Traditionally, multiple sclerosis has been categorised by distinct clinical descriptors-relapsing-remitting, secondary progressive, and primary progressive-for patient care, research, and regulatory approval of medications. Accumulating evidence suggests that the clinical course of multiple sclerosis is better considered as a continuum, with contributions from concurrent pathophysiological processes that vary across individuals and over time. The apparent evolution to a progressive course reflects a partial shift from predominantly localised acute injury to widespread inflammation and neurodegeneration, coupled with failure of compensatory mechanisms, such as neuroplasticity and remyelination. Ageing increases neural susceptibility to injury and decreases resilience. These observations encourage a new consideration of the course of multiple sclerosis as a spectrum defined by the relative contributions of overlapping pathological and reparative or compensatory processes. New understanding of key mechanisms underlying progression and measures to quantify progressive pathology will potentially have important and beneficial implications for clinical care, treatment targets, and regulatory decision-making.
 The factor that is most relevant and strongly associated with the clinical course of multiple sclerosis is chronological age. Very young patients exclusively have relapsing remitting disease, whereas those with later onset disease face a more rapid development of permanent disability. For people with progressive multiple sclerosis, the poor response to current disease modifying therapies might be related to ageing in the immune system and CNS. Ageing is also associated with increased risks of side-effects caused by some multiple sclerosis therapies. Both somatic and reproductive ageing processes might contribute to development of progressive multiple sclerosis. Understanding the role of ageing in immune and neural cell function in patients with multiple sclerosis might be key to halting non-relapse-related progression. The growing literature on potential therapies that target senescent cells and ageing processes might provide effective strategies for remyelination and neuroprotection.
 Multiple sclerosis is a complex autoimmune disease, and several therapies for multiple sclerosis have been developed and widely used. However, existing medications for multiple sclerosis were far from satisfactory due to their failure to suppress relapses and alleviate disease progression. Novel drug targets for multiple sclerosis prevention are still needed. We performed Mendelian randomization to explore potential drug targets for multiple sclerosis using summary statistics from the International Multiple Sclerosis Genetics Consortium (nCase = 47 429, nControl = 68 374) and further replicated in UK Biobank (nCase = 1356, nControl = 395 209) and FinnGen cohorts (nCase = 1326, nControl = 359 815). Genetic instruments for 734 plasma and 154 CSF proteins were obtained from recently published genome-wide association studies. The reverse causality detection using bidirectional Mendelian randomization analysis and Steiger filtering, Bayesian co-localization, and phenotype scanning that searched previously reported genetic variant-trait associations were implemented to consolidate the Mendelian randomization findings further. In addition, the protein-protein interaction network was performed to reveal potential associations among proteins and/or present multiple sclerosis medications. At Bonferroni significance (P < 5.63 × 10-5), Mendelian randomization analysis revealed six protein-multiple sclerosis pairs. In plasma, per standard deviation increase in FCRL3, TYMP and AHSG had a protective effect. Odds ratios for the proteins above were 0.83 (95% CI, 0.79-0.89), 0.59 (95% CI, 0.48-0.71) and 0.88 (95% CI, 0.83-0.94), respectively. In CSF, per 10-fold increase in MMEL1 (OR, 5.03; 95% CI, 3.42-7.41) increased the risk of multiple sclerosis, while SLAMF7 (OR, 0.42; 95% CI, 0.29-0.60) and CD5L (OR, 0.30; 95%CI, 0.18-0.52) decreased the risk. None of the six proteins had reverse causality. Bayesian co-localization suggested that FCRL3 [coloc.abf-posterior probability of hypothesis 4 (PPH4) = 0.889], TYMP (coloc.susie-PPH4 = 0.896), AHSG (coloc.abf-PPH4 = 0.957, coloc.susie-PPH4 = 0.973), MMEL1 (coloc.abf-PPH4 = 0.930) and SLAMF7 (coloc.abf-PPH4 = 0.947) shared the same variant with multiple sclerosis. FCRL3, TYMP and SLAMF7 interacted with target proteins of current multiple sclerosis medications. MMEL1 was replicated in both UK Biobank and FinnGen cohorts. Our integrative analysis suggested that genetically determined levels of circulating FCRL3, TYMP, AHSG, CSF MMEL1 and SLAMF7 had causal effects on multiple sclerosis risk. These findings suggested those five proteins might be promising drug targets for multiple sclerosis and warrant further clinical investigation, especially FCRL3 and SLAMF7.
 The multiple sclerosis (MS) neurotherapeutic landscape is rapidly evolving. New disease-modifying therapies (DMTs) with improved efficacy and safety, in addition to an expanding pipeline of agents with novel mechanisms, provide more options for patients with MS. While treatment of MS neuroinflammation is well tailored in the existing DMT armamentarium, concerted efforts are currently underway for identifying neuropathological targets and drug discovery for progressive MS. There is also ongoing research to develop agents for remyelination and neuroprotection. Further insights are needed to guide DMT initiation and sequencing as well as to determine the role of autologous stem cell transplantation in relapsing and progressive MS. This review provides a summary of these updates.
 Observational studies have suggested a suspected association between varicella-zoster virus (VZV) infection and multiple sclerosis (MS), but the connection has remained unclear. The aim of the present study is to evaluate the causal relationship between chickenpox which is caused by VZV infection and MS. We performed a two-sample Mendelian randomization analysis to investigate the association of chickenpox with MS using summary statistics from genome-wide association studies (GWAS). The GWAS summary statistics data for chickenpox was from the 23andMe cohort including 107 769 cases and 15 982 controls. A large summary of statistical data from the International Multiple Sclerosis Genetics Consortium (IMSGC) was used as the outcome GWAS data set, including 14 802 MS cases and 26 703 controls. We found evidence of a significant association between genetically predicted chickenpox and risk of MS (odds ratio [OR] = 35.27, 95% confidence interval [CI] = 22.97-54.17, p = 1.46E-59). Our findings provided evidence indicating a causal effect of chickenpox on MS. Further elucidations of this association and underlying mechanisms are needed for identifying feasible interventions to promote MS prevention.
 The current diagnostic criteria for pediatric onset multiple sclerosis (POMS) are summarized, as well as the evidence for performance of the most recent iteration of McDonald criteria in the pediatric population. Next, the varied roles of MRI in POMS are reviewed, including diagnostic considerations and research-based utilization. The primary role of bloodwork and cerebrospinal fluid studies in the diagnosis of POMS is to rule out disease mimics. Prognostically, POMS portends a more inflammatory course with higher relapse rate and disability reached at younger ages compared with AOMS counterparts. As such, there is an emerging trend toward the earlier use of highly efficacious disease modifying therapies to target prompt immunomodulatory disease control. Current POMS disease modifying therapies (DMTs) and active clinical POMS trials are detailed.
 Multiple sclerosis is a chronic inflammatory disease of the CNS that results from the interplay between heritable and environmental factors. Mounting evidence from different fields of research supports the pivotal role of the Epstein-Barr virus (EBV) in the development of multiple sclerosis. However, translating this knowledge into clinically actionable information requires a better understanding of the mechanisms linking EBV to pathophysiology. Ongoing research is trying to clarify whether EBV causes neuroinflammation via autoimmunity or antiviral immunity, and if the interaction of EBV with genetic susceptibility to multiple sclerosis can explain why a ubiquitous virus promotes immune dysfunction in susceptible individuals. If EBV also has a role in driving disease activity, the characterisation of this role will help diagnosis, prognosis, and treatment in people with multiple sclerosis. Ongoing clinical trials targeting EBV and new anti-EBV vaccines provide hope for future treatments and preventive interventions.
 Multiple sclerosis is often diagnosed in patients who are planning on having children. Although multiple sclerosis does not negatively influence most pregnancy outcomes, less is known regarding the effects of fetal exposure to novel disease-modifying therapies (DMTs). The withdrawal of some DMTs during pregnancy can modify the natural history of multiple sclerosis, resulting in a substantial risk of pregnancy-related relapse and disability. Drug labels are typically restrictive and favour fetal safety over maternal safety. Emerging data reporting outcomes in neonates exposed to DMTs in utero and through breastfeeding will allow for more careful and individualised treatment decisions. This emerging research is particularly important to guide decision making in women with high disease activity or who are treated with DMTs associated with risk of discontinuation rebound. As increasing data are generated in this field, periodic updates will be required to provide the most up to date guidance on how best to achieve multiple sclerosis stability during pregnancy and post partum, balanced with fetal and newborn safety.
 BACKGROUND AND PURPOSE: Multiple sclerosis (MS) is an unpredictable disease characterised by a highly variable disease onset and clinical course. Three main clinical phenotypes have been described. However, distinguishing between the two progressive forms of MS can be challenging for clinicians. This article examines how the diagnostic definitions of progressive MS impact clinical research, the design of clinical trials and, ultimately, treatment decisions. METHODS: We carried out an extensive review of the literature highlighting differences in the definition of progressive forms of MS, and the importance of assessing the extent of the ongoing inflammatory component in MS when making treatment decisions. RESULTS: Inconsistent results in phase III clinical studies of treatments for progressive MS, may be attributable to differences in patient characteristics (e.g., age, clinical and radiological activity at baseline) and endpoint definitions. In both primary and secondary progressive MS, patients who are younger and have more active disease will derive the greatest benefit from the available treatments. CONCLUSIONS: We recommend making treatment decisions based on the individual patient's pattern of disease progression, as well as functional, clinical and imaging parameters, rather than on their clinical phenotype. Because the definition of progressive MS differs across clinical studies, careful selection of eligibility criteria and study endpoints is needed for future studies in patients with progressive MS.
 Multiple sclerosis (MS) is the most prevalent nontraumatic disabling neurologic condition among young adults worldwide. The diagnosis and management of MS is complex. The goal of this review is to provide an updated and practical approach to the diagnosis and treatment approaches in MS, emphasizing current understanding of immunopathogenesis, recent advances, and future directions, for both MS and non-MS clinicians.
 Epidemiological studies have provided compelling evidence that multiple sclerosis (MS) is a rare complication of infection with the Epstein-Barr virus (EBV), a herpesvirus that infects more than 90% of the global population. This link was long suspected because the risk of MS increases markedly after infectious mononucleosis (symptomatic primary EBV infection) and with high titres of antibodies to specific EBV antigens. However, it was not until 2022 that a longitudinal study demonstrated that MS risk is minimal in individuals who are not infected with EBV and that it increases over 30-fold following EBV infection. Over the past few years, a number of studies have provided clues on the underlying mechanisms, which might help us to develop more targeted treatments for MS. In this Review, we discuss the evidence linking EBV to the development of MS and the mechanisms by which the virus is thought to cause the disease. Furthermore, we discuss implications for the treatment and prevention of MS, including the use of antivirals and vaccines.
 In recent years, the use of magnetic resonance imaging (MRI) for the diagnostic work-up of multiple sclerosis (MS) has evolved considerably. The 2017 McDonald criteria show high sensitivity and accuracy in predicting a second clinical attack in patients with a typical clinically isolated syndrome and allow an earlier diagnosis of MS. They have been validated, are evidence-based, simplify the clinical use of MRI criteria and improve MS patients' management. However, to limit the risk of misdiagnosis, they should be applied by expert clinicians only after the careful exclusion of alternative diagnoses. Recently, new MRI markers have been proposed to improve diagnostic specificity for MS and reduce the risk of misdiagnosis. The central vein sign and chronic active lesions (i.e., paramagnetic rim lesions) may increase the specificity of MS diagnostic criteria, but further effort is necessary to validate and standardize their assessment before implementing them in the clinical setting. The feasibility of subpial demyelination assessment and the clinical relevance of leptomeningeal enhancement evaluation in the diagnostic work-up of MS appear more limited. Artificial intelligence tools may capture MRI attributes that are beyond the human perception, and, in the future, artificial intelligence may complement human assessment to further ameliorate the diagnostic work-up and patients' classification. However, guidelines that ensure reliability, interpretability, and validity of findings obtained from artificial intelligence approaches are still needed to implement them in the clinical scenario. This review provides a summary of the most recent updates regarding the application of MRI for the diagnosis of MS.
 PURPOSE OF REVIEW: In this review, we provide a comprehensive update on current scientific advances and emerging therapeutic approaches in the field of multiple sclerosis. RECENT FINDINGS: Multiple sclerosis (MS) is a common disorder characterized by inflammation and degeneration within the central nervous system (CNS). MS is the leading cause of non-traumatic disability in the young adult population. Through ongoing research, an improved understanding of the disease underlying mechanisms and contributing factors has been achieved. As a result, therapeutic advancements and interventions have been developed specifically targeting the inflammatory components that influence disease outcome. Recently, a new type of immunomodulatory treatment, known as Bruton tyrosine kinase (BTK) inhibitors, has surfaced as a promising tool to combat disease outcomes. Additionally, there is a renewed interested in Epstein-Barr virus (EBV) as a major potentiator of MS. Current research efforts are focused on addressing the gaps in our understanding of the pathogenesis of MS, particularly with respect to non-inflammatory drivers. Significant and compelling evidence suggests that the pathogenesis of MS is complex and requires a comprehensive, multilevel intervention strategy. This review aims to provide an overview of MS pathophysiology and highlights the most recent advances in disease-modifying therapies and other therapeutic interventions.
 Across its clinical development program, ocrelizumab demonstrated efficacy in improving clinical outcomes in multiple sclerosis, including annualized relapse rates and confirmed disability progression. However, as with any new treatment, it was unclear how this efficacy would translate into real-world clinical practice. The objective of this study was to systematically collate the published real-world clinical effectiveness data for ocrelizumab in relapsing remitting multiple sclerosis and primary progressive multiple sclerosis. A search strategy was developed in MEDLINE and Embase to identify articles reporting real-world evidence in people with relapsing remitting multiple sclerosis or primary progressive multiple sclerosis receiving treatment with ocrelizumab. The search focused on English language articles only but was not limited by the country in which the study was conducted or the time frame of the study. Additional manual searches of relevant websites were also performed. Fifty-two studies were identified reporting relevant evidence. Real-world effectiveness data for ocrelizumab were consistently favorable, with reductions in relapse rate and disease progression rates similar to those reported in the OPERA I/OPERA II and ORATORIO clinical trials, including in studies with more diverse patient populations not well represented in the pivotal trials. Although direct comparisons are confounded by lack of randomization of treatments, outcomes reported suggest that ocrelizumab has a similar or greater efficacy than other therapy options. Initial real-world effectiveness data for ocrelizumab appear favorable and consistent with results reported in clinical trials, providing clinicians with an efficacious option to treat patients with multiple sclerosis.
 Main target in palliative care (PC) is burden care of patients and their families, with the aim to reduce suffering through the management of symptoms, rehabilitation, psychosocial issues, and spiritual well-being, using a multidisciplinary approach. Multiple sclerosis (MS) is a chronic disease which induces physical and psychosocial symptoms, with a significant impact on the quality of life. As a consequence, despite advances in research in disease-modifying drugs, MS remains a life-limiting disease with symptoms negatively impacting the lives of MS patients and their families. PC has been developed for end-of-life treatment in oncology, being little used in MS. Specific issues in MS, like pain due to spasticity, requires a different approach respect to cancer pain management. Moreover, it is difficult to anticipate life expectancy in people with severe MS, who often need palliative care for a long extended period. PC teams are trained to keep open full and competent lines of communication about symptoms and disease progression, advanced care planning, and end-of-life issues and wishes. Many studies investigated the effects of home-based PC in advanced MS, showing weak evidences about the efficacy of PC versus usual care in MS. However, current evidence does not support or refute the routine use of PC interventions for people with MS.
 BACKGROUND: Anxiety symptoms and anxiety disorders are prevalent and burdensome, yet poorly managed in multiple sclerosis (MS). Indeed, anxiety disorders occur in 22% of people with MS, and anxiety can negatively impact physical function, cognition, and quality of life. Currently, there are no treatment guidelines available for anxiety in MS, based on limited information regarding the efficacy of pharmacotherapy and psychotherapy. Exercise training may be a promising avenue for treatment of anxiety in MS, and this is based, in part, on a wealth of evidence in the general population of adults. This review provides an overview of anxiety and evidence from meta-analyses and systematic reviews for current treatments options in the general population and MS. We further make a case for exercise as a novel treatment approach that requires focal examination in persons with MS. METHODS: We conducted a scoping review of available research, including systematic reviews and meta-analyses, on anxiety and its prevalence, predictors, consequences, and treatments in MS. We then noted limitations with existing evidence regarding treatment options, and then provided a backdrop based on evidence from the general population for the novel proposition of exercise as treatment of anxiety in MS. RESULTS: Pharmacotherapy and psychotherapy treatments of anxiety may be efficacious, but come with significant limitations, especially for persons with MS. Exercise is a promising novel avenue for treatment of anxiety in MS, and has a positive side-effect profile. CONCLUSION: Anxiety is under-investigated and poorly treated in MS. There is a paucity of evidence for the relationship between exercise training and anxiety in MS, but the evidence in the general population supports the urgent need for systematic examination of the efficacy of exercise in treating anxiety symptoms and disorders in persons with MS.
 PURPOSE OF REVIEW: Polypharmacy, the use of ≥ 5 medications, is common in people with multiple sclerosis and is associated with negative outcomes. The use of multiple medications is common for symptom management in people with multiple sclerosis, but risks drug-drug interactions and additive side effects. Multiple sclerosis providers should therefore focus on the appropriateness and risks versus benefits of pharmacotherapy in each patient. This review describes the prevalence and risks associated with polypharmacy in people with multiple sclerosis and offers strategies to identify and mitigate inappropriate polypharmacy. RECENT FINDINGS: Research in people with multiple sclerosis has identified risk factors and negative outcomes associated with polypharmacy. Medication class-specific investigations highlight their contribution to potentially inappropriate polypharmacy in people with multiple sclerosis. People with multiple sclerosis are at risk for inappropriate polypharmacy. Multiple sclerosis providers should review medications and consider their appropriateness and potential for deprescribing within the context of each patient.
 Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) that results in significant neurodegeneration in the majority of those affected and is a common cause of chronic neurological disability in young adults(1,2). Here, to provide insight into the potential mechanisms involved in progression, we conducted a genome-wide association study of the age-related MS severity score in 12,584 cases and replicated our findings in a further 9,805 cases. We identified a significant association with rs10191329 in the DYSF-ZNF638 locus, the risk allele of which is associated with a shortening in the median time to requiring a walking aid of a median of 3.7 years in homozygous carriers and with increased brainstem and cortical pathology in brain tissue. We also identified suggestive association with rs149097173 in the DNM3-PIGC locus and significant heritability enrichment in CNS tissues. Mendelian randomization analyses suggested a potential protective role for higher educational attainment. In contrast to immune-driven susceptibility(3), these findings suggest a key role for CNS resilience and potentially neurocognitive reserve in determining outcome in MS.
 The last thirty years have led to the introduction of treatments that reduce the frequency of relapses and slow the progression of multiple sclerosis. They must be prescribed early, chosen according to the form of the disease and actively monitored. Symptomatic treatments complete the treatment.
 PURPOSE OF REVIEW: Cortical lesions are an established pathological feature of multiple sclerosis, develop from the earliest disease stages and contribute to disease progression. Here, we discuss current imaging approaches for detecting cortical lesions in vivo and their contribution for improving our understanding of cortical lesion pathogenesis as well as their clinical significance. RECENT FINDINGS: Although a variable portion of cortical lesions goes undetected at clinical field strength and even at ultra-high field MRI, their evaluation is still clinically relevant. Cortical lesions are important for differential multiple sclerosis (MS) diagnosis, have relevant prognostic value and independently predict disease progression. Some studies also show that cortical lesion assessment could be used as a therapeutic outcome target in clinical trials. Advances in ultra-high field MRI not only allow increased cortical lesion detection in vivo but also the disclosing of some interesting features of cortical lesions related to their pattern of development and evolution as well to the nature of associated pathological changes, which might prove relevant for better understanding the pathogenesis of these lesions. SUMMARY: Despite some limitations, imaging of cortical lesions is of paramount importance in MS for elucidating disease mechanisms as well as for improving patient management in clinic.
 The emphasis on mechanisms driving multiple sclerosis (MS) symptomatic worsening suggests that we move beyond categorical clinical classifiers such as relapsing-remitting MS (RR-MS) and progressive MS (P-MS). Here, we focus on the clinical phenomenon progression independent of relapse activity (PIRA), which begins early in the disease course. PIRA occurs throughout MS, becoming more phenotypically evident as patients age. The underlying mechanisms for PIRA include chronic-active demyelinating lesions (CALs), subpial cortical demyelination, and nerve fiber injury following demyelination. We propose that much of the tissue injury associated with PIRA is driven by autonomous meningeal lymphoid aggregates, present before disease onset and unresponsive to current therapeutics. Recently, specialized magnetic resonance imaging (MRI) has identified and characterized CALs as paramagnetic rim lesions in humans, enabling novel radiographic-biomarker-clinical correlations to further understand and treat PIRA.

 BACKGROUND: Obesity reportedly increases the risk for developing multiple sclerosis (MS), but little is known about its association with disability accumulation. METHODS: This nationwide longitudinal cohort study included 1066 individuals with newly diagnosed MS from the German National MS cohort. Expanded Disability Status Scale (EDSS) scores, relapse rates, MRI findings and choice of immunotherapy were compared at baseline and at years 2, 4 and 6 between obese (body mass index, BMI ≥30 kg/m(2)) and non-obese (BMI <30 kg/m(2)) patients and correlated with individual BMI values. RESULTS: Presence of obesity at disease onset was associated with higher disability at baseline and at 2, 4 and 6 years of follow-up (p<0.001). Median time to reach EDSS 3 was 0.99 years for patients with BMI ≥30 kg/m(2) and 1.46 years for non-obese patients. Risk to reach EDSS 3 over 6 years was significantly increased in patients with BMI ≥30 kg/m(2) compared with patients with BMI <30 kg/m(2) after adjustment for sex, age, smoking (HR 1.87; 95% CI 1.3 to 2.6; log-rank test p<0.001) and independent of disease-modifying therapies. Obesity was not significantly associated with higher relapse rates, increased number of contrast-enhancing MRI lesions or higher MRI T2 lesion burden over 6 years of follow-up. CONCLUSIONS: Obesity in newly diagnosed patients with MS is associated with higher disease severity and poorer outcome. Obesity management could improve clinical outcome of MS.
 IMPORTANCE: Ocrelizumab, a humanized monoclonal antibody targeted against CD20+ B cells, reduces the frequency of relapses by 46% and disability worsening by 40% compared with interferon beta 1a in relapsing-remitting multiple sclerosis (MS). Rituximab, a chimeric monoclonal anti-CD20 agent, is often prescribed as an off-label alternative to ocrelizumab. OBJECTIVE: To evaluate whether the effectiveness of rituximab is noninferior to ocrelizumab in relapsing-remitting MS. DESIGN, SETTING, AND PARTICIPANTS: This was an observational cohort study conducted between January 2015 and March 2021. Patients were included in the treatment group for the duration of study therapy and were recruited from the MSBase registry and Danish MS Registry (DMSR). Included patients had a history of relapsing-remitting MS treated with ocrelizumab or rituximab, a minimum 6 months of follow-up, and sufficient data to calculate the propensity score. Patients with comparable baseline characteristics were 1:6 matched with propensity score on age, sex, MS duration, disability (Expanded Disability Status Scale), prior relapse rate, prior therapy, disease activity (relapses, disability accumulation, or both), magnetic resonance imaging lesion burden (missing values imputed), and country. EXPOSURE: Treatment with ocrelizumab or rituximab after 2015. MAIN OUTCOMES AND MEASURES: Noninferiority comparison of annualized rate of relapses (ARRs), with a prespecified noninferiority margin of 1.63 rate ratio. Secondary end points were relapse and 6-month confirmed disability accumulation in pairwise-censored groups. RESULTS: Of the 6027 patients with MS who were treated with ocrelizumab or rituximab, a total of 1613 (mean [SD] age; 42.0 [10.8] years; 1089 female [68%]) fulfilled the inclusion criteria and were included in the analysis (898 MSBase, 715 DMSR). A total of 710 patients treated with ocrelizumab (414 MSBase, 296 DMSR) were matched with 186 patients treated with rituximab (110 MSBase, 76 DMSR). Over a pairwise censored mean (SD) follow-up of 1.4 (0.7) years, the ARR ratio was higher in patients treated with rituximab than in those treated with ocrelizumab (rate ratio, 1.8; 95% CI, 1.4-2.4; ARR, 0.20 vs 0.09; P < .001). The cumulative hazard of relapses was higher among patients treated with rituximab than those treated with ocrelizumab (hazard ratio, 2.1; 95% CI, 1.5-3.0). No difference in the risk of disability accumulation was observed between groups. Results were confirmed in sensitivity analyses. CONCLUSION: In this noninferiority comparative effectiveness observational cohort study, results did not show noninferiority of treatment with rituximab compared with ocrelizumab. As administered in everyday practice, rituximab was associated with a higher risk of relapses than ocrelizumab. The efficacy of rituximab and ocrelizumab administered at uniform doses and intervals is being further evaluated in randomized noninferiority clinical trials.
 Multiple sclerosis (MS) is a chronic progressive demyelinating disease of the central nervous system (CNS), which also affects the autonomic nervous system (ANS). Manifestations of MS in the ANS include urological, sexual, gastrointestinal, cardiovascular, and thermoregulatory disorders as well as increased fatigue. These problems are common yet are often underestimated due to the non-specificity of the symptoms and the limited evaluation of the ANS in the usual clinical practice. Most of these symptoms seem to be related to localized lesions in the CNS. However, the mechanisms by which these disorders are caused in MS have not been fully investigated, thus preventing any focused etiological treatment. The most common disorders of the ANS in MS represent a challenge for clinicians due to the variability of the clinical picture and our minimal data on their diagnosis and treatment. Early diagnosis and initiation of individualized treatment regimens, often in need of multiple approaches, seem to yield the best results in managing ANS dysfunction in MS patients.
 OBJECTIVE: Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the central nervous system (CNS). The most common clinical manifestations of MS are spasticity, pain, vesico-urethral disorders, cognitive impairments, chronic fatigue and sexual dysfunction. This review aims to explore the possible therapeutic options for managing sexual dysfunction in people with MS (PwMS). METHOD: A thorough search of the PubMed Medline database was performed. Records were limited to clinical studies published between 01/01/2010 up to 01/01/2022. The results were screened by the authors in pairs. RESULTS: The search identified 36 records. After screening, 9 records met the inclusion-exclusion criteria and were assessed. The pharmacological approaches investigated the effectiveness of sildenafil, tadalafil and onabotulinumtoxinA. Of the interventional studies the non-pharmacological investigated, the effectiveness of aquatic exercises, the application of pelvic floor exercises,the combination of pelvic floor exercises and mindfulness technique, the combination of pelvic floor exercises and electro muscular stimulation with electromyograph biofeedback, the application of yoga techniques and the efficacy of assistive devices like the clitoral vacuum suction device and the vibration device. CONCLUSION: The management of sexual dysfunction in PwMS needs to be further investigated. A team of healthcare professionals should be involved in the management of SD in order to address not only the primary (MS-related) SD symptoms but the secondary and tertiary as well. The main limitations that were identified in the existing literature were related to MS disease features, sample characteristics and evaluation tools and batteries.

 Multiple sclerosis (MS) represents a chronic immune-mediated neurodegenerative disease of the central nervous system that generally debuts around the age of 20-30 years. Still, in recent years, MS has been increasingly recognized among the pediatric population, being characterized by several peculiar features compared to adult-onset disease. Unfortunately, the etiology and disease mechanisms are poorly understood, rendering the already limited MS treatment options with uncertain efficacy and safety in pediatric patients. Thus, this review aims to shed some light on the progress in MS therapeutic strategies specifically addressed to children and adolescents. In this regard, the present paper briefly discusses the etiology, risk factors, comorbidities, and diagnosis possibilities for pediatric-onset MS (POMS), further moving to a detailed presentation of current treatment strategies, recent clinical trials, and emerging alternatives. Particularly, promising care solutions are indicated, including new treatment formulations, stem cell therapies, and cognitive training methods.
 BACKGROUND: Epidemiological studies have shown conflicting results between antibiotic use and multiple sclerosis (MS) risks. The present systematic review and meta-analysis were conducted to assess the association between antibiotic use and the risk of MS. METHODS: PubMed, Scopus, Embase, Web of Science, and Google Scholar as well as reference lists of retrieved studies were searched systematically to identify studies were assessed the relationship between antibiotic use and MS up to September 24, 2022. Random-effects model was used for the calculation of pooled Odds ratio (OR) and 95% confidence intervals (CI). RESULTS: Five independent studies containing 47,491 participants were included in the meta-analysis. The overall results of included studies showed a non-significant positive association between antibiotic use (OR overall=1.01, 95%CI: 0.75-1.37) and a non-significant negative association between penicillin use (OR overall= 0.83; 95%CI: 0.62-1.13) and MS risk. Heterogeneity was (I(2)=90.1, P (heterogeneity) < 0.001) and (I(2)=90.7, P (heterogeneity) < 0.001) in antibiotics and penicillin use groups respectively. CONCLUSION: Our meta-analysis did not show a significant association between antibiotic or penicillin use with the risk of MS. However, due to the limitations of this study, further well-designed studies are required to confirm our findings.
 PURPOSE OF REVIEW: Multiple sclerosis is characterized by a diverse and complex pathology. Clinical relapses, the hallmark of the disease, are accompanied by focal white matter lesions with intense inflammatory and demyelinating activity. Prevention of these relapses has been the major focus of pharmaceutical development, and it is now possible to dramatically reduce this inflammatory activity. Unfortunately, disability accumulation persists for many people living with multiple sclerosis owing to ongoing damage within existing lesions, pathology outside of discrete lesions, and other yet unknown factors. Understanding this complex pathological cascade will be critical to stopping progressive multiple sclerosis. Positron emission tomography uses biochemically specific radioligands to quantitatively measure pathological processes with molecular specificity. This review examines recent advances in the understanding of multiple sclerosis facilitated by positron emission tomography and identifies future avenues to expand understanding and treatment options. RECENT FINDINGS: An increasing number of radiotracers allow for the quantitative measurement of inflammatory abnormalities, de- and re-myelination, and metabolic disruption associated with multiple sclerosis. The studies have identified contributions of ongoing, smoldering inflammation to accumulating tissue injury and clinical worsening. Myelin studies have quantified the dynamics of myelin loss and recovery. Lastly, metabolic changes have been found to contribute to symptom worsening. The molecular specificity facilitated by positron emission tomography in people living with multiple sclerosis will critically inform efforts to modulate the pathology leading to progressive disability accumulation. Existing studies show the power of this approach applied to multiple sclerosis. This armamentarium of radioligands allows for new understanding of how the brain and spinal cord of people is impacted by multiple sclerosis.
 Multiple sclerosis (MS) is heterogeneous with respect to outcomes, and evaluating possible heterogeneity of treatment effect (HTE) is of high interest. HTE is non-random variation in the magnitude of a treatment effect on a clinical outcome across levels of a covariate (i.e. a patient attribute or set of attributes). Multiple statistical techniques can evaluate HTE. The simplest but most bias-prone is conventional one variable-at-a-time subgroup analysis. Recently, multivariable predictive approaches have been promoted to provide more patient-centered results, by accounting for multiple relevant attributes simultaneously. We review approaches used to estimate HTE in clinical trials of MS.
 More than 10 disease-modifying therapies (DMT) are approved by the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA) for the treatment of multiple sclerosis (MS) and new therapeutic options are on the horizon. Due to different underlying therapeutic mechanisms, a more individualized selection of DMTs in MS is possible, taking into account the patient's current situation. Therefore, concomitant treatment of various comorbid conditions, including autoimmune mediated disorders such as rheumatoid arthritis, should be considered in MS patients. Because the pathomechanisms of autoimmunity partially overlap, DMT could also treat concomitant inflammatory diseases and simplify the patient's treatment. In contrast, the exacerbation and even new occurrence of several autoimmune diseases have been reported as a result of immunomodulatory treatment of MS. To simplify treatment and avoid disease exacerbation, knowledge of the beneficial and adverse effects of DMT in other autoimmune disorders is critical. Therefore, we conducted a literature search and described the beneficial and adverse effects of approved and currently studied DMT in a large number of comorbid autoimmune diseases, including rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel diseases, cutaneous disorders including psoriasis, Sjögren´s syndrome, systemic lupus erythematosus, systemic vasculitis, autoimmune hepatitis, and ocular autoimmune disorders. Our review aims to facilitate the selection of an appropriate DMT in patients with MS and comorbid autoimmune diseases.
 Previous studies revealed a latitudinal gradient of multiple sclerosis (MS) prevalence, increasing by moving from the equator to the poles. The duration and quality of an individual's exposure to sunlight vary with latitude. Skin exposure to sunlight activates vitamin D synthesis, while light absence, as perceived by the eyes, activates melatonin synthesis in the pineal gland. Vitamin D or melatonin deficiency/insufficiency or overdose can occur at any latitude due to specific lifestyles and diets. Moving away from the equator, especially beyond 37°, decreases vitamin D while raising melatonin. Furthermore, melatonin synthesis increases in cold habitats like northern countries. Since melatonin's beneficial role was shown in MS, it is expected that northern countries whose individuals have higher endogenous melatonin should show a lower MS prevalence; however, these are ranked with the highest scores. In addition, countries like the United States and Canada have uncontrolled over-the-counter usage. In high latitudes, vitamin D deficiency and a higher MS prevalence persist even though vitamin D is typically compensated for by supplementation and not sunlight. Recently, we found that prolonged darkness increased MS melatonin levels, mimicking the long-term increase in northern countries. This caused a reduction in cortisol and increased infiltration, inflammation, and demyelination, which were all rescued by constant light therapy. In this review, we explain melatonin and vitamin D's possible roles in MS prevalence. The possible causes in northern countries are then discussed. Finally, we suggest strategies to treat MS by manipulating vitamin D and melatonin, preferably with sunlight or darkness, not supplements.
 Multiple sclerosis (MS) is the most common chronic inflammatory neurological disease. The emergence of disease-modifying therapies (DMTs) has greatly improved disease activity control and progression of disability in MS patients. DMTs differ in their mode of action, route of administration, efficacy, and safety profiles, offering multiple options for clinicians. Personalized medicine aims at tailoring the therapeutic strategy to patients' characteristics and disease activity but also patients' needs and preferences. New therapeutic options have already changed treatment paradigms for patients with active relapsing MS (RMS). The traditional approach consists in initiating treatment with moderate-efficacy DMTs and subsequently, escalating to higher-efficacy DMTs when there is evidence of clinical and/or radiological breakthrough activity. Recent real-world studies suggest that initiation of high-efficacy DMTs from disease onset can improve long-term outcomes for RMS patients. In this article, we review different treatment strategies and discuss challenges associated with personalized therapy.

 Depressive disorders can occur in up to 50% of people with multiple sclerosis in their lifetime. If left untreated, comorbid major depressive disorders may not spontaneously remit and is associated with an increased morbidity and mortality. Conversely, epidemiological evidence supports increased psychiatric visit as a significant prodromal event prior to diagnosis of MS. Are there common molecular pathways that contribute to the co-development of MS and psychiatric illnesses? We discuss immune cells that are dysregulated in MS and how such dysregulation can induce or protect against depressive symptoms. This is not meant to be a comprehensive review of all molecular pathways but rather a framework to guide future investigations of immune responses in depressed versus euthymic people with MS. Currently, there is weak evidence supporting the use of antidepressant medication in comorbid MS patients. It is our hope that by better understanding the neuroimmune crosstalk in the context of depression in MS, we can enhance the potential for future therapeutic options.
 BACKGROUND: Phase 3 clinical trials for disease-modifying therapies in relapsing-remitting multiple sclerosis (RRMS) have utilized a limited number of conventional designs with a high degree of success. However, these designs limit the types of questions that can be addressed, and the time and cost required. Moreover, trials involving people with progressive multiple sclerosis (MS) have been less successful. OBJECTIVE: The objective of this paper is to discuss complex innovative trial designs, intermediate and composite outcomes and to improve the efficiency of trial design in MS and broaden questions that can be addressed, particularly as applied to progressive MS. METHODS: We held an international workshop with experts in clinical trial design. RESULTS: Recommendations include increasing the use of complex innovative designs, developing biomarkers to enrich progressive MS trial populations, prioritize intermediate outcomes for further development that target therapeutic mechanisms of action other than peripherally mediated inflammation, investigate acceptability to people with MS of data linkage for studying long-term outcomes of clinical trials, use Bayesian designs to potentially reduce sample sizes required for pediatric trials, and provide sustained funding for platform trials and registries that can support pragmatic trials. CONCLUSION: Novel trial designs and further development of intermediate outcomes may improve clinical trial efficiency in MS and address novel therapeutic questions.
 Extracellular vesicles (EVs) are a heterogeneous family of extracellular structures bounded by a phospholipid bilayer, released by all cell types in various biological fluids, such as blood and cerebrospinal fluid (CSF), playing important roles in intercellular communication, both locally and systemically. EVs carry and deliver a variety of bioactive molecules (proteins, nucleic acids, lipids and metabolites), conferring epigenetic and phenotypic changes to the recipient cells and thus resulting as important mediators of both homeostasis and pathogenesis. In neurological diseases, such as multiple sclerosis (MS), the EV ability to cross Blood-Brain Barrier (BBB), moving from central nervous system (CNS) to the peripheral circulation and vice versa, has increased the interest in EV study in the neurological field. In the present review, we will provide an overview of the recent advances made in understanding the pathogenic role of EVs regarding the immune response, the BBB dysfunction and the CNS inflammatory processes.
 Multiple sclerosis (MS) is an autoimmune, neurodegenerative disease that is driven by immune system-mediated demyelination of nerve axons. While diseases such as cancer, HIV, malaria and even COVID have realised notable benefits from the attention of the mathematical community, MS has received significantly less attention despite the increasing disease incidence rates, lack of curative treatment, and long-term impact on patient well-being. In this review, we highlight existing, MS-specific mathematical research and discuss the outstanding challenges and open problems that remain for mathematicians. We focus on how both non-spatial and spatial deterministic models have been used to successfully further our understanding of T cell responses and treatment in MS. We also review how agent-based models and other stochastic modelling techniques have begun to shed light on the highly stochastic and oscillatory nature of this disease. Reviewing the current mathematical work in MS, alongside the biology specific to MS immunology, it is clear that mathematical research dedicated to understanding immunotherapies in cancer or the immune responses to viral infections could be readily translatable to MS and might hold the key to unlocking some of its mysteries.
 BACKGROUND: Multiple Sclerosis (MS) is a chronic neuroinflammatory disease that affects the central nervous system. Asymmetry is one of the finding in brain MRI of these patients, which is related to the debilitating symptoms of the disease. This study aimed to investigate and compare the thalamic asymmetry in MS patients and its relationship with other MRI and clinical findings of these patients. METHODS: This cross-sectional study conducted on 83 patients with relapse-remitting MS (RRMS), 43 patients with secondary progressive MS (SPMS), and 89 healthy controls. The volumes of total intracranial, total gray matter, total white matter, lesions, thalamus, and also the thalamic asymmetry indices were calculated. The 9-hole peg test (9-HPT) and Expanded Disability Status Scale (EDSS) were assessed as clinical findings. RESULTS: We showed that the normalized whole thalamic volume in healthy subjects was higher than MS patients (both RRMS and SPMS). Thalamic asymmetry index (TAI) was significantly different between RRMS patients and SPMS patients (p = 0.011). The absolute value of TAI was significantly lower in healthy subjects than in RRMS (p < 0.001) and SPMS patients (p < 0.001), and SPMS patients had a higher absolute TAI compared to RRMS patients (p = 0.037). CONCLUSIONS: In this cross-sectional study we showed a relationship between normalized whole thalamic volume and MS subtype. Also, we showed that the asymmetric indices of the thalamus can be related to the progression of the disease. Eventually, we showed that thalamic asymmetry can be related to the disease progression and subtype changes in MS.
 Multiple sclerosis (MS) has a longitudinal and heterogeneous course, with an increasing number of therapy options and associated risk profiles, leading to a constant increase in the number of parameters to be monitored. Even though important clinical and subclinical data are being generated, treating neurologists may not always be able to use them adequately for MS management. In contrast to the monitoring of other diseases in different medical fields, no target-based approach for a standardized monitoring in MS has been established yet. Therefore, there is an urgent need for a standardized and structured monitoring as part of MS management that is adaptive, individualized, agile, and multimodal-integrative. We discuss the development of an MS monitoring matrix which can help facilitate data collection over time from different dimensions and perspectives to optimize the treatment of people with MS (pwMS). In doing so, we show how different measurement tools can combined to enhance MS treatment. We propose to apply the concept of patient pathways to disease and intervention monitoring, not losing track of their interrelation. We also discuss the use of artificial intelligence (AI) to improve the quality of processes, outcomes, and patient safety, as well as personalized and patient-centered care. Patient pathways allow us to track the patient's journey over time and can always change (e.g., when there is a switch in therapy). They therefore may assist us in the continuous improvement of monitoring in an iterative process. Improving the monitoring process means improving the care of pwMS.
 The 2022 ECTRIMS lecture focused on pediatric-onset multiple sclerosis (POMS), in recognition of the pivotal importance of prompt recognition and treatment of children and youth diagnosed with multiple sclerosis (MS), enabled over the past decade by the formal inclusion of pediatric patients in the McDonald diagnostic criteria. Epidemiologic, genetic and immunologic research has supported the concept that MS is a single disease across the age span and that clues to the inciting and early facets of MS pathobiology might be uniquely discerned through study of the youngest MS patients. Pediatric trials of pharmaceutical agents approved in adult-onset MS are emerging, although innovative study designs, alignment of regulatory agency requirements for trial design, family-centric models for study visits and emphasis on long-term safety and tolerability are essential. Evidence of safety and efficacy of key therapies is key if POMS patients are to be availed of the full armamentarium of MS therapeutic options. Finally, the rarity of POMS necessitates an international community effort to advance care and research. Such collaborations have been facilitated through the International Pediatric Multiple Sclerosis Group, Multiple Sclerosis International Federation, and by national multiple sclerosis societies. International efforts and priorities for the next decade will be highlighted.

 The CNS is very susceptible to oxidative stress; the gut microbiota plays an important role as a trigger of oxidative damage that promotes mitochondrial dysfunction, neuroinflammation, and neurodegeneration. In the current review, we discuss recent findings on oxidative-stress-related inflammation mediated by the gut-brain axis in multiple sclerosis (MS). Growing evidence suggests targeting gut microbiota can be a promising strategy for MS management. Intricate interaction between multiple factors leads to increased intra- and inter-individual heterogeneity, frequently painting a different picture in vivo from that obtained under controlled conditions. Following an evidence-based approach, all proposed interventions should be validated in clinical trials with cohorts large enough to reach significance. Our review summarizes existing clinical trials focused on identifying suitable interventions, the suitable combinations, and appropriate timings to target microbiota-related oxidative stress. Most studies assessed relapsing-remitting MS (RRMS); only a few studies with very limited cohorts were carried out in other MS stages (e.g., secondary progressive MS-SPMS). Future trials must consider an extended time frame, perhaps starting with the perinatal period and lasting until the young adult period, aiming to capture as many complex intersystem interactions as possible.
 BACKGROUND: Ocrelizumab is a recombinant humanized anti-CD20 monoclonal IgG1, approved by FDA and EMA for adult patients with multiple sclerosis (MS). The data on the efficacy and safety of Ocrelizumab for pediatric MS cases are limited. OBJECTIVE: Here, we describe pediatric relapsing-remitting MS (P-RRMS) cases who were treated with Ocrelizumab as a disease-modifying drug. METHOD: P-RRMS cases who were started Ocrelizumab below 18 years-of-age and followed-up >12 months with Ocrelizumab treatment were included. The primary end-points were annualized relapse rate (ARR) and magnetic resonance imaging (MRI) activity (new/enlarging T2 lesions and new gadolinium (Gd) enhancing lesions). The secondary end-points were the percentage of patients who remain relapse-free and/or free from Gd enhancing lesions, Expanded Disability Status Scale (EDSS) score, and the safety profile of Ocrelizumab. RESULTS: Of 18 P-RRMS cases receiving Ocrelizumab, 10 patients fulfilled the inclusion criteria for our study. The median duration of follow-up under Ocrelizumab was 28,3 months (min: 15 months, max: 46 months). Mean ARR decreased from 2.01 (±0.71) to 0 during the follow-up of Ocrelizumab treatment (P < 0.0001). None of the patients had MRI activity during the treatment. Mean EDSS decreased from 1.75 (±1.09) to 1.20 (±0.63) from the initiation of Ocrelizumab to the last follow-up of the patients (P = 0.024). None of the patients had serious side effects, except one patient who experienced anaphylaxis. CONCLUSION: Ocrelizumab can be considered a safe and effective treatment option in highly active P-RRMS.

 BACKGROUND: The optimal treatment strategy of multiple sclerosis (MS) is a matter of debate. The classical approach is the escalating (ESC) strategy, which consists of starting with low- to moderate-efficacy disease-modifying drugs (DMDs) and upscale to high-efficacy DMDs when noting some evidence of active disease. Another approach, the early intensive (EIT) strategy, is starting with high-efficiency DMDs as first-line therapy. Our goal was to compare effectiveness, safety, and cost of ESC and EIT strategies. METHODS: We searched MEDLINE, EMBASE and SCOPUS until September 2022, for studies comparing EIT and ESC strategies in adult participants with relapsing-remitting MS and a minimum follow-up of 5 years. We examined the Expanded Disability Severity Scale (EDSS), the proportion of severe adverse events, and cost in a 5-year period. Random-effects meta-analysis summarized the efficacy and safety and an EDSS-based Markov model estimated the cost. RESULTS: Seven studies with 3,467 participants showed a 30% reduction in EDSS worsening in 5 years (RR 0.7; [0.59-0.83]; p < 0.001) in the EIT group vs in the ESC group. Two studies with 1,118 participants suggested a similar safety profile for these strategies (RR 1.92; [0.38-9.72]; p = 0.4324). EIT with natalizumab in extended interval dosing, rituximab, alemtuzumab, and cladribine demonstrated cost-effectiveness in our model. DISCUSSION: EIT presents higher efficacy in preventing disability progression, a similar safety profile, and can be cost-effective within a 5-year timeline.
 Magnetic resonance imaging is a fundamental tool to reach a diagnosis of multiple sclerosis and monitoring its progression. Although several attempts have been made to segment multiple sclerosis lesions using artificial intelligence, fully automated analysis is not yet available. State-of-the-art methods rely on slight variations in segmentation architectures (e.g. U-Net, etc.). However, recent research has demonstrated how exploiting temporal-aware features and attention mechanisms can provide a significant boost to traditional architectures. This paper proposes a framework that exploits an augmented U-Net architecture with a convolutional long short-term memory layer and attention mechanism which is able to segment and quantify multiple sclerosis lesions detected in magnetic resonance images. Quantitative and qualitative evaluation on challenging examples demonstrated how the method outperforms previous state-of-the-art approaches, reporting an overall Dice score of 89% and also demonstrating robustness and generalization ability on never seen new test samples of a new dedicated under construction dataset.
 BACKGROUND: Observational investigations examining cancer risk among multiple sclerosis (MS) patients have produced contradictory findings. Herein, we performed an extensive review and meta-analysis to evaluate the correlation and causation between MS and cancer incidence. METHODS: We systematically screened for published articles examining cancer incidences among MS patients within the Cochrane Library, PubMed, and Embase databases. Next, we employed STATA v.16.0 for data analysis. Following meta-analysis, we performed a two-sample Mendelian randomization (MR) analysis to uncover the underlying mechanism behind the MS-mediated regulation of certain cancers. RESULTS: Overall, we selected 18 articles encompassing 14 individual cancers incidences and a total of 368,952 patients for meta-analysis. Based on our analysis, there was reduced pancreatic (ES = 0.68; 95% CI: 0.49-0.93; I 2 = 0%) and ovarian cancer (ES = 0.65; 95% CI: 0.53-0.80; I 2 = 86.7%) co-occurrences among MS patients. Meanwhile, the incidences of breast (ES = 1.10; 95% CI: 1.01-1.21; I 2 = 60.9%) and brain cancers (ES = 1.94; 95% CI: 1.12-3.37; I 2 = 56.1%) were elevated among the same population. However, MR analysis revealed the opposite relation between MS and breast cancer risk (OR = 0.94392; 95% CI: 0.91011-0.97900, P = 0.002). Moreover, it revealed strong incidence of lung cancer (OR = 1.0004; 95% CI: 1.0001-1.0083, P = 0.001) among MS patients, as evidenced by the inverse variance weighting estimator. Lastly, MR found that other forms of cancers were not significantly related to MS. CONCLUSIONS: Using meta-analysis, we demonstrated that MS patients exhibited enhanced pancreatic and ovarian cancer risk, and diminished breast and brain cancer risk. However, using MR analysis, we discovered an inverse relation between MS and breast cancer risk, and additionally saw an uptick in lung cancer co-occurrence among MS patients.
 BACKGROUND: Although multiple sclerosis is the most common chronic inflammatory demyelinating disease of the central nervous system, the rate of misdiagnosis in clinical practice is high. This is usually due to the inadequate application of the McDonald criteria and misinterpretation of images. OBJECTIVE: This review focuses on typical clinical symptoms, choice of magnetic resonance imaging (MRI) sequences, correct application of the McDonald criteria, and finally interpretation of the images.
 AIM: To report an analysis of the concept of prognostic uncertainty in patients with multiple sclerosis (MS). BACKGROUND: The complexity and ambiguity involved in a diagnosis of MS lead to the occurrence of prognostic uncertainty among patients. A concept analysis is presented that analyses what prognostic uncertainty means to those experiencing the transition between relapsing-remitting multiple sclerosis and secondary progressive multiple sclerosis. DESIGN: Concept analysis. DATA SOURCES: PubMed, Ovid Medline, Cumulative Index for Nursing and Allied Health Literature databases were searched for literature published within the last 10 years using combinations of the terms prognostic and diagnostic uncertainty, and multiple sclerosis along with archival referencing. METHODS: The Walker and Avant method was used to analyse the concept of prognostic uncertainty in patients with MS. RESULTS: The defining attributes identified that provide additional context to prognostic uncertainty are illness uncertainty, intolerance of uncertainty and progressive dwindling. Related, contrary, model and borderline cases are presented to further discuss the application of the key attributes to the concept. CONCLUSION: There are limited data on prognostic uncertainty and multiple sclerosis; however, patients and physicians express uncertainty in understanding one's disease trajectory and determining when a patient with relapsing-remitting multiple sclerosis has entered the secondary progressive multiple sclerosis disease course leading to ineffective communication and frustration. RELEVANCE TO CLINICAL PRACTICE: Genetics and genomics have the potential to provide a prognostic factor for addressing the concept of uncertainty as it relates to persons with multiple sclerosis. Moving beyond the concept analysis, a case is made for nurse involvement in genetic and genomic research to conduct trials, translate, and apply these findings to clinical practice and nursing curricula, addressing the uncertainty experienced by those afflicted with chronic illnesses, such as multiple sclerosis.
 BACKGROUND: Multiple sclerosis patients experience 3-6 times more seizures than the general population, but observations vary among studies. Seizure risk in disease-modifying therapy recipients remains unknown. OBJECTIVE: The objective of this study was to compare seizure risk in multiple sclerosis patients receiving disease-modifying therapy versus placebo. METHODS: MEDLINE(OVID), Embase, CINAHL, and ClinicalTrials.gov were searched from database inception until August 2021. Phase 2-3 randomized, placebo-controlled trials reporting efficacy and safety data for disease-modifying therapies were included. Network meta-analysis followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, using Bayesian random effects model for individual and pooled (by drug target) therapies. Main outcome was log(e) seizure risk ratios [95% credible intervals]. Sensitivity analysis included meta-analysis of non-zero-event studies. RESULTS: A total of 1993 citations and 331 full-texts were screened. Fifty-six included studies (29,388 patients-disease-modifying therapy = 18,909; placebo = 10,479) reported 60 seizures (therapy = 41; placebo = 19). No individual therapy was associated with altered seizure risk ratio. Exceptions were daclizumab (-17.90 [-65.31; -0.65]) and rituximab (-24.86 [-82.71; -1.37]) trending toward lower risk ratio; cladribine (25.78 [0.94; 4.65]) and pegylated interferon-beta-1a (25.40 [0.78; 85.47]) trended toward higher risk ratio. Observations had wide credible intervals. Sensitivity analysis of 16 non-zero-event studies revealed no difference in risk ratio for pooled therapies (l0.32 [-0.94; 0.29]). CONCLUSION: No evidence of association was found between disease-modifying therapy and seizure risk-this informs seizure management in multiple sclerosis patients.


 BACKGROUND: Although often overlooked, patient and public involvement (PPI) is vital when considering the design and delivery of complex and adaptive clinical trial designs for chronic health conditions such as multiple sclerosis (MS). METHODS: We conducted a rapid review to assess current status of PPI in the design and conduct of clinical trials in MS over the last 5 years. We provide a case study describing PPI in the development of a platform clinical trial in progressive MS. RESULTS: We identified only eight unique clinical trials that described PPI as part of articles or protocols; nearly, all were linked with funders who encourage or mandate PPI in health research. The OCTOPUS trial was co-designed with people affected by MS. They were central to every aspect from forming part of a governance group shaping the direction and strategy, to the working groups for treatment selection, trial design and delivery. They led the PPI strategy which enabled a more accessible, acceptable and inclusive design. CONCLUSION: Active, meaningful PPI in clinical trial design increases the quality and relevance of studies and the likelihood of impact for the patient community. We offer recommendations for enhancing PPI in future MS clinical trials.
 Tuberous sclerosis (TS) is a monogenic disorder which causes disabling neurological symptoms. Similarly, multiple sclerosis (MS) may result in disability, but in contrast, is diagnosed without genetic testing. Clinicians are advised to exercise caution in diagnosing MS in the presence of a pre-existing genetic disorder, as it may be a potential 'red flag'. A dual diagnosis of MS and TS has not previously been reported in the literature. We provide two cases of known cases of TS who presented with new neurological symptoms and associated physical signs compatible with a dual diagnosis of TS/MS.
 The purpose of this literature review was to summarise relevant findings regarding the clinical management of multiple sclerosis (MS) in the COVID-19 pandemic, with the focus on patient risks, and the implications of disease-modifying treatment, both on COVID-19 severity and on the response to the SARS-CoV-2 vaccinations. Although MS per se does not seem to put patients at risk for more severe COVID-19, alongside the risk factors known to apply to the general population, progressive disease course, higher disability status, and B-cell depleting therapies may all negatively affect infection severity. The question of COVID-19 sequelae in patients with MS (pwMS) remains unresolved, challenging researchers to further explore this area. The safety profile of COVID-19 vaccinations in pwMS is similar to that of the general population. The efficacy of the vaccination might be affected by B-cell depletion, as well as by S1PR-modulating medications that attenuate humoral responses to the COVID-19 vaccination. Future research should focus on gathering evidence regarding the clinical course of MS following COVID-19 infection and vaccination in larger studies, as well as on establishing the safest and most efficient schedule of COVID-19 vaccination in pwMS on cell-depleting therapies.
 Multiple sclerosis (MS) is a progressive disease that often affects the cerebellum. It is characterised by demyelination, inflammation, and neurodegeneration within the central nervous system. Damage to the cerebellum in MS is associated with increased disability and decreased quality of life. Symptoms include gait and balance problems, motor speech disorder, upper limb dysfunction, and oculomotor difficulties. Monitoring symptoms is crucial for effective management of MS. A combination of clinical, neuroimaging, and task-based measures is generally used to diagnose and monitor MS. This paper reviews the present and new tools used by clinicians and researchers to assess cerebellar impairment in people with MS (pwMS). It also describes recent advances in digital and home-based monitoring for people with MS.
 Radiologically isolated syndrome refers to the clinical scenario in which individuals have imaging concerning for multiple sclerosis and would otherwise satisfy radiographic dissemination in space criteria, but do not have any attributable signs or symptoms. Radiologically isolated syndrome has been increasingly recognized in the pediatric population and it is understood certain individuals will transition to a formal diagnosis of multiple sclerosis over time. This review aims to outline the available data within this unique population including the diagnostic criteria, epidemiology, risk factors associated with transitioning to multiple sclerosis, and the current therapeutic landscape. Radiologically isolated syndrome will also be positioned within a broader spectrum of demyelinating disease as recent data has pointed towards a likely prodromal phase that precedes a first clinical event and diagnosis of multiple sclerosis. Characterizing the radiographic features, clinical symptoms, and biomarkers that constitute this prodromal phase of multiple sclerosis would help identify patients who may most benefit from early intervention in the future.
 Comorbid conditions commonly affect people with multiple sclerosis (MS). Population-based studies indicate that people with MS have an increased incidence of ischemic heart disease, cerebrovascular disease, peripheral vascular disease, and psychiatric disorders as compared to people without MS. People with MS from underrepresented minority and immigrant groups have higher comorbidity burdens. Comorbidities exert effects throughout the disease course, from symptom onset through diagnosis to the end of life. At the individual level, comorbidity is associated with higher relapse rates, greater physical and cognitive impairments, lower health-related quality of life, and increased mortality. At the level of the health system and society, comorbidity is associated with increased health care utilization, costs and work impairment. A nascent literature suggests that MS affects outcomes from comorbidities. Comorbidity management needs to be integrated into MS care, and this would be facilitated by determining optimal models of care.

 BACKGROUND: In 2018 multiple sclerosis (MS) care unit (MSCU) recommendations were defined. Nevertheless, the information on MS care, and whether MS centres fulfil the international recommendation is limited. Thus our objectives were to assess whether centres meet the MSCU recommendations and gain a comprehensive overview of MS care in Central-Eastern European countries. METHODS: A self-report questionnaire assessing aspects of the MSCU recommendations, disease-modifying therapy (DMT) and registry use and the patient number was assembled and sent to nine Central-Eastern European countries. Furthermore, one Danish and one German centre were contacted as a reference. RESULTS: In 9/9 countries, MS care was pursued in centres by MS neurologists and MS nurses. In Austria and the Czech Republic, management of MS was conducted under strict regulations displaying a referral centre system, fundamentally similar to but independent of the MSCU criteria. Several centres fulfilled all aspects of the MSCU criteria, while others had similar insufficiencies consisting of a speech therapist, continence, pain and spasticity specialist, neuro-ophthalmologist, and oto-neurologist. In 9/9 countries, DMTs were reimbursed. However, some centres did not provide every available DMT. A national registry was available in 4/9 countries with mandatory registry use only in Austria and the Czech Republic. CONCLUSION: In countries where MSCU recommendations are not fulfilled, a strictly regulated centre system similar to the Austrian and Czech model with a registry-based quality control might ensure appropriate care for people with MS.

 Multiple sclerosis is a severe demyelinating disease mediated by cells of the innate and adaptive immune system, especially pathogenic T lymphocytes that produce the pro-inflammatory cytokine granulocyte-macrophage colony stimulating factor (GM-CSF). Although the factors and molecules that drive the genesis of these cells are not completely known, some were discovered and shown to promote the development of such cells, such as dietary factors. In this regard, iron, the most abundant chemical element on Earth, has been implicated in the development of pathogenic T lymphocytes and in MS development via its effects on neurons and glia. Therefore, the aim of this paper is to revise the state-of-art regarding the role of iron metabolism in cells of key importance to MS pathophysiology, such as pathogenic CD4(+) T cells and CNS resident cells. Harnessing the knowledge of iron metabolism may aid in the discovery of new molecular targets and in the development of new drugs that tackle MS and other diseases that share similar pathophysiology.
 Microorganisms in human life play a huge role: in particular, those that coexist with the host organism, inhabiting the skin, upper respiratory tract, external genitalia and especially the digestive tract. The intestinal microbiota, including bacteriome, mycobiome and virome, not only takes part in the digestion process, but also provides the synthesis of a number of vitamins. The intestinal microbiome also serves as the basis for a system of extensive bidirectional neuroendocrine pathways that connect microbiota with various regions of the central nervous system, the hypothalamic-pituitary-adrenal system, and the peripheral parts of the autonomic nervous system. This system of connections has got the name of gut-brain axis and has attracted close attention of scientists over the past two decades, since a targeted impact on the intestinal flora is potentially capable of changing the nature of nervous system regulatory influences on the whole body. It is especially important to study patterns of functioning of the gut-brain axis in patients with the nervous system pathology, namely neurodegenerative and demyelinating diseases. Methods for their treatment continue to improve, and perhaps the correction of the gut microbiotic composition will serve as an additional therapeutic approach. The review article describes current views on the role of the intestinal microbiota, provides the latest data on the composition of bacteriome, mycobiome, and virome in patients with relapsing-remitting multiple sclerosis.
 BACKGROUND: Dysphagia is a major disorder observed in patients with multiple sclerosis (MS), yet different prevalence rates are reported for it. Therefore, we designed this study to estimate the pooled prevalence of dysphagia in patients with MS. METHOD: We searched PubMed, Scopus, EMBASE, Web of Science, and gray literature including references from the identified studies, reviews studies, and conference abstracts which were published up to May 2022. Articles that were relevant to our topic and could provide information regarding the prevalence of dysphagia among MS patients were included; however, articles with self-report screening strategies were excluded. RESULTS: The literature search found 997 articles. After eliminating duplicates, 672 articles remained. Two conference abstracts were included for final analysis. A total of 11,266 MS cases and 5047 MS patients with dysphagia were included in the meta-analysis. The overall prevalence of dysphagia across all 54 studies was 44.8 % (95 % CI: [40.4 %-49.2 %]), with a high level of heterogeneity between countries (Q=; I(2) = 94.96 %; p < 0.001). CONCLUSION: The results of this systematic review shows that the prevalence of dysphagia in MS patients is 45% which is greatly higher compared to the general population.
 INTRODUCTION: The Multiple Sclerosis Screening Questionnaire (MSNQ) is a self-report measure used to assess cognitive difficulties in people with Multiple Sclerosis (PwMS). The aim of this systematic review was to determine the associations between the MSNQ and: objective measures of cognition, measures of mood, and quality of life measures. METHOD: A comprehensive search was done across three databases (PsycINFO, MEDLINE, and CINAHL). A total of 15 studies, including 1992 participants, were selected for final inclusion. Meta-analyses were conducted to determine the pooled effect size of associations. Where data were not available for meta-analyses, a narrative synthesis approach was taken. RESULTS: Significant, but small (r = -0.17), associations were found between the MSNQ and objective measures of cognition. Significant, moderate associations (r = 0.47) were found between the MSNQ and measures of mood. CONCLUSIONS: The small association between the MSNQ and objective measures of cognition shows that the measures do not converge well. However, their divergence may be important to map the broad construct of "cognitive ability" more fully. Limitations include a lack of reporting of non-significant effect sizes in individual studies. Clinical implications include the potential for the MSNQ to be used beyond being solely a proxy measure for objective cognition. Future research should investigate the associations between the informant version of the MSNQ and objective measures.
 Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system and the association with other autoimmune diseases is well-documented. There are many therapeutic options for the treatment of MS. Most of the available drugs cause drug-induced liver injury (DILI) to variable extents with heterogeneous clinical and biological manifestations, including liver injury with or without signs of hypersensitivity and autoimmunity. The diagnosis of DILI may be particularly difficult because MS is frequently associated with idiopathic autoimmune hepatitis. Recent advances suggest that MS and immune-mediated DILI could be promoted by genetic factors, including HLA genotype. In addition, some of these drugs may promote hepatitis B virus reactivation. This review explores the potential hepatotoxicity of drugs used to treat MS and the criteria to distinguish DILI from idiopathic autoimmune hepatitis associated with MS. The role of susceptible genes both promoting MS and causing the hepatotoxicity of the drug used for MS treatment is also discussed.

 Pediatric-onset multiple sclerosis (POMS), is the manifestation of multiple sclerosis in individuals before 18 years of age. About a third of children with POMS show some form of lower cognitive performance. The purpose of this study is to examine using quantitative meta-analyses the effect size of altered performance between children with and without POMS on overall intelligence quotient (IQ), information processing speed, and language functions. We searched the literature for studies that reported scores on cognitive tests administered to children with and without POMS. Studies were systematically reviewed using PRISMA guidelines. We analyzed data from 14 studies that examined 1283 children with and without POMS when cognitive categories consisted of five or more studies. Effect sizes, publication bias and potential confounds were considered. Significant cognitive differences are revealed for all categories with the strongest effect observed for overall IQ. A moderate effect is observed for information processing speed, and small effects for verbal fluency and verbal memory. Cognitive abilities present differently in children with POMS and a better understanding of this manifestation will inform intervention and remediation tools that can improve clinical and educational practice for the benefit of children with POMS.
 BACKGROUND: Physical activity is encouraged for people with Multiple Sclerosis. Yoga is a popular form of physical activity and is chosen by some people with Multiple Sclerosis. However, little is known about the impact of yoga for this population, alongside what influences ongoing engagement. AIM: The aim of this study is to qualitatively explore the impact of online home-based yoga on people with Multiple Sclerosis and to explore factors that influence engagement. METHODS: A qualitative study using semi-structured interviews and focus groups with people with Multiple Sclerosis and a yoga teacher. Thematic analysis was used to analyse the data. Ethical Approval was gained from Northumbria University. FINDINGS: Three overarching themes emerged from the analysis. 'Yoga as engagement in physical activity' captured the reasoning for participating in yoga and how this method of physical activity was an alternative to physical activity done prior to diagnosis. Frustration was apparent within this theme that some individuals were unable to engage in the range of physical activity that they wished to. 'Yoga is a personalised approach' demonstrated the flexibility and inclusivity of yoga, for individuals with varying symptoms to be able to engage with. Finally, 'yoga impacts individuals both physically and psychologically' captured the focus on the psychological impact of yoga, improving wellbeing and control. CONCLUSIONS: Yoga gives people with Multiple Sclerosis the feeling of control over their symptoms and a means to engage with meaningful physical activity. Prior involvement in physical activity influenced engagement in yoga and wanting to push themselves. There was reluctance among this group to engage with aerobic activity, which warrants future investigation and support from health and exercise professionals.
 Multiple sclerosis (MS) was once considered an untreatable disease. Through years of research, many drugs have been discovered and are widely used for the treatment of MS. However, the current treatment can only alleviate the clinical symptoms of MS and has serious side effects. Mesenchymal stem cells (MSCs) provide neuroprotection by migrating to injured tissues, suppressing inflammation, and fostering neuronal repair. Therefore, MSCs therapy holds great promise for MS treatment. This review aimed to assess the feasibility and safety of use of MSCs in MS treatment as well as its development prospect in clinical treatment by analysing the existing clinical studies.
 BACKGROUND: Current cognitive monitoring of people with multiple sclerosis (pwMS) is sporadic, resource intensive and insensitive for detection of real-world cognitive performance and decline. Smartphone applications may provide us with a more sensitive biomarker for cognitive decline that reflects real-world performance. The goal of this study was to perform a systematic review and qualitative synthesis of all current smartphone apps monitoring cognition in pwMS. METHODS: A systematic search of five major online databases (PubMed/Medline, Scopus, Web of Science, Cumulative Index of Nursing and Allied Health Literature and IEEE Xplore) was performed in accordance with the Cochrane Handbook and Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. We included all studies with at least one measure of phone-based digital biomarkers for monitoring cognition in pwMS above the age of 18. Two authors independently screened the articles retrieved. Data on test-retest reliability, validity coefficients, feasibility and practice effects were extracted from the studies identified. Critical appraisal of the studies was performed using the National Institute of Health quality assessment tool for observational cohort and cross-sectional studies. RESULTS: 12 articles covering six smartphone apps were included in this review. All articles had a low risk of bias, though sample size calculation was rarely performed. Of the six apps, five used smartphone versions of the symbol digit modalities test. The final app examined keystroke features passively. Test-retest reliability ranged from good to excellent. Concurrent validity was demonstrated through moderate to strong correlation with neuropsychological tests and weak to moderate correlations with EDSS, radiological biomarkers and patient-reported outcomes. Mobile apps performed comparably, and in some cases outperformed established cognitive tests. Whilst reported acceptability was high, significant attrition rates were present in longitudinal cohorts. There were significant short and long-term practice effects. Overall, smartphone versions of the SDMT showed strong psychometric properties across multiple apps. CONCLUSION: Smartphone applications are reliable and valid biomarkers of real-world cognition in pwMS. Further longitudinal data would allow for a better understanding of their predictive and ecological validity.
 BACKGROUND: Trigeminal neuralgia (TN) is a well-recognized symptom of multiple sclerosis (MS), yet its clinical characteristics related to MS subtype is poorly studied. Our aim was to evaluate whether development and clinical outcome of TN are influenced by MS phenotype. METHODS: In this retrospective cohort study, our database from 2007 to 2022 was reviewed to identify patients who had both the diagnosis of MS and TN, whether TN was an initial symptom of MS or developed later in diagnosis. A detailed medical history and treatment outcome was obtained. Pain status was assessed retrospectively using the Barrow Neurological Institute Pain Scale (BNI-PS), with BNI-PS I-III considered as good pain control and BNI-PS IV-V as poor pain control. RESULTS: 58 patients had MS-related TN. 44 patients had relapsing remitting multiple sclerosis (RRMS) at the time of TN diagnosis, 11 had secondary progressive multiple sclerosis (SPMS) at the time of TN diagnosis, and type of MS was not clear in 3 patients at the time of TN diagnosis (either RRMS or SPMS). Over a mean follow up of 18.8 (SD=10.9) years, 30 transitioned to SPMS. TN was refractory to medical management in 9 RRMS and 22 SPMS patients (p = 0.001). TN patients with RRMS required lower median number of pain medications compared to SPMS (p = 0.014). Brain MRI was available in 41 of the entire cohort. Of these, 27 patients had demyelinating lesions in the trigeminal sensory pathway and 14 did not. Patients with existing lesions had a higher chance of failure of medical management (74% versus 36%, p = 0.017) and required surgical intervention (55% versus 7%, p = 0.003). DISCUSSION: TN was not seen in primary progressive multiple sclerosis (PPMS). In patients who transitioned to SPMS, TN was more likely to be refractory to medical management. TN was more refractory in the presence of demyelinating plaque involving trigeminal sensory pathway.
 PURPOSE OF REVIEW: Autologous haematopoietic stem cell transplantation (AHSCT) is increasingly considered a treatment option for patients with multiple sclerosis (MS), an autoimmune demyelinating and degenerative disease of the central nervous system (CNS). AHSCT persistently suppresses inflammation and improves the disease course in large proportions of patients with relapsing-remitting (RR) MS. Aim of this article is to review the relevant new knowledge published during the last 3 years. RECENT FINDINGS: Laboratory studies reported confirmatory and new insights into the immunological and biomarker effects of AHSCT. Retrospective clinical studies confirmed excellent outcomes in RRMS, showing possible superior effectiveness over standard therapies and suggesting a possible benefit in early secondary progressive (SP) MS with inflammatory features. New data on risks of infertility and secondary autoimmunity were also reported. Further evidence on the high effectiveness and acceptable safety of AHSCT strengthens its position as a clinical option for aggressive RRMS. Further research is needed to better define its role in treatment-naïve and progressive forms of MS, ideally within randomised clinical trials (RCTs).


 BACKGROUND: Multiple sclerosis (MS) is a chronic demyelinating/neurodegenerative disease associated with change in cognitive function (CF) over time. This systematic review aims to describe the instruments used to measure change in CF over time in people with MS (PwMS). METHODS: PubMed, OVID, Web of Science, and Scopus databases were searched in English until May 2021. Articles were included if they had at least 100 participants and at least a 1-year interval between baseline and last follow-up measurement of CF. Results were quantitatively synthesized, presented in tables and risk of bias was assessed with the Newcastle-Ottawa Scale. RESULTS: Fifty-seven articles met the inclusion criteria (41,623 PwMS and 1105 controls). An intervention (drug/rehabilitation) was assessed in 22 articles. In the studies that used a test battery, Visual and verbal learning and memory were the most frequently measured domains, but when studies that used test battery or a single test are combined, Information processing speed was the most measured. The Symbol Digit Modalities Test (SDMT) was the most frequently used test as a single test and in a test battery combined. Most studied assessed "change in CF" as cognitive decline defined as 1 or more tests measured as ≥ 1.5 SD from the study control or normative mean in a test battery at baseline and follow-up. Meta-analysis of change in SDMT scores with seven articles indicated a nonstatistically significant -0.03 (95% CI -0.14, 0.09) decrease in mean SDMT score per year. CONCLUSION: This study highlights the slow rate of measured change in cognition in PwMS and emphasizes the lack of a gold standard test and consistency in measuring cognitive change at the population level. More sensitive testing utilizing multiple domains and longer follow-up may define subgroups where CF change follows different trajectories thus allowing targeted interventions to directly support those where CF is at greatest risk of becoming a clinically meaningful issue.


 Multiple Sclerosis (MS) is a chronic, inflammatory demyelinating disease of the central nervous system (CNS) driven by a complex interplay of genetic and environmental factors. While the therapeutic arsenal has expanded significantly for management of relapsing forms of MS, treatment of individuals with progressive MS is suboptimal. This treatment inequality is in part due to an incomplete understanding of pathomechanisms at different stages of the disease-underscoring the critical need for new biomarkers. Extracellular vesicles (EVs) and their bioactive cargo have emerged as endogenous nanoparticles with great theranostic potential-as diagnostic and prognostic biomarkers and ultimately as therapeutic candidates for precision nanotherapeutics. The goals of this review are to: 1) summarize the current data investigating the role of EVs and their bioactive cargo in MS pathogenesis, 2) provide a high level overview of advances and challenges in EV isolation and characterization for translational studies, and 3) conclude with future perspectives on this evolving field.
 Multiple sclerosis (MS) is an inflammatory disease related to the central nervous system (CNS) with a significant global burden. In this illness, the immune system plays an essential role in its pathophysiology and progression. The currently available treatments are not recognized as curable options and, at best, might slow the progression of MS injuries to the CNS. However, stem cell treatment has provided a new avenue for treating MS. Stem cells may enhance CNS healing and regulate immunological responses. Likewise, stem cells can come from various sources, including adipose, neuronal, bone marrow, and embryonic tissues. Choosing the optimal cell source for stem cell therapy is still a difficult verdict. A type of stem cell known as mesenchymal stem cells (MSCs) is obtainable from different sources and has a strong immunomodulatory impact on the immune system. According to mounting data, the umbilical cord and adipose tissue may serve as appropriate sources for the isolation of MSCs. Human amniotic epithelial cells (hAECs), as novel stem cell sources with immune-regulatory effects, regenerative properties, and decreased antigenicity, can also be thought of as a new upcoming contender for MS treatment. Overall, the administration of stem cells in different sets of animal and clinical trials has shown immunomodulatory and neuroprotective results. Therefore, this review aims to discuss the different types of stem cells by focusing on MSCs and their mechanisms, which can be used to treat and improve the outcomes of MS disease.
 PURPOSE: MRI is integral to the diagnosis of multiple sclerosis (MS) and is important for clinical prognostication. Quantitative volumetric reporting tools (QReports) can improve the accuracy and objectivity of MRI-based assessments. Several QReports are commercially available; however, validation can be difficult to establish and does not currently follow a common pathway. To aid evidence-based clinical decision-making, we performed a systematic review of commercial QReports for use in MS including technical details and published reports of validation and in-use evaluation. METHODS: We categorized studies into three types of testing: technical validation, for example, comparison to manual segmentation, clinical validation by clinicians or interpretation of results alongside clinician-rated variables, and in-use evaluation, such as health economic assessment. RESULTS: We identified 10 companies, which provide MS lesion and brain segmentation and volume quantification, and 38 relevant publications. Tools received regulatory approval between 2006 and 2020, contextualize results to normative reference populations, ranging from 620 to 8000 subjects, and require T1- and T2-FLAIR-weighted input sequences for longitudinal assessment of whole-brain volume and lesions. In MS, six QReports provided evidence of technical validation, four companies have conducted clinical validation by correlating results with clinical variables, only one has tested their QReport by clinician end-users, and one has performed a simulated in-use socioeconomic evaluation. CONCLUSION: We conclude that there is limited evidence in the literature regarding clinical validation and in-use evaluation of commercial MS QReports with a particular lack of clinician end-user testing. Our systematic review provides clinicians and institutions with the available evidence when considering adopting a quantitative reporting tool for MS.
 Multiple Sclerosis (MS) is a multifactorial, neurodegenerative, and inflammatory demyelination disease with incomplete remyelination in the CNS. It would be more informative to reveal the underlying molecular mechanisms of MS. Molecular mechanisms involving epigenetic changes play a pivotal role in this disease. Epigenetic changes impact gene expression without altering the underlying DNA sequence. The main epigenetic modifications that play a key role in the regulation of gene expression principally include DNA methylation, histone modifications, and microRNA- associated post-transcriptional gene silencing. In this review, we summarize the dynamics of epigenetic changes and their relation to environmental risk factors in MS pathogenesis. Studies suggest that epigenetic changes have a role in the development of MS and environmental risk factors, such as vitamin D, smoking, and Epstein-Barr virus infection seem to influence the development and susceptibility to MS. Investigating epigenetic and environmental factors can provide new opportunities for the molecular basis of the diseases, which shows complicated pathogenesis. Epigenetic research has the potential to complete our understanding of MS initiation and progression. Increased understanding of MS molecular pathways leads to new insights into potential MS therapies. However, there is a need for in vivo evaluation of the role of epigenetic factors in MS therapy. It would be more valuable to indicate the role of various epigenetic factors in MS.


 Multiple sclerosis is clinically characterized by relapses and remissions (relapsing-remitting multiple sclerosis) that over time may evolve to a progressive course (secondary progressive multiple sclerosis) or as having a progressive course from disease onset (primary progressive multiple sclerosis). At present, it is not definitively known whether these clinical entities constitute a single pathological disease or whether these manifestations represent two distinct disease entities sharing inflammatory demyelination as a pathological feature. Here we show using a novel mouse model that CSF of primary progressive multiple sclerosis patients is unique in its capacity to induce motor disability and spinal cord pathology including demyelination, impaired remyelination, reactive astrogliosis and axonal damage. Notably, removal of immunoglobulin G from primary progressive multiple sclerosis CSF via filtration or immunodepletion attenuates its pathogenic capacity. Furthermore, injection of recombinant antibodies derived from primary progressive multiple sclerosis CSF recapitulates the pathology. Our findings suggest that the clinical and pathological features of primary progressive multiple sclerosis are antibody-mediated and pathogenically distinct from relapsing-remitting and secondary progressive multiple sclerosis. Our study has potentially important implications for the development of specific therapies for patients with primary progressive multiple sclerosis.
 BACKGROUND: In the last years, research on pharmacotherapy and non-pharmacological approaches to Multiple Sclerosis (MS) has significantly increased, along with a greater attention to sleep as a clinical outcome measure. This review aims to update the state of the art on the effects of MS treatments on sleep, but above all to evaluate the role of sleep and its management within the current and future therapeutic perspectives for MS patients. METHOD: A comprehensive MEDLINE (PubMed)-based bibliographic search was conducted. This review includes the 34 papers that met the selection criteria. RESULTS: First-line disease modifying therapies (especially the interferon-beta) seem to have a negative impact on sleep, assessed subjectively or objectively, while second-line treatments (in particular, natalizumab) do not seem to lead to the onset of daytime sleepiness (also evaluated objectively) and, in some cases, an improvement in sleep quality has been observed as well. Management of sleep is considered a major factor in modifying disease progression in pediatric MS; however, probably because only fingolimod has recently been approved in children, information is still scarce in this group of patients. CONCLUSIONS: Studies on the effect of drugs and non-pharmacological treatments for MS on sleep are still insufficient and there is a lack of investigations on the most recent therapies. However, there is preliminary evidence that melatonin, chronotherapy, cognitive-behavioral therapy, and non-invasive brain stimulation techniques might be further assessed as adjuvant therapies, thus representing a promising field of research.
 Despite extensive research into the pathophysiology of multiple sclerosis (MS) and recent developments in potent disease-modifying therapies (DMTs), two-thirds of relapsing-remitting MS patients transition to progressive MS (PMS). The main pathogenic mechanism in PMS is represented not by inflammation but by neurodegeneration, which leads to irreversible neurological disability. For this reason, this transition represents a critical factor for the long-term prognosis. Currently, the diagnosis of PMS can only be established retrospectively based on the progressive worsening of the disability over a period of at least 6 months. In some cases, the diagnosis of PMS is delayed for up to 3 years. With the approval of highly effective DMTs, some with proven effects on neurodegeneration, there is an urgent need for reliable biomarkers to identify this transition phase early and to select patients at a high risk of conversion to PMS. The purpose of this review is to discuss the progress made in the last decade in an attempt to find such a biomarker in the molecular field (serum and cerebrospinal fluid) between the magnetic resonance imaging parameters and optical coherence tomography measures.
 INTRODUCTION: Multiple sclerosis is a chronic, demyelinating, inflammatory, and neurodegenerative disease of the central nervous system that affects over 2 million people worldwide. Considerable advances have been made in the availability of disease modifying therapies for relapsing-remitting multiple sclerosis since their introduction in the 1990s. This has led to debate regarding the optimal first-line treatment approach: a strategy of escalation versus early highly effective treatment. AREAS COVERED: This review defines the strategies of escalation and early highly effective treatment, outlines the pros and cons of each, and provides an analysis of both the current literature and expected future directions of the field. EXPERT OPINION: There is growing support for using early highly effective treatment as the initial therapeutic approach in relapsing-remitting multiple sclerosis. However, much of this support stems from observational real-world studies that use historic data and lack safety outcomes or randomized control trials that compare individual high versus low-moderate efficacy therapies, instead of the approaches themselves. Randomized control trials (DELIVER-MS, TREAT-MS) are needed to systemically and prospectively compare contemporary escalation versus early highly effective treatment approaches.
 INTRODUCTION: In addition to physical and cognitive symptoms, patients with multiple sclerosis (MS) have an increased risk of experiencing mental health problems. METHODS: This narrative review provides an overview of the appearance and epidemiology of affective symptoms in MS such as depression, anxiety, bipolar disorder, euphoria, and pseudobulbar affect. Furthermore, the association between affective symptoms and quality of life and the currently used diagnostic instruments for assessing these symptoms are considered whereby relevant studies published between 2009 and 2021 were included in the review. RESULTS: Patients with mild and moderate disability more frequently reported severe problems with depression and anxiety than severe mobility problems. Apart from the occurrence of depression, little is known about the association of other affective symptoms such as anxiety, bipolar disorder, euphoria, and pseudobulbar affect and subsyndromal symptoms, which fail to meet the diagnostic criteria but are nevertheless a significant source of distress. Although there are a few recommendations in the research to perform routine screenings for diagnosable affective disorders, a standardized diagnostic procedure to assess subsyndromal symptoms is still lacking. As the applied measurements are diverse and show low accuracy to detect these symptoms, patients who experience affective symptoms are less likely to be identified. DISCUSSION: In addition to the consideration of definite psychiatric diagnoses, there is an unmet need for a common definition and assessment of disease-related affective symptoms in MS. Future studies should focus on the improvement and standardization of a common diagnostic procedure for subsyndromal affective symptoms in MS to enable integrated and optimal care for patients.

 BACKGROUND: There is a clinical association between migraine and multiple sclerosis. MAIN BODY: Migraine and MS patients share similar demographics, with the highest incidence among young, female and otherwise healthy patients. The same hormonal constellations/changes trigger disease exacerbation in both entities. Migraine prevalence is increased in MS patients, which is further enhanced by disease-modifying treatment. Clinical data show that onset of migraine typically starts years before the clinical diagnosis of MS, suggesting that there is either a unidirectional relationship with migraine predisposing to MS, and/or a "shared factor" underlying both conditions. Brain imaging studies show white matter lesions in both MS and migraine patients. Neuroinflammatory mechanisms likely play a key role, at least as a shared downstream pathway. In this review article, we provide an overview of the literature about 1) the clinical association between migraine and MS as well as 2) brain MRI studies that help us better understand the mechanistic relationship between both diseases with implications on their underlying pathophysiology. CONCLUSION: Studies suggest a migraine history predisposes patients to develop MS. Advanced brain MR imaging may shed light on shared and distinct features, while helping us better understand mechanisms underlying both disease entities.
 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune-mediated disease characterized by complicated neuropsychiatric symptoms and the detection of cerebrospinal fluid antibodies against the GluN1 subunit of the NMDAR. With the proposed clinical method, more anti-NMDAR encephalitis patients have been discovered since its first report. However, anti-NMDAR encephalitis overlapping with multiple sclerosis (MS) is rare. Herein we report a male patient with anti-NMDAR encephalitis who developed MS in mainland China. Furthermore, we summarized the characteristics of patients who were diagnosed with overlapping MS and anti-NMDAR encephalitis in previous studies. Additionally, we pioneered the use of mycophenolate mofetil in immunosuppressive therapy, providing a novel therapeutic alternative for overlapping anti-NMDAR encephalitis and MS.
 INTRODUCTION: Cognitive impairment (CI) is a core feature of Multiple Sclerosis (MS), being detectable in up to 65% of subjects. Treatment of CI can be considered of paramount importance. However, no standardized strategies are available to date to define the best treatment approach, especially for the pharmacological management. AREAS COVERED: In this narrative review, the authors outline the latest advances in pharmacological management of CI in MS, including Disease Modifying Treatments (DMTs) which indirectly may or may not influence CI and symptomatic drugs. Selected publications were restricted to those written in English, reporting on an adult relapsing-remitting MS or progressive MS sample, assessing the effects of (at least) 1 DMT or treatment in a longitudinal design, reporting data on (at least) one standardized cognitive test performed at baseline and follow-up, and published between January 2018 and May 2022. EXPERT OPINION: Recent data can be considered encouraging and inspiring for future studies. Overall, there is preliminary evidence of a beneficial effect of DMTs on cognition, particularly for high-efficacy DMTs. As for symptomatic treatments, dalfampridine appears to be the only medication with robust evidence of a positive effect on cognition. However, the definition of clinically meaningful change/improvement in cognitive functions remains an unmet need. Future studies should assess the role of other patient-related factors that can be associated with a better cognitive response to treatments and investigate the possible positive effect of multimodal interventions on cognition.
 BACKGROUND: Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease that causes significant disabilities. Latest MS epidemiological data in Australia reveal rising prevalence. No epidemiological study of MS has been conducted so far in the Illawarra region. AIM: To calculate prevalence and incidence of MS in the Illawarra region and compare with data from other regions, states and the national prevalence. METHODS: Data of MS patients in the Illawarra region were collected from hospital medical records, ambulatory care units and hospital pharmacy. Prevalence was calculated for alive MS patients on 30 June 2018 expressed per 100 000 population. Yearly adjusted incidence rate was calculated for 10 years (2009-2019), expressed as cases per 100 000 population-years. RESULTS: Estimated MS prevalence in the Illawarra region was 116.6 per 100 000 population with yearly incidence (2009-2019) of 5.06 cases per 100 000 population-years (female to male, 3:1). Relapsing-remitting MS (RRMS) was the most common type (277/397; 69.7%) with primary progressive MS (PPMS) in 52/397 (13%), and secondary progressive MS (SPMS) in 45/397 (11.3%; unknown in 23). The commonest age at diagnosis ranged between 30 and 39 years for all types with RRMS and PPMS between 30-39 years and 40-49 years respectively. The most common recorded treatment was natalizumab (103 patients), followed by fingolimod (82 patients) and interferon (58 patients). CONCLUSION: The calculated MS prevalence in the Illawarra region is higher than New South Wales and the Australian average MS prevalence. Further epidemiological studies focussing on MS risk factors and other factors bearing on MS prevalence in the Illawarra region are required.
 BACKGROUND: As their disease evolves, most patients with progressive forms of multiple sclerosis (MS) develop particular healthcare needs that are not always addressed with usual follow-up. To adapt neurological care to these patients, we created a specific consultation for patients with progressive MS in our centre in 2019. OBJECTIVES: To explore the main unmet care needs of patients with progressive MS in our setting, and to establish the usefulness of the specific consultation to address them. METHODS: Literature review and interviews with patients and healthcare professionals were conducted to identify the main unmet needs in routine follow-up. Two questionnaires were developed, assessing the importance of the unmet needs identified and the usefulness of the consultation to meet them, for patients under follow-up in the specific consultation and their informal caregivers. RESULTS: Forty-one patients and nineteen informal caregivers participated. The most important unmet needs were the information about the disease, access to social services and coordination between specialists. A positive correlation was found between the importance of these unmet needs and the responsiveness to each of them in the specific consultation. CONCLUSIONS: The creation of a specific consultation may improve attention to the healthcare needs of patients with progressive MS.

 Multiple sclerosis is a chronic neuroinflammatory demyelinating disease of the central nervous system (CNS) of unknown etiology and still incompletely clarified pathogenesis. The disease is generally considered a disorder resulting from a complex interplay between environmental risk factors and predisposing causal genetic variants. To examine the etiopathogenesis of the disease, two complementary pre-clinical models are currently discussed: the "outside-in" model proposing a peripherally elicited inflammatory/autoimmune attack against degraded myelin as the cause of the disease, and the "inside-out" paradigm implying a primary cytodegenerative process of cells in the CNS that triggers secondary reactive inflammatory/autoimmune responses against myelin debris. In this review, the integrating pathogenetic role of damage-associated molecular patterns (DAMPs) in these two scenario models is examined by focusing on the origin and sources of these molecules, which are known to promote neuroinflammation and, via activation of pattern recognition receptor-bearing antigen-presenting cells, drive and shape autoimmune responses. In particular, environmental factors are discussed that are conceptually defined as agents which produce endogenous DAMPs via induction of regulated cell death (RCD) or act themselves as exogenous DAMPs. Indeed, in the field of autoimmune diseases, including multiple sclerosis, recent research has focused on environmental triggers that cause secondary events in terms of subroutines of RCD, which have been identified as prolific sources of DAMPs. Finally, a model of a DAMP-driven positive feed-forward loop of chronic inflammatory demyelinating processes is proposed, aimed at reconciling the competing "inside-out" and "outside-in" paradigms.
 New treatment options are available for active progressive multiple sclerosis (MS), including primary and secondary progressive forms. Several pieces of evidence have recently suggested a "window of beneficial treatment opportunities," principally in the early stages of progression. However, for progressive MS, which is characterised by an inevitable tendency to get worse, it is crucial to redefine the "response to treatment" beyond the concept of "no evidence of disease activity" (NEDA-3), which was initially conceived to evaluate disease outcomes in relapsing-remitting form, albeit it is currently applied to all MS cases in clinical practice. This review examines the current perspectives and limitations in assessing the effectiveness of DMTs and disease outcomes in progressive MS, the current criteria applied in defining the response to DMTs, and the strengths and limitations of clinical scales and tools for evaluating MS evolution and patient perception. Additionally, the impact of age and comorbidities on the assessment of MS outcomes was examined.
 The link between vitamin D and multiple sclerosis (MS) has been suggested in epidemiological, genetic, immunological, and clinical studies. The aim of the present systematic review of the literature was to assess the effects of vitamin D supplementation on clinical and imaging outcomes in patients with MS. The outcomes we assessed included relapse events, disability progression, and magnetic resonance imaging (MRI) lesions. The search was conducted using PubMed, ClinicalTrials.gov, and EudraCT databases, and it included records published up until 28 February 2023. The systematic review was reported according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) 2020 guidelines. Nineteen independent clinical studies (corresponding to 24 records) were included in the systematic review. The risk of bias in randomized controlled trials (RCTs) was analyzed using the Cochrane risk-of-bias tool. Fifteen trials investigated relapse events, and most of them reported no significant effect of vitamin D supplementation. Eight of 13 RCTs found that vitamin D supplementation had no effect on disability [assessed by Expanded Disability Status Scale (EDSS) scores] compared to controls. Interestingly, recent RCTs reported a significant reduction in new MRI lesions in the central nervous system of MS patients during supplementation with vitamin D3.
 BACKGROUND: Sexual function is often impaired following neurological disorders such as multiple sclerosis (MS). Young women with MS encourage disruptions in sexual function, sexual behaviors, and family formation as common global problems. Thus, the aim of the present systematic review and meta-analysis study was to investigate the global prevalence of female sexual dysfunction (FSD) worldwide. METHODS: Various databases (PubMed, Scopus, Web of Science, Embase, and ScienceDirect) along with Google Scholar search engine were hired for systematic searching in the field of the prevalence of FSD (by July 2022). The heterogeneity of the studies was assessed using I(2) index, and random effects model was used to perform the analysis (CMA software, v.2). RESULTS: Following assessment of 14 included studies with the sample size of 2115 women, a total prevalence of sexual dysfunction (SD) in women with MS was reported 62.5% (95% CI 53.9-70.5). Meta-regression assessment also showed that FSD accelerates following increasing the sample size and the year of the studies. CONCLUSION: The total prevalence of SD in women with MS was found considerably high (62.5%) in the world, which needs more serious attention by health policymakers. Correct implementation of health policies can potentially increase the society's awareness and successful treatment of SD in MS patients.

 BACKGROUND: Late-onset multiple sclerosis (LOMS) is defined as the onset of symptoms above 50 years, corresponding to an increasingly recognized subset of MS. This study aimed at comparing demographic and clinical data of patients with LOMS to those of early-onset MS (EOMS) from a Portuguese cohort. METHODS: Retrospective chart review of an MS cohort from a Portuguese tertiary center. RESULTS: From 746 patients with MS (61.7% female), we identified 39 cases with presentation after 50 years of age (22 males and 17 females), corresponding to 5.3%. The mean age at onset was 55.4 (±5.0) for LOMS and 29.5 (±8.9) for EOMS. There was no significant difference in disease duration. The most common type was relapsing-remitting MS, accounting for 51.5% and 83.9% of LOMS and EOMS patients, respectively. Primary-progressive MS (PPMS) was significantly more represented in the LOMS group (41.0%) (p < 0.01). The median EDSS was significantly higher in the LOMS group (4.75, 0.0-7.5) when compared to the EOMS group (2.0, 0.0-9,0). The most frequent presenting feature was myelitis in both LOMS (48.7%) and EOMS patients (47.4%), resulting in significantly higher EDSS (p = 0.003). CONCLUSIONS: LOMS is associated with higher EDSS when considering the same disease duration, translating into increased disability.

 Multiple sclerosis (MS) is an autoimmune inflammatory condition affecting the central nervous system (CNS). A systematic review following the PRISMA guidelines was performed to explore the effect of metabolic and bariatric surgery (MBS) on the clinical course and outcomes in patients with multiple sclerosis. Eleven articles examining 394 patients were included in the final analysis. The mean MS duration at the time of surgery was 7.6 ± 4.6 years, and the mean postoperative follow-up was 35.5 ± 5.3 months. MBS leads to the same weight loss with the same complication rate as in patients without MS. Most of patients experienced improvement in clinical course of MS after MBS, compared to non-surgical group. However, there is a risk for MS exacerbation in a number of patients after MBS; they should not be disadvantaged from having MBS, since surgery leads to the same weight loss outcomes with the same complication rate as in patients without MS.
 The impact of pregnancy and breastfeeding on the development and outcomes of Multiple sclerosis (MS) has been debated for decades. Since several factors can influence the evolution of the disease, the protective role of multiparity and breastfeeding remains uncertain, as well the role of hormone replacement therapy in the perimenopausal period. We report two cases of relatively late-onset MS in two parous women, who developed their first neurological symptoms after six and nine pregnancies, respectively. Both women breastfed each of their children for 3 to 12 months. One of them underwent surgical menopause and received hormone replacement therapy for 7 years before MS onset. We performed a systematic literature review to highlight the characteristics shared by women who develop the disease in similar conditions, after unique hormonal imbalances, and to collect promising evidence on this controversial issue. Several studies suggest that the beneficial effects of pregnancy and breastfeeding on MS onset and disability accumulation may only be realized when several pregnancies occur. However, these data on pregnancy and breastfeeding and their long-term benefits on MS outcomes suffer from the possibility of reverse causality, as women with milder impairment might choose to become pregnant more readily than those with a higher level of disability. Thus, the hypothesis that multiparity might have a protective role on MS outcomes needs to be tested in larger prospective cohort studies of neo-diagnosed women, evaluating both clinical and radiological features at presentation.
 BACKGROUND: Quality of life (QoL) is commonly impaired among people with multiple sclerosis (PwMS). The aim of this study was to evaluate via meta-analysis the efficacy of Mindfulness-based interventions (MBIs) for improving QoL in PwMS. METHODS: Eligible randomized controlled trials (RCTs) were identified via searching six major electronic databases (MEDLINE, EMBASE, CINAHL, Cochrane Central Register of Controlled Trials, AMED, and PsycINFO) in April 2022. The primary outcome was QoL. Study quality was determined using the Cochrane Collaboration risk of bias tool. Meta-analysis using a random effects model was undertaken. Effect sizes are reported as Standardized Mean Difference (SMD). Prospero ID: 139835. RESULTS: From a total of 1312 individual studies, 14 RCTs were eligible for inclusion in the meta-analysis, total participant n = 937. Most studies included PwMS who remained ambulatory. Cognitively impaired PwMS were largely excluded. Comorbidities were inconsistently reported. Most MBIs were delivered face-to face in group format, but five were online. Eight studies (n = 8) measured MS-specific QoL. In meta-analysis, overall effect size (SMD) for any QoL measure (n = 14) was 0.40 (0.18-0.61), p = 0.0003, I(2) = 52%. SMD for MS-specific QoL measures (n = 8) was 0.39 (0.21-0.57), p < 0.0001, I(2) = 0%. MBI effect was largest on subscale measures of mental QoL (n = 8), SMD 0.70 (0.33-1.06), p = 0.0002, I(2) = 63%. Adverse events were infrequently reported. CONCLUSIONS: MBIs effectively improve QoL in PwMS. The greatest benefits are on mental health-related QoL. However, more research is needed to characterize optimal formatting, mechanisms of action, and effects in PwMS with more diverse social, educational, and clinical backgrounds.
 BACKGROUND: Comorbid conditions are common in people with multiple sclerosis (pwMS). They can delay diagnosis and negatively impact the disease course, progression of disability, therapeutic management, and adherence to treatment. OBJECTIVE: To quantify the economic impact of comorbidity in multiple sclerosis (MS), based on cost-of-illness estimates made using a bottom-up approach. METHODS: A retrospective study was carried out in two northern Italian areas. The socio-demographic and clinical information, including comorbidities data, were collected through ad hoc anonymous self-assessment questionnaire while disease costs (direct and indirect costs of disease and loss of productivity) were estimated using a bottom-up approach. Costs were compared between pwMS with and without comorbidity. Adjusted incremental costs associated with comorbidity were reported using generalized linear models with log-link and gamma distributions or two-part models. RESULTS: 51.0% of pwMS had at least one comorbid condition. Hypertension (21.0%), depression (15.7%), and anxiety (11.7%) were the most prevalent. PwMS with comorbidity were more likely to use healthcare resources, such as hospitalizations (OR = 1.21, p < 0.001), tests (OR = 1.59, p < 0.001), and symptomatic drugs and supplements (OR = 1.89, p = 0.012), and to incur non-healthcare costs related to investment (OR = 1.32, p < 0.001), transportation (OR = 1.33, p < 0.001), services (OR = 1.33, p < 0.001), and informal care (OR = 1.43, p = 0.16). Finally, they experienced greater productivity losses (OR = 1.34, p < 0.001) than pwMS without comorbidity. The adjusted incremental annual cost per patient due to comorbidity was €3,106.9 (13% of the overall costs) with MS disability found to exponentially affect annual costs. CONCLUSION: Comorbidity has health, social, and economic consequences for pwMS.
 BACKGROUND: Several studies report mixed associations between the retinal nerve fiber layer (RNFL) thickness with cognitive and physical disability in persons with multiple sclerosis (PwMS). Systematic synthesis of these findings is crucial in deriving credible conclusions. METHODS: Five databases were searched from their inception to March 2022. The inclusion criteria for studies were MS-specific and required RNFL and cognitive performance data in order to be analyzed. The selection processes followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. RESULTS: The systematic review yielded 31 studies that investigated the association between RNFL thickness and cognitive performance. Twenty-two studies reported positive associations, and nine did not. The meta-analysis included 11 studies with a total of 782 PwMS with mean age of 40.5 years, mean Expanded Disability Status Scale (EDSS) of 2.7, and disease duration of 11.3 years. RNFL thickness was significantly associated Symbol Digit Modalities Test (pooled r = 0.306, p < 0.001), Paced Auditory Serial Addition Test (pooled r = 0.374, p < 0.001) and Word List Generation (WLG, pooled r = 0.177, p < 0.001). RNFL was also significantly correlated with visuospatial learning and memory tests (pooled r = 0.148, p = 0.042) and verbal learning and memory tests (pooled r = 0.245, p = 0.005). Within three eligible studies, no significant association between ganglion cell inner-plexiform layer and SDMT 0.083 (95% CI - 0.186, 0.352) was noted. The heterogeneity was high in all correlation studies (I(2) > 63% and p < 0.008) except for the WLG and visuospatial memory findings. CONCLUSION: RNFL thickness is associated with cognitive processing speed, verbal learning and memory, visual learning and memory, as well as verbal fluency in PwMS. The number of studies included in the meta-analyses were limited due to non-standardized reporting.
 Multiple sclerosis(MS) shows the pathological characteristics of &quot;inflammatory injury of white matter&quot; and &quot;myelin repair disability&quot; in the central nervous system(CNS). It is very essential for MS treatment and reduction of disease burden to strengthen repair, improve function, and reduce disability. Accordingly, different from the simple immunosuppression, we believe that key to strengthening remyelination and maintaining the &quot;damage-repair&quot; homeostasis of tissue is to change the current one-way immunosuppression strategy and achieve the &quot;moderate pro-inflammation-effective inflammation removal&quot; homeostasis. Traditional Chinese medicine shows huge potential in this strategy. Through literature research, this study summarized the research on remyelination, discussed the &quot;mode-rate pro-inflammation-effective inflammation removal&quot; homeostasis and the &quot;damage-repair&quot; homeostasis based on microglia, and summed up the key links in remyelination in MS. This review is expected to lay a theoretical basis for improving the function of MS patients and guide the application of traditional Chinese medicine.
 BACKGROUND: A contemporary understanding of disability evolution in multiple sclerosis (MS) is an essential tool for individual disease management and planning of interventional studies. We have used prospectively collected longitudinal data to analyse disability progression and variation in a British MS cohort. METHODS: Cox proportional hazards regression was used to estimate hazard of Expanded Disability Status Scale (EDSS) 4.0 and 6.0. A continuous Markov model was used to estimate transitional probabilities for individual EDSS scores. Models were adjusted for age at MS onset, sex and disease-modifying treatments (DMTs) exposure. RESULTS: 2135 patients were included (1487 (70%) female, 1922 (89%) relapsing onset). 865 (41%) had used DMTs. Median time to EDSS 4.0 and 6.0 was 18.2 years (95% CI 16.3 to 20.2) and 22.1 years (95% CI 20.5 to 24.5). In the Markov model, the median time spent at EDSS scores of <6 (0.40-0.98 year) was shorter than the time spent at EDSS scores of ≥6 (0.87-4.11 year). Hazard of change in EDSS was greatest at EDSS scores <6 (HR for increasing EDSS: 1.02-1.33; decreasing EDSS: 0.34-1.27) compared with EDSS scores ≥6 (HR for increasing EDSS: 0.08-0.61; decreasing EDSS: 0.18-0.54). CONCLUSIONS: These data provide a detailed contemporary model of disability outcomes in a representative population-based MS cohort. They support a trend of increasing time to disability milestones compared with historical reference populations, and document disability variation with the use of transitional matrices. In addition, they provide essential information for patient counselling, clinical trial design, service planning and offer a comparative baseline for assessment of therapeutic interventions.
 The earlier the diagnosis of multiple sclerosis (MS), the sooner disease-modifying treatments can be initiated. However, significant delays still occur in developing countries. We aimed to identify factors leading to delayed diagnosis of MS in Upper Egypt. One hundred forty-two patients with remitting relapsing MS (RRMS) were recruited from 3 MS units in Upper Egypt. Detailed demographic and clinical data were collected. Neurological examination and assessment of the Disability Status Scale (EDSS) were performed. The mean age was 33.52 ± 8.96 years with 72.5% of patients were females. The mean time from symptom onset to diagnosis was 18.63 ± 27.87 months and the median was 3 months. Seventy-two patients (50.7%) achieved diagnosis within three months after the first presenting symptom (early diagnosis), while seventy patients (49.3%) had more than three months delay in diagnosis (delayed diagnosis). Patients with a delayed diagnosis frequently presented in the period before 2019 and had a significantly higher rate of initial non-motor presentation, initial non-neurological consultations, prior misdiagnoses, and a higher relapse rate. Another possible factor was delayed MRI acquisition following the initial presentation in sixty-six (46.5%) patients. Multivariable logistic regression analysis demonstrated that earlier presentation, initial non-neurological consultation, and prior misdiagnosis were independent predictors of diagnostic delay. Despite advances in MS management in Egypt, initial non-neurological consultation and previous misdiagnoses are significant factors responsible for delayed diagnosis in Upper Egypt.
 INTRODUCTION: MRI activity is less frequent among secondary progressive multiple sclerosis (SPMS) patients. In the current study, we aimed to identify SPMS patients with higher radiological disease activity (RDA) and determine their clinical characteristics. METHODS: We evaluated the occurrence of RDA in SPMS patients followed at the Sheba Multiple Sclerosis Center between January 1, 2015, and December 31, 2020. All patients underwent brain and spinal cord MRI examinations as a routine follow-up unrelated to clinical disease activity. Patients were subdivided into RDA and non-RDA MRI groups based on the presence of active gadolinium-enhancing T1 lesions and/or new/enlarging T2 lesions. Demographic variables and disease-related data were compared. RESULTS: One hundred consecutive SPMS patients, 74 females, median age of 50 years, disease duration of 19.5 years, and neurological disability by the Expanded Disability Status Scale (EDSS) score of 6.0, were included in the study. The RDA group comprised 35 patients (35%), of them 65.7% (n = 23) exhibited only brain MRI activity, 22.8% (n = 8) only spinal cord MRI activity, and 11.4% (n = 4) had both. Patients in the RDA group were diagnosed at a younger mean (SD) age of 28.2 (8.9) versus 33.7 (10.1) years and were younger with a mean (SD) age of 47.8 (9.9) versus 53.4 (10.1) years, as compared with the non-RDA group. No significant differences were found in relation to disease duration, EDSS, exposure to immunomodulatory treatments, and duration of immunomodulatory treatments. CONCLUSIONS: RDA unrelated to clinical symptomatology was more frequent in a subgroup of young SPMS patients.
 BACKGROUND AND OBJECTIVES: Depression is common in multiple sclerosis (MS) and is associated with faster disability progression. The etiology of comorbid depression in MS remains poorly understood. Identification of individuals with a high risk of depression, through polygenic scores (PGS), may facilitate earlier identification. Previous genetic studies of depression considered depression as a primary disorder, not a comorbidity, and thus, findings may not generalize to MS. Body mass index (BMI) is a risk factor of both MS and depression, and its association may highlight differences in depression in MS. To improve the understanding of comorbid depression in MS, we will investigate PGS in people with MS, with the hypothesis that a higher depression PGS is associated with increased odds for comorbid depression in MS. METHODS: Samples from 3 sources (Canada, UK Biobank, and the United States) were used. Individuals were grouped into cases (MS/comorbid depression) and compared with 3 control groups: MS/no depression, depression/no immune disease, and healthy persons. We used 3 depression definitions: lifetime clinical diagnoses, self-reported diagnoses, and depressive symptoms. The PGS were tested in association with depression using regression. RESULTS: A total of 106,682 individuals of European genetic ancestry were used: Canada (n = 370; 213 with MS), UK Biobank (n = 105,734; 1,390 with MS), and the United States (n = 578 with MS). Meta-analyses revealed individuals with MS and depression had a higher depression PGS compared with both individuals with MS without depression (odds ratio range per SD 1.29-1.38, p < 0.05) and healthy controls (odds ratio range per SD 1.49-1.53, p < 0.025), regardless of the definition applied and when sex stratified. The BMI PGS was associated with depressive symptoms (p ≤ 0.001). The depression PGS did not differ between depression occurring as a comorbid condition with MS or as the primary condition (odds ratio range per SD 1.03-1.13, all p > 0.05). DISCUSSION: A higher depression genetic burden was associated with approximately 30%-40% increased odds of depression in European genetic ancestry participants with MS compared with those without depression and was no different compared with those with depression and no comorbid immune disease. This study paves the way for further investigations into the possible use of PGS for assessing psychiatric disorder risk in MS and its application to non-European genetic ancestries.

 OBJECTIVE: This research was conducted to assess Neurofilament light chain (NfL) as prognostic factor for Multiple Sclerosis and effect of Fingolimod on plasma levels of NfL. MATERIALS AND METHODS: A systemic search was conducted from electronic databases (PubMed/Medline, Cochrane Library, and Google Scholar) from inception to 7th September 2022. All statistical analyses were conducted in Review Manager 5.4.1. Studies meeting inclusion criteria were selected. Only those studies that involved Multiple sclerosis patients in which plasma levels of NfL was provided and Fingolimod was used in the treatment group. Fixed-effect model was used to pool the studies to assess NfL as prognostic factor, which was reported in the Hazards ratio (HR) and their corresponding 95% confidence interval (CI). Moreover, effect of Fingolimod on NfL levels was analysed qualitatively. RESULTS: Five Randomized Controlled Trials were used in the study. Four studies were used in quantitative analysis which showed increased NfL was related to significant increase in cognitive disability worsening (HR= 1.66 [1.35, 2.05]; p< 0.00001; I(2)= 0%). The qualitative analysis method was employed to evaluate the factors correlating with increased NfL levels in Multiple Sclerosis patients. Five studies evaluated that there was significant decrease in NfL levels when Fingolimod was used as compared to placebo. 4 studies were included to correlated NfL levels with clinical and MRI parameters and association was found between increasing NfL levels and relapses, active/new T2 lesions and percentage of brain volume change. CONCLUSION: The results of our meta-analysis and systematic review demonstrated statistically significant effect of NfL as a prognostic marker with its level being decreased significantly when Fingolimod was used for treating Multiple Sclerosis.
 BACKGROUND: The current standard endpoint to assess disability accumulation in multiple sclerosis (MS) clinical trials is the time to the first confirmed disability progression, which excludes subsequent progression events. Including recurrent progression events may permit a more comprehensive assessment of treatment effects on disability progression. OBJECTIVE: To propose a definition of recurrent disability progression events and to compare time-to-first and recurrent event analysis. METHODS: Recurrent disability progression events were defined by expanding the recommended first event definition. Marginal recurrent event methods (negative binomial model, Lin-Wei-Yang-Ying model) were compared with Cox regression in data from three randomized controlled trials in relapsing multiple sclerosis (RMS) and primary progressive multiple sclerosis (PPMS), and in simulated randomized controlled trial data. RESULTS: The recurrent event analyses included a substantially larger number of progression events compared with the time-to-first-event analyses (+7.5% and +9.9% in the RMS trials and +22.7% in the PPMS trial). The increase in the number of events resulted in more precise treatment effect estimates and a corresponding gain in statistical power. CONCLUSION: Our results support the use of recurrent event data analysis, especially in progressive MS trials, to improve estimates of treatment effects, increase statistical power, and better capture the clinically meaningful long-term disability progression experience.
 OBJECTIVE: As personality changes and personality disorders are frequently observed in multiple sclerosis (MS), personality may be a prognostic factor for this disease. The present study investigated the influence of personality on disability, progression, and treatment adherence in MS. METHOD: Personality was assessed in 41 patients with Relapsing-Remitting MS (30 females; mean age = 42.63 years) using the NEO Personality Inventory-3rd edition. Disability was measured with the Expanded Disability Status Scale, and treatment adherence information was collected from the Swiss MS Cohort. Correlation, multiple linear and partial least square regressions were performed to examine relations between personality, disability, and treatment adherence in MS. RESULTS: After accounting for age and time since disease onset, our analysis revealed that Neuroticism (β = 0.32, p = 0.01) and its Vulnerability facet (β = 0.28, p < 0.05) predicted greater disability, whereas Extraversion (β = -0.25, p = 0.04) and its Activity facet (β = -0.23, p < 0.05) predicted milder disability. Regarding disability progression, correlational analysis revealed that it was negatively correlated with Extraversion (r = -0.44, p = 0.02) and the Feelings facet of Openness (r = -0.41, p = 0.03), but regressions failed to highlight any predictive links. No significant results could be demonstrated for treatment adherence. CONCLUSIONS: Overall, our study showed that some personality traits can impact disability in MS, indicating that these should be considered in clinical practice, as they could be used to adapt and improve patients' clinical support.
 OBJECTIVE: A growing body of research examining the effect of exercise on cognitive function in people with multiple sclerosis (MS), while findings of available studies were conflicting. We aimed to explore the effect of exercise on cognitive function in MS patients. METHODS: For this systematic review and meta-analysis, we searched PubMed, Web of Science, EBSCO, Cochrane, and Scopus electronic databases, through July 18, 2022. Cochrane risk assessment tool was used to evaluate the methodological quality of the included literature. RESULTS: Twenty-one studies with a total of 23 experimental groups and 21 control groups met the inclusion criteria. There was a significant effect of exercise on improving cognitive function in MS patients, while the effect size was small (Cohen's d = 0.20, 95% CI 0.06-0.34, p < 0.001, I(2) = 39.31%). Subgroup analysis showed that exercise significantly improved memory (Cohen's d = 0.17, 95% CI 0.02-0.33, p = 0.03, I(2) = 7.59%). In addition, multicomponent training, exercise conducted 8 weeks and 10 weeks, up to 60 min per session, 3 times or more per week, 180 min or more per week increased cognitive function significantly. Furthermore, a worse basal MS status (defined by the Expanded Disability Status Scale) and an older age were associated with greater improvement in cognitive function. CONCLUSION: MS patients are recommended to participate in at least three multicomponent training sessions per week, with each session lasting up to 60 min, and the exercise goal of 180 min per week can be achieved by increasing the frequency of exercise. Exercise lasting 8 or 10 weeks is best for cognitive function improvement. Additionally, a worse basal MS status, or the older the age, the greater effect on cognitive function.
 SIGNIFICANCE: Unilateral gaze-evoked nystagmus is a rare neurologic finding that is largely diagnosed in connection with ischemic stroke. Gazed-evoked nystagmus is also a rare initial presentation of multiple sclerosis. PURPOSE: This study aimed to report a rare presentation of gaze-evoked nystagmus in a patient with multiple sclerosis and review the mechanism underlying the gaze-evoked nystagmus. CASE REPORT: A 32-year-old man presented with a 1-week history of diplopia. Neurologic examination revealed right-sided gaze-evoked nystagmus and right-sided ataxia. Laboratory test revealed a positive result for oligoclonal bands. Contrast brain MRI revealed multiple hyperintense T2 lesions including a hyperintense patch at the right inferior cerebellar peduncle. A diagnosis of multiple sclerosis was made. The patient received methylprednisolone 500 mg intravenously for 14 days. The diplopia and gaze-evoked nystagmus resolved and remained stable 2 months later. CONCLUSIONS: Our case demonstrates that damage to the inferior cerebellar peduncle may result in ipsilesional gaze-evoked nystagmus and ipsilesional ataxia, in contrast to ipsilesional gaze-evoked nystagmus and contralesional ataxia.
 Cerebellar dysfunction is likely to cause severe and treatment-resistant disability in multiple sclerosis (MS). Certain spinocerebellar ataxia (SCA)-related alleles can increase MS susceptibility, and channel polymorphisms can impact disability measures. Following an index patient with the coexistence of MS and SCA Type-8 (SCA8) in the MS clinic, an institutional engine search for MS and hereditary ataxia coexistence was conducted but did not reveal any other cases. This extremely rare coexistence of MS and SCA8 in our index patient may be incidental; however, a yet-to-be-identified contribution of coexistent hereditary ataxia(s) to the susceptibility of a prominent progressive ataxia MS phenotype cannot be ruled out.
 OBJECTIVE: Multiple sclerosis (MS) is a chronic disease with different clinical courses and a tendency to worsening. The relapsing-remitting MS presents acute onset and relapses of neurological symptoms, followed by their remission. This form can convert to secondary progressive MS (SPMS) with irreversible neurological worsening and disability. The identification of signs, symptoms, markers of progression, and strategies to manage MS patients is mandatory to allow early identification of those at higher risk of conversion to SPMS, for prompt intervention to cope with the progression of the disease. METHODS: A panel of Italian experts from Southern Italy have reviewed the current knowledge on MS and its management and identified the crucial tools for SPMS recognition. RESULTS: More effective communication between patients and clinicians should be established, with the support of digital tools. Moreover, the improvement in the clinical use of biomarkers for progression (cellular structures and tissue organization, such as neurofilaments and chitinase 3-like 1, axonal and neurons density) and of instrumental analyses for recognition of whole-brain atrophy, chronic active lesions, spinal cord lesions and atrophy, and the improvement the combination of the Expanded Disability Status Scale and the evaluation of cognitive dysfunction are discussed. CONCLUSION: Given the availability of a pharmacological option, adequate education both for patients, regarding the evolution of the disease and the specific treatment, and for professionals, to allow more effective and sensitive communication and the best use of diagnostic and management tools, could represent a strategy to improve patient management and their quality of life.
 Isolated cognitive relapses (ICRs) have been a matter of debate for the past few years. Currently, there is no clear consensus on such an entity, as cognitive decline usually accompanies typical multiple sclerosis (MS) relapses. Herein, we present the neuropsychological and neurophysiological manifestations of a patient who suddenly complained of confusion and memory loss, showing insight into her deficit, in absence of sensorimotor disturbances. Neuroimaging revealed a large tumefactive gadolinium-enhancing lesion localized in the left medial temporal lobe. The patient's symptoms persisted for months afterwards, despite corticosteroid treatment. We believe our patient experienced a true ICR. ICRs are rare entities in MS, but we should be alert to their existence in order to treat them promptly. Deepening their pathophysiology is equally important and neuropsychology combined with neurophysiology may be useful in this regard.
 BACKGROUND: Music Therapy (MT) is a unique treatment method for Persons with Multiple Sclerosis (PwMS) that can accelerate their functional recovery. MT has been proven to adjust the gait performance of PwMS in a short period. Its therapeutic effects in gait disorders of PwMS for long-term intervention are also starting to draw interest, but it has yet to be investigated. AIM: This review aimed to systematically examine the outcomes of PwMS with gait disorders after receiving MT intervention. METHODS: A systematic review has been performed using several academic databases with keywords such as music therapy, multiple sclerosis, and gait. The study protocol was registered on PROSPERO (CRD42022365668). RESULTS: A total of 405 studies were initially identified. After applying the inclusion and exclusion criteria, twelve studies were finally included. The results showed that all PwMS received MT intervention with different strategies, and ten studies confirmed that gait disorders of PwMS were effectively improved by MT intervention. CONCLUSION: Most previous studies focused on the transient effects of MT on the gait performance of PwMS. This review bridges gaps in the long-term intervention of MT on gait disorders of PwMS and offers references for therapists to design treatment plans. According to this review, MT intervention has positive therapeutic effects on gait disorders in PwMS.
 BACKGROUND: Dysesthetic or ongoing extremity pain is a common symptom in all multiple sclerosis (MS) types. Although the pathology of the disease is the demyelination of central neurons, the patients may also complain of neuropathic pain in distal extremities that is generally related to A-delta and C fiber dysfunction. It is not known whether thinly myelinated and unmyelinated fibers are affected in MS patients. We aim to investigate the small fiber loss and its length dependency. METHODS: We evaluated the skin biopsy taken from proximal and distal leg of MS patients with neuropathic pain. Six patients with primary progressive MS (PPMS), seven with relapsing-remitting MS (RRMS), seven with secondary progressive MS (SPMS) and as a control group ten age and sex-matched healthy controls were included. Neurological examination, electrophysiological evaluation and DN4 questionnaire were performed. Subsequently, skin punch biopsy from 10 cm above the lateral malleolus and proximal thigh were done. The biopsy samples were stained with PGP9.5 antibody and intraepidermal nerve fiber density (IENFD) was determined. RESULTS: The mean proximal IENFD was 8.58±3.58 fibers/mm among MS patients and 14.72±2.89 fiber/mm among healthy controls (p=0.001). However, the mean distal IENFD did not differ between MS patients and healthy controls (9.26±3.24 and 9.75±1.6 fiber/mm respectively. Although proximal and distal IENFD tends to be lower in MS patients with neuropathic pain, there was no statistically significant difference between MS patients with and without neuropathic pain CONCLUSION: Although MS is a demyelinating disease, unmyelinated fibers can also be affected. Our findings suggest non-length dependent small fiber neuropathy in MS patients.
 Cognitive disorders are present in 30 to 45% of relapsing-remitting forms of multiple sclerosis and in up to 50-75% of progressive forms. They bear a negative impact on the quality of life and predict an unfavorable disease progression. According to guidelines, screening based on objective measurement such as the Single Digit Modality Test (SDMT) should be performed at the time of diagnosis and then on an annual basis. Confirmation of diagnosis and management are performed in collaboration with neuropsychologists. Increased awareness from patients and healthcare professionals is important to ensure earlier management and prevent negative consequences on the patients professional and family life.

 INTRODUCTION: The prevalence of restless legs syndrome (RLS) is reported to vary in patients with multiple sclerosis (MS) in studies which are conducted in different populations. The goal of this systematic review and meta-analysis is to update the prevalence of RLS in MS cases. METHODS: We searched PubMed, Scopus, EMBASE, CINAHL, Web of Science, Google Scholar, and gray literature including references from identified studies and conference abstracts which were published up to June 2021. Data on the total number of participants, first author, country, disease duration, number of controls, mean patient age, male and female numbers, mean EDSS, and number of cases and/or controls with RLS were extracted from the included studies. RESULTS: The literature search revealed 855 articles; after deleting duplicates, 530 remained. For the meta-analysis, 75 studies were included (Fig. 1). In six articles, the authors did not differentiate between CIS and MS cases when reporting RLS cases. In total, 15,411 MS/CIS patients were evaluated and 4309 had RLS. The pooled prevalence of RLS was 28% (95% CI: 24-33%). The pooled prevalence of RLS in men was 22% (95% CI: 17-26%), and the pooled prevalence of RLS in women was 30% (95% CI: 25-35%). The pooled prevalence of RLS in controls was 8% (95% CI: 6-10%). CONCLUSION: The results of this systematic review and meta-analysis show that the pooled prevalence of RLS is 28% in MS cases and 8%. The pooled prevalence is higher in women than men (30% vs 22%).


 BACKGROUND: Seizures in people with multiple sclerosis (MS) are reported; however, the risk of epilepsy in adults with MS remains poorly defined. METHODS: We performed a systematic review and meta-analysis to evaluate the incidence and prevalence of epilepsy in adults (≥ 18 years) with MS compared to those without. We searched MEDLINE and EMBASE from inception to July 1, 2022 to include observational studies that reported the prevalence or incidence of epilepsy in adults with MS and a comparator group, consisting of adults without MS or the general population. We used the Newcastle Ottawa Scale to evaluate quality of the included studies. We performed random-effects meta-analyses to determine the prevalence and incidence of epilepsy in adults with MS compared to the non-MS group. RESULTS: We identified 17 studies consisting of 192,850 adults with MS, across nine countries. Most studies were of moderate quality as they did not specify the MS type or type of seizures. Compared to a comparison group, both the prevalence (pooled OR 2.04; 95% confidence interval 1.59-2.63, I(2) = 95.4, n = 12) and the incidence of epilepsy (pooled RR 3.34; 3.17-3.52, I(2) = 4.6%, n = 6) was higher in people with MS. Heterogeneity in estimates was not explained by additional analyses. CONCLUSIONS: MS is an independent risk factor for both incident and prevalent epilepsy, suggesting variation in grey matter involvement over the disease course. Longitudinal studies are required to help identify patient and disease characteristics associated with epilepsy.
 BACKGROUND: Low serum 25(OH)D(3) (vD) is an environmental risk factor for multiple sclerosis (MS). Lower vD levels during early disease may be associated with long-term disability. Determinants of serum vD levels in healthy individuals include supplementation behaviour and genetic factors. These determinants have been less well studied in people with MS (pwMS). METHODS: We developed a vD-weighted genetic risk score (GRS) and validated this in 373,357 UK Biobank participants without MS. We measured serum 25(OH)D(3) and genotyped six vD-associated SNPs (rs12785878, rs10741657, rs17216707, rs10745742, rs8018720, rs2282679) in a cohort of pwMS (n = 315) with age and geographically matched controls (n = 232). We then assessed predictors of serum vD concentration in this cohort. RESULTS: The GRS was strongly associated with vD status in the Biobank cohort (p < 2 × 10(-16)). vD supplementation, having MS, lower BMI, increased age and supplementation dose were associated with higher vD levels (false discovery rate, FDR < 5%). In multivariable models adjusting for supplementation, BMI, age, sex, and MS status, the GRS was strongly associated with vD level (p = 0.004), but not in those who supplemented (p = 0.47). CONCLUSIONS: Our findings suggest that vD supplementation is the major determinant of vD level in pwMS, with genetic determinants playing a far smaller role.
 BACKGROUND: Current procedures for diagnosing multiple sclerosis (MS) present a series of limitations, making it critically important to identify new biomarkers. The aim of the study was to identify new biomarkers for the early diagnosis of MS using spectral-domain optical coherence tomography (OCT) and artificial intelligence. METHODS: Spectral domain OCT was performed on 79 patients with relapsing-remitting multiple sclerosis (RRMS) (disease duration ≤ 2 years, no history of optic neuritis) and on 69 age-matched healthy controls using the posterior pole protocol that incorporates the anatomic Positioning System. Median retinal thickness values in both eyes and inter-eye difference in healthy controls and patients were evaluated by area under the receiver operating characteristic (AUROC) curve analysis in the foveal, parafoveal and perifoveal areas and in the overall area spanned by the three rings. The structures with the greatest discriminant capacity - retinal thickness and inter-eye difference - were used as inputs to a convolutional neural network to assess the diagnostic capability. RESULTS: Analysis of retinal thickness and inter-eye difference in RRMS patients revealed that greatest alteration occurred in the ganglion cell (GCL), inner plexiform (IPL), and inner retinal (IRL) layers. By using the average thickness of the GCL (AUROC = 0.82) and the inter-eye difference in the IPL (AUROC = 0.71) as inputs to a two-layer convolutional neural network, automatic diagnosis attained accuracy = 0.87, sensitivity = 0.82, and specificity = 0.92. CONCLUSION: This study adds weight to the argument that neuroretinal structure analysis could be incorporated into the diagnostic criteria for MS.
 Comorbidity is highly prevalent in people with multiple sclerosis (MS) throughout their disease course. In the last 15 years, our understanding of the association between comorbidity and outcomes such as relapses, disability progressive, health-related quality of life, health care use, and mortality has grown substantially. The broad adverse impacts of comorbidity on these outcomes point to the need to prevent and treat comorbidity effectively in people with MS. This requires having the necessary tools to evaluate comorbidity, an understanding of how MS affects management of comorbidity now, testing of interventions tailored to people with MS, and determining the best models of care to optimize comorbidity management.
 In multiple sclerosis, remyelination trials have yet to deliver success like that achieved for relapse rates with disease course modifying treatment trials. The challenge is to have a clinical, functional outcome measure. Currently, there are none that have been validated, other than visual evoked potentials in optic neuritis. Like vision, quick eye movements (saccades) are heavily dependent on myelination. We proposed that it is possible to extrapolate from demyelination of the medial longitudinal fasciculus in the brainstem to quantitative assessment of cortical networks governing saccadic eye movements in multiple sclerosis. We have developed and validated a double-step saccadic test, which consists of a pair of eye movements towards two stimuli presented in quick succession (the demonstrate eye movement networks with saccades protocol). In this single-centre, cross-sectional cohort study we interrogated the structural and functional relationships of double-step saccades in multiple sclerosis. Data were collected for double-step saccades, cognitive function (extended Rao's Brief Repeatable Battery), disability (Expanded Disability Status Scale) and visual functioning in daily life (National Eye Institute Visual Function Questionnaire). MRI was used to quantify grey matter atrophy and multiple sclerosis lesion load. Multivariable linear regression models were used for analysis of the relationships between double-step saccades and clinical and MRI metrics. We included 209 individuals with multiple sclerosis (mean age 54.3 ± 10.5 years, 58% female, 63% relapsing-remitting multiple sclerosis) and 60 healthy control subjects (mean age 52.1 ± 9.2 years, 53% female). The proportion of correct double-step saccades was significantly reduced in multiple sclerosis (mean 0.29 ± 0.22) compared to controls (0.45 ± 0.22, P < 0.001). Consistent with this, there was a significantly larger double-step dysmetric saccadic error in multiple sclerosis (mean vertical error -1.18 ± 1.20°) compared to controls (-0.54 ± 0.86°, P < 0.001). Impaired double-step saccadic metrics were consistently associated with more severe global and local grey matter atrophy (correct responses-cortical grey matter: β = 0.42, P < 0.001), lesion load (vertical error: β = -0.28, P < 0.001), progressive phenotypes, more severe physical and cognitive impairment (correct responses-information processing: β = 0.46, P < 0.001) and visual functioning. In conclusion, double-step saccades represent a robust metric that revealed a novel eye-movement impairment in individuals with multiple sclerosis. Double-step saccades outperformed other saccadic tasks in their statistical relationship with clinical, cognitive and visual functioning, as well as global and local grey matter atrophy. Double-step saccades should be evaluated longitudinally and tested as a potential novel outcome measure for remyelination trials in multiple sclerosis.
 OBJECTIVE: Previous work on temporally sparse multifocal methods suggests that the results are correlated with disability and progression in people with multiple sclerosis (PwMS). Here, we assess the diagnostic power of three cortically mediated sparse multifocal pupillographic objective perimetry (mfPOP) methods that quantified response-delay and light-sensitivity at up to 44 regions of both visual fields concurrently. METHODS: One high-spatial-resolution mfPOP method, P129, and two rapid medium-resolution methods, W12 and W20, were tested on 44 PwMS and controls. W12 and W20 took 82 s to test both visual fields concurrently, providing response delay and sensitivity at each field location, while P129 took 7 min. Diagnostic power was assessed using areas under the receiver operating characteristic (AUROC) curves and effect-size (Hedges' g). Linear models examined significance. Concurrent testing of both eyes permitted assessment of between-eye asymmetries. RESULTS: Per-region response delays and asymmetries achieved AUROCs of 86.6% ± 4.72% (mean ± SE) in relapsing-remitting MS, and 96.5% ± 2.30% in progressive MS. Performance increased with increasing disability scores, with even moderate EDSS 2 to 4.5 PwMS producing AUROCs of 82.1 to 89.8%, Hedge's g values up to 2.06, and p = 4.0e - 13. All tests performed well regardless of any history of optic neuritis. W12 and W20 performed as well or better than P129. CONCLUSION: Overall, the 82-s tests (W12 and W20) performed better than P129. The results suggest that mfPOP assesses a correlate of disease severity rather than a history of inflammation, and that it may be useful in the clinical management of PwMS.


 Introduction: Multiple sclerosis (MS) is the most common progressive neurological condition with onset in young adulthood. Because people with MS (PwMS) are often separated from specialty care by distance or disability, telemedicine can help alleviate that burden by removing obstacles to accessing care. Methods: We surveyed 762 PwMS in the iConquerMS research network about their use of in-person and telemedicine services prepandemic (January-February 2020) and during the coronavirus disease 2019 (COVID-19) pandemic (September-November 2020). The survey asked PwMS about their use of in-person and telemedicine services, technology access, perceptions and preferences of telemedicine, their most recent telemedicine encounter, and reasons for not using telemedicine. Results: Prepandemic, the most cited reason for not using telemedicine was providers not offering remote visits. During the pandemic, there was a decrease in the use of in-person health care (100% to ∼78%) and an increase in telemedicine utilization (25% to ∼80%). Most participants had access to telemedicine-enabling technologies and a large portion indicated a preference for using telemedicine for some or most/all of their MS health care (41-57%). Before the pandemic, telemedicine utilization was highest for primary care, while during the pandemic, utilization of telemedicine was greatest for general MS care. Mental health telemedicine encounters increased during the pandemic. Discussion: The dramatic increase in telemedicine utilization during the COVID-19 pandemic has provided access for PwMS to multispecialty care. Maintaining the policy changes that enabled remote health care to expand during the pandemic will be critical for sustained access to MS specialty care for this vulnerable population.
 BACKGROUND: The relation of sarcopenia and disability in MS is unknown. OBJECTIVE: To investigate the relation of temporal muscle thickness (TMT) and disability. METHODS: A cohort of 132 people who presented with a clinically isolated syndrome (CIS) suggestive of MS at a mean age of 30.0 years, were prospectively followed clinically and with MRI over 30-years. TMT and expanded disability status scale (EDSS) were assessed at baseline, one- five- ten- fourteen- twenty- and thirty-year follow-up. RESULTS: At 30-years, 27 participants remained classified as having had a CIS, 34 converted to relapsing remitting MS, 26 to secondary progressive MS, and 16 had died due to MS. Using linear mixed effect models with subject nested in time, greater annualized TMT-thinning was seen in individuals who developed MS (-0.04 mm/a, 95%CI: -0.07 to -0.01, p = 0.023). In those who converted to MS, a thinner TMT was reached at 14- (p = 0.008), 20- (p = 0.002) and 30-years (p< 0.001). TMT was negatively correlated with EDSS at 20-years (R=-0.18, p = 0.032) and 30-years (R-0.244, p = 0.005). Longitudinally, TMT at earlier timepoints was not predictive for 30-year clinical outcomes. CONCLUSION: TMT thinning is accelerated in MS and correlated with disability in later disease stages, but is not predictive of future disability.

 OBJECTIVE: To determine the influence of multiple sclerosis (MS) on in-hospital outcomes of patients with hemorrhagic strokes using a large, nationally representative database. MATERIALS AND METHODS: This population-based, retrospective study extracted data of adults with hemorrhagic stroke from the US Nationwide Inpatient Sample (NIS) database from 2016 to 2018. Patients with/without MS were then compared. Hemorrhagic stroke and MS were identified by the International Classification of Diseases, Tenth editions (ICD-10) codes. In-hospital outcomes (i.e., in-hospital mortality, discharge destination, length of stay [LOS], total hospital cost, and major complications) were compared between subjects with and without MS using logistic regression analysis. RESULTS: Among 107,573 patients with hemorrhagic stroke, 0.3% (n=337) had MS. After 1:10 propensity-score (PS) matching, 3,707 patients remained in the analytic sample. Multivariable analysis revealed that patients with MS had significantly shorter LOS (adjusted β=-1.34 days; 95% CI: -2.41 to -0.26, p=0.015), and lower total hospital costs (adjusted β=-28.82; 95% CI: -43.57 to -14.06, p<0.001) than those without MS. No significant different risks of any major complications, in-hospital mortality, or transfer to nursing homes/long-term care facilities were observed. For major complications, patients with MS had a significantly lower risk of cerebral edema than those without MS (adjusted odds ratio [aOR] = 0.66, 95%CI: 0.51 to 0.86, p =0.002) CONCLUSIONS: In hospitalized patients with hemorrhagic stroke, those with MS have shorter LOS, lower costs, and a lower risk of cerebral edema compared to no MS. More relevant experiments and studies are needed to confirm results of this study.
 BACKGROUND: Today, it is estimated that around 5% of multiple sclerosis (MS) patients are in the late-onset category (age at disease onset ≥ 50). Diagnosis and treatment in this group could be challenging. Here, we report the latest update on the characteristics of Iranian patients with late-onset MS (LOMS). METHODS: This cross-sectional study used the information provided by the nationwide MS registry of Iran (NMSRI). The registrars from 14 provinces entered data of patients with a confirmed diagnosis of MS by neurologists. Patients with disease onset at or later than 50 years of age were considered LOMS. RESULTS: Of 20,036 records, the late-onset category included 321 patients (1.6%). The age-standardized LOMS prevalence was around 75 per 100,000 people. 215 patients (67%) were female. Median Expanded Disability Status Scale (EDSS) was 3 (interquartile range: 1.5-5). The majority of the cases (56%) suffered from relapsing-remitting (RR) course while 20% were diagnosed with primary progressive (PP) MS. Significantly higher proportion of male sex, PPMS, and higher EDSS were seen in the late-onset group compared with early-onset and adult-onset cases (p-value < 0.05). Seventy-five (23%) patients did not receive any disease-modifying treatment. DISCUSSION: The more prominent degenerative pathology of LOMS may be the underlying mechanism of the observed differences in comparison to non-LOMS. CONCLUSION: There are substantial differences and knowledge gaps regarding LOMS which could be the subject of further research.
 After 2 weeks of treatment, a woman with multiple sclerosis treated with dimethyl fumarate developed alopecia. Considering the adverse events, the therapy was discontinued, leading to alopecia regression during the next 3 months. Although the precise mechanism has not been completely elucidated, glutathione depletion or downregulation of aerobic glycolysis are considered to be potential reasons for hair loss induction. The incidence and mechanism of this uncommon adverse reaction to dimethyl fumarate should be further investigated.
 BACKGROUND: Multiple Sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The most common type of MS is the relapsing-remitting MS (RRMS) where relapses are the main component of the disease course. However, the relationship between the characteristics of the relapses on one hand and their severity and outcome on the other hand has not been fully characterized. OBJECTIVES: To explore the characteristics of relapses among a cohort of Egyptian MS patients and their relation to the severity and outcome of the disease. SUBJECTS AND METHODS: We analyzed 300 attacks from 223 patients in a retrospective study to identify demographic, clinical and paraclinical (laboratory and radiological) factors affecting: 1- Severity of relapses (the difference between the EDSS at the day of maximum worsening and the EDSS before the onset of the attack). 2- Outcome of relapses (the difference between the EDSS at the day of maximum improvement and the EDSS before the onset of the relapse). RESULTS: Severe attacks were most likely to occur in patients who are males, single, presenting with poly-symptomatic presentation, slower tempo of evolution of attack symptoms, longer duration of the attack, absence of DMTs at the time of the attack. The risk of having a severe relapse is more than 3 times when the patient is single. Regarding attack outcome, poorly recovered attacks were more common in patients with older age at disease onset and at attack onset, male sex, higher number of relapses, longer duration of illness prior to the attack, severe relapses, polysymptomatic presentation, associated cognitive symptoms, slower tempo of symptom evolution, longer duration of the attack, patients on OCPs, smoking, and presence of black holes in brain MRI. The risk of having relapses with partial or no recovery is more than five times when the patient has black holes in brain MRI and more than 4 times when the patient is a smoker. CONCLUSION: Bearing in mind the demographic characteristics as well as the clinical and paraclinical characteristics of each attack and their relation to attack severity and outcome are a key to understanding the individual disease course of every patient and hence tailoring the best therapeutic plan suitable for his individual needs. In other words, prompt, rapid intervention in male patients, polysymptomatic attacks, slower tempo of evolution of attack symptoms and longer duration of the attack should be adopted since these factors are predictive of severe relapses as well as poor relapse outcome.


 Multiple sclerosis (MS) is an autoimmune disease of the central nervous system still lacking a cure. Treatment typically focuses on slowing the progression and managing MS symptoms. Single-cell transcriptomics allows the investigation of the immune system-the key player in MS onset and development-in great detail increasing our understanding of MS mechanisms and stimulating the discovery of the targets for potential therapies. Still, de novo drug development takes decades; however, this can be reduced by drug repositioning. A promising approach is to select potential drugs based on activated or inhibited genes and pathways. In this study, we explored the public single-cell RNA data from an experiment with six patients on single-cell RNA peripheral blood mononuclear cells (PBMC) and cerebrospinal fluid cells (CSF) of patients with MS and idiopathic intracranial hypertension. We demonstrate that AIM2 inflammasome, SMAD2/3 signaling, and complement activation pathways are activated in MS in different CSF and PBMC immune cells. Using genes from top-activated pathways, we detected several promising small molecules to reverse MS immune cells' transcriptomic signatures, including AG14361, FGIN-1-27, CA-074, ARP 101, Flunisolide, and JAK3 Inhibitor VI. Among these molecules, we also detected an FDA-approved MS drug Mitoxantrone, supporting the reliability of our approach.

 BACKGROUND: Multiple sclerosis (MS) prevalence is rising in the Middle East. Most MS medications are available in the region, but not all, possibly affecting neurologists' prescribing habits. OBJECTIVES: To provide an overview of the current practices of Near East (NE) healthcare practitioners by probing their prescribing decisions, to report the COVID-19 impacts on neurologists' prescribing habits, and to explore the future relevance of current medication used in MS management among other newcomers. METHODS: A cross-sectional study was carried out using an online survey from April 27, 2022, to July 5, 2022. The questionnaire was designed with the input of five neurologists representing five NE countries (Iran, Iraq, Lebanon, Jordan & Palestine). They identified several factors that play a crucial role in the optimal care of MS patients. The link was shared among neurologists using snowball sampling. RESULTS: The survey included 98 neurologists. Effectiveness and safety balance was the most important factor considered when selecting the MS treatment. Among patients with MS, the most challenging factor for the patients was thought to be related to family planning, followed by affordability and tolerability of side effects. In the treatment of mild to moderate relapsing remitting multiple sclerosis (RRMS) in men, Interferon beta 1a SC, Fingolimod, and Glatiramer acetate were the most commonly recommended treatments. Dimethyl fumarate substituted fingolimod in female patients. Interferon beta 1a SC was the safest treatment for mild to moderate RRMS. Interferon beta 1a SC was preferred over other treatments for patients with mild to moderate MS and planning for pregnancy (56.6%) or breastfeeding (60.2%). Fingolimod was not a choice for these patients. Neurologists seemed to discuss the top three treatments of Natalizumab, Ocrelizumab, and Cladribine with patients with highly active MS. When asked to position future disease-modifying therapies five years from today, more than 45% of physicians expressed a lack of information on Bruton's tyrosine kinase (BTK) inhibitors. CONCLUSIONS: Most neurologists in the NE region followed Middle East North Africa Committee for Treatment and Research in Multiple Sclerosis (MENACTRIMS) recommendations for prescribing treatment. The treatment choice also depended on the availability of disease-modifying therapies (DMTs) in the region. Regarding the use of upcoming DMTs, there is a clear need for real-world data, long-term extension studies, and comparative studies to support their efficacy and safety profiles in treating patients with MS.
 Gut microbiota, the total microorganisms in our gastrointestinal tract, might have an implication in multiple sclerosis (MS), a demyelinating neurological disease. Our study included 50 MS patients and 21 healthy controls (HC). Twenty patients received a disease modifying therapy (DMT), interferon beta1a or teriflunomide, 19 DMT combined with homeopathy and 11 patients accepted only homeopathy. We collected in total 142 gut samples, two for each individual: at the study enrolment and eight weeks after treatment. We compared MS patients' microbiome with HC, we analysed its evolution in time and the effect of interferon beta1a, teriflunomide and homeopathy. There was no difference in alpha diversity, only two beta diversity results related to homeopathy. Compared to HC, untreated MS patients had a decrease of Actinobacteria, Bifidobacterium, Faecalibacterium prauznitzii and increased Prevotella stercorea, while treated patients presented lowered Ruminococcus and Clostridium. Compared to the initial sample, treated MS patients had a decrease of Lachnospiraceae and Ruminococcus and an increased Enterococcus faecalis. Eubacterium oxidoreducens was reduced after homeopathic treatment. The study revealed that MS patients may present dysbiosis. Treatment with interferon beta1a, teriflunomide or homeopathy implied several taxonomic changes. DMTs and homeopathy might influence the gut microbiota.
 BACKGROUND AND PURPOSE: Brain pseudoatrophy has been shown to play a pivotal role in the interpretation of brain atrophy measures during the first year of disease-modifying therapy in multiple sclerosis. Whether pseudoatrophy also affects the spinal cord remains unclear. The aim of this study was to analyze the extent of pseudoatrophy in the upper spinal cord during the first 2 years after therapy initiation and compare this to the brain. METHODS: A total of 129 patients from a prospective longitudinal multicentric national cohort study for whom magnetic resonance imaging scans at baseline, 12 months, and 24 months were available were selected for brain and spinal cord volume quantification. Annual percentage brain volume and cord area change were calculated using SIENA (Structural Image Evaluation of Normalized Atrophy) and NeuroQLab, respectively. Linear mixed model analyses were performed to compare patients on interferon-beta therapy (n = 84) and untreated patients (n = 45). RESULTS: Patients treated with interferon-beta demonstrated accelerated annual percentage brain volume and cervical cord area change in the first year after treatment initiation, whereas atrophy rates stabilized to a similar and not significantly different level compared to untreated patients during the second year. CONCLUSIONS: These results suggest that pseudoatrophy occurs not only in the brain, but also in the spinal cord during the first year of interferon-beta treatment.
 INTRODUCTION: The Omicron variant of COVID-19 is highly transmissible, triggering unprecedented infection rates. The present study aimed to investigate the course of multiple sclerosis (MS) in the Omicron era among Iranian patients with MS. METHODS: This observational study was designed on MS patients of the national MS registry of Iran through a self-designed online questionnaire. A questionnaire was prepared as a Google Form for MS patients during the Omicron outbreak from 1 March to 30 April 2022. RESULTS: One hundred seventy-four patients with a mean age of 37.3 ± 9.04 were enrolled. Of the patients, 95.97% used DMT, the most common of which were rituximab and fingolimod. Of the patients, 77.58% were fully vaccinated for COVID-19. Regardless of the COVID-19 vaccination status, 76 patients developed COVID-19, which was mild to moderate. Except for recent corticosteroid therapy and secondary progressive MS (SPMS), other demographic and MS characteristics were not significantly associated with the severity of COVID-19. There was also a marginal association between the Expanded Disability Status Scale (EDSS) and the severity of COVID-19. In addition, 17.10% of patients reported MS relapse following COVID-19 leading to escalation therapy in eight patients. CONCLUSION: Our study demonstrated that in the Omicron era, most patients developed mild COVID-19. Although the predominant COVID-19 variant in this period was Omicron, we could not separate the pathogenic variants. The risk factors for COVID-19 during the Omicron era were not different from other pandemic waves. Our preliminary results revealed that the MS relapse following COVID-19 was higher than in previous waves.
 BACKGROUND: We propose a randomized controlled trial (RCT) that examines the effects of a remotely-delivered, cultrally-tailored exercise training program for immediate and sustained improvements in patient-reported outcomes (PROs) of walking dysfunction, symptoms, and health-related quality of life (HRQOL) among African-Americans with multiple sclerosis (MS). METHODS/DESIGN: The study will be conducted using a parallel group RCT design. The RCT examines the effects of a remotely-delivered, culturally-tailored exercise training program compared with an active control condition among 100 African-Americans with MS. The primary PROs focus on walking dysfunction. The secondary PROs include symptoms of fatigue, depression, anxiety, and HRQOL. The tertiary PROs include exercise behavior and mediator variables based on social cognitive theory. Participants will be randomly assigned into one of two conditions, intervention (Aerobic and Resistance Exercise Training) or active control (Stretching and Flexibility), using a random numbers sequence with concealed allocation. The conditions will be administered over four months by a trained behavioral coach who will be uninvolved in recruitment, screening, random assignment, and outcome assessment. We will monitor the outcomes of interest before and after the 4-month intervention period, and then again 4 months after intervention cessation for capturing stability of intervention effects. The data analysis will follow intent-to-treat principles with a linear mixed model. DISCUSSION: If successful, this RCT will provide initial evidence for the uptake and implementation of the program in clinics/environments providing healthcare for African-Americans with MS.
 BACKGROUND AND OBJECTIVE: Neuromuscular fatigue contributes to decrements in quality of life in Multiple Sclerosis (MS), yet available treatments demonstrate limited efficacy. Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique which presents promise in managing fatigue, possibly related to its capacity to modulate corticospinal excitability. There is evidence for capitalising on metaplasticity using tDCS for improving outcomes. However, this remains to be explored with fatigue in people with MS (pwMS). We investigated cathodal tDCS (ctDCS) priming on anodal tDCS (atDCS)-induced corticospinal excitability and fatigue modulation in pwMS. METHODS: 15 pwMS and 15 healthy controls completed fatiguing exercise whilst receiving either ctDCS or sham (stDCS) primed atDCS to the motor cortex. We assessed change in contraction force and motor evoked potential (MEP) amplitude across time to represent changes in fatigue and corticospinal excitability. RESULTS AND CONCLUSION: ctDCS primed atDCS induced MEP elevation in healthy participants but not in pwMS, possibly indicating impaired metaplasticity in pwMS. No tDCS-mediated change in the magnitude of fatigue was observed, implying that development of fatigue may not rely on changes in corticospinal excitability. SIGNIFICANCE: These findings expand understanding of tDCS effects in pwMS, highlighting differences that may be relevant in the disease pathophysiology.
 Fingolimod has been approved as a disease-modifying drug in multiple sclerosis since 2010. There are a few reports of melanoma as a side effect of Fingolimod in the literature. Herein we aim to report a known case of multiple sclerosis under Fingolimod presenting with persistent nasal congestion who was eventually diagnosed with soft palate malignant melanoma.
 INTRODUCTION: Multiple Sclerosis (MS) as one of the most common causes of disability around the world requires a uniform standardized information registry system to help policy-makers systematically plan for care quality improvements. The aim of this study is to verify aspects and methodological scopes of MS registry system in Iran. METHODS: The National MS Registry System in Iran (NMSRI) is a population-based registry system that systemically identifies and collects all MS patients' data in a specific geographical area. It supports 22 medical science universities and 13 MS societies in 18 provinces of Iran. The information items taken from each patient to collect the data set and data are gathered from all available sources including public and private hospitals, clinics, neurologists' offices, and all MS societies. They are recorded in District Health Information System 2 (DHIS2) software. DISCUSSION: The NMSRI is a successful system of collecting MS patients' data. It can lead to positive results, such as updating patients' data to receive new treatments, fair allocation of treatment budgets, and providing researchers with novel ideas to carry out research projects.
 INTRODUCTION: Intellectual enrichment and brain reserve modulate the expression of cognitive and motor disability in multiple sclerosis (MS). Their association with fatigue, one of the most debilitating and common symptoms of MS, has never been explored. MATERIALS AND METHODS: Forty-eight MS patients underwent clinical and MRI examination at baseline and after 1 year. Physical and cognitive MS-related fatigue were evaluated via Modified Fatigue Impact subscales (MFIS-P and MFIS-C). Differences in reserve indexes between fatigued and non-fatigued patients were tested. The relationship between clinico-demographic features, global brain structural damage, indexes of reserve (age-adjusted intracranial volume and cognitive reserve index) and fatigue were tested via correlations and hierarchical linear/binary logistic regression, to predict MFIS-P and MFIS-C (at baseline) or new-onset fatigue and meaningful worsening in MFIS (at follow-up). RESULTS: At baseline, although a significant difference was identified for cognitive reserve questionnaire between fatigued and non-fatigued patients (18.19 ± 4.76 versus 15.15 ± 3.56, p = 0.015), only depression accounted for significant variance in MFIS-P and MFIS-C (R(2)=0.248, p = 0.002; R(2)=0.252, p<0.001). MFIS-T, MFIS-P and MFIS-C changes over time were associated to depression changes over time (r = 0.56, r = 0.55, and r = 0.57, respectively; all p<0.001). Indexes of reserve did not differ between non-fatigued patients and patients developing new-onset fatigue at follow-up. None of the baseline features was able to predict the new-onset fatigue or meaningful worsening in MFIS at follow-up. CONCLUSIONS: Among the explored features, only depression was strongly associated to both physical and cognitive fatigue. Intellectual enrichment and brain reserve did not seem to affect fatigue symptoms in MS patients.
 Since 1996, a debate regarding the cause of disability in Multiple Sclerosis (MS) and the accuracy of the current definitions of MS types has not subsided. Recently, many researchers presented evidence supporting that relapses are a significant causative factor of the increased disability in multiple sclerosis (MS), primarily, but not exclusively, indicating that the disease's progression, which is independent of any relapse activity, plays a significant role in the patient's deterioration mainly in adult MS cases, and this gradually becomes the principle pathway with which disabilities compound in MS patients. We propose an updated definition of the types of MS, highlighting the central role of the disease's progression.
 Background and Objectives: Multiple sclerosis (MS) starts quite rarely in childhood, comprising just 3-10% of all diagnosed cases of MS population. The age of onset of the disease may be related to the initial phenotype and the prognosis of MS. The aim of the study is to assess the characteristics of the manifestation of MS in children. Materials and Methods: Two groups of patients were analyzed: those diagnosed with MS in childhood (0 < 18 years of age) and who developed MS in 2005-2021, and those diagnosed in adulthood (≥18 years old). The data were collected from the database of the Lithuanian University of Health Sciences Kauno Klinikos. Results: For the analysis, 105 patients were selected: 35 children (group A) and 70 adults (group B). At the onset of the disease, 62.9% of children and 70.0% of adults experienced visual disturbances (p > 0.05). Isolated symptoms were more common in children (65.7%) as compared to adults (28.6%), p < 0.001. Sensory disorders were more common in adults than in children (p < 0.001). Optic nerve and cerebral hemispheres were the most affected in group A (p < 0.05). During the first year after diagnosis, the median number of relapses in group A was higher (3, range 1-5) as compared to group B (1, range 1-2) (p < 0.001). Recovery time after a relapse was shorter in children as compared to adults (p < 0.001). Oligoclonal bands were found in 85.7% of children and in 98.6% of adults. Oligoclonal bands were less common in the childhood-onset than in the adult-onset group (p = 0.007). Conclusions: The initial symptoms of multiple sclerosis in pediatric patients usually appeared around the age of 16, with a similar frequency in boys and girls, and in most of the childhood cases the initial symptoms were limited to the dysfunction of a single part of the nervous system children usually started with visual disorders, while sensory, coordination and motor disorders were less common. The course of the disease in juvenile patients with MS was more aggressive in the first year as there were more relapses, but the functional impairment recovered faster as compared to adults.

 BACKGROUND: The application of machine learning (ML) to predict cognitive evolution is exceptionally scarce. Computer-based self-administered cognitive tests provide the opportunity to set up large longitudinal datasets to aid in developing ML prediction models of risk for Multiple Sclerosis-related cognitive decline. OBJECTIVE: to analyze to what extent clinically feasible models can be built with standard clinical practice features and subsequently used for reliable prediction of cognitive evolution. METHODS: This prospective longitudinal study includes 1184 people with MS who received a Processing Speed (PS) evaluation at 12 months of follow-up measured by the iPad®-based Processing Speed Test (PST). Six of the most potent classification models built with routine clinical practice features were trained and tested to predict the 12-month patient class label (PST worsening (PSTw) versus PST stable). A rigorous scheme of all the preprocessing steps run to obtain reliable generalization performance is detailed. RESULTS: Based on a 12-month reduction of 10% of the PST raw score, 187/1184 (15.8%) people with MS were classified as PSTw. The trees-based models (random forest and the eXtreme Gradient Boosting) achieved the best performance, with an area under the receiver operating characteristic curve (AUC) of 0.90 and 0.89, respectively. The timing of high-efficacy disease-modifying therapies (heDMTs) was identified as one of the top importance predictors in all the models evaluated. CONCLUSION: Using trees-based machine learning models to predict individual future information processing speed deterioration in MS could become a reality in clinical practice.
 There is a growing need to discover the characteristics that predict prognostic factors after the first demyelinating event. In this study of 141 patients that met the 2017 McDonald criteria, a higher number of oligoclonal bands, cervical spinal cord demyelinating lesions, and sensory involvement were identified as independent predictors of the second demyelinating event during the 5-year follow-up period in patients who experienced the first demyelinating event. The identification of the aforementioned risk variables will make it possible to identify patients who are more likely to exhibit early second demyelinating event, implying more frequent monitoring and consideration of early application of highly effective disease-modifying treatment.
 BACKGROUND: Impairments in speech and social cognition have been reported in people with multiple sclerosis (pwMS), although their relationships with neuropsychological outcomes and their clinical utility in MS are unclear. OBJECTIVES: To evaluate word finding, prosody and social cognition in pwMS relative to healthy controls (HC). METHODS: We recruited people with relapsing MS (RMS, n = 21), progressive MS (PMS, n = 24) and HC (n = 25) from an outpatient MS clinic. Participants completed a battery of word-finding, social cognitive, neuropsychological and clinical assessments and performed a speech task for prosodic analysis. RESULTS: Of 45 pwMS, mean (SD) age was 49.4 (9.4) years, and median (range) Expanded Disability Severity Scale score was 3.5 (1.0-6.5). Compared with HC, pwMS were older and had slower information processing speed (measured with the Symbol Digit Modalities Test, SDMT) and higher depression scores. Most speech and social cognitive measures were associated with information processing speed but not with depression. Unlike speech, social cognition consistently correlated with intelligence and memory. Visual naming test mean response time (VNT-MRT) demonstrated worse outcomes in MS versus HC (p = .034, Nagelkerke's R(2)  = 65.0%), and in PMS versus RMS (p = .009, Nagelkerke's R(2)  = 50.2%). Rapid automatised object naming demonstrated worse outcomes in MS versus HC (p = .014, Nagelkerke's R(2)  = 49.1%). These word-finding measures showed larger effect sizes than that of the SDMT (MS vs. HC, p = .010, Nagelkerke's R(2)  = 40.6%; PMS vs. RMS, p = .023, Nagelkerke's R(2)  = 43.5%). Prosody and social cognition did not differ between MS and HC. CONCLUSIONS: Word finding, prosody and social cognition in MS are associated with information processing speed and largely independent of mood. Impairment in visual object meaning perception is potentially a unique MS disease-related deficit that could be further explored and cautiously considered as an adjunct disability metric for MS.
 INTRODUCTION: Cerebral vasculitides are often devastating conditions that require immediate diagnosis and treatment. CASE REPORT: We report a pathologically proven clinical case of primary central nervous system vasculitis in a 50-year-old man with a diagnosis of relapsing-remitting multiple sclerosis after alemtuzumab therapy, which required additional immunosuppression to control this life-threatening condition. CONCLUSION: In patients presenting subacute neurological deterioration after alemtuzumab therapy, primary central nervous system vasculitis should be considered as a differential diagnosis among other autoimmune conditions.
 Objective: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that frequently affects cognition. Persons with MS (PwMS) complain of difficulties with prospective memory (PM), the capacity to remember to perform an intended action at the appropriate moment in the future. The objective of this study was to assess the clinical utility of the Miami Prospective Memory Test (MPMT) in detecting PM deficits in MS. The test is brief, easy to administer and accessible, and allows direct comparison between scores on event- and time-based conditions. A secondary objective was to examine the relationship between PM performance and cognitive functioning. Method: Eighty-four PwMS between 27 and 78 years old were compared to 50 age-, sex- and education-matched healthy adults on the MPMT. Results: Time-based (TB) scores, but not event-based (EB) scores, were significantly lower in PwMS than in healthy adults. The MPMT showed good internal consistency, and correlations were found with disability assessed by the Expanded Disability Status Scale (EDSS). PM was also correlated with memory and executive/attention functioning. Conclusions: This study supports the clinical utility of the MPMT in assessing the presence of PM deficits in PwMS especially under TB constraints.

 Multiple sclerosis (MS) is one of the most serious neurological diseases. It is the most frequent reason of non-traumatic disability among young adults. MS is an autoimmune disease wherein the central nervous system wrongly destructs the myelin sheath surrounding and protecting axons of nerve cells of the brain and the spinal cord which results in presence of lesions called plaques. The damage of myelin sheath alters the normal transmission of nerve flow at the plaques level, consequently, a loss of communication between the brain and other organs. The consequence of this poor transmission of nerve impulses is the occurrence of various neurological symptoms. MS lesions cause mobility, vision, cognitive, and memory disorders. Indeed, early detection of lesions provides an accurate MS diagnosis. Consequently, and with the adequate treatment, clinicians will be able to deal effectively with the disease and reduce the number of relapses. Therefore, the use of magnetic resonance imaging (MRI) is primordial which is proven as the relevant imaging tool for early diagnosis of MS patients. But, low contrast MRI images can hide important objects in the image such lesions. In this paper, we propose a new automated contrast enhancement (CE) method to ameliorate the low contrast of MRI images for a better enhancement of MS lesions. This step is very important as it helps radiologists in confirming their diagnosis. The developed algorithm called BDS is based on Brightness Preserving Dynamic Fuzzy Histogram Equalization (BPDFHE) and Singular Value Decomposition with Discrete Wavelet Transform (SVD-DWT) techniques. BDS is dedicated to improve the low quality of MRI images with preservation of the brightness level and the edge details from degradation and without added artifacts or noise. These features are essential in CE approaches for a better lesion recognition. A modified version of BDS called MBDS is also implemented in the second part of this paper wherein we have proposed a new method for computing the correction factor. Indeed, with the use of the new correction factor, the entropy has been increased and the contrast is greatly enhanced. MBDS is specially dedicated for very low contrast MRI images. The experimental results proved the effectiveness of developed methods in improving low contrast of MRI images with preservation of brightness level and edge information. Moreover, performances of both proposed BDS and MBDS algorithms exceeded conventional CE methods.

 RNA oxidation has been implicated in neurodegeneration, but the underlying mechanism for such effects is unclear. Extensive RNA oxidation occurs within the neurons in multiple sclerosis (MS) brains. Here, we identified selectively oxidized mRNAs in neuronal cells that pertained to neuropathological pathways. N-acetyl aspartate transferase 8 like (NAT8L) is one such transcript, whose translation product enzymatically synthesizes N-acetyl aspartic acid (NAA), a neuronal metabolite important for myelin synthesis. We reasoned that impediment of translation of an oxidized NAT8L mRNA will result in a reduction in its cognate protein, thus lowering the NAA level. This hypothesis is supported by our studies on cells, an animal model, and postmortem human MS brain. Reduced brain NAA level hampers myelin integrity making neuronal axons more susceptible to damage, which contributes to MS neurodegeneration. Overall, this work provides a framework for a mechanistic understanding of the link between RNA oxidation and neurodegeneration.
 BACKGROUND: The multi-order visual system represents an excellent testing site regarding the process of trans-synaptic degeneration. The presence and extent of global versus trans-synaptic neurodegeneration in people with multiple sclerosis (pwMS) is not clear. OBJECTIVE: To explore cross-sectional and longitudinal relationships between retinal, thalamic and cortical changes in pwMS with and without MS-related optic neuritis (pwMSON and pwoMSON) using MRI and optical coherence tomography (OCT). METHODS: 162 pwMS and 47 healthy controls (HCs) underwent OCT and brain MRI at baseline and 5.5-years follow-up. Peripapillary retinal nerve fiber layer (pRNFL) and macular ganglion cell inner plexiform layer (mGCIPL) thicknesses were determined. Global volume measures of brain parenchymal volume (BPV)/percent brain volume change (PBVC), thalamic volume and T2-lesion volume (LV) were derived using standard analysis protocols. Regional cortical thickness was determined using FreeSurfer. Cross-sectional and longitudinal relationship between the retinal measures, thalamic volume and cortical thickness were assessed using age, BPV/PBVC and T2-LV adjusted correlations and regressions. RESULTS: After age, BPV and T2-LV adjustment, the thalamic volume explained additional variance in the thickness of pericalcarine (R(2) increase of 0.066, standardized β = 0.299, p = 0.039) and lateral occipital (R2 increase of 0.024, standardized β = 0.299, p = 0.039) gyrii in pwMSON. In pwoMSON, the thalamic volume was a significant predictor only of control (frontal) regions of pars opercularis. There was no relationship between thalamic atrophy and cortical thinning over the follow-up in both pwMS with and without MSON. While numerically lower in the pwMSON group, the inter-eye difference was not able to predict the presence of MSON. CONCLUSIONS: MSON can induce a measurable amount of trans-synaptic pathology on second-order cortical regions.
 INTRODUCTION: Quantifying a significant cognitive change on a neuropsychological battery is essential to assess patients' decline or recovery and offer appropriate care. The reliability of change indices is particularly important in multiple sclerosis (MS), as the course of cognitive impairment is quite unpredictable, due at least in part to substantial interindividual variability. The main objective of this study was to compare six different methods for assessing cognitive change in an MS sample: the SD method, two reliable change indices, two standardized regression-based methods (SRB), and the generalized regression-based method (GSRB). METHOD: One hundred and twenty-three patients with clinically definite MS and 89 healthy controls underwent a battery of standardized neuropsychological tests assessing cognitive functions that are frequently affected in this disease (i.e., verbal episodic memory, working memory, processing speed and verbal fluency). RESULTS: We observed fairly similar proportions of improvement, decline or stability in the control group whatever the method. By contrast, in the MS sample, regression-based methods with one predictor (i.e., score at T1) and four predictors (i.e., score at T1 and demographic factors: age, sex, education level) detected a significant worsening more often than the reliable change indices while the GSRB method was more consistent with the RCI methods in tasks associated with ceiling effects. CONCLUSIONS: The interpretation of a patient's cognitive changes depends on which method is used. The (G)SRB methods appear to be relevant indicators for assessing cognitive change in MS. The addition of demographic factors does not seem to play an important role in the prediction of significant worsening in the MS sample, regardless of cognitive domain. For clinicians, an easy-to-use free shiny app is provided.
 Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by central nervous (CNS) demyelination resulting in axonal injury and neurological deficits. Essentially, MS is driven by an auto-amplifying mechanism of inflammation and cell death. Current therapies mainly focus on disease modification by immunosuppression, while no treatment specifically focuses on controlling cell death injury. Here, we report that ferroptosis, an iron-catalyzed mode of regulated cell death (RCD), contributes to MS disease progression. Active and chronic MS lesions and cerebrospinal fluid (CSF) of MS patients revealed several signs of ferroptosis, reflected by the presence of elevated levels of (labile) iron, peroxidized phospholipids and lipid degradation products. Treatment with our candidate lead ferroptosis inhibitor, UAMC-3203, strongly delays relapse and ameliorates disease progression in a preclinical model of relapsing-remitting MS. In conclusion, the results identify ferroptosis as a detrimental and targetable factor in MS. These findings create novel treatment options for MS patients, along with current immunosuppressive strategies.
 OBJECTIVES: The incidence of early onset multiple sclerosis (EOMS) is increasing. We therefore aimed to compare the demographic, clinical, and magnetic resonance imaging features of early onset and adult onset multiple sclerosis patients. Furthermore, the effects of age of onset were evaluated for patients who reached an expanded disability status scale (EDSS) scores of six. PATIENTS AND METHODS: This was a retrospective study of MS patient medical charts between 1977 and 2021, which were registered in the MS database. Only patients with relapsing remitting MS longer than 1 year were included in the study. The patients included in the study were divided into the EOMS and adult onset MS (AOMS) groups. General demographic datas, clinical datas such as the characteristics of the first clinical period, the time between the first two attacks, the attack rate in the first 2 and 3 years, the treatment status, the EDSS at the first evaluation, the EDSS score at 6 month intervals, the time to reach an EDSS score of six, and magnetic resonance imaging features such brain and spinal T2 lesions were recorded. RESULTS: Total of 3477 including 353 (10.2 %) EOMS and 3124 (89.8 %) AOMS patients were analyzed. There was no statistically significant difference in symptom patterns between the EOMS and AOMS groups ( p = 0.649). Supratentorial clinical features at first attack were more common in AOMS patients, while optic neuropathy at first attack was more common in EOMS patients. Using univariable analysis, clinical supratentorial features at first attack, clinical optic neuropathy at first attack, clinical spinal cord at fist attack, spinal cord lesions, first EDSS score, relapse in the first 3 years, and onset patterns in terms of age were found to be statistically significant risk factors. In multivariable-adjusted analysis, clinical supratentorial features at first attack, clinical spinal cord lesions at first attack, first EDSS scores relapses in the first 3 years, and onset patterns in terms of age were found to be independent risk factors for EDSS in reaching a score of six. Early treatment start was associated with reduced hazard rate of reaching an EDSS score of 6. CONCLUSION: Onset pattern in terms of age was an independent prognostic factor for neurological disabilities in MS patients.
 OBJECTIVES: To compare the clinical and radiological effectiveness of ocrelizumab in primary progressive multiple sclerosis (PPMS) and relapsing-remitting multiple sclerosis (RRMS) in a clinical practice setting and describe its tolerability and adverse events. METHODS: A retrospective observational cohort study was conducted comparing clinical and magnetic resonance imaging (MRI) data of all patients with (pw)PPMS and RRMS who had received treatment with ocrelizumab at least one cycle and have been followed up for one year at minimum. RESULTS: 42 patients (27 women) treated with ocrelizumab: 29 had RRMS and 13 PPMS. The follow-up period was 26.4 ± 8.4 months. The proportion of pwRRMS with no evidence of disease activity (NEDA) in the first year was 69.2% and in the second was 80%. In the first year, radiological activity was reduced by 80.0% in pwRRMS and 91.7% in pwPPMS. In the second year, radiological activity was completely reduced in both groups. A statistically significant difference (p<0.05) was observed between the pre-ocrelizumab rate of disability progression vs. the first year rate of progression for pwRRMS and pwPPMS. However, an increase in the disability progression rate in the second year of treatment was found in pwPPMS. Ocrelizumab was mostly well tolerated and some adverse effects were reported: infusion-related reactions (IRRs) were the most frequent adverse event, followed by infections and hematological side effects. Discontinuations were due to infections, hematological complications, and perception of ineffectiveness. CONCLUSIONS: Ocrelizumab was very effective in reducing relapses and MRI activity. The rate of progression was slowed down; however, the effect was more evident for pwRRMS than for pwPPMS over time.


 OBJECTIVE: Multiple sclerosis (MS) is a disease with higher female prevalence, and the majority of patients are of childbearing age. Thus, pregnancy concerns are important for patients with MS and their families. Improving the understanding of the effects of pregnancy on the progress of MS could improve the knowledge about pregnancy-related issues in MS patients. The aim of this study is to evaluate the general knowledge of Saudi adults living in the Qassim region regarding pregnancy-related relapses in relapsing-remitting MS (RRMS) and to identify misconceptions regarding pregnancy, breastfeeding, and the use of oral hormonal contraceptives among female MS patients. SUBJECTS AND METHODS: A representative random cluster sample of 337 participants was used in this cross-sectional study. All participants were living in one of the following cities in the Qassim region: Buraydah, Unaizah, and Alrrass. Data collection was done between February 2022 and March 2022 using a self-administered questionnaire. RESULTS: The overall mean knowledge score was 7.42 (SD 4.21), with poor, moderate, and good knowledge representing 77.2%, 187%, and 4.2% of the sample, respectively. Higher knowledge scores were associated with age less than 40 years, being a student, knowing about MS, and knowing someone with MS. Other variables such as gender, educational level, and residence location did not show significant differences regarding the knowledge score. CONCLUSIONS: Our results demonstrate that knowledge and attitude are suboptimal among the Qassim population regarding the effects of MS on pregnant patients, pregnancy outcomes, breastfeeding, and usage of contraceptive methods, with 77.2% showing poor total knowledge scores.
 BACKGROUND AND PURPOSE: Functional neurological disorders (FNDs) have attracted much attention from the neurological medical community over the last decades as new developments in neurosciences have reduced stigma around these by showing brain network dysfunctions. An overlap with other neurological conditions such as multiple sclerosis (MS) is well known by clinicians but there is a lack of clinical and fundamental research in this field to better define diagnosis and therapeutic decisions, as well as a lack of deep understanding of the underlying pathophysiology. AIM: We aimed to provide a critical commentary on the state of knowledge about the borderland between FNDs and MS. METHODS: We based our commentary on a joint point of view between an FND specialist and an MS expert. RESULTS: A brief review of the previous literature and relevant new studies covering the overlap between FNDs and MS is presented, along with suggestions for future research directions. CONCLUSION: There are clear diagnostic criteria for both FNDs and MS and a strict application of these will help better diagnosis and prevent unnecessary treatment escalation in MS or absence of referral to multimodal therapy in FND. Better teaching of younger neurologists is needed as well as prospective research focusing on pathophysiology.

 In this work we present BIANCA-MS, a novel tool for brain white matter lesion segmentation in multiple sclerosis (MS), able to generalize across both the wide spectrum of MRI acquisition protocols and the heterogeneity of manually labeled data. BIANCA-MS is based on the original version of BIANCA and implements two innovative elements: a harmonized setting, tested under different MRI protocols, which avoids the need to further tune algorithm parameters to each dataset; and a cleaning step developed to improve consistency in automated and manual segmentations, thus reducing unwanted variability in output segmentations and validation data. BIANCA-MS was tested on three datasets, acquired with different MRI protocols. First, we compared BIANCA-MS to other widely used tools. Second, we tested how BIANCA-MS performs in separate datasets. Finally, we evaluated BIANCA-MS performance on a pooled dataset where all MRI data were merged. We calculated the overlap using the DICE spatial similarity index (SI) as well as the number of false positive/negative clusters (nFPC/nFNC) in comparison to the manual masks processed with the cleaning step. BIANCA-MS clearly outperformed other available tools in both high- and low-resolution images and provided comparable performance across different scanning protocols, sets of modalities and image resolutions. BIANCA-MS performance on the pooled dataset (SI: 0.72 ± 0.25, nFPC: 13 ± 11, nFNC: 4 ± 8) were comparable to those achieved on each individual dataset (median across datasets SI: 0.72 ± 0.28, nFPC: 14 ± 11, nFNC: 4 ± 8). Our findings suggest that BIANCA-MS is a robust and accurate approach for automated MS lesion segmentation.
 OBJECTIVE: There is some evidence implicating diet in the development of inflammatory diseases. We aimed to study the influence of dietary habits on the risk of developing multiple sclerosis (MS). METHODS: We used a population-based case-control study recruiting incident cases of MS (1953 cases, 3557 controls). Subjects with different dietary habits 5 years prior to MS diagnosis were compared regarding MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Adjustment was made for a large number of environmental and lifestyle habits, including ancestry, smoking, alcohol consumption, body mass index, physical activity, and sun exposure habits. RESULTS: Mediterranean diet was associated with lower risk of developing MS (adjusted OR = 0.54, 95% CI: 0.34-0.86, p = 0.009), compared with Western-style diet. There was no significant association between vegetarian/vegan diet and MS risk (adjusted OR = 0.96, 95% CI: 0.75-1.24, p = 0.976), nor between diet with low glycemic index and MS risk (adjusted OR = 0.93, 95% CI: 0.60-1.42, p = 0.518). CONCLUSIONS: Mediterranean diet may exert a protective influence regarding the risk of subsequently developing MS compared with Western-style diet.
 BACKGROUND: Cognitive impairment (CI) frequently occurs in multiple sclerosis (MS) and is assumed to increase over time. However, recent studies have suggested that the evolution of cognitive status in patients with MS may be more heterogeneous than expected. Predicting CI remains also challenging, and longitudinal studies exploring the baseline determinants of cognitive performances are limited. No studies have explored the predictive value of patient-reported outcome measures (PROMs) regarding future CI. OBJECTIVE: To explore the evolutionary patterns of cognitive status in a cohort of RRMS patients initiating a new disease modifying treatment (DMT), and to determine whether PROMs may have a predictive value for future CI. METHODS: The present prospective study is a 12-month follow-up of a cohort of 59 RRMS patients who underwent yearly a comprehensive, multiparametric assessment combining clinical (with EDSS assessment), neuropsychological (BVMT-R, SDMT, CVLT-II), MRI-derived metrics and a set of self-reported questionnaires. Lesion and brain volumes were analyzed and processed by the automated MSmetrix® software (Icometrix®, Leuven, Belgium). Spearman's correlation coefficient was used to evaluate the association of collected variables. A longitudinal logistic regression analysis was performed to find baseline correlates of CI at 12 months (T1). RESULTS: A total of 33 patients (56%) were defined as cognitively impaired at baseline, and 20 (38%) were defined as impaired at follow-up after 12 months. The mean raw scores and Z-scores of all the cognitive tests were significantly improved at T1 (p < 0.05). There was a statistically significant improvement in most PROM scores at T1 (p < 0.05) in comparison with baseline scores. Among the variables assessed, lower education and physical disability level at baseline correlated with impaired SDMT (OR: 1.68, p = 0.01; OR: 3.10, p = 0.02, respectively) and impaired BVMT-R (OR: 4.08, p=<0.001; OR: 4.82, p = 0.001, respectively) at T1. Neither baseline PROMs nor MRI volumetric parameters were predictive of cognitive performances at T1. CONCLUSIONS: These findings provide additional evidence that evolution of CI in MS may be a dynamic phenomenon and will not usually follow an inevitable, declining trajectory, and do not support the utility of PROMs in predicting CI in RRMS. The present study is still ongoing to determine whether our findings are confirmed at 2 and 3 years of follow-up.
 BACKGROUND: Patients with multiple sclerosis (MS) who discontinue fingolimod might present with rebound activity. The reasons for the development of rebound have been identified, but there are limited data on the long-term clinical outcomes of these patients. This study aimed to compare the long-term outcomes of patients with MS with and without rebound activity after fingolimod discontinuation. METHODS: A total of 31 patients who discontinued fingolimod for various reasons with a minimum follow-up of 5 years were included in the study. Of these, 10 were assigned to the rebound group and 21 to the non-rebound group. Clinical and demographic data and 5-year clinical outcomes of both groups were prospectively examined. RESULTS: At fingolimod initiation, there were no significant differences in age, disease duration, and Expanded Disability Status Scale (EDSS) score. The annualized relapse rate (ARR) was significantly higher in the rebound group than in the non-rebound group before the fingolimod treatment (p = 0.005). In the rebound group, EDSS scores 2 months after rebound treatment and at the 5-year follow-up were not significantly different than before fingolimod initiation (p = 0.14 and p = 0.46, respectively). The last recorded EDSS was significantly higher in the non-rebound group than in the rebound group (3.6 ± 2.3 vs. 2.15 ± 1.4, p = 0.045). At the last follow-up, one patient was diagnosed with secondary progressive multiple sclerosis in the rebound group (10%), and 11 patients were in the non-rebound group (52.4%, p = 0.05). CONCLUSION: When rebound activity is well-monitored and treated after fingolimod discontinuation, no overall EDSS change is expected in the long-term follow-up.
 BACKGROUND: Metabolic syndrome and multiple sclerosis [MS] share the presence of chronic inflammation in their pathogenic mechanisms. This study aimed to estimate the prevalence of metabolic syndrome parameters in MS and their association with disease disability, cognitive function, and Neurofilament Light chain [NfL] levels. METHODS: Clinical, analytical, and magnetic resonance imaging data were obtained through medical records. Disease disability was measured by the Expanded Disability Status Scale [EDSS], the MS Severity Scale [MSSS] along with cognitive impairment by the Brief International Cognitive Assessment for MS [BICAMS] and Word List Generation test [WLG]. Metabolic syndrome parameters were evaluated by fasting blood glucose, triglycerides, high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol, total cholesterol, blood pressure, and waist circumference [WC]. We also analysed serum leptin and ghrelin and cerebrospinal fluid NfL. RESULTS: Our sample included 51 people with MS, 34 (66.7%) females, mean age of 38.20±12.12 years and median disease duration of 3 years (P25=2.0, P75=5.0). Multivariate linear regression analysis confirmed that WC correlates with EDSS (β=0.04, p=.001) and MSSS (β=0.07, p=.002) as well as Brief Visuospatial Memory Test-Revised (β=-0.29, p=.008), WLG (β=-0.20, p=.039). NfL is also negatively associated with HDL-C (β=-4.51, p=.038). CONCLUSIONS: Waist circumference is associated with disability and deficits in cognitive tests. A decrease in HDL-C is associated with an increase in NfL. This suggests metabolic syndrome might be an important factor in MS disease course.
 OBJECTIVE: We aim to validate an algorithm based on routinely-collected healthcare data to detect incidence of multiple sclerosis (MS) in the Campania Region (South Italy) and to explore its spatial and temporal variations. METHODS: We included individuals resident in the Campania Region who had at least one MS record in administrative datasets (drug prescriptions, hospital discharge, outpatients), from 2015 to 2020. We merged administrative to the clinical datasets to ascertain the actual date of diagnosis, and validated the minimum interval from our study baseline (Jan 1, 2015) to first MS records in administrative datasets to detect incident cases. We used Bayesian approach to explore geographical distribution, also including deprivation index as a covariate in the estimation model. We used the capture-recapture method to estimate the proportion of undetected cases. RESULTS: The best performance was achieved by the 12-month interval algorithm, detecting 2,150 incident MS cases, with 74.4% sensitivity (95%CI = 64.1%, 85.9%) and 95.3% specificity (95%CI = 90.7%, 99.8%). The cumulative incidence was 36.68 (95%CI = 35.15, 38.26) per 100,000 from 2016 to 2020. The mean annual incidence was 7.34 (95%CI = 7.03, 7.65) per 100,000 people-year. The geographical distribution of MS relative risk shows a decreasing east-west incidence gradient. The number of expected MS cases was 11% higher than the detected cases. CONCLUSIONS: We validated a case-finding algorithm based on administrative data to estimate MS incidence, and its spatial/temporal variations. This algorithm provides up-to-date estimates of MS incidence, and will be used in future studies to evaluate changes in MS incidence in relation to different risk factors.

 OBJECTIVES: Neurological disabilities, especially physical issues, can adversely affect the daily lives of people with multiple sclerosis (MS) and negatively impact their health-related quality of life (HRQOL). On the other hand, physical and psychiatric symptoms are variable in people with MS, and QOL can be influenced by cultural and educational background. This study aimed to evaluate the association of HRQOL with disabilities, fatigue, and depression in Japanese subjects with MS. METHODS: Evaluation of HRQOL, fatigue, and depression was performed in 184 Japanese individuals with MS, using the Functional Assessment of MS (FAMS), Fatigue Severity Scale (FSS), and Beck Depression Inventory-Second Edition (BDI-II), respectively. RESULTS: Multiple linear regression analysis demonstrated negative correlations of the Expanded Disability Status Scale (EDSS) with scores on the FAMS subscales of mobility, symptoms, thinking and fatigue, total FAMS, and additional concerns. The FSS score had negative correlations with mobility, symptoms, emotional well-being, thinking and fatigue, total FAMS, and additional concerns. There were negative correlations between BDI-II scores and all items of FAMS. CONCLUSIONS: HRQOL had relatively close correlations with disabilities and fatigue, and depression had an especially close relationship with HRQOL.
 BACKGROUND: People with MS (pwMS) have higher prevalence of comorbidities at disease onset and face increased risk of developing cardiovascular disorders. Stroke is of particular concern for this population with previous neurological disability. However, data on stroke outcomes and resource utilization in those pwMS remains scarce. OBJECTIVE: To assess the risk of adverse stroke outcomes and hyperacute treatment utilization for pwMS in a U.S. population-based sample of hospitalized patients. METHODS: This study identified patients discharged with a diagnosis of ischemic stroke in the 2018 National Inpatient Sample. We compared the discharge outcomes and hyperacute stroke treatment utilization in MS (n = 2,795) versus non-MS patients (n = 682.730). Regression models adjusted for cardiovascular risk factors and hospital characteristics were used to account for the complex sampling design. RESULTS: The odds of a good discharge were 32% less likely to occur in pwMS (adj.OR 0.68 [95%CI 0.58-0.81], p<0.001). However, this was not associated with an increased risk of mortality. PwMS had a 57% reduction in the risk of receiving endovascular thrombectomy (EVT) (adj.OR 0.43 [95%CI 0.22-0.83], p = 0.01) but no difference in rates of thrombolysis. CONCLUSION: Patients with MS have lower rates of good discharge outcomes and EVT with ischemic stroke, despite similar rates of thrombolysis.
 Retinal periphlebitis (RPP) is a long-known entity in patients with multiple sclerosis (MS) and has not been revisited in the context of recent developments in MS pathogenesis and heterogeneity. We present six cases of RPP in three female and three male MS patients. They all have relapsing-remitting MS and did not have or had minor ocular symptoms. It is important to perform a thorough retinal examination in patients with MS, as peripheral and sectorial lesions could be unseen. A better knowledge on the concomitant involvement of retinal veins contributes to the understanding of immunopathology, with potentially distinct autoantigenic targets. RPP might serve as a subphenotype marker that may influence treatment choices in MS. Further research is needed.
 BACKGROUND: Natalizumab is a widely used high-efficacy treatment in multiple sclerosis (MS). Real-world evidence regarding long-term effectiveness and safety is warranted. We performed a nationwide study evaluating prescription patterns, effectiveness, and adverse events. METHODS: A nationwide cohort study using the Danish MS Registry. Patients initiating natalizumab between June 2006 and April 2020 were included. Patient characteristics, annualized relapse rates (ARRs), confirmed Expanded Disability Status Scale (EDSS) score worsening, MRI activity (new/enlarging T2- or gadolinium-enhancing lesions), and reported adverse events were evaluated. Further, prescription patterns and outcomes across different time periods ("epochs") were analysed. RESULTS: In total, 2424 patients were enrolled, with a median follow-up time of 2.7 years (interquartile range (IQR) 1.2-5.1). In recent epochs, patients were younger, had lower EDSS scores, had fewer pre-treatment relapses and were more often treatment naïve. At 13 years of follow-up, 36% had a confirmed EDSS worsening. On-treatment ARR was 0.30, corresponding to a 72% reduction from pre-initiation. MRI activity was rare, 6.8% had activity within 2-14 months from treatment start, 3.4% within 14-26 months, and 2.7% within 26-38 months. Approximately 14% of patients reported adverse events, with cephalalgia constituting the majority. During the study, 62.3% discontinued treatment. Of these, the main cause (41%) was due to JCV antibodies, while discontinuations due to disease activity (9%) or adverse events (9%) were less frequent. CONCLUSION: Natalizumab is increasingly used earlier in the disease course. Most patients treated with natalizumab are clinically stable with few adverse events. JCV antibodies constitute the main cause for discontinuation.
 BACKGROUND: Multiple sclerosis is a chronic, autoimmune, degenerative disease. Therapies targeting B-cells have been shown to be effective in its treatment; however, there are few studies evaluating their efficacy in the Mexican population. OBJECTIVE: To evaluate the clinical impact of rituximab in patients with newly-diagnosed relapsing-remitting multiple sclerosis (RRMS). MATERIAL AND METHODS: Real life, descriptive study, in which rituximab was evaluated as treatment for RRMS over a 24-month period. Pre- and post-treatment clinical variables were analyzed; a comparison was made between treatment-naïve and non-treatment-naïve patients. RESULTS: Twenty-eight patients with RRMS were included. Mean age at diagnosis was 30.7 years, and 22 patients were treatment-naïve (78.5 %). After 24 months, there was a mean reduction of 1.8 points in the EDSS scale and a decrease in the number of active lesions on magnetic resonance imaging; a significant difference in both variables could be established (p < 0.05). However, the logistic regression model did not show a relationship between the variables for achieving NEDA-3 criteria. No serious adverse events were observed. CONCLUSIONS: Treatment with rituximab resulted in significant clinical and radiological improvement in treatment-naïve and non-treatment-naïve Mexican patients with RRMS.
 BACKGROUND: Anxiety represents one of the most prevalent psychiatric symptoms in multiple sclerosis (MS), impacting the overall disease burden and quality of life. This psychopathological feature can be expressed as state (S-ANX) and trait (T-ANX) anxiety, but few studies specifically evaluated these two components in MS. The present study was aimed at investigating the prevalence and specific correlates of S-ANX and T-ANX in a cohort of people with MS (PwMS). METHODS: 88 in- and out-patients with MS were consecutively recruited. S-ANX and T-ANX were evaluated with the two subscales of the State and Trait Anxiety Inventory. Bivariate analyses were performed to compare PwMS who displayed clinically significant S-ANX and T-ANX and those who did not. Two logistic regression models were run in order to identify variables significantly associated with S-ANX and T-ANX. RESULTS: S-ANX and T-ANX presented a prevalence of 42% and 45.5%, respectively. S-ANX was more frequent in subjects hospitalized due to recent MS onset. PwMS and S-ANX more frequently had a recent relapse, as well as evidence of disease activity on brain magnetic resonance imaging. Subjects with T-ANX were more often females and displayed higher severity of fatigue. Depressive features at the Beck Depression Inventory were more severe in both S-ANX and T-ANX subjects. PwMS with S-ANX reported a higher prevalence of T-ANX and vice versa. At the logistic regressions, depression severity displayed a significant association with S-ANX and T-ANX. We also detected positive associations between S-ANX and inpatient status, as well as between T-ANX and female sex. CONCLUSION: Both S-ANX and T-ANX are highly prevalent features in PwMS. These two components of anxiety should be adequately identified and discriminated in the clinical practice. The higher severity of depression in PwMS with clinically significant anxiety should not be neglected.
 BACKGROUND: Timely initiation of disease modifying therapy is crucial for managing multiple sclerosis (MS). OBJECTIVE: We aimed to validate a previously published predictive model of individual treatment response using a non-overlapping cohort from the Middle East. METHODS: We interrogated the MSBase registry for patients who were not included in the initial model development. These patients had relapsing MS or clinically isolated syndrome, a recorded date of disease onset, disability and dates of disease modifying therapy, with sufficient follow-up pre- and post-baseline. Baseline was the visit at which a new disease modifying therapy was initiated, and which served as the start of the predicted period. The original models were used to translate clinical information into three principal components and to predict probability of relapses, disability worsening or improvement, conversion to secondary progressive MS and treatment discontinuation as well as changes in the area under disability-time curve (ΔAUC). Prediction accuracy was assessed using the criteria published previously. RESULTS: The models performed well for predicting the risk of disability worsening and improvement (accuracy: 81%-96%) and performed moderately well for predicting the risk of relapses (accuracy: 73%-91%). The predictions for ΔAUC and risk of treatment discontinuation were suboptimal (accuracy < 44%). Accuracy for predicting the risk of conversion to secondary progressive MS ranged from 50% to 98%. CONCLUSION: The previously published models are generalisable to patients with a broad range of baseline characteristics in different geographic regions.
 Effective learning from performance feedback is vital for adaptive behavior regulation necessary for successful cognitive performance. Yet, how this learning operates in clinical groups that experience cognitive dysfunction is not well understood. Multiple sclerosis (MS) is an autoimmune, degenerative disease of the central nervous system characterized by physical and cognitive dysfunction. A highly prevalent impairment in MS is cognitive fatigue (CF). CF is associated with altered functioning within cortico-striatal regions that also facilitate feedback-based learning in neurotypical (NT) individuals. Despite this cortico-striatal overlap, research about feedback-based learning in MS, its associated neural underpinnings, and its sensitivity to CF, are all lacking. The present study investigated feedback-based learning ability in MS, as well as associated cortico-striatal function and connectivity. MS and NT participants completed a functional magnetic resonance imaging (fMRI) paired-word association task during which they received trial-by-trial monetary, non-monetary, and uninformative performance feedback. Despite reporting greater CF throughout the task, MS participants displayed comparable task performance to NTs, suggesting preserved feedback-based learning ability in the MS group. Both groups recruited the ventral striatum (VS), caudate nucleus, and ventromedial prefrontal cortex in response to the receipt of performance feedback, suggesting that people with MS also recruit cortico-striatal regions during feedback-based learning. However, compared to NT participants, MS participants also displayed stronger functional connectivity between the VS and task-relevant regions, including the left angular gyrus and right superior temporal gyrus, in response to feedback receipt. Results indicate that CF may not interfere with feedback-based learning in MS. Nonetheless, people with MS may recruit alternative connections with the striatum to assist with this form of learning. These findings have implications for cognitive rehabilitation treatments that incorporate performance feedback to remediate cognitive dysfunction in clinical populations.
 INTRODUCTION: Multiple sclerosis is a disease with a heterogeneous evolution. The early identification of secondary progressive multiple sclerosis is a clinical challenge, which would benefit from the definition of biomarkers and diagnostic tools applicable in the transition phase from relapsing-remitting multiple sclerosis to secondary progressive multiple sclerosis. We aimed to reach a Portuguese national consensus on the monitoring of patients with multiple sclerosis and on the more relevant clinical variables for the early identification of its progression. MATERIAL AND METHODS: A Delphi panel which included eleven Portuguese Neurologists participated in two rounds of questions between July and August of 2021. In the first round, 39 questions which belonged to the functional, cognitive, imaging, biomarkers and additional evaluations were included. Questions for which no consensus was obtained in the first round (less than 80% of agreement), were appraised by the panel during the second round. RESULTS: The response rate was 100% in both rounds and consensus was reached for a total of 33 questions (84.6%). Consensus was reached for monitoring time, evaluation scales and clinical variables such as the degree of brain atrophy and mobility reduction, changes suggestive of secondary progressive multiple sclerosis. Additionally, digital devices were considered tools with potential to identify disease progression. Most questions for which no consensus was obtained referred to the cognitive assessment and the remaining referred to both functional and imaging domains. CONCLUSION: Consensus was obtained for the determination of the monitorization interval and for most of the clinical variables. Most questions that did not reach consensus were related with the confirmation of progression taking into account only one test/domain, reinforcing the multifactorial nature of multiple sclerosis.
 Mendelian randomization (MR) is a powerful approach for assessing the causal effect of putative risk factors on an outcome, using genetic variants as instrumental variables. The methodology and application developed in the framework of MR have been dramatically improved, taking advantage of the many public genome-wide association study (GWAS) data. The availability of summary-level data allowed to perform numerous MR studies especially for complex diseases, pinpointing modifiable exposures causally related to increased or decreased disease risk. Multiple sclerosis (MS) is a complex multifactorial disease whose aetiology involves both genetic and non-genetic risk factors and their interplay. Previous observational studies have revealed associations between candidate modifiable exposures and MS risk; although being prone to confounding, and reverse causation, these studies were unable to draw causal conclusions. MR analysis addresses the limitations of observational studies and allows to establish reliable and accurate causal conclusions. Here, we systematically reviewed the studies evaluating the causal effect, through MR, of genetic and non-genetic exposures on MS risk. Among 107 papers found, only 42 were eligible for final evaluation and qualitative synthesis. We found that, above all, low vitamin D levels and high adult body mass index (BMI) appear to be uncontested risk factors for increased MS risk.
 OBJECTIVES: To investigate the correlation between choroid plexus volume and whole brain morphology in patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). METHODS: Fifty-one patients with MS, 42 patients with NMOSD, and 56 healthy controls (HC) were recruited. The morphological changes in choroid plexus and whole brain tissue were compared between three groups and the correlations between choroid plexus volume and brain atrophy were further investigated. The longitudinal alterations of brain morphology in 25 MS and 20 NMOSD patients were compared. RESULTS: Compared to the HC group, the choroid plexus volumes were increased in the MS group (p < 0.001) but not in the NMOSD group (p > 0.05). Compared to the HC group, the MS group showed reduced cortex thickness, deep gray matter volume, and increased ventricle system volume, and the NMOSD group showed increased third ventricle volume (all p < 0.05, false discovery rate corrected). In the MS group, there were widespread correlations between enlarged choroid plexus volume and reduced cerebral cortex thickness (p < 0.05, r = -0.292~-0.538, false discovery rate corrected). The interval time was not significantly different between the MS (median: 1.37 years) and NMOSD group (median: 1.25 years) (p > 0.05). In MS, compared with the baseline, the right hippocampus and nucleus accumbens volumes were decreased in long follow-up, and bilateral lateral ventricle volumes were increased both in short and long follow-up (all p < 0.05, false discovery rate corrected). CONCLUSIONS: The enlarged choroid plexus related to reduced cortical thickness and progressive local brain atrophy are shown in MS patients, but not obvious in NMOSD patients. KEY POINTS: • MS and NMOSD have different altered patterns in choroid plexus volume and brain atrophy. • The enlarged choroid plexus related to brain atrophy is shown in MS patients, but not obvious in NMOSD patients. • Progressive local brain atrophy is shown in MS patients, but not obvious in NMOSD patients.
 BACKGROUND: Patients with multiple sclerosis (MS) may experience decisional conflict during treatment choice. Shared decision making (SDM), whereby patients and health professionals, primarily nurses, collaborate in making decisions, reduces this decisional conflict. It requires understanding large amounts of information and may be complex, especially when decisions affect patients' autonomy and quality and prolongation of life. Patient decision aids are tools in facilitating SDM. This study aimed to identify the key elements from the perspective of patients with relapsing-remitting MS to create a patient decision aid in the Spanish sociocultural context. METHODS: This is a qualitative study using focus groups led by a clinical nurse specialist. Semistructured interviews included healthcare needs and demands, the SDM process, and general characteristics of a peer support program. After the transcription of interview recordings, data were analyzed by thematic analysis and a constructivist naturalistic approach. RESULTS: Patients with MS (27) from Spain participated in 4 focus groups of 90 to 120 minutes each. Three overarching themes were identified: information access to sufficient high-quality data; knowledge of available treatment options, including efficacy, adverse effects, frequency, administration route, and the impact on daily life; decision-making role, engaged versus nonengaged patients. The former require support in facilitating their active involvement in decisions, whereas the latter prefer more passive health models. CONCLUSION: The needs identified by patients with relapsing-remitting MS regarding treatment choice in the Spanish setting align with those reported by other studies. The identified themes provide valuable information to design and develop a virtual patient decision aid jointly by clinical MS nurses and patients according to the International Patient Decision Aid Standards Collaboration criteria. This aid will help improve understanding between nurses and patients during SDM and facilitate the process.
 OBJECTIVE: To re-explore the responsiveness of the Persian version of Multiple Sclerosis Walking Scale-12 (MSWS-12p) to physiotherapy intervention and determine the minimally clinically important change (MCIC). This study followed a prospective cohort design. Patients with MS (PwMS) underwent physiotherapy treatment for 10 sessions. The outcome measures were the MSWS-12p and Timed 25-Foot Walk test (T25-FW). Data was collected before and after ten sessions of physiotherapy. The effect sizes and the area under receiver operating characteristics curve (AUC) and MCIC were calculated. RESULTS: Thirty PwMS (16 female, mean age 43.07 years) participated in the study. The effect sizes for MSWS-12p were moderate (0.52, 0.64). The change scores of MSWS-12p showed excellent correlation with the dichotomized smallest detectable change (SDC) criterion (Eta coefficient test = 0.84). There was no correlation between the MSWS-12p total change scores and the T25-FW (r = - 0.14, p = 0.45). The AUC was perfect and the MCIC for the MSWS-12p was calculated 10.0 points. The MSWS-12p is responsive and demonstrates changes after physiotherapy. Changes > 10.0 points on MSWS-12p total score should be considered as true improvement after physiotherapy.
 OBJECTIVE: To explore longitudinal changes in brain volumetric measures and retinal layer thicknesses following acute optic neuritis (AON) in people with multiple sclerosis (PwMS), to investigate the process of trans-synaptic degeneration, and determine its clinical relevance. METHODS: PwMS were recruited within 40 days of AON onset (n = 49), and underwent baseline retinal optical coherence tomography and brain magnetic resonance imaging followed by longitudinal tracking for up to 5 years. A comparator cohort of PwMS without a recent episode of AON were similarly tracked (n = 73). Mixed-effects linear regression models were used. RESULTS: Accelerated atrophy of the occipital gray matter (GM), calcarine GM, and thalamus was seen in the AON cohort, as compared with the non-AON cohort (-0.76% vs -0.22% per year [p = 0.01] for occipital GM, -1.83% vs -0.32% per year [p = 0.008] for calcarine GM, -1.17% vs -0.67% per year [p = 0.02] for thalamus), whereas rates of whole-brain, cortical GM, non-occipital cortical GM atrophy, and T2 lesion accumulation did not differ significantly between the cohorts. In the AON cohort, greater AON-induced reduction in ganglion cell+inner plexiform layer thickness over the first year was associated with faster rates of whole-brain (r = 0.32, p = 0.04), white matter (r = 0.32, p = 0.04), and thalamic (r = 0.36, p = 0.02) atrophy over the study period. Significant relationships were identified between faster atrophy of the subcortical GM and thalamus, with worse visual function outcomes after AON. INTERPRETATION: These results provide in-vivo evidence for anterograde trans-synaptic degeneration following AON in PwMS, and suggest that trans-synaptic degeneration may be related to clinically-relevant visual outcomes. ANN NEUROL 2023;93:76-87.

 Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system which, in addition to affecting motor and cognitive functions, may also lead to specific changes in the speech of patients. Speech production, comprehension, repetition and naming tasks, as well as structural and content changes in narratives, might indicate a limitation of executive functions. In this study we present a speech-based machine learning technique to distinguish speakers with relapsing-remitting subtype MS and healthy controls (HC). We exploit the fact that MS might cause a motor speech disorder similar to dysarthria, which, with our hypothesis, might affect the phonetic posterior estimates supplied by a Deep Neural Network acoustic model. From our experimental results, the proposed posterior posteriorgram-based feature extraction approach is useful for detecting MS: depending on the actual speech task, we obtained Equal Error Rate values as low as 13.3%, and AUC scores up to 0.891, indicating a competitive and more consistent classification performance compared to both the x-vector and the openSMILE 'ComParE functionals' attributes. Besides this discrimination performance, the interpretable nature of the phonetic posterior features might also make our method suitable for automatic MS screening or monitoring the progression of the disease. Furthermore, by examining which specific phonetic groups are the most useful for this feature extraction process, the potential utility of the proposed phonetic features could also be utilized in the speech therapy of MS patients.
 Multiple sclerosis (MS) is a chronic inflammatory pathology of the central nervous system, which affects young subjects. MS requires a multidisciplinary care coordinated between specialists and allied health professionals. A close collaboration is needed between the various praticians. The last decades have been marked by very significant progress, the diagnosis being established earlier and disease-modifying treatments introduced earlier, with the use of high-efficiency treatments. These therapeutic advances are exciting, however efforts are still needed to better understand the mechanisms of myelin repair and neurodegeneration.
 This study was conducted in order to examine the effect of acupressure applied to patients with multiple sclerosis on fatigue. The patients meeting the inclusion criteria were assigned to intervention (n = 30) and control (n = 30) groups. The data of the study were collected using a questionnaire and the Fatigue Severity Scale. During the study, the control group received its routine treatment; on the other hand, the intervention group received routine treatment and also the certified researcher, receiving the acupressure training, applied acupressure to the intervention group by using the points Li4, ST36 and SP6 3 times a week for a total of 4 weeks. The postacupressure fatigue mean score was 5.2 ± 0.7 in the intervention group and 5.9 ± 0.7 in the control group, and there was a significant difference in the control and intervention groups in terms of postacupressure fatigue mean scores (P < .05). According to these results of the study, it can be recommended to provide acupressure training to patients with multiple sclerosis in order to decrease the fatigue associated with multiple sclerosis.
 BACKGROUND: Informal and formal volunteering engagement is a proxy for social integration and may have beneficial effects for physical and mental well-being in persons with multiple sclerosis (pwMS). As literature on the topic among the pwMS is lacking, this study aimed to determine frequency and type of volunteering performed by pwMS and to identify factors associated with volunteering. METHODS: Cross-sectional, self-reported data of 615 pwMS participating in the Swiss Multiple Sclerosis Registry were analyzed using descriptive statistics to determine frequency and type of volunteering engagement. Univariable and multivariable generalized linear models with binomial distribution and log link function were used to identify factors associated with volunteering. Age, sex, employment status and gait disability were added to the multivariable model as fixed confounders. Sociodemographic, health-, work- and daily activity-related factors were included in the analysis. RESULTS: About one third (29.4%) of participants reported engagement in volunteering activities, most often through charities (16.02%) and cultural organizations (14.36%). In the multivariable model, participants who had a university degree were more likely to volunteer than those with lower level of education (RR = 1.48 95% CI [1.14; 1.91]). The ability to pursue daily activities (as measured by the EQ-5D subscale) was strongly associated with participation in volunteering among pwMS. Compared with pwMS who had no or only slight limitations in daily activities, those with severe problems were markedly less likely to engage in volunteering (RR = 0.41, 95% CI [0.21; 0.80]) . Finally, pwMS who reported caring for and supporting their family (i.e., being a homemaker) were more likely to engage in volunteering activities than those who did not (RR = 1.52, 95% CI [1.15; 2.01]). CONCLUSION: Nearly one in three pwMS engaged in diverse volunteering activities. Having a university degree, being less limited in daily activities and being a homemaker increased the probability of pursuing volunteering activities. Contingent on individual-level motivations, resources or physical abilities, pwMS who experience challenges in performing daily activities or social barriers should be made aware of barrier-free offers of socially inclusive and volunteering activities, often provided by the national MS societies and health leagues.
 OBJECTIVE: Illness personification theory posits that individuals suffering from chronic illness ascribe human characteristics to their illness, which impacts their adaptation. Whereas negative or malevolent personification of chronic illness derails adaptation, positive or benevolent personification yields a complex pattern with aspects of adaptation. This study aimed to examine, for the first time, the role of personification of multiple sclerosis (MS). METHOD: A two-wave design was implemented with 90 people with MS (PwMS) at T1 (2019) and 60 at T2 (2020). The Ben-Gurion University Illness Personification Scale (BGU-IPS) was administered alongside a host of adaptation-related variables relating to salutogenic, psychological, psychopathological and health aspects. The intent was to replicate the 2-factor structure of the IPS and examine associations with adaptation variables. RESULTS: The 2-factor structure of the BGU-IPS was replicated by Principal Component Analysis and Confirmatory Factor Analysis, with good to excellent test-retest reliability. for negative (ICC = 0.81; p < .001) as well as for positive personification scale (ICC = 0.76; p < .001). Negative personification was associated with elevated levels of psychological and psychopathological aspects, as well as low levels of heath related-adaption and salutogenic adaption. Positive personification was associated with salutogenic adaption. In addition, exploratory longitudinal analyses revealed that negative personification at T1 significantly predicted anxiety, physical problems, pain frequency and fatigue frequency at T2, while controlling for the variable's T1 measurements, while positive personification at T1 significantly predicted intolerance of uncertainty at T2. CONCLUSION: The findings depict negative personification as a risk factor for adaptation in MS and call for a detailed exploration of the meaning of positive personification.

 BACKGROUND: Nabiximols (Sativex®) is a cannabinoid approved for multiple sclerosis (MS)-related spasticity. Its mechanism of action is partially understood, and efficacy is variable. OBJECTIVE: To conduct an exploratory analysis of brain networks connectivity changes on resting state (RS) functional MRI (fMRI) of MS patients treated with nabiximols. METHODS: We identified a group of MS patients treated with Sativex® at Verona University Hospital, who underwent RS brain fMRI in the 4 weeks before (T0) and 4-8 weeks after (T1) treatment start. Sativex® response was defined as ≥ 20% spasticity Numerical Rating Scale score reduction at T1 vs. T0. Connectivity changes on fMRI were compared between T0 and T1 in the whole group and according to response status. ROI-to-ROI and seed-to-voxel connectivity were evaluated. RESULTS: Twelve MS patients (7 males) were eligible for the study. Seven patients (58.3%) resulted Sativex® responders at T1. On fMRI analysis, Sativex® exposure was associated with global brain connectivity increase (particularly in responders), decreased connectivity of motor areas, and bidirectional connectivity changes of the left cerebellum with a number of cortical areas. CONCLUSIONS: Nabiximols administration is associated with brain connectivity increase of MS patients with spasticity. Modulation of sensorimotor cortical areas and cerebellum connectivity could play a role in nabiximols effect.
 Ocrelizumab is a humanized monoclonal anti-CD20 antibody, approved for the treatment of relapsing and primary-progressive multiple sclerosis. We reported a case of pericarditis in an RRMS patient treated with ocrelizumab, who presented with chest pain, high body temperature and laboratory findings of systemic inflammation, with a favorable clinical outcome.
 INTRODUCTION AND AIMS: Nicolau syndrome, or embolia cutis medicamentosa, is a rare cutaneous complication of drug injection that has been rarely described in relation to medication used in multiple sclerosis. PATIENTS AND METHODS: We conducted a retrospective study of patients with Nicolau syndrome receiving self-injectable multiple sclerosis medication from 2010 to October 2022. RESULTS: From January 2010 to October 2022, 449 patients were followed up in our demyelinating pathology unit with self-injectable drugs - 317 with beta interferons and 132 with glatiramer acetate (GA). In this period of time, 10 episodes of Nicolau syndrome were recorded in seven patients (six men and one woman) receiving GA, which represents 5.3% of the total number of patients receiving this treatment. The most commonly affected areas were the buttocks (n = 4) and the arms (n = 3). Three patients (42.8%) suffered a second episode. CONCLUSION: Nicolau syndrome is a complication unique to GA and more frequent in men in our cohort of multiple sclerosis patients. This cutaneous complication frequently recurs in the same patient, which is a factor to be taken into account in the decision to maintain the drug or switch to another therapeutic strategy.
 Late-onset neutropaenia is defined as an absolute neutrophil count of <1.5×10(3)cells/μL starting>4 weeks after the last dose of rituximab, in the absence of other identifiable causes. Late-onset neutropaenia is a rare adverse reaction to rituximab (observed in approximately 5% of patients). Rheumatic diseases constitute the main indication for rituximab; in these patients, neutropaenia appears after a mean of>28 days. Ocrelizumab is another monoclonal antibody that binds to CD20 (a glycosylated phosphoprotein mainly expressed on the membranes of B-lymphocytes); in January 2018, it was approved for the treatment of relapsing-remitting and primary progressive multiple sclerosis. We present a case of neutropaenia following intravenous infusion of ocrelizumab in a patient with primary progressive multiple sclerosis who presented with neutropaenic fever, herpetic stomatitis, and ecthyma gangrenosum only 20 days after infusion.
 Multiple sclerosis (MS) affects more than 2.8 million people worldwide and is an incurable, heterogeneous, chronic, degenerative, demyelinating, immune-mediated neurological disease of the central nervous system. It affects the physical, mental, psychosocial, financial, and spiritual dimensions of patients and their families. Given this illness trajectory and the multiple complex symptoms associated with MS, palliative care services would improve the quality of life for MS patients. Palliative care is a human right for all patients with a life-limiting, progressive disease. The goal of palliative care is the prevention and relief of suffering by means of assessment and treatment that holistically addresses symptoms and suffering. Thus, this article argues for the early integration of palliative care for persons given a diagnosis of MS. This argument is underscored by the analysis of a case study of a typical patient with MS who would have benefited from conjunctive palliative care.
 Heritability studies represent an important tool to investigate the main sources of variability for complex diseases, whose etiology involves both genetics and environmental factors. In this paper, we aimed to estimate multiple sclerosis (MS) narrow-sense heritability (h(2)), on a liability scale, using extended families ascertained from affected probands sampled in the Sardinian province of Nuoro, Italy. We also investigated the sources of MS liability variability among shared environment effects, sex, and categorized year of birth (<1946, ≥1946). The latter can be considered a proxy for different early environmental exposures. To this aim, we implemented a Bayesian liability threshold model to obtain posterior distributions for the parameters of interest adjusting for ascertainment bias. Our analysis highlighted categorized year of birth as the main explanatory factor, explaining ~70% of MS liability variability (median value = 0.69, 95% CI: 0.64, 0.73), while h(2) resulted near to 0% (median value = 0.03, 95% CI: 0.00, 0.09). By performing a year of birth-stratified analysis, we found a high h(2) only in individuals born on/after 1946 (median value = 0.82, 95% CI: 0.68, 0.93), meaning that the genetic variability acquired a high explanatory role only when focusing on this subpopulation. Overall, the results obtained highlighted early environmental exposures, in the Sardinian population, as a meaningful factor involved in MS to be further investigated.
 PURPOSE: To report our experience with a case of a very atypical clinical onset of multiple sclerosis in a young boy during a COVID-19 infection. CASE REPORT: A 16-year-old boy was referred to our ophthalmology clinic with a complete isolated bilateral horizontal gaze palsy. The condition had onset suddenly 2 weeks prior and he had no associated symptoms, as well as no significant medical history. His corrected visual acuity was 0.0 logMAR in both eyes. While hospitalized, he was found infected with COVID-19. Subsequent brain MRI showed multiple lesions typical of a yet undiagnosed MS, as well as an active pontine plaque which was highly probable the cause of the horizontal gaze palsy. High-dose steroid treatment was initiated 1 week later, after the patient exhibited negative COVID-19 test results. CONCLUSION: Clinical manifestations of MS are rarely seen in male teenagers and only a few cases of isolated bilateral horizontal gaze palsy have been reported as the initial manifestation, but never during concomitant COVID-19 infection. We presume that the presence of COVID-19 may have been a neuroinflammatory trigger of underlying MS.
 BACKGROUND: Facial emotion recognition (FER) may be impaired in patients with multiple sclerosis (MS). Nevertheless, the literature is heterogeneous, with studies not highlighting this kind of impairment. Moreover, most studies have not explored differences between MS spectrum disorders (radiologically isolated syndrome (RIS), clinically-isolated syndrome (CIS), relapsing-remitting (RRMS), and progressive (primary - (PPMS) and secondary - (SPMS)). One hypothesis would be that FER impairment results from an alteration of eye-gaze strategies while observing emotional faces. Consequently, a FER deficit would be found in MS patients for whom these observation strategies would be disturbed and more frequent in the progressive forms. METHODS: We prospectively enroled 52 patients (10 RIS, 10 CIS, 12RRMS, 10 SPMS, 10 PPMS) and 23 healthy controls (HC) to assess FER using Ekman Faces Test. Eye movements (number and duration of fixations) were recorded with an eye-tracking device. RESULTS: 21% of the MS participants had significant FER impairment. This impairment was observed in all phenotypes. In progressive forms, FER impairment was more frequent, more severe, and associated with modified emotional face observation strategies. MS participants with significant FER impairment had significantly more modification of eye-gaze strategies during observation of expressive faces than MS participants without FER impairment. CONCLUSION: FER impairment seems to be linked to a deficit of attention orientation in MS. Remediation of eye-gaze strategies during observation of emotional faces could be beneficial, as observed in other neurological diseases.
 Judicious multiple sclerosis (MS) diagnosis and early start of disease modifying therapy significantly improves long-term disability outcomes in persons with MS (pwMS). Retrospective analysis based on 25-year New York State MS Consortium (NYSMSC) data determined the effect of changes in the respective diagnostic criteria in shortening the time between symptom onset to MS diagnosis. Based on 9378 current and historical MS cases, there was a significant decrease in time to diagnosis in pwMS from 1982-2001 to >2017 periods (average 4.2 vs. 1.1 years, p < 0.001). Additional improvements and better implementation of the MS diagnostic criteria can further decrease the diagnosis lag.

 BACKGROUND: Although cervical spinal cord (cSC) area is an established biomarker in MS, there is currently a lack of longitudinal assessments of cSC gray and white matter areas. OBJECTIVE: We conducted an explorative analysis of longitudinal changes of cSC gray and white matter areas in MS patients. METHODS: 65 MS patients (33 relapsing-remitting; 20 secondary progressive and 12 primary progressive) and 20 healthy controls (HC) received clinical and upper cSC MRI assessments over 1.10±0.28 years. cSC compartments were quantified on MRI using the novel averaged magnetization inversion recovery acquisitions sequence (in-plane resolution=0.67 × 0.67mm(2)), and in-house developed post-processing methods. Patients were stratified regarding clinical progression. RESULTS: Patients with clinical progression showed faster reduction of cSC areas over time at the level of cSC enlargement (approximate vertebral level C4-C5) compared to stable patients (p<0.05). In addition, when compared to the rostral-cSC (approximate vertebral level C2-C3), a preferential reduction of cSC and white matter areas over time at the level of cSC enlargement (p<0.05 and p<0.01, respectively) was demonstrated only in patients with clinical progression, but not in stable MS patients and HC. Compared to HC, MS patients showed comparable changes over time in all cSC compartments. CONCLUSIONS: MS patients with clinical disease progression demonstrate subtle signs of a more pronounced tissue loss at the level of cSC enlargement. Future studies should consider larger sample sizes and more extended observation periods.
 BACKGROUND: Cognitive impairment (CI) is frequent in persons with multiple sclerosis (PwMS) and is linked to neurodegeneration. Cholesterol pathway biomarkers (CPB) are associated with blood-brain barrier breakdown, lesions, and neurodegeneration in multiple sclerosis (MS). CPB could influence CI. METHODS: This cross-sectional study (n = 163) included 74 relapsing-remitting MS (RR-MS), 48 progressive MS (P-MS) and 41 healthy control (HC) subjects. The assessed physical disability and cognitive measures were: Nine-hole Peg Test (NHPT), Timed 25-Foot Walk, Symbol Digit Modalities Test (SDMT), Paced Auditory Serial Addition Test-3, and Beck Depression Inventory-Fast Screen. CPB panel included plasma total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and the apolipoproteins (Apo), ApoA-I, ApoA-II, ApoB, ApoC-II and ApoE. Disability and cognitive measures were assessed as dependent variables in regression analyzes with age, sex, body mass index, years of education, HC vs. RR-MS vs. P-MS status, CPB, and a HC vs. RR-MS vs. P-MS status × CPB interaction term as predictors. RESULTS: SDMT was associated with the interaction terms for HDL-C (p = 0.045), ApoA-I (p = 0.032), ApoB (p = 0.032), TC/HDL-C (p = 0.013), and ApoB/ApoA-I (p = 0.008) ratios. CPB associations of SDMT were not abrogated upon adjusting for brain parenchymal volume. NHPT performance was associated with the interaction terms for TC (p = 0.047), LDL-C (p = 0.017), ApoB (p = 0.001), HDL-C (p = 0.035), ApoA-I (p = 0.032), ApoC-II (p = 0.049) and ApoE (p = 0.037), TC/HDL-C (p < 0.001), and ApoB/ApoA-I ratios (p < 0.001). CONCLUSIONS: The LDL to HDL proportion is associated with SDMT and NHPT in MS. The findings are consistent with a potential role for CPB in CI.

 Brain atrophy in multiple sclerosis (MS), as measured by percentage brain volume change (PBVC) from brain magnetic resonance imaging (MRI), has been established as an outcome parameter in clinical trials. It is unknown to what extent volume changes within different brain tissue compartments contribute to PBVC. We analyzed pairs of MRI scans (at least 6 months apart) in 600 patients with relapsing-remitting MS. Multiple regression revealed that PBVC mainly reflects volume loss of white and cortical gray matter, while deep gray matter and white matter lesions were less represented. Our findings aid the interpretation of PBVC changes in MS.
 Fingolimod-induced lymphopenia is a risk factor for severe monkeypox infection. As monkeypox was recently declared a Public Health Emergency of International Concern, vaccination should be evaluated in patients with MS before immunosuppressive treatment, particularly in patients receiving sphingosine-1-phosphate receptor modulators.(,)
 OBJECTIVE: To investigate monoaminergic network abnormalities in patients with multiple sclerosis (MS) according to their fatigue and depressive status through a positron emission tomography (PET)-based constrained independent component analysis (ICA) on resting state (RS) functional MRI (fMRI). METHODS: In this prospective study, 213 patients with MS (mean age=40.6±12.5 years; 94/119 men/women; 153 relapsing-remitting; 60 progressive) and 62 healthy controls (HCs, mean age=39.0±10.4 years; 30/32 men/women) underwent neurological, fatigue, depression and RS fMRI assessment. Patterns of dopamine, norepinephrine-related and serotonin-related RS functional connectivity (FC) were derived by ICA, constrained to PET atlases for dopamine, norepinephrine and serotonin transporters, obtained in HCs' brain. RESULTS: Compared with HCs, patients with MS showed abnormalities in all three explored monoaminergic networks, mostly with decreased RS FC within PET-guided monoaminergic networks in frontal regions and subcortical areas including the cerebellum and thalamus, and increased RS FC in temporo-parieto-occipital cortical areas, including bilateral precunei.MS-related fatigue was associated with decreased RS FC within the PET-guided dopamine network in the left thalamus and left cerebellum, and with increased RS FC within the PET-guided serotonin network in the left middle occipital gyrus. MS-related depression was associated with more distributed abnormalities involving the three explored monoaminergic networks, resulting in overall reduced RS FC in the frontal lobe, limbic areas and the precuneus. CONCLUSIONS: Patients with MS present diffuse dysregulation in the monoaminergic networks. Specific alterations in these networks were associated with fatigue and depression, providing a pathological marker for these bothersome symptoms and putative targets for their treatment.
 BACKGROUND: The number of patients diagnosed with multiple sclerosis (MS) has increased significantly over the last decade. The challenge is to identify the transition from relapsing-remitting to secondary progressive MS. Since available methods to examine patients with MS are limited, both the diagnostics and prognostication of disease progression would benefit from the multimodal approach. The latter combines the evidence obtained from disparate radiologic modalities, neurophysiological evaluation, cognitive assessment and molecular diagnostics. In this systematic review we will analyse the advantages of multimodal studies in predicting the risk of conversion to secondary progressive MS. METHODS AND ANALYSIS: We will use peer-reviewed publications available in Web of Science, Medline/PubMed, Scopus, Embase and CINAHL databases. In vivo studies reporting the predictive value of diagnostic methods will be considered. Selected publications will be processed through Covidence software for automatic deduplication and blind screening. Two reviewers will use a predefined template to extract the data from eligible studies. We will analyse the performance metrics (1) for the classification models reflecting the risk of secondary progression: sensitivity, specificity, accuracy, area under the receiver operating characteristic curve, positive and negative predictive values; (2) for the regression models forecasting disability scores: the ratio of mean absolute error to the range of values. Then, we will create ranking charts representing performance of the algorithms for calculating disability level and MS progression. Finally, we will compare the predictive power of radiological and radiomical correlates of clinical disability and cognitive impairment in patients with MS. ETHICS AND DISSEMINATION: The study does not require ethical approval because we will analyse publicly available literature. The project results will be published in a peer-review journal and presented at scientific conferences. PROSPERO REGISTRATION NUMBER: CRD42022354179.
 OBJECTIVE: To estimate the pooled prevalence of sexual dysfunction (SD) in women with multiple sclerosis (MS). METHODS: We systematically searched PubMed, Scopus, EMBASE, Web of Science, and google scholar and also gray literature up to October 2021. The search strategy includes: ("Multiple Sclerosis" OR "MS" OR "Disseminated Sclerosis" OR (Disseminated AND Sclerosis) OR (Sclerosis AND Multiple)) AND ("Sexual Dysfunction" OR (Sexual AND Dysfunction) OR (Sexual AND Dysfunctions) OR (Sexual AND Disorders) OR (Sexual AND Disorder) OR "Sexual Dysfunctions" OR "Sexual Disorders" OR "Sexual Disorder" OR "Psychosexual Dysfunctions" OR (Dysfunction AND Psychosexual) OR (Dysfunctions AND Psychosexual) OR "Psychosexual Dysfunction" OR "Psychosexual Disorders" OR (Disorder AND Psychosexual) OR (Disorders AND Psychosexual) OR "Psychosexual Disorder" OR "Hypoactive Sexual Desire Disorder" OR "Sexual Aversion Disorder" OR (Aversion Disorders AND Sexual) OR (Disorders AND Sexual Aversion) OR "Sexual Aversion Disorders" OR "Orgasmic Disorder" OR (Disorders AND Orgasmic) OR "Orgasmic Disorders" OR "Sexual Arousal Disorder" OR (Arousal Disorders AND Sexual) OR (Disorders AND Sexual Arousal) OR "Sexual Arousal Disorders" OR "Frigidity"). RESULTS: We found 2150 articles by literature search, after deleting duplicates 1760 remained. Fifty-six articles remained for meta-analysis. The pooled prevalence of SD in MS patients estimated as 61% (95%CI:56-67%) (I(2):95.7%, P < 0.001). The pooled prevalence of Anorgasmia in MS patients estimated as 29% (95%CI:20-39%) (I(2):85.3%, P < 0.001). The pooled odds of developing SD in MS women estimated as 3.05(95%CI: 1.74-5.35) (I(2):78.3%, P < 0.001). The pooled prevalence of decreased vaginal lubrication in MS patients estimated as 32%(95%CI:27-37%) (I(2) = 94.2%, P < 0.001). The pooled prevalence of reduced libido was 48%(95%CI:36-61%) (I(2):92.6%, P < 0.001). The pooled prevalence of arousal problems was 40%(95%CI: 26-54%) (I(2):97.4%, P < 0.001). The pooled prevalence of intercourse satisfaction was 27% (95%CI: 8-46%) (I(2):99%, P < 0.001). CONCLUSION: The result of this systematic review and meta-analysis show that the pooled prevalence of SD in women with MS is 61% and the odds of developing SD in comparison with controls is 3.05.
 BACKGROUND: Timing of disease-modifying therapy affects clinical disability in multiple sclerosis, but it is not known whether patient reported outcomes are also affected. This study investigates the relationship between treatment timing and patient-reported symptoms and health-related quality of life. METHODS: This was a nationwide observational cohort study of adults with relapsing multiple sclerosis, with disease onset between 2001 and 2016, and commenced on disease-modifying treatment within 4 years from disease onset. Patients commencing treatment within 0-2 years were compared with patients commencing treatment at 2-4 years. Indication bias was mitigated by propensity matching. Outcomes were patient-reported symptoms and health-related quality of life as measured by the Multiple Sclerosis Impact Scale (MSIS-29) and EuroQol-5 Dimensions-3 Level (EQ-5D). The follow-up period was 4-10 years from disease onset. RESULTS: There were 2648 patients (69% female, median age 32.8) eligible for matching. Mean follow-up time was 3.7 years. Based on 780 matched patients, each year of treatment delay was associated with a worse MSIS physical score by 2.75 points (95% CI 1.29 to 4.20), and worse MSIS psychological score by 2.02 points (95% CI 0.03 to 3.78), in the adjusted models.Among 690 matched patients, earlier treatment start was not associated with EQ-5D score during the follow-up. CONCLUSIONS: Earlier commencement of disease-modifying treatment was associated with better patient-reported physical symptoms when measured using a disease-specific metric; however, general quality of life was not affected. This indicates that other factors may inform patients' overall quality of life.
 BACKGROUND: It is not known if and when first-line disease modifying therapy (DMT) can safely be discontinued in relapse onset multiple sclerosis (MS) patients. OBJECTIVES: To investigate the characteristics of patients who discontinued first-line DMT, and the occurrence of clinical and radiological inflammatory disease activity after discontinuation. METHODS: We collected clinical and MRI parameters from patients with relapse onset MS in the MS Center Amsterdam and Rijnstate Hospital Arnhem who discontinued first-line DMT with no intention of restarting or switching treatment. RESULTS: In total, 130 patients were included in the analyses. After discontinuation, 78 patients (60%) experienced disease activity. Sixty-three patients (48.5%) showed MRI activity after DMT discontinuation, 40 patients (30.8%) experienced relapse(s), and 29 patients (22.3%) restarted DMT. Higher age at DMT discontinuation was associated with a lower risk of MRI activity (45 -55 vs. <45 years: OR 0.301, p = 0.007, >55 vs. <45 years, OR: 0.296, p = 0.044), and with a lower risk of relapse(s) after discontinuation (45-55 vs. <45 years: OR=0.495, p = 0.106, >55 vs. <45 years: OR=0.081, p = 0.020). CONCLUSION: Higher age at first-line DMT discontinuation is associated with lower risk and severity of radiological disease activity in MS, and a lower risk of relapse(s) after discontinuation.
 BACKGROUND AND OBJECTIVES: Ten years after its authorization, data about fingolimod use in real-world setting is still scarce. Here we describe the long-term evolution of fingolimod-treated relapsing-remitting MS (RRMS) patients and determine baseline characteristics associated with risk of relapses or disability. METHODS: We analyzed baseline characteristics and clinical evolution of 1227 patients with RRMS treated with fingolimod from 2010 to 2019 in 4 French MS referral centers. We used Cox models to determine risks factors of relapses and sustained EDSS worsening. RESULTS: Median follow-up duration was 50 months, and 63% of patients remained fingolimod-treated at the end of follow-up. Mean 5-years annualized relapse rate (ARR) decreased from 0.63 (0.60-0.67) to 0.26 (0.24-0.29, P<0.001), while the mean EDSS rose from 2.5 (2.4-2.6) to 3.0 (2.8-3.1, P<0.001). Female sex, lower age, higher EDSS and use of natalizumab were associated with relapse risk. Female sex was associated with sustained EDSS increase risk. CONCLUSIONS: Based on a large real-world cohort, our results confirm the durable reduction of the ARR described in pivot studies. Switching from moderate-efficacy DMT to fingolimod decreased the relapse risk. Switching patients from high-efficacy DMT increased risk of relapse, but the overall five-years ARR remained stable.
 BACKGROUND: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system characterized by two major and interconnected hallmarks: inflammation and progressive neurodegeneration. OBJECTIVE: The aim of this work was to compare neurodegenerative processes, in the form of global and regional brain volume loss rates, in healthy controls (HCs) and in patients with relapsing MS (RMS) treated with ocrelizumab, which suppresses acute inflammation. METHODS: Whole brain, white matter, cortical gray matter, thalamic, and cerebellar volume loss rates were assessed in 44 HCs that were part of a substudy in the OPERA II randomized controlled trial (NCT01412333) and 59 patients with RMS enrolled in the same substudy as well as age- and sex-matched patients in OPERA I (NCT01247324) and II. Volume loss rates were computed using random coefficients models over a period of 2 years. RESULTS: Ocrelizumab-treated patients showed global and regional brain volume loss rates that were approaching that of HCs. CONCLUSION: These findings are consistent with an important role of inflammation on overall tissue loss and the role of ocrelizumab in reducing this phenomenon.
 Multiple sclerosis is a common immune-mediated inflammatory and demyelinating disease. Lower cholecalciferol levels are an established environmental risk factor in multiple sclerosis. Although cholecalciferol supplementation in multiple sclerosis is widely accepted, optimal serum levels are still debated. Moreover, how cholecalciferol affects pathogenic disease mechanisms is still unclear. In the present study, we enrolled 65 relapsing-remitting multiple sclerosis patients who were double-blindly divided into two groups with low and high cholecalciferol supplementation, respectively. In addition to clinical and environmental parameters, we obtained peripheral blood mononuclear cells to analyze DNA, RNA, and miRNA molecules. Importantly, we investigated miRNA-155-5p, a previously published pro-inflammatory miRNA in multiple sclerosis known to be correlated to cholecalciferol levels. Our results show a decrease in miR-155-5p expression after cholecalciferol supplementation in both dosage groups, consistent with previous observations. Subsequent genotyping, gene expression, and eQTL analyses reveal correlations between miR-155-5p and the SARAF gene, which plays a role in the regulation of calcium release-activated channels. As such, the present study is the first to explore and suggest that the SARAF miR-155-5p axis hypothesis might be another mechanism by which cholecalciferol supplementation might decrease miR-155 expression. This association highlights the importance of cholecalciferol supplementation in multiple sclerosis and encourages further investigation and functional cell studies.
 INTRODUCTION: Multiple sclerosis (MS) is an autoimmune disease that can affect balance, gait, and improve fall risk. The aim of this study was to investigate peripheral vestibular system involvement in MS and associations with the disease severity. METHODS: Thirty-five adult patients with MS and 14 age- and gender-matched healthy controls were evaluated using video head impulse test (v-HIT), cervical vestibular evoked myogenic potential (c-VEMP), ocular vestibular evoked myogenic potentials (o-VEMPs), and sensory organization test (SOT) of computerized dynamic posturography (CDP). The results of both groups were compared, and association with EDSS scores was evaluated. RESULTS: There was no significant difference between the groups regarding v-HIT and c-VEMP results (p > 0.05). There was no association of the v-HIT, c-VEMP, and o-VEMP results with EDSS scores (p > 0.05). There was no significant difference between the o-VEMP results of the groups (p > 0.05) except for N1-P1 amplitudes (p = 0.01). The amplitudes of N1-P1 were significantly lower in the patients compared to controls (p = 0.01). There was no significant difference between the SOT results of the groups (p > 0.05). However, significant differences were found within and between groups when the patients were categorized according to their EDSS scores with a cutoff point of 3 (p < 0.05). There were negative correlations between the EDSS scores and composite (r = -396, p = 0.02) and somatosensory (SOM) scores (r = -487, p = 0.04) of CDP in the MS group. CONCLUSION: Although central and peripheral balance-related systems are affected in MS, the impact of disease on the peripheral vestibular end organ is subtle. In particular, the v-HIT, which was mentioned previously as a detector of brainstem dysfunction could not be a reliable tool in the detection of brainstem pathologies in MS patients. The o-VEMP amplitudes may be affected in the early stages of the disease, possibly due to the crossed ventral tegmental tract, oculomotor nuclei, or interstitial nucleus of Cajal involvements. An EDSS score >3 seems a cutoff level indicating abnormalities in balance integration.
 BACKGROUND: Fingolimod became the first disease-modifying therapy approved by Health Canada for pediatric multiple sclerosis in 2018, but the impact of that approval on treatment patterns in Canada is unknown. The aim of this study was to describe trends in the epidemiology and treatment of pediatric-onset multiple sclerosis in Alberta, Canada. METHODS: This study entailed a retrospective review of administrative health databases using 2 case definitions of multiple sclerosis. Those <19 years of age at a date of diagnosis between January 1, 2011, and December 31, 2020, were included. Incidence and prevalence estimates were calculated and stratified by sex and age cohort. Pharmacy dispenses of disease-modifying therapies were identified. RESULTS: 106 children met one or both case definitions. In 2020, the age-standardized incidence using the 2 case definitions was 0.47 and 0.57 per 100 000, and the age-standardized prevalence was 2.84 and 3.41 per 100 000, respectively. Seventy-nine incident cases were identified, 38 (48%) of whom were dispensed a disease-modifying therapy prior to age 19 years. Injectables accounted for all initial pediatric disease-modifying therapy dispenses prior to 2019, whereas in 2019-2020 injectables accounted for only 3 of 15 (20%) initial dispenses, and instead B-cell therapies were the most common initial disease-modifying therapy (6 of 15, 40%). In 2020, B-cell therapies were the most common disease-modifying therapy dispensed overall (9 of 22 dispenses, 41%) followed by fingolimod (6 of 22, 27%). CONCLUSION: The treatment of children with multiple sclerosis in Alberta has evolved, with a rapid shift in 2019 away from injectables to newer agents, although B-cell therapies-not fingolimod-are now most commonly dispensed.
 INTRODUCTION: Neurodegeneration is likely to be present from the earliest stages of multiple sclerosis (MS). MS responds poorly to disease-modifying treatments (DMTs) and leads to irreversible brain volume loss (BVL), which is a reliable predictor of future physical and cognitive disability. Our study aimed to discover the relationship between BVL, disease activity, and DMTs in a cohort of patients with MS. MATERIAL AND METHODS: A total of 147 patients fulfilled our inclusion criteria. Relevant demographic and clinical data (age, gender, time of MS onset, time of treatment initiation, DMT characteristics, Expanded Disability Status Scale (EDSS), number of relapses in the last two years prior to MRI examination) were correlated with MRI findings. RESULTS: Patients with progressive MS had significantly lower total brain and grey matter volumes (p = 0.003; p < 0.001), and higher EDSS scores (p < 0.001), compared to relapsing-remitting patients matched by disease duration and age. There was no association between MRI atrophy and MRI activity (c2 = 0.013, p = 0.910). Total EDSS negatively correlated with the whole brain (rs = -0.368, p < 0.001) and grey matter volumes (rs = -0.308, p < 0.001), but was not associated with the number of relapses in the last two years (p = 0.278). Delay in DMT negatively correlated with whole brain (rs = -0.387, p < 0.001) and grey matter volumes (rs = -0.377, p < 0.001). Treatment delay was connected with a higher risk for lower brain volume (b = -3.973, p < 0.001), and also predicted a higher EDSS score (b = 0.067, p < 0.001). CONCLUSIONS: Brain volume loss is a major contributor to disability progression, independent of disease activity. Delay in DMT leads to higher BVL and increased disability. Brain atrophy assessment should be translated into daily clinical practice to monitor disease course and response to DMTs. The assessment of BVL itself should be considered a suitable marker for treatment escalation.
 BACKGROUND AND OBJECTIVES: Recent data suggest increasing global prevalence of multiple sclerosis (MS). Early diagnosis of MS reduces the burden of disability-adjusted life years and associated health care costs. Yet diagnostic delays persist in MS care and even within national health care systems with robust resources, comprehensive registries, and MS subspecialist referral networks. The global prevalence and characteristics of barriers to expedited MS diagnosis, particularly in resource-restricted regions, have not been extensively studied. Recent revisions to MS diagnostic criteria demonstrate potential to facilitate earlier diagnosis, but global implementation remains largely unknown. METHODS: The Multiple Sclerosis International Federation third edition of the Atlas of MS was a survey that assessed the current global state of diagnosis including adoption of MS diagnostic criteria; barriers to diagnosis with respect to the patient, health care provider, and health system; and existence of national guidelines or national standards for speed of MS diagnosis. RESULTS: Coordinators from 107 countries (representing approximately 82% of the world population), participated. Eighty-three percent reported at least 1 "major barrier" to early MS diagnosis. The most frequently reported barriers included the following: "lack of awareness of MS symptoms among general public" (68%), "lack of awareness of MS symptoms among health care professionals" (59%), and "lack of availability of health care professionals with knowledge to diagnose MS" (44%). One-third reported lack of "specialist medical equipment or diagnostic tests." Thirty-four percent reported the use of only 2017 McDonald criteria (McD-C) for diagnosis, and 79% reported 2017 McD-C as the "most commonly used criteria." Sixty-six percent reported at least 1 barrier to the adoption of 2017 McD-C, including "neurologists lack awareness or training" by 45%. There was no significant association between national guidelines pertaining to MS diagnosis or practice standards addressing the speed of diagnosis and presence of barriers to early MS diagnosis and implementation of 2017 McD-C. DISCUSSION: This study finds pervasive consistent global barriers to early diagnosis of MS. While these barriers reflected a lack of resources in many countries, data also suggest that interventions designed to develop and implement accessible education and training can provide cost-effective opportunities to improve access to early MS diagnosis.
 BACKGROUND: Spasticity is common among people with multiple sclerosis (MS), but there are few studies of spasticity treatment patterns. We aim to describe associations with spasticity treatment measured primarily by oral baclofen use. METHODS: This cohort study using Swedish registers included 1826 and 3519 people with incident and prevalent MS (pwIMS, pwPMS) respectively, followed from 2005 to 2014. Cox regression assessed factors associated with new baclofen prescriptions and its discontinuation. RESULTS: A total of 10% of pwIMS and 19% of pwPMS received baclofen, a drug prescribed specifically for spasticity in Sweden, of which many patients had relapsing-remitting course. Prescriptions occurred soon after MS diagnosis: pwIMS received baclofen typically within 6 months of diagnosis, and pwPMS within 3 years. Younger patients compared with older patients were three times more likely to receive baclofen with similar disability level measured using Expanded Disability Severity Scores (EDSS). Patients aged 18-44 years with EDSS 3.0-5.0 have an HR for baclofen use of 5.62 (95% CI 2.91 to 10.85) and EDSS 6+ have an HR of 15.41 (95% CI 7.07 to 33.58) compared with individuals with EDSS 0-2.5. In comparison, patients aged 45+ years with EDSS 3.0-5.0 have an HR of 2.05 (95% CI 1.10 to 3.82) and EDSS 6+ an HR of 4.26 (95% CI 1.96 to 9.17). Baclofen discontinuation was high: 49% (95% CI 0.42 to 0.57) of pwIMS discontinued within 150 days of dispensation, 90% discontinued within 2 years including patients with progressive course or higher EDSS. Associations among pwPMS and sensitivity analyses including additional treatments were similar. CONCLUSIONS: Younger patients with MS are more likely to receive baclofen compared with older patients with MS. High rates of baclofen discontinuation highlight the need for more tolerable and efficacious spasticity treatments and monitoring of spasticity among people with MS.
 BACKGROUND: Information on performance of multiple sclerosis (MS) diagnostic criteria is scarce for populations from Latin America, Asia, or the Caribbean. OBJECTIVE: To assess performance of revised 2017 McDonald criteria as well as evaluate genetic ancestry in a group of MS patients from Argentina experiencing a debut demyelinating event. METHODS: Demographic and clinical characteristics, cerebrospinal fluid (CSF), and magnetic resonance imaging (MRI) findings and new T2 lesions were recorded at baseline and during relapses. Diagnostic accuracy in predicting conversion to clinically defined MS (CDMS) based on initial imaging applying revised 2017 criteria was evaluated and genetic ancestry-informative markers analyzed. RESULTS: Of 201 patients experiencing their first demyelinating event (median follow-up 60 months), CDMS was confirmed in 67. We found 2017 diagnostic criteria were more sensitive (84% vs 67%) and less specific (14% vs 33%) than 2010 criteria, especially in a group of patients revised separately, presenting positive oligoclonal bands (88% vs 8%). Genetic testing performed in 128 cases showed 72% of patients were of European ancestry and 27% presented genetic admixture. CONCLUSION: 2017 McDonald criteria showed higher sensitivity and lower specificity compared with 2010 criteria, shortening both time-to-diagnosis and time-to-treatment implementation.
 Treating MS has been difficult. One successful drug is Ocrelizumab (anti-CD20), used for the chronic relapsing MS (RMS) and the progressive MS (PMS) forms. TH40 cells are pathogenic effector T cells that increase in percentage and numbers during chronic inflammation. Here we show that in the earliest MS course, clinically isolated syndrome (CIS), TH40 cells expand in number. In PMS TH40 cell numbers remain expanded demonstrating sustained chronic inflammation. In RMS TH40 cells were found in CSF and express CD20. Ocrelizumab reduced TH40 cells to healthy control levels in patients. During treatment inflammatory cytokine producing TH40 cells were decreased.
 BACKGROUND AND PURPOSE: This study assessed the effect of patient characteristics on the response to disease-modifying therapy (DMT) in multiple sclerosis (MS). METHODS: We extracted data from 61,810 patients from 135 centers across 35 countries from the MSBase registry. The selection criteria were: clinically isolated syndrome or definite MS, follow-up ≥ 1 year, and Expanded Disability Status Scale (EDSS) score ≥ 3, with ≥1 score recorded per year. Marginal structural models with interaction terms were used to compare the hazards of 12-month confirmed worsening and improvement of disability, and the incidence of relapses between treated and untreated patients stratified by their characteristics. RESULTS: Among 24,344 patients with relapsing MS, those on DMTs experienced 48% reduction in relapse incidence (hazard ratio [HR] = 0.52, 95% confidence interval [CI] = 0.45-0.60), 46% lower risk of disability worsening (HR = 0.54, 95% CI = 0.41-0.71), and 32% greater chance of disability improvement (HR = 1.32, 95% CI = 1.09-1.59). The effect of DMTs on EDSS worsening and improvement and the risk of relapses was attenuated with more severe disability. The magnitude of the effect of DMT on suppressing relapses declined with higher prior relapse rate and prior cerebral magnetic resonance imaging activity. We did not find any evidence for the effect of age on the effectiveness of DMT. After inclusion of 1985 participants with progressive MS, the effect of DMT on disability mostly depended on MS phenotype, whereas its effect on relapses was driven mainly by prior relapse activity. CONCLUSIONS: DMT is generally most effective among patients with lower disability and in relapsing MS phenotypes. There is no evidence of attenuation of the effect of DMT with age.
 BACKGROUND: In multiple sclerosis (MS), iron rim lesions (IRLs) are associated with pronounced tissue damage, higher disease severity and have been suggested as an imaging marker of chronic active inflammation behind the blood-brain barrier indicating progression. Furthermore, chronic intrathecal compartmentalized inflammation has been suggested to be a mediator of a cerebrospinal fluid (CSF)-related tissue damage. OBJECTIVE: To investigate CSF markers of intrathecal inflammation in patients with at least one IRL compared to patients without IRLs and to investigate tissue damage in lesions and normal-appearing white matter (NAWM) with proximity to CSF spaces. METHODS: A total of 102 patients (51 with at least 1 IRL and 51 age-/sex-matched patients without IRL) scanned with the same 3T magnetic resonance imaging (MRI) and having CSF analysis data were included. RESULTS: Patients with at least one IRL had higher disability scores, higher lesion volumes, lower brain volumes and a higher intrathecal immunoglobulin G (IgG) synthesis. Apparent diffusion coefficient (ADC) values in IRLs were higher compared to non-IRLs. We observed a negative linear correlation of ADC values in all tissue classes and distance to CSF, which was stronger in patients with high IgG quotients. CONCLUSION: IRLs are associated with higher intrathecal IgG synthesis. CSF-mediated intrathecal smouldering inflammation could explain a CSF-related gradient of tissue damage.
 BACKGROUND: Alemtuzumab, a humanized anti-CD52 monoclonal antibody, has been approved as a treatment in persons with active relapsing-remitting multiple sclerosis (RRMS). Real-world data in middle east is very limited. We aimed to evaluate the effectiveness and safety of alemtuzumab in a real-world clinical setting. METHODS: This observational, registry based study assessed persons with multiple sclerosis (PwMS) who were treated with alemtuzumab and completed at least follow up one year after second course. Baseline clinical and radiological characteristics within one year prior to alemtuzumab initiation were collected. The relapse rate, disability measures, radiological activity and adverse events at last follow-up visits were assessed. RESULTS: Data of seventy-three persons with multiple sclerosis (MS) was analyzed, of which 53 (72.6%) were females. Mean age and mean disease duration were 34.25 ± 7.62 and 9.23 ± 6.20 years respectively. Alemtuzumab was started in 32 (43.8%) naïve patients due to highly active disease and in 25 (34.2%) (PwMS) who were on prior therapies and  in 16 (22%) patients due to adverse events on prior medications. Mean follow-up period was 4 ± 1.67 years. In the last follow-up visits, most of our cohort was relapse free (79.5% vs. 17.8%; p < 0.001) compared to baseline before alemtuzumab treatment while mean EDSS score was reduced (2.21 ± 2.15 vs. 2.41 ± 1.85; p < 0.059). The proportion of PwMS who had MRI activity (new T2/ Gd-enhancing) lesions were significantly reduced compared to baseline (15.1% vs. 82.2%; p < 0.001). NEDA-3 was achieved in 57.5% of (PwMS). NEDA-3 was significantly better in naïve patients (78% versus. 41.5%; p < 0.002) and in patients with disease duration < 5 years, (82.6% v 43.2%; p < 0.002). Several adverse events such as infusion reactions (75.3%), autoimmune thyroiditis (16.4%) and glomerulonephritis (2.7%) were reported. CONCLUSION: The effectiveness and safety profile of alemtuzumab in this cohort were consistent with data of clinical trials. Early initiation of Alemtuzumab is associated with favorable outcome.


 Pediatric multiple sclerosis (MS) accounts for 3%-10% of all patients diagnosed with MS. Complex interplay between environmental factors impacts the risk for MS and may also affect disease course. Many of these environmental factors are shared with adult-onset MS. However, children with MS are in closer temporal proximity to the biological onset of MS and have less confounding environmental exposures than their adult counterparts. Environmental factors that contribute to MS risk include: geographical latitude, viral exposures, obesity, vitamin deficiencies, smoking, air pollution, perinatal factors, gut microbiome, and diet. More recently, research efforts have shifted to studying the impact of these risk determinants on the clinical course of MS. In this article we will examine relevant environmental risk determinants of pediatric MS and review the current knowledge on how these factors may contribute to pediatric MS disease evolution.
 Multiple sclerosis (MS) is a disease of the central nervous system (CNS) that affects the brain and spinal cord. It is estimated that the average prevalence of MS is 35.9 cases per 100,000 and a total of 2.8 million people worldwide have MS. Brain atrophy is usually seen in the early stages of MS, and its progress is faster than healthy people. The present study was a numerical study that uses the Fluid-structure interaction (FSI) model to investigate the effect of brain atrophy on brain injury in MS. Firstly, a healthy model was constructed from MRI images and validated by experimental data. Then three models with different degrees of brain atrophy, which showed the rate of brain atrophy in different years in MS patients, were developed to model the brain atrophy in MS. The models were subjected to two different types of impact conditions. Type I, which only produced a translational motion and the HIC value of 744, was applied to each model. Type II produced both translational and rotational motion. In this type of impact, the experimental kinematics, with peaks of 450 g for the translational acceleration and 26.2 krad/s2 for the rotational acceleration, were applied to the nodes that located in the center of gravity of the head models and the results were extracted from each one. According to the results of impact type I, the pressure of the frontal lobe of the brain is 149,647 Pa in the health model and 137,690 Pa in the model with severe atrophy.
 The aim of this qualitative study is to gain insight into the perspectives of persons with multiple sclerosis on social support. Semi-structured interviews were conducted with eleven persons with multiple sclerosis. The results on informal support for persons with multiple sclerosis reveal perceived support and the lack of support from different persons. The results on formal support for persons with multiple sclerosis show perceived support from healthcare professionals, professionals working outside healthcare and social care systems, and associations of persons with MS, but also inadequate support from healthcare professionals and social workers. Close emotional relationship, empathy, knowledge and understanding are the basis for provision of all types of support from informal support system, while perceived support from formal support system is based on professionals´ empathy, their professionalism and knowledge. Persons with multiple sclerosis need accurate and timely emotional, informational, practical and financial support.
 BACKGROUND: Multiple sclerosis (MS) is an aggressive disease characterized by central nervous system (CNS) inflammatory and demyelinating lesions. Tolerance failure is implicated in the development of several autoimmune disorders, including MS. Due to their involvement in maintaining environmental tolerance, regulatory T cells (Tregs) are regarded as efficient immune cells. We examined the frequency of Tregs in this study using CD4/CD25/forkhead box protein P3 (FOXP3)/Helios markers. METHODS: Fifty participants, including 25 patients with secondary progressive MS (SPMS) and 25 healthy controls (HCs), were enrolled in this study, and their demographic characteristics were recorded. Peripheral blood samples ranging from 5 to 6 mL were obtained, and the Ficoll technique was used to extract peripheral blood mononuclear cells (PBMCs). Then, the percentage of CD4(+)CD25(+)FOXP3(+)Helios(+) regulatory T lymphocytes was examined by flow cytometry in the study groups. Real-time polymerase chain reaction (PCR) was also used to assess the Helios gene expression level. RESULTS: This study showed that the percentage of Tregs with CD4 and CD25 markers did not reveal a significant difference compared with HCs despite the decrease in SPMS patients (P = 0.6). However, lymphocytes with CD4/CD25/FOXP3/Helios markers were significantly reduced in the patients (P = 0.01). Additionally, SPMS patients had statistically significantly lower Helios gene expression levels (P = 0.002). CONCLUSION: In SPMS patients, a decrease in the frequency of the CD4(+)CD25(+)FOXP3(+)Helios(+) Treg population can result in an imbalanced immune system. In other words, one of the immunological mechanisms involved in this disease may be a deficiency in Tregs. Helios gene expression was also decreased in these patients, which may exacerbate functional defects in Tregs.
 The runt-related transcription factor-1 (RUNX1) gene with its lncRNA RUNXOR are recently becoming a research focus in various diseases, specifically immune-related diseases as they are implicated in multiple pathways. Interestingly, their role in multiple sclerosis (MS) remains unstudied. The present study explored the role of RUNXOR/RUNX1 in the development and progression of MS and investigated their possible mechanism of action. We measured the serum expression levels of lncRNA RUNXOR, as well as RUNX1, microtubule associated protein 2 (MAP2), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) mRNAs in 30 healthy controls and 120 MS patients subdivided into 4 groups: 30 clinically isolated syndrome patients, 30 relapsing-remitting MS (RRMS) patients in relapse, 30 RRMS patients in remission and 30 secondary progressive MS patients. Additionally, we measured the serum protein levels of RUNX1, MAP2, NGF, BDNF and interleukin-10 (IL-10). All measured RNA expression levels were markedly downregulated and, consequently, the protein levels of RUNX1, MAP2, NGF, BDNF and IL-10 were significantly decreased in MS patients compared to healthy controls. Moreover, the levels of the measured parameters varied significantly within the MS groups. According to receiver-operating-characteristic (ROC) curve and logistic regression analyses, lncRNA RUNXOR, RUNX1 mRNA and its protein levels were predictors of disease progression, in addition to RUNX1 mRNA exhibiting a diagnostic potential. Altogether, this study suggests the implication of the RUNXOR-RUNX1 axis in MS development, progression, and increased MS-related disability, and highlights the potential utility of the studied parameters as promising diagnostic/prognostic biomarkers for MS.
 BACKGROUND: Covid-19 pandemic impacted on management of people with Multiple Sclerosis (pwMS). Level of satisfaction of pwMS regarding the care received by the staff of Multiple Sclerosis Centers (MSCs) during the pandemic was not fully investigated. In a large patient-centered multicenter study, the therapeutic adherence and quality of care of MSCs was assessed. METHODS: In April-May 2021, an online survey was widespread by 16 Italian MSCs. Frequencies, percentages and/or means and standard deviations were calculated to describe the sample. ANOVAs were performed to evaluate the effect of sociodemographic and clinical variables on overall pwMS' rating of MSC assistance. RESULTS: 1670 pwMS completed the survey (67.3% women). During the pandemic, 88% did not change their disease modifying therapy schedule, and 89.1% reached their MSCs with no or little difficulties. Even if only 1.3% of participants underwent a tele-health follow-up visit with their MSC staff, the 80.1% believed that tele-health services should be improved regardless of pandemic. 92% of participants were satisfied of how their MSC took charge of their needs; ANOVAs revealed an effect of disease duration on pwMS' level of satisfaction on MSCs management during the pandemic. CONCLUSIONS: The results revealed an efficient MSCs response to Covid-19 pandemic and provided the basis for the implementing of tele-health services that would further improve the taking charge of patients, particularly those with longer disease, higher disability, and/or living far from their MSC.
 OBJECTIVE: We aimed at examining the effects of a known metacognitive training in MS (MaTiMS) and its modification with an additional neuroeducational module and mindfulness-based exercises (MaTiMS-modified) on neuropsychiatric and cognitive outcomes in people with progressive multiple sclerosis (pwpMS). Exploratively, we investigated whether the modification may show an additional benefit. METHODS: Both interventions were administered in small groups of ambulatory patients. Neuropsychological testing before and after the 3- to 4-week intervention phase comprised patient reported outcomes and cognitive tests. After 3, 6 and 12 months, participants completed online surveys. Analysis of change scores (between baseline and retest) with t-tests (Mann-Whitney U and Wilcoxon tests, respectively) and mixed ANCOVAs with repeated measures for comparison of both interventions were conducted. RESULTS: A total of 65 pwpMS turned to a final sample of 50 (n = 15 excluded due to drop-outs, occurrence of relapse or steroid treatment). Change scores within MaTiMS revealed no significant effect on the PDQ-20 total score and only a significant effect on the subscale retrospective memory lasting 3 months with a moderate effect size. In contrast, MaTiMS-modified revealed a highly significant change in PDQ-20 total compared to baseline and significant improvements with small to moderate effect sizes on all PDQ-20 subscales (lasting until 3 months), in self-efficacy, stress, visuo-spatial working memory (moderate effect sizes), and fatigue (small effect size). While no interaction effect between time and group could be revealed, a significant main effect for time was found in PDQ-20 total. CONCLUSION: Both MaTiMS and MaTiMS-modified positively affected perceived cognitive deficits. However, our data speak in favor of additional benefits by adding neuroeducational and mindfulness-based exercises thus being valuable methods to support brain health including self-efficacy, perceived stress, and fatigue, even in patients with a chronic and progressive brain disease.
 Multiple sclerosis is a disease that tends to affect women during their childbearing years. Although relapse risk decreases during pregnancy, patients should still be optimized on disease-modifying therapy before and after pregnancy to minimize gaps in treatment. Exclusive breastfeeding may reduce the chances of disease relapse postpartum, and many disease-modifying therapies are considered to be safe while breastfeeding. Treatments for other neuroimmunologic disorders such as neuromyelitis optica spectrum disorder, myelin oligodendrocyte glycoprotein antibody-associated disease, neurosarcoidosis, and central nervous system vasculitis may require rituximab before and prednisone or intravenous immunoglobulin therapy during pregnancy.
 BACKGROUND: Hyperreflective granular elements with a transient presence in the retina can be detected non-invasively by optical coherence tomography (OCT). Such foci or dots may represent aggregates of activated microglia. However, in multiple sclerosis an increased number of hyperreflective foci has so far not been demonstrated in the intrinsically hyporeflective and avascular outer nuclear layer of the retina where there are no fixed elements in healthy eyes. Therefore, the present study intended to investigate the presence of hyperreflective foci in the outer nuclear layer in patients with relapsing- remitting multiple sclerosis (RRMS) by using a high-resolution OCT scanning protocol. METHODS: This cross-sectional exploratory study examined 88 eyes in 44 RRMS patients and 106 eyes in 53 age- and sex-matched healthy subjects. None of the patients had any sign of retinal disease. All patients and healthy subjects each underwent one session of spectral domain OCT imaging. A total of 23,200 B-scans extracted from 8 × 8 mm blocks of linear B-scans at 60 μm intervals were analysed for hyperreflective foci in the outer nuclear layer of the retina. Analyses were made of the total block scan and a circular 6-mm diameter fovea-centered field in each eye. Multivariate logistic regression analysis was used to assess associations between parameters. RESULTS: Hyperreflective foci were observed in 31 out of 44 (70.5 %) multiple sclerosis patients compared to 1 out of 53 (1.8%) healthy subjects (p < 0.0001). From analyses of the total block scans, the median number of hyperreflective foci in the outer nuclear layer was 1 (range 0-13) in patients and 0 (range 0-2) in healthy subjects (p < 0.0001). In total, 66.2% of all hyperreflective foci were located within 6 mm of the center of the macula. There was no detectable association between the presence of hyperreflective foci and retinal nerve fiber layer or ganglion cell layer thickness. CONCLUSION: Hyperreflective granular foci in the avascular outer nuclear layer of the retina seen by OCT were almost completely absent in healthy subjects, whereas they were found, albeit at low density, in the majority of patients with RRMS. Hyperreflective foci can be repeatedly examined by non-invasive means and without pupil dilation, which opens a new field of investigation of infiltrating elements in an unmyelinated part of the central nervous system.
 BACKGROUND: Multiple sclerosis (MS) has two pathophysiological processes, one inflammatory and the other degenerative. We investigated the relationship between active lesions on magnetic resonance imaging showing the inflammatory phase in MS patients and serum parameters that can be used as inflammatory biomarkers. Thus, we aim to detect the inflammatory period in clinical and radiological follow-up and to reveal the period in which disease-modifying treatments are effective with serum parameters. METHODS: One hundred eighty-six MS patients presented to our hospital between January 2016 and November 2021 and 94 age- and sex-matched healthy volunteers were recruited for our study. While 99 patients had active lesions on magnetic resonance imaging, 87 patients did not have any active lesions. Neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and monocyte/lymphocyte ratio (MLR) were determined. The SII (systemic immune inflammatory index) value was calculated according to the platelet X neutrophil/lymphocyte ratio formula. RESULTS: NLR, MLR, PLR and SII values were found to be statistically significantly higher in MS patients than in the control group. The NLR, MLR, PLR and SII were higher in the active group with gadolonium than in the group without active lesions. In addition, the cutoff values that we can use to determine the presence of active lesions were 1.53, 0.18, 117.15, and 434.45 for NLR, MLR PLR and SII, respectively. CONCLUSIONS: We found that all parameters correlated with radiological activity. In addition, we showed that we can detect the inflammatory period with high sensitivity and specificity with the cutoff value used for SII and PLR. Among these easily accessible and inexpensive evaluations, we concluded that SII, including the values in the PLR formula, can come to the fore.

 Our research studied relapsing-remitting multiple sclerosis (RRMS). In half of the RRMS cases, mild cognitive difficulties are present, but often remain undetected despite their adverse effects on individuals' daily life. Detecting subtle cognitive alterations using speech analysis have rarely been implemented in MS research. We applied automatic speech recognition technology to devise a speech task with potential diagnostic value. Therefore, we used two narrative tasks adjusted for the neural and cognitive characteristics of RRMS; namely narrative recall and personal narrative. In addition to speech analysis, we examined the information processing speed, working memory, verbal fluency, and naming skills. Twenty-one participants with RRMS and 21 gender-, age-, and education-matched healthy controls took part in the study. All the participants with RRMS achieved a normal performance on Addenbrooke's Cognitive Examination. The following parameters of speech were measured: articulation and speech rate, the proportion, duration, frequency, and average length of silent and filled pauses. We found significant differences in the temporal parameters between groups and speech tasks. ROC analysis produced high classification accuracy for the narrative recall task (0.877 and 0.866), but low accuracy for the personal narrative task (0.617 and 0.592). The information processing speed affected the speech of the RRMS group but not that of the control group. The higher cognitive load of the narrative recall task may be the cause of significant changes in the speech of the RRMS group relative to the controls. Results suggest that narrative recall task may be effective for detecting subtle cognitive changes in RRMS.
 BACKGROUND AND OBJECTIVE: Multiple sclerosis (MS) is a lifelong demyelinating disorder with a varying disease course, resulting in different degrees of physical disability for affected patients. This study aimed to present the initial clinicoradiological features of Omani MS patients presenting to a tertiary care center in Oman. METHODS: In this retrospective study, all Omani patients diagnosed with MS from January 2006 to December 2020, whose treatment and followup were conducted in our center, were included. Data was retrieved from the patients' medical records. Disability status was assessed according to the Expanded Disability Status Scale. RESULTS: A total of N = 155 Omani patients were diagnosed with MS of whom 68.4% were female. The mean age at diagnosis was 28.6 ± 8 years. The mean duration from symptoms to diagnosis was 1.9 years. Relapsing-remitting MS was diagnosed in 97.4% patients. Most common presenting symptoms were unifocal (84.5%), supratentorial (34.2%) and optic pathway (33.5%). At first assessment, 94.8% patients had no to mild disabilities and 3.2% had severe disabilities. During the mean follow up period of 61.2 months, the frequency of severe disabilities increased to 12.9%. Out of 155 patients, 98 (63.2%) had their initial brain magnetic resonance (MRI) report available for review, 62/98 (63%) of whom showed ≥ 20 T2-weighted (T2W) lesions. Of these lesions, 75/98 (76.5%) were periventricular, 66 (67.3%) juxtacortical, and 56 (57.1%) infratentorial. The most common initially prescribed disease modifying therapies (DMT) were interferons (104/155; 67%), followed by fingolimod (16; 10.3%), natalizumab (14; 9%) and dimethyl fumarate (4; 2.6%). CONCLUSIONS: The results of this study indicate that the demographic and clinicoradiological features of MS patients in Oman are similar to those reported elsewhere in the Arabian Gulf region.
 BACKGROUND AND PURPOSE: The differences in cognitive function between primary progressive and secondary progressive multiple sclerosis (MS) remain unclear. We compared cognitive performance between primary progressive multiple sclerosis (PPMS) and secondary progressive multiple sclerosis (SPMS), and explored the structural and functional magnetic resonance imaging (MRI) correlates of their cognitive functions. METHODS: Seventy-five healthy controls and 183 MS patients (60 PPMS and 123 SPMS) underwent 3.0-T MRI. MS patients were administered the Brief Repeatable Battery of Neuropsychological Tests; cognitive domain z-scores were calculated and then averaged to obtain a measure of global cognition. Using hierarchical linear regression analysis, the contribution of lesion volumes, normalized brain volumes, white matter (WM) fractional anisotropy (FA) and mean diffusivity abnormalities, and resting state (RS) functional connectivity (FC) alterations to global cognition in PPMS and SPMS was investigated. RESULTS: PPMS and SPMS had similar z-scores in all investigated cognitive domains. Poor global cognitive function was associated with decreased FA of the medial lemniscus (ΔR (2)  = 0.11, p = 0.011) and lower normalized gray matter volume (ΔR (2)  = 0.29, p < 0.001) in PPMS, and with decreased FA of the fornix (ΔR (2)  = 0.35, p < 0.001) and lower normalized WM volume (ΔR (2)  = 0.05; p = 0.034) in SPMS. CONCLUSIONS: PPMS and SPMS had similar neuropsychological performance. Cognitive dysfunction in PPMS and SPMS was related to distinct patterns of structural MRI abnormalities and involvement of different WM tracts, whereas RS FC alterations did not contribute to explaining their global cognitive functioning.
 BACKGROUND: Cognitive impairment (CI) is common in Multiple Sclerosis (MS), and its prevalence rate ranges between 22% and 70%. Because CI significantly impacts vocational status, caregiver burden, and quality of life, an accurate neuropsychological assessment is required. Three widely used and validated batteries for MS-associated CI are the Brief Repeatable Neuropsychological Battery (BRN-B), the Minimal Assessment of Cognitive Function (MACFIMS), and the Brief International Cognitive Assessment (BICAMS). Although similar, these batteries differ in time-consuming and in specific tests employed. This study aims to assess the sensitivity of cognitive tests included in these batteries through an Item Response Theory approach. METHODS: Ninety-seven patients with MS and 91 demographically matched controls (HC) were consecutively assessed using the three neuropsychological batteries (i.e., BRN-B, MACFIMS, and BICAMS). Continuous Response Model (CRM) was used to identify the cognitive test(s) that best discriminate patients with MS from HC. Receiver Operating Characteristic (ROC) curve analysis was used to determine the accuracy of the CRM results. RESULTS: Cognitive tests loaded on two different latent variables: the 'higher-order executive functioning,' consisting of tests assessing concept formation, problem-solving, and inhibitory control, and the 'memory and information processing speed,' comprising tests assessing long-term, working memory, and information processing speed. The Delis Kaplan Executive Functioning System-Sorting Test and the Stroop Test were the most sensitive tests in differentiating cognitive functioning between MS and HC. CONCLUSIONS: This study confirms the importance of including a more extensive executive assessment in MS clinical practice since higher-order executive functions (e.g., abstraction and inhibitory control) significantly impact patients' quality of life and functional autonomy. Clinical implications of careful dissection of executive functioning in MS neuropsychological assessment are discussed.
 BACKGROUND: There is a significant increase in the parenchymal microvessel blood volume in the earliest forms of multiple sclerosis (MS) which may be due to venular dilatation. Increased cortical venous pressure could account for this finding. Venous pressure is also implicated in the physiology of fatigue. The purpose of this study is to discover if there is dilatation of the veins within the subarachnoid space in multiple sclerosis and to estimate the pressures required to maintain any enlargement found. These findings will be correlated with the fatigue symptoms found in MS. METHODS: 103 patients with MS were compared with a control group of 50 patients. Post contrast 3DT1 images were used. The cross-sectional area of the bridging cortical veins and the vein of Galen were measured. RESULTS: In MS, the superficial territory cortical veins were 29% larger and the veins of Galen were 25% larger than the controls. CONCLUSION: There is evidence of a significant increase in the bridging vein transmural pressure in MS, estimated to be approximately 6.5 mmHg in the superficial cortical veins. MS patients with significant fatigue have larger cortical veins than those who are not significantly fatigued.
 INTRODUCTION: Little is known about the molecular profiling associated with the effect of cladribine in patients with multiple sclerosis (MS). Here, we aimed first to characterize the transcriptomic and proteomic profiles induced by cladribine in blood cells, and second to identify potential treatment response biomarkers to cladribine in patients with MS. METHODS: Gene, protein and microRNA (miRNA) expression profiles were determined by microarrays (genes, miRNAs) and mass spectrometry (proteins) in peripheral blood mononuclear cells (PBMCs) from MS patients after in vitro treatment with cladribine in its active and inactive forms. Two bioinformatics approaches to integrate the three obtained datasets were applied: (i) a multiomics discriminant analysis (DIABLO - Data Integration Analysis for Biomarker discovery using Latent variable approaches for Omics studies); and (ii) a multi-stage integration of features selected in differential expression analysis on each dataset and then merged. Selected molecules from the in vitro study were quantified by qPCR ex vivo in PBMCs from MS patients receiving cladribine. RESULTS: PBMCs treated in vitro with cladribine were characterized by a major downregulation of gene, protein, and miRNA expression compared with the untreated cells. An intermediate pattern between the cladribine-treated and untreated conditions was observed in PBMCs treated with cladribine in its inactive form. The differential expression analysis of each dataset led to the identification of four genes and their encoded proteins, and twenty-two miRNAs regulating their expression, that were associated with cladribine treatment. Two of these genes (PPIF and NHLRC2), and three miRNAs (miR-21-5p, miR-30b-5p, and miR-30e-5p) were validated ex vivo in MS patients treated with cladribine. DISCUSSION: By using a combination of omics data and bioinformatics approaches we were able to identify a multiomics molecular profile induced by cladribine in vitro in PBMCs. We also identified a number of biomarkers that were validated ex vivo in PBMCs from patients with MS treated with cladribine that have the potential to become treatment response biomarkers to this drug.
 Purpose: Although the cognitive sequelae of multiple sclerosis have been recognized for more than four decades, the focus of research has been on studying the more common deficits of the disease, including those involving memory and information processing speed. Less understood and investigated are the visual-spatial perceptual disturbances of multiple sclerosis, which can be difficult to assess and interpret given the potential confounds associated with the physical problems and other cognitive disturbances of the disorder.Materials and methods: This study examined the visual-spatial perceptual deficits of multiple sclerosis in 40 participants diagnosed with this condition using two measures generally unaffected by the aforementioned confounds, the Hooper Visual Organization Test and Visual Form Discrimination.Results: Results revealed both measures to be sensitive to the impairments of multiple sclerosis but suggested that they are assessing somewhat different aspects of visual-spatial perception in this population, given their relationship with one another and with disease-related variables.Conclusions: In this light, findings indicate that a complete and accurate understanding of the visual-spatial perceptual sequelae of multiple sclerosis requires the administration of more than a single measure.
 Multiple Sclerosis is a neurodegenerative disease which shows different phenotypes making difficult for clinicians to make short-term decisions related with treatment and prognosis. Diagnosis is usually retrospective. Learning Healthcare Systems (LHS) can support clinical practice as they are devised as constantly improving modules. LHS can identify insights which allow evidence-based clinical decisions and more accurate prognosis. We are developing a LHS with the aim of reducing uncertainty. We are using ReDCAP to collect patients' data, both from Clinical Reported Outcomes (CRO) and from Patients Reported Outcomes (PRO). Once analyzed, this data will serve as a foundation to our LHS. We conducted bibliographical research to select those CRO and PRO collected in clinical practice or identified as possible risk factors. We designed a data collection and management protocol based on using ReDCAP. We are following a cohort of 300 patients for 18 months. At the moment, we have included 93 patients and received 64 complete responses and 1 partial response. This data will be used to develop a LHS, able to accurate prognosis as well as to automatically include new data and improve its algorithm.
 This paper presents a study that examined desired functionality, content, and design of a mobile application for young Czech adults living with Multiple Sclerosis (MS). The study was structured around a high-fidelity prototype developed for the corresponding user group in Norway. Both groups were active on social media and willing to contribute to designing an application promoting a healthy lifestyle and well-being. Adopting the content analysis, the study first compared the social content shared within the Facebook communities in the Norwegian and Czech user groups that were active. Regardless of the similarities, the Czech group expected that solutions regarding main functionalities and content should stand out from other competitive applications offered on the market. Most of all, they would like to see healthcare staff being engaged in content creation by providing credible information, especially regarding new treatments and clinical trials. Enhanced interaction between all the stakeholders (patients, and healthcare providers) would add value and relevance to the content already provided by social media.
 BACKGROUND: Autologous mesenchymal stem cell neurotrophic factor-secreting cells (NurOwn(®)) have the potential to modify underlying disease mechanisms in progressive multiple sclerosis (PMS). OBJECTIVE: This open-label phase II study was conducted to evaluate safety/efficacy of three intrathecal cell treatments. METHODS: Eighteen participants with non-relapsing PMS were treated. The primary endpoint was safety. Secondary endpoints included: cerebrospinal fluid (CSF) biomarkers; timed 25-foot walk speed, nine-hole peg test (9-HPT), low-contrast letter acuity, symbol digit modalities test, and 12-item multiple sclerosis (MS) walking scale. Seventeen participants received all treatments. RESULTS: No deaths/adverse events related to worsening of MS, clinical/magnetic resonance imaging (MRI) evidence of disease activation, and clinically significant changes in safety lab results were reported. Two participants developed symptoms of low back and leg pain, consistent with a diagnosis of arachnoiditis, occurring in one of three intrathecal treatments in both participants. Nineteen percent of treated participants achieved pre-specified ⩾ 25% improvements in timed 25-foot walk speed/nine-HPT at 28 weeks compared to baseline, along with consistent efficacy signals for pre-specified response criteria across other secondary efficacy outcomes. CSF neuroprotective factors increased, and inflammatory biomarkers decreased after treatment, consistent with the proposed mechanism of action. CONCLUSION: Based on these encouraging preliminary findings, further confirmation in a randomized study is warranted.
 This study designed to investigate the protective effects of L-theanine on experimental Multiple sclerosis in mice. Frothy Male C57BL/6 mice were allocated into 4 experimental groups: control no treatment received a regular chew pellet, and the cuprizone (CPZ) group received a standard chew pellet containing 0.2% (w/w) CPZ. In group 3, mice were fed a regular diet and administered p.o. with L-theanine (50mg/kg). In group 4, mice received a diet containing CPZ and were administered p.o. with L-theanine (50mg/kg). Finally, reflexive motor behavior and serum antioxidant levels were determined. Based on findings, CPZ significantly decreased ambulation score, hind-limb suspension, front limb suspension, and grip strength (P<0.05). The CPZ + L-theanine reduced the adverse effect of the CPZ on ambulation score, hind-limb foot angle, surface righting, and negative geotaxis (P<0.05). The CPZ + L-theanine increased front and hind-limb suspension, grip strength, number of the cross, and duration of a stay on the rotarod compared to the control animal (P<0.05). CPZ administration significantly elevated serum malondialdehyde (MDA) while superoxide dismutase (SOD) and glutathione peroxidase (GPx) and total antioxidant status (TAS) levels decreased compared to control mice (P<0.05). The CPZ + L-theanine leads to the cessation of MDA production while increasing SOD, GPx, and TAS levels (P<0.05). These results suggested L-theanine has a protective effect against CPZ-induced MS in mice.
 OBJECTIVE: To compare the incidence of multiple sclerosis (MS) among women who had undergone assisted reproductive technology (ART) treatment with the women who had conceived a child without previous ART treatment. DESIGN: A register-based nationwide cohort study. PATIENT(S): Women with a first ovarian stimulation cycle before in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) (i.e., ART treatment) recorded in the Danish IVF register between 1996 and 2018; and women recorded in the Danish Medical Birth Register with the birth of their first child where date of conception is between 1996 and 2018. The cohort was observed until March 10, 2021. INTERVENTION(S): Mainly included IVF, ICSI, and fresh embryo transfer with hormone stimulation. MAIN OUTCOME MEASURES: A diagnosis of MS recorded in the Danish Multiple Sclerosis Registry. Crude and adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs) were calculated. RESULTS: A total of 585,716 women were included in the cohort of which 63,791 (11%) were exposed to at least one initiated IVF or ICSI cycle during the study period. Cycles with oocyte donation were excluded. The median follow-up time for the entire cohort was 12.4 years (Q1-Q3= 6.6-18.1). Compared with women conceiving without previous ART, ART treated women were older (31.8 years vs. 27.5 years), more often had a university degree (45% vs. 36%), and more often had received other fertility treatments than IVF or ICSI before cohort entry (26% vs. 3%). We found no association between incident MS and exposure to ART compared with non-ART pregnancy (aHR=1.08; 95 % CI, 0.93-1.25). An analysis following intention-to-treat principle on a propensity score matched sub cohort confirmed our results. In subgroup analysis including all ART cycles among the ART treated women, we found no increased risk of MS within 2 years of ART cycle start for successful ART cycles (pregnancy) compared with failed ART cycles (no pregnancy) (aHR=1.01; 95% CI, 0.58-1.76). We found a non-significant trend toward increased risk of MS with increasing numbers of ART cycles although based on small numbers. CONCLUSION(S): Women treated with ART do not seem to be at increased risk of developing MS compared with the women not exposed to ART.
 BACKGROUND: Cognitive impairment occurs in 40%-70% of persons with multiple sclerosis (MS). OBJECTIVE: To examine the effectiveness of natalizumab compared with other disease-modifying treatments (DMTs) on improving cognition as measured by the Symbol Digit Modalities Test (SDMT). METHODS: Data were collected as part of Swedish nationwide phase IV surveillance studies (2007-2020). An increase in SDMT score by ⩾10% of the difference between maximum score possible (110) and the baseline value was defined as cognitive improvement. The likelihood of improvement was compared between natalizumab-treated individuals and individuals treated with other DMTs using mixed effect logistic regression. Trend in odds of improvement was investigated using slope analyses. RESULTS: We included 2100 persons with relapsing-remitting MS treated with natalizumab and 2622 persons treated with other DMTs. At 6 months, 45% reached improvement. The natalizumab group showed largest odds of improvement during follow-up (odds ratio: 2.3, 95% confidence interval (CI): 1.5-3.5). The odds of improvement increased by 7% (95% CI: 6-7) per month of natalizumab treatment. The equivalent estimate was 4% (95% CI: 2-5) for other monoclonal antibodies and nonsignificant for oral or platform therapies. CONCLUSION: Treatment with natalizumab or other monoclonal antibodies is associated with a significantly faster likelihood of cognitive improvement than platform or oral DMTs.
 INTRODUCTION: Cognitive impairment is a core symptom of multiple sclerosis, leading to disability in 40-70% of patients. The most common cognitive domains affected by MS are information processing speed, complex attention, executive functions and less frequently, episodic declarative memory. Cardiovascular disease comorbidities have been shown to increase the decline rate in many neurological conditions. Our study aims to examine the possible impact of CVD risk factors in the cognitive decline rate of PwMS. METHODS: Over the course of a year, 248 PwMS with and without Cardiovascular comorbidity were cognitively evaluated using the written version of SDMT and the MoCA. RESULTS: Compared to control, MS patients with comorbid CVD had greater general cognitive decline and decreased processing speed. Patients with comorbid diabetes and dyslipidemia had the highest impairment, followed by those with hypertension, compared to the control group and those patients with a high BMI. CONCLUSION: The presence of cardiovascular comorbidities and especially dyslipidemia increases the rate of cognitive decline in MS patients. In such cases, patients should be evaluated every 6 months instead of a year and the use of the SDMT is advised since it's time efficient,it requires minimal training and correlates with MRI findings.
 INTRODUCTION: Multiple sclerosis (MS) is a chronic, demyelinating disease of the central nervous system. Its clinical courses are clinically isolated syndrome (CIS), relapsing remitting (RRMS), secondary progressive (SPMS), and primary progressive (PPMS). The differentiation of MS types is crucial for adequate treatment. OBJECTIVES: To evaluate antioxidant parameters of MS patients' serum according to MS type. MATERIALS AND METHODS: The study included 84 patients diagnosed with MS. The study group was divided into three subgroups corresponding to MS courses RRMS, SPMS, and PPMS. Sulfhydryl groups (SH), ceruloplasmin (CER), and superoxide dismutase (SOD) and its isoforms were identified in study participants' sera. RESULTS: CuZnSOD levels were significantly higher in SPMS patients than in PPMS patients, but there was no difference between SMPS and treatment-naive PPMS patients. MnSOD activity was significantly lower in SPMS patients than in PPMS patients. Our results show that SH levels were decreased in SPMS patients compared with RRMS patients, but this difference was significant only for male participants. SH concentration was reversely correlated with age, BMI, disease duration, EDSS, and in smoking patients with pack-years. CER serum levels waere elevated in SPMS patients compared with RRMS patients, but this difference was significant only for male participants. Our results show correlation between CER and EDSS levels. CONCLUSION: Oxidative stress plays a limited role in all disease stages, particularly in smokers as a confounding factor.
 BACKGROUND: Cholesterol and lipids are essential components of nerve cells. Myelin synthesis and stabilization is a cholesterol-dependent process. It has been shown in several studies that high plasma cholesterol levels may be associated with clinical deterioration in Multiple Sclerosis (MS). There is scarce information about the effects of disease-modifying treatment (DMTs) on lipid profile. In this study, we aimed to investigate the effect of DMTs on plasma lipid profiles in MS patients. METHOD: The records of 380 MS patients who were still under follow-up were analyzed in terms of age, sex, disease duration, EDSS scores, serum lipid levels, and used DMTs. The data of patients receiving Interferon (n = 53), Glatiramer acetate (n = 25), Fingolimod (n = 44), Teriflunomide (n = 24), Dimethyl fumarate (n = 7) and Ocrelizumab (n = 14) were compared with the data of control group (n = 53). RESULTS: A total of 220 patients, 157 women, and 63 men, were included in the study. The average age of the participants in the study was 39.83 ± 10.21 years, mean disease duration was 8.45 ± 6.56 years, and the EDSS score was 2.25 ± 1.97. Although, Lipid parameters were higher in MS patients using Fingolimod the difference cannot reach the statistical significance. CONCLUSION: No significant relationship was found between the DMTs that MS patients had been using for the last six months and their cholesterol levels.
 BACKGROUND: Virchow-Robin spaces (VRS) have been associated with neurodegeneration and neuroinflammation. However, it remains uncertain to what degree non-dilated or dilated VRS reflect specific features of neuroinflammatory pathology. Thus, we aimed at investigating the clinical relevance of VRS as imaging biomarker in multiple sclerosis (MS) and to correlate VRS to their histopathologic signature. METHODS: In a cohort study comprising 142 MS patients and 30 control subjects, we assessed the association of non-dilated and dilated VRS to clinical and magnetic resonance imaging (MRI) outcomes. Findings were corroborated in a validation cohort comprising 63 MS patients. Brain blocks from 6 MS patients and 3 non-MS controls were histopathologically processed to correlate VRS to their tissue substrate. FINDINGS: In our actively treated clinical cohort, the count of dilated centrum semiovale VRS was associated with increased T1 and T2 lesion volumes. There was no systematic spatial colocalization of dilated VRS with MS lesions. At tissue level, VRS mostly corresponded to arteries and were not associated with MS pathological hallmarks. Interestingly, in our ex vivo cohort comprising mostly progressive MS patients, dilated VRS in MS were associated with signs of small vessel disease. INTERPRETATION: Contrary to prior beliefs, these observations suggest that VRS in MS do not associate with an accumulation of immune cells. But instead, these findings indicate vascular pathology as a driver and/or consequence of neuroinflammatory pathology for this imaging feature. FUNDING: NIH, Swedish Society for Medical Research, Swiss National Science Foundation and University of Zurich.
 Patients with multiple sclerosis (MS) present a spectrum of nutritional disorders from obesity to malnutrition. The purpose of this study was an assessment of the nutritional status of MS patients by NRS-2002 and GLIM criteria. METHODS: 147 patients were included in the study. The nutritional status was assessed by NRS 2002, GLIM, and body composition analysis. The routine biochemical parameters were measured. RESULTS: Deterioration of the nutritional status was observed in 87.8% of patients. GLIM criteria indicated that 20% of patients were malnourished and 80% were at risk. The percentage of patients with excess body mass was 46.8%, and of underweight patients was 6.6%. The risk of malnutrition was positively associated with low content of adipose tissue (R=-0.24; p=0.00), low BMI (R=-0.22; p=0.00), and higher weight loss in the last 6 months (R=0.47; p=0.00). Additionally, a significant (p<0.05) correlation between malnutrition state and s-albumin (R=-0.2) and CRP (R=0.23) was observed. CONCLUSION: Overweight and obesity concerned a large proportion of the studied group of MS patients, but this does not exclude the risk of malnutrition. Dietary care and regular outpatient nutritional status assessment should be provided throughout the disease.
 BACKGROUND: Cognitive impairment occurs in up to 70% of people with MS (pwMS) and has a large impact on quality of life and working capacity. As part of the development of a smartphone-app (dreaMS) for monitoring MS disease activity and progression, we assessed the feasibility and acceptance of using cognitive games as assessment tools for cognitive domains. METHODS: We integrated ten cognitive games in the dreaMS app. Participants were asked to play these games twice a week for 5 weeks. All subjects underwent a battery of established neuropsychological tests. User feedback on acceptance was obtained via a five-point Likert-scale questionnaire. We correlated game performance measures with predetermined reference tests (Spearman's rho) and analyzed differences between pwMS and Healthy Controls (rank biserial correlation). RESULTS: We included 31 pwMS (mean age 43.4 ± 12.0 years; 68% females; median Expanded Disability Status Scale score 3.0, range 1.0-6.0) and 31 age- and sex-matched HC. All but one game showed moderate-strong correlations with their reference tests, (|r(s)|= 0.34-0.77). Performance improved in both groups over the 5 weeks. Average ratings for overall impression and meaningfulness were 4.6 (range 4.2-4.9) and 4.7 (range 4.5-4.8), respectively. CONCLUSION: Moderate-strong correlations with reference tests suggest that adaptive cognitive games may be used as measures of cognitive domains. The practice effects observed suggest that game-derived measures may capture change over time. All games were perceived as enjoyable and meaningful, features crucial for long-term adherence. Our results encourage further validation of adaptive cognitive games as monitoring tools for cognition in larger studies of longer duration. STUDY REGISTER: ClinicalTrials.gov: NCT04413032.
 BACKGROUND: Real-word evidence from diverse data sources is increasingly important in terms of generating rapid insights to effectively manage patient populations, especially during major public health disruptions such as the ongoing COVID-19 pandemic. Patients with chronic and inflammatory diseases - such as multiple sclerosis (MS) - were reported to experience potentially negative effects due to the use of immunosuppressive drugs in combination with a COVID-19 infection. In this research, we explored the impact of the COVID-19 pandemic on medication use in patients with MS in Germany. METHODS: Patient-level pharmacy dispensing data from the Permea platform - covering approximately 44% of all community pharmacy dispensing in Germany - were analysed from 2019 - 2021. Longitudinal use patterns of MS medication and antidepressants and patient demographics were assessed. Daily variation in MS medication use was specifically studied around the dates of the first and second lockdowns in Germany. RESULTS: We included data from 539,400 prescriptions which included at least 1 MS drug. The medication data showed a stable level of monthly prescriptions for MS medication at 2.02 ± 0.03 prescriptions per pharmacy during the study period. Although there was a sharp increase in daily prescriptions before the first lockdown (from an average 660.08 ± 137.59 daily prescriptions in the observed period to a maximum dispensing number of 998 daily prescriptions), the overall number of prescriptions remained at pre-pandemic levels (603 ± 90.31 daily prescriptions in 2019). Similar trends were observed for monthly co-prescribed antidepressant use per pharmacy (0.10 ± 0.01 in 2019-0.11 ± 0.02 in 2020). CONCLUSION: Throughout the COVID-19 pandemic, the use of MS medications and co-prescribed antidepressants was stable. These insights from real-world data demonstrate the value of evidence-based insights for managing patient care.
 We investigate structural properties of neurons in the granular layer of human cerebellum with respect to their involvement in multiple sclerosis (MS). To this end we analyze data recorded by X-ray phase contrast tomography from tissue samples collected post mortem from a MS and a healthy control group. Using automated segmentation and histogram analysis based on optimal transport theory (OT) we find that the distributions representing nuclear structure in the granular layer move to a more compact nuclear state, i.e. smaller, denser and more heterogeneous nuclei in MS. We have previously made a similar observation for neurons of the dentate gyrus in Alzheimer's disease, suggesting that more compact structure of neuronal nuclei which we attributed to increased levels of heterochromatin, may possibly represent a more general phenomenon of cellular senescence associated with neurodegeneration.
 Crocin is the main bioactive components of the saffron which has positive role in the nervous system; however, its neuroprotective activity is not fully elicited. So, the aim of the current study was to determine effects of the crocin on reflexive motor and anti-depressive behaviors as well as serum and brain tissue antioxidant activities in cuprizone-induced (CPZ) model of multiple sclerosis (MS) mice. Forty male C57BL/6 mice were randomly assigned into 4 groups. Mice in the control group were received normal diet. In group 2, mice received normal diet and orally received crocin (100 mg/kg) 3 times per week for 5 weeks. In group 3, CPZ-induced demyelination was done by chew palate containing 0.2% (w/w) CPZ for 5 weeks. In group 4, mice feed CPZ containing diet and orally received crocin (100 mg/kg) three times per for 5 weeks. After determination of the MS signs, reflexive motor behavior and depressive tests were done. Also, serum and brain tissue antioxidant activity was determined. According to the data, CPZ had negative effects on hind-limb foot angle, hind- and front-limb suspension, surface righting, grip strength, and negative geotaxis while crocin improved it. Co-administration of the CPZ + crocin reversed effect of the CPZ on the reflexive motor behaviors. CPZ increased immobility time in the forced swimming test (FST) and tail suspension test (TST), while co-administration of the CPZ + crocin reversed effect of the CPZ on immobility time. CPZ decreased number of cross in open field test (OFT) and spending time on rotarod, while co-administration of the CPZ + crocin reversed effect of the CPZ. Malondialdehyde (MDA) production increased, and glutathione peroxidase (GPx), superoxide dismutase (SOD), and total antioxidant status (TAS) levels decreased in serum and brain tissue of the mice treated with CPZ. Pretreatment with crocin decreased adverse effect of the CPZ on serum and brain tissue antioxidants. These results suggested crocin has protective effect against CPZ-induced MS in mice.
 BACKGROUND: Understanding when multiple sclerosis (MS) lesions become clinically symptomatic may provide insight into disease pathophysiology. Our objective was to temporally associate lesion formation and trigeminal neuralgia (TN) symptom onset in MS. METHODS: This is a retrospective case series of patients with MS, analysing time difference between TN symptom onset and oldest MRI showing a correlative lesion. RESULTS: For the 26 patients with MS, a correlative lesion was noted on MRI on average 5±4 years prior to TN symptom onset; 57% had primary or secondary progressive MS. CONCLUSIONS: TN lesions can be present years prior to symptom onset, suggestive of alternative explanations than typical relapses. This phenomenon may hint at alternative pathophysiology of progressive MS in comparison to relapsing-remitting MS.
 BACKGROUND: Whilst there is research on psychotherapy and professional psychological support (PPS) in people with Multiple Sclerosis (pwMS) in discrete randomised controlled trials, little is known about the different types of PPS pwMS access throughout the trajectory of their illness and their perceived helpfulness. Additionally, research on what pwMS's preferences are with regard to PPS is lacking. METHOD: In an online cross-sectional survey study with 565 pwMS, we asked about the types of PPS pwMS had accessed and their preferences. RESULTS: Although 88% of the sample wanted PPS, only 53% of the sample had managed to access PPS. 40% of the entire sample currently wanted PPS but did not access it previously. The most common reason for this was because they were happy with the support they received from other sources (51%) and/or they were unaware of what was available to them (33%). 59% of those who had accessed PPS had accessed more than one type. The perceived level of helpfulness from PPS was rated as higher amongst those who had accessed more types of PPS. The most common combination of PPS accessed was a mixture of counselling with either cognitive behavioural therapy and/or mindfulness-based therapies. Counselling was the single-most accessed type of PPS. Most pwMS wanted PPS as a proactive means to either preserve and boost psychological well-being (37%) or learn skills to manage future difficulties as and when they arise (23%), rather than as a reaction to immediate pressing concerns (18%). The majority of pwMS showed a broad range of preferences regarding PPS and selected more than 5 types, with high interest in programmes with a self-management component, counselling and mindfulness-based interventions in particular. CONCLUSIONS: Patient preferences for PPS highlight the need to take a proactive and preventative approach to preserve psychological wellbeing rather than only being provided in response to mental health crises. Psychological support should be made more readily available early on to fulfil this presently unmet need.
 INTRODUCTION: Dimethyl fumarate treatment is approved in Europe for patients with relapsing-remitting multiple sclerosis (MS) and in the US for relapsing forms of MS. We recently published the results of the first randomized placebo-controlled trial of 48 weeks of treatment with dimethyl fumarate or placebo in primary progressive MS (PPMS) (clinicaltrial.gov NCT02959658). The placebo-controlled phase of the trial did not meet its primary endpoint (reduction in cerebrospinal fluid concentrations of neurofilament light chain [NFL]). AIM: To investigate the effects of dimethyl fumarate treatment in the open-label extension phase of the trial (week 48-96), where all patients were treated with DMF. METHODS: Reported data are from screening, week 48, and week 96 visits. Patients were clinically evaluated with Expanded Disability Status Scale (EDSS), 9-Hole Peg Test (9HPT), Timed 25-Foot Walk (T25FW) test, Symbol Digit Modalities Test (SDMT), California Verbal Learning Test, and Brief Visuospatial Memory-Revised. Serum NFL concentrations were measured by single-molecule array analysis. MRI was performed on a 3 tesla MRI scanner and included: new/enlarging lesions, volume of lesions, cortical grey matter, putamen, thalamus, and normal-appearing white matter, and additional diffusion tensor imaging and magnetization transfer ratio measures. RESULTS: Forty-two patients entered the open-label treatment phase, and 33 patients (61%) had complete data sets at week 96. The remaining 39% did not complete the trial and were not evaluated at week 96. We found no evidence of differences in clinical and MRI measures between patients initially treated with dimethyl fumarate and patients initially treated with placebo from baseline to week 48 and from week 48-96, where all patients were treated with dimethyl fumarate. Serum NFL concentrations remained stable in both groups over 96 weeks. Assessed with either EDSS, T25FW, or 9HPT at week 96, progression was observed for 14 patients (45%). Interestingly, another 15 patients (46%) had improvement in one or more of these domains. Applying a cut-off of 8 points, 2 (6%) patients worsened on SDMT, 25 (78%) did not change, and 5 (16%) improved. CONCLUSIONS: Dimethyl fumarate treatment showed no effects on neither clinical nor MRI outcomes or changes in serum concentrations of NFL. An expected number of patients showed evidence of progression on standard clinical scales; however, this was matched by an equal number of patients improving. The reasons for the physical improvement in an unexpectedly high proportion of patients must be addressed in future studies.
 BACKGROUND: Fatigue is a common complaint in patients with multiple sclerosis (PwMS) and reduces quality of life. Several hypotheses for the pathogenesis of fatigue in MS are proposed ranging from neurological lesions to malnutrition, but none has been conclusively validated through clinical research. OBJECTIVES: The goal of this study was to examine the correlation between fatigue and nutritional status and dietary habits in PwMS. METHODS: This was a cross-sectional, multicenter study conducted at 10 French MS centers and enrolling PwMS with an Expanded Disability Status Scale (EDSS) score between 0 and 7. Plasma level of albumin, magnesium, calcium, iron, vitamin D and B12 evaluated nutritional status. A semi-structured eating behavior questionnaire has been developed to evaluate dietary habits. Evaluation of fatigue used specific questionnaire (EMIF-SEP). Quality of sleep was evaluated by visual analogue scale (VAS), depression with Beck Depression Inventory (BDI-II); dysphagia by DYsphagia in MUltiple Sclerosis questionnaire (DYMUS) and taste disorders by gustometry. Association between nutritional deficiencies and different data such as socio-demographic data, disease characteristics, swallowing and taste disorders, food intake, depression and sleep quality was investigated. RESULTS: A total of 352 patients mean age: 48.1±10.1 years, mean duration of MS: 15.3±9.1 years and median EDSS: 4 were analyzed. Bivariate and multivariate analyses showed a statistically significant correlation between fatigue and depression and use of sleeping pills, while none of the variables related to dietary habits or nutritional status correlated significantly with fatigue. CONCLUSIONS: Dietary habits and nutritional status have little impact on fatigue and general population nutrition recommendations remain the rule for PwMS. In cases of fatigue, specific attention should be paid to depression and use of sleeping pills.
 Understanding the associations and potential drivers of long-term disability in Multiple Sclerosis (MS) is of clinical and prognostic value. Previous data have suggested a link between depression and disability accrual in MS. We aimed to determine whether depression in early MS predicts subsequent accrual of disability. Using data from the UK MS Register, we identified individuals with and without symptoms of depression and anxiety close to disease onset. We used Cox proportional hazards regression to evaluate whether early depressive or anxiety symptoms predict subsequent physical disability worsening, measured using the Expanded Disability Status Scale (EDSS). We analysed data from 862 people with MS of whom 134 (15.5%) reached an EDSS of ≥ 6.0. Early depressive symptoms were associated with an increased risk of reaching an EDSS of 6.0 (HR 2.42, 95% CI 1.49-3.95, p < 0.001), however this effect dissipated when adjusting for baseline EDSS (HR 1.40, 95% CI 0.84-2.32, p = 0.2). These data suggest that early depressive symptoms in MS are associated with subsequent disability accrual, but are likely the result of disability rather than its cause.
 BACKGROUND: Pregnancy planning is a relevant issue in the management of Multiple Sclerosis (MS), which commonly involves women of childbearing age. Increased knowledge and a wider therapeutic scenario could have changed the approach of neurologists towards this topic over time. Our aim was to describe how pregnancy planning and management for women with MS have changed in the last 15 years. METHODS: We retrospectively collected clinical data of female patients with relapsing-remitting MS (RRMS), referred to the Neurology Clinic of the University-Hospital "Policlinico G. Rodolico" of Catania, who became pregnant between 2005-2020. We compared data about MS and pregnancy between two time periods according to pregnancy onset (2005-2012; 2013-2020). RESULTS: 190 patients with RRMS carried 253 pregnancies in the observation period. Women undergoing a pregnancy in the last period (2013-2020), as compared to women who had pregnancy in the first period (2005-2012), were older (p<0.01), more often treated before and during pregnancy with high-efficacy disease-modifying drugs (DMD) (p<0.001), and exhibited lower annualized relapse rates (ARR) before (p=0.01) and after pregnancy (p<0.001). CONCLUSION: Results from our experience suggest that nowadays DMD are more frequently used in women of childbearing age, even during pregnancy, leading to a reduced ARR before and after delivery in absence of increased obstetric complications.
 BACKGROUND: Multiple sclerosis (MS) is the most common disabling neurological disease in young adults worldwide with majority of patients manifest symptoms between 20 and 40 years of age. The aims of this study are to explore physicians' perspectives, views, and behaviors in diagnosing and treating patients with MS in Saudi Arabia and investigate the prescribing pattern of disease-modifying therapies (DMTs). METHODS: A sequential explanatory mixed-method approach was used to achieve the study objectives. The quantitative arm of the study consisted of patient data extracted from the Saudi MS registry from 2015 to 2018. The qualitative study consisted of in-depth semi-structured interviews with physicians using a validated interview topic guide comprising 28 open-ended questions. RESULTS: We extracted data of 2,507 patients from 20 different hospitals across Saudi Arabia. Patients' mean age was 34 ± 10 years; two-thirds (n = 1,668) were female. 92% (n = 2,292) had relapsing-remitting multiple sclerosis, and 5% (n = 126) had secondary-progressive multiple sclerosis. In general, patients with MS received at least one drug as the DMT or DMTs and corticosteroids for those with relapse. Qualitatively, nine physicians agreed to participate in the interviews. Of them, five (55%) were male and four were female from different regions. Thematic analysis yielded three main themes: practice, views, and challenges. CONCLUSIONS: The prevalence of MS in Saudi Arabia is raising but is still much lower than that reported in the Gulf region. A national MS guideline is needed to streamline diagnosis and treatment criteria, avoid any delay in treatment, and guide physicians who provide care for patients with MS.
 BACKGROUND AND PURPOSE: Cortical demyelinated lesions are prevalent in multiple sclerosis (MS), associated with disability, and have recently been incorporated into MS diagnostic criteria. Presently, advanced and ultrahigh-field MRIs-not routinely available in clinical practice-are the most sensitive methods for detection of cortical lesions. Approaches utilizing MRI sequences obtainable in routine clinical practice remain an unmet need. We plan to assess the sensitivity of the ratio of T(1) -weighted and T(2) -weighted (T(1) /T(2) ) signal intensity for focal cortical lesions in comparison to other high-field imaging methods. METHODS: 3-Tesla and 7-Tesla MRI collected from 10 adults with MS were included in the study. T(1) /T(2) images were calculated by dividing 3T T(1) -weighted (T(1) w) images by 3T T(2) -weighted (T(2) w) fluid-attenuated inversion recovery images for each participant. A total of 614 cortical lesions were identified using 7T T(2) *w and T(1) w images and corresponding voxels were assessed on registered 3T images. Signal intensities were compared across 3T imaging sequences, including T(1) /T(2) , T(1) w, T(2) w, and inversion recovery susceptibility-weighted imaging with enhanced T(2) weighting (IR-SWIET) images. RESULTS: T(1) /T(2) images demonstrated a larger contrast between median lesional and nonlesional cortical signal intensity (median ratio = 1.29, range: 1.19-1.38) when compared to T(1) w (1.01, 0.97-1.10, p < .002), T(2) w (1.17, 1.07-1.26, p < .002), and IR-SWIET (1.21, 1.01-1.29, p < .03). CONCLUSION: T(1) /T(2) images are sensitive to cortical lesions. Approaches incorporating T(1) /T(2) could improve the accessibility of cortical lesion detection in research settings and clinical practice.
 BACKGROUND: Bowel symptoms are commonly experienced by patients with Multiple sclerosis (PwMS), but no specific questionnaire validated in this population allows a rigorous assessment. OBJECTIVE: Validation of a multidimensional questionnaire assessing bowel disorders in PwMS. METHODS: A prospective, multicenter study was conducted between April 2020 and April 2021. The STAR-Q (Symptoms' assessmenT of AnoRectal dysfunction Questionnaire), was built in 3 steps. First, literature review and qualitative interviews were performed to create the first version, discussed with a panel of experts. Then, a pilot study assessed comprehension, acceptation and pertinence of items. Finally, the validation study was designed to measure content validity, internal consistency reliability (alpha coefficient of Cronbach) and test-retest reliability [intraclass correlation coefficient (ICC)]. The primary outcome was good psychometric properties with Cronbach's α>0.7 and ICC>0.7. RESULTS: We included 231 PwMS. Comprehension, acceptation and pertinence were good. STAR-Q showed a very good internal consistency reliability (Cronbach's α=0.84) and test-retest reliability (ICC=0.89). Final version of STAR-Q was composed of 3 domains corresponding in symptoms (Q1-Q14), treatment and constraints (Q15-Q18) and impact on quality of life (Q19). Three categories of severity were determined (STAR-Q≤16: minor, between 17 and 20: moderate, and≥21: severe). CONCLUSIONS: STAR-Q presents very good psychometric properties and allows a multidimensional assessment of bowel disorders in PwMS.
 BACKGROUND: Vascular management in People with Multiple Sclerosis (PwMS) is important given the higher vascular burden than the general population, associated with increased disability and mortality. OBJECTIVES: We assessed differences in the prevalence of type 2 diabetes and hypertension; and the use of antidiabetic, antihypertensive and lipid-lowering medications at the time of the MS diagnosis. METHODS: This is a population-based study including PwMS and matched controls between 1987 and 2018 in England. RESULTS: We identified 12,251 PwMS and 72,572 matched controls. PwMS had a 30% increased prevalence of type 2 diabetes (95% confidence interval (CI) = 1.19, 1.42). Among those with type 2 diabetes, PwMS had a 56% lower prevalence of antidiabetic usage (95% CI = 0.33, 0.58). Prevalence of hypertension was 6% greater in PwMS (95% CI = 1.05, 1.06), but in those with hypertension, usage of antihypertensive was 66% lower in PwMS (95% CI = 0.28, 0.42) than controls. Treatment with lipid-lowering medications was 63% lower in PwMS (95% CI = 0.54, 0.74). PwMS had a 0.4-mm Hg lower systolic blood pressure (95% CI = -0.60, -0.13). 3.8% of PwMS were frail. CONCLUSION: At the time of diagnosis, PwMS have an increased prevalence of vascular risk factors, including hypertension and diabetes though paradoxically, there is poorer treatment. Clinical guidelines supporting appropriate vascular assessment and management in PwMS should be developed.
 Current research and drug development for multiple sclerosis (MS) is fully influenced by the self-nonself (SNS) model of immunity, suggesting that breakage of immunological tolerance towards self-antigens expressed in the central nervous system (CNS) is responsible for pathogenesis of MS; thus, immune suppressive drugs are recommended for the management of the disease. However, this model provides incomplete understanding of the causes and pathways involved in the onset and progression of MS and limits our ability to effectively treat this neurological disease. Some pre-clinical and clinical reports have been misunderstood; some others have been underappreciated because of the lack of a theoretical model that can explain them. Also, current immunotherapies are guided according to the models that are not designed to explain the functional outcomes of an immune response. The adaptation model of immunity is proposed to offer a new understanding of the existing data and galvanize a new direction for the treatment of MS. According to this model, the immune system continuously communicates with the CNS through the adaptation receptors (AdRs) and adaptation ligands (AdLs) or co-receptors, signal IV, to support cell growth and neuroplasticity. Alterations in the expression of the neuronal AdRs results in MS by shifting the cerebral inflammatory immune responses from remyelination to demyelination. Therefore, novel therapeutics for MS should be focused on the discovery and targeting of the AdR/AdL axis in the CNS rather than carrying on with immune suppressive interventions.
 Multiple sclerosis (MS) is a chronic neurological disease that may cause several different symptoms, some which may entail the need for help in daily life. The aim of this study was to explore the association between sociodemographic background factors and the use of personal assistance and home help services (home help) among persons with MS in Sweden. The study was based on cross-sectional survey data merged with register data and included 3,863 persons with MS aged 20-51. Binary logistic regression analyses were performed to identify factors associated with the use of personal assistance and home help. The central finding of this study was that grade of impairment, as determined by the Expanded Disability Status Scale for Multiple Sclerosis (EDSS), was the most important variable associated with the use of both personal assistance (p < 0.001, OR 18.83) and home help (p < 0.001, OR 6.83). Living alone and receiving sickness benefit were also both associated with the use of personal assistance (p < 0.001, OR 3.32; p 0.001, OR 3.32) and home help (p 0.004, OR 2.56; p 0.011, OR 2.56). Stating a visible symptom of MS as being the most limiting factor of the disease (p 0.001, OR 2.73) and having a disposable income below the limit for poverty risk (p 0.02, OR 2.16) was associated with the use of personal assistance. Receiving informal, meaning unpaid, help (p 0.049, OR 1.89) was associated with the use of home help. Several background factors were controlled for but were not related to differences in the usage of formal help. The results indicated no significant differences in demographic characteristics that could be linked to unequal distribution. However, differences were found between those using personal assistance and home help. The latter were mainly affected by invisible symptoms, suggesting a plausible influencing factor in the chances of obtaining more comprehensive help in the form of personal assistance. Users of home help were also more likely to receive informal help than users of personal assistance, which may suggest that home help is not sufficient.

 INTRODUCTION: Multiple Sclerosis (MS) has a complex pathophysiology that involves genetic and environmental factors. DNA methylation (DNAm) is one epigenetic mechanism that can reversibly modulate gene expression. Cell specific DNAm changes have been associated with MS, and some MS therapies such as dimethyl fumarate can influence DNAm. Interferon Beta (IFNβ), was one of the first disease modifying therapies in multiple sclerosis (MS). However, how IFNβ reduces disease burden in MS is not fully understood and little is known about the precise effect of IFNβ treatment on methylation. METHODS: The objective of this study was to determine the changes in DNAm associated with INFβ use, using methylation arrays and statistical deconvolutions on two separate datasets (total n(treated) = 64, n(untreated) = 285). RESULTS: We show that IFNβ treatment in people with MS modifies the methylation profile of interferon response genes in a strong, targeted, and reproducible manner. Using these identified methylation differences, we constructed a methylation treatment score (MTS) that is an accurate discriminator between untreated and treated patients (Area under the curve = 0.83). This MTS is time-sensitive and in consistent with previously identified IFNβ treatment therapeutic lag. This suggests that methylation changes are required for treatment efficacy. Overrepresentation analysis found that IFNβ treatment recruits the endogenous anti-viral molecular machinery. Finally, statistical deconvolution revealed that dendritic cells and regulatory CD4+ T cells were most affected by IFNβ induced methylation changes. DISCUSSION: In conclusion, our study shows that IFNβ treatment is a potent and targeted epigenetic modifier in multiple sclerosis.
 Decision-making for reimbursement and clinical guidelines (CGs) serves different purposes although the decision-criteria and required evidence largely overlap. This study aimed to assess similarities and discrepancies between health technology assessment (HTA) reports as compared to CGs for multiple sclerosis (MS) medicines. All HTA reports and corresponding CGs for MS from the UK, France, Germany, the Netherlands, Poland, Sweden, and the European Union were assessed to identify synergies in recommendations for MS medicines (approved 1995-2020). A content analysis of HTA reports and CGs was performed to identify similarities and discrepancies in wording of treatment recommendations across documents. We assessed 132 HTA reports and 9 CGs for 16 MS treatments. Final recommendations for reimbursement and inclusion in CGs were mostly similar (90%), albeit with considerable differences in treatment lines and subindications. Since 2010, HTA reports refer to the use of CGs in 42% (55/132) and to consultations with clinicians in 43% (57/132) of cases. Six of nine CGs referred to HTA reports and two referred to HTA consultations, in one case having a formal relation to the HTA organization. CGs referenced pharmacoeconomic studies (4/9) for costs and cost-effectiveness. To date, not all new HTA recommendations for MS treatments are included in CGs. Some synergy exists between treatment recommendations in HTA reports and CGs, although discrepancies were seen in timelines and in recommended treatment lines and subindications. More stakeholder dialogue and/or consultation of each other's publications may further improve synergy, facilitate transparency, and enhance patient access.
 Aim: Describe demographics, clinical characteristics, healthcare resource utilization (HCRU) and costs in people with multiple sclerosis (pwMS) switching to alemtuzumab from other disease-modifying therapies (DMTs). Patients & methods: Retrospective, observational study of IBM(®)MarketScan(®) claims database. PwMS previously treated with DMTs and initiating alemtuzumab (1 January 2013 to 31 December 2019) were identified. "Index" was date of alemtuzumab initiation (prescription filled). Results: The study cohort (n = 341) was primarily female (72%) with (mean ± standard deviation) age 45.1 ± 9.5 years. At index, duration of MS was 5.3 ± 2.8 years. HCRU (inpatient/outpatient services), outpatient costs (including MS-specific MRI and emergency room visits) and annualized relapse rate significantly reduced over the 2 years following initiation of alemtuzumab. DMT costs reduced over the same period. Conclusion: Health economic and clinical benefits were seen following switching to alemtuzumab from other DMTs for treatment of MS, in this cohort from the USA.

 BACKGROUND: Multiple sclerosis (MS), which is frequently seen in young adults, affects mental health because of disease symptoms and cognitive disorders. This study was conducted to evaluate the presence of alexithymia and problem- or emotion-focused coping strategies with stress in MS patients, determine the relationship between these variables, and compare the results of MS patients with those of healthy individuals. METHODS: This descriptive, cross-sectional, and comparative study was carried out with the participation of 120 MS patients presenting to a neurology clinic and outpatient clinic of a university hospital and 120 healthy individuals. Data were collected using a personal information form, the Toronto Alexithymia Scale, and the Ways of Coping Scale. RESULTS: The 40.8% rate of alexithymia in the MS patients was higher than that in the healthy individuals (21.7%). Compared with healthy individuals, MS patients use emotion-focused coping methods, such as a lack of self-confidence approach and a submissive approach, more frequently ( P < .05). A significant negative correlation was found between the alexithymia and problem-focused coping strategies of MS patients ( P < .01). CONCLUSION: Alexithymia is more common in MS patients than in healthy individuals. Alexithymia negatively affects the methods patients use to cope with stress. In the treatment and care of MS patients, nurses should plan interventions for the ability of these patients to recognize and express their emotions and develop positive coping methods.
 BACKGROUND AND PURPOSE: The aim was to study brain innate immune cell activation in teriflunomide-treated patients with relapsing-remitting multiple sclerosis. METHODS: Imaging with 18-kDa translocator protein positron emission tomography (TSPO-PET) using the [(11) C]PK11195 radioligand was employed to assess microglial activity in the white matter, thalamus and areas surrounding chronic white matter lesions in 12 patients with relapsing-remitting multiple sclerosis who had been treated with teriflunomide for at least 6 months before inclusion. Magnetic resonance imaging (MRI) was used to measure lesion load and brain volume, and quantitative susceptibility mapping (QSM) was used to detect iron rim lesions. These evaluations were repeated after 1 year of inclusion. Twelve age- and gender-matched healthy control subjects were imaged for comparison. RESULTS: Half of the patients had iron rim lesions. In TSPO-PET, the proportion of active voxels indicating innate immune cell activation was slightly greater amongst patients compared with healthy individuals (7.7% vs. 5.4%, p = 0.033). The mean distribution volume ratio of [(11) C]PK11195 was not significantly different in the normal-appearing white matter or thalamus amongst patients versus controls. Amongst the treated patients, no significant alteration was observed in positron emission tomography distribution volume ratio, the proportion of active voxels, the number of iron-rim-positive lesions, lesion load or brain volume during follow-up. CONCLUSIONS: Compared to controls, treated patients exhibited modest signs of diffuse innate immune cell activity, which was unaltered during follow-up. Lesion-associated smoldering inflammation was negligible at both timepoints. To our knowledge, this is the first study applying both TSPO-PET and QSM-MRI to longitudinally evaluate smoldering inflammation.
 BACKGROUND: In multiple sclerosis (MS), determination of regional brain atrophy is clinically relevant. However, analysis of large datasets is rare because of the increased variability in multicenter data. PURPOSE: To compare different methods to correct for center effects. To investigate regional gray matter (GM) volume in relapsing-remitting MS in a large multicenter dataset. METHODS: MRI scans of 466 MS patients and 279 healthy controls (HC) were retrieved from the Italian Neuroimaging Network Initiative repository. Voxel-based morphometry was performed. The center effect was accounted for with different methods: (a) no correction, (b) factor in the statistical model, (c) ComBat method and (d) subsampling procedure to match single-center distributions. By applying the best correction method, GM atrophy was assessed in MS patients vs HC and according to clinical disability, disease duration and T(2) lesion volume. Results were assessed voxel-wise using general linear model. RESULTS: The average residuals for the harmonization methods were 5.03 (a), 4.42 (b), 4.26 (c) and 2.98 (d). The comparison between MS patients and HC identified thalami and other deep GM nuclei, the cerebellum and several cortical regions. At single-center analysis, the thalami were always involved, whereas different other regions were found in each center. Cerebellar atrophy correlated with clinical disability, while deep GM nuclei atrophy correlated with T(2)-lesion volume. CONCLUSION: Harmonization based on subsampling more effectively decreased the residuals of the statistical model applied. In comparison with findings from single-center analysis, the multicenter results were more robust, highlighting the importance of data repositories from multiple centers.
 BACKGROUND AND OBJECTIVES: Immune responses in the central nervous system (CNS) are highly compartmentalized and cerebrospinal fluid (CSF) in particular often reflects CNS pathology better than peripheral blood. While CSF leukocytes are known to be distinct from blood, the immediate effects of peripheral leukocyte depletion on CSF leukocytes have not been studied in humans. METHODS: We here analyzed CSF and blood from two relapsing-remitting multiple sclerosis (RRMS) patients early after peripheral leukocyte depletion with the anti-CD52 antibody alemtuzumab compared to untreated RRMS and control patients using single cell RNA-sequencing. RESULTS: As expected for alemtuzumab, most leukocyte lineages including T cells were synchronously depleted from CSF and blood, while - surprisingly - pDCs were maintained in CSF but depleted from blood by alemtuzumab. Transcriptionally, genes associated with migration were elevated only in the CSF after alemtuzumab. Predicted cellular interactions indicated a central role of pDCs and enhanced migration signaling in the CSF after alemtuzumab. DISCUSSION: The CSF and blood compartments are thus partially uncoupled, emphasizing that the CNS is only partially accessible even for treatments profoundly affecting the blood.
 INTRODUCTION: Magnetic resonance imaging (MRI) is widely used for the diagnosis and follow-up of patients with multiple sclerosis (MS). Coordination between neurology and neuroradiology departments is crucial for performing and interpreting radiological studies as efficiently and as accurately as possible. However, improvements can be made in the communication between these departments in many Spanish hospitals. METHODS: A panel of 17 neurologists and neuroradiologists from 8 Spanish hospitals held in-person and online meetings to draft a series of good practice guidelines for the coordinated management of MS. The drafting process included 4 phases: 1) establishing the scope of the guidelines and the methodology of the study; 2) literature review on good practices or recommendations on the use of MRI in MS; 3) discussion and consensus between experts; and 4) validation of the contents. RESULTS: The expert panel agreed a total of 9 recommendations for improving coordination between neurology and neuroradiology departments. The recommendations revolve around 4 main pillars: 1) standardising the process for requesting and scheduling MRI studies and reports; 2) designing common protocols for MRI studies; 3) establishing multidisciplinary committees and coordination meetings; and 4) creating formal communication channels between both departments. CONCLUSIONS: These consensus recommendations are intended to optimise coordination between neurologists and neuroradiologists, with the ultimate goal of improving the diagnosis and follow-up of patients with MS.
 Aim: To assess bridging glatiramer acetate (GA) or IFN-β for relapse prevention in women with relapsing multiple sclerosis planning pregnancy. Materials & methods: Participants discontinued disease-modifying therapies (DMTs) and received GA/IFN (early- or delayed-start) or no DMT (control) until pregnancy. Results: Annualized relapse rate was lower in delayed-start GA/IFN cohort versus control during washout/bridging. During washout/bridging, bridging with GA/IFN in this cohort reduced clinical activity, while disease activity increased in controls versus baseline. Conclusion: More data on GA/IFN bridging are needed. Women with low relapsing multiple sclerosis activity in the year prior to DMT discontinuation due to pregnancy planning benefited from GA/IFN bridging with lower annualized relapse rate versus no treatment and reduced clinical activity versus baseline during washout/bridging and pregnancy.
 OBJECTIVE: This study aimed to evaluate safety (infusion-related reactions [IRRs]) and patient satisfaction (patient-reported outcomes [PROs]) for at-home ocrelizumab administration for patients with multiple sclerosis (MS). METHODS: This open-label study included adult patients with an MS diagnosis who had completed a ≥ 600-mg ocrelizumab dose, had a patient-determined disease steps score of 0 to 6 and had completed PROs. Eligible patients received a 600-mg ocrelizumab home-based infusion over 2 h, followed by 24-h and 2-week post-infusion follow-up calls. IRRs and adverse events (AEs) were documented during infusions and follow-up calls. PROs were completed before and 2 weeks post infusion. RESULTS: Overall, 99 of 100 expected patients were included (mean [SD] age, 42.3 [7.7] years; 72.7% female; 91.9% White). The mean (SD) infusion time was 2.5 (0.6) hours, and 75.8% of patients completed their ocrelizumab infusion between 2 to 2.5 h. The IRR incidence rate was 25.3% (95% CI: 16.7%, 33.8%)-similar to other shorter ocrelizumab infusion studies-and all AEs were mild/moderate. In total, 66.7% of patients experienced AEs, including itch, fatigue, and grogginess. Patients reported significantly increased satisfaction with the at-home infusion process and confidence in the care provided. Patients also reported a significant preference for at-home infusion compared with prior infusion center experiences. INTERPRETATION: IRRs and AEs occurred at acceptable rates during in-home infusions of ocrelizumab over a shorter infusion time. Patients reported increased confidence and comfort with the home infusion process. Findings from this study provide evidence of the safety and feasibility of home-based ocrelizumab infusion over a shorter infusion period.
 BACKGROUND: Chitinase -3-like 1-protein (CHI3L1) is a glycoside secreted by monocytes, microglia, and activated astrocytes. Its distribution in inflammatory lesions denotes its role in astrocytic response to modulate CNS inflammation. In multiple sclerosis (MS), CHI3L1 levels have been found to be influenced by disease severity, activity, and progression. We aimed to measure CSF level of CHI3L1 in patients with MS and correlate its level with disability measures for a possible role as a biomarker for disease progression. METHODS: Fifty-two MS patients (30 relapsing-remitting MS and 22 progressive MS) and thirty-five age and sex-matched healthy controls were included. They all underwent full clinical assessment (including disability and cognitive scales), radiological assessment, and CSF level of CHI3L1. RESULTS: Patients with MS had higher CSF level of CHI3L1 than controls. Patients with progressive forms had higher levels than relapsing forms. There were positive correlations between disease duration, number of attacks, total EDSS, and CSF level of CHI3L1. Patients who had higher level of CSF CHI3L1 showed worse performance in MMSE and BICAMS and more lesions in T2 MRI brain. A cut off value of 154 ng/mL was found between patients with RRMS and PMS patients. CONCLUSION: CHI3L1 can be considered as a biomarker of disease progression. CHI3L1 level increases in progressive MS more than RRMS. Also, high CSF level of CHI3L1 was associated with more disability including motor, cognitive, and radiological aspects.
 OBJECTIVE: Cognitive impairment is common in multiple sclerosis (MS), significantly impacts daily functioning, is time-consuming to assess, and is prone to practice effects. We examined whether the alpha band power measured with magnetoencephalography (MEG) is associated with the different cognitive domains affected by MS. METHODS: Sixty-eight MS patients and 47 healthy controls underwent MEG, T1- and FLAIR-weighted magnetic resonance imaging (MRI), and neuropsychological testing. Alpha power in the occipital cortex was quantified in the alpha1 (8-10 Hz) and alpha2 (10-12 Hz) bands. Next, we performed best subset regression to assess the added value of neurophysiological measures to commonly available MRI measures. RESULTS: Alpha2 power significantly correlated with information processing speed (p < 0.001) and was always retained in all multilinear models, whereas thalamic volume was retained in 80% of all models. Alpha1 power was correlated with visual memory (p < 0.001) but only retained in 38% of all models. CONCLUSIONS: Alpha2 (10-12 Hz) power in rest is associated with IPS, independent of standard MRI parameters. This study stresses that a multimodal assessment, including structural and functional biomarkers, is likely required to characterize cognitive impairment in MS. Resting-state neurophysiology is thus a promising tool to understand and follow up changes in IPS.
 BACKGROUND: Multiple sclerosis (MS) is an immune-mediated demyelinating disorder of the central nervous system. The glycosphingolipid sulfatide, a lipid particularly enriched in the myelin sheath, has been shown to be involved the maintenance of this specific membrane structure. Sulfatide in cerebrospinal fluid (CSF) may reflect demyelination, a dominating feature of MS. We investigated the diagnostic utility of CSF sulfatide isoform levels to separate different courses or phenotypes of MS disease. MATERIAL AND METHODS: This was a mono-center, cross-sectional study of relapsing-remitting MS (RRMS) (n = 45) and progressive MS (PMS) (n = 42) patients (consisting of primary PMS (n = 17) and secondary PMS (n = 25)) and healthy controls (n = 19). In total, 20 sulfatide isoforms were measured in CSF by liquid chromatography-mass spectrometry. RESULTS: CSF total sulfatide concentrations, as well as CSF sulfatide isoform distribution, did not differ across the study groups, and their levels were independent of disease course/phenotype, disease duration, time to conversion to secondary PMS, age, and disability in MS patients. CONCLUSION: CSF sulfatide isoforms lack diagnostic and prognostic utility as a biomarker for progressive MS.
 OBJECTIVE: Disease-modifying therapies (DMTs) in multiple sclerosis (MS) may affect the course and outcome of COVID-19, but withholding them could permit disease activity. This study aimed to understand the course of COVID-19 in unvaccinated patients with MS on disease-modifying therapies. SUBJECTS AND METHODS: This descriptive study examined the course of COVID-19 among infected patients with MS followed up at a large tertiary center in Kuwait between March 1, 2020, and March 1, 2021. All subjects were outpatients at the time of data collection. RESULTS: We studied 51 patients with MS confirmed to be infected with SARS-CoV-2 using real-time polymerase chain reaction. Of these patients, 33/51 were female, median age was 35 years (IQR 27-39 years), median Expanded Disability Status Scale score was 1.5 (IQR zero-3), and 47/51 had RRMS. B-cell-depleting agents (ocrelizumab and rituximab) were given to 19 patients, another 19 were on immune cell traffickers (fingolimod and natalizumab), and 13 were on other DMT treatments (alemtuzumab, cladribine, interferon-beta, dimethyl fumarate, and teriflunomide). 43/51 of these patients experienced mild COVID-19, not requiring hospitalization. None of the subjects experienced MS relapses during infection. Two patients on rituximab had a moderate course of the illness, which required hospitalization for oxygen support, but did not need mechanical ventilation; the rest of the subjects remained asymptomatic. CONCLUSIONS: These findings suggest that DMT may not adversely affect the course of COVID-19 in MS patients; however, patients on B-cell-depleting agents trended toward a worse outcome.
 Introduction. Multiple sclerosis (MS) is a neurodegenerative disease that, despite mainly affecting women, is more severe in men and causes motor, cognitive and emotional alterations. The objective of this study was to determine the possible relationship between motor, cognitive and emotional alterations. Materials and Methods. This is a descriptive, observational and cross-sectional study, with 67 patients with MS (20 men and 47 women), who were given the following questionnaires: Expanded Disability Status Scale (EDSS), Two-Minute Walk Test (2MWT), Berg Balance Scale, Beck’s Depression Inventory (BDI-II), State-Trait Anxiety Inventory (STAI) and Prefrontal Symptoms Inventory (PSI) to analyze their cognitive level, body mass index (BMI) and percentage of muscle mass. In addition, regression analysis was conducted to study the relationship among variables. Results. No significant differences were found between men and women in any of the variables. Regarding the relationship between parameters, the regression analysis was statistically significant, showing an effect of age on the walking and balance performance (β ≅ −0.4, p < 0.05); in addition, there was a relationship between 2MWT and STAI A/S, indicating that both older age and a high anxiety state could impact walking performance. On the other hand, prefrontal symptoms showed moderate relationships with both anxiety and depression (β ≅ 0.6, p < 0.05); thus, high levels of anxiety and depression could increase prefrontal alterations. Conclusions. There is a relationship between motor and emotional variables. Specifically, state anxiety is related to walking resistance. No relationship was found between depression and cognitive alteration and balance or walking ability. Only age has an effect in these relationships.
 Multiple sclerosis (MS) is a debilitating disease that causes inflammation of the central nervous system, resulting in myelin damage and axon degeneration. Although the cause of MS remains unknown, various factors such as sex, latitude, sun exposure, serum vitamin D levels, Epstein Barr Virus infection, diet, microbiota and ethnicity are being studied for their potential roles in the development of the disease. While chronobiological factors such as circadian rhythm and seasonality have been explored for their potential influence on the onset, exacerbation, and/or relapses of MS, the potential influence of the lunar cycle on MS has yet to be studied. Therefore, the authors of this letter call for future studies to investigate the possible effects of the lunar cycle on MS activity and course, given evidence suggesting that the lunar cycle may affect sleep, fatigue, melatonin secretion, and mood state in humans. A deeper understanding of the chronobiology of MS could have practical implications for the development of chronotherapeutic strategies and the prevention or mitigation of MS relapses, potentially improving the quality of life of MS patients.
 BACKGROUND: The Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) is the most widely used screening tool for cognitive impairment in Multiple Sclerosis (MS). However, the administration and scoring procedures of the paper version are time consuming and prone to errors. Aim of our study was to develop a tablet version of BICAMS (iBICAMS), and to assess its reliability compared to the paper version. METHODS: We administered both BICAMS and iBICAMS to 139 MS patients in two different sessions. We compared scores on both versions using a paired t-test. We used a repeated measures ANOVA to test the impact of rater, order of administration and test-retest time on test-retest performances. We used the Intraclass Correlation Coefficient (ICC) to assess the reliability between BICAMS and iBICAMS. RESULTS: All three sub-tests of the BICAMS (SDMT, CVLT-II and BVMT-R) were different between the paper and the tablet versions. Order of administration influenced test-retest performances at the SDMT (p<0.001), CVLT- II (p<0.001) and BVMT-R (p<0.001). Intraclass coefficient correlation (ICC) revealed a high level of agreement between the paper BICAMS and the iPad version for all three tests: SDMT (0.92), CVLT-II (0.83) and BVMT-R (0.82). CONCLUSIONS: We found a high reliability between BICAMS and iBICAMS. Considering the inherent advantages of automated scoring, digital storage of data, standardized timing, the iBICAMS could become a standard in clinical practice.
 A 23-year-old man, under treatment for relapsing remitting multiple sclerosis, presented with sudden drop in vision in the left eye for the past 1 week. We noted optic atrophy with sclerosed vessels in multiple quadrants in both eyes, moderate vitreous haze, and active retinal vasculitis in left eye. The patient received therapeutic pars plana vitrectomy in the left eye, and the vitreous sample was analyzed for immunophenotypes by flow cytometry (T-cells) and immunohistochemistry (B-cells). 65.1% of total vitreous cells were CD3(+) T-cells. These included 42.4% CD4(+), and 20.6% CD8(+) T-cells. Immunohistochemistry detected CD20(+) B-cells (not quantifiable). Our analysis demonstrated a mixed B- and T-lymphocyte vitreous infiltrate in multiple sclerosis-associated uveitis.
 OBJECTIVES: The study aimed to investigate inner retinal changes in multiple sclerosis (MS) patients by comparing them with healthy controls. The study also aimed to assess regional differences of inner retinal layer involvement in eyes with and without optic neuritis (ON). MATERIALS AND METHODS: This retrospective, cross-sectional study consisted of 141 eyes of 74 relapsing-remitting MS patients and 80 eyes of 40 healthy controls. The study group was separated into two subgroups according to the presence of ON history. Peripapillary retinal nerve fiber layer (pRNFL) thickness, total macular thickness, and thicknesses of the macular retinal nerve fiber layer (mRNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), and inner nuclear layer were compared between the MS and healthy control groups and between eyes with and without ON history. RESULTS: Mean pRNFL, total macular, mRNFL, GCL, and IPL thicknesses were significantly thinner in the MS group than in the control group (p<0.001) and in eyes with ON compared to those without ON (p<0.05). Comparison of inner retinal layer thicknesses in the inner 3-mm ring subfields of the ETDRS grid revealed significant thinning in all subfields of the GCL and IPL of eyes with ON (p<0.05). The inferior subfield demonstrated the highest difference. CONCLUSION: The study demonstrated that GCL and IPL thinning is a robust and reliable biomarker in all MS patients. The thinning was significantly greater in eyes with ON than in eyes without ON. The study also documented that the inferior region showed significantly greater GCL and IPL thinning in eyes with previous ON attacks.
 BACKGROUND AND PURPOSE: Modifiable lifestyle factors, including diet, have been implicated in multiple sclerosis (MS) progression, but prospective evidence is limited. The aim of this study was to examine prospective relationships between quality of diet and subsequent disability over 7.5 years in an international cohort of people living with MS (pwMS). METHODS: Data from 602 participants in the HOLISM (Health Outcomes and Lifestyle In a Sample of people with Multiple sclerosis) study were analysed. Quality of diet was assessed using the modified Diet Habits Questionnaire (DHQ). Disability was assessed using the Patient-determined MS Severity Score (P-MSSS). Characteristics of disability were assessed by log-binomial, log-multinomial and linear regression, adjusted for demographic and clinical covariates, as appropriate. RESULTS: Higher baseline total DHQ scores (>80-89, >89%) were associated with lower risks of increased P-MSSS at 7.5 years (adjusted risk ratio [aRR] 0.46, 95% confidence interval [CI] 0.23, 0.91 and aRR 0.48, 95% CI 0.26, 0.89, respectively), and with less P-MSSS accrual (aβ = -0.38, 95% CI -0.78, 0.01 and aβ = -0.44, 95% CI -0.81, -0.06). Of the DHQ domains, fat subscore was most strongly associated with subsequent disability. Participants with reducing baseline-to-2.5- years total DHQ scores had greater risk of increased P-MSSS at 7.5 years (aRR 2.77, 95% CI 1.18, 6.53) and higher P-MSSS accrual (aβ = 0.30, 95% CI 0.01, 0.60). Participants reporting baseline meat and dairy consumption had greater risk of increased P-MSSS at 7.5 years (aRR 2.06, 95% CI 1.23, 3.45 and aRR 2.02, 95% CI 1.25, 3.25) and higher P-MSSS accrual (aβ = 0.28, 95% CI 0.02, 0.54 and aβ = 0.43, 95% CI 0.16, 0.69, respectively). However, reported meat consumption was confounded by quality of diet. Changes in meat or dairy consumption from baseline were inconsistently associated with subsequent disability. CONCLUSIONS: We show for the first time robust long-term associations between quality of diet and subsequent disability progression in pwMS. Subject to replication, dietary modification may represent a point of intervention for reducing disability in pwMS.
 BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that particularly affects people in their 30s. Oral disease-modifying therapy (DMT) offers a simple dosage form, good efficacy and safety. Dimethyl fumarate (DMF) is a frequently prescribed oral DMT medication worldwide. The aim of this study was to evaluate the impact of medication adherence on health outcomes in Slovenian persons with MS treated with DMF. METHODS: Our retrospective cohort study included persons with relapsing-remitting MS on DMF treatment. The medication adherence was evaluated by AdhereR software package using the proportion of days covered (PDC) measure. The threshold was set at 90%. Health outcomes after treatment initiation were represented by relapse occurrence, disability progression and occurrence of active (new T2 and T1/Gadolinium (Gd) enhancing) lesions between first two outpatient visits and first two brain magnetic resonance imaging (MRI), respectively. For each health outcome a separate multivariable regression model was built. RESULTS: The study included 164 patients. Their mean age (SD) was 36.7 (8.8) years, and the majority of patients were women (114 or 70%). Eighty-one patients were treatment naive. The mean (SD) PDC value was 0.942 (0.08) and 82% of patients were considered adherent above the 90% threshold. Older age (OR 1.06 per one year, P = 0.017, 95% CI (1.01-1.11)) and treatment naivety (OR 3.93, P = 0.004, 95% CI (1.64-10.4)) were related to higher adherence. In the 6-year follow-up period after DMF treatment initiation, 33 patients experienced a relapse. Among those, 19 required an emergency visit. Sixteen patients had a 1-point disability progression on the Expanded Disability Status Scale (EDSS) score between two consecutive outpatient visits. Thirty-seven patients were found to have active lesions between first and second brain MRI. Medication adherence showed no impact on relapse occurrence or disability progression. Lower medication adherence (10% lower PDC) was associated with higher occurrence of active lesions (OR 1.25, P=0.038, 95% CI: 1.01-1.56). Higher disability prior to DMF initiation was related to a higher risk for relapse occurrence and EDSS progression. CONCLUSION: Our study showed high medication adherence among Slovenian persons with relapse-remitting MS on DMF treatment. Higher adherence was associated with lower incidence of the radiological progression of MS. Interventions for improving medication adherence should be intended for younger patients with higher disability prior treatment with DMF and those switching from alternative DMTs.
 Theranostic imaging methods could greatly enhance our understanding of the distribution of CNS-acting drugs in individual patients. Fluorine-19 magnetic resonance imaging ((19)F MRI) offers the opportunity to localize and quantify fluorinated drugs non-invasively, without modifications and without the application of ionizing or other harmful radiation. Here we investigated siponimod, a sphingosine 1-phosphate (S(1)P) receptor antagonist indicated for secondary progressive multiple sclerosis (SPMS), to determine the feasibility of in vivo (19)F MR imaging of a disease modifying drug. Methods: The (19)F MR properties of siponimod were characterized using spectroscopic techniques. Four MRI methods were investigated to determine which was the most sensitive for (19)F MR imaging of siponimod under biological conditions. We subsequently administered siponimod orally to 6 mice and acquired (19)F MR spectra and images in vivo directly after administration, and in ex vivo tissues. Results: The (19)F transverse relaxation time of siponimod was 381 ms when dissolved in dimethyl sulfoxide, and substantially reduced to 5 ms when combined with serum, and to 20 ms in ex vivo liver tissue. Ultrashort echo time (UTE) imaging was determined to be the most sensitive MRI technique for imaging siponimod in a biological context and was used to map the drug in vivo in the stomach and liver. Ex vivo images in the liver and brain showed an inhomogeneous distribution of siponimod in both organs. In the brain, siponimod accumulated predominantly in the cerebrum but not the cerebellum. No secondary (19)F signals were detected from metabolites. From a translational perspective, we found that acquisitions done on a 3.0 T clinical MR scanner were 2.75 times more sensitive than acquisitions performed on a preclinical 9.4 T MR setup when taking changes in brain size across species into consideration and using equivalent relative spatial resolution. Conclusion: Siponimod can be imaged non-invasively using (19)F UTE MRI in the form administered to MS patients, without modification. This study lays the groundwork for more extensive preclinical and clinical investigations. With the necessary technical development, (19)F MRI has the potential to become a powerful theranostic tool for studying the time-course and distribution of CNS-acting drugs within the brain, especially during pathology.
 BACKGROUND AND PURPOSE: There has been scant research on the consequences of discontinuing second-line disease-modifying treatment (DMT) in middle-aged patients with multiple sclerosis (MS). The objective was therefore to examine the occurrence of focal inflammatory activity after the discontinuation of second versus first-line DMT in patients over 45 years. METHODS: Patients who had been treated for at least 6 months with second (natalizumab, fingolimod, anti CD20) or first-line DMT and who stopped their DMT were retrospectively included. Kaplan-Meier survival curves were used to study the occurrence of relapse and MRI activity according to the type of DMT stopped. Proportional hazard Cox models were calculated to identify factors associated with focal inflammatory activity. The annualized relapse rate was calculated under treatment and for every 3 months after DMT discontinuation. RESULTS: We included 232 patients (median age: 52.8 years), 49 of whom stopped second-line DMT. The probability of having a relapse within the year following discontinuation was 6% for first-line DMT, 9% for fingolimod and 43% for natalizumab. In multivariate analysis, the probability of relapse after DMT discontinuation was significantly increased with natalizumab compared to first-line DMT (HR = 3.24; 95% CI [1.52; 6.90]). A peak of relapse was observed at 0-3 months after stopping natalizumab or fingolimod. CONCLUSION: Our study suggests that the risk of inflammatory activity is greater after discontinuation of natalizumab compared to other DMT even in middle-aged patients. As for younger patients, natalizumab discontinuation should only be considered if there is an adequate substitution of a different therapy. .
 BACKGROUND: MicroRNAs (miRs) are involved in the autoimmune and neurological diseases, including multiple sclerosis (MS), through modulating post-transcriptional gene regulation. Accumulating evidence indicates that miR-10, miR-24a, miR-124, and miR-21 play an imperative role in MS pathogenesis. Therefore, the current research aimed to analyze the expression of the selected miRNAs for MS in Iranian population. METHODS AND RESULTS: Blood sample of 75 relapsing-remitting MS (RRMS) patients and 75 healthy individuals suffering no neurodegenerative illness was collected. Subsequently, the isolation of peripheral blood mononuclear cells (PBMCs) was performed by employing Ficoll-Hypaque density gradient method. Afterward, total RNA was extracted and subjected to qRT-PCR analysis. The obtained results evidenced that the relative expression of miR-10 (P = 0.0002), miR-21 (P = 0.0014), and miR-124 (P = 0.0091) significantly decreased in RRMS patients compared to healthy participants. On the contrary, no notable change was observed between the studies groups regarding miR-24a expression levels (P = 0.107). ROC curve analysis estimated an area under the curve (AUC) value equal to 0.75 with P = 0.0006 for miR-10, while it was decreased for miR-21 (AUC = 0.67 and P = 0.0054) and miR-124 (AUC = 0.66 and P = 0.012). CONCLUSION: The change in miR-10, miR-124, and miR-21 expression patterns was implied to participate in MS development. Further large scale observational studies are recommended.
 BACKGROUND: Fatigue is experienced by more than 65% of individuals with multiple sclerosis (MS). Some studies have supported the effectiveness of acupuncture in improving the symptoms of MS. OBJECTIVE: The present research was intended to investigate the effectiveness of acupuncture plus amantadine compared with amantadine alone on fatigue in patients with relapsing-remitting MS (RRMS) in the remission stage of the disease. METHODS: In this randomized controlled trial, 60 participants with RRMS suffering from fatigue were recruited and randomized equally to acupuncture (n = 30) and control (n = 30) groups. The acupuncture group received treatment 2 to 3 times per week for 10 sessions over 4 weeks. Both the acupuncture and control groups received amantadine 100 mg daily and routine treatment with immuno-modulators. The primary outcome was the fatigue severity scale (FSS) score, which was evaluated at baseline, and after 2 and 4 weeks. The secondary outcome was the Multiple Sclerosis Quality of Life 54 (MSQOL-54) questionnaire score, measured at baseline and the end of the 4-week treatment period. RESULTS: The severity of fatigue was reduced in both groups. However, after 4 weeks of treatment, the reduction of fatigue in the acupuncture group was more significant than in the control group (P < 0.01, mean difference (MD) = -1.14, 95% confidence interval (CI): -1.83 to -0.45). Quality of life, including mental and physical status, was significantly improved in the acupuncture group compared with the control group (P < 0.05, MD = 9.09, 95% CI: 0.46 to 17.73). No adverse events occurred in any of the participants. CONCLUSIONS: Acupuncture combined with amantadine and routine care compared with amantadine and routine care alone appears to be an effective short-term treatment for reducing fatigue and enhancing quality of life, including physical function and mental status, in patients with RRMS.
 INTRODUCTION: Multiple Sclerosis, known main cause of non-traumatic neurological disability in adults, leads to changes in muscle strength, especially in the lower limbs. Assessing muscle strength in these patients is thus essential and can be achieved by the Five Times Sit to Stand Test (FTSST), commonly performed in person. Due to the COVID-19 pandemic and social distancing measured adopted, Brazilian physiotherapists turned to remote monitoring and assessment, supported by Resolution n° 516/2020, which required proving the reliability of tests. Given this scenario, this study sought to evaluate the intra- and inter-rater reliability of the Five Times Sit to Stand Test performed remotely and synchronously by multiple sclerosis patients. METHODS: A sample of 33 individuals with relapsing-remitting Multiple Sclerosis (18 women and 15 men, mean age 43.7 ± 13.4 years) were remotely and synchronously by video call. Inter-rater reliability was evaluated by analyzing FTSST execution time, in seconds, timed by two different raters on the same video call. In turn, intra-rater reliability was assessed by analyzing the execution time recorded in two different video calls made by the same rater, within a 24-28-h interval. Descriptive and inferential data analysis were performed using SPSS 20.0 software. Means and standard deviation were calculated for descriptive statistic. Intraclass correlation coefficient (ICC), with a 0.05 significance level, standard error of measurement (SEM) and minimal detectable change (MDC) were calculated for inferential analysis. RESULTS: Data analysis showed excellent ICC values and low SEM and MDC values regarding inter-rater reliability (ICC: 0.993 (0.986-0.996); p-value: <0.001; SEM: 0.6 s; MDC: 1.6 s) and intra-rater reliability (ICC: 0.962 (0.925-0.981); p-value: <0.001; SEM: 1.4 s; MDC: 3.8 s). CONCLUSION: Based on these values, FTSST performed remotely and synchronously by relapsing-remitting Multiple Sclerosis patients is reliable and can be used both by different raters, for assessment, or by the same rater, in pre- and post-test situations.
 BACKGROUND AND PURPOSE: Cerebral gray matter (GM) atrophy is a proposed measure of neuroprotection in multiple sclerosis (MS). Glatiramer acetate (GA) limits clinical relapses, MRI lesions, and whole brain atrophy in relapsing-remitting MS (RRMS). The effect of GA on GM atrophy remains unclear. We assessed GM atrophy in patients with RRMS starting GA therapy in comparison to a cohort of patients with clinically benign RRMS (BMS). DESIGN/METHODS: We studied 14 patients at GA start [age (mean ± SD) 44.2 ± 7.0 years, disease duration (DD) 7.2 ± 6.4 years, Expanded Disability Status Scale score (EDSS) (median,IQR) 1.0,2.0] and 6 patients with BMS [age 43.0 ± 6.1 years, DD 18.1 ± 8.4 years, EDSS 0.5,1.0]. Brain MRI was obtained at baseline and one year later (both groups) and two years later in all patients in the GA group except one who was lost to follow-up. Semi-automated algorithms assessed cerebral T2 hyperintense lesion volume (T2LV), white matter fraction (WMF), GM fraction (GMF), and brain parenchymal fraction (BPF). The exact Wilcoxon-Mann-Whitney test compared the groups. The Wilcoxon signed rank test assessed longitudinal changes within groups. RESULTS: During the first year, MRI changes did not differ significantly between groups (p > 0.15). Within the BMS group, WMF and BPF decreased during the first year (p = 0.03). Within the GA group, there was no significant change in MRI measures during each annual period (p > 0.05). Over two years, the GA group had a significant increase in T2LV and decrease in WMF (p < 0.05), while GMF and BPF remained stable (p > 0.05). MRI changes in brain volumes (GMF or WMF) in the first year in the GA group were not significantly different from those in the BMS group (p > 0.5). CONCLUSIONS: In this pilot study with a small sample size, patients with RRMS started on GA did not show significant GM or whole brain atrophy over 2 years, resembling MS patients with a clinically benign disease course.
 Background and Objectives: We aimed to determine the link between brain volumetry results and functional disability calculated using the Expanded Disability Status Scale (EDSS) among multiple sclerosis (MS) patients in relation to the provided treatment (disease-modifying therapies (DMTs)) during a 5-year follow-up period. Materials and Methods: A retrospective cohort study was performed enrolling 66 consecutive patients with a confirmed diagnosis of MS, predominantly females (62% (n = 41)). Relapsing-remitting (RR) MS was noted in 92% (n = 61) of patients, with the rest being patients with secondary progressive (SP) MS. The mean age was 43.3 years (SD 8.3 years). All patients were evaluated clinically using the EDSS and "FreeSurfer© 7.2.0" radiologically during a 5-year follow-up. Results: A significant increase in patient functional disability was noted, calculated using the EDSS during a 5-year follow-up. The baseline EDSS ranged between 1 and 6 with a median of 1.5 (IQR 1.5-2.0), and after 5 years, the EDSS was between 1 and 7, with a median EDSS of 3.0 (IQR 2.4-3.6). Compared with RRMS patients, SPMS patients demonstrated a significant increase in EDSS score during a 5-year period, with a median EDSS of 2.5 in RRMS patients (IQR 2.0-3.3) and 7.0 (IQR 5.0-7.0) among SPMS patients. Significantly lower brain volumetry results in different brain areas were found, including cortical, total grey and white matter, p < 0.05. Statistically significant differences were observed between baseline volumetry results of the hippocampus and the middle anterior part of the corpus callosum and their volumetry results after 5 years, p < 0.001. In this study population, the thalamus did not demonstrate significant changes in volumetry results during follow-up, p > 0.05. The provided treatment (DMTs) did not demonstrate a significant impact on the brain MRI volumetry results during a 5-year follow-up, p > 0.05. Conclusions: Brain MRI volumetry seriously impacts the early detection of brain atrophic changes. In this study, significant relationship between brain magnetic resonance volumetry results and disability progression among MS patients with no important impact of the provided treatment was described. Brain MRI volumetry may aid in the identification of early disease progression among MS patients, as well as enrich the clinical evaluation of MS patients in clinical patient care.
 INTRODUCTION: Prior studies have suggested that cardiovascular risk factors (CVRFs) can affect the prognosis of multiple sclerosis (MS). The aim of this study was to assess if CVRFs affect the early course of MS. METHODS: A retrospective observational study was performed, including patients diagnosed with relapsing-remitting MS (RRMS) from 2010 to 2020, with at least 2 years of disease and 6 months follow-up. Age at onset, disease duration, number of relapses, time to confirmed Expanded Disability Status Scale (EDSS) 3.0 and 6.0, and time to secondary progressive MS (SPMS) were collected. Presence and date at onset of hypertension (HT), diabetes mellitus (DM), high low-density lipoprotein cholesterol (LDLc), and smoking during the study period were collected. The primary objective was to assess if CVRFs at the onset of MS are associated with lower time to EDSS 3.0, time to EDSS 6.0, and time to SPMS, using bivariate and multivariate analysis. RESULTS: 281 RRMS patients were included; median age at onset was 33 (IQR 26-39); 69.4% were female. Median EDSS at onset was 1.5 (IQR 1-2.5). Nine patients reached SPMS; 24 patients were diagnosed with HT, 9 with DM, 109 with high LDLc, and 123 were smokers during follow-up. No statistically significant association was found between the presence of CVRF at MS onset and the mentioned clinical outcomes during the MS course. CONCLUSION: No association was found between CVRFs and the early course of MS in our cohort.
 BACKGROUND: Magnetic resonance spectroscopic imaging (MRSI) of the brain enables in vivo assessment of metabolic alterations in multiple sclerosis (MS). This provides complementary insights into lesion pathology that cannot be obtained via T1- and T2-weighted conventional magnetic resonance imaging (cMRI). PURPOSE: The aims of this study were to assess focal metabolic alterations inside and at the periphery of lesions that are visible or invisible on cMRI, and to correlate their metabolic changes with T1 hypointensity and the distance of lesions to cortical gray matter (GM). METHODS: A 7 T MRSI was performed on 51 patients with relapsing-remitting MS (30 female/21 male; mean age, 35.4 ± 9.9 years). Mean metabolic ratios were calculated for segmented regions of interest (ROIs) of normal-appearing white matter, white matter lesions, and focal regions of increased mIns/tNAA invisible on cMRI. A subgroup analysis was performed after subdividing based on T1 relaxation and distance to cortical GM. Metabolite ratios were correlated with T1 and compared between different layers around cMRI-visible lesions. RESULTS: Focal regions of, on average, 2.8-fold higher mIns/tNAA than surrounding normal-appearing white matter and with an appearance similar to that of MS lesions were found, which were not visible on cMRI (ie, ~4% of metabolic hotspots). T1 relaxation was positively correlated with mIns/tNAA ( P ≤ 0.01), and negatively with tNAA/tCr ( P ≤ 0.01) and tCho/tCr ( P ≤ 0.01). mIns/tCr was increased outside lesions, whereas tNAA/tCr distributions resembled macroscopic tissue damage inside the lesions. mIns/tCr was -21% lower for lesions closer to cortical GM ( P ≤ 0.05). CONCLUSIONS: 7 T MRSI allows in vivo visualization of focal MS pathology not visible on cMRI and the assessment of metabolite levels in the lesion center, in the active lesion periphery and in cortical lesions. This demonstrated the potential of MRSI to image mIns as an early biomarker in lesion development.
 BACKGROUND: Research is needed to identify the unmet disease education and communication needs of people with multiple sclerosis (PwMS) to support informed decision-making, enable self-management and maintain independence for PwMS for as long as possible. METHODS: An Expert Steering Group co-developed two studies for PwMS aged 18 years and over: a qualitative, online, patient community activity and a quantitative anonymised online survey. The quantitative survey was conducted in the UK from 12 September 2019 to 18 November 2019 amongst PwMS recruited via the Multiple Sclerosis (MS) Trust newsletter and their closed Facebook group. Questions explored the goals, desires, and knowledge gaps of PwMS. Self-reported data from people with relapsing-remitting multiple sclerosis (RRMS) were collated and reviewed, and discussed by the Steering Group. This paper presents descriptive statistics of the quantitative survey findings. RESULTS: The sample consisted of 117 participants with RRMS. Most respondents (73%) had personal goals related to lifestyle and many (69%) were concerned about maintaining independence. More than half of respondents were worried about planning for the future in relation to income (56%), housing (40%) and most respondents also indicated MS had a negative impact on their lives, including their work life (73%) and social life (69%). Limited occupational support was forthcoming (17% were not provided with any support and only 27% report their work environment being adjusted to suit their needs). The ability to plan for the future and to understand the course of MS were highlighted as key priorities by respondents. A positive trend was observed between those who felt able to plan for the future and their knowledge of MS progression. The proportion of patients who report knowing a 'great deal' about MS prognosis and disability progression was low (16% and 9%, respectively), suggesting an increased role for clinical teams to provide information and education for PwMS. Communication between respondents and their clinical teams highlighted the role of specialist nurses for PwMS to provide holistic, informative support and demonstrated the level of comfort that PwMS have in discussing less clinical topics with these providers. CONCLUSION: This UK nationwide survey highlighted some of the unmet needs in disease education and communication in a subgroup of UK patients with RRMS, which can impact quality of life. Discussing goals and planning alongside prognosis and disability progression with MS care teams may enable people with RRMS not only to make informed treatment decisions, but also to self-manage and plan for the future, factors which are important to maintain independence.
 BACKGROUND: Disease and treatment-associated immune system abnormalities may confer higher risk of Coronavirus disease 2019 (COVID-19) to people with multiple sclerosis (PwMS). We assessed modifiable risk factors associated with COVID-19 in PwMS. METHODS: Among patients referring to our MS Center, we retrospectively collected epidemiological, clinical and laboratory data of PwMS with confirmed COVID-19 between March 2020 and March 2021 (MS-COVID, n = 149). We pursued a 1:2 matching of a control group by collecting data of PwMS without history of previous COVID-19 (MS-NCOVID, n = 292). MS-COVID and MS-NCOVID were matched for age, expanded disability status scale (EDSS) and line of treatment. We compared neurological examination, premorbid vitamin D levels, anthropometric variables, life-style habits, working activity, and living environment between the two groups. Logistic regression and Bayesian network analyses were used to evaluate the association with COVID-19. RESULTS: MS-COVID and MS-NCOVID were similar in terms of age, sex, disease duration, EDSS, clinical phenotype and treatment. At multiple logistic regression, higher levels of vitamin D (OR 0.93, p < 0.0001) and active smoking status (OR 0.27, p < 0.0001) emerged as protective factors against COVID-19. In contrast, higher number of cohabitants (OR 1.26, p = 0.02) and works requiring direct external contact (OR 2.61, p = 0.0002) or in the healthcare sector (OR 3.73, p = 0.0019) resulted risk factors for COVID-19. Bayesian network analysis showed that patients working in the healthcare sector, and therefore exposed to increased risk of COVID-19, were usually non-smokers, possibly explaining the protective association between active smoking and COVID-19. CONCLUSIONS: Higher Vitamin D levels and teleworking may prevent unnecessary risk of infection in PwMS.
 BACKGROUND: Neurofilament light (NfL) levels reflect inflammatory disease activity in multiple sclerosis (MS), but it is less clear if NfL also can serve as a biomarker for MS progression in treated patients without relapses and focal lesion accrual. In addition, it has not been well established if clinically effective treatment re-establishes an age and sex pattern for cerebrospinal fluid NfL (cNfL) as seen in controls, and to what degree levels are affected by disability level and magnetic resonance imaging (MRI) atrophy metrics. METHODS: We included subjects for whom cNfL levels had been determined as per clinical routine or in clinical research, classified as healthy controls (HCs, n = 89), MS-free disease controls (DCs, n = 251), untreated MS patients (uMS; n = 296), relapse-free treated MS patients (tMS; n = 78), and ProTEct-MS clinical trial participants (pMS; n = 41). RESULTS: Using linear regression, we found a positive association between cNfL and age, as well as lower concentrations among women, in all groups, except for uMS patients. In contrast, disability level in the entire MS cohort, or T1 and T2 lesion volumes, brain parenchymal fraction, thalamic fraction, and cortical thickness in the pMS trial cohort, did not correlate with cNfL concentrations. Furthermore, the cNfL levels in tMS and pMS groups did not differ. CONCLUSIONS: In participants with MS lacking signs of inflammatory disease activity, disease modulatory therapy reinstates an age and sex cNfL pattern similar to that of control subjects. No significant association was found between cNfL levels and clinical worsening, disability level, or MRI metrics.
 Multiple sclerosis (MS) is one of the most common neurodegenerative diseases showing various symptoms both of physical and cognitive type. In this work, we used attenuated total reflection Fourier transformed infrared (ATR-FTIR) spectroscopy to analyze plasma samples for discriminating MS patients from healthy control individuals, and identifying potential spectral biomarkers helping the diagnosis through a quick non-invasive blood test. The cohort of the study consists of 85 subjects, including 45 MS patients and 40 healthy controls. The differences in the spectral features both in the fingerprint region (1800-900 cm(-1)) and in the high region (3050-2800 cm(-1)) of the infrared spectra were highlighted also with the support of different chemometric methods, to capture the most significant wavenumbers for the differentiation. The results show an increase in the lipid/protein ratio in MS patients, indicating changes in the level (metabolism) of these molecular components in the plasma. Moreover, the multivariate tools provided a promising rate of success in the diagnosis, with 78% sensitivity and 83% specificity obtained through the random forest model in the fingerprint region. The MS diagnostic tools based on biomarkers identification on blood (and blood component, like plasma or serum) are very challenging and the specificity and sensitivity values obtained in this work are very encouraging. Overall, the results obtained suggest that ATR-FTIR spectroscopy on plasma samples, requiring minimal or no manipulation, coupled with statistical multivariate approaches, is a promising analytical tool to support MS diagnosis through the identification of spectral biomarkers.
 BACKGROUND: Annualized relapse rate (ARR) is used as an outcome measure in multiple sclerosis (MS) clinical trials. Previous studies demonstrated that ARR has reduced in placebo groups between 1990 and 2012. This study aimed to estimate real-world ARRs from contemporary MS clinics in the UK, in order to improve the feasibility estimations for clinical trials and facilitate MS service planning. METHODS: A multicentre observational, retrospective study of patients with MS from 5 tertiary neuroscience centres in the UK. We included all adult patients with a diagnosis of MS that had a relapse between 01/04/2020 and 30/06/2020. RESULTS: One hundred thirteen out of 8783 patients had a relapse during the 3-month study period. Seventy-nine percent of the patients with a relapse were female, the mean age was 39 years, and the median disease duration was 4.5 years; 36% of the patients that had a relapse were on disease-modifying treatment. The ARR from all study sites was estimated at 0.05. The ARR for relapsing remitting MS (RRMS) was estimated at 0.08, while the ARR for secondary progressive MS (SPMS) was 0.01. CONCLUSIONS: We report a lower ARR compared to previously reported rates in MS.
 OBJECTIVE: To further investigate objective measures of cognitive fatigue (CF), defined as the inability to sustain performance over time, in newly diagnosed multiple sclerosis (MS) patients, by conducting a performance analysis on the Paced Auditory Serial Addition Test (PASAT) based on the type of errors (omissions vs. incorrect responses) committed. METHOD: Sixty-two newly diagnosed patients with MS (pwMS) and 41 healthy controls (HC) completed the PASAT. Analysis of the change in performance during the test was performed by comparing the number of correct responses, incorrect responses, and omissions in the 1(st) versus the 3(rd) tertile of the PASAT. RESULTS: A significant decline in accuracy over time was observed to be related to an increment in the number of omissions, significantly more pronounced in pwMS than in HC. No change in the number of incorrect responses throughout the PASAT was observed for either group. CONCLUSIONS: CF can be detected even in newly diagnosed pwMS and might objectively manifest as a progressive increase in omissions during a sustained highly demanding task (i.e., PASAT). This pattern may reflect slowed processing speed and increased fatigue in pwMS. Focusing on omissions on the PASAT instead of correct responses only may improve its specificity as an objective measure of CF.
 BACKGROUND: Teriflunomide is a disease modifying treatment (DMT) approved for relapsing-remitting multiple sclerosis (RRMS) in adults and children. It reduces lymphocyte proliferation by inhibiting the mitochondrial enzyme dihydroorotate dehydrogenase (DHODH) and thereby the pyrimidine synthesis. Although most DMTs in multiple sclerosis (MS) modulate or inhibit the immune system in the periphery, the efficacy may improve if the agent also targets immune activity within the central nervous system (CNS), acts as a neuro-protective and enhances neuro-regeneration. The objective of this study was to determine the passage of teriflunomide over the blood-cerebrospinal fluid barrier (BCSFB). METHODS: Plasma and cerebrospinal fluid (CSF) teriflunomide concentrations were determined at steady state in 12 patients with RRMS, treated with oral teriflunomide 14 mg once daily. Included patients were all clinically stable without relapse or disability worsening within 6 months prior from baseline and were on no other immune modulating or immunosuppressive drugs. RESULTS: The mean teriflunomide concentrations in plasma and CSF were 38775 (SEM ± 7256) ng/mL and 68 (SEM ± 15) ng/mL, respectively. The passage over the BCSFB was 0.17 % (SEM ± 0.01). While no correlation was found between the function of the BCSFB assessed with the albumin ratio and the CSF teriflunomide concentration, the CSF and plasma teriflunomide concentrations were highly correlated (r(s) = 0.90, < 0.0001). CONCLUSIONS: Further studies are warranted to determine if the obtained CSF teriflunomide concentration reflects that in the CNS and is able to influence inflammatory and degenerative processes within the CNS.
 BACKGROUND AND PURPOSE: Although cognitive impairment (CI) is frequent in multiple sclerosis (MS) patients, few studies (and with conflicting results) have evaluated early predictors of CI in the long term. We aimed at determining associations between early clinical/neuroradiological variables with reference to CI after 20 years of MS. METHODS: We investigated in 170 MS patients the relationship between clinical/magnetic resonance imaging (MRI) data at diagnosis and cognitive status almost 20 years after MS onset. Among others, number and volume of both white matter lesions (WMLs) and cortical lesions (CLs) were evaluated at diagnosis and after 2 years. All MS patients were followed over time and underwent a comprehensive neuropsychological assessment at the end of study. Advanced statistical methods (unsupervised cluster analysis and random forest model) were conducted. RESULTS: CI patients showed higher focal cortical pathology at diagnosis compared to cognitively normal subjects (p < 0.001). Volumes of both WMLs and CLs emerged as the MRI metrics most associated with long-term CI. Moreover, number of CLs (especially ≥3) was also strongly associated with long-term CI (≥3 CLs: odds ratio [OR] = 3.7, 95% confidence interval = 1.8-7.5, p < 0.001), more than number of WMLs; the optimal cutoff of three CLs (area under the curve = 0.67, specificity = 75%, sensitivity = 55%) was estimated according to the risk of developing CI. CONCLUSIONS: These results highlight the impact of considering both white and gray matter focal damage from early MS stages. Given the low predictive value of WML number and the poor clinical applicability of lesion volume estimation in the daily clinical context, the evaluation of number of CLs could represent a reliable prognostic marker of CI.
 PURPOSE: Fatigue is a common symptom of multiple sclerosis (MS) and can adversely affect all aspect of quality of life. The etiology of fatigue remains unclear, and its treatments are suboptimal. Characterizing the phenotypes of fatigued persons with MS may help advance research on fatigue's etiology and identify ways to personalize fatigue interventions to improve quality of life. The purpose of this study was to identify fatigue phenotypes; examine phenotype stability overtime; and characterize phenotypes by health and function, social and environmental determinants, psychosocial factors, and engagement in healthy behaviors. METHODS: We conducted a longitudinal study over a 3-month period with 289 fatigued participants with MS. To identify fatigue phenotypes and determine transition probabilities, we used latent profile and transition analyses with valid self-report measures of mental and physical fatigue severity, the mental and physical impact of fatigue, depression, anxiety, and sleep quality. We used ANOVAs and effect sizes to characterize differences among phenotypes. RESULTS: The best fitting model included six subgroups of participants: Mild Phenotype, Mild-to-Moderate Phenotype, Moderate-to-Severe Phenotype, Severe Phenotype, Fatigue-dominant Phenotype, and Mental Health-dominant Phenotype. The transition analysis indicated that phenotypic membership was highly stable. Variables with a large eta squared effect size included environmental barriers, self-efficacy, and fatigue catastrophizing. CONCLUSION: These results indicate that the magnitude of fatigue experienced may be more important to consider than the type of fatigue when characterizing fatigue phenotypes. Future research should explore whether tailoring interventions to environmental barriers, self-efficacy, and fatigue catastrophizing reduce the likelihood of transitioning to a more severe phenotype.
 INTRODUCTION: Cognitive dysfunction can be seen in patients with MS (PwMS) and has been gaining attention in recent years. This study aimed to assess cognitive function and its determinants in PwMS using Addenbrooke Cognitive Assessment Battery (ACE-R). MATERIAL AND METHODS: This case-control study was conducted at an outpatient MS clinic in Istanbul. The sample consisted of 60 consecutive patients with definite MS and 60 matched controls. Cognitive function was evaluated by using the ACE-R. Subjective cognitive function, anxiety, depression, and fatigue were evaluated by validated scales. RESULTS: The mean age of the patients was 38.8, and the time since diagnosis was nine years. The majority of the patients had relapsing-remitting MS. Compared to age, sex, and education-matched healthy controls, all ACE-R scores, attention/orientation (p = 0.020), memory (p = 0.003), verbal fluency (p = 0.002), language (p = 0.002), visuospatial (p = 0.001), and general cognitive functioning (p < 0.001), were found to be lower in PwMS. The patients obtained the lowest scores in memory and fluency and the highest in the visuospatial domain. Age, education, mobility, subjective cognitive dysfunction, anxiety, depression, and fatigue were associated with cognitive test scores. However, only education, depression, and fatigue remained significant in the multivariable analysis. CONCLUSION: This study revealed impaired domains of cognitive functioning and its predictors in PwMS. Understanding cognitive dysfunction and its predictors in PwMS may enable healthcare providers to identify patients who might benefit from interventions to improve cognitive function. Assessment of PwMS at outpatient clinics with a practical cognitive test that does not require special competence can be suggested.
 OBJECTIVE: We tested for the presence of differential item functioning (DIF) in commonly used measures of depressive symptoms, in people with multiple sclerosis (MS) versus people with a psychiatric disorder without MS. METHODS: Participants included individuals with MS, or with a lifetime history of a depressive or anxiety disorder (Dep/Anx) but no immune-mediated inflammatory disease. Participants completed the Patient Health Questionnaire (PHQ-9), Hospital Anxiety and Depression Scale (HADS), and the Patient Reported Outcome Measurement Information System (PROMIS)-Depression. We assessed unidimensionality of the measures using factor analysis. We evaluated DIF using logistic regression, with and without adjustment for age, gender and body mass index (BMI). RESULTS: We included 555 participants (MS: 252, Dep/Anx: 303). Factor analysis showed that each depression symptom measure had acceptable evidence of unidimensionality. In unadjusted analyses comparing the MS versus Dep/Anx groups we identified multiple items with evidence of DIF, but few items showed DIF effects that were large enough to be clinically meaningful. We observed non-uniform DIF for one PHQ-9 item, and three HADS-D items. We also observed DIF with respect to gender (one HADS-D item), and BMI (one PHQ-9 item). For the MS versus Dep/Anx groups, we no longer observed DIF post-adjustment for age, gender and BMI. On unadjusted and adjusted analyses, we did not observe DIF for any PROMIS-D item. CONCLUSION: Our findings suggest that DIF exists for the PHQ-9 and HADS-D with respect to gender and BMI in clinical samples that include people with MS whereas DIF was not observed for the PROMIS-Depression scale.
 Current understanding of Multiple Sclerosis (MS) pathophysiology implicates perturbations in adaptive cellular immune responses, predominantly T cells, in Relapsing-Remitting forms (RRMS). Nevertheless, from a clinical perspective MS is a heterogeneous disease reflecting the heterogeneity of involved biological systems. This complexity requires advanced analysis tools at the single-cell level to discover biomarkers for better patient-group stratification. We designed a novel 44-parameter mass cytometry panel to interrogate predominantly the role of effector and regulatory subpopulations of peripheral blood myeloid subsets along with B and T-cells (excluding granulocytes) in MS, assessing three different patient cohorts: RRMS, PPMS (Primary Progressive) and Tumefactive MS patients (TMS) (n=10, 8, 14 respectively). We further subgrouped our cohort into inactive or active disease stages to capture the early underlying events in disease pathophysiology. Peripheral blood analysis showed that TMS cases belonged to the spectrum of RRMS, whereas PPMS cases displayed different features. In particular, TMS patients during a relapse stage were characterized by a specific subset of CD11c+CD14+ CD33+, CD192+, CD172+-myeloid cells with an alternative phenotype of monocyte-derived macrophages (high arginase-1, CD38, HLA-DR-low and endogenous TNF-a production). Moreover, TMS patients in relapse displayed a selective CD4 T-cell lymphopenia of cells with a Th2-like polarised phenotype. PPMS patients did not display substantial differences from healthy controls, apart from a trend toward higher expansion of NK cell subsets. Importantly, we found that myeloid cell populations are reshaped under effective disease-modifying therapy predominantly with glatiramer acetate and to a lesser extent with anti-CD20, suggesting that the identified cell signature represents a specific therapeutic target in TMS. The expanded myeloid signature in TMS patients was also confirmed by flow cytometry. Serum neurofilament light-chain levels confirmed the correlation of this myeloid cell signature with indices of axonal injury. More in-depth analysis of myeloid subsets revealed an increase of a subset of highly cytolytic and terminally differentiated NK cells in PPMS patients with leptomeningeal enhancement (active-PPMS), compared to those without (inactive-PPMS). We have identified previously uncharacterized subsets of circulating myeloid cells and shown them to correlate with distinct disease forms of MS as well as with specific disease states (relapse/remission).
 BACKGROUND: Treatment of pediatric-onset multiple sclerosis (POMS) is challenging given the lack of safety and efficacy data in the pediatric population for many of the disease-modifying treatments (DMTs) approved for use in adults with MS. Our objective was to describe the demographic features and clinical and radiologic course of patients with POMS treated with the commonly used newer DMTs within the US Network of Pediatric MS Centers (NPMSC). METHODS: This is an analysis of prospectively collected data from patients who initiated treatment before age 18 with the DMTs listed below at the 12 regional pediatric MS referral centers participating in the NPMSC. RESULTS: One hundred sixty-eight patients on dimethyl fumarate, 96 on fingolimod, 151 on natalizumab, 166 on rituximab, and 37 on ocrelizumab met criteria for analysis. Mean age at DMT initiation ranged from 15.2 to 16.5 years. Disease duration at the time of initiation of index DMT ranged from 1.1 to 1.6 years with treatment duration of 0.9-2.0 years. Mean annualized relapse rate (ARR) in the year prior to initiating index DMT ranged from 0.4 to 1.0. Mean ARR while on index DMT ranged from 0.05 to 0.20. New T2 and enhancing lesions occurred in 75%-88% and 55%-73% of the patients, respectively, during the year prior to initiating index DMT. After initiating index DMT, new T2 and enhancing lesions occurred in 0%-46% and 11%-34% patients, respectively. Rates of NEDA-2 (no evidence of disease activity) ranged from 76% to 91% at 6 months of treatment with index DMTs and 66% to 84% at 12 months of treatment with index DMTs. CONCLUSIONS: Though limited by relatively short treatment duration with the index DMTs, our data suggest clinical and MRI benefit, as well as high rates of NEDA-2, in a large number of POMS patients, which can be used to guide future studies in this population.
 BACKGROUND: Spinal cord lesions have been associated with progressive disease in individuals with typical relapsing remitting MS (RRMS). OBJECTIVE: In the current study, we aimed to determine if progressive disease is associated with spinal cord lesions in those with tumefactive multiple sclerosis (MS). METHODS: Retrospective chart review of individuals presenting to Mayo Clinic with tumefactive MS with spinal cord MRIs available (n=159). Clinical data were extracted by chart review. Brain and spinal cord MRIs were reviewed to characterize the tumefactive demyelinating lesion(s) and assess the burden of spinal cord disease. RESULTS: A total of 69 (43%) had spinal cord lesions. Progressive demyelinating disease was documented in 13 (8%); the majority (11/13) with secondary progressive disease. The method of progression was myelopathic in 8/13 (62%), cognitive in 3/13 (23%), motor from a supratentorial lesion in 2/13 (16%). EDSS at last follow-up was higher in those with progression than those without (median 6.0 (2.0-10.0) vs. 2.5 (0-10.0), p = < 0.001). Progressive demyelinating disease occurred in a minority. CONCLUSIONS: Patients with progression typically experienced progressive motor impairment, and this occurred exclusively in individuals with lesions in the corticospinal tracts of the brain and/or the spinal cord.
 Determining the validity of data during clinical neuropsychological assessment is crucial for proper interpretation, and extensive literature has emphasized myriad methods of doing so in diverse samples. However, little research has considered noncredible presentation in persons with multiple sclerosis (pwMS). PwMS often experience one or more factors known to impact validity of data, including major neurocognitive impairment, psychological distress/psychogenic interference, and secondary gain. This case series aimed to illustrate the potential relationships between these factors and performance validity testing in pwMS. Six cases from an IRB-approved database containing pwMS referred for neuropsychological assessment at a large, academic medical center involving at least one of the above-stated factors were identified. Backgrounds, neuropsychological test data, and clinical considerations for each were reviewed. Interestingly, no pwMS diagnosed with major neurocognitive impairment was found to have noncredible performance, nor was any patient with noncredible performance in the absence of notable psychological distress. Given the variability of noncredible performance and multiplicity of factors affecting performance validity in pwMS, clinicians are strongly encouraged to consider psychometrically appropriate methods for evaluating validity of cognitive data in pwMS. Additional research aiming to elucidate base rates of, mechanisms begetting, and methods for assessing noncredible performance in pwMS is imperative.
 BACKGROUND: Naming difficulty is commonly reported by patients with multiple sclerosis (pwMS). Though many cognitive batteries recommended for pwMS include fluency tasks, they do not include naming tasks. The aim of this study was to examine the prevalence of naming impairment in pwMS by using a measure of confrontation naming and to identify correlates with neuroimaging. METHODS: One-hundred-eighty-five pwMS (M(age) = 48.75 ± 11.23) completed neuropsychological testing and fifty had brain MRI scans within one year of neuropsychological testing. Controlling for demographic variables, partial correlations and hierarchical regressions with language tests as the outcome variables and neuroimaging variables as predictors were performed. RESULTS: Performance on language tasks ranged within low average to average, with impairment most frequently found on a measure of confrontation naming (Boston Naming Test [BNT];27.6%), followed by a measure of phonemic fluency (Controlled Oral Word Association Test [COWAT]; 24.3%) and semantic fluency (animals [AF]; 18.3%). In the subset of patients with neuroimaging, thalamic volume had the strongest relationship with language variables, followed by white matter volume and T2 lesion volume. Language variables had no association with fractional gray matter volume. Of the language measures, BNT demonstrated the strongest relationship with MRI variables, followed by AF. There were no significant associations between neuroimaging variables and COWAT. Regression results revealed that fractional thalamic volume significantly contributed to BNT scores after adjusting for demographics, while T2 lesion volume predicted AF and no neuroimaging variables emerged as predictors for COWAT after controlling for demographics. CONCLUSIONS: Objective naming impairment is common in pwMS and are more strongly associated with neuroimaging of MS brain pathology than verbal fluency tasks that are commonly used in cognitive batteries for pwMS. Continued research on language (especially naming) deficits and neuroimaging correlates (particularly thalamic involvement) in pwMS is needed.
 BACKGROUND: Autologous hematopoietic stem cell treatment (AHSCT) is considered an effective treatment option for patients with aggressive relapsing-remitting multiple sclerosis (RRMS). Still there are few randomized and controlled studies of AHSCT to shed light on the safety and efficacy of the treatment, and therefore experiences from single centers are important. AIM: To describe the Danish experience with AHSCT regarding patient characteristics, safety, and efficacy. METHOD: Nationwide retrospective single center study of patients with multiple sclerosis (MS) treated with AHSCT. RESULTS: A total of 32 patients were treated with AHSCT from May 2011 to May 2021. Seven were treated with carmustine, etoposide, cytarabine arabinoside, and melphalan (BEAM) as well as antithymocyte globulin (ATG). Twenty-five patients were treated with cyclophosphamide (CY) and ATG. In the whole cohort, relapse-free survival (RFS) was 77% (95% CI: 64-94%), worsening-free survival (WFS) was 79% (95% CI: 66-96%), MRI event-free survival (MFS) was 93% (95% CI: 85-100%), and no evidence of disease (NEDA-3) was 69% (95% CI: 54-89%) at the end of year two post-AHSCT. We had no treatment related mortality and only few severe adverse events (AEs). CONCLUSION: AHSCT of patients with aggressive RRMS was an effective and relatively safe treatment with few serious AEs and no mortality in Danish patients.
 BACKGROUND: Information processing speed is commonly impaired in people with multiple sclerosis (PwMS). However, depression and fatigue can affect the cognitive profile of patients: fatigue has a negative impact from the disease's earliest stage and a reduced information processing speed is often associated with higher levels of depression. Therefore, the aim of this study was to investigate the correlations between information processing speed and physical fatigue in a cohort of Italian PwMS from a single center, considering the effect of depression. METHODS: Two hundred (W = 128; mean age = 39.83 years; SD = 11.86) PwMS, from the Bari University Hospital, underwent testing for processing speed (Symbol Digit Modalities Test [SDMT]), fatigue level (Fatigue Severity Scale [FSS]), and depression (Beck's Depression Inventory [BDI]). RESULTS: Statistically significant correlations emerged between SDMT and FSS, SDMT and BDI, FSS and BDI. Mediation analyses revealed that while physical fatigue had no significant direct negative effect on information processing speed (z=-0.891; p > 0.05), depression predicted the relationship between fatigue and information processing speed (z=-2.181; p < 0.05). CONCLUSION: Our findings showed that cognitive performance at SDMT was not affected by patients' perceived level of physical fatigue, but by depression. The presence of a high BDI score mediates the physical fatigue on cognitive performance impact.
 OBJECTIVE: This study proposes a comprehensive quantitative evaluation of the efficacy of drugs and placebo in clinical trials for primary progressive multiple sclerosis (PPMS). METHODS: A literature search was conducted using the PubMed, EMBASE, and Cochrane library databases and the clinical studies reporting drug efficacy in the treatment of PPMS were included in the analyses. The cumulative proportion of patients without confirmed disability progression (wCDP%) was used as the main efficacy endpoint. The model-based meta-analysis method was used to describe the time course of each drug (as well as placebo) in order to rank the drug efficacy for the treatment of PPMS. RESULTS: Fifteen studies involving 3779 patients were included, of which, nine were placebo-controlled and six were single-arm trials. Twelve drugs were included in the study. The results showed that, except for biotin, interferon β-1a, and interferon β-1b, whose efficacy was comparable to the placebo, the efficacy of the other 9 drugs were significantly better than placebo. Among these, ocrelizumab showed outstanding performance, with wCDP% of 72.6 at 96 weeks, while the proportions of rest of the drugs ranged between approximately 55-70%. CONCLUSION: The results of this study provide the necessary quantitative information for both the rational clinical use of drugs and future clinical trials in primary progressive multiple sclerosis.
 INTRODUCTION: Natalizumab is associated with a risk of progressive multifocal leukoencephalopathy (PML) in multiple sclerosis (MS) patients infected with John Cunningham virus (JCV). Ocrelizumab has demonstrated efficacy to treat MS; however, its safety in patients previously treated with natalizumab is unclear. OBJECTIVE: To evaluate the safety and efficacy of ocrelizumab in patients with relapsing MS (RMS) previously treated with natalizumab. METHODS: Clinically and radiographically stable RMS patients, ages 18-65 treated with natalizumab for ⩾ 12 months, were enrolled in the study and initiated ocrelizumab 4-6 weeks after their final dose of natalizumab. Relapse assessment, expanded disability status scale, and brain magnetic resonance imaging (MRI) were performed prior to starting ocrelizumab and at months 3, 6, 9, and 12. RESULTS: Forty-three patients were enrolled, and 41 (95%) completed the study. Two patients had a relapse while on ocrelizumab, one at month 9 and the other at month 12, without changes on brain MRI. Two additional patients had new brain MRI lesions detected at month 3, with no new symptoms. Thirteen serious adverse events (SAEs) were recorded, four of which were considered possibly related to ocrelizumab. CONCLUSION: Overall, our study indicates clinical and MRI stability for most patients transitioning from natalizumab to ocrelizumab. CLINICALTRIALS.GOV IDENTIFIER: NCT03157830.
 BACKGROUND: Sexual dysfunction (SD) is one of the most common complications of multiple sclerosis (MS). The aim of this study was to evaluate the effects of bupropion on SD among female patients with MS. METHODS: This double-blind placebo-control randomized clinical trial was conducted on MS patients with SD complaint. Diagnosis was based on the secondary SD subscale scores of the Multiple Sclerosis Intimacy and Sexuality Questionnaire-19 (MSISQ-19). Accordingly, individuals scoring above 27 based on this scale were diagnosed with SD. The subjects were randomly assigned to the bupropion and placebo groups. Bupropion was administered 75 mg twice daily for twelve weeks. As for the study outcomes, besides MSISQ-19, quality of life (Multiple Sclerosis Quality Of Life-54 (MSQOL-54)), fatigue (Multidimensional Fatigue Inventory (MFI)), depression and anxiety (Hospital Anxiety and Depression Scale), and bupropion tolerability were assessed at baseline as well as at weeks 6 and 12. RESULTS: From 84 patients who met the inclusion criteria, 64 patients completed the trial and were analyzed. Demographics and baseline clinical characteristics were not significantly differed between the two groups. The results showed the mean score of MSISQ-19 from baseline to the end of the study period significantly improved in the bupropion group compared with the placebo (week 6: P: 0.03; week 12: P: 0.03). Similarly, MFI scores showed significant improvement in the bupropion group compared with the placebo group (P: 0.001). Both anxiety and depression scores showed significant alterations at study interval between the two groups (Anxiety: weeks 6 and 12: P:0.04; depression: week 6: 0.01, week 12: 0.02). However, there was no significant change in the MSQOL-54 score between the two groups. CONCLUSION: The results of the study substantiated that bupropion can be an effective agent for SD improvement in female patients with MS. Further clinical trials with larger sample sizes can more accurately evaluate the observed findings.
 The support provided at the Germaine-Revel medical center in the Rhône region involves assessing the patient as a whole, which is a key aspect of implementing personalized rehabilitation focused on one or more objectives. The team offers multidisciplinary and multimodal care, because the clinical symptoms of people with multiple sclerosis are very varied: they can include neuromotor, neurosensory, neurosensory and cognitive disorders, as well as bladder and bowel and genital disorders.

 INTRODUCTION: With the approval of natalizumab in Europe in 2006, the Austrian Multiple Sclerosis Therapy Registry (AMSTR) was established. Here, we present data from this registry about effectiveness and safety of natalizumab in patients treated up to 14 years. PATIENTS/METHODS: Data retrieved from the AMSTR contained baseline characteristics and biannual documentation of annualised relapse rate (ARR) and Expanded Disability Status Scale (EDSS) score as well as adverse events and reasons for discontinuation on follow-up visits. RESULTS: A total of 1596 natalizumab patients (71% women, n = 1133) were included in the analysis and the observed treatment duration ranged from 0 to 164 months (13.6 years). The mean ARR was 2.0 (SD = 1.13) at baseline, decreasing to 0.16 after 1 year and 0.01 after 10 years. A total of 325 patients (21.6%) converted to secondary progressive multiple sclerosis (SPMS) during the observational period. Of 1502 patients, 1297 (86.4%) reported no adverse events (AE) during follow-up visits. The most common reported AEs were infections and infusion-related reactions. John Cunningham virus (JCV) seropositivity was the most common specified reason for treatment discontinuation (53.7%, n = 607). There were five confirmed cases of Progressive Multifocal Leukoencephalopathy (PML) with 1 death. CONCLUSION: The effectiveness of natalizumab in patients with active relapsing-remitting multiple sclerosis (RRMS) could be confirmed in our real-world cohort even after follow-up of up to 14 years, though after year 10, there were less than 100 remaining patients. A low number of AE were reported in this nationwide registry study, establishing Natalizumab's favourable safety profile during long-term use.
 Brain morphometry is usually based on non-enhanced (pre-contrast) T1-weighted MRI. However, such dedicated protocols are sometimes missing in clinical examinations. Instead, an image with a contrast agent is often available. Existing tools such as FreeSurfer yield unreliable results when applied to contrast-enhanced (CE) images. Consequently, these acquisitions are excluded from retrospective morphometry studies, which reduces the sample size. We hypothesize that deep learning (DL)-based morphometry methods can extract morphometric measures also from contrast-enhanced MRI. We have extended DL+DiReCT to cope with contrast-enhanced MRI. Training data for our DL-based model were enriched with non-enhanced and CE image pairs from the same session. The segmentations were derived with FreeSurfer from the non-enhanced image and used as ground truth for the coregistered CE image. A longitudinal dataset of patients with multiple sclerosis (MS), comprising relapsing remitting (RRMS) and primary progressive (PPMS) subgroups, was used for the evaluation. Global and regional cortical thickness derived from non-enhanced and CE images were contrasted to results from FreeSurfer. Correlation coefficients of global mean cortical thickness between non-enhanced and CE images were significantly larger with DL+DiReCT (r = 0.92) than with FreeSurfer (r = 0.75). When comparing the longitudinal atrophy rates between the two MS subgroups, the effect sizes between PPMS and RRMS were higher with DL+DiReCT both for non-enhanced (d = -0.304) and CE images (d = -0.169) than for FreeSurfer (non-enhanced d = -0.111, CE d = 0.085). In conclusion, brain morphometry can be derived reliably from contrast-enhanced MRI using DL-based morphometry tools, making additional cases available for analysis and potential future diagnostic morphometry tools.
 BACKGROUND: Impairment of cardiovascular control is common in multiple sclerosis (MS), possibly due to damage of strategic brain regions such as the insula. Aerobic training (AT) targets cardiopulmonary system and may represent a neuroprotective strategy. PURPOSE: To investigate whether insular damage (T2-hyperintense lesions and volume) is associated with cardiovascular fitness (CF) and influences AT effects in MS. METHODS: Sixty-one MS patients were randomized to an AT intervention group (MS-AT) and a motor training control group (MS-C). At baseline and after training (24 sessions over 2-3 months), peak of oxygen consumption (VO2max), heart rate reserve (HRR), 6-min walk test (6MWT) and whole brain and insula MRI data were collected. Two healthy control (HC) groups were enrolled for CF and MRI data analysis. RESULTS: At baseline, MS patients vs HC showed impaired VO2max, HRR and 6MWT (p < 0.001) and widespread gray matter atrophy, including bilateral insula. In MS patients, left insula T2-lesion volume correlated with HRR (r = 0.27, p = 0.042). After training, MS-AT, especially those without insular T2-hyperintense lesions, showed 6MWT improvement (p < 0.05) and a stable insular volume, whereas MS-C showed left insular volume loss (p < 0.001). CONCLUSIONS: By increasing 6MWT performance, our results suggest that AT may improve walking capacity and submaximal measure of CF in MS patients. Such beneficial effect may be modulated by insula integrity.
 BACKGROUND: Remote administration of the Symbol Digit Modalities Test (SDMT) requires validation. OBJECTIVES: Examine interchangeability of remote and in-person SDMT administrations in persons with MS. METHODS: After in-person baseline administration, follow-up administration was either performed in-person (n = 72) or remotely via videoconferencing (n = 143). We examined whether raw score change from baseline to follow-up differed between in-person and remote follow-up modalities. RESULTS: SDMT raw score change did not differ between in-person and remote follow-up modalities (-0.1 ± 5.9 vs -0.2 ± 6.2, p = 0.995, d = 0.008), and correlations between baseline and follow-up were comparable across modalities (0.86 vs 0.88). CONCLUSIONS: Remote and in-person SDMT administrations appear interchangeable.
 BACKGROUND: Black/African American patients with multiple sclerosis (BpwMS) and Hispanic/Latino patients with multiple sclerosis (HpwMS), who historically have been underrepresented in multiple sclerosis (MS) clinical trials, exhibit greater disease severity and more rapid disease progression than White patients with MS (WpwMS). The lack of diversity and inclusion in clinical trials, which may be due to barriers at the system, patient and study levels, impacts the ability to effectively assess risks, benefits and treatment responses in a generalized patient population. METHODS: CHIMES (Characterization of Ocrelizumab in Minorities With Multiple Sclerosis), an open-label, single-arm, multicenter, phase IV study of self-identified BpwMS and HpwMS aged 18-65 years with relapsing MS and an Expanded Disability Status Score (EDSS) of ≤5.5, was developed in collaboration with patients with MS, national advocacy groups and clinical researchers. Patients were enrolled at study centers across the US, including Puerto Rico, and 1 site in Kenya. RESULTS: A total of 182 patients enrolled in CHIMES: 113 (62.1%) were BpwMS, and 69 (37.9%) were HpwMS; the mean (SD) baseline EDSS score was 2.4 (1.4), and 62.6% of patients were treatment naive. Using the pooled non-BpwMS/HpwMS group in the OPERA ocrelizumab trials as a reference population, patients enrolled in CHIMES were younger, had a higher mean body mass and had a greater T2 lesion volume but similar T2 lesion number on MRI. CONCLUSION: BpwMS and HpwMS have been consistently underrepresented in clinical trials, limiting the understanding of disease biology and response to treatment in this population. Data from the CHIMES study revealed differences in demographics and some baseline disease characteristics and disease burden between BpwMS and HpwMS vs WpwMS. These differences could have an impact when assessing clinical outcomes in BpwMS and HpwMS. GOV IDENTIFIER: NCT04377555.
 BACKGROUND: Spinal cord (SC) gray and white matter pathology plays a central role in multiple sclerosis (MS). OBJECTIVE: We aimed to investigate the extent, pattern, and clinical relevance of SC gray and white matter atrophy in vivo. METHODS: 39 relapsing-remitting patients (RRMS), 40 progressive MS patients (PMS), and 24 healthy controls (HC) were imaged at 3T using the averaged magnetization inversion recovery acquisitions sequence. Total and lesional cervical gray and white matter, and posterior (SCPH) and anterior horn (SCAH) areas were automatically quantified. Clinical assessment included the expanded disability status scale, timed 25-foot walk test, nine-hole peg test, and the 12-item MS walking scale. RESULTS: PMS patients had significantly reduced cervical SCAH - but not SCPH - areas compared with HC and RRMS (both p < 0.001). In RRMS and PMS, the cervical SCAH areas increased significantly less in the region of cervical SC enlargement compared with HC (all p < 0.001). This reduction was more pronounced in PMS compared with RRMS (both p < 0.001). In PMS, a lower cervical SCAH area was the most important magnetic resonance imaging (MRI)-variable for higher disability scores. CONCLUSION: MS patients show clinically relevant cervical SCAH atrophy, which is more pronounced in PMS and at the level of cervical SC enlargement.
 Multiple sclerosis (MS) is a neurodegenerative disease with a complex pathogenesis. Re-lapsing-remitting multiple sclerosis (RRMS) is the most common subset of MS, accounting for approximately 85% of cases. Recent studies have shown that ferroptosis may contribute to the progression of RRMS, but the underlying mechanism remains to be elucidated. Herein, this study intended to explore the molecular network of ferroptosis associated with RRMS and establish a predictive model for efficacy diagnosis. Firstly, RRMS-related module genes were identified using weighted gene co-expression network analysis (WGCNA). Secondly, the optimal machine learning model was selected from four options: the generalized linear model (GLM), random forest model (RF), support vector machine model (SVM), and extreme gradient boosting model (XGB). Subsequently, the predictive efficacy of the diagnostic model was evaluated using receiver operator characteristic (ROC) analysis. Finally, a SVM diagnostic model based on five genes (JUN, TXNIP, NCOA4, EIF2AK4, PIK3CA) was established, and it demonstrated good predictive performance in the validation dataset. In summary, our study provides a systematic exploration of the complex relationship between ferroptosis and RRMS, which may contribute to a better understanding of the role of ferroptosis in the pathogenesis of RRMS and provide promising diagnostic strategies for RRMS patients.
 INTRODUCTION: The relationship between fatigue and (socio-)cognitive deficits in neurological diseases has sparked increasing research interest in the past years. So far, findings are inconsistent. Most studies focused on general cognitive functioning in specific disorders, particularly cancer or multiple sclerosis (MS). METHODS: This study aims to examine the relationship between fatigue, social cognition and social activity, also taking into account general cognition, more closely, including a stroke patient group (n = 57), a MS patient group (n = 31) and a healthy control group (n = 20). The participants underwent a comprehensive (socio-)cognitive test battery and completed questionnaires on fatigue and psychopathology which, in addition to fatigue, can also affect (socio-)cognitive performance. RESULTS: In both MS and stroke patients high fatigue scores were observed. Irrespective of aetiology, patients with high and low fatigue did not differ with regard to general cognition and social cognition. However, high fatigue scores were associated with a reduction of social activities in both patient groups. No other significant relationships were observed between fatigue and (socio-)cognitive measures. CONCLUSIONS: Future studies ought to further explore the potentially complex nature of fatigue symptoms and their relationship with (socio-)cognitive performance and social activity in neurological populations.
 BACKGROUND: Multiple sclerosis typically has onset in young adults and new disease activity diminishes with age. Most clinical trials of disease-modifying therapies for multiple sclerosis have not enrolled individuals older than 55 years. Observational studies suggest that risk of return of disease activity after discontinuation of a disease-modifying therapies is greatest in younger patients with recent relapses or MRI activity. We aimed to determine whether risk of disease recurrence in older patients with no recent disease activity who discontinue disease-modifying therapy is increased compared to those who remain on disease-modifying therapy. METHODS: DISCOMS was a multicentre, randomised, controlled, rater-blinded, phase 4, non-inferiority trial. Individuals with multiple sclerosis of any subtype, 55 years or older, with no relapse within the past 5 years or new MRI lesion in the past 3 years while continuously taking an approved disease-modifying therapy were enrolled at 19 multiple sclerosis centres in the USA. Participants were randomly assigned (1:1 by site) with an interactive response technology system to either continue or discontinue disease-modifying therapy. Relapse assessors and MRI readers were masked to patient assignment; patients and treating investigators were not masked. The primary outcome was percentage of individuals with a new disease event, defined as a multiple sclerosis relapse or a new or expanding T2 brain MRI lesion, over 2 years. We assessed whether discontinuation of disease-modifying therapy was non-inferior to continuation using a non-inferiority, intention-to-treat analysis of all randomly assigned patients, with a predefined non-inferiority margin of 8%. This trial is registered at ClinicalTrials.gov, NCT03073603, and is completed. FINDINGS: 259 participants were enrolled between May 22, 2017, and Feb 3, 2020; 128 (49%) were assigned to the continue group and 131 (51%) to the discontinue group. Five participants were lost to follow-up (continue n=1, discontinue n=4). Six (4·7%) of 128 participants in the continue group and 16 (12·2%) of 131 in the discontinue group had a relapse or a new or expanding brain MRI lesion within 2 years. The difference in event rates was 7·5 percentage points (95% CI 0·6-15·0). Similar numbers of participants had adverse events (109 [85%] of 128 vs 104 [79%] of 131) and serious adverse events (20 [16%] vs 18 [14%]), but more adverse events (422 vs 347) and serious adverse events (40 vs 30) occurred in the discontinue group. The most common adverse events were upper respiratory infections (20 events in 19 [15%] participants in the continue group and 37 events in 30 [23%] participants in the discontinue group). Three participants in the continue group and four in the discontinue group had treatment-related adverse events, of which one in each group was a serious adverse event (multiple sclerosis relapse requiring admission to hospital). One participant in the continue group and two in the discontinue group died; no deaths were deemed to be related to treatment. INTERPRETATION: We were unable to reject the null hypothesis and could not conclude whether disease-modifying therapy discontinuation is non-inferior to continuation in patients older than 55 years with multiple sclerosis and no recent relapse or new MRI activity. Discontinuation of disease-modifying therapy might be a reasonable option in patients older than 55 years who have stable multiple sclerosis, but might be associated with a small increased risk of new MRI activity. FUNDING: Patient-Centered Outcomes Research Institute and the National Multiple Sclerosis Society.
 INTRODUCTION: The Expanded Disability Status Scale (EDSS) is the gold standard for evaluating clinical disability in multiple sclerosis (MS) in daily practice. However, more precise clinical assessment tools are needed. We assessed a new, automated rating of the neurological examination obtained with a mobile application (Quantified Neurological Examination - QNE). METHOD: Consecutive MS patients were assessed for EDSS score and QNE application that calculates, from the description of the examination, a global score and subscores (qFSS) corresponding to the EDSS functional system scores (FSS). Brain MRI was analysed to obtain automatic measures of brain atrophy. RESULTS: We performed 200 examinations and included 78 patients in the MRI analysis. The global QNE score was strongly correlated with the EDSS. qFSS was statistically different according to the corresponding FSS for each function, except for the visual FSS. EDSS was predominantly correlated to the pyramidal function of the lower limbs. QNE score and qFSS had at least equivalent correlation to MRI measures than EDSS, particularly regarding the gray matter and cortical volumes. DISCUSSION: We propose an automated method to rate neurological disability in MS. While QNE strongly correlates with EDSS, it may allow a more precise way to monitor the evolution of disability.
 Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease characterized by the appearance of focal lesions across the central nervous system. The discrimination of acute from chronic MS lesions may yield novel biomarkers of inflammatory disease activity which may support patient management in the clinical setting and provide endpoints in clinical trials. On a single timepoint and in the absence of a prior reference scan, existing methods for acute lesion detection rely on the segmentation of hyperintense foci on post-gadolinium T1-weighted magnetic resonance imaging (MRI), which may underestimate recent acute lesion activity. In this paper, we aim to improve the sensitivity of acute MS lesion detection in the single-timepoint setting, by developing a novel machine learning approach for the automatic detection of acute MS lesions, using single-timepoint conventional non-contrast T1- and T2-weighted brain MRI. The MRI input data are supplemented via the use of a convolutional neural network generating "lesion-free" reconstructions from original "lesion-present" scans using image inpainting. A multi-objective statistical ranking module evaluates the relevance of textural radiomic features from the core and periphery of lesion sites, compared within "lesion-free" versus "lesion-present" image pairs. Then, an ensemble classifier is optimized through a recursive loop seeking consensus both in the feature space (via a greedy feature-pruning approach) and in the classifier space (via model selection repeated after each pruning operation). This leads to the identification of a compact textural signature characterizing lesion phenotype. On the patch-level task of acute versus chronic MS lesion classification, our method achieves a balanced accuracy in the range of 74.3-74.6% on fully external validation cohorts.
 OBJECTIVE: The present study aimed to investigate the findings of cervical, ocular and masseter vestibular evoked myogenic potentials (cVEMP, oVEMP and mVEMP) among Multiple sclerosis (MS) and correlate with clinical and MRI findings. DESIGN: Standard group comparison research design. STUDY SAMPLE: Individuals with relapsing-remitting MS (n = 45) and age-sex-matched controls (n = 45) were the participants. All of them underwent case history, neurological examination, cVEMP, oVEMP and mVEMP testing. MRI was obtained only for MS participants. RESULTS: Abnormal result on at least one vestibular evoked myogenic potential (VEMP) sub-type was evidenced in 95.56% of participants whereas, unilateral or bilateral abnormal result on all three VEMP sub-types was observed in 60% of participants. The mVEMP abnormality was higher (82.22%) than cVEMP (75.56%) and oVEMP (75.56%) abnormalities but the differences were not significant (p > 0.05). There was no significant association of VEMP abnormalities with the presence of the brainstem symptoms, the brainstem signs, or the MRI lesions (p > 0.05). In the MS group, 38% had normal brainstem MRI; however, mVEMP, cVEMP and oVEMP abnormalities were evidenced in 82.4%, 64.7% and 52.94%, respectively. CONCLUSIONS: Among the three VEMP sub-types, mVEMP appears to be of greater value in identifying silent brainstem dysfunction undetected by clinical and MRI findings in the MS population.

 Autologous hematopoietic stem cell transplantation (AHSCT) has been approved for multiple sclerosis (MS) in many European countries. A large proportion of patients are women of child-bearing age. For them, AHSCT may have negative consequences for reproductive health, since the ovaries are particularly susceptible to alkylating agents. Anti-Müllerian hormone (AMH) reflects the ovarian reserve and has been suggested as a potential biomarker of fertility in women. The aim of this study was to investigate AMH levels in relation to age and reproductive potential in MS patients treated with AHSCT. The study cohort comprised 38 female patients, aged 20-44 years, who underwent AHSCT for MS using a cyclophosphamide (200 mg/kg)/rabbit-anti-thymocyte globulin (6 mg/kg) conditioning regimen between 2013-2020. Clinal follow-up visits were made 3 months after AHSCT and then yearly. AMH was analysed in blood samples. The median age at transplantation was 28 years (interquartile range, IQR 25-33). The median AMH concentration was 23 pmol/l at baseline (IQR 6.0-30), 0.5 pmol/l at 3 months (IQR 0-1.5) and 1.1 pmol/l at 2 years (IQR 0-2.9). A multiple linear regression model was used to determine if age and/or AHSCT influenced AMH values; both significantly did (age, -0.21 per year, p = 0.018; AHSCT -19, p <0.0001). Seven women became pregnant, six spontaneously and one both spontaneously and with IVF. One patient underwent an abortion, all other pregnancies led to live births. Six of the women became pregnant despite low or very low post-AHSCT serum concentrations of AMH, suggesting that low serum AMH concentrations do not necessarily reflect impaired fertility in patients treated with high-dose cyclophosphamide.
 BACKGROUND: Altered thalamic volumes and resting state (RS) functional connectivity (FC) might be associated with physical activity (PA) and cardiorespiratory fitness (CRF) in people with progressive multiple sclerosis (PMS). OBJECTIVES: To assess thalamic structural and functional alterations and investigate their correlations with PA/CRF levels in people with PMS. METHODS: Seven-day accelerometry and cardiopulmonary exercise testing were used to assess PA/CRF levels in 91 persons with PMS. They underwent 3.0 T structural and RS fMRI acquisition with 37 age/sex-matched healthy controls (HC). Between-group comparisons of MRI measures and their correlations with PA/CRF variables were assessed. RESULTS: PMS people had lower volumes compared to HC (all p < 0.001). At corrected threshold, PMS showed decreased intra- and inter-thalamic RS FC, and increased RS FC between the thalamus and the hippocampus, bilaterally. At uncorrected threshold, decreased thalamic RS FC with caudate nucleus, cerebellum and anterior cingulate cortex (ACC), as well as increased thalamic RS FC with occipital regions, were also detected. Lower CRF, measured as peak oxygen consumption (VO(2peak)), correlated with lower white matter volume (r = 0.31, p = 0.03). Moreover, lower levels of light PA correlated with increased thalamic RS FC with the right hippocampus (r = - 0.3, p = 0.05). DISCUSSION: People with PMS showed widespread brain atrophy, as well as pronounced intra-thalamic and thalamo-hippocampal RS FC abnormalities. White matter atrophy correlated with CRF, while increased thalamo-hippocampal RS FC was associated to worse PA levels. Thalamic RS FC might be used to monitor physical impairment and efficacy of rehabilitative and disease-modifying treatments in future studies.
 BACKGROUND: Ozanimod and ponesimod are sphingosine 1-phosphate receptor modulators approved by the U.S. Food and Drug Administration for treatment of relapsing forms of multiple sclerosis (MS). Given that no head-to-head trials have assessed these two treatments, we performed a matching-adjusted indirect comparison (MAIC) to compare efficacy and safety outcomes between ozanimod and ponesimod for MS. METHODS: A MAIC compared efficacy and safety of ozanimod and ponesimod at 2 years. Outcomes included annualized relapse rate (ARR) and percentage change from baseline in brain volume loss (BVL) as well as rates of any treatment-emergent adverse events (TEAEs), serious adverse events (AEs), AEs leading to discontinuation, and other safety outcomes. Individual patient-level data were obtained for ozanimod from the RADIANCE-B trial, while aggregate-level patient data were obtained for ponesimod from the OPTIMUM trial. The MAIC was not anchored owing to lack of a common comparator across the two trials. The following characteristics were matched between the trials' populations: age, sex, time since MS symptom onset, relapses in prior year, Expanded Disability Status Scale score, disease-modifying therapies received in the prior 2 years, absence of gadolinium-enhancing T1 lesions, and percentage of patients from Eastern Europe. RESULTS: After matching, key baseline characteristics were balanced between patients receiving ozanimod and ponesimod. Compared with ponesimod, ozanimod had a numerically lower ARR (rate ratio: 0.80 [95% CI: 0.57, 1.10]) and was associated with a significant reduction in BVL (% change difference: 0.20 [95% CI: 0.05, 0.36]). Additionally, ozanimod was associated with a significantly lower risk of TEAEs (risk difference: -11.9% [95% CI: -16.8%, -7.0%]), AEs leading to discontinuation (-6.1% [95% CI: -8.9%, -3.4%]), and lymphocyte count <0.2 K/μL (-2.3% [95% CI: -4.2%, -0.5%]). There were no statistically significant differences in the other safety outcomes. CONCLUSION: The MAIC results suggest that, compared with ponesimod, ozanimod is more effective in preserving brain volume, is comparable in terms of reducing relapse rates, and has a favorable safety profile.
 Reliable remote cognitive testing could provide a safer assessment of cognitive impairment in multiple sclerosis (MS) during the COVID-19 pandemic and thereafter. Here we aimed to investigate the reliability and feasibility of administering Brief International Cognitive Assessment for MS (BICAMS) and the Trail-Making Test (TMT) to people with MS online. Between-group differences on BICAMS and the TMT were examined in a sample of 68 participants. Group 1 (N = 34) was tested in-person pre-pandemic. Group 2 was tested remotely. Within-group differences for in-person and virtual administrations were examined for Group 1. No significant differences between virtual and in-person administrations of the CVLT-II and SDMT were detected. BVMT-R scores were significantly higher for virtual administrations (M = 20.59, SD = 6.65) compared to in-person administrations (M = 16.35, SD = 6.05), possibly indicating inter-rater differences. Strong positive correlations were found for in-person and virtual scores within Group 1 on the CVLT-II (r = .84), SDMT (r = .85), TMT-A (r = .88), TMT-B (r = .76) and BVMT-R (r = .72). No significant differences between in-person and remote administrations of CVLT-II and SDMT in people living with MS were detected. Recommendations for future studies employing the TMT and BVMT-R online are provided.
 BACKGROUND: Frontal cortico-subcortical dysfunction may contribute to fatigue and dual-task impairment of walking and cognition in progressive multiple sclerosis (PMS). PURPOSE: To explore the associations among fatigue, dual-task performance and structural and functional abnormalities of frontal cortico-subcortical network in PMS. METHODS: Brain 3 T structural and functional MRI sequences, Modified Fatigue Impact Scale (MFIS), dual-task motor and cognitive performances were obtained from 57 PMS patients and 10 healthy controls (HC). The associations of thalamic, caudate nucleus and dorsolateral prefrontal cortex (DLPFC) atrophy, microstructural abnormalities of their connections and their resting state effective connectivity (RS-EC) with fatigue and dual-task performance were investigated using random forest. RESULTS: Thirty-seven PMS patients were fatigued (F) (MFIS ≥ 38). Compared to HC, non-fatigued (nF) and F-PMS patients had significantly worse dual-task performance (p ≤ 0.002). Predictors of fatigue (out-of-bag [OOB]-accuracy = 0.754) and its severity (OOB-R(2) = 0.247) were higher Expanded Disability Status scale (EDSS) score, lower RS-EC from left-caudate nucleus to left-DLPFC, lower fractional anisotropy between left-caudate nucleus and left-thalamus, higher mean diffusivity between right-caudate nucleus and right-thalamus, and longer disease duration. Microstructural abnormalities in connections among thalami, caudate nuclei and DLPFC, mainly left-lateralized in nF-PMS and more bilateral in F-PMS, higher RS-EC from left-DLPFC to right-DLPFC in nF-PMS and lower RS-EC from left-caudate nucleus to left-DLPFC in F-PMS, higher EDSS score, higher WM lesion volume, and lower cortical volume predicted worse dual-task performances (OOB-R(2) from 0.426 to 0.530). CONCLUSIONS: In PMS, structural and functional frontal cortico-subcortical abnormalities contribute to fatigue and worse dual-task performance, with different patterns according to the presence of fatigue.

 BACKGROUND: Although cannabis has become an increasingly common method for pain management among people with multiple sclerosis (PwMS), there is a dearth of knowledge regarding the types of cannabis products used as well as the characteristics of cannabis users. The current study aimed to (1) describe the prevalence of cannabis use and the routes of administration of cannabis products in adults with an existing chronic pain condition and MS, (2) to examine differences in demographic and disease-related variables between cannabis users and non-users, and (3) to examine differences between cannabis users and non-users in pain-related variables, including pain intensity, pain interference, neuropathic pain, pain medication use, and pain-related coping. METHODS: Secondary analysis of baseline data from participants with multiple sclerosis (MS) and chronic pain (N = 242) enrolled in an RCT comparing mindfulness-based cognitive therapy (MBCT), cognitive-behavioral therapy (CBT), and usual care for chronic pain. Statistical methods included t-tests, Mann-Whitney tests, chi-square tests, and Fisher's exact tests to assess for differences in demographic, disease-related, and pain-related variables between cannabis users and non-users. RESULTS: Of the 242 participants included in the sample, 65 (27%) reported the use of cannabis for pain management. The most common route of administration was oil/tincture (reported by 42% of cannabis users), followed by vaped (22%) and edible (17%) products. Cannabis users were slightly younger than non-users (Med(age) 51.0 vs 55.0, p = .019) and reported higher median pain intensity scores (6.0 vs 5.0, p = .022), higher median pain interference scores (5.9 vs 5.4, p = .027), and higher median levels of neuropathic pain (20.0 vs 16.0, p = .001). CONCLUSIONS: The current study identified factors that may intersect with cannabis use for pain management and adds to our current knowledge of the types of cannabis products used by PwMS. Future research should continue to investigate trends in cannabis use for pain management, especially as the legality and availability of products continue to shift. Additionally, longitudinal studies are needed to examine the effects of cannabis use on pain-related outcomes over time.
 BACKGROUND: T lymphocytes exhibit numerous alterations in relapsing-remitting (RRMS), secondary progressive (SPMS), and primary progressive multiple sclerosis (PPMS). The NKG2D pathway has been involved in MS pathology. NKG2D is a co-activating receptor on subsets of CD4(+) and most CD8(+) T lymphocytes. The ligands of NKG2D are expressed at low levels in normal tissues but are elevated in MS postmortem brain tissues compared with controls. Whether the NKG2D pathway shows specific changes in different forms of MS remains unclear. METHODS: We performed unsupervised and supervised flow cytometry analysis to characterize peripheral blood T lymphocytes from RRMS, SPMS, and PPMS patients and healthy controls (HC). We used an in vitro microscopy approach to assess the role of NKG2D in the interactions between human CD8(+)T lymphocytes and human astrocytes. RESULTS: Specific CD8(+), CD4(+), and CD4(-)CD8(-) T cell populations exhibited altered frequency in MS patients' subgroups. The proportion of NKG2D(+) T lymphocytes declined with age in PPMS patients but not in RRMS and HC. This reduced percentage of NKG2D(+) cells was due to lower abundance of γδ and αβ CD4(-)CD8(-) T lymphocytes in PPMS patients. NKG2D(+) T lymphocytes were significantly less abundant in RRMS than in HC; this was caused by a decreased frequency of CD4(-)CD8(-) and CD8(+) T lymphocytes and was not linked to age. Blocking NKG2D increased the motility of CD8(+) T lymphocytes co-cultured with astrocytes expressing NKG2D ligand. Moreover, preventing NKG2D from interacting with its ligands increased the proportion of CD8(+) T lymphocytes exhibiting a kinapse-like behavior characterized by short-term interaction while reducing those displaying a long-lasting synapse-like behavior. These results support that NKG2D participates in the establishment of long-term interactions between activated CD8(+) T lymphocytes and astrocytes. CONCLUSION: Our data demonstrate specific alterations in NKG2D(+) T lymphocytes in MS patients' subgroups and suggest that NKG2D contributes to the interactions between human CD8(+) T lymphocytes and human astrocytes.
 BACKGROUND: Multiple sclerosis (MS) leads to demyelination and neurodegeneration with autoimmune responses in central nervous system. Patients begin with a relapsing-remitting (RR) course, and more than 80% of them may advance to secondary progressive MS (SPMS), which is characteristic for the gradual decline of neurological functions without demonstrated treating method to prevent. This study aims to investigate the contribution of peripheral CD8 + T cells during the conversion from RRMS to SPMS, as well as reveal potential diagnostic signature in distinguishing SPMS. METHODS: Single-cell RNA sequencing was employed to reveal the heterogeneity of CD8 + T cells between SPMS and RRMS. In addition, flow cytometry was used to further characterized CD8 + T cell dynamic changes in patients. T cell receptor sequencing was performed to detect the clonal expansion of MS. Using Tbx21 siRNA, T-bet was confirmed to manipulate GzmB expression. The correlation between GzmB + CD8 + T cell subsets and clinical characteristics of MS and their potential diagnostic value for SPMS were evaluated by generalized linear regression models and receiver operating characteristic (ROC) curve respectively. RESULTS: Other than diminished naïve CD8 + T cell, elevating of activated CD8 + T cell subsets were observed in SPMS patients. Meanwhile, this aberrant amplified peripheral CD8 + T cells not only exhibited terminal differentiated effector (EMRA) phenotype with GzmB expression, but also possessed distinct trajectory from clonal expansion. In addition, T-bet acted as a key transcriptional factor that elicited GzmB expression in CD8 + T(EMRA) cells of patients with SPMS. Finally, the expression of GzmB in CD8 + T cells was positively correlated with disability and progression of MS, and could effectively distinguish SPMS from RRMS with a high accuracy. CONCLUSIONS: Our study mapped peripheral immune cells of RRMS and SPMS patients and provided an evidence for the involvement of GzmB + CD8 + T(EMRA) cells in the progression of MS, which could be used as a diagnostic biomarker for distinguishing SPMS from RRMS.
 BACKGROUND: Falls are common among people living with multiple sclerosis (MS) who use wheelchairs or scooters. Falls may lead to severe consequences including physical injuries. However, very little is known about the circumstances associated with injurious falls in this population. Therefore, we aimed to explore the differences in fall-related characteristics between injurious and non-injurious falls among people with MS who use wheelchairs or scooters. METHODS: A convenience sample of 48 people with MS (age = 62.0 [13.0] years, gender = 81.3% female, primary mobility aid = power wheelchair) completed a fall-history survey that examined the characteristics and consequences of their most recent fall. Participants also completed standard questionnaires on quality of life, community participation, and fear of falling. RESULTS: Most falls (85.4%) reported by participants occurred inside the house. Twelve (25.0%) participants reported experiencing fall-related injuries such as bruises, cuts, muscle strains, and fractures. People who reported being injured after a fall had a higher proportion of falls that occurred during transfers compared to those who were not injured (n = 10, 83.3% vs n = 17, 47.2%). Most participants (45.8%) did not receive any information from healthcare professionals on how to manage their fall-risk after their fall experience. No differences between injurious and non-injurious fallers in quality of life, community participation, and fear of falling were observed. CONCLUSIONS: This cross-sectional investigation provides compelling evidence that people with MS who use wheelchairs or scooters are at high risk of fall-related injuries. The study findings underscore the importance of increasing health care providers' awareness about the frequency and consequences of falls. Further, it demonstrates the critical need for evidence-based interventions specifically designed to minimize fall-related injuries in this vulnerable population.
 OBJECTIVES AND AIMS: Quantitative MRI (qMRI) has greatly improved the sensitivity and specificity of microstructural brain pathology in multiple sclerosis (MS) when compared to conventional MRI (cMRI). More than cMRI, qMRI also provides means to assess pathology within the normal-appearing and lesion tissue. In this work, we further developed a method providing personalized quantitative T1 (qT1) abnormality maps in individual MS patients by modeling the age dependence of qT1 alterations. In addition, we assessed the relationship between qT1 abnormality maps and patients' disability, in order to evaluate the potential value of this measurement in clinical practice. METHODS: We included 119 MS patients (64 relapsing-remitting MS (RRMS), 34 secondary progressive MS (SPMS), 21 primary progressive MS (PPMS)), and 98 Healthy Controls (HC). All individuals underwent 3T MRI examinations, including Magnetization Prepared 2 Rapid Acquisition Gradient Echoes (MP2RAGE) for qT1 maps and High-Resolution 3D Fluid Attenuated Inversion Recovery (FLAIR) imaging. To calculate personalized qT1 abnormality maps, we compared qT1 in each brain voxel in MS patients to the average qT1 obtained in the same tissue (grey/white matter) and region of interest (ROI) in healthy controls, hereby providing individual voxel-based Z-score maps. The age dependence of qT1 in HC was modeled using linear polynomial regression. We computed the average qT1 Z-scores in white matter lesions (WMLs), normal-appearing white matter (NAWM), cortical grey matter lesions (GMcLs) and normal-appearing cortical grey matter (NAcGM). Lastly, a multiple linear regression (MLR) model with the backward selection including age, sex, disease duration, phenotype, lesion number, lesion volume and average Z-score (NAWM/NAcGM/WMLs/GMcLs) was used to assess the relationship between qT1 measures and clinical disability (evaluated with EDSS). RESULTS: The average qT1 Z-score was higher in WMLs than in NAWM. (WMLs: 1.366 ± 0.409, NAWM: -0.133 ± 0.288, [mean ± SD], p < 0.001). The average Z-score in NAWM in RRMS patients was significantly lower than in PPMS patients (p = 0.010). The MLR model showed a strong association between average qT1 Z-scores in white matter lesions (WMLs) and EDSS (R(2) = 0.549, β = 0.178, 97.5 % CI = 0.030 to 0.326, p = 0.019). Specifically, we measured a 26.9 % increase in EDSS per unit of qT1 Z-score in WMLs in RRMS patients (R(2) = 0.099, β = 0.269, 97.5 % CI = 0.078 to 0.461, p = 0.007). CONCLUSIONS: We showed that personalized qT1 abnormality maps in MS patients provide measures related to clinical disability, supporting the use of those maps in clinical practice.
 OBJECTIVE: To measure the knee range of motion (ROM) in the sagittal plane by video analysis in patients with multiple sclerosis (MS) after a course of medical rehabilitation and determine the minimal clinically important differences (MCID). MATERIAL AND METHODS: We examined 45 patients (37 women, 8 men) with relapsing-remitting (n=38) and secondary-progressive MS before and after a course of medical rehabilitation. Gait parameters were recorded on video analysis system Physiomed Smart («Physiomed», Germany, the Davis protocol). RESULTS: The course of complex medical rehabilitation contributes to an increase knee ROM in MS patients in a wide range of disability (EDSS <6.5 points). MCID is estimated as 7.14° in mild (EDSS ≤4.0) and as 7.67° in moderate (EDSS=4.5-5.5) gait impairment. CONCLUSION: The results will assist clinicians and researchers in interpreting the significance of observed kinematic changes in the knee joint in MS patients after medical intervention.
 BACKGROUND: Hispanics with multiple sclerosis (MS) experience disproportionate rates of mobility disability compared to non-Hispanic Whites with MS. Physical activity (PA) is highlighted as a potential adjuvant therapy for improving MS symptoms and disease progression, however less than 30% of Hispanics with MS report sufficient levels of PA. OBJECTIVES: The current study aimed to examine the correlates of PA behavior among Hispanics with MS in the North American Research Committee on Multiple Sclerosis Registry (NARCOMS). METHODS: In Spring 2015, 136 NARCOMS participants identified as Hispanic and completed the International Physical Activity Questionnaire (IPAQ). IPAQ scores were converted to Health Contribution Scores (HCS) for estimating PA. The association between the HCS scores and MS symptoms (i.e., mobility, cognition, fatigue, spasticity, hand function, bowel/bladder, sensory, tremors, depression, and pain), quality of life (QOL), comorbid conditions, and disability status were evaluated using Pearson or Spearman correlation coefficients with follow-up multivariable regression analyses. RESULTS: The mean age among participants was 58 years and 79% identified as female. The mean MS disease duration was 20 years and 68% reported relapsing disease course. The mean HCS score among participants was 15.6 ± 20.9. HCS was moderately associated with disability status (r(s) = -0.39), mobility (r(s) = -0.37), bowel/bladder function (r(s) = -0.33), and physical health related QOL (r = 0.32). There were small associations between HCS and hand function (r(s) = -0.29), fatigue (r(s) = -0.20), and tremor (r(s) = -0.25). Multivariable regression analyses indicated that disability status, mobility, bowel/bladder function, and physical health related QOL were all associated with HCS but did not independently contribute to the models when controlling for age, sex, and employment. CONCLUSIONS: This study highlights correlates of PA behavior among Hispanics with MS. Researchers and clinicians may consider disability status, mobility, and physical health related QOL in future studies examining PA among Hispanics with MS.
 Multiple Sclerosis (MS) is characterised by significant symptom diversity and complexity. The unpredictability of the symptoms and the emotional and cognitive facets of the disease have a significant impact on the patients' quality of life, relationships and other significant areas of living. Psychological interventions have been found to have moderate effects on quality of life, depression, stress reduction, improvement of wellbeing, anxiety, fatigue, sleep disturbances and emotion regulation. Most interventions so far are based on generic models of therapy which cannot always cover the complexity and unpredictability of MS. The present research project follows from an exploratory mixed method study on the experience of psychological interventions and the impact on the management of MS. The results of that study generated themes that led to the development of an integrative group psychological intervention named MyMS-Ally. The current study aims to explore the feasibility and acceptability of MyMS-Ally intervention and obtain preliminary data on the effects on quality of life, emotion regulation, depression and anxiety through the application of a convergent mixed methods design. People with MS will be recruited at the Bristol and Avon Multiple Sclerosis centre, North Bristol NHS Trust. They will participate in MyMS-Ally group intervention for 8 weeks. Individual semi-structured interviews drawing on Interpretative Phenomenological methodology will be conducted before and after the intervention and at three months follow up. Participants will complete quantitative measures on quality of life, emotion regulation, depression and anxiety before and after the intervention and at one and three months follow up. The aim is to explore the relevance, sustainability and adherence to the intervention and study processes (feasibility) as well as the appropriateness of the intervention based on the emotional and cognitive responses, satisfaction and perceived effectiveness (acceptability). It is aspired that this patient-centred psychological intervention will address needs and preferences of people with MS. The results of the present study will provide data for further development of the intervention and will lead to a big scale evaluation study.
 BACKGROUND: Multiple sclerosis (MS) is an inflammatory demyelinating condition of the central nervous system that leads to neurological disability and a poor quality of life (QoL). Rituximab has been used off-label in many countries to treat MS because of its high efficacy and affordability. However, there is no evidence of its effectiveness in Thailand. Therefore, the objective of this study was to evaluate the efficacy and additional benefits of rituximab in Thai patients with MS. METHODS: This was a prospective cohort study of patients diagnosed with MS who started treatment with rituximab between November 1, 2020, and October 31, 2022. Patients with MS eligible for the study received intravenous rituximab with a starting dose of 1000 mg at the first visit and another 1000 mg dose 2 weeks later. Thereafter, 1000 mg rituximab was administered every 6 months until the end of the study. The primary outcome was the annualized relapse rate (ARR). In addition, magnetic resonance imaging (MRI) activity of the gadolinium-enhancing lesion, QoL, number of hospital visits, and treatment costs were considered secondary outcomes. RESULTS: Ten patients diagnosed with relapsing-remitting multiple sclerosis were included in the study. The median ARR markedly decreased from 2.14 (0-4) to 0 (0-0.5) (p=0.005). The median Expanded Disability Status Scale score improved from 3.25 (1.5-6.0) to 1 (1-4) (p=0.005). The median number of enhancing lesions decreased from 1 (0-7) to 0 (0-3) (p=0.017). In addition, the median EuroQoL 5 Dimension 5 Level score, indicating QoL, improved from 0.7 (0.41-0.85) to 0.88 (0.68-1.00) (p=0.005). The median number of outpatient department visits significantly decreased from 6 (4-12) to 3 (2-5) (p=0.009). Hospitalization or inpatient department visits diminished from 1 (0-2) to 0 (0-1) (p=0.007). The total direct medical cost of rituximab treatment was not significantly different from that of the pre-treatment condition: 70,891 THB (65,391-116,358) VS 66,961 THB (33,927-109,248) or 1,904 USD (1,756-3,125 USD) VS 1,798 USD (911-2,934) (p=0.173). CONCLUSION: Rituximab was effective in the treatment of MS in Thailand. The use of rituximab reduced the number of relapses, reduced disability, decreased the number of active MRI lesions, and improved QoL. Moreover, the benefit of rituximab in treating MS in Thailand surpasses the current cost of treatment.
 BACKGROUND: Performance feedback is vital to rehabilitation interventions that treat cognitive impairments from multiple sclerosis (MS). Optimal treatment relies on participants' motivation to learn from feedback throughout these interventions. Cognitive fatigue, a prevalent symptom of MS, is associated with aberrant reward processing, which necessitates research into how fatigue affects perceived reward value of feedback in these individuals. The current study investigated how trait fatigue influences subjective valuation of feedback and subsequent feedback-seeking behavior in people with MS. METHODS: 33 MS and 32 neurotypical (NT) participants completed a willingness-to-pay associative memory paradigm that assessed feedback valuation via trial-by-trial decisions to either purchase or forego feedback in service of maximizing a performance-contingent monetary reward. Participant ratings of trait fatigue were also collected. Generalized logistic mixed modeling was used to analyze factors that influenced trial-wise feedback purchase decisions and task performance. RESULTS: Despite reporting greater trait fatigue, MS participants purchased comparable amounts of feedback as NT participants. Like NT participants, MS participants were more likely to purchase feedback when they were less confident about response accuracy. MS participants also performed comparably to NT participants, who both particularly benefited from purchase decisions that yielded negative feedback (i.e., indicating a response error). CONCLUSIONS: Trait cognitive fatigue may not impact performance feedback valuation in people with MS. Nonetheless, confidence in performance may drive their feedback-seeking behavior and may serve as a target for improving learning throughout cognitive rehabilitation and maximizing treatment success.
 OBJECTIVE: This study was conducted to evaluate the effectiveness of self-acupressure on quality of life, physical and cognitive functions in individuals with Relapsing-Remitting Multiple Sclerosis (RRMS). METHODS: In our randomized controlled study; participants in the study group were asked to perform self-acupressure on 6 points. They were asked to perform a total of 16 sessions, 2 days a week, for an average of 27 min each session in the morning and evening. No intervention was made in the control group during the study. Data were collected using Descriptive Information Form, Multiple Sclerosis Functional Composite Test (MSFC), and Multiple Sclerosis Quality of Life 54 Scale (MSQL-54). RESULTS: Thirty-one individuals with RRMS in each group, 25 women in the study group and 21 women in the control group, were included in the study. After the self-acupressure application, a positive and significant difference was detected in all MSFC sub-parameters (9-Hole Peg Test, Timed 25-foot Walk Test, Paced Auditory Serial Addition Test) values of the study group compared to the control group. In addition, after self-acupressure application, the study group was found to have statistically significantly higher scores in both the combined physical health and composite mental health sub-parameters of MSQOL-54 compared to the control group (p < 0.05). CONCLUSION: We found that self-acupressure was effective in improving physical function, cognitive function and quality of life in RRMS patients. Additionally, self-acupressure is a feasible, accessible and inexpensive method in the disease management of multiple sclerosis, which needs to be treated or supported continuously.
 BACKGROUND: The use of telemedicine has quickly increased during of the COVID-19 pandemic. Given that unmet needs and barriers to multiple sclerosis (MS) care have been reported, telemedicine has become an interesting option to the care of these patients. The objective of these consensus recommendations was to elaborate a guideline for the management of people with MS using telemedicine in order to contribute to an effective and high-quality healthcare. METHODS: A panel of Argentinean neurologist's experts in neuroimmunological diseases and dedicated to the diagnosis, management,and care of MS patients gathered virtually during 2021 and 2022 to conduct a consensus recommendation on the use of telemedicine in clinical practice in adult people with MS. To reach consensus, the methodology of "formal consensus RAND/UCLA Appropriateness method" was used. RESULTS: Recommendations were established based on relevant published evidence and expert opinion focusing on definitions, general characteristics and ethical standards, diagnosis of MS, follow-up (evaluation of disability and relapses of MS), identification and treatment of relapses, and finally disease-modifying treatments using telemedicine. CONCLUSION: The recommendations of this consensus would provide a useful guide for the proper use of telemedicine for the assessment, follow-up, management, and treatment of people with MS. We suggest the use of these guidelines to all the Argentine neurologists committed to the care of people with MS.
 BACKGROUND: Cognitive impairment (CI) is prevalent in Chinese patients with relapsing-remitting multiple sclerosis (RRMS). METHODS: A decision analytic model was constructed to simulate Chinese patients with newly diagnosed RRMS and their matched control cohort without MS for the risks of developing CI, developing secondary progressive MS (SPMS), and mortality. Both English and Chinese bibliographic databases were searched for evidence to estimate model inputs. Base case analysis and sensitivity analysis were conducted for the point estimations and uncertainty of the measured burden outcomes. RESULTS: Model simulations estimated that the lifetime cumulative risk of CI in newly diagnosed RRMS patients was 85.2%. Relative to the matched control cohort, newly diagnosed RRMS patients were associated with a lower life expectancy (33.2 years vs. 41.7 years, difference: -8.5 years), lower quality-adjusted life years (QALY) (18.4 QALY vs. 38.4 QALY, difference: -19.9 QALY), and higher lifetime medical costs (¥613,883 vs. ¥202,726, difference: ¥411,157) and indirect costs (¥1,099,021 vs. ¥94,612, difference: ¥1,004,410). Patients who developed CI accounted for at least half of the measured burden. The disease burden outcomes were mainly driven by the risk of developing CI, progression risk from RRMS to SPMS, hazard ratios of mortality associated with CI relative to no CI, utility of patients with RRMS, annual relapse risk, and annual costs of personal care. CONCLUSION: Most Chinese patients with newly diagnosed RRMS are likely to develop CI in their lifetime, and such patients that develop CI could significantly contribute to the disease burden of RRMS.
 AIM: The aim of this study was to identify whether NfL and CXCL13 cerebrospinal fluid (CSF) concentrations at diagnostic lumbar puncture can predict the course of multiple sclerosis (MS) in terms of relapses, higher expanded disability status scale (EDSS) and magnetic resonance imaging (MRI) activity. METHODS: We conducted a single-centre prospective observational cohort study at the MS center, University Hospital Ostrava, Czech Republic. CSF NfL (cNfL) and CXCL13 concentrations were examined (ELISA method) in patients with clinically isolated syndrome (CIS) and relapsing-remitting MS (RRMS) at the time of diagnostic lumbar puncture. RESULTS: A total of 44 patients with CIS or early RRMS were enrolled, 31 (70.5%) of whom were women. The median age at the time of CSF sampling was 31.21 years (IQR 25.43-39.32), and the follow-up period was 54.6 months (IQR 44.03-59.48). In the simple and multiple logistic regression models, CXCL13 levels did not predict relapses, MRI activity or EDSS > 2.5. Similarly, cNfL concentrations did not predict relapses or MRI activity in either model. In the multiple regression, higher cNfL levels were associated with reaching EDSS > 2.5 (odds ratio [OR] 1.002, 95% confidence interval [CI] 1.000 to 1.003). CONCLUSIONS: Our data did not confirm cNfL and/or CXCL13 CSF levels were predictive factors for disease activity such as relapses and MRI activity at the time of diagnostic lumbar puncture in patients with RRMS. While cNfL CSF levels predicted higher disability only after adjustment for other known risk factors, elevated CSF CXCL13 did not predict higher disability at all.
 Interferon (IFN)-β-1a (Avonex) and longer half-life, polyethylene glycol-conjugated IFN-β-1a (PEG-IFN-β-1a, Plegridy), may generate different molecular responses. We identified different short-term and long-term in vivo global RNA signatures of IFN-stimulated genes in multiple sclerosis (MS) peripheral blood mononuclear cells and in selected paired serum immune proteins. At 6 h, non-PEGylated IFN-β-1a injection upregulated expression of 136 genes and PEG-IFN-β-1a upregulated 85. At 24 h, induction was maximal; IFN-β-1a upregulated 476 genes and PEG-IFN-β-1a now upregulated 598. Long-term PEG-IFN-β-1a therapy increased expression of antiviral and immune-regulatory genes (IFIH1, TLR8, IRF5, TNFSF10 [TRAIL], STAT3, JAK2, IL15, and RB1) and IFN signaling pathways (IFNB1, IFNA2, IFNG, IRF7), but downregulated expression of inflammatory genes (TNF, IL1B, and SMAD7). Long-term PEG-IFN-β-1a induced longer and stronger expression of Th1, Th2, Th17, chemokine, and antiviral proteins than long-term IFN-β-1a. Long-term therapy also primed the immune system, evoking higher gene and protein induction after IFN reinjection at 7 months than at 1 month of PEG-IFN-β-1a treatment. Both forms of IFN-β balanced correlations of expression among these genes and proteins, with positive correlations between Th1 and Th2 families, quelling the "cytokine storm" of untreated MS. Both IFNs induced long-term, potentially beneficial, molecular effects on immune and possibly neuroprotective pathways in MS.
 INTRODUCTION: Diroximel fumarate (DRF), ponesimod (PON), and teriflunomide (TERI) are oral disease-modifying therapies approved for the treatment of relapsing multiple sclerosis. No randomized trials have compared DRF versus PON or TERI. OBJECTIVES: The objectives of this analysis were to compare DRF versus PON and DRF versus TERI for clinical and radiological outcomes. METHODS: We used individual patient data from EVOLVE-MS-1, a 2-year, open-label, single-arm, phase III trial of DRF (n = 1057), and aggregated data from OPTIMUM, a 2-year, double-blind, phase III trial comparing PON (n = 567) and TERI (n = 566). To account for cross-trial differences, EVOLVE-MS-1 data were weighted to match OPTIMUM's average baseline characteristics using an unanchored matching-adjusted indirect comparison. We examined the outcomes of annualized relapse rate (ARR), 12-week confirmed disability progression (CDP), 24-week CDP, absence of gadolinium-enhancing (Gd+) T1 lesions, and absence of new/newly enlarging T2 lesions. RESULTS: After weighting, we did not observe strong evidence of differences between DRF and PON for ARR [DRF versus PON incidence rate difference (IRD) -0.02; 95% confidence interval (CI) -0.08, 0.04; incidence rate ratio (IRR) 0.92; 95% CI 0.61, 1.2], 12-week CDP [risk difference (RD) -2.5%; 95% CI -6.3, 1.2; risk ratio (RR) 0.76; 95% CI 0.38, 1.1], 24-week CDP (RD -2.7%; 95% CI -6.0, 0.63; RR 0.68; 95% CI 0.28, 1.0), and absence of new/newly enlarging T2 lesions (RD -2.5%; 95% CI -13, 7.4; RR 0.94; 95% CI 0.70, 1.2). However, a higher proportion of DRF-treated patients were free of Gd+ T1 lesions than PON-treated patients (RD 11%; 95% CI 6.0, 16; RR 1.1; 95% CI 1.06, 1.2). Compared with TERI, DRF showed improved ARR (IRD -0.08; 95% CI -0.15, -0.01; IRR 0.74; 95% CI 0.50, 0.94), 12-week CDP (RD -4.2%; 95% CI -7.9, -0.48; RR 0.67; 95% CI 0.38, 0.90), 24-week CDP (RD -4.3%; 95% CI -7.7, -1.1; RR 0.57; 95% CI 0.26, 0.81), and absence of Gd+ T1 lesions (RD 25%; 95% CI 19, 30; RR 1.4; 95% CI 1.3, 1.5). However, DRF and TERI did not appear to differ significantly with respect to absence of new/newly enlarging T2 lesions when based on comparisons using the overall EVOLVE-MS-1 sample (RD 8.5%; 95% CI -0.93, 18; RR 1.3; 95% CI 0.94, 1.6), or in a sensitivity analysis restricted to newly enrolled EVOLVE-MS-1 patients (RD 2.7%; 95% CI -9.1, 14; RR 1.1; 95% CI 0.68, 1.5). CONCLUSIONS: We did not observe differences between DRF and PON for ARR, CDP, and absence of new/newly enlarging T2 lesions, but there was a higher proportion of patients free of Gd+ T1 lesions among DRF-treated patients than PON-treated patients. DRF had improved efficacy versus TERI for all clinical and radiological outcomes, except for absence of new/newly enlarging T2 lesions. CLINICAL TRIALS REGISTRATION: EVOLVE-MS-1 (ClinicalTrials.gov identifier: NCT02634307); OPTIMUM (ClinicalTrials.gov identifier: NCT02425644).

 BACKGROUND: Natalizumab is effective in the treatment of multiple sclerosis (MS). In 2021, the European Medicines Agency approved the subcutaneous (SC) variant of natalizumab which can be used instead of intravenous administration. However, the course of drug levels varies between administration routes, and the Food and Drug Administration rejected the request for approval of natalizumab SC for reasons that were not disclosed. Our objective was to evaluate the course of natalizumab trough drug levels in patients who switched from natalizumab intravenous to SC on various treatment intervals. METHODS: The NEXT-MS trial (N=382) investigates personalised treatment of natalizumab, in which infusion intervals are prolonged based on individual natalizumab trough drug levels. In 2021, an amendment was approved allowing participants to switch from intravenous to SC administration with frequent measurements of natalizumab drug levels and antidrug antibodies (ADAs). Results were compared with linear mixed model analyses. RESULTS: Until December 2022, 15 participants switched to SC natalizumab. Natalizumab drug levels with SC administration were on average 55% lower compared with intravenous administration (Exp (estimate) 0.45, 95% CI 0.39 to 0.53, p<0.001), leading to very low trough drug levels in three patients on extended treatment intervals. No natalizumab ADAs were detected during intravenous or SC treatment. None of the participants on natalizumab SC showed evidence of MS disease activity. CONCLUSIONS: Natalizumab trough drug levels can decrease after switching from natalizumab intravenous to SC administration. We advise to monitor trough drug levels in patients with low natalizumab drug levels during intravenous treatment, patients with higher body mass index or patients on extended treatment intervals who switch to SC administration of natalizumab.
 This study was done to evaluate the diagnostic accuracy of cerebrospinal fluid kappa free light chain (KFLC) for diagnosis of multiple sclerosis, against isoelectrofocusing (IEF) to detect oligoclonal bands (OCB) as gold standard. 64 cases were divided into positive and negative based on the OCB results. Diagnostic accuracy was calculated for the 1 mg/L cut-off. The 1 mg/L cut-off yielded a percent agreement of 86.1% and Cohen's kappa value of 0.8. Youden's index, yielded a cut-off of 0.92 mg/L as optimal (90.3% specificity and 90.9% sensitivity). The analytical time was 3 hours and 55 min for IEF and 25 min for KFLC. The cost of a single OCB test was PKR12 000 (US$68.17) compared with PKR4150 (US$23.58) for KFLC. KFLC proved to be an accurate, cheaper and time-saving alternative and can be performed prior to the contemporary testing.
 BACKGROUND: Healthcare utilization and satisfaction are important for health outcomes among people living with multiple sclerosis (PwMS). However, there is little current evidence around healthcare utilization among PwMS, and less comparing PwMS to those not living with MS. OBJECTIVE: To evaluate healthcare utilization and satisfaction among Understanding MS online course enrolees and to identify factors associated with healthcare satisfaction. METHOD: In this international cross-sectional study, we evaluated participant characteristics (including health literacy and quality of life), healthcare utilization (number of visits, number of provider types), and satisfaction with healthcare (perceived healthcare sufficiency, quality, accessibility) among enrolees in the Understanding MS online course (N = 1068). We evaluated study outcomes using summary statistics. We compared participant characteristics and study outcomes between PwMS and those not living with MS using chi square and t-tests. RESULTS: In this study cohort, PwMS were older, less likely to have a university degree, had lower health literacy, and lower quality of life. PwMS had significantly more healthcare visits in the previous year and visited a more diverse range of provider types than those not living with MS. PwMS were also more likely to report being satisfied with the healthcare they received. Among both PwMS and those not living with MS, higher health literacy and higher healthcare utilization were significantly associated with satisfaction with healthcare sufficiency, quality, and accessibility. CONCLUSION: PwMS were more likely to be satisfied with the healthcare they received compared to those not living with MS. This may be due in part to the differences in health literacy and healthcare utilization between the two groups. We recommend that these relationships be rigorously assessed in future research.
 BACKGROUND: The QuantiFERON®-Monitor (QFM) is an assay that measures interferon-γ production and was developed to provide an objective marker of complex immune response. In this study, we evaluated the use of the QFM test in patients with two forms of multiple sclerosis (MS), relapsing-remitting form treated with fingolimod (fMS) and secondarily progressive form not treated pharmacologically (pMS), and in healthy controls (HC). We hypothesized that IFN-γ levels would be lower in those subjects who are relatively more immunosuppressed and higher in those with normal or activated immune function. METHODS: This single-center observational study was conducted from November 2020 to October 2021 and compared results in three groups of patients: 86 healthy controls, 96 patients with pMS, and 78 fMS. Combination of lyophilized stimulants was added to 1 ml heparinized whole blood within 8 hr of collection. Plasmatic IFN-γ was measured using the ELISA kit for the QFM and data were obtained in IU/ml. RESULTS: The results showed that controls had nearly 2-fold higher levels of IFN-γ (QFM score) in median (q25, q75) 228.00 (112.20, 358.67) than the MS patient groups: pMS 144.80 (31.23, 302.00); fMS 130.50 (39.95, 217.07) which is statistically significant difference P-value: HC vs. pMS = 0.0071; HC vs. fMS = 0.0468. This result was also confirmed by a validation analysis to exclude impact of variable factors, such as disease duration and Expanded Disability Status Scale scores. CONCLUSIONS: Results showed that controls had higher levels of IFN-γ production than the MS patient groups and suggest that MS patients included in this study have a lower ability of immune system activation than HC. Results confirm that fingolimod is able to suppress production of IFN-γ. The fact that the QFM score of MS patients is significantly lower than that of HC may indicate a dysfunctional state of the immune system in baseline conditions.
 OBJECTIVE: Cognitive impairment (CI) and executive dysfunction (ED) are prevalent in patients with multiple sclerosis (PwMS). The Minimal Assessment of Cognitive Function in Multiple Sclerosis (MACFIMS) is the gold standard neuropsychological battery (NPB) for detecting CI. Delis-Kaplan Executive Function System (DKEFS) NPB evaluates ED. We aimed to find practical test(s) from DKEFS with acceptable diagnostic utility for early detection of impairment in cognitive and executive domains. METHODS: Cognitive and executive tasks, physical disability, and depression scores of 30 PwMS were assessed (17 women, age: 38.1). Symbol Digit Modalities Test (SDMT), Paced Auditory Serial Addition Test (PASAT), and Controlled Oral Word Association Test (COWAT) from MACFIMS and Trail Making Test (TMT), Design Fluency Test (DFT), and Verbal Fluency Test (VFT) from DKEFS were selected. The association between patients' characteristics and performance in tests, and diagnostic accuracy of DKEFS tests in detecting impairment in cognitive tasks were evaluated, using Pearson correlation and receiver operator characteristic curve analyses, respectively. RESULTS: A significant correlation was found between disease duration and SDMT and TMT subtests. Expanded Disability Status Scale was significantly related to SDMT, VFT-switching, and TMT subtests. Beck Depression Inventory was significantly related to DFT. TMT-switching detected abnormalities in SDMT and PASAT with 100% sensitivity, 93.3% (for SDMT), and 85.7% specificity (for PASAT). TMT-letter showed 100% sensitivity and 90% specificity in identifying abnormalities in COWAT. CONCLUSIONS: TMT, particularly the switching condition, is a practical paper-based test that could predict impairment in cognitive tasks. Clinicians may use TMT as a screening tool among PwMS.
 PURPOSE: Genetic studies of multiple sclerosis (MS) susceptibility and severity have focused on populations of European ancestry. Studying MS genetics in other ancestral groups is necessary to determine the generalisability of these findings. The genetic Association study in individuals from Diverse Ancestral backgrounds with Multiple Sclerosis (ADAMS) project aims to gather genetic and phenotypic data on a large cohort of ancestrally-diverse individuals with MS living in the UK. PARTICIPANTS: Adults with self-reported MS from diverse ancestral backgrounds. Recruitment is via clinical sites, online (https://app.mantal.co.uk/adams) or the UK MS Register. We are collecting demographic and phenotypic data using a baseline questionnaire and subsequent healthcare record linkage. We are collecting DNA from participants using saliva kits (Oragene-600) and genotyping using the Illumina Global Screening Array V.3. FINDINGS TO DATE: As of 3 January 2023, we have recruited 682 participants (n=446 online, n=55 via sites, n=181 via the UK MS Register). Of this initial cohort, 71.2% of participants are female, with a median age of 44.9 years at recruitment. Over 60% of the cohort are non-white British, with 23.5% identifying as Asian or Asian British, 16.2% as Black, African, Caribbean or Black British and 20.9% identifying as having mixed or other backgrounds. The median age at first symptom is 28 years, and median age at diagnosis is 32 years. 76.8% have relapsing-remitting MS, and 13.5% have secondary progressive MS. FUTURE PLANS: Recruitment will continue over the next 10 years. Genotyping and genetic data quality control are ongoing. Within the next 3 years, we aim to perform initial genetic analyses of susceptibility and severity with a view to replicating the findings from European-ancestry studies. In the long term, genetic data will be combined with other datasets to further cross-ancestry genetic discoveries.
 BACKGROUND: Cognitive difficulties experienced by people with multiple sclerosis (MS) impact on quality of life and daily functioning, from childcare and work to social and self-care activities. The Cognitive Occupation-Based programme for people with MS (COB-MS) was developed as a holistic, individualised cognitive rehabilitation intervention to address the wide-ranging symptoms and functional difficulties that present in MS, including the ability to maintain employment, social activities, home management and self-care. The aim of the research is to evaluate the feasibility and preliminary efficacy of COB-MS for people with MS. METHODS: Due to the impacts of COVID-19, trial activities that were planned for in-person delivery were completed remotely. One hundred and twenty people with MS will be assigned to participate in either the COB-MS programme or a treatment-as-usual, wait-list control group as part of this single-blind, cluster-randomised controlled feasibility and preliminary efficacy trial of the COB-MS programme. The COB-MS group will participate in an eight-session occupational-based cognitive rehabilitation programme over 9 weeks. The COB-MS intervention was planned for in-person delivery but was delivered online by occupational therapists to small groups of people with MS. The primary outcome measure is the Goal Attainment Scaling at 12 weeks. Participants will be assessed pre-intervention, post-intervention, 12 weeks post-intervention and 6 months post-intervention. Qualitative evaluations of participants' perspectives will also be examined as part of the feasibility study. Data, due to be collected in-person, was collected online or by post. The original study design, including the statistical analysis plan, remains unchanged despite the shift to a remote trial conduct. DISCUSSION: Results will provide recommendations for a future definitive trial of COB-MS, with respect to both feasibility and preliminary, clinical efficacy. TRIAL REGISTRATION: ISRCTN ISRCTN11462710 . Registered on 9 September 2019 and updated on 23 September 2020 to account for changes outlined here.
 Multiple sclerosis (MS) presents a high prevalence, a marked increase worldwide, and a relevant impact on patients, public health, and society. Anxiety often cooccurs with MS and can contribute to the worsening of MS symptoms. However, knowledge about predictors of anxiety in Patients with MS (PwMS) is scarce. OBJECTIVE: This preliminary study explored a novel model for anxiety symptoms in PwMS, including neuropathic pain (NeP), cognitive fusion (CF), experiential avoidance (EA), and alexithymia as explanatory factors. METHOD: This cross-sectional study integrated two independent convenience samples: 107 PwMS recruited from the Portuguese Society for Multiple Sclerosis and 97 age- and gender-matched participants without the MS diagnosis (no-MS sample) recruited from the Portuguese general population. Self-report questionnaires that measured the constructs included in the model were administered to both groups. RESULTS: PwMS showed significantly higher values regarding anxiety symptoms and their explanatory variables (NeP, CF, EA, alexithymia) in comparison to non-MS participants. In the MS sample, no correlations were found between anxiety symptoms and sociodemographic and clinical characteristics. NeP, CF, and alexithymia showed significant correlations with anxiety symptoms and significantly explained this symptomatology in simple linear regression models. Thus, these variables were retained in the multiple linear regression model and emerged as significant regressors that together explained 38% of the variance in anxious symptomatology in PwMS. CONCLUSIONS: This preliminary study provides novel evidence on NeP and some maladaptive emotion regulation strategies related to EA/psychological inflexibility, as vulnerability to anxiety in PwMS can be considerably increased by CF and alexithymia. Clinical implications were discussed.
 OBJECTIVES: To evaluate medication adherence to oral and parenteral disease-modifying therapies (DMTs) and to explore factors associated with medication non-adherence in patients with multiple sclerosis (MS). METHODS: A cross-sectional multicentre study was conducted among patients with MS. Patients who attended outpatient clinics of neurology departments from three major referral centres were invited to participate in the study. Medication adherence was measured using the Multiple Sclerosis Treatment Adherence Questionnaire. KEY FINDINGS: A total of 319 patients with MS on DMT were included in the final analyses, their average age was 35 years and more than two-thirds (72.1%) of them were women. The adherent group comprised 46.7% of patients. The results of association analyses showed that factors that were associated with adherence level were female gender (P = 0.034), non-smoking/x-smoking (P = 0.007), school education (P = 0.019), unemployment (P = 0.006), history of previous DMT (P = 0.020), longer previous treatment duration (P = 0.008), and type of current DMT (P = 0.020). Among the non-adherent patients, there were significant differences between oral and parenteral DMT users in the importance of barriers to adherence (P < 0.001). Additionally, the degree of treatment satisfaction was higher in oral users than in parenteral users (P < 0.001). CONCLUSIONS: The adherence level was quite low. Gender, smoking status, education, employment status, history of previous DMT, previous treatment duration and type of current DMT were associated with medication non-adherence in our patients with MS. These factors should be considered when evaluating medication adherence, and the modifiable factors may represent potential targets for interventions to improve pharmaceutical care planning in patients with MS.
 Mesenchymal stem cell-neural progenitors (MSC-NP) are a neural derivative of MSCs that are being investigated in clinical trials as an autologous intrathecal cell therapy to treat patients with secondary progressive (SP) or primary progressive (PP) multiple sclerosis (MS). MSC-NPs promote tissue repair through paracrine mechanisms, however which secreted factors mediate the therapeutic potential of MSC-NPs and how this cell population differs from MSCs remain poorly understood. The objective of this study was to define the transcriptional profile of MSCs and MSC-NPs from MS and non-MS donors to better characterize each cell population. MSCs derived from SPMS, PPMS, or non-MS bone marrow donors demonstrated minimal differential gene expression, despite differences in disease status. MSC-NPs from both MS and non-MS-donors exhibited significant differential gene expression compared to MSCs, with 2,156 and 1,467 genes upregulated and downregulated, respectively. Gene ontology analysis demonstrated pronounced downregulation of cell cycle genes in MSC-NPs compared to MSC consistent with reduced proliferation of MSC-NPs in vitro. In addition, MSC-NPs demonstrated significant enrichment of genes involved in cell signaling, cell communication, neuronal differentiation, chemotaxis, migration, and complement activation. These findings suggest that increased cell signaling and chemotactic capability of MSC-NPs may support their therapeutic potential in MS.
 CSF1R-related leukoencephalopathy is an autosomal dominant neurologic disorder causing microglial dysfunction with a wide range of neurologic complications, including motor dysfunction, dementia, and seizures. This case report highlights an unusual presentation of CSF1R-related leukoencephalopathy with radiographic spinal cord involvement initially diagnosed as multiple sclerosis. This case highlights the importance of considering adult-onset neurogenetic disorders in the setting of white matter disease. Genetic testing provides a confirmatory diagnosis for an expanding number of adult-onset leukoencephalopathies and informs therapeutic decision-making.
 BACKGROUND AND PURPOSE: There is an absence of data from large population-based cohort studies on the incidence of radiologically isolated syndrome (RIS). The incidence of RIS and the subsequent risk for multiple sclerosis (MS) were investigated. METHODS: A population-based, retrospective cohort study was conducted using a data-lake-based analysis of digitalized radiology reports. All brain and spinal cord magnetic resonance imaging (MRI) in people aged 16-70 during the years 2005-2010 (n = 102,224) were screened using optimized search terms to detect cases with RIS. The subjects with RIS were followed up until January 2022. RESULTS: The cumulative incidence of RIS was 0.03% when all MRI modalities were included and 0.06% when only brain MRI was included according to MAGNIMS 2018 recommendation criteria. With the Okuda 2009 criteria, the respective figures were 0.03% and 0.05% (86% concordance). The overall risk for MS after RIS was similar, 32% by using the MAGNIMS and 32% by using the Okuda definition of RIS. Individuals aged <35.5 years exhibited the most significant predisposition to MS (80%), whilst those >35.5 years had less than 10% risk of MS. MS diagnosed after RIS constituted 0.8% of the incident MS cases in the population during 2005-2010. CONCLUSIONS: A population-wide context was provided for the incidence of RIS and its relationship to MS. MAGNIMS recommendations were only slightly more sensitive to detect RIS compared to the Okuda criteria. RIS has a subtle effect on the overall incidence of MS, yet the risk for MS in individuals under the age of 35.5 years is substantial.
 BACKGROUND: Multiple sclerosis (MS) is traditionally managed using disease-modifying pharmaceutical therapies as a first line approach for treatment, yet there is increasing interest in lifestyle factors, particularly diet, for managing disease outcomes. Lutein has neuroprotective properties in healthy adults, but no previous research has examined the effects of lutein supplementation in persons with MS. OBJECTIVES: This study aimed to investigate the efficacy of 4-mo lutein supplementation on carotenoid status and cognition in persons with relapse-remitting MS (RRMS). METHODS: A randomized controlled, single-blind research design was used among adults with RRMS (N = 21). Participants were randomized into placebo (n = 9) or treatment (20-mg/d lutein, n = 12) groups with outcomes measured before and after 4 mo. Macular pigment optical density (MPOD) was assessed using heterochromatic flicker photometry. Skin carotenoids were assessed using reflection spectroscopy. Serum lutein was measured using high-performance liquid chromatography. Cognition was assessed via the Eriksen flanker with event-related potentials, spatial reconstruction, and the symbol digit modalities tests. RESULTS: There was a significant group by time interaction for MPOD (F = 6.74, P = 0.02), skin carotenoids (F = 17.30, P < 0.01), and serum lutein (F = 24.10, P < 0.01), whereby the treatment group improved in all carotenoid outcomes. There were no significant group by time interactions for cognitive and neuroelectric outcomes. However, increase in MPOD was positively associated with accuracy during the flanker incongruent trials (r = 0.55, P = 0.03) and the spatial memory task (r = 0.58, P = 0.02) among treatment participants. CONCLUSIONS: Lutein supplementation increases carotenoid status among persons with RRMS. There is no significant effect on cognitive function but change in macular carotenoids is selectively associated with improved attention and memory. This study provides preliminary support for a fully powered study targeting retinal and neural carotenoids for cognitive benefits in persons with MS. This trial was registered at clinicaltrials.gov as NCT04843813.
 BACKGROUND: As disease-modifying therapies do not reverse the course of multiple sclerosis (MS), assessment of therapeutic success involves documenting patient-reported outcomes (PROs) concerning health-related quality of life, disease and treatment-related symptoms, and the impact of symptoms on function. Interpreting PRO data involves going beyond statistical significance to calculate within-patient meaningful change scores. These thresholds are needed for each PRO in order to fully interpret the PRO data. This analysis of PRO data from the PROMiS AUBAGIO study, which utilized 8 PRO instruments in teriflunomide-treated relapsing-remitting MS (RRMS) patients, was designed to estimate clinically meaningful within-individual improvement thresholds in the same manner, for 8 PRO instruments. RESULTS: The analytical approach followed a triangulation exercise that considered results from anchor- and distribution-based methods and graphical representations of empirical cumulative distribution functions in PRO scores in groups defined by anchor variables. Data from 8 PRO instruments (MSIS-29 v2, FSMC, MSPS, MSNQ, TSQM v1.4, PDDS, HRPQ-MS v2, and HADS) were assessed from 434 RRMS patients. For MSIS-29 v2, FSMC, MSPS, and MSNQ total scores, available anchor variables enabled both anchor- and distribution-based methods to be applied. For instruments with no appropriate anchor available, distribution-based methods were applied. A recommended value for meaningful within-individual improvement was defined by comparing mean change in PRO scores between participants showing improvement of one or two categories in the anchor variable or those showing no change. A "lower bound" estimate was calculated using distribution-based methods. An improvement greater than the lower-bound estimate was considered "clinically meaningful". CONCLUSION: This analysis produced estimates for assessing meaningful within-individual improvements for 8 PRO instruments used in MS studies. These estimates should be useful for interpreting scores and communicating study results and should facilitate decision-making by regulatory and healthcare authorities where these 8 PROs are commonly employed.
 BACKGROUND: There are currently no specific biomarkers for multiple sclerosis (MS). Identifying robust biomarkers for MS is crucial to improve disease diagnosis and management. METHODS: This study first used six Mendelian randomisation methods to assess causal relationship of 174 metabolites with MS, incorporating data from European-ancestry metabolomics (n=8569-86 507) and MS (n=14 802 MS cases, 26 703 controls) genomewide association studies. Genetic scores for identified causal metabolite(s) were then computed to predict MS disability progression in an independent longitudinal cohort (AusLong study) of 203 MS cases with up to 15-year follow-up. RESULTS: We found a novel genetic causal effect of serine on MS onset (OR=1.67, 95% CI 1.51 to 1.84, p=1.73×10(-20)), such that individuals whose serine level is 1 SD above the population mean will have 1.67 times the risk of developing MS. This is robust across all sensitivity methods (OR ranges from 1.49 to 1.67). In an independent longitudinal MS cohort, we then constructed time-dynamic and time-fixed genetic scores based on serine genetic instrument single-nucleotide polymorphisms, where higher scores for raised serum serine level were associated with increased risk of disability worsening, especially in the time-dynamic model (RR=1.25, 95% CI 1.10 to 1.42, p=7.52×10(-4)). CONCLUSIONS: These findings support investigating serine as an important candidate biomarker for MS onset and disability progression.
 BACKGROUND: Paramagnetic rim lesions (PRLs) and slowly expanding lesions (SELs) have been posited as markers of chronic active lesions (CALs). OBJECTIVE: To assess the lesion-level concordance of PRLs and SELs in MS and to characterize changes in brain tissue integrity in CALs over time. METHODS: MRIs were analyzed from a substudy of AFFINITY [NCT03222973], a phase 2 trial of opicinumab in relapsing MS. Assessments included (1) identification of SELs based on longitudinal MRIs over 72 weeks, and identification of PRLs on susceptibility-weighted imaging (SWI) filtered phase images at week 72; (2) evaluation of subject-level correlation of SEL and PRL counts, volumes, and degree of lesion-level overlap between SELs and PRLs; and (3) characterization of tissue integrity over time in overlapping and non-overlapping SELs and PRLs. RESULTS: In 41 subjects, 119 chronic PRLs and 267 SELs were detected. Of 119 (39.5%) chronic PRLs, 47 co-localized with a SEL; 46/267 (17.2%) SELs co-localized with a PRL. PRLs co-localized with SELs showed expansion and worsening microstructural damage over time. SELs with and without co-localization with PRLs showed ongoing tissue damage. CONCLUSIONS: Chronic MS lesions identified as both PRL and SEL were associated with the most severe accumulation of tissue damage. TRIAL REGISTRATION: AFFINITY [NCT03222973].
 Automated co-registration and subtraction techniques have been shown to be useful in the assessment of longitudinal changes in multiple sclerosis (MS) lesion burden, but the majority depend on T2-fluid-attenuated inversion recovery sequences. We aimed to investigate the use of a novel automated temporal color complement imaging (CCI) map overlapped on 3D double inversion recovery (DIR), and to assess its diagnostic performance for detecting disease progression in patients with multiple sclerosis (MS) as compared to standard review of serial 3D DIR images. We developed a fully automated system that co-registers and compares baseline to follow-up 3D DIR images and outputs a pseudo-color RGB map in which red pixels indicate increased intensity values in the follow-up image (i.e., progression; new/enlarging lesion), blue-green pixels represent decreased intensity values (i.e., disappearing/shrinking lesion), and gray-scale pixels reflect unchanged intensity values. Three neuroradiologists blinded to clinical information independently reviewed each patient using standard DIR images alone and using CCI maps based on DIR images at two separate exams. Seventy-six follow-up examinations from 60 consecutive MS patients who underwent standard 3 T MR brain MS protocol that included 3D DIR were included. Median cohort age was 38.5 years, with 46 women, 59 relapsing-remitting type MS, and median follow-up interval of 250 days (interquartile range: 196-394 days). Lesion progression was detected in 67.1% of cases using CCI review versus 22.4% using standard review, with a total of 182 new or enlarged lesions using CCI review versus 28 using standard review. There was a statistically significant difference between the two methods in the rate of all progressive lesions (P < 0.001, McNemar's test) as well as cortical progressive lesions (P < 0.001). Automated CCI maps using co-registered serial 3D DIR, compared to standard review of 3D DIR alone, increased detection rate of MS lesion progression in patients undergoing clinical brain MRI exam.

 BACKGROUND: The decision of initiating treatment for multiple sclerosis (MS) with a high-efficacy DMT (HE DMT) or non-high-efficacy DMT (non-HE DMT) is influenced by several factors, including risk perception of patients and physicians. OBJECTIVE: Investigate the influence of physicians' risk perception on decision-making when switching treatments for MS and the reasons for switching. METHODS: Data were drawn from the Adelphi Real-World MS Disease-Specific Program (a retrospective survey) and analysis included people with RMS identified between 2017- 2021. RESULTS: Of 4129 patients with reasons for switch available, 3538 switched from non-HE DMT and 591 from HE DMT. Overall, 4.7% of patients were switched treatment by their physicians due to the risk of malignancies and infections including PML risk. The proportion of switches that were made due to the risk of PML were 23.9% in the HE DMT and 0.5% in the non-HE DMT groups. The top reasons for switching were relapse frequency (non-HE DMT vs HE-DMT: 26.8% vs 15.2%), lack of efficacy (20.9 vs 11.7) and increased number of MRI lesions (20.3% vs 12.4%). CONCLUSIONS: Physicians' risk perception of malignancies and infection excluding PML was not a leading factor when switching treatment. The risk of PML was a key factor, especially for switching patients from HE DMTs. In both groups, lack of efficacy was the key contributing factor for switching. Initiating the treatment with HE DMTs may potentially reduce the number of switches due to sub-optimal efficacy. These findings might help physicians to engage more in discussions with patients about the benefit/risk profile of DMTs.
 BACKGROUND AND PURPOSE: It is still debated whether the COVID-19 pandemic affected disease activity in people with autoimmune diseases, including multiple sclerosis (MS). The aim of this study, therefore, was to explore the impact of COVID-19 in people with MS (pwMS) not receiving continuative disease-modifying therapy (DMT) after previous treatment with autologous hematopoietic stem cell transplantation (AHSCT). MATERIALS AND METHODS: We included pwMS treated with AHSCT who were in disease remission without receiving DMTs during the pandemic and who were followed up at our centre during the study period. Data on SARS-CoV-2 infection and vaccination were recorded, with details of adverse events and clinical-radiological disease activity. RESULTS: A total of 36 pwMS (31 females; 86%) were included, of whom 23 (64%) had relapsing-remitting (RR-MS) and 13 had secondary progressive MS (SP-MS). Thirty-three pwMS (92%) received anti-SARS-CoV-2 mRNA vaccines. Thirteen patients (36%) developed mild to moderate COVID-19 a median (range) of 58 (4-224) months after AHSCT; seven (54%) of these patients were not yet vaccinated. Transient neurological symptoms after vaccination or infection were reported in 9% and 36% of the patients, respectively. The rate of new inflammatory events (relapses or asymptomatic magnetic resonance imaging [MRI] activity) after AHSCT increased from 0.006 (one asymptomatic new lesion/159 patient-years) before the pandemic to 0.083 (five relapses plus two cases of asymptomatic MRI activity/84 patient-years) since the pandemic start (p = 0.004). CONCLUSIONS: People with MS with a history of highly active disease, who are untreated or receiving moderate-efficacy DMTs might be more vulnerable to disease reactivation, possibly elicited by exogenous triggers. Careful monitoring and further investigation are warranted to ascertain whether special precautions are needed in these cases.
 Primary central nervous system lymphoma (PCNSL) is an uncommon lymphoproliferative disease associated with immunosuppression. Here, we report the case of a patient with multiple sclerosis, under treatment with fingolimod (FTY720, Gilenya) for 4 years, who developed this condition. Although the causal relationship cannot be established, there are cases in the literature that describe the appearance of lymphoma after the use of this medication. Considering the high mortality of PCNSL, epidemiological studies are necessary to establish a relationship between its arising and the use of immunosuppressants.
 BACKGROUND: The local divergence exponent (LDE) has been used to assess gait stability in people with multiple sclerosis (pwMS). Although previous studies have consistently found that stability is lower in pwMS, inconsistent methodologies have been used to assess patients with a broad range of disability levels. QUESTIONS: What sensor location and movement direction(s) are better able to classify pwMS at early stages of the disease? METHODS: 49 pwMS with EDSS ≤ 2.5 and 24 healthy controls walked overground for 5 min while 3D acceleration data was obtained from sensors placed at the sternum (STR) and lumbar (LUM) areas. Unidirectional (vertical [VT], mediolateral [ML], and anteroposterior [AP]) and 3-dimensional (3D) LDEs were calculated using STR and LUM data over 150 strides. ROC analyses were performed to assess classification models using single and combined LDEs, with and without velocity per lap (VEL(LAP)) as a covariate. RESULTS: Four models performed equally well by using combinations of VEL(LAP), LUM(3D), LUM(VT), LUM(ML), LUM(AP), STR(ML), and STR(AP) (AUC = 0.879). The best model using single sensor LDEs included VEL(LAP), STR(3D), STR(ML), and STR(AP) (AUC = 0.878), whereas using VEL(LAP) + STR(VT) (AUC = 0.869) or VEL(LAP) + STR(3D) (AUC=0.858) performed best using a single LDE. SIGNIFICANCE: The LDE offers an alternative to currently insensitive tests of gait impairment in pwMS at early stages, when deterioration is not clinically evident. For clinical purposes, the implementation of this measure can be simplified using a single sensor at the sternum and a single LDE measure, but speed should be considered. Longitudinal studies to determine the predictive power and responsiveness of the LDE to MS progression are still needed.
 BACKGROUND AND PURPOSE: MR imaging provides information on the number and extend of focal lesions in multiple sclerosis (MS) patients. This study explores whether total brain T2 lesion volume or lesion number shows a better correlation with serum and cerebrospinal fluid (CSF) biomarkers of disease activity. MATERIALS AND METHODS: In total, 52 patients suffering from clinically isolated syndrome (CIS)/relapsing-remitting multiple sclerosis (RRMS) were assessed including MRI markers (total brain T2 lesion volume semi-automatically outlined on 3D DIR/FLAIR sequences, number of lesions), serum and CSF biomarkers at the time of neuroimaging (neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP)), and clinical parameters. After log-transformation and partial correlations adjusted for the covariates patients' age, BMI, EDSS-score and diagnosis, the Fisher's r-to-Z transformation was used to compare different correlation coefficients. RESULTS: The correlation between lesion volume and serum NfL (r = 0.6, p < 0.001) was stronger compared to the association between the number of T2 lesions and serum NfL (r = 0.4, p < 0.01) (z = -2.0, p < 0.05). With regard to CSF NfL, there was a moderate, positive relationship for both number of T2 lesions and lesion volume (r = 0.5 respectively, p < 0.01). We found no significant association between MRI markers and GFAP levels. CONCLUSION: Our findings suggest that there is a stronger association between serum NfL and T2 lesion volume, than there is between serum NfL and T2 lesion number. Improving robustness and accuracy of fully-automated lesion volume segmentation tools can expedite implementation into clinical routine and trials.
 BACKGROUND: Multiple sclerosis (MS) is a leading cause of neurological disability in young and middle-aged populations, associated with substantial burden of illness. Because a growing literature now shows that this burden extends to poorer oral health, oral health-related quality of life (OHRQoL) may be reduced as well. OBJECTIVES: To test whether people with relapsing-remitting MS (RRMS) have poorer OHRQoL than demographically matched controls, and to establish which variables are associated with worse OHRQoL. MATERIALS AND METHODS: In total, 64 people with RRMS and 69 demographically matched controls participated. Both groups completed the Oral Health Impact Profile (OHIP-14), a validated measure of OHRQoL, as well as an objective oral health examination performed by a qualified dentist, a measure of dental-related functionality and a measure of mental health. RESULTS: OHRQoL was significantly poorer in the RRMS relative to the control group. However, although poorer OHRQoL in the RRMS group was moderately associated with objectively assessed oral health (r = .30), it was more strongly associated with mental health (r = .61). For the control group, the reverse pattern of association was evident, with OHRQoL more strongly associated with oral health (r = .48) relative to mental health (r = .20). CONCLUSION: People with RRMS report poorer OHRQoL than demographically matched controls, but these appraisals are more strongly linked to mental health than to objective oral health indicators.
 INTRODUCTION: The discontinuation of disease-modifying therapies (DMTs) in multiple sclerosis (MS) is commonly seen in real-world settings due to several factors. AREA COVER: The aim of this study is to describe the frequency of disease activity after discontinuation of DMTs in MS patients included in the Argentinean MS and NMOSD registry. DISCUSION: Patients with relapsing remitting MS (RRMS) and active secondary progressive MS (SPMS) were included based on the following criteria: they discontinued treatment for more than 6 months, they had been treated with a DMT for ≥2 years, and they had at least 6 months of follow-up in the registry after discontinuation. Demographic and clinical data were collected. Disease activity during follow-up was defined as the presence of a clinical relapse or a new magnetic resonance (MRI) lesion (either new lesions on T2-weighted sequence and/or contrast enhancement). Bivariate analysis was applied to identify clinical and demographic factors related to disease activity. CONCLUSION: We included 377 patients (75.5% RRMS, 22.5% SPMS) who had discontinued DMTs. The mean (SD) follow-up after discontinuation was 15.7 (7.9) months. After discontinuation, the presence of relapse was detected in 18.8% and 3.5% in RRMS and SPMS, respectively; and new MRI activity in 22% and 3.5%, respectively. We found that higher risk of relapse and MRI activity was associated with younger age (p < 0.001), shorter disease duration (p < 0.001), and RRMS phenotype (p = 0.006). Males showed higher MRI activity (p 0.011). This study provides real-world data that can guide physicians when considering discontinuation of DMTs.
 BACKGROUND: This study examined the feasibility and efficacy of reactive balance training for improving stepping performance and reducing laboratory-induced falls in people with multiple sclerosis (MS). METHODS: Thirty people diagnosed with MS (18-70 years) participated in a blinded randomized controlled trial (ACTRN12618001436268). The intervention group (n = 14) underwent two 50-minute sessions (total 100 min) that exposed them to a total of 24 trips and 24 slips in mixed order, over one week. The control group (n = 16) received sham training (stepping over foam obstacles) with equivalent dosage. The primary outcome was falls into the harness (defined as >30% body weight) when exposed to trips and slips that were unpredictable in timing, location and type at post-assessment. Physical and psychological measures were also assessed at baseline and post assessments. RESULTS: The intervention and control groups completed 86% and 95% of the training protocols respectively. Incidence rate ratios (95% confidence intervals) of the intervention group relative to the control group were 0.57 (0.25, 1.26) for all falls, 0.80 (0.30, 2.11) for slip falls and 0.20 (0.04, 0.96) for trip falls in the laboratory. Kinematic analyses indicated the intervention participants improved dynamic stability, with higher centre of mass position and reduced trunk sway during recovery steps following a trip, compared to control. There were no significant differences between the intervention and control participants at post-assessment for other secondary outcome measures. CONCLUSIONS: Reactive balance training improved trip-induced dynamic stability, limb support, trunk control and reduced falls in people with MS. More research is required to optimise the training protocol and determine whether the beneficial effects of reactive balance training can be retained long term and generalize to fewer daily-life falls.
 BACKGROUND: In the context of the COVID-19 pandemic, French health authorities allowed the home administration of natalizumab by a healthcare-at-home service. We evaluated the patients' perception of care quality following the transition from day-hospital to home natalizumab administration. METHODS: Thirty relapsing-remitting multiple sclerosis (MS) patients treated with natalizumab were prospectively evaluated for one year after changing onto a home treatment procedure, using MusiCare, the first MS-specific questionnaire to evaluate patient experience and MusiQol. A numerical rating scale score for satisfaction and a dedicated questionnaire concerning patient experience were completed after each infusion. The primary endpoint was the mean difference in MusiCare score between baseline and 12 months. RESULTS: From June 2020 to November 2021, 306 infusions were performed at home. Three patients withdrew from the study (one lost to follow-up and two preferred to return at the day hospital). No worsening of patient experience or quality of life was observed. The mean scores of the Musicare dimensions were higher at 12 months than at baseline, significantly for the "relationship with healthcare professionals" (p = 0.0203). The MusiQol global score remained stable but the coping and friendship dimensions were significantly better at M12 than at baseline (p = 0.0491 and p = 0.0478, respectively). The satisfaction questionnaire highlighted some pain during the infusions (21.8%) and contradictions between healthcare professionals (17.2%). The mean score for satisfaction with care was 9.1/10. No safety concerns were identified. CONCLUSION: The positive experience of patients with home natalizumab administration provides an important opportunity to improve the quality of patient care.
 OBJECTIVE: To examine differences in the therapeutic response to ocrelizumab in multiple sclerosis (MS) patients who self-identified as either White or Black, assessed longitudinally by expanded disability status scale (EDSS) progression and MRI brain volume loss. METHODS: MS subjects treated with ocrelizumab were retrospectively identified. Clinical data were available for 229 subjects (White 146; Black 83) and MRI data from for 48 subjects (White 31; Black 17). Outcome measures were changes in the EDSS and brain volume over time. EDSS were analyzed as raw scores, ambulatory (EDSS <5.0) vs. ambulatory with assistance (5.5 ≤ EDSS ≤ 6.5) status, and EDSS severity (< 3.0, 3.0-5.0, and > 5.5 ≤ 6.5). General linear mixed model was used for statistical analysis. FreeSurfer was used for volumetric analysis. RESULTS: The Black cohort had overrepresentation of females (78% vs. 62%, p = 0.013), lower age (median, 45 (IQR 39-51) vs. 49 (38-58), p = 0.08), lower Vitamin D levels (33 (21-45) vs. 40 (29-52), p = 0.002), and higher EDSS (4 (2-6) vs. 2.5 (1-6), p = 0.019). There was no progression of EDSS scores over the 2-year observation period. The covariates with significant influence on the baseline EDSS scores were older age, race, longer disease duration, prior MS treatment, and lower vitamin D levels. No differences were observed between the racial groups over time in the cortical, thalamic, caudate, putamen, and brainstem gray matter volumes nor in the cortical thickness or total lesion volume. CONCLUSION: In this real-world clinical and radiological study, ocrelizumab treatment was highly effective in stabilizing clinical and MRI measures of disease progression in Blacks and Whites, despite higher baseline disability in the Black cohort.
 BACKGROUND: Heterogeneous processes may contribute to cognitive impairment in multiple sclerosis (MS). OBJECTIVE: To apply a longitudinal multiparametric MRI approach to identify mechanisms associated with cognitive worsening in MS patients. METHODS: 3 T brain functional and structural MRI scans were acquired at baseline and after a median follow-up of 3.4 years in 35 MS patients and 22 healthy controls (HC). Associations between cognitive worsening (reliable change index score < - 1.25 at the Rao's battery) and longitudinal changes in regional T2-hyperintense white matter (WM) lesions, diffusion tensor microstructural WM damage, gray matter (GM) atrophy and resting state (RS) functional connectivity (FC) were explored. RESULTS: At follow-up, HC showed no clusters of significant microstructural WM damage progression, GM atrophy or changes in RS FC. At follow-up, 10 MS patients (29%) showed cognitive worsening. Compared to cognitively stable, cognitively worsened MS patients showed more severe GM atrophy of the right anterior cingulate cortex and bilateral supplementary motor area (p < 0.001). Cognitively worsened vs cognitively stable MS patients showed also decreased RS FC in the right hippocampus of the right working memory network and in the right insula of the default mode network. Increased RS FC in the left insula of the executive control network was found in the opposite comparison (p < 0.001). No significant regional accumulation of focal WM lesions nor microstructural WM abnormalities occurred in both patients' groups. CONCLUSIONS: GM atrophy progression in cognitively relevant brain regions combined with functional impoverishment in networks involved in cognitive functions may represent the substrates underlying cognitive worsening in MS.
 OBJECTIVE: In multiple sclerosis (MS), iron rim lesions (IRLs) on magnetic resonance imaging (MRI) are associated with pronounced intralesional tissue damage. The aim of this study was to investigate (peri-)lesional and structural connectivity tissue damage in IRLs compared to non-IRLs. MATERIAL AND METHODS: MRI was acquired on a 3 T system. Tissue integrity was assessed using the T1/T2-weighted (T1/T2w) ratio. Furthermore, we assessed the impact on structural network connectivity accounting for differences in lesion volumes and T1/T2w values. RESULTS: Seventy-six patients (38 with at least one IRL and 38 age- and sex-matched patients without IRLs) were included. In the IRL-group, T1/T2w ratios of IRLs were significantly lower compared to non-IRLs (p < 0.05). When comparing the T1/T2w ratios in non-IRLs between the IRL-group and non-IRL group, there was no significant difference (p = 0.887). We observed a centrifugal decrease in microstructural damage from lesions to the perilesional white matter. In the IRL-group, T1/T2w ratios in the perilesional white matter 3-8 mm distant to the lesion were significantly lower in IRLs compared to non-IRLs. We found no significant differences in the amount of network disruption between both lesion types (p = 0.122). CONCLUSION: T1/T2w represents an interesting candidate to capture a pronounced intra- and perilesional tissue damage of IRLs. However, our preliminary results suggest that a pronounced tissue damage might not result in a higher disruption to structural connectivity networks in IRLs.
 BACKGROUND: Follow-on disease modifying therapies (FO-DMTs) do not always require Phase III studies. There are concerns that cheaper FO-DMTs are only used to reduce healthcare costs. However, the well-being of people with MS (pwMS) should be a priority. We aimed to evaluate the efficacy, safety and treatment satisfaction of one of the FO- Fingolimod (FTY) used in Turkey with the approval of Turkish Ministry of Health. METHODS: PwMS under FTY were recruited from 13 centers and real-world data and answers of satisfaction and adherence statements of pwMS on FTY treatment were analyzed. RESULTS: Data of 239 pwMS were obtained. The duration of FTY treatment was 2.5 ± 0.8 (1-4) years in pwMS who were included in the study and whose treatment continued for at least one year. Significant decreases in annual relapse rate (p < 0.001), Expanded Disability Status Scale (p < 0.001) and neuroimaging findings (p < 0.001) were observed. While 64% of the patients were satisfied and 71.5% were found to adherent with this FO-FTY. CONCLUSION: This multicenter retrospective study found that the efficacy, safety and treatment adherence of a prescribed FO-FTY were consistent with the results of real-world studies. Studies including real-world data may provide guidance to address issues related to FO-FTY use.
 BACKGROUND: Multiple sclerosis (MS) is characterized by a complex etiology that is reflected in the lack of consistently predictable treatment responses across patients of seemingly similar characteristics. Approaches to demystify the underlying predictors of aberrant treatment responses have made use of genome-wide association studies (GWAS), with imminent progress made in identifying single nucleotide polymorphisms (SNPs) associated with MS risk, disease progression, and treatment response. Ultimately, such pharmacogenomic studies aim to utilize the approach of personalized medicine to maximize patient benefit and minimize rate of disease progression. OBJECTIVE: Very limited research is available around the long intergenic non-coding RNA (linc)00513, recently being reported as a novel positive regulator of the type-1 interferon (IFN) pathway, following its overexpression in the presence of two polymorphisms: rs205764 and rs547311 in the promoter region of this gene. We attempt to provide data on the prevalence of genetic variations at rs205764 and rs547311 in Egyptian MS patients, and correlate these polymorphisms with the patients' responses to disease-modifying treatments. METHODS: Genomic DNA from 144 RRMS patients was isolated and analyzed for genotypes at the positions of interest on linc00513 using RT-qPCR. Genotype groups were compared with regards to their response to treatment; additional secondary clinical parameters including the estimated disability status score (EDSS), and onset of the disease were examined in relation to these polymorphisms. RESULTS: Polymorphisms at rs205764 were associated with a significantly higher response to fingolimod and a significantly lower response to dimethylfumarate. Moreover, the average EDSS of patients carrying polymorphisms at rs547311 was significantly higher, whereas no correlation appeared to exist with the onset of MS. CONCLUSION: Understanding the complex interplay of factors influencing treatment response is pivotal in MS. One of the factors contributing to a patient's response to treatment, as well as disease disability, may be polymorphisms on non-coding genetic material, such as rs205764 and rs547311 on linc00513. Through this work, we propose that genetic polymorphisms may partially drive disease disability and inconsistent responses to treatment in MS; we also aim to draw attention towards genetic approaches, such as screening for specific polymorphisms, to possibly direct treatment choices in such a complex disease.
 Central nervous system (CNS) atrophy provides valuable additional evidence of an ongoing neurodegeneration independent of lesion accrual in persons with multiple sclerosis (PwMS). However, there are limitations for interpretation of CNS volume changes at individual patient-level. Patients are receiving information on the topic of atrophy through various sources, including media, patient support groups and conferences, and discussions with their providers. Whether or not the topic of CNS atrophy should be proactively discussed with PwMS during office appointments is currently controversial. This commentary/perspective article represents perspectives of PwMS, providers and researchers with recommendations for minimizing confusion and anxiety, and facilitating proactive discussion about brain atrophy, as an upcoming routine measure in evaluating disease progression and treatment response monitoring. The following recommendations were created based on application of patient's and provider's surveys, and various workshops held over a period of 2 years: (1) PwMS should receive basic information on understanding of brain functional anatomy, and explanation of inflammation and neurodegeneration; (2) the expertise for atrophy measurements should be characterized as evolving; (3) quality patient education materials on these topics should be provided; (4) the need for standardization of MRI exams has to be explained and communicated; (5) providers should discuss background on volumetric changes, including references to normal aging; (6) the limitations of brain volume assessments at an individual-level should be explained; (7) the timing and language used to convey this information should be individualized based on the patient's background and disease status; (8) a discussion guide may be a very helpful resource for use by providers/staff to support these discussions; (9) understanding the role of brain atrophy and other MRI metrics may elicit greater patient satisfaction and acceptance of the value of therapies that have proven efficacy around these outcomes; (10) the areas that represent possibilities for positive self-management of MS symptoms that foster hope for improvement should be emphasized, and in particular regarding use of physical and mental exercise that build or maintain brain reserve through increased network efficiency, and (11) an additional time during clinical visits should be allotted to discuss these topics, including creation of specific educational programs.
 BACKGROUND: There is limited information on the trajectories of disease-modifying therapy (DMT) use and their association with sickness absence and/or disability pension (SADP) among people with multiple sclerosis (PwMS). The objective of the study was to identify trajectories of DMT use over 10 years among PwMS, identify sociodemographic and clinical factors associated with the trajectories, and to assess the association between identified trajectories and SADP days. METHODS: A longitudinal register-based study was conducted, on a prospective data set linked across six nationwide registers, assessing treatment courses of PwMS with DMTs for the 10 years following multiple sclerosis (MS) onset. The study included 1923 PwMS with MS onset in 2007-2010, when aged 19-56 years. In each 6-month-period, their treatment was categorized as before treatment, high-efficacy, non-high-efficacy, or no DMT. Sequence analysis was performed to identify sequences of the treatment categories and cluster them into different DMT trajectories. Cluster belonging, in relation to demographic and clinical characteristics, was assessed through log-multinomial regression analysis. The association of trajectories/cluster-belonging with SADP net days was assessed using generalized estimating equation (GEE) models. RESULTS: Cluster analyses identified 4 trajectories of DMT use: long-term non-high-efficacy DMTs (38.6%), escalation to high-efficacy DMTs (31.2%), delayed start and escalation to high-efficacy DMTs (15.4%), and discontinued/ no DMT (14.2%). Age, MS type, expanded disability status scale (EDSS) score and the number of DMT switches were associated with cluster belonging. The youngest age group (18-25) were more likely to be in the escalation to high-efficacy cluster. People with primary progressive MS were more likely to be in the delayed start or discontinued/ no DMT cluster. Higher EDSS scores were associated to being in the other three clusters than in the long-term non-high-efficacy DMTs cluster. Higher number of DMT switches were associated with being in the escalation to high-efficacy DMTs cluster but less likely to be in the delayed start or discontinued/ no DMT clusters. Descriptive analyses showed a trend of fewer mean SADP days among PwMS using non-high-efficacy DMT than the other clusters about 9 years after onset. PwMS in the escalation to high-efficacy and discontinued/no DMT clusters had more SADP days. PwMS in the delayed start and escalation to high-efficacy DMTs cluster, started with fewer SADP days which increased over time. SADP days adjusted through GEE models showed trends comparable with the descriptive analysis. CONCLUSION: This study described the long-term real-world trajectories of DMT use among PwMS in Sweden using sequence analysis and showed the association of the trajectories with SADP days as well as sociodemographic and clinical characteristics.
 OBJECTIVE: To identify specific white matter tracts (WMTs) whose disruption is associated with the severity of neurogenic lower urinary tract dysfunction (NLUTD) in two independent cohorts of women with multiple sclerosis (MS) and NLUTD. METHODS: Cohort 1 consisted of twenty-eight women with MS and NLUTD. The validation cohort consisted of 10 women with MS and NLUTD. Eleven healthy women served as controls. Participants of both MS cohorts had the same inclusion and exclusion criteria. Both MS cohorts and the healthy controls underwent the same clinical assessment and functional MRI (fMRI) protocol, except that the validation MS cohort underwent 7-Tesla fMRI scan. Fifteen WMTs (six coursing to relevant brainstem areas) involved in bladder control were a priori regions of interest (ROI). Spearman's correlation test was performed between each the Fractional Anisotropy (FA) and mean diffusivity (MD) of each WMT and the clinical parameters. RESULTS: Overall, we found a very high degree of overlap (100% of a priori ROI) in the tracts identified by our correlation analysis as having the greatest contribution to NLUTD symptoms in MS women. The right inferior cerebellar peduncle, left posterior limb of internal capsule, and left superior cerebellar peduncle displayed significant associations to the greatest number of clinical parameters. CONCLUSIONS: Our correlation analysis supports the role of specific WMT disruptions in the contribution of symptoms in women with MS and NLUTD, as confirmed in two independent MS cohorts.
 BACKGROUND AND PURPOSE: Inflammatory disease activity in multiple sclerosis (MS) decreases with advancing age. Previous work found a decrease in contrast-enhancing lesions (CELs) with age. Here, we describe the relation of age and magnetic resonance imaging (MRI) measures of inflammatory disease activity during long-term follow-up in a large real-world cohort of people with relapse onset MS. METHODS: We investigated MRI data from the long-term observational Amsterdam MS cohort. We used logistic regression models and negative binomial generalized estimating equations to investigate the associations between age and radiological disease activity after a first clinical event. RESULTS: We included 1063 participants and 10,651 cranial MRIs. Median follow-up time was 6.1 years (interquartile range = 2.4-10.9 years). Older participants had a significantly lower risk of CELs on baseline MRI (40-50 years vs. <40 years: odds ratio [OR] = 0.640, 95% confidence interval [CI] = 0.45-0.90; >50 years vs. <40 years: OR = 0.601, 95% CI = 0.33-1.08) and a lower risk of new T2 lesions or CELs during follow-up (40-50 years vs. <40 years: OR = 0.563, 95% CI = 0.47-0.67; >50 years vs. <40 years: OR = 0.486, 95% CI = 0.35-0.68). CONCLUSIONS: Greater age is associated with a lower risk of inflammatory MRI activity at baseline and during long-term follow-up. In patients aged >50 years, a less aggressive treatment strategy might be appropriate compared to younger patients.
 BACKGROUND: Video-oculography (VOG) is used to quantify functional deficits in internuclear ophthalmoplegia (INO), whereas MRI can detect the corresponding structural lesions in the medial longitudinal fasciculus (MLF). This study investigates the diagnostic agreement of MRI compared to VOG measurements. METHODS: We prospectively compared structural MRI findings and functional VOG measures of 63 MS patients to assess their diagnostic agreement for INO. RESULTS: MRI detected 12 true-positive and 92 true-negative MLF lesions for INO compared to VOG (12 true-positive and 38 true-negative patients) but identified one-third of the MLF lesions on the wrong side. MRI ratings were specific (92.0%) to detect MLF lesions but not sensitive (46.2%) for diagnosing INO (86.4% and 63.2% by patient). Accordingly, MRI has a high positive likelihood ratio of 5.77 but a modest negative likelihood ratio of 0.59 for the probability of INO (4.63 and 0.43) with an accuracy of 82.5% (79.4%). CONCLUSION: MRI assessments are highly specific but not sensitive for detecting INO compared to VOG. While MRI identifies MLF lesions in INO, VOG quantifies the deficit. As a simple, quick, and non-invasive test for diagnosing and tracking functional INO deficits, it will hopefully find its place in the diagnostic and therapeutic pathways of MS.
 OBJECTIVE: The aim is to compare the effects of different electrical stimulations on pain, functional capacity and quality of life in patients with Multiple Sclerosis (pwMS). METHOD: 40 pwMS were included in the study, randomized by simple random method and divided into 2 groups. Low-frequency Transkutaneal Electric Stimulation (TENS) was applied to 1st group and Interferential current was applied to 2nd group for 30 min 5 days/a week for 4 weeks. For pain severity Visual Analogue Scale (VAS), for neuropathic pain the LANSS questionnaire was used. Functional capacity was evaluated with the 2-minute walk test (2MWT) and quality of life was evaluated with the 'Multiple Sclerosis International Quality of Life Scale (MusiQol)'. RESULTS: The most severe and mean VAS and LANSS results significiantly decreased, 2MWT results significiantly increased in two groups (p<0.05). A significiant increase was found in all sub-headings of the MusiQol, except for the relationship with the health system in TENS group (p<0.05). An increase was found in the total score, activities of daily living, well-being, relationship with friends, relationship with family, sexual life, rejection sub-headings of the MusiQol in IFC group (p<0.05). There was no significant difference between the groups in terms of VAS, LANSS, 2MWT and MusiQol (p>0.05). CONCLUSION: In this study, it was found that interference current and TENS applications decrease pain and increase functional capacity. However, it was determined that TENS application was a more effective method in increasing the quality of life. CLINICALTRIALS: NCT05110586.
 BACKGROUND: Cognitive dysfunction is relatively common in patients with multiple sclerosis (MS). Although it occurs in all stages and all phenotypes of MS, it is more prevalent in secondary progressive MS (SPMS) compared to relapsing MS (RMS). It is unclear whether the higher frequency of cognitive impairment in SPMS is linked to the progressive phenotype or other clinical factors. In this study, we compared working memory in patients with RMS, SPMS, and healthy subjects. We also investigated the effects of age, disease duration, and disability on working memory performance. METHODS: This case-control study enrolled 134 MS patients, 69 patients were diagnosed with RMS and 65 patients with SPMS, and 77 healthy control subjects. We designed two working memory tasks with different sets of stimuli (face vs. checkerboard) and different instructions (same or different vs. which one is the same). RESULTS: Accuracy was significantly more impaired in SPMS patients than in RMS patients and both groups were worse than healthy subjects. This finding was similar between both tasks. Age and overall cognitive functions (measured with MoCA) also affected accuracy, but disease duration and disability only affected accuracy in working memory task with checkerboard stimuli. CONCLUSION: MS patients are impaired in keeping the information in the visual working memory for a few seconds. Progressive phenotype significantly affected working memory accuracy, and this effect did not explain out with other demographic or clinical factors. Future studies are needed to reveal underlying mechanisms of working memory dysfunction in SPMS and working memory dysfunction as a biomarker of disease progression.
 Multiple sclerosis (MS) causes gait and cognitive impairments that are partially normalized by compensatory mechanisms. We aimed to identify the gait tasks that unmask gait disturbance and the underlying neural correlates in MS. We included 25 patients with MS (Expanded Disability Status Scale score: median 2.0, interquartile range 1.0-2.5) and 19 healthy controls. Fast-paced gait examinations with inertial measurement units were conducted, including straight or circular walking with or without cognitive/motor tasks, and the timed up and go test (TUG). Receiver operating characteristic curve analysis was performed to distinguish both groups by the gait parameters. The correlation between gait parameters and cortical thickness or fractional anisotropy values was examined by using three-dimensional T1-weighted imaging and diffusion tensor imaging, respectively (corrected p < .05). Total TUG duration (>6.0 s, sensitivity 88.0%, specificity 84.2%) and stride velocity during cognitive dual-task circular walking (<1.12 m/s, 84.0%, 84.2%) had the highest discriminative power of the two groups. Deterioration of these gait parameters was correlated with thinner cortical thickness in regional areas, including the left precuneus and left temporoparietal junction, overlapped with parts of the default mode network, ventral attention network, and frontoparietal network. Total TUG duration was negatively correlated with fractional anisotropy values in the deep cerebral white matter areas. Turning and multitask gait may be optimal to unveil partially compensated gait disturbance in patients with mild-to-moderate MS through dynamic balance control and multitask processing, based on the structural damage in functional networks.
 OBJECTIVES: To investigate the normal-appearing white matter (NAWM) susceptibility in a cohort of newly diagnosed multiple sclerosis (MS) patients and to evaluate possible correlations between NAWM susceptibility and disability progression. METHODS: Fifty-nine patients with a diagnosis of MS (n = 53) or clinically isolated syndrome (CIS) (n = 6) were recruited and followed up. All participants underwent neurological examination, blood sampling for serum neurofilament light chain (sNfL) level assessment, lumbar puncture for the quantification of cerebrospinal fluid (CSF) β-amyloid(1-42) (Aβ) levels, and brain MRI. T2-weighted scans were used to quantify white matter (WM) lesion loads. For each scan, we derived the NAWM volume fraction and the WM lesion volume fraction. Quantitative susceptibility mapping (QSM) of the NAWM was calculated using the susceptibility tensor imaging (STI) suite. Susceptibility maps were computed with the STAR algorithm. RESULTS: Primary progressive patients (n = 9) showed a higher mean susceptibility value in the NAWM than relapsing-remitting (n = 44) and CIS (n = 6) (p = 0.01 and p = 0.02). Patients with a higher susceptibility in the NAWM showed increased sNfL concentration (ρ = 0.38, p = 0.004) and lower CSF Aβ levels (ρ = -0.34, p = 0.009). Mean NAWM susceptibility turned out to be a predictor of the expanded disability status scale (EDSS) worsening at follow-up (β = 0.41, t = 2.66, p = 0.01) and of the MS severity scale (MSSS) (β = 0.38, t = 2.43, p = 0.019). CONCLUSIONS: QSM in the NAWM seems to predict the EDSS increment over time. This finding might provide evidence on the role of QSM in identifying patients with an increased risk of early disability progression. KEY POINTS: • NAWM-QSM is higher in PPMS patients than in RRMS. • NAWM-QSM seems to be a predictor of EDSS worsening over time. • Patients with higher NAWM-QSM show increased sNfL concentration and lower CSF Aβ levels.
 INTRODUCTION: The emergence of several therapeutic options in multiple sclerosis (MS), which significantly modify the immune system functioning, has led to the need for the consideration of additional factors, such as risk of infections, in the decision-making process. The aim of these consensus recommendations was to discuss and perform a practical guide to Latin American neurologists on the risk of infections at diagnosis, follow-up and prior to initiation of DMDs. METHODS: A panel of Latin American neurologists, experts in demyelinating diseases and dedicated to management and care of MS patients, gathered during 2021 and 2022 to make consensus recommendations on the risk of infections in PwMS treated with DMDs in Latin America. The RAND/UCLA methodology was developed to synthesize the scientific evidence and expert opinions on health care topics and was used for reaching a formal agreement. RESULTS: Recommendations were established based on relevant published evidence and expert opinion, focusing on: 1- baseline infection disease and vaccination status; 2- opportunistic infections; 3- progressive multifocal leukoencephalopathy; 4- genitourinary system infections; 5- respiratory tract infections; 6- digestive system infections, 7-others local infections and 8- COVID-19. CONCLUSION: The recommendations of this consensus seek to optimize the care, management and treatment of PwMS in Latin America. The standardized evidence-based care of pwMS infections will allow better outcomes.
 PURPOSE: To report a case of severe, recurrent bilateral panuveitis secondary to primary progressive multiple sclerosis responsive to ocrelizumab infusions. OBSERVATION: We describe the clinical progression of a 40 year old female who presented with a 3-week history of insidious bilateral visual loss that was clinically consistent with panuveitis. A diagnosis of multiple sclerosis was established with serial magnetic resonance imaging (MRI) that coincided with focal neurological events separated by time. There was initially good response to high dose oral prednisolone; however, the patient would have recurrent uveitis each time the dose was weaned. Under guidance of neurology, we had initiated treatment with ocrelizumab with stability of ocular inflammation for the past 24 months. CONCLUSION: Six-monthly 600mg ocrelizumab infusions may be effective as a steroid sparing option for patients with severe, recurrent bilateral panuveitis secondary to primary progressive multiple sclerosis.
 BACKGROUND: Multiple sclerosis is a diffuse chronic demyelinating disease of the central nervous system. It is relatively uncommon in the Asian population and even more so in males. Despite the usual involvement of the brainstem, eight-and-a-half syndrome remains a rare first presentation in multiple sclerosis. Only a few cases have been reported previously, but none involving the Asian population. Eight-and-a-half syndrome, a neuro-ophthalmological condition, is characterized by one-and-a-half syndrome with ipsilateral lower facial nerve palsy, which localizes lesions to the pontine tegmentum. This case report demonstrates the first case of eight-and-a-half syndrome as the first presentation of multiple sclerosis in an Asian male. CASE PRESENTATION: A healthy 23-year-old Asian man presented with sudden onset of diplopia followed by left-sided facial asymmetry for 3 days. Assessment of extraocular movement revealed left conjugate horizontal gaze palsy. On right gaze, there was limited left eye adduction and horizontal nystagmus of the right eye. These findings were consistent with a left-sided one-and-a-half syndrome. Prism cover test revealed left esotropia of 30 prism diopters. Cranial nerve examination showed left lower motor neuron facial nerve palsy, while other neurological examination was normal. Magnetic resonance imaging brain showed multifocal T2 fluid attenuated inversion recovery hyperintense lesions, involving bilateral periventricular, juxtacortical, and infratentorial regions. A focal gadolinium contrast-enhanced lesion with open ring sign on T1 sequence was seen at the left frontal juxtacortical region. Multiple sclerosis was diagnosed on the basis of the clinical and radiological evidence, which fulfilled the 2017 McDonald criteria. Positive oligoclonal bands in cerebrospinal fluid analysis further confirmed our diagnosis. He had a complete resolution of symptoms 1 month after a course of pulsed corticosteroid therapy, and was subsequently placed on maintenance therapy with interferon beta-1a. CONCLUSION: This case illustrates eight-and-a-half syndrome as the first presentation of a diffuse central nervous system pathology. A wide range of differential diagnoses needs to be considered in such a presentation as based on the patient's demographics and risk factors.
 OBJECTIVE: To evaluate the association of traumatic brain injury (TBI) before the multiple sclerosis (MS) onset with the rate of progression of neurological disorders and cerebrospinal fluid markers of blood-brain barrier permeability, inflammation, demyelination, and gliosis. MATERIAL AND METHODS: Patients with relapsing-remitting MS in the Altai region of Russia with/without TBI before the MS onset (n=44; 19 men, 25 women in each group) participated in a prospective, controlled, randomized study. Disability rate was assessed retrospectively. Pleocytosis, levels of protein, albumin, C-reactive protein, TNF-alpha, myelin basic protein, S100 protein were measured in the cerebrospinal fluid in subgroups of patients (n=14 in each group) in MS remission and exacerbation. RESULTS: Concussion and mild brain contusion were documented in the group of patients with TBI before the MS onset in 35 (79.5%) and 9 (20.5%) patients, respectively. Traumatic brain injury was over the age of 15 in 72.5% of patients. The rate of MS progression was higher in the group with TBI compared to the group without TBI (0.76±1.28 and 0.40±0.43 EDSS points per year, respectively; p=0.014). TBI before the MS onset increases the risk of disability by more than 0.25 EDSS points per year (OR 2.74; 95 CI 1.10-6.85; p=0.029). Intergroup differences in cerebrospinal fluid parameters were not found either during MS exacerbation or remission. CONCLUSION: Concussion or mild brain contusion before the MS onset may be factors influencing the progression of neurological deficit in MS. It seems relevant to study the mechanisms of adverse effects of TBI on the MS progression.
 BACKGROUND: We undertook a phase-III, randomized controlled trial (RCT) that examined the effectiveness of a behavioral intervention based on social cognitive theory (SCT) and delivered through the Internet using e-learning approaches for immediate and sustained increases in physical activity among persons with multiple sclerosis (MS). METHOD: The study followed a parallel group RCT design. Persons with MS (N = 318) were randomized into either behavioral intervention (n = 159) or attention/social contact control (n = 159) conditions. The conditions were administered over a 6-month period by persons who were uninvolved in screening, recruitment, random assignment, and outcome assessment. There was a 6-month follow-up period without access of conditions. We collected outcome data every 6 months over the 12-month period. The primary outcome was device-measured minutes/day of moderate-to-vigorous physical activity (MVPA). The data analysis involved a modified intent-to-treat approach (i.e. those who received the allocated conditions) using a linear mixed model. RESULTS: There was a significant group by time interaction on the primary outcome of device-measured minutes/day of MVPA (p < 0.005). MVPA was increased immediately after the 6-month period in the behavioral intervention compared with control, and this difference was sustained over the 6-month follow-up. CONCLUSION: This study provides evidence for the effectiveness of a widely scalable approach for increasing MVPA in persons with MS.
 BACKGROUND: Spinal cord and gadolinium (Gd)-enhanced magnetic resonance imaging (MRI) can provide additional information to brain MRI to determine prognosis of multiple sclerosis (MS). However, the real-world impact of routine use of brain MRI with spinal cord and/or Gd sequences is unknown. Our aim was to evaluate the effect of brain, spinal cord and Gd MRI on treatment decisions in MS. METHODS: In this 2015-2020 population-based study, we performed a retrospective analysis on MS patients resident in the Campania Region (South Italy), with disease modifying treatment (DMT) prescription (n = 6,161). DMTs were classified as platform (dimethyl fumarate, glatiramer acetate, interferon-beta, peg-interferon-beta, teriflunomide), or high-efficacy (alemtuzumab, cladribine, fingolimod, natalizumab, ocrelizumab). We evaluated the association between binary MRI variables and switch from platform to high-efficacy DMT using multivariable logistic regression. RESULTS: The likelihood of switch from platform to high-efficacy DMT was 47% higher when including post-Gd acquisitions to brain and/or spinal cord MRI, 59% higher when including spinal cord acquisitions to brain MRI, and 132% higher when including any MRI compared with no MRI (all p < 0.05). The likelihood of switch to high-efficacy DMT decreased over time from treatment start. CONCLUSION: Our results show that spinal cord and Gd MRI acquisitions can provide relevant information to influence subsequent treatment decisions, especially in early treatment phases, compared with stand-alone brain MRI.
 BACKGROUND: Patient stratification and individualized treatment decisions based on multiple sclerosis (MS) clinical phenotypes are arbitrary. Subtype and Staging Inference (SuStaIn), a published machine learning algorithm, was developed to identify data-driven disease subtypes with distinct temporal progression patterns using brain magnetic resonance imaging; its clinical utility has not been assessed. The objective of this study was to explore the prognostic capability of SuStaIn subtyping and whether it is a useful personalized predictor of treatment effects of natalizumab and dimethyl fumarate. METHODS: Subtypes were available from the trained SuStaIn model for 3 phase 3 clinical trials in relapsing-remitting and secondary progressive MS. Regression models were used to determine whether baseline SuStaIn subtypes could predict on-study clinical and radiological disease activity and progression. Differences in treatment responses relative to placebo between subtypes were determined using interaction terms between treatment and subtype. RESULTS: Natalizumab and dimethyl fumarate reduced inflammatory disease activity in all SuStaIn subtypes (all p < 0.001). SuStaIn MS subtyping alone did not discriminate responder heterogeneity based on new lesion formation and disease progression (p > 0.05 across subtypes). CONCLUSION: SuStaIn subtypes correlated with disease severity and functional impairment at baseline but were not predictive of disability progression and could not discriminate treatment response heterogeneity.
 BACKGROUND: Optic pathway is considered an ideal model to study the interaction between inflammation and neurodegeneration in multiple sclerosis (MS). METHODS: Optical Coherence Tomography (OCT) and 3.0 T magnetic resonance imaging (MRI) were acquired in 92 relapsing remitting (RR) MS at clinical onset. Peripapillary RNFL (pRNFL) and macular layers were measured. White matter (WM) and gray matter (GM) lesion volumes (LV), lateral geniculate nucleus (LGN) volume, optic radiations (OR) WM LV, thickness of pericalcarine cortex were evaluated. OCT and MRI control groups (healthy controls [HC]-OCT and HC-MRI) were included. RESULTS: A significant thinning of temporal pRNFL and papillo-macular bundle (PMB) was observed (p<0.001) in 16 (17%) patients presented with monocular optic neuritis (MSON+), compared to 76 MSON- and 30 HC (-15 μm). In MSON-, PMB was reduced (-3 μm) compared to HC OCT (p<0.05). INL total volume was increased both in MSON+ (p<0.001) and MSON- (p = 0.033). Inner retinal layers volumes (macular RNFL, GCL and IPL) were significantly decreased in MSON+ compared to HC (p<0.001) and MSON- (p<0.001). Reduced GCL volume in the parafoveal ring was observed in MSON- compared to HCOCT (p < 0.05). LGN volume was significantly reduced only in MSON+ patients compared to HC-MRI (p<0.001) and MSON- (p<0.007). GCL, IPL and GCIP volumes associated with ipsilateral LGN volume in MSON+ and MSON-. Finally, LGN volume associated with visual cortex thickness with no significant difference between MSON+ and MSON-. CONCLUSIONS: Anterograde trans-synaptic degeneration is early detectable in RRMS presenting with optic neuritis but does not involve LGN.
 BACKGROUND: White matter (WM) lesions and brain atrophy are present early in multiple sclerosis (MS). However, their spatio-temporal relationship remains unclear. METHODS: Yearly magnetic resonance images were analysed in 387 patients with a first clinical demyelinating event (FCDE) from the 5-year REFLEXION study. Patients received early (from baseline; N = 258; ET) or delayed treatment (from month-24; N = 129; DT) with subcutaneous interferon beta-1a. FSL-SIENA/VIENA were used to provide yearly percentage volume change of brain (PBVC) and ventricles (PVVC). Yearly total lesion volume change (TLVC) was determined by a semi-automated method. Using linear mixed models and voxel-wise analyses, we firstly investigated the overall relationship between TLVC and PBVC and between TLVC and PVVC in the same follow-up period. Analyses were then separately performed for: the untreated period of DT patients (first two years), the first year of treatment (year 1 for ET and year 3 for DT), and a period where patients had received at least 1 year of treatment (stable treatment; ET: years 2, 3, 4, and 5; DT: years 4 and 5). RESULTS: Whole brain: across the whole study period, lower TLVC was related to faster atrophy (PBVC: B = 0.046, SE = 0.013, p < 0.001; PVVC: B = -0.466, SE = 0.118, p < 0.001). Within the untreated period of DT patients, lower TLVC was related to faster atrophy (PBVC: B = 0.072, SE = 0.029, p = 0.013; PVVC: B = -0.917, SE = 0.306, p = 0.003). A similar relationship was found within the first year of treatment of ET patients (PBVC: B = 0.081, SE = 0.027, p = 0.003; PVVC: B = -1.08, SE = 0.284, p < 0.001), consistent with resolving oedema and pseudo-atrophy. Voxel-wise: overall, higher TLVC was related to faster ventricular enlargement. Lower TLVC was related to faster widespread atrophy in year 1 in both ET (first year of treatment) and DT (untreated) patients. In the second untreated year of DT patients and within the stable treatment period of ET patients (year 4), faster periventricular and occipital lobe atrophy was associated with higher TLVC. CONCLUSIONS: WM lesion changes and atrophy occurred simultaneously in early MS. Spatio-temporal correspondence of these two processes involved mostly the periventricular area. Within the first year of the study, in both treatment groups, faster atrophy was linked to lower lesion volume changes, consistent with higher shrinking and disappearing lesion activity. This might reflect the pseudo-atrophy phenomenon that is probably related to the therapy driven (only in ET patients, as they received treatment from baseline) and "natural" (both ET and DT patients entered the study after a FCDE) resolution of oedema. In an untreated period and later on during stable treatment, (real) atrophy was related to higher lesion volume changes, consistent with increased new and enlarging lesion activity.
 BACKGROUND: The motor symptoms affecting upper and lower extremity functioning in people with multiple sclerosis (PwMS) are considered the cardinal symptoms of multiple sclerosis. There is still a need for outcome measures that can sensitively evaluate these symptoms. We aimed to investigate the sensitivity of the isometric outcomes (maximum force; Fmax, maximum rate of force development; RFDmax, rate of force development scaling factor; RFD-SF, and rate of force relaxation scaling factor; RFR-SF) and standard clinical tests (9-hole peg test; 9HPT and timed 25-feet walk test; T25FW) in detecting the upper and lower extremity motor deficiencies in PwMS and also in a subgroup of mildly affected PwMS whose performance in standard clinical tests were similar to controls. METHODS: Twenty-nine PwMS (age: 47.9 (8.6) years, relapsing-remitting type, expanded disability status scale: 2.5 (1.5)) and their age- and gender-matched controls completed an identical testing protocol in the upper (grip force muscles) and lower (knee extensors) extremities. For each extremity, we assessed Fmax, RFDmax, RFD-SF, and RFR-SF. Additionally, participants completed standard clinical tests for the evaluation of upper- (9HPT) and lower-extremity (T25FW) function. Comparisons were made between controls and PwMS 1) using all study participants and 2) including only mildly affected PwMS whose performance in standard functional tests was comparable to controls. Independent sample t-tests were utilized to compare groups, with a p-value set at 0.01 to correct for multiple comparisons. P-values and effect sizes were used to evaluate the sensitivity of the outcome measures in detecting group differences. RESULTS: Our results indicate that most isometric outcomes and standard functional tests were sensitive in detecting motor deficiencies in both upper and lower extremities between groups (p<0.001). Among participants, 16 PwMS in 9HPT and 11 PwMS in T25FW demonstrated performance similar to that of the control group (9HPT: 18.85 (2.20) s vs 17.81 (2.19) s; p=0.19) and (T25FW: 3.60 (0.42) s vs 3.58 (0.29) s; p=0.92). The results of the comparisons between mildly affected PwMS and their controls indicate that RFR-SF is the only sensitive isometric outcome to detect differences between groups in the upper (-8.24 (0.76) 1/s vs -8.93 (0.6) 1/s; p=0.008) and lower extremity (-5.86 (1.13) 1/s vs -7.71 (1.11) 1/s; p<0.001). CONCLUSION: The rate of force relaxation scaling factor, which assesses the ability to rapidly relax muscle forces after quick contractions, demonstrates high sensitivity in detecting motor deficiencies in PwMS, even when the current standard clinical outcomes fail to detect these differences. Our findings emphasize the importance of future randomized controlled trials focusing on rehabilitative and therapeutic interventions that specifically target muscle force relaxation to enhance motor functioning in PwMS.
 BACKGROUND: We evaluated imaging features suggestive of neurodegeneration within the brainstem and upper cervical spinal cord (UCSC) in non-progressive multiple sclerosis (MS). METHODS: Standardized 3-Tesla three-dimensional brain magnetic resonance imaging (MRI) studies were prospectively acquired. Rates of change in volume, surface texture, curvature were quantified at the pons and medulla-UCSC. Whole and regional brain volumes and T2-weighted lesion volumes were also quantified. Independent regression models were constructed to evaluate differences between those of Black or African ancestry (B/AA) and European ancestry (EA) with non-progressive MS. RESULTS: 209 people with MS (pwMS) having at least two MRI studies, 29% possessing 3-6 timepoints, resulted in 487 scans for analysis. Median follow-up time between MRI timepoints was 1.33 (25th-75th percentile: 0.51-1.98) years. Of 183 non-progressive pwMS, 88 and 95 self-reported being B/AA and EA, respectively. Non-progressive pwMS demonstrated greater rates of decline in pontine volume (p < 0.0001) in B/AA and in medulla-UCSC volume (p < 0.0001) for EA pwMS. Longitudinal surface texture and curvature changes suggesting reduced tissue integrity were observed at the ventral medulla-UCSC (p < 0.001), dorsal pons (p < 0.0001) and dorsal medulla (p < 0.0001) but not the ventral pons (p = 0.92) between groups. CONCLUSIONS: Selectively vulnerable regions within the brainstem-UCSC may allow for more personalized approaches to disease surveillance and management.
 PURPOSE: This study aims to identify common and distinct hemodynamic and functional connectivity (FC) features for self-rated fatigue and depression symptoms in patients with clinically isolated syndrome (CIS) and relapsing-remitting multiple sclerosis (RR-MS). METHODS: Twenty-four CIS, 29 RR-MS patients, and 39 healthy volunteers were examined using resting-state fMRI (rs-fMRI) to obtain whole-brain maps of (i) hemodynamic response patterns (through time shift analysis), (ii) FC (via intrinsic connectivity contrast maps), and (iii) coupling between hemodynamic response patterns and FC. Each regional map was correlated with fatigue scores, controlling for depression, and with depression scores, controlling for fatigue. RESULTS: In CIS patients, the severity of fatigue was associated with accelerated hemodynamic response in the insula, hyperconnectivity of the superior frontal gyrus, and evidence of reduced hemodynamics-FC coupling in the left amygdala. In contrast, depression severity was associated with accelerated hemodynamic response in the right limbic temporal pole, hypoconnectivity of the anterior cingulate gyrus, and increased hemodynamics-FC coupling in the left amygdala. In RR-MS patients, fatigue was associated with accelerated hemodynamic response in the insula and medial superior frontal cortex, increased functional role of the left amygdala, and hypoconnectivity of the dorsal orbitofrontal cortex, while depression symptom severity was linked to delayed hemodynamic response in the medial superior frontal gyrus; hypoconnectivity of the insula, ventromedial thalamus, dorsolateral prefrontal cortex, and posterior cingulate; and decreased hemodynamics-FC coupling of the medial orbitofrontal cortex. CONCLUSION: There are distinct FC and hemodynamic responses, as well as different magnitude and topography of hemodynamic connectivity coupling, associated with fatigue and depression in early and later stages of MS.
 CLINICAL CASE: A 49-year-old man (MM72) affected by Secondary Progressive Multiple Sclerosis (SP-MS) since 1998. On last 3 years, neurologists valued 9.0 the patient MM72's EDSS. METHODS: MM72 was treated by acoustic waves, modulated in frequency and power by the MAM device, according to an ambulatory intensive protocol. Patient's treatments schedule was organized in thirty cycles of DrenoMAM and AcuMAM, and manual cervical spinal adjustments. Before and after treatments, MSIS-29, Barthel, FIM, EDSS, ESS, and FSS questionnaires were administered to the patient. RESULTS: MM72 patient had improvements in all index score (MSIS-29, Barthel, FIM, EDSS, ESS and FSS) after 30 treatments by MAM plus cervical spine chiropractic adjustments. He showed a significative improvement of his disability and the restore of many functions. After MAM treatments, MM72's cognitive sphere improved of 370%. Fur-thermore, after 5 years of paraplegy, he regained his lower limbs and feet fingers movements with an increase of 230%. CONCLUSION: We suggest ambulatory intensive treatments by fluid dynamic MAM protocol in SP-MS patients. Statistical analyses are in progress on a larger sample of SP-MS patients.
 OBJECTIVES: To evaluate the combined contribution of brain and cervical cord damage in predicting 5-year clinical worsening in a multicentre cohort of definite multiple sclerosis (MS) patients. METHODS: Baseline 3.0T brain and cervical cord T2-weighted and three-dimensional T1-weighted MRI was acquired in 367 patients with MS (326 relapse-onset and 41 progressive-onset) and 179 healthy controls. Expanded Disability Status Scale (EDSS) score was obtained at baseline and after a median follow-up of 5.1 years (IQR=4.8-5.2). At follow-up, patients were classified as clinically stable/worsened according to EDSS changes. Generalised linear mixed models identified predictors of clinical worsening, evolution to secondary progressive (SP) MS and reaching EDSS=3.0, 4.0 and 6.0 milestones at 5 years. RESULTS: At follow-up, 120/367 (33%) patients with MS worsened clinically; 36/256 (14%) patients with relapsing-remitting evolved to SPMS. Baseline predictors of EDSS worsening were progressive-onset versus relapse-onset MS (standardised beta (β)=0.97), higher EDSS (β=0.41), higher cord lesion number (β=0.41), lower normalised cortical volume (β=-0.15) and lower cord area (β=-0.28) (C-index=0.81). Older age (β=0.86), higher EDSS (β=1.40) and cord lesion number (β=0.87) independently predicted SPMS conversion (C-index=0.91). Predictors of reaching EDSS=3.0 after 5 years were higher baseline EDSS (β=1.49), cord lesion number (β=1.02) and lower normalised cortical volume (β=-0.56) (C-index=0.88). Baseline age (β=0.30), higher EDSS (β=2.03), higher cord lesion number (β=0.66) and lower cord area (β=-0.41) predicted EDSS=4.0 (C-index=0.92). Finally, higher baseline EDSS (β=1.87) and cord lesion number (β=0.54) predicted EDSS=6.0 (C-index=0.91). CONCLUSIONS: Spinal cord damage and, to a lesser extent, cortical volume loss helped predicting worse 5-year clinical outcomes in MS.
 Purpose: The purpose of this case report is to describe spasticity and encephalopathy that developed in a multiple sclerosis patient following carbapenem administration. Summary: A 55-year-old female with multiple sclerosis developed spasticity and encephalopathy within 24 hours of meropenem and ertapenem administration. This was the second time that she had developed encephalopathy following carbapenem administration. The patient gradually recovered over four days following discontinuation of carbapenem therapy. Conclusion: Carbapenem neurotoxicity, a well-documented adverse effect, has been linked to several risk factors, including central nervous system lesions. Despite this, there is little evidence describing the risk of neurotoxicity in patients with multiple sclerosis. It is important to understand the potential adverse effects of carbapenems in specific patient populations to help guide appropriate treatment of infections.
 BACKGROUND: MS is the most common CNS inflammatory demyelinating disease. Plasma exchange (PLEX) has well-demonstrated efficacy in acute corticosteroid-refractory attacks of demyelination but identifying the factors that predict favorable PLEX response remains elusive. We aimed to determine if apparent diffusion coefficient (ADC) restriction on brain MRI predicts clinical response to PLEX in individuals with an acute cerebral attack of MS. METHODS: Retrospective chart review of individuals with a cerebral attack of MS who underwent PLEX at Mayo Clinic. RESULTS: We identified 34 individuals who fulfilled the inclusion criteria. Twenty-seven (79%) responded to plasma exchange, with 16/34 (47%) having moderate and 11/34 (32%) marked improvement. Twenty-three (68%) people had ADC restriction on brain MRI prior to PLEX.  ADC restriction did not predict response (p = 0.51). Several other pre-PLEX factors, including sex, Expanded Disability Status Scale (EDSS) at initial attack, time to PLEX, and concurrent spinal cord attack, also failed to predict response. Plasma-exchange responders had less disability at 6-month follow-up compared to non-responders (median EDSS 2.5 (range 1.0-10.0) vs. 7.5 (5.5-10.0), p<0.001). CONCLUSION: Acute cerebral attacks of MS have a high rate of plasma exchange response resulting in a lower EDSS at 6-months. ADC restriction does not predict response to plasma exchange.
 OBJECTIVE: This study aimed to investigate the effects of multi-task training on motor and cognitive performance in People with Multiple Sclerosis (PwMS) without clinical disability compared to single-task training and a control group. METHODS: A total of 42 patients were randomly assigned to three groups labeled as Multi-Task Training Group (MTTG, n:14), Single-Task Training Group (STTG, n:14), and Control Group (CG, n:14). The STTG performed only motor tasks based on the task-oriented training program twice a week for 6 weeks while the MTTG performed the same tasks concurrently with additional motor and cognitive tasks. The CG performed relaxation exercises at home. Postural stability by posturography, walking by Timed Up-and-Go, manual dexterity by Nine-Hole Peg Test, mental tracking by Counting Backward, and verbal fluency by Word List Generation were assessed before and after the intervention under single and dual-task conditions. RESULTS: In the MTTG, both single cognitive and single motor task performances increased, and, moreover, the cognitive Dual-Task Costs (DTCs) decreased although the motor DTCs were not changed significantly. There were significant group-by-time interactions in favor of MTTG only on the mental tracking DTC during walking compared to the STTG. Moreover, the changes in postural and walking DTCs were associated with changes in single-motor task performance. CONCLUSION: This study suggests that multi-task training is effective in reducing cognitive DTC rather than motor DTC under dual-task conditions in PwMS without clinical disability. TRIAL REGISTRATION NUMBER: NCT03512886.
 PURPOSE: The current pilot, single-blind, randomized controlled trial (RCT) examined the feasibility of remotely-delivered and supported aerobic walking exercise training compared with an active control condition on cognitive processing speed (CPS) in 19 fully-ambulatory persons with multiple sclerosis (pwMS) who were pre-screened for impaired CPS. METHODS: Feasibility was assessed in the domains of process (e.g., recruitment), resource (e.g., monetary costs), management (e.g., time requirements), and scientific outcomes (i.e., treatment effect). Fully-ambulatory, but CPS-impaired pwMS were randomly assigned into either 16-weeks of home-based aerobic walking exercise or home-based stretching and range-of-motion activities. Both conditions involved delivery of informational newsletters and one-on-one, online video chats with a behavior coach. Participants across both conditions tracked their activity using highly accurate wearable motion sensors. Treatment-blinded assessors administered the Symbol Digit Modalities Test (SDMT) remotely before and after the 16-week study period. RESULTS: The study was cost-effective, accessible, and acceptable. The intervention further was safe. Adherence and compliance rates across both conditions exceeded 80%. There was an overall moderate effect for change in SDMT score between the conditions (d = 0.42). The intervention was associated with a 4.8-point improvement in SDMT scores (d = 0.70; 10% increase) compared with a 1-point improvement for the control condition (d = 0.09; 2% increase). CONCLUSIONS: This remotely-delivered and supported aerobic walking exercise training intervention was safe and feasible for fully-ambulatory, CPS-impaired pwMS. The pattern of results, including the promising effects on CPS, support the design and implementation of an appropriately-powered RCT on this approach for managing CPS impairment in a large MS sample.
 PURPOSE: Spectral-domain optical coherence tomography (SD-OCT) was used to evaluate, in patients with multiple sclerosis without a history of optic neuritis (MSNON), the proportion of the different macular ganglion cell-inner plexiform layer complex (mGCIP) defect patterns. The results were compared with those of healthy controls (HCs). METHODS: In this cross-sectional case-control study, 34 eyes of 34 individuals, 17 with MSNON and 17 HCs, were evaluated. All participants underwent mGCIP thickness measurement using SD-OCT (Zeiss Cirrus HD-OCT 4000, macular cube protocol). The mGCIP defect patterns were classified in nine types (minimal, inner, outer, diffuse mild, diffuse severe inferior confined, inferior dominant, superior confined, and superior dominant), according to the shape derived by the deviation map of the instrument, and the proportion of each type was assessed. RESULTS: A mGCIP defect pattern was detected in 70.5% of MSNON eyes, with an inner type as the most frequent pattern (47%), followed by the outer type (11.7%) and the inferior confined type (11.7%). No defect was found in Hcs. CONCLUSIONS: A significant thinning of the mGCIP with the frequent presence of an inner defect was seen in MSNON patients. The presence of this defect may serve as a biomarker of subclinical optic nerve involvement in MS patients.
 It has been shown that transcranial ultrasound stimulation (TUS) is capable of attenuating myelin loss and providing neuroprotection in animal models of brain disorders. In this study, we investigated the ability of TUS to promote remyelination in the lysolecithin (LPC)-induced local demyelination in the hippocampus. Demyelination was induced by the micro-injection of 1.5 μL LPC (1%) into the rat hippocampus and the treated group received daily TUS for 5 or 12 days. Magnetic resonance imaging techniques, including magnetization transfer ratio (MTR) and T2-weighted imaging, were used to longitudinally characterize the demyelination model. Furthermore, the therapeutic effects of TUS on LPC-induced demyelination were assessed by Luxol fast blue (LFB) staining. Our data revealed that reductions in MTR values observed during demyelination recover almost completely upon remyelination. The MTR values in demyelinated lesions were significantly higher in TUS-treated rats than in the LPC-only group after undergoing TUS. Form histological observation, TUS significantly reduced the size of demyelinated lesion 7 days after LPC administration. This study demonstrated that MTR was a sensitive and reproducible quantitative marker to assess remyelination process in vivo during TUS treatment. These findings might open new promising treatment strategies for demyelinating diseases such as multiple sclerosis.
 BACKGROUND: Neurofilament light chain (NfL), a neuronal cytoskeletal protein that is released upon neuroaxonal injury, is associated with multiple sclerosis (MS) relapsing activity and has demonstrated some prognostic ability for future relapse-related disease progression, yet its value in assessing non-relapsing disease progression remains unclear. METHODS: We examined baseline and longitudinal blood NfL levels in 1421 persons with relapsing MS (RMS) and 596 persons with primary progressive MS (PPMS) from the pivotal ocrelizumab MS trials. NfL treatment-response and risk for disease worsening (including disability progression into the open-label extension period and slowly expanding lesions [SELs] on brain MRI) at baseline and following treatment with ocrelizumab were evaluated using time-to-event analysis and linear regression models. FINDINGS: In persons from the RMS control arms without acute disease activity and in the entire PPMS control arm, higher baseline NfL was prognostic for greater whole brain and thalamic atrophy, greater volume expansion of SELs, and clinical progression. Ocrelizumab reduced NfL levels vs. controls in persons with RMS and those with PPMS, and abrogated the prognostic value of baseline NfL on disability progression. Following effective suppression of relapse activity by ocrelizumab, NfL levels at weeks 24 and 48 were significantly associated with long-term risk for disability progression, including up to 9 years of observation in RMS and PPMS. INTERPRETATION: Highly elevated NfL from acute MS disease activity may mask a more subtle NfL abnormality that reflects underlying non-relapsing progressive biology. Ocrelizumab significantly reduced NfL levels, consistent with its effects on acute disease activity and disability progression. Persistently elevated NfL levels, observed in a subgroup of persons under ocrelizumab treatment, demonstrate potential clinical utility as a predictive biomarker of increased risk for clinical progression. Suppression of relapsing biology with high-efficacy immunotherapy provides a window into the relationship between NfL levels and future non-relapsing progression. FUNDING: F. Hoffmann-La Roche Ltd.
 BACKGROUND: Alemtuzumab is effective in reducing relapse rate and disability, but limited data exist on its effect on cognitive function in relapsing multiple sclerosis (RMS). The present study assessed neurocognitive function and safety associated with alemtuzumab treatment in RMS. METHODS: This longitudinal, single-arm, prospective study included people with RMS (aged 25-55 years) who were treated with alemtuzumab in clinical practice in the United States of America and Canada. The first participant was enrolled in December 2016. The primary endpoint was the change from baseline to post-baseline (month [M] 12/24) in MS-COGnitive (MS-COG) composite score. Secondary endpoints included Paced Auditory Serial Addition Test (PASAT), Symbol Digit Modalities Test (SDMT), Brief Visuospatial Memory Test-Revised (BVMT-R), Selective Reminding Test (SRT), Controlled Oral Word Association Test (COWAT), and Automated Neuropsychological Assessment Metrics (ANAM) scores. Depression and fatigue were assessed using Hamilton Rating Scale-Depression (HAM-D) and Fatigue Severity Scale (FSS)/Modified Fatigue Impact Scale (MFIS), respectively. Magnetic resonance imaging (MRI) parameters were assessed when available. Safety was assessed throughout the study. Descriptive statistics were used for the pre-specified statistical analyses. Since the study was terminated early (November 2019) because of operational and resource difficulties, post hoc analyses for statistical inference were performed among participants who had a baseline value and at least one complete post-baseline assessment for cognitive parameters, fatigue, or depression. RESULTS: Of the 112 participants enrolled, 39 were considered as the primary analysis population at M12. At M12, a mean change of 0.25 (95% confidence interval [CI]: 0.04, 0.45; p = 0.0049; effect size [ES]: 0.39) was observed in the MS-COG composite score. Improvements were observed in processing speed (based on PASAT and SDMT; p < 0.0001; ES: 0.62), as well as in individual PASAT, SDMT and COWAT scores. An improvement was also noted in HAM-D (p = 0.0054; ES: -0.44), but not in fatigue scores. Among MRI parameters, decreases in burden of disease volume (BDV; ES: -0.12), new gadolinium-enhancing lesions (ES: -0.41) and newly active lesions (ES: -0.07) were observed at M12. About 92% of participants showed stable or improved cognitive status at M12. There were no new safety signals reported in the study. The most common adverse events (≥10% of participants) were headache, fatigue, nausea, insomnia, urinary tract infection, pain in extremity, chest discomfort, anxiety, dizziness, arthralgia, flushing, and rash. Hypothyroidism (3.7%) was the most frequent adverse event of special interest. CONCLUSION: The findings from this study suggest that alemtuzumab has a positive impact on cognitive function with significant improvements in processing speed and depression in people with RMS over a period of 12 months. The safety profile of alemtuzumab was consistent with previous studies.
 BACKGROUND AND OBJECTIVES: Ganglion cell + inner plexiform layer (GCIPL) thinning, measured by optical coherence tomography (OCT), reflects global neurodegeneration in multiple sclerosis (MS). Atrophy of the inner (INL) and outer nuclear layer (ONL) may also be prominent in progressive MS (PMS). The phase 2, SPRINT-MS trial found reduced brain atrophy with ibudilast therapy in PMS. In this post hoc analysis of the SPRINT-MS trial, we investigate (1) retinal atrophy (2) differences in response by subtype and (3) associations between OCT and MRI measures of neurodegeneration. METHODS: In the multicenter, double-blind SPRINT-MS trial, participants with secondary progressive MS (SPMS) or primary progressive MS (PPMS) were randomized to ibudilast or placebo. OCT and MRI data were collected every 24 weeks for 96 weeks. Extensive OCT quality control and algorithmic segmentation produced consistent results across Cirrus HD-OCT and Spectralis devices. Primary endpoints were GCIPL, INL, and ONL atrophy, assessed by linear mixed-effects regression. Secondary endpoints were associations of OCT measures, brain parenchymal fraction, and cortical thickness, assessed by partial Pearson correlations. RESULTS: One hundred thirty-four PPMS and 121 SPMS participants were included. GCIPL atrophy was 79% slower in the ibudilast (-0.07 ± 0.23 µm/y) vs placebo group (-0.32 ± 0.20 µm/y, p = 0.003). This effect predominated in the PPMS cohort (ibudilast: -0.08 ± 0.29 µm/y vs placebo: -0.60 ± 0.29 µm/y, a decrease of 87%, p < 0.001) and was not detected in the SPMS cohort (ibudilast: -0.21 ± 0.28 µm/y vs placebo: -0.14 ± 0.27 µm/y, p = 0.55). GCIPL, INL, and ONL atrophy rates correlated with whole brain atrophy rates across the cohort (r = 0.27, r = 0.26, and r = 0.20, respectively; p < 0.001). Power calculations from these data show future trials of similar size and design have ≥80% power to detect GCIPL atrophy effect sizes of approximately 40%. DISCUSSION: Ibudilast treatment decreased GCIPL atrophy in PMS, driven by the PPMS cohort, with no effect seen in SPMS. Modulated atrophy of retinal layers may be detectable in sample sizes smaller than the SPRINT-MS trial and correlate with whole brain atrophy in PMS, further highlighting their utility as outcomes in PMS. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that ibudilast reduces composite ganglion cell + inner plexiform layer atrophy, without reduction of inner or outer nuclear layer atrophy, in patients with primary progressive MS but not those with secondary progressive MS.
 T2 lesion quantification plays a crucial role in monitoring disease progression and evaluating treatment response in multiple sclerosis (MS). We developed a 3D, multi-arm U-Net for T2 lesion segmentation, which was trained on a large, multicenter clinical trial dataset of relapsing MS. We investigated its generalization to other relapsing and primary progressive MS clinical trial datasets, and to an external dataset from the MICCAI 2016 MS lesion segmentation challenge. Additionally, we assessed the model's ability to reproduce the separation of T2 lesion volumes between treatment and control arms; and the association of baseline T2 lesion volumes with clinical disability scores compared with manual lesion annotations. The trained model achieved a mean dice coefficient of ≥ 0.66 and a lesion detection sensitivity of ≥ 0.72 across the internal test datasets. On the external test dataset, the model achieved a mean dice coefficient of 0.62, which is comparable to 0.59 from the best model in the challenge, and a lesion detection sensitivity of 0.68. Lesion detection performance was reduced for smaller lesions (≤ 30 μL, 3-10 voxels). The model successfully maintained the separation of the longitudinal changes in T2 lesion volumes between the treatment and control arms. Such tools could facilitate semi-automated MS lesion quantification; and reduce rater burden in clinical trials.
 PURPOSE: Recent studies suggest an involvement of the peripheral nervous system (PNS) in multiple sclerosis (MS). Here, we characterize the proximal-to-distal distribution pattern of peripheral nerve lesions in relapsing-remitting MS (RRMS) by quantitative magnetic resonance neurography (MRN). METHODS: A total of 35 patients with RRMS were prospectively included and underwent detailed neurologic and electrophysiologic examinations. Additionally, 30 age- and sex-matched healthy controls were recruited. 3T MRN with anatomical coverage from the proximal thigh down to the tibiotalar joint was conducted using dual-echo 2‑dimensional relaxometry sequences with spectral fat saturation. Quantification of PNS involvement was performed by evaluating microstructural (proton spin density (ρ), T2-relaxation time (T2(app))), and morphometric (cross-sectional area, CSA) MRN markers in every axial slice. RESULTS: In patients with RRMS, tibial nerve lesions at the thigh and the lower leg were characterized by a decrease in T2(app) and an increase in ρ compared to controls (T2(app) thigh: p < 0.0001, T2(app) lower leg: p = 0.0040; ρ thigh: p < 0.0001; ρ lower leg: p = 0.0098). An additional increase in nerve CSA was only detectable at the thigh, while the semi-quantitative marker T2w-signal was not altered in RRMS in both locations. A slight proximal-to-distal gradient was observed for T2(app) and T2-signal, but not for ρ. CONCLUSION: PNS involvement in RRMS is characterized by a decrease in T2(app) and an increase in ρ, occurring with proximal predominance at the thigh and the lower leg. Our results indicate microstructural alterations in the extracellular matrix of peripheral nerves in RRMS and may contribute to a better understanding of the pathophysiologic relevance of PNS involvement.
 BACKGROUND AND OBJECTIVES: Excessive activation of certain lipid mediator (LM) pathways plays a role in the complex pathogenesis of multiple sclerosis (MS). However, the relationship between bioactive LMs and different aspects of CNS-related pathophysiologic processes remains largely unknown. Therefore, in this study, we assessed the association of bioactive LMs belonging to the ω-3/ω-6 lipid classes with clinical and biochemical (serum neurofilament light [sNfL] and serum glial fibrillary acidic protein [sGFAP]) parameters and MRI-based brain volumes in patients with MS (PwMS) and healthy controls (HCs). METHODS: A targeted high-performance liquid chromatography-tandem mass spectrometry approach was used on plasma samples of PwMS and HCs of the Project Y cohort, a cross-sectional population-based cohort that contains PwMS all born in 1966 in the Netherlands and age-matched HCs. LMs were compared between PwMS and HCs and were correlated with levels of sNfL, sGFAP, disability (Expanded Disability Status Scale [EDSS]), and brain volumes. Finally, significant correlates were included in a backward multivariate regression model to identify which LMs best related to disability. RESULTS: The study sample consisted of 170 patients with relapsing remitting MS (RRMS), 115 patients with progressive MS (PMS), and 125 HCs. LM profiles of patients with PMS significantly differed from those of patients with RRMS and HCs, particularly patients with PMS showed elevated levels of several arachidonic acid (AA) derivatives. In particular, 15-hydroxyeicosatetraenoic acid (HETE) (r = 0.24, p < 0.001) correlated (average r = 0.2, p < 0.05) with clinical and biochemical parameters such as EDSS and sNfL. In addition, higher 15-HETE levels were related to lower total brain (r = -0.24, p = 0.04) and deep gray matter volumes (r = -0.27, p = 0.02) in patients with PMS and higher lesion volume (r = 0.15, p = 0.03) in all PwMS. DISCUSSION: In PwMS of the same birth year, we show that ω-3 and ω-6 LMs are associated with disability, biochemical parameters (sNfL, GFAP), and MRI measures. Furthermore, our findings indicate that, particularly, in patients with PMS, elevated levels of specific products of the AA pathway, such as 15-HETE, associate with neurodegenerative processes. Our findings highlight the potential relevance of ω-6 LMs in the pathogenesis of MS.

 BACKGROUND: Fatigue is common and disabling in multiple sclerosis (MS), yet its mechanisms are poorly understood. In particular, overlap in measures of fatigue and depression complicates interpretation. We applied a multivariate network approach to quantify relationships between fatigue and other variables in early MS. METHODS: Data were collected from patients with newly diagnosed immunotherapy-naïve relapsing-remitting MS at baseline and month 12 follow-up in FutureMS, a Scottish nationally representative cohort. Subjective fatigue was assessed by Fatigue Severity Scale. Detailed phenotyping included measures assessing each of physical disability, affective disorders, cognitive performance, sleep quality, and structural brain imaging. Network analysis was conducted to estimate partial correlations between variables. Baseline networks were compared between those with persistent and remitted fatigue at one-year follow up. RESULTS: Data from 322 participants at baseline, and 323 at month 12, were included. At baseline, 154 patients (47.8%) reported clinically significant fatigue. In the network analysis, fatigue severity showed strongest connections with depression, followed by Expanded Disability Status Scale. Conversely, fatigue severity was not linked to objective cognitive performance or brain imaging variables. Even after controlling for measurement of "tiredness" in our measure of depression, four specific depressive symptoms remained linked to fatigue. Results were consistent at baseline and month 12. Overall network strength was not significantly different between groups with persistent and remitted fatigue (4.89 vs 2.90, p = 0.11). CONCLUSIONS: Our findings support robust links between subjective fatigue and depression in early relapsing-remitting MS. Shared mechanisms between specific depressive symptoms and fatigue could be key targets of treatment and research in MS-related fatigue.
 INTRODUCTION: Quantitative MRI quantifies tissue microstructural properties and supports the characterization of cerebral tissue damages. With an MPM protocol, 4 parameter maps are constructed: MTsat, PD, R1 and R2*, reflecting tissue physical properties associated with iron and myelin contents. Thus, qMRI is a good candidate for in vivo monitoring of cerebral damage and repair mechanisms related to MS. Here, we used qMRI to investigate the longitudinal microstructural changes in MS brain. METHODS: Seventeen MS patients (age 25-65, 11 RRMS) were scanned on a 3T MRI, in two sessions separated with a median of 30 months, and the parameters evolution was evaluated within several tissue classes: NAWM, NACGM and NADGM, as well as focal WM lesions. An individual annual rate of change for each qMRI parameter was computed, and its correlation to clinical status was evaluated. For WM plaques, three areas were defined, and a GLMM tested the effect of area, time points, and their interaction on each median qMRI parameter value. RESULTS: Patients with a better clinical evolution, that is, clinically stable or improving state, showed positive annual rate of change in MTsat and R2* within NAWM and NACGM, suggesting repair mechanisms in terms of increased myelin content and/or axonal density as well as edema/inflammation resorption. When examining WM lesions, qMRI parameters within surrounding NAWM showed microstructural modifications, even before any focal lesion is visible on conventional FLAIR MRI. CONCLUSION: The results illustrate the benefit of multiple qMRI data in monitoring subtle changes within normal appearing brain tissues and plaque dynamics in relation with tissue repair or disease progression.
 OBJECTIVES: The purpose of this work was to evaluate the influence of residual quadrupolar interaction on the determination of human brain apparent tissue sodium concentrations (aTSCs) using quantitative sodium magnetic resonance imaging ( 23 Na MRI) in healthy controls (HCs) and patients with multiple sclerosis (MS). Especially, it was investigated if the more detailed examination of residual quadrupolar interaction effects enables further analysis of the observed 23 Na MRI signal increase in MS patients. MATERIALS AND METHODS: 23 Na MRI with a 7 T MR system was performed on 21 HC and 50 MS patients covering all MS subtypes (25 patients with relapsing-remitting MS, 14 patients with secondary progressive MS, and 11 patients with primary progressive MS) using 2 different 23 Na pulse sequences for quantification: a commonly used standard sequence (aTSC Std ) as well as a sequence with shorter excitation pulse length and lower flip angle for minimizing signal loss resulting from residual quadrupolar interactions (aTSC SP ). Apparent tissue sodium concentration was determined using the same postprocessing pipeline including correction of the receive profile of the radiofrequency coil, partial volume correction, and relaxation correction. Spin dynamic simulations of spin-3/2 nuclei were performed to aid in the understanding of the measurement results and to get deeper insight in the underlying mechanisms. RESULTS: In normal-appearing white matter (NAWM) of HC and all MS subtypes, the aTSC SP values were approximately 20% higher than the aTSC Std values ( P < 0.001). In addition, the ratio aTSC SP /aTSC Std was significantly higher in NAWM than in normal-appearing gray matter (NAGM) for all subject cohorts ( P < 0.002). In NAWM, aTSC Std values were significantly higher in primary progressive MS compared with HC ( P = 0.01) as well as relapsing-remitting MS ( P = 0.03). However, in contrast, no significant differences between the subject cohorts were found for aTSC SP . Spin simulations assuming the occurrence of residual quadrupolar interaction in NAWM were in good accordance with the measurement results, in particular, the ratio aTSC SP /aTSC Std in NAWM and NAGM. CONCLUSIONS: Our results showed that residual quadrupolar interactions in white matter regions of the human brain have an influence on aTSC quantification and therefore must be considered, especially in pathologies with expected microstructural changes such as loss of myelin in MS. Furthermore, the more detailed examination of residual quadrupolar interactions may lead to a better understanding of the pathologies themselves.
 Pilot trials have suggested that repetitive transcranial magnetic stimulation (rTMS) may reduce limb spasticity in multiple sclerosis (MS). We carried out the current meta-analysis to synthesize currently available evidence regarding such correlation. Up to November 2022, five international electronic databases (Cochrane CENTRAL, PubMed, Embase, Web of Science, and CINAHL) and four Chinese electronic databases (CBM, CNKI, WanFang Data, and VIP) were systematically searched to identify randomized trials comparing active rTMS and sham stimulation in patients with MS-related spasticity. Two reviewers independently selected studies and extracted data on study design, quality, clinical outcomes, and time points measured. The primary outcome was clinical spasticity relief after intervention. Secondary outcomes included spasticity at the follow-up visit 2 weeks later and post-treatment fatigue. Of 831 titles found, we included 8 studies (181 participants) in the quantitative analysis. Pooled analyses showed that rTMS therapy was associated with significant spasticity relief in the early post-intervention period [standardized mean differences (SMD): -0.67; 95%CI: -1.12 to -0.21], but there was insufficient evidence for rTMS in reducing spasticity at the follow-up visit 2 weeks later (SMD: -0.17; 95%CI: -0.52 to 0.17) and fatigue (SMD: -0.26; 95%CI: -0.84 to 0.31). This evidence supports the recommendations to treat MS-related spasticity with rTMS, but underlines the need for further large randomized trials.
 BACKGROUND: The effect of disease modifying therapies (DMTs) on brain atrophy in persons with multiple sclerosis (pwMS) is typically investigated in highly standardized clinical trial settings or single-center academic institutions. We aimed at utilizing artificial intelligence (AI)-based volumetric analysis on routine unstandardized T2-FLAIR scans in determining the effect of DMTs on lateral ventricular volume (LVV) and thalamic volume (TV) changes in pwMS. METHODS: The DeepGRAI (Deep Gray Rating via Artificial Intelligence) registry is a multi-center, longitudinal, observational, real-word study with a convenience sample of 1002 relapsing-remitting (RR) pwMS from 30 United States sites. Brain MRI exams acquired as part of the routine clinical management were collected at baseline and on average at 2.6-years follow-up. The MRI scans were acquired either on 1.5T or 3T scanners with no prior harmonization. TV was determined using the DeepGRAI tool and lateral ventricular volume LVV was measured using NeuroSTREAM software. RESULTS: After propensity matching based on baseline age, disability and time of follow-up, untreated pwRRMS had significantly greater TV change when compared to treated pwRRMS (-1.2% vs. -0.3%, p = 0.044). PwRRMS treated with high-efficacy DMTs had significant and two-fold lower% LVV change when compared to pwRRMS treated on moderate-efficacy DMTs (3.5% vs. 7.0%, p = 0.001). PwRRMS who stopped DMT during the follow-up had significantly greater annualized% TV change compared to pwRRMS who remained on their DMT (-0.73% vs. -0.14%, p = 0.012) and significantly greater annualized% LVV change (3.4% vs. 1.7%, p = 0.047). These findings were also observed in a propensity analysis that additionally incorporated matching for scanner model at both baseline and follow-up visits. CONCLUSIONS: LVV and TV measured on T2-FLAIR scans can detect treatment-induced short-term neurodegenerative changes measured in a real-word unstandardized, multicenter, clinical routine setting.
 BACKGROUND AND OBJECTIVES: Inflammation of the choroid plexus (CP) has been reported in multiple sclerosis (MS). The AU1 association between CP inflammation and clinical disability progression is still under debate. The objective of the current study was to assess the relationship between measures of CP inflammation and investigate their associations with clinical disability progression in MS. METHODS: In this retrospective analysis of a longitudinal study, 174 patients with MS (118 with relapsing-remitting MS and 56 with progressive MS [PMS]) and 56 healthy controls (HCs), group matched for age and sex, were imaged on a 3T MRI scanner at baseline and after an average of 5.5 years of follow-up. T2 lesion volume (T2-LV) was assessed. Regional tissue volumes were calculated. CP volume was measured, and pseudo-T2 (pT2) mapping was performed to asses CP inflammation. Group comparisons and correlations were adjusted for age and sex. RESULTS: Patients with MS presented with significantly larger CP volume (p = 0.01) and increased CP pT2 (<0.001) at baseline, when compared with HCs. CP volume and CP pT2 did not significantly increase over the follow-up in the MS sample. However, baseline CP pT2 was associated with clinical disability progression at follow-up (p = 0.001), even after controlling for all other factors significantly associated with disability progression (p = 0.030), including T2-LV, normalized brain volume, normalized gray matter volume, and normalized thalamic volumes. Changes in CP volume and CP pT2 were not related to changes in clinical parameters such as relapse rate over the course of the follow-up. DISCUSSION: CP inflammation, as evidenced by MRI, is clinically relevant in MS. CP inflammation may have a relevant role in driving disease progression.
 OBJECTIVES: To evaluate the impact of early (at first-line) vs delayed (3-year delay) ofatumumab initiation and long-term clinical, societal, and economic outcomes of ofatumumab vs teriflunomide in relapsing multiple sclerosis (RMS) patients from a Spanish societal perspective. METHODS: A cost-consequence analysis was conducted using an Expanded Disability Status Scale (EDSS)-based Markov model. Inputs were sourced from ASCLEPIOS I and II trials and published literature. RESULTS: At the end of 10 years, compared with first-line teriflunomide treatment, early first-line ofatumumab initiation was projected to result in 35.6% fewer patients progressing to EDSS ≥ 7 and 27.8% fewer relapses. The ofatumumab cohort required 7.3% reduced informal care time and had 19% fewer disability-adjusted life years (DALYs) than the teriflunomide cohort. A 3-year delay in ofatumumab treatment (3-year teriflunomide + 7-year ofatumumab) was projected to result in 32.2% more patients progressing to EDSS ≥ 7, 20.2% more relapses, 5.4% increased informal care time, and 16.6% more DALYs compared with early ofatumumab initiation. Early ofatumumab initiation was associated with total annual cost savings (excluding disease-modifying-therapies' acquisition costs) of €35,328 ($34,549; conversion factor 1€= $1.02255) and €24,373 ($23,836) per patient vs teriflunomide and 3-year delayed ofatumumab initiation, respectively. CONCLUSIONS: This study highlights the benefits of early initiation of high-efficacy therapy such as ofatumumab vs its delayed initiation for improving the outcomes in RMS patients (having characteristics similar to those of patients included in the ASCLEPIOS trials). Ofatumumab treatment was projected to provide improved long-term clinical, societal, and economic outcomes vs teriflunomide treatment in RMS patients from a Spanish societal perspective.

 BACKGROUND: Sensoready® autoinjector pen facilitates self-administration of subcutaneous ofatumumab injections at home. We aim to investigate patient and nurse preference for using Sensoready® versus comparator autoinjectors in multiple sclerosis (MS). METHODS: A pilot survey was conducted in Germany followed by in-field interviews across United States, Germany, France, and Italy. The survey recruited 80 MS patients and 50 MS nurses. Respondents were interviewed for 45-min on qualitative open-ended and quantitative close-ended survey consisting of 31 questions for patients and 41 for nurses. Ratings were measured on Likert scale from 1 (not at all important) to 10 (extremely important). RESULTS: "Easy to perform self-injection with the pen" and "Patient able to use independently" (both, mean overall score 9.4) were the most important attributes for both patients and nurses. Sensoready® scored high across most important attributes for both patients and nurses (p < 0.05). Sensoready® was preferred over comparator devices across majority of the important attributes (84%; p < 0.05), especially ease of use of the pen (mean overall score 9.4). Sensoready® was preferred over their current device by 9/10 nurses and 8/10 patients if they had to choose a treatment based on the device alone. CONCLUSION: Both MS patients and nurses preferred the Sensoready® (ofatumumab) over comparator autoinjectors for their treatment, mostly driven by ease of administration.
 BACKGROUND: The added value of patient-reported outcome measures (PROMs) in addition to standard clinical outcome tools in the assessment of relapsing-remitting multiple sclerosis (RRMS) patients' status is increasingly recognized. PROMs facilitate the detection of hidden aspects of MS and help to integrate the patient's subjective experience of health-related quality of life (HRQoL) status and treatment satisfaction in a holistic way. However, the relationship between PROMs and clinical and cognitive status has been scarcely investigated up to now. OBJECTIVE: To investigate the association of PROMs with physical and cognitive disability in a cohort of RRMS patients at initiation of a new disease-modifying treatment. METHODS: In this cross-sectional bicenter study, 59 consecutive RRMS patients underwent neurological examination with EDSS assessment, comprehensive cognitive tests (BVMT-R, SDMT, CVLT-II) and a set of self-reported questionnaires. Lesion and brain volumes were analyzed and processed by the automated MSmetrix(®) software (Icometrix(®), Leuven, Belgium). Spearman's correlation coefficient was used to evaluate the association of collected variables. A cross-sectional logistic regression analysis was performed to find baseline correlates of cognitive impairment. RESULTS: Of the 59 RRMS patients (mean age 39 ± 9.8 years, 79.7% female, median EDSS 2.0), 33 (56%) had cognitive impairment. While almost all dimensions of health, explored by PROMs, were impacted in the overall sample, no significant difference was observed in patients with and without cognitive impairment. All PROMs were significantly associated with EDSS (R = 0.37-0.55; p < 0.05), except for the psychological component of MSIS-29, BDI and DEX-Q scores. No significant correlation was found between PROMs and cognitive performances. The cross-sectional logistic regression analysis included age, gender (female), education, EDSS, hippocampus and FLAIR lesion volumes as significant predictors of cognitive impairment. CONCLUSIONS: The data highlight that PROMs provide valuable information on the well-being of PwMS closely paralleling the extent of MS-related disability, as measured by the EDSS. Additional research should determine the relevance of PROMs as longitudinal outcome measures.
 OBJECTIVE: To study the efficacy of ocrelizumab (OCR) and natalizumab (NAT) using indicators of activity and progression in patients with highly active multiple sclerosis (HAMS) during the first year of therapy in real clinical practice. MATERIAL AND METHODS: The study included 110 patients with HAMS and 13 patients with rapidly progressive MS (RPMS), aged 19 to 60 years, who received monoclonal antibody (MAT) therapy for 12 months. Group 1 consisted of 77 patients receiving NAT therapy, group 2 of 46 patients receiving OCR therapy. To assess the efficacy of therapy, we used indicators of the average frequency of exacerbations per year, EDSS estimates, and MRI data. RESULTS: EDSS score at the time of initiation of MAT therapy was 2.4±1.0 in group 1 and 2.8±1.2 in group 2 (p=0.047); 12 months after the start of MAT therapy, EDSS score in group 1 decreased slightly (p=0.001), in group 2 it has not changed. The frequency of exacerbations per year after the start of MAT therapy was 0.04±0.2 in group 1 and 0.07±0.2 in group 2 (p<0.0001 in both groups). The number of foci accumulating gadolinium detected during the year was 3 in group 1, one in group 2 (p=0.629 between groups). Subgroups of patients who received line 1 DMT (n=22) or NAT (n=21) before the start of OCR therapy were considered separately. In both subgroups, a stable assessment of EDSS was noted, the average annual number of exacerbations did not differ (p=0.117). In patients with RPMS after a year of MAT therapy, EDSS scores were stable, the average annual frequency of exacerbations was 0.08±0.3 per year. CONCLUSION: The administration of MAT therapy led to a statistically significant decrease in the number of exacerbations and stabilization of neurological deficits during the first year of follow-up. After 12 months of therapy, both groups experienced a dramatic decrease in the average annual number of exacerbations, no increase in disability, and positive dynamics according to MRI results. A similar level of OCR efficacy was found in patients who switched from DMT 1 line therapy and NAT.
 In experimental autoimmune encephalomyelitis, neurological deficit correlates with axonal loss and the CD8+ T cells are a likely mediator of axonal damage. In relapsing-remitting multiple sclerosis, there is a correlation of the immune inflammatory activity in the lesion foci with the axon transection.
 The patient was a 44-year-old man who developed cognitive impairment beginning at the age of 35 years that gradually worsened. The cognitive impairment led to a difficult social life, and he retired from his company. After hospitalization and workup, he was diagnosed with primary progressive multiple sclerosis (PPMS) that presented only with cognitive impairment for 10 years. Since he had multiple predictive factors for poor prognosis, anti-CD20 monoclonal antibody therapy was implemented. Cognitive impairment and cerebral blood flow SPECT findings improved, and he returned to a social life 3 months later. Anti-CD20 monoclonal antibody therapy was effective in improving cognitive impairment in a case of an advanced stage of PPMS.



 OBJECTIVE: This article discusses obstetric and gynecologic associations with common neurologic disorders. LATEST DEVELOPMENTS: Neurologic complications of obstetric and gynecologic disorders can arise throughout the lifespan. Caution should be exercised when prescribing fingolimod and natalizumab to patients with multiple sclerosis who are of childbearing potential because of the risk of disease rebound when they are discontinued. OnabotulinumtoxinA is considered safe in pregnancy and lactation based on long-term observational data. Hypertensive disorders of pregnancy are associated with higher subsequent cerebrovascular risk, likely via multiple mechanisms. ESSENTIAL POINTS: Neurologic disorders may present in a variety of obstetric and gynecologic contexts, with meaningful implications for recognition and treatment. These interactions must be considered when treating women with neurologic conditions.
 BACKGROUND: Natalizumab is a high-efficacy therapy for recurrent multiple sclerosis (RMS) with a four-week administration interval. Controlled trials have shown that extending this interval to six weeks led to better safety without increasing the risk of relapse. We aimed to analyze the safety of extending the natalizumab interdose interval from 4 to 6 weeks in a real-life setting. METHODS: This monocentric retrospective self-controlled study included adult patients with RMS treated with natalizumab with a four-week interval between infusions for a minimum of six months, before switching to a six-week interval. The main outcomes were the incidence of MS relapse, new MRI lesions, and MRI activity signs during the two periods, with patients being their own controls. RESULTS: Fifty-seven patients were included in the analysis. The mean (95%CI) annualized relapse rate (AAR) before natalizumab introduction was 1.03 (0.52; 1.55). During the four-week interval dosing period, no patient presented with an MS relapse, and seven (13.5%) patients had new MRI lesions. During the six-week interval dosing period, no relapse was observed and two (3.6%) patients had new MRI lesions. CONCLUSION: We did not observe more relapses or signs of MRI activity when extending the interval between natalizumab infusions from four to six weeks.
 BACKGROUND AND OBJECTIVE: Cognitive and physical functions correlate and delineate aging and disease trajectories. Whereas cognitive reserve (CR) is well-established, physical reserve (PR) is poorly understood. We, therefore, developed and evaluated a novel and more comprehensive construct, individual reserve (IR), comprised of residual-derived CR and PR in older adults with and without multiple sclerosis (MS). We hypothesized that: (a) CR and PR would be positively correlated; (b) low CR, PR, and IR would be associated with worse study outcomes; (c) associations of brain atrophy with study outcomes would be stronger in lower compared to higher IR due to compensatory mechanisms conferred by the latter. METHODS: Older adults with MS (n = 66, mean age = 64.48 ± 3.84 years) and controls (n = 66, mean age = 68.20 ± 6.09 years), underwent brain MRI, cognitive assessment, and motoric testing. We regressed the repeatable battery for the assessment of neuropsychological status and short physical performance battery on brain pathology and socio-demographic confounders to derive independent residual CR and PR measures, respectively. We combined CR and PR to define a 4-level IR variable. The oral symbol digit modalities test (SDMT) and timed-25-foot-walk-test (T25FW) served as outcome measures. RESULTS: CR and PR were positively correlated. Low CR, PR and IR were associated with worse SDMT and T25FW performances. Reduced left thalamic volume, a marker of brain atrophy, was associated with poor SDMT and T25FW performances only in individuals with low IR. The presence of MS moderated associations between IR and T25FW performance. CONCLUSION: IR is a novel construct comprised of cognitive and physical dimensions representing collective within-person reserve capacities.
 Oligodendrocytes are responsible for myelinating central nervous system (CNS) axons and rapid electrical transmission through saltatory conduction of action potentials. Myelination and myelin repair rely partially on oligodendrogenesis, which comprises oligodendrocyte precursor cell (OPC) migration, maturation, and differentiation into oligodendrocytes (OL). In multiple sclerosis (MS), demyelination occurs due to an inflammatory cascade with auto-reactive T-cells. When oligodendrogenesis fails, remyelination becomes aberrant and conduction impairments are no longer restored. Although current disease modifying therapies have achieved results in modulating the faulty immune response, disease progression continues because of chronic inflammation, neurodegeneration, and failure of remyelination. Therapies have been tried to promote remyelination. Modulation of neuronal activity seems to be a very promising strategy in preclinical studies. Additionally, studies in people with MS (pwMS) have shown symptom improvement following non-invasive brain stimulation. (NIBS) techniques. The aforementioned mechanisms are yet unknown and probably involve both the activation of neurons and glial cells. Noting neuronal activity contributes to myelin plasticity and that NIBS modulates neuronal activity; we argue that NIBS is a promising research horizon for demyelinating diseases. We review the hypothesized pathways through which NIBS may affect both neuronal activity in the CNS and how the resulting activity can affect oligodendrogenesis and myelination.
 The association between trigeminal neuralgia (TN) and multiple sclerosis (MS) is well established. Many MS patients with TN have magnetic resonance imaging (MRI) evidence of a symptomatic demyelinating lesion. Although infratentorial presentations are included in the diagnostic criteria for MS, there remains confusion in clinical practice as to whether TN should be considered a clinically isolated syndrome for the application of McDonald criteria. In this case series, we discuss this diagnostic quandary in patients presenting with TN and additional MRI findings suggestive of MS and highlight the unmet need for data in such patients to optimally guide their care.
 OBJECTIVE: To investigate a disease-modifying drugs (DMD) response in multiple sclerosis (MS) in the Tomsk region population and detect clinical factors associated with the treatment response. MATERIAL AND METHODS: A 5-year prospective clinical study included 363 MS patients of the Tomsk region taking DMDs of the «first-line» and «second-line treatments». The response to DMDs therapy and the impact of MS clinical characteristics on response to treatment were assessed. RESULTS: Clinical factors associated with resistance to DMD are male gender, partial reduce of the MS onset symptoms, short period of the first remission, severe neurological impairment, high relapse rate and disease progression rate. CONCLUSION: Clinical features of MS are crucial factors associated with DMD response and should be used to prescribe DMD. This factor assessment can improve efficacy of the personalized MS treatment.

 Genchi et al.(1) report the first phase 1 trial of neural stem cell transplantation in multiple sclerosis showing a reduction in gray matter atrophy. Results give hope for a new era of induced neuroprotection, especially in progressive multiple sclerosis.
 BACKGROUND: Knowledge within the field of multiple sclerosis treatment during pregnancy is vital to ensure the most optimal clinical practice. Immunomodulatory treatment in pregnancy could in theory affect the normal development and maturation of the immune system of the fetus with a potential increased risk of infections, consequently. We therefore set out to investigate whether exposure to interferon-beta in utero affected the risk of acquiring infections in early childhood. METHODS: This retrospective matched cohort study utilized data from the Danish Multiple Sclerosis Registry linked with national Danish registries to identify all children born of mothers with MS in Denmark from 1998 to 2018. The study included 510 children exposed to interferon-beta in utero. The children were matched 1:1 on various of demographic characteristics with children born to mothers with untreated MS and 1:3 with children born to mothers without MS. Each child was followed for up to five years. Using individual-level data, we investigated all-cause mortality, rate of hospital admissions due to infections, and redeemed prescriptions of antibiotics. The primary statistical model applied was a negative binomial regression analysis. RESULTS: We found no differences in childhood mortality, for hospital admissions the rate ratio compared to healthy controls was 0.79 (0.62-1.00). Regarding antibiotic prescriptions, the results were similar (RR 1.00 (0.90-1.11). Furthermore, we found no certain dose-response relationship between interferon-beta exposure duration and hospital admission rate (P = 0.47) or redeemed antibiotic prescription (P = 0.71). CONCLUSION: Exposure to interferon-beta during gestation has little to no impact on the risk of acquiring significant infections during the first five years of childhood.
 BACKGROUND: The clinical transition from relapsing-remitting multiple sclerosis (RRMS) to secondary progressive MS (SPMS) is often related to a period of diagnostic uncertainty delaying diagnosis. With emerging treatment options for SPMS how to identify RRMS patients at risk of SPMS and when to assign a SPMS diagnosis has become a matter of growing clinical concern. This study aimed to determine the period of diagnostic uncertainty among Danish MS patients. Secondly, this study examined the performance of two objective classifiers in a longitudinal setting regarding their ability to shorten the period of diagnostic uncertainty. METHODS: By using the Danish Multiple Sclerosis Registry, we identified all patients linked to Rigshospitalet with clinically assigned SPMS from 2010 to 2021. We reviewed all patient records and identified the first mentioned sign of progression (FMP). The time between the dates of FMP and clinically assigned SPMS was defined as the period of diagnostic uncertainty. Secondly, we applied two objective classifiers (the Karolinska Decision tree and the MSBase criteria) to generate suggested transition dates and compared them to the ones obtain from the patient records. Detailed descriptions of the population were made at all mentioned timepoints. RESULTS: In total 138 patients were included. We found a median period of diagnostic uncertainty of 2.12 years. The objective classifiers generated a median suggested transition date 3.44 and 4.48 years earlier than the date of clinically assigned SPMS, but they only provided an earlier SPMS transition date in 50.72% and 55.80% of cases. CONCLUSIONS: Our findings emphasize the uncertainty related to the transition from RRMS to SPMS illustrating the need of an improved diagnostic approach. Objective classifiers might have the potential to help reduce the period of diagnostic uncertainty in the future, but in their current form they do not perform satisfactorily enough to solve all difficulties related to detecting SPMS-transition.
 BACKGROUND: To analyze the 100 most cited articles (T100) on ocrelizumab using bibliometric methods to determine the current situation and identify research hotspots. METHODS: Articles with "ocrelizumab" in their title were searched for in the Web of Science (WoS) database, identifying 900 articles. After the exclusion criteria were applied, 183 original articles and reviews were obtained. The T100 were selected from among these articles. Data on these articles (author, source, institution, country, scientific category, citation number, and citation density) were analyzed. RESULTS: The number of articles showed a fluctuating upward trend from 2006 to 2022. The total number of citations for the T100 ranged from two to 923. The average number of citations per article was 45.11. The most articles were published in 2021 (n = 31). The "Ocrelizumab versus Placebo in Primary Progressive Multiple Sclerosis" study (T1) was the most cited article among the T100 and had the highest annual average number of citations. T1, T2, and T3 were clinical trials on treating multiple sclerosis. The USA was the most productive and influential research country, with 44 articles. Multiple Sclerosis and Related Disorders was the most productive journal (n = 22). Clinical neurology ranked first among the WoS categories (n = 70). Hauser Stephen and Kappos Ludwig were the most influential authors, with 10 articles each. Biotechnology company Roche was at the top of the publication list, with 36 articles. CONCLUSION: This study's results can give researchers an idea about current developments and research collaborations on ocrelizumab. These data can help researchers easily obtain publications that have become classics. We conclude that the clinical and academic communities have shown a growing interest in ocrelizumab for treating primary progressive multiple sclerosis in recent years.
 BACKGROUND: Fatigue, a multidimensional and challenging symptom associated with various underlying conditions, can manifest as a subjective feeling and a performance fatigability. The latter is often defined as an objectively measurable performance decline with time on task. Both syndromes are highly prevalent in people with multiple sclerosis (pwMS) and are often resistant to medical therapy. In the absence of valid and reliable objective parameters, the current cognitive fatigue diagnosis remains purely subjective. Assessing brain wave activity changes has repeatedly been a viable strategy for monitoring cognitive fatigue in healthy subjects. In this study, we aimed to investigate oscillatory brain activity changes and their associations with subjective fatigue in pwMS. METHODS: We enrolled 21 pwMS and 21 healthy controls (HC) in this study. Subjects performed a sustained attention task divided into six blocks over the course of 30 minutes, and underwent resting state EEGs before and after the task. During the task, subjects were repeatedly asked to rate their subjective levels of mental fitness, mental exhaustion, and mind wandering. Using Linear Mixed Models, we explored fatigability-related changes by focusing on the time course of changes in reaction time variability, subjective ratings of fatigability, as well as frontomedial theta, and occipital alpha power. We further investigated initial and fatigability-induced differences between pwMS and HC at rest. Finally, Pearson correlations were used to examine the relationship between subjective fatigue and objective fatigability parameters. RESULTS: Our results revealed a systematically stronger fatigability development in pwMS that was objectively measurable. PwMS reported lower mental fitness levels and demonstrated greater variability in reaction times with time on task. Occipital alpha power significantly increased during the task. Especially for upper alpha power, this increase was significantly more prominent in pwMS compared to HC. However, the time-on-task-induced changes in our study were not associated with the subjective fatigue ratings. CONCLUSIONS: The results of this study expand the understanding of the neural mechanisms underlining cognitive fatigability and may complement the fatigue diagnosis and therapy monitoring with quantitative objective methods.
 INTRODUCTION: The influence of breastfeeding and it´s duration on the course of multiple sclerosis (MS) is unclear. Here we analyzed a real-world data for breastfeeding women with MS and their disease course collected from a Czech national registry ReMuS. OBJECTIVES: To identify risk factors associated with not initiating breastfeeding after delivery, to analyze the impact of breastfeeding on the MS disease course, evaluate the assumption, that breastfeeding is not harmful in MS patients, and compare the disease course by breastfeeding status. MATERIALS AND METHODS: Using propensity score matching we compared Expanded Disability Status Scale (EDSS), confirmed disease worsening (CDW) and annual relapse rate (ARR) in breastfeeding and non-breastfeeding MS patients according to disease duration, disease modifying treatment (DMT) before pregnancy, last EDSS score before conception, age, and ARR during pregnancy. We also compared these parameters between breastfeeding patients not using a DMT and non-breastfeeding patients who resumed DMT within 3 months after delivery. EDSS, ARR, and CDW were collected at 12, 24, and 36 months after delivery. RESULTS: A total of 1681 pregnancies that ended in delivery were analyzed from 2013 through 2020. Change in ARR and EDSS values and 6-months CDW did not significantly differ between the analyzed groups. Compared with non-breastfeeding women who resumed DMT early after delivery, breastfeeding women with MS did not experience worse clinical outcomes even without initiating a DMT. DISCUSSION: Breastfeeding in Czech women with MS did not negatively affect the disease course and can be supported. Patients with MS can be treated with certain DMTs alongside breastfeeding and there is no need to stop breastfeeding, if the patient is clinically stable.
 Neuroprotective, anti-inflammatory, and remyelinating properties of androgens are well-characterized in demyelinated male mice and men suffering from multiple sclerosis. However, androgen effects mediated by the androgen receptor (AR), have been only poorly studied in females who make low androgen levels. Here, we show a predominant microglial AR expression in demyelinated lesions from female mice and women with multiple sclerosis, but virtually undetectable AR expression in lesions from male animals and men with multiple sclerosis. In female mice, androgens and estrogens act in a synergistic way while androgens drive microglia response towards regeneration. Transcriptomic comparisons of demyelinated mouse spinal cords indicate that, regardless of the sex, androgens up-regulate genes related to neuronal function integrity and myelin production. Depending on the sex, androgens down-regulate genes related to the immune system in females and lipid catabolism in males. Thus, androgens are required for proper myelin regeneration in females and therapeutic approaches of demyelinating diseases need to consider male-female differences.
 OBJECTIVE: The role of CSF lymphocytic pleocytosis in predicting the clinical outcome of multiple sclerosis is unclear. We explored the impact of CSF pleocytosis at diagnosis on long-term disease progression in a large UK cohort. METHODS: We extracted demographic, clinical and CSF data of people with MS attending the MS clinics between 1996 and 2014 at two MS centres from the English Midlands. We compared EDSS at onset, follow up EDSS and progression indices Multiple Sclerosis Severity Score (MSSS), annualized change in EDSS and transition to secondary progression in the presence/absence of pleocytosis. Two-tailed student t-test, Mann-Whitney U test, Chi-Square or Fisher's exact tests were used for detecting the differences. RESULTS: A total of 247 patients with MS (178 females; mean age 42.4; 217 with relapsing onset) were followed up for an average of 13.56 years (median 12 years). Almost 18% had lymphocytic CSF ≥ 5 per microliter. CSF pleocytosis was not associated with higher EDSS at the time of LP or at follow up, and other progression indices like MSSS, annualized change in EDSS or transition to secondary progression. DISCUSSION: CSF pleocytosis at MS diagnosis does not predict higher long-term disability and has no long-term prognostic value in routine clinical circumstances. Differences between MS populations and potential differences in disease activity at the time of CSF analysis may account for differences between studies.
 BACKGROUND: Patient-reported outcomes (PROs) are increasingly being used as outcomes in secondary progressive multiple sclerosis (SPMS) trials. We examined how PROs reflect disease burden in SPMS. METHODS: In this observational prospective study, 65 SPMS patients were examined by five different PROs (Fatigue Scale Motor Cognition (FSMC), Multiple Sclerosis Impact Scale version 2 (MSIS-29v2), 36-Item Short Form Health Survey version 2 (SF-36v2), EQ-5D-5L and Work Productivity and Activity Impairment Questionnaire: Multiple Sclerosis version 2.0 (WPAI:MS)); two different rating scales, Multiple Sclerosis Impairment Scale (MSIS) and Expanded Disability Status Scale (EDSS); functional tests of mobility (Timed-25-Foot Walk (T-25FW), 6-Spot Step Test (6-SST) and (9-Hole Peg Test (9-HPT)); cognitive tests (Symbol Digital Modalities Test (SDMT) and Brief Visuospatial Memory Test-Revised (BVMT-R)); and multimodal Magnetic Resonance Imaging (MRI). RESULTS: When the PROs were divided into physical and psychological subscores, the PRO physical subscores of FSMC, MSIS-29v2 and SF-36v2 correlated with physical rating scales (EDSS, MSIS) and physical measures of upper (9-HPT) and lower extremity function (T-25FW and 6-SST)) (p = 0.04-0.0001). 9-HPT correlated the least with physical subscores of PROs but showed the strongest correlation with activity impairment (subscore of WPAI:MS). In contrast, psychological PRO subscores of FSMC, MSIS-29v2 and SF-36v2 did not reflect the cognitive outcomes (SDMT and BVMT-R), although the cognitive scores correlated with disease burden indicated by MRI lesion volumes. The psychological PRO subscores did not correlate with fatigue, physical and MRI outcomes either. CONCLUSION: Correlation between PRO physical subscores and physical outcomes supports PROs as potentially useful clinical endpoints in SPMS. The results of this study indicate that patients with SPMS highly perceive their mobility on function of their lower extremities, while they perceive their daily activities highly dependent on function of the upper extremities. Psychological subscores of MS specific PROs may be less suitable as surrogate markers for the cognitive status and should be considered as a mental quality of life measurement independent of disease burden.
 BACKGROUND AND OBJECTIVES: Limited data is available on children with evidence of silent central nervous system demyelination on MRI. We sought to characterize the population in a US cohort and identify predictors of clinical and radiologic outcomes. METHODS: We identified 56 patients such patients who presented with incidental MRI findings suspect for demyelination, enrolled through our US Network of Pediatric Multiple Sclerosis Centers, and conducted a retrospective review of 38 patients with MR images, and examined risk factors for development of first clinical event or new MRI activity. MRI were rated based on published MS and radiologically isolated syndrome (RIS) imaging diagnostic criteria. RESULTS: One-third had a clinical attack and ¾ developed new MRI activity over a mean follow-up time of 3.7 years. Individuals in our cohort shared similar demographics to those with clinically definite pediatric-onset MS. We show that sex, presence of infratentorial lesions, T1 hypointense lesions, juxtacortical lesion count, and callosal lesions were predictors of disease progression. Interestingly, the presence of T1 hypointense and infratentorial lesions typically associated with worse outcomes were instead predictive of delayed disease progression on imaging in subgroup analysis. Additionally, currently utilized diagnostic criteria (both McDonald 2017 and RIS criteria) did not provide statistically significant benefit in risk stratification. CONCLUSION: Our findings underscore the need for further study to determine if criteria currently used for pediatric patients with purely radiographic evidence of demyelination are sufficient.
 BACKGROUND: Paediatric-onset multiple sclerosis (POMS) is increasing worldwide and represents approximately 5% of all MS cases. Although this patient group has similar characteristics to the adult group, it is important for this patient group to receive effective treatment due to the early onset of cognitive involvement, higher lesion burden, and secondary progression at an earlier age than adults. In this study, we aimed to evaluate the factors that cause treatment change in POMS patients. MATERIAL AND METHOD: Adult patients with a first MS attack at age 18 years or younger who were followed up with the diagnosis of MS at the Clinical Neuroimmunology and Demyelinating Diseases outpatient clinic of Cerrahpaşa Medical School between 1987 and 2020 were included in our study. Patient files were reviewed retrospectively, and demographic and clinical characteristics, imaging, first attack characteristics, and treatment change were noted. We included 269 patients with a definite diagnosis of MS in the study, and these patients were evaluated in two groups: negative for treatment change and positive for treatment change. RESULTS: Multifocal involvement was detected more frequently in the group with treatment change (p = 0,049). Cerebellar involvement as a first attack symptom was more common in male patients (p = 0,023) The age at first MS attack was found to be younger (p = 0,006), and the disease duration was longer in the positive for treatment change group (p = 0,003). Spinal cord involvement was more common in the positive for treatment change group (p = 0,016). Abnormal VEP findings were observed more frequently in the group without treatment change (p = 0.018). In multivariant analysis, spinal cord involvement, younger age at first attack, and abnormal VEP findings in the group without treatment change were found to be significant. Among the reasons for treatment change, the most common reason was radiological and clinical progression. CONCLUSION: The higher inflammatory load in POMS patients compared with adults necessitates early initiation of treatment in this group and timely treatment change to prevent disability. Furthermore, this patient group should be followed closely and receive effective treatment.
 BACKGROUND: Many patients treated with Natalizumab experience wearing-off symptoms (WoS) towards the end of the administration cycle. During the pandemic we advised and asked patients undergoing treatment with Natalizumab if they wanted to be shifted from a standard interval dosing (StID of 4 weeks) to an extended interval dosing (ExID of 5-6 weeks), regardless of their JCV index. Our main objective was to study prevalence and incidence of WoS when ExID was adopted. METHODS: We enrolled 86 patients, from May 2020 to January 2021, evaluated at baseline and during a 6 months follow-up with a survey focused on WoS, Fatigue Severity Scale (FSS), Expanded Disability Status Scale (EDSS) and MRI. RESULTS: Among the 86 patients, 32 (37.2%) reported WoS. Most common one was fatigue (93.7%). Mean EDSS was higher in the group reporting WoS (3.8 WoS vs 3.1 non-WoS, p < 0.05). Sphincterial function was the EDSS item that significantly differed between the WoS group and the non-WoS group (1.4 WoS vs 0.6 non-WoS, p < 0.001). WoS correlate with the FSS scale (p < 0.001). CONCLUSION: Adopting an extended interval dosing does not result in significantly different occurrence of WoS between the ExID and the StID populations, in our cohort of patients. Interestingly, there is a strong correlation between WoS and a higher EDSS and FSS. Safety and efficacy of Natalizumab with ExID are relatively preserved in our study.

 OBJECTIVES: We investigated choroid plexus (CP) volume in patients presenting with optic neuritis (ON) as a clinically isolated syndrome (CIS), compared to a cohort with established relapsing-remitting multiple sclerosis (RRMS) and healthy controls (HCs). METHODS: Three-dimensional (3D) T1, T2-FLAIR and diffusion-weighted sequences were acquired from 44 ON CIS patients at baseline, 1, 3, 6 and 12 months after the onset of ON. Fifty RRMS patients and 50 HCs were also included for comparison. RESULTS: CP volumes was larger in both ON CIS and RRMS groups compared to HCs, but not significantly different between ON CIS and RRMS patients (analysis of covariance (ANCOVA) adjusted for multiple comparisons). Twenty-three ON CIS patients who converted to clinically definite MS (MS) demonstrated CP volume similar to RRMS patients, but significantly larger compared to HCs. In this sub-group, CP volume was not associated with the severity of optic nerve inflammation or long-term axonal loss, not with brain lesion load. A transient increase of CP volume was observed following an occurrence of new MS lesions on brain magnetic resonance imaging (MRI). INTERPRETATION: Enlarged CP can be observed very early in a disease. It transiently reacts to acute inflammation, but not associated with the degree of tissue destruction.
 BACKGROUND: Definitions of trial measures are consequential to accurately capturing outcomes and cross-trial comparability, particularly for derivative measures. OBJECTIVE: Using CombiRx, examine the impact of relapse definition on endpoints and evaluate the durability of progression measures in Relapsing Remitting Multiple Sclerosis (RRMS). METHODS: CombiRx relapse types were distinguished by the presence or timing of Expanded Disability Status Scale (EDSS) increase. Using the broadest definition of relapse, progression endpoints were assessed in patients without relapses on trial. Durability compared EDSS at study end and time of worsening. RESULTS: Broadening relapse definition to the most inclusive definition increased annualized relapse rate (ARR) threefold in all arms and decreased progression independent of relapse activity (PIRA), defined as 6-month confirmed disability worsening (6M CDW) without relapse, by 44%. Neither PIRA nor PIA (progression independent of any inflammatory activity) guaranteed durable worsening, with 43% and 40%, respectively, improving by end of study. Multivariate analysis showed two CDW events, not relapse, predicted durability among patients meeting 6M CDW. CONCLUSIONS: The stringency of relapse definition impacted absolute ARR and composite endpoints in RRMS. Despite the most generous relapse definition, 43% of patients meeting PIRA on trial did not have durable worsening suggesting that relapse definition and durability should be considered to avoid overestimating progression in RRMS trials.
 BACKGROUND: Fatigue is a prominent and disabling symptom of multiple sclerosis (MS), impairing quality of life. The disease course of relapsing remitting MS (RRMS) is individual. OBJECTIVES: We aimed to study the effects of demographic and clinical characteristics, as well as lifestyle risk factors on experienced fatigue and health-related quality of life (HRQoL) among RRMS patients, comparing benign and severe disease types. METHODS: Altogether 198 Finnish RRMS patients were recruited for this real-life cross-sectional study. Self-reported questionnaires were used to evaluate fatigue and HRQoL by using Fatigue Scale for Motor and Cognitive Functions and 15D health-related quality of life questionnaires. Patients were categorized into subgroups based on the current disability status measured by the Expanded Disability Status Scale (EDSS) cut-off value of 4.5, and by retrospective clinical course divided into benign and aggressive RRMS. RESULTS: All in all, 73% of the RRMS patients suffered from fatigue. Lower HRQoL had a strong correlation with more prominent fatigue (r = -0.719). Higher EDSS was associated with more prominent fatigue and lower HRQoL in the whole RRMS cohort. Older age at the disease onset was associated with more prominent fatigue and decreased HRQoL in the groups of aggressive RRMS and EDSS > 4.5. In the groups of EDSS ≤ 4.5 and benign RRMS, a higher number of used disease-modifying treatments (DMTs) was associated with more pronounced fatigue and reduced HRQoL. In addition, higher BMI was associated with lower HRQoL in patients with benign RRMS. Side effects (45 %) and lack of efficacy (26 %) were the most common reasons for discontinuing a DMT. Cessation due to side effects was the only reason that was significantly associated with more prominent fatigue and lower HRQoL. Use of nicotine products, gender, or disease duration were not associated with fatigue or HRQoL. CONCLUSIONS: Individuals with severe RRMS and higher EDSS scores are more prone to experience fatigue and lower HRQoL. In addition, fatigue and lower HRQoL are more commonly observed among RRMS patients with older age at disease onset and in those with multiple DMT switches.
 BACKGROUND: Leptomeningeal inflammation in patients with multiple sclerosis (MS) mainly affects meningeal B-cell follicle-like structures linked to cortical and subpial lesions and can be visualized as leptomeningeal enhancement (LME). OBJECTIVE: To evaluate the evolution of LME under different MS immunotherapies. METHODS: A total of 214 MS patients treated with anti-CD20 therapies or fingolimod at the university hospital Bern were screened for LME. Magnetic resonance imaging (MRI) and medical records were retrospectively evaluated, and comparative statistics were applied. RESULTS: We compared MS patients treated with anti-CD20 therapies (128 patients (59.8%)) or fingolimod (86 patients (40.2%)). Of 128 anti-CD20-treated patients, 108 (84.4%) had no LME, 11 (8.6%) had persistent LME, and 9 (7.0%) showed resolution of LME. Of 86 fingolimod-treated MS patients, 81 (94.2%) had no LME and 5 (5.8%) persistent LME. Patients with LME persistence were older than those without or resolution of LME (p = 0.039). Resolution of LME was more frequent during anti-CD20 compared with fingolimod treatment (p = 0.019). CONCLUSION: We observed LME resolution under treatment with anti-CD20 therapies. As LME might play an important role in cerebral gray matter pathology in MS, further investigations including extensions to higher field strengths, correlation with clinical phenotypes, and comparison with other immunotherapies are needed.
 BACKGROUND: Cognitive impairment is common in patients with multiple sclerosis, even in the early stages of the disease. The Brief International Cognitive Assessment for multiple sclerosis (BICAMS) is a short screening tool developed to assess cognitive function in everyday clinical practice. OBJECTIVE: To investigate associations between volumetric brain measures derived from a magnetic resonance imaging (MRI) examination and performance on BICAMS subtests in early stages of multiple sclerosis (MS). METHODS: BICAMS was used to assess cognitive function in 49 MS patients at baseline and after one and two years. The patients were separated into two groups (with or without cognitive impairment) based on their performances on BICAMSs subtests. MRI data were analysed by a software tool (MSMetrix), yielding normalized measures of global brain volumes and lesion volumes. Associations between cognitive tests and brain MRI measures were analysed by running correlation analyses, and differences between subgroups and changes over time with independent and paired samples tests, respectively. RESULTS: The strongest baseline correlations were found between the BICAMS subtests and normalized whole brain volume (NBV) and grey matter volume (NGV); processing speed r = 0.54/r = 0.48, verbal memory r = 0.49/ r = 0.42, visual memory r = 0.48 /r = 0.39. Only the verbal memory test had significant correlations with T2 and T1 lesion volumes (LV) at both time points; T2LV r = 0.39, T1LV r = 0.38. There were significant loss of grey matter and white matter volume overall (NGV p<0.001, NWV p = 0.003), as well as an increase in T1LV (p = 0.013). The longitudinally defined confirmed cognitively impaired (CCI) and preserved (CCP) patients showed significant group differences on all MRI volume measures at both time points, except for NWV. Only the CCI subgroup showed significant white matter atrophy (p = 0.006) and increase in T2LV (p = 0.029). CONCLUSIONS: The present study found strong correlations between whole brain and grey matter volumes and performance on the BICAMS subtests as well as significant changes in global volumes from baseline to follow-up with clear differences between patients defined as cognitively impaired and preserved at both baseline and follow-up.
 BACKGROUND AND PURPOSE: Diffusion MRI (dMRI) is sensitive to microstructural changes in white matter of people with relapse-remitting multiple sclerosis (pw-RRMS) that lead to progressive disability. The role of diffusion in assessing the efficacy of different therapies requires more investigation. This study aimed to evaluate selected dMRI metrics in normal-appearing white matter and white matter-lesion in pw-RRMS and healthy controls longitudinally and compare the effect of therapies given. MATERIAL AND METHODS: Structural and dMRI scans were acquired from 78 pw-RRMS (29 injectables, 36 fingolimod, 13 dimethyl fumarate) and 43 HCs at baseline and 2-years follow-up. Changes in dMRI metrics and correlation with clinical parameters were evaluated. RESULTS: Differences were observed in most clinical parameters between pw-RRMS and HCs at both timepoints (p ≤ 0.01). No significant differences in average changes over time were observed for any dMRI metric between treatment groups in either tissue type. Diffusion metrics in NAWM and WML correlated negatively with most cognitive domains, while FA correlated positively at baseline but only for NAWM at follow-up (p ≤ 0.05). FA correlated negatively with disability in NAWM and WML over time, while MD and RD correlated positively only in NAWM. CONCLUSIONS: This is the first DTI study comparing the effect of different treatments on dMRI parameters over time in a stable cohort of pw-RRMS. The results suggest that brain microstructural changes in a stable MS cohort are similar to HCs independent of the therapies used.

 INTRODUCTION: Asymptomatic optic nerve lesions are frequent in multiple sclerosis (MS) and their impact on cognition and/or brain volume has never been taken into account. PATIENTS AND METHODS: We used the data from the cross-sectional Visual Ways in MS (VWIMS) study including relapsing remitting MS. All patients underwent brain and optic nerve Magnetic Resonance Imaging (MRI) including Double Inversion Recuperation (DIR) sequence, retinal OCT, and cognitive evaluation with the Brief International Cognitive Assessment in MS (BICAMS). We measured the association between OCT findings (thickness/volume of retinal layers) and extra-visual parameters (cerebral volumes and BICAMS scores) in optic nerves with and/or without the presence of DIR asymptomatic optic nerve hypersignal. RESULTS: Between March and December 2017, we included 98 patients. Two patients were excluded. Over the 192 eyes, 73 had at least one clinical history of optic neuritis (ON-eyes) whereas 119 were asymptomatic (NON-eyes). Among the 119 NON-eyes, 58 had 3D-DIR optic nerve hypersignal (48.7%). We confirmed significant associations between some retinal OCT measures and some extra-visual parameters (cerebral volumes, cognitive scores) in NON-eyes. Unexpectedly, these associations were found when an asymptomatic optic nerve DIR-hypersignal was present on MRI, but not when it was absent. CONCLUSION: Our study showed a relation between OCT measures and extra-visual parameters in NON-eyes MS patients. As a confusion factor, asymptomatic optic nerve lesions may be the explanation of the relation between OCT measures and extra-visual parameters. Retinal OCT seems to be far more a "window over the optic nerve" than a "window over the brain".


 Intrathecal inflammation plays a key role in the pathogenesis of multiple sclerosis (MS). To better elucidate its relationship with peripheral inflammation, we investigated the correlation between cerebrospinal fluid (CSF) and serum levels of 61 inflammatory proteins. Paired CSF and serum samples were collected from 143 treatment-naïve MS patients at diagnosis. A customized panel of 61 inflammatory molecules was analyzed by a multiplex immunoassay. Correlations between serum and CSF expression levels for each molecule were performed by Spearman's method. The expression of sixteen CSF proteins correlated with their serum expression (p-value < 0.001): only five molecules (CXCL9, sTNFR2, IFNα2, Pentraxin-3, and TSLP) showed a Rho value >0.40, suggesting moderate CSF/serum correlation. No correlation between inflammatory serum patterns and Q(alb) was observed. Correlation analysis of serum expression levels of these sixteen proteins with clinical and MRI parameters pinpointed a subset of five molecules (CXCL9, sTNFR2, IFNα2, IFNβ, and TSLP) negatively correlating with spinal cord lesion volume. However, following FDR correction, only the correlation of CXCL9 remained significant. Our data support the hypothesis that the intrathecal inflammation in MS only partially associates with the peripheral one, except for the expression of some immunomodulators that might have a key role in the initial MS immune response.
 BACKGROUND / AIMS: The benefit of disease-modifying therapy (DMT) is unclear for older patients with multiple sclerosis (MS), namely those who have not experienced clinical disease activity for a prolonged time. We aimed to compare baseline differences and clinical outcomes between DMT discontinuers and continuers in a cohort of MS patients older than 60 years. METHODS: Retrospective, observational study identifying MS patients aged over 60 years, stable on DMT> 24 months. Additional inclusion criteria were a previous diagnosis of relapsing MS and a minimum follow-up period of 24 months. Differences between groups (continuers/discontinuers) were assessed. For risk of relapse and of confirmed disability worsening at follow up, a time to outcome survival model was constructed using Cox proportional hazards regression, testing for possible risk predictors. RESULTS: Thirty-five patients were included (68.6% female), with a mean age at diagnosis of 42.1 ( ± 9.5) years and a median EDSS score of 3 (IQR 2) at the age of 60 years (baseline). Thirteen patients discontinued DMT after baseline, in a mean follow-up time of 77.1 months ( ± 40.2). No differences were found between DMT continuers vs discontinuers. DMT discontinuation did not predict risk to relapse (HR 0.38, 95%CI 0.04-3.80, p = 0.408) or disability worsening at follow-up (HR 0.83, 95%CI 0.31-2.22, p = 0.712). MRI gadolinium-enhancing lesions and EDSS score > 3 at baseline were found to be independent predictors of risk to relapse and disability worsening at follow-up, respectively. CONCLUSION: DMT discontinuation did not seem to influence clinical outcome, equating with the perceived limited effect of continued immunomodulation on older stable and/or progressive patients.
 BACKGROUND: Although cognitive evaluation has been incorporated in recent MS clinical trials, the definition of cognitive progression is not clear and recent data are questioning the 4-point cutoff using the SDMT at the individual level. We aimed to evaluate the behavior of cognitive performance over time using different cutoffs. METHODS: Cognitive performance over six years was analyzed in a cohort of 42 relapsing-remitting MS patients and 30 controls using verbal/visual memory and information processing speed tests. Fixed cutoffs were: 10% and 20% change (all tests) and a 4- and 8-point change (SDMT). The relative cutoff established by regression-based models was a 1SD change. RESULTS: The distributions of "worsening", "stability", and "improvement" showed low concordance rates across the cutoffs (p < 0.001 for most comparisons). Most patients classified with worsening initially using fixed cutoffs had subsequent improvement in all cognitive tests, yielding a low sensitivity to predict later cognitive worsening. Using the relative cutoff, the proportion of patients with subsequent improvement was noticeably smaller. CONCLUSIONS: Fixed cutoffs classify a high proportion of patients with cognitive improvement. Most patients categorized with worsening initially presented subsequent improvement. Instead, the relative cutoff generally had a better performance. These data raise concerns about how we are defining cognitive worsening so far, especially at the individual level.
 Multiple sclerosis (MS) is a debilitating, demyelinating disease of the central nervous system, with manifestations ranging from numbness and blindness to paralysis. Typical MS is a slowly progressive demyelinating disease, causing significant morbidity spanning over many years. In contrast, "Marburg's disease" is a rare variant of MS which demonstrates a malignant monophasic disease progression leading to death within weeks to months. We present a rapidly fatal demyelinating disease with the clinicopathological findings on par with the handful of reported cases of "Marburg's disease" in the literature. A previously healthy 30-year-old mother of two children was extensively investigated for focal neurological signs succumbing to death 5 weeks after the onset. Antemortem investigations for tuberculosis, autoimmune diseases, and viral studies were negative. Magnetic resonance imaging of the brain showed hyperintense lesions with contrast enhancement compatible with MS. Histopathologic examination confirmed numerous inflammatory and demyelination foci scattered throughout the brain and brain stem predominantly involving the white matter. There were extensive perivascular inflammatory cell cuffs containing lymphocytes admixed with histiocytes. Also, a few foci of vasculitis with fibrinoid necrosis, mediated by lymphocytes and neutrophils were noted associated with parenchymal haemorrhages. Considered a rare variant of MS, the case of Marburg's disease presented here shows an infrequent association with active vasculitis and haemorrhage, described only a few times in the literature. This wide spectrum of rapidly fatal demyelinating diseases consisting of rare variants with overlapping clinicopathological features makes diagnosis challenging. Therefore, it is important to correlate clinical-radiological and histopathological findings to arrive at an accurate final diagnosis.
 OBJECTIVES: Multiple sclerosis is diagnosed based on clinical and laboratory findings, including cerebrospinal fluid (CSF) oligoclonal banding (OCB) analysis. The lack of updated CSF OCB laboratory guidelines in Canada has likely led to variation in processes and reporting across clinical laboratories. As a first step to developing harmonized laboratory recommendations, we examined current CSF OCB processes, reporting, and interpretation across all Canadian clinical laboratories currently performing this test. DESIGN AND METHODS: A survey of 39 questions was sent to clinical chemists at all 13 Canadian clinical laboratories performing CSF OCB analysis. The survey included questions regarding quality control processes, reporting practices for CSF gel electrophoresis pattern interpretation, and associated tests and calculated indices. RESULTS: The survey response rate was 100%. Most (10/13) laboratories use ≥2 CSF-specific bands (2017 McDonald Criteria) as their CSF OCB positivity cut-off and only 2/13 report the number of bands with every report. Most (8/13 and 9/13) laboratories report an inflammatory response pattern and monoclonal gammopathy pattern, respectively. However, the process for reporting and/or confirming a monoclonal gammopathy varies widely. Variation was observed for reference intervals, units, and the panel of reported associated tests and calculated indices. The maximum acceptable time interval between paired CSF and serum collections varied from 24 h to no limit. CONCLUSIONS: Profound variation exists in processes, reporting, and interpretation of CSF OCB and associated tests and indices across Canadian clinical laboratories. Harmonization of CSF OCB analysis is required to ensure continuity and quality of patient care. Our detailed assessment of current practice variation highlights the need for clinical stakeholder engagement and further data analysis to support optimal interpretation and reporting practices, which will aid in developing harmonized laboratory recommendations.

 30 years ago the first disease-modifying therapy for relapsing multiple sclerosis was approved for use in the United States and soon thereafter across the globe. Since then the field of MS therapeutics, and studies of immunopathogenesis and genetics, have advanced our understanding of the disease and raised the hope of better addressing the next challenges of treating progressive disease, enhancing repair of the damaged nervous system and, hopefully, of a cure. Thirty years into the MS treatment era, the field continues to debate fundamental aspects of MS, and there exists a widening chasm between the triumphs in relapsing disease and the desolation of MS progression, which remains the principal unmet need. In this Personal Viewpoint, we outline lessons learned from the first era of great therapeutic development, as we look to the future of MS research and therapeutics.
 INTRODUCTION: Several studies have suggested the possibility that disease prodromes might occur months or even years before a multiple sclerosis diagnosis. OBJECTIVES: To describe the profile of prodromal symptoms and the possible relationship between the occurrence of individual symptoms and clinical course characteristics in patients with relapsing-remitting multiple sclerosis (RRMS), and to assess their role as predictors of further disease course. MATERIAL AND METHODS: The cohort included 564 patients with RRMS. Patients were stratified based on their current EDSS score, and the annual EDSS growth rate was calculated. Logistic Regression Analysis was used to study the relationship between prodromal symptoms and disease progression. RESULTS: The most commonly reported prodromal symptom was fatigue (42%). The following symptoms were significantly more common in women than in men: headache (39.7% vs. 26.5%, p < 0.05), excessive sleepiness (19.1% vs. 11.1%, p < 0.05) and constipation (18.0% vs. 11.1%, p < 0.05). Prodromal urinary and cognitive disturbances, fatigue and pain complaints were significantly more common in patients with the highest annual EDSS increase (p < 0.05). Multivariate analysis revealed some potential predictors of long-term disability progression: hesitancy in starting urination predicted EDSS increase by 0.6 point (p < 0.05), while deterioration in everyday functioning because of cognitive disturbances, and pain complaints, were associated with an EDSS increase of 0.5 (p < 0.05), and 0.4 (p < 0.05), respectively. CONCLUSIONS: Prodromal pain, urinary and cognitive complaints (especially when these lead to deterioration of everyday functioning) were associated with a higher EDSS increase rate, and may thus be regarded as possible predictors of worse clinical outcomes in RRMS patients.
 BACKGROUND AND PURPOSE: The timed 25-foot walk (T25FW) and nine-hole peg test (NHPT) exhibit random variability in the short term. A threshold of ≥20% change from baseline has been used to indicate true disability change, but other threshold definitions may be better suited to exclude false and include true change events. The aim of this study was to use patient-level original trial data to investigate the short-term variation in T25FW and NHPT, and to compare its extent with disability change at 12-month follow-up in people with primary progressive multiple sclerosis (PPMS). METHODS: We used original patient-level data from PROMISE, a large PPMS trial. In this trial, three separate T25FW and NHPT measurements were performed 1 week apart during screening. We used these repeated measures to describe the extent of short-term variation. We used binary logistic regression models to investigate the association between screening characteristics and unacceptable short-term variation. RESULTS: The traditional 20% threshold excluded a reasonable number of false change events, while also yielding a large number of change events at follow-up. Increasing index values on the T25FW and NHPT were associated with higher short-term variation. CONCLUSIONS: The traditional ≥20% change threshold for the T25FW and NHPT represents a reasonable compromise between reducing the number of false change events and achieving the largest number of change events in people with PPMS. Our analyses inform the design of clinical trials in PPMS.
 Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system (CNS) whose aetiology is only partly understood. Investigating the intricate transcriptional changes occurring in MS brains is critical to unravel novel pathogenic mechanisms and therapeutic targets. Unfortunately, this process is often hindered by the difficulty in retrieving an adequate number of samples. However, by merging data from publicly available datasets, it is possible to identify alterations in gene expression profiles and regulatory pathways that were previously overlooked. Here, we merged microarray gene expression profiles obtained from CNS white matter samples taken from MS donors to identify novel differentially expressed genes (DEGs) linked with MS. Data from three independent datasets (GSE38010, GSE32915, and GSE108000) were combined and used to detect novel DEGs using the Stouffer's Z-score method. Corresponding regulatory pathways were analysed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway databases. Finally, top up- and down-regulated transcripts were validated by real-time quantitative PCR (qPCR) using an independent set of white matter tissue samples obtained from MS donors with different disease subtypes. There were a total of 1446 DEGs, of which 742 were up-regulated and 704 genes were down-regulated. DEGs were associated with several myelin-related pathways and protein metabolism pathways. Validation studies of selected top up- or down-regulated genes highlighted MS subtype-specific differences in the expression of some of the identified genes, underlining a more complex scenario of white matter pathology amongst people afflicted by this devastating disease.
 Choroid Plexuses (ChP) are structures located in the ventricles that produce the cerebrospinal fluid (CSF) in the central nervous system. They are also a key component of the blood-CSF barrier. Recent studies have described clinically relevant ChP volumetric changes in several neurological diseases including Alzheimer's, Parkinson's disease, and multiple sclerosis (MS). Therefore, a reliable and automated tool for ChP segmentation on images derived from magnetic resonance imaging (MRI) is a crucial need for large studies attempting to elucidate their role in neurological disorders. Here, we propose a novel automatic method for ChP segmentation in large imaging datasets. The approach is based on a 2-step 3D U-Net to keep preprocessing steps to a minimum for ease of use and to lower memory requirements. The models are trained and validated on a first research cohort including people with MS and healthy subjects. A second validation is also performed on a cohort of pre-symptomatic MS patients having acquired MRIs in routine clinical practice. Our method reaches an average Dice coefficient of 0.72 ± 0.01 with the ground truth and a volume correlation of 0.86 on the first cohort while outperforming FreeSurfer and FastSurfer-based ChP segmentations. On the dataset originating from clinical practice, the method reaches a Dice coefficient of 0.67 ± 0.01 (being close to the inter-rater agreement of 0.64 ± 0.02) and a volume correlation of 0.84. These results demonstrate that this is a suitable and robust method for the segmentation of the ChP both on research and clinical datasets.
 BACKGROUND: Wellness is a promising area of research in multiple sclerosis (MS); however, considerable questions remain regarding the efficacy of behavioral interventions to improve wellness and which delivery methods yield favorable results. OBJECTIVE: To evaluate the efficacy of a wellness intervention consisting of diet, stress reduction techniques, sleep hygiene, and exercise, delivered via a 7-week web-based program with no tailored intervention support (e.g., counseling or resources) from the study team, on quality of life (QoL) and fatigue among people with MS. METHODS: Individuals (n = 100) with self-reported physician's diagnosis of relapsing-remitting MS or clinically isolated syndrome were recruited to enroll in this randomized waitlist-control trial consisting of three timepoints at 0, 12, and 24 weeks. Participants were randomized to begin the intervention at baseline (INT; n = 51) or to a waitlist to begin the intervention after the 12-week timepoint (WLC; n = 49), and both groups were followed for 24 weeks. RESULTS: At 12-weeks, 95 participants (46 INT and 49 WLC) completed the primary endpoint and 86 (42 INT and 44 WLC) completed the 24-week follow-up. Compared to baseline, the INT group had a significant increase in physical QoL (5.43 ± 1.85; P = 0.003) at 12-weeks which was maintained at 24-weeks. Physical QoL values in the WLC group did not significantly increase between weeks 12 and 24 (3.24 ± 2.03; P = 0.11); however, physical QoL values significantly improved compared to week 0 values (4.00 ± 1.87; P = 0.033). Neither group had significant changes in mental QoL. The INT group had a mean baseline to 12-week change of ‑5.06 ± 1.79 (P = 0.005) for MFIS and -0.68 ± 0.21 (P = 0.002) for FSS, both of which were maintained at 24-weeks. The 12- to 24-week changes for the WLC group were -4.50 ± 1.81 (P = 0.013) for MFIS and -0.44 ± 0.17 (P = 0.011) for FSS. At 12-weeks, the INT group had significantly greater reductions in fatigue compared to the WLC (P = 0.009 for both MFIS and FSS). There were no between-group mean differences for physical or mental QoL, but a significantly higher proportion of participants had clinically significant improvement in physical QoL in the INT group (50%) compared to the WLC group (22.5%) at 12-weeks (P = 0.006). The 12-week intervention effect was similar during the active intervention phase (i.e., baseline to 12 weeks for INT and 12 to 24 weeks for WLC) in each group. Course completion rates significantly differed between groups with 47.9% of the INT group and 18.8% of the WLC group completing the course (P = 0.01). CONCLUSION: A wellness intervention delivered via a web-based program, without tailored support, resulted in significant improvements in fatigue compared to control. TRIAL REGISTRATION: Clinicaltrials.gov Identifier: NCT05057676.
 BACKGROUND: Alemtuzumab is a highly effective treatment for relapsing remitting multiple sclerosis (RRMS), but in recent years safety-related concerns had emerged due to description of novel serious side effects not registered in CARE-MS I and CARE-MS II phase 3 studies, nor in TOPAZ extension study. Data about alemtuzumab use in real clinical practice are limited and based mainly on retrospective studies with small sample sizes. Therefore, more information about effectiveness and safety of alemtuzumab in this context is needed. METHODS: A multicenter observational prospective study to investigate effectivity and safety of alemtuzumab in a real-world setting was performed. Primary endpoints were the change in annualized relapse rate (ARR), and in disability measured by EDSS score. Secondary endpoints were the cumulative probability of confirmed 6-month disability improvement and worsening. Disability worsening and disability improvement were considered when the EDSS score was increased or decreased, respectively, in 1 point if baseline EDSS score was <5.0, or in 0.5 point if baseline EDSS score was ≥5.5, confirmed over 6 months. Other secondary endpoint was the proportion of patients who achieved NEDA-3 status (absence of clinical relapses, disability EDSS progression, and MRI disease activity as depicted by new/enlarging T2 lesions or Gadolinium enhancing T1 lesions). Adverse events also were recorded. RESULTS: A total of 195 RRMS patients (70% female) who started alemtuzumab treatment were included. Mean of follow-up was 2.38 years. Alemtuzumab significantly reduced the annualized relapse rate from baseline with risk reductions of 86%, 83.5%, and 84%, at 12, 24, and 36 months of follow-up respectively (Friedman test, p-value < 0.05 for all comparisons). Alemtuzumab also significantly reduced EDSS score over one and two years after starting alemtuzumab treatment (Friedman test, p-value<0.001 for both comparisons). A high proportion of patients presented confirmed 6-month stability or disability improvement (92%, 82%, and 79%, over 1, 2 and 3 years of follow-up respectively). The proportion of patients who retained NEDA-3 status at 12, 24 and 36 months were 61%, 49%, and 42%, respectively. Baseline characteristics associated with a lower probability of achieving NEDA-3 were younger age, sex female, high ARR, elevated number of previous treatments, and switch from a second line therapy. Infusion related reactions were the most frequent adverse event observed. The most common infections were urinary tract infections (50%), and upper respiratory tract infections (19%) over the 3 years of follow- up. Secondary thyroid autoimmunity was developed in 18.5% of patients. CONCLUSION: Alemtuzumab has demonstrated in real clinical practice high effectiveness in controlling multiple sclerosis activity, and no unexpected adverse events were observed.
 BACKGROUND: As a modulator of the sphingosine 1-phosphate receptor, siponimod is administered as a therapeutic intervention for multiple sclerosis. A previous phase 3 study first reported siponimod-associated macular edema. Since that report, there were only few relevant reports in clinical settings. Here, we report a case of secondary progressive multiple sclerosis developed macular edema after siponimod treatment. We also review the progress of sphingosine 1-phosphate receptor modulators, elaborate on accepted mechanisms in treating multiple sclerosis, and discuss the causation of siponimod-associated macular edema. CASE PRESENTATION: A 38-year-old Chinese female patient with secondary progressive multiple sclerosis, who had recurrent numbness of the limbs and right leg fatigue, developed mild macular edema following 4 months of siponimod treatment. The macular edema resolved after discontinuing the medication, and did not recur after resuming siponimod. CONCLUSION: Although siponimod-associated macular edema may be rare, mild, transitory, and manageable, it cannot be ignored and requires ongoing vigilance.
 PURPOSE: To evaluate the classifiability of small multiple sclerosis (MS)-like lesions in simulated sodium ((23) Na) MRI for different (23) Na MRI contrasts and reconstruction methods. METHODS: (23) Na MRI and (23) Na inversion recovery (IR) MRI of a phantom and simulated brain with and without lesions of different volumes (V = 1.3-38.2 nominal voxels) were simulated 100 times by adding Gaussian noise matching the SNR of real 3T measurements. Each simulation was reconstructed with four different reconstruction methods (Gridding without and with Hamming filter, Compressed sensing (CS) reconstruction without and with anatomical (1) H prior information). Based on the mean signals within the lesion volumes of simulations with and without lesions, receiver operating characteristics (ROC) were determined and the area under the curve (AUC) was calculated to assess the classifiability for each lesion volume. RESULTS: Lesions show higher classifiability in (23) Na MRI than in (23) Na IR MRI. For typical parameters and SNR of a 3T scan, the voxel normed minimal classifiable lesion volume (AUC > 0.9) is 2.8 voxels for (23) Na MRI and 19 voxels for (23) Na IR MRI, respectively. In terms of classifiability, Gridding with Hamming filter and CS without anatomical (1) H prior outperform CS reconstruction with anatomical (1) H prior. CONCLUSION: Reliability of lesion classifiability strongly depends on the lesion volume and the (23) Na MRI contrast. Additional incorporation of (1) H prior information in the CS reconstruction was not beneficial for the classification of small MS-like lesions in (23) Na MRI.
 BACKGROUND: Fingolimod is indicated for the treatment of relapsing-remitting multiple sclerosis (RRMS) and also targets cardiovascular system due to receptors on cardiomyocytes. Results of previous studies are controversial for the effect of fingolimod in terms of ventricular arrhythmias. Index of cardio-electrophysiological balance (iCEB) is a risk marker for predicting malignant ventricular arrhythmia. There is no evidence on the effect of fingolimod on iCEB in patients with relapsing-remitting multiple sclerosis (RRMS). The aim of this study was to evaluate iCEB in patients with RRMS treated with fingolimod . METHODS: A total of 86 patients with RRMS treated with fingolimod were included in the study. All patients underwent a standard 12-lead surface electrocardiogram at initiation of treatment and 6 h after treatment. Heart rate, RR interval, QRS duration, QT, QTc (heart rate corrected QT), T wave peak-to-end (Tp-e) interval, Tp-e/QT, Tp-e/QTc, iCEB (QT/QRS) and iCEBc (QTc/QRS) ratios were calculated from the electrocardiogram. QT correction for heart rate was performed using both the Bazett and Fridericia formulas. Pre-treatment and post-treatment values were compared. RESULTS: Heart rate was significantly lower after fingolimod treatment (p< 0.001). While the post-treatment values of RR and QT intervals were significantly longer (p< 0.001) and post-treatment iCEB was higher (median [Q1-Q3], 4.23 [3.95-4.50] vs 4.53 [4.18-5.14]; p< 0.001), it was found that there was no statistically significant change in iCEB and other study parameters derived using QT after correcting for heart rate using both of two formulas. CONCLUSIONS: In this study, it was found that fingolimod did not statistically significantly change any of the heart rate-corrected ventricular repolarization parameters, including iCEBc, and it is safe in terms of ventricular arrhythmia.
 BACKGROUND: In relapsing-remitting multiple sclerosis (RRMS) the most common treatment strategy has been to start with low-moderate efficacy disease modifying therapy (LE-DMT) and to escalate to more efficacious treatments in cases of breakthrough disease activity. However, recent evidence suggests a better outcome in patients commencing with moderate-high efficacy DMT (HE-DMT) immediately after clinical onset. OBJECTIVE: The aim of this study is to compare disease activity and disability outcomes in patients treated with the two alternative strategies using the Swedish and Czech national multiple sclerosis registries, taking advantage of the fact that the relative frequency of each strategy differs markedly between these two countries. METHODS: Adult RRMS patients who initiated their first-ever DMT between 2013 and 2016 and were included in the Swedish MS register were compared with a similar cohort from the MS register of the Czech Republic using propensity score overlap weighting as a balancing method. The main outcomes of interest were time to confirmed disability worsening (CDW), time to achieve an expanded disability status scale (EDSS) value of 4, time to relapse, and time to confirmed disability improvement (CDI). To support the results, a sensitivity analysis focusing solely on patients from Sweden starting with HE-DMT and patients from the Czech Republic starting with LE-DMT was performed. RESULTS: In the Swedish cohort, 42% of patients received HE-DMT as initial therapy compared to 3.8% of patients in the Czech cohort. The time to CDW was not significantly different between the Swedish and Czech cohorts (p-value 0.2764), with hazard ratio (HR) of 0.89 and a 95% confidence interval (CI) of 0.77-1.03. Patients from the Swedish cohort exhibited better outcomes for all remaining variables. The risk of reaching EDSS 4 was reduced by 26% (HR 0.74, 95%CI 0.6-0.91, p-value 0.0327), the risk of relapse was reduced by 66% (HR 0.34, 95%CI 0.3-0.39, p-value <0.001), and the probability of CDI was three times higher (HR 3.04, 95%CI 2.37-3.9, p-value <0.001). CONCLUSION: The analysis of the Czech and the Swedish RRMS cohorts confirmed a better prognosis for patients in Sweden, where a significant proportion of patients received HE-DMT as initial treatment.
 BACKGROUND: Falls as well as fall-related injuries (e.g., bone fractures) are common in persons with multiple sclerosis (pwMS). Whilst some studies have identified lower extremity maximal muscle strength (Fmax) as one among several risk factors, no previous studies have investigated the association between rate of force development (RFD; ability to generate a rapid rise in muscle force) and falls in pwMS. Not only is RFD substantially compromised (and more so than Fmax) in pwMS, studies involving other neurodegenerative populations have shown that RFD - to a greater extent than Fmax - is crucial for counteracting unexpected perturbations and avoiding falling. OBJECTIVE: To explore whether knee extensor RFD (and Fmax) can discriminate fallers from non-fallers in pwMS. METHODS: Knee extensor neuromuscular function (comprising RFD(50ms) and RFD(200ms) (force developed in the interval 0-50 ms and 0-200 ms, respectively) as well as Fmax) of the weaker leg was assessed by isokinetic dynamometry. Falls were determined by 1-year patient recall, with pwMS subsequently being classified as non-fallers (0 falls), fallers (1-2 falls), or recurrent fallers (≥3 falls). RESULTS: A total of n=53 pwMS were enrolled in the study, with n=24 classified as non-fallers (63% females, 48 years, EDSS 2.2), n=16 as fallers (88% females, 57 years, EDSS 3.3), and n=13 as recurrent fallers (46% females, 60 years, EDSS 4.2). Compared with non-fallers, neuromuscular function was reduced in both fallers (RFD(50) -4.42 [-7.47;-1.37] Nm(.)s(-1.)kg(-1), -48%; RFD(200) -1.45 [-2.98;0.07] Nm(.)s(-1.)kg(-1), -24%; Fmax -0.42 [-0.81;-0.03] Nm(.)kg(-1), -21%) and recurrent fallers (RFD(50) -5.69 [-8.94;-2.43] Nm(.)s(-1.)kg(-1), -62%; RFD(200) -2.26 [-3.89;-0.63] Nm(.)s(-1.)kg(-1), -38%; Fmax -0.38 [-0.80;0.03] Nm(.)kg(-1), -19%). Across all participants, associations were observed between RFD(50ms) and falls (r(s) = -0.46 [-0.67;-0.24], between RFD(200ms) and falls (r(s) = -0.34 [-0.59;-0.09]), and between Fmax and falls (r(s) = -0.24 [-0.48;0.01]). CONCLUSION: In this exploratory study, knee extensor neuromuscular function was able to discriminate fallers from non-fallers in pwMS, with RFD being superior to Fmax. Routine assessment of lower extremity neuromuscular function (RFD(50ms) in particular) may be a helpful tool in identifying pwMS at future risk of falling.
 BACKGROUND: Information processing speed (IPS) deterioration is common in relapsing-remitting multiple sclerosis (RRMS) patients [1] and might severely affect quality of life and occupational activity. However, understanding of its neural substrate is not fully elucidated. We aimed to investigate the associations between MRI-derived metrics of neuroanatomical structures, including the tracts, and IPS. METHODS: Symbol Digit Modalities Test (SDMT), Paced Auditory Serial Addition Test (PASAT), and Color Trails Test (CTT) were used to evaluate IPS in 73 RRMS consecutive patients, all undergoing only interferon beta (IFN-β) therapy during the study. At the same time, 1.5T MRI including diffusion tensor imaging (DTI) data was acquired for each recruited subject. We analyzed volumetric and diffusion MRI measures (FreeSurfer 6.0) including normalized brain volume (NBV), cortical thickness (thk), white matter hypointensities (WMH), volume (vol), diffusion parameters: mean (MD), radial (RD), axial (AD) diffusivities, and fractional anisotropy (FA) of 18 major white-matter (WM) tracts. Multiple linear regression model with interaction resulted in distinguishing the neural substrate of IPS deficit in the IPS impaired subgroup of patients. RESULTS: The most significant tract abnormalities contributing to IPS deficit were right inferior longitudinal fasciculus (R ILF) FA, forceps major (FMAJ) FA, forceps minor (FMIN) FA, R uncinate fasciculus (UNC) AD, R corticospinal tract (CST) FA, and left superior longitudinal fasciculus FA (L SLFT). Among volumetric MRI metrics, IPS deficit was associated with L and R thalamic vol. and cortical thickness of insular regions. CONCLUSION: In this study, we showed that disconnection of the selected WM tracts, in addition to cortical and deep gray matter (GM) atrophy, might underlie IPS deficit in RRMS patients but more extensive studies are needed for precise associations.
 Accurate diagnosis of multiple sclerosis requires careful attention to its differential diagnosis-many disorders can mimic the clinical manifestations and paraclinical findings of this disease. A collaborative effort, organised by The International Advisory Committee on Clinical Trials in Multiple Sclerosis in 2008, provided diagnostic approaches to multiple sclerosis and identified clinical and paraclinical findings (so-called red flags) suggestive of alternative diagnoses. Since then, knowledge of disorders in the differential diagnosis of multiple sclerosis has expanded substantially. For example, CNS inflammatory disorders that present with syndromes overlapping with multiple sclerosis can increasingly be distinguished from multiple sclerosis with the aid of specific clinical, MRI, and laboratory findings; studies of people misdiagnosed with multiple sclerosis have also provided insights into clinical presentations for which extra caution is warranted. Considering these data, an update to the recommended diagnostic approaches to common clinical presentations and key clinical and paraclinical red flags is warranted to inform the contemporary clinical evaluation of patients with suspected multiple sclerosis.

 The article presents a clinical observation of a schizophrenia-like disorder in a patient with multiple sclerosis (MS). The patient had highly active MS with a relapsing course, the diagnosis was made based on the McDonald 2017 criteria. During the course of a demyelinating disease of the nervous system, the patient developed an episode of psychotic disorders with symptoms of mutism, hallucinations, delusions and impaired thinking, which was quickly stopped in stationary conditions. This case is of particular interest to neurologists and psychiatrists, since psychotic disorders occur in MS patients and cause difficulties in diagnosis and treatment.
 Since multiple sclerosis (MS) is characterized by an unpredictable disease course, accurate prognosis and personalized treatment constitute an important challenge in clinical practice. We performed a qualitative systematic review to assess the predictive value of retinal layer measurement by spectral-domain optical coherence tomography (SD-OCT) in MS patients. Longitudinal MS cohort studies that determined the risk of clinical deterioration based on peripapillary retinal nerve fiber layer (pRNFL) and/or macular ganglion cell-inner plexiform layer (mGCIPL) atrophy were included. Our search strategy and selection process yielded eight articles in total. Of those, five studies only focused on patients with a relapsing-remitting disease pattern (RRMS). After correction for confounders such as disease duration, we found that (1) cross-sectional measurement of pRNFL thickness ≤ 88 µm; (2) cross-sectional measurement of mGCIPL thickness < 77 µm; (3) longitudinal measurement of pRNFL thinning > 1.5 µm/year; and (4) longitudinal measurement of mGCIPL thinning ≥ 1.0 µm/year is associated with an increased risk for disability progression in subsequent years. Longitudinal mGCIPL assessment consistently resulted in the highest risk estimates in our analysis. Within these studies, inclusion and exclusion criteria accounted for the retinal degeneration inherent to (acute) optic neuritis (ON). This small systematic review provides additional evidence that OCT-measured pRNFL and/or mGCIPL atrophy can predict disability progression in RRMS patients. We therefore recommend close clinical follow-up or initiation/change of treatment in RRMS patients with increased risk for clinical deterioration based on retinal layer thresholds, in particular when other poor prognostic signs co-occur.
 BACKGROUND: Dysphagia is a common symptom in multiple sclerosis that can occur even early in the disease course and can lead to serious complications. Early recognition and treatment can promote comfort, safety and optimal nutritional status. Few dysphagia rating scales are available in Spanish. The aim of this study was to translate the Dysphagia in Multiple Sclerosis Questionnaire (DYMUS) into Spanish and to validate it. METHODS: Forward and backward translation method was used to translate the original English version of DYMUS into Spanish. A pilot-study with 10 PwMS was carried on in order to improve the intelligibility of the instrument, comprehensibility and content validity of the questionnaire. The questionnaire was filled out by 100 PwMS who were asked a dichotomous question on their swallowing ("Do you have swallowing troubles?"). Descriptive data are presented as median and quartiles for continuous variables and frequency and percentage for categorical ones. Internal consistency reliability was estimated by Cronbach's alfa. Test-retest reliability was estimated by intraclass correlation coefficient. Concurrent validity with a speech and language therapy assessment (SLT-A) was measured with the weighted kappa statistic for the concordance for both dysphagia type and degree categories. Confirmatory factor analysis by means of structural equation models was used to verify the two-factor (solids and liquids) structure of the DYMUS questionnaire. As the goodness of fit evaluation was poor, an additional exploratory factor analysis was carried out. RESULTS: Internal consistency was high. The globus sensation question and the weight loss questions (item 3 and 10) are the least specific with dysphagia symptomatology so they are worst correlated with the sum of the others (item-rest correlation, 0.243 and 0.248, respectively). The test-retest reliability of the DYMUS among 40 patients using ICC was 0.75 (95% CI 0.57 - 0.86). Concurrent validity with SLT-A was poor (weighted kappa 0.37 for dysphagia type and 0.38 for dysphagia degree). The DYMUS questionnaire detected three times more dysphagia (53% versus 17%) than the dichotomous question. Confirmatory factors analysis failed to confirm the bidimensional structure (solid and liquid items) often reported in other validation studies. The subsequent exploratory factor analysis also identified two factors, but with poor interpretability. CONCLUSION: DYMUS-SP scale is not a sufficiently useful scale to detect dysphagia in PwMS due to the poor concurrent validity and the probable overdiagnosis of the condition; however, it can be helpful as a screening tool when combined with other measures.


 Obesity is associated with chronic mild-grade systemic inflammation and neuroinflammation. Obesity in early childhood and adolescence is also a significant risk factor for multiple sclerosis (MS) development. However, the underlying mechanisms that explain the link between obesity and MS development are not fully explored. An increasing number of studies call attention to the importance of gut microbiota as a leading environmental risk factor mediating inflammatory central nervous system demyelination, particularly in MS. Obesity and high-calorie diet are also associated with disturbances in gut microbiota. Therefore, gut microbiota alteration is a plausible connection between obesity and the increased risk of MS development. A greater understanding of this connection could provide additional therapeutic opportunities, like dietary interventions, microbiota-derived products, and exogenous antibiotics and probiotics. This review summarizes the current evidence regarding the relationships between MS, obesity, and gut microbiota. We discuss gut microbiota as a potential link between obesity and increased risk for MS. Additional experimental studies and controlled clinical trials targeting gut microbiota are warranted to unravel the possible causal relationship between obesity and increased risk of MS.
 The gut microbiota is involved in the development of the immune system and can modulate the risk for immune-mediated disorders such as multiple sclerosis (MS). Dysbiosis has been demonstrated in MS patients and its restoration by disease-modifying treatments (DMTs) is hypothesized. We aimed to study the changes in gut microbiota composition during the first 6 months of treatment with dimethyl fumarate (DMF), an oral DMT, and to identify the microorganisms associated with DMF side effects. We collected and analyzed the gut microbiota of 19 MS patients at baseline and after 1, 3, and 6 months of DMF treatment. We then cross-sectionally compared gut microbiota composition according to the presence of gastrointestinal (GI) symptoms and flushing. Overall, the gut microbiota biodiversity showed no changes over the 6-month follow-up. At the genus level, DMF was associated with decreased Clostridium abundance after 6 months. In subjects reporting side effects, a higher abundance of Streptococcus, Haemophilus, Clostridium, Lachnospira, Blautia, Subdoligranulum, and Tenericutes and lower of Bacteroidetes, Barnesiella, Odoribacter, Akkermansia, and some Proteobacteria families were detected. Our results suggest that gut microbiota may be involved in therapeutic action and side effects of DMF, representing a potential target for improving disease course and DMT tolerability.
 INTRODUCTION: An association between intercurrent viral respiratory infections and exacerbations of Multiple Sclerosis (MS) disease activity has been proposed by several studies. Considering the rapid spread of SARS-CoV2 worldwide and the systematic effort to immediately detect all incident cases with specific diagnostic tests, the pandemic can represent an interesting experimental model to assess the relationship between viral respiratory infections and MS disease activity. AIMS AND METHODS: In this study, we have performed a propensity score matched case-control study with a prospective clinical/MRI follow-up, on a cohort of relapsing-remitting MS (RRMS) patients who tested positive for SARS-CoV2 in the period 2020-2022, with the aim to evaluate if the SARS-CoV2 infection influences the short-term risk of disease activity. Controls (RRMS patients not exposed to SARS-CoV-2, using 2019 as the reference period) were matched 1:1 with cases for age, EDSS, sex and disease-modifying treatment (DMT) (moderate efficacy vs high efficacy). Differences in relapses, MRI disease activity and confirmed disabilty worsening (CDW) between cases in the 6 months following the SARS-CoV-2 infection, and controls in a similar 6 months reference period in 2019 were compared. RESULTS: We identified 150 cases of SARS-CoV2 infection in the period March 2020 - March 2022, out of a total population of approximately 1500 MS patients, matched with 150 MS patients not exposed to SARS-CoV2 (controls). Mean age was 40.9 ± 12.0 years in cases and 42.0 ± 10.9 years in controls, mean EDSS was 2.54±1.36 in cases and 2.60±1.32 in controls. All patients were treated with a DMT, and a considerable proportion with a high efficacy DMT (65.3% in cases and 66% in controls), reflecting a typical real world RRMS population. 52.8% of patients in this cohort had been vaccinated with a mRNA Covid-19 vaccine. We did not observe a significant difference in relapses (4.0% cases, 5.3% controls; p = 0.774), MRI disease activity (9.3% cases, 8.0% controls; p = 0.838), CDW (5.3% cases, 6.7% controls; p = 0.782) in the 6 months after SARS-CoV-2 infection between cases and controls. CONCLUSION: Using a propensity score matching design and including both clinical and MRI data, this study does not suggest an increased risk of MS disease activity following SARS-CoV-2 infection. All MS patients in this cohort were treated with a DMT, and a considerable number with a high efficacy DMT. These results therefore may not be applicable to untreated patients, for which the risk of increased MS disease activity after SARS-CoV-2 infection may not be excluded. A possible hypothesis explaining these results could be that SARS-CoV2 is less prone, compared to other viruses, to induce exacerbations of MS disease activity; another possible interpretation of these data might be that DMT is able to effectively suppress the increase of disease activity triggered by SARS-CoV2 infection.

 BACKGROUND: Surgical patients with preexisting neurological diseases create greater challenges to perioperative management, and choice of anesthetic is often complicated. We investigated neuraxial anesthesia use in total knee and hip arthroplasty (TKA/THA) recipients with multiple sclerosis or myasthenia gravis compared to the general population. METHODS: We retrospectively analyzed patients undergoing a TKA/THA with a diagnosis of multiple sclerosis or myasthenia gravis (Premier Health Database, 2006-2019). The primary outcome was neuraxial anesthesia use in multiple sclerosis or myasthenia gravis patients compared to the general population. Secondary outcomes were length of stay, intensive care unit admission, and mechanical ventilation. We measured the association between the aforementioned subgroups and neuraxial anesthesia use. Subsequently, subgroup-specific associations between neuraxial anesthesia and secondary outcomes were measured. We report odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Among 2,184,193 TKA/THAs, 7559 and 3176 had a multiple sclerosis or myasthenia gravis diagnosis, respectively. Compared to the general population, neuraxial anesthesia use was lower in multiple sclerosis patients (OR, 0.61; CI, 0.57-0.65; P < .0001) and no different in myasthenia gravis patients (OR, 1.05; CI, 0.96-1.14; P = .304). Multiple sclerosis patients administered neuraxial anesthesia (compared to those without neuraxial anesthesia) had lower odds of prolonged length of stay (OR, 0.63; CI, 0.53-0.76; P < .0001) mirroring neuraxial anesthesia benefits seen in the general population. CONCLUSIONS: Neuraxial anesthesia use was lower in surgical patients with multiple sclerosis compared to the general population but no different in those with myasthenia gravis. Neuraxial use was associated with lower odds of prolonged length of stay.
 BACKGROUND AND OBJECTIVES: Although MRI-based markers of neuroinflammation have proven crucial for the diagnosis of multiple sclerosis (MS), predicting clinical progression with inflammation remains difficult. Neurodegenerative markers such as brain volume loss show stronger clinical (predictive) correlations, but also harbor age-related variation that must be disentangled from disease duration. In this study we investigated how clinical disability is related to volumetric MRI measures in a cohort of MS patients and healthy controls (HC) of the same age: Project Y. METHODS: This study included 234 MS patients born in 1966 and 112 HC born between 1965 and 1967 in the Netherlands. Disability was quantified using the expanded disability status scale (EDSS), nine hole peg test (9HPT), and timed 25 foot walking test (T25FWT). Volumes were quantified on 3T MRI as normalized whole brain (NBV) and regional gray matter (GM) volumes using the same scanner and MRI protocol: cortical (normalized cortical gray matter volume; NCGMV), deep (NDGMV), thalamic (NThalV), and cerebellar (NCbV) GM volumes. In addition, mean upper cervical cord area (MUCCA), white matter lesion volume (LV), and spinal cord lesions were assessed. These measures were compared between patients and HC, and related to disability measures using linear regression. RESULTS: Mean age of people with MS (PwMS) was 52.8 years (SD 0.9) and median disease duration 15.8 years (IQR 8.7-24.8). All global and regional brain measures were lower in MS patients compared to HC. Univariate regression models showed that NDGMV (β = -0.20) and MUCCA (β = -0.38) were most strongly related to the EDSS in all PwMS. After subtype stratification, MUCCA was most strongly related to the EDSS (β = -0.60) and 9HPT (β = -0.55) in secondary progressive PwMS. Multivariate regression models demonstrated that in all PwMS, the EDSS was best explained by lower MUCCA, longer disease durations and a progressive disease course (adjusted-R (Sastre-Garriga et al., 2017) = 0.26, p < 0.001). MUCCA was a consistent correlate in separate models of the EDSS for all PwMS, relapsing and progressive onset PwMS. The 9HPT (adjusted-R (Sastre-Garriga et al., 2017) = 0.20, p < 0.001) was best explained by lower MUCCA, higher LV and pack years, while lower limb disability (adjusted-R (Sastre-Garriga et al., 2017) = 0.11, p < 0.001) was best explained by lower MUCCA, progressive onset MS and female sex. DISCUSSION: Our results indicate that in a cohort unbiased by age differences, spinal cord and deep gray matter volumes best related to physical disability. Our results support the use of these measures in clinical practice and trials.
 BACKGROUND: Cladribine tablets are a highly effective immune reconstitution therapy licensed for treating relapsing multiple sclerosis (RMS) in Europe since 2017. Currently, there is a high demand for real-world data from different clinical settings on the effectiveness and safety profile of cladribine in MS. METHODS: Within this report, we retrospectively evaluated the outcomes of RMS patients who received cladribine between August 2018 and November 2021 at our Belgian institute. Patients with data for three effectiveness endpoints, more specifically, relapses, MRI observations, and confirmed disability worsening were incorporated into the analysis of 'no evidence of disease activity' (NEDA-3) re-baselined at 3 months. Safety endpoints included lymphopenia, liver transaminases, and adverse events (AEs) during follow-up. Descriptive statistics and time-to-event analysis were performed, including subgroup analysis by pre-treatment. RESULTS: Of the 84 RMS patients included in this study (age 42 [33-50], 64.3% female, diagnosis duration 6 [2-11] years, baseline EDSS 2.5 [1.5-3.6]), 14 (16.7%) patients experienced relapses, while disability progression and brain MRI activity occurred in 8.5% (6/71) and 6.3% (5/79). This resulted in 72.6% (n = 69, standard error 6%) retaining NEDA-3 status at the mean follow-up time of 22.6 ± 11.5 months. During the first year after cladribine initiation, disease activity prevailed more in patients with ≥2 prior DMTs and those switching from fingolimod, although both trends were not statistically significant. In terms of safety, 67.9% reported at least one AE during follow-up, the most frequent being fatigue (64.9%) and skin-related problems (38.6%). CONCLUSION: Overall, our research results confirm cladribine's safety and effectiveness among RMS patients in real-world conditions. After the re-baseline, we observed high rates of NEDA-3-retention, and no new safety signals were noted.
 BACKGROUND AND OBJECTIVES: Primary progressive multiple sclerosis (PPMS) displays a highly variable disease progression with a characteristic accumulation of disability, what makes difficult its diagnosis and efficient treatment. The identification of microRNAs (miRNAs)-based signature for the early detection in biological fluids could reveal promising biomarkers to provide new insights into defining MS clinical subtypes and potential therapeutic strategies. The objective of this cross-sectional study was to describe PPMS miRNA profiles in CSF and serum samples compared with other neurologic disease individuals (OND) and relapsing-remitting MS (RRMS). METHODS: First, a screening stage analyzing multiple miRNAs in few samples using OpenArray plates was performed. Second, individual quantitative polymerase chain reactions (qPCRs) were used to validate specific miRNAs in a greater number of samples. RESULTS: A specific profile of dysregulated circulating miRNAs (let-7b-5p and miR-143-3p) was found downregulated in PPMS CSF samples compared with OND. In addition, in serum samples, miR-20a-5p and miR-320b were dysregulated in PPMS against RRMS and OND, miR-26a-5p and miR-485-3p were downregulated in PPMS vs RRMS, and miR-142-5p was upregulated in RRMS compared with OND. DISCUSSION: We described a 2-miRNA signature in CSF of PPMS individuals and several dysregulated miRNAs in serum from patients with MS, which could be considered valuable candidates to be further studied to unravel their actual role in MS. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that specific miRNA profiles accurately distinguish PPMS from RRMS and other neurologic disorders.
 Addressing a person in the context of their disease must be done respectfully. As a person with multiple sclerosis (MS), my preference is to be referred to as such. Some people with MS refer to themselves as MSers, MS warriors, MS sufferers, and that's fine. A person with MS can refer to themselves in the context of their disease in the manner they choose. People without MS should use terminology most respectful and acceptable to the broadest of the minority. Academics sometimes use persons with MS to refer to an infinite number of people. Not only is this incorrect but use of persons has broadly fallen out of favour in recent decades. In this personal viewpoint I discuss these issues from a lived experience perspective.

 BACKGROUND: Dimethyl fumarate (DMF) is a first-line oral therapy for relapsing-remitting multiple sclerosis (RRMS). This retrospective study aims to determine the utility of routine complete blood counts (CBC) in predicting lymphopenia, adverse effects and efficacy in a real-world clinical setting. METHODS: The Calgary Multiple Sclerosis (MS) Clinic manages over 1800 people with MS on disease-modifying therapies (DMT). Data of patients with relapsing-remitting MS (pwMS) who initiated DMF between July 1, 2013 and December 31, 2014 were included. Patients were followed for one year. DMT use is carefully monitored and pwMS need a screening CBC and have regular CBCs done at follow-up. Demographic, clinical, MRI and relapse information are collected prospectively in a clinic database. We analyzed CBCs at baseline and month 3. RESULTS: We identified 139 pwMS in the study period who started DMF. Median follow-up time on-drug was 12 (0.16-12) months. In our study, 15.8% of pwMS developed lymphopenia grade 2 or higher. Baseline lymphocyte counts and older age were significant predictors of lymphopenia. Higher baseline eosinophil counts predicted flushing/gastrointestinal adverse effects, and higher baseline monocyte counts were predictive of breakthrough disease activity. Neutrophil and platelet to lymphocyte ratios, markers that have been associated with overall mortality in the general population, were increased at month 3. CONCLUSIONS: Routinely obtained CBCs during the screening and monitoring of people with MS starting DMF offer clinically useful information and generate interesting hypotheses. Age and baseline lymphocyte counts are reinforced as clinically useful predictors of lymphopenia. Our novel findings that baseline eosinophil and monocyte counts could offer insights into usual adverse effects and efficacy, respectively, should be further investigated as a potentially new set of biomarkers.
 Levamisole-associated multifocal inflammatory encephalopathy (LAMIE) is a devastating adverse effect of levamisole (LEV) treatment. In Russia, people often use LEV without a doctor's prescription for anthelmintic prophylaxis. LAMIE often misdiagnosed as the first episode of MS or acute disseminated encephalomyelitis (ADEM). The aim of our study was to describe clinical, laboratory and morphological characteristics of LAMIE, magnetic resonance imaging (MRI) patterns and create an algorithm for the differential diagnosis. This study was a prospective observational study with retrospective analysis of cases. It was performed at two hospitals with ambulatory service for MS. We included 43 patients with LAMIE with follow-up was from 1 year to 5 years. Age was 19-68 y.o. with female predominance. The most typical manifestations of LAMIE were cerebellar, pyramidal and cognitive symptoms, and majority of patients had biphasic course of the disease. Three main types of MRI patterns were described: ADEM-like, MS-like, atypical demyelination. About 40% of patients had CSF specific oligoclonal bands synthesis, but only 20 % of them converted to MS during the period from 1 month until 2 years. The CSF albumin levels and immunoglobulin G index were elevated in LAMIE patients compared to reference values. We described results of brain biopsy in two cases. Therefore LAMIE should be considered in patients with demyelinating or inflammatory conditions with biphasic onset of the disease and variable MRI presentation.
 The MOTIV-SEP therapeutic education program for people with multiple sclerosis integrates the cognitive, emotional, behavioral and social components of therapeutic compliance. These components allow for an approach centered on the individual, in order to help him or her better support the important stage of starting treatment, but also to anticipate and reduce the obstacles to compliance.
 Glatiramer acetate is one of the oldest and safest disease modifying therapies used to treat relapsing-remitting multiple sclerosis. Urticarial vasculitis is a rare complication of treatment with glatiramer acetate, having been reported by only two others previously. Here, we describe a case of normocomplementemic urticarial vasculitis diagnosed on skin punch biopsy in a patient with multiple sclerosis treated with glatiramer acetate for five years. Upon treatment with steroids and an antihistamine along with discontinuation of glatiramer acetate, the urticaria resolved.

 The application of convolutional neural networks (CNNs) to MRI data has emerged as a promising approach to achieving unprecedented levels of accuracy when predicting the course of neurological conditions, including multiple sclerosis, by means of extracting image features not detectable through conventional methods. Additionally, the study of CNN-derived attention maps, which indicate the most relevant anatomical features for CNN-based decisions, has the potential to uncover key disease mechanisms leading to disability accumulation. From a cohort of patients prospectively followed up after a first demyelinating attack, we selected those with T1-weighted and T2-FLAIR brain MRI sequences available for image analysis and a clinical assessment performed within the following six months (N = 319). Patients were divided into two groups according to expanded disability status scale (EDSS) score: ≥3.0 and < 3.0. A 3D-CNN model predicted the class using whole-brain MRI scans as input. A comparison with a logistic regression (LR) model using volumetric measurements as explanatory variables and a validation of the CNN model on an independent dataset with similar characteristics (N = 440) were also performed. The layer-wise relevance propagation method was used to obtain individual attention maps. The CNN model achieved a mean accuracy of 79% and proved to be superior to the equivalent LR-model (77%). Additionally, the model was successfully validated in the independent external cohort without any re-training (accuracy = 71%). Attention-map analyses revealed the predominant role of frontotemporal cortex and cerebellum for CNN decisions, suggesting that the mechanisms leading to disability accrual exceed the mere presence of brain lesions or atrophy and probably involve how damage is distributed in the central nervous system.

 BACKGROUND AND OBJECTIVES: Cognitive impairment is a common and impactful symptom of relapsing-remitting multiple sclerosis (RRMS). Cognitive outcome measures are often used in cross-sectional studies, but their performance as longitudinal outcome measures in clinical trials is not widely researched. In this study, we used data from a large clinical trial to describe change on the Symbol Digit Modalities Test (SDMT) and the Paced Auditory Serial Addition Test (PASAT) over up to 144 weeks of follow-up. METHODS: We used the data set from DECIDE (clinicaltrials.gov identifier NCT01064401), a large randomized controlled RRMS trial to describe change on the SDMT and PASAT over 144 weeks of follow-up. We compared change on these cognitive outcomes with change on the timed 25-foot walk (T25FW), a well-established physical outcome measure. We investigated several definitions for clinically meaningful change: any change, 4-point change, 8-point change, and 20% change for the SDMT, any change, 4-point change, and 20% change for the PASAT, and 20% change for the T25FW. RESULTS: DECIDE included 1,814 trial participants. SDMT and PASAT scores steadily improved throughout follow-up: the SDMT from a mean 48.2 (SD, 16.1) points at baseline to 52.6 (SD 15.2) at 144 weeks and the PASAT from 47.0 (SD 11.3) at baseline to 50.0 (SD 10.8) at 144 weeks. This improvement in scores is most likely due to a practice effect. Throughout the trial, participants were more likely to experience improvement than worsening of their SDMT and PASAT performance, whereas the number of worsening events on the T25FW steadily increased. Changing the definition of clinically meaningful change for the SDMT and PASAT or using a 6-month confirmation changed the overall number of worsening or improvement events but did not affect the overall behavior of these measures. DISCUSSION: Our findings suggest that the SDMT and PASAT scores do not accurately reflect the steady cognitive decline that people with RRMS experience. Both outcomes show postbaseline increases in scores, which complicates the interpretation of these outcome measures in clinical trials. More research into the size of these changes is needed before recommending a general threshold for clinically meaningful longitudinal change.
 BACKGROUND: Cognitive impairment in people with MS (PwMS) has primarily been investigated using conventional imaging markers or fluid biomarkers of neurodegeneration separately. However, the single use of these markers do only partially explain the large heterogeneity found in PwMS. OBJECTIVE: To investigate the use of multimodal (bio)markers: i.e., serum and cerebrospinal fluid (CSF) levels of neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) and conventional imaging markers in predicting cognitive functioning in PwMS. METHODS: Eighty-two PwMS (56 females, disease duration = 14 ± 9 years) underwent neuropsychological and neurological examination, structural magnetic resonance imaging, blood sampling and lumbar puncture. PwMS were classified as cognitively impaired (CI) if scoring ≥ 1.5SD below normative scores on ≥ 20% of test scores. Otherwise, PwMS were defined as cognitively preserved (CP). Association between fluid and imaging (bio)markers were investigated, as well as binary logistics regression to predict cognitive status. Finally, a multimodal marker was calculated using statistically important predictors of cognitive status. RESULTS: Only higher NfL levels (in serum and CSF) correlated with worse processing speed (r = - 0.286, p = 0.012 and r = - 0.364, p = 0.007, respectively). sNfL added unique variance in the prediction of cognitive status on top of grey matter volume (NGMV), p = 0.002). A multimodal marker of NGMV and sNfL yielded most promising results in predicting cognitive status (sensitivity = 85%, specificity = 58%). CONCLUSION: Fluid and imaging (bio)markers reflect different aspects of neurodegeneration and cannot be used interchangeably as markers for cognitive functioning in PwMS. The use of a multimodal marker, i.e., the combination of grey matter volume and sNfL, seems most promising for detecting cognitive deficits in MS.
 Fatigue is a common disabling symptom of relapsing remitting multiple sclerosis (RRMS). Many studies have linked grey matter atrophy to fatigue, but white matter lesion load (WM-LL) has received less attention. Here we assess the relation between fatigue and regional WM-LL volumetric measures. 63 patients with RRMS participated in this study; mean age was 31.9 ± 8.1 years. Each patient provided demographic details and was scored on the expanded disability status scale (EDSS) and fatigue severity scale (FSS). VolBrain, a fully automated, operator-independent tool was used to assess WM-LL and whole brain volume. The patients were classified into three groups: no fatigue (FSS < 4), low to moderate fatigue (FSS ≥ 4 ≤ 5) and high fatigue (FSS > 5). 33.3% of patients had no significant fatigue, 25.4% had mild-to-moderate fatigue, and 41.3% had significant fatigue. Age, disease duration, relapses, and EDSS were positively correlated to fatigue severity (P = 0.034, 0.002, 0.009 and 0.001 respectively). Whole brain volume, total and regional WM-LL (juxtacortical, periventricular, infratentorial) were also correlated with fatigue severity. Ordinal regression analysis for fatigue severity showed EDSS and infratentorial lesion volume were the best predictors. In conclusion, EDSS and infratentorial lesion volume (cerebellar and brainstem) are the best predictors of fatigue severity.
 BACKGROUND: Individual genetic variability may influence the course of multiple sclerosis (MS). The interleukin (IL)-8C>T rs2227306 single nucleotide polymorphism (SNP) regulates IL-8 activity in other clinical conditions; however, its role in MS has never been investigated. OBJECTIVES: To explore the association between IL-8 SNP rs2227306, cerebrospinal fluid (CSF) IL-8 concentrations, clinical, and radiological characteristics in a group of newly diagnosed MS patients. METHODS: In 141 relapsing-remitting (RR)-MS patients, rs2227306 polymorphism, CSF levels of IL-8, clinical, and demographical characteristics were determined. In 50 patients, structural magnetic resonance imaging (MRI) measures were also assessed. RESULTS: An association between CSF IL-8 and Expanded Disability Status Scale (EDSS) at diagnosis was found in our set of patients (r = 0.207, p = 0.014). CSF IL-8 concentrations were significantly higher in patients carrying the T variant of rs2227306 (p = 0.004). In the same group, a positive correlation emerged between IL-8 and EDSS (r = 0.273, p = 0.019). Finally, a negative correlation between CSF levels of IL-8 and cortical thickness emerged in rs2227306T carriers (r = -0.498, p = 0.005). CONCLUSION: We describe for the first time a role of SNP rs2227306 of IL-8 gene in regulating the expression and the activity of this inflammatory cytokine in MS.
 BACKGROUND: The Rowland Universal Dementia Assessment Scale (RUDAS) is a cognitive test with favorable diagnostic properties for detecting dementia and a low influence of education and cultural biases. OBJECTIVE: We aimed to validate the RUDAS in people with Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). METHODS: We enrolled one hundred and fifty participants (60 with AD, 30 with PD, 60 with MS, and 120 healthy controls (HC)). All clinical groups completed a comprehensive neuropsychological battery, RUDAS, and standard cognitive tests of each disorder: MMSE, SCOPA-COG, and Symbol Digit Modalities Test. Intergroup comparisons between clinical groups and HC and ROC curves were estimated. Random Forest algorithms were trained and validated to detect cognitive impairment using RUDAS and rank the most relevant scores. RESULTS: The RUDAS scores were lower in patients with AD, and patients with PD and MS showed cognitive impairment compared to healthy controls. Effect sizes were generally large. The total score was the most discriminative, followed by the memory score. Correlations with standardized neuropsychological tests were moderate to high. Random Forest algorithms obtained accuracies over 80-90% using the RUDAS for diagnosing AD and cognitive impairment associated with PD and MS. CONCLUSION: Our results suggest the RUDAS is a valid test candidate for multi-disease cognitive screening tool in AD, PD, and MS.
 BACKGROUND: Choroid plexus (CP) enlargement has been suggested as a reliable marker of neuroinflammation in adult multiple sclerosis (MS). We investigated CP volume in patients with paediatric MS compared with matched healthy controls (HC), possible sex-related effect, and the associations with clinical and structural MRI variables. METHODS: Brain 3.0 T dual-echo and three-dimensional (3D) T1-weighted sequences were selected retrospectively from 69 patients with paediatric MS and 23 age-matched and sex-matched HC. CP volume was manually obtained from 3D T1-weighted scans by two expert raters. RESULTS: CP segmentation was highly reproducible (intraobserver agreement: rater I=0.963, rater II=0.958; interobserver agreement=0.968). Compared with HC, patients with paediatric MS showed higher normalised CP volume (p<0.001). Both female and male patients with paediatric MS showed higher normalised CP volume compared with sex-matched HC (women: p<0.001 and men: p=0.021), with a significant disease×sex interaction (p=0.040). In patients with MS, a higher normalised CP volume was significantly associated with higher brain lesional volume (β=0.252, p=0.017), larger lateral ventricle volume (β=0.470, false discovery rate (FDR)-p<0.001), lower normalised brain volume (β=-0.413, FDR-p=0.002) and lower normalised thalamic volume (β=0.291, FDR-p=0.046). No associations with disease duration, Expanded Disability Status Scale score, normalised cortical and white matter volumes were found (FDR-p≥0.172). A significant effect of the disease in the negative association between normalised volumes of CP and thalami was observed (FDR-p=0.046). CONCLUSIONS: CP enlargement occurs in paediatric MS, suggesting its early involvement in the pathophysiology of the disease. The higher CP volume, which is found especially in female patients, supports the hypothesis of sex-related differences occurring already in paediatric MS.
 INTRODUCTION: Cladribine is approved for the treatment of active relapsing MS (RRMS), but its positioning in MS therapeutic scenario still needs to be fully elucidated. METHODS: This is a monocentric, observational, real-world study on RRMS patients treated with cladribine. Relapses, magnetic resonance imaging (MRI) activity, disability worsening, and loss of no-evidence-of-disease-activity-3 (NEDA-3) status were assessed as outcomes. White blood cell, lymphocyte counts and side effects were also evaluated. Patients were analyzed overall and in subgroups according to the last treatment before cladribine. The relationship between baseline characteristics and outcomes was tested to identify predictors of response. RESULTS: Among the 114 patients included, 74.9% were NEDA-3 at 24 months. We observed a reduction of relapses and MRI activity, along with a stabilization of disability. A higher number of gadolinium-enhancing lesions at baseline was the only risk factor for loss of NEDA-3 during follow-up. Cladribine was more efficacious in switchers from first-line therapies or naïves. Grade I lymphopenia was more frequent at month 3 and 15. No grade IV lymphopenia cases were observed. Independent predictors of grade III lymphopenia were a lower baseline lymphocyte count and a higher number of previous treatments. Sixty-two patients presented at least one side effect and globally 111 adverse events were recorded, none of them was serious. CONCLUSIONS: Our study confirms previous data on cladribine effectiveness and safety. Cladribine is more effective when placed early in the treatment algorithm. Real-world data on larger populations with longer follow-up are needed to confirm our findings.

 BACKGROUND AND PURPOSE: The overall disability in patients with relapsing-remitting multiple sclerosis is likely to be partly rather than entirely attributed to relapse. MATERIALS AND METHODS: The aim was to investigate the determinants of recovery from first relapse and relapse-associated worsening (RAW) in relapsing-remitting multiple sclerosis patients from the Italian MS Registry during a 5-year epoch from the beginning of first-line disease-modifying therapy. To determine recovery, the functional system (FS) score was used to calculate the difference between the score on the date of maximum improvement and the score before the onset of relapse. Incomplete recovery was defined as a combination of partial (1 point in one FS) and poor recovery (2 points in one FS or 1 point in two FSs or any other higher combination). RAW was indicated by a confirmed disability accumulation measured by the Expanded Disability Status Scale score confirmed 6 months after the first relapse. RESULTS: A total of 767 patients had at least one relapse within 5 years of therapy. Of these patients, 57.8% experienced incomplete recovery. Age (odds ratio [OR] 1.02, 95% confidence interval [CI] 1.01-1.04; p = 0.007) and pyramidal phenotype were associated with incomplete recovery (OR = 2.1, 95% CI 1.41-3.14; p < 0.001). RAW was recorded in 179 (23.3%) patients. Age (OR = 1.02, 95% CI 1.01-1.04; p = 0.029) and pyramidal phenotype (OR = 1.84, 95% CI 1.18-2.88; p = 0.007) were the strongest predictors in the multivariable model. CONCLUSIONS: Age and pyramidal phenotype were the strongest determinants of RAW in early disease epochs.
 Multiple sclerosis (MS) is a complex autoimmune disease of central nervous system, which is degenerative in nature usually appears between 20-40years of age. The exact cause of MS is still not clearly known. Loss of myelin sheath and axonal damage are the main features of MS that causes induction of inflammatory process and blocks free conduction of impulses. Till date FDA has approved 18 drugs to treat or modify MS symptoms. These medicines are disease-modifying in nature directed to prevent relapses or slow down the progression of disease. The use of the synthetic drug over an extended period causes undesirable effects that prompt us to look at Mother Nature. Complementary and alternative medicine involves the use of medicinal plants as an alternative to the existing modern medical treatment. However, modern drugs cannot be replaced completely with medicinal plants, but the two types of drugs can be used harmoniously with later one can be added as an adjuvant to the existing treatment. These medicinal plants have the potential to prevent progression and improve the symptoms of MS. Various plants such like Nigella sativa, ginger, saffron, pomegranate, curcumin, resveratrol, ginsenoside have been tested as therapeutics for many neurodegenerative diseases. The purpose of this write-up is to make information available about medicinal plants in their potential to treat or modify the symptoms of MS. Chronically ill patients tend to seek medicinal plants as they are easily available and there is a general perception about these medicines of having fewer undesirable effects.
 An antigen panel consisting of Epstein-Barr, measles, mumps, varicella zoster and rubella viruses (EMMRZ) was recently presented, which may aid in the diagnosis of multiple sclerosis (MS). The aim of this study was to validate and extend the EMMRZ panel. Various candidates, such as Cytomegalovirus and John Cunningham virus were analysed in relapsing-remitting MS (RRMS) and optic neuritis (ON) samples by enzyme-linked immunosorbent assay. IgG levels were elevated in RRMS samples and correlations were found between serum and cerebrospinal fluid levels. Cohort-dependent optimized panels were obtained for RRMS and ON, which obtained the highest sensitivity when combined with the status of oligoclonal bands.
 BACKGROUND: Low sexual function and satisfaction are common problems among people with multiple sclerosis (PwMS), but the literature on which patient variables are associated with these issues is inconsistent. OBJECTIVE: To investigate the associations between sexual function and satisfaction in PwMS with clinical, demographic, and patient-reported quality of life (QOL) measures and determine if sex differences exist. METHODS: This analysis includes PwMS enrolled in the Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital (CLIMB), who completed patient-reported outcome measures: Multiple Sclerosis Quality of Life-54 (MSQOL-54), Modified Fatigue Impact Scale (MFIS), and Center for Epidemiologic Studies Depression Scale (CES-D). Regression models were used to analyze associations between patient variables and function and satisfaction. Results were stratified by sex. Cross-sectional and longitudinal data were used. RESULTS: 702 PwMS (526 females,176 males, mean age 42.2 +/-11.1, median EDSS 1.5) were included in the cross-sectional analysis. Data from 341 PwMS were used in the three-year longitudinal analysis. Increasing age, disease duration, and disability were associated with reduced sexual function and satisfaction to the same degree in males and females. However, sex differences existed in the strength of associations with QOL variables. There was no significant longitudinal change in females or males. CONCLUSIONS: Age and disease duration were associated with reduced sexual function and satisfaction in males and females. In females, function was significantly associated with disability and satisfaction with fatigue. Males had stronger associations with sexual function in domains related to emotional well-being, health perceptions, and overall QOL. Males had stronger associations with satisfaction in emotional and social functioning and physical health domains. These findings can help better understand the multidimensional problems of sexual function and satisfaction in PwMS and better guide patient care.
 OBJECTIVES: This study aimed to determine the cost-utility of ocrelizumab versus rituximab in patients with RRMS, from the perspective of the Colombian healthcare system. METHODOLOGY: Cost-utility study based on a Markov model, with a 50-year horizon and payer perspective. The currency was the US dollar for the year 2019, with a cost-effectiveness threshold of $5180 defined for Colombian health system. The model used annual cycles according to the health status determined by the disability scale. Direct costs were considered, and the incremental cost-effectiveness ratio per 1 quality-adjusted life-year (QALY) gained was used as the outcome measure. A discount rate of 5% was applied to costs and outcomes. Multiple one-way deterministic sensitivity analyses and 10 000 Monte Carlo simulation were conducted. RESULTS: For the treatment of patients with RRMS, ocrelizumab versus rituximab had an incremental cost-effectiveness ratio of $73 652 for each QALY gained. After 50 years, 1 subject treated with ocrelizumab earns 4.8 QALYs >1 subject treated with rituximab, but at a higher cost of $521 759 versus $168 752, respectively. Ocrelizumab becomes a cost-effective therapy if its price is discounted > 86% or if there is a high willingness to pay. CONCLUSIONS: Ocrelizumab was not a cost-effective drug as compared with rituximab in treating patients with RRMS in Colombia.
 BACKGROUND AND PURPOSE: Defects in the mitochondrial respiratory chain (MRC) can lead to combined MRC dysfunctions (COXPDs) with heterogenous genotypes and clinical features. We report a patient carrying heterozygous variants in the TUFM gene who presented with clinical features compatible with COXPD4 and radiological findings mimicking multiple sclerosis (MS). METHODS: A 37-year-old French Canadian woman was investigated for recent onset of gait and balance problems. Her previous medical history included recurrent episodes of hyperventilation associated with lactic acidosis during infections, asymptomatic Wolff-Parkinson-White syndrome, and nonprogressive sensorineural deafness. RESULTS: Neurological examinations revealed fine bilateral nystagmus, facial weakness, hypertonia, hyperreflexia, dysdiadochokinesia, dysmetria, and ataxic gait. Brain magnetic resonance imaging (MRI) showed multifocal white matter abnormalities in cerebral white matter as well as cerebellar hemispheres, brainstem, and middle cerebellar peduncles, some of which mimicked MS. Analysis of native-state oxidative phosphorylation showed a combined decrease in CI/CII, CIV/CII, and CVI/CII. Exome sequencing detected two heterozygous TUFM gene variants. Little clinical progression was noted over a 5-year follow-up. Brain MRI remained unchanged. CONCLUSIONS: Our report broadens the phenotypic and radiological spectrum of TUFM-related disorders by adding milder, later onset forms to the previously known early onset, severe presentations. The presence of multifocal white matter abnormalities can be misinterpreted as due to acquired demyelinating diseases, and thus TUFM-related disorders should be added to the list of mitochondrial MS mimickers.
 OBJECTIVE: To exp lore changes in immunoglobulin (Ig) levels for people with relapsing-multiple sclerosis (RMS) treated with ocrelizumab or ofatumumab and the relationship between Ig levels and infections. METHODS: A systematic literature review (SLR) was conducted to identify clinical trials and real-world evidence (RWE) studies on Ig levels over time and studies on associations with infections for ocrelizumab and ofatumumab for people with RMS through 10 September 2021. Searches were conducted in Embase, MEDLINE, Cochrane Library, trial registries, and recent conference abstracts. RESULTS: Of 1,580 articles identified, 30 reporting on 11 trials and 5 RWE studies were included. Ocrelizumab trials (n = 4) had 24-336 weeks of follow-up and reported decreasing Ig G (IgG) levels, while RWE (n = 5) had 52-78 weeks of follow-up and reported IgG to be stable or decrease only slightly. IgG levels were stable in ofatumumab trials (n = 5; 104-168 weeks of follow-up), but no RWE or longer-term studies were identified. No apparent association between decreased Ig levels and infections was observed during ofatumumab treatment (ASCLEPIOS I/II), while for ocrelizumab, the only data on apparent associations between decreased IgG levels and serious infection rates were for a pooled population of people with RMS or primary progressive MS. CONCLUSION: Decreasing IgG levels have been correlated with increased infection risk over time. IgG levels appeared to decrease over time in ocrelizumab trials but remained relatively stable over time in ofatumumab trials. Additional research is needed to understand differences between ocrelizumab and ofatumumab and identify people at risk of decreasing IgG levels and infection.
 BACKGROUND AND PURPOSE: The aim was to evaluate the potential of retinal nerve fiber layer thickness (RNFLT) measured with optical coherence tomography in predicting disease progression in relapsing-remitting multiple sclerosis (RRMS). METHODS: Analyses were conducted post hoc of this 24-month, phase III, double-blind study, in which RRMS patients were randomized (1:1:1) to once daily oral fingolimod 0.5 mg, 1.25 mg or placebo. The key outcomes were the association between baseline RNFLT and baseline clinical characteristics and clinical/imaging outcomes up to 24 months. Change of RNFLT with fingolimod versus placebo within 24 months and time to retinal nerve fiber layer (RNFL) thinning were evaluated. RESULTS: Altogether 885 patients were included. At baseline, lower RNFLT was correlated with higher Expanded Disability Status Scale score (r = -1.085, p = 0.018), lower brain volume (r = 0.025, p = 0.006) and deep gray matter volume (r = 0.731, p < 0.0001), worse visual acuity (r = -19.846, p < 0.0001) and longer duration since diagnosis (r = -0.258, p = 0.018). At month 12, low baseline RNFLT (<86 μm) versus high baseline RNFLT (≥99 μm) was associated with a greater brain volume loss (percentage change -0.605% vs. -0.315%, p = 0.035) in patients without optic neuritis history. At month 24, low baseline RNFLT versus high baseline RNFLT was associated with a higher number of new or newly enlarged T2 lesions (mean number 4.0 vs. 2.8, p = 0.014) and a higher risk of subsequent RNFL thinning (hazard ratio 2.55; 95% confidence interval 1.84-3.53; p < 0.001). The atrophy of the RNFL in the inferior quadrant was alleviated with fingolimod 0.5 mg versus placebo at month 24 (Δ(least squares mean) = 1.8, p = 0.047). CONCLUSION: Retinal nerve fiber layer thickness could predict disease progression in RRMS. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT00355134, https://clinicaltrials.gov/ct2/show/NCT00355134.
 BACKGROUND: Ketogenic diets have anti-inflammatory and neuroprotective properties which make these diets an attractive complimentary treatment approach for patients living with multiple sclerosis (MS). The objective of this study was to assess the impact of ketogenic diets on neurofilament light chain (NfL), a biomarker of neuroaxonal injury. METHODS: Thirty-nine subjects with relapsing MS completed a 6-month ketogenic diet intervention. NfL levels were assayed at both baseline (pre-diet) and 6-months on-diet. In addition, ketogenic diet study participants were compared to a cohort (n = 31) of historical, untreated MS controls. RESULTS: Baseline (pre-diet) mean NfL was 5.45 pg/ml (95% CI 4.59 - 6.31). After 6 months on ketogenic diet, mean NfL was not significantly changed (5.49 pg/ml; 95% CI 4.82 - 6.19). Compared to untreated MS controls (mean 15.17 pg/ml), NfL levels for the ketogenic diet cohort were relatively low. MS subjects with higher levels of ketosis (as measured by serum beta-hydroxybutyrate) exhibited greater reductions in NfL between baseline and 6-months on ketogenic diet. CONCLUSIONS: Ketogenic diets do not worsen biomarkers of neurodegeneration in relapsing MS patients, with stable, low levels of NfL observed throughout the diet intervention. Subjects with greater biomarkers of ketosis experienced a higher degree of improvement in serum NfL. CLINICAL TRIAL IDENTIFIER: NCT03718247 - "Utilization of the Ketogenic Diet in Patients with Relapsing-Remitting MS" https://clinicaltrials.gov/ct2/show/NCT03718247.
 Multiple sclerosis (MS) is a chronic autoimmune demyelinating and neurodegenerative disease of the central nervous system with a wide variety of clinical phenotypes. In spite of the phenotypic classification of MS patients, current data provide evidence that diffuse neuroinflammation and neurodegeneration coexist in all MS forms, the latter gaining increasing clinical relevance in progressive phases. Given that the transition phase of relapsing-remitting MS (RRMS) to secondary progressive MS (SPMS) is not well defined, and widely accepted criteria for SPMS are lacking, randomised controlled trials (RCTs) specifically designed for the transition phase have not been conducted. This review summarizes primary and secondary analyses and reports derived from phase III prospective clinical RCTs listed in PubMed of compounds authorised through the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA) for the treatment of MS. The best data are available for interferon beta-1a (IFNb-1a) subcutaneous (s.c.), IFNb-1b s.c., mitoxantrone and siponimod, the latter being the most modern compound with likely the best risk-to-effect ratio. Moreover, there is a labels discrepancy for many disease-modifying treatments (DMTs) between the FDA and EMA, which have to be taken into consideration when opting for a specific DMT.
 BACKGROUND: Multiple sclerosis (MS) is a neurological disease in which the myelin lining the central nervous system is damaged. The complex and unpredictable nature of MS disease makes the diagnosis process more difficult for the patient. The aim of this study was to review the lived experiences of patients with multiple sclerosis when receiving the diagnosis. METHODS: We followed the guidelines of the Preferred Reporting Items for Systematic Reviews (PRISMA) statement. A systematic search was performed using four databases including PubMed, Scopus, Web of Science, and psych info on April 2022. RESULTS: We found 537 articles. After Applying relevant exclusion criteria removing duplicate and irrelevant articles, 13 studies were included in our systematic review after the abstract and full-text screening. Our findings collected data from 10 sub-themes in the following 3 themes to capture patients' experiences after receiving the diagnosis. These included: Emotional reactions to receiving the diagnosis; Communication with health professionals and knowledge about MS and Fear of being different. CONCLUSION: It is important to understand patients' experiences with the disease and identifying problems to help and support families, patients, and health care personnel's. Therefore, it is necessary to design or implement therapeutic interventions for patients at the time of receiving the diagnosis to reduce psychological problems.
 PURPOSE: Physical activity (PA) has been found to be beneficial for people with multiple sclerosis (pwMS) outside of the relapse period. However, little is known about how people experience PA during a relapse. This study investigates the experiences of pwMS engaging with PA during a relapse. MATERIALS AND METHODS: The study followed an interpretivist approach, adopting a qualitative exploratory design. Semi-structured interviews were conducted with a purposive sample of 15 adults following a recent relapse. Transcripts were analysed in NVivo using framework analysis. RESULTS: The experiences of participants were synthesised in three overarching themes: "on the road to recovery", "getting active but fearing repercussions", and "self-directed versus guided recovery". Barriers to PA included: feeling unwell, physical limitations, concerns about causing deterioration, worries that others would recognise their disability, and lack of professional support. Facilitators included: awareness of the benefits of PA, access to exercise resources, individualised advice and support from practitioners, and PA pitched at the right level. CONCLUSIONS: Relapses can disrupt normal PA routines, making it challenging to return to PA. This article makes recommendations for supporting people to undertake PA, the timing and form of support, along with suggestions for further research exploring the safety of PA during a relapse. Implications for rehabilitationPeople with RRMS find it difficult to be physically active during a relapse.There are complex personal, social and environmental reasons why people find it hard to engage with physical activity (PA).Improved timely advice and customised support during a relapse can help reduce fears and enhance confidence with returning to PA.Physical activity recommendations should be tailored to individual's abilities to make them achievable, giving a sense of accomplishment and boosting motivation.
 OBJECTIVES: Long-term immunomodulatory therapy of pediatric onset-multiple sclerosis (POMS) is based mainly on published case series and internationally agreed guidelines. Relevant studies in the Greek population are absent from the literature. The purpose of this study is to present data on the efficacy and safety of the 1st line immunomodulatory drugs in the treatment of POMS patients. MATERIALS AND METHODS: The present study included 27 patients meeting the IPMSSG criteria for POMS and who are monitored at the outpatient clinic of the Multiple Sclerosis and Demyelinating Diseases Unit (MSDDU), of the 1st Neurological Department, University Hospital of Aeginition. All patients received 1st line immunomodulatory drugs as initial therapy. Clinical, laboratory, and imaging parameters of the disease were recorded before and after treatment. RESULTS: Post-treatment, a significant reduction of the relapse number (mean ± SD: 2.0 ± 1.0 vs 1.2 ± 1.6, p = 0.002), EDSS progression (mean ± SD: 1.5 ± 0.8 vs 0.9 ± 0.7, p = 0.005) and ARR (mean ± SD: 1.5 ± 0.7 vs 0.4 ± 0.5, p = 0.0001) was observed, while no changes were observed in the EDSS score, (mean ± SD: 1.8 ± 0.6 vs 1.9. 0.6, p = 0.60). Advanced age at treatment initiation increased the risk for drug discontinuation before 24 months of therapy (HR = 0.6, 95% CI (0.35-0.99), p = 0.04). CONCLUSIONS: Most pediatric patients are forced to switch to either more efficacious 1st line or 2nd line drugs. Additionally, our study suggests that older age at the time of the 1st line treatment initiation, contributes to earlier drug discontinuation.
 IMPORTANCE: Many disease-modifying therapies (DMTs) have been approved for multiple sclerosis (MS) in the past 2 decades. Research evaluating how these approvals have changed real-world prescribing patterns is scarce. OBJECTIVE: To evaluate patterns in DMT initiations between 2001 and 2020 among commercially insured US adults and children with MS. DESIGN, SETTING, AND PARTICIPANTS: This serial cross-sectional study was conducted from 2001 through 2020 (mean patient enrollment duration, 4.8 years) and used US commercial claims data (MarketScan). Analysis took place between January 2022 and March 2023. Of 287 084 patients with MS identified, 113 583 patients (113 095 adults and 488 children) with MS newly initiated at least 1 DMT. EXPOSURE: New initiation episode of a DMT, defined as no claim for the same DMT in the previous year. MAIN OUTCOME MEASURE: The proportion of total DMT initiations per year attributable to each DMT. Trends in initiations were evaluated annually. RESULTS: The study team identified 153 846 DMT initiation episodes among adults (median age, 46 [IQR, 38-53) years]; 86 133 female [76.2%]) and 583 among children (median age, 16 (IQR, 14-17) years; 346 female [70.9%]). Among adults, use of platform injectables showed an absolute decline of 73.8% over the study period, driven by a 61.2% reduction in interferon β initiations (P < .001 for trend). In contrast, the 2010 introduction of oral DMTs led to a rise in their use from 1.1% (2010) to 62.3% (2020) of all DMT initiations (P = .002 for trend). Infusion therapy initiations remained relatively low, accounting for 3.2% of all initiations since their introduction in 2004 but increased modestly annually after ocrelizumab was introduced (2017), reaching 8.2% of all initiations in 2020 (P < .001 for trend). Children showed similar initiation patterns, except for preferred oral therapy. Between 2019 and 2020, dimethyl fumarate was the most commonly initiated DMT in adults (23.3% to 27.2% of all initiations), while in children fingolimod was the most commonly initiated (34.8% to 68.8%). CONCLUSIONS AND RELEVANCE: Current MS treatment guidelines emphasize shared decision-making between patients and clinicians to balance treatment efficacy, safety, cost, and convenience. This study found that oral DMTs were the predominant DMT type initiated by 2020. The cause of this shift cannot be determined from this study, but may reflect several factors, including convenience of administration, direct-to-consumer advertising, or insurance restrictions.
 BACKGROUND AND PURPOSE: During the COVID-19 pandemic, ocrelizumab administration was frequently postponed because of a lack of safety information and to favour vaccination. The clinical implications of ocrelizumab administration delay in multiple sclerosis (MS) patients were assessed. METHODS: Relapsing (RMS) and primary progressive (PPMS) MS patients receiving ocrelizumab for at least 6 months at our centre were retrospectively classified, according to the possible occurrence of a delay (≥4 weeks) in treatment administration. Patients were categorized in the extended-interval dosing (EID) group in the presence of at least one delayed infusion; otherwise they were considered as part of the standard interval dosing (SID) cohort. MS history, magnetic resonance imaging examinations and B-cell counts were also retrospectively collected and analysed. RESULTS: A total of 213 RMS and 61 PPMS patients were enrolled; 115 RMS and 29 PPMS patients had been treated according to the SID regimen, whilst 98 RMS and 32 PPMS patients were included in the EID cohort. Average follow-up after delay was 1.28 ± 0.7 years in the EID cohort. In RMS, comparing SID and EID patients, no differences were found considering the occurrence of clinical relapses (9.6% vs. 16.3%, p = 0.338), magnetic resonance imaging activity (9.8% vs. 14.1%, p = 0.374) or disability progression (11.3% vs. 18.4%, p = 0.103). Similar findings were observed in PPMS patients. In the pooled EID group, treatment delay correlated with CD19-positive relative (r = 0.530, p < 0.001) and absolute (r = 0.491, p < 0.001) cell counts, without implications on disease activity. CONCLUSIONS: Sporadic ocrelizumab administration delay granted sustained treatment efficacy in our cohort. Prospective data should be obtained to confirm these observations and set up systematic extended-interval regimens.
 Ublituximab (ublituximab-xiiy; BRIUMVI(™)) is a glycoengineered anti-CD20 monoclonal antibody developed by TG Therapeutics, Inc. for the treatment of multiple sclerosis (MS). The mechanism of action of ublituximab involves the depletion of B cells via antibody-dependent cellular cytotoxicity, as B cells have a key role in the pathogenesis of MS. Ublituximab is the first anti-CD20 treatment that is administered twice-yearly as one hour infusions, following the initial doses. In December 2022, ublituximab received its first global approval in the USA for the treatment of adults with relapsing forms of MS, including clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease. This article summarizes the milestones in the development of ublituximab leading to this first approval in this indication.
 Many challenges exist in the precise diagnosis and clinical management of secondary progressive multiple sclerosis (SPMS) because of the lack of definitive clinical, imaging, immunologic, or pathologic criteria that demarcate the transition from relapsing-remitting MS to SPMS. This review provides an overview of the diagnostic criteria/definition and the heterogeneity associated with different SPMS patient populations; it also emphasizes the importance of available prospective/retrospective tools to identify patients with SPMS earlier in the disease course so that approved disease-modifying therapies and nonpharmacological strategies will translate into better outcomes. Delivery of such interventions necessitates an evolving patient-clinician dialog within the context of a multidisciplinary team.
 BACKGROUND: Choroid plexus (CP) is considered to be linked to inflammation of multiple sclerosis (MS), but its connection with markers of inflammation in vivo in MS is unclear, the markers such as lesions load and brain atrophy, particularly the white matter lesions (WMLs) edge surrounded by an iron rim, termed as iron rim lesions (IRLs). PURPOSE: To investigate the association between CP volume and brain lesions load, especially IRLs load and atrophy in MS, and its relationship with clinical characteristics. METHODS: 3.0 T brain MRI images were acquired from 99 relapsing-remitting MS (RRMS) and 60 healthy controls (HCs) to obtain the volumes of CP, whole brain and lesions. Volumes were expressed as a ratio of intracranial volume. Expanded Disability Status Scale (EDSS), Montreal Cognitive Assessment (MoCA) and Symbol Digit Modalities Test (SDMT) were used to assess the severity of disability and cognitive function. Student's t-test and Multivariable regression analyses were performed to evaluate the difference of CP volumes between RRMS and HC and the association between CP volume and lesions load, brain volumes and clinical scale scores in RRMS. RESULTS: CP volume was 30% larger in patients with RRMS than HCs (p < 0.001) and was 20% larger in patients with IRLs than those without IRLs (p = 0.007). Moreover, the larger CP volume was related to greater WMLs volume in the whole RRMS (r = 0.46, p < 0.001). Further analysis in patients with IRLs showed a positive correlation between CP volume and WMLs volume (r = 0.45, p = 0.003), and IRLs volume (r = 0.51, p < 0.001). Meanwhile, enlarged CP was related to lower volumes in the whole brain (r = -0.30, p = 0.006), deep gray matter (r = -0.51, p < 0.001) and most regional deep gray matter nuclei (except amygdala), but no correlation with cortical lesions or cortex volume (both p > 0.05). In addition, CP volume was significantly higher in patients with cognitive impairment than those with cognitive preservation by MoCA scores (p = 0.011); the larger CP volume was associated with higher EDSS scores (r = 0.25, p = 0.014) and lower SDMT Z scores in RRMS (r = -0.26, p = 0.014). CONCLUSION: The enlargement of CP in RRMS had close correlations with inflammatory lesions, especially IRLs and deep gray matter atrophy, but not the cortex. Meanwhile, the larger CP volume was associated with higher disability and lower cognitive scores. CP volume may be a surrogate imaging marker for MS disease activity.
 Impairment in persons with multiple sclerosis (PwMS) can often be attributed to symptoms of motor instability and fatigue. Symptom monitoring and queued interventions often target these symptoms. Clinical metrics are currently limited to objective physician assessments or subjective patient reported measures. Recent research has turned to wearables for improving the objectivity and temporal resolution of assessment. Our group has previously observed wearable assessment of supervised and unsupervised standing transitions to be predictive of fall-risk in PwMS. Here we extend the application of standing transition quantification to longitudinal home monitoring of symptoms. Subjects (N=23) with varying degrees of MS impairment were recruited and monitored with accelerometry for a total of  ∼  6 weeks each. These data were processed using a preexisting framework, applying a deep learning activity classifier to isolate periods of standing transition from which descriptive features were extracted for analysis. Participants completed daily and biweekly assessments describing their symptoms. From these data, Canonical Correlation Analysis was used to derive digital phenotypes of MS instability and fatigue. We find these phenotypes capable of distinguishing fallers from non-fallers, and further that they demonstrate a capacity to characterize symptoms at both daily and sub-daily resolutions. These results represent promising support for future applications of wearables, which may soon augment or replace current metrics in longitudinal monitoring of PwMS.
 BACKGROUND: We previously reported an association between household chemical exposures and an increased risk of paediatric-onset multiple sclerosis. METHODS: Using a case-control paediatric multiple sclerosis study, gene-environment interaction between exposure to household chemicals and genotypes for risk of paediatric-onset multiple sclerosis was estimated.Genetic risk factors of interest included the two major HLA multiple sclerosis risk factors, the presence of DRB1*15 and the absence of A*02, and multiple sclerosis risk variants within the metabolic pathways of common household toxic chemicals, including IL-6 (rs2069852), BCL-2 (rs2187163) and NFKB1 (rs7665090). RESULTS: 490 paediatric-onset multiple sclerosis cases and 716 controls were included in the analyses. Exposures to insect repellent for ticks or mosquitos (OR 1.47, 95% CI 1.06 to 2.04, p=0.019), weed control products (OR 2.15, 95% CI 1.51 to 3.07, p<0.001) and plant/tree insect or disease control products (OR 3.25, 95% CI 1.92 to 5.49, p<0.001) were associated with increased odds of paediatric-onset multiple sclerosis. There was significant additive interaction between exposure to weed control products and NFKB1 SNP GG (attributable proportions (AP) 0.48, 95% CI 0.10 to 0.87), and exposure to plant or disease control products and absence of HLA-A*02 (AP 0.56; 95% CI 0.03 to 1.08). There was a multiplicative interaction between exposure to weed control products and NFKB1 SNP GG genotype (OR 2.30, 95% CI 1.00 to 5.30) but not for other exposures and risk variants. No interactions were found with IL-6 and BCL-2 SNP GG genotypes. CONCLUSIONS: The presence of gene-environment interactions with household toxins supports their possible causal role in paediatric-onset multiple sclerosis.
 OBJECTIVES: Nabiximols represents an increasingly employed add-on treatment option for spasticity in people with multiple sclerosis (PwMS) who either were unresponsive or reported excessive adverse reactions to other therapies. While several studies performed in the last decade demonstrated its effectiveness, safety, and tolerability, few quantitative data are available on the impact on motor dysfunctions. In this open-label, not concurrently controlled study, we aimed to assess the impact of a 4-week treatment with nabiximols on upper limb functionality. METHODS: Thirteen PwMS (9 female, 4 male) with moderate-severe spasticity underwent a combination of clinical tests (i.e., Box and Block, BBT and Nine-Hole Peg test, 9HPT) and instrumental kinematic analysis of the "hand to mouth" (HTM) movement by means of optical motion capture system. RESULTS: After the treatment, improvements in gross and fine dexterity were found (BBT + 3 blocks/min, 9HPT - 2.9 s, p < 0.05 for both cases). The kinematic analysis indicated that HTM movement was faster (1.69 vs. 1.83 s, p = 0.05), smoother, and more stable. A significant reduction of the severity of spasticity, as indicated by the 0-10 numerical rating scale (4.2 vs. 6.3, p < 0.001), was also observed. CONCLUSION: The findings from the present pilot study suggest that a 4-week treatment with nabiximols ameliorates the spasticity symptoms and the overall motor function of upper limb in PwMS with moderate-severe spasticity. The use of quantitative techniques for human movement analysis may provide valuable information about changes originated by the treatment in realistic upper limb motor tasks involved in activities of daily living.
 BACKGROUND: A growing body of compelling evidence has emerged to validate a set of signs and symptoms that indicates the onset of disease before more typical signs and symptoms present to fulfill a diagnosis of MS. On 24 June 2021, a group of international researchers, patient advocates, and Society representatives led by Professors Helen Tremlett (University of British Columbia) and Ruth Ann Marrie (University of Manitoba) convened virtually for a workshop. OBJECTIVE: Identify key gaps in knowledge, opportunities, and research priorities regarding the prodromal stage of MS. METHODS: The group developed a new framework for MS that includes the stage of early signs and symptoms of MS-and outlined a roadmap to guide future research, with the "goal of preventing the progression to onset of typical symptoms of MS in those who present during the prodromal stage of MS". RESULTS: If high-risk individuals in the early stages of MS can be identified with a high degree of certainty, there is an opportunity to intervene and minimize the risk of progressing to typical MS symptoms and a diagnosis of MS. CONCLUSION: Standardized criteria must be developed, validated, and point of intervention found to better recognize, better diagnose, and better treat MS.
 BACKGROUND: Disease-Modifying Therapies (DMTs) for Multiple Sclerosis (MS) are widely used given their proven efficacy in the relapsing form of the disease, while recently, Siponimod and Ocrelizumab have been approved for the progressive forms of the disease. Currently, 22 diseasemodifying drugs are approved by the FDA, while in 2012, only nine were present in the market. From March 2019 until August 2020, six new drugs were approved. This rapid development of new DMTs highlighted the need to update our knowledge about their short and long-term safety. OBJECTIVE: This review summarizes the available safety data for all the Disease-Modifying Therapies for Multiple Sclerosis and presents the monitoring plan before and during the treatment. METHODS: A literature search was conducted using PUBMED and COCHRANE databases. Key journals and abstracts from major annual meetings of Neurology, references of relevant reviews, and relative articles were also manually searched. We prioritized systematic reviews, large randomized controlled trials (RCTs), prospective cohort studies, and other observational studies. Special attention was paid to guidelines and papers focusing on the safety and monitoring of DMTs. CONCLUSION: Data for oral (Sphingosine 1-phosphate (S1P) receptor modulators, Fumarates, Teriflunomide, Cladribine), injectables (Interferons, Glatiramer acetate, Ofatumumab), and infusion therapies (Natalizumab, Ocrelizumab, Alemtuzumab) are presented.
 BACKGROUND: Consistent findings on underlying brain features or specific structural atrophy patterns contributing to depression in multiple sclerosis (MS) are limited. OBJECTIVE: To investigate how deep gray matter (DGM) features predict depressive symptom trajectories in MS patients. METHODS: We used data from the MS Partners Advancing Technology and Health Solutions (MS PATHS) network in which standardized patient information and outcomes are collected. We performed whole-brain segmentation using SLANT-CRUISE. We assessed if DGM structures were associated with elevated depressive symptoms over follow-up and with depressive symptom phenotypes. RESULTS: We included 3844 participants (average age: 46.05 ± 11.83 years; 72.7% female) of whom 1905 (49.5%) experienced ⩾1 periods of elevated depressive symptoms over 2.6 ± 0.9 years mean follow-up. Higher caudate, putamen, accumbens, ventral diencephalon, thalamus, and amygdala volumes were associated with lower odds of elevated depressive symptoms over follow-up (odds ratio (OR) range per 1 SD (standard deviation) increase in volume: 0.88-0.94). For example, a 1 SD increase in accumbens or caudate volume was associated with 12% or 10% respective lower odds of having a period of elevated depressive symptoms over follow-up (for accumbens: OR: 0.88; 95% confidence interval (CI): 0.83-0.93; p < 0.001; for caudate: OR: 0.90; 95% CI: 0.85-0.96; p = 0.003). CONCLUSION: Lower DGM volumes were associated with depressive symptom trajectories in MS.
 Baclofen (BAC) is the first-line recommendation to treat spasticity in people with multiple sclerosis whose treatment goals include improving mobility or easing pain. The short half-life of BAC calls for multiple daily dosing which may be eliminated by the development of a transdermal system. This study aimed to assess the effect of transdermal microneedle patches on improving the skin permeation of BAC. Nanosuspension-loaded microneedle patch containing BAC was fabricated and characterized. In vitro permeation of BAC across intact and microneedle-treated dermatomed porcine ear skin was evaluated. In vitro passive permeation of BAC solution after 72 h was observed to be 92.56 ± 11.24 µg/cm(2). A near 9-fold enhancement was observed when employing the strategy of microneedle-mediated delivery of the solution. To increase drug loading, two strategies, nanosizing and microneedle-mediated delivery, were combined and permeation of BAC after 72 h resulted to be 1951.95 ± 82.01 µg/cm(2) (p < 0.05). Microneedle-mediated transdermal delivery of BAC holds potential for sustained management of multiple sclerosis-related spasticity. Nanosizing of BAC particles facilitated higher drug loading in MN patches and an eventual increase in cumulative drug permeation from the patches.
 PURPOSE: This meta-synthesis aimed to synthesise qualitative evidence on experiences of people with Multiple Sclerosis (MS) in receiving a diagnosis, to derive a conceptual understanding of adjustment to MS diagnosis. METHODS: Five electronic databases were systematically searched to identify qualitative studies that explored views and experiences around MS diagnosis. Papers were quality-appraised using a standardised checklist. Data synthesis was guided by principles of meta-ethnography, a well-established interpretive method for synthesising qualitative evidence. RESULTS: Thirty-seven papers were selected (with 874 people with MS). Synthesis demonstrated that around the point of MS diagnosis people experienced considerable emotional upheaval (e.g., shock, denial, anger, fear) and difficulties (e.g., lengthy diagnosis process) that limited their ability to make sense of their diagnosis, leading to adjustment difficulties. However, support resources (e.g., support from clinicians) and adaptive coping strategies (e.g., acceptance) facilitated the adjustment process. Additionally, several unmet emotional and informational support needs (e.g., need for personalised information and tailored emotional support) were identified that, if addressed, could improve adjustment to diagnosis. CONCLUSIONS: Our synthesis highlights the need for providing person-centred support and advice at the time of diagnosis and presents a conceptual map of adjustment for designing interventions to improve adjustment following MS diagnosis.Implications for RehabilitationThe period surrounding Multiple Sclerosis diagnosis can be stressful and psychologically demanding.Challenges and disruptions at diagnosis can threaten sense of self, resulting in negative emotions.Adaptive coping skills and support resources could contribute to better adjustment following diagnosis.Support interventions should be tailored to the needs of newly diagnosed people.
 BACKGROUND: Research suggests that serious infections (SIs), comorbidities, and advanced disability represent key drivers of early death in people with Multiple Sclerosis (pwMS). Nevertheless, further research is warranted to better characterize and quantify the risk of SI among pwMS compared to the general population. METHODS: Our study consisted of a retrospective analysis of claims data provided by a German statutory health insurance fund, AOK PLUS, covering 3.4 million individuals in Saxony and Thuringia from 01/01/2015-31/12/2019. A propensity score (PS) matching method was used to compare the incidence of SIs among people with and without MS. PwMS were required to have ≥1 inpatient or ≥2 confirmed outpatient diagnoses of MS (ICD-10 G35) from a neurologist from 01/01/2016-31/12/2018, while people from the general population could not have any inpatient/outpatient codes for MS during the entire study period. The index date was defined as the first observed MS diagnosis or, in the case of the non-MS cohort, a randomly assigned date within the inclusion period. For both cohorts a PS was assigned, corresponding with their probabilistic likelihood of having MS based on observable factors including patient characteristics, comorbidities, medication use and other variables. People with and without MS were matched using a 1:1 nearest neighbor strategy. An exhaustive list of ICD-10 codes was created in association with 11 main SI categories. SIs were those recorded as the main diagnosis during an inpatient stay. ICD-10 codes from the 11 main categories were sorted into smaller classification units, used to distinguish between infections. A 60-day threshold for measuring new cases was defined to account for the potential risk of re-infection. Patients were observed until the end of the study period (31/12/2019) or death. Cumulative incidence, incidence rates (IRs) and IR ratios (IRRs) were reported during follow-up and at 1-, 2- and 3-years post-index. RESULTS: A total of 4250 and 2,098,626 patients were included in the unmatched cohorts of people with and without MS. Ultimately, one match was identified for all 4,250 pwMS, corresponding with a final population of 8,500 patients. On average, patients were 52.0/52.2 years in the matched MS/non-MS cohorts; the gender breakdown was 72% female. Overall, IRs of SIs per 100 patient years (PY) were higher in pwMS than in those without MS (1 year: 7.6 vs. 4.3; 2 years: 7.1 vs. 3.8; 3 years: 6.9 vs. 3.9). During follow-up, the most common infection types in pwMS were of a bacterial/parasitic origin (2.3 per 100 PY), followed by respiratory (2.0) and genitourinary (1.9) infections. Respiratory infections were most common in patients without MS (1.5 per 100 PY). Differences in the IRs of SIs were statistically significant (p<0.01) at each measurement window, with IRRs ranging from 1.7-1.9. PwMS had a higher risk of hospitalized genitourinary infections (IRR: 3.3-3.8) and bacterial/parasitic infections (2.0-2.3). CONCLUSIONS: The incidence of SIs is much higher in pwMS, than comparators from the general population in Germany. Differences in hospitalized infection rates were largely driven by higher levels of bacterial/parasitic and genitourinary infections in the MS population.
 PURPOSE: Dalfampridine (DFP) is used to improve motor functions in patients with multiple sclerosis (MS). Overdose of DFP can occur for a variety of reasons and can lead to a state of epilepsy. CASE REPORT: A 24-year-old woman with MS was admitted to hospital with severe sweating and delirium after attempting suicide by overdosing on DFP. At the time of hospitalization, she developed a tonic-clonic seizure that did not respond to immediate intravenous (IV) diazepam injection, followed by intravenous sodium valproate. Therefore, according to the hospital protocol of the neurology department, the patient was intubated and IV infusion of midazolam was started, Due to the persistence of seizures, sodium thiopental began and the patient was admitted to the intensive care unit (ICU). In the ICU, she received an infusion of sodium thiopental and intravenous sodium valproate, monitored by a daily electroencephalogram (EEG). The patient was discharged after four days due to her stable medical condition. CONCLUSION: Epilepsy in case of overuse of DFP should be considered as a life-threatening side effect and timely treatment should be done to prevent damage to the nervous system.
 WHAT IS THIS SUMMARY ABOUT? Patient registries contain anonymous data from people who share the same medical condition. The MSBase registry contains information from over 80,000 people living with multiple sclerosis (MS) across 41 countries. Using information from the MSBase registry, the GLIMPSE (Generating Learnings In MultiPle SclErosis) study looked at real-life outcomes in 3475 people living with MS who were treated with cladribine tablets (Mavenclad(®)) compared with other oral treatments. WHAT WERE THE RESULTS? Results showed that people treated with cladribine tablets stayed on treatment for longer than other treatments given by mouth. They also had fewer relapses (also called flare ups of symptoms) than people who received a different oral treatment for their MS. WHAT DO THE RESULTS MEAN? The results provide evidence that, compared with other oral treatments for MS, cladribine tablets are an effective medicine for people living with MS.

 INTRODUCTION: Wells syndrome, also known as eosinophilic cellulitis, is a rare dermatosis with approximately 200 cases previously described in the literature. Here, we present a case of a patient with multiple sclerosis with Wells syndrome induced by dimethyl fumarate (DMF). CASE REPORT: A 41-year-old Caucasian woman was treated with DMF in July 2021. One week later, she experienced itching on her upper and lower right arm, followed by the appearance of erythematous plaques covered with vesicles. The complete blood count showed an increased eosinophil count of up to 2,000 µL. The histological images demonstrated dermal eosinophil infiltration concordant with Wells syndrome. The clinical course was benign, with complete resolution of the lesions and normalization of the eosinophil count within four weeks. Administration of corticosteroids was not necessary. CONCLUSIONS: Eosinophilia is rare in patients with multiple sclerosis treated with DMF and usually does not require dosage adjustments. Although clinical manifestations of eosinophilia in these patients are very rare, it is important for practitioners to recognize the symptoms. Many neuroleptic drugs can induce eosinophilia and systemic symptoms; therefore, physicians must be aware of the risks associated with DMF and neuroleptic drugs, particularly for quetiapine, which contains fumarate.
 Multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) are autoimmune inflammatory disorders of the central nervous system (CNS) with similar characteristics. The differential diagnosis between MS and NMOSD is critical for initiating early effective therapy. In this study, we developed a deep learning model to differentiate between multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) using brain magnetic resonance imaging (MRI) data. The model was based on a modified ResNet18 convolution neural network trained with 5-channel images created by selecting five 2D slices of 3D FLAIR images. The accuracy of the model was 76.1%, with a sensitivity of 77.3% and a specificity of 74.8%. Positive and negative predictive values were 76.9% and 78.6%, respectively, with an area under the curve of 0.85. Application of Grad-CAM to the model revealed that white matter lesions were the major classifier. This compact model may aid in the differential diagnosis of MS and NMOSD in clinical practice.
 Multiple sclerosis is a recurrent and progressive inflammatory autoimmune disease causing demyelination in the central nervous system. Nowadays, the number of MS patients is increasing, but the diagnostic process and disease management are still quite difficult and costly and time consuming. The combination of methods used for clinical MS diagnosis mainly relies on MRI, that cannot be used as routine analysis. Classical methods of biological liquids analysis used for disease diagnosis and monitoring, include electrophoretic and labeled antibody-based techniques requiring professional personnel for analysis performing and results interpretation. In line with that, there is a need for reliable, sensitive and cost-effective methods that would be easier to take for both the staff and the patient. Biosensors application for MS biomarkers detection would provide such advantages. This review aimed to summarize studies carried out in this field available at the literature so far, evaluate current situation and emphasize possible perspectives for research and clinical application. Since this is multidisciplinary area of research, including development of biosensors, their use in clinical practice and making diagnostic clues, this review is expected to help different specialists, medical doctors, engineers, biochemists to use the results of each other's work for common good. Possible transition to the use biosensors in clinical practice may be associated with some difficulties that must be taken into account were either considered.
 In multiple sclerosis (MS), demyelination occurs in the cerebral cortex, and cerebral cortex atrophy correlates with clinical disabilities. Treatments are needed in MS to induce remyelination. Pregnancy is protective in MS. Estriol is made by the fetoplacental unit, and maternal serum estriol levels temporally align with fetal myelination. Here, we determined the effect of estriol treatment on the cerebral cortex in the preclinical model of MS, experimental autoimmune encephalomyelitis (EAE). Estriol treatment initiated after disease onset decreased cerebral cortex atrophy. Neuropathology of the cerebral cortex showed increased cholesterol synthesis proteins in oligodendrocytes, more newly formed remyelinating oligodendrocytes, and increased myelin in estriol-treated EAE mice. Estriol treatment also decreased the loss of cortical layer V pyramidal neurons and their apical dendrites and preserved synapses. Together, estriol treatment after EAE onset reduced atrophy and was neuroprotective in the cerebral cortex.
 OBJECTIVE: Clarification of the characteristics and dynamics of changes in the main indicators of visual evoked potentials (VEP) for a reverse chess pattern in patients with multiple sclerosis (MS) at various stages of the disease and severity of disability. MATERIAL AND METHODS: The study of VEP was carried out on 477 subjects, 120 of which were healthy volunteers and 357 patients with MS, including those with clinically isolated syndrome (CIS; 22.7%), remitting course (RT; 55.7%), primary progressive course (PPT; 8.4%), secondary progressive course (VPT; 13.2%). Disability was assessed using the Expanded Disability Status Scale (EDSS). RESULTS: A high sensitivity of VEP in the detection of demyelinating damage to the visual pathways, including subclinical, was noted already at the initial stages of MS, which increases with the progression of the disease from 77.8 to 97.8%. There was a significant increase in latency (r=0.42, p<0.05) and a decrease in amplitude (r= -0.26, p<0.05) of the P100 peak as the EDSS score increased. In patients with MS, 5 patterns of VEP were identified depending on the level and severity of damage to the visual pathways, where pattern 1 is normative VEP, pattern 5 is the absence of VEP recording in case of a pronounced axonal-demyelinating lesion of the visual pathways (prechiasmal/postchiasmal levels). Patterns 1 and 2 are most typical for CIS (22.2 and 53.1%) or RT (20.1 and 26.6%). Patterns 3 and 4 are typical for APT (70 and 20%) and VPT (48.9 and 21.3%), pattern 5 - for VPT (19.1%). Patterns 3-5 predominated in patients with higher EDSS (r=0.54, p<0.05). CONCLUSION: The classification of VEP changes into patterns makes it possible to identify the dissemination of a focal lesion in the projections of the visual pathways, which increases the diagnostic efficiency of the study and makes it possible to assess the severity of MS.
 INTRODUCTION: Stress and adversity during childhood, adolescence, and adulthood could impact the present and future health and well-being of people with multiple sclerosis (PwMS); however, a lifespan approach and nuanced stressor data are scarce in this nascent area of research. Our aim was to examine relationships among comprehensively measured lifetime stressors and two self-reported MS outcomes: (1) disability and (2) relapse burden changes since COVID-19 onset. METHODS: Cross-sectional data were collected from a nationally distributed survey of U.S.-based adults with MS. Hierarchical block regressions were used to sequentially evaluate contributions to both outcomes independently. Likelihood ratio (LR) tests and Akaike information criterion (AIC) were used to evaluate additional predictive variance and model fit. RESULTS: A total of 713 participants informed either outcome. Most respondents (84%) were female, 79% had relapsing remitting multiple sclerosis (MS), and mean (SD) age was 49 (12.7) years. Childhood (R(2)  = .261, p < .001; AIC = 1063, LR p < .05) and adulthood stressors (R(2)  = .2725, p < .001, AIC = 1051, LR p < .001) contributed significantly to disability, above and beyond prior nested models. Only adulthood stressors (R(2)  = .0534, p < .001; AIC = 1572, LR p < .01) significantly contributed above the nested model for relapse burden changes since COVID-19. CONCLUSIONS: Stressors across the lifespan are commonly reported in PwMS and could contribute to disease burden. Incorporating this perspective into the "lived experience with MS" could facilitate personalized health care by addressing key stress-related exposures and inform intervention research to improve well-being.
 BACKGROUND: Granulocyte invasion into the brain is a pathoanatomical feature differentiating neuromyelitis optica spectrum disorder (NMOSD) from multiple sclerosis (MS). We aimed to determine whether granulocyte activation markers (GAM) in cerebrospinal fluid (CSF) can be used as a biomarker to distinguish NMOSD from MS, and whether levels associate with neurological impairment. METHODS: We quantified CSF levels of five GAM (neutrophil elastase, myeloperoxidase, neutrophil gelatinase-associated lipocalin, matrixmetalloproteinase-8, tissue inhibitor of metalloproteinase-1), as well as a set of inflammatory and tissue-destruction markers, known to be upregulated in NMOSD and MS (neurofilament light chain, glial fibrillary acidic protein, S100B, matrix metalloproteinase-9, intercellular adhesion molecule-1, vascular cellular adhesion molecule-1), in two cohorts of patients with mixed NMOSD and relapsing-remitting multiple sclerosis (RRMS). RESULTS: In acute NMOSD, GAM and adhesion molecules, but not the other markers, were higher than in RRMS and correlated with actual clinical disability scores. Peak GAM levels occurred at the onset of NMOSD attacks, while they were stably low in MS, allowing to differentiate the two diseases for ≤21 days from onset of clinical exacerbation. Composites of GAM provided area under the curve values of 0.90-0.98 (specificity of 0.76-1.0, sensitivity of 0.87-1.0) to differentiate NMOSD from MS, including all anti-aquaporin-4 protein (aAQP4)-antibody-negative patients who were untreated. CONCLUSIONS: GAM composites represent a novel biomarker to reliably differentiate NMOSD from MS, including in aAQP4(-) NMOSD. The association of GAM with the degree of concurrent neurological impairment provides evidence for their pathogenic role, in turn suggesting them as potential drug targets in acute NMOSD.
 Despite the high incidence of optic neuritis (ON), and the growing number of therapeutic options for the long-term treatment of diseases associated with ON including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD) and MOG antibody associated disease (MOGAD), there are still only limited therapeutic options for treating an acute event of optic neuritis. These include steroids, plasma exchange (PLEX) and intravenous immunoglobulin (IVIG). High-dose steroids remain the mainstay of acute treatment. However, evidence is emerging that when optic neuritis is accompanied with certain atypical features that suggest a more unfavorable outcome this mandates special consideration such as early addition of other therapeutic agents or tapering the steroid very slowly. This review will distinguish between typical and atypical neuritis and discuss acute treatment options.
 INTRODUCTION: The number of elderly people with multiple sclerosis (MS) has increased in line with population ageing. As the immune system presents profound changes over an individual's lifetime, it is important to understand the differences between these patients and younger patients. DEVELOPMENT: Immunosenescence, defined as age-related alterations naturally occurring in the immune system, particularly influences tolerance, response, and adverse effects of disease-modifying treatments for MS. Thymic involution is the most noteworthy characteristic of this phenomenon. This process leads to a reduction in the number of virgin T cells. Other effects include an inverted CD4+/CD8+ cell ratio, severe alterations in NK cell functioning, and reduced tissue repair capacity in the brain. CONCLUSIONS: The number of older people with MS is increasing due to population ageing, advances in disease-modifying treatments, and improved health and social care of these patients. Ageing of the immune system increases the risk of infections, tumours, and autoimmune diseases in elderly individuals. Furthermore, neurodegeneration is accelerated in patients with MS due to the nervous system's loss of remyelination capacity. Understanding of the changes affecting the immune system in the elderly population is essential to improving the care provided to this ever-growing patient group.
 BACKGROUND: Although the relapse risk is increased after birth in women with relapsing multiple sclerosis (RMS), only a very few disease-modifying therapies (DMTs) are approved during breastfeeding. Glatiramer acetate (GA, Copaxone®) is one of three DMTs that can be used in breastfeeding. The real-world safety of Copaxone® in Offsprings of Breastfeeding and treated RMS pAtients (COBRA) study demonstrated that offspring parameters (hospitalisations, antibiotic use, developmental delays, growth parameters) were similar between offspring breastfed by mothers taking GA or no DMT (control) during breastfeeding. COBRA data analyses were extended to provide further safety data on the impact of maternal GA treatment during breastfeeding on offspring. METHODS: COBRA was a non-interventional, retrospective study using German Multiple Sclerosis and Pregnancy Registry data. Participants had RMS, gave birth and had GA or no DMT during breastfeeding. Offspring total adverse events (AEs), non-serious AEs (NAEs) and serious AEs (SAEs) up to 18 months postpartum were assessed. Reasons for offspring hospitalisations and antibiotic treatments were explored. RESULTS: Baseline maternal demographics and disease characteristics were similar between cohorts. Each cohort had 60 offspring. Numbers of offspring AEs were comparable between cohorts; total AEs: 82 (GA) vs 83 (control); NAEs: 59 vs 61; SAEs: 23 vs 22. AEs in both cohorts were diverse with no specific patterns. Duration of GA-exposed breastfeeding was 6 to >574 days for offspring with any AE. For all-cause hospitalisations, 11 offspring had 12 hospitalisations (GA cohort) and 12 control offspring had 16 hospitalisations. Most common reason for hospitalisation was infection: 5/12 (41.7%; GA) vs 4/16 (25.0%, control). Two out of 12 (16.7%) hospitalisations due to infection occurred during GA-exposed breastfeeding; the others occurred 70, 192 and 257 days after discontinuation of GA-exposed breastfeeding. Median (range) duration of GA-exposed breastfeeding was 110 (56 to ≥285) days for offspring hospitalised for infections and 137 (88-396) days for those hospitalised for other reasons. Nine offspring had 13 antibiotic treatments (GA cohort) and nine control offspring had 10 treatments. Ten out of 13 (76.9%) antibiotic treatments occurred during GA-exposed breastfeeding, of which four were primarily due to double kidney with reflux. Other antibiotic treatments occurred 193, 229 and 257 days after discontinuation of GA-exposed breastfeeding. CONCLUSIONS: GA treatment of mothers with RMS during breastfeeding did not increase AEs, hospitalisations or antibiotic use in their offspring versus control offspring. These data support previous COBRA data that the benefit of maternal RMS treatment with GA during breastfeeding outweighs the potential, apparently low risk of untoward events, in their breastfed offspring.
 OBJECTIVE: To explore and describe the basis and implications of genetic and environmental susceptibility to multiple sclerosis (MS) using the Canadian population-based data. BACKGROUND: Certain parameters of MS-epidemiology are directly observable (e.g., the recurrence-risk of MS in siblings and twins, the proportion of women among MS patients, the population-prevalence of MS, and the time-dependent changes in the sex-ratio). By contrast, other parameters can only be inferred from the observed parameters (e.g., the proportion of the population that is "genetically susceptible", the proportion of women among susceptible individuals, the probability that a susceptible individual will experience an environment "sufficient" to cause MS, and if they do, the probability that they will develop the disease). DESIGN/METHODS: The "genetically susceptible" subset (G) of the population (Z) is defined to include everyone with any non-zero life-time chance of developing MS under some environmental conditions. The value for each observed and non-observed epidemiological parameter is assigned a "plausible" range. Using both a Cross-sectional Model and a Longitudinal Model, together with established parameter relationships, we explore, iteratively, trillions of potential parameter combinations and determine those combinations (i.e., solutions) that fall within the acceptable range for both the observed and non-observed parameters. RESULTS: Both Models and all analyses intersect and converge to demonstrate that probability of genetic-susceptibitly, P(G), is limited to only a fraction of the population {i.e., P(G) ≤ 0.52)} and an even smaller fraction of women {i.e., P(G│F) < 0.32)}. Consequently, most individuals (particularly women) have no chance whatsoever of developing MS, regardless of their environmental exposure. However, for any susceptible individual to develop MS, requires that they also experience a "sufficient" environment. We use the Canadian data to derive, separately, the exponential response-curves for men and women that relate the increasing likelihood of developing MS to an increasing probability that a susceptible individual experiences an environment "sufficient" to cause MS. As the probability of a "sufficient" exposure increases, we define, separately, the limiting probability of developing MS in men (c) and women (d). These Canadian data strongly suggest that: (c < d ≤ 1). If so, this observation establishes both that there must be a "truly" random factor involved in MS pathogenesis and that it is this difference, rather than any difference in genetic or environmental factors, which primarily accounts for the penetrance difference between women and men. CONCLUSIONS: The development of MS (in an individual) requires both that they have an appropriate genotype (which is uncommon in the population) and that they have an environmental exposure "sufficient" to cause MS given their genotype. Nevertheless, the two principal findings of this study are that: P(G) ≤ 0.52)} and: (c < d ≤ 1). Threfore, even when the necessary genetic and environmental factors, "sufficient" for MS pathogenesis, co-occur for an individual, they still may or may not develop MS. Consequently, disease pathogenesis, even in this circumstance, seems to involve an important element of chance. Moreover, the conclusion that the macroscopic process of disease development for MS includes a "truly" random element, if replicated (either for MS or for other complex diseases), provides empiric evidence that our universe is non-deterministic.
 PURPOSE: To evaluate amide proton transfer weighted (APTw) signal differences between multiple sclerosis (MS) lesions and contralateral normal-appearing white matter (cNAWM). Cellular changes during the demyelination process were also assessed by comparing APTw signal intensity in T1weighted isointense (ISO) and hypointense (black hole -BH) MS lesions in relation to cNAWM. METHODS: Twenty-four people with relapsing-remitting MS (pw-RRMS) on stable therapy were recruited. MRI/APTw acquisitions were undertaken on a 3 T MRI scanner. The pre and post-processing, analysis, co-registration with structural MRI maps, and identification of regions of interest (ROIs) were all performed with Olea Sphere 3.0 software. Generalized linear model (GLM) univariate ANOVA was undertaken to test the hypotheses that differences in mean APTw were entered as dependent variables. ROIs were entered as random effect variables, which allowed all data to be included. Regions (lesions and cNAWM) and/or structure (ISO and BH) were the main factor variables. The models also included age, sex, disease duration, EDSS, and ROI volumes as covariates. Receiver operating characteristic (ROC) curve analyses were performed to evaluate the diagnostic performance of these comparisons. RESULTS: A total of 502 MS lesions manually identified on T2-FLAIR from twenty-four pw-RRMS were subcategorized as 359 ISO and 143 BH with reference to the T1-MPRAGE cerebral cortex signal. Also, 490 ROIs of cNAWM were manually delineated to match the MS lesion positions. A two-tailed t-test showed that mean APTw values were higher in females than in males (t = 3.52, p < 0.001). Additionally, the mean APTw values of MS lesions were higher than those of cNAWM after accounting for covariates (mean lesion = 0.44, mean cNAWM = 0.13, F = 44.12, p < 0.001).The mean APTw values of ISO lesions were higher than those of cNAWM after accounting for covariates (mean ISO lesions = 0.42, mean cNAWM = 0.21, F = 12.12, p < 0.001). The mean APTw values of BH were also higher than those of cNAWM (mean BH lesions = 0.47, mean cNAWM = 0.033, F = 40.3, p < 0.001). The effect size (i.e., difference between lesion and cNAWM) for BH was found to be higher than for ISO (14 vs. 2). Diagnostic performance showed that APT was able to discriminate between all lesions and cNAWM with an accuracy of >75% (AUC = 0.79, SE = 0.014). Discrimination between ISO lesions and cNAWM was accomplished with an accuracy of >69% (AUC = 0.74, SE = 0.018), while discrimination between BH lesions and cNAWM was achieved at an accuracy of >80% (AUC = 0.87, SE = 0.021). CONCLUSIONS: Our results highlight the potential of APTw imaging for use as a non-invasive technique that is able to provide essential molecular information to clinicians and researchers so that the stages of inflammation and degeneration in MS lesions can be better characterized.
 BACKGROUND: Multiple sclerosis (MS) is a chronic disease affecting multiple functional aspects of patients' lives. Depression and anxiety are common amongst persons with MS (PwMS). There has been an interest in utilizing patient-reported outcome measures (PROMs) to capture and systematically assess patient's perceptions of their MS experience in addition to other clinical measures, but PROMs are not usually collected in routine clinical practice. Therefore, this study aims to systematically incorporate periodic electronically administered PROMs into the care of PwMS to evaluate its effects on depression and anxiety. METHODS: A randomized controlled trial will be conducted with patients allocated 1:1 to either intervention or conservative treatment groups. Patients in the intervention group will complete PROMs at the start of the study and then every 6 months for 1 year, in addition to having their MS healthcare provider prompted to view their scores. The conservative treatment group will complete PROMs at the start of the study and again after 12 months, and their neurologist will not be able to view their scores. For both groups, pre-determined critical PROM scores will trigger an alert to the patient's MS provider. The difference in change in Hospital Anxiety and Depression Scale score between the intervention and conservative treatment groups at 12 months will be the primary outcome, along with difference in Consultation Satisfaction Questionnaire and CollaboRATE scores at 12 months, and proportion and type of healthcare provider intervention/alerts initiated by different PROMs as secondary outcomes. DISCUSSION: This study will determine the feasibility of utilizing PROMs on an interval basis and its effects on the psychological well-being of PwMS. Findings of this study will provide evidence on use of PROMs in future MS clinical practice. TRIAL REGISTRATION: This trial is registered at the National Institutes of Health United States National Library of Medicine, ClinicalTrials.gov NCT04979546 . Registered on July 28, 2021.
 The relationship between structural connectivity (SC) and functional connectivity (FC) captured from magnetic resonance imaging, as well as its interaction with disability and cognitive impairment, is not well understood in people with multiple sclerosis (pwMS). The Virtual Brain (TVB) is an open-source brain simulator for creating personalized brain models using SC and FC. The aim of this study was to explore SC-FC relationship in MS using TVB. Two different model regimes have been studied: stable and oscillatory, with the latter including conduction delays in the brain. The models were applied to 513 pwMS and 208 healthy controls (HC) from 7 different centers. Models were analyzed using structural damage, global diffusion properties, clinical disability, cognitive scores, and graph-derived metrics from both simulated and empirical FC. For the stable model, higher SC-FC coupling was associated with pwMS with low Single Digit Modalities Test (SDMT) score (F=3.48, P$\lt$0.05), suggesting that cognitive impairment in pwMS is associated with a higher SC-FC coupling. Differences in entropy of the simulated FC between HC, high and low SDMT groups (F=31.57, P$\lt$1e-5), show that the model captures subtle differences not detected in the empirical FC, suggesting the existence of compensatory and maladaptive mechanisms between SC and FC in MS.
 BACKGROUND: Little is known about polypharmacy and multiple sclerosis (MS). OBJECTIVES: To estimate polypharmacy prevalence in a population-based MS cohort and compare persons with/without polypharmacy. METHODS: Using administrative and pharmacy data from Canada, we estimated polypharmacy prevalence (⩾5 concurrent medications for >30 consecutive days) in MS individuals in 2017. We compared the characteristics of persons with/without polypharmacy and described the number of polypharmacy days, the most common medication classes contributing to polypharmacy and hyper-polypharmacy prevalence (⩾10 medications). RESULTS: Of 14,227 included individuals (75% women), mean age = 55.4 (standard deviation (SD): 13.2) years; 28% (n = 3995) met criteria for polypharmacy (median polypharmacy days = 273 (interquartile range (IQR): 120-345)). Odds of polypharmacy were higher for women (adjusted odds ratio (aOR) = 1.14; 95% confidence intervals (CI):1.04-1.25), older individuals (aORs 50-64 years = 2.04; 95% CI:1.84-2.26; ⩾65 years = 3.26; 95% CI: 2.92-3.63 vs. <50 years), those with more comorbidities (e.g. ⩾3 vs. none, aOR = 6.03; 95% CI: 5.05-7.22) and lower socioeconomic status (SES) (e.g. most (SES-Q1) vs. least deprived (SES-Q5) aOR = 1.64; 95% CI: 1.44-1.86). Medication classes most commonly contributing to polypharmacy were as follows: antidepressants (66% of polypharmacy days), antiepileptics (47%), and peptic ulcer drugs (41%). Antidepressants were most frequently co-prescribed with antiepileptics (34% of polypharmacy days) and peptic ulcer drugs (27%). Five percent of persons (716/14,227) experienced hyper-polypharmacy. CONCLUSION: More than one in four MS persons met criteria for polypharmacy. The odds of polypharmacy were higher for women, older persons, and those with more comorbidities, but lower SES.
 BACKGROUND AND PURPOSE: Fully automatic quantification methods of spinal cord compartments are needed to study pathologic changes of the spinal cord GM and WM in MS in vivo. We propose a novel method for automatic spinal cord compartment segmentation (SCORE) in patients with MS. MATERIALS AND METHODS: The cervical spinal cords of 24 patients with MS and 24 sex- and age-matched healthy controls were scanned on a 3T MR imaging system, including an averaged magnetization inversion recovery acquisition sequence. Three experienced raters manually segmented the spinal cord GM and WM, anterior and posterior horns, gray commissure, and MS lesions. Subsequently, manual segmentations were used to train neural segmentation networks of spinal cord compartments with multidimensional gated recurrent units in a 3-fold cross-validation fashion. Total intracranial volumes were quantified using FreeSurfer. RESULTS: The intra- and intersession reproducibility of SCORE was high in all spinal cord compartments (eg, mean relative SD of GM and WM: ≤ 3.50% and ≤1.47%, respectively) and was better than manual segmentations (all P < .001). The accuracy of SCORE compared with manual segmentations was excellent, both in healthy controls and in patients with MS (Dice similarity coefficients of GM and WM: ≥ 0.84 and ≥0.92, respectively). Patients with MS had lower total WM areas (P < .05), and total anterior horn areas (P < .01 respectively), as measured with SCORE. CONCLUSIONS: We demonstrate a novel, reliable quantification method for spinal cord tissue segmentation in healthy controls and patients with MS and other neurologic disorders affecting the spinal cord. Patients with MS have reduced areas in specific spinal cord tissue compartments, which may be used as MS biomarkers.
 OBJECTIVES: To evaluate the effects of rituximab treatment on innate immune cell activation in primary progressive multiple sclerosis (PPMS). METHODS: A 48-year-old woman with PPMS was started on rituximab shortly after diagnosis. [(11)C]PK11195 PET imaging was employed to assess innate immune cell activation with special interest in the white matter around chronic lesions. PET, MRI, and disability measurements were performed at baseline and after 18 months of rituximab treatment. Specific binding of [(11)C]PK11195 was quantified using mean distribution volume ratios (DVRs), and at voxel-level based on proportions of active voxels. RESULTS: The PPMS patient had higher PK11195 DVRs and higher proportions of active voxels in the thalamus and the normal appearing white matter compared to the healthy control group. The thalamic and perilesional white matter DVRs and the proportions of active voxels decreased after rituximab treatment. The patient remained clinically stable during the 5-years follow-up. CONCLUSIONS: This case suggests that while a degree of smoldering activity persists, high efficacy B-cell-targeting therapy may contribute to reduced innate immune cell activation in PPMS brain areas relevant for disease progression. This case supports the therapeutic concept that controlling smoldering brain inflammation is beneficial for slowing down progression independent of relapses.
 Cognitive impairment is a common and debilitating feature of multiple sclerosis (MS), and the dysregulation of synaptic plasticity is one of its direct causes. Long non-coding RNAs (lncRNAs) have been shown to play a role in synaptic plasticity, but their role in cognitive impairment in MS has not been fully explored. In this study, using quantitative real-time PCR, we examined the relative expression of two specific lncRNAs, BACE1-AS and BC200, in the serum of two cohorts of MS patients with and without cognitive impairment. Both lncRNAs were overexpressed in both cognitively impaired and non-cognitively impaired MS patients, with consistently higher levels in the cohort with cognitive impairment. We also found a strong positive correlation between the expression levels of these two lncRNAs. Notably, BACE1-AS was consistently higher in the remitting cases of both relapsing-remitting MS (RRMS) and secondary progressive MS (SPMS) groups than in the respective relapse cases of the same subtype, with the SPMS-Remitting group of cognitively impaired MS patients showing the highest expression of BACE1-AS among all MS groups. Additionally, we observed that the primary progressive MS (PPMS) group had the highest expression of BC200 in both cohorts of MS. Furthermore, we developed a model called Neuro_Lnc-2, which showed better diagnostic performance than either BACE1-AS or BC200 alone in predicting MS. Our findings suggest that these two lncRNAs may have a significant impact on the pathogenesis of the progressive types of MS and on the cognitive function of the patients. Future research is required to confirm these findings.
 OBJECTIVE: To find the optimal therapeutic dose of the anti-B cell mAb divozilimab (DIV) based on the efficacy and safety data of intravenous administration at a dose of 125 mg or 500 mg in patients with relapsing remitting multiple sclerosis (RRMS) compared to placebo (PBO) and teriflunomide (TRF). To study the efficacy and safety of DIV within 24 weeks of treatment. MATERIAL AND METHODS: A multicenter, randomized, double-blind and double-masked, placebo-controlled phase 2 clinical trial (CT) BCD-132-2 involved 271 adult patients with RRMS from 25 centres In Russia. Patients were randomly assigned (2:2:2:1) into 4 groups: TRF, DIV 125 mg, DIV 500 mg and PBO. After screening patients entered to the main period, which consisted of one cycle of therapy for 24 weeks. The primary endpoint was the total number of gadolinium-enhancing T1 lesions (Gd+) observed on brain MRI scans after 24 weeks (per scan - involves estimating the mean value of the score from all the MRI assessments performed for each participant in the study). RESULTS: 263 patients completed 24 weeks of treatment. Most of the patients in the DIV groups had no lesions on T1-weighted MRI after 24 weeks of treatment (94.44% on 125 mg and 93.06% on 500 mg). In the TRF and PBO groups the values were significantly lower: 68.06% and 56.36% respectively (both p<0.05). The proportions of relapse-free patients in the DIV groups were 93.06% and 97.22% (125 mg and 500 mg, respectively). As expected, DIV reduced the CD19+ B-cells. However, the repopulation rate of CD19+ B-cells in the 125 mg group was more pronounced (mainly due to the recovering pool of CD27-naive B-cells) compared to the 500 mg group. DIV showed a favorable safety profile at both doses. CONCLUSION: Thus, the assessment of 24 weeks treatment demonstrated that DIV is a highly effective, safe and convenient option for the treatment of RRMS patients, both naive and previously treated with disease modifying therapy. A dose of 500 mg is recommended for further efficacy and safety evaluation during phase 3 CT.
 OBJECTIVES: The aim of this study was to assess peripheral nerve involvement in patients with multiple sclerosis (MS) at first clinical presentation using quantitative magnetic resonance (MR) neurography in correlation with clinical, laboratory, electrophysiological, and central nervous MR imaging data. MATERIALS AND METHODS: In this prospective monocentric study, 30 patients first diagnosed with MS according to the McDonald criteria (19 women; mean age, 32.4 ± 8.8 years) and 30 age- and sex-matched healthy volunteers were examined with high-resolution 3 T MR neurography using a dual-echo T2-relaxometry sequence covering the tibial and peroneal nerves from proximal thigh to distal calf. Magnetic resonance biomarkers of T2 relaxation time (T2 app ), proton spin density (PSD), and nerve cross-sectional area (CSA) were correlated with clinical symptoms, intrathecal immunoglobulin (Ig) synthesis, nerve conduction study, and lesion load on brain and spine MR imaging. The diagnostic accuracy of MR biomarkers was assessed using receiver-operating characteristic curves. RESULTS: Diffuse nerve changes were detected along the tibial and peroneal nerves in MS patients, who showed decreased PSD ( P < 0.001), increased T2 app ( P < 0.001), and smaller tibial nerve CSA ( P < 0.001) compared with healthy subjects. Tibial PSD was identified as best parameter separating patients from controls (area under the curve = 0.876). Intrathecal IgG and IgM synthesis correlated with PSD values ( r = -0.44, P = 0.016, and r = -0.42, P = 0.022). Contrast-enhancement of brain or spine lesions was related to larger tibial and peroneal CSA ( P < 0.001, P = 0.033). Abnormal electrophysiology correlated with higher tibial and peroneal T2 app ( P < 0.001 and P = 0.033), lower tibial and peroneal PSD ( P = 0.018 and P = 0.002), and smaller peroneal CSA ( P < 0.001). CONCLUSIONS: Quantitative MR neurography reveals peripheral nerve changes in patients with initial diagnosis of MS. Correlation of imaging findings with intrathecal immunoglobulin synthesis may indicate a primary coaffection of the peripheral nervous system in MS.
 Despite the wide range of clinical, instrumental and laboratory methods used in modern ophthalmology, the problem of diagnosing optic neuropathy and identifying its etiology remains relevant. A complex multidisciplinary approach involving various specialists is required in the differential diagnosis of immune-mediated optic neuritis, for example in multiple sclerosis, neuromyelitis optica spectrum disorder, and MOG-associated diseases. Of special interest is differential diagnosis of optic neuropathy in demyelinating diseases of the central nervous system, hereditary optic neuropathies and ischemic optic neuropathy. The article presents a summary of scientific and practical results of differential diagnosis of optic neuropathies with various etiologies. Timely diagnosis and early therapy start reduces the degree of disability in patients with optic neuropathies of different etiologies.

 OBJECTIVES: Numerous studies have indicated that chronic cerebrospinal venous insufficiency is a potential factor in causing multiple sclerosis in recent years, but this conclusion remains unconfirmed. This meta-analysis examined the correlation between multiple sclerosis and chronic cerebrospinal venous insufficiency. METHODS: We searched Embase and Medline (Ovid) for publications published from 1 January 2006 to 1 May 2022. The meta-analysis was performed following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. RESULTS: Eligible studies (n=20) included 3069 participants from seven countries. Pooled analysis indicated that chronic cerebrospinal venous insufficiency was more frequent in patients with multiple sclerosis than in healthy controls (OR 3.36; 95% CI 1.92 to 5.85; p<0.001) with remarkable heterogeneity among studies (I(2)=79%). Results were more strongly correlated in subsequent sensitivity analyses, but heterogeneity was also more substantial. We removed studies that initially proposed a chronic cerebrospinal venous insufficiency team as well as studies by authors involved in or advocating endovascular therapies. CONCLUSIONS: Chronic cerebrospinal venous insufficiency is significantly associated with multiple sclerosis and it is more prevalent in patients with multiple sclerosis than in healthy individuals, but considerable heterogeneity of results is still observed.
 BACKGROUND: Fatigue is one of the most common symptoms of people with Multiple Sclerosis (MS). However, currently-used medications for the treatment of fatigue probably do not work better than a placebo. In a pilot trial, we showed that one infusion of low-dose ketamine significantly improved fatigue severity measured four weeks after the infusion. METHODS: The proposed study is a single-center, phase II, randomized, double-blind, parallel-group, active-placebo-controlled trial of intravenous low-dose ketamine in patients with MS fatigue. Participants will be randomized 1:1:1 into three groups: receiving either one or two infusions of ketamine (0.5 mg/kg over 40 min) or zero to one infusion of the active placebo (midazolam, 0.05 mg/kg over 40 min). Eligibility criteria include adult patients diagnosed with MS based on the latest criteria, complaining of fatigue as one of the main symptoms, and having a screening MFIS score higher than a pre-specified threshold. RESULTS: One hundred and ten participants will be randomized over 30 months at Johns Hopkins MS Center. Complete enrollment is expected by mid-2025. The study's primary outcome will be the MFIS score at the end of week 4, comparing two-thirds of the participants who received ketamine with one-third who received midazolam. The secondary and exploratory outcomes (measured four weeks after the second infusion) will show how long the effects of a single infusion last and if two infusions of ketamine are better than one in improving MS fatigue. CONCLUSION: This study can show whether intervening in the glutamatergic pathways would improves MS fatigue.
 BACKGROUND: Vascular disease risk factors (VDRF) such as hypertension, hyperlipidemia, obesity, diabetes and heart disease likely play a role in disease progression in people with multiple sclerosis (PwMS) (Marrie, Rudick et al. 2010). Studies exploring the mechanistic connection between vascular disease and MS disease progression are scant. We hypothesized that phosphate energy metabolism impairment in PwMS with VDRFs (VDRF+) will be greater compared to PwMS without VDRFs (VDRF-) and is related to increased brain atrophy in VDRF+. To test this hypothesis, we planned to study the differences in the high energy phosphate (HEP) metabolites in cerebral gray matter as assessed by (31)P magnetic resonance spectroscopic imaging (MRSI) and MRI brain volumetric in the VDRF+ and VDRF- PwMS at four different timepoints over a 3 yearlong period using a 7T MR system. We present here the results from the cross-sectional evaluation of HEP metabolites and brain volumes. We also evaluated the differences in clinical impairment, blood metabolic biomarkers and quality of life in VDRF+ and VDRF- PwMS in this cohort. METHODS: Group differences in high energy phosphate metabolites were assessed from a volume of interest in the occipital region using linear mixed models. Brain parenchymal and white matter lesion volumes were determined from MR anatomic images. We present here the cross-sectional analysis of the baseline data collected as part of a longitudinal 3 yearlong study where we obtained baseline and subsequent 6-monthly clinical and laboratory data and annual 7T MRI volumetric and (31)P MR spectroscopic imaging (MRSI) data on 52 PwMS with and without VDRF. Key clinical and laboratory outcomes included: body mass index (BMI), waist and thigh circumferences and disability [Expanded Disability Status Scale (EDSS)], safety (complete blood count with differential, complete metabolic), lipid panel including total cholesterol and HbA1C. We analyzed clinical and laboratory data for the group differences using student's t or χ2 test. We investigated relationship between phosphate metabolites and VDRF using mixed effect linear regression. RESULTS: Complete MRI data were available for 29 VDRF+, age 56.3 (6.8) years [mean (SD)] (83% female), and 23 VDRF-, age 52.5 (7.5) years (57% female) individuals with MS. The mean value of normalized adenosine triphosphate (ATP) (calculated as the ratio of ATP to total phosphate signal in a voxel) was decreased by 4.5% (p < .05) in VDRF+ compared to VDRF- MS group. White matter lesion (WML) volume fraction in VDRF+ individuals {0.007 (0.007)} was more than doubled compared to VDRF- participants {0.003 (0.006), p= .02}. CONCLUSIONS: We found significantly lower brain ATP and higher inorganic phosphate (Pi) in those PwMS with VDRFs compared to those without. ATP depletion may reflect mitochondrial dysfunction. Ongoing longitudinal data analysis from this study, not presented here, will evaluate the relationship of phosphate metabolites, brain atrophy and disease progression in PwMS with and without vascular disease.
 Multiple sclerosis (MS) is an autoimmune disorder that affects the central nervous system (CNS), including the brain, spinal cord, and optic nerves. The symptoms can vary from muscle weakness to vision loss. In the case of MS, the immune system attacks the myelin sheath, which protects the nerve fiber and causes inflammation resulting in demyelination. The myelin sheath has the composition of various proteins including membrane proteins and glycoproteins. The four main proteins namely Myelin Basic Protein (MBP), Myelin associated Oligodendrocyte Basic protein (MOBP), Myelin Proteolipid Protein (PLP) and Myelin Associated Glycoprotein (MAG) are known to be critical auto-antigens in causing demyelination in CNS leading to MS. Three out of these four proteins are intrinsically disordered proteins and in this review, we attempted to understand how these proteins play a crucial role in maintaining the integrity of myelin, by exploring its structural and functional aspects and also their auto-antigenicity leading to multiple sclerosis.
 OBJECTIVES: The prevalence of multiple sclerosis (MS) in East Asia is thought to be lower than in Western countries. Globally, there is a trend of increasing MS prevalence. We investigated the changes in the prevalence and clinical phenotype of MS in the Tokachi province of Hokkaido in northern Japan, from 2001 to 2021. METHODS: Data processing sheets were sent to all related institutions inside and outside the Tokachi area of Hokkaido island in Japan and were collected from April to May 2021. The prevalence according to the Poser's diagnostic criteria for MS was determined on March 31, 2021. RESULTS: In 2021, the crude MS prevalence in northern Japan was 22.4/100,000 (95% confidence interval, 17.6-28.0). The prevalences of MS standardized by the Japanese national population in 2001, 2006, 2011, 2016, and 2021 were 6.9, 11.5, 15.3, 18.5, and 23.3, respectively. The female/male ratio was 4.0 in 2021, increased from 2.6 in 2001. We checked the prevalence using the 2017 revised McDonald criteria, and found only additional male patient who had not fulfilled Poser's criteria. The age- and sex-adjusted incidence of MS per 100,000 individuals increased from 0.09 in 1980-1984 to 0.99 in 2005-2009; since then, it has remained stable. The proportions of primary-progressive, relapsing-remitting, and secondary-progressive MS types in 2021 were 3%, 82%, and 15%, respectively. CONCLUSION: Our results demonstrated a consistent increase in the prevalence of MS among the northern Japanese over 20 years, particularly in females, and consistently lower rates of progressive MS in northern Japan than elsewhere in the world.
 Vitamin D supplementation has been considered a possible treatment to reduce the risk of disease activity and progression in people with multiple sclerosis (MS). However, its effect on disease symptoms remains unclear. The aim of this meta-analysis was to conduct a systematic review to assess the effect of vitamin D on fatigue in this population. The systematic review was conducted using the MEDLINE, Cochrane Library, Embase and Web of Science databases from inception to May 2023. Randomized controlled trials (RCTs) reporting pre-post changes in fatigue after vitamin D supplementation were included. Pooled effect sizes and 95% confidence intervals (95% CIs) were calculated by applying a random effects model with Stata/SE (Version 16.0; StataCorp., College Station, TX, USA). The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed. A total of five studies with 345 individuals (271 females; age range: 25.4-41.1 years) were included. A significant reduction in fatigue was perceived when vitamin D supplementation was compared with a control group: -0.18 (95% CI: -0.36 to -0.01; I(2) = 0%). Thus, our findings show that the therapeutic use of vitamin D on fatigue in people with MS could be considered. Nevertheless, due to the lack of agreement on the dose to be applied, it is recommended to use it under medical prescription.

 OBJECTIVE: Gadolinium-enhanced T1-weighted lesions are a well-established marker of areas with acute inflammatory activity. A majority of these gadolinium-enhanced T1 lesions are isointense relative to the surrounding white matter, but 20-40% of such active lesions will evolve during one year into areas of low signal ("black hole"). This study sought to characterize evolution of "black hole" lesions in patients with relapsing-remitting multiple sclerosis (MS) using the magnetic resonance imaging (MRI), which measures active lesions via the count of new or enlarged T2 and gadolinium-enhanced T1-weighted lesions. MATERIALS AND METHODS: This was a prospective, observational case-series study which utilized pre- and post-gadolinium contrast T1-weighted and Proton density MRI scans. Twenty-nine patients (8 males and 21 females) with average age of 38.86 ± 6.58 years and disease duration of 5.75 ± 7.00 years were used to analyze 196 acute demyelinating plaques detected on MRI images during the 24-month follow-up of post-gadolinium signal intensity enhancement of MS plaques. RESULTS: Significant difference in black hole development was found between the shapes of acute and chronic "black holes". Ring-shaped and patchy plaques were 4.09 (1.87-8.91) times more likely and 1.49 (0.71-3.12) times less likely to develop an acute "black holes" than homogeneous plaques, respectively. Acute plaques with higher lesion-to-CSF SI ratio and larger surface area showed a greater tendency to develop into acute and chronic "black holes". CONCLUSIONS: The value of lesion-to-CSF SI ratio and surface area were found as the predictors of the "black hole" formation.
 BACKGROUND: Cladribine is a nucleoside analogue interfering with synthesis and repair of DNA. Treatment with cladribine leads to a preferential reduction in lymphocytes, resulting in profound depletion of B-cells with a rapid recovery of naïve B-cells, while T-cell show a lesser but long-lasting depletion It is approved for treatment of relapsing multiple sclerosis (MS). Cladribine tablets 3.5 mg/kg bodyweight are administered in two yearly treatment courses, each including two treatment series lasting 4 or 5 days, one at the start of the first month and the other at the start of the second month. OBJECTIVE: To describe treatment patterns of cladribine in a real-world setting. METHODS: Registry based observational cohort study with prospectively enrolled cases from December 2017 through June 2021. The data source is The Danish Multiple Sclerosis Registry, which is a near complete nationwide population-based registry. Outcomes were length of the treatment, preceding and following treatments, treatment response, and safety data. RESULTS: In total 268 patients had started therapy with cladribine tablets, 89 men and 179 women, with a median age of 40 years (interquartile range (IQR) 32-48. The disease course was relapsing-remitting MS in 97.8% of the patients, and at treatment start the median time from disease onset was 8.1 years (IQR 4.2-14.5) and EDSS 2.5 (IQR 1.5-3.5). Thirty-four patients (12.7%) were treatment naïve while 56 (20.9%) had received one previous disease-modifying therapy (DMT), 67 (25.0%) two, and 111 (41.4%) three or more previous DMTs. In total, 214 (80.0%) patients had completed the full treatment of two courses of cladribine, while 54 (20.0%) had received only one course of cladribine tablets. The median follow-up time after cladribine initiation was 34.7 months (IQR 23.3-43.7). Compared with an annualized relapse rate (ARR) of 0.67 (95% CI [0.56, 0.79]) in the year prior to start of cladribine, ARR was reduced to 0.11 (95% CI [0.08, 0.15]) in year 0-2 after 3-month re-baseline with cladribine (84.8% reduction). Adverse events, reported in 44 (16.4%) of the patients, were mild or moderate, and herpes zoster was only reported in 2 patients. In total, 30 (11.2%) patients discontinued cladribine treatment, of whom 7 (2.6%) discontinued because of adverse effects and 12 (4.5%) discontinued because of disease activity. CONCLUSION: In this nationwide review of all Danish patients starting therapy with cladribine tablets in a real-world setting, cladribine treatment was safe, and the therapeutic response was as expected from previous clinical trials. A prolonged observation period is necessary to assess the long-term benefit and risk of cladribine.
 BACKGROUND AND PURPOSE: Measures of atrophy in the whole brain can be used to reliably assess treatment effect in clinical trials of patients with multiple sclerosis (MS). Trials assessing the effect of treatment on grey matter (GM) and white matter (WM) atrophy are very informative, but hindered by technical limitations. This study aimed to measure GM and WM volume changes, using a robust longitudinal method, in patients with relapsing MS randomized to cladribine tablets 3.5 mg/kg or placebo in the CLARITY study. METHODS: We analysed T1-weighted magnetic resonance sequences using SIENA-XL, from 0 to 6 months (cladribine, n = 267; placebo, n = 265) and 6 to 24 months (cladribine, n = 184; placebo, n = 186). Mean percentage GM and WM volume changes (PGMVC and PWMVC) were compared using a mixed-effect model. RESULTS: More GM and WM volume loss was found in patients taking cladribine versus those taking placebo in the first 6 months of treatment (PGMVC: cladribine: -0.53 vs. placebo: -0.25 [p = 0.045]; PWMVC: cladribine: -0.49 vs. placebo: -0.34 [p = 0.137]), probably due to pseudoatrophy. However, over the period 6 to 24 months, GM volume loss was significantly lower in patients on cladribine than in those on placebo (PGMVC: cladribine: -0.90 vs. placebo: -1.27 [p = 0.026]). In this period, volume changes in WM were similar in the two treatment arms (p = 0.52). CONCLUSIONS: After a short period of pseudoatrophy, treatment with cladribine 3.5 mg/kg significantly reduced GM atrophy in comparison with placebo. This supports the relevance of GM damage in MS and may have important implications for physical and cognitive disability progression.
 Alemtuzumab is an anti-CD52 monoclonal antibody used to treat relapsing-remitting multiple sclerosis following failure of second-line medications. It is administered intravenously in 2 treatment sequences 1 year apart. This drug is frequently associated with mild infusion reactions within days of administration, increased infection risk, and long term adverse events from secondary autoimmunity. Alemtuzumab-induced serious immune-mediated thrombocytopenia (ITP) is well-reported and occurred in 1.0-2.2% of participants in initial phase 2 and 3 trials for multiple sclerosis. Significant neutropenia, however, is rare and was only observed in 0.1% of study participants. Delayed neutropenia and/or ITP is thought to occur from secondary autoimmunity. Few case reports have described severe neutropenia occurring beyond 2 months of last alemtuzumab dose. We present an unusual case of delayed combined neutropenia and thrombocytopenia that occurred 15 months after the second infusion of alemtuzumab. The patient was asymptomatic and presented following discovery of neutropenia and thrombocytopenia during routine laboratory studies. The patient responded to steroids initially and was discharged, although outpatient cell counts subsequently revealed recurrent neutropenia and ITP. The adverse drug reaction probability (Naranjo) scale was completed and showed probable likelihood that the adverse event was alemtuzumab-related. Long term screening for delayed hematologic abnormalities, at least 4 years after initial dose, is necessary when using alemtuzumab. Greater research is needed to understand the mechanism of drug-associated neutropenia.
 BACKGROUND: Therapeutic plasma exchange (TPE) is a conventional second-line treatment for patients with multiple sclerosis (MS) or clinically isolated syndrome with steroid-refractory relapses. METHODS: MS and clinically isolated syndrome patients with a steroid-refractory relapse, who fulfilled the indications for TPE were enrolled in this study. An expert nurse recorded the data comprising age, sex, type of MS, disease modifying therapy, disease duration, relapse rate, vital signs at the beginning, during and at the end of each plasma exchange session, plasma exchange volume, normal saline volume, and TPE complications. Ultimately, the statistical association was estimated amongst the variables. RESULTS: A total of 122 cases were assessed. Twelve cases (9.8%) received plasmapheresis for the second time. The mean age was 32.2±8.7 years and 107 (87.7%) were female. In total, 609 plasma exchange sessions were completed. Hypotension and skin reaction were the most clinical complications. Hemoglobin loss and hypokalemia were the most laboratory complications. Fifty-four cases (44.3%) had no complications, 40 (32.8%) had 1 complication, 21 (17.2%) 2 complications, 6 (4.9%) had 3 complications, and 1 (0.8%) disclosed 4 complications. The relapse rate in the past 12 months and the mean plasma volume exchange were significantly different between the groups. CONCLUSIONS: We revealed that TPE could be considered as a safe second-line therapy in MS relapses. Hypotension, skin reaction, hemoglobin loss, and hypokalemia were the most complications of TPE in our patients.

 BACKGROUND: A rapid and reliable diagnosis of multiple sclerosis (MS) is crucial to initiate adapted disease-modifying treatment. The 2017 McDonald criteria were revised with the aim of further improving the diagnostic performance. OBJECTIVE: In this article the published studies comparing the use of the 2017 and 2010 McDonald criteria were reviewed and analyzed in terms of diagnostic performance. MATERIAL AND METHODS: A total of 20 studies and 1 review article with a total of 3006 evaluated patients were identified by means of a literature search in the PubMed database (search term: McDonald criteria 2010 and McDonald criteria 2017). RESULTS: Using the 2017 McDonald criteria, a diagnosis of MS was made in more patients (2277/3006 patients, 76%) and in an earlier stage (3-10 months) compared with the 2010 revision (1562/3006 patients, 52%). Of the additional MS diagnoses, 193/715 were due to the adjustment of the imaging criteria of temporal dissemination and 536/715 were due to the introduction of oligoclonal bands as a diagnostic criterion. CONCLUSION: The revised McDonald criteria of 2017 have achieved their goal and enable the diagnosis of MS in a higher proportion of patients at the first clinical event.

 The review presents current data on the use of positron emission tomography and single-photon emission computed tomography in multiple sclerosis (MS) to assess the activity of the pathological process, including neuroinflammation, demyelination, activation of microglia, neurodegeneration and local blood flow disorders. These methodologies are a new approach for studying the mechanisms of action and evaluating the clinical effect of disease modifying therapy of MS, especially those capable of penetrating into brain tissue. Among them, the most attention is attracted by cladribine tablets acting on the mechanism of immune reconstitution therapy, most likely with the modulation of immune reactions directly in the brain tissue.
 BACKGROUND AND PURPOSE: Randomized controlled trials and observational studies of nabiximols oromucosal spray in patients with multiple sclerosis (MS) spasticity have shown improvement in a range of associated symptoms (pain, spasms, fatigue, bladder dysfunction, and sleep disturbances). This study evaluated the effectiveness and tolerability of add-on nabiximols in the routine management of patients with MS spasticity in Austria, with a focus on spasticity-associated symptoms. METHODS: This was an open, prospective, multicenter, observational, non-interventional study of patients with MS spasticity receiving add-on treatment with nabiximols oromucosal spray. Main endpoints were patient-reported changes from baseline in the frequency (counts) or severity (mean Numerical Rating Scale [NRS] scores) of spasticity-associated symptoms, and patient-reported changes from baseline in impairment of daily activities due to spasticity, after 1 and 3 months of nabiximols treatment. No analyses were conducted for statistical significance. RESULTS: There were 55 patients in the effectiveness population, and 62 in the safety population. Patients reported clinically relevant reductions from baseline to month 3 in the average number of spasms/day (-68.2%) and number of urinary incontinence episodes (-69.3%) in the week prior to the clinic visit, and reductions in mean 0-10 NRS scores for sleep impairment (-47.2%), fatigue (-26.4%), pain (40.4%), and spasticity severity (39.0%). There was no change from baseline in daily activity impairment due to spasticity. The majority of patients were at least partly satisfied with add-on nabiximols for spasticity-associated symptoms. There were 31 adverse events (27 treatment related) reported in 19 patients, with no new safety signals. CONCLUSIONS: Add-on nabiximols improved the severity of MS spasticity and a range of spasticity-associated symptoms during real-world use in Austria. Nabiximols is an option for patients with MS spasticity who fail first-line oral antispasticity treatment.
 BACKGROUND: Chronic periodontitis (CP) is a multifactorial, chronic inflammatory disease of microbial etiology that manifests as a result of the dysfunction of the immune mechanism, culminating in the destruction of the alveolar bone of the jaws. Multiple sclerosis (MS) is an autoimmune disorder that affects the central nervous system (CNS), leads to demyelination and degeneration of nerve axons and often causes severe physical and/or cognitive impairment. As CP and MS involve inflammatory mechanisms and immune dysfunction, researchers have attempted to study the association between them. AIM: To systematically review the literature on the epidemiological association between CP and MS in adults. METHODS: PRISMA 2020 statement was used in the study protocol. The design was done according to the Cochrane methodology. A comprehensive literature search was performed in PubMed, Scopus and Cochrane databases; a manual search and evaluation of the gray literature was also performed. The meta-analysis was performed by Review Manager (RevMan) 5.4. Odds ratio (OR) with 95% confidence interval (CI) was defined as the effect size of the outcome. Heterogeneity was assessed by Chi-square and I(2). The articles evaluated were written in English, without a time limit, concern observational studies (patient-controls) and report the diagnostic criteria of the diseases. Duplicate entries were excluded. To evaluate the reliability of the results of each study, Newcastle-Ottawa Scale (NOS) and GRADE tools were used. Two independent reviewers did all evaluations with a resolution of discrepancies by a third. RESULTS: Meta-analysis included three observation studies examined 3376 people. MS patients are significantly more likely to be diagnosed with CP than healthy controls (OR 1.93, 95% CI 1.54-2.42, p<0.0001). CONCLUSION: A high prevalence of CP was found among MS patients compared with healthy controls. Healthcare professionals should be aware of the association between these pathological entities to provide patients with high-quality care through an effective and holistic diagnostic and therapeutic approach.
 BACKGROUND: Women of fertile age who receive autologous hematopoietic stem cell transplantation (AHSCT) due to multiple sclerosis (MS) are at risk of loss of ovarian function and infertility because of the conditioning regimen with alkylating agents. OBJECTIVE: To present our data on fertility preservation by ovarian tissue cryopreservation (OTC) in young women with MS before AHSCT. METHODS: Retrospective, observational cohort study RESULTS: Eight women had OTC. After AHSCT four had premature ovarian insufficiency (POI), and two of these had autotransplantation of their cryopreserved ovarian tissue. Both women regained ovarian function, and a spontaneous pregnancy was achieved resulting in the delivery of a healthy baby. CONCLUSION: OTC preserves fertility in young women with MS at risk of POI.
 BACKGROUND & OBJECTIVES: MS is not only a demyelinating disease of central nervous system, but it also affects cortical and deep gray matter (GM). Furthermore, it causes axonal damage in the brain and spinal cord through inflammation and axonal degeneration. It is mostly seen between the ages of 20 and 40 and prevalence of the disease is higher among females than males. In the present study, we measured different parameters in the brains of patients with multiple sclerosis (MS) and healthy controls in both genders to determine the amount of brain atrophy quantitatively in MS patients. METHODS: We used T2-weighted MRI scans of 40 MS patients (25 females + 15 males) with clinically definite relapsing-remitting multiple sclerosis that was determined according to Poser criteria in multiple parts of the brain, and we compared these data with those of sex-matched healthy controls in the same numbers. RESULTS: Wideness of the lateral and third ventricles and the volumes of cerebral sulci in MS patients were significantly increased compared to both male and female controls. Brain width, corpus callosum area and the total brain/cerebellum + brain stem volumes of MS patients were decreased considerably. INTERPRETATION & CONCLUSIONS: The present measurements indicated that MS caused parenchymal destruction in the cortex, axonal degeneration and myelin loss in the white matter of the brain. Consequently, the current observations correlate well with worsening disability in MS patients.
 BACKGROUND: Fingolimod, natalizumab, and ocrelizumab are commonly used in the second-line treatment of relapsing-remitting multiple sclerosis (RRMS). However, these have only been compared in observational studies, not in controlled trials, with limited and inconclusive results being reported. A comparison of their effect on relapse and disability in a real-world setting is therefore needed. OBJECTIVES: The objective of this study was to compare the efficacy of fingolimod, natalizumab, and ocrelizumab in reducing disease activity in RRMS. METHODS: This multicenter, retrospective observational study was carried out with prospectively collected data from 16 centers. All consecutive RRMS patients treated with fingolimod, natalizumab, and ocrelizumab were included. Data for relapses, Expanded Disability Status Scale (EDSS) scores, and brain magnetic resonance imaging (MRI) scans were collected. Patients were matched using propensity scores. Annualized relapse rates (ARR), time to first relapse, and disability accumulation were compared. RESULTS: Propensity score matching retained 736 patients in the fingolimod versus 370 in the natalizumab groups, 762 in the fingolimod versus 434 in the ocrelizumab groups, and 310 in the natalizumab versus 310 in the ocrelizumab groups for final analyses. Mean ARR decreased markedly from baseline after treatment in all three treatment groups. Mean on-treatment ARR was lower in natalizumab-treated patients (0.09, 95% confidence interval (CI), 0.07-0.12) than in those treated with fingolimod (0.17, 0.15-0.19, p<0.001), ocrelizumab (0.08, 0.06-0.11), and fingolimod (0.14, 0.12-0.16, p=0.001). No significant difference was observed in mean on-treatment ARR between patients treated with natalizumab (0.08, 0.06-0.11) and ocrelizumab (0.09, 0.07-0.12, p=0.54). Compared to fingolimod, the natalizumab and ocrelizumab groups exhibited a higher percentage of relapse-free patients and a lower percentage of MRI-active patients at year 1. No significance differences in disability accumulation were determined between the therapies. CONCLUSION: Natalizumab and ocrelizumab exhibited similar effects on relapse control, and both were associated with better relapse control than fingolimod. The effects of the three therapies on disability outcomes were similar.
 BACKGROUND: The clinical relevance of serum glial fibrillary acidic protein (sGFAP) concentration as a biomarker of MS disability progression independent of acute inflammation has yet to be quantified. OBJECTIVE: To test whether baseline values and longitudinal changes in sGFAP concentration are associated with disability progression without detectable relapse of magnetic resonance imaging (MRI) inflammatory activity in participants with secondary-progressive multiple sclerosis (SPMS). METHODS: We retrospectively analyzed longitudinal sGFAP concentration and clinical outcome data from the Phase 3 ASCEND trial of participants with SPMS, with no detectable relapse or MRI signs of inflammatory activity at baseline nor during the study (n = 264). Serum neurofilament (sNfL), sGFAP, T2 lesion volume, Expanded Disability Status Scale (EDSS), Timed 25-Foot Walk (T25FW), 9-Hole Peg Test (9HPT), and composite confirmed disability progression (CDP) were measured. Linear and logistic regressions and generalized estimating equations were used in the prognostic and dynamic analyses. RESULTS: We found a significant cross-sectional association between baseline sGFAP and sNfL concentrations and T2 lesion volume. No or weak correlations between sGFAP concentration and changes in EDSS, T25FW, and 9HPT, or CDP were observed. CONCLUSION: Without inflammatory activity, changes in sGFAP concentration in participants with SPMS were neither associated with current nor predictive of future disability progression.
 Relapsing-remitting Multiple Sclerosis is the most common demyelinating neurodegenerative disease and is characterized by periods of relapses and generation of various motor symptoms. These symptoms are associated with the corticospinal tract integrity, which is quantified by means of corticospinal plasticity which can be probed via transcranial magnetic stimulation and assessed with corticospinal excitability measures. Several factors, such as exercise and interlimb coordination, can influence corticospinal plasticity. Previous work in healthy and in chronic stroke survivors showed that the greatest improvement in corticospinal plasticity occurred during in-phase bilateral exercises of the upper limbs. During in-phase bilateral movement, both upper limbs are moving simultaneously, activating the same muscle groups and triggering the same brain region respectively. Altered corticospinal plasticity due to bilateral cortical lesions is common in MS, yet, the impact of these type of exercises in this cohort is unclear. The aim of this concurrent multiple baseline design study is to investigate the effects of in-phase bilateral exercises on corticospinal plasticity and on clinical measures using transcranial magnetic stimulation and standardized clinical assessment in five people with relapsing-remitting MS. The intervention protocol will last for 12 consecutive weeks (30-60 minutes /session x 3 sessions/week) and include in-phase bilateral movements of the upper limbs, adapted to different sports activities and to functional training. To define functional relation between the intervention and the results on corticospinal plasticity (central motor conduction time, resting motor threshold, motor evoked potential amplitude and latency) and on clinical measures (balance, gait, bilateral hand dexterity and strength, cognitive function), we will perform a visual analysis and if there is a potential sizeable effect, we will perform statistical analysis. A possible effect from our study, will introduce a proof-of-concept for this type of exercise that will be effective during disease progression. Trial registration: ClinicalTrials.gov NCT05367947.

 Multiple sclerosis (MS) is a heterogeneous disease of the central nervous system that is governed by neural tissue loss and dystrophy during its progressive phase, with complex reactive pathological cellular changes. The immune-mediated mechanisms that promulgate the demyelinating lesions during relapses of acute episodes are not characteristic of chronic lesions during progressive MS. This has limited our capacity to target the disease effectively as it evolves within the central nervous system white and gray matter, thereby leaving neurologists without effective options to manage individuals as they transition to a secondary progressive phase. The current review highlights the molecular and cellular sequelae that have been identified as cooperating with and/or contributing to neurodegeneration that characterizes individuals with progressive forms of MS. We emphasize the need for appropriate monitoring via known and novel molecular and imaging biomarkers that can accurately detect and predict progression for the purposes of newly designed clinical trials that can demonstrate the efficacy of neuroprotection and potentially neurorepair. To achieve neurorepair, we focus on the modifications required in the reactive cellular and extracellular milieu in order to enable endogenous cell growth as well as transplanted cells that can integrate and/or renew the degenerative MS plaque.
 BACKGROUND: To provide a comprehensive assessment of the treatment effects of nabiximols oromucosal spray on multiple sclerosis spasticity in two clinical trials, GWSP0604 and SAVANT. METHODS: Both studies enriched for responders before randomization, defined by a ≥20% improvement in Spasticity 0-10 numeric rating scale (NRS) score. Additionally, SAVANT used randomized re-titration following washout. Spasticity NRS outcomes, spasm count, and modified Ashworth scale (MAS) scores were analyzed. RESULTS: Mean change from baseline in average daily Spasticity NRS scores was significantly larger for nabiximols than placebo at all postbaseline timepoints, ranging from -0.36 to -0.89 in GWSP0604 and -0.52 to -1.96 in SAVANT. Percent reduction in geometric mean change from baseline in average daily spasm count for nabiximols ranged from 19-35% versus placebo. A treatment difference favoring nabiximols was observed in overall MAS scores during the randomized part of each study. Treatment effect was larger for combinations of lower limb muscle groups (ranging between -0.16 and -0.37). CONCLUSIONS: Nabiximols leads to improvement in spasticity that was sustained over the 12-week treatment period as measured by average daily Spasticity NRS scores, daily spasm counts, and MAS scores for combinations of muscle groups, especially the combination of the 6 key muscle groups in the lower limbs in NRS responders to nabiximols treatment.

 The improved understanding of multiple sclerosis (MS) neurobiology alongside the development of novel markers of disease will allow precision medicine to be applied to MS patients, bringing the promise of improved care. Combinations of clinical and paraclinical data are currently used for diagnosis and prognosis. The addition of advanced magnetic resonance imaging and biofluid markers has been strongly encouraged, since classifying patients according to the underlying biology will improve monitoring and treatment strategies. For example, silent progression seems to contribute significantly more than relapses to overall disability accumulation, but currently approved treatments for MS act mainly on neuroinflammation and offer only a partial protection against neurodegeneration. Further research, involving traditional and adaptive trial designs, should strive to halt, repair or protect against central nervous system damage. To personalize new treatments, their selectivity, tolerability, ease of administration, and safety must be considered, while to personalize treatment approaches, patient preferences, risk-aversion, and lifestyle must be factored in, and patient feedback used to indicate real-world treatment efficacy. The use of biosensors and machine-learning approaches to integrate biological, anatomical, and physiological parameters will take personalized medicine a step closer toward the patient's virtual twin, in which treatments can be tried before they are applied.
 Neuropsychiatric abnormalities may be broadly divided in two categories: disorders of mood, affect, and behavior and abnormalities affecting cognition. Among these conditions, clinical depression, anxiety and neurocognitive disorders are the most common in multiple sclerosis (MS), with a substantial impact on patients' quality of life and adherence to treatments. Such manifestations may occur from the earliest phases of the disease but become more frequent in MS patients with a progressive disease course and more severe clinical disability. Although the pathogenesis of these neuropsychiatric manifestations has not been fully defined yet, brain structural and functional abnormalities, consistently observed with magnetic resonance imaging (MRI), together with genetic and immunologic factors, have been suggested to be key players. Even though the detrimental clinical impact of such manifestations in MS patients is a matter of crucial importance, at present, they are often overlooked in the clinical setting. Moreover, the efficacy of pharmacologic and non-pharmacologic approaches for their amelioration has been poorly investigated, with the majority of studies showing marginal or no beneficial effect of different therapeutic approaches, possibly due to the presence of multiple and heterogeneous underlying pathological mechanisms and intrinsic methodological limitations. A better evaluation of these manifestations in the clinical setting and improvements in the understanding of their pathophysiology may offer the potential to develop tools for differentiating these mechanisms in individual patients and ultimately provide a principled basis for treatment selection. This review provides an updated overview regarding the pathophysiology of the most common neuropsychiatric symptoms in MS, the clinical and MRI characteristics that have been associated with mood disorders (i.e., depression and anxiety) and cognitive impairment, and the treatment approaches currently available or under investigation.
 PURPOSE: Volume measurement using MRI is important to assess brain atrophy in multiple sclerosis (MS). However, differences between scanners, acquisition protocols, and analysis software introduce unwanted variability of volumes. To quantify theses effects, we compared within-scanner repeatability and between-scanner reproducibility of three different MR scanners for six brain segmentation methods. METHODS: Twenty-one people with MS underwent scanning and rescanning on three 3 T MR scanners (GE MR750, Philips Ingenuity, Toshiba Vantage Titan) to obtain 3D T1-weighted images. FreeSurfer, FSL, SAMSEG, FastSurfer, CAT-12, and SynthSeg were used to quantify brain, white matter and (deep) gray matter volumes both from lesion-filled and non-lesion-filled 3D T1-weighted images. We used intra-class correlation coefficient (ICC) to quantify agreement; repeated-measures ANOVA to analyze systematic differences; and variance component analysis to quantify the standard error of measurement (SEM) and smallest detectable change (SDC). RESULTS: For all six software, both between-scanner agreement (ICCs ranging 0.4-1) and within-scanner agreement (ICC range: 0.6-1) were typically good, and good to excellent (ICC > 0.7) for large structures. No clear differences were found between filled and non-filled images. However, gray and white matter volumes did differ systematically between scanners for all software (p < 0.05). Variance component analysis yielded within-scanner SDC ranging from 1.02% (SAMSEG, whole-brain) to 14.55% (FreeSurfer, CSF); and between-scanner SDC ranging from 4.83% (SynthSeg, thalamus) to 29.25% (CAT12, thalamus). CONCLUSION: Volume measurements of brain, GM and WM showed high repeatability, and high reproducibility despite substantial differences between scanners. Smallest detectable change was high, especially between different scanners, which hampers the clinical implementation of atrophy measurements.
 OBJECTIVE: Neurodegenerative conditions often manifest radiologically with the appearance of premature aging. Multiple sclerosis (MS) biomarkers related to lesion burden are well developed, but measures of neurodegeneration are less well-developed. The appearance of premature aging quantified by machine learning applied to structural MRI assesses neurodegenerative pathology. We assess the explanatory and predictive power of "brain age" analysis on disability in MS using a large, real-world dataset. METHODS: Brain age analysis is predicated on the over-estimation of predicted brain age in patients with more advanced pathology. We compared the performance of three brain age algorithms in a large, longitudinal dataset (>13,000 imaging sessions from >6,000 individual MS patients). Effects of MS, MS disease course, disability, lesion burden, and DMT efficacy were assessed using linear mixed effects models. RESULTS: MS was associated with advanced predicted brain age cross-sectionally and accelerated brain aging longitudinally in all techniques. While MS disease course (relapsing vs. progressive) did contribute to advanced brain age, disability was the primary correlate of advanced brain age. We found that advanced brain age at study enrollment predicted more disability accumulation longitudinally. Lastly, a more youthful appearing brain (predicted brain age less than actual age) was associated with decreased disability. INTERPRETATION: Brain age is a technically tractable and clinically relevant biomarker of disease pathology that correlates with and predicts increasing disability in MS. Advanced brain age predicts future disability accumulation.
 We describe a woman with a history of relapsing acute optic neuritis and perineuritis. Testing failed to confirm a specific diagnosis; hence, she was diagnosed with seronegative neuromyelitis optica spectrum disorder and treated with the immunotherapy rituximab, later in conjunction with mycophenolate mofetil. She achieved a durable remission for 9 years until she presented with paresthesia affecting her left fifth digit, right proximal thigh, and left foot, while also reporting a 25-pound weight loss over the prior 3 months. New imaging demonstrated a longitudinally extensive and enhancing optic nerve, in conjunction with multifocal enhancing lesions within the spinal cord, in a skip-like distribution. The differential diagnosis is discussed.
 BACKGROUND: Interferon beta therapies are well-established disease-modifying treatments for patients with relapsing multiple sclerosis (MS). Based on clinical evidence from two large cohort studies, both, the EMA and FDA updated the labels of the interferon beta class in terms of pregnancy and breastfeeding in 2019 and 2020, respectively. To complement pregnancy label updates with patient-reported real-world data, this study examined German pregnancy and outcome reports including available data on child development from women with MS treated with peginterferon beta-1a or intramuscular (IM) interferon beta-1a. METHODS: The post-authorisation safety study PRIMA included adult women diagnosed with relapsing-remitting MS or clinically isolated syndrome, who were treated with peginterferon beta-1a or IM interferon beta-1a before or during pregnancy and registered in the marketing authorisation holder's MS Service center patient support program. In the prospective part of the study, conducted from April to October 2021, data on developmental milestones of the newborns were collected via telephone interview from mothers reporting live births. RESULTS: In total, 426 women were enrolled, reporting 542 pregnancies that resulted in 466 live births. A total of 162 women completed the questionnaire for 192 live births (53.1% male). Newborns had Apgar scores indicative of healthy infants. Weight, length and head circumference at birth and physical growth curves up to 48 months lay within the expected range of the German general population. Most newborn screenings and examinations during check-ups were inconspicuous over the study period of 48 months. Out of 158 breastfed infants, 112 (70.9%) were breastfed exclusively until month 5. CONCLUSION: Study results confirmed former reports indicating that exposure to interferon beta therapies during pregnancy or lactation had no adverse effects on intrauterine growth and child development over the study period, which covered the first 4 years of life. These real-world data obtained within the scope of a patient support program for peginterferon beta-1a or IM interferon beta-1a corroborate German and Scandinavian registry data and support the label update of all interferon beta therapies. REGISTRATION: NCT04655222, EUPAS38347.
 INTRODUCTION: Multiple sclerosis (MS) is a disabling disease that affects young adults. Treatments for MS have increased exponentially in number, efficacy and risk. Autologous hematopoietic stem cell transplantation (aHSCT) can change the natural history of the disease. To analyze if aHSCT should be done early in the course of the disease or after failing of other therapies, we have studied the long-term results of aHSCT in a cohort of persons with MS who were given, or not, immunosuppressive drugs before the transplant. MATERIALS AND METHODS: Patients with MS referred to our center for aHSCT between June 2015 and January 2023 were prospectively entered in the study. All phenotypes of MS were included (relapsing remitting, primary progressive and secondary progressive). The follow up was assessed with the patient reported EDSS score in an online form; only patients followed by three or more years were included in the analysis. Patients were divided into two groups: Given or not disease modifying treatments (DMT) before the aHSCT. RESULTS: 1132 subjects were prospectively enrolled. 74 patients were followed for more than 36 months, and the subsequent analysis was done in this cohort. The response rate (RR = improvement + stabilization) at 12, 24 and 36 mo was 84%, 84% and 58% respectively for patients not receiving prior DMT and 72%, 90% and 67% for patients receiving DMT. In the whole group, the EDSS score dropped from a mean of 5.5 to 4.5 at 12 mo, to 5.0 at 24 mo and to 5.5 at 36 mo, after the aHSCT. The EDSS score was on average worsening in patients before the aHSCT, but the transplant stabilized the EDSS score at 3 years in patients with prior exposure to DMT, whereas in persons not given DMT, the transplant resulted in a significant decrease (p = .01) of the EDSS score. This indicates a positive response in all patients given aHSCT, but significantly better in those not exposed to DMT before the graft. CONCLUSION: The response to aHSCT was better for persons not exposed to immunosuppressive DMT before the transplant, thus suggesting that aHSCT should be done early in the course of the disease and probably before the treatment with DMT. Additional studies are needed to further analyze the impact of the use of DMT therapies before the aHSCT in MS, as well as the timing of the procedure.
 BACKGROUND: People with relapsing-remitting multiple sclerosis can benefit from disease-modifying treatments (DMTs). Several DMTs are available that vary in their efficacy, side-effect profile and mode of administration. OBJECTIVE: We aimed to measure the preferences of people with relapsing-remitting multiple sclerosis for DMTs using a discrete choice experiment and to assess which stated preference attributes correlate with the attributes of the DMTs they take in the real world. METHODS: Discrete choice experiment attributes were developed from literature reviews, interviews and focus groups. In a discrete choice experiment, participants were shown two hypothetical DMTs, then chose whether they preferred one of the DMTs or no treatment. A mixed logit model was estimated from responses and individual-level estimates of participants' preferences conditional on their discrete choice experiment choices calculated. Logit models were estimated with stated preferences predicting current real-world on-treatment status, DMT mode of administration and current DMT. RESULTS: A stated intrinsic preference for taking a DMT was correlated with currently taking a DMT, and stated preferences for mode of administration were correlated with the modes of administration of the DMTs participants were currently taking. Stated preferences for treatment effectiveness and adverse effects were not correlated with real-world behaviour. CONCLUSIONS: There was variation in which discrete choice experiment attributes correlated with participants' real-world DMT choices. This may indicate patient preferences for treatment efficacy/risk are not adequately taken account of in prescribing. Treatment guidelines must ensure they take into consideration patients' preferences and improve communication around treatment efficacy/risk.
 BACKGROUND: Multiple sclerosis (MS) is a neuroinflammatory disease with debilitating manifestations that may predispose patients to hip fracture and osteoarthritis, and may affect recovery from total hip arthroplasty (THA). With increased longevity of MS patients and growth in demand for arthroplasty in this population, it is important to understand outcomes of THA in patients with MS. AIM: We sought to compare outcomes of THA among persons with MS and without MS. METHODS: International Classification of Diseases, Ninth Revision Procedure Coding System (ICD-9-PCS) codes for hip arthroplasty (815.1) were used to identify all patients in the New York Statewide Planning and Research Cooperative System (SPARCS) database who underwent THA between 2000 and 2014. Patients with MS, the primary exposure, were identified using ICD-9-Clinical Modification (CM) code 340. The study outcomes of length of stay (days), discharge disposition, index admission mortality, 90-day readmission, 1-year revision arthroplasty, and 1-year all-cause mortality were evaluated using multivariable regression analyses inclusive of basic demographics, admission source, disposition, payer, comorbidity, and socioeconomic status (SES). RESULTS: Compared to patients without MS, those with MS had marginally longer lengths of stay (mean ratio [MR] 1.05; 95% confidence interval [CI], 1.01-1.10; p = 0.0142), higher risk for institutional discharge disposition (odds ratio [OR] 2.03; 95% CI, 1.54-2.70; p < 0.0001) and higher risk of readmission for revision hip arthroplasty (OR 2.60; 95% CI, 1.07-6.35; p = 0.035). However, MS patients had similar risk for 90-day readmission and one-year all-cause mortality as compared with non-MS patients. CONCLUSIONS: Although patients with MS who underwent THA had a 90-day complication risk that was similar to those without MS, the risk for requiring revision surgery was more than 2-fold higher. Additional studies are needed to understand the reasons for revision surgery and for developing strategies to mitigate the risk of complications.

 BACKGROUND: Multiple sclerosis (MS) is an immune-mediated disease that has been related to several risk factors such as various viral infections. We carried out this study in order to establish a relationship between COVID-19 infection and MS severity. METHODS: In a case-control study, we recruited patients with relapsing-remitting multiple sclerosis (RRMS). Patients were divided into two groups based on positive COVID-19 PCR at the end of the enrollment phase. Each patient was prospectively followed for 12 months. Demographical, clinical, and past medical history were collected during routine clinical practice. Assessments were performed every six months; MRI was performed at enrollment and 12 months later. RESULTS: Three hundred and sixty-two patients participated in this study. MS patients with COVID-19 infection had significantly higher increases in the number of MRI lesions (p: 0.019, OR(CI): 6.37(1.54-26.34)) and EDSS scores (p: 0.017), but no difference was found in total annual relapses or relapse rates. COVID-19 infections were positively correlated with EDSS progression (p: 0.02) and the number of new MRI lesions (p: 0.004) and predicted the likelihood of the number of new MRI lesions by an odds of 5.92 (p: 0.018). CONCLUSION: COVID-19 may lead to higher disability scores in the RRMS population and is associated with developing new Gd-enhancing lesions in MRI imaging. However, no difference was observed between the groups regarding the number of relapses during follow-up.
 Psychiatric symptoms frequently occur in multiple sclerosis (MS), presenting with a complex phenomenology that encompasses a large clinical spectrum from clear-cut psychiatric disorders up to isolated psychopathological manifestations. Despite their relevant impact on the overall disease burden, such clinical features are often misdiagnosed, receive suboptimal treatment and are not systematically evaluated in the quantification of disease activity. The development of psychiatric symptoms in MS underpins a complex pathogenesis involving both emotional reactions to a disabling disease and structural multifocal central nervous system damage. Here, we review MS psychopathological manifestations under a biological perspective, highlighting the pathogenic relevance of synaptic and neural network dysfunction. Evidence obtained from human and experimental disease models suggests that MS-related psychiatric phenomenology is part of a disconnection syndrome due to diffuse inflammatory and neurodegenerative brain damage.
 Personalized longitudinal disease assessment is central to quickly diagnosing, appropriately managing, and optimally adapting the therapeutic strategy of multiple sclerosis (MS). It is also important for identifying idiosyncratic subject-specific disease profiles. Here, we design a novel longitudinal model to map individual disease trajectories in an automated way using smartphone sensor data that may contain missing values. First, we collect digital measurements related to gait and balance, and upper extremity functions using sensor-based assessments administered on a smartphone. Next, we treat missing data via imputation. We then discover potential markers of MS by employing a generalized estimation equation. Subsequently, parameters learned from multiple training datasets are ensembled to form a simple, unified longitudinal predictive model to forecast MS over time in previously unseen people with MS. To mitigate potential underestimation for individuals with severe disease scores, the final model incorporates additional subject-specific fine-tuning using data from the first day. The results show that the proposed model is promising to achieve personalized longitudinal MS assessment; they also suggest that features related to gait and balance as well as upper extremity function, remotely collected from sensor-based assessments, may be useful digital markers for predicting MS over time.
 BACKGROUND: Teriflunomide (TER) (Aubagio™) is an FDA-approved disease-modifying therapy (DMT) for relapsing-remitting multiple sclerosis (RRMS). The mechanism of action of TER is thought to be related to the inhibition of dihydroorotate dehydrogenase (DHODH), a key mitochondrial enzyme in the de novo pyrimidine synthesis pathway required by rapidly dividing lymphocytes. Several large pivotal studies have established the efficacy and safety of TER in patients with RRMS. Despite this, little is known about how the adaptive and innate immune cell subsets are affected by the treatment in patients with MS. METHODS: We recruited 20 patients with RRMS who were newly started on TER and performed multicolor flow cytometry and functional assays on peripheral blood samples. A paired t-test was used for the statistical analysis and comparison. RESULTS: Our data showed that TER promoted a tolerogenic environment by shifting the balance between activated pathogenic and naïve or immunosuppressive immune cell subsets. In our cohort, TER increased the expression of the immunosuppressive marker CD39 on regulatory T cells (Tregs) while it decreased the expression of the activation marker CXCR3 on CD4(+) T helper cells. TER treatment also reduced switched memory (sm) B cells while it increased naïve B cells and downregulated the expression of co-stimulatory molecules CD80 and CD86. Additionally, TER reduced the percentage and absolute numbers of natural killer T (NKT) cells, as well as the percentage of natural killer (NK) cells and showed a trend toward reducing the CD56(dim) NK pathogenic subset. CONCLUSION: TER promotes the tolerogenic immune response and suppresses the pathogenic immune response in patients with RRMS.
 BACKGROUND: In a recent trial, hydroxychloroquine (HCQ) treatment reduced the expected rate of disability worsening at 18 months in primary progressive multiple sclerosis (PPMS). Neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) are emerging biomarkers in multiple sclerosis. METHODS: We measured NfL and GFAP levels in serum samples from 39 patients with inactive PPMS included in a phase II clinical trial of HCQ treatment in PPMS at multiple time points over 18 months, and investigated the association of these biomarkers with clinical disability at screening and during follow-up. Screening and 12-month retinal nerve fiber layer (RNFL) thickness was also recorded and analyzed. RESULTS: NfL and GFAP levels increased over time, but only significantly from screening to month 6. NfL and GFAP levels did not significantly increase from month 6 up to month 18. At screening, NfL and GFAP levels did not correlate with the Expanded Disability Status Scale (EDSS), and GFAP but not NfL modestly correlated with Timed 25-Foot Walk test (T25FW). Screening NfL and GFAP levels did not predict disability worsening (≥20% worsening on the T25FW) at month 18. RNFL thickness decreased significantly from screening to month 12 and independently predicted disability worsening. CONCLUSIONS: In this cohort of people with inactive PPMS, HCQ treatment attenuated the increase of NfL and GFAP after 6 months of treatment and up to 18 months of follow-up, suggesting a treatment effect of HCQ over these biomarkers. RNFL thickness, a marker of neuroaxonal atrophy, was associated with disability worsening, and should be explored further as a prognostic marker in this population.
 BACKGROUND: Sleep disorders in multiple sclerosis (MS) patients are common. Dimethylfumarate is an oral disease-modifying drug (DMT), whose impact on sleep is unknown. OBJECTIVE: The aim of this study was to characterize actigraphic patterns in MS patients treated with dimethylfumarate. METHODS: Twenty relapsing-remitting MS patients with low to a mild disability, aged 20-50y, treated with dimethylfumarate for more than 6 months, were enrolled. All subjects had no history of sleep disorders. Actigraphy was used to study sleep patterns during a seven-day period. Sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI). Twenty healthy subjects served as controls. RESULTS: Our results showed statistically significant differences between some actigraphic patterns in MS patients treated with dimethylfumarate and healthy subjects, but the values for patients were still within normal limits. PSQI score was higher in MS patients compared to controls. CONCLUSION: Our findings suggest that dimethylfumarate, an oral DMT with a favourable benefit-risk profile, does not strongly alter sleep patterns in MS patients with low to mild disability and with no history of sleep disorders. Actigraphy is a simple diagnostic tool, able to support an objective measure of sleep parameters. The simplicity of application may allow considering its use for a screening of sleep disorders in MS patients.
 Multiple sclerosis (MS) is a chronic autoimmune-mediated demyelinating disease of the central nervous system (CNS) that is usually associated with varying degrees of progressive disability. Chitinase-3-like protein-1 (CHI3L1) has attracted growing attention as a marker of ongoing inflammation and oncogenic transformation. The aim of this work was to assess the diagnostic accuracy of CHI3L1 versus IgG oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) of newly diagnosed relapsing remitting MS (RRMS) patients to throw light on a new simpler non subjective potential diagnostic marker in MS. This cross-sectional study of MS patients was carried at Ain Shams University Hospitals during the period from January 2021 till January 2022. Subjects included in this study were 40 patients diagnosed as having RRMS, based on their magnetic resonance imaging (MRI) findings, clinical presentation and according to the revised McDonald criteria 2017. The group included 10 males and 30 females; their ages ranged from 20 to 45 years. We found a significant correlation between CSF CHI3L1 levels and presence of oligoclonal bands (p=0.001), and that a cut off value of 30 ng/ml could be used for diagnosis of MS with sensitivity 84.85% and specificity 85.71%. A significant association was also found between CHI3L1 levels in CSF and Expanded Disability Status Scale (EDSS) score (p=0.002). We concluded that there were high levels of CHI3L1 in the CSF of MS patients and there was a significant correlation between CHI3L1 and oligoclonal bands and that CHI3L1 may be considered a promising diagnostic marker of MS.
 BACKGROUND: Multiple sclerosis is a chronic demyelinating autoimmune disease accompanied by inflammation and loss of axons and neurons. Toll-like receptors play crucial roles in the innate immune system and inflammation. However, few studies have explored the specific effects of toll-like receptor 7 signaling pathway in multiple sclerosis. To explore underlying effects to develop a new therapeutic target, we use Vesatolimod, a safe and well-tolerated agonist of toll-like receptor 7, to assess the possible effects in Experimental autoimmune encephalomyelitis (EAE) animal model. METHODS: EAE animal model was induced by injection of MOG35-55 and monitored daily for clinical symptoms, and the treatment group was given Vesatolimod at the onset of illness. The therapeutic effects of Vesatolimod on EAE inflammation, demyelination, CD107b cells and T cells infiltration, and microglia activation was evaluated. Autophagy within the spinal cords of EAE mice was also preliminarily assessed. RESULTS: Treatment with Vesatolimod significantly alleviated clinical symptoms of EAE from day 18 post-immunization and decreased the expression levels of inflammatory cytokines, particularly Eotaxin and IL-12 (P40), in peripheral blood. It also inhibited demyelination in spinal cords. Moreover, VES treatment reduced activation of microglia, infiltration of CD3 + T cells and CD107b + cells, as well as inhibited the autophagy-related proteins expression in the spinal cords of EAE mice. CONCLUSION: Our results indicate that Vesatolimod exhibits protective effects on EAE mice and is promising for treatment of MS.
 BACKGROUND: The correlation between fatigue and disability in multiple sclerosis (MS) with the hypothalamus-pituitary-adrenal axis is known. This study aimed to investigate the relationship between the morphometric dimensions of the pituitary gland with fatigue and disability. METHOD: This research, designed as a prospective and case-control study, included 85 MS patients and 45 healthy controls. The disability was evaluated using the expanded disability rating scale (EDSS), while fatigue was determined using the fatigue severity scale (FSS) and the neurological fatigue index (NFI-MS). The morphometric structure of the pituitary gland was measured using a coronal, T2-weighted, turbo-spin-echo sequence of magnetic resonance imaging. RESULTS: FSS and NFI-MS scores were higher in MS patients than in the control group (p = 0.001). Patients with a progressive and moderate-to-severe disability had a higher FSS score (p = 0.015; p = 0.002, respectively). A positive correlation was determined between disease duration, attack frequency, and EDSS and physical fatigue subscale score (p = 0.001; r = 0.383; 0.373; 0.545, respectively). The height and width of the pituitary gland were higher in MS patients (p = 0.021; p = 0.001, respectively). Pituitary gland height was higher in fatigued patients (p = 0.041). A low-positive correlation was determined between the number of attacks and the height of the pituitary gland (p = 0.027, r = 0.231). CONCLUSION: The difference in the dimensions of the pituitary gland in MS patients, especially in the fatigued group, supports the relationship of fatigue with morphometric features as well as the hypothalamus-pituitary-adrenal axis.
 BACKGROUND: The clinical evaluation of a new diagnosis of MS typically includes serologic testing to evaluate for its many mimics, yet there is little data to guide approaches to such testing. OBJECTIVE: To evaluate for the frequency and clinical significance of serologic testing for MS diagnostic evaluations. METHODS: In a single MS subspeciality center retrospective study, new patient evaluations for MS over the course of a year were identified, and the results of serologic testing and diagnostic evaluation extracted. Retrospective longitudinal diagnostic assessment was performed to confirm the accuracy of initial serological testing assessments. RESULTS: 150 patients had 823 serologic tests. 40 (5%) tests were positive, and resulted in 117 additional serologic tests, 10 radiographs, and 2 biopsies. 77 (51%) patients were diagnosed with a non-demyelinating disorder. Serologic testing results did not change any diagnosis, yet in some patients, it resulted in unnecessary additional testing and diagnostic delay. CONCLUSIONS: Serologic testing in the clinical assessment for routine MS resulted in unnecessary diagnostic delay, additional testing, and considerable healthcare cost.
 Cognitive skill learning (CSL) refers to the capacity to improve performance on specific cognitive operations through repeated practice. We hypothesized that high CSL aptitude may promote accumulation of cognitive reserve, and resiliency to cognitive decline, in people with Multiple Sclerosis (MS). Using an adaptive working memory training paradigm, we obtained CSL aptitude indices (amount of improvement on the training task over time) in MS patients for a single session of practice (25-30 min), and longer-term practice (twenty sessions). Neuropsychological performance was assessed with the Symbol Digit Modalities Test (SDMT), Paced Auditory Serial Addition Test (PASAT), and the Raven's Advanced Progressive Matrices (RAPM). CSL aptitude measures were positively correlated with neuropsychological performance, and had high diagnostic accuracy for classifying cognitive impairment in MS, defined as 1.5 SD below the demographics-corrected normative mean of the SDMT. Positive relationships between CSL aptitude measures and neuropsychological performance tended to be more pronounced for individuals with high estimated cognitive reserve, suggesting that high CSL aptitude is a a factor that promotes the protective effects of cognitive reserve. Furthermore, regression analyses indicated that CSL aptitude is separable from baseline cognitive capacity. The findings suggest that CSL aptitude impacts the neuropsychological profile in MS, and may be a factor underlying variance in cognitive resiliency.
 BACKGROUND: The role of infectious agents, including Chlamydia pneumoniae (Cpn), in the development of multiple sclerosis (MS), is still a matter of major contention. OBJECTIVE: This meta-analysis study aimed to assess the actual involvement of Cpn in MS development. METHODS: We undertook a search of international scientific databases to identify eligible studies. We used a random-effects meta-analysis model (REM) to generate the pooled odds ratio (OR) and 95% confidence intervals (CIs). Heterogeneity was calculated using the I(2) statistic. Sensitivity and subgroup analyses were applied to assess the effects of study characteristics and socio-demographic variables on the pooled OR. RESULTS: We identified 37 studies comprising 51 datasets that satisfied the inclusion criteria. Considering diagnostic methods for Cpn, 26 and 25 datasets used PCR- and serological-based methods, respectively. In PCR-based datasets, REM showed a significant positive association between Cpn infection and the development of MS (OR, 5.29; 95% CI, 3.12-8.97), while a non-significant positive association was achieved in serological-based datasets (OR, 1.34; 95% CI, 0.88-2.03). In subgroup analyses on PCR-based datasets, results were significant for both CSF (OR, 5.70) and serum (OR, 4.84) samples; both healthy (OR, 16.11) and hospital-based (OR, 2.88) controls; and both moderate (OR, 5.14) and high (OR, 5.48) quality studies. In serological-based datasets, only those that used CSF samples yielded significant results (OR, 3.41). CONCLUSIONS: Our findings verify the significant positive relationship between Cpn infection and MS. We advocate prospective cohort studies with lifelong follow-ups and also experimental studies to better understand the role of Cpn in MS development.
 BACKGROUND: In the OPTIMUM trial in patients with relapsing MS, treatment differences in annualized relapse rate (ARR, 0.088) and change in fatigue at week 108 (3.57 points, measured using the Fatigue Symptoms and Impacts Questionnaire-Relapsing Multiple Sclerosis, symptom domain (FSIQ-RMS-S)) favored ponesimod over teriflunomide. However, the importance of the fatigue outcome to patients was unclear. OBJECTIVE: To assess the importance of the OPTIMUM FSIQ-RMS-S results using data from an MS discrete choice experiment (DCE). METHODS: The DCE included components to correlate levels of physical and cognitive fatigue with FSIQ-RMS-S scores. Changes in relapses/year and time to MS progression equivalent to the treatment difference in fatigue in OPTIMUM were determined for similar fatigue levels as mean baseline fatigue in OPTIMUM. RESULTS: DCE participants would accept 0.06 more relapses/year or a 0.15-0.17 year decrease in time to MS progression for a 3.57-point difference in physical fatigue on the FSIQ-RMS-S. To improve cognitive fatigue by 3.57-points on the FSIQ-RMS-S, DCE participants would accept 0.09-0.10 more relapses/year or a 0.24-0.28 year decrease in time to MS progression. CONCLUSION: MS patients would accept 0.06 more relapses/year to change their fatigue by a similar magnitude as the between-treatment difference observed in the OPTIMUM trial.
 Myelin repair is an unrealized therapeutic goal in the treatment of multiple sclerosis (MS). Uncertainty remains about the optimal techniques for assessing therapeutic efficacy and imaging biomarkers are required to measure and corroborate myelin restoration. We analyzed myelin water fraction imaging from ReBUILD, a double-blind, randomized placebo-controlled (delayed treatment) remyelination trial, that showed a significant reduction in VEP latency in patients with MS. We focused on brain regions rich in myelin. Fifty MS subjects in two arms underwent 3T MRI at baseline and months 3 and 5. Half of the cohort was randomly assigned to receive treatment from baseline through 3 mo, whereas the other half received treatment from 3 mo to 5 mo post-baseline. We computed myelin water fraction changes occurring in normal-appearing white matter of corpus callosum, optic radiations, and corticospinal tracts. An increase in myelin water fraction was documented in the normal-appearing white matter of the corpus callosum, in correspondence with the administration of the remyelinating treatment clemastine. This study provides direct, biologically validated imaging-based evidence of medically induced myelin repair. Moreover, our work strongly suggests that significant myelin repair occurs outside of lesions. We therefore propose myelin water fraction within the normal-appearing white matter of the corpus callosum as a biomarker for clinical trials looking at remyelination.
 Multiple sclerosis (MS) is a common neurological disease, especially among people of young working age, and the number of MS cases registered in the world and in the Russian Federation tends to increase. The pathogenesis of MS is based on the theory of damage to its own myelin sheath as a result of activation of autoreactive T cells, which also leads to damage to both oligodendrocytes and axons. In addition, the role of vascular factor in the pathogenesis of MS is discussed in the literature periodically and several areas of research of vascular dysfunction in patients are identified. This article provides a retrospective analysis of the available literature dating from the 19th century to the present time in order to find the relationship between MS and changes in venous circulation.

 OBJECTIVES: To identify genes that confer MS risk via the alteration of cis-regulated protein abundance and verify their aberrant expression in human brain. METHODS: Utilizing a two-stage proteome-wide association study (PWAS) design, MS GWAS data (N = 41,505) was respectively integrated with two distinct human brain proteomes from the dorsolateral prefrontal cortex, including ROSMAP (N = 376) in the discovery stage and Banner (N = 152) in the confirmation stage. In the following, Bayesian colocalization analysis was conducted for GWAS and protein quantitative trait loci signals to prioritize candidate genes. Differential expression analysis was then used to verify the dysregulation of risk genes in white matter and gray matter for evidence at the transcription level. RESULTS: A total of 51 genes whose protein abundance had association with the MS risk were identified, of which 18 genes overlapped in the discovery and confirmation PWAS. Bayesian colocalization indicated six causal genes with genetic risk variants for the MS risk. The differential expression analysis of SHMT1 (P(FDR)  = 4.82 × 10(-2) ), FAM120B (P(FDR)  = 8.13 × 10(-4) ) in white matter and ICA1L (P(FDR)  = 3.44 × 10(-2) ) in gray matter confirmed the dysregulation at the transcription level. Further investigation of expression found SHMT1 significantly up-regulated in white matter lesion, and FAM120B up-regulated in both white matter lesion and normal appearing white matter. ICA1L was down-regulated in both gray matter lesion and normal appearing gray matter. INTERPRETATION: Dysregulation of SHMT1, FAM120B and ICA1L may confer MS risk. Our findings shed new light on the pathogenesis of MS and prioritized promising targets for future therapy research.
 BACKGROUND: Characterization of cognitive impairment (CI) in multiple sclerosis into distinct phenotypes holds promise for individualized treatments and biomarker exploration. OBJECTIVE: Apply a previously validated, neuropsychologically driven diagnostic algorithm to identify a taxonomy of the type of cognitive phenotypes in multiple sclerosis. METHODS: An algorithm developed and validated in other neurological diseases was applied to a cohort of 1281 people with multiple sclerosis who underwent clinical neuropsychological evaluation across three multiple sclerosis centers. A domain was marked impaired if scores on two tests within the domain fell below one of the two thresholds of interest (compared to controls; -1.0 SD and -1.5 SD below the mean). Results were then tabulated for each participant to determine the type of impairments across the sample. RESULTS: At -1 SD threshold, 48.7% were intact, 21.6% had single-domain, 14.3% bi-domain, and 15.4% multi-domain impairment. At -1.5 SD threshold, 72.9% were intact, 14.0% had single-domain, 8.2% bi-domain, and 5.0% multi-domain impairment. Processing speed was the most frequent single-domain impairment, followed by executive function and memory. CONCLUSIONS: These findings advance the taxonomy of cognitive phenotypes in multiple sclerosis and clarify the type and distribution of possible cognitive diagnoses, pave the way for further investigation of associated biomarkers, and provide clinically meaningful information to guide individualized treatment and rehabilitation.
 BACKGROUND: Neurologists' perceptions of the presence of cognitive impairment (CI) in people with multiple sclerosis (PwMS) may not always align with findings of objective cognitive assessment. The accuracy of self-reported CI in PwMS can also be highly variable across individuals, and may not align with objective measurement of cognitive disturbances. Research suggests that additional factors impact perceived cognitive ability, such as depression and fatigue. Objective cognitive screening regardless of patient or neurologist perception has been recommended but still is often limited in routine care. Moreover, comprehensive neuropsychological assessment is even less routinely done. OBJECTIVE: To explore how neurologists' perceptions of PwMS' CI compare to the perception of the patient by determining whether PwMS and their clinicians are accurate in detecting the presence and degree of CI as defined by a multi-domain validated computerized test battery in PwMS, as well as investigate what factors influence perception of CI in each group. METHODS: PwMS completed a computerized multi-domain cognitive testing battery, and self-reported measures of disease impact (MSIS-29), fatigue (MFIS), and depression (BDI-II). Disability was assessed by the clinician using the Expanded Disability Status Scale (EDSS). Clinicians and patients also provided an estimation of cognitive deficits along a Likert scale. RESULTS: In this cohort of PwMS (N=202, age range: 20 to 88, gender: 71% female), their level of accuracy in detecting attention deficits (k = -.028, p = .010) was low but statistically significant. In contrast, clinicians' accuracy in detecting global CI (k = -.037, p < .001) and a number of specific domain deficits was moderate. Fatigue (p < .001) and cognitive performance (p = .012) significantly predicted patient perceived cognitive deficits. Clinician perceived cognitive performance was significantly predicted by multiple factors: cognitive scores (p < .001), physical disability (p = .011), age (p = .021), and depression (p = .038). CONCLUSION: The need to objectively screen for CI in PwMS, regardless of perception, can be aided by a better understanding of the agreement and discrepancies between the patient and clinician regarding perceived cognitive disturbances and the presence of CI defined by a multi-dimensional objective screening battery.
 INTRODUCTION: Optical coherence tomography (OCT)-derived peripapillary retinal nerve fiber layer (pRNFL) and ganglion cell+inner plexiform layer (GCIPL) thickness inter-eye differences (IEDs) are robust measurements for identifying clinical history acute ON in people with MS (PwMS). This study investigated the utility and durability of these measures as longitudinal markers to identify optic nerve lesions. METHODS: Prospective, multi-center international study of PwMS (with/without clinical history of ON) and healthy controls. Data from two sites in the International MS Visual System Consortium (IMSVISUAL) were analyzed. Mixed-effects models were used to compare inter-eye differences based on MS and acute ON history. RESULTS: Average age of those with MS (n = 210) was 39.1 ± 10.8 and 190 (91%) were relapsing-remitting. Fifty-nine (28.1%) had a history of acute unilateral ON, while 9/210 (4.3%) had >1 IB episode. Median follow-up between OCT scans was 9 months. By mixed-effects modeling, IEDs were stable between first and last visits within groups for GCIPL for controls (p = 0.18), all PwMS (p = 0.74), PwMs without ON (p = 0.22), and PwMS with ON (p = 0.48). For pRNFL, IEDs were within controls (p = 0.10), all PwMS (p = 0.53), PwMS without ON history (p = 0.98), and PwMS with history of ON (p = 0.81). CONCLUSION: We demonstrated longitudinal stability of pRNFL and GCIPL IEDs as markers for optic nerve lesions in PwMS, thus reinforcing the role for OCT in demonstrating optic nerve lesions.
 BACKGROUND AND PURPOSE: The discovery of glymphatic function in the human brain has generated interest in waste clearance mechanisms in neurological disorders such as multiple sclerosis (MS). However, noninvasive in vivo functional assessment is currently lacking. This work studies the feasibility of a novel intravenous dynamic contrast MRI method to assess the dural lymphatics, a purported pathway contributing to glymphatic clearance. METHODS: This prospective study included 20 patients with MS (17 women; age = 46.4 [27, 65] years; disease duration = 13.6 [2.1, 38.0] years, expanded disability status score (EDSS) = 2.0 [0, 6.5]). Patients were scanned on a 3.0T MRI system using intravenous contrast-enhanced fluid-attenuated inversion recovery MRI. Signal in the dural lymphatic vessel along the superior sagittal sinus was measured to calculate peak enhancement, time to maximum enhancement, wash-in and washout slopes, and the area under the time-intensity curve (AUC). Correlation analysis was performed to examine the relationship between the lymphatic dynamic parameters and the demographic and clinical characteristics, including the lesion load and the brain parenchymal fraction (BPF). RESULTS: Contrast enhancement was detected in the dural lymphatics in most patients 2-3 min after contrast administration. BPF had a significant correlation with AUC (p < .03), peak enhancement (p < .01), and wash-in slope (p = .01). Lymphatic dynamic parameters did not correlate with age, BMI, disease duration, EDSS, or lesion load. Moderate trends were observed for correlation between patient age and AUC (p = .062), BMI and peak enhancement (p = .059), and BMI and AUC (p = .093). CONCLUSION: Intravenous dynamic contrast MRI of the dural lymphatics is feasible and may be useful in characterizing its hydrodynamics in neurological diseases.
 BACKGROUND: There is a paucity of information on maternal multiple sclerosis (MS) and risk of adverse pregnancy and perinatal outcomes. OBJECTIVE: The aim of this study was to determine the association between MS and risks of adverse pregnancy and perinatal outcomes in women with MS. In women with MS, the influence of exposure to disease-modifying therapy (DMT) was also investigated. METHODS: Population-based retrospective cohort study on singleton births to mothers with MS and matched MS-free mothers from the general population in Sweden between 2006 and 2020. Women with MS were identified through Swedish health care registries, with MS onset before child's birth. RESULTS: Of 29,568 births included, 3418 births were to 2310 mothers with MS. Compared with MS-free controls, maternal MS was associated with increased risks of elective caesarean sections, instrumental delivery, maternal infection and antepartum haemorrhage/ placental abruption. Compared with offspring of MS-free women, neonates of mothers with MS were at increased risks of medically indicated preterm birth and being born small for gestational age. DMT exposure was not associated with increased risks of malformations. CONCLUSIONS: While maternal MS was associated with a small increased risk of few adverse pregnancy and neonatal outcomes, DMT exposure close to pregnancy was not associated with major adverse outcomes.
 BACKGROUND: Multiple Sclerosis (MS) affects people in their most productive years of life. Consequently, MS can substantially affect employment and work-related outcomes. OBJECTIVES: This study characterizes productivity loss and employment status of people with multiple sclerosis (pwMS) and investigates associated factors. METHODS: We used baseline data collected as part of the Canadian Prospective Cohort Study to Understand Progression in Multiple Sclerosis (CanProCo). Using the Valuation of Lost Productivity questionnaire, we measured MS-related paid work productivity loss for those employed, productivity losses incurred by those unemployed (i.e. lost employment time), and unpaid work productivity losses for all. A set of sociodemographic, disease, and performance-related factors were investigated using a two-part regression model for productivity loss and a multinomial logistic model for employment status. RESULTS: From the cohort of 888 pwMS enrolled at baseline (mostly showing mild to moderate disability), 75% were employed, and of those unemployed, 69% attributed their unemployment to health-related issues. Total productivity loss over a 3-month period averaged 64 and 395 hours for those employed and unemployed, respectively. Some factors that affected productivity loss and employment status included use of disease-modifying therapies, fatigue, and performance indicators such as cognitive processing speed. CONCLUSION: Productivity loss experienced by employed and unemployed pwMS is substantial. Targeting the identified modifiable factors is likely to improve work productivity and permanence of MS patients in the workforce.
 Multiple sclerosis (MS) is a chronic inflammatory and degenerative disease of the central nervous system afflicting nearly three million individuals worldwide. Neuroimmune interactions between glial, neural, and immune cells play important roles in MS pathology and offer potential targets for therapeutic intervention. Here, we review underlying risk factors, mechanisms of MS pathogenesis, available disease modifying therapies, and examine the value of emerging technologies, which may address unmet clinical needs and identify novel therapeutic targets.
 Multiple sclerosis (MS), an autoimmune disease, has been considered an inflammatory disorder of the central nervous system (CNS) with demyelination and axonal damage. Although there are certain first-line therapies to treat MS, their unsatisfactory efficacy is partly due to the limited CNS access after systemic administration. Besides, there is an urgent need to treat MS by enhancing remyelination or neuroprotection, or dampen the activity of microglia. Astragaloside IV (ASI) bears anti-inflammatory, antioxidant, remyelination and neuroprotective activity. While its poor permeability, relatively high molecular weight and low lipophilicity restrict it to reach the brain. Therefore, β-asarone modified ASI loaded chitosan nanoparticles (ASI-βCS-NP) were prepared to enhance the nose-to-brain delivery and therapeutic effects of ASI on EAE mice. The prepared ASI-βCS-NP showed mean size of about 120 nm, and zeta potential from +19 to +25 mV. DiR-βCS-NP was confirmed with good nose-to-brain targeting ability. After intranasal administration, the ASI-βCS-NP significantly reduced behavioral scores, decreased weight loss, suppressed inflammatory infiltration and astrocyte/microglial activation, reduced demyelination and increased remyelination on a mice EAE model. Our findings indicate that ASI-βCS-NP may be a potent treatment for MS after nose-to-brain drug delivery.
 The prevalence of multiple sclerosis (MS) has significantly increased in recent decades. People with MS have a high risk of falling; these falls may lead to serious injuries, affecting their quality of life PURPOSE: The aim of this study is to assess the factors affecting falls in people with MS and map out the most significant ones. This study also aims to determine whether fatigue has a moderation effect and balance has a mediation effect on falls in people with MS METHODS: In total, 103 people with MS with a mean age of 32.09 ± 7.17 were enrolled. All subjects were assessed for multiple variables including balance using the Berg Balance Scale (BBS), speed of gait using the Timed Up and Go (TUG) test, fear of falling using the Falls Efficacy Scale-International (FES-I), level of fatigue using the Modified Fatigue Impact Scale (MFIS), and lower limb muscle strength using a handheld digital dynamometer RESULTS: Simple binary logistic regression analysis showed significant results for BBS (OR: 10.88; 95% CI: 4.24-27.96; p < 0.0001), TUG (OR: 1.18; 95% CI: 1.09-1.28; p < 0.0001), FES-I (OR: 1.06; 95% CI: 1.02-1.10; p = 0.001), and MFIS (OR: 1.04; 95% CI: 1.02-1.07; p < 0.0001) as factors affecting falls. According to multivariate analysis, balance (OR: 3.924; 95% CI: 1.307-11.780, p = 0.015), speed of gait (OR: 1.122; 95% CI: 1.023-1.231; p = 0.015), and fatigue (OR: 1.029; 95% CI: 1.002-1.058; p = 0.038) were the strongest predicting factors of falls. Hayes's PROCESS analysis showed that fatigue had a significant moderation effect on the relationship between gait speed and falls (MFIS; β; 0.10; p < 0.0001; 95% CI: 0.07-0.14) and balance had a mediation effect on the relationship between gait speed and falls (BBS; indirect effect; 0.08; 95% CI: 0.02-0.13) CONCLUSIONS: People with MS with impaired balance, slower gait speeds, higher levels of fatigue, and a fear of falling were at a high risk of falling. The relationship between gait speed and falls can be mediated by impaired balance and moderated by the level of fatigue. Our data suggest that targeting balance and fatigue while developing rehabilitation interventions could decrease the incidence of falls among people with MS.
 Multiple sclerosis may present an increased risk for venous thromboembolism. Ophthalmological symptoms include loss of vision, visual field loss, changes in color vision, diplopia and nystagmus. First-line treatments for multiple sclerosis are beta-interferon, glatiramer acetate, dimethyl fumarate and teriflunomide. To the best of our knowledge, no ophthalmologic side effects have been reported with glatiramer acetate. We present a woman with multiple sclerosis on glatiramer acetate therapy with a central retinal vein occlusion in the absence of other risk factors.
 Multiple sclerosis (MS) is an autoimmune disease of the CNS, featuring inflammation and demyelination with variable recovery. In this issue of the JCI, Kapell, Fazio, and authors address the potential for targeting neuron-oligodendrocyte potassium shuttling at the nodes of Ranvier as a neuroprotective strategy during inflammatory demyelination of the CNS in experimental MS. Their extensive and impressive study could serve as a template for defining the physiologic properties of a putative protective pathway. The authors examined MS features in existent disease models, investigated the impact of pharmacologic intervention, and evaluated its status in tissues from patients with MS. We await future studies that will tackle the challenge of translating these findings into a clinical therapy.
 Neurologists have long recognized the importance of the visual system in the diagnosis and monitoring of neurologic disorders. This is particularly true because approximately 50% of the brain's pathways subserve afferent and efferent aspects of vision. During the past 30 years, researchers and clinicians have further refined this concept to include investigation of the visual system for patients with specific neurologic diagnoses, including multiple sclerosis (MS), concussion, Parkinson disease (PD), and conditions along the spectrum of Alzheimer disease (AD, mild cognitive impairment, and subjective cognitive decline). This review highlights the visual "toolbox" that has been developed over the past 3 decades and beyond to capture both structural and functional aspects of vision in neurologic disease. Although the efforts to accelerate the emphasis on structure-function relationships in neurologic disorders began with MS during the early 2000s, such investigations have broadened to recognize the need for outcomes of visual pathway structure, function, and quality of life for clinical trials of therapies across the spectrum of neurologic disorders. This review begins with a patient case study highlighting the importance using the most modern technologies for visual pathway assessment, including optical coherence tomography. We emphasize that both structural and functional tools for vision testing can be used in parallel to detect what might otherwise be subclinical events or markers of visual and, perhaps, more global neurologic decline. Such measures will be critical because clinical trials and therapies become more available across the neurologic disease spectrum.
 BACKGROUND: Rehabilitation is an essential health care service and a critical component of comprehensive multiple sclerosis (MS) care. OBJECTIVE: As part of a 2-day meeting hosted by the International Advisory Committee on Clinical Trials in MS in December 2022, a panel initiated a discussion on the conceptual and practical issues related to selecting intermediate outcomes for clinical trials of MS rehabilitation interventions. RESULTS: The overarching goal of rehabilitation - optimal functioning - was acknowledged as a complex biopsychosocial phenomenon that varies with patient priorities and environmental context. This complexity means that multiple causal pathways and potential intermediate outcomes must be carefully considered during the design of clinical trials in MS rehabilitation that aim to improve functioning. In addition, practical issues must be considered such as psychometric properties of outcome measures, measure type, and characteristics of the target population, including severity of dysfunction. CONCLUSION: This article uses the International Classification of Functioning, Disability and Health as a foundation for determining relevant intermediate outcomes for clinical trials of MS rehabilitation interventions.
 While the genetics of MS risk susceptibility are well-described, and recent progress has been made on the genetics of disease severity, the genetics of disease progression remain elusive. We therefore investigated the genetic determinants of MS progression on longitudinal brain MRI: change in brain volume (BV) and change in T2 lesion volume (T2LV), reflecting progressive tissue loss and increasing disease burden, respectively. We performed genome-wide association studies of change in BV (N = 3401) and change in T2LV (N = 3513) across six randomized clinical trials from Biogen and Roche/Genentech: ADVANCE, ASCEND, DECIDE, OPERA I & II, and ORATORIO. Analyses were adjusted for randomized treatment arm, age, sex, and ancestry. Results were pooled in a meta-analysis, and were evaluated for enrichment of MS risk variants. Variant colocalization and cell-specific expression analyses were performed using published cohorts. The strongest peaks were in PTPRD (rs77321193-C/A, p = 3.9 × 10(-7)) for BV change, and NEDD4L (rs11398377-GC/G, p = 9.3 × 10(-8)) for T2LV change. Evidence of colocalization was observed for NEDD4L, and both genes showed increased expression in neuronal and/or glial populations. No association between MS risk variants and MRI outcomes was observed. In this unique, precompetitive industry partnership, we report putative regions of interest in the neurodevelopmental gene PTPRD, and the ubiquitin ligase gene NEDD4L. These findings are distinct from known MS risk genetics, indicating an added role for genetic progression analyses and informing drug discovery.
 PURPOSE: To quantify the associations of myopia with longitudinal changes in retinal layer thicknesses in people with multiple sclerosis (PwMS) and healthy controls (HC). METHODS: A cohort of PwMS and HC with recorded refractive error (RE) prospectively scanned on Cirrus HD-OCT at the Johns Hopkins MS Center was assessed for inclusion. Exclusion criteria included OCT follow-up < 6 months, ocular comorbidities, incidental OCT pathologies, and inadequate scan quality. Eyes were classified as having high myopia (HM) (RE≤ -6 diopters), low myopia (LM) (RE> -6 and ≤ -3 diopters), or no myopia (NM) (RE> -3 and ≤ +2.75). Linear mixed-effects regression models were used in analyses. RESULTS: A total of 213 PwMS (eyes: 67 HM, 98 LM, 207 NM) and 80 HC (eyes: 26 HM, 37 LM, 93 NM) were included. Baseline average ganglion cell/inner plexiform (GCIPL) and peri-papillary retinal nerve fiber layer (pRNFL) thicknesses were lower in MS HM compared with MS NM (diff: -3.2 µm, 95% CI: -5.5 to -0.8, p = 0.008 and -5.3 µm, 95% CI: -9.0 to -1.7, p = 0.004, respectively), and similarly in HC HM, as compared with HC NM. Baseline superior, inferior, and nasal pRNFL thicknesses were lower in HM compared with NM, while temporal pRNFL thickness was higher, both in MS and HC (MS: 7.1 µm, 95% CI: 2.7-11.6, p = 0.002; HC: 4.7 µm, 95% CI: -0.3 to 9.7, p = 0.07). No longitudinal differences in rates of GCIPL change were noted between HM and LM vs. NM, either in MS or HC. CONCLUSION: Cross-sectional differences in average GCIPL and pRNFL thicknesses are commonly seen in people with HM as compared to reference normative values from people with NM and can lead to false attribution of pathology if RE is not taken into account. However, our study suggests that longitudinal changes in average GCIPL thickness in PwMS with myopia are similar in magnitude to PwMS with NM, and therefore are appropriate for monitoring disease-related pathology.
 Symptomatic treatment of Multiple Sclerosis (MS) is crucial, since it helps to lessen the limitations that affect patients' daily lives. Tremors are a significant and frequent symptom in MS patients. However, there is still a lack of evidence supporting a specific therapeutic approach for MS patients' tremors. A 41-year-old man with a history of MS is presented in this study. He exhibited stiffness and tremors at the follow-up clinic, which affected his daily activities. For his spasticity, he received intrathecal baclofen (ITB). The patient's symptoms responded well to this treatment, as both stiffness and tremors decreased. In an MS patient, ITB therapy thus unexpectedly reduced and improved tremor symptoms.
 Transorbital sonography (TOS) could be a swift and convenient method to detect the atrophy of the optic nerve, possibly providing a marker that might reflect other quantitative structural markers of multiple sclerosis (MS). Here we evaluate the utility of TOS as a complementary tool for assessing optic nerve atrophy, and investigate how TOS-derived measures correspond to volumetric brain markers in MS. We recruited 25 healthy controls (HC) and 45 patients with relapsing-remitting MS and performed B-mode ultrasonographic examination of the optic nerve. Patients additionally underwent MRI scans to obtain T1-weighted, FLAIR and STIR images. Optic nerve diameters (OND) were compared between HC, MS patients with and without history of optic neuritis (non-ON) using a mixed-effects ANOVA model. The relationship between within-subject-average OND and global and regional brain volumetric measures was investigated using FSL SIENAX, voxel-based morphometry and FSL FIRST. OND was significantly different between HC-MS (HC = 3.2 ± 0.4 mm, MS = 3 ± 0.4 mm; p < 0.019) and we found significant correlation between average OND and normalised whole brain (β = 0.42, p < 0.005), grey matter (β = 0.33, p < 0.035), white matter (β = 0.38, p < 0.012) and ventricular cerebrospinal fluid volume (β = - 0.36, p < 0.021) in the MS group. History of ON had no impact on the association between OND and volumetric data. In conclusion, OND is a promising surrogate marker in MS, that can be simply and reliably measured using TOS, and its derived measures correspond to brain volumetric measures. It should be further explored in larger and longitudinal studies.
 BACKGROUND: Pathologically specific MRI measures may elucidate in-vivo the heterogeneous processes contributing to cognitive impairment in multiple sclerosis (MS). PURPOSE: Using diffusion tensor and neurite orientation dispersion and density imaging (NODDI), we explored the contribution of focal lesions and normal-appearing (NA) tissue microstructural abnormalities to cognitive impairment in MS. METHODS: One hundred and fifty-two MS patients underwent 3 T brain MRI and a neuropsychological evaluation. Forty-eight healthy controls (HC) were also scanned. Fractional anisotropy (FA), mean diffusivity (MD), intracellular volume fraction (ICV_f) and orientation dispersion index (ODI) were assessed in cortical and white matter (WM) lesions, thalamus, NA cortex and NAWM. Predictors of cognitive impairment were identified using random forest. RESULTS: Fifty-two MS patients were cognitively impaired. Compared to cognitively preserved, impaired MS patients had higher WM lesion volume (LV), lower normalized brain volume (NBV), cortical volume (NCV), thalamic volume (NTV), and WM volume (p ≤ 0.021). They also showed lower NAWM FA, higher NAWM, NA cortex and thalamic MD, lower NAWM ICV_f, lower WM lesion ODI, and higher NAWM ODI (false discovery rate-p ≤ 0.026). Cortical lesion number and microstructural abnormalities were not significantly different. The best MRI predictors of cognitive impairment (relative importance) (out-of-bag area under the curve = 0.727) were NAWM FA (100%), NTV (96.0%), NBV (84.7%), thalamic MD (43.4%), NCV (40.6%), NA cortex MD (26.0%), WM LV (23.2%) and WM lesion ODI (17.9%). CONCLUSIONS: Our multiparametric MRI study including NODDI measures suggested that neuro-axonal damage and loss of microarchitecture integrity in focal WM lesions, NAWM, and GM contribute to cognitive impairment in MS.
 BACKGROUND: Neurologically-based muscle weakness is a common symptom in people with multiple sclerosis MS (MS), who may also exhibit muscle morphology changes and intrinsic muscle dysfunction. Diagnostic ultrasound (sonography) is a non-invasive, inexpensive, and clinically feasible method to measure muscle morphology. The purpose of this study was to investigate possible asymmetries in lower limb muscle morphology and performance in people with MS, and to assess the relationships of muscle morphology measures with individual patient characteristics, muscle performance, and functional mobility. METHODS: This cross-sectional study was conducted at the Washington, DC Veterans Affairs Medical Center. The study participants were 29 Veterans with MS (52% female, 79% African-American, 48.6 ± 11.2 years old, Mean Expanded Disability Status Scale: 3.6 ± 1.4) who completed seated knee extension isokinetic strength and power tests, functional assessments (Timed 25-Foot Walk - T25FW, 5-Times Sit-to-Stand - 5STS), and quantitative B-mode ultrasound image acquisition of the rectus femoris muscle to derive morphology measures (thickness and echogenicity). The limb with weaker knee extension strength was identified as the more-involved limb. Differences between the more and less-involved limb were quantified using a t-test for all muscle morphology and muscle performance measures. Relationships between muscle morphology and patient characteristics, muscle performance, and functional mobility were evaluated using bivariate and multivariate analyses. RESULTS: The rectus femoris thickness from the more-involved limb was lower (p<0.001) than that of the less-involved limb, whereas echogenicity was not different between the two limbs (p=0.147). Rectus femoris thickness of the more-involved limb was directly related to age (r=-0.63, p<0.001), muscle strength (r=0.53, p=0.003) and power (r=0.53, p=0.003), and gait speed (r=0.42, p=0.024); whereas its echogenicity was positively associated only with muscle strength (r=-0.46, p=0.013) and power (r=-0.50, p=0.006). Together rectus femoris thickness and echogenicity of the more involved limb explained 44% and 48% of the variance in muscle strength and power, respectively (p<0.001). CONCLUSION: This study supports the ability of sonography to measure muscle morphology in people with MS, identify asymmetries, and quantify associations with important clinical correlates. Compared with more invasive and costly alternatives, sonography is a clinically feasible, relatively low-cost tool that can be used to assess muscle morphology in people with MS. Further research is warranted to determine the potential clinical utility of sonographic measures of muscle morphology in evaluating changes due to disease progression or therapeutic interventions in this population.

 Recurrent neuroinflammation in relapsing-remitting MS (RRMS) is thought to lead to neurodegeneration, resulting in progressive disability. Repeated magnetic resonance imaging (MRI) of the brain provides non-invasive measures of atrophy over time, a key marker of neurodegeneration. This study investigates regional neurodegeneration of the brain in recently-diagnosed RRMS using volumetry and voxel-based morphometry (VBM). RRMS patients (N = 354) underwent 3T structural MRI <6 months after diagnosis and 1-year follow-up, as part of the Scottish multicentre 'FutureMS' study. MRI data were processed using FreeSurfer to derive volumetrics, and FSL for VBM (grey matter (GM) only), to establish regional patterns of change in GM and normal-appearing white matter (NAWM) over time throughout the brain. Volumetric analyses showed a decrease over time (q<0.05) in bilateral cortical GM and NAWM, cerebellar GM, brainstem, amygdala, basal ganglia, hippocampus, accumbens, thalamus and ventral diencephalon. Additionally, NAWM and GM volume decreased respectively in the following cortical regions, frontal: 14 out of 26 regions and 16/26; temporal: 18/18 and 15/18; parietal: 14/14 and 11/14; occipital: 7/8 and 8/8. Left GM and NAWM asymmetry was observed in the frontal lobe. GM VBM analysis showed three major clusters of decrease over time: 1) temporal and subcortical areas, 2) cerebellum, 3) anterior cingulum and supplementary motor cortex; and four smaller clusters within the occipital lobe. Widespread GM and NAWM atrophy was observed in this large recently-diagnosed RRMS cohort, particularly in the brainstem, cerebellar GM, and subcortical and occipital-temporal regions; indicative of neurodegeneration across tissue types, and in accord with limited previous studies in early disease. Volumetric and VBM results emphasise different features of longitudinal lobar and loco-regional change, however identify consistent atrophy patterns across individuals. Atrophy measures targeted to specific brain regions may provide improved markers of neurodegeneration, and potential future imaging stratifiers and endpoints for clinical decision making and therapeutic trials.
 BACKGROUND: With millions of victims worldwide, multiple sclerosis is the second most common cause of disability among young adults. Although formidable advancements have been made in understanding the disease, the neurodegeneration associated with multiple sclerosis is only partially counteracted by current treatments, and effective therapy for progressive multiple sclerosis remains an unmet need. Therefore, new approaches are required to delay demyelination and the resulting disability and to restore neural function by promoting remyelination and neuronal repair. AIMS: The article reviews the latest literature in this field. MATERIALS AND METHODS: The fibroblast growth factor (FGF) signaling pathway is a promising target in progressive multiple sclerosis. DISCUSSION: FGF signal transduction contributes to establishing the oligodendrocyte lineage, neural stem cell proliferation and differentiation, and myelination of the central nervous system. Furthermore, FGF signaling is implicated in the control of neuroinflammation. In recent years, interventions targeting FGF, and its receptor (FGFR) have been shown to ameliorate autoimmune encephalomyelitis symptoms in multiple sclerosis animal models moderately. CONCLUSION: Here, we summarize the recent findings and investigate the role of FGF/FGFR signaling in the onset and progression, discuss the potential therapeutic advances, and offer fresh insights into managing multiple sclerosis.
 Context: To counteract cumulative weight gain, a female veteran with multiple sclerosis with spinal cord involvement initiated a program of time restricted eating (TRE), eating all calories within a daily 6-hour window.Findings: The patient experienced significant weight loss and improved cardiometabolic markers.Conclusion/Clinical Relevance: Additional research is warranted to study TRE to mitigate obesity.
 BACKGROUND: People with MS (PwMS) can experience a number of diverse needs which may be met by community-based services such as those delivered by MS Ireland (MSI), where Community Workers (CWs) provide support to PwMS on an individualised basis. However, while such support may be critical in helping PwMS adapt and cope with the challenges of living with MS, there has been little evaluation of the outcomes and impacts of this service to date. This study aimed to explore the perceived effectiveness and impacts of community work from the perspectives of both PwMS and CWs. METHODS: Using stakeholder engagement and public and patient involvement (PPI), two surveys were developed for (1) CWs, and (2) services users of MSI. A series of open and closed questions centred on the effectiveness of community work in meeting twelve distinct categories of needs taken from an adapted framework of rehabilitation and healthcare needs of PwMS. Both CWs and service users rated the extent to which these various needs were met through community work, as well as describing the mechanisms by which needs were met, and the challenges faced in meeting these needs. Separately, both groups described the perceived impacts of community work using open-text responses. RESULTS: Fifteen CWs and 367 PwMS, 269 (73%) of whom knew their CW, participated. Both groups rated community work positively in meeting the needs for information, emotional/psychological support and coordination of care, with lower perceived capacity for community work to meet needs for employment accommodations, caregiver support and homecare. Mann Whitney U tests did not find any significant difference between groups in the perceived capacity of community work to meet the various needs examined (p>.05). Core mechanisms by which CWs meet needs are by signposting to relevant services, listening, and facilitating peer support. Difficulty accessing external services was the primary challenge identified in meeting needs. Positive impacts of community work included the role that CWs play in fostering confidence and acceptance of MS, and in helping service users overcome the challenges of MS. CONCLUSION: Results suggest how CWs can help meet the needs of PwMS, while also highlighting the numerous positive impacts that community work has for this group. While it is clear that a number of unmet needs may remain due to a lack of access to other external services, this study shows how community-based services may play an important role in helping PwMS adapt to living with MS.

 OBJECTIVE: Multiple sclerosis (MS) is associated with cognitive impairment (CI) such as slowed information processing speed (IPS). Currently, no immunocellular or molecular markers have been established in cerebrospinal fluid and serum analysis as surrogate biomarkers with diagnostic or predictive value for the development of CI. This systematic review and meta-analysis aims to sum up the evidence regarding currently discussed markers for CI in MS. METHODS: A literature search was conducted on molecular biomarkers of CI in MS, such as neurofilament light chain, chitinases, and vitamin D. RESULTS: 5543 publications were screened, of which 77 entered the systematic review. 13 studies were included in the meta-analysis. Neurofilament light chain (CSF: r(p) = -0.294, p = 0.003; serum: r(p) = -0.137, p = 0.001) and serum levels of vitamin D (r(p) = 0.190, p = 0.014) were associated with IPS outcomes. CONCLUSIONS: Neurofilament light chain and vitamin D are promising biomarkers to track impairments in IPS in MS. Further longitudinal research is needed to establish the use of molecular biomarkers to monitor cognitive decline.
 BACKGROUND: Limb apraxia is an acquired cognitive-motor disorder characterized by spatial and temporal disorganization of limb movements, negatively affecting the quality of life of patients, including those with multiple sclerosis (MS). Although recent studies have shown the potential role of VR in increasing cognitive and motor functions, only a few studies have been carried out on the rehabilitation of upper limb apraxia. Hence, our study aims to evaluate the potential efficacy of VR training to improve upper limb ideomotor apraxia in patients with MS. METHODS: One hundred and six patients, affected by secondary progressive MS, who attended our Robotic and Behavioral Neurorehabilitation Service from March 2019 to February 2020, were enrolled in this study and randomly divided into two groups: the control group (CG: 53 patients) performed traditional therapy whereas the experimental group (EG:53 patients) received training using semi-immersive VR. All patients underwent the same amount of cognitive training, 3 times a week for 8 weeks. They were submitted to a specific neuropsychological assessment before (T0) and after the rehabilitation treatment (T1). RESULTS: The VR training led to a significant improvement in global cognitive functions, with regard to constructive and ideomotor apraxia. On the contrary, the CG achieved significant improvements only in ideomotor apraxia. Moreover, only in the EG, we observed an improvement in the mood at the end of training. CONCLUSION: The present study demonstrates that VR rehabilitation can be an effective tool for the treatment of apraxia, which is a neuropsychological problem often underestimated in MS patients. Further studies with long-term follow-up periods are needed to confirm the effect of this promising approach.
 BACKGROUND: In relapsing-remitting multiple sclerosis (RRMS), early identification of suboptimal responders can prevent disability progression. OBJECTIVE: We aimed to develop and validate a dynamic score to guide the early decision to switch from first- to second-line therapy. METHODS: Using time-dependent propensity scores (PS) from a French cohort of 12,823 patients with RRMS, we constructed one training and two validation PS-matched cohorts to compare the switched patients to second-line treatment and the maintained patients. We used a frailty Cox model for predicting individual hazard ratios (iHRs). RESULTS: From the validation PS-matched cohort of 348 independent patients with iHR ⩽ 0.69, we reported the 5-year relapse-free survival at 0.14 (95% confidence interval (CI) 0.09-0.22) for the waiting group and 0.40 (95% CI 0.32-0.51) for the switched group. From the validation PS-matched cohort of 518 independent patients with iHR > 0.69, these values were 0.37 (95% CI 0.30-0.46) and 0.44 (95% CI 0.37-0.52), respectively. CONCLUSIONS: By using the proposed dynamic score, we estimated that at least one-third of patients could benefit from an earlier switch to prevent relapse.
 BACKGROUND: The in vivo relation between microglia activation and demyelination in multiple sclerosis is still unclear. OBJECTIVE: We combined (11)C-PBR28 positron emission tomography and rapid estimation of myelin for diagnostic imaging (REMyDI) to characterize the relation between these pathological processes in a heterogeneous MS cohort. METHODS: (11)C-PBR28 standardized uptake values normalized by a pseudo-reference region (SUVR) were used to measure activated microglia. A voxelwise analysis compared (11)C-PBR28 SUVR in the white matter of 38 MS patients and 16 matched healthy controls. The relative difference in SUVR served as a threshold to classify patients' lesioned, perilesional and normal-appearing white matter as active or inactive. REMyDI was acquired in 27 MS patients for assessing myelin content in active and inactive white matter and its relationship with SUVR. Finally, we investigated the contribution of radiological metrics to clinical outcomes. RESULTS: (11)C-PBR28 SUVR were abnormally higher in several white matter areas in MS. Myelin content was lower in active compared to inactive corresponding white matter regions. An inverse correlation between SUVR and myelin content was found. Radiological metrics correlated with both neurological and cognitive impairment. CONCLUSION: our data suggest an inverse relation of microglia activation and myelination, particularly in perilesional white matter tissue.
 The objective of this study was to determine the potential usefulness of an animal model to predict the appropriate dose of newly developed drugs for treating relapsing remitting multiple sclerosis (RRMS). Conversion of the lowest effective dose (LEffD) for mice and rats in the experimental autoimmune encephalomyelitis (EAE) model was used to predict the human effective dose utilizing the body surface area correction factor found in the 2005 US Food and Drug Administration (FDA) Guidance for Industry in selecting safe starting doses for clinical trials. Predictions were also tested by comparison with doses estimated by scaling up the LEffD in the model by the human to animal clearance ratio. Although initial proof-of-concept studies of oral fingolimod tested the efficacy and safety of 1.25 and 5 mg in treating RRMS, the EAE animal model predicted the approved dose of this drug, 0.5 mg daily. This approach would have also provided useful predictions of the approved human oral doses for cladribine, dimethyl fumarate, ozanimod, ponesimod, siponimod, and teriflunomide, drugs developed with more than one supposed mechanism of action. The procedure was not useful for i.v. dosed drugs, including monoclonal antibodies. We maintain that drug development scientists should always examine a simple allometric method to predict the therapeutic effective dose in humans. Then, following clinical studies, we believe that the animal model might be expected to yield useful predictions of other drugs developed to treat the same condition. The methodology may not always be predictive, but the approach is so simple it should be investigated.
 OBJECTIVE: Multiple sclerosis (MS) causes impairment of respiratory function, trunk control, and functional mobility. The purpose of this study was to investigate the relationship between functional mobility and respiratory function and trunk control in MS patients and to compare the findings with those in healthy individuals. METHODS: Thirty MS patients and 30 healthy subjects were included in this case-control study. All participants were evaluated with a pulmonary function test, maximal inspiratory and expiratory pressure (MIP, MEP), core stability tests, a lumbopelvic stability test (LST), a 2-minute walk test (2MWT), and the Timed Up and Go test (TUG). The disability level of the MS patients was assessed with the Expanded Disability Status Scale (EDSS). RESULTS: Respiratory function, respiratory muscle strength, trunk control, and functional mobility were lower in the MS patients than in the controls (p < 0.05). TUG values had a significant negative correlation and the 2MWT values had a significant positive correlation with MEP, core stability tests, and the LST (p < 0.05). Of the variance in the 2MWT distance, 69% was explained by the LST, EDSS, and MEP; of the variance in TUG time, 40% was explained by the EDSS and MEP (p < 0.05). CONCLUSIONS: To preserve and develop functional mobility in MS patients, approaches to increase respiratory function and trunk control should be included in rehabilitation programs. CLINICALTRIALS.GOV REGISTRATION NUMBER: NCT03826095.
 Background Cortical multiple sclerosis lesions are clinically relevant but inconspicuous at conventional clinical MRI. Double inversion recovery (DIR) and phase-sensitive inversion recovery (PSIR) are more sensitive but often unavailable. In the past 2 years, artificial intelligence (AI) was used to generate DIR and PSIR from standard clinical sequences (eg, T1-weighted, T2-weighted, and fluid-attenuated inversion-recovery sequences), but multicenter validation is crucial for further implementation. Purpose To evaluate cortical and juxtacortical multiple sclerosis lesion detection for diagnostic and disease monitoring purposes on AI-generated DIR and PSIR images compared with MRI-acquired DIR and PSIR images in a multicenter setting. Materials and Methods Generative adversarial networks were used to generate AI-based DIR (n = 50) and PSIR (n = 43) images. The number of detected lesions between AI-generated images and MRI-acquired (reference) images was compared by randomized blinded scoring by seven readers (all with >10 years of experience in lesion assessment). Reliability was expressed as the intraclass correlation coefficient (ICC). Differences in lesion subtype were determined using Wilcoxon signed-rank tests. Results MRI scans of 202 patients with multiple sclerosis (mean age, 46 years ± 11 [SD]; 127 women) were retrospectively collected from seven centers (February 2020 to January 2021). In total, 1154 lesions were detected on AI-generated DIR images versus 855 on MRI-acquired DIR images (mean difference per reader, 35.0% ± 22.8; P < .001). On AI-generated PSIR images, 803 lesions were detected versus 814 on MRI-acquired PSIR images (98.9% ± 19.4; P = .87). Reliability was good for both DIR (ICC, 0.81) and PSIR (ICC, 0.75) across centers. Regionally, more juxtacortical lesions were detected on AI-generated DIR images than on MRI-acquired DIR images (495 [42.9%] vs 338 [39.5%]; P < .001). On AI-generated PSIR images, fewer juxtacortical lesions were detected than on MRI-acquired PSIR images (232 [28.9%] vs 282 [34.6%]; P = .02). Conclusion Artificial intelligence-generated double inversion-recovery and phase-sensitive inversion-recovery images performed well compared with their MRI-acquired counterparts and can be considered reliable in a multicenter setting, with good between-reader and between-center interpretative agreement. Published under a CC BY 4.0 license. Supplemental material is available for this article. See also the editorial by Zivadinov and Dwyer in this issue.
 The central vein sign (CVS) has been proposed as a biomarker of multiple sclerosis (MS). In adult-onset MS (AOMS), 40%-threshold of CVS positive (+) lesions demonstrated high accuracy for MS diagnosis. However, CVS+ lesions' performance has not been characterized in paediatric-onset (POMS) yet. We compared the CVS contribution to MS diagnosis in 10 POMS and 12 disease-duration-matched AOMS patients. Three POMS patients did not meet the 40%-threshold, while all AOMS patients were correctly diagnosed as having MS. The high proportion of periventricular confluent lesions, excluded from the CVS assessment, seemed to impair CVS sensitivity in POMS diagnosis.
 Multiple sclerosis (MS) is an inflammatory and demyelinating disease which leads to impairment in several functional systems including cognition. Alteration of brain networks is linked to disability and its progression. However, results are mostly cross-sectional and yet contradictory as putative adaptive and maladaptive mechanisms were found. Here, we aimed to explore longitudinal reorganization of brain networks over 2-years by combining diffusion tensor imaging (DTI), resting-state functional MRI (fMRI), magnetoencephalography (MEG), and a comprehensive neuropsychological-battery. In 37 relapsing-remitting MS (RRMS) and 39 healthy-controls, cognition remained stable over-time. We reconstructed network models based on the three modalities and analyzed connectivity in relation to the hierarchical topology and functional subnetworks. Network models were compared across modalities and in their association with cognition using linear-mixed-effect-regression models. Loss of hub connectivity and global reduction was observed on a structural level over-years (p < .010), which was similar for functional MEG-networks but not for fMRI-networks. Structural hub connectivity increased in controls (p = .044), suggesting a physiological mechanism of healthy aging. Despite a general loss in structural connectivity in RRMS, hub connectivity was preserved (p = .002) over-time in default-mode-network (DMN). MEG-networks were similar to DTI and weakly correlated with fMRI in MS (p < .050). Lower structural (β between .23-.33) and both lower (β between .40-.59) and higher functional connectivity (β = -.54) in DMN was associated with poorer performance in attention and memory in RRMS (p < .001). MEG-networks involved no association with cognition. Here, cognitive stability despite ongoing neurodegeneration might indicate a resilience mechanism of DMN hubs mimicking a physiological reorganization observed in healthy aging.
 BACKGROUND: Pregnancy in women with multiple sclerosis (wwMS) is associated with a reduction of long-term disability progression. The mechanism that drives this effect is unknown, but converging evidence suggests a role for epigenetic mechanisms altering immune and/or central nervous system function. In this study, we aimed to identify whole blood and immune cell-specific DNA methylation patterns associated with parity in relapse-onset MS. RESULTS: We investigated the association between whole blood and immune cell-type-specific genome-wide methylation patterns and parity in 192 women with relapse-onset MS, matched for age and disease severity. The median time from last pregnancy to blood collection was 16.7 years (range = 1.5-44.4 years). We identified 2965 differentially methylated positions in whole blood, 68.5% of which were hypermethylated in parous women; together with two differentially methylated regions on Chromosomes 17 and 19 which mapped to TMC8 and ZNF577, respectively. Our findings validated 22 DMPs and 366 differentially methylated genes from existing literature on epigenetic changes associated with parity in wwMS. Differentially methylated genes in whole blood were enriched in neuronal structure and growth-related pathways. Immune cell-type-specific analysis using cell-type proportion estimates from statistical deconvolution of whole blood revealed further differential methylation in T cells specifically (four in CD4(+) and eight in CD8(+) T cells). We further identified reduced methylation age acceleration in parous women, demonstrating slower biological aging compared to nulligravida women. CONCLUSION: Differential methylation at genes related to neural plasticity offers a potential molecular mechanism driving the long-term effect of pregnancy on MS outcomes. Our results point to a potential 'CNS signature' of methylation in peripheral immune cells, as previously described in relation to MS progression, induced by parity. As the first epigenome-wide association study of parity in wwMS reported, validation studies are needed to confirm our findings.
 The IL-10/IL-10 receptor (IL-10R) axis plays an important role in attenuating neuroinflammation in animal models of Multiple Sclerosis (MS) and increased IL-10 has been associated with a positive response to MS disease modifying therapy. Because environmental factors play an important role in MS susceptibility and disease course, identification of environmental factors that impact the IL-10/IL-10R axis has therapeutic potential. In this review, we provide historical and updated perspectives of how IL-10R signaling impacts neuroinflammation, discuss environmental factors and intestinal microbes with known impacts on the IL-10/IL-10R axis, and provide a hypothetical model for how B cells, via their production of IL-10, may be important in conveying environmental "information" to the inflamed central nervous system.
 BACKGROUND AND OBJECTIVES: B cell-depleting therapies are highly effective in relapsing-remitting multiple sclerosis (RRMS) but are associated with increased infection risk and blunted humoral vaccination responses. Extension of dosing intervals may mitigate such negative effects, but its consequences on MS disease activity are yet to be ascertained. The objective of this study was to determine clinical and neuroradiologic disease activity, as well as B-cell repopulation dynamics, after implementation of extended rituximab dosing in RRMS. METHODS: We conducted a prospective observational study in a specialized-care, single-center setting, including patients with RRMS participating in the COMBAT-MS and MultipleMS observational drug trials, who had received at least 2 courses of rituximab (median follow-up 4.2 years, range 0.1-8.9 years). Using Cox regression, hazard ratios (HRs) of clinical relapse and/or contrast-enhancing lesions on MRI were calculated in relation to time since last dose of rituximab. RESULTS: A total of 3,904 dose intervals were accumulated in 718 patients and stratified into 4 intervals: <8, ≥8 to 12, ≥12 to 18, and ≥18 months. We identified 24 relapses of which 20 occurred within 8 months since previous infusion and 4 with intervals over 8 months. HRs for relapse when comparing ≥8 to 12, ≥12 to 18, and ≥18 months with <8 months since last dose were 0.28 (95% CI 0.04-2.10), 0.38 (95% CI 0.05-2.94), and 0.89 (95% CI 0.20-4.04), respectively, and thus nonsignificant. Neuroradiologic outcomes mirrored relapse rates. Dynamics of total B-cell reconstitution varied considerably, but median total B-cell counts reached lower level of normal after 12 months and median memory B-cell counts after 16 months. DISCUSSION: In this prospective cohort of rituximab-treated patients with RRMS exposed to extended dosing intervals, we could not detect a relation between clinical or neuroradiologic disease activity and time since last infusion. Total B- and memory B-cell repopulation kinetics varied considerably. These findings, relevant for assessing risk-mitigation strategies with anti-CD20 therapies in RRMS, suggest that relapse risk remains low with extended infusion intervals. Further studies are needed to investigate the relation between B-cell repopulation dynamics and adverse event risks associated with B-cell depletion.

 BACKGROUND: Evolving evidence suggests that measurement of cerebrospinal fluid (CSF) kappa free light chain (KFLC) synthesis has high diagnostic sensitivity and specificity for multiple sclerosis (MS), but its prognostic ability is less investigated. The usefulness of KFLC in predicting cognitive impairment (CI) is still unknown. METHODS: In a monocentric longitudinal retrospecitve cohort study, KFLC-index ([CSF KFLC/serum KFLC]/[CSF albumin/serum albumin]) measured by latex-enhanced immunonephelometry was prospectively determined as part of the diagnostic workup in patients with early relapsing-remitting MS (RRMS, n=77). The ability of KFLC-index to predict information processing speed (IPS) worsening as assessed with the symbol digit modalities test (SDMT) was investigated in univariable and multivariable models. RESULTS: In patients with KFLC-index>100 (n=31), 11 subjects (35.5%) showed reduced SDMT scores by ≥8 points at follow-up (mean follow-up time 7.3 ± 2.6 years), compared with their baseline scores (p=0.01). Baseline KFLC-index>100 was strongly associated with a higher hazard of SDMT score reduction at follow-up (adjusted hazard ratio 10.5, 95% confidence interval 2.2-50.8, p=0.003; median time to SDMT reduction 7 years). CONCLUSION: Intrathecal KFLC synthesis has become an attractive diagnostic tool for MS. We show for the first time that in a real-world setting of early RRMS, KFLC-index predicted cognitive decline. Whether this predictive ability of KFLC-index also concerns other cognitive domains than IPS, warrants further investigations.
 BACKGROUND AND OBJECTIVE: Despite accumulating evidence of intrathecal inflammation in patients with primary progressive multiple sclerosis (PPMS), immunomodulatory and suppressive treatment strategies have proven unsuccessful. With this study, we investigated the involvement of CD20(+) T cells and the effect of dimethyl fumarate on CD20(+) T cells in PPMS. METHODS: The main outcomes in this observational, case-control study were flow cytometry assessments of blood and CSF CD20(+) T cells and ELISA measurements of myelin basic protein and neurofilament light chain in untreated patients with PPMS and patients treated for 48 weeks with dimethyl fumarate or placebo. MRI measures included new and enlarging T2-weighted lesions over 48 weeks and lesion, normal-appearing white matter, cortical, and thalamic volume. RESULTS: Assessing CD20(+) T cells in patients with PPMS and controls showed an increased percentage of CD20(+) T cells in the blood of untreated patients and a strong enrichment in the CSF. In addition, a higher frequency of CD8(+)CD20(+) T cells in the CSF correlated with a higher concentration of myelin basic protein and T2-weighted lesion volume and with a lower normal-appearing white matter and thalamus volume. Furthermore, CD8(+)CD20(+) T cells were associated with the development of new T2 lesions. After 48 weeks of treatment with dimethyl fumarate, total T cells in CSF were reduced; however, CD20(+) T cells were unaffected. DISCUSSION: This study shows an association between intrathecal CD8(+)CD20(+) T cells, white matter injury, and thalamic atrophy in PPMS, suggesting a role of CD8(+)CD20(+) T cells in the immunopathogenesis of PPMS. The results also suggest that limited efficacy of dimethyl fumarate in PPMS may, at least partly, be a consequence of failure to suppress CD8(+)CD20(+) T cells in CSF.
 BACKGROUND: Theory of Mind (ToM) processing in Multiple Sclerosis (MS) is still poorly understood due to the difficulty of most tasks in qualifying the mentalizing deficit net of cognitive load. METHODS: In this study, we administered the New False Belief Animation Task (NFBAT) to 50 MS and 33 healthy controls (HC) to investigate spontaneous mentalizing in ToM and goal-directed interactions. The global cognitive level was assessed by the Montreal Cognitive Assessment (MoCA). NFBAT appropriateness and intentionality scores were computed to investigate the ToM accuracy and intentionality attribution difficulties. NFBAT answers were qualitatively analyzed and categorized into kinetically and socially coherent/not coherent responses to test a low-level perceptual deficit. RESULTS: The main result showed dysfunctional mentalizing reasoning in MS compared to HC in the NFBAT Intentionality score in ToM conditions (p = 0.028, d = 0.501), while the two groups were equally proficient in mentalization accuracy. The Intentionality underperformance in MS was related to social low-level perceptual processing (β =0.06, p < 0.001) and visuospatial functions (β =0.05, p =0.002). A predictive role of memory and executive functions on NFBAT Intentionality scores was not observed. CONCLUSION: These results strengthen the hypothesis that ToM in MS is likely related to low-level social processing.
 OBJECTIVE: To examine (1) the association between childhood diet and developing MS, age of onset and onset type and (2) the association between diet at age 50 and disability and MRI volumes in people with MS (PwMS). METHODS: The study enrolled 361 PwMS born in 1966 and 125 age- and sex-matched healthy controls (HCs). Information on individual dietary components (fruit, vegetables, red meat, oily fish, whole-grain bread and candy, snacks and fast food) and MS risk factors at the age of 10 and 50 years were collected using questionnaires. Overall diet quality score was calculated for each participant. Multivariable regression analyses were used to evaluate the association between diet at childhood and developing MS, age of onset and onset type and to evaluate diet at age 50, disability and MRI outcomes. RESULTS: Poorer overall diet quality and individual dietary components during childhood (less whole-grain bread, more candy, snacks and fast food and oily fish) were associated with developing MS and onset type (all p < 0.05), but not with the age of onset. Fruit consumption at age 50 was associated with lower disability (Q3 vs. Q1: -0.51; 95% CI: -0.89 to -0.13). Furthermore, several individual dietary components at age 50 were associated with MRI volumetric measures. Higher-diet quality at age 50 was only associated with lower lesion volumes in PwMS (Q2 vs. Q1: -0.3 mL; 95% CI: -0.5 to -0.02). INTERPRETATION: We demonstrate significant associations between dietary factors in childhood and developing MS, age of onset and onset type and between dietary factors at age 50 and disability and MRI-derived volumes.
 BACKGROUND: Multiple sclerosis (MS) is associated with regulatory T cells (Tregs) insufficiency while low-dose interleukin-2 (IL2(LD)) activates Tregs and reduces disease activity in autoimmune diseases. METHODS: We aimed at addressing whether IL2(LD) improved Tregs from MS patients. MS-IL2 was a single-center double-blind phase-2 study. Thirty patients (mean [SD] age 36.8 years [8.3], 16 female) with relapsing-remitting MS with new MRI lesions within 6 months before inclusion were randomly assigned in a 1:1 ratio to placebo or IL-2 at 1 million IU, daily for 5 days and then fortnightly for 6 months. The primary endpoint was change in Tregs at day-5. RESULTS: Unlike previous trials of IL2(LD) in more than 20 different autoimmune diseases, Tregs were not expanded at day-5 in IL2(LD) group, but only at day-15 (median [IQR] fold change from baseline: 1.26 [1.21-1.33] in IL2(LD) group; 1.01 [0.95-1.05] in placebo group, p < 0.001). At day-5, however, Tregs had acquired an activated phenotype (fold change of CD25 expression in Tregs: 2.17 [1.70-3.55] in IL2(LD) versus 0.97 [0.86-1.28] in placebo group, p < 0.0001). Regulator/effector T cells ratio remained elevated throughout treatment period in the IL2(LD) group (p < 0.001). Number of new active brain lesions and of relapses tended to be reduced in IL2(LD) treated patients, but the difference did not reach significance in this trial not powered to detect clinical efficacy. CONCLUSION: The effect of IL2(LD) on Tregs in MS patients was modest and delayed, compared to other auto-immune diseases. This, together with findings that Tregs improve remyelination in MS models and recent reports of IL2(LD) efficacy in amyotrophic lateral sclerosis, warrants larger studies of IL2(LD) in MS, notably with increased dosages and/or modified modalities of administration. TRIAL REGISTRATION INFORMATION: ClinicalTrials.gov: NCT02424396; EU Clinical trials Register: 2014-000088-42.
 Relapsing-remitting multiple sclerosis (RRMS) is the most common clinical course of multiple sclerosis (MS), characterized by a chronic inflammatory state and elevated levels of oxidative markers. Food supplements with potential anti-inflammatory, antioxidant and neuroprotective effects have been tested as possible adjuvants in the treatment of MS. In this sense, this pilot study was carried out with the aim of verifying whether a minimum daily dose of a guarana, selenium and l-carnitine (GSC) based multi supplement, mixed in cappuccino-type coffee, administered for 12 weeks to 28 patients with RRMS could differentially modulate oxidative blood markers (lipoperoxidation, protein carbonylation and DNA oxidation) and inflammatory blood markers (protein levels of cytokines IL-1β, IL-6, TNF-α, IFN-γ, IL-10, gene expression of these cytokines, and NLRP3 and CASP-1 molecules, and C-reactive protein levels). The results indicate that a low concentration of GSC is capable of decreasing the plasma levels of oxidized DNA and pro-inflammatory cytokines of RRMS patients. The results support further research into the action of GSC on clinical symptoms, not only in patients with MS, but also with other neurological conditions.

 OBJECTIVE: To assess the level of microbiota markers in the blood and cerebrospinal fluid (CSF) of patients with different types of multiple sclerosis (MS), people with radiologically isolated syndrome (RIS) and control subjects. MATERIAL AND METHODS: We used gas chromatography-mass spectrometry (GC-MS) to evaluate the levels of microbiota markers in 69 patients with different types of MS (27 patients in the acute stage, 35 patients with MS in remission, 7 patients with primary-progressive MS), 10 people with RIS, and 47 control subjects (different diseases of the nervous system of a non-autoimmune or inflammatory nature). RESULTS: We showed a statistically significant increase in the content of various microbiota markers in the CSF of patients with MS compared with the control group. We found no change in the content of these markers in blood of patients with MS. This suggests a change of markers of microbial load at the level of the central nervous system, but not at the level of the whole organism. The greatest number of statistically significant differences with the control group was found in the content of markers in CSF of patients with MS in remission. In the acute stage, on the contrary, we found no statistically significant differences compared to the control group. In particular, in CSF of patients with MS in remission, a statistically significant increase in the content of bacterial plasmalogen (4.5 times), and increase in the level of microbial markers specific to Peptostreptococcus anaerobius, Pseudomonas aeruginosa, Eubacterium, Bifidobacterium, Butirivibrio, Moraxella, Acinetobacter, Propionibacterium acnes, as well as an increase of markers of the Epstein-Barr virus were found. In addition, there was an increase of campesterol, the likely source of which is campesterol-producing microfungi. In the CSF of subjects with RIS there were a statistically significant increase in the level of markers of the Epstein-Barr virus, Propionibacterium acnes, as well as Pseudomonas, Moraxella, and Acinetobacter. CONCLUSION: An association of MS with polymicrobial infection is possible. It is also likely that there is a certain pattern of increase of microbiota markers in the CSF of patients with MS, but not in blood.
 OBJECTIVE: The radiologically isolated syndrome (RIS) represents the earliest detectable pre-clinical phase of multiple sclerosis (MS). This study evaluated the impact of therapeutic intervention in preventing first symptom manifestation at this stage in the disease spectrum. METHODS: We conducted a multi-center, randomized, double-blinded, placebo-controlled study involving people with RIS. Individuals without clinical symptoms typical of MS but with incidental brain MRI anomalies consistent with central nervous system (CNS) demyelination were included. Within 12 MS centers in the United States, participants were randomly assigned 1:1 to oral dimethyl fumarate (DMF) 240 mg twice daily or placebo. The primary endpoint was the time to onset of clinical symptoms attributable to a CNS demyelinating event within a follow-up period of 96 weeks. An intention-to-treat analysis was applied to all participating individuals in the primary and safety investigations. The study is registered at ClinicalTrials.gov, NCT02739542 (ARISE). RESULTS: Participants from 12 centers were recruited from March 9, 2016, to October 31, 2019, with 44 people randomized to dimethyl fumarate and 43 to placebo. Following DMF treatment, the risk of a first clinical demyelinating event during the 96-week study period was highly reduced in the unadjusted Cox proportional-hazards regression model (hazard ratio [HR] = 0.18, 95% confidence interval [CI] = 0.05-0.63, p = 0.007). More moderate adverse reactions were present in the DMF (34 [32%]) than placebo groups (19 [21%]) but severe events were similar (DMF, 3 [5%]; placebo, 4 [9%]). INTERPRETATION: This is the first randomized clinical trial demonstrating the benefit of a disease-modifying therapy in preventing a first acute clinical event in people with RIS. ANN NEUROL 2023;93:604-614.
 AIM: To compare the efficacy and safety of newer and/or second-line disease-modifying treatments (DMTs) with interferon beta-1a. METHOD: This observational retrospective study included patients younger than 18 years old in the French KIDBIOSEP cohort who had a diagnosis of relapsing multiple sclerosis between 2008 and 2019 and received at least one DMT. Primary outcome was the annualized relapse rate (ARR). Secondary outcomes were the risk of new T2 or gadolinium-enhanced lesions on brain MRI. RESULTS: Among 78 patients enrolled, 50 were exposed to interferon and 76 to newer DMTs. Mean ARR went from 1.65 during pre-treatment period to 0.45 with interferon (p < 0.001). Newer DMTs reduced ARR compared to interferon: fingolimod 0.27 (p = 0.013), teriflunomide 0.25 (p = 0.225), dimethyl-fumarate 0.14 (p = 0.045), natalizumab 0.03 (p = 0.007). Risk of new lesions on MRI was reduced with interferon compared to pre-treatment period; it decreased even more with newer DMTs for T2 lesions. Regarding risk of new gadolinium-enhanced lesions, the added value of new treatments compared to interferon was less obvious, except for natalizumab (p = 0.031). CONCLUSION: In this real-world setting, newer DMTs showed better efficacy than interferon beta-1a on ARR and risk of new T2 lesions, with a good safety profile. Natalizumab tend to emerge as the most effective treatment.
 BACKGROUND: The COVID-19 pandemic has led to reorganization or reduction of neurorehabilitation services for people with multiple sclerosis (PwMS). The aim of this study was to explore the changes in the organizational framework and technology usage in physiotherapy services for PwMS during the COVID-19 pandemic. METHODS: This international cross-sectional survey study was designed, developed, and disseminated by RIMS European Network for Best Practice and Research in Multiple Sclerosis Rehabilitation. Physiotherapists from nine countries (Australia, Belgium, Czech Republic, Ireland, Israel, Italy, Norway, Spain, Turkey) who provided physiotherapy services to PwMS, were invited to complete an online survey to compare physiotherapy delivery to PwMS prior to and during the pandemic period. RESULTS: The survey was completed by 215 physiotherapists. Accessibility, the average number, length and perceived effectiveness of physiotherapy sessions provided to PwMS were significantly reduced during the COVID-19 pandemic (p=0.001). Physiotherapists increased the advice of mobile apps, recorded videos for rehabilitation and exercise websites during the pandemic (p<0.001) while the use of telerehabilitation and virtual reality technology did not change. CONCLUSION: There was of a reduction in the number, duration and perceived effectiveness of rehabilitation sessions for people with multiple sclerosis during the COVID-19 pandemic while use of remote technologies for physiotherapy did not change. To ensure the continuity of physiotherapy for PwMS with complex healthcare needs also during pandemics, the provision of guidelines and training in telehealth technologies in professional education becomes crucial.
 Aim: The costs and consequences of initial and delayed ofatumumab treatment were evaluated in relapsing-remitting multiple sclerosis with active disease in Canada. Materials & methods: A Markov cohort model was used (10-year horizon, annual cycle length, 1.5% discounting). Scenario analyses examined ofatumumab as first-line treatment versus 3 and 5 years following switch from commonly used first-line therapies. Results: Ofatumumab resulted in improvements in clinical outcomes (relapses and disease progression) and productivity (employment and full-time work), and reduction of economic burden (administration, monitoring and non-drug costs) that were comparable to other high-efficacy therapies (ocrelizumab, cladribine and natalizumab). Switching to ofatumumab earlier in the disease course may improve these outcomes. Conclusion: Results highlight the value of a high-efficacy therapy such as ofatumumab as initial treatment (i.e., first-line) in newly diagnosed relapsing-remitting multiple sclerosis patients with active disease.
 BACKGROUND: Spasticity and urinary disturbances can profoundly impact the daily lives of persons with multiple sclerosis (pwMS). Cannabis has been associated with improvement in sphincteric disturbances. To our knowledge, few studies have evaluated the effect of nabiximols oromucosal spray (Sativex®) on urinary disturbances by instrumental methods. OBJECTIVES: This longitudinal study was conducted to assess the effect of nabiximols oromucosal spray on urinary disturbances by clinical and urodynamic evaluation in pwMS. MATERIALS AND METHODS: Neurological, spasticity, and quality of life (QoL) assessments were performed before (T0), and at one (T1) and six (T6) months after the start of nabiximols treatment. At these same time points, patients were assessed for urinary disturbances by the International Prostatic Symptoms Score (IPSS) and a urodynamic test evaluating maximum detrusor pressure (P(det)), bladder filling capacity (CC(max)), uninhibited detrusor contractions (UDC), bladder volume at first desire (BVFD), post-void residual volume (PVR) and voluntary abdominal pressure (PA). RESULTS: Of 31 pwMS enrolled in the study, 25 reached T1 and 18 reached T6. Mean IPSS total score, its subscores, and IPSS QoL decreased significantly from T0 to T6 (p = 0.000), with no differences according to sex, age, MS type, disease duration and disability at baseline. P(det) improved significantly from T0 to T6 (p = 0.0171), and CC(max) changed only marginally (p = 0.0494); results were similar in patient subgroups naïve to or previously exposed to urological treatment. All patients with overactive bladder showed improvement in their urodynamic assessment based on significant reduction of P(det) (p = 0.0138). In patients with mainly hypotonic bladder, mean P(det) decreased from T0 to T6 without reaching statistical significance; most urodynamic parameters showed a trend to improve. Mean numerical scale scores for MS spasticity, and for spasms, pain and tremors, decreased significantly from T0 to T6. The mean 'physical health composite' score of the MS Quality of Life-54 questionnaire increased significantly from T0 to T6 (p = 0.0126). DISCUSSION AND CONCLUSION: Our data suggest that nabiximols has an appreciable effect on ameliorating subjective perception of urinary disturbances and appears to have a positive effect on objective urodynamic parameters, particularly in patients with hyperactive bladder.
 BACKGROUND: Susceptibility-weighted imaging (SWI) is efficient in detecting multiple sclerosis (MS) plaques and evaluating the level of disease activity. PURPOSE: To automatically detect active and inactive MS plaques in SWI images using a Bayesian approach. MATERIAL AND METHODS: A 1.5-T scanner was used to evaluate 147 patients with MS. The area of the plaques along with their active or inactive status were automatically identified using a Bayesian approach. Plaques were given an orange color if they were active and a blue color if they were inactive, based on the preset signal intensity. RESULTS: Experimental findings show that the proposed method has a high accuracy rate of 91% and a sensitivity rate of 76% for identifying the type and area of plaques. Inactive plaques were properly identified in 87% of cases, and active plaques in 76% of cases. The Kappa analysis revealed an 80% agreement between expert diagnoses based on contrast-enhanced and FLAIR images and Bayesian inferences in SWI. CONCLUSION: The results of our study demonstrated that the proposed method has good accuracy for identifying the MS plaque area as well as for identifying the types of active or inactive plaques in SWI. Therefore, it might be helpful to use the proposed method as a supplemental tool to accelerate the specialist's diagnosis.
 BACKGROUND: Complete and timely publication of clinical trials ensures that patients and the medical community are fully informed when making treatment decisions. The aim of this study is to assess the publication of phase III and IV clinical trials on multiple sclerosis (MS) drugs that have been carried out between 2010 and 2019 and to identify the factors associated with their publication in peer-reviewed journals. METHODS: An advanced search in ClinicalTrials.gov was performed and consecutive searches in PubMed, EMBASE and Google Scholar were conducted looking for the associated publications of all completed trials. Study design characteristics, results and other relevant information were extracted. Data was analysed following a case-control design. Clinical trials with associated publications in peer-reviewed journals were the cases and unpublished trials were the controls. A multivariate logistic regression analysis was performed to identify factors associated with trial publication. RESULTS: One hundred and fifty clinical trials were included in the analysis. Ninety-six of them (64.0%) were published in peer-reviewed journals. In the multivariate analysis, factors associated with trial publication were a favourable primary outcome (OR 12.49, 95% CI 1.28 to 122.29) and reaching the originally estimated sample size (OR 41.97, 95% CI 1.96 to 900.48), while those associated with a lower odds of publication were having 20% or more patients lost to follow-up (OR 0.03, 95% CI 0.01 to 0.52) and evaluating drugs intended to improve treatment tolerability (OR 0.01, 95% CI 0.00 to 0.74). CONCLUSIONS: Phase III and IV clinical trials on MS drugs are prone to under-reporting and publication bias. Efforts must be made to promote a complete and accurate dissemination of data in MS clinical research.
 OBJECTIVES: Neurofilament light (NfL) chain is a marker of neuroaxonal damage in various neurological diseases. Here we quantitated NfL levels in the cerebrospinal fluid (CSF) and serum from patients with multiple sclerosis (MS) and controls, using the R-PLEX NfL assay, which employs advanced Meso Scale Discovery(®) (MSD) electrochemiluminescence (ECL)-based detection technology. METHODS: NfL was quantitated in samples from 116 individuals from two sites (Ottawa Hospital Research Institute and Mayo Clinic), consisting of patients with MS (n=71) and age- and sex-matched inflammatory neurological controls (n=13) and non-inflammatory controls (n=32). Correlation of NfL levels between CSF and serum was assessed in paired samples in a subset of MS patients and controls (n=61). Additionally, we assessed the correlation between NfL levels obtained with MSD's R-PLEX(®) and Quanterix's single molecule array (Simoa(®)) assays in CSF and serum (n=32). RESULTS: Using the R-PLEX, NfL was quantitated in 99% of the samples tested, and showed a broad range in the CSF (82-500,000 ng/L) and serum (8.84-2,014 ng/L). Nf-L levels in both biofluids correlated strongly (r=0.81, p<0.0001). Lastly, Nf-L measured by MSD's R-PLEX and Quanterix's Simoa assays were highly correlated for both biofluids (CSF: r=0.94, p<0.0001; serum: r=0.95, p<0.0001). CONCLUSIONS: We show that MSD's R-PLEX NfL assay can reliably quantitate levels of NfL in the CSF and serum from patients with MS and controls, where levels correlate strongly with Simoa.
 Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system (CNS) and the most common non-traumatic cause of neurological disability in young adults. Multiple sclerosis clinical care has improved considerably due to the development of disease-modifying therapies that effectively modulate the peripheral immune response and reduce relapse frequency. However, current treatments do not prevent neurodegeneration and disease progression, and efforts to prevent multiple sclerosis will be hampered so long as the cause of this disease remains unknown. Risk factors for multiple sclerosis development or severity include vitamin D deficiency, cigarette smoking and youth obesity, which also impact vascular health. People with multiple sclerosis frequently experience blood-brain barrier breakdown, microbleeds, reduced cerebral blood flow and diminished neurovascular reactivity, and it is possible that these vascular pathologies are tied to multiple sclerosis development. The neurovascular unit is a cellular network that controls neuroinflammation, maintains blood-brain barrier integrity, and tightly regulates cerebral blood flow, matching energy supply to neuronal demand. The neurovascular unit is composed of vessel-associated cells such as endothelial cells, pericytes and astrocytes, however neuronal and other glial cell types also comprise the neurovascular niche. Recent single-cell transcriptomics data, indicate that neurovascular cells, particular cells of the microvasculature, are compromised within multiple sclerosis lesions. Large-scale genetic and small-scale cell biology studies also suggest that neurovascular dysfunction could be a primary pathology contributing to multiple sclerosis development. Herein we revisit multiple sclerosis risk factors and multiple sclerosis pathophysiology and highlight the known and potential roles of neurovascular unit dysfunction in multiple sclerosis development and disease progression. We also evaluate the suitability of the neurovascular unit as a potential target for future disease modifying therapies for multiple sclerosis.
 BACKGROUND: People with multiple sclerosis (PwMS) have recurrent stays in rehabilitation clinics because of progressive disease. Nurses are key players in supporting PwMS through self-management interventions. However, little is known about the effectiveness, or sustainability of nursing interventions. The aim of this study was to develop a nurse-led self-management intervention and its programme theory for PwMS in one Swiss rehabilitation clinic. METHODS: On the basis of the Medical Research Council framework, we developed a theory-based programme for a nurse-led intervention. As key element of the intervention, we created a consulting guidance. RESULTS: As part of the programme theory, we created a systematic plan (action model) to illustrate how contextual resources (e.g., skills of the MS nurse and responsibilities of the multidisciplinary team) need to be coordinated. The change model shows how changes in the intervention lead to the achievement of outcomes (e.g., increased self-efficacy). The consulting guidance was refined by PwMS and four Swiss MS experts. CONCLUSIONS: An initial programme theory is a solid foundation for the next phases of the theory-based evaluations to refine the programme theory and sustainable implementation of the intervention.
 INTRODUCTION: Multiple sclerosis (MS) is a progressive inflammatory autoimmune disease that involves young individuals. The drug delivery systems now are available for this disease have chronic and non-targeted effects on the patients. Because of the presence of BBB (blood-brain-barrier), their concentration in the CNS (central nervous system) is low. Because of this flaw, it is critical to use innovative active targeted drug delivery methods. RESULT: Platelets are blood cells that circulate freely and play an important role in blood hemostasis. In this review, we emphasize the various roles of activated platelets in the inflammatory condition to recruit other cells to the injured area and limit inflammation. Besides, the activated platelets in the different stages of the MS disease play a significant role in limiting the progression of inflammation in the peripheral area and CNS. DISCUSSION: This evidence indicates that a platelet-based drug delivery system can be an efficient biomimetic candidate for drug targeting to the CNS and limiting the inflammation in the peripheral and central areas for MS therapy.
 BACKGROUND: Physical activity (PA) research in multiple sclerosis (MS) typically has not focused on persons newly diagnosed with the disease. This is noteworthy as PA might be most amenable for change in the early stages of MS and further yield long-term benefits over the disease course. PURPOSE: This study examined correlates of PA based on the Capability-Opportunity-Motivation-Behavior (COM-B) model in persons newly diagnosed with MS. METHODS: Participants newly diagnosed with MS (i.e., ≤ 2 years; n = 152) completed an online Qualtrics survey that assessed PA levels and COM-B constructs. Multivariate Analysis of Variance and Discriminant Function Analysis identified the constructs that differentiated PA groups. RESULTS: The results indicated that 39.5% and 34.2% of the sample were classified as Insufficiently Active and Not Regularly Active, respectively. The results further identified Intention, Action Control, Action Self-efficacy, Action Planning, Outcome Expectation, Goal Setting, and Recovery Self-efficacy, and Fatigue as the primary correlates of PA in persons newly diagnosed with MS. CONCLUSIONS: Our results identified COM-B constructs in the Capability and Motivation domains as the primary correlates of physical activity in persons newly diagnosed with MS. Such research might inform interventions for changing physical activity in this MS subpopulation.
 INTRODUCTION AND OBJECTIVES: Multiple sclerosis (MS) is a disease of the central nervous system associated with immune dysfunction, demyelination, and neurodegeneration. The disease has heterogeneous clinical phenotypes such as relapsing-remitting MS (RRMS) and progressive multiple sclerosis (PMS), each with unique pathogenesis. Metabolomics research has shown promise in understanding the etiologies of MS disease. However, there is a paucity of clinical studies with follow-up metabolomics analyses. This 5-year follow-up (5YFU) cohort study aimed to investigate the metabolomics alterations over time between different courses of MS patients and healthy controls and provide insights into metabolic and physiological mechanisms of MS disease progression. METHODS: A cohort containing 108 MS patients (37 PMS and 71 RRMS) and 42 controls were followed up for a median of 5 years. Liquid chromatography-mass spectrometry (LC-MS) was applied for untargeted metabolomics profiling of serum samples of the cohort at both baseline and 5YFU. Univariate analyses with mixed-effect ANCOVA models, clustering, and pathway enrichment analyses were performed to identify patterns of metabolites and pathway changes across the time effects and patient groups. RESULTS AND CONCLUSIONS: Out of 592 identified metabolites, the PMS group exhibited the most changes, with 219 (37%) metabolites changed over time and 132 (22%) changed within the RRMS group (Bonferroni adjusted P < 0.05). Compared to the baseline, there were more significant metabolite differences detected between PMS and RRMS classes at 5YFU. Pathway enrichment analysis detected seven pathways perturbed significantly during 5YFU in MS groups compared to controls. PMS showed more pathway changes compared to the RRMS group.
 BACKGROUND: Magnetic resonance imaging (MRI) diagnosis is usually performed by analyzing contrast-weighted images, where pathology is detected once it reached a certain visual threshold. Computer-aided diagnosis (CAD) has been proposed as a way for achieving higher sensitivity to early pathology. PURPOSE: To compare conventional (i.e., visual) MRI assessment of artificially generated multiple sclerosis (MS) lesions in the brain's white matter to CAD based on a deep neural network. STUDY TYPE: Prospective. POPULATION: A total of 25 neuroradiologists (15 males, age 39 ± 9, 9 ± 9.8 years of experience) independently assessed all synthetic lesions. FIELD STRENGTH/SEQUENCE: A 3.0 T, T(2) -weighted multi-echo spin-echo (MESE) sequence. ASSESSMENT: MS lesions of varying severity levels were artificially generated in healthy volunteer MRI scans by manipulating T(2) values. Radiologists and a neural network were tasked with detecting these lesions in a series of 48 MR images. Sixteen images presented healthy anatomy and the rest contained a single lesion at eight increasing severity levels (6%, 9%, 12%, 15%, 18%, 21%, 25%, and 30% elevation in T(2) ). True positive (TP) rates, false positive (FP) rates, and odds ratios (ORs) were compared between radiological diagnosis and CAD across the range lesion severity levels. STATISTICAL TESTS: Diagnostic performance of the two approaches was compared using z-tests on TP rates, FP rates, and the logarithm of ORs across severity levels. A P-value <0.05 was considered statistically significant. RESULTS: ORs of identifying pathology were significantly higher for CAD vis-à-vis visual inspection for all lesions' severity levels. For a 6% change in T(2) value (lowest severity), radiologists' TP and FP rates were not significantly different (P = 0.12), while the corresponding CAD results remained statistically significant. DATA CONCLUSION: CAD is capable of detecting the presence or absence of more subtle lesions with greater precision than the representative group of 25 radiologists chosen in this study. LEVEL OF EVIDENCE: 1 TECHNICAL EFFICACY: Stage 3.
 BACKGROUND: Predicting the long-term disability outcomes of multiple sclerosis (MS) cases is challenging. OBJECTIVE: We prospectively analysed our previous MS cohort with initial cerebrospinal fluid (CSF) proteomics data to reveal disability markers after 8.2±2.2 years of follow-up. METHODS: Patients with regular follow-up visits were assigned into two groups: those with an age-related MS severity (ARMSS) score ≥5 (unfavourable course group, N = 27) and ARMSS score <5 (favourable course group, N = 67). A machine learning-based algorithm was applied to reveal candidate poor prognosis-associated initial CSF proteins, which were measured in an independent MS cohort (verification group, N = 40) by ELISA. Additionally, the correlation of initial clinical and radiological parameters with long-term disability was analysed. RESULTS: CSF alpha-2-macroglobulin (P = 0.0015), apo-A1 (P = 0.0016), and haptoglobin (P = 0.0003) protein levels, as well as cerebral lesion load (>9 lesions) on magnetic resonance imaging, gait disturbance (P = 0.04), and bladder/bowel symptoms (P = 0.01) were significantly higher in the unfavourable course group than in the favourable course group. Optic nerve involvement evident on initial magnetic resonance imaging (P = 0.002) and optic neuritis (P = 0.01) were more frequent in the favourable course group. CONCLUSION: The herein identified initial CSF protein levels, in addition to the clinical and radiological parameters at disease onset, have predictive value for long-term disability in MS cases.
 OBJECTIVE: To develop a multiple sclerosis (MS)-specific model of balance and examine differences between (1) MS and neurotypical controls and (2) people with MS (PwMS) with (MS-F) and without a fall history (MS-NF). DESIGN AND SETTING: A cross-sectional study was conducted at the Gait and Balance Laboratory at the University of Kansas Medical Center. Balance was measured from the instrumented sway system (ISway) assessment. PARTICIPANTS: In total, 118 people with relapsing-remitting MS (MS-F=39; MS-NF=79) and 46 age-matched neurotypical controls. INTERVENTION: Not applicable. OUTCOME MEASURES: A total of 22 sway measures obtained from the ISway were entered into an exploratory factor analysis to identify underlying balance domains. The model-derived balance domains were compared between (1) PwMS and age-matched, neurotypical controls and (2) MS-F and MS-NF. RESULTS: Three distinct balance domains were identified: (1) sway amplitude and velocity, (2) sway frequency and jerk mediolateral, and (3) sway frequency and jerk anteroposterior, explaining 81.66% of balance variance. PwMS exhibited worse performance (ie, greater amplitude and velocity of sway) in the sway velocity and amplitude domain compared to age-matched neurotypical controls (P=.003). MS-F also exhibited worse performance in the sway velocity and amplitude domain compared to MS-NF (P=.046). The anteroposterior and mediolateral sway frequency and jerk domains were not different between PwMS and neurotypical controls nor between MS-F and MS-NF. CONCLUSIONS: This study identified a 3-factor, MS-specific balance model, demonstrating that PwMS, particularly those with a fall history, exhibit disproportionate impairments in sway amplitude and velocity. Identifying postural stability outcomes and domains that are altered in PwMS and clinically relevant (eg, related to falls) would help isolate potential treatment targets.
 BACKGROUND: The common inflammatory disease multiple sclerosis (MS) is a disease of the central nervous system. For more than 25 years autologous hematopoietic stem cell transplantation (AHSCT) has been used to treat MS. It has been shown to be highly effective in suppressing inflammatory activity in relapsing-remitting MS (RRMS) patients. This treatment is thought to lead to an immune system reset, inducing a new, more tolerant system; however, the precise mechanism behind the treatment effect in MS patients is unknown. In this study, the effect of AHSCT on the metabolome and lipidome in peripheral blood from RRMS patients was investigated. METHODS: Peripheral blood samples were collected from 16 patients with RRMS at ten-time points over the five months course of AHSCT and 16 MS patients not treated with AHSCT. Metabolomics and lipidomics analysis were performed using liquid-chromatography high-resolution mass spectrometry. Mixed linear models, differential expression analysis, and cluster analysis were used to identify differentially expressed features and groups of features that could be of interest. Finally, in-house and in-silico libraries were used for feature identification, and enrichment analysis was performed. RESULTS: Differential expression analysis found 657 features in the lipidomics dataset and 34 in the metabolomics dataset to be differentially expressed throughout AHSCT. The administration of cyclophosphamide during mobilization and conditioning was associated with decreased concentrations in glycerophosphoinositol species. Thymoglobuline administration was associated with an increase in ceramide and glycerophosphoethanolamine species. After the conditioning regimen, a decrease in glycerosphingoidlipids concentration was observed, and following hematopoietic stem cell reinfusion glycerophosphocholine concentrations decreased for a short period of time. Ceramide concentrations were strongly associated with leukocyte levels during the procedure. The ceramides Cer(d19:1/14:0) and Cer(d20:1/12:0) were found to be increased (P < .05) in concentration at the three-month follow-up compared to baseline. C16 ceramide, Cer(D18:2/16:0), and CerPE(d16:2(4E,6E)/22:0) were found to be significantly increased in concentration after AHSCT compared to prior to treatment as well as compared to newly diagnosed RRMS patients. CONCLUSION: AHSCT had a larger impact on the lipids in peripheral blood compared to metabolites. The variation in lipid concentration reflects the transient changes in the peripheral blood milieu during the treatment, rather than the changes in the immune system that are assumed to be the cause of clinical improvement within RRMS patients treated with AHSCT. Ceramide concentrations were affected by AHSCT and associated with leukocyte counts and were altered three months after treatment, suggesting a long-lasting effect.

 Quantitative assessment of brain myelination has gained attention for both research and diagnosis of neurological diseases. However, conventional pulse sequences cannot directly acquire the myelin-proton signals due to its extremely short T2 and T2* values. To obtain the myelin-proton signals, dedicated short T2 acquisition techniques, such as ultrashort echo time (UTE) imaging, have been introduced. However, it remains challenging to isolate the myelin-proton signals from tissues with longer T2. In this article, we extended our previous two-dimensional ultrashort echo time magnetic resonance fingerprinting (UTE-MRF) with dual-echo acquisition to three dimensional (3D). Given a relatively low proton density (PD) of myelin-proton, we utilized Cramér-Rao Lower Bound to encode myelin-proton with the maximal SNR efficiency for optimizing the MR fingerprinting design, in order to improve the sensitivity of the sequence to myelin-proton. In addition, with a second echo of approximately 3 ms, myelin-water component can be also captured. A myelin-tissue (myelin-proton and myelin-water) fraction mapping can be thus calculated. The optimized 3D UTE-MRF with dual-echo acquisition is tested in simulations, physical phantom and in vivo studies of both healthy subjects and multiple sclerosis patients. The results suggest that the rapidly decayed myelin-proton and myelin-water signal can be depicted with UTE signals of our method at clinically relevant resolution (1.8 mm isotropic) in 15 min. With its good sensitivity to myelin loss in multiple sclerosis patients demonstrated, our method for the whole brain myelin-tissue fraction mapping in clinical friendly scan time has the potential for routine clinical imaging.
 Spasticity is one of the main symptoms that is most common in patients with Multiple Sclerosis and causes increased disability. The aim of this study is to understand the experiences of patients with Multiple Sclerosis about their spasticity from their perspective. This study was conducted as a qualitative study with a Hermeneutic phenomenological framework. The data were evaluated by using VanManen's thematic analysis method. As a result of the data analysis, four main themes were elicited, namely, "the meaning of spasticity for the patient," "the difficulties of living with spasticity," 'coping with spasticity," and "the new me created by spasticity." It was understood that spasticity is a symptom that brings about difficulties in psychological, social, and working life as well as physical difficulties. Nurses should be aware of the psychological symptoms as well as the physical symptoms that patients experience due to spasticity and should create a patient-specific management program.
 OBJECTIVES: Immobility and its physiological and psychological consequences are common problems in patients with multiple sclerosis. The aim of this study was to investigate the effect of 8 weeks of combined training on Adipsin and lipid profile and the possible relationship between these indicators and psychological function in women with multiple sclerosis. METHODS: In this quasi-experimental study, 40 women with multiple sclerosis were selected by purposeful sampling method and randomly divided into two equal control and exercise groups (n=20). Exercise was performed for 8 weeks (two resistance sessions and one endurance session per week). Before and after the intervention, blood samples were taken and the DASS-21 questionnaire was completed to assess anxiety, depression and stress. Data were analyzed using analysis of covariance, t-test, Bonferroni post hoc test and Pearson correlation test at a significance level of p≤0.05. RESULTS: In the exercise group, levels of Adipsin, total cholesterol, LDL, TG, weight, fat percentage, WHR, BMI, depression, anxiety and stress were significantly reduced and HDL levels were significantly increased after 8 weeks of combined exercise (p≤0.05). Also, BMI (p=0.01), fat percentage (p=0.01) and WHR (p=0.01) levels had significant positive correlation with Adipsin. There was a significant positive relationship between Total cholesterol level with depression index (p=0.04). CONCLUSIONS: Performing combination exercises through improving body composition can increase the risk of obesity and cardiovascular risk factors and improve the psychological function of patients with multiple sclerosis. Specialists can use these exercises as an adjunct to drug therapy for MS patients.
 PURPOSE: Studies on hypothalamic changes in patients with relapsing remitting multiple sclerosis (RRMS) are very scarce, despite the fact that the relationship with the hypothalamus is frequently reported. The aim of the study was to determine the volume of the hypothalamic subunits and the total hypothalamus and its relationship with the total demyelinating lesion volume (TLV) and expanded disability status scale (EDSS) in RRMS patients. METHODS: In this cross-sectional study, anterior-superior, superior tubular, posterior hypothalamus, anterior-inferior, inferior tubular subunits of hypothalamus, and total hypothalamus volume were calculated, with fully automatic analysis methods using volumetric T1 images of 65 relapsed RRMS patients and 68 healthy controls (HC). Volume changes in the hypothalamus and its subunits in RRMS patients were examined using multivariate analysis of covariance (MANCOVA). The relationship of these volumes with EDSS and TLV was investigated by partial correlation analysis. RESULTS: There is volume reduction in total hypothalamus (F = 13.87, p < 0.001), anterior-superior (F = 19.2, p < 0.001), superior tubular (F = 10.1, p = 0.002) subunits, and posterior hypothalamus (F = 19.2, p < 0.001) volume in RRMS patients. EDSS correlates negatively with anterior-superior (p = 0.017, r =  - 0.333), superior tubular subunits (p = 0.023, r =  - 0.439), posterior hypothalamus (p < 0.001, r =  - 0.511), and whole hypothalamus volume (p = 0.001, r =  - 0.439). TLV correlates negatively with anterior superior (p < 0.001, r =  - 0.565), anterior inferior (p = 0.002, r =  - 0.431), superior tubular subunits (p = 0.002, r =  - 0.432), posterior hypothalamus (p < 0.001, r =  - 0.703), and whole hypothalamus (p < 0.001, r =  - 0.627) volumes. CONCLUSION: This study demonstrates a reduction in total hypothalamus volume, anterior-superior, superior tubular, and posterior hypothalamus in patients with RRMS. Anterior-superior and superior tubular subunit, posterior hypothalamus, and total hypothalamus volume were negatively correlated with TLV and EDSS scores.
 Multiple Sclerosis (MS) is, to date, an incurable disease of the nervous system characterized by demyelination. Several genetic mutations are associated with the disease but they are not able to explain all the diagnosticated cases. Thus, it is suggested that altered gene expression may play a role in human pathologies. In this review, we explored the role of the transcriptomic profile in MS to investigate the main altered biological processes and pathways involved in the disease. Herein, we focused our attention on RNA-seq methods that in recent years are producing a huge amount of data rapidly replacing microarrays, both with bulk and single-cells. The studies evidenced that different MS stages have specific molecular signatures and non-coding RNAs may play a key role in the disease. Sex-dependence was observed before and after treatments used to alleviate symptomatology activating different biological processes in a drug-dependent manner. New pathways, such as neddylation, were found deregulated in MS and inflammation was linked to neuron degeneration areas through spatial transcriptomics. It is evident that the use of RNA-seq in the study of complex pathologies, such as MS, is a valid strategy to shed light on new involved mechanisms.
 BACKGROUND: Soma and neurite density imaging (SANDI) is a new biophysical model that incorporates soma in addition to neurite density, thus possibly providing more specific information about the complex pathological processes of multiple sclerosis (MS). PURPOSE: To discriminate the pathological abnormalities of MS white matter (WM) lesions, normal-appearing (NA) WM and cortex and to evaluate the associations among SANDI-derived measures, clinical disability, and conventional MRI variables. METHODS: Twenty healthy controls (HC) and 23 MS underwent a 3 T brain MRI. Using SANDI on diffusion-weighted sequence, the fractions of neurite (f(neurite)) and soma (f(soma)) were assessed in WM lesions, NAWM, and cortex. RESULTS: Compared to HC WM, MS NAWM showed lower f(neurite) (false discovery rate [FDR]-p = 0.011). In MS patients, WM lesions showed lower f(neurite) and f(soma) compared to both HC and MS NAWM (FDR-p < 0.001 for all). In the cortex, MS patients had lower f(neurite) and f(soma) compared to HC (FDR-p ≤ 0.009). Compared to both HC and RRMS, PMS patients had lower f(neurite) in NAWM (vs HC: FDR-p < 0.001; vs RRMS: FDR-p = 0.003) and cortex (vs HC: FDR-p < 0.001; vs RRMS: p = 0.031, not surviving FDR correction), and lower cortical f(soma) (vs HC: FDR-p < 0.001; vs RRMS: FDR-p = 0.009). Compared to HC, PMS also showed a higher f(soma) in NAWM (FDR-p = 0.015). F(neurite) and f(soma) in the different brain compartments were correlated with age, phenotype, disease duration, disability, WM lesion volumes, normalized brain, cortical, and WM volumes (r from - 0.761 to 0.821, FDR-p ≤ 0.4). CONCLUSIONS: SANDI may represent a clinically relevant model to discriminate different neurodegenerative phenomena that gradually accumulate through MS disease course.
 Current therapies for multiple sclerosis (MS) reduce both relapses and relapse-associated worsening of disability, which is assumed to be mainly associated with transient infiltration of peripheral immune cells into the central nervous system (CNS). However, approved therapies are less effective at slowing disability accumulation in patients with MS, in part owing to their lack of relevant effects on CNS-compartmentalized inflammation, which has been proposed to drive disability. Bruton tyrosine kinase (BTK) is an intracellular signalling molecule involved in the regulation of maturation, survival, migration and activation of B cells and microglia. As CNS-compartmentalized B cells and microglia are considered central to the immunopathogenesis of progressive MS, treatment with CNS-penetrant BTK inhibitors might curtail disease progression by targeting immune cells on both sides of the blood-brain barrier. Five BTK inhibitors that differ in selectivity, strength of inhibition, binding mechanisms and ability to modulate immune cells within the CNS are currently under investigation in clinical trials as a treatment for MS. This Review describes the role of BTK in various immune cells implicated in MS, provides an overview of preclinical data on BTK inhibitors and discusses the (largely preliminary) data from clinical trials.
 BACKGROUND: Multiple sclerosis (MS) is a demyelinating disease of the central nervous system, rare during childhood. MS variations, like tumefactive MS and Balo concentric sclerosis, constitute puzzling to treat diagnostic dilemmas for pediatric patients. Differential diagnosis, mainly from brain tumors, is an absolute necessity. In addition, apart from treating acute attacks, immunomodulatory alternatives are limited. CASE: We present a 12.5-year-old boy diagnosed, 5 years ago, with tumefactive relapsing-remitting MS, with severe recurrent clinical attacks. Definite diagnosis of demyelination was achieved via combined brain imaging including magnetic resonance (MR) imaging, MR spectroscopy and computed tomography, avoiding brain biopsy. Acute attacks showed satisfactory response to aggressive treatment choices, like plasmapheresis and cyclophosphamide, but age-appropriate immunomodulating treatment was available, only 2 years later. Finally, after a last radiological relapse, when he was 10 years old, fingolimod was initiated. He has been clinically and radiologically stable since, presenting an excellent treatment tolerance.
 The article discusses the possibility and expediency of validating translations into Russian of objective and subjective neurological scales, the advantages and disadvantages of such translations, which is extremely relevant at the present time. As an example, the expediency of «validating» the translation into Russian of the objective neurological scale for assessing the severity of symptoms of the Expanded Disability Status Scale, which is widely used in patients with multiple sclerosis is discussed. The results of assessing the severity of neurological disorders according to these neurological scales do not depend on translation into other languages and therefore do not need validation.
 INTRODUCTION: Multiple sclerosis (MS) is a chronic autoimmune disease with a substantial impact on quality of life and functional capability. The prognosis of MS has changed over time due to the development of increasingly effective therapies. As the knowledge and perceptions of persons living with chronic conditions increasingly have been acknowledged, it has become important to understand lived experiences with a focus on everyday events and experiences as a way of knowing and interpreting the world. Exploring context-specific lived experiences as a source of knowledge about the disease and care may contribute to more precision in designing care services. The aim of this study was to explore the lived experience of persons living with MS in a Swedish context. MATERIALS AND METHODS: A qualitative interview study was conducted with both purposeful and random sampling strategies, resulting in 10 interviews. Data were analyzed using inductive thematic content analysis. RESULTS: The analysis generated 4 overarching themes with 12 subthemes, the 4 themes were: perspectives on life and health, influence on everyday life, relations with healthcare, and shared healthcare processes. The themes are concerned with the patients' own perspectives and context as well as medical and healthcare-related perspectives. Patterns of shared experiences were found, for example, in the diagnosis confirmation, future perspectives, and planning and coordination. More diverse experiences appeared concerning relations with others, one's individual requirements, symptoms and consequences, and knowledge building. CONCLUSION: The findings suggest a need for a more diverse and coproduced development of healthcare services to meet diverse needs in the population with greater acknowledgement of the person's lived experience, including consideration of the complexity of the disease, personal integrity, and different ways of knowing. Findings from this study will be further explored together with other quantitative and qualitative data.
 BACKGROUND: Several disease-modifying treatments (DMTs) for relapsing-remitting multiple sclerosis (RRMS) reduce relapse rates and slow disease progression. RRMS DMTs have varying efficacy and administration routes; DMTs prescribed first may not be the most effective on relapses or disease progression. Here, we aimed to quantify the benefit of initiating ofatumumab, a high-efficacy DMT, earlier in the treatment pathway. METHODS: Aggregate data from a real-world cohort of patients with RRMS, who were eligible for dimethyl fumarate (DMF) or ofatumumab treatment within the UK National Health Service (N = 615), were used to produce a simulated patient cohort. The cohort was tracked through a discrete event simulation (DES) model, based on the Expanded Disability Status Scale (EDSS), with a lifetime time horizon. Outcomes assessed were: mean number of relapses, time to wheelchair (EDSS ≥7), and time to death. Two modeling approaches were used. The first compared outcomes between two treatment sequences (base case: ofatumumab to natalizumab versus DMF to ofatumumab). The second incorporated a time-specific delay of 1-5 years for switching from DMF to ofatumumab; the difference in outcomes as a function of increasing delay to ofatumumab are reported. RESULTS: Compared with delayed ofatumumab, fewer relapses and increased time to wheelchair were predicted for earlier ofatumumab in the treatment-sequence approach (mean relapses over the lifetime time horizon: 8.63 versus 9.00; time to wheelchair: 17.55 versus 16.60 years). Time to death was similar for both sequences. At Year 10, a numerically greater proportion of patients receiving earlier ofatumumab had mild disease (EDSS 0-3: 44.12% versus 40.06%). Greater differences, reflecting poorer outcomes, were predicted for relapses and time to wheelchair with increasing delays to ofatumumab treatment. CONCLUSIONS: The DES model provided a means by which the magnitude of benefit associated with earlier ofatumumab initiation could be quantified; fewer relapses and a prolonged time to wheelchair were predicted.
 Cognitive impairment (CI) has been recognized as one of the core multiple sclerosis (MS) symptoms that profoundly impact lives of people with MS (PwMS). Clinical trials have begun to focus on cognition as a primary or secondary outcome, but translating improvements in cognitive testing scores to functioning in the real world is difficult. Performance-based functional assessments and virtual reality (VR) assessments, which incorporate real-world challenges, have been proposed as a way to better assess functional cognition (i.e., cognitive performance and its impact on real-life cognitive functioning of PwMS) and could address the difficulty in evaluating the impact of a treatment on real-world functioning. In this narrative review, we identify and summarize some of the promising recent research applications of performance-based functional assessments and VR tools to assess functional cognition in MS. Overall, most of the studies suggest that functional and VR assessments can detect cognitive differences between people with and without MS and between PwMS with and without CI. Furthermore, performance on some of the functional and VR assessments was associated with performance on standard cognitive assessments. However, developing any guidelines on how to implement these assessments in clinical practice is difficult because of the relatively small sample size across these studies. Performance-based functional and VR assessments represent an innovative approach to increasing sensitivity of how cognitive impairments/abilities present in the daily life of PwMS. More studies, with a larger sample size, robust research methods, and pre- and post-treatment assessments, are warranted to validate relevant, accessible functional and VR assessments before implementing these assessment approaches in clinical practice.

 BACKGROUND: Mobility impairment is common in older persons with multiple sclerosis (MS), and further compounded by general age-related mobility decline but its underlying brain substrates are poorly understood. OBJECTIVE: Examine fronto-striatal white matter (WM) integrity and lesion load as imaging correlates of mobility outcomes in older persons with and without MS. METHODS: Fifty-one older MS patients (age 64.9 ± 3.7 years, 29 women) and 50 healthy, matched controls (66.2 ± 3.2 years, 24 women), participated in the study, which included physical and cognitive test batteries and 3T MRI imaging session. Primary imaging measures were fractional anisotropy (FA) and WM lesion load. The relationship between mobility impairment, defined using a validated short physical performance battery cutoff score, and neuroimaging measures was assessed with stratified logistic regression models. FA was extracted from six fronto-striatal circuits (left/right): dorsal striatum (dStr)-to-anterior dorsolateral prefrontal cortex (aDLPFC), dStr-to-posterior DLPFC, and ventral striatum (vStr)-to-ventromedial prefrontal cortex (VMPFC). RESULTS: Mobility impairment was significantly associated with lower FA in two circuits, left dStr-aDLPFC (P = .003) and left vStr-VMPFC (P = .004), in healthy controls but not in MS patients (P > .20), for fully adjusted regression models. Conversely, in MS patients but not in healthy controls, mobility impairment was significantly associated with greater lesion volume (P < .02). CONCLUSIONS: Comparing older persons with and without MS, we provide compelling evidence of a double dissociation between the presence of mobility impairment and two neuroimaging markers of white matter integrity, fronto-striatal fractional anisotropy, and whole brain lesion load.
 In addition to the classical neurourological diseases multiple sclerosis and paraplegia/spina bifida, there are many and also widely spread diseases of the neurological spectrum that can result in significant dysfunctions of the urinary tract. Depending on the location (cerebral/suprapontine, spinal/suprasacral, spinal infrasacral and peripheral), different disorders can result (detrusor overactivity and underactivity, sphincter dyssynergia and low compliance). Changes can also occur over the course of an illness and thus make the analysis of the respective disorder even more difficult. Not all patients present directly to a neurourological center and in some cases the connection is not directly apparent. Firstly, this article focuses on the urological relevance of the respective neurological disease. Secondly, the basic neurourological information should support the initial assessment of the disorder.
 INTRODUCTION: Family caregivers of patients with multiple sclerosis (MS) are at risk of care burden that may lead to a detrimental effect on their quality of life (QoL), physical and mental well-being. This study aimed to determine the effect of the family-centered empowerment model (FCEM) on the care burden of caregivers of patients with MS. METHODS: This quasi-experimental study was conducted using convenience sampling on 60 caregivers of patients referring to the Multiple Sclerosis Clinic in Ghaem Hospital, Mashhad, Iran. The participants were assigned to FCEM and control groups based on the days they were referred to the MS clinic. Data collection tools included the Zarit Caregiver Burden Inventory (CBI), completed in the intervention and control groups before and 1 month after the intervention. The support based on FCEM was provided during eight 45-60-min sessions, and the control group received the medical center's routine training. Data were analyzed by Chi-square, independent t-test, analysis of covariance, and repeated measure tests. RESULTS: The results of the present study showed that all demographic characteristics were homogeneous at the baseline. Before the intervention, no significant difference was observed between the two groups regarding mean scores of care burden. Based on the repeated measure test, there was no significant treatment and time interaction in changes in care burden. CONCLUSION: The FCEM has no significant effect in alleviating the care burden. It is recommended to observe the necessary considerations regarding the context of this type of intervention and to carry out further investigations in different intervals.
 BACKGROUND: Multiple sclerosis is a chronic progressive disease of the central nervous system that affects the patients' quality of life. The disease's complications reduce the quality of life in patients by creating physical, psychological, social and economic problems for the patient and his/her family and reducing the patient's individual and social functioning. The aim of the present study is designing, implementing and evaluating an intervention based on the PRECEDE-PROCEED model to promote the quality of life in people with multiple sclerosis. This paper summarizes the study protocol. METHODS: We will use the PRECEDE-PROCEED model for designing the study. In the first step, the factors affecting quality of life in people with multiple sclerosis will be determined by a qualitative study. In the second step, these factors will be prioritized based on their importance and variability, then behavioral and environmental factors of the most important priority will be identified. In the third step, the predisposing, enabling and reinforcing factors related to the identified priority will be determined by a qualitative directed content analysis. In the fourth step, a questionnaire will be designed and psychometric based on the results of the previous step. The fifth step will be about planning to implement the intervention. In the sixth step, the intervention will be implemented and its effectiveness will be evaluated by process, impact and outcome evaluations. DISCUSSION: The results of this study will provide information about patients' needs and concerns and thus will contribute to policymakers, government, community, health professionals and families to take the necessary measures to improve quality of life in these patients.
 Hepatocyte nuclear factor 4 α (HNF4α), a transcription factor (TF) essential for embryonic development, has been recently shown to regulate the expression of inflammatory genes. To characterize HNF4a function in immunity, we measured the effect of HNF4α antagonists on immune cell responses in vitro and in vivo. HNF4α blockade reduced immune activation in vitro and disease severity in the experimental model of multiple sclerosis (MS). Network biology studies of human immune transcriptomes unraveled HNF4α together with SP1 and c-myc as master TF regulating differential expression at all MS stages. TF expression was boosted by immune cell activation, regulated by environmental MS risk factors and higher in MS immune cells compared to controls. Administration of compounds targeting TF expression or function demonstrated non-synergic, interdependent transcriptional control of CNS autoimmunity in vitro and in vivo. Collectively, we identified a coregulatory transcriptional network sustaining neuroinflammation and representing an attractive therapeutic target for MS and other inflammatory disorders.
 BACKGROUND: Natalizumab via subcutaneous administration was recently approved for patients with multiple sclerosis. OBJECTIVE: In light of personalized extended dosing, in which treatment intervals are prolonged to a concentration cut-off, it would be preferable to measure natalizumab drug concentrations in capillary blood. METHODS: In this cross-sectional study in patients treated with intravenous (IV) natalizumab, capillary blood samples by fingerprick and venous blood samples were collected in 30 participants prior to IV administration of natalizumab. RESULTS: Natalizumab concentrations were similar with a mean bias of -0.36 μg/mL (95% CI: 1.3 to -2 μg/mL). CONCLUSIONS: This study shows that physicians can monitor natalizumab drug concentrations by a fingerprick, which could be used for personalized extended dosing.
 BACKGROUND: As cladribine is contraindicated in pregnancy, data to pregnancy outcomes and disease control are scarce. OBJECTIVE: To investigate the effects of Cladribine use, in the last 6 months prior (56.4%) to or after (43.6%) the last menstrual period in a population of women with multiple sclerosis, on pregnancy outcomes and relapse rate during pregnancy and postpartum. METHODS: Data were collected prospectively in regular telephone interviews. RESULTS: Of 39 pregnancies, 27 babies have been born so far and one major congenital malformation occurred. Disease control was excellent among the cohort both during pregnancy and the postpartum period, with only one relapse recorded in each time period. CONCLUSIONS: Although most newborns are healthy, reinforced councelling on effective contraception 6 months after the last cladribine dosing is necessary.
 PURPOSE: To evaluate the corneal nerve fiber morphology in patients with multiple sclerosis (MS) by in vivo corneal confocal microscopy (CCM). METHODS: Retinal nerve fiber layer thickness (RNFLT), central macular thickness (CMT), corneal nerve fiber length (CNFL), corneal nerve fiber density (CNFD), corneal nerve branch density (CNBD) and corneal nerve fiber tortuosity (CNFT) were measured. Correlation of corneal nerve findings with duration and clinical severity of MS was calculated. RESULTS: CNFL (9.50 ± 0.60 vs. 11.20 ± 0.57 mm/mm(2), P = 0.046) and CNBD (57.46 ± 5.04 vs. 77.65 ± 3.41 no/mm(2), P = 0.001) were significantly lower with no significant difference in CNFD (21.24 ± 1.20 vs. 23.62 ± 0.95 no/mm(2), P = 0.125), CNFT (2.00 ± 0.15 vs. 1.73 ± 0.12, P = 0.180), CMT (269.57 ± 12.53 vs. 271.10 ± 18.84 μm, P = 0.716) or RNFLT (102.82 ± 6.98 vs. 105.33 ± 12.70 μm, P = 0.351) between patients with RRMS compared to controls. There was no significant correlation between CCM parameters with EDSS and duration of disease in MS patients. CONCLUSION: The current study demonstrated that a decrease in CNFL, CNFD and CNBD in CCM analysis in the early course of MS.
 BACKGROUND: Circular RNAs (circRNAs) are a class of non-coding RNAs increasingly emerging as crucial actors in the pathogenesis of human diseases, including autoimmune and neurological disorders as multiple sclerosis (MS). Despite several efforts, the mechanisms regulating circRNAs expression are still largely unknown and the circRNA profile and regulation in MS-relevant cell models has not been completely investigated. In this work, we aimed at exploring the global landscape of circRNA expression in MS patients, also evaluating a possible correlation with their genetic and epigenetic background. METHODS: We performed RNA-seq experiments on circRNA-enriched samples, derived from peripheral blood mononuclear cells (PBMCs) of 10 MS patients and 10 matched controls and performed differential circRNA expression. The genetic background was evaluated using array genotyping, and an expression quantitative trait loci (eQTL) analysis was carried out. RESULTS: Expression analysis revealed 166 differentially expressed circRNAs in MS patients, 125 of which are downregulated. One of the top dysregulated circRNAs, hsa_circ_0007990, derives from the PGAP3 gene, encoding a protein relevant for the control of autoimmune responses. The downregulation of this circRNA was confirmed in two independent replication cohorts, suggesting its implementation as a possible RNA-based biomarker. The eQTL analysis evidenced a significant association between 89 MS-associated loci and the expression of at least one circRNA, suggesting that MS-associated variants could impact on disease pathogenesis by altering circRNA profiles. Finally, we found a significant correlation between exon methylation and circRNA expression levels, supporting the hypothesis that epigenetic features may play an important role in the definition of the cell circRNA pool. CONCLUSION: We described the circRNA expression profile of PBMCs in MS patients, suggesting that MS-associated variants may tune the expression levels of circRNAs acting as "circ-QTLs", and proposing a role for exon-based DNA methylation in regulating circRNA expression.

 BACKGROUND: Depression and anxiety are common psychiatric comorbidities among people with multiple sclerosis (MS). Emerging data suggest abnormal serum homocysteine, vitamin B(12), and folate levels in people with MS, which are related to a range of neurological disorders, including mood and mental illnesses. Evidence suggests that dietary interventions could affect mood disorders via several pathways. This study aimed to evaluate the impact of the low-saturated fat (Swank) and modified Paleolithic elimination (Wahls) diets, along with a supplement regimen, on mood as assessed by Hospital Anxiety and Depression Scale (HADS), and Mental Health Inventory (MHI). The secondary objective was to identify changes in serum levels of homocysteine, folate, and vitamin B(12) and the association and mediation effects between their changes and HADS and MHI scores and their subscales among people with relapsing-remitting MS (RRMS). METHODS: In a previously conducted randomized parallel-arm trial, participants with RRMS (n = 77) were randomly allocated to either the Swank or Wahls diets at baseline and followed for 24 weeks. Blood was drawn at four study visits spaced 12 weeks apart: (1) run-in, (2) baseline, (3) 12 weeks, and (4) 24 weeks. Serum vitamin B(12), folate, and homocysteine were analyzed. HADS and MHI questionnaires were also completed by participants at the four study visits to assess symptoms of depression and anxiety, behavioral control and positive affect respectively. RESULTS: Significant improvement in severity of depression (HADS-D) and anxiety (HADS-A) symptoms, MHI total, and MHI subscores were seen at 12 and 24 weeks in each diet group. Further, a significant within-group reduction in serum homocysteine and a significant increase in serum vitamin B(12) level were observed in both groups at 12 and 24 weeks compared to corresponding baseline values (p ≤ 0.05 for all). All participants exceeded the analytical maximum threshold for folate of 20 nmol/L at 12 and 24 weeks. Changes in serum levels of homocysteine and vitamin B(12) were not associated with and did not mediate changes in HADS depression, anxiety, MHI total and four subscales scores (p > 0.05). CONCLUSION: Participants on both Swank and Wahls dietary interventions, including folate and vitamin B(12) supplements, showed significant improvement in mood. However, the favorable effects of both diets on mood were not associated with or mediated by the effect of the diets on serum levels of homocysteine, folate, and vitamin B(12) (p > 0.05).
 OBJECTIVES: Recent studies supported coagulation involvement in multiple sclerosis, an inflammatory-demyelinating and degenerative disease of the central nervous system. The main objectives of this observational study were to identify the most specific pro-coagulative/vascular factors for multiple sclerosis pathogenesis and to correlate them with brain hemodynamic abnormalities. METHODS: We compared i) serum/plasma levels of complement(C)/coagulation/vascular factors, viral/microbiological assays, fat-soluble vitamins and lymphocyte count among people with multiple sclerosis sampled in a clinical remission (n=30; 23F/7M, 40 ± 8.14 years) or a relapse (n=30; 24F/6M, age 41 ± 10.74 years) and age/sex-matched controls (n=30; 23F/7M, 40 ± 8.38 years); ii) brain hemodynamic metrics at dynamic susceptibility contrast-enhanced 3T-MRI during relapse and remission, and iii) laboratory data with MRI perfusion metrics and clinical features of people with multiple sclerosis. Two models by Partial Least Squares Discriminant Analysis were performed using two groups as input: (1) multiple sclerosis vs. controls, and (2) relapsing vs. remitting multiple sclerosis. RESULTS: Compared to controls, multiple sclerosis patients had a higher Body-Mass-Index, Protein-C and activated-C9; and a lower activated-C4. Levels of Tissue-Factor, Tie-2 and P-Selectin/CD62P were lower in relapse compared to remission and HC, whereas Angiopoietin-I was higher in relapsing vs. remitting multiple sclerosis. A lower number of total lymphocytes was found in relapsing multiple sclerosis vs. remitting multiple sclerosis and controls. Cerebral-Blood-Volume was lower in normal-appearing white matter and left caudatum while Cerebral-Blood-Flow was inferior in bilateral putamen in relapsing versus remitting multiple sclerosis. The mean-transit-time of gadolinium-enhancing lesions negatively correlated with Tissue-Factor. The top-5 discriminating variables for model (1) were: EBV-EBNA-1 IgG, Body-Mass-Index, Protein-C, activated-C4 and Tissue-Factor whereas for model (2) were: Tissue-Factor, Angiopoietin-I, MCHC, Vitamin A and T-CD3. CONCLUSION: Tissue-factor was one of the top-5 variables in the models discriminating either multiple sclerosis from controls or multiple sclerosis relapse from remission and correlated with mean-transit-time of gadolinium-enhancing lesions. Tissue-factor appears a promising pro-coagulative/vascular biomarker and a possible therapeutic target in relapsing-remitting multiple sclerosis. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, identifier NCT04380220.

 The widespread use of magnetic resonance imaging (MRI) has led to an increase in incidental findings in the central nervous system. Radiologically isolated syndrome (RIS) is a condition where imaging reveals lesions suggestive of demyelinating disease without any clinical episodes consistent with multiple sclerosis (MS). The prognosis for RIS patients is uncertain, with some remaining asymptomatic while others progress to MS. Several risk factors for disease progression have been identified, including male sex, younger age at diagnosis, and spinal cord lesions. This article reviews two promising biomarkers, the central vein sign (CVS) and the paramagnetic rim sign (PRS), and their potential role in the diagnosis and prognosis of MS and RIS. Both CVS and PRS have been shown to be accurate diagnostic markers in MS, with high sensitivity and specificity, and have been useful in distinguishing MS from other disorders. Further research is needed to validate these findings and determine the clinical utility of these biomarkers in routine practice.
 BACKGROUND AND OBJECTIVES: In multiple sclerosis (MS), contrast enhancement lesions and chronic active lesions have been demonstrated to have different degrees of inflammation. Accordingly, they exist different degrees of tissue damage, one is short and acute, and another is slow and longstanding. This study aimed to explore whether diffusion parameters can differentiate different types of lesions, and investigate the microstructural damage between different types of MS lesions by using diffusion magnetic resonance imaging (dMRI) and its correlation with clinical biomarkers of disability and cognitive states. METHODS: We retrospectively identified 77 contrast enhancement lesions (CELs), 384 iron rim lesions (IRLs), 393 non-iron rim lesions (NIRLs), their corresponding perilesional white matter (PLWM), and 68 normal-appearing white matter (NAWM) from 68 relapsing-remitting MS (RRMS). Additionally, 44 white matter in healthy controls (WM in HCs) were also enrolled in this study. The DTI and DKI parameters were measured in the above white matter, including kurtosis fractional anisotropy (KFA), fractional anisotropy (FA), mean kurtosis (MK), and mean diffusivity (MD). All the patients were assessed with the Digital Span Test (DST), the Symbol Digit Modalities Test (SDMT), the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA), and the Expanded Disability Status Scale (EDSS). RESULTS: The lowest KFA, FA, MK values and the highest MD values were found in CELs, followed by IRLs, NIRLs, NAWM, and WM in HCs. In KFA and FA values, there were significant differences between each type of lesion, as well as each type of PLWM (P < 0.05). The MK values of CELs and IRLs were significantly lower than NIRLs, but inversely for MD (P < 0.05). There were no differences between CELs and IRLs for MK (P = 1) and MD (P = 0.261). The results of MK and MD values in CELs-PLWM and IRLs-PLWM were similar to the CELs and IRLs. There were no significant differences between NAWM and WM in HCs in all the enrolled diffusion parameters (P >0.05) and the FA values between NIRLs-PLWM and NAWM or between NIRLs-PLWM and WM in HCs were no significant differences (P >0.05). The KFA and MD values in IRLs-PLWM (r =0.443, P =0.021; r =-0.518, P =0.006) were correlated with the DST scores and the KFA of CELs-PLWM (r =0.396, P =0.041) was correlated with SDMT scores. CONCLUSION: Our findings demonstrate that the KFA values have the potential to distinguish different types of MS white matter tissues. Furthermore, the diffusion parameters can reflect the microstructure abnormalities in different MS lesions and might help us better understand the pathological mechanism and lesion evolution.
 B cell depletion is becoming a preferred long-term treatment even in early multiple sclerosis, but concerns about the risks of impaired immune competence persist. In their observational study Schuckmann et al. thoroughly assessed the impact of B cell-adapted extended interval dosing on immunoglobulin levels as a surrogate of adverse immunosuppressive effects.
 BACKGROUND: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct central nervous system (CNS) disorder that shares features with multiple sclerosis (MS) and may be misdiagnosed as MS. MOGAD and MS share a frequently relapsing clinical course and lesions with inflammatory demyelinating pathology. One key feature of MS pathology is tissue damage in normal-appearing white matter (NAWM) outside of discrete lesions, whereas the extent to which similar non-lesional damage occurs in MOGAD is not known and could be assessed using qGRE. The goal of this study was to examine the brains of people with MOGAD using quantitative gradient-recalled echo (qGRE) magnetic resonance imaging and to compare tissue damage with MS patients matched for disability. METHODS: MOGAD and MS patients were recruited to match in terms of age and disability. Similarly aged healthy control (HC) data were drawn from existing studies. qGRE brain imaging of HC (N = 15), MOGAD (N = 17), and MS (N = 15) patients was used to examine the severity and extent of tissue damage within and outside of discrete lesions. The qGRE metric R2t* is sensitive to changes in tissue microstructure and was measured in white matter lesions (WMLs), NAWM, cortical (CGM) and deep gray matter (DGM). Statistical inference was performed with linear models. RESULTS: R2t* was reduced in CGM (p = 0.00047), DGM (p = 0.0055) and NAWM (p = 0.0019) in MOGAD and MS compared to similar regions in age-matched HCs. However, the degree of R2t* reduction in all these regions was less in the MOGAD patients compared with MS. WMLs in MOGAD demonstrated reduced R2t* compared to NAWM but this reduction was modest compared to changes associated with WMLs in MS (p = 0.026). CONCLUSION: These results demonstrate abnormalities in lesional and non-lesional CNS tissues in MOGAD that are not detectable on standard MRI. The abnormalities seen in NAWM, CGM, and DGM were less severe in MOGAD compared to MS. MOGAD-related WMLs showed reduced R2t*, but were less abnormal than WMLs in MS. These data reveal damage to non-lesional tissues in two different demyelinating diseases, suggesting that damage outside of WMLs may be a common feature of demyelinating diseases. The lesser degree of R2t* abnormality in MOGAD tissues compared to MS suggests less underlying tissue damage and may underlie the greater propensity for recovery in MOGAD.
 INTRODUCTION: Multiple sclerosis is an inflammatory and demyelinating disease caused by a pathogenic immune response against the myelin sheath surfaces of oligodendrocytes. The demyelination has been classically associated with pathogenic B cells residing in the central nervous system that release autoreactive antibodies against myelin. The aim of the present study was to investigate whether extracellular vesicles (EVs) mediate delivery of myelin autoreactive antibodies from peripheral B cells against oligodendrocytes in multiple sclerosis (MS) and to analyze whether these EVs could mediate demyelination in vitro. We also studied the role of these EV-derived myelin antibodies as a diagnostic biomarker in MS. METHODS: This is a prospective, observational, and single-center study that includes patients with MS and two control groups: patients with non-immune white matter lesions and healthy controls. We isolated B-cell-derived EVs from the blood and cerebrospinal fluid (CSF) and analyzed their myelin antibody content. We also studied whether antibody-loaded EVs reach oligodendrocytes in patients with MS and the effect on demyelination of B-cell-derived EVs containing antibodies in vitro. RESULTS: This study enrolled 136 MS patients, 23 white matter lesions controls, and 39 healthy controls. We found autoreactive myelin antibodies in EVs that were released by peripheral B cells, but not by populations of B cells resident in CSF. We also identified a cut-off of 3.95 ng/mL of myelin basic protein autoantibodies in EVs from peripheral B cells, with 95.2% sensitivity and 88.2% specificity, which allows us to differentiate MS patients from healthy controls. EV-derived myelin antibodies were also detected in the oligodendrocytes of MS patients. Myelin antibody-loaded EVs from B cells induced myelin markers decrease of oligodendrocytes in vitro. DISCUSSION: Peripheral reactive immune cells could contribute remotely to MS pathogenesis by delivering myelin antibodies to oligodendrocytes. EV-derived myelin antibodies could play a role as diagnostic biomarker in MS.
 The purpose of this study was to examine whether myeloid dendritic cells (mDCs) from patients with multiple sclerosis (MS) and healthy controls (HCs) become similarly tolerogenic when exposed to IL-27 as this may represent a potential mechanism of autoimmune dysregulation. Our study focused on natural mDCs that were isolated from HCs and MS patient peripheral blood mononuclear cells (PBMCs). After a 24-h treatment with IL-27 ± lipopolysaccharide (LPS), the mDCs were either harvested to identify IL-27-regulated gene expression or co-cultured with naive T-cells to measure how the treated DC affected T-cell proliferation and cytokine secretion. mDCs isolated from HCs but not untreated MS patients became functionally tolerogenic after IL-27 treatment. Although IL-27 induced both HC and untreated MS mDCs to produce similar amounts of IL-10, the tolerogenic HC mDCs expressed PD-L2, IDO1, and SOCS1, while the non-tolerogenic untreated MS mDCs expressed IDO1 and IL-6R. Cytokine and RNA analyses identified two signature blocks: the first identified genes associated with mDC tolerizing responses to IL-27, while the second was associated with the presence of MS. In contrast to mDCs from untreated MS patients, mDCs from HCs and IFNb-treated MS patients became tolerogenic in response to IL-27. The genes differentially expressed in the different donor IL-27-treated mDCs may contain targets that regulate mDC tolerogenic responses.

 Introduction: different lines of evidence have shown that ginger administration may be beneficial for patients with multiple sclerosis (MS). Therefore, we aimed to investigate the effect of ginger supplementation on disability, physical and psychological quality of life (QoL), body mass index (BMI), neurofilament light chain (NfL), interlukin-17 (IL-17), matrix metalloproteinase-9 (MMP-9), and neutrophil to lymphocyte ratio (NLR) in patients with relapsing-remitting MS. Methods: this was a 12 week double-blind parallel randomized placebo-controlled trial with a 3 week run-in period. The treatment (n = 26) and control (n = 26) groups received 500 mg ginger and placebo (corn) supplements 3 times daily, respectively. Disability was evaluated using the Expanded Disability Status Scale (EDSS). QoL was rated using the Multiple Sclerosis Impact Scale (MSIS-29). BMI was calculated by dividing weight by height squared. Serum levels of NfL, IL-17, and MMP-9 were measured using the enzyme-linked immunosorbent assay. NLR was determined using a Sysmex XP-300™ automated hematology analyzer. All outcomes were assessed before and after the intervention and analyzed using the intention-to-treat principle. Results: in comparison with placebo, ginger supplementation caused a significant reduction in the EDSS (-0.54 ± 0.58 vs. 0.08 ± 0.23, P < 0.001), the MSIS-29 physical scale (-8.15 ± 15.75 vs. 4.23 ± 8.46, P = 0.001), the MSIS-29 psychological scale (-15.71 ± 19.59 vs. 6.68 ± 10.41, P < 0.001), NfL (-0.14 ± 0.97 vs. 0.38 ± 1.06 ng mL(-1), P = 0.049), IL-17 (-3.34 ± 4.06 vs. 1.77 ± 6.51 ng L(-1), P = 0.003), and NLR (-0.09 ± 0.53 vs. 0.53 ± 1.90, P = 0.038). Nevertheless, the differences in BMI and MMP-9 were not significant between the groups. Conclusion: ginger supplementation may be an effective adjuvant therapy for patients with relapsing-remitting MS.
 BACKGROUND: The selection and description of participants in clinical trials enables health care providers to determine generalizability of findings to the populations they serve. Limited diversity of participants in trials restricts evidence-based decision-making. OBJECTIVES: To determine the extent to which diverse participants are being included in clinical trials of rehabilitation interventions for people with multiple sclerosis (MS). METHODS: We conducted a scoping review of MS rehabilitation trials published since January 2002 using MEDLINE, CINAHL, and Web of Science. Covidence was used to facilitate the review. Article selection required randomized control design, a rehabilitation intervention, and a functional status outcome. Data extracted included details of intervention(s), outcomes, and participant selection and description using a social determinants of health framework. RESULT: A total of 243 studies were included. Exercise interventions and impairment-focused outcomes were most common. Most studies used only a MS Clinic for recruitment. Common exclusion criteria were physical or mental comorbidities, disability, age, and cognitive impairment. Participant age and sex were reported for almost all trials; reporting of other social determinants of health was atypical. CONCLUSION: MS rehabilitation trials have used limited recruitment methods, restricted samples, and reported few participant descriptors. Changes are required to enhance participant diversity and the descriptions of participant characteristics.
 OBJECTIVE: To evaluate the efficacy and safety of the anti-CD20 monoclonal antibody divozilimab (DIV) used as an intravenous infusion at a dose of 500 mg for the treatment of patients with relapsing-remitting multiple sclerosis (RRMS) in comparison with the teriflunomide (TRF). The study of the efficacy and safety of the use of the drug DIV was carried out for 48 weeks of therapy. MATERIAL AND METHODS: The multicenter, randomized, double-blind and double-masked phase III clinical trial (CT) BCD-132-4/MIRANTIBUS included 338 adult patients with RRMS distributed in a 1:1 ratio into two groups: DIV 500 mg and TRF 14 mg. After screening, subjects were included in the main CT period, which consisted of two cycles of therapy over 48 weeks. The primary end point was «Mean annualized relapse rate 48 weeks after the last patient is randomized in the study». RESULTS: 321 subjects completed 48 weeks of therapy according to the study protocol. The analysis of the of efficacy data for the primary endpoint successively proved the hypothesis of superiority of the test drug DIV at a dose of 500 mg over the reference drug TRF. A rapid suppression of acute disease activity according to the brain MRI and clinical manifestations of the disease was shown after the first infusion of DIV in patients with RRMS. Thus, after 48 weeks of therapy in patients treated with DIV, there were no T1 gadolinium-enhancing lesions, while in the TRF group such lesions were observed in 20.7% (35/169) of subjects. Evaluation of the CUA per scan showed that the mean values for the estimated period were statistically significantly lower in the DIV drug group compared to the TRF group: the ratio of the adjusted per scan rates (DIV/TRF) was 0.125 [95% CI: 0.089; 0.177]. Over the 48 weeks of therapy, the proportion of subjects with relapses was 9.5% (n=16/169) in the DIV group and 19.5% (33/169) in the TRF group (p=0.0086). DIV has shown a favorable safety profile. Among the adverse reactions (AR), infusion reactions and deviations of laboratory data, such as a decrease in the number of leukocytes, neutrophils, and lymphocytes, were most often recorded. Identified AR were expected, had mild to moderate severity, and resolved without any negative consequences. CONCLUSION: The results of the clinical study indicate the high efficacy and safety of DIV in comparison with TRF.
 The progressive forms of multiple sclerosis (MS) primary progressive MS (PPMS) and secondary progressive MS (SPMS) are clinically distinguished by the rate at which symptoms worsen. Little is however known about the pathological mechanisms underlying the differential rate of accumulation of pathological changes. In this study, (1)H NMR spectroscopy was used to measure low-molecular-weight metabolites in paired cerebrospinal fluid (CSF) and serum of PPMS, SPMS, and control patients, as well as to determine lipoproteins and glycoproteins in serum samples. Additionally, neurodegenerative and inflammatory markers, neurofilament light (NFL) and chitinase-3-like protein 1 (CHI3L1), and the concentration of seven metal elements, Mg, Mn, Cu, Fe, Pb, Zn, and Ca, were also determined in both CSF and serum. The results indicate that the pathological changes associated with progressive MS are mainly localized in the central nervous system (CNS). More so, PPMS and SPMS patients with comparable disability status are pathologically similar in relation to neurodegeneration, neuroinflammation, and some metabolites that distinguish them from controls. However, the rapid progression of PPMS from the onset may be driven by a combination of neurotoxicity induced by heavy metals coupled with diminished CNS antioxidative capacity associated with differential intrathecal ascorbate retention and imbalance of Mg and Cu.
 Multiple sclerosis is a leading cause of neurological disability in adults. Heterogeneity in multiple sclerosis clinical presentation has posed a major challenge for identifying genetic variants associated with disease outcomes. To overcome this challenge, we used prospectively ascertained clinical outcomes data from the largest international multiple sclerosis registry, MSBase. We assembled a cohort of deeply phenotyped individuals of European ancestry with relapse-onset multiple sclerosis. We used unbiased genome-wide association study and machine learning approaches to assess the genetic contribution to longitudinally defined multiple sclerosis severity phenotypes in 1813 individuals. Our primary analyses did not identify any genetic variants of moderate to large effect sizes that met genome-wide significance thresholds. The strongest signal was associated with rs7289446 (β = -0.4882, P = 2.73 × 10-7), intronic to SEZ6L on chromosome 22. However, we demonstrate that clinical outcomes in relapse-onset multiple sclerosis are associated with multiple genetic loci of small effect sizes. Using a machine learning approach incorporating over 62 000 variants together with clinical and demographic variables available at multiple sclerosis disease onset, we could predict severity with an area under the receiver operator curve of 0.84 (95% CI 0.79-0.88). Our machine learning algorithm achieved positive predictive value for outcome assignation of 80% and negative predictive value of 88%. This outperformed our machine learning algorithm that contained clinical and demographic variables alone (area under the receiver operator curve 0.54, 95% CI 0.48-0.60). Secondary, sex-stratified analyses identified two genetic loci that met genome-wide significance thresholds. One in females (rs10967273; βfemale = 0.8289, P = 3.52 × 10-8), the other in males (rs698805; βmale = -1.5395, P = 4.35 × 10-8), providing some evidence for sex dimorphism in multiple sclerosis severity. Tissue enrichment and pathway analyses identified an overrepresentation of genes expressed in CNS compartments generally, and specifically in the cerebellum (P = 0.023). These involved mitochondrial function, synaptic plasticity, oligodendroglial biology, cellular senescence, calcium and G-protein receptor signalling pathways. We further identified six variants with strong evidence for regulating clinical outcomes, the strongest signal again intronic to SEZ6L (adjusted hazard ratio 0.72, P = 4.85 × 10-4). Here we report a milestone in our progress towards understanding the clinical heterogeneity of multiple sclerosis outcomes, implicating functionally distinct mechanisms to multiple sclerosis risk. Importantly, we demonstrate that machine learning using common single nucleotide variant clusters, together with clinical variables readily available at diagnosis can improve prognostic capabilities at diagnosis, and with further validation has the potential to translate to meaningful clinical practice change.
 BACKGROUND: Mobile health applications (apps) are promising condition self-management tools for people living with multiple sclerosis (MS). However, most existing apps do not include health tracking features. This gap has been raised as a priority research topic, but the development of new self-management apps will require designers to understand the context and needs of those living with MS. Our aim was to conduct a content analysis of publicly available user reviews of existing MS self-management apps to understand desired features and guide the design of future apps. METHODS: We systematically reviewed MS self-management apps which were publicly available in English on the Google Play and iOS app stores. We then conducted sentiment and content analysis of recent user reviews which referenced health tracking and data visualization to understand self-reported experiences and feedback. RESULTS: Searches identified 75 unique apps, of which six met eligibility criteria and had reviews. One hundred and thirty-seven user reviews of these apps were eligible, though most were associated with a single app (n=108). Overall, ratings and sentiment scores skewed highly positive (Median [IQR]: Ratings - 5 [4-5], Sentiment scores - 0.70 [0.44-0.86]), though scores of individual apps varied. Content analysis revealed five themes: reasons for app usage, simple user experience, customization and flexibility, feature requests, and technical issues. Reviewers suggested that app customization, interconnectivity, and consolidated access to desired features should be considered in the design of future apps. User ratings weakly correlated with review sentiment scores (ρ = 0.27 [0.11-0.42]). CONCLUSIONS: Self-tracking options in MS apps are currently limited, though the apps that offer these functions are considered useful by individuals with MS. Additional qualitative research is required to understand how specific app features and opportunities for personalization should be incorporated into new self-management tools for this population.
 PURPOSE: The relevance of self-concept change in the process of psychosocial adjustment following multiple sclerosis (MS) diagnosis has become more apparent in recent years. The current study aimed to investigate the experience of self-concept change as described by an MS sample. METHODS: Sixteen people (aged 26-67 years, 62.5% female) who had been living with MS for an average of 12 years, participated in a single online semi-structured interview. All interviews were audio-recorded and transcribed verbatim. RESULTS: Thematic analysis guided by phenomenology produced three superordinate themes: 1) Changing life (salient external events that were related to changing views of self), 2) Changing self (the experience of self-concept change), and 3) Changing thoughts (the internal thought processes that served as the filter between changing life circumstances and changing self-views). Overall, external events appeared to facilitate a process of internally driven revaluations and redefinitions of self-concept both globally and within specific self domains. CONCLUSION: Self-concept change due to MS emerges as a complex internal process, often arising from external challenges and changes in everyday life. These novel findings illustrate the need to better support people with MS to make sense of changes to their self-concept, particularly during key transitions across the illness.Implications for RehabilitationSelf-concept change following MS diagnosis and throughout the disease course has wide-ranging impacts on psychological adjustment.Several key external events contribute to changing the self-views of people living with MS.While external events prompt change, key internal processes likely facilitate the redefinition of self-concept.Targeted support during key transitional periods to assist pwMS to productively renegotiate and manage these changes to their self-concept is needed.
 OBJECTIVE: To validate the smartphone sensor-based Draw a Shape Test - a part of the Floodlight Proof-of-Concept app for remotely assessing multiple sclerosis-related upper extremity impairment by tracing six different shapes. METHODS: People with multiple sclerosis, classified functionally normal/abnormal via their Nine-Hole Peg Test time, and healthy controls participated in a 24-week, nonrandomized study. Spatial (trace accuracy), temporal (mean and variability in linear, angular, and radial drawing velocities, and dwell time ratio), and spatiotemporal features (trace celerity) were cross-sectionally analyzed for correlation with standard clinical and brain magnetic resonance imaging (normalized brain volume and total lesion volume) disease burden measures, and for capacity to differentiate people with multiple sclerosis from healthy controls. RESULTS: Data from 69 people with multiple sclerosis and 18 healthy controls were analyzed. Trace accuracy (all shapes), linear velocity variability (circle, figure-of-8, spiral shapes), and radial velocity variability (spiral shape) had a mostly fair/moderate-to-good correlation (|r| = 0.14-0.66) with all disease burden measures. Trace celerity also had mostly fair/moderate-to-good correlation (|r| = 0.18-0.41) with Nine-Hole Peg Test performance, cerebellar functional system score, and brain magnetic resonance imaging. Furthermore, partial correlation analysis related these results to motor impairment. People with multiple sclerosis showed greater drawing velocity variability, though slower mean velocity, than healthy controls. Linear velocity (spiral shape) and angular velocity (circle shape) potentially differentiate functionally normal people with multiple sclerosis from healthy controls. INTERPRETATION: The Draw a Shape Test objectively assesses upper extremity impairment and correlates with all disease burden measures, thus aiding multiple sclerosis-related upper extremity impairment characterization.
 Remyelination is crucial to recover from inflammatory demyelination in multiple sclerosis (MS). Investigating remyelination in vivo using magnetic resonance imaging (MRI) is difficult in MS, where collecting serial short-interval scans is challenging. Using experimental autoimmune encephalomyelitis (EAE) in common marmosets, a model of MS that recapitulates focal cerebral inflammatory demyelinating lesions, we investigated whether MRI is sensitive to, and can characterize, remyelination. In six animals followed with multisequence 7 T MRI, 31 focal lesions, predicted to be demyelinated or remyelinated based on signal intensity on proton density-weighted images, were subsequently assessed with histopathology. Remyelination occurred in four of six marmosets and 45% of lesions. Radiological-pathological comparison showed that MRI had high statistical sensitivity (100%) and specificity (90%) for detecting remyelination. This study demonstrates the prevalence of spontaneous remyelination in marmoset EAE and the ability of in vivo MRI to detect it, with implications for preclinical testing of pro-remyelinating agents.
 INTRODUCTION: Natalizumab and fingolimod are well-established, sequestrating disease-modifying treatments (DMTs), widely used as a second-line treatment in patients with relapse remitting multiple sclerosis (RRMS). However, there is no standard strategy for managing treatment failure on these agents. The present study aimed to evaluate the effectiveness of rituximab after natalizumab and fingolimod withdrawal. METHODS: A retrospective cohort was accomplished on RRMS patients treated with natalizumab and fingolimod who were switched to rituximab. RESULTS: 100 patients (50 cases in each group) were analyzed. After six months of follow-up, a substantial decline in clinical relapse and disability progression was observed in both groups. However, no significant change was demonstrated in the pattern of MRI activity (P = 1.000) in natalizumab pretreated patients. After adjusting for the baseline characteristics, a head-to-head comparison found a non-significant trend of lower EDSS in the pretreated fingolimod group compared to those previously treated with natalizumab(P = 0.057). However, in terms of clinical relapse and MRI activity, the clinical outcomes were comparable in both groups ((P = 0.194), (P = 0.957). Moreover, rituximab was well-tolerated, and no serious adverse events were reported. CONCLUSION: The present study revealed the effectiveness of rituximab as an appropriate alternative option for escalation therapy after fingolimod and natalizumab discontinuation.
 OBJECTIVES: Ambiguity exists about the impact of multiple sclerosis (MS) on fertility and pregnancy. We explored female and male patients' experiences with MS regarding family planning to understand information needs and opportunities to improve informed decision-making. METHODS: Semi-structured interviews were conducted with Australian female (n = 19) and male (n = 3) patients of reproductive age diagnosed with MS. Transcripts were analysed thematically, adopting a phenomenological approach. RESULTS: Four main themes emerged: 'reproductive planning', revealing inconsistent experiences about pregnancy intention discussions with health care professionals (HCPs), and involvement in decisions about MS management and pregnancy; 'reproductive concerns', about the impact of the disease and its management; 'information awareness and accessibility', with participants generally reporting they had limited access to desired information and received conflicting information about family planning; and 'trust and emotional support', with continuity of care and engagement with peer-support groups about family planning needs valued. CONCLUSION: Patients with MS want consistent engagement with HCPs regarding discussion of pregnancy intent and desire improvements in quality and accessibility of available resources and support services to address reproductive concerns. PRACTICE IMPLICATIONS: Family planning conversations should be a part of routine care planning for MS patients and contemporary resources are required to support these discussions.
 BACKGROUND: Teriflunomide, the active metabolite of leflunomide, is a disease-modifying therapy drug used for the treatment of multiple sclerosis (MS), yet the complications associated with this drug remain not fully understood. Here we present the rare case of a 28-year-old female MS patient who developed subacute cutaneous lupus erythematosus (SCLE) following teriflunomide treatment. Though SCLE has been reported to be associated with leflunomide, the current report represents the first documented evidence demonstrating SCLE as a potential teriflunomide treatment-related complication. Additionally, a literature review on the leflunomide-induced SCLE was conducted to emphasize the association of SCLE with teriflunomide, specifically amongst the female demographic with a preexisting autoimmune diathesis. CASE PRESENTATION: A 28-year-old female first presented with MS symptoms in the left upper limb along with blurred vision in the left eye. Medical and family histories were unremarkable. The patient exhibited positive serum biomarkers including ANA, Ro/SSA, La/SSB, and Ro-52 antibodies. Relapsing-remitting MS was diagnosed according to the 2017 McDonald's diagnostic criteria, and remission was achieved upon intravenous administration of methylprednisolone followed by teriflunomide sequential therapy. Three months post-teriflunomide treatment, the patient developed multiple facial cutaneous lesions. SCLE was subsequently diagnosed and was attributed to treatment-related complication. Interventions include oral administration of hydroxychloroquine and tofacitinib citrate effectively resolved cutaneous lesions. Discontinuation of hydroxychloroquine and tofacitinib citrate treatment led to recurring SCLE symptoms under continuous teriflunomide treatment. Full remission of facial annular plaques was achieved after re-treatment with hydroxychloroquine and tofacitinib citrate. The patient's clinical condition remained stable in long-term outpatient follow-ups. CONCLUSIONS: As teriflunomide has become a standard disease-modifying therapy for MS, the current case report highlights the importance of monitoring treatment-related complications, specifically in relation to SCLE symptoms.
 BACKGROUND: Although multiple sclerosis (MS) is an immune-related disorder, pharmaceutical interventions targeting the immune system do not stop or reverse disability progression; the major challenge for this condition. Studies show that disability progression in MS is associated with vascular comorbidity and brain volume loss, indicating that a multi-targeted approach is required to prevent debilitation. The aim of the present study was to examine the associations between vascular ultrasound, disability, biochemistry and lifestyle data in people with MS (pwMS). METHODS: Extracranial vascular ultrasound was performed on 51 pwMS and 25 age-matched controls. Sonographic interrogation determined carotid intima-media thickness (cIMT) and abnormal blood flow patterns. Disability was assessed using the Expanded Disability Status Scale (EDSS). Biochemical and lifestyle data were obtained for all participants. RESULTS: The EDSS had a highly significant positive association with the cIMT of the right (r = 0.63; p = 0.001) and left (r = 0.49; p = 0.001) common carotid arteries and negative associations with the peak systolic blood flow velocity of the right vertebral artery (r = -0.42; p = 0.01) as well as end-diastolic velocity of the left internal carotid artery (r = -0.47; p = 0.01). These associations were significantly influenced by biochemical and lifestyle factors. Both cIMT and age showed significant associations with the EDSS. When cIMT was adjusted for age in a regression analysis, the association between the EDSS and the cIMT remained significant (p < 0.01), while the age association was reduced to being significant only at 10% (p = 0.06). There was no association between the use of MS medication and the EDSS (p = 0.56). CONCLUSION: PwMS who had increased cIMT, a surrogate marker for atherosclerosis, and reduced carotid artery blood flow velocities were at risk for greater disability over and above the effect of aging. These findings provide important information for disease management and disability prevention in pwMS. Modification of diet and lifestyle may promote the unhindered flow of essential nutritional factors into the brain in pwMS.

 INTRODUCTION: During the COVID-19 pandemic, electronic health record (EHR) data has been used to investigate disease severity and risk factors for severe COVID-19 in people with multiple sclerosis (pwMS). Methodological challenges including sampling bias, and residual confounding should be considered when conducting EHR-based studies. We aimed to address these limitations related to the use of EHR data in order to identify risk factors, including the use of disease modifying therapies (DMTs), associated with hospitalization for COVID-19 amongst pwMS. METHODS: We performed a retrospective cohort study including a sample of 47,051 pwMS using a large US-based EHR and claims linked database. Follow-up started at the beginning of the pandemic, February 20th 2020, and continued until September 30th 2020. COVID-19 diagnosis was determined by the presence of ICD-10 diagnostic code for COVID-19, or a positive diagnostic laboratory test, or an ICD-10 diagnostic code for coronaviruses. We used Cox regression modeling to assess the impact of baseline demographics, MS disease history and pre-existing comorbidities on the risk of hospitalization for COVID-19. Then, we identified 5,169 pwMS using ocrelizumab (OCR) and 3,351 pwMS using dimethyl fumarate (DMF) at baseline, and evaluated the distribution of the identified COVID-19 risk factors between the two groups. Finally, we used Cox regression models, adjusted for the identified confounders, to estimate the risk of hospitalization for COVID-19 in pwMS treated with OCR compared to DMF. RESULTS: Among the pwMS cohort, we identified 799 COVID-19 cases (1.7%) which resulted in 182 hospitalizations for COVID-19 (0.4%). Population differences between the pwMS and COVID-19 cohorts were observed. Statistical modeling identified older age, male gender, African-American race, walking with assistance, non-ambulatory status, severe relapse requiring hospitalization in year prior to baseline, and specific comorbidities to be associated with a higher risk of COVID-19 related-hospitalization. Comparing the COVID-19 risk factors between OCR users and DMF users, MS characteristics including ambulatory status and MS subtype were highly imbalanced, likely arising from key differences in the labelled indications for these therapies. Compared to DMF use, in unadjusted (HR 1.58, 95% CI 0.73 - 3.44), adjusted (HR 1.28, 95% CI 0.58 - 2.83), propensity score weighted (HR 1.25, 95% CI 0.56 - 2.80), and doubly robust models (HR 1.29, 95% CI 0.57 - 2.89), no significantly increased risk of hospitalization for COVID-19 was associated with OCR use. CONCLUSION: We observed significant population differences when comparing all pwMS to COVID-19 cases, as well as significant differences in key confounders between OCR and DMF treated patients. In unadjusted analyses we did not observe a statistically significant higher risk of COVID-19 hospitalization in pwMS treated with OCR compared to DMF, with further attenuation of risk when adjusting for the key confounders. This study re-emphasises the importance to appropriately consider both sampling and confounding bias in EHR-based MS research.
 BACKGROUND: Multiple Sclerosis (MS) is a chronic neurodegenerative disorder. People living with MS (plwMS) require long-term, multidisciplinary care in both clinical and community settings. MS-specific mHealth interventions have advanced in the form of clinical treatments, rehabilitation, disease monitoring and self-management of disease. However, mHealth interventions for plwMS appear to have limited proof of clinical efficacy. As native mobile apps target specific mobile operating systems, they tend to have better interactive designs leveraging platform-specific guidelines. Thus, to improve such efficacy, it is pivotal to explore the design characteristics of native mobile apps used for plwMS. OBJECTIVES: This study aimed to explore the design characteristics of native mobile apps used for adults living with MS in academic settings. METHODS: A scoping review of studies was conducted. A literature search was performed through PubMed, CINAHL, MEDLINE and Cochrane Library. Per native mobile apps, characteristics, persuasive technology elements and evaluations were summarized. RESULTS: A total of 14 native mobile apps were identified and 43% of the identified apps were used for data collection (n=6). Approximately 70% of the included apps involved users (plwMS) whilst developing (n=10). A total of three apps utilized embedded sensors. Videos or photos were used for physical activity interventions (n=2) and gamification principles were applied for cognitive and/or motor rehabilitation interventions (n=3). Behavior change theories were integrated into the design of the apps for fatigue management and physical activity. Regarding persuasive technology, the design principles of primary support were applied across all identified apps. The elements of dialogue support and social support were the least applied. The methods for evaluating the identified apps were varied. CONCLUSION: The findings suggest that the identified apps were in the early stages of development and had a user-centered design. By applying the persuasive systems design model, interaction design qualities and features of the identified mobile apps in academic settings were systematically evaluated at a deeper level. Identifying the digital functionality and interface design of mobile apps for plwMS will help researchers to better understand interactive design and how to incorporate these concepts in mHealth interventions for improvement of clinical efficacy.
 BACKGROUND AND PURPOSE: People with multiple sclerosis (pwMS) report reduced quality of life (QoL). Engagement with healthy lifestyle behaviours, including consuming a healthy diet, regular physical activity, and adequate vitamin D exposure, is associated with higher QoL. We aim to assess whether individual lifestyle behaviours are more beneficial to QoL than others, and whether there are additive benefits to QoL by engaging in multiple healthy behaviours concurrently. METHODS: Data from pwMS who completed an online survey at baseline, and at 2.5-, 5- and 7.5-year follow-up, were analysed. Behaviours assessed were consumption of a no-meat/dairy-plus-omega-3 supplementation diet, meditation practice, physical activity, non-smoking, and vitamin D exposure. Mental QoL (mQoL) and physical QoL (pQoL) were assessed by the Multiple Sclerosis Quality of Life (MSQOL-54) questionaire. Linear regression analyses were performed to assess associations of individual behaviours at baseline and follow-up time points with QoL, as well as between number of behaviours and QoL. RESULTS: At baseline, healthy diet and regular physical activity were associated with higher mQoL (5.3/100 and 4.0/100) and higher pQoL (7.8/100 and 6.7/100). Prospectively, diet was positively associated with mQoL, and physical activity with both mQoL and pQoL. At baseline, engagement with ≥3 behaviours was positively associated with mQoL and pQoL, with additive positive associations for each additional behaviour. Prospectively, engagement with ≥3 behaviours was positively associated with mQoL and pQoL, with strongest associations observed with engagement with five behaviours. CONCLUSION: Consumption of a healthy diet, and regular physical activity, are both potential interventions to improve QoL. Engagement with multiple lifestyle behaviours may provide additional benefits and should be encouraged and supported for multiple sclerosis management.
 BACKGROUND AND OBJECTIVES: Uncontrolled evidence suggests that autologous hematopoietic stem cell transplantation (AHSCT) can be effective in people with active secondary progressive multiple sclerosis (SPMS). In this study, we compared the effect of AHSCT with that of other anti-inflammatory disease-modifying therapies (DMTs) on long-term disability worsening in active SPMS. METHODS: We collected data from the Italian Bone Marrow Transplantation Study Group and the Italian Multiple Sclerosis Register. Patients were considered eligible if treatment had been started after the diagnosis of SPMS. Disability worsening was assessed by the cumulative proportion of patients with a 6-month confirmed disability progression (CDP) according to the Expanded Disability Status Scale (EDSS) score. Key secondary endpoints were the EDSS time trend after treatment start and the prevalence of disability improvement over time. Time to first CDP was assessed by means of proportional hazard Cox regression models. A linear mixed model with a time × treatment group interaction was used to assess the longitudinal EDSS time trends. Prevalence of improvement was estimated using a modified Kaplan-Meier estimator and compared between groups by bootstrapping the area under the curve. RESULTS: Seventy-nine AHSCT-treated patients and 1975 patients treated with other DMTs (beta interferons, azathioprine, glatiramer-acetate, mitoxantrone, fingolimod, natalizumab, methotrexate, teriflunomide, cyclophosphamide, dimethyl fumarate, and alemtuzumab) were matched to reduce treatment selection bias using propensity score and overlap weighting approaches. Time to first CDP was significantly longer in transplanted patients (hazard ratio [HR] = 0.50; 95% CI = 0.31-0.81; p = 0.005), with 61.7% of transplanted patients free from CPD at 5 years. Accordingly, EDSS time trend over 10 years was higher in patients treated with other DMTs than in AHSCT-treated patients (+0.157 EDSS points per year compared with -0.013 EDSS points per year; interaction p < 0.001). Patients who underwent AHSCT were more likely to experience a sustained disability improvement: 34.7% of patients maintained an improvement (a lower EDSS than baseline) 3 years after transplant vs 4.6% of patients treated by other DMTs (p < 0.001). DISCUSSION: The use of AHSCT in people with active SPMS is associated with a slowing of disability progression and a higher likelihood of disability improvement compared with standard immunotherapy. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that autologous hematopoietic stem cell transplants prolonged the time to CDP compared with other DMTs.
 The current study-within-a-trial explored individuals' decisions to decline participation in research trialling a chronic illness-focused therapy (i.e. multiple sclerosis). Four themes were identified from seven semi-structured interviews with participation decliners and were confirmed by the host trial's Patient & Public Involvement (PPI) panel: acknowledgement of the value of research; 'fit' of the study; misinterpretation of participant information; and 'ignorance is bliss' - discussed in light of theory and research. This study-within-a-trial extends research on trial recruitment and participation decline; while also suggesting that PPI can be utilised in both a practical and impactful manner.
 Aim: Patients with relapsing-remitting multiple sclerosis (RRMS) treated with natalizumab have anecdotally reported a 'feel-good experience' (FGE). The authors characterized the FGE using survey data from patients with RRMS treated with natalizumab or other disease-modifying therapies (other-DMT). Methods: Questionnaire data from RRMS patients who use MyMSTeam, an online patient social network, were analyzed. Results: The survey included 347 patients (95 natalizumab; 252 other-DMT). More natalizumab than other-DMT patients self-reported having an FGE (62.1 vs 44.8%; p = 0.001) as well as other physical, emotional and cognitive benefits. Conclusion: This study demonstrates that physical, emotional and cognitive benefits were more commonly reported by patients treated with natalizumab than those treated with other disease-modifying therapies and helps characterize patient-reported factors associated with the FGE.
 BACKGROUND AND PURPOSE: Autoantibodies have been found to contribute to pathology and are used in the diagnosis of some neurological diseases. We examined the prevalence of autoantibodies in patients with various neurological diseases and whether patients who had autoantibodies differed in age, sex, or disability from those who did not. METHODS: We examined the prevalence of neural surface and onconeural autoantibodies in cerebrospinal fluid (CSF) and serum from patients with multiple sclerosis (n = 64), Parkinson disease plus atypical parkinsonism (n = 150), amyotrophic lateral sclerosis (n = 43), or autoimmune encephalitis (positive control; n = 7) and a healthy control group (n = 37). A total of 12 onconeural autoantibodies and six neural surface autoantibodies were tested in all participants. RESULTS: Autoantibodies were present in all cohorts. The prevalence of autoantibodies was high (>80%) in the autoimmune encephalitis cohort but low (<20%) in all other cohorts. When comparing patients within cohorts who were positive for autoantibodies to patients who were not, there was no difference in age, sex, and disability. This was apart from the multiple sclerosis and Parkinson disease plus atypical parkinsonism cohorts, where those with positivity for autoantibodies in the CSF were significantly older. CONCLUSIONS: The presence of the autoantibodies examined does not appear to have a substantial clinical impact within the diseases examined in this study. The presence of autoantibodies in all cohorts presents a risk for misdiagnosis when the method is used incorrectly on patients with atypical clinical presentation.
 PURPOSE: To examine evidence-based nontraditional and home-based interventions and their efficacy for use in individuals with MS to improve performance in their daily activities. MATERIALS AND METHODS: A search of five databases including PubMed, CINAHL, Cochrane Library, OT Seeker, and Ovid Medline produced 924 research articles. Thirty-two articles were selected for full-text review, of which 15 were included in this systematic review. INCLUSION CRITERIA: Articles were level 2B or higher evidence, had a minimum of 19 participants with MS, addressed ADLs or body functions supporting ADL performance, and were published since 2010. EXCLUSION CRITERIA: Articles not written in English and not identified as nontraditional or home-based programming. RESULTS: The review uncovered strong evidence for the use of the nontraditional interventions of vestibular rehabilitation, self-management, yoga, musical production, and ELEVIDA to improve ADL performance in individuals with MS. Strong evidence supported the use of home-based programs that included cognitive behavioral therapy, cooling suits, manual dexterity, strengthening, vestibular rehabilitation, and physical activity. CONCLUSIONS: High levels of evidence support the use of nontraditional or home-based interventions to improve ADL performance in clients with MS. Innovation and technology continue to expand the occupational therapist's toolbox of interventions.
 BACKGROUND AND OBJECTIVES: Ocrelizumab (OCR), a humanized anti-CD20 monoclonal antibody, is highly efficient in patients with relapsing-remitting multiple sclerosis (RR-MS). We assessed early cellular immune profiles and their association with disease activity at treatment start and under therapy, which may provide new clues on the mechanisms of action of OCR and on the disease pathophysiology. METHODS: A first group of 42 patients with an early RR-MS, never exposed to disease-modifying therapy, was included in 11 centers participating to an ancillary study of the ENSEMBLE trial (NCT03085810) to evaluate the effectiveness and safety of OCR. The phenotypic immune profile was comprehensively assessed by multiparametric spectral flow cytometry at baseline and after 24 and 48 weeks of OCR treatment on cryopreserved peripheral blood mononuclear cells and analyzed in relation to disease clinical activity. A second group of 13 untreated patients with RR-MS was included for comparative analysis of peripheral blood and CSF. The transcriptomic profile was assessed by single-cell qPCRs of 96 genes of immunologic interest. RESULTS: Using an unbiased analysis, we found that OCR as an effect on 4 clusters of CD4(+) T cells: one corresponding to naive CD4(+) T cells was increased, the other clusters corresponded to effector memory (EM) CD4(+)CCR6(-) T cells expressing homing and migration markers, 2 of them also expressing CCR5 and were decreased by the treatment. Of interest, one CD8(+) T-cell cluster was decreased by OCR corresponding to EM CCR5-expressing T cells with high expression of the brain homing markers CD49d and CD11a and correlated with the time elapsed since the last relapse. These EM CD8(+)CCR5(+) T cells were enriched in the CSF of patients with RR-MS and corresponded to activated and cytotoxic cells. DISCUSSION: Our study provides novel insights into the mode of action of anti-CD20, pointing toward the role of EM T cells, particularly a subset of CD8 T cells expressing CCR5.
 BACKGROUND: In relapsing-remitting multiple sclerosis (RRMS), smoking is a known risk factor for disease susceptibility and disability progression. However, its impact on the efficacy of oral disease-modifying drugs (DMDs) is unclear. Therefore, we initiated a single-center, retrospective, observational study to investigate the relationship between smoking and disease activity in RRMS patients under oral DMDs. METHODS: We retrospectively enrolled RRMS patients who initiated oral DMDs (fingolimod or dimethyl fumarate) at our hospital between January 2012 and December 2019. Clinical data and smoking status at oral DMD initiation were collected up to December 2020. We conducted survival analyses for relapse and any disease activity, defined as relapse or MRI disease activity, among patients with distinct smoking statuses. RESULTS: We enrolled 103 RRMS patients under oral DMDs including 19 (18.4%) current smokers at baseline. Proportions of relapses and any disease activity during follow-up were higher in current smokers (relapse: p = 0.040, any disease activity: p = 0.004) and time from initiating oral DMDs to relapse was shorter in current smokers (log-rank test: p = 0.011; Cox proportional hazard analysis: hazard ratio (HR) 2.72 [95% confidence interval (CI) 1.22-6.09], p = 0.015) than in non-smokers. Time from initiating oral DMDs to any disease activity was also shorter in current smokers (log-rank test: p = 0.016; Cox proportional hazard analysis: HR 2.18 [95% CI 1.14-4.19], p = 0.019) than in non-smokers. The survival curves for relapse and any disease activity were not different between the former smoker and never-smoker groups. Multivariate survival analysis showed current smoking was an independent risk factor for relapse or any disease activity after adjusting for covariates (relapse: HR 2.54 [95% CI 1.06-6.10], p = 0.037; any disease activity: HR 3.47 [95% CI 1.27-9.50], p = 0.015). CONCLUSION: Smoking was a risk factor for disease activity in RRMS patients under oral DMD treatment. RRMS patients should be advised to stop smoking even after the initiation of DMDs.
 OBJECTIVES: To compare in a nationwide observational cohort the effectiveness, frequency and reasons for treatment interruption of dimethylfumarate (DMF) and teriflunomide (TERI) (horizontal switchers) versus alemtuzumab (AZM), cladribine (CLAD), fingolimod (FTY), natalizumab (NTZ), ocrelizumab (OCR) and ozanimod (OZA) (vertical switchers) in patients with relapsing-remitting multiple sclerosis (pwRRMS) and prior interferon beta (IFN-beta) or glatiramer-acetate (GLAT) treatment. MATERIALS AND METHODS: The "horizontal switch cohort" included 669 and the "vertical switch cohort" 800 RRMS patients. We used propensity scores for inverse probability weighting in generalized linear (GLM) and Cox proportional hazards models to correct for bias in this non-randomized registry study. RESULTS: Estimated mean annualized relapse rates (ARR) were 0.39 for horizontal and 0.17 for vertical switchers. The incidence rate ratio (IRR) in the GLM model showed an increased relapse probability of 86% for horizontal versus vertical switchers (IRR = 1.86; 95% CI 1.38-2.50; p < 0.001). Analyzing the time to the first relapse after treatment switch by Cox regression, a hazard ratio of 1.58 (95% CI 1.24-2.02; p < 0.001) indicated an increased risk of 58% for horizontal switchers. The hazard ratios for treatment interruption comparing horizontal versus vertical switchers were 1.78 (95% CI 1.46-2.18; p < 0.001). CONCLUSIONS: Horizontal switching after a platform therapy resulted in a higher relapse and interrupt probability and was associated with a trend towards less EDSS improvement comparing to vertical switching in Austrian RRMS patients.
 After natalizumab (NAT) cessation, some multiple sclerosis (MS) patients experience a severe disease rebound. The rebound pathophysiology is still unclear; however, it has been linked to interleukin-17-producing T-helper (Th17) cells. We demonstrate that during NAT treatment, MCAM+CCR6+Th17 cells gradually acquire a pathogenic profile, including proinflammatory cytokine production, pathogenic transcriptional signatures, brain endothelial barrier impairment, and oligodendrocyte damage via induction of apoptotic pathways. This is accompanied by an increase in Th17 cell frequencies in the cerebrospinal fluid of NAT-treated patients. Notably, Th17 cells derived from NAT-treated patients, who later developed a disease rebound upon treatment cessation, displayed a distinct transcriptional pathogenicity profile associated with altered migratory properties. Accordingly, increased brain infiltration of patient Th17 cells was illustrated in a humanized mouse model and brain histology from a rebound patient. Therefore, peripheral blood-accumulated MCAM+CCR6+Th17 cells might be involved in rebound pathophysiology, and monitoring of changes in Th17 cell pathogenicity in patients before/during NAT treatment cessation might enable rebound risk assessment in the future.
 AIM: We reviewed the clinical features of a sample of pediatric acquired demyelinating syndromes with the purpose of determining the appropriate protocol for follow-up after the first episode. METHODS: A multicenter retrospective observational study was conducted on a cohort of 40 children diagnosed with a first episode of acquired demyelinating syndrome over the period 2012-2021. Patients were evaluated with clinical and neuroradiologic assessment after 3, 6, and 12 months, with a median follow-up of 4.0 years. RESULTS: At the first acquired demyelinating syndrome episode, 18 patients (45%) were diagnosed with acute disseminated encephalomyelitis, 18 (45%) with clinical isolated syndrome, and 4 (10%) with multiple sclerosis. By month 12, 12 patients (30%) had progressed from an initial diagnosis of acute disseminated encephalomyelitis (2) or clinical isolated syndrome (10) to multiple sclerosis. Of these, 6 had clinical relapse and 6 radiologic relapse only. The first relapse occurred after a median of 3 months. Among the patients who had evolved toward multiple sclerosis, there was a prevalence of females (P = .014), higher oligoclonal bands positivity (P = .009), and older median age (P < .001) as compared with those who had remained stable. INTERPRETATION: Both clinical and radiologic follow-up of children with acquired demyelinating syndromes is crucial, especially during the first year after acute onset, for early identification of multiple sclerosis and prompt initiation of disease-modifying treatment to delay axonal damage and to limit disability.
 Although the causes of multiple sclerosis are largely unknown, genetic and environmental components play an important role. Geographic distribution, varying with latitude, reflects both genetic and environmental influences. We conducted a retrospective exploratory observational study to characterize the disability progression of 2396 Jewish patients with relapsing-remitting multiple sclerosis, followed at the Sheba Multiple Sclerosis Center, Tel-Aviv, Israel; 188 patients who originated in Iraq and 2207 patients who originated in northern Europe. Peripheral blood microarray gene expression analysis was performed in a subgroup of patients to identify molecular pathways associated with faster disability progression. During a follow-up period of 18.8 and 19.8 years, respectively, 51.6% of patients with an Iraqi origin progressed to moderate disability defined as expanded disability status scale (EDSS) score of 3.0 to 5.5, compared to 44.2% of patients with a northern European origin (odds ratio 1.347, 95% CI 1.0-1.815, p = 0.049). An Iraqi origin was associated with increased risk of progression to moderate disability adjusted for sex, disease duration, age at onset, and treatment with immunomodulatory drugs (hazard ratio 1.323; 95% CI, 1.049-1.668, p = 0.02), but not to severe disability defined as EDSS score > = 6.0 (i.e., walking aids are required for a distance of 100 meters, (hazard ratio 1.311; 95% CI, 0.918-1.874, p = 0.136). Gene expression analysis disclosed 98 differentially expressed genes (79 over-expressed and 19 under-expressed) between relapsing-remitting multiple sclerosis patients of Iraqi origin (N = 17) and northern European (N = 34) origin. Interestingly, this gene expression was enriched with genes related to neuronal pathways associated with morphology of axons, branching of neurites, proliferation of neocortical neurons, and formation of myelin sheath, suggesting an augmented process of neurodegeneration in relapsing-remitting multiple sclerosis patients with an Iraqi origin. The study results suggest that relapsing-remitting multiple sclerosis patients with an Iraqi origin progress faster to disability possibly due to an enhanced process of neurodegeneration.
 OBJECTIVE: To describe the safety, efficacy, and potential role in therapy of ponesimod, which was recently approved by the Food and Drug Administration (FDA) as a therapeutic option for the treatment of multiple sclerosis (MS). DATA SOURCES: A PubMed literature search using the following terms: ponesimod and MS (January 1, 2012-October 31, 2022). FDA product labeling was also reviewed for pertinent data sources. STUDY SELECTION AND DATA EXTRACTION: All relevant English-language articles examining efficacy and/or safety of ponesimod were considered for inclusion. DATA SYNTHESIS: Ponesimod is an orally administered second-generation sphingosine 1-phospate (S1-P) receptor modulator classified as a disease modifying treatment (DMT) for MS. Clinical studies have shown that ponesimod prevents relapse in patients with relapsing-remitting MS (RRMS) and has superior efficacy compared with teriflunomide. Nasopharyngitis, upper respiratory tract infections, headache, high blood pressure, and liver dysfunction were some of the common adverse effects associated with ponesimod. Dyspnea, bradyarrhythmias, atrioventricular conduction delays, and macular edema were some of the rare but serious adverse effects associated with ponesimod. RELEVANCE TO PATIENT CARE AND CLINICAL PRACTICE IN COMPARISON WITH EXISTING AGENTS: Some advantages of ponesimod over other S1-P receptor modulators approved for RRMS include selectivity for the S1-P(1) receptor and short half-life, which allows for quick reversal of immunosuppressive effects. However, data from long-term efficacy and safety studies and more direct comparison studies with other DMTs are required. CONCLUSION: Currently available data suggest that ponesimod is a useful addition to other high-efficacy DMTs available to treat patients with MS.
 Real-world data sources offer opportunities to compare the effectiveness of treatments in practical clinical settings. However, relevant outcomes are often recorded selectively and collected at irregular measurement times. It is therefore common to convert the available visits to a standardized schedule with equally spaced visits. Although more advanced imputation methods exist, they are not designed to recover longitudinal outcome trajectories and typically assume that missingness is non-informative. We, therefore, propose an extension of multilevel multiple imputation methods to facilitate the analysis of real-world outcome data that is collected at irregular observation times. We illustrate multilevel multiple imputation in a case study evaluating two disease-modifying therapies for multiple sclerosis in terms of time to confirmed disability progression. This survival outcome is derived from repeated measurements of the Expanded Disability Status Scale, which is collected when patients come to the healthcare center for a clinical visit and for which longitudinal trajectories can be estimated. Subsequently, we perform a simulation study to compare the performance of multilevel multiple imputation to commonly used single imputation methods. Results indicate that multilevel multiple imputation leads to less biased treatment effect estimates and improves the coverage of confidence intervals, even when outcomes are missing not at random.
 BACKGROUND: Understanding the experiences of people with MS taking part in physical activity interventions is critical to inform future interventions. AIM: The aim was to gain insight into the experiences of people with MS taking part in a behavior change group physical activity intervention with a novel social cognitive theory component. METHODS: A qualitative semi-structured interview format was utilized. Questions focussed on expectations, views and beliefs at being involved in the study, beliefs on physical activity, and subjective evaluation of the trial content and delivery. Seventeen people were interviewed and data were analyzed using thematic analysis. RESULTS: Three themes were generated: psychological and social factors, intervention processes, and MS identity. The acceptance of MS as an identity acted as an initial barrier to exercise, with a more positive, exercise-enabling identity post-intervention. Psychological factors such as self-efficacy and anxiety, as well as social factors such as social support, were found to play an important role in how participants experienced the program. Similarly, intervention processes included support for group-based activities and structure of exercise classes, and were also inter-linked to the other themes. CONCLUSION: It appears that group-based exercise interventions are acceptable and feasible for people with MS. The qualitative findings support previously reported quantitative findings that the Step it Up intervention is effective at promoting physical activity and improving psychological outcomes.
 BACKGROUND: Townsville (population=195,564, latitude=19.3°S) is the largest city in the Northern Queensland region of Australia, an area previously defined as a low/medium-prevalence zone for multiple sclerosis (MS). However, the epidemiology of MS in this region since 1981 is unknown. AIMS: To assess the 2012 to 2022 epidemiology of MS in Townsville. METHODS: Demographic/clinical data extracted from medical records of MS cases identified by public and private clinicians. Prevalence, and incidence and mortality rates estimated for 2012 and 2022 and age-standardised to the 2022 Australian population. Differences in estimates assessed by Poisson regression. RESULTS: Females and relapsing-remitting MS comprised most cases. The 2012 prevalence was 45.0/100,000 (50.4/100,000 age-standardised, F/M sex ratio=2.0). Prevalence increased by 188% in 2022, with a crude prevalence of 86.9/100,000 (91.7/100,000 age-standardised, F/M sex ratio=2.7). 2012-22 MS onset incidence rate was 3.8/100,000 person-years (age-standardised 3.5/100,000, F/M sex ratio=2.7). Mean age increased from 49.4 to 57.3 years. Age-standardised mortality rate was 0.9/100,000 person-years, with standardised mortality ratio=1.0. DISCUSSION: These results show that Townsville is a high-frequency region for MS, with prevalence and incidence on par with that seen at higher latitudes in Australia. These results have implications for clinical practice in the region and for organisational resource allocation.
 BACKGROUND: The SARS-CoV-2 pandemic represents one of the most challenging issues that have recently influenced everyday life in countries all over the world. Understanding the risk of this disease is of high importance in patients with multiple sclerosis (MS) as they represent a vulnerable population through their treatment with disease-modifying therapies (DMTs). Infective episodes may trigger relapses and lead to deterioration of the health condition. SUMMARY: Vaccination is an important preventive measure against infectious diseases. In MS patients, concerns have been raised about the effectiveness of vaccines in patients on various immunomodulatory drugs and about their possible adverse effects including impairment of neurological functions. The objectives of this article were to summarize the current knowledge on immune responses to the COVID-19 vaccines and their safety in MS patients and to provide practical guidance based on the data available to date. KEY MESSAGES: Although MS is not associated with a higher risk of COVID-19, this infection can trigger relapses or pseudo-relapses. Vaccines against SARS-CoV-2 are recommended for all MS patients who are not in the active phase of the disease, despite the fact that there is still a lack of long-term reliable data on the effectiveness and safety of vaccines against COVID-19. Some DMTs can reduce vaccine humoral responses, but might still provide some protection and adequate T-cell response. To optimize the effectiveness of vaccination, the ideal timing of vaccine application and DMTs dosing regimen is crucial.
 OBJECTIVES: The precise location of multiple sclerosis (MS) cortical lesions can be very challenging at 3 T, yet distinguishing them from subcortical lesions is essential for the diagnosis and prognosis of the disease. Compressed sensing-accelerated fluid and white matter suppression imaging (CS-FLAWS) is a new magnetic resonance imaging sequence derived from magnetization-prepared 2 rapid acquisition gradient echo with promising features for the detection and classification of MS lesions. The objective of this study was to compare the diagnostic performances of CS-FLAWS (evaluated imaging) and phase sensitive inversion recovery (PSIR; reference imaging) for classification of cortical lesions (primary objective) and infratentorial lesions (secondary objective) in MS, in combination with 3-dimensional (3D) double inversion recovery (DIR). MATERIALS AND METHODS: Prospective 3 T scans (MS first diagnosis or follow-up) acquired between March and August 2021 were retrospectively analyzed. All underwent 3D CS-FLAWS, axial 2D PSIR, and 3D DIR. Double-blinded reading sessions exclusively in axial plane and final consensual reading were performed to assess the number of cortical and infratentorial lesions. Wilcoxon test was used to compare the 2 imaging datasets (FLAWS + DIR and PSIR + DIR), and intraobserver and interobserver agreement was assessed using the intraclass correlation coefficient. RESULTS: Forty-two patients were analyzed (38 with relapsing-remitting MS, 29 women, 42.7 ± 12.6 years old). Compressed sensing-accelerated FLAWS allowed the identification of 263 cortical lesions versus 251 with PSIR ( P = 0.74) and 123 infratentorial lesions versus 109 with PSIR ( P = 0.63), corresponding to a nonsignificant difference between the 2 sequences. Compressed sensing-accelerated FLAWS exhibited fewer false-negative findings than PSIR either for cortical lesions (1 vs 13; P < 0.01) or infratentorial lesions (1 vs 15; P < 0.01). No false-positive findings were found with any of the 2 sequences. Diagnostic confidence was high for each contrast. CONCLUSION: Three-dimensional CS-FLAWS is as accurate as 2D PSIR imaging for classification of cortical and infratentorial MS lesions, with fewer false-negative findings, opening the way to a reliable full brain MS exploration in a clinically acceptable duration (5 minutes 15 seconds).
 BACKGROUND AND PURPOSE: Thinning of the retinal combined ganglion cell and inner plexiform layer (GCIP) as measured by optical coherence tomography (OCT) is a common finding in patients with multiple sclerosis. This study aimed to investigate whether a single retinal OCT analysis allows prediction of future disease activity after a first demyelinating event. METHODS: This observational cohort study included 201 patients with recently diagnosed clinically isolated syndrome or relapsing-remitting multiple sclerosis from two German tertiary referral centers. Individuals underwent neurological examination, magnetic resonance imaging, and OCT at baseline and at yearly follow-up visits. RESULTS: Patients were included at a median disease duration of 2.0 months. During a median follow-up of 59 (interquartile range = 43-71) months, 82% of patients had ongoing disease activity as demonstrated by failing the no evidence of disease activity 3 (NEDA-3) criteria, and 19% presented with confirmed disability worsening. A GCIP threshold of ≤77 μm at baseline identified patients with a high risk for NEDA-3 failure (hazard ratio [HR] = 1.7, 95% confidence interval [CI] = 1.1-2.8, p = 0.04), and GCIP measures of ≤69 μm predicted disability worsening (HR = 2.2, 95% CI = 1.2-4.3, p = 0.01). Higher rates of annualized GCIP loss increased the risk for disability worsening (HR = 2.5 per 1 μm/year increase of GCIP loss, p = 0.03). CONCLUSIONS: Ganglion cell thickness as measured by OCT after the initial manifestation of multiple sclerosis may allow early risk stratification as to future disease activity and progression.
 BACKGROUND: Growing evidence has suggested the involvement of gut microbiota in the pathophysiology of multiple sclerosis (MS). Disease-modifying therapies (DMTs) exert a parallel effect on the gut microenvironment with subsequent modulation of the intestinal and systemic immune system. Herein, we summarize the current literature on the effect of DMTs on the gut microbiome and possible implications for MS. METHODS: All the literature available in PubMed on the effects of DMTs on the gut microbiota composition in patients with MS was reviewed. We used multiple combinations of the following keywords: "multiple sclerosis; demyelinating disease; gut microbiome; microbiome; brain-gut axis; diet; fecal microbiome; disease modifying therapy; immunomodulator; interferon; glatiramer acetate; teriflunomide; dimethyl fumarate; natalizumab; alemtuzumab; anti-CD20; fingolimod". All the original research articles available in English were included in this narrative review. RESULTS: Ten original full-text articles were considered eligible, including seven case-control and three cohort studies. First-line DMTs, including oral and subcutaneous treatments (dimethyl fumarate, glatiramer acetate, and interferon β 1b) were considered, while a small number of patients with MS were under natalizumab, fingolimod and anti-CD20 treatments. CONCLUSIONS: Emerging evidence reported changes in the gut microbiome during exposition to DMTs. However, the association between DMTs exposure and microbial changes was mostly indirect, and the results of the different studies needed to be more consistent. The mitigation of methodological bias is necessary for future studies to allow the identification of a "microbial signature" related to MS pathophysiology, the role of DMTs, and possible prognostic implications.
 OBJECTIVES: Cytokines play a key role in neuroinflammation, which is present in every subset of multiple sclerosis (MS). The aim of the study was to assess levels of selected interleukins and proinflammatory factors in cerebrospinal fluid (CSF) among patients diagnosed with relapsing-remitting multiple sclerosis (RRMS). METHODS: One hundred eighteen patients diagnosed de novo with RRMS were enrolled in the study. We analysed the relationships between selected cytokines' levels depending on the age at diagnosis, time from the first symptoms to diagnosis and presence of MRI lesions. RESULTS: Among the study group the levels of IL-5 and IL-13 increased with the age at the diagnosis of MS. The concentration of IL-10 was lower in group of patients over the age of 35. The levels of IFN-γ, TNF-α, IL-5, IL-10 and IL-15 increased with the longer time from the first symptoms to diagnosis. Positive correlations were found between the levels of IL-2 and IL-12, IL-17, IL-4, IL-1RA as well as IL-1 and IL-4, IL-17. The concentration of IL-5 correlated positively with IL-4, IL-9 and IL-13. The level of IL-10 increased with IL-6 and IL-9 concentrations. A negative correlation was found for IL-10 and IL-4. In turn, between IL-13 and both IL-5 and IL-9, the relationship was positive. The level of IL-2 was significantly higher among patients without gadolinium-enhanced (Gd(+)) MRI lesions. CONCLUSIONS: The results of the study provide new insight into the role of selected molecules in the development of inflammation in MS. It might be crucial in planning the most adequate immunomodulatory therapy.
 Given that multiple sclerosis (MS) is a complex disease with an unclear etiology, a single animal model is unlikely to accurately represent all aspects of pathology and clinical features of the human condition. However, the availability of three major types of murine models of MS, that is, experimental autoimmune encephalomyelitis (EAE), viral models, and toxic models, enables studies of several relevant features of this debilitating disease. Researchers have recently begun to combine magnetic resonance imaging (MRI) technologies with other experimental strategies to acquire complementary information, for example, anatomical and functional, and study the effect of experimental manipulations longitudinally in a noninvasive way. This review summarizes the latest MRI studies investigating critical aspects of MS, such as atrophy, demyelination, neuroaxonal damage, and neuroinflammation, in mouse models of MS. Advanced techniques will be briefly discussed, providing references to specialized literature for the readers. Thus, this review aims to describe different imaging protocols used to study critical aspects of MS in a research laboratory, discussing the main related findings in the most significant murine models of the disease.
 OBJECTIVES: It is now well recognized that brain damage and/or atrophy apparent on MRI is only moderately correlated to cognitive functioning. The cognitive reserve (CR) hypothesis has been proposed to explain this functional heterogeneity, but it has only been addressed recently in the MS literature and has not yet been thoroughly investigated. The objective of this study is to examine the protective role of CR in cognition using a standardized CR tool in a population with a wide age range. METHODS: A neuropsychological evaluation was performed on 84 pwMS aged between 27 and 78 years old and the CR Index questionnaire (CRIq) was used to estimate CR. The EDSS scale was used to assess the degree of neurologic impairment and estimate the disease burden. RESULTS: A moderating effect of CR was observed in the relationship between EDSS score and specific cognitive domains: processing efficiency, visuospatial learning and memory, as well as a tendency for verbal memory. In pwMS with a high level of CR, there was no negative relationship between these cognitive domains and EDSS. CONCLUSION: The results support the protective role of CR in a sample of pwMS with a wide age range. This role seems to be limited to specific cognitive tasks that pose a greater challenge and therefore require greater adaptability.
 Multiple sclerosis (MS) is a chronic, debilitating disease characterised by demyelination of the nerves of the central nervous system that results in patients progressively losing the ability to perform daily tasks. As there is no cure for this disease, rehabilitation therapy is an important aspect of care; assisting patients to regain or retain function and improve their physical, mental and social wellbeing. At present there is no current consistent model of care for MS, likely due to the variable symptom presentation. Various forms of rehabilitation therapy are available, and these include physical rehabilitation methods, such as balance and gait therapy, speech and respiration rehabilitation, and occupational therapy. Contrary to previous understanding, exercise-based therapies have shown various benefits for patients with MS, and in addition to improving MS-related physical symptoms, have been shown to reduce the risk of developing cardiovascular disease and can improve cognitive function. Cognition rehabilitation therapy specifically focuses on behavioural tasks and is divided into two main forms: compensatory rehabilitation, which offers cognitive functioning benefits, and restorative rehabilitation, which offers memory benefits. Excitation therapies include cranial stimulation and other stimulation rehabilitation methods such as focal muscle vibration therapy and these non-invasive techniques may improve patient's physical ability. Additionally, more novel rehabilitation methods include robot-assisted gait therapy and telerehabilitation, both of which are expected to play progressively more prominent roles in the future of rehabilitation therapy. The structure of the care team has been found to impact patient outcomes, and both in- and out-patient care settings have been found to be beneficial, dependant on the patient's circumstances, with certain patients better suited to a particular setting. While a single point of care is recommended for patients, a multidisciplinary care team and regular reassessment is recommended to manage changing symptoms and ensure continuity of care. The importance of the critical components of rehabilitation have been identified, and these are of vital importance in achieving beneficial outcomes. These components include the patients' participation in the treatment, goal setting with a multidisciplinary care team, a guiding-light purpose for the patient, which focusses on recognizing their personal potential and obtaining improvements through a tailored plan. The final critical component of rehabilitation is the results measurement, which highlights the need for a quantifiable reduction in impairment and improvement in activity and participation. Overall, a lack of standardisation in outcome measurements makes comparison challenging. This is particularly important when comparing standard methods of care with more novel rehabilitation techniques. However, within the broad area of rehabilitation therapies, it is clear that patients with MS can benefit from rehabilitation practices; physically, mentally and socially.
 BACKGROUND: Using reliable contrast-enhanced T1 sequences is crucial to detect enhancing brain lesions for multiple sclerosis (MS) at the time of diagnosis and over follow-up. Contrast-enhanced 3D gradient-recalled echo (GRE) T1-weighted imaging (WI) and 3D turbo spin echo (TSE) T1-WI are both available for clinical practice and have never been compared within the context of this diagnosis. PURPOSE: The aim of this study was to compare contrast-enhanced 3D GRE T1-WI and 3D TSE T1-WI for the detection of enhancing lesions in the brains of MS patients. METHODS: This single-center prospective study enrolled patients with MS who underwent a 3.0 T brain MRI from August 2017 to April 2021 for follow-up. Contrast-enhanced 3D GRE T1-WI and 3D TSE T1-WI were acquired in randomized order. Two independent radiologists blinded to all data reported all contrast-enhanced lesions in each sequence. Their readings were compared with a reference standard established by a third expert neuroradiologist. Interobserver agreement, contrast ratio, and contrast-to-noise ratio were calculated for both sequences. RESULTS: A total of 158 MS patients were included (mean age, 40 ± 11 years; 95 women). Significantly more patients had at least 1 contrast-enhanced lesion on 3D TSE T1-WI than on 3D GRE T1-WI for both readers (61/158 [38.6%] vs 48/158 [30.4%] and 60/158 [38.6%] vs 47/158 [29.7%], P < 0.001). Significantly more contrast-enhanced lesions per patient were detected on 3D TSE T1-WI (mean 2.47 vs 1.56 and 2.56 vs 1.39, respectively, P < 0.001). Interobserver agreement was excellent for both sequences, κ = 0.96 (confidence interval [CI], 0.91-1.00) for 3D TSE T1-WI and 0.92 (CI, 0.86-0.99) for 3D GRE T1-WI. Contrast ratio and contrast-to-noise ratio were significantly higher on 3D TSE T1-WI (0.84 vs 0.53, P < 0.001, and 87.9 vs 57.8, P = 0.03, respectively). CONCLUSIONS: At 3.0 T, contrast-enhanced 3D TSE-T1-WI supports the detection of significantly more enhancing lesions than 3D GRE T1-WI and should therefore be used for MS patients requiring contrast-enhanced examination.
 Multiple sclerosis (MS) is an auto-immune inflammatory disorder affecting the central nervous system. The cause of the disease is unknown but both genetic and environmental factors are implicated in the pathogenesis. We derived cerebral organoids from induced pluripotent stem cells (iPSC) of healthy control subjects as well as from primary progressive MS (PPMS), secondary progressive MS (SPMS) and relapsing remitting MS (RRMS) patients to better understand the pathologic basis of the varied clinical phenotypic expressions of MS. In MS organoids, most notably in PPMS, we observed a decrease of proliferation marker Ki67 and a reduction of the SOX2+ stem cell pool associated with an increased expression of neuronal markers CTIP2 and TBR1 as well as a strong decrease of oligodendrocyte differentiation. This dysregulation of the stem cell pool is associated with a decreased expression of the cell cycle inhibitor p21. Our findings show that the genetic background of a patient can directly alter stem cell function, provides new insights on the innate cellular dysregulation in MS and identifies p21 pathway as a new potential target for therapeutic strategies in MS.
 INTRODUCTION: Multiple Sclerosis (MS) is a neurological disorder with an increasing global prevalence and severe complications. MS14® is a Persian-medicine-derived natural product with herbal and marine origin which has shown beneficial effects in the management of MS complications. In this study, its effect on physical activity of MS patients was investigated. METHODS: A triple-blind placebo-controlled clinical trial was conducted. Participants used either MS14 capsule or placebo 3 times a day for 3 weeks. At baseline and end of the study, physical activity indices were assessed using international physical activity questionnaire (IPAQ). Secondary outcome measures were Fatigue Severity Scale (FSS), timed 10 m walk, Ashworth scale, and Timed Get up and Go. RESULTS: A total number of 80 MS patients completed the study. At the end of study, improvement of general physical activity (p-value=0.047) and Timed 10 m walk index (p-value=0.003) in the MS14 group was significant when compared to placebo. No serious adverse effects were observed in this study. CONCLUSION: Considering the improvement of some physical activity indices, MS14® is seems to be a safe natural product which could be considered as a supplementary treatment in MS patients. Future larger trials are suggested to further evaluate its efficacy.
 This study aimed to compare the changes in psychological status and cortisol level between multiple sclerosis (MS) patients and a healthy control group (HC). One hundred and fifty-five MS patients and 165 HC subjects had completed questionnaires consisting of 36-Item short health survey (SF-36), Hamilton Anxiety Rating Scale (HAM-A), Beck Depression Inventory-II (BDI-II), and fatigue severity score (FSS) before and after (one year from onset) COVID-19 pandemic. The salivary cortisol level was also measured again in 26 MS patients and 14 control individuals. MS patients had lower scores of mental and physical components of quality of life (MCS and PCS), but higher HAM-A, FSS, and BDII scores than HC Before and after COVID-19. There were significant changes in scores of MCS, BDI-II, HAM-A, and FSS after the COVID-19 outbreak in MS patients, but not in PCS score. In HC group, we observed significant changes in scores of MCS, BDI-II, and FSS, but not in scores of PCS and HAM-A. Compared to HC, the MS patients reported greater deterioration in the overall mental health component of their health-related quality of life, and their levels of anxiety and fatigue over the study period. The change of cortisol levels was non-significant with a small effect size.
 Multiple Sclerosis (MS) is a chronic, inflammatory, neurodegenerative disease that is characterized by a complex etiology. Efforts towards the management of MS have long been directed towards symptomatic relief, as well as the use of immune-modulatory, disease modifying therapies; however, inconsistent treatment responses still prevail, increasing the risk for disease progression. While a great deal of research attempted to unravel the complexity of treatment responses in light of epigenetic variability, parallel efforts in the direction of alternative medicine may be as paramount. Herbal compounds have long been regarded as safe and versatile options for aiding in various disorders, including neurodegenerative conditions like MS. Numerous studies have taken interest in a myriad of herbal plants for their potential benefit in alleviating some of the most common MS symptoms such as spasticity and fatigue, delaying the progression of the disease, as well as influencing the overall quality of life for MS patients. This review aims to provide a comprehensive overview of recent clinical studies examining the effects of various herbal plants on different aspects of MS, in an attempt to shed light on an important tool for aiding in the management of this complex and multifactorial disease.
 BACKGROUND: Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that leads to neurological impairment and disability, mostly in young-aged people. Depression and anxiety are important associated mental disorders for people with MS (PwMS), which influence their life quality. During the COVID-19 pandemic, fear and stress levels enhanced dramatically for the general population, but mostly in progressive chronic pathologies such as MS. AIM: This study aimed to analyze the dynamic of psychological aspects in PwMS pre-pandemic and during pandemic, their connection with clinical outcomes, and with the coronavirus disease. METHODS: We included 95 PwMS with relapsing-remitting MS (RRMS) and secondary progressive MS (SPMS), who were first evaluated 4 years before the pandemic outbreak and the second time 2 years after. They completed a series of psychological tests for depression, anxiety, negative automatic thoughts, and stress: Beck Depression Inventory-II (BDI-II), Beck Anxiety Inventory (BAI), Endler Multidimensional Anxiety Scales (EMAS), Automatic Thoughts Questionnaire (ATQ). A neurologist evaluated the Expanded Disability Status Scale (EDSS) and a COVID-19 survey was completed by 78 patients. RESULTS: During the pandemic, depression was encountered in 9.47% of PwMS, only 1.05% with a severe form, and 6.3% with suicidal thoughts, while anxiety was more frequent (39% of cases). Compared to the pre-pandemic period, depression levels remained stable over time (p = 0.55), anxiety was reduced (p<0.001), and stress levels significantly increased (p = 0.001). Some social aspects, such as having sufficient income, reduced the risk for psychological comorbidities. There was a mild correlation between emotional well-being and neurological disability. Of all patients who responded to the survey, 53.84% had previous COVID-19 infections, no patient was hospitalized and 69.23% were vaccinated. There was no relationship between the COVID-19 infection and psychological test results. CONCLUSION: During the pandemic, in the MS population depression remained stable, anxiety decreased, and stress levels were enhanced compared to the pre-pandemic period. Psychiatric comorbidities were not influenced by the coronavirus infection.
 Rapid and accurate diagnosis of any illness determines the success of treatment. The same applies to multiple sclerosis (MS), chronic, inflammatory, and neurodegenerative diseases (ND) of the central nervous system (CNS). Unfortunately, the definitive diagnosis of MS is prolonged and involves mainly clinical symptoms observation and magnetic resonance imaging (MRI) of the CNS. However, as we previously reported, Attenuated Total Reflectance Fourier Transform Infrared (ATR-FTIR) spectroscopy shed new light on the minimally invasive, label-free, and rapid diagnosis of this illness through blood fraction. Herein we introduce Raman spectroscopy coupled with chemometric analysis to provide more detailed information about the biochemical changes behind MS. This pilot study demonstrates that mentioned combination may provide a new diagnostic biomarker and bring closer to rapid MS diagnosis. It has been shown that Raman spectroscopy provides lipid and carotenoid molecules as useful biomarkers which may be applied for both diagnosis and treatment monitoring.
 AIM: N-acetylcysteine (NAC), a thiol-containing antioxidant and glutathione (GSH) precursor, attenuates oxidative stress, and possibly improves psychiatric disorders. This study aimed to evaluate the effects of oral NAC on oxidative stress, depression, and anxiety symptoms in patients with multiple sclerosis (MS). METHODS: This clinical trial was conducted on 42 MS patients randomly assigned to intervention (n = 21) and control (n = 21) groups. The intervention group received 600 mg of NAC twice daily for 8 weeks, and the control group received a placebo with the same prescription form. An analysis of serum malondialdehyde (MDA), serum nitric oxide (NO), and erythrocyte GSH was carried out on both groups, along with a complete blood count. The Hospital Anxiety and Depression Scale (HADS) was used to assess symptoms of depression (HADS-D) and anxiety (HADS-A). RESULTS: Compared to the control group, NAC consumption significantly decreased serum MDA concentrations (-0.33 [-5.85-2.50] vs. 2.75 [-0.25-5.22] μmol/L; p = 0.03) and HADS-A scores (-1.6 ± 2.67 vs. 0.33 ± 2.83; p = 0.02). No significant changes were observed in serum NO concentrations, erythrocyte GSH levels, and HADS-D scores (p > 0.05). CONCLUSIONS: Based on the findings of the present study, NAC supplementation for 8 weeks decreased lipid peroxidation and improved anxiety symptoms in MS patients. The aforementioned results suggest that adjunctive therapy with NAC can be considered an effective strategy for MS management. Further randomized controlled studies are warranted.
 BACKGROUND: The Multiple Sclerosis Intimacy and Sexuality Questionnaire-15 (MSISQ-15) is a valid and reliable tool to assess the sexuality of people with multiple sclerosis. The objectives of this study were: 1) to cross-culturally adapt and examine the psychometric properties of the MSISQ-15 in the Spanish context and 2) to examine the association between sexual dysfunction and other related factors. METHODS: We conducted a instrumental study. People diagnosed with multiple sclerosis and members of multiple sclerosis associations in Spain were included. The linguistic adaptation of the questionnaire was performed through a translation-back translation procedure. For the psychometric validation, the confirmatory factor analysis was used while the internal consistency was examined by the ordinal alpha test. The construct validity was examined by correlating the results with the Male Sexual Function (FSH), Female Sexual Function-2 (FSM-2), Dyadic Adjustment Scale-13 (EAD-13) and Multiple Sclerosis International Quality of Life Questionnaire (MusiQoL) questionnaires. RESULTS: A total of 208 participants were included. Both the fit of the Spanish version of the MSISQ-15 to the original scale and the internal consistency were adequate (α = 0.89). The construct validity showed correlations with the FSH, FSM-2, and MusiQoL but not with the EAD-13. CONCLUSIONS: The Spanish version of the MSISQ-15 is a valid and reliable tool to assess the sexuality of people with multiple sclerosis in the Spanish context.
 BACKGROUND: To compare the rate of retinal atrophy over time in patients with relapsing-remitting multiple sclerosis (RRMS) treated with various disease-modifying therapies (DMT). METHODS: Patients with RRMS on various DMT and those observed without treatment were prospectively enrolled into the study between September 2015 and June 2018. All subjects with follow-up of 1-4 years were included and categorized into groups as "no drug", "low efficacy drug", "high efficacy drug", or "dimethyl fumarate" (DMF), based on treatment modality used for the longest duration of their follow-up. Ocular coherence tomography (OCT) was used to measure peripapillary retinal nerve fiber layer thickness (RNFL) and ganglion cell/inner plexiform layer (GC-IPL) thickness at baseline and every 6 months. A linear mixed effects regression model was performed to compare rates of retinal atrophy across treatment groups. RESULTS: Out of 67 participants who met inclusion criteria (mean age = 37; 76% female), 13 were untreated, 12 on low efficacy therapy, 18 on DMF, and 24 on high efficacy therapy. History of optic neuritis was associated with lower baseline GC-IPL thickness (p = 0.003). Higher baseline GC-IPL thickness was associated with increased rate of GC-IPL thinning (p = 0.009). Age, disease duration, and ethnicity were not predictors of baseline RNFL or GC-IPL thickness, or rate of atrophy of these layers. CONCLUSIONS: There were no differences in rate of GC-IPL atrophy between patients with RRMS on different treatments in this cohort. Age, disease duration, and ethnicity also did not predict retinal atrophy. History of ON was associated with reduced GC-IPL thickness at baseline, consistent with previous research. Rate of GC-IPL thinning was higher for subjects with higher baseline GC-IPL thickness, suggesting a plateau effect.
 BACKGROUND AND OBJECTIVES: To identify biomarkers associated with treatment response in patients with multiple sclerosis (MS) treated with the oral therapies teriflunomide, dimethyl fumarate (DMF), and fingolimod. METHODS: Serum levels of IL-6, IL-17, TNF-α, granulocyte-macrophage colony-stimulating factor, IL-10, interferon-gamma (IFN-γ) IL-1β, and chemokine ligand 13 (CXCL13) were measured at baseline and 12 months with single molecule array (Simoa) assays in a cohort of patients with MS treated with teriflunomide (N = 19), DMF (N = 22), and fingolimod (N = 25) and classified into "no evidence of disease activity" (NEDA) and EDA patients after 1 year of treatment. RESULTS: Serum CXCL13 and TNF-α levels were significantly decreased after treatment with teriflunomide in NEDA compared with EDA patients after 1 year of treatment (p = 0.008 for both cytokines). These findings were validated in an independent cohort of patients with MS treated with teriflunomide (N = 36) and serum CXCL13, and TNF-α levels were again significantly reduced in NEDA patients (p < 0.0001 for CXCL13 and p = 0.003 for TNF-α). CXCL13, but not TNF-α, showed good performance to classify NEDA and EDA patients according to a cut-off value of 9.64 pg/mL based on the change in CXCL13 levels between baseline and 12 months, with a sensitivity of 75% and specificity of 82% in the original cohort, and sensitivity of 65.4% and specificity of 60% in the validation cohort. DISCUSSION: Altogether, these results point to CXCL13 as a treatment response biomarker to teriflunomide in relapsing-remitting patients with MS, and the change in CXCL13 levels during the first year of treatment can be used in clinical practice to identify optimal responders to teriflunomide.
 It has been shown that the dysbiosis of the gut's microbes substantially impacts CNS illnesses, including Alzheimer's, Parkinson's, autism, and autoimmune diseases like multiple sclerosis (MS). MS is a CNS-affected autoimmune demyelination condition. Through a two-way communication pathway known as the gut-brain axis, gut microbes communicate with the CNS. When there is a disruption in the gut microbiome, cytokines and other immune cells are secreted, which affects the BBB and gastrointestinal permeability. Recent research using animal models has revealed that the gut microbiota may greatly influence the pathophysiology of EAE/MS. Any change in the gut might increase inflammatory cytokinesand affect the quantity of SCFAs, and other metabolites that cause neuroinflammation and demyelination. In- vivo and in-vitro studies have concluded that probiotics affect the immune system and can be utilized to treat gastrointestinal dysbiosis. Any alteration in the gut microbial composition caused by probiotic intake may serve as a preventive and treatment strategy for MS. The major goal of this review is to emphasize an overview of recent research on the function of gut microbiota in the onset of MS and how probiotics have a substantial impact on gastrointestinal disruption in MS and other neuro disorders. It will be easier to develop new therapeutic approaches, particularly probiotic-based supplements, for treating multiple sclerosis (MS) if we know the link between the gut and CNS.
 Multiple sclerosis (MS) is a multifactorial neurological disease characterized by chronic inflammation and immune-driven demyelination of the central nervous system (CNS). The rising number of MS cases in the last decade could be partially attributed to environmental changes, among which the alteration of the gut microbiome driven by novel dietary habits is now of particular interest. The intent of this review is to describe how diet can impact the development and course of MS by feeding the gut microbiome. We discuss the role of nutrition and the gut microbiota in MS disease, describing preclinical studies on experimental autoimmune encephalomyelitis (EAE) and clinical studies on dietary interventions in MS, with particular attention to gut metabolites-immune system interactions. Possible tools that target the gut microbiome in MS, such as the use of probiotics, prebiotics and postbiotics, are analyzed as well. Finally, we discuss the open questions and the prospects of these microbiome-targeted therapies for people with MS and for future research.
 BACKGROUND: Rituximab (RTX) is an extensively used off-label drug for multiple sclerosis (MS), whereas the induction and maintenance regimens vary widely among studies. Few data are available on efficacy and safety of repeated low-dose RTX therapy in MS patients. OBJECTIVE: This study aimed to evaluate the efficacy and safety of repeated low-dose RTX therapy for relapsing-remitting MS (RRMS), the most common form of MS affecting approximately 85% of patients. METHODS: Nine RRMS patients were enrolled and the medical records were retrospectively reviewed. RTX at 100 mg per week for three consecutive weeks was used as induction therapy. Maintenance therapy was reinfusions of RTX at 100 mg every 6 months during the first year, followed by 100 mg every 6 to 12 months. Main outcome measures included annualized relapse rate (ARR), expanded disability status scale (EDSS) score, and T2 lesion burden on MRI for evaluating the efficacy of low-dose RTX regimen. Meanwhile, adverse events (AEs) were recorded to assess the safety of repeated RTX infusions. RESULTS: All patients were females with an average onset age of 25.4 ± 6.7 years. The median disease duration before the first RTX infusion was 56 (range, 3-108) months and the median follow-up period was 30 (range, 15-40) months. No relapses were recorded in all patients after RTX therapy. Repeated low-dose RTX therapy resulted in a dramatic reduction of median ARR (pre-RTX vs post-RTX, 1.1 vs 0, p = 0.012), median EDSS score (2.0 vs 0, p = 0.007), and the number of T2 lesions on MRI (35.6 ± 18.0 vs 29.4 ± 18.1, p = 0.001). A total of 35 episodes of AEs occurred during repeated low-dose RTX therapy, and all of them were mild and transient. CONCLUSION: Repeated low-dose RTX therapy is cost-effective for RRMS patients and shows a good safety profile. It may be a promising option for those having no access or poor response to first-line disease-modified drugs (DMDs), particularly in low- or middle-income countries.
 BACKGROUND: Cognitive decline is inadequately captured by the standard neurological examination. Serum neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP) are biomarkers of neuronal damage and astrocytic reactivity that may offer an accessible measure of the multiple sclerosis (MS) pathology linked to cognitive decline. OBJECTIVE: To investigate the association of sNfL and sGFAP with cognitive decline in MS patients at high risk for progressive pathology. METHODS: We included 94 MS patients with sustained Expanded Disability Status Score (EDSS) ⩾ 3, available serum samples and cognitive assessment performed by symbol digit modalities test (SDMT) over a median of 3.1 years. The visit for sGFAP/sNfL quantification was at confirmed EDSS ⩾ 3. Linear regression analysis on log-transformed sGFAP/sNfL assessed the association with current and future SDMT. Analyses were adjusted for age, sex, EDSS, treatment group, and recent relapse. RESULTS: sNfL was significantly associated with concurrent SDMT (adjusted change in mean SDMT = -4.5; 95% confidence interval (CI): -8.7, -0.2; p = 0.039) and predicted decline in SDMT (adjusted change in slope: -1.14; 95% CI: -1.83, -0.44; p = 0.001), particularly in active patients. sGFAP was not associated with concurrent or future SDMT. CONCLUSIONS: Higher levels of sNfL were associated with cognitive impairment and predicted cognitive decline in MS patients at high risk for having an underlying progressive pathology.
 The aim of this study is to examine the relationship between body mass index (BMI) and intelligence quotient scores (IQ). The sample included 11 patients with pediatric multiple sclerosis between 8 and 17 years, mean age 14.45 years (SD = 2.69). The BMI was calculated as weight in kilograms divided by the square of height in meters. The Wechsler Intelligence Scale for Children V and the Abbreviated Weschler Intelligence Scale were used to measure total IQ. Average sample BMI and IQ were 24.61 (SD = 5.53) (range: 19-39.4) and 86.63 (SD = 14.79) (range: 66-111), respectively. Results of the Pearson correlation indicated that there was a significant negative association between BMI and IQ, (r = -0.608, p = 0.042). R-squared was 0.370. We discuss if lower IQ lead to BMI gains or whether overweight/obesity lead to intellectual functioning changes. Implication for practice and future research are presented.
 BACKGROUND AND OBJECTIVES: The specificity of novel blood biomarkers for multiple sclerosis (MS)-related neurodegeneration is unclear because neurodegeneration also occurs during normal aging. To understand which aspects of neurodegeneration the serum biomarkers neurofilament light (sNfL), serum glial fibrillary acidic protein (sGFAP), and serum contactin-1 (sCNTN1) reflect, we here explore their cross-sectional association with disability outcome measures and MRI volumes in a unique cohort of people with MS (PwMS) of the same age. METHODS: sNfL, sGFAP (both singe-molecule array technology) and sCNTN1 (Luminex) were measured in serum samples of 288 PwMS and 125 healthy controls (HCs) of the Project Y cohort, a population-based cross-sectional study of PwMS born in the Netherlands in 1966 and age-matched HC. RESULTS: sNfL (9.83 pg/mL [interquartile range {IQR}: 7.8-12.0]) and sGFAP (63.7 pg/mL [IQR: 48.5-84.5]) were higher in PwMS compared with HC (sNfL: 8.8 pg/mL [IQR: 7.0-10.5]; sGFAP: 51.7 pg/mL [IQR: 40.1-68.3]) (p < 0.001), whereas contactin-1 (7,461.3 pg/mL [IQR: 5,951.8-9,488.6]) did not significantly differ between PwMS compared with HC (7,891.2 pg/mL [IQR: 6,120.0-10,265.8]) (p = 0.068). sNfL and sGFAP levels were 1.2-fold higher in secondary progressive patients (SPMS) compared with relapsing remitting patients (p = 0.009 and p = 0.043). Stratified by MS subtype, no relations were seen for CNTN1, whereas sNfL and sGFAP correlated with the Expanded Disability Status Scale (ρ = 0.43 and ρ = 0.39), Nine-Hole Peg Test, Timed 25-Foot Walk Test, and Symbol Digit Modalities Test (average ρ = 0.38) only in patients with SPMS. Parallel to these clinical findings, correlations were only found for sNfL and sGFAP with MRI volumes. The strongest correlations were observed between sNfL and thalamic volume (ρ = -0.52) and between sGFAP with deep gray matter volume (ρ = - 0.56) in primary progressive patients. DISCUSSION: In our cohort of patients of the same age, we report consistent correlations of sNfL and sGFAP with a range of metrics, especially in progressive MS, whereas contactin-1 was not related to clinical or MRI measures. This demonstrates the potential of sNfL and sGFAP as complementary biomarkers of neurodegeneration, reflected by disability, in progressive MS.

 OBJECTIVE: To address the diagnostic performances of cerebrospinal fluid (CSF) free light chains (FLC) measurements compared to oligoclonal bands (OCB) to support multiple sclerosis (MS) diagnosis. RESULTS: kFLC index showed the highest diagnostic accuracy to detect MS patients with the highest AUC compared to OCB, IgG index, IF kFLC R, kFLC H, λFLC index and IF λFLC. CONCLUSIONS: FLC indices are biomarkers of intrathecal Immunoglobulin synthesis and central nervous system (CNS) inflammation. kFLC index can discriminate between MS and other CNS inflammatory disorders, while λFLC index is less informative for MS but can play a role to support the diagnosis of other inflammatory CNS disorders.
 BACKGROUND: The expansion of the availability of advanced imaging methods needs more time, expertise, and resources which is in contrast to the primary goal of the imaging techniques. To overcome most of these difficulties, artificial intelligence (AI) can be used. A number of studies used AI models for multiple sclerosis (MS) diagnosis and reported diverse results. Therefore, we aim to perform a comprehensive systematic review and meta-analysis study on the role of AI in the diagnosis of MS. METHODS: We performed a systematic search using four databases including PubMed, Scopus, Web of Science, and IEEE. Studies that applied deep learning or AI to the diagnosis of MS based on any modalities were considered eligible in our study. The accuracy, sensitivity, specificity, precision, and area under curve (AUC) were pooled with a random-effects model and 95% confidence interval (CI). RESULTS: After the screening, 41 articles with 5989 individuals met the inclusion criteria and were included in our qualitative and quantitative synthesis. Our analysis showed that the overall accuracy among studies was 94% (95%CI: 93%, 96%). The pooled sensitivity and specificity were 92% (95%CI: 90%, 95%) and 93% (95%CI: 90%, 96%), respectively. Furthermore, our analysis showed 92% precision in MS diagnosis for AI studies (95%CI: 88%, 97%). Also, the overall pooled AUC was 93% (95%CI: 89%, 96%). CONCLUSION: Overall, AI models can further improve our diagnostic practice in MS patients. Our results indicate that the use of AI can aid the clinicians in accurate diagnosis of MS and improve current diagnostic approaches as most of the parameters including accuracy, sensitivity, specificity, precision, and AUC were considerably high, especially when using MRI data.
 The severe adult respiratory syndrome virus type 2 (SARS-CoV-2) related acute respiratory distress syndrome (ARDS) has a strong immunological and inflammatory component; accordingly investigators are employing monoclonal antibodies to ameliorate the virus-induced cytokine storm such as antibodies against interleukin 6 (IL-6), tumor necrosis factors alpha (TNF-alpha) and CC chemokine receptor 5 (CCR5) (1). Cyclophosphamide (Cy) has proven its role in various settings including autoimmune diseases, and in the post-haploidentical stem cell transplant setting; Cy depletes cytotoxic and effector T cell populations while relatively sparing the regulatory T cells (Tregs) and could tip the balance away from the overtly pro-inflammatory setting (1). We present here the cases of three persons who were infected by the SARS-CoV-2 virus during the Cy-induced pancytopenia of an autologous hematopoietic stem cell transplantation (HSCT), aimed to down-regulate the immune response in multiple sclerosis (MS) (2). The surprisingly benign course of the COVID-19 in the three cases suggest that the Cy could have had a role in abrogating the inflammatory response in these persons.
 A number of studies have suggested that multiple sclerosis (MS) can be associated with serious vascular complications, for which pulmonary thromboembolism (PTE) is a potentially lethal complication. The purpose of this study is to establish a current literature-based estimate of the incidence of venous thromboembolism (VTE), deep vein thrombosis (DVT), and PTE in patients with MS (pwMS) due to the lack of systematic reviews and meta-analyses on this topic. In this systematic review and meta-analysis, studies were assessed regarding the association between MS and the incidence of VTE. The studies were identified through a systematic search of major electronic databases spanning the period from 1950 to February 2022. A random-effects analysis was conducted to calculate the pooled effect size (ES) and 95% confidence intervals (CI) using STATA software. Nine out of 4605 studies were included in the meta-analysis, with an overall sample size of 158,546 individuals. Meta-analysis revealed that the pooled incidence of VTE was 1.8% (95% CI 1.4-2.3) among pwMS. Also, there was an incidence of 0.9% (95% CI 0.4-1.4) and 1.5% (95% CI 1-2.2) for PTE and DVT, respectively in pwMS. Analysis showed MS would be significantly associated with a twofold increased risk of VTE [risk ratios (RR) = 2.12 (95% CI 1.53-2.93)]. Although MS is not typically considered a major risk factor for VTE, the meta-analysis of cohort studies shows that MS has a relative association with an increased incidence of VTE. Future research should focus on the investigation of the effects of MS and its treatments on VTE risk, and also a full range of confounding adjustments will be needed.
 Two-thirds of people with Multiple Sclerosis (PwMS) have walking disabilities. Considering the literature, prolonged tests, such as the 6 min walk test, better reflect their everyday life walking capacities and endurance. However, in most studies, only the distance traveled during the 6MWT was measured. This study aims to analyze spatio-temporal (ST) walking patterns of PwMS and healthy people in the 6MWT. Participants performed a 6MWT with measures of five ST variables during three 1 min intervals (initial: 0'-1', middle: 2'30″-3'30″, end: 5'-6') of the 6MWT, using the GAITRite system. Forty-five PwMS and 24 healthy people were included. We observed in PwMS significant changes between initial and final intervals for all ST parameters, whereas healthy people had a rebound pattern but the changes between intervals were rather negligible. Moreover, ST variables' changes were superior to the standard measurement error only for PwMS between initial and final intervals for all ST parameters. This result suggests that the modification in PwMS' walking pattern is effectively due to their walking ability and not to a measurement, and suggests that PwMS could not manage their walking efficiently compared to healthy people, who could maintain their rhythm throughout the 6MWT. Further studies are needed to detect these patterns changes in the early evolution of the disease, identify clinical determinants involved in PwMS' walking pattern, and investigate whether interventions can positively impact this pattern.
 Multiple sclerosis (MS) is the most common chronic central nervous system inflammatory disease. Individual courses are highly variable, with complete remission in some patients and relentless progression in others. We generated induced pluripotent stem cells (iPSCs) to investigate possible mechanisms in benign MS (BMS), compared with progressive MS (PMS). We differentiated neurons and astrocytes that were then stressed with inflammatory cytokines typically associated with MS phenotypes. TNF-α/IL-17A treatment increased neurite damage in MS neurons from both clinical phenotypes. In contrast, TNF-α/IL-17A-reactive BMS astrocytes cultured with healthy control neurons exhibited less axonal damage compared with PMS astrocytes. Accordingly, single-cell transcriptomic BMS astrocyte analysis of cocultured neurons revealed upregulated neuronal resilience pathways; these astrocytes showed differential growth factor expression. Furthermore, supernatants from BMS astrocyte/neuronal cocultures rescued TNF-α/IL-17-induced neurite damage. This process was associated with a unique LIF and TGF-β1 growth factor expression, as induced by TNF-α/IL-17 and JAK-STAT activation. Our findings highlight a potential therapeutic role of modulation of astrocyte phenotypes, generating a neuroprotective milieu. Such effects could prevent permanent neuronal damage.
 BACKGROUND: In 2020, the French Multiple Sclerosis (MS) Society (SFSEP) decided to develop a national evidence-based consensus on pregnancy in MS. As neuromyelitis optica spectrum disorders (NMOSD) shares a series of commonalities with MS, but also some significant differences, specific recommendations had to be developed. OBJECTIVES: To establish recommendations on pregnancy in women with NMOSD. METHODS: The French Group for Recommendations in Multiple Sclerosis (France4MS) reviewed PubMed and universities databases (January 1975 through June 2021). The RAND/UCLA appropriateness method, which was developed to synthesise the scientific literature and expert opinions on health care topics, was used to reach a formal agreement. Fifty-six MS experts worked on the full-text review and initial wording of recommendations. A sub-group of nine NMOSD experts was dedicated to analysing available data on NMOSD. A group of 62 multidisciplinary healthcare specialists validated the final proposal of summarised evidence. RESULTS: A strong agreement was reached for all 66 proposed recommendations. They cover diverse topics, such as pregnancy planning, follow-up during pregnancy and postpartum, delivery routes, loco-regional analgesia or anaesthesia, prevention of postpartum relapses, breastfeeding, vaccinations, reproductive assistance, management of relapses, and disease-modifying treatments. CONCLUSION: Physicians and patients should be aware of the new and specific evidence-based recommendations of the French MS Society for pregnancy in women with NMOSD. They should help harmonise counselling and treatment practise, allowing for better individualised choices.
 PURPOSE: Walking difficulties in people with multiple sclerosis (pwMS) are one of the most pronounced predictors affecting patients' quality of life. The study objective was to determine the psychometric properties of the Croatian version of the Multiple Sclerosis Walking Scale (MSWS-12) among pwMS in Croatia and to examine the association between MSWS-12 and Depression, Anxiety, and Stress Scale-21 (DASS-21), and Multiple Sclerosis Impact Scale-29 (MSIS-29). MATERIALS AND METHODS: A cross-sectional study included a sample of pwMS (N = 148). Psychometric properties were examined by estimating the validity and reliability of the MSWS-12. The predictive validity of MSWS-12 and demographic and disease-related factors were assessed by a hierarchical regression model using MSIS-29 and DASS-21 as criterion variables. RESULTS: Scale reliability was good for the MSWS-12 scale, expressed by Cronbach's alpha coefficient (α = 0.98). Correlations between MSWS-12 and DASS-21 (0.20-0.27) and between MSWS-12 and MSIS-29 subscales (0.47-0.83) provided initial support for the convergent validity. Factor analysis demonstrated the unidimensional structure of the MSWS-12. CONCLUSIONS: The Croatian version of the MSWS-12 is a reliable, valid, and clinically useful tool for assessing walking impairments in pwMS.Implications for rehabilitationWalking difficulties in people with multiple sclerosis (pwMS) are one of the most pronounced predictors affecting patients' quality of life.Multiple Sclerosis Walking Scale (MSWS-12) is a measure of the disease's impact on walking abilities from the patient's perspective.MSWS-12 is a reliable scale for assessing walking speed, endurance, and gait quality in multiple sclerosis and is validated in several languages (Korean, Italian, Brazilian, and Persian).The Croatian version of the MSWS-12 is a reliable, predictive, and valid tool for screening walking impairments in pwMS.
 Multiple Sclerosis (MS) is a chronic neurodegenerative disease with limited therapeutic options. Recombinant Fc multimers (rFc), designed to mirror many of the anti-inflammatory activities of Intravenous Immunoglobulin (IVIG), have been shown to effectively treat numerous immune-mediated diseases in rodents. In this study we used the experimental autoimmune encephalomyelitis (EAE) murine model of MS to test the efficacy of a rFc, M019, that consists of multimers of the Fc portion of IgG2, in inhibiting disease severity. We show that M019 effectively reduced clinical symptoms when given either pre- or post-symptom onset compared to vehicle treated EAE induced mice. M019 was effective in reducing symptoms in both SJL model of relapsing remitting MS as well as the B6 model of chronic disease. M019 binds to FcγR bearing-monocytes both in vivo and in vitro and prevented immune cell infiltration into the CNS of treated mice. The lack of T cell infiltration into the spinal cord was not due to a decrease in T cell priming; there was an equivalent frequency of Th17 cells in the spleens of M019 and vehicle treated EAE induced mice. Surprisingly, there was an increase in chemokines in the sera but not in the CNS of M019 treated mice compared to vehicle treated animals. We postulate that M019 interacts with a FcγR rich monocyte intermediary to prevent T cell migration into the CNS and demyelination.
 This systematic review aimed to present the comparison of the impacts of conventional exercise and virtual reality (VR) exergaming on the physical and cognitive abilities of people with multiple sclerosis (PwMS). The literature search was conducted in the EMBASE, PubMed, Scopus, CINAHL, and Cochrane Library databases. Eligible studies were identified by independent reviewers based on the title, abstract and full-texts. Studies were limited to randomized clinical trials published in peer-reviewed journals in English that compared conventional exercise with VR-exergaming for improving the physical and cognitive abilities of PwMS. Selected studies were assessed for their risk of bias and the major findings of the reviewed studies were analyzed descriptively. The search identified 239 articles of which 10 studies met the eligibility criteria. Despite these studies employing strategies to control biases, some risks of bias remain. Various gaming platforms and conventional exercises were used based on the extent of technologies and therapy regimens. The selected studies used measures of physical and cognitive abilities to compare VR-exergaming with conventional exercise. This review suggests positive impacts of both VR-exergaming and conventional exercise in MS rehabilitation. We also found that VR-exergaming generally exceeded conventional exercise for improving physical and cognitive abilities, psychosocial status, and fatigue.
 BACKGROUND: The treatment paradigm for multiple sclerosis (MS), particularly relapsing-remitting MS, is heavily reliant on biologic disease-modifying therapies (DMTs). However, the current cost of treatment acts as a significant barrier to access for patients. Over the next few years exclusivity periods for key biologic medicines used in MS are likely to end, opening the door for biosimilar medicines to enter the market. METHODS: In this review, we discuss what biosimilar medicines are, and how the existing experience with biosimilar medicines across multiple therapy areas can inform the assimilation of biosimilar medicines into the MS treatment landscape in Europe and the US. RESULTS: There is currently a lack of knowledge and awareness around the distinctions and similarities between small molecules, non-biological complex drugs, and biological medicines, as well as the different categories of follow-on successor medicines. These include biosimilar medicines that offer a matching efficacy and safety profile to the reference biologic. Understanding and recognition of the stringency of the approval pathways required for drug categories such as biosimilars are key in building confidence in treatment outcomes. For example, biosimilar medicines are sometimes perceived only as 'copies' of their reference biologic despite undergoing an extensive approval process requiring that no clinically meaningful differences are observed between the biosimilar medicine and the reference medicine. For MS, introduction of biosimilar medicines in the future will enable more people with MS to receive effective treatment, and also expand access to biologic DMTs in MS. Experiences from the use of biosimilars in multiple therapy areas have shown us that this can result in cost-saving benefits for a healthcare system. Introduction of biosimilar medicines in other therapy areas has also demonstrated the importance of appropriate, accurate education and information for their successful integration into clinical practice. CONCLUSION: In order to realize optimized treatment outcomes in MS in coming years and to find the appropriate place for biosimilar medicines in the changing MS landscape, it is essential that clinicians and people with MS understand the fundamentals of biosimilars, their potential benefits and consistency of treatment provided by a biosimilar medicine, given the matching efficacy and safety profile to its reference medicine. As evidenced in other therapy areas, biosimilar medicines may reduce key barriers to access by providing a cost-effective alternative to the MS treatment arsenal, while providing the same treatment outcomes as reference biologics.
 ABSTRACTEvidence supporting the direct therapeutic benefits of neuropsychological assessment (NPA) feedback relies mostly upon post-feedback consumer surveys. This randomized-controlled trial with cross-over investigated the benefits of NPA feedback in multiple sclerosis (MS). Seventy-one participants were randomly allocated to NPA with feedback or a "delayed-treatment" control group. The primary hypotheses were that NPA feedback would lead to improved knowledge of cognitive functioning and improved coping. Outcome instruments were administered by a research assistant blinded to group allocation. At 1-week post-NPA feedback there were no significant group-by-time interaction effects, indicating no improvement. But nor was there any significant deterioration in psychological wellbeing, despite most participants receiving "bad news" confirming cognitive impairment. At 1-month follow-up, within-subjects' analyses not only found no evidence of any delayed deterioration, but showed clinically significant improvement (small-medium effects) in perceived everyday cognitive functioning, MS self-efficacy, stress and depression. Despite lack of improvement in the RCT component at 1-week post-NPA feedback, the absence of deterioration at this time, in addition to significant improvements in perceived cognitive functioning, self-efficacy and mood at follow-up, together with high satisfaction ratings, all support NPA feedback as a safe psycho-educational intervention that is followed by improved psychological wellbeing over time.Trial registration: Uniform Trial Number identifier: U1111-1127-1585.Trial registration: Australian New Zealand Clinical Trials Registry identifier: ACTRN12612000161820.
 Patients with multiple sclerosis (MS) typically experience varying degrees of impairments and disabilities. Task-oriented training (TOT) has been used for those patients to improve their motor skills. This review aimed to evaluate the primary research on the effectiveness of TOT in improving upper limb functions in patients with MS. The systematic search was performed using PubMed, Cochrane library and Physical therapy Evidence Database (PEDro) databases up to 2022. Only randomized controlled trials that used TOT alone for UL functions of adult patients with MS were included. Two independent reviewers screened records, extracted data and assessed studies' quality by using PEDro scale. The meta-analysis was based on the standardized mean differences and the random effect. The search screened 9148 records; only five randomized controlled trials were eligible; four of them were of good quality. The trials included 147 patients with MS; 66% of them were females, their mean average age was 47 years. TOT duration ranged from 40 to 210 min with total period of 10 days to 8 weeks; it was applied alone without conventional physical therapy. Meta-analyses compared TOT alone versus control interventions revealed non-significant difference in the improvement of UL functions on Nine-Hole Peg Test, Action Reach Arm Test, Motor Activity Log-Amount Of Use scale, and Manual Ability Measurement. This review concluded that TOT alone can be effective for improving UL functions in patients with MS but meta-analyses showed non-significant differences when it was compared with conventional physical therapy.
 Transcranial magnetic stimulation (TMS) is a noninvasive technique mainly used for the assessment of corticospinal tract integrity and excitability of the primary motor cortices. Motor evoked potentials (MEPs) play a pivotal role in TMS studies. TMS clinical guidelines, concerning the use and interpretation of MEPs in diagnosing and monitoring corticospinal tract integrity in people with multiple sclerosis (pwMS), were established almost ten years ago and refer mainly to the use of TMS implementation; this comprises the magnetic stimulator connected to a standard EMG unit, with the positioning of the coil performed by using the external landmarks on the head. The aim of the present work was to conduct a narrative literature review on the MEP assessment and outcome measures in clinical and research settings, assessed by TMS Methodological characteristics of different TMS system implementations (TMS without navigation, line-navigated TMS and e-field-navigated TMS); these were discussed in the context of mapping the corticospinal tract integrity in MS. An MEP assessment of two case reports, by using an e-field-navigated TMS, was presented; the results of the correspondence between the e-field-navigated TMS with MRI, and the EDSS classifications were presented. Practical and technical guiding principles for the improvement of TMS studies in MEP assessment for MS are discussed, suggesting the use of e-field TMS assessment in the sense that it can improve the accuracy of corticospinal tract integrity testing by providing a more objective correspondence of the neurophysiological (e-field-navigated TMS) and clinical (Expanded Disability Status Scale-EDSS) classifications.
 BACKGROUND: The clinical utility of the Trendelenburg Test remains unknown in people with multiple sclerosis (MS). OBJECTIVE: To measure (1) intra-rater reliability, (2) agreement of goniometer-assessed Trendelenburg pelvis-on-femur angle (POF) with motion capture, and (3) concurrent validity of Trendelenburg POF and hip abduction strength with POF during walking and step negotiation. METHODS: Trendelenburg POF was measured in 20 people with MS using goniometry and motion analysis. In addition, peak POF was measured using motion analysis during walking, step ascent, and step descent. Intra-rater reliability of goniometer-assessed Trendelenburg POF and agreement with motion analysis-assessed POF were analyzed. Pearson's r was used to determine the relationships between Trendelenburg POF and hip abduction strength with peak POF during each functional activity. RESULTS: Goniometer-assessed Trendelenburg POF demonstrated very strong reliability (ICC: 0.948), strong agreement with 3D motion analysis (ICC: 0.792), correlated moderately with peak POF during walking (r = 0.519) and step ascent (r = 0.572), and weakly with step descent (r = 0.463). Hip abductor strength correlated weakly with peak POF during step ascent (r = -0.307) and negligibly during walking (r = -0.270) and step descent (r = -0.249). CONCLUSIONS: Goniometer-assessed Trendelenburg POF was reliable, agreed with motion analysis, and may provide insight into hip abduction muscle performance during functional activities in people with MS.
 BACKGROUND: In 2019 and 2020, over 17 million hectares of Australia burned, and half of the Australian population was affected by toxic bushfire smoke. Then in 2020, restrictions designed to curtail the spread of COVID-19 resulted in significant changes to healthcare access. There is no Australian emergency management standard for persons with disabilities, including those with multiple sclerosis (MS). Persons with MS often require multidisciplinary and complex care, with continuity of treatment essential to prevent disease progression. OBJECTIVE: To identify limitations in access to healthcare from the perspective of persons with MS as well as MS care providers during recent crises and make recommendations for policy to improve MS healthcare access during a crisis. METHOD: In mid-2020, we undertook online surveys and interviews with persons with MS, their carers, healthcare professionals and staff of MS service providers (i.e., care providers). We used descriptive analysis for quantitative, and a general inductive approach for qualitative data. RESULTS: One-hundred and thirteen persons with MS and a total of 63 MS care providers, who were close carers, healthcare professionals and service providers provided survey responses. For participants with MS, limited access to general practitioners and medical tests were of the most significant concern during the bushfires and the pandemic. In contrast, during the pandemic accessing physiotherapy was another top concern. Twenty-nine people participated in in-depth interviews, revealing that reduced healthcare access during the bushfire and the pandemic caused concern. The use of telehealth received both positive and negative reviews. All participants indicated a need for preparation and planning for healthcare access before a crisis. Persons with MS recommended centralised information sources, prioritised access to healthcare and increased levels of MS nurses and other allied healthcare. Care providers recommended centralised information sources, more nursing and mental health care access, and increased opportunities for multidisciplinary telehealth delivery. CONCLUSIONS: We recommend the involvement of the MS community in creating and designing disaster preparation plans, which should cater to a range of disaster types, to improve disaster preparedness in a community that is vulnerable to increasingly common community crises.
 BACKGROUND: Previous studies have shown that there is a relationship between cognitive impairment (CI) and motor dysfunction (MD) in neurological diseases, such as Alzheimer's and Parkinson's disease. However, there whether CI and MD are associated in patients with multiple sclerosis (MS) is unknown. Here we studied the association between CI and MD in patients with MS and examined if muscle weakness or incoordination, balance impairment, gait abnormalities, and/or increased fall risk are indicators of CI in patients with MS. METHODS: Seventy patients with MS were included in this cross-sectional study. Cognitive impairment was assessed using the Montreal Cognitive Assessment Scale (MoCA), muscle strength using a hand-held dynamometer, and balance, gait, and fall risk assessment using the Tinetti scale. Motor coordination was assessed using the timed rapid alternating movement test for the upper extremity and the timed alternate heel-to-knee test for the lower extremity. RESULTS: There was a significant association between CI and motor coordination, balance, gait, and risk of fall (p < 0.005) but not muscle strength. Stepwise multiple linear regression showed that 22.7% of the variance in the MoCA was predicted by the fall risk and incoordination of the upper extremities in the MS population. CONCLUSIONS: CI is significantly associated with motor incoordination, balance impairment, gait abnormality, and increased fall risk. Furthermore, the risk of fall and upper extremity incoordination appeared to be best indicators of CI in patients with MS.
 B-cell depleting therapies such as rituximab and ocrelizumab are widely used for the treatment of Multiple Sclerosis but have increased risks of adverse reactions compared to earlier MS therapies. One rarely reported reaction is pyoderma gangrenosum (PG), an inflammatory, ulcerative, skin disease of unclear etiology. Here we describe a male and female patient, each with Relapsing-Remitting Multiple Sclerosis, and both of whom developed PG while on rituximab. Both PG diagnoses were supported by persistent fever, biopsy reports of sterile neutrophilia, and leukocytosis in the absence of an identifiable infectious agent. The diagnoses were further confirmed by dramatic clinical improvement following initiation of high dose steroids and intravenous immunoglobulins, and discontinuation of rituximab.
 BACKGROUND: Self-administration of subcutaneous interferon beta-1a (sc IFN β-1a) can be achieved with the RebiSmart® electromechanical autoinjector. This study investigated adherence to, and duration of persistence with, the newest version of the device (v1.6) among 2644 people receiving sc IFN β-1a for multiple sclerosis (MS). RESEARCH DESIGN AND METHODS: This retrospective, observational study utilized data from RebiSmart® devices, recorded on the MSdialog database, between January 2014 and November 2019. Adherence and persistence were evaluated over a 3-year period and assessed in relation to age, sex, injection type, and injection depth. RESULTS: The population of RebiSmart® users (N = 2644) comprised of 1826 (69.1%) females and mean age was 39 (range 16-83) years. Adherence to RebiSmart® use and data transfer to the MSdialog database was consistently high (mean 91.7%; range 86.8-92.6%), including across all variables (81.6-100%). Mean (±SD) persistence during the study period was 1.35 ± 1.06 years, with a maximum recorded persistence of 5.1 years. In multivariate analysis, the longest durations of persistence were observed among older individuals and males (p < 0.0001 and p = 0.0078, respectively). CONCLUSIONS: People living with MS were highly adherent to use of the RebiSmart® device, with higher persistence generally observed for older and/or male individuals.
 BACKGROUND: Older age and longer disease duration (DD) may impact the effectiveness of disease-modifying therapies in patients with multiple sclerosis (MS). Siponimod is a sphingosine 1-phosphate receptor modulator approved for the treatment of active secondary progressive MS (SPMS) in many countries. The pivotal phase 3 EXPAND study examined siponimod versus placebo in a broad SPMS population with both active and non-active disease. In this population, siponimod demonstrated significant efficacy, including a reduction in the risk of 3-month confirmed disability progression (3mCDP) and 6-month confirmed disability progression (6mCDP). Benefits of siponimod were also observed across age and DD subgroups in the overall EXPAND population. Herein we sought to assess the clinical impact of siponimod across age and disease duration subgroups, specifically in participants with active SPMS. METHODS: This study is a post hoc analysis of a subgroup of EXPAND participants with active SPMS (≥ 1 relapse in the 2 years before the study and/or ≥ 1 T1 gadolinium-enhancing magnetic resonance imaging lesion at baseline) receiving oral siponimod (2 mg/day) or placebo during EXPAND. Data were analyzed for participant subgroups stratified by age at baseline (primary cut-off: < 45 year ≥ 45 years; and secondary cut-off: < 50 years or ≥ 50 years) and by DD at baseline (< 16 years or ≥ 16 years). Efficacy endpoints were 3mCDP and 6mCDP. Safety assessments included adverse events (AEs), serious AEs, and AEs leading to treatment discontinuation. RESULTS: Data from 779 participants with active SPMS were analyzed. All age and DD subgroups had 31-38% (3mCDP) and 27-43% (6mCDP) risk reductions with siponimod versus placebo. Compared with placebo, siponimod significantly reduced the risk of 3mCDP in participants aged ≥ 45 years (hazard ratio [HR]: 0.68; 95% confidence interval [CI]: 0.48-0.97), < 50 years (HR: 0.69; 95% CI: 0.49-0.98), ≥ 50 years (HR: 0.62; 95% CI: 0.40-0.96), and in participants with < 16 years DD (HR: 0.68; 95% CI: 0.47-0.98). The risk of 6mCDP was significantly reduced with siponimod versus placebo for participants aged < 45 years (HR: 0.60; 95% CI: 0.38-0.96), ≥ 45 years (HR: 0.67; 95% CI: 0.45-0.99), < 50 years (HR: 0.62; 95% CI: 0.43-0.90), and in participants with < 16 years DD (HR: 0.57; 95% CI: 0.38-0.87). Increasing age or longer MS duration did not appear to increase the risk of AEs, with an observed safety profile that remained consistent with the overall active SPMS and overall SPMS populations in EXPAND. CONCLUSIONS: In participants with active SPMS, treatment with siponimod demonstrated a statistically significant reduction in the risk of 3mCDP and 6mCDP compared with placebo. Although not every outcome reached statistical significance in the subgroup analyses (possibly a consequence of small sample sizes), benefits of siponimod were seen across a spectrum of ages and DD. Siponimod was generally well tolerated by participants with active SPMS, regardless of baseline age and DD, and AE profiles were broadly similar to those observed in the overall EXPAND population.
 OBJECTIVE: Compassion is widely regarded as an important component of high-quality healthcare. However, its conceptualization, use, and associated outcomes in the care of people with multiple sclerosis (PwMS) have not been synthesized. The aim of this review is to scope the peer reviewed academic literature on the conceptualization, use, and outcomes associated with compassion in the care of PwMS. METHODS: Studies were eligible for inclusion if reporting primary research data from quantitative, qualitative, or mixed-methods studies on the conceptualization, use, and outcomes associated with compassion in the care of PwMS. Relevant studies were identified through searching five electronic databases (CINAHL, Cochrane Library, EMBASE, MEDLINE, and PsycINFO) in January 2022. We followed the guidance outlined in the Joanna Briggs Institute (JBI) manual for evidence synthesis, and also referred to the Preferred Reporting Items for Systematic Reviews and Meta-analyses extension for Scoping Reviews Checklist (PRISMA-ScR). Simple descriptive methods were used to chart quantitative findings, and a descriptive approach with basic content analysis was employed to describe qualitative findings. RESULTS: Fifteen studies were included (participant n = 1722): eight quantitative, six mixed-methods, one exclusively qualitative. Synthesized qualitative data revealed that PwMS conceptualize compassion as involving self-kindness, agency, and acceptance. PwMS report using self-compassion in response to unpleasant sensations and experiences. Quantitative findings suggest that compassion may mediate benefit finding, reduced distress, and improved quality of life (QoL) in PwMS, that those with the condition may become more compassionate through time, and that self-compassion specifically can be increased through training in mindfulness. In this context, greater self-compassion in PwMS correlates with less depression and fatigue, better resilience and QoL. Among studies, self-compassion was the most common outcome measure for PwMS. CONCLUSIONS: A nascent literature exists on the conceptualization, use, and outcomes associated with compassion in the care of PwMS. Further research is required to better understand what compassion means to PwMS and those caring for them. However, self-compassion can be cultivated among PwMS and may be helpful for managing unpleasant somatic symptoms and in benefit finding. Impact on other health outcomes is less clear. The use of compassion by health care providers in the care of PwMS is unstudied.
 BACKGROUND: Assessment of motor and cognitive functions is recommended before clean intermittent catheterization training. Two validated instruments, the Functional Independence Measure (FIM) and the Pencil and Paper Test (PP-Test), are associated with the ability to learn self-catheterization in people with multiple sclerosis. OBJECTIVES: We aimed to compare the performance of these tools in predicting the outcome of clean intermittent catheterization training in multiple sclerosis. METHODS: All people with multiple sclerosis attending a tertiary neuro-urology department between 2011 and 2019 and eligible for clean intermittent catheterization were included in this retrospective study. The reference standard was the ability to perform at least 2 trials of self-catheterization at the end of the training session. The 2 index tests, the FIM and PP-Test, were administered before the teaching session. Their diagnostic performance was estimated by calculating sensitivity, specificity, and area under the receiver operating characteristic curve (AUC). The AUC values were compared by a two-sided DeLong test. RESULTS: We included 395 individuals (mean [SD] age 49.8 [12] years; 70% women). At the end of the session, 87% of the patients succeeded in learning self-catheterization. The optimal cut-offs for the FIM (107) and PP-Test (13) were estimated, resulting in sensitivity of 73% (95% confidence interval [68-77) and 73% (67-77) and specificity 73% (59-84) and 63% (49-76), respectively. The AUC values for the FIM and PP-Test were significantly different (0.79 vs 0.73, p = 0.049). The effect size was large for both the FIM (Cohen's d = 1.14) and PP-Test (Cohen's d = 0.87). CONCLUSIONS: An FIM value ≥107 has the best specificity to predict outcome after clean intermittent catheterization training for people with multiple sclerosis. The sensitivity of the FIM and PP-Test is similar, and both have a large effect size for the outcome of self-catheterization training in multiple sclerosis.
 BACKGROUND: Multiple sclerosis (MS), is prevalent across many racial and ethnic groups, and disproportionately impacts racially minoritized populations. Rehabilitation interventions are an important component of comprehensive MS care. Yet, we do not know the extent to which MS rehabilitation trials consider race and ethnicity in defining eligibility criteria, planning recruitment strategies, selecting outcome measures, supporting intervention delivery, and designing approaches to promote adherence and retention. METHODS: We conducted a scoping review of five databases (MEDLINE, CINAHL, Cochrane Central, EMBASE, and Web of Science) to locate randomized controlled rehabilitation trials published from January 2002 to March 2022. We extracted data from relevant studies, assessed their methodological quality, and narratively summarized results. Reporting of this review is in line with the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR). RESULTS: Fifty-six studies of neurorehabilitation (n = 3), cognitive rehabilitation (n = 6), exercise training (n = 9) and self-management (n = 38) interventions were included in this review. The studies were predominantly from North America (n = 44; 73%) or Europe (n = 12; 20%) and included 4280 participants. Most participants (n = 3669; 86%) were Caucasians. Less than 10% of participants were Black (n = 282), Latinx/Hispanic (n = 60), Asian (n = 46), Indigenous (n = 7), or Arab (n = 2). Few studies discussed how race and/or ethnicity were considered in trial planning or execution. CONCLUSIONS: Without consistent and systematic attention to race and ethnicity, both in terms of trial design and reporting, it is impossible to know how MS rehabilitation interventions will translate into real-world applications. This call to action - to the MS rehabilitation research community to ensure trial and intervention processes that accommodate the needs of diverse racial and ethnic groups - is an important first step in addressing inequities in rehabilitation care for persons with MS.
 BACKGROUND: Multiple sclerosis (MS) impacts education, future career pathways and working capability and therefore may negatively impact the financial situation of persons with MS (pwMS) in Switzerland. We therefore investigated the financial situation and its influencing sociodemographic and disease-specific factors of pwMS compared to the general Swiss population with focus on material deprivation (MD). METHODS: Data on the financial situation of pwMS were collected via a specific questionnaire added to the regular, semi-annual follow-up assessments of the Swiss Multiple Sclerosis Registry. Questions were taken in an unmodified format from the standardized "Statistics on Income and Living Conditions" (SILC) questionnaire 2019 of the Federal Statistical Office of Switzerland which evaluates the financial situation of the general Swiss population, enabling a direct comparison of pwMS with the general Swiss population. RESULTS: PwMS were 1.5 times more frequently affected by MD than the general Swiss population (6.3% of pwMS versus 4.2% of the general Swiss population) which was confirmed in a multivariable logistic regression analysis of pooled SILC and Swiss Multiple Sclerosis Registry (SMSR) data. High symptom burden, having only mandatory schooling, well as having a pending disability insurance application (as opposed to no application or receiving benefits) were associated with a higher odds of MD whereas higher education, older age, having a Swiss citizenship, living with a spouse or a partner or being currently employed were independently associated with a lower odds of MD. CONCLUSION: MS has a negative impact on the financial situation and is associated with MD. PwMS with a high symptom burden at the transition from work force to receiving disability benefits appeared to be vulnerable for MD. Higher education, older age, having a Swiss citizenship, living with a spouse or a partner or being currently employed were independently associated with a lower odds of MD.
 Typical assessments of balance impairment are subjective or require data from cumbersome and expensive force platforms. Researchers have utilized lower back (sacrum) accelerometers to enable more accessible, objective measurement of postural sway for use in balance assessment. However, new sensor patches are broadly being deployed on the chest for cardiac monitoring, opening a need to determine if measurements from these devices can similarly inform balance assessment. Our aim in this work is to validate postural sway measurements from a chest accelerometer. To establish concurrent validity, we considered data from 16 persons with multiple sclerosis (PwMS) asked to stand on a force platform while also wearing sensor patches on the sacrum and chest. We found five of 15 postural sway features derived from the chest and sacrum were significantly correlated with force platform-derived features, which is in line with prior sacrum-derived findings. Clinical significance was established using a sample of 39 PwMS who performed eyes-open, eyes-closed, and tandem standing tasks. This cohort was stratified by fall status and completed several patient-reported measures (PRM) of balance and mobility impairment. We also compared sway features derived from a single 30-second period to those derived from a one-minute period with a sliding window to create individualized distributions of each postural sway feature (ID method). We find traditional computation of sway features from the chest is sensitive to changes in PRMs and task differences. Distribution characteristics from the ID method establish additional relationships with PRMs, detect differences in more tasks, and distinguish between fall status groups. Overall, the chest was found to be a valid location to monitor postural sway and we recommend utilizing the ID method over single-observation analyses.
 Exercise improves a wide range of symptoms experienced by those living with multiple sclerosis (MS) and may foster community and a positive sense of disability identity. However, exercise rates remain low. Sustained exercise participation has the greatest likelihood of improving symptoms and requires a theory-based approach accounting for the barriers faced by people with MS that impede exercise participation long-term. MOVE MS is a once weekly group exercise program based on Social Cognitive Theory supporting long-term exercise participation through peer instruction, behavior change education, multiple exercise modalities, and seated instruction. This feasibility study evaluated MOVE MS with a 7-month trial. The primary scientific outcome was exercise participation and the secondary outcomes were MS symptoms/impact, self-efficacy, depression, anxiety, disability identity, and quality of life, among others. We further conducted semi-structured formative interviews post-intervention. Thirty-three participants began the program. The onset of COVID-19 necessitated a shift toward online delivery. Seventeen participants completed the program. There were non-significant improvements in exercise participation (Godin Leisure-Time Exercise Questionnaire, baseline mean = 14.2 (SD = 11.8), post-intervention mean = 16.6 (SD = 11.2), F-value = 0.53 (Partial Eta(2) = 0.08), and several secondary outcomes (including the MS Impact Scale, MS Walking Scale, and the Leeds MS Quality of Life Scale). Sixteen participants were interviewed, and analysis yielded five themes on program components and feedback. MOVE MS-delivered in-person or online-may be a feasible option for long-term exercise programming for people with MS.
 BACKGROUND: Remote smartphone-based 2-minute walking tests (s2MWTs) allow frequent and potentially sensitive measurements of ambulatory function. OBJECTIVE: To investigate the s2MWT on assessment of, and responsiveness to change in ambulatory function in MS. METHODS: One hundred two multiple sclerosis (MS) patients and 24 healthy controls (HCs) performed weekly s2MWTs on self-owned smartphones for 12 and 3 months, respectively. The timed 25-foot walk test (T25FW) and Expanded Disability Status Scale (EDSS) were assessed at 3-month intervals. Anchor-based (using T25FW and EDSS) and distribution-based (curve fitting) methods were used to assess responsiveness of the s2MWT. A local linear trend model was used to fit weekly s2MWT scores of individual patients. RESULTS: A total of 4811 and 355 s2MWT scores were obtained in patients (n = 94) and HC (n = 22), respectively. s2MWT demonstrated large variability (65.6 m) compared to the average score (129.5 m), and was inadequately responsive to anchor-based change in clinical outcomes. Curve fitting separated the trend from noise in high temporal resolution individual-level data, and statistically reliable changes were detected in 45% of patients. CONCLUSIONS: In group-level analyses, clinically relevant change was insufficiently detected due to large variability with sporadic measurements. Individual-level curve fitting reduced the variability in s2MWT, enabling the detection of statistically reliable change in ambulatory function.
 BACKGROUND: Previously, several studies investigated the effect of cladribine among patients with multiple sclerosis (MS) as a treatment option. Due to the contradictory results of previous studies regarding the efficacy and safety of cladribine in the MS population, we aimed to conduct a systematic review and meta-analysis by including clinical trials and observational studies in terms of having more confirmative results to make a general decision. METHODS: The three databases including PubMed, Scopus, and Web of Science were comprehensively searched in May 2022. We included the studies that investigated the efficacy and safety of cladribine in patients with MS. Eligible studies have to provide sufficient details on MS diagnosis and appropriate follow-up duration. We investigated the efficacy of cladribine with several outcomes including Expanded Disability Status Scale (EDSS) change, progression-free survival (PFS), relapse-free survival (RFS), and MRI-free activity survival (MFAS). RESULTS: After two-step reviewing, 23 studies were included in our qualitative and quantitative synthesis. The pooled SMD for EDSS before and after treatment was - 0.54 (95%CI: - 1.46, 0.39). Our analysis showed that the PFS after cladribine use is 79% (95%CI 71%, 86%). Also, 58% of patients with MS who received cladribine remained relapse-free (95%CI 31%, 83%). Furthermore, the MFAS after treatment was 60% (95%CI 36%, 81%). Our analysis showed that infection is the most common adverse event after cladribine treatment with a pooled prevalence of 10% (95%CI 4%, 18%). Moreover, the pooled prevalence of infusion-related adverse events was 9% (95%CI 4%, 15%). Also, the malignancies after cladribine were present in 0.4% of patients (95%CI 0.25%, 0.75%). CONCLUSION: Our results showed acceptable safety and efficacy for cladribine for the treatment of MS except in terms of reducing EDSS. Combination of our findings with the results of previous studies which compared cladribine to other disease-modifying therapies (DMTs), cladribine seems to be a safe and effective drug in achieving better treatment for relapsing-remitting MS (RRMS) patients.
 Alemtuzumab is a humanized monoclonal antibody indicated for treatment of highly active relapsing-remitting multiple sclerosis (HA-RRMS). It binds to CD52 antigen and produces a rapid and prolonged lymphocyte depletion followed by a different pattern of T and B cell repopulation. Among others, its adverse events are autoimmune diseases.In this article, we present a patient with HA-RRMS, who was subsequently treated with alemtuzumab and afterwards developed hemophagocytic lymphohistiocytosis (HLH). Albeit rarely, HLH can be triggered by alemtuzumab treatment.HLH can favourably respond to prompt immunosuppressant therapy.Multidisciplinary approach by a team consisting of a neurology, hematology and rheumatology specialist is needed to treat this potentially lethal condition.
 Multiple sclerosis (MS) is a central nervous system (CNS) disease characterized by inflammation, axonal demyelination, and neurodegeneration, which can have a strong impact on all aspects of the life of the patient. Multiple sclerosis causes motor, sensory, cerebellar, and autonomic dysfunctions, as well as cognitive and psychoemotional impairment. The most frequently compromised cognitive domains are complex attention/information processing, memory, executive and visuospatial functions. Recently, alterations have also been evidenced in complex cognitive functions, such as social cognition, moral judgment, and decision-making. Cognitive impairment is characterized by high variability and can affect work skills, social interactions, coping strategies and more generally the quality of life of patients and their families. With the use of sensitive and easy-to-administer test batteries, an increasingly accurate and early diagnosis is feasible: this allows to determine the effectiveness of possible preventive measures, to predict the future progression of the disease and to improve the quality of life of patients. There is currently limited evidence regarding the efficacy, on cognitive impairment, of disease-modifying therapies. The most promising approach, which has received strong empirical support, is cognitive rehabilitation.
 Teriflunomide belongs to disease-modifying drugs and is used in treatment of multiple sclerosis. According to in vitro studies more than 99.4 % of drug is binding to plasma proteins and only less than 1 % is free for clinical activity. The rapid and simple ultra-performance liquid chromatography-tandem mass spectrometry method (UPLC-MS/MS) was developed and validated for determination of total and free teriflunomide (TFM) in serum of patients with multiple sclerosis. To determine the total teriflunomide samples were precipitated with a precipitation reagent consisting of 11 % solution of ZnSO(4) in acetonitrile/methanol (40:60, v/v). To determine the free fraction of teriflunomide, an ultracentrifugation method was used. The analysis was performed on a UPLC system connected to a XEVO TQ-XS mass spectrometer. Chromatographic separation was carried out on an Acquity UPLC BEH C18 1.7 µm (100 × 2.1 mm) column heated to 30 °C and teriflunomide-D4 was used as an internal standard. Ionization was performed by electrospray in negative ion mode. The developed methods were validated according to the rules of the European Medicines Agency (EMA) for the analytical method validation of bioanalytical methods. The coefficients of variation were in the range of 0.53-14.84 % and the recovery 97.92-108.33 %, respectively. Share of free teriflunomide was 0.15-0.40 % (mean 0.25 ± 0.05 %) of total teriflunomide and there was a significant correlation between free and total teriflunomide r(2) = 0.9083 (p < 0.0001). This newly developed method allows the rapid and easy determination of the teriflunomide concentration with high sensitivity and can be applied to clinical samples of patients with multiple sclerosis.
 Multiple sclerosis (MS) is a complex dysimmune disorder of the central nervous system. Genome-wide association studies (GWAS) have identified 233 genetic variations associated with MS at the genome-wide significant level. Epigenetic studies have pinpointed differentially methylated CpG sites in MS patients. However, the interplay between genetic risk factors and epigenetic regulation remains elusive. Here, we employed a network model to integrate GWAS summary statistics of 14 802 MS cases and 26 703 controls with DNA methylation profiles from 140 MS cases and 139 controls and the human interactome. We identified differentially methylated genes by aggregating additive effects of differentially methylated CpG sites within promoter regions. We reconstructed a gene regulatory network (GRN) using literature-curated transcription factor knowledge. Colocalization of the MS GWAS and methylation quantitative trait loci (mQTL) was performed to assess the GRN. The resultant MS-associated GRN highlighted several single nucleotide polymorphisms with GWAS-mQTL colocalization: rs6032663, rs6065926 and rs2024568 of CD40 locus, rs9913597 of STAT3 locus, and rs887864 and rs741175 of CIITA locus. Moreover, synergistic mQTL and expression QTL signals were identified in CD40, suggesting gene expression alteration was likely induced by epigenetic changes. Web-based Cell-type Specific Enrichment Analysis of Genes (WebCSEA) indicated that the GRN was enriched in T follicular helper cells (P-value = 0.0016). Drug target enrichment analysis of annotations from the Therapeutic Target Database revealed the GRN was also enriched with drug target genes (P-value = 3.89 × 10-4), revealing repurposable candidates for MS treatment. These candidates included vorinostat (HDAC1 inhibitor) and sivelestat (ELANE inhibitor), which warrant further investigation.
 BACKGROUND: To effectively manage sexual dysfunction in women reporting overactive bladder, it is essential to know how patients perceive these problems, their lives, and their strategies. AIM: In this study we aimed to understand the sexual life experiences of women with multiple sclerosis (MS) who report overactive bladder from their point of view. METHODS: This study included 12 women with MS and was conducted as a qualitative study with a hermeneutic phenomenological framework. The data were evaluated by using Van Manen's thematic analysis method. The Consolidated Criteria for Reporting Qualitative Research checklist was used. OUTCOMES: In this study, thematic codes of sexual symptoms in women with MS with overactive bladder were defined and evaluated. RESULTS: As a result of the analysis of the data, four main themes and nine subthemes were identified. The main themes were "sexual self-concept," "sexual relationships," "sexual function," and "coping with problems". Subthemes such as body image, sexual esteem, the meaning of sexuality, communication, intimacy, coping with overactive bladder and sexual problems, and getting support showed that overactive bladder symptoms negatively affected women's sexual health. CLINICAL IMPLICATIONS: Given the variety of sexual problems experienced by women with MS who report overactive bladder, these problems should be a routine part of clinical evaluation. STRENGTHS AND LIMITATIONS: This study is to our knowledge the first to examine the sexual life experiences of MS women reporting overactive bladder in depth based on the holistic view of sexuality theory. However, the sample is small and includes only women with MS who have reported overactive bladder. CONCLUSIONS: The sexual experience of women with MS who reported overactive bladder was multi-dimensional. Women with MS cope with their sexual problems alone and cannot receive the necessary support from their husbands, nurses, or other health professionals.
 Fatigue is associated with a dramatically decreased quality of life in people with multiple sclerosis (pwMS). It refers to a constant subjective feeling of exhaustion and performance decline, known as fatigability. However, inconsistency and heterogeneity in defining and assessing fatigue have led to limited advances in understanding and treating MS-associated fatigue. Transcranial direct current stimulation (tDCS) has emerged as a promising, non-pharmaceutical treatment strategy for subjective fatigue. However, whether repetitive tDCS also have long-term effects on time-on-task performance has not yet been investigated. This pseudorandomized, single-blinded, and sham-controlled study investigated tDCS effects on behavioral and electrophysiological parameters. 18 pwMS received eight twice-weekly 30 min stimulations over the left dorsolateral prefrontal cortex. Fatigability was operationalized as time-on-task-related changes in reaction time variability and P300 amplitude. Additionally, subjective trait and state fatigue ratings were assessed. The results revealed an overall decrease in subjective trait fatigue ratings that lasted at least four weeks after the stimulations. However, the ratings declined after both anodal and sham tDCS. No effects were found on subjective state fatigue and objective fatigability parameters. Linear Mixed Models and Bayesian Regression models likewise favored the absence of a tDCS effect on fatigability parameters. The results confirm the complex relationship between MS-associated fatigue and fatigability. Reliable and clinically relevant parameters need to be established to extend the potential of tDCS for treating fatigability. Furthermore, our results indicate that consecutive stimulations rather than twice-weekly stimulations should be the preferred stimulation scheme in future studies.
 BACKGROUND AND OBJECTIVES: Patients with multiple sclerosis (MS) may seek fertility treatment (FT)-including in vitro fertilization (IVF). Variable relapse risk after IVF has been reported in small historical cohorts, with more recent studies suggesting no change in annualized relapse rate (ARR). The objective of this study was to evaluate ARR 12 months pre-FT and 3 months post-FT in a multicenter cohort and identify factors associated with an increased risk of relapse. METHODS: Patients with clinically isolated syndrome (CIS) or MS aged 18-45 years with at least 1 FT from January 1, 2010, to October 14, 2021, were retrospectively identified at 4 large academic MS centers. The exposed period of 3 months after FT was compared with the unexposed period of 12 months before FT. FTs included controlled ovarian stimulation followed by fresh embryo transfer (COS-ET), COS alone, embryo transfer (ET) alone, and oral ovulation induction (OI). The Wilcoxon signed rank test and mixed Poisson regression models with random effects were used to compare ARR pre-FT vs post-FT, with the incidence rate ratio (IRR) and 95% CI reported. RESULTS: One hundred twenty-four FT cycles among 65 patients with MS (n = 56) or CIS (n = 9) were included: 61 COS-ET, 19 COS alone, 30 ET alone, and 14 OI. The mean age at FT was 36.5 ± 3.8 years, and the mean disease duration was 8.2 ± 5.0 years. Across 80 cycles with COS, only 5 relapses occurred among 4 unique patients within 3 months of treatment. The mean ARR after COS and before was not different (0.26 vs 0.25, p = 0.37), and the IRR was 0.95 (95% CI: 0.52-1.76, p = 0.88). No cycles with therapeutic disease-modifying therapies (DMTs) during COS had 3 months relapse (ARR 0 post-COS vs 0.18 pre-COS, p = 0.02, n = 34). Relapse rates did not vary by COS protocol. Among COS-ET cycles that achieved pregnancy (n = 43), ARR decreased from 0.26 to 0.09 (p = 0.04) within the first trimester of pregnancy. There were no relapses 3 months after ET alone and 1 relapse after OI. DISCUSSION: In this modern multicenter cohort of patients with MS undergoing diverse FTs, which included 43% on DMTs, we did not observe an elevated relapse risk after FT.
 OBJECTIVE: Identification of a complex of genetic predictors of multiple sclerosis (MS) based on previously obtained results in genome-wide association studies of disease markers (GWAS markers) in a population of MS patients and healthy individuals of the Republic of Bashkortostan (Russian Federation) using polygenic detection. MATERIAL AND METHODS: The total study group consisted of 2048 people (641 patients with MS and 1407 healthy individuals) who permanently resided in the Republic of Bashkortostan and belonged to the Bashkir (n=325), Russian (n=772) or Tatar (n=951) nationalities. The analysis of association between MS and polymorphisms previously associated with the disease according to GWAS data was performed. Of the 641 MS patients, 247 were the subject of a 20-year prospective clinical follow-up. RESULTS: The C6orf10 rs3129934*T allele was most significantly associated with MS in Russians (OR=2.00, P=5.85·10(-5)) and Tatars (OR=2.38, P=8.61·10(-7)). An increased MS risk in Russians was also associated with the EOMES rs11129295*T (OR=1.56, P=0.007) and IL7R rs1494558*I (OR=1.61, P=0.003) alleles. Meta-analysis confirmed the association of the C6orf10 rs3129934*T, EOMES rs11129295*T and IL7R rs1494558*I alleles with MS in the total group, as well as revealed associations of the INAVA rs7522462*G, IL7R rs10624573*I, CD6 rs17824933*G, GPC5 rs9523762*A and GPR65 rs2119704*C alleles with the disease. Using polygenic analysis, we identified a complex predictor C6orf10 rs3129934*C + INAVA rs7522462*G + CD6 rs17824933*C with a pronounced protective effect against MS in the total group (OR=0.34, P(FDR)=2.65·10(-7)). CONCLUSION: We reproduced the association of eight polymorphisms (C6orf10 rs3129934, INAVA rs7522462, IL7R rs10624573, EOMES rs11129295, GPR65 rs2119704, GPC5 rs9523762, CD6 rs17824933 and CD58 rs2300747) with MS, previously identified in GWAS in European populations. Whole exome or genome sequencing may help to reveal the mechanisms underlying the pathogenesis of MS in populations of the Russian Federation.
 Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS). Anxiety and depression are the most common psychiatric comorbidities of MS, which seriously affect patients' quality of life, treatment compliance, and prognosis. However, current treatments for anxiety and depression in MS show low therapeutic efficacy and significant side effects. In the present study, we explored the therapeutic effects of a novel low-toxic anti-inflammatory drug, nanoparticulate magnesium hydride (MgH(2)), on mood disorders of MS. We observed that anxiety/depression-like behaviors in experimental autoimmune encephalomyelitis (EAE) mice were alleviated by MgH(2) treatment. In addition, disease severity and inflammatory demyelination were also diminished. Furthermore, we confirmed the suppressive effect of MgH(2) on depression in the acute restraint stress model. Mechanistically, MgH(2) may play a therapeutic role by promoting microglial M2 polarization, inhibiting microglial M1 polarization, and reducing oxidative stress and mitochondrial damage. Therefore, nanoparticulate MgH(2) may be a promising therapeutic drug for psychiatric comorbidities of MS.
 INTRODUCTION: The diagnosis of the progression phase of Multiple Sclerosis (MS) is still retrospective and based on the objectivation of clinical disability accumulation. OBJECTIVES: To assess whether the Patient Reported Outcomes Measures (PROMs) scores predict the occurrence of disease progression within three years of follow-up. METHODS: Observational prospective multicenter study. Stable Relapsing-Remitting MS (RRMS) patients were enrolled. At enrollment, patients completed the following PROMs: Beck Depression Inventory- II, The Treatment Satisfaction Questionnaire for Medications, Medical Outcomes Study Short Form 36- Item (SF36), Fatigue Severity Scale. EDSS was assessed at enrollment and three years later. The outcome measure was defined as the occurrence of confirmed disability progression (CDP) within three years of follow-up. Univariable and multivariable logistic regression models were performed to study the association between the final score of each test and the outcome. RESULTS: SF36-Physical Functioning (SF36-PF) was the only independent variable associated with the outcome. The ROC curve analysis determined a score of 77.5 at SF36-PF as the cut-off point identifying patients experiencing CDP within three years of follow-up [AUC: 0.66 (95% CI: 0.56-0.75)]. CONCLUSIONS: RRMS patients scoring higher (>77.5) at SF36-PF subscale have a higher likelihood to experience CDP within the next three years.
 BACKGROUND: The presence of subclinical optic nerve (ON) injury in youth living with pediatric-onset MS has not been fully elucidated. Magnetization transfer saturation (MTsat) is an advanced magnetic resonance imaging (MRI) parameter sensitive to myelin density and microstructural integrity, which can be applied to the study of the ON. OBJECTIVE: The objective of this study was to investigate the presence of subclinical ON abnormalities in pediatric-onset MS by means of magnetization transfer saturation and evaluate their association with other structural and functional parameters of visual pathway integrity. METHODS: Eleven youth living with pediatric-onset MS (ylPOMS) and no previous history of optic neuritis and 18 controls underwent standardized brain MRI, optical coherence tomography (OCT), Magnetoencephalography (MEG)-Visual Evoked Potentials (VEPs), and visual battery. Data were analyzed with mixed effect models. RESULTS: While ON volume, OCT parameters, occipital MEG-VEPs outcomes, and visual function did not differ significantly between ylPOMS and controls, ylPOMS had lower MTsat in the supratentorial normal appearing white matter (-0.26 nU, p = 0.0023), and in both in the ON (-0.62 nU, p < 0.001) and in the normal appearing white matter of the optic radiation (-0.56 nU, p = 0.00071), with these being positively correlated (+0.57 nU, p = 0.00037). CONCLUSIONS: Subclinical microstructural injury affects the ON of ylPOMS. This may appear as MTsat changes before being detectable by other currently available testing.
 BACKGROUND: Effective communication is essential for multiple sclerosis (MS) disease management. Improving communication about MS may improve healthcare and service quality. OBJECTIVE: To evaluate confidence in communicating about MS in a cohort of MS community members and to assess the impact of participation in the Understanding MS massive open online course (MOOC) on communication confidence. The Understanding MS MOOC is a freely available six-week online course that covers a range of topics related to MS, including its underlying pathology, symptoms, risk factors, and management. METHODS: We assessed communication confidence among Understanding MS MOOC enrolees (N = 905) at three timepoints: prior to their participation in the course, immediately following course completion, and six months following course completion. Communication confidence was quantified using 5-point Likert scale questions. We identified factors that were associated with communication confidence using chi square and t-tests. Among course completers who also completed all three study surveys (N = 88), we assessed the impact of course participation using paired t-tests and we assessed effect size using Cohen's D. We assessed the relationship between changes in primary and secondary outcomes (i.e., MS-related knowledge, health literacy, quality of life, perceived healthcare quality, and self-efficacy) using Pearson correlation. RESULTS: We found that at baseline, communication confidence was positively associated with MS knowledge, health literacy and quality of life. We also found that men and people with MS were more likely to report being confident. Among study participants who completed the course and all three study surveys, we found that course participation improved communication confidence and that this improvement was maintained at the six-month follow-up. The improvement in communication confidence was positively correlated with changes in MS knowledge and health literacy. CONCLUSION: Confidence in communicating about MS is associated with MS knowledge and health literacy. By improving MS knowledge and health literacy, online educational interventions such as the Understanding MS MOOC can improve communication confidence in the MS community.
 BACKGROUND: Adherence to prescribed treatment in chronic diseases, as occurs in multiple sclerosis (MS), is a critical factor for a successful therapeutic response. This study aimed to investigate the effect of educational program based on Theory of Planned Behavior (TPB) on treatment adherence in patients with multiple sclerosis (MS) receiving injectable immunomodulatory drugs. METHODS: The present study is an educational randomized controlled trial research that was conducted on 100 patients with MS who had gone to MS clinic in Tehran city (Iran). The samples were randomly assigned to the intervention (N = 50) and control groups (N = 50). Data collection instrument was a researcher-made questionnaire based on TPB. Then, educational program was performed for the intervention group through four educational sessions. After three months, data collection was repeated for the two groups and data were analyzed. RESULTS: The knowledge and performance of the intervention group on treatment adherence drugs increased from 56.25 ± 20.3 to 78.31 ± 15.57 and 56.22 ± 5.76 to 71.62 ± 12.01 after the education respectively (p < 0.001). The mean of construct of TPB in the intervention group also increased after the intervention (p < 0.05). CONCLUSION: Applying the TPB model proved is very effective in developing an educational program for patients with MS, to enhance treatment adherence drugs. Besides such programs, follow-up education for controlling and monitoring are highly recommended. TRIAL REGISTRATION: This trial has been registered at Iranian Registry of Clinical Trials, IRCT20210808052109N1. Prospectively registered at 12-Aug-2021, (12/8/2021) available at: URL: https://en.irct.ir/trial/57994.
 Axonal loss in multiple sclerosis (MS) is a key component of disease progression and permanent neurologic disability. MS is a heterogeneous demyelinating and neurodegenerative disease of the central nervous system (CNS) with varying presentation, disease courses, and prognosis. Immunomodulatory therapies reduce the frequency and severity of inflammatory demyelinating events that are a hallmark of MS, but there is minimal therapy to treat progressive disease and there is no cure. Data from patients with MS, post-mortem histological analysis, and animal models of demyelinating disease have elucidated patterns of MS pathogenesis and underlying mechanisms of neurodegeneration. MRI and molecular biomarkers have been proposed to identify predictors of neurodegeneration and risk factors for disease progression. Early signs of axonal dysfunction have come to light including impaired mitochondrial trafficking, structural axonal changes, and synaptic alterations. With sustained inflammation as well as impaired remyelination, axons succumb to degeneration contributing to CNS atrophy and worsening of disease. These studies highlight the role of chronic demyelination in the CNS in perpetuating axonal loss, and the difficulty in promoting remyelination and repair amidst persistent inflammatory insult. Regenerative and neuroprotective strategies are essential to overcome this barrier, with early intervention being critical to rescue axonal integrity and function. The clinical and basic research studies discussed in this review have set the stage for identifying key propagators of neurodegeneration in MS, leading the way for neuroprotective therapeutic development. This article is categorized under: Immune System Diseases > Molecular and Cellular Physiology Neurological Diseases > Molecular and Cellular Physiology.
 BACKGROUND: Self- and informant-report measures are often useful in predicting objective cognitive performance; however, the relationship between these reports and mood, anxiety, and fatigue requires further examination. Additionally, it remains unclear as to how these factors might be associated with objective neurocognitive performance. METHODS: Eighty-six persons with multiple sclerosis (PwMS; F = 65, M = 21) completed a comprehensive neuropsychological battery that included objective neurocognitive measures, subjective reports of neurocognitive function with the Multiple Sclerosis Neuropsychological Screening Questionnaire (MSNQ) Self-Report (MSNQ-S) and Informant-Report (MSNQ-I), and self-report measures of anxiety, depression, and fatigue. Hierarchical linear regressions were conducted with depression, anxiety, the interaction between depression and anxiety, cognitive fatigue, and physical fatigue as predictors. Outcome variables included the MSNQ-S, MSNQ-I, each of five neurocognitive composites, and global intraindividual variability (IIV). RESULTS: Although greater cognitive fatigue was associated with greater reported cognitive dysfunction, it was not associated with objective neurocognitive impairment. Greater depression predicted poorer performance on measures of processing speed and verbal memory, though the effects became non-significant once accounting for anxiety. The interaction between depression and anxiety predicted greater neurocognitive IIV; those with high levels of depression and anxiety demonstrated greater dispersion of scores. CONCLUSIONS: Cognitive fatigue may skew one's perception of their cognition, though it is not associated with objective impairment. However, co-occurring depression and anxiety were associated with greater variability which is a marker of poorer neurocognitive integrity. Our findings highlight the importance of accounting for depression, anxiety, and cognitive fatigue in PwMS, given that they are all potentially modifiable factors.
 In this prospective longitudinal study, we quantified regional brain volume and susceptibility changes during the first two years after the diagnosis of multiple sclerosis (MS) and identified their association with cerebrospinal fluid (CSF) markers at baseline. Seventy patients underwent MRI (T1 and susceptibility weighted images processed to quantitative susceptibility maps, QSM) with neurological examination at the diagnosis and after two years. In CSF obtained at baseline, the levels of oxidative stress, products of lipid peroxidation, and neurofilaments light chain (NfL) were determined. Brain volumetry and QSM were compared with a group of 58 healthy controls. In MS patients, regional atrophy was identified in the striatum, thalamus, and substantia nigra. Magnetic susceptibility increased in the striatum, globus pallidus, and dentate and decreased in the thalamus. Compared to controls, MS patients developed greater atrophy of the thalamus, and a greater increase in susceptibility in the caudate, putamen, globus pallidus and a decrease in the thalamus. Of the multiple calculated correlations, only the decrease in brain parenchymal fraction, total white matter, and thalamic volume in MS patients negatively correlated with increased NfL in CSF. Additionally, negative correlation was found between QSM value in the substantia nigra and peroxiredoxin-2, and QSM value in the dentate and lipid peroxidation levels.
 Background: Multivoxel pattern analysis (MVPA) has emerged as a powerful unbiased approach for generating seed regions of interest (ROIs) in resting-state functional connectivity (RSFC) analysis in a data-driven manner. Studies exploring RSFC in multiple sclerosis have produced diverse and often incongruent results. Objectives: The aim of the present study was to investigate RSFC differences between people with relapsing-remitting multiple sclerosis (RRMS) and healthy controls (HC). Methods: We performed a whole-brain connectome-wide MVPA in 50 RRMS patients with expanded disability status scale ≤4 and 50 age and gender-matched HCs. Results: Significant group differences were noted in RSFC in three clusters distributed in the following regions: anterior cingulate gyrus, right middle frontal gyrus, and frontal medial cortex. Whole-brain seed-to-voxel RSFC characterization of these clusters as seed ROIs revealed network-specific abnormalities, specifically in the anterior cingulate cortex and the default mode network. Conclusions: The network-wide RSFC abnormalities we report agree with the previous findings in RRMS, the cognitive and clinical implications of which are discussed herein. Impact statement This study investigated resting-state functional connectivity (RSFC) in relapsing-remitting multiple sclerosis (RRMS) people with mild disability (expanded disability status scale ≤4). Whole-brain connectome-wide multivoxel pattern analysis was used for assessing RSFC. Compared with healthy controls, we were able to identify three regions of interest for significant differences in connectivity patterns, which were then extracted as a mask for whole-brain seed-to-voxel analysis. A reduced connectivity was noted in the RRMS group, particularly in the anterior cingulate cortex and the default mode network regions, providing insights into the RSFC abnormalities in RRMS.
 OBJECTIVE: To evaluate the clinical significance of deep learning-derived brain age prediction in neuromyelitis optica spectrum disorder (NMOSD) relative to relapsing-remitting multiple sclerosis (RRMS). METHODS: This cohort study used data retrospectively collected from 6 tertiary neurological centres in China between 2009 and 2018. In total, 199 patients with NMOSD and 200 patients with RRMS were studied alongside 269 healthy controls. Clinical follow-up was available in 85 patients with NMOSD and 124 patients with RRMS (mean duration NMOSD=5.8±1.9 (1.9-9.9) years, RRMS=5.2±1.7 (1.5-9.2) years). Deep learning was used to learn 'brain age' from MRI scans in the healthy controls and estimate the brain age gap (BAG) in patients. RESULTS: A significantly higher BAG was found in the NMOSD (5.4±8.2 years) and RRMS (13.0±14.7 years) groups compared with healthy controls. A higher baseline disability score and advanced brain volume loss were associated with increased BAG in both patient groups. A longer disease duration was associated with increased BAG in RRMS. BAG significantly predicted Expanded Disability Status Scale worsening in patients with NMOSD and RRMS. CONCLUSIONS: There is a clear BAG in NMOSD, although smaller than in RRMS. The BAG is a clinically relevant MRI marker in NMOSD and RRMS.
 This pretest-posttest, descriptive pilot study examined the feasibility and perceived impact of an 8-week online adaptive yoga program on patients diagnosed with multiple sclerosis. The program incorporated yoga poses, breathing practices, and relaxation techniques. Participants rated their perceived and actual symptom severity, overall quality of life, and perception of program impact, and contributed open-ended narrative comments about the program. All participants reported an overall perceived benefit from study participation and expressed enjoyment in interacting with other patients with multiple sclerosis. The program was found to be safe and rewarding for all participants.
 BACKGROUND: A previous comparative analysis of the time trends of Hodgkin lymphoma (HL), multiple sclerosis (MS), Crohn's disease (CD), and ulcerative colitis (UC) suggested that the occurrence of all four diseases was precipitated by exposure to similar environmental risk factors during early lifetime. In the present cross-sectional study, it was hypothesized that besides their resembling temporal variations the four diseases would also show similar geographic distributions. METHODS: Using the vital statistics of 21 countries from 1951 to 2020, overall and age-specific death rates from the four diseases were calculated for each individual country. The death rates of different countries were compared using linear regression analysis. RESULTS: The data revealed strikingly similar geographic distributions of all four diseases. Their occurrence was common in Europe and relatively uncommon in countries outside Europe. Further stratification by consecutive age groups showed that for each disease analyzed separately, there were significant correlations amongst each two sequential age groups. In HL and UC, the inter-age correlations started at age 5 years or less. In MS and CD, the inter-age correlations only started at age 15 years. CONCLUSIONS: The similarities in the geographic distributions of death rates from HL, MS, CD, and UC suggest that these four diseases share a set of one or more common environmental risk factors. The data also support the contention that the exposure to such shared risk factors starts during an early period of lifetime.
 Multiple sclerosis (MS) is an immune-mediated disease that targets the myelin sheath of central nervous system (CNS) neurons leading to axon injury, neuronal death, and neurological progression. Though women are more highly susceptible to developing MS, men that develop this disease exhibit greater cognitive impairment and accumulate disability more rapidly than women. Magnetic resonance imaging and pathology studies have revealed that the greater neurological progression seen in males correlates with chronic immune activation and increased iron accumulation at the rims of chronic white matter lesions as well as more intensive whole brain and grey matter atrophy and axon loss. Studies in humans and in animal models of MS suggest that male aged microglia do not have a higher propensity for inflammation, but may become more re-active at the rim of white matter lesions as a result of the presence of pro-inflammatory T cells, greater astrocyte activation or iron release from oligodendrocytes in the males. There is also evidence that remyelination is more efficient in aged female than aged male rodents and that male neurons are more susceptible to oxidative and nitrosative stress. Both sex chromosome complement and sex hormones contribute to these sex differences in biology.
 Oligodendrocyte (OL) injury and loss are central features of evolving lesions in multiple sclerosis. Potential causative mechanisms of OL loss include metabolic stress within the lesion microenvironment. Here we use the injury response of primary human OLs (hOLs) to metabolic stress (reduced glucose/nutrients) in vitro to help define the basis for the in situ features of OLs in cases of MS. Under metabolic stress in vitro, we detected reduction in ATP levels per cell that precede changes in survival. Autophagy was initially activated, although ATP levels were not altered by inhibitors (chloroquine) or activators (Torin-1). Prolonged stress resulted in autophagy failure, documented by non-fusion of autophagosomes and lysosomes. Consistent with our in vitro results, we detected higher expression of LC3, a marker of autophagosomes in OLs, in MS lesions compared to controls. Both in vitro and in situ, we observe a reduction in nuclear size of remaining OLs. Prolonged stress resulted in increased ROS and cleavage of spectrin, a target of Ca(2+)-dependent proteases. Cell death was however not prevented by inhibitors of ferroptosis or MPT-driven necrosis, the regulated cell death (RCD) pathways most likely to be activated by metabolic stress. hOLs have decreased expression of VDAC1, VDAC2, and of genes regulating iron accumulation and cyclophilin. RNA sequencing analyses did not identify activation of these RCD pathways in vitro or in MS cases. We conclude that this distinct response of hOLs, including resistance to RCD, reflects the combined impact of autophagy failure, increased ROS, and calcium influx, resulting in metabolic collapse and degeneration of cellular structural integrity. Defining the basis of OL injury and death provides guidance for development of neuro-protective strategies.
 (1) Background: Radial RARE-EPI MRI facilitates simultaneous T(2) and T(2)* mapping (2in1-RARE-EPI). With modest undersampling (R = 2), the speed gain of 2in1-RARE-EPI relative to Multi-Spin-Echo and Multi-Gradient-Recalled-Echo references is limited. Further reduction in scan time is crucial for clinical studies investigating T(2) and T(2)* as imaging biomarkers. We demonstrate the feasibility of further acceleration, utilizing compressed sensing (CS) reconstruction of highly undersampled 2in1-RARE-EPI. (2) Methods: Two-fold radially-undersampled 2in1-RARE-EPI data from phantoms, healthy volunteers (n = 3), and multiple sclerosis patients (n = 4) were used as references, and undersampled (R(extra) = 1-12, effective undersampling R(eff) = 2-24). For each echo time, images were reconstructed using CS-reconstruction. For T(2) (RARE module) and T(2)* mapping (EPI module), a linear least-square fit was applied to the images. T(2) and T(2)* from CS-reconstruction of undersampled data were benchmarked against values from CS-reconstruction of the reference data. (3) Results: We demonstrate accelerated simultaneous T(2) and T(2)* mapping using undersampled 2in1-RARE-EPI with CS-reconstruction is feasible. For R(extra) = 6 (TA = 01:39 min), the overall MAPE was ≤8% (T(2)*) and ≤4% (T(2)); for R(extra) = 12 (TA = 01:06 min), the overall MAPE was <13% (T(2)*) and <5% (T(2)). (4) Conclusion: Substantial reductions in scan time are achievable for simultaneous T(2) and T(2)* mapping of the brain using highly undersampled 2in1-RARE-EPI with CS-reconstruction.
 PURPOSE: Interest in fractures in patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) has considerably increased in the last decade. However, few studies have compared the incidence of fractures between patients with MS and NMOSD using a nationwide database. This study aimed to evaluate the differences in the risk of fracture between patients with NMOSD and MS compared to that in healthy controls using cohort data from a Korean nationwide database. METHODS: In this retrospective cohort study, data from the National Health Insurance Service (NHIS) database from January 2010 to December 2017 were analyzed. A total of 1,217/1,329 patients with MS/NMOSD free of fractures at the index date were included. Matched controls were selected based on age, sex, and the presence of hypertension, diabetes mellitus, and dyslipidemia. The mean follow-up durations after the index date were 4.40/4.08 years for patients with MS/NMOSD and 4.73/4.28 for their matched controls. RESULTS: The adjusted hazard ratios (aHRs) with 95% confidence intervals of any, hip, and vertebral fractures were 1.81 (1.43-2.28), 3.36 (1.81-6.24), and 2.01 (1.42-2.99) times higher for patients with MS than for controls, respectively, and they were 1.85 (1.47-2.34), 3.82 (2.05-7.11), and 2.84 (1.92-4.21) times higher for patients with NMOSD than for controls, respectively. No significant differences were observed in the incidence of fractures between the MS and NMOSD groups. Patients with MS/NMOSD had a 1.8-fold higher risk of fracture than matched controls, and the risk of hip fracture was especially high (3- to 4-fold higher). CONCLUSIONS: Clinicians need to regularly assess patients with MS/NMOSD for the risk of fractures and take preventative measures to reduce it.
 BACKGROUND: There is concern that immune checkpoint inhibitors (ICPIs) can provoke relapses in people with multiple sclerosis (pwMS). OBJECTIVE: Analyze outcomes of pwMS who received ICPI treatment for malignancy. METHODS: We electronically identified pwMS who received ICPI treatment at Mass General Brigham hospital system. We retrospectively obtained information about patients' MS, cancer, treatment, and outcomes. RESULTS: Sixteen patients were identified with an average (standard deviation (SD)) age of 67.4 (11.9) years. Eleven (68.8%) had no relapses since MS diagnosis. None had MS relapses after ICPI treatment or new MS lesions. CONCLUSION: ICPI use was not associated with increased clinical disease activity in this cohort of older patients with inactive MS.
 OBJECTIVES: Among people with immune-mediated inflammatory disease (IMID), including multiple sclerosis (MS), inflammatory bowel disease (IBD) and rheumatoid arthritis (RA) most research has focused on mental illness rather than on mental health. We assessed dimensions of mental health among persons with IMID and compared them across IMID. We also evaluated demographic and clinical characteristics associated with flourishing mental health. DESIGN: Participants: Adults with an IMID (MS, 239; IBD, 225; RA 134; total 598) who were participating in a cohort study. SETTING: Tertiary care centre in Manitoba, Canada. PRIMARY OUTCOME MEASURE: Participants completed the Mental Health Continuum Short-Form (MHC-SF), which measures emotional, psychological and social well-being, and identifies flourishing mental health. This outcome was added midway through the study on the advice of the patient advisory group. Depression, anxiety, pain, fatigue and physical function were also assessed. RESULTS: Total MHC-SF and subscale scores were similar across IMID groups. Nearly 60% of participants were considered to have flourishing mental health, with similar proportions across disease types (MS 56.5%; IBD 58.7%; RA 59%, p=0.95). Older age was associated with a 2% increased odds of flourishing mental health per year of age (OR 1.02; 95% CI: 1.01 to 1.04). Clinically meaningful elevations in anxiety (OR 0.25; 95% CI: 0.12 to 0.51) and depressive symptoms (OR 0.074; 95% CI: 0.009 to 0.61) were associated with lower odds. Higher levels of pain, anxiety and depressive symptoms were associated with lower total Mental Health Continuum scores at the 50th quantile. CONCLUSIONS: Over half of people with MS, IBD and RA reported flourishing mental health, with levels similar across the disease groups. Interventions targeting symptoms of depression and anxiety, and upper limb impairments, as well as resilience training may help a higher proportion of the IMID population achieve flourishing mental health.
 Background: Lipid metabolism may impact disability in people with multiple sclerosis (pwMS). Methods: Fifty-one pwMS entered an ultrasound and MRI study, of whom 19 had followed a pathology-supported genetic testing program for more than 10 years (pwMS-ON). Genetic variation, blood biochemistry, vascular blood flow velocities, diet and exercise were investigated. Results: pwMS-ON had significantly lower (p < 0.01) disability (Expanded Disability Status Scale) than pwMS not on the program (1.91 ± 0.75 vs 3.87 ± 2.32). A genetic variant in the lipid transporter FABP2 gene (rs1799883; 2445G>A, A54T) was significantly associated (p < 0.01) with disability in pwMS not on the program, but not in pwMS-ON (p = 0.88). Vascular blood flow velocities were lower in the presence of the A-allele. Conclusion: Pathology-supported genetic testing may provide guidance for lifestyle interventions with a significant impact on improved disability in pwMS.
 Ocrelizumab is a B cell-depleting drug widely used in relapsing-remitting multiple sclerosis (RRMS) and primary-progressive MS. In RRMS, it is becoming increasingly apparent that accumulation of disability not only manifests as relapse-associated worsening (RAW) but also as progression independent of relapse activity (PIRA) throughout the disease course. This study's objective was to investigate the role of PIRA in RRMS patients treated with ocrelizumab. We performed a single-center, retrospective, cross-sectional study of clinical data acquired at a German tertiary multiple sclerosis referral center from 2018 to 2022. All patients with RRMS treated with ocrelizumab for at least six months and complete datasets were analyzed. Confirmed disability accumulation (CDA) was defined as a ≥ 12-week confirmed increase from the previous expanded disability status scale (EDSS) score of ≥ 1.0 if the previous EDSS was ≤  5.5 or a ≥ 0.5-point increase if the previous EDSS was > 5.5. PIRA was defined as CDA without relapse since the last EDSS measurement and at least for the preceding 12 weeks. RAW was defined as CDA in an interval of EDSS measurements with ≥ 1 relapses. Cox proportional hazard models were used to analyze the probability of developing PIRA depending on various factors, including disease duration, previous disease-modifying treatments (DMTs), and optical coherence tomography-assessed retinal degeneration parameters. 97 patients were included in the analysis. Mean follow-up time was 29 months (range 6 to 51 months). 23.5% developed CDA under ocrelizumab therapy (n = 23). Of those, the majority developed PIRA (87.0% of CDA, n = 20) rather than RAW (13.0% of CDA, n = 3). An exploratory investigation using Cox proportional hazards ratios revealed two possible factors associated with an increased probability of developing PIRA: a shorter disease duration prior to ocrelizumab (p = 0.02) and a lower number of previous DMTs prior to ocrelizumab (p = 0.04). Our data show that in ocrelizumab-treated RRMS patients, the main driver of disability accumulation is PIRA rather than RAW. Furthermore, these real-world data show remarkable consistency with data from phase 3 randomized controlled trials of ocrelizumab in RRMS, which may increase confidence in translating results from tightly controlled RCTs into the real-world clinical setting.
 Little is known about how the brain's functional organization changes over time with respect to structural damage. Using multiple sclerosis as a model of structural damage, we assessed how much functional connectivity (FC) changed within and between preselected resting-state networks (RSNs) in 122 subjects (72 with multiple sclerosis and 50 healthy controls). We acquired the structural, diffusion, and functional MRI to compute functional connectomes and structural disconnectivity profiles. Change in FC was calculated by comparing each multiple sclerosis participant's pairwise FC to controls, while structural disruption (SD) was computed from abnormalities in diffusion MRI via the Network Modification tool. We used an ordinary least squares regression to predict the change in FC from SD for 9 common RSNs. We found clear differences in how RSNs functionally respond to structural damage, namely that higher-order networks were more likely to experience changes in FC in response to structural damage (default mode R2 = 0.160-0.207, P < 0.001) than lower-order sensory networks (visual network 1 R2 = 0.001-0.007, P = 0.157-0.387). Our findings suggest that functional adaptability to structural damage depends on how involved the affected network is in higher-order processing.
 BACKGROUND: People with multiple sclerosis (PwMS) show an increased risk of sexual dysfunction (SD), both in women and men. OBJECTIVE: The aim of the present study was to apply the Multiple Sclerosis Intimacy and Sexuality Questionnaire-19 (MSISQ-19) and evaluate our results by comparing them with those in in the literature, as well as to assess the ease of applying the scale and the engagement of the patients in discussing the topic of sexuality. METHODS: We developed and applied a web-based Google form questionnaire that the respondents completed online, which included the MSISQ-19, for the assessment of sexual function. Baseline characteristics were reported as proportions and mean ± standard deviation (SD) or median ± interquartile range (IQR) as appropriate according to data distribution. Categorical variables were stratified by sex and compared with chi-squared tests. Statistical analyses were performed using STATA v. 16 (StataCorp., College Station, TX, USA). RESULTS: Of the 621 respondents, 541 were included in the analysis. Among the patients with MS, a total of 347 (64.14%) exhibited SD. When stratified by gender, the frequencies of SD were not significantly different. CONCLUSION: There is a high incidence of sexual dysfunction among PwMS and we need to identify the reasons for this and implement strategies to treat and counsel our patients. The MSISQ-19 can be used to help clinicians to assess sexual functioning in a quick and easy way and give patients the possibility to address this topic and receive appropriate help and support.
 BACKGROUND: Patients with relapsing-remitting multiple sclerosis commonly switch between disease-modifying therapies (DMTs). Identifying predictors of relapse when switching could improve outcomes. OBJECTIVE: To determine predictors of relapse hazard when switching to cladribine. METHODS: Data of patients who switched to cladribine, grouped by prior disease-modifying therapy (pDMT; interferon-β/glatiramer acetate, dimethyl fumarate, teriflunomide, fingolimod or natalizumab (NTZ)), were extracted from the MSBase Registry. Predictors of relapse hazard during the treatment gap and the first year of cladribine therapy were determined. RESULTS: Of 513 patients, 22 relapsed during the treatment gap, and 38 within 1 year of starting cladribine. Relapse in the year before pDMT cessation predicted treatment gap relapse hazard (hazard ratio (HR) = 2.43, 95% confidence interval (CI)  = 1.03-5.71). After multivariable adjustment, relapse hazard on cladribine was predicted by relapse before pDMT cessation (HR = 2.00, 95% CI = 1.01-4.02), treatment gap relapse (HR = 6.18, 95% confidence interval (CI) = 2.65-14.41), switch from NTZ (HR compared to injectable therapies 4.08, 95% CI = 1.35-12.33) and age at cladribine start (HR = 0.96, 95% CI = 0.91-0.99). CONCLUSION: Relapse during or prior to the treatment gap, and younger age, are of prognostic relevance in the year after switching to cladribine. Switching from NTZ is also independently associated with greater relapse hazard.
 OBJECTIVE: Job loss is common in multiple sclerosis (MS) and frequently associated with depression, fatigue, and cognitive dysfunction. Identifying these modifiable risk factors and providing "at-risk" women with a neuropsychologically-based intervention may improve employment outcomes. Our study seeks to investigate the utility of a neuropsychologically-based intervention with varying levels of treatment and follow-up, and evaluate treatment and employment outcomes among groups. METHOD: In this longitudinal, quasi-randomized controlled trial, employed women with MS meeting criteria on screening measures were considered "at-risk" for job instability and randomized to one of two neuropsychological testing interventions (standard-care group received testing and phone feedback of results and recommendations; experimental group received testing and in-person feedback with subsequent care-coordinator calls from a nurse to help coordinate recommendation completion). Participants who did not meet criteria were considered "low-risk" and only followed over time. RESULTS: 56 women in the treatment groups (standard-care = 23; experimental = 33) and 63 women in the follow-only group were analyzed at 1 year. Rates of decreased employment were similar between standard-care (17.4%) and experimental (21.2%) groups (OR = .782, 95% CI .200-3.057). However, the experimental group completed significantly more treatment recommendations, t(53) = -3.237, p = .002. Rates of decreased employment were also similar between the "low-risk" (17.5%) and "at-risk" groups (19.6%), (OR = .721, 95% CI .285-1.826). CONCLUSION: Employment outcomes were similar at 1 year between treatment groups receiving differing levels of a neuropsychologically-based intervention, however treatment adherence significantly improved in the experimental group. Treatment groups also had similar employment outcomes as compared to a "low-risk," no intervention group, suggesting that engaging in either neuropsychological intervention may have impacted job stability.
 BACKGROUND: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system(CNS). It is widely accepted that the development and progression of MS result from aberrant activation of potentially encephalitogenic reactive-T cells against CNS antigens. The pathologic roles of both CD4+ (T helper; Th) and CD8+ T cells have been demonstrated in MS lesions. OBJECTIVE: In the present work, we applied a series of bioinformatics tools to design a dendritic cell (DC)-targeting Tregitope-based multi-epitope vaccine for MS to induce tolerance in pathogenic myelin-specific T cells. METHODS: The 3D structure of anti-DEC205 scFv and the remaining part of the vaccine were modeled by ROSIE Antibody server and ITASSER software, respectively. AIDA web server (ab initio domain assembly server) was applied to assemble two parts of the vaccine and build the full construct. Following modeled structure refinement and validation, physicochemical properties, and allergenicity of the vaccine were assessed. In the final step, in silico cloning was done to ensure high-level expression in the desired host. RESULTS: This vaccine consists of three main parts; 1) Anti-DEC205 scFv antibody, 2) multiepitope vaccine part composed of multiple pathogenic CD4+, and CD8+ T cell epitopes originated from multiple known antigens in MS patients, as well as T-regulatory (Treg)-inducing epitopes (Tregitopes), and 3) vasoactive intestinal peptide (VIP). All parts of the final vaccine were joined together with the help of proper linkers. After vaccine construction, the three-D structure, as well as different physicochemical and immunological features of the vaccine were predicted. Finally, in silico gene cloning was also carried out to assure efficient production of protein vaccine in Escherichia coli K12 expression strain. CONCLUSION: Computational study revealed that this vaccination can regulate MS disease progression and even relapse by harnessing pathogenic T cells.
 INTRODUCTION: The advent of new disease-modifying therapies (DMTs), such as monoclonal antibodies (mAbs), resulted in significant changes in the treatment guidelines for Multiple sclerosis (MS) and improvement in the clinical outcomes. However, mAbs, such as rituximab, natalizumab, and ocrelizumab, are expensive with variable effectiveness rates. Thus, the present study aimed to compare the direct medical cost and consequences (e.g., clinical relapse, disability progression, and new MRI lesions) between rituximab and natalizumab in managing relapsing-remitting multiple sclerosis (RRMS) in Saudi Arabia. Also, the study aimed to explore the cost and consequence of ocrelizumab in managing RRMS as a second-choice treatment. METHODS: The electronic medical records (EMRs) of patients with RRMS were retrospectively reviewed to retrieve the patients' baseline characteristics and disease progression from two tertiary care centers in Riyadh, Saudi Arabia. Biologic-naïve patients treated with rituximab or natalizumab or those switched to ocrelizumab and treated for at least six months were included in the study. The effectiveness rate was defined as no evidence of disease activity (NEDA-3) (i.e., absence of new T2 or T1 gadolinium (Gd) lesions as demonstrated by the Magnetic Resonance Imaging (MRI), disability progression, and clinical relapses), while the direct medical costs were estimated based on the utilization of healthcare resources. In addition, bootstrapping with 10,000 replications and inverse probability weighting based on propensity score were conducted. RESULTS: Ninety-three patients met the inclusion criteria and were included in the analysis (natalizumab (n = 50), rituximab (n = 26), ocrelizumab (n = 17)). Most of the patients were otherwise healthy (81.72%), under 35 years of age (76.34%), females (61.29%), and on the same mAb for more than one year (83.87%). The mean effectiveness rates for natalizumab, rituximab, and ocrelizumab were 72.00%, 76.92%, and 58.83%, respectively. Natalizumab mean incremental cost compared to rituximab was $35,383 (95% CI: $25,401.09- $49,717.92), and its mean effectiveness rate was 4.92% lower than rituximab (95% CI: -30-27.5) with 59.41% confidence level that rituximab will be dominant. CONCLUSIONS: Rituximab seems to be more effective and is less costly than natalizumab in the management of RRMS. Ocrelizumab does not seem to slow the rates of disease progression among patients previously treated with natalizumab.
 BACKGROUND: Demographic characteristics, social determinants of health (SDoH), health inequities, and health disparities substantially influence the general and disease-specific health outcomes of people with multiple sclerosis (MS). Participants in clinical trials do not represent all people with MS treated in practice. OBJECTIVE: To provide recommendations for enhancing diversity and inclusion in clinical trials in MS. METHODS: We held an international workshop under the Auspices of the International Advisory Committee on Clinical Trials in MS (the "Committee") to develop recommendations regarding diversity and inclusivity of participants of clinical trials in MS. Workshop attendees included members of the Committee as well as external participants. External participants were selected based on expertise in trials, SDoH, health equity and regulatory science, and diversity with respect to gender, race, ethnicity, and geography. RESULTS: Recommendations include use of diversity plans, community engagement and education, cultural competency training, biologically justified rather than templated eligibility criteria, adaptive designs that allow broadening of eligibility criteria over the course of a trial, and logistical and practical adjustments to reduce study participant burden. Investigators should report demographic and SDoH characteristics of participants. CONCLUSION: These recommendations provide sponsors and investigators with methods of improving diversity and inclusivity of clinical trial populations in MS.
 BACKGROUND: The majority of patients with multiple sclerosis on ocrelizumab have B-cell depletion after standard interval dosing of 26 weeks. With B-cell-guided dosing patients receive their next dose when B-cell repopulation occurs. Prediction of B-cell repopulation using ocrelizumab concentrations could aid in personalising treatment regimes. The objectives of this study were to evaluate the association between ocrelizumab drug concentration, antidrug antibodies (ADAs) and CD19 B-cell count, and to define a cut-off ocrelizumab concentration for start of B-cell repopulation (defined by ≥10 CD19+ B cells/µL). METHODS: In this investigator-initiated prospective study, blood samples at various time points during ocrelizumab treatment were collected from a biobank. Serum ocrelizumab concentrations and ADAs were measured with two different assays developed for this study. Data were analysed using linear mixed effect models. An receiver operating characteristic (ROC) curve was used to determine a cut-off ocrelizumab concentration for start of B-cell repopulation (defined by ≥10 cells/µL). RESULTS: A total of 452 blood samples from 72 patients were analysed. Ocrelizumab concentrations were detectable up until 53.3 weeks after last infusion and ranged between <0.0025 and 204 µg/mL after 1-67 weeks. Ocrelizumab concentration was negatively associated with B-cell count, with body mass index identified as effect modifier. We found a cut-off value of 0.06 µg/mL for start of B-cell repopulation of ≥10 cells/µL. Ocrelizumab ADAs were detectable in four patients (5.7%) with corresponding low ocrelizumab concentrations and start of B-cell repopulation. CONCLUSIONS: Serum ocrelizumab concentration was strongly associated with B-cell count. Measurement of ocrelizumab drug concentrations and ADAs could play an important role to further personalise treatment and predict the start of B-cell repopulation.
 OBJECTIVE: Psoriasis and multiple sclerosis (MS) are complex immune diseases that are mediated by T cells and share multiple comorbidities. Previous studies have suggested psoriatic patients are at higher risk of MS; however, causal relationships between the two conditions remain unclear. Through epidemiology and genetics, we provide a comprehensive understanding of the relationship, and share molecular factors between psoriasis and MS. METHODS: We used logistic regression, trans-disease meta-analysis and Mendelian randomization. Medical claims data were included from 30 million patients, including 141,544 with MS and 742,919 with psoriasis. We used genome-wide association study summary statistics from 11,024 psoriatic, 14,802 MS cases, and 43,039 controls for trans-disease meta-analysis, with additional summary statistics from 5 million individuals for Mendelian randomization. RESULTS: Psoriatic patients have a significantly higher risk of MS (4,637 patients with both diseases; odds ratio [OR] 1.07, p = 1.2 × 10(-5) ) after controlling for potential confounders. Using inverse variance and equally weighted trans-disease meta-analysis, we revealed >20 shared and opposing (direction of effect) genetic loci outside the major histocompatibility complex that showed significant genetic colocalization (in COLOC and COLOC-SuSiE v5.1.0). Co-expression analysis of genes from these loci further identified distinct clusters that were enriched among pathways for interleukin-17/tumor necrosis factor-α (OR >39, p < 1.6 × 10(-3) ) and Janus kinase-signal transducers and activators of transcription (OR 35, p = 1.1 × 10(-5) ), including genes, such as TNFAIP3, TYK2, and TNFRSF1A. Mendelian randomization found psoriasis as an exposure has a significant causal effect on MS (OR 1.04, p = 5.8 × 10(-3) ), independent of type 1 diabetes (OR 1.05, p = 4.3 × 10(-7) ), type 2 diabetes (OR 1.08, p = 2.3 × 10(-3) ), inflammatory bowel disease (OR 1.11, p = 1.6 × 10(-11) ), and vitamin D level (OR 0.75, p = 9.4 × 10(-3) ). INTERPRETATION: By investigating the shared genetics of psoriasis and MS, along with their modifiable risk factors, our findings will advance innovations in treatment for patients suffering from comorbidities. ANN NEUROL 2023;94:384-397.
 BACKGROUND: Multiple sclerosis (MS) is a disabling autoimmune demyelinating disorder affecting young people and causing significant disability. In the last decade, different microRNA (miRNA) expression patterns have been associated to several treatment response therapies such as interferon and glatiramer acetate. Nowadays, there is increasing interest in the potential role of miRNA as treatment response biomarkers to the most recent oral and intravenous treatments. In this study, we aimed to evaluate serum miRNAs as biomarkers of No Evidence of Disease Activity (NEDA-3) at 2 years in patients with relapsing remitting MS (RRMS) treated with fingolimod. MAIN BODY: A Discovery cohort of 31 RRMS patients treated with fingolimod were identified from the CLIMB study and classified as No Evidence of Disease Activity (NEDA-3) or Evidence of Disease Activity (EDA-3) after 2 years on treatment. Levels of miRNA expression were measured at 6 months using human serum miRNA panels and compared in EDA-3 and NEDA-3 groups using the Wilcoxon rank sum test. A set of differentially expressed miRNA was further validated in an independent cohort of 22 fingolimod-treated patients. We found that 548a-3p serum levels were higher levels in fingolimod-treated patients classified as NEDA-3, compared to the EDA-3 group in both the Discovery (n = 31; p = 0.04) and Validation (n = 22; p = 0.03) cohorts 6 months after treatment initiation; miR-548a-3p provided an AUC of 0.882 discriminating patients with NEDA-3 at 2 years in the Validation cohort. CONCLUSION: Our results show differences in miR-548a-3p expression at 6 months after fingolimod start in patients with MS with NEDA-3 at 2 years. These results provide class III evidence of the use of miR-548a-3p as biomarker of NEDA-3 in patients with fingolimod.
 OBJECTIVE: The purpose of this study was to examine the association between frailty and the quantity and quality of free-living walking and the mediating effect of frailty on the relationship between disability and walking performance in people with multiple sclerosis (MS). METHODS: Ninety-nine people with relapsing-remitting MS (mean age = 49.3 [SD = 9.8] years; 73.7% women; Expanded Disability Status Scale [EDSS] score range = 2.0-6.0) wore a triaxial accelerometer for 7 days. Recorded measures reflected the quantity (daily step counts, number of 30-second walking bouts, and signal vector magnitude [SVM]) and quality (gait speed, step cadence, step and stride regularity, and sample entropy) of walking. For each walking quality measure, the typical (median), best (90th percentile), and worst (10th percentile) values were calculated. Frailty was evaluated through a 38-item frailty index. RESULTS: Participants were classified as not frail (n = 31), moderately frail (n = 34), and severely frail (n = 34) on the basis of established procedures. Patients who were moderately and severely frail exhibited poorer performance in all measures of walking quantity and quality, except for sample entropy, than individuals who were not frail. No differences in free-living walking performance were observed between the moderately and severely frail groups. Frailty did not mediate the relationship between disability (EDSS) and measures of walking quality. Conversely, frailty had a significant mediating effect on the relationship between disability and measures of walking quantity, such as daily step counts (indirect effect: b = -220.42, 95% CI = -452.03 to -19.65) and SVM (indirect effect: b = -1.00, 95% CI = -1.86 to -0.30). CONCLUSION: Frailty is associated with poorer free-living walking performance in people with MS. The study findings suggest that frailty, rather than disability, may be primarily responsible for the lower amount of physical activity performed by people with MS in the real world. IMPACT: The observation that frailty and disability are differently related to measures of walking quality and quantity underscores the importance of a targeted approach to rehabilitation in people with MS.
 Background: Spasticity continues to be a very prevalent, highly invalidating, and difficult-to-manage symptom in patients with multiple sclerosis (MS). The aim of this systematic review is to evaluate the effectiveness of the use of cannabis and cannabinoids in these patients, evaluating its use as an additional therapy. Methods: We performed a systematic review of the literature searching in the major scientific databases (PubMed, Scopus, EMBASE, WOS, and Cochrane Library) for articles from January 2017 to May 2022 containing information about the effectiveness of cannabis and cannabinoids in patients with insufficient response to first-line oral antispastic treatment. Results: A total of five medium high-quality articles were selected to be part of the study and all evaluated the effectiveness of the tetrahydrocannabinol (THC) and cannabidiol (CBD) spray. The effectiveness of this drug and the significant improvements are produced on the patient-related spasticity assessment scales, obtaining improvement up to 45%; and on quality of life, producing a decrease in the appearance of symptoms related to spasticity, as well as an increase in the development of basic activities of daily living. The average dose is 5-7 sprays/day. The discontinuation rate for these treatments is around 40% due to lack of effectiveness and adverse events. All reported adverse effects are mild to moderate in severity and their incidence is ∼17%, although this figure tends to decrease with drug use. Conclusions: Adding the THC:CBD sprays have been shown to be more effective in treating MS spasticity than optimizing the dose of first-line antispastic drugs in selected responders patients. The safety and tolerability profiles remain in line with those obtained in other trials. More patients would benefit from treatment if the initial response search period was extended.
 BACKGROUND: Lesions in the periventricular, (juxta)cortical, and infratentorial region, as visible on brain MRI, are part of the diagnostic criteria for Multiple sclerosis (MS) whereas lesions in the subcortical region are currently only a marker of disease activity. It is unknown whether MS lesions follow individual spatial patterns or whether they occur in a random manner across diagnostic regions. AIM: First, to describe cross-sectionally the spatial lesion patterns in patients with MS. Second, to investigate the spatial association of new lesions and lesions at baseline across diagnostic regions. METHODS: Experienced neuroradiologists analyzed brain MRI (3D, 3T) in a cohort of 330 early MS patients. Lesions at baseline and new solitary lesions after two years were segmented (manually and by consensus) and classified as periventricular, (juxta)cortical, or infratentorial (diagnostic regions) or subcortical-with or without Gadolinium-enhancement. Gadolinium enhancement of lesions in the different regions was compared by Chi square test. New lesions in the four regions served as dependent variable in four zero-inflated Poisson models each with the six independent variables of lesions in the four regions at baseline, age and gender. RESULTS: At baseline, lesions were most often observed in the subcortical region (mean 13.0 lesions/patient), while lesion volume was highest in the periventricular region (mean 2287 µl/patient). Subcortical lesions were less likely to show gadolinium enhancement (3.1 %) than juxtacortical (4.3 %), periventricular (5.3 %) or infratentorial lesions (7.2 %). Age was inversely correlated with new periventricular, juxtacortical and subcortical lesions. New lesions in the periventricular, juxtacortical and infratentorial region showed a significant autocorrelative behavior being positively related to the number of lesions in the respective regions at baseline. New lesions in the subcortical region showed a different behavior with a positive association with baseline periventricular lesions and a negative association with baseline infratentorial lesions. CONCLUSION: Across regions, new lesions do not occur randomly; instead, new lesions in the periventricular, juxtacortical and infratentorial diagnostic region are associated with that at baseline. Lesions in the subcortical regions are more closely related to periventricular lesions. Moreover, subcortical lesions substantially contribute to lesion burden in MS but are less likely to show gadolinium enhancement (than lesions in the diagnostic regions).
 Multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) are two prevalent autoimmune diseases of the central nervous system that predominantly affect women during childbearing age. Patients of childbearing age affected by conditions, such as MS and NMOSD, should consider the potential implications of pregnancy. The selection of treatment options should be carefully evaluated, considering preconception care and assessing the risk-benefit profile for both the mother and fetus. In recent years, there has been growing interest and need to address pregnancy and delivery in the context of these diseases, leading to the development of several internationally reported guidelines. The management of MS and NMOSD has entered a new era in Japan, with the inclusion of monoclonal antibodies and various biological agents, including B-cell depletion therapy, which is covered by insurance. Furthermore, there has been increasing focus on myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), which has been reported to be associated with pregnancy. In this article, we aim to discuss the characteristics of MS, NMOSD, and MOGAD in the context of pregnancy, while providing updated insights on managing pregnancy and lactation with disease-modifying drugs and biologic agents.
 BACKGROUND: Over the decades, several natural history studies on patients with primary (PPMS) or secondary progressive multiple sclerosis (SPMS) were reported from international registries. In PPMS, a consistent heterogeneity on long-term disability trajectories was demonstrated. The aim of this study was to identify subgroups of patients with SPMS with similar longitudinal trajectories of disability over time. METHODS: All patients with MS collected within Big MS registries who received an SPMS diagnosis from physicians (cohort 1) or satisfied the Lorscheider criteria (cohort 2) were considered. Longitudinal Expanded Disability Status Scale (EDSS) scores were modelled by a latent class growth analysis (LCGA), using a non-linear function of time from the first EDSS visit in the range 3-4. RESULTS: A total of 3613 patients with SPMS were included in the cohort 1. LCGA detected three different subgroups of patients with a mild (n=1297; 35.9%), a moderate (n=1936; 53.6%) and a severe (n=380; 10.5%) disability trajectory. Median time to EDSS 6 was 12.1, 5.0 and 1.7 years, for the three groups, respectively; the probability to reach EDSS 6 at 8 years was 14.4%, 78.4% and 98.3%, respectively. Similar results were found among 7613 patients satisfying the Lorscheider criteria. CONCLUSIONS: Contrary to previous interpretations, patients with SPMS progress at greatly different rates. Our identification of distinct trajectories can guide better patient selection in future phase 3 SPMS clinical trials. Additionally, distinct trajectories could reflect heterogeneous pathological mechanisms of progression.
 BACKGROUND: Diet-dependent acid-base load has been associated with worsening in mental health, but to date no study has examined this in people with multiple sclerosis (PwMS). We examined the association between potential renal acid load (PRAL) and net endogenous acid production (NEAP) scores and depression, anxiety, and fatigue in PwMS. METHODS: Participants with a first clinical diagnosis of CNS demyelination were followed prospectively as part of the AusLong Study (aged 18-59 years at cohort entry). At baseline, 5- and 10-year reviews, PRAL and NEAP scores were calculated using dietary intake in the preceding 12 months calculated from a food frequency questionnaire. At 5- and 10-year reviews, the Hospital Anxiety and Depression Scale was used to assess depression and anxiety, and the Fatigue Severity Scale assessed fatigue. RESULTS: Higher PRAL and NEAP scores were associated with increased subsequent absolute value and change in HADS depression scores over five years' follow-up (e.g., highest vs lowest PRAL quartile, 5-year change in HADS-D score: β=+3.01, 95%CI= 1.54, 4.48, p<0.001). The level of depression at the 10-year review was determined by both the baseline dietary acid scores and baseline-5-year changes in dietary acid scores (e.g., PRAL change from baseline to 5-year review, 10-year review HADS-D score: β=+0.09, 95%CI= 0.03, 0.15, p<0.001, NEAP change from baseline to 5-year review, 10-year review HADS-D score: β=+0.07, 95%CI= 0.01, 0.14, p=0.03). Some associations were observed with anxiety and fatigue but were much weaker and less consistent. CONCLUSION: Our findings indicate that a higher dietary acid load potentially has a long-term influence on the level of depression in PwMS. The evidence is less convincing for anxiety and fatigue.
 PURPOSE: To investigate the immediate effects of wearing novel sensory-stimulating textured insoles on balance and gait in 41 people with multiple sclerosis (pwMS). MATERIALS AND METHODS: Assessments of balance (firm/foam surface; eyes open/closed) and walking (when negotiating even/uneven surfaces) were performed wearing textured insoles, smooth insoles, shoes only, and barefoot. Outcome measures were centre of pressure (CoP) movement during standing (elliptical area, sway path velocity) and spatiotemporal gait patterns (stride/step width, stride time, double-limb support time, stride length, velocity). RESULTS: Wearing textured insoles led to reductions in CoP velocity measures when standing on foam with eyes open and closed when compared to barefoot (p values ≤0.02). Textured insoles did not appear to be consistently superior to smooth insoles or shoes only for improving gait. Relative to the insole/shoe conditions, walking barefoot led to poorer gait performance for the even and uneven surface tasks (p values ≤0.03). CONCLUSIONS: For pwMS, stimulating the foot with "texture" appears to provide enhanced sensory input with the capacity to improve CoP movement control during standing; offering a potential new treatment option for balance rehabilitation. Further research is needed to identify which individuals may benefit most from textured insoles.Implications for rehabilitationTextured shoe insoles, designed to stimulate plantar mechanoreceptors, are a novel approach to improve standing balance and walking patterns in people with multiple sclerosis (pwMS).Wearing textured insoles for the first time can lead to improvements in centre of pressure movement control when standing on an unstable compliant supporting surface.Textured insoles offer a potential new treatment technique for balance rehabilitation in pwMS who show early signs of diminished foot sensation.
 BACKGROUND: Multiple sclerosis (MS) quality of care guidelines are consensus-based. The effectiveness of the recommendations is unknown. OBJECTIVE: To determine whether clinic-level quality of care affects clinical and patient-reported outcomes. METHODS: This nationwide observational cohort study included patients with adult-onset MS in the Swedish MS registry with disease onset 2005-2015. Clinic-level quality of care was measured by four indicators: visit density, magnetic resonance imaging (MRI) density, mean time to commencement of disease-modifying therapy, and data completeness. Outcomes were Expanded Disability Status Scale (EDSS) and patient-reported symptoms measured by the Multiple Sclerosis Impact Scale (MSIS-29). Analyses were adjusted for individual patient characteristics and disease-modifying therapy exposure. RESULTS: In relapsing MS, all quality indicators benefitted EDSS and physical symptoms. Faster treatment, frequent visits, and higher data completeness benefitted psychological symptoms. After controlling for all indicators and individual treatment exposures, faster treatment remained independently associated with lower EDSS (-0.06, 95% confidence interval (CI): -0.01, -0.10) and more frequent visits were associated with milder physical symptoms (MSIS-29 physical score: -16.2%, 95% CI: -1.8%, -29.5%). Clinic-level quality of care did not affect any outcomes in progressive-onset disease. CONCLUSION: Certain quality of care indicators correlated to disability and patient-reported outcomes in relapse-onset but not progressive-onset disease. Future guidelines should consider recommendations specific to disease course.
 BACKGROUND AND OBJECTIVES: Multiple sclerosis (MS), a leading cause of nontraumatic neurologic disability in young adults, exerts a substantial economic burden on the health care system. The objective of this study was to quantify the excess health care costs of MS in British Columbia, Canada. METHODS: A retrospective-matched cohort study of patients with MS was conducted using population-based administrative health data from 2001 to 2020. Patients with MS who satisfied a validated case definition were matched to 5 unique controls without MS on sex, age, and cohort entry date. Patients and controls were followed to the end of 2020 or to their last health care resource use, whichever came first. We calculated the direct medical costs for each individual, including outpatient services use, hospital admissions, and dispensed medications. We used generalized linear models with an identity link and normal distribution to estimate the excess cost of MS as the mean cost difference between patients with MS and controls. All costs were reported in 2020 Canadian dollars. RESULTS: A total of 17,071 patients with MS were matched to 85,355 controls. Overall, 72.4% were female, and the mean age at cohort entry date was 46.1 years. The excess cost of MS was $6,881 (95% CI: $6,713, $7,049) per patient-year. Inpatient, outpatient, and medication costs accounted for 25%, 10%, and 65% of excess costs, respectively. Excess costs were higher in patients with MS with at least one disease-modifying therapy (DMT) prescription ($13,267; 95% CI: $12,992-$13,542) compared with non-DMT users ($3,469; 95% CI: $3,297-$3,641) and even higher among frequent DMT users ($24,835; 95% CI: $24,528-$25,141). Patients with MS with a history of at least one relapse requiring hospitalization had higher excess costs ($10,543; 95% CI: $10,136-$10,950) compared with patients with MS without a relapse; hospitalizations accounted for 51% of the costs in this group. The excess cost of hospitalizations was $1,391 lower among frequent DMT users than non-DMT users. DISCUSSION: The economic burden of MS is considerable, with medications, particularly DMTs, being the largest cost driver. Future studies should investigate how disease management strategies, including early diagnosis and timely use of DMTs, could offset future and ongoing costs while improving patients' quality of life.
 BACKGROUND: Over one-third of multiple sclerosis (MS) patients are post-menopausal women, the primary demographic affected by breast cancer. After breast cancer diagnosis, there is little information about patients' clinical experiences with both diseases. OBJECTIVE: Utilize a case series of MS patients diagnosed with breast cancer to characterize oncologic and MS trajectories, and generate novel insights about clinical considerations using qualitative analysis. METHODS: A single-center retrospective review was performed on medical record data of patients with MS and breast cancer. Thematic analysis was used to characterize experiences with the concurrent diagnoses. RESULTS: For the 43 patients identified, mean age was 56.7 years at cancer diagnosis and MS duration was 16.5 years. Approximately half were treated with MS disease modifying therapy at cancer diagnosis, and half of these subsequently discontinued or changed therapy. Altogether 14% experienced MS relapse(s) during follow-up (with 2 relapses in the first 2 years), with mean annualized relapse rate of 0.03. Cohort Expanded Disability Status Scale (EDSS) scores remained stable during follow-up. Qualitative insights unique to this population were identified regarding immunosuppression use and neurologic symptoms. CONCLUSIONS: MS relapses were infrequent, and there was modest progression during breast cancer treatment. Oncologic outcomes were comparable to non-MS patients with similarly staged cancer.
 BACKGROUND: The phase 3 TERIKIDS study demonstrated efficacy and manageable safety for teriflunomide versus placebo in children with relapsing multiple sclerosis (RMS). OBJECTIVE: Evaluate plasma neurofilament light chain (pNfL) concentrations in TERIKIDS. METHODS: Patients received placebo or teriflunomide (14 mg adult equivalent) for up to 96 weeks in the double-blind (DB) period. In the open-label extension (OLE), all patients received teriflunomide until up to 192 weeks after randomization. pNfL was measured using single-molecule array assay (Simoa(®) NF-light(™)). RESULTS: Baseline mean age was 14.5 years; 69.4% were female. Baseline geometric least square mean pNfL levels were similar for teriflunomide (n = 78) and placebo (n = 33) patients (19.83 vs 18.30 pg/mL). Over the combined DB and OLE periods, pNfL values were lower for teriflunomide versus placebo (analysis of variance p < 0.01; Week 192: 10.61 vs 17.32 pg/mL). Observed between-group pNfL differences were attenuated upon adjustment for gadolinium (Gd)-enhancing or new/enlarged T2 lesion counts at DB Week 24. Higher baseline pNfL levels were associated with shorter time since first MS symptom onset, higher baseline Gd-enhancing lesion counts and T2 lesion volume, and increased hazard of high magnetic resonance imaging activity or clinical relapse during the DB period. CONCLUSION: Teriflunomide treatment was associated with significantly reduced pNfL levels in children with RMS. CLINICALTRIALS.GOV IDENTIFIER: NCT02201108.
 Multiple sclerosis (MS) is a clinically heterogenous disease. Currently, we cannot identify patients with more active disease who may potentially benefit from earlier interventions. Previous data from our lab identified the CXCL13 index (I(CXCL13)), a measure of intrathecal production of CXCL13, as a potential biomarker to predict future disease activity in MS patients two years after diagnosis. Patients with clinically isolated syndrome (CIS) or radiologically isolated syndrome (RIS) underwent a lumbar puncture and blood draw, and the I(CXCL13) was determined. They were then followed for at least 5 years for MS activity. Patients with high I(CXCL13) were more likely to convert to clinically definite MS (82.4%) compared to those with low I(CXCL13) (10.0%). The data presented below demonstrate that this predictive ability holds true in CIS and RIS patients, and for at least five years compared to our initial two-year follow-up study. These data support the concept that I(CXCL13) has the potential to be used to guide immunomodulatory therapy in MS.
 WHAT IS THIS SUMMARY ABOUT? This is a summary of an article originally published in the Multiple Sclerosis Journal. Cladribine tablets (MAVENCLAD(®)) are an oral (taken by mouth) medication, approved for the treatment of people with relapsing forms of multiple sclerosis (MS, with episodes of new or worsening symptoms). They are administered for a maximum of 10 days per year, over a period of 2 years. Cladribine tablets work by temporarily reducing the number of lymphocytes, which are immune cells that help to fight off infections. Because of this, people with MS (also called PwMS) may have concerns about the effect of cladribine tablets on vaccines, as these work via immune cells to build protection against infection. WHAT HAPPENED IN THE MAGNIFY-MS STUDY? A study called MAGNIFY-MS investigated how long it takes for cladribine tablets to begin to work in people with a type of MS called highly active relapsing MS. During the study, some participants received their usual vaccinations against flu (influenza) and against the chickenpox virus (also called varicella zoster virus) as part of their routine medical care. The MAGNIFY-MS study gave the researchers an opportunity to look at how cladribine tablets affect the way the flu and chickenpox virus vaccines work in the body. WHAT WERE THE RESULTS? Cladribine tablets do not affect how well the body responds to flu and chickenpox vaccines. WHAT DO THE RESULTS MEAN? PwMS taking cladribine tablets who are vaccinated against chickenpox, flu or both can be protected against these diseases.
 In the emerging context of gut-brain control of multiple sclerosis (MS), developing therapeutics targeting proinflammatory proteins controlling the gut-brain immunomodulation is welcoming. One such immunomodulator is glia maturation factor-β (GMF-β). GMF-β activation following GMF-β-ser-83 phosphorylation upregulates proinflammatory responses and exacerbates experimental autoimmune encephalomyelitis (EAE). Notably, GMF-β(-/-) mice exhibited no EAE symptoms. Thus, we identified 1H-indazole-4-yl-methanol (GMFBI.1) inhibitor which blocked GMF-β-ser-83 phosphorylation critical in EAE suppression. To establish gut GMF-β's role in EAE in the context of gut-brain involvement in neurodegenerative diseases, we altered gut GMFBI.1 bioavailability as an index of EAE suppression. At first, we identified Miglyol 812N as a suitable biocompatible GMFBI.1 carrier compared to other FDA-approved carriers using in silico molecular docking analysis. GMFBI.1 administration in Miglyol 812N enhanced its retention/brain permeability. Subsequently, we administered GMFBI.1-Miglyol 812N by subcutaneous/oral routes at different doses with differential GMFBI.1 bioavailability in gut and brain to assess the role of local GMFBI.1 bioavailability in EAE reversal by a pharmacokinetic approach. Deprival of gut GMFBI.1 bioavailability led to partial EAE suppression despite having sufficient GMFBI.1 in circulation to inhibit brain GMF-β activity. Restoration of gut GMFBI.1 bioavailability led to complete EAE reversal. Molecular pathology behind partial/full EAE reversal was associated with differential GMF-β-Ser-83 phosphorylation/GM-CSF expression levels in enteric glial cells owing to GMFBI.1 bioavailability. In addition, we observed leaky gut reversal, tight junction protein ZO-1 restoration, beneficial gut microbiome repopulation, recovery from gut dysbiosis, and upregulation of Treg cells. GMFBI.1's dual gut/brain targeting of GMF-β has therapeutical/translational potential in controlling autoimmunity in MS.
 BACKGROUND: Gait imbalance is one of the frequent complications in subjects with multiple sclerosis (MS). Fampridine (4-aminopyridine) is a potassium-channel blocker that is administered for gait imbalance in MS. Different studies showed the effects of fampridine on gait status based on various tests in subjects with MS. Some showed significant improvement after treatment, and others did not. So, we designed this systematic review, and meta-analysis to estimate the pooled effects of fampridine on gait status in patients with MS. METHODS: The main goal is the evaluation of times of different gait test pre and post fampridine treatment. Two independent expert researchers conducted a systematic and comprehensive search in PubMed, Scopus, EMBASE, Web of Science, and Google Scholar and also gray literature, including references of the references and conference abstracts. The search was done on September 16, 2022. Before-after studies trials reporting scores of the walking tests. We extracted data regarding the total number of participants, first author, publication year, country of origin, mean age, Expanded Disability Status Scale (EDSS), and the results of walking tests. RESULTS: The literature search revealed 1963 studies; after deleting duplicates, 1098 studies remained. Seventy-seven full texts were evaluated. Finally, 18 studies were included for meta-analysis, while most of them were not placebo-controlled trials. The most frequent country of origin was Germany, and the mean age and EDSS ranged between 44 and 56 years and 4 and 6, respectively. The studies were published between 2013 and 2019. The pooled standardized mean difference (SMD) (after-before) of the MS Walking Scale (MSWS-12) was - 1.97 (95%CI: - 1.7, - 1.03) (I(2) = 93.1%, P < 0.001). The pooled SMD (after-before) of the six-minute walk test (6MWT) was 0.49 (95%CI: 0.22, - 0.76) (I(2) = 0%, P = 0.7). The pooled SMD (after-before) of T Timed 25-Foot Walk (T25FW) was - 0.99(95%CI: - 1.52, - 0.47) (I(2) = 97.5%, P < 0.001). CONCLUSION: This systematic review and meta-analysis show that fampridine improves gait imbalance in patients with MS.
 BACKGROUND AND PURPOSE: Data on pregnancy outcomes following fetal exposure to disease-modifying drugs (DMDs) in women with multiple sclerosis (MS) are sparse although growing. METHODS: Data from the Danish Multiple Sclerosis Registry were linked with nationwide registries enabling an investigation of adverse pregnancy outcomes in newborns of women with MS following fetal exposure to injectable first-line treatments, dimethyl fumarate, glatiramer acetate, or natalizumab. Logistic regression models accounting for clustered data were used to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for individual and composite adverse outcomes after adjusting for relevant covariates. RESULTS: A total of 1009 DMD-exposed pregnancies were compared with 1073 DMD-unexposed pregnancies as well as 91,112 pregnancies from the general population. No association of an increased risk of any perinatal outcome was found when comparing newborns with fetal exposure with the general population, including preterm birth (OR = 1.19, 95% CI = 0.86-1.64), small for gestational age (OR = 1.38, 95% CI = 0.92-2.07), spontaneous abortion (OR = 1.04, 95% CI = 0.84-1.27), congenital malformation (OR = 0.99, 95% CI = 0.68-1.45), low Apgar score (OR = 0.62, 95% CI = 0.23-1.65), stillbirth (OR = 1.05, 95% CI = 0.33-3.31), placenta complication (OR = 0.53, 95% CI = 0.22-1.27), and any adverse event (OR = 1.10, 95% CI = 0.93-1.30). Similar results were found when comparing DMD-exposed pregnancies with DMD-unexposed pregnancies. CONCLUSIONS: We found no increased association of adverse pregnancy outcomes in newborns with fetal exposure to DMDs when compared with either DMD-unexposed pregnancies or the general population.
 Background and Objectives: Multiple sclerosis (MS) is a widely spread and debilitating disease with 2.8 million people worldwide currently affected. However, the exact pathogenesis of the disease and its progression remains incompletely understood. According to the revised McDonald criteria, cerebrospinal fluid oligoclonal bands (CSF OCBs) magnetic resonance imaging (MRI) results, in conjunction with clinical presentation, remain the gold standard of MS diagnostics. Therefore, this study aims to evaluate the association between CSF OCB status and features of radiological and clinical findings in patients with multiple sclerosis in Lithuania. Materials and Methods: The selection of 200 MS patients was performed in order to find associations between CSF OCB status, MRI data and various disease features. The data were acquired from outpatient records and a retrospective analysis was performed. Results: OCB positive patients were diagnosed with MS earlier and had spinal cord lesions more frequently than OCB negative patients. Patients with lesions in the corpus callosum had a greater increase in the Expanded Disability Status Scale (EDSS) score between their first and last visit. Patients with brainstem lesions had higher EDSS scores during their first and last visit. Even so, the progression of the EDSS score was not greater. The time between the first symptoms and diagnosis was shorter for patients who had juxtacortical lesions than patients who did not. Conclusions: CSF OCBs and MRI data remain irreplaceable tools when diagnosing multiple sclerosis as well as prognosing the development of the disease and disability.
 Vitamin D (VD) is the most discussed antioxidant supplement for multiple sclerosis (MS) patients and many studies suggest correlations between a low VD serum level and onset and progression of the disease. While many studies in animals as well as clinical studies focused on the role of VD in the relapsing-remitting MS, knowledge is rather sparse for the progressive phase of the disease and the development of cortical pathology. In this study, we used our established rat model of cortical inflammatory demyelination, resembling features seen in late progressive MS, to address the question about whether VD could have positive effects on reducing cortical pathology, oxidative stress, and neurofilament light chain (NfL) serum levels. For this purpose, we used male Dark Agouti (DA) rats, with one group being supplemented with VD (400 IE per week; VD(+)) from the weaning on at age three weeks; the other group received standard rodent food. The rat brains were assessed using immunohistochemical markers against demyelination, microglial activation, apoptosis, neurons, neurofilament, and reactive astrocytes. To evaluate the effect of VD on oxidative stress and the antioxidant capacity, we used two different oxidized lipid markers (anti- Cu(++) and HOCl oxidized LDL antibodies) along with colorimetric methods for protective polyphenols (PP) and total antioxidative capacity (TAC). NfL serum levels of VD(+) and VD(-) animals were analyzed by fourth generation single-molecule array (SIMOA) analysis. We found significant differences between the VD(+) and VD(-) animals both in histopathology as well as in all serum markers. Myelin loss and microglial activation is lower in VD(+) animals and the number of apoptotic cells is significantly reduced with a higher neuronal survival. VD(+) animals show significantly lower NfL serum levels, a higher TAC, and more PP. Additionally, there is a significant reduction of oxidized lipid markers in animals under VD supplementation. Our data thus show a positive effect of VD on cellular features of cortical pathology in our animal model, presumably due to protection against reactive oxygen species. In this study, VD enhanced remyelination and prevented neuroaxonal and oxidative damage, such as demyelination and neurodegeneration. However, more studies on VD dose relations are required to establish an optimal response while avoiding overdosing.

 People identified with Black/African American or Hispanic/Latinx ethnicity are more likely to exhibit a more severe multiple sclerosis disease course relative to those who identify as White. While social determinants of health account for some of this discordant severity, investigation into contributing immunobiology remains sparse. The limited immunologic data stands in stark contrast to the volume of clinical studies describing ethnicity-associated discordant presentation, and to advancement made in our understanding of MS immunopathogenesis over the past several decades. In this perspective, we posit that humoral immune responses offer a promising avenue to better understand underpinnings of discordant MS severity among Black/African American, and Hispanic/Latinx-identifying patients.
 BACKGROUND AND OBJECTIVES: In the past decade, autologous hematopoietic stem cell transplantation (AHSCT) has emerged as a treatment for relapsing-remitting multiple sclerosis (RRMS). How this procedure affects biomarkers of B- and T-cell activation is currently unknown. The objective of this study was to investigate CXCL13 and sCD27 concentrations in CSF before and after AHSCT. METHODS: This prospective cohort study was conducted at a specialized MS clinic in a university hospital. Patients with a diagnosis of RRMS, treated with AHSCT between January 1, 2011, and December 31, 2018, were evaluated for participation. Patients were included if CSF samples from baseline plus at least 1 follow-up were available on June 30, 2020. A control group of volunteers without neurologic disease was included as a reference. CSF concentrations of CXCL13 and sCD27 were measured with ELISA. RESULTS: The study comprised 29 women and 16 men with RRMS, aged 19-46 years at baseline, and 15 women and 17 men, aged 18-48 years, in the control group. At baseline, patients had higher CXCL13 and sCD27 concentrations than controls, with a median (IQR) of 4 (4-19) vs 4 (4-4) pg/mL (p < 0.0001) for CXCL13 and 352 (118-530) vs 63 (63-63) pg/mL (p < 0.0001) for sCD27. After AHSCT, the CSF concentrations of CXCL13 were considerably lower at the first follow-up at 1 year than at baseline, with a median (IQR) of 4 (4-4) vs 4 (4-19) pg/mL (p < 0.0001), and then stable throughout follow-up. The CSF concentrations of sCD27 were also lower at 1 year than at baseline, with a median (IQR) of 143 (63-269) vs 354 (114-536) pg/mL (p < 0.0001). Thereafter, sCD27 concentrations continued to decrease and were lower at 2 years than at 1 year, with a median (IQR) of 120 (63-231) vs 183 (63-290) pg/mL (p = 0.017). DISCUSSION: After AHSCT for RRMS, CSF concentrations of CXCL13 were rapidly normalized, whereas sCD27 decreased gradually over the course of 2 years. Thereafter, the concentrations remained stable throughout follow-up, indicating that AHSCT induced long-lasting biological changes.
 BACKGROUND: The aim of this study was to evaluate how many MS patients treated with an approved DMD in routine care would have fulfilled the inclusion and exclusion criteria of phase III clinical trial and would therefore be eligible for the respective drug trial. Further, adverse events and disease progression for these patients were compared. METHODS: A comparison of patients fulfilling phase III clinical trial inclusion and exclusion criteria and those who do not with regard to sociodemographic and clinical characteristics, adverse events and disease progression. Database was the REGIMS register, a national, prospective, observational, clinical multicentre registry. 1248 MS Patients were included. RESULTS: 27.2% patients would have been eligible for inclusion into a phase III clinical trial of their indication. Patients who did not meet the criterion age are more likely to have a serious adverse event (SAE), whereas patients who did not fulfil the criterion relapse had a significant lower occurrence of an adverse event (AE). Non-fulfilment of other inclusion criteria (EDSS Score; medication history and MS type) did not show any significant differences in drug safety variables, AE and SAE. CONCLUSION: Our results suggest that a low transferability of phase III clinical trial criteria, to patients in routine care with the exception of age, does not imply a higher risk with regard to adverse and serious adverse events.
 Background: The Sensoready(®) pen is intended for self-administration of subcutaneous 20 mg ofatumumab at home. This human factors summative study assessed the usability of the Sensoready pen in relapsing multiple sclerosis patients. Methods: 32 patients (injection-experienced [n = 17] and injection-naive [n = 15]) across five locations in the USA were asked to complete two simulated injections using the Sensoready pen. Results: In the first and second simulated injections, 90.6 and 96.9% of patients, respectively, successfully delivered a full dose, while 81.3 and 84.4%, respectively, successfully performed the injection without any use errors. Conclusion: The Sensoready pen is safe and effective for its intended use by intended users and in the intended use environment. This pen has a low harm potential and high injection success rate in patients, even without prior training or experience.
 OBJECTIVE: Cognitive involvement in pediatric multiple sclerosis (MS) relative to adult MS is less defined. This study advances our understanding by measuring cognitive performances in pediatric MS, adult MS, and pediatric healthy controls. METHODS: Consecutive relapsing pediatric MS participants from the United States Network of Pediatric MS Centers were compared with pediatric healthy controls and adults with relapsing MS. Participants were compared on two screening batteries: the Brief International Cognitive Assessment for MS and the Cogstate Brief Battery. Results were transformed to age-normative z scores. RESULTS: The pediatric groups (MS vs. Healthy Controls) did not differ on either battery's composite mean score or individual test scores (ps > 0.32), nor in the proportions impaired on either battery, Brief International Cognitive Assessment for MS (26% vs. 24%, p = 0.83); Cogstate Brief Battery (26% vs. 32%, p = 0.41). The pediatric versus adult MS group even after controlling for differences in disease duration performed better on the Brief International Cognition Assessment for MS composite (p = 0.03), Symbol Digit Modalities Test (p = 0.02), Rey Auditory Verbal Learning Test (p = 0.01), and Cogstate choice reaction time (p < 0.001). CONCLUSION: Pediatric MS patients do not differ from healthy pediatric controls on cognitive screens but perform better than adults with MS.
 OBJECTIVES: Several studies indicated leukocyte telomere length (LTL) as a biomarker of multiple sclerosis (MS) evolution. This study aimed to investigate LTL in women with multiple sclerosis (MS) compared to that in healthy women (HW) across different reproductive phases, and to evaluate its relationship with MS activity. METHODS: Blood samples were collected from women with MS and HW during the fertile phase, pregnancy, and puerperium. LTL was determined using quantitative fluorescence in situ hybridization (Q-FISH). RESULTS: Blood samples from 68 women with MS (22 during fertile life, 23 during pregnancy, and 23 post-partum) and 52 HW (23 during fertile life, 20 during pregnancy, and 9 post-partum) were analyzed. During pregnancy, LTL in MS women and HW was 84.7 ± 10.5 and 77.6 ± 11.5, respectively (p < 0.005). Regression analysis showed that shorter LTL was associated with pregnancy in HW (p = 0.021); this relationship was not observed in MS women, for whom shorter LTL was related to a higher EDSS (p = 0.036). A longitudinal analysis was performed in eight MS women, showing LTL shortening from pregnancy to puerperium (p = 0.003), which was related to MS reactivation (p = 0.042). CONCLUSION: Our results highlight the possible associations between LTL, reproductive biological phases, and MS activity after delivery.
 OBJECTIVES: Heat sensitivity (HS) describes a temporary worsening of multiple sclerosis (MS) symptoms with increased body temperature. The pathophysiology may relate to central nervous system conduction deficits and autonomic dysfunction. We conducted deep clinical phenotyping of a cohort of persons with MS to identify predictors of HS. METHODS: We recruited 59 MS participants with HS or No HS. Participants self-reported symptom severity (Hospital Anxiety and Depression Scale, Multiple Sclerosis Impact Scale, and fatigue visual analog scale) and underwent maximal exercise and transcranial magnetic stimulation testing to characterize autonomic and corticospinal function. We examined associations with HS using binomial logistic regression. RESULTS: People with HS (36/59) had significantly greater disability, depression, fatigue, and physical and psychological functional effects of MS. They also had significantly lower corticospinal excitability but not conduction. After controlling for disease-modifying therapy (DMT), disability, and disease type, self-reported difficulty using hands in everyday tasks was significantly associated with a large increase in the odds of HS. Autonomic and corticospinal dysfunction were not associated with HS. Lack of DMT use alone was also associated with a large increase in the odds of HS. DISCUSSION: Following a comprehensive assessment of plausible contributors to HS, HS was most strongly associated with lack of a DMT prescription and self-reported hand dysfunction. Surprisingly, objective measurement of autonomic and corticospinal integrity did not contribute to HS.
 OBJECTIVES: Understanding distress and quality of life (QOL) is important in improving the lives of people with multiple sclerosis (MS), and investigating their antecedents is very important. The present study aimed to examine the role of multiple sclerosis self-efficacy and difficulties in emotion regulation in predicting distress and QOL in people with MS. Also, this study compared types of MS (RRMS, PPMS, and SPMS) in terms of MS self-efficacy, difficulties in emotion regulation, distress, and QOL. METHODS: This study included 122 people with three types of MS (RRMS=33, PPMS=62, and SPMS=25). Data were collected by the use of four scales: Quality of Life (QOL), Psychological Distress (DASS), Difficulties in Emotion Regulation (DERS), and Multiple Sclerosis Self-Efficacy (MSSE). Pearson's correlation, path analysis, MANOVA, and Tukey's post hoc test were used for data analysis. RESULTS: Findings indicated MS self-efficacy had negative and significant effects on difficulties in emotion regulation and distress and had a positive and significant effect on QOL. Difficulties in emotion regulation had a negative and significant effect on QOL and a positive and significant effect on distress. Also, the indirect effect (through difficulties in emotion regulation) of MS self-efficacy on distress and QOL was significant. In addition, the comparisons showed that differences between RRMS and SPMS in terms of MS self-efficacy and distress were significant. CONCLUSIONS: Self-efficacy and emotion regulation are key components in improving the life (reducing distress and increasing QOL) of people with MS, although it depends to some extent on the type of MS disease.
 BACKGROUND: Substantial evidence supports therapeutic exercise for improving health and function in people with multiple sclerosis (MS). However, few studies have considered the patients' perspective. OBJECTIVE: This study explored perspectives of adults with MS following participation in a 3-month clinic- and home-based exercise rehabilitation program. METHODS: Twenty participants with MS were interviewed using a semi-structured interview guide on the design and implementation processes of the exercise programs as well as any perceived facilitators or barriers to exercise. Data analysis was conducted using a thematic analysis approach to generate themes from the transcribed interviews. RESULTS: Key facilitators of exercise for people with MS included perceived improvements in physical health and function, activity participation, and psychosocial health. Mismatched level of exercise with their stage of post-diagnosis and/or functional ability and limited human interaction emerged as barriers to exercise. CONCLUSIONS: Participation in the exercise program was a positive experience for people with MS. Despite the provision of a high level of adaptation and tailored exercise plan and delivery, self-directed exercise continued to present challenges for people with MS. Additionally, the importance of seeking cost-effective ways to maintain motivational support was implicit in participant responses. The findings provided an improved understanding of personal experiences and exercise perspectives that can inform future intervention strategies aimed at promoting sustained exercise participation.
 BACKGROUND: Progressive multiple sclerosis (PMS) is a debilitating condition characterized by progressively worsening symptoms. Monoclonal antibodies are novel therapies for MS, but their safety and efficacy in the progressive form have not been comprehensively studied. In this systematic review, we aimed to evaluate the available evidence regarding monoclonal antibody treatment for PMS. METHODS: After registration of the study protocol in PROSPERO, we systematically searched three major databases for clinical trials involving monoclonal antibodies administration for PMS treatment. All the retrieved results were imported into the EndNote reference manager. After removing the duplicates, two independent researchers did the study selection and data extraction. The risk of bias was assessed using the Joanna Briggs Institute (JBI) checklist. RESULTS: Of the 1846 studies in the preliminary search, 13 clinical trials investigating monoclonal antibodies (Ocrelizumab, Natalizumab, Rituximab, and Alemtuzumab) in PMS patients were included. Ocrelizumab was significantly effective in reducing clinical disease progression measures in primary PMS patients. The results for Rituximab were not completely reassuring and only showed significant changes for some endpoints on MRI and clinical measures. Natalizumab decreased the relapse rate and improved MRI features for secondary PMS patients, but not clinical endpoints. The studies on Alemtuzumab treatment revealed conflicting outcomes, with improvements observed in MRI endpoints but clinical worsening in patients. Additionally, among the studied adverse events, upper respiratory infections, urinary tract infections, and nasopharyngitis were frequently reported. CONCLUSION: Based on our findings, Ocrelizumab is the most efficient monoclonal antibody for primary PMS, although it is associated with a higher risk of infection. While other monoclonal antibodies did not show significant promise in treating PMS, more research is necessary.
 A 28-year-old woman presented with subacute relapsing left-sided weakness. MRI demonstrated both enhancing C3-C6 and nonenhancing T2-T4 lesions. Initial provisional diagnosis was inflammatory/autoimmune. Her left-sided weakness progressed despite immunosuppressive therapies. We reassessed our original suspected diagnosis because of an atypical clinicoradiologic course, leading to biopsy and a definitive diagnosis.
 BACKGROUND: Detecting new and enlarged lesions in multiple sclerosis (MS) patients is needed to determine their disease activity. LeMan-PV is a software embedded in the scanner reconstruction system of one vendor, which automatically assesses new and enlarged white matter lesions (NELs) in the follow-up of MS patients; however, multicenter validation studies are lacking. PURPOSE: To assess the accuracy of LeMan-PV for the longitudinal detection NEL white-matter MS lesions in a multicenter clinical setting. STUDY TYPE: Retrospective, longitudinal. SUBJECTS: A total of 206 patients with a definitive MS diagnosis and at least two follow-up MRI studies from five centers participating in the Swiss Multiple Sclerosis Cohort study. Mean age at first follow-up = 45.2 years (range: 36.9-52.8 years); 70 males. FIELD STRENGTH/SEQUENCE: Fluid attenuated inversion recovery (FLAIR) and T1-weighted magnetization prepared rapid gradient echo (T1-MPRAGE) sequences at 1.5 T and 3 T. ASSESSMENT: The study included 313 MRI pairs of datasets. Data were analyzed with LeMan-PV and compared with a manual "reference standard" provided by a neuroradiologist. A second rater (neurologist) performed the same analysis in a subset of MRI pairs to evaluate the rating-accuracy. The Sensitivity (Se), Specificity (Sp), Accuracy (Acc), F1-score, lesion-wise False-Positive-Rate (aFPR), and other measures were used to assess LeMan-PV performance for the detection of NEL at 1.5 T and 3 T. The performance was also evaluated in the subgroup of 123 MRI pairs at 3 T. STATISTICAL TESTS: Intraclass correlation coefficient (ICC) and Cohen's kappa (CK) were used to evaluate the agreement between readers. RESULTS: The interreader agreement was high for detecting new lesions (ICC = 0.97, Pvalue < 10(-20) , CK = 0.82, P value = 0) and good (ICC = 0.75, P value < 10(-12) , CK = 0.68, P value = 0) for detecting enlarged lesions. Across all centers, scanner field strengths (1.5 T, 3 T), and for NEL, LeMan-PV achieved: Acc = 61%, Se = 65%, Sp = 60%, F1-score = 0.44, aFPR = 1.31. When both follow-ups were acquired at 3 T, LeMan-PV accuracy was higher (Acc = 66%, Se = 66%, Sp = 66%, F1-score = 0.28, aFPR = 3.03). DATA CONCLUSION: In this multicenter study using clinical data settings acquired at 1.5 T and 3 T, and variations in MRI protocols, LeMan-PV showed similar sensitivity in detecting NEL with respect to other recent 3 T multicentric studies based on neural networks. While LeMan-PV performance is not optimal, its main advantage is that it provides automated clinical decision support integrated into the radiological-routine flow. EVIDENCE LEVEL: 4 TECHNICAL EFFICACY: Stage 2.
 BACKGROUND: Identifying the meaningful goals of people with multiple sclerosis (PwMS) can facilitate tailored treatment plans. OBJECTIVES: To describe and compare the goals set by PwMS during two interventions, and explore the strategies used to meet their goals, the barriers and facilitators influencing goal achievement. METHODS: Data from 56 community-dwelling PwMS were used in this secondary analysis: 45 used an interactive fatigue self-management website (MS INFoRm), and 11 received MS INFoRm coupled with occupational performance coaching (OPC) for 3 months. The International Classification of Functioning, Disability and Health (ICF) was used to map and compare the goals, strategies, facilitators and obstacles to goal achievement between the groups. Goals were also evaluated for being Specific, Measurable, Attainable, Relevant and Timely (SMART). RESULTS: Most goals were related to 'looking after one's health' (n = 35) and 'recreation and leisure' (n = 17). Participants who received OPC set more SMART goals (75 vs. 24%, p < 0.01). Fatigue management strategies were identified. Personal and environmental factors were found as facilitators and obstacles to goal achievement. CONCLUSION AND SIGNIFICANCE: Coaching can help PwMS with goal setting, and to adapt strategies to achieve their goals. Increased awareness of goals set by PwMS may equip clinicians to better assess their clients' needs.
 Multiple sclerosis (MS) is a chronic, inflammatory, and degenerative disease of the central nervous system (CNS). Inflammation is observed in all stages of MS, both within and around the lesions, and can have beneficial and detrimental effects on MS pathogenesis. A possible mechanism for the neuroprotective effect in MS involves the release of brain-derived neurotrophic factor (BDNF) by immune cells in peripheral blood and inflammatory lesions, as well as by microglia and astrocytes within the CNS. BDNF is a neurotrophic factor that plays a key role in neuroplasticity and neuronal survival. This review aims to analyze the current understanding of the role that inflammation plays in MS, including the factors that contribute to both beneficial and detrimental effects. Additionally, it explores the potential role of BDNF in MS, as it may modulate neuroinflammation and provide neuroprotection. By obtaining a deeper understanding of the intricate relationship between inflammation and BDNF, new therapeutic strategies for MS may be developed.
 BACKGROUND AND PURPOSE: People with multiple sclerosis (MS) suffer from higher infection-related mortality compared to the general population; however, sparse data are available on the increased risk of death associated with coronavirus disease 2019 (COVID-19) and other common types of infections. METHODS: All mortality records and multiple-cause-of-death data in 2010-2021 of residents in the Veneto region (northeastern Italy) were extracted. Mention of specific infections was compared between death certificates reporting MS or not. Odds ratios (OR) with 95% confidence intervals (95% CI) were estimated by conditional logistic regression matching by age, sex and calendar year. The bimonthly averages of MS-related deaths in 2010-2019 were compared with those registered during the pandemic (2020-2021). RESULTS: Of 580,015 deaths through 2010-2021, MS was mentioned in 850 cases (0.15%), 59.3% women. Influenza and pneumonia were reported in 18.4% of MS-related compared to 11.0% non-MS-related deaths (OR 2.72, 95% CI 2.28-3.25). The odds of mention of urinary tract infections was significantly greater in MS-related deaths of men (OR 8.16, 95% CI 5.23-12.7) than women (OR 3.03, 95% CI 1.82-5.02). Aspiration pneumonia, pressure ulcers/skin infections and sepsis were also significantly associated with MS-related deaths. Reporting of COVID-19 as a cause of death did not significantly differ between deaths with and without mention of MS (approximately 11% of both). However, compared to 2010-2019, peaks in MS-related deaths were observed during the pandemic waves. CONCLUSIONS: Infections continue to play a significant role in MS-related deaths, underlying the need to improve prevention and management strategies.
 OBJECTIVE: The present study aims to analyse the bidirectional hypothesis between stress and multiple sclerosis with several measures of stress, impairment and functionality, considering also the interaction role of stress-related psychosocial factors such as anxiety, coping and social support. METHODS: A one-year follow-up was conducted with 26 people with multiple sclerosis. Participants reported i) at baseline, anxiety (State-Trait Anxiety Inventory), and social support (Multidimensional Scale of Perceived Social Support); ii) daily, Ecological Momentary Assessment through self-reported diaries of stressful events and coping strategies; iii) monthly, the perceived stress (Perceived Stress Scale), iv) trimonthly, the self-reported functionality (Functionality Assessment in multiple sclerosis) and v) at baseline and at the end, neurologist rated impairment (Expanded Disability Status Scale). Mixed-effect regression models were conducted. RESULTS: The bidirectional hypothesis was confirmed with perceived stress and self-reported functionality, which were negatively related in both directions. Coping and anxiety showed an interaction effect: active coping increased functionality only with high levels of stress, and high-trait anxiety showed lower functionality whereas low-trait anxiety showed higher functionality but only with low stress levels. CONCLUSION: People with multiple sclerosis may benefit from different types of psychological therapies, from gold-standard therapies like Cognitive Behavioural Therapy to third-waves therapies like Dialectical Behaviour Therapy or mindfulness, that focus on dealing with stress and affective symptoms, adjusting to the disease, and to improving their overall quality of life. More research is needed in this field under the biopsychosocial model.

 BACKGROUND: Comorbid conditions, particularly vascular comorbidity, are common in MS and may hasten the CNS damage and disease manifestations. We undertook a preliminary examination of the association between blood pressure (BP) and cognitive function in samples of older adults with MS and healthy controls. METHODS: Older adults with MS (n = 29) and healthy controls (n = 29) completed the Brief International Cognitive Assessment for MS (BICAMS) battery and underwent assessment of BP. The data were analyzed using the Baron and Kenny approach for examining blood pressure as an explanatory variable for group differences in cognition. RESULTS: The MS group, as expected, had significantly lower California Verbal Learning Test-II (CVLT-II) z-scores from the BICAMS and higher diastolic BP (DBP) than healthy controls. DBP had statistically significant correlations with CVLT-II z-scores in the overall sample (r =  - .42) and MS subsample (r =  - .51), but not healthy controls(r =  - .29); the correlation was not attenuated when controlling for age and disability status in the MS subsample (pr =  - .48). Group initially explained 6% of the variance in z-scores from the CVLT-II (β =  - 0.24). The inclusion of DBP accounted for an additional 14% of the variance in z-scores from the CVLT-II, and DBP(β =  - 0.39), but not group (β =  - 0.13), was a significant correlate of CVLT-II z-scores; the results were unchanged when controlling for anxiety and depression scores. CONCLUSION: Our results provide preliminary, cross-sectional support for future population-based research examining DBP, hypertension, and verbal memory in older adults with MS.
 BACKGROUND AND PURPOSE: Multiple sclerosis (MS) is associated with abnormal B-cell function, and MS genetic risk alleles affect multiple genes that are expressed in B cells. However, how these genetic variants impact the B-cell compartment in early childhood is unclear. In the current study, we aim to assess whether polygenic risk scores (PRSs) for MS are associated with changes in the blood B-cell compartment in children from the general population. METHODS: Six-year-old children from the population-based Generation R Study were included. Genotype data were used to calculate MS-PRSs and B-cell subset-enriched MS-PRSs, established by designating risk loci based on expression and function. Analyses of variance were performed to examine the effect of MS-PRSs on total B-cell numbers (n = 1261) as well as naive and memory subsets (n = 675). RESULTS: After correction for multiple testing, no significant associations were observed between MS-PRSs and total B-cell numbers and frequencies of subsets therein. A naive B-cell-MS-PRS (n = 26 variants) was significantly associated with lower relative, but not absolute, naive B-cell numbers (p = 1.03 × 10(-4) and p = 0.82, respectively), and higher frequencies and absolute numbers of CD27(+) memory B cells (p = 8.83 × 10(-4) and p = 4.89 × 10(-3) , respectively). These associations remained significant after adjustment for Epstein-Barr virus seropositivity and the HLA-DRB1*15:01 genotype. CONCLUSIONS: The composition of the blood B-cell compartment is associated with specific naive B-cell-associated MS risk variants during childhood, possibly contributing to MS pathophysiology later in life. Cell subset-specific PRSs may offer a more sensitive tool to define the impact of genetic risk on the immune system in diseases such as MS.
 BACKGROUND: The 30-Second Sit-To-Stand (30SSTS) is a quick, inexpensive, safe, and widely used clinical measure of lower extremity function. To date, there is limited evidence regarding the use of 30SSTS in multiple sclerosis (MS). The purpose of this study was to examine the construct validity of the 30SSTS test in persons with MS compared with non-MS healthy controls. METHODS: Twenty ambulatory persons with MS and twenty age- and sex-matched healthy controls completed the 30SSTS, Timed 25-Foot Walk (T25FW), Timed Up and Go (TUG), Six-Minute Walk (6MW), and Godin Leisure-Time Exercise Questionnaire (GLTEQ). Persons with MS also completed the Patient Determined Disease Steps (PDDS) and 12-item MS Walking Scale (MSWS-12). RESULTS: Persons with MS had significantly worse performance on the TUG (mean difference [95% confidence interval] = 1.4 [0.5, 2.3] sec) and 6MW (-259.2 [-450.8, -67.6] ft), but not on the 30SSTS (-1.6 [-1.5, 4.6] reps) and T25FW (-0.59 [-0.1, 1.2] ft/sec) compared with controls. There were significant moderate-to-strong correlations between the 30SSTS with T25FW, TUG, and 6MW scores in persons with MS (r = 0.48, -0.65 and 0.61, respectively), whereas the 30SSTS was only significantly associated with 6MW scores (r = 0.43) in controls. The 30SSTS was negatively associated with MS-related walking disability assessed by the PDDS and MSWS-12 (r(s) = -0.52 and -0.64, respectively), but was not significantly associated with the GLTEQ in MS and controls (r = 0.30 and 0.17, respectively). CONCLUSION: This study provides initial support for the construct validity of the 30SSTS as a measure of lower extremity function in persons with MS. Our findings warrant the inclusion of the 30SSTS as a feasible and valid measure of physical function in clinical research and practice involving persons with MS.
 Inflammatory demyelinating diseases (IDDs) are among the main causes of inflammatory and neurodegenerative injury of the central nervous system (CNS) in young adult patients. Of these, multiple sclerosis (MS) is the most frequent and studied, as it affects about a million people in the USA alone. The understanding of the mechanisms underlying their pathology has been advancing, although there are still no highly effective disease-modifying treatments for the progressive symptoms and disability in the late stages of disease. Among these mechanisms, the action of glial cells upon lesion and regeneration has become a prominent research topic, helped not only by the discovery of glia as targets of autoantibodies, but also by their role on CNS homeostasis and neuroinflammation. In the present article, we discuss the participation of glial cells in IDDs, as well as their association with demyelination and synaptic dysfunction throughout the course of the disease and in experimental models, with a focus on MS phenotypes. Further, we discuss the involvement of microglia and astrocytes in lesion formation and organization, remyelination, synaptic induction and pruning through different signaling pathways. We argue that evidence of the several glia-mediated mechanisms in the course of CNS demyelinating diseases supports glial cells as viable targets for therapy development.
 Multiple sclerosis (MS) is a progressive inflammatory neurodegenerative disease of the nervous system accompanied by demyelination. MS-associated cognitive impairments mainly involve recent memory, information processing speed, stable memory, and executive function. Moreover, MS is associated with impaired glucose and insulin metabolism, which can exacerbate cognitive decline. The present study aimed to compare the cognitive status of MS patients with and without insulin resistance. In this cross-sectional study, 74 relapsing-remitting multiple sclerosis diagnosed patients were enrolled. Indicators of insulin resistance, including fasting blood glucose, insulin level, and homeostatic model assessment of insulin resistance (HOMA-IR) index, were measured. They were then divided into two groups based on the results of the HOMA-IR index. Cognition status was evaluated by the minimal assessment of cognitive function in multiple sclerosis battery. The prevalence of insulin resistance was 37.8%, and the prevalence of cognitive decline was estimated to be 67.56%. Mean scores of the California verbal learning test (CVLT), CVLT delayed free recall, controlled oral word association test, and judgment of line orientation tests were significantly lower in MS patients with insulin resistance than without. In addition, a negative correlation was demonstrated between the results of the CVLT, CVLT delayed free recall, controlled oral word association test, judgment of line orientation tests, brief visuospatial memory test, and Delis-Kaplan executive function system sorting tests and fasting insulin levels. Greater verbal memory and spatial comprehension impairments were observed in MS patients with insulin resistance.
 INTRODUCTION: The incidence, prevalence and outcomes of multiple sclerosis (MS) are unclear in Indigenous Peoples (IP) who are more likely to be underrepresented in research. We completed a systematic review of MS in IP of the Americas. METHODS: A systematic review was conducted using PubMed, Web of Science, and Cochrane databases as well as references of retrieved papers. Inclusion criteria were: peer-reviewed publications (January 1990- December 2021), incidence, prevalence, or clinical outcome measures of MS in self-identified IP in the Americas. Incidence, prevalence, morbidity and mortality data were summarized and stratified by location and year of publication. Study quality was evaluated by risk of bias or confounding. RESULTS: Out of 416 titles, thirteen studies met inclusion criteria. Four studies evaluated incidence, seven prevalence, three clinical outcomes and one mortality. Most studies were completed in Canada or the United States (US). Incidence rates per 100,000 ranged from 0.48 (in US Indian Health Service records) to 8.15 (First Nations Manitoban Canadians). Prevalence ranged from 0 (Lacandonian Mexicans and Panamanians) to 188.5 (First Nations Manitoban Canadians). Incidence and prevalence are consistently lower in IP than comparator White populations. IP with MS were reported to have higher disability and faster disability progression than non-Indigenous comparators. MS-related mortality is low compared to White people. CONCLUSION: There is an absence of high-quality studies evaluating MS in IP. Available evidence indicates low, but increasing incidence and prevalence of MS in IP of the Americas. IP with MS may have worse disability than non-Indigenous comparators. Future studies should evaluate the factors influencing the increases in incidence and prevalence as well as better characterize possible disparities in MS care among IP.
 Cerebral energy deficiency is increasingly recognised as an important feature of multiple sclerosis (MS). Until now, we have lacked non-invasive imaging methods to quantify energy utilisation and mitochondrial function in the human brain. Here, we used novel dual-calibrated functional magnetic resonance imaging (dc-fMRI) to map grey-matter (GM) deoxy-haemoglobin sensitive cerebral blood volume (CBV(dHb)), cerebral blood flow (CBF), oxygen extraction fraction (OEF), and cerebral metabolic rate of oxygen consumption (CMRO(2)) in patients with MS (PwMS) and age/sex matched controls. By integrating a flow-diffusion model of oxygen transport, we evaluated the effective oxygen diffusivity of the capillary network (D(C)) and the partial pressure of oxygen at the mitochondria (PmO(2)). Significant between-group differences were observed as decreased CBF (p = 0.010), CMRO(2) (p < 0.001) and D(C) (p = 0.002), and increased PmO(2) (p = 0.043) in patients compared to controls. No significant differences were observed for CBV(dHb) (p = 0.389), OEF (p = 0.358), or GM volume (p = 0.302). Regional analysis showed widespread reductions in CMRO(2) and D(C) for PwMS. Our findings may be indicative of reduced oxygen demand or utilisation in the MS brain and mitochondrial dysfunction. Our results suggest changes in brain physiology may precede MRI-detectable GM loss and may contribute to disease progression and neurodegeneration.
 BACKGROUND: Although the use of Virtual Reality (VR) has received increasing interest as an add-on treatment in neurorehabilitation programs in the last fifteen years, there is scarce information about the effectiveness of fully immersive VR-based treatments on upper limb (UL) motor function in people with Multiple Sclerosis (PwMS). METHODS: In this bicentric 2-period interventional crossover study, 19 PwMS with moderate to severe disability (mean EDSS score 5.5) and relevant UL impairment underwent 12 immersive-VR sessions over a period of 4 weeks, using commercially available VR platform (Oculus Quest) and games (Fruit Ninja, Beat Saber and Creed - Rise to Glory). Possible changes associated with the treatment were objectively assessed through instrumental kinematic analysis of the "hand-to-mouth" (HTM) movement by means of optical motion capture system. Clinical tests to assess gross and fine manual dexterity (i.e., the Box and Blocks and Nine Hole Peg Test) were also administered. RESULTS: The results of the kinematic analysis suggest that the VR training positively impacted the ability of the tested PwMS to perform the HTM task. In particular, a significant reduction of the overall time required to complete the task of approximately 20% for both most and least affected limb, and an improved degree of precision and stability of the movement, as indicated by the reduced value of adjusting sway, especially for the most affected limb (-60%). CONCLUSION: Based on the results of the quantitative analysis, a 4-week treatment with immersive VR is able to improve speed and stability of the HTM movement in PwMS. This suggests that such an approach might be considered suitable to facilitate an immediate transfer of the possible positive effects associated with the training to common activities of daily living.
 OBJECTIVE: Teriflunomide is an oral medication approved for the treatment of patients with multiple sclerosis. The primary effect of teriflunomide is to reduce de novo pyrimidine synthesis by inhibiting mitochondrial dihydroorotate dehydrogenase, thereby causing cell-cycle arrest. We aimed to investigate the occurrence of peripheral neuropathy, a rare side effect of teriflunomide, in patients receiving teriflunomide. METHODS: Multiple sclerosis patients receiving teriflunomide (n=42) or other disease modifying therapies (n=18) and healthy controls (n=25) were enrolled in this cross-sectional study between January 2020 and 2021. The mean duration of teriflunomide treatment was 26 months (ranging from 6 to 54 months). All participants underwent neurological examination and nerve conduction studies of tibial, peroneal, sural, superficial peroneal, median, and ulnar nerves by using surface recording bar and bipolar stimulating electrodes. RESULTS: The mean superficial peroneal nerve distal latency and conduction velocity were significantly slower, and the mean superficial peroneal nerve action potential amplitude was lower in patients using teriflunomide (2.50 ms, p<0.001; 47.35 m/s, p=0.030; and 11.05 μV, p<0.001, respectively). The mean peroneal motor nerve distal latency was significantly longer and amplitude was lower in teriflunomide patients (3.68 ms, p<0.001, and 5.25 mV, p=0.009, respectively). During the study period, treatment switching to another disease-modifying therapy was planned in 10 patients, and all neuropathic complaints were reversed after switching. CONCLUSION: Teriflunomide has the potential to cause peripheral neuropathy. The awareness of peripheral neuropathy, questioning the symptoms, and if suspected, evaluation with electromyography and switching the therapy in patients under teriflunomide treatment are crucial.
 BACKGROUND: Early risk-stratification in multiple sclerosis (MS) may impact treatment decisions. Current predictive models have identified that clinical and imaging characteristics of aggressive disease are associated with worse long-term outcomes. Serum biomarkers, neurofilament (sNfL) and glial fibrillary acidic protein (sGFAP), reflect subclinical disease activity through separate pathological processes and may contribute to predictive models of clinical and MRI outcomes. METHODS: We conducted a retrospective analysis of the Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital (CLIMB study), where patients with multiple sclerosis are seen every 6 months and undergo Expanded Disability Status Scale (EDSS) assessment, have annual brain MRI scans where volumetric analysis is conducted to calculate T2-lesion volume (T2LV) and brain parenchymal fraction (BPF), and donate a yearly blood sample for subsequent analysis. We included patients with newly diagnosed relapsing-remitting MS and serum samples obtained at baseline visit and 1-year follow-up (both within 3 years of onset), and were assessed at 10-year follow-up. We measured sNfL and sGFAP by single molecule array at baseline visit and at 1-year follow-up. A predictive clinical model was developed using age, sex, Expanded Disability Status Scale (EDSS), pyramidal signs, relapse rate, and spinal cord lesions at first visit. The main outcome was odds of developing of secondary progressive (SP)MS at year 10. Secondary outcomes included 10-year EDSS, brain T2LV and BPF. We compared the goodness-of-fit of the predictive clinical model with and without sNfL and sGFAP at baseline and 1-year follow-up, for each outcome by area under the receiver operating characteristic curve (AUC) or R-squared. RESULTS: A total 144 patients with median MS onset at age 37.4 years (interquartile range: 29.4-45.4), 64% female, were included. SPMS developed in 25 (17.4%) patients. The AUC for the predictive clinical model without biomarker data was 0.73, which improved to 0.77 when both sNfL and sGFAP were included in the model (P = 0.021). In this model, higher baseline sGFAP associated with developing SPMS (OR=3.3 [95%CI:1.1,10.6], P = 0.04). Adding 1-year follow-up biomarker levels further improved the model fit (AUC = 0.79) but this change was not statistically significant (P = 0.15). Adding baseline biomarker data also improved the R-squared of clinical models for 10-year EDSS from 0.24 to 0.28 (P = 0.032), while additional 1-year follow-up levels did not. Baseline sGFAP was associated with 10-year EDSS (ß=0.58 [95%CI:0.00,1.16], P = 0.05). For MRI outcomes, baseline biomarker levels improved R-squared for T2LV from 0.12 to 0.27 (P<0.001), and BPF from 0.15 to 0.20 (P = 0.042). Adding 1-year follow-up biomarker data further improved T2LV to 0.33 (P = 0.0065) and BPF to 0.23 (P = 0.048). Baseline sNfL was associated with T2LV (ß=0.34 [95%CI:0.21,0.48], P<0.001) and 1-year follow-up sNfL with BPF (ß=-2.53% [95%CI:-4.18,-0.89], P = 0.003). CONCLUSIONS: Early biomarker levels modestly improve predictive models containing clinical and MRI variables. Worse clinical outcomes, SPMS and EDSS, are associated with higher sGFAP levels and worse MRI outcomes, T2LV and BPF, are associated with higher sNfL levels. Prospective study implementing these predictive models into clinical practice are needed to determine if early biomarker levels meaningfully impact clinical practice.
 Antigen-specific therapies allow for modulation of the immune system in a disease relevant context without systemic immune suppression. These therapies are especially valuable in autoimmune diseases such as multiple sclerosis (MS), where autoreactive T cells destroy myelin sheath. This work shows that an antigen-specific dual-sized microparticle (dMP) system can effectively halt and reverse disease progression in a mouse model of MS. Current MS treatments leave patients immunocompromised, but the dMP formulation spares the immune system as mice can successfully clear a Listeria Monocytogenes infection. Furthermore, we highlight design principles for particle based immunotherapies including the importance of delivering factors specific for immune cell recruitment (GM-CSF or SDF-1), differentiation (GM-CSF or FLT3L) and suppression (TGF-β or VD3) in conjunction with disease relevant antigen, as the entire formulation is required for maximum efficacy. Lastly, the dMP scheme relies on formulating phagocytosable and non-phagocytosable MP sizes to direct payload to target either cell surface receptors or intracellular targets, as the reverse sized dMP formulation failed to reverse paralysis. We also challenge the design principles of the dMP system showing that the size of the MPs impact efficacy and that GM-CSF plays two distinct roles and that both of these must be replaced to match the primary effect of the dMP system. Overall, this work shows the versatile nature of the dMP system and expands the knowledge in particle science by emphasizing design tenets to guide the next generation of particle based immunotherapies.
 INTRODUCTION: There is limited local information on the risk of severe COVID-19 infection in patients with multiple sclerosis (MS) who are receiving disease-modifying treatments (DMT). The aim of the study was to assess the impact of COVID-19 disease (severity and lethality) in MS patients receiving DMT. METHODS: The study was performed on a prospective cohort with EM. We included 111 patients with MS and a confirmed diagnosis of COVID-19 treated with DMT and followed up until the resolution of COVID-19. RESULTS: A total of six patients (5.4%; 95% CI: 2-11.4%) developed severe COVID-19 defined as requiring hospitalization in intensive care unit or death and three died (crude case fatality rate of 2.7%; 95% CI: 1.1-4.3%). The age-adjusted case fatality rate was 1.5% (95% CI: 0.6-2.4%). The factor that was independently associated with severe COVID-19 was age (OR 1.1; CI 1.0-1.3; p < 0.05) with a trend in the Expanded Disability Status Scale (EDSS) = 6 (OR 6.2; CI 0.6-56.4; p = 0.10). CONCLUSION: The lethality due to COVID-19 in MS patients is low, and severity was significantly associated with age and showed a trend with EDSS = 6.
 Multiple sclerosis (MS) is known as a chronic inflammatory disease (CID) that affects the central nervous system and leads to nerve demyelination. However, the exact cause of MS is unknown, but immune system regulation and inhibiting the function of inflammatory pathways may have a beneficial effect on controlling and improving the disease. Studies show that probiotics can alter the gut microbiome, thereby improving and affecting the immune system and inflammatory responses in patients with MS. The results show that probiotics have a good effect on the recovery of patients with MS in humans and animals. The present study investigated the effect of probiotics and possible therapeutic mechanisms of probiotics on immune cells and inflammatory cytokines. This review article showed that probiotics could improve immune cells and inflammatory cytokines in patients with MS and can play an effective role in disease management and control.
 Motor disability is a dominant and restricting symptom in multiple sclerosis, yet its neuroimaging correlates are not fully understood. We apply statistical and machine learning techniques on multimodal neuroimaging data to discriminate between multiple sclerosis patients and healthy controls and to predict motor disability scores in the patients. We examine the data of sixty-four multiple sclerosis patients and sixty-five controls, who underwent the MRI examination and the evaluation of motor disability scales. The modalities used comprised regional fractional anisotropy, regional grey matter volumes, and functional connectivity. For analysis, we employ two approaches: high-dimensional support vector machines run on features selected by Fisher Score (aiming for maximal classification accuracy), and low-dimensional logistic regression on the principal components of data (aiming for increased interpretability). We apply analogous regression methods to predict symptom severity. While fractional anisotropy provides the classification accuracy of 96.1% and 89.9% with both approaches respectively, including other modalities did not bring further improvement. Concerning the prediction of motor impairment, the low-dimensional approach performed more reliably. The first grey matter volume component was significantly correlated (R = 0.28-0.46, p < 0.05) with most clinical scales. In summary, we identified the relationship between both white and grey matter changes and motor impairment in multiple sclerosis. Furthermore, we were able to achieve the highest classification accuracy based on quantitative MRI measures of tissue integrity between patients and controls yet reported, while also providing a low-dimensional classification approach with comparable results, paving the way to interpretable machine learning models of brain changes in multiple sclerosis.
 PURPOSE: Multiple sclerosis (MS) is associated with different ocular disorders. This study aimed to investigate the retinal microvascular changes detected by optical coherence tomography angiography (OCTA) in eyes with MS with or without a history of optic neuritis (ON). METHODS: A comprehensive literature search was conducted in the Web of Science, Embase, PubMed, and Cochrane Library databases on September 26, 2021 for articles focused on OCTA manifestations in the eyes of MS patients compared with healthy controls. RevMan Manager (v.5.4) and Stata (v.14.1) were used to analyze the main differences and publication risks. Weighted mean differences and 95% confidence intervals were calculated for continuous estimates. This study also included subgroup analysis between three groups: eyes with multiple sclerosis and with optic neuritis (MSON); eyes with multiple sclerosis and without optic neuritis (MSNON); and healthy controls. RESULTS: Thirteen studies with a total of 1803 eyes were identified, including 957 eyes with MS and 846 eyes of healthy controls. The vessel density of the MS eyes decreased significantly in most areas of the radial peripapillary capillary. A marked reduction in the macular superficial capillary plexus of MS eyes regardless of ON history was also confirmed. CONCLUSION: The results suggest that MS patients demonstrated significant retinal microvasculature impairment regardless of ON history, compared to healthy controls. Retinal vessel density attenuation detected by OCTA may serve as a reliable early marker of MS.
 It has been indicated that calorie restriction (CR) leads to several neuroprotective effects against physiological aging and different neurodegenerative disorders. Unfortunately, the definite therapeutic strategy is not introduced for Multiple sclerosis (MS) as an autoimmune disease of central nervous system (CNS) and researchers are striving to find the best treatment procedures and then optimize them. More recently, several preclinical studies have reported beneficial effects of CR on MS. It was stated that CR can decline demyelination, improve remyelination and decrease neuroinflammation in animal model of MS, as well as reduce body weight and enhance emotional wellbeing in MS patients. In this context we designed this review to examine studies exploring the effects of CR on MS disease based on the clinical and animal models to highlight involved mechanistic implications and future prospective.
 Analogs of immunodominant myelin peptides involved in multiple sclerosis (MS: the most common autoimmune disease) have been extensively used to modify the immune response over the progression of the disease. The immunodominant 35-55 epitope of myelin oligodendrocyte glycoprotein (MOG(35-55) ) is an autoantigen appearing in MS and stimulates the encephalitogenic T cells, whereas mannan polysaccharide (Saccharomyces cerevisiae) is a carrier toward the mannose receptor of dendritic cells and macrophages. The conjugate of mannan-MOG(35-55) has been extensively studied for the inhibition of chronic experimental autoimmune encephalomyelitis (EAE: an animal model of MS) by inducing antigen-specific immune tolerance against the clinical symptoms of EAE in mice. Moreover, it presents a promising approach for the immunotherapy of MS under clinical investigation. In this study, a competitive enzyme-linked immunosorbent assay (ELISA) was developed to detect the MOG(35-55) peptide that is conjugated to mannan. Intra- and inter-day assay experiments proved that the proposed ELISA methodology is accurate and reliable and could be used in the following applications: (i) to identify the peptide (antigen) while it is conjugated to mannan and (ii) to adequately address the alterations that the MOG(35-55) peptide may undergo when it is bound to mannan during production and stability studies.

 INTRODUCTION: On 4 and 5 November 2022, Madrid hosted the 15th edition of the Post-ECTRIMS Meeting, where neurologists specialised in multiple sclerosis (MS) outlined the most relevant novelties presented at the 2022 ECTRIMS Congress, held in Amsterdam from 26 to 28 October. AIM: To synthesise the content presented at the 15th edition of the Post-ECTRIMS Meeting, in an article broken down into two parts. DEVELOPMENT: In this first part, the initial events involved in the onset of MS, the role played by lymphocytes and the migration of immune system cells into the central nervous system are presented. It describes emerging biomarkers in body fluids and imaging findings that are predictive of disease progression and useful in the differential diagnosis of MS. It also discusses advances in imaging techniques which, together with a better understanding of the agents involved in demyelination and remyelination processes, provide a basis for dealing with remyelination in the clinical setting. Finally, the mechanisms triggering the inflammatory reaction and neurodegeneration involved in MS pathology are reviewed.
 OBJECTIVE: This article summarizes neuroimaging findings in demyelinating disease, the most common being multiple sclerosis. Revisions to criteria and treatment options have been ongoing, and MRI plays a pivotal role in diagnosis and disease monitoring. The common antibody-mediated demyelinating disorders with their respective classic imaging features are reviewed, as well as the differential diagnostic considerations on imaging. LATEST DEVELOPMENTS: The clinical criteria of demyelinating disease rely heavily on imaging with MRI. With novel antibody detection, the range of clinical demyelinating syndromes has expanded, most recently with myelin oligodendrocyte glycoprotein-IgG antibodies. Imaging has improved our understanding of the pathophysiology of multiple sclerosis and disease progression, and further research is underway. The importance of increased detection of pathology outside of the classic lesions will have an important role as therapeutic options are expanding. ESSENTIAL POINTS: MRI has a crucial role in the diagnostic criteria and differentiation among common demyelinating disorders and syndromes. This article reviews the typical imaging features and clinical scenarios that assist in accurate diagnosis, differentiation between demyelinating diseases and other white matter diseases, the importance of standardized MRI protocols in clinical practice, and novel imaging techniques.
 BACKGROUND: Paramagnetic rim lesions (PRL) may be linked to relapse risk of people with relapsing-remitting multiple sclerosis (pwRRMS). OBJECTIVE: To determine the relationship between presence of PRL lesions and cognitive recovery after relapse. METHODS: PRL load was compared between acutely relapsing pwRRMS and matched stable pwRRMS controls (each group n = 21). In addition, cognitive recovery was compared between acutely relapsing pwRRMS with at least one PRL (PRL+) and those without any PRL (PRL-). RESULTS: Acutely relapsing pwRRMS had significantly greater prevalence and number of PRL (p = 0.004 and p = 0.003) compared with stable controls. These findings remained significant after adjusting for global neuroinflammatory burden (enhancing and non-enhancing lesions). In addition, acutely relapsing PRL + pwRRMS (n = 10) had worse recovery of verbal memory following relapse compared with acutely relapsing PRL - pwRRMS (n = 7; p = 0.027). CONCLUSION: These findings may partially explain previously suggested associations between presence of PRL with more severe disease course.
 Multiple Sclerosis (MS) is a degenerative disorder of the central nervous system (CNS) with complicated etiology that has not been clearly analyzed until nowadays. Apart from anti-inflammatory, immune modulatory and symptomatic treatments, which are the main tools towards MS control, antioxidant molecules may be of interest. Oxidative stress is a key condition implicated in the disease progression. Reactive species production is associated with immune cell activation in the brain as well as in the periphery, accounting for demyelinating and axonal disruptive processes. This review refers to research articles, of the last decade. It describes biological evaluation of antioxidant drugs, and molecules with pharmaceutical interest, which are not designed for MS treatment, however they seem to have potency against MS. Their antioxidant effect is accompanied, in most of the cases, by anti-inflammatory, immune-modulatory and neuroprotective properties. Compounds with such characteristics are expected to be beneficial in the treatment of MS, alone or as complementary therapy, improving some clinical and mechanistic aspects of the disease. This review also summarizes some of the pathobiological characteristics of MS, as well as the role of oxidative stress and inflammation in the progression of neurodegeneration. It presents known drugs and bioactive compounds with antioxidant, and in many cases, pleiotropic activity that have been tested for their efficacy in MS progression or the experimentally induced MS. Antioxidants may offer reduction or prevention of the disease symptoms and progression. Thus, their results may, combined with already applied treatments, be beneficial for the development of new molecules or the repurposing of drugs and supplements that are used with other indication so far.
 A pilot analysis of the tear fluid of patients with multiple sclerosis (MS) collected by glass microcapillary was performed using various experimental methods: liquid chromatography-mass spectrometry, Raman spectroscopy, infrared spectroscopy, and atomic-force microscopy. Infrared spectroscopy found no significant difference between the tear fluid of MS patients and the control spectra; all three significant peaks were located at around the same positions. Raman analysis showed differences between the spectra of the tear fluid of MS patients and the spectra of healthy subjects, which indicated a decrease in tryptophan and phenylalanine content and changes in the relative contributions of the secondary structures of the polypeptide chains of tear proteins. Atomic-force microscopy exhibited a surface fern-shaped dendrite morphology of the tear fluid of patients with MS, with less roughness on both oriented silicon (100) and glass substrates compared to the tear fluid of control subjects. The results of liquid chromatography-mass spectrometry showed downregulation of glycosphingolipid metabolism, sphingolipid metabolism, and lipid metabolism. Proteomic analysis identified upregulated proteins in the tear fluid of patients with MS such as cystatine, phospholipid transfer protein, transcobalamin-1, immunoglobulin lambda variable 1-47, lactoperoxidase, and ferroptosis suppressor protein 1; and downregulated proteins such as haptoglobin, prosaposin, cytoskeletal keratin type I pre-mRNA-processing factor 17, neutrophil gelatinase-associated lipocalin, and phospholipase A2. This study showed that the tear proteome in patients with MS is modified and can reflect inflammation. Tear fluid is not a commonly used biological material in clinico-biochemical laboratories. Experimental proteomics has the potential to become a promising contemporary tool for personalized medicine, and it might be applied in clinical practice by providing a detailed analysis of the tear-fluid proteomic profile of patients with MS.
 BACKGROUND: Self-management programs have been used with success in several clinical populations, and there is a growing body of evidence to support their use among persons with multiple sclerosis (MS). This group aimed to develop a novel self-management program, Managing My MS My Way (M(4)W), which is based in social cognitive theory and contains evidence-based strategies that have been shown to be effective for persons with MS. Furthermore, persons with MS would serve as stakeholders throughout the development process to ensure that the program would be useful and encourage adoption. This paper outlines the initial development stages of M(4)W, including determining 1) stakeholders' interest in a self-management program, 2) the general focus of the program, 3) the delivery method of the program, 4) the content of the program, and 5) potential barriers and adaptations. METHODS: A three-stage study consisting of an anonymous survey (n = 187) to determine interest, topic, and delivery format; semi-structured interviews (n = 6) to follow-up on the survey results; and semi-structured interviews (n = 10) to refine the content and identify barriers. RESULTS: Over 80% of survey participants were somewhat or very interested in a self-management program. Fatigue was the topic with the greatest amount of interest (64.7%). An internet-based program (e.g., mobile health or mHealth) was the most preferred delivery method (37.4%), with the first group of stakeholders proposing a module-based system with an initial in-person orientation session. The second group of stakeholders were overall enthusiastic about the program, giving moderate to high confidence scores for each of the proposed interventional strategies. Suggestions included skipping sections that were not applicable to them, setting reminders, and seeing their progress (e.g., visualizing their fatigue scores as they move through the program). In addition, stakeholders recommended larger font sizes and speech-to-text entry. CONCLUSIONS: Input from the stakeholders has been incorporated into the prototype of M(4)W. The next steps will be to test this prototype with another group of stakeholders to assess its initial usability and identify issues before developing the functional prototype.
 PURPOSE: To assess the ability of a new posterior pole protocol to detect areas with significant differences in retinal nerve fiber layer (RNFL) and ganglion cell layer (GCL) thickness in patients with multiple sclerosis versus healthy control subjects; in addition, to assess the correlation between RNFL and GCL thickness, disease duration, and the Expanded Disability Status Scale (EDSS). METHODS: We analyzed 66 eyes of healthy control subjects and 100 eyes of remitting-relapsing multiple sclerosis (RR-MS) patients. Double analysis based on first clinical symptom onset (CSO) and conversion to clinically definite MS (CDMS) was performed. The RR-MS group was divided into subgroups by CSO and CDMS year: CSO-1 (≤ 5 years) and CSO-2 (≥ 6 years), and CDMS-1 (≤ 5 years) and CDMS-2 (≥ 6 years). RESULTS: Significant differences in RNFL and GCL thickness were found between the RR-MS group and the healthy controls and between the CSO and CDMS subgroups and in both layers. Moderate to strong correlations were found between RNFL and GCL thickness and CSO and CDMS. Furthermore, we observed a strong correlation with EDSS 1 year after the OCT examination. CONCLUSIONS: The posterior pole protocol is a useful tool for assessing MS and can reveal differences even in early stages of the disease. RNFL thickness shows a strong correlation with disability status, while GCL thickness correlates better with disease duration.
 BACKGROUND AND PURPOSE: The endocannabinoid system (ECS) has been found altered in patients with multiple sclerosis (MS). However, whether the ECS alteration is present in the early stage of MS remains unknown. First, we aimed to compare the ECS profile between newly diagnosed MS patients and healthy controls (HCs). Next, we explored the association of the ECS, biomarkers of inflammation, and clinical parameters in newly diagnosed MS patients. METHODS: Whole blood gene expression of ECS components and levels of endocannabinoids in plasma were measured by real-time quantitative polymerase chain reaction and ultra-high-pressure liquid chromatography-mass spectrometry, respectively, in 66 untreated MS patients and 46 HCs. RESULTS: No differences were found in the gene expression or plasma levels of the selected ECS components between newly diagnosed MS patients and HCs. Interferon-γ, encoded by the gene IFNG, correlated positively (ρ = 0.60) with the expression of G protein-coupled receptor 55 (GPR55), and interleukin1β (IL1B) correlated negatively (ρ = -0.50) with cannabinoid receptor 2 (CNR2) in HCs. CONCLUSIONS: We found no alteration in the peripheral ECS between untreated patients with MS and HC. Furthermore, our results indicate that the ECS has a minor overall involvement in the early stage of MS on inflammatory markers and clinical parameters when compared with HCs.
 BACKGROUND AND PURPOSE: The long-term impact of gadolinium retention in the dentate nuclei of patients undergoing administration of seriate gadolinium-based contrast agents is still widely unexplored. The aim of this study was to evaluate the impact of gadolinium retention on motor and cognitive disability in patients with MS during long-term follow-up. MATERIALS AND METHODS: In this retrospective study, clinical data were obtained from patients with MS followed in a single center from 2013 to 2022 at different time points. These included the Expanded Disability Status Scale score to evaluate motor impairment and the Brief International Cognitive Assessment for MS battery to investigate cognitive performances and their respective changes with time. The association with qualitative and quantitative MR imaging signs of gadolinium retention (namely, the presence of dentate nuclei T1-weighted hyperintensity and changes in longitudinal relaxation R1 maps, respectively) was probed using different General Linear Models and regression analyses. RESULTS: No significant differences in motor or cognitive symptoms emerged between patients showing dentate nuclei hyperintensity and those without visible changes on T1WIs (P  = .14 and 0.92, respectively). When we tested possible relationships between quantitative dentate nuclei R1 values and both motor and cognitive symptoms, separately, the regression models including demographic, clinical, and MR imaging features explained 40.5% and 16.5% of the variance, respectively, without any significant effect of dentate nuclei R1 values (P  = .21 and 0.30, respectively). CONCLUSIONS: Our findings suggest that gadolinium retention in the brains of patients with MS is not associated with long-term motor or cognitive outcomes.
 OBJECTIVE: Depressive disorder occurs in up to 50% of persons with Multiple Sclerosis (PwMS). Accurate assessment of depression in MS is essential in clinical settings because depressive symptomatology can affect the clinical course of the disease. METHODS: We translated, adapted, and tested the Spanish version of the Chicago Multiscale Depression Inventory (CMDI), a specific test to assess depression in neurological disorders. We compare our results with those obtained with previous versions of the questionnaire (English and Italian). Finally, we also analyze the relationship between the results obtained on the CMDI and demographic, clinical, and cognitive variables. RESULTS: The results obtained with the Spanish version of the CMDI were similar to those observed in previous published versions. We also observed higher depression scores in PwMS (especially in progressive forms) compared with healthy controls. Moreover, depression symptomatology was related to higher disability and fatigue and worse cognitive performance in PwMS. CONCLUSIONS: The results support the validity of the CDMI in the Spanish population, as well as the association between depression and other characteristic symptoms of MS. These findings also emphasize the importance of good assessment and multidisciplinary treatment of depression in PwMS.
 Despite the importance of blood group compatibility in solid organ transplantation, the role of ABO antigens is less critical in hematopoietic stem cell transplantation (HSCT). However, ABO-mismatch HSCT can present specific conditions and challenges for the recipient. One of the possible consequences of ABO-mismatch HSCT is pure red cell aplasia (PRCA). Although there are different treatment strategies to manage PRCA, each may carry its own risk. Here, we report a patient who developed PRCA after ABO-mismatch allogeneic HSCT from her sibling with multiple sclerosis history. PRCA improved with tapering immunosuppressive agents. Although the patient developed manageable graft versus host disease (GVHD), she eventually recovered from both PRCA and GVHD.
 BACKGROUND: Rituximab (RTX) is largely used as a long-term maintenance therapy in various inflammatory neurological diseases. Reducing the dose of maintenance therapy of RTX from 2 grams every 6 months (traditional regimen) to 1 gram every 6 months (reduced regimen) is a widely applied practice, with the assumption that it decreases the risk of side effects while maintaining efficacy. METHODS: In order to better describe the biological consequences of this strategy, we retrospectively compared, in a single center, the B-cell count after the traditional regimen and after the reduced regimen in patients who underwent both (n = 161). RESULTS: The rate of patients with B-cell repopulation was not significantly different between traditional and reduced regimens (9.9% vs 15.6%, p = 0.18). Among the 145 patients who did not have B-cell repopulation following the traditional regimen, B-cell repopulation following the reduced regimen occurred in only 16 cases (11.0%) and was usually slight: 11/16 patients had only 1% of CD19+ cells. CONCLUSION: These data emphasize the relevance of 1 g of RTX as maintenance therapy and the fact that 2 g of RTX is generally an overtreatment in inflammatory neurological diseases.
 Substantial cortical gray matter tissue damage, which correlates with clinical disease severity, has been revealed in multiple sclerosis (MS) using advanced magnetic resonance imaging (MRI) methods at 3 T and the use of ultra-high field, as well as in histopathology studies. While clinical assessment mainly focuses on lesions using T1 - and T2 -weighted MRI, quantitative MRI (qMRI) methods are capable of uncovering subtle microstructural changes. The aim of this ultra-high field study is to extract possible future MR biomarkers for the quantitative evaluation of regional cortical pathology. Because of their sensitivity to iron, myelin, and in part specifically to cortical demyelination, T1 , T2 , R2* , and susceptibility mapping were performed including two novel susceptibility markers; in addition, cortical thickness as well as the volumes of 34 cortical regions were computed. Data were acquired in 20 patients and 16 age- and sex-matched healthy controls. In 18 cortical regions, large to very large effect sizes (Cohen's d ≥ 1) and statistically significant differences in qMRI values between patients and controls were revealed compared with only four regions when using more standard MR measures, namely, volume and cortical thickness. Moreover, a decrease in all susceptibility contrasts ( χ , χ+ , χ-) and R2* values indicates that the role of cortical demyelination might outweigh inflammatory processes in the form of iron accumulation in cortical MS pathology, and might also indicate iron loss. A significant association between susceptibility contrasts as well as R2* of the caudal middle frontal gyrus and disease duration was found (adjusted R(2) : 0.602, p = 0.0011). Quantitative MRI parameters might be more sensitive towards regional cortical pathology compared with the use of conventional markers only and therefore may play a role in early detection of tissue damage in MS in the future.
 Aim: To assess the relative efficacy of disease-modifying therapies (DMTs) for relapsing multiple sclerosis (RMS) including newer therapies (ozanimod, ponesimod, ublituximab) using network meta-analysis (NMA). Materials & methods: Bayesian NMAs for annualised relapse rate (ARR) and time to 3-month and 6-month confirmed disability progression (3mCDP and 6mCDP) were conducted. Results: For each outcome, the three most efficacious treatments versus placebo were monoclonal antibody (mAb) therapies: alemtuzumab, ofatumumab, and ublituximab for ARR; alemtuzumab, ocrelizumab, and ofatumumab for 3mCDP; and alemtuzumab, natalizumab, and either ocrelizumab or ofatumumab (depending on the CDP definition used for included ofatumumab trials) for 6mCDP. Conclusion: The most efficacious DMTs for RMS were mAb therapies. Of the newer therapies, only ublituximab ranked among the three most efficacious treatments (for ARR).
 Exercise training is an effective and safe second-line therapy for improving multiple sclerosis (MS) symptoms and disease progression among adults. This study aimed to determine the appropriateness of a novel exercise training program for wheelchair users with MS. Ten wheelchair users with MS were recruited from a previous cross-sectional research study to attend one of three focus groups with 3-4 participants that lasted between 69 and 87 min. The focus groups were conducted online using a semi-structured format and participants were invited to complete an evaluation survey. During the focus groups, participants provided qualitative feedback regarding the exercise prescription, exercise modes (resistance and aerobic), training manual, exercise equipment, fitness tracker, rating scale, newsletters, logbook, and coaching. Most feedback focused on minor considerations such as avoiding the color red as it can be an issue for individuals with optic neuritis. Among quantitative evaluation survey ratings, coaching calls were rated the highest 4.7 ± 0.4 on a 5-point scale, followed by the exercise prescription (4.4 ± 0.8) and fitness tracker (4.3 ± 0.9). Focus group participants provided invaluable feedback for finalizing a novel exercise training program for wheelchair users with MS and provided focal suggestions for further improvements.
 NEUROMYELITIS OPTICA. Neuromyelitis optica (NMO) or neuromyelitis optica spectrum disorder (NMOSD) includes different inflammatory conditions of the central nervous system distinct from multiple sclerosis. It is characterized by the association of typical clinical manifestations, such as optic neuritis, extensive transverse myelitis, involvement of the area postrema, and by the presence of anti-aquaporin 4 antibodies. It evolves with relapses. These can be lethal and justify emergency treatment with the administration of high dose of intravenous corticosteroids possibly associated with plasma exchange sessions. A disease modifying treatment is then started to prevent the occurrence of a new relapse.
 The purpose of this study was to characterize the ponesimod effect on the heart rate (HR) in patients with multiple sclerosis (MS). A previous pharmacokinetic (PK) and pharmacodynamic model developed in healthy participants was updated using data from phase II and III trials conducted in patients with MS. Clinically relevant covariates were assessed. Simulations were conducted to evaluate the impact of the lack of adherence to ponesimod treatment and provide guidance in cases of treatment re-initiation. The maximal effect parameter of the PK/HR model was lower in patients with MS (23.5% decrease) compared with healthy volunteers (43.2%). The effect of patient covariates on PK/HR was similar to those identified in healthy participants and not clinically relevant in patients with MS. The population PK/HR model well characterized the effect of ponesimod on the time course of HR in patients with MS. After 2 weeks of treatment with 10 mg or higher doses, the model indicated full tolerance development. After repeated dosing at 20 mg, tolerance was maintained > 60% of the steady-state tolerance for up to 4 days after the last dose. Re-initiating with gradual uptitration is recommended if drug discontinuation lasts ≥ 4 days. This managed the negative chronotropic effects of ponesimod. No bradycardia events were observed within the first 2 weeks of treatment in patients with relapsing MS with a baseline HR > 55 bpm. This justifies the recommendation included in the human prescription drug labeling to monitor HR after the first ponesimod dose in these patients.

 This study examined whether an alteration in the effort-reward relationship, a theoretical framework based on cognitive neuroscience, could explain cognitive fatigue. Forty persons with MS and 40 healthy age- and education-matched cognitively healthy controls (HC) participated in a computerized switching task with orthogonal high- and low-demand (effort) and reward manipulations. We used the Visual Analog Scale of Fatigue (VAS-F) to assess subjective state fatigue before and after each condition during the task. We used mixed-effects models to estimate the association and interaction between effort and reward and their relationship to subjective fatigue and task performance. We found the high-demand condition was associated with increased VAS-F scores (p < .001), longer response times (RT) (p < .001) and lower accuracy (p < .001). The high-reward condition was associated with faster RT (p = .006) and higher accuracy (p = .03). There was no interaction effect between effort and reward on VAS-F scores or performance. Participants with MS reported higher VAS-F scores (p = .02). Across all conditions, participants with MS were slower (p < .001) and slower as a function of condition demand compared with HC (p < .001). This behavioural study did not find evidence that an effort-reward interaction is associated with cognitive fatigue. However, our findings support the role of effort in subjective cognitive fatigue and both effort and reward on task performance. In future studies, more salient reward manipulations could be necessary to identify effort-reward interactions on subjective cognitive fatigue.
 We report a 57-year-old man with multiple sclerosis since his 30s who was treated with fingolimod for 9 years. He developed left hemiparesis and consciousness disturbance. Brain MRI revealed a mass lesion in the right frontal lobe with gadolinium enhancement. Cerebrospinal fluid examination showed no pleocytosis. The lesion continued to expand after admission, and on the 9th day after admission, decompressive craniectomy and brain biopsy were performed. Brain pathology revealed demyelination in the lesion, leading to the diagnosis of a tumefactive demyelinating lesion. Corticosteroid therapy ameliorated the brain lesion, and we inducted natalizumab. Tumefactive demyelinating lesions requiring decompressive craniotomy are rare, and we report this case for the further accumulation of similar cases.

 The importance of circulating immune cells to primary progressive multiple sclerosis (PPMS) pathophysiology is still controversial because most immunotherapies were shown to be ineffective in treating people with PPMS (pwPPMS). Yet, although controversial, data exist describing peripheral immune system alterations in pwPPMS. This study aims to investigate which alterations might be present in pwPPMS free of disease-modifying drugs (DMD) in comparison to age- and sex-matched healthy controls. A multicentric cross-sectional study was performed using 23 pwPPMS and 23 healthy controls. The phenotype of conventional CD4(+) and CD8(+) T cells, regulatory T cells (Tregs), B cells, natural killer (NK) T cells and NK cells was assessed. Lower numbers of central memory CD4(+) and CD8(+) T cells and activated HLA-DR(+) Tregs were observed in pwPPMS. Regarding NK and NKT cells, pwPPMS presented higher percentages of CD56(dim)CD57(+) NK cells expressing NKp46 and of NKT cells expressing KIR2DL2/3 and NKp30. Higher disease severity scores and an increasing time since diagnosis was correlated with lower numbers of inhibitory NK cells subsets. Our findings contribute to reinforcing the hypotheses that alterations in peripheral immune cells are present in pwPPMS and that changes in NK cell populations are the strongest correlate of disease severity.
 INTRODUCTION: Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) that affects young adults, causing a variety of symptoms (motor alterations, visual alterations, loss of sphincter control, gait alterations) that impair the patient's functional status. However, other symptoms, such as sexual dysfunction, can also have an effect on quality of life. DEVELOPMENT: Sexual dysfunction can occur at any time during the course of the disease; its prevalence varies between 50% and 90%, and it can be secondary to demyelinating lesions in the spinal cord and/or brain or caused by symptoms that do not directly involve the nervous system (fatigue; psychological, social, and cultural factors; etc.). Although its prevalence and impact on quality of life are well known, sexual dysfunction is still frequently underestimated. Therefore, in this article we review the different scales for assessing presence or severity of sexual dysfunction, in order to offer early multidisciplinary management. CONCLUSION: We evaluated 5 questionnaires that could identify the presence of sexual dysfunction in patients with MS and determine its aetiology, assisting in treatment decision making. MS must be understood as a complex disease that encompasses and compromises different aspects of patients' health, and goes beyond simply measuring disability.
 OBJECTIVE: To measure the cranial volume differences from 15 different parts in the follow-up of relapsing-remitting multiple sclerosis (RRMS) patients and correlate them with clinical parameters. METHODS: Forty-seven patients with RRMS were included in the study. Patients were grouped into two categories; low Expanded Disability Status Scale (EDSS) (< 3; group 1), and moderate-high EDSS (≥ 3; group 2). Patients were evaluated with Beck Depression Inventory (BDI), Montreal Cognitive Assessment (MOCA), Symbol Digit Modalities Test (SDMT), Fatigue Severity Scale (FSS), and calculated Annualized Relapse Rate (ARR) scores. Magnetic resonance imaging (MRI) was performed with a 1.5T MRI device (Magnetom AERA, Siemens, Erlangen, Germany) twice in a 1-year period. Volumetric analysis was performed by a free, automated, online MRI brain volumetry software. The differences in volumetric values between the two MRI scans were calculated and correlated with the demographic and clinical parameters of the patients. RESULTS: The number of attacks, disease duration, BDI, and FSS scores were higher in group 2; SDMT was higher in group 1. As expected, volumetric analyses have shown volume loss in total cerebral white matter in follow-up patients (p < 0.001). In addition, putaminal volume loss was related to a higher number of attacks. Besides, a negative relation between FSS with total amygdala volumes, a link between atrophy of globus pallidus and ARR, and BDI scores was found with the aid of network analysis. CONCLUSIONS: Apart from a visual demonstration of volume loss, cranial MRI with volumetric analysis has a great potential for revealing covert links between segmental volume changes and clinical parameters.
 Cumulative evidence along several lines indicates that B cells play an important role in the pathological course of multiple sclerosis (MS), neuromyelitisoptica spectrum disorders (NMOSD) and related CNS diseases. This has prompted extensive research in exploring the utility of targeting B cells to contain disease activity in these disorders. In this review, we first recapitulate the development of B cells from their origin in the bone marrow to their migration to the periphery, including the expression of therapy-relevant surface immunoglobulin isotypes. Not only the ability of B cells to produce cytokines and immunoglobulins seems to be essential in driving neuroinflammation, but also their regulatory functions strongly impact pathobiology. We then critically assess studies of B cell depleting therapies, including CD20 and CD19 targeting monoclonal antibodies, as well as the new class of B cell modulating substances, Bruton´s tyrosinekinase (BTK) inhibitors, in MS, NMOSD and MOGAD.
 AIMS: The laboratory diagnosis of demyelinating inflammatory disorders (DIDs) relies on both intrathecal oligoclonal band (OCB) positivity and IgG index. Although OCB typing remains the gold-standard test for DIDs, it can be laborious and ambiguous, complicating diagnostics, and unduly increasing diagnostic time. We examined whether serum or cerebrospinal fluid (CSF) parameters can classify OCB types and, thus, be used as a replacement test to standard OCB typing. METHODS: We retrospectively analysed >1000 prospectively collected samples of patients with DIDs and quantified albumin and IgG levels in the CSF and serum. We determined OCB types by isoelectric focusing combined with immunofixation and evaluated the diagnostic accuracies of IgG and albumin indices in discriminating OCB types by receiver operating characteristic curves and multinomial regression. RESULTS: An IgG index cut-off of 0.589 differentiated types 2/3 from types 1/4 (area under the curve 0.780, 95% CI 0.761 to 0.812, p<0.001; specificity: 71.10%, sensitivity: 73.45%). Albumin quotient cut-off values of 6.625 and of 6.707 discriminated type 1 from type 4 and type 2 from type 3, respectively (specificity: <55%, sensitivity: <75%). Female sex, age, IgG index, CSF IgG and serum albumin were associated with different OCB types. CONCLUSIONS: Our study reveals that IgG and albumin index can differentiate OCB types with adequate accuracy, especially if refined by age and gender.
 OBJECTIVE: To assess the efficacy and safety of sampeginterferon-β1a (samPEG-IFN-β1a) 180 μg and 240 μg administered once every 2 weeks compared to placebo and low dose interferon beta-1a (LIB) 30 μg administered once weekly. MATERIAL AND METHODS: Patients with relapsing-remitting multiple sclerosis aged 18-60 years, with Expanded Disability Status Scale score ≤5.5 were randomized at a ratio of 2:2:2:1 to the following groups: samPEG-IFN-β1a 180 µg, samPEG-IFN-β1a 240 µg, LIB, placebo. After 20 weeks, the placebo group completed the study. After week 52, the final analysis was performed, which included the primary endpoint analysis, the LIB group patients completed their participation in the study. The patients in samPEG-IFN-β1a groups continued to receive therapy with samPEG-IFN-β1a 240 µg until week 100 inclusive. The results of the final analysis after 52 weeks have been previously published. The current article presents a long-term efficacy and safety of samPEG-IFN-β1a after 104 weeks of the trial. RESULTS: The annualized relapse rate over the second year was 0.16 in the samPEG-IFN-β1a 180 μg group and 0.09 in the samPEG-IFN-β1a 240 μg group. By week 104, the proportion of relapse-free patients was 77.0% (87/113) and 83.3% (95/114) in the samPEG-IFN-β1a 180 μg and 240 μg groups, respectively. There were no negative dynamics of MRI markers, neurological deficit parameters and cognitive functions by scales and tests. The safety profile of samPEG-IFN-β1a was consistent with the known safety profile of IFN-β therapy. CONCLUSION: Treatment with samPEG-IFN-β1a is an effective and safe first-line therapy for relapsing-remitting multiple sclerosis patients.
 OBJECTIVE: To assess the benefits of neurological rehabilitation and the dose-response relationship for the treatment of mobility and balance in multiple sclerosis. METHODS: We included studies investigating the effects of neurological rehabilitation on mobility and balance with the following eligibility criteria for inclusion: Population, People with Multiple Sclerosis (PwMS); Intervention, method of rehabilitation interventions; Comparison, experimental (specific balance intervention) vs control (no intervention/no specific balance intervention); Outcome, balance clinical scales; Study Design, randomised controlled trials. We conducted a random effects dose-response meta-analysis to assess linear trend estimations and a one stage linear mixed effects meta-regression for estimating dose-response curves. RESULTS: We retrieved 196 studies from a list of 5020 for full text review and 71 studies (n subjects=3306) were included. One study was a cross-over and 70 studies were randomized controlled trials and the mean sample size per study was 46.5 ± 28.6 (mean±SD) with a mean age of 48.3 ± 7.8years, disease duration of 11.6 ± 6.1years, and EDSS of 4.4 ± 1.4points. Twenty-nine studies (40.8%) had the balance outcome as the primary outcome, while 42 studies (59.1%) had balance as secondary outcome or did not specify primary and secondary outcomes. Thirty-three trials (46.5%) had no active intervention as comparator and 38 trials (53.5%) had an active control group. Individual level data from 20 studies (n subjects=1016) were analyzed showing a medium pooled effect size for balance interventions (SMD=0.41; 95% CIs 0.22 to 0.59). Moreover, we analyzed 14 studies (n subjects=696) having balance as primary outcome and BBS as primary endpoint yielding a mean difference of 3.58 points (95% CIs 1.79 to 5.38, p<0.0001). Finally, we performed meta regression of the 20 studies showing an association between better outcome, log of intensity defined as minutes per session (β=1.26; SEβ=0.51; p = 0.02) and task-oriented intervention (β=0.38; SEβ=0.17; p = 0.05). CONCLUSION: Our analyses provide level 1 evidence on the effect of balance intervention to improve mobility. Furthermore, according to principles of neurological rehabilitation, high intensity and task-specific interventions are associated with better treatment outcomes.
 Multiple Sclerosis (MS), a neurodegenerative disease of unknown etiology, which affects approximately 450 of every 100 000 women in the USA. Using an ecological observational study design and publicly available data from the Center for Disease Control and Prevention in the USA, we assessed trends in county-level, age-adjusted female MS mortality rates between 1999 and 2006 to determine if they were correlated with environmental factors, including the county's PM2.5. In counties with colder winters, there was a significant positive association between the average PM2.5 index and the MS mortality rate, after controlling for the county's UV index and median household income. This relationship was not apparent in counties with warmer winters. We also found that colder counties had higher MS mortality rates, even after controlling for the UV and PM2.5 indices. The findings from this study provide county-level evidence for a temperature-dependent association between PM2.5 pollution and MS mortality rates, which should be further investigated.
 Presence of EBV infected B cells and EBV-specific CD8 T cells in the multiple sclerosis (MS) brain suggests a role for virus-driven immunopathology in brain inflammation. Tissue-resident memory (Trm) T cells differentiating in MS lesions could provide local protection against EBV reactivation. Using immunohistochemical techniques to analyse canonical tissue residency markers in postmortem brains from control and MS cases, we report that CD103 and/or CD69 are mainly expressed in a subset of CD8+ T cells that intermingle with and contact EBV infected B cells in the infiltrated MS white matter and meninges, including B-cell follicles. Some Trm-like cells were found to express granzyme B and PD-1, mainly in white matter lesions. In the MS brain, Trm cells could fail to constrain EBV infection while contributing to sustain inflammation.
 Background: Many female people with multiple sclerosis (pwMS) are in childbearing age; however, only few data exist about the situation of breastfeeding in pwMS. Objective: Our study analyzed breastfeeding rate and duration, reasons for weaning, and the impact of disease severity on successful breastfeeding in pwMS. Methods: The study included pwMS giving birth within 3 years before study participation. Data were collected by structured questionnaire. Results: Compared to published data, we found a significant difference (p = 0.0007) between the nursing rate in the general population (96.6%) and females with MS (85.9%). However, a higher rate of exclusive breastfeeding could be observed in our study population for 5-6 months in 40.6% of pwMS versus 9% for 6 months in the general population. In contrast, total breastfeeding duration in our study population was shorter (18.8% for 11-12 months) than in the general population (41.1% for 12 months). Reasons for weaning were predominantly (68.7%) related to breastfeeding barriers based on MS. No significant impact of prepartum or postpartum education on the breastfeeding rate could be observed. Prepartum relapse rate and prepartum disease-modifying drugs had no effect on breastfeeding success. Conclusion: Our survey provides an insight into the situation of breastfeeding in pwMS in Germany.
 There is increasing interest in the application of neuroimaging technology in exercise neurorehabilitation research among persons with multiple sclerosis (MS). The inclusion and focus on neuroimaging outcomes in MS exercise training research is critical for establishing a biological basis for improvements in functioning and elevating exercise within the neurologist's clinical armamentarium alongside disease modifying therapies as an approach for treating the disease and its consequences. Indeed, the inclusion of selective neuroimaging approaches and sensor-based technology among physical activity, mobility, and balance outcomes in such MS research might further allow for detecting specific links between the brain and real-world behavior. This paper provided a scoping review on the application of neuroimaging in exercise training research among persons with MS based on searches conducted in PubMed, Web of Science, and Scopus. We identified 60 studies on neuroimaging-technology-based (primarily MRI, which involved a variety of sequences and approaches) correlates of functions, based on multiple sensor-based measures, which are typically targets for exercise training trials in MS. We further identified 12 randomized controlled trials of exercise training effects on neuroimaging outcomes in MS. Overall, there was a large degree of heterogeneity whereby we could not identify definitive conclusions regarding a consistent neuroimaging biomarker of MS-related dysfunction or singular sensor-based measure, or consistent neural adaptation for exercise training in MS. Nevertheless, the present review provides a first step for better linking correlational and randomized controlled trial research for the development of high-quality exercise training studies on the brain in persons with MS, and this is timely given the substantial interest in exercise as a potential disease-modifying and/or neuroplasticity-inducing behavior in this population.
 Neurofilament light chain (NfL), is a neuron-specific cytoskeletal protein detected in extracellular fluid following axonal damage. Extensive research has focused on NfL quantification in CSF, establishing it as a prognostic biomarker of disability progression in Multiple Sclerosis (MS). Our study used a new commercially available Enzyme-Linked Immunosorbent Assay (ELISA) kit and Single Molecular Array (Simoa) advanced technology to assess serum NfL levels in MS patients and Healthy Controls (HC). Verifying the most accurate, cost-effective methodology will benefit its application in clinical settings. Blood samples were collected from 54 MS patients and 30 HC. Protocols accompanying the kits were followed. The ELISA thershold was set as 3 S.D. above the mean of the HC. For Simoa, the Z-score calculation created by Jens Kuhle's group was applied (with permission). Samples exceeding the threshold or z-score ≥1.5 indicated subclinical disease activity. To our knowledge, this is the first study to find strong-positive correlation between ELISA and Simoa for the quantification of NfL in serum (r = 0.919). Despite the strong correlation, Simoa has better analytical sensitivity and can detect small changes in samples making it valuable in clinical settings. Further research is required to evaluate whether serum NfL quantification using ELISA could be utilized to predict disability progression.
 BACKGROUND: Pathophysiology of multiple sclerosis (MS) is dominated by both inflammation and neurodegeneration. A correlation between inflammation and regulated cell death has been suggested previously. Shadow cells in the cerebrospinal fluid (CSF) are considered apoptotic cells. OBJECTIVE: To assess the occurrence of shadow cells in MS patients in comparison to other neurological diseases (OND). METHODS: We conducted cytological examination of CSF in 114 MS patients and 125 patients with OND, who had diagnostic lumbar puncture at the Department of Neurology, Medical University of Innsbruck, with time to laboratory processing ≤0.5 h, showed a CSF white blood cell (WBC) count ≤50/µl and a red blood cell (RBC) count ≤500/µl. Shadow cells were counted by two blinded, independent, experienced investigators, using a standardized approach on microscopic slides. RESULTS: The number of shadow cells did not statistically significantly differ between patients with MS (median: 12, IQR: 0-85) and OND (median 6, IQR: 0-94; p = 0.106). Multivariable regression analysis including age, sex, time to laboratory processing, CSF WBC and RBC count, CSF/serum glucose ratio, CSF/serum albumin quotient and disease group as independent variables, identified WBC count as significant predictor of shadow cells (β [ln WBC count]=0.73, p<10(-9)), whereas the disease group had no impact (p = 0.466). CONCLUSIONS: Occurrence of shadow cells in the CSF seems to depend on the extent of inflammatory cells rather than MS disease-specific mechanisms.
 BACKGROUND: Pediatric onset multiple sclerosis patients (POMS) are defined as multiple sclerosis with an onset before the age of 18 years. Compared to adult onset multiple sclerosis (AOMS), POMS has more severe disease activity at onset, but better recovery. Little is known about the molecular mechanism responsible for the differences in the clinical presentations. METHODS: Peripheral Blood Mononuclear Cells samples were taken from 22 POMS patients (mean age 14.1 ± 2.4 years, 15 females, 7 male), and 16 AOMS patients, (mean age 30.8 ± 6.1 years,10 females, 6 males), and gene-expression were analyzed using Affymetrix Inc. HU-133-A2 microarrays. Differentially Expressed Genes (DEGs) that significantly distinguished between POMS and AOMS with pvalue <0.05 after false discovery rate correction were evaluated using Partek software. Twenty-one matched age and gender control was applied to clarify age-related changes. Clinical assessment was performed by analysis of expanded disability status scale (EDSS) and brain MRI lesion loads. Gene functional analysis was performed by Ingenuity Pathway Analysis software. RESULTS: Compared to AOMS, POMS had higher EDSS (3.0 IQR 2.0-3.0 and 2.0 IQR 2.0-3.0, p = 0.005), volume of T1 (2.72 mm(3), IQR 0.44-8.39 mm(3) and 0.5 mm(3) IQR 0-1.29 mm(3) respectively, p = 0.04) and T2 (3.70 mm(3), IQR 1.3-9.6 and 0.96 mm(3), IQR 0.24-4.63 respectively, p = 0.02) brain MRI lesions. The POMS transcriptional profile was characterized by 551 DEGs, enriched by cell cycling, B lymphocyte signaling and senescent pathways (p < 0.02). Of these, 183 DEGs significantly correlated with T2 lesions volume. The POMS MRI correlated DEGs (n = 183) and their upstream regulators (n = 718) has overlapped with age related DEGs obtained from healthy subjects (n = 497). This evaluated common DEGs (n = 29) defined as POMS age-related regulators, suggesting to promote effect on disease severity. CONCLUSION: Our finding of higher transcriptional levels of genes involved in cell cycle, cell migration and B cell proliferation that promoted by transcriptional level of age-associated genes and transcription factors allows better understanding of the more aggressive clinical course that defines the POMS.
 It is known that the thalamus plays an important role in pathological brain conditions involved in demyelinating, inflammatory and neurodegenerative diseases such as Multiple Sclerosis (MS). Beside immune cells and cytokines, ion channels were found to be key players in neuroinflammation. MS is a prototypical example of an autoimmune disease of the central nervous system that is classified as a channelopathy where abnormal ion channel function leads to symptoms and clinical signs. Here we review the influence of the cytokine-ion channel interaction in the thalamocortical system in demyelination and inflammation.

 BACKGROUND AND PURPOSE: There is increasing evidence that cardiovascular risk (CVR) contributes to disability progression in multiple sclerosis (MS). CVR is particularly prevalent in secondary progressive MS (SPMS) and can be quantified through validated composite CVR scores. The aim was to examine the cross-sectional relationships between excess modifiable CVR, whole and regional brain atrophy on magnetic resonance imaging, and disability in patients with SPMS. METHODS: Participants had SPMS, and data were collected at enrolment into the MS-STAT2 trial. Composite CVR scores were calculated using the QRISK3 software. Prematurely achieved CVR due to modifiable risk factors was expressed as QRISK3 premature CVR, derived through reference to the normative QRISK3 dataset and expressed in years. Associations were determined with multiple linear regressions. RESULTS: For the 218 participants, mean age was 54 years and median Expanded Disability Status Scale was 6.0. Each additional year of prematurely achieved CVR was associated with a 2.7 mL (beta coefficient; 95% confidence interval 0.8-4.7; p = 0.006) smaller normalized whole brain volume. The strongest relationship was seen for the cortical grey matter (beta coefficient 1.6 mL per year; 95% confidence interval 0.5-2.7; p = 0.003), and associations were also found with poorer verbal working memory performance. Body mass index demonstrated the strongest relationships with normalized brain volumes, whilst serum lipid ratios demonstrated strong relationships with verbal and visuospatial working memory performance. CONCLUSIONS: Prematurely achieved CVR is associated with lower normalized brain volumes in SPMS. Future longitudinal analyses of this clinical trial dataset will be important to determine whether CVR predicts future disease worsening.
 A woman presented at age 18 years with partial myelitis and diplopia and experienced multiple subsequent relapses. Her MRI demonstrated T2 abnormalities characteristic of multiple sclerosis (MS) (white matter ovoid lesions and Dawson fingers), and CSF demonstrated an elevated IgG index and oligoclonal bands restricted to the CSF. Diagnosed with clinically definite relapsing-remitting MS, she was treated with various MS disease-modifying therapies and eventually began experiencing secondary progression. At age 57 years, she developed an acute longitudinally extensive transverse myelitis and was found to have AQP4 antibodies by cell-based assay. Our analysis of the clinical course, radiographic findings, molecular diagnostic methods, and treatment response characteristics support the hypothesis that our patient most likely had 2 CNS inflammatory disorders: MS, which manifested as a teenager, and neuromyelitis optica spectrum disorder, which evolved in her sixth decade of life. This case emphasizes a key principle in neurology practice, which is to reconsider whether the original working diagnosis remains tenable, especially when confronted with evidence (clinical and/or paraclinical) that raises the possibility of a distinctively different disorder.
 INTRODUCTION: Multiple sclerosis is a chronic neurological disease with numerous disease-modifying treatments available, including dimethyl fumarate (DMF), a first-line therapy for relapsing-remitting multiple sclerosis. Although rates of discontinuation of DMF are generally low in clinical trials, non-adherence to treatment is associated with poorer clinical outcomes. Assessing real-world adherence and predictive factors is critical to be able to improve clinical outcomes for patients. This study evaluated adherence to DMF over 24 months in a cohort of patients treated in a Portuguese healthcare centre. PATIENTS AND METHODS: A prospective, non-interventional, single-centre study with 24 months' follow-up was conducted. The study included adult patients with relapsing-remitting multiple sclerosis treated with DMF in routine clinical practice. Adherence to DMF was calculated and patients were considered to have adhered if the value was above 80%. Clinical and socio-demographic variables were compared between groups. RESULTS: Of the 80 patients included, 74% were women, with a mean age of 39 years and a mean age of 32 years at diagnosis. Twenty-six patients had not received any previous treatment. Adherence varied between 93, 82 and 87.5% at 6, 12 and 24 months, respectively. No differences were found between patients who had not received any prior treatment and those who had been treated. CONCLUSION: This real-world analysis showed significant adherence to DMF treatment by Portuguese patients over a period of two years. However, these results must be interpreted in the light of the substantial changes in outpatient consultations and the various periodic restrictions due to the COVID-19 pandemic, which had an important effect on patient follow-up and data collection.
 BACKGROUND: A gap in research about the trajectories of function among men and women aging with functional limitations because of multiple sclerosis (MS) hinders ability to plan for future needs. OBJECTIVES: Using a biopsychosocial model, we characterize how men and women with MS report changes over time in their function and test how person-level differences in age, diagnosis duration, and sex influence perceived function. METHODS: A longitudinal study with multiple waves of surveys was used to collect data on participant perceptions of function, as well as demographic and contextual variables. Self-reported functional limitation was measured over a decade. The study participants were community residing with physician-diagnosed MS. RESULTS: The people with MS had a diagnosis duration of about 13 years and were around 51 years of age, on average, at the start of the study. They were primarily women and non-Hispanic White. We analyzed the data using mixed-effects models. Subject-specific, functional limitation trajectories were described best with a quadratic growth model. Relative to men, women reported lower functional limitation and greater between-person variation and rates of acceleration in functional limitation scores. DISCUSSION: Results suggest function progressed through two pathways for over a decade, particularly closer to diagnoses. Variability in trajectories between individuals based on sex and years since diagnosis of disease indicates that men and women with MS may experience perceptions of their function with age differently. This has implications for clinician advice to men and women with MS.
 WHAT IS THIS SUMMARY ABOUT? This summary explains the findings from a recent investigation that combined the results of over 1000 people from three clinical studies to understand the safety of evobrutinib. Evobrutinib is an oral medication (taken by mouth), being researched as a potential treatment for multiple sclerosis (MS). This medication was also investigated in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Over 1000 people have taken evobrutinib as part of three separate phase 2 clinical studies. These studies looked at how much of the drug should be taken, how safe the drug is, and how well it might work for treating a certain medical condition. WHAT WERE THE RESULTS? Evobrutinib was well-tolerated by participants in all three studies. The number of side effects reported by participants taking the medication was very similar to those reported by participants taking the placebo (a 'dummy' treatment without a real drug). The most common side effects in clinical studies were urinary tract infections, headache, swelling of the nose and throat, diarrhoea and blood markers of potential liver damage (these returned to normal once the treatment was stopped). WHAT DO THE RESULTS MEAN? The safety data from all three clinical studies are encouraging and can be used to inform further research into using evobrutinib in MS. Clinical Trial Registration: NCT02975349 (multiple sclerosis), NCT03233230 (rheumatoid arthritis), NCT02975336 (systemic lupus erythematosus) (ClinicalTrials.gov).
 Interferon-beta (IFN-β) subtypes are widely used as immunomodulatory agents for relapsing-remitting multiple sclerosis (MS). Although generally well tolerated, a growing number of reports have recently shown association of long-term IFN-β therapy with several types of glomerulonephritis. Here, we present the case of a 42-year-old woman with MS who developed nephrotic-range proteinuria after taking IFN-β1b for nine years. Initially, due to the presence of histological features consistent with immunoglobulin A (IgA) nephropathy (granular IgA deposits in mesangial lesions), a tonsillectomy plus steroid pulse therapy was performed. However, proteinuria did not significantly decrease after these treatments. Therefore, a second renal biopsy was performed after three years, revealing a membranoproliferative glomerulonephritis-like pattern without immune complex. Further immunofluorescence analysis showed attenuated IgA staining. Consequently, IFN-β1b was replaced with dimethyl fumarate, resulting in complete remission, with proteinuria decreasing to the level of 0.2 g/day. Although it is a rare adverse effect, physicians should pay careful attention to the symptoms and findings of nephritis during the follow-up of patients under treatment with this agent.
 BACKGROUND: Multiple Sclerosis (MS) is a chronic debilitating disease that targets the central nervous system. Globally it is estimated that 2.8 million people live with MS (2018) and as there is no known cure; therefore, identifying methods to increase a patient's quality of life (QoL) is of considerable importance. Non-pharmacological interventions are a viable and effective option to increase QoL in patients with MS, however, to date, the literature lacks a complete systematic review of these interventions. METHODS: A literature search was conducted for studies published up until March 4th 2022 in Scopus, Web of Science, CINAHL Plus, The Cochrane Library, Medline, and Embase. Studies were included if they were randomized control trials (RCTs) assessing a non-pharmacological intervention in adults with MS and measured QoL using the MSQOL-54, SF-36 or MSQLI tools for at least two time points. Quality assessment of each study was completed as well as a review of publication bias. Where possible, meta-analysis was conducted using a random effects model and for other studies a qualitative synthesis was presented. RESULTS: Thirty studies were included in the meta-analysis and eleven studies were summarized qualitatively. The pooled effects across all non-pharmacological interventions showed a modest improvement in both the physical and mental components of QoL, with a standardized mean difference (SMD) of 0.44 (95% CI 0.26-0.61) and 0.42 (95% CI 0.24-0.60), respectively. Non-pharmacological interventions based around a physical activity were found to be particularly effective in improving both the physical composite score (PCS) and mental composite score (MCS), with an SMD of 0.40 (95% CI 0.14-0.66) and 0.31 (95% CI 0.08-0.55), respectively. Interventions incorporating balance exercises presented a significant advantageous solution for improving QoL, with an SMD of 1.71 (95% CI 1.22, 2.20) and 1.63(95% CI 1.15-2.12) for PCS and MCS respectively. CONCLUSIONS: This systematic review and meta-analysis identified that non-pharmacological interventions can be an effective method of improving QoL in patients with MS, especially modalities with a physical activity component and balance interventions.

 BACKGROUND: Multiple sclerosis (MS) is frequently diagnosed in people of reproductive age, many of whom will become pregnant following diagnosis. Although many women report an improvement in symptoms and relapses during pregnancy, symptoms such as fatigue and spasticity are commonly reported and can worsen. Prescribing medications during pregnancy and breastfeeding presents unique challenges and guidance on the use of symptomatic therapies is limited. OBJECTIVES: This paper aims to provide a consensus on the current evidence base to facilitate informed decision-making and optimise pre-conception counselling. METHODS: A list of most commonly prescribed medications for symptom management in MS was created using pregnancy and MS-related READ codes in the Welsh GP Dataset, followed by a review by MS neurologists. RESULTS: A final list of 24 medications was generated for review. Searches were performed on each medication, and evidence graded using standardised criteria. Evidence-based recommendations were developed and distributed to experts in the field and revised according to feedback using modified Delphi criteria. CONCLUSIONS: Our guidelines provide evidence-based recommendations on the safety of symptomatic therapies during pregnancy and breastfeeding for general practitioners and specialist teams working with people with MS who are hoping to embark on pregnancy or are currently pregnant. Individual risk-benefit ratios should be considered during pre-conception counselling to optimise symptom burden and minimise harm to both parent and child.
 Multiple sclerosis (MS) is a neurological condition characterized by severe structural brain damage and by functional reorganization of the main brain networks that try to limit the clinical consequences of structural burden. Resting-state (RS) functional connectivity (FC) abnormalities found in this condition were shown to be variable across different MS phases, according to the severity of clinical manifestations. The article describes a system exploiting machine learning on RS FC matrices to discriminate different MS phenotypes and to identify relevant functional connections for MS stage characterization. To this end, the system exploits some mathematical properties of covariance-based RS FC representation, which can be described by a Riemannian manifold. The classification performance of the proposed framework was significantly above the chance level for all MS phenotypes. Moreover, the proposed system was successful in identifying relevant RS FC alterations contributing to an accurate phenotype classification.
 BACKGROUND: Many clinical studies have shown a correlation between plasma cortisol and neurological disorders. This study explored the causal relationship between plasma cortisol and dementia, epilepsy and multiple sclerosis based on Mendelian randomization (MR) method. METHODS: Data were taken from the summary statistics of a genome-wide association study, FinnGen consortium and United Kingdom Biobank. Dementia, epilepsy, and multiple sclerosis were used as outcomes, and genetic variants associated with plasma cortisol were used as instrumental variables. The main analysis was performed using the inverse variance weighted method, and the results were assessed according to the odds ratio (OR) and 95% confidence interval. Heterogeneity tests, pleiotropy tests, and leave-one-out method were conducted to evaluate the stability and accuracy of the results. RESULTS: In two-sample MR analysis, the inverse variance weighted method showed that plasma cortisol was associated with Alzheimer's disease (AD) [odds ratio (95% confidence interval) = 0.99 (0.98-1.00), P = 0.025], vascular dementia (VaD) [odds ratio (95% confidence interval) = 2.02 (1.00-4.05), P = 0.049)], Parkinson's disease with dementia (PDD) [odds ratio (95% confidence interval) = 0.24 (0.07-0.82), P = 0.023] and epilepsy [odds ratio (95% confidence interval) = 2.00 (1.03-3.91), P = 0.042]. There were no statistically significant associations between plasma cortisol and dementia with Lewy bodies (DLB), frontotemporal dementia (FTD) and multiple sclerosis. CONCLUSION: This study demonstrates that plasma cortisol increase the incidence rates of epilepsy and VaD and decrease the incidence rates of AD and PDD. Monitoring plasma cortisol concentrations in clinical practice can help prevent diseases, such as AD, PDD, VaD and epilepsy.
 OBJECTIVE: to evaluate associations between neurocognitive impairment and electroencephalography (EEG) data in Multiple Sclerosis (MS). METHODS: patients aged between 18 and 65 years, diagnosed with MS accordingly to the McDonald 2017 criteria and who were in remission for at least one month were included. Cognitive functions were evaluated by validated neuropsychological tests for Tunisian population. Electroencephalography data of each patient were analysed, Grand Total EEG (GTE) score was calculated and we evaluated their statistical links with cognitive impairment. RESULTS: Thirty five patients were included. Slower background activity was associated with presence of: reduced information processing speed (IPS) (p = 0,03), verbal memory impairment (p = 0,04) and executive dysfunction (p = 0,016). The score 3 of GTE (reactivity of background activity) was associated with reduced IPS (p = 0,007) and executive dysfunction (p = 0,014). We found a positive correlation between background activity and Tunisian Verbal Test (TVLT) (ρ =0,46 ; p = 0,005) and Symbol Digit Modalities Test (SDMT) (ρ =0,35 ; p = 0,03). Sensitivity of GTE score was 68,4% for executive dysfunction (cut-off=2,5) and 66,7% for reduced IPS (cut-off=2,5). CONCLUSIONS: Our results have shown utility of EEG in detecting cortical involvement and its correlation with cognitive impairment in MS patients. SIGNIFICANCE: EEG could be a tool for monitoring cortical involvement during MS and predict cognitive impairment.
 Aim: To analyze the cost-effectiveness of treatment of relapsing remitting multiple sclerosis (RRMS) with cladribine tablets (CladT) and dimethyl fumarate (DMF) from the perspective of the Spanish National Health System (NHS). Methods: A probabilistic Markov model (second-order Monte Carlo simulation) with a 10-year time horizon and annual Markov cycles was performed. Results: CladT was the dominant treatment, with lower costs (-74,741 € [95% CI: -67,247; -85,661 €]) and greater effectiveness (0.1920 [95% CI: -0.1659; 0.2173] QALY) per patient, compared with DMF. CladT had a 95.1% probability of being cost-effective and a 94.1% chance of being dominant compared with DMF. Conclusion: CladT is the dominant treatment (lower costs, with more QALYs) compared with DMF in the treatment of RRMS in Spain.
 OBJECTIVES: Disease-modifying therapies (DMTs) can slow disease progression in multiple sclerosis (MS). The objective of this study was to explore the cost-of-illness (COI) progression among newly diagnosed people with MS in relation to the first DMT received. DESIGN AND SETTING: A cohort study using data from nationwide registers in Sweden. PARTICIPANTS: People with MS (PwMS) in Sweden first diagnosed in 2006-2015, when aged 20-55, receiving first-line therapy with interferons (IFN), glatiramer acetate (GA) or natalizumab (NAT). They were followed up through 2016. OUTCOME MEASURES: Outcomes (in Euros, €) were: (1) secondary healthcare costs: specialised outpatient and inpatient care including out-of-pocket expenditure, DMTs including hospital-administered MS therapies, and prescribed drugs, and (2) productivity losses: sickness absence and disability pension. Descriptive statistics and Poisson regression were computed, adjusting for disability progression using the Expanded Disability Status Scale. RESULTS: 3673 newly diagnosed PwMS who were treated with IFN (N=2696), GA (N=441) or NAT (N=536) were identified. Healthcare costs were similar for the INF and GA groups, while the NAT group had higher costs (p value<0.05), owing to DMT and outpatient costs. IFN had lower productivity losses than NAT and GA (p value>0.05), driven by fewer sickness absence days. NAT had a trend towards lower disability pension costs compared with GA (p value>0.05). CONCLUSIONS: Similar trends over time for healthcare costs and productivity losses were identified across the DMT subgroups. PwMS on NAT maintained their work capacity for a longer time compared with those on GA, potentially leading to lower disability pension costs over time. COI serves as an objective measure to explore the importance of DMTs in maintaining low levels of progression of MS over time.
 Multiple sclerosis (MS) is a debilitating disease that requires prolonged treatment with often severe side effects. One experimental MS therapeutic currently under development is a single amino acid mutant of a plant peptide termed kalata B1, of the cyclotide family. Like all cyclotides, the therapeutic candidate [T20K]kB1 is highly stable as it contains a cyclic backbone that is cross-linked by three disulfide bonds in a knot-like structure. This stability is much sought after for peptide drugs, which despite exquisite selectivity for their targets, are prone to rapid degradation in human serum. In preliminary investigations, it was found that [T20K]kB1 retains oral activity in experimental autoimmune encephalomyelitis, a model of MS in mice, thus opening up opportunities for oral dosing of the peptide. Although [T20K]kB1 can be synthetically produced, a recombinant production system provides advantages, specifically for reduced scale-up costs and reductions in chemical waste. In this study, we demonstrate the capacity of the Australian native Nicotiana benthamiana plant to produce a structurally identical [T20K]kB1 to that of the synthetic peptide. By optimizing the co-expressed cyclizing enzyme, precursor peptide arrangements, and transgene regulatory regions, we demonstrate a [T20K]kB1 yield in crude peptide extracts of ~ 0.3 mg/g dry mass) in whole plants and close to 1.0 mg/g dry mass in isolated infiltrated leaves. With large-scale plant production facilities coming on-line across the world, the sustainable and cost-effective production of cyclotide-based therapeutics is now within reach.
 INTRODUCTION: Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS). Although there are several disease-modifying therapies that can effectively manage MS relapses, the treatment of chronic progressive MS remains a difficult task. CNS-compartmentalized inflammation plays a primary role in progressive MS, especially by activated microglia. In this context, Bruton's tyrosine kinase (BTK) inhibition may be a promising therapeutic approach, as the enzyme is centrally involved in the activation of B cells as well as myeloid cells, such as macrophages and microglia. AREAS COVERED: This paper discusses a novel and promising approach for MS treatment. We discuss the factors assumed to promote progression in MS and how this process could be counteracted by BTK inhibition, as well as summarize all available clinical data on the usefulness of this therapeutic approach for halting MS progression. EXPERT OPINION: Current therapeutic approaches in MS are effective for treating relapses but fail to halt progression of the disease. This reflects the emerging concept that the underlying pathophysiology of chronic progressive MS differs from that of relapsing-remitting MS. Understanding the CNS intrinsic process in more detail provides novel therapeutic targets, and one of these may be the inhibition of the enzyme BTK.

 BACKGROUND AND OBJECTIVES: Relapsing-remitting multiple sclerosis (RRMS), aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) may have overlapping clinical features. There is an unmet need for imaging markers that differentiate between them when serologic testing is unavailable or ambiguous. We assessed whether imaging characteristics typical of MS discriminate RRMS from AQP4-NMOSD and MOGAD, alone and in combination. METHODS: Adult, nonacute patients with RRMS, APQ4-NMOSD, and MOGAD and healthy controls were prospectively recruited at the National Hospital for Neurology and Neurosurgery (London, United Kingdom) and the Walton Centre (Liverpool, United Kingdom) between 2014 and 2019. They underwent conventional and advanced brain, cord, and optic nerve MRI and optical coherence tomography (OCT). RESULTS: A total of 91 consecutive patients (31 RRMS, 30 APQ4-NMOSD, and 30 MOGAD) and 34 healthy controls were recruited. The most accurate measures differentiating RRMS from AQP4-NMOSD were the proportion of lesions with the central vein sign (CVS) (84% vs 33%, accuracy/specificity/sensitivity: 91/88/93%, p < 0.001), followed by cortical lesions (median: 2 [range: 1-14] vs 1 [0-1], accuracy/specificity/sensitivity: 84/90/77%, p = 0.002) and white matter lesions (mean: 39.07 [±25.8] vs 9.5 [±14], accuracy/specificity/sensitivity: 78/84/73%, p = 0.001). The combination of higher proportion of CVS, cortical lesions, and optic nerve magnetization transfer ratio reached the highest accuracy in distinguishing RRMS from AQP4-NMOSD (accuracy/specificity/sensitivity: 95/92/97%, p < 0.001). The most accurate measures favoring RRMS over MOGAD were white matter lesions (39.07 [±25.8] vs 1 [±2.3], accuracy/specificity/sensitivity: 94/94/93%, p = 0.006), followed by cortical lesions (2 [1-14] vs 1 [0-1], accuracy/specificity/sensitivity: 84/97/71%, p = 0.004), and retinal nerve fiber layer thickness (RNFL) (mean: 87.54 [±13.83] vs 75.54 [±20.33], accuracy/specificity/sensitivity: 80/79/81%, p = 0.009). Higher cortical lesion number combined with higher RNFL thickness best differentiated RRMS from MOGAD (accuracy/specificity/sensitivity: 84/92/77%, p < 0.001). DISCUSSION: Cortical lesions, CVS, and optic nerve markers achieve a high accuracy in distinguishing RRMS from APQ4-NMOSD and MOGAD. This information may be useful in clinical practice, especially outside the acute phase and when serologic testing is ambiguous or not promptly available. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that selected conventional and advanced brain, cord, and optic nerve MRI and OCT markers distinguish adult patients with RRMS from AQP4-NMOSD and MOGAD.
 Multiple Sclerosis (MS) is a progressive demyelinating disease of the central nervous system characterised by a wide range of motor and non-motor symptoms. The level of disability of people with MS (pwMS) is based on a wide range of clinical measures, though their frequency of evaluation and inaccuracies coming from objective and self-reported evaluations limits these assessments. Alternatively, remote health monitoring through devices can offer a cost-efficient solution to gather more reliable, objective measures continuously. Measuring smartphone keyboard interactions is a promising tool since typing and, thus, keystroke dynamics are likely influenced by symptoms that pwMS can experience. Therefore, this paper aims to investigate whether keyboard interactions gathered on a person's smartphone can provide insight into the clinical status of pwMS leveraging machine learning techniques. In total, 24 Healthy Controls (HC) and 102 pwMS were followed for one year. Next to continuous data generated via smartphone interactions, clinical outcome measures were collected and used as targets to train four independent multivariate binary classification pipelines in discerning pwMS versus HC and estimating the level of disease severity, manual dexterity and cognitive capabilities. The final models yielded an AUC-ROC in the hold-out set above 0.7, with the highest performance obtained in estimating the level of fine motor skills (AUC-ROC=0.753). These findings show that keyboard interactions combined with machine learning techniques can be used as an unobtrusive monitoring tool to estimate various levels of clinical disability in pwMS from daily activities and with a high frequency of sampling without increasing patient burden.
 Multiple sclerosis (MS) results from an autoimmune attack on the central nervous system (CNS). Dysregulated immune cells invade the CNS, causing demyelination, neuronal and axonal damage, and subsequent neurological disorders. Although antigen-specific T cells mediate the immunopathology of MS, innate myeloid cells have essential contributions to CNS tissue damage. Dendritic cells (DCs) are professional antigen-presenting cells (APCs) that promote inflammation and modulate adaptive immune responses. This review focuses on DCs as critical components of CNS inflammation. Here, evidence from studies is summarized with animal models of MS and MS patients that support the critical role of DCs in orchestrating CNS inflammation.
 OBJECTIVE: The aim of this study was to assess the presence of detectable changes of skin thickness on clinical brain magnetic resonance imaging (MRI) scans in patients with MS, history of multiple gadolinium-based contrast agents (GBCAs) administrations, and evidence of gadolinium deposition in the brain. MATERIALS AND METHODS: In this observational cross-sectional study, 71 patients with MS who underwent conventional brain MRI with an imaging protocol including enhanced 3D volumetric interpolated breath-hold examination (VIBE) T1-weighted with fat saturation were assessed. Patients with bilateral isointense dentate nucleus on unenhanced T1-weighted images were assigned to group A (controls without MRI evidence of gadolinium deposition), and patients with visually hyperintense dentate nuclei were assigned to group B. Qualitative and quantitative assessment of the skin thickness were performed. RESULTS: Group A included 27 patients (median age, 33 years [IQR, 27-46]; 20 women), and group B included 44 patients (median age, 42 years [IQR, 35-53]; 29 women). Qualitative and quantitative assessment of the skin revealed significant differences between group A and group B. The average skin-to-scalp thickness ratios was significantly higher in group B than in group A (mean ± standard deviation = 0.52 ± 0.02 in group B vs 0.41 ± 0.02 in group A, P < 0.0001) and showed a positive correlation with the total number of enhanced MRI scans ( r = 0.39; 95% confidence interval, 0.17-0.57, P < 0.01). CONCLUSIONS: Brain MRI detects increased skin thickness of the scalp in patients with MS and dentate nucleus high signal intensity on unenhanced T1-weighted images and shows positive association with previous exposures to linear GBCAs rather than macrocyclic GBCAs.
 BACKGROUND AND OBJECTIVES: B cell-depleting antibodies were proven as effective strategy for the treatment of relapsing multiple sclerosis (RMS). The monoclonal antibody ocrelizumab was approved in 2017 in the United States and in 2018 in the European Union, but despite proven efficacy in randomized, controlled clinical trials, its effectiveness in the real-world setting remains to be fully elucidated. In particular, most study patients were treatment naive or switched from injectable therapies, whereas oral substances or monoclonal antibodies made up >1% of previous treatments. METHODS: We evaluated ocrelizumab-treated patients with RMS enrolled in the prospective cohorts at the University Hospitals Duesseldorf and Essen, Germany. Epidemiologic data at baseline were compared, and Cox proportional hazard models were applied to evaluate outcomes. RESULTS: Two hundred eighty patients were included (median age: 37 years, 35% male patients). Compared with using ocrelizumab as a first-line treatment, its use as a third-line therapy increased hazard ratios (HRs) for relapse and disability progression, whereas differences between first- vs second-line and second- vs third-line remained smaller. We stratified patients according to their last previous disease-modifying treatment and here identified fingolimod (FTY) (45 patients, median age 40 years, 33% male patients) as a relevant risk factor for ongoing relapse activity despite 2nd-line (HR: 3.417 [1.007-11.600]) or 3rd-line (HR: 5.903 [2.489-13.999]) ocrelizumab treatment, disability worsening (2nd line: HR: 3.571 [1.013-12.589]; 3rd line: HR: 4.502 [1.728-11.729]), and occurrence of new/enlarging MRI lesions (2nd line: HR: 1.939 [0.604-6.228]; 3rd line: HR: 4.627 [1.982-10.802]). Effects were persistent throughout the whole follow-up. Neither peripheral B-cell repopulation nor immunoglobulin G levels were associated with rekindling disease activity. DISCUSSION: Our prospectively collected observational data suggest suboptimal effectiveness of ocrelizumab in patients switching from FTY compared with those switching from other substances or having been treatment naive. These findings support previous studies indicating abated effectiveness of immune cell-depleting therapies following FTY treatment in patients with RMS. CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that for patients with RMS, previous treatment with FTY compared with previous treatment with other immunomodulating therapies decreases the effectiveness of ocrelizumab.
 Since the early 1980s, Epstein-Barr virus (EBV) infection has been described as one of the main risk factors for developing multiple sclerosis (MS), and recently, new epidemiological evidence has reinforced this premise. EBV seroconversion precedes almost 99% of the new cases of MS and likely predates the first clinical symptoms. The molecular mechanisms of this association are complex and may involve different immunological routes, perhaps all running in parallel (i.e., molecular mimicry, the bystander damage theory, abnormal cytokine networks, and coinfection of EBV with retroviruses, among others). However, despite the large amount of evidence available on these topics, the ultimate role of EBV in the pathogenesis of MS is not fully understood. For instance, it is unclear why after EBV infection some individuals develop MS while others evolve to lymphoproliferative disorders or systemic autoimmune diseases. In this regard, recent studies suggest that the virus may exert epigenetic control over MS susceptibility genes by means of specific virulence factors. Such genetic manipulation has been described in virally-infected memory B cells from patients with MS and are thought to be the main source of autoreactive immune responses. Yet, the role of EBV infection in the natural history of MS and in the initiation of neurodegeneration is even less clear. In this narrative review, we will discuss the available evidence on these topics and the possibility of harnessing such immunological alterations to uncover predictive biomarkers for the onset of MS and perhaps facilitate prognostication of the clinical course.
 Motor fatigue is one of the most common symptoms in multiple sclerosis (MS) patients. Previous studies suggested that increased motor fatigue in MS may arise at the central nervous system level. However, the mechanisms underlying central motor fatigue in MS are still unclear. This paper investigated whether central motor fatigue in MS reflects impaired corticospinal transmission or suboptimal primary motor cortex (M1) output (supraspinal fatigue). Furthermore, we sought to identify whether central motor fatigue is associated with abnormal M1 excitability and connectivity within the sensorimotor network. Twenty-two patients affected by relapsing-remitting MS and 15 healthy controls (HCs) performed repeated blocks of contraction at different percentages of maximal voluntary contraction with the right first dorsal interosseus muscle until exhaustion. Peripheral, central, and supraspinal components of motor fatigue were quantified by a neuromuscular assessment based on the superimposed twitch evoked by peripheral nerve and transcranial magnetic stimulation (TMS). Corticospinal transmission, excitability and inhibition during the task were tested by measurement of motor evoked potential (MEP) latency, amplitude, and cortical silent period (CSP). M1 excitability and connectivity was measured by TMS-evoked electroencephalography (EEG) potentials (TEPs) elicited by M1 stimulation before and after the task. Patients completed fewer blocks of contraction and showed higher values of central and supraspinal fatigue than HCs. We found no MEP or CSP differences between MS patients and HCs. Patients showed a post-fatigue increase in TEPs propagation from M1 to the rest of the cortex and in source-reconstructed activity within the sensorimotor network, in contrast to the reduction observed in HCs. Post-fatigue increase in source-reconstructed TEPs correlated with supraspinal fatigue values. To conclude, MS-related motor fatigue is caused by central mechanisms related explicitly to suboptimal M1 output rather than impaired corticospinal transmission. Furthermore, by adopting a TMS-EEG approach, we proved that suboptimal M1 output in MS patients is associated with abnormal task-related modulation of M1 connectivity within the sensorimotor network. Our findings shed new light on the central mechanisms of motor fatigue in MS by highlighting a possible role of abnormal sensorimotor network dynamics. These novel results may point to new therapeutical targets for fatigue in MS.
 OBJECTIVE: Nutrition modulation can reduce multiple sclerosis (MS) related symptoms and fatigue severity. Mediterranean diet may be beneficial regarding anti-inflammatory components. However, previous studies are limited. This study aims to investigate the relationship between Mediterranean diet adherence and MS-related symptoms and fatigue severity. METHODS: One hundred and two adult MS patients were enrolled in this cross-sectional study. Dietary adherence was assessed using the Mediterranean diet assessment tool (MEDAS). MS-related symptoms were determined using the MS-related symptom checklist (MS-RS), and the fatigue severity scale (FSS) was applied. Linear regression models were established to assess predicted factors of MS-RS and FSS. RESULTS: The mean age of the participants was 33.1  ±  9.81 years. Being female and having higher education degree was 71.6% and 60.8%, respectively. In the linear regression model, MEDAS were not associated with MS-RS but negatively associated with FSS scores. MS-RS scores were significantly higher among participants who consumed more than one serving of red meat or products per day. Those who consumed less than one serving of butter, margarine, or cream per day reported lower FSS scores. Some trend significances were shown to consume limited sweet and lower FSS scores. Likewise, MS-RS scores were lower in those ≥three serving/week intake of fish. CONCLUSION: Following a Mediterranean-style diet should be encouraged to improve fatigue severity. Components, such as reduced consumption of red meat, saturated fatty acids, sweets and increased fish consumption, could be promising to reduce MS symptoms or fatigue severity. These findings should be proven with further intervention studies.
 BACKGROUND: The central vein sign (CVS) on brain magnetic resonance imaging (MRI) is a promising diagnostic marker for distinguishing adult multiple sclerosis (MS) from other demyelinating conditions, but its prevalence is not well-established in pediatric-onset multiple sclerosis (POMS) versus myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). MOGAD can mimic MS radiologically. This study seeks to determine the utility of CVS, together with other radiological findings, in distinguishing POMS from MOGAD in children. METHODS: Children with POMS or MOGAD were identified in a pediatric demyelinating database. Two reviewers, blinded to diagnosis, fused fluid-attenuated inversion recovery sequences and susceptibility-weighted imaging from clinical imaging to identify CVS. Agreement in CVS number was reported using intraclass correlation coefficients (ICC). We performed topographic analyses as well as characterization of the clinical information and lesions on brain, spinal cord, and orbital MRI when available. RESULTS: Twenty children, 10 with POMS and 10 with MOGAD, were assessed. The median lesion percentage of CVS was higher in POMS versus MOGAD for both raters (rater 1: 80% vs 9.8%; rater 2: 22.7% vs 7.5%). Inter-rater reliability for identifying total white matter lesions was strong (ICC 0.94 [95% confidence interval [CI] 0.84, 0.97]); however, it was poor for detecting CVS lesions (ICC -0.17 [95% CI: -0.37, 0.58]). CONCLUSION: The CVS can be a useful diagnostic tool for differentiating POMS from MOGAD. However, advanced clinical imaging tools that can better detect CVS are needed to increase inter-rater reliability before clinical application.
 The ongoing developments of psychiatric classification systems have largely improved reliability of diagnosis, including that of schizophrenia. However, with an unknown pathophysiology and lacking biomarkers, its validity still remains low, requiring further advancements. Research has helped establish multiple sclerosis (MS) as the central nervous system (CNS) disorder with an established pathophysiology, defined biomarkers and therefore good validity and significantly improved treatment options. Before proposing next steps in research that aim to improve the diagnostic process of schizophrenia, it is imperative to recognize its clinical heterogeneity. Indeed, individuals with schizophrenia show high interindividual variability in terms of symptomatic manifestation, response to treatment, course of illness and functional outcomes. There is also a multiplicity of risk factors that contribute to the development of schizophrenia. Moreover, accumulating evidence indicates that several dimensions of psychopathology and risk factors cross current diagnostic categorizations. Schizophrenia shares a number of similarities with MS, which is a demyelinating disease of the CNS. These similarities appear in the context of age of onset, geographical distribution, involvement of immune-inflammatory processes, neurocognitive impairment and various trajectories of illness course. This article provides a critical appraisal of diagnostic process in schizophrenia, taking into consideration advancements that have been made in the diagnosis and management of MS. Based on the comparison between the two disorders, key directions for studies that aim to improve diagnostic process in schizophrenia are formulated. All of them converge on the necessity to deconstruct the psychosis spectrum and adopt dimensional approaches with deep phenotyping to refine current diagnostic boundaries.
 Automated methods for segmentation-based brain volumetry may be confounded by the presence of white matter (WM) lesions, which introduce abnormal intensities that can alter the classification of not only neighboring but also distant brain tissue. These lesions are common in pathologies where brain volumetry is also an important prognostic marker, such as in multiple sclerosis (MS), and thus reducing their effects is critical for improving volumetric accuracy and reliability. In this work, we analyze the effect of WM lesions on deep learning based brain tissue segmentation methods for brain volumetry and introduce techniques to reduce the error these lesions produce on the measured volumes. We propose a 3D patch-based deep learning framework for brain tissue segmentation which is trained on the outputs of a reference classical method. To deal more robustly with pathological cases having WM lesions, we use a combination of small patches and a percentile-based input normalization. To minimize the effect of WM lesions, we also propose a multi-task double U-Net architecture performing end-to-end inpainting and segmentation, along with a training data generation procedure. In the evaluation, we first analyze the error introduced by artificial WM lesions on our framework as well as in the reference segmentation method without the use of lesion inpainting techniques. To the best of our knowledge, this is the first analysis of WM lesion effect on a deep learning based tissue segmentation approach for brain volumetry. The proposed framework shows a significantly smaller and more localized error introduced by WM lesions than the reference segmentation method, that displays much larger global differences. We also evaluated the proposed lesion effect minimization technique by comparing the measured volumes before and after introducing artificial WM lesions to healthy images. The proposed approach performing end-to-end inpainting and segmentation effectively reduces the error introduced by small and large WM lesions in the resulting volumetry, obtaining absolute volume differences of 0.01 ± 0.03% for GM and 0.02 ± 0.04% for WM. Increasing the accuracy and reliability of automated brain volumetry methods will reduce the sample size needed to establish meaningful correlations in clinical studies and allow its use in individualized assessments as a diagnostic and prognostic marker for neurodegenerative pathologies.
 Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease that affects the nervous system. Peripheral blood leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNA-CN) are potential biomarkers of neurological disability and neural damage. Our objective was to assess the LTL and mtDNA-CN in relapsing-remitting MS (RRMS). We included 10 healthy controls, 75 patients with RRMS, 50 of whom had an Expanded Disability Status Scale (EDSS) from 0 to 3 (mild to moderate disability), and 25 had an EDSS of 3.5 to 7 (severe disability). We use the Real-Time Polymerase Chain Reaction (qPCR) technique to quantify absolute LTL and absolute mtDNA-CN. ANOVA test show differences between healthy control vs. severe disability RRMS and mild-moderate RRMS vs. severe disability RRMS (p = 0.0130). LTL and mtDNA-CN showed a linear correlation in mild-moderate disability RRMS (r = 0.378, p = 0.007). Furthermore, we analyzed LTL between RRMS groups with a ROC curve, and LTL can predict severe disability (AUC = 0.702, p = 0.0018, cut-off < 3.0875 Kb, sensitivity = 75%, specificity = 62%), whereas the prediction is improved with a logistic regression model including LTL plus age (AUC = 0.762, p = 0.0001, sensitivity = 79.17%, specificity = 80%). These results show that LTL is a biomarker of disability in RRMS and is correlated with mtDNA-CN in mild-moderate RRMS patients.
 Multiple sclerosis (MS) is a chronic disease affecting the central nervous system (CNS) due to an autoimmune attack on axonal myelin sheaths. Epigenetics is an open research topic on MS, which has been investigated in search of biomarkers and treatment targets for this heterogeneous disease. In this study, we quantified global levels of epigenetic marks using an ELISA-like approach in Peripheral Blood Mononuclear Cells (PBMCs) from 52 patients with MS, treated with Interferon beta (IFN-β) and Glatiramer Acetate (GA) or untreated, and 30 healthy controls. We performed media comparisons and correlation analyses of these epigenetic markers with clinical variables in subgroups of patients and controls. We observed that DNA methylation (5-mC) decreased in treated patients compared with untreated and healthy controls. Moreover, 5-mC and hydroxymethylation (5-hmC) correlated with clinical variables. In contrast, histone H3 and H4 acetylation did not correlate with the disease variables considered. Globally quantified epigenetic DNA marks 5-mC and 5-hmC correlate with disease and were altered with treatment. However, to date, no biomarker has been identified that can predict the potential response to therapy before treatment initiation.
 BACKGROUND: Figure of 8 Walk Test (F8WT) assesses the multidirectional and adaptive requirements of both straight and curved path walking. The study aimed to examine the reliability, validity, and minimal detectable change (MDC) of the F8WT in patients with Multiple Sclerosis (pwMS). METHODS: 45 mildly disabled pwMS (10 male, 35 female) were included in the study. Reliability of F8WT test was evaluated with Intraclass Correlation Coefficient (ICC). MDC estimates were calculated using baseline data. The correlation between the F8WT and Berg Balance Scale (BBS), The Timed Up and Go test (TUG), The Timed 25-Foot Walk Test (T25FW), The Four Square Step Test (FSST) was used for the validity. RESULTS: The intra-rater (ICC 0.980-0.983) and inter-rater (ICC 0.976-0.985) reliability of the F8WT was determined to be excellent. MDC values for intra-rater were 1.04-1.08 s, and MDC values for inter-rater were 1.16-0.99 s. The correlation with F8WT and BBS (p = 0.000, r = -0.702), TUG (p = 0.000, r = 0.854), T25FW (p = 0.000, r = 0.784), FSST (p = 0.000, r = 0.748) was found to be statistically significant. CONCLUSION: The F8WT has good reliability and validity in mildly disabled pwMS. According to the MDC results, small differences in pwMS can be adequately detected with F8WT. Therefore, it may be a clinically suitable test for detecting balance and walking.
 STUDY OBJECTIVES: This study aims to explore the polysomnographically measured sleep differences between patients with multiple sclerosis (MS) and healthy control patients. METHODS: An electronic literature search was conducted in EMBASE, MEDLINE, all EBM databases, CINAHL, and PsycINFO from inception to March 2022. A random-effects model was applied to explore the pooled effect sizes of polysomnographic differences between patients with MS and control patients. RESULTS: Thirteen studies were identified for meta-analysis. The meta-analyses revealed significant reductions in stage N2 sleep and sleep efficiency and increases in wake time after sleep onset, the periodic limb movement index, and the periodic limb movement arousal index in patients with MS compared with control patients. Meta-regression analyses showed that some of the heterogeneity was explained by age and daytime sleepiness of patients with MS. CONCLUSIONS: Our study showed that polysomnographic abnormalities are present in MS. Our findings also underscore the need for a comprehensive polysomnographic assessment of sleep changes in patients with MS. Furthermore, the effects of age and daytime sleepiness in patients with MS on sleep changes should also be carefully considered and closely monitored in the management of MS. CITATION: Zhang Y, Ren R, Yang L, et al. Sleep in multiple sclerosis: a systematic review and meta-analysis of polysomnographic findings. J Clin Sleep Med. 2023;19(2):253-265.
 Objectives: Difficulties with prospective memory (PM) are not routinely assessed in persons with multiple sclerosis (MS) even though they can impact daily functioning. This study aimed to examine the preliminary criterion and ecological validity of a highly abbreviated Memory for Intentions Test (MIST) intended to serve as an initial screening of PM in persons with MS. Methods: Participants (n = 112) were classified as impaired if they performed 1.5 standard deviations below the normative mean on the MIST. Individual MIST trials with adequate difficulty and discriminability were examined using receiver operating characteristic analyses, with their classification accuracies, sensitivities, and specificities compared to each other. Regressions were run to evaluate their ecological validity, with appointment attendance and employment as the outcomes. Results: Two trials had a classification accuracy of ≥80%: Trial 3 (79% sensitivity, 84% specificity) and Trial 4 (57% sensitivity, 91% specificity). These two trials had comparable specificity (p=.127), with Trial 3 having slightly higher sensitivity (p=.083). Only Trial 4 was significantly associated with appointment attendance (b = 1.63, p=.047) and unemployment (aOR = 11.20, p=.027). Discussion:Trial 4 of the MIST, a verbal task with a time-based cue that requires participants to complete a pre-specified response after a 15-minute delay, has the potential to be a screener for PM.
 Multiple Sclerosis (MS) is an autoimmune disease that causes brain and spinal cord lesions, which magnetic resonance imaging (MRI) can detect and characterize. Recently, deep learning methods have achieved remarkable results in the automated segmentation of MS lesions from MRI data. Hence, this study proposes a novel dense residual U-Net model that combines attention gate (AG), efficient channel attention (ECA), and Atrous Spatial Pyramid Pooling (ASPP) to enhance the performance of the automatic MS lesion segmentation using 3D MRI sequences. First, convolution layers in each block of the U-Net architecture are replaced by residual blocks and connected densely. Then, AGs are exploited to capture salient features passed through the skip connections. The ECA module is appended at the end of each residual block and each downsampling block of U-Net. Later, the bottleneck of U-Net is replaced with the ASSP module to extract multi-scale contextual information. Furthermore, 3D MR images of Fluid Attenuated Inversion Recovery (FLAIR), T1-weighted (T1-w), and T2-weighted (T2-w) are exploited jointly to perform better MS lesion segmentation. The proposed model is validated on the publicly available ISBI2015 and MSSEG2016 challenge datasets. This model produced an ISBI score of 92.75, a mean Dice score of 66.88%, a mean positive predictive value (PPV) of 86.50%, and a mean lesion-wise true positive rate (LTPR) of 60.64% on the ISBI2015 testing set. Also, it achieved a mean Dice score of 67.27%, a mean PPV of 65.19%, and a mean sensitivity of 74.40% on the MSSEG2016 testing set. The results show that the proposed model performs better than the results of some experts and some of the other state-of-the-art methods realized related to this particular subject. Specifically, the best Dice score and the best LTPR are obtained on the ISBI2015 testing set by using the proposed model to segment MS lesions.
 Introduction: Multiple sclerosis (MS) is a progressive disease of the central nervous system that can result in highly variable effects on mobility and sensorimotor function. Persons with MS (pwMS) often use complementary and alternative approaches, such as acupuncture, to address these symptoms. However, studies of acupuncture on these symptoms have been hindered by methodologic flaws, which have limited the ability to draw conclusions about its efficacy. The purpose of this study was to examine the feasibility of an acupuncture intervention on a wide range of sensorimotor and mobility measurements in pwMS. Methods: Using a randomized crossover design, subjects experienced acupuncture or a no treatment control condition twice weekly for 4 weeks, followed by a 4-week washout period, and then crossed over to the other condition for 4 weeks. Strength, sensation, spasticity, gait, and balance were measured for all subjects, both before and after each condition. Results: Seven of the 12 subjects who started the program completed all phases. No subjects experienced adverse effects. No statistically significant changes were observed in the gait or balance measures. Small statistically significant changes were observed in upper extremity strength. Sensation and spasticity were unaffected. Discussion: The variability of MS suggests that a wide array of testing procedures be utilized, however, this may have led to difficulty with completing all phases of the study. Acupuncture did not result in changes in mobility in pwMS. Some improvements in upper extremity strength were observed. It is unclear whether these changes represent the effect of acupuncture or the inherent variability of MS.
 DISCLOSURES: Ms McKenna, Dr Lin, Dr Whittington, Mr Nikitin, Ms Herron-Smith, Dr Campbell, and Dr Peterson report grants from Arnold Ventures, grants from Blue Cross Blue Shield of MA, grants from California Healthcare Foundation, grants from The Commonwealth Fund, and grants from The Peterson Center on Healthcare, during the conduct of the study; other from America's Health Insurance Plans, other from Anthem, other from AbbVie, other from Alnylam, other from AstraZeneca, other from Biogen, other from Blue Shield of CA, other from CVS, other from Editas, other from Express Scripts, other from Genentech/Roche, other from GlaxoSmithKline, other from Harvard Pilgrim, other from Health Care Service Corporation, other from Kaiser Permanente, other from LEO Pharma, other from Mallinckrodt, other from Merck, other from Novartis, other from National Pharmaceutical Council, other from Premera, other from Prime Therapeutics, other from Regeneron, other from Sanofi, other from United Healthcare, other from HealthFirst, other from Pfizer, other from Boehringer-Ingelheim, other from uniQure, other from Envolve Pharmacy Solutions, other from Humana, and other from Sun Life, outside the submitted work.
 The prevalence of multiple sclerosis (MS) in Asian countries is thought to be lower than in Western countries, with Asian populations presenting 80% less risk of MS than white populations. Incidence and prevalence rates in Asian countries are therefore not well defined and their association with rates in neighboring countries, as well as with ethnic, environmental, and socioeconomic factors, are not well understood. We performed a comprehensive literature review of epidemiological data from China and neighbouring countries to study the frequency of the disease, focusing on prevalence, and the progression over time and the influence of sex-related, environmental, dietary, and sociocultural factors. Prevalence rates in China range between 0.88 cases/100,000 population in 1986 and 5.2 cases/100,000 population in 2013, with a non-significant upwards trend (p = .08). The increase observed in Japan, where figures ranged between 8.1 and 18.6 cases/100,000 population was highly significant (p < .001). Prevalence rates in countries with predominantly white populations are considerably higher and have increased over time, reaching 115 cases/100,000 population in 2015 (r(2) = 0.79, p < .0001). In conclusion, the prevalence of MS in China appears to have risen in recent years, although Asian populations (including Chinese and Japanese populations, among others) appear to present less risk than other populations. Within Asia, geographical latitude appears not to be a determining factor for developing MS.
 PURPOSE: This study aims to investigate the role of in vivo corneal confocal microscopy (IVCCM) in the detection of corneal inflammatory activity and subbasal nerve alterations in patients with multiple sclerosis (MS) and to further determine whether IVCCM can be used to detect (acute) disease relapse. DESIGN: Prospective cross-sectional study, with a subgroup follow-up. METHODS: This single-center study included 58 patients with MS (MS-Relapse group [n = 27] and MS-Remission group [n = 31]), and 30 age- and sex-matched healthy control subjects. Patients with a history of optic neuritis or trigeminal symptoms were excluded. Corneal nerve fiber density (CNFD), corneal nerve branch density (CNBD), corneal nerve fiber length (CNFL), and dendritic cell (DC) density were evaluated in all patients with MS and control subjects by IVCCM. Patients in the MS-Relapse group who were in remission for ≥6 months after the MS incident underwent a repeat IVCCM. RESULTS: No statistical difference was observed between the MS-Relapse and MS-Remission groups regarding age, sex, MS duration, and the number of relapses (P > .05). Compared with healthy control subjects, all subbasal nerve parameters were significantly lower (CNFD: P < .001, CNFL: P < .001, CNBD: P < .001), and the DC density was significantly higher (P = .023) in patients with MS. However, no significant difference was observed between MS-Relapse and MS-Remission groups in terms of CNFD (mean [SE] difference -2.05 [1.69] fibers/mm(2) [95% confidence interval {CI} -1.32 to 5.43]; P < .227), CNFL (mean [SE] difference -1.10 [0.83] mm/mm(2) [95% CI -0.56 to 2.75]; P < .190), CNBD (mean [SE] difference -3.91 [2.48] branches/mm(2) [95% CI -1.05 to 8.87]; P < .120), and DC density (median [IQR], 59.38 [43.75-85.0] vs 75.0 [31.25-128.75]; P = .596). The repeat IVCCM in relapse patients (n = 16 [59.3%]) showed a significant increase in CNFD (P = .036) and CNBD (P = .018), but no change was observed in CNFL (P = .075) and DC density (P = .469). CONCLUSION: Although increased inflammation and neurodegeneration can be demonstrated in patients with MS compared with healthy control subjects, a single time point evaluation of IVCCM does not seem to be sufficient to confirm the occurrence of relapse in patients with MS. However, IVCCM holds promise for demonstrating early neuroregeneration in patients with MS.
 Although multiple sclerosis (MS) and multiple system atrophy (MSA) are both characterized by impaired oligodendrocytes (OLs), the aetiological relevance remains obscure. Given inherent stressors affecting OLs, the objective of the present study was to discuss the possible role of amyloidogenic evolvability (aEVO) in these conditions. Hypothetically, in aEVO, protofibrils of amyloidogenic proteins (APs), including β-synuclein and β-amyloid, might form in response to diverse stressors in parental brain. Subsequently, the AP protofibrils might be transmitted to offspring via germ cells in a prion-like fashion. By virtue of the stress information conferred by protofibrillar APs, the OLs in offspring's brain might be more resilient to forthcoming stressors, perhaps reducing MS risk. aEVO could be comparable to a gene for the inheritance of acquired characteristics. On the contrary, during ageing, MSA risk is increased through antagonistic pleiotropy. Consistently, the expression levels of APs are reduced in MS, but are increased in MSA compared to controls. Furthermore, β-synuclein, the non-amyloidogenic homologue of β-synuclein, might exert a buffering effect on aEVO, and abnormal β-synuclein could also increase MS and MSA disease activity. Collectively, a better understanding of the role of aEVO in the OL diseases might lead to novel interventions for such chronic degenerative conditions.
 INTRODUCTION: Our study aimed to evaluate whether assessing α-synuclein expression levels in blood samples could provide a reliable and straightforward alternative to existing diagnostic and prognostic methods for neurodegenerative disorders, including multiple sclerosis (MS). We specifically investigated if α-synuclein and IL-6 expression levels from serum and peripheral blood mononuclear cells (PBMCs) could accurately predict MS severity in patients using a two-dimensional approach. METHODS: We designed a case-control study to analyze the expression of α-synuclein and IL-6 in the peripheral blood of an MS patient group (n = 51) and a control group (n = 51). We statistically evaluated the PBMCs and serum profiles of α-synuclein and IL-6 in MS patients, along with their age of onset, disease duration, tobacco exposure, and Expanded Disability Status Scale (EDSS) score, using SPSS V22.0 software and GraphPad Prism V9.0. RESULTS: Our findings indicate that α-synuclein production was significantly downregulated in MS patients. Principal component analysis also revealed distinct profiles between MS patients and controls. PBMCs and serum profiles of α-synuclein correlated with the EDSS score, suggesting that disease severity can be predicted using α-synuclein profiles. Moreover, α-synuclein showed a significant correlation with IL-6 and age of onset. Lastly, receiver operating characteristic curves of PBMCs and serum activity of α-synuclein profiles displayed discrimination with area under the curve values of 0.856 and 0.705, respectively. CONCLUSION: Our results imply that measuring α-synuclein levels in both serum and PBMCs could be a valuable method for diagnosing and predicting MS severity, potentially serving as a non-invasive biomarker for the disease.
 BACKGROUND: There is no study in the world on the relationship between consuming black and green tea as beverages containing polyphenols and the risk of MS. This study aimed to determine the association between the consumption of green and black tea, coffee, non-alcoholic beer, milk, fruit juices and carbonated beverages with the risk of MS. METHODS AND MATERIALS: This case-control study was performed on 150 patients with MS and 300 healthy individuals as a control group among patients who were referred to the ophthalmology ward of a referral hospital in Ahvaz with the groups matching for age. The data collection tool was a researcher-made questionnaire including demographic information and beverage consumption. Analysis was performed using univariate and multiple logistic regression models. RESULTS: The mean age of patients at the time of diagnosis was 38.55 ± 8.88 years. The results showed that drinking milk (OR = 5.46), natural juice (OR = 2.49), and carbonated beverages (OR = 16.17) were associated with an increased chance of developing MS. However, drinking non-alcoholic beer (OR = 0.48), black tea (OR = 0.20), green tea (OR = 0.29) and coffee (OR = 0.07) were associated with a reduced chance of developing MS. CONCLUSION: The results show that drinking black and green tea, non-alcoholic beer, and coffee are associated with a decrease in the chance of developing MS. The results of this study can be used to design interventional research and to change people's lifestyles to prevent MS.
 BACKGROUND: Patients with relapsing-remitting multiple sclerosis (RRMS) who experience relapses on a first-line therapy (interferon, glatiramer acetate, dimethyl fumarate, or teriflunomide; collectively, "BRACETD") often switch to another therapy, including natalizumab or fingolimod. Here we compare the effectiveness of switching from a first-line therapy to natalizumab or fingolimod after ≥1 relapse. METHODS: Data collected prospectively in the MSBase Registry, a global, longitudinal, observational registry, were extracted on February 6, 2018. Included patients were adults with RRMS with ≥1 relapse on BRACETD therapy in the year before switching to natalizumab or fingolimod. Included patients received natalizumab or fingolimod for ≥3 months after the switch. RESULTS: Following 1:1 propensity score matching, 1000 natalizumab patients were matched to 1000 fingolimod patients. Mean (standard deviation) follow-up time was 3.02 (2.06) years after switching to natalizumab and 2.58 (1.64) years after switching to fingolimod. Natalizumab recipients had significantly lower annualized relapse rate (relative risk=0.66; 95% confidence interval [CI], 0.59-0.74), lower risk of first relapse (hazard ratio [HR]=0.69; 95% CI, 0.60-0.80), and higher confirmed disability improvement (HR=1.27; 95% CI, 1.03-1.57) than fingolimod recipients. No difference in confirmed disability worsening was observed. CONCLUSIONS: Patients with RRMS switching from BRACETD demonstrated better outcomes with natalizumab than with fingolimod.
 Neurologists increasingly use anti-CD20 therapies, including for women of childbearing age, despite these medications being unlicensed for use in pregnancy. Current evidence suggests that women can safely conceive while taking anti-CD20 therapy. Women should not be denied treatment during pregnancy when it is clinically indicated, although they should be counselled regarding live vaccinations for their infant. Women receiving regular ocrelizumab for multiple sclerosis should preferably wait 3 months before trying to conceive. There are few data around ofatumumab in pregnancy, and while there is probably a class effect across all anti-CD20 therapies, ofatumumab may need to be continued during pregnancy to maintain efficacy. We recommend that anti-CD20 therapies can be safely given while breast feeding. It is important to make time to discuss treatments with women of childbearing age to help them choose their most suitable treatment. Outcomes should be monitored in pregnancy registries.
 This study aimed to investigate the association between dietary acid load (DAL) and multiple sclerosis (MS), through the potential renal acid load (PRAL) and net endogenous acid production (NEAP) scores. In a hospital-based case-control study of 109 patients with MS and 130 healthy individuals, a validated 168-item semi-quantitative food frequency questionnaire and a logistic regression model were used to evaluate the association between the DAL and MS. After adjusting for age (years), gender (male/female), body mass index (Kg/m(2)), and total calories (Kcal), the MS odds were 92% lower for those in the highest tertile of total plant-based protein (OR: 0.08, 95%CI: 0.03, 0.23; p-value < 0.001) and about four times higher for those in the highest tertile of the PRAL (OR: 4.16, 95%CI: 1.94, 8.91; p-value < 0.001) and NEAP scores (OR: 3.57, 95%CI: 1.69, 7.53; p-value < 0.001), compared to those in the lowest tertile. After further adjusting for sodium, saturated fatty acid, and fiber intake, the results remained significant for total plant-based protein intake (OR: 0.07, 95%CI: 0.01, 0.38; p-value = 0.002). In conclusion, a higher NEAP or PRAL score may be associated with increased odds of MS, while a higher intake of plant-based protein instead of animal-based protein may be protective.
 Multiple sclerosis is an inflammatory demyelinating disease of unknown cause that affects the central nervous system. Although it was once deemed "incurable," many disease-modifying therapies have been introduced since the beginning of the 20th century; eight of these are now available in Japan. Treatment for multiple sclerosis is undergoing a significant shift from the safety-oriented "escalation strategy," in which the patient is initially administered medications with low risks of side effects but moderate efficacy, to a "personalized approach" based on individual prognostic factors followed by an "early top-down strategy" in which higher efficacy treatments are initiated first. Disease-modifying drugs for multiple sclerosis can be high- (fingolimod, ofatumumab, natalizumab) or moderate-efficacy (interferon beta, glatiramer acetate, dimethyl fumarate), and there are also disease-modifying therapies for secondary progressive multiple sclerosis (siponimod and ofatumumab). Approximately 20,000 Japanese patients have multiple sclerosis, and this number continues to increase. Many neurologists are expected to prescribe high-efficacy drugs in the future. The risk management of adverse events, particularly progressive multifocal leukoencephalopathy, is required to ensure that the importance of safety never be underestimated, even though treatment efficacy is the main focus.
 OBJECTIVE: The objective of this study was to develop evidence-based recommendations on pregnancy management for persons with multiple sclerosis (MS). BACKGROUND: MS typically affects young women in their childbearing years. Increasing evidence is available to inform questions raised by MS patients and health professionals about pregnancy issues. METHODS: The French Group for Recommendations in Multiple Sclerosis (France4MS) reviewed PubMed and university databases (January 1975 through June 2021). The RAND/UCLA appropriateness method was developed to synthesise the scientific literature and expert opinions on healthcare topics; it was used to reach a formal agreement. Fifty-six MS experts worked on the full-text review and initial wording of recommendations. A group of 62 multidisciplinary healthcare specialists validated the final proposal of summarised evidence. RESULTS: A strong agreement was reached for all 104 proposed recommendations. They cover diverse topics, such as pregnancy planning, follow-up during pregnancy and postpartum, delivery routes, locoregional analgesia or anaesthesia, prevention of postpartum relapses, breastfeeding, vaccinations, reproductive assistance, management of relapses and disease-modifying treatments. CONCLUSION: The 2022 recommendations of the French MS society should be helpful to harmonise counselling and treatment practice for pregnancy in persons with MS, allowing for better and individualised choices.
 BACKGROUND: Clinicians are increasingly recognizing the importance of shared decision-making in complex treatment choices, highlighting the importance of the patient's rationale and motivation for switching therapies. This study aimed to evaluate the association between different modalities of changing multiple sclerosis (MS) treatments, cognitive profile and attitude and preferences of patients concerning treatment choice. METHODS: This multicenter cross-sectional study was conducted at 28 Italian MS centers in the period between June 2016 and June 2017. We screened all MS patients treated with any DMT, with a treatment compliance of at least 80% of therapy administered during the 3 last months who needed to modify MS therapy because of efficacy, safety or other reasons during a follow-up visit. At the time of switching the symbol digit modalities test (SDMT) and the Control Preference Scale (CPS) were evaluated. According to the CPS, patients were classified as "active" (i.e. who prefer making the medical decision themselves), "collaborative" (i.e. who prefer decisions be made jointly with the physician), or "passive" (i.e. who prefer the physician make the decision). RESULTS: Out of 13,657 patients recorded in the log, 409 (3%) changed therapy. Of these, 336 (2.5%) patients, 69.6% were female and with mean age 40.6 ± 10.5 years, were enrolled. According to the CPS score evaluation, a significant high percentage of patients (51.1%) were considered collaborative, 74 patients (22.5%) were passive, and 60 (18.2%) patients were active. Stratifying according to CPS results, we found a higher SDMT score among collaborative patients compared to active and passive ones (45.8 ± 12.3 versus 41.0 ± 13.2 versus 41.7 ± 12.8, p < 0.05). CONCLUSION: In this study, the CPS evaluation showed that more than 50% of patients who needed to change therapy chose a "collaborative" role in making treatment decision. Cognitive profile with SDMT seems to correlate with patients' preference on treatment decision, showing better scores in collaborative patients.
 BACKGROUND AND PURPOSE: With the new highly active drugs available for people with multiple sclerosis (pwMS), vaccination becomes an essential part of the risk management strategy. We aimed to develop a European evidence-based consensus for the vaccination strategy of pwMS who are candidates for disease-modifying therapies (DMTs). METHODS: This work was conducted by a multidisciplinary working group using formal consensus methodology. Clinical questions (defined as population, interventions and outcomes) considered all authorized DMTs and vaccines. A systematic literature search was conducted and quality of evidence was defined according to the Oxford Centre for Evidence-Based Medicine Levels of Evidence. The recommendations were formulated based on the quality of evidence and the risk-benefit balance. RESULTS: Seven questions, encompassing vaccine safety, vaccine effectiveness, global vaccination strategy and vaccination in subpopulations (pediatric, pregnant women, elderly and international travelers) were considered. A narrative description of the evidence considering published studies, guidelines and position statements is presented. A total of 53 recommendations were agreed by the working group after three rounds of consensus. CONCLUSION: This first European consensus on vaccination in pwMS proposes the best vaccination strategy according to current evidence and expert knowledge, with the goal of homogenizing the immunization practices in pwMS.
 BACKGROUND AND PURPOSE: Individuals with multiple sclerosis (MS) want health advice regarding participation in their choice of exercise. To address this need, a flexible exercise participation programme (FEPP) was developed, underpinned by the MS aerobic exercise guidelines and supported by a physiotherapist using behaviour change techniques. The aim of this study was to investigate the feasibility of the FEPP for individuals with minimal disability from MS. METHODS: A feasibility study utilising a single group pre/post-intervention design was conducted. The 12-week FEPP was completed by 10 individuals with MS (EDSS 0-3.5). Exercise progression in duration, intensity or frequency of exercise (in line with MS exercise guidelines) was guided by a self-perceived weekly energy level score, and weekly telephone coaching sessions using behavioural change techniques. Trial feasibility was assessed via measures of process (recruitment and retention), resources/management (communication time; data entry) and scientific feasibility (safety; compliance). Secondary FEPP feasibility outcomes included the Goal Attainment Scale (GAS) T-score, exercise participation (weekly exercise diary), high-level mobility (HiMAT), vitality (Subjective Vitality Scale), biomarkers for inflammation (cytokines levels [IL2, IL4, IL6, IL10, TNF and IFNγ]), and acceptability (participant survey). RESULTS: Process: In total, 11 (85%) of 13 eligible participants enroled at baseline with 10 (91%) completing the study. Resources/management: Coaching sessions included a baseline interview-mean 39 min (SD: 6.6) and telephone coaching-mean 10 min (SD: 3.8) per week. Outcome measure data collection time-mean 44 min (SD: 2.1). Scientific feasibility: Two participants experienced a fall during their exercise participation. Self-reported compliance was high (99%). GAS T-scores increased significantly, indicating achievement of exercise participation goals. Secondary outcomes showed trends towards improvement. DISCUSSION: The FEPP was feasible, safe and highly acceptable for use with individuals with MS and warrants a larger trial to explore effectiveness.
 BACKGROUND: We undertook a randomized controlled trial (RCT) that investigated the effectiveness of a theory-based, Internet-delivered, behavioral intervention focusing on physical activity promotion for immediate and sustained improvements in secondary, patient-reported outcomes (PROs) of function, symptoms, and quality of life (QOL) in multiple sclerosis (MS). METHOD: Persons with MS (N = 318) were recruited from throughout the United States and randomized into behavioral intervention (n = 159) or attention/social contact control (n = 159) conditions. The conditions were administered over a 6-month period by persons who were uninvolved in screening, recruitment, random assignment, and outcome assessment. There was a 6-month follow-up period without intervention access/content. We collected PROs data every 6 months over the 12-month period. The PROs included validated measures of walking and cognitive function, symptoms of fatigue, depression, anxiety, pain, and sleep quality, and QOL. The data analysis involved a modified intent-to-treat approach using a linear mixed model in JMP Pro 16.0. RESULTS: There was a significant group by time interaction on Fatigue Severity Scale scores (p < .01) and physical subscale scores of the Modified Fatigue Impact Scale (p < .05). Scores on both measures decreased immediately after the 6-month period in the behavioral intervention compared with no change in the control condition, and this differential pattern of change was sustained over the 6-month follow-up. There were no group by time interactions on the other PROs. DISCUSSION: This study provides evidence for the effectiveness of a novel, widely scalable approach for physical activity promotion and fatigue management in persons with MS, yet this must be contextualized with the absence of improvements in the other PROs.
 BACKGROUND: The potential of neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) as biomarkers of disease activity and severity in progressive forms of multiple sclerosis (MS) is unclear. OBJECTIVE: To investigate the relationship between serum concentrations of NfL, GFAP, and magnetic resonance imaging (MRI) in progressive MS. METHODS: Serum concentrations of NfL and GFAP were measured in 32 healthy controls and 32 patients with progressive MS from whom clinical and MRI data including diffusion tensor imaging (DTI) were obtained during three years of follow-up. RESULTS: Serum concentrations of NfL and GFAP at follow-up were higher in progressive MS patients than in healthy controls and serum NfL correlated with the EDSS score. Decreasing fractional anisotropy (FA) in normal-appearing white matter (NAWM) correlated with worsening EDSS scores and higher serum NfL. Higher serum NfL and increasing T2 lesion volume correlated with worsening paced autitory serial addition test scores. In multivariable regression analyses with serum GFAP and NfL as independent factors and DTI measures of NAWM as dependent factors, we showed that high serum NfL at follow-up was independently associated with decreasing FA and increasing MD in NAWM. Moreover, we found that high serum GFAP was independently associated with decreasing MD in NAWM and with decreasing MD and increasing FA in cortical gray matter. CONCLUSION: Serum concentrations of NfL and GFAP are increased in progressive MS and are associated with distinct microstructural changes in NAWM and CGM.

 BACKGROUND: The prevalence of multiple sclerosis (MS) in older people is increasing due to population aging and availability of effective disease-modifying therapies (DMTs). Treating older people with MS is complicated by age-related and MS-related comorbidities, immunologic effects of prior DMTs, and immunosenescence. Teriflunomide is a once-daily oral immunomodulator that has demonstrated efficacy and acceptable safety in clinical trials of adults with relapsing forms of MS (RMS). However, there are limited clinical trial and real-world data regarding teriflunomide use in people with MS aged >55 years. We analyzed real-world data to assess the effectiveness and safety of teriflunomide in older people with RMS who had switched to this agent from other DMTs. METHODS: People with RMS (relapsing remitting and active secondary progressive MS) aged ≥55 years who had switched from other DMTs to teriflunomide (7 mg or 14 mg) for ≥1 year were identified retrospectively by chart review at four sites in the United States. Data were extracted from medical records from 1 year pre-index to 2 years post-index (index defined as the teriflunomide start date). Assessments of effectiveness included annualized relapse rate (ARR), Expanded Disability Status Scale (EDSS) score, and magnetic resonance imaging (MRI) outcomes. Assessments of safety included lymphocyte counts, infections, and malignancies. We examined the effectiveness outcomes and lymphocyte counts within sub-groups defined by age (55-64, ≥65 years), sex, MS type, and prior route of DMT administration (oral, injectable, infusible). RESULTS: In total, 182 patients with RMS aged ≥55 years who switched from other DMTs to teriflunomide were identified (mean [SD] age: 62.5 [5.4] years). Mean ARR decreased from the start of teriflunomide treatment (mean [SD]: 0.43 [0.61]) to year 1 post-index (0.13 [0.65]) and year 2 post-index (0.05 [0.28]). Mean EDSS score remained unchanged from index (mean [SD]: 4.5 [1.8]) to 1 year post-treatment (4.5 [1.8]) and increased slightly at 2 years post-treatment (4.7 [1.7]). MRI scans from index and years 1 and 2 post-index compared with scans from the previous year indicated that most patients had stable or improved MRI outcomes at index (87.7%) and remained stable or improved at years 1 (96.0%) and 2 (93.6%). Lymphopenia decreased at years 1 (21.4%) and 2 post-index (14.8%, compared to index (23.5%). By 1 year post-index, fewer patients had grade 3 or 4 lymphopenia, and at 2 years post-index, there were no patients with grade 3 or 4 lymphopenia. Infection incidence was low (n = 40, 22.0%) and none were related to teriflunomide. The decreases in lymphopenia were driven by decreases among people who switched from a prior oral DMT; there were no notable differences in lymphopenia across the other sub-groups examined. ARR, EDSS score, and MRI outcomes across all sub-groups were similar to the results of the overall population. CONCLUSION: Our multicenter, longitudinal, retrospective study demonstrated that patients with RMS aged 55 or older switching to teriflunomide from other DMTs had significantly improved ARR, stable disability, and stable or improved MRI over up to 2 years' follow up. Safety results were acceptable with fewer patients exhibiting lymphopenia at years 1 and 2 post-index.
 Multiple sclerosis (MS) is a demyelinating disorder in which the myelin sheath covering the central nervous system axons is damaged or lost, disrupting action potential conduction and leading to various neurological complications. The pathogenesis of MS remains unclear, and no effective therapies are currently available. MS is triggered by environmental factors in genetically susceptible individuals. DNA damage and DNA repair failure have been proposed as MS genetic risk factors; however, inconsistent evidence has been found in multiple studies. Therefore, more investigations are needed to ascertain whether DNA damage/repair is altered in this disorder. In this context, therapies that prevent DNA damage or enhance DNA repair could be effective strategies for MS treatment. The overactivation of the extracellular-signal-related kinase 1 and 2 (Erk1/2) pathway can lead to DNA damage and has been linked to MS pathogenesis. In our study, we observed substantially elevated oxidative DNA damage and slower DNA repair rates in an experimentally autoimmune encephalomyelitis animal model of MS (EAE). Moreover, statistical decreases in oxidative DNA strand breaks and faster repair rates were observed in EAE animals injected with the Erk1/2 inhibitor PD98059 (PD). Moreover, the expression of several genes associated with DNA strand breaks and repair changed in EAE mice at both the mRNA and protein levels, as revealed by the RT(2) Profiler PCR array and verified by RT-PCR and protein analyses. The treatment with PD mitigated these changes and improved DNA repair gene expression. Our results demonstrate clear associations between Erk1/2 activation, DNA damage/repair, and MS pathology, and further suggest that PD therapy may be a promising adjuvant therapeutic strategy.
 BACKGROUND: Biomarkers of disease activity have been intensively studied in multiple sclerosis (MS) but knowledge on predictors of disability improvement is limited. The aim of this pilot study was to explore whether increased brain-derived neurotrophic factor concentrations in serum and CSF (sBDNF/cBDNF) precede neurological and cognitive improvement in MS. METHODS: In this pilot, monocentric prospective cohort study we collected serum/CSF samples at baseline together with EDSS (n = 36) and cognitive testing (n = 34) in patients with relapsing-remitting/primary progressive MS or clinically isolated syndrome. BDNF was assessed in serum and CSF with a single molecule array (SIMOA) HD-1 analyser (Quanterix). Twelve months later EDSS and cognitive testing were repeated. BDNF concentrations of patients with vs. without disability or cognitive improvement (disability improvement: decrease in EDSS ≥ 0.5; cognitive improvement: average z-score increase in neuropsychological performance ≥ 0.5) were compared using univariate ANOVAs adjusting for covariates. RESULTS: Compared to subjects without, patients with disability improvement had higher sBDNF at baseline (q = 0.04). Subjects with cognitive improvement had higher cBDNF at baseline than those without cognitive improvement (q = 0.004). Secondary analysis demonstrated significant correlations between sBDNF and EDSS change (q = 0.036), cBDNF and average z-score change (q = 0.04) and cBDNF and number of cognitive tests with improvement (q = 0.04), while controlling for covariates. CONCLUSIONS: Our findings suggest a possible role for BDNF in neurological and cognitive improvement in MS. These findings have to be confirmed in a larger sample but they already highlight the potential of BDNF as a biomarker for disability improvement and neuroplasticity in MS.
 Multiple sclerosis (MS) is a chronic, progressive neuroinflammatory disease with a complex pathophysiological background. A variety of diverse factors have been attributed to the propagation of inflammation and neurodegeneration in MS, mainly genetic, immunological, and environmental factors such as vitamin D deficiency, infections, or hormonal disbalance. Recently, the importance of the gut-brain axis for the development of many neurological conditions, including stroke, movement disorders, and neuroinflammatory disorders, has been postulated. The purpose of our paper was to summarize current evidence confirming the role of the gut microbiome in the pathophysiology of MS and related disorders, such as neuromyelitis optica spectrum disorder (NMO-SD). For this aim, we conducted a systematic review of the literature listed in the following databases: Medline, Pubmed, and Scopus, and were able to identify several studies demonstrating the involvement of the gut microbiome in the pathophysiology of MS and NMO-SD. It seems that the most relevant bacteria for the pathophysiology of MS are those belonging to Pseudomonas, Mycoplasma, Haemophilus, Blautia, Dorea, Faecalibacterium, Methanobrevibacter, Akkermansia, and Desulfovibrionaceae genera, while Clostridium perfringens and Streptoccocus have been demonstrated to play a role in the pathophysiology of NMO-SD. Following this line of evidence, there is also some preliminary data supporting the use of probiotics or other agents affecting the microbiome that could potentially have a beneficial effect on MS/NMO-SD symptoms and prognosis. The topic of the gut microbiome in the pathophysiology of MS is therefore relevant since it could be used as a biomarker of disease development and progression as well as a potential disease-modifying therapy.
 OBJECTIVE: Multiple sclerosis (MS) is a debilitating neurological disease associated with a variety of psychological, cognitive, and motoric symptoms. Walking is among the most important functions compromised by MS. Dual-task walking (DTW), an everyday activity in which people walk and engage in a concurrent, discrete task, has been assessed in MS, but little is known about how it relates to other MS symptoms. Self-awareness theory suggests that DTW may be a function of the interactions among psychological, cognitive, and motor processes. METHOD: Cognitive testing, self-report assessments for depression and falls self-efficacy (FSE), and walk evaluations [DTW and single-task walk (STW)] were assessed in seventy-three people with MS in a clinical care setting. Specifically, we assessed whether psychological factors (depression and FSE) that alter subjective evaluations regarding one's abilities would moderate the relationships between physical and cognitive abilities and DTW performance. RESULTS: DTW speed is related to diverse physical and cognitive predictors. In support of self-awareness theory, FSE moderated the relationship between STW and DTW speeds such that lower FSE attenuated the strength of the relationship between them. DTW costs - the change in speed normalized by STW speed - did not relate to cognitive and motor predictors. DTW costs did relate to depressive symptoms, and depressive symptoms moderated the effect of information processing on DTW costs. CONCLUSIONS: Findings indicate that an interplay of physical ability and psychological factors - like depression and FSE - may enhance understanding of walking performance under complex, real-world, DTW contexts.
 This study aimed to assess the possible association between cognitive impairment and two important biochemical biomarkers of oxidative stress, thiol-disulfide homeostasis (TDH), and ischemia-modified albumin (IMA) in patients with multiple sclerosis (MS). This study included 85 patients with MS (38 treatment-naïve relapsing-remitting MS (RRMS), 31 RRMS on fingolimod therapy, and 16 secondary progressive MS (SPMS)) and 33 healthy controls. Cognitive evaluation was carried out by applying the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) test battery and the scores were adjusted for age and years of education. Plasma TDH was assessed using an automated method and plasma IMA levels were determined using the cobalt-albumin binding assay. Plasma native thiol and total thiol levels were significantly decreased in patients with SPMS when compared with the naïve patients and healthy controls. Cognitive impairment was detected in 47.4% of naïve patients, 64.5% of patients on fingolimod therapy, and 80% of patients with SPMS. Naïve patients or patients on fingolimod therapy who were cognitively impaired had significantly decreased levels of native thiol and total thiol compared to the cognitively normal patients. Logistic regression analysis revealed total thiol and native thiol to be significantly associated with cognitive impairment in naïve patients and patients on fingolimod therapy. Significant correlations were determined between BICAMS scores, TDH, IMA, clinical indices of disease severity (EDSS and MSSS), and magnetic resonance imaging parameters. This study has shown for the first time that plasma TDH parameters are associated with cognitive impairment in MS.
 BACKGROUND AND PURPOSE: Sexual dysfunction (SD) in people with multiple sclerosis (pwMS) is common and an often underestimated issue in the care of pwMS. The objective of the study was to evaluate risk factors for SD in pwMS, correlate its prevalence with patient-reported measures (quality of life and physical activity) and analyse its association with hormonal status. METHODS: Sexual dysfunction was determined in 152 pwMS using the Multiple Sclerosis Intimacy and Sexuality Questionnaire 19. A logistical regression model was used to identify independent risk factors for SD. RESULTS: The prevalence of SD in pwMS was 47%. Independent risk factors for the development of SD were ever-smoking (odds ratio [OR] 3.4, p = 0.023), disability as measured by the Expanded Disability Status Scale (OR 2.0, p < 0.001), depression (OR 4.3, p = 0.047) and bladder and bowel dysfunction (OR 8.8, p < 0.001); the use of disease-modifying treatment was associated with a lower risk for SD (OR 0.32, p = 0.043). SD was associated with worse quality of life (Multiple Sclerosis Impact Scale 29: physical score 6.3 vs. 40.0; psychological score 8.3 vs. 33.3; both p < 0.001) and lower physical activity (Baecke questionnaire, p < 0.001). Laboratory analysis revealed significantly higher luteinizing hormone and follicle-stimulating hormone levels and lower 17-beta oestradiol, androstenedione, dehydroepiandrosterone sulfate, oestrone and anti-Mullerian hormone levels in female pwMS with SD. In male pwMS and SD, there was a significant decrease in inhibin B levels. CONCLUSIONS: Our findings highlight the requirement of a holistic approach to SD in MS including physical, neurourological and psychosocial factors. Active screening for SD, especially in patients with disability, depression or bladder and bowel dysfunction, is recommended.
 BACKGROUND AND OBJECTIVE: There has been growing interest in quality of life associated with multiple sclerosis but the research has been overwhelmingly carried out in developed countries. This study aimed to assess quality of life of multiple sclerosis patients in Trinidad and Tobago. METHODS: All multiple sclerosis patients were asked to complete demographic, EQ-5D-5L and MSQOL-54 questionnaires. EQ-5D data were compared with population norms for Trinidad and Tobago. MSQOL-54 data were compared with results from a matching cohort of non-MS respondents. Regression analyses were used to explore the association between MSQOL-54 scales and EQ-5D utility. RESULTS: The 97 patients were mainly urban, highly educated and 75% female. EQ-5D-5L data showed more frequent and more severe problems and lower index values than the population and patients of other chronic illness clinics in Trinidad and Tobago. MSQOL-54 results showed that patients were more affected by physical items, but had high scores on mental and emotional items when compared with the matching cohort and patients in other countries. CONCLUSION: The low prevalence and demographics of patients suggest the possibility of undetected cases in rural areas and/or among less educated groups. Further investigation into the high levels of mental and emotional health among patients may lead to the design of interventions to help patients of multiple sclerosis and other illnesses.
 In MS patients with a progressive form of the disease, the slow deterioration of neurological functions is thought to result from a combination of neuronal cell death, axonal damages and synaptic dysfunctions [...].
 Better knowledge about the possible role of genetic factors in modulating the response to multiple sclerosis (MS) treatment, including rehabilitation, known to promote neural plasticity, could improve the standard of care for this disease. Vitamin D receptor (VDR) gene polymorphisms are associated with MS risk, probably because of the role played by vitamin D in regulating inflammatory and reparative processes. The aim of this study was to evaluate the association of the most important functional VDR SNPs (TaqI (T/C), ApaI (A/C), and FokI (C/T)) with functional outcome in MS patients undergoing multidisciplinary inpatient rehabilitation (MDR) treatment, in order to determine whether genetic profiling might be useful to identify subjects with a higher chance of recovery. To this end, 249 MS inpatients with a diagnosis of either progressive (pMS; n = 155) or relapsing remitting (RRMS; n = 94) disease who underwent MDR treatment (average duration = 5.1 weeks) were genotyped for VDR SNPs by real-time allelic discrimination. The rehabilitation outcome was assessed using the modified Barthel Index (mBI), Expanded Disability Status Scale (EDSS), and pain numerical rating scores (NRS) at the beginning and the end of MDR treatment. A positive correlation was observed in RRMS patients between the VDR TaqI major allele (TT) and mBI increase (i.e., better functional recovery), as assessed by the linear and logistic regression analysis adjusted for gender, age, disease duration, time of hospitalization, HLA-DRB1*15.01 positivity, and number of rehabilitative interventions (Beta = 6.35; p = 0.0002). The VDR-1 TaqI, ApaI, FokI: TCC haplotype was also associated with mBI increase in RRMS patients (Beta = 3.24; p = 0.007), whereas the VDR-2: CAC haplotype was correlated with a lower mBI increase (Beta = -2.18 p = 0.04) compared with the other haplotypes. VDR TaqI major allele (TT), as well as the VDR-1 TaqI, ApaI, FokI: TCC haplotype could be associated with a better rehabilitation outcome in RRMS patients.
 BACKGROUND: Fatigue is a debilitating symptom of multiple sclerosis (MS), but its relation to sociodemographic and disease-related characteristics has not been investigated in larger studies. The objectives of this study were to evaluate predictors of self-reported fatigue in a Swedish nationwide register-based MS cohort. METHODS: Using a repeated cross-sectional design, we included 2,165 persons with relapsing- remitting and secondary progressive MS with one or multiple Fatigue Scale for Motor and Cognitive Functions (FSMC) scores, which was modelled using multivariable linear regressions for multiple predictors. RESULTS: Only associations to expanded disability status scale (EDSS) and Symbol Digit Modalities Test (SDMT) were considered clinically meaningful among MS-associated characteristics in our main model; compared to mild disability (EDSS 0-2.5), those with severe disability (EDSS ≥6) scored 17.6 (95% CI 13.1-22.2) FSMC points higher, while the difference was 10.7 (95% CI 8.0-13.4) points for the highest and lowest quartiles of SDMT. Differences between highest and lowest quartiles of health-related quality of life (HRQoL) instruments were even greater and considered clinically meaningful; EuroQoL Visual Analogue Scale (EQ-VAS) 31.9 (95% CI 29.9-33.8), Multiple Sclerosis Impact Scale (MSIS-29) psychological component 35.6 (95% CI 33.8-37.4) and MSIS-29 physical component 45.5 (95% CI 43.7-47.4). CONCLUSION: Higher self-reported fatigue is associated with higher disability level and worse cognitive processing speed, while associations to other MS-associated characteristics including MS type, line of disease modifying therapy (DMT), MS duration, relapse and new cerebral lesions are weak. Furthermore, we found a strong correlation between high fatigue rating and lower ratings on health-related quality of life instruments.
 BACKGROUND: Multiple sclerosis (MS) is a progressive neurodegenerative disease of the central nervous system (CNS) with varying degrees of axonal and neuronal damage. The onset and progression of the disease are influenced by several environmental and genetic variables. Long non-coding RNAs (lncRNAs) have a crucial role in the pathophysiology of MS. Our study aimed to assess the levels of HAR1A and HAR1B lncRNA expression in the blood samples of MS patients and investigate the relationship between these lncRNAs and disease activity. METHODS AND RESULTS: The blood samples of 100 MS patients, including 82 relapsing-remitting (RR), 8 primary progressive (PP), and 10 secondary progressive (SP) MS cases, and 100 healthy controls were collected. Quantitative real-time PCR was used for the evaluation of gene expression. ROC curve analysis was performed to evaluate the diagnostic potential of lncRNA levels. A significant decrease was detected in HAR1A expressions (P < 0.0001), and a moderate increase was also shown in HAR1B of SPMS patients (P value = 0.0189). HAR1A showed different expression levels in patients over forty (P value = 0.034). The expression levels of HAR1A and HAR1B were positively correlated in MS patients (r = 0.2003, P value = 0.0457). In addition, ROC curve results suggested that HAR1A can be introduced as a novel biomarker for MS diagnosis (AUC = 0.776). CONCLUSION: The low serum level of HAR1A may be a potential molecular biomarker for MS diagnosis; however, no discernible difference was detected in the expression level of HAR1B in the blood samples of MS patients.
 BACKGROUND AND PURPOSE: In multiple sclerosis (MS), iron rim lesions (IRLs) are characterized by pronounced tissue matrix damage. The T1/T2-weighted (T1/T2w) ratio represents a postprocessing MRI approach to investigate tissue integrity, but studies investigating spinal cord pathology are missing until now. The aim of this study was to characterize tissue integrity using the T1/T2w ratio in lesions and the normal-appearing white and gray matter (NAWM, NAGM) in the spinal cord and brain in MS patients with and without brain IRLs. METHODS: Forty MS patients (20 patients with at least one brain IRL and 20 age- and sex-matched patients without IRLs) were included. Normalized cross-sectional area (nCSA) of the upper cervical cord was calculated in addition to T1/T2w values and standard brain and spinal cord MRI parameters. RESULTS: Patients with IRLs had higher disability scores, a smaller nCSA, and a higher cervical T2 lesion volume. T1/T2w values of brain IRLs were significantly lower compared to non-IRLs (p < .001). Furthermore, T1/T2w values of lesions were significantly lower compared to the NAGM and NAWM, both in the brain and the spinal cord (p < .05 for all comparisons). T1/T2w values of the NAGM and NAWM in the brain and spinal cord did not statistically differ between the IRL group and the non-IRL group. CONCLUSION: IRLs constitute an imaging marker of disease severity. T1/T2w ratio maps represent an interesting technique to capture diffuse tissue properties. Calculation of T1/T2w ratio maps of the spinal cord might provide additional insights into the pathophysiological processes of MS.
 Multiple sclerosis (MS) pathophysiology includes inflammation, demyelination and neurodegeneration, but the exact mechanisms of disease initiation and progression are unknown. A major feature of lesions is lack of myelin, which increases axonal energy demand and requires adaptation in number and size of mitochondria. Outside lesions, subtle and diffuse alterations are observed in normal appearing white matter (NAWM) and normal appearing grey matter (NAGM), including increased oxidative stress, reduced axon density and changes in myelin composition and morphology. On an ultrastructural level, only limited data is available on alterations in myelinated axons. We generated large scale 2D scanning transmission electron microscopy images ('nanotomy') of non-demyelinated brain tissue of control and progressive MS donors, accessible via an open-access online repository. We observed a reduced density of myelinated axons in NAWM, without a decrease in cross-sectional axon area. Small myelinated axons were less frequently and large myelinated axons were more frequently present in NAWM, while the g-ratio was similar. The correlation between axonal mitochondrial radius and g-ratio was lost in NAWM, but not in NAGM. Myelinated axons in control GM and NAGM had a similar g-ratio and radius distribution. We hypothesize that axonal loss in NAWM is likely compensated by swelling of the remaining myelinated axons and subsequent adjustment of myelin thickness to maintain their g-ratio. Failure of axonal mitochondria to adjust their size and fine-tuning of myelin thickness may render NAWM axons and their myelin more susceptible to injury.

 BACKGROUND: Natalizumab (TYSABRI®) 300 mg administered intravenously every-4-weeks (Q4W) is approved for treatment of relapsing-remitting multiple sclerosis but is associated with increased risk of progressive multifocal leukoencephalopathy (PML). Extended natalizumab dosing intervals of approximately every-6-weeks (Q6W) are associated with a lower risk of PML. Primary and secondary clinical outcomes from the NOVA randomized clinical trial (NCT03689972) suggest that effective disease control is maintained in patients who were stable during treatment with natalizumab Q4W for ≥12 months and who then switched to Q6W dosing. We compared additional exploratory clinical and patient-reported outcomes (PROs) from NOVA to assess the efficacy of Q6W dosing. METHODS: Prespecified exploratory clinical efficacy endpoints in NOVA included change from baseline in Expanded Disability Status Scale (EDSS) score, Timed 25-Foot Walk (T25FW), dominant- and nondominant-hand 9-Hole Peg Test (9HPT), and Symbol Digit Modalities Test (SDMT). Exploratory patient-reported outcome (PRO) efficacy endpoints included change from baseline in the Treatment Satisfaction Questionnaire for Medication (TSQM), Neuro-QoL fatigue questionnaire, Multiple Sclerosis Impact Scale (MSIS-29), EuroQol 5 Dimensions (EQ-5D-5 L) index score, Clinical Global Impression (CGI)-Improvement (patient- and clinician-assessed) and CGI-Severity (clinician-assessed) rating scales. Estimated proportions of patients with confirmed EDSS improvement were based on Kaplan-Meier methods. Estimates of mean treatment differences for Q6W versus Q4W in other outcomes were assessed by least squares mean (LSM) and analyzed using a linear mixed model of repeated measures or ordinal logistic regression (CGI-scale). RESULTS: Exploratory clinical and patient-reported outcomes were assessed in patients who received ≥1 dose of randomly assigned study treatment and had ≥1 postbaseline efficacy assessment (Q6W group, n = 247, and Q4W group, n = 242). Estimated proportions of patients with EDSS improvement at week 72 were similar for Q6W and Q4W groups (11.7% [19/163] vs 10.8% [17/158]; HR 1.02 [95% confidence interval [CI], 0.53-1.98]; P = 0.9501). At week 72, there were no significant differences between Q6W and Q4W groups in LSM change from baseline for T25FW (0.00, P = 0.975), 9HPT (dominant [0.22, P = 0.533] or nondominant [0.09, P = 0.862] hand), or SDMT (-1.03, P = 0.194). Similarly, there were no significant differences between Q6W and Q4W groups in LSM change from baseline for any PRO (TSQM, -1.00, P = 0.410; Neuro-QoL fatigue, 0.52, P = 0.292; MSIS-29 Psychological, 0.67, P = 0.572; MSIS-29 Physical, 0.74, P = 0.429; EQ-5D-5 L, 0.00, P = 0.978). For the EQ-5D-5 L, a higher proportion of Q6W patients than Q4W patients demonstrated worsening (≥0.5 standard deviation increase in the EQ-5D-5 L index score; P = 0.0475). From baseline to week 72 for Q6W versus Q4W, odds ratio (ORs) of LSM change in CGI scores did not show meaningful differences between groups (CGI-Improvement [patient]: OR [95% CI] 1.2 [0.80-1.73]; CGI-Improvement [physician]: 0.8 [0.47-1.36]; CGI-Severity [physician]: 1.0 [0.71-1.54]). CONCLUSIONS: No significant differences were observed in change from baseline to week 72 between natalizumab Q6W and Q4W groups for all exploratory clinical or PRO-related endpoints assessed. For the EQ-5D-5 L, a higher proportion of Q6W than Q4W patients demonstrated worsening.
 BACKGROUND: Fatigue is one of the most common problems in patients with multiple sclerosis (MS) and has adverse effects on their sleep status and self-efficacy. This study aimed to determine the effect of distance nurse-led fatigue management on fatigue, sleep quality, and self-efficacy in patients with MS. METHODS: This quasi-experimental study was performed on 60 patients with MS in Arak, Iran. Subjects were randomly assigned into intervention and control groups. The intervention group received eight sessions of nurse-led fatigue management training through the Skyroom platform. The control group received only the usual programs. Data were collected before and two months after the intervention using the Fatigue Severity Scale, the Pittsburgh Sleep Quality Index, and the Multiple Sclerosis Self-Efficacy Scale. The significance level in this study was determined 0.05. RESULTS: After the intervention, the mean score of fatigue severity in the intervention group was significantly lower than the control group (2.52 ± 0.40 vs 5.65 ± 0.52) (P < 0.001). Also, after the intervention, the mean score of self-efficacy in the intervention group was significantly higher than the control group (49.37 ± 3.25 vs 24.43 ± 2.52) (P < 0.001). Furthermore, after the intervention the mean score of sleep quality was lower in intervention group (11.92 ± 2.01) than the control group (15.46 ± 1.40) (P < 0.001). CONCLUSION: Distance nurse-led fatigue management improved fatigue, sleep quality, and self-efficacy in patients with MS. We recommend the use of these courses as an important step toward improving fatigue, sleep quality, and self-efficacy among these patients.
 Curative therapies against autoimmune diseases are lacking. Indeed, most of the currently available treatments are only targeting symptoms. We have developed a novel strategy for a therapeutic vaccine against autoimmune diseases based on intranasal administration of a fusion protein tolerogen, which consists of a mutant, enzymatically inactive, cholera toxin A1 (CTA1)-subunit genetically fused to disease-relevant high-affinity peptides and a dimer of D-fragments from protein A (DD). The CTA1 R7K mutant - myelin oligodendrocyte glycoprotein (MOG), or proteolipid protein (PLP) - DD (CTA1R7K-MOG/PLP-DD) fusion proteins effectively reduced clinical symptoms in the experimental autoimmune encephalitis model of multiple sclerosis. The treatment induced Tr1 cells, in the draining lymph node, which produced interleukin (IL)-10 and suppressed effector clusters of differentiation 4(+) T-cell responses. This effect was dependent on IL-27 signaling because treatment was ineffective in bone marrow chimeras lacking IL-27Ra within their hematopoietic compartment. Single-cell RNA sequencing of dendritic cells in draining lymph nodes demonstrated distinct gene transcriptional changes of classic dendritic cells 1, including enhanced lipid metabolic pathways, induced by the tolerogenic fusion protein. Thus, our results with the tolerogenic fusion protein demonstrate the possibility to vaccinate and protect against disease progression by reinstating tolerance in multiple sclerosis and other autoimmune diseases.
 PURPOSE: The purpose of this study was to compare a highly-accelerated double inversion recovery (fast-DIR) sequence using a recent parallel imaging technique (CAIPIRINHA) with a conventional DIR (conv-DIR) sequence for image quality and the detection of juxtacortical and infratentorial multiple sclerosis (MS) lesions. MATERIALS AND METHODS: A total of 38 patients with MS who underwent brain MRI at 3 T between 2020 and 2021 were included. There were 27 women and 12 men with a mean age of 40 ± 12.8 (standard deviation) years (range: 20-59 years). All patients underwent conv-DIR sequence and fast-DIR sequence. Fast-DIR was obtained with a T(2)-preparation module to improve contrast and an iterative denoising algorithm to compensate noise enhancement. Two blinded readers reported the number of juxtacortical and infratentorial MS lesions for fast-DIR and conv-DIR, confirmed by further consensus reading that was used as the standard of reference. Image quality and contrast were evaluated for fast-DIR and conv-DIR sequences. Comparisons between fast-DIR and conv-DIR sequences were performed using Wilcoxon test and Lin concordance correlation coefficient. RESULTS: Thirty-eight patients were analyzed. Fast-DIR imaging allowed detection of 289 juxtacortical lesions vs. 238 with conv-DIR, corresponding to a significant improved detection rate with fast-DIR (P < 0.001). Conversely, 117 infratentorial lesions were detected with conv-DIR sequence vs. 80 with fast-DIR sequence (P < 0.001). Inter-observer agreement for lesion detection with fast-DIR and conv-DIR was very high (Lin concordance correlation coefficient ranging between 0.86 and 0.96). CONCLUSION: Fast-DIR improves the detection of juxtacortical MS lesions, but is limited for the detection of infratentorial MS lesions.

 OBJECTIVE: Mindfulness is an established approach to reduce distress and stress reactivity by improving awareness and tolerability of thoughts and emotions. This study compares mindfulness training to sleep hygiene in persons with multiple sclerosis (PWMS) who report chronic insomnia, examining sleep efficiency (SE), self-reported sleep quality and quality of life. METHODS: Fifty-three PWMS were randomized (1:1) in a single-blinded, parallel group design to ten, two-hour weekly sessions of Mindfulness Based Stress Intervention for Insomnia (MBSI-I) over a span of ten weeks or a single, one hour sleep hygiene (SH) session over one day. The primary outcome measure was SE, measured by the Fitbit™ Charge 2 wrist device, at 10 and 16 weeks from the start of study interventions. Self-report outcomes included the Pittsburg Sleep Quality Rating Scale (PSQI), Insomnia Severity Index (ISI) and the Multiple Sclerosis Quality of Life Inventory (MSQLI). Nineteen participants in the MBSI-I group and 24 in the SH group completed the primary study. Subsequently, ten participants in the original SH group participated in the 10-week MSBI-I course and their data was added to the MBSI-I cohort (eMSBI-I). RESULTS: While neither SE nor the PSQI showed significant differences between MBSI-I, eMBSI-I and SH groups, ISI improved in both the MSBI-I and eMBSI-I vs SH at 10 weeks (p = 0.0014 and p = 0.0275) but not 16 weeks. However, pre and post assessments within the MBSI-I and eMBSI-I cohorts did show significant improvement in the PSQI and ISI at 10 and 16 weeks, while SH was significant in the ISI only at 16 weeks. Several quality of life measurements, including fatigue, mental health and cognitive function favored the mindfulness cohorts. CONCLUSION: This pilot study demonstrates beneficial effects of MBSR on insomnia, sleep quality and quality of life in PWMS. TRIAL REGISTRATION: NCT03949296. 14 May 2019.
 OBJECTIVES: The neuropsychiatric sequelae of multiple sclerosis (MS) are important predictors of morbidity and mortality. The authors examined how symptoms of depression, anxiety, fatigue, subjective cognitive impairment, and objective cognitive dysfunction varied with disease duration. They also explored changes in the use of disease-modifying therapies, psychotropic medications, and psychotherapies in relation to disease duration. METHODS: A retrospective sample of 464 people with MS was stratified into three groups based on disease duration: <5 years (N=129), 5-10 years (N=101), and >10 years (N=234). Symptoms of depression and anxiety were recorded with the Hospital Anxiety and Depression Scale (HADS); fatigue, with the five-item version of the Modified Fatigue Impact Scale (MFIS-5); subjective cognitive impairment, with the five-item version of the Perceived Deficits Questionnaire (PDQ-5); and cognition, with the Minimal Assessment of Cognitive Function in MS (MACFIMS). RESULTS: There were between-group differences in anxiety symptoms (p<0.01) and degree of cognitive impairment (p=0.03), but there were no differences in depressive symptoms, fatigue, or subjective cognitive difficulties. Anxiety was higher during the first 5 years after diagnosis, and cognitive dysfunction was higher when assessed more than 10 years after diagnosis. With longer disease duration, a greater proportion of participants received psychotropic medications (p<0.01), and lower proportions received disease-modifying therapies (p<0.01) or psychotherapies (p<0.01). CONCLUSIONS: Findings indicated that rates of some neuropsychiatric symptoms, such as anxiety and cognitive dysfunction, may shift with disease duration, whereas other symptoms, such as fatigue and depression, may not. These findings highlight the importance of closely monitoring the mental state of people with MS over time.
 In this prospective case control study, relationship of detailed cerebellar volumetric data and cognition in patients with multiple sclerosis considering falling status using 3 D MRI and network analysis were evaluated. Participants consist of 106 adults with relapsing-remitting multiple sclerosis. Scores of Montreal cognitive assessment test, symbol digit modality Test, nine-hole peg test, berg balance scale test, timed up and go test, timed 25-foot walk test were worse in faller group than non faller group (p < 0.05 for all tests). There was no significant difference in terms of cerebellar lobule volumes between groups. But using artificial intelligence (AI) based network analysis, we brought a new perspective to interpreting the relationship between the cerebellum, cognition, gait, and balance. Overall, data from the study suggest a possible relationship between cerebellar volume changes and cognitive dysfunction through connectivity analysis in patients with multiple sclerosis. Further studies are needed to examine this issue by using connectivity analysis.
 BACKGROUND: Gait and cognition impairments are common problems among People with Multiple Sclerosis (PwMS). Previous studies have investigated cross-sectional associations between gait and cognition. However, there is a lack of evidence regarding the longitudinal association between these factors in PwMS. Therefore, the objective of this study was to explore this longitudinal relationship using smartphone-based data from the Floodlight study. METHODS: Using the publicly available Floodlight dataset, which contains smartphone-based longitudinal data, we used a linear mixed model to investigate the longitudinal relationship between cognition, measured by the Symbol Digit Modalities Test (SDMT), and gait, measured by the 2 Minute Walking test (2 MW) step count and Five-U-Turn Test (FUTT) turning speed. Four mixed models were fitted to explore the association between: 1) SDMT and mean step count; 2) SDMT and variability of step count; 3) SDMT and mean FUTT turning speed; and 4) SDMT and variability of FUTT turningt speed. RESULTS: After controlling for age, sex, weight, and height, there were significant correlations between SDMT and the variability of 2 MW step count, the mean of FUTT turning speed. No significant correlation was observed between SDMT and the 2 MW mean step count. SIGNIFICANCE: Our findings support the evidence that gait and cognition are associated in PwMS. This may support clinicians to adjust treatment and intervention programs that address both gait and cognitive impairments.


 BACKGROUND: Cancer is a major cause of death, but how cancer influences mortality risk in Multiple Sclerosis (MS) is unclear. OBJECTIVES: Determine all-cause mortality and mortality following a cancer diagnosis among MS patients compared with matched population controls. METHODS: Norwegian MS patients born 1930 - 1979 (n= 6950) followed-up 1953 - 2016, were matched with 37 922 controls. We compared incident cancer diagnosis from the Cancer Registry of Norway, date of death from the Cause of Death Registry, education from the National Education Database, by multivariate Cox proportional hazard regression. RESULTS: Hazard ratio (HR) and 95% confidence interval (CI) for all-cause mortality among MS patients was 4.97 (4.64 - 5.33), and 2.61 (2.29 - 2.98) for mortality following a cancer diagnosis. Mortality in MS was highest following urinary- (2.53: 1.55 - 4.14), colorectal- (2.14: 1.47 - 3.11), hematological- (1.76: 1.08 - 2.88), ovarian - 2.30 (1.73-3.06) and breast cancer diagnosis (2.61: 1.85 - 3.68), compared to controls. High education was inversely associated with mortality among MS patients. CONCLUSIONS: All-cause mortality was five- fold and mortality following a cancer diagnosis was two- fold increased among MS patients. Mortality following specific cancers raises the possibility of diagnostic neglect.
 BACKGROUND: Prevalence of multiple sclerosis has been increased during the last decades throughout the world. Epidemiological studies could improve our understanding relating to its intrinsic and extrinsic causes. OBJECTIVES: The current study has been conducted to determine the epidemiological features of MS in south-eastern Iran which is a semi-tropical area with different ethnicities. METHODS: This longitudinal descriptive study was carried out in south-eastern Iran, based on information of MS patients registered at Zahedan University of Medical Sciences database from 1990 to 2020. RESULTS: A total of 1045 cases were enrolled into the study. The age-standardized prevalence ratio of MS increased to 42.2/100,000 population by 2020. These figures showed increasing trends both in females and males and reached to 61.5 and 22.6 per 100,000 population, respectively by the year 2020. Likewise, the total incidence rate grew to its maximum amount of 4.5 in 2015. Female incidence also revealed an upward trend and peaked in 2016 to 6.4 while male incidence rate reached at its highest level of 1.8 in 2009. CONCLUSION: MS prevalence ratios and incidence rates in south-eastern Iran have been increasing steadily, especially in women during the last three decades. The south-eastern part of Iran should be considered a high-risk region.
 INTRODUCTION: B cells are acknowledged as crucial players in the pathogenesis of multiple sclerosis (MS). Several disease modifying drugs including cladribine have been shown to exert differential effects on peripheral blood B cell subsets. However, little is known regarding functional changes within the peripheral B cell populations. In this study, we obtained a detailed picture of B cell repertoire changes under cladribine treatment on a combined immunoglobulin (Ig) transcriptome and proteome level. METHODS: We performed next-generation sequencing of Ig heavy chain (IGH) transcripts and Ig mass spectrometry in cladribine-treated patients with relapsing-remitting multiple sclerosis (n = 8) at baseline and after 6 and 12 months of treatment in order to generate Ig transcriptome and Ig peptide libraries. Ig peptides were overlapped with the corresponding IGH transcriptome in order to analyze B cell clones on a combined transcriptome and proteome level. RESULTS: The analysis of peripheral blood B cell percentages pointed towards a significant decrease of memory B cells and an increase of naive B cells following cladribine therapy. While basic IGH repertoire parameters (e.g. variable heavy chain family usage and Ig subclasses) were only slightly affected by cladribine treatment, a significantly decreased number of clones and significantly lower diversity in the memory subset was noticeable at 6 months following treatment which was sustained at 12 months. When looking at B-cell clones comprising sequences from the different time-points, clones spanning between all three time-points were significantly more frequent than clones including sequences from two time-points. Furthermore, Ig proteome analyses showed that Ig transcriptome specific peptides could mostly be equally aligned to all three time-points pointing towards a proportion of B-cell clones that are maintained during treatment. DISCUSSION: Our findings suggest that peripheral B cell related treatment effects of cladribine tablets might be exerted through a reduction of possibly disease relevant clones in the memory B cell subset without disrupting the overall clonal composition of B cells. Our results -at least partially- might explain the relatively mild side effects regarding infections and the sustained immune response after vaccinations during treatment. However, exact disease driving B cell subsets and their effects remain unknown and should be addressed in future studies.
 BACKGROUND: Factors driving differences in disease burden between African American and White people with multiple sclerosis (pwMS) remain unclear. Here, we explored whether differences in disability outcomes could be observed after controlling for major sociodemographic factors and comorbidities, and assessed the presence of a possible interaction between MS and race. METHODS: In this cross-sectional study, 120 pwMS within 6 years from disease onset and 82 healthy controls between 18 and 70 years of age, self-identified as either African American or White, were prospectively enrolled. Inclusion criteria for pwMS were: diagnosis of MS according to the revised McDonald criteria, relapsing-remitting phenotype and Expanded Disability Status Scale (EDSS) < 6.5. Study outcomes included: (i) global disability (EDSS); (ii) quantitative mobility and leg function (Timed 25 Foot Walk Test-T25FWT); (iii) quantitative finger dexterity (9-Hole Peg Test-9HPT); (iv) cognitive efficiency and speed performance (Symbol Digit Modalities Test-SDMT). Differences in disability outcomes were assessed employing multivariable linear regression models. Based on their association with MS or disability, covariates included age, gender, race, years of education, total income, body mass index, comorbidities. The interaction between MS and race on disability outcomes was estimated via relative excess risk of interaction and attributable proportion. RESULTS: Accounting for age, gender, total income, education, body mass index and comorbidities, African American pwMS showed significantly worse performances in manual dexterity and cognition than White pwMS (White pwMS coeff. 3.24, 95% CI 1.55, 4.92 vs African American pwMS coeff. 5.52, 95% CI 3.55, 7.48 and White pwMS coeff. -5.87, 95% CI -8.86, -2.87 vs African American pwMS coeff. -7.99, 95% CI -11.58,-4.38). MS and race independently contributed to the observed gradient in disability severity. CONCLUSIONS: Complex social disparities and systemic racism might contribute to clinical heterogeneity in MS.
 Clostridium perfringens epsilon toxin is associated with enterotoxaemia in livestock. More recently, it is proposed to play a role in multiple sclerosis (MS) in humans. Compared to matched controls, strains of C. perfringens which produce epsilon toxin are significantly more likely to be isolated from the gut of MS patients and at significantly higher levels; similarly, sera from MS patients are significantly more likely to contain antibodies to epsilon toxin. Epsilon toxin recognises the myelin and lymphocyte (MAL) protein receptor, damaging the blood-brain barrier and brain cells expressing MAL. In the experimental autoimmune encephalomyelitis model of MS, the toxin enables infiltration of immune cells into the central nervous system, inducing an MS-like disease. These studies provide evidence that epsilon toxin plays a role in MS, but do not yet fulfil Koch's postulates in proving a causal role.
 BACKGROUND: People living with multiple sclerosis (MS) need access to high quality healthcare and support services. However, many people with MS do not have access to the services that they need. OBJECTIVE: To survey healthcare utilisation and perceived quality and accessibility amongst people living with MS who enroled in a free online course about MS (the Understanding MS massive open online course (MOOC)) and to evaluate the impact of course completion on these outcomes. METHODS: This longitudinal cohort study evaluated participants before they began the course, immediately following completion, and six months following completion. We describe baseline healthcare utilisation and perceived accessibility and quality (N = 813) and identify factors associated with satisfaction using chi-square and t-tests. We evaluate the impact of course completion amongst a sub-group (N = 123) of participants who both completed the course and completed all three assessments using paired t-tests. We determined effect size using Cohen's D. RESULTS: Most participants accessed at least one healthcare service in the month before beginning the course and were satisfied with their healthcare accessibility and quality. Participants who reported being satisfied with their healthcare quality and accessibility had more healthcare visits, and greater MS knowledge, health literacy, quality of life and self-efficacy. Completing the Understanding MS MOOC had no effect on perceived healthcare accessibility or quality. CONCLUSION: Our study suggests that people with MS who access online educational resources are likely to be well resourced in other areas as well. Our findings also suggest that a more targeted intervention may be necessary to improve healthcare accessibility and quality outcomes in people with MS.
 BACKGROUND: Multiple sclerosis (MS) is the most frequent non-traumatic neurological debilitating disease among young adults with no cure. Over recent decades, efforts to treat neurodegenerative diseases have shifted to regenerative cell therapy. Adipose tissue-derived stromal vascular fraction (SVF) comprises a heterogeneous cell population, considered an easily accessible source of MSCs with therapeutic potential in autoimmune diseases. This study aimed to assess the regenerative capacity of low-level laser-activated SVF in an MS cat model. METHODS: Fifteen adult Persian cats were used in this study: Group I (control negative group, normal cats), Group II (EB-treated group, induced for MS by ethidium bromide (EB) intrathecal injection), and Group III (SVF co-treated group, induced for MS then treated with SVF on day 14 post-induction). The SVF was obtained after digesting the adipose tissue with collagenase type I and injecting it intrathecal through the foramen magnum. RESULTS: The results showed that the pelvic limb's weight-bearing locomotion activity was significantly (P ≤ 0.05) recovered in Group III, and the Basso, Beattie, and Bresnahan (BBB) scores of hindlimb locomotion were significantly higher in Group III (14 ± 0.44) than Group II (4 ± 0.31). The lesion's extent and intensity were reduced in the magnetic resonance imaging (MRI) of Group III. Besides, the same group showed a significant increase in the expression of neurotrophic factors: BDNF, SDF and NGF (0.61 ± 0.01, 0.51 ± 0.01 and 0.67 ± 0.01, respectively) compared with Group II (0.33 ± 0.01, 0.36 ± 0.006 and 0.2 ± 0.01, respectively). Furthermore, SVF co-treated group revealed a significant (P ≤ 0.05) increase in oligodendrocyte transcription factor (Olig2) and myelin basic protein (4 ± 0.35 and 6 ± 0.45, respectively) that was decreased in group II (1.8 ± 0.22 and 2.9 ± 0.20, respectively). Moreover, group III showed a significant (P ≤ 0.05) reduction in Bax and glial fibrillary acidic protein (4 ± 0.53 and 3.8 ± 0.52, respectively) as compared with group II (10.7 ± 0.49 and 8.7 ± 0.78, respectively). The transmission electron microscopy demonstrated regular more compact, and markedly (P ≤ 0.05) thicker myelin sheaths (mm) in Group III (0.3 ± 0.006) as compared with group II (0.1 ± 0.004). Based on our results, the SVF co-treated group revealed remyelination and regeneration capacity with a reduction in apoptosis and axonal degeneration. CONCLUSION: SVF is considered an easy, valuable, and promising therapeutic approach for treating spinal cord injuries, particularly MS.

 INTRODUCTION: Fingolimod is the first approved oral therapy for relapsing-remitting multiple sclerosis (RRMS). The present study aimed to further characterize fingolimod's safety profile, and to assess the patient-reported treatment satisfaction and impact of fingolimod on the quality of life (QoL) of patients with multiple sclerosis (MS) treated in routine care in Greece. METHODS: This was a multicenter, prospective, observational, 24-month study conducted in Greece by hospital-based and private practice neurologists who specialize in MS. Eligible patients had initiated fingolimod within 15 days in accordance with the locally approved label. Safety outcomes included any adverse event (AE) observed during the study period and efficacy outcomes included both objective (disability progression and 2-year annualized relapse rate) and patient-reported assessments (Treatment Satisfaction Questionnaire for Medication (TSQM) v1.4 and the EuroQol (EQ)-5-dimension (5D) 3-level instruments). RESULTS: A total of 489 eligible patients (age 41.2 ± 9.8 years; 63.7% female; 4.2% treatment-naive) were exposed to fingolimod for a median of 23.7 months. During the observation period, 20.5% of the participants experienced 233 AEs. Lymphopenia (8.8%), leukopenia (4.2%), hepatic enzyme increased (3.4%), and infections (3.0%) were the most common. Most patients (89.3%) did not experience disability progression; the 2-year annualized relapse rate decreased by 94.7% compared to baseline. The median EQ-visual analogue scale (VAS) was 74.5 at month 24 vs. 65.0 at enrollment (p < 0.001) and the EQ-5D index score was 0.80 vs. 0.78, respectively. Significant improvements were noted in the TSQM global satisfaction and effectiveness domain scores between 6 and 24 months post enrollment (median scores at month 24, 71.4 and 66.7, respectively) (p < 0.001). Significant increases from enrollment to the 24th month were also noted in the patients' global satisfaction and effectiveness domain scores [mean change of 7.4 ± 17.7 (p = 0.005) and mean increase of 5.4 ± 16.2) (p = 0.043), respectively]. CONCLUSION: In the real-world setting of Greece, fingolimod demonstrates a clinical benefit and a predictable and manageable safety profile, which contribute towards high patient-reported treatment satisfaction and improvements in the QoL of patients with MS.
 Hormonal imbalance may be an important factor in the severity of multiple sclerosis (MS) disease. In this context, hormone therapy has been shown to have immunoregulatory potential in various experimental approaches. There is increasing evidence of potentially beneficial effects of thyroid, melatonin, and sex hormones in MS models. These hormones may ameliorate the neurological impairment through immunoregulatory and neuroprotective effects, as well as by reducing oxidative stress. Expanding our knowledge of hormone therapy may be an effective step toward identifying additional molecular/cellular pathways in MS disease. In this review, we discuss the role of several important hormones in MS pathogenesis in terms of their effects on immunoregulatory aspects and neuroprotection.
 BACKGROUND: Balance and mobility impairment are two of the most common and debilitating symptoms among people with multiple sclerosis (MS). Somatosensory symptoms, including reduced plantar cutaneous sensation, have been identified in this cohort. Given the importance of the somatosensory system in gait, it is likely that impaired plantar sensation may play a role in the walking adaptations commonly observed in people with MS, including decreased stride length and increased stride width and dual support time, often described as a cautious gait strategy. Understanding the contributions of plantar sensation to these alterations may provide targets for interventions that seek to improve sensory feedback and normalize gait patterns. This cross-sectional study determined whether individuals with MS who demonstrate reduced sensitivity of the plantar surfaces also demonstrate altered plantar pressure distributions during walking compared to a control cohort. METHODS: Twenty individuals with MS and twenty age- and sex-matched control participants walked barefoot at preferred and three matched speeds. Participants walked across a walkway with an embedded pressure plate used to quantify pressures within ten plantar zones. In addition, vibration perception thresholds were assessed at four sites on the plantar surface. RESULTS: Individuals with MS demonstrated increased peak total plantar pressures compared to control participants, that increased with walking speed. For the MS group, plantar pressures were higher on the less sensitive foot, although pressures on both feet exceeded those of the control cohort. Positive correlations between vibration perception threshold and peak total pressure were evident, although generally stronger in the MS cohort. CONCLUSION: A relationship between plantar vibration sensitivity and pressure could indicate that individuals with MS seek to increase plantar sensory feedback during walking. However, because proprioception may also be impaired, increased plantar pressure could result from inaccurate foot placement. Interventions targeting improved somatosensation may have the potential to normalize gait patterns and should be investigated.
 AIM: The aim of this study was to investigate the prevalence and potential association between infection with different herpes viruses and multiple sclerosis (MS). METHODS: A systematic literature search was performed by finding relevant cross-sectional and case-control studies from a large online database. Heterogeneity, Odds ratio (OR), and corresponding 95% Confidence interval (CI) were applied to all studies by meta-analysis and forest plots. The analysis was performed using Stata Software v.14. RESULTS: One hundred and thirty-four articles (289 datasets) were included in the meta-analysis, 128 (245 datasets) of which were case/control and the rest were cross-sectional. The pooled prevalence of all human herpes viruses among MS patients was 50% (95% CI: 45-55%; I2 = 96.91%). In subgroup analysis, the pooled prevalence of Herpes simplex virus (HSV), Varicella-zoster virus (VZV), Epstein-Barr virus (EBV), Cytomegalovirus (CMV), Human herpes virus 6 (HHV-6), Human herpes virus 7 (HHV-7), and Human herpes virus 8 (HHV-8) was 32%, 52%, 74%, 41%, 39% 28%, and 28%, respectively. An association was found between infection with human herpes viruses and MS [summary OR 2.07 (95% CI (1.80-2.37); I2 = 80%)]. CONCLUSION: The results of the present study showed that EBV, VZV, and HHV-6 infection are associated with multiple sclerosis and can be considered as potential risk factors for MS. Although the exact molecular mechanism of the role of herpes viruses in the development of MS is still unknown, it seems that molecular mimicry, the release of autoreactive antibodies, and inflammation in the CNS following viral infection can be important factors in the induction of MS.
 Multiple sclerosis (MS) is commonly diagnosed in young adults during their reproductive years. Consequently, concerns about family planning and MS management related to pregnancy and breastfeeding are often encountered in clinical practice. Pregnancy itself is not harmful for women with MS. However, disease-modifying therapies (DMTs) have implications for reproductive planning, including stopping treatment while trying to conceive and during pregnancy, as well as managing fetal risks. People with MS and their care team must engage in collaborative decision-making before, during, and after pregnancy. Based on the results of a consensus-building initiative, answers are provided to 20 frequently asked questions regarding the management of MS during pregnancy planning, pregnancy, and the postpartum period.

 OBJECTIVES: The objective of this study was to report on the development of neuroinvasive West Nile virus (WNV) infection in the context of anti-CD20 monotherapy for multiple sclerosis (MS). METHODS: This is a case series study. RESULTS: In 2021-2022, we observed 4 cases of neuroinvasive WNV infection in our patient population of 2009 patients with MS on ocrelizumab, compared with a total of 46 cases of neuroinvasive WNV infection reported in Pennsylvania and 40 in New Jersey. Odds were 258 times that of the general population (95% confidence interval 97-691), χ(2) p < 0.0001). All were women aged 41-61 years with variable disease duration, level of disability, and duration of anti-CD20 therapy. All presented in summer/early fall with fever, headache, and encephalopathy consistent with meningoencephalitis. Three patients had acute cerebellitis. Two had anterior nerve root involvement progressing to quadriparesis, and 1 developed refractory nonconvulsive status epilepticus. All required intubation and experienced significant morbidity. All had CSF pleocytosis. Two patients were WNV IgM positive in both the serum and CSF, 1 patient had positive serum IgM and CSF metagenomic next-generation sequencing (mNGS), while 1 had positive CSF mNGS with negative serum and CSF antibodies. DISCUSSION: Neuroinvasive WNV infection can develop with anti-CD20 monotherapy in the absence of additional immunosuppression. WNV serologies may be negative in the setting of anti-CD20 treatment; in the appropriate clinical context, one should consider direct detection methods such as PCR or mNGS-based testing.
 BACKGROUND: Multiple sclerosis (MS) is one of the most prevalent chronic inflammatory diseases caused by demyelination and axonal damage in the central nervous system. Structural retinal imaging via optical coherence tomography (OCT) shows promise as a noninvasive biomarker for monitoring of MS. There are successful reports regarding the application of Artificial Intelligence (AI) in the analysis of cross-sectional OCTs in ophthalmologic diseases. However, the alteration of thicknesses of various retinal layers in MS is noticeably subtle compared to other ophthalmologic diseases. Therefore, raw cross-sectional OCTs are replaced with multilayer segmented OCTs for discrimination of MS and healthy controls (HCs). METHODS: To conform to the principles of trustworthy AI, interpretability is provided by visualizing the regional layer contribution to classification performance with the proposed occlusion sensitivity approach. The robustness of the classification is also guaranteed by showing the effectiveness of the algorithm while being tested on the new independent dataset. The most discriminative features from different topologies of the multilayer segmented OCTs are selected by the dimension reduction method. Support vector machine (SVM), random forest (RF), and artificial neural network (ANN) are used for classification. Patient-wise cross-validation (CV) is utilized to evaluate the performance of the algorithm, where the training and test folds contain records from different subjects. RESULTS: The most discriminative topology is determined to square with a size of 40 pixels and the most influential layers are the ganglion cell and inner plexiform layer (GCIPL) and inner nuclear layer (INL). Linear SVM resulted in 88% Accuracy (with standard deviation (std) = 0.49 in 10 times of execution to indicate the repeatability), 78% precision (std=1.48), and 63% recall (std=1.35) in the discrimination of MS and HCs using macular multilayer segmented OCTs. CONCLUSION: The proposed classification algorithm is expected to help neurologists in the early diagnosis of MS. This paper distinguishes itself from other studies by employing two distinct datasets, which enhances the robustness of its findings in comparison with previous studies with lack of external validation. This study aims to circumvent the utilization of deep learning methods due to the limited quantity of the available data and convincingly demonstrates that favorable outcomes can be achieved without relying on deep learning techniques.
 BACKGROUND: People with multiple sclerosis (pwMS) treated with certain disease-modifying therapies (DMTs) have attenuated IgG response following COVID-19 vaccination; however, the clinical consequences remain unclear. OBJECTIVE: To report COVID-19 rates in pwMS according to vaccine serology. METHODS: PwMS with available (1) serology 2-12 weeks following COVID-19 vaccine 2 and/or vaccine 3 and (2) clinical data on COVID-19 infection/hospitalisation were included. Logistic regression was performed to examine whether seroconversion following vaccination predicted risk of subsequent COVID-19 infection after adjusting for potential confounders. Rates of severe COVID-19 (requiring hospitalisation) were also calculated. RESULTS: A total of 647 pwMS were included (mean age 48 years, 500 (77%) female, median Expanded Disability Status Scale (EDSS) 3.5% and 524 (81%) exposed to DMT at the time of vaccine 1). Overall, 472 out of 588 (73%) were seropositive after vaccines 1 and 2 and 222 out of 305 (73%) after vaccine 3. Seronegative status after vaccine 2 was associated with significantly higher odds of subsequent COVID-19 infection (odds ratio (OR): 2.35, 95% confidence interval (CI): 1.34-4.12, p = 0.0029), whereas seronegative status after vaccine 3 was not (OR: 1.05, 95% CI: 0.57-1.91). Five people (0.8%) experienced severe COVID-19, all of whom were seronegative after most recent vaccination. CONCLUSION: Attenuated humoral response to initial COVID-19 vaccination predicts increased risk of COVID-19 in pwMS, but overall low rates of severe COVID-19 were seen.
 OBJECTIVE: Falls are common in people with multiple sclerosis. There is rising interest in how the multifactorial and chronic nature of fall risk among people with multiple sclerosis can be addressed through self-management. Thus, the aims were to investigate the extent and the scope of publications on self-management of falls in people with multiple sclerosis, and to identify how the concept of self-management was defined and used. DATA SOURCES: A systematic literature search in Medline, Cochrane, Web of Science and PsycInfo was conducted to identify publications until July 2022. REVIEW METHODS: Published methodological guidance was followed. Articles targeting: (1) people with multiple sclerosis, (2) falls, and (3) self-management were selected. Of 1656 records, 203 publications were assessed for eligibility, of which 173 did not meet the inclusion criteria, and 16 publications did not contain empirical data. The type of publication, study focus, and study design was extracted. If applicable, key findings, self-management tasks and skills, and the definition of self-management were extracted. RESULTS: Fourteen original articles met all inclusion criteria. Ten articles represented six different fall prevention interventions. Three publications were randomized controlled trials. Self-management content was variable and not comprehensive in nature. None of the 14 publications included a self-management definition. CONCLUSION: The limited number of original articles and the even fewer intervention studies show that the research on self-management of falls in people with multiple sclerosis is in its infancy. To progress in the research area of self-management of falls, a more robust, consensus-based description of self-management frameworks and activities is needed.
 BACKGROUND: Most people with multiple sclerosis (MS) are employed at the time of their diagnosis; however, due to the unpredictable nature of MS, most exit the workforce shortly thereafter. A plethora of research has examined factors that negatively affect employment outcomes for people with MS. However, little is known about how hope, a modifiable positive psychology factor, affects employment. OBJECTIVE: This study examined the role of hope and its association with employment outcomes for people with MS. METHODS: Two-hundred and fifty-five adults with MS (mean ± SD age, 45.45 years ± 10.28) completed surveys about their MS, employment, disability-related stress, and hope. A three-step hierarchical logistic regression was conducted to examine the extent to which hope explains the variance in employment, over and above demographic and disability related covariates. RESULTS: The final model explained 28% of the variance in employment, suggesting that the model was able to distinguish people with MS who were employed versus those who were unemployed. Higher levels of hope were associated with an increased probability of being employed (OR = 4.65; 95% CI [1.98, 10.92]). CONCLUSION: This study supports that hope is associated with favorable employment outcomes for people with MS. Persons with MS may benefit from working with rehabilitation professionals to enhance their hope, and this study provides a foundation for the development of hope-based interventions to improve employment outcomes among this population.
 BACKGROUND: Currently, there are several studies showing that wearable inertial sensors are highly sensitive in the detection of gait disturbances in people with multiple sclerosis (PwMS), showing excellent reliability within one or 7-14 days. However, it is not known how stable these gait parameters remain over a longer period of time. This is surprising, because many treatments last longer than two weeks. Thus, the purpose of the current study was to examine gait parameters obtained by means of wearable inertial sensors during a 6-min walk and to reassess these parameters after a period of one year. METHODS: Fifty PwMS (without a relapse or a recent change in the Expanded Disability Status Scale (EDSS) or treatment) and 20 healthy participants were examined at two assessment points (interval between assessments: 14.4 ± 6.6 months). At each assessment point, all participants had to complete a 6-min walking test, an observer-rater test (Berg Balance Scale, BBS) and a Timed-up and Go Test (TUG). To measure mean gait parameters (i.e. walking speed, stride length, stride time, the duration of the stance and swing phase and minimum toe-to-floor distance), as well as the intraindividual standard deviation of each mean gait parameter, wearable inertial sensors were utilized. RESULTS: We found that even after one year all mean gait parameters showed excellent Intraclass Correlation Coefficients (ICC between 0.75 and 0.95) in PwMS. Looking at MS subgroups, the ICCs were slightly higher in MS subgroup 2 (EDSS 2.0-5.0) than those in MS subgroup 1 (EDSS 0.0-1.5) and healthy controls. Compared to the mean gait parameters, parameters of gait variability showed only good-to-fair ICC values in PwMS. Concerning BBS and TUG, the ICC values after one year were close to the ICC values of the measured mean gait parameters. CONCLUSIONS: Due to the excellent stability of mean gait parameters after one year, these sensor-based gait parameters can be identified as clinically relevant markers to evaluate treatment effects over a longer (several months) period of time in MS.
 BACKGROUND: Depression and anxiety are commonly experienced in individuals with multiple sclerosis (MS) yet little is known about factors associated with psychological help-seeking attitudes in those with MS. METHOD: The current study investigated whether increased stigma related to chronic illness, internalized shame, and autonomous motivation mediated the relationship between depressive and anxiety symptoms and psychological help-seeking attitudes in individuals with MS. Two hundred fifty-four participants with MS completed an online questionnaire assessing depressive and anxiety symptoms, stigma related to chronic illness, internalized shame, autonomous motivation, and psychological help-seeking attitudes. RESULTS: Stigma related to chronic illness, internalized shame, and autonomous motivation mediated the relationships between increased depressive symptoms and anxiety symptoms and psychological help-seeking attitudes. The study also found that higher levels of chronic illness-related stigma and internalized shame were associated with more negative psychological help-seeking attitudes and higher autonomous motivation was associated with more positive psychological help-seeking attitudes. There were no direct effects of depressive or anxiety symptoms on psychological help-seeking attitudes. CONCLUSION: The significant mediating roles of stigma-related chronic illness, internalized shame, and autonomous motivation indicate that these factors may be useful to include in future depression and anxiety intervention studies targeting MS populations.
 BACKGROUND: CLASSIC-MS evaluated the long-term efficacy of cladribine tablets in patients with relapsing multiple sclerosis. OBJECTIVE: Report long-term mobility and disability beyond treatment courses received in CLARITY/CLARITY Extension. METHODS: This analysis represents CLASSIC-MS patients who participated in CLARITY with/without participation in CLARITY Extension, and received ⩾1 course of cladribine tablets or placebo (N = 435). Primary objective includes evaluation of long-term mobility (no wheelchair use in the 3 months prior to first visit in CLASSIC-MS and not bedridden at any time since last parent study dose (LPSD), i.e. Expanded Disability Status Scale (EDSS) score <7). Secondary objective includes long-term disability status (no use of an ambulatory device (EDSS < 6) at any time since LPSD). RESULTS: At CLASSIC-MS baseline, mean ± standard deviation EDSS score was 3.9 ± 2.1 and the median time since LPSD was 10.9 (range = 9.3-14.9) years. Cladribine tablets-exposed population: 90.6% (N = 394), including 160 patients who received a cumulative dose of 3.5 mg/kg over 2 years. Patients not using a wheelchair and not bedridden: exposed, 90.0%; unexposed, 77.8%. Patients with no use of an ambulatory device: exposed, 81.2%; unexposed, 75.6%. CONCLUSION: With a median 10.9 years' follow-up after CLARITY/CLARITY Extension, findings suggest the sustained long-term mobility and disability benefits of cladribine tablets.
 BACKGROUND: Multiple sclerosis (MS) is a chronic, inflammatory and neurodegenerative disease that leads to irreversible damage to the brain and spinal cord. The goal of so-called "immune reconstitution therapies" (IRTs) is to achieve long-term disease remission by eliminating a pathogenic immune repertoire through intense short-term immune cell depletion. B cells are major targets for effective immunotherapy in MS. OBJECTIVES: The aim of this study was to analyze the gene expression pattern of B cells before and during IRT (i.e., before B-cell depletion and after B-cell repopulation) to better understand the therapeutic effects and to identify biomarker candidates of the clinical response to therapy. METHODS: B cells were obtained from blood samples of patients with relapsing-remitting MS (n = 50), patients with primary progressive MS (n = 13) as well as healthy controls (n = 28). The patients with relapsing MS received either monthly infusions of natalizumab (n = 29) or a pulsed IRT with alemtuzumab (n = 15) or cladribine (n = 6). B-cell subpopulation frequencies were determined by flow cytometry, and transcriptome profiling was performed using Clariom D arrays. Differentially expressed genes (DEGs) between the patient groups and controls were examined with regard to their functions and interactions. We also tested for differences in gene expression between patients with and without relapse following alemtuzumab administration. RESULTS: Patients treated with alemtuzumab or cladribine showed on average a > 20% lower proportion of memory B cells as compared to before IRT. This was paralleled by profound transcriptome shifts, with > 6000 significant DEGs after adjustment for multiple comparisons. The top DEGs were found to regulate apoptosis, cell adhesion and RNA processing, and the most highly connected nodes in the network of encoded proteins were ESR2, PHB and RC3H1. Higher mRNA levels of BCL2, IL13RA1 and SLC38A11 were seen in patients with relapse despite IRT, though these differences did not pass the false discovery rate correction. CONCLUSIONS: We show that B cells circulating in the blood of patients with MS undergoing IRT present a distinct gene expression signature, and we delineated the associated biological processes and gene interactions. Moreover, we identified genes whose expression may be an indicator of relapse risk, but further studies are needed to verify their potential value as biomarkers.
 OBJECTIVE: Persons with multiple sclerosis (PwMS) are at increased risk for cognitive dysfunction. Considering the impact and potential ramifications of cognitive dysfunction, it is important that cognition is routinely assessed in PwMS. Thus, it is also important to identify a screener that is accurate and sensitive to MS-related cognitive difficulties, which can inform decisions for more resource-intensive neuropsychological testing. However, research focused on available self-report screeners has been mixed, such as with the Multiple Sclerosis Neuropsychological Screening Questionnaire (MSNQ). This study aims to clarify the relationship between subjective and objective assessment of cognitive functioning in MS by examining domain-specific performance and intraindividual variability (IIV). METHODS: 87 PwMS (F = 65, M = 22) completed a comprehensive neuropsychological battery which included self- and informant-report measures of neurocognitive functioning. Scores were examined in relation to mean performance on five domains of cognitive functioning and two measures of IIV. RESULTS: The MSNQ-Self was inversely associated with executive function, verbal memory, and visual memory; it was not associated with IIV. The MSNQ-Informant was inversely associated with executive function and verbal memory, and positively associated with one measure of IIV. The MSNQ-Self showed a correlation of moderate effect size with depression (r = .39) while the MSNQ-Informant did not. CONCLUSIONS: Results suggest that the MSNQ-Self and MSNQ-Informant show similar utility. Our findings also suggest that domains of executive function and memory may be most salient, thus more reflected in subjective reports of cognitive functioning. Future work should further examine the impact of mood disturbance with cognitive performance and IIV.
 BACKGROUND: A pro-inflammatory diet has been posited to induce chronic inflammation within the central nervous system (CNS), and multiple sclerosis (MS) is an inflammatory disease of the CNS. OBJECTIVE: We examined whether Dietary Inflammatory Index (DII(®))) scores are associated with measures of MS progression and inflammatory activity. METHODS: A cohort with a first clinical diagnosis of CNS demyelination was followed annually (10 years, n = 223). At baseline, 5- and 10-year reviews, DII and energy-adjusted DII (E-DII(TM)) scores were calculated (food frequency questionnaire) and assessed as predictors of relapses, annualised change in disability (Expanded Disability Status Scale) and two magnetic resonance imaging measures; fluid-attenuated inversion recovery (FLAIR) lesion volume and black hole lesion volume. RESULTS: A more pro-inflammatory diet was associated with a higher relapse risk (highest vs. lowest E-DII quartile: hazard ratio = 2.24, 95% confidence interval (CI) = -1.16, 4.33, p = 0.02). When we limited analyses to those assessed on the same manufacturer of scanner and those with a first demyelinating event at study entry (to reduce error and disease heterogeneity), an association between E-DII score and FLAIR lesion volume was evident (β = 0.38, 95% CI = 0.04, 0.72, p = 0.03). CONCLUSION: There is a longitudinal association between a higher DII and a worsening in relapse rate and periventricular FLAIR lesion volume in people with MS.
 INTRODUCTION: Progressive multifocal leukoencephalopathy is a rare but often fatal complication of some multiple sclerosis treatments. Although it has mainly been associated with natalizumab treatment, its appearance with other immunosuppressive therapies has also been reported. AIMS: The aim of this case report is to describe the development of progressive multifocal encephalopathy in a patient with relapsing-remitting multiple sclerosis treated with ocrelizumab without previous use of natalizumab. CONCLUSIONS: A summary of the presentation and disease course is provided, presented in the context of the current literature and likely pathophysiology.
 Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS). Although emerging evidence has shown that changes in neurotransmitter levels in the synaptic gap may contribute to the pathophysiology of MS, their specific role has not been elucidated yet. In this review, we aim to analyze preclinical and clinical evidence on the structural and functional changes in neurotransmitters in MS and critically discuss their potential role in MS pathophysiology. Preclinical studies have demonstrated that alterations in glutamate metabolism may contribute to MS pathophysiology, by causing excitotoxic neuronal damage. Dysregulated interaction between glutamate and GABA results in synaptic loss. The GABAergic system also plays an important role, by regulating the activity and plasticity of neural networks. Targeting GABAergic/glutamatergic transmission may be effective in fatigue and cognitive impairment in MS. Acetylcholine (ACh) and dopamine can also affect the T-mediated inflammatory responses, thereby being implicated in MS-related neuroinflammation. Also, melatonin might affect the frequency of relapses in MS, by regulating the sleep-wake cycle. Increased levels of nitric oxide in inflammatory lesions of MS patients may be also associated with axonal neuronal degeneration. Therefore, neurotransmitter imbalance may be critically implicated in MS pathophysiology, and future studies are needed for our deeper understanding of their role in MS.
 BACKGROUND: Multiple sclerosis (MS) is a chronic neurodegenerative disorder of the central nervous system (CNS) that commonly affects young and middle-aged adults. Neurodegeneration of the CNS affects its functions such as sensorimotor, autonomic and cognitive functions. Affectation of motor function can result in disability in performance of daily life activities. Thus, effective rehabilitation interventions are needed to help prevent disability in patients with MS. One of these interventions is the constraint induced movement therapy (CIMT). The CIMT is used to improve motor function in patients with stroke and other neurological conditions. Recently, its use in patients with MS is gaining ground. The aim of this study is to carry out a systematic review and meta-analysis to determine from the literature, the effects of CIMT on upper limb function in patients with MS. METHODS: PubMED, Embase, Web of Science (WoS), PEDro, and CENTRAL were searched until October 2022. Randomized controlled trials in patients with MS who were 18 years and above were included. Data on the characteristics of the study participants such as disease duration, type of MS, the mean scores of the outcomes of interest such as motor function and use of the arm in daily activities, and white matter integrity were extracted. Methodological quality and risks of bias of the included studies were assessed using PEDro scale and Cochrane risks of bias tool. The data was analysed using both narrative and quantitative syntheses. In the quantitative synthesis, random effect model meta-analysis of the mean and standard deviation of the scores on the outcomes of interest and the study sample size (for both the CIMT and the control group) post intervention was carried out. In addition, percentage of variation across the studies due to heterogeneity (I(2)) was considered significant when it is between 50% and 90% at p < 0.05. RESULTS: Two studies comprising of 4 published articles with good methodological quality were included in the study. The results showed that, CIMT is safe and improved white matter integrity, motor function, muscle strength, dexterity, real-world arm use and biomechanical parameters post intervention. However, although there was a trend towards better improvement in the CIMT group in all the outcomes, there was no statistically significant difference between groups in motor function (SMD=0.44, 95% CI=-0.20 to 1.07, p = 0.18) and quality of movement (SMD=0.96, -1.15 to 3.07, p = 0.37). CONCLUSION: CIMT can be used in patients with MS since it is safe as well as effective at improving functional outcomes. However, more studies are required to confirm its safety and effectiveness.
 BACKGROUND: Currently, outcomes of Multiple Sclerosis (MS) are not standardized and it is unclear which outcomes matter most to people living with MS. A consensus between patients and healthcare professionals on which outcomes to measure and how, would facilitate a move towards value-based MS care. OBJECTIVE: to develop an internationally accepted, patient-relevant Standard Outcome Set for MS (S.O.S.MS). METHODS: A mixed-method design was used, including a systematic literature review, four patient focus groups (n=30) and a RAND-modified Delphi process with seventeen MS experts of five disciplines from seven countries (the Netherlands, United States of America, Portugal, Ireland, India, New Zealand, Switzerland and Turkey). RESULTS: A standard outcome set for MS was defined, consisting of fourteen outcomes divided in four domains: disease activity (n=3), symptoms (n=4), functional status (n=6), and quality of life (n=1). For each outcome, an outcome measure was selected and the measurement protocol was defined. In addition, seven case-mix variables were selected. CONCLUSION: This standard outcome set provides a guideline for measuring outcomes of MS in clinical practice and research. Using this set to monitor and (inter)nationally benchmark real-world outcomes of MS can support improvement of patient value and ultimately guide the transition towards value-based MS care.
 Ocrelizumab is a humanized monoclonal antibody designed to bind to the CD20 molecule, resulting in a rapid depletion of B-cells; however, it has been shown that lymphocyte subpopulations other than B-cells are affected by the drug. To review the effects of ocrelizumab on circulating lymphocytes and identify candidate biomarkers to predict and monitor treatment response. A literature search for the most relevant articles from 2006 to 2022 was conducted in PubMed and Scopus. The effect of ocrelizumab on the peripheral immune system goes beyond B-cells; it also depletes T CD20 + lymphocytes. Further, ocrelizumab reshapes the T-cell response toward a low inflammatory profile and induces an increase in T CD8 + regulatory cell percentage. A higher Body Mass Index and higher B-cell count at baseline have been associated with early B-cell reappearance. Serum neurofilament light chain reduction has been associated with treatment response. Ocrelizumab treatment exerts a broad immunomodulatory effect and may be tailored based on patients' clinical and biological profiles.
 Growing evidence points to the importance of cholesterol in preserving brain homeostasis. Cholesterol makes up the main component of myelin in the brain, and myelin integrity is vital in demyelinating diseases such as multiple sclerosis. Because of the connection between myelin and cholesterol, the interest in cholesterol in the central nervous system increased during the last decade. In this review, we provide a detailed overview on brain cholesterol metabolism in multiple sclerosis and its role in promoting oligodendrocyte precursor cell differentiation and remyelination.
 INTRODUCTION: Mechanical methods aimed at the filtration of the cerebrospinal fluid (CSF) are a group of therapies that have been proposed to treat neurological conditions where pathogens are present in the CSF. Even though the industry of medical devices has not been very active in this field, there is a lack of systematization of the different systems and procedures that can be applied. AREAS COVERED: First, we systematize the classification and definitions of procedures and systems for mechanical filtration of the CSF. Then, we made a literature review in search of clinical or preclinical studies where any system of mechanical CSF clearance was proposed or applied. EXPERT OPINION: We found mechanical filtration of the CSF has been explored in subarachnoid hemorrhage, CNS infections (bacterial, viral, and fungal), meningeal carcinomatosis, multiple sclerosis, autoimmune encephalitis, and polyradiculomyelitis. Brain aging and neurodegenerative diseases are additional potential conditions of interest. While there is some preliminary positive evidence for many of these conditions, more advanced systems, detailed descriptions of procedures, and rigorous validations are needed to make these therapies a reality in the next decades.
 BACKGROUND: Patients with pediatric-onset multiple sclerosis (PwPOMS) frequently experience motor, sensory, and cognitive problems. Although exercise is known to be effective in adult patients with MS, there are still no studies investigating the effectiveness of exercise in PwPOMS. To examine the effectiveness of online exercise training on physical activity, muscle strength, functionality, gait, fatigue, and quality of life in PwPOMS. METHODS: Twenty-one individuals were included and randomly divided into two groups. The online exercise training program (OETP) group received exercise training including aerobics, strengthening, and balance training for 8 weeks, and the control group received no intervention. Outcomes were assessed at baseline, 8 weeks, and 32 weeks. RESULTS: Significant improvements were recorded in physical activity, muscle strength, functionality, gait, fatigue, and quality of life in the OETP group after treatment (p<0.05). Between groups, the OETP group was superior to the control group in terms of physical activity, muscle strength, functionality, and quality of life (p<0.05). The OETP group remained superior to the control group in follow-up. CONCLUSION: OETP performed under the supervision of a physiotherapist is effective in PwPOMS. Even if these patients have no disabilities, it would be beneficial to refer them to rehabilitation from an early period.
 Immune Cell Deconvolution methods utilizing gene expression profiling to quantify immune cells in tissues and blood are an appealing alternative to flow cytometry. Our objective was to investigate the applicability of deconvolution approaches in clinical trial settings to better investigate the mode of action of drugs for autoimmune diseases. Popular deconvolution methods CIBERSORT and xCell were validated using gene expression from the publicly available GSE93777 dataset that has comprehensive matching flow cytometry. As shown in the online tool, ~ 50% of signatures show strong correlation (r > 0.5) with the remainder showing moderate correlation, or in a few cases, no correlation. Deconvolution methods were then applied to gene expression data from the phase III CLARITY study (NCT00213135) to evaluate the immune cell profile of relapsing multiple sclerosis patients treated with cladribine tablets. At 96 weeks after treatment, deconvolution scores showed the following changes vs placebo: naïve, mature, memory CD4(+) and CD8(+) T cells, non-class switched, and class switched memory B cells and plasmablasts were significantly reduced, naïve B cells and M2 macrophages were more abundant. Results confirm previously described changes in immune cell composition following cladribine tablets treatment and reveal immune homeostasis of pro- vs anti-inflammatory immune cell subtypes, potentially supporting long-term efficacy.
 Epigenetic mechanisms can regulate how DNA is expressed independently of sequence and are known to be associated with various diseases. Among those epigenetic mechanisms, DNA methylation (DNAm) is influenced by genotype and the environment, making it an important molecular interface for studying disease etiology and progression. In this study, we examined the whole blood DNA methylation profiles of a large group of people with (pw) multiple sclerosis (MS) compared to those of controls. We reveal that methylation differences in pwMS occur independently of known genetic risk loci and show that they more strongly differentiate disease (AUC = 0.85, 95% CI 0.82-0.89, p = 1.22 × 10(-29)) than known genetic risk loci (AUC = 0.72, 95% CI: 0.66-0.76, p = 9.07 × 10(-17)). We also show that methylation differences in MS occur predominantly in B cells and monocytes and indicate the involvement of cell-specific biological pathways. Overall, this study comprehensively characterizes the immune cell-specific epigenetic architecture of MS.
 OBJECTIVE: To determine the prognostic value of persisting neuroinflammation in multiple sclerosis (MS) lesions, we developed a 18 kDa-translocator-protein-positron emission tomography (PET) -based classification of each lesion according to innate immune cell content and localization. We assessed the respective predictive value of lesion phenotype and diffuse inflammation on atrophy and disability progression over 2 years. METHODS: Thirty-six people with MS (disease duration 9 ± 6 years; 12 with relapsing-remitting, 13 with secondary-progressive, and 11 with primary-progressive) and 19 healthy controls (HCs) underwent a dynamic [(18) F]-DPA-714-PET. At baseline and after 2 years, the patients also underwent a magnetic resonance imaging (MRI) and neurological examination. Based on a threshold of significant inflammation defined by a comparison of [(18) F]-DPA-714 binding between patients with MS and HCs, white matter lesions were classified as homogeneously active (active center), rim-active (inactive center and active periphery), or nonactive. Longitudinal cortical atrophy was measured using Jacobian integration. RESULTS: Patients with MS had higher innate inflammation in normal-appearing white matter (NAWM) and cortex than HCs (respective standardized effect size = 1.15, 0.89, p = 0.003 and < 0.001). Out of 1,335 non-gadolinium-enhancing lesions, 53% were classified as homogeneously-active (median = 17 per patient with MS), 6% rim-active (median = 1 per patient with MS), and 41% non-active (median = 14 per patient with MS). The number of homogenously-active lesions was the strongest predictor of longitudinal changes, associating with cortical atrophy (β = 0.49, p = 0.023) and Expanded Disability Status Scale (EDSS) changes (β = 0.35, p = 0.023) over 2 years. NAWM and cortical binding were not associated to volumetric and clinical changes. INTERPRETATION: The [(18) F]-DPA-714-PET revealed that an unexpectedly high proportion of MS lesions have a smoldering component, which predicts atrophy and clinical progression. This suggests that following the acute phase, most lesions develop a chronic inflammatory component, promoting neurodegeneration and clinical progression. ANN NEUROL 2023;94:366-383.
 Multiple sclerosis (MS) is an autoimmune, demyelinating disease with the highest incidence in women of childbearing age. The effect of pregnancy on disease activity and progression is a primary concern for women with MS and their clinical teams. It is well established that inflammatory disease activity is naturally suppressed during pregnancy, followed by an increase postpartum. However, the long-term effect of pregnancy on disease progression is less understood. Having had a pregnancy before MS onset has been associated with an older age at first demyelinating event, an average delay of 3.4 years. After MS onset, there is conflicting evidence about the impact of pregnancy on long-term outcomes. The study with the longest follow-up to date showed that pregnancy was associated with a 0.36-point lower disability score after 10-years of disease in 1830 women. Understanding the biological mechanism by which pregnancy induces long-term beneficial effects on MS outcomes could provide mechanistic insights into the elusive determinants of secondary progression. Here, we review potential biological processes underlying this effect, including evidence that acute sex hormone exposure induces lasting changes to neurobiological and DNA methylation patterns, and how sustained methylation changes in immune cells can alter immune composition and function long-term.
 Multiple sclerosis (MS) is the most common inflammatory, demyelinating and neurodegenerative disease of the central nervous system in young adults. Chronic-relapsing experimental autoimmune encephalomyelitis (crEAE) in Biozzi ABH mice is an experimental model of MS. This crEAE model is characterized by an acute phase with severe neurological disability, followed by remission of disease, relapse of neurological disease and remission that eventually results in a chronic progressive phase that mimics the secondary progressive phase (SPEAE) of MS. In both MS and SPEAE, the role of microglia is poorly defined. We used a crEAE model to characterize microglia in the different phases of crEAE phases using morphometric and RNA sequencing analyses. At the initial, acute inflammation phase, microglia acquired a pro-inflammatory phenotype. At the remission phase, expression of standard immune activation genes was decreased while expression of genes associated with lipid metabolism and tissue remodeling were increased. Chronic phase microglia partially regain inflammatory gene sets and increase expression of genes associated with proliferation. Together, the data presented here indicate that microglia obtain different features at different stages of crEAE and a particularly mixed phenotype in the chronic stage. Understanding the properties of microglia that are present at the chronic phase of EAE will help to understand the role of microglia in secondary progressive MS, to better aid the development of therapies for this phase of the disease.
 PURPOSE: To explore the end users' experiences of foot drop electrical stimulator use for people with neurological conditions. MATERIALS AND METHODS: Electronic databases MEDLINE, EMBASE, CINAHL, Scopus, and Google Scholar were searched in March 2022. Included articles were quality assessed using the Critical Appraisal Skills Programme (CASP) checklist. A thematic synthesis approach was used to synthesise the review findings and establish analytical themes. A Confidence in the Evidence from Reviews of Qualitative Research (CERQual) Approach was used to assess the level of confidence of analytical themes. RESULTS: Seven qualitative studies were included with 67 participants with stroke and multiple sclerosis. The outcomes to foot drop stimulator use were enhanced walking ability, independence, confidence, and social participation. Main barriers to use were device aesthetics, usability challenges, trustworthiness of device in complex environments, and cost of the device. A conceptual model was created illustrating the barriers and outcomes in managing foot drop. CONCLUSIONS: We recommend that the outcomes to continued use of foot drop electrical stimulators are carefully considered against the barriers. Our conceptual model may be useful to guide clinical conversations around the possible use of FES for managing foot drop in people with multiple sclerosis and stroke.Implications for rehabilitationThe key outcomes to foot drop electrical stimulator use were enhanced walking ability, improved independence and confidence, and enhanced social participation.The main barriers to foot drop electrical stimulator use were device aesthetics, usability challenges, trustworthiness of device in complex environments, and cost of the device.We created a conceptual model that may be useful to guide clinical conversations around the possible use of FES for managing foot drop in people with multiple sclerosis and stroke.
 BACKGROUND: Magnetic resonance imaging (MRI) markers for chronic active lesions in MS include slowly expanding lesions (SELs) and paramagnetic rim lesions (PRLs). OBJECTIVES: To identify the relationship between SELs and PRLs in MS, and their association with disability. METHODS: 61 people with MS (pwMS) followed retrospectively with MRI including baseline susceptibility-weighted imaging, and longitudinal T1 and T2-weighted scans. SELs were computed using deformation field maps; PRLs were visually identified. Mixed-effects models assessed differences in Expanded Disability Status Scale (EDSS) score changes between the group defined by the presence of SELs and or PRLs. RESULTS: The median follow-up time was 3.2 years. At baseline, out of 1492 lesions, 616 were classified as SELs, and 80 as PRLs. 92% of patients had ⩾ 1 SEL, 56% had ⩾ 1 PRL, while both were found in 51%. SELs compared to non-SELs were more likely to also be PRLs (7% vs. 4%, p = 0.027). PRL counts positively correlated with SEL counts (ρ= 0.28, p = 0.03). SEL + PRL + patients had greater increases in EDSS over time (beta = 0.15/year, 95% confidence interval (0.04, 0.27), p = 0.009) than SEL+PRL-patients. CONCLUSION: SELs are more numerous than PRLs in pwMS. Compared with either SELs or PRLs found in isolation, their joint occurrence was associated with greater clinical progression.
 Serum antibodies directed against myelin oligodendrocyte glycoprotein (MOG) are found in patients with acquired CNS demyelinating syndromes that are distinct from multiple sclerosis and aquaporin-4-seropositive neuromyelitis optica spectrum disorder. Based on an extensive literature review and a structured consensus process, we propose diagnostic criteria for MOG antibody-associated disease (MOGAD) in which the presence of MOG-IgG is a core criterion. According to our proposed criteria, MOGAD is typically associated with acute disseminated encephalomyelitis, optic neuritis, or transverse myelitis, and is less commonly associated with cerebral cortical encephalitis, brainstem presentations, or cerebellar presentations. MOGAD can present as either a monophasic or relapsing disease course, and MOG-IgG cell-based assays are important for diagnostic accuracy. Diagnoses such as multiple sclerosis need to be excluded, but not all patients with multiple sclerosis should undergo screening for MOG-IgG. These proposed diagnostic criteria require validation but have the potential to improve identification of individuals with MOGAD, which is essential to define long-term clinical outcomes, refine inclusion criteria for clinical trials, and identify predictors of a relapsing versus a monophasic disease course.
 BACKGROUND: The "Managing Fatigue" (MF) programme can help people living with Multiple sclerosis (MS) manage fatigue in their everyday lives. The programme has been proven feasible with Swedish occupational therapists, but there is a lack of knowledge of how MS participants experience the programme, and what they learned from participating in the programme. AIM: To describe how Swedish MS participants experience the content and structure of the Swedish MF programme, as well as what they learned from participating in the programme. MATERIAL AND METHODS: Qualitative interviews were performed with nine MS participants, and data were analysed according to direct content analysis. RESULTS: Participants experienced programme material was relevant, and they valued the structured sessions that utilised different teaching forms. Participants described the group format and the experienced course leader nurtured their learning process. They learned occupational skills to save energy, to re-value daily occupations, and initiated a process of change, but individual support is needed after programme completion. CONCLUSION AND SIGNIFICANCE: Findings support programme feasibility among MS participants, and show the importance of being able to practice skills to handle fatigue in everyday life. Future studies should consider adding outcome measures focussing on engagement in occupations when evaluating programme effectiveness.
 BACKGROUND: Several studies indicate that the anterior visual pathway provides information about the dynamics of axonal degeneration in Multiple Sclerosis (MS). Current research in the field is focused on the quest for the most discriminative features among patients and controls and the development of machine learning models that yield computer-aided solutions widely usable in clinical practice. However, most studies are conducted with small samples and the models are used as black boxes. Clinicians should not trust machine learning decisions unless they come with comprehensive and easily understandable explanations. MATERIALS AND METHODS: A total of 216 eyes from 111 healthy controls and 100 eyes from 59 patients with relapsing-remitting MS were enrolled. The feature set was obtained from the thickness of the ganglion cell layer (GCL) and the retinal nerve fiber layer (RNFL). Measurements were acquired by the novel Posterior Pole protocol from Spectralis Optical Coherence Tomography (OCT) device. We compared two black-box methods (gradient boosting and random forests) with a glass-box method (explainable boosting machine). Explainability was studied using SHAP for the black-box methods and the scores of the glass-box method. RESULTS: The best-performing models were obtained for the GCL layer. Explainability pointed out to the temporal location of the GCL layer that is usually broken or thinning in MS and the relationship between low thickness values and high probability of MS, which is coherent with clinical knowledge. CONCLUSIONS: The insights on how to use explainability shown in this work represent a first important step toward a trustworthy computer-aided solution for the diagnosis of MS with OCT.
 BACKGROUND AND PURPOSE: Commonly used fatigue-lowering medications have not been proven effective in treating multiple sclerosis (MS)-related fatigue. A neuroanatomical basis for treatment-resistant fatigue in MS has not been explored. The aim of this study was to investigate the association between brain diffusion abnormality patterns and resistance to fatigue-lowering treatment. METHODS: Retrospective patient stratification: 1. treatment-resistant (n = 22) received anti-fatigue and/or anti-depressant and/or anxiolytic medication and the latest two Modified Fatigue Impact Scale (MFIS) score≥38; 2. responder (n = 16): received anti-fatigue and/or antidepressant and/or anxiolytic medication while the latest MFIS was <38, and minimum one previous MFIS was ≥38; 3. non-treated never-fatigued (n = 26): received none of the above-mentioned medications and MFIS was always<38 (over minimum four years assessed with MFIS every 1-2 years). 3T brain MRI was used to perform a cross-sectional voxel-wise comparison of fractional anisotropy (FA) between the groups. RESULTS: Treatment-resistant versus responder patients showed more extensive brain damage (ie, lower FA) favoring the fronto-striatal pathways. Both groups showed more widespread brain damage than non-treated never-fatigued patients. A mean fronto-striatal FA value of 0.26 could perfectly predict response to modafinil/armodafinil. CONCLUSION: Fronto-striatal damage may play a role in the development of resistance to fatigue-lowering treatment. Fronto-striatal FA may serve as a biomarker to predict response to fatigue-lowering medications in MS.
 BACKGROUND AND OBJECTIVE: Clinical overlap is observed between multiple sclerosis (MS) and myelin oligodendrocyte glycoprotein immunoglobulin-G (MOG-IgG) associated disease (MOGAD) and the difficulty in distinguishing between the two diseases. Here, we measured and compared the readily available neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and monocyte to lymphocyte ratio (MLR) to determine whether these three biomarkers can help to distinguish MOGAD and MS at disease onset. The impact of these three biomarkers on MOGAD and MS relapse also needs to be explored. METHODS: In this retrospective analysis, we obtained clinical and paraclinical data from the first attacks of MOGAD (N = 31) and MS (N = 50). Electronic medical records were used to collect demographic data (gender, age at onset), clinical symptoms, EDSS at onset, and medical treatments. The primary outcome was relapse within one year of onset. Four hematological parameters were recorded, including neutrophil count, platelet count, lymphocyte count, and monocyte count. NLR, PLR, and MLR were calculated and compared between MOGAD, MS, and HC. Receiver operator curve (ROC) analysis was performed to assess the ability of NLR, PLR, and MLR to distinguish between MOGAD and MS, MOGAD and HC, respectively. A logistic regression analysis was performed to determine the impact of NLR/PLR/MLR on MOGAD/MS relapse within one year of onset. RESULTS: Compared to HC, NLR is significantly higher in MOGAD and MS (p<0.001, p = 0.04, respectively). The PLR and MLR are elevated in MOGAD compared to HC (p<0.001, p<0.001, respectively), and MLR in MS are also statistically higher than in HC (p = 0.023). It is worth noting that NLR and PLR were much higher in MOGAD compared to MS (p<0.001, p = 0.001, respectively), but a significant difference regarding MLR has not been found between MOGAD and MS. Based on ROC curve analyses, we found that using NLR, PLR, and MLR to discriminate between MOGAD and MS yielded a ROC-plot area under the curve (AUC) value of 0.794, 0.727, and 0.681, respectively. Meanwhile, the AUC of NLR, PLR, and MLR to discriminate between MOGAD and HC were 0.926, 0.772, and 0.786. Furthermore, the logistics analysis revealed a significant positive association between PLR and MOGAD relapse. CONCLUSION: NLR helps differentiate MOGAD and MS in disease onset, and higher PLR was related to MOGAD relapse.
 BACKGROUND: To date, few cases of multiple sclerosis (MS) patients with concomitant Human Immunodeficiency Virus (HIV) infection have been described. However, none of the previously described cases has been treated with Natalizumab, probably due to the increasing risk of progressive multifocal leukoencephalopathy (PML). CASE: We report the case of a patient concomitantly diagnosed for HIV infection and MS treated with combined antiretroviral therapy (cART) and Natalizumab for 19 months, without clinical or radiological MS activity. CONCLUSIONS: Our case might suggest considering Natalizumab in patients with concomitant HIV infection, especially for those with significant disease activity requiring a high efficacy disease modifying treatment.
 Despite the large number of immunomodulatory or immunosuppressive treatments available to treat relapsing-remitting multiple sclerosis (MS), treatment of the progressive phase of the disease has not yet been achieved. This lack of successful treatment approaches is caused by our poor understanding of the mechanisms driving disease progression. Emerging concepts suggest that a combination of persisting focal and diffuse inflammation within the CNS and a gradual failure of compensatory mechanisms, including remyelination, result in disease progression. Therefore, promotion of remyelination presents a promising intervention approach. However, despite our increasing knowledge regarding the cellular and molecular mechanisms regulating remyelination in animal models, therapeutic increases in remyelination remain an unmet need in MS, which suggests that mechanisms of remyelination and remyelination failure differ fundamentally between humans and demyelinating animal models. New and emerging technologies now allow us to investigate the cellular and molecular mechanisms underlying remyelination failure in human tissue samples in an unprecedented way. The aim of this Review is to summarize our current knowledge regarding mechanisms of remyelination and remyelination failure in MS and in animal models of the disease, identify open questions, challenge existing concepts, and discuss strategies to overcome the translational roadblock in the field of remyelination-promoting therapies.
 Multiple sclerosis (MS) is an inflammatory disease of the CNS. In this issue of the JCI, Ma and Sannino et al. show that two strains of intestinal Clostridium perfringens, known to produce epsilon toxin (ETX), were frequently found in patients with MS. Tiny amounts of this toxin added to immunization with myelin antigens provoked MS-like brain lesions in mice. The distribution of these lesions was diffuse, as in MS, in contrast to the spinal cord-restricted lesions of most animal models. ETX bound to endothelial cells of the CNS to enhance immune cell trafficking through the blood-brain barrier into inflammatory brain lessons. ETX also binds to human, but not murine, white blood cells, perhaps altering immune responses. Barrier disruption and changes in immunity due to the toxin could alter the benefits of immune-modulatory MS therapies and are likely to interact with the complex genetics and environmental influences seen in MS.
 Multiple sclerosis is mediated by the immune system that damages the myelin sheath. Most patients experience inflammation. Since one of the factors that have a role in reducing inflammation is acetylcholine, and according to the benefits of saliva, in this study, the level of salivary and serum cholinesterase activity in patients with multiple sclerosis and healthy were evaluated. Thirty women with multiple sclerosis who were hospitalized in the neurology ward of Imam Reza and Hazrat Rasoul Hospitals and 30 healthy females participated in the study. The severity of multiple sclerosis was calculated by expanded disability status scale (EDSS). Saliva and serum samples were collected in the morning. Cholinesterase activity was assessed by a photometric method. The mean cholinesterase activity in stimulated and unstimulated saliva and serum significantly reduced in the multiple sclerosis group. The cutoff for differentiation of multiple sclerosis patients from healthy individuals by assessing cholinesterase activity (IU/L) was 3577 in serum, 241 in unstimulated saliva, and 266 in stimulated saliva. It seems that cholinesterase activity decreases in patients with multiple sclerosis.
 Multiple sclerosis (MS) symptoms and unpredictability can damage patient well-being. This study is aimed to investigate the relation between sociodemographic and clinical characteristics and the use of coping strategies as well as social support on health-related quality of life (HRQOL). We evaluated 314 MS outpatients of Virgen Macarena University Hospital in Sevilla/Spain (mean age 45 years, 67.8% women) twice over an 18-months period by Brief COPE Questionnaire (COPE-28), Multidimensional Scale of Perceived Social Support (MSPSS) and 12-Item Short Form Health Survey (SF-12). Female gender was significantly related to religion (r= 0.175, p< 0.001), self-distraction (r= 0.160, p< 0.001) and self-blame (r= 0.131, p< 0.05). Age correlated positively with religion (r= 0.240, p< 0.001), and self-blame (r= 0.123, p< 0.05). Progressive MS as well as functional impairment (EDSS) showed a positive relation with denial (r= 0.125, p< 0.05; r= 0.150, p< 0.001). Longer duration since diagnosis was related to lower perceived support from family (r= -0.123, p< 0.05). EDSS (β= -0.452, p< 0.001) was the strongest negative predictor of physical HRQOL followed by age (β= -0.123, p< 0.001), whereas family support was a protective factor (β= 0.096, p< 0.001). Denial (β= -0.132, p< 0.05), self-blame (β= -0.156, p< 0.05), female gender (β= -0.115, p< 0.05) and EDSS (β= -0.108, p< 0.05) negatively impacted on mental HRQOL 18 months later, whereas positive reframing (β= 0.142, p< 0.05) was a protective factor. Our study could identify sociodemographic and clinical variables associated with dysfunctional coping strategies, such as self-blame and denial, which specifically predict worse mental HRQOL as opposed to positive reframing. Diminishing dysfunctional coping and supporting cognitive reframing may contribute to improve HRQOL in MS.
 BACKGROUND: Kinesiophobia can be a barrier for physical activity in patients with multiple sclerosis (PwMS) and it can develop as a result of fear and avoidance reactions due to fatigue. However, there is no valid and reliable scale available to assess kinesiophobia due to fatigue in PwMS. AIMS: To investigate the test-retest reliability and construct validity of the Tampa Scale of Kinesiophobia-Fatigue (TSK-F) in PwMS. METHODS: Eighty-seven PwMS were included in the study. In addition to TSK-F, the following measurements were used for construct validity: Expanded Disability Status Scale (EDSS), Fatigue Severity Scale (FSS), Fatigue Impact Scale (FIS), 6-Minute Walking Test (6MWT), International Physical Activity Questionnaire (IPAQ), Beck Depression Inventory (BDI), Multiple Sclerosis Quality of Life Scale-54 (MSQoL-54). TSK-F was administered twice (3-7 days apart) to measure test-retest reliability. RESULTS: The intraclass correlation coefficient of the TSK-F was 0.867. It had a weak correlation with the IPAQ and EDSS, moderate correlation with the MSQoL-54 and 6MWT, and strong correlation with the BDI, FSS, and FIS (respectively, rho - 0.345, rho 0.365, rho 0.544, rho - 0.449, rho 0.690, rho 0.602, rho 0.650). The scale had good performance to discriminate the disease severity with the area under the curve (AUC) value 0.730. CONCLUSIONS: TSK-F has excellent reliability and moderate-to-good validity in evaluating kinesiophobia and the scale may be a useful outcome measurement for assessment of kinesiophobia due to fatigue in PwMS.
 INTRODUCTION: There is an urgent need for remyelinating therapies that restore function in people with multiple sclerosis (pwMS). Aerobic exercise is a promising remyelinating strategy because it promotes remyelination in animal models both independently and synergistically with medications. Here, in this study, we present an innovative, randomised, single-blind, clinical trial designed to explore: the relationship between demyelination and mobility (part 1), and if 24 weeks of aerobic exercise promotes remyelination in pwMS (part 2). METHODS AND ANALYSIS: Sedentary participants (n=60; aged 18-64 years) with stable MS will undergo a baseline visit with the following outcomes to assess associations between demyelination and mobility (part 1): spinal cord demyelination (somatosensory-evoked potentials, SSEPs), mobility (6-Minute Timed Walk, Timed 25-Foot Walk, Timed Up and Go, 9-Hole Peg Test) and patient-reported outcomes (PROs). After baseline testing, participants with significantly prolonged SSEP latency will advance to the clinical exercise trial (part 2) and will be randomised 1:1 to active or control conditions for 24 weeks. The active condition will be aerobic stationary cycling three times per week with graded virtual supervision. The control condition will be monthly virtual MS symptom education groups (six sessions). SSEP latency (remyelination endpoint), mobility outcomes and PROs will be measured at 12 and 24 weeks in all clinical trial participants. A subset of 11 active and 11 control participants will undergo a brain MRI with quantitative T(1) myelin water fraction at baseline and 24 weeks (exploratory remyelination endpoint). ETHICS AND DISSEMINATION: Ethical approval was obtained from the Oregon Health & Science University Institutional Review Board (#21045). Dissemination of findings will include peer-reviewed publications, conference presentations and media releases. The proposed study will inform the feasibility, study design and sample size for a fully powered clinical trial of aerobic exercise to promote remyelination in pwMS. TRIAL REGISTRATION NUMBER: NCT04539002.
 This review summarizes recent findings related to the role of the sympathetic nervous system (SNS) in pathogenesis of multiple sclerosis (MS) and its commonly used experimental model - experimental autoimmune encephalomyelitis (EAE). They indicate that noradrenaline, the key end-point mediator of the SNS, acting through β-adrenoceptor, has a contributory role in the early stages of MS/EAE development. This stage is characterized by the SNS hyperactivity (increased release of noradrenaline) reflecting the net effect of different factors, such as the disease-associated inflammation, stress, vitamin D hypovitaminosis, Epstein-Barr virus infection and dysbiosis. Thus, the administration of propranolol, a non-selective β-adrenoceptor blocker, readily crossing the blood-brain barrier, to experimental rats before the autoimmune challenge and in the early (preclinical/prodromal) phase of the disease mitigates EAE severity. This phenomenon has been ascribed to the alleviation of neuroinflammation (due to attenuation of primarily microglial activation/proinflammatory functions) and the diminution of the magnitude of the primary CD4+ T-cell autoimmune response (the effect associated with impaired autoantigen uptake by antigen presenting cells and their migration into draining lymph nodes). The former is partly related to breaking of the catecholamine-dependent self-amplifying microglial feed-forward loop and the positive feedback loop between microglia and the SNS, leading to down-regulation of the SNS hyperactivity and its enhancing influence on microglial activation/proinflammatory functions and the magnitude of autoimmune response. The effects of propranolol are shown to be more prominent in male EAE animals, the phenomenon important as males (like men) are likely to develop clinically more severe disease. Thus, these findings could serve as a firm scientific background for formulation of a new sex-specific immune-intervention strategy for the early phases of MS (characterized by the SNS hyperactivity) exploiting anti-(neuro)inflammatory and immunomodulatory properties of propranolol and other relatively cheap and safe adrenergic drugs with similar therapeutic profile.
 BACKGROUND: Sexual and physical violence against disabled individuals is widespread and linked to negative public health and social outcomes. The real-world prevalence of abuse in women with multiple sclerosis (MS) has not been well studied. OBJECTIVES: To explore abuse prevalence in a real-world cohort of females with MS attending an academic MS Center. METHODS: Prospective and retrospective abuse data were confidentially collected during neurology clinic visits and extracted from medical records for women attending an academic MS Center. Self-reported and provider-documented prevalence of abuse experiences were correlated with socio-economic and disease-specific factors. RESULTS: In total, 200 women completed prospective questionnaires, and 121 non-overlapping independent health records were retrospectively reviewed. Mean age (SD) was 49.055 (11.39). Seventy-six (38%) reported lifetime abuse incidents; 15% were abused within the previous year. Intimate partners were the most likely verbal (p ⩽ 0.01)) and physical (p = 0.04) abuse perpetrators. Neurologic disability correlated with greater likelihood of verbal abuse (p = 0.021) in prospective cohort. There was no billing or encounter documentation for any form of abuse. CONCLUSION: Intimate partner violence is common in women with MS, correlates with neurologic disability, and is underreported by the health system. Future research needs to focus on abuse detection and mitigation strategies.
 The influence of pregnancy on the course of multiple sclerosis (MS) has long been controversial. While historical evidence suggests a substantial decline in relapse rates during pregnancy followed by a rebound in the postpartum period, more recent work yielded equivocal results. We performed a systematic review and meta-analysis on data from cohort studies to determine whether women with MS experience increased relapse rates after delivery. A systematic literature search was conducted in the databases MEDLINE and Epistemonikos on the topic 'motherhood choice in MS' in March 2022. We included cohort studies assessing the association between pregnancy and MS relapse activity defined by the annualised relapse rate after 3, 6, 9 and 12 months post partum. Furthermore, information about disease-modifying therapies (DMT) and breast feeding was considered, if available. 5369 publications were identified. Of these, 93 full-text articles on MS relapse activity during the postpartum period were screened. 11 studies including 2739 pregnancies were eligible. Women with MS showed a significantly increased relapse rate in the first 6 months post partum, compared with preconception with the incidence rate ratio (IRR) almost doubled in the first 3 months post partum (1.87, 95% CI 1.40 to 2.50). However, at 10-12 months post partum, the IRR decreased significantly (0.81, 95% CI 0.67 to 0.98). Subanalysis on influencing parameters suggested that preconceptional DMTs (IRR for highly-effective DMTs 2.76, 95% CI 1.34 to 5.69) and exclusive breast feeding (risk ratio 0.39, 95% CI 0.18 to 0.86) significantly influenced postpartum relapse risk. Increased postpartum annualised relapse rate and possible modifiers should be considered in counselling women with MS who are considering pregnancy.
 The term 'neuromyelitis optica spectrum disorders' (NMOSD) is used as an umbrella term that refers to aquaporin-4 immunoglobulin G (AQP4-IgG)-positive neuromyelitis optica (NMO) and its formes frustes and to a number of closely related clinical syndromes without AQP4-IgG. NMOSD were originally considered subvariants of multiple sclerosis (MS) but are now widely recognized as disorders in their own right that are distinct from MS with regard to immunopathogenesis, clinical presentation, optimum treatment, and prognosis. In part 1 of this two-part article series, which ties in with our 2014 recommendations, the neuromyelitis optica study group (NEMOS) gives updated recommendations on the diagnosis and differential diagnosis of NMOSD. A key focus is on differentiating NMOSD from MS and from myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis (MOG-EM; also termed MOG antibody-associated disease, MOGAD), which shares significant similarity with NMOSD with regard to clinical and, partly, radiological presentation, but is a pathogenetically distinct disease. In part 2, we provide updated recommendations on the treatment of NMOSD, covering all newly approved drugs as well as established treatment options.
 INTRODUCTION: Multiple sclerosis mainly affects women of childbearing age, and the pregnancy and postpartum period is of special interest because of the peculiarities of the disease course and the therapeutic consequences that derive from it. During the period of breastfeeding (BF), the choice of treatment strategy must weigh up the well-established benefits of BF for both the newborn and the mother against the safety profile and potential adverse effects on the infant resulting from exposure to disease-modifying drugs transferred through breast milk. DEVELOPMENT: The study reviews the current evidence on the safety of disease-modifying drugs available for the treatment of multiple sclerosis during the BF period, and gathers data on the transfer of the different drugs into breast milk, as well as the potential adverse effects described in the infant. The drugs of first choice during this period are interferon beta and glatiramer acetate. The rest of the disease modifying drugs are not accepted for use in the BF period according to their summary of product characteristics. However, in recent years, data from studies of clinical practice and case series have been published suggesting that some of these drugs could be used safely during this period. CONCLUSIONS: Given the recognised health benefits of BF for both mother and infant, exclusive breastfeeding is recommended whenever possible. It is essential to carry out an individualised assessment prior to pregnancy and to evaluate the different treatment options depending on each patient.
 Multiple sclerosis (MS) is an autoimmune neurodegenerative disease affecting numerous people worldwide. While the relapsing subtypes of MS are to some extent treatable, the disease remains incurable leading to progressive disability. Limited efficacy of current small molecule drugs necessitates development of efficient and safe MS medications. Accordingly, drug repurposing is an invaluable strategy that recognizes new targets for known drugs especially in the field of poorly addressed therapeutic areas. Drug discovery largely depends on the identification of potential binding molecules to the intended biomolecular target(s). In this regard, current study was devoted to in silico repurposing of 263 small molecule CNS drugs to achieve superior binders to some MS-related targets. On the basis of molecular docking scores, thioxanthene and benzisothiazole-based antipsychotics could be identified as potential binders to sphingosine-1-phosphate lyase (S1PL) and cyclophilin D (CypD). Tightest interaction modes were observed for zuclopenthixol-S1PL (ΔG(b) -7.96 kcal/mol) and lurasidone-CypD (ΔG(b) -8.84 kcal/mol) complexes. Molecular dynamics (MD) simulations proved the appropriate and stable accommodation of top-ranked drugs inside enzyme binding sites during 100 ns. Hydroxyethyl piperazine of zuclopenthixol and benzisothiazole of lurasidone flipped inside the binding pocket to interact with adjacent polar and apolar residues. Solvent accessible surface area (SASA) fluctuations confirmed the results of binding trajectory analysis and showed that non-polar hydrophobic interactions played significant roles in acquired stabilities. Our results on lurasidone binding pattern were interestingly in accordance with previous reports on X-ray structures of other norbornane maleimide derivatives as CypD inhibitors. According to this, Asn144, Phe102 and Phe155 served as important residues in providing stable binding pose of lurasidone through both exo and endo conformations. Although experimental results are necessary to be achieved, the outcomes of this study proposed the potentiality of some thioxanthene and benzisothiazole-based antipsychotics for binding to S1PL and CypD, respectively, as MS-related targets.
 Coronavirus disease-2019 (COVID-19) is associated with cytokine storm and is characterized by acute respiratory distress syndrome (ARDS) and pneumonia problems. The respiratory system is a place of inappropriate activation of the immune system in people with multiple sclerosis (MS), and this may cause damage to the lung and worsen both MS and infections.The concerns for patients with multiple sclerosis are because of an enhance risk of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The MS patients pose challenges in this pandemic situation, because of the regulatory defect of autoreactivity of the immune system and neurological and respiratory tract symptoms. In this review, we first indicate respiratory issues associated with both diseases. Then, the main mechanisms inducing lung damages and also impairing the respiratory muscles in individuals with both diseases is discussed. At the end, the leading role of physical exercise on mitigating respiratory issues inducing mechanisms is meticulously evaluated.
 Ocrelizumab, an anti-CD20 monoclonal antibody, counteracts induction of humoral immune responses after severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) vaccinations in patients with multiple sclerosis (MS). We aimed to assess if serum ocrelizumab concentration measured at the time of vaccination could predict the humoral response after SARS-CoV-2 vaccination. In 52 patients with MS, we found ocrelizumab concentration at the time of vaccination to be a good predictor for SARS-CoV-2 IgG anti-RBD titers after vaccination (comparable to B-cell count). As the course of ocrelizumab concentration may be predicted using pharmacokinetic models, this may be a superior biomarker to guide optimal timing for vaccinations in B-cell depleted patients with MS. ANN NEUROL 2023;93:103-108.
 Malfunctions in the immune system cause multiple sclerosis (MS), which initiates mild to severe nerve damage. MS will disturb the signal communication between the brain and other body parts, and early diagnosis will help reduce the harshness of MS in humankind. Magnetic resonance imaging (MRI) supported MS detection is a standard clinical procedure in which the bio-image recorded with a chosen modality is considered to assess the severity of the disease. The proposed research aims to implement a convolutional neural network (CNN) supported scheme to detect MS lesions in the chosen brain MRI slices. The stages of this framework include (i) image collection and resizing, (ii) deep feature mining, (iii) hand-crafted feature mining, (iii) feature optimization with firefly algorithm, and (iv) serial feature integration and classification. In this work, five-fold cross-validation is executed, and the final result is considered for the assessment. The brain MRI slices with/without the skull section are examined separately, presenting the attained results. The experimental outcome of this study confirms that the VGG16 with random forest (RF) classifier offered a classification accuracy of >98% MRI with skull, and VGG16 with K-nearest neighbor (KNN) provided an accuracy of >98% without the skull.
 BACKGROUND: Multiple sclerosis (MS), a chronic auto-immune, inflammatory, and degenerative disease of the central nervous system, affects both males and females; however, females suffer from a higher risk of developing MS (2-3:1 ratio relative to males). The precise sex-based factors influencing risk of MS are currently unknown. Here, we explore the role of sex in MS to identify molecular mechanisms underlying observed MS sex differences that may guide novel therapeutic approaches tailored for males or females. METHODS: We performed a rigorous and systematic review of genome-wide transcriptome studies of MS that included patient sex data in the Gene Expression Omnibus and ArrayExpress databases following PRISMA statement guidelines. For each selected study, we analyzed differential gene expression to explore the impact of the disease in females (IDF), in males (IDM) and our main goal: the sex differential impact of the disease (SDID). Then, for each scenario (IDF, IDM and SDID) we performed 2 meta-analyses in the main tissues involved in the disease (brain and blood). Finally, we performed a gene set analysis in brain tissue, in which a higher number of genes were dysregulated, to characterize sex differences in biological pathways. RESULTS: After screening 122 publications, the systematic review provided a selection of 9 studies (5 in blood and 4 in brain tissue) with a total of 474 samples (189 females with MS and 109 control females; 82 males with MS and 94 control males). Blood and brain tissue meta-analyses identified, respectively, 1 (KIR2DL3) and 13 (ARL17B, CECR7, CEP78, IFFO2, LOC401127, NUDT18, RNF10, SLC17A5, STMP1, TRAF3IP2-AS1, UBXN2B, ZNF117, ZNF488) MS-associated genes that differed between males and females (SDID comparison). Functional analyses in the brain revealed different altered immune patterns in females and males (IDF and IDM comparisons). The pro-inflammatory environment and innate immune responses related to myeloid lineage appear to be more affected in females, while adaptive responses associated with the lymphocyte lineage in males. Additionally, females with MS displayed alterations in mitochondrial respiratory chain complexes, purine, and glutamate metabolism, while MS males displayed alterations in stress response to metal ion, amine, and amino acid transport. CONCLUSION: We found transcriptomic and functional differences between MS males and MS females (especially in the immune system), which may support the development of new sex-based research of this disease. Our study highlights the importance of understanding the role of biological sex in MS to guide a more personalized medicine.
 BACKGROUND: Since the advent of disease-modifying therapies (DMTs), people with MS are living longer. The management of MS requires use of DMTs, symptom management, and prevention for those with access to these aspects of health care. Although DMTs are used as part of early intervention to manage disease pathophysiology in those with MS, physical rehabilitation still focuses on symptomatic management of MS (tertiary prevention) and has not embraced a primary or secondary prevention approach to holistically manage MS. Although rehabilitation has been found to be beneficial for people with MS, there is currently limited information for persons in their early years of MS diagnosis. More importantly there is limited engagement of persons with early MS in rehabilitation care. Thus, the purpose of this study was to elucidate the perceptions of people living with early MS and their overall experiences with physical rehabilitation for MS management. METHODS: The study team used semi-structured interviews to collect qualitative data to ascertain the experiences and perceptions of 15 persons with early MS who were within 5 years of diagnosis (mean age 36.5 ± 10.4 years). Using a phenomenological approach, the researchers sought to understand the lived experiences of 15 people living with early MS. Using inductive thematic analysis, authors coded each interview separately and arrived at themes with consensus. RESULTS: Our study discovered six main themes and several subthemes offering insight into the lived experiences of the participants. Themes uncovered included: insight to condition, awareness of rehabilitation, resource availability, information seeking, clinician expertise in MS, and therapeutic use of self. CONCLUSIONS: Our study offered a small but poignant glimpse into the lived experiences of people living with early MS. There is still poor public awareness of MS-specific rehabilitation and its benefits for people with early MS. People with early MS seek information about their diagnosis but information and resources that are reliable and easily accessible are still needed, especially from their neurologists, to improve engagement in MS-specific rehabilitation. More research exploring these experiences and more diversity in the participant pool would lead to best practices in physical rehabilitation.

 Astrocytes, the most abundant group of glia cells in the brain, provide support for neurons and indicate multiple various functions in the central nervous system (CNS). Growing data additionally describe their role in the regulation of immune system activity. They exert their function not only by direct contact with other cell types, but also through an indirect method, e.g., by secreting various molecules. One such structure is extracellular vesicles, which are important mediators of crosstalk between cells. In our study, we observed that the impact of exosomes derived from astrocytes with various functional phenotype differently affect the immune response of CD4+ T cells, both from healthy individuals and from patients with multiple sclerosis (MS). Astrocytes, by modulating exosome cargo, impacts the release of IFN-γ, IL-17A and CCL2 in our experimental conditions. Considering the proteins concentration in cell culture supernatants and the cellular percentage of Th phenotypes, it could be stated that human astrocytes, by the release of exosomes, are able to modify the activity of human T cells.
 Multiple sclerosis patients treated with anti-CD20 therapy (aCD20-MS) are considered especially vulnerable to complications from SARS-CoV-2 infection due to severe B-cell depletion with limited viral antigen-specific immunoglobulin production. Therefore, multiple vaccine doses as part of the primary vaccination series and booster updates have been recommended for this group of immunocompromised individuals. Even though much less studied than antibody-mediated humoral responses, T-cell responses play an important role against CoV-2 infection and are induced efficiently in vaccinated aCD20-MS patients. For individuals with such decoupled adaptive immunity, an understanding of the contribution of T-cell mediated immunity is essential to better assess protection against CoV-2 infection. Here, we present results from a prospective, single-center study for the assessment of humoral and cellular immune responses induced in aCD20-MS patients (203 donors/350 samples) compared to a healthy control group (43/146) after initial exposure to CoV-2 spike antigen and subsequent re-challenges. Low rates of seroconversion and RBD-hACE2 blocking activity were observed in aCD20-MS patients, even after multiple exposures (responders after 1st exposure = 17.5%; 2nd exposure = 29.3%). Regarding cellular immunity, an increase in the number of spike-specific monofunctional IFNγ(+)-, IL-2(+)-, and polyfunctional IFNγ(+)/IL-2(+)-secreting T-cells after 2nd exposure was found most noticeably in healthy controls. Nevertheless, a persistently higher T-cell response was detected in aCD20-MS patients compared to control individuals before and after re-exposure (mean fold increase in spike-specific IFNγ(+)-, IL-2(+)-, and IFNγ(+)/IL-2(+)-T cells before re-exposure = 3.9X, 3.6X, 3.5X/P< 0.001; after = 3.2X, 1.4X, 2.2X/P = 0.002, P = 0.05, P = 0.004). Moreover, cellular responses against sublineage BA.2 of the currently circulating omicron variant were maintained, to a similar degree, in both groups (15-30% T-cell response drop compared to ancestral). Overall, these results highlight the potential for a severely impaired humoral response in aCD20-MS patients even after multiple exposures, while still generating a strong T-cell response. Evaluating both humoral and cellular responses in vaccinated or infected MS patients on B-cell depletion therapy is essential to better assess individual correlations of immune protection and has implications for the design of future vaccines and healthcare strategies.

 BACKGROUND: The efficacy of stereotactic radiosurgery (SRS) for the relief of trigeminal neuralgia (TN) is well established. Much less is known, however, about the benefit of SRS for multiple sclerosis (MS)-related TN (MS-TN). OBJECTIVE: To compare outcomes in patients who underwent SRS for MS-TN vs classical/idiopathic TN and identify relative risk factors for failure. METHODS: We conducted a retrospective, case-control study of patients who underwent Gamma Knife radiosurgery at our center for MS-TN between October 2004 and November 2017. Cases were matched 1:1 to controls using a propensity score predicting MS probability using pretreatment variables. The final cohort consisted of 154 patients (77 cases and 77 controls). Baseline demographics, pain characteristics, and MRI features were collected before treatment. Pain evolution and complications were obtained at follow-up. Outcomes were analyzed using the Kaplan-Meir estimator and Cox regressions. RESULTS: There was no statistically significant difference between both groups with regards to initial pain relief (modified Barrow National Institute IIIa or less), which was achieved in 77% of patients with MS and 69% of controls. In responders, 78% of patients with MS and 52% of controls eventually had recurrence. Pain recurred earlier in patients with MS (29 months) than in controls (75 months). Complications were similarly distributed in each group and consisted, in the MS group, of 3% of new bothersome facial hypoesthesia and 1% of new dysesthesia. CONCLUSION: SRS is a safe and effective modality to achieve pain freedom in MS-TN. However, pain relief is significantly less durable than in matched controls without MS.
 BACKGROUND: The Epstein-Barr virus (EBV) plays a role in the causation of Hodgkin lymphoma (HL) and multiple sclerosis (MS). A previous study showed that the time trends of mortality from Crohn's disease (CD) and MS shared striking similarities. It was hypothesized that such similarities would also involve the time trends of ulcerative colitis and HL. AIMS: To compare the time trends of CD and UC with those of HL and MS in 6 different countries. METHODS: Using the vital statistics of England, Canada, Netherlands, Scotland, Switzerland, and United States from 1951 to 2020, the time trends of mortality from these 4 diseases were compared. The time-dependent changes of death rates were subjected to a birth-cohort analysis. RESULTS: Similar trends were observed in all 6 countries. UC mortality rose among generations born during the nineteenth century and decreased among all generations born subsequently during the twentieth century. CD mortality was similarly characterized by a birth-cohort pattern with a rise and fall that were shifted by 20-30 years towards more recent generations when compared to UC. The birth-cohort pattern of UC was matched by a similar pattern of HL, whereas the birth-cohort pattern of CD was matched by a similar pattern of MS. CONCLUSIONS: The similarities in the ubiquitous birth-cohort patterns of UC, CD, HL, and MS suggest that these 4 diseases share a common environmental risk factor. Such risk factor may be linked to EBV or its acquisition during an early period of a patient's lifetime.

 Many studies indicate an important role of microglia and their cytokines in the pathophysiology of multiple sclerosis (MS). Microglia are the macrophages of the central nervous system (CNS). They have many functions, such as being "controllers" of the CNS homeostasis in pathological and healthy conditions, playing a key role in the active immune defense of the CNS. Macroglia exhibit a dual role, depending on the phenotype they adopt. First, they can exhibit neurotoxic effects, which are harmful in the case of MS. However, they also show neuroprotective and regenerative effects in this disease. Many of the effects of microglia are mediated through the cytokines they secrete, which have either positive or negative properties. Neurotoxic and pro-inflammatory effects can be mediated by microglia via lipopolysaccharide and gamma interferon. On the other hand, the mediators of anti-inflammatory and protective effects secreted by microglia can be, for example, interleukin-4 and -13. Further investigation into the role of microglia in MS pathophysiology may perhaps lead to the discovery of new therapies for MS, as recent research in this area has been very promising.
 BACKGROUND: Multiple sclerosis (MS) is a neuroinflammatory disease in which pregnancy leads to a temporary amelioration in disease activity as indicated by the profound decrease in relapses rate during the 3rd trimester of pregnancy. CD4(+) and CD8(+) T cells are implicated in MS pathogenesis as being key regulators of inflammation and brain lesion formation. Although Tcells are prime candidates for the pregnancy-associated improvement of MS, the precise mechanisms are yet unclear, and in particular, a deep characterization of the epigenetic and transcriptomic events that occur in peripheral T cells during pregnancy in MS is lacking. METHODS: Women with MS and healthy controls were longitudinally sampled before, during (1st, 2nd and 3rd trimesters) and after pregnancy. DNA methylation array and RNA sequencing were performed on paired CD4(+) and CD8(+) T cells samples. Differential analysis and network-based approaches were used to analyze the global dynamics of epigenetic and transcriptomic changes. RESULTS: Both DNA methylation and RNA sequencing revealed a prominent regulation, mostly peaking in the 3rd trimester and reversing post-partum, thus mirroring the clinical course with improvement followed by a worsening in disease activity. This rebound pattern was found to represent a general adaptation of the maternal immune system, with only minor differences between MS and controls. By using a network-based approach, we highlighted several genes at the core of this pregnancy-induced regulation, which were found to be enriched for genes and pathways previously reported to be involved in MS. Moreover, these pathways were enriched for in vitro stimulated genes and pregnancy hormones targets. CONCLUSION: This study represents, to our knowledge, the first in-depth investigation of the methylation and expression changes in peripheral CD4(+) and CD8(+) T cells during pregnancy in MS. Our findings indicate that pregnancy induces profound changes in peripheral T cells, in both MS and healthy controls, which are associated with the modulation of inflammation and MS activity.
 BACKGROUND: Motor and cognitive impairments impact the everyday functioning of people with MS (pwMS). The present randomized controlled trial (RCT) evaluated the benefits of a combined motor-cognitive virtual reality training program on key motor and cognitive symptoms and related outcomes in pwMS. METHODS: In a single-blinded, two-arm RCT, 124 pwMS were randomized into a treadmill training with virtual reality (TT + VR) group or a treadmill training alone (TT) (active-control) group. Both groups received three training sessions per week for 6 weeks. Dual-tasking gait speed and cognitive processing speed (Symbol Digit Modalities Test, SDMT, score) were the primary outcomes. Secondary outcomes included additional tests of cognitive function, mobility, and patient-reported questionnaires. These were measured before, after, and 3 months after training. RESULTS: Gait speed improved (p < 0.005) in both groups, similarly, by about 10 cm/s. The TT + VR group (n = 53 analyzed per-protocol) showed a clinically meaningful improvement of 4.4 points (95% CI 1.9-6.8, p = 0.001) in SDMT, compared to an improvement of only 0.8 points in the TT (n = 51 analyzed per-protocol) group (95% CI 0.9-2.5 points, p = 0.358) (group X time interaction effect p = 0.027). Furthermore, TT + VR group-specific improvements were seen in depressive symptoms (lowered by 31%, p = 0.003), attention (17%, p < 0.001), and verbal fluency (11.6% increase, p = 0.002). DISCUSSION: These findings suggest that both TT and TT + VR improve usual and dual-task gait in pwMS. Nonetheless, a multi-modal approach based on VR positively impacts multiple aspects of cognitive function and mental health, more than seen after treadmill-treading alone. Trial registered at ClinicalTrials.Gov NCT02427997.
 INTRODUCTION: Adverse childhood experiences (ACEs) are proposed to increase the risk of developing multiple sclerosis (MS) later in life. This systematic review aimed to explore the correlation between ACEs and MS development, age of onset, quality of life in MS patients and MS relapse rates. METHODS: We searched a total of six databases in June 2022 and retrieved the relevant studies. The population included adult (18+) individuals who either had been diagnosed or were at risk for developing MS and also had exposure to ACEs. Our primary outcomes include the risks of MS development, age of MS onset, and MS relapse rate in patients who were exposed to different types of ACEs. RESULTS: A total of 11 studies were included in our review. A study reported that among 300 women diagnosed with MS, 71 (24%) reported a history of childhood abuse; moreover, with further research, it was concluded that ACEs were associated with the development of MS. Abuse that occurred 2-3 times per week was associated with an 18.81-fold increased risk of having MS when compared to the unexposed sample. The relapse rate of MS was found to be substantially greater in severe cases of ACEs compared to individuals who did not report any ACEs. CONCLUSIONS: Results support a significant association between ACEs and the development of MS; individuals with a positive history of ACEs develop MS symptoms earlier. Moreover, the severity of ACEs is also linked with increased relapse rates of MS.
 PURPOSE: To develop a general unsupervised anomaly detection method based only on MR images of normal brains to automatically detect various brain abnormalities. MATERIALS AND METHODS: In this study, a novel method based on three-dimensional deep autoencoder network is proposed to automatically detect and segment various brain abnormalities without being trained on any abnormal samples. A total of 578 normal T2w MR volumes without obvious abnormalities were used for model training and validation. The proposed 3D autoencoder was evaluated on two different datasets (BraTs dataset and in-house dataset) containing T2w volumes from patients with glioblastoma, multiple sclerosis and cerebral infarction. Lesions detection and segmentation performance were reported as AUC, precision-recall curve, sensitivity, and Dice score. RESULTS: In anomaly detection, AUCs for three typical lesions were as follows: glioblastoma, 0.844; multiple sclerosis, 0.858; cerebral infarction, 0.807. In anomaly segmentation, the mean Dice for glioblastomas was 0.462. The proposed network also has the ability to generate an anomaly heatmap for visualization purpose. CONCLUSION: Our proposed method was able to automatically detect various brain anomalies such as glioblastoma, multiple sclerosis, and cerebral infarction. This work suggests that unsupervised anomaly detection is a powerful approach to detect arbitrary brain abnormalities without labeled samples. It has the potential to support diagnostic workflow in radiology as an automated tool for computer-aided image analysis.
 Research on the markers of immunoregulatory response in multiple sclerosis (MS) is still of great importance. The aim of our study was the evaluation of leptin, fibronectin, and UCHL1 concentrations as potential biomarkers of a relapsing-remitting type of MS (RRMS). Surface Plasmon Resonance Imaging (SPRI) biosensors were used for the evaluation of proteins concentrations in 100 RRMS patients and 46 healthy volunteers. Plasma leptin, fibronectin, and UCHL1 concentrations were significantly higher in RRMS patients compared to the control group (p < 0.001, respectively). UCHL1 concentration evaluation revealed the highest diagnostic sensitivity (100%) and negative predictive value (100%) in differentiating MS patients from healthy individuals. There was no significant difference in the UCHL1 concentrations depending on the patient's sex, the presence of relapse within the last 24 months, and the EDSS value (p > 0.05, respectively). In RRMS patients UCHL1 concentration positively correlated with fibronectin levels (r = 0.3928; p < 0.001). In the current cohort of patients plasma UCHL1 concentration was independent of the time of MS relapse and the severity of neurological symptoms. Thus current study may indicate that plasma UCHL1, besides leptin and fibronectin, also could be a promising high-sensitive potential biomarker of relapsing-remitting type of MS. However, these results should be validated with a larger group of patients, taking into account neuroimaging and cerebrospinal fluid analysis data, and by comparing them to patients with other neurological diseases as a control group.
 BACKGROUND: Due to the growing number of people aging with multiple sclerosis (MS), there has been a call for rehabilitation specially targeted older adults with MS in order to support them in better wellbeing, despite physical and cognitive impairment. However, the existing research within the area of rehabilitation has primarily focused on the physical and psychological aspects of aging with MS, omitting the social element. OBJECTIVE: This study aims to examine how social relations and engagement in leisure activities predict wellbeing among older adults with MS living in Denmark. Furthermore, the study aims to identify which sociodemographic and health-related factors are the most important in predicting whether older adults with MS face challenges in participating in leisure activities and experiencing different kinds of social relations. METHOD: A cross-sectional survey was designed to measure social relations, wellbeing, and engagement in leisure activities among older adults with MS. Of the 4,329 people over 65 years diagnosed with MS in Denmark in 2022, 2,574 (59.46%) were invited to participated in the study, and 1,107 (43.03%) ended up answering the survey. Linear and logistic regression analyses and dominance analyses were conducted to examine the associations between wellbeing, leisure activities, social relations, sociodemographic and health-related factors. RESULTS: The results of the study show that perceived emotional social support (mean difference 8.69, 95% CI 5.23; 12.14) and perceived instrumental social support (mean difference 4.15, 95% CI 0.95; 7.35), were associated with better wellbeing among older adults with MS. Perceived strained social relations (mean difference -7.95, 95% CI -10.66; -5.26) were on the contrary associated with lower levels of wellbeing. Strained social relations were the most important predictors of wellbeing accounting for 59% of the predicted variance. Experiencing social emotional support from friends, coworkers, or neighbors (39% of the predicted variance), experiencing instrumental social support from children or children in law (43% of the predicted variance), and experiencing strained social relations with partner (48% of the predicted variance) constituted he most important predictor of wellbeing. Engagement in five out of fourteen leisure activities were associated with better wellbeing among the participants. The leisure activities there was found to be the most important predictor of wellbeing represented both social (37% of the predicted variance), physical (18% of the predicted variance), and creative elements (13% of the predicted variance). Finally, cohabitation was found to be the most important predictor of having perceived emotional social support (59% of the predicted variance), instrumental social support (78.9% of the predicted variance) and strained social relations (18.8% of the predicted variance) and mobility was found to be the most important predictor of challenges in participating in leisure activities (81.8% of the predicted variance). CONCLUSION: The findings of the study highlight that rehabilitation targeting older adults with MS should focus on both physical, psychological, and social elements of peoples' everyday life. Further, the results indicate that future rehabilitation focusing on social elements of aging with MS should take into account health and sociodemographic characteristics such as cohabitation, mobility, age, and sex, as these potentially relate to participation in leisure activities as well as social relations among older adults.
 Understanding how variations in the plasma and brain proteome contribute to multiple sclerosis susceptibility can provide important insights to guide drug repurposing and therapeutic development for the disease. However, the role of genetically predicted protein abundance in multiple sclerosis remains largely unknown. Integrating plasma proteomics (n = 3301) and brain proteomics (n = 376 discovery; n = 152 replication) into multiple sclerosis genome-wide association studies (n = 14 802 cases and 26 703 controls), we employed summary-based methods to identify candidate proteins involved in multiple sclerosis susceptibility. Next, we evaluated associations of the corresponding genes with multiple sclerosis at tissue-level using large gene expression quantitative trait data from whole-blood (n = 31 684) and brain (n = 1194) tissue. Further, to assess transcriptional profiles for candidate proteins at cell-level, we examined gene expression patterns in immune cell types (Dataset 1: n = 73 cases and 97 controls; Dataset 2: n = 31 cases and 31 controls) for identified plasma proteins, and in brain cell types (Dataset 1: n = 4 cases and 5 controls; Dataset 2: n = 5 cases and 3 controls) for identified brain proteins. In a longitudinal multiple sclerosis cohort (n = 203 cases followed up to 15 years), we also assessed the corresponding gene-level associations with the outcome of disability worsening. We identified 39 novel proteins associated with multiple sclerosis risk. Based on five identified plasma proteins, four available corresponding gene candidates showed consistent associations with multiple sclerosis risk in whole-blood, and we found TAPBPL upregulation in multiple sclerosis B cells, CD8+ T cells and natural killer cells compared with controls. Among the 34 candidate brain proteins, 18 were replicated in a smaller cohort and 14 of 21 available corresponding gene candidates also showed consistent associations with multiple sclerosis risk in brain tissue. In cell-specific analysis, six identified brain candidates showed consistent differential gene expression in neuron and oligodendrocyte cell clusters. Based on the 39 protein-coding genes, we found 23 genes that were associated with disability worsening in multiple sclerosis cases. The findings present a set of candidate protein biomarkers for multiple sclerosis, reinforced by high concordance in downstream transcriptomics findings at tissue-level. This study also highlights the heterogeneity of cell-specific transcriptional profiles for the identified proteins and that numerous candidates were also implicated in disease progression. Together, these findings can serve as an important anchor for future studies of disease mechanisms and therapeutic development.
 BACKGROUND: In the absence of evidence from randomised controlled trials, observational data can be used to emulate clinical trials and guide clinical decisions. Observational studies are, however, susceptible to confounding and bias. Among the used techniques to reduce indication bias are propensity score matching and marginal structural models. OBJECTIVE: To use the comparative effectiveness of fingolimod vs natalizumab to compare the results obtained with propensity score matching and marginal structural models. METHODS: Patients with clinically isolated syndrome or relapsing remitting MS who were treated with either fingolimod or natalizumab were identified in the MSBase registry. Patients were propensity score matched, and inverse probability of treatment weighted at six monthly intervals, using the following variables: age, sex, disability, MS duration, MS course, prior relapses, and prior therapies. Studied outcomes were cumulative hazard of relapse, disability accumulation, and disability improvement. RESULTS: 4608 patients (1659 natalizumab, 2949 fingolimod) fulfilled inclusion criteria, and were propensity score matched or repeatedly reweighed with marginal structural models. Natalizumab treatment was associated with a lower probability of relapse (PS matching: HR 0.67 [95% CI 0.62-0.80]; marginal structural model: 0.71 [0.62-0.80]), and higher probability of disability improvement (PS matching: 1.21 [1.02 -1.43]; marginal structural model 1.43 1.19 -1.72]). There was no evidence of a difference in the magnitude of effect between the two methods. CONCLUSIONS: The relative effectiveness of two therapies can be efficiently compared by either marginal structural models or propensity score matching when applied in clearly defined clinical contexts and in sufficiently powered cohorts.
 Multiple sclerosis (MS) is one of the most common neurological diseases in North America and it is frequently associated with sensory processing difficulties, cognitive deficits, and psychiatric illness. While many studies have examined cognitive deficits in MS measured by behavioural responses and neuroimaging techniques, only a few studies have examined neurophysiological measures of auditory functioning in MS, such as the mismatch negativity (MMN). The MMN is an event-related potential that indicates automatic auditory change detection. This study examined whether MMN endpoints measured by electroencephalography (EEG) differ in individuals with relapsing-remitting MS compared to healthy controls and whether the symptomatology of MS, including symptoms of depression and fatigue, are related to MMN measures. A multi-feature MMN paradigm, which includes five distinct deviant tones, was used to assess auditory cortex function in MS. There were no significant differences in MMN amplitudes or latencies between the MS and control group (p < 0.05) and corresponding effect sizes were small. However, there was a correlation between reduced MMN amplitudes in response to an intensity deviant and physician-reported disability. The intensity MMN may be more sensitive to deterioration in this population. Ultimately, this study provides a comprehensive profile of early auditory processing abilities in MS and suggests that a reduction in the MMN response may be representative of disease severity in MS.
 INTRODUCTION: Vaccine hesitancy promotes the spread of infectious diseases including COVID-19 virus, limiting the herd immunity. Complications caused by COVID-19 in people with multiple sclerosis forced governments to ensure them prior access to vaccinations. Their propensity to be vaccinated needs to be assessed to promote adhesion to vaccination programs. The aim of this study was to explore the COVID-19 vaccine hesitancy rate in pwMS. METHODS: We conducted an observational study recruiting patients affected by multiple sclerosis followed at MS Clinical and Research Unit of Tor Vergata University, Rome. We invited them to fill in an online survey about their intent to get COVID-19 vaccination. Fisher's exact test and Kruskal-Wallis test were performed to explore differences in sociodemographic, clinical, and emotional variables relative to the opinions about vaccinations. An exploratory factor analysis (EFA) was performed to assess the factorial structure of the questionnaire; Pearson's correlations between the factors and Big Five personality dimensions were also calculated. RESULTS: Of 276 respondents, 90% was willing to get vaccinated, while only 1.4% was sure to refuse the vaccination. Education level, opinions on safety and efficacy of vaccines, and emotional status were found to be associated to the propensity of getting the COVID-19 vaccination (respectively: p = 0.012, p < 0.001, and p = 0.0001). Moreover, general opinions on healthcare system were related to the intention to get vaccinated. CONCLUSION: Our results reinforce the importance of a good relationship between doctor and patient and the need to adapt doctors' communication strategy to patients' personalities and beliefs.

 Multiple sclerosis (MS) is one of the organ-specific autoimmune diseases in which immune cells invade the neurons in the central nervous system (CNS) due to loss of tolerance to self-antigens. Consequently, inflammation and demyelination occur in the central nervous system. The pathogenesis of MS is not completely understood. However, it seems that T cells, especially Th17 cells, have an important role in disease development. In recent years, studies on the manipulation of metabolic pathways with therapeutic targets have received increasing attention and have had promising results in some diseases, such as cancers. Glycolysis is a central metabolic pathway and plays an important role in the differentiation of T CD4+ cells to their subsets, especially Th17 cells. This suggests that manipulation of glycolysis, for example, using appropriate safe inhibitors of this pathway can represent a means to affect the differentiation of T CD4+, thus reducing inflammation and disease activity in MS patients. Hence, in this study, we aimed to discuss evidence showing that using inhibitors of 6-phosphofructo-2- kinase/fructose-2,6-biphosphatase 3(PFKFB3) as the main regulator of glycolysis may exert beneficial therapeutic effects on MS patients.
 PURPOSE: Fingolimod, an oral treatment for relapsing-remitting multiple sclerosis (RRMS), has been associated with a significant rebound in disease activity after therapy cessation. We described a patient with neuromyelitis optica spectrum disorder (NMOSD) who was previously diagnosed with RRMS and experienced fatal rebound syndrome after cessation of fingolimod. CASE REPORT: A 54-year-old woman, previously diagnosed with RRMS, experienced relapse after orthopedic surgery. The diagnosis was later revised to NMOSD based on a positive aquaporin-4 antibody. Three weeks after converting the immunomodulator from fingolimod to azathioprine, severe disease reactivation was observed. Considering the multiple new and enlarging magnetic resonance imaging lesions, the temporal relationship between fingolimod cessation and symptom onset, and the relatively low possibility of disease reactivation within a short time, the diagnosis of fingolimod withdrawal syndrome was proposed. Although immediate steroid pulse therapy and plasma exchange were performed, the patient eventually died owing to a fulminant clinical course. CONCLUSION: Fingolimod withdrawal syndrome is well known in patients with multiple sclerosis (MS). It can also occur in patients with NMOSD. Recognizing patients with NMOSD who present with MS-like manifestations, and avoiding drugs that may be harmful to patients with NMOSD, are important.
 Multiple Sclerosis (MS) is the most common non-traumatic disabling disease in young people. The prediction active plaque has the potential to offer new biomarkers for assessing the activity of MS disease. Consequently it supports patient management in the clinical setting and trials. This study aims to investigate the predictive capability of radiomics features for identifying active plaques in these patients using T2 FLAIR (Fluid Attenuated Inversion Recovery) images. For this purpose, a dataset images from 82 patients with 122 lesions was analyzed. Feature selection was performed using the Least Absolute Shrinkage and Selection Operator (LASSO) method. Six different classifier algorithms, namely K-Nearest Neighbors (KNN), Logistic Regression (LR), Decision Tree (DT), Support Vector Machine (SVM), Naive Bayes (NB), and Random Forest (RF), were employed for modeling. The models were evaluated using 5-fold cross-validation, and performance metrics including sensitivity, specificity, accuracy, area under the curve (AUC), and mean squared error were computed. A total of 107 radiomics features were extracted for each lesion, and 11 robust features were identified through the feature selection process. These features consisted of four shape features (elongation, flatness, major axis length, mesh volume), one first-order feature (energy), one Gray Level Co-occurrence Matrix feature (correlation), two Gray Level Run Length Matrix features (gray level non-uniformity, gray level non-uniformity normalized), and three Gray Level Size Zone Matrix features (low gray level zone emphasis, size zone non-uniformity, small area low gray level emphasis). The NB classifier demonstrated the best performance with an AUC, sensitivity, and specificity of 0.85, 0.82, and 0.66, respectively. The findings indicate the potential of radiomics features in predicting active MS plaques in T2 FLAIR images.
 BACKGROUND: The prognostic significance of non-disabling relapses in people with relapsing-remitting multiple sclerosis (RRMS) is unclear. OBJECTIVE: To determine whether early non-disabling relapses predict disability accumulation in RRMS. METHODS: We redefined mild relapses in MSBase as 'non-disabling', and moderate or severe relapses as 'disabling'. We used mixed-effects Cox models to compare 90-day confirmed disability accumulation events in people with exclusively non-disabling relapses within 2 years of RRMS diagnosis to those with no early relapses; and any early disabling relapses. Analyses were stratified by disease-modifying therapy (DMT) efficacy during follow-up. RESULTS: People who experienced non-disabling relapses within 2 years of RRMS diagnosis accumulated more disability than those with no early relapses if they were untreated (n = 285 vs 4717; hazard ratio (HR) = 1.29, 95% confidence interval (CI) = 1.00-1.68) or given platform DMTs (n = 1074 vs 7262; HR = 1.33, 95% CI = 1.15-1.54), but not if given high-efficacy DMTs (n = 572 vs 3534; HR = 0.90, 95% CI = 0.71-1.13) during follow-up. Differences in disability accumulation between those with early non-disabling relapses and those with early disabling relapses were not confirmed statistically. CONCLUSION: This study suggests that early non-disabling relapses are associated with a higher risk of disability accumulation than no early relapses in RRMS. This risk may be mitigated by high-efficacy DMTs. Therefore, non-disabling relapses should be considered when making treatment decisions.
 BACKGROUND: Clinically Isolated Syndrome (CIS) is the first clinical episode suggestive of Clinical Definite Multiple Sclerosis (CDMS). There are no reports on possible predictors of conversion to CDMS in Mexican mestizo patients. AIM OF THE STUDY: To investigate immunological markers, clinical and paraclinical findings, and the presence of herpesvirus DNA to predict the transition from CIS to CDMS in Mexican patients. METHODS: A single-center prospective cohort study was conducted with newly diagnosed patients with CIS in Mexico between 2006 and 2010. Clinical information, immunophenotype, serum cytokines, anti-myelin protein immunoglobulins, and herpes viral DNA were determined at the time of diagnosis. RESULTS: 273 patients diagnosed with CIS met the enrolment criteria; after 10 years of follow-up, 46% met the 2010 McDonald criteria for CDMS. Baseline parameters associated with conversion to CDMS were motor symptoms, multifocal syndromes, and alterations of somatosensory evoked potentials. The presence of at least one lesion on magnetic resonance imaging was the main factor associated with an increased risk of conversion to CDMS (RR 15.52, 95% CI 3.96-60.79, p = 0.000). Patients who converted to CDMS showed a significantly lower percentage of circulating regulatory T cells, cytotoxic T cells, and B cells, and the conversion to CDMS was associated with the presence of varicella-zoster virus and herpes simplex virus 1 DNA in cerebrospinal fluid and blood. CONCLUSION: There is scarce evidence in Mexico regarding the demographic and clinical aspects of CIS and CDMS. This study shows several predictors of conversion to CDMS to be considered in Mexican patients with CIS.
 Autonomic dysfunction (AD) in people with MS (pwMS) is a frequent finding. This narrative review will present an overview of central neural mechanisms involved in the control of cardiovascular and thermoregulatory systems, and methods of autonomic nervous system testing will be discussed thereafter. Since the need for standardization of autonomic nervous system (ANS) testing, we will focus on the standard battery of tests (blood pressure and heart rate response to Valsalva maneuver and head-up tilt, and heart rate response to deep breathing test plus one of the tests for sudomotor function), which can detect ANS pathology in the majority of pwMS. The review will briefly discuss the other types of AD in pwMS and the use of appropriate tests. While performing ANS testing in pwMS one has to consider the multiple sclerosis phenotypes, disease duration, and its activity, the degree of clinical disability of patients included in the study, and the disease-modifying therapies taken, as these factors may have a great influence on the results of ANS testing. In other words, detailed patient characteristics presentation and patient stratification are beneficial when reporting results of ANS testing in pwMS.
 CONTEXT: Stress and chronic pain are the factors that most influence the quality of life and well-being of people with MS, and 90% of adults with MS suffer from persistent fatigue. These symptoms can be associated with other disorders such as depression, and drug treatments provide inadequate comfort for most people with them. OBJECTIVE: The study intended to examine the impact of hypnosis and hypnotherapy in the management of symptoms of people with multiple sclerosis (MS), such as stress, chronic pain, an inferior quality of life, and a lack of psychological well-being. DESIGN: The research team performed a systematic narrative review by searching the PubMed and Web of Science databases, including review articles and other studies for additional citations. SETTING: The study was conducted at our Scientific Institute for Research (IRCCS) in Messina. RESULTS: Only 14 of 121 publications met the inclusion criteria and were selected. Hypnotic treatment is an effective therapy that has beneficial impacts on the intensity of perceived pain, psychological well-being, mood disorders, and fatigue, and in addition, it significantly improves physical functioning in MS patients. The same effects haven't been obtained with other nonpharmacological techniques. CONCLUSION: Hypnosis is an appropriate psychological therapy for the management of MS patients' symptoms.
 OBJECTIVE: To study the whole-genome DNA methylation profiles of peripheral blood mononuclear blood cells (PBMCs) of patients with relapsing-remitting multiple sclerosis (RRMS) in remission and relapse in order to assess the contribution of this epigenetic mechanism of gene expression regulation to the activity of the pathological process. MATERIAL AND METHODS: Eight patients with RRMS in remission and 6 patients in relapse were included in the study. Methylation levels of DNA CpG sites in PBMCs were analyzed using Infinium HumanMethylation450 BeadChip DNA microarrays. RESULTS: Seven differentially methylated positions (DMPs) were identified, of which 3 were hypermethylated (cg02981003, cg18486102, cg19533582) and 4 were hypomethylated (cg16814680, cg1964802, cg18584440, cg08291996) during RRMS relapse. Five DMPs are located in protein-coding genes (GPR123, FAIM2, BTNL2, ZNF8, ASAP2), one in microRNA gene (MIR548N), and one in an intergenic region. For all identified DMPs, we observed a change in DNA methylation levels of more than 20% (range 20.2-57.5%). Hierarchical clustering of DNA samples on the heatmap shows their clear aggregation into separate clusters corresponding to RRMS patients in the stages of relapse and remission. CONCLUSION: For the first time it was shown that during relapse and remission of RRMS there are differences in the DNA methylation profile that allow discrimination between these clinical stages. These data indicate the involvement of the epigenetic mechanism of DNA methylation in the activation of the pathological process in RRMS.
 Background Use of χ-separation imaging can provide surrogates for iron and myelin that relate closely to abnormal changes in multiple sclerosis (MS) lesions. Purpose To evaluate the appearances of MS and neuromyelitis optica spectrum disorder (NMOSD) brain lesions on χ-separation maps and explore their diagnostic value in differentiating the two diseases in comparison with previously reported diagnostic criteria. Materials and Methods This prospective study included individuals with MS or NMOSD who underwent χ-separation imaging from October 2017 to October 2020. Positive (χ(pos)) and negative (χ(neg)) susceptibility were estimated separately by using local frequency shifts and calculating R2' (R2' = R2* - R2). R2 mapping was performed with a machine learning approach. For each lesion, presence of the central vein sign (CVS) and paramagnetic rim sign (PRS) and signal characteristics on χ(neg) and χ(pos) maps were assessed and compared. For each participant, the proportion of lesions with CVS, PRS, and hypodiamagnetism was calculated. Diagnostic performances were assessed using receiver operating characteristic (ROC) curve analysis. Results A total of 32 participants with MS (mean age, 34 years ± 10 [SD]; 25 women, seven men) and 15 with NMOSD (mean age, 52 years ± 17; 14 women, one man) were evaluated, with a total of 611 MS and 225 NMOSD brain lesions. On the χ(neg) maps, 80.2% (490 of 611) of MS lesions were categorized as hypodiamagnetic versus 13.8% (31 of 225) of NMOSD lesions (P < .001). Lesion appearances on the χ(pos) maps showed no evidence of a difference between the two diseases. In per-participant analysis, participants with MS showed a higher proportion of hypodiamagnetic lesions (83%; IQR, 72-93) than those with NMOSD (6%; IQR, 0-14; P < .001). The proportion of hypodiamagnetic lesions achieved excellent diagnostic performance (area under the ROC curve, 0.96; 95% CI: 0.91, 1.00). Conclusion On χ-separation maps, multiple sclerosis (MS) lesions tend to be hypodiamagnetic, which can serve as an important hallmark to differentiate MS from neuromyelitis optica spectrum disorder. © RSNA, 2022 Supplemental material is available for this article.
 Genome-wide association studies (GWAS) successfully identified multiple sclerosis (MS) susceptibility variants. Despite this notable progress, understanding the biological context of these associations remains challenging, due in part to the complexity of linking GWAS results to causative genes and cell types. Here, we aimed to address this gap by integrating GWAS data with single-cell and bulk chromatin accessibility data and histone modification profiles from immune and nervous systems. MS-GWAS associations are significantly enriched in regulatory regions of microglia and peripheral immune cell subtypes, especially B cells and monocytes. Cell-specific polygenic risk scores were developed to examine the cumulative impact of the susceptibility genes on MS risk and clinical phenotypes, showing significant associations with risk and brain white matter volume. The findings reveal enrichment of GWAS signals in B cell and monocyte/microglial cell-types, consistent with the known pathology and presumed targets of effective MS therapeutics.
 Because of the wide use of Fingolimod for the treatment of multiple sclerosis (MS) and its cardiovascular side effects such as bradycardia, second-generation sphingosine 1-phosphate receptor 1 (S1P1) agonist drugs for MS have been developed and approved by FDA. The issue of bradycardia is still present with the new drugs, however, which necessitates further exploration of S1P1 agonists with improved safety profiles for next-generation MS drugs. Herein, we report a tetrahydroisoquinoline or a benzo[c]azepine core-based S1P1 agonists such as 32 and 60 after systematic examination of hydrophilic groups and cores. We investigated the binding modes of our representative compounds and their molecular interactions with S1P1 employing recent S1P1 cryo-EM structures. Also, favorable ADME properties of our compounds were shown. Furthermore, in vivo efficacy of our compounds was clearly demonstrated with PLC and EAE studies. Also, the preliminary in vitro cardiovascular safety of our compound was verified with human iPSC-derived cardiomyocytes.
 The transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel that is activated by capsaicin (CAP), the main component of chili pepper. Despite studies in several neurological diseases, the role of TRPV1 in demyelinating diseases remains unknown. Herein, we reported that TRPV1 expression was increased within the corpus callosum during demyelination in a cuprizone (CPZ)-induced demyelination mouse model. TRPV1 deficiency exacerbated motor coordinative dysfunction and demyelination in CPZ-treated mice, whereas the TRPV1 agonist CAP improved the behavioral performance and facilitated remyelination. TRPV1 was predominantly expressed in Iba1(+) microglia/macrophages in human brain sections of multiple sclerosis patients and mouse corpus callosum under demyelinating conditions. TRPV1 deficiency decreased microglial recruitment to the corpus callosum, with an associated increase in the accumulation of myelin debris. Conversely, the activation of TRPV1 by CAP enhanced the recruitment of microglia to the corpus callosum and potentiated myelin debris clearance. Using real-time live imaging we confirmed an increased phagocytic function of microglia following CAP treatment. In addition, the expression of the scavenger receptor CD36 was increased, and that of the glycolysis regulators Hif1a and Hk2 was decreased. We conclude that TRPV1 is an important regulator of microglial function in the context of demyelination and may serve as a promising therapeutic target for demyelinating diseases such as multiple sclerosis.
 With recent findings connecting the Epstein-Barr virus to an increased risk of multiple sclerosis and growing concerns regarding the neurological impact of the coronavirus pandemic, we examined potential links between viral exposures and neurodegenerative disease risk. Using time series data from FinnGen for discovery and cross-sectional data from the UK Biobank for replication, we identified 45 viral exposures significantly associated with increased risk of neurodegenerative disease and replicated 22 of these associations. The largest effect association was between viral encephalitis exposure and Alzheimer's disease. Influenza with pneumonia was significantly associated with five of the six neurodegenerative diseases studied. We also replicated the Epstein-Barr/multiple sclerosis association. Some of these exposures were associated with an increased risk of neurodegeneration up to 15 years after infection. As vaccines are currently available for some of the associated viruses, vaccination may be a way to reduce some risk of neurodegenerative disease.
 There is increasing evidence of Epstein-Barr virus (EBV) being conditional in multiple sclerosis (MS) pathogenesis and influential for disease activity. Interferon-beta (IFNβ) is a cytokine with antiviral effects used to treat MS, in which a possible antiviral effect against EBV has been questioned. In this study, we investigated the effect of IFNβ-1a treatment on serum EBV antibody levels in 84 patients with relapsing-remitting MS. In the 18 months following IFNβ-1a treatment initiation, there were no significant associations between treatment and serum levels of Epstein-Barr nuclear antigen 1 (EBNA-1) immunoglobulin (Ig) G, early antigen (EA) IgG, viral capsid antigen (VCA) IgG or VCA IgM. The findings suggest that IFNβ-1a treatment does not influence the humoral response to EBV in patients with MS.
 Glucocorticoids (GCs) are used to treat inflammatory disorders such as multiple sclerosis (MS) by exerting prominent activities in T cells including apoptosis induction and suppression of cytokine production. However, little is known about their impact on energy metabolism, although it is widely accepted that this process is a critical rheostat of T cell activity. We thus tested the hypothesis that GCs control genes and processes involved in nutrient transport and glycolysis. Our experiments revealed that escalating doses of dexamethasone (Dex) repressed energy metabolism in murine and human primary T cells. This effect was mediated by the GC receptor and unrelated to both apoptosis induction and Stat1 activity. In contrast, treatment of human T cells with rapamycin abolished the repression of metabolic gene expression by Dex, unveiling mTOR as a critical target of GC action. A similar phenomenon was observed in MS patients after intravenous methylprednisolon (IVMP) pulse therapy. The expression of metabolic genes was reduced in the peripheral blood T cells of most patients 24 h after GC treatment, an effect that correlated with disease activity. Collectively, our results establish the regulation of T cell energy metabolism by GCs as a new immunomodulatory principle.
 PURPOSE: To characterize and analytically validate the MSDA Test, a multi-protein, serum-based biomarker assay developed using Olink(®) PEA methodology. EXPERIMENTAL DESIGN: Two lots of the MSDA Test panel were manufactured and subjected to a comprehensive analytical characterization and validation protocol to detect biomarkers present in the serum of patients with multiple sclerosis (MS). Biomarker concentrations were incorporated into a final algorithm used for calculating four Disease Pathway scores (Immunomodulation, Neuroinflammation, Myelin Biology, and Neuroaxonal Integrity) and an overall Disease Activity score. RESULTS: Analytical characterization demonstrated that the multi-protein panel satisfied the criteria necessary for a fit-for-purpose validation considering the assay's intended clinical use. This panel met acceptability criteria for 18 biomarkers included in the final algorithm out of 21 biomarkers evaluated. VCAN was omitted based on factors outside of analytical validation; COL4A1 and GH were excluded based on imprecision and diurnal variability, respectively. Performance of the four Disease Pathway and overall Disease Activity scores met the established acceptability criteria. CONCLUSIONS AND CLINICAL RELEVANCE: Analytical validation of this multi-protein, serum-based assay is the first step in establishing its potential utility as a quantitative, minimally invasive, and scalable biomarker panel to enhance the standard of care for patients with MS.
 BACKGROUND: Multiple sclerosis (MS) is an immune-mediated, neurodegenerative disease of the central nervous system that manifests in symptoms that compromise health-related quality of life (HRQOL). HRQOL focuses on a person's overall, subjective evaluation of health status primarily in the physical and mental domains. Exercise training is a form of rehabilitation for managing MS-related outcomes that might influence HRQOL. Reviews on exercise training are available, but we are unaware of a recent comprehensive review and meta-analysis of exercise effects for improving physical and mental domains of HRQOL. This analysis provides an updated review and meta-analysis of randomized controlled trials (RCTs) examining interventions consisting of aerobic, resistance and combined exercise training for improving HRQOL in persons with MS. This systematic review 1) assessed the overall strength of evidence for exercise interventions on HRQOL, 2) evaluated the relative effect of exercise interventions on physical and mental domains of HRQOL, and 3) determined moderators of exercise intervention effects on HRQOL. METHODS: Seven databases were searched for RCTs evaluating physical and/or mental domains of HRQOL with adults diagnosed with MS and undergoing an intervention of aerobic, resistance or combined exercise training compared with a non-exercise comparator. Data extraction included participant and intervention characteristics, and pre- and post-intervention HRQOL outcome data. Effect sizes (ESs) were calculated as standardized mean differences (SMDs) and a multilevel random-effects model was used to generate an aggregated SMD that compared exercise with non-exercise control conditions. RESULTS: Twelve RCTs met the inclusion criteria and yielded 23 ESs to be analyzed. Participants (N = 593; 308 intervention vs. 285 control conditions) had a mean (±standard deviation) age of 42.4 (6.5) years and 80% (18.3%) were female. Results generated a medium effect of exercise for improving overall HRQOL (ES=0.64, p = 0.0001) with high heterogeneity (Q(11)=58.8, I(2)=86.7%). Exercise training yielded a large effect on the physical domain (k = 12, ES=0.82, p<0.0009) and a medium effect on the mental domain (k = 11, ES=0.41, p<0.0001). Moderator analyses identified exercise modality, supervision level, intervention delivery and length, HRQOL tool, and number of participants with relapsing-remitting MS as significant influences of ES for HRQOL. CONCLUSIONS: Exercise training is clinically effective for improving overall HRQOL in MS and produces greater improvements in the physical domain of HRQOL than the mental domain. The moderator analysis suggests that supervised, aerobic, and group-delivered exercise training of ≥3 months yields the most influence on HRQOL. Such results may have major implications for MS treatment and care.
 OBJECTIVE: To study the effect of the RS6265 polymorphism of BDNF gene on the risk of development, main clinical characteristics and DMT response in MS patients in Tomsk region. MATERIAL AND METHODS: The study group included 321 patients, the control group consisted of 266 healthy volunteers. Deoxyribonucleic acid (DNA) was isolated from venous blood using the standard phenol-chloroform method. Genotyping was carried out by real-time polymerase chain reaction (PCR) using competing TaqMan probes complementary to the polymorphic nucleotide sequence. RESULTS: Carriage of the C allele and CC genotype of the RS6265 polymorphism of the BDNF gene was found to be a factor determining a more favorable MS course. CONCLUSION: Carriers of the indicated genotype had a low rate of MS progression, a lower frequency of relapses and a less pronounced degree of disability with a comparable MS duration, and significantly more often demonstrated a more optimal response to first and second line of DMT.
 INTRODUCTION: Pain and cognitive dysfunction are separately known to be important manifestations of multiple sclerosis (MS). Although pain is a complex subjective phenomenon with affective and cognitive aspects, it is not known if people with MS reporting pain are at greater risk of reduced performance in objective tests of cognition. The presence or direction of any association remains to be clarified, as do the roles of confounders such as fatigue, medication and mood. METHODS: We conducted a systematic review of studies examining the relationship between pain and objectively measured cognition in adults with confirmed MS, according to a pre-registered protocol (PROSPERO 42,020,171,469). We carried out searches in MEDLINE, Embase and PsychInfo. Studies of adults with any subtype of MS, with chronic pain and in which cognitive evaluation was conducted by validated instruments were included. We evaluated the role of potential confounders (medication, depression, anxiety, fatigue and sleep) and described findings by eight pre-specified cognitive domains. Risk of bias was assessed using the Newcastle-Ottawa Scale. RESULTS: 11 studies (n = 3714 participants, range 16 to 1890 per study) were included in the review. Four studies included longitudinal data. Nine studies identified a relationship between pain and objectively measured cognitive performance. In seven of these studies, higher pain scores were associated with poorer cognitive performance. However, no evidence was available for some cognitive domains. Heterogeneous study methodology precluded meta-analysis. Studies infrequently controlled for the specified confounders. Most studies were judged to be at risk of bias. DISCUSSION: Several studies, but not all, identified a negative relationship between pain severity and objectively measured cognitive performance. Our ability to further characterise this relationship is limited by study design and lack of evidence in many cognitive domains. Future studies should better establish this relationship and delineate the neurological substrate underpinning it.
 BACKGROUND: The presence of contrast enhancement (CE) on magnetic resonance imaging (MRI) is one of the principal criteria for diagnosis and disease activity of multiple sclerosis (MS). Therefore, MS patients are frequently exposed to contrast agents, which may cause deposition in the brain, restricting its use in repeat examinations. Thus, serum biomarkers may be valuable as surrogate parameters to evaluate MS activity. METHODS: REDUCE-GAD was a prospective, multicentric, biobanking study to determine whether established serum markers (neurofilament light chain [NfL], glial fibrillary acidic protein [GFAP], tau protein, ubiquitin-carboxyl-terminal-hydrolase (UCH-L1), S100B and matrix-metalloproteinase 9 [MMP9]) are predictive of CE-positive MRI lesions. Blood samples were obtained from patients undergoing MRI 5 days before or after collection. RESULTS: Patients (N = 102) from four different centers with confirmed MS or related disorders were included; n = 57 (55.9%) showed CE on MRI versus n = 45 (44.1%) without CE. Only higher NfL values indicated CE (odds ratio [OR] 1.05; 95% CI 1.0-1.09) and were correlated with number (ρ = 0.47; p < 0.001) and diameter of CE lesions (ρ = 0.58; p < 0.001). Nfl Z-scores improved diagnostic accuracy (OR 1.52; 95% CI 1.06-2.18). Receiver operator characteristic analysis revealed a reasonable cut-off value for NfL at 14.1 pg/mL (sensitivity 49.1%; specificity 82.2%; positive predictive value 77.8%; negative predictive value 56.0%). NfL ≥59.2 pg/mL was exclusively observed in patients with CE. CONCLUSIONS: Evaluation of several possible serum biomarkers for CE in MS patients provided the most robust results for NfL, particularly as Z-scores. Following further evaluation, biomarkers may help stratify the application of contrast agents for brain imaging in MS patients.
 BACKGROUND: Smoking and occupational pulmonary irritants contribute to multiple sclerosis (MS) development. We aimed to study the association between ambient air pollution and MS risk and potential interaction with the human leukocyte antigen (HLA)-DRB1*15:01 allele. METHODS: Exposure to combustion-related air pollution was estimated as outdoor levels of nitrogen oxides (NOx) at the participants' residence locations, by spatially resolved dispersion modelling for the years 1990-18. Using two population-based case-control studies (6635 cases, 8880 controls), NOx levels were associated with MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Interaction between high NOx levels and the HLA-DRB1*15:01 allele regarding MS risk was calculated by the attributable proportion due to interaction (AP). In addition, a register study was performed comprising all MS cases in Sweden who had received their diagnosis between 1993 and 2018 (n = 22 173), with 10 controls per case randomly selected from the National Population register. RESULTS: Residential air pollution was associated with MS risk. NOx levels (3-year average) exceeding the 90th percentile (24.6 µg/m3) were associated with an OR of 1.37 (95% CI 1.10-1.76) compared with levels below the 25th percentile (5.9 µg/m3), with a trend of increasing risk of MS with increasing levels of NOx (P <0.0001). A synergistic effect was observed between high NOx levels (exceeding the lower quartile among controls) and the HLA-DRB1*15:01 allele regarding MS risk (AP 0.26, 95% CI 0.13-0.29). CONCLUSIONS: Our findings indicate that moderate levels of combustion-related ambient air pollution may play a role in MS development.
 Neuroinflammation caused by COVID-19 negatively impacts brain metabolism and function, while pre-existing brain pathology may contribute to individuals' vulnerability to the adverse consequences of COVID-19. We used summary statistics from genome-wide association studies (GWAS) to perform Mendelian randomization (MR) analyses, thus assessing potential associations between multiple sclerosis (MS) and two COVID-19 outcomes (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] infection and COVID-19 hospitalization). Genome-wide risk genes were compared between the GWAS datasets on hospitalized COVID-19 and MS. Literature-based analysis was conducted to construct molecular pathways connecting MS and COVID-19. We found that genetic liability to MS confers a causal effect on hospitalized COVID-19 (odd ratio [OR]: 1.09, 95% confidence interval: 1.03-1.16) but not on SARS-CoV-2 infection (1.03, 1.00-1.05). Genetic liability to hospitalized COVID-19 confers a causal effect on MS (1.15, 1.02-1.30). Hospitalized COVID-19 and MS share five risk genes within two loci, including TNFAIP8, HSD17B4, CDC37, PDE4A, and KEAP1. Pathway analysis identified a panel of immunity-related genes that may mediate the links between MS and COVID-19. Our study suggests that MS was associated with a 9% increased risk for COVID-19 hospitalization, while hospitalized COVID-19 was associated with a 15% increased risk for MS. Immunity-related pathways may underlie the link between MS on COVID-19.
 RATIONALE: Multiple sclerosis (MS) is a central nervous system disease mainly mediated by immunity, which is one of the most common causes of neurological dysfunction in young people worldwide. In the acute phase, high-dose steroid therapy is effective. There are few reports about cerebral venous thrombosis (CVT) after high-dose steroid therapy. PATIENT CONCERNS: We present a case of a 19-year-old female diagnosed with MS who developed a headache after high-dose steroid therapy was diagnosed with CVT. Headache symptoms improved after anticoagulant treatment. DIAGNOSES: MS comorbid CVT. INTERVENTIONS: Anticoagulant therapy was added and hormone therapy was reduced. OUTCOMES: Clinical symptoms such as headache, limb numbness, and involuntary tremors in the right hand were improved, and the muscle strength of the right limb recovered to grade 4. The patient did not suffer from headaches after discharge and no abnormality in the computed tomography (CT) scan of the cephalic vein at the 5-months follow-up. LESSONS: High-dose steroid therapy may be a risk factor for CVT in patients with MS. MS patients who develop headaches during high-dose steroid therapy should undergo further cranial CTV to rule out CVT.
 BACKGROUND: Multiple sclerosis (MS) is a chronic demyelinating autoimmune disorder which may cause long-term disability. MicroRNA (miRNA) are stable, non-coding molecules that have been identified in our Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital (CLIMB)-cohort, as well as other international cohorts, as potential disease biomarkers in MS. However, few studies have evaluated the association of miRNA expression early in the MS disease course with long-term outcomes. Therefore, we aimed to evaluate the potential role of three candidate serum miRNAs previously correlated with MS disability in patients with MS, miR-320b, miR-25-3p and miRNA 486-5p, as early biomarkers of MS disability at 10-year follow-up. MAIN BODY: We included 144 patients with serum obtained within three years of MS onset. miRNA expression was measured by RNA extraction followed by RT-PCR. Demographic, clinical, brain MRI and other biomarkers were collected. The primary outcome was the association between early miRNA expression and retaining benign MS, defined as EDSS ≤ 2 at 10-year follow-up. Among the 144 patients, 104 were benign and 40 were not benign at 10-year follow-up. 89 (62%) were women, with mean age at onset 37.7 (SD: 9.6) years. Patients who retained benign MS had lower values of miR-25-3p (p = 0.047) and higher miR-320b (p = 0.025) values. Development of SPMS was associated with higher miR-320b (p = 0.002) levels. Brain parenchymal fraction at year 10 was negatively correlated with miR-25-3p (p = 0.0004) and positively correlated with miR-320b (p = 0.006). No association was found between miR-486-5p and any outcome, and 10-year T2-lesion volume was not associated with any miRNA. CONCLUSIONS: Our results show that miR-320b and miR-25-3p expression are early biomarkers associated with MS severity and brain atrophy. This study provides class III evidence of that miR-320b and miR-25-3p are associated with long-term MS disability which may be a potential tool to risk-stratify patients with MS for early treatment decisions.
 Multiple sclerosis is a chronic neurological disease characterized by inflammation and degeneration within the central nervous system. Over the course of the disease, most MS patients successively accumulate inflammatory lesions, axonal damage, and diffuse CNS pathology, along with an increasing degree of motor disability. While the pharmacological approach to MS targets inflammation to decrease relapse rates and relieve symptoms, disease-modifying therapy and immunosuppressive medications may not prevent the accumulation of pathology in most patients leading to long-term motor disability. This has been met with recent interest in promoting plasticity-guided concepts, enhanced by neurophysiological and neuroimaging approaches to address the preservation of motor function.
 BACKGROUND: Since multiple sclerosis (MS) is often diagnosed in young women, pregnancy is a common topic for women with MS (wwMS). The study aimed to assess the measurement properties of two patient-reported outcome measures on motherhood choice in MS, and to explore the information and support needs of wwMS concerning motherhood. METHODS: We conducted an anonymous web-based survey to validate the motherhood/pregnancy choice and worries questionnaire (MPWQ, 31 items plus up to 3 additional items) and the motherhood choice knowledge questionnaire (MCKQ, 16 items). We used mailing lists and social media for nationwide recruitment in Germany, and included women of childbearing age with relapsing-remitting MS, clinically isolated syndrome or suspected MS who were considering pregnancy or were pregnant. For the MPWQ, we assessed item difficulty, discriminatory power, and internal consistency (Cronbach's alpha; CA). We analysed construct validity using the Leipzig Questionnaire of Motives to have a Child, the Decisional Conflict Scale, the Hospital Anxiety and Depression Scale, and the Pregnancy-Related Anxiety Questionnaire-revised 2. We studied the structural validity using exploratory factor analysis (EFA). The MCKQ was evaluated descriptively. We explored the information and support needs of wwMS on motherhood descriptively. We examined correlations between MCKQ, MPWQ and clinical characteristics and performed exploratory group comparisons considering the following binary variables: having children and being pregnant. RESULTS: 325 wwMS started the survey; 232 wwMS met our inclusion criteria and were analysed. Their mean age was 30 years (SD 5). Most women had relapsing-remitting MS (n = 218; 94%), 186 (80%) had no children, and 38 (16%) were pregnant. Internal consistency was good for the worries subscale (CA>0.8), while it was unsatisfactory for the attitude and coping subscales (CA<0.7). The EFA did not support the three-scale structure (coping, attitude, and worries). Due to these findings, we decided to keep the worries scale without any subscale. The items from the coping scale and attitude scale could be assessed as additional descriptive items. Convergent and divergent construct validity of the MPWQ was satisfactory. 206 wwMS (89%) completed the MCKQ. On average, 9 of 16 (56%) items were answered correctly (range 2-15), and the questionnaire showed a good balance between easy and difficult items. Questions on immunotherapy, disease activity, and breastfeeding were the most challenging. WwMS were confident in getting pregnant and raising a child (n = 222; 96%). Most wwMS were worried about postpartum relapses (n = 200; 86%) and the long-term effects of pregnancy on disease evolution (n = 149; 64%). About half of the wwMS (n = 124; 54%) did not know where to find professional help and 127 (55%) had no strategies to cope with future impairments so that they could take care of a child. CONCLUSION: Our results support the suitability and acceptability of both questionnaires as potential patient-reported measures for assessment of knowledge and worries around motherhood/pregnancy in MS. The survey results highlight the need for evidence-based information on motherhood in MS to increase knowledge, reduce worries and support wwMS in making informed decisions.
 BACKGROUND: Relapsing-remitting multiple sclerosis (RRMS) is the most common phenotype of multiple sclerosis (MS), and its active stage is characterized by active T2 lesions with or without gadolinium (Gd) enhancement on magnetic resonance imaging (MRI). Natalizumab is indicated as monotherapy in adults with active RRMS in Japan. The main objective of this study was to investigate the long-term effect of natalizumab on disease progression in Japanese patients with RRMS using MRI data. METHODS: This retrospective, chart review study was conducted at a single center in Japan. The main study outcome was the yearly proportion of patients with active T2-weighted image lesions detected with or without Gd enhancement on brain MRI (incidence rate) after treatment initiation for up to 5 years. Additional endpoints included annual relapse rate (ARR) and expanded disability status scale (EDSS) score. RESULTS: This study included data from 85 patients with RRMS who had received natalizumab for ≥ 1 year; of these, 65 (76.5%) were female and the mean ± standard deviation (SD) age at baseline was 37.5 ± 10.0 years. The incidence rate of active T2 lesions was 52.9% (45/85) in the year prior to natalizumab treatment (Year - 1), which decreased to 2.4% and 1.6% in Year 0.5-1.5 and Year 1.5-2.5, respectively. No active T2 lesions were detected in Year 2.5-5.5 in patients who continued natalizumab treatment. EDSS score was stable, improved, and worsened in 61.8%, 26.3%, and 11.8% of patients, respectively. The median (range) EDSS score was 2.0 (0.0-7.0) at baseline (n = 85) and remained within a similar range (median score between 1.0 and 2.25 during Years 1-5). ARR decreased from 1.12 relapses per year at baseline to 0.12 relapses per year during Year 1 and remained below 0.15 relapses per year up to Year 5. CONCLUSION: The results of this first long-term study evaluating the effect of natalizumab on MRI activity and clinical outcomes in Japanese patients with RRMS suggest that natalizumab markedly reduced disease activity and maintained effectiveness over several years.
 INTRODUCTION: Multiple sclerosis (MS) is characterized by the destruction of the blood-brain barrier, loss of myelin sheath, and contribution of inflammatory interleukins such as TNF-alpha, interleukin-17, and interleukin-6. METHODS: The current study investigated the effect of antigen B of hydatid cyst fluid on the reduction of anti-inflammatory cytokines and nerve conduction velocity in rats with experimental autoimmune encephalomyelitis (EAE)-induced MS. After isolation of antigen B from sterile cyst fluid, the rats were randomly divided into four groups: saline, EAE, EAE + teriflunomide (EAE + TF), and EAE + antigen B (EAE + AngB). The EAE model was induced using cow spinal cord homogenization, in combination with Freund's complete adjuvant. The serum concentration of cytokines including IL-1B and IL-17, IL-10, IL-6, and TNF-X was measured by the ELISA method, and real-time PCR was performed to study gene expression. Electrophysiological, behavioral, and neuropathological tests were also conducted. RESULTS: Nerve conduction velocity and IL-10 concentration were increased in the antigen B group. The results of this study showed that antigen B reduced the inflammatory component of the EAE MS animal model by modulating the immune system compared to teriflunomide, which eventually led to a reduction in symptoms at the behavioral and electrophysiological level. CONCLUSIONS: It seems that antigen B plays a critical role in regulating immunity and it can be used as a possible therapeutic agent to modulate the immune system in MS patients. It might be rational to consider hydatid cyst fluid antigen as a modifier in MS.
 BACKGROUND: An imbalance of adipokines, hormones secreted by white adipose tissue, is suggested to play a role in the immunopathology of multiple sclerosis (MS). In people with MS (PwMS) of the same age, we aimed to determine whether the adipokines adiponectin, leptin, and resistin are associated with MS disease severity. Furthermore, we aimed to investigate whether these adipokines mediate the association between body mass index (BMI) and MS disease severity. METHODS: Adiponectin, resistin, and leptin were determined in serum using ELISA. 288 PwMS and 125 healthy controls (HC) were included from the Project Y cohort, a population-based cross-sectional study of people with MS born in the Netherlands in 1966, and age and sex-matched HC. Adipokine levels and BMI were related to demographic, clinical and disability measures, and MRI-based brain volumes. RESULTS: Adiponectin levels were 1.2 fold higher in PwMS vs. HC, especially in secondary progressive MS. Furthermore, we found a sex-specific increase in adiponectin levels in primary progressive (PP) male patients compared to male controls. Leptin and resistin levels did not differ between PwMS and HC, however, leptin levels were associated with higher disability (EDSS) and resistin strongly related to brain volumes in progressive patients, especially in several grey matter regions in PPMS. Importantly, correction for BMI did not significantly change the results. CONCLUSION: In PwMS of the same age, we found associations between adipokines (adiponectin, leptin, and resistin) and a range of clinical and radiological metrics. These associations were independent of BMI, indicating distinct mechanisms.
 BACKGROUND AND OBJECTIVES: Recent literature on multiple sclerosis (MS) demonstrates the growing implementation of optical coherence tomography-angiography (OCT-A) to discover potential qualitative and quantitative changes in the retina and optic nerve. In this review, we analyze OCT-A studies in patients with MS and examine its utility as a surrogate or precursor to changes in central nervous system tissue. METHODS: PubMed and EMBASE were systematically searched to identify articles that applied OCT-A to evaluate the retinal microvasculature measurements in patients with MS. Quantitative data synthesis was performed on all measurements which were evaluated in at least two unique studies with the same OCT-A devices, software, and study population compared to controls. A fixed-effects or random-effects model was applied for the meta-analysis based on the heterogeneity level. RESULTS: The study selection process yielded the inclusion of 18 studies with a total of 1552 evaluated eyes in 673 MS-associated optic neuritis (MSON) eyes, 741 MS without optic neuritis (MSNON eyes), and 138 eyes without specification for the presence of optic neuritis (ON) in addition to 1107 healthy control (HC) eyes. Results indicated that MS cases had significantly decreased whole image superficial capillary plexus (SCP) vessel density when compared to healthy control subjects in the analyses conducted on Optovue and Topcon studies (both P < 0.0001). Likewise, the whole image vessel densities of deep capillary plexus (DCP) and radial peripapillary capillary (RPC) were significantly lower in MS cases compared to HC (all P < 0.05). Regarding optic disc area quadrants, MSON eyes had significantly decreased mean RPC vessel density compared to MSNON eyes in all quadrants except for the inferior (all P < 0.05). Results of the analysis of studies that used prototype Axsun machine revealed that MSON and MSNON eyes both had significantly lower ONH flow index compared to HC (both P < 0.0001). CONCLUSIONS: This systematic review and meta-analysis of the studies reporting OCT-A measurements of people with MS confirmed the tendency of MS eyes to exhibit reduced vessel density in the macular and optic disc areas, mainly in SCP, DCP, and RPC vessel densities.
 PURPOSE: Lexical characteristics of speech stimuli can significantly impact intelligibility. However, lexical characteristics of the widely used Speech Intelligibility Test (SIT) are unknown. We aimed to (a) define variation in neighborhood density, word frequency, grammatical word class, and type-token ratio across a large corpus of SIT sentences and tests and (b) determine the relationship of lexical characteristics to speech intelligibility in speakers with multiple sclerosis (MS), Parkinson's disease (PD), and neurologically healthy controls. METHOD: Using an extant database of 92 speakers (32 controls, 30 speakers with MS, and 30 speakers with PD), percent correct intelligibility scores were obtained for the SIT. Neighborhood density, word frequency, word class, and type-token ratio were calculated and summed for each of the 11 sentences of each SIT test. The distribution of each characteristic across SIT sentences and tests was examined. Linear mixed-effects models were performed to assess the relationship between intelligibility and the lexical characteristics. RESULTS: There was large variability in the distribution of lexical characteristics across this large corpus of SIT sentences and tests. Modeling revealed a relationship between intelligibility and the lexical characteristics, with word frequency and word class significantly contributing to the model. CONCLUSIONS: Three primary findings emerged: (a) There was considerable variability in lexical characteristics both within and across the large corpus of SIT tests; (b) there was not a robust association between intelligibility and the lexical characteristics; and (c) findings from a study demonstrating an effect of neighborhood density and word frequency on intelligibility were replicated. Clinical and research implications of the findings are discussed, and three exemplar SIT tests systematically controlling for neighborhood density and word frequency are provided.
 INTRODUCTION: Double inversion recovery (DIR) has been validated as a sensitive magnetic resonance imaging (MRI) contrast in multiple sclerosis (MS). Deep learning techniques can use basic input data to generate synthetic DIR (synthDIR) images that are on par with their acquired counterparts. As assessment of longitudinal MRI data is paramount in MS diagnostics, our study's purpose is to evaluate the utility of synthDIR longitudinal subtraction imaging for detection of disease progression in a multicenter data set of MS patients. METHODS: We implemented a previously established generative adversarial network to synthesize DIR from input T1-weighted and fluid-attenuated inversion recovery (FLAIR) sequences for 214 MRI data sets from 74 patients and 5 different centers. One hundred and forty longitudinal subtraction maps of consecutive scans (follow-up scan-preceding scan) were generated for both acquired FLAIR and synthDIR. Two readers, blinded to the image origin, independently quantified newly formed lesions on the FLAIR and synthDIR subtraction maps, grouped into specific locations as outlined in the McDonald criteria. RESULTS: Both readers detected significantly more newly formed MS-specific lesions in the longitudinal subtractions of synthDIR compared with acquired FLAIR (R1: 3.27 ± 0.60 vs 2.50 ± 0.69 [ P = 0.0016]; R2: 3.31 ± 0.81 vs 2.53 ± 0.72 [ P < 0.0001]). Relative gains in detectability were most pronounced in juxtacortical lesions (36% relative gain in lesion counts-pooled for both readers). In 5% of the scans, synthDIR subtraction maps helped to identify a disease progression missed on FLAIR subtraction maps. CONCLUSIONS: Generative adversarial networks can generate high-contrast DIR images that may improve the longitudinal follow-up assessment in MS patients compared with standard sequences. By detecting more newly formed MS lesions and increasing the rates of detected disease activity, our methodology promises to improve clinical decision-making.
 BACKGROUND: In recent meta-analyses, robot-assisted gait training for patients with multiple sclerosis (MS) have yielded limited clinical benefits compared with conventional overground gait training. OBJECTIVE: To investigate the effect of robot-assisted gait training for patients with MS on clinical outcomes through a systematic review and meta-analysis. METHODS: We searched for relevant studies in the PubMed, EMBASE, Cochrane Library, and Physiotherapy Evidence Database databases from their inception to April 7, 2022. We selected studies that (1) included participants with MS, (2) used robot-assisted gait training as the intervention, (3) included conventional overground gait training or another gait training protocol as control treatment, and (4) reported clinical outcomes. Continuous variables are expressed as standardized mean differences with 95% confidence intervals. Statistical analyses were performed using RevMan 5.4 software. RESULTS: We included 16 studies enrolling 536 participants. Significant improvement was observed in the intervention group, with low heterogeneity at the end of the intervention with regard to walking velocity (standardized mean difference [SMD]: 0.38, 95% confidence interval [CI]: [0.15, 0.60]), walking endurance (SMD: 0.26, 95% CI [0.04, 0.48]), mobility (SMD: -0.37, 95% CI [-0.60, -0.14]), balance (SMD: 0.26, 95% CI [0.04, 0.48]), and fatigue (SMD: -0.27, 95% CI [-0.49, -0.04]). The results of subgroup analyses revealed improvements in these outcomes for the intervention group using grounded exoskeletons. No significant differences were noted in all the outcomes between the groups at follow-up. CONCLUSIONS: Robot-assisted gait training with grounded exoskeletons exerts a positive short-term effect and is an adequate treatment option for patients with MS.
 The establishment of surrogate markers to detect disability progression in persons with multiple sclerosis (PwMS) is important to improve monitoring of clinical deterioration. Optical coherence tomography (OCT) could be such a tool. However, sufficient longitudinal data of retinal neuroaxonal degeneration as a marker of disease progression exist only for PwMS with a relapsing-remitting course (RRMS) so far. In contrast, longitudinal data of retinal layers in patients with primary-progressive MS (PPMS) are inconsistent, and the association of OCT parameters with ambulatory performance in PwMS has rarely been investigated. We aimed to investigate the relative annual rates of change in retinal layers in PwMS (RRMS and PPMS) compared with healthy controls (HC) using OCT and to evaluate their association with ambulatoryfunctionalscore (AS) worsening in PPMS. A retrospective analysis of a longitudinal OCT dataset of the retinal layers of PwMS and HC from two MS centers in Germany was performed. Walking ability was measured over a standardized distance of 500 m, and changes during the observation period were categorized using the AS and the expanded disability status scale (EDSS). 61 HC with 121 eyes and 119 PwMS (PPMS: 57 patients with 108 eyes; RRMS: 62 patients with 114 eyes) were included. The median follow-up time for PwMS was 3 years. The relative annual change of pRNFL (peripapillary retinal nerve fiber layer) and INL (inner nuclear layer) was significantly different in PwMS compared with HC. RRMS and PPMS subgroups did not differ in the annual atrophy rates. In patients with PPMS, worsening of the AS was significantly associated with increased thinning of the TMV (total macular volume), GCIP (ganglion cell and inner plexiform layer), and ONPL (outer nuclear and outer plexiform layer) (all p-value < 0.05, r > 0.30). For every -0.1% decrease in the TMV, GCIP, and ONPL, the risk of a deterioration in the AS increased by 31% (hazard ratio (HR): 1.309), 11% (HR: 1.112), and 16% (HR: 1.161), respectively. In addition, worsening EDSS in PPMS was significantly associated with the relative annual atrophy rates of pRNFL, TMV, and GCIP (all p-value < 0.05). Disability progression in PPMS can be measured using OCT, and increasing annual atrophy rates of the inner retinal layers are associated with worsening ambulation. OCT is a robust and side-effect-free imaging tool, making it suitable for routine monitoring of PwMS.
 BACKGROUND: Although ongoing exercise is known to reduce disability in people with multiple sclerosis (MS), participation in lower-extremity exercise programs can be limited by their existing mobility impairments. Lower-extremity exoskeletons could address this problem by facilitating home and community locomotion and enhancing exercise capability but little data is available on the potential of this technology for reducing disability of people with MS. METHODS: We evaluated the Keeogo™ exoskeleton for people with MS using an open-label randomised cross-over design. The trial design allowed us to quantify rehabilitation effects (tested without device) and training effects (tested with device) using functional outcomes: 6-minute walk test (6MWT), timed stair test (TST), and timed up-and-go (TUG). Baseline and post-study self-report instruments included Medical Outcomes Survey Short Form-36 (SF36), MS Walking Scale (MSWS), and others. Amount of home use was documented by daily activity log. Partial correlation analysis was used to explore the relationships between changes in functional outcomes and self-report disability, controlling for amount of home use of the device. RESULTS: Twenty-nine participants with MS completed the trial. Change scores for MSWS, SF36 physical function and SF36 emotional well-being correlated positively with changes in 6MWT which was explained by amount of home use. CONCLUSIONS: The benefits in physical functioning and emotional well-being from using the exoskeleton at home were linked to amount of device usage. Low-profile robotic exoskeletons could be used to deliver facilitated exercise while assisting with locomotor activities of daily living, such as walking and stair climbing in the home and community environment.IMPLICATIONS FOR REHABILITATIONExoskeletons for home use may have the potential to benefit people with MS in terms of physical functioning and emotional well-being.The benefits in physical functioning and emotional well-being appeared to be linked to amount of usage.Exoskeletons might be useful for delivering facilitated exercise while assisting with walking and stair climbing in the home.

 The relationship between brain diffusion microstructural changes and disability in multiple sclerosis (MS) remains poorly understood. We aimed to explore the predictive value of microstructural properties in white (WM) and grey matter (GM), and identify areas associated with mid-term disability in MS patients. We studied 185 patients (71% female; 86% RRMS) with the Expanded Disability Status Scale (EDSS), timed 25-foot walk (T25FW), nine-hole peg test (9HPT), and Symbol Digit Modalities Test (SDMT) at two time-points. We used Lasso regression to analyse the predictive value of baseline WM fractional anisotropy and GM mean diffusivity, and to identify areas related to each outcome at 4.1 years follow-up. Motor performance was associated with WM (T25FW: RMSE = 0.524, R(2) = 0.304; 9HPT dominant hand: RMSE = 0.662, R(2) = 0.062; 9HPT non-dominant hand: RMSE = 0.649, R(2) = 0.139), and SDMT with GM diffusion metrics (RMSE = 0.772, R(2) = 0.186). Cingulum, longitudinal fasciculus, optic radiation, forceps minor and frontal aslant were the WM tracts most closely linked to motor dysfunction, and temporal and frontal cortex were relevant for cognition. Regional specificity related to clinical outcomes provide valuable information that can be used to develop more accurate predictive models that could improve therapeutic strategies.
 BACKGROUND AND OBJECTIVES: The question of the long-term safety of pregnancy is a major concern in patients with multiple sclerosis (MS), but its study is biased by reverse causation (women with higher disability are less likely to experience pregnancy). Using a causal inference approach, we aimed to estimate the unbiased long-term effects of pregnancy on disability and relapse risk in patients with MS and secondarily the short-term effects (during the perpartum and postpartum years) and delayed effects (occurring beyond 1 year after delivery). METHODS: We conducted an observational cohort study with data from patients with MS followed in the Observatoire Français de la Sclérose en Plaques registry between 1990 and 2020. We included female patients with MS aged 18-45 years at MS onset, clinically followed up for more than 2 years, and with ≥3 Expanded Disease Status Scale (EDSS) measurements. Outcomes were the mean EDSS score at the end of follow-up and the annual probability of relapse during follow-up. Counterfactual outcomes were predicted using the longitudinal targeted maximum likelihood estimator in the entire study population. The patients exposed to at least 1 pregnancy during their follow-up were compared with the counterfactual situation in which, contrary to what was observed, they would not have been exposed to any pregnancy. Short-term and delayed effects were analyzed from the first pregnancy of early-exposed patients (who experienced it during their first 3 years of follow-up). RESULTS: We included 9,100 patients, with a median follow-up duration of 7.8 years, of whom 2,125 (23.4%) patients were exposed to at least 1 pregnancy. Pregnancy had no significant long-term causal effect on the mean EDSS score at 9 years (causal mean difference [95% CI] = 0.00 [-0.16 to 0.15]) or on the annual probability of relapse (causal risk ratio [95% CI] = 0.95 [0.93-1.38]). For the 1,253 early-exposed patients, pregnancy significantly decreased the probability of relapse during the perpartum year and significantly increased it during the postpartum year, but no significant delayed effect was found on the EDSS and relapse rate. DISCUSSION: Using a causal inference approach, we found no evidence of significantly deleterious or beneficial long-term effects of pregnancy on disability. The beneficial effects found in other studies were probably related to a reverse causation bias.
 BACKGROUND AND PURPOSE: Parkinson's disease (PD) and multiple sclerosis (MS) can impair driving. However, we lack evidence on car accidents associated with these diseases. The aims of this study were to examine what types of car accident were associated with drivers with PD and MS, compared to individuals with ulcerative colitis (UC; the comparison group), and to evaluate the occurrence of car accidents in relation to years since diagnosis. METHODS: This retrospective nationwide, registry-based study included drivers involved in car accidents between 2010 and 2019, based on the Swedish Traffic Accident Data Acquisition database. Data on pre-existing diagnoses were retrieved retrospectively from the National Patient Registry. Data analyses included group comparisons, time-to-event analysis, and binary logistic regression. RESULTS: In total, 1491 drivers, including 199 with PD, 385 with MS, and 907 with UC, were registered to have been involved in a car accident. The mean time from diagnosis to the car accident was 5.6 years for PD, 8.0 years for MS, and 9.4 years for UC. Time to car accident since diagnosis differed significantly (p < 0.001) among groups (adjusted for age). Drivers with PD had more than twice the odds of a single-car accident than drivers with MS or UC, but no differences were observed between MS and UC. CONCLUSIONS: Drivers with PD were older and experienced the car accident within a shorter timeframe after disease diagnosis. Although several factors may cause a car accident, fitness to drive could be more thoroughly evaluated for patients with PD by physicians, even early after the diagnosis.
 BACKGROUND: Certain classes of multiple sclerosis (MS) disease modifying therapies (DMTs) have been associated with an increased risk of severe COVID-19, resulting in prescribers considering changes in their practice habits during the COVID-19 pandemic. This study assessed for differences in prescribing patterns of DMTs along with the reason(s) for modification of therapy over time. METHODS: A retrospective review of medical records at Johns Hopkins Health System was performed. The timeframe of the study, April 2019 to December 2021, was divided into three subcategories: pre-pandemic (April 2019-March 2020), pre-vaccine availability (April 2020-March 2021), and post-vaccine availability (April 2021-December 2021). Patients were identified through dispense reports from the pharmacy dispensing system, and prescribing report from the health-system electronic health record (EHR). The health-system EHR was also utilized to conduct chart reviews for a subset of patients that had a modification in their therapy during the specified timeframes. The study included adult patients that were prescribed at least one DMT through the Johns Hopkins Pharmacy Services during the study timeframe and those who stayed on their DMT for at least 2 months without tolerability issues. Descriptive statistics were used to compare the prescribing practices during the timeframes with the percentage of prescribing for each type of treatment and to assess the percentage of patients that switched therapies in the different time periods. RESULTS: Based on prescribing report data, 670 patients were prescribed a DMT during the pre-pandemic period with infusion therapies being the most prescribed therapies during this timeframe (38%), followed by oral therapies at 35%. In comparison, a total of 620 patients were prescribed a DMT during pre-vaccine pandemic and the percentage of prescriptions of infusion therapies decreased to 28% (-10%) during this timeframe, whereas oral prescriptions increased to 42% (+7%). These trends continued during the post-vaccine timeframe where infusion therapies decreased to 26% (-12%) and oral therapies increased to 43% (+8%) in reference to the pre-pandemic period. Prescribing patterns of self-injectable therapies remained stable throughout the 3 timeframes. A dispensing report cohort of 500 patients were randomly selected for chart reviews to assess therapy modifications due to COVID-19. The percentage of therapy change due to COVID-19 increased to 45.2% during pre-vaccine period and remained at 38.4% during post-vaccine period when compared to the pre-pandemic reference period. The majority of changes due to COVID-19 were delays in infusion therapies (96% during pre-vaccine, and 94% during post-vaccine), not medication changes. CONCLUSION: Prescribing patterns and therapy modifications of DMTs for MS patients were impacted by COVID-19, with the greatest changes observed for the infusion therapies, including reduction in percentage of infusion prescriptions and delays in infusion therapies. Prescribing patterns of lower efficacy self-injectable therapies (interferon-beta and glatiramer acetate) remained stable. The outcomes of this study provide background for future outcomes-focused research studies in MS.
 In this issue of JNO, Drs. Mark L. Moster, Marc J. Dinkin, and Deborah I. Friedman discuss the following 6 articles:Piehl F, Eriksson-Dufva A, Budzianowska A, Feresiadou A, Hansson W, Hietala MA, Håkansson I, Johansson R, Jons D, Kmezic I, Lindberg C, Lindh J, Lundin F, Nygren I, Punga AR, Press R, Samuelsson K, Sundström P, Wickberg O, Brauner S, Frisell T. Efficacy and safety of rituximab for new-onset generalized myasthenia gravis: the RINOMAX randomized clinical trial. JAMA Neurol. 2022;79:1105-1112.Cortese R, Carrasco FP, Tur C, Bianchi A, Brownlee W, De Angelis F, De La Paz I, Grussu F, Haider L, Jacob A, Kanber B, Magnollay L, Nicholas RS, Trip A, Yiannakas M, Toosy AT, Hacohen Y, Barkhof F, Ciccarelli O. Differentiating multiple sclerosis from AQP4-neuromyelitis optica spectrum disorder and MOG-antibody disease with imaging. Neurology. 2022. doi: 10.1212/WNL.0000000000201465.Carelli V, Newman NJ, Yu-Wai-Man P, Biousse V, Moster ML, Subramanian PS, Vignal-Clermont C, Wang AG, Donahue SP, Leroy BP, Sergott RC, Klopstock T, Sadun AA, Rebolleda Fernández G, Chwalisz BK, Banik R, Girmens JF, La Morgia C, DeBusk AA, Jurkute N, Priglinger C, Karanjia R, Josse C, Salzmann J, Montestruc F, Roux M, Taiel M, Sahel JA; the LHON Study Group. Indirect comparison of Lenadogene Nolparvovec gene therapy versus natural history in patients with leber hereditary optic neuropathy carrying the m.11778G>A MT-ND4 mutation. Ophthalmol Ther. 2022. doi: 10.1007/s40123-022-00611-x.Noll C, Hiltensperger M, Aly L, Wicklein R, Afzali AM, Mardin C, Gasperi C, Berthele A, Hemmer B, Korn T, Knier B. Association of the retinal vasculature, intrathecal immunity, and disability in multiple sclerosis. Front Immunol. 2022;13:997043.Mitchell JL, Buckham R, Lyons H, Walker JK, Yiangou A, Sassani M, Thaller M, Grech O, Alimajstorovic Z, Julher M, Tsermoulas G, Brock K, Mollan SP, Sinclair AJ. Evaluation of diurnal and postural intracranial pressure employing telemetric monitoring in idiopathic intracranial hypertension. Fluids Barriers CNS. 2022;19:85.Pan Y, Chen YX, Zhang J, Lin ML, Liu GM, Xu XL, Fan XQ, Zhong Y, Li Q, Ai SM, Xu W, Tan J, Zhou HF, Xu DD, Zhang HY, Xu B, Wang S, Ma JJ, Zhang S, Gan LY, Cui JT, Li L, Xie YY, Guo X, Pan-Doh N, Zhu ZT, Lu Y, Shi YX, Xia YW, Li ZY, Liang D. Doxycycline vs placebo at 12 weeks in patients with mild thyroid-associated ophthalmopathy: a randomized clinical trial. JAMA Ophthalmol. 2022;140:1076-1083.
 BACKGROUND AND OBJECTIVES: Large-scale observational studies have shown that, in patients with multiple sclerosis (MS), the risk of becoming more severely ill from coronavirus disease 2019 (COVID-19) is determined by older age, male sex, cardiovascular comorbidities, African American ethnicity, progressive disease, recent use of corticosteroids, and B cell-depleting disease-modifying treatment. In contrast, the effect of COVID-19 on the disease course of MS has been studied much less extensively. Our main goal was to explore whether COVID-19 is associated with accelerated clinical disability worsening in patients with MS. METHODS: Since March 2020, demographics and infectious outcome (categorized as ambulatory, hospitalized, and/or death) of patients with MS who developed COVID-19 have been collected at the Belgian National MS Center in Melsbroek. On February 28, 2022, this database was locked and complemented with clinical disability measures-Expanded Disability Status Scale (EDSS), Timed 25-Foot Walk Test (T25FWT), 9-Hole Peg Test (9HPT), and Symbol Digit Modalities Test (SDMT)-that were available from a larger local database, obtained during routine medical follow-up. For each parameter, the first 2 assessments before COVID-19 diagnosis (T0 and T1; T1 is the closest to COVID-19 diagnosis), and the first thereafter (T2), were retrieved. RESULTS: We identified 234 unique cases of COVID-19. Thirty-one patients were hospitalized (13.2%), and 5 died (2.1%) as a result of their infection. Among survivors with complete EDSS results (N = 138), mean annualized T1-to-T2 EDSS worsening was more pronounced, compared with the respective change between T0 and T1 (0.3 ± 0.9 vs 0.1 ± 0.9, p = 0.012). No such differences were found for the T25FWT, 9HPT, and SDMT scores. Severe COVID-19 (hospitalization) was associated with clinically relevant T1-to-T2 EDSS worsening (OR 2.65, p = 0.042). Vaccination coverage in the total cohort was 53.8%. Being unprotected by vaccination at the time of infection was associated with a worse COVID-19 outcome (hospitalization and/or death; OR 3.52, p = 0.002) but not with clinically relevant T1-to-T2 EDSS worsening. DISCUSSION: The occurrence and severity of COVID-19 are both associated with clinical disability worsening in patients with MS. Vaccination protects against a more severe course of COVID-19 in this specific population. TRIAL REGISTRATION INFORMATION: The study has been registered at ClinicalTrials.gov (study registration number: NCT05403463).
 OBJECTIVES: Cladribine is a selective and oral immunological reconstitution treatment, approved in Europe for very active multiple sclerosis (MS) with relapses. Aims were to assess the safety and effectiveness of cladribine in real-world setting, during treatment follow-up. METHODS: This was a multicentric, longitudinal, observational study with retrospective and prospective data collection of clinical, laboratory, and imaging data. This interim analysis reports data from July 1, 2018 (study onset), to March 31, 2021. RESULTS: A total of 182 patients were enrolled: 68.7% were female; mean age at onset was 30.1 ± 10.0 years, and mean age at first cycle of cladribine treatment was 41.1 ± 12.1; 88.5% were diagnosed with relapse-remitting MS and 11.5% with secondary progressive MS. Mean disease duration at cladribine start was 8.9 ± 7.7 years. Most patients (86.1%) were not naive, and median number of previous disease-modifying therapies was 2 (interquartile range, 1-3). At 12 months, we observed no significant Expanded Disability Status Scale score worsening ( P = 0.843, Mann-Whitney U test) and a significantly lower annualized relapse rate (0.9 at baseline to 0.2; 78% reduction). Cladribine treatment discontinuation was registered in 8% of patients, mainly (69.2%) due to disease activity persistence. Most frequent adverse reactions were lymphocytopenia (55%), infections (25.2%), and fatigue (10.7%). Serious adverse effects were reported in 3.3%. No patient has discontinued cladribine treatment because of adverse effects. CONCLUSION: Our study confirms the clinical efficacy and the safety profile of cladribine for treating MS patients with a long-term active disease in the real-world setting. Our data contribute to the body of knowledge of the clinical management of MS patients and the improvement of related clinical outcomes.
 BACKGROUND: Multiple sclerosis (MS) is an immune-mediated central nervous system disease whose course is unpredictable. Finding biomarkers that help to better comprehend the disease's pathogenesis is crucial for supporting clinical decision-making. Blood extracellular vesicles (EVs) are membrane-bound particles secreted by all cell types that contain information on the disease's pathological processes. PURPOSE: To identify the immune and nervous system-derived EV profile from blood that could have a specific role as biomarker in MS and assess its possible correlation with disease state. RESULTS: Higher levels of T cell-derived EVs and smaller size of neuron-derived EVs were associated with clinical relapse. The smaller size of the oligodendrocyte-derived EVs was related with motor and cognitive impairment. The proteomic analysis identified mannose-binding lectin serine protease 1 and complement factor H from immune system cell-derived EVs as autoimmune disease-associated proteins. We observed hepatocyte growth factor-like protein in EVs from T cells and inter-alpha-trypsin inhibitor heavy chain 2 from neurons as white matter injury-related proteins. In patients with MS, a specific protein profile was found in the EVs, higher levels of alpha-1-microglobulin and fibrinogen β chain, lower levels of C1S and gelsolin in the immune system-released vesicles, and Talin-1 overexpression in oligodendrocyte EVs. These specific MS-associated proteins, as well as myelin basic protein in oligodendrocyte EVs, correlated with disease activity in the patients with MS. CONCLUSION: Neural-derived and immune-derived EVs found in blood appear to be good specific biomarkers in MS for reflecting the disease state.
 This project sought to explore the potential association between medical history and the development of multiple sclerosis (MS) by conducting a retrospective study. This population-based case-control study included 200 MS cases and 2 control groups of 200 patients and healthy individuals each. Data was collected through face-to-face interviews, medical file reviews, and an electronic checklist. Multivariable analysis was used to calculate odds ratios and 95% confidence intervals to estimate the risk of each medical history on MS occurrences. Of 600 participants, 381 (63.5%) individuals were female. The mean age of the participants was 36.5 ± 11.9 years. The adjusted risks of MS were 4.40; 95% CI: 1.73 to 11.1 for measles and 4.75; 95% CI: 2.05 to 11 for amoxicillin consumption. The adjusted MS odds for autoimmune disease including 4.63; 95% CI: 0.35 to 60.6 for psoriasis and 7.15; 95% CI: 1.87 to 27.2 for myasthenia gravis. On the other hand, the calculated adjusted odds of MS occurrence were 0.14; 95% CI: 0.03 to 0.69 for seizure and 0.17; 95% CI: 0.02 to 1.49 for epilepsy. This study suggested that individuals with autoimmune diseases should be monitored more closely, as they may be at an increased risk of developing other autoimmune conditions, particularly MS.
 BACKGROUND: There is growing interest and evidence for high intensity training (HIT) in clinical populations, including persons with multiple sclerosis (MS). While HIT has been shown to be a safe modality in this group, it is still unclear what collective knowledge exists for HIT on functional outcomes. This study examined HIT modalities (e.g., aerobic, resistance, functional training) on functional outcomes such as walking, balance, postural control, and mobility in persons with MS. METHODS: High intensity training studies, including RCTs and non-RCTs, that targeted functional outcomes in persons with MS were included in the review. A literature search was conducted in MEDLINE, EMBASE, PsycINFO, SPORTSDiscus, and CINAHL in April 2022. Other literature search methods were performed via website and citation searching. The methodological quality of included studies was assessed by TESTEX for RCTs and ROBINS-I for non-RCTs. This review synthesized the following data: study design and characteristics, participant characteristics, intervention characteristics, outcome measures, and effect sizes. RESULTS: Thirteen studies (6 RCTs and 7 non-RCTs) were included in the systematic review. The included participants (N = 375) had varying functional levels (EDSS range: 0-6.5) and phenotypes (relapsing remitting, secondary progressive, primary progressive). HIT modalities involving high intensity aerobic training (n = 4), high intensity resistance training (n = 7), and high intensity functional training (n = 2), revealed a significant and consistent benefit on walking speed and walking endurance in response to HIT, while the evidence regarding balance and mobility improvement was less clear. CONCLUSION: Persons with MS can successfully tolerate and adhere to HIT. While HIT appears to be an effective modality for improving some functional outcomes, the heterogeneous testing protocols, HIT modalities, and exercise doses among the studies preclude any conclusive evidence for its effectiveness thus necessitating future inquiry.
 Numerous disorders are characterised by fatigue as a highly disabling symptom. Fatigue plays a particularly important clinical role in multiple sclerosis (MS) where it exerts a profound impact on quality of life. Recent concepts of fatigue grounded in computational theories of brain-body interactions emphasise the role of interoception and metacognition in the pathogenesis of fatigue. So far, however, for MS, empirical data on interoception and metacognition are scarce. This study examined interoception and (exteroceptive) metacognition in a sample of 71 persons with a diagnosis of MS. Interoception was assessed by prespecified subscales of a standard questionnaire (Multidimensional Assessment of Interoceptive Awareness [MAIA]), while metacognition was investigated with computational models of choice and confidence data from a visual discrimination paradigm. Additionally, autonomic function was examined by several physiological measurements. Several hypotheses were tested based on a preregistered analysis plan. In brief, we found the predicted association of interoceptive awareness with fatigue (but not with exteroceptive metacognition) and an association of autonomic function with exteroceptive metacognition (but not with fatigue). Furthermore, machine learning (elastic net regression) showed that individual fatigue scores could be predicted out-of-sample from our measurements, with questionnaire-based measures of interoceptive awareness and sleep quality as key predictors. Our results support theoretical concepts of interoception as an important factor for fatigue and demonstrate the general feasibility of predicting individual levels of fatigue from simple questionnaire-based measures of interoception and sleep.
 Background Annualized Relapse Rate (ARR) is one of the most important indicators of disease progression in patients with Multiple Sclerosis (MS). However, imaging markers that can effectively predict ARR are currently unavailable. In this study, we developed a deep learning-based method for the automated extraction of radiomics features from Positron Emission Computed Tomography (PET) and Magnetic Resonance (MR) images to predict ARR in patients with MS. Methods Twenty-five patients with a definite diagnosis of Relapsing-Remitting MS (RRMS) were enrolled in this study. We designed a multi-branch fully convolutional neural network to segment lesions from PET/MR images. After that, radiomics features were extracted from the obtained lesion volume of interest. Three feature selection methods were used to retain features highly correlated with ARR. We combined four classifiers with different feature selection methods to form twelve models for ARR classification. Finally, the model with the best performance was chosen. Results Our network achieved precise automatic lesion segmentation with a Dice Similarity Coefficient (DSC) of 0.81 and a precision of 0.86. Radiomics features from lesions filtered by Recursive Feature Elimination (RFE) achieved the best performance in the Support Vector Machines (SVM) classifier. The classification model performance was best when radiomics from both PET and MR were combined to predict ARR, with high accuracy at 0.88 and Area Under the ROC curves (AUC) at 0.96, which outperformed MR or PET-based model and clinical indicators-based model. Conclusion Our automatic segmentation masks can replace manual ones with excellent performance. Furthermore, the deep learning and PET/MR radiomics-based model in our research is an effective tool in assisting ARR classification of MS patients.
 BACKGROUND: In recent years dramatic changes in multiple sclerosis (MS) incidence have been reported in different provinces in Iran. This study was conducted to assess MS incidence temporal trends from March 21, 2005, to March 20, 2020, and provide a forecast until the end of 2025 in Shahroud county. METHODS: This longitudinal study was carried out based on the data obtained from the MS registration system in Shahroud county. First, the annual incidence rates were calculated based on the year of diagnosis and smoothed using the Empirical Bayesian Method. Then temporal trends and annual percent change (APC) of MS incidence were analyzed using Joinpoint (JP) regression. Finally, the univariate time series model analysis was used to estimate the MS incidence trend until the end of 2025. RESULTS: A total of 234 newly diagnosed cases (60 [25.64%] males and 174 [74.36.4%] females) were examined in this study. The mean age of patients at the time of diagnosis was 31.40 ± 3.78. It was 32.01 ± 6.35 and 30.66 ± 4.27 years for males and females, respectively (P<0.22). The mean annual MS incidence was 5.99 ± 1.46, 3.03 ± 0.21, and 8.98 ± 2.79 per 100,000 in overall, males and females respectively. The MS incidence increased significantly from 5.67 (95% CI: 3.63-7.99) in 2005 to 7.58 (95% CI: 5.17-10.28) in 2020 with an APC of 4.5 (2.8 - 6.1). The MS incidence had a non-linear time trend in the study period and the best time trend fitted to the annual MS incidence trend was the non-linear quadratic curve. Based on this model, the annual MS incidence is expected to increase until the end of 2025. CONCLUSION: Shahroud county is one of the high-risk areas for MS and the increasing trend of MS incidence in it is similar to regional and global changes. This study, also, showed that MS incidence in Shahroud county will be increasing in the coming years.
 Dysphagia is a common symptom of neurological disease, including multiple sclerosis (MS). The DYsphagia in MUltiple Sclerosis (DYMUS) questionnaire was developed as a screening tool for swallowing problems. The purpose of the present study was to validate the Czech version of the DYMUS questionnaire. We validated the questionnaire on a sample of 435 patients with MS and 135 healthy controls (HC) chosen by accidental sampling from larger, long-term studies conducted by the Prague MS Center. For the purposes of this study, we used both electronic (primary method of distribution) and paper-based (backup) versions of the questionnaire. The internal consistency of the whole scale was satisfactory (Cronbach's α =0.833). The DYMUS mean score in HC was 0.215 (standard deviation [SD] = 0.776). Normative data suggested a cut-off value for dysphagia between 1 and 2 points. Principal component analysis (PCA) showed a two-factor structure of the adapted scale. However, the structure did not completely correspond to the originally proposed dimensions of dysphagia for solids and liquids; our data supported dropout of item Q10. Criterion validity was proved by the difference in dysphagia between HC and patients MS (U = 25,546, p < 0.001) and by a positive correlation with the EDSS (Kendall's tau-b = 0.169, p < 0.001) and other patient-reported outcomes. The Czech version of the DYMUS questionnaire is a valid and reliable tool for evaluating swallowing impairment in Czech-speaking patients with MS. Moreover, the questionnaire can be administered electronically, with a paper-based backup.
 We aimed to study the influence of smoking habits, exposure to passive smoking and snuff use on disease progression, cognitive performance and quality of life in patients with multiple sclerosis (MS). METHOD: Patients from two population-based case-control studies were categorised based on tobacco exposure at diagnosis and were followed up to 15 years post diagnosis through the Swedish MS registry (n=9089) regarding changes in Expanded Disability Status Scale (EDSS), Multiple Sclerosis Impact Scale 29 and Symbol Digit Modalities Test. We used linear mixed models to analyse long-term changes, and Cox regression models with 95% CI using 24-week confirmed disability worsening, reaching EDSS 3 and EDSS 4, respectively, physical and psychological worsening and cognitive disability worsening as end points. The influence of smoking cessation post diagnosis was also investigated. RESULTS: Compared with non-smokers, current smokers had a faster EDSS progression (β(current smoking×time)=0.03, 95% CI 0.02 to 0.04). A faster EDSS progression was also associated with passive smoking (β(current passive smoking×time)=0.04, 95% CI 0.03 to 0.06). Smoke exposure negatively impacted all secondary outcomes. Those who continued smoking had worse outcomes than those who stopped smoking post diagnosis. Snuff users had a more favourable EDSS progression, compared with never users. CONCLUSIONS: Our findings indicate that both smoking and passive smoking have a negative influence on MS and that smoking cessation post diagnosis may be an important secondary preventive measure. Snuff use was associated with slower disease progression, suggesting that nicotine replacement therapy could be an attractive way to increase the chance of quitting smoking among patients with MS.
 BACKGROUND: Multiple sclerosis (MS) is an inflammatory, degenerative, demyelinating disease that ranges from benign to rapidly progressive forms. A striking characteristic of the disease is the clinical-radiological paradox. OBJECTIVES: The present study was conducted to determine whether, in our cohort, the clinical-radiological paradox exists and whether lesion location is related to clinical disability in patients with MS. METHODS: Retrospective data from 95 patients with MS (60 women and 35 men) treated at a single center were examined. One head-and-spine magnetic resonance imaging (MRI) examination from each patient was selected randomly, and two independent observers calculated lesion loads (LLs) on T2/fluid attenuation inversion recovery sequences manually, considering the whole brain and four separate regions (periventricular, juxtacortical, posterior fossa, and spinal cord). The LLs were compared with the degree of disability, measured by the Kurtzke Expanded Disability Status Scale (EDSS), at the time of MRI examination in the whole cohort and in patients with relapsing-remitting (RR), primarily progressive, and secondarily progressive MS. RESULTS: High LLs correlated with high EDSS scores in the whole cohort (r = 0.34; p < 0.01) and in the RRMS group (r = 0.27; p = 0.02). The EDSS score correlated with high regional LLs in the posterior fossa (r = 0.31; p = 0.002) and spinal cord (r = 0.35; p = 0.001). CONCLUSIONS: Our results indicate that the clinical-radiological paradox is a myth and support the logical connection between lesion location and neurological repercussion.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) misdiagnosis (i.e. the incorrect diagnosis of patients who truly have NMOSD) remains an issue in clinical practice. We determined the frequency and factors associated with NMOSD misdiagnosis in patients evaluated in a cohort from Latin America. METHODS: We retrospectively reviewed the medical records of patients with NMOSD, according to the 2015 diagnostic criteria, from referral clinics in six Latin American countries (Argentina, Chile, Paraguay, Colombia, Ecuador, and Venezuela). Diagnoses prior to NMOSD and ultimate diagnoses, demographic, clinical and paraclinical data, and treatment schemes were evaluated. RESULTS: A total of 469 patients presented with an established diagnosis of NMOSD (73.2% seropositive) and after evaluation, we determined that 56 (12%) patients had been initially misdiagnosed with a disease other than NMOSD. The most frequent alternative diagnoses were multiple sclerosis (MS; 66.1%), clinically isolated syndrome (17.9%), and cerebrovascular disease (3.6%). NMOSD misdiagnosis was determined by MS/NMOSD specialists in 33.9% of cases. An atypical MS syndrome was found in 86% of misdiagnosed patients, 50% had NMOSD red flags in brain and/or spinal magnetic resonance imaging (MRI), and 71.5% were prescribed disease-modifying drugs. CONCLUSIONS: NMOSD misdiagnosis is relatively frequent in Latin America (12%). Misapplication and misinterpretation of clinical and neuroradiological findings are relevant factors associated with misdiagnosis.
 BACKGROUND: It is assumed that people with multiple sclerosis (MS) who participate in programs of physical exercise improve their physical fitness. OBJECTIVE: The aim of this network meta-analysis (NMA) was to analyze the effect of different types of exercise on muscular fitness and cardiorespiratory fitness (CRF) among people with MS and to determine the best type of exercise according to disease severity. METHODS: MEDLINE, the Physiotherapy Evidence Database, the Cochrane Library, SPORTDiscus, Scopus, and Web of Science were searched from inception to April 2022 to identify randomized controlled trials (RCTs) concerning the effect of physical exercise on fitness in people with MS. We ranked the types of physical exercise by calculating the surface under the cumulative ranking (SUCRA). RESULTS: We included 72 RCTs involving 2543 MS patients in this NMA. A ranking of five types of physical exercise (aerobic, resistance, combined [aerobic and resistance], sensorimotor training, and mind-body exercises) was achieved. Combined and resistance training had the highest effect sizes (0.94, 95% CI 0.47, 1.41, and 0.93, 95% CI 0.57, 1.29, respectively) and the highest SUCRA (86.2% and 87.0%, respectively) for muscular fitness. The highest effect size (0.66, 95% CI 0.34, 0.99) and SUCRA (86.9%) for CRF was for aerobic exercise. CONCLUSIONS: Combined and resistance training seem to be the most effective exercises to improve muscular fitness and aerobic exercise for CRF in people with MS.
 BACKGROUND: Cognitive problems, both complaints and objective impairments, are frequent and disabling in patients with multiple sclerosis (MS) and profoundly affect daily living. However, intervention studies that focus on cognitive problems that patients experience in their daily lives are limited. This study therefore aimed to investigate the effectiveness of cognitive rehabilitation therapy (CRT) and mindfulness-based cognitive therapy (MBCT) on patient-reported cognitive complaints in MS. METHODS: In this randomized-controlled trial, MS patients with cognitive complaints completed questionnaires and underwent neuropsychological assessments at baseline, post-treatment and 6-month follow-up. Patient-reported cognitive complaints were primarily investigated. Secondary outcomes included personalized cognitive goals and objective cognitive function. CRT and MBCT were compared to enhanced treatment as usual (ETAU) using linear mixed models. RESULTS: Patients were randomized into CRT (n = 37), MBCT (n = 36) or ETAU (n = 37), of whom 100 completed the study. Both CRT and MBCT positively affected patient-reported cognitive complaints compared to ETAU at post-treatment (p<.05), but not 6 months later. At 6-month follow-up, CRT had a positive effect on personalized cognitive goals (p=.028) and MBCT on processing speed (p=.027). Patients with less cognitive complaints at baseline benefited more from CRT on the Cognitive Failures Questionnaire (i.e. primary outcome measuring cognitive complaints) at post-treatment (p=.012-.040), and those with better processing speed at baseline benefited more from MBCT (p=.016). CONCLUSION: Both CRT and MBCT alleviated cognitive complaints in MS patients immediately after treatment completion, but these benefits did not persist. In the long term, CRT showed benefits on personalized cognitive goals and MBCT on processing speed. These results thereby provide insight in the specific contributions of available cognitive treatments for MS patients.
 Relapsing-remitting multiple sclerosis progresses by relapse. It is therefore necessary to know how to identify this phenomenon in order to be able to provide the best possible support to patients. The term "relapse" is used to characterize the period of a few days to a few weeks during which an attack of inflammation of the myelin occurs. Depending on the area affected, the symptoms will be different. To qualify as a relapse, the patient must have had new, permanent symptoms for at least 24 hours without fever or signs of infection and within 30 days of the last relapse.
 Ublituximab, an intravenous glycoengineered chimeric anti-CD20 IgG1 monoclonal antibody (mAb), is a new FDA-approved treatment for relapsing forms of Multiple Sclerosis (MS). Reassembling the other three anti-CD20 mAbs already in use for MS (rituximab, ocrelizumab and ofatumumab), ublituximab leads to depletion of B cells but spars long-lived plasma cells. Here, we discuss the main findings obtained during the phase 3 clinical trials (ULTIMATE I and II) for ublituximab versus teriflunomide. The current emergence and approval of new anti-CD20 mAbs with different dose regimens, routes of application, glycoengineering and mechanisms of action may contribute to different clinical outcomes.
 To prioritize circulating metabolites that likely play causal roles in the pathogenesis of multiple sclerosis (MS). Two-sample Mendelian randomization analysis was performed to estimate the causal effects of 571 circulating metabolites on the risk of MS. Genetic instruments for circulating metabolites were obtained from three previous genome-wide association studies (GWAS) of the blood metabolome (N = 7824; 24,925; and 115,078; respectively), while genetic associations with MS were from a large GWAS by the International Multiple Sclerosis Genetics Consortium (14,802 cases and 26,703 control). The primary analysis was performed with the multiplicative random-effect inverse variance-weighted method, while multiple sensitivity analyses were conducted with the weighted median, weighted mode, MR-Egger, and MR-PRESSO. A total of 29 metabolites had suggestive evidence of causal associations with MS. Genetically instrumented levels of serine (OR = 1.56, 95% CI = 1.25-1.95), lysine (OR = 1.18, 95% CI = 1.01-1.38), acetone (OR = 2.45, 95% CI = 1.02-5.90), and acetoacetate (OR = 2.47, 95% CI = 1.14-5.34) were associated with a higher MS risk. Total cholesterol and phospholipids in large very-low-density lipoprotein were associated with a lower MS risk (OR = 0.83, 95% CI = 0.69-1.00; OR = 0.80, 95% CI = 0.68-0.95), but risk-increasing associations (OR = 1.20, 95% CI = 1.04-1.40; OR = 1.13, 95% CI = 1.00-1.28) were observed for the same two lipids in very large high-density lipoprotein. Our metabolome-wide Mendelian randomization study prioritized a list of circulating metabolites, such as serine, lysine, acetone, acetoacetate, and lipids, that likely have causal associations with MS.
 BACKGROUND: Natalizumab, a therapeutic antibody used to treat multiple sclerosis, undergoes in vivo Fab arm exchange to form a monovalent bispecific antibody. Although highly efficacious, the immunosuppressive activity of natalizumab has been associated with JC polyomavirus-driven progressive multifocal leukoencephalopathy (PML). Development of assays that can distinguish between and quantify bivalent (unexchanged) and monovalent (exchanged) forms of natalizumab in clinical samples may be useful for optimizing extended interval dosing and reducing the risk of PML. METHODS: In vitro natalizumab arm exchange was conducted, along with peptide mimotope and anti-idiotype surface capture chemistry, to enable the development of enzyme-linked immunosorbent assays. RESULTS: An assay using a unique peptide Veritope TM was developed, which can exclusively bind to bivalent natalizumab. In combination with enzyme-linked immunosorbent assays that quantifies total natalizumab, the assay system allows quantification of both natalizumab forms. CONCLUSIONS: In this article, a novel assay for the quantification of unexchanged and exchanged natalizumab variants in clinical samples was developed. This assay will enable investigations into the clinical significance of the relationship of PK/PD with the monovalent-to-bivalent ratio, as it relates to the efficacy of the drug and risk of PML.
 Multiple sclerosis (MS) is an autoimmune neurodegenerative disease. Since the modulation of the immune system by parasites has been proven, and there have been reports of a reduction in the clinical symptoms of MS in people with toxoplasmosis, this study aimed to investigate the effect of toxoplasmosis on MS in an animal model. MS model was induced by the ethidium bromide injection in the areas specified in the Rat's brain in the stereotaxic device and Toxoplasma gondii RH strain injection of the rat's peritoneal for creation of toxoplasmosis. The effect of acute and chronic toxoplasmosis on the MS model was evaluated by examining the development of clinical symptoms of MS, body weight, changes in the levels of inflammatory cytokines, inflammatory cell infiltration, cell density, and spongy tissue in the brain. The body weight in the acute toxoplasmosis with MS was the same as the MS group, and a significant decrease was observed, but no weight loss was observed in the chronic toxoplasmosis with MS. In the chronic toxoplasmosis, the progress of clinical signs such as Immobility of limbs, including tail, hands, and feet, was observed less compared to other groups. The histology results in the group of chronic toxoplasmosis showed high cell density and inhibition of spongy tissue formation, and the infiltration of inflammatory cells in this group was less. TNF-α and INF-γ decreased in MS with chronic toxoplasmosis compared to the MS group. Our findings showed that chronic toxoplasmosis with inhibition of spongy tissue formation and prevention of cell infiltration and. As a result, the reduction of inflammatory cytokines could reduce clinical symptoms in MS in the animal model.
 INTRODUCTION: Treatment with cladribine tablets is indicated in highly active relapsing-remitting multiple sclerosis (RRMS). Cladribine tablets proved safe and effective in the pivotal CLARITY trial, but that trial included primarily treatment-naïve patients. In clinical practice however, cladribine tablets are often given to patients who have failed other treatments. Therefore, this study investigated the real-world safety and efficacy of cladribine tablets. MATERIAL AND METHODS: We gathered data from nine MS clinical centres across Poland for patients with RRMS who started treatment with cladribine tablets from December 2019 to June 2022. RESULTS: We enrolled 140 patients, with follow-up data available for 136 in year 1 and for 66 in year 2. At baseline, the mean age was 35.6 years, mean disease duration was 7.3 years, median EDSS score was 2.5, and 94% of patients were treatment- -experienced. Thirty-nine patients (27.9%) had undergone COVID-19, and 94 (67.1%) were vaccinated against COVID-19. The annualised relapse rate (ARR) decreased from 1.49 at baseline to 0.33 in year 1 (p < 0.001) and to 0.25 in year 2 (p < 0.001). The percentage of relapse-free patients increased from 11.5% at baseline to 70.2% in year 1 and 82.1% in year 2. The percentage of patients with active lesions decreased from 91.4% at baseline to 36.2% in year 1 and 18.2% in year 2. EDSS score remained stable or improved in 83.7% of patients in year 1 and 89.6% in year 2. No evidence of disease activity (NEDA-3) was achieved in 42.7% of patients in year 1 and 66.7% in year 2. Only one patient (0.72%) had grade 4 lymphopenia and 21 (15.1%) had grade 3 lymphopenia. Varicella zoster virus infections occurred in three patients. Eight patients discontinued treatment with cladribine: five due to inefficacy, one due to lymphopenia, and two due to a personal decision. CONCLUSIONS: Cladribine tablets proved safe and effective in a real-world cohort of treatment-experienced patients. However, the efficacy measures improved to a lesser extent in our cohort than in the pivotal clinical trial, which is probably due to a higher proportion of treatment-experienced patients in our cohort.
 Multiple sclerosis is accompanied by decreased mobility and various adaptations affecting neural structure and function. Therefore, the purpose of this project was to understand how motor cortex thickness and corticospinal excitation and inhibition contribute to turning performance in healthy controls and people with multiple sclerosis. In total, 49 participants (23 controls, 26 multiple sclerosis) were included in the final analysis of this study. All participants were instructed to complete a series of turns while wearing wireless inertial sensors. Motor cortex gray matter thickness was measured via magnetic resonance imaging. Corticospinal excitation and inhibition were assessed via transcranial magnetic stimulation and electromyography place on the tibialis anterior muscles bilaterally. People with multiple sclerosis demonstrated reduced turning performance for a variety of turning variables. Further, we observed significant cortical thinning of the motor cortex in the multiple sclerosis group. People with multiple sclerosis demonstrated no significant reductions in excitatory neurotransmission, whereas a reduction in inhibitory activity was observed. Significant correlations were primarily observed in the multiple sclerosis group, demonstrating lateralization to the left hemisphere. The results showed that both cortical thickness and inhibitory activity were associated with turning performance in people with multiple sclerosis and may indicate that people with multiple sclerosis rely on different neural resources to perform dynamic movements typically associated with fall risk.

 Purpose The aim was to carry out a systematic review dedicated to describing the work barriers and the job adjustments that are particularly sensitive to people with Multiple Sclerosis (PwMS). Methods Four electronic databases (PubMed/MEDLINE, Scopus, SciVerse ScienceDirect, and Web of Science) were searched for peer-reviewed original articles reporting the barriers at work and/or the job adjustments used by PwMS. MS must have been diagnosed according to accepted international criteria at the time of the study and/or confirmed by a doctor. No time limits were set for the search. Articles that were published in English, Italian, Spanish, French, and Portuguese were accepted. Each article was screened by three experienced and trained investigators. The protocol was registered in PROSPERO (CRD42022299994). Results The initial systematic search yielded 104,228 results, of which 49 articles provided sufficient information and were considered suitable for inclusion in the study. Overall, the studies included 30283 participants with MS. Thirteen (27.1%) studies reported on barriers to work, 14 (29.2%) addressed reasonable adjustments and 21 (43.7%) assessed both outcomes. Job characteristics are the most important barriers for PwMS. Other reported barriers concern the work environment, social relationships at work, negative work events and lack of information. PwMS are more vulnerable to the need for adjustments at the workplace, being the management of the workload the most commonly used one. Conclusions PwMS are exposed to a wide variety of work barriers and job adjustments. Future studies are still highly encouraged on the topic.
 BACKGROUND AND OBJECTIVES: Antibodies to CD20 efficiently reduce new relapses in multiple sclerosis (MS), and ocrelizumab has been shown to be effective also in primary progressive MS. Although anti-CD20 treatments efficiently deplete B cells in blood, some B cells and CD20(-) plasma cells persist in lymphatic organs and the inflamed CNS; their survival is regulated by the B cell-activating factor (BAFF)/A proliferation-inducing ligand (APRIL) system. The administration of a soluble receptor for BAFF and APRIL, atacicept, unexpectedly worsened MS. Here, we explored the long-term effects of ocrelizumab on immune cell subsets as well as on cytokines and endogenous soluble receptors comprising the BAFF-APRIL system. METHODS: We analyzed immune cell subsets and B cell-regulating factors longitudinally for up to 2.5 years in patients with MS treated with ocrelizumab. In a second cohort, we determined B-cell regulatory factors in the CSF before and after ocrelizumab. We quantified the cytokines BAFF and APRIL along with their endogenous soluble receptors soluble B-cell maturation antigen (sBCMA) and soluble transmembrane activator and calcium-modulator and cyclophilin ligand (CAML) interactor (sTACI) using enzyme-linked immunosorbent assays (ELISAs). In addition, we established an in-house ELISA to measure sTACI-BAFF complexes. RESULTS: Ocrelizumab treatment of people with MS persistently depleted B cells and CD20(+) T cells. This treatment enhanced BAFF and reduced the free endogenous soluble receptor and decoy sTACI in both serum and CSF. Levels of sTACI negatively correlated with BAFF levels. Reduction of sTACI was associated with formation of sTACI-BAFF complexes. DISCUSSION: We describe a novel effect of anti-CD20 therapy on the BAFF-APRIL system, namely reduction of sTACI. Because sTACI is a decoy for APRIL, its reduction may enhance local APRIL activity, thereby promoting regulatory IgA(+) plasma cells and astrocytic interleukin (IL)-10 production. Thus, reducing sTACI might contribute to the beneficial effect of anti-CD20 as exogenous sTACI (atacicept) worsened MS. CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that endogenous sTACI in blood and CSF is decreased after ocrelizumab treatment.
 INTRODUCTION: On 4 and 5 November 2022, Madrid hosted the 15th edition of the Post-ECTRIMS Meeting, where neurologists specialised in multiple sclerosis outlined the latest developments presented at the 2022 ECTRIMS Congress, held in Amsterdam from 26 to 28 October. AIM: To synthesise the content presented at the 15th edition of the Post-ECTRIMS Meeting, in an article broken down into two parts. DEVELOPMENT: This second part describes the new developments in terms of therapeutic strategies for escalation and de-escalation of disease-modifying therapies (DMT), when and in whom to initiate or switch to highly effective DMT, the definition of therapeutic failure, the possibility of treating radiologically isolated syndrome and the future of personalised treatment and precision medicine. It also considers the efficacy and safety of autologous haematopoietic stem cell transplantation, different approaches in clinical trial design and outcome measures to assess DMT in progressive stages, challenges in the diagnosis and treatment of cognitive impairment, and treatment in special situations (pregnancy, comorbidity and the elderly). In addition, results from some of the latest studies with oral cladribine and evobrutinib presented at ECTRIMS 2022 are shown.
 Becoming unfit for work or losing one's job because of multiple sclerosis is not inevitable. Many tools are available and occupational health professionals are now specifically mandated to support workers, whether or not they are employees, in maintaining their jobs, thanks in particular to the prevention of professional displacement unit, the recommendations of the French National Authority for Health and better coordination.
 BACKGROUND: Memory disturbance is common in people with multiple sclerosis (pwMS). Currently, a range of memory rehabilitation approaches alone or as a component of cognitive rehabilitation is utilized clinically. OBJECTIVE: To evaluate the effectiveness of memory rehabilitation in improving health outcomes (memory, cognitive function, functional ability, quality of life) in pwMS. METHODS: A summary of the Cochrane Review "Memory rehabilitation for people with multiple sclerosis" by Taylor et al from a rehabilitation perspective. RESULTS: The review included 44 studies (with 2714 participants). The memory rehabilitation approaches varied amongst the included primary studies for memory retraining techniques (computerized programs, training using internal and external memory aids, etc.). Overall, the risk of bias amongst the included trials was low. The findings suggest high-certainty evidence for a beneficial effect of memory rehabilitation in improving subjective memory at intermediate- (1-6 months) and longer-term (> 6 months); and moderate-certainty evidence at immediate post-intervention. The evidence of the effect of memory rehabilitation on other outcomes showed mixed results. CONCLUSION: The evidence suggests some beneficial effects of memory rehabilitation in improving subjective memory and quality of life in pwMS. However, further evidence is required for the evaluation of memory strategies for other outcomes.

 At the age of 27, Jeanne woke up one morning blind in her left eye. It took almost a year for her to be diagnosed with multiple sclerosis (MS) and to receive proper treatment. She then had to adapt, rethink some of her life plans and go through different stages of the disease. Today, at the age of 45, she feels she is "surviving well". She tells us the story of her MS.
 BACKGROUND: In the general population, maternal SARS-CoV-2 infection during pregnancy is associated with worse maternal outcomes; however, only one study so far has evaluated COVID-19 clinical outcomes in pregnant and postpartum women with multiple sclerosis, showing no higher risk for poor COVID-19 outcomes in these patients. OBJECTIVE: In this multicenter study, we aimed to evaluate COVID-19 clinical outcomes in pregnant patients with multiple sclerosis. METHODS: We recruited 85 pregnant patients with multiple sclerosis who contracted COVID-19 after conception and were prospectively followed-up in Italian and Turkish Centers, in the period 2020-2022. A control group of 1354 women was extracted from the database of the Multiple Sclerosis and COVID-19 (MuSC-19). Univariate and subsequent logistic regression models were fitted to search for risk factors associated with severe COVID-19 course (at least one outcome among hospitalization, intensive care unit [ICU] admission and death). RESULTS: In the multivariable analysis, independent predictors of severe COVID-19 were age, body mass index ⩾ 30, treatment with anti-CD20 and recent use of methylprednisolone. Vaccination before infection was a protective factor. Vaccination before infection was a protective factor. Pregnancy was not a risk nor a protective factor for severe COVID-19 course. CONCLUSION: Our data show no significant increase of severe COVID-19 outcomes in patients with multiple sclerosis who contracted the infection during pregnancy.
 BACKGROUND: Primary progressive multiple sclerosis (PPMS) is the least prevalent multiple sclerosis (MS) phenotype. For persons with PPMS (pwPPMS), pharmacological treatment options are limited. As a complementary non-pharmacological treatment, endurance training improves the health-related quality of life (HRQoL), numerous MS symptoms, and MS-related performance impediments. High-intensity interval training (HIIT) has been shown to induce superior effects compared to moderate-intensity continuous training (MCT). As current evidence is based on MS samples with mixed phenotypes, generalizability to pwPPMS remains unclear. METHODS: CYPRO is a parallel-group, single-center, and single-blind randomized controlled superiority trial evaluating the effects of HIIT compared to MCT in pwPPMS. Sixty-one pwPPMS are randomized (1:1) to perform volume-matched HIIT or MCT sessions on bicycle ergometers two to three times per week in addition to standard rehabilitative care during their three-week inpatient stay at Valens rehabilitation clinic, Switzerland. Standard rehabilitative care comprises endurance and strength training, physiotherapy, and occupational therapy. HIIT sessions include six 90-second intervals at 95% peak heart rate (HR(peak)), interspersed by 90-second active breaks with unloaded pedaling, aimed to reach 60%HR(peak). MCT represents the standard treatment at Valens rehabilitation clinic and is performed as continuous cycling at 60%HR(peak) for the duration of 26 minutes. The primary outcome is cardiorespiratory fitness, assessed as peak oxygen consumption (V̇O(2peak)) during cardiopulmonary exercise testing (CPET). Secondary outcomes include peak power output during CPET, walking capacity, cognitive performance, HRQoL, fatigue, anxiety and depressive symptoms, and blood-derived biomarkers (e.g., serum neurofilament light chain, glial fibrillary acidic protein, kynurenine pathway metabolites) related to MS pathophysiology. All outcomes are assessed at baseline and discharge after three weeks. Venous blood sampling is additionally performed immediately and two hours after the first HIIT or MCT session. DISCUSSION: CYPRO will expand current knowledge on symptom management and rehabilitation in MS to the subpopulation of pwPPMS, and will contribute to the exploration of potential disease-modifying effects of endurance training in MS. The superiority design of CYPRO will allow deriving explicit recommendations on endurance training design in pwPPMS that can be readily translated into clinical practice. TRIAL REGISTRATION: CYPRO has been prospectively registered at ClinicalTrials.gov on 8 February 2022 (NCT05229861).
 BACKGROUND: Somatosensory evoked potentials (SSEP) are still broadly used, although not explicitly recommended, for the diagnostic work-up of suspected multiple sclerosis (MS). OBJECTIVE: To relate disability, SSEP, and lesions on T2-weighted magnetic resonance imaging (MRI) in patients with early MS. METHODS: In this monocentric retrospective study, we analyzed a cohort of patients with relapsing-remitting MS or clinically isolated syndrome, with a maximum disease duration of two years, as well as with available data on the score at the expanded disability status scale (EDSS), on SSEP, on whole spinal cord (SC) MRI, and on brain MRI. RESULTS: Complete data of 161 patients were available. Tibial nerve SSEP (tSSEP) were less frequently abnormal than SC MRI (22% vs. 68%, p < 0.001). However, higher EDSS scores were significantly associated with abnormal tSSEP (median, 2.0 vs. 1.0; p = 0.001) but not with abnormal SC MRI (i.e., at least one lesion; median, 1.5 vs. 1.5; p = 0.7). Of the 35 patients with abnormal tSSEP, 32 had lesions on SC MRI, and 2 had corresponding lesions on brain MRI. CONCLUSION: Compared to tSSEP, SC MRI is the more sensitive diagnostic biomarker regarding SC involvement. In early MS, lesions as detectable by T2-weighted MRI are the main driver of abnormal tSSEP. However, tSSEP were more closely associated with disability, which is compatible with a potential role of tSSEP as prognostic biomarker in complementation of MRI.
 BACKGROUND: With the new highly active drugs available for people with multiple sclerosis (pwMS), vaccination becomes an essential part of the risk management strategy. OBJECTIVE: To develop a European evidence-based consensus for the vaccination strategy of pwMS who are candidates for disease-modifying therapies (DMTs). METHODS: This work was conducted by a multidisciplinary working group using formal consensus methodology. Clinical questions (defined as population, interventions, and outcomes) considered all authorized DMTs and vaccines. A systematic literature search was conducted and quality of evidence was defined according to the Oxford Centre for Evidence-Based Medicine Levels of Evidence. The recommendations were formulated based on the quality of evidence and the risk-benefit balance. RESULTS: Seven questions, encompassing vaccine safety, vaccine effectiveness, global vaccination strategy and vaccination in sub-populations (pediatric, pregnant women, elderly and international travelers) were considered. A narrative description of the evidence considering published studies, guidelines, and position statements is presented. A total of 53 recommendations were agreed by the working group after three rounds of consensus. CONCLUSION: This first European consensus on vaccination in pwMS proposes the best vaccination strategy according to current evidence and expert knowledge, with the goal of homogenizing the immunization practices in pwMS.
 BACKGROUND: Intrathecal immunoglobulin-G synthesis is a hallmark of multiple sclerosis (MS), which can be detected by oligoclonal IgG bands (OCB) or by κ-free light chains (κ-FLC) in cerebrospinal fluid. OBJECTIVE: To perform a systematic review and meta-analysis to evaluate whether κ-FLC index has similar diagnostic value to identify patients with clinically isolated syndrome (CIS) or MS compared to OCB, and to determine κ-FLC index cut-off. METHODS: PubMed was searched for studies that assessed diagnostic sensitivity and specificity of κ-FLC index and OCB to discriminate CIS/MS patients from control subjects. Two reviewers following preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines performed study eligibility assessment and data extraction. Findings from studies were analyzed with bivariate mixed models. RESULTS: A total of 32 studies were included in the meta-analysis to evaluate diagnostic value of κ-FLC index. Sensitivity and specificity ranged from 52% to 100% (weighted average: 88%) and 69% to 100% (89%) for κ-FLC index and from 37% to 100% (85%) and 74% to 100% (92%) for OCB. Mean difference of sensitivity and specificity between κ-FLC index and OCB was 2 and -4 percentage points. Diagnostic accuracy determined by mixed models revealed no significant difference between κ-FLC index and OCB. A discriminatory cut-off for κ-FLC index was determined at 6.1. CONCLUSION: The findings indicate that κ-FLC index has similar diagnostic accuracy in MS as OCB.
 BACKGROUND: Though there are several disease-modifying therapy (DMT) options for patients with multiple sclerosis (MS), treatment outcomes rely on patient adherence and persistence. Previous studies have demonstrated suboptimal adherence rates and high rates of early treatment discontinuation. Health-system specialty pharmacies (HSPPs) are a growing practice model that have demonstrated adherence and persistence benefits through single site evaluations. Research is needed across multiple HSSPs to understand and validate the outcomes of this practice model. METHODS: A multisite prospective cohort study was performed including patients with at least three fills of a DMT between January 2020 and June 2021 at an HSSP. Patients were excluded due to pregnancy or death. Enrollment occurred for 6 months followed by 12 months of follow-up. Adherence was measured using pharmacy claims to calculate proportion of days covered (PDC) during the follow-up period. Time to non-persistence was calculated as the time from an index DMT fill to the first date of a gap of >60 days between medication exhaust and fulfillment dates. Adherence and persistence calculations were assessed at the therapeutic class level (any self-administered DMT dispensed by the HSSPs). The Kaplan-Meier method was used to present the probability of being persistent, and Cox proportional hazards regression analysis was used to estimate hazard ratios of factors associated with non-persistence, which included age, sex, study site, insurance type, and whether the patient switched medication as potential factors. RESULTS: The most common self-administered DMTs filled among 968 patients were glatiramer acetate (32%), fingolimod (18%), and dimethyl fumarate (18%). Most patients (96%) did not switch DMT during the study period. The median PDC was 0.97 (interquartile range 0.90-0.99), which was similar across all sites. Patients who had at least one DMT switch were 76% less likely to have a higher PDC than those who did not have any switch after adjusting for other covariates (Odds ratio: 0.24, 95% confidence interval [CI]: 0.14-0.40, p<0.001). Most patients (86%) were persistent to DMT over the 12-month study period. Among those non-persistent, median time to non-persistence was 231 (IQR 177-301) days. Patients who switched medications were 2.4 times more likely to be non-persistent (95% CI: 1.3 - 4.5, p = 0.005). The most common reasons for non-persistence were discontinuation/medication held for an extended period (30%), often due to patient or prescriber decision (75%). CONCLUSION: High rates of DMT adherence and persistence were seen among patients serviced by HSSPs, indicating potential benefits of this model for patients with MS. Switching DMTs was associated with lower adherence and persistence and may be an opportunity for added care coordination or resources to optimize therapy transitions.
 INTRODUCTION: Osteopontin (OPN) is involved in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). The aim of this study was to investigate the expression of OPN in spinal cords of mice in the successive phases of EAE, to compare it with the density of inflammatory cells, oligodendrocytes and with the expression of interleukin (IL)-17A and to assess the effect of anti-α4β1 integrin (VLA-4) treatment. MATERIAL AND METHODS: Experimental autoimmune encephalomyelitis (EAE) mice were injected with anti-VLA-4 antibodies or, as treatment control, with immunoglobulin G (IgG). Spinal cords were sectioned and immunostained for OPN, CD45 (overall leukocytes), CD3 (T cells), Iba1 (activated macrophages/microglia), IL-17A, and CNP1 (oligodendrocytes). Microscopic images were analysed and the percentage of immunopositive areas encompassing the whole spinal cord cross-sectional area were assessed in images for each antigen. RESULTS: Osteopontin was expressed by inflammatory cells and by a minority of neurons and blood vessels. Most of the studied parameters followed the temporal pattern of clinical scores: increase in the peak phase and decrease in the chronic phase. Only OPN and IL-17A remained at a high level in the chronic phase, while CNP1 expression gradually decreased in the successive phases. Anti-VLA-4 treatment lowered the expression of the studied antigens in the peak and chronic phases with the exception of oligodendrocyte marker CNP1 which in both phases showed an increased expression. CONCLUSIONS: Involvement of OPN is particularly significant in advanced EAE. Anti-VLA-4 treatment not only inhibits migration of myelin-reactive T cells, but also downregulates OPN and inhibits loss of oligodendrocytes.
 BACKGROUND: Familial Mediterranean Fever (FMF) is associated with increased risk of multiple sclerosis (MS). Optimal treatment of patients with comorbid FMF and MS remains uncertain. CASE: A 28-year-old woman with FMF, treated with colchicine, had symptomatic onset of relapsing remitting MS following four simultaneous vaccines. MRI brain with a 7-Tesla magnet demonstrated several areas of leptomeningeal enhancement with predominant linear, spread/fill and rare nodular patterns. Central vein signs were present in supratentorial white matter lesions. She received four cycles of ocrelizumab and achieved no evidence of disease activity (NEDA-3) at 20 months' follow up. DISCUSSION: FMF with incident CNS demyelinating disease demonstrated neuroimaging features typical for classic RRMS including the central vein sign and leptomeningeal enhancement. Treatment with B-cell depleting therapy for FMF-MS led to clinical stability and symptomatic improvement at 20 months' follow up. We add to the sparse literature characterizing the course of FMF as a genetic risk factor for CNS demyelinating disease, demonstrating pathognomonic imaging features of MS on 7 T imaging and treatment efficacy with B-cell depletion.
 Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease of the central nervous system (CNS) that often progresses to severe disability. Previous studies have highlighted the role of T cells in disease pathophysiology; however, the success of B-cell-targeted therapies has led to an increased interest in how B cells contribute to disease immunopathology. In this review, we summarize evidence of B-cell involvement in MS disease mechanisms, starting with pathology and moving on to review aspects of B cell immunobiology potentially relevant to MS. We describe current theories of critical B cell contributions to the inflammatory CNS milieu in MS, namely (i) production of autoantibodies, (ii) antigen presentation, (iii) production of proinflammatory cytokines (bystander activation), and (iv) EBV involvement. In the second part of the review, we summarize medications that have targeted B cells in patients with MS and their current position in the therapeutic armamentarium based on clinical trials and real-world data. Covered therapeutic strategies include the targeting of surface molecules such as CD20 (rituximab, ocrelizumab, ofatumumab, ublituximab) and CD19 (inebilizumab), and molecules necessary for B-cell activation such as B cell activating factor (BAFF) (belimumab) and Bruton's Tyrosine Kinase (BTK) (evobrutinib). We finally discuss the use of B-cell-targeted therapeutics in pregnancy.
 BACKGROUND: The Multiple Sclerosis Quality of Life-54 (MSQOL-54) is one of the most commonly-used MS-specific health-related quality of life (HRQOL) measures. It is a multidimensional, MS-specific HRQOL inventory, which includes the generic SF-36 core items, supplemented with 18 MS-targeted items. Availability of an adaptive short version providing immediate item scoring may improve instrument usability and validity. However, multidimensional computerized adaptive testing (MCAT) has not been previously applied to MSQOL-54 items. We thus aimed to apply MCAT to the MSQOL-54 and assess its performance. METHODS: Responses from a large international sample of 3669 MS patients were assessed. We calibrated 52 (of the 54) items using bifactor graded response model (10 group factors and one general HRQOL factor). Then, eight simulations were run with different termination criteria: standard errors (SE) for the general factor and group factors set to different values, and change in factor estimates from one item to the next set at < 0.01 for both the general and the group factors. Performance of the MCAT was assessed by the number of administered items, root mean square difference (RMSD), and correlation. RESULTS: Eight items were removed due to local dependency. The simulation with SE set to 0.32 (general factor), and no SE thresholds (group factors) provided satisfactory performance: the median number of administered items was 24, RMSD was 0.32, and correlation was 0.94. CONCLUSIONS: Compared to the full-length MSQOL-54, the simulated MCAT required fewer items without losing precision for the general HRQOL factor. Further work is needed to add/integrate/revise MSQOL-54 items in order to make the calibration and MCAT performance efficient also on group factors, so that the MCAT version may be used in clinical practice and research.
 BACKGROUND: Epstein-Barr Virus (EBV) is strongly associated with multiple sclerosis (MS). After initial infection, EBV maintains a life-long latent infection in B lymphocytes. Depletion of B lymphocytes from the blood with the anti-CD20 antibody ocrelizumab (OCR) markedly reduces disease activity in MS. Our objective was to measure the effect of OCR treatment on the antibody response to EBV and human antigens that are cross-reactive with EBV. METHODS: Blood was collected from MS patients before and during OCR treatment. Antibodies to three EBV antigens (EBNA-1, BFRF3, and gp350) and three human proteins that are cross-reactive with EBV (septin-9, DLST, and HNRNPL) were quantified with Western blots. Antibodies to EBNA-1 and BFRF3 were also quantified with ELISA. RESULTS: Antibodies to the EBV proteins BFRF3 and EBNA-1 measured on Western blot were significantly decreased after 12 months on OCR. Subsequent testing with ELISA confirmed the decrease for both BFRF3 and EBNA-1. With Western blots, there was a trend to decreased antibody response to septin-9 and DLST, but not HNRNPL. Total IgG concentration did not change. CONCLUSION: The antibody response to some EBV antigens decreases in OCR treated patients. The benefit of OCR for MS may be through removal of EBV antigenic stimulus.
 OBJECTIVE: Evaluate the effect of subcutaneous interferon β-1a (sc IFN β-1a) versus placebo on the evolution of T1-weighted MRI lesions and central brain atrophy in in patients with a first clinical demyelinating event (FCDE). METHODS: Post hoc analysis of baseline-to-24 month MRI data from patients with an FCDE who received sc IFN β-1a 44 μg once- (qw) or three-times-weekly (tiw), or placebo, in REFLEX. Patients were grouped according to treatment regimen or conversion to clinically definite MS (CDMS) status. The intensity of new lesions on unenhanced T1-weighted images was classified as T1 iso- or hypo-intense (black holes) and percentage ventricular volume change (PVVC) was assessed throughout the study. RESULTS: In patients not converting to CDMS, sc IFN β-1a tiw or qw, versus placebo, reduced the overall number of new lesions (P < 0.001 and P = 0.005) and new T1 iso-intense lesions (P < 0.001 and P = 0.002) after 24 months; only sc IFN β-1a tiw was associated with fewer T1 hypo-intense lesions versus placebo (P < 0.001). PVVC findings in patients treated with sc IFN β-1a suggested pseudo-atrophy that was ~ fivefold greater versus placebo in the first year of treatment (placebo 1.11%; qw 4.28%; tiw 6.76%; P < 001); similar findings were apparent for non-converting patients. CONCLUSIONS: In patients with an FCDE, treatment with sc IFN β-1a tiw for 24 months reduced the number of new lesions evolving into black holes.
 Resilience; Progressive multiple sclerosis; Genomics.
 BACKGROUND: Some studies comparing primary and secondary progressive multiple sclerosis (PPMS, SPMS) report similar ages at onset of the progressive phase and similar rates of subsequent disability accrual. Others report later onset and/or faster accrual in SPMS. Comparisons have been complicated by regional cohort effects, phenotypic differences in sex ratio and management and variable diagnostic criteria for SPMS. METHODS: We compared disability accrual in PPMS and operationally diagnosed SPMS in the international, clinic-based MSBase cohort. Inclusion required PPMS or SPMS with onset at age ≥18 years since 1995. We estimated Andersen-Gill hazard ratios for disability accrual on the Expanded Disability Status Scale (EDSS), adjusted for sex, age, baseline disability, EDSS score frequency and drug therapies, with centre and patient as random effects. We also estimated ages at onset of the progressive phase (Kaplan-Meier) and at EDSS milestones (Turnbull). Analyses were replicated with physician-diagnosed SPMS. RESULTS: Included patients comprised 1872 with PPMS (47% men; 50% with activity) and 2575 with SPMS (32% men; 40% with activity). Relative to PPMS, SPMS had older age at onset of the progressive phase (median 46.7 years (95% CI 46.2-47.3) vs 43.9 (43.3-44.4); p<0.001), greater baseline disability, slower disability accrual (HR 0.86 (0.78-0.94); p<0.001) and similar age at wheelchair dependence. CONCLUSIONS: We demonstrate later onset of the progressive phase and slower disability accrual in SPMS versus PPMS. This may balance greater baseline disability in SPMS, yielding convergent disability trajectories across phenotypes. The different rates of disability accrual should be considered before amalgamating PPMS and SPMS in clinical trials.
 BACKGROUND: Chronic fatigue is a significant symptom in several diseases including traumatic and degenerative neurological disorders. While several studies have investigated the correlates of chronic fatigue, there is as yet no unifying framework to explain chronic fatigue. METHODS: In this narrative review, I investigate the role of selective attention in the development of chronic fatigue and discuss results within the framework of the sensory attenuation model of fatigue, which posits that fatigue is the phenomenological output of altered attention to sensory input. Following a short introduction of this framework, I present results from investigations that address attentional mechanisms in fatigue in multiple sclerosis, stroke, traumatic brain injury and Parkinson's disease. RESULTS: Attention was quantified in all four disease models using a variety of outcome measures, including behavioural, neurophysiological, structural and functional brain connectivity. The range of measures precluded direct comparison of results across disease conditions; however, in all four disease models there was evidence of poor selective attention that explained levels of chronic fatigue, supporting the sensory attenuation model of fatigue as a disease-independent mechanism of fatigue. Evidence was lacking to draw any conclusions about the direction of causality. CONCLUSION: The role of selective attention in development of fatigue is indicated. Future studies must focus on establishing causality and exploring attentional circuitry as a potential therapeutic target.
 BACKGROUND AND OBJECTIVE: Nearly 40-65% patients with MS develop cognitive impairment during the disease. There is no treatment clearly effective in improving the cognitive deficits. To evaluate the efficacy and safety of Rivastigmine in cognitively impaired MS patients. MATERIALS AND METHODS: This was a parallel group randomized open label study with blinded end-point assessment. The patient allocation to treatment and control arm was done by telephonic contact with an independent statistician who used a computer to generate a random sequence of allocation using permuted block randomization (varying block size of 4 and 6) in 1:1 ratio. The outcome assessor was blinded to this allocation. A total of 60 patients were in included in the study (30 in each arm). Primary outcome was improvement in memory functions (using logical memory subset of Wechsler Memory Scale III, India) assessed after 12 weeks. Secondary outcomes included fatigue, depression, and safety. RESULTS: In modified intention to treat analysis (N = 22), treatment arm showed statistically significant improvement in memory function with mean difference of 7.56 [95% CI (0.67,14.46), p 0.032] as compared to control arm. There was no statistically significant difference in outcomes such as fatigue and depression. Vomiting was the most common side effect. No major adverse events were observed in either group. CONCLUSION: Rivastigmine is safe and effective in improving memory functions in cognitively impaired MS patients. However, our study has a small sample size and tested only a single domain. Larger studies with a validated single comprehensive neuropsychological test are needed.
 Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease associated with axonal injury, and neurofilament light chains in serum (sNfL) are considered a biomarker for this damage. We aimed to investigate the relationship between sNfL and the axonal damage in early MS lesions in a special cohort of biopsied patients. sNfL from 106 biopsied patients with 26 follow-up samples were analyzed using single-molecule array (SiMoA) technology. Findings were correlated with clinical parameters and histological findings of acute axonal damage (APP-positive spheroids) and axonal loss in different lesion stages. A median of 59 pg/ml sNfL was found (range 8-3101 pg/ml). sNfL levels correlated with APP-positive spheroids in early active demyelinating lesions that represent the earliest lesion stages (p < 0.01). A significant negative correlation between sNfL levels in follow-up blood samples and axonal density in normal-appearing white matter was also observed (p = 0.02). sNfL levels correlated with the Expanded Disability Status Score at biopsy (p < 0.01, r = 0.49) and at last clinical follow-up (p < 0.01, r = 0.66). In conclusion, sNfL likely represent a compound measure of recent and ongoing neuroaxonal damage. We found that sNfL in biopsied MS patients correlate with acute axonal damage in the earliest MS lesion stages. Determination of sNfL levels thus allows insight into brain pathology and underlines the relevance of relapse-associated lesional pathology. Axonal loss in normal-appearing white matter contributes to sNfL levels independent of relapses. Since sNfL levels correlate with clinical disability, they may predict the future disability of patients and help with individual treatment decisions.
 Multiple sclerosis (MS) is a disabling neurodegenerative disease that causes demyelination and axonal degeneration of the central nervous system. Current treatments are partially effective in managing MS relapses and have a negligible impact on treating MS cognitive deficits and cannot enhance neuronal remyelination, imposing a need for a new MS remedy. Semaglutide, a novel glucagon-like peptide-1 agonist, has recently displayed a neuroprotective effect on several neurodegenerative diseases, suggesting that it may have a protective effect in MS. Therefore, this study was conducted to investigate the influence of semaglutide on experimental autoimmune encephalomyelitis (EAE)-induced MS in mice. Here, EAE was induced in mice using spinal cord homogenate, which eventually altered the mice's cognitive and motor functions, similar to what is observed in MS. Interestingly, intraperitoneally administered semaglutide (25 nmol/kg/day) amended EAE-induced cognitive and motor deficits observed in novel object recognition, open field, rotarod, and grip strength tests. Moreover, histological examination revealed that semaglutide treatment attenuated hippocampal damage and corpus callosum demyelination caused by EAE. Additionally, biochemical testing revealed that semaglutide activates the PI3K/Akt axis, which eventually hampers GSK-3β activity. GSK-3β activity inhibition attenuates demyelination and triggers remyelination through CREB/BDNF; furthermore, it boosts Nrf2 and SOD levels, protecting the mice from EAE-induced oxidative stress. Additionally, GSK-3β inhibition minimizes neuroinflammation, as reflected by decreased NF-kβ and TNF-α levels. In conclusion, semaglutide has a neuroprotective effect in EAE-induced MS in mice, which is mediated by activating the ramified PI3K/Akt/GSK-3β pathway.
 BACKGROUND: The application of neuroprotective agents in combination with stem cells is considered a potential effective treatment for multiple sclerosis (MS). Therefore, the effects of lithium chloride as a neuroprotective agent and a GSK3-β inhibitor were evaluated in combination with human adipose derived stem cells on re-myelination, oligodendrocyte differentiation, and functional recovery. METHODS: After inducing a mouse model of MS and proving it by the hanging wire test, the mice were randomly assigned to five experimental groups: Cup, Sham, Li, hADSC, and Li + hADSC. Additionally, a control group with normal feeding was considered. Finally, toluidine blue staining was carried out to estimate the level of myelination. Furthermore, immunofluorescent staining was used to evaluate the mean of OLIG2 and MOG positive cells. The mRNA levels of β-Catenin, myelin and oligodendrocyte specific genes were determined via the Real-Time PCR. RESULTS: The results of the hanging wire test and toluidine blue staining showed a significant increase in myelin density and improvements in motor function in groups, which received lithium and stem cells, particularly in the Li + hADSC group compared with the untreated groups (P < 0.01). Moreover, immunostaining results indicated that the mean percentages of MOG and OLIG2 positive cells were significantly higher in the Li + hADSC group than in the other groups (P < 0.01). Finally, gene expression studies indicated that the use of lithium could increase the expression of β-Catenin, myelin and oligodendrocyte specific genes. CONCLUSION: The use of Lithium Chloride can increase stem cells differentiation into oligodendrocytes and improve re-myelination in MS.
 Many patients with multiple sclerosis (MS) experience information processing speed (IPS) deficits, and the Symbol Digit Modalities Test (SDMT) has been recommended as a valid screening test. Magnetic resonance imaging (MRI) has markedly improved the understanding of the mechanisms associated with cognitive deficits in MS. However, which structural MRI markers are the most closely related to cognitive performance is still unclear. We used the multicenter 3T-MRI data set of the Italian Neuroimaging Network Initiative to extract multimodal data (i.e., demographic, clinical, neuropsychological, and structural MRIs) of 540 MS patients. We aimed to assess, through machine learning techniques, the contribution of brain MRI structural volumes in the prediction of IPS deficits when combined with demographic and clinical features. We trained and tested the eXtreme Gradient Boosting (XGBoost) model following a rigorous validation scheme to obtain reliable generalization performance. We carried out a classification and a regression task based on SDMT scores feeding each model with different combinations of features. For the classification task, the model trained with thalamus, cortical gray matter, hippocampus, and lesions volumes achieved an area under the receiver operating characteristic curve of 0.74. For the regression task, the model trained with cortical gray matter and thalamus volumes, EDSS, nucleus accumbens, lesions, and putamen volumes, and age reached a mean absolute error of 0.95. In conclusion, our results confirmed that damage to cortical gray matter and relevant deep and archaic gray matter structures, such as the thalamus and hippocampus, is among the most relevant predictors of cognitive performance in MS.
 BACKGROUND: Pediatric-onset multiple sclerosis (POMS) accounts for 3 to 10% of all MS diagnoses. POMS is usually characterized by prominent disease activity, and patients are at higher risk of developing physical disability and cognitive impairment. OBJECTIVE: This article characterizes a cohort of POMS patients followed at the pediatric neurology unit of a Portuguese tertiary hospital. METHODS: Retrospective observational study. Clinical records of all patients with POMS between 2011 and 2020 were revised. RESULTS: A total of 21 patients, with a female:male ratio of 11:10 and a mean age of onset of 14.8 years were included. Clinical manifestations at presentation included myelitis in eight patients (two with associated brainstem syndrome), optic neuritis in six (one with associated cerebellar syndrome), supratentorial symptoms in four, and isolated brainstem syndrome in two. Twenty patients had oligoclonal immunoglobulin G bands in cerebrospinal fluid. Supra- and infratentorial involvement was identified in the first brain magnetic resonance imaging of nine patients. Initial relapses were treated with intravenous steroids in 19 patients. The mean time for diagnosis was 2.8 months. Eleven patients were on first-line treatment (nine on β-interferon, two on teriflunomide) and 10 on second-line treatment (six on natalizumab, three on fingolimod, one on ocrelizumab). The mean annual relapse rate was 0.29 (range, 0.01-3), and the median Expanded Disability Status Scale was 1. Four patients reported learning disabilities and/or cognitive deficits. CONCLUSION: About half of patients in this cohort were on second-line disease-modifying treatment, with 19% showing cognitive impairment. Efforts to establish an early diagnosis are crucial to improving these patients' outcomes.
 Cerebrospinal fluid (CSF) analysis is of utmost importance for diagnosis and differential diagnosis of patients with suspected multiple sclerosis (MS). Evidence of intrathecal immunoglobulin G (IgG) synthesis proves the inflammatory nature of the disease, increases diagnostic certainty and substitutes for dissemination in time according to current diagnostic criteria. The gold standard to determine intrathecal IgG synthesis is the detection of CSF-restricted oligoclonal bands (OCBs). However, advances in laboratory methods brought up κ-free light chains (FLCs) as a new biomarker, which are produced in excess over intact immunoglobulins and accumulate in CSF in the case of central nervous system-derived inflammation. Overwhelming evidence showed a high diagnostic accuracy of intrathecal κ-FLC synthesis in MS with sensitivity and specificity of approximately 90% similar to OCB. κ-FLCs have advantages as its detection is fast, easy, cost-effective, reliable, rater-independent and returning quantitative results which might also improve the value of predicting MS disease activity. An international panel of experts in MS and CSF diagnostics developed a consensus of all participants. Six recommendations are given for establishing standard CSF evaluation in patients suspected of having MS. The panel recommended to include intrathecal κ-FLC synthesis in the next revision of MS diagnostic criteria as an additional tool to measure intrathecal immunoglobulin synthesis.
 BACKGROUND: Few reports have examined the feasibility of a post-contrast double inversion recovery (DIR) magnetic resonance (MR) sequence in patients with multiple sclerosis (MS) because of partial or complete signal loss of enhancing MS lesions. PURPOSE: To compare subtracted images of DIR (pre-contrast - post-contrast DIR images) with contrast enhanced T1-weighted (CE-T1W) images in the depiction of contrast enhancement of MS lesions. MATERIAL AND METHODS: In total, 27 patients were included. Two neuroradiologists interpreted both images of CE-T1W imaging and subtracted DIR, and interpretation of the images was classified into a score of 1-5 (from 5, definitely superior contrast of lesions on DIR subtraction compared to conventional CE-T1W imaging, to 1, definitely superior contrast of lesions on CE-T1W imaging. The interrater agreement (κ coefficient) was measured. The signal-to-noise ratio (SNR) and contrast-noise-ratio (CNR) of the lesion were compared. RESULTS: A significant difference (P < 0.001) in scoring was seen between conventional CE-T1W imaging (2.1 ± 1.5 with one reviewer and 2.4 ± 1.5 with the other) and DIR subtraction (4.4 ± 1.0 with one reviewer and 4.7 ± 0.8 with the other). SNR from conventional CE-T1W imaging (24.8 ± 14.7) was significantly superior to that from DIR subtraction (4.0 ± 1.0; P < 0.001). CNR in DIR subtraction (326.4 ± 250.0) was significantly superior to that in conventional CE-T1W imaging (0.8 ± 5.5; P < 0.001). For interrater agreement in the evaluation of contrast enhancement of the lesions, κ coefficients were 0.84 for conventional CE-T1W imaging and 0.72 for DIR subtraction. CONCLUSION: Subtracted DIR image enables more obvious contrast enhancement of the MS lesions compared with conventional CE-T1W imaging.
 Multiple sclerosis (MS) is an incurable autoimmune disease and is currently treated by systemic immunosuppressants with off-target side effects. Although aberrant myeloid function is often observed in MS plaques in the central nervous system (CNS), the role of myeloid cells in therapeutic intervention is currently overlooked. Here, we developed a myeloid cell-based strategy to reduce the disease burden in experimental autoimmune encephalomyelitis (EAE), a mouse model of progressive MS. We developed monocyte-adhered microparticles ("backpacks") for activating myeloid cell phenotype to an anti-inflammatory state through localized interleukin-4 and dexamethasone signals. We demonstrate that backpack-laden monocytes infiltrated into the inflamed CNS and modulated both the local and systemic immune responses. Within the CNS, backpack-carrying monocytes regulated both the infiltrating and tissue-resident myeloid cell compartments in the spinal cord for functions related to antigen presentation and reactive species production. Treatment with backpack-monocytes also decreased the level of systemic pro-inflammatory cytokines. Additionally, backpack-laden monocytes induced modulatory effects on T(H)1 and T(H)17 populations in the spinal cord and blood, demonstrating cross talk between the myeloid and lymphoid arms of disease. Backpack-carrying monocytes conferred therapeutic benefit in EAE mice, as quantified by improved motor function. The use of backpack-laden monocytes offers an antigen-free, biomaterial-based approach to precisely tune cell phenotype in vivo, demonstrating the utility of myeloid cells as a therapeutic modality and target.
 Multiple sclerosis (MS) is a chronic progressive disabling disease of the central nervous system (CNS) characterized by demyelination and neuronal injury. Dyslipidemia is observed as one of the imperative risk factors involved in MS neuropathology. Also, chronic inflammation in MS predisposes to the progress of dyslipidemia. Therefore, treatment of dyslipidemia in MS by statins may attenuate dyslipidemia-induced MS and avert MS-induced metabolic changes. Therefore, the present review aimed to elucidate the possible effects of statins on the pathogenesis and outcomes of MS. Statins adversely affect the cognitive function in MS by decreasing brain cholesterol CoQ10, which is necessary for the regulation of neuronal mitochondrial function. However, statins could be beneficial in MS by shifting the immune response from pro-inflammatory Th17 to an anti-inflammatory regulatory T cell (Treg). The protective effect of statins against MS is related to anti-inflammatory and immunomodulatory effects with modulation of fibrinogen and growth factors. In conclusion, the effects of statins on MS neuropathology seem to be conflicting, as statins seem to be protective in the acute phase of MS through anti-inflammatory and antioxidant effects. However, statins lead to detrimental effects in the chronic phase of MS by reducing brain cholesterol and inhibiting the remyelination process.
 BACKGROUND: The relapsing-remitting multiple sclerosis (RRMS) is the most common type of MS with prevalence rate 20-60 patients/100.000 individuals in Egypt. Poor postural control and cognitive dysfunctions are well-established complications of RRMS without potent remedy yet. The latest evidence highlighted the potential and independent immune-modulating effects of vitamin D(3) and ultraviolet radiation in the management of RRMS. OBJECTIVE: To investigate the efficacy of broadband ultraviolet B radiation (UVBR) versus moderate loading dose of vitamin D(3) supplementation in improving postural control and cognitive functions. DESIGN: Pretest-posttest randomized controlled study. SETTING: Multiple sclerosis outpatient unit of Kasr Al-Ainy Hospital. PARTICIPANTS: Forty-seven patients with RRMS were recruited from both genders, yet only 40 completed the study. INTERVENTIONS: Patients were randomized into two groups: UVBR group involved 24 patients, received sessions for 4 weeks and vitamin D(3) group involved 23 patients, took vitamin D(3) supplementation (50 000 IU/week) for 12 weeks. MAIN OUTCOME MEASURES: Overall balance system index (OSI) and symbol digit modalities test (SDMT). RESULTS: Highly significant decrease (P < 0.001) of the OSI in both groups post-treatment, indicating improved postural control. Moreover, highly significant improvement in the SDMT scores was noted, indicating information processing speed enhancement. Nonetheless, no statistically significant (P ≥ 0.05) differences were evident between the two groups post-treatment in all tested measures. CONCLUSION: Both therapeutic programs were statistically equal in improving postural control and cognitive functions. However, clinically, UVBR therapy was more convenient owing to its shorter treatment time and higher percentage of change for all tested measures.
 BACKGROUND: A study was undertaken to evaluate remote monitoring via smartphone sensor-based tests in people with multiple sclerosis (PwMS). This analysis aimed to explore regional neural correlates of digital measures derived from these tests. METHODS: In a 24-week, non-randomized, interventional, feasibility study (NCT02952911), sensor-based tests on the Floodlight Proof-of-Concept app were used to assess cognition (smartphone-based electronic Symbol Digit Modalities Test), upper extremity function (Draw a Shape Test, Pinching Test), and gait and balance (Static Balance Test, Two-Minute Walk Test, U-Turn Test). In this post-hoc analysis, digital measures and standard clinical measures (e.g., Nine-Hole Peg Test [9HPT]) were correlated against regional structural magnetic resonance imaging outcomes. Seventy-six PwMS aged 18-55 years with an Expanded Disability Status Scale score of 0.0-5.5 were enrolled from two different sites (USA and Spain). Sixty-two PwMS were included in this analysis. RESULTS: Worse performance on digital and clinical measures was associated with smaller regional brain volumes and larger ventricular volumes. Whereas digital and clinical measures had many neural correlates in common (e.g., putamen, globus pallidus, caudate nucleus, lateral occipital cortex), some were observed only for digital measures. For example, Draw a Shape Test and Pinching Test measures, but not 9HPT score, correlated with volume of the hippocampus (r = 0.37 [drawing accuracy over time on the Draw a Shape Test]/ - 0.45 [touching asynchrony on the Pinching Test]), thalamus (r = 0.38/ - 0.41), and pons (r = 0.35/ - 0.35). CONCLUSIONS: Multiple neural correlates were identified for the digital measures in a cohort of people with early MS. Digital measures showed associations with brain regions that clinical measures were unable to demonstrate, thus providing potential novel information on functional ability compared with standard clinical assessments.
 BACKGROUND: It is unclear which patients with multiple sclerosis (MS) are most susceptible for omicron breakthrough infections. METHODS: We assessed omicron breakthrough infections in vaccinated patients with MS with and without disease-modifying therapies enrolled in an ongoing large prospective study. We longitudinally studied humoral responses after primary and booster vaccinations and breakthrough infections. RESULTS: Omicron breakthrough infections were reported in 110/312 (36%) patients with MS, and in 105/110 (96%) infections were mild. Omicron breakthrough infections occurred more frequently in patients treated with anti-CD20 therapies and sphingosine-1 phosphate receptor (S1PR) modulators, patients with impaired humoral responses after primary immunisation (regardless of treatment) and patients without prior SARS-CoV-2 infections. After infection, antibody titres increased in patients on S1PR modulator treatment while anti-CD20 treated patients did not show an increase. CONCLUSIONS: SARS-COV-2 omicron breakthrough infections are more prevalent in patients with MS on anti-CD20 therapies and S1PR modulators compared with other patients with MS, which correlated with decreased humoral responses after vaccination. Humoral responses after infection were higher in S1PR modulator-treated patients in comparison to patients on anti-CD20 therapies, suggesting that immunological protection from contracting infection or repeated exposures may differ between these therapies.
 IMPORTANCE: The value of serum neurofilament light chain (sNfL) levels for predicting long-term disability in patients with multiple sclerosis (MS) remains controversial. OBJECTIVE: To assess whether high sNfL values are associated with disability worsening in patients who underwent their first demyelinating MS event. DESIGN, SETTING, AND PARTICIPANTS: This multicenter cohort study included patients who underwent their first demyelinating event suggestive of MS at Hospital Universitario Ramón y Cajal (development cohort; June 1, 1994, to September 31, 2021, with follow-up until August 31, 2022) and 8 Spanish hospitals (validation cohort; October 1, 1995, to August 4, 2020, with follow-up until August 16, 2022). EXPOSURES: Clinical evaluations at least every 6 months. MAIN OUTCOMES AND MEASURES: The main outcomes were 6-month confirmed disability worsening (CDW) and an Expanded Disability Status Scale (EDSS) score of 3. Levels of sNfL were measured in blood samples obtained within 12 months after disease onset using a single molecule array kit. The cutoffs used were sNfL level of 10 pg/mL and a standardized score (z score) of 1.5. Multivariable Cox proportional hazards regression models were used to evaluate outcomes. RESULTS: Of the 578 patients included in the study, 327 were in the development cohort (median age at sNfL analysis, 34.1 years [IQR, 27.2-42.7 years]; 226 female [69.1%]) and 251 patients were in the validation cohort (median age at sNfL analysis, 33.3 years [IQR, 27.4-41.5 years]; 184 female [73.3%]). The median follow-up was 7.10 years (IQR, 4.18-10.0 years). Levels of sNfL greater than 10 pg/mL were independently associated with higher risk of 6-month CDW and an EDSS of 3 in the development cohort (6-month CDW: hazard ratio [HR], 2.39; 95% CI, 1.39-4.12; P = .002; EDSS of 3: HR, 4.12; 95% CI, 2.18-7.77; P < .001) and the validation cohort (6-month CDW: HR, 1.61; 95% CI, 1.07-2.42; P = .02; EDSS of 3: HR, 2.03; 95% CI, 1.23-3.33; P = .005). Highly effective disease-modifying treatments were associated with lower risks of 6-month CDW and an EDSS of 3 in patients with high baseline sNfL values. CONCLUSIONS AND RELEVANCE: This cohort study found that high sNfL values obtained within the first year of disease were associated with long-term disability worsening in MS, suggesting that sNfL level measurement may help identify optimal candidates for highly effective disease-modifying treatments.

 BACKGROUND: Chronological age is associated with disability accumulation in multiple sclerosis (MS). Biological age may give more precise estimates of aging pathways associations with MS severity. Both normal aging and accelerated aging from MS may negatively impact disease course. Multi-marker indices of aging, such as the NHANES biological age index (BAI), may be more robust than single biomarkers in capturing biological age and are strongly associated with mortality risk and aging-related diseases. OBJECTIVE: We sought to investigate whether the NHANES BAI, utilizing readily available measures in the clinic, captures accelerating aging and correlates with disability in MS participants. METHODS: We conducted a prospective, cross-sectional case-control pilot study. Consecutive patients who met the 2017 McDonald's Criteria for MS were recruited from May 2020 to May 2022 along with age-similar healthy controls. BAI components included blood pressure, FEV1, serum creatinine, C-reactive protein, blood-urea nitrogen, albumin, alkaline phosphatase, cholesterol, CMV IgG, and hemoglobin A1c. The index was calculated using the Klemara and Doubal method. Spearman correlation and multivariable linear regression models were used to assess the association between BAI and MS clinical outcomes. RESULTS: A total of 51 MS (68.6% female) and 38 control (68.4% female) participants were recruited. BAI correlated with chronological age (CA) in MS (r(2)=0.90,p<0.0001) and control participants (r(2) =0.87,p<0.0001). The mean BAI was 1.4 years older than CA in MS participants (range +15 to -10.5 years) and 2.2 years younger in control participants (range +11.2 to -14.1 years). In unadjusted Spearman analyses, BAI correlated with the timed 25-foot walk (T25FW, rho(s)(=)0.31, p = 0.045) and symbol digit modalities test (SDMT rho(s) = 0.35, p = 0.018). In a multivariable regression model, a 5-year older BAI was associated with a 1.2-point lower score on SDMT (95%CI -2.2 to -0.25, p = 0.014). CONCLUSIONS: MS participants were biologically older than their own chronological age and age-similar controls. In this modest-sized pilot sample, there was strongest correlation for MS outcome measures between BAI and the SDMT. These results support further study of the BAI as a marker of biological age variability in MS.
 Central nervous system diseases (CNSDs) lead to significant disability worldwide. Mobile app interventions have recently shown the potential to facilitate monitoring and medical management of patients with CNSDs. In this direction, the characteristics of the mobile apps used in research studies and their level of clinical effectiveness need to be explored in order to advance the multidisciplinary research required in the field of mobile app interventions for CNSDs. A systematic review of mobile app interventions for three major CNSDs, i.e., Parkinson's disease (PD), multiple sclerosis (MS), and stroke, which impose significant burden on people and health care systems around the globe, is presented. A literature search in the bibliographic databases of PubMed and Scopus was performed. Identified studies were assessed in terms of quality, and synthesized according to target disease, mobile app characteristics, study design and outcomes. Overall, 21 studies were included in the review. A total of 3 studies targeted PD (14%), 4 studies targeted MS (19%), and 14 studies targeted stroke (67%). Most studies presented a weak-to-moderate methodological quality. Study samples were small, with 15 studies (71%) including less than 50 participants, and only 4 studies (19%) reporting a study duration of 6 months or more. The majority of the mobile apps focused on exercise and physical rehabilitation. In total, 16 studies (76%) reported positive outcomes related to physical activity and motor function, cognition, quality of life, and education, whereas 5 studies (24%) clearly reported no difference compared to usual care. Mobile app interventions are promising to improve outcomes concerning patient's physical activity, motor ability, cognition, quality of life and education for patients with PD, MS, and Stroke. However, rigorous studies are required to demonstrate robust evidence of their clinical effectiveness.
 BACKGROUND: Suboptimal performance during neuropsychological testing frequently occurs in multiple sclerosis (MS), leading to unreliable cognitive outcomes. Neurophysiological alterations correlate with MS-related cognitive impairment, but studies have not yet considered performance validity. OBJECTIVES: To investigate neurophysiological markers of cognitive impairment in MS, while explicitly addressing performance validity. METHODS: Magnetoencephalography recordings, neuropsychological assessments, and performance validity testing were obtained from 90 MS outpatients with cognitive complaints. Spectral and resting-state functional connectivity (rsFC) properties were compared between cognitively impaired (CI), cognitively preserved (CP), and suboptimally performing (SUB) patients using regression models and permutation testing. RESULTS: CI had higher power in low-frequency bands and lower power in high bands compared to CP, indicating neuronal slowing. CI also showed lower beta power compared to SUB. Overall power spectra visually differed between CI and CP, and SUB showed overlap with both groups. CI had lower rsFC than CP and SUB patients. CP and SUB patients showed no differences. CONCLUSION: Neuronal slowing and altered rsFC can be considered cognitive markers in MS. Patients who performed suboptimally showed resemblance with patients with and without cognitive impairments, and although their overall neurophysiological profile was more similar to patients without impairments, it suggests heterogeneity regarding their pathophysiology.
 BACKGROUND: Stigma experienced by persons living with multiple sclerosis (PwMS) is underrepresented in the literature. Discovering how the experience of stigma impacts quality of life and mood symptoms in PwMS may guide future care considerations with the goal of improving overall quality of life. METHODS: A retrospective review of data from the Quality of Life in Neurological Disorders (Neuro-QoL) set of measures and PROMIS Global Health (PROMIS-GH) scale was conducted. Multivariable linear regression was used to assess relationships between baseline (first visit) Neuro-QoL Stigma, Anxiety, Depression, and PROMIS-GH. Mediation analyses examined whether mood symptoms mediated the relationship between stigma and quality of life (PROMIS-GH). RESULTS: 6,760 patients (mean age 60.2 ± 8.9 years, 27.7% male, 74.2% white) were included. Neuro-QoL Stigma was significantly related to PROMIS-GH Physical Health (beta=-0.390, 95% CI [-0.411, -0.368]; p < 0.001) and PROMIS-GH Mental Health (beta=-0.595, 95% CI [-0.624, -0.566]; p < 0.001). Neuro-QoL Stigma was also significantly related to Neuro-QoL Anxiety (beta=0.721, 95% CI [0.696, 0.746]; p < 0.001) and Neuro-QoL Depression (beta=0.673, 95% CI [0.654, 0.693]; p < 0.001). Mediation analyses revealed that both Neuro-QoL Anxiety and Depression partially mediated the relationship between Neuro-QoL Stigma and PROMIS-GH Physical and Mental Health. CONCLUSION: Results demonstrate stigma is associated with decreased quality of life in both physical and mental health domains in PwMS. Stigma was also associated with more significant symptoms of anxiety and depression. Finally, anxiety and depression play a mediating role in the relationship between stigma and both physical and mental health in PwMS. Therefore, tailoring interventions to effectively reduce symptoms of anxiety and depression in PwMS may be warranted, as it will likely improve overall quality of life and reduce negative impacts of stigma.
 BACKGROUND: Mortality data from Europe and North America show a shorter life expectancy for people with multiple sclerosis (MS). It is not known if a similar mortality risk exists in the southern hemisphere. We analysed the mortality outcomes of a comprehensive New Zealand (NZ) MS cohort, 15 years postrecruitment. METHODS: All participants of the nationwide 2006 NZ MS prevalence study were included and mortality outcomes were compared with life table data from the NZ population using classic survival analyses, standardised mortality ratios (SMRs) and excess death rates (EDRs). RESULTS: Of 2909 MS participants, 844 (29%) were deceased at the end of the 15-year study period. Median survival age for the MS cohort was 79.4 years (78.5, 80.3), compared with 86.6 years (85.5, 87.7) for the age-matched and sex-matched NZ population. The overall SMR was 1.9 (1.8, 2.1)). Symptom onset between 21 and 30 years corresponded to an SMR of 2.8 and a median survival age 9.8 years lower than the NZ population. Progressive-onset disease was associated with a survival gap of 9 years compared with 5.7 years for relapsing onset. The EDR for those diagnosed in 1997-2006 was 3.2 (2.6, 3.9) compared with 7.8 (5.8, 10.3) for those diagnosed between 1967 and 1976. CONCLUSIONS: New Zealanders with MS have a median survival age 7.2 years lower than the general population and twice the mortality risk. The survival gap was greater for progressive-onset disease and for those with an early age of onset.
 Clinical symptom worsening in patients with multiple sclerosis (MS) is driven by inflammation compartmentalized within the CNS, which results in chronic neuronal damage owing to insufficient repair mechanisms. The term 'smouldering inflammation' summarizes the biological aspects underlying this chronic, non-relapsing and immune-mediated mechanism of disease progression. Smouldering inflammation is likely to be shaped and sustained by local factors in the CNS that account for the persistence of this inflammatory response and explain why current treatments for MS do not sufficiently target this process. Local factors that affect the metabolic properties of glial cells and neurons include cytokines, pH value, lactate levels and nutrient availability. This Review summarizes current knowledge of the local inflammatory microenvironment in smouldering inflammation and how it interacts with the metabolism of tissue-resident immune cells, thereby promoting inflammatory niches within the CNS. The discussion highlights environmental and lifestyle factors that are increasingly recognized as capable of altering immune cell metabolism and potentially responsible for smouldering pathology in the CNS. Currently approved MS therapies that target metabolic pathways are also discussed, along with their potential for preventing the processes that contribute to smouldering inflammation and thereby to progressive neurodegenerative damage in MS.
 Multiple Sclerosis (MS) is a demyelinating disease of the central nervous system that disturbs the flow of brain signals to other parts of the body. The actual cause of the disease is still not apparent. The intrinsically disordered proteins (IDP) play a crucial role in neurodegenerative diseases like Alzheimer's, Lewy bodies, Parkinson's, Amyotrophic Lateral Sclerosis, Multiple Sclerosis, etc. In MS, it was known that the immune system attacks the proteins like Myelin Basic Protein (MBP), Myelin-associated Oligodendrocyte Basic protein (MOBP), Myelin-Associated Protein (MAG), and Myelin Proteolipid Protein (PLP) and this leads to demyelination causing MS. Here the proteins MBP and MOBP are both moonlighting intrinsically disordered proteins and exist between the myelin sheath, unlike MAG which is a transmembrane protein. The main focus of the article was to examine the significant role of proteins intrinsically disordered regions (IDR) in maintaining their function. Molecular dynamics simulation studies were performed to study the conformational dynamics of these protein IDRs both in water and near the myelin sheath. The results suggest that the IDR dominates the structural dynamics of these proteins and IDR in both proteins was responsible for their interaction with the myelin sheath. Interestingly, it was noted that the known epitopes MBP(83-96) and MOBP(65-87) in the IDR have no interaction with the myelin sheath. Thus when the protein remains intrinsically disordered it maintains the proper function and myelin integrity and if it adopts folds the region was identified as an epitope by the immune system leading to demyelination causing MS.
 BACKGROUND: Recently, concern has been raised about the influence of the previous disease-modifying treatments (DMTs) on the clinical efficacy of ocrelizumab (OCR). We aimed to evaluate whether the previous DMT affects the lymphocyte subset kinetics in people with Multiple Sclerosis (MS) switching to OCR. METHODS: This is a multicenter, retrospective, real-world study on consecutive MS patients who started or switched to OCR. We grouped them by prior DMT in: (i) naïve-to-treatment (NTT), (ii) switching from fingolimod (SF) and (iii) switching from natalizumab (SN). Differences in absolute lymphocyte count and lymphocyte subset count changes, considering the period from baseline to 6 months, over all the three groups were assessed with an inverse-probability-weighted regression adjustment model. RESULTS: Mean T CD4+ cell count reduction from baseline to the six-month follow-up was more pronounced in the SN group compared to the NTT (p = 0,026). Further, patients in the SF group experienced a less pronounced CD4 T cell number decrease than both NTT and SN groups (p = 0,04 and p < 0,001, respectively). Patients in the SF group experienced an increase in CD8 T cell absolute number, whereas those in the NTT and SN groups experienced a significant decrease (p = 0,015 and p < 0,001, respectively). Patients experiencing early inflammatory activity showed a lower CD8+ cell count at baseline than stable patients (p = 0,02). CONCLUSIONS: Previous DMTs influence the lymphocyte kinetics in people with MS switching to OCR. Reassessment of these findings over a larger population may help optimize the switch.
 BACKGROUND AND PURPOSE: The association between socioeconomic status (SES) and the risk of multiple sclerosis (MS) is unclear. The aim was to study whether a potential association between indicators of SES and MS risk in Sweden is explained by lifestyle/environmental factors. METHODS: Using the Swedish MS registry and the Swedish patient registries, a register study was performed comprising all cases diagnosed with MS in Sweden between 1990 and 2018 (N = 24,729) and five randomly selected controls per case, matched by year and age at disease onset, sex and residential area at disease onset. Data from two matched case-control studies combined comprising data on environment/lifestyle factors (7193 cases, 9609 controls, inclusion period 2005-2018) were also utilized. For all participants, information regarding ancestry, formal education (available 1990-2018) and family income (available 1998-2018) was retrieved from the National Board of Health and Welfare. RESULTS: The registry study revealed no association between education and MS risk, whereas an income exceeding the upper quartile was associated with lower MS risk compared to having an income in the lowest quartile (odds ratio 0.86, 95% confidence interval 0.82-0.90). These findings were replicated in the crude analyses of the case-control study. However, after adjustment for confounding, no association was observed between income and risk of MS. CONCLUSIONS: Education and income were not associated with occurrence of MS after adjustment for a few lifestyle-related factors (smoking, alcohol consumption, body mass index and sun exposure habits), indicating that SES has no influence on MS risk besides its association with these lifestyle factors in the Swedish context.
 Predicting the long-term outcome of multiple sclerosis (MS) remains an important challenge to this day. As the gut microbiota is emerging as a potential player in MS, we investigated in this study whether gut microbial composition at baseline is related to long-term disability worsening in a longitudinal cohort of 111 MS patients. Fecal samples and extensive host metadata were collected at baseline and 3 months post-baseline, with additional repeated neurological measurements performed over (median) 4.4 y. Worsening (with EDSS-Plus) occurred in 39/95 patients (outcome undetermined for 16 individuals). The inflammation-associated, dysbiotic Bacteroides 2 enterotype (Bact2) was detected at baseline in 43.6% of worsened patients, while only 16.1% of non-worsened patients harbored Bact2. This association was independent of identified confounders, and Bact2 was more strongly associated with EDSS-Plus than neurofilament light chain (NfL) plasma levels. Furthermore, using fecal sampling performed 3 months post-baseline, we observed Bact2 to be relatively stable, suggesting its potential use as a prognostic biomarker in MS clinical practice.
 Thyroid hormones are essential during developmental myelination and may play a direct role in remyelination and repair in the adult central nervous system by promoting the differentiation of oligodendrocyte precursor cells into mature oligodendrocytes. Since tri-iodothyronine (T3) is believed to mediate the majority of important thyroid hormone actions, liothyronine (synthetic T3) has the potential to induce reparative mechanisms and limit neurodegeneration in multiple sclerosis (MS). We completed a phase 1b clinical trial to determine the safety and tolerability of ascending doses of liothyronine in individuals with relapsing and progressive MS. A total of 20 people with MS were enrolled in this single-center trial of oral liothyronine. Eighteen participants completed the 24-week study. Our study cohort included mostly women (11/20), majority relapsing MS (12/20), mean age of 46, and baseline median EDSS of 3.5. Liothyronine was tolerated well without treatment-related severe/serious adverse events or evidence of disease activation/clinical deterioration. The most common adverse events included gastrointestinal distress and abnormal thyroid function tests. No clinical thyrotoxicosis occurred. Importantly, we did not observe a negative impact on secondary clinical outcome measures. The CSF proteomic changes suggest a biological effect of T3 treatment within the CNS. We noted changes primarily in proteins associated with immune cell function and angiogenesis. Liothyronine appeared safe and was well tolerated in people with MS. A larger clinical trial will help assess whether liothyronine can promote oligodendrogenesis and enhance remyelination in vivo, limit axonal degeneration, or improve function.
 BACKGROUND: Individuals with peripheral vestibulopathy are known to have difficulty with volitional head turns. This leads to differences in head and body turning kinematics, compared to those without vestibular dysfunction. Multiple sclerosis (MS), a neuro-inflammatory disease affecting the central nervous system, can cause vestibular dysfunction (dizziness, unsteadiness, gaze instability). However, head and trunk turning kinematics in people with MS (PwMS) have not been assessed. RESEARCH QUESTION: Will PwMS, demonstrate head and body kinematics alterations similar to individuals with a peripheral dysfunction compared to vestibular healthy individuals? METHODS: Eleven individuals with a recent vestibular schwannoma resection (VSR), fourteen PwMS, and 10 healthy control (HC) participants were fitted with head and trunk worn inertial measurement units (IMUs) and performed walking and turning tasks. Head and trunk peak turning speed and amplitude were extracted. Regression models controlling for gait speed were fit per outcome with post hoc corrections applied to significant models. RESULTS: Yaw plane head turn speed and amplitude were significantly less in the VSR group compared to HC. Pitch plane head turn amplitude was significantly smaller in PwMS compared to HC (p = 0.04), however pitch plane speed did not differ between the groups. There was no difference between PwMS and the VSR group in yaw or pitch plane speed and amplitude. Both PwMS and the VSR group turned significantly slower than HC during the 180d body turn as measured at the head and trunk (head speed model p = 0.009 and <0.001; trunk speed model p < 0.001 for both groups) however the MS and VSR groups did not differ from each other. SIGNIFICANCE: Turning kinematics while walking in PwMS are altered compared to HC and are similar to individuals with unilateral vestibular hypofunction. Centrally mediated vestibular dysfunction in PwMS may alter movement kinematics and should be considered during examination and treatment.
 BACKGROUND AND PURPOSE: The heterogeneous symptoms of multiple sclerosis (MS) can considerably impact the lives of people with MS (PwMS). The aim of this study was to describe the extent of restrictions in different life domains that PwMS experience in relation to their symptoms and level of disability. METHODS: A cross-sectional survey was conducted among working-age PwMS in Sweden. The 4052 participants who answered the questions on restrictions in work and private life domains (family, leisure activities, and contact with friends/acquaintances) were included. Predictors of restrictions in the four domains were determined through multinomial logistic regression. RESULTS: Approximately one-third of the PwMS reported no restrictions in the domains of work (35.7%), family (38.7%), leisure activities (31.1%) or contact with friends/acquaintances (40.3%), the remaining participants reported moderate to severe restrictions. Tiredness/fatigue was the most commonly reported most-limiting symptom (49.5%). PwMS with Expanded Disability Status Scale (EDSS) scores of zero reported restrictions in life domains ranging from 39.6% (friends/acquaintances) to 45.7% (leisure activities). Age, sex, education, type of living area, MS type, type of most-limiting symptom, and EDSS score predicted restrictions in work and private life domains. CONCLUSIONS: Most PwMS reported similar levels of restrictions in both their work and private lives. Restrictions in these life domains were also reported by PwMS with low disability levels (EDSS = 0) and were often associated with invisible symptoms such as fatigue. Even in a contemporary MS cohort, close to 90% of PwMS report limitations due to MS.



 PURPOSE OF REVIEW: Choroid plexuses (ChPs) are key actors of the blood-to-cerebrospinal-fluid barrier and serve as brain immune checkpoint. The past years have seen a regain of interest about their potential involvement in the physiopathology of neuroinflammatory disorders like multiple sclerosis (MS). This article offers an overview of the recent findings on ChP alterations in MS, with a focus on the imaging tools able to detect these abnormalities and on their involvement in inflammation, tissue damage and repair. RECENT FINDINGS: On MRI, ChPs are enlarged in people with MS (PwMS) versus healthy individuals. This size increase is an early event, already detected in presymptomatic and pediatric MS. Enlargement of ChPs is linked to local inflammatory infiltrates, and their dysfunction selectively impacts periventricular damage, larger ChPs predicting the expansion of chronic active lesions, smoldering inflammation and remyelination failure in tissues surrounding the ventricles. ChP volumetry may add value for the prediction of disease activity and disability worsening. SUMMARY: ChP imaging metrics are emerging as possible biomarkers of neuroinflammation and repair failure in MS. Future works combining multimodal imaging techniques should provide a more refined characterization of ChP functional changes, their link with tissue damage, blood to cerebrospinal-fluid barrier dysfunction and fluid trafficking in MS.
 Multiple sclerosis (MS) is characterized by a complex etiology that is mirrored by the perplexing and inconsistent treatment responses observed across different patients. Although epigenetic research has garnered rightful interest in its efforts towards demystifying and understanding aberrant responses to treatment, the interim undoubtedly requires alternative non-pharmacological approaches towards attaining more effective management strategies. Of particular interest in this review is resistance training (RT) as a non-pharmacological exercise-based interventional strategy and its potential role as a disease-modifying tool. RT has been reported across literature to positively influence numerous aspects in the quality of life (QoL) and functional capacity of MS patients, and one of the attributes of these benefits may be a shift in the immune system of these individuals. RT has also been proven to affect different immune system key players associated with MS pathology. Ultimately, this brief review aims to provide a potential yet crucial link between RT, alterations in the expression profile of the immune system, and finally an imminent improvement in the overall well-being and QoL of MS patients, suggesting that utilizing RT as an interventional exercise modality may be an effective strategy that would aid in managing such a complex and debilitating disease.
 Innovative pro-regenerative treatment strategies for progressive multiple sclerosis (PMS), combining neuroprotection and immunomodulation, represent an unmet need. Neural precursor cells (NPCs) transplanted in animal models of multiple sclerosis have shown preclinical efficacy by promoting neuroprotection and remyelination by releasing molecules sustaining trophic support and neural plasticity. Here we present the results of STEMS, a prospective, therapeutic exploratory, non-randomized, open-label, single-dose-finding phase 1 clinical trial ( NCT03269071 , EudraCT 2016-002020-86), performed at San Raffaele Hospital in Milan, Italy, evaluating the feasibility, safety and tolerability of intrathecally transplanted human fetal NPCs (hfNPCs) in 12 patients with PMS (with evidence of disease progression, Expanded Disability Status Scale ≥6.5, age 18-55 years, disease duration 2-20 years, without any alternative approved therapy). The safety primary outcome was reached, with no severe adverse reactions related to hfNPCs at 2-year follow-up, clearly demonstrating that hfNPC therapy in PMS is feasible, safe and tolerable. Exploratory secondary analyses showed a lower rate of brain atrophy in patients receiving the highest dosage of hfNPCs and increased cerebrospinal fluid levels of anti-inflammatory and neuroprotective molecules. Although preliminary, these results support the rationale and value of future clinical studies with the highest dose of hfNPCs in a larger cohort of patients.
 BACKGROUND: Upper and lower limb disabilities are hypothesized to have partially independent underlying (network) disturbances in multiple sclerosis (MS). OBJECTIVE: This study investigated functional network predictors and longitudinal network changes related to upper and lower limb progression in MS. METHODS: Two-hundred fourteen MS patients and 58 controls underwent functional magnetic resonance imaging (fMRI), dexterity (9-Hole Peg Test) and mobility (Timed 25-Foot Walk) measurements (baseline and 5 years). Patients were stratified into progressors (>20% decline) or non-progressors. Functional network efficiency was calculated using static (over entire scan) and dynamic (fluctuations during scan) approaches. Baseline measurements were used to predict progression; significant predictors were explored over time. RESULTS: In both limbs, progression was related to supplementary motor area and caudate efficiency (dynamic and static, respectively). Upper limb progression showed additional specific predictors; cortical grey matter volume, putamen static efficiency and posterior associative sensory (PAS) cortex, putamen, primary somatosensory cortex and thalamus dynamic efficiency. Additional lower limb predictors included motor network grey matter volume, caudate (dynamic) and PAS (static). Only the caudate showed a decline in efficiency over time in one group (non-progressors). CONCLUSION: Disability progression can be predicted using sensorimotor network measures. Upper and lower limb progression showed unique predictors, possibly indicating different network disturbances underlying these types of progression in MS.
 BACKGROUND: Multiple sclerosis risk has been shown to have seasonal variations that are more pronounced in higher latitudes. However, this phenomenon has not been adequately studied near the Equator. OBJECTIVE: To explore the risk of multiple sclerosis associated with month, season of birth, and sunlight exposure variables in Colombia. METHODS: In this case-control study, 668 multiple sclerosis cases were matched to 2672 controls by sex and age. Association of multiple sclerosis with each month/season of birth and sunlight exposure variables was estimated with multilevel mixed-effects logistic regression and ecological regression models, respectively. Seasonality in the births of multiple sclerosis was assessed with a non-parametric seasonality test. RESULTS: We found a higher probability of multiple sclerosis in September (0.25; 95% confidence interval (CI) = 0.21-0.31) and lower in March (0.15; 95% CI = 0.10-0.18), which turned non-significant after a multiple comparisons test. Sunlight exposure variables had no significant effect on the risk of MS, and the tests of seasonality in the births of MS did not show significant results. CONCLUSION: Our results show no seasonality in the risk of multiple sclerosis near the Equator, supporting the hypothesis that this phenomenon is latitude dependent.
 Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS), diagnosed at a mean age of 32 years. CNS glia are crucial players in the onset of MS, primarily involving astrocytes and microglia that can cause/allow massive oligodendroglial cells death, without immune cell infiltration. Current therapeutic approaches are aimed at modulating inflammatory reactions during relapsing episodes, but lack the ability to induce very significant repair mechanisms. In this review article, different experimental approaches based mainly on the application of different cell types as therapeutic strategies applied for the induction of myelin repair and/or the amelioration of the disease are discussed. Regarding this issue, different cell sources were applied in various experimental models of MS, with different results, both in significant improvements in remyelination and the reduction of neuroinflammation and glial activation, or in neuroprotection. All cell types tested have advantages and disadvantages, which makes it difficult to choose a better option for therapeutic application in MS. New strategies combining cell-based treatment with other applications would result in further improvements and would be good candidates for MS cell therapy and myelin repair.
 BACKGROUND: Somatosensory evoked potentials (SEPs) are widely used for the diagnosis and evaluation of neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). However, whether the parameters of tibial nerve SEPs can help to distinguish NMOSD from MS remains unclear. Thus, the aim of this study was to investigate the utility of tibial nerve SEP parameters in differentiating patients with NMOSD and MS. METHODS: The clinical data of patients with NMOSD or MS treated in our institution between 2005 and 2021 were retrospectively extracted from our electronic database. Additional inclusion criteria were presentation with sensory symptoms in the lower extremities with corresponding lesions in the magnetic resonance images as well as available data on anti-aquaporin-4 antibodies and tibial nerve SEPs. The Z-scores of the N21-P38 interval (central sensory conduction time), P38 latency, and P38 amplitude were compared between the patients with NMOSD and MS. The relationship of disease severity with the parameters of the tibial nerve SEPs was also evaluated. RESULTS: Twenty patients with NMOSD and 13 patients with MS were enrolled. The Z-scores of the N21-P38 interval and P38 latency were significantly higher in the MS group than in the NMOSD group (p < 0.05 and p < 0.01, respectively), whereas there was no difference in the Z-scores of the P38 amplitude between the two groups. In the MS group, only the N21-P38 interval and P38 latency were significantly correlated with disease severity (p < 0.05 and p < 0.01, respectively). In contrast, none of the tibial nerve SEP parameters were significantly correlated with disease severity in the NMOSD group. CONCLUSION: Evaluation of the N21-P38 interval and P38 latency in tibial nerve SEPs potentially helps in differentiating between NMOSD and MS.
 T cells play an important role in the development and progression of multiple sclerosis (MS), an autoimmune disease of the central nervous system. In the present study, the immunomodulatory impacts of two Lactobacillus strains, L paracasei DSM 13434 and L plantarum DSM 15312, on the frequency and cytokine production of CD4+ T cells in MS patients were explored. Thirty MS patients were enrolled in this study. The CD4+ T cells were isolated, cultured, and exposed to the media containing cell-free supernatants of L plantarum (group1), L paracasei (group 2), the mixture group of cell-free supernatants of both probiotics (group 3), and vehicle (control) group (group 4). The frequencies of T helper (Th) 1, Th17, Th2, and T regulatory type 1 (Tr1) cells and mean fluorescent intensity (MFI) of the associated cytokines were assessed using flow cytometry. The levels of interleukin 17 (IL-17), transforming growth factor β (TGF-β), and interferon-gamma (IFN-γ) cytokines in supernatants of all groups were measured by enzyme-linked immunosorbent assay. The percentage of Th1 cells and the MFI of IFN-γ in Th1 cells (CD4+ IFN-γ+) in all three probiotic treatment groups were significantly decreased compared to the control group. However, no significant changes were observed in the proportion and MFI of Th2, Th17, and Tr1 cells. A significant decrease was observed in IL-17 secretion in the supernatant of cultured CD4+ T cells in all three treatment groups in comparison with control. The levels of TGF-β and IFN-γ were not significantly different among any of the study groups.  Collectively, cell-free supernatants of the lactobacilli showed an in vitro anti-inflammatory effect. However, further studies are needed to prove the real effects of probiotics on MS.
 BACKGROUND: Risk factors for aquaporin-4 (AQP4+) antibody neuromyelitis optica spectrum disorder (NMOSD) are not well-established. OBJECTIVE: To investigate demographic and environmental factors associated with NMOSD using a validated questionnaire and case-control design. METHODS: We enrolled patients with AQP4 + NMOSD through six Canadian Multiple Sclerosis Clinics. Participants completed the validated Environmental Risk Factors in Multiple Sclerosis Study (EnvIMS) questionnaire. Their responses were compared to those of 956 unaffected controls from the Canadian arm of EnvIMS. We calculated odds ratios (ORs) for the association between each variable and NMOSD using logistic regression and Firth's procedure for rare events. RESULTS: In 122 participants (87.7% female) with NMOSD, odds of NMOSD in East Asian and Black participants were ⩾8 times that observed in White participants. Birthplace outside Canada was associated with an increased risk of NMOSD (OR = 5.5, 95% confidence interval (CI) = 3.6-8.3) as were concomitant autoimmune diseases (OR = 2.7, 95% CI = 1.4-5.0). No association was observed with reproductive history or age at menarche. CONCLUSION: In this case-control study, risk of NMOSD in East Asian and Black versus White individuals was greater than that observed in many previous studies. Despite the preponderance of affected women, we did not observe any association with hormonal factors such as reproductive history or age at menarche.
 BACKGROUND. The central vein sign (CVS) is a proposed MRI biomarker of multiple sclerosis (MS). The impact of gadolinium-based contrast agent (GBCA) administration on CVS evaluation remains poorly investigated. OBJECTIVE. The purpose of this study was to assess the effect of GBCA use on CVS detection and on the diagnostic performance of the CVS for MS using a 3-T FLAIR* sequence. METHODS. This study was a secondary analysis of data from the pilot study for the prospective multicenter Central Vein Sign: A Diagnostic Biomarker in Multiple Sclerosis (CAVS-MS), which recruited adults with suspected MS from April 2018 to February 2020. Participants underwent 3-T brain MRI including FLAIR and precontrast and post-contrast echo-planar imaging T2*-weighted acquisitions. Postprocessing was used to generate combined FLAIR and T2*-weighted images (hereafter, FLAIR*). MS diagnoses were established using the 2017 McDonald criteria. Thirty participants (23 women, seven men; mean age, 45 years) were randomly selected from the CAVS-MS pilot study cohort. White matter lesions (WMLs) were marked using FLAIR* images. A single observer, blinded to clinical data and GBCA use, reviewed marked WMLs on FLAIR* images for the presence of the CVS. RESULTS. Thirteen of 30 participants had MS. Across participants, on precontrast FLAIR* imaging, 218 CVS-positive and 517 CVS-negative WMLs were identified; on post-contrast FLAIR* imaging, 269 CVS-positive and 459 CVS-negative WMLs were identified. The fraction of WMLs that were CVS-positive on precontrast and postcontrast images was 48% and 58% in participants with MS and 7% and 10% in participants without MS, respectively. The median patient-level CVS-positivity rate on precontrast and postcontrast images was 43% and 67% for participants with MS and 4% and 8% for participants without MS, respectively. In a binomial model adjusting for MS diagnoses, GBCA use was associated with an increased likelihood of at least one CVS-positive WML (odds ratio, 1.6; p < .001). At a 40% CVS-positivity threshold, the sensitivity of the CVS for MS increased from 62% on precontrast images to 92% on postcontrast images (p = .046). Specificity was not significantly different between precontrast (88%) and postcontrast (82%) images (p = .32). CONCLUSION. GBCA use increased CVS detection on FLAIR* images, thereby increasing the sensitivity of the CVS for MS diagnoses. CLINICAL IMPACT. The postcontrast FLAIR* sequence should be considered for CVS evaluation in future investigational trials and clinical practice.
 INTRODUCTION: Physical rehabilitation restores lost function and promotes brain plasticity in people with Multiple Sclerosis (MS). Research groups worldwide are testing the therapeutic effects of combining non-invasive neuromodulation with physical therapy (PT) to further improve functional outcomes in neurological disorders but with mixed results. Whether such devices enhance function is not clear. We present the rationale and study design for a randomized controlled trial evaluating if there is additional benefit to the synergistic pairing of translingual neurostimulation (TLNS) with PT to improve walking and balance in MS. METHODS AND ANALYSIS: A parallel group [PT + TLNS or PT + Sham], quadruple-blinded, randomized controlled trial. Participants (N = 52) with gait and balance deficits due to relapsing-remitting or progressive MS, who are between 18 and 70 years of age, will be recruited through patient registries in Newfoundland & Labrador and Saskatchewan, Canada. All participants will receive 14 weeks of PT while wearing either a TLNS or sham device. Dynamic Gait Index is the primary outcome. Secondary outcomes include fast walking speed, subjective ratings of fatigue, MS impact, and quality of life. Outcomes are assessed at baseline (Pre), after 14 weeks of therapy (Post), and 26 weeks (Follow Up). We employ multiple methods to ensure treatment fidelity including activity and device use monitoring. Primary and secondary outcomes will be analyzed using linear mixed-effect models. We will control for baseline score and site to test the effects of Time (Post vs. Follow-Up), Group and the Group x Time interaction as fixed effects. A random intercept of participant will account for the repeated measures in the Time variable. Participants must complete the Post testing to be included in the analysis. ETHICS AND DISSEMINATION: The Human Research Ethics Boards in Newfoundland & Labrador (HREB#2021.085) & Saskatchewan (HREB Bio 2578) approved the protocol. Dissemination avenues include peer-reviewed journals, conferences and patient-oriented communications.
 OBJECTIVE: Aim: Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative disease resulting in cognitive impairment, physical disabilities, and neurological symptoms. Ocrelizumab is an effective drug used in MS treatment. However, it causes a risk of hepatitis B reactivation in anti-HBc positive patients. We describe the impact of entecavir and tenofovir on HBV reactivation during treatment with ocrelizumab. PATIENTS AND METHODS: Materials and methods: Our study included eight patients (aged 18-70 years) with positive anti-HBc antibodies who were diagnosed with MS based on the 2017 McDonald criteria. The subjects were treated with ocrelizumab and were given anti-HBV prophylaxis with nucleoside analogs. The mean time from the beginning of therapy with nucleoside analogs to the initiation of ocrelizumab treatment was 27.5 days. Patients were administered ocrelizumab and none of them was diagnosed with HBV reactivation. RESULTS: Results: None of the laboratory parameters worsened. No severe adverse effects were observed. These results suggest that entecavir and tenofovir are effective in HBV reactivation prophylaxis. Additionally, positive anti-HBc antibodies do not rule out treatment with ocrelizumab. CONCLUSION: Conclusions: In patients with positive anti-HBc antibodies, nucleoside analogs, such as entecavir or tenofovir, should be administered before ocrelizumab administration to reduce the risk of viral reactivation. Further studies on simultaneous treatment with ocrelizumab and nucleoside analogs are required to confirm our findings.
 Multiple sclerosis (MS) is a complex neurological condition that involves both inflammatory demyelinating and neurodegenerative components. MS research and treatments have traditionally focused on immunomodulation, with less investigation of neuroprotection, and this holds true for the role of vitamin D in MS. Researchers have already established that vitamin D plays an anti-inflammatory role in modulating the immune system in MS. More recently, researchers have begun investigating the potential neuroprotective role of vitamin D in MS. The active form of vitamin D, 1,25(OH)(2)D(3), has a range of neuroprotective properties, which may be important in remyelination and/or the prevention of demyelination. The most notable finding relevant to MS is that 1,25(OH)(2)D(3) promotes stem cell proliferation and drives the differentiation of neural stem cells into oligodendrocytes, which carry out remyelination. In addition, 1,25(OH)(2)D(3) counteracts neurodegeneration and oxidative stress by suppressing the activation of reactive astrocytes and M1 microglia. 1,25(OH)(2)D(3) also promotes the expression of various neuroprotective factors, including neurotrophins and antioxidant enzymes. 1,25(OH)(2)D(3) decreases blood-brain barrier permeability, reducing leukocyte recruitment into the central nervous system. These neuroprotective effects, stimulated by 1,25(OH)(2)D(3), all enhance neuronal survival. This review summarizes and connects the current evidence supporting the vitamin D-mediated mechanisms of action for neuroprotection in MS.
 Multiple sclerosis (MS) is a complex and long-lasting neurodegenerative disease of the central nervous system (CNS), characterized by the loss of myelin within the white matter and cortical fibers, axonopathy, and inflammatory responses leading to consequent sensory-motor and cognitive deficits of patients. While complete resolution of the disease is not yet a reality, partial tissue repair has been observed in patients which offers hope for therapeutic strategies. To address the molecular and cellular events of the pathomechanisms, a variety of animal models have been developed to investigate distinct aspects of MS disease. Recent advances of multiscale intravital imaging facilitated the direct in vivo analysis of MS in the animal models with perspective of clinical transfer to patients. This review gives an overview of MS animal models, focusing on the current imaging modalities at the microscopic and macroscopic levels and emphasizing the importance of multimodal approaches to improve our understanding of the disease and minimize the use of animals.
 BACKGROUND: Overactive bladder (OAB), cognitive dysfunction, depression and anxiety are common problems encountered in MS. This study was planned to investigate the relationship between the severity of OAB symptoms and cognitive function, anxiety and depression in MS. METHODS: 100 patients with MS diagnosis with OAB symptoms were recruited. OAB symptoms was assessed with the OAB-V8 questionnaire. Symbol Digit Modalites Test (SDMT), California Verbal Learning Test II (CVLT-II) and Brief Vasospatial Memory Test-Revised (BVMT-R) in BICAMS Battery were used to evaluate cognitive function. Depression and anxiety were assessed with the Hospital Anxiety Depression (HAD) Scale. RESULTS: The mean age of the patients was 40.9±12.3, the duration of the disease was 9.03±6.89 years, and the mean OAB-V8 score was 17.6±8.9. SDMT test (r=-0.299, p<0.01) showed a moderately significant, CVLT-II (r= -0.219, p<0.05) and BVMT-R (r=-0.218, p<0.05) tests showed a weakly significant negative correlation with OAB-V8 score. There was a moderate positive correlation between the OAB-V8 score and HAD-D (r=0.279, p=0.005) and HAD-A (r=0.318, p=0.001) scores. SDMT and BVMT-R scores were significantly lower in anticholinergic (Ach) drug users (especially oxybutynin users) compared to those who did not use Ach drugs. CONCLUSIONS: It has been observed that the severity of OAB symptoms is related to worsening of information processing speed and an increase in depression and anxiety. It has been determined that there is a significant effect on information processing speed, visual learning and memory in patients using Ach drugs, especially in those using oxybutynin, compared to those who do not use Ach drugs.
 BACKGROUND: Pain and fatigue are highly prevalent in multiple sclerosis (MS) and are associated with adverse physical, social, and psychological outcomes. There is a critical need to identify modifiable factors that can reduce the impact of these symptoms on daily life. PURPOSE: This study examined the moderating role of dispositional coping in the relationships between daily fluctuations (i.e., deviations from a person's usual level) in pain and fatigue and same-day functional/affective outcomes. METHODS: Adults with MS (N = 102) completed a self-report measure of dispositional coping (Brief COPE), followed by 7 days of ecological momentary assessment of pain and fatigue and end-of-day diaries assessing same-day pain interference, fatigue impact, social participation, upper extremity and lower extremity functioning, depressive symptoms, and positive affect and well-being (PAWB). Multilevel models tested interactions between daily symptom fluctuations and dispositional coping (avoidant/approach) in predicting same-day outcomes. RESULTS: Higher approach coping mitigated the same-day association between pain and pain interference, whereas higher avoidant coping augmented this association. Daily PAWB benefits were seen for those who reported high approach coping and low avoidant coping; effects were only observed on days of low pain (for approach coping) and low fatigue (for avoidant coping). Avoidant coping was associated with worse fatigue impact, social participation, lower extremity functioning, and depressive symptoms. CONCLUSIONS: When faced with pain and fatigue, avoidant coping is associated with increased, and approach coping with decreased, functional/affective difficulties in the daily lives of individuals with MS. Altering coping strategy use may reduce the impact of pain and fatigue.
 BACKGROUND AND PURPOSE: Upper limb (UL) function is often affected in people with multiple sclerosis (PwMS) and is typically assessed through objective measures, including the Nine Hole Peg Test (9-HPT), Box and Block Test (BBT), and Hand Grip Strength (HGS). It is important to include the subjective perspective of PwMS in the assessment. This study aims to evaluate associations between Manual Ability Measure-36 (MAM-36) and 9-HPT, BBT, and HGS in MS. METHODS: The cross-sectional study included five Italian centers. Inclusion criteria were age ≥ 18 years, MS diagnosis, and stable disease course. Exclusion criteria were bilateral UL paralysis, and concomitant orthopedic or neurological diseases. RESULTS: A total of 199 PwMS were included: 128 female, mean age = 50.7 ± 13.0 years, 119 relapsing-remitting MS (RRMS), 31 primary and 49 secondary progressive MS, mean disease duration = 14.0 ± 10.4, years, mean Expanded Disability Status Scale (EDSS) = 4.6 ± 2.0. The MAM-36 showed small correlations with 9-HPT, BBT, and HGS. Correlations between MAM-36 and 9-HPT and BBT were highest among subjects with EDSS ≥ 6 and progressive MS. MAM-36 and HGS showed the highest correlations in subjects with EDSS ≤ 5 and RRMS. Combining 9-HPT and HGS provided the strongest predictive power over the MAM-36. CONCLUSIONS: Correlations between objective measures and MAM-36 were small to moderate, meaning that objective measures do not match subjects' perception of UL function. The combination of 9-HPT and HGS measures can help improve the assessment of UL function in activities of daily living.
 OBJECTIVES: The primary aim of this study was to assess the degree to which discrepancies between self-reported and actigraphy-based measures of sleep are associated with specific demographic, disease characteristics, and clinical features in a sample of individuals with multiple sclerosis (MS) reporting clinically significant insomnia symptoms. METHODS: Participants were 90 community-based participants with MS and insomnia. Measures included the Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory-Fast Screen (BDI-FS), Modified Fatigue Impact Scale (MFIS), and MS Neuropsychological Screening Questionnaire (MSNQ), and wrist actigraphy-derived sleep parameters. Discrepancy scores were calculated by subtracting actigraphy-derived values from PSQI-derived values for sleep latency (SL), total sleep time (TST), and sleep efficiency (SE). RESULTS: Correlations between PSQI and actigraphy-derived values were weak. Significant discrepancies, with moderate-to-large effect sizes, were observed between PSQI and actigraphy for SL, TST, and SE, whereby the PSQI yielded longer SL, shorter TST, and less SE than actigraphy. MSNQ elevations correlated with greater PSQI-actigraphy discrepancies in SL and TST. MFIS elevations correlated with greater discrepancies in TST. Discrepancies were not significantly related to BDI-FS, gender, race, education level, or MS type. CONCLUSIONS: Results emphasize the importance of assessing fatigue with sleep, and when feasible, inclusion of both self-report and actigraphy measures.
 BACKGROUND: Multiple sclerosis (MS) is a chronic neurodegenerative inflammatory disease that requires long-term commitment to treatment for optimal outcomes. A variety of disease-modifying therapies (DMTs) are now available that reduce relapses and delay disease progression in people with MS. However, adherence remains a significant issue, with a variety of mental, physical, and emotional factors contributing to non-adherence. In a large number of studies, non-adherence has been associated with worse clinical outcomes (relapses and disease severity), a higher economic burden, and loss of work productivity. However, many of these studies were short-term (1-2 years) or cross-sectional studies; thus, more data are needed on the long-term clinical and economic impacts of DMT non-adherence. The objective of this study was to determine the longer-term impact of adherence to DMTs on disease activity and healthcare resource utilization (HCRU) in people with MS. The study hypothesis was that non-adherence to DMTs would be associated long-term with worse clinical outcomes and a higher economic burden. METHODS: A retrospective administrative claims analysis of the US MarketScan® Commercial database (2011-2017) in individuals (18-65 years) with MS (based on International Classification of Disease coding) was conducted. Adherence was classified by proportion of days covered (PDC) ≥0.8 and non-adherence by PDC <0.8; sensitivity analyses helped further categorize as moderately (PDC ≥0.6-<0.8) or highly (PDC <0.6) non-adherent. Cohorts were matched using propensity score matching. Time to first relapse, annualized relapse rate (ARR), time to use of assistive devices (cane/walker or wheelchair), and annual HCRU (inpatient, emergency room [ER], outpatient, and MRI visits and costs) were compared between cohorts. RESULTS: 10,248 MS cases were identified; 58% met adherence criteria, and 42% met non-adherence criteria. Mean follow-up from diagnosis or first DMT claim was 5.3 years. Adherent individuals had a longer time to first relapse (hazard ratio [HR] 0.83; 95% confidence interval [CI]: 0.77-0.90; p<0.0001), a lower ARR (0.13 vs. 0.18, respectively; rate ratio [RR] 0.75 [95% CI: 0.71-0.79]; p<0.0001), and longer lag times to cane/walker use (HR 0.79 [95% CI: 0.66-0.94]; p=0.0067) and wheelchair use (HR 0.68 [95% CI: 0.55-0.83]; p=0.0002) than non-adherent individuals. Adherent individuals had fewer annual inpatient and ER visits and lower total costs than those who were non-adherent (p<0.0001). Sensitivity analyses showed that differences in disease activity and HCRU were generally more pronounced between matched adherent and highly non-adherent pairs than between matched adherent and moderately non-adherent pairs. CONCLUSION: Significant differences in MS disease activity and HCRU were observed based on adherence to DMTs. Our study underscores the negative impact of non-adherence to DMTs on long-term clinical and economic outcomes in MS.
 BACKGROUND: Although surface electromyography (sEMG) is the method used to assess muscle fatigue in patients with multiple sclerosis (PwMS), no pattern of signal change has been established. The differences shown in the parameters of other neurophysiological tests between PwMS and control groups (CG) suggest the differentiation of the sEMG signal. AIM: The purpose of the study was to verify potential differences in the fatigue sEMG signal in PwMS compared to CG. DESIGN: Cross-sectional study. SETTING: Chair and Department of Functional Diagnostics and Physical Medicine. POPULATION: A randomised group of patients diagnosed with MS (30, 20-41 years). A random sample of young, healthy adults (median 28, 20-39 years). METHODS: Measurement of sEMG was performed from extensor carpi radialis (ECR) and FCR (flexor carpi radialis) during 60-80% of maximum voluntary contraction (MVC) of extension and then flexion for 60sec, accordance with the fatigue protocol in Research XP Master Edition software (v. 1.08.27). RESULTS: Root mean square amplitude (A<inf>RMS</inf>) were lower for muscle in the PwMS compared to the CG (ECR P=0.0001, FCU P<0.0001). In the CG, the A<inf>RMS</inf> value increases during fatigue contraction (ECR P=0.0003, FCU P<0.0001), while in the PwMS) the A<inf>RMS</inf> value decreases (ECR: P<0.0001, FCU P<0.0001. CONCLUSIONS: The PwMS show an opposite pattern of preservation of the absolute value of A<inf>RMS</inf> during prolonged contraction to fatigue, compared with healthy subjects. CLINICAL REHABILITATION IMPACT: The results are important for clinical trials using sEMG to assess fatigue in PwMS. Knowledge of the differences in the time domain changes in sEMG signal between healthy subjects and PwMS is crucial for correctly interpreting the results.
 OBJECTIVE: To determine the concordance and statistical precision in gait velocity in people with multiple sclerosis (pwMS), measured with FeetMe® (insoles with pressure and motion sensors) compared with GAITRite® (classic reference system of gait analysis) in the timed 25-Feet Walk test (T25WT). METHODS: This observational, cross-sectional, prospective, single center study was conducted between September-2018 and April-2019 in pwMS aged 18-55 years, with Expanded Disability Status Scale (EDSS) 0-6.5 and relapse free ≥30 days at baseline. Primary endpoint was gait velocity. Secondary endpoints were ambulation time, cadence, and stride length assessment, while the correlation between gait variables and the clinical parameters of MS subjects was assessed as an exploratory endpoint. RESULTS: A total of 207 MS subjects were enrolled, of whom, 205 were considered in primary analysis. Most subjects were women (66.8%) and had relapsing-remitting MS (RRMS) (82.9%), with overall mean (standard deviation [SD]) age of 41.5 (8.0) year and EDSS 3.1 (2.0). There was a statistically significant (p<0.0001) and strong agreement (intra-class correlation coefficient (ICC) >0.830) in gait velocity, ambulation time and cadence assessment between FeetMe® and GAITRite®. CONCLUSIONS: Agreement between devices was strong (ICC≥0.800). FeetMe® is the first validated wearable medical device that allows gait monitoring in MS subjects, being potentially able to assess disease activity, progression, and treatment response.
 AIMS: Interferon-beta (IFNβ), the most widely prescribed medication for multiple sclerosis, is generally considered safe. Nevertheless, rare serious and/or life-threatening side effects have been reported such as thrombotic microangiopathy. A few mechanisms have been proposed to explain how interferon causes thrombotic microangiopathy, but immunological studies have been unable to pin this phenomenon down to a single pathophysiologic pathway. The aim of this article was to report a new mechanism explaining Interferon beta related thrombotic microangiopathy. METHODS: We report thrombotic microangiopathy in a 28-year-old male receiving interferon-beta treatment for multiple sclerosis. RESULTS: After three years of starting interferon beta therapy, the patient presented with malignant hypertension causing seizures, rapidly progressive renal failure requiring haemodialysis and haemolytic anaemia. Corticosteroid and plasma exchange sessions permitted haemolysis control. Nonetheless, the patient remained hemodialysis-dependent. Exploration of the complement system found a complement factor I deficiency whose activity normalized at the control carried out after 2 years. CONCLUSION: IFNβ treatment may cause complement factor I deficit, which can lead to thrombotic microangiopathy and severe renal failure.
 Dimethyl fumarate (DMF) is a well-characterized molecule that exhibits immuno-modulatory, anti-inflammatory, and antioxidant properties and that is currently approved for the treatment of psoriasis and multiple sclerosis. Due to its Nrf2-dependent and independent mechanisms of action, DMF has a therapeutic potential much broader than expected. In this comprehensive review, we discuss the state-of-the-art and future perspectives regarding the potential repurposing of DMF in the context of chronic inflammatory diseases of the intestine, such as inflammatory bowel disorders (i.e., Crohn's disease and ulcerative colitis) and celiac disease. DMF's mechanisms of action, as well as an exhaustive analysis of the in vitro/in vivo evidence of its beneficial effects on the intestine and the gut microbiota, together with observational studies on multiple sclerosis patients, are here reported. Based on the collected evidence, we highlight the new potential applications of this molecule in the context of inflammatory and immune-mediated intestinal diseases.
 OBJECTIVE: The primary objective was to study the association between fingolimod and the frequency of depression, anxiety, and insomnia symptoms among a cohort of Multiple Sclerosis (MS) patients with stress. The secondary objective was to examine the association between patient characteristics and these psychiatric symptoms. PATIENTS AND METHODS: Patients with MS and stress were recruited according to the Arabic version of the Perceived Stress Scale (PSS). Psychiatric outcomes were measured by validated scales. Logistic regression was used to estimate adjusted odds ratios (aORs) with 95% confidence intervals (CIs). Data from 324 participants were analyzed. RESULTS: Fingolimod was associated with a significantly lower adjusted odds ratio for depression (aOR 0.58, 95% CI 0.35-0.97, p<0.05) but less associated with anxiety (aOR 0.63, 95% CI 0.35-1.01, p=0.05) and insomnia (aOR 0.88, 95% CI 0.52-1.51, p=0.64). CONCLUSIONS: Close monitoring of mental health is required for patients with MS using disease-modifying therapies.
 INTRODUCTION: Epidemiological studies have suggested an increased vascular risk in patients with multiple sclerosis (MS). There is increasing evidence of the beneficial effects of GLP-1 agonists (GLP-1a) in preventing vascular complications and slowing the progression of neurodegeneration. Our objective was to explore the changes in the endothelial function of MS patients after 12 months of GLP-1a therapy. We also explored the role of lipoprotein subfractions and the antioxidant capacity of plasma. METHODS: MS patients were enrolled in a prospective, unicentric study. GLP-1a (dulaglutide) was administered to 13 patients. The control population consisted of 12 subjects. Endothelial function was determined by peripheral arterial tonometry and expressed as reperfusion hyperemia index (RHI). Trolox equivalent antioxidant capacity (TEAC) was used to assess the total antioxidant capacity of the plasma. The levels of lipoprotein subfractions were evaluated. RESULTS: The GLP-1a group did not have a significant change in their RHIs after 12 months (2.1 ± 0.6 vs. 2.1 ± 0.7; p = 0.807). However, a significant increase in their TEACs was observed (4.1 ± 1.4 vs. 5.2 ± 0.5 mmol/L, p = 0.010). On the contrary, the subjects in the control group had a significant worsening of their RHIs (2.1 ± 0.5 vs. 1.8 ± 0.6; p = 0.030), without significant changes in their TEACs. Except for a significant decrease in very-low-density lipoprotein (VLDL) (30.8 ± 10.2 vs. 22.6 ± 8.3 mg/dL, p = 0.043), no other significant changes in the variables were observed in the control group. VLDL levels (beta = -0.637, p = 0.001), the use of GLP-1a therapy (beta = 0.560, p = 0.003), and small LDL (beta = 0.339, p = 0.043) were the only significant variables in the model that predicted the follow-up RHI. CONCLUSION: Our results suggest that the application of additional GLP-1a therapy may have atheroprotective and antioxidant effects in MS patients with high MS activity and thus may prospectively mitigate their vascular risk. However, the lipoprotein profile may also play an important role in the atherogenic risk of MS subjects.
 BACKGROUND: Performing cognitive-motor dual tasks (DTs) may result in reduced walking speed and cognitive performance. The effect in persons with progressive multiple sclerosis (pwPMS) having cognitive dysfunction is unknown. OBJECTIVE: To profile DT-performance during walking in cognitively impaired pwPMS and examine DT-performance by disability level. METHODS: Secondary analyses were conducted on baseline data from the CogEx-study. Participants, enrolled with Symbol Digit Modalities Test 1.282 standard deviations below normative value, performed a cognitive single task ([ST], alternating alphabet), motor ST (walking) and DT (both). Outcomes were number of correct answers on the alternating alphabet task, walking speed, and DT-cost (DTC: decline in performance relative to the ST). Outcomes were compared between EDSS subgroups (≤ 4, 4.5-5.5, ≥ 6). Spearman correlations were conducted between the DTC(motor) with clinical measures. Adjusted significance level was 0.01. RESULTS: Overall, participants (n = 307) walked slower and had fewer correct answers on the DT versus ST (both p < 0.001), with a DTC(motor) of 15.8% and DTC(cognitive) of 2.7%. All three subgroups walked slower during the DT versus ST, with DTC(motor) different from zero (p's < 0.001). Only the EDSS ≥ 6 group had fewer correct answers on the DT versus ST (p < 0.001), but the DTC(cognitive) did not differ from zero for any of the groups (p ≥ 0.039). CONCLUSION: Dual tasking substantially affects walking performance in cognitively impaired pwPMS, to a similar degree for EDSS subgroups.
 BACKGROUND: Neuroinflammation and neurodegeneration are pathological hallmarks of multiple sclerosis (MS). Brain-derived neurotrophic factor (BDNF), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) are blood-based biomarkers for neurogenesis, axonal damage and astrocyte reactivity, respectively. We hypothesize that exercise has a neuroprotective effect on MS reflected by normalization of BDNF, NfL and GFAP levels. OBJECTIVES: To investigate the neuroprotective effect of aerobic training (AT) compared to a control intervention on blood-based biomarkers (i.e. BDNF, NfL, GFAP) in people with MS (pwMS). METHODS: In the TREFAMS-AT (Treating Fatigue in Multiple Sclerosis - Aerobic Training) study, 89 pwMS were randomly allocated to either a 16-week AT intervention or a control intervention (3 visits to a MS nurse). In this secondary analysis, blood-based biomarker concentrations were measured in 55 patients using Simoa technology. Changes in pre- and post-intervention concentrations were compared and between-group differences were assessed using analysis of covariance (ANCOVA). Confounding effects of age, sex, MS-related disability assessed using the Expanded Disability Status Scale (EDSS), MS duration, use of disease-modifying medication, and Body Mass Index were considered. RESULTS: Blood samples were available for 30 AT and 25 control group participants (mean age 45.6 years, 71% female, median disease duration 8 years, median EDSS score 2.5). Within-group changes in both study groups were small and non-significant, with the exception of BDNF in the control group (median (interquartile range) -2.1 (-4.7; 0)). No between-group differences were found for any biomarker: BDNF (β = 0.11, 95%CI (-3.78 to 4.00)), NfL (β = -0.04, 95%CI (-0.26 to 0.18)), and GFAP (β = -0.01, 95%CI (-0.16 to 0.15)), adjusted for confounders. CONCLUSION: Aerobic exercise therapy did not result in statistically significant changes in the tested neuro-specific blood-based biomarkers in people with MS. TRIAL REGISTRATION: this study is registered under number ISRCTN69520623 (https://www.isrctn.com/ISRCTN695206).
 BACKGROUND: There is an unmet need for reliable and sensitive measures for better monitoring people with multiple sclerosis (PwMS) to detect disease progression early and adapt therapeutic measures accordingly. OBJECTIVE: To assess reliability of extracted features and meaningfulness of 11 tests applied through a smartphone application ("dreaMS"). METHODS: PwMS (age 18-70 and EDSS ≤ 6.5) and matched healthy volunteers (HV) were asked to perform tests installed on their smartphone once or twice weekly for 5 weeks. Primary outcomes were test-retest reliability of test features (target: intraclass correlation [ICC] ≥ 0.6 or median coefficient of variation [mCV] < 0.2) and reported meaningfulness of the tests by PwMS. Meaningfulness was self-assessed for each test on a 5-point Likert scale (target: mean score of > 3) and by a structured interview. CLINICALTRIALS: gov Identifier: NCT04413032. RESULTS: We included 31 PwMS (21 [68%] female, mean age 43.4 ± 12.0 years, median EDSS 3.0 [range 1.0-6.0]) and 31 age- and sex-matched healthy volunteers. Out of 133 features extracted from 11 tests, 89 met the preset reliability criteria. All 11 tests were perceived as highly meaningful to PwMS. CONCLUSION: The dreaMS app reliably assessed features reflecting key functional domains meaningful to PwMS. More studies with longer follow-up are needed to prove validity of these measures as digital biomarkers in PwMS.
 OBJECTIVES: To develop an automatic method for accurate and robust thalamus segmentation in T1w-MRI for widespread clinical use without the need for strict harmonization of acquisition protocols and/or scanner-specific normal databases. METHODS: A three-dimensional convolutional neural network (3D-CNN) was trained on 1975 T1w volumes from 170 MRI scanners using thalamus masks generated with FSL-FIRST as ground truth. Accuracy was evaluated with 18 manually labeled expert masks. Intra- and inter-scanner test-retest stability were assessed with 477 T1w volumes of a single healthy subject scanned on 123 MRI scanners. The sensitivity of 3D-CNN-based volume estimates for the detection of thalamus atrophy was tested with 127 multiple sclerosis (MS) patients and a normal database comprising 4872 T1w volumes from 160 scanners. The 3D-CNN was compared with a publicly available 2D-CNN (FastSurfer) and FSL. RESULTS: The Dice similarity coefficient of the automatic thalamus segmentation with manual expert delineation was similar for all tested methods (3D-CNN and FastSurfer 0.86 ± 0.02, FSL 0.87 ± 0.02). The standard deviation of the single healthy subject's thalamus volume estimates was lowest with 3D-CNN for repeat scans on the same MRI scanner (0.08 mL, FastSurfer 0.09 mL, FSL 0.15 mL) and for repeat scans on different scanners (0.28 mL, FastSurfer 0.62 mL, FSL 0.63 mL). The proportion of MS patients with significantly reduced thalamus volume was highest for 3D-CNN (24%, FastSurfer 16%, FSL 11%). CONCLUSION: The novel 3D-CNN allows accurate thalamus segmentation, similar to state-of-the-art methods, with considerably improved robustness with respect to scanner-related variability of image characteristics. This might result in higher sensitivity for the detection of disease-related thalamus atrophy. KEY POINTS: • A three-dimensional convolutional neural network was trained for automatic segmentation of the thalamus with a heterogeneous sample of T1w-MRI from 1975 patients scanned on 170 different scanners. • The network provided high accuracy for thalamus segmentation with manual segmentation by experts as ground truth. • Inter-scanner variability of thalamus volume estimates across different MRI scanners was reduced by more than 50%, resulting in increased sensitivity for the detection of thalamus atrophy.
 Multiple sclerosis (MS) is a disease in which the immune system damages components of the central nervous system (CNS), leading to the destruction of myelin and the formation of demyelinating plaques. This often occurs in episodic "attacks" precipitated by the transmigration of leukocytes across the blood-brain barrier (BBB), and repeated episodes of demyelination lead to substantial losses of axons within and removed from plaques, ultimately leading to progressive neurological dysfunction. Within leukocyte populations, macrophages and T and B lymphocytes are the predominant effectors. Among current immunotherapies, oral cladribine's impact on lymphocytes is well characterised, but little is known about its impact on other leukocytes such as monocytes and dendritic cells (DCs). The aim of this study was to determine the transmigratory ability of monocyte and DC subsets in healthy subjects and untreated and cladribine-treated relapse-remitting MS (RRMS) patients using a well-characterised model of the BBB. Peripheral blood mononuclear cells from subjects were added to an in vitro transmigration assay to assess cell migration. Our findings show that while prior treatment with oral cladribine inhibits the migration of intermediate monocytes, it has no impact on the transmigration of DC subsets. Overall, our data indicate a previously unrecognised role of cladribine on intermediate monocytes, known to accumulate in the brain active MS lesions.
 BACKGROUND: Primary progressive multiple sclerosis (PPMS) is characterised by gradual worsening of disability from symptom onset. Knowledge about the natural course of PPMS remains limited. METHODS: PPMS patients from the German NeuroTransData (NTD) MS registry with data from 56 outpatient practices were employed for retrospective cross-sectional and longitudinal analyses. The cross-sectional analysis included a contemporary PPMS cohort with a documented visit within the last 2 years before index date (1 Jan 2021). The longitudinal analysis included a disease modifying therapy (DMT)-naïve population and focused on the evolution of expanded disability status scale (EDSS) from the first available assessment at or after diagnosis within the NTD registry to index date. Outcome measures were estimated median time from first EDSS assessment to first 24-week confirmed EDSS ≥ 4 and ≥ 7. Besides EDSS change, the proportion of patients on disability pension were described over time. RESULTS: The cross-sectional analysis included 481 PPMS patients (59.9% female, mean [standard deviation, SD] age 60.5 [11.5] years, mean [SD] EDSS 4.9 [2.1]). Estimated median time from first EDSS assessment after diagnosis to reach 24-week confirmed EDSS ≥ 4 for DMT-naïve patients was 6.9 years. Median time to EDSS ≥ 7 was 9.7 years for 25% of the population. Over a decade mean (SD) EDSS scores increased from 4.6 (2.1) to 5.7 (2.0); the proportion of patients on disability pension increased from 18.9% to 33.3%. CONCLUSIONS: This study provides first insights into the German NTD real-world cohort of PPMS patients. Findings confirm the steadily deteriorating course of PPMS accompanied by increasingly limited quality of life.
 OBJECTIVE: It has been reasoned that stressful life events tend to alter immune function thereby increasing the susceptibility to autoimmune diseases including multiple sclerosis (MS). Using the database of Kuwait National MS Registry, this quasi-experimental study assessed the impact of the first Gulf War (Iraqi invasion of Kuwait in 1990) on MS risk in Kuwait. METHODS: MS incidence data from 1980 to 2019 were obtained from the Kuwait National MS Registry. Annual age-standardized incidence rates (ASIRs) (per 10(5) person-years) were computed using the World Standard Population as a reference. Interrupted time series analysis with the option of autoregressive order (1) was used to evaluate the impact of the first Gulf War on MS risk by treating 1990 as an intervention year. RESULTS: Estimated baseline annual ASIR (per 10(5) person-years) was 0.38 (95% CI: -1.02, 1.78; p = 0.587). MS ASIRs (per 10(5) person-years) tended to increase significantly every year prior to 1990 by 0.45 (ASIR per 10(5) person-years = 0.45; 95% CI: 0.15, 0.76; p = 0.005). During the first year of the first Gulf War, there seemed to be a non-significant increase (step change) in ASIRs (per 10(5) person-years) of MS (ASIR per 10(5) person-years = 0.85; 95% CI: - 5.16, 6.86; p = 0.775) followed by a non-significant increase in the annual trend in MS ASIRs per 10(5) person-years (relative to the preintervention trend i.e., the difference between the pre-first Gulf War versus the post-first Gulf War trends) by 0.65 (ASIR per 10(5) person-years = 0.65; 95% CI: - 0.22, 1.52; p = 0.138). However, a postestimation measure of the post-first Gulf War trend was statistically significant (ASIR per 10(5) person-years = 1.10; 95% CI: 0.40, 1.80; p = 0.003), which implies that the post-first Gulf War trend in the annual ASIRs (per 10(5) person-years) inclined to be the same as was the pre-first Gulf War (i.e., counterfactual of the pre-first Gulf War trend in annual ASIRs (per 10(5) person-years) as if no first Gulf War took place).The Durbin-Watson test statistic (d = 1.89) showed almost non-significant autocorrelations across the time series observations on ASIRs (per 10(5) person-years). CONCLUSIONS: This study suggests that the first Gulf War was not significantly associated with the increasing trend in MS risk at population level in Kuwait neither with any short-term change nor with secular trend. Future studies may consider confirming the role of conflict-related stress or other stressful life events in potential exacerbation of MS risk along with unraveling biologically plausible mechanistic pathways.

 BACKGROUND AND PURPOSE: Reduced cerebral perfusion has been observed in multiple sclerosis (MS) and may contribute to tissue loss both acutely and chronically. Here, we test the hypothesis that hypoperfusion occurs in MS and relates to the presence of irreversible tissue damage. METHODS: In 91 patients with relapsing MS and 26 healthy controls (HC), gray matter (GM) cerebral blood flow (CBF) was assessed using pulsed arterial spin labeling. GM volume, T1 hypointense and T2 hyperintense lesion volumes (T1LV and T2LV, respectively), and the proportion of T2-hyperintense lesion volume that appears hypointense on T1-weighted magnetic resonance imaging (T1LV/T2LV) were quantified. GM CBF and GM volume were evaluated globally, as well as regionally, using an atlas-based approach. RESULTS: Global GM CBF was lower in patients (56.9 ± 12.3 mL/100 g/min) than in HC (67.7 ± 10.0 mL/100 g/min; p < 0.001), a difference that was widespread across brain regions. Although total GM volume was comparable between groups, significant reductions were observed in a subset of subcortical structures. GM CBF negatively correlated with T1LV (r = -0.43, p = 0.0002) and T1LV/T2LV (r = -0.37, p = 0.0004), but not with T2LV. CONCLUSIONS: GM hypoperfusion occurs in MS and is associated with irreversible white matter damage, thus suggesting that cerebral hypoperfusion may actively contribute and possibly precede neurodegeneration by hampering tissue repair abilities in MS.
 BACKGROUND: This study was conducted with the aim of identifying the burden of psychosocial factors on the worsening symptoms of multiple sclerosis. METHODS: This as conducted with a qualitative approach and conventional content analysis among patients with Multiple sclerosis in Mashhad. Data were collected through semi-structured interviews with patients with Multiple sclerosis. Twenty-one patients with Multiple sclerosis were selected through purposive sampling and snowball sampling. The data were analyzed using Graneheim and Lundman method. Guba and Lincoln's criteria were used for evaluating research transferability. The data collection and management was performed by using the MAXQADA 10 software. RESULTS: In explanation of the psychosocial factors of patients with Multiple sclerosis, one category (psychosocial tensions) and three subcategories of stress (physical symptoms, emotional symptoms, and behavioral symptoms), agitation (family disorder, treatment-related concerns, and social relationship concerns), and stigmatization (social stigma and internalized stigma) were extracted. CONCLUSION: The results of this study show that patients with Multiple sclerosis are faced with concerns such as stress, agitation, and fear of stigma, and need support and understanding from the family and community to overcome these concerns. Society must base its health policies on addressing the challenges faced by patients. Accordingly, the authors argue that health policies, and consequently, healthcare systems, need to address patients' ongoing challenges as a priority in caring for patients with Multiple sclerosis.
 Virtual Reality (VR) has emerged as a new treatment approach in neurorehabilitation (NR). REAVITELEM Study is a specific NR intervention program based on VR at center (VRC) and tele-rehabilitation (TR) in Argentina. Methods First national multicenter study with a 12-week program intervention of VRC and TR. Participants were assessed at baseline, at 6th and 12th week. Phase I: recruitment and gather of 5 NR Centers from Argentina by the coordinator center (INEBA) to unify evaluation and intervention criteria. Phase II, all centers completed VRC an TR programs. Intervention was 30-minute session, twice a week for 12 weeks. Outcome measures: Expanded Disability Status Scale (EDSS), Fist and Key Pinch Dynamometry, Beck Depression Inventory-Fast Screen, Fatigue Severity Scale, Functional Independence Measure (FIM), International Questionnaire investigating Quality of life in MS (MusiQol) and a Visual Analogue Scale (VAS) of satisfaction after treatment. Results A total of 54 PWMS (23 males) were recruited for VRC. Afterwards, 14 completed TR. The mean age for VRC was 44.72 (SD ± 13.74) and 41.71 (SD ± 10.5) for TR. The median EDSS was 4, 75 for VR. At VRC, 42 have RRMS, 8 have SPMS and 4 PPMS. At TR, 13 have RRMS and 1 have SPMS. The VAS reported an excellent level of satisfaction after treatment with an average of 9, 02 (SD±1.35) in VRC and 9.42 (SD±0.66) in TR. There were significant differences for MusiQol, which improved from baseline to the post-intervention assessment at VRC (p=<0.001) and at TR (p = 0.004) as well as FIM post-intervention assessment at VCR (p = 0.02) and TR (p = 0.04). Conclusion this study suggest that the NR treatment based on VR in MS in Argentina, is an additional effective tool, which favors improvements in the level of functioning in activities of daily living, quality of life, mood, and satisfaction with the treatment.
 BACKGROUND: Cognitive dysfunction, including reduced Information processing speed (IPS), is relatively common in multiple sclerosis(MS). IPS deficits have profound effects on several aspects of patients' life. Previous studies showed that deep gray matter atrophy is highly correlated with overall cognitive impairment in MS. However, the effect of deep gray matter atrophy on IPS deficits is not well understood. In this study, we evaluated the effects of deep gray matter volume changes on IPS in people with early relapse-remitting MS (RRMS) compared to healthy control. METHODS: In this case-control study, we enrolled 63 case with RRMS and 36 healthy controls. All patients were diagnosed within 6 years. IPS was evaluated using the Integrated Cognitive Assessment (ICA) test. We also performed a 1.5T MRI to evaluate deep gray matter structures. RESULTS: People with RRMS had lower accuracy in the ICA test (p = .01). However, the reaction time did not significantly differ between RRMS and control groups (p = .6). Thalamus volume was significantly lower in the RRMS group with impaired IPS compared to the RRMS with normal IPS and control groups (p < 10(-4)). Other deep gray matter structures were not significantly different between the RRMS with impaired IPS group and the RRMS with normal IPS group. CONCLUSION: Some people with MS are impaired in IPS even in the early stages of the disease. Thalamic atrophy affected IPS in these patients, however atrophy in other deep gray matter structures, including caudate, putamen, globus pallidus, hippocampus, amygdala, accumbens, and cerebellum, were not significantly correlated with IPS impairment in early RRMS.
 BACKGROUND: Effectiveness of cladribine tablets, an oral disease-modifying treatment (DMT) for multiple sclerosis (MS), was established in clinical trials and confirmed with real-world experience. OBJECTIVES: Use real-world data to compare treatment patterns and clinical outcomes in people with MS (pwMS) treated with cladribine tablets versus other oral DMTs. METHODS: Retrospective treatment comparisons were based on data from the international MSBase registry. Eligible pwMS started treatment with cladribine, fingolimod, dimethyl fumarate, or teriflunomide tablets from 2018 to mid-2021 and were censored at treatment discontinuation/switch, death, loss to follow-up, pregnancy, or study period end. Treatment persistence was evaluated as time to discontinuation/switch; relapse outcomes included time to first relapse and annualized relapse rate (ARR). RESULTS: Cohorts included 633 pwMS receiving cladribine tablets, 1195 receiving fingolimod, 912 receiving dimethyl fumarate, and 735 receiving teriflunomide. Individuals treated with fingolimod, dimethyl fumarate, or teriflunomide switched treatment significantly more quickly than matched cladribine tablet cohorts (adjusted hazard ratio (95% confidence interval): 4.00 (2.54-6.32), 7.04 (4.16-11.93), and 6.52 (3.79-11.22), respectively). Cladribine tablet cohorts had significantly longer time-to-treatment discontinuation, time to first relapse, and lower ARR, compared with other oral DMT cohorts. CONCLUSION: Cladribine tablets were associated with a significantly greater real-world treatment persistence and more favorable relapse outcomes than all oral DMT comparators.
 BACKGROUND AND OBJECTIVES: Migraine is common among people with multiple sclerosis (MS), but the reasons for this are unknown. We tested 3 hypothesized mechanisms for this observed comorbidity, including migraine is a risk factor of MS, genetic variants are shared between the conditions, and migraine is because of MS. METHODS: Data were from 2 sources: publicly available summary statistics from genome-wide association studies of MS (N = 115,748) and migraine (N = 375,752 and N = 361,141) and a case-control study of MS recruited from the Kaiser Permanente Northern California Health Plan (N = 1,991). For the latter participants, migraine status was ascertained using a validated electronic health record migraine probability algorithm or self-report. Using the public summary statistics, we used 2-sample Mendelian randomization to test whether a migraine genetic instrumental variable was associated with MS. We used linkage disequilibrium score regression and LOGODetect to ascertain whether MS and migraine shared genetic variants across the genome and regionally. Using the Northern California MS cohort, we used logistic regression to identify whether people with both MS and migraine had different odds of clinical characteristics (e.g., age at MS onset, Perceived Deficits Questionnaire, and depression) or MS-specific risk factors (e.g., body mass index, smoking status, and infectious mononucleosis status) compared with people with MS without migraine. RESULTS: We did not find evidence supporting migraine as a causal risk factor of MS (p = 0.29). We did, however, identify 4 major histocompatibility complex (MHC) loci shared between MS and migraine. Among the Northern California MS cohort, 774 (39%) experienced migraine. People with both MS and migraine from this cohort were more likely to ever smoke (odds ratio [OR] = 1.30, 95% CI: 1.08-1.57), have worse self-reported cognitive deficits (OR = 1.04, 95% CI: 1.02-1.06), and ever experience depression (OR = 1.48, 95% CI: 1.22-1.80). DISCUSSION: Our findings do not support migraine as a causal risk factor of MS. Several genetic variants, particularly in the MHC, may account for some of the overlap. It seems likely that migraine within the context of MS is because of MS. Identifying what increases the risk of migraine within MS might lead to an improved treatment and quality of life.
 BACKGROUND: Multiple sclerosis (MS) is an autoimmune, T-cell-dependent, inflammatory, demyelinating disease of the central nervous system, with an unpredictable course. Current MS therapies focus on treating and preventing exacerbations, and avoiding the progression of disability. At present, there is no treatment that is capable of safely and effectively reaching these objectives. Clinical trials suggest that alemtuzumab, a humanized monoclonal antibody, could be a promising option for MS. OBJECTIVES: To evaluate the benefits and harms of alemtuzumab alone or associated with other treatments in people with any form of MS. SEARCH METHODS: We used standard, extensive Cochrane search methods. The latest search date was 21 June 2022. SELECTION CRITERIA: We included randomized controlled trials (RCTs) in adults with any subtype of MS comparing alemtuzumab alone or associated with other medications versus placebo; another active drug; or alemtuzumab in another dose, regimen, or duration. DATA COLLECTION AND ANALYSIS: We used standard Cochrane methods. Our co-primary outcomes were 1. relapse-free survival, 2. sustained disease progression, and 3. number of participants experiencing at least one adverse event. Our secondary outcomes were 4. participants free of clinical disability, 5. quality of life, 6. change in disability, 7. fatigue, 8. new or enlarging lesions on resonance imaging, and 9. dropouts. We used GRADE to assess certainty of evidence for each outcome. MAIN RESULTS: We included three RCTs (1713 participants) comparing intravenous alemtuzumab versus subcutaneous interferon beta-1a for relapsing-remitting MS. Participants were treatment-naive (two studies) or had experienced at least one relapse after interferon or glatiramer (one study). Alemtuzumab was given at doses of 12 mg/day or 24 mg/day for five days at months 0 and 12, or 24 mg/day for three days at months 12 and 24. Participants in the interferon beta-1a group received 44 μg three times weekly. Alemtuzumab 12 mg: 1. may improve relapse-free survival at 36 months (hazard ratio [HR] 0.31, 95% confidence interval [CI] 0.18 to 0.53; 1 study, 221 participants; low-certainty evidence); 2. may improve sustained disease progression-free survival at 36 months (HR 0.25, 95% CI 0.11 to 0.56; 1 study, 223 participants; low-certainty evidence); 3. may make little to no difference on the proportion of participants with at least one adverse event at 36 months (risk ratio [RR] 1.00, 95% CI 0.98 to 1.02; 1 study, 224 participants; low-certainty evidence), although the proportion of participants with at least one adverse event was high with both drugs; 4. may slightly reduce disability at 36 months (mean difference [MD] -0.70, 95% CI -1.04 to -0.36; 1 study, 223 participants; low-certainty evidence). The evidence is very uncertain regarding the risk of dropouts at 36 months (RR 0.81, 95% CI 0.57 to 1.14; 1 study, 224 participants; very low-certainty evidence). Alemtuzumab 24 mg: 1. may improve relapse-free survival at 36 months (HR 0.21, 95% CI 0.11 to 0.40; 1 study, 221 participants; low-certainty evidence); 2. may improve sustained disease progression-free survival at 36 months (HR 0.33, 95% CI 0.16 to 0.69; 1 study, 221 participants; low-certainty evidence); 3. may make little to no difference on the proportion of participants with at least one adverse event at 36 months (RR 0.99, 95% CI 0.97 to 1.02; 1 study, 215 participants; low-certainty evidence), although the proportion of participants with at least one adverse event was high with both drugs; 4. may slightly reduce disability at 36 months (MD -0.83, 95% CI -1.16 to -0.50; 1 study, 221 participants; low-certainty evidence); 5. may reduce the risk of dropouts at 36 months (RR 0.08, 95% CI 0.01 to 0.57; 1 study, 215 participants; low-certainty evidence). For quality of life, fatigue, and participants free of clinical disease activity, the studies either did not consider these outcomes or they used different measuring tools to those planned in this review. AUTHORS' CONCLUSIONS: Compared with interferon beta-1a, alemtuzumab may improve relapse-free survival and sustained disease progression-free survival, and make little to no difference on the proportion of participants with at least one adverse event for people with relapsing-remitting MS at 36 months. The certainty of the evidence for these results was very low to low.
 Epstein-Barr virus infection, and perhaps almost exclusively delayed Epstein-Barr virus infection, seems to be a prerequisite for the development of multiple sclerosis. Siblings provide protection against infectious mononucleosis by occasionally preventing delayed primary Epstein-Barr virus infection, with its associated high risk of infectious mononucleosis. Each additional sibling provides further protection according to the age difference between the index child and the sibling. The closer the siblings are in age, the higher the protection, with younger siblings being more protective against infectious mononucleosis than older siblings. If the hypothesis that delayed Epstein-Barr virus infection is necessary for the development of multiple sclerosis is true, then the relative risk of multiple sclerosis as a function of sibship constellation should mirror the relative risk of infectious mononucleosis as a function of sibship constellation. Such an indirect hypothesis test is necessitated by the fact that age at primary Epstein-Barr virus infection is unknown for practically all people who have not experienced infectious mononucleosis. In this retrospective cohort study using nationwide registers, we followed all Danes born during the period 1971-2018 (n = 2 576 011) from 1977 to 2018 for hospital contacts with an infectious mononucleosis diagnosis (n = 23 905) or a multiple sclerosis diagnosis (n = 4442), defining two different end points. Relative risks (hazard ratios) of each end point as a function of sibship constellation were obtained from stratified Cox regression analyses. The hazard ratios of interest for infectious mononucleosis and multiple sclerosis could be assumed to be identical (test for homogeneity P = 0.19), implying that having siblings, especially of younger age, may protect a person against multiple sclerosis through early exposure to the Epstein-Barr virus. Maximum protection per sibling was obtained by having a 0-2 years younger sibling, corresponding to a hazard ratio of 0.80, with a 95% confidence interval of 0.76-0.85. The corresponding hazard ratio from having an (0-2 years) older sibling was 0.91 (0.86-0.96). Our results suggest that it may be possible essentially to eradicate multiple sclerosis using an Epstein-Barr virus vaccine administered before the teenage years. Getting there would require both successful replication of our study findings and, if so, elucidation of why early Epstein-Barr virus infection does not usually trigger the immune mechanisms responsible for the association between delayed Epstein-Barr virus infection and multiple sclerosis risk.
 BACKGROUND: Mounting evidence suggests differences in the disease characteristics of multiple sclerosis (MS) across ethnic and racial groups. Although it is widely recognized that falls are a significant concern for people with MS (PwMS), no study has explored if the fall risk is related to race/ethnicity in PwMS. The primary purpose of this pilot study was to examine whether the risk of falls is different between age-matched White, Black, and Latinx PwMS. METHODS: Fifteen White, 16 Black, and 22 Latinx, age-matched ambulatory PwMS were selected from previous studies. Demographic and disease information, the fall risk (annual fall prevalence, proportion of recurrent fallers, and the number of falls) in the preceding year, and a battery of fall risk factors (including the disability level, gait speed, and cognition) were compared between race/ethnicity groups. The fall history was gathered using the valid fall questionnaire. The disability level was assessed by the Patient Determined Disease Steps score. Gait speed was measured using the Timed 25-Foot Walk test. The short Blessed Orientation-Memory-Concentration test evaluates participants' cognitive function. SPSS 28.0 was used for all statistical analyses and a significance level of 0.05 was applied. RESULTS: Among the demographic measurements, age (p = 0.052), sex (p = 0.17), body mass (p = 0.338), age at diagnosis (p = 0.623), and disease duration (p = 0.280) were comparable across groups while the body height was significantly different between racial groups (p < 0.001). Binary logistic regression analysis did not detect a significant relationship between the faller status and racial/ethnic group (p = 0.571) after controlling the body height and age. Similarly, the recurrent faller status was not associated with our participants' race/ethnicity (p = 0.519). There was no difference in the number of falls in the past year between racial groups (p = 0.477). The fall risk factors of disability level (p = 0.931) and gait speed (p = 0.252) were similar among the groups. However, the White group had a significantly better Blessed Orientation-Memory-Concentration score than the Black (p = 0.037) and Latinx (p = 0.036) groups. No significant difference in the Blessed Orientation-Memory-Concentration score was observed between the Black and Latinx groups (p = 0.857). CONCLUSION: As the initial attempt, our preliminary study suggests that the annual risk of being a faller or recurrent faller may not be affected by PwMS' race/ethnicity. Similarly, the physical functions (quantified by the Patient Determined Disease Steps and the gait speed) are comparable between racial/ethnic groups. However, the cognitive function may differ among age-matched racial groups of PwMS. Given the small sample size, caution is warranted when interpreting our findings. Despite the limitations, our study provides pilot knowledge about how race/ethnicity affects the fall risk in PwMS. Due to the limited sample size, it is too soon to definitively conclude that race/ethnicity has ignorable impacts on fall risk in PwMS. Further studies with larger sample sizes and more fall risk metrics are needed to clarify the effects of race/ethnicity on fall risk in this population.
 The negative effects of thermal stress on Multiple Sclerosis (MS)' symptoms have long been known. However, the underlying mechanisms of MS heat and cold intolerance remain unclear. The aim of this study was to evaluate body temperatures, thermal comfort, and neuropsychological responses to air temperatures between 12 and 39 °C in people with MS compared to healthy controls (CTR). Twelve MS (5 males/7 females; age: 48.3 ± 10.8 years; EDSS range: 1-7) and 11 CTR participants (4 males /7 females; age: 47.5 ± 11.3 years) underwent two 50-min trials in a climatic chamber. Air temperature was ramped from 24 °C to either 39 °C (HEAT) or 12 °C (COLD) and we continuously monitored participants' mean skin (T(sk)) and rectal temperatures (T(rec)), heart rate and mean arterial pressure. We recorded participants' self-reported thermal sensation and comfort, mental and physical fatigue, and we assessed their cognitive performance (information processing). Changes in mean T(sk) and T(rec) did not differ between MS and CTR neither during HEAT nor COLD. However, at the end of the HEAT trial, 83% of MS participants and 36% of CTR participants reported being "uncomfortable". Furthermore, self-reports of mental and physical fatigue increased significantly in MS but not CTR (p < 0.05), during both HEAT and COLD. Information processing was lower in MS vs. CTR (p < 0.05); yet this cognitive impairment was not exacerbated by HEAT nor COLD (p > 0.05). Our findings indicate that neuropsychological factors (i.e. discomfort and fatigue) could contribute to MS heat and cold intolerance in the absence of deficits in the control of body temperature.
 BACKGROUND AND PURPOSE: Magnetic resonance imaging (MRI) plays a key role in diagnosing and monitoring multiple sclerosis (MS). Double inversion recovery (DIR) is a pulse sequence that has proven highly effective at detecting cortical lesions but is understudied in the spinal cord. We hypothesize that DIR images obtained during brain MRI can be of value in assessing the upper spinal cord of MS patients. METHODS: We retrospectively examined brain MRI exams of 64 patients with established MS, who had also undergone cervical spine MRI. Two blinded MS expert readers, who assessed the scans for lesion numbers and rated lesion visibility and overall image quality, reviewed brain 3-dimensional DIR sagittal and coronal images. Standardized mean contrast-to-noise ratios (C/N) and standard deviation (SD) were calculated in representative lesions for each patient and compared to those of 3-dimensional FLAIR images. RESULTS: For the analysis of lesions categorized as "definite lesions," the sensitivity was 87%, specificity was 61%, and negative predictive value was 80%. On the other hand, for "definite" plus "probable" lesions, the sensitivity was 91%, the specificity was 54%, and negative predictive value was 86%. DIR demonstrated lesions with an average C/N of 7.56 with an SD of 1.77. FLAIR sequence demonstrated lesions with an average C/N of 0.67 and SD of 1.27. CONCLUSIONS: Sagittally acquired brain DIR can provide useful information on upper spinal cord lesions, with high C/N. In theory, this should facilitate the attainment of McDonald's or the Magnetic Resonance Imaging in MS (MAGNIMS) criteria in some cases, without a dedicated cervical spine MRI exam.
 BACKGROUND: Accumulating evidence has demonstrated that an association between chronic pain and autoimmune diseases (AIDs). Nevertheless, it is unclear whether these associations refer to a causal relationship. We used a two-sample Mendelian randomization (MR) method to determine the causal relationship between chronic pain and AIDs. METHODS: We assessed genome-wide association study (GWAS) summary statistics for chronic pain [multisite chronic pain (MCP) and chronic widespread pain (CWP)], and eight common AIDs, namely, amyotrophic lateral sclerosis (ALS), celiac disease (CeD), inflammatory bowel disease (IBD), multiple sclerosis (MS), rheumatoid arthritis (RA), systemic lupus Erythematosus (SLE), type 1 diabetes (T1D) and psoriasis. Summary statistics data were from publicly available and relatively large-scale GWAS meta-analyses to date. The two-sample MR analyses were first performed to identify the causal effect of chronic pain on AIDs. The two-step MR and multivariable MR were used to determine if mediators (BMI and smoking) causally mediated any connection and to estimate the proportion of the association mediated by these factors combined. RESULTS: With the utilization of MR analysis, multisite chronic pain was associated with a higher risk of MS [odds ratio (OR) = 1.59, 95% confidence interval (CI) = 1.01-2.49, P = 0.044] and RA (OR = 1.72, 95% CI = 1.06-2.77, P = 0.028). However, multisite chronic pain had no significant effect on ALS (OR = 1.26, 95% CI = 0.92-1.71, P = 0.150), CeD (OR = 0.24, 95% CI = 0.02-3.64, P = 0.303), IBD (OR = 0.46, 95% CI = 0.09-2.27, P = 0.338), SLE (OR = 1.78, 95% CI = 0.82-3.88, P = 0.144), T1D (OR = 1.15, 95% CI = 0.65-2.02, P = 0.627) or Psoriasis (OR = 1.59, 95% CI = 0.22-11.26, P = 0.644). We also found positive causal effects of MCP on BMI and causal effects of BMI on MS and RA. Moreover, there were no causal connections between genetically predicted chronic widespread pain and the risk of most types of AIDs disease. CONCLUSION: Our MR analysis implied a causal relationship between MCP and MS/RA, and the effect of MCP on MS and RA may be partially mediated by BMI.
 Studies indicate differences in the clinical phenotypes and neuroimaging of children with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) compared to multiple sclerosis; however, there are limited data assessing the socioeconomic and paraclinical differences between these distinct disorders. This retrospective study identified patients aged <18 years at time of diagnosis with MOGAD or multiple sclerosis. Demographics, birth history, socioeconomic factors (insurance type, median income, parental education level), and paraclinical features (clinical manifestations, laboratory evaluation) were recorded for eligible participants. Seventy-eight patients (28 MOGAD, 50 multiple sclerosis) met inclusion criteria. Mothers of MOGAD children were more likely to have attended college compared to the mothers of children with multiple sclerosis (80% vs 49%; P = .02). Though MOGAD patients had greater rates of day care attendance (81% vs 57%), lower rates of birth complications (7% vs 21%), and higher rates of being breastfed (65% vs 46%), these findings did not meet predefined statistical significance. Clinically, children with MOGAD exhibited a lower body mass index percentile at presentation (58th ± 27th percentile vs 83rd ± 20th percentile; P = .0001) and were younger (7.6 ± 4.1 vs 14.8 ± 1.6 years; P < .0001) and more likely to exhibit an infectious prodrome (57% vs 10%; P < .0001). MOGAD patients were less likely to have evidence of remote Epstein-Barr virus infection (29% vs 100%; P < .0001) and less likely to have ≥3 unique oligoclonal bands in the cerebrospinal fluid (5% vs 87%; P < .001). Compared with multiple sclerosis, children with MOGAD exhibit lower body mass index percentiles at presentation, are more likely to have mothers with higher education levels, and are less likely to have had prior Epstein-Barr virus infection. Our data confirm that MOGAD patients are younger, more likely to exhibit infectious prodrome, and are less likely to exhibit intrathecal synthesis of oligoclonal bands. These features provide new insights into the differentiating pathobiology of MOGAD and may be helpful in differentiating these children from multiple sclerosis early in the diagnostic evaluation.

 Multiple sclerosis (MS) is a severely debilitating disease which requires accurate and timely diagnosis. MRI is the primary diagnostic vehicle; however, it is susceptible to noise and artifact which can limit diagnostic accuracy. A myriad of denoising algorithms have been developed over the years for medical imaging yet the models continue to become more complex. We developed a lightweight algorithm which utilizes the image's inherent noise via dictionary learning to improve image quality without high computational complexity or pretraining through a process known as orthogonal matching pursuit (OMP). Our algorithm is compared to existing traditional denoising algorithms to evaluate performance on real noise that would commonly be encountered in a clinical setting. Fifty patients with a history of MS who received 1.5 T MRI of the spine between the years of 2018 and 2022 were retrospectively identified in accordance with local IRB policies. Native resolution 5 mm sagittal images were selected from T2 weighted sequences for evaluation using various denoising techniques including our proposed OMP denoising algorithm. Peak signal to noise ratio (PSNR) and structural similarity index (SSIM) were measured. While wavelet denoising demonstrated an expected higher PSNR than other models, its SSIM was variable and consistently underperformed its comparators (0.94 ± 0.10). Our pilot OMP denoising algorithm provided superior performance with greater consistency in terms of SSIM (0.99 ± 0.01) with similar PSNR to non-local means filtering (NLM), both of which were superior to other comparators (OMP 37.6 ± 2.2, NLM 38.0 ± 1.8). The superior performance of our OMP denoising algorithm in comparison to traditional models is promising for clinical utility. Given its individualized and lightweight approach, implementation into PACS may be more easily incorporated. It is our hope that this technology will provide improved diagnostic accuracy and workflow optimization for Neurologists and Radiologists, as well as improved patient outcomes.

 INTRODUCTION: Optic neuritis (ON), an acute inflammation of the optic nerve resulting in eye pain and temporary vision loss, is one of the leading causes of vision-related hospital bed days in the U.S. Military and may be a harbinger of multiple sclerosis (MS). We developed a case identification algorithm to estimate incidence rates of ON and the conversion rate to MS based on a retrospective assessment of medical records of service members (SMs) of the U.S. Armed Force. MATERIALS AND METHODS: Electronic medical records (EMRs) from 2006 to 2018 in the Defense Medical Surveillance System were screened using the case identification algorithms for ON and MS diagnosis. The incidences rates of ON were calculated. The rates of conversion to MS was modeled using the Kaplan-Meier survival analysis. RESULTS: The overall incidence rate of ON was 8.1 per 100,000 from 2006 to 2018. Females had a rate (16.9 per 100,000) three times higher than males. Most (68%) of subsequent diagnoses of MS were made within 1 year after diagnosis of ON. The overall 5-year risk of progression to MS was 15% (11%-16% for 95% CI). The risk of conversion to MS in females was significantly higher than in males. CONCLUSIONS: We developed an efficient tool to explore the EMR database to estimate the burden of ON in the U.S. Military and the MS conversion based on a dynamic cohort. The estimated conversion rates to MS feeds into inform retention and fitness-for-duty policy in these SMs.
 INTRODUCTION: This study assessed the societal costs of multiple sclerosis (MS) in Lebanon, categorized by disease severity. METHODS: This was a cross-sectional, prevalence-based, bottom-up study using a face-to-face questionnaire. Patients were stratified by disease severity using the expanded disability status scale (EDSS); EDSS scores of 0-3, 4-6.5, and 7-9 indicating respectively mild, moderate, and severe MS. All direct medical, nonmedical, and indirect costs related to reduced productivity were accounted for regardless of who bore them. Costs, collected from various sources, were presented in international US dollars (US$) using the purchasing power parity (PPP) conversion rate. RESULTS: We included 210 Lebanese patients (mean age: 43.3 years; 65.7% females). The total annual costs per patient were PPP US$ 33,117 for 2021, 12.4 times higher than the nominal GDP per capita. Direct costs represented 52% (US$ 17,185), direct nonmedical costs 8% (US$ 2,722), and indirect costs 40% (US$ 13, 211) of the mean annual costs. The total annual costs per patient increased with disease severity and were PPP US$ 29,979, PPP US$ 36,125, PPP US$ 39,136 for mild, moderate, and severe MS, respectively. CONCLUSION: This study reveals the huge economic burden of MS on the Lebanese healthcare system and society.
 BACKGROUND: On May 2017, two generic drugs for fingolimod were introduced into the market in Israel, and most MS patients treated with Gilenya® (Novartis) were switched to fingolimod (Teva), or to Finolim (Rafa). In this study we analyzed the consequences of switching to generic fingolimod in a single MS center. METHODS: Study population included relapsing MS patients who were treated with Gilenya® for at least two year before May 2017, switched to generic fingolimod and remained on treatment for at least 2 years thereafter. Data before and after the switch were compared. RESULTS: Twenty-seven patients fulfilled the inclusion criteria (F = 20, RRMS=20, SPMS=7, average age 49±11.4 years, average disease duration=16.6 ± 7.6 years). Seventeen patients had to be switched back to the original Gilenya® due to intolerable new or worsening clinical adverse events (n = 9), clinical relapse (n = 1), clinical relapse with adverse events (n = 3), elevation of liver enzymes > X3 ULN (n = 3) and elevation of amylase (n = 1). Expanded Disability Status Scale (EDSS) score increased in 4 patients during the year before the switch, and in 12 patients during the year of treatment with generic fingolimod (p = 0.036). CONCLUSION: The tolerability, retention rate and probably efficacy of generic fingolimod seems to be lower than the original Gilenya®.

 Introduction: Patient-reported outcomes (PROs) are valuable measures for routine clinical care of people with multiple sclerosis (pwMS). Materials: 646 pwMS treated with interferon-β-1a (IFN-β-1a) were retrospectively included from the New York State Multiple Sclerosis Consortium. Clinical and PRO data at enrollment and 3 year follow-up were collected. PwMS with stable disease and disability worsening were matched (1:1) based on age, Expanded Disability Status Scale (EDSS) scores and disease duration. Disability worsening was determined based on trial criteria. Results: PwMS with future EDSS worsening had higher baseline and follow-up timed-25-foot walk (6.6 vs 5.5 s; 9.1 vs 5.5 s; p < 0.001) when compared with stable pwMS. Worsening pwMS reported higher baseline difficulties in getting up (odds ratio [OR] = 2.4; p = 0.009), climbing stairs (OR = 1.6; p = 0.024) and standing (OR = 2.2; p < 0.001). Worsening pwMS reported greater lower limb limitations (OR = 2.3; p = 0.004) and fatigue (OR = 1.8; p = 0.002). Conclusion: Higher fatigue and lower limb functional limitations are significant predictors of future disability worsening in pwMS.
 BACKGROUND AND OBJECTIVES: In women with highly active multiple sclerosis (MS), suspending rituximab (RTX) for planning pregnancy is associated with low disease reactivation. Whether this strategy reduces the risk of disease reactivity as compared with suspending natalizumab (NTZ) 3 months after conception is unclear. METHODS: We retrospectively included women with MS followed in our department during pregnancy and 1 year after birth who suspended NTZ at the end of the first trimester (option mostly proposed before 2016) or suspended RTX/ocrelizumab (RTX/OCR) in the year before conception (option proposed since 2016). RESULTS: In women who suspended NTZ, 45 pregnancies resulted in 3 miscarriages and 42 live births, including 1 newborn with major malformations. In women who suspended RTX/OCR, 37 pregnancies resulted in 3 miscarriages and 33 live births; 1 pregnancy was terminated for malformation. During pregnancy, relapse occurred in 3/42 (7.1%) patients of the NTZ group and 1/33 (3%) of the RTX/OCR group (p = 0.6). After delivery, relapse occurred in 9/42 (21.4%) patients of the NTZ group and 0/33 of the RTX/OCR group (p < 0.01). In the NTZ group, 8/9 relapses occurred in patients who restarted NTZ less than 4 weeks after delivery. The proportion of patients with gadolinium-enhanced and/or new T2 lesions on brain or spinal cord MRI performed after delivery was higher in the NTZ than RTX/OCR group (14/40 [35%] vs 1/31 [3%] patients, p = 0.001), the proportion with EDSS score progression during the period including pregnancy and the year after delivery was higher (7/42 [17%] vs 0/33 patients, p = 0.01), and the proportion fulfilling NEDA-3 during this period was lower (21/40 [53%] vs 30/31 [97%] patients, p < 0.001). DISCUSSION: Suspending RTX/OCR in the year before conception in women with highly active MS was associated with no disease reactivation during and after pregnancy. As previously reported, stopping NTZ at the end of the first trimester was associated with disease reactivation. In women receiving NTZ who are planning pregnancy, a bridge to RTX/OCR for pregnancy or continuing NTZ until week 34 are both reasonable clinical decisions. The RTX/OCR option is more comfortable for women and reduces the exposure of infants to monoclonal antibodies.
 INTRODUCTION: The authors aimed to analyze the possible relationship of the late response of trigemino-cervical reflex (TCR) with various clinical conditions having brainstem lesions and lesion localizations in the brainstem. METHODS: The authors enrolled 30 healthy subjects, 16 patients with stroke, 14 patients with multiple sclerosis (MS), and 9 patients with neuro-Behçet disease. All patients had at least one MRI, and lesion localization was classified into midbrain, pons, medulla oblongata, or their combinations. The TCR was recorded simultaneously from bilateral sternocleidomastoid and splenius capitis muscles. RESULTS: There was no significant difference based on lesion localization within the brainstem. Trigemino-cervical reflex latency was significantly longer in patients with MS compared with all other groups (P < 0.005 for each comparison). The Receiver Operating Characteristic curve analysis of sternocleidomastoid showed a cut-off value of 76.9 ms with 44% sensitivity and 92.7% specificity to predict MS. Similarly, the authors determined a cut-off value of 61.5 ms of splenius capitis latency with 38.5% sensitivity and 91.5% specificity to predict MS. CONCLUSIONS: This study showed that TCR might be abnormal in a given patient with one brainstem lesion, independently from the lesion localization. This may be attributed to a broad network of TCR at the brainstem. Thus, abnormally delayed TCR responses can be used as a tool for the discrimination of MS among other brainstem lesions.
 BACKGROUND: The cerebellum plays key roles in the pathology of multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), but the way in which these conditions affect how the cerebellum communicates with the rest of the brain (its connectome) and associated genetic correlates remains largely unknown. METHODS: Combining multimodal MRI data from 208 MS patients, 200 NMOSD patients and 228 healthy controls and brain-wide transcriptional data, this study characterized convergent and divergent alterations in within-cerebellar and cerebello-cerebral morphological and functional connectivity in MS and NMOSD, and further explored the association between the connectivity alterations and gene expression profiles. RESULTS: Despite numerous common alterations in the two conditions, diagnosis-specific increases in cerebellar morphological connectivity were found in MS within the cerebellar secondary motor module, and in NMOSD between cerebellar primary motor module and cerebral motor- and sensory-related areas. Both diseases also exhibited decreased functional connectivity between cerebellar motor modules and cerebral association cortices with MS-specific decreases within cerebellar secondary motor module and NMOSD-specific decreases between cerebellar motor modules and cerebral limbic and default-mode regions. Transcriptional data explained > 37.5% variance of the cerebellar functional alterations in MS with the most correlated genes enriched in signaling and ion transport-related processes and preferentially located in excitatory and inhibitory neurons. For NMOSD, similar results were found but with the most correlated genes also preferentially located in astrocytes and microglia. Finally, we showed that cerebellar connectivity can help distinguish the three groups from each other with morphological connectivity as predominant features for differentiating the patients from controls while functional connectivity for discriminating the two diseases. CONCLUSIONS: We demonstrate convergent and divergent cerebellar connectome alterations and associated transcriptomic signatures between MS and NMOSD, providing insight into shared and unique neurobiological mechanisms underlying these two diseases.
 Vaccines play a crucial role in preventing infections in patients with multiple sclerosis (MS), although concerns have been raised about potential worsening of the underlying disease. To investigate this, we conducted a prospective, multicentre, non-randomized observational study assessing changes in disease activity, safety, and clinical tolerability of vaccination in 222 MS patients on disease-modifying drugs. The majority of patients were female (76.6%) and 89.6% had relapsing-remitting MS. The vaccines administered were primarily seasonal influenza (56.3%) or tetanus-based vaccines (33.8%). Disease activity, as measured by annualized relapse rate, decreased significantly from 0.64 the year prior to vaccination to 0.38 in the following year. Moreover, the extended disability status scale remained stable within six months after vaccination in comparison to pre-vaccination values. Side effects were reported in 19.2% of vaccinated subjects, most commonly local side effects (65.2%) or flu-like symptoms (34.8%). Our findings suggest that standard non-live vaccines are safe and well-tolerated in MS patients and do not negatively impact disease activity.
 Multiple sclerosis (MS) is frequently misdiagnosed based on MRI abnormalities detected in the brain white matter. Cortical lesions have been well described neuropathologically, but remain challenging to detect in clinical practice. Therefore, the ability to detect cortical lesions offers real potential to reduce misdiagnosis. Cortical lesions have been shown to have a predilection for regions with CSF stasis - such as the insula and cingulate gyrus. This pathological observation forms the basis of our current pilot MR imaging study, which successfully uses high spatial resolution imaging of these two anatomical regions to clearly identify cortical lesions in MS.
 BACKGROUND: Patients with multiple sclerosis (MS) are commonly treated with anti-CD20 therapies. Reduced seroconversion following COVID-19 vaccination in patients receiving certain anti-CD20 therapies has been reported; however, the immune response following natural infection is poorly characterised. This study aimed to retrospectively evaluate COVID-19 antibody responses after vaccination and natural infection in patients treated with anti-CD20 therapies. METHODS: We performed a retrospective review evaluating COVID-19 seroconversion and anti-spike glycoprotein antibody titres in double-vaccinated patients with MS, or related neuroinflammatory conditions, treated with anti-CD20 therapies (N = 30) with a confirmed history of natural severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (n = 14) or without infection (control; n = 16). This single-centre study was performed at the Yale Multiple Sclerosis Center, where patients treated with anti-CD20 therapies (ocrelizumab, n = 21; rituximab, n = 5; ofatumumab, n = 4) were systematically checked for SARS-CoV-2 anti-spike antibody levels throughout the pandemic. Data were collected from March 2020 to March 2022. All patients had received at least two doses of a Food and Drug Administration (FDA)-approved COVID-19 vaccine. Qualitative anti-spike antibody seropositivity was determined based on test-specific laboratory reference ranges. For a subset of patients (n = 18), quantitative anti-spike antibody levels were assessed via DiaSorin LIAISON® chemiluminescence immunoassay (positive titre was defined as ≥ 13). Vaccination and infection dates were also recorded, and patients were monitored for adverse COVID-19-related health effects. RESULTS: Overall, 15/30 (50.0%) patients seroconverted following double vaccination. After infection, 13/14 (92.9%) seroconverted, while 6/16 (37.5%) uninfected patients seroconverted after vaccination. For the 18 patients with quantitative anti-spike antibody titres, mean titre post-vaccination was 37.4. Mean antibody titres were significantly higher after infection: 540.3 versus 20.1 in the control group (p < 0.05). Of the 14 infected patients, 13 had mild COVID-19 symptoms and one was asymptomatic. No hospitalisations or deaths were reported. CONCLUSIONS: This study reports that SARS-CoV-2 anti-spike antibody titres in double-vaccinated MS patients treated with anti-CD20 therapies were significantly increased post-infection compared with the control group. Patients treated with anti-CD20 therapy who had confirmed infections displayed mild or asymptomatic infection. These results provide reassurance that anti-CD20 therapies in double-vaccinated patients do not preclude an appropriate SARS-CoV-2 antibody response post-infection.
 INTRODUCTION: Multiple sclerosis (MS) is an immune-mediated disorder of the CNS manifested by recurrent attacks of neurological symptoms (related to focal inflammation) and gradual disability accrual (related to progressive neurodegeneration and neuroinflammation). Sphingosine-1-phosphate-receptor (S1PR) modulators are a class of oral disease-modifying therapies (DMTs) for relapsing MS. The first S1PR modulator developed and approved for MS was fingolimod, followed by siponimod, ozanimod, and ponesimod. All are S1P analogues with different S1PR-subtype selectivity. They restrain the S1P-dependent lymphocyte egress from lymph nodes by binding the lymphocytic S1P-subtype-1-receptor. Depending on their pharmacodynamics and pharmacokinetics, they can also interfere with other biological functions. AREAS COVERED: Our narrative review covers the PubMed English literature on S1PR modulators in MS until August 2022. We discuss their pharmacology, efficacy, safety profile, and risk management recommendations based on the results of phase II and III clinical trials. We briefly address their impact on the risk of infections and vaccines efficacy. EXPERT OPINION: S1PR modulators decrease relapse rate and may modestly delay disease progression in people with relapsing MS. Aside their established benefit, their place and timing within the long-term DMT strategy in MS, as well as their immunological effects in the new and evolving context of the post-COVID-19 pandemic and vaccination campaigns warrant further study.
 BACKGROUND: Persons with Multiple Sclerosis (pwMS) frequently experience walking difficulties, often expressed as a slower walking speed during the 6 Minute Walking Test (6MWT). In addition, slower walking speeds are also related to higher levels of perceived exertion. PwMS are also known to have a higher energetic Cost of walking (Cw) and may experience muscle fatigue during prolonged walking. In this study, we aimed to explore changes in Rate of Perceived Exertion (RPE) and the Cw within participants during the 6MWT in pwMS. Additionally, concomitant changes in the mean and variability of gait characteristics and changes in muscle activation describing muscle fatigue were assessed. METHODS: The 6MWT was performed on an instrumented treadmill while three-dimensional motion capture and gas exchange were measured continuously. RPE on the 6-20 borg-scale was questioned directly before and after the 6MWT. Cost of walking was expressed in Joules/kg/m. Muscle fatigue was assessed by increases in Root Median Square (RMdS) and decreases in Median Frequency (MF) of the recorded EMGs. Wilcoxon-Signed Rank test was used to assess a difference in RPE before and after the 6MWT. Linear mixed models, while controlling for walking speed, were used to assess changes in Cw, mean and variability of gait characteristics and RMdS and MF of muscle activation. RESULTS: 28 pwMS (23 females, mean ± standard deviation age 46 ± 10 years, height 1.69 ± 0.08 meter, weight 76 ± 18 kilogram, EDSS 2.7 ± 1.3) were included. Although the RPE increased from 8 to 12, no changes in Cw were found. Walking speed was the only spatiotemporal parameter which increased during the 6MWT and RMdS of the gastrocnemius and tibialis anterior muscles increased. The soleus muscle decreased in MF over time. CONCLUSION: The increases in RPE and walking speed was not accompanied by a change in Cw during the 6MWT which indicates that the perceived exertion was not accompanied by an increased physical exertion. Changes in muscle activation might give an indication for muscle fatigue but were inconclusive. Although the 6MWT reflects daily life walking challenges for pwMS, this test did not show the expected changes in gait parameters in our sample.
 The peptide spanning residues 35 to 55 of the protein myelin oligodendrocyte glycoprotein (MOG) has been studied extensively in its role as a key autoantigen in the neuroinflammatory autoimmune disease multiple sclerosis. Rodents and nonhuman primate species immunized with this peptide develop a neuroinflammatory condition called experimental autoimmune encephalomyelitis, often used as a model for multiple sclerosis. Over the last decade, the role of citrullination of this antigen in the disease onset and progression has come under increased scrutiny. We recently reported on the ability of these citrullinated MOG35-55 peptides to aggregate in an amyloid-like fashion, suggesting a new potential pathogenic mechanism underlying this disease. The immunodominant region of MOG is highly conserved between species, with the only difference between the murine and human protein, a polymorphism on position 42, which is serine in mice and proline for humans. Here, we show that the biophysical and biochemical behavior we previously observed for citrullinated murine MOG35-55 is fundamentally different for human and mouse MOG35-55. The citrullinated human peptides do not show amyloid-like behavior under the conditions where the murine peptides do. Moreover, we tested the ability of these peptides to stimulate lymphocytes derived from MOG immunized marmoset monkeys. While the citrullinated murine peptides did not produce a proliferative response, one of the citrullinated human peptides did. We postulate that this unexpected difference is caused by disparate antigen processing. Taken together, our results suggest that further study on the role of citrullination in MOG-induced experimental autoimmune encephalomyelitis is necessary.
 BACKGROUND: Fampridine is a potassium channel blocker drug used to improve walking ability in patients with multiple sclerosis (MS). We evaluated the effect of fampridine in patients with MS in the acute phase of transverse myelitis. METHODS: In a randomized, placebo-controlled trial, 30 patients who had their first episode of cervical myelitis with quadriparesis presentation, with the final diagnosis of MS, were randomly divided into two equal groups. The intervention group received intravenous methylprednisolone (IVMP) for 7 days plus fampridine. The placebo group received IVMP for 7 days plus placebo. To compare the treatment results, we compared the Barthel index (BI) scores of the groups at the start of the trial and the 21st day after the start of treatment. RESULTS: There was no significant difference in baseline characteristics between the intervention and placebo groups in terms of mean age, sex, and mean admission BI (p > 0.05). Mean (SD) admission BI in placebo and intervention groups was 27.20 (7.341) and 27.87(5.78), respectively (p = 0.784). The measured mean (SD) BI after treatment was 48.73 (15.54) in the placebo and 64.93 (11.81) in the intervention group (p = 0.003) after 3 weeks. CONCLUSION: Using fampridine plus IVMP in the acute phase of transverse myelitis in MS patients improved the disease's symptoms and increased the daily activity ability of patients.
 Demyelinating and inflammatory myelopathies represent a group of diseases with characteristic patterns in neuroimaging and several differential diagnoses. The main imaging patterns of demyelinating myelopathies (multiple sclerosis, neuromyelitis optica spectrum disorder, acute disseminated encephalomyelitis, and myelin oligodendrocyte glycoprotein antibody-related disorder) and inflammatory myelopathies (systemic lupus erythematosus-myelitis, sarcoidosis-myelitis, Sjögren-myelitis, and Behçet's-myelitis) will be discussed in this article, highlighting key points to the differential diagnosis.
 Both genetic susceptibility and environmental exposures are thought to be involved in multiple sclerosis (MS) pathogenesis. Of all viruses potentially relevant to MS aetiology, Epstein-Barr virus (EBV) is the best-studied. EBV is a B cell lymphotropic virus which is able to evade the immune system by establishing latent infection in memory B cells, and EBV reactivation is restricted by CD8 cytotoxic T cell (CTL) responses in immune competent individuals. Autologous haematopoietic stem cell transplantation (AHSCT) is considered to be the most effective therapy in the treatment of relapsing MS even though chemotherapy-induced lymphopenia can associate with the re-emergence of latent viruses. Despite the increasing interest in EBV and MS pathogenesis the relationship between AHSCT, EBV and viral immunity in people with MS has not been investigated to date. This study analysed immune responses to EBV in a well characterised cohort of 13 individuals with MS by utilising pre-AHSCT, and 6-, 12- and 24-month post AHSCT bio-banked peripheral blood mononuclear cells and plasma samples. It is demonstrated that the infused stem cell product contains latently EBV-infected memory B cells, and that EBV viremia occurs in the immune-compromised recipient post-transplant. High throughput TCR analysis detected expansion and diversification of the CD8 CTL responses reactive with EBV lytic and latent antigens from 6 to 24 months following AHSCT. Increased levels of latent EBV infection found within the B cell pool following treatment, as measured by EBV genomic detection, did not associate with disease relapse. This is the first study of EBV immunity following application of AHSCT in the treatment of MS and not only raises important questions about the role of EBV infection in MS pathogenesis, but is of clinical importance given the expanding clinical trials of adoptive EBV-specific CTLs in MS.
 PURPOSE: A combined resting state functional connectivity MRI (fcMRI) and diffusion tensor imaging (DTI) metric called structural and functional connectivity index (SFCI) was recently proposed for tracking disease status and progression in multiple sclerosis (MS). The metric combines fcMRI and transverse diffusivity (TD) along different functional pathways involved in principle symptomatic domains of MS. In a longitudinal study of patients with MS receiving the same MS therapy, initial worsening of transcallosal (TC) motor and frontoparietal (FP) cognitive networks, as measured by fcMRI and DTI over the first year was followed by stabilization in the second year of follow-up. In this study we have (i) probed relationships between individual and composite neurological measures of MS with SFCI and its individual components along TC motor and FP cognitive pathways and (ii) compared sensitivity of SFCI to treatment-induced longitudinal changes with each individual imaging measure. METHODS: Twenty five patients with MS (15 female, age 42 ± 8 y) participated in this study and were scanned at 3 T whole body MRI scanner with diffusion tensor imaging (DTI) and resting-state functional connectivity MRI (fcMRI) scan protocol at baseline and 6, 12, 18 and 24 months after starting fingolimod. fcMRI and TD along TC and FP pathways were combined to form structural and functional connectivity index (SFCI) at each time point. Correlations between individual/combined neurological measures and individual imaging components/SFCI at baseline and were evaluated and compared. In addition, efficacies of individual and combined imaging metrics in tracking network integrity were compared. RESULTS: Individual TD along the TC pathway was significantly inversely correlated with all individual/composite neurological scores. There were moderate correlations of TC and FP components of SFCI with most of the neurological scores, and the pathway-combined SFCI was significantly correlated with all neurological scores. Trend-level increases of both TC and FP fcMRI were observed during the second year of follow-up, both TC and FP TD increased significantly in the first year and then stabilized during the second year. A trend toward a decrease in combined imaging metrics along TC and FP were observed during the first year, followed by a trend toward an increase in these metrics during the second year, while a significant decrease in SFCI during the first year followed by a significant increase during the second year was observed. CONCLUSIONS: SFCI was more effective in tracking network integrity/disease progression than individual pathway-specific components, which supports its use as an imaging marker for MS disease status and progression.
 BACKGROUND: Factors driving increased innate immune cell activation in multiple sclerosis (MS) brain are not well understood. As higher prevalence of microglial/macrophage activation in association with chronic lesions and diffusely in the normal appearing white matter predict more rapid accumulation of clinical disability, it is of high importance to understand processes behind this. Objective of the study was to explore demographic, clinical and paraclinical variables associating with later positron emission tomography (PET)-measurable innate immune cell activation. METHODS: PET-imaging using a TSPO-binding [(11)C]PK11195 was performed to evaluate microglial activation in patients with relapsing-remitting MS aged 40-55 years with a minimum disease duration of five years (n = 37). Medical records and diagnostic MR images were reviewed for relevant early MS disease-related clinical and paraclinical parameters. RESULTS: More prominent microglial activation was associated with higher number of T2 lesions in the diagnostic MRI, a higher immunoglobulin G (IgG) index in the diagnostic CSF and Expanded Disability Status Scale (EDSS) ≥ 2.0 five years after diagnosis. CONCLUSION: The number of T2 lesions in MRI, and CSF immunoglobulin content measured by IgG index at the time of MS diagnosis associated with later TSPO-PET-measurable innate immune cell activation. This suggests that both focal and diffuse early inflammatory phenomena impact the development of later progression-related pathology.

 BACKGROUND: Demyelinating diseases (DD) are a group of chronic neurological diseases associated with loss and injury of brain or spinal cord regions. These conditions could trigger impairment of neurological functions and disability from earlier stages of life. Epidemiological data on DD remains insufficient for decision-making in the Mexican healthcare system. This study aims to describe the epidemiology of DD based on data from Mexico's National Registry of Demyelinating Diseases. METHODS: A cross-sectional, registry-based, observational study was performed. We analyzed 408 reports of multiple sclerosis (331, 81%), neuromyelitis optica spectrum disorder (67, 16%), chronic recurrent inflammatory optic neuropathy (5, 1%), clinically isolated syndrome (4, 0.9%), and autoimmune encephalitis (1, 0.2%) reported across 2021. RESULTS: The time from first symptoms to diagnosis of any DD was about 3 years. A treatment failure history was detected in 40% of patients. It was estimated that NMOSD accounts for 20% of all disorders. There was evidence that the use of brand-name and generic IFN drug products lead to increased therapeutic failures. CONCLUSION: Our research team suggests reinforcing educational programs and activities based on diagnosis and clinical management improvement to first-contact physicians and specialty doctors and promoting awareness in the whole population.
 BACKGROUND: Biotin is a commonly used supplement for hair, nail, and skin. Recent literature suggests that high-dose biotin therapy for neurological diseases like Multiple sclerosis can interfere with lab results that use biotin/streptavidin immunoassay, called biotin interference. Biotin interference can affect thyroid lab results, giving biochemical hyperthyroidism. CASE PRESENTATION: Our patient, a 64-year-old white man with a known history of multiple sclerosis, presented with elevated free T3, free T4, and low TSH that resembled hyperthyroidism. He had no symptoms of hyperthyroidism except some fatigue and tachycardia on the first encounter. He was started on anti-thyroid medications. He was then re-evaluated since his lab results remained the same after two months of anti-thyroid medications. It was found that he was on biotin, 10000mcg/day, for his multiple sclerosis. Biotin was discontinued, and five days later his lab results returned to normal values. CONCLUSION: The lack of knowledge of biotin use by patients can lead to misdiagnosis of patients' thyroid lab results and improper management. Awareness about biotin interference and abnormal thyroid lab values should be a priority among clinicians and the public. If the biotin is discontinued on time, such misdiagnosis can be avoided.
 OBJECTIVES: Investigating differential vulnerability of thalamic nuclei in multiple sclerosis (MS). METHODS: In a secondary analysis of prospectively collected datasets, we pooled 136 patients with MS or clinically isolated syndrome and 71 healthy controls all scanned with conventional 3D-T1 and white-matter-nulled magnetization-prepared rapid gradient echo (WMn-MPRAGE) and tested for cognitive performance. T1-based thalamic segmentation was compared with the reference WMn-MPRAGE method. Volumes of thalamic nuclei were compared according to clinical phenotypes and cognitive profile. RESULTS: T1- and WMn-MPRAGE provided comparable segmentations (0.84 ± 0.13 < volume-similarity-index < 0.95 ± 0.03). Medial and posterior thalamic groups were significantly more affected than anterior and lateral groups. Cognitive impairment related to volume loss of the anterior group. CONCLUSION: Thalamic nuclei closest to the third ventricle are more affected, with cognitive consequences.
 Foot-drop is one of the most diagnosed and physically limiting symptoms persons with multiple sclerosis (pwMS) experience. Clinicians prescribe ankle-foot orthosis (AFO) and functional electrical stimulation (FES) devices to help alleviate the effects of foot drop, but it is unclear how their clinical and functional gait improvements compare given the user's level of disability, type of multiple sclerosis, walking environment, or desired physical activity. The research questions explored were what is the current state of AFO and FES research for pwMS? What are the prevailing research trends? What definitive clinical and functional device comparisons exist for pwMS? eight databases were systematically searched for relevant literature published between 2009 and 2021. The American Association of Orthotists and Prosthetists and Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines for systematic literature reviews were followed. A team of 3 researchers critically evaluated 17 articles that passed eligibility criteria. This review discusses the current state and trends of research, provides evidence statements on device effects, and recommends improvements for future studies. A meta-analysis would be informative, but study variability across the literature makes directly comparing AFO and FES device effects unreliable. This review contributes new and useful information to multiple sclerosis literature that can be used by both clinicians and researchers. Clinicians can use the provided insights to prescribe more effective, customized treatments, and other researchers can use them to evaluate and design future studies.
 BACKGROUND: Menopause is a physiologic phase in women's lives. Findings regarding multiple sclerosis (MS) course through menopause are diverse. So, we designed this systematic review and meta-analysis to estimate the impact of menopause on relapse rate, and disability status in women with MS. METHODS: PubMed, Scopus, EMBASE, Web of Science, and google scholar were systematically searched by two independent researchers on January 1st, 2023. They also evaluated conference abstracts, and references of the included studies. In addition, data regarding the total number of participants, name of the first author of the publication, publication year, country of origin, disease duration, disease type, annual relapse rate, and Expanded Disability Status Scale (EDSS) before and after menopause were recorded. RESULTS: A literature search revealed 1024 records. Twenty-one full texts were evaluated, and finally, four studies were included for meta-analysis. Mean ARR before menopause ranged between 0.21 and 0.37, and after menopause ranged between 0.13 and 0.08. The SMD of mean ARR ranged between - 1.04, and - 0.29, while the pooled SMD was estimated as -0.52(95% CI: -0.88, -0.15) (I(2) = 73.6%, P = 0.02). The mean EDSS before menopause ranged between 1.5 and 2, and after menopause ranged between 2 and 3.1. The SMD of EDSS ranged between 0.46, and 0.71. The pooled SMD of EDSS change (after menopause-before menopause) estimated as 0.56(95% CI: 0.38, 0.73)(I(2) = 0, P = 0.4). CONCLUSION: The result of this systematic review and meta-analysis show that menopause can be associated with relapse rate reduction, unlike increase in disease-related disability in women with MS.
 Immune responses in people with multiple sclerosis (pwMS) receiving disease-modifying therapies (DMTs) have been of significant interest throughout the COVID-19 pandemic. Lymphocyte-targeting immunotherapies, including anti-CD20 treatments and sphingosine-1-phosphate receptor (S1PR) modulators, attenuate Ab responses after vaccination. Evaluation of cellular responses after vaccination, therefore, is of particular importance in these populations. In this study, we used flow cytometry to analyze CD4 and CD8 T cell functional responses to SARS-CoV-2 spike peptides in healthy control study participants and pwMS receiving 5 different DMTs. Although pwMS receiving rituximab and fingolimod therapies had low Ab responses after both 2 and 3 vaccine doses, T cell responses in pwMS taking rituximab were preserved after a third vaccination, even when an additional dose of rituximab was administered between vaccine doses 2 and 3. PwMS taking fingolimod had low detectable T cell responses in peripheral blood. CD4 and CD8 T cell responses to SARS-CoV-2 variants of concern Delta and Omicron were lower than to the ancestral Wuhan-Hu-1 variant. Our results indicate the importance of assessing both cellular and humoral responses after vaccination and suggest that, even in the absence of robust Ab responses, vaccination can generate immune responses in pwMS.
 BACKGROUND: Chronic active lesions (CAL) in multiple sclerosis (MS) have been observed even in patients taking high-efficacy disease-modifying therapy, including B-cell depletion. Given that CAL are a major determinant of clinical progression, including progression independent of relapse activity (PIRA), understanding the predicted activity and real-world effects of targeting specific lymphocyte populations is critical for designing next-generation treatments to mitigate chronic inflammation in MS. METHODS: We analyzed published lymphocyte single-cell transcriptomes from MS lesions and bioinformatically predicted the effects of depleting lymphocyte subpopulations (including CD20 B-cells) from CAL via gene-regulatory-network machine-learning analysis. Motivated by the results, we performed in vivo MRI assessment of PRL changes in 72 adults with MS, 46 treated with anti-CD20 antibodies and 26 untreated, over ∼2 years. FINDINGS: Although only 4.3% of lymphocytes in CAL were CD20 B-cells, their depletion is predicted to affect microglial genes involved in iron/heme metabolism, hypoxia, and antigen presentation. In vivo, tracking 202 PRL (150 treated) and 175 non-PRL (124 treated), none of the treated paramagnetic rims disappeared at follow-up, nor was there a treatment effect on PRL for lesion volume, magnetic susceptibility, or T1 time. PIRA occurred in 20% of treated patients, more frequently in those with ≥4 PRL (p = 0.027). INTERPRETATION: Despite predicted effects on microglia-mediated inflammatory networks in CAL and iron metabolism, anti-CD20 therapies do not fully resolve PRL after 2-year MRI follow up. Limited tissue turnover of B-cells, inefficient passage of anti-CD20 antibodies across the blood-brain-barrier, and a paucity of B-cells in CAL could explain our findings. FUNDING: Intramural Research Program of NINDS, NIH; NINDS grants R01NS082347 and R01NS082347; Dr. Miriam and Sheldon G. Adelson Medical Research Foundation; Cariplo Foundation (grant #1677), FRRB Early Career Award (grant #1750327); Fund for Scientific Research (FNRS).
 Central nervous system (CNS) inflammation is a key factor in multiple sclerosis (MS). Invasion of peripheral immune cells into the CNS resulting from an unknown signal or combination of signals results in activation of resident immune cells and the hallmark feature of the disease: demyelinating lesions. These lesion sites are an amalgam of reactive peripheral and central immune cells, astrocytes, damaged and dying oligodendrocytes, and injured neurons and axons. Sustained inflammation affects cells directly located within the lesion site and further abnormalities are apparent diffusely throughout normal-appearing white matter and grey matter. It is only relatively recently, using animal models, new tissue sampling techniques, and next-generation sequencing, that molecular changes occurring in CNS resident cells have been broadly captured. Advances in cell isolation through Fluorescence Activated Cell Sorting (FACS) and laser-capture microdissection together with the emergence of single-cell sequencing have enabled researchers to investigate changes in gene expression in astrocytes, microglia, and oligodendrocytes derived from animal models of MS as well as from primary patient tissue. The contribution of some dysregulated pathways has been followed up in individual studies; however, corroborating results often go unreported between sequencing studies. To this end, we have consolidated results from numerous RNA-sequencing studies to identify and review novel patterns of differentially regulated genes and pathways occurring within CNS glial cells in MS. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology.
 Programmed cell death 1 (PD-1) is an immune checkpoint and has been reported to be associated with several autoimmune diseases. We aimed to investigate the association between human PD-1 gene (PDCD1) polymorphisms and multiple sclerosis (MS). This case-control study was conducted on 229 MS patients and 246 healthy controls. Genotyping of rs36084323 (PD-1.1 G/A), rs11568821 (PD-1.3 G/A) and rs2227981 (PD-1.5 C/T) polymorphisms was performed by PCR-RFLP technique. The frequency difference of PD-1.1 genotypes and alleles (-536 G/A) between patients and healthy controls was not significant. Regarding PD-1.3, the AA + AG genotype was found to be relatively higher in the control group. Concerning PD-1.5 (+7785 C/T), the frequency of T allele carriers (TT + CT) was relatively higher in MS patients, which was marginally insignificant (p = .07). PD-1 gene polymorphisms may be associated with MS; however, accurate conclusions require further studies with a larger number of samples.

 Multiple sclerosis (MS) is a progressive inflammatory demyelinating disease of the CNS. Increasing evidence suggests that vulnerable neurons in MS exhibit fatal metabolic exhaustion over time, a phenomenon hypothesized to be caused by chronic hyperexcitability. Axonal Kv7 (outward-rectifying) and oligodendroglial Kir4.1 (inward-rectifying) potassium channels have important roles in regulating neuronal excitability at and around the nodes of Ranvier. Here, we studied the spatial and functional relationship between neuronal Kv7 and oligodendroglial Kir4.1 channels and assessed the transcriptional and functional signatures of cortical and retinal projection neurons under physiological and inflammatory demyelinating conditions. We found that both channels became dysregulated in MS and experimental autoimmune encephalomyelitis (EAE), with Kir4.1 channels being chronically downregulated and Kv7 channel subunits being transiently upregulated during inflammatory demyelination. Further, we observed that pharmacological Kv7 channel opening with retigabine reduced neuronal hyperexcitability in human and EAE neurons, improved clinical EAE signs, and rescued neuronal pathology in oligodendrocyte-Kir4.1-deficient (OL-Kir4.1-deficient) mice. In summary, our findings indicate that neuron-OL compensatory interactions promoted resilience through Kv7 and Kir4.1 channels and identify pharmacological activation of nodal Kv7 channels as a neuroprotective strategy against inflammatory demyelination.
 The radiologically isolated syndrome (RIS) was defined in 2009 as the presence of asymptomatic, incidentally identified demyelinating-appearing white matter lesions in the CNS within individuals lacking symptoms typical of multiple sclerosis (MS). The RIS criteria have been validated and predict the transition to symptomatic MS reliably. The performance of RIS criteria that require fewer MRI lesions is unknown. 2009-RIS subjects, by definition, fulfil three to four of four criteria for 2005 dissemination in space (DIS) and subjects fulfilling only one or two lesions in at least one 2017 DIS location were identified within 37 prospective databases. Univariate and multivariate Cox regression models were used to identify predictors of a first clinical event. Performances of different groups were calculated. Seven hundred and forty-seven subjects (72.2% female, mean age 37.7 ± 12.3 years at the index MRI) were included. The mean clinical follow-up time was 46.8 ± 45.4 months. All subjects had focal T2 hyperintensities suggestive of inflammatory demyelination on MRI; 251 (33.6%) fulfilled one or two 2017 DIS criteria (designated as Groups 1 and 2, respectively), and 496 (66.4%) fulfilled three or four 2005 DIS criteria representing 2009-RIS subjects. Group 1 and 2 subjects were younger than the 2009-RIS group and were more likely to develop new T2 lesions over time (P < 0.001). Groups 1 and 2 were similar regarding survival distribution and risk factors for transition to MS. At 5 years, the cumulative probability for a clinical event was 29.0% for Groups 1 and 2 compared to 38.7% for 2009-RIS (P = 0.0241). The presence of spinal cord lesions on the index scan and CSF-restricted oligoclonal bands in Groups 1-2 increased the risk of symptomatic MS evolution at 5 years to 38%, comparable to the risk of development in the 2009-RIS group. The presence of new T2 or gadolinium-enhancing lesions on follow-up scans independently increased the risk of presenting with a clinical event (P < 0.001). The 2009-RIS subjects or Groups 1 and 2 with at least two of the risk factors for a clinical event demonstrated better sensitivity (86.0%), negative predictive value (73.1%), accuracy (59.8%) and area under the curve (60.7%) compared to other criteria studied. This large prospective cohort brings Class I evidence that subjects with fewer lesions than required in the 2009 RIS criteria evolve directly to a first clinical event at a similar rate when additional risk factors are present. Our results provide a rationale for revisions to existing RIS diagnostic criteria.

 BACKGROUND: Multiple sclerosis imposes a heavy burden on the person who suffers from it and on the relatives, due to the caregiving load involved. The objective was to analyse whether the inclusion of social costs in economic evaluations of multiple sclerosis-related interventions changed results and/or conclusions. METHODS: A systematic review was launched using Medline and the Cost-Effectiveness Analysis Registry of Tufts University (2000-2019). Included studies should: (1) be an original study published in a scientific journal, (2) be an economic evaluation of any multiple sclerosis-related intervention, (3) include productivity losses and/or informal care costs (social costs), (4) be written in English, (5) use quality-adjusted life years as outcome, and (6) separate the results according to the perspective applied. RESULTS: Twenty-nine articles were selected, resulting in 67 economic evaluation estimations. Social costs were included in 47% of the studies. Productivity losses were assessed in 90% of the estimations (the human capital approach was the most frequently used method), whereas informal care costs were included in nearly two-thirds of the estimations (applying the opportunity and the replacement-cost methods equally). The inclusion of social costs modified the figures for incremental costs in 15 estimations, leading to a change in the conclusions in 10 estimations, 6 of them changing from not recommended from the healthcare perspective to implemented from the societal perspective. The inclusion of social costs also altered the results from cost-effective to dominant in five additional estimations. CONCLUSIONS: The inclusion of social costs affected the results/conclusions in multiple sclerosis-related interventions, helping to identify the most appropriate interventions for reducing its economic burden from a broader perspective.
 PURPOSE: The current study attempted to expand the literature on cognition and mood in MS by determining if illness intrusiveness may potentially serve as an intermediary factor in the well-established cognition-mood relationship in people with MS. METHOD: This study employed a retrospective cross-sectional design to answer this question. Baseline neuropsychological test data and mood questionnaires from 199 participants with clinically definite MS were used in this study. The sample was middle-aged (M = 48.4, SD = 11.8), highly educated (M = 14.6, SD = 2.2), majority female (76.9%) and majority White (74.5%). Assumptions for parametric statistics and ordinary least squares regression were met. Conditional process models evaluated whether illness intrusiveness mediated the relationship between cognitive functioning and psychiatric symptoms. RESULTS: In total, 33.2% of the sample met criteria for clinically significant anxiety, 41.7% met criteria for depression, and 27.8% of the sample met criteria for processing speed impairment, consistent with other MS samples. Illness intrusiveness was found to mediate the relationship between processing speed and depression, ab = -.07, 95% CI [-.15, -.002], processing speed and anxiety, ab = -.06, 95% CI [-.12, -.02], and processing speed and more general mood disturbance, ab = -.08, 95% CI [-.13, -.0005]. CONCLUSIONS: Illness intrusiveness was found to be a potential important intermediary mechanism by which the primary cognitive impairment in MS, processing speed, impacts mood in this disease population. Conclusions, treatment implications, and directions for future research in light of these findings were discussed. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 Gender differences in earnings exist worldwide. Gender segregation or familial status have been previously stated as possible explanations for these differences as well as health differences between women and men. Women are diagnosed with multiple sclerosis (MS) as twice much as men. Moreover, MS limitations may affect the work capacity of people with MS (PwMS) implying a reduction in their earnings. We aimed to explore gender differences in earnings among people with MS and without MS and between groups of those diagnosed while also considering types of occupation and family composition, and how these possible differences relate to sickness absence (SA) and disability pension (DP). We conducted a population-based cohort study in Sweden with microdata from several nationwide registers. PwMS aged 19-57 years (n = 5128) living in Sweden and 31,767 matched references from the population without MS. Outcome measures included earnings, number of SA and DP days combined (SA/DP). A four-way weighted least-squares analysis of covariance was performed to explore the associations of gender, MS, type of occupation, and family composition with earnings. Risk of SA and DP days was assessed with logistic regression. Overall, and across all occupations, women earned less than men, although less so among managers with MS. Annual gender differences in earnings were larger if living with children at home compared to not living with children. Nevertheless, these gender differences decreased after adjusting for SA/DP, both among PwMS and references. PwMS had considerably more SA/DP days than references. Women also had more SA/DP days than men. We observed that working women earned less than working men, and that gender differences in earnings were present in all occupations, although less evident among PwMS in managerial positions. The combination of gender, occupation, family composition, and MS, was associated with earnings, even when adjusting for the number of SA and DP days.
 Fungal infection or proliferation in our body is capable of initiation of strong inflammation and immune responses that result in different consequences, including infection-trigged organ injury and inflammation-related remote organ dysfunction. Fungi associated infectious diseases have been well recognized in the clinic. However, whether fungi play an important role in non-infectious central nervous system disease is still to be elucidated. Recently, a growing amount of evidence point to a non-negligible role of peripheral fungus in triggering unique inflammation, immune response, and exacerbation of a range of non-infectious CNS disorders, including Multiple sclerosis, Neuromyelitis optica, Parkinson's disease, Alzheimer's disease, and Amyotrophic lateral sclerosis et al. In this review, we summarized the recent advances in recognizing patterns and inflammatory signaling of fungi in different subsets of immune cells, with a specific focus on its function in CNS autoimmune and neurodegeneration diseases. In conclusion, the fungus is capable of triggering unique inflammation by multiple mechanisms in the progression of a body of CNS non-infectious diseases, suggesting it serves as a key factor and critical novel target for the development of potential therapeutic strategies.
 BACKGROUND AND OBJECTIVES: Long lasting immune response to anti-SARS-CoV-2 vaccination in people with Multiple Sclerosis (pwMS) is still largely unexplored. Our study aimed at evaluating the persistence of the elicited amount of neutralizing antibodies (Ab), their activity and T cell response after three doses of anti-SARS-CoV-2 vaccine in pwMS. METHODS: We performed a prospective observational study in pwMS undergoing SARS-CoV-2 mRNA vaccinations. Anti-Region Binding Domain (anti-RBD) of the spike (S) protein immunoglobulin G (IgG) titers were measured by ELISA. The neutralization efficacy of collected sera was measured by SARS-CoV-2 pseudovirion-based neutralization assay. The frequency of Spike-specific IFNγ-producing CD4+ and CD8+ T cells was measured by stimulating Peripheral Blood Mononuclear Cells (PBMCs) with a pool of peptides covering the complete protein coding sequence of the SARS-CoV-2 S. RESULTS: Blood samples from 70 pwMS (11 untreated pwMS, 11 under dimethyl fumarate, 9 under interferon-γ, 6 under alemtuzumab, 8 under cladribine, 12 under fingolimod and 13 under ocrelizumab) and 24 healthy donors were collected before and up to six months after three vaccine doses. Overall, anti-SARS-CoV-2 mRNA vaccine elicited comparable levels of anti-RBD IgGs, neutralizing activity and anti-S T cell response both in untreated, treated pwMS and HD that last six months after vaccination. An exception was represented by ocrelizumab-treated pwMS that showed reduced levels of IgGs (p<0.0001) and a neutralizing activity under the limit of detection (p<0.001) compared to untreated pwMS. Considering the occurrence of a SARS-CoV-2 infection after vaccination, the Ab neutralizing efficacy (p=0.04), as well as CD4+ (p=0.016) and CD8+ (p=0.04) S-specific T cells, increased in treated COVID+ pwMS compared to uninfected treated pwMS at 6 months after vaccination. DISCUSSION: Our follow-up provides a detailed evaluation of Ab, especially in terms of neutralizing activity, and T cell responses after anti-SARS-CoV-2 vaccination in MS context, over time, considering a wide number of therapies, and eventually breakthrough infection. Altogether, our observations highlight the vaccine response data to current protocols in pwMS and underline the necessity to carefully follow-up anti-CD20- treated patients for higher risk of breakthrough infections. Our study may provide useful information to refine future vaccination strategies in pwMS.
 BACKGROUND: Individuals with multiple sclerosis (MS) are vulnerable to all types of infection, because MS itself involves immunodeficiency, in addition to involving treatment with immunosuppressants. Simple predictive variables for infection that are easily assessed in daily examinations are warranted. Lymphocyte area under the curve (L_AUC), defined as the sum of serial absolute lymphocyte counts under the lymphocyte count-time curve, has been established as a predictive factor for several infections after allogenic hematopoietic stem cell transplantation. We assessed whether L_AUC could also be a useful factor for predicting severe infection in MS patients. METHODS: From October 2010 to January 2022, MS patients, diagnosed based on the 2017 McDonald criteria, were retrospectively reviewed. We extracted patients with infection requiring hospitalization (IRH) from medical records and matched with controls in a 1:2 ratio. Variables including clinical severity and laboratory data were compared between the infection group and controls. L_AUC was calculated along with the AUC of total white blood cells (W_AUC), neutrophils (N_AUC), lymphocytes (L_AUC), and monocytes (M_AUC). To correct for different times of blood examination and extract mean values of AUC per time point, we divided the AUC by follow-up duration. For example, in evaluating lymphocyte counts, we defined the ratio of [L_AUC] to [follow-up duration] as [L_AUC/t]. Multivariate regression analysis was conducted to extract predictive factors associated with IRH. Also, discriminative analysis was conducted using candidate variables from multivariate analysis. RESULTS: The total case-control sample included 177 patients of MS with IRH (n=59) and non-IRH (controls) (n=118). Adjusted odds ratios (OR) for the risk of serious infection in patients with MS with higher baseline expanded disability status scale (EDSS) (OR 1.340, 95% confidence interval [CI] 1.070-1.670, p = 0.010) and lower ratio of L_AUC/t to M_AUC/t (OR 0.766, 95%CI 0.591-0.993, p = 0.046) were significant. Notably, the kind of treatment, including glucocorticoids (GCs), disease-modifying drugs (DMDs) and other immunosuppressants agents, and dose of GCs were not significantly associated with serious infection after correlated with EDSS and ratio of L_AUC/t to M_AUC/t. In discriminative analysis, sensitivity was 88.1% (95%CI 76.5-94.7%) and specificity was 35.6% (95%CI 27.1-45.0%), using EDSS ≥ 6.0 or ratio of L_AUC/t to M_AUC/t ≤ 3.699, while sensitivity was 55.9% (95%CI 42.5-68.6%) and specificity was 83.9% (95%CI 75.7-89.8%), using both EDSS ≥ 6.0 and ratio of L_AUC/t to M_AUC/t ≤ 3.699. CONCLUSION: Our study revealed the impact of the ratio L_AUC/t to M_AUC/t as a novel prognostic factor for IRH. Clinicians should pay more attention to laboratory data such as lymphocyte or monocyte counts itself, directly presenting individual immunodeficiency, rather than the kind of drug to prevent infection as a clinical manifestation.
 Multiple sclerosis (MS) is a demyelinating disease caused by auto-antigen recognizing CD4(+) T cells. However, IL-17A-producing CD4(+) T cells that are bystander-activated by IL-1β and IL-23, and T cell receptors independently, could contribute to experimental autoimmune encephalomyelitis. Here, we studied the differences in the frequency and function of bystander-activated CD4(+) T cells in patients with MS. A significantly higher frequency of CD4 + IL-1Rl + T cells was found in memory than in naïve CD4(+) T cells and in Th17/Th17.1 than in Th1/Th2 subtypes in both MS and healthy controls (HC). Following IL-1β and IL-23 stimulation, IL-1Rl expression was markedly increased in both memory and Th17/Th17.1 cells, and their IL-17A-production was increased after bystander-activation, which was significantly higher in MS compared with HC. Our study suggests a potential role of IL-17A-producing bystander-activated CD4(+)IL-1Rl(+) T cells in MS.
 Natalizumab is a humanized recombinant monoclonal IgG4 antibody used in the treatment of multiple sclerosis. Commonly used methods for natalizumab and anti-natalizumab antibodies quantification are enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay, respectively. Measurement of therapeutic monoclonal antibodies can be challenging due to the resemblance to human plasma immunoglobulins. Recent developments in mass spectrometry enables to analyze vast variety of large protein molecules. The aim of this study was to develop a LC-MS/MS method for determining natalizumab in human serum and cerebrospinal fluid (CSF) and apply it to clinical settings. For successful quantification, it was necessary to find specific sequences of peptides in natalizumab. This immunoglobulin was treated with dithiothreitol and iodoacetamide, cleaved with trypsin into short specific peptides and determined on a UPLC-MS/MS system. An Acquity UPLC BEH C18 column at 55 °C and gradient elution was used for analysis. Intra- and interassay accuracies and precisions were tested at four concentration levels. Precision was determined by coefficients of variation and was in the range of 0.8-10.2 %, with accuracy in the range of 89.8-106.4 %. The concentration of natalizumab in patient samples ranged from 1.8 to 193.3 μg/mL. The method was validated according to the European Medicines Agency (EMA) guideline, met all acceptance criteria for accuracy and precision, and is suitable for clinical applications. In comparison to immunoassay, which can be elevated by cross-reaction with endogenous immunoglobulins, the results of developed LC-MS/MS method are more accurate and specific.
 Microglia are resident macrophages of the central nervous system (CNS). It plays a significant role in immune surveillance under physiological conditions. On stimulation by pathogens, microglia change their phenotypes, phagocytize toxic molecules, secrete pro-inflammatory/anti-inflammatory factors, promotes tissue repair, and maintain the homeostasis in CNS. Accumulation of myelin debris in multiple sclerosis (MS)/experimental autoimmune encephalomyelitis (EAE) inhibits remyelination by decreasing the phagocytosis by microglia and prevent the recovery of MS/EAE. Drug induced microglia phagocytosis could be a novel therapeutic intervention for the treatment of MS/EAE. But the abnormal phagocytosis of neurons and synapses by activated microglia will lead to neuronal damage and degeneration. It indicates that the phagocytosis of microglia has many beneficial and harmful effects in central neurodegenerative diseases. Therefore, simply promoting or inhibiting the phagocytic activity of microglia may not achieve ideal therapeutic results. However, limited reports are available to elucidate the microglia mediated phagocytosis and its underlying molecular mechanisms. On this basis, the present review describes microglia-mediated phagocytosis, drug-induced microglia phagocytosis, molecular mechanism, and novel approach for MS/EAE treatment.
 In multiple sclerosis (MS), gray matter (GM) atrophy progresses in a non-random manner, possibly in regions with a high distribution of specific neurotransmitters involved in several relevant central nervous system functions. We investigated the associations among regional GM atrophy, atlas-based neurotransmitter distributions and clinical manifestations in a large MS patients' group. Brain 3 T MRI scans, neurological examinations and neuropsychological evaluations were obtained from 286 MS patients and 172 healthy controls (HC). Spatial correlations among regional GM volume differences and atlas-based nuclear imaging-derived neurotransmitter maps, and their associations with MS clinical features were investigated using voxel-based morphometry and JuSpace toolbox. Compared to HC, MS patients showed widespread GM atrophy being spatially correlated with the majority of neurotransmitter maps (false discovery rate [FDR]-p ≤ 0.004). Patients with a disease duration ≥ 5 vs < 5 years had significant cortical, subcortical and cerebellar atrophy, being spatially correlated with a higher distribution of serotoninergic and dopaminergic receptors (FDR-p ≤ 0.03). Compared to mildly-disabled patients, those with Expanded Disability Status Scale ≥ 3.0 or ≥ 4.0 had significant cortical, subcortical and cerebellar atrophy being associated with serotonergic, dopaminergic, opioid and cholinergic maps (FDR-p ≤ 0.04). Cognitively impaired vs cognitively preserved patients had widespread GM atrophy being spatially associated with serotonergic, dopaminergic, noradrenergic, cholinergic and glutamatergic maps (FDR-p ≤ 0.04). Fatigued vs non-fatigued MS patients had significant cortical, subcortical and cerebellar atrophy, not associated with neurotransmitter maps. No significant association between GM atrophy and neurotransmitter maps was found for depression. Regional GM atrophy with specific neurotransmitter systems may explain part of MS clinical manifestations, including locomotor disability, cognitive impairment and fatigue.
 Epidemiological studies show that omega-3 fatty acid consumption is associated with improved conditions in neurodegenerative diseases such as multiple sclerosis (MS). However, the mechanism of this association is not well understood. Emerging evidence suggests that parent molecules such as docosahexaenoic acid are converted into downstream metabolites that are capable of directly modulating immune responses. In vitro, we found that docosahexaenoyl ethanolamide (DHEA), another dietary component and its epoxide metabolite, reduced the polarization of naïve T-cells toward proinflammatory Th1 and Th17 phenotypes. Furthermore, we identified that DHEA and related endocannabinoids are changing during the disease progression in mice undergoing relapse-remitting experimental autoimmune encephalomyelitis (RR-EAE). In addition, daily administration of DHEA to mice delayed the onset of disease, the rate of relapse, and the severity of clinical scores at relapse in RR-EAE, an animal model of MS. Collectively, these data indicate that DHEA and their downstream metabolites reduce the disease severity in the RR-EAE model of MS and can be potential dietary adjuvants to existing MS therapeutics.
 All currently licensed medications for multiple sclerosis (MS) target the immune system. Albeit promising preclinical results demonstrated disease amelioration and remyelination enhancement via modulating oligodendrocyte lineage cells, most drug candidates showed only modest or no effects in human clinical trials. This might be due to the fact that remyelination is a sophistically orchestrated process that calls for the interplay between oligodendrocyte lineage cells, neurons, central nervous system (CNS) resident innate immune cells, and peripheral immune infiltrates and that this process may somewhat differ in humans and rodent models used in research. To ensure successful remyelination, the recruitment and activation/repression of each cell type should be regulated in a highly organized spatio-temporal manner. As a result, drug candidates targeting one single pathway or a single cell population have difficulty restoring the optimal microenvironment at lesion sites for remyelination. Therefore, when exploring new drug candidates for MS, it is instrumental to consider not only the effects on all CNS cell populations but also the optimal time of administration during disease progression. In this review, we describe the dysregulated mechanisms in each relevant cell type and the disruption of their coordination as causes of remyelination failure, providing an overview of the complex cell interplay in CNS lesion sites.
 The medicinal properties of cannabis and cannabinoid-derivative are entirely investigated and known. In addition, the identification of psychotropic plant cannabinoids has led to more studies regarding the cannabinoid system and its therapeutic features in the treatment and management of clinical symptoms of neuroinflammatory disorders, such as multiple sclerosis (MS), Parkinsons disease (PD), and Alzheimers disease (AD). In fact, cannabinoid agonists are able to control and regulate inflammatory responses. In contrast to the cannabinoid receptor type 1 (CB1) and its unwanted adverse effects, the cannabinoid receptor type 2 (CB2) and its ligands hold promise for new and effective therapeutic approaches. So far, some successes have been achieved in this field. This review will discuss an outline of the endocannabinoid system's involvement in neuroinflammatory disorders. Moreover, the pharmacological efficacy of different natural and synthetic preparations of phytocannabinoids acting on cannabinoid receptors, particularly in MS, PD, and AD, will be updated. Also, the reasons for targeting CB2 for neurodegeneration will be explained.
 Multiple sclerosis (MS) is a chronic, autoimmune, demyelinating disease of the central nervous system (CNS) that leads to axonal damage and accumulation of disability. Relapsing-remitting MS (RR-MS) is the most frequent presentation of MS and this form of MS is three times more prevalent in females than in males. This female bias in MS is apparent only after puberty, suggesting a role for sex hormones in this regulation; however, very little is known of the biological mechanisms that underpin the sex difference in MS onset. Experimental autoimmune encephalomyelitis (EAE) is an animal model of RR-MS that presents more severely in females in certain mouse strains and thus has been useful to study sex differences in CNS autoimmunity. Here, we overview the immunopathogenesis of MS and EAE and how immune mechanisms in these diseases differ between a male and female. We further describe how females exhibit more robust myelin-specific T helper (Th) 1 immunity in MS and EAE and how this sex bias in Th cells is conveyed by sex hormone effects on the T cells, antigen presenting cells, regulatory T cells, and innate lymphoid cell populations.
 OBJECTIVE: To study the effect of fluoxetine on Th17- and Th1-immune response, which plays an important role in the pathogenesis of multiple sclerosis (MS). MATERIAL AND METHODS: Ten patients with relapsing-remitting MS and ten healthy subjects were examined. The functions of Th17- and Th1-immune responses were assessed by the production of cytokines interleukin-17 (IL-17) and interferon-gamma (IFN-γ) by CD4(+) T cells stimulated with macrophages or microbeads coated with anti-CD3 and anti-CD28-antibodies. To assess the effect of fluoxetine on the macrophages-induced Th17- and Th1-immune response, macrophages were pre-incubated in the presence of fluoxetine and co-cultured with autologous CD4(+) T-cells. In the case of stimulation of CD4(+) T-cells with anti-CD3/CD28-microbeads, fluoxetine was added directly to the T-helper cells before adding of microbeads. In addition, we evaluated the effect of fluoxetine on the production of the factors of differentiation of Th17-cells cytokines IL-6 and IL-1β by macrophages. The levels of cytokines in the cell culture supernatants were measured by ELISA. RESULTS: The production of IL-17 and IFN-γ by CD4(+) T-cells stimulated with macrophages or anti-CD3/CD28-microbeads was comparable between the groups. Fluoxetine suppressed the production of IL-17 and IFN-γ by anti-CD/CD28-stimulated CD4(+) T-cells in both groups. Fluoxetine also suppressed the production of IL-6 and IL-1β by macrophages as well as their ability to induce IL-17 and IFN-γ production by CD4(+) T-cells in both groups. CONCLUSIONS: Fluoxetine may have an anti-inflammatory effect in MS that could be mediated by suppression of Th17- and Th1-cells or macrophage-induced Th17- and Th1-immune response.
 INTRODUCTION: Medical treatments for trigeminal neuralgia secondary to multiple sclerosis have low efficacy and tolerability and scientific evidence regarding efficacy of neurosurgery is scarce. We aimed to assess neurosurgical outcome and complications in trigeminal neuralgia secondary to multiple sclerosis. METHODS: Patients with trigeminal neuralgia secondary to multiple sclerosis who underwent microvascular decompression, glycerol rhizolysis or balloon compression were prospectively and consecutively included from 2012 to 2019. Preoperatively, we systematically obtained clinical characteristics and performed a 3.0 Tesla MRI. Follow-up at three, six and 12 months was performed by independent assessors. RESULTS: We included 18 patients. Of the seven patients treated with microvascular decompression, two patients (29%) had an excellent outcome (both had neurovascular contact with morphological changes), three patients (43%) had a good outcome, one patient (14%) had treatment failure and one patient (14%) had a fatal outcome. Three patients (43%) had major complications. Of 11 patients treated with percutaneous procedures, seven patients (64%) had an excellent or good outcome with major complications in three patients (27%). CONCLUSION: Percutaneous procedures provided acceptable outcome and complication rates and should be offered to the majority of patients with trigeminal neuralgia secondary to multiple sclerosis who need surgery. Microvascular decompression is less effective and has a higher complication rate in trigeminal neuralgia secondary to multiple sclerosis compared to microvascular decompression in classical and idiopathic trigeminal neuralgia. Microvascular decompression should only be considered in patients with trigeminal neuralgia secondary to multiple sclerosis when they have neurovascular contact with morphological changes.
 Multiple sclerosis (MS) is a neurological, immune-mediated demyelinating disease that affects people in the prime of life. Environmental, infectious, and genetic factors have been implicated in its etiology, although a definitive cause has yet to be determined. Nevertheless, multiple disease-modifying therapies (DMTs: including interferons, glatiramer acetate, fumarates, cladribine, teriflunomide, fingolimod, siponimod, ozanimod, ponesimod, and monoclonal antibodies targeting ITGA4, CD20, and CD52) have been developed and approved for the treatment of MS. All the DMTs approved to date target immunomodulation as their mechanism of action (MOA); however, the direct effects of some DMTs on the central nervous system (CNS), particularly sphingosine 1-phosphate (S1P) receptor (S1PR) modulators, implicate a parallel MOA that may also reduce neurodegenerative sequelae. This review summarizes the currently approved DMTs for the treatment of MS and provides details and recent advances in the molecular pharmacology, immunopharmacology, and neuropharmacology of S1PR modulators, with a special focus on the CNS-oriented, astrocyte-centric MOA of fingolimod.
 This figure presents a comparison of molecular imaging of the translocator protein (TSPO) and contrast-enhanced MRI in 2 patients with tumefactive multiple sclerosis and glioblastoma, respectively. In the case of the tumefactive multiple sclerosis patient, TSPO uptake is primarily located centrally, while in the glioblastoma patient, TSPO uptake is predominantly situated peripherally to the central necrotic area. These findings suggest that TSPO imaging could be a noninvasive imaging technique for distinguishing between these 2 diagnoses.
 INTRODUCTION: Gait disturbance in central nervous system (CNS) demyelinating disorders, including multiple sclerosis (MS) and neuromyelitis optica (NMO) is one of the most troublesome problems that has a direct impact on the quality of life. However, the associations between gait disturbance and other clinical variables of these two diseases have not been fully elucidated. OBJECTIVE: This study aimed to evaluate gait disturbance using a computerized gait analysis system and its association with various clinical variables in patients with MS and NMO. METHODS: A total of 33 patients (14 with MS and 19 with NMO) with minor disabilities, who were able to walk independently and had passed their acute phase, were enrolled in the study. Gait analysis were performed using a computer-based instrumented walkway system. (Walk-way MG-1000, Anima, Japan) Clinical variables, such as disease duration, medication, body mass index (BMI), hand grip power, and muscle mass were recorded. The Montreal Cognitive Assessment (MOCA), Beck Depression Inventory score-II (BDI), and fatigue scale were measured using the Functional Assessment of Chronic Illness Therapy-fatigue scale (FACIT-fatigue) scale. A trained neurologist scored the Expanded Disability Status Scale (EDSS). RESULTS: Gait speed was the single parameter that showed a significant positive correlation with MOCA (p < 0.001). The stance phase time was the single parameter that showed a significant negative correlation with EDSS (p < 0.001). Hand grip strength showed a significant positive correlation with skeletal muscle mass as assessed by bioimpedance analysis (p < 0.05). The FACIT-fatigue scale score showed a significant negative correlation with the BDI (p < 0.001). CONCLUSION: In our patients with MS/NMO with mild disability, cognitive impairment was significantly correlated with gait speed, and the degree of disability was significantly correlated with stance phase time. Our findings may imply that early detection of a decrease in gait speed and an increase in stance phase time can predict the progression of cognitive impairment in patients with MS/NMO with mild disability.
 Demyelinating optic neuritis and hereditary optic neuropathy (HON) take a leading place among the diseases, the leading clinical syndrome of which is bilateral optic neuropathy with a simultaneous or sequential significant decrease in visual acuity. Optic neuritis can occur at the onset or be one of the syndromes within multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOGAD). HON are a group of neurodegenerative diseases, among which the most common variants are Leber's hereditary optic neuropathy (LHON), associated with mitochondrial DNA (mtDNA) mutations, and autosomal recessive optic neuropathy (ARON), caused by nuclear DNA (nDNA) mutations in DNAJC30. There are phenotypes of LHON «plus», one of which is the association of HON and CNS demyelination in the same patient. In such cases, the diagnosis of each of these diseases causes significant difficulties, due to the fact that in some cases there are clinical and radiological coincidences between demyelinating and hereditary mitochondrial diseases.
 Multiple sclerosis (MS) is a complex chronic disease with an unknown etiology. It is considered an inflammatory demyelinating and neurodegenerative disorder of the central nervous system (CNS) characterized, in most cases, by an unpredictable onset of relapse and remission phases. The disease generally starts in subjects under 40; it has a higher incidence in women and is described as a multifactorial disorder due to the interaction between genetic and environmental risk factors. Unfortunately, there is currently no definitive cure for MS. Still, therapies can modify the disease's natural history, reducing the relapse rate and slowing the progression of the disease or managing symptoms. The limited access to human CNS tissue slows down. It limits the progression of research on MS. This limit has been partially overcome over the years by developing various experimental models to study this disease. Animal models of autoimmune demyelination, such as experimental autoimmune encephalomyelitis (EAE) and viral and toxin or transgenic MS models, represent the most significant part of MS research approaches. These models have now been complemented by ex vivo studies, using organotypic brain slice cultures and in vitro, through induced Pluripotent Stem cells (iPSCs). We will discuss which clinical features of the disorders might be reproduced and investigated in vivo, ex vivo, and in vitro in models commonly used in MS research to understand the processes behind the neuropathological events occurring in the CNS of MS patients. The primary purpose of this review is to give the reader a global view of the main paradigms used in MS research, spacing from the classical animal models to transgenic mice and 2D and 3D cultures.
 OBJECTIVE: We aim to evaluate 3-year effects of ocrelizumab (humanized anti-CD20 monoclonal antibody for the treatment of multiple sclerosis (MS)) on lymphocytes, neutrophils and immunoglobulins: (1) when compared with pre-infusion assessment; (2) over the course of treatment; and (3) possible clinical correlates of the observed immunological modifications. METHODS: This real-world observational cohort study has been conducted on prospectively collected data from 78 MS patients (mean age 47.8 ± 10.5 years; females 48.7%) commencing on ocrelizumab from 2018, with mean follow-up of 36.5 ± 6.8 months. Clinical data and blood samples were collected every three months. Total lymphocyte count and subpopulations were assessed on peripheral blood using flow cytometry. Serum immunoglobulins were evaluated with nephelometry. RESULTS: When compared with pre-infusion values, we observed reduction of total, CD19 and CD20 lymphocyte counts; however, after the first infusion, their levels remained substantially stable. Over time we observed a progressive reduction of CD8 lymphocytes, while no changes were observed for CD4, CD27, CD3CD27, and CD19CD27. After the first infusion, we observed reduction in IgG, which further decreased during the follow-up. Higher probability of EDSS progression was associated with reduced modulation of CD8 lymphocytes. INTERPRETATION: Ocrelizumab affects both humoral and cellular immune responses. Disability progression over the follow-up was associated with lower CD8 cytotoxic T-lymphocyte reduction. Changes in humoral response are immediate and sustained, while modulation of cellular immunity occurs progressively through regular re-treatment, and is related to clinical stability.
 Multiple sclerosis (MS) is a chronic neuroinflammatory disease of the central nervous system (CNS) affecting nearly three million humans worldwide. In MS, cells of an auto-reactive immune system invade the brain and cause neuroinflammation. Neuroinflammation triggers a complex, multi-faceted harmful process not only in the white matter but also in the grey matter of the brain. In the grey matter, neuroinflammation causes synapse dysfunctions. Synapse dysfunctions in MS occur early and independent from white matter demyelination and are likely correlates of cognitive and mental symptoms in MS. Disturbed synapse/glia interactions and elevated neuroinflammatory signals play a central role. Glutamatergic excitotoxic synapse damage emerges as a major mechanism. We review synapse/glia communication under normal conditions and summarize how this communication becomes malfunctional during neuroinflammation in MS. We discuss mechanisms of how disturbed glia/synapse communication can lead to synapse dysfunctions, signaling dysbalance, and neurodegeneration in MS.
 OBJECTIVE: Neurodegeneration induced by inflammatory stress in multiple sclerosis (MS) leads to long-term neurological disabilities that are not amenable to current immunomodulatory therapies. METHODS AND RESULTS: Here, we report that neuronal downregulation of Splicing factor 3b subunit 2 (SF3B2), a component of U2 small nuclear ribonucleoprotein (snRNP), preserves retinal ganglion cell (RGC) survival and axonal integrity in experimental autoimmune encephalomyelitis (EAE)-induced mice. By employing an in vitro system recapitulating the inflammatory environment of MS lesion, we show that when SF3B2 levels are downregulated, cell viability and axon integrity are preserved in cortical neurons against inflammatory toxicity. Notably, knockdown of SF3B2 suppresses the expression of injury-response and necroptosis genes and prevents activation of Sterile Alpha and TIR Motif Containing 1 (Sarm1), a key enzyme that mediates programmed axon degeneration. INTERPRETATION: Together, these findings suggest that the downregulation of SF3B2 is a novel potential therapeutic target to prevent secondary neurodegeneration in MS.
 BACKGROUND: The objective of the present study was to estimate the effectiveness of the BBIBP-CorV vaccine (VE) in preventing SARS-CoV-2 infection, related hospitalization, and death among people living with multiple sclerosis (PLWMS). METHODS: In this population-based retrospective observational study, data on all PLWMS, vaccination, SARS-CoV-2 tests, hospitalization, and deaths were collected in Isfahan, Iran between February 9, 2021, and November 4, 2021. We estimated the hazard ratio between vaccinated (partially and fully) and unvaccinated groups using the Andersen-Gill extension of the Cox proportional hazards model. We also performed Cox proportional hazards analysis to identify risk factors for breakthrough infection and COVID-19-related hospitalization in fully-immunized group. RESULTS: Of the 9869 PLWMS, 1368 were in partially-vaccinated group, 4107 were in the fully-vaccinated group, and 3794 were in the unvaccinated group. In the partially-vaccinated group, the estimated VE against COVID-19 infection was 39.3% (16%, 56.1%), hospitalization was 64.9% (1.3%, 87.5%), and mortality was 92.7% (88.8%, 100%). The respective results for the fully-vaccinated group were 63.9% (56%, 70.3%), 75.7% (57.5%, 86.1%), and 100%. Progressive MS was independently associated with a greater risk of breakthrough infection (HR=1.952, 95%CI: 1.174-3.246, p = 0.010). Older adults (≥50 years vs. 18-49 years, HR=3.115, 95%CI: 1.145-8.470, p = 0.026) and those on rituximab (HR=7.584; 95% CI: 1.864-30.854; p = 0.005) were at an increased risk of COVID-19-related hospitalization. CONCLUSION: This study showed that two doses of the BBIBP-CorV vaccine can effectively prevent COVID-19 infection and hospitalization among PLWMS. Old PLWMS and those who treating with rituximab are at increased risk of hospitalization after receiving two doses of the vaccine.
 BACKGROUND: Multiple sclerosis (MS) is an incurable autoimmune inflammatory demyelinating disease of the central nervous system. Several MS medications can modify disease course through effects on adaptive immune cells, while drugs targeting innate immunity are under investigation. Myeloid-derived suppressor cells (MDSCs) which arise during chronic inflammation, are defined by their T-cell immunosuppressive functions. MiR-223 modulates myeloid cell maturation and expansion, including MDSCs. METHODS: MDSCs isolated from healthy controls (HC) and people with MS (pwMS) were co-cultured with CD4+ T-cells to study their immunosuppressive activities in vitro. Cytokines and chemokines concentration were evaluated by Luminex assay in the serum of HC, pwMS, and other neuroinflammatory diseases and correlated with MDSC activities. RESULTS: MDSC suppressive functions are dysregulated in pwMS compared to HC, which was reversed by glucocorticoids (GC). GC specifically downregulated miR-223 levels in MDSCs and increased the expression of STAT3. In vitro assay showed that miR-223 inhibition enhanced MDSC suppressive activity, STAT3 dependently. By multiple linear regression analysis, we demonstrated that MDSC phosphorylated STAT3 was correlated with serum GM-CSF in HC and pwMS. CONCLUSIONS: These results suggest that miR-223 could be a therapeutic target for enhancing MDSC's suppressive activities as an alternative to GC.
 OBJECTIVE: Changes in the normal-appearing white matter (NAWM) in multiple sclerosis (MS) may contribute to disease progression. Here, we systematically quantified ultrastructural and subcellular characteristics of the axon-myelin unit in MS NAWM and determined how this correlates with low-grade inflammation. METHODS: Human brain tissue obtained with short postmortem delay and fixation at autopsy enables systematic quantification of ultrastructural characteristics. In this study, we performed high-resolution immunohis tochemistry and quantitative transmission electron microscopy to study inflammation and ultrastructural characteristics of the axon-myelin unit in MS NAWM (n = 8) and control white matter (WM) in the optic nerve. RESULTS: In the MS NAWM, there were more activated and phagocytic microglia cells (HLA(+) P2RY12(-) and Iba1(+) CD68(+) ) and more T cells (CD3(+) ) compared to control WM, mainly located in the perivascular space. In MS NAWM compared to control WM, there were, as expected, longer paranodes and juxtaparanodes and larger overlap between paranodes and juxtaparanodes. There was less compact myelin wrapping, a lower g-ratio, and a higher frequency of axonal mitochondria. Changes in myelin and axonal mitochondrial frequency correlated positively with the number of active and phagocytic microglia and lymphocytes in the optic nerve. INTERPRETATION: These data suggest that in MS NAWM myelin detachment and uncompact myelin wrapping occurs, potassium channels are unmasked at the nodes of Ranvier, and axonal energy demand is increased, or mitochondrial transport is stagnated, accompanied by increased presence of activated and phagocytic microglia and T cells. These subclinical alterations to the axon-myelin unit in MS NAWM may contribute to disease progression. ANN NEUROL 2023;93:856-870.
 BACKGROUND: Although growing evidence has shown beneficial effects of motor imagery (MI) training in different populations including people with multiple sclerosis (pwMS), not all patients with neurological diseases may benefit from MI. OBJECTIVES: To investigate factors and strategies affecting and enhancing MI ability in pwMS. DATA SOURCES: MEDLINE/PubMed, PsycINFO, Cochrane Library, Scopus, EMBASE, EBSCOhost, Web of Science and REHABDATA databases, clinical trials registries, dissertation repositories, study bibliographies and internet search engines were searched through August 2021. STUDY SELECTION: Any study type but single case studies investigating factors or strategies contributing to MI ability in pwMS. STUDY APPRAISAL AND SYNTHESIS METHODS: Risk of bias (RoB) was assessed using the Joanna Briggs Institute Checklist for Case-Control and Analytical Cross-Sectional Studies and Cochrane RoB-2.0 tool for randomised trials. A qualitative synthesis was performed summarising main results. RESULTS: Eight databases, 4 trial registries, 9 dissertation repositories, and 1 internet search engine were searched. Fourteen studies including 366 pwMS and 236 healthy controls were included. Most frequently, cognitive impairment was reported as a negative factor influencing MI ability in pwMS. Other negative factors were cognitive fatigue and disability. Inconsistent evidence was found on the contribution of MS phenotype, anxiety, and depression. Using a theory-based MI framework and familiarisation to MI and external cueing may enhance MI ability. LIMITATIONS: Eligible studies were highly heterogeneous. CONCLUSION AND IMPLICATIONS OF KEY FINDINGS: Cognitive impairment, cognitive fatigue and disability negatively influence MI ability in pwMS. Visual and/or auditory cueing of MI are strategies for facilitating MI ability. SYSTEMATIC REVIEW REGISTRATION NUMBER: PROSPERO CRD42020173081 CONTRIBUTION OF THE PAPER.
 Neurodegenerative and inflammatory processes influence the clinical course of multiple sclerosis (MS). The β-site amyloid precursor protein cleaving enzyme 1 (BACE1) has been associated with cognitive dysfunction, amyloid deposition and neuroinflammation in Alzheimer's disease. We explored in a group of 50 patients with relapsing-remitting MS the association between the cerebrospinal fluid (CSF) levels of BACE1, clinical characteristics at the time of diagnosis and prospective disability after three-years follow-up. In addition, we assessed the correlations between the CSF levels of BACE 1, amyloid β (Aβ) 1-40 and 1-42, phosphorylated tau (pTau), lactate, and a set of inflammatory and anti-inflammatory molecules. BACE1 CSF levels were correlated positively with depression as measured with Beck Depression Inventory-Second Edition scale, and negatively with visuospatial memory performance evaluated by the Brief Visuospatial Memory Test-Revised. In addition, BACE CSF levels were positively correlated with Bayesian Risk Estimate for MS at onset, and with Expanded Disability Status Scale score assessed three years after diagnosis. Furthermore, a positive correlation was found between BACE1, amyloid β 42/40 ratio (Spearman's r = 0.334, p = 0.018, n = 50), pTau (Spearman's r = 0.304, p = 0.032, n = 50) and lactate concentrations (Spearman's r = 0.361, p = 0.01, n = 50). Finally, an association emerged between BACE1 CSF levels and a group of pro and anti-inflammatory molecules, including interleukin (IL)-4, IL-17, IL-13, IL-9 and interferon-γ. BACE1 may have a role in different key mechanisms such as neurodegeneration, oxidative stress and inflammation, influencing mood, cognitive disorders and disability progression in MS.
 BACKGROUND: Pediatric-onset multiple sclerosis (POMS) represents the earliest stage of disease pathogenesis. Investigating the cerebrospinal fluid (CSF) proteome in POMS may provide novel insights into early MS processes. OBJECTIVE: To analyze CSF obtained from children at time of initial central nervous system (CNS) acquired demyelinating syndrome (ADS), to compare CSF proteome of those subsequently ascertained as having POMS versus monophasic acquired demyelinating syndrome (mADS). METHODS: Patients were selected from two prospective pediatric ADS studies. Liquid chromatography-mass spectrometry (LC-MS) was performed in a Dutch discovery cohort (POMS n = 28; mADS n = 39). Parallel reaction monitoring-mass spectrometry (PRM-MS) was performed on selected proteins more abundant in POMS in a combined Dutch and Canadian validation cohort (POMS n = 48; mADS n = 106). RESULTS: Discovery identified 5580 peptides belonging to 576 proteins; 58 proteins were differentially abundant with ⩾2 peptides between POMS and mADS, of which 28 more abundant in POMS. Fourteen had increased abundance in POMS with ⩾8 unique peptides. Five selected proteins were all confirmed within validation. Adjusted for age, 2 out of 5 proteins remained more abundant in POMS, that is, Carboxypeptidase E (CPE) and Semaphorin-7A (SEMA7A). CONCLUSION: This exploratory study identified several CSF proteins associated with POMS and not mADS, potentially reflecting neurodegeneration, compensatory neuroprotection, and humoral response in POMS. The proteins associated with POMS highly correlated with age at CSF sampling.
 CLINICAL RATIONALE FOR THE STUDY: The course of COVID-19 in people with multiple sclerosis (PwMS) has been described, while the serological status after SARS-CoV-2 infection or vaccination, especially in patients treated with disease-modifying therapies (DMT), is still under investigation. This is a significant clinical problem, as certain DMTs may predispose to a severe course of viral infections. AIM OF THE STUDY: We analyzed the presence of antibodies against spike (S) and nucleocapsid (N) proteins of SARS-CoV-2 in relapsing-remitting PwMS treated with DMT, especially dimethyl fumarate, interferon beta, and glatiramer acetate, in a single multiple sclerosis (MS) centre in north-eastern Poland (the Department of Neurology, Medical University of Bialystok). MATERIAL AND METHODS: The presence of antibodies against S and N proteins in PwMS was assessed twice: on visit one (between May and June 2020) (n = 186) and on visit two (between May and June 2021) (n = 88). Samples were taken from 68 individuals on both visits. Demographic and clinical data was collected: duration of MS, Expanded Disability Status Scale Score (EDSS), type of DMT, history of COVID-19 (positive PCR or antigen test in the past), vaccination status, and the type of vaccine. RESULTS: It was shown that on visit one: 3.7% (n = 7) PwMS were positive for IgA against S protein (IgA-S), 3.2% (n = 6) for IgG against S (IgG-S) protein, and none of those examined was positive for IgG against N protein (IgG-N). On visit two, the most common detected antibodies were IgG-S (71.3%; n = 62), then IgA-S (65.1%; n = 55), and the least common was IgG-N (18.2%; n = 16). On visit two: 20.45% of PwMS had a history of a positive SARS-CoV-2 PCR or antigen test during the last year. By the time of visit two, 42.05% (n = 37) of patients who participated in visit two had been full-course vaccinated against COVID-19. It was demonstrated that vaccination against SARS-CoV-2 significantly induces the production of IgG-S and IgA-S (p < 0.0001), while no difference between vaccinated and unvaccinated patients was shown in the detection of IgG-N. There was no correlation between COVID-19 infection and antibodies against proteins S and N in the study group. Moreover, the presented study did not show any relationship between the ability to produce antibodies against the S protein with any of the used DMTs. CONCLUSIONS AND CLINICAL IMPLICATIONS: According to our study, PwMS treated with dimethyl fumarate, interferon beta, or glatiramer acetate can efficiently produce antibodies against SARS-CoV-2 both after infection and after vaccination.
 Multiple Sclerosis (MS) is a common immune-mediated disorder of the central nervous system that affects young adults and is characterized by demyelination and neurodegeneration. Recent studies have associated C9orf72 intermediate repeat expansions with MS. The objective of this study was to investigate whether C9orf72 repeat length is associated with MS or with a specific disease course in a monocentric Austrian MS cohort. Genotyping of 382 MS patients and 643 non-neurological controls for C9orf72 repeat expansions was performed. The study did not find a difference in the distribution of repeat numbers between controls and MS cases (median repeat units = 2; p = 0.39). Additionally, sub-analysis did not establish a link between intermediate repeats and MS (p = 0.23) and none of the patients with progressive disease course carried an intermediate allele (20-30 repeat units). Exploratory analysis for different cut-offs (of ≥7, ≥17, and ≥24) did not reveal any significant differences in allele frequencies between MS and controls. However, the study did identify a progressive MS patient with a pathogenic C9orf72 expansion and probable co-existing behavioral variant frontotemporal dementia (bvFTD) in a retrospective chart review. In conclusion, this study did not find evidence supporting an association between C9orf72 repeat length and MS or a specific disease course in the Austrian MS cohort. However, the identification of a progressive MS patient with a pathogenic C9orf72 expansion and probable co-existing with FTD highlights the complexity and challenges involved in recognizing distinct neurodegenerative diseases that may co-occur in MS patients.

 INTRODUCTION: Derangement of axonal mitochondrial bioenergetics occurs during progressive multiple sclerosis (PMS). However, whether this is a delayed epiphenomenon or an early causative event of disease progression waits to be understood. Answering this question might further our knowledge of mechanisms underlying neurobiology of PMS and related therapy. METHODS: MOG(35-55)-immunized NOD and PLP(139-151)-immunized SJL female mice were adopted as models of progressive or relapsing-remitting experimental autoimmune encephalomyelitis (EAE), respectively. Multiple parameters of mitochondrial homeostasis were analyzed in the mouse spinal cord during the early asymptomatic stage, also evaluating the effects of scavenging mitochondrial reactive oxygen species with Mito-TEMPO. RESULTS: Almost identical lumbar spinal cord immune infiltrates consisting of Th1 cells and neutrophils without B and Th17 lymphocytes occurred early upon immunization in both mouse strains. Still, only NOD mice showed axon-restricted dysregulation of mitochondrial homeostasis, with reduced mtDNA contents and increased cristae area. Increased expression of mitochondrial respiratory complex subunits Nd2, Cox1, Atp5d, Sdha also exclusively occurred in lumbar spinal cord of NOD and not SJL mice. Accordingly, in this region genes regulating mitochondrial morphology (Opa1, Mfn1, Mfn2 and Atp5j2) and mitochondriogenesis (Pgc1α, Foxo, Hif-1α and Nrf2) were induced early upon immunization. A reduced extent of mitochondrial derangement occurred in the thoracic spinal cord. Notably, the mitochondrial radical scavenger Mito-TEMPO reduced H(2)O(2) content and prevented both mtDNA depletion and cristae remodeling, having no effects on dysregulation of mitochondrial transcriptome. DISCUSSION: We provide here the first evidence that axonal-restricted derangement of mitochondrial homeostasis already occurs during the asymptomatic state exclusively in a mouse model of PMS. Data further our understanding of mechanisms related to EAE progression, and point to very early axonal mitochondrial dysfunction as central to the neuropathogenesis of MS evolution.
 In this study, toll-like receptor 10 (TLR10) and Epstein-Barr virus (EBV) were determined in the peripheral blood of 43 patients with relapsing-remitting multiple sclerosis and 41 age- and gender-matched controls. Serum TLR10 levels were assessed using an enzyme-linked immunosorbent assay kit. EBV DNA and viral load were detected using a real-time polymerase chain reaction assay kit. Results revealed that median TLR10 levels were significantly lower in patients than in controls (318 vs. 574 pg/mL; p < 0.001). Most patients were classified as low producers of TLR10 (≤ median of controls) compared to controls (84.0 vs. 51.0%; p < 0.001). Logistic regression analysis revealed that participants with low TLR10 production had an odds ratio of 4.52. Receiver operating characteristic curve analysis indicated that TLR10 is a good predictor of multiple sclerosis (area under the curve = 0.778; p < 0.001). Prevalence of EBV was less frequent in patients than in controls but the difference was not significant (23.3 vs. 41.5%; p = 0.102), while median EBV load was significantly higher in patients compared to controls (8.55 vs. 1.29 DNA copy/100 cells). When TLR10 levels were stratified according to age group, gender, EBV positivity, Expanded Disability Status Scale (EDSS), or therapy, no significant differences were found in each stratum. Further, no significant correlation was found between TLR10 levels and EDSS or EBV load. In conclusions, TLR10 was down-regulated in serum of multiple sclerosis patients, and this down-regulation was not affected by age, gender, EBV load, EDSS, or therapy.
 BACKGROUND: People with MS (PwMS) and related conditions treated with anti-CD20 and S1P modulating therapies exhibit attenuated immune responses to SARS-CoV-2 vaccines. It remains unclear whether humoral/T-cell responses are valid surrogates for postvaccine immunity. OBJECTIVE: To characterize COVID-19 vaccine-breakthrough infections in this population. METHODS: We conducted a prospective multicenter cohort study of PwMS and related CNS autoimmune conditions with confirmed breakthrough infections. Postvaccination antibody response, disease-modifying therapies (DMTs) at the time of vaccination, and DMT at the time of infection were assessed. RESULTS: Two hundred nine patients had 211 breakthrough infections. Use of anti-CD20 agents at time of infection was associated with increased infection severity (p = 0.0474, odds ratio (OR) = 5.923) for infections during the Omicron surge and demonstrated a trend among the total cohort (p = 0.0533). However, neither use of anti-CD20 agents at the time of vaccination nor postvaccination antibody response was associated with hospitalization risk. Anti-CD20 therapies were relatively overrepresented compared to a similar prevaccination-era COVID-19 cohort. CONCLUSION: Use of anti-CD20 therapies during vaccine breakthrough COVID-19 infection is associated with higher severity. However, the attenuated postvaccination humoral response associated with anti-CD20 therapy use during vaccination may not drive increased infection severity. Further studies are necessary to determine if this attenuated vaccine response may be associated with an increased likelihood of breakthrough infection.

 The purpose of this exploratory qualitative study was to provide insight on the use of yoga in occupational therapy (OT) for people with multiple sclerosis (PwMS). This study aimed to answer how and why OT practitioners (OTPs) integrate yoga into clinical practice for PwMS. Eight OTPs, half of whom have also completed yoga teacher training, participated in a semi-structured telephone interview. Interviews were transcribed verbatim, inductively open-coded, and analyzed using thematic data analysis. Themes that emerged were: (a) OT and yoga are a natural fit; (b) improved performance and participation; (c) leveraging personal ties to yoga; and (d) influenced by client factors and clinical environment. The qualitative data provide valuable information about OTPs' justification for, and unique application of, yoga in clinical practice for PwMS. Future researchers should further explore the use of yoga for OT-related outcomes and the experience of PwMS.
 Approximately 15% of multiple sclerosis (MS) patients develop a progressive form of disease from onset; this condition (primary progressive-PP) MS is difficult to diagnose and treat, and is associated with a poor prognosis. Extracellular vesicles (EVs) of brain origin isolated from blood and their protein cargoes could function as a biomarker of pathological conditions. We verified whether MBP and MOG content in oligodendrocytes-derived EVs (ODEVs) could be biomarkers of MS and could help in the differential diagnosis of clinical MS phenotypes. A total of 136 individuals (7 clinically isolated syndrome (CIS), 18 PPMS, 49 relapsing remitting (RRMS)) and 70 matched healthy controls (HC) were enrolled. ODEVs were enriched from serum by immune-capture with anti-MOG antibody; MBP and MOG protein cargoes were measured by ELISA. MBP concentration in ODEVs was significantly increased in CIS (p < 0.001), RRMS (p < 0.001) and PPMS (p < 0.001) compared to HC and was correlated with disease severity measured by EDSS and MSSS. Notably, MBP concentration in ODEVs was also significantly augmented in PPMS compared to RRMS (p = 0.004) and CIS (p = 0.03). Logistic regression and ROC analyses confirmed these results. A minimally invasive blood test measuring the concentration of MBP in ODEVs is a promising tool that could facilitate MS diagnosis.
 Human T lymphotropic virus-associated myelopathy/tropical spastic paraparesis (HTLV/TSP), also known as HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP), and multiple sclerosis (MS) are chronic debilitating diseases of the central nervous system; although the etiology of which is different, similarities have been observed between these two demyelinating diseases, especially in clinical manifestation and immunopathogenesis. Exorbitant response of the immune system to the virus and neurons in CNS is the causative agent of HAM/TSP and MS, respectively. Helper T lymphocyte-17 cells (Th17s), a component of the immune system, which have a proven role in immunity and autoimmunity, mediate protection against bacterial/fungal infections. The role of these cells has been reviewed in several CNS diseases. A pivotal role for Th17s is presented in demyelination, even more axial than Th1s, during MS. The effect of Th17s is not well determined in HTLV-1-associated infections; however, the evidence that we have supplied in this review illustrates the attendance, also the role of Th17 cells during HAM/TSP. Furthermore, for better conception concerning the trace of these cells in HAM/TSP, a comparative characterization with MS, the resembling disease, has been applied here.
 INTRODUCTION: Multiple sclerosis (MS) is a severe inflammatory neuroimmune degenerative condition affecting more than 2 million individuals worldwide. The purpose of this study was to assess the prevalence of acute periapical abscesses in patients with MS and to evaluate whether acute periapical abscesses (PAs) are more likely to affect patients who were previously infected by Epstein-Barr virus (EBV). METHODS: Integrated data of hospital patients were used. Data from the corresponding diagnosis codes for MS and acute PA were retrieved by querying the appropriate International Classification of Diseases, Tenth Revision codes in the database. RESULTS: Of the total hospital patient population, 0.18% were diagnosed with a history of MS. Females were more affected than males 3.25-fold. Whites were more affected than African Americans 6-fold. Whites were more affected than African Americans combined with other ethnicities 3.6-fold. The odds ratio (OR) for acute PAs in patients with a history of MS was 2.2 (P < .0001). After adjustment for diabetes mellitus comorbidity, the OR for acute PAs in patients with a history of MS was 2.6. After adjustment for cardiovascular disease comorbidity, the OR for acute PAs in patients with a history of MS was 1.27. Of the patients who presented with PAs, 0.2% were diagnosed with a history of EBV infection. The OR was 3.98, and the difference in prevalence was statistically significant (P < .0001). CONCLUSIONS: Under the conditions of this cross-sectional study, it appears that the prevalence of acute PAs is higher in patients with MS and that EBV may play a role.
 Plasma exchange (PLEX) is a therapeutic apheresis modality in which the plasma is separated from inflammatory factors such as circulating autoreactive immunoglobulins, the complement system, and cytokines, and its therapeutic effect is based on the removal of these mediators of pathological processes. Plasma exchange is well established for various neurological disorders, and it is applied successfully in central nervous system inflammatory demyelinating diseases (CNS-IDD). It mainly modulates the humoral immune system; thus, it has a greater theoretical effect in diseases with prominent humoral mechanisms, such as neuromyelitis optica (NMO). However, it also has a proven therapeutic effect in multiple sclerosis (MS) attacks. Several studies have suggested that patients with severe attacks of CNS-IDD have poor response to steroid therapy but show clinical improvement after the PLEX treatment. Currently, PLEX is generally established only as a rescue therapy for steroid unresponsive relapses. However, there are still research gaps in the literature regarding plasma volume, number of sessions, and how early the apheresis treatment needs to started. Thus, in the present article, we summarize the clinical studies and meta-analyses, especially about MS and NMO, outlining clinical data regarding the experience with therapeutic PLEX in severe attacks of CNS-IDD, the clinical improvement rates, the prognostic factors of a favorable response, and highlighting the likely role of the early apheresis treatment. Further, we have gathered this evidence and suggested a protocol for the treatment of CNS-IDD with PLEX in the routine clinical practice.
 BACKGROUND: Multiple sclerosis (MS) is a neurological disorder marked by accumulating immune-mediated damage to the central nervous system. The dysregulated immune system in MS combined with immune effects of disease-modifying therapies (DMTs) used in MS treatment could alter responses to infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19). Most of the literature on immune response to SARS-CoV-2 infection and COVID-19 vaccination, in both the general population and patients with MS on DMTs, has focused on humoral immunity. However, immune response to COVID-19 involves multiple lines of defense, including T cells. OBJECTIVE AND METHODS: We review innate and adaptive immunity to COVID-19 and expand on the role of T cells in mediating protective immunity against SARS-CoV-2 infection and in responses to COVID-19 vaccination in MS. RESULTS: Innate, humoral, and T cell immune responses combat COVID-19 and generate protective immunity. Assays detecting cytokine expression by T cells show an association between SARS-CoV-2-specific T cell responses and milder/asymptomatic COVID-19 and protective immune memory. CONCLUSION: Studies of COVID-19 immunity in people with MS on DMTs should ideally include comprehensive assessment of innate, humoral, and T cell responses.
 OBJECTIVES: Multiple sclerosis (MS) is a potentially disabling autoimmune disease of the central nervous system. Neither the pathogenesis nor the effectiveness of treatment of MS has been fully understood. This in vitro trial evaluated the beneficial immunomodulatory effects of single and combined treatments of all-trans retinoic acid (ATRA) and docosahexaenoic acid (DHA) on the peripheral blood mononuclear cells (PBMCs) of relapsing-remitting MS (RRMS) patients who were receiving interferon beta (IFN-β). METHODS: The PBMCs of 15 RRMS patients were isolated, cultured, and treated with single and combined treatments of ATRA and DHA. The expressions of IL-2, IL-4, T-bet, and GATA3 genes were evaluated using real-time PCR. RESULTS: The results showed that a single treatment of ATRA could significantly suppress the gene expression of the pro-inflammatory cytokine, IL-2 (P < 0.05), and related transcription factor, T-bet (P < 0.001). The gene expression level of the anti-inflammatory cytokine, IL-4, and its transcription factor, GATA3, were not significantly changed. The expression of IL-2 and T-bet genes was significantly decreased in combination treatments of ATRA and DHA (P < 0.001). Significant suppression of IL-2 and T-bet (P < 0.001) was observed in ATRA and DHA combination therapy with half doses of their single treatment, which suggested a synergistic effect of these components. DISCUSSION: Co-administration of vitamin A and DHA, an omega-3 fatty acid derivative, may exert a synergistic effect in modulating the immune system in MS patients; however, more studies are needed to evaluate the exact effects and mechanism of their actions on the immune cells.
 BACKGROUND: Smoking is associated with an increased risk of multiple sclerosis (MS) and disability worsening. The relationship between smoking, cognitive processing speed, and brain atrophy remains uncertain. OBJECTIVE: To quantify the impact of smoking on processing speed and brain volume in MS and to explore the longitudinal relationship between smoking and changes in processing speed. METHODS: A retrospective study of MS patients who completed the processing speed test (PST) between September 2015 and March 2020. Demographics, disease characteristics, smoking history, and quantitative magnetic resonance imaging (MRI) were collected. Cross-sectional associations between smoking, PST performance, whole-brain fraction (WBF), gray matter fraction (GMF), and thalamic fraction (TF) were assessed using multivariable linear regression. The longitudinal relationship between smoking and PST performance was assessed by linear mixed modeling. RESULTS: The analysis included 5536 subjects of whom 1314 had quantitative MRI within 90 days of PST assessment. Current smokers had lower PST scores than never smokers at baseline, and this difference persisted over time. Smoking was associated with reduced GMF but not with WBF or TF. CONCLUSION: Smoking has an adverse relationship with cognition and GMF. Although causality is not demonstrated, these observations support the importance of smoking cessation counseling in MS management.
 BACKGROUND: Limb weakness is a major impairment that affects mobility in persons with multiple sclerosis (PwMS). Specifically, lower limb (LL) weakness can greatly affect gait and balance, while increasing fall risk and decreasing quality of life. Numerous studies have compared LL strength of PwMS to healthy controls, however none have objectively measured strength in all major LL joints (hip, knee, and ankle) in a large number of PwMS. Additionally, while discrete normative values exist for knee extensors in PwMS, there has yet to be regression-based normative isometric strength values for all major LL muscle groups. Therefore, this study aimed to develop gender-specific regression-based normative prediction equations, with 95% confidence intervals, for maximal isometric peak torque of major LL muscles in PwMS. A secondary aim was to characterize the prevalence of LL weakness in PwMS, defined as ≥ 2 SD below values reported for healthy individuals. METHODS: A convenience sample of 175 (women: n = 135) PwMS participated in a prospective, cross-sectional study where isometric peak torque of hip flexors, extensors, and abductors, knee flexors and extensors, and ankle plantarflexors and dorsiflexors were measured using the Biodex System 4 Pro-Dynamometer®. Demographics (age, height, and weight) and disease characteristics (disease duration and disability) were collected. Performances were separated for each muscle group into strongest limb and weakest limb. For each gender, regression-based equations were generated for the LL muscle groups by limb with age, height, weight, disability, and disease duration as the covariates. Descriptive statistics were used to examine the frequency of LL weakness by gender and disability level. For comparison purposes, age-stratified (<30, 30-39, 40-49, 50-59, 60-69, >70 years) and disability-stratified (mild, moderate, and severe ambulant) discrete peak torque values were also generated for each gender. RESULTS: Regression-based normative data are presented for men and women, accounting for age, height, weight, disability, and disease duration. Men were significantly stronger (P < 0.001) than women for all LL, with the men's models accounting for a greater percent of muscle strength variation than women's models for all muscle groups, except for hip extension. Disability was inversely related to strength in all of the models. LL weakness was prevalent in hip flexion (m: 47.5%; w: 63.0%) and extension (m: 92.5%; w: 88.1%), knee extension (m: 30.0%; w: 33.3%) and flexion (m: 25.0%; w: 34.8%), and ankle plantarflexion (m: 15.0%; w: 10.4%) and dorsiflexion (m: 100.0%; w: 96.3%). PwMS with mild disability had a high prevalence of ankle dorsiflexion (94.9-100.0%) and hip extension (81.4-90.0%) weakness. CONCLUSIONS: This study is the first to provide regression-based normative data of bilateral strength in all major LL muscle groups and clinically useful prevalence data on the occurrence of weakness in these muscles. Of note, PwMS had a high prevalence of ankle dorsiflexion and hip extension weakness even when they were only mildly disabled. These findings can help guide the direction of future interventions and treatments to improve muscle function in PwMS.
 BACKGROUND: Progressive motor impairment anatomically associated with a "critical" lesion has been described in primary demyelinating disease. Most "critical" lesions occur within the spinal cord. OBJECTIVE: To describe the clinical and radiological features of "critical" lesions of the cervicomedullary junction (CMJ). METHODS: Observational study on people presenting with a CMJ lesion associated with primary demyelinating disease-related progressive motor impairment. Clinical data were extracted by chart review. Brain and spinal cord magnetic resonance images were reviewed to characterize the CMJ lesion and determine additional demyelination burden. RESULTS: Forty-one people were included: 29 (71%) had progression from onset and 12 (29%) had a relapse onset (secondary progressive) course. Most had progressive hemiparesis (21 (51%)) or progressive quadriparesis (15 (37%)) with a median Expanded Disability Status Scale (EDSS) of 5.5 (2.0-8.5) at last follow-up. No "critical" CMJ lesion enhanced; most were bilateral (25 (61%)). Brain magnetic resonance images were otherwise normal in 16 (39%) or with a restricted demyelination burden in 15 (37%). Cervical and thoracic cord MRIs were without additional lesions in 25 (61%) and 22/37 (59%), respectively. CONCLUSION: CMJ "critical" lesions can correlate with progressive motor impairment even with few or no additional magnetic resonance imaging (MRI) lesions. Lesion location is an important determinant of progressive motor impairment in demyelinating disease.
 BACKGROUND: The prevalence of dysphagia in the early phases of multiple sclerosis is 30-40%, with an estimated of 30% of cases going undiagnosed cases. Such complications can lead to malnutrition, dehydration, and aspiration pneumonia and have a great impact on the quality of life and psychosocial status of a person with MS. The aim of this study was the validation of dysphagia in multiple sclerosis self-assessment questionnaire (DYMUS) in the Croatian language. METHODS AND PATIENTS: The cross-cultural adaptation process included a back-forward translation technique of the English language version of DYMUS to the Croatian language, with pilot testing on 30 participants. The validity and reliability of the Croatian version of DYMUS (DYMUS-Hr) was applied to 106 MS patients, with comparison to the Eating Assessment Tool (EAT10), the Water Swallowing Test (WST), and a dichotomous self-assessment question. In the assessment of test-retest reliability, 99 MS patients were included. RESULTS: Internal consistency of DYMUS-Hr was very good (Cronbach's alpha-0.837); Cronbach's alpha was 0.819 for the "dysphagia for solids", and 0.562 for "dysphagia for liquids" subscale. A significant correlation (p < 0.001) was found between DYMUS-Hr and EAT10 (Spearman's rho-0.787), and WST (Spearman's rho-0.483). Construct validity was assessed with the self-assessment question and interpreted with the Mann-Whitney U test. Test-retest reliability showed moderate to substantial Cohen's Kappa reliability for each item. CONCLUSION: DYMUS-Hr is a valid and reliable screening assessment tool for patients with MS. There is a general lack of awareness about dysphagia symptoms among patients with MS; consequently, this disorder receives inadequate attention and often goes untreated.
 BACKGROUND: Rare genetic variants are emerging as important contributors to the heritability of multiple sclerosis (MS). Whether rare variants also contribute to pediatric-onset multiple sclerosis (POMS) is unknown. OBJECTIVE: To test whether genes harboring rare variants associated with adult-onset MS risk (PRF1, PRKRA, NLRP8, and HDAC7) and 52 major histocompatibility complex (MHC) genes are associated with POMS. METHODS: We analyzed DNA samples from 330 POMS cases and 306 controls from the US Network of Pediatric MS Centers and Kaiser Permanente Northern California for which Illumina ExomeChip genotypes were available. Using the gene-based method "SKAT-O," we tested the association between candidate genes and POMS risk. RESULTS: After correction for multiple comparisons, one adult-onset MS gene (PRF1, p = 2.70 × 10(-3)) and two MHC genes (BRD2, p = 5.89 × 10(-5) and AGER, p = 7.96 × 10(-5)) were significantly associated with POMS. Results suggest these are independent of HLA-DRB1*1501. CONCLUSION: Findings support a role for rare coding variants in POMS susceptibility. In particular, rare minor alleles within PRF1 were more common among individuals with POMS compared to controls while the opposite was true for rare variants within significant MHC genes, BRD2 and AGER. These genes would not have been identified by common variant studies, emphasizing the merits of investigating rare genetic variation in complex diseases.
 Multiple sclerosis (MS) is a debilitating neurodegenerative autoimmune disease of the central nervous system (CNS). The current study aimed to investigate the neuroprotective properties of Ajugarin-I (Aju-I) against the experimental autoimmune encephalomyelitis (EAE) model of MS and explored the underlying mechanism involved. The protective potential of Aju-I was first confirmed against glutamate-induced HT22 cells and hydrogen peroxide (H(2) O(2) )-induced BV2 cells. Next, an EAE model has been established to investigate the mechanisms of MS and identify potential candidates for MS treatment. The behavioral results demonstrated that Aju-I post-immunization treatment markedly reduced the EAE-associated clinical score, motor impairment, and neuropathic pain. Evans blue and fluorescein isothiocyanate extravasation in the brain were markedly reduced by Aju-I. It effectively restored the EAE-associated histopathological changes in the brain and spinal cord. It markedly attenuated EAE-induced inflammation in the CNS by reducing the expression levels of p-38/JNK/NF-κB but increased the expression of IkB-α. It suppressed oxidative stress by increasing the expression of Nrf2 but decreasing the expression of keap-1. It suppressed EAE-induced apoptosis in the CNS by regulating Bax/Bcl-2 and Caspase-3 expression. Taken together, this study suggests that Aju-I treatment exhibits neuroprotective properties in the EAE model of MS via regulation of MAPK/NF-κB, Nrf2/Keap-1, and Bcl2/Bax signaling.
 Multiple sclerosis is a chronic inflammatory disease of the central nervous system ultimate to neurodegeneration and demyelination. Ibudilast is a phosphodiesterase inhibitor, effective on the function of glial cells and lymphocytes, and inhibits the release of TNF-α by inflammatory cells. Dysregulation of glia is one of the most important pathological causes of MS. Therefore, ibudilast as a glial attenuator can be a useful treatment. The objective of the present study was to investigate the effect of nasal spray of polydopamine coated micelles of surfactin, a biosurfactant, loaded with ibudilast on its brain targeted delivery and effectiveness in remylination and neuroprotection in animal model of MS. In animal studies the micelles were administrated intranasally in different doses of 10, 25 and 50 mg/kg/day in C57/BL6 mice immunized by experimental autoimmune encephalomyelitis (EAE) model. The results of Luxol fast blue staining indicated increment in myelin fiber percent more significantly (p < 0.05) in the groups treated with the polydopamine coated micelles (PDAM) compared to nasal spray of free drug or oral administration. These formulations also increased expression of Mbp, Olig2 and Mog genes in the corpus callosum. These results suggest a positive outcome of polydopamine coated micelles loaded with ibudilast in active MS as an anti-inflammatory and neuroprotective agent.
 BACKGROUND AND PURPOSE: Myelin water fraction (MWF) deficits as measured by myelin water imaging (MWI) have been related to worse motor function in persons with multiple sclerosis (PwMS). However, it is unknown if measures from MWI metrics in motor areas relate to fall risk measures in PwMS. The objective of this study was to examine the relationship between MWI measures in motor areas to performance on clinical measures of fall risk and disability in PwMS. METHODS: Sixteen individuals with relapsing-remitting MS participated (1 male, 15 female; age 47.1 years [12.3]; Expanded Disability Status Scale 4.0 [range 0-6.5]) and completed measures of walking and fall risk (Timed 25 Foot Walk [T25FW] and Timed Up and Go). MWF and the geometric mean of the intra-/extracellular water T(2) (geomT(2IEW) ) values reflecting myelin content and contribution of large-diameter axons/density, respectively, were assessed in three motor-related regions. RESULTS: The geomT(2IEW) of the corticospinal tract (r = -.599; p = .018) and superior cerebellar peduncles (r = -.613; p = .015) demonstrated significant inverse relationships with T25FW, suggesting that decreased geomT(2IEW) was related to slower walking. Though not significant, MWF in the corticospinal tract and superior cerebellar peduncles also demonstrated fair relationships with the T25FW, suggesting that worse performance on the T25FW was associated with lower MWF values. CONCLUSIONS: MWI of key motor regions was associated with walking performance in PwMS. Further MWI studies are needed to identify relationships between pathology and clinical function in PwMS to guide targeted rehabilitation therapies aimed at preventing falls.
 AIM: Evaluate the real-world costs over two years and costs by site of care for ocrelizumab (OCR), natalizumab (NTZ), and alemtuzumab (ATZ) in patients with multiple sclerosis (MS). METHODS: This retrospective study used HealthCore Integrated Research Database and included continuously enrolled adults with MS initiating OCR, NTZ, and ATZ between April 2017 and July 2019 (i.e. patient identification period). Annual total cost of care (pharmacy and medical costs) was evaluated for the first- and second-year of follow-up, further stratified by site of care. Costs were measured using health plan allowed amount and adjusted to 2019 US dollars. Sensitivity analyses were conducted in patients who completed yearly dosing schedule according to Food and Drug Administration approved prescribing information. RESULTS: Overall, 1,058, 166, and 46 patients were included in OCR, NTZ, and ATZ cohorts, respectively. Mean (standard deviation [SD]) total cost of care during first- and second-year follow-up were $125,597 ($72,274) and $109,618 ($75,085) for OCR, $117,033 ($57,102) and $106,626 ($54,872) for NTZ, and $179,809 ($97,530) and $108,636 ($77,973) for ATZ. Infusible drug cost was the main driver in all three cohorts accounting for >78% of the total costs. Annual total cost of care increased substantially after patients started/switched to infusible DMTs. Across site of care, hospital outpatient infusion was common (OCR 58%, NTZ 37%, ATZ 49%) and expensive followed by physician office infusion (OCR 28%, NTZ 40%, ATZ 16%); home infusion was the least common (<10%) and least expensive. LIMITATIONS: The results were limited to commercially insured patients (specifically those with Anthem-affiliated health plans). CONCLUSIONS: Real-world costs increased after patients started/switched to infusible DMTs. Drug cost is the main driver for the total costs, which varied substantially by site of care. Controlling drug cost markups and using home setting for infusion can reduce costs in the treatment of MS patients.
 In multiple sclerosis, spontaneous remyelination is generally incomplete and heterogeneous across patients. A high heterogeneity in remyelination may also exist across lesions within the same individual, suggesting the presence of local factors interfering with myelin regeneration. In this study we explored in vivo the regional distribution of myelin repair and investigated its relationship with neurodegeneration. We first took advantage of the myelin binding property of the amyloid radiotracer 11C-PiB to conduct a longitudinal 11C-PiB PET study in an original cohort of 19 participants with a relapsing-remitting form of multiple sclerosis, followed-up over a period of 1-4 months. We then replicated our results on an independent cohort of 40 people with multiple sclerosis followed-up over 1 year with magnetization transfer imaging, an MRI metrics sensitive to myelin content. For each imaging method, voxel-wise maps of myelin content changes were generated according to modality-specific thresholds. We demonstrated a selective failure of remyelination in periventricular white matter lesions of people with multiple sclerosis in both cohorts. In both the original and the replication cohort, we estimated that the probability of demyelinated voxels to remyelinate over the follow-up increased significantly as a function of the distance from ventricular CSF. Enlarged choroid plexus, a recently discovered biomarker linked to neuroinflammation, was found to be associated with the periventricular failure of remyelination in the two cohorts (r = -0.79, P = 0.0018; r = -0.40, P = 0.045, respectively), suggesting a role of the brain-CSF barrier in affecting myelin repair in surrounding tissues. In both cohorts, the failure of remyelination in periventricular white matter lesions was associated with lower thalamic volume (r = 0.86, P < 0.0001; r = 0.33; P = 0.069, respectively), an imaging marker of neurodegeneration. Interestingly, we also showed an association between the periventricular failure of remyelination and regional cortical atrophy that was mediated by the number of cortex-derived tracts passing through periventricular white matter lesions, especially in patients at the relapsing-remitting stage. Our findings demonstrate that lesion proximity to ventricles is associated with a failure of myelin repair and support the hypothesis that a selective periventricular remyelination failure in combination with the large number of tracts connecting periventricular lesions with cortical areas is a key mechanism contributing to cortical damage in multiple sclerosis.
 BACKGROUND: Multiple sclerosis (MS) is an immune-mediated disease that affects the central nervous system, and is potentially disabling. Women experience MS more frequently than men at a 3:1 ratio. Current literature suggests that women may experience health, social determinants of health, and disability differentially, and there is a gap in the research examining how gender intersects with MS. METHODS: Interviews were conducted with 23 women with MS. van Manen's hermeneutic phenomenology was used to inform and analyze the data to understand the nature and meaning of health and well-being for participants. RESULTS: A key theme of "enhancing wholeness for women with MS" emerged from the data, which suggests that women with MS view themselves as healthy and "whole" despite living with MS. Supporting factors for physical, mental, and social well-being include the ability to enact human agency within social structures such as with employment or seeking care with MS clinics. The findings informed the development of a figure that depicts the supporting factors of health and well-being for women living with MS. CONCLUSION: The health and well-being of women with MS may be optimally supported by nurses and interdisciplinary healthcare teams through careful consideration as to how agency is enacted within social structures, for example, MS clinics, employment, and social support systems, as well as considerations for social determinants of health.

 Multiple sclerosis (MS) is a neurological disease that leads to severe physical and cognitive disabilities. Drugs used in the treatment of MS vary from small synthetic molecules to large macromolecules such as antibodies. Sphingosine 1-phosphate receptor modulators are frequently used for the treatment of MS. These medicines prevent the egress of lymphocytes from secondary lymphoid organs leading to immune system suppression. Currently, four S1PR modulators are on the market and several potential drug candidates are in clinical trials for the treatment of MS. These compounds differ in chemical structure, adverse effects, and efficacy points of view. The current article reviews the latest studies on S1PR1 modulators and compares them with other MS drugs in terms of efficacy, tolerability, and safety. A special focus was dedicated to discussing the structure-activity relationships of these compounds and performing a three-dimensional quantitative structure-activity relationship (3D-QSAR) analysis to gain better insight into the ligand-receptor interaction mode.
 BACKGROUND: Spasticity is a frequent symptom of multiple sclerosis (MS), which may negatively influence daily living activities (ADL). OBJECTIVES: To (1) explore the feasibility to conduct a structured interview by specialist nurses about limitations in ADL; (2) determine the percentage of people with MS (PwMS) with limitations in ADL related to spasticity; (3) to assess the knowledge about spasticity and describe its clinical features. DESIGN: Observational, cross-sectional, multicentre study in 16 MS units of Catalonia (Spain). Participants were recruited from the outpatient facility and day-care hospital between July 2018 and June 2019 and met the following criteria: (1) age 18 or older, (2) diagnosis of MS according to McDonald criteria 2010 and (3) no clinical relapse in previous 30 days. METHODS: Specialist nurses conducted a structured interview divided in two parts: the assessment of (1) limitations in the ADL and (2) the presence of spasticity and associated symptoms. The usefulness of this intervention was requested. This study met the STROBE reporting guidelines checklist for observational studies. RESULTS: Three hundred sixty eight pwMS (244 women) with a mean age of 46 years and a median Expanded Disability Status Scale score of 2.5 (range, 0-8.5) were included. 262 (71%) pwMS had limitations in the ADL, and spasticity was reported as the most limiting symptom in 59 (23%). As a result of the interview, spasticity was observed in 199 (76%) participants; 47 (24%) of them were unaware that they had spasticity and 102 (51%) would not have reported it spontaneously. The level of the interview satisfaction was high (90%). CONCLUSIONS: Spasticity is a complex and limiting symptom in MS. The structured interview conducted by specialist nurses is feasible and has good acceptance. PATIENT CONTRIBUTION: Specialist nurses can be proactive in MS clinical assessment, which may help to detect symptoms with negative impact on quality of life.
 PURPOSE: The purpose of this study was to explore the lived experience of dancing with Parkinson's and Multiple Sclerosis in an inclusive dance group called ReDiscoverMe (RDM). METHODS: Participatory research approaches and interpretative phenomenological analysis were used to make sense of the lived experience captured in interviews and observations. Arthur Frank's conceptual framework on embodied storytelling from his book The Wounded Storyteller was the study's theoretical lens. Themes are both described and represented in images made by an RDM participant. FINDINGS: Dancing in a nonjudgmental environment was described by participants as a way to rediscover themselves while continually adapting to living with chronic illness. We interpreted this experience of rediscovery as an active, recursive process involving three "movements": escaping, expanding, and embracing. Through these movements, participants could rise above the self and illness. CONCLUSIONS: The lived experience of dancing in this group was characterized by transformations of the body, self, and life. Through escaping, expanding, and embracing, participants could more easily embrace the body's contingency, integrate the self and body by becoming dancers, connect with others living with illness, and produce desire through passion. Participants could therefore experience illness as a journey and gain something from the experience.
 An 18-protein multiple sclerosis (MS) disease activity (DA) test was validated based on associations between algorithm scores and clinical/radiographic assessments (N = 614 serum samples; Train [n = 426; algorithm development] and Test [n = 188; evaluation] subsets). The multi-protein model was trained based on presence/absence of gadolinium-positive (Gd+) lesions and was also strongly associated with new/enlarging T2 lesions, and active versus stable disease (composite of radiographic and clinical evidence of DA) with improved performance (p < 0.05) compared to the neurofilament light single protein model. The odds of having ≥1 Gd+ lesions with a moderate/high DA score were 4.49 times that of a low DA score, and the odds of having ≥2 Gd+ lesions with a high DA score were 20.99 times that of a low/moderate DA score. The MSDA Test was clinically validated with improved performance compared to the top-performing single-protein model and can serve as a quantitative tool to enhance the care of MS patients.
 Aging is a significant risk factor associated with the progression of CNS neurodegenerative diseases including multiple sclerosis (MS). Microglia, the resident macrophages of the CNS parenchyma, are a major population of immune cells that accumulate in MS lesions. While they normally regulate tissue homeostasis and facilitate the clearance of neurotoxic molecules including oxidized phosphatidylcholines (OxPCs), their transcriptome and neuroprotective functions are reprogrammed by aging. Thus, determining the factors that instigate aging associated microglia dysfunction can lead to new insights for promoting CNS repair and for halting MS disease progression. Through single-cell RNA sequencing (scRNAseq), we identified Lgals3, which encodes for galectin-3 (Gal3), as an age upregulated gene by microglia responding to OxPC. Consistently, excess Gal3 accumulated in OxPC and lysolecithin-induced focal spinal cord white matter (SCWM) lesions of middle-aged mice compared with young mice. Gal3 was also elevated in mouse experimental autoimmune encephalomyelitis (EAE) lesions and more importantly in MS brain lesions from two male and one female individuals. While Gal3 delivery alone into the mouse spinal cord did not induce damage, its co-delivery with OxPC increased cleaved caspase 3 and IL-1β within white matter lesions and exacerbated OxPC-induced injury. Conversely, OxPC-mediated neurodegeneration was reduced in Gal3(-/-) mice compared with Gal3(+/+) mice. Thus, Gal3 is associated with increased neuroinflammation and neurodegeneration and its overexpression by microglia/macrophages may be detrimental for lesions within the aging CNS.SIGNIFICANCE STATEMENT Aging accelerates the progression of neurodegenerative diseases such as multiple sclerosis (MS). Understanding the molecular mechanisms of aging that increases the susceptibility of the CNS to damage could lead to new strategies to manage MS progression. Here, we highlight that microglia/macrophage-associated galectin-3 (Gal3) was upregulated with age exacerbated neurodegeneration in the mouse spinal cord white matter (SCWM) and in MS lesions. More importantly, co-injection of Gal3 with oxidized phosphatidylcholines (OxPCs), which are neurotoxic lipids found in MS lesions, caused greater neurodegeneration compared with injection of OxPC alone, whereas genetic loss of Gal3 reduced OxPC damage. These results demonstrate that Gal3 overexpression is detrimental to CNS lesions and suggest its deposition in MS lesions may contribute to neurodegeneration.
 As a result of technical developments and greater availability of imaging equipment, the number of neuroradiological examinations is steadily increasing [1]. Due to improved image quality and sensitivity, more details can be detected making reporting more complex and time-intensive. At the same time, reliable algorithms increasingly allow quantitative image analysis that should be integrated in reports in a standardized manner. Moreover, increasing digitalization is resulting in a decrease in the personal exchange between neuroradiologists and referring disciplines, thereby making communication more difficult. The introduction of structured reporting tailored to the specific disease and medical issue [2, 3] and corresponding to at least the second reporting level as defined by the German Radiological Society (https://www.befundung.drg.de/de-DE/2908/strukturierte-befundung/) is therefore desirable to ensure that the quality standards of neuroradiological reports continue to be met.The advantages of structured reporting include a reduced workload for neuroradiologists and an information gain for referring physicians. A complete and standardized list with relevant details for image reporting is provided to neuroradiologists in accordance with the current state of knowledge, thereby ensuring that important points are not forgotten [4]. A time savings and increase in efficiency during reporting were also seen [5]. Further advantages include report clarity and consistency and better comparability in follow-up examinations regardless of the neuroradiologist's particular reporting style. This results in better communication with the referring disciplines and makes clinical decision significantly easier [6, 7]. Although the advantages are significant, any potential disadvantages like the reduction of autonomy in reporting and inadequate coverage of all relevant details and any incidental findings not associated with the main pathology in complex cases or in rare diseases should be taken into consideration [4]. Therefore, studies examining the advantages of structured reporting, promoting the introduction of this system in the clinical routine, and increasing the acceptance among neuroradiologists are still needed.Numerous specific templates for structured reporting, e. g., regarding diseases in cardiology and oncology, are already available on the website www.befundung.drg.de . Multiple sclerosis (MS) is an idiopathic chronic inflammatory and neurodegenerative disease of the central nervous system and is the most common non-trauma-based inflammatory neurological disease in young adults. Therefore, it has significant individual and socioeconomic relevance [8]. Magnetic resonance imaging (MRI) plays an important role in the diagnosis, prognosis evaluation, and follow-up of this disease. MRI is established as the central diagnostic method in the diagnostic criteria. Therefore, specific changes are seen on MRI in almost all patients with a verified MS diagnosis [9]. Reporting of MRI datasets regarding the brain and spinal cord of patients with MS includes examination of the images with respect to the relevant medical issue in order to determine whether the McDonald criteria, which were revised in 2017 [10] and define dissemination in time and space clinically as well as with respect to MRI based on the recommendations of the MAGNIMS groups [11, 12], are fulfilled. A more precise definition of lesion types and locations according to the recommendations of an international expert group [13] is discussed in the supplementary material. Spinal cord signal abnormalities are seen in up to 92 % of MS patients [14-16] and are primarily located in the cervical spine [15]. The recommendations of the MAGNIMS-CMSC-NAIMS working group published in 2021 [11] explicitly recommend the use of structured reporting for MS patients.Therefore, a reporting template for evaluating MRI examinations of the brain and spinal cord of patients with MS was created as part of the BMBF-funded DIFUTURE consortium in consensus with neuroradiological and neurological experts in concordance with the recommendations mentioned above [11] and was made available for broad use (https://github.com/DRGagit/ak_befundung). The goal is to facilitate efficient and comprehensive evaluation of patients with MS in the primary diagnostic workup and follow-up imaging. These reporting templates are consensus-based recommendations and do not make any claim to general validity or completeness. The information technology working group (@GIT) of the German Radiological Society and the German Society for Neuroradiology strive to keep the reporting templates presented here up-to-date with respect to new research data and recommendations of the MAGNIMS-CMSC-NAIMS group [11]. KEY POINTS:: · consensus-based reporting templates. · template for the structured reporting of MRI examinations of patients with multiple sclerosis. · structured reporting might facilitate communication between neuroradiologists and referring disciplines. CITATION FORMAT: · Riederer I, Mühlau M, Wiestler B et al. Structured Reporting in Multiple Sclerosis - Consensus-Based Reporting Templates for Magnetic Resonance Imaging of the Brain and Spinal Cord. Fortschr Röntgenstr 2023; 195: 135 - 138.
 BACKGROUND: The multiple sclerosis (MS) community is highly interested in diet as a potential protective factor against disability, but empirical evidence remains limited. OBJECTIVE: Evaluate associations between patient-reported Mediterranean diet alignment and objective disability in a real-world MS cohort. METHODS: Data were analyzed from persons with MS, aged 18-65, who completed the Mediterranean Diet Adherence Screener (MEDAS), MS Functional Composite (MSFC; primary disability metric), and patient-reported outcomes (PROs; disability, gait disturbance, fatigue, anxiety, and depression) as part of our Comprehensive Annual Assessment Program. Multiple regression predicted MSFC (and PROs) with MEDAS after adjusting for demographic (age, sex, race, ethnicity, and socioeconomic status) and health-related (body mass index (BMI), exercise, sleep disturbance, hypertension, diabetes, hyperlipidemia, and smoking) covariates. RESULTS: Higher MEDAS independently predicted better outcomes across MSFC (z-score, B = 0.10 (95% confidence interval (CI): 0.06, 0.13), β = 0.18, p < 0.001), MSFC components, and PROs in 563 consecutive patients. Each MEDAS point was associated with 15.0% lower risk for MSFC impairment (⩽ 5th percentile on ⩾ 2 tasks; odds ratio (OR) = 0.850; 95% CI: 0.779, 0.928). Higher MEDAS attenuated effects of progressive disease and longer disease duration on disability. CONCLUSION: With robust control for potential confounds, higher Mediterranean diet alignment predicted lower objective and patient-reported disability. Findings lay the necessary groundwork for longitudinal and interventional studies to guide clinical recommendations in MS.
 Epidemiological studies support the idea that multiple sclerosis (MS) is a multifactorial disease, overlapping genetic, epigenetic, and environmental factors. A better definition of environmental risks is critical to understand both etiology and the sex-related differences of MS. Exposure to endocrine-disrupting compounds (EDCs) fully represents one of these risks. EDCs are natural or synthetic exogenous substances (or mixtures) that alter the functions of the endocrine system. Among synthetic EDCs, exposure to bisphenol A (BPA) has been implicated in the etiology of MS, but to date, controversial data has emerged. Furthermore, nothing is known about bisphenol S (BPS), one of the most widely used substitutes for BPA. As exposure to bisphenols will not disappear soon, it is necessary to clarify their role also in this pathological condition defining their role in disease onset and course in both sexes. In this study, we examined, in both sexes, the effects of perinatal exposure to BPA and BPS in one of the most widely used mouse models of MS, experimental autoimmune encephalomyelitis (EAE). Exposure to bisphenols seemed to be particularly deleterious in males. In fact, both BPA- and BPS-treated males showed anticipation of the disease onset and an increased motoneuron loss in the spinal cord. Overall, BPA-treated males also displayed an exacerbation of EAE course and an increase in inflammation markers in the spinal cord. Analyzing the consequences of bisphenol exposure on EAE will help to better understand the role of both xenoestrogens and endogenous estrogens on the sexually dimorphic characteristics of MS.
 BACKGROUND: Serum neurofilament light chain (sNfL) is an emerging multiple sclerosis (MS) biomarker which measures neuro-axonal damage. However, understanding its temporal association with disease activity in pediatric-onset MS (POMS) and Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) remains limited. OBJECTIVE: To investigate the association of sNfL levels and time from disease activity in children with MS and MOGAD. METHODS: POMS and MOGAD cases with onset before 18 years of age were enrolled at the University of California San Francisco (UCSF) Regional Pediatric MS Center. Frequency-matched healthy subjects were recruited from general pediatric clinics. Serum samples were tested for MOG-IgG at Mayo Clinic using a live cell-based fluorescent activated cell sorting assay. sNfL levels were measured using single-molecule array (Simoa) technology measured in pg/mL. Data on demographics, clinical features, MRI, CSF, and treatment data were collected by chart review. RESULTS: We included 201 healthy controls healthy controls, 142 POMS, and 20 confirmed MOGAD cases with available sNfL levels. The median (IQR) age at the time of sampling was 15.6 (3.9), 15.5 (3.1), and 8.8 (4.1) years for controls, POMS, and MOGAD, respectively. Median sNfL levels (pg/ml) were higher in POMS (19.6) and MOGAD (32.7) cases compared to healthy controls (3.9) (p<0.001). sNfL levels ≥100 pg/ml were only detected within four months of a clinical event or MRI activity in both POMS and MOGAD cases. In addition, sNfL levels were higher in POMS patients with new/enlarged T2 and gadolinium-enhanced lesions than those without MRI activity within four months of sampling in POMS cases. CONCLUSION: High sNfL levels were observed close to clinical or MRI events in POMS and MOGAD. Our findings support sNfL as a biomarker of disease activity in pediatric demyelinating disorders.
 BACKGROUND: Disease-modifying treatments (DMT) are used to prevent future relapses and disability. High long-term adherence to treatment is important to achieve disease control. This study aims to investigate and compare adherence, adverse event (AE) profiles, and frequencies, main reasons for treatment discontinuation under Teriflunomide (TERI), Dimethyl Fumarate (DMF), and Fingolimod (FNG) for relapsing-remitting MS (RRMS) patients. This study is designed to explore patient-reported experiences in real-life settings. METHODS: Patients who were older than 18 years with a definite diagnosis of RRMS and no history of stem-cell transplantation were included. Outpatient clinic data files at the Neurology Department of Marmara University from June 2012 to June 2019 were examined retrospectively. RESULTS: One hundred and ninety MS patients were enrolled. 118 FNG, 51 DMF, 44 TERI treatment cycles were recorded. Time sincedisease onset, time since diagnosis, and treatment duration were significantly longer for FNG (p = 0.012, p = 0.004, p < 0.001). 72.8% of all the treatment cycles were continued. There was no significant difference in treatment continuity between the 3 DMT groups. The most common reasons for treatment discontinuation in order of frequency were adverse events, the progression of the disease, and the persistence of relapses. No significant difference was found for treatment discontinuation reasons. 32% of the patients reported at least one AE. 28% FNG, 49 % DMF, and 27.3% TERI using patients reported AEs. AEs were much more frequently reported for DMF (p = 0.015). The most common adverse events for each DMT were alopecia (n = 6, 13.6%) for TERI, flushing for DMF (n = 20, 39.2%), and persistent lymphopenia for FNG (n = 9, 7.6%). No severe or life-threatening AE was reported for DMF, one patient experienced pancreatitis under TERI, and 11 (9.3%) patients using FNG had to stop treatment due to serious or life-threatening AEs including cardiac adverse events, opportunistic infections, and dysplasia. DISCUSSION: Overall treatment discontinuation because of AEs is as low as 10.3% in this study. However, AEs are still the main reason for treatment drop-out.

 BACKGROUND: Inter-individual courses of multiple sclerosis (MS) are extremely variable. The objective of this study was to investigate whether κ-free light chain (κ-FLC) index and serum neurofilament light (sNfL) have an additive predictive value for MS disease activity. METHODS: Patients with early MS who had cerebrospinal fluid (CSF) and serum sampling at disease onset were followed for four years. At baseline, age, sex, disease duration, number of T2-hyperintense (T2L), and contrast-enhancing T1 lesions (CEL) on MRI were determined. During follow-up, the occurrence of a second clinical attack and start of disease-modifying treatment (DMT) were registered. κ-FLC was measured by nephelometry, and κ-FLC index calculated as [CSF κ-FLC/serum κ-FLC]/albumin quotient. sNfL was determined by single-molecule array, and age- and body-mass-index adjusted Z scores were calculated. FINDINGS: A total of 86 patients at a mean age of 33 ± 10 years and with a female predominance of 67% were included; 36 (42%) patients experienced a second clinical attack during follow-up. Cox regression analysis adjusted for age, sex, T2L, CEL, disease and follow-up duration, and DMT use during follow-up revealed that both κ-FLC index as well as sNfL Z score independently predict time to second clinical attack. The chance for freedom of relapse within 12 months was 2% in patients with high levels of κ-FLC index (>100) and high sNfL Z score (>3), 30% in patients with high κ-FLC index (>100) and lower sNfL Z score (≤3), 70% in patients with lower κ-FLC index (≤100) but high sNfL Z score (>3), and 90% in patients with lower levels of κ-FLC index (≤100) and sNfL Z score (≤3). INTERPRETATION: κ-FLC index and sNfL Z score have an additive predictive value for early MS disease activity that is independent of known predictors. FUNDING: This study was funded by a grant of the charitable foundation of the Austrian Multiple Sclerosis Society.
 Polygenic inheritance plays a pivotal role in driving multiple sclerosis susceptibility, an inflammatory demyelinating disease of the CNS. We developed polygenic risk scores (PRS) of multiple sclerosis and assessed associations with both disease status and severity in cohorts of European descent. The largest genome-wide association dataset for multiple sclerosis to date (n = 41 505) was leveraged to generate PRS scores, serving as an informative susceptibility marker, tested in two independent datasets, UK Biobank [area under the curve (AUC) = 0.73, 95% confidence interval (CI): 0.72-0.74, P = 6.41 × 10-146] and Kaiser Permanente in Northern California (KPNC, AUC = 0.8, 95% CI: 0.76-0.82, P = 1.5 × 10-53). Individuals within the top 10% of PRS were at higher than 5-fold increased risk in UK Biobank (95% CI: 4.7-6, P = 2.8 × 10-45) and 15-fold higher risk in KPNC (95% CI: 10.4-24, P = 3.7 × 10-11), relative to the median decile. The cumulative absolute risk of developing multiple sclerosis from age 20 onwards was significantly higher in genetically predisposed individuals according to PRS. Furthermore, inclusion of PRS in clinical risk models increased the risk discrimination by 13% to 26% over models based only on conventional risk factors in UK Biobank and KPNC, respectively. Stratifying disease risk by gene sets representative of curated cellular signalling cascades, nominated promising genetic candidate programmes for functional characterization. These pathways include inflammatory signalling mediation, response to viral infection, oxidative damage, RNA polymerase transcription, and epigenetic regulation of gene expression to be among significant contributors to multiple sclerosis susceptibility. This study also indicates that PRS is a useful measure for estimating susceptibility within related individuals in multicase families. We show a significant association of genetic predisposition with thalamic atrophy within 10 years of disease progression in the UCSF-EPIC cohort (P < 0.001), consistent with a partial overlap between the genetics of susceptibility and end-organ tissue injury. Mendelian randomization analysis suggested an effect of multiple sclerosis susceptibility on thalamic volume, which was further indicated to be through horizontal pleiotropy rather than a causal effect. In summary, this study indicates important, replicable associations of PRS with enhanced risk assessment and radiographic outcomes of tissue injury, potentially informing targeted screening and prevention strategies.
 Multiple sclerosis (MS) is a neuroinflammatory disease characterized by loss of myelin (demyelination) and, to a certain extent, subsequent myelin repair (remyelination). To better understand the pathomechanisms underlying de- and remyelination and to monitor the efficacy of treatments aimed at regenerating myelin, techniques offering noninvasive visualizations of myelin are warranted. Magnetic resonance (MR) imaging has long been at the forefront of efforts to visualize myelin, but it has only recently become feasible to access the rapidly decaying resonance signals stemming from the myelin lipid-protein bilayer itself. Here, we show that direct MR mapping of the bilayer yields highly specific myelin maps in brain tissue from patients with MS. Furthermore, examination of the bilayer signal behavior is found to reveal pathological alterations in normal-appearing white and gray matter. These results indicate promise for in vivo implementations of the myelin bilayer mapping technique, with prospective applications in basic research, diagnostics, disease monitoring, and drug development.
 OBJECTIVE: It remains unclear whether viral infections interfere with multiple sclerosis (MS) disease progression. We evaluated the prognostic role of antibody responses toward viruses determined at disease onset on long-term disease outcomes. METHODS: Humoral immune responses against Epstein-Barr virus (EBV)-encoded nuclear antigen EBNA1, viral capsid antigen (VCA) and early antigen, and toward cytomegalovirus (HCMV), human herpesvirus 6 and measles were investigated in a cohort of 143 patients with MS for their association with long-term disability and inflammation disease outcomes. RESULTS: Median (IQR) follow-up was 20 (17.2-22.8) years. In univariable analysis, increased HCMV levels were associated with a lower risk to Expanded Disability Status Scale 4.0 (HR 0.95; 95% CI 0.91 to 0.99; p=0.03), to develop a secondary progressive MS (HR 0.94; 95% CI 0.90 to 0.99; p=0.02) and to first-line treatment (HR 0.98; 95% CI 0.96 to 0.99; p=0.04). High HCMV IgG levels were associated with a longer time to first-line treatment (p=0.01). Increased immune responses against EBV-VCA were associated with higher risk for first-line (HR 1.45; 95% CI 1.12 to 1.88; p=0.005) and second-line treatments (HR 2.03; 95% CI 1.18 to 3.49; p=0.01), and high VCA IgG levels were associated with shorter time to first-line (p=0.004) and second-line (p=0.02) therapies. EBNA1-specific IgG levels correlated with disease severity (0.17; p=0.04) and with an increased relapse rate during follow-up (relapse rate 1.26; 95% CI 1.03 to 1.56; p=0.02) that remained stable in multivariable analysis. CONCLUSIONS: These results indicate that elevated immune responses against HCMV at disease onset have protective effects on long-term disability and inflammation disease outcomes. Our data also indicate that increased immune responses against EBV in early phases may influence long-term disease prognosis.
 Transplantation of human neural stem cells (hNSCs) is a promising regenerative therapy to promote remyelination in patients with multiple sclerosis (MS). Transplantation of hNSCs has been shown to increase the number of CD4+CD25+Foxp3+ T regulatory cells (Tregs) in the spinal cords of murine models of MS, which is correlated with a strong localized remyelination response. However, the mechanisms by which hNSC transplantation leads to an increase in Tregs in the CNS remains unclear. We report that hNSCs drive the conversion of T conventional (Tconv) cells into Tregs in vitro. Conversion of Tconv cells is Ag driven and fails to occur in the absence of TCR stimulation by cognate antigenic self-peptides. Furthermore, CNS Ags are sufficient to drive this conversion in the absence of hNSCs in vitro and in vivo. Importantly, only Ags presented in the thymus during T cell selection drive this Treg response. In this study, we investigate the mechanisms by which hNSC Ags drive the conversion of Tconv cells into Tregs and may provide key insight needed for the development of MS therapies.
 AIMS: Axonal injury in multiple sclerosis (MS) and experimental models is most frequently detected in acutely demyelinating lesions. We recently reported a compensatory neuronal response, where mitochondria move to the acutely demyelinated axon and increase the mitochondrial content following lysolecithin-induced demyelination. We termed this homeostatic phenomenon, which is also evident in MS, the axonal response of mitochondria to demyelination (ARMD). The aim of this study is to determine whether ARMD is consistently evident in experimental demyelination and how its perturbation relates to axonal injury. METHODS: In the present study, we assessed axonal mitochondrial content as well as axonal mitochondrial respiratory chain complex IV activity (cytochrome c oxidase or COX) of axons and related these to axonal injury in nine different experimental disease models. We used immunofluorescent histochemistry as well as sequential COX histochemistry followed by immunofluorescent labelling of mitochondria and axons. RESULTS: We found ARMD a consistent and robust phenomenon in all experimental disease models. The increase in mitochondrial content within demyelinated axons, however, was not always accompanied by a proportionate increase in complex IV activity, particularly in highly inflammatory models such as experimental autoimmune encephalomyelitis (EAE). Axonal complex IV activity inversely correlated with the extent of axonal injury in experimental disease models. CONCLUSIONS: Our findings indicate that ARMD is a consistent and prominent feature and emphasise the importance of complex IV activity in the context of ARMD, especially in autoimmune inflammatory demyelination, paving the way for the development of novel neuroprotective therapies.
 Menopause, defined as the permanent cessation of ovarian function, represents a period of significant fluctuation in sex hormone concentrations. Sex hormones including oestrogen, progesterone, testosterone and anti-Mullerian hormone are thought have neuroinflammatory effects and are implicated in both neuroprotection and neurodegeneration. Sex hormones have a role in modifying clinical trajectory in multiple sclerosis (MS) throughout the lifespan. MS predominantly effects women and is typically diagnosed early in a woman's reproductive life. Most women with MS will undergo menopause. Despite this, the effect of menopause on MS disease course remains unclear. This review examines the relationship between sex hormones and MS disease activity and clinical course, particularly around the time of menopause. It will consider the role of interventions such as exogenous hormone replacement therapy in modulating clinical outcomes in this period. Understanding the impact of menopause on multiple sclerosis is fundamental for delivering optimal care to women with MS as they age and will inform treatment decisions with the aim of minimising relapses, disease accrual and improving quality of life.
 Obesity-induced insulin resistance (OIR) has been associated with an increased prevalence of neurodegenerative disorders such as multiple sclerosis. Obesity results in increased blood-brain barrier (BBB) permeability, specifically in the hypothalamic regions associated with the control of caloric intake. In obesity, the chronic state of low-grade inflammation has been implicated in several chronic autoimmune inflammatory disorders. However, the mechanisms that connect the inflammatory profile of obesity with the severity of experimental autoimmune encephalomyelitis (EAE) are poorly defined. In this study, we show that obese mice are more susceptible to EAE, presenting a worse clinical score with more severe pathological changes in the spinal cord when compared with control mice. Analysis of immune infiltrates at the peak of the disease shows that high-fat diet (HFD)- and control (chow)-fed groups do not present any difference in innate or adaptive immune cell compartments, indicating the increased severity occurs prior to disease onset. In the setting of worsening EAE in HFD-fed mice, we observed spinal cord lesions in myelinated regions and (blood brain barrier) BBB disruption. We also found higher levels of pro-inflammatory monocytes, macrophages, and IFN-γ(+)CD4(+) T cells in the HFD-fed group compared to chow-fed animals. Altogether, our results indicate that OIR promotes BBB disruption, allowing the infiltration of monocytes/macrophages and activation of resident microglia, ultimately promoting CNS inflammation and exacerbation of EAE.
 OBJECTIVE: Analyse the integrated safety profile of evobrutinib, a Bruton's tyrosine kinase inhibitor (BTKi), using pooled data from multiple sclerosis (MS), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) trials. METHODS: Phase II, randomised, double-blind, placebo-controlled trial data were analysed (N=1083; MS: n=213, 48 weeks (W); RA: n=390, 12W; SLE: n=480, 52W). The analysis included all patients who received ≥1 dose of evobrutinib (25 mg or 75 mg once daily, or 50 mg or 75 mgtwice daily) or placebo. Descriptive statistics and exposure-adjusted incidence rates (EAIR) were used to report treatment-emergent adverse events (TEAEs). RESULTS: Data from 1083 patients were pooled: evobrutinib, n=861; placebo, n=271 (sum >1083 due to MS trial design: n=49 received both placebo (W0-24) and evobrutinib 25 mg (W25-48)); median follow-up time (pt-years): evobrutinib, 0.501; placebo, 0.463. Across indications, the proportion of patients with TEAEs and the EAIR were similar for evobrutinib and placebo (66.2% (247.6 events/100 pt-years) vs 62.4% (261.4 events/100 pt-years)). By indication, the EAIR (events/100 pt-years) of TEAEs for evobrutinib versus placebo were: MS: 119.7 vs 148.3; RA: 331.8 vs 306.8; SLE: 343.0 vs 302.1. Two fatal events occurred (in SLE). The serious infections EAIR was 2.7 and 2.1 events/100 pt-years for evobrutinib and placebo. For previously reported BTKi-class effects, the EAIR of transient elevated alanine aminotransferase/aspartate aminotransferase TEAEs (events/100 pt-years) with evobrutinib versus placebo was 4.8 vs 2.8/3.5 vs 0.7, respectively. IgG levels were similar in evobrutinib/placebo-treated patients. CONCLUSIONS: This is the first BTKi-integrated safety analysis that includes patients with MS. Overall, evobrutinib treatment (all doses) was generally well tolerated across indications. TRIAL REGISTRATION NUMBERS: NCT02975349, NCT03233230, NCT02975336.
 AIMS: It is aimed to investigate the psychometric properties of Mini-BESTestTR in Turkish patients with neurological disorders. METHODS: A total of 61 people between the ages of 42 and 80, who were patients with Parkinson's disease, stroke or multiple sclerosis for more than 1 year, were included in the study. For inter-rater reliability, two independent researchers applied the scale two times within 5 days for test-retest reliability. The relationship of mini-BESTestTR with Berg Balance Scale (BBS) to assess concurrent validity, and Timed Get up and Go (TUG), Functional Reach Test (FRT) and Functional Ambulation Classification (FAC) for convergent validity was investigated. RESULTS: The scores of the two evaluators were within the range of agreement (mean = - 0.278 ± 1.484, p > 0.05), and the Mini-BESTestTR had excellent inter-rater reliability [ICC (95% CI) = 0.989 (0.981-0.993)] and test-retest reliability [ICC (95% CI) = 0.998 (0.996-0.999)]. Mini-BESTestTR had a strong correlation with BBS (r = 0.853, p < 0.001) and TUG (r =  - 0.856, p < 0.001), had a moderate correlation with FAC (r = 0.696, p < 0.001) and FRT (r = 0.650, p < 0.001). CONCLUSIONS: Mini-BESTestTR showed significant correlations with other balance assessment measures, and concurrent and convergent validity of Mini-BESTestTR was demonstrated when administered to a sample of patients with chronic stroke, Parkinson's disease and multiple sclerosis.
 BACKGROUND: Retinal degeneration leading to optical coherence tomography (OCT) changes is frequent in patients with multiple sclerosis (PwMS). OBJECTIVE: To investigate associations among OCT changes, MRI measurements of global and regional brain volume loss, and physical and cognitive impairment in PwMS. METHODS: 95 PwMS and 52 healthy controls underwent OCT and MRI examinations. Mean peripapillary retinal nerve fiber layer (pRNFL) thickness and ganglion cell/inner plexiform layer (GCIPL) volume were measured. In PwMS disability was quantified with the Expanded Disability Status Scale (EDSS) and Symbol Digit Modalities Test (SDMT). Associations between OCT, MRI, and clinical measures were investigated with multivariable regression models. RESULTS: In PwMS, pRNFL and GCIPL were associated with the volume of whole brain (p < 0.04), total gray matter (p < 0.002), thalamus (p ≤ 0.04), and cerebral cortex (p ≤ 0.003) -both globally and regionally-, but not white matter. pRNFL and GCIPL were also inversely associated with T2-lesion volume (T2LV), especially in the optic radiations (p < 0.0001). The brain volumes associated with EDSS and SDMT significantly overlapped with those correlating with pRNFL and GCIPL. CONCLUSIONS: In PwMS, pRNFL and GCIPL reflect the integrity of clinically-relevant gray matter structures, underling the value of OCT measures as markers of neurodegeneration and disability in multiple sclerosis.
 Conflicting results on melatonin synthesis in multiple sclerosis (MS) have been reported due to variabilities in patient lifestyles, which are not considered when supplementing melatonin. Since melatonin acts through its receptors, we identified melatonin receptors in oligodendrocytes (OLs) in the corpus callosum, where demyelination occurs; the subventricular zone, where neural stem/progenitor cells (NSPCs) are located; and the choroid plexus, which functions as a blood-cerebrospinal fluid barrier. Moreover, using chimeric mice, resident macrophages were found to express melatonin receptors, whereas bone marrow-derived macrophages lost this expression in the demyelinated brain. Next, we showed that cuprizone-fed mice, which is an MS model, tended to have increased melatonin levels. While we used different approaches to alter the circadian rhythm of melatonin and cortisol, only the constant light approach increased NSPC proliferation and differentiation to oligodendrocyte precursor cells (OPCs), OPCs maturation to OLs and recruitment to the site of demyelination, the number of patrolling monocytes, and phagocytosis. In contrast, constant darkness and exogenous melatonin exacerbated these events and amplified monocyte infiltration. Therefore, melatonin should not be considered a universal remedy, as is currently claimed. Our data emphasize the importance of monitoring melatonin/cortisol oscillations in each MS patient by considering diet and lifestyle to avoid melatonin overdose.
 Multiple sclerosis (MS) is a complex disease of the CNS thought to require an environmental trigger. Gut dysbiosis is common in MS, but specific causative species are unknown. To address this knowledge gap, we used sensitive and quantitative PCR detection to show that people with MS were more likely to harbor and show a greater abundance of epsilon toxin-producing (ETX-producing) strains of C. perfringens within their gut microbiomes compared with individuals who are healthy controls (HCs). Isolates derived from patients with MS produced functional ETX and had a genetic architecture typical of highly conjugative plasmids. In the active immunization model of experimental autoimmune encephalomyelitis (EAE), where pertussis toxin (PTX) is used to overcome CNS immune privilege, ETX can substitute for PTX. In contrast to PTX-induced EAE, where inflammatory demyelination is largely restricted to the spinal cord, ETX-induced EAE caused demyelination in the corpus callosum, thalamus, cerebellum, brainstem, and spinal cord, more akin to the neuroanatomical lesion distribution seen in MS. CNS endothelial cell transcriptional profiles revealed ETX-induced genes that are known to play a role in overcoming CNS immune privilege. Together, these findings suggest that ETX-producing C. perfringens strains are biologically plausible pathogens in MS that trigger inflammatory demyelination in the context of circulating myelin autoreactive lymphocytes.
 Multiple sclerosis (MS) is a multifactorial, immune-mediated disease caused by complex gene-environment interactions. Dietary factors modulating the inflammatory status through the control of the metabolic and inflammatory pathways and the composition of commensal gut microbiota, are among the main environmental factors involved in the pathogenesis of MS. There is no etiological therapy for MS and the drugs currently used, often accompanied by major side effects, are represented by immunomodulatory substances capable of modifying the course of the disease. For this reason, nowadays, more attention is paid to alternative therapies with natural substances with anti-inflammatory and antioxidant effects, as adjuvants of classical therapies. Among natural substances with beneficial effects on human health, polyphenols are assuming an increasing interest due to their powerful antioxidant, anti-inflammatory, and neuroprotective effects. Beneficial properties of polyphenols on the CNS are achieved through direct effects depending on their ability to cross the blood-brain barrier and indirect effects exerted in part via interaction with the microbiota. The aim of this review is to examine the literature about the molecular mechanism underlying the protective effects of polyphenols in MS achieved by experiments conducted in vitro and in animal models of the disease. Significant data have been accumulated for resveratrol, curcumin, luteolin, quercetin, and hydroxytyrosol, and therefore we will focus on the results obtained with these polyphenols. Clinical evidence for the use of polyphenols as adjuvant therapy in MS is restricted to a smaller number of substances, mainly curcumin and epigallocatechin gallate. In the last part of the review, a clinical trial studying the effects of these polyphenols in MS patients will also be revised.

 The nature and unpredictable prognosis of multiple sclerosis (MS) make pregnancy and motherhood challenging experiences for women with the disease. Using the thematic synthesis method, we aimed to systematically interpret and synthesize data from qualitative research examining the motherhood experiences of women with MS. The analyses revealed three analytical themes: "Deciding to become a mother," "The journey during pregnancy, childbirth, and the postpartum period," and "Surviving as a mother with multiple sclerosis." For women with MS, being a mother, pregnancy, and the postpartum period were complex and challenging issues. During this period, most women felt lonely, thought that they were contradictory and inadequately informed by healthcare professionals and that they could not get enough social support. Despite all the difficulties, being a mother was a source of motivation for them. This meta-synthesis study provides healthcare professionals with an in-depth understanding of the experiences of women with MS with pregnancy, childbirth, postpartum period, and motherhood from their perspectives.
 MRI plays a central role in the diagnosis of multiple sclerosis (MS) and in the monitoring of disease course and treatment response. Advanced MRI techniques have shed light on MS biology and facilitated the search for neuroimaging markers that may be applicable in clinical practice. MRI has led to improvements in the accuracy of MS diagnosis and a deeper understanding of disease progression. This has also resulted in a plethora of potential MRI markers, the importance and validity of which remain to be proven. Here, five recent emerging perspectives arising from the use of MRI in MS, from pathophysiology to clinical application, will be discussed. These are the feasibility of noninvasive MRI-based approaches to measure glymphatic function and its impairment; T1-weighted to T2-weighted intensity ratio to quantify myelin content; classification of MS phenotypes based on their MRI features rather than on their clinical features; clinical relevance of gray matter atrophy versus white matter atrophy; and time-varying versus static resting-state functional connectivity in evaluating brain functional organization. These topics are critically discussed, which may guide future applications in the field.
 BACKGROUND: Paramagnetic rim lesions (PRLs) are chronic active lesions associated with a more severe disease course in multiple sclerosis (MS). Retinal layer thinning measured by optical coherence tomography (OCT) is a biomarker of neuroaxonal damage associated with disability progression in MS. OBJECTIVE: We aimed to determine a potential association between OCT parameters (peripapillary retinal nerve fiber layer (pRNFL) ganglion cell-inner plexiform layer (GCIPL), inner nuclear layer (INL) thickness), and PRLs in patients with MS (pwMS). METHODS: In this cross-sectional retrospective study, we included pwMS with both 3T brain MRI and an OCT scan. Regression models were calculated with OCT parameters (pRNFL, GCIPL, INL) as dependent variables, and the number of PRLs as an independent variable adjusted for covariates. RESULTS: We analyzed data from 107 pwMS (mean age 34.7 years (SD 10.9), 64.5% female, median disease duration 6 years (IQR 1-13), median EDSS 1.5 (range 0-6.5)). Higher number of PRLs was associated with lower pRNFL (β = -0.18; 95% CI -0.98, -0.03; p = 0.038) and GCIPL thickness (β = -0.21; 95% CI -0.58, -0.02; p = 0.039). CONCLUSION: The association between higher number of PRLs and lower pRNFL and GCIPL thicknesses provides additional evidence that pwMS with PRLs are affected by a more pronounced neurodegenerative process.
 BACKGROUND: Risk factors such as low vitamin D level has been implicated in the etiology of multiple sclerosis (MS) and may be relevant to myopia, such that there may be an association between myopia and MS. METHODS: Using linked Swedish national register data, we conducted a cohort study of men who were born in Sweden between 1950 and 1992, lived in Sweden between 1990 and 2018, and enrolled in military conscription assessment (n = 1,847,754). Myopia was defined based on the spherical equivalent refraction measured at conscription assessment, around age 18 years. Multiple sclerosis was identified using the Patient Register. Cox regression produced hazard ratios (HR) with 95% confidence intervals (95% CI), with adjustment for demographic and childhood socioeconomic characteristics and residential region. Due to changes in the assessment of refractive error, the analysis was stratified into two groups by the year of conscription assessment: 1969-1997 and 1997-2010. RESULTS: Among 1,559,859 individuals during a maximum of 48 years of follow-up from age 20 to 68 years (44,715,603 person-years), there were 3,134 MS events, and the incidence rate 7.0 (95% CI [6.8, 7.3] per 100,000 person-years). Among individuals with conscription assessments during 1997-2010, there were 380 MS events. There was no evidence of an association between myopia and MS, with HR 1.09 (95% CI 0.83, 1.43). Among individuals who underwent conscription assessment in 1969-1997, there were 2754 MS events. After adjusting for all covariates, there was no evidence of an association between myopia and MS (HR 0.99 [95% CI 0.91, 1.09]). CONCLUSION: Myopia in late adolescence is not associated with a subsequent raised risk of MS and thus there does not appear to be important shared risk factors.
 BACKGROUND AND PURPOSE: Conventional MRI measures of multiple sclerosis (MS) disease severity, such as lesion volume and brain atrophy, do not provide information about microstructural tissue changes, which may be driving physical and cognitive progression. Myelin damage in normal-appearing white matter (NAWM) is likely an important contributor to MS disability. Myelin water fraction (MWF) provides quantitative measurements of myelin. Mean MWF reflects average myelin content, while MWF standard deviation (SD) describes variation in myelin within regions. The myelin heterogeneity index (MHI = SD/mean MWF) is a composite metric of myelin content and myelin variability. We investigated how mean MWF, SD, and MHI compare in differentiating MS from controls and their associations with physical and cognitive disability. METHODS: Myelin water imaging data were acquired from 91 MS participants and 31 healthy controls (HC). Segmented whole-brain NAWM and corpus callosum (CC) NAWM, mean MWF, SD, and MHI were compared between groups. Associations of mean MWF, SD, and MHI with Expanded Disability Status Scale and Symbol Digit Modalities Test were assessed. RESULTS: NAWM and CC MHI had the highest area under the curve: .78 (95% confidence interval [CI]: .69, .86) and .84 (95% CI: .76, .91), respectively, distinguishing MS from HC. CONCLUSIONS: Mean MWF, SD, and MHI provide complementary information when assessing regional and global NAWM abnormalities in MS and associations with clinical outcome measures. Examining all three metrics (mean MWF, SD, and MHI) enables a more detailed interpretation of results, depending on whether regions of interest include areas that are more heterogeneous, earlier in the demyelination process, or uniformly injured.
 Dealing with patients with both multiple sclerosis (MS) and inflammatory rheumatic disorders (IRDs) is not uncommon for a rheumatologist, as there is a statistical association between SpA and MS. As several CNS demyelinating events have been reported in patients treated with TNF inhibitor (TNFi), the pre-existing demyelinating disease was considered a contraindication for TNFi. However, this contraindication is mainly based on a randomized controlled trial in MS and not on large epidemiological studies. According to the last epidemiological studies, TNFi might not be an inducer of MS. Moreover, there are no clear recommendations on the use of the other DMARDs in patients suffering from an IRD and MS. In this review, we summarize the link between MS and IRDs and the impact of DMARDs on MS, especially TNFi. We also look at the impact of disease-modifying drugs for adults with MS and IRDs.
 Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are often accompanied by optic neuritis associated with neurofilament disruption. In this study, the stiffness of the optic nerve was investigated by atomic force microscopy (AFM) in mice with induced EAE in the successive phases of the disease: onset, peak, and chronic. AFM results were compared with the intensity of the main pathological processes in the optic nerve: inflammation, demyelination, and axonal loss, as well as with the density of astrocytes, assessed by quantitative histology and immunohistochemistry. Optic nerve tissue and serum levels of neurofilament light chain protein (NEFL) were also examined by immunostaining and ELISA, respectively. The stiffness of the optic nerve in EAE mice was lower than that in control and naïve animals. It increased in the onset and peak phases and sharply decreased in the chronic phase. Serum NEFL level showed similar dynamics, while tissue NEFL level decreased in the onset and peak phases, indicating a leak of NEFL from the optic nerve to body fluids. Inflammation and demyelination gradually increased to reach the maximum in the peak phase of EAE, and inflammation slightly declined in the chronic phase, while demyelination did not. The axonal loss also gradually increased and had the highest level in the chronic phase. Among these processes, demyelination and especially axonal loss most effectively decrease the stiffness of the optic nerve. NEFL level in serum can be regarded as an early indicator of EAE, as it rapidly grows in the onset phase of the disease.
 PURPOSE: To translate Preference-Based Multiple Sclerosis Index (PBMSI) into Turkish, investigate its psychometric properties and differences between its two scoring algorithms: PBMSI-Rating Scale (PBMSI-RS) and PBMSI-Standard Gamble (PBMSI-SG). METHODS: An expert committee supervised the translation process. Psychometric properties were evaluated in 104 people with multiple sclerosis. Exploratory common factor analysis was used to investigate structural validity. Convergent validity was assessed by formulating hypotheses about correlations between PBMSI and other HRQL measures, disability level, walking-related measures, and MS symptoms. Known-groups validity was assessed against different measures of disability and walking capacity. Test-retest reliability was assessed by calculating the intraclass correlation coefficient (ICC), standard error of measurement (SEM), and minimal detectable change (MDC95%). RESULTS: Factor analysis revealed one factor (Eigenvalue = 2.46). PBMSI-RS and PBMSI-SG correlated significantly with other measures (p < .001). Both could differentiate between individuals with different levels of disability and walking capacity (p < .05, d  ≥  0.50). Relative test-retest reliability was moderate for PBMSI-RS (ICC = 0.75) and good for PBMSI-SG (ICC = 0.83). SEM and MDC95% values were 0.16 and 0.44 for PBMSI-RS and 0.10 and 0.28 for PBMSI-SG, respectively. CONCLUSION: Turkish version of PBMSI has good psychometric properties to assess health-related quality of life in people with multiple sclerosis. PBMSI-SG should be preferred over PBMSI-RS.IMPLICATIONS FOR REHABILITATIONHealth-related quality of life is often used as a primary or secondary endpoint in multiple sclerosis research.The Preference-Based Multiple Sclerosis Index is the first preference-based health-related quality of life measure developed in multiple sclerosis using patient preferences.Preference-Based Multiple Sclerosis Index was translated to Turkish and demonstrated good psychometric properties, including structural, convergent, known-groups validity, internal consistency, and test-retest reliability.Professionals working in the field of multiple sclerosis research and rehabilitation may benefit from using the Preference-Based Multiple Sclerosis Index as it is a short and psychometrically robust instrument.
 The immune system plays a significant role in multiple sclerosis. While MS was historically thought to be T cell-mediated, multiple pieces of evidence now support the view that B cells are essential players in multiple sclerosis pathogenic processes. High-efficacy disease-modifying therapies that target the immune system have emerged over the past two decades. Anti-CD20 monoclonal antibodies selectively deplete CD20+ B and CD20+ T cells and efficiently suppress inflammatory disease activity. These monotherapies prevent relapses, reduce new or active magnetic resonance imaging brain lesions, and lessen disability progression in patients with relapsing multiple sclerosis. Rituximab, ocrelizumab, and ofatumumab are currently used in clinical practice, while phase III clinical trials for ublituximab have been recently completed. In this review, we compare the four anti-CD20 antibodies in terms of their mechanisms of action, routes of administration, immunological targets, and pharmacokinetic properties. A deeper understanding of the individual properties of these molecules in relation to their efficacy and safety profiles is critical for their use in clinical practice.
 BACKGROUND: Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating, degenerative disease of the central nervous system that affects approximately 2.8 million people worldwide. Compelling evidence from observational studies and clinical trials indicates a strong association between brain volume loss (BVL) and the accumulation of disability in MS. However, the considerable heterogeneity in study designs and methods of assessment of BVL invites questions concerning the generalizability of the reported findings. Therefore, we conducted this systematic review to characterize the relationship between BVL and physical disability in patients with MS. METHODS: A systematic literature search of MEDLINE and EMBASE databases was performed supplemented by gray literature searches. The following study designs were included: prospective/retrospective cohort, cross-sectional and case-control. Only English language articles published from 2010 onwards were eligible for final inclusion. There were no restrictions on MS subtype, age, or ethnicity. Of the 1620 citations retrieved by the structured searches, 50 publications met our screening criteria and were included in the final data set. RESULTS: Across all BVL measures, there was considerable heterogeneity in studies regarding the underlying study population, the definitions of BVL and image analysis methodologies, the physical disability measure used, the measures of association reported and whether the analysis conducted was univariable or multivariable. A total of 36 primary studies providing data on the association between whole BVL and physical disability in MS collectively suggest that whole brain atrophy is associated with greater physical disability progression in MS patients. Similarly, a total of 15 primary studies providing data on the association between ventricular atrophy and physical disability in MS suggest that ventricular atrophy is associated with greater physical disability progression in MS patients. Along similar lines, the existing evidence based on a total of 13 primary studies suggests that gray matter atrophy is associated with greater physical disability progression in MS patients. Four primary studies suggest that corpus callosum atrophy is associated with greater physical disability progression in MS patients. The majority of the existing evidence (6 primary studies) suggests no association between white matter atrophy and physical disability in MS. It is difficult to assign a relationship between basal ganglia volume loss and physical disability as well as medulla oblongata width and physical disability in MS due to very limited data. CONCLUSION: The evidence gathered from this systematic review, although very heterogeneous, suggests that whole brain atrophy is associated with greater physical disability progression in MS patients. Our review can help define future imaging biomarkers for physical disability progression and treatment monitoring in MS.
 OBJECTIVES: Natalizumab (NTZ), a monoclonal antibody against very late antigen-4 (VLA-4), is one of the most efficient therapies to prevent acute relapses in multiple sclerosis (MS). VLA-4 is the key adhesion molecule for peripheral immune cells, especially lymphocytes to enter the CNS. While its blockade thus virtually abrogates CNS infiltration of these cells, long-term exposure to natalizumab may also affect immune cell function. METHODS: In this study, we report that in patients with MS, NTZ treatment is associated with an enhanced activation status of peripheral monocytes. RESULTS: Expression of 2 independent activation markers, CD69 and CD150, was significantly higher on blood monocytes from NTZ-treated patients when compared with those from matched untreated patients with MS, while other properties such as cytokine production remained unchanged. DISCUSSION: These findings consolidate the concept that peripheral immune cells remain fully competent on NTZ treatment, an excellent asset rare among MS treatments. However, they also suggest that NTZ may exert nondesirable effects on the progressive aspect of MS, where myeloid cells and their chronic activation are attributed a prominent pathophysiologic role.
 IMPORTANCE: Racial, ethnic, and geographic differences in multiple sclerosis (MS) are important factors to assess when determining the disease burden and allocating health care resources. OBJECTIVE: To calculate the US prevalence of MS in Hispanic, non-Hispanic Black (hereafter referred to as Black), and non-Hispanic White individuals (hereafter referred to as White) stratified by age, sex, and region. DESIGN, SETTING, AND PARTICIPANTS: A validated algorithm was applied to private, military, and public (Medicaid and Medicare) administrative health claims data sets to identify adult cases of MS between 2008 and 2010. Data analysis took place between 2019 and 2022. The 3-year cumulative prevalence overall was determined in each data set and stratified by age, sex, race, ethnicity, and geography. The insurance pools included 96 million persons from 2008 to 2010. Insurance and stratum-specific estimates were applied to the 2010 US Census data and the findings combined to calculate the 2010 prevalence of MS cumulated over 10 years. No exclusions were made if a person met the algorithm criteria. MAIN OUTCOMES AND MEASUREMENTS: Prevalence of MS per 100 000 US adults stratified by demographic group and geography. The 95% CIs were approximated using a binomial distribution. RESULTS: A total of 744 781 persons 18 years and older were identified with MS with 564 426 cases (76%) in females and 180 355 (24%) in males. The median age group was 45 to 54 years, which included 229 216 individuals (31%), with 101 271 aged 18 to 24 years (14%), 158 997 aged 35 to 44 years (21%), 186 758 aged 55 to 64 years (25%), and 68 539 individuals (9%) who were 65 years or older. White individuals were the largest group, comprising 577 725 cases (77%), with 80 276 Black individuals (10%), 53 456 Hispanic individuals (7%), and 33 324 individuals (4%) in the non-Hispanic other category. The estimated 2010 prevalence of MS per 100 000 US adults cumulated over 10 years was 161.2 (95% CI, 159.8-162.5) for Hispanic individuals (regardless of race), 298.4 (95% CI, 296.4-300.5) for Black individuals, 374.8 (95% CI, 373.8-375.8) for White individuals, and 197.7 (95% CI, 195.6-199.9) for individuals from non-Hispanic other racial and ethnic groups. During the same time period, the female to male ratio was 2.9 overall. Age stratification in each of the racial and ethnic groups revealed the highest prevalence of MS in the 45- to 64-year-old age group, regardless of racial and ethnic classification. With each degree of latitude, MS prevalence increased by 16.3 cases per 100 000 (95% CI, 12.7-19.8; P < .001) in the unadjusted prevalence estimates, and 11.7 cases per 100 000 (95% CI, 7.4-16.1; P < .001) in the direct adjusted estimates. The association of latitude with prevalence was strongest in women, Black individuals, and older individuals. CONCLUSIONS AND RELEVANCE: This study found that White individuals had the highest MS prevalence followed by Black individuals, individuals from other non-Hispanic racial and ethnic groups, and Hispanic individuals. Inconsistent racial and ethnic classifications created heterogeneity within groups. In the United States, MS affects diverse racial and ethnic groups. Prevalence of MS increases significantly and nonuniformly with latitude in the United States, even when adjusted for race, ethnicity, age, and sex. These findings are important for clinicians, researchers, and policy makers.
 BACKGROUND: Whether genetic factors influence the long-term course of multiple sclerosis (MS) is unresolved. OBJECTIVE: To determine the influence of HLA-DRB1*1501 on long-term disease course in a homogeneous cohort of clinically isolated syndrome (CIS) patients. METHODS: One hundred seven patients underwent clinical and MRI assessment at the time of CIS and after 1, 3, 5 and 15 years. HLA-DRB1*1501 status was determined using Sanger sequencing and tagging of the rs3135388 polymorphism. Linear/Poisson mixed-effects models were used to investigate rates of change in EDSS and MRI measures based on HLA-DRB1*1501 status. RESULTS: HLA-DRB1*1501 -positive (n = 52) patients showed a faster rate of disability worsening compared with the HLA-DRB1*1501 -negative (n = 55) patients (annualised change in EDSS 0.14/year vs. 0.08/year, p < 0.025), and a greater annualised change in T2 lesion volume (adjusted difference 0.45 mL/year, p < 0.025), a higher number of gadolinium-enhancing lesions, and a faster rate of brain (adjusted difference -0.12%/year, p < 0.05) and spinal cord atrophy (adjusted difference -0.22 mm(2)/year, p < 0.05). INTERPRETATION: These findings provide evidence that the HLA-DRB1*1501 allele plays a role in MS severity, as measured by long-term disability worsening and a greater extent of inflammatory disease activity and tissue loss. HLA-DRB1*1501 may provide useful information when considering prognosis and treatment decisions in early relapse-onset MS.
 STUDY OBJECTIVE: This study compared the adherence trajectories of fingolimod (FIN), teriflunomide (TER), and dimethyl fumarate (DMF) users with multiple sclerosis (MS) as there is limited evidence regarding the comparative adherence patterns of different oral disease-modifying agents (DMAs). DESIGN: A retrospective cohort study DATA SOURCE: 2015-2019 IBM MarketScan Commercial Claims Database. PATIENTS: Adults (≥18 years) with MS (International Classification of Diseases [ICD]-9/10-Clinical Modification [CM]:340/G35) diagnosis and ≥1 DMA prescription. INTERVENTION: Incident FIN-, TER-, or DMF use based on the index DMA with 1 year of washout period. MEASUREMENTS: The DMA adherence trajectories based on the proportion of days covered (PDC) were examined using the Group-Based Trajectory Modeling (GBTM) one year after the treatment initiation. Generalized boosting models (GBM)-based inverse probability treatment weights (IPTW) were incorporated in multinomial logistic regression to assess the comparative adherence trajectories across oral DMAs with FIN group as a reference category. MEASUREMENTS AND MAIN RESULTS: The study cohort consisted of 1913 patients with MS who were initiated with FIN (24.2%, n = 462), TER (24.0%, n = 458), and DMF (51.9%, n = 993) during 2016-2018. The adherence rate (PDC ≥ 0.8) among FIN, TER, and DMF users was found to be 70.8% (n = 327), 59.6% (n = 273), and 61.0% (n = 606), respectively. The GBTM grouped patients into three adherence trajectories: Complete Adherers-59.1%, Slow Decliners-22.6%, and Rapid Discontinuers-18.3%. The multinomial logistic regression model involving GBM-based IPTW revealed that DMF (adjusted odds ratio [aOR]: 2.32, 95% confidence interval [CI]:1.57-3.42) and TER (aOR: 2.50, 95% CI: 1.62-3.88) users had higher odds to be rapid discontinuers relative to FIN users. In addition, TER users were more likely (aOR: 1.50, 95% CI: 1.06-2.13) to be slow decliners compared with FIN users. CONCLUSION: Teriflunomide and DMF were associated with poorer adherence trajectories than FIN. More research is needed to evaluate the clinical implications of these adherence trajectories of oral DMAs to optimize the management of MS.
 OBJECTIVE: This study was undertaken to describe the safety, tolerability, pharmacokinetics, and immunogenicity of elezanumab (ABT-555), a fully human monoclonal antibody (mAb) directed against repulsive guidance molecule A (RGMa), in healthy and multiple sclerosis (MS) study participants. METHODS: The single-center, first-in-human, single ascending dose (SAD) study evaluated elezanumab (50-1,600mg intravenous [IV] and 150mg subcutaneous) in 47 healthy men and women. The multicenter multiple ascending dose (MAD; NCT02601885) study evaluated elezanumab (150mg, 600mg, and 1,800mg) in 20 adult men and women with MS, receiving either maintenance or no immunomodulatory treatment. RESULTS: No pattern of study drug-related adverse events was identified for either the SAD or MAD elezanumab regimens. Across both studies, the T(max) occurred within 4 hours of elezanumab IV infusion, and the harmonic mean of t(1/2) ranged between 18.6 and 67.7 days. Following multiple dosing, elezanumab C(max) , area under the curve, and C(trough) increased dose-proportionally and resulted in dose-dependent increases in elezanumab cerebrospinal fluid (CSF) concentrations. Elezanumab CSF penetration was 0.1% to 0.4% across both studies, with CSF levels of free RGMa decreased by >40%. Changes in CSF interleukin-10 (IL-10) and free RGMa demonstrated dose/exposure-dependence. INTERPRETATION: The elezanumab pharmacokinetic profile supports monthly, or bimonthly, administration of up to 1,800mg with the option of a loading dose of 3,600mg. Elezanumab partitioning into CSF is within the range expected for mAbs. Reduced CSF levels of free RGMa demonstrate central nervous system target binding of elezanumab with an apparent maximal effect at 1,800mg IV. Exposure-associated increases in CSF IL-10, an anti-inflammatory cytokine with neuroprotective/neurorestorative properties, support potential pathway modulation in MS participants. ANN NEUROL 2023;93:285-296.
 BACKGROUND: Several MRI findings of optic neuritis (ON) have been described and correlated with specific underlying etiologies. Specifically, optic nerve enhancement is considered an accurate biomarker of acute ON. OBJECTIVE: To identify differences in MRI patterns of optic nerve enhancement in certain demyelinating etiologies presenting with acute ON. METHODS: Retrospective analysis of enhancement patterns on fat-suppressed T1-weighted images from patients presenting clinical and radiological acute ON, treated at our institution between January 2014 and June 2022. Location and extension of enhancing optic nerve segments, as well as presence of perineural enhancement were evaluated in three predetermined demyelinating conditions. Fisher's exact test and chi(2) were calculated. RESULTS: Fifty-six subjects met eligibility criteria. Mean age was 31 years (range 6-79) and 70% were females. Thirty-four (61%) patients were diagnosed with multiple sclerosis (MS), 8 (14%) with neuromyelitis optica (NMO), and 14 (25%) with anti-myelin oligodendrocyte glycoprotein disease (MOGAD). Bilateral involvement was more frequent in MOGAD, compared to MS and NMO (43 vs 3% and 12.5% respectively, p = 0.002). MS patients showed shorter optic nerve involvement, whereas MOGAD showed more extensive lesions (p = 0.006). Site of involvement was intraorbital in 63% MS, 89% NMO, 90% MOGAD (p = 0.051) and canalicular in 43% MS, 33% NMO and 75% MOGAD (p = 0.039). Intracranial or chiasmatic involvement and presence of perineural enhancement were not statistically different between entities. CONCLUSION: In the setting of acute ON, patients presenting MOGAD were more likely to show bilateral, longitudinally extended and anterior (intraorbital and canalicular) optic nerve involvement compared to patients with MS or NMO.
 THE AIM: To investigate the role of Sirtuin 1 (SIRT1) level and SIRT1 (rs3818292, rs3758391, rs7895833) gene polymorphisms in patients with optic neuritis (ON) and multiple sclerosis (MS). METHODS: 79 patients with ON and 225 healthy subjects were included in the study. ON patients were divided into 2 subgroups: patients with MS (n = 30) and patients without MS (n = 43). 6 ON patients did not have sufficient data for MS diagnosis and were excluded from the subgroup analysis. DNA was extracted from peripheral blood leukocytes and genotyped by real-time polymerase chain reaction. Results were analysed using the program "IBM SPSS Statistics 27.0". RESULTS: We discovered that SIRT1 rs3758391 was associated with a twofold increased odds of developing ON under the codominant (p = 0.007), dominant (p = 0.011), and over-dominant (p = 0.008) models. Also, it was associated with a threefold increased odds ofON with MS development under the dominant (p = 0.010), twofold increased odds under the over-dominant (p = 0.032) models and a 1.2-fold increased odds of ON with MS development (p = 0.015) under the additive model. We also discovered that the SIRT1 rs7895833 was significantly associated with a 2.5-fold increased odds of ON development under the codominant (p = 0.001), dominant (p = 0.006), and over-dominant (p < 0.001) models, and a fourfold increased odds of ON with MS development under the codominant (p < 0.001), dominant (p = 0.001), over-dominant (p < 0.001) models and with a twofold increased odds of ON with MS development (p = 0.013) under the additive genetic model. There was no association between SIRT1 levels and ON with/without MS development. CONCLUSIONS: SIRT1 rs3758391 and rs7895833 polymorphisms are associated with ON and ON with MS development.
 BACKGROUND: Diagnosing multiple sclerosis (MS) can be a lengthy process, which can negatively affect psychological well-being, condition management, and future engagement with health services. Therefore, providing timely and appropriate emotional support may improve adjustment and health outcomes. PURPOSE: To develop a patient care pathway for providing emotional support around the point of diagnosing MS, and to explore potential barriers and facilitators to delivery and implementation. METHODS: Focus groups were conducted with 26 stakeholders, including 16 people living with MS, 5 carers/family members and 5 professionals working with people living with MS (3 MS nurses, 1 psychiatrist, and 1 charity staff member). Discussions were audio-recorded, transcribed verbatim and analyzed using framework analysis. RESULTS: Participants suggested that a patient care pathway should include comprehensive information provision as a part of emotional support at diagnosis, and follow-up sessions with a healthcare professional. Barriers including increasing staff workloads and financial costs to health services were acknowledged, thus participants suggested including peer support workers to deliver additional emotional support. All participants agreed that elements of a care pathway and embedded interventions should be individually tailored, yet provided within a standardized system to ensure accessibility. CONCLUSIONS: A patient care pathway was developed with stakeholders, which included an embedded MS Nurse support intervention supplemented with peer support sessions. Participants suggested that the pathway should be delivered within a standardized system to ensure equity of service provision across the country. PATIENT OR PUBLIC CONTRIBUTION: This research was conceptualized and designed collaboratively with Nottingham Multiple Sclerosis Patient and Public Involvement and Engagement (PPIE) group members. One member is a co-author and was actively involved in every key stage of the research process, including co-design of the pathway and research protocol, data collection (including presenting to participants and moderating group discussions), analysis and write-up. Authors consulted with PPIE members at two meetings (9 and 11 PPIE attendees per meeting) where they gave feedback on the research design, findings and the resulting pathway. People living with MS and carers of people with MS were included in the focus groups as participants.
 Current data emphasize the immunomodulating role of vitamin D in enhancing the anti-inflammatory response. Vitamin D deficiency is an established risk factor for developing multiple sclerosis-the autoimmune demyelinating and degenerative disease of the central nervous system. Several studies confirmed that higher vitamin D serum level is associated with better clinical and radiological outcomes in patients with multiple sclerosis, whereas vitamin D supplementation benefits in multiple sclerosis remain inconclusive. Despite that, many experts suggest regular measurements of vitamin D serum levels and supplementation in patients with multiple sclerosis. In this study, 133 patients with multiple sclerosis (relapsing-remitting subtype) were prospectively observed in a 0-, 12- and 24-month time span in a clinical setting. The study group consisted of 71.4% of patients (95 out of 133) supplementing vitamin D. The associations between vitamin D serum levels, clinical outcomes (disability status expressed by EDSS, number of relapses and time to relapse) and radiological outcomes (new T2-weighted lesions and number of gadolinium-enhanced lesions) were evaluated. There were no statistically significant correlations between clinical outcomes and vitamin D serum levels or supplementations. Fewer new T2-weighted lesions were observed in patients with vitamin D supplementations (p = 0.034) in 24 months of observation. Moreover, an optimal or higher level of vitamin D (>30 ng/mL) maintained throughout the entire observation period was associated with a lower number of new T2-weighted lesions in 24 months of observation (p = 0.045). These results support vitamin D implementation commencement and amelioration in patients with multiple sclerosis.

 BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) in which genetic and environmental factors contribute to disease progression. Both innate and adaptive immune cells, including T cells, B cells, activated macrophages and microglia, have been identified to be involved in the pathogenesis of MS, leading to the CNS inflammation, neurodegeneration and demyelination. In recent years, there has been considerable progress in understanding the contribution of tissue-resident immune cells in the pathogenesis of MS. METHODS: We performed a keyword-based search in PubMed database. We combined "multiple sclerosis" with keywords, such as tissue-resident memory T cells, microglia to search for relevant literatures in PubMed. RESULTS AND CONCLUSION: In this review, we comprehensively describe the characteristics of tissue-resident memory T cells and microglia, summarize their role in the pathogenesis of MS, and discuss their interaction with other immune cells in the CNS.
 Amplitude of low-frequency fluctuations (ALFF) is defined as changes of BOLD signal during resting state (RS) brain activity. Previous studies identified differences in RS activation between healthy and multiple sclerosis (MS) participants. However, no research has investigated the relationship between ALFF and learning in MS. We thus examine this here. Twenty-five MS and nineteen healthy participants performed a paired-associate word learning task where participants were presented with extrinsic or intrinsic performance feedback. Compared to healthy participants, MS participants showed higher local brain activation in the right thalamus. We also observed a positive correlation in the MS group between ALFF and extrinsic feedback within the left inferior frontal gyrus, and within the left superior temporal gyrus in association with intrinsic feedback. Healthy participants showed a positive correlation in the right fusiform gyrus between ALFF and extrinsic feedback. Findings suggest that while MS participants do not show a feedback learning impairment compared to the healthy participants, ALFF differences might suggest a general maladaptive pattern of task unrelated thalamic activation and adaptive activation in frontal and temporal regions. Results indicate that ALFF can be successfully used at capturing pathophysiological changes in local brain activation in MS in association with learning through feedback.
 OCS-05 (aka BN201) is a peptidomimetic that binds to serum glucocorticoid kinase-2 (SGK2), displaying neuroprotective activity. The objective of this randomized, double-blind 2-part study was to test safety and pharmacokinetics of OCS-05 administered by intravenous (i.v.) infusion in healthy volunteers. Subjects (n = 48) were assigned to receive placebo (n = 12) or OCS-05 (n = 36). , Doses tested were 0.05, 0.2, 0.4, 0.8, 1.6, 2.4 and 3.2 mg/kg in the single ascending dose (SAD) part. In the multiple ascending dose (MAD) part, 2.4 and 3.0 mg/kg doses were administered with 2 h i.v. infusion for 5 consecutive days. Safety assessments included adverse events, blood tests, ECG, Holter monitoring, brain MRI and EEG. No serious adverse events were reported in the OCS-05 group (there was one serious adverse event in the placebo group). Adverse events reported in the MAD part were not clinically significant, and no changes on the ECG, EEG or brain MRI were observed. Single-dose (0.05-3.2 mg/kg) exposure (C(max) and AUC) increased in a dose-proportional manner. Steady state was reached by Day 4 and no accumulation was observed. Elimination half-life ranged from 3.35 to 8.23 h (SAD) and 8.63 to 12.2 h (MAD). Mean individual C(max) concentrations in the MAD part were well below the safety thresholds. OCS-05 administered as 2-h i.v. infusions of multiple doses up to 3.0 mg/Kg daily for up to 5 consecutive days was safe and well tolerated. Based on this safety profile, OCS-05 is currently being tested in a phase 2 trial in patient with acute optic neuritis (NCT04762017, date registration 21/02/2021).
 We aimed to assess the long-term safety and effectiveness of ocrelizumab in a cohort of patients with multiple sclerosis (MS) at high risk of progressive multifocal leukoencephalopathy (PML), previously treated with natalizumab in extending interval dosing (EID), who switched to ocrelizumab and to compare them with patients who continued EID-natalizumab. Thirty MS patients previously treated with natalizumab in EID (every 8 weeks) were included in this observational retrospective cohort study. Among them, 17 patients were switched to ocrelizumab and 13 continued with EID-natalizumab. Except for the John Cunningham virus (JCV) index, no significant differences were detected between both groups. Main outcome measures included: annualized relapse rate (ARR), radiological activity, disability progression, and the NEDA-3 index. Patients were followed for 96 weeks. The median washout period in ocrelizumab-switchers was 6 weeks. Among them, AAR and radiological activity during follow-up were 0.03, without significant differences in comparison with the previous period on natalizumab-EID. The comparison between ocrelizumab-switchers and patients continuing on EID-natalizumab showed no significant differences in AAR, radiological activity, or disability progression. However, the proportion of patients maintaining a NEDA-3 status in week 96 was slightly superior among ocrelizumab-switchers (94 vs 69%). No serious adverse events were observed in any group. In conclusion, switching from EID-natalizumab to ocrelizumab can be considered as a therapeutic option, particularly in patients with MS at high risk of PML, to mitigate the risks of both PML and disease reactivation.
 We recently discovered that superparamagnetic iron oxide nanoparticles (SPIONs) can levitate plasma biomolecules in the magnetic levitation (MagLev) system and cause formation of ellipsoidal biomolecular bands. To better understand the composition of the levitated biomolecules in various bands, we comprehensively characterized them by multi-omics analyses. To probe whether the biomolecular composition of the levitated ellipsoidal bands correlates with the health of plasma donors, we used plasma from individuals who had various types of multiple sclerosis (MS), as a model disease with significant clinical importance. Our findings reveal that, while the composition of proteins does not show much variability, there are significant differences in the lipidome and metabolome profiles of each magnetically levitated ellipsoidal band. By comparing the lipidome and metabolome compositions of various plasma samples, we found that the levitated biomolecular ellipsoidal bands do contain information on the health status of the plasma donors. More specifically, we demonstrate that there are particular lipids and metabolites in various layers of each specific plasma pattern that significantly contribute to the discrimination of different MS subtypes, i.e., relapsing-remitting MS (RRMS), secondary-progressive MS (SPMS), and primary-progressive MS (PPMS). These findings will pave the way for utilization of MagLev of biomolecules in biomarker discovery for identification of diseases and discrimination of their subtypes.
 INTRODUCTION: Balance disorders are common in people with Multiple Sclerosis (PwMS) and, together with other impairments and disabilities, often prevent PwMS from performing their daily living activities. Besides clinical scales and performance tests, robotic platforms can provide more sensitive, specific, and objective monitoring. Validated technologies have been adopted as gold standard, but innovative robotic solutions would represent an opportunity to detect balance impairment in PwMS. AIM: Study's aim was to compare postural assessment of 46 PwMS with a relapsing-remitting form during static tasks performed with the novel robotic platform hunova® and the gold standard EquiTest®, METHODS: Pearson's r was run on Center of Pressure (COP)-related parameters and global static balance measures computed from hunova® and EquiTest® in eyes-open (EO) and eyes-closed (EC) conditions. In addition, agreeableness level toward the use of both devices was tested through numeric rating scale. RESULTS: Considering COP-related parameters, correlations were significant for all measures (p < .001). Interestingly, in EO, a strong correlation was shown for sway area (r = .770), while Medio-Lateral (ML) and Anterior-Posterior (AP) oscillation range, path length, ML and AP speed, ML and AP root mean square distance had a relatively strong association (.454 ≤ r ≤ .576). In EC, except for ML oscillation range showing a relatively strong correlation (r = .532), other parameters were strongly associated (.603 ≤ r ≤ .782). Correlations between global balance indexes of hunova® and EquiTest® revealed a relatively strong association between the Somatosensory Score in EquiTest® and the Somatosensory Index in hunova® (r = - .488). While in EO Static Balance Index from hunova® was highly correlated with Equilibrium score of EquiTest® (r = .416), Static Balance Index had a relatively strong association with both the Equilibrium (r = .482) and Strategy Score (r = .583) of EquiTest® in EC. Results from agreeableness rating scale revealed that hunova® was highly appreciated compared to EquiTest® (p = .044). CONCLUSIONS: hunova® represents an innovative adjunct to standard robotic balance evaluation for PwMS. This confirms that combining traditional and robotic assessments can more accurately detect balance impairments in MS.
 Ocrelizumab is an anti-CD20 monoclonal antibody used in the treatment of primary progressive and relapsing multiple sclerosis (MS). Although cases of organizing pneumonia have been reported in association with other antiCD20 agents such as rituximab, there is insufficient data in the literature on Ocrelizumab-associated lung involvement. Herein, we present a case of organizing pneumonia in a 37-year-old female patient with multiple sclerosis following Ocrelizumab use.
 Numerous studies relate the onset and severity of multiple sclerosis (MS) with viral infections. Herpes simplex virus type 1 (HSV-1), which is neurotropic and highly prevalent in the brain of healthy individuals, has been proposed to relate to MS. Here, we review and discuss the reported connections between HSV-1 and MS.
 Multiple sclerosis (MS) is a progressive neuro-inflammatory and neuro-autoimmune disease. Although hydrogen sulfide has recently shown potential therapeutic impacts in different neurological diseases, its effects on MS are still obscure. MiR-146a is considered a vital target for different therapeutic approaches in treating MS. The present study is directed to explore the therapeutic effects of NaHS (hydrogen sulfide donor) on cuprizone-induced MS and to explore whether NaHS can mediate its effects via regulating miR-146a expression. A total of 28 male C57Bl/6 mice were divided into 4 groups; control, cuprizone-intoxicated, NaHS control (100 μmol/kg/day, i.p), and NaHS-treated groups. Intriguingly, NaHS treatment managed to improve locomotor coordination and curb neuronal inflammation and demyelination as evidenced by hematoxylin & eosin, and Luxol fast blue staining and the increased myelin basic protein (MBP) content. Additionally, NaHS reduced interleukin-1 receptor-associated kinase-1 (IRAK-1), nuclear transcription factor kappa B (NF-κB), interleukin (IL)-17, and IL-1β brain levels along with downregulation of miR-146a expression compared with the untreated cuprizone-intoxicated group. Furthermore, NaHS-treated animals revealed much less oxidative stress compared to the untreated animals as evidenced by elevated glutathione and reduced malondialdehyde contents. Altogether, the current work reported that NaHS could improve motor dysfunction and reduce axonal demyelination, oxidative stress, as well as neuro-inflammation in mice with MS. Thus, using H(2)S-releasing compounds could be a promising approach in MS treatment strategies. The mechanism of these beneficial effects may involve the regulation of miR-146a/NF-κB/IL-1β axis.
 BACKGROUND: Shift work, which often results in sleep deprivation and circadian desynchrony, has been associated with increased risk of multiple sclerosis (MS). We aimed at studying the impact of sleep duration, circadian disruption and sleep quality on MS risk. METHODS: We used a Swedish population-based case-control study (2075 cases, 3164 controls). Aspects of sleep were associated with MS risk by calculating OR with 95% CIs using logistic regression models. RESULTS: Compared with sleeping 7-9 hours/night during adolescence, short sleep (<7 hours/night) was associated with increased risk of developing MS (OR 1.4, 95% OR 1.1-1.7). Similarly, subjective low sleep quality during adolescence increased the risk of subsequently developing MS (OR 1.5, 95% CI 1.3 to 1.9), whereas phase shift did not significantly influence the risk. Our findings remained similar when those who worked shifts were excluded. CONCLUSIONS: Insufficient sleep and low sleep quality during adolescence seem to increase the risk of subsequently developing MS. Sufficient restorative sleep at young age, needed for adequate immune functioning, may be a preventive factor against MS.
 AIM: To validate a French version of the Multiple Sclerosis Intimacy and Sexuality Questionnaire 15 which examines patients' perception of the effect of multiple sclerosis symptoms on their sexual activity. METHODS: After completing a translation/re-translation process to ensure linguistic and content validity, the Multiple Sclerosis Intimacy and Sexuality Questionnaire 15 French (MSISQ-15Fr) was completed by patients with multiple sclerosis. The validity of the construction, reliability, stability and reproducibility of the translation was evaluated. EXPLANATORY MIXED OBSERVATIONAL STUDY: Validation of a French assessment tool for sexual disorders (borrowed theoretical framework): the Multiple Sclerosis Intimacy and Sexuality Questionnaire 15 (MSISQ 15) RESULTS: The normed χ(2) was 1.21, the root mean square error of approximation was 0.046 [0.00; 0.07], the comparative fit index was 0.974, and the standardized root mean square was 0.065. The calculated Cronbach's coefficients indicated strong internal coherence, and the intraclass correlation coefficient was satisfactory at 0.9. Translations of the Multiple Sclerosis Intimacy and Sexuality Questionnaire 15 (MSISQ-15) have already been validated in five languages. This French version is valid, stable and reproducible. It provides French-speaking nurses an accessible and appropriate tool that will enable them to play an active role in the sexual health strategy recommended by the World Health Organization.
 BACKGROUND: Multiple sclerosis (MS) is a chronic debilitating disease characterized by inflammatory demyelination of the central nervous system. Grey matter (GM) lesions have been shown to be closely related to MS motor deficits and cognitive impairment. In this study, GM lesion-related genes for diagnosis and immune status in MS were investigated. METHODS: Gene Expression Omnibus (GEO) databases were utilized to analyze RNA-seq data for GM lesions in MS. Differentially expressed genes (DEGs) were identified. Weighted gene co-expression network analysis (WGCNA), least absolute shrinkage and selection operator (LASSO) algorithm and protein-protein interaction (PPI) network were used to screen related gene modules and candidate genes. The abundance of immune cell infiltration was analyzed by the CIBERSORT algorithm. Candidate genes with strong correlation with immune cell types were determined to be hub genes. A diagnosis model of nomogram was constructed based on the hub genes. Gene set enrichment analysis (GSEA) was performed to identify the biological functions of hub genes. Finally, an MS mouse model was induced to verify the expression levels of immune hub genes. RESULTS: Nine genes were identified by WGCNA, LASSO regression and PPI network. The infiltration of immune cells was significantly different between the MS and control groups. Four genes were identified as GM lesion-related hub genes. A reliable prediction model was established by nomogram and verified by calibration, decision curve analysis and receiver operating characteristic curves. GSEA indicated that the hub genes were mainly enriched in cell adhesion molecules, cytokine-cytokine receptor interaction and the JAK-STAT signaling pathway, etc. CONCLUSIONS: TLR9, CCL5, CXCL8 and PDGFRB were identified as potential biomarkers for GM injury in MS. The effectively predicted diagnosis model will provide guidance for therapeutic intervention of MS.
 BACKGROUND: To date, little is known about the prevalence of itch in multiple sclerosis (MS) and its characteristics. OBJECTIVES: In this cross-sectional study, we assessed the prevalence, intensity and characteristics of chronic pruritus in MS patients and its effect on quality-of-life and association with MS symptoms, clinical signs, comorbidities and MRI findings. METHODS: MS patients presenting to an outpatient neurology clinic were asked about their current symptoms. Those who experienced chronic pruritus were administered the Standardized Itch Questionnaire and Itch Quality of Life forms. All patients' medical records were reviewed. Patients with any medical conditions associated with chronic itch were excluded. RESULTS: Seventy-seven total MS patients were included, and 27 (35%) reported pruritus. The average itch NRS severity was 5.42 (range 0-10). The most affected body parts were the extremities, face or scalp, and trunk. Itch was characterized as acute (74%), paroxysmal (59%) and tingling (55%). Heat (52%) was the most common aggravating factor, while cold temperatures had no effect. Compared with MS patients without itch, itch patients reported more fatigue (77% vs 44%, p = 0.004), heat sensitivity (48% vs 20%, p = 0.0177), cognitive impairment (62% vs 26%, p = 0.0029) and depression or anxiety (48% vs 16%, p = 0.0063). Additionally, itch patients had more T2 hyperintensities in the posterior cervical cord and anterior pons/ventromedial medulla (74.1% vs 46.0%, p = 0.018 and 29.6% vs 8.0%, p = 0.020, respectively). Finally, T2 hyperintensities in the anterior pons/ventromedial medulla were strongly associated with itch localized to the face or scalp (OR 11.3, 95% CI 1.6-78.6, p = 0.025). CONCLUSION: MS patients experience paroxysmal neuropathic pruritus that is most frequently localized to the extremities, face or scalp. Patients with itch were more likely to have MS-related comorbidities and demyelinating lesions in the spinal cord or brainstem.
 Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases.
 Zinc (Zn(2+)) is the second most abundant necessary trace element in the human body, exerting a critical role in many physiological processes such as cellular proliferation, transcription, apoptosis, growth, immunity, and wound healing. It is an essential catalyst ion for many enzymes and transcription factors. The maintenance of Zn(2+) homeostasis is essential for the central nervous system, in which Zn(2+) is abundantly distributed and accumulates in presynaptic vesicles. Synaptic Zn(2+) is necessary for neural transmission, playing a pivotal role in neurogenesis, cognition, memory, and learning. Emerging data suggest that disruption of Zn(2+) homeostasis is associated with several central nervous system disorders including Alzheimer's disease, depression, Parkinson's disease, multiple sclerosis, schizophrenia, epilepsy, and traumatic brain injury. Here, we reviewed the correlation between Zn(2+) and these central nervous system disorders. The potential mechanisms were also included. We hope that this review can provide new clues for the prevention and treatment of nervous system disorders.
 BACKGROUND: Multiple sclerosis (MS) is the most common nontraumatic debilitating disease in young adults. This study aimed to determine the effect of distance empowerment programs on self-efficacy in MS patients. METHODS: Sixty-four MS patients participated in this quasi-experimental study. Patients were first entered into the study using the convenience sampling method and then were randomly allocated to control (32) and intervention (32) groups. The intervention group underwent a distance empowerment program (via WhatsApp, Telegram, and blog) and weekly telephone follow-up for 2 months. Self-efficacy was evaluated before, and immediately after, the empowerment program using the MS Self-Efficacy Scale. RESULTS : Data from 59 participants were analyzed. Before implementation of the empowerment program, the mean scores of self-efficacy in the intervention and control groups were not significantly different. After implementing the empowerment program, the mean score of self-efficacy in the intervention group was higher than that of the control group ( P < .05). CONCLUSION : Distance empowerment has an effect on the self-efficacy of patients with MS and may lead to an increase in self-efficacy scores after implementing an empowerment program.
 BACKGROUND: People living with multiple sclerosis (plwMS) seek access to information on evidence-based lifestyle-related risk factors associated with multiple sclerosis (MS). As the internet has made delivery of lifestyle information increasingly accessible and cost-effective, we designed the Multiple Sclerosis Online Course (MSOC) to deliver a multimodal lifestyle modification program for plwMS. Two MS online courses were developed: the intervention course based on lifestyle recommendations of the Overcoming Multiple Sclerosis (OMS) program and the standard-care course representing standard lifestyle recommendations from other MS websites. We examined for feasibility in a pilot randomised controlled trial (RCT), where satisfactory completion and accessibility were achieved across both study arms. From this success, a protocol for a larger RCT was developed to examine the effectiveness of MSOC in improving health-related quality of life (HRQoL) and other health outcomes in plwMS. METHODS/DESIGN: This single-blinded RCT will recruit n = 1,054 plwMS. Participants in the intervention arm will receive access to a MSOC with seven modules providing evidence-based information on the OMS program. Participants in the control group will receive access to a MSOC of identical format, with seven modules providing general MS-related information and lifestyle recommendations sourced from popular MS websites, e.g. MS societies. Participants will complete questionnaires at baseline and at 6, 12, and 30 months after course completion. The primary endpoint is HRQoL, as measured by MSQOL-54 (both physical and mental health domains) at 12 months following course completion. Secondary outcomes are changes to depression, anxiety, fatigue, disability, and self-efficacy as measured by Hospital Anxiety and Depression Scale, Patient-Determined Disease Steps and University of Washington Self-Efficacy Scale, respectively, assessed at each timepoint. Further assessments will include quantitative post-course evaluation, adoption and maintenance of behaviour change from follow-up survey data, and qualitative analysis of participants' outcomes and reasons for course completion or non-completion. DISCUSSION: This RCT aims to determine whether an online intervention course delivering evidence-based lifestyle modification recommendations based on the Overcoming Multiple Sclerosis program to plwMS is more effective at improving HRQoL, and other health outcomes post-intervention, compared with an online standard-care course. TRIAL REGISTRATION: This trial was registered prospectively with the Australian New Zealand Clinical Trials Registry, www.anzctr.org.au , identifier ACTRN12621001605886. DATE OF REGISTRATION: 25 November 2021.
 This study examined levels of depression and anxiety symptoms (Hospital Anxiety and Depression Scale scores), and self-reported (Godin Leisure-Time Exercise Questionnaire), and accelerometer-measured physical activity in older adults with multiple sclerosis (n = 40) compared with age- and sex-matched healthy controls (n = 40). We observed differences in depression, anxiety, and physical activity between groups and further observed that minutes/day of moderate to vigorous physical activity partially accounted for group differences in depression scores. We provide preliminary support for research examining approaches for increasing moderate to vigorous physical activity and possibly reducing depression symptoms in older adults with multiple sclerosis.
 BACKGROUND: Multiple sclerosis is an inflammatory, autoimmune, and progressive neurodegenerative disease of the central nervous system with an unknown etiology. Based on the gender differences in epidemiological, clinical, and pathological features of multiple sclerosis, the role of sex hormones and their receptors in this disease has been considered. A single nucleotide polymorphism located in the exon 4 of progesterone receptor, rs1042838 (G/T -Val660Leu), was associated with reduced progesterone receptor activity. We aimed to investigate the association of this polymorphism with the risk of multiple sclerosis. METHOD: A total of 426 individuals were included in the present study, including 200 patients and 226 age and sex adjusted healthy controls in Iranian population. The target SNP was genotyped using PCR-RFLP, and statistical analysis was performed using SPSS 21.0 and by ꭓ2 and logistic regression tests. RESULTS: The results showed that the allele T acts as a risk allele, so that the genotypes TG and TT significantly increase RRMS susceptibility compared to the genotype GG. CONCLUSION: Our data suggest that Val660Leu polymorphism might be a risk factor for the development of RRMS.
 Shared decision making is a way of incorporating patients' preferences and values into the decisions regarding the treatment and follow-up plan for the condition that affects them. It is currently applied mainly in the context of chronic disorders for which there is no cure available but nevertheless many therapeutic alternatives, such as multiple sclerosis (MS). Current views and opinions on shared decision making for the treatment of MS are discussed in this consensus based on a modified Delphi method that included a group of neurologists from Argentina. A set of statements was defined by the experts and seeks to serve as a guide to apply this concept in clinical practice.

 Despite exosome promise as endogenous drug delivery vehicles, the current understanding of exosome may be insufficient to develop their various applications. Here we synthesized five sialic acid analogues with different length N-acyl side chains and screened out the optimal metabolic precursor for exosome labeling via bio-orthogonal click chemistry. In proof-of-principle labeling experiments, exosomes derived from macrophages (RAW-Exo) strongly co-localized with central nervous system (CNS) microglia. Inspired by this discovery, we developed a resveratrol-loaded RAW-Exo formulation (RSV&Exo) for multiple sclerosis (MS) treatment. Intranasal administration of RSV&Exo significantly inhibited inflammatory responses in the CNS and peripheral system in a mouse model of MS and effectively improved the clinical evolution of MS in vivo. These findings suggested the feasibility and efficacy of engineered RSV&Exo administration for MS, providing a potential therapeutic strategy for CNS diseases.
 Multiple sclerosis (MS) is regarded as a chronic inflammatory disease that leads to demyelination and eventually to neurodegeneration. Activation of innate immune cells and other inflammatory cells in the brain and spinal cord of people with MS has been well described. However, with the innovation of technology in glial cell research, we have a deep understanding of the mechanisms of glial cells connecting inflammation and neurodegeneration in MS. In this review, we focus on the role of glial cells, including microglia, astrocytes, and oligodendrocytes, in the pathogenesis of MS. We mainly focus on the connection between glial cells and immune cells in the process of axonal damage and demyelinating neuron loss.
 It has now been established that a perturbation in gut microbiome composition exists in multiple sclerosis (MS) and its interplay with the immune system and brain could potentially contribute to the development of the disease and influence its course. The effects of the gut microbiota on the disease may be mediated by direct interactions between bacteria and immune cells or through interactions of products of bacterial metabolism with immune and CNS cells. In this review article we summarize the ways in which the gut microbiome of people with MS differs from controls and how bacterial metabolites can potentially play a role in MS pathogenesis, and examine approaches to alter the composition of the gut microbiota potentially alleviating gut dysbiosis and impacting the course of MS.
 Multiple sclerosis (MS) is a neurodegenerative and autoimmune disease affecting the central nervous system (CNS). The precise etiology of MS is still undeciphered, and signs and symptoms of the disease are varied and complex, ranging from axonal degeneration, synaptic, and neuronal loss to demyelination. Inflammation plays a critical role in determining the onset and the progression of MS, but there is still a lot of information missing before scientists come to understand what are the factors that contribute to the establishment of the neuroinflammation. Thus, various murine models, each representative of a specific hallmark of MS, are used to study the processes underlying the pathogenetic mechanisms of the disease in an attempt to find effective drugs for its treatment. Among the many causes of MS, viral infections appear to be one of the most prominent ones. In this scenario, the comprehension of the role of receptors activated upon the recognition of viral, and in general microbial, components in determining onset and progression of the neuroinflammation is of paramount importance. Toll-like receptors (TLRs) are evolutionarily conserved receptors that recognize several pathogen-associated molecular patterns (PAMPs), common structures of the pathogens, or the damage caused by the pathogens within the host. TLRs are thus directly involved in the regulation of inflammatory reactions and in the activation of the innate and, subsequently, the adaptive immune responses crucial for the elimination of infectious pathogens. The role of TLR activation in the development of MS is widely studied in various murine models of MS, as well as in MS patients. In this chapter, we will summarize the current knowledge about the contribution of TLRs to the development or progression of MS, and we will illustrate different methods commonly used for the investigation of the role of different TLRs in various murine models of the disease.
 BACKGROUND: Bruton's tyrosine kinase (BTK) is a key signaling node in B cell receptor (BCR) and Fc receptor (FcR) signaling. BTK inhibitors (BTKi) are an emerging oral treatment option for patients suffering from multiple sclerosis (MS). Remibrutinib (LOU064) is a potent, highly selective covalent BTKi with a promising preclinical and clinical profile for MS and other autoimmune or autoallergic indications. METHODS: The efficacy and mechanism of action of remibrutinib was assessed in two different experimental autoimmune encephalomyelitis (EAE) mouse models for MS. The impact of remibrutinib on B cell-driven EAE pathology was determined after immunization with human myelin oligodendrocyte glycoprotein (HuMOG). The efficacy on myeloid cell and microglia driven neuroinflammation was determined in the RatMOG EAE. In addition, we assessed the relationship of efficacy to BTK occupancy in tissue, ex vivo T cell response, as well as single cell RNA-sequencing (scRNA-seq) in brain and spinal cord tissue. RESULTS: Remibrutinib inhibited B cell-dependent HuMOG EAE in dose-dependent manner and strongly reduced neurological symptoms. At the efficacious oral dose of 30 mg/kg, remibrutinib showed strong BTK occupancy in the peripheral immune organs and in the brain of EAE mice. Ex vivo MOG-specific T cell recall response was reduced, but not polyclonal T cell response, indicating absence of non-specific T cell inhibition. Remibrutinib also inhibited RatMOG EAE, suggesting that myeloid cell and microglia inhibition contribute to its efficacy in EAE. Remibrutinib did not reduce B cells, total Ig levels nor MOG-specific antibody response. In brain and spinal cord tissue a clear anti-inflammatory effect in microglia was detected by scRNA-seq. Finally, remibrutinib showed potent inhibition of in vitro immune complex-driven inflammatory response in human microglia. CONCLUSION: Remibrutinib inhibited EAE models by a two-pronged mechanism based on inhibition of pathogenic B cell autoreactivity, as well as direct anti-inflammatory effects in microglia. Remibrutinib showed efficacy in both models in absence of direct B cell depletion, broad T cell inhibition or reduction of total Ig levels. These findings support the view that remibrutinib may represent a novel treatment option for patients with MS.
 INTRODUCTION AND HYPOTHESIS: Urinary incontinence following a pelvic floor muscle (PFM) dysfunction is a common disorder in women with multiple sclerosis (MS). Concurrent anodal transcranial direct current stimulation (a-tDCS) of the primary motor cortex (M1) may prime the effects of PFM training (PFMT) in MS patients. This study was aimed at investigating the effects of M1 a-tDCS on the effectiveness of PFMT in the treatment of female MS patients with urinary incontinence and PFM dysfunctions. METHODS: In a randomized double-blinded, control trial study, 30 women with MS were divided into two groups (experimental group: concurrent active M1 a-tDCS and PFMT; control group: concurrent sham M1 a-tDCS and PFMT). Over the course of 8 weeks, these patients received 20-min interventions three times a week. As an indication of PFM function, the bladder base displacement was measured by ultrasonography before, during the 4th week, immediately, and 1 month after the intervention ended. Urinary incontinence was also measured by Incontinence Questionnaire-Urinary Incontinence Short Form (ICIQ-UISF) before, immediately, and 1 month after the intervention ended. RESULTS: A significant improvement in PFM function occurred in the 4th week of intervention and remained 1 month after the intervention in the experimental group when compared with the control group (p<0.05). Compared with baseline, both groups reported significant improvements in PFM function at 8 weeks (p<0.05). Also, both groups were found to have decreased ICIQ-UIS scores after the intervention and at 1-month follow-up (p<0.05). CONCLUSIONS: In MS patients, M1 a-tDCS can significantly enhance the effects of PFMT on the PFM function and urinary incontinence.
 Aim: The presence of two or more publications that report on overlapping patient cohorts poses a challenge for quantitatively synthesizing real-world evidence (RWE) studies. Thus, we evaluated eight approaches for handling such related publications in network meta-analyses (NMA) of RWE studies. Methods: Bayesian NMAs were conducted to estimate the annualized relapse rate (ARR) of disease-modifying therapies in multiple sclerosis. The NMA explored the impact of hierarchically selecting one pivotal study from related publications versus including all of them while adjusting for correlations. Results: When selecting one pivotal study from related publications, the ARR ratios were mostly similar regardless of the pivotal study selected. When including all related publications, there were shifts in the point estimates and the statistical significance. Conclusion: An a priori hierarchy should guide the selection among related publications in NMAs of RWE. Sensitivity analyses modifying the hierarchy should be considered for networks with few or small studies.
 BACKGROUND AND PURPOSE: The clinical correlation of gadolinium-based contrast agents (GBCAs) has not been well studied in multiple sclerosis (MS). We investigated the extent to which the number of GBCA administrations relates to self-reported disability and performance measures. METHODS: A cohort of MS patients was analyzed in this retrospective observational study. The main outcome was the association between the cumulative number of GBCA exposures (linear or macrocyclic GBCA), Patient-Determined Disease Steps (PDDS), and measures of physical and cognitive performance (walking speed test, manual dexterity test [MDT], and processing speed test [PST]). The analysis was performed first cross-sectionally and then longitudinally. RESULTS: The cross-sectional data included 1059 MS patients with a mean age of 44.0 years (standard deviation = 11.2). While the contrast ratio in globus pallidus weakly correlated with PDDS, MDT, and PST in a univariate correlational analysis (coefficients, 95% confidence interval [CI] = 0.11 [0.04, 0.18], 0.15 [0.08, 0.21], and -0.16 [-0.10, -0.23], respectively), the associations disappeared after covariate adjustment. A significant association was found between number of linear GBCA administrations and PDDS (coefficient [CI] = -0.131 [-0.196, -0.067]), and MDT associated with macrocyclic GBCA administrations (-0.385 [-0.616, -0.154]), but their signs indicated better outcomes in patients with greater GBCA exposures. The longitudinal data showed no significant detrimental effect of macrocyclic GBCA exposures. CONCLUSION: No detrimental effects were observed between GBCA exposure and self-reported disability and standardized objective measures of physical and cognitive performance. While several weak associations were found, they indicated benefit on these measures.
 BACKGROUND AND OBJECTIVES: The optic nerve has been recommended as an additional region for demonstrating dissemination in space (DIS) in diagnostic criteria for multiple sclerosis (MS). The aim of this study was to investigate whether adding the optic nerve region as determined by optical coherence tomography (OCT) as part of the DIS criteria improves the 2017 diagnostic criteria. METHODS: From a prospective observational study, we included patients with a first demyelinating event who had complete information to assess DIS and a spectral domain OCT scan obtained within 180 days. Modified DIS criteria (DIS + OCT) were constructed by adding the optic nerve to the current DIS regions based on validated thresholds for OCT intereye differences. Time to second clinical attack was the primary endpoint. RESULTS: We analyzed 267 patients with MS (mean age 31.3 years [SD 8.1], 69% female) during a median observation period of 59 months (range: 13-98). Adding the optic nerve as a fifth region improved the diagnostic performance by increasing accuracy (DIS + OCT 81.2% vs DIS 65.6%) and sensitivity (DIS + OCT 84.2% vs DIS 77.9%) without lowering specificity (DIS + OCT 52.2% vs DIS 52.2%). Fulfilling DIS + OCT criteria (≥2 of 5 DIS + OCT regions involved) indicated a similar risk of a second clinical attack (hazard ratio [HR] 3.6, CI 1.4-14.5) compared with a 2.5-fold increased risk when fulfilling DIS criteria (HR 2.5, CI 1.2-11.8). When the analysis was conducted according to topography of the first demyelinating event, DIS + OCT criteria performed similarly in both optic neuritis and nonoptic neuritis. DISCUSSION: Addition of the optic nerve, assessed by OCT, as a fifth region in the current DIS criteria improves diagnostic performance by increasing sensitivity without lowering specificity. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that adding the optic nerve as determined by OCT as a fifth DIS criterion to the 2017 McDonald criteria improves diagnostic accuracy.
 OBJECTIVE: To analyze anti-SARS-CoV-2-S1-IgG levels, avidity, Omicron BA.2 variant neutralizing capacity, and SARS-CoV-2-specific T cells in anti-CD20-treated patients with multiple sclerosis (aCD20pwMS) after two, three, or four COVID-19 vaccinations. RESULTS: Frequencies of aCD20pwMS with detectable SARS-CoV-2-S1-IgG increased moderately between two (31/61 (51%)), three (31/57 (54%)), and four (17/26 (65%)) vaccinations. However, among patients with detectable SARS-CoV-2-S1-IgG, frequencies of high avidity (6/31 (19%) vs 11/17 (65%)) and Omicron neutralizing antibodies (0/10 (0%) vs 6/10 (60%)) increased strongly between two and four vaccinations. SARS-CoV-2-specific T cells were detectable in >92% after two or more vaccinations. CONCLUSION: Additional vaccinations qualitatively improve SARS-CoV-2 antibody responses.
 BACKGROUND AND PURPOSE: Serum neurofilament light chain (sNfL) is a promising biomarker of neuroaxonal damage in persons with multiple sclerosis (pwMS). In cross-sectional studies, sNfL has been associated with disease activity and brain magnetic resonance imaging (MRI) changes; however, it is still unclear to what extent in particular high sNfL levels impact on subsequent disease evolution. METHODS: sNfL was quantified by an ultrasensitive single molecule array (Simoa) in 199 pwMS (median age = 34.2 years, 64.3% female) and 49 controls. All pwMS underwent 3-T MRI to assess global and compartmental normalized brain volumes, T2-lesion load, and cortical mean thickness. Follow-up data and serum samples were available in 144 pwMS (median follow-up time = 3.8 years). Linear and binary logistic models were used to estimate the independent contribution of sNfL for changes in MRI and Expanded Disability Status Scale (EDSS). Age-corrected sNfL z-scores from a normative database of healthy controls were used for sensitivity analyses. RESULTS: High sNfL levels at baseline were associated with atrophy measures of the whole brain (standardized beta coefficient βj = -0.352, p < 0.001), white matter (βj = -0.229, p = 0.007), thalamus (βj = -0.372, p = 0.004), and putamen (βj = -1.687, p = 0.012). pwMS with high levels of sNfL at baseline and follow-up had a greater risk of EDSS worsening (p = 0.007). CONCLUSIONS: Already single time point elevation of sNfL has a distinct effect on brain volume changes over a short-term period, and repeated high levels of sNfL indicate accumulating physical disability. Serial assessment of sNfL may provide added value in the clinical management of pwMS.
 Multiple sclerosis (MS) is a chronic inflammatory and demyelinating autoimmune disease. MS patients deal with motor and sensory impairments, visual disabilities, cognitive disorders, and speech and language deficits. The study aimed to record, enhance, update, and delve into our present comprehension of speech deficits observed in patients with MS and the methodology (assessment tools) studies followed. The method used was a search of the literature through the databases for May 2015 until June 2022. The reviewed studies offer insight into speech impairments most exhibited by MS patients. Patients with MS face numerous communication changes concerning the phonation system (changes observed concerning speech rate, long pause duration) and lower volume. Moreover, the articulation system was affected by the lack of muscle synchronization and inaccurate pronunciations, mainly of vowels. Finally, there are changes regarding prosody (MS patients exhibited monotonous speech). Findings indicated that MS patients experience communication changes across various domains. Based on the reviewed studies, we concluded that the speech system of MS patients is impaired to some extent, and the patients face many changes that impact their conversational ability and the production of slower and inaccurate speech. These changes can affect MS patients' quality of life.
 BACKGROUND: No studies to date have examined if macular xanthophyll accumulation and retinal integrity are independently associated with cognitive function in individuals with multiple sclerosis (MS). This study explored whether macular xanthophyll accumulation and structural morphometry in the retina were associated with behavioral performance and neuroelectric function during a computerized cognitive task among persons with MS and healthy controls (HCs). METHODS: 42 HCs and 42 individuals with MS aged 18-64 years were enrolled. Macular pigment optical density (MPOD) was measured using heterochromatic flicker photometry. Optic disc retinal nerve fiber layer (odRNFL), macular retinal nerve fiber layer, and total macular volume were assessed via optical coherence tomography. Attentional inhibition was assessed using an Eriksen flanker task while underlying neuroelectric function was recorded using event-related potentials. RESULTS: Persons with MS had a slower reaction time, lower accuracy, and delayed P3 peak latency time during both congruent and incongruent trials compared with HCs. Within the MS group, MPOD explained variance in incongruent P3 peak latency, and odRNFL explained variance in congruent reaction time and congruent P3 peak latency. CONCLUSIONS: Persons with MS exhibited poorer attentional inhibition and slower processing speed, yet higher MPOD and odRNFL levels were independently associated with greater attentional inhibition and faster processing speed among persons with MS. Future interventions are necessary to determine if improvements in these metrics may promote cognitive function among persons with MS.
 BACKGROUND: The potential mediating and moderating effects of sleep disorders on cognitive outcomes in multiple sclerosis (MS) have been insufficiently studied. OBJECTIVES: To determine direct and indirect longitudinal associations between sleep disorders and perceived cognitive dysfunction in women with MS. METHODS: The 2013 and 2017 waves of the Nurses' Health Study (n = 63,866) were utilized. All diagnoses and symptoms including MS (n = 524) were self-reported. Subjective cognitive function was measured using a composite score of four memory items and three binary outcomes that assessed difficulty following instructions, conversations/plots, and street navigation. Moderating and mediating effects of diagnosed/suspected obstructive sleep apnea (OSA), sleepiness, and insomnia between MS and cognition were estimated using the four-way decomposition method. RESULTS: Prevalence of diagnosed/suspected OSA, sleepiness, and insomnia in 2013 were higher for nurses with MS (NwMS). NwMS were more likely to report cognitive difficulties in 2017. Insomnia mediated 5.4%-15.1% of the total effect between MS and following instructions, conversations/plots, and memory impairment, while sleepiness mediated 8.6%-12.3% of the total effect for these outcomes. In interaction analyses, OSA significantly accounted for 34% of the total effect between MS and following instructions. CONCLUSION: Prevalent OSA, insomnia, and sleepiness could differentially moderate or mediate the effect of MS on cognition in women with MS.
 BACKGROUND: Disease-modifying therapies (DMT) for multiple sclerosis (MS) influence SARS-CoV-2 vaccination response, which might have implications for vaccination regimens in individual patients. Expanding the knowledge of predictors for an insufficient vaccination response as a surrogate for protection against severe disease courses of infection in people with MS (pwMS) under DMT is of great importance in identifying high-risk populations. METHODS: Cross-sectional analysis of vaccination titre and its modifiers, in a prospective real-world cohort of 386 individuals (285 pwMS and 101 healthy controls) by two independent immunoassays between October 2021 and June 2022. FINDINGS: In our cohort, no difference in vaccination antibody level was evident between healthy controls (HC) and untreated pwMS. In pwMS lymphocyte levels, times vaccinated and DMT influence SARS-CoV-2 titre following vaccination. Those treated with selective sphingosine-1-phosphate receptor modulators (S1P) showed comparable vaccination titres to untreated; higher CD8 T cell levels prior to vaccination in B cell-depleted patients resulted in increased anti-spike SARS-CoV2 antibody levels. INTERPRETATION: PwMS under DMT with anti-CD20 treatment, in particular those with decreased CD8 levels before vaccination, as well as non-selective S1P but not selective S1P are at increased risk for insufficient SARS-CoV-2 vaccination response. This argues for a close monitoring of anti-spike antibodies in order to customize individual vaccination regimens within these patients. FUNDING: This work was supported by the German Research Foundation (DFG, CRC-TR-128 to TU, SB, and FZ).
 BACKGROUND: The presence of meningeal ectopic lymphoid structures (ELS) in a subgroup of patients diagnosed with secondary progressive multiple sclerosis (SPMS) corresponds to a pronounced cortical inflammation and an aggravated disease course. In MP4-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS), B cell aggregates develop in the central nervous system (CNS) in the chronic stage of the disease. Therefore, the model is suitable for studying key molecules of ELS development and maintenance. Here, we investigated whether there is a specific cytokine and chemokine signature in paired cerebrospinal fluid (CSF) and serum samples associated with the presence of cerebellar B cell and T cell pathology and B cell aggregates of MP4-immunized mice. METHODS: Paired CSF and serum samples were collected from the cisterna magna and periphery of MP4-immunized mice at the chronic stage of disease. A control group with mice immunized only with the adjuvant (vehicle) was included in the study. A selected panel of 34 cytokines and chemokines were measured by MAGPIX® for both cohorts. For the assessment of B cell and T cell infiltration, immunohistochemical staining was performed and analyzed using light microscopy. To detect specific chemokine receptors additional staining was conducted. RESULTS: While we detected several upregulated cytokines and chemokines in the CSF of MP4-immunized mice independent of the extent of B cell and T cell pathology compared to vehicle-immunized mice, C-C motif chemokine ligand (CCL)-1 was associated with high B cell and T cell infiltration. Furthermore, the level of certain chemokines, including CCL1, CCL5, CCL7, CCL12, CCL22 and C-X-C motif chemokine ligand (CXCL)-13, was significantly increased (p < 0.05) in MP4-immunized mice showing a high number of B cell aggregates. While C-C motif chemokine receptor (CCR)5 had a ubiquitous expression independent of the extent of B cell and T cell pathology, C-X-C motif chemokine receptor (CXCR)-5 and CXCR6 expression was specifically associated with high B cell and T cell pathology. CONCLUSION: Our data suggest that multiple cytokines and chemokines are involved in the pathophysiology of MP4-induced EAE. Furthermore, the presence of B cell aggregates was associated with a specific chemokine profile in the CSF, which might be useful for predicting the presence of these aggregates without the necessity to histologically screen the CNS tissue.
 PURPOSE: This study aimed to investigate the alterations of brain volumetry and associated structural covariance in subcortical regions in multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD). MATERIALS AND METHODS: Fourty MS patients, 35 NMOSD patients and 34 healthy controls (HC) underwent 3D T1-weighted image and 3D T2 FLAIR of MRI. The volume differences in subcortical regions were compared between the MS, NMOSD, and HC groups by automated brain volumetry. Structural covariance analysis was performed with each pair of these regions to investigate the alterations of anatomical connections in MS and NMOSD compared to HC. RESULTS: Compared with HC, MS patients presented significantly smaller volume in some subcortical and infratentorial regions (P<0.05), while NMOSD patients showed no significant difference of volumetry in any of the brain regions (P>0.05), although they had no significant difference in disease duration (MS 3.95±3.73 ys; NMOSD 3.11±4.61 ys; P>0.05). In addition, the structural covariance analyses revealed synergic volume alteration in subcortical regions both in the MS and NMOSD groups. More extensive additional connections compared with HC were found in MS patients and more extensive missing connections compared with HC were found in NMOSD patients. CONCLUSION: This study revealed distinct patterns of brain structural damage and reorganization in MS and NMOSD, which could facilitate a better distinction between these two entities.
 Oligodendrocytes and their progenitors upregulate MHC pathways in response to inflammation, but the frequency of this phenotypic change is unknown and the features of these immune oligodendroglia are poorly defined. We generated MHC class I and II transgenic reporter mice to define their dynamics in response to inflammatory demyelination, providing a means to monitor MHC activation in diverse cell types in living mice and define their roles in aging, injury, and disease.
 BACKGROUND: Little is known about COVID-19 course and outcomes after a third booster dose of mRNA vaccine against SARS-CoV-2 (mRNA-Vax) in patients with multiple sclerosis (pwMS) treated with ocrelizumab (OCR) and fingolimod (FNG), which showed a weakened immune response to mRNA-vax. OBJECTIVES: The aim of this study was to evaluate COVID-19 course and outcomes in pwMS on OCR and FNG after receiving the third dose of mRNA-Vax and to compare it with pwMS on natalizumab (NTZ). METHODS: Inclusion criteria: >18 years of age, being treated with OCR/FNG/NTZ since the first mRNA-Vax dose; COVID-19 after a third booster dose of mRNA-Vax; no steroids use. RESULTS: Overall, 290 pwMS (79 NTZ, 126 OCR, and 85 FNG) from 17 Italian MS centers were included. Age, Expanded Disability Status Scale (EDSS) score, MS phenotype, disease, and treatment duration were significantly different across groups. PwMS who had COVID-19 on OCR and FNG compared with those on NTZ were slightly more symptomatic with higher hospitalization rates (11.1% vs 7.1% vs 1.3%, respectively). Regression models showed that the majority of the differences observed were not related to the disease-modifying treatments (DMTs) used. No fatal cases were observed. CONCLUSION: Our results support the effectiveness of the third booster dose of mRNA-Vax against severe forms of COVID-19 in pwMS treated with OCR and FNG.
 Upper limb function is one of the most affected domains in people with multiple sclerosis (PwMS), as self-reported by 50% of patients. Heterogeneous results have been found about the correlation between objective and subjective upper limb function. The aim of the present study is to perform a systematic review and meta-analysis of studies presenting data on the strength of association between the gold standard for 9-Hole Peg Test scores and Patient-Reported Outcome Measures (PROMs) of manual ability. Primary research studies including assessments of 9-Hole Peg Test scores and Patient-Reported Outcome Measures were searched in Scopus, Web of Science, and PubMed. Meta analytical calculations were performed using a random-effects model. We retrieved n = 27 studies including n = 75 distinct effect sizes (N of subjects = 3263). The central tendency analysis showed a strong correlation between 9-HPT scores and PROMs (r = 0.51, 95% CI [0.44, 0.58]). Moderator analysis showed the effect size to be significantly larger in studies with a mean or median EDSS level indicating severe disability. The publication bias hypothesis was not supported; instead, we noted that studies based on larger samples also tend to report stronger effect sizes. Results of the study indicate that the correlation between 9-HPT and PROMs is strong, although the constructs measured by these instrument does not fully overlap. The correlation between 9-HPT and PROMs was stronger in larger studies and when samples include a sizeable subgroup of PwMS with severe disability, pointing out the importance of sample diversity.
 BACKGROUND AND OBJECTIVE: Emerging evidence suggests a role for diet in multiple sclerosis (MS) care; however, owing to methodological issues and heterogeneity of dietary interventions in preliminary trials, the current state of evidence does not support dietary recommendations for MS. The objective of this study was to assess the efficacy of different dietary approaches on MS-related fatigue and quality of life (QoL) through a systematic review of the literature and network meta-analysis (NMA). METHODS: Electronic database searches were performed in May 2021. Inclusion criteria were (1) randomized trial with a dietary intervention, (2) adults with definitive MS based on McDonald criteria, (3) patient-reported outcomes for fatigue and/or QoL, and (4) minimum intervention period of 4 weeks. For each outcome, standardized mean differences (SMDs) were calculated and included in random effects NMA to determine the pooled effect of each dietary intervention relative to each of the other dietary interventions. The protocol was registered at PROSPERO (CRD42021262648). RESULTS: Twelve trials comparing 8 dietary interventions (low-fat, Mediterranean, ketogenic, anti-inflammatory, Paleolithic, fasting, calorie restriction, and control [usual diet]), enrolling 608 participants, were included in the primary analysis. The Paleolithic (SMD -1.27; 95% CI -1.81 to -0.74), low-fat (SMD -0.90; 95% CI -1.39 to -0.42), and Mediterranean (SMD -0.89; 95% CI -1.15 to -0.64) diets showed greater reductions in fatigue compared with control. The Paleolithic (SMD 1.01; 95% CI 0.40-1.63) and Mediterranean (SMD 0.47; 95% CI 0.08-0.86) diets showed greater improvements in physical QoL compared with control. For improving mental QoL, the Paleolithic (SMD 0.81; 95% CI 0.26-1.37) and Mediterranean (SMD 0.36; 95% CI 0.06-0.65) diets were more effective compared with control. However, the NutriGRADE credibility of evidence for all direct comparisons is very low because of most of the included trials having high or moderate risk of bias, small sample sizes, and the limited number of studies included in this NMA. DISCUSSION: Several dietary interventions may reduce MS-related fatigue and improve physical and mental QoL; however, because of the limitations of this NMA, which are driven by the low quality of the included trials, these findings must be confirmed in high-quality, randomized, controlled trials.
 Multiple sclerosis (MS) is an autoimmune and demyelinating disease of the central nervous system that results from complex interactions between genetic and environmental determinants. Patients with MS exhibit a high risk of depression, however, the exact pathomechanisms remain largely unknown. It is becoming widely accepted that the gut-brain axis (GBA) disorders may exert an influence on neuroinflammation and psychiatric symptoms, including so-called MS-related depression. The element suggested as a bridge between intestinal disorders, depression, and MS is an inflammatory response with the central role of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. The pro-inflammatory activity of effector cytokines of the NLRP3 inflammasome forms the hypothesis that it is actively involved in the development of inflammatory and autoimmune diseases. Despite extensive reviews considering the possible origins of MS-related depression, its complex pathophysiology prevents any easy determination of its underlying mechanisms. This paper aims to discuss molecular mechanisms related to the GBA axis that can mediate dysbiosis, intestinal barrier dysfunction, disruption of blood-brain barrier integrity, neuroinflammation, and subsequent manifestation of MS-related major depressive disorder.
 INTRODUCTION: Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative disease mediated by autoimmune reactions against myelin proteins and gangliosides in the grey and white matter of the brain and spinal cord. It is considered one of the most common neurological diseases of non-traumatic origin in young people, especially in women. Recent studies point to a possible association between MS and gut microbiota. Intestinal dysbiosis has been observed, as well as an alteration of short-chain fatty acid-producing bacteria, although clinical data remain scarce and inconclusive. OBJECTIVE: To conduct a systematic review on the relationship between gut microbiota and multiple sclerosis. METHOD: The systematic review was conducted in the first quarter of 2022. The articles included were selected and compiled from different electronic databases: PubMed, Scopus, ScienceDirect, Proquest, Cochrane, and CINAHL. The keywords used in the search were: "multiple sclerosis", "gut microbiota", and "microbiome". RESULTS: 12 articles were selected for the systematic review. Among the studies that analysed alpha and beta diversity, only three found significant differences with respect to the control. In terms of taxonomy, the data are contradictory, but confirm an alteration of the microbiota marked by a decrease in Firmicutes, Lachnospiraceae, Bifidobacterium, Roseburia, Coprococcus, Butyricicoccus, Lachnospira, Dorea, Faecalibacterium, and Prevotella and an increase in Bacteroidetes, Akkermansia, Blautia, and Ruminocococcus. As for short-chain fatty acids, in general, a decrease in short-chain fatty acids, in particular butyrate, was observed. CONCLUSIONS: Gut microbiota dysbiosis was found in multiple sclerosis patients compared to controls. Most of the altered bacteria are short-chain fatty acid (SCFA)-producing, which could explain the chronic inflammation that characterises this disease. Therefore, future studies should consider the characterisation and manipulation of the multiple sclerosis-associated microbiome as a focus of both diagnostic and therapeutic strategies.
 BACKGROUND: Exercise positively affects multiple sclerosis (MS) symptoms, physiological systems, and potentially cognition. However, an uninvestigated "window of opportunity" exists for exercise therapy early in the disease. OBJECTIVE: This study presents secondary analyses from the Early Multiple Sclerosis Exercise Study, and aims to investigate the efficacy of exercise on physical function, cognition, and patient-reported measures of disease and fatigue impact early in the disease course of MS. METHODS: This randomized controlled trial (n = 84, time since diagnosis <2 years) included 48 weeks of aerobic exercise or an active control condition (health education) and between-group changes are based on repeated measurement mixed regression models. Physical function tests included measures of aerobic fitness, walking (6-minute walk, Timed 25-foot walk, Six-spot step test), and upper-limb dexterity. Tests of processing speed and memory evaluated cognition. The questionnaires Multiple Sclerosis Impact Scale and Modified Fatigue Impact Scale assessed perception of disease and fatigue impact. RESULTS: Following early exercise aerobic fitness showed superior between-group physiological adaptations (4.0 [1.7; 6.3] ml O(2)/min/kg; large effect size [ES = 0.90]). No other outcomes showed significant between-group differences, yet all measures of walking and upper-limb function showed small-to-medium effect sizes in favor of exercise (ES = 0.19-0.58). Overall disability status as well as cognition were unaffected by exercise, whereas perception of disease and fatigue impact were reduced in both groups. CONCLUSION: In early MS, 48 weeks of supervised aerobic exercise seem to positively modify physical function, but not cognitive function. Perception of disease and fatigue impact may be modifiable by exercise in early MS. TRIAL REGISTRATION: Clinicaltrials.gov (identifier: NCT03322761).
 BACKGROUND: The spinal cord (SC) is a preferential target of multiple sclerosis (MS) damage highly relevant towards disability. Differential impact of such damage could be due to the initial amount of SC tissue, as described for the brain parenchyma (brain reserve concept). We aimed to test the existence of SC reserve by using spinal canal area (SCaA) as a proxy. METHODS: Brain sagittal three-dimensional T1-weighted scans covering down to C5 level were acquired in 2930 people with MS and 43 healthy controls (HCs) in a cross-sectional, multicentre study. SC area (SCA) and SCaA were obtained with the Spinal Cord Toolbox. Demographical data and patient-derived disability scores were obtained. SC parameters were compared between groups with age-adjusted and sex-adjusted linear regression models. The main outcome of the study, the existence of an association between SCaA and Patient Determined Disease Steps, was tested with scaled linear models. RESULTS: 1747 persons with MS (mean age: 46.35 years; 73.2% female) and 42 HCs (mean age: 45.56 years; 78.6% female) were analysed after exclusion of post-processing errors and application of quality criteria. SCA (60.41 mm(2) vs 65.02 mm(2), p<0.001) was lower in people with MS compared with HC; no differences in SCaA were observed (213.24 mm(2) vs 212.61 mm(2), p=0.125). Adjusted scaled linear models showed that a larger SCaA was significantly associated with lower scores on Patient Determined Disease Steps (beta coefficient: -0.12, p=0.0124) independently of spinal cord atrophy, brain T2 lesion volume, age and sex. CONCLUSIONS: A larger SCaA may be protective against disability in MS, possibly supporting the existence of SC reserve.
 PURPOSE: To analyze the effectiveness of resistance training programs (RTP) on strength, functional capacity, balance, general health perception, and fatigue for people with Multiple Sclerosis (MS) and to determine the most effective dose of RTP in this population. METHODS: Studies examining the effect of RTP on strength, functional capacity, balance, general health perception, and fatigue in MS patients were included. 44 studies were included. The meta-analysis, subgroup analysis and meta-regression methods were used to calculate the mean difference and standardized mean difference. RESULTS: Significant group differences were observed in knee extensor (p = 0.01) and flexor (p < 0.001), but not in 1-repetition maximum. Regarding functional capacity and balance, differences between groups, in favour of the RTP group, were found in the Timed Up and Go Test (p = 0.001), walking endurance, (p = 0.02) gait speed (p = 0.02) and balance (p = 0.02). No significant differences between groups were observed in fatigue or general health perception. The results regarding the optimal dose are inconsistent. CONCLUSIONS: RTP improves strength, functional capacity, balance, and fatigue in people with MS. Registration: (PROSPERO): CRD42020182781Implications for rehabilitationResistance training is a valid strategy to improve isometric strength and functional capacity in MS patients.RTP using long durations (more than 6 weeks), high intensity (more than 80% 1-RM) and two-day weekly training frequency may be a correct stimulus to improve strength, functional capacity, balance, and fatigue in people with MS.Trainers and rehabilitators should consider these indicators in order to maximize muscular and functional adaptations in this population.
 BACKGROUND: Translocator protein (TSPO)-PET and neurofilament light (NfL) both report on brain pathology, but their potential association has not yet been studied in multiple sclerosis (MS) in vivo. We aimed to evaluate the association between serum NfL (sNfL) and TSPO-PET-measurable microglial activation in the brain of patients with MS. METHODS: Microglial activation was detected using PET and the TSPO-binding radioligand [(11)C]PK11195. Distribution volume ratio (DVR) was used to evaluate specific [(11)C]PK11195-binding. sNfL levels were measured using single molecule array (Simoa). The associations between [(11)C]PK11195 DVR and sNfL were evaluated using correlation analyses and false discovery rate (FDR) corrected linear regression modelling. RESULTS: 44 patients with MS (40 relapsing-remitting and 4 secondary progressive) and 24 age-matched and sex-matched healthy controls were included. In the patient group with elevated brain [(11)C]PK11195 DVR (n=19), increased sNfL associated with higher DVR in the lesion rim (estimate (95% CI) 0.49 (0.15 to 0.83), p(FDR)=0.04) and perilesional normal appearing white matter (0.48 (0.14 to 0.83), p(FDR)=0.04), and with a higher number and larger volume of TSPO-PET-detectable rim-active lesions defined by microglial activation at the plaque edge (0.46 (0.10 to 0.81), p(FDR)=0.04 and 0.50 (0.17 to 0.84), p(FDR)=0.04, respectively). Based on the multivariate stepwise linear regression model, the volume of rim-active lesions was the most relevant factor affecting sNfL. CONCLUSIONS: Our demonstration of an association between microglial activation as measured by increased TSPO-PET signal, and elevated sNfL emphasises the significance of smouldering inflammation for progression-promoting pathology in MS and highlights the role of rim-active lesions in promoting neuroaxonal damage.
 IMPORTANCE: Autologous hematopoietic stem cell transplant (AHSCT) is available for treatment of highly active multiple sclerosis (MS). OBJECTIVE: To compare the effectiveness of AHSCT vs fingolimod, natalizumab, and ocrelizumab in relapsing-remitting MS by emulating pairwise trials. DESIGN, SETTING, AND PARTICIPANTS: This comparative treatment effectiveness study included 6 specialist MS centers with AHSCT programs and international MSBase registry between 2006 and 2021. The study included patients with relapsing-remitting MS treated with AHSCT, fingolimod, natalizumab, or ocrelizumab with 2 or more years study follow-up including 2 or more disability assessments. Patients were matched on a propensity score derived from clinical and demographic characteristics. EXPOSURE: AHSCT vs fingolimod, natalizumab, or ocrelizumab. MAIN OUTCOMES: Pairwise-censored groups were compared on annualized relapse rates (ARR) and freedom from relapses and 6-month confirmed Expanded Disability Status Scale (EDSS) score worsening and improvement. RESULTS: Of 4915 individuals, 167 were treated with AHSCT; 2558, fingolimod; 1490, natalizumab; and 700, ocrelizumab. The prematch AHSCT cohort was younger and with greater disability than the fingolimod, natalizumab, and ocrelizumab cohorts; the matched groups were closely aligned. The proportion of women ranged from 65% to 70%, and the mean (SD) age ranged from 35.3 (9.4) to 37.1 (10.6) years. The mean (SD) disease duration ranged from 7.9 (5.6) to 8.7 (5.4) years, EDSS score ranged from 3.5 (1.6) to 3.9 (1.9), and frequency of relapses ranged from 0.77 (0.94) to 0.86 (0.89) in the preceding year. Compared with the fingolimod group (769 [30.0%]), AHSCT (144 [86.2%]) was associated with fewer relapses (ARR: mean [SD], 0.09 [0.30] vs 0.20 [0.44]), similar risk of disability worsening (hazard ratio [HR], 1.70; 95% CI, 0.91-3.17), and higher chance of disability improvement (HR, 2.70; 95% CI, 1.71-4.26) over 5 years. Compared with natalizumab (730 [49.0%]), AHSCT (146 [87.4%]) was associated with marginally lower ARR (mean [SD], 0.08 [0.31] vs 0.10 [0.34]), similar risk of disability worsening (HR, 1.06; 95% CI, 0.54-2.09), and higher chance of disability improvement (HR, 2.68; 95% CI, 1.72-4.18) over 5 years. AHSCT (110 [65.9%]) and ocrelizumab (343 [49.0%]) were associated with similar ARR (mean [SD], 0.09 [0.34] vs 0.06 [0.32]), disability worsening (HR, 1.77; 95% CI, 0.61-5.08), and disability improvement (HR, 1.37; 95% CI, 0.66-2.82) over 3 years. AHSCT-related mortality occurred in 1 of 159 patients (0.6%). CONCLUSION: In this study, the association of AHSCT with preventing relapses and facilitating recovery from disability was considerably superior to fingolimod and marginally superior to natalizumab. This study did not find evidence for difference in the effectiveness of AHSCT and ocrelizumab over a shorter available follow-up time.
 PURPOSE: The Australian multiple sclerosis (MS) community experienced two recent major crises, widespread bushfires and the COVID 19 pandemic. We aimed to understand the needs of persons with MS during times of crisis. MATERIALS AND METHODS: A consumer-directed mixed-method study. We included an online survey, semi-structured interviews, and a workshop with persons with MS, carers, healthcare professionals, and disability advocates. Data were collected via: (1) 176 people completing online surveys to identify crisis concerns and communications, (2) 29 people completing online interviews on bushfire and pandemic impact, and (3) 13 people participating in a crises-priorities workshop. Descriptive data were calculated for survey response, and a general inductive analytical approach was taken with interview and workshop responses. RESULTS: The most significant concerns were bushfire smoke exposure and disease-modifying-medication and susceptibility to COVID-19 (66% and 63% mean concern score, respectively). Interviews indicated crises experiences from the bushfires, and the pandemic overlapped respective of changes in mood and symptom stability. For bushfires, a need for future preparations, and for the pandemic, the benefits of social restrictions, disclosing personal health information and increased care burden were important. CONCLUSIONS: Multiple crises challenged the MS community but offered lessons for healthcare in future crises. Continued progress in centralised crisis information, with considered use of telehealth and rural healthcare support, is needed.Implications for rehabilitationThe MS community showed high concerns for the effect of toxic smoke from the 2019/2020 Australian bushfires and, separately, for the disease-modifying-medication and susceptibility to COVID-19.The MS community placed priority on a crisis management plan for individuals.Reduced social activity due to restrictions was beneficial for MS symptom self-awareness and may help overall fatigue management.Healthcare system preparation must prepare to alleviate increased carer workload at times of crisis.
 The indirect contribution of multiple sclerosis (MS) relapses to disability worsening outcomes, and vice-versa, remains unclear. Disease modifying therapies (DMTs) are potential modulators of this association. Understanding how these endo-phenotypes interact may provide insights into disease pathogenesis and treatment practice in relapse-onset MS (ROMS). Utilising a unique, prospectively collected clinical data from a longitudinal cohort of 279 first demyelinating event cases followed for up to 15 years post-onset, we examined indirect associations between relapses and treatment and the risk of disability worsening, and vice-versa. Indirect association parameters were estimated using joint models for longitudinal and survival data. Early relapses within 2.5 years of MS onset predicted early disability worsening outcomes (HR = 3.45, C.I 2.29-3.61) per relapse, but did not contribute to long-term disability worsening thereinafter (HR = 0.21, C.I 0.15-0.28). Conversely, disability worsening outcomes significantly contributed to relapse risk each year (HR = 2.96, C.I 2.91-3.02), and persisted over time (HR = 3.34, C.I 2.90-3.86), regardless of DMT treatments. The duration of DMTs significantly reduced the hazards of relapses (1st-line DMTs: HR = 0.68, C.I 0.58-0.79; 3rd-line DMTs: HR = 0.37, C.I 0.32-0.44) and disability worsening events (1st-line DMTs: HR = 0.74, C.I 0.69-0.79; 3rd-line DMTs: HR = 0.90, C.I 0.85-0.95), respectively. Results from time-dynamic survival probabilities further revealed individuals having higher risk of future relapses and disability worsening outcomes, respectively. The study provided evidence that in ROMS, relapses accrued within 2.5 years of MS onset are strong indicators of disability worsening outcomes, but late relapses accrued 2.5 years post onset are not overt risk factors for further disability worsening. In contrast, disability worsening outcomes are strong positive predictors of current and subsequent relapse risk. Long-term DMT use and older age strongly influence the individual outcomes and their associations.
 BACKGROUND: Multiple sclerosis (MS) is a prototype neuroinflammatory disorder with increasingly recognized role for neurodegeneration. Most first-line treatments cannot prevent the progression of neurodegeneration and the resultant disability. Interventions can improve symptoms of MS and might provide insights into the underlying pathology. OBJECTIVE: To investigate the effect of intermittent caloric restriction on neuroimaging markers of MS. METHODS: We randomized ten participants with relapsing remitting MS to either a 12-week intermittent calorie restriction (iCR) diet (n = 5) or control (n = 5). Cortical thickness and volumes were measured through FreeSurfer, cortical perfusion was measured by arterial spin labeling and neuroinflammation through diffusion basis spectrum imaging. RESULTS: After 12 weeks of iCR, brain volume increased in the left superior and inferior parietal gyri (p: 0.050 and 0.049, respectively) and the banks of the superior temporal sulcus (p: 0.01). Similarly in the iCR group, cortical thickness improved in the bilateral medial orbitofrontal gyri (p: 0.04 and 0.05 in right and left, respectively), the left superior temporal gyrus (p: 0.03), and the frontal pole (p: 0.008) among others. Cerebral perfusion decreased in the bilateral fusiform gyri (p: 0.047 and 0.02 in right and left, respectively) and increased in the bilateral deep anterior white matter (p: 0.03 and 0.013 in right and left, respectively). Neuroinflammation, demonstrated through hindered and restricted water fractions (HF and RF), decreased in the left optic tract (HF p: 0.02), and the right extreme capsule (RF p: 0.007 and HF p: 0.003). CONCLUSION: These pilot data suggest therapeutic effects of iCR in improving cortical volume and thickness and mitigating neuroinflammation in midlife adults with MS.
 Multiple sclerosis (MS) is a common autoimmunity disease of the central nervous system (CNS) that mostly happens in young adults. The chronic clinical features of MS include inflammatory demyelination, infiltration of immune cells, and secretion of inflammatory cytokines, which have been proved to be associated with CD4(+) T cells. Ferroptosis is a newly discovered programmed cell death mediated by the massive lipid peroxidation and more sensitive to CD4(+) T cells. However, the effect of ferroptosis of CD4(+) T cells on the occurrence and progression of MS retains unclear. Here, the experimental autoimmune encephalomyelitis (EAE) model was used to investigate the role of GPX4, a leading inhibitor of ferroptosis, which plays in the function of CD4(+) T cells. Our results showed that GPX4 was highly expressed in CD4(+) T cells of MS patients based on existing databases. Strikingly, conditional knockout of GPX4 in CD4(cre) mice (cKO mice) significantly alleviated the average symptom scores and immunopathology of EAE. The infiltration of immune cells, including CD4(+) T and CD8(+) T cells, and the generation of GM-CSF, TNF-α, and IL-17A, were remarkably reduced in the CNS from cKO mice compared with WT mice. These findings further revealed the vital role of GPX4 in the expansion and function of CD4(+) T cells. Moreover, GPX4-deficient CD4(+) T cells were susceptible to ferroptosis in EAE model. Overall, this study provided novel insights into therapeutic strategies targeting GPX4 in CD4(+) T cells for inhibiting CNS inflammation and treating MS.
 Herein, a tolerogenic nanovaccine is developed and tested on an animal model of multiple sclerosis. The nanovaccine is constructed to deliver the self-antigen, myelin oligodendrocyte glycoprotein (MOG) peptide, and dexamethasone on an abatacept-modified polydopamine core nanoparticle (AbaLDPN-MOG). AbaLDPN-MOG can target dendritic cells and undergo endocytosis followed by trafficking to lysosomes. AbaLDPN-MOG blocks the interaction between CD80/CD86 and CD28 in antigen-presenting cells and T cells, leading to decreased interferon gamma secretion. The subcutaneous administration of AbaLDPN-MOG to mice yields significant biodistribution to lymph nodes and, in experimental-autoimmune encephalomyelitis (EAE) model mice, increases the integrity of the myelin basic sheath and minimizes the infiltration of immune cells. EAE mice are treated with AbaLDPN-MOG before or after injection of the autoantigen, MOG. Preimmunization of AbaLDPN-MOG before the injection of MOG completely blocks the development of clinical symptoms. Early treatment with AbaLDPN-MOG at three days after injection of MOG also completely blocks the development of symptoms. Notably, treatment of EAE symptom-developed mice with AbaLDPN-MOG significantly alleviates the symptoms, indicating that the nanovaccine has therapeutic effects. Although AbaLDPN is used for MOG peptide delivery in the EAE model, the concept of AbaLDPN can be widely applied for the prevention and alleviation of other autoimmune diseases.
 BACKGROUND: In severe conditions of limited motor abilities, frequent position changes for work or passive and active rest are essential bedside activities to prevent further health complications. We aimed to develop a system using eye movements for bed positioning and to verify its functionality in a control group and a group of patients with significant motor limitation caused by multiple sclerosis. METHODS: The eye-tracking system utilized an innovative digital-to-analog converter module to control the positioning bed via a novel graphical user interface. We verified the ergonomics and usability of the system by performing a fixed sequence of positioning tasks, in which the leg and head support was repeatedly raised and then lowered. Fifteen women and eleven men aged 42.7 ± 15.9 years in the control group and nine women and eight men aged 60.3 ± 9.14 years in the patient group participated in the experiment. The degree of disability, according to the Expanded Disability Status Scale (EDSS), ranged from 7 to 9.5 points in the patients. We assessed the speed and efficiency of the bed control and the improvement during testing. In a questionnaire, we evaluated satisfaction with the system. RESULTS: The control group mastered the task in 40.2 s (median) with an interquartile interval from 34.5 to 45.5 s, and patients mastered the task in in 56.5 (median) with an interquartile interval from 46.5 to 64.9 s. The efficiency of solving the task (100% corresponds to an optimal performance) was 86.3 (81.6; 91.0) % for the control group and 72.1 (63.0; 75.2) % for the patient group. Throughout testing, the patients learned to communicate with the system, and their efficiency and task time improved. A correlation analysis showed a negative relationship (rho = - 0.587) between efficiency improvement and the degree of impairment (EDSS). In the control group, the learning was not significant. On the questionnaire survey, sixteen patients reported gaining confidence in bed control. Seven patients preferred the offered form of bed control, and in six cases, they would choose another form of interface. CONCLUSIONS: The proposed system and communication through eye movements are reliable for positioning the bed in people affected by advanced multiple sclerosis. Seven of 17 patients indicated that they would choose this system for bed control and wished to extend it for another application.
 PURPOSE: The purpose was to evaluate the psychometric properties of physical activity measures in persons with multiple sclerosis (PwMS). METHODS: Adults with multiple sclerosis were recruited, n = 30 (validation) and n = 57 (test-retest). Steps measured with PiezoRX, Yamax SW200 and ActiGraph GT9X Link (AGlink) and time in different positions measured with AGlink were validated against data from video analysis. Psychometric properties of the Physical Activity and Disability Survey - Revised Swedish version (PADS-R(Sw)) was evaluated. RESULTS: The most valid measures were AGlink using the low-frequency extension filter, and PiezoRX with median absolute percentage errors (MeAPEs) of 0.9-3.1% and 1.3-3.3%. The MeAPEs were higher for Yamax SW200 (2.9-21.0%), AGlink display (3.6-44.8%) and AGlink normal filter (8.9-48.9%), indicating low validity. AGlink was not valid in measurements of sitting (MeAPE 12.0-12.5%) or lying (MeAPE 31.0-41.7%). The correlation between PADS-R(Sw) and AGlink steps was r = 0.492 (p = .009). The relative reliability of PADS-R(Sw) was ICC(2,1) 0.85 (CI 0.76-0.91), and absolute reliability was SEM 0.54. CONCLUSION: AGlink and PiezoRX were valid measures of steps in PwMS. The questionnaire PADS-R(Sw) was valid, with high relative reliability, but its absolute reliability was unsatisfactory.
 Tandem gait is widely used during clinical exams to evaluate dynamic balance in chronic diseases, such as multiple sclerosis (MS). The early detection of balance impairments in MS is challenging to improve the understanding of patients' complaints. The objective was to propose two indexes to quantify the contributions and inefficiency of limb and trunk movements during tandem gait in early-stage MS patients. Fifteen patients with remitting-relapsed MS, with a median Expanded Disability Status Scale of 2.5 [0-4] were compared to 15 matched healthy participants. Three-dimensional motion analysis was performed during tandem gait to calculate spatiotemporal parameters, contribution and inefficiency indexes, based on the linear momentum of body segments. Compared to healthy participants, MS patients at the early stage of disease executed tandem gait with higher speed (p = 0.03) and increased step length (p = 0.03). The contribution indexes of upper limbs were significantly decreased during swing phase in MS patients. The inefficiency index for the upper limbs were around twice higher for MS patients compared to healthy participants. Since the additional movements concerned only light body segments and not contribute to the whole-body forward progression during tandem gait, they could reflected more both upper limb movements alterations and restoring movements to avoid loss of balance during tandem gait around swing phase in MS. These quantified indexes could be used as physical markers to quantify both the balance deterioration and the efficiency of rehabilitation program during the follow up of MS from the early stage of their disease.
 Multiple sclerosis is a slowly progressive disease, immunosuppressants and other drugs can delay the progression and progression of the disease, but the most patients will be left with varying degrees of neurological deficit symptoms, such as muscle weakness, muscle spasm, ataxia, sensory impairment, dysphagia, cognitive dysfunction, psychological disorders, etc. From the early stage of the disease to the stage of disease progression, professional rehabilitation treatment can reduce the functional dysfunction of multiple sclerosis patients, improve neurological function, and reduce family and social burdens. With the development of various new rehabilitation technologies such as transcranial magnetic stimulation, virtual reality technology, robot-assisted gait, telerehabilitation and transcranial direct current stimulation, the advantages of rehabilitation therapy in multiple sclerosis treatment have been further established, and more treatment means have also been provided for patients.
 Remyelination and neurodegeneration prevention mitigate disability in Multiple Sclerosis (MS). We have shown acute intermittent hypoxia (AIH) is a novel, non-invasive and effective therapy for peripheral nerve repair, including remyelination. Thus, we posited AIH would improve repair following CNS demyelination and address the paucity of MS repair treatments. AIH's capacity to enhance intrinsic repair, functional recovery and alter disease course in the experimental autoimmune encephalomyelitis (EAE) model of MS was assessed. EAE was induced by MOG(35-55) immunization in C57BL/6 female mice. EAE mice received either AIH (10 cycles-5 min 11% oxygen alternating with 5 min 21% oxygen) or Normoxia (control; 21% oxygen for same duration) once daily for 7d beginning at near peak EAE disease score of 2.5. Mice were followed post-treatment for an additional 7d before assessing histopathology or 14d to examine maintenance of AIH effects. Alterations in histopathological correlates of multiple repair indices were analyzed quantitatively in focally demyelinated ventral lumbar spinal cord areas to assess AIH impacts. AIH begun at near peak disease significantly improved daily clinical scores/functional recovery and associated histopathology relative to Normoxia controls and the former were maintained for at least 14d post-treatment. AIH enhanced correlates of myelination, axon protection and oligodendrocyte precursor cell recruitment to demyelinated areas. AIH also effected a dramatic reduction in inflammation, while polarizing remaining macrophages/microglia toward a pro-repair state. Collectively, this supports a role for AIH as a novel non-invasive therapy to enhance CNS repair and alter disease course following demyelination and holds promise as a neuroregenerative MS strategy.
 Multiple sclerosis is an autoimmune neurodegenerative disease of the CNS that causes progressive disabilities, owing to CNS axon degeneration as a late result of demyelination. In the search for the prevention of axonal loss, mitigating inflammatory attacks in the CNS and myelin restoration are two possible approaches. As a result, therapies that target diverse signaling pathways involved in neuroprotection and remyelination have the potential to overcome the challenges in the development of multiple sclerosis treatments. LINGO1 (Leucine rich repeat and Immunoglobulin domain containing, Nogo receptor- interaction protein), AKT/PIP3/mTOR, Notch, Wnt, RXR (Retinoid X receptor gamma), and Nrf2 (nuclear factor erythroid 2-related factor 2) signaling pathways are highlighted in this section. This article reviews the present knowledge regarding numerous signaling pathways and their functions in regulating remyelination in multiple sclerosis pathogenesis. These pathways are potential biomarkers and therapeutic targets in MS.
 Oligodendrocytes are a type of glial cells that produce a lipid-rich membrane called myelin. Myelin assembles into a sheath and lines neuronal axons in the brain and spinal cord to insulate them. This not only increases the speed and efficiency of nerve signal transduction but also protects the axons from damage and degradation, which could trigger neuronal cell death. Demyelination, which is caused by a loss of myelin and oligodendrocytes, is a prominent feature of many neurological conditions, including Multiple sclerosis (MS), spinal cord injuries (SCI), and leukodystrophies. Demyelination is followed by a time of remyelination mediated by the recruitment of endogenous oligodendrocyte precursor cells, their migration to the injury site, and differentiation into myelin-producing oligodendrocytes. Unfortunately, endogenous remyelination is not sufficient to overcome demyelination, which explains why there are to date no regenerative-based treatments for MS, SCI, or leukodystrophies. To better understand the role of oligodendrocytes and develop cell-based remyelination therapies, human oligodendrocytes have been derived from somatic cells using cell reprogramming. This review will detail the different cell reprogramming methods that have been developed to generate human oligodendrocytes and their applications to disease modeling and cell-based remyelination therapies. Recent developments in the field have seen the derivation of brain organoids from pluripotent stem cells, and protocols have been devised to incorporate oligodendrocytes within the organoids, which will also be reviewed.
 Proteasomes exist in mammalian cells in multiple combinatorial variants due to the diverse regulatory particles and exchange of catalytic subunits. Here, using biotin carboxyl carrier domain of transcarboxylase from Propionibacterium shermanii fused with different proteasome subunits of catalytic and regulatory particles, we report comprehensive characterization of highly homogenous one-step purified human constitutive and immune 20S and 26S/30S proteasomes. Hydrolysis of a multiple sclerosis (MS) autoantigen, myelin basic protein (MBP), by engineered human proteasomes with different catalytic phenotypes, revealed that peptides which may be directly loaded on the HLA class I molecules are produced mainly by immunoproteasomes. We detected at least five MBP immunodominant core regions, namely, LPRHRDTGIL, SLPQKSHGR, QDENPVVHFF, KGRGLSLSRF and GYGGRASDY. All peptides, except QDENPVVHFF, which originates from the encephalitogenic MBP part, were associated with HLA I alleles considered to increase MS risk. Prediction of the affinity of HLA class I to this peptide demonstrated that MS-protective HLA-A*44 and -B*35 molecules are high-affinity binders, whereas MS-associated HLA-A*23, -A*24, -A*26 and -B*51 molecules tend to have moderate to low affinity. The HLA-A*44 molecules may bind QDENPVVHFF and its deamidated form in several registers with unprecedently high affinity, probably linking its distinct protective phenotype with thymic depletion of the repertoire of autoreactive cytotoxic T cells or induction of CD8+ regulatory T cells, specific to the encephalitogenic MBP peptide.
 Tumor necrosis factor-alpha (TNF-α) is a pleiotropic immune cytokine that belongs to the TNF superfamily of receptor ligands. The cytokine exists as either a transmembrane or a soluble molecule, and targets two distinct receptors, TNF-α receptor 1 (TNFR1) and TNF-α receptor 2 (TNFR2), which activate different signaling cascades and downstream genes. TNF-α cellular responses depend on its molecular form, targeted receptor, and concentration levels. TNF-α plays a multifaceted role in normal physiology that is highly relevant to human health and disease. In the central nervous system (CNS), this cytokine regulates homeostatic functions, such as neurogenesis, myelination, blood-brain barrier permeability and synaptic plasticity. However, it can also potentiate neuronal excitotoxicity and CNS inflammation. The pleiotropism of TNF-α and its various roles in the CNS, whether homeostatic or deleterious, only emphasizes the functional complexity of this cytokine. Anti-TNF-α therapy has demonstrated effectiveness in treating various autoimmune inflammatory diseases and has emerged as a significant treatment option for CNS autoimmune diseases. Nevertheless, it is crucial to recognize that the effects of this therapeutic target are diverse and complex. Contrary to initial expectations, anti-TNF-α therapy has been found to have detrimental effects in multiple sclerosis. This article focuses on describing the various roles, both physiological and pathological, of TNF-α in the CNS. Additionally, it discusses the specific disease processes that are dependent or regulated by TNF-α and the rationale of its use as a therapeutic target.
 BACKGROUND: The global rising prevalence and incidence of multiple sclerosis (MS) has been reported during the past decades. However, details regarding the evolution of MS burden have not been fully studied. This study aimed to investigate the global, regional, and national burden and temporal trends in MS incidence, deaths, and disability-adjusted life years (DALYs) from 1990 to 2019 using the age-period-cohort analysis. METHODS: We performed a secondary comprehensive analysis of incidence, deaths, and DALYs of MS by calculating the estimated annual percentage change from 1990 to 2019 obtained from the Global Burden of Disease (GBD) 2019 study. The independent age, period, and birth cohort effects were evaluated by an age-period-cohort model. RESULTS: In 2019, there were 59,345 incident MS cases and 22,439 MS deaths worldwide. The global number of incidences, deaths, and DALYs of MS followed an upward trend, whereas the age-standardized rates (ASR) slightly declined from 1990 to 2019. High socio-demographic index (SDI) regions had the highest ASR of incidences, deaths, and DALYs in 2019, while the rate of deaths and DALYs in medium SDI regions are the lowest. Six regions which include high-income North America, Western Europe, Australasia, Central Europe, and Eastern Europe had higher ASR of incidences, deaths, and DALYs than other regions in 2019. The age effect showed that the relative risks (RRs) of incidence and DALYs reached the peak at ages 30-39 and 50-59, respectively. The period effect showed that the RRs of deaths and DALYs increased with the period. The cohort effect showed that the later cohort has lower RRs of deaths and DALYs than the early cohort. CONCLUSION: The global cases of incidence, deaths, and DALYs of MS have all increased, whereas ASR has declined, with different trends in different regions. High SDI regions such as European countries have a substantial burden of MS. There are significant age effects for incidence, deaths, and DALYs of MS globally, and period effects and cohort effects for deaths and DALYs.
 Cyclophosphamide (CYC) may be an effective treatment in patients who fail first line therapy for severe central nervous system (CNS) inflammatory disorders including CNS vasculitis, neuromyelitis optica, autoimmune encephalitis, tumefactive and aggressive multiple sclerosis (MS). We performed a retrospective analysis of 46 patients treated with CYC after failing first line therapy for severe CNS inflammatory conditions. Primary outcomes included modified Rankin Scale (mRS) for patients classified into a non-MS group, Expanded Disability Status Score (EDSS) for MS patients, and Targeted Neurological Deficit score (TND) for all patients. Secondary outcome included neuroimaging studies following CYC treatment. By the second follow up period (average of 7 months) mRS in the non-MS group improved from 3.7 to 2.2 and EDSS in the MS group improved from 5.6 to 3.8. Average TND score at 7 months was 2.8 (mild-marked improvement). At first follow up (average 5.6 months), 76.2% (32/42) patients had either stable or improving imaging, and 83.3% (30/36) patients had stable or improving imaging at second follow up (average 13.6 months). Adverse events were reported by 31.9% of patients with most common being nausea and vomiting, headache, alopecia, and hyponatremia. Treatment with CYC can result in disease stabilization of severe CNS inflammatory diseases and is generally well tolerated.
 INTRODUCTION: Data on structural brain changes after infection with SARS-CoV-2 is sparse. We postulate multiple sclerosis as a model to study the effects of SARS-CoV-2 on brain atrophy due to the unique availability of longitudinal imaging data in this patient group, enabling assessment of intraindividual brain atrophy rates. METHODS: Global and regional cortical gray matter volumes were derived from structural MRIs using FreeSurfer. A linear model was fitted to the measures of the matching pre-SARS-CoV-2 images with age as an explanatory variable. The residuals were used to determine whether the post-SARS-CoV-2 volumes differed significantly from the baseline. RESULTS: Fourteen RRMS patients with a total of 113 longitudinal magnetic resonance images were retrospectively analyzed. We found no acceleration of brain atrophy after infection with SARS-CoV-2 for global gray matter volume (p = 0.17). However, on the regional level, parahippocampal gyri showed a tendency toward volume reduction (p = 0.0076), suggesting accelerated atrophy during or after infection. CONCLUSIONS: Our results illustrate the opportunity of using longitudinal MRIs from existing MS registries to study brain changes associated with SARS-CoV-2 infections. We would like to address the global MS community with a call for action to use the available cohorts, reproduce the proposed analysis, and pool the results.
 The study was designed to examine microglia morphology in early and late forms of multiple sclerosis (MS). Archival paraffin embedded tissue samples from 25 cases were examined immunohistochemically. Pío del Río Hortega reported that phagocytes in acute focal destructive CNS lesions develop from microglia with no early contribution from infiltrating monocytes. In this study, we were unable to identify the changes cited by del Río Hortega in support of his theory. Instead, myelin phagocytes in MS appear to originate chiefly from infiltrating monocytes. In 4 cases, walls composed of MHC class II antigen-positive "wall microglia" were observed at plaque margins separating demyelinated and bordering myelinated tissue. Wall microglia in 2 plaques were accompanied by AQP4-positive fiber-forming astrocytes. In chronic but not early disease MS cases, microglia were seen to interact with infiltrating monocytes to form microglial nodules of several types. Also, MHC II-positive "activated" microglia in bordering intact tissue were exceptionally prominent where there was little evidence of ongoing myelin loss. It is concluded that myelin phagocytes in MS derive entirely from infiltrating MRP14-positive monocytes and not from resident microglia and that Río Hortega's microglia play an anti-inflammatory role in MS and not the destructive role favored by the current literature.
 Multiple sclerosis (MS) is a debilitating chronic disease of unknown etiology. There are limited treatment options due to an incomplete understanding of disease pathology. The disease is shown to have seasonal exacerbation of clinical symptoms. The mechanisms of such seasonal worsening of symptoms remains unknown. In this study, we applied targeted metabolomics analysis of serum samples using LC-MC/MC to determine seasonal changes in metabolites throughout the four seasons. We also analyzed seasonal serum cytokine alterations in patients with relapsed MS. For the first time, we can demonstrate seasonal changes in various metabolites in MS compared to the control. More metabolites were affected in MS in the fall season followed by spring, while summer MS was characterized by the smallest number of affected metabolites. Ceramides were activated in all seasons, suggesting their central role in the disease pathogenesis. Substantial changes in glucose metabolite levels were found in MS, indicating a potential shift to glycolysis. An increased serum level of quinolinic acid was demonstrated in winter MS. Histidine pathways were affected, suggesting their role in relapse of MS in the spring and fall. We also found that spring and fall seasons had a higher number of overlapping metabolites affected in MS. This could be explained by patients having a relapse of symptoms during these two seasons.
 Compelling evidence indicates that Epstein Barr virus (EBV) infection is a prerequisite for multiple sclerosis (MS). The disease may arise from a complex interplay between latent EBV infection, genetic predisposition, and various environmental and lifestyle factors that negatively affect immune control of the infection. Evidence of gene-environment interactions and epigenetic modifications triggered by environmental factors in genetically susceptible individuals supports this view. This review gives a short introduction to EBV and host immunity and discusses evidence indicating EBV as a prerequisite for MS. The role of genetic and environmental risk factors, and their interactions, in MS pathogenesis is reviewed and put in the context of EBV infection. Finally, possible preventive measures are discussed based on the findings presented.
 This study comprehensively addresses the involvement of the protein CKLF-like Marvel transmembrane domain-containing family member 5 (CMTM5) in the context of demyelination and cytodegenerative autoimmune diseases, particularly multiple Sclerosis (MS). An observed reduction in CMTM5 expression in post-mortem MS lesions prompted further investigations in both in vitro and in vivo animal models. In the cuprizone animal model, we detected a decrease in CMTM5 expression in oligodendrocytes that is absent in other members of the CMTM protein family. Our findings also confirm these results in the experimental autoimmune encephalomyelitis (EAE) model with decreased CMTM5 expression in both cerebellum and spinal cord white matter. We also examined the effects of a Cmtm5 knockdown in vitro in the oligodendroglial Oli-neu mouse cell line using the CRISPR interference technique. Interestingly, we found no effects on cell response to thapsigargin-induced endoplasmic reticulum (ER) stress as determined by Atf4 activity, an indicator of cellular stress responses. Overall, these results substantiate previous findings suggesting that CMTM5, rather than contributing to myelin biogenesis, is involved in maintaining axonal integrity. Our study further demonstrates that the knockdown of Cmtm5 in vitro does not modulate oligodendroglial responses to ER stress. These results warrant further investigation into the functional role of CMTM5 during axonal degeneration in the context of demyelinating conditions.

 BACKGROUND: Data are sparse regarding the safety of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines in patients with multiple sclerosis (MS). OBJECTIVE: To estimate (1) the pooled proportion of MS patients experiencing relapse among vaccine recipients; (2) the rate of transient neurological worsening, adverse events, and serious adverse events; (3) the previous outcomes of interest for different SARS-CoV-2 vaccine types. METHODS: Systematic review and meta-analysis of pharmacovigilance registries and observational studies. RESULTS: Nineteen observational studies comprising 14,755 MS patients who received 23,088 doses of COVID-19 vaccines were included. Mean age was 43.3 years (95% confidence interval (CI): 40-46.6); relapsing-remitting, secondary-progressive, primary-progressive MS and clinically isolated syndrome were diagnosed in 82.6% (95% CI: 73.9-89.8), 12.6% (95% CI: 6.3-20.8), 6.7% (95% CI: 4.2-9.9), and 2.9% (95% CI: 1-5.9) of cases, respectively. The pooled proportion of MS patients experiencing relapse at a mean time interval of 20 days (95% CI: 12-28.2) from vaccination was 1.9% (95% CI: 1.3%-2.6%; I(2) = 78%), with the relapse risk being independent of the type of administered SARS-CoV-2-vaccine (p for subgroup differences = 0.7 for messenger RNA (mRNA), inactivated virus, and adenovector-based vaccines). After vaccination, transient neurological worsening was observed in 4.8% (95% CI: 2.3%-8.1%) of patients. Adverse events and serious adverse events were reported in 52.8% (95% CI: 46.7%-58.8%) and 0.1% (95% CI: 0%-0.2%) of vaccinations, respectively. CONCLUSION: COVID-19 vaccination does not appear to increase the risk of relapse and serious adverse events in MS. Weighted against the risks of SARS-CoV-2-related complications and MS exacerbations, these safety data provide compelling pro-vaccination arguments for MS patients.
 Multiple sclerosis (MS) is an autoimmune inflammatory and neurodegenerative disease of the central nervous system (CNS) with increasing incidence and prevalence. MS is associated with inflammatory and metabolic disturbances that, as preliminary human and animal data suggest, might be mediated by disruption of circadian rhythmicity. Nutrition habits can influence the risk for MS, and dietary interventions may be effective in modulating MS disease course. Chronotherapeutic approaches such as time-restricted eating (TRE) may benefit people with MS by stabilizing the circadian clock and restoring immunological and metabolic rhythms, thus potentially counteracting disease progression. This review provides a summary of selected studies on dietary intervention in MS, circadian rhythms, and their disruption in MS, including clock gene variations, circadian hormones, and retino-hypothalamic tract changes. Furthermore, we present studies that reported diurnal variations in MS, which might result from circadian disruption. And lastly, we suggest how chrononutritive approaches like TRE might counteract MS disease activity.
 BACKGROUND: Vaccination in patients with multiple sclerosis (MS) treated with immunosuppressive drugs is highly recommended. Regarding COVID-19 vaccination, no specific concern has been raised. OBJECTIVES: We aimed to evaluate if COVID-19 vaccination or infection increased the risk of disease activity, either radiological or clinical, with conversion to MS in a cohort of people with a radiologically isolated syndrome (RIS). METHODS: This multicentric observational study analyzed patients in the RIS Consortium cohort during the pandemic between January 2020 and December 2022. We compared the occurrence of disease activity in patients according to their vaccination status. The same analysis was conducted by comparing patients' history of COVID-19 infection. RESULTS: No difference was found concerning clinical conversion to MS in the vaccinated versus unvaccinated group (6.7% vs 8.5%, p > 0.9). The rate of disease activity was not statistically different (13.6% and 7.4%, respectively, p = 0.54). The clinical conversion rate to MS was not significantly different in patients with a documented COVID-19 infection versus non-infected patients. CONCLUSION: Our study suggests that COVID-19 infection or immunization in RIS individuals does not increase the risk of disease activity. Our results support that COVID-19 vaccination can be safely proposed and repeated for these subjects.
 INTRODUCTION AND OBJECTIVE: While part of the care for neurological patients is done by telephone, it is not well known what neurological diseases and which part of that care is provided by telephone. Our goal is to find it out through a bibliographic review. MATERIALS AND METHODS: References on telephone care for neurological diseases accessible through the PubMed, Embase, and Cochrane platforms have been systematically reviewed, with an unspecified start date and up to March 2022. We found 618 references, and as 219 did not pass the exclusion criteria, 399 were finally included in the review. RESULTS: Dementia is the area of neurology with more publications about its telephone assistance. It is followed by stroke, head trauma, multiple sclerosis, Parkinson's disease and movement disorders, epilepsy, neuromuscular disorders, and others. DISCUSSION AND CONCLUSIONS: Dementias are the diseases with more bibliographic references on their telephone assistance despite not being the most prevalent. The telephone is frequently used to administer diagnostic scales or support caregivers and is particularly useful in diseases that limit mobility and attending a medical practice.
 BACKGROUND: Relatively little is known about how global and regional brain volumes changes in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) compare with Multiple Sclerosis (MS), Neuromyelitis optica spectrum disorder (NMOSD), and healthy controls (HC). OBJECTIVE: To compare global and regional brain volumes in MOGAD, MS, NMOSD, and HC cross-sectionally as well as longitudinally in a subset of patients. METHODS: We retrospectively reviewed all adult MOGAD and NMOSD patients with brain MRI performed in stable remission and compared them with MS patients and HC. Volumetric parameters were assessed using the FDA-approved icobrain software. adjusted for age and sex. RESULTS: Twenty-four MOGAD, 47 NMOSD, 40 MS patients, and 37 HC were included in the cross-sectional analyses. Relative to HC, the age-adjusted whole brain (WB) volume was significantly lower in patients with MOGAD (p=0.0002), NMOSD (p=0.042), and MS (p=0.01). Longitudinal analysis of a subset of 8 MOGAD, 22 NMOSD, and 34 MS patients showed a reduction in the WB and cortical gray matter (CGM) volumes over time in all three disease groups, without statistically significant differences between groups. The MOGAD group had a greater loss of thalamic volume compared to MS (p=0.028) and NMOSD (p=0.023) and a greater loss of hippocampal volumes compared to MS (p=0.007). CONCLUSIONS: Age-adjusted WB volume loss was evident in all neuroinflammatory conditions relative to HC in cross-sectional comparisons. In longitudinal analyses, MOGAD patients had a higher thalamic atrophy rate relative to MS and NMOSD, and a higher hippocampal atrophy rate relative to MS. Larger studies are needed to validate these findings and to investigate their clinical implications.
 OBJECTIVE: To assess marked central canal T2-hyperintensity in patients with myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) myelitis compared to myelitis patients with aquaporin-4-antibody-positive neuromyelitis optica spectrum disorder (AQP4 + NMOSD) and multiple sclerosis (MS). MATERIAL/METHODS: Two blinded raters evaluated spinal cord magnetic resonance imaging (MRIs) of myelitis patients with MOGAD (n = 63), AQP4 + NMOSD (n = 37), and MS (n = 26), assessing for marked central canal T2-hyperintensity and its evolution. If there were conflicting results, a third neurologist assessed the MRI. RESULTS: Marked central canal T2-hyperintensity was more frequent in patients with MOGAD (18/63[29%]) than MS (1/26[4%]; p = 0.01) myelitis but did not differ from AQP4 + NMOSD (13/37[35%]; p = 0.49). Marked central canal T2-hyperintensity had completely resolved on follow-up axial MRI for most MOGAD (12/14[86%]) and AQP4 + NMOSD (10/10[100%]; p = 0.49) patients. CONCLUSIONS: Marked central canal T2-hyperintensity is a common transient radiologic accompaniment of MOGAD and AQP4 + NMOSD myelitis, but not MS myelitis.
 The reinforcer pathology model posits that core behavioral economic mechanisms, including delay discounting and behavioral economic demand, underlie adverse health decisions and related clinical disorders. Extensions beyond substance use disorder and obesity, however, are limited. Using a reinforcer pathology framework, this study evaluates medical adherence decisions in patients with multiple sclerosis. Participants completed behavioral economic measures, including delay discounting, probability discounting, and a medication purchase task. A medical decision-making task was also used to evaluate how sensitivity to mild side effect risk and efficacy contributed to the likelihood of taking a hypothetical disease-modifying therapy. Less steep delay discounting and more intense (greater) medication demand were independently associated with greater adherence to the medication decision-making procedure. More generally, the pattern of interrelations between the medication-specific and general behavioral economic metrics was consistent with and contributes to the reinforcer pathology model. Additional research is warranted to expand these models to different populations and health behaviors, including those of a positive health orientation (i.e., medication adherence).
 BACKGROUND: The earliest detection of progressive multifocal leukoencephalopathy (PML) is crucial in Natalizumab (NTZ)-treated Multiple Sclerosis (MS) patients. This study aims to assess serum Neurofilaments (sNFL) ability to early detect PML in longitudinal patients' follow-up. METHODS: NFL were retrospectively measured in four PML cases occurred at the Regional Referring Center for MS (CRESM, Italy), in samples collected since one year before PML diagnosis, at PML diagnosis, during PML and in post-PML follow-up. sNFL levels were interpreted according to previously defined reference values. Clinical examination and EDSS were performed at each NTZ infusion. Routinary MRI was undertaken every six months; after PML diagnosis, MRI was performed according to clinical evaluation. sNFL were also measured in 45 NTZ-treated patients experiencing NEDA-3 status for at least 12 months. RESULTS: Patients showed different PML onsets and manifestations: in 3 patients routinary brain MRI revealed radiological signs of PML preceding different clinical manifestations, while in one patient brain MRI was performed after the clinical onset. PML diagnosis was defined at the time of the first detection of JCV DNA in cerebrospinal fluid. The following different PML phases were considered: 1. Basal (up to 4 months before PML diagnosis): sNFL values were in the normal range in all patients' samples, except for one (median 9.1 pg/ml, range 6.2-15.1 pg/ml) 2. Pre-PML (within 3 months before PML diagnosis): sNFL were elevated in all available samples (median 19.50 pg/ml, range 15.50-33.80 pg/ml). 3. PML diagnosis: sNFL were elevated in all patients (median 59.20 pg/ml, range 11.1-101.50 pg/ml). 4. PML/IRIS: during this phase, sNFL levels reached their peak (median 96.35 pg/ml, range 20.5-272.9) in all patients. 5. Post-PML (recovery phase, starting from the first MRI without enhancement, up to the end of follow-up): sNFL levels showed a decrease (median 12.80 pg/ml, range 9.30-30.60); however, based on reference values, sNFL were still elevated in 2 out of 4 patients at the end of their follow-up (622 and 887 days after PML diagnosis). sNFL were always elevated when MRI scan suggested a suspicious of PML. In NEDA-3 patients, sNFL levels were in the normal range in all patients' samples (median 4.7 pg/ml, range 1.4-8.6 pg/ml). CONCLUSION: Elevated sNFL were observed not only at PML diagnosis, but also in pre-PML phase. At PML recovery, sNFL weren't normalized in all patients' samples, suggesting ongoing neuronal degeneration. sNFL represent a reliable biomarker and should be introduced in clinical practice as an additional/alternative parameter to MRI to early detect and monitor PML.
 In carefully selected patients, autologous haematopoietic stem cell transplantation (HSCT) is a safe, highly effective and cost-saving treatment modality for treatment-resistant, and potentially treatment-naïve, immune-mediated neurological disorders. Although the evidence base has been growing in the last decade, limited understanding has led to confusion, mistrust and increasing use of health tourism. In this article, we discuss what autologous HSCT is, which immune-mediated conditions can be treated with it, how to select patients, what are the expected outcomes and potential adverse effects, and how cost-effective this treatment is.
 Movement slowness is a common and disruptive symptom of multiple sclerosis (MS). A potential cause is that individuals with MS slow down to conserve energy as a behavioral adjustment to heightened metabolic costs of movement. To investigate this prospect, we measured the metabolic costs of both walking and seated arm reaching at five speeds in persons with mild MS (pwMS; n = 13; 46.0 ± 7.7 yr) and sex- and age-matched controls (HCs; n = 13; 45.8 ± 7.8 yr). Notably, the cohort of pwMS was highly mobile and no individuals required a cane or aid when walking. We found that the net metabolic power of walking was approximately 20% higher for pwMS across all speeds (P = 0.0185). In contrast, we found no differences in the gross power of reaching between pwMS and HCs (P = 0.492). Collectively, our results suggest that abnormal slowness of movement in MS-particularly reaching-is not the consequence of heightened effort costs and that other sensorimotor mechanisms are playing a considerable role in slowing.NEW & NOTEWORTHY Individuals with multiple sclerosis (MS) often move more slowly than those without the disease. A possible cause is that movements in MS are more energetically expensive and slowing is an adaptation to conserve metabolic resources. Here, we find that while walking is more costly for persons with MS, arm-reaching movements are not. These results bring into question the driving force of movement slowness in MS and implicate other motor-related networks contributing to slowing.
 BACKGROUND: Multiple sclerosis is a chronic immune-mediated disease of the brain and spinal cord resulting in physical and cognitive impairment in young adults. It is hypothesized that a disrupted bacterial and viral gut microbiota is a part of the pathogenesis mediating disease impact through an altered gut microbiota-brain axis. The aim of this study is to explore the characteristics of gut microbiota in multiple sclerosis and to associate it with disease variables, as the etiology of the disease remains only partially known. METHODS: Here, in a case-control setting involving 148 Danish cases with multiple sclerosis and 148 matched healthy control subjects, we performed shotgun sequencing of fecal microbial DNA and associated bacterial and viral microbiota findings with plasma cytokines, blood cell gene expression profiles, and disease activity. RESULTS: We found 61 bacterial species that were differentially abundant when comparing all multiple sclerosis cases with healthy controls, among which 31 species were enriched in cases. A cluster of inflammation markers composed of blood leukocytes, CRP, and blood cell gene expression of IL17A and IL6 was positively associated with a cluster of multiple sclerosis-related species. Bacterial species that were more abundant in cases with disease-active treatment-naïve multiple sclerosis were positively linked to a group of plasma cytokines including IL-22, IL-17A, IFN-β, IL-33, and TNF-α. The bacterial species richness of treatment-naïve multiple sclerosis cases was associated with number of relapses over a follow-up period of 2 years. However, in non-disease-active cases, we identified two bacterial species, Faecalibacterium prausnitzii and Gordonibacter urolithinfaciens, whose absolute abundance was enriched. These bacteria are known to produce anti-inflammatory metabolites including butyrate and urolithin. In addition, cases with multiple sclerosis had a higher viral species diversity and a higher abundance of Caudovirales bacteriophages. CONCLUSIONS: Considerable aberrations are present in the gut microbiota of patients with multiple sclerosis that are directly associated with blood biomarkers of inflammation, and in treatment-naïve cases bacterial richness is positively associated with disease activity. Yet, the finding of two symbiotic bacterial species in non-disease-active cases that produce favorable immune-modulating compounds provides a rationale for testing these bacteria as adjunct therapeutics in future clinical trials.
 BACKGROUND AND OBJECTIVES: Patients with multiple sclerosis (PwMS) receiving extended dosing of rituximab (RTX) have exhibited no return of disease activity, which suggests that maintenance of deep depletion of circulating B cells is not necessary to maintain the efficacy of RTX in MS. METHODS: This was a prospective monocentric observational study including all consecutive PwMS who started or continued RTX after 2019, when the medical staff decided to extend the dosing interval up to 24 months for all patients. Circulating B-cell subsets were monitored regularly and systematically in case of relapse. The first extended interval was analyzed. RESULTS: We included 236 PwMS (81% with relapsing-remitting MS; mean [SD] age 43 [12] years; median [range] EDSS score 4 [0-8]; mean relapse rate during the year before RTX start 1.09 [0.99]; 41.5% with MRI activity). The median number of RTX infusions before extension was 4 (1-13). At the time of the analysis, the median delay in dosing was 17 months (8-39); the median proportion of circulating CD19(+) B cells was 7% (0-25) of total lymphocytes and that of CD27(+) memory B cells was 4% (0-16) of total B cells. The mean annual relapse rate did not differ before and after the extension: 0.03 (0.5) and 0.04 (0.15) (p = 0.51). Similarly, annual relapse rates did not differ before and after extension in patients with EDSS score ≤3 (n = 79) or disease duration ≤5 years (n = 71) at RTX onset. During the "extended dosing" period, MRI demonstrated no lesion accrual in 228 of the 236 patients (97%). Five patients experienced clinical relapse, which was confirmed by MRI. In these patients, the level of B-cell subset reconstitution at the time of the relapse did not differ from that for patients with the same extension window. DISCUSSION: The efficacy of RTX outlasted substantial reconstitution of circulating B cells in PwMS, which suggests that renewal of the immune system underlies the prolonged effect of RTX in MS. These findings suggest that extended interval dosing of RTX that leads to a significant reconstitution of circulating B cells is safe in PwMS, could reduce the risk of infection, and could improve vaccine efficacy.
 This study employed systems biology and high-throughput technologies to analyze complex molecular components of MS pathophysiology, combining data from multiple omics sources to identify potential biomarkers and propose therapeutic targets and repurposed drugs for MS treatment. This study analyzed GEO microarray datasets and MS proteomics data using geWorkbench, CTD, and COREMINE to identify differentially expressed genes associated with MS disease. Protein-protein interaction networks were constructed using Cytoscape and its plugins, and functional enrichment analysis was performed to identify crucial molecules. A drug-gene interaction network was also created using DGIdb to propose medications. This study identified 592 differentially expressed genes (DEGs) associated with MS disease using GEO, proteomics, and text-mining datasets. 37 DEGs were found to be important by topographical network studies, and 6 were identified as the most significant for MS pathophysiology. Additionally, we proposed six drugs that target these key genes. Crucial molecules identified in this study were dysregulated in MS and likely play a key role in the disease mechanism, warranting further research. Additionally, we proposed repurposing certain FDA-approved drugs for MS treatment. Our in silico results were supported by previous experimental research on some of the target genes and drugs. SIGNIFICANCE: As the long-lasting investigations continue to discover new pathological territories in neurodegeneration, here we apply a systems biology approach to determine multiple sclerosis's molecular and pathophysiological origin and identify multiple sclerosis crucial genes that contribute to candidating new biomarkers and proposing new medications.
 Multiple sclerosis (MS) is an incurable, progressive chronic autoimmune demyelinating disease. Therapy for MS is based on slowing down the processes of neurodegeneration and suppressing the immune system of patients. MS is accompanied by inflammation, axon-degeneration and neurogliosis in the central nervous system. One of the directions for a new effective treatment for MS is cellular, subcellular, as well as gene therapy. We investigated the therapeutic potential of adipose mesenchymal stem cell (ADMSC) derived, cytochalasin B induced artificial microvesicles (MVs) expressing nerve growth factor (NGF) on a mouse model of multiple sclerosis experimental autoimmune encephalomyelitis (EAE). These ADMSC-MVs-NGF were tested using histological, immunocytochemical and molecular genetic methods after being injected into the tail vein of animals on the 14th and 21st days post EAE induction. ADMSC-MVs-NGF contained the target protein inside the cytoplasm. Their injection into the caudal vein led to a significant decrease in neurogliosis at the 14th and 21st days post EAE induction. Artificial ADMSC-MVs-NGF stimulate axon regeneration and can modulate gliosis in the EAE model.
 Progressive multifocal leukoencephalopathy (PML) is a rare viral central nervous system (CNS) demyelinating disease primarily associated with a compromised immune system. PML is seen mainly in individuals with human immunodeficiency virus, lymphoproliferative disease, and multiple sclerosis. Patients on immunomodulators, chemotherapy, and solid organ or bone marrow transplants are predisposed to PML. Recognition of various PML-associated typical and atypical imaging abnormalities is critical for early diagnosis and differentiating it from other conditions, especially in high-risk populations. Early PML recognition should expedite efforts at immune-system restoration, allowing for a favorable outcome. This review aims to provide a practical overview of radiological abnormalities in PML patients and address differential considerations.
 Proteomics has the potential to identify pharmacodynamic (PD) biomarkers for similarity assessment of proposed biosimilars without relying on clinical efficacy end points. In this study, with 36 healthy participants randomized to therapeutic doses of interferon-beta 1a products (IFNβ-1a) or pegylated-IFNβ-1a (pegIFNβ-1a) approved to treat multiple sclerosis or placebo, we evaluated the utility of a proteomic assay that profiles > 7,000 plasma proteins. IFNβ-1a and pegIFNβ-1a resulted in 248 and 528 differentially expressed protein analytes, respectively, between treatment and placebo groups over the time course. Thirty-one proteins were prioritized based on a maximal fold change ≥ 2 from baseline, baseline adjusted area under the effect curve (AUEC) and overlap between the 2 products. Of these, the majority had a significant AUEC compared with placebo in response to either product; 8 proteins showed > 4-fold maximal change from baseline. We identified previously reported candidates, beta-2microglobulin and interferon-induced GTP-binding protein (Mx1) with ~ 50% coefficient of variation (CV) for AUEC, and many new candidates (including I-TAC, C1QC, and IP-10) with CVs ranging from 26%-129%. Upstream regulator analysis of differentially expressed proteins predicted activation of IFNβ1 signaling as well as other cytokine, enzyme, and transcription signaling networks by both products. Although independent replication is required to confirm present results, our study demonstrates the utility of proteomics for the identification of individual and composite candidate PD biomarkers that may be leveraged to support clinical pharmacology studies for biosimilar approvals, especially when biologics have complex mechanisms of action or do not have previously characterized PD biomarkers.
 BACKGROUND: The decline of humoral response to COVID-19 vaccine led to authorise a booster dose. Here, we characterised the kinetics of B-cell and T-cell immune responses in patients with multiple sclerosis (PwMS) after the booster dose. METHODS: We enrolled 22 PwMS and 40 healthcare workers (HCWs) after 4-6 weeks from the booster dose (T3). Thirty HCWs and 19 PwMS were also recruited 6 months (T2) after the first dose. Antibody response was measured by anti-receptor-binding domain (RBD)-IgG detection, cell-mediated response by an interferon (IFN)-γ release assay (IGRA), Th1 cytokines and T-cell memory profile by flow cytometry. RESULTS: Booster dose increased anti-RBD-IgG titers in fingolimod-treated, cladribine-treated and IFN-β-treated patients, but not in ocrelizumab-treated patients, although antibody titres were lower than HCWs. A higher number of fingolimod-treated patients seroconverted at T3. Differently, T-cell response evaluated by IGRA remained stable in PwMS independently of therapy. Spike-specific Th1-cytokine response was mainly CD4(+) T-cell-mediated, and in PwMS was significantly reduced (p<0.0001) with impaired IL-2 production compared with HCWs at T3. In PwMS, total Th1 and IFN-γ CD4(+) T-cell responders to spike protein were increased from T2 to T3.Compared with HCWs, PwMS presented a higher frequency of CD4(+) and CD8(+) terminally differentiated effector memory cells and of CD4(+) effector memory (T(EM)) cells, independently of the stimulus suggesting the association of this phenotype with MS status. CD4(+) and CD8(+) T(EM) cell frequency was further increased at T3 compared with T2. CONCLUSIONS: COVID-19 vaccine booster strengthens humoral and Th1-cell responses and increases T(EM) cells in PwMS.
 OBJECTIVES: This is the first study to estimate the prevalence and predictors of spouse and patient perceptions of global/overall personality change (PC) in patients with multiple sclerosis (MS). METHODS: 69 clinic patients and their spouses completed parallel measures of perceived PC and semantic differential scales measuring pre-MS and current specific behaviours. We correlated perceived personality changes with the following measures of perceived physical, cognitive, emotional, and social functioning: MS Impact Scale, MS Neuropsychological Questionnaire, Beck Depression Inventory-FastScreen; Hospital Anxiety and Depression Scale; Family Questionnaire, McMaster Assessment Device; and Social Provisions Scale. RESULTS: Spouses and patients reported comparable levels of substantial change. Both associated PC with patient distress, perceived cognitive impairment, spouse distress, and poorer family functioning. Spouse, but not patient, PC ratings predicted severity of physical symptoms and social support. Principal component analysis of semantic differential ratings yielded a Compassionate Empathy component correlating with PC within spouse, but not patient, data. CONCLUSIONS: These partially overlapping potential triggers for spouse and patient PC judgments raise questions about the extent they overlap with clinicians' criteria for PC, since spouses did not link impulsivity with PC. It is also suggested that the initial focus of treatment of PC should focus on partner-agreed changes.
 BACKGROUND: Pediatric patients with multiple sclerosis (POMS) and related disorders, clinically isolated syndrome (CIS), myelin oligodendrocyte glycoprotein antibody disorder (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD), are commonly treated with immunosuppressants. Understanding the impact of SARS-CoV-2 infection in patients may inform treatment decisions. OBJECTIVE: Characterize SARS-CoV-2 infection prevalence and severity among a cohort of patients with POMS and related disorders, as well as the impact of disease-modifying therapies (DMTs). METHODS: POMS and related disorders patients enrolled in a large, prospective registry were screened for COVID-19 during standard-of-care neurology visits. If confirmed positive of having infection, further analysis was undertaken. RESULTS: Six hundred and sixty-nine patients were surveyed between March 2020 and August 2021. There were 73 confirmed COVID-19 infections. Eight of nine hospitalized patients (89%), and all patients admitted to the ICU were treated with B cell depleting therapy. The unadjusted odds ratio of hospitalization among those who tested positive of having had COVID-19 was 15.27 among those on B-cell-depleting therapy (p = 0.016). CONCLUSIONS: B-cell-depleting treatment was associated with a higher risk of COVID-19, higher rates of hospitalization, and ICU admission, suggesting this therapy carries a higher risk of severe infection in POMS and related disorders.
 OBJECTIVES: To evaluate, in a Saudi Arabian context, how the COVID-19 pandemic psychologically impacted persons with multiple sclerosis (PwMS). METHODS: A cross-sectional study was undertaken during the period from October 2021 to March 2022. 738 participants resident in the Kingdom of Saudi Arabia (KSA) completed a self-administered online questionnaire. The research focused on persons diagnosed with MS. RESULTS: Participant ages spanned from 18 to over 55. The mean was 36.1±12.9 years old. Four hundred eighty-nine (66.3%) of the 738 participants were female. Two hundred sixty-four (35.8%) were single. Four hundred twelve (55.8%) were married. Six hundred eighty-five (92.8%) had received a COVID-19 vaccine. Regarding MS duration, 117 (15.9%) had been diagnosed for less than 2 years, 171 (23.2%) for 2-5 years, while 251 (34%) had the condition for 10 or more years. Regarding psychological health, 11.2% of participants complained of minimal/no depression, 33.3% of mild depression, 28.3% of moderate depression, and 27.1% of moderately severe to severe depression symptoms. Concerning anxiety, 17.2% of participants reported minimal anxiety, 36.9% mild, 23.3% moderate, while 22.6% suffered from severe anxiety symptoms. CONCLUSION: A high prevalence of depression and anxiety was found, along with high prevalence of co-occurrence of these disorders among PwMS.
 Multiple sclerosis (MS) is an immune-mediated, chronic inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS). Immune cell infiltration can lead to permanent activation of macrophages and microglia in the parenchyma, resulting in demyelination and neurodegeneration. Thus, neurodegeneration that begins with acute lymphocytic inflammation may progress to chronic inflammation. This chronic inflammation is thought to underlie the development of so-called smouldering lesions. These lesions evolve from acute inflammatory lesions and are associated with continuous low-grade demyelination and neurodegeneration over many years. Their presence is associated with poor disease prognosis and promotes the transition to progressive MS, which may later manifest clinically as progressive MS when neurodegeneration exceeds the upper limit of functional compensation. In smouldering lesions, in the presence of only moderate inflammatory activity, a toxic environment is clearly identifiable and contributes to the progressive degeneration of neurons, axons, and oligodendrocytes and, thus, to clinical disease progression. In addition to the cells of the immune system, the development of oxidative stress in MS lesions, mitochondrial damage, and hypoxia caused by the resulting energy deficit and iron accumulation are thought to play a role in this process. In addition to classical immune mediators, this chronic toxic environment contains high concentrations of oxidants and iron ions, as well as the excitatory neurotransmitter glutamate. In this review, we will discuss how these pathobiochemical markers and mechanisms, alone or in combination, lead to neuronal, axonal, and glial cell death and ultimately to the process of neuroinflammation and neurodegeneration, and then discuss the concepts and conclusions that emerge from these findings. Understanding the role of these pathobiochemical markers would be important to gain a better insight into the relationship between the clinical classification and the pathomechanism of MS.
 Demyelinating diseases alter myelin or the coating surrounding most nerve fibers in the central and peripheral nervous systems. The grouping of human central nervous system demyelinating disorders today includes multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) as distinct disease categories. Each disease is caused by a complex combination of genetic and environmental variables, many involving an autoimmune response. Even though these conditions are fundamentally similar, research into genetic factors, their unique clinical manifestations, and lesion pathology has helped with differential diagnosis and disease pathogenesis knowledge. This review aims to synthesize the genetic approaches that explain the differential susceptibility between these diseases, explore the overlapping clinical features, and pathological findings, discuss existing and emerging hypotheses on the etiology of demyelination, and assess recent pathogenicity studies and their implications for human demyelination. This review presents critical information from previous studies on the disease, which asks several questions to understand the gaps in research in this field.
 The COVID-19 pandemic had a profound impact on mental health symptoms and quality of life (QoL) in the general population due to necessary public health restrictions such as social distancing. The psychosocial effect of the pandemic on vulnerable groups such as people living with Multiple Sclerosis (PwMS) has been scarcely explored in countries with additional socioeconomical burdens such as access to healthcare disparities METHODS: A questionnaire exploring sociodemographic variables, quality of life, mental health determinants and sleep quality was applied to 92 PwMS to explore changes prior and during the pandemic regarding these domains RESULTS: 58.8% of the subjects were female, median age was 37.1 (± 8.5) years and relapsing-remitting MS was the predominant clinical subtype (83.5%). Unemployment rate significantly increased during the pandemic (12.3% vs 27.8%; p= 0.001). Only 46.4% received medical follow-up care during the pandemic. QoL was affected predominantly due to limitations in instrumented activities of daily life (IADL). Neuropsychiatric symptoms, requiring healthcare during the pandemic, anxiety prior to the pandemic and restricted IADL were predictors of MS-related physical impact worsening, while decreased physical/emotional wellbeing selfcare, neuropsychiatric symptoms, bad sleep quality, anxiety prior to the pandemic and restricted non-instrumental ADL predicted aggravation of MS-related psychological impact measured by the MSIS-29. Curiously, specific items regarding anxiety were more prevalent prior to the pandemic (anxious mood; p=0.02, helplessness; p=0.01), sleep problems; p=0.001 and cardiovascular symptoms; p=0.001, nevertheless, stability was observed for most items. Importantly, 77.3% of PwMS reported at least one neuropsychiatric symptom CONCLUSION: The deleterious effects of the COVID-19 pandemic on psychosocial wellbeing in PwMS, QoL and mental health outcomes are frequently overseen in vulnerable populations such as PwMS. Albeit the limitations of this study, our results may help implement policies that prevent negative outcomes on psychosocial wellbeing due to public health measures (e.g., social distancing) in MS and other neurological diseases that inexorably need constant follow-up.
 Current available treatments of Multiple Sclerosis (MS) reduce neuroinflammation acting on different targets on the immune system, but potentially lead to severe side effects and have a limited efficacy in slowing the progression of the disease. Here, we evaluated in vitro the immunomodulatory potential of a new class of nanoparticles - liposomes, constituted by a double-layer of phosphatidylserine (PSCho/PS), and double-faced, with an outer layer of phosphatidylserine and an inner layer of phosphatidic acid (PSCho/PA), either alone or in the presence of the myelin basic protein (MBP) peptide (residues 85-99) (PSCho/PS-MBP and PSCho/PA-MBP). Results showed that PSCho/PS are equally and efficiently internalized by pro- and anti-inflammatory macrophages (M1 and M2 respectively), while PSCho/PA were internalized better by M2 than M1. PSCho/PS liposomes were able to inhibit the secretion of innate pro-inflammatory cytokine IL-1β. PSCho/PS liposomes expanded Tregs, reducing Th1 and Th17 cells, while PSCho/PA liposomes were unable to dampen pro-inflammatory T cells and to promote immune-regulatory phenotype (Treg). The ability of PSCho/PS liposomes to up-regulate Treg cells was more pronounced in MS patients with high basal expression of M2 markers. PSCho/PS liposomes were more effective in decreasing Th1 (but not Th17) cells in MS patients with a disease duration >3 months. On the other hand, down-modulation of Th17 cells was evident in MS patients with active, Gadolinium enhancing lesions at MRI and in MS patients with a high basal expression of M1-associated markers in the monocytes. The same findings were observed for the modulation of MBP-driven Th1/Th17/Treg responses. These observations suggest that early MS associate to a hard-wired pro-Th1 phenotype of M1 that is lost later during disease course. On the other hand, acute inflammatory events reflect a temporary decrease of M2 phenotype that however is amenable to restauration upon treatment with PSCho/PS liposomes. Thus, together these data indicate that monocytes/macrophages may play an important regulatory function during MS course and suggest a role for PSCho/PS and PSCho/PS-MBP as new therapeutic tools to dampen the pro-inflammatory immune responses and to promote its regulatory branch.
 OBJECTIVES: Define the cutoff thresholds of the Kappa (K) and Lambda (L) free light chains (FLC) indices for the detection of intrathecal immunoglobulin synthesis (IIS) using the new K and L FLC ELISA from SEBIA. The reference technique, which is not readily standardized between laboratories, is based on the demonstration of oligoclonal banding (OCB) in cerebrospinal fluid (CSF) which is absent in serum. For the past 6 years, we have also routinely calculated the K FLC index using The Binding Site (TBS) reagents on an Optilite instrument, an approach increasingly used as an alternative and/or a complement to electrophoretic analysis. METHODS: We analyzed 391 serum/CSF pairs divided into three groups. The first group were cases without OCB and with normal albumin CSF/serum ratio (n=174). The second group were cases with specific OCB (n=73). The last group included patients with increased albumin CSF/sera ratio without OCB (n=142). RESULTS: Analysis of the first group determined that the cutoffs for detection of IIS are respectively 2.55 and 1.02 for the K FLC and L FLC indices. Of the 73 cases with IIS, only 2 had a K FLC index below this threshold (sensitivity of 97.26%), while 16 out of 73 cases (78.08%) and 13 out of 72 cases (81.94%) had an IgG and L FLC index below the cutoffs, respectively. Additionally, we illustrate equivalent performances for prediction of the presence of OCB between SEBIA and TBS methods. CONCLUSIONS: Sebia K FLC and L FLC assays are adequate alternative methods for the diagnosis of IIS.
 BACKGROUND AND PURPOSE: Optimal reporting is a critical element of scholarly communications. Several initiatives, such as the EQUATOR checklists, have raised authors' awareness about the importance of adequate research reports. On these premises, we aimed at appraising the reporting quality of published randomized controlled trials (RCTs) dealing with rehabilitation interventions. Given the breadth of such literature, we focused on rehabilitation for multiple sclerosis (MS), which was taken as a model of a challenging condition for all the rehabilitation professionals.A thematic methodological survey was performed to critically examine rehabilitative RCTs published in the last 2 decades in MS populations according to 3 main reporting themes: (1) basic methodological and statistical aspects; (2) reproducibility and responsiveness of measurements; and (3) clinical meaningfulness of the change. SUMMARY OF KEY POINTS: Of the initial 526 RCTs retrieved, 370 satisfied the inclusion criteria and were included in the analysis. The survey revealed several sources of weakness affecting all the predefined themes: among these, 25.7% of the studies complemented the P values with the confidence interval of the change; 46.8% reported the effect size of the observed differences; 40.0% conducted power analyses to establish the sample size; 4.3% performed retest procedures to determine the outcomes' reproducibility and responsiveness; and 5.9% appraised the observed differences against thresholds for clinically meaningful change, for example, the minimal important change. RECOMMENDATIONS FOR CLINICAL PRACTICE: The RCTs dealing with MS rehabilitation still suffer from incomplete reporting. Adherence to evidence-based checklists and attention to measurement issues and their impact on data interpretation can improve study design and reporting in order to truly advance the field of rehabilitation in people with MS.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1 available at: http://links.lww.com/JNPT/A424 ).
 Apoptosis is a natural physiological process that can maintain the homeostasis of the body and immune system. This process plays an important role in the system's resistance to autoimmune development. Because of the dysfunction of cell apoptosis mechanism, the number of autoreactive cells in the peripheral tissue increases along with their accumulation. This will lead to the development of autoimmune diseases, such as multiple sclerosis (MS). MS is an immune-mediated disease of the central nervous system characterized by severe white matter demyelination. Because of the complexity of its pathogenesis, there is no drug to cure it completely. Experimental autoimmune encephalomyelitis (EAE) is an ideal animal model for the study of MS. Carboplatin (CA) is a second-generation platinum anti-tumor drug. In this study, we attempted to assess whether CA could be used to ameliorate EAE. CA reduced spinal cord inflammation, demyelination, and disease scores in mice with EAE. Moreover, the number and proportion of pathogenic T cells especially Th1 and Th17 in the spleen and draining lymph nodes were reduced in CA-treated EAE mice. Proteomic differential enrichment analysis showed that the proteins related to apoptosis signal changed significantly after CA treatment. CFSE experiment showed that CA significantly inhibited the T cell proliferation. Finally, CA also induced apoptosis in activated T cells and MOG-specific T cells in vitro. Overall, our findings indicated that CA plays a protective role in the initiation and progression of EAE and has the potential to be a novel drug in the treatment of MS.
 In this study, we investigated whether regional distribution of white matter (WM) lesions, normal-appearing [NA] WM microstructural abnormalities and gray matter (GM) atrophy may differently contribute to cognitive performance in multiple sclerosis (MS) patients according to sex. Using the same scanner, brain 3.0T MRI was acquired for 287 MS patients (females = 173; mean age = 42.1 [standard deviation, SD = 12.7] years; relapsing-remitting = 196, progressive = 91; median Expanded Disability Status Scale = 2.5 [interquartile range, IQR = 1.5-5.0]; median disease duration = 12.1 [IQR = 6.3-19.0] years; treatment: none = 70, first-line = 130, second-line = 87) and 172 healthy controls (HC) (females = 92; mean age = 39.3 [SD = 14.8] years). MS patients underwent also Rao's neuropsychological battery. Using voxel-wise analyses, we investigated in patients sex-related differences in the association of cognitive performances with WM lesions, NAWM fractional anisotropy (FA) and GM volumes (p < 0.01, family-wise error [FWE]). Sixty-six female (38%) and 48 male (42%) MS patients were cognitively impaired, with no significant between-group difference (p = 0.704). However, verbal memory performance was worse in males (p = 0.001), whereas verbal fluency performance was worse in females (p = 0.004). In both sexes, a higher T2-hyperintense lesion prevalence in cognitively-relevant WM tracts was significantly associated with worse cognitive performance (p ≤ 0.006), with stronger associations in females than males in global cognition (p ≤ 0.004). Compared to sex-matched HC, male and female MS patients had widespread lower NAWM FA and GM volume (p < 0.01). In both sexes, worse cognitive performance was associated with widespread reduced NAWM FA (p < 0.01), with stronger associations in females than males in global cognition and verbal memory (p ≤ 0.009). Worse cognitive performance was significantly associated with clusters of cortical GM atrophy in males (p ≤ 0.007) and mainly with deep GM atrophy in females (p ≤ 0.006). In this study, only limited differences in cognitive performances were found between male and female MS patients. A disconnection syndrome due to focal WM lesions and diffuse NAWM microstructural abnormalities seems to be more relevant in female MS patients to explain cognitive impairment.
 BACKGROUND: Cognitive impairment is common in people living with neuromyelitis optica spectrum disease (NMOSD) and multiple sclerosis (MS). However, there is little published data on intelligence quotient (IQ) in NMOSD patients. Therefore, we performed the present study to compare IQ scores across NMOSD, MS, and control groups. METHOD: In this cross-sectional study, 49 NMOSD (30 with positive aquaporin4 antibody), 41 MS, and 20 control individuals were recruited. The IQ score for each person was measured using Wechsler Adult Intelligence Scale-Revised (WAIS-R). Participants were reported on eleven scores of subsets, verbal IQ (VIQ), performance IQ (PIQ), and full score IQ (FSIQ). RESULT: The scores of FSIQ, VIQ, PIQ, vocabulary, similarities, and digit-symbol in NMOSD and MS individuals were lower than the control group. Relative to control, NMOSD patients reported a lower score of information. We found no difference between NMOSD and MS groups, except in vocabulary and similarities. No significant difference between seropositive and seronegative NMOSD groups was observed except for the information and block design. In NMOSD group, a greater EDSS score was associated with decreased scores of FSIQ, VIQ, and PIQ. Being employed and being married were associated with greater scores of VIQ and PIQ, respectively. In both NMOSD and MS groups, advanced education was associated with increased scores of FSIQ and VIQ. CONCLUSION: Our study showed decreased IQ scores in NMOSD and MS. Further studies are required to examine intellectual quotient in people with NMOSD and MS.
 BACKGROUND: Remote activity monitoring has the potential to evaluate real-world, motor function, and disability at home. The relationships of daily physical activity with spinal cord white matter and gray matter (GM) areas, multiple sclerosis (MS) disability and leg function, are unknown. OBJECTIVE: Evaluate the association of structural central nervous system pathology with ambulatory disability. METHODS: Fifty adults with progressive or relapsing MS with motor disability who could walk >2 minutes were assessed using clinician-evaluated, patient-reported outcomes, and quantitative brain and spinal cord magnetic resonance imaging (MRI) measures. Fitbit Flex2, worn on the non-dominant wrist, remotely assessed activity over 30 days. Univariate and multivariate analyses were performed to assess correlations between physical activity and other disability metrics. RESULTS: Mean age was 53.3 years and median Expanded Disability Status Scale (EDSS) was 4.0. Average daily step counts (STEPS) were highly correlated with EDSS and walking measures. Greater STEPS were significantly correlated with greater C2-C3 spinal cord GM areas (ρ = 0.39, p = 0.04), total cord area (TCA; ρ = 0.35, p = 0.04), and cortical GM volume (ρ = 0.32, p = 0.04). CONCLUSION: These results provide preliminary evidence that spinal cord GM area is a neuroanatomical substrate associated with STEPS. STEPS could serve as a proxy to alert clinicians and researchers to possible changes in structural nervous system pathology.
 OBJECTIVE: To assess the characteristics of Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disorder (MOGAD) with brainstem involvement in the first event (BSIFE) and make comparisons with aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder (AQP4-IgG-NMOSD) and multiple sclerosis (MS). METHODS: From 2017 to 2022, this study identified MOG-IgG-positive patients with brainstem or both brainstem and cerebellum lesions in the first episode. As a comparison group, AQP4-IgG-NMOSD (n = 30) and MS (n = 30) patients with BSIFE were enroled. RESULTS: Thirty-five patients (35/146, 24.0%) were the BSIFE of MOGAD. Isolated brainstem episodes occurred in 9 of the 35 (25.7%) MOGAD patients, which was similar to MS (7/30, 23.3%) but was lower than AQP4-IgG-NMOSD (17/30, 56.7%, P = 0.011). Pons (21/35, 60.0%), medulla oblongata (20/35, 57.1%) and middle cerebellar peduncle (MCP, 19/35, 54.3%) were the most frequently affected areas. Intractable nausea (n = 7), vomiting (n = 8) and hiccups (n = 2) happened in MOGAD patients, but EDSS of MOGAD was lower than AQP4-IgG-NMOSD (P = 0.001) at the last follow-up. MOGAD patients with or without BSIFE did not significantly differ in terms of the ARR (P = 0.102), mRS (P = 0.823), or EDSS (P = 0.598) at the most recent follow-up. Specific oligoclonal bands appeared in MOGAD (13/33, 39.4%) and AQP4-IgG-NMOSD (7/24, 29.2%) in addition to MS (20/30, 66.7%). Fourteen MOGAD patients (40.0%) experienced relapse in this study. When the brainstem was involved in the first attack, there was an increased likelihood of a second attack occurring at the same location (OR=12.22, 95%CI 2.79 to 53.59, P = 0.001). If the first and second events were both in the brainstem, the third event was likely to occur at the same location (OR=66.00, 95%CI 3.47 to 1254.57, P = 0.005). Four patients experienced relapses after the MOG-IgG turned negative. CONCLUSION: BSIFE occurred in 24.0% of MOGAD. Pons, medulla oblongata and MCP were the most frequently involved regions. Intractable nausea, vomiting and hiccups occurred in MOGAD and AQP4-IgG-NMOSD, but not MS. The prognosis of MOGAD was better than AQP4-IgG-NMOSD. In contrast to MS, BSIFE may not indicate a worse prognosis for MOGAD. When patients with BSIFE, MOGAD tent to reoccur in the brainstem. Four of the 14 recurring MOGAD patients relapsed after the MOG-IgG test turned negative.
 BACKGROUND: Long-term B cell depletion with ocrelizumab in multiple sclerosis (MS) is associated with severe side effects such as hypogammaglobulinemia and infections. Our study therefore aimed to assess immunoglobulin levels under treatment with ocrelizumab and implement an extended interval dosing (EID) scheme. METHODS: Immunoglobulin levels of 51 patients with ≥24 months of treatment with ocrelizumab were analyzed. After ≥4 treatment cycles, patients chose to either continue on the standard interval dosing (SID) regimen (n = 14) or, in the case of clinically and radiologically stable disease, switch to B cell-adapted EID (n = 12, next dose at CD19(+) B cells >1% of peripheral blood lymphocytes). FINDINGS: Levels of immunoglobulin M (IgM) declined rapidly under ocrelizumab treatment. Risk factors for IgM and IgA hypogammaglobulinemia were lower levels at baseline and more previous disease-modifying therapies. B cell-adapted EID of ocrelizumab increased the mean time until next infusion from 27.3 to 46.1 weeks. Ig levels declined significantly in the SID group over 12 months but not in the EID group. Previously stable patients remained stable under EID as measured by expanded disability status scale (EDSS), neurofilament light chain, timed 25-foot walk (T25-FW), 9-hole peg test (9-HPT), symbol digit modalities test (SDMT), and multiple sclerosis impact scale (MSIS-29). CONCLUSIONS: In our pilot study, B cell-adapted EID of ocrelizumab prevented the decline of Ig levels without affecting disease activity in previously stable patients with MS. Based on these findings, we propose a new algorithm for long-term ocrelizumab treatment. FUNDING: This study was supported by the Deutsche Forschungsgemeinschaft (SFB CRC-TR-128, SFB 1080, and SFB CRC-1292) and the Hertie Foundation.
 INTRODUCTION: The understanding of the pathophysiology of multiple sclerosis (MS) has evolved alongside the characterization of cytokines and chemokines in cerebrospinal fluid (CSF) and serum. However, the complex interplay of pro- and anti-inflammatory cytokines and chemokines in different body fluids in people with MS (pwMS) and their association with disease progression is still not well understood and needs further investigation. Therefore, the aim of this study was to profile a total of 65 cytokines, chemokines, and related molecules in paired serum and CSF samples of pwMS at disease onset. METHODS: Multiplex bead-based assays were performed and baseline routine laboratory diagnostics, magnetic resonance imaging (MRI), and clinical characteristics were assessed. Of 44 participants included, 40 had a relapsing-remitting disease course and four a primary progressive MS. RESULTS: There were 29 cytokines and chemokines that were significantly higher in CSF and 15 in serum. Statistically significant associations with moderate effect sizes were found for 34 of 65 analytes with sex, age, CSF, and MRI parameters and disease progression. DISCUSSION: In conclusion, this study provides data on the distribution of 65 different cytokines, chemokines, and related molecules in CSF and serum in newly diagnosed pwMS.
 Th17/Treg imbalance is closely related to the occurrence and development of multiple sclerosis (MS), and the transdifferentiation of Th17 cells into Treg cells may contribute to the resolution of inflammation, presenting a therapeutic strategy for MS. To modulate this phenotypic shift in situ, a "Trojan horse"-like hybrid system, nanocapsule-coupled Th17 cells, is reported for MS treatment. Following intravenous injection into MS mice, the hybrid system efficiently transmigrates across the blood-brain barrier and homes to the inflamed MS niche. (Aminooxy)-acetic acid, a transdifferentiation inducer, is locally released upon the production of ROS and in turn taken up by Th17 cells. It is demonstrated that the Trojan horse hybrid system enables in situ phenotypic transdifferentiation of Th17 cells into anti-inflammatory Treg cells. This phenotypic conversion leads to a domino-like immune response that is conducive to MS therapy. Overall, this work highlights a new pathway for accurate modulation of the phenotypes of adoptively transferred cells in situ, from proinflammatory to anti-inflammatory for MS therapy, and may be broadly applicable for patients suffering from other autoimmune diseases.
 Several biomarkers from multiple sclerosis (MS) patients' biological fluids have been considered to support diagnosis, predict disease course, and evaluate treatment response. In this study, we assessed the CSF concentration of selected molecules implicated in the MS pathological process. To investigate the diagnostic and prognostic significance of CSF concentration of target candidate biomarkers in both relapsing (RMS, n = 107) and progressive (PMS, n = 18) MS patients and in other inflammatory (OIND, n = 10) and non-inflammatory (ONIND, n = 15) neurological disorders. We measured the CSF concentration of APRIL, BAFF, CHI3L1, CCL-2, CXCL-8, CXCL-10, CXCL-12, CXCL-13 through a Luminex Assay. MS patients were prospectively evaluated, and clinical and radiological activity were recorded. CHI3L1 and CXCL13 CSF levels were significantly higher in both MS groups compared to control groups, while CCL2, BAFF, and APRIL concentrations were lower in RMS patients compared to PMS and OIND. Considering RMS patients with a single demyelinating event, higher concentrations of CHI3L1, CXCL10, CXCL12, and CXCL13 were recorded in patients who converted to clinically defined MS(CDMS). RMS patients in the CXCL13 and CHI3L1 high concentration group had a significantly higher risk of relapse (HR 12.61 and 4.57), MRI activity (HR 7.04 and 2.46), and of any evidence of disease activity (HR 12.13 and 2.90) during follow-up. CSF CXCL13 and CHI3L1 levels represent very good prognostic biomarkers in RMS patients, and therefore can be helpful in the treatment choice. Higher CSF concentrations of neuro-inflammatory biomarkers were associated with a higher risk of conversion to CDMS in patients with a first clinical demyelinating event. Differential CSF BAFF and APRIL levels between RMS and PMS suggest a different modulation of B-cells pathways in the different phases of the disease.
 Background and Objectives: Neurofilament light chain (NfL) is a sensitive biomarker of neuroaxonal damage. This study aimed to assess the relationship between the annual change in plasma NfL (pNfL) and disease activity in the past year, as defined by the concept no evidence of disease activity (NEDA) in a cohort of multiple sclerosis (MS) patients. Materials and Methods: Levels of pNfL (SIMOA) were examined in 141 MS patients and analyzed in relationship to the NEDA-3 status (absence of relapse, disability worsening, and MRI activity) and NEDA-4 (NEDA-3 extended by brain volume loss ≤ 0.4%) during the last 12 months. Patients were divided into two groups: annual pNfL change with an increase of less than 10% (group 1), and pNfL increases of more than 10% (group 2). Results: The mean age of the study participants (n = 141, 61% females) was 42.33 years (SD, 10.17), and the median disability score was 4.0 (3.5-5.0). The ROC analysis showed that a pNfL annual change ≥ 10% correlates with the absence of the NEDA-3 status (p < 0.001; AUC: 0.92), and the absence of the NEDA-4 status (p < 0.001; AUC: 0.839). Conclusions: Annual plasma NfL increases of more than 10% appear to be a useful tool for assessing disease activity in treated MS patients.
 Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an exceptionally transmissible and pathogenic coronavirus that appeared at the end of 2019 and triggered a pandemic of acute respiratory disease, known as coronavirus disease 2019 (COVID-19). COVID-19 can evolve into a severe disease associated with immediate and delayed sequelae in different organs, including the central nervous system (CNS). A topic that deserves attention in this context is the complex relationship between SARS-CoV-2 infection and multiple sclerosis (MS). Here, we initially described the clinical and immunopathogenic characteristics of these two illnesses, accentuating the fact that COVID-19 can, in defined patients, reach the CNS, the target tissue of the MS autoimmune process. The well-known contribution of viral agents such as the Epstein-Barr virus and the postulated participation of SARS-CoV-2 as a risk factor for the triggering or worsening of MS are then described. We emphasize the contribution of vitamin D in this scenario, considering its relevance in the susceptibility, severity and control of both pathologies. Finally, we discuss the experimental animal models that could be explored to better understand the complex interplay of these two diseases, including the possible use of vitamin D as an adjunct immunomodulator to treat them.
 INTRODUCTION: Multiple sclerosis is associated with decrease in health-promoting behaviors (HPBs) and require appropriate nursing interventions. Telenursing can play an important role in education of patients during the COVID-19 pandemic in which face-to-face education is limited. This study aimed to investigate the effect of self-care education with telenursing approach on HPBs in patients with MS. MATERIALS AND METHODS: In this clinical trial, 68 patients with MS were selected using simple random sampling from Jahrom MS Society and randomly assigned to the intervention (n = 34) and control (n = 34) groups. In the intervention group, educational sessions were held three days a week for six weeks. Data were collected using demographic information and Walker's Health-Promoting Lifestyle questionnaires before and immediately after the intervention. Data were analyzed by Mann-Whitney and Wilcoxon tests using SPSS software (Ver. 21). RESULTS: Based on the findings, immediately after the intervention, the mean score of HPBs was significantly higher (p = 0.005) in the intervention group (145.38 ± 26.66) than the control group (129.18 ± 22.35). The means of nutrition, exercise, health responsibility, and stress management were significantly different between the intervention and control groups immediately after the intervention (p < 0.05). CONCLUSION: results this study indicated that self-care education with telenursing approach was effective on HPBs in patients with MS. It can be beneficial to employ as an educative-supportive approach in MS patients.
 Resveratrol is a natural polyphenol which may be useful for treating neurodegenerative diseases such as multiple sclerosis (MS). To date, current immunomodulatory treatments for MS aim to reduce inflammation with limited effects on the neurodegenerative component of this disease. The purpose of the current study is to develop a novel nanoparticle formulation of resveratrol to increase its solubility, and to assess its ability to prevent optic nerve and spinal cord degeneration in an experimental autoimmune encephalomyelitis (EAE) mouse model of MS. Resveratrol nanoparticles (RNs) were made using a thin rehydration technique. EAE mice received a daily oral administration of vehicle, RNs or unconjugated resveratrol for one month. They were assessed daily for clinical signs of paralysis and weekly for their visual acuity with optokinetic responses (OKR). After one month, their spinal cords and optic nerves were stained for inflammation and demyelination and retinal ganglion cells immunostained for Brn3a. RNs were stable for three months. The administration of RNs did not have any effect on clinical manifestation of EAE and did not preserve OKR scores but reduced the intensity of the disease. It did not reduce inflammation and demyelination in the spinal cord and the optic nerve. However, RNs were able to decrease RGC loss compared to the vehicle. Results demonstrate that resveratrol is neuroprotective by reducing RGC loss. Interestingly, neuroprotective effects and decreased disease severity occurred without reduction of inflammation or demyelination, suggesting this therapy may fill an unmet need to limit the neurodegenerative component of MS.
 BACKGROUND: While intravesical injections of botulinum neurotoxin A (BoNT-A) are currently recommended for patients experiencing refractory neurogenic overactive bladder and/or detrusor overactivity (OAB/DO), it is unclear how much this therapy is effective and sustainable in the long-term in patients with multiple sclerosis (MS). OBJECTIVES: To assess the mid-term continuation rate of BoNT-A injections to treat neurogenic OAB/DO in MS patients and to investigate MS-specific risk factors for discontinuation. METHODS: This retrospective study involved 11 French university hospital centers. All MS patients who received BoNT-A to treat neurogenic OAB/DO between 2008 and 2013 and were subsequently followed up for at least 5 years were eligible. RESULTS: Of the 196 MS patients included, 159 (81.1%) were still under BoNT-A 5 years after the first injection. The combination of the Expanded Disability Status Scale (EDSS < 6 or ⩾ 6) and of the MS type (relapsing-remitting vs progressive) predicted the risk of discontinuation. This risk was 5.5% for patients with no risk factor, whereas patients presenting with one or two risk factors were 3.3 and 5.7 times more likely to discontinue, respectively. CONCLUSION: BoNT-A is a satisfying mid-term neurogenic OAB/DO therapy for most MS patients. Combining EDSS and MS type could help predict BoNT-A discontinuation.
 PURPOSE: Physical activity (PA) participation offers many benefits for persons with multiple sclerosis (MS). Persons with MS are significantly less active than the general population; however, there is insufficient evidence regarding the association between geographical remoteness and PA participation in persons with MS. We identify PA levels across levels of rurality in an Australian MS population. MATERIALS AND METHODS: The Australian MS Longitudinal Study collects regular survey data from persons with MS in Australia, including demographic, clinical, and health behavioural data. Physical activity engagement was identified with the International Physical Activity Questionnaire-short form and geographical remoteness was identified from participants' postcode using the Access and Remoteness Index for Australia. Hurdle regression analysis examined the relationship between remoteness and PA participation, and level of PA, after controlling for confounding. RESULTS: Data from 1260 respondents showed that 24% of persons with MS did not participate in any PA. Remoteness was not associated with the participation in any PA (OR 1.04; 89% highest density probability interval (HDPI) estimate 0.88, 1.22). Amongst those with any PA (n = 960), those living in more remote areas had, on average, higher levels of PA (RR 1.21; 89% HDPI estimate 1.11, 1.34). CONCLUSIONS: Physical activity promotion does not need to differ based on geographical location. Implications for rehabilitationAlmost one quarter of persons with MS in our study recorded no participation in any physical activity (PA).Healthcare practitioners are encouraged to include the promotion of PA as part of MS management.Physical activity participation is similar for persons with MS across different geographical locations.Physical activity promotion does not need to differ based on geographical location.
 INTRODUCTION: Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS). The pathophysiology of MS is complex and is said to be influenced by multiple environmental determinants, including diet. We and others have previously demonstrated how consumption of bovine milk can aggravate disease severity in MS patients, which can be explained by molecular mimicry between milk antigens and those expressed within the CNS. In this study we set out to identify alternatives to drinking cow milk which might be less detrimental to MS patients who have a genetic predisposition towards developing antibody titers against bovine milk antigens that cross-react with CNS antigens. METHODS: To this end, we screened 35 patients with MS and 20 healthy controls for their IgG reactivity against an array of animal-sourced milk, plant-based alternatives as well as individual antigens from bovine milk. RESULTS: We demonstrate that MS patients have a significantly higher IgG response to animal-sourced milk, especially cow milk, in comparison to healthy donors. We also show that the reactivity to cow milk in MS patients can be attributed to reactivity against different bovine milk antigens. Finally, our correlation data indicate the co-existence of antibodies to individual bovine milk antigens and their corresponding cross-reactive CNS antigens. DISCUSSION: Taken together, we suggest screening of blood from MS patients for antibodies against different types of milk and milk antigens in order to establish a personalized diet regimen.
 A 62-year-old man with relapsing-remitting multiple sclerosis developed progressive multifocal leukencephalopathy (PML) after 6 years on fingolimod. The fingolimod was immediately discontinued and preexisting mirtazepine increased. Three weeks later, with brain magnetic resonance imaging (MRI) appearances worsening and cerebrospinal fluid (CSF) JC virus (JCV) titres increasing, maraviroc was introduced. At 6 weeks, subtle punctate contrast enhancement raised the possibility of immune reconstitution inflammatory syndrome (IRIS), followed by a single focal-to-generalised tonic clonic seizure and a further deterioration in clinical disability. Mefloquine was commenced alongside three doses of pembrolizumab administered a month apart. Serial CSF examinations and several imaging modalities including spectroscopy and fused FDG-PET-MRI (18F-fluoro-deoxy-glucose-positron emission tomography-magnetic resonance imaging) were used to help distinguish between PML, PML-IRIS and rebound MS activity and guide optimal management at each stage. A handful of small, enhancing ovoid lesions developed between the first two doses of pembrolizumab, probably representative of a mild rebound phenomenon. A sustained improvement became obvious thereafter with CSF JCV-DNA undetectable 16 weeks following fingolimod withdrawal. To our knowledge, this is the first case of combined therapy and use of pembrolizumab in a fingolimod-associated PML.
 BACKGROUND AND PURPOSE: This study was undertaken to investigate baseline peripapillary retinal nerve fiber layer (pRNFL) and macular ganglion cell and inner plexiform layer (GCIPL) thickness for prediction of disability accumulation in early relapsing multiple sclerosis (RMS). METHODS: From a prospective observational study, we included patients with newly diagnosed RMS and obtained spectral-domain optical coherence tomography scan within 90 days after RMS diagnosis. Impact of pRNFL and GCIPL thickness for prediction of disability accumulation (confirmed Expanded Disability Status Scale [EDSS] score ≥ 3.0) was tested by multivariate (adjusted hazard ratio [HR] with 95% confidence interval [CI]) Cox regression models. RESULTS: We analyzed 231 MS patients (mean age = 30.3 years, SD = 8.1, 74% female) during a median observation period of 61 months (range = 12-93). Mean pRNFL thickness was 92.6 μm (SD = 12.1), and mean GCIPL thickness was 81.4 μm (SD = 11.8). EDSS ≥ 3 was reached by 28 patients (12.1%) after a median 49 months (range = 9-92). EDSS ≥ 3 was predicted with GCIPL < 77 μm (HR = 2.7, 95% CI = 1.6-4.2, p < 0.001) and pRNFL thickness ≤ 88 μm (HR = 2.0, 95% CI = 1.4-3.3, p < 0.001). Higher age (HR = 1.4 per 10 years, p < 0.001), incomplete remission of first clinical attack (HR = 2.2, p < 0.001), ≥10 magnetic resonance imaging (MRI) lesions (HR = 2.0, p < 0.001), and infratentorial MRI lesions (HR = 1.9, p < 0.001) were associated with increased risk of disability accumulation, whereas highly effective disease-modifying treatment was protective (HR = 0.6, p < 0.001). Type of first clinical attack and presence of oligoclonal bands were not significantly associated. CONCLUSIONS: Retinal layer thickness (GCIPL more than pRNFL) is a useful predictor of future disability accumulation in RMS, independently adding to established markers.
 Multiple sclerosis (MS) is an inflammatory and demyelinating disease of the central nervous system (CNS) that remains incurable. Herein, we demonstrated that ilepcimide (Antiepilepsirine), an antiepileptic drug used for decades, protects mice from experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Our studies found that ilepcimide treatment effectively ameliorates demyelination, blood-brain barrier leakage and infiltration of CD4(+) and CD8(+) T cells in EAE mice. On the one hand, ilepcimide can inhibit dihydroorotate dehydrogenase (DHODH), an important therapeutic target for MS. Computer molecular docking, thermal shift and fluorescence quenching assay demonstrated the directly interaction between ilepcimide and DHODH. Accordingly, ilepcimide observably repressed T cell proliferation in mixed lymphocyte reaction (MLR) assay and concanavalin A (Con-A) model in a DHODH-dependent manner. On the other hand, ilepcimide exhibited neuroprotective effect possibly through activating NRF2 antioxidant pathway in mouse neural crest-derived Neuro2a cells. Collectively, our findings have revealed the therapeutic potential of ilepcimide in EAE mouse model via restricting inflammatory response and oxidative stress, offering a potential opportunity for repurposing existing drug ilepcimide for MS therapy.
 BACKGROUND: In multiple sclerosis (MS), pathological processes affecting brain gray (GM) and white matter (WM) are heterogeneous. OBJECTIVE: To apply a multimodal MRI approach to investigate the regional distribution of the different pathological processes occurring in the brain WM and GM of relapse-onset MS patients. METHODS: Fifty-seven MS patients (forty-two relapsing remitting [RR], fifteen secondary progressive [SP]) and forty-seven age- and sex-matched healthy controls (HC) underwent a multimodal 3 T MRI acquisition. Between-group voxel-wise differences of brain WM and GM volumes, magnetization transfer ratio (MTR), T(1)-weighted(w)/T(2)w ratio, intracellular volume fraction (ICV_f), and quantitative susceptibility mapping (QSM) maps were investigated. RESULTS: Compared to HC, RRMS showed significant WM, deep GM and cortical atrophy, significantly lower MTR and T(1)w/T(2)w ratio of periventricular and infratentorial WM, deep GM and several cortical areas, lower ICV_f in supratentorial and cerebellar WM and in some cortical areas, and lower QSM values in bilateral periventricular WM (p < 0.001). Compared to RRMS, SPMS patients showed significant deep GM and widespread cortical atrophy, significantly lower MTR of periventricular WM, deep GM and cerebellum, lower T(1)w/T(2)w ratio of fronto-temporal WM regions, lower ICV_f of some fronto-tempo-occipital WM and cortical areas. They also had increased QSM and T(1)w/T(2)w ratio in the pallidum, bilaterally (p < 0.001). CONCLUSION: A periventricular pattern of demyelination and widespread GM and WM neuro-axonal loss are detectable in RRMS and are more severe in SPMS. Higher T(1)w/T(2)w ratio and QSM in the pallidum, possibly reflecting iron accumulation and neurodegeneration, may represent a relevant MRI marker to differentiate SPMS from RRMS.
 BACKGROUND: There has yet to be an examination of how appointment attendance behaviors in multiple sclerosis (MS) are related to scheduling metrics and certain demographic, clinical, and behavioral factors such as cognitive functioning and personality traits. This study aimed to examine the factors that differ between no shows (NS), short notice cancellations (SNC), and attended appointments. METHODS: Participants (n = 110) were persons with MS who were enrolled in a larger cross-sectional study, during which they completed a battery of neuropsychological measures. Data about their appointments in three MS-related clinics the year prior to their study evaluation were extracted from the medical record. Bivariate analyses were done, with post-hoc tests conducted with Bonferroni corrections if there was an overall group difference. RESULTS: A higher number of SNC were noted during the winter, with 22.4% being due to the weather. SNC were also more common on Thursdays, but less frequent during the early morning time slots (7am to 9am). In contrast, NS were associated with lower annual income, weaker healthcare provider relationships, lower self-efficacy, higher levels of neuroticism, depressive symptom severity, and health distress, and greater cognitive difficulties, particularly with prospective memory. CONCLUSIONS: While SNC are related to clinic structure and situational factors like the weather, NS may be more influenced by behavioral issues, such as difficulty remembering an appointment and high levels of distress. These findings highlight potential targets for reducing the number of missed appointments in the clinic, providing opportunities for improved healthcare efficiency and most importantly health.
 BACKGROUND: Although distinct brain-homing B cells have been identified in multiple sclerosis (MS), it is unknown how these further evolve to contribute to local pathology. We explored B-cell maturation in the central nervous system (CNS) of MS patients and determined their association with immunoglobulin (Ig) production, T-cell presence, and lesion formation. METHODS: Ex vivo flow cytometry was performed on post-mortem blood, cerebrospinal fluid (CSF), meninges and white matter from 28 MS and 10 control brain donors to characterize B cells and antibody-secreting cells (ASCs). MS brain tissue sections were analysed with immunostainings and microarrays. IgG index and CSF oligoclonal bands were measured with nephelometry, isoelectric focusing, and immunoblotting. Blood-derived B cells were cocultured under T follicular helper-like conditions to evaluate their ASC-differentiating capacity in vitro. FINDINGS: ASC versus B-cell ratios were increased in post-mortem CNS compartments of MS but not control donors. Local presence of ASCs associated with a mature CD45(low) phenotype, focal MS lesional activity, lesional Ig gene expression, and CSF IgG levels as well as clonality. In vitro B-cell maturation into ASCs did not differ between MS and control donors. Notably, lesional CD4(+) memory T cells positively correlated with ASC presence, reflected by local interplay with T cells. INTERPRETATION: These findings provide evidence that local B cells at least in late-stage MS preferentially mature into ASCs, which are largely responsible for intrathecal and local Ig production. This is especially seen in active MS white matter lesions and likely depends on the interaction with CD4(+) memory T cells. FUNDING: Stichting MS Research (19-1057 MS; 20-490f MS), National MS Fonds (OZ2018-003).
 INTRODUCTION: In multiple sclerosis (MS), chronic disability primarily stems from axonal and neuronal degeneration, a condition resistant to conventional immunosuppressive or immunomodulatory treatments. Recent research has indicated that selective sphingosine-1-phosphate receptor S1PR-1 and -5 modulators yield positive effects in progressive MS and mechanistic models of inflammation-driven neurodegeneration and demyelination. METHODS: In this study, the S1PR-1/-5 modulator RP-101074 was evaluated as a surrogate for ozanimod in the non-inflammatory, primary degenerative animal model of light-induced photoreceptor loss (LI-PRL) in CX3CR1-GFP mice to assess potential neuroprotective effects, independent of its immunomodulatory mechanism of action. RESULTS: Prophylactic administration of RP-101074 demonstrated protective effects in the preclinical, non-inflammatory LI-PRL animal model, following a bell-shaped dose-response curve. RP-101074 treatment also revealed activity-modulating effects on myeloid cells, specifically, CX3CR1+ cells, significantly reducing the marked infiltration occurring one week post-irradiation. Treatment with RP-101074 produced beneficial outcomes on both retinal layer thickness and visual function as evidenced by optical coherence tomography (OCT) and optomotor response (OMR) measurements, respectively. Additionally, the myelination status and the quantity of neural stem cells in the optic nerve suggest that RP-101074 may play a role in the activation and/or recruitment of neural stem cells and oligodendrocyte progenitor cells, respectively. CONCLUSION/DISCUSSION: The data from our study suggest that RP-101074 may have a broader role in MS treatment beyond immunomodulation, potentially offering a novel approach to mitigate neurodegeneration, a core contributor to chronic disability in MS.
 MOTIVATION: Identifying and prioritizing disease-related proteins is an important scientific problem to develop proper treatments. Network science has become an important discipline to prioritize such proteins. Multiple sclerosis, an autoimmune disease for which there is still no cure, is characterized by a damaging process called demyelination. Demyelination is the destruction of myelin, a structure facilitating fast transmission of neuron impulses, and oligodendrocytes, the cells producing myelin, by immune cells. Identifying the proteins that have special features on the network formed by the proteins of oligodendrocyte and immune cells can reveal useful information about the disease. RESULTS: We investigated the most significant protein pairs that we define as bridges among the proteins providing the interaction between the two cells in demyelination, in the networks formed by the oligodendrocyte and each type of two immune cells (i.e. macrophage and T-cell) using network analysis techniques and integer programming. The reason, we investigated these specialized hubs was that a problem related to these proteins might impose a bigger damage in the system. We showed that 61%-100% of the proteins our model detected, depending on parameterization, have already been associated with multiple sclerosis. We further observed the mRNA expression levels of several proteins we prioritized significantly decreased in human peripheral blood mononuclear cells of multiple sclerosis patients. We therefore present a model, BriFin, which can be used for analyzing processes where interactions of two cell types play an important role. AVAILABILITY AND IMPLEMENTATION: BriFin is available at https://github.com/BilkentCompGen/brifin.
 Wobbly hedgehog syndrome (WHS) has been long considered to be a myelin disease primarily affecting the four-toed hedgehog. In this study, we have shown for the first time that demyelination is accompanied by extensive remyelination in WHS. However, remyelination is not enough to compensate for the axonal degeneration and neuronal loss, resulting in a progressive neurodegenerative disease reminiscent of progressive forms of multiple sclerosis (MS) in humans. Thus, understanding the pathological features of WHS may shed light on the disease progression in progressive MS and ultimately help to develop therapeutic strategies for both diseases.
 Disability in multiple sclerosis (MS) is driven in part by the failure of remyelination and progressive neurodegeneration. Microglia, and specifically triggering receptor expressed on myeloid cells 2 (TREM2), a factor highly expressed in microglia, have been shown to play an important role in remyelination. Here, using a focal demyelination model in the brain, we demonstrate that demyelination is persistent in TREM2 knockout mice, lasting more than 6 weeks after lysolecithin injection and resulting in substantial neurodegeneration. We also find that TREM2 knockout mice exhibit an altered glial response following demyelination. TREM2 knockout microglia demonstrate defects in migration and phagocytosis of myelin debris. In addition, human monocyte-derived macrophages from subjects with a TREM2 mutation prevalent in human disease also show a defect in myelin debris phagocytosis. Together, we highlight the central role of TREM2 signaling in remyelination and neuroprotection. These findings provide insights into how chronic demyelination might lead to axonal damage and could help identify novel neuroprotective therapeutic targets for MS.
 INTRODUCTION: Multiple sclerosis (MS) is the most frequent demyelinating disease of the central nervous system. Although there is currently no definite cure for MS, new therapies have recently been developed based on a continuous search for new biomarkers. DEVELOPMENT: MS diagnosis relies on the integration of clinical, imaging and laboratory findings as there is still no singlepathognomonicclinical feature or diagnostic laboratory biomarker. The most commonly laboratory test used is the presence of immunoglobulin G oligoclonal bands (OCB) in cerebrospinal fluid of MS patients. This test is now included in the 2017 McDonald criteria as a biomarker of dissemination in time. Nevertheless, there are other biomarkers currently in use such as kappa free light chain, which has shown higher sensitivity and specificity for MS diagnosis than OCB. In addition, other potential laboratory tests involved in neuronal damage, demyelination and/or inflammation could be used for detecting MS. CONCLUSIONS: CSF and serum biomarkers have been reviewed for their use in MS diagnosis and prognosis to stablish an accurate and prompt MS diagnosis, crucial to implement an adequate treatment and to optimize clinical outcomes over time.
 PURPOSE: Previous studies have shown that tetrahydrocannabinol (THC), the main psychoactive component of cannabis, can impair cognitive abilities. There is also some evidence that cannabidiol (CBD), the most abundant non-intoxicating constituent of cannabis, can attenuate these effects. The purpose of this study was to investigate the effects of THC:CBD oromucosal spray (with equal parts THC and CBD) on cognition compared with control conditions in human studies. METHODS: A systematic literature search was performed on four major bibliographic databases. Studies were included in the present review if they evaluated the cognitive effects of THC:CBD oromucosal spray compared with a control condition. RESULTS: Ten studies were identified (7 on patients with multiple sclerosis, 1 on those with Huntington, and 2 on healthy volunteers) with 510 participants in total. There was considerable heterogeneity among the studies in terms of dose and duration of administration. All studies have used an equal or nearly equal dose of THC and CBD. CONCLUSIONS: Although the results across studies were somewhat inconsistent, most evidence revealed that there is no significant difference between THC:CBD oromucosal spray and control treatments in terms of cognitive outcomes. However, more trials are needed with longer follow-up periods, and dose considerations, particularly comparing lower and higher doses of the spray.
 In recent decades, multiple sclerosis (MS) diseases have been significantly prevalent in some industrial areas of Iran, such as steel industrial areas in Isfahan province (central Iran). In this study, the environmental impacts of two steel mill factories in Isfahan province and their effects on the spread of MS in the region were investigated. To examine the extent of exposure, seasonal dust samples were collected from 15 sites around the two investigated factories. The annual dust deposition rate (DDR) was then determined and the concentrations of lead (Pb), cadmium (Cd), nickel (Ni), cobalt (Co), and manganese (Mn) in the dust samples were measured. Furthermore, the concentration of the mentioned elements was determined in the nail samples taken from 40 MS patients and 40 healthy people (control) living in the study region. The interpolated map extracted from the DDR values showed the highest dust deposition around the two studied steel factories, which decreases with increasing distance from them. The enrichment factor (EF) of heavy metals was the highest at the distance between the two steel factories, decreasing by moving away from them which indicate that these two steel factories are the source of investigated heavy metals in the region. The statistical analysis also revealed significant differences (P < 0.01) between the concentration of heavy metals measured in nail samples taken from MS patients and healthy people. The mean Pb concentration measured in the nail sample taken from MS patients was more than 18 times that of healthy people (93.45 and 5.02 mg/kg, respectively). These results revealed a buildup of heavy metals in the body of MS patients much more than usual, originating from the activities of two investigated steel companies in the region.

 PURPOSE: There is a gap in research on how best to support exercise in moderate to severe MS. The objective of this study is to share perspectives of people living with MS and physiotherapists on their experiences in a randomized clinical trial of online physiotherapy vs. an active comparator. METHODS: Semi-structured exit interviews were conducted with volunteer participants from the online and comparator arms of the trial, and focus groups were held with study physiotherapists. Transcripts were analyzed using reflexive thematic analysis. RESULTS: Perspectives from participants with MS yielded three themes: usability of their program, utility of their program, and motivation to participate. Visual and dexterity impairments limited the usability of the online program. Having an opportunity "to be pushed" was valued by participants in both trial arms. Motivation to exercise was variable, and participants desired periodic face-to-face contact with their physiotherapists. Perspectives from trial physiotherapists yielded similar and complementary findings concerning usability and utility. CONCLUSIONS: Participants with MS and physiotherapists found the online physiotherapy platform useful for supporting exercise, yet they identified some limitations. As the appeal of online platforms has increased since the pandemic, it will be important to consider the needs of people with moderate to severe MS. TRIAL REGISTRATION NUMBER: NCT03039400.IMPLICATIONS FOR REHABILITATIONPeople with moderate-to-severe MS and physiotherapists involved in a clinical trial found online physiotherapy useful for supporting exercise. Physiotherapists and participants using the online program desired improved platform accommodations for people living with MS with visual and dexterity impairments.Physiotherapists and people living with MS from both the online exercise program and comparator groups perceived a need for more face-to-face contact and opportunities to build therapeutic alliance.Perspectives from prescribing physiotherapists and people living with MS about supporting exercise online may have practice implications during and post-pandemic.
 The advent of highly effective disease modifying therapy has transformed the landscape of multiple sclerosis (MS) care over the last two decades. However, there remains a critical, unmet need for sensitive and specific biomarkers to aid in diagnosis, prognosis, treatment monitoring, and the development of new interventions, particularly for people with progressive disease. This review evaluates the current data for several emerging imaging and liquid biomarkers in people with MS. MRI findings such as the central vein sign and paramagnetic rim lesions may improve MS diagnostic accuracy and evaluation of therapy efficacy in progressive disease. Serum and cerebrospinal fluid levels of several neuroglial proteins, such as neurofilament light chain and glial fibrillary acidic protein, show potential to be sensitive biomarkers of pathologic processes such as neuro-axonal injury or glial-inflammation. Additional promising biomarkers, including optical coherence tomography, cytokines and chemokines, microRNAs, and extracellular vesicles/exosomes, are also reviewed, among others. Beyond their potential integration into MS clinical care and interventional trials, several of these biomarkers may be informative of MS pathogenesis and help elucidate novel targets for treatment strategies.
 The corpus callosum (CC) is the major commissure interconnecting the two hemispheres and is particularly affected in multiple sclerosis (MS). In the present review, we aimed to investigate the role played by callosal damages in the pathogenesis of MS-related dysfunctions and examine whether a model of callosal disconnection syndrome is a valid model for MS. For this purpose, we will first review structural and functional evidence of callosal pathology in MS. Second, we will account for the potential role of CC abnormalities in MS-related dysfunctions. Finally, we will report data concurring with a "multiple disconnection hypothesis" that has been proposed to explain those dysfunctions, and we will examine evidence pointing toward MS as a "callosal disconnection syndrome." We will end by discussing the contribution of this interpretation to the understanding of MS and MS-related deficits.
 INTRODUCTION: A contribution of neutrophil granulocytes to the pathogenesis of multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) is recognized. Anti-CD20 treatments applied in these diseases are associated with infectious complications and neutropenia. No data is available about functional characteristics of neutrophils obtained from patients with anti-CD20 treatments. METHODS: In neutrophils isolated from 13 patients with anti-CD20 treatment (9 MS, 4 NMOSD), 11 patients without anti-CD20 treatment (9 MS, 2 NMOSD) and 5 healthy controls, we analyzed chemotaxis, production of reactive oxygen species (ROS), phagocytosis, and formation of neutrophil extracellular traps (NET) in vitro. RESULTS: Chemotaxis and ROS production were found unchanged between patients with and without anti-CD20 treatment or between patients and healthy controls. We found a higher proportion of non-phagocytosing cells in patients without anti-CD20 treatment compared to patients with anti-CD20 treatment and healthy controls. As compared to healthy controls, a higher proportion of neutrophils from patients without anti-CD20 treatments underwent NET formation, either unstimulated or stimulated with phorbol 12-myristate 3-acetate for 3 h. In about half of patients with anti-CD20 treatment (n = 7), NET formation of unstimulated neutrophils occurred already within 20 min of incubation. This was not observed in patients without anti-CD20 treatment and healthy controls. CONCLUSION: Anti-CD20 treatment in MS and NMOSD patients does not alter chemotaxis and ROS production of neutrophils in vitro but might restore their impaired phagocytosis in these diseases. Our study reveals a predisposition to early NET formation in vitro of neutrophils obtained from patients with anti-CD20 treatment. This may contribute to associated risks of neutropenia and infections.
 Although several immunomodulatory drugs are available for multiple sclerosis (MS), most present significant side effects with long-term use. Therefore, delineation of nontoxic drugs for MS is an important area of research. β-Hydroxy β-methylbutyrate (HMB) is accessible in local GNC stores as a muscle-building supplement in humans. This study underlines the importance of HMB in suppressing clinical symptoms of experimental autoimmune encephalomyelitis (EAE) in mice, an animal model of MS. Dose-dependent study shows that oral HMB at a dose of 1 mg/kg body weight/d or higher significantly suppresses clinical symptoms of EAE in mice. Accordingly, orally administered HMB attenuated perivascular cuffing, preserved the integrity of the blood-brain barrier and blood-spinal cord barrier, inhibited inflammation, maintained the expression of myelin genes, and blocked demyelination in the spinal cord of EAE mice. From the immunomodulatory side, HMB protected regulatory T cells and suppressed Th1 and Th17 biasness. Using peroxisome proliferator-activated receptor (PPAR)α-/- and PPARβ-/- mice, we observed that HMB required PPARβ, but not PPARα, to exhibit immunomodulation and suppress EAE. Interestingly, HMB reduced the production of NO via PPARβ to protect regulatory T cells. These results describe a novel anti-autoimmune property of HMB that may be beneficial in the treatment of MS and other autoimmune disorders.
 Multiple Sclerosis (MS) is characterized by chronic deterioration of the nervous system, mainly the brain and the spinal cord. An individual with MS develops the condition when the immune system begins attacking nerve fibers and the myelin sheathing that covers them, affecting the communication between the brain and the rest of the body and eventually causing permanent damage to the nerve. Patients with MS (pwMS) might experience different symptoms depending on which nerve was damaged and how much damage it has sustained. Currently, there is no cure for MS; however, there are clinical guidelines that help control the disease and its accompanying symptoms. Additionally, no specific laboratory biomarker can precisely identify the presence of MS, leaving specialists with a differential diagnosis that relies on ruling out other possible diseases with similar symptoms. Since the emergence of Machine Learning (ML) in the healthcare industry, it has become an effective tool for uncovering hidden patterns that aid in diagnosing several ailments. Several studies have been conducted to diagnose MS using ML and Deep Learning (DL) models trained using MRI images, achieving promising results. However, complex and expensive diagnostic tools are needed to collect and examine imaging data. Thus, the intention of this study is to implement a cost-effective, clinical data-driven model that is capable of diagnosing pwMS. The dataset was obtained from King Fahad Specialty Hospital (KFSH) in Dammam, Saudi Arabia. Several ML algorithms were compared, namely Support Vector Machine (SVM), Decision Tree (DT), Logistic Regression (LR), Random Forest (RF), Extreme Gradient Boosting (XGBoost), Adaptive Boosting (AdaBoost), and Extra Trees (ET). The results indicated that the ET model outpaced the rest with an accuracy of 94.74%, recall of 97.26%, and precision of 94.67%.
 BACKGROUND: Multiple sclerosis (MS) is a lifelong deteriorating disease characterized by multiple heterogeneous symptoms. Being an autoimmune disease of the central nervous system, mainly affecting the myelin sheath of the nerves ordinarily results in neurological symptoms. GABA has numerous effects on the immune cells, altering cytokine production, cell migration and proliferation. Immune cells express GABA receptors making GABA an inflammation modulator. Therefore, GABAergic- associated agents could provide a compatible add-on therapy for MS patients alleviating their symptoms and providing better quality years. OBJECTIVE: This review aims to highlight and provide evidence of the potential benefits of a secondary treatment option in MS patients, aiming to better manage this disease. METHODS: We conducted a literature search through PubMed, Scopus and Google Scholar for GABA agonists, antagonists and modulators used in the in vivo model of experimental autoimmune encephalomyelitis (EAE), taking into consideration certain inclusion and exclusion criteria. RESULTS: In vivo studies for GABA-a and GABA-b agonists and modulators showed regulation of the autoimmune response in EAE mice. Increased preservation of myelinated sensitive fibers and diminished axonal damage in the CNS was also demonstrated. Further, decreased mononuclear inflammatory infiltration, pro-inflammatory cytokines reduction and reduced levels of Reactive oxygen species (ROS) were also reported. Biological results included decreased peak disease severity, duration, clinical scores and EAE incidence in the treatment groups. CONCLUSION: GABA agonists and modulators efficiently challenged different aspects of disease pathophysiology in vivo models of EAE. The studies showed a significant relevance of neuroprotection via modulation of the autoimmune response in EAE rats, indicating that they should be considered proper therapeutic candidates for clinical use, while also further clinical studies could empower their administration in clinical practice.
 OBJECTIVE: In this observational study on a cohort of biopsy-proven central nervous system demyelinating disease consistent with MS, we examined the relationship between early-active demyelinating lesion immunopattern (IP) with subsequent clinical course, radiographic progression, and cognitive function. METHODS: Seventy-five patients had at least one early-active lesion on biopsy and were pathologically classified into three immunopatterns based on published criteria. The median time from biopsy at follow-up was 11 years, median age at biopsy - 41, EDSS - 4.0. At last follow-up, the median age was 50, EDSS - 3.0. Clinical examination, cognitive assessment (CogState battery), and 3-Tesla-MRI (MPRAGE/FLAIR/T2/DIR/PSIR/DTI) were obtained. RESULTS: IP-I was identified in 14/75 (19%), IP-II was identified in 41/75 (56%), and IP-III was identified in 18/75 (25%) patients. Patients did not differ significantly by immunopattern in clinical measures at onset or last follow-up. The proportions of disease courses after a median of 11 years were similar across immunopatterns, relapsing-remitting being most common (63%), followed by monophasic (32%). No differences in volumetric or DTI measures were found. CogState performance was similar for most tasks. A slight yet statistically significant difference was identified for episodic memory scores, with IP-III patients recalling one word less on average. INTERPRETATION: In this study, immunopathological heterogeneity of early-active MS lesions identified at biopsy does not correlate with different long-term clinical, neuroimaging or cognitive outcomes. This could be explained by the fact that while active white matter lesions are pathological substrates for relapses, MS progression is driven by mechanisms converging across immunopatterns, regardless of pathogenic mechanisms driving the acute demyelinated plaque.
 BACKGROUND: The nine-hole peg test (NHPT) is the outcome measure with the least change in secondary and primary progressive MS (SPMS and PPMS) trials. The Standard NHPT is defined as the average of four measurements, two in each hand. Little is known about the performance of alternative NHPT scoring methods as longitudinal outcome measures in progressive MS. Non-ambulatory people with progressive MS are now generally excluded from clinical trials, and there is little information on longitudinal NHPT change in this patient group. In this investigation, we used patient-level data from two large randomized controlled trials in progressive MS to explore alternative NHPT scoring methods and NHPT change in non-ambulatory people with progressive MS. METHODS: We used patient-level data from the ASCEND (SPMS, n = 889) and PROMISE (PPMS, n = 943) clinical trials to compare significant change on the Standard NHPT with the alternatives dominant hand (DH), non-dominant hand (NDH), and either hand (EH) NHPT in ambulatory and non-ambulatory trial participants. RESULTS: The Standard NHPT changed slowly and showed few worsening events, as did the DH and NDH alternatives. Using the EH NHPT resulted in a substantial increase of worsening events. Non-ambulatory trial participants with PPMS experienced more NHPT worsening than ambulatory participants, especially when using the EH NHPT. CONCLUSION: Using the EH NHPT yielded substantially more worsening events in people with progressive MS. Clinical trials in non-ambulatory people may be possible with the NHPT as the primary outcome measure. More research into the precision of these measures in this patient group is necessary.
 PURPOSE/OBJECTIVE: The first year following a new multiple sclerosis (MS) diagnosis may be a critical time for individuals as they learn to manage their disease. Effective self-management of MS likely requires healthy self-efficacy levels, yet little is known about self-efficacy in the postdiagnosis period. This study aims to improve our understanding of self-efficacy in individuals newly diagnosed with MS by examining self-efficacy trajectories and identifying patient characteristics associated with trajectories in the first postdiagnosis year. RESEARCH METHOD/DESIGN: Newly diagnosed adults with MS/clinically isolated syndrome (CIS) (N = 230) completed a battery of questionnaires, including the University of Washington Self-Efficacy Scale, at 1, 2, 3, 6, 9, and 12 months, postdiagnosis. Sankey diagrams characterized self-efficacy trajectories and a multiple regression model tested patient characteristics as predictors of self-efficacy change scores. RESULTS: Mean self-efficacy T-scores ranged from 50.79 to 52.04 (SD = 9.40 and 10.12, respectively) across the postdiagnosis year. MS diagnosis (vs. CIS), higher disability levels, and higher MS symptom severity were associated with lower self-efficacy levels at baseline. Baseline symptom severity predicted change in self-efficacy levels from baseline to month 12 (B = -0.05, p = .030). CONCLUSIONS/IMPLICATIONS: Self-efficacy remains relatively stable in the first year following a MS diagnosis, though high symptom severity is associated with decreased self-efficacy at 12-months postdiagnosis. Clinical characteristics (e.g., MS diagnosis, disability level) also appear to play a role in setting the course of self-efficacy in this postdiagnosis year. Timely interventions that enhance self-efficacy and/or improve certain clinical characteristics may promote healthy self-management of MS that carries forward in disease course. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 The aim of this study was to investigate the feasibility of automatically assessing the 2-Minute Walk Distance (2MWD) for monitoring people with multiple sclerosis (pwMS). For 154 pwMS, MS-related clinical outcomes as well as the 2MWDs as evaluated by clinicians and derived from accelerometer data were collected from a total of 323 periodic clinical visits. Accelerometer data from a wearable device during 100 home-based 2MWD assessments were also acquired. The error in estimating the 2MWD was validated for walk tests performed at hospital, and then the correlation (r) between clinical outcomes and home-based 2MWD assessments was evaluated. Robust performance in estimating the 2MWD from the wearable device was obtained, yielding an error of less than 10% in about two-thirds of clinical visits. Correlation analysis showed that there is a strong association between the actual and the estimated 2MWD obtained either at hospital (r = 0.71) or at home (r = 0.58). Furthermore, the estimated 2MWD exhibits moderate-to-strong correlation with various MS-related clinical outcomes, including disability and fatigue severity scores. Automatic assessment of the 2MWD in pwMS is feasible with the usage of a consumer-friendly wearable device in clinical and non-clinical settings. Wearable devices can also enhance the assessment of MS-related clinical outcomes.
 INTRODUCTION: Substantial links between autoimmune diseases have been shown by an increasing number of studies, and one hypothesis for this comorbidity is that there is a common genetic cause. METHODS: In this paper, a large-scale cross-trait Genome-wide Association Studies (GWAS) was conducted to investigate the genetic overlap among rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease and type 1 diabetes. RESULTS AND DISCUSSION: Through the local genetic correlation analysis, 2 regions with locally significant genetic associations between rheumatoid arthritis and multiple sclerosis, and 4 regions with locally significant genetic associations between rheumatoid arthritis and type 1 diabetes were discovered. By cross-trait meta-analysis, 58 independent loci associated with rheumatoid arthritis and multiple sclerosis, 86 independent loci associated with rheumatoid arthritis and inflammatory bowel disease, and 107 independent loci associated with rheumatoid arthritis and type 1 diabetes were identified with genome-wide significance. In addition, 82 common risk genes were found through genetic identification. Based on gene set enrichment analysis, it was found that shared genes are enriched in exposed dermal system, calf, musculoskeletal, subcutaneous fat, thyroid and other tissues, and are also significantly enriched in 35 biological pathways. To verify the association between diseases, Mendelian randomized analysis was performed, which shows possible causal associations between rheumatoid arthritis and multiple sclerosis, and between rheumatoid arthritis and type 1 diabetes. The common genetic structure of rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease and type 1 diabetes was explored by these studies, and it is believed that this important discovery will lead to new ideas for clinical treatment.
 Experimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis (MS) in which Th17 cells have a crucial but unclear function. Here we show that choline acetyltransferase (ChAT), which synthesizes acetylcholine (ACh), is a critical driver of pathogenicity in EAE. Mice with ChAT-deficient Th17 cells resist disease progression and show reduced brain-infiltrating immune cells. ChAT expression in Th17 cells is linked to strong TCR signaling, expression of the transcription factor Bhlhe40, and increased Il2, Il17, Il22, and Il23r mRNA levels. ChAT expression in Th17 cells is independent of IL21r signaling but dampened by TGFβ, implicating ChAT in controlling the dichotomous nature of Th17 cells. Our study establishes a cholinergic program in which ACh signaling primes chronic activation of Th17 cells, and thereby constitutes a pathogenic determinant of EAE. Our work may point to novel targets for therapeutic immunomodulation in MS.
 BACKGROUND AND PURPOSE: Retina thickness has been studied in patients with neuromyelitis optica spectrum disorders (NMOSD) without distinguishing serostatus and limited data are available in unaffected eyes. We aimed to investigate retina thickness in eyes of aquaporin-4 immunoglobulin G antibody seropositive (AQP4-IgG(+)) NMOSD patients with optic neuritis (AQP4-ON) and without (AQP4-NON). METHODS: Eligible studies were identified by searching PubMed and Embase. Mean difference (MD, μm) with corresponding 95% confidence interval (CI) was pooled with random-effect models. The primary measures were average thickness of peripapillar retinal nerve fiber layer (pRNFL) centered on optic disc and the combination of ganglion cell layer and inner plexiform layer (GCIPL) at macula. RESULTS: We included 21 studies enrolling 787 AQP4-IgG(+) NMOSD patients. Compared with healthy control, pRNFL was thinner in eyes of AQP4-ON (- 32.78, 95% CI [- 36.24, - 29.33]) and AQP4-NON (- 2.76, 95% CI [- 3.94, - 1.58]), so was GICPL in AQP4-ON (-21.38, 95% CI [- 24.01, - 18.74]) and AQP4-NON (95% CI - 2.96, [- 3.91, - 2.00]). Compared with multiple sclerosis with ON, AQP4-ON had thinner pRNFL (- 13.56, 95%CI [- 16.51, - 10.60]) and GCIPL (- 9.12, 95% CI [- 11.88, - 6.36]). AQP4-ON and myelin oligodendrocyte glycoprotein antibody-associated demyelination with ON (MOG-ON) had similar pRNFL (0.59, 95% CI [- 6.61, 7.79]) and GCIPL thickness (- 0.55, 95% CI [- 2.92, 1.82]). AQP4-NON had similar pRNFL and GCIPL thickness to MOG-NON and multiple sclerosis without ON. CONCLUSIONS: The average thickness of pRNFL and GICPL decreased both in AQP4-ON and AQP4-NON eyes. AQP4-ON eyes had a similar level of pRNFL and GICPL thinning to MOG-ON eyes, so did AQP4-NON to MOG-NON eyes.
 BACKGROUND: The relationship between socioeconomic status (SES) and mortality among persons with multiple sclerosis (PwMS) is poorly understood. OBJECTIVE: To investigate the association between SES and mortality risk in PwMS. METHODS: From health-administrative data, we identified 12,126 incident MS cases with a first demyelinating event (MS 'onset') occurring between 1994 and 2017. Cox proportional hazard model assessed the association between socioeconomic status quintiles (SES-Qs) at MS onset and all-cause mortality. RESULTS: Lower SES-Qs were associated with higher mortality risk; adjusted hazard ratios: SES-Q1 (most deprived) =1.61 (95% confidence interval (CI) = 1.36-1.91); SES-Q2 = 1.26 (95% CI = 1.05-1.50); SES-Q3 = 1.22 (95% CI = 1.02-1.46); SES-Q4 = 1.13 (95% CI = 0.94-1.35) versus SES-Q5 (least deprived). CONCLUSION: A lower SES was associated with higher mortality risk in PwMS.
 A 62-year-old woman with a history of multiple sclerosis (MS) presented with recurrent episodes of confusion, dysarthria and gait difficulties. These episodes occurred about 3 days after administration of pegylated interferon-beta-1a (Plegridy®) and resolved spontaneously in around 4 days. The brain MRI scan, laboratory findings and cerebrospinal fluid analysis during these episodes were negative for other causes of encephalopathy. She discontinued treatment with interferon and was started on teriflunomide, experiencing no recurrence of symptoms. We believe that interferon was responsible for this patient's recurrent encephalopathic syndrome, possibly due to its effects on inflammatory cytokines and endothelial dysfunction.
 BACKGROUND AND OBJECTIVES: Observational studies suggest low levels of 25-hydroxyvitamin D (25[OH]D) may be associated with increased disease activity in people with multiple sclerosis (PwMS). Large-scale genome-wide association studies (GWAS) suggest 25(OH)D levels are partly genetically determined. The resultant polygenic scores (PGSs) could serve as a proxy for 25(OH)D levels, minimizing potential confounding and reverse causation in analyses with outcomes. Herein, we assess the association of genetically determined 25(OH)D and disease outcomes in MS. METHODS: We generated 25(OH)D PGS for 1,924 PwMS with available genotyping data pooled from 3 studies: the CombiRx trial (n = 575), Johns Hopkins MS Center (n = 1,152), and Immune-Mediated Inflammatory Diseases study (n = 197). 25(OH)D-PGS were derived using summary statistics (p < 5 × 10(-8)) from a large GWAS including 485,762 individuals with circulating 25(OH)D levels measured. We included clinical and imaging outcomes: Expanded disability status scale (EDSS), timed 25-foot walk (T25FW), nine-hole peg test (9HPT), radiologic activity, and optical coherence tomography-derived ganglion cell inner plexiform layer (GCIPL) thickness. A subset (n = 935) had measured circulating 25(OH)D levels. We fitted multivariable models based on the outcome of interest and pooled results across studies using random effects meta-analysis. Sensitivity analyses included a modified p value threshold for inclusion in the PGS (5 × 10(-5)) and applying Mendelian randomization (MR) rather than using PGS. RESULTS: Initial analyses demonstrated a positive association between generated 25(OH)D-PGS and circulating 25(OH)D levels (per 1SD increase in 25[OH]D PGS: 3.08%, 95% CI: 1.77%, 4.42%; p = 4.33e-06; R(2) = 2.24%). In analyses with outcomes, we did not observe an association between 25(OH)D-PGS and relapse rate (per 1SD increase in 25[OH]D-PGS: 0.98; 95% CI: 0.87-1.10), EDSS worsening (per 1SD: 1.05; 95% CI: 0.87-1.28), change in T25FW (per 1SD: 0.07%; 95% CI: -0.34 to 0.49), or change in 9HPT (per 1SD: 0.09%; 95% CI: -0.15 to 0.33). 25(OH)D-PGS was not associated with new lesion accrual, lesion volume or other imaging-based outcomes (whole brain, gray, white matter volume loss or GCIPL thinning). The results were similarly null in analyses using other p value thresholds or those applying MR. DISCUSSION: Genetically determined lower 25(OH)D levels were not associated with worse disease outcomes in PwMS and raises questions about the plausibility of a treatment effect of vitamin D in established MS.
 Peripheral B cell depletion via anti-CD20 treatment is a highly effective disease-modifying treatment for reducing new relapses in multiple sclerosis (MS) patients. A drawback of rituximab (RTX) and other anti-CD20 antibodies is a poor immune response to vaccination. While this can be mitigated by treatment interruption of at least six months prior to vaccination, the timing to resume treatment while maintaining subsequent vaccine responses remains undetermined. Here, we characterized SARS-CoV-2 S-directed antibody and B cell responses throughout three BNT162b2 mRNA vaccine doses in RTX-treated MS patients, with the first two doses given during treatment interruption. We examined B-cell mediated immune responses in blood samples from patients with RTX-treated MS throughout three BNT162b2 vaccine doses, compared to an age- and sex-matched healthy control group. The first vaccine dose was given 1.3 years (median) after the last RTX infusion, the second dose one month after the first, and the third dose four weeks after treatment re-initiation. We analyzed SARS-CoV-2 S-directed antibody levels using enzyme-linked immunosorbent assay (ELISA), and the neutralization capacity of patient serum against SARS-CoV-2 S-pseudotyped lentivirus using luciferase reporter assay. In addition, we assessed switched memory (CD19(+)CD20(+)CD27(+)IgD(-)), unswitched memory (CD19(+)CD20(+)CD27(+)IgD(+)), naïve (CD19(+)CD20(+)CD27(-)IgD(+)), and double negative (DN, CD19(+)CD20(+)CD27(-)IgD(-)) B cell frequencies, as well as their SARS-CoV-2 S-specific (CoV(+)) and Decay Accelerating Factor-negative (DAF(-)) subpopulations, using flow cytometry. After two vaccine doses, S-binding antibody levels and neutralization capacity in SARS-CoV-2-naïve MS patients were comparable to vaccinated healthy controls, albeit with greater variation. Higher antibody response levels and CoV(+)-DN B cell frequencies after the second vaccine dose were predictive of a boost effect after the third dose, even after re-initiation of rituximab treatment. MS patients also exhibited lower frequencies of DAF(-) memory B cells, a suggested proxy for germinal centre activity, than control individuals. S-binding antibody levels in RTX-treated MS patients after two vaccine doses could help determine which individuals would need to move up their next vaccine booster dose or postpone their next RTX infusion. Our findings also offer first indications on the potential importance of antigenic stimulation of DN B cells and long-term impairment of germinal centre activity in rituximab-treated MS patients.
 Multiple sclerosis (MS) is a chronic demyelinating and neuroinflammatory disease of the human central nervous system with complex pathoetiology, heterogeneous presentations and an unpredictable course of disease progression. There remains an urgent need to identify and validate a biomarker that can reliably predict the initiation and progression of MS as well as identify patient responses to disease-modifying treatments/therapies (DMTs). Studies exploring biomarkers in MS and other neurodegenerative diseases currently focus mainly on cerebrospinal fluid (CSF) analyses, which are invasive and impractical to perform on a repeated basis. Recent studies, replacing CSF with peripheral blood samples, have revealed that the elevation of serum neurofilament light chain (sNfL) in the clinical stages of MS is, potentially, an ideal prognostic biomarker for predicting disease progression and for possibly guiding treatment decisions. However, there are unresolved factors (the definition of abnormal values of sNfL concentration, the standardisation of measurement and the amount of change in sNfL concentration that is significant) that are preventing its use as a biomarker in routine clinical practice for MS. This updated review critiques these recent findings and highlights areas for focussed work to facilitate the use of sNfL as a prognostic biomarker in MS management.
 BACKGROUND AND PURPOSE: Vitamin D is considered to play a role in multiple sclerosis (MS) etiopathogenesis. A polymorphism in the CYP24A1 gene, rs2762943, was recently identified that was associated with an increased MS risk. CYP24A1 encodes a protein involved in the catabolism of the active form of vitamin D. The immunological effects of carrying the rs2762943 risk allele were investigated, as well as its role as genetic modifier. METHODS: Serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D (1,25(OH)(2) D) were measured in a cohort of 167 MS patients. In a subgroup of patients, expression levels of major histocompatibility complex class II and co-stimulatory molecules were determined by flow cytometry, and serum levels of pro-inflammatory (interferon gamma, granulocyte macrophage colony-stimulating factor, C-X-C motif chemokine ligand 13) and anti-inflammatory (interleukin 10) cytokines and neurofilament light chain were measured by single-molecule array assays. The effect of the rs2762943 polymorphism on disease activity and disability measures was evaluated in 340 MS patients. RESULTS: Compared to non-carriers, carriers of the rs2762943 risk allele were characterized by reduced levels of 1,25(OH)(2) D (p = 0.0001) and elevated levels of interferon gamma (p = 0.03) and granulocyte macrophage colony-stimulating factor (p = 0.008), whereas no significant differences were observed for the other markers. The presence of the rs2762943 risk allele had no significant impact on disease activity and disability outcomes during follow-up. However, risk allele carriers were younger at disease onset (p = 0.04). CONCLUSIONS: These findings suggest that the CYP24A1 rs2762943 polymorphism plays a more important role in MS susceptibility than in disease prognosis and is associated with lower 1,25(OH)(2) D levels and a heightened pro-inflammatory environment in MS patients.
 INTRODUCTION: The association between multiple sclerosis (MS) and non-small cell lung cancer (NSCLC) has been the subject of investigation in clinical cohorts, yet the molecular mechanisms underpinning this relationship remain incompletely understood. To address this, our study aimed to identify shared genetic signatures, shared local immune microenvironment, and molecular mechanisms between MS and NSCLC. METHODS: We selected multiple Gene Expression Omnibus (GEO) datasets, including GSE19188, GSE214334, GSE199460, and GSE148071, to obtain gene expression levels and clinical information from patients or mice with MS and NSCLC. We employed Weighted Gene Co-expression Network Analysis (WGCNA) to investigate co-expression networks linked to MS and NSCLC and used single-cell RNA sequencing (scRNA-seq) analysis to explore the local immune microenvironment of MS and NSCLC and identify possible shared components. RESULTS: Our analysis identified the most significant shared gene in MS and NSCLC, phosphodiesterase 4A (PDE4A), and we analyzed its expression in NSCLC patients and its impact on patient prognosis, as well as its molecular mechanism. Our results demonstrated that high expression of PDE4A was associated with poor prognoses in NSCLC patients, and Gene Set Enrichment Analysis (GSEA) revealed that PDE4A is involved in immune-related pathways and has a significant regulatory effect on human immune responses. We further observed that PDE4A was closely linked to the sensitivity of several chemotherapy drugs. CONCLUSION: Given the limitation of studies investigating the molecular mechanisms underlying the correlation between MS and NSCLC, our findings suggest that there are shared pathogenic processes and molecular mechanisms between these two diseases and that PDE4A represents a potential therapeutic target and immune-related biomarker for patients with both MS and NSCLC.
 BACKGROUND: Health state utilities (HSU) are a health-related quality-of-life (HRQoL) input for cost-utility analyses used for resource allocation decisions, including medication reimbursement. New Zealand (NZ) guidelines recommend the EQ-5D instruments; however, the EQ-5D-5L may not sufficiently capture psychosocial health. We evaluated HRQoL among people with multiple sclerosis (MS) in NZ using the EQ-5D-5L and assessed the instrument's discriminatory sensitivity for a NZ MS cohort. METHODS: Participants were recruited from the NZ MS Prevalence Study. Participants self-completed a 45-min online survey that included the EQ-5D-5L/EQ-VAS. Disability severity was classified using the Expanded Disability Status Scale (EDSS) to categorise participant disability as mild (EDSS: 0-3.5), moderate (EDSS: 4.0-6.0) and severe (EDSS: 6.5-9.5). Anxiety/depression were also measured using the Hospital Anxiety and Depression Score (HADS). In the absence of an EQ-5D-5L NZ tariff, HSUs were derived using an Australian tariff. We evaluated associations between HSUs and participant characteristics with linear regression models. RESULTS: 254 participants entered the study. Mean age was 55.2 years, 79.5% were female. Mean (SD) EQ-5D-5L HSU was 0.58 (0.33). Mean (SD) HSUs for disability categories were: mild 0.80 ± 0.17, moderate 0.57 ± 0.21 and severe 0.14 ± 0.32. Twelve percent reported HSU = 1.0 (i.e., no problems in any domain). Participants who had never used a disease-modifying therapy reported a lower mean HSU. Multivariable modelling found that the HADS anxiety score was not associated with EQ-5D-5L. CONCLUSIONS: HRQoL for people with MS in NZ was lower than comparable countries, including Australia. We suggest a comparison with other generic tools that may have improved sensitivity to mental health.
 BACKGROUND: Observational studies have associated obesity with an increased risk of multiple sclerosis (MS). However, the role of genetic factors in their comorbidity remains largely unknown. Our study aimed to investigate the shared genetic architecture underlying obesity and MS. METHODS: By leveraging data from genome-wide association studies, we investigated the genetic correlation of body mass index (BMI) and MS by linkage disequilibrium score regression and genetic covariance analyser. The casualty was identified by bidirectional Mendelian randomisation. Linkage disequilibrium score regression in specifically expressed genes and multimarker analysis of GenoMic annotation was utilised to explore single-nucleotide polymorphism (SNP) enrichment at the tissue and cell-type levels. Shared risk SNPs were derived using cross-trait meta-analyses and Heritability Estimation from Summary Statistics. We explored the potential functional genes using summary-data-based Mendelian randomization (SMR). The expression profiles of the risk gene in tissues were further examined. FINDINGS: We found a significantly positive genetic correlation between BMI and MS, and the causal association of BMI with MS was supported (β = 0.22, P = 8.03E-05). Cross-trait analysis yielded 39 shared risk SNPs, and the risk gene GGNBP2 was consistently identified in SMR. We observed tissue-specific level SNP heritability enrichment for BMI mainly in brain tissues for MS in immune-related tissues, and cell-type-specific level SNP heritability enrichment in 12 different immune cell types in brain, spleen, lung, and whole blood. The expressions of GGNBP2 were significantly altered in the tissues of patients with obesity or MS compared to those of control subjects. INTERPRETATION: Our study indicates the genetic correlation and shared risk genes between obesity and MS. These findings provide insights into the potential mechanisms behind their comorbidity and the future development of therapeutics. FUNDING: This work was funded by the National Natural Science Foundation of China (82171698, 82170561, 81300279, and 81741067), the Program for High-level Foreign Expert Introduction of China (G2022030047L), the Natural Science Foundation for Distinguished Young Scholars of Guangdong Province (2021B1515020003), Natural Science Foundation of Guangdong Province (2022A1515012081), the Foreign Distinguished Teacher Program of Guangdong Science and Technology Department (KD0120220129), the Climbing Programme of Introduced Talents and High-level Hospital Construction Project of Guangdong Provincial People's Hospital (DFJH201803, KJ012019099, KJ012021143, and KY012021183), and in part by VA Clinical Merit and ASGE clinical research funds (FWL).
 Ferroptosis is a form of lipid peroxidation-mediated cell death and damage triggered by excess iron and insufficiency in the glutathione antioxidant pathway. Oxidative stress is thought to play a crucial role in progressive forms of multiple sclerosis (MS) in which iron deposition occurs. In this study we assessed if ferroptosis plays a role in a chronic form of experimental autoimmune encephalomyelitis (CH-EAE), a mouse model used to study MS. Changes were detected in the mRNA levels of several ferroptosis genes in CH-EAE but not in relapsing-remitting EAE. At the protein level, expression of iron importers is increased in the earlier stages of CH-EAE (onset and peak). While expression of hemoxygenase-1, which mobilizes iron from heme, likely from phagocytosed material, is increased in macrophages at the peak and progressive stages. Excess iron in cells is stored safely in ferritin, which increases with disease progression. Harmful, redox active iron is released from ferritin when shuttled to autophagosomes by 'nuclear receptor coactivator 4' (NCOA4). NCOA4 expression increases at the peak and progressive stages of CH-EAE and accompanied by increase in redox active ferrous iron. These changes occur in parallel with reduction in the antioxidant pathway (system xCT, glutathione peroxidase 4 and glutathione), and accompanied by increased lipid peroxidation. Mice treated with a ferroptosis inhibitor for 2 weeks starting at the peak of CH-EAE paralysis, show significant improvements in function and pathology. Autopsy samples of tissue sections of secondary progressive MS (SPMS) showed NCOA4 expression in macrophages and oligodendrocytes along the rim of mixed active/inactive lesions, where ferritin+ and iron containing cells are located. Cells expressing NCOA4 express less ferritin, suggesting ferritin degradation and release of redox active iron, as indicated by increased lipid peroxidation. These data suggest that ferroptosis is likely to contribute to pathogenesis in CH-EAE and SPMS.
 AIMS: The aim of this study was to explore the experiences, values and preferences of people living with relapsing multiple sclerosis (PLwRMS) focusing on their treatments and what drives their treatment preferences. METHODS: In-depth, semi-structured, qualitative telephone interviews were conducted using a purposive sampling approach with 72 PLwRMS and 12 health care professionals (HCPs, MS specialist neurologists and nurses) from the United Kingdom, United States, Australia and Canada. Concept elicitation questioning was used to elicit PLwRMS' attitudes, beliefs and preferences towards features of disease-modifying treatments. Interviews with HCPs were conducted to inform on HCPs' experiences of treating PLwRMS. Responses were audio recorded and transcribed verbatim and then subjected to thematic analysis. RESULTS: Participants discussed numerous concepts that were important to them when making treatment decisions. Levels of importance participants placed on each concept, as well as reasons underpinning importance, varied substantially. The concepts with the greatest variability in terms of how much PLwRMS found them to be important in their decision-making process were mode of administration, speed of treatment effect, impact on reproduction and parenthood, impact on work and social life, patient engagement in decision making, and cost of treatment to the participant. Findings also demonstrated high variability in what participants described as their ideal treatment and the most important features a treatment should have. HCP findings provided clinical context for the treatment decision-making process and supported patient findings. CONCLUSIONS: Building upon previous stated preference research, this study highlighted the importance of qualitative research in understanding what drives patient preferences. Characterized by the heterogeneity of the RMS patient experience, findings indicate the nature of treatment decisions in RMS to be highly individualized, and the subjective relative importance placed on different treatment factors by PLwRMS to vary. Such qualitative patient preference evidence could offer valuable and supplementary insights, alongside quantitative data, to inform decision making related to RMS treatment.
 Nowadays the problem of comorbidity is still relevant. In this review, we describe clinical cases of the disease of the neuromuscular junction (myasthenia gravis (MG) generalized form) and the demyelinating disease of the central nervous system (DD CNS) (multiple sclerosis, neuromyelitis optica spectrum disorder (NMOSD), etc.) combinations registered in our practice with precise pathogenetic analysis. Although the number of the described associations is growing every year, the exact development mechanisms of this cross syndrome as well as the nature of the association between the discussed autoimmune diseases remain unknown. At the beginning of both disorders there is a considerable loss of auto tolerance of the immune system and, as a result, an increased response from autoreactive T-lymphocytes to the structures of the nervous system: brain cells and neuromuscular synapses. There are three main theories for comorbidity: initial predisposition, direct case relationship with disease-modifying therapy (DMT) application, and coincidence. It is known that early diagnostics of MG and timely administration of necessary adequate treatment reduce the risk of process generalization and lead to a decline in mortality. Therefore, the offer to examine MS patients with atypical symptoms for possible MG identification seems very rational. Similarly, MG patients having uncharacteristic symptoms that can be indicative of other autoimmune nervous system diseases also demand special diagnostics. Considering the presence of similar pathogenetic links, several authors propose a possibility of a new nosological unit establishment, including described comorbidity.
 Several reports have pointed out that Chitinases are expressed and secreted by various cell types of central nervous system (CNS), including activated microglia and astrocytes. These cells play a key role in neuroinflammation and in the pathogenesis of many neurodegenerative disorders. Increased levels of Chitinases, in particular Chitotriosidase (CHIT-1) and chitinase-3-like protein 1 (CHI3L1), have been found increased in several neurodegenerative disorders. Although having important biological roles in inflammation, to date, the molecular mechanisms of Chitinase involvement in the pathogenesis of neurodegenerative disorders is not well-elucidated. Several studies showed that some Chitinases could be assumed as markers for diagnosis, prognosis, activity, and severity of a disease and therefore can be helpful in the choice of treatment. However, some studies showed controversial results. This review will discuss the potential of Chitinases in the pathogenesis of some neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis, to understand their role as distinctive biomarkers of neuronal cell activity during neuroinflammatory processes. Knowledge of the role of Chitinases in neuronal cell activation could allow for the development of new methodologies for downregulating neuroinflammation and consequently for diminishing negative neurological disease outcomes.

 Multiple sclerosis (MS) may impact quality of life, careers and family plans of the affected individuals. The current treatments with disease modifying therapies aim to prevent people with MS (pwMS) from disability accumulation and progression. Different countries have different reimbursement policies resulting in inequalities in patient care among geographical regions. Access to anti-CD20 therapies for relapsing MS is restricted in Hungary because therapy of individual cases only is reimbursed. In the light of the latest research and national guidelines, 17 Hungarian MS experts agreed on 8 recommendations regarding relapsing pwMS using the Delphi round method. Strong agreement (> 80%) was achieved in all except one recommendation after three rounds, which generated a fourth Delphi round. The experts agreed on treatment initiation, switch, follow-up and discontinuation, as well as on special issues such as pregnancy, lactation, elderly population, and vaccination. Well-defined national consensus protocols may facilitate dialogue between policymakers and healthcare professionals and thus contribute to better patient care in the long run.
 MRI and clinical features of myelin oligodendrocyte glycoprotein (MOG)-antibody disease may overlap with those of other inflammatory demyelinating conditions posing diagnostic challenges, especially in non-acute phases and when serologic testing for MOG antibodies is unavailable or shows uncertain results. We aimed to identify MRI and clinical markers that differentiate non-acute MOG-antibody disease from aquaporin 4 (AQP4)-antibody neuromyelitis optica spectrum disorder and relapsing remitting multiple sclerosis, guiding in the identification of patients with MOG-antibody disease in clinical practice. In this cross-sectional retrospective study, data from 16 MAGNIMS centres were included. Data collection and analyses were conducted from 2019 to 2021. Inclusion criteria were: diagnosis of MOG-antibody disease; AQP4-neuromyelitis optica spectrum disorder and multiple sclerosis; brain and cord MRI at least 6 months from relapse; and Expanded Disability Status Scale (EDSS) score on the day of MRI. Brain white matter T2 lesions, T1-hypointense lesions, cortical and cord lesions were identified. Random forest models were constructed to classify patients as MOG-antibody disease/AQP4-neuromyelitis optica spectrum disorder/multiple sclerosis; a leave one out cross-validation procedure assessed the performance of the models. Based on the best discriminators between diseases, we proposed a guide to target investigations for MOG-antibody disease. One hundred and sixty-two patients with MOG-antibody disease [99 females, mean age: 41 (±14) years, median EDSS: 2 (0-7.5)], 162 with AQP4-neuromyelitis optica spectrum disorder [132 females, mean age: 51 (±14) years, median EDSS: 3.5 (0-8)], 189 with multiple sclerosis (132 females, mean age: 40 (±10) years, median EDSS: 2 (0-8)] and 152 healthy controls (91 females) were studied. In young patients (<34 years), with low disability (EDSS < 3), the absence of Dawson's fingers, temporal lobe lesions and longitudinally extensive lesions in the cervical cord pointed towards a diagnosis of MOG-antibody disease instead of the other two diseases (accuracy: 76%, sensitivity: 81%, specificity: 84%, P < 0.001). In these non-acute patients, the number of brain lesions < 6 predicted MOG-antibody disease versus multiple sclerosis (accuracy: 83%, sensitivity: 82%, specificity: 83%, P < 0.001). An EDSS < 3 and the absence of longitudinally extensive lesions in the cervical cord predicted MOG-antibody disease versus AQP4-neuromyelitis optica spectrum disorder (accuracy: 76%, sensitivity: 89%, specificity: 62%, P < 0.001). A workflow with sequential tests and supporting features is proposed to guide better identification of patients with MOG-antibody disease. Adult patients with non-acute MOG-antibody disease showed distinctive clinical and MRI features when compared to AQP4-neuromyelitis optica spectrum disorder and multiple sclerosis. A careful inspection of the morphology of brain and cord lesions together with clinical information can guide further analyses towards the diagnosis of MOG-antibody disease in clinical practice.
 The human endogenous retrovirus type W (HERV-W) has been identified and repeatedly confirmed as human-specific pathogenic entity affecting many cell types in multiple sclerosis (MS). Our recent contributions revealed the encoded envelope (ENV) protein to disturb myelin repair by interfering with oligodendroglial precursor differentiation and by polarizing microglial cells toward an axon-damage phenotype. Indirect proof of ENV's antiregenerative and degenerative activities has been gathered recently in clinical trials using a neutralizing anti-ENV therapeutic antibody. Yet direct proof of its mode of action can only be presented here based on transgenic ENV expression in mice. Upon demyelination, we observed myelin repair deficits, neurotoxic microglia and astroglia, and increased axon degeneration. Experimental autoimmune encephalomyelitis activity progressed faster in mutant mice equally accompanied by activated glial cells. This study therefore provides direct evidence on HERV-W ENV's contribution to the overall negative impact of this activated viral entity in MS.
 BACKGROUND: The global COVID-19 pandemic began in March 2019, and given the number of casualties and adverse effects on the economy, society, and all aspects of the health system, efforts have been made to develop vaccines from the beginning of the pandemic. Numerous vaccines against COVID-19 infection have been developed in several technologies and have spread rapidly. There have been reported multiple complications of the COVID-19 vaccines as with other vaccines. A number of studies have reported multiple sclerosis (MS ) and neuromyelitis optica spectrum disorder (NMOSD) as complications of COVID-19 vaccines. METHODS: First, we found 954 studies from 4 databases (PubMed, Embase, Scopus, and Web of Science) from inception to March 1(st), 2022. Next, duplicate articles were eliminated, and 476 studies remained. Then 412 studies were removed according to inclusion and exclusion criteria. After obtaining the full text of 64 articles, 12 studies were selected finally. RESULTS: The data were extracted from included studies in a table. Our data includes demographic data, comorbidities, vaccines information and side effects, NMOSD and MS symptoms, laboratory and cerebrospinal fluid (CSF) findings, magnetic resonance imaging (MRI) results, treatment, and outcome of all cases. CONCLUSION: MS and NMOSD are two neuroinflammatory disorders that arise in the CNS. Cases of MS and NMOSD have been reported following COVID-19 vaccination. Nevertheless, more studies with more subjects are needed to assess any possible relationship between the COVID-19 vaccine and central nervous system demyelination.
 OBJECTIVE: To compare the effects of core stabilization (CS) and dynamic neuromuscular stabilization (DNS) on balance, trunk function, mobility, falling, and spasticity, in people with multiple sclerosis (PWMS). DESIGN: Two-group randomized controlled trial. SETTING: General community and referral center. PARTICIPANTS: A total of 64 PWMS, between 30 and 50 years old, and an expanded disability status scale between 2 and 5, participated in this study (N=64). INTERVENTIONS: Participants were randomly assigned to CS (n=32) and DNS (n=32) groups. Both groups received a total of 15 sessions of CS or DNS exercises, 60 minutes per session, 3 times a week during the 5 weeks. OUTCOME MEASURES: Balance function was measured as the primary outcome measure. Trunk function, postural stability, falling rate, fear of falling, falling index, mobility, and spasticity were measured as secondary outcomes. RESULTS: DNS group had significant improvement in Berg balance scale, trunk impairment scale, postural stability, activities-specific balance confidence, reduced falling rate, the timed Up and Go (TUG), multiple sclerosis walking scale-12, and multiple sclerosis spasticity scale in PWMS compared with the CS group, (P<.0001) after 5 weeks of intervention and 17 weeks of follow-up. Except for the modified Ashworth scale (MAS), significant improvements were seen in all outcome measures in both groups after 5 weeks of intervention. CONCLUSION: This is the first clinical evidence to support the importance of DNS exercise in improving balance, trunk function, and fall prevention in PWMS. This study provides clinical evidence that DNS may be more effective for PWMS than CS.
 OBJECTIVE: The COVID-19 pandemic continues to impact communities around the world. In this study, we explored the COVID-19 experiences of persons with multiple sclerosis (MS) and carers. METHODS: Using a qualitative approach, interviews were undertaken with 27 participants residing in Australia (10 persons with MS, 10 carers and 7 MS service providers). Demographic and background data were also collected. Interviews were analysed using an inductive iterative thematic analysis. RESULTS: Across all groups, participants consistently recognized pandemic challenges and impacts for persons with MS and carers, especially due to disruption to routines and services. Emotional and mental health impacts were also highlighted, as anxiety, fear of contracting COVID-19 and stress, including relationship stress between persons with MS and carers and family members. Some persons with MS also mentioned physical health impacts, while for carers, the challenge of disruptions included increased demands and reduced resources. In addition to acknowledging challenges, persons with MS and carers also gave examples of resilience. This included coping and adapting by finding new routines and creating space through rest and breaks and through appreciating positives including the benefits of access to telehealth. CONCLUSION: Additional support is required for persons with MS and carers in navigating the impacts of COVID-19 as the pandemic progresses. In addition to addressing challenges and disruptions, such support should also acknowledge and support the resilience of people with MS and carers and enhance resilience through supporting strategies for coping and adaptation. PATIENT AND PUBLIC CONTRIBUTION: Service user stakeholders were consulted at the beginning and end of the study. They provided feedback on interview questions and participant engagement, as well as service user perspectives on the themes identified in the current study. Participants were provided with summaries of key themes identified and invited to provide comments.
 BACKGROUND: Walking on different slopes is a common daily activity for many ambulatory people with multiple sclerosis (pwMS) AIM: Investigate energy expenditure measures of walking on level, uphill and downhill slopes in pwMS. DESIGN: Observational case-control study. SETTING: Sheba Multiple Sclerosis Center, Tel-Hashomer, Israel. POPULATION: Eighteen pwMS; 10 women and 8 men, aged 39.7 (SD=6.8), mean EDSS was 2.9 (SD=1.2) and 23 healthy adults; 8 women and 15 men, aged 37.1 (S.D.=5.3). METHODS: Energy expenditure values were obtained via a metabolic device during four conditions: sitting, comfortable walking, uphill and downhill walking. Each walking trial, obtained on a treadmill, lasted 6-min and were separated by10-min recovery intervals. RESULTS: For both pwMS and healthy controls, the O2 rate and O2 cost was higher during uphill walking compared to level walking and lower during downhill walking compared with level walking. O2 rate and net O2 cost during uphill walking was lower in pwMS compared with the healthy controls. The most demanding effort was during uphill walking, with pwMS rating it more demanding compared with the healthy controls. CONCLUSIONS: Perceived effort of walking on different slopes is not consistent with changes in the energy expenditure values in pwMS. CLINICAL REHABILITATION IMPACT: pwMS describe the effort of walking on different slopes higher than normal, regardless of the energy expenditure values.
 Oligodendrocyte (OL) damage and death are prominent features of multiple sclerosis (MS) pathology, yet mechanisms contributing to OL loss are incompletely understood. Dysfunctional RNA binding proteins (RBPs), hallmarked by nucleocytoplasmic mislocalization and altered expression, have been shown to result in cell loss in neurologic diseases, including in MS. Since we previously observed that the RBP heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) was dysfunctional in neurons in MS, we hypothesized that it might also contribute to OL pathology in MS and relevant models. We discovered that hnRNP A1 dysfunction is characteristic of OLs in MS brains. These findings were recapitulated in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS, where hnRNP A1 dysfunction was characteristic of OLs, including oligodendrocyte precursor cells and mature OLs in which hnRNP A1 dysfunction correlated with demyelination. We also found that hnRNP A1 dysfunction was induced by IFNγ, indicating that inflammation influences hnRNP A1 function. To fully understand the effects of hnRNP A1 dysfunction on OLs, we performed siRNA knockdown of hnRNP A1, followed by RNA sequencing. RNA sequencing detected over 4000 differentially expressed transcripts revealing alterations to RNA metabolism, cell morphology, and programmed cell death pathways. We confirmed that hnRNP A1 knockdown was detrimental to OLs and induced apoptosis and necroptosis. Together, these data demonstrate a critical role for hnRNP A1 in proper OL functioning and survival and suggest a potential mechanism of OL damage and death in MS that involves hnRNP A1 dysfunction.
 BACKGROUND: Cognitive fatigue is highly prevalent in people with multiple sclerosis (pwMS) and significantly limits their quality of life. Fatigue can be subdivided into a subjective feeling of constant (trait) or current (state) exhaustion, as well as an objective performance decline, also known as fatigability. However, the current fatigue diagnosis in pwMS is purely subjective, leaving fatigability mostly unattended. Sensorimotor and sensory gating deficits have recently been described as possible objective markers for fatigability in healthy subjects. Thus, this study aimed to investigate the potential of prepulse inhibition (PPI) ratios and the P50 sensory gating suppression as surrogate markers for cognitive fatigue in pwMS. METHODS: PPI and P50 sensory gating ratios were assessed before and after a 30-min fatigability-inducing AX- continuous performance task. Subjective trait fatigue was operationalized via self-report questionnaires, subjective state fatigue via visual analog scales (VAS), and fatigability via the change in both gating ratios. The data were analyzed using Linear Mixed Models and Pearson correlations. RESULTS: We included 18 pwMS and 20 healthy controls (HC) in the final analyses. The task-induced fatigability was more pronounced in pwMS. While the initial PPI and P50 ratios were similar in both groups, P50 sensory gating was significantly disrupted after fatigability induction in pwMS. PPI, on the other hand, decreased in both groups. Moreover, initial P50 sensory gating ratios were negatively associated with subjective trait fatigue in pwMS, indicating that higher trait fatigue is associated with disrupted sensory gating. Finally, fatigability-related changes in P50 sensory gating were associated with the changes in VAS ratings, but only in HC. CONCLUSIONS: This study demonstrated that P50 sensory gating is a promising objective fatigue and fatigability parameter. Importantly, P50 sensory gating correlated with subjective trait and state fatigue ratings. Our results extend the subjective fatigue diagnosis and broaden the understanding of pathophysiological neuronal mechanisms in MS-related fatigue. This is the first study to present fatigue-related disruption of sensory gating in pwMS.
 BACKGROUND: There is considerable evidence that persons with multiple sclerosis (PwMS) who experience cognitive impairments (CIs) are at risk of having significant limitations in activities of daily living (ADLs). However, ADL assessment often consists of proxies or self-report of ADLs. This study examined whether the performance of instrumental ADLs (I-ADL) is impaired in PwMS with and without CI. METHODS: Participants included 72 PwMS and 48 matched healthy controls (HCs). PwMS were divided into MS-CI (n = 25) and MS-not-impaired (n = 47) groups based on the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) scores. All participants performed the Actual Reality(TM) (AR) test, measuring I-ADL using authentic websites. RESULTS: The MS-CI performed significantly worse on AR compared with HC and MS-not-impaired. In addition, the MS-not-impaired performed significantly worse than HC on AR. AR differentiates well between PwMS with and without CI. CONCLUSIONS: While CI in MS results in significant limitations in the performance of I-ADL, PwMS who do not show evidence of CI can have limitations in I-ADL. AR assessment is a valid and reliable tool sensitive to CI. It should be used in addition to traditional cognitive assessments to detect early functional deterioration through the course of MS.
 Zika virus (ZIKV) is an arbovirus of the Flaviviridae genus that has rapidly disseminated from across the Pacific to the Americas. Robust evidence has indicated a crucial role of ZIKV in congenital virus syndrome, including neonatal microcephaly. Moreover, emerging evidence suggests an association between ZIKV infection and the development of an extensive spectrum of central nervous system inflammatory demyelinating diseases (CNS IDD), such as multiple sclerosis-like clinical phenotypes. However, the underlying mechanisms of host-pathogen neuro-immune interactions remain to be elucidated. This study aimed to identify common transcriptional signatures between multiple sclerosis (MS) and ZIKV infection to generate molecular interaction networks, thereby leading to the identification of deregulated processes and pathways, which could give an insight of these underlying molecular mechanisms. Our investigation included publicly available transcriptomic data from MS patients in either relapse or remission (RR-MS) and datasets of subjects acutely infected by ZIKV for both immune peripheral cells and central nervous system cells. The protein-protein interaction (PPI) analysis showed upregulated AP-1 transcription factors (JUN and FOS) among the top hub and bottleneck genes in RR-MS and ZIKV data. Gene enrichment analysis retrieved a remarkable presence of ontologies and pathways linked to oxidative stress responses, immune cell function, inflammation, interleukin signaling, cell division, and transcriptional regulation commonly enriched in both scenarios. Considering the recent findings concerning AP-1 function in immunological tolerance breakdown, regulation of inflammation, and its function as an oxidative stress sensor, we postulate that the ZIKV trigger may contribute as a boost for the activation of such AP-1-regulated mechanisms that could favor the development of MS-like phenotypes following ZIKV infection in a genetically susceptible individual.
 Interferon-beta (IFN-β) for Multiple Sclerosis (MS) is turning 30. The COVID-19 pandemic rejuvenated the interest in interferon biology in health and disease, opening translational opportunities beyond neuroinflammation. The antiviral properties of this molecule are in accord with the hypothesis of a viral etiology of MS, for which a credible culprit has been identified in the Epstein-Barr Virus. Likely, IFNs are crucial in the acute phase of SARS-CoV-2 infection, as demonstrated by inherited and acquired impairments of the interferon response that predispose to a severe COVID-19 course. Accordingly, IFN-β exerted protection against SARS-CoV-2 in people with MS (pwMS). In this viewpoint, we summarize the evidence on IFN-β mechanisms of action in MS with a focus on its antiviral properties, especially against EBV. We synopsize the role of IFNs in COVID-19 and the opportunities and challenges of IFN-β usage for this condition. Finally, we leverage the lessons learned in the pandemic to suggest a role of IFN-β in long-COVID-19 and in special MS subpopulations.
 IMPORTANCE: Progression independent of relapse activity (PIRA) is the main event responsible for irreversible disability accumulation in relapsing multiple sclerosis (MS). OBJECTIVE: To investigate clinical and neuroimaging predictors of PIRA at the time of the first demyelinating attack and factors associated with long-term clinical outcomes of people who present with PIRA. DESIGN, SETTING, AND PARTICIPANTS: This cohort study, conducted from January 1, 1994, to July 31, 2021, included patients with a first demyelinating attack from multiple sclerosis; patients were recruited from 1 study center in Spain. Patients were excluded if they refused to participate, had alternative diagnoses, did not meet protocol requirements, had inconsistent demographic information, or had less than 3 clinical assessments. EXPOSURES: Exposures included (1) clinical and neuroimaging features at the first demyelinating attack and (2) presenting PIRA, ie, confirmed disability accumulation (CDA) in a free-relapse period at any time after symptom onset, within (vs after) the first 5 years of the disease (ie, early/late PIRA), and in the presence (vs absence) of new T2 lesions in the previous 2 years (ie, active/nonactive PIRA). MAIN OUTCOMES AND MEASURES: Expanded Disability Status Scale (EDSS) yearly increase rates since the first attack and adjusted hazard ratios (HRs) for predictors of time to PIRA and time to EDSS 6.0. RESULTS: Of the 1128 patients (mean [SD] age, 32.1 [8.3] years; 781 female individuals [69.2%]) included in the study, 277 (25%) developed 1 or more PIRA events at a median (IQR) follow-up time of 7.2 (4.6-12.4) years (for first PIRA). Of all patients with PIRA, 86 of 277 (31%) developed early PIRA, and 73 of 144 (51%) developed active PIRA. Patients with PIRA were slightly older, had more brain lesions, and were more likely to have oligoclonal bands than those without PIRA. Older age at the first attack was the only predictor of PIRA (HR, 1.43; 95% CI, 1.23-1.65; P < .001 for each older decade). Patients with PIRA had steeper EDSS yearly increase rates (0.18; 95% CI, 0.16-0.20 vs 0.04; 95% CI, 0.02-0.05; P < .001) and an 8-fold greater risk of reaching EDSS 6.0 (HR, 7.93; 95% CI, 2.25-27.96; P = .001) than those without PIRA. Early PIRA had steeper EDSS yearly increase rates than late PIRA (0.31; 95% CI, 0.26-0.35 vs 0.13; 95% CI, 0.10-0.16; P < .001) and a 26-fold greater risk of reaching EDSS 6.0 from the first attack (HR, 26.21; 95% CI, 2.26-303.95; P = .009). CONCLUSIONS AND RELEVANCE: Results of this cohort study suggest that for patients with multiple sclerosis, presenting with PIRA after a first demyelinating event was not uncommon and suggests an unfavorable long-term prognosis, especially if it occurs early in the disease course.
 Epstein-Barr virus (EBV) is a ubiquitous human lymphotropic herpesvirus with a well-established causal role in several cancers. Recent studies have provided compelling epidemiological and mechanistic evidence for a causal role of EBV in multiple sclerosis (MS). MS is the most prevalent chronic inflammatory and neurodegenerative disease of the central nervous system and is thought to be triggered in genetically predisposed individuals by an infectious agent, with EBV as the lead candidate. How a ubiquitous virus that typically leads to benign latent infections can promote cancer and autoimmune disease in at-risk populations is not fully understood. Here we review the evidence that EBV is a causal agent for MS and how various risk factors may affect EBV infection and immune control. We focus on EBV contributing to MS through reprogramming of latently infected B lymphocytes and the chronic presentation of viral antigens as a potential source of autoreactivity through molecular mimicry. We consider how knowledge of EBV-associated cancers may be instructive for understanding the role of EBV in MS and discuss the potential for therapies that target EBV to treat MS.
 Today's medicine strives to be personalized, preventive, predictive and participatory. This implies to have access to multimodal data to better characterize patients groups and to combine clinical and imaging data with high-quality biological samples. Collecting such data is one of the objectives of the Observatoire français de la sclérose en plaques (OFSEP), the French MS registry. On December 2022, the OFSEP biocollection includes 4,888 patients with scientific characteristics and about 90,000 samples. Thanks to its richness, this biocollection open for the scientific community, contributes to address unmet needs in MS through identification of multiomics determinants of MS activity, progression and secondary effects.
 BACKGROUND: Cerebrospinal fluid (CSF) is an important sampling site for putative biomarkers and contains immune cells. CXCL10 is a multiple sclerosis (MS)-relevant chemokine that is present in the injured central nervous system and recruits CXCR3+ immune cells toward injured tissues. OBJECTIVE: Perform a comprehensive evaluation to determine a potential relationship between CXCL10 and various immune cell subsets in the CNS of MS and control cases. METHODS: In MS and control cases, CXCL10 was measured in the CSF and plasma by ELISA. Immune cells within both the CSF and peripheral blood were quantified by flow cytometry. RESULTS: Compared to non-inflammatory neurological disease (NIND) cases, MS cases had significantly higher CXCL10 in CSF (p = 0.021); CXCL10 was also correlated with total cell numbers in CSF (p = 0.04) and T cell infiltrates (CD3+, p = 0.01; CD4+, p = 0.01; CD8+, p = 0.02); expression of CXCR3 on peripheral immune cell subsets was not associated with CSF CXCL10. CONCLUSIONS: Elevated levels of CXCL10 in the CSF of MS cases are associated with increased T cells but appear to be independent of peripheral CXCR3 expression. These results support the importance of elevated CXCL10 in MS and suggest the presence of an alternative mechanism of CXCL10 outside of solely influencing immune cell trafficking.
 Multiple sclerosis (MS) is a severe chronic autoimmune demyelinating disease of the central nervous system, mediated by Th1/Th17 lymphocytes as well as B lymphocytes, macrophages and other immune cells. Some patients with MS are treated with alemtuzumab, a monoclonal antibody against CD52+ cells, which belongs to the disease-modifying therapies (DMTs). The main effect of alemtuzumab is related to changes in immune recruitment. Alemtuzumab therapy can induce secondary autoimmunity against the background of immune rebalancing. The thyroid gland is generally involved in the autoimmune process. Graves' disease (GD) develops most often, followed by autoimmune thyroiditis.We present a clinical case of a patient with GD developed after alemtuzumab therapy for MS. The patient was referred to a radiologist at the Department of Radionuclide Therapy of Endocrinology Research Centre for radioiodine therapy (RAIT) due to relapse of thyrotoxicosis after anti-thyroid drug therapy for GD. The goal of treatment was achieved in 2 months, thyroid hormone therapy was initiated, against the background of this, there was compensation of thyroid function.
 Therapeutic approaches providing effective medication for Alzheimer's disease (AD) patients after disease onset are urgently needed. Previous studies in AD mouse models and in humans suggested that physical exercise or changed lifestyle can delay AD-related synaptic and memory dysfunctions when treatment started in juvenile animals or in elderly humans before onset of disease symptoms. However, a pharmacological treatment that can reverse memory deficits in AD patients was thus far not identified. Importantly, AD disease-related dysfunctions have increasingly been associated with neuro-inflammatory mechanisms and searching for anti-inflammatory medication to treat AD seems promising. Like for other diseases, repurposing of FDA-approved drugs for treatment of AD is an ideally suited strategy to reduce the time to bring such medication into clinical practice. Of note, the sphingosine-1-phosphate analogue fingolimod (FTY720) was FDA-approved in 2010 for treatment of multiple sclerosis patients. It binds to the five different isoforms of Sphingosine-1-phosphate receptors (S1PRs) that are widely distributed across human organs. Interestingly, recent studies in five different mouse models of AD suggest that FTY720 treatment, even when starting after onset of AD symptoms, can reverse synaptic deficits and memory dysfunction in these AD mouse models. Furthermore, a very recent multi-omics study identified mutations in the sphingosine/ceramide pathway as a risk factor for sporadic AD, suggesting S1PRs as promising drug target in AD patients. Therefore, progressing with FDA-approved S1PR modulators into human clinical trials might pave the way for these potential disease modifying anti-AD drugs.
 Multiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), characterized by demyelination and neurodegeneration. Oligodendrocytes play a vital role in maintaining the integrity of myelin, the protective sheath around nerve fibres essential for efficient signal transmission. However, in MS, oligodendrocytes become dysfunctional, leading to myelin damage and axonal degeneration. Emerging evidence suggests that metabolic changes, including mitochondrial dysfunction and alterations in glucose and lipid metabolism, contribute significantly to the pathogenesis of MS. Mitochondrial dysfunction is observed in both immune cells and oligodendrocytes within the CNS of MS patients. Impaired mitochondrial function leads to energy deficits, affecting crucial processes such as impulse transmission and axonal transport, ultimately contributing to neurodegeneration. Moreover, mitochondrial dysfunction is linked to the generation of reactive oxygen species (ROS), exacerbating myelin damage and inflammation. Altered glucose metabolism affects the energy supply required for oligodendrocyte function and myelin synthesis. Dysregulated lipid metabolism results in changes to the composition of myelin, affecting its stability and integrity. Importantly, low levels of polyunsaturated fatty acids in MS are associated with upregulated lipid metabolism and enhanced glucose catabolism. Understanding the intricate relationship between these mechanisms is crucial for developing targeted therapies to preserve myelin and promote neurological recovery in individuals with MS. Addressing these metabolic aspects may offer new insights into potential therapeutic strategies to halt disease progression and improve the quality of life for MS patients.
 BACKGROUND AND OBJECTIVES: To evaluate whether the kappa free light chain index (K-index) can predict the occurrence of new T2-weighted MRI lesions (T2L) and clinical events in clinically isolated syndrome (CIS) and radiologically isolated syndrome (RIS). METHODS: All consecutive patients presenting for the diagnostic workup, including CSF analysis, of clinical and/or MRI suspicion of multiple sclerosis (MS) since May 1, 2018, were evaluated. All patients diagnosed with CIS and RIS with at least 1-year follow-up were included. Clinical events and new T2L were collected during follow-up. The K-index performances in predicting new T2L and a clinical event were evaluated using time-dependent ROC analyses. The time to clinical event or new T2L was estimated using survival analysis according to the binarized K-index using an independent cutoff of 8.9, and the ability of each variable to predict outcomes was compared using the Harrell c-index. RESULTS: One hundred and eighty two patients (146 CIS and 36 RIS, median age 39 [30; 48] y-o, 70% females) were included with a median follow-up of 21 [13, 33] months. One hundred five (58%) patients (85 CIS and 20 RIS) experienced new T2L, and 28 (15%; 21 CIS and 7 RIS) experienced a clinical event. The K-index could predict new T2L over time in CIS (area under the curve [AUC] ranging from 0.86 to 0.96) and in RIS (AUC ranging from 0.84 to 0.54) but also a clinical event in CIS (AUC ranging from 0.75 to 0.87). Compared with oligoclonal bands (OCBs), the K-index had a better sensitivity and a slight lower specificity in predicting new T2L and clinical events in both populations. In the predictive model, the K-index was the variable that best predict new T2L in both CIS and RIS but also clinical events in CIS (c-index ranging from 0.70 to 0.77), better than the other variables, including OCB. DISCUSSION: This study provides evidence that the K-index predicts new T2L in CIS and RIS but also clinical attack in patients with CIS. We suggest adding the K-index in the further MS diagnosis criteria revisions as a dissemination-in-time biomarker.
 BACKGROUND: Research interest in the impact of comorbidities in MS has been expanding. Based on studies, certain comorbidities are more prevalent in MS population such as depression, anxiety, hypertension and hypercholesterolemia, diabetes, and hypothyroidism. OBJECTIVE: This study aims to describe the prevalence of comorbidities in MS population based on the health insurance claims data. METHOD: This retrospective database analysis was conducted using patient-level medicinal and pharmacy claims data from a leading insurance group (Iranian health insurance) in 2007-2016. MS population was identified based on their Disease Modifying Therapies prescribed by a neurologist (qualified to diagnose MS). Comorbidities in MS and non-MS population were assessed by their prescriptions. Crude and age-standardized prevalence rate (ASPR) of coverage of comorbidities in different age and sex groups and their odds ratio versus non-MS population were assessed. RESULTS: The most common comorbidities were depression (15.50%) and anxiety (10.1%). Hypercholesterolemia, diabetes, hypertension, and hypothyroidism were prevalent in 6%, 3.6%, 3.5%, and 2.7% respectively. Anxiety and depression were more prevalent in middle age group (45-65 years old). But other comorbidities were more prevalent in older age groups. All comorbidities were more prevalent in female except hypertension in patients ≥45 years old. The odds of all comorbidities were higher for male patients with MS rather than their parallel age group in non-MS patients. These also applied for female patients with MS 18-44 years old (except hypertension). CONCLUSION: Using claims data, the prevalence of taking treatment for selected comorbidities in MS population and their association with sex and age, can guide patients, healthcare providers, and policy makers to help improve MS patients' wellbeing.
 BACKGROUND: The impact of disease-modifying therapies on the efficacy to mount appropriate immune responses to COVID-19 vaccination in patients with multiple sclerosis (MS) is currently under investigation. OBJECTIVE: To characterize long-term humoral and cellular immunity in mRNA-COVID-19 MS vaccinees treated with teriflunomide or alemtuzumab. METHODS: We prospectively measured SARS-COV-2 IgG, memory B-cells specific for SARS-CoV-2 RBD, and memory T-cells secreting IFN-γ and/or IL-2, in MS patients vaccinated with BNT162b2-COVID-19 vaccine before, 1, 3 and 6 months after the second vaccine dose, and 3-6 months following vaccine booster. RESULTS: Patients were either untreated (N = 31, 21 females), under treatment with teriflunomide (N = 30, 23 females, median treatment duration 3.7 years, range 1.5-7.0 years), or under treatment with alemtuzumab (N = 12, 9 females, median time from last dosing 15.9 months, range 1.8-28.7 months). None of the patients had clinical SARS-CoV-2 or immune evidence for prior infection. Spike IgG titers were similar between untreated, teriflunomide and alemtuzumab treated MS patients both at 1 month (median 1320.7, 25-75 IQR 850.9-3152.8 vs. median 901.7, 25-75 IQR 618.5-1495.8, vs. median 1291.9, 25-75 IQR 590.8-2950.9, BAU/ml, respectively), at 3 months (median 1388.8, 25-75 1064.6-2347.6 vs. median 1164.3 25-75 IQR 726.4-1399.6, vs. median 837.2, 25-75 IQR 739.4-1868.5 BAU/ml, respectively), and at 6 months (median 437.0, 25-75 206.1-1161.3 vs. median 494.3, 25-75 IQR 214.6-716.5, vs. median 176.3, 25-75 IQR 72.3-328.8 BAU/ml, respectively) after the second vaccine dose. Specific SARS-CoV-2 memory B cells were detected in 41.9%, 40.0% and 41.7% of subjects at 1 month, in 32.3%, 43.3% and 25% at 3 months, and in 32.3%, 40.0%, 33.3% at 6 months following vaccination in untreated, teriflunomide treated and alemtuzumab treated MS patients, respectively. Specific SARS-CoV-2 memory T cells were found in 48.4%, 46.7% and 41.7 at 1 month, in 41.9%, 56.7% and 41.7% at 3 months, and in 38.7%, 50.0%, and 41.7% at 6 months, of untreated, teriflunomide-treated and alemtuzumab -treated MS patients, respectively. Administration of a third vaccine booster significantly increased both humoral and cellular responses in all patients. CONCLUSIONS: MS patients treated with teriflunomide or alemtuzumab achieved effective humoral and cellular immune responses up to 6 months following second COVID-19 vaccination. Immune responses were reinforced following the third vaccine booster.
 Cladribine has been approved for the treatment of multiple sclerosis (MS) and its administration results in a long-lasting depletion of lymphocytes. As lymphopenia is known to hamper immune responses to vaccination, we evaluated the immunogenicity of the influenza vaccine in patients undergoing cladribine treatment at different stages vs. controls. The antibody response in 90 cladribine-treated MS patients was prospectively compared with 10 control subjects receiving platform immunotherapy (NCT05019248). Serum samples were collected before and six months after vaccination. Response to vaccination was determined by the hemagglutination-inhibition test. Postvaccination seroprotection rates against influenza A were comparable in cladribine-treated patients and controls (H1N1: 94.4% vs. 100%; H3N2: 92.2% vs. 90.0%). Influenza B response was lower in the cladribine cohort (61.1% vs. 80%). The increase in geometric mean titers was lower in the cladribine group vs. controls (H1N1: +98.5 vs. +188.1; H3N2: +225.3 vs. +300.0; influenza B: +40.0 vs. +78.4); however, titers increased in both groups for all strains. Seroprotection was achieved irrespective of vaccination timing and lymphocyte subset counts at the time of vaccination in the cladribine cohort. To conclude, cladribine-treated MS patients can mount an adequate immune response to influenza independently of treatment duration and time interval to the last cladribine administration.
 Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system). The aim of this study was to investigate the effect of 6 weeks of aerobic training on the main proteins of myelin including myelin basic protein (MBP), myelin oligodendrocyte (MOG), myelin associated glycoprotein (MAG), and myelin proteolipid protein (PLP) at hippocampus of C57BL/6 mouse model of cuprizone-induced MS. Twenty-eight female C57BL/6 mice (23 ± 3 g) were randomly divided into four groups (n = 7 per group): control, exercise (Exe), cuprizone (CPZ), and cuprizone with exercise (CPZ + Exe). Exercise groups performed treadmill aerobic exercise training 5 days a week, 15-22 m/min, and 15-60 min, during 6 weeks. Cuprizone were fed to mice at CPZ and CPZ + Exe groups for 6 weeks. Animals were sacrificed after 6 weeks. Biochemical and molecular biology analyses were performed. Mice at CPZ group had decreased myelination of nerve cells in the hippocampus. In addition, the use of CPZ in the hippocampus caused a decrease in the MBP, MOG gene expression, as well as a decrease in the MAG and PLP gene and protein expression compared to the healthy control group. However, performing aerobic exercise with CPZ consumption increased MBP gene expression and increased MAG and PLP protein expression, as well as increased myelination of nerve cells in the hippocampus compared to the CPZ group (p < 0.05). It seems that regular aerobic exercise in the MS model controls the destruction of myelin in the nerve cells of hippocampus by upregulating MBP, MAG and PLP, which can have positive effects on cognitive and motor performance.
 BACKGROUND AND OBJECTIVES: In multiple sclerosis (MS), accelerated aging of the immune system (immunosenescence) may be associated with disease onset or drive progression. DNA methylation (DNAm) is an epigenetic factor that varies among lymphocyte subtypes, and cell-specific DNAm is associated with MS. DNAm varies across the life span and can be used to accurately estimate biological age acceleration, which has been linked to a range of morbidities. The objective of this study was to test for cell-specific epigenetic age acceleration (EAA) in people with MS. METHODS: This was a case-control study of EAA using existing DNAm data from several independent previously published studies. Data were included if .idat files from Illumina 450K or EPIC arrays were available for both a case with MS and an age-matched and sex-matched control, from the same study. Multifactor statistical modeling was performed to assess the primary outcome of EAA. We explored the relationship of EAA and MS, including interaction terms to identify immune cell-specific effects. Cell-sorted DNA methylation data from 3 independent datasets were used to validate findings. RESULTS: We used whole blood DNA methylation data from 583 cases with MS and 643 non-MS controls to calculate EAA using the GrimAge algorithm. The MS group exhibited an increased EAA compared with controls (approximately 9 mths, 95% CI 3.6-14.4), p = 0.001). Statistical deconvolution showed that EAA is associated with MS in a B cell-dependent manner (β (int) = 1.7, 95% CI 0.3-2.8), p = 0.002), irrespective of B-cell proportions. Validation analysis using 3 independent datasets enriched for B cells showed an EAA increase of 5.1 years in cases with MS compared with that in controls (95% CI 2.8-7.4, p = 5.5 × 10(-5)). By comparison, there was no EAA difference in MS in a T cell-enriched dataset. We found that EAA was attributed to the DNAm surrogates for Beta-2-microglobulin (difference = 47,546, 95% CI 10,067-85,026; p = 7.2 × 10(-5)), and smoking pack-years (difference = 8.1, 95% CI 1.9-14.2, p = 0.002). DISCUSSION: This study provides compelling evidence that B cells exhibit marked EAA in MS and supports the hypothesis that premature B-cell immune senescence plays a role in MS. Future MS studies should focus on age-related molecular mechanisms in B cells.
 BACKGROUND: Vitamin D is an important regulator of calcium. Mendelian randomization (MR) studies exclusively focused on the circulating total 25-hydroxyvitamin D (25(OH)D) as a biomarker of vitamin D status, and have found the causal association between 25(OH)D and the risk of multiple sclerosis (MS). However, it currently remains unclear about the causal association of the 25(OH)D subtypes including 25(OH)D3 and C3-epi-25(OH)D3, as well as calcium with the risk of MS. METHODS: We performed a two-sample MR study to evaluate the causal association of circulating total 25(OH)D, 25(OH)D3, C3-epi-25(OH)D3, and calcium with the risk of MS using large-scale genome-wide association studies (GWAS) datasets from total 25(OH)D (n = 417,580), 25(OH)D3 (n = 40,562), C3-epi-25(OH)D3 (n = 40,562), calcium (n = 305,349), and MS (14,802 MS and 26,703 controls). We selected five MR methods including inverse-variance weighted (IVW), simple median, weighted median, MR-Egger, MR-PRESSO (Mendelian Randomization Pleiotropy Residual Sum and Outlier), and contamination mixture method. RESULTS: IVW showed that the genetically increased circulating 25(OH)D level (OR = 0.81, 95% CI: 0.70-0.94, P = 4.00E-03), circulating 25(OH)D3 level (OR = 0.85, 95% CI: 0.76-0.95, P = 5.00E-03), and circulating C3-epi-25(OH)D3 level (OR = 0.85, 95% CI: 0.74-0.98, P = 2.30E-02) were causally associated with reduced risk of MS. However, IVW showed no causal association between circulating calcium level and the risk of MS with OR = 2.85, 95% CI: 0.42-19.53, P = 2.85E-01. CONCLUSIONS: Our current findings together with evidence from other MR studies support the use of vitamin D but not calcium supplementation for the prevention of MS.
 BACKGROUND: Identifying mutual neuroinflammatory axis in different experimental models of multiple sclerosis (MS) is essential to evaluate the de- and re-myelination processes and improve therapeutic interventions' reproducibility. METHODS: The expression profile data set of EAE (GSE47900) and cuprizone (GSE100663) models were downloaded from the Gene Expression Omnibus database. The R package and GEO2R software processed these raw chip data. Gene Ontology (GO) functional analysis, KEGG pathway analysis, and protein-protein interaction network analysis were performed to investigate interactions between common differentially expressed genes (DEGs) in all models. Finally, the ELISA method assessed the protein level of highlighted mutual cytokines in serum. RESULTS: Our data introduced 59 upregulated [CXCL10, CCL12, and GBP6 as most important] and 17 downregulated [Serpinb1a, Prr18, and Ugt8a as most important] mutual genes. The signal transducer and activator of transcription 1 (STAT1) and CXCL10 were the most crucial hub proteins among mutual upregulated genes. These mutual genes were found to be mainly involved in the TNF-α, TLRs, and complement cascade signaling, and animal models shared 26 mutual genes with MS individuals. Finally, significant upregulation of serum level of TNF-α/IL-1β/CXCL10 cytokines was confirmed in all models in a relatively similar pattern. CONCLUSION: For the first time, our study revealed the common neuroinflammatory pathway in animal models of MS and introduced candidate hub genes for better evaluating the preclinical efficacy of pharmacological interventions and designing prospective targeted therapies.
 STUDY DESIGN: Scoping review. OBJECTIVE: To identify and provide systematic overviews of partnership principles and strategies identified from health research about spinal cord injury (SCI) and related health conditions. METHODS: Four health electronic databases (Medline, Embase, CINAHL, PsycINFO) were searched from inception to March 2019. We included articles that described, reflected, and/or evaluated one or more collaborative research activities in health research about SCI, stroke, multiple sclerosis, Parkinson's disease, amputation, cerebral palsy, spina bifida, amyotrophic lateral sclerosis, acquired brain injury, or wheelchair-users. Partnership principles (i.e. norms or values) and strategies (i.e. observable actions) were extracted and analyzed using directed qualitative content analysis. RESULTS: We included 39 articles about SCI (n = 13), stroke (n = 15), multiple sclerosis (n = 5), amputation (n = 2), cerebral palsy (n = 2), Parkinson's disease (n = 1), and wheelchair users (n = 1). We extracted 110 principles and synthesized them into 13 overarching principles. Principles related to building and maintaining relationships between researchers and research users were most frequently reported. We identified 32 strategies that could be applied at various phases of the research process and 26 strategies that were specific to a research phase (planning, conduct, or dissemination). CONCLUSION: We provided systematic overviews of principles and strategies for research partnerships. These could be used by researchers and research users who want to work in partnership to plan, conduct and/or disseminate their SCI research. The findings informed the development of the new SCI Integrated Knowledge Translation Guiding Principles (www.iktprinciples.com) and will support the implementation of these Principles within the SCI research system.
 BACKGROUND AND OBJECTIVES: Ocrelizumab improved clinical and MRI measures of disease activity and progression in three phase 3 multiple sclerosis (MS) studies. Post hoc analyses demonstrated a correlation between the ocrelizumab serum concentration and the degree of blood B-cell depletion, and body weight was identified as the most influential covariate on ocrelizumab pharmacokinetics. The magnitude of ocrelizumab treatment benefit on disability progression was greater in lighter vs heavier patients. These observations suggest that higher ocrelizumab serum levels provide more complete B-cell depletion and a greater delay in disability progression. The current post hoc analyses assessed population exposure-efficacy/safety relationships of ocrelizumab in patients with relapsing and primary progressive MS. METHODS: Patients in OPERA I/II and ORATORIO were grouped in exposure quartiles based on their observed individual serum ocrelizumab level over the treatment period. Exposure-response relationships were analyzed for clinical efficacy (24-week confirmed disability progression (CDP), annualized relapse rate [ARR], and MRI outcomes) and adverse events. RESULTS: Ocrelizumab reduced new MRI lesion counts to nearly undetectable levels in patients with relapsing or primary progressive MS across all exposure subgroups, and reduced ARR in patients with relapsing MS to very low levels (0.13-0.18). A consistent trend of higher ocrelizumab exposure leading to lower rates of CDP was seen (0%-25% [lowest] to 75%-100% [highest] quartile hazard ratios and 95% confidence intervals; relapsing MS: 0.70 [0.41-1.19], 0.85 [0.52-1.39], 0.47 [0.25-0.87], and 0.34 [0.17-0.70] vs interferon β-1a; primary progressive MS: 0.88 [0.59-1.30], 0.86 [0.60-1.25], 0.77 [0.52-1.14], and 0.55 [0.36-0.83] vs placebo). Infusion-related reactions, serious adverse events, and serious infections were similar across exposure subgroups. DISCUSSION: The almost complete reduction of ARR and MRI activity already evident in the lowest quartile, and across all ocrelizumab-exposure groups, suggests a ceiling effect. A consistent trend of higher ocrelizumab exposure leading to greater reduction in risk of CDP was observed, particularly in the relapsing MS trials, and was not associated with a higher rate of adverse events. Higher ocrelizumab exposure may provide improved control of disability progression by reducing disease activity below that detectable by ARR and MRI, and/or by attenuating other B-cell-related pathologies responsible for tissue damage. CLASSIFICATION OF EVIDENCE: This analysis provides Class III evidence that higher ocrelizumab serum levels are related to greater reduction in risk of disability progression in patients with multiple sclerosis. The study is rated Class III because of the initial treatment randomization disclosure that occurred after inclusion in the open-label extension. TRIAL REGISTRATION INFORMATION: ClinicalTrials.gov Identifier: NCT01247324 (OPERA I), NCT01412333 (OPERA II), and NCT01194570 (ORATORIO).
 The high-mobility-group domain-containing transcription factor Sox9 confers glial competence to neuroepithelial precursors in the developing central nervous system and is an important determinant of astroglial and oligodendroglial specification. In oligodendroglial cells, it remains expressed in oligodendrocyte progenitor cells (OPCs) of the developing nervous system, but is shut off in differentiating oligodendrocytes as well as in OPCs that persist in the adult nervous system. To better understand the role of Sox9 in OPCs, we generated mouse models that allowed oligodendroglial expression of a Sox9 transgene during development or in the adult. With transgene expression beginning in the last trimester of pregnancy, the number of OPCs increased dramatically, followed by comparable gains in the number of pre-myelinating and myelinating oligodendrocytes as assessed by marker gene expression. This argues that Sox9 boosts oligodendrogenesis during ontogenetic development at all stages, including terminal oligodendrocyte differentiation. When Sox9 transgene expression started in the adult, many transgene-expressing OPCs failed to maintain their progenitor cell identity and instead converted into myelinating oligodendrocytes. As infrequent and inefficient differentiation of adult OPCs is one of the main obstacles to effective remyelination in demyelinating diseases such as Multiple Sclerosis, increased Sox9 levels in adult OPCs may substantially increase their remyelination capacity.
 Aluminium (Al) is the most ubiquitous metal in the Earth's crust. Even though its toxicity is well-documented, the role of Al in the pathogenesis of several neurological diseases remains debatable. To establish the basic framework for future studies, we review literature reports on Al toxicokinetics and its role in Alzheimer's disease (AD), autism spectrum disorder (ASD), alcohol use disorder (AUD), multiple sclerosis (MS), Parkinson's disease (PD), and dialysis encephalopathy (DE) from 1976 to 2022. Despite poor absorption via mucosa, the biggest amount of Al comes with food, drinking water, and inhalation. Vaccines introduce negligible amounts of Al, while the data on skin absorption (which might be linked with carcinogenesis) is limited and requires further investigation. In the above-mentioned diseases, the literature shows excessive Al accumulation in the central nervous system (AD, AUD, MS, PD, DE) and epidemiological links between greater Al exposition and their increased prevalence (AD, PD, DE). Moreover, the literature suggests that Al has the potential as a marker of disease (AD, PD) and beneficial results of Al chelator use (such as cognitive improvement in AD, AUD, MS, and DE cases).
 PURPOSE: To compare the effects of exergaming versus conventional exercises on cognition, lower-limb functional coordination, and stepping time in people with multiple sclerosis (PwMS). METHODS: Thirty-six PwMS were randomly assigned to either intervention (n = 18) or control (n = 18) group and received 18 training sessions during six weeks. The intervention group performed exergames that required multidirectional timed-stepping, weight-shifting, and walking while the control group performed conventional matched exercises. Trail making test (TMT part A, B; TMT-A, TMT-B, TMT B-A), six-spot step test (SSST), and choice stepping reaction time (CSRT-including reaction time (RT), movement time (MVT), and total response time (TRT)) were assessed pre- and post-intervention (short-term), and after three-month follow-up (mid-term). RESULTS: The intervention group showed faster TMT-B (p = 0.003) and TMT B-A (p = 0.002) at post-intervention and faster SSST at both post-intervention (p = 0.002) and follow-up (p = 0.04). The CSRT components showed no between-group differences at post-intervention; however, at follow-up, the intervention group had lower TRT (p = 0.046) and MVT (p = 0.015). TMT-A and RT had no significant between-group differences. CONCLUSIONS: In short-term, exergames led to more improvements in complex attention, executive function, and lower-limb functional coordination comparing to the matched conventional exercises. In mid-term, exergaming was more effective for improving stepping time and lower-limb functional coordination. However, the two approaches did not show any superiority over each other for improving simple attention and RT.Implications for rehabilitationWhen designed properly, exergames have great potential to improve attention and executive function of people with multiple sclerosis (PwMS), at least in the short-term.Exergames seem like an appropriate option for improving lower limb coordination and decreasing choice stepping response time among PwMS in the mid-term.Exergames do not have superiority in improving the choice stepping reaction time compared to their matched conventional treatment.
 OBJECTIVES: Knowledge about multiple sclerosis (MS) is crucial for those who provide care and support as caregivers. However, despite the key benefits of acquiring relevant information to properly assume the caregiving role, caregivers' knowledge of MS is poorly investigated. The aim of this study was to develop and validate the Caregivers' Knowledge of Multiple Sclerosis (CareKoMS), a self-assessed questionnaire, to test MS knowledge in caregivers of people with MS. DESIGN: Cross-sectional study. SETTING: Italy. PARTICIPANTS: Two-hundred caregivers (female: 49%) were asked to self-administer the 32-item CareKoMS questionnaire; they had a median age of 60 years (IQR: 51-68 years) and a medium-high educational level (36.5% primary school and 63.5% high school/university). Item analysis using item difficulty index, item discrimination index, Kuder-Richardson-20 coefficient and item-total correlation were assessed. Once excluding less useful items, reliability, floor and ceiling effects and construct validity were calculated on the 21-item CareKoMS final version. RESULTS: Psychometric evaluation indicates that the 21-item CareKoMS was a good questionnaire with no ceiling or floor effects registered. Internal consistency was satisfactory and acceptable as indicated by the mean value of 0.74 of Kuder-Richardson-20. No ceiling or floor effects have been observed. Interestingly, educational level and disease duration correlated with MS knowledge. CONCLUSION: CareKoMS is a valid self-assessed questionnaire on MS knowledge for caregivers that may be used in clinical practice and research. Assessing knowledge of MS among caregivers is essential to facilitate their caregiving role and thus decrease the burden of disease management.
 OBJECTIVES: The clinical impact of brain microstructural abnormalities in multiple sclerosis (MS) remains elusive. We aimed to characterize the topography of longitudinal relaxation rate (R1) and quantitative susceptibility (χ) changes, as indices of iron and myelin, together with brain atrophy, and to clarify their contribution to cognitive and motor disability in MS. METHODS: In this cross-sectional study, voxel-based morphometry, and voxel-based quantification analyses of R1 and χ maps were conducted in gray matter (GM) and white matter (WM) of 117 MS patients and 53 healthy controls. Voxel-wise between-group differences were assessed with nonparametric permutation tests, while correlations between MRI metrics and clinical variables (global disability, cognitive and motor performance) were assessed both globally and voxel-wise within clusters emerging from the between-group comparisons. RESULTS: MS patients showed widespread R1 decrease associated with more limited modifications of χ, with atrophy mainly involving deep GM, posterior and infratentorial regions (p < 0.02). While R1 and χ showed a parallel reduction in several WM tracts (p < 0.001), reduced GM R1 values (p < 0.001) were associated with decreased thalamic χ (p < 0.001) and small clusters of increased χ in the caudate nucleus and prefrontal cortex (p < 0.02). In addition to the atrophy, χ values in the cingulum and corona radiata correlated with global disability and motor performance, while focal demyelination correlated with cognitive performance (p < 0.04). CONCLUSIONS: We confirmed the presence of widespread R1 changes, involving both GM and WM, and atrophy in MS, with less extensive modifications of tissue χ. While atrophy and χ changes are related to global and motor disability, R1 changes are meaningful correlates of cognition. KEY POINTS: • Compared to healthy controls, multiple sclerosis patients showed R1 and χ changes suggestive of iron increase within the basal ganglia and reduced iron and myelin content within (subnuclei of) the thalamus. • Thalamic volume and χ changes significantly predicted clinical disability, as well as pulvinar R1 and χ changes, independently from atrophy. • Atrophy-independent R1 and χ changes, suggestive of thalamic iron and myelin depletion, may represent a sensitive marker of subclinical inflammation.
 BACKGROUND: Magnetic resonance imaging (MRI) T2-lesions resolve more often in myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) than aquaporin-4 IgG-positive neuromyelitis optica spectrum disorder (AQP4 + NMOSD) and multiple sclerosis (MS) in adults but few studies analyzed children. OBJECTIVE: The main objective of this study is to investigate MRI T2-lesion evolution in pediatric MOGAD, AQP4 + NMOSD, and MS. METHODS: Inclusion criteria were as follows: (1) first clinical attack; (2) abnormal MRI (⩽6 weeks); (3) follow-up MRI beyond 6 months without relapses in that region; and (4) age < 18 years. An index T2-lesion (symptomatic/largest) was identified, and T2-lesion resolution or persistence on follow-up MRI was determined. RESULTS: We included 56 patients (MOGAD, 21; AQP4 + NMOSD, 8; MS, 27) with 69 attacks. Index T2-lesion resolution was more frequent in MOGAD (brain 9 of 15 [60%]; spine 8 of 12 [67%]) than AQP4 + NMOSD (brain 1 of 4 [25%]; spine 0 of 7 [0%]) and MS (brain 0 of 18 [0%]; spine 1 of 13 [8%]), p < 0.01. Resolution of all T2-lesions occurred more often in MOGAD (brain 6 of 15 [40%]; spine 7 of 12 [58%]) than AQP4 + NMOSD (brain 1 of 4 [25%]; spine 0 of 7 [0%]), and MS (brain 0 of 18 [0%]; spine 1 of 13 [8%]), p < 0.01. Reductions in median index T2-lesion area were greater in MOGAD (brain, 305 mm; spine, 23 mm) than MS (brain, 42 mm [p<0.001]; spine, 10 mm [p<0.001]) without differing from AQP4 + NMOSD (brain, 133 mm [p=0.42]; spine, 19.5 mm [p=0.69]). CONCLUSION: In children, MRI T2-lesions resolved more often in MOGAD than AQP4 + NMOSD and MS which is similar to adults suggesting these differences are related to pathogenesis rather than age.
 BACKGROUND AND OBJECTIVES: Multiple sclerosis (MS) is a neuroinflammatory and neurodegenerative disease characterized by infiltration of immune cells in multifocal areas of the CNS. The specific molecular processes allowing autoreactive immune cells to enter the CNS compartment through the blood-brain barrier remain elusive. METHODS: Using endothelial cell (EC) enrichment and single-cell RNA sequencing, we characterized the cells implicated in the neuroinflammatory processes in experimental autoimmune encephalomyelitis, an animal model of MS. Validations on human MS brain sections of the most differentially expressed genes in venous ECs were performed using immunohistochemistry and confocal microscopy. RESULTS: We found an upregulation of genes associated with antigen presentation and interferon in most populations of CNS-resident cells, including ECs. Interestingly, instead of transcriptionally distinct profiles, a continuous gradient of gene expression separated the arteriovenous zonation of the brain vasculature. However, differential gene expression analysis presented more transcriptomic alterations on the venous side of the axis, suggesting a prominent role of venous ECs in neuroinflammation. Furthermore, analysis of ligand-receptor interactions identified important potential molecular communications between venous ECs and infiltrated immune populations. To confirm the relevance of our observation in the context of human disease, we validated the protein expression of the most upregulated genes (Ackr1 and Lcn2) in MS lesions. DISCUSSION: In this study, we provide a landscape of the cellular heterogeneity associated with neuroinflammation. We also present important molecular insights for further exploration of specific cell processes that promote infiltration of immune cells inside the brain of experimental autoimmune encephalomyelitis mice.
 BACKGROUND: Research on reflexology therapy for multiple sclerosis (MS) is limited, and the evaluation is mixed. Our aim is to confirm the efficacy of reflexology therapy for MS. METHODS: The preferred reporting items for systematic reviews and meta-analyses guidelines were followed. The search strategy was conducted in PubMed, Embase, the Cochrane Library, and the Science Citation Index. The quality of the included trials was assessed by the Cochrane Handbook. The main results were summarized and analyzed in RevMan 5.4. RESULTS: A total of 11 studies were included in the final analysis. There were significant differences [mean difference (MD) -0.90, 95% confidence interval (CI) -1.37 to -0.43, heterogeneity I2  = 0%] between the Precision Reflexology and Sham Reflexology groups in visual analogue scale pain. There was a significant difference (MD -1.00, 95% CI -1.42 to -0.58, heterogeneity I2  = 93%) between the Precision Reflexology and Sham Reflexology groups on the fatigue severity scale. There was no difference between the Precision Reflexology and Sham Reflexology groups in physical function (MD 6.88, 95% CI -3.36 to 17.13, heterogeneity I2  = 31%), role disorder due to physical problems (MD 10.20, 95% CI -4.91 to 25.30, heterogeneity I2  = 0%), physical pain (MD 7.68, 95% CI -0.09 to 15.45, heterogeneity I2  = 0%), role disorder due to emotional problems (MD 3.41, 95% CI -11.55 to 18.37, heterogeneity I2  = 0%), energy (MD 3.27, 95% CI -4.32 to 10.87, heterogeneity I2  = 0%), emotional well-being (MD 1.79, 95% CI -4.76 to 8.34, heterogeneity I2  = 0%), social function (MD 5.72, 95% CI -3.48 to 14.91, heterogeneity I2  = 0%), or general health (MD 2.63, 95% CI -4.36 to 9.62, heterogeneity I2  = 0%). CONCLUSIONS: Reflexology therapy can be used as an effective intervention for the pain and fatigue of MS patients while improving the quality of life.
 BACKGROUND: Neurogenic detrusor overactivity incontinence (NDOI) is often inadequately managed with oral therapy. OBJECTIVE: To assess efficacy and safety of abobotulinumtoxinA (aboBoNT-A; Dysport®; Ipsen Ltd.) according to etiology of NDOI. DESIGN, SETTING, AND PARTICIPANTS: Two phase III, randomized, double-blind studies (CONTENT1 [NCT02660138] conducted in Asia, Europe and North America; CONTENT2 [NCT02660359] conducted in the Americas, Asia, Europe and Oceania) both included patients with spinal cord injury (SCI) or multiple sclerosis (MS), with inadequately managed NDOI, regularly performing clean intermittent catheterization (CIC). INTERVENTION: Patients in CONTENT1 and CONTENT2 received aboBoNT-A injections 600 U (n = 162)/800 U (n = 161), or placebo (n = 162) into the detrusor muscle. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Primary endpoint: mean change from baseline in number of NDOI episodes/week at Week 6. Secondary endpoints: proportion of patients with no NDOI episodes; incontinence-related quality of life (I-QoL); urodynamic parameters; and time-to-retreatment. Safety was also assessed. Statistical analyses were conducted for pooled populations by etiology (aboBoNT-A doses vs. placebo). RESULTS AND LIMITATIONS: Of 485 randomized patients, 341 (70%) and 144 (30%) had SCI and MS etiologies, respectively. A significant reduction was observed in mean NDOI episodes/week at Week 6 with both aboBoNT-A doses versus placebo in the SCI (all p < 0.001) and MS (all p < 0.01) groups, as well as significant improvements in I-QoL and urodynamic parameters. Median time-to-retreatment was longer in patients with MS (48-62 weeks across doses) than those with SCI (39-44 weeks). Safety data were similar between etiologies. Urinary tract infection was the most frequent adverse event; similar numbers were reported across treatment groups. CONCLUSIONS: AboBoNT-A was well tolerated and significantly improved continence and bladder function, and QoL, in patients with SCI or MS with NDOI performing regular CIC. PATIENT SUMMARY: AboBoNT-A injections improved QoL, symptoms, and bladder function in patients with SCI or MS with bladder muscle overactivity that causes incontinence.
 In our study, we aimed to investigate the relationship between microRNA (miRNA) expression levels and serum iron (Fe), copper (Cu), and zinc (Zn) levels in Multiple sclerosis (MS) patients. Total RNA was isolated from peripheral venous blood containing ethylenediaminetetraacetic acid (EDTA) of MS patients and controls. Total RNA was labeled with Cy3-CTP fluorescent dye. Hybridization of samples was performed on microarray slides and arrays were scanned. Data argument and bioinformatics analysis were performed. Atomic absorption spectrophotometer method was used to measure serum Fe, Cu, and Zn levels. In our study, in bioinformatics analysis, although differently expressed miRNAs were not detected between 16 MS patients and 16 controls, hsa-miR-744-5p upregulation was detected between 4 MS patients and 4 controls. This may be stem from the patient group consisting of MS patients who have never had an attack for 1 year. Serum iron levels were detected significantly higher in the 16 MS patients compared to the 16 controls. This may be stem from the increase in iron accumulation based on inflammation in MS disease. According to the findings in our study, hsa-miR-744-5p upregulation has been determined as an early diagnostic biomarker for the development together of insulin resistance, diabetes mellitus associated with insulin signaling, and Alzheimer's diseases. Therefore, hsa-miR-744-5p is recommended as an important biomarker for the development together of diabetes mellitus, Alzheimer's disease, and MS disease. In addition, increased serum Fe levels may be suggested as an important biomarker for neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and MS disease.
 The novel coronavirus SARS-CoV-2 continues to cause death and disease throughout the world, underscoring the necessity of understanding the virus and host immune response. From the start of the pandemic, a prominent pattern of central nervous system (CNS) pathologies, including demyelination, has emerged, suggesting an underlying mechanism of viral mimicry to CNS proteins. We hypothesized that immunodominant epitopes of SARS-CoV-2 share homology with proteins associated with multiple sclerosis (MS). Using PEPMatch, a newly developed bioinformatics package which predicts peptide similarity within specific amino acid mismatching parameters consistent with published MHC binding capacity, we discovered that nucleocapsid protein shares significant overlap with 22 MS-associated proteins, including myelin proteolipid protein (PLP). Further computational evaluation demonstrated that this overlap may have critical implications for T cell responses in MS patients and is likely unique to SARS-CoV-2 among the major human coronaviruses. Our findings substantiate the hypothesis of viral molecular mimicry in the pathogenesis of MS and warrant further experimental exploration.
 PURPOSE: To explore the acceptability and potential efficacy of orthotic shorts in people with multiple sclerosis. MATERIALS AND METHODS: This mixed-methods, cross-over study utilised qualitative data to investigate acceptability, including perceived effectiveness. Quantitative data included wear times, self-selected walking speed, spatiotemporal gait parameters, and participant-perceived walking ability. Fifteen participants were assessed with and without two pairs of custom-made shorts: one designed as an orthotic and a second looser pair. Each were worn at home for two weeks. Semi-structured interviews were conducted at the first and final appointments. Quantitative data were analysed using Cohen's d; qualitative analysis used a thematic framework. A triangulation protocol integrated qualitative and quantitative data. RESULTS: Orthotic shorts were acceptable to most users who described improved control, stability, and function. Where shorts were less acceptable, this was due to restriction of hip flexion or appearance. Effect sizes were in the moderate category for participant-perceived walking ability and for those spatiotemporal gait parameters that reflect mediolateral stability. Small effect sizes were seen for walking speed and related spatiotemporal parameters, such as step length. CONCLUSION: Orthotic shorts are acceptable and potentially efficacious for improving walking, stability, and function in people with multiple sclerosis. Further research and design development are warranted.Implications for rehabilitationOrthotic shorts are a type of fabric orthosis that have not been previously researched but might assist pelvic stability.Orthotic shorts appear to be acceptable to those people with multiple sclerosis who perceive themselves to be unstable around the trunk and hips.Orthotic shorts might improve gait stability and self-perceived walking ability.
 BACKGROUND: People with multiple sclerosis (pwMS) on anti-CD20 therapies (aCD20) and fingolimod have shown inadequate humoral responses to COVID-19 vaccines. OBJECTIVE: The objective of the study was to pilot larger studies by demonstrating the safety and comparing the immunogenicity of different types of third doses in seronegative pwMS after two doses of BBIBP-CorV inactivated vaccine. METHODS: In December 2021, subject to receiving their third dose, being COVID-19-naiive, and receiving no corticosteroid within two months, we measured the level of anti-SARS-CoV-2-Spike IgG in pwMS seronegative after two shots of BBIBP-CorV inactivated vaccine. RESULTS: We included 20/29 pwMS who received adenoviral vector (AV), 7/29 who received inactivated, and 2/29 who received conjugated third doses. No serious adverse events were reported two weeks post-third dose. The pwMS receiving AV third doses showed significantly increased IgG concentrations, while only the ones not on aCD20 and fingolimod responded to inactivated third doses. An ordinal logistic multivariable generalized linear model indicated that age (per year β: -0.10, P = 0.04), type of disease-modifying therapy (aCD20 β: -8.36, P <0.01; fingolimod β: -8.63, P = 0.01; others: reference), and type of third dose (AV or conjugated β: 2.36, P = 0.02; inactivated: reference) are predictive of third dose immunogenicity among pwMS who remain seronegative after two shots of BBIBP-CorV vaccine. Statistical significance was not achieved for variables sex, MS duration, EDSS, duration of DMT, duration of third dose to IgG test, and duration from last aCD20 infusion to third dose. CONCLUSION: This preliminary pilot study highlights the need for further research to determine the optimal COVID-19 third dose vaccination strategy for pwMS living in areas where BBIBP-CorV vaccine has been used.
 BACKGROUND AND OBJECTIVE: Discontinuation of fingolimod ≥2 months before pregnancy is recommended to minimize potential teratogenicity. The magnitude of MS pregnancy relapse risk, particularly severe relapses, after fingolimod cessation is unclear, as is whether this risk is reduced by pregnancy or modifiable factors. METHODS: Pregnancies who stopped fingolimod treatment within 1 year before or during pregnancy were identified from the German MS and Pregnancy Registry. Data were collected through structured telephone-administered questionnaires and neurologists' notes. Severe relapses were defined as a ≥2.0 increase in Expanded Disability Status Scale (EDSS) or new or worsening relapse-related ambulatory impairment. Women who continued to meet this definition 1 year postpartum were classified as reaching the Severe Relapse Disability Composite Score (SRDCS). Multivariable models accounting for measures of disease severity and repeated events were used. RESULTS: Of the 213 pregnancies among 201 women (mean age at pregnancy onset 32 years) identified, 56.81% (n = 121) discontinued fingolimod after conception. Relapses during pregnancy (31.46%) and the postpartum year (44.60%) were common. Nine pregnancies had a severe relapse during pregnancy and additional 3 during the postpartum year. One year postpartum, 11 of these (6.32% of n = 174 with complete EDSS information) reached the SRDCS. Adjusted relapse rates during pregnancy were slightly higher compared with the year before pregnancy (relapse rate ratio = 1.24, 95% CI 0.91-1.68). Neither exclusive breastfeeding nor resuming fingolimod within 4 weeks of delivery were associated with a reduced risk of postpartum relapses. Most pregnancies relapsed during the first 3 months postpartum (n = 55/204, 26.96%). DISCUSSION: Relapses during pregnancy after fingolimod cessation are common. Approximately 6% of women will retain clinically meaningful disability from these pregnancy-related, fingolimod cessation relapses 1 year postpartum. This information should be shared with women on fingolimod desiring pregnancy, and optimizing MS treatment with nonteratogenic approaches should be discussed.
 BACKGROUND: Wearable sensor technologies have the potential to improve monitoring in people with multiple sclerosis (MS) and inform timely disease management decisions. Evidence of the utility of wearable sensor technologies in people with MS is accumulating but is generally limited to specific subgroups of patients, clinical or laboratory settings, and functional domains. OBJECTIVE: This review aims to provide a comprehensive overview of all studies that have used wearable sensors to assess, monitor, and quantify motor function in people with MS during daily activities or in a controlled laboratory setting and to shed light on the technological advances over the past decades. METHODS: We systematically reviewed studies on wearable sensors to assess the motor performance of people with MS. We scanned PubMed, Scopus, Embase, and Web of Science databases until December 31, 2022, considering search terms "multiple sclerosis" and those associated with wearable technologies and included all studies assessing motor functions. The types of results from relevant studies were systematically mapped into 9 predefined categories (association with clinical scores or other measures; test-retest reliability; group differences, 3 types; responsiveness to change or intervention; and acceptability to study participants), and the reporting quality was determined through 9 questions. We followed the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) reporting guidelines. RESULTS: Of the 1251 identified publications, 308 were included: 176 (57.1%) in a real-world context, 107 (34.7%) in a laboratory context, and 25 (8.1%) in a mixed context. Most publications studied physical activity (196/308, 63.6%), followed by gait (81/308, 26.3%), dexterity or tremor (38/308, 12.3%), and balance (34/308, 11%). In the laboratory setting, outcome measures included (in addition to clinical severity scores) 2- and 6-minute walking tests, timed 25-foot walking test, timed up and go, stair climbing, balance tests, and finger-to-nose test, among others. The most popular anatomical landmarks for wearable placement were the waist, wrist, and lower back. Triaxial accelerometers were most commonly used (229/308, 74.4%). A surge in the number of sensors embedded in smartphones and smartwatches has been observed. Overall, the reporting quality was good. CONCLUSIONS: Continuous monitoring with wearable sensors could optimize the management of people with MS, but some hurdles still exist to full clinical adoption of digital monitoring. Despite a possible publication bias and vast heterogeneity in the outcomes reported, our review provides an overview of the current literature on wearable sensor technologies used for people with MS and highlights shortcomings, such as the lack of harmonization, transparency in reporting methods and results, and limited data availability for the research community. These limitations need to be addressed for the growing implementation of wearable sensor technologies in clinical routine and clinical trials, which is of utmost importance for further progress in clinical research and daily management of people with MS. TRIAL REGISTRATION: PROSPERO CRD42021243249; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=243249.
 Multiple sclerosis (MS) is a highly heterogeneous demyelinating disease of the central nervous system (CNS) that needs for reliable biomarkers to foresee disease severity. Recently, myeloid-derived suppressor cells (MDSCs) have emerged as an immune cell population with an important role in MS. The monocytic-MDSCs (M-MDSCs) share the phenotype with Ly-6C(hi)-cells in the MS animal model, experimental autoimmune encephalomyelitis (EAE), and have been retrospectively related to the severity of the clinical course in the EAE. However, no data are available about the presence of M-MDSCs in the CNS of MS patients or its relation with the future disease aggressiveness. In this work, we show for the first time cells exhibiting all the bona-fide phenotypical markers of M-MDSCs associated with MS lesions, whose abundance in these areas appears to be directly correlated with longer disease duration in primary progressive MS patients. Moreover, we show that blood immunosuppressive Ly-6C(hi)-cells are strongly related to the future severity of EAE disease course. We found that a higher abundance of Ly-6C(hi)-cells at the onset of the EAE clinical course is associated with a milder disease course and less tissue damage. In parallel, we determined that the abundance of M-MDSCs in blood samples from untreated MS patients at their first relapse is inversely correlated with the Expanded Disability Status Scale (EDSS) at baseline and after a 1-year follow-up. In summary, our data point to M-MDSC load as a factor to be considered for future studies focused on the prediction of disease severity in EAE and MS.
 When the Coronavirus Disease 2019 (COVID-19) appeared, it was unknown what impact it would have on the condition of patients with autoimmunological disorders. Attention was focused on the course of infection in patients suffering from multiple sclerosis (MS), specially treated with disease-modifying therapies (DMTs) or glucocorticoids. The impact of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection on the occurrence of MS relapses or pseudo-relapses was important. This review focuses on the risk, symptoms, course, and mortality of COVID-19 as well as immune response to vaccinations against COVID-19 in patients with MS (PwMS). We searched the PubMed database according to specific criteria. PwMS have the risk of infection, hospitalization, symptoms, and mortality due to COVID-19, mostly similar to the general population. The presence of comorbidities, male sex, a higher degree of disability, and older age increase the frequency and severity of the COVID-19 course in PwMS. For example, it was reported that anti-CD20 therapy is probably associated with an increased risk of severe COVID-19 outcomes. After SARS-CoV-2 infection or vaccination, MS patients acquire humoral and cellular immunity, but the degree of immune response depends on applied DMTs. Additional studies are necessary to corroborate these findings. However, indisputably, some PwMS need special attention within the context of COVID-19.
 BACKGROUND: Immunogenicity data shows blunted responses to COVID-19 vaccination among people with MS (pwMS) on certain disease-modifying therapies (DMTs). Still, it is uncertain how this data translates into the clinic. OBJECTIVE: To assess the effect of DMTs and other factors on the effectiveness of inactivated vaccination in pwMS. METHODS: This cohort study was conducted in a period in which Iran experienced two COVID-19 peaks caused by the Delta variant. We used multivariable cox regression to compare COVID-19-free survivals, and an ordinal logistic model to compare COVID-19 severity between vaccinated pwMS on different DMTs. RESULTS: A total of 617 pwMS were included in the final analysis, with a mean [SD] follow-up of 25.59 weeks [5.48] after their second dose. Laboratory/imaging-confirmed breakthrough COVID-19 occurred in 15/277 (5.41%) of injectable-treated (reference), 10/61 (16.39%) of fingolimod-treated (adjusted hazard ratio (aHR) [95% confidence interval (CI)]: 2.80 [1.24, 6.29]; P = 0.01), 9/128 (7.03%) of other oral-treated (aHR [95%CI]: 1.16 [0.50, 2.68]; P = 0.73), 19/145 (13.10%) of anti-CD20-treated (aHR [95%CI]: 2.11 [1.05, 4.22]; P = 0.04), and 6/56 (10.71%) of non-treated pwMS (aHR [95%CI]: 1.52 [0.57, 4.04]; P = 0.40). Age (adjusted Odds Ratio [aOR] [95%CI]: 1.05 [1.00, 1.10], P = 0.05) number of comorbidities (aOR [95%CI]: 2.05 [1.06, 3.96], P = 0.03), fingolimod therapy (aOR [95%CI]: 10.39 [2.47, 43.62], P < 0.01), and anti-CD20 therapy (aOR [95%CI]: 4.44 [1.49, 13.23], P < 0.01) were independently associated with a more severe COVID-19 course. CONCLUSION: The observed results stress the importance of developing personalized vaccination schedules and reservation of COVID-19 treatment resources for older pwMS with comorbidities receiving fingolimod or anti-CD20 therapies.
 The gut-associated lymphoid tissue is a primary activation site for immune responses to infection and immunomodulation. Experimental evidence using animal disease models suggests that specific gut microbes significantly regulate inflammation and immunoregulatory pathways. Furthermore, recent clinical findings indicate that gut microbes' composition, collectively named gut microbiota, is altered under disease state. This review focuses on the functional mechanisms by which gut microbes promote immunomodulatory responses that could be relevant in balancing inflammation associated with autoimmunity in the central nervous system. We also propose therapeutic interventions that target the composition of the gut microbiota as immunomodulatory mechanisms to control neuroinflammation.
 The primary chemical components of Astragalus membranaceus include polysaccharides, saponins, flavonoids, and amino acids. Recent studies have shown that Astragalus membranaceus has multiple functions, including improving immune function and exerting antioxidative, anti-radiation, anti-tumor, antibacterial, antiviral, and hormone-like effects. Astragalus membranaceus and its extracts are widely used in clinical practice because they have obvious therapeutic effects against various autoimmune diseases and relatively less adverse reaction. Multiple sclerosis (MS) is an autoimmune disease of central nervous system (CNS), which mainly caused by immune disorder that leads to inflammatory demyelination, inflammatory cell infiltration, and axonal degeneration in the CNS. In this review, the authors analyzed the clinical manifestations of MS and experimental autoimmune encephalomyelitis (EAE) and focused on the efficacy of Astragalus membranaceus and its chemical components in the treatment of MS/EAE.
 Ozanimod is approved in multiple countries for the treatment of adults with either relapsing multiple sclerosis or moderately to severely active ulcerative colitis. Ozanimod is metabolized in humans to form seven active plasma metabolites, including two major active metabolites CC112273 and CC1084037, and an inactive metabolite. Here, the binding and activity of ozanimod and its metabolites across human sphingosine 1-phosphate receptors were determined. Binding affinity was assessed in Chinese hamster ovary cell membranes expressing recombinant human sphingosine 1-phosphate receptors 1 and 5 via competitive radioligand binding using tritium-labeled ozanimod; selectivity via functional potency assessment was performed using [(35)S]-guanosine-5'-(γ-thio)-triphosphate binding assays. Receptor internalization was assessed in human embryonic kidney 293 cells overexpressing sphingosine 1-phosphate receptor 1-green fluorescent protein and Chinese hamster ovary cells overexpressing sphingosine 1-phosphate receptor 5-hemagglutinin via fluorescence activated cell sorting. Functional activity was assessed in primary cultures of human astrocytes via phosphorylation assays. Ozanimod and its functionally active metabolites bound to the same sites within sphingosine 1-phosphate receptors 1 and 5, with metabolites displaying the same selectivity profile as ozanimod. Agonism at sphingosine 1-phosphate receptor 1 induced receptor internalization, whereas sphingosine 1-phosphate receptor 5 did not. Ozanimod, CC112273, and CC1084037 elicited functional intracellular signaling in human astrocytes, pharmacologically characterized to be mediated by sphingosine 1-phosphate receptor 1. The active plasma metabolites of ozanimod bound to sphingosine 1-phosphate receptors 1 and 5 and displayed similar pharmacologic profiles as their parent compound, likely contributing to clinical efficacy in patients with relapsing multiple sclerosis or moderately to severely active ulcerative colitis.
 Recent approaches in gait analysis involve the use of wearable motion sensors to extract spatio-temporal parameters that characterize multiple aspects of an individual's gait. In particular, the medical community could largely benefit from this type of devices as they could provide the clinicians with a valuable tool for assessing gait impairment. Motion sensor data are however complex and there is an urgent unmet need to develop sound statistical methods for analyzing such data and extracting clinically relevant information. In this article, we measure gait by following the hip rotation over time and the resulting statistical unit is a time series of unit quaternions. We explore the possibility to form groups of patients with similar walking impairment by taking into account their walking data and their global decease severity with semi-supervised clustering. We generalize a compromise-based method named hclustcompro to unit quaternion time series by combining it with the proper dissimilarity quaternion dynamic time warping. We apply this method on patients diagnosed with multiple sclerosis to form groups of patients with similar walking deficiencies while accounting for the clinical assessment of their overall disability. We also compare the compromise-based clustering approach with the method mergeTrees that falls into a sub-class of ensemble clustering named collaborative clustering. The results provide a first proof of both the interest of using wearable motion sensors for assessing gait impairment and the use of prior knowledge to guide the clustering process. It also demonstrates that compromise-based clustering is a more appropriate approach in this context.
 Multiple sclerosis (MS) is an inflammatory demyelinating disease characterized by multiple lesions in the central nervous system. Although the role of B cells in MS pathogenesis has attracted much attention, but the detailed mechanisms remain unclear. To investigate the effects of B cells on demyelination, we analyzed a cuprizone-induced demyelination model, and found that demyelination was significantly exacerbated in B cell-deficient mice. We next investigated whether immunoglobulin affected the myelin formation process using organotypic brain slice cultures and revealed that remyelination was improved in immunoglobulin-treated groups compared with the control group. Analysis of oligodendrocyte-precursor cell (OPC) monocultures showed that immunoglobulins directly affected on OPCs and promoted their differentiation and myelination. Furthermore, OPCs expressed FcγRI and FcγRIII, two receptors that were revealed to mediate the effects of IgG. To the best of our knowledge, this is the first study to demonstrate that B cells act in an inhibitory manner against cuprizone-induced demyelination, while immunoglobulins enhance remyelination following demyelination. Analysis of the culture system revealed that immunoglobulins directly act on OPCs to promote their differentiation and myelination. Future studies to elucidate the effects of immunoglobulins on OPCs in vivo and the detailed mechanisms of these effects may lead to new treatments for demyelinating diseases.
 Vitamin D deficiency is involved in the pathogenesis of multiple sclerosis (MS), a severe autoimmune demyelinating disease of the central nervous system. The gene polymorphism Cdx-2 (rs11568820, G/A) seriously influences the trancriptional activity of the vitamin D receptor (VDR) that binds the vitamin D responsive elements of target genes including HLA-DRB1*15. The aim of the present study in Slovaks was to analyse the association of Cdx-2 variants with the risk of MS and disability progression, and to assess the DRB1*15:01 allele as a possible confounding factor. In total, 493 MS patients and 417 healthy controls were involved in this study. The genotyping of Cdx-2 was performed using restriction analysis; DRB1*15:01 positivity was determined by a high-resolution melting analysis of its surrogate marker rs3135388 (G/A). Our results did not prove any allelic association between Cdx-2 and a risk of MS (minor allele A - 0.181 in patients vs. 0.161 in controls, OR = 1.15, .95 CI = 0.90-1.47, p = 0.289). The logistic regression analysis, adjusted for sex and age, showed no differences in Cdx-2 genotype counts when using an additive, dominant or recessive genetic model (p = 0.351, 0.150, 0.240 respectively). The Cdx-2 variants were also not associated with disease disability progression, evaluated using the Multiple Sclerosis Severity Score. The HLA-DRB1*15:01 allele was found to strongly increase the risk of MS in our study (0.300 in patients vs. 0.101 in controls, OR = 3.83, .95 CI = 2.94-4.99, p = 1.016 × 10(-26), dominant genetic model OR = 4.62, .95 CI = 3.40-6.26, p = 9.1 × 10(-23)). In summary, we found the Cdx-2 as a single genetic marker not to be associated with MS development or progression in Slovaks, independently of HLA-DRB1*15:01 status.
 Inflammation induced by autoreactive CD4(+) T lymphocytes is a major factor in the pathogenesis of multiple sclerosis (MS). Immunosuppressive drugs, such as FTY720, are subsequently developed to prevent the migration of CD4(+) T lymphocytes to the central nervous system (CNS). However, these immunosuppressive drugs have limited accumulation in lymph nodes (LNs), resulting in poor efficacy. Here, this work develops a nanoplatform for delivering immunosuppressive drugs to LNs for durable MS treatment. Human CD47 peptide and L-selectin targeting aptamer are modified on the nanoparticles encapsulated with FTY720 (clnFTY) for self-passivation and the targeting of L-selectin on lymphocytes, a homing receptor for T-cells entering LNs. Using this natural process, clnFTY nanoparticles efficiently deliver FTY720 to LNs and delay disease progression in experimental autoimmune encephalomyelitis (EAE) mice following a single dose treatment over a 42-day observational period. Considering the daily dosing requirement of FTY720, this strategy greatly improves its therapeutic efficiency. The ability of clnFTY nanoparticles to target lymphocytes, reduce sphingosine-1-phosphate receptor 1 (S1PR1) expression, and suppress inflammatory cytokines release are demonstrated in clinical blood samples from MS patients. Taken together, this study demonstrates that targeted LNs delivery may greatly extend the treatment cycle of immunosuppressive drugs for durable MS treatment.
 Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS), characterized by the presence of localized demyelinating lesions accompanied by an inflammatory reaction, evidently leading to neurodegeneration. A number of ion channels have been implicated in the progression of MS, most notably in cell types involved in the immune response. In the present study, we investigated the implication of two ion channel isoforms, Kv1.1 and Kv1.3, in experimental models of neuroinflammation and demyelination. Immunohistochemical staining of brain sections from the mouse cuprizone model displayed high levels Kv1.3 expression. In an astroglial cellular model of inflammation, stimulation with LPS resulted also in a higher expression of Kv1.1 and Kv1.3, while the introduction of 4-Aminopyridine (4-AP) exacerbated the release of pro-inflammatory chemokine CXCL10. In the oligodendroglial cellular model of demyelination, the alteration in expression levels of Kv1.1 and Kv1.3 may be correlated with that of MBP levels. Indirect co-culture was attempted to further understand the communication between astrocytes and oligodendrocytes, The addition of reactive astrocytes' secretome significantly inhibited the production of MBP, this inhibition was accompanied by an alteration in the expression of Kv1.1 and Kv1.3. The addition of 4-AP in this case did not alleviate the decrease in MBP production. In conclusion, the use of 4-AP generated controversial results, suggesting 4-AP may be used in the early stages of the disease or in the remission phases to stimulate myelination, yet in induced toxic inflammatory environment, 4-AP exacerbated this effect.
 Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as Coronavirus-19 (COVID-19) infection, has been associated with several neurological symptoms, including acute demyelinating syndromes (ADS). There is a growing body of literature discussing COVID-19 and demyelinating conditions in adults; however, there is less published about COVID-19 demyelinating conditions in the pediatric population. This review aims to discuss the impact of COVID-19 in pediatric patients with central nervous system ADS (cADS) and chronic demyelinating conditions. We reviewed PubMed, Google Scholar, and Medline for articles published between December 1, 2019 and October 25, 2022 related to COVID-19 and pediatric demyelinating conditions. Of 56 articles reviewed, 20 cases of initial presentation of ADS associated with COVID-19 were described. The most commonly described cADS associated with COVID-19 infection in children was Acute Disseminated Encephalomyelitis followed by Transverse Myelitis. Cases of Myelin Oligodendrocyte Glycoprotein Antibody Disease, Neuromyelitis Optica Spectrum Disorder, and Multiple Sclerosis are also described. The risk of severe COVID-19 in pediatric patients with demyelinating conditions appears low, including in patients on disease modifying therapies, but studies are limited. The pandemic did affect disease modifying therapies in ADS, whether related to changes in prescriber practice or access to medications. COVID-19 is associated with ADS in children and the COVID-19 pandemic has impacted pediatric patients with demyelinating conditions in various ways.
 BACKGROUND AND AIMS: Patients with multiple sclerosis (PwMS) may suffer severely from falling and gait disturbance. Cognitive dysfunction, a common condition in MS patients, may also increase falling rates, regardless of physical disability. We planned this study to determine the fall rate and risk factors in MS patients, follow patients for falls, and reveal the relationship between falls and cognitive dysfunction. METHODS: The study was conducted on 124 patients who have RRMS diagnoses. Patients' gait speed, simultaneous gait speed during other tasks, functions of the upper extremity, balance rating, and fear of falling were evaluated with dual-task Timed-Up-and-Go-3 versions (TUG, TUG-C, TUG-M), Timed 25 Foot Walk (T25WFT), Nine Hole Peg Test (9HPT), Berg Balance Scale (BBS) and Falls Efficacy Scale-International (FES-I) tests. Cognitive functions, fatigue levels, and quality of life were measured with the Symbol Digit Modalities Test (SDMT), Fatigue Severity Scale (FSS), and Multiple Sclerosis Quality of Life (MSQoL) test. Two groups were formed as "fallers" and "non-faller patients". We monitored the patients in six months period. RESULTS: Forty-six patients fell at least once in the last one year before the study began. Fallers were older, less educated, had lower SDMT scores and higher disability scores. Non-faller patients scored lower in FES-I, TUG, and FSS tests. SDMT scores showed statistically significant, linear, positive, and moderate correlation with BBS and 9HPT scores (r = 0.307, p = 0.038, and r = 0.320, p = 0.030, respectively). CONCLUSION: We determined that advanced age, lower education level, and cognitive dysfunction adversely affect gait speed and balance. Among the fallers, those with lower SDMT and MoCA scores had higher falling rates. We determined that EDSS and BBS scores are predictive factors for falls in patients with MS. In conclusion, patients with cognitive impairment should be closely monitored for the risk of falling. Consideration of falls during follow-up examinations might be predictive of cognitive deterioration in patients with MS.
 BACKGROUND: Delineating the specific components of the existing balance training interventions in people with multiple sclerosis (PwMS) may contribute to a framework for future design and reporting of such interventions. Thus, we aimed to systematically synthesize how balance training frequency, intensity, time, type, duration, and progression are reported in balance training interventions for PwMS. METHODS: A systematic literature search was conducted in Medline, Embase, Web of Science, and Cinahl. Search terms were MS, postural balance, walking, gait, and randomized/quasi-randomized controlled or clinical trials. Articles including ambulatory PwMS and interventions designed to challenge the balance control system were eligible. Two investigators screened, selected, and extracted data independently. Data on study characteristics such as design, population, and balance training content were extracted. Categorization of balance training based on balance control components was performed. RESULTS: We included 40 studies grouped under five balance training categories. Balance interventions were well described regarding frequency, session time, and duration, but only two interventions described training intensity, and no systematic, gradual progression approach was reported for balance training adaptation over time. However, the balance training interventions included many sensory and motor components of the balance control system. Still, little focus was on reactive motor strategies, vestibular sense, and cognitive dual-tasking. CONCLUSIONS: Existing balance training interventions in PwMS primarily consist of practicing sensory and motor strategies. Future balance training interventions are encouraged to systematically monitor individual advancements in balance training adaptations and to apply the progressive overload principle (i.e. continuous increase in balance exercise stimulus over time). Furthermore, we suggest that balance training in PwMS is performed with high intensity near an individual's balance capacity limits. Finally, individualized balance training is recommended to cover all relevant components of balance control using the proposed framework.
 The purpose of this study was to assess the efficacy of a combined training program (CTP) in reducing the effects of dual tasking on the temporal parameters and kinematics of gait, as compared with single-task gait. A controlled, randomized, intervention study was performed in an intervention group and a control group. The intervention group attended three weekly CTP sessions for 24 weeks. Gait pattern was evaluated prior to the baseline intervention, at 12 weeks, and at 24 weeks (Repost). The sample was composed of 22 subjects diagnosed with multiple sclerosis with an Expanded Disability Status Scale score of 0-5.5. A total of 12 patients were allocated to the intervention group and another 10 to the control group. A three-dimensional photogrammetry scanner was connected to a selective attention system designed to present a dual-task gait condition. Dual tasking had an impact on all spatiotemporal parameters of gait, and the most remarkable effect of dual tasking was on double-support time, which increased by 9% with respect to normal walking. In contrast, dual tasking had a trivial effect on single-support time. The CTP was effective in reducing the effects of dual tasking on stride length and velocity of the center of mass after Repost of training (p < .05). The CTP reduced time in double-support phase, whereas single-support time increased after Repost of intervention. The application of the CTP had no effect on the cost of the double task after 12 weeks of intervention. It is suggested to increase the application time over Repost.
 In multiple sclerosis, while remarkable progress has been accomplished to control the inflammatory component of the disease, repair of demyelinated lesions is still an unmet need. Despite encouraging results generated in experimental models, several candidates favouring or promoting remyelination have not reached the expected outcomes in clinical trials. One possible reason for these failures is that, in most cases, during preclinical testing, efficacy was evaluated on histology only, while functional recovery had not been assessed. We have generated a Xenopus laevis transgenic model Tg(mbp:GFP-NTR) of conditional demyelination in which spontaneous remyelination can be accelerated using candidate molecules. Xenopus laevis is a classic model for in vivo studies of myelination because tadpoles are translucent. We reasoned that demyelination should translate into loss of sensorimotor functions followed by behavioural recovery upon remyelination. To this end, we measured the swimming speed and distance travelled before and after demyelination and during the ongoing spontaneous remyelination and have developed a functional assay based on the visual avoidance of a virtual collision. Here we show that alteration of these functional and clinical performances correlated well with the level of demyelination and that histological remyelination, assayed by counting in vivo the number of myelinating oligodendrocytes in the optic nerve, translated in clinical-functional recovery. This method was further validated in tadpoles treated with pro-remyelinating agents (clemastine, siponimod) showing that increased remyelination in the optic nerve was associated with functional improvement. Our data illustrate the potential interest of correlating histopathological parameters and functional-clinical parameters to screen molecules promoting remyelination in a simple in vivo model of conditional demyelination.
 OBJECTIVE: We aimed to explore and describe the experiences of people with multiple sclerosis (MS) living with impaired balance control and how balance impairment can be managed in everyday life. METHODS: A qualitative design was used. Data were collected through semistructured interviews. Transcripts were analyzed using qualitative inductive content analysis. Sixteen participants (12 women) with MS and variation in level of balance control were interviewed. Age ranged between 35 and 64 years, and overall MS-disability ranged between 2.0 (mild) and 5.5 (moderate) according to the Expanded Disability Status Scale. RESULTS: Five main categories emerged: Balance is an automatic skill that now requires attention; contributors to balance impairment; burdens of balance impairment; management of balance impairment; and negotiation between capacity and ambition for continuing the good life. Body functions emphasized as central to keeping balance were somatosensory-motor functions, vision, and management of fatigue. Day-to-day variation in capacity and being in stimuli-rich environments were conditions highlighted as impacting balance. The main categories yielded the overarching theme of being restrained by impaired balance control and struggling to keep up. CONCLUSION: Participants with MS described balance impairment as balance no longer being an automatic skill and having an adverse impact on everyday life. A strong effort was shown to not let shortcomings control and determine quality of life. To manage limitations and restrictions and to move forward in the struggle to keep up a good life, an extensive toolbox of strategies aiming to minimize the impact of balance impairment was used to maintain quality of life. IMPACT: This study highlights the importance of person-centered health care in MS, with increased awareness of the individual perspective of how balance impairment is perceived. The person-centered focus increases both quality and efficiency in therapy since it involves the individual's thoughts of a life where participation in valued activities is less restricted.
 Many scientific studies reveal a significant connection between human intestinal microbiota, eating habits, and the development of chronic-degenerative diseases; therefore, alterations in the composition and function of the microbiota may be accompanied by different chronic inflammatory mechanisms. Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS), in which autoreactive immune cells attack the myelin sheaths of the neurons. The purpose of this paper was to describe the main changes that occur in the gut microbiota of MS patients, with a focus on both microbiota and its implications for health and disease, as well as the variables that influence it. Another point stressed by this paper is the role of microbiota as a triggering factor to modulate the responses of the innate and adaptive immune systems, both in the intestine and in the brain. In addition, a comprehensive overview of the taxa modified by the disease is presented, with some points on microbiota modulation as a therapeutic approach for MS. Finally, the significance of gastro-intestinal pains (indirectly related to dysbiosis) was assessed using a case study (questionnaire for MS patients), as was the willingness of MS patients to modulate gut microbiota with probiotics.
 OBJECTIVE: Cladribine tablet therapy is an efficacious treatment for multiple sclerosis (MS), however, its mechanism of action on T and B cell subsets remains unclear. The purpose of this study was to investigate the treatment effects of cladribine on the peripheral pool of T and B cells subsets and reactivity toward central nervous system (CNS) antigens. METHODS: In this cross-sectional exploratory study, frequencies and absolute counts of peripheral T and B cell subsets and B cell cytokine production from untreated patients with relapsing-remitting MS (RRMS) and patients treated with cladribine for 1 year were measured using flow cytometry. Autoreactivity was assessed using a FluoroSpot assay. RESULTS: We found that 1 year after initiation of cladribine treatment, a lower number of CD4(+) T cells was persisting whereas CD19(+) B cell counts were normalized compared to untreated patients with RRMS. Follicular helper T cells and their effecter subsets producing cytokines exerting distinct B cell helper activity were lower and, additionally, the peripheral B cell pool was skewed toward a naïve and anti-inflammatory phenotype. Finally, reactivity to the recently identified CNS-enriched autoantigen RAS guanyl-releasing protein 2 (RASGRP2), but not to myelin basic protein and myelin oligodendrocyte glycoprotein, was lower in cladribine-treated patients. INTERPRETATION: Together, these investigations on T and B cell subsets suggest that cladribine treatment impairs the B-T cell crosstalk and reduces their ability to mediate pathogenic effector functions. This may result in specific reduction of autoreactivity to RASGRP2 which is expressed in B cells and brain tissue. ANN NEUROL 2023;94:518-530.
 BACKGROUND: Muscle strength and dexterity impairments are common among patients with multiple sclerosis (MS) producing limitations in activities of daily living related to the upper limb (UL). This study aimed to evaluate the effectiveness of serious games specifically developed for the MYO Armband® capture sensor in improving forearm and wrist mobility, UL muscle strength, dexterity, fatigue, functionality, quality of life, satisfaction, adverse effects and compliance. METHODS: A double-blinded (allocation concealment was performed by a blinded investigator and by blinding for assessors) randomised controlled trial was conducted. The sample was randomised into two groups: an experimental group that received treatment based on UL serious games designed by the research team and controlled by the MYO Armband® gesture capture sensor, along with conventional rehabilitation and a control group that received the same conventional rehabilitation for the UL. Both groups received two 60-min sessions per week over an eight-week period. Wrist range of motion (goniometry), grip muscle strength (Jamar® dynamometer), coordination and gross UL dexterity (Box and Block Test), fatigue (Fatigue Severity Scale), functionality (ABILHAND), quality of life (Multiple Sclerosis Impact Scale-29), adverse effects (Simulator Sickness Questionnaire, SSQ), perceived workload (NASA-Task load index), satisfaction (Client Satisfaction Questionnaire-8 (CSQ-8), Satisfaction with Technology Scale, System Usability Scale (SUS) and QUEST 2.0) and compliance (attendance) were assessed in both groups pre-treatment, post-treatment and during a follow-up period of 2 weeks without receiving any treatment. RESULTS: Significant differences were observed in the experimental group compared to the control group in the assessment of forearm supination (p = .004) and grip strength (p = .004). Adverse effects were minimal (SSQ: 7/100 points) and perceived workload was low (NASA-Task Load Index: 25/100 points) in the experimental group. The MYO Armband® technology proved to be useful for the participants (SUS: 80.66/100) and the satisfaction scales received high scores (QUEST 2.0: 59.4/70 points; Satisfaction with Technology: 84.36/100 points). There were significant differences between the groups in terms of attendance percentage (p = .029). CONCLUSIONS: An experimental protocol using MYO Armband®-based serious games designed for UL rehabilitation showed improvements in active wrist range of motion and handgrip strength in patients with MS, with high satisfaction, minimal adverse effects and workload and excellent compliance. TRIAL REGISTRATION NUMBER: This randomised controlled trial has been registered at ClinicalTrials.gov Identifier: NCT04171908.
 Potentially toxic elements such as lead and aluminium have been proposed to play a role in the pathogenesis of multiple sclerosis (MS), since their neurotoxic mechanisms mimic many of the pathogenetic processes in MS. We therefore examined the distribution of several potentially toxic elements in the autopsied brains of people with and without MS, using two methods of elemental bio-imaging. Toxicants detected in the locus ceruleus were used as indicators of past exposures. Autometallography of paraffin sections from multiple brain regions of 21 MS patients and 109 controls detected inorganic mercury, silver, or bismuth in many locus ceruleus neurons of both groups, and in widespread blood vessels, oligodendrocytes, astrocytes, and neurons of four MS patients and one control. Laser ablation-inductively coupled plasma-mass spectrometry imaging of pons paraffin sections from all MS patients and 12 controls showed that combinations of iron, silver, lead, aluminium, mercury, nickel, and bismuth were present more often in the locus ceruleus of MS patients and were located predominantly in white matter tracts. Based on these results, we propose that metal toxicants in locus ceruleus neurons weaken the blood-brain barrier, enabling multiple interacting toxicants to pass through blood vessels and enter astrocytes and oligodendroglia, leading to demyelination.

 AIMS: The objective of the study is to explore the importance of tissue hypoxia in causing neurological deficits and demyelination in the inflamed CNS, and the value of inspiratory oxygen treatment, using both active and passive experimental autoimmune encephalomyelitis (EAE). METHODS: Normobaric oxygen treatment was administered to Dark Agouti rats with either active or passive EAE, compared with room air-treated, and naïve, controls. RESULTS: Severe neurological deficits in active EAE were significantly improved after just 1 h of breathing approximately 95% oxygen. The improvement was greater and more persistent when oxygen was applied either prophylactically (from immunisation for 23 days), or therapeutically from the onset of neurological deficits for 24, 48, or 72 h. Therapeutic oxygen for 72 h significantly reduced demyelination and the integrated stress response in oligodendrocytes at the peak of disease, and protected from oligodendrocyte loss, without evidence of increased oxidative damage. T-cell infiltration and cytokine expression in the spinal cord remained similar to that in untreated animals. The severe neurological deficit of animals with passive EAE occurred in conjunction with spinal hypoxia and was significantly reduced by oxygen treatment initiated before their onset. CONCLUSIONS: Severe neurological deficits in both active and passive EAE can be caused by hypoxia and reduced by oxygen treatment. Oxygen treatment also reduces demyelination in active EAE, despite the autoimmune origin of the disease.
 BACKGROUND: Most people with Multiple Sclerosis (pwMS) are subjected to immunomodulatory disease-modifying treatments (DMTs). As a result, immune responses to COVID-19 vaccinations could be compromised. There are few data on cellular immune responses to the use of COVID-19 vaccine boosters in pwMS under a broad spectrum of DMTs. METHODS: In this prospective study, we analysed cellular immune responses to SARS-CoV-2 mRNA booster vaccinations in 159 pwMS with DMT, including: ocrelizumab, rituximab, fingolimod, alemtuzumab, dimethyl fumarate, glatiramer acetate, teriflunomide, natalizumab and cladribine. RESULTS: DMTs, and particularly fingolimod, interact with cellular responses to COVID-19 vaccination. One booster dose does not increase cellular immunity any more than two doses, except in the cases of natalizumab and cladribine. SARS-CoV-2 infection combined with two doses of vaccine resulted in a greater cellular immune response, but this was not observed after supplementary booster jabs. Ocrelizumab-treated pwMS who had previously received fingolimod did not develop cellular immunity, even after receiving a booster. The time after MS diagnosis and disability status negatively correlated with cellular immunity in ocrelizumab-treated pwMS in a booster dose cohort. CONCLUSIONS: After two doses of SARS-CoV-2 vaccination, a high response yield was achieved, except in patients who had received fingolimod. The effects of fingolimod on cellular immunity persisted for more than 2 years after a change to ocrelizumab (which, in contrast, conserved cellular immunity). Our results confirmed the need to find alternative protective measures for fingolimod-treated people and to consider the possible failure to provide protection against SARS-CoV-2 when switching from fingolimod to ocrelizumab.
 Multiple sclerosis (MS) is a systemic inflammatory illness of the central nervous system that involves demyelinating lesions in the myelin-rich white matter and pathology in the grey matter. Despite significant advancements in drug research for MS, the disease's complex pathophysiology makes it difficult to treat the progressive forms of the disease. In this study, we identified a natural flavonoid compound icariin (ICA) as a potent effective agent for MS in ameliorating the deterioration of symptoms including the neurological deficit score and the body weight in a murine experimental autoimmune encephalomyelitis (EAE) model. These improvements were associated with decreased demyelination in the corpus callosum and neuron loss in the hippocampus and cortex confirmed by immunohistochemistry analysis. Meanwhile, it was observed that the activation of microglia in cerebral cortex and hippocampus were inhibited followed by the neuroinflammatory cytokines downregulation such as IL-1β, IL-6 and TNF-α after ICA treatment, which was probably attributable to the suppression of microglial NLRP3 inflammasome activation. Additionally, molecular docking also revealed the binding force of ICA to NLRP3 inflammasome protein complexes in vitro. Taken together, our findings have demonstrated that ICA, as pleiotropic agent, prevents EAE-induced MS by improving demyelination and neuron loss, which interferes with the neuroinflammation via microglial NLRP3 inflammasome activation.
 BACKGROUND AND OBJECTIVES: Fingolimod, an oral therapy for MS, decreases expression of membrane S1P1 receptors on CD4(+) memory cells, causing their retention and deactivation in lymph nodes. We determined fingolimod effects on the number and proportion of potentially CNS-damaging CD8(+)CD28(+) cytolytic T lymphocyte cells (CTLs) and on MS-depleted and dysfunctional CD8(+)CD28(-) anti-inflammatory suppressor/regulatory T cells (Treg) and on CD8(+) T-cell expression of the CD69 activation/lymph node retention protein in MS. METHODS: CD8, CD28, CD4, and CD69 expression on peripheral blood mononuclear cells was measured with flow cytometry. In vitro concanavalin A (ConA) activation of T cells, including CD8(+)CD28(-) cells, was used to mimic inflammation. RESULTS: Fifty-nine patients with MS, 35 therapy-naive (16 clinically stable; 19 exacerbating) and 24 fingolimod-treated (19 clinically stable; 5 exacerbating), and 26 matched healthy controls (HCs) were compared. In therapy-naive patients, the CD8(+) Treg percent of total lymphocytes was only 1/4 of HC levels. In fingolimod-treated patients, however, CD8(+) Treg percentages rose to 2.5-fold higher than in HC and 10-fold higher than in therapy-naive MS. With fingolimod therapy, in contrast, CD8(+) CTL levels were less than half of levels in HCs and therapy-naive patients. In HCs and all MS, activation with ConA strongly induced CD69 expression on CD4(+) cells and induced 3-fold higher CD69 levels on CD8(+) CTL than on CD8(+) Treg. Fingolimod and analogs in vitro did not modify lymphocyte CD69 expression. Lower levels of CD69 on CD8(+) Treg than on CTL may allow easier Treg egress from lymph nodes and enhance control of peripheral inflammation. In vitro activation reduced the already low CD8(+) Treg population in therapy-naive MS, but only slightly altered Treg levels in fingolimod-treated MS. DISCUSSION: Fingolimod therapy markedly increases the percentage of CD8(+) Treg in MS, reversing the low CD8(+) Treg:CTL ratio seen in untreated MS. The increase in immune regulatory cells has potential therapeutic benefit in MS. Activation in vitro depletes CD8(+)CD28(+)CTL in patients with MS; the loss is more pronounced in older patients with MS. This suggests that inflammation can disrupt the tenuous immune regulation in MS, especially in older patients.
 BACKGROUND: Neuroinflammation is involved in the pathophysiology of Alzheimer's disease (AD), including immune-linked genetic variants and molecular pathways, microglia and astrocytes. Multiple Sclerosis (MS) is a chronic, immune-mediated disease with genetic and environmental risk factors and neuropathological features. There are clinical and pathobiological similarities between AD and MS. Here, we investigated shared genetic susceptibility between AD and MS to identify putative pathological mechanisms shared between neurodegeneration and the immune system. METHODS: We analysed GWAS data for late-onset AD (N cases = 64,549, N controls = 634,442) and MS (N cases = 14,802, N controls = 26,703). Gaussian causal mixture modelling (MiXeR) was applied to characterise the genetic architecture and overlap between AD and MS. Local genetic correlation was investigated with Local Analysis of [co]Variant Association (LAVA). The conjunctional false discovery rate (conjFDR) framework was used to identify the specific shared genetic loci, for which functional annotation was conducted with FUMA and Open Targets. RESULTS: MiXeR analysis showed comparable polygenicities for AD and MS (approximately 1800 trait-influencing variants) and genetic overlap with 20% of shared trait-influencing variants despite negligible genetic correlation (rg = 0.03), suggesting mixed directions of genetic effects across shared variants. conjFDR analysis identified 16 shared genetic loci, with 8 having concordant direction of effects in AD and MS. Annotated genes in shared loci were enriched in molecular signalling pathways involved in inflammation and the structural organisation of neurons. CONCLUSIONS: Despite low global genetic correlation, the current results provide evidence for polygenic overlap between AD and MS. The shared loci between AD and MS were enriched in pathways involved in inflammation and neurodegeneration, highlighting new opportunities for future investigation.
 BACKGROUND: There is increasing need for evidence-based data on reproduction for women with multiple sclerosis (MS). First-trimester (first 13 weeks) miscarriages are relatively common in the general population. It is therefore important to have information on the frequency with which this occurs in women with MS. METHODS: The Canadian Multiple Sclerosis Pregnancy Study (CANPREG-MS) is a prospective study on women with MS who are pregnant or actively trying to conceive. As far as we are aware, this is the first study on miscarriages for this population that takes into account each woman's entire pregnancy history (i.e. before and after the MS diagnosis as well as during enrollment in CANPREG-MS). RESULTS: There were 208 pregnancies during the study and 36 resulted in first-trimester miscarriage for a rate of 17.31%, within the expected range of 15%-20% for the general population. CONCLUSIONS: CANPREG-MS provides real world data that there does not appear to be an increase in first-trimester miscarriages for women with MS. This information will be helpful to women with MS and their healthcare providers.
 In multiple sclerosis and the experimental autoimmune encephalomyelitis (EAE) model, both resident microglia and infiltrating macrophages contribute to demyelination as well as spontaneous remyelination. Nevertheless, the specific roles of microglia versus macrophages are unknown. We investigated the influence of microglia in EAE using the colony stimulating factor 1 receptor (CSF-1R) inhibitor, PLX5622, to deplete microglial population and Ccr2(RFP/+) fms(EGFP/+) mice, to distinguish blood-derived macrophages from microglia. PLX5622 treatment depleted microglia and meningeal macrophages, and provoked a massive infiltration of CCR2(+) macrophages into demyelinating lesions and spinal cord parenchyma, albeit it did not alter EAE chronic phase. In contrast, microglia and meningeal macrophages depletion reduced the expression of major histocompatibility complex II and CD80 co-stimulatory molecule in dendritic cells, macrophages and microglia. In addition, it diminished T cell reactivation and proliferation in the spinal cord parenchyma, inducing a significant delay in EAE onset. Altogether, these data point to a specific role of CNS microglia and meningeal macrophages in antigen presentation and T cell reactivation at initial stages of EAE.
 AIM: The frequency of olfactory dysfunction in patients with Multiple Sclerosis (MS) has revealed very different results in studies. Some studies have shown that olfactory dysfunction may be associated with cognitive impairment and poor quality of life. In these studies, different odor tests and cognitive tests were used and different results were obtained. MATERIALS AND METHODS: Forty literate patients over the age of 18 and 24 healthy volunteers of similar age and education were included in the study. Sniffin' Sticks Odor Test, California Verbal Learning Test II, Symbol Digit Modalities Test, Revised Brief Visuospatial Memory Test, Trail-Making Test, Quality of Life Short Form-36, Fatigue Impact Scale, Beck Depression Inventory, and Beck Anxiety Inventory were applied to the individuals. RESULTS: Olfactory dysfunction was detected in 50 % of the patients. High disability rate, low cognitive functions, low quality of life, and fatigue were identified as the factors affecting olfactory function negatively. Odor discrimination and identification abilities were associated with disability level and cognitive functions, whereas quality of life was linked to odor threshold scores. The olfactory function and cognitive abilities of patients with progressive MS (n = 5) were worse than those of patients with relapsing remitting MS (n = 35). CONCLUSION: Olfactory dysfunction is common in patients with MS and is associated with disability and quality of life. Olfactory function can be used in the follow-up of patients and olfactory dysfunction deserves further study as a metric that might emerge as a biomarker.
 BACKGROUND: The link between tobacco smoking and Multiple Sclerosis (MS) onset and progression is well-established. While clinical levels of depression and anxiety are highly prevalent in people living with MS (plwMS), and both are recognized as common MS-related symptoms, the relationships between smoking behavior and depression and anxiety are unclear. This systematic review aimed to synthesize evidence on the relationships between current-smoking and former-smoking and depression and anxiety in plwMS. METHODS: Systematic review of all studies investigating associations between tobacco smoking and depression and anxiety in plwMS was conducted. Relevant studies published before 26 April 2022 were identified by searching seven databases; MEDLINE® (Ovid and PubMed), Embase, CINAHL®, Cochrane Library and PsycInfo), and citation and reference list checking. Joanna Briggs Institute Critical Appraisal Checklists for respective study designs assessed the risk of bias. RESULTS: Thirteen publications reporting on 12 studies met study inclusion criteria. Nine of 12 studies examining current-smoking and depression in plwMS identified a positive association. Four prospective studies provided evidence supporting a causal smoking-depression relationship, with 1.3-2.3-fold higher depression prevalence found in current-smokers than non-smokers. Three cross-sectional studies found no smoking-depression association. Four of five included studies found current-smoking was associated with anxiety, with three prospective studies indicating anxiety prevalence was around 20% higher in current-smokers. Former-smoking was associated with increased prevalence of depression, but not anxiety. CONCLUSION: We provide strong evidence for increased depression prevalence in plwMS who are either current-smokers or former-smokers. However, only current-smoking was associated with increased prevalence of anxiety.
 BACKGROUND: Natalizumab (NTZ) and ocrelizumab (OCR) can be used for the treatment of relapsing-remitting multiple sclerosis (RRMS). In patients treated with NTZ, screening for JC virus (JCV) is mandatory, and a positive serology usually requires a change in treatment after 2 years. In this study, JCV serology was used as a natural experiment to pseudo-randomize patients into NTZ continuation or OCR. METHODS: An observational analysis of patients who had received NTZ for at least 2 years and were either changed to OCR or maintained on NTZ, depending on JCV serology status, was performed. A stratification moment (STRm) was established when patients were pseudo-randomized to either arm (NTZ continuation if JCV negativity, or change to OCR if JCV positivity). Primary endpoints include time to first relapse and presence of relapses after STRm and OCR initiation. Secondary endpoints include clinical and radiological outcomes after 1 year. RESULTS: Of the 67 patients included, 40 continued on NTZ (60%) and 27 were changed to OCR (40%). Baseline characteristics were similar. Time to first relapse was not significantly different. Ten patients in the JCV + OCR arm presented a relapse after STRm (37%), four during the washout period, and 13 patients in the JCV-NTZ arm (32.5%, p = 0.701). No differences in secondary endpoints were detected in the first year after STRm. CONCLUSIONS: The JCV status can be used as a natural experiment to compare treatment arms with a low selection bias. In our study, switching to OCR versus NTZ continuation led to similar disease activity outcomes.
 BACKGROUND: Multiple sclerosis (MS) typically has its onset in early and middle adulthood, but the population is steadily becoming more dominated by older adults. One of the primary consequences of both MS and aging involves declines of lower extremity physical function and mobility. This cross-sectional study compared physical function status based on Short Physical Performance Battery (SPPB) summary and component scores between persons with MS and healthy controls across 6 age groups. We further examined associations between SPPB summary scores and component scores as well as associations between summary scores and measures of physical and cognitive function for identifying the strongest correlates of SPPB summary scores. METHODS: The study involved secondary analysis of cross-sectional data from multiple studies. Ambulatory adults with MS who were relapse-free for the last 30 days were recruited, and controls were recruited based on similar criteria to adults with MS except without the diagnosis of MS or relapses. The sample of 345 persons with MS and 174 controls completed questionnaires regarding demographic and clinical information and underwent assessments of physical and cognitive function including the SPPB, 6-Minute Walk, Timed 25-Foot Walk, Symbol Digit Modalities Test, California Verbal Learning Test-Second Edition, and Brief Visuospatial Memory Test-Revised. RESULTS: The two-way ANOVA indicated a main effect of MS status (F(5,500)=34.74, p<.01, η(2)=0.065), a main effect of age (F(1,500)=3.88, p<.01, η(2)=0.037), and no MS status by age interaction (F(5,500)=1.20, p=.31, η(2)=0.012) on SPPB scores. The bivariate correlation analysis indicated that summary SPPB scores were associated with component SPPB scores in the overall samples of persons with MS (r(s)=0.71 to 0.83) and controls (r(s)=0.42 to 0.91) as well as within most age groups of MS (r(s)=0.63 to 0.91) and controls (r(s)=0.34 to 1.00). The associations between SPPB scores and physical function outcomes were larger in the sample of persons with MS (r(s)=-0.72 to 0.76) than controls (r(s)=-0.47 to 0.48). SPPB scores were further significantly associated with scores on cognitive outcomes in persons with MS (r(s)=0.31 to 0.43), whereas these associations were weaker in controls (r(s)=0.09 to 0.32). Overall, the associations between SPPB scores and physical function outcomes were stronger than the associations between SPPB scores and cognitive function outcomes. CONCLUSION: Overall, MS status and aging have additive effects on physical function, and the summary SPPB score may be driven by a specific component within each age group. SPPB scores may be driven more by mobility rather than cognition, and are consistent with cognitive-motor coupling in MS. The novelty of this study provides evidence of worsening physical function based on the application of the SPPB and its scores across the lifespan in persons with MS and controls, and this has important implications particularly given the increasing prevalence of older adults with MS.
 OBJECTIVE: This study aims to conduct a meta-analysis to assess the effect of virtual reality-based therapy (VRBT) on balance dimensions and fear of falling in patients with multiple sclerosis (PwMS). Secondarily, to determine the most recommendable dose of VRBT to improve balance. METHODS: PubMed Medline, Web of Science, Scopus, CINAHL and PEDro were screened, without publication date restrictions, until September 30th, 2021. Randomized controlled trials (RCTs) comparing the effectiveness of VRBT against other interventions in PwMS were included. Functional and dynamic balance, confidence of balance, postural control in posturography, fear of falling and gait speed were the variables assessed. A meta-analysis was performed by pooling the Cohen's standardized mean difference (SMD) with 95% confidence interval (95% CI) using Comprehensive Meta-Analysis 3.0. RESULTS: Nineteen RCTs, reporting 858 PwMS, were included. Our findings reported that VRBT is effective in improving functional balance (SMD = 0.8; 95%CI 0.47 to 1.14; p < 0.001); dynamic balance (SMD = - 0.3; 95%CI - 0.48 to - 0.11; p = 0.002); postural control with posturography (SMD = - 0.54; 95%CI - 0.99 to - 0.1; p = 0.017); confidence of balance (SMD = 0.43; 95%CI 0.15 to 0.71; p = 0.003); and in reducing fear of falling (SMD = - 1.04; 95%CI - 2 to - 0.07; p = 0.035); but not on gait speed (SMD = - 0.11; 95%CI: - 0.35 to 0.14; p = 0.4). Besides, the most adequate dose of VRBT to achieve the greatest improvement in functional balance was at least 40 sessions, five sessions per week and 40-45 min per sessions; and for dynamic balance, it would be between 8 and 19 weeks, twice a week and 20-30 min per session. CONCLUSION: VRBT may have a short-term beneficial role in improving balance and reducing fear of falling in PwMS.
 INTRODUCTION: Multiple sclerosis (MS) is an acute demyelinating disease with an autoimmune nature, followed by gradual neurodegeneration and enervating scar formation. Dysregulated immune response is a crucial dilemma contributing to the pathogenesis of MS. The role of chemokines and cytokines, such as transforming growth factor-β (TGF-β), have been recently highlighted regarding their altered expressions in MS. TGF-β has three isoforms, TGF-β1, TGF-β2, and TGF-β3, that are structurally similar; however, they can show different functions. RESULTS: All three isoforms are known to induce immune tolerance by modifying Foxp3(+) regulatory T cells. Nevertheless, there are controversial reports concerning the role of TGF-β1 and 2 in the progression of scar formation in MS. At the same time, these proteins also improve oligodendrocyte differentiation and have shown neuroprotective behavior, two cellular processes that suppress the pathogenesis of MS. TGF-β3 shares the same properties but is less likely contributes to scar formation, and its direct role in MS remains elusive. DISCUSSION: To develop novel neuroimmunological treatment strategies for MS, the optimal strategy could be the one that causes immune modulation, induces neurogenesis, stimulates remyelination, and prevents excessive scar formation. Therefore, regarding its immunological properties, TGF-β could be an appropriate candidate; however, contradictory results of previous studies have questioned its role and therapeutic potential in MS. In this review article, we provide an overview of the role of TGF-β in immunopathogenesis of MS, related clinical and animal studies, and the treatment potential of TGF-β in MS, emphasizing the role of different TGF-β isoforms.
 Positron emission tomography (PET) imaging of the myelin sheath is a powerful tool to investigate multiple sclerosis, monitor its evolution, and support drug development. Radiotracers based on N,N-dimethylaminostilbene (MeDAS) fluorinated analogs have been designed for myelin PET imaging but were never translated to humans. We have synthesized three original fluorinated analogs of MeDAS with low metabolic rates for which binding to myelin in a healthy rat brain was demonstrated by fluorescence microscopy. A tosyl precursor was synthesized for the lead compound PEGMeDAS and automated fluorine-18 radiolabeling afforded [(18)F]PEGMeDAS in 25 ± 5% radiochemical yield and 102 ± 15 GBq/μmol molar activity. Biodistribution in healthy rats demonstrated the brain penetration with low penetration of radiometabolites. However, E to Z isomerization observed in plasma hampers further investigations of this family of molecules and requires complementary data on the in vivo behavior of the Z isomer.
 Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS), characterized by demyelinating neuropathy. Despite a long period of research on the immune mechanisms involved in CNS diseases, the etiology of MS remains unknown. MS may present with different clinical and pathological manifestations due to the involvement of different pathogenic processes, including balance and mobility disorders, psychiatric abnormalities, and intestinal dysfunction. We used an animal model of MS, experimental autoimmune encephalomyelitis (EAE), to assess clinical symptoms of MS with the aim of creating new indicators for the assessment of EAE. Our results show that EAE mice develop severe bone loss, anxiety-like moods, and intestinal inflammation in addition to clinical phenomena such as inflammatory infiltration and demyelination of the spinal cord. Our new indicators aim to provide a more comprehensive assessment of MS to avoid the pitfalls of a single intervention and also to provide a more systematic assessment of the effectiveness of drugs used to treat MS.
 BACKGROUND: The chronic nature of multiple sclerosis (MS) affects patient's activities of daily living (ADL) and quality of life (QOL). Nursing interventions based on patients' active participation in goal-setting can be beneficial in improving ADL and QOL. AIMS: This study aimed to determine the effect of applying the nursing process based on King's Theory of Goal Attainment (TGA) on ADL and QOL of persons with multiple sclerosis (PwMS) during the COVID-19 pandemic. METHODS: In this clinical trial, 70 patients referred to the MS Society of Hamadan, Iran, were recruited using the convenience sampling method and randomly assigned into 2 groups. A 4-stage TGA was developed and implemented for the intervention group for a month. Data were gathered by ADL, instrumental ADL (IADL), and QOL questionnaires, and Goal of Attainment Scale (GAS) before and 2 months after the intervention. RESULTS: Intervention group achieved a higher number of prioritized goals (p < 0.001) and reported higher QOL (P < 0.001) and instrumental ADL (IADL; P = 0.002) than the control group. CONCLUSIONS: Given the results, TGA could effectively promote mutual goal attainment, QOL, and IADL for PwMS during the COVID-19 pandemic. TRIAL REGISTRATION: ClinicalTriasl.gov Identifier: IRCT20201210049668N1.
 BACKGROUND AND PURPOSE: Although two doses of COVID-19 vaccine elicited a protective humoral response in most persons with multiple sclerosis (pwMS), a significant group of them treated with immunosuppressive disease-modifying therapies (DMTs) showed less efficient responses. METHODS: This prospective multicenter observational study evaluates differences in immune response after a third vaccine dose in pwMS. RESULTS: Four hundred seventy-three pwMS were analyzed. Compared to untreated patients, there was a 50-fold decrease (95% confidence interval [CI] = 14.3-100.0, p < 0.001) in serum SARS-CoV-2 antibody levels in those on rituximab, a 20-fold decrease (95% CI = 8.3-50.0, p < 0.001) in those on ocrelizumab, and a 2.3-fold decrease (95% CI = 1.2-4.6, p = 0.015) in those on fingolimod. As compared to the antibody levels after the second vaccine dose, patients on the anti-CD20 drugs rituximab and ocrelizumab showed a 2.3-fold lower gain (95% CI = 1.4-3.8, p = 0.001), whereas those on fingolimod showed a 1.7-fold higher gain (95% CI = 1.1-2.7, p = 0.012), compared to patients treated with other DMTs. CONCLUSIONS: All pwMS increased their serum SARS-CoV-2 antibody levels after the third vaccine dose. The mean antibody values of patients treated with ocrelizumab/rituximab remained well below the empirical "protective threshold" for risk of infection identified in the CovaXiMS study (>659 binding antibody units/mL), whereas for patients treated with fingolimod this value was significantly closer to the cutoff.
 A hallmark of multiple sclerosis (MS) is the formation of multiple focal demyelinating lesions within the central nervous system (CNS). These lesions mainly consist of phagocytes that play a key role in lesion progression and remyelination, and therefore represent a promising therapeutic target in MS. We recently showed that unsaturated fatty acids produced by stearoyl-CoA desaturase-1 induce inflammatory foam cell formation during demyelination. These fatty acids are elongated by the "elongation of very long chain fatty acids" proteins (ELOVLs), generating a series of functionally distinct lipids. Here, we show that the expression and activity of ELOVLs are altered in myelin-induced foam cells. Especially ELOVL6, an enzyme responsible for converting saturated and monounsaturated C16 fatty acids into C18 species, was found to be up-regulated in myelin phagocytosing phagocytes in vitro and in MS lesions. Depletion of Elovl6 induced a repair-promoting phagocyte phenotype through activation of the S1P/PPARγ pathway. Elovl6-deficient foamy macrophages showed enhanced ABCA1-mediated lipid efflux, increased production of neurotrophic factors, and reduced expression of inflammatory mediators. Moreover, our data show that ELOVL6 hampers CNS repair, as Elovl6 deficiency prevented demyelination and boosted remyelination in organotypic brain slice cultures and the mouse cuprizone model. These findings indicate that targeting ELOVL6 activity may be an effective strategy to stimulate CNS repair in MS and other neurodegenerative diseases.
 BACKGROUND: Hemodynamics in the prefrontal cortex (PFC) while walking forward and backward, with and without an additional cognitive task (motor single-task [ST] and motor cognitive dual-task [DT]) have not been studied in people with multiple sclerosis (pwMS). AIM: To investigate the PFC hemodynamics during forward and as well as backward walking, with and without a cognitive task, in pwMS and healthy controls. DESIGN: Observational case-control study. SETTING: Sheba Multiple Sclerosis Center, Tel-Hashomer, Israel. POPULATION: Eighteen pwMS (36.1±11.7 years, 66.6% female) and 17 healthy controls (37.5±13.8 years, 76.5% female). METHODS: Each subject completed four walking trials: ST forward walking, DT forward walking, ST backward walking, DT backward walking. PFC activity for all trials was recorded using functional near-infrared spectroscopy (fNIRS). The PFC was subdivided in the frontal eye field (FEF), frontopolar cortex (FPC) and the dorsolateral PFC (DLPFC). RESULTS: The relative oxygenated hemoglobin (HbO) concentration was higher during the DT forward walking in all PFC subareas compared with the ST forward walking for both groups. The relative HbO concentration was higher during ST backward walking compared with ST forward walking in pwMS (DLPFC, FEF) and the healthy controls (FEF, FPC), specifically during the initial part of the trial. CONCLUSIONS: ST backward walking and DT forward walking impact the hemodynamics at the PFC, although, the difference between pwMS and healthy adults requires further clarification. Future RCT's are encouraged to examine the impact of an intervention program based on DT forward and backward walking on PFC activity in pwMS. CLINICAL REHABILITATION IMPACT: Backward walking increases activity in the PFC region in pwMS. Similarly, when performing a cognitive task while walking forward.
 This study characterizes antibody and T-cell immune responses over time until the booster dose of COronaVIrus Disease 2019 (COVID-19) vaccines in patients with multiple sclerosis (PwMS) undergoing different disease-modifying treatments (DMTs). We prospectively enrolled 134 PwMS and 99 health care workers (HCWs) having completed the two-dose schedule of a COVID-19 mRNA vaccine within the last 2-4 weeks (T0) and followed them 24 weeks after the first dose (T1) and 4-6 weeks after the booster (T2). PwMS presented a significant reduction in the seroconversion rate and anti-receptor-binding domain (RBD)-Immunoglobulin (IgG) titers from T0 to T1 (p < 0.0001) and a significant increase from T1 to T2 (p < 0.0001). The booster dose in PwMS showed a good improvement in the serologic response, even greater than HCWs, as it promoted a significant five-fold increase of anti-RBD-IgG titers compared with T0 (p < 0.0001). Similarly, the T-cell response showed a significant 1.5- and 3.8-fold increase in PwMS at T2 compared with T0 (p = 0.013) and T1 (p < 0.0001), respectively, without significant modulation in the number of responders. Regardless of the time elapsed since vaccination, most ocrelizumab- (77.3%) and fingolimod-treated patients (93.3%) showed only a T-cell-specific or humoral-specific response, respectively. The booster dose reinforces humoral- and cell-mediated-specific immune responses and highlights specific DMT-induced immune frailties, suggesting the need for specifically tailored strategies for immune-compromised patients to provide primary prophylaxis, early SARS-CoV-2 detection and the timely management of COVID-19 antiviral treatments.
 Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Although various viruses have been proposed to contribute to MS pathology, the etiology of MS remains unknown. Since intrathecal antibody synthesis is well documented in chronic viral infection and neuroinflammatory diseases, we hypothesized whether the patterns of antigen-specific antibody responses associated with various viral exposures may define patients with CNS chronic immune dysregulation. The pan-viral antibody profiling in cerebrospinal fluid (CSF) and serum of patients with MS showed significant differences from those in healthy volunteers and a pattern of antibody responses against multiple viruses, including the previously identified Epstein-Barr virus. These findings demonstrate that virus-specific antibody signatures might be able to reflect disease-associated inflammatory milieu in CSF of subjects with neuroinflammatory diseases.
 BACKGROUND: The disturbed metabolism of ceramide (Cer) is supposed to evoke the autoimmune response, contributing to MS pathology. OBJECTIVES: To determine levels of anti-Cer immunoglobulins G (IgGs) in the CSF and serum of subjects with various phenotypes of MS, and to investigate relationships between levels of anti-Cer antibodies and MS-related variables. METHODS: IgGs isolated from serum and the CSF of 68 MS patients and appropriate controls were examined for their reactivity to Cer subspecies. Their levels were compared between the studied groups and compartments, and analyzed with regard to clinical variables. RESULTS: Increased levels of anti-C16:0-, C18:0-, C18:1-, C24:0- and C24:1-Cer IgGs were detected in the CSF and serum of MS patients in comparison with controls. For IgGs against particular Cer subspecies, correlations were found between their CSF and serum level, as well as with the Link index. Serum and the CSF anti-Cer IgGs differed between patients with clinically isolated syndrome (CIS) and relapsing-remitting MS from those with progressive MS. No correlations were found between anti-Cer IgGs and other MS-related clinical variables. CONCLUSION: Patients with MS have shown altered panels of anti-Cer IgGs in the CSF and serum, which might suggest a relevant, though limited role of Cer as a target for autoimmune humoral response. Utility of antibodies against Cer subspecies as potential markers for MS activity and progression deserves further investigations.
 BACKGROUND: Rituximab is extensively used off-label to treat multiple sclerosis (MS), and long-term vigilance for adverse events is needed. This study was conducted to determine frequencies and predictors of hematological adverse events, including hypogammaglobulinemia, severe lymphopenia, neutropenia, and infections leading to hospitalization. METHODS: This retrospective cohort study included all patients with MS initiating rituximab treatment at Haukeland University Hospital between January 1(st), 2017, and July 1(st), 2021. Patients were followed by clinical monitoring and repeated blood sampling every six months. Clinical outcomes and laboratory results were retrieved from the Norwegian MS Registry and Biobank and the patient administrative system at Haukeland University Hospital. RESULTS: Five hundred and fifty-six patients were included, 515 with relapsing-remitting MS (RRMS) and 41 with progressive MS. Overall, 33 patients (5.9%) experienced 56 episodes of infections requiring hospital admission. Sixty patients (10.8%) had confirmed hypogammaglobulinemia, 17 (3.1%) had confirmed severe lymphopenia, and 10 (1.8%) had confirmed severe neutropenia. Predictors of infection requiring hospital admission were progressive MS (adjusted OR (aOR): 4.81; 95%CI: 1.25-18.48), duration of treatment with rituximab (aOR: 1.52; 95%CI: 1.11-2.09) and confirmed severe lymphopenia (aOR: 13.58; 95%CI: 3.41-54.06) and neutropenia (aOR: 13.40; 95%CI: 2.93-61.25). Of the hematological abnormalities, only hypogammaglobulinemia was associated with treatment duration (aOR: 1.35; 95%CI: 1.09-1.69). CONCLUSION: The risk of hospitalization due to infection is associated with time on rituximab treatment, in patients with lympho- or neutropenia, and in patients with primary progressive MS. We observed a time-dependent decline in IgG values, in contrast to neutrophil and lymphocyte count, suggesting a cumulative dose-dependent response. These predictors can assist clinicians in assessing and monitoring MS patients receiving rituximab.
 BACKGROUND/PURPOSE: Health state utilities (HSU) are a subjective measure of an individual's health-related quality of life (HRQoL), adjusted by societal or patient relative preference weights for living in different states of health-related quality of life (HRQoL), derived from patient-reported responses to multi-attribute utility instrument (MAUI), and can be used as inputs for cost-utility analyses and in clinical assessment. This research assessed associations of diet with subsequent HSU in a large international cohort of people living with multiple sclerosis (MS), a progressive autoimmune condition of the central nervous system. METHODS: HSUs were generated from responses to Short-Form Six-Dimension (SF-6D) MAUI, and quality-of-the-diet by Diet Habits Questionnaire (DHQ). Cross-sectional, and short- and long-term prospective associations of DHQ with HSU evaluated by linear regression at 2.5- and 5-years. Pooled prospective associations between DHQ and HSU evaluated using linear and quantile regression. Analyses adjusted for relevant demographic and clinical covariates. RESULTS: Among 839 participants, baseline DHQ scores showed short- and long-term associations with subsequent HSU, each 10-unit increase in total DHQ score associated with 0.008-0.012 higher HSU (out of 1.00). These associations were dose-dependent, those in the top two quartiles of baseline DHQ scores having 0.01-0.03 higher HSU at follow-up, 0.03 being the threshold for a minimally clinically important difference. Fat, fiber, and fruit/vegetable DHQ subscores were most strongly and consistently associated with better HSU outcomes. However, baseline meat and dairy consumption were associated with 0.01-0.02 lower HSU at subsequent follow-up. CONCLUSIONS: A higher quality-of-the-diet showed robust prospective relationships with higher HSUs 2.5- and 5-years later, substantiating previous cross-sectional relationships in this cohort. Subject to replication, these results suggest interventions to improve the quality-of-the-diet may be effective to improve HRQoL in people living with MS.
 OBJECTIVE: To study the attitude of patients with multiple sclerosis (MS) to vaccination as a method of preventing infectious diseases, in particular, COVID-19. MATERIAL AND METHODS: The data of a survey of 408 patients with MS in the Sverdlovsk region in relation to vaccination against COVID-19, conducted using the original questionnaire, were analyzed. RESULTS: According to the survey data, 266 (65.2%) patients with MS are positive about vaccination. 222 (54.4%) patients with MS refused vaccination. The most common reasons for refusal were - fear that the vaccine could worsen the state of health - 44.1%, coronavirus infection in the last 6 months - 14.85%, «I was always told that I should not be vaccinated» - 14.4%, a combination of the above answers - 16.65%. The accumulated world experience and our observations demonstrate the important role of vaccination of patients with MS from COVID-19. CONCLUSIONS: It is necessary to rise the awareness of vaccination among patients with MS, since until recently this has been given insufficient attention.
 Impaired mobility is amongst the most debilitating symptoms reported by people with multiple sclerosis (MS). Historically, it has been viewed that walking impairments in people with MS are directly caused by the physical damage to the neurons in the central nervous system (CNS) which results from the immunopathology of MS. However, research from over the past 4 decades has revealed that physical function in people with MS is also affected by skeletal muscle dysfunction characterized by a reduced capacity to produce, regulate, and sustain the force-generating muscle contractions that propel human movement. While the immediate CNS damage caused by MS can alter the neural activation of muscle by disrupting neuromotor transmission, chronic reductions in mobility and extreme fatigue can lead to physically inactive lifestyles that negatively affect skeletal muscle through mechanisms of deconditioning. Consequently, people with MS can experience alterations in activation patterns, muscle mass and tissue composition, contractility, metabolism, and perfusion that contribute to reductions in muscle function that ultimately impair key physical functions such as walking. This article provides an overview of the cellular mechanisms that contribute to skeletal muscle dysfunction in people with MS and a discussion of the current evidence suggesting that skeletal muscle may be a key physiological target for interventions aiming to improve mobility in this population. We specifically highlight recent evidence demonstrating the potential for rehabilitation and exercise interventions to induce muscle plasticity in people with MS who have moderate to severe levels of disability. In conclusion, we discuss future directions in basic science and clinical research that may advance our understanding of muscle dysfunction in MS and lead to the development of more precise and effective treatment strategies.
 PURPOSE: Computerised rehabilitation programs can be used to address cognitive deficits typically caused by multiple sclerosis (MS). However, there are still doubts on their effectiveness, due to mixed results obtained in clinical trials. The objective of this paper is to improve cognitive rehabilitation (CR) practices in MS, by presenting and assessing a MS-specific cognitive rehabilitation software. METHODS: We conducted a detailed analysis of how CR is carried out in practice in MS rehabilitation centres. From the analysis, we elicited a reference CR process, and identified the essential features a software supporting the process should have. We designed and implemented MS-rehab, a novel MS-specific computerised rehabilitation system having the identified features. We experimented MS-rehab in a pilot study involving eight MS patients. To highlight the improvement with respect to the state of the art, we compared MS-rehab with available professional tools selected using well defined criteria. RESULTS: This paper has three main contributions: (1) the identification of a set of essential features a computerised tool for CR in MS should provide; (2) MS-rehab, a novel CR system designed for MS therapists and patients, which embodies innovative MS specific features; (3) the assessment of MS-rehab efficacy in a pilot study with MS patients. CONCLUSIONS: The availability of a MS-specific CR system like MS-rehab fosters the design of more rigorous clinical studies on the effectiveness of computerised rehabilitation in MS. MS-rehab demonstrated its potential and innovativeness as a tool for cognitive rehabilitation in MS.IMPLICATIONS FOR REHABILITATIONComputerized tools for cognitive rehabilitation (CR) in multiple sclerosis (MS) can be improved by a set of MS-specific features.The availability of advanced home-based cognitive rehabilitation mechanisms is fundamental for supporting standardized cognitive rehabilitation protocols in MS.A MS-specific CR system has given promising results in a pilot study involving MS patients.Hardly do state-of-the-art professional tools include all the required MS specific features.
 BACKGROUND: Galectins are a family of endogenous mammalian lectins involved in pathogen recognition, killing, and facilitating the entry of microbial pathogens and parasites into the host. They are the intermediators that decipher glycan-containing information about the host immune cells and microbial structures to modulate signaling events that cause cellular proliferation, chemotaxis, cytokine secretion, and cell-to-cell communication. They have subgroups that take place in different roles in the immune system. The effect of galectin-8 on multiple sclerosis disease (MS) has been studied in the literature, but the results seemed unclear. In this study, we aimed to determine anti-galectin-8 (anti-Gal-8) levels in MS and their potential use as biomarkers. METHODS: In this experimental study, 45 MS patients diagnosed according to McDonald criteria were included in the patient group. The healthy control group contained 45 people without MS diagnosis and any risk factors. Demographic data, height, weight, body mass index, blood glucose, thyroid-stimulating hormone, alanine transaminase, aspartate transaminase, creatinine, low-density lipoprotein, anti-Gal-8 levels, the prevalence of hypertension, diabetes mellitus and coronary artery disease were recorded. In addition, the expanded disability status scale and disease duration were evaluated in the patient group. Data were presented as mean ± standard deviations. RESULTS: The mean blood anti-galectin-8 value of the patient group was 4.84 ± 4.53 ng/mL, while it was 4.67 ± 3.40 ng/mL in the control group, and the difference in these values was found statistically insignificant (P > .05). Moreover, body mass index, glucose, alanine transaminase, aspartate transaminase, thyroid-stimulating hormone, and low-density lipoprotein levels were also statistically insignificant (P > .05). CONCLUSION: This study examined anti-Gal-8 levels in MS patients. The relationship between MS and galectin-8 and anti-Gal-8 levels in patients needs further clarification. As a result, the study's results could help elucidate the pathogenesis of MS and give more evidence for diagnosis.
 Objectives: To assess quality of life or factors related to the foot and general health and to determine the impact taking into account foot health status in people with multiple sclerosis (MS). Methods: 50 subjects with MS and 50 healthy subjects were studied using the Foot Health Status Questionnaire, that is a validated and is reliable tool was used to assess foot health and quality of life. This instrument comprise four domains for evaluate the foot health (foot function, foot pain, footwear and general foot health) in the first section and for measure the general health comprise four domains (general health, physical activity, social capacity and vigor) for second section and was use for all participants. Results: In both groups of the sample, 50% (n = 15) were men and 50% (n = 35) women, and the mean age in the case group was 48.04 ± 10.49 and the control group was 48.04 ± 10.45 were recruited. A statistically significant difference (p < 0.05) was shown for foot function, general foot health, general health, physical activity and vigor domains, stating that people with MS have a lower related to foot health (lower FHSQ scores) compared to healthy subjects who have higher FHSQ scores. There were no statistically significant differences (p > 0.05) for the scores of the other domains of the FHSQ (foot pain, footwear and social capacity). Conclusion: Patients with MS suffer a negative impact on the quality of life related to foot health, which appears to be associated with the chronic disease.
 BACKGROUND AND PURPOSE: This study's purpose was to investigate the reliability, validity, and responsiveness of the Patient-Specific Functional Scale (PSFS) for measuring mobility-related goals in people with multiple sclerosis (MS). METHODS: Data from 32 participants with MS who underwent 8 to 10 weeks of rehabilitation were analyzed (Expanded Disability Status Scale scores 1.0-7.0). For the PSFS, participants identified 3 mobility-related areas where they had difficulty and rated them at baseline, 10 to 14 days later (before starting intervention), and immediately after intervention. Test-retest reliability and response stability of the PSFS were calculated using the intraclass correlation coefficient (ICC 2,1 ) and minimal detectable change (MDC 95 ), respectively. Concurrent validity of the PSFS was determined with the 12-item Multiple Sclerosis Walking Scale (MSWS-12) and the Timed 25-Foot Walk Test (T25FW). PSFS responsiveness was determined using Cohen's d , and minimal clinically important difference (MCID) was calculated based on patient-reported improvements on a Global Rating of Change (GRoC) scale. RESULTS: The PSFS total score demonstrated moderate reliability (ICC 2,1 = 0.70, 95% CI: 0.46 to 0.84) and the MDC was 2.1 points. At baseline, the PSFS was fairly and significantly correlated with the MSWS-12 ( r = -0.46, P = 0.008) but not with the T25FW. Changes in the PSFS were moderately and significantly correlated with the GRoC scale (ρ = 0.63, P < 0.001), but not with MSWS-12 or T25FW changes. The PSFS was responsive ( d = 1.7), and the MCID was 2.5 points or more to identify patient-perceived improvements based on the GRoC scale (sensitivity = 0.85, specificity = 0.76). DISCUSSION AND CONCLUSIONS: This study supports the use of the PSFS as an outcome measure in people with MS to assess mobility-related goals.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A423 ).
 The US Food and Drug Administration (FDA) recently issued a warning regarding ocrelizumab due to reports of colitis among patients taking this medication. Since it is the only FDA-approved therapy for primary progressive multiple sclerosis (PPMS), further research on this adverse event is necessary, and healthcare professionals should be informed of potential treatment options. In this review, we summarize the available data on the incidence of inflammatory colitis associated with anti-CD20 monoclonal antibodies (mAbs), such as ocrelizumab and rituximab, used in MS treatment. Although the exact pathophysiology of anti-CD20-induced colitis remains unknown, immunological dysregulation through treatment-mediated B-cell depletion has been proposed as a possible mechanism. Our study highlights the importance of clinicians being aware of this potential side effect, and patients taking these medications should be closely monitored for any new-onset gastrointestinal symptoms or diarrheal illness. Research indicates that prompt intervention with endoscopic examination and medical or surgical therapies can ensure timely and effective management, thus improving patient outcomes. However, large-scale studies are still needed to determine the associated risk factors and to establish definitive guidelines for the clinical evaluation of MS patients on anti-CD20 medications.
 Autoimmune Encephalitis (AE) spans a group of non-infectious inflammatory conditions of the central nervous system due to an imbalanced immune response. Aiming to elucidate the pathophysiological mechanisms of AE, we applied an unsupervised proteomic approach to analyze the cerebrospinal fluid (CSF) protein profile of AE patients with autoantibodies against N-methyl-d-aspartate receptor (NMDAR) (n = 9), leucine-rich glioma-inactivated protein 1 (LGI1) (n = 9), or glutamate decarboxylase 65 (GAD65) (n = 8) compared to 9 patients with relapsing-remitting multiple sclerosis as inflammatory controls, and 10 patients with somatic symptom disorder as non-inflammatory controls. We found a dysregulation of the complement system, a disbalance between pro-inflammatory and anti-inflammatory proteins on the one hand, and dysregulation of proteins involved in synaptic transmission, synaptogenesis, brain connectivity, and neurodegeneration on the other hand to a different extent in all AE subtypes compared to non-inflammatory controls. Furthermore, elevated levels of several proteases and reduction in protease inhibitors could be detected in all AE subtypes compared to non-inflammatory controls. Moreover, the different AE subtypes showed distinct protein profiles compared to each other and inflammatory controls which may facilitate future identification of disease-specific biomarkers. Overall, CSF proteomics provides insights into the complex pathophysiological mechanisms of AE, including immune dysregulation, neuronal dysfunction, neurodegeneration, and altered protease function.
 BACKGROUND: Impaired manual dexterity is frequent and disabling in patients with multiple sclerosis (MS), affecting activities of daily living and quality of life. OBJECTIVE: The aim of this study was to evaluate the feasibility, usability and patient engagement/satisfaction of a home-based immersive virtual reality (VR) headset-based dexterity training in persons with multiple sclerosis (pwMS). In addition, preliminary efficacy data on the impact of this new training on manual dexterity were collected. METHODS: Single arm prospective study. After a waiting period of two weeks, pwMS performed a specifically developed home-based VR headset-based dexterity training using the Oculus quest 2 for two weeks with five training sessions/week, each session for approximately 20 minutes. Primary endpoints were feasibility (measured by the adherence rate), usability (System Usability Scale, SUS) and patient engagement/satisfaction (Custom User Engagement Questionnaire, CUEQ). Secondary exploratory efficacy endpoints, measured before and after the waiting period as well as after the training intervention, were the Nine-hole-Peg-Test (9HPT), Coin rotation task (CRT), Handheld JAMAR dynamometer, Arm Function in Multiple Sclerosis Questionnaire (AMSQ) and the Multiple Sclerosis Impact Scale 29 (MSIS 29). RESULTS: Eleven pwMS (mean age 49 ± 10.87 SD, mean EDSS 4.28 ± 1.48 SD) participated in the study. Feasibility (adherence rate: 81.8%), usability (median SUS score 94 (IQR = 78-96)) and patient engagement/satisfaction (median 8 on scale of 1-10) of the VR training was very high. In addition, the CRT for the dominant hand improved significantly after training (p = 0.03). CONCLUSIONS: The good results on feasibility, usability, and patient engagement/satisfaction qualify this home-based immersive VR headset-based dexterity training approach for the use in home-based neurorehabilitation in pwMS. Improved fine motor skills for the dominant hand suggest preliminary efficacy, but this needs to be proven in a future randomized-controlled trials.
 Inflammatory processes are involved in the pathophysiology of both Alzheimer's disease (AD) and multiple sclerosis (MS) but their exact contribution to disease progression remains to be deciphered. Biomarkers are needed to define pathophysiological processes of these disorders, who may increasingly co-exist in the elderly generations of the future, due to the rising prevalence in both and ameliorated treatment options with improved life expectancy in MS. The purpose of this review was to provide a systematic overview of inflammatory biomarkers, as measured in the cerebrospinal fluid (CSF), that are associated with clinical disease progression. International peer-reviewed literature was screened using the PubMed and Web of Science databases. Disease progression had to be measured using clinically validated tests representing baseline functional and/or cognitive status, the evolution of such clinical scores over time and/or the transitioning from one disease stage to a more severe stage. The quality of included studies was systematically evaluated using a set of questions for clinical, neurochemical and statistical characteristics of the study. A total of 84 papers were included (twenty-five for AD and 59 for MS). Elevated CSF levels of chitinase-3-like protein 1 (YKL-40) were associated with disease progression in both AD and MS. Osteopontin and monocyte chemoattractant protein-1 were more specifically related to disease progression in AD, whereas the same was true for interleukin-1 beta, tumor necrosis factor alpha, C-X-C motif ligand 13, glial fibrillary acidic protein and IgG oligoclonal bands in MS. We observed a broad heterogeneity of studies with varying cohort characterization, non-disclosure of quality measures for neurochemical analyses and a lack of adequate longitudinal designs. Most of the retrieved biomarkers are related to innate immune system activity, which seems to be an important mediator of clinical disease progression in AD and MS. Overall study quality was limited and we have framed some recommendations for future biomarker research in this field. SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/prospero/, identifier CRD42021264741.
 Axonal degeneration determines the clinical outcome of multiple sclerosis and is thought to result from exposure of denuded axons to immune-mediated damage. Therefore, myelin is widely considered to be a protective structure for axons in multiple sclerosis. Myelinated axons also depend on oligodendrocytes, which provide metabolic and structural support to the axonal compartment. Given that axonal pathology in multiple sclerosis is already visible at early disease stages, before overt demyelination, we reasoned that autoimmune inflammation may disrupt oligodendroglial support mechanisms and hence primarily affect axons insulated by myelin. Here, we studied axonal pathology as a function of myelination in human multiple sclerosis and mouse models of autoimmune encephalomyelitis with genetically altered myelination. We demonstrate that myelin ensheathment itself becomes detrimental for axonal survival and increases the risk of axons degenerating in an autoimmune environment. This challenges the view of myelin as a solely protective structure and suggests that axonal dependence on oligodendroglial support can become fatal when myelin is under inflammatory attack.
 INTRODUCTION: The purpose of this study was to investigate the effects of two different technology-supported rehabilitation approaches which are mobile application based telerehabilitation (TR) and virtual reality supported task oriented circuit therapy groups (V-TOCT) on the upper limb (UL), trunk function, and functional activity kinematics in patients with Multiple Sclerosis (PwMS). METHODS: Thirty-four patients with PwMS were included in this study. The participants were evaluated at baseline and after eight weeks of treatment by an experienced physiotherapist using the Trunk Impairment Scale (TIS), kinetic function sub-parameter of the International Cooperative Ataxia Rating Scale (K-ICARS), ABILHAND, Minnesota Manual Dexterity tests (MMDT), and trunk and UL kinematics using inertial sensors. The participants were randomized into the TR and V-TOCT groups with a 1:1 allocation ratio. All participants received interventions for 1 hour per session, 3 sessions per week, for 8 weeks. RESULTS: Trunk impairment, ataxia severity, UL, and hand function showed statistically significant improvement in both groups. The functional range of motion (FRoM) of shoulder and wrist increased transversal plane and the FRoM of shoulder increased on sagittal plane in V-TOCT. Log Dimensionless Jerk (LDJ) decreased on transversal plane in V-TOCT group. The FRoM of the trunk joints increased on the coronal plane and the FRoM of the trunk joints increased on the transversal plane in TR. Dynamic balance of the trunk and K-ICARS improved better in V-TOCT than in TR (p < 0,05). CONCLUSIONS: V-TOCT and TR improved UL function, TIS, and ataxia severity in PwMS. The V-TOCT was more effective than the TR in terms of dynamic trunk control and kinetic function. The clinical results were confirmed using the kinematic metrics of motor control.
 PURPOSE: The purpose of this study was to provide a patient-reported outcome measure for people with multiple sclerosis (MS) comprehensively reflecting the construct of fatigue and developed upon the assumptions of the Rasch model. The Neurological Fatigue Index - Multiple Sclerosis (NFI-MS) is based on both a medical and patient-described symptom framework of fatigue and has been validated. Therefore, in this study the German version of the NFI-MS (NFI-MS-G) consisting of a physical and cognitive subscale and a summary scale was validated. METHOD: In this bi-centre-study, 309 people with MS undergoing outpatient rehabilitation or being≥2 months before or after their inpatient rehabilitation completed the German NFI-MS-G twice within 14-21 days together with other questionnaires. Correlation with established questionnaires and Rasch analysis were used for its validation. Additionally, psychometric properties of known-groups validity, internal consistency, test-retest reliability, measurement precision and readability were tested. Finally, the English NFI-MS and German NFI-MS-G were compared with each other to equate the language versions. RESULTS: The NFI-MS-G showed good internal construct validity, convergent and known-groups validity and internal consistency (Cronbach's alpha 0.84-0.93). The physical subscale showed minor local dependencies between items 1 and 7, 2 and 3 and 4 to 6, that could be treated by combining the respective items to testlets. Unidimensionality was found for the physical and cognitive subscales but not for the summary scale. Replacing the summary scale, a 2-domains subtest measuring the higher-order construct of fatigue was created. Good test-retest reliability (Lin's concordance correlation coefficient of 0.86-0.90) and low floor and ceiling effects were demonstrated. The NFI-MS-G was found easily readable and invariant across groups of gender, age, disease duration, timepoint and centre. CONCLUSION: The German version of the NFI-MS comprehensively represents the construct of fatigue and has adequate psychometric properties. The German version differs from the English original version with respect to a lack of unidimensionality of the summary scale and minor local dependencies of the physical subscale that could be canceled out using a testlet analysis.
 PURPOSE/OBJECTIVE: Within the framework of the Salutogenic Model of Health, this study aimed to investigate sense of coherence among caregiving partners of persons with multiple sclerosis (PwMS), and its relationship with perceived social support and illness beliefs conceived as generalized resistance resources in tension management. RESEARCH METHOD/DESIGN: In this cross-sectional study, 398 caregiving partners of PwMS (M(age) = 44.62; 34.9% women and 65.1% men) filled in questionnaires measuring sense of coherence (Sense of Coherence Scale-13), perceived social support from family, friends and significant others (Multidimensional Scale of Perceived Social Support), and illness beliefs (Revised Illness Perception Questionnaire). Hierarchical linear regression analysis was performed to assess the contribution of perceived support and illness beliefs to sense of coherence, controlling for sociodemographic and clinical variables. RESULTS: Perceived support from family and beliefs concerning illness-related emotional representations, illness coherence, and treatment control emerged as significant predictors of participants' sense of coherence. Higher perceived support from family and stronger beliefs in illness coherence and treatment control were associated with higher sense of coherence, while more negative emotional representations were related to lower sense of coherence values. CONCLUSIONS/IMPLICATIONS: Findings lend support to the relevance of a salutogenic approach to caregiving in multiple sclerosis. They further suggest the usefulness of interventions that can promote caregivers' sense of coherence and successful coping in life by benefitting from family support, favoring the construction of a coherent illness view, offering comprehensive information and expert guidance on treatment and rehabilitation opportunities, and promoting adaptive management of negative emotions. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 In the progressive phase of multiple sclerosis (MS), the hampered differentiation capacity of oligodendrocyte precursor cells (OPCs) eventually results in remyelination failure. We have previously shown that DNA methylation of Id2/Id4 is highly involved in OPC differentiation and remyelination. In this study, we took an unbiased approach by determining genome-wide DNA methylation patterns within chronically demyelinated MS lesions and investigated how certain epigenetic signatures relate to OPC differentiation capacity. We compared genome-wide DNA methylation and transcriptional profiles between chronically demyelinated MS lesions and matched normal-appearing white matter (NAWM), making use of post-mortem brain tissue (n = 9/group). DNA methylation differences that inversely correlated with mRNA expression of their corresponding genes were validated for their cell-type specificity in laser-captured OPCs using pyrosequencing. The CRISPR-dCas9-DNMT3a/TET1 system was used to epigenetically edit human-iPSC-derived oligodendrocytes to assess the effect on cellular differentiation. Our data show hypermethylation of CpGs within genes that cluster in gene ontologies related to myelination and axon ensheathment. Cell type-specific validation indicates a region-dependent hypermethylation of MBP, encoding for myelin basic protein, in OPCs obtained from white matter lesions compared to NAWM-derived OPCs. By altering the DNA methylation state of specific CpGs within the promotor region of MBP, using epigenetic editing, we show that cellular differentiation and myelination can be bidirectionally manipulated using the CRISPR-dCas9-DNMT3a/TET1 system in vitro. Our data indicate that OPCs within chronically demyelinated MS lesions acquire an inhibitory phenotype, which translates into hypermethylation of crucial myelination-related genes. Altering the epigenetic status of MBP can restore the differentiation capacity of OPCs and possibly boost (re)myelination.
 INTRODUCTION: It is generally recommended to avoid live attenuated vaccines in patients treated with high efficacy disease-modifying treatment (DMT). However, a delay in starting DMT in highly active or aggressive multiple sclerosis (MS) might lead to a significant disability. OBJECTIVE: We aimed to report a case series of 16 highly active RRMS patients who received the live-attenuated varicella-zoster virus (VZV) vaccine during treatment with natalizumab. METHODS: This retrospective case series was conducted between September 2015 and February 2022 at the MS Research Center of Sina and Qaem hospital, Tehran, Mashhad, Iran, to identify the outcome of highly active MS patients who received the live-attenuated VZV vaccine on natalizumab. RESULTS: Two males and 14 females were included in this study, with a mean age of 25.5 ± 8.4-year-old. 10 patients were naïve cases of highly active MS, and six were escalated to natalizumab. The patients received two doses of live attenuated VZV vaccine after a mean of 6.72 cycles of natalizumab treatment. Except for the one who experienced mild chickenpox infection, no serious adverse event or disease activity was evident after vaccination. CONCLUSION: While our data do not confirm the safety of the live attenuated VZV vaccine in natalizumab recipients, it highlights the importance of case-by-case decision-making in MS management based on the risk-benefit assessment.
 This study examined the effectiveness of a vision-based framework for multiple sclerosis (MS) and Parkinson's disease (PD) gait dysfunction prediction. We collected gait video data from multi-view digital cameras during self-paced walking from MS, PD patients and age, weight, height and gender-matched healthy older adults (HOA). We then extracted characteristic 3D joint keypoints from the collected videos. In this work, we proposed a data-driven methodology to classify strides in persons with MS (PwMS), persons with PD (PwPD) and HOA that may generalize across different walking tasks and subjects. We presented a comprehensive quantitative comparison of 16 diverse traditional machine and deep learning (DL) algorithms. When generalizing from comfortable walking (W) to walking-while-talking (WT), multi-scale residual neural network achieved perfect accuracy and AUC for classifying individuals with a given gait disorder; for subject generalization in W trials, residual neural network resulted in the highest accuracy and AUC of 78.1% and 0.87 (resp.), and 1D convolutional neural network (CNN) had highest accuracy of 75% in WT trials. Finally, when generalizing over new subjects in different tasks, again 1D CNN had the top classification accuracy and AUC of 79.3% and 0.93 (resp.). This work is the first attempt to apply and demonstrate the potential of DL with a multi-view digital camera-based gait analysis framework for neurological gait dysfunction prediction. This study suggests the viability of inexpensive vision-based systems for diagnosing certain neurological disorders.
 Multiple sclerosis (MS) is a chronic inflammatory neurologic disease characterized by the demyelinating injury of the central nervous system (CNS). It was reported that the mutant peptide came from myelin proteolipid protein (PLP) and myelin basic protein (MBP) might play a critical role in immunotherapy function of MS. However, endogenous peptides in demyelinating brain tissue of MS and their role in the pathologic process of MS have not been revealed. Here, we performed peptidomic analysis of freshly isolated corpus callosum (CC) from the brains of CPZ-treated mice and normal diet controls of male C57BL/6 mice by LC-MS/MS. Identified a total of 217 peptides were expressed at different levels in MS mice model compared with controls. By performed GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis, we found that the precursor protein of these differently expressed peptides (DEPs) were associated with myelin sheath and oxidative phosphorylation. Our study is the first brain peptidomic of MS mice model, revealing the distinct features of DEPs in demyelination brain tissue. These DPEs may provide further insight into the pathogenesis and complexity of MS, which would facilitate the discovery of the potential novel and effective strategy for the treatment of MS.
 Multiple sclerosis (MS) is a neurodegenerative disease that progressively decreases the muscular and functional capacity. Thus, there is an alteration in the ability to walk that affects balance, speed and resistance. Since MS pathology involves neuroinflammation, cellular oxidation and mitochondrial alterations, the objective of the study was to assess the impact of a nutritional intervention with coconut oil and epigallocatechin gallate (EGCG) on gait and balance. In order to do this, 51 patients with MS were enrolled and randomly distributed into an intervention group and a control group, which received either a daily dose of 800 mg of EGCG and 60 ml of coconut oil, or a placebo, all during a period of 4 months and which followed a Mediterranean isocaloric diet. Initial and final assessments consisted of the evaluation of quantitative balance (Berg scale), perceived balance (ABC scale), gait speed (10MWT) and resistance (2MWT). Besides, muscle strength was measured using a dynamometer and levels of β-hydroxybutyrate (BHB) were measured in serum samples. In the intervention group, there was a significant improvement in the gait speed, quantitative balance and muscle strength of the right quadriceps; an improvement in gait resistance was observed in both groups. There were also significant and positive correlations between balance and gait scales. In conclusion, the administration of EGCG and coconut oil seems to improve gait speed and balance in MS patients, although the latter was not perceived by them. Furthermore, these variables appear to be related and contribute to functionality.
 BACKGROUND: Face masks protrude into the lower visual field causing reduced perception of visual stimuli, potentially making obstacle avoidance during walking more difficult and increasing fall risk. Recommendations on walking and mask wearing for older adults have been debated, with no clear consensus on the various factors interacting and influencing walking safety while wearing a face mask. It is particularly important to address this issue in populations at an increased risk of falls. Therefore, this study aims to investigate the effects of mask-wearing on objectively measured walking adaptability in people with Parkinson's disease and Multiple Sclerosis. METHODS: 50 patients with either Parkinson's disease or Multiple Sclerosis attending inpatient neurorehabilitation will be recruited to participate in this crossover study. Performance during a standardized gait adaptability (C-Gait) test on a VR-based treadmill (C-Mill+VR), as well as during clinical mobility tests (10-meter walk test, Timed Up & Go test, and stair ambulation) will be measured with and without an FFP2- mask (order randomized). In addition, participants will be asked about their perceived performance and perceived safety during the tests with and without a mask. Performance on the seven C-Gait subtests is based on centre of pressure-derived measures of foot placement in relation to the different tasks. These are averaged and added to a cognitive C-Gait task to give the overall composite score (primary outcome). Secondary outcomes will include the different subscores and clinical mobility tests. POTENTIAL SIGNIFICANCE: This study will make an important contribution to an ongoing debate regarding recommendations persons with and without a neurological disease should be given regarding wearing a face mask while walking. Furthermore, the study will complement the existing scientific discourse with clinical data from people with a neurological disease for whom falls, mobility deficits and mask wearing may be more frequent, which can help inform evidence-based recommendations. TRIAL REGISTRATION: German clinical trial register: DRKS00030207.
 The trafficking of autoreactive leucocytes across the blood-brain barrier endothelium is a hallmark of multiple sclerosis pathogenesis. Although the blood-brain barrier endothelium represents one of the main CNS borders to interact with the infiltrating leucocytes, its exact contribution to neuroinflammation remains understudied. Here, we show that Mcam identifies inflammatory brain endothelial cells with pro-migratory transcriptomic signature during experimental autoimmune encephalomyelitis. In addition, MCAM was preferentially upregulated on blood-brain barrier endothelial cells in multiple sclerosis lesions in situ and at experimental autoimmune encephalomyelitis disease onset by molecular MRI. In vitro and in vivo, we demonstrate that MCAM on blood-brain barrier endothelial cells contributes to experimental autoimmune encephalomyelitis development by promoting the cellular trafficking of TH1 and TH17 lymphocytes across the blood-brain barrier. Last, we showcase ST14 as an immune ligand to brain endothelial MCAM, enriched on CD4+ T lymphocytes that cross the blood-brain barrier in vitro, in vivo and in multiple sclerosis lesions as detected by flow cytometry on rapid autopsy derived brain tissue from multiple sclerosis patients. Collectively, our findings reveal that MCAM is at the centre of a pathological pathway used by brain endothelial cells to recruit pathogenic CD4+ T lymphocyte from circulation early during neuroinflammation. The therapeutic targeting of this mechanism is a promising avenue to treat multiple sclerosis.
 BACKGROUND: Despite the wide range of existing performance measures to evaluate functional status of patients with multiple sclerosis, the heterogeneous nature of the disease hinders clinical characterization and monitoring of disease severity. Speckle tracking ultrasonography is a non-invasive technique to assess isolated muscle function by evaluating the contractile properties of muscle tissue, i.e. muscle strain. The aim of this study was to investigate whether muscle strain measured by speckle tracking ultrasonography could be a useful quantitative measure of muscle function in patients with multiple sclerosis. The criterion validity of muscle strain was compared to that of validated performance measures of upper and lower extremity function. METHODS: This cross-sectional study used baseline data from an explorative observational cohort study (the MUST study). Participants recruited from a hospital outpatient MS clinic underwent speckle tracking ultrasonography of the biceps brachii, supraspinatus, and soleus muscles of the dominant side according to pre-defined submaximal isometric contractions. Participants also completed the Timed 25-Foot Walk Test, the Six Spot Step Test, the 2-minute walking test, the Nine-Hole Peg Test, the 12-item Multiple Sclerosis Walking Scale, and the Oxford Shoulder Score. Gaussian distribution was investigated by visual inspection of normal probability plots and the Shapiro-Wilk test. The Timed 25-Foot Walk Test and Nine-Hole Peg Test were selected as gold standards for function of the lower and upper extremities, respectively. Criterion validity was assessed using Spearman's rank-order correlation coefficient ρ (rho), comparing the muscle strain and performance measures against predefined gold standards. Differences in criterion validity were estimated using squared correlations on the Fischer's Z-scale, with non-parametric bootstrapping to obtain bias-corrected, accelerated bootstrap confidence intervals (95% BCa). RESULTS: Criterion validity showed good to excellent correlations between the gold standard for lower extremity function and the 2-minute walking test and Six Spot Step Test, and a fair correlation to the 12-item Multiple Sclerosis Walking Scale. No significant correlation was found between the gold standard for upper extremity function and the performance measure. There were no significant correlations between the gold standards and muscle strain. CONCLUSION: The absence of criterion validity for muscle strain alongside fair to strong criterion validity for the performance measures indicates that speckle tracking ultrasonography assessment of muscle strain is either invalid or evaluates other constructs of multiple sclerosis. Muscle strain assessed by speckle tracking ultrasonography cannot be recommended for the evaluation of treatment effects or disease progression in multiple sclerosis.
 BACKGROUND AND OBJECTIVE: Erythropoietin (EPO) is a candidate neuroprotective drug. We assessed its long-term safety and efficacy as an adjunct to methylprednisolone in patients with optic neuritis and focused on conversions to multiple sclerosis (MS). METHODS: The TONE trial randomized 108 patients with acute optic neuritis but without previously known MS to either 33,000 IU EPO or placebo in conjunction with 1,000 mg methylprednisolone daily for 3 days. After reaching the primary end point at 6 months, we conducted an open-label follow-up 2 years after randomization. RESULTS: The follow-up was attended by 83 of 103 initially analyzed patients (81%). There were no previously unreported adverse events. The adjusted treatment difference of peripapillary retinal nerve fiber layer atrophy in relation to the fellow eye at baseline was 1.27 µm (95% CI -6.45 to 8.98, p = 0.74). The adjusted treatment difference in low-contrast letter acuity was 2.87 on the 2.5% Sloan chart score (95% CI -7.92 to 13.65). Vision-related quality of life was similar in both treatment arms (National Eye Institute Visual Functioning Questionnaire median score [IQR]: 94.0 [88.0 to 96.9] in the EPO and 93.4 [89.5 to 97.4] in the placebo group). The rate of multiple sclerosis-free survival was 38% in the placebo and 53% in the EPO group (hazard ratio: 1.67, 95% CI 0.96 to 2.88, p = 0.068). DISCUSSION: In line with the results at 6 months, we found neither structural nor functional benefits in the visual system of patients with optic neuritis as a clinically isolated syndrome, 2 years after EPO administration. Although there were fewer early conversions to MS in the EPO group, the difference across the 2-year window was not statistically significant. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that for patients with acute optic neuritis, EPO as an adjunct to methylprednisolone is well tolerated and does not improve long-term visual outcomes. TRIAL REGISTRATION INFORMATION: The trial was preregistered before commencement at clinicaltrials.gov (NCT01962571).
 20 yr ago, a tribute appeared in this journal on the 70th anniversary of an animal model of disseminated encephalomyelitis, abbreviated EAE for experimental autoimmune encephalomyelitis. "Observations on Attempts to Produce Disseminated Encephalomyelitis in Monkeys" appeared in the Journal of Experimental Medicine on February 21, 1933. Rivers and colleagues were trying to understand what caused neurological reactions to viral infections like smallpox, vaccinia, and measles, and what triggered rare instances of encephalomyelitis to smallpox vaccines. The animal model known as EAE continues to display its remarkable utility. Recent research, since the 70th-anniversary tribute, helps explain how Epstein-Barr virus triggers multiple sclerosis via molecular mimicry to a protein known as GlialCAM. Proteins with multiple domains similar to GlialCAM, tenascin, neuregulin, contactin, and protease kinase C inhibitors are present in the poxvirus family. These observations take us a full circle back to Rivers' first paper on EAE, 90 yr ago.
 BACKGROUND AND OBJECTIVES: Patients with anti-GABA-A receptor encephalitis characteristically experience therapy-refractory epileptic seizures. General anesthesia is often required to terminate refractory status epilepticus. The immunologic mechanisms leading to antibody formation remain to be elucidated. Described triggers of anti-GABA-A autoimmunity are tumors, mainly thymomas, and herpes simplex encephalitis. METHODS: We present a young woman with prediagnosis of relapse remitting multiple sclerosis (MS), treated with interferons, natalizumab, and alemtuzumab. Six months after one and only cycle of alemtuzumab, speech arrest and behavioral changes with aggressive and anxious traits appeared. She showed increasing motor convulsions resulting in focal status epilepticus. RESULTS: Anti-GABA-A receptor antibodies in CSF and serum were confirmed in different external laboratories, in a more extensive analysis after antibodies against NMDAR, CASPR2, LGI1, GABABR, and AMPAR were ruled out during in-house examination. Clinical condition improved temporarily with cortisone therapy, plasmapheresis, and IVIG but deteriorated rapidly after steroid discontinuation, resulting in brain biopsy. On histopathologic confirmation consistent with anti-GABA-A receptor antibody-associated CNS inflammation, completing the first rituximab cycle, continuing oral corticosteroids and supplementing immunosuppression with cyclosporine A led to quick recovery. DISCUSSION: Our case describes a severe autoantibody-induced encephalitis in a young patient with MS, with alemtuzumab as a potential trigger for anti-GABA-A receptor encephalitis.
 [(18)F]3-fluoro-4-aminopyridine ([(18)F]3F4AP) is a positron emission tomography (PET) tracer for imaging demyelination based on the multiple sclerosis drug 4-aminopyridine (4AP, dalfampridine). This radiotracer was found to be stable in rodents and nonhuman primates imaged under isoflurane anesthesia. However, recent findings indicate that its stability is greatly decreased in awake humans and mice. Since both 4AP and isoflurane are metabolized primarily by cytochrome P450 enzymes, particularly cytochrome P450 family 2 subfamily E member 1 (CYP2E1), we postulated that this enzyme may be responsible for the metabolism of 3F4AP. Here, we investigated the metabolism of [(18)F]3F4AP by CYP2E1 and identified its metabolites. We also investigated whether deuteration, a common approach to increase the stability of drugs, could improve its stability. Our results demonstrate that CYP2E1 readily metabolizes 3F4AP and its deuterated analogs and that the primary metabolites are 5-hydroxy-3F4AP and 3F4AP N-oxide. Although deuteration did not decrease the rate of the CYP2E1-mediated oxidation, our findings explain the diminished in vivo stability of 3F4AP compared with 4AP and further our understanding of when deuteration may improve the metabolic stability of drugs and PET ligands. SIGNIFICANCE STATEMENT: The demyelination tracer [(18)F]3F4AP was found to undergo rapid metabolism in humans, which could compromise its utility. Understanding the enzymes and metabolic products involved may offer strategies to reduce metabolism. Using a combination of in vitro assays and chemical syntheses, this report shows that cytochrome P450 enzyme CYP2E1 is likely responsible for [(18)F]3F4AP metabolism, that 4-amino-5-fluoroprydin-3-ol (5-hydroxy-3F4AP, 5OH3F4AP) and 4-amino-3-fluoropyridine 1-oxide (3F4AP N-oxide) are the main metabolites, and that deuteration is unlikely to improve the stability of the tracer in vivo.
 Multiple sclerosis is a chronic inflammatory disease of the central nervous system(1). Astrocytes are heterogeneous glial cells that are resident in the central nervous system and participate in the pathogenesis of multiple sclerosis and its model experimental autoimmune encephalomyelitis(2,3). However, few unique surface markers are available for the isolation of astrocyte subsets, preventing their analysis and the identification of candidate therapeutic targets; these limitations are further amplified by the rarity of pathogenic astrocytes. Here, to address these challenges, we developed focused interrogation of cells by nucleic acid detection and sequencing (FIND-seq), a high-throughput microfluidic cytometry method that combines encapsulation of cells in droplets, PCR-based detection of target nucleic acids and droplet sorting to enable in-depth transcriptomic analyses of cells of interest at single-cell resolution. We applied FIND-seq to study the regulation of astrocytes characterized by the splicing-driven activation of the transcription factor XBP1, which promotes disease pathology in multiple sclerosis and experimental autoimmune encephalomyelitis(4). Using FIND-seq in combination with conditional-knockout mice, in vivo CRISPR-Cas9-driven genetic perturbation studies and bulk and single-cell RNA sequencing analyses of samples from mouse experimental autoimmune encephalomyelitis and humans with multiple sclerosis, we identified a new role for the nuclear receptor NR3C2 and its corepressor NCOR2 in limiting XBP1-driven pathogenic astrocyte responses. In summary, we used FIND-seq to identify a therapeutically targetable mechanism that limits XBP1-driven pathogenic astrocyte responses. FIND-seq enables the investigation of previously inaccessible cells, including rare cell subsets defined by unique gene expression signatures or other nucleic acid markers.
 Gait analysis is often used to study locomotor alterations in people with multiple sclerosis (PwMS), but the large number of extracted variables challenges the interpretability. In this paper, we analysed gait alterations by combining the Gait Profile Score (GPS), which summarizes kinematic locomotor deviations, and Statistical Parametric Mapping (SPM), which compares kinematics and kinetics over the whole gait cycle. Eleven PwMS and 11 speed-matched Healthy Controls (HC) underwent overground gait analysis. GPS were compared through independent-samples t-tests; sagittal-plane kinematics and power at hip, knee, and ankle were compared through SPM Hotelling's-T2 and SPM t-tests. Spearman's correlation coefficients (r) between GPS and clinical outcomes were also calculated. PwMS had higher GPS than HC (PwMS = 8.74 ± 2.13°; HC = 5.01 ± 1.41°;p < 0.001). Multivariate SPM found statistically significant differences at 0-49%, 70-80%, and 93-99% of stride (p < 0.05) and univariate analysis showed reduced ankle dorsiflexion, and lower knee flexion during pre-swing and swing. GPS correlated with Expanded Disability Status Scale (r = 0.65; 95%C.I.[0.04,0.91]; p = 0.04) and 2-Minute Walking Test (r = -0.65; 95%C.I.[-0.91,-0.04]; p = 0.04). GPS in conjunction with SPM revealed multi-joint kinematic alterations on sagittal plane involving distal joint angles, ankle and knee, during the stance phase with no changes at the proximal level. Gait deviations were more pronounced in PwMS with higher disability and walking limitations.
 Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease of the central nervous system (CNS) that mostly manifests as irreversible disability. The aetiopathogenesis of MS is still unclear, although it was initially thought to be primarily mediated by T-cells. Research into the immune concepts of MS pathophysiology in recent years has led to a shift in the understanding of its origin i.e. from a T-cell-mediated to a B-cell-mediated molecular background. Thus, the use of B-cell-selective therapies, such as anti- -CD20 antibody therapy, as expanded therapeutic options for MS is now strongly supported. This review provides an up-to-date discussion on the use of anti-CD20 targeted therapy in MS treatment. We present a rationale for its use and summarise the results of the main clinical trials showing the efficacy and safety of rituximab, ocrelizumab, ofatumumab, and ublituximab. Future directions that show selectivity to a broader population of lymphocytes, such as the use of anti-CD19 targeted antibodies, as well as the concept of extended interval dosing (EID) of anti-CD20 drugs, are also discussed in this review.
 Dysbiotic oral microbiota has been associated with multiple sclerosis. However, the role and mechanism of oral microbiota in the development of multiple sclerosis are still elusive. Here, we demonstrated that ligature-induced periodontitis (LIP) aggravated experimental autoimmune encephalomyelitis (EAE) in mice, and this was likely dependent on the expansion of T helper 17 (Th17) cells. LIP increased the splenic richness of Enterobacter sp., which was able to induce the expansion of splenic Th17 cells and aggravate EAE in mice. LIP also led to enrichment of Erysipelotrichaceae sp. in the gut and increased Th17 cells in the large intestinal lamina propria of EAE mice. Fecal microbiota transplantation from EAE mice with LIP also promoted EAE symptoms. In conclusion, periodontitis exacerbates EAE, likely through ectopic colonization of oral pathobionts and expansion of Th17 cells.
 Epstein-Barr virus (EBV) is known to be associated with several cancers along with neurological modalities like Alzheimer's disease (AD) and multiple sclerosis (MS). Previous study from our group revealed that a 12 amino acid peptide fragment ((146)SYKHVFLSAFVY(157)) of EBV glycoprotein M (gM) exhibits amyloid-like self-aggregative properties. In the current study, we have investigated its effect on Aβ(42) aggregation along with its effect on neural cell immunology and disease markers. EBV virion was also considered for the above-mentioned investigation. An increase in the aggregation of Aβ(42) peptide was observed upon incubation with gM(146-157). Further, the exposure of EBV and gM(146-157) onto neuronal cells indicated the upregulation of inflammatory molecules like IL-1β, IL-6, TNF-α, and TGF-β that suggested neuroinflammation. Besides, host cell factors like mitochondrial potential and calcium ion signaling play a crucial role in cellular homeostasis and alterations in these factors aid in neurodegeneration. Changes in mitochondrial membrane potential manifested a decrease while elevation in the level of total Ca(2+) ions was observed. Amelioration of Ca(2+) ions triggers excitotoxicity in neurons. Subsequently, neurological disease-associated genes APP, ApoE4, and MBP were found to be increased at the protein level. Additionally, demyelination of neurons is a hallmark of MS and the myelin sheath consists of ∼70% of lipid/cholesterol-associated moieties. Hereby, genes associated with cholesterol metabolism indicated changes at the mRNA level. Enhanced expression of neurotropic factors like NGF and BDNF was discerned postexposure to EBV and gM(146-157). Altogether, this study delineates a direct connection of EBV and its peptide gM(146-157) with neurological illnesses.
 BACKGROUND: During multiple sclerosis (MS) treatment different modes of action such as lateral (interferon beta to glatiramer acetate or glatiramer acetate to interferon beta) or vertical (interferon beta/glatiramer acetate to fingolimod) drug switch can be performed. This study aims to investigate the clinical effectiveness of switching from the first-line injectable disease modifying treatments (iDMTs) to fingolimod (FNG) compared to switching between first-line iDMTs. METHODS: This is a multicenter, observational and retrospective study of patients with relapsing-remitting MS who had lateral and vertical switch. The observation period included three key assessment time points (before the switch, at switch, and after the switch). Data were collected from the MS patients' database by neurologists between January 2018 and June 2019. The longest follow-up period of the patients was determined as 24 months after the switch. RESULTS: In 462 MS patients that were included in the study, both treatments significantly decreased the number of relapses during the postswitch 12 months versus preswitch one year while patients in the FNG group experienced significantly fewer relapses compared to iDMT cohort in the postswitch 12 months period. FNG cohort experienced fewer relapses than in the iDMT cohort within the postswitch 2 year. The mean time to first relapse after the switch was significantly longer in the FNG group. DISCUSSION: The present study revealed superior effectiveness of vertical switch over lateral switch regarding the improvement in relapse outcomes. Patients in the FNG cohort experienced sustainably fewer relapses during the follow-up period after the switch compared the iDMT cohort. Importantly, switching to FNG was more effective in delaying time to first relapse when compared with iDMTs.
 BACKGROUND: The health-related quality of life (HRQoL) of children with multiple sclerosis (MS) is mediated by the HRQoL of their parents. Understanding factors that modify the relationship between the child's MS diagnosis and parental HRQoL would inform interventions to improve the HRQoL of both parents and children living with MS. OBJECTIVE: We evaluated whether the association between an MS diagnosis during childhood and parental HRQoL is modified by the presence of a family health condition or low socioeconomic position (SEP). METHODS: Parents of children with MS or the transient illness, monophasic-acquired demyelinating syndromes (monoADS), were enrolled in a prospective Canadian study. Multivariable models evaluated whether the association between a child's MS diagnosis (vs. monoADS) and parental HRQoL was modified by ⩾1 family health conditions or low SEP. RESULTS: Two hundred seven parents and their children with MS (n = 65) or monoADS (n = 142) were included. We found a synergistic effect of an MS diagnosis and a family health condition on parental HRQoL. We also found a synergistic effect of having MS and a low SEP on parental HRQoL. CONCLUSION: Parents of children with MS who have another family health condition or a low SEP are at particularly high risk for low HRQoL.
 PURPOSE OF REVIEW: The primary aim of this review is to describe the clinical course, salient imaging features, and relevant serological profiles of common optic neuritis (ON) subtypes. Key diagnostic challenges and treatment options will also be discussed. RECENT FINDINGS: ON is a broad term that describes an inflammatory optic nerve injury arising from a variety of potential causes. ON can occur sporadically, however there is particular concern for co-associated central nervous system (CNS) inflammatory syndromes including multiple sclerosis (MS), neuromyelitis optic spectrum disorders (NMOSD), and myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD). The ON subtypes that often herald MS, NMOSD, and MOGAD differ with respect to serological antibody profile and neuroimaging characteristics, yet there is significant overlap in their clinical presentations. A discerning history and thorough examination are critical to rendering the correct diagnosis. SUMMARY: Optic neuritis subtypes vary with respect to their long-term prognosis and accordingly, require different acute treatment strategies. Moreover, delays in identifying MOGAD, and certainly NMOSD, can be highly detrimental because affected individuals are vulnerable to permanent vision loss and neurologic disability from relapses.
 OBJECTIVE: The aim of the study is to characterize patient-reported signs and symptoms of urinary tract infections in patients with neurogenic bladder to inform development of an intervention to improve the accuracy of urinary tract infection diagnosis. DESIGN: This is a retrospective cohort study of adults with neurogenic bladder due to spinal cord injury/disorder, multiple sclerosis, and/or Parkinson disease and urinary tract infection encounters at four medical centers between 2017 and 2018. Data were collected through medical record review and analyzed using descriptive statistics and unadjusted logistic regression. RESULTS: Of 199 patients with neurogenic bladder and urinary tract infections, 37% were diagnosed with multiple sclerosis, 36% spinal cord injury/disorder, and 27% Parkinson disease. Most patients were men (88%) in inpatient or long-term care settings (60%) with bladder catheters (67%). Fever was the most frequent symptom (32%). Only 38% of patients had a urinary tract-specific symptom; 48% had only nonspecific to the urinary tract symptoms. Inpatient encounter setting (odds ratio, 2.5; 95% confidence interval, 1.2-5.2) was associated with greater odds of only having nonspecific urinary tract symptoms. CONCLUSIONS: In patients with neurogenic bladder and urinary tract infection encounters, nonspecific signs and symptoms are most frequently reported. These results can inform interventions to help providers better elicit and document urinary tract-specific symptoms in patients with neurogenic bladder presenting with possible urinary tract infection, particularly among hospitalized patients. TO CLAIM CME CREDITS: Complete the self-assessment activity and evaluation online at http://www.physiatry.org/JournalCME. CME OBJECTIVES: Upon completion of this article, the reader should be able to: (1) Describe patient-reported signs and symptoms of urinary tract infection (UTI) in adults with neurogenic bladder (NB) due to spinal cord injury/disorder (SCI/D), multiple sclerosis (MS), and Parkinson disease (PD); (2) Differentiate urinary tract specific symptoms and nonspecific symptoms reported by adults with NB for suspected UTI and recognize how this may impact UTI diagnosis in this population; and (3) Recognize differences in UTI signs and symptoms reported by patients with NB based on patient and encounter characteristics. LEVEL: Advanced. ACCREDITATION: The Association of Academic Physiatrists is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.The Association of Academic Physiatrists designates this Journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s) ™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
 BACKGROUND/OBJECTIVES: This cross-sectional study examined the relationship between the oxygen (O(2)) cost of walking and body composition metrics, while considering potential covariates such as disability status, step length, and cadence, in persons with multiple sclerosis (MS). SUBJECTS/METHODS: The sample included 63 persons with MS across a wide distribution of body mass index (BMI). O(2) cost of walking was assessed using portable, indirect calorimetry, and percent body fat (%Fat), fat-free mass (FFM), bone mineral content, bone mineral density (BMD), and weight/FFM were determined from dual-energy x-ray absorptiometry. Other outcome measures included step length, cadence, physical activity, and disability status. RESULTS: The O(2) cost of walking had small-to-moderate associations with BMI (r(s) = -31, p = 0.015), %Fat (r(s) = -0.26, p = 0.041), and BMD (r(s) = -0.31, p = 0.013). O(2) cost of walking was significantly associated with these outcomes even after controlling for age, sex, disability status, and gait outcomes. The O(2) cost of walking was further significantly associated with shorter step length (r(s) = -0.40, p = 0.001), slower cadence (r(s) = -0.38, p = 0.002), and higher disability status (r(s) = 0.44, p < 0.001), but not physical activity. Body composition metrics were not associated with gait parameters, physical activity or disability status in our sample of persons with mild-to-moderate MS. CONCLUSIONS: The results indicated that higher O(2) cost of walking was associated with lower fat and worse bone health after taking factors such as disability status into consideration. Researchers may focus on interventions that change body composition, or perhaps gait profiles, as possible approaches for changing O(2) cost of walking and its consequences such as disability status in persons with MS.
 central nervous system (CNS) inflammation triggers activation of the integrated stress response (ISR). We previously reported that prolonging the ISR protects remyelinating oligodendrocytes and promotes remyelination in the presence of inflammation. However, the exact mechanisms through which this occurs remain unknown. Here, we investigated whether the ISR modulator Sephin1 in combination with the oligodendrocyte differentiation enhancing reagent bazedoxifene (BZA) is able to accelerate remyelination under inflammation, and the underlying mechanisms mediating this pathway. We find that the combined treatment of Sephin1 and BZA is sufficient to accelerate early-stage remyelination in mice with ectopic IFN-γ expression in the CNS. IFN-γ, which is a critical inflammatory cytokine in multiple sclerosis (MS), inhibits oligodendrocyte precursor cell (OPC) differentiation in culture and triggers a mild ISR. Mechanistically, we further show that BZA promotes OPC differentiation in the presence of IFN-γ, while Sephin1 enhances the IFN-γ-induced ISR by reducing protein synthesis and increasing RNA stress granule formation in differentiating oligodendrocytes. Finally, pharmacological suppression of the ISR blocks stress granule formation in vitro and partially lessens the beneficial effect of Sephin1 on disease progression in a mouse model of MS, experimental autoimmune encephalitis (EAE). Overall, our findings uncover distinct mechanisms of action of BZA and Sephin1 on oligodendrocyte lineage cells under inflammatory stress, suggesting that a combination therapy may effectively promote restoring neuronal function in MS patients.
 BACKGROUND AND OBJECTIVES: Cladribine tablets cause a reduction in lymphocytes with a predominant effect on B-cell and T-cell counts. The MAGNIFY-MS substudy reports the dynamic changes on multiple peripheral blood mononuclear cell (PBMC) subtypes and immunoglobulin (Ig) levels over 12 months after the first course of cladribine tablets in patients with highly active relapsing multiple sclerosis (MS). METHODS: Immunophenotyping was performed at baseline (predose) and at the end of months 1, 2, 3, 6, and 12 after initiating treatment with cladribine tablets. Assessments included lymphocyte subtype counts of CD19(+) B cells, CD4(+) and CD8(+) T cells, CD16(+) natural killer cells, plasmablasts, and Igs. Immune cell subtypes were analyzed by flow cytometry, and serum IgG and IgM were analyzed by nephelometric assay. Absolute cell counts and percentage change from baseline were assessed. RESULTS: The full analysis set included 57 patients. Rapid reductions in median CD19(+), CD20(+), memory, activated, and naive B-cell counts were detected, reaching nadir by month 2. Thereafter, total CD19(+), CD20(+), and naive B-cell counts subsequently reconstituted, but memory B cells remained reduced by 93%-87% for the remainder of the study. The decrease in plasmablasts was slower, reaching nadir at month 3. Decrease in T-cell subtypes was also slower and more moderate compared with B-cell subtypes, reaching nadir between months 3 and 6. IgG and IgM levels remained within the normal range over the 12-month study period. DISCUSSION: Cladribine tablets induce a specific pattern of early and sustained PBMC subtype dynamics in the absence of relevant Ig changes: While total B cells were reduced dramatically, T cells were affected significantly less. Naive B cells recovered toward baseline, naive CD4 and CD8 T cells did not, and memory B cells remained reduced. The results help to explain the unique immune depletion and repopulation architecture regarding onset of action and durability of effects of cladribine tablets while largely maintaining immune competence. TRIAL REGISTRATION INFORMATION: ClinicalTrials.gov Identifier: NCT03364036. Date registered: December 06, 2017.
 Immune mechanisms play an essential role in driving multiple sclerosis (MS) and altered trafficking and/or activation of dendritic cells (DC) were observed in the central nervous system and cerebrospinal fluid of MS patients. Interferon β (IFNβ) has been used as a first-line therapy in MS for almost three decades and vitamin D deficiency is a recognized environmental risk factor for MS. Both IFNβ and vitamin D modulate DC functions. Here, we studied the response to 1,25-dihydoxyvitamin D3 (1,25(OH)(2)D3) of DC obtained with IFNβ/GM-CSF (IFN-DC) compared to classically derived IL4-DC, in three donor groups: MS patients free of therapy, MS patients undergoing IFNβ therapy, and healthy donors. Except for a decreased CCL2 secretion by IL4-DC from the MS group, no major defects were observed in the 1,25(OH)(2)D3 response of either IFN-DC or IL4-DC from MS donors compared to healthy donors. However, the two cell models strongly differed for vitamin D receptor level of expression as well as for basal and 1,25(OH)(2)D3-induced cytokine/chemokine secretion. 1,25(OH)(2)D3 up-modulated IL6, its soluble receptor sIL6R, and CCL5 in IL4-DC, and down-modulated IL10 in IFN-DC. IFN-DC, but not IL4-DC, constitutively secreted high levels of IL8 and of matrix-metalloproteinase-9, both down-modulated by 1,25(OH)(2)D3. DC may contribute to MS pathogenesis, but also provide an avenue for therapeutic intervention. 1,25(OH)(2)D3-induced tolerogenic DC are in clinical trial for MS. We show that the protocol of in vitro DC differentiation qualitatively and quantitatively affects secretion of cytokines and chemokines deeply involved in MS pathogenesis.
 Background The human cerebellum has a large, highly folded cortical sheet. Its visualization is important for various disorders, including multiple sclerosis and spinocerebellar ataxias. The derivation of the cerebellar cortical surface in vivo is impeded by its high foliation. Purpose To image the cerebellar cortex, including its foliations and lamination, in less than 20 minutes, reconstruct the cerebellocortical surface, and extract cortical measures with use of motion-corrected, high-spatial-resolution 7.0-T MRI. Materials and Methods In this prospective study, conducted between February 2021 and July 2022, healthy participants underwent an examination with either a 0.19 × 0.19 × 0.5-mm(3), motion-corrected fast low-angle shot (FLASH) sequence (14.5 minutes) or a whole-cerebellum 0.4 × 0.4 × 0.4-mm(3), motion-corrected magnetization-prepared 2 rapid gradient-echo (MP2RAGE) sequence (18.5 minutes) at 7.0 T. Four participants underwent an additional FLASH sequence without motion correction. FLASH and MP2RAGE sequences were used to visualize the cerebellar cortical layers, derive cerebellar gray and white matter segmentations, and examine their fidelity. Quantitative measures were compared using repeated-measures analyses of variance or paired t tests. Results Nine participants (median age, 36 years [IQR, 25-42 years; range, 21-62 years]; five women) underwent examination with the FLASH sequence. Nine participants (median age, 37 years [IQR, 34-42 years; range, 25-62 years]; five men) underwent examination with the MP2RAGE sequence. A susceptibility difference between the expected location of the granular and molecular cerebellar layers was visually detected in the FLASH data in all participants. The segmentations derived from the whole-cerebellum MP2RAGE sequence showed the characteristic anatomic features of the cerebellum, like the transverse fissures and splitting folds. The cortical surface area (median, 949 cm(2) [IQR, 825-1021 cm(2)]) was 1.8 times larger, and the cortical thickness (median, 0.88 mm [IQR, 0.81-0.93 mm]) was five times thinner than previous in vivo estimates and closer to ex vivo reference data. Conclusion In vivo imaging of the cerebellar cortical layers and surface and derivation of quantitative measures was feasible in a clinically acceptable acquisition time with use of motion-corrected 7.0-T MRI. Published under a CC BY 4.0 license. Supplemental material is available for this article. See also the editorial by Dietrich in this issue.
 Randomised controlled trials (RCTs) play an important role in multiple sclerosis (MS) research, ensuring that new interventions are safe and efficacious before their introduction into clinical practice. Trials have been evolving to improve the robustness of their designs and the efficiency of their conduct. Advances in digital and mobile technologies in recent years have facilitated this process and the first RCTs with decentralised elements became possible. Decentralised clinical trials (DCTs) are conducted remotely, enabling participation of a more heterogeneous population who can participate in research activities from different locations and at their convenience. DCTs also rely on digital and mobile technologies which allows for more flexible and frequent assessments. While hospitals quickly adapted to e-health and telehealth assessments during the COVID-19 pandemic, the conduct of conventional RCTs was profoundly disrupted. In this paper, we review the existing evidence and gaps in knowledge in the design and conduct of DCTs in MS.
 BACKGROUND: Caregivers of people with Multiple Sclerosis are required to provide ongoing assistance especially during the advanced stages of the disease. They have to manage interventions and assume responsibilities which significantly impact both their personal quality of life and family's dynamics. OBJECTIVE: A qualitative phenomenological study was carried out to understand the experience of burden in caregivers and their resources to manage it. The study also explores how healthcare services involved in the Multiple Sclerosis Clinical Pathway respond to the needs of well-being of patients and family members. METHODS: 17 caregivers were involved in focus groups and in semi-structured individual interviews. RESULTS: Fatigue is experienced by all respondents and it starts when physical disabilities increase or when people become aware of them. Many caregivers declare that they refer to intrinsic (love towards their relatives, patience and dedication) or extrinsic (family members, hobbies) resources to cope with the burden of assistance. Patient associations and the Multiple Sclerosis Clinical Pathway play a significant role in supporting caregivers. CONCLUSIONS: Fatigue, loneliness, and isolation are experienced by caregivers and strongly affect their quality of life and health status. The study highlights caregivers' need to reconcile working times with care times, to give more space to self-care and to have moments to share their experiences with someone else. These needs should be at the core of health policies in order to avoid physical and emotional breakdowns which could lead to the rupture of the relational balance on which home care is based.
 INTRODUCTION: While it is recommended that patients with multiple sclerosis (MS) be vaccinated against COVID-19, it is unknown what the vaccine response is in MS patients treated with fingolimod, an agent which modulates the humoral response. We aimed to characterize the immune response to the COVID-19 vaccine in MS patients treated with fingolimod and to explore which factors influenced response. METHOD: We collected the following data from 59 MS patients treated with fingolimod and vaccinated against COVID-19: age, sex, duration of treatment, number of vaccine doses, date of last vaccination, type of vaccine, lymphocyte count, history of COVID-19, and serology to measure the vaccine response. We used Student's t-test and Chi(2) test to see whether there was a relationship between these variables and seropositivity. A multivariate logistic regression model was used to identify factors influencing the serology result. A multivariate linear regression model was used to identify factors influencing the antibody titer. RESULTS: Twenty-eight participants (47%) developed a positive serology. Age (P<0.001) and the duration of treatment (P=0.002) were significantly related to seropositivity. Gender (P=0.73), number of vaccinations (P=0.78), lymphocyte count (P=0.46), and the time between the last vaccine dose and blood sampling (P=0.84) were not significant variables. Multivariate analysis using logistic regression (n=59) showed that age (P=0.003, RR = 2.28, 95%CI = 1.28, 4.07) and duration of treatment (P=0.04, RR=1.91, 95%CI=1.04, 3.50) were significantly and independently correlated with COVID serology. Multivariate linear regression analysis of the antibody titer (n=59) found the duration of treatment to be significant (P = 0.015), but not age (P = 0.53). After removing three outliers, age (P = 0.005, RR=6.82, 95%CI=1.66, 27.98) and duration of treatment (P = 0.008, RR=5.12, 95%CI=1.24, 21.03) were significantly correlated with the antibody titer. CONCLUSION: COVID-19 seropositivity was present in 47% of our sample of 59 MS patients on fingolimod. A strong relationship was found between antibody development, age, and duration of treatment, as well as between antibody titer and age and duration of treatment.
 BACKGROUND: Multiple sclerosis often leads to proprioceptive impairments of the hand. However, it is challenging to objectively assess such deficits using clinical methods, thereby also impeding accurate tracking of disease progression and hence the application of personalized rehabilitation approaches. OBJECTIVE: We aimed to evaluate test-retest reliability, validity, and clinical usability of a novel robotic assessment of hand proprioceptive impairments in persons with multiple sclerosis (pwMS). METHODS: The assessment was implemented in an existing one-degree of freedom end-effector robot (ETH MIKE) acting on the index finger metacarpophalangeal joint. It was performed by 45 pwMS and 59 neurologically intact controls. Additionally, clinical assessments of somatosensation, somatosensory evoked potentials and usability scores were collected in a subset of pwMS. RESULTS: The test-retest reliability of robotic task metrics in pwMS was good (ICC=0.69-0.87). The task could identify individuals with impaired proprioception, as indicated by the significant difference between pwMS and controls, as well as a high impairment classification agreement with a clinical measure of proprioception (85.00-86.67%). Proprioceptive impairments were not correlated with other modalities of somatosensation. The usability of the assessment system was satisfactory (System Usability Scale ≥73.10). CONCLUSION: The proposed assessment is a promising alternative to commonly used clinical methods and will likely contribute to a better understanding of proprioceptive impairments in pwMS.
 While inflammation may not be the cause of disease, it is well known that it contributes to disease pathogenesis across a multitude of peripheral and central nervous system disorders. Chronic and overactive inflammation due to an effector T-cell-mediated aberrant immune response ultimately leads to tissue damage and neuronal cell death. To counteract peripheral and neuroinflammatory responses, research is being focused on regulatory T cell enhancement as a therapeutic target. Regulatory T cells are an immunosuppressive subpopulation of CD4+ T helper cells essential for maintaining immune homeostasis. The cells play pivotal roles in suppressing immune responses to maintain immune tolerance. In so doing, they control T cell proliferation and pro-inflammatory cytokine production curtailing autoimmunity and inflammation. For nervous system pathologies, Treg are known to affect the onset and tempo of neural injuries. To this end, we review recent findings supporting Treg's role in disease, as well as serving as a therapeutic agent in multiple sclerosis, myasthenia gravis, Guillain-Barre syndrome, Parkinson's and Alzheimer's diseases, and amyotrophic lateral sclerosis. An ever-broader role for Treg in the control of neurologic disease has been shown for traumatic brain injury, stroke, neurotrophic pain, epilepsy, and psychiatric disorders. To such ends, this review serves to examine the role played by Tregs in nervous system diseases with a focus on harnessing their functional therapeutic role(s).
 BACKGROUND AND OBJECTIVES: Prospective, deeply phenotyped research cohorts monitoring individuals with chronic neurologic conditions, such as multiple sclerosis (MS), depend on continued participant engagement. The COVID-19 pandemic restricted in-clinic research activities, threatening this longitudinal engagement, but also forced adoption of televideo-enabled care. This offered a natural experiment in which to analyze key dimensions of remote research: (1) comparison of remote vs in-clinic visit costs from multiple perspectives and (2) comparison of the remote with in-clinic measures in cross-sectional and longitudinal disability evaluations. METHODS: Between March 2020 and December 2021, 207 MS cohort participants underwent hybrid in-clinic and virtual research visits; 96 contributed 100 "matched visits," that is, in-clinic (Neurostatus-Expanded Disability Status Scale [NS-EDSS]) and remote (televideo-enabled EDSS [tele-EDSS]; electronic patient-reported EDSS [ePR-EDSS]) evaluations. Clinical, demographic, and socioeconomic characteristics of participants were collected. RESULTS: The costs of remote visits were lower than in-clinic visits for research investigators (facilities, personnel, parking, participant compensation) but also for participants (travel, caregiver time) and carbon footprint (p < 0.05 for each). Median cohort EDSS was similar between the 3 modalities (NS-EDSS: 2, tele-EDSS: 1.5, ePR-EDSS: 2, range 0.6.5); the remote evaluations were each noninferior to the NS-EDSS within ±0.5 EDSS point (TOST for noninferiority, p < 0.01 for each). Furthermore, year to year, the % of participants with worsening/stable/improved EDSS scores was similar, whether each annual evaluation used NS-EDSS or whether it switched from NS-EDSS to tele-EDSS. DISCUSSION: Altogether, the current findings suggest that remote evaluations can reduce the costs of research participation for patients, while providing a reasonable evaluation of disability trajectory longitudinally. This could inform the design of remote research that is more inclusive of diverse participants.
 There is vast evidence for the effect of NOD-like receptor protein-3 (NLRP3) inflammasome on multiple sclerosis (MS) pathogenesis. Clemastine (CLM) targets NLRP3 in hypoxic brain injury and promotes oligodendrocyte differentiation. However, no previous study pointed to the link of CLM with inflammasome components in MS. Herein, the study aimed to verify the action of CLM on NLRP3 signaling in experimental autoimmune encephalomyelitis (EAE) as an MS rat model. Homogenate of spinal cord with complete Freund's adjuvant was administered on days 0 and 7 to induce EAE. Rats received either CLM (5 mg/kg/day; p.o.) or MCC950 (2.5 mg/kg/day; i.p) for 15 days starting from the first immunization day. In EAEs' brains, NLRP3 pathway components; total and phosphorylated p38 mitogen-activated protein kinase (MAPK), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, interleukins 1β and -18 along with pyroptotic marker; gasdermin D (GSDMD) were upregulated. These were accompanied with diminished nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and total antioxidant capacity levels. CLM improved these perturbations as well as signs of MS; weight loss, clinical scores, and motor disorders observed in the open field, hanging wire and rotarod tests. Histopathological examinations revealed improvement in H&E abnormalities and axonal demyelination as shown by luxol fast blue stain in lumbar sections of spinal cord. These CLM's actions were studied in comparison to MCC950 as a well-established selective blocker of the NLRP3 inflammasome. Conclusively, CLM has a protective role against neuroinflammation and demyelination in EAE via its anti-inflammatory and anti-pyroptotic actions.
 BACKGROUND AND OBJECTIVES: Studies on tumefactive brain lesions in myelin oligodendrocyte glycoprotein-immunoglobulin G (IgG)-associated disease (MOGAD) are lacking. We sought to characterize the frequency clinical, laboratory, and MRI features of these lesions in MOGAD and compare them with those in multiple sclerosis (MS) and aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD). METHODS: We retrospectively searched 194 patients with MOGAD and 359 patients with AQP4+NMOSD with clinical/MRI details available from the Mayo Clinic databases and included those with ≥1 tumefactive brain lesion (maximum transverse diameter ≥2 cm) on MRI. Patients with tumefactive MS were identified using the Mayo Clinic medical record linkage system. Binary multivariable stepwise logistic regression identified independent predictors of MOGAD diagnosis; Cox proportional regression models were used to assess the risk of relapsing disease and gait aid in patients with tumefactive MOGAD vs those with nontumefactive MOGAD. RESULTS: We included 108 patients with tumefactive demyelination (MOGAD = 43; AQP4+NMOSD = 16; and MS = 49). Tumefactive lesions were more frequent among those with MOGAD (43/194 [22%]) than among those with AQP4+NMOSD (16/359 [5%], p < 0.001). Risk of relapse and need for gait aid were similar in tumefactive and nontumefactive MOGAD. Clinical features more frequent in MOGAD than in MS included headache (18/43 [42%] vs 10/49 [20%]; p = 0.03) and somnolence (12/43 [28%] vs 2/49 [4%]; p = 0.003), the latter also more frequent than in AQP4+NMOSD (0/16 [0%]; p = 0.02). The presence of peripheral T2-hypointense rim, T1-hypointensity, diffusion restriction (particularly an arc pattern), ring enhancement, and Baló-like or cystic appearance favored MS over MOGAD (p ≤ 0.001). MRI features were broadly similar in MOGAD and AQP4+NMOSD, except for more frequent diffusion restriction in AQP4+NMOSD (10/15 [67%]) than in MOGAD (11/42 [26%], p = 0.005). CSF analysis revealed less frequent positive oligoclonal bands in MOGAD (2/37 [5%]) than in MS (30/43 [70%], p < 0.001) and higher median white cell count in MOGAD than in MS (33 vs 6 cells/μL, p < 0.001). At baseline, independent predictors of MOGAD diagnosis were the presence of somnolence/headache, absence of T2-hypointense rim, lack of T1-hypointensity, and no diffusion restriction (Nagelkerke R (2) = 0.67). Tumefactive lesion resolution was more common in MOGAD than in MS or AQP4+NMOSD and improved model performance. DISCUSSION: Tumefactive lesions are frequent in MOGAD but not associated with a worse prognosis. The clinical, MRI, and CSF attributes of tumefactive MOGAD differ from those of tumefactive MS and are more similar to those of tumefactive AQP4+NMOSD with the exception of lesion resolution, which favors MOGAD.
 BACKGROUND AND OBJECTIVES: Pediatric-acquired demyelination of the CNS associated with antibodies directed against myelin oligodendrocyte glycoprotein (MOG; MOG antibody-associated disease [MOGAD]) occurs as a monophasic or relapsing disease and with variable but often extensive T2 lesions in the brain. The impact of MOGAD on brain growth during maturation is unknown. We quantified the effect of pediatric MOGAD on brain growth trajectories and compared this with the growth trajectories of age-matched and sex-matched healthy children and children with multiple sclerosis (MS, a chronic relapsing disease known to lead to failure of normal brain growth and to loss of brain volume) and monophasic seronegative demyelination. METHODS: We included children enrolled at incident attack in the prospective longitudinal Canadian Pediatric Demyelinating Disease Study who were recruited at the 3 largest enrollment sites, underwent research brain MRI scans, and were tested for serum MOG-IgG. Children seropositive for MOG-IgG were diagnosed with MOGAD. MS was diagnosed per the 2017 McDonald criteria. Monophasic seronegative demyelination was confirmed in children with no clinical or MRI evidence of recurrent demyelination and negative results for MOG-IgG and aquaporin-4-IgG. Whole and regional brain volumes were computed through symmetric nonlinear registration to templates. We computed age-normalized and sex-normalized z scores for brain volume using a normative dataset of 813 brain MRI scans obtained from typically developing children and used mixed-effect models to assess potential deviation from brain growth trajectories. RESULTS: We assessed brain volumes of 46 children with MOGAD, 26 with MS, and 51 with monophasic seronegative demyelinating syndrome. Children with MOGAD exhibited delayed (p < 0.001) age-expected and sex-expected growth of thalamus, caudate, and globus pallidus, normalized for the whole brain volume. Divergence from expected growth was particularly pronounced in the first year postonset and was detected even in children with monophasic MOGAD. Thalamic volume abnormalities were less pronounced in children with MOGAD compared with those in children with MS. DISCUSSION: The onset of MOGAD during childhood adversely affects the expected trajectory of growth of deep gray matter structures, with accelerated changes in the months after an acute attack. Further studies are required to better determine the relative impact of monophasic vs relapsing MOGAD and whether relapsing MOGAD with attacks isolated to the optic nerves or spinal cord affects brain volume over time.
 As resident macrophages of the CNS, microglia are critical immune effectors of inflammatory lesions and associated neural dysfunctions. In multiple sclerosis (MS) and its animal models, chronic microglial inflammatory activity damages myelin and disrupts axonal and synaptic activity. In contrast to these detrimental effects, the potent phagocytic and tissue-remodelling capabilities of microglia support critical endogenous repair mechanisms. Although these opposing capabilities have long been appreciated, a precise understanding of their underlying molecular effectors is only beginning to emerge. Here, we review recent advances in our understanding of the roles of microglia in animal models of MS and demyelinating lesions and the mechanisms that underlie their damaging and repairing activities. We also discuss how the structured organization and regulation of the genome enables complex transcriptional heterogeneity within the microglial cell population at demyelinating lesions.
 Several recent studies have applied machine learning techniques to develop risk algorithms that predict subsequent suicidal behavior based on electronic health record data. In this study we used a retrospective cohort study design to test whether developing more tailored predictive models-within specific subpopulations of patients-would improve predictive accuracy. A retrospective cohort of 15,117 patients diagnosed with multiple sclerosis (MS), a diagnosis associated with increased risk of suicidal behavior, was used. The cohort was randomly divided into equal sized training and validation sets. Overall, suicidal behavior was identified among 191 (1.3%) of the patients with MS. A Naïve Bayes Classifier model was trained on the training set to predict future suicidal behavior. With 90% specificity, the model detected 37% of subjects who later demonstrated suicidal behavior, on average 4.6 years before the first suicide attempt. The performance of a model trained only on MS patients was better at predicting suicide in MS patients than that a model trained on a general patient sample of a similar size (AUC of 0.77 vs. 0.66). Unique risk factors for suicidal behavior among patients with MS included pain-related codes, gastroenteritis and colitis, and history of smoking. Future studies are needed to further test the value of developing population-specific risk models.
 BACKGROUND: Despite strong recommendations for coronavirus disease 2019 (Covid-19) vaccination by multiple sclerosis (MS) organizations, some persons with MS (pwMS) remain vaccine hesitant. The Swiss MS Registry conducted a survey to explore Covid-19 vaccine hesitancy, self-reported side effects and changes in MS symptoms following vaccination in adult pwMS. METHODS: Self-reported data were analyzed cross-sectionally. Multivariable logistic regression was used to explore participant characteristics associated with Covid-19 vaccine hesitancy. RESULTS: Of 849 respondents, 73 (8.6%) were unvaccinated. Hesitation to vaccinate was most often a personal preference (N = 42, 57.53%). Factors negatively associated with vaccine hesitancy included older age (OR = 0.97 per year, 95% CI [0.94, 0.99]) and regularly seeing healthcare professionals (OR = 0.25, 95% CI [0.07, 0.85]). A history of confirmed Covid-19 infection (OR = 3.38, 95% CI [1.69, 6.77]) and being underweight (OR = 4.50, 95% CI [1.52, 13.36]) were positively associated with vaccine hesitancy. Of 768 participants who provided information, 320 (41.2%) and 351 (45.2%) reported vaccination side effects after the first and second vaccinations, respectively. Changes in MS symptoms were reported by 49 (6.3%) participants after the first and 67 (9.0%) participants after the second vaccination, and were most often described as increased or new-onset fatigue (N = 17/49 (34.7%) after the first and N = 21/67 (31.3%) after the second dose). CONCLUSIONS: Covid-19 vaccine hesitancy was low among surveyed pwMS. The risk of vaccine hesitancy was higher among younger pwMS, those with a history of Covid-19 infection, and those without regular contact with healthcare professionals.
 BACKGROUND: The neutrophil-to-lymphocyte ratio (NLR) and monocyte-to-lymphocyte ratio (MLR) are inflammatory biomarkers that may predict disease course in neuroinflammatory diseases. We examine whether NLR or MLR at the time of the first attack predicts longitudinal disease outcomes in pediatric neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). METHODS: Clinical data were collected retrospectively at a single institution. NLR (ratio of percent neutrophils to percent lymphocytes) and MLR (ratio of percent monocytes to percent lymphocytes) were calculated in the complete blood cell count at the time of presentation before treatments. Expanded Disability Status Scale (EDSS) score and time to next relapse were used as the outcome assessments. RESULTS: Twenty-eight patients with MS and eight patients with aquaporin-4-positive NMOSD were included. For NMOSD, NLR at presentation associated with EDSS at six months (P = 0.003) and one year (P = 0.032) even when adjusting for age at presentation. MLR associated with EDSS at six months (P = 0.0203) and EDSS at one year (P = 0.0079). However, NLR and MLR did not predict EDSS scores in MS. MLR and NLR did not predict time to next relapse or did not associate with magnetic resonance imaging activity in MS and NMOSD. Changes in MLR and NLR were observed with disease-modifying therapies but did not predict disease activity. CONCLUSIONS: NLR and MLR associated with six-month and one-year EDSS in children with NMOSD but not in MS. Future studies should explore whether changes in NLR and MLR could predict disease activity or treatment efficacy.
 Macrophage M2 (MP2)-based cell therapy is a novel medicinal treatment for animals with Experimental Autoimmune Encephalomyelitis (EAE) as an experimental model of multiple sclerosis (MS). This systematic review and meta-analysis study was designed to assess the overall therapeutic effects of MP2 cell therapy on Clinical Score and motor impairment in EAE-induced animals. All experiments on MP2 cell therapy in animals with EAE were gathered (by October 2, 2022) from English (PubMed, Scopus, WoS, Science Direct, and ISC) and Persian (MagIran and SID) databases. The searching strategy was designed using "Experimental Autoimmune Encephalomyelitis," "Multiple Sclerosis," and "Macrophage M2" keywords. Following primary and secondary screenings, eligible papers were selected based on the PRISMA 2020 guideline, and the study quality was assessed using the Animal Research: Reporting of In Vivo Experiments (ARRIVE) checklist. The difference in means of Clinical Score (score 0-5) as the effect size (ES) was analyzed based on the random effect model (CMA software, v.2). Subgrouping (EAE phases of Onset, Peak, and Recovery) was applied, and I(2) index was used to assess the heterogeneity index. Publication bias and sensitivity indices were also evaluated. P < 0.05 was considered significant, and the confidence interval (CI) was determined 95%. Among 22 gathered papers, medium to high quality studies were selected for meta-analysis. Difference in means, P value, and I(2) for Onset, Peak, and Recovery phases were 0.082 (CI95%: -0.323-0.159, P value: 0.504, I(2) : 67.961%), -0.606 (CI95%: -1.518 to -0.305, P value: 0.192, I(2) : 96.070%), and -1.103 (CI95%: -1.390 to -0.816, P value: 0.000, I(2) : 30.880%), respectively and Overall Effect was found -0.509 (CI95%: -0.689 to -0.328, P value < 0.001). Also, P value (two-tailed) indices for publication bias were 0.366 and 0.583 for Egger's regression intercept and Begg rank correlation, respectively. The P value for sensitivity was detected 0.003. Cell therapy procedure using MP2 can potentially alleviate the Clinical Scores Index and correct the motor defects in Recovery phase of EAE animals. In healthy mice, the brain and myelin surrounding neurons are in a healthy and physiological state (1). To evaluate MS in humans, it is necessary to model this type of disease in animals using EAE procedure through subcutaneous injection of CFA, MOG(35-55) , MT, and Pert. Thus, inflammation and autoimmunity occur, which finally lead to myelin destruction and motor symptoms (2). By aspiration of progenitor cells available in bone marrow, the MP2 can be isolated and cultured. By activation of these types of cells, a rich collection of MP2 can be prepared for the cell-therapy process (3). After injection through the tail vein or intra-peritoneal procedure, these cells can be located in CNS through crossing from the BBB. They begin their anti-inflammatory activities and help repair the damaged myelin (4). Eventually, the clinical symptoms can be modified considerably, and the animal motor function improves (5). CFA, complete Freund's adjuvant; MOG(35-55) , myelin oligodendrocyte glycoprotein; MT, Mycobacterium tuberculosis; Pert, pertussis; EAE, Experimental Autoimmune Encephalomyelitis; BM, bone marrow; MP2, macrophage M2; and BBB, blood brain barrier.
 Multiple sclerosis is an autoimmune disease in which the immune system attacks the nerve myelin sheath. The balance between pathogenic Th17 cells and regulatory Treg cells, both of which express the chemokine receptor CCR6 is critical for determining disease activity. It has been postulated that CCL20, the cognate ligand of CCR6, produced by the blood-brain barrier attracts these immune cells to the central nervous system (CNS). However, the pathological phenotypes of the experimental model of multiple sclerosis in CCR6-knockout (KO) mice are inconclusive, while this has not been addressed in CCL20-KO mice. To address this, we generated CCL20-KO and CCR6-KO mice using the CRISPR/Cas9 system. Clinical phenotypes of experimental autoimmune encephalomyelitis (EAE) in the chronic phase were slightly exacerbated in both mutant mice relative to those in wild-type (WT) mice. Inflammatory cell infiltration and demyelination in the CNS were similar in the KO and WT mice. CNS CD4(+) T cell counts were the same for mutant and WT mice. The mutant and WT mice did not differ significantly in the proportions of Th17 and Treg cells in the CNS, or in IL-17 and TGF-β mRNA expression in the CNS. These findings suggest that CCL20/CCR6-mediated cell migration is not necessarily required for the onset of EAE, and may be compensated for by other chemokine signals.
 BACKGROUND AND OBJECTIVE: Dimethyl fumarate (DMF) is an immunomodulatory drug approved for the therapy of multiple sclerosis (MS). The identification of response biomarkers to DMF is a necessity in the clinical practice. With this aim, we studied the immunophenotypic and transcriptomic changes produced by DMF in peripheral blood mononuclear cells (PBMCs) and its association with clinical response. MATERIAL AND METHODS: PBMCs were obtained from 22 RRMS patients at baseline and 12 months of DMF treatment. Lymphocyte and monocyte subsets, and gene expression were assessed by flow cytometry and next-generation RNA sequencing, respectively. Clinical response was evaluated using the composite measure "no evidence of disease activity" NEDA-3 or "evidence of disease activity" EDA-3 at 2 years, classifying patients into responders (n=15) or non-responders (n=7), respectively. RESULTS: In the whole cohort, DMF produced a decrease in effector (TEM) and central (TCM) memory T cells in both the CD4+ and CD8+ compartments, followed by an increase in CD4+ naïve T cells. Responder patients presented a greater decrease in TEM lymphocytes. In addition, responder patients showed an increase in NK cells and were resistant to the decrease in the intermediate monocytes shown by non-responders. Responder patients also presented differences in 3 subpopulations (NK bright, NK dim and CD8 TCM) at baseline and 4 subpopulations (intermediate monocytes, regulatory T cells, CD4 TCM and CD4 TEMRA) at 12 months. DMF induced a mild transcriptional effect, with only 328 differentially expressed genes (DEGs) after 12 months of treatment. The overall effect was a downregulation of pro-inflammatory genes, chemokines, and activators of the NF-kB pathway. At baseline, no DEGs were found between responders and non-responders. During DMF treatment a differential transcriptomic response was observed, with responders presenting a higher number of DEGs (902 genes) compared to non-responders (189 genes). CONCLUSIONS: Responder patients to DMF exhibit differences in monocyte and lymphocyte subpopulations and a distinguishable transcriptomic response compared to non-responders that should be further studied for the validation of biomarkers of treatment response to DMF.
 Inflammation in the central nervous system can impair the function of neuronal mitochondria and contributes to axon degeneration in the common neuroinflammatory disease multiple sclerosis (MS). Here we combine cell-type-specific mitochondrial proteomics with in vivo biosensor imaging to dissect how inflammation alters the molecular composition and functional capacity of neuronal mitochondria. We show that neuroinflammatory lesions in the mouse spinal cord cause widespread and persisting axonal ATP deficiency, which precedes mitochondrial oxidation and calcium overload. This axonal energy deficiency is associated with impaired electron transport chain function, but also an upstream imbalance of tricarboxylic acid (TCA) cycle enzymes, with several, including key rate-limiting, enzymes being depleted in neuronal mitochondria in experimental models and in MS lesions. Notably, viral overexpression of individual TCA enzymes can ameliorate the axonal energy deficits in neuroinflammatory lesions, suggesting that TCA cycle dysfunction in MS may be amendable to therapy.
 BACKGROUND: Serum levels of neurofilament light chain (sNfL) are a potentially useful biomarker for assessing the efficacy of multiple sclerosis (MS) treatments. OBJECTIVE: To compare levels of sNfL in patients with MS who switched from natalizumab every 4 weeks (Q4W) to extended interval dosing (EID) and patients who remained on Q4W dosing in real-world clinical practice. METHODS: This was a retrospective analysis of samples from patients treated with natalizumab from 2010 to 2015 at a single center in the United States. Levels of sNfL were compared in patients who stayed on Q4W dosing or who switched to EID (parallel-arm analyses) and during Q4W and EID periods in patients who switched to EID (pre- and post-switch analyses). RESULTS: The analysis included 139 patients (Q4W: n = 79; EID: n = 60). After adjustment, levels of sNfL did not significantly differ between patients who remained on Q4W dosing and those who switched to EID in parallel-arm analyses (adjusted Q4W-EID difference = 0.51 pg/mL; p = 0.60) or pre- and post-switch analyses (adjusted difference = 0.96 pg/mL; p = 0.10). CONCLUSION: These sNfL biomarker results suggest that the effectiveness of natalizumab is maintained in patients who switch from Q4W dosing to EID.
 Multiple sclerosis (MS) is the most common demyelinating central nervous system (CNS) disease affecting young adults, often resulting in neurological deficits and disability as the disease progresses. B lymphocytes play a complex and critical role in MS pathology and are the target of several therapeutics in clinical trials. Currently, there is no way to accurately select patients for specific anti-B cell therapies or to non-invasively quantify the effects of these treatments on B cell load in the CNS and peripheral organs. Positron emission tomography (PET) imaging has enormous potential to provide highly specific, quantitative information regarding the in vivo spatiotemporal distribution and burden of B cells in living subjects. This paper reports methods to synthesize and employ a PET tracer specific for human CD19(+) B cells in a well-established B cell-driven mouse model of MS, experimental autoimmune encephalomyelitis (EAE), which is induced with human recombinant myelin oligodendrocyte glycoprotein 1-125. Described here are optimized techniques to detect and quantify CD19(+) B cells in the brain and spinal cord using in vivo PET imaging. Additionally, this paper reports streamlined methods for ex vivo gamma counting of disease-relevant organs, including bone marrow, spinal cord, and spleen, together with high-resolution autoradiography of CD19 tracer binding in CNS tissues.
 IMPORTANCE: Immunological response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination is important, especially in people with multiple sclerosis (pwMS) on immunosuppressive therapies. OBJECTIVE: This study aims to determine whether adjuvanted protein-based vaccine NVX-CoV2373 is able to induce an immune response to SARS-CoV-2 in pwMS with inadequate responses to prior triple mRNA/viral vector vaccination. DESIGN SETTING AND PARTICIPANTS: We conducted a single-center, prospective longitudinal cohort study at the MS Center in Dresden, Germany. In total, 65 participants were included in the study in accordance with the following eligibility criteria: age > 18 years, immunomodulatory treatment, and insufficient T-cellular and humoral response to prior vaccination with at least two doses of SARS-CoV-2 mRNA (BNT162b2, mRNA-1273) or viral vector vaccines (AZD1222, Ad26.COV2.S). INTERVENTIONS: Intramuscular vaccination with two doses of NVX-CoV2373 at baseline and 3 weeks of follow-up. MAIN OUTCOMES AND MEASURES: The development of SARS-CoV-2-specific antibodies and T-cell responses was evaluated. RESULTS: For the final analysis, data from 47 patients on stable treatment with sphingosine-1-phosphate receptor (S1PR) modulators and 17 on ocrelizumab were available. The tolerability of the NVX-CoV2373 vaccination was overall good and comparable to the one reported for the general population. After the second NVX-CoV2373 vaccination, 59% of S1PR-modulated patients developed antispike IgG antibodies above the predefined cutoff of 200 binding antibody units (BAU)/ml (mean, 1,204.37 [95% CI, 693.15, 2,092.65] BAU/ml), whereas no clinically significant T-cell response was found. In the subgroup of the patients on ocrelizumab treatment, 23.5% developed antispike IgG > 200 BAU/ml (mean, 116.3 [95% CI, 47.04, 287.51] BAU/ml) and 53% showed positive spike-specific T-cellular responses (IFN-gamma release to antigen 1: mean, 0.2 [95% CI, 0.11, 0.31] IU/ml; antigen 2: mean, 0.24 [95% CI, 0.14, 0.37]) after the second vaccination. CONCLUSIONS: Vaccination with two doses of NVX-CoV2373 was able to elicit a SARS-CoV-2-specific immune response in pwMS lacking adequate immune responses to previous mRNA/viral vector vaccination. For patients receiving S1PR modulators, an increase in anti-SARS-CoV-2 IgG antibodies was detected after NVX-CoV2373 vaccination, whereas in ocrelizumab-treated patients, the increase of antiviral T-cell responses was more pronounced. Our data may impact clinical decision-making by influencing the preference for NVX-CoV2373 vaccination in pwMS receiving treatment with S1PR modulation or anti-CD20 treatment.
 We present an autopsy case of a 19-year-old man with a history of epilepsy whose unwitnessed sudden death occurred unexpectedly in the night. About 4 years before death, he was diagnosed with unilateral optic neuritis (ON). Demyelinating disease was suspected, but he was lost to follow up after the recovery. Six months before death, he received a second dose of mRNA coronavirus disease 2019 (COVID-19) vaccine. Three months before death, he experienced epileptic seizures for the first time. Seventeen days before death, he was infected with COVID-19, which showed self-limited course under home isolation. Several days before death, he complained of seizures again at night. Autopsy revealed multifocal gray-tan discoloration in the cerebrum. Histologically, the lesions consisted of active and inactive demyelinated plaques in the perivenous area of the white matter. Perivascular lymphocytic infiltration and microglial cell proliferation were observed in both white matter and cortex. The other major organs including heart and lung were unremarkable. Based on the antemortem history and postmortem findings, the cause of death was determined to be multiple sclerosis with suspected exacerbation. The direct or indirect involvement of cortex and deep gray matter by exacerbated multiple sclerosis may explain the occurrence of seizures. Considering the absence of other structural abnormalities except the inflammatory demyelination of the cerebrum, fatal arrhythmia or laryngospasm in the terminal epileptic seizure may explain his sudden unexpected death in the benign circumstances. In this case, the onset of seizure was preceded by COVID-19 vaccination, and the exacerbation of seizure was preceded by COVID-19 infection, respectively. Literature reporting first manifestation or relapse of multiple sclerosis temporally associated with COVID-19 vaccination or infection are reviewed.
 OBJECTIVE: Accumulating evidence suggests that dysfunctional adipose tissue (AT) plays a major role in the risk of developing multiple sclerosis (MS), the most common immune-mediated and demyelinating disease of the central nervous system. However, the contribution of adipose tissue to the etiology and progression of MS is still obscure. This study aimed at deciphering the responses of AT in experimental autoimmune encephalomyelitis (EAE), the best characterized animal model of MS. RESULTS AND METHODS: We observed a significant AT loss in EAE mice at the onset of disease, with a significant infiltration of M1-like macrophages and fibrosis in the AT, resembling a cachectic phenotype. Through an integrative and multilayered approach, we identified lipocalin2 (LCN2) as the key molecule released by dysfunctional adipocytes through redox-dependent mechanism. Adipose-derived LCN2 shapes the pro-inflammatory macrophage phenotype, and the genetic deficiency of LCN2 specifically in AT reduced weight loss as well as inflammatory macrophage infiltration in spinal cord in EAE mice. Mature adipocytes downregulating LCN2 reduced lipolytic response to inflammatory stimuli (e.g. TNFα) through an ATGL-mediated mechanism. CONCLUSIONS: Overall data highlighted a role LCN2 in exacerbating inflammatory phenotype in EAE model, suggesting a pathogenic role of dysfunctional AT in MS.
 BACKGROUND AND OBJECTIVES: In the multiple sclerosis (MS) brain, chronic active lesions can be detected using MRI- and PET-based methods. In this study, we investigated whether the frequency of TSPO-PET-detectable chronic active lesions associates with disease progression measured using the Expanded Disability Status Scale (EDSS) at 5-year follow-up. METHODS: Chronic lesion-associated innate immune cell activation was evaluated using TSPO-PET in 82 patients with MS. Chronic lesions were categorized into rim-active, inactive, and overall active lesion subtypes based on innate immune cell activation patterns in the lesion core and at the 2-mm perilesional rim. Logistic regression was used to identify best predictors of progression. RESULTS: Twenty-one patients experienced disability progression during the follow-up. These patients had a significantly higher proportion of rim-active lesions (p < 0.001) and a significantly lower proportion of inactive lesions (p = 0.001) compared with nonprogressed patients. The results were similar in the patient group having no relapses during the follow-up (60 patients, 14 experienced progression). In logistic regression modeling, the categorized variable "patients with >10% rim-active lesions and ≤50% inactive lesions of all chronic lesions" predicted disease progression in the entire cohort (OR = 26.8, p < 0.001) and in the group free of relapses (OR = 34.8, p = 0.002). DISCUSSION: The results show that single TSPO-PET-based in vivo lesion phenotyping of chronic MS lesions provides a strong predictor for MS disease progression. This emphasizes the significance of chronic active lesions in disability accumulation in MS.
 There are limited real-world data on the use of botulinum toxin type A (BoNT-A) in patients with multiple sclerosis (MS). Accordingly, this nationwide, population-based, retrospective cohort study aimed to describe BoNT-A treatment trends in patients with MS between 2014 and 2020 in France. This study extracted data from the French National Hospital Discharge Database (Programme de Médicalisation des Systèmes d'Information, PMSI) covering the entire French population. Among 105,206 patients coded with MS, we identified those who received ≥1 BoNT-A injection, administered within striated muscle for MS-related spasticity and/or within the detrusor smooth muscle for neurogenic detrusor overactivity (NDO). A total of 8427 patients (8.0%) received BoNT-A injections for spasticity, 52.9% of whom received ≥3 BoNT-A injections with 61.9% of the repeated injections administered every 3 to 6 months. A total of 2912 patients (2.8%) received BoNT-A injections for NDO, with a mean of 4.7 injections per patient. Most repeated BoNT-A injections within the detrusor smooth muscle (60.0%) were administered every 5 to 8 months. There were 585 patients (0.6%) who received both BoNT-A injections within striated muscle and the detrusor smooth muscle. Overall, our study highlights a broad range of BoNT-A treatment practices between 2014 and 2020 in patients with MS.
 BACKGROUND: Multiple sclerosis (MS) is one of the most common neurological diseases that cause chronic inflammation of the central nervous system and demyelination of the myelin sheath. At present, microRNAs (miRNAs) are considered not only a diagnostic and prognostic indicator of diseases but also a new goal in gene therapy. This study aims to find a simple, non-invasive, valuable biomarker for early detection and potential treatment of MS. METHODS: In the present study, 30 patients with MS were included. The qRT-PCR method was performed to evaluate the expression level of miR-193a, RhoA, and ROCK1. Besides, western blotting was performed to determine the expression level of RhoA and ROCK1 at protein levels. Moreover, we aimed to clarify the possible correlation between miR-193a-5p and its-regulated target genes so that miR-193a-5p mimic was transfected into MS-derived cultured PBMSs, and the expression level of RhoA and ROCK1 were then evaluated by qRT-PCR and Western blotting. In the final step, the correlation between miR-193a-5p and clinicopathological features of patients was investigated. RESULTS: Results showed that miR-193a was decreased while RhoA and ROCK1 were up-regulated in PBMCs obtained from patients with MS compared to the control group. It was also revealed that miR-193a transfection reduced RhoA and ROCK1 expression at mRNA and protein levels. The results from the Chi-square analysis showed that down-regulation of miR-193a was associated with increased CRP level, CSF IgG positivity, and MSSS (Multiple Sclerosis Severity Score), suggesting miR-193a is a potential diagnostic and prognostic indicator. CONCLUSION: We implied that miR-193a could modulate RhoA and ROCK 1 expression in MS patients, in which its down-regulation leads to increased expression of RhoA and ROCK1 and poor prognosis of patients with MS. Therefore, miR-193a and its associated targets could serve potential prognostic, diagnostic, and therapeutic efficacy in MS patients.
 OBJECTIVE: This article provides an overview of the growing body of evidence showing bidirectional relationships between sleep and various neurologic disorders. LATEST DEVELOPMENTS: Mounting evidence demonstrates that disrupted sleep can negatively impact various neurologic disease processes, including stroke, multiple sclerosis, epilepsy, neuromuscular disorders including amyotrophic lateral sclerosis, and headache syndromes. Abnormal sleep can also be a precursor to Alzheimer disease and neurodegenerative disease states such as Parkinson disease and dementia with Lewy bodies. Interventions to improve sleep and treat obstructive sleep apnea may play a vital role in preventing neurologic disease development and progression. ESSENTIAL POINTS: Sleep disorders are common among patients with neurologic disorders. To provide comprehensive care to patients with neurologic conditions, neurologists must ask patients about sleep issues that may warrant further diagnostic testing, treatment, and sleep medicine referral when indicated.
 BACKGROUND AND PURPOSE: Regular physical activity (PA) helps to reduce the severity of physical and mental symptoms and improves quality of life in people with multiple sclerosis (PwMS). Based on current evidence and expert opinion, the recent multiple sclerosis guidelines recommend at least 150 minutes/week of PA. This study presents the results of a survey analyzing whether and how PwMS met the guidelines before and during the pandemic. METHODS: We developed and disseminated an international online survey between December 2020 and July 2021, investigating changes in self-reported PA type, duration, frequency, and intensity due to the COVID-19 outbreak in PwMS with differing disability levels. RESULTS: Among respondents (n = 3810), 3725 were eligible. The proportion of those who conducted at least one activity decreased with increasing disability level at both time points (pre and during). Overall 60% of respondents met the guidelines before the pandemic (mild: 64.43%; moderate: 51.53%; severe: 39.34%; χ 2(2) = 109.13, P < 0.01); a reduction of approximately 10% occurred during the pandemic in all disability groups (mild: 54.76%; moderate: 42.47%; severe: 29.48%; χ 2(2) = 109.67, P < 0.01). Respondents with higher disability participated more in physical therapy and less in walking, cycling, and running at both time points. Most respondents reported practicing PA at a moderate intensity at both time points; frequency and duration of sessions decreased as disability level increased. DISCUSSION AND CONCLUSIONS: The percentage of those meeting the guidelines reduced with increasing disability level and during the pandemic. PA type and intensity varied widely across the disability categories. Interventions accounting for disability level are required to enable more PwMS to reap the benefits of PA.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, http://links.lww.com/JNPT/A415 ).
 INTRODUCTION: The effect of disease-modifying therapies (DMT) on vaccine responses is largely unknown. Understanding the development of protective immunity is of paramount importance to fight the COVID-19 pandemic. OBJECTIVE: To characterise humoral immunity after mRNA-COVID-19 vaccination of people with multiple sclerosis (pwMS). METHODS: All pwMS in Norway fully vaccinated against SARS-CoV-2 were invited to a national screening study. Humoral immunity was assessed by measuring anti-SARS-CoV-2 SPIKE RBD IgG response 3-12 weeks after full vaccination, and compared with healthy subjects. RESULTS: 528 pwMS and 627 healthy subjects were included. Reduced humoral immunity (anti-SARS-CoV-2 IgG <70 arbitrary units) was present in 82% and 80% of all pwMS treated with fingolimod and rituximab, respectively, while patients treated with other DMT showed similar rates as healthy subjects and untreated pwMS. We found a significant correlation between time since the last rituximab dose and the development of humoral immunity. Revaccination in two seronegative patients induced a weak antibody response. CONCLUSIONS: Patients treated with fingolimod or rituximab should be informed about the risk of reduced humoral immunity and vaccinations should be timed carefully in rituximab patients. Our results identify the need for studies regarding the durability of vaccine responses, the role of cellular immunity and revaccinations.
 Multiple sclerosis (MS) is a central nervous system (CNS) demyelinating disease. Failure to remyelinate successfully is common in MS lesions, often with consequent neuronal/axonal damage. CNS myelin is normally produced by oligodendroglial cells. Remyelination by Schwann cells (SchC) has been reported in spinal cord demyelination, in which SchCs are in close proximity to CNS myelin. We identified an MS cerebral lesion that was remyelinated by SchCs. This prompted us to query the extent of SchC remyelination in the brain and spinal cords of additional autopsied MS specimens. CNS tissues were obtained from the autopsies of 14 MS cases. Remyelinated lesions were identified by Luxol fast blue-periodic-acid Schiff and solochrome cyanine staining. Deparaffinized sections containing remyelinated lesions were stained with anti-glial fibrillary acid protein to identify reactive astrocytes. Glycoprotein P zero (P0) is a protein exclusive to peripheral but not CNS myelin. Areas of SchC remyelination were identified by staining with anti-P0. Myelinated regions in the index case cerebral lesion were confirmed to be of SchC origin using anti-P0 staining. Subsequently, 64 MS lesions from 14 autopsied MS cases were examined, and 23 lesions in 6 cases showed remyelination by SchCs. Lesions from the cerebrum, brainstem, and spinal cord were examined in each case. When present, SchC remyelination was most commonly located adjacent to the venules and associated with a lower surrounding density of glial fibrillary acid protein(+) reactive astrocytes than areas of only oligodendroglial cell remyelination. The difference was significant only for spinal cord and brainstem lesions but not for lesions located in the brain. In conclusion, we demonstrated SchC remyelination in the cerebrum, brainstem, and spinal cord of 6 autopsied MS cases. To our knowledge, this is the first report of supratentorial SchC remyelination in MS.
 Multiple sclerosis (MS) is an autoimmune disease that develops when dysfunctional autoreactive lymphocytes attack the myelin sheath in the central nervous system. There are no cures for MS, and existing treatments are associated with unwanted side effects. One approach for treating MS is presenting distinct immune signals (i.e., self-antigen and immunomodulatory cues) to innate and adaptive immune cells to engage multiple signaling pathways involved in MS. We previously developed immune polyelectrolyte multilayer (iPEM) complexes built through layer-by-layer deposition of self-antigen - myelin oligodendrocyte glycoprotein (MOG) - and toll-like receptor antagonist, GpG to treat MS. Here, glutaraldehyde-mediated stable cross-links were integrated into iPEMs to load multiple classes of therapeutics. These cross-linked iPEMs maintain their immunological features, including the ability of GpG to blunt toll-like-receptor 9 signaling and MOG to expand T cells expressing myelin-specific T cell receptors. Lastly, we show that these functional assemblies can be loaded with a critical class of drug - mTOR inhibitors - associated with inducing regulatory T cells. These studies demonstrate the ability to incorporate small molecule drugs in reinforced self-assembled immune signals juxtaposed at high densities. This precision technology contributes new technologies that could drive antigen-specific immune response by simultaneously modulating innate and adaptive immunity.
 Multiple sclerosis (MS) is an inflammatory disease of the central nervous system, for which and Epstein-Barr virus (EBV) infection is a likely prerequisite. Due to the homology between Epstein-Barr nuclear antigen 1 (EBNA1) and alpha-crystallin B (CRYAB), we examined antibody reactivity to EBNA1 and CRYAB peptide libraries in 713 persons with MS (pwMS) and 722 matched controls (Con). Antibody response to CRYAB amino acids 7 to 16 was associated with MS (OR = 2.0), and combination of high EBNA1 responses with CRYAB positivity markedly increased disease risk (OR = 9.0). Blocking experiments revealed antibody cross-reactivity between the homologous EBNA1 and CRYAB epitopes. Evidence for T cell cross-reactivity was obtained in mice between EBNA1 and CRYAB, and increased CRYAB and EBNA1 CD4(+) T cell responses were detected in natalizumab-treated pwMS. This study provides evidence for antibody cross-reactivity between EBNA1 and CRYAB and points to a similar cross-reactivity in T cells, further demonstrating the role of EBV adaptive immune responses in MS development.
 Recent evidence suggests that the glucagon-like peptide-1 receptor (GLP-1R) agonists have neuroprotective activities in the CNS in animal models of Parkinson's disease, Alzheimer's disease, and multiple sclerosis (MS). This study aimed to investigate whether a novel long-acting GLP-1R agonist, NLY01, could limit demyelination or improve remyelination as occurs in MS using the cuprizone (CPZ) mouse model. Herein, we assessed the expression of GLP-1R on oligodendrocytes in vitro and found that mature oligodendrocytes (Olig2(+)PDGFRa(-)) express GLP-1R. We further confirmed this observation in the brain by immunohistochemistry and found that Olig2(+)CC1(+) cells express GLP-1R. We next administered NLY01 twice per week to C57B6 mice while on CPZ chow diet and found that NLY01 significantly reduced demyelination with greater weight loss than vehicle-treated controls. Because GLP-1R agonists are known to have anorexigenic effect, we then administered CPZ by oral gavage and treated the mice with NLY01 or vehicle to ensure the dose consistency of CPZ ingestion among mice. Using this modified approach, NLY01 was no longer effective in reducing demyelination of the corpus callosum (CC). We next sought to examine the effects of NLY01 treatment on remyelination after CPZ intoxication and during the recovery period using an adoptive transfer-CPZ (AT-CPZ) model. We found no significant differences between the NLY01 and vehicle groups in the amount of myelin or the number of mature oligodendrocytes in the CC. In summary, despite the promising anti-inflammatory and neuroprotective effects of GLP-1R agonists that have been previously described, our experiments provided no evidence to support a beneficial effect of NLY01 on limiting demyelination or enhancing remyelination. This information may be useful in selecting proper outcome measures in clinical trials of this promising class of drugs in MS.
 Multiple sclerosis (MS) is an autoimmune demyelinating disease that leads to axon degeneration as the major cause of everlasting neurological disability. The cis-phosphorylated tau (cis-p-tau) is an isoform of tau phosphorylated on threonine 231 and causes tau fails to bind micro-tubules and promotes assembly. It gains toxic function and forms tangles in the cell which finally leads to cell death. An antibody raised against cis- p-tau (cis mAb) detects this isoform and induces its clearance. Here, we investigated the formation of cis-p-tau in a lysophosphatidylcholine (LPC)-induced prolonged demyelination model as well as the beneficial effects of its clearance using cis mAb. Cis -p-tau was increased in the lesion site, especially in axons and microglia. Behavioral and functional studies were performed using visual cliff test, visual placing test, and visual evoked potential recording. Cis-p-tau clearance resulted in decreased gliosis, protected myelin and reduced axon degeneration. Analysis of behavioral and electrophysiological data showed that clearance of cis-p-tau by cis mAb treatment improved the visual acuity along with the integrity of the optic pathway. Our results highlight the opportunity of using cis mAb as a new therapy for protecting myelin and axons in patients suffering from MS.
 Clostridium perfringens epsilon toxin (ETX) is the third most lethal bacterial toxin and has been suggested to be an environmental trigger of multiple sclerosis, an immune-mediated disease of the human central nervous system. However, ETX cytotoxicity on primary human cells has not been investigated. In this article, we demonstrate that ETX preferentially binds to and kills human lymphocytes expressing increased levels of the myelin and lymphocyte protein MAL. Using flow cytometry, ETX binding was determined to be time and dose dependent and was highest for CD4+ cells, followed by CD8+ and then CD19+ cells. Similar results were seen with ETX-induced cytotoxicity. To determine if ETX preference for CD4+ cells was related to MAL expression, MAL gene expression was determined by RT-qPCR. CD4+ cells had the highest amount of Mal gene expression followed by CD8+ and CD19+ cells. These data indicate that primary human cells are susceptible to ETX and support the hypothesis that MAL is a main receptor for ETX. Interestingly, ETX bindings to human lymphocytes suggest that ETX may influence immune response in multiple sclerosis.
 OBJECTIVES: Previous studies suggested a higher rate of COVID-19 infection in patients with multiple sclerosis than in the general population, and limited studies addressed the impact of COVID-19 and its vaccination in patients with multiple sclerosis in Iran. We decided to investigate the factors associated with COVID-19 infection, the effects and side effects of the COVID-19 vaccination in patients with multiple sclerosis (MS). METHODS: We used the data of the patients with multiple sclerosis registered in a referral clinic in Kerman, one of the large cities in Iran (a population of 537,000 inhabitants), to explore the association between demographic variables, the history of COVID-19 vaccination, and the clinical outcomes. RESULTS: Of the 367 participants in this study, 88.3% received the COVID-19 vaccine, 35.4% were confirmed COVID-19 cases, and the incidence of COVID-19 was much higher before vaccination (24.5% before vaccination versus 10.1% after vaccination). The multivariable logistic regression model showed that male gender (OR = 2.64, 95% confidence interval: 1.21, 5.74) and current employment (OR = 3.04, 95% confidence interval: 1.59, 5.80) were associated with an increased risk of COVID-19. The only factor associated with the adverse effects of COVID-19 vaccination was the type of vaccine (AstraZeneca). CONCLUSION: Our findings showed that the vaccination protected MS cases considerably against COVID-19. In addition, the side effects of the vaccines were not noticeably high in these cases as well. Among all COVID-19 vaccines, AstraZeneca had the most common side effects, so people must be aware of them before vaccination. The male gender and employment were the most important variables in the prevalence of COVID-19 in patients with multiple sclerosis in our study.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a progressive demyelinating disease of the central nervous system that has overlapping symptoms with multiple sclerosis (MS) but differs from it in a variety of ways. Previous studies have reported conflicting results trying to estimate the number of individuals affected by them which is why we designed this systematic review and meta-analysis to estimate the worldwide prevalence and incidence of NMOSD/NMO based on current evidence. METHODS: We searched PubMed, Scopus, EMBASE, Web of Science, and gray literature including references from the identified studies, review studies, and conference abstracts which were published up to February 1, 2022. We used all MeSH terms pertaining to "NMOSD," "NMO," and all the terms on "prevalence," "incidence," and "epidemiology" to identify the search components. Pooled effect sizes were measured using random-effect model by DerSimonian-Laird. RESULTS: The prevalence and incidence rates of NMOSD/NMO ranged from 0.07 to 10 and 0.029 to 0.880 per 100,000 population, respectively. The overall pooled prevalence of NMO per 100,000 population was 1.54 (I(2): 98.4%, 95% CI: 1.13-1.96, P< 0.001) based on the 2006 criteria, 1.51 (I(2): 99.4%, 95% CI: 1.21-1.81, P < 0.001) based on the 2015 criteria and 2.16 (I(2): 89.4%, 95% CI: 1.46-2.86, P < 0.001) based on the 2006/2015 criteria. The overall annual incidence of NMO per 100,000 population was 0.155 (I(2): 95%, 95% CI: 0.115-0.195, P < 0.001) based on the 2006 criteria and 0.278 (I(2): 100%, 95% CI: 0.135-0.420, P < 0.001) based on the 2015 criteria. The prevalence rates were highest in French West Indies and South Korea, and lowest in Cuba and Australia, based on the 2006 and 2015 criteria, respectively. Also, the highest annual incidence rates were obtained for Sweden and Slovak republic and the lowest for Cuba and Australia based on the 2006 and 2015 criteria, respectively. All estimated rates were higher among females compared to males. CONCLUSION: Although rare, NMOSD/NMO impact affected individuals in devastating ways. Several large-scale prospective studies are required to reach a comprehension of the epidemiological aspects of these notorious demyelinating conditions.
 BACKGROUND: Cognitive dysfunction is one of the most common consequences of multiple sclerosis (MS). Recent studies have noted a high incidence of vascular comorbidity that might be associated with cognitive decline among persons with MS. However, there is a lack of evidence on vascular biomarkers (e.g., arterial stiffness indices) that are associated with cognition in MS. The current study characterized differences in vascular function between persons with MS and healthy controls, and examined the association between vascular and cognitive function in persons with MS compared with healthy controls. RESULTS: The MS group had significantly worse cognitive performance and higher cfPWV than healthy controls. There were significant bivariate correlations between the Symbol Digit Modalities Test (SDMT) score with AIx75 (r(s) = -0.45) and cfPWV (r(s) = 0.30) in the MS sample, but not in healthy controls. Regression analyses further indicated a nonlinear association between cfPWV and the SDMT in the MS sample (p-values for β coefficients < 0.05; adjusted R(2) = 0.10). No significant associations were observed among other cognitive and vascular outcomes. CONCLUSION: Our findings suggest significant associations between arterial stiffness and cognitive processing speed in MS. This preliminary examination provides initial, cross-sectional support for future population-based research on cognitive and vascular function in persons with MS. Such results may be clinically important for developing interventions that focus on regulating vascular dysfunction as an early treatment for preventing cognitive impairment in the MS population.
 AIMS AND OBJECTIVES: We aimed to identify correlates of cannabinoid-based products (CBP) use in patients with multiple sclerosis (MS) in France and Spain. BACKGROUND: MS is responsible for a wide range of symptoms, including pain. Access to CBP differs according to local legislation. The French context is more restrictive than the Spanish one, and no data regarding cannabis use among MS patients has yet been published. Characterizing MS patients who use CBP constitutes a first step toward identifying persons most likely to benefit from them. DESIGN: An online cross-sectional survey was submitted to MS patients who were members of a social network for people living with chronic diseases and were living in France or Spain. METHODS: Two study outcomes measured therapeutic CBP use and daily therapeutic CBP use. Seemingly unrelated bivariate probit regression models were used to test for associations between the outcomes and patients' characteristics while accounting for country-related differences. STROBE guidelines were followed in reporting this study. RESULTS: Among 641 study participants (70% from France), the prevalence of CBP use was similar in both countries (23.3% in France vs. 20.1% in Spain). MS-related disability was associated with both outcomes, with a gradient observed between different degrees of disability. MS-related pain level was associated with CBP use only. CONCLUSIONS: CBP use is common in MS patients from both countries. The more severe the MS, the more participants turned to CBP to alleviate their symptoms. Easier access to CBP should be ensured for MS patients in need of relief, especially from pain. RELEVANCE TO CLINICAL PRACTICE: This study highlights the characteristics of MS patients using CBP. Such practices should be discussed by healthcare professional with MS patients.
 Multiple sclerosis is an autoimmune disease that affects the central nervous system. Because of its complexity and the difficulty to treat, searching for immunoregulatory responses that reduce the clinical signs of disease by non-aggressive mechanisms and without adverse effects is a scientific challenge. Herein we propose a protocol of oral tolerance induction that prevented and controlled MOG-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. The genetically modified strain HSP65-producing Lactococcus lactis was orally administered for 5 consecutive days either before or during disease development in mice. Both protocols of feeding HSP65 resulted in significant reduction in the clinical score of EAE. Frequencies of LAP+CD4+Foxp3- regulatory T cells were higher in spleens and inguinal lymph nodes of fed mice. In addition, intravital microscopy showed that adherence of leukocytes to venules in the spinal cord was reduced in orally treated mice. Oral treatment with HSP65-producing L.lactis prevented leukocytes to leave the secondary lymphoid organs, therefore they could not reach the central nervous system. Despite the inhibition of pathological immune response that drive EAE development, activated T cells were at normal frequencies suggesting that oral tolerance did not induce general immunosuppression, but it led to specific control of pathogenic T cells. Our results indicate a novel therapeutic strategy to prevent and control autoimmune diseases such as multiple sclerosis.
 Multiple sclerosis (MS) is the most common demyelinating autoimmune disease of the central nervous system (CNS). Immune-mediated myelin and axonal damage that is accompanied by chronic axonal loss causing destruction of the myelin sheaths are hallmarks of MS. While great strides have been made in understanding the molecular underpinnings of re-/myelination, currently no remyelination therapy is available for MS. As myelination is a complex process that is not fully understood, we sought to develop a systematic, reliable, automated and quantitative higher throughput screening method. We aimed to quantitate myelin sheaths in vitro with high sensitivity at the single cell level suitable for testing small compound libraries. To this end, we miniaturised in vitro retinal ganglion cell-oligodendrocyte precursor cell (RGC-OPC) co-cultures into a multi-well plate format. This allowed us to maintain the reciprocal interaction of live axons and oligodendrocytes (OLs) to ensure compact myelin formation. To quantify our co-cultures, we developed a novel computer vision algorithm to precisely measure myelination. We demonstrated efficacy of our system with known pro-differentiating compounds BQ3020 and XAV939 which exhibited robust, efficient, and dose dependent effects on myelination. Through this combination of experimental and technical advances, we have developed a method allowing systematic and reliable testing of remyelinating compound efficacy.
 In the absence of head-to-head comparison trials, we aimed to compare the effectiveness of two largely prescribed oral platform disease-modifying treatments for relapsing-remitting multiple sclerosis, namely, dimethyl fumarate (DMF) and teriflunomide (TRF). We searched scientific databases to identify real-world studies reporting a direct comparison of DMF versus TRF. We fitted inverse-variance weighted meta-analyses with random effects models to estimate the risk ratio (RR) of relapse, confirmed disability worsening (CDW), and treatment discontinuation. Quantitative synthesis was accomplished on 14 articles yielding 11,889 and 8133 patients treated with DMF and TRF, respectively, with a follow-up ranging from 1 to 2.8 years. DMF was slightly more effective than TRF in reducing the short-term relapse risk (RR = 0.92, p = 0.01). Meta-regression analyses showed that such between-arm difference tends to fade in studies including younger patients and a higher proportion of treatment-naïve subjects. There was no difference between DMF and TRF on the short-term risk of CDW (RR = 0.99, p = 0.69). The risk of treatment discontinuation was similar across the two oral drugs (RR = 1.02, p = 0.63), but it became slightly higher with DMF than with TRF (RR = 1.07, p = 0.007) after removing one study with a potential publication bias that altered the final pooled result, as also confirmed by a leave-one-out sensitivity analysis. Discontinuation due to side effects and adverse events was reported more frequently with DMF than with TRF. Our findings suggest that DMF is associated with a lower risk of relapses than TRF, with more nuanced differences in younger naïve patients. On the other hand, TRF is associated with a lower risk of treatment discontinuation for side effects and adverse events.
 In multiple sclerosis (MS), glial cells astrocytes interact with the autoreactive immune cells that attack the central nervous system (CNS), which causes and sustains neuroinflammation. However, little is known about the direct interaction between these cells when they are in close proximity in the inflamed CNS. By using an experimental autoimmune encephalomyelitis (EAE) model of MS, we previously found that in the proximity of autoreactive CNS-infiltrated immune cells (CNS-IICs), astrocytes respond with a rapid calcium increase that is mediated by the autocrine P2X7 receptor (P2X7R) activation. We now reveal that the mechanisms regulating this direct interaction of astrocytes and CNS-IICs involve the coupling between P2X7R, connexin-43, and β(3)-integrin. We found that P2X7R and astroglial connexin-43 interact and concentrate in the immediate proximity of the CNS-IICs in EAE. P2X7R also interacts with β(3)-integrin, and the block of astroglial α(v)β(3)-integrin reduces the P2X7R-dependent calcium response of astrocytes upon encountering CNS-IICs. This interaction was dependent on astroglial mitochondrial activity, which regulated the ATP-driven P2X7R activation and facilitated the termination of the astrocytic calcium response evoked by CNS-IICs. By further defining the interactions between the CNS and the immune system, our findings provide a novel perspective toward expanding integrin-targeting therapeutic approaches for MS treatment by controlling the cell-cell interactions between astrocytes and CNS-IICs.
 Background: CD4(+) T cells play an important role in body development and homeostasis. Quantitative and functional changes in CD4(+) T cells result in abnormal immune responses, which lead to inflammation, cancer, or autoimmune diseases, such as multiple sclerosis (MS). Ubiquitination plays an essential role in the differentiation and functioning of CD4(+) T cells. However, the function of several E3 ubiquitin ligases in CD4(+) T cell differentiation and T cell-mediated pathological diseases remains unclear. Methods: RNA sequencing data were analyzed to identify the E3 ubiquitin ligases that participate in the pathogenesis of MS. Furthermore, conditional knockout mice were generated. Specifically, flow cytometry, qPCR, western blot, CO-IP and cell transfer adoptive experiments were performed. Results: In this study, we identified The RING finger 157 (RNF157) as a vital regulator of CD4(+) T cell differentiation; it promoted Th1 differentiation but attenuated Th17 differentiation and CCR4 and CXCR3 expressions in CD4(+) T cells, thereby limiting experimental autoimmune encephalomyelitis development. Mechanistically, RNF157 in CD4(+) T cells targeted HDAC1 for K48-linked ubiquitination and degradation. Notably, RNF157 expression was significantly decreased and showed a significant negative correlation with RORγt expression in patients with MS. Conclusions: Our study highlights the critical role of RNF157 in regulating CD4(+) T cell functions in autoimmune diseases and suggests RNF157 as a potential target in adaptive immune responses against MS and other autoimmune disorders.
 BACKGROUND: Numerous studies addressed the prevalence of multiple sclerosis, but prevalence studies of NMOSD and, particularly, MOGAD are scarce. We aimed to estimate the prevalence of NMOSD and MOGAD in the city of São Paulo, based on the known prevalence of MS. METHODS: In this observational study, we determined the total number of patients with central nervous system demyelinating disease on regular follow-up in a university referral center in São Paulo, from May 2019 to May 2021 according to the diagnosis of multiple sclerosis (MS), NMOSD and MOGAD using the current diagnostic criteria for these diseases. We used the MS: NMOSD and MS: MOGAD ratios to estimate the ratio of these diseases in São Paulo, Brazil. RESULTS: We identified 968 patients with MS, 133 patients with AQP4 positive NMOSD, and 28 patients with MOGAD. We found the MS: NMOSD ratio of 7,28 and the MS: MOGAD ratio of 34,57. We estimated a prevalence of 2,1 per 100,000 inhabitants for NMOSD and of 0,4 per 100,000 inhabitants for MOGAD. CONCLUSION: The prevalence of NMOSD is high in São Paulo, but the prevalence of MOGAD is low when compared with the prevalence found in most of the studies reported to date.
 INTRODUCTION: The Andalusian Registry of Pregnancies in patients with multiple sclerosis is the largest Spanish registry on multiple sclerosis (MS) and family planning. For the first time, it includes information on the fertility of men with MS. The influence of the use of a disease-modifying treatment (DMT) on the health of the foetus/newborn and the impact of breastfeeding on MS are also analysed. SUBJECTS AND METHODS: This is a multicentre, prospective and observational study. Recruitment of patients took place between December 2018 and December 2020. Women were followed up for one year after delivery. Altogether 100 women and 16 men were included, with a total of 103 newborn infants. RESULTS: The annualised relapse rate of the women with MS decreased significantly during pregnancy (from 0.23 to 0.065). A total of 11.2% of patients resorted to assisted reproductive techniques in order to conceive a child. No association was found between the use of a DMT at conception and/or pregnancy and the risk of miscarriage, prematurity or low birth weight. Over half the women with MS (54.2%) chose to breastfeed (26.7% of them while on a DMT). CONCLUSIONS: MS does not affect the fertility of men. Neither does the use of a DMT at the time of conception affect their fertility or their children's health. Assisted reproductive techniques did not have a negative impact on the course of MS. Breastfeeding is a common practice among women with MS and there is no evidence of positive or negative effects on disease progression.
 BACKGROUND: Currently, 19 disease-modifying therapies (DMTs) have been approved for the treatment of patients with relapsing forms of multiple sclerosis (RMS). OBJECTIVE: The objective of this study was to conduct a systematic review and network meta-analysis to evaluate the efficacy and safety of DMTs in adults with RMS. METHODS: We searched PubMed, Embase, the Cochrane Central Register of Controlled Trials, ClinicalTrials.gov, the Food and Drug Administration, and European Medicines Agency websites for randomized controlled trials (RCTs) (from inception to July 2021). Eligible RCTs evaluated approved treatments for RMS as monotherapy and reported at least one of the primary outcome measures of interest. The primary outcome was efficacy (annualized relapse rate and 12-week confirmed disability progression) and safety (serious adverse events [AEs] and discontinuation due to AEs). We assessed the risk of bias (RoB) of included studies using the Cochrane RoB tool version 2.0 (https://www.bmj.com/content/343/bmj.d5928) for RCTs. Surface under the cumulative ranking (SUCRA) was used to rank therapies and to assess quality of general evidence, respectively. The Grading of Recommendations Assessment, Development and Evaluation framework was used to rank therapies and to assess quality of general evidence. RESULTS: A total of 43 records represent 45 RCTs selected for network meta-analysis. In total, 30,720 participants (median of 732; interquartile range: 248-931) were included, of which 67% were female. By SUCRA analysis, alemtuzumab (94.3%) presented the highest probability of being the best alternative for annualized relapse rate, whereas ofatumumab (93.5%) presented the highest probability of being the best alternative for 12-week confirmed disability progression. Interferon beta-1b subcutaneous (87.0%) presented the highest probability of the best safety among all DMTs for serious AEs, whereas alemtuzumab (92.4%) presented the highest probability of the best safety among all DMTs for discontinuation due to AEs. CONCLUSION: Network meta-analysis shows that alemtuzumab and ofatumumab present the highest efficacy among DMTs. Because there is little difference between these probabilities for many treatments, health professionals should use clinical shared decision making when formulating treatment plans with patients.
 The appearance of new foci on MRI, the increase in neurological deficits, including the appearance of cognitive disorders and disturbances in the level of consciousness in patients with multiple sclerosis during the «washing period» when transferring from natalizumab (NZ) to another drug, may be due to both progressive multifocal leukoencephalopathy (PML) and exacerbation of the disease in the absence of therapy. Discontinuation of NS is fraught not only with a resumption, but with an increase in disease activity, the development of an immune reconstitution inflammatory syndrome (IRIS) due to the opening of the blood-brain barrier. Often, the processes of differential diagnosis of IRIS and natalizumab-associated PML are complex and require the use of additional methods of examination and monitoring of the dynamics of the patient's condition. However, the severity of the condition and the severity of the consequences caused by incorrect therapeutic tactics significantly reduce the time for diagnosis and require an immediate decision. The difficulties of differential diagnosis of IRIS and PML are reflected in the clinical case.
 BACKGROUND: Most current disease-modifying therapies approved for multiple sclerosis (MS) are immunomodulatory drugs that counteract the aberrant activity of the immune system. Hence, new pharmacological interventions that drive anti-inflammatory activity and neuroprotection would represent interesting alternative therapeutic approaches or complementary strategies to treat progressive forms of MS. There is evidence of reduced noradrenaline levels and alterations to locus coeruleus (LC) noradrenergic neurons in MS patients, as well as in animal models of this disease, potentially factors contributing to the pathophysiology. Drugs that enhance noradrenaline appear to have some beneficial effects in MS, suggesting their potential to dampen the underlying pathology and disease progression. METHODS: Therefore, we explored the consequences of chronic LC noradrenergic neurons activation by chemogenetics in experimental autoimmune encephalomyelitis (EAE) mice, the most widely used experimental model of MS. LC activation from the onset or the peak of motor symptoms was explored as two different therapeutic approaches, assessing the motor and non-motor behavioral changes as EAE progresses, and studying demyelination, inflammation and glial activation in the spinal cord and cerebral cortex during the chronic phase of EAE. RESULTS: LC activation from the onset of motor symptoms markedly alleviated the motor deficits in EAE mice, as well as their anxiety-like behavior and sickness, in conjunction with reduced demyelination and perivascular infiltration in the spinal cord and glial activation in the spinal cord and prefrontal cortex (PFC). When animals exhibited severe paralysis, LC activation produced a modest alleviation of EAE motor symptoms and it enhanced animal well-being, in association with an improvement of the EAE pathology at the spinal cord and PFC level. Interestingly, the reduced dopamine beta-hydroxylase expression associated with EAE in the spinal cord and PFC was reversed through chemogenetic LC activation. CONCLUSION: Therefore, clear anti-inflammatory and neuroprotective effects were produced by the selective activation of LC noradrenergic neurons in EAE mice, having greater benefits when LC activation commenced earlier. Overall, these data suggest noradrenergic LC neurons may be targets to potentially alleviate some of the motor and non-motor symptoms in MS.
 Serum neurofilament light chain (sNfL) is an intensely investigated biomarker in multiple sclerosis (MS). The aim of this study was to explore the impact of cladribine (CLAD) on sNfL and the potential of sNfL as a predictor of long-term treatment response. Data were gathered from a prospective, real-world CLAD cohort. We measured sNfL at baseline (BL-sNfL) and 12 months (12Mo-sNfL) after CLAD start by SIMOA. Clinical and radiological assessments determined fulfilment of "no evidence of disease activity" (NEDA-3). We evaluated BL-sNfL, 12M-sNfL and BL/12M sNfL ratio (sNfL-ratio) as predictors for treatment response. We followed 14 patients for a median of 41.5 months (range 24.0-50.0). NEDA-3 was fulfilled by 71%, 57% and 36% for a period of 12, 24 and 36 months, respectively. We observed clinical relapses in four (29%), MRI activity in six (43%) and EDSS progression in five (36%) patients. CLAD significantly reduced sNfL (BL-sNfL: mean 24.7 pg/mL (SD ± 23.8); 12Mo-sNfL: mean 8.8 pg/mL (SD ± 6.2); p = 0.0008). We found no correlation between BL-sNfL, 12Mo-sNfL and ratio-sNfL and the time until loss of NEDA-3, the occurrence of relapses, MRI activity, EDSS progression, treatment switch or sustained NEDA-3. We corroborate that CLAD decreases neuroaxonal damage in MS patients as determined by sNfL. However, sNfL at baseline and at 12 months failed to predict clinical and radiological treatment response in our real-world cohort. Long-term sNfL assessments in larger studies are essential to explore the predictive utility of sNfL in patients treated with immune reconstitution therapies.
 BACKGROUND: Data on corpus callosum involvement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are limited. OBJECTIVE: The objective of the study was to compare callosal lesions in MOGAD, multiple sclerosis (MS), and aquaporin-4-IgG positive neuromyelitis optica spectrum disorder (AQP4+NMOSD). RESULTS: Callosal lesion frequency was similar in MOGAD (38/171 (22%)), MS (24/72 (33%)), and AQP4+NMOSD (18/63 (29%)). Clinical phenotypes included encephalopathy (47%) and focal supratentorial (21%) or infratentorial (45%) deficits. None had callosal-disconnection syndromes. Maximal callosal-T2-lesion diameter (median (range)) in millimeter was similar in MOGAD (21 (4-77)) and AQP4+NMOSD (22 (5-49); p = 0.93) but greater than in MS (10.5 (2-64)). Extracallosal extension (21/38 (55%)) and T2-lesion resolution (19/34 (56%)) favored MOGAD. CONCLUSIONS: Despite similar frequency and imaging overlap, larger lesions, sagittal midline involvement, and lesion resolution favored MOGAD.
 BACKGROUND AND PURPOSE: Valid measurements of cardiorespiratory fitness in persons with multiple sclerosis (pwMS) are essential during inpatient rehabilitation for a precise evaluation of the current health status, for defining appropriate exercise intensities, and for evaluation of exercise intervention studies. We aim (i) to examine the proportion of pwMS who attain the American College of Sports Medicine (ACSM) criteria for maximal effort during graded cardiopulmonary exercise testing (CPET) and (ii) to provide insight into participant characteristics that limit maximal exercise performance. METHODS: This cross-sectional study comprises a retrospective examination of ACSM criteria for maximal effort during graded CPET of n = 380 inpatient pwMS (mean age = 48 ± 11 years, 66% female). Chi-squared or Fisher's exact tests were conducted to compare differences in the distribution of criteria achieved. Participants' characteristics were examined as potential predictors using binary logistic regression. RESULTS: Only 60% of the overall sample attained a respiratory exchange ratio ≥ 1.10. With regard to the definition applied, only 24% or 40% of the participants achieved an oxygen consumption plateau, and 17% or 50% attained the heart rate criterion. Forty-six percent met at least two of three criteria. Disability status, gender, disease course, and body mass index were associated with the attainment of maximal effort. CONCLUSIONS: Our findings suggest that a relevant proportion of inpatient pwMS do not attain common criteria utilized to verify maximal oxygen consumption. Identified predictors for criteria attainment can be used to create models to predict cardiorespiratory fitness and to optimize CPET protocols in restrictive groups of pwMS.
 Multiple Sclerosis (MS) is a chronic inflammatory disease that affects the brain and spinal cord. Inflammation, demyelination, synaptic alteration, and neuronal loss are hallmarks detectable in MS. Experimental autoimmune encephalomyelitis (EAE) is an animal model widely used to study pathogenic aspects of MS. Autophagy is a process that maintains cell homeostasis by removing abnormal organelles and damaged proteins and is involved both in protective and detrimental effects that have been seen in a variety of human diseases, such as cancer, neurodegenerative diseases, inflammation, and metabolic disorders. This study is aimed at investigating the autophagy signaling pathway through the analysis of the main autophagic proteins including Beclin-1, microtubule-associated protein light chain (LC3, autophagosome marker), and p62 also called sequestosome1 (SQSTM1, substrate of autophagy-mediated degradation) in the hippocampus of EAE-affected mice. The expression levels of Beclin-1, LC3, and p62 and the Akt/mTOR pathway were examined by Western blot experiments. In EAE mice, compared to control animals, significant reductions of expression levels were detectable for Beclin-1 and LC3 II (indicating the reduction of autophagosomes), and p62 (suggesting that autophagic flux increased). In parallel, molecular analysis detected the deregulation of the Akt/mTOR signaling. Immunofluorescence double-labeling images showed co-localization of NeuN (neuronal nuclear marker) and Beclin-1, LC3, and p62 throughout the CA1 and CA3 hippocampal subfields. Taken together, these data demonstrate that activation of autophagy occurs in the neurons of the hippocampus in this experimental model.
 BACKGROUND: Core stability exercise programs have become popular in recent years for preserving balance and functional independence in people with multiple sclerosis (PwMS); however, their real impact is not well-known as the main intervention target (i.e., core stability) theoretically responsible for balance or functional improvements is not measured. The objective of this study was to test the reliability of accelerometers integrated into smartphones for quantifying core stability and developing exercise progressions in PwMS. METHODS: Twenty participants with MS [age: 47.5±8.0 years; height: 1.62±0.07 m; mass: 63.4±10.9 kg; EDSS: 3.0 (1.5-6)] participated voluntarily in this study. CS was assessed in different variations of the front, side, and back bridges and bird-dog exercises by measuring the mean lumbopelvic acceleration in two testing sessions, separated by one week. Relative and absolute reliability of lumbopelvic acceleration of those exercise variations performed by more than 60% of the participants was analyzed by the intraclass correlation coefficient (ICC(3,1)), and the standard error of measurement (SEM) and the minimal detectable change (MDC), respectively. Repeated measures ANOVAs were performed to detect a potential learning effect between test-retest assessments. Statistical significance was set at p < 0.05. RESULTS: Reliability analyses revealed that good to excellent relative and absolute scores (0.85<ICC<0.96; 7.8%≤SEM≤19.2%; 21.6%≤MDC≤53.2%) for the mean lumbopelvic acceleration obtained during 10 of the 12 CS exercise variations performed by more than 60% of the participants. A non-significant between-session learning effect was detected in all the variables considered (all p values >0.05). CONCLUSION: Smartphone accelerometry seems a low cost, portable and easy-to-use tool to objectively and reliably track core stability changes in PwMS through. However, in spite of the popularity of bridging and bird-dog exercises, only the short and long bridges and the three-point bird-dog positions proved feasible for most participants. Overall, this study provides useful information to evaluate and guide the prescription of core stability exercise programs in PwMS with mild-to-moderate impairment.
 BACKGROUND: The kappa free light chains index (κ-index) is increasing in importance as a fast, easy, cost-effective, and quantitative biomarker in multiple sclerosis (MS), which can replace cerebrospinal fluid (CSF)-restricted oligoclonal bands (OCB) detection. In previous studies, controls often included mixed patients with several inflammatory central nervous system disorders. The aim of the present study was to assess the κ-index in patients with serum aquaporin-4 (AQP4)-IgG or myelin-oligodendrocyte-glycoprotein (MOG)-IgG. METHODS: We analyzed CSF/serum samples of patients with AQP4-IgG or MOG-Ig and evaluated distinct κ-index cut-offs. We described clinical and magnetic resonance imaging (MRI) features of patients with the highest κ-index values. RESULTS: In 11 patients with AQP4-IgG, median κ-index was 16.8 (range 0.2; 63) and 6/11 (54.5%) had κ-index >12. Among 42 patients with MOG-IgG, 2 had low positive MOG-IgG titers, were ultimately diagnosed with MS, and had a markedly increased κ-index (54.1 and 102.5 respectively). For the remaining 40 MOG-IgG-positive patients the median κ-index was 0.3 (range 0.1; 15.5). Some 6/40 (15%) and 1/40 (2.5%) patients had a κ-index >6 and >12, respectively. None fulfilled MRI dissemination in space and dissemination in time (DIS/DIT) criteria and the final diagnosis was MOG-IgG-associated disease (MOGAD) for these 40 patients. Four of the 40 (10%) MOG-IgG-positive patients had OCB. CONCLUSION: While a marked increase in κ-index could discriminate MS from MOGAD, a low κ-index threshold could lead to confusion between MS and MOGAD or AQP4 antibody-positive neuromyelitis optica spectrum disorder.
 IMPORTANCE: Currently, disease-modifying therapies for multiple sclerosis (MS) use 4 mechanisms of action: immune modulation, suppressing immune cell proliferation, inhibiting immune cell migration, or cellular depletion. Over the last decades, the repertoire substantially increased because of the conceptual progress that not only T cells but also B cells play an important pathogenic role in MS, fostered by the empirical success of B cell-depleting antibodies against the surface molecule CD20. Notwithstanding this advance, a continuous absence of B cells may harbor safety risks, such as a decline in the endogenous production of immunoglobulins. Accordingly, novel B cell-directed MS therapies are in development, such as inhibitors targeting Bruton tyrosine kinase (BTK). OBSERVATIONS: BTK is centrally involved in the B cell receptor-mediated activation of B cells, one key requirement in the development of autoreactive B cells, but also in the activation of myeloid cells, such as macrophages and microglia. Various compounds in development differ in their binding mode, selectivity and specificity, relative inhibitory concentration, and potential to enter the central nervous system. The latter may be important in assessing whether BTK inhibition is a promising strategy to control inflammatory circuits within the brain, the key process that is assumed to drive MS progression. Accordingly, clinical trials using BTK inhibitors are currently conducted in patients with relapsing-remitting MS as well as progressive MS, so far generating encouraging data regarding efficacy and safety. CONCLUSIONS AND RELEVANCE: While the novel approach of targeting BTK is highly promising, several questions remain unanswered, such as the long-term effects of using BTK inhibitors in the treatment of inflammatory CNS disease. Potential changes in circulating antibody levels should be evaluated and compared with B cell depletion. Also important is the potential of BTK inhibitors to enter the CNS, which depends on the given compound. Remaining questions involve where BTK inhibitors fit in the landscape of MS therapeutics. A comparative analysis of their distinct properties is necessary to identify which inhibitors may be used in relapsing vs progressive forms of MS as well as to clarify which agent may be most suitable for sequential use after anti-CD20 treatment.
 Genes associated with increased susceptibility to multiple sclerosis (MS) have been identified, but their functions are incompletely understood. One of these genes codes for the RNA helicase DExD/H-Box Polypeptide 39B (DDX39B), which shows genetic and functional epistasis with interleukin-7 receptor-α gene (IL7R) in MS-risk. Based on evolutionary and functional arguments, we postulated that DDX39B enhances immune tolerance thereby decreasing MS risk. Consistent with such a role we show that DDX39B controls the expression of many MS susceptibility genes and important immune-related genes. Among these we identified Forkhead Box P3 (FOXP3), which codes for the master transcriptional factor in CD4(+)/CD25(+) T regulatory cells. DDX39B knockdown led to loss of immune-regulatory and gain of immune-effector expression signatures. Splicing of FOXP3 introns, which belong to a previously unrecognized type of introns with C-rich polypyrimidine tracts, was exquisitely sensitive to DDX39B levels. Given the importance of FOXP3 in autoimmunity, this work cements DDX39B as an important guardian of immune tolerance.
 PURPOSE: Persons with Multiple Sclerosis (PwMS) are physically inactive and spend more time in sedentary behaviours than healthy persons, which increases the risk of developing cardiometabolic diseases. In this randomised crossover study, the cardiometabolic health effects of replacing sitting with light-intensity physical activity (LIPA) and exercise (EX) were investigated. MATERIALS AND METHODS: Twenty-eight mildly disabled PwMS performed four 4-day activity regimens in free-living conditions; CONTROL (habitual activity), SIT, LIPA, and EX. Plasma glucose and insulin (oral glucose tolerance test), plasma lipids, inflammation, resting heart rate, blood pressure, body weight, and perceived exertion were measured (clinical-trials.gov: NCT03919058). RESULTS: CONTROL: 9.7 h sitting/day, SIT: 13.3 h sitting/day, LIPA: 8.3 h sitting, 4.7 h standing, and 2.7 h light-intensity walking/day, and EX: 11.6 h sitting/day with 1.3 h vigorous-intensity cycling. Compared to SIT, improvements (p < 0.001) after LIPA and EX were found for insulin total area under the curve (-17 019 ± 5708 and -23 303 ± 7953 pmol/L*min), insulin sensitivity (Matsuda index +1.8 ± 0.3 and +1.9 ± 0.4) and blood lipids (triglycerides: -0.4 ± 0.1 and -0.5 ± 0.1 mmol/L; non-high-density lipoprotein cholesterol: -0.3 ± 0.1 and -0.5 ± 0.1 mmol/L), with no difference between LIPA and EX. Perceived exertion was higher after EX compared to LIPA (Borg score [6-20]: +2.6 ± 3.3, p = 0.002). CONCLUSION: Replacing sitting with LIPA throughout the day exerts similar cardiometabolic health effects as a vigorous-intensity exercise in PwMS.IMPLICATIONS FOR REHABILITATIONIncreasing light-intensity physical activity (LIPA) throughout the day improves cardiometabolic health to the same extent as one vigorous-intensity exercise sessionIncreasing LIPA induces less exertion than performing a vigorous-intensity exercise.
 BACKGROUND: Genome-wide association studies (GWAS) have highlighted over 200 autosomal variants associated with multiple sclerosis (MS). However, variants in non-coding regions such as those encoding microRNAs have not been explored thoroughly, despite strong evidence of microRNA dysregulation in MS patients and model organisms. This study explores the effect of microRNA-associated variants in MS, through the largest publicly available GWAS, which involved 47,429 MS cases and 68,374 controls. METHODS: We identified SNPs within the coordinates of microRNAs, ± 5-kb microRNA flanking regions and predicted 3'UTR target-binding sites using miRBase v22, TargetScan 7.0 RNA22 v2.0 and dbSNP v151. We established the subset of microRNA-associated SNPs which were tested in the summary statistics of the largest MS GWAS by intersecting these datasets. Next, we prioritised those microRNA-associated SNPs which are among known MS susceptibility SNPs, are in strong linkage disequilibrium with the former or meet a microRNA-specific Bonferroni-corrected threshold. Finally, we predicted the effects of those prioritised SNPs on their microRNAs and 3'UTR target-binding sites using TargetScan v7.0, miRVaS and ADmiRE. RESULTS: We have identified 30 candidate microRNA-associated variants which meet at least one of our prioritisation criteria. Among these, we highlighted one microRNA variant rs1414273 (MIR548AC) and four 3'UTR microRNA-binding site variants within SLC2A4RG (rs6742), CD27 (rs1059501), MMEL1 (rs881640) and BCL2L13 (rs2587100). We determined changes to the predicted microRNA stability and binding site recognition of these microRNA and target sites. CONCLUSIONS: We have systematically examined the functional, structural and regulatory effects of candidate MS variants among microRNAs and 3'UTR targets. This analysis allowed us to identify candidate microRNA-associated MS SNPs and highlights the value of prioritising non-coding RNA variation in GWAS. These candidate SNPs could influence microRNA regulation in MS patients. Our study is the first thorough investigation of both microRNA and 3'UTR target-binding site variation in multiple sclerosis using GWAS summary statistics.
 The XCL1-XCR1 axis has a potential role in the recruitment of immune cells to the site of inflammation. The present study aimed to examine the relation of XCL1 serum levels with Multiple sclerosis (MS) and HTLV-1-associated myelopathy (HAM), as chronic inflammatory diseases of the central nervous system (CNS). DNA was extracted to evaluate HTLV-1 proviral load (PVL) using real-time PCR. Serum levels of XCL1 was determined by using an ELISA assay. The serum level of XCL1 was significantly higher in patients with HAM than that of asymptomatic carriers (ACs) and healthy controls (HCs) (p < 0.001 and p < 0.0001, respectively) and was also higher in MS patients compared to HCs (p < 0.0001). Moreover, the concentration of XCL1 serum level was significantly different between the ACs and HCs group (p < 0.0001). In conclusion, increased expression of XCL1 might contribute to the migration of autoreactive T cells to the central nervous system and play a critical role in the development and pathogenesis of inflammatory neurological diseases including HAM and MS.
 INTRODUCTION: Using tele-rehabilitation methods to deliver exercise, physical activity (PA) and behaviour change interventions for people with multiple sclerosis (pwMS) has increased in recent years, especially since the SARS-CoV-2 pandemic. This scoping review aims to provide an overview of the literature regarding adherence to therapeutic exercise and PA delivered via tele-rehabilitation for pwMS. METHODS AND ANALYSIS: Frameworks described by Arksey and O'Malley and Levac et al underpin the methods. The following databases will be searched from 1998 to the present: Medline (Ovid), Embase (Ovid), CINAHL (EBSCOhost), Health Management Information Consortium Database, ProQuest Dissertations and Theses Global, Pedro, Cochrane Central Register of Controlled Trials, US National Library of Medicine Registry of Clinical Trials, WHO International Clinical Trials Registry Platform portal and The Cochrane Database of Systematic Reviews. To identify papers not included in databases, relevant websites will be searched. Searches are planned for 2023. With the exception of study protocols, papers on any study design will be included. Papers reporting information regarding adherence in the context of prescribed therapeutic exercise and PA delivered via tele-rehabilitation for pwMS will be included. Information relating to adherence may comprise; methods of reporting adherence, adherence levels (eg, exercise diaries, pedometers), investigation of pwMS' and therapists' experiences of adherence or a discussion of adherence. Eligibility criteria and a custom data extraction form will be piloted on a sample of papers. Quality assessment of included studies will use Critical Appraisal Skills Programme checklists. Data analysis will involve categorisation, enabling findings relating to study characteristics and research questions to be presented in narrative and tabular format. ETHICS AND DISSEMINATION: Ethical approval was not required for this protocol. Findings will be submitted to a peer-reviewed journal and presented at conferences. Consultation with pwMS and clinicians will help to identify other dissemination methods.
 PURPOSE: This cross-sectional observational pilot study investigated egocentric social networks for 10 paired sex- and age-matched adults with and without multiple sclerosis (MS). This study also investigated the relationship between social network measures and various disease factors associated with MS. The relationship between social network measures and communication participation restrictions was also examined. METHOD: Participants completed a seven-item social network survey. Social network structure and composition were quantified. The network organization measures (structure analysis) included the total number of members (network size) and extent to which members are connected (network density). The measured characteristics of people around a participant (composition analysis) included the amount of kin relative to network size (proportion of kin), gender variation (gender diversity index), and age variation (standard deviation of age). Standard clinical neuropsychological, psychosocial, and speech metrics quantified processing speed, memory, depression, fatigue, and sentence intelligibility. Measures of communication participation and MS severity were also obtained. RESULTS: Matched-pairs tests indicated that the proportion of kin significantly differed between paired participants, whereas all other social network measures were similar. For participants with MS, correlation analyses indicated weak associations between proportion of kin and cognitive, psychosocial, and speech measures. However, strong correlations were found between social network size and processing speed, memory, fatigue, MS severity, and communication participation. Gender diversity index also strongly correlated with depression. CONCLUSIONS: Results from this pilot study highlight the importance of evaluating egocentric networks in the clinical management of MS, as maintaining nonkin friendships may be difficult for adults with MS making them vulnerable to social isolation. Furthermore, those with small and less diverse networks may experience more severe cognitive and psychosocial problems and limited communication participation.
 OBJECTIVE: This study examined individual and co-occurring behavioral risk factors (diet, exercise, and stress) in wheelchair users with multiple sclerosis (MS) and potential association with MS symptoms (ie, fatigue, depression, anxiety, pain, sleep, and health-related quality of life [HRQOL]). DESIGN: Survey. SETTING: General Community. PARTICIPANTS: One hundred twenty-three wheelchair users with MS completed this study (N=123). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Participants were mailed instructions for accessing online questionnaires (demographic and clinical characteristics, Godin Leisure-Time Exercise Questionnaire, Perceived Stress Scale, Automated Self-Administered 24-Hour Dietary Assessment Tool, and MS symptoms). RESULTS: Standard cut-points were used to categorize behavioral risk factors and then identify the extent and distribution of these behaviors both individually and co-occurring. We then analyzed the associations between behavioral risk factors and MS symptoms using bivariate correlation analyses and Mann-Whitney U tests. The mean age of participants was 60.6±10.0 years, 76% identified as women, 82% had a progressive disease course, and the mean MS duration was 23.0±9.7 years. Seven participants were classified as having 0 negative health behaviors, 41 participants had 1 negative health behavior, 49 participants had 2 negative health behaviors, and 26 participants had 3 negative health behaviors. The number of negative health behaviors was significantly correlated with HRQOL (physical, r=.30; psychological, r=.47), sleep (r=.25), depressive symptoms (r=.36), and anxiety (r=.43). Mann-Whitney U tests indicated greater fatigue, depression, and anxiety as well as lower sleep quality and HRQOL among participants who reported 2 or 3 behavioral risk factors compared with 0 or 1 behavioral risk factor. CONCLUSIONS: Future research should examine the design and implementation of multiple health behavior change interventions targeting co-occurring behavioral risk factors among wheelchair users with MS.
 There is emerging evidence that microbiota and its metabolites play an important role in helath and diseases. In this regard, gut microbiota has been found as a crucial component that influences immune responses as well as immune-related disorders such as autoimmune diseases. Gut bacterial dysbiosis has been shown to cause disease and altered microbiota metabolite synthesis, leading to immunological and metabolic dysregulation. Of note, microbiota in the gut produce short-chain fatty acids (SCFAs) such as acetate, butyrate, and propionate, and remodeling in these microbiota metabolites has been linked to the pathophysiology of a number of autoimmune disorders such as type 1 diabetes, multiple sclerosis, inflammatory bowel disease, rheumatoid arthritis, celiac disease, and systemic lupus erythematosus. In this review, we will address the most recent findings from the most noteworthy studies investigating the impact of microbiota SCFAs on various autoimmune diseases.
 AIM: To describe burden, and to explore cross-country inequalities across sociodemographic development levels for four autoimmune diseases (ADs) including rheumatoid arthritis (RA), inflammatory bowel disease (IBD), multiple sclerosis (MS) and psoriasis (PS). METHODS: The estimates and their 95% uncertainty interval (UI) for disability-adjusted life-years (DALYs) of RA, IBD, MS and PS were extracted from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. Age-standardized DALYs rate (ASDR) across 204 countries, as well as age and sex distribution of global DALYs rate of these four ADs were illustrated. Slope index of inequality and concentration index, which are two standard metrics of absolute and relative gradient inequality recommended by World Health Organization (WHO), were utilized to quantify the distributive inequalities in the burden of ADs. RESULTS: In 2019, the ASDR of RA, IBD, MS and PS varied remarkably across 204 countries, with different age and sex distribution of global DALYs rate. The slope index of inequality changed from 26.7 (95% CI: 20.7 to 32.8) in 1990 to 40.3 (95% CI: 31.9 to 48.7) in 2019 for RA, from 17.1 (95% CI: 12.4 to 21.7) in 1990 to 25.2 (95% CI: 20.1 to 30.2) in 2019 for IBD, from 19.3 (95% CI: 15.2 to 23.4) in 1990 to 28.9 (95% CI: 24.2 to 33.5) in 2019 for MS, from 42.3 (95% CI: 33.1 to 51.6) in 1990 to 40.2 (95% CI: 32.5 to 48.0) in 2019 for PS. Moreover, the concentration index showed 20.4 (95% CI: 18.9 to 22.0) in 1990 and 18.2 (95% CI: 16.7 to 19.6) in 2019 for RA, 25.0 (95% CI: 23.0 to 27.1) in 1990 and 33.5 (95% CI: 31.6 to 35.5) in 2019 for IBD, 46.7 (95% CI: 44.0 to 49.3) in 1990 and 41.8 (95% CI: 39.6 to 44.1) in 2019 for MS, 31.7 (95% CI: 29.0 to 34.4) in 1990 and 32.6 (95% CI: 29.9 to 35.2) in 2019 for PS. CONCLUSIONS: There is a strong heterogeneity in ASDR across all countries, as well as in age and sex distribution of global DALYs rate for four ADs including RA, IBD, MS and PS. Countries with higher sociodemographic development levels shouldered disproportionately higher burden of ADs, and the magnitude of this sociodemographic development level-related inequalities exacerbated over time.

 IL-17 is one of the major proinflammatory cytokine implicated in the pathophysiology of various chronic inflammatory diseases. However, a clear association between the levels of IL-17 and various neurodegenerative diseases is inconclusive due to lack of consistent results reported in several studies. Therefore, we designed and performed a meta-analysis study to assess the levels of IL-17 cytokine in various neurodegenerative diseases. The aim of this meta-analysis study was to assess the level of IL-17 in cerebrospinal fluid/serum of the patients with neurodegenerative diseases such as Alzheimer's disease, Parkinson disease, multiple sclerosis, and amyotrophic lateral sclerosis. An extensive search was performed on electronic databases including PubMed, Cochrane, and Google Scholar to find out the relevant studies for analysis. The quality of selected studies was assessed by Newcastle-Ottawa scale for cohort and case control studies. The standardized mean difference of level of IL-17 in patients with neurodegenerative diseases and control was calculated using RevMan 5 software. A significant increase in the level of serum IL-17 was found to in the patients with neurodegenerative diseases like Alzheimer's disease (p = 0.001) and amyotrophic lateral sclerosis (p = 0.009), whereas IL-17 level in serum of Parkinson's disease (p = 0.22), multiple sclerosis (p = 0.09), and in peripheral blood mononuclear cells of MS patients (p = 0.34) was not found to be significant. IL-17 may be involved in regulation of neuronal inflammation during the pathogenesis of these neurodegenerative disease, and its specific inhibition could be a potential therapeutic target.
 PURPOSE/AIM: Although Five Times-Sit-To-Stand test (FTSST) performance is known to be a valid and reliable method in people with chronic stroke, Parkinson's disease, and balance disorder, it has not been widely studied in patients with Multiple sclerosis (MS). The main aim of this study was to evaluate validity and reliability of the FTSST in patients with MS. METHODS: The first outcome measure of the study was the FTSST, which was conducted by two different researchers. Secondary outcome measures were Biodex Stability System (BSS), 10-meter walk test, time up go test (TUG), EDSS scoring, Fatigue Severity Scale (FSS), Barthel Index, Quadriceps Muscle strength test, Functional Reach test. Intraclass correlation coefficient (ICC) was used for the validity and reliability of the FTSST, which was made by two different researchers, and Pearson Correlation Analysis was used to determine its relationship with other measurements. RESULTS: Interrater and test-retest reliability for the FTSST were excellent (Intraclass correlation coefficients of 0.98 and 0.99, respectively). A statistically significant correlation was found between all secondary outcome measures and FTSST (p < 0.05). CONCLUSION: FTSST is considered to be a valid, reliable, easy, and rapid method for evaluating lower extremity muscle strength and balance in patients with MS.
 Multiple sclerosis (MS) has been considered as a T cell-mediated autoimmune disease. However, the signaling pathways regulating effector T cells in MS have yet to be elucidated. Janus kinase 2 (JAK2) plays a crucial role in hematopoietic/immune cytokine receptor signal transduction. Here, we tested the mechanistic regulation of JAK2 and the therapeutic potential of pharmacological JAK2 inhibition in MS. Both inducible whole-body JAK2 knockout and T cell-specific JAK2 knockout completely prevented the onset of experimental autoimmune encephalomyelitis (EAE), a widely used MS animal model. Mice with JAK2 deficiency in T cells exhibited minimal demyelination and minimal CD45(+) leukocyte infiltration in the spinal cord, accompanied by a remarkable reduction of T helper cell type 1 (T(H)1) and type 17 (T(H)17) in the draining lymph nodes and spinal cord. In vitro experiments showed that disruption of JAK2 markedly suppressed T(H)1 differentiation and IFNγ production. The phosphorylation of signal transducer and activator of transcription 5 (STAT5) was reduced in JAK2 deficient T cells, while STAT5 overexpression significantly increased T(H)1 and IFNγ production in STAT5 transgenic mice. Consistent with these results, JAK1/2 inhibitor baricitinib or selective JAK2 inhibitor fedratinib attenuated the frequencies of T(H)1 as well as T(H)17 in the draining lymph nodes and alleviated the EAE disease activity in mice. Our findings suggest that overactive JAK2 signaling in T lymphocytes is the culprit in EAE, which may serve as a potent therapeutic target for autoimmune disease.
 This French National Diagnostic and Care Protocol (NDPC) includes both pediatric and adult patients with non-infectious chronic uveitis (NICU) or non-infectious recurrent uveitis (NIRU). NICU is defined as uveitis that persists for at least 3 months or with frequent relapses occurring less than 3 months after cessation of treatment. NIRU is repeated episodes of uveitis separated by periods of inactivity of at least 3 months in the absence of treatment. Some of these NICU and NIRU are isolated. Others are associated with diseases that may affect various organs, such as uveitis associated with certain types of juvenile idiopathic arthritis, adult spondyloarthropathies or systemic diseases in children and adults such as Behçet's disease, granulomatoses or multiple sclerosis. The differential diagnoses of pseudo-uveitis, sometimes related to neoplasia, and uveitis of infectious origin are discussed, as well as the different forms of uveitis according to their main anatomical location (anterior, intermediate, posterior or panuveitis). We also describe the symptoms, known physiopathological mechanisms, useful complementary ophthalmological and extra-ophthalmological examinations, therapeutic management, monitoring and useful information on the risks associated with the disease or treatment. Finally, this protocol presents more general information on the care pathway, the professionals involved, patient associations, adaptations in the school or professional environment and other measures that may be implemented to manage the repercussions of these chronic diseases. Because local or systemic corticosteroids are usually necessary, these treatments and the risks associated with their prolonged use are the subject of particular attention and specific recommendations. The same information is provided for systemic immunomodulatory treatments, immunosuppressive drugs, sometimes including anti-TNFα antibodies or other biotherapies. Certain particularly important recommendations for patient management are highlighted in summary tables.
 Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS) that causes substantial morbidity and diminished quality of life. Evidence highlights the central role of myeloid lineage cells in the initiation and progression of MS. However, existing imaging strategies for detecting myeloid cells in the CNS cannot distinguish between beneficial and harmful immune responses. Thus, imaging strategies that specifically identify myeloid cells and their activation states are critical for MS disease staging and monitoring of therapeutic responses. We hypothesized that positron emission tomography (PET) imaging of triggering receptor expressed on myeloid cells 1 (TREM1) could be used to monitor deleterious innate immune responses and disease progression in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. We first validated TREM1 as a specific marker of proinflammatory, CNS-infiltrating, peripheral myeloid cells in mice with EAE. We show that the (64)Cu-radiolabeled TREM1 antibody-based PET tracer monitored active disease with 14- to 17-fold higher sensitivity than translocator protein 18 kDa (TSPO)-PET imaging, the established approach for detecting neuroinflammation in vivo. We illustrate the therapeutic potential of attenuating TREM1 signaling both genetically and pharmacologically in the EAE mice and show that TREM1-PET imaging detected responses to an FDA-approved MS therapy with siponimod (BAF312) in these animals. Last, we observed TREM1(+) cells in clinical brain biopsy samples from two treatment-naïve patients with MS but not in healthy control brain tissue. Thus, TREM1-PET imaging has potential for aiding in the diagnosis of MS and monitoring of therapeutic responses to drug treatment.
 BACKGROUND: Peripapillary hyperreflective ovoid mass-like structures (PHOMS) have recently been described as new optical coherence tomography (OCT) marker. It is not yet clear whether the occurrence of PHOMS is disease-specific or disease-spanning. PHOMS have been described in 16-18% of patients with multiple sclerosis (MS). Currently, no data on the prevalence of PHOMS in other demyelinating diseases including aquaporine-4-IgG-positive neuromyelitis optica spectrum disease (AQP4 + NMOSD) or myelin oligodendrocyte glycoprotein-IgG-associated disease (MOGAD) are reported. METHODS: We performed a cross-sectional, retrospective spectral domain OCT study evaluating the frequency of PHOMS in AQP4 + NMOSD (n = 47) and MOGAD (n = 44) patients. To test the association with retinal neuroaxonal damage, we compared demographic and clinical data as well as retinal layer thicknesses between eyes with vs. eyes without PHOMS. RESULTS: PHOMS were detected in 17% of AQP4 + NMOSD and 14% of MOGAD patients. Intra-cohort analysis revealed that AQP4 + NMOSD patients with PHOMS were significantly older [mean (years): 57.5 vs. 50.0; p value = 0.04]. We found no association of PHOMS with retinal neuroaxonal degeneration. In addition, in subjects with only one eye affected by PHOMS compared with the unaffected fellow eye, no differences in retinal parameters were observed (n = 4). CONCLUSIONS: In summary, we found PHOMS in 17% of AQP4 + NMOSD and 14% of MOGAD patients. This is comparable to the prevalence of published MS PHOMS data. Therefore, a disease-specific occurrence of PHOMS is unlikely. Interestingly, PHOMS do not seem to depend on retinal neuroaxonal degeneration.
 We describe the case of a 24-year-old male patient with multiple sclerosis (MS) who was treated with Teriflunomide for eight months. However, due to MS progression, treatment was switched to Ocrelizumab. After 15 months of therapy with Ocrelizumab the patient developed edema and nephrotic-range albuminuria. Kidney biopsy showed focal segmental glomerulosclerosis (FSGS) and Ocrelizumab treatment was stopped. Teriflunomide is less likely to have caused FSGS due to a three week wash-out period and a timespan of 15 months between the last Teriflunomide dose and development of albuminuria. Treatment with Ocrelizumab has been associated with organ-specific inflammation in MS-patients, thus an association between the development of FSGS and Ocrelizumab therapy is possible, and this case suggests considering this potential association.
 BACKGROUND AND OBJECTIVES: Antitumor necrosis factor α (TNFα) agents are a class of biologic drugs used for the treatment of several immune-mediated conditions. An increased risk of multiple sclerosis (MS) with their use has been suggested, but studies have been limited. Relevant population-based epidemiologic data linking anti-TNFα to MS are scarce. The objective was to compare the risk of MS in anti-TNFα users with nonusers among patients with rheumatic disease (RD) or inflammatory bowel disease (IBD). METHODS: A nested case-control study was conducted. Population-based health care-linked databases from 4 Canadian provinces were used. All patients with RD or IBD residing within a participating province between January 2000 and March 2018 were identified by validated case definitions. Any anti-TNFα dispensation in the 2 years before the index date (MS onset) was identified. Incident onset MS cases were ascertained using a validated algorithm. Up to 5 controls were matched to each MS case based on birth year ±3 years, disease duration, and health authority (based on region of residence). Conditional logistic regressions were used to calculate the incidence rate ratio (IRR) after adjusting for potential confounders. A meta-analysis was conducted to provide pooled estimates across provinces using random-effects models. RESULTS: Among 296,918 patients with RD patients, 462 MS cases (80.1% female, mean [SD] age, 47.4 [14.6] years) were matched with 2,296 controls (59.5% female, mean [SD] age, 47.4 [14.5] years). Exposure to anti-TNFα occurred in 18 MS cases and 42 controls. After adjusting for matching variables, sex, and the Charlson Comorbidity Index, the pooled IRR was 2.05 (95% CI, 1.13-3.72). Among 84,458 patients with IBD, 190 MS cases (69.5% female, mean [SD] age, 44.3 [12.3] years) were matched with 943 controls (54.1% female, mean [SD] age, 44.2 [12.2] years). Exposure to anti-TNFα occurred in 23 MS cases and 98 controls. The pooled adjusted IRR was 1.35 (95% CI, 0.70-2.59). DISCUSSION: The use of anti-TNFα was associated with an increased risk of MS compared with nonusers, especially among patients with RD. These findings could help clinicians and patients with RD to make more informed treatment decisions. Further studies are needed to validate these results for patients with IBD.
 Neurodegenerative disorders are typically characterized by late onset progressive damage to specific (sub)populations of cells of the nervous system that are essential for mobility, coordination, strength, sensation, and cognition. Addressing this selective cellular vulnerability has become feasible with the emergence of single-cell-omics technologies, which now represent the state-of-the-art approach to profile heterogeneity of complex tissues including human post-mortem brain at unprecedented resolution. In this review, we briefly recapitulate the experimental workflow of single-cell RNA sequencing and summarize the recent knowledge acquired with it in the most common neurodegenerative diseases: Parkinson's, Alzheimer's, Huntington's disease, and multiple sclerosis. We also discuss the possibility of applying single-cell approaches in the diagnostics and therapy of neurodegenerative disorders, as well as the limitations. While we are currently at the point of deeply exploring the transcriptomic changes in the affected cells, further technological developments hold a promise of manipulating the affected pathways once we understand them better.
 BACKGROUND AND PURPOSE: Oxidative stress biomarkers are increased in multiple sclerosis (MS) lesions. Antioxidant defense enzymes regulate reactive oxygen species that can cause tissue injury in MS. METHODS: The study of 91 subjects included 64 relapsing-remitting MS (RR-MS; 72% female, baseline age ± SD = 44.6 ± 11 years, disease duration = 13.3 ± 8.8 years, median Expanded Disability Status Scale [EDSS] = 2.0, interquartile range = 1.8) and 27 healthy controls (HC) at baseline and 5-year follow-up (5YFU). Serum glutathione peroxidase (GPX), glutathione-S-transferase (GST), glutathione reductase (GSHR), superoxide dismutase, and paraoxonase-1 (PON1) arylesterase and paraoxonase activities were measured using kinetic enzyme assays. Total cholesterol (TC), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDL-C), and an apolipoprotein (Apo) panel with ApoA-I, ApoA-II, ApoB, ApoC-II, and ApoE were obtained. Serum neurofilament (sNfL) was used to assess axonal injury. Disability was measured on the EDSS. RESULTS: GSHR activity was lower in HC compared to RR-MS at baseline and 5YFU. GPX (p = 0.008) and PON1 arylesterase and paraoxonase activities (both p = 0.05) increased between baseline and 5YFU in HC but did not increase in RR-MS. At baseline and 5YFU, GPX and GST were associated with TC, LDL-C, and ApoA-II; GSHR was associated with ApoA-II and ApoC-II. Antioxidant enzymes were not associated with sNfL or EDSS in RR-MS. CONCLUSIONS: RR-MS patients did not exhibit the changes in antioxidant enzyme activities over 5YFU found in HC; however, the differences were modest. Antioxidant enzyme activities are not associated with disability.
 People with multiple sclerosis (pwMS) frequently present with deficits in binaural processing used for sound localization. This study examined spatial release from speech-on-speech masking in pwMS, which involves binaural processing and additional higher level mechanisms underlying streaming, such as spatial attention. 26 pwMS with mild severity (Expanded Disability Status Scale score <3) and 20 age-matched controls listened via headphones to pre-recorded sentences from a standard list presented simultaneously with eight-talker babble. Virtual acoustic techniques were used to simulate sentences originating from 0°, 20°, or 50° on the interaural horizontal plane around the listener whilst babble was presented continuously at 0° azimuth, and participants verbally repeated the target sentence. In a separate task, two simultaneous sentences both containing a colour and number were presented, and participants were required to report the target colour and number. Both competing sentences could originate from 0°, 20°, or 50° on the azimuthal plane. Participants also completed a series of neuropsychological assessments, an auditory questionnaire, and a three-alternative forced-choice task that involved the detection of interaural time differences (ITDs) in noise bursts. Spatial release from masking was observed in both pwMS and controls, as response accuracy in the two speech discrimination tasks improved in the spatially separated conditions (20° and 50°) compared with the co-localised condition. However, pwMS demonstrated significantly less spatial release (18%) than controls (28%) when discriminating colour/number coordinates. At 50° separation, pwMS discriminated significantly fewer coordinates (77%) than controls (89%). In contrast, pwMS had similar performances to controls when sentences were presented in babble, and for the basic ITD discrimination task. Significant correlations between speech discrimination performance and standardized neuropsychological scores were observed across all spatial conditions. Our findings suggest that spatial hearing is likely to be implicated in pwMS, thereby affecting the perception of competing speech originating from various locations.

 BACKGROUND: Multiple sclerosis (MS) is an autoimmune disease for which bone marrow mesenchymal stem cells (BM-MSCs) have become one of the most promising tools for treatment. Cuprizone(CPZ) induces demyelination in the central nervous system and its use has established a demyelination sheath animal model which is particularly suitable for studying the effects of BM-MSCs on the remyelination and mood improvement of a demyelinating model mice. METHODS: 70 C57BL/6 male mice were selected and divided into 4 groups: the normal control (n = 20), chronic demyelination (n = 20), myelin repair (n = 15) and cell-treated groups (n = 15). Mice in the normal control group were given a normal diet; the chronic demyelination group mice were given a 0.2% CPZ mixed diet for 14 weeks, mice in the myelin repair and cell-treated groups mice were given a 0.2% CPZ diet for 12 weeks and normal diet for 2 weeks, while the cell-treated group mice were injected with BM-MSCs from the 13th week. The cuprizone-induced demyelination model was successfully established and BM-MSCs extracted, behavioural changes of the mice were detected by open field test, elevated plus maze test and tail suspension test, demyelination and repair of the corpus callosum and astrocyte changes were observed by immunofluorescence and electron microscopy and the concentrations of monoamine neurotransmitters and their metabolites detected by enzyme-linked immunosorbent assay (ELISA) and high performance liquid chromatography-electrochemistry (HPLC-ECD). RESULTS: Results suggest BM-MSCs were successfully extracted and cultured, and migrated to the demyelinating area of brain tissue after cell transplantation. Compared with the normal control group, the mice in the chronic demyelination group showed obvious anxiety and depression behaviours (p < 0.05); compared with the chronic demyelination group, the anxiety and depression behaviours of the cell-treated group mice were improved (p < 0.05); compared with the normal control group, the demyelination of the corpus callosum region of the chronic demyelination group mice was significant (p < 0.01), while the myelin sheath of the cell-treated and myelin repair groups was repaired when compared with the chronic demyelination group (p < 0.05), and the cell-treated group had a more significant effect than the myelin repair group (p < 0.05). Compared with the normal control group, the number of astrocytes in the corpus callosum of the chronic demyelination group mice was significantly increased (p < 0.01), and the expression of glial fibrillary acidic protein (GFAP) in the cell-treated group was lower than that in the chronic demyelination and myelin repair groups (p < 0.05); the serum concentrations of norepinephrine (NE), 5-hydroxytryptamine (5-HT) and 5-Hydroxyindole-3-acetic acid (5-HIAA) between the normal control and the chronic demyelination groups were significantly different (p < 0.05). CONCLUSIONS: The CPZ-induced model can be used as an experimental carrier for MS combined with anxiety and depression, and BM-MSC transplantation promotes the repair of myelin sheath and the recovery of emotional disorders in the model.
 BACKGROUND: Experimental autoimmune encephalomyelitis (EAE), as an autoimmune disease in the central nervous system (CNS), is an animal model for multiple sclerosis (MS) mediated by T lymphocytes. OBJECTIVE: To investigate ginger extract's effect on reducing inflammation and improving the symptoms in the EAE model. METHODS: The EAE was induced by injecting MOG35-55 and pertussis toxin into eight-week-old female C57BL6 mice. The mice were treated with an intraperitoneal injection of 300 mg/kg/day of hydroalcoholic extract of ginger for 21 days. The disease severity and weight changes were measured daily. Then, the mice spleens were removed; the gene expressions of interleukin (IL)-17, transforming growth factor beta (TGF-β), interferon-γ (IFN-γ), and tumor necrosis factor α (TNF-α) were analyzed by Real-time PCR and the percentage of regulatory T lymphocytes (Treg cells) was determined by flow cytometry. Serum nitric oxide and antioxidant capacity were measured, and brain tissue sections were prepared to investigate the leukocyte infiltration and plaque formation. RESULTS: The severity of symptoms in the intervention group was lower than in the control. The gene expression levels of inflammatory cytokines, including IL-17 (P=0.04) and IFN-γ (P=0.01), were reduced. The Treg cells increased significantly, and the serum nitric oxide level was lower in the ginger-treated group. There was no significant difference in lymphocyte infiltration in the brain between the two groups. CONCLUSION: The present study indicated that ginger extract could effectively reduce inflammatory mediators and modulate immune responses in EAE.
 BACKGROUND: COVID-19 vaccines are recommended for people with multiple sclerosis (pwMS). Adequate humoral responses are obtained in pwMS receiving disease-modifying therapies (DMTs) after vaccination, with the exception of those receiving B-cell-depleting therapies and non-selective S1P modulators. However, most of the reported studies on the immunity of COVID-19 vaccinations have included mRNA vaccines, and information on inactivated virus vaccine responses, long-term protectivity, and comparative studies with mRNA vaccines are very limited. Here, we aimed to investigate the association between humoral vaccine responses and COVID-19 infection outcomes following mRNA and inactivated virus vaccines in a large national cohort of pwMS receiving DMTs. METHODS: This is a cross-sectional and prospective multicenter study on COVID-19-vaccinated pwMS. Blood samples of pwMS with or without DMTs and healthy controls were collected after two doses of inactivated virus (Sinovac) or mRNA (Pfizer-BioNTech) vaccines. PwMS were sub-grouped according to the mode of action of the DMTs that they were receiving. SARS-CoV-2 IgG titers were evaluated by chemiluminescent microparticle immunoassay. A representative sample of this study cohort was followed up for a year. COVID-19 infection status and clinical outcomes were compared between the mRNA and inactivated virus groups as well as among pwMS subgroups. RESULTS: A total of 1484 pwMS (1387 treated, 97 untreated) and 185 healthy controls were included in the analyses (male/female: 544/1125). Of those, 852 (51.05%) received BioNTech, and 817 (48.95%) received Sinovac. mRNA and inactivated virus vaccines result in similar seropositivity; however, the BioNTech vaccination group had significantly higher antibody titers (7.175±10.074) compared with the Sinovac vaccination group (823±1.774) (p<0.001). PwMS under ocrelizumab, fingolimod, and cladribine treatments had lower humoral responses compared with the healthy controls in both vaccine types. After a mean of 327±16 days, 246/704 (34.9%) of pwMS who were contacted had COVID-19 infection, among whom 83% had asymptomatic or mild disease. There was no significant difference in infection rates of COVID-19 between participants vaccinated with BioNTech or Sinovac vaccines. Furthermore, regression analyses show that no association was found regarding age, sex, Expanded Disability Status Scale score (EDSS), the number of vaccination, DMT type, or humoral antibody responses with COVID-19 infection rate and disease severity, except BMI Body mass index (BMI). CONCLUSION: mRNA and inactivated virus vaccines had similar seropositivity; however, mRNA vaccines appeared to be more effective in producing SARS-CoV-2 IgG antibodies. B-cell-depleting therapies fingolimod and cladribine were associated with attenuated antibody titer. mRNA and inactive virus vaccines had equal long-term protectivity against COVID-19 infection regardless of the antibody status.
 BACKGROUND: People with Multiple Sclerosis (PwMS) find it more difficult to engage in physical activity (PA) than healthy controls. Accelerometers can be used to measure sedentary time and free-living physical activity, understanding the differences between PwMS and controls can help inform changes such as interventions to promote a more active lifestyle. This in turn will help prevent secondary conditions and reduce symptom progression. OBJECTIVE: To conduct a systematic review and meta-analysis on accelerometer measured sedentary behavior and physical activity between PwMS and healthy controls. METHODS: A systematic search of five databases (PubMed, Web of Science, Ovid, Science Direct and CINAHIL) from inception until 22nd November 2019. Inclusion criteria was (1) included a group of participants with a definite diagnosis of multiple sclerosis of any type; (2) have 3 or more days of PA monitoring using accelerometers during free living conditions; (3) include age matched healthy controls; (4) assess adults over the age of 18; (5) reported data had to have been reported in a manner suitable for quantitative pooling including: percent of time spent sedentary, minutes per day of sedentary, light, moderate, vigorous activity (moderate and vigorous totaled together), steps per day or counts per day. RESULTS: Initial search produced 9021 papers, after applying inclusion criteria 21 eligible papers were included in the study. One paper was a longitudinal study from which only baseline data was included. One paper was a reliability and validity study, with data for PwMS versus controls in the validity section. All other papers are cross sectional, with one being a pilot study and another a random control study. One paper used two devices in unison, only one set of data is included in the statistics. Outcome data was available for 1098 participants, 579 PwMS and 519 healthy controls. Significant differences were seen in all categories tested: (1) sedentary time (min/day), standard mean difference -0.286, P = 0.044, n = 4 studies; (2) relative sedentary time (%/day), standard mean difference -0.646, P = 0.000, n = 5 studies; (3) LPA (min/day), standard mean difference 0.337, P = 0.039, n = 5 studies; (4) relative LPA (%/day), standard mean difference 0.211, P = 0.152, n = studies; (5) MVPA (min/day), standard mean difference 0.801, P = 0.000, n = 8 studies; (6) relative MVPA (%/day), mean difference 0.914, P = 0.000, n = 5 studies; (7) step count, standard mean difference 0.894, P = 0.000, n = 8 studies; (8) activity count, standard mean difference 0.693, P = 0.000, n = 13 studies. CONCLUSION: PwMS are more sedentary and engage in less LPA, MVPA, steps per day and accelerometer counts per day than healthy controls when measured using accelerometers during free-living conditions.
 BACKGROUND: Sleep disorders are common in people with multiple sclerosis (PwMS) and could contribute to cognitive dysfunction. However, effects of pathological sleep on cognitive domains are insufficiently characterized. OBJECTIVE: To evaluate associations between cognitive performance and polysomnographic (PSG)-based sleep disturbances in PwMS. METHODS: PwMS with known/suspected untreated obstructive sleep apnea (OSA, N = 131) underwent PSG and cognitive tests: Symbol Digit Modalities Test (SDMT), Paced Auditory Serial Addition Test (PASAT), California Verbal Learning Test-II (CVLT-II), Brief Visuospatial Memory Test-Revised (BVMT-R Total and Delayed), Judgment of Line Orientation (JLO), Controlled Oral Word Association Test (COWAT), Trail Making Test, Go/No-Go, and Nine-Hole Peg Test (NHPT). RESULTS: Apnea severity measures were associated with worse processing speed, attention, and working memory (SDMT); immediate and delayed visual memory (BVMT-R Total and Delayed); attention, psychomotor speed, and cognitive flexibility (Trails); and manual dexterity and visuomotor coordination (NHPT) (ps ⩽ 0.011). Sleep macrostructure measures showed stronger associations with verbal memory and response inhibition (CVLT-II Total Recognition Discriminability Index), and immediate visual memory (BVMT-R Total) (ps ⩽ 0.011). CONCLUSIONS: Pathological sleep, including hypoxia, sleep fragmentation, and disturbances in sleep/wake states, are differentially associated with worse cognitive performance in PwMS. These findings could inform future personalized approaches to cognitive impairment in PwMS with sleep disorders. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02544373 (https://clinicaltrials.gov/ct2/show/NCT02544373).
 Recent cross-sectional investigations suggest a relationship between frailty, as measured by Frailty Index (FI), and multiple sclerosis (MS). However, if and how frailty is associated with relapse activity in MS is still unknown. To explore this issue, a one-year follow-up study involving 471 patients was conducted. A univariate regression model showed an inverse association between baseline FI score and the presence of relapse, which was also confirmed in the multivariate model. These results suggest that frailty may reflect pathophysiological mechanisms involved in MS disease activity and that the FI may be used as an enrichment criterion in clinical trials.
 BACKGROUND: Functional exercise capacity evaluation is crucial to monitor treatment effects and disease progression in people with multiple sclerosis (pwMS). Compared to other tests, the incremental shuttle walking test (ISWT), which more accurately reflects cardiovascular responses, may be more useful for assessing exercise capacity. The aim of the study is to investigate the reliability and validity of the ISWT. METHODS: Thirty-six pwMS with an Expanded Disability Status Scale (EDSS) score<4.5 between the ages of 25 and 65 were included in the study. The subjects underwent practice (ISWT-p) before undergoing the test-retest protocol in order to rule out the ISWT learning effect (ISWT-1 - ISWT-2). ISWT-1 and ISWT-2 were administered with a 3-7 day interval for test-retest reliability. Six-minutes walking test (6MWT) were applied for concurrent validity. The EDSS, pulmonary function tests, Fatigue Impact Scale (FIS), respiratory muscle strength [maximum inspiratory and expiratory pressure (MIP-MEP)] measurements were made for convergent validity. RESULTS: ISWT was found to have excellent test-retest reliability with an ICC value of 0.97. The area under the curve value was 0.904 indicating that ISWT has a good performance for predicting disease severity. The moderate correlation between ISWT and 6MWT (rho: 0.68, p<0,001) proved concurrent validity. It was also moderately correlated with EDSS, MEP (rho: -0.58 and 0.47 respectively), weakly correlated with MIP and FIS (rho:0.37 and -0.36, respectively) while not correlated with pulmonary function tests. CONCLUSION: The ISWT had excellent test-retest reliability, acceptable criterion and construct validity in ambulatory MS patients.
 BACKGROUND: Within the past 10 years, immune mechanisms associated with acute ischemic stroke (AIS) have been brought into focus, but data on B cell activation and intrathecal Ig production is still scarce. In this study, we determined the prevalence of an elevated IgG index, positive oligoclonal bands (OCBs) and chemokine C-X-C motif ligand 13 (CXCL13) levels in the cerebrospinal fluid (CSF) as markers of intrathecal IgG synthesis and B cell activation in patients with AIS. METHODS: In a retrospective study we analyzed the cerebrospinal fluid (CSF) from 212 patients with AIS from December 2013 to May 2018 assessing intrathecal Ig synthesis, OCBs and CXCL13 concentrations. RESULTS: Overall, 5.7% (12/212) of AIS patients showed an intrathecal IgG synthesis, 0.5% (1/212) with isolated elevated IgG index, 5.2% (7/136) isolated positive OCBs and 2.9% (4/136) both elevated IgG index and positive OCBs. CXCL13 levels were elevated in 3.6% (3/83) of the patients. Approximately one third of these patients had simultaneously chronic inflammatory CNS disease (multiple sclerosis, neuromyelitis optica spectrum disorder, neurosarcoidosis). There was no significant association between CSF findings and stroke characteristics including vascular territory, localization, volume, etiology, acute treatment, or blood-brain barrier dysfunction. Intrathecal IgG synthesis was more common in patients with prior stroke. Longitudinal CSF analysis did not reveal any newly-occurring, but instead mostly persistent or even disappearing intrathecal IgG synthesis after AIS. CONCLUSIONS: We found no evidence of a relevant B cell recruitment and intrathecal IgG synthesis in patients with AIS. In fact, the occurrence of intrathecal IgG synthesis was associated with concurrent chronic inflammatory CNS disease or previous stroke. Consequently, in patients with first-ever AIS and intrathecal IgG synthesis, physicians should search for concomitant inflammatory CNS disease.
 INTRODUCTION: Robotic-assisted upper limb rehabilitation might improve upper limb recovery in people with multiple sclerosis (PwMS) with moderate-to-severe disability. In the few existing studies, the training effects have been related to the type of intervention, if intensive, repetitive, or task-oriented training might promote neuroplasticity and recovery. Notably, most of these devices operate within a serious game context providing different feedback. Since feedback is a key component of motor control and thus involved in motor and cognitive rehabilitation, clinicians cannot desist from considering the potential contribution of feedback in the upper limb robot-assisted rehabilitation effects. AREA COVERED: In this systematic review, we reported the rehabilitation protocols used in the robot-assisted upper limb training in PwMS to provide state-of-the-art on the role of feedback in robotic-assisted Upper Limb rehabilitation. PubMed, the Cochrane Library, and the Physiotherapy Evidence Database databases were systematically searched from inception to March 2022. After a literature search, the classification systems for feedback and the serious game were applied. EXPERT OPINION: There is a need for sharing standard definitions and components of feedback and serious game in technologically assisted upper limb rehabilitation. Indeed, improving these aspects might further improve the effectiveness of such training in the management of PwMS.
 INTRODUCTION: Vaccination against the coronavirus disease 2019 (COVID-19) is recommended for patients with multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). However, vaccine safety in these patients taking immunotherapeutic agents is unclear as they were not included in the vaccine trials. OBJECTIVES: To evaluate the safety of COVID-19 vaccines in patients with MS, NMOSD, and MOGAD. METHODS: We reviewed the medical records of MS, NMOSD, and MOGAD patients at the Keimyung University Dongsan Hospital. Information regarding vaccination schedules and adverse events was collected. RESULTS: A total of 56 patients (19, 22, and 15 patients with MS, NMOSD, and MOGAD, respectively) with a median age of 48.18 ± 15.72 years (range, 16-81 years) were included. Of them, 42 (75.0%) were female. In total, 76.8% (43/56) of all patients were vaccinated, and the vaccination rate was the highest for NMOSD patients (81.8%) and the lowest for MS patients (68.4%). All vaccinated patients were administered mRNA vaccines at least once in single or multiple vaccination doses. Only 3 of 43 (7.0%) vaccinated patients experienced clinical relapse following vaccination. Facial sensory changes with a brainstem lesion developed in an MS patient taking dimethyl fumarate, while myelitis occurred in a MOGAD patient receiving azathioprine maintenance therapy. The first episode of optic neuritis occurred in a patient who was later diagnosed with MOGAD. CONCLUSIONS: Our study demonstrated a favorable safety profile with no serious adverse events associated with COVID-19 vaccines in patients with MS, NMOSD, and MOGAD.
 Multiple sclerosis (MS) is a neurodegenerative disease characterized by degradation of the myelin sheath resulting in impaired neural communication throughout the body. As a result, most people with MS (PwMS) experience gait asymmetries between their legs leading to an increased risk of falls. Recent work indicates that split-belt treadmill adaptation, where the speed of each leg is controlled independently, can decrease gait asymmetries for other neurodegenerative impairments. The purpose of this study was to test the efficacy of split-belt treadmill training to improve gait symmetry in PwMS. In this study, 35 PwMS underwent a 10 min split-belt treadmill adaptation paradigm, with the faster paced belt moving under the more affected limb. Step length asymmetry (SLA) and phase coordination index (PCI) were the primary outcome measures used to assess spatial and temporal gait symmetries, respectively. It was predicted that participants with a worse baseline symmetry would have a greater response to split-belt treadmill adaptation. Following this adaptation paradigm, PwMS experienced aftereffects that improved gait symmetry, with a significant difference between predicted responders and nonresponders in both SLA and PCI change (p < 0.001). Additionally, there was no correlation between SLA and PCI change. These findings suggest that PwMS retain the ability for gait adaptation, with those most asymmetrical at baseline demonstrating the greatest improvement, and that there may be separate neural mechanisms for spatial and temporal locomotor adjustments.
 PURPOSE/OBJECTIVES: Care and case management (CCM) aims to provide optimal care for patients and their caregivers on an individual and superordinate level of health care providers and authorities. To facilitate a clear and systematic CCM process as part of a clinical study intervention, a semistructured manual is the prerequisite. PRIMARY PRACTICE SETTINGS: The ongoing COCOS-MS (Communication, Coordination and Security for People with Multiple Sclerosis) study is a randomized controlled Phase II clinical intervention study. The CCM manual is being tested on the intervention group consisting of severely affected individuals with multiple sclerosis (MS; Expanded Disability Status Scale [EDSS] >5) and their caregivers receiving CCM for 12 months in addition to standard care. The intervention comprises monthly personal visits and weekly telephone calls during which the CCM manual is applied. FINDINGS/CONCLUSIONS: The CCM manual has been developed on the basis of previous literature and well-established questionnaires following theoretical aspects and prior scientific work covering individual domains of life of people with MS. Within the COCOS-MS study, its feasibility is being tested meticulously. It allows for a standardized assessment while being tailored to the individual. At the end of the intervention period, it will be analyzed statistically and qualitatively. Consequently, conclusions can be drawn as to whether the CCM manual is feasible or has to be adapted for use in standard care after analyzation. IMPLICATIONS FOR CASE MANAGEMENT PRACTICE: The CCM manual serves as a tool for the continuous, long-term, cross-sectoral care for patients suffering from severe MS and their caregivers. The manual provides guidance in adequately addressing patients' complex symptoms, problems, and needs, as well as assessing existing resources both at the individual patient level and at a superordinate level.
 BACKGROUND: To have country-wide information about multidrug resistance (MDR) in isolates from community-acquired urinary tract infections (CAUTI) of Turkey, in terms of resistance rates and useful options. METHODS: We used a geocode standard, nomenclature of territorial units for statistics (NUTS), and a total of 1588 community-acquired isolates of 20 centres from 12 different NUTS regions between March 2019 and March 2020 were analysed. RESULTS: Of the 1588 culture growths, 1269 (79. 9%) were Escherichia coli and 152 (9.6%) were Klebsiella spp. Male sex, advancedage, and having two or more risk factors showed a statistically significant relation with MDR existence (p < 0.001, p: 0.014, p < 0.001, respectively) that increasing number of risk factors or degree of advancing in age directly affects the number of antibiotic groups detected to have resistance by pathogens. In total, MDR isolates corresponded to 36.1% of our CAUTI samples; MDR existence was 35.7% in E. coli isolates and 57.2% in Klebsiella spp. isolates. Our results did not show an association between resistance or MDR occurrence rates and NUTS regions. DISCUSSION: The necessity of urine culture in outpatient clinics should be taken into consideration, at least after evaluating risk factorsfor antibacterial resistance individually. Community-acquired UTIs should be followed up time- and region-dependently. Antibiotic stewardship programmes should be more widely and effectively administrated.
 The neuroinflammatory process characterizing multiple sclerosis (MS) is associated with changes in excitatory synaptic transmission and altered central concentrations of the primary excitatory amino acid, L-glutamate (L-Glu). Recent findings report that cerebrospinal fluid (CSF) levels of L-Glu positively correlate with pro-inflammatory cytokines in MS patients. However, to date, there is no evidence about the relationship between the other primary excitatory amino acid, L-aspartate (L-Asp), its derivative D-enantiomer, D-aspartate, and the levels of pro-inflammatory and anti-inflammatory cytokines in the CSF of MS. In the present study, we measured by HPLC the levels of these amino acids in the cortex, hippocampus, cerebellum, and spinal cord of mice affected by experimental autoimmune encephalomyelitis (EAE). Interestingly, in support of glutamatergic neurotransmission abnormalities in neuroinflammatory conditions, we showed reduced L-Asp levels in the cortex and spinal cord of EAE mice and increased D-aspartate/total aspartate ratio within the cerebellum and spinal cord of these animals. Additionally, we found significantly decreased CSF levels of L-Asp in both relapsing-remitting (n = 157) MS (RR-MS) and secondary progressive/primary progressive (n = 22) (SP/PP-MS) patients, compared to control subjects with other neurological diseases (n = 40). Importantly, in RR-MS patients, L-Asp levels were correlated with the CSF concentrations of the inflammatory biomarkers G-CSF, IL-1ra, MIP-1β, and Eotaxin, indicating that the central content of this excitatory amino acid, as previously reported for L-Glu, reflects a neuroinflammatory environment in MS. In keeping with this, we revealed that CSF L-Asp levels were positively correlated with those of L-Glu, highlighting the convergent variation of these two excitatory amino acids under inflammatory synaptopathy occurring in MS.
 BACKGROUND: Decision curve analysis can be used to determine whether a personalized model for treatment benefit would lead to better clinical decisions. Decision curve analysis methods have been described to estimate treatment benefit using data from a single randomized controlled trial. OBJECTIVES: Our main objective is to extend the decision curve analysis methodology to the scenario in which several treatment options exist and evidence about their effects comes from a set of trials, synthesized using network meta-analysis (NMA). METHODS: We describe the steps needed to estimate the net benefit of a prediction model using evidence from studies synthesized in an NMA. We show how to compare personalized versus one-size-fit-all treatment decision-making strategies, such as "treat none" or "treat all patients with a specific treatment" strategies. First, threshold values for each included treatment need to be defined (i.e., the minimum risk difference compared with control that renders a treatment worth taking). The net benefit per strategy can then be plotted for a plausible range of threshold values to reveal the most clinically useful strategy. We applied our methodology to an NMA prediction model for relapsing-remitting multiple sclerosis, which can be used to choose between natalizumab, dimethyl fumarate, glatiramer acetate, and placebo. RESULTS: We illustrated the extended decision curve analysis methodology using several threshold value combinations for each available treatment. For the examined threshold values, the "treat patients according to the prediction model" strategy performs either better than or close to the one-size-fit-all treatment strategies. However, even small differences may be important in clinical decision making. As the advantage of the personalized model was not consistent across all thresholds, improving the existing model (by including, for example, predictors that will increase discrimination) is needed before advocating its clinical usefulness. CONCLUSIONS: This novel extension of decision curve analysis can be applied to NMA-based prediction models to evaluate their use to aid treatment decision making. HIGHLIGHTS: Decision curve analysis is extended into a (network) meta-analysis framework.Personalized models predicting treatment benefit are evaluated when several treatment options are available and evidence about their effects comes from a set of trials.Detailed steps to compare personalized versus one-size-fit-all treatment decision-making strategies are outlined.This extension of decision curve analysis can be applied to (network) meta-analysis-based prediction models to evaluate their use to aid treatment decision making.
 BACKGROUND AND PURPOSE: An enhanced severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine regimen could improve humoral vaccine response in patients with multiple sclerosis (MS) treated by anti-CD20. The aim was to evaluate the serological response and the neutralizing activity after BNT162b2 primary and booster vaccination in MS patients, including patients on anti-CD20 receiving a primary vaccine regimen enhanced with three injections. METHODS: In this prospective longitudinal cohort study of 90 patients (47 on anti-CD20, 10 on fingolimod, 33 on natalizumab, dimethylfumarate or teriflunomide), anti-SARS-CoV-2 receptor binding domain (RBD) immunoglobulin G antibodies were quantified and their neutralization capacity was evaluated by enzyme-linked immunosorbent assay (GenScript) and a virus neutralization test against B.1 historical strain, Delta and Omicron variants, before and after three to four BNT162b2 injections. RESULTS: After the primary vaccination scheme, the anti-RBD positivity rate was strongly decreased in patients on anti-CD20 (28% [15%; 44%] after two shots, 45% [29%; 62%] after three shots) and fingolimod (50% [16%; 84%]) compared to other treatments (100% [90%; 100%]). Neutralization activity was also decreased in patients on anti-CD20 and fingolimod, and notably low for the Omicron variant in all patients (0%-22%). Delayed booster vaccination was performed in 54 patients, leading to a mild increase of anti-RBD seropositivity in patients on anti-CD20 although it was still lower compared to other treatments (65% [43%; 84%] vs. 100% [87%; 100%] respectively). After a booster, Omicron neutralization activity remained low on anti-CD20 and fingolimod treated patients but was strongly increased in patients on other treatments (91% [72%; 99%]). DISCUSSION: In MS patients on anti-CD20, an enhanced primary vaccination scheme moderately increased anti-RBD seropositivity and anti-RBD antibody titre, but neutralization activity remained modest even after a fourth booster injection. TRIAL REGISTRATION INFORMATION: COVIVAC-ID, NCT04844489, first patient included on 20 April 2021.
 BACKGROUND: Rituximab (RTX) and ocrelizumab (OCR), B cell-depleting therapy targeting CD20 molecules, affect the humoral immune response after vaccination. How these therapies influence T-cell-mediated immune response against SARS-CoV-2 after immunization remains unclear. We aimed to evaluate the humoral and cellular immune response to the COVID-19 vaccine in a cohort of patients with multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and myasthenia gravis (MG). METHODS: Patients with MS (83), NMOSD (19), or MG (7) undergoing RTX (n=47) or OCR (n=62) treatment were vaccinated twice with the mRNA BNT162b2 vaccine. Antibodies were quantified using the SARS-CoV-2 IgG chemiluminescence immunoassay, targeting the spike protein. SARS-CoV-2-specific T cell responses were quantified by interferon γ release assays (IGRA). The responses were evaluated at two different time points (4-8 weeks and 16-20 weeks following the 2nd dose of the vaccine). Immunocompetent vaccinated individuals (n=41) were included as controls. RESULTS: Almost all immunocompetent controls developed antibodies against the SARS-CoV-2 trimeric spike protein, but only 34.09% of the patients, without a COVID-19 history and undergoing anti-CD20 treatment (via RTX or OCR), seroconverted. This antibody response was higher in patients with intervals of longer than 3 weeks between vaccinations. The duration of therapy was significantly shorter in seroconverted patients (median 24 months), than in the non-seroconverted group. There was no correlation between circulating B cells and the levels of antibodies. Even patients with a low proportion of circulating CD19(+) B cells (<1%, 71 patients) had detectable SARS-CoV-2 specific antibody responses. SARS-CoV-2 specific T cell response measured by released interferon γ was detected in 94.39% of the patients, independently of a humoral immune response. CONCLUSION: The majority of MS, MG, and NMOSD patients developed a SARS-CoV-2-specific T cell response. The data suggest that vaccination can induce SARS-CoV-2-specific antibodies in a portion of anti-CD20 treated patients. The seroconversion rate was higher in OCR-treated patients compared to those on RTX. The response represented by levels of antibodies was better in individuals, with intervals of longer than 3 weeks between vaccinations.
 BACKGROUND AND PURPOSE: Evidence of brain gadolinium retention has affected gadolinium-based contrast agent usage. It is, however, unclear to what extent macrocyclic agents are retained and whether their in vivo detection may necessitate nonconventional MRI. Magnetization transfer (MT) could prove suitable to detect gadolinium-related signal changes since dechelated gadolinium ions bind to macromolecules. Therefore, this study aimed to investigate associations of prior gadolinium administrations with MT and T1 signal abnormalities. METHODS: A cohort of 23 persons with multiple sclerosis (MS) (18 females, 5 males, 57 ± 8.0 years) with multiple past gadolinium administrations (median 6, range 3-12) and 23 age- and sex-matched healthy controls underwent 1.5 Tesla MRI with MT, T1-weighted 2-dimensional spin echo, and T1-weighted 3-dimensional gradient echo. The signal intensity index was assessed by MRI in gadolinium retention predilection sites. RESULTS: There were dose-dependent associations of the globus pallidus signal on gradient echo (r = .55, p < .001) and spin echo (r = .38, p = .013) T1-weighted imaging, but not on MT. Relative to controls, MS patients had higher signal intensity index in the dentate nucleus on T1-weighted gradient echo (1.037 ± 0.040 vs. 1.016 ± 0.023, p = .04) with a similar trend in the globus pallidus on T1-weighted spin echo (1.091 ± 0.034 vs. 1.076 ± 0.014, p = .06). MT detected no group differences. CONCLUSIONS: Conventional T1-weighted imaging provided dose-dependent associations with gadolinium administrations in MS, while these could not be detected with 2-dimensional MT. Future studies could explore newer MT techniques like 3D and inhomogenous MT. Notably, these associations were identified with conventional MRI even though most patients had not received gadolinium administrations in the preceding 9 years, suggestive of long-term retention.
 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently described CNS inflammatory disorder that may manifest with optic neuritis, myelitis, seizures, and/or acute disseminated encephalomyelitis. While MOG-specific antibodies in patients with MOGAD are IgG1, a T-cell-dependent antibody isotype, immunologic mechanisms of this disease are not fully understood. Thymic hyperplasia can be associated with certain autoimmune diseases. In this report we describe a case of MOGAD associated with thymic hyperplasia in a young adult.
 Multiple sclerosis (MS) is a CNS inflammatory demyelinating disease. Recent investigations highlight the gut-brain axis as a communication network with crucial implications in neurological diseases. Thus, disrupted intestinal integrity allows the translocation of luminal molecules into systemic circulation, promoting systemic/brain immune-inflammatory responses. In both, MS and its preclinical model, the experimental autoimmune encephalomyelitis (EAE) gastrointestinal symptoms including "leaky gut" have been reported. Oleacein (OLE), a phenolic compound from extra virgin olive oil or olive leaves, harbors a wide range of therapeutic properties. Previously, we showed OLE effectiveness preventing motor defects and inflammatory damage of CNS tissues on EAE mice. The current studies examine its potential protective effects on intestinal barrier dysfunction using MOG(35-55)-induced EAE in C57BL/6 mice. OLE decreased EAE-induced inflammation and oxidative stress in the intestine, preventing tissue injury and permeability alterations. OLE protected from EAE-induced superoxide anion and accumulation of protein and lipid oxidation products in colon, also enhancing its antioxidant capacity. These effects were accompanied by reduced colonic IL-1β and TNFα levels in OLE-treated EAE mice, whereas the immunoregulatory cytokines IL-25 and IL-33 remained unchanged. Moreover, OLE protected the mucin-containing goblet cells in colon and the serum levels of iFABP and sCD14, markers that reflect loss of intestinal epithelial barrier integrity and low-grade systemic inflammation, were significantly reduced. These effects on intestinal permeability did not draw significant differences on the abundance and diversity of gut microbiota. However, OLE induced an EAE-independent raise in the abundance of Akkermansiaceae family. Consistently, using Caco-2 cells as an in vitro model, we confirmed that OLE protected against intestinal barrier dysfunction induced by harmful mediators present in both EAE and MS. This study proves that the protective effect of OLE in EAE also involves normalizing the gut alterations associated to the disease.
 Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory infiltration and demyelination in the central nervous system (CNS). IFN-gamma (IFN-γ), a critically important immunomodulator, has been widely studied in MS pathology. The confusing and complex effects of IFN-γ in MS patients and rodent models, however, cause us to look more closely at its exact role in MS. In this study, we identified the role of the IFN-γ signaling in the choroid plexus (CP) in the experimental autoimmune encephalomyelitis (EAE) model. We found that the IFN-γ signal was rapidly amplified when CNS immune cell infiltration occurred in the CP during the progressive stage. Furthermore, using two CP-specific knockdown strategies, we demonstrated that blocking the IFN-γ signal via knockdown of IFN-γR1 in the CP could protect mice against EAE pathology, as evidenced by improvements in clinical scores and infiltration. Notably, knocking down IFN-γR1 in the CP reduced the local expression of adhesion molecules and chemokines. This finding suggests that IFN-γ signaling in the CP may participate in the pathological process of EAE by preventing pathological T helper (Th) 17(+) cells from infiltrating into the CNS. Finally, we showed that the unbalanced state of IFN-γ signaling between peripheral lymphocytes and the choroid plexus may determine whether IFN-γ has a protective or aggravating effect on EAE pathology. Above all, we discovered that IFN-γR1-mediated IFN-γ signaling in the CP was a vital pathway in the pathological process of EAE.
 AIM: To describe current situation and analyze temporal trends of prevalence for four autoimmune diseases including rheumatoid arthritis (RA), inflammatory bowel disease (IBD), multiple sclerosis (MS) and psoriasis, at the global, continental, and national levels. METHODS: The estimates and 95% uncertainty interval (UI) for age-standardized prevalence rate (ASPR) of RA, IBD, MS and psoriasis were obtained from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. ASPR of RA, IBD, MS and psoriasis in 2019 was illustrated at the global, continental, and national levels. Joinpoint regression analysis was adopted to analyze the 1990-2019 temporal trends by calculating the annual percentage change (APC) and average APC (AAPC), as well as their 95% confidence interval (CI). RESULTS: In 2019, the global ASPR of RA, IBD, MS and psoriasis was 224.25 (95% UI: 204.94 to 245.99), 59.25 (95% UI: 52.78 to 66.47), 21.25 (95% UI: 18.52 to 23.91) and 503.62 (95% UI: 486.92 to 519.22), respectively, with ASPRs generally higher in Europe and America than in Africa and Asia. From 1990 to 2019, the global ASPR increased significantly for RA (AAPC = 0.27%, 95% CI: 0.24 to 0.30; P < 0.001) and decreased significantly for IBD (AAPC = -0.73%, 95% CI: -0.76 to -0.70; P < 0.001), MS (AAPC = -0.22%, 95% CI: -0.25 to -0.18; P < 0.001) and psoriasis (AAPC = -0.93%, 95% CI: -0.95 to -0.91; P < 0.001), with the most substantial changes occurring at different continents and periods. The trends of ASPR of these four autoimmune diseases varied significantly across 204 countries and territories. CONCLUSIONS: There is a strong heterogeneity in prevalence (2019), as well as their temporal trends (1990-2019) of autoimmune diseases across the world, highlighting the strong distributive inequities of autoimmune diseases worldwide, which may be instructive for better understanding the epidemiology of these diseases, appropriately allocating the medical resources, as well as making relevant health policies.
 The Italian Neuroimaging Network Initiative (INNI) is an expanding repository of brain MRI data from multiple sclerosis (MS) patients recruited at four Italian MRI research sites. We describe the raw data quality of resting-state functional MRI (RS-fMRI) time-series in INNI and the inter-site variability in functional connectivity (FC) features after unified automated data preprocessing. MRI datasets from 489 MS patients and 246 healthy control (HC) subjects were retrieved from the INNI database. Raw data quality metrics included temporal signal-to-noise ratio (tSNR), spatial smoothness (FWHM), framewise displacement (FD), and differential variation in signals (DVARS). Automated preprocessing integrated white-matter lesion segmentation (SAMSEG) into a standard fMRI pipeline (fMRIPrep). FC features were calculated on pre-processed data and harmonized between sites (Combat) prior to assessing general MS-related alterations. Across centers (both groups), median tSNR and FWHM ranged from 47 to 84 and from 2.0 to 2.5, and median FD and DVARS ranged from 0.08 to 0.24 and from 1.06 to 1.22. After preprocessing, only global FC-related features were significantly correlated with FD or DVARS. Across large-scale networks, age/sex/FD-adjusted and harmonized FC features exhibited both inter-site and site-specific inter-group effects. Significant general reductions were obtained for somatomotor and limbic networks in MS patients (vs. HC). The implemented procedures provide technical information on raw data quality and outcome of fully automated preprocessing that might serve as reference in future RS-fMRI studies within INNI. The unified pipeline introduced little bias across sites and appears suitable for multisite FC analyses on harmonized network estimates.
 Neuroinflammation plays a crucial role in the development and progression of neurological disorders. MicroRNA-155 (miR-155), a miR is known to play in inflammatory responses, is associated with susceptibility to inflammatory neurological disorders and neurodegeneration, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis as well as epilepsy, stroke, and brain malignancies. MiR-155 damages the central nervous system (CNS) by enhancing the expression of pro-inflammatory cytokines, like IL-1β, IL-6, TNF-α, and IRF3. It also disturbs the blood-brain barrier by decreasing junctional complex molecules such as claudin-1, annexin-2, syntenin-1, and dedicator of cytokinesis 1 (DOCK-1), a hallmark of many neurological disorders. This review discusses the molecular pathways which involve miR-155 as a critical component in the progression of neurological disorders, representing miR-155 as a viable therapeutic target.
 BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that affects millions of people worldwide. The disease course varies greatly across individuals and many disease-modifying treatments with different safety and efficacy profiles have been developed recently. Prognostic models evaluated and shown to be valid in different settings have the potential to support people with MS and their physicians during the decision-making process for treatment or disease/life management, allow stratified and more precise interpretation of interventional trials, and provide insights into disease mechanisms. Many researchers have turned to prognostic models to help predict clinical outcomes in people with MS; however, to our knowledge, no widely accepted prognostic model for MS is being used in clinical practice yet. OBJECTIVES: To identify and summarise multivariable prognostic models, and their validation studies for quantifying the risk of clinical disease progression, worsening, and activity in adults with MS. SEARCH METHODS: We searched MEDLINE, Embase, and the Cochrane Database of Systematic Reviews from January 1996 until July 2021. We also screened the reference lists of included studies and relevant reviews, and references citing the included studies. SELECTION CRITERIA: We included all statistically developed multivariable prognostic models aiming to predict clinical disease progression, worsening, and activity, as measured by disability, relapse, conversion to definite MS, conversion to progressive MS, or a composite of these in adult individuals with MS. We also included any studies evaluating the performance of (i.e. validating) these models. There were no restrictions based on language, data source, timing of prognostication, or timing of outcome. DATA COLLECTION AND ANALYSIS: Pairs of review authors independently screened titles/abstracts and full texts, extracted data using a piloted form based on the Checklist for Critical Appraisal and Data Extraction for Systematic Reviews of Prediction Modelling Studies (CHARMS), assessed risk of bias using the Prediction Model Risk Of Bias Assessment Tool (PROBAST), and assessed reporting deficiencies based on the checklist items in Transparent Reporting of a Multivariable Prediction Model for Individual Prognosis or Diagnosis (TRIPOD). The characteristics of the included models and their validations are described narratively. We planned to meta-analyse the discrimination and calibration of models with at least three external validations outside the model development study but no model met this criterion. We summarised between-study heterogeneity narratively but again could not perform the planned meta-regression. MAIN RESULTS: We included 57 studies, from which we identified 75 model developments, 15 external validations corresponding to only 12 (16%) of the models, and six author-reported validations. Only two models were externally validated multiple times. None of the identified external validations were performed by researchers independent of those that developed the model. The outcome was related to disease progression in 39 (41%), relapses in 8 (8%), conversion to definite MS in 17 (18%), and conversion to progressive MS in 27 (28%) of the 96 models or validations. The disease and treatment-related characteristics of included participants, and definitions of considered predictors and outcome, were highly heterogeneous amongst the studies. Based on the publication year, we observed an increase in the percent of participants on treatment, diversification of the diagnostic criteria used, an increase in consideration of biomarkers or treatment as predictors, and increased use of machine learning methods over time. Usability and reproducibility All identified models contained at least one predictor requiring the skills of a medical specialist for measurement or assessment. Most of the models (44; 59%) contained predictors that require specialist equipment likely to be absent from primary care or standard hospital settings. Over half (52%) of the developed models were not accompanied by model coefficients, tools, or instructions, which hinders their application, independent validation or reproduction. The data used in model developments were made publicly available or reported to be available on request only in a few studies (two and six, respectively). Risk of bias We rated all but one of the model developments or validations as having high overall risk of bias. The main reason for this was the statistical methods used for the development or evaluation of prognostic models; we rated all but two of the included model developments or validations as having high risk of bias in the analysis domain. None of the model developments that were externally validated or these models' external validations had low risk of bias. There were concerns related to applicability of the models to our research question in over one-third (38%) of the models or their validations. Reporting deficiencies Reporting was poor overall and there was no observable increase in the quality of reporting over time. The items that were unclearly reported or not reported at all for most of the included models or validations were related to sample size justification, blinding of outcome assessors, details of the full model or how to obtain predictions from it, amount of missing data, and treatments received by the participants. Reporting of preferred model performance measures of discrimination and calibration was suboptimal. AUTHORS' CONCLUSIONS: The current evidence is not sufficient for recommending the use of any of the published prognostic prediction models for people with MS in clinical routine today due to lack of independent external validations. The MS prognostic research community should adhere to the current reporting and methodological guidelines and conduct many more state-of-the-art external validation studies for the existing or newly developed models.
 For a long time, technical obstacles have hampered the acquisition of high-resolution images and the development of reliable processing protocols for spinal cord (SC) MRI. Fortunately, this scenario has changed in the past 5-10 years, due to hardware and software improvements. Nowadays, with advanced protocols, SC MRI is considered a useful tool for several inherited and acquired neurologic diseases, not only for diagnosis approach but also for pathophysiological unraveling and as a biomarker for disease monitoring and clinical trials. In this review, we address advanced SC MRI sequences for macrostructural and microstructural evaluation, useful semiautomatic and automatic processing tools and clinical applications on several neurologic conditions such as hereditary cerebellar ataxia, hereditary spastic paraplegia, motor neuron diseases and multiple sclerosis.
 During inflammatory, demyelinating diseases such as multiple sclerosis (MS), inflammation and axonal damage are prevalent early in the course. Axonal damage includes swelling, defects in transport, and failure to clear damaged intracellular proteins, all of which affect recovery and compromise neuronal integrity. The clearance of damaged cell components is important to maintain normal turnover and restore homeostasis. In this study, we used mass spectrometry to identify insoluble proteins within high-speed/mercaptoethanol/sarcosyl-insoluble pellets from purified white matter plaques isolated from the brains of individuals with relapsing-remitting MS (RRMS). We determined that the transmembrane protein 106B (TMEM106B), normally lysosome-associated, is insoluble in RRMS plaques relative to normal-appearing white matter from individuals with Alzheimer's disease and non-neurologic controls. Relative to wild-type mice, hypomorphic mice with a reduction in TMEM106B have increased axonal damage and lipid droplet accumulation in the spinal cord following myelin-oligodendrocyte-glycoprotein-induced experimental autoimmune encephalomyelitis. Additionally, the corpora callosa from cuprizone-challenged hypomorphic mice fail to clear lipid droplets efficiently during remyelination, suggesting that when TMEM106B is compromised, protein and lipid clearance by the lysosome is delayed. As TMEM106B contains putative lipid- and LC3-binding sites, further exploration of these sites is warranted.
 INTRODUCTION: Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system. However, the limitations of available therapeutic strategies are frustrating, both in terms of their low efficacy and multiple side effects. Previous studies showed that natural compounds such as Chalcones possess neuroprotective effects on neurodegenerative disorders. However, few studies have so far been published on the potential effects of Chalcones on treating demyelinating disease. The present study was designed to investigate the effects of Chalcones from Ashitaba (ChA) on cuprizone-induced noxious changes in the C57BL6 mice model of MS. METHODS: The mice received normal diets (Control group: CNT), or Cuprizone-supplemented diets either without ChA (Cuprizone group: CPZ) or with low or high (300, 600 mg/kg/day) doses of ChA (ChA-treated groups: CPZ+ChA300/600). Brain-derived neurotrophic factor (BDNF) and tumor necrosis factor alpha (TNFα) levels, demyelination scores in the corpus callosum (CC), and cognitive impairment were evaluated using the enzyme-linked immunosorbent assay, histological, and Y-maze tests, respectively. RESULTS: The findings showed that ChA Co-treatment significantly reduced the extent of demyelination in the CC and the serum and brain levels of TNFα in the ChA-treated groups compared to the CPZ group. Besides, treatment with a higher dose of ChA significantly improved the behavioral responses and BDNF levels in the serum and brain of the CPZ+ChA600 group when compared with the CPZ group. CONCLUSION: The present study provided evidence for the neuroprotective effects of ChA on cuprizone-induced demyelination and behavioral dysfunction in C57BL/6 mice, possibly by modulating TNFα secretion and BDNF expression.
 Multiple sclerosis (MS) is a widespread chronic neuroinflammatory and neurodegenerative disease. Microglia play a crucial role in the pathogenesis of MS via the release of cytokines and reactive oxygen species, e.g., nitric oxide. Research involving the role of phytocannabinoids in neuroinflammation is currently receiving much attention. Cannabigerol is a main phytocannabinoid, which has attracted significant pharmacological interest due to its non-psychotropic nature. In this research, we studied the effects of cannabigerol on microglial inflammation in vitro, followed by an in vivo study. Cannabigerol attenuated the microglial production of nitric oxide in BV2 microglia and primary glial cells; concomitant treatment of the cells with cannabigerol and telmisartan (a neuroprotective angiotensin receptor blocker) decreased nitric oxide production additively. Inducible nitric oxide synthase (iNOS) expression was also reduced by cannabigerol. Moreover, tumor necrosis factor-α (TNF-α), a major cytokine involved in MS, was significantly reduced by cannabigerol in both cell cultures. Next, we studied the effects of cannabigerol in vivo using a mice model of MS, experimental autoimmune encephalomyelitis (EAE). The clinical scores of EAE mice were attenuated upon cannabigerol treatment; additionally, lumbar sections of EAE mice showed enhanced neuronal loss (relative to control mice), which was restored by cannabigerol treatment. Altogether, the set of experiments presented in this work indicates that cannabigerol possesses an appealing therapeutic potential for the treatment of MS.
 B cells contribute to chronic inflammatory conditions as source of antibody-secreting plasma cells and as antigen-presenting cells activating T cells, making anti-CD20-mediated B cell depletion a widely used therapeutic option. B cells or B cell subsets may, however, exert regulatory effects, while to date, the immunological and/or clinical impact of these observations remained unclear. We found that in multiple sclerosis (MS) patients, B cells contain regulatory features and that their removal enhanced activity of monocytes. Using a co-culture system, we identified B cell-provided interleukin (IL)-10 as key factor in controlling pro-inflammatory activity of peripheral myeloid cells as well as microglia. Depleting B cells via anti-CD20 in a mouse model of MS unleashed the activity of myeloid cells and microglia and accelerated disease severity; in contrast, adoptive transfer of IL-10-providing B cells restored in vivo control of central nervous system (CNS) macrophages and microglia and reversed clinical exacerbation. These findings suggest that B cells exert meaningful regulatory properties, which should be considered when designing novel B cell-directed agents.
 The recent SARS-CoV-2 pandemic and related vaccines have raised several issues. Among them, the potential role of the viral infection (COVID-19) or anti-SARS-CoV-2 vaccines as causal factors of dysimmune CNS disorders, as well as the safety and efficacy of vaccines in patients affected by such diseases and on immune-active treatments have been analyzed. The aim is to better understand the relationship between SARS-CoV-2 infection/vaccines with dysimmune CNS diseases by describing 12 cases of multiple sclerosis/myelitis onset or reactivation after exposure to SARS-CoV-2 infection/vaccines and reviewing all published case reports or case series in which MS onset or reactivation was temporally associated with either COVID-19 (8 case reports, 3 case series) or anti-SARS-CoV-2 vaccines (13 case reports, 6 case series). All the cases share a temporal association between viral/vaccine exposure and symptoms onset. This finding, together with direct or immune-based mechanisms described both during COVID-19 and MS, claims in favor of a role for SARS-CoV-2 infection/vaccines in unmasking dysimmune CNS disorders. The most common clinical presentations involve the optic nerve, brainstem and spinal cord. The preferential tropism of the virus together with the presence of some host-related genetic/immune factors might predispose to the involvement of specific CNS districts.
 Hippocampal demyelination in multiple sclerosis (MS) has been linked with cognitive deficits, however, patients could benefit from treatment that induces oligodendroglial cell function and promotes remyelination. We investigated the role of A(1) and A(2A) adenosine receptors (AR) in regulating oligodendrocyte precursor cells (OPCs) and myelinating oligodendrocyte (OL) in the demyelinated hippocampus using the cuprizone model of MS. Spatial learning and memory were assessed in wild type C57BL/6 mice (WT) or C57BL/6 mice with global deletion of A(1) (A(1)AR-/-) or A(2A) AR (A(2A)AR-/-) fed standard or cuprizone diet (CD) for four weeks. Histology, immunofluorescence, Western blot and TUNEL assays were performed to evaluate the extent of demyelination and apoptosis in the hippocampus. Deletion of A(1) and A(2A) AR alters spatial learning and memory. In A(1)AR-/- mice, cuprizone feeding led to severe hippocampal demyelination, A(2A)AR-/- mice had a significant increase in myelin whereas WT mice had intermediate demyelination. The A(1)AR-/- CD-fed mice displayed significant astrocytosis and decreased expression of NeuN and MBP, whereas these proteins were increased in the A(2A)AR-/- CD mice. Furthermore, Olig2 was upregulated in A(1)AR-/- CD-fed mice compared to WT mice fed the standard diet. TUNEL staining of brain sections revealed a fivefold increase in the hippocampus of A(1)AR-/- CD-fed mice. Also, WT mice fed CD showed a significant decrease expression of A(1) AR. A(1) and A(2A) AR are involved in OPC/OL functions with opposing roles in myelin regulation in the hippocampus. Thus, the neuropathological findings seen in MS may be connected to the depletion of A(1) AR.
 BACKGROUND: The circulating metabolome is altered in multiple sclerosis (MS), but its prognostic capabilities have not been extensively explored. Lipid metabolites might be of particular interest due to their multiple roles in the brain, as they can serve as structural components, energy sources, and bioactive molecules. Gaining a deeper understanding of the disease may be possible by examining the lipid metabolism in the periphery, which serves as the primary source of lipids for the brain. OBJECTIVE: To determine if altered serum lipid metabolites are associated with the risk of relapse and disability in children with MS. METHODS: We collected serum samples from 61 participants with pediatric-onset MS within 4 years of disease onset. Prospective longitudinal relapse data and cross-sectional disability measures (Expanded Disability Status Scale [EDSS]) were collected. Serum metabolomics was performed using untargeted liquid chromatography and mass spectrometry. Individual lipid metabolites were clustered into pre-defined pathways. The associations between clusters of metabolites and relapse rate and EDSS score were estimated utilizing negative binomial and linear regression models, respectively. RESULTS: We found that serum acylcarnitines (relapse rate: normalized enrichment score [NES] = 2.1, q = 1.03E-04; EDSS: NES = 1.7, q = 0.02) and poly-unsaturated fatty acids (relapse rate: NES = 1.6, q = 0.047; EDSS: NES = 1.9, q = 0.005) were associated with higher relapse rates and EDSS, while serum phosphatidylethanolamines (relapse rate: NES = -2.3, q = 0.002; EDSS: NES = -2.1, q = 0.004), plasmalogens (relapse rate: NES = -2.5, q = 5.81E-04; EDSS: NES = -2.1, q = 0.004), and primary bile acid metabolites (relapse rate: NES = -2.0, q = 0.02; EDSS: NES = -1.9, q = 0.02) were associated with lower relapse rates and lower EDSS. CONCLUSION: This study supports the role of some lipid metabolites in pediatric MS relapses and disability.
 BACKGROUND AND OBJECTIVES: The major histocompatibility complex (MHC) locus has a predominant role in the genetic predisposition to multiple sclerosis (MS), with 32 associations found to be involved. We aimed to investigate the impact of MHC MS-risk alleles on T-cell repertoire in patients with MS. METHODS: We studied 161 untreated patients with relapsing-remitting MS for whom Class I and II human leukocyte antigen (HLA) alleles were inferred from whole-genome genotyping data, and T-cell receptor (TCR) CDR3 sequences were obtained through next-generation sequencing. T-cell repertoire features including diversity, public clones, and architecture were evaluated. RESULTS: We identified 5 MS-risk loci associated with TCR diversity: HLA-DRB1*15:01 (7.65 × 10(-3)), rs9271366 (1.96 × 10(-3)), rs766848979 A (1.89 × 10(-2)), rs9277626 (2.95 × 10(-2)), and rs11751659 (1.92 × 10(-2)), with evidence of expanded clonotypes in carriers of risk alleles. Moreover, HLA-DRB1*15:01 (4.99 × 10(-3)), rs9271366 (6.54 × 10(-3)), rs1049079 C (4.37 × 10(-2)), AA DQΒ1 position -5 L (1.05 × 10(-3)), and AA DQΒ1 position 221 Q (9.39 × 10(-4)) showed an association with the CDR3 aminoacidic sequence architecture, suggesting an impact on the antigen recognition breadth as well. Evaluating the sharing of clones across MS-risk allele carrier individuals revealed the presence of highly shared clonotypes predicted to target viral antigens, including Epstein-Barr virus. DISCUSSION: Our study supports the association between MHC-risk alleles and macrofeatures of the T-cell repertoire in the context of MS. Further studies are needed to understand the underlying molecular mechanisms.
 BACKGROUND AND PURPOSE: Falls are a common and persistent concern among people with neurological disorders (PwND), as they frequently result in mobility deficits and may lead to loss of functional independence. This study investigated the ceiling and floor effects, internal consistency, and convergent validity of 2 patient-reported fall prevention strategy scales in PwND. METHODS: This is a prospective cohort study. Two-hundred and ninety-nine PwND (111 people with multiple sclerosis, 94 people with Parkinson's disease, and 94 people with stroke) were seen for rehabilitation and assessed. The number of retrospective and prospective falls, use of walking assistive devices, scores on the Fall Prevention Strategy Survey (FPSS), Falls Behavioural Scale (FaB), and balance and mobility scales (Berg Balance Scale, Dynamic Gait Index, Timed Up and Go, 10-m walking test, and Activities-specific Balance Confidence) were analyzed. RESULTS: Total score distributions showed negligible ceiling and floor effects for both the FPSS (ceiling: 0.3%, floor: 0.3%) and the FaB (ceiling: 0%, floor: 0%). The Cronbach α (CI) was of 0.87 (0.85-0.89) for the FPSS and 0.86 (0.84-0.88) for the FaB. In terms of convergent validity, the FPSS and FaB were moderately correlated (Spearman correlation coefficient = 0.65). Moreover, the correlations between the FPSS and FaB and balance and mobility scales ranged from 0.25 to 0.49 ( P < .01). Both scales are slightly better able to distinguish between retrospective fallers/nonfallers [area under the curve, AUC (95% CI): FPSS: 0.61 (0.5-0.7); FaB: 0.60 (0.5-0.6)] compared with prospective fallers/nonfallers [AUC (95% CI): FPSS: 0.56 (0.4-0.6); FaB: 0.57 (0.4-0.6)]. Both scales accurately identified individuals who typically required the use of a walking assistive device for daily ambulation [AUC (95% CI): FPSS: 0.74 (0.7-0.8); FaB: 0.69 (0.6-0.7)]. Multiple regression analysis showed that previous falls, use of an assistive device, and balance confidence significantly predicted participants' prevention strategies (FPSS: R2 = 0.31, F(8,159) = 10.5, P < .01; FaB: R2 = 0.31, F(8,164) = 10.89, P < .01). CONCLUSION: The FPSS and the FaB appear to be valid tools to assess fall prevention strategies in people with neurological disorders. Both scales provide unique and added value in providing information on individual behavior for fall prevention.
 Multiple sclerosis (MS) is the most common demyelinating disease that attacks the central nervous system. Dietary intake of cuprizone (CPZ) produces demyelination resembling that of patients with MS. Given the role of the vagus nerve in gut-microbiota-brain axis in development of MS, we performed this study to investigate whether subdiaphragmatic vagotomy (SDV) affects demyelination in CPZ-treated mice. SDV significantly ameliorated demyelination and microglial activation in the brain compared with sham-operated CPZ-treated mice. Furthermore, 16S ribosomal RNA analysis revealed that SDV significantly improved the abnormal gut microbiota composition of CPZ-treated mice. An untargeted metabolomic analysis demonstrated that SDV significantly improved abnormal blood levels of metabolites in CPZ-treated mice compared with sham-operated CPZ-treated mice. Notably, there were correlations between demyelination or microglial activation in the brain and the relative abundance of several microbiome populations, suggesting a link between gut microbiota and the brain. There were also correlations between demyelination or microglial activation in the brain and blood levels of metabolites. Together, these data suggest that CPZ produces demyelination in the brain through the gut-microbiota-brain axis via the subdiaphragmatic vagus nerve.
 B cells have emerged as an important immune cell type that can be targeted for therapy in multiple sclerosis (MS). Depleting B cells with anti-CD20 antibodies is effective in treating MS. Yet, atacicept treatment, which blocks B-cell Activating Factor (BAFF) and A Proliferation-Inducing Ligand (APRIL), two cytokines important for B cell development and function, paradoxically increases disease activity in MS patients. The reason behind the failure of atacicept is not well understood. The stark differences in clinical outcomes with these therapies demonstrate that B cells have both inflammatory and anti-inflammatory functions in MS. In this review, we summarize the importance of B cells in MS and discuss the different B cell subsets that perform inflammatory and anti-inflammatory functions and how therapies modulate B cell functions in MS patients. Additionally, we discuss the potential anti-inflammatory functions of BAFF and APRIL on MS disease.
 Multiple sclerosis (MS) is the chronic inflammatory demyelinating disease of the CNS. Relapsing-remitting MS (RRMS) is the most common type of MS. However, the mechanisms of relapse and remission in MS have not been fully understood. While SJL mice immunized with proteolipid protein (PLP) develop relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), we have recently observed that some of these mice were resistant to the active induction of relapsing EAE after initial clinical and histological symptoms of EAE with a severity similar to the relapsing EAE mice. To clarify the mechanism of relapsing, we examined myelin morphology during PLP(139-151)-induced RR-EAE in the SJL mice. While RR-EAE mice showed an increased EAE severity (relapse) with CNS inflammation, demyelination with abnormal myelin morphology in the spinal cord, the resistant mice exhibited a milder EAE phenotype with diminished relapse. Compared with the RR-EAE mice, the resistant mice showed less CNS inflammation, demyelination, and abnormalities of the myelin structure. In addition, scanning electron microscopic (SEM) analysis with the osmium-maceration method displayed ultrastructural abnormalities of the myelin structure in the white matter of the RR-EAE spinal cord, but not in that of the resistant mice. While the intensity of myelin staining was reduced in the relapsing EAE spinal cord, immunohistochemistry and immunoblot analysis revealed that the 21.5 kDa isoform of degenerating myelin basic protein (MBP) was specifically induced in the relapsing EAE spinal cord. Taken together, the neuroinflammation-induced degenerating 21 kDa isoform of MBP sheds light on the development of abnormal myelin on the relapse of MS pathogenesis.
 Multiple sclerosis (MS) is a chronic inflammatory demyelinating disorder of the central nervous system. The immunopathology of MS involves both T and B lymphocytes. Rituximab is one of the anti-CD20 monoclonal antibody therapies which deplete B-cells. Although some anti-CD20 therapies have been approved by the Food and Drug Administration for treatment of MS, rituximab is used off-label. Several studies have shown that rituximab has a good efficacy and safety in MS, including certain specific patient conditions such as treatment-naïve patients, treatment-switching patients, and the Asian population. However, there are still questions about the optimal dose and duration of rituximab in MS due to the different dosing regimens used in each study. Moreover, many biosimilars have become available at a lower cost with comparable physicochemical properties, pharmacokinetics, pharmacodynamics, efficacy, safety, and immunogenicity. Thus, rituximab may be considered as a potential therapeutic option for patients without access to standard treatment. This narrative review summarized the evidence of both original and biosimilars of rituximab in MS treatment including pharmacokinetics, pharmacodynamics, clinical efficacy, safety, and dosing regimen.
 Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system characterized by remyelination failure, axonal degeneration, and progressive worsening of motor functions. Animal models of demyelination are frequently used to develop and evaluate therapies for MS. We recently reported that focal internal capsule (IC) demyelination in mice with lysophosphatidylcholine injection induced acute motor deficits followed by recovery through remyelination. However, it remains unknown whether the IC demyelination mouse model can be used to evaluate changes in motor functions caused by pharmacological treatments that promote remyelination using behavioral testing and histological analysis. In this study, we examined the effect of clemastine, an anti-muscarinic drug that promotes remyelination, in the mouse IC demyelination model. Clemastine administration improved motor function and changed forepaw preference in the IC demyelinated mice. Moreover, clemastine-treated mice showed increased mature oligodendrocyte density, reduced axonal injury, an increased number of myelinated axons and thicker myelin in the IC lesions compared with control (PBS-treated) mice. These results suggest that the lysophosphatidylcholine-induced IC demyelination model is useful for evaluating changes in motor functions following pharmacological treatments that promote remyelination.
 BACKGROUND: Tryptophan is an essential amino acid primarily metabolized by the kynurenine pathway in mammals. Intermediate metabolites emerging in this pathway have been associated with many neurogenerative diseases. This study aimed to compare tryptophan pathway metabolite levels in patients with multiple sclerosis (MS) and healthy controls and reveal the relationship of tryptophan metabolites with disease subtype and the Expanded Disability Status Scale (EDSS) score. METHODS: The study included a total of 80 MS cases [53 with relapsing remitting MS (RRMS) and 27 with secondary progressive MS (SPMS)] and 41 healthy volunteers. The patients with RRMS were further divided into relapse (RRMS-attack) and non-attack (RRMS-stable) groups. Using liquid chromatography mass spectrometry, tryptophan, kynurenine, kynurenic acid, quinolinic acid, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid levels were measured. The serum metabolite levels of the patient and control groups were compared. In addition, the link and relationship between the EDSS score and disease duration of the patients and their plasma tryptophan metabolite levels were examined. RESULTS: The tryptophan level of the patient group was significantly lower than that of the healthy controls (p<0.05). The kynurenine (105.38±65.43), quinolinic acid (10.42±3.56), kynurenine/tryptophan ratio (0.0218±0.019), and quinolinic acid/kynurenic acid ratio (1.7054±0.96141) of the patients with MS were significantly higher compared to the controls (p<0.05). In the receiver operating characteristic analysis of the power of kynurenine/tryptophan and quinolinic acid/kynurenic acid ratios in predicting the disease, both ratios predicted the diagnosis of MS (area under the curve: 0.793 and 0.645, respectively; p<0.05), albeit at low sensitivity and specificity. The parameters were similar between the RRMS-attack and RRMS-stable patient groups (p>0.05). There was also no significant difference between the RRMS and SPMS patient groups in terms of tryptophan metabolites (p>0.05). Lastly, no significant relationship was observed between tryptophan metabolites and MS subtype and the EDSS score. CONCLUSION: Our findings revealed that the kynurenine pathway involved in the tryptophan metabolism differed between the patients with MS and healthy controls, and this difference may be a limited guide in the diagnosis of MS, due to major overlaps in values for MS versus Controls, and is insufficient to determine the disease subtype.
 Optic neuritis is an inflammatory optic neuropathy that is commonly indicative of autoimmune neurological disorders including multiple sclerosis, myelin-oligodendrocyte glycoprotein antibody-associated disease, and neuromyelitis optica spectrum disorder. Early clinical recognition of optic neuritis is important in determining the potential aetiology, which has bearing on prognosis and treatment. Regaining high-contrast visual acuity is common in people with idiopathic optic neuritis and multiple sclerosis-associated optic neuritis; however, residual deficits in contrast sensitivity, binocular vision, and motion perception might impair vision-specific quality-of-life metrics. In contrast, recovery of visual acuity can be poorer and optic nerve atrophy more severe in individuals who are seropositive for antibodies to myelin oligodendrocyte glycoprotein, AQP4, and CRMP5 than in individuals with typical optic neuritis from idiopathic or multiple-sclerosis associated optic neuritis. Key clinical, imaging, and laboratory findings differentiate these disorders, allowing clinicians to focus their diagnostic studies and optimise acute and preventive treatments. Guided by early and accurate diagnosis of optic neuritis subtypes, the timely use of high-dose corticosteroids and, in some instances, plasmapheresis could prevent loss of high-contrast vision, improve contrast sensitivity, and preserve colour vision and visual fields. Advancements in our knowledge, diagnosis, and treatment of optic neuritis will ultimately improve our understanding of autoimmune neurological disorders, improve clinical trial design, and spearhead therapeutic innovation.
 BACKGROUND: Increasing evidence indicates the importance of CD8(+) T cells in autoimmune attack against CNS myelin and axon in multiple sclerosis (MS). Previous research has also discovered that myelin-reactive T cells have memory phenotype functions in MS patients. However, limited evidence is available regarding the role of CD8(+) memory T cell subsets in MS. This study aimed to explore potential antigen-specific memory T cell-related biomarkers and their association with disease activity. METHODS: The myelin oligodendrocyte glycoprotein (MOG)-specific CD8(+) memory T cell subsets and their related cytokines (perforin, granzyme B, interferon (IFN)-γ) and negative co-stimulatory molecules (programmed cell death protein 1 (PD-1), T- cell Ig and mucin domain 3 (Tim-3)) were analyzed by flow cytometry and real-time PCR in peripheral blood of patients with relapsing-remitting MS. RESULTS: We found that MS patients had elevated frequency of MOG-specific CD8(+) T cells, MOG-specific central memory T cells (T(CM)), MOG-specific CD8(+) effector memory T cells (T(EM)), and MOG-specific CD8(+) terminally differentiated cells (T(EMRA)); elevated granzyme B expression on MOG-specific CD8(+) T(CM); and, on MOG-specific CD8(+) T(EM), elevated granzyme B and reduced PD-1 expression. The Expanded Disability Status Scale score (EDSS) in MS patients was correlated with the frequency of MOG-specific CD8(+) T(CM), granzyme B expression in CD8(+) T(CM), and granzyme B and perforin expression on CD8(+) T(EM), but with reduced PD-1 expression on CD8(+) T(EM). CONCLUSION: The dysregulation of antigen-specific CD8(+) memory T cell subsets, along with the abnormal expression of their related cytokines and negative co-stimulatory molecules, may reflect an excessive or persistent inflammatory response induced during early stages of the illness. Our findings strongly suggest positive regulatory roles for memory T cell populations in MS pathogenesis, probably via molecular mimicry to trigger or promote abnormal peripheral immune responses. Furthermore, downregulated PD-1 expression may stimulate a positive feedback effect, promoting MS-related inflammatory responses via the interaction of PD-1 ligands. Therefore, these parameters are potential serological biomarkers for predicting disease development in MS.
 Autoimmune disorders of the central nervous system following COVID-19 infection include multiple sclerosis (MS), neuromyelitis optica spectrum disorder, myelin oligodendrocyte glycoprotein antibody-associated disease, autoimmune encephalitis, acute disseminated encephalomyelitis, and other less common neuroimmunologic disorders. In general, these disorders are rare and likely represent postinfectious phenomena rather than direct consequences of the SARS-CoV-2 virus itself. The impact of COVID-19 infection on patients with preexisting neuroinflammatory disorders depends on both the disorder and disease-modifying therapy use. Patients with MS do not have an increased risk for severe COVID-19, though patients on anti-CD20 therapies may have worse clinical outcomes and attenuated humoral response to vaccination. Data are limited for other neuroinflammatory disorders, but known risk factors such as older age and medical comorbidities likely play a role. Prophylaxis and treatment for COVID-19 should be considered in patients with preexisting neuroinflammatory disorders at high risk for developing severe COVID-19.
 Glial cells and central nervous system (CNS)-infiltrating leukocytes contribute to multiple sclerosis (MS). However, the networks that govern crosstalk among these ontologically distinct populations remain unclear. Here, we show that, in mice and humans, CNS-resident astrocytes and infiltrating CD44(hi)CD4(+) T cells generated interleukin-3 (IL-3), while microglia and recruited myeloid cells expressed interleukin-3 receptor-ɑ (IL-3Rɑ). Astrocytic and T cell IL-3 elicited an immune migratory and chemotactic program by IL-3Rɑ(+) myeloid cells that enhanced CNS immune cell infiltration, exacerbating MS and its preclinical model. Multiregional snRNA-seq of human CNS tissue revealed the appearance of IL3RA-expressing myeloid cells with chemotactic programming in MS plaques. IL3RA expression by plaque myeloid cells and IL-3 amount in the cerebrospinal fluid predicted myeloid and T cell abundance in the CNS and correlated with MS severity. Our findings establish IL-3:IL-3RA as a glial-peripheral immune network that prompts immune cell recruitment to the CNS and worsens MS.
 Multiple sclerosis (MS) is an inflammatory-demyelinating disease of the central nervous system (CNS) mediated by aberrant auto-reactive immune responses. The current immune-modulatory therapies are unable to protect and repair immune-mediated neural tissue damage. One of the therapeutic targets in MS is the sphingosine-1-phosphate (S1P) pathway which signals via sphingosine-1-phosphate receptors 1-5 (S1P(1-5)). S1P receptors are expressed predominantly on immune and CNS cells. Considering the potential neuroprotective properties of S1P signaling, we utilized S1P(1)-GFP (Green fluorescent protein) reporter mice in the cuprizone-induced demyelination model to investigate in vivo S1P - S1P(1) signaling in the CNS. We observed S1P(1) signaling in a subset of neural stem cells in the subventricular zone (SVZ) during demyelination. During remyelination, S1P(1) signaling is expressed in oligodendrocyte progenitor cells in the SVZ and mature oligodendrocytes in the medial corpus callosum (MCC). In the cuprizone model, we did not observe S1P(1) signaling in neurons and astrocytes. We also observed β-arrestin-dependent S1P(1) signaling in lymphocytes during demyelination and CNS inflammation. Our findings reveal β-arrestin-dependent S1P(1) signaling in oligodendrocyte lineage cells implying a role of S1P(1) signaling in remyelination.
 BACKGROUND: Neurological conditions represent an important driver of paediatric disability burden worldwide. Measurement of serum neurofilament light chain (sNfL) concentrations, a specific marker of neuroaxonal injury, has the potential to contribute to the management of children with such conditions. In this context, the European Medicines Agency recently declared age-adjusted reference values for sNfL a top research priority. We aimed to establish an age-adjusted sNfL reference range database in a population of healthy children and adolescents, and to validate this database in paediatric patients with neurological conditions to affirm its clinical applicability. METHODS: To generate a paediatric sNfL reference dataset, sNfL values were measured in a population of healthy children and adolescents (aged 0-22 years) from two large cohorts in Europe (the Coronavirus Antibodies in Kids from Bavaria study, Germany) and North America (a US Network of Paediatric Multiple Sclerosis Centers paediatric case-control cohort). Children with active or previous COVID-19 infection or SARS-CoV-2 antibody positivity at the time of sampling, or a history of primary systemic or neurological conditions were excluded. Linear models were used to restrospectively study the effect of age and weight on sNfL concentrations. We modelled the distribution of sNfL concentrations as a function of age-related physiological changes to derive reference percentile and Z score values via a generalised additive model for location, scale, and shape. The clinical utility of the new reference dataset was assessed in children and adolescents (aged 1-19 years) with neurological diseases (epilepsy, traumatic brain injury, bacterial CNS infections, paediatric-onset multiple sclerosis, and myelin oligodendrocyte glycoprotein antibody-associated disease) from the paediatric neuroimmunology clinic at the University of California San Francisco (San Francisco, CA, USA) and the Children's Hospital of the University of Regensburg (Regensburg, Germany). FINDINGS: Samples from 2667 healthy children and adolescents (1336 [50·1%] girls and 1331 [49·9%] boys; median age 8·0 years [IQR 4·0-12·0]) were used to generate the reference database covering neonatal age to adolescence (target age range 0-20 years). In the healthy population, sNfL concentrations decreased with age by an estimated 6·8% per year until age 10·3 years (estimated multiplicative effect per 1 year increase 0·93 [95% CI 0·93-0·94], p<0·0001) and was mostly stable thereafter up to age 22 years (1·00 [0·52-1·94], p>0·99). Independent of age, the magnitude of the effect of weight on sNfL concentrations was marginal. Samples from 220 children with neurological conditions (134 [60·9%] girls and 86 [39·1%] boys; median age 14·7 years [IQR 10·8-16·5]) were used to validate the clinical utility of the reference Z scores. In this population, age-adjusted sNfL Z scores were higher than in the reference population of healthy children and adolescents (p<0·0001) with higher effect size metrics (Cohen's d=1·56) compared with the application of raw sNfL concentrations (d=1·28). INTERPRETATION: The established normative sNfL values in children and adolescents provide a foundation for the clinical application of sNfL in the paediatric population. Compared with absolute sNfL values, the use of sNfL Z score was associated with higher effect size metrics and allowed for more accurate estimation of the extent of ongoing neuroaxonal damage in individual patients. FUNDING: Swiss National Science Foundation, US National Institutes of Health, and the National Multiple Sclerosis Society.
 BACKGROUND AND PURPOSE: Patients with multiple sclerosis (MS) under certain disease-modifying therapies (DMT) show a higher risk of infection and a lower immune response to vaccination. Hence, assessing immunization status prior to DMT start and, where necessary, performing vaccinations is  recommended. We aimed to determine the immunization status in MS patients and to identify factors associated with low vaccination rates. METHODS: Patients with MS who were seen at the MS clinic of the Medical University of Innsbruck throughout a period of 14 months in 2020 and 2021 were eligible for inclusion into this prospective, single-center study. Immunization status against 17 different pathogens was obtained from vaccination certificate and by patient questionnaire. Antibody detection against seven antigens was performed in peripheral blood. RESULTS: Of 424 patients with MS at a mean age of 43 ± 12 years, the vast majority had vaccinations against tetanus (94%), diphtheria (92%), and poliomyelitis (90%), whereas a lower proportion had vaccinations against tick-borne encephalitis (70%), pertussis (69%), hepatitis B (65%), rubella (55%), hepatitis A (50%), measles (49%), mumps (47%), and only a minority against influenza (10%), pneumococcal (6%) and meningococcal disease (4%), human papillomavirus (4%), yellow fever (2%), and varicella zoster virus (1%). A total of 87% received vaccination against SARS-CoV-2. Overall, higher vaccination rates were associated with younger age, relapsing disease course, and education level. Misinformation on infectious diseases and vaccines was associated with lower vaccination rates. CONCLUSIONS: The majority of MS patients did not fulfil vaccination recommendations. Efforts to increase vaccination rates, preferentially before DMT start, should be promoted.
 Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system. Artemisinin (ART) is a natural sesquiterpene lactone with an endoperoxide bond that is well-known for its anti-inflammatory effects in experimental autoimmune encephalomyelitis (EAE), the most commonly used animal model of MS. Tehranolide (TEH) is a novel compound with structural similarity to ART. In this study, we aimed to investigate the ameliorating effect of TEH on EAE development by targeting proteins and genes involved in this process and compare its effects with ART. Female C57BL/6 mice were immunized with MOG35-55. Twelve days post-immunization, mice were treated with 0.28 mg/kg/day TEH and 2.8 mg/kg/day ART for 18 consecutive days, and the clinical score was measured daily. The levels of pro-inflammatory and anti-inflammatory cytokines were assessed in mice serum and splenocytes by ELISA. We also evaluated the mRNA expression level of cytokines, as well as genes involved in T cell differentiation and myelination in the spinal cord tissue by qRT-PCR. Administration of TEH and ART significantly alleviated EAE signs. A significant reduction in IL-6 and IL-17 secretion and IL-17 and IL-1 gene expression in spinal cord were observed in the TEH-treated group. ART had similar or less significant effects. Moreover, TGF-β, IL-4, and IL-10 genes were stimulated by ART and TEH in the spinal cord, while the treatments did not affect IFN-γ expression. Both treatments dramatically increased the expression of FOXP3, GATA3, MBP, and AXL. Additionally, the T-bet gene was reduced after TEH administration. The compounds made no changes in RORγt, nestin, Gas6, Tyro3, and Mertk mRNA expression levels in the spinal cord. The study revealed that both TEH and ART can effectively modulate the genes responsible for inflammation and myelination that play a crucial role in EAE. Interestingly, TEH demonstrated a greater potency compared to ART and hence may have the potential to be evaluated in interventions for the management of MS.
 Maladjusted immune responses to the coronavirus disease 2019 (COVID-19), for example, cytokine release syndrome, may result in immunopathology and acute respiratory distress syndrome. Sphingosine-1-phosphate (S1P), a bioactive lipid mediator, and its S1P receptor (S1PR) are crucial in maintaining endothelial cell chemotaxis and barrier integrity. Apart from the S1P1 receptor-mediated mechanisms of sequestration of cytotoxic lymphocytes, including Th-17 and S1P1/2/3-mediated endothelial barrier functions, S1PR modulators may also attenuate cytokine release via activation of serine/threonine protein phosphatase 2A and enhance the pulmonary endothelial barrier via the c-Abl tyrosine kinase pathway. Chronic treatment with fingolimod (S1PR1,3,4,5 modulator) and siponimod (S1PR1,5 modulator) has demonstrated efficacy in reducing inflammatory disease activity and slowing down disease progression in multiple sclerosis. The decision to selectively suppress the immunity of a critically ill patient with COVID-19 remains a difficult choice. It has been suggested that treatment with fingolimod or siponimod may be appropriate to attenuate severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)-induced hyperinflammation in patients with COVID-19 since these patients are already monitored in an intensive care setting. Here, we review the use of S1PR modulators, fingolimod and siponimod, in regulating the inflammatory response to SARS-CoV-2 with the aim of understanding their potential rationale use in patients with COVID-19.
 BACKGROUND: Multiple sclerosis (MS) is an inflammatory, neurodegenerative disease of the central nervous system which results in disability over time and reduced quality of life. To increase the sensitivity of the EQ-5D-5L for psychosocial health, four bolt-on items from the AQoL-8D were used to create the nine-item EQ-5D-5L-Psychosocial. We aimed to externally validate the EQ-5D-5L-Psychosocial in a large cohort of people with MS (pwMS) and explore the discriminatory power of the new instrument with EQ-5D-5L/AQoL-8D. METHODS: A large representative sample from the Australian MS Longitudinal Study completed the AQoL-8D and EQ-5D-5L (including EQ VAS) and both instruments health state utilities (HSUs) were scored using Australian tariffs. Sociodemographic/clinical data were also collected. External validity of EQ-5D-5L-Psychosocial scoring algorithm was assessed with mean absolute errors (MAE) and Spearman's correlation coefficient. Discriminatory sensitivity was assessed with an examination of ceiling/floor effects, and disability severity classifications. RESULTS: Among 1683 participants (mean age: 58.6 years; 80% female), over half (55%) had moderate or severe disability. MAE (0.063) and the distribution of the prediction error were similar to the original development study. Mean (± standard deviation) HSUs were EQ-5D-5L: 0.58 ± 0.32, EQ-5D-5L-Psychosocial 0.62 ± 0.29, and AQoL-8D: 0.63 ± 0.20. N = 157 (10%) scored perfect health (i.e. HSU = 1.0) on the EQ-5D-5L, but reported a mean HSU of 0.90 on the alternative instruments. The Sleep bolt-on dimension was particularly important for pwMS. CONCLUSIONS: The EQ-5D-5L-Psychosocial is more sensitive than the EQ-5D-5L in pwMS whose HSUs approach those reflecting full health. When respondent burden is taken into account, the EQ-5D-5L-Psychosocial is preferential to the AQoL-8D. We suggest a larger confirmatory study comparing all prevalent multi-attribute utility instruments for pwMS.
 The intracerebral infection of mice with Theiler's murine encephalomyelitis virus (TMEV) represents a well-established animal model for multiple sclerosis (MS). Because CD28 is the main co-stimulatory molecule for the activation of T cells, we wanted to investigate its impact on the course of the virus infection as well as on a potential development of autoimmunity as seen in susceptible mouse strains for TMEV. In the present study, 5 weeks old mice on a C57BL/6 background with conventional or tamoxifen-induced, conditional CD28-knockout were infected intracerebrally with TMEV-BeAn. In the acute phase at 14 days post TMEV-infection (dpi), both CD28-knockout strains showed virus spread within the central nervous system (CNS) as an uncommon finding in C57BL/6 mice, accompanied by histopathological changes such as reduced microglial activation. In addition, the conditional, tamoxifen-induced CD28-knockout was associated with acute clinical deterioration and weight loss, which limited the observation period for this mouse strain to 14 dpi. In the chronic phase (42 and 147 dpi) of TMEV-infection, surprisingly only 33% of conventional CD28-knockout mice showed chronic TMEV-infection with loss of motor function concomitant with increased spinal cord inflammation, characterized by T- and B cell infiltration, microglial activation and astrogliosis at 33-42 dpi. Therefore, the clinical outcome largely depends on the time point of the CD28-knockout during development of the immune system. Whereas a fatal clinical outcome can already be observed in the early phase during TMEV-infection for conditional, tamoxifen-induced CD28-knockout mice, only one third of conventional CD28-knockout mice develop clinical symptoms later, accompanied by ongoing inflammation and an inability to clear the virus. However, the development of autoimmunity could not be observed in this C57BL/6 TMEV model irrespective of the time point of CD28 deletion.
 Cluster of differentiation 38 (CD38) is a multifunctional cell surface protein involved in nicotinamide adenine dinucleotide (NAD(+)) homeostasis in types of cells and tissues, which can be found in many immune cells and non-immune cells. Previous studies have shown that CD38 plays an important role in regulating innate immunity. Recently, many studies have revealed the importance of CD38 in autoimmune diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), multiple sclerosis (MS), type 1 diabetes (T1D) and inflammatory bowel disease, among others. In this report, we will briefly discuss the complex immunological functions of CD38 and focus on recent advances in the role of CD38 in the development and pathogenesis of autoimmune diseases, as well as their potential as therapeutic targets for systemic diseases, intending to make a comprehensive understanding of CD38 and its promising therapeutic potential in these systemic diseases.
 Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterised by acute inflammation and subsequent neuro-axonal degeneration resulting in progressive neurological impairment. Aberrant immune system activation in the periphery and subsequent lymphocyte migration to the CNS contribute to the pathophysiology. Recent research has identified metabolic dysfunction as an additional feature of MS. It is already well known that energy deficiency in neurons caused by impaired mitochondrial oxidative phosphorylation results in ionic imbalances that trigger degenerative pathways contributing to white and grey matter atrophy. However, metabolic dysfunction in MS appears to be more widespread than the CNS. This review focuses on recent research assessing the metabolism and mitochondrial function in peripheral immune cells of MS patients and lymphocytes isolated from murine models of MS. Emerging evidence suggests that pharmacological modulation of lymphocytic metabolism may regulate their subtype differentiation and rebalance pro- and anti-inflammatory functions. As such, further understanding of MS immunometabolism may aid the identification of novel treatments to specifically target proinflammatory immune responses.
 Recent studies have strengthened the evidence for Epstein-Barr Virus (EBV) as an important contributing factor in the development of multiple sclerosis (MS). Chronic inflammation is a key feature of MS. EBV(+) B cells can express cytokines and exosomes that promote inflammation, and EBV is known to be reactivated through the upregulation of cellular inflammasomes. Inflammation is a possible cause of the breakdown of the blood-brain barrier (BBB), which allows the infiltration of lymphocytes into the central nervous system. Once resident, EBV(+) or EBV-specific B cells could both plausibly exacerbate MS plaques through continued inflammatory processes, EBV reactivation, T cell exhaustion, and/or molecular mimicry. Another virus, SARS-CoV-2, the cause of COVID-19, is known to elicit a strong inflammatory response in infected and immune cells. COVID-19 is also associated with EBV reactivation, particularly in severely ill patients. Following viral clearance, continued inflammation may be a contributor to post-acute sequelae of COVID-19 infection (PASC). Evidence of aberrant cytokine activation in patients with PASC supports this hypothesis. If unaddressed, long-term inflammation could put patients at risk for reactivation of EBV. Determining mechanisms by which viruses can cause inflammation and finding treatments for reducing that inflammation may help reduce the disease burden for patients suffering from PASC, MS, and EBV diseases.
 Multiple sclerosis (MS) is an inflammatory and autoimmune disorder, in which an antibody-mediated demyelination mechanism plays a critical role. We prepared two glucosylated peptides derived from the human myelin proteins, that is, oligodendrocyte-myelin glycoprotein (OMGp) and reticulon-4 receptor (RTN4R), selected by a bioinformatic approach for their conformational homology with CSF114(Glc), a designed β-turn antigenic probe derived from myelin oligodendrocyte glycoprotein (MOG), a glycoprotein present in the CNS. This synthetic antigen is specifically recognized by antibodies in sera of MS patients. We report herein the antigenic properties of these peptides, showing, on the one hand, that MS patient antibodies recognize the two glucosylated peptides and, on the other hand, that these antibodies cross-react with CSF114(Glc) and with the previously described hyperglucosylated nontypeable Haemophilus influenzae bacterial adhesin protein HMW1ct(Glc). These observations point to an immunological association between human and bacterial protein antigens, underpinning the hypothesis that molecular mimicry triggers the breakdown of self-tolerance in MS and suggesting that RTN4R and OMGp can be considered as autoantigens.
 OBJECTIVE: Mirror patterns are incidental types that accompany the analysis of the oligoclonal band (OCB) in cerebrospinal fluid (CSF). However, their interpretation remains controversial. In this study, we analyzed all graphic results of mirror patterns from 86 patients to provide an optimal interpretation scheme for mirror patterns. METHODS: Matched CSF and serum specimens were obtained from patients with various neurological disorders that required OCB analysis. A total of 86 patients were screened and serum immunofixation electrophoresis (IFE) was performed in all 86. The interobserver agreement for interpreting mirror patterns by visual inspection was tested. The method agreement between the visual inspection and IFE was also evaluated. The CSF/serum albumin quotient (QALB) was calculated to determine the blood-brain barrier integrity of all patients. RESULTS: Of the 86 patients with mirror patterns, 19.8% (17/86) had typical mirror bands and most (80.2%) had atypical mirror bands. There was a good agreement between the 2 observers in interpreting typical mirror patterns. However, kappa statistics analysis showed poor agreement regarding the interpretation of atypical mirror bands by visual observation alone (kappa value, -0.026 to 0.314 between 2 observers). The disagreement was pronounced between the visual inspection and validation of IFE (kappa value, -0.0238 to 0.176 between the first observer and IFE; -0.322 to 0.118 between the second observer and IFE). The normal QALB rates in the type V groups were significantly higher than those in the type IV group and the positive QALB rates in the type IV were significantly higher than those in the type V. CONCLUSION: Visual inspection to interpret mirror pattern bands is unreliable. Considering the completely different clinical significance between type IV and type V and high risk of potential misinterpretations, it is necessary to perform IFE on all the atypical mirror types to discriminate atypical type IV from atypical type V.
 Multiple sclerosis (MS) is a focal inflammatory and demyelinating disease. The inflammatory infiltrates consist of macrophages/microglia, T and B cells. Remyelination (RM) is an endogenous repair process which frequently fails in MS patients. In earlier studies, T cells either promoted or impaired RM. Here, we used the combined cuprizone/MOG-EAE model to further dissect the functional role of T cells for RM. The combination of MOG immunization with cuprizone feeding targeted T cells to the corpus callosum and increased the extent of axonal injury. Global gene expression analyses demonstrated significant changes in the inflammatory environment; however, additional MOG immunization did not alter the course of RM. Our results suggest that the inflammatory environment in the combined model affects axons and oligodendrocytes differently and that oligodendroglial lineage cells might be less susceptible to T cell mediated injury.
 OBJECTIVE: Multiple sclerosis (MS) is an immune disease in the central nervous system (CNS) associated with Th17 cells. Moreover, STAT3 initiates Th17 cell differentiation and IL-17A expression through facilitating RORγt in MS. Here, we reported that magnolol, isolated from Magnolia officinalis Rehd. Et Wils, was regarded as a candidate for MS treatment verified by both in vitro and in vivo studies. METHODS: In vivo, experimental autoimmune encephalomyelitis (EAE) model in mice was employed to evaluate the alleviation of magnolol on myeloencephalitis. In vitro, FACS assay was employed to evaluate the effect of magnolol on Th17 and Treg cell differentiation and IL-17A expression; network pharmacology-based study was applied to probe the involved mechanisms; western blotting, immunocytochemistry, and luciferase reporter assay was used to further confirm the regulation of magnolol on JAK/STATs signaling pathway; surface plasmon resonance (SPR) assay and molecular docking were applied to manifest affinity with STAT3 and binding sites; overexpression of STAT3 was employed to verify whether magnolol attenuates IL-17A through STAT3 signaling pathway. RESULTS: In vivo, magnolol alleviated loss of body weight and severity of EAE mice; magnolol improved lesions in spinal cords and attenuated CD45 infiltration, and serum cytokines levels; correspondingly, magnolol focused on inhibiting Th17 differentiation and IL-17A expression in splenocyte of EAE mice; moreover, magnolol selectively inhibited p-STAT3(Y705) and p-STAT4(Y693) of both CD4(+) and CD8(+) T cells in splenocyte of EAE mice. In vitro, magnolol selectively inhibited Th17 differentiation and IL-17A expression without impact on Treg cells; network pharmacology-based study revealed that magnolol perhaps diminished Th17 cell differentiation through regulating STAT family members; western blotting further confirmed that magnolol inhibited p-JAK2(Y1007) and selectively antagonized p-STAT3(Y705) and slightly decreased p-STAT4(Y693); magnolol antagonized both STAT3 nucleus location and transcription activity; magnolol had a high affinity with STAT3 and the specific binding site perhaps to be at SH2 domain; overexpression of STAT3 resulted in failed inhibition of magnolol on IL-17A. CONCLUSION: Magnolol selectively inhibited Th17 differentiation and cytokine expression through selectively blocking of STAT3 resulting in decreased the ratio of Th17/Treg cells for treating MS, suggesting that the potential of magnolol for treating MS as novel STAT3 inhibitor.
 BACKGROUND: Long latency reflexes (LLRs) are impaired in a wide array of clinical conditions. We aimed to illustrate the clinical applications and recent advances of LLR in various neurological disorders from a systematic review of published literature. METHODS: We reviewed the literature using appropriately chosen MeSH terms on the database platforms of MEDLINE, Web of Sciences, and Google Scholar for all the articles from 1st January 1975 to 2nd February 2021 using the search terms "long loop reflex", "long latency reflex" and "C-reflex". The included articles were analyzed and reported using synthesis without meta-analysis (SWiM) guidelines. RESULTS: Based on our selection criteria, 40 articles were selected for the systematic review. The various diseases included parkinsonian syndromes (11 studies, 217 patients), Huntington's disease (10 studies, 209 patients), myoclonus of varied etiologies (13 studies, 127 patients) including progressive myoclonic epilepsy (5 studies, 63 patients) and multiple sclerosis (6 studies, 200 patients). Patients with parkinsonian syndromes showed large amplitude LLR II response. Enlarged LLR II was also found in myoclonus of various etiologies. LLR II response was delayed or absent in Huntington's disease. Delayed LLR II response was present in multiple sclerosis. Among the other diseases, LLR response varied according to the location of cerebellar lesions while the results were equivocal in patients with essential tremor. CONCLUSIONS: Abnormal LLR is observed in many neurological disorders. However, larger systematic studies are required in many neurological disorders in order to establish its role in diagnosis and management.
 Tumor necrosis factor (TNF) is a pleiotropic cytokine with a major role in immune system homeostasis and is involved in many inflammatory and autoimmune diseases, such as rheumatoid arthritis (RA), psoriasis, Alzheimer's disease (AD), and multiple sclerosis (MS). Thus, TNF and its receptors, TNFR1 and TNFR2, are relevant pharmacological targets. Biologics have been developed to block TNF-dependent signaling cascades, but they display serious side effects, and their pharmacological effectiveness decreases over time because of their immunogenicity. In this review, we present recent discoveries in small molecules targeting TNF and its receptors and discuss alternative strategies for modulating TNF signaling.
 Dynamic balance disorders are common impairments in People with Multiple Sclerosis (PwMS) leading to gait disorders and a higher risk of falling. However, the assessment of dynamic balance is still challenging and instrumented indexes provide objective and quantitative data of CoM movement and Base of Support, which are considered that are two key factors describing dynamic balance. This study aims at validating recent instrumented indexes based on the inverted pendulum model and characterizing dynamic balance disorders in PwMS. We clinically assessed 20 PwMS and we collected instrumented gait data through an optoelectronic system. Data from 20 Healthy Subjects (HS) were also considered as normative reference. Margin of Stability by HoF (MoS_Hof) and by Terry (MoS_Terry) at midstance, and Foot Placement Estimator (D(FPE)) at heel strike were calculated in mediolateral (ML) and anteroposterior (AP) directions, for both less affected and most affected sides for PwMS and for dominant and non-dominant side for HS. MoS_HOF well discriminated between PwMS and HS, followed by MoS_TERRY in ML direction (Mos_HOF: PwMS = 130.0 ± 27.2 mm, HS = 106.5 ± 18.6 mm, p < 0.001, MoS_TERRY: PwMS = 75.1 ± 24.3 mm, HS = 56.5 ± 23.4 mm, p < 0.02). MoS_HOF and MoS_TERRY discriminated between sides in both directions in PwMS. D(FPE) did not discriminate between groups and sides. Moderate correlations were found between all three indexes and clinical balance scales (from r = 0.02 to r = 0.66), energy recovery (from r = -0.77 to r = -0.11), single stance time (from r = -0.11 to r = 0.80) and step length (from r = -0.83 to r = -0.20). MoS_HOF resulted in the best index to describe dynamic balance disorders in PwMS: they keep CoM position far from the lateral and as close as possible to the anterior boundary of the Base of Support as preventive strategies to control balance perturbations. Furthermore, PwMS seem to use different preventive strategies in accordance with the specific lower limb impairments. This alters the physiological gait mechanisms increasing the energy expenditure and decreasing gait quality and dynamic balance.
 Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) coined by inflammation and neurodegeneration. The actual cause of the neurodegenerative component of the disease is however unclear. We investigated here the direct and differential effects of inflammatory mediators on human neurons. We used embryonic stem cell-derived (H9) human neuronal stem cells (hNSC) to generate neuronal cultures. Neurons were subsequently treated with tumour necrosis factor alpha (TNFα), interferon gamma (IFNγ), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 17A (IL-17A) and interleukin 10 (IL-10) separately or in combination. Immunofluorescence staining and quantitative polymerase chain reaction (qPCR) were used to assess cytokine receptor expression, cell integrity and transcriptomic changes upon treatment. H9-hNSC-derived neurons expressed cytokine receptors for IFNγ, TNFα, IL-10 and IL-17A. Neuronal exposure to these cytokines resulted in differential effects on neurite integrity parameters with a clear decrease for TNFα- and GM-CSF-treated neurons. The combinatorial treatment with IL-17A/IFNγ or IL-17A/TNFα induced a more pronounced effect on neurite integrity. Furthermore, combinatorial treatments with two cytokines induced several key signalling pathways, i.e. NFκB-, hedgehog and oxidative stress signalling, stronger than any of the cytokines alone. This work supports the idea of immune-neuronal crosstalk and the need to focus on the potential role of inflammatory cytokines on neuronal cytoarchitecture and function.
 The post-translational modification citrullination has been proposed to play a role in the pathogenesis of multiple sclerosis (MS). Myelin basic protein (MBP) is a candidate autoantigen which is citrullinated to a minor extent under physiological conditions and hypercitrullinated in MS. We examined immune cell responses elicited by hypercitrullinated MBP (citMBP) in cultures of mononuclear cells from 18 patients with MS and 42 healthy donors (HDs). The immunodominant peptide of MBP, MBP85-99, containing citrulline in position 99, outcompeted the binding of native MBP85-99 to HLA-DR15, which is strongly linked to MS. Moreover, using the monoclonal antibody MK16 as probe, we observed that B cells and monocytes from HLA-DR15(+) patients with MS presented MBP85-99 more efficiently after challenge with citMBP than with native MBP. Both citMBP and native MBP induced proliferation of CD4(+) T cells from patients with MS as well as TNF-α production by their B cells and CD4(+) T cells, and citrullination of MBP tended to enhance TNF-α secretion by CD4(+) T cells from HLA-DR15(+) patients. Unlike native MBP, citMBP induced differentiation into Th17 cells in cultures from HDs, while neither form of MBP induced Th17-cell differentiation in cultures from patients with MS. These data suggest a role for citrullination in the breach of tolerance to MBP in healthy individuals and in maintenance of the autoimmune response to MBP in patients with MS.
 BACKGROUND: Meningoencephalitis of unknown origin (MUO) is an inflammatory disease of the canine central nervous system (CNS) that shares several features with multiple sclerosis (MS) in humans. In approximately 95% of MS patients, ≥ two immunoglobulin G (IgG) oligoclonal bands (OCBs) are detectable exclusively in the cerebrospinal fluid (CSF). HYPOTHESIS/OBJECTIVES: To investigate OCBs in CSF and serum in dogs affected by MUO, intervertebral disc disease (IVDD), idiopathic epilepsy (IE), intracranial neoplasia (IN), steroid-responsive meningitis-arteritis (SRMA), and diseases outside the CNS. We hypothesize that the highest prevalence of CSF-specific OCBs (≥ two OCBs uniquely in the CSF) would be found in dogs affected by MUO. ANIMALS: Client-owned dogs (n = 121) presented to the neurology service due to neurological deficits. METHODS: Prospective study. Measurement of IgG concentration in CSF and serum via a canine IgG ELISA kit. OCB detection via isoelectric focusing (IEF) and immunoblot. RESULTS: Presence of CSF-specific OCBs was significantly higher in dogs with MUO (57%) compared to 22% in IN, 6% in IE, 15% in SRMA, 13% in IVDD, and 0% in the non-CNS group (p < .001). Dogs with MUO were 9.9 times more likely to show CSF-specific OCBs than all other diseases together (95% confidence interval, 3.7-26.4; p < .001). CONCLUSIONS AND CLINICAL IMPORTANCE: MUO showed the highest prevalence of CSF-specific OCBs, indicating an inflammatory B cell response. Future studies are needed to evaluate the prevalence in the specific MUO subtypes and a possible similarity with human MS.
 Signaling by insulin-like growth factor-1 (IGF-1) is essential for the development of the central nervous system (CNS) and regulates neuronal survival and myelination in the adult CNS. In neuroinflammatory conditions including multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE), IGF-1 can regulate cellular survival and activation in a context-dependent and cell-specific manner. Notwithstanding its importance, the functional outcome of IGF-1 signaling in microglia/macrophages, which maintain CNS homeostasis and regulate neuroinflammation, remains undefined. As a result, contradictory reports on the disease-ameliorating efficacy of IGF-1 are difficult to interpret, together precluding its potential use as a therapeutic agent. To fill this gap, we here investigated the role of IGF-1 signaling in CNS-resident microglia and border associated macrophages (BAMs) by conditional genetic deletion of the receptor Igf1r in these cell types. Using a series of techniques including histology, bulk RNA sequencing, flow cytometry and intravital imaging, we show that absence of IGF-1R significantly impacted the morphology of both BAMs and microglia. RNA analysis revealed minor changes in microglia. In BAMs however, we detected an upregulation of functional pathways associated with cellular activation and a decreased expression of adhesion molecules. Notably, genetic deletion of Igf1r from CNS-resident macrophages led to a significant weight gain in mice, suggesting that absence of IGF-1R from CNS-resident myeloid cells indirectly impacts the somatotropic axis. Lastly, we observed a more severe EAE disease course upon Igf1r genetic ablation, thus highlighting an important immunomodulatory role of this signaling pathway in BAMs/microglia. Taken together, our work shows that IGF-1R signaling in CNS-resident macrophages regulates the morphology and transcriptome of these cells while significantly decreasing the severity of autoimmune CNS inflammation.
 BACKGROUND AND OBJECTIVE: The Nine-Hole Peg Test (NHPT) is the most used test to assess hand dexterity in clinical practice and is considered the gold standard but only evaluates the time needed to complete the task. The aim of this work is to describe a graphic test on a smart tablet to assess in a quantitative as well qualitative way the dominant hand dexterity and to validate it in a cohort of neurological subjects and healthy controls. METHODS: The task consists in asking the subject to connect with a graphic line the start and the end point of a pre-defined path, with two different widths, in the most precise and fastest way possible. The path is constituted by a 'meander' and a 'spiral' part. The subjects perform the task on a smart tablet with a capacitive pen four times. The three parameters of interest considered at each trial are the execution time, length path, and number of interactions with the border. The app automatically computes these three parameters and stores the completed test files. The results of the digital graphic test are compared to the NHPT results. Healthy and pathological subjects are compared to each other, and performances obtained in different repetitions are compared to assess the learning effect in each population. RESULTS: 53 subjects with a definitive diagnosis of neurodegenerative/genetic neurological disorders (34 men, mean age 59.1 ± 16.1) and 78 healthy controls (33 men, mean age 42.5 ± 16.3) were recruited. Among the pathological subjects, 31 also performed the NHPT. The graphic test clearly distinguish between the two populations for all parameters of interest. Moreover, compared to the gold standard NHPT, time has a moderate positive correlation (r = 0.57, p ≤ 0.001), whereas interactions and length have a strong positive correlation (r = 0.81, p ≤ 0.001) and (r = 0.69, p ≤ 0.001), respectively. CONCLUSIONS: The proposed digital test can measure in an accurate, quantitative and qualitative way dominant hand disability and can result more informative with respect to the gold standard NHPT. In homogeneous cohort of subjects (for example affected by multiple sclerosis or Parkinson disease), the digital test can be used as an outcome measure in clinical trials as well as a tool for monitoring disease progression at the dominant hand level.
 BACKGROUND: Restless legs syndrome (RLS) is a sensory-motor disorder characterized by an uncomfortable sensation in the lower extremity, triggered by sitting and lying positions and release with motion. There is strong evidence that RLS prevalence is higher in persons with multiple sclerosis (MS, pwMS) than in the general population. Current literature has shown that exergaming as non-pharmacological therapy may be an effective method for symptoms such as balance, walking, fatigue, cognitive functions in pwMS, but the effects on RLS are not known. Therefore, the study's main aim is to investigate the effects of exergaming in pwMS with RLS. METHODS: Thirty-one pwMS with RLS and 34 pwMS without RLS were randomly divided as exergaming group and control group. The outcome measures were International RLS Study Group Rating Scale, Modified Fatigue Impact Scale, MS Walking Scale, Timed 25-Foot Walk Test, Hospital Anxiety and Depression Scale, Godin-Shephard Leisure-Time Physical Activity Questionnaire, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, 6 min Walk Test, Timed and Up Go, MS International Quality of Life questionnaire, MS-Related Symptom Checklist. RESULTS: 26 pwMS with RLS (11 exergaming group, 15 control group) and 27 pwMS without RLS (12 exergaming group, 15 control group) were included in 8-week post-treatment analyses. After an 8-week long-term follow-up, 16 pwMS with and without RLS completed the protocol. The RLS severity (p = 0.004), anxiety level (p = 0.024), sleep quality (0.005), walking (0.004), and balance functions (0.041) were improved in pwMS with RLS exergaming group, while RLS severity increased in control group (p = 0.004). At 8-week follow-up, the effect of exergaming on RLS severity, quality of life, sleep quality, and walking capacity was preserved. There was significant improvement in gait and balance functions in pwMS without RLS exergaming group, there was no significant differences control group. In 8-week follow-up, improvement obtained in pwMS without RLS exergaming group was not preserved. CONCLUSIONS: This study suggests that exergaming training could be an effective method for managing RLS severity, anxiety, sleep quality, gait, balance, and quality of life in pwMS with RLS.
 BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic created an urgency for an effective vaccine. The FDA approved vaccines offered by Pfizer-BioNTech (BNT162b2), ModernaTX (mRNA-1273) and Janssen/Johnson & Johnson (Ad26.COV2.S) have shown minimal side effects (SE) in general population studies. Multiple sclerosis (MS) patients were not specifically represented in the above studies. The MS community is interested in how these vaccines behave in people with MS. In this study, we compare the SE experienced by MS to that of the general population after SARS-CoV-2 vaccination and evaluate their risk of relapses or pseudo-relapses. METHODS: A retrospective, single-site, cohort study of 250 MS patients who received the initial cycle of FDA approved SARS-CoV-2 vaccines with 151 of whom also received an additional booster dose. SE resulting immediately after COVID-19 vaccination were collected as part of the standard clinical care during patient visits. RESULTS: Out of the studied 250 MS patients, 135 received the first and second doses of BNT162b2 with less than 1% and 4% pseudo-relapses respectively and 79 received the third BNT162b2 dose with a pseudo-relapse rate of 3%. 88 received the mRNA-1273 vaccine with a pseudo-relapse frequency of 2% and 5% after the first and second doses respectively. 70 patients had the mRNA-1273 vaccine booster with a 3% pseudo-relapse rate. 27 received the Ad26.COV2.S first dose, 2 of whom received a second Ad26.COV2.S booster dose, with no reports of MS worsening. No acute relapses were reported in our patient population. All patients experiencing pseudo-relapse symptoms returned to baseline within 96 h. CONCLUSION: COVID-19 vaccine is safe in patients with MS. Cases of temporary worsening of MS symptoms following SARS-CoV-2 are rare. Our findings support those reported by other recent studies and the CDC recommendation for MS patients to receive the FDA-approved COVID-19 vaccines, including the boosters.
 MicroRNAs (miRNAs) have been established as key players in various biological processes regulating differentiation, proliferation, inflammation, and autoimmune disorders. Emerging evidence suggests the critical role of miRNAs in the pathogenesis of multiple sclerosis (MS). Here, we provide a comprehensive overview of miRNAs, which are differentially expressed in MS patients or experimental autoimmune encephalomyelitis (EAE) mice and contribute to MS pathogenesis through regulating diverse pathways, including CD4+ T cells proliferation, differentiation, and activation in three subtypes of CD4+ T cells, including Th1, Th17 and regulatory T cells (Tregs). Moreover, the regulation of oligodendrocyte precursor cells (OPC) differentiation as a crucial player in MS pathogenesis is also described. Our literature research showed that miR-223 could affect different pathways involved in MS pathogenesis, such as promoting Th1 differentiation, activating the M2 phenotype of myeloid cells, and clearing myelin debris. MiR-223 was also identified as a potential biomarker, distinguishing relapsing-remitting multiple sclerosis (RRMS) from progressive multiple sclerosis (PMS), and thus, it may serve as an attractive target for further investigations. Our overview provides novel potential therapeutic targets for the treatment and new insights into miRNAs' role in MS pathogenesis.
 In multiple sclerosis, an inflammatory attack results in myelin loss, which can be partially reversed by remyelination. Recent studies suggest that mature oligodendrocytes could contribute to remyelination by generating new myelin. Here, we show that in a mouse model of cortical multiple sclerosis pathology, surviving oligodendrocytes can indeed extend new proximal processes but rarely generate new myelin internodes. Furthermore, drugs that boost myelin recovery by targeting oligodendrocyte precursor cells did not enhance this alternate mode of myelin regeneration. These data indicate that the contribution of surviving oligodendrocytes to myelin recovery in the inflamed mammalian CNS is minor and inhibited by distinct remyelination brakes.
 INTRODUCTION: Multiple Sclerosis (MS) is a chronic inflammatory and degenerative disease of the central nervous system (CNS). The severity of disability in people with MS (PwMS) is generally measured with the Expanded Disability Status Scale (EDSS). A variant of MS known as 'benign MS' (BMS) has been defined as an EDSS score of 3 or lower, combined with a disease duration of 10 years or longer; however, there is disagreement in the field about whether BMS really exists. Given that the EDSS does not capture cognitive issues, communication dysfunction, fatigue, depression, or anxiety properly, its ability to accurately represent disability in all PwMS, including BMS, remains questionable. METHODS: In this study, 141 persons with BMS (PwBMS) were included, consisting of 115 females (82%) and 26 males (18%) with a mean age of 50.8 (±8.68). A computerized test battery (NeuroTrax®) was used to assess cognition, covering seven cognitive domains (memory, executive function, visual-spatial processing, verbal function, attention, information processing, and motor skills). Fatigue was measured using the Fatigue Severity Scale (FSS). The Beck Depression Inventory (BDI) was used to assess symptoms of depression. Cognitive impairment was defined for this study as when someone has a score lower than 85 in at least two subdomains of the cognitive test battery. Rates of impairment were compared to 158 persons with non-benign MS (PwNBMS; with a disease duration of 10 years and longer and an EDSS score higher than 3) and 487 PwMS with a disease duration of fewer than 10 years. RESULTS: Cognitive impairment was found in 38% of PwBMS and in 66% of PwNBMS (p<0.001). In PwBMS, the lowest rate of impairment was found in the verbal function domain (18%) and the highest rate of impairment in the domain of information processing (32%). Fatigue and depression were found in 78% and 55% of all PwBMS, with no difference in these rates between PwBMS and PwNBMS (p = 0.787 and p = 0.316 resp.) CONCLUSION: Cognitive impairment, fatigue and depression are common among people with an EDSS-based definition of benign MS. These aspects should be incorporated into a new and better definition of truly benign MS.
 BACKGROUND: Bornyl acetate (BA), a chemical component of essential oil in the Pinus family, has yet to be actively studies in terms of its therapeutic effect on numerous diseases, including autoimmune diseases. PURPOSE: This study aimed to investigate the pharmacological effects and molecular mechanisms of BA on myelin oligodendrocyte glycoprotein (MOG(35-55))-induced experimental autoimmune encephalomyelitis (EAE) mice in an animal model of multiple sclerosis (MS), a representative autoimmune disease in central nervous system. METHODS: BA (100, 200, or 400 mg/kg) was orally treated to EAE mice once daily for 30 days after immunization for the behavioral test and for the 16th-18th days for the histopathological and molecular analyses, from the onset stage (8th day) of EAE symptoms. RESULTS: BA mitigated behavioral dysfunction (motor disability) and demyelination in the spinal cord that were associated with the down-regulation of representative pro-inflammatory cytokines (interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha), enzymes (cyclooxygenase-2 and inducible nitric oxide synthase), and chemokines (monocyte chemotactic protein-1, macrophage inflammatory protein-1 alpha, and regulated on activation), and decreased infiltration of microglia (CD11b(+)/CD45(+(low))) and macrophages (CD11b(+)/CD45(+(high))). The anti-inflammatory effect of BA was related to the inhibition of mitogen-activated protein kinases and nuclear factor-kappa B pathways. BA also reduced the recruitment/infiltration rates of CD4(+) T, Th1, and Th17 cells into the spinal cords of EAE mice, which was related to reduced blood-spinal cord barrier (BSCB) disruption. CONCLUSION: These findings strongly suggest that BA may alleviate EAE due to its anti-inflammatory and BSCB protective activities. This indicates that BA is a potential therapeutic agent for treating autoimmune demyelinating diseases including MS.
 INTRODUCTION: Multiple sclerosis (MS) is a potentially disabling disease that damages the brain and spinal cord, inducing paralysis of the body. While MS has been known as a T-cell mediated disease, recent attention has been drawn to the involvement of B cells in its pathogenesis. Autoantibodies from B cells are closely related with the damage lesion of central nervous system and worse prognosis. Therefore, regulating the activity of antibody secreting cell could be related with the severity of the MS symptoms. METHODS: Total mouse B cells were stimulated with LPS to induce their differentiation into plasma cells. The differentiation of plasma cells was subsequently analyzed using flow cytometry and quantitative PCR analysis. To establish an experimental autoimmune encephalomyelitis (EAE) mouse model, mice were immunized with MOG(35-55)/CFA emulsion. RESULTS: In this study, we found that plasma cell differentiation was accompanied by upregulation of autotaxin, which converts sphingosylphosphorylcholine (SPC) to sphingosine 1-phosphate in response to LPS. We observed that SPC strongly blocked plasma cell differentiation from B cells and antibody production in vitro. SPC downregulated LPS-stimulated IRF4 and Blimp 1, which are required for the generation of plasma cells. SPC-induced inhibitory effects on plasma cell differentiation were specifically blocked by VPC23019 (S1PR1/3 antagonist) or TY52159 (S1PR3 antagonist), but not by W146 (S1PR1 antagonist) and JTE013 (S1PR2 antagonist), suggesting a crucial role of S1PR3 but not S1PR1/2 in the process. Administration of SPC against an EAE mouse model significantly attenuated the symptoms of disease, showing decreased demyelinated areas of the spinal cord and decreased numbers of cells infiltrated into the spinal cord. SPC markedly decreased plasma cell generation in the EAE model, and SPC-induced therapeutic effects against EAE were not observed in μMT mice. CONCLUSION: Collectively, we demonstrate that SPC strongly inhibits plasma cell differentiation, which is mediated by S1PR3. SPC also elicits therapeutic outcomes against EAE, an experimental model of MS, suggesting SPC as a new material to control MS.
 Multiple sclerosis (MS) is an autoimmune demyelinating disease of the CNS that is linked with both genetic and environmental factors. A Western-style diet rich in fat and simple sugars is hypothesized as a potential factor contributing to the increased incidence of inflammatory autoimmune diseases, such as MS, in developed countries. Although the adverse effects of a high-fat diet in MS have been studied extensively, the effect of a fructose-rich diet (FRD) on MS etiology is unknown. We hypothesized that an FRD will alter the gut microbiome, influence immune populations, and negatively impact disease in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. To test this, we fed C57BL/6 mice either an FRD or normal feed for 4 or 12 wk and analyzed the effect of an FRD on gut microbiota, immune populations, and EAE. An FRD significantly influenced the gut microbiota, with reduced abundance of beneficial bacteria and enrichment of potentially proinflammatory bacteria. We also observed immune modulation in the gut and periphery. Of particular interest was a population of Helios-RORγt+Foxp3+CD4+ T cells that was enriched in the small intestine lamina propria of FRD-fed mice. However, despite gut microbiota and immune modulations, we observed only a subtle effect of an FRD on EAE severity. Overall, our data suggest that in C57Bl6/J mice, an FRD modulates the gut microbiota and immune system without significantly impacting myelin oligodendrocyte glycoprotein 35-55/CFA-induced EAE.
 BACKGROUND AND OBJECTIVES: To increase the validity of biomarker measures in multiple sclerosis (MS), factors affecting their concentration need to be identified. Here, we test whether the volume of distribution approximated by the patients' estimated blood volume (BV) and body mass index (BMI) affect the serum concentrations of glial fibrillary acidic protein (GFAP). As a control, we also determine the relationship between BV/BMI and GFAP concentrations in CSF. To confirm earlier findings, we test the same hypotheses for neurofilament light chain (NfL). METHODS: NfL and GFAP concentrations were measured in serum and CSF (sNFL/sGFAP and cNFL/cGFAP) in 157 patients (n = 106 with MS phenotype and n = 51 with other neurologic/somatoform diseases). Using multivariate linear regressions, BV was tested in the MS cohort as a predictor for each of the biomarkers while controlling for age, sex, MS phenotype, Expanded Disability Status Scale score, gadolinium-enhancing lesions, and acute relapse. In addition, overweight/obese patients (BMI ≥25 kg/m(2)) were compared with patients with BMI <25 kg/m(2) using the general linear model. The analyses were repeated including the neurologic/somatoform controls. RESULTS: In the MS cohort, BV predicted sGFAP (ß = -0.301, p = 0.014). Overweight/obese patients with MS had lower sGFAP concentrations compared with patients with MS and BMI <25 kg/m(2) (F = 4.732, p = 0.032). Repeating the analysis after adding patients with other neurologic/somatoform diseases did not change these findings (ß = -0.276, p = 0.009; F = 7.631, p = 0.006). Although sNfL was inversely correlated with BV (r = -0.275, p = 0.006) and body weight (r = -0.258, p = 0.010), those results did not remain significant after adjusting for covariates. BV and BMI were not associated with cGFAP or cNfL concentrations. DISCUSSION: These findings support the notion that the volume of distribution of sGFAP approximated by BV and BMI is a relevant variable and should therefore be controlled for when measuring sGFAP in MS, while this might not be necessary when measuring cGFAP concentrations.
 OBJECTIVE: Neurological manifestations of autoimmune connective tissue diseases (CTD) are poorly understood and difficult to diagnose. We here aimed to address this shortcoming by studying immune cell compositions in CTD patients with and without neurological manifestation. METHODS: Using flow cytometry, we retrospectively investigated paired cerebrospinal fluid (CSF) and blood samples of 28 CTD patients without neurological manifestation, 38 CTD patients with neurological manifestation (N-CTD), 38 non-inflammatory controls, and 38 multiple sclerosis (MS) patients, a paradigmatic primary neuroinflammatory disease. RESULTS: We detected an expansion of plasma cells in the blood of both N-CTD and CTD compared to non-inflammatory controls and MS. Blood plasma cells alone distinguished the clinically similar entities N-CTD and MS with high discriminatory performance (AUC: 0.81). Classical blood monocytes indicated higher disease activity in systemic lupus erythematosus (SLE) patients. Surprisingly, immune cells in the CSF did not differ significantly between N-CTD and CTD, while CD4(+) T cells and the CD4(+)/CD8(+) ratio were elevated in the blood of N-CTD compared to CTD. Several B cell-associated parameters partially overlapped in the CSF in MS and N-CTD. We built a machine learning model that distinguished N-CTD from MS with high discriminatory power using either blood or CSF. CONCLUSION: We here find that blood flow cytometry alone surprisingly suffices to distinguish CTD with neurological manifestations from clinically similar entities, suggesting that a rapid blood test could support clinicians in the differential diagnosis of N-CTD.
 Some autoimmune (AI) conditions affect white blood cell (WBC) counts. Whether a genetic predisposition to AI disease associates with WBC counts in populations expected to have low numbers of AI cases is not known. We developed genetic instruments for 7 AI diseases using genome-wide association study summary statistics. Two-sample inverse variance weighted regression (IVWR) was used to determine associations between each instrument and WBC counts. Effect size represents change in transformed WBC counts per change in log odds-ratio of the disease. For AI diseases with significant associations by IVWR, polygenic risk scores (PRS) were used to test for associations with measured WBC counts in individuals of European ancestry in a community-based (ARIC, n = 8926), and a medical-center derived cohort (BioVU, n = 40,461). The IVWR analyses revealed significant associations between 3 AI diseases and WBC counts: systemic lupus erythematous (Beta = - 0.05 [95% CI, - 0.06, - 0.03]), multiple sclerosis (Beta =  - 0.06 [- 0.10, - 0.03]), and rheumatoid arthritis (Beta = 0.02 [0.01, 0.03]). PRS for these diseases showed associations with measured WBC counts in ARIC and BioVU. Effect sizes tended to be larger among females, consistent with the known higher prevalence of these diseases among this group. This study shows that genetic predisposition to systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis was associated with WBC counts, even in populations expected to have very low numbers of disease cases.
 The failure of remyelination in the human CNS contributes to axonal injury and disease progression in multiple sclerosis (MS). In contrast to regions of chronic demyelination in the human brain, remyelination in murine models is preceded by abundant oligodendrocyte progenitor cell (OPC) repopulation, such that OPC density within regions of demyelination far exceeds that of normal white matter (NWM). As such, we hypothesized that efficient OPC repopulation was a prerequisite of successful remyelination, and that increased lesion volume may contribute to the failure of OPC repopulation in human brain. In this study, we characterized the pattern of OPC activation and proliferation following induction of lysolecithin-induced chronic demyelination in adult rabbits. The density of OPCs never exceeded that of NWM and oligodendrocyte density did not recover even at 6 months post-injection. Rabbit OPC recruitment in large lesions was further characterized by chronic Sox2 expression in OPCs located in the lesion core and upregulation of quiescence-associated Prrx1 mRNA at the lesion border. Surprisingly, when small rabbit lesions of equivalent size to mouse were induced, they too exhibited reduced OPC repopulation. However, small lesions were distinct from large lesions as they displayed an almost complete lack of OPC proliferation following demyelination. These differences in the response to demyelination suggest that both volume dependent and species-specific mechanisms are critical in the regulation of OPC proliferation and lesion repopulation and suggest that alternate models will be necessary to fully understand the mechanisms that contribute to failed remyelination in MS.
 Background: Transient receptor potential ankyrin 1 (TRPA1) activation is implicated in neuropathic pain-like symptoms. However, whether TRPA1 is solely implicated in pain-signaling or contributes to neuroinflammation in multiple sclerosis (MS) is unknown. Here, we evaluated the TRPA1 role in neuroinflammation underlying pain-like symptoms using two different models of MS. Methods: Using a myelin antigen, Trpa1(+)(/+) or Trpa1(-)(/-) female mice developed relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) (Quil A as adjuvant) or progressive experimental autoimmune encephalomyelitis (PMS)-EAE (complete Freund's adjuvant). The locomotor performance, clinical scores, mechanical/cold allodynia, and neuroinflammatory MS markers were evaluated. Results: Mechanical and cold allodynia detected in RR-EAE, or PMS-EAE Trpa1(+)(/+) mice, were not observed in Trpa1(-)(/-) mice. The increased number of cells labeled for ionized calcium-binding adapter molecule 1 (Iba1) or glial fibrillary acidic protein (GFAP), two neuroinflammatory markers in the spinal cord observed in both RR-EAE or PMS-EAE Trpa1(+)(/+) mice, was reduced in Trpa1(-)(/-) mice. By Olig2 marker and luxol fast blue staining, prevention of the demyelinating process in Trpa1(-)(/-) induced mice was also detected. Conclusions: Present results indicate that the proalgesic role of TRPA1 in EAE mouse models is primarily mediated by its ability to promote spinal neuroinflammation and further strengthen the channel inhibition to treat neuropathic pain in MS.
 BACKGROUND: Although previous sporadic studies have reported the associations between a few autoimmune diseases and nasal polyps, these studies have limitations such as conflicting results, small sample sizes, and low levels of evidence. METHODS: Several autoimmune diseases were selected as exposures while the nasal polyps were selected as outcomes. Bidirectional univariable Mendelian randomization and multivariable Mendelian randomization analyses were performed after rigorous screening of instrumental variables. Then mediation analyses were conducted to further investigate the underlying mechanisms. RESULTS: For the first time, we investigated the causal relationships between nine autoimmune diseases and nasal polyps in different genders and found: (1) there was a causal association between adult-onset Still's disease and nasal polyps; (2) sarcoidosis, ulcerative colitis, type 1 diabetes, and Crohn's disease had no significant associations with nasal polyps; (3) celiac disease showed a suggestive positive association with female nasal polyps, whereas juvenile arthritis and multiple sclerosis showed suggestive positive associations with male nasal polyps. By contrast, arthropathic psoriasis showed a suggestive negative association with nasal polyps. In addition to these nine diseases, previous controversial issues were further investigated: (1) there was a causal relationship between rheumatoid arthritis and nasal polyps, which was partially mediated by "BAFF-R for IgD+ B cells"; (2) ankylosing spondylitis showed suggestive positive associations with the female but not the male nasal polyps. Besides, we validated that there was no causal effect of autoimmune hyperthyroidism on nasal polyps. CONCLUSION: Specific conclusions regarding the causal effects of multiple autoimmune diseases on nasal polyps are the same as above. By comparing results between different genders, we have initially observed the sex bimodality in the causal effects between autoimmune diseases and nasal polyps, with those on male nasal polyps being stronger than those on female nasal polyps. Our study lays a solid foundation for further research in the future, not only helping identify individuals susceptible to nasal polyps early but also improving our understanding of the immunopathogenesis of these heterogeneous diseases.
 BACKGROUND AND OBJECTIVE: Depleting CD20(+) B cells is the primary mechanism by which ocrelizumab (OCRE) is efficient in persons with multiple sclerosis (pwMS). However, the exact role of OCRE on other immune cell subsets directly or indirectly remains elusive. The purpose of this study is to characterize the dynamics of peripheral immune cells of pwMS on OCRE. METHODS: We collected blood samples from 38 pwMS before OCRE onset (T0) and at 6 and 12 months (T6, T12) after initiation. To cover the immune cell diversity, using mass cytometry time of flight, we designed a 38-parameter panel to analyze B, T, and innate immune cell markers and CNS migratory markers. In parallel, viral-specific CD8(+) T-cell responses were assessed by the quantification of interferon-γ secretion using the enzyme-linked immunospot assay on cytomegalovirus, Epstein-Barr virus, and influenza stimulations. RESULTS: Beside B-cell depletion, we observed a loss in memory CD8(+)CD20(+) and central memory CD8(+) T cells but not in CD4(+)CD20(+) T cells already at T6 and T12 (p < 0.001). The loss of memory CD8(+) T cells correlated with a lower CXCR3 expression (p < 0.001) and CNS-related LFA-1 integrin expression (p < 0.001) as well as a reduced antiviral cellular immune response observed at both time points (p < 0.001). Of note, we did not observe major changes in the phenotype of the other cell types studied. Seven of 38 (18.4%) patients in our cohort presented with infections while on OCRE; 4 of which were switched from dimethyl fumarate. Finally, using a mixed linear model on mass cytometry data, we demonstrated that the immunomodulation induced by previous disease-modifying therapies (DMTs) was prolonged over the period of the study. DISCUSSION: In addition to its well-known role on B cells, our data suggest that OCRE also acts on CD8(+) T cells by depleting the memory compartment. These changes in CD8(+) T cells may be an asset in the action of OCRE on MS course but might also contribute to explain the increased occurrence of infections in these patients. Finally, although more data are needed to confirm this observation, it suggests that clinicians should pay a special attention to an increased infection risk in pwMS switched from other DMTs to OCRE.
 Axonal injury and demyelination occur in demyelinating diseases, such as multiple sclerosis, and the detachment of myelin from axons precedes its degradation. Paranodes are the areas at which each layer of the myelin sheath adheres tightly to axons. The destruction of nodal and paranodal structures during inflammation is an important pathophysiology of various neurological disorders. However, the underlying pathological changes in these structures remain unclear. Kallikrein 6 (KLK6), a serine protease produced by oligodendrocytes, is involved in demyelinating diseases. In the present study, we intraperitoneally injected mice with LPS for several days and examined changes in the localization of KLK6. Transient changes in the intracellular localization of KLK6 to paranodes in the spinal cord were observed during LPS-induced systemic inflammation. However, these changes were not detected in the upper part of brain white matter. LPS-induced changes were suppressed by minocycline, suggesting the involvement of microglia. Moreover, nodal lengths were elongated in LPS-treated wild-type mice, but not in LPS-treated KLK6-KO mice. These results demonstrate the potential involvement of KLK6 in the process of demyelination.
 (1) Multiple sclerosis (MS) is a chronic inflammatory disease of autoimmune origin. The Epstein−Barr virus (EBV) is associated with the onset of MS, as almost all patients have high levels of EBV-specific antibodies as a result of a previous infection. We evaluated longitudinally the effects of dimethyl fumarate (DMF), a first-line treatment of MS, on the quantity and quality of EBV-specific IgG in MS patients. (2) Serum samples from 17 MS patients receiving DMF were taken before therapy (T0) and after 1 week (T1) and 1 (T2), 3 (T3) and 6 (T4) months of treatment. Anti-EBV nuclear antigen (EBNA)-1 and capsid antigen (CA) IgG levels and anti-CA IgG avidity were measured in all samples. (3) Serum levels of anti-CA IgG were lower at T1 (p = 0.0341), T2 (p = 0.0034), T3 (p < 0.0001) and T4 (p = 0.0023) than T0. These differences were partially confirmed also in anti-EBNA-1 IgG levels (T3 vs. T0, p = 0.0034). All patients had high-avidity anti-CA IgG at T0, and no changes were observed during therapy. (4): DMF can reduce the amount but not the avidity of the anti-EBV humoral immune response in MS patients from the very early stages of treatment.
 BACKGROUND AND OBJECTIVES: Immunomodulatory therapies reduce the relapse rate but only marginally control disability progression in patients with MS. Although serum neurofilament light chain (sNfL) levels correlate best with acute signs of inflammation (e.g., relapses and gadolinium-enhancing [Gd+] lesions), their role in predicting progressive biology and irreversible axonal damage is less clear. We aimed to determine the ability of sNfL to dissect distinct measures of disease severity and predict future (no) evidence of disease activity (EDA/no evidence of disease activity [NEDA]). METHODS: One hundred fifty-three of 221 patients with relapsing-remitting MS initially enrolled in the Neurofilament and longterm outcome in MS cohort at the MS outpatient clinic of the University Medical Center Mainz (Germany) met the inclusion criteria for this prospective observational cohort study with a median follow-up of 6 years (interquartile range 4-7 years). Progressive disease forms were excluded. Inclusion criteria consisted of Expanded Disability Status Scale (EDSS) assessment within 3 months and MRI within 12 months around blood sampling at baseline (y0) and follow-up (y6). EDSS progression at y6 had to be confirmed 12 weeks later. sNfL was measured by single-molecule array, and the following additional variables were recorded: therapy, medical history, and detailed MRI parameters (T2 hyperintense lesions, Gd+ lesions, and new persistent T1 hypointense lesions). RESULTS: Patients experiencing EDSS progression or new persistent T1 lesions at y6 showed increased sNfL levels at y0 compared with stable patients or patients with inflammatory activity only. As a potential readily accessible marker of neurodegeneration, we incorporated the absence of persistent T1 lesions to the NEDA-3 concept (NEDA-3(T1): n = 54, 35.3%; EDA(T1): n = 99, 64.7%) and then evaluated a risk score with factors that distinguish patients with and without NEDA-3(T1) status. Adding sNfL to this risk score significantly improved NEDA-3(T1) prediction (0.697 95% CI 0.616-0.770 vs 0.819 95% CI 0.747-0.878, p < 0.001). Patients with sNfL values ≤8.6 pg/mL showed a 76% risk reduction for EDA(T1) at y6 (hazard ratio 0.244, 95% CI 0.142-0.419, p < 0.001). DISCUSSION: sNfL levels associate with severe focal axonal damage as reflected by development of persistent T1 lesions. Baseline sNfL values predicted NEDA-3(T1) status at 6-year follow-up.
 OBJECTIVE: The purpose of this study was to determine the frequency of myelin oligodendrocyte glycoprotein (MOG)-IgG and aquaporin-4 (AQP4)-IgG among patients with pediatric-onset multiple sclerosis (POMS) and healthy controls, to determine whether seropositive cases fulfilled their respective diagnostic criteria, to compare characteristics and outcomes in children with POMS versus MOG-IgG-associated disease (MOGAD), and identify clinical features associated with final diagnosis. METHODS: Patients with POMS and healthy controls were enrolled at 14 US sites through a prospective case-control study on POMS risk factors. Serum AQP4-IgG and MOG-IgG were assessed using live cell-based assays. RESULTS: AQP4-IgG was negative among all 1,196 participants, 493 with POMS and 703 healthy controls. MOG-IgG was positive in 30 of 493 cases (6%) and zero controls. Twenty-five of 30 patients positive with MOG-IgG (83%) had MOGAD, whereas 5 of 30 (17%) maintained a diagnosis of multiple sclerosis (MS) on re-review of records. MOGAD cases were more commonly in female patients (21/25 [84%] vs 301/468 [64%]; p = 0.044), younger age (mean = 8.2 ± 4.2 vs 14.7 ± 2.6 years; p < 0.001), more commonly had initial optic nerve symptoms (16/25 [64%] vs 129/391 [33%]; p = 0.002), or acute disseminated encephalomyelitis (ADEM; 8/25 [32%] vs 9/468 [2%]; p < 0.001), and less commonly had initial spinal cord symptoms (3/20 [15%] vs 194/381 [51%]; p = 0.002), serum Epstein-Barr virus (EBV) positivity (11/25 [44%] vs 445/468 [95%]; p < 0.001), or cerebrospinal fluid oligoclonal bands (5/25 [20%] vs 243/352 [69%]; p < 0.001). INTERPRETATION: MOG-IgG and AQP4-IgG were not identified among healthy controls confirming their high specificity for pediatric central nervous system (CNS) demyelinating disease. Five percent of those with prior POMS diagnoses ultimately had MOGAD; and none had AQP4-IgG positivity. Clinical features associated with a final diagnosis of MOGAD in those with suspected MS included initial ADEM phenotype, younger age at disease onset, and lack of EBV exposure. ANN NEUROL 2023;93:271-284.
 Circulating proteins have important functions in inflammation and a broad range of diseases. To identify genetic influences on inflammation-related proteins, we conducted a genome-wide protein quantitative trait locus (pQTL) study of 91 plasma proteins measured using the Olink Target platform in 14,824 participants. We identified 180 pQTLs (59 cis, 121 trans). Integration of pQTL data with eQTL and disease genome-wide association studies provided insight into pathogenesis, implicating lymphotoxin-α in multiple sclerosis. Using Mendelian randomization (MR) to assess causality in disease etiology, we identified both shared and distinct effects of specific proteins across immune-mediated diseases, including directionally discordant effects of CD40 on risk of rheumatoid arthritis versus multiple sclerosis and inflammatory bowel disease. MR implicated CXCL5 in the etiology of ulcerative colitis (UC) and we show elevated gut CXCL5 transcript expression in patients with UC. These results identify targets of existing drugs and provide a powerful resource to facilitate future drug target prioritization.
 The respiratory tract is home to a diverse microbial community whose influence on local and systemic immune responses is only beginning to be appreciated. The airways have been linked with the trafficking of myelin-specific T-cells in the preclinical stages of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Th17 cells are important pathogenic effectors in MS and EAE but are innocuous immediately following differentiation. Upregulation of the cytokine GM-CSF appears to be a critical step in their acquisition of pathogenic potential, but little is known about the mechanisms that mediate this process. Here, primed myelin-specific Th17 cells were transferred to congenic recipient mice prior to exposure to various human respiratory tract-associated bacteria and T-cell trafficking, phenotype and the severity of resulting EAE were monitored. Disease was exacerbated in mice exposed to the Proteobacteria Moraxella catarrhalis and Klebsiella pneumoniae, but not the Firmicute Veillonella parvula, and this was associated with significantly increased GM-CSF(+) and GM-CSF(+)IFNγ(+) ex-Th17-like donor CD4 T cells in the lungs and central nervous system (CNS) of these mice. These findings support the concept that respiratory bacteria may contribute to the pathophysiology of CNS autoimmunity by modulating pathogenicity in crucial T-cell subsets that orchestrate neuroinflammation.
 Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system and is marked by inflammation and damage to the myelin sheath surrounding nerve fibers. Recent studies have highlighted the therapeutic value of exosomes (Exos) obtained from bone marrow mesenchymal stem cells (BMSCs) in MS treatment. These BMSC-Exos contain biologically active molecules that show promising results in preclinical evaluations. The aim of this study was to investigate the mechanism of BMSC-Exos containing miR-23b-3p in both LPS-stimulated BV2 microglia and in experimental autoimmune encephalomyelitis (EAE), an animal model for MS. Exos were isolated from BMSCs, and their effects were evaluated in vitro by co-culturing with BV2 microglia. The interaction between miR-23b-3p and its downstream targets was also explored. The efficacy of BMSC-Exos was further verified in vivo by injecting the Exos into EAE mice. The results showed that BMSC-Exos containing miR-23b-3p reduced microglial pyroptosis in vivo by specifically binding to and suppressing the expression of NEK7. In vivo, BMSC-Exos containing miR-23b-3p alleviated the severity of EAE by decreasing microglial inflammation and pyroptosis via the repression of NEK7. These findings provide new insights into the therapeutic potential of BMSC-Exos containing miR-23b-3p for MS.
 OBJECTIVE: To investigate the incidence of and factors associated with SARS-CoV-2 testing and infection in immune-mediated inflammatory disease (IMID) patients versus matched non-IMID comparators from the general population. METHODS: We conducted a population-based, matched cohort study among adult residents from Ontario, Canada, from January 2020 to December 2020. We created cohorts for the following IMIDs: rheumatoid arthritis (RA), psoriasis, psoriatic arthritis, ankylosing spondylitis, systemic autoimmune rheumatic diseases, multiple sclerosis (MS), iritis, inflammatory bowel disease (IBD), polymyalgia rheumatica, and vasculitis. Each patient was matched with 5 patients without IMIDs based on sociodemographic factors. We estimated the incidence of SARS-CoV-2 testing and infection in IMID patients and non-IMID patients. Multivariable logistic regressions assessed odds of SARS-CoV-2 infection. RESULTS: We studied 493,499 patients with IMIDs and 2,466,946 patients without IMIDs. Patients with IMIDs were more likely to have at least 1 SARS-CoV-2 test versus patients without IMIDs (27.4% versus 22.7%), but the proportion testing positive for SARS-CoV-2 was identical (0.9% in both groups). Overall, IMID patients had 20% higher odds of being tested for SARS-CoV-2 (odds ratio 1.20 [95% confidence interval 1.19-1.21]). The odds of SARS-CoV-2 infection varied across IMID groups but was not significantly elevated for most IMID groups compared with non-IMID comparators. The odds of SARS-CoV-2 infection was lower in IBD and MS and marginally higher in RA and iritis. CONCLUSION: Patients across all IMIDs were more likely to be tested for SARS-CoV-2 versus those without IMIDs. The risk of SARS-CoV-2 infection varied across disease subgroups.
 Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) have recently been established to define a new disease entity, MOG-antibody-associated disease (MOGAD), which is clinically overlapping with multiple sclerosis. MOG-specific antibodies (Abs) from patients are pathogenic, but the precise effector mechanisms are currently still unknown and no therapy is approved for MOGAD. Here, we determined the contributions of complement and Fc-receptor (FcR)-mediated effects in the pathogenicity of MOG-Abs. Starting from a recombinant anti-MOG (mAb) with human IgG1 Fc, we established MOG-specific mutant mAbs with differential FcR and C1q binding. We then applied selected mutants of this MOG-mAb in two animal models of experimental autoimmune encephalomyelitis. First, we found MOG-mAb-induced demyelination was mediated by both complement and FcRs about equally. Second, we found that MOG-Abs enhanced activation of cognate MOG-specific T cells in the central nervous system (CNS), which was dependent on FcR-, but not C1q-binding. The identification of complement-dependent and -independent pathomechanisms of MOG-Abs has implications for therapeutic strategies in MOGAD.
 Neuropathic pain is the most difficult-to-treat pain syndrome in multiple sclerosis. Evidence relates neuropathic pain to demyelination, which often originates from unresolved neuroinflammation or altered immune response. Posttranscriptional regulation of gene expression might play a fundamental role in the regulation of these processes. The ELAV RNA-binding proteins HuR and HuD are involved in the promotion of inflammatory phenomena and in neuronal development and maintenance, respectively. Thus, the aim of this study was to investigate the role of HuR and HuD in demyelination-associated neuropathic pain in the mouse experimental autoimmune encephalomyelitis (EAE) model. HuR resulted overexpressed in the spinal cord of MOG(35-55)-EAE and PLP(139-151)-EAE mice and was detected in CD11b + cells. Conversely, HuD was largely downregulated in the MOG-EAE spinal cord, along with GAP43 and neurofilament H, while in PLP-EAE mice, HuD and neuronal markers remained unaltered. Intranasal antisense oligonucleotide (ASO) delivery to knockdown HuR, increased myelin basic protein expression, and Luxol Fast Blue staining in both EAE models, an indication of increased myelin content. These effects temporally coincided with attenuation of pain hypersensitivity. Anti-HuR ASO increased the expression of HuD in GAP43-expressing cells and promoted a HuD-mediated neuroprotective activity in MOG-EAE mice, while in PLP-EAE mice, HuR silencing dampened pro-inflammatory responses mediated by spinal microglia activation. In conclusion, anti-HuR ASO showed myelin protection at analgesic doses with multitarget mechanisms, and it deserves further consideration as an innovative agent to counteract demyelination in neuropathic pain states.
 Gradual loss of neuronal structure and function due to impaired blood-brain barrier (BBB) and neuroinflammation are important factors in multiple sclerosis (MS) progression. Our previous studies demonstrated that the C16 peptide and angiopoietin 1 (Ang-1) compound (C + A) could modulate inflammation and vascular protection in many models of MS. In this study, nanotechnology and a novel nanovector of the leukocyte chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLP) were used to examine the effects of C + A on MS. The acute experimental autoimmune encephalomyelitis (EAE) model of MS was established in Lewis rats. The C + A compounds were conjugated to control nano-carriers and fMLP-nano-carriers and administered to animals by intravenous injection. The neuropathological changes in the brain cortex and spinal cord were examined using multiple approaches. The stimulation of vascular injection sites was examined using rabbits. The results showed that all C + A compounds (C + A alone, nano-carrier C + A, and fMLP-nano-carrier C + A) reduced neuronal inflammation, axonal demyelination, gliosis, neuronal apoptosis, vascular leakage, and BBB impairment induced by EAE. In addition, the C + A compounds had minimal side effects on liver and kidney functions. Furthermore, the fMLP-nano-carrier C + A compound had better effects compared to C + A alone and the nano-carrier C + A. This study indicated that the fMLP-nano-carrier C + A could attenuate inflammation-related pathological changes in EAE and may be a potential therapeutic strategy for the treatment of MS and EAE.
 BACKGROUND: Treatment with fingolimod for multiple sclerosis (MS) reduces the efficacy of COVID-19 vaccination. The aim of this exploratory study was to evaluate whether main lymphocyte subsets and demographic features correlated to the subsequent increase in anti-SARS-CoV2 antibodies following the third dose of COVID-19 vaccination in fingolimod-treated MS patients. METHODS: This was a prospective single-center observational exploratory study including a subgroup of adult patients with MS (pwMS) in treatment with fingolimod who underwent COVID-19 vaccination. The association of anti-SARS-CoV2 antibody levels (reported as the Log10 of the difference between the post and pre third dose levels) with the total number and percentage of CD3+ T and CD19+ B was assessed by a linear regression model adjusted for age and sex. RESULTS: We found that peripheral blood CD19+ B lymphocytes before the third dose of vaccination in pwMS treated with fingolimod predict the subsequent increase of anti-SARS-CoV2 antibodies. CONCLUSION: This work suggests that evaluating the percentage of CD19+ B cells may be important to identify patients at risk of not producing SARS-CoV-2 antibodies, with possible reduced protection from COVID-19.
 Grey matter pathology is central to the progression of multiple sclerosis (MS). We discovered that MS plasma immunoglobulin G (IgG) antibodies, mainly IgG1, form large aggregates (>100 nm) which are retained in the flow-through after binding to Protein A. Utilizing an annexin V live-cell apoptosis detection assay, we demonstrated six times higher levels of neuronal apoptosis induced by MS plasma IgG aggregates (n = 190, from two cohorts) compared to other neurological disorders (n = 116) and healthy donors (n = 44). MS IgG aggregate-mediated, complement-dependent neuronal apoptosis was evaluated in multiple model systems including primary human neurons, primary human astrocytes, neuroblastoma SH-SY5Y cells, and newborn mouse brain slices. Immunocytochemistry revealed the co-deposition of IgG, early and late complement activation products (C1q, C3b, and membrane attack complex C5b9), as well as active caspase 3 in treated neuronal cells. Furthermore, we found that MS plasma cytotoxic antibodies are not present in Protein G flow-through, nor in the paired plasma. The neuronal apoptosis can be inhibited by IgG depletion, disruption of IgG aggregates, pan-caspase inhibitor, and is completely abolished by digestion with IgG-cleaving enzyme IdeS. Transmission electron microscopy and nanoparticle tracking analysis revealed the sizes of MS IgG aggregates are greater than 100 nm. Our data support the pathological role of MS IgG antibodies and corroborate their connection to complement activation and axonal damage, suggesting that apoptosis may be a mechanism of neurodegeneration in MS.
 Besides antiviral functions, type I IFN expresses potent anti-inflammatory properties and is being widely used to treat certain autoimmune conditions, such as multiple sclerosis. In a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis, administration of IFN-β effectively attenuates the disease development. However, the precise mechanisms underlying IFN-β-mediated treatment remain elusive. In this study, we report that IFN-induced protein with tetratricopeptide repeats 2 (Ifit2), a type I and type III IFN-stimulated gene, plays a previously unrecognized immune-regulatory role during autoimmune neuroinflammation. Mice deficient in Ifit2 displayed greater susceptibility to experimental autoimmune encephalomyelitis and escalated immune cell infiltration in the CNS. Ifit2 deficiency was also associated with microglial activation and increased myeloid cell infiltration. We also observed that myelin debris clearance and the subsequent remyelination were substantially impaired in Ifit2-/- CNS tissues. Clearing myelin debris is an important function of the reparative-type myeloid cell subset to promote remyelination. Indeed, we observed that bone marrow-derived macrophages, CNS-infiltrating myeloid cells, and microglia from Ifit2-/- mice express cytokine and metabolic genes associated with proinflammatory-type myeloid cell subsets. Taken together, our findings uncover a novel regulatory function of Ifit2 in autoimmune inflammation in part by modulating myeloid cell function and metabolic activity.
 Growing evidence from cerebrospinal fluid samples and post-mortem brain tissue from individuals with multiple sclerosis (MS) and rodent models indicates that the meninges have a key role in the inflammatory and neurodegenerative mechanisms underlying progressive MS pathology. The subarachnoid space and associated perivascular spaces between the membranes of the meninges are the access points for entry of lymphocytes, monocytes and macrophages into the brain parenchyma, and the main route for diffusion of inflammatory and cytotoxic molecules from the cerebrospinal fluid into the brain tissue. In addition, the meningeal spaces act as an exit route for CNS-derived antigens, immune cells and metabolites. A number of studies have demonstrated an association between chronic meningeal inflammation and a more severe clinical course of MS, suggesting that the build-up of immune cell aggregates in the meninges represents a rational target for therapeutic intervention. Therefore, understanding the precise cell and molecular mechanisms, timing and anatomical features involved in the compartmentalization of inflammation within the meningeal spaces in MS is vital. Here, we present a detailed review and discussion of the cellular, molecular and radiological evidence for a role of meningeal inflammation in MS, alongside the clinical and therapeutic implications.
 White blood cell (WBC) count profiles in anti-aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) and anti-myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are still unknown. This study evaluated the total WBC count, differential WBC counts, monocyte-to-lymphocyte ratio (MLR), and neutrophil-to-lymphocyte ratio (NLR) in patients with these diseases within three months from an attack before acute treatment or relapse prevention and compared the profiles with those in matched volunteers or in multiple sclerosis (MS) patients. AQP4-NMOSD patients (n = 13) had a higher neutrophil count (p = 0.0247), monocyte count (p = 0.0359), MLR (p = 0.0004), and NLR (p = 0.0037) and lower eosinophil (p = 0.0111) and basophil (p = 0.0283) counts than those of AQP4-NMOSD-matched volunteers (n = 65). Moreover, patients with MOGAD (n = 26) had a higher overall WBC count (p = 0.0001), neutrophil count (p < 0.0001), monocyte count (p = 0.0191), MLR (p = 0.0320), and NLR (p = 0.0002) than those of MOGAD-matched volunteers (n = 130). The three demyelinating diseases showed similar levels of the total and differential WBC counts; however, MOGAD and MS showed different structures in the hierarchical clustering and distributions on a two-dimensional canonical plot using differential WBC counts from the other three groups. WBC count profiles were similar in patients with MOGAD and MS but differed from profiles in matched volunteers or patients with AQP4-NMOSD.
 BACKGROUND: The Neurogenic Bladder Symptom Score-Short Form (NBSS-SF) evaluates the impact of disease-specific symptoms on the quality of life (QoL) in individuals with neurogenic bladder (NB). There is no data on the validity and reliability of the NBSS-SF questionnaire in the Arabic language, so this study aimed at providing the translation, cultural adaptation, and validation of the Arabic NBSS-SF in patients with multiple sclerosis (MS) and spinal cord injury (SCI). METHODS: The original English language version of the NBSS-SF was translated into Arabic according to the cultural and linguistic adaptation algorithm. People with SCI and MS completed the NBSS-SF, demographic and clinical information, and Qualiveen QoL questionnaire. Responses were recorded twice within a 14-day period. Psychometric properties such as content validity, construct validity, internal consistency, and test-retest reliability were tested. Internal consistency and test-retest reliability was evaluated using Cronbach's alpha, and the intraclass correlation coefficient (ICC), respectively. Construct validity was assessed by comparing the NBSS-SF with the Qualiveen questionnaire. RESULTS: Thirty-nine patients with MS and 97 with SCI participated in the study. The internal consistency for the overall NBSS-SF score (Cronbach's α of 0.82) and for each subdomain was variable (urinary incontinence 0.82; storage/voiding 0.73; consequences 0.53). ICC was 0.93 for the overall score and 0.96 for the urinary incontinence subdomain, 0.74 for storage/voiding, and 0.91 for consequences. The correlation analysis showed a significantly strong correlation between the QoL item of NBSS-SF and the Qualiveen total score (r = 0.72, p < 0.000). There was a significant moderate positive correlation between the total scores on the Arabic version of the NBSS-SF and the subdomains of the Qualiveen, including limitations (r = 0.51, p = 0.04), fears (r = 0.57, p = 0.04), feelings (r = 0.46, p = 0.01), and constraints (r = 0.59, p = 0.03). CONCLUSIONS: Our results showed that the Arabic version of NBSS-SF is a valid and reliable instrument for evaluating neurogenic lower urinary tract dysfunction symptoms in the Arabic population suffering from SCI and MS.
 BACKGROUND AND OBJECTIVES: Although the diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is based on serum MOG antibodies (MOG-Abs) positivity, patients with coexisting or restricted MOG-Abs in the CSF have been reported. The aim of this study is to characterize the relevance of CSF MOG-Abs positivity in clinical practice. METHODS: Eleven medical centers retrospectively collected clinical and laboratory data of adult and pediatric patients with suspected inflammatory CNS disease and MOG-Abs positivity in serum and/or CSF using live cell-based assays. Comparisons were performed using parametric or nonparametric tests, as appropriate. Potential factors of unfavorable outcomes were explored by Cox proportional hazard models and logistic regression. RESULTS: The cohort included 255 patients: 139 (55%) women and 132 (52%) children (i.e., <18-year-old). Among them, 145 patients (56.8%) had MOG-Abs in both serum and CSF (MOG-Abs seropositive and CSF positive), 79 (31%) only in serum (MOG-Abs seropositive and CSF negative), and 31 (12%) only in CSF (MOG-Abs seronegative and CSF positive). MOG-Abs seronegative and CSF positive predominated in adults (22% vs 3% of children), presented more commonly with motor (n = 14, 45%) and sensory symptoms (n = 13, 42%), and all but 4 (2 multiple sclerosis, 1 polyradiculoneuritis, and 1 Susac syndrome) had a final diagnosis compatible with MOGAD. When comparing seropositive patients according to MOG-Abs CSF status, MOG-Abs seropositive and CSF positive patients had a higher Expanded Disability Status Scale (EDSS) at nadir during the index event (median 4.5, interquartile range [IQR] 3.0-7.5 vs 3.0, IQR 2.0-6.8, p = 0.007) and presented more commonly with sensory (45.5% vs 24%, p = 0.002), motor (33.6% vs 19%, p = 0.021), and sphincter symptoms (26.9% vs 7.8%, p = 0.001) than MOG-Abs seropositive and CSF negative. At the last follow-up, MOG-Abs seropositive and CSF positive cases had more often persistent sphincter dysfunction (17.3% vs 4.3%, p = 0.008). Compared with seropositive patients, those MOG-Abs seronegative and CSF positive had higher disability at the last follow-up (p ≤ 0.001), and MOG-Abs seronegative and CSF positive status were independently associated with an EDSS ≥3.0. DISCUSSION: Paired serum and CSF MOG-Abs positivity are common in MOGAD and are associated with a more severe clinical presentation. CSF-only MOG-Abs positivity can occur in patients with a phenotype suggestive of MOGAD and is associated with a worse outcome. Taken together, these data suggest a clinical interest in assessing CSF MOG-Abs in patients with a phenotype suggestive of MOGAD, regardless of the MOG-Abs serostatus.
 BACKGROUND AND PURPOSE: Serum levels of neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP) are promising neuro-axonal damage and astrocytic activation biomarkers. Susac syndrome (SS) is an increasingly recognized neurological condition and biomarkers that can help assess and monitor disease evolution are highly needed for the adequate management of these patients. sNfL and sGFAP levels were evaluated in patients with SS and their clinical relevance in the relapse and remission phase of the disease was assessed. METHODS: As part of a multicentre study that enrolled patients diagnosed with SS from six international centres, sNfL and sGFAP levels were assessed in 22 SS patients (nine during a relapse and 13 in remission) and 59 age- and sex-matched healthy controls using SimoaTM assay Neurology 2-Plex B Kit. RESULTS: Serum NfL levels were higher than those of healthy controls (p < 0.001) in SS patients and in both subgroups of patients in relapse and in remission (p < 0.001 for both), with significantly higher levels in relapse than in remission (p = 0.008). sNfL levels showed a negative correlation with time from the last relapse (r = -0.663; p = 0.001). sGFAP levels were slightly higher in the whole group of patients than in healthy controls (p = 0.046) and were more pronounced in relapse than in remission (p = 0.013). CONCLUSION: In SS patients, both sNFL and sGFAP levels increased compared with healthy controls. Both biomarkers had higher levels during clinical relapse and much lower levels in remission. sNFL was shown to be time sensitive to clinical changes and can be useful to monitor neuro-axonal damage in SS.
 BACKGROUND: Previous cross-sectional studies have reported distinct clinical and radiological features among the different acute optic neuritis (ON) aetiologies. Nevertheless, these reports often included the same number of patients in each group, not taking into account the disparity in frequencies of ON aetiologies in a real-life setting and thus, it remains unclear what are the truly useful features for distinguishing the different ON causes. To determine whether clinical evaluation, ophthalmological assessment including the optical coherence tomography (OCT), CSF analysis, and MRI imaging may help to discriminate the different causes of acute ON in a real-life cohort. METHODS: In this prospective monocentric study, adult patients with recent acute ON (<1 month) underwent evaluation at baseline and 1 and 12 months, including, high- and low-contrast visual acuity, visual field assessment and OCT measurements, baseline CSF analysis and MRI. RESULTS: Among 108 patients, 71 (65.7%) had multiple sclerosis (MS), 19 (17.6%) had idiopathic ON, 13 (12.0%) and 5 (4.6%) had myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies, at last follow up respectively.At baseline, the distribution of bilateral ON, CSF-restricted oligoclonal bands, optic perineuritis, optic nerve length lesions and positive dissemination in space and dissemination in time criteria on MRI were significantly different between the four groups (p <0.001). No significant difference in visual acuity nor inner retinal layer thickness was found between the different ON aetiologies. CONCLUSIONS: In this large prospective study, bilateral visual involvement, CSF and MRI results are the most useful clues in distinguishing the different aetiologies of acute ON, whereas ophthalmological assessments including OCT measurements revealed no significant difference between the aetiologies.
 Neurodegenerative disease refers to a group of disorders that predominantly damage the neurons in the brain. Despite significant progress in the knowledge of neurodegenerative diseases, there is currently no disease-modifying drug available. Vitamin K was first established for its involvement in blood clotting, but there is now compelling evidence indicating its role in the neurological system. In particular, the results of recent studies on the effects of vitamin K2 on preventing apoptosis, oxidative stress, and microglial activation in neuron cells through its role in electron transport are very promising against Alzheimer's disease. In addition to its protective effect on cognitive functions, its inhibitory effects on inflammation and α-synuclein fibrillization in Parkinson's disease, which has been revealed in recent years, are remarkable. Although there are many studies on the mechanism and possible treatment methods of neurodegenerative diseases, especially Parkinson's and Alzheimer's disease, studies on the relationship between vitamin K and neurodegenerative diseases are very limited, yet have promising findings. Vitamin K has also been proposed for therapeutic use in multiple sclerosis patients to lower the intensity or to slow down the progression of the disease. Accordingly, the aim of this study is to review the current evidence for the use of vitamin K supplementation in neurodegenerative diseases, in particular Alzheimer's disease, Parkinson's disease, and multiple sclerosis.
 Interferon-induced protein with tetratricopeptide repeats 2, Ifit2, is critical in restricting neurotropic murine-β-coronavirus, RSA59 infection. RSA59 intracranial injection of Ifit2-deficient (-/-) compared to wild-type (WT) mice results in impaired acute microglial activation, reduced CX3CR1 expression, limited migration of peripheral lymphocytes into the brain, and impaired virus control followed by severe morbidity and mortality. While the protective role of Ifit2 is established for acute viral encephalitis, less is known about its influence during the chronic demyelinating phase of RSA59 infection. To understand this, RSA59 infected Ifit2(-/-) and Ifit2(+/+) (WT) were observed for neuropathological outcomes at day 5 (acute phase) and 30 post-infection (chronic phase). Our study demonstrates that Ifit2 deficiency causes extensive RSA59 spread throughout the spinal cord gray and white matter, associated with impaired CD4(+) T and CD8(+) T cell infiltration. Further, the cervical lymph nodes of RSA59 infected Ifit2(-/-) mice showed reduced activation of CD4(+) T cells and impaired IFNγ expression during acute encephalomyelitis. Interestingly, BBB integrity was better preserved in Ifit2(-/-) mice, as evidenced by tight junction protein Claudin-5 and adapter protein ZO-1 expression surrounding the meninges and blood vessels and decreased Texas red dye uptake, which may be responsible for reduced leukocyte infiltration. In contrast to sparse myelin loss in WT mice, the chronic disease phase in Ifit2(-/-) mice was associated with severe demyelination and persistent viral load, even at low inoculation doses. Overall, our study highlights that Ifit2 provides antiviral functions by promoting acute neuroinflammation and thereby aiding virus control and limiting severe chronic demyelination. IMPORTANCE Interferons execute their function by inducing specific genes collectively termed as interferon-stimulated genes (ISGs), among which interferon-induced protein with tetratricopeptide repeats 2, Ifit2, is known for restricting neurotropic viral replication and spread. However, little is known about its role in viral spread to the spinal cord and its associated myelin pathology. Toward this, our study using a neurotropic murine β-coronavirus and Ifit2-deficient mice demonstrates that Ifit2 deficiency causes extensive viral spread throughout the gray and white matter of the spinal cord accompanied by impaired microglial activation and T cell infiltration. Furthermore, infected Ifit2-deficient mice showed impaired activation of T cells in the cervical lymph node and relatively intact blood-brain barrier integrity. Overall, Ifit2 plays a crucial role in mounting host immunity against neurotropic murine coronavirus in the acute phase while preventing mice from developing viral-induced severe chronic neuroinflammatory demyelination, the characteristic feature of human neurological disease multiple sclerosis (MS).
 Epstein-Barr virus (EBV) infection is prevalent in global population and associated with multiple malignancies and autoimmune diseases. During the infection, EBV-harbored or infected cell-expressing antigen could elicit a variety of antibodies with significant role in viral host response and pathogenesis. These antibodies have been extensively evaluated and found to be valuable in predicting disease diagnosis and prognosis, exploring disease mechanisms, and developing antiviral agents. In this review, we discuss the versatile roles of EBV antibodies as important biomarkers for EBV-related diseases, potential driving factors of autoimmunity, and promising therapeutic agents for viral infection and pathogenesis.
 BACKGROUND: Mesenchymal stem cells (MSCs) are partially differentiated multipotent cells. They can be derived from various tissues such as the umbilical cord, bone marrow, and adipose tissue. Intrathecal administration of MSCs has shown efficacy for various neurological conditions including multiple sclerosis, autism, traumatic brain injury, and many more. OBJECTIVE: This review will seek to determine whether there are any serious adverse events associated with spinal intrathecal administration of MSCs. METHODS: PubMed was used to search the scientific literature for serious adverse events that are related to spinal intrathecal administration of MSCs. Disease specific searches were performed for neurological conditions that could benefit from intrathecal administration of MSCs. In addition, a general serious adverse events search was performed to identify any additional adverse events. RESULTS AND DISCUSSION: A total of 39 studies were included in our analysis. None of the studies reported serious adverse events related to spinal intrathecal administration of MSCs. Notably, no infections, clinical rejection, or tumors were identified. CONCLUSION: Properly performed spinal intrathecal injection of MSCs is exceedingly safe, with no serious adverse events reported based on our exhaustive literature search.
 INTRODUCTION: Clinical validation studies have demonstrated the ability of accelerated MRI sequences to decrease acquisition time and motion artifact while preserving image quality. The operational benefits, however, have been less explored. Here, we report our initial clinical experience in implementing fast MRI techniques for outpatient brain imaging during the COVID-19 pandemic. METHODS: Aggregate acquisition times were extracted from the medical record on consecutive imaging examinations performed during matched pre-implementation (7/1/2019-12/31/2019) and post-implementation periods (7/1/2020-12/31/2020). Expected acquisition time reduction for each MRI protocol was calculated through manual collection of acquisition times for the conventional and accelerated sequences performed during the pre- and post-implementation periods. Aggregate and expected acquisition times were compared for the five most frequently performed brain MRI protocols: brain without contrast (BR-), brain with and without contrast (BR+), multiple sclerosis (MS), memory loss (MML), and epilepsy (EPL). RESULTS: The expected time reductions for BR-, BR+, MS, MML, and EPL protocols were 6.6 min, 11.9 min, 14 min, 10.8 min, and 14.1 min, respectively. The overall median aggregate acquisition time was 31 [25, 36] min for the pre-implementation period and 18 [15, 22] min for the post-implementation period, with a difference of 13 min (42%). The median acquisition time was reduced by 4 min (25%) for BR-, 14.0 min (44%) for BR+, 14 min (38%) for MS, 11 min (52%) for MML, and 16 min (35%) for EPL. CONCLUSION: The implementation of fast brain MRI sequences significantly reduced the acquisition times for the most commonly performed outpatient brain MRI protocols.
 Multiple Sclerosis (MS) is a chronic autoimmune disease of the central nervous system caused by the excessive activation of T cells. Procyanidins are polyphenols that exhibit anti-inflammatory activity. Procyanidin B2 (PCB2) gallate [specifically, PCB2 3,3″-di-O-gallate (PCB2DG)] inhibits cytokine production in T cells by suppressing the acceleration of glycolysis. In this study, we determined the effect of PCB2DG on T cell-mediated autoimmune disease in vivo. We examined the immunosuppressive effects of PCB2DG using an experimental autoimmune encephalomyelitis (EAE) model, which is a classic animal model for MS. Our results indicated that the clinical score for EAE symptoms improved significantly following the oral administration of PCB2DG. This effect was associated with the suppression of T cell-mediated cytokines (e.g., IFN-γ, TNF-α, and IL-17) and infiltrating T cells into the spinal cord, which ameliorated spinal cord injury. In addition, spleen cell culture experiments revealed that the increase of T cell-mediated pro-inflammatory cytokines in EAE mice was significantly decreased following PCB2DG treatment. We further analyzed the glycolytic activity of spleen cells to identify the mechanism of the immunosuppressive effects of PCB2DG. The production of lactate and the expression of glycolytic enzymes and transporters were increased following EAE induction, but not in PCB2DG-treated EAE mice. Collectively, our results indicate that a dietary polyphenol, which has a unique structure, improves the onset of EAE symptoms and inhibits the excessive activation of T cells by influencing glycolysis.
 Demyelinating disorders, with a particular focus on multiple sclerosis (MS), have a multitude of detrimental cognitive and physical effects on the patients. Current treatment options that involve substances promoting remyelination fail in the clinics due to difficulties in reaching the central nervous system (CNS). Here, the dual encapsulation of retinoic acid (RA) into lipid nanocapsules with a nominal size of 70 nm, and a low PdI of 0.1, coupled with super paramagnetic iron oxide nanoparticles (SPIONs) was accomplished, and joined by an external functionalization process with a transferrin-receptor binding peptide. This nanosystem showed a 3-fold improved internalization by endothelial cells compared to the free drug, ability to interact with oligodendrocyte progenitor cells and microglia, and improvements in the permeability through the blood-brain barrier by 5-fold. The lipid nanocapsules also induced the differentiation of oligodendrocyte progenitor cells into more mature, myelin producing oligodendrocytes, as evaluated by high-throughput image screening, by 3-5-fold. Furthermore, the ability to tame the inflammatory response was verified in lipopolysaccharide-stimulated microglia, suppressing the production of pro-inflammatory cytokines by 50-70%. Overall, the results show that this nanosystem can act in both the inflammatory microenvironment present at the CNS of affected patients, but also stimulate the differentiation of new oligodendrocytes, paving the way for a promising platform in the therapy of MS.
 BACKGROUND AND OBJECTIVES: With the increasing use of visually evoked potentials (VEPs) as quantitative outcome parameters for myelin in clinical trials, an in-depth understanding of longitudinal VEP latency changes and their prognostic potential for subsequent neuronal loss will be required. In this longitudinal multicenter study, we evaluated the association and prognostic potential of VEP latency for retinal neurodegeneration, measured by optical coherence tomography (OCT), in relapsing-remitting MS (RRMS). METHODS: We included 293 eyes of 147 patients with RRMS (age [years, median ± SD] 36 ± 10, male sex 35%, F/U [years, median {IQR} 2.1 {1.5-3.9}]): 41 eyes had a history of optic neuritis (ON) ≥6 months before baseline (CHRONIC-ON), and 252 eyes had no history of ON (CHRONIC-NON). P100 latency (VEP), macular combined ganglion cell and inner plexiform layer volume (GCIPL), and peripapillary retinal nerve fiber layer thickness (pRNFL) (OCT) were quantified. RESULTS: P100 latency change over the first year predicted subsequent GCIPL loss (36 months) across the entire chronic cohort (p = 0.001) and in (and driven by) the CHRONIC-NON subset (p = 0.019) but not in the CHRONIC-ON subset (p = 0.680). P100 latency and pRNFL were correlated at baseline (CHRONIC-NON p = 0.004, CHRONIC-ON p < 0.001), but change in P100 latency and pRNFL were not correlated. P100 latency did not differ longitudinally between protocols or centers. DISCUSSION: VEP in non-ON eyes seems to be a promising marker of demyelination in RRMS and of potential prognostic value for subsequent retinal ganglion cell loss. This study also provides evidence that VEP may be a useful and reliable biomarker for multicenter studies.
 Multiple sclerosis is the most common immune-mediated disorder affecting the central nervous system in young adults but still has no cure. Bacillus Calmette-Guérin (BCG) vaccine is reported to have non-specific anti-inflammatory effects and therapeutic benefits in autoimmune disorders including multiple sclerosis. However, the precise mechanism of action of BCG and the host immune response to it remain unclear. In this study, we aimed to investigate the efficacy of the BCG Tokyo-172 vaccine in suppressing experimental autoimmune encephalomyelitis (EAE). Groups of young and mature adult female C57BL/6J mice were BCG-vaccinated 1 month prior or 6 days after active EAE induction using myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. Another group of 2D2 TCRMOG transgenic female mice was BCG-vaccinated before and after the onset of spontaneous EAE. BCG had an age-associated protective effect against active EAE only in wild-type mice vaccinated 1 month before EAE induction. Furthermore, the incidence of spontaneous EAE was significantly lower in BCG vaccinated 2D2 mice than in non-vaccinated controls. Protection against EAE was associated with reduced splenic T-cell proliferation in response to MOG35-55 peptide together with high frequency of CD8+ interleukin-10-secreting T cells in the spleen. In addition, microglia and astrocytes isolated from BCG-vaccinated mice showed polarization to anti-inflammatory M2 and A2 phenotypes, respectively. Our data provide new insights into the cell-mediated and humoral immune mechanisms underlying BCG vaccine-induced neuroprotection, potentially useful for developing better strategies for the treatment of MS.
 The pathogenic role B cells play in multiple sclerosis is underscored by the success of B cell depletion therapies. Yet, it remains unclear how B cells contribute to disease, although it is increasingly accepted that mechanisms beyond Ab production are involved. Better understanding of pathogenic interactions between B cells and autoreactive CD4 T cells will be critical for novel therapeutics. To focus the investigation on B cell:CD4 T cell interactions in vivo and in vitro, we previously developed a B cell-dependent, Ab-independent experimental autoimmune encephalomyelitis (EAE) mouse model driven by a peptide encompassing the extracellular domains of myelin proteolipid protein (PLPECD). In this study, we demonstrate that B cell depletion significantly inhibited PLPECD-induced EAE disease, blunted PLPECD-elicited delayed-type hypersensitivity reactions in vivo, and reduced CD4 T cell activation, proliferation, and proinflammatory cytokine production. Further, PLPECD-reactive CD4 T cells sourced from B cell-depleted donor mice failed to transfer EAE to naive recipients. Importantly, we identified B cell-mediated Ag presentation as the critical mechanism explaining B cell dependence in PLPECD-induced EAE, where bone marrow chimeric mice harboring a B cell-restricted MHC class II deficiency failed to develop EAE. B cells were ultimately observed to restimulate significantly higher Ag-specific proliferation from PLP178-191-reactive CD4 T cells compared with dendritic cells when provided PLPECD peptide in head-to-head cultures. We therefore conclude that PLPECD-induced EAE features a required pathogenic B cell-mediated Ag presentation function, providing for investigable B cell:CD4 T cell interactions in the context of autoimmune demyelinating disease.
 BACKGROUND: Treatment with cladribine tablets (CladT), an immune reconstitution therapy for relapsing multiple sclerosis (RMS), involves two short courses of treatment in Year 1 and Year 2. Most patients achieve sustained efficacy with CladT, but a small proportion may experience new disease activity (DA). Following completion of the indicated dose, physicians may have questions relating to the long-term management of these patients. Since the EU approval of CladT over 5 years ago, real-world evidence (RWE) is increasing and may provide some insights and guidance for clinical practice. We describe a systematic literature review (SLR) of RWE and provide expert opinions relating to six questions regarding the long-term use of CladT. METHODS: Pertinent clinical questions were developed by a steering committee (SC) of 14 international multiple sclerosis (MS) experts regarding breakthrough DA in Year 1, new DA after 2 years or more of treatment, long-term management of stable patients, and whether additional courses of CladT may be required or safe. An SLR was performed in EMBASE and PubMed using the population, intervention, comparators, outcomes, study design (PICOS) framework to identify relevant studies within the last 15 years. Searches of key congress proceedings for the last 2-3 years were also performed. Following review of the results and RWE, the SC drafted and agreed on expert opinion statements for each question. RESULTS: A total of 35 publications reporting RWE for CladT were included in this review. In the real world, breakthrough DA in Year 1 is of low incidence (1.1-21.9%) but can occur, particularly in patients switching from anti-lymphocyte trafficking agents. In most patients, this DA did not lead to treatment discontinuation. Reported rates of DA after the full therapeutic effect of CladT has been achieved (end of Year 2, 3 or 4) range from 12.0 to 18.7% in the few studies identified. No RWE was identified to support management decisions for stable patients in Year 5 or later. Views among the group were also diverse on this question and voting on expert opinion statements was required. Only two studies reported the administration of additional courses of CladT, but detailed safety outcomes were not provided. CONCLUSIONS: RWE for the long-term use of CladT in the treatment of RMS is increasing, however, gaps in knowledge remain. Where possible, the RWE identified through the SLR informed expert statements, but, where RWE is still lacking, these were based solely on experiences and opinion, providing some guidance on topics and questions that occur in daily clinical practice. More real-world studies with longer-term follow-up periods are needed and highly anticipated.
 BACKGROUND AND OBJECTIVES: Anti-CD20 monoclonal antibody (mAb) B-cell depletion is a remarkably successful multiple sclerosis (MS) treatment. Chimeric antigen receptor (CAR)-T cells, which target antigens in a non-major histocompatibility complex (MHC)-restricted manner, can penetrate tissues more thoroughly than mAbs. However, a previous study indicated that anti-CD19 CAR-T cells can paradoxically exacerbate experimental autoimmune encephalomyelitis (EAE) disease. We tested anti-CD19 CAR-T cells in a B-cell-dependent EAE model that is responsive to anti-CD20 B-cell depletion similar to the clinical benefit of anti-CD20 mAb treatment in MS. METHODS: Anti-CD19 CAR-T cells or control cells that overexpressed green fluorescent protein were transferred into C57BL/6 mice pretreated with cyclophosphamide (Cy). Mice were immunized with recombinant human (rh) myelin oligodendrocyte protein (MOG), which causes EAE in a B-cell-dependent manner. Mice were evaluated for B-cell depletion, clinical and histologic signs of EAE, and immune modulation. RESULTS: Clinical scores and lymphocyte infiltration were reduced in mice treated with either anti-CD19 CAR-T cells with Cy or control cells with Cy, but not with Cy alone. B-cell depletion was observed in peripheral lymphoid tissue and in the CNS of mice treated with anti-CD19 CAR-T cells with Cy pretreatment. Th1 or Th17 populations did not differ in anti-CD19 CAR-T cell, control cell-treated animals, or Cy alone. DISCUSSION: In contrast to previous data showing that anti-CD19 CAR-T cell treatment exacerbated EAE, we observed that anti-CD19 CAR-T cells ameliorated EAE. In addition, anti-CD19 CAR-T cells thoroughly depleted B cells in peripheral tissues and in the CNS. However, the clinical benefit occurred independently of antigen specificity or B-cell depletion.
 Neuronal oxidative stress has been implicated in aging and neurodegenerative disease. Here we investigated the impact of elevated oxidative stress induced in mouse spinal cord by deletion of Mn-Superoxide dismutase (MnSOD) using a neuron specific Cre recombinase in Sod2 floxed mice (i-mn-Sod2 KO). Sod2 deletion in spinal cord neurons was associated with mitochondrial alterations and peroxide generation. Phenotypically, i-mn-Sod2 KO mice experienced hindlimb paralysis and clasping behavior associated with extensive demyelination and reduced nerve conduction velocity, axonal degeneration, enhanced blood brain barrier permeability, elevated inflammatory cytokines, microglia activation, infiltration of neutrophils and necroptosis in spinal cord. In contrast, spinal cord motor neuron number, innervation of neuromuscular junctions, muscle mass, and contractile function were not altered. Overall, our findings show that loss of MnSOD in spinal cord promotes a phenotype of demyelination, inflammation and progressive paralysis that mimics phenotypes associated with progressive multiple sclerosis.
 A small proportion of multiple sclerosis (MS) patients develop new disease activity soon after starting anti-CD20 therapy. This activity does not recur with further dosing, possibly reflecting deeper depletion of CD20-expressing cells with repeat infusions. We assessed cellular immune profiles and their association with transient disease activity following anti-CD20 initiation as a window into relapsing disease biology. Peripheral blood mononuclear cells from independent discovery and validation cohorts of MS patients initiating ocrelizumab were assessed for phenotypic and functional profiles using multiparametric flow cytometry. Pretreatment CD20-expressing T cells, especially CD20(dim)CD8(+) T cells with a highly inflammatory and central nervous system (CNS)-homing phenotype, were significantly inversely correlated with pretreatment MRI gadolinium-lesion counts, and also predictive of early disease activity observed after anti-CD20 initiation. Direct removal of pretreatment proinflammatory CD20(dim)CD8(+) T cells had a greater contribution to treatment-associated changes in the CD8(+) T cell pool than was the case for CD4(+) T cells. Early disease activity following anti-CD20 initiation was not associated with reconstituting CD20(dim)CD8(+) T cells, which were less proinflammatory compared with pretreatment. Similarly, this disease activity did not correlate with early reconstituting B cells, which were predominantly transitional CD19(+)CD24(high)CD38(high) with a more anti-inflammatory profile. We provide insights into the mode-of-action of anti-CD20 and highlight a potential role for CD20(dim)CD8(+) T cells in MS relapse biology; their strong inverse correlation with both pretreatment and early posttreatment disease activity suggests that CD20-expressing CD8(+) T cells leaving the circulation (possibly to the CNS) play a particularly early role in the immune cascades involved in relapse development.
 Multiple sclerosis (MS) is a T cell-driven autoimmune disease that attacks the myelin of the central nervous system (CNS) and currently has no cure. MS etiology is linked to both the gut flora and external environmental factors but this connection is not well understood. One immune system regulator responsive to nonpathogenic external stimuli is the aryl hydrocarbon receptor (AHR). The AHR, which binds diverse molecules present in the environment in barrier tissues, is a therapeutic target for MS. However, AHR's precise function in T lymphocytes, the orchestrators of MS, has not been described. Here, we show that in a mouse model of MS, T cell-specific Ahr knockout leads to recovery driven by a decrease in T cell fitness. At the mechanistic level, we demonstrate that the absence of AHR changes the gut microenvironment composition to generate metabolites that impact T cell viability, such as bile salts and short chain fatty acids. Our study demonstrates a newly emerging role for AHR in mediating the interdependence between T lymphocytes and the microbiota, while simultaneously identifying new potential molecular targets for the treatment of MS and other autoimmune diseases.
 TNF signaling is an essential regulator of cellular homeostasis. Through its two receptors TNFR1 and TNFR2, soluble versus membrane-bound TNF enable cell death or survival in a variety of cell types. TNF-TNFRs signaling orchestrates important biological functions such as inflammation, neuronal activity as well as tissue de- and regeneration. TNF-TNFRs signaling is a therapeutic target for neurodegenerative diseases such as multiple sclerosis (MS) and Alzheimer's disease (AD), but animal and clinical studies yielded conflicting findings. Here, we ask whether a sequential modulation of TNFR1 and TNFR2 signaling is beneficial in experimental autoimmune encephalomyelitis (EAE), an experimental mouse model that recapitulates inflammatory and demyelinating aspects of MS. To this end, human TNFR1 antagonist and TNFR2 agonist were administered peripherally at different stages of disease development in TNFR-humanized mice. We found that stimulating TNFR2 before onset of symptoms leads to improved response to anti-TNFR1 therapeutic treatment. This sequential treatment was more effective in decreasing paralysis symptoms and demyelination, when compared to single treatments. Interestingly, the frequency of the different immune cell subsets is unaffected by TNFR modulation. Nevertheless, treatment with only a TNFR1 antagonist increases T-cell infiltration in the central nervous system (CNS) and B-cell cuffing at the perivascular sites, whereas a TNFR2 agonist promotes Treg CNS accumulation. Our findings highlight the complicated nature of TNF signaling which requires a timely balance of selective activation and inhibition of TNFRs in order to exert therapeutic effects in the context of CNS autoimmunity.
 BACKGROUND: Impaired cerebrospinal fluid (CSF) homeostasis is central to the pathogenesis of idiopathic intracranial hypertension (IIH), although the precise mechanisms involved are still not completely understood. The aim of the current study was to assess the CSF/serum ratio of neurofilament light chain levels (QNfL) as a potential indicator of functional CSF outflow obstruction in IIH patients. METHODS: NfL levels were measured by single molecule array in CSF and serum samples of 87 IIH patients and in three control groups, consisting of 52 multiple sclerosis (MS) patients with an acute relapse, 21 patients with an axonal polyneuropathy (PNP), and 41 neurologically healthy controls (HC). QNfL was calculated as the ratio of CSF and serum NfL levels. Similarly, we also assessed the CSF/serum ratio of glial fibrillary acidic protein (QGFAP) levels to validate the QNfL data. Routine CSF parameters including the CSF/serum albumin ratio (QAlb) were determined in all groups. Lumbar puncture opening pressure of IIH patients was measured by manometry. RESULTS: CSF-NfL levels (r = 0.29, p = 0.008) and QNfL (0.40, p = 0.0009), but not serum NfL (S-NfL) levels, were associated with lumbar puncture opening pressure in IIH patients. CSF-NfL levels were increased in IIH patients, MS patients, and PNP patients, whereas sNfL levels were normal in IIH, but elevated in MS and PNP. Remarkably, QNfL (p < 0.0001) as well as QGFAP (p < 0.01) were only increased in IIH patients. QNfL was positively correlated with CSF-NfL levels (r = 0.51, p = 0.0012) and negatively correlated with S-NfL levels (r = - 0.51, p = 0.0012) in HC, while it was only positively associated with CSF-NfL levels in IIH patients (r = 0.71, p < 0.0001). An increase in blood-CSF barrier permeability assessed by QAlb did not lead to a decrease in QNfL in any cohort. CONCLUSIONS: The observed elevation of QNfL in IIH patients, which was associated with lumbar puncture opening pressure, indicates a reduced NfL transition from the CSF to serum compartment. This supports the hypothesis of a pressure-dependent CSF outflow obstruction to be critically involved in IIH pathogenesis.
 Endoplasmic reticulum (ER) stress and mitochondrial dysfunction are found in lesions of multiple sclerosis (MS) and animal models of MS such as experimental autoimmune encephalomyelitis (EAE), and may contribute to the neuronal loss that underlies permanent impairment. We investigated whether glatiramer acetate (GA) can reduce these changes in the spinal cords of chronic EAE mice by using routine histology, immunostaining, and electron microscopy. EAE spinal cord tissue exhibited increased inflammation, demyelination, mitochondrial dysfunction, ER stress, downregulation of NAD+ dependent pathways, and increased neuronal death. GA reversed these pathological changes, suggesting that immunomodulating therapy can indirectly induce neuroprotective effects in the CNS by mediating ER stress.
 BACKGROUND AND PURPOSE: In MS, it is common to acquire brain and spinal cord MR imaging sequences separately to assess the extent of the disease. The goal of this study was to see how replacing the traditional brain T1-weighted images (brain-T1) with an acquisition that included both the brain and the cervical spinal cord (cns-T1) affected brain- and spinal cord-derived measures. MATERIALS AND METHODS: Thirty-six healthy controls (HC) and 42 patients with MS were included. Of those, 18 HC and 35 patients with MS had baseline and follow-up at 1 year acquired on a 3T magnet. Two 3D T1-weighted images (brain-T1 and cns-T1) were acquired at each time point. Regional cortical thickness and volumes were determined with FastSurfer, and the percentage brain volume change per year was obtained with SIENA. The spinal cord area was estimated with the Spinal Cord Toolbox. Intraclass correlation coefficients (ICC) were calculated to check for consistency of measures obtained from brain-T1 and cns-T1. RESULTS: Cortical thickness measures showed an ICC >0.75 in 94% of regions in healthy controls and 80% in patients with MS. Estimated regional volumes had an ICC >0.88, and the percentage brain volume change had an ICC >0.79 for both groups. The spinal cord area measures had an ICC of 0.68 in healthy controls and 0.92 in patients with MS. CONCLUSIONS: Brain measurements obtained from 3D cns-T1 are highly equivalent to those obtained from a brain-T1, suggesting that it could be feasible to replace the brain-T1 with cns-T1.
 The spectrum of MOG-IgG-associated disease (MOGAD) includes optic neuritis (ON), myelitis (MY), acute disseminated encephalomyelitis (ADEM), brainstem encephalitis, cerebral cortical encephalitis (CE) and AQP4-IgG-negative neuromyelitis optica spectrum disorder (NMOSD). In MOGAD, MOG-IgG are usually detected in sera (MOG-IgGSERUM), but there have been some seronegative MOGAD cases with MOG-IgG in CSF (MOG-IgGCSF), and its diagnostic implications remains unclear. In this cross-sectional study, we identified patients with paired serum and CSF sent from all over Japan for testing MOG-IgG. Two investigators blinded to MOG-IgG status classified them into suspected MOGAD (ADEM, CE, NMOSD, ON, MY and Others) or not based on the current recommendations. The MOG-IgGSERUM and MOG-IgGCSF titres were assessed with serial 2-fold dilutions to determine end point titres [≥1:128 in serum and ≥1:1 (no dilution) in CSF were considered positive]. We analysed the relationship between MOG-IgGSERUM, MOG-IgGCSF and the phenotypes with multivariable regression. A total of 671 patients were tested [405 with suspected MOGAD, 99 with multiple sclerosis, 48 with AQP4-IgG-positive NMOSD and 119 with other neurological diseases (OND)] before treatment. In suspected MOGAD, 133 patients (33%) tested MOG-IgG-positive in serum and/or CSF; 94 (23%) double-positive (ADEM 36, CE 15, MY 8, NMOSD 9, ON 15 and Others 11); 17 (4.2%) serum-restricted-positive (ADEM 2, CE 0, MY 3, NMOSD 3, ON 5 and Others 4); and 22 (5.4%) CSF-restricted-positive (ADEM 3, CE 4, MY 6, NMOSD 2, ON 0 and Others 7). None of AQP4-IgG-positive NMOSD, multiple sclerosis or OND cases tested positive for MOG-IgGSERUM, but two with multiple sclerosis cases were MOG-IgGCSF-positive; the specificities of MOG-IgGSERUM and MOG-IgGCSF in suspected MOGAD were 100% [95% confidence interval (CI) 99-100%] and 99% (95% CI 97-100%), respectively. Unlike AQP4-IgG-positive NMOSD, the correlation between MOG-IgGSERUM and MOG-IgGCSF titres in MOGAD was weak. Multivariable regression analyses revealed MOG-IgGSERUM was associated with ON and ADEM, whereas MOG-IgGCSF was associated with ADEM and CE. The number needed to test for MOG-IgGCSF to diagnose one additional MOGAD case was 13.3 (14.3 for ADEM, 2 for CE, 19.5 for NMOSD, infinite for ON, 18.5 for MY and 6.1 for Others). In terms of MOG-IgGSERUM/CSF status, most cases were double-positive while including either serum-restricted (13%) or CSF-restricted (17%) cases. These statuses were independently associated with clinical phenotypes, especially in those with ON in serum and CE in CSF, suggesting pathophysiologic implications and the utility of preferential diagnostic testing. Further studies are warranted to deduce the clinical and pathological significance of compartmentalized MOG-IgG.
 IMPORTANCE: In patients with multiple sclerosis (MS), factors associated with severe COVID-19 include anti-CD20 therapies and neurologic disability, but it is still unclear whether these 2 variables are independently associated with severe COVID-19 or whether the association depends on MS clinical course. OBJECTIVE: To assess the association between anti-CD20 therapies and COVID-19 severity in patients with relapsing-remitting MS (RRMS) and progressive MS (PMS). DESIGN, SETTING, AND PARTICIPANTS: This multicenter, retrospective cohort study used data from the COVISEP study, which included patients with MS and COVID-19 from February 1, 2020, to June 30, 2022, at 46 French MS expert centers, general hospitals, and private neurology practices. Eligible patients with RRMS were those treated with high-efficacy MS therapy (ie, anti-CD20, fingolimod, or natalizumab), and eligible patients with PMS were those younger than 70 years with an Expanded Disability Status Scale (EDSS) score of 8 or lower. Patients were monitored from COVID-19 symptom onset until recovery or death. EXPOSURES: Current anti-CD20 therapy (ocrelizumab or rituximab). MAIN OUTCOMES AND MEASURES: The main outcome was severe COVID-19 (ie, hospitalization with any mode of oxygenation or death). All analyses were conducted separately in patients with RRMS and PMS using propensity score-weighted logistic regression. Subgroup analyses were performed according to COVID-19 vaccine status, sex, EDSS score, and age. RESULTS: A total of 1400 patients, 971 with RRMS (median age, 39.14 years [IQR, 31.38-46.80 years]; 737 [76.1%] female) and 429 with PMS (median age, 54.21 years [IQR, 48.42-60.14 years]; 250 [58.3%] female) were included in the study. A total of 418 patients with RRMS (43.0%) and 226 with PMS (52.7%) were treated with anti-CD20 therapies. In weighted analysis, 13.4% and 2.9% of patients with RRMS treated and not treated with anti-CD20 had severe COVID-19, respectively, and anti-CD20 treatment was associated with increased risk of severe COVID-19 (odds ratio [OR], 5.20; 95% CI, 2.78-9.71); this association persisted among vaccinated patients (7.0% vs 0.9%; OR, 8.85; 95% CI, 1.26-62.12). Among patients with PMS, 19.0% and 15.5% of patients treated and not treated with anti-CD20 had severe COVID-19, respectively, and there was no association between anti-CD20 treatment and severe COVID-19 (OR, 1.28; 95% CI, 0.76-2.16). In PMS subgroup analysis, anti-CD20 exposure interacted negatively with EDSS score (P = .009 for interaction) and age (P = .03 for interaction); anti-CD20 therapies were associated with risk of severe COVID-19 only in patients with less neurologic disability and younger patients with PMS. CONCLUSIONS AND RELEVANCE: In this cohort study, risk of severe COVID-19 was higher in patients with PMS than in those with RRMS. Use of anti-CD20 therapies was associated with an increased risk of severe COVID-19 among patients with RRMS. In patients with PMS, there was no association between anti-CD20 therapies and risk of severe COVID-19.
 BACKGROUND AND OBJECTIVES: Patients of low individual socioeconomic status (SES) are at a greater risk of unfavorable health outcomes. However, the association between neighborhood socioeconomic deprivation and health outcomes for patients with neurologic disorders has not been studied at the population level. Our objective was to determine the association between neighborhood socioeconomic deprivation and 30-day mortality and readmission after hospitalization for various neurologic conditions. METHODS: This was a retrospective study of nationwide Medicare claims from 2017 to 2019. We included patients older than 65 years hospitalized for the following broad categories based on diagnosis-related groups (DRGs): multiple sclerosis and cerebellar ataxia (DRG 058-060); stroke (061-072); degenerative nervous system disorders (056-057); epilepsy (100-101); traumatic coma (082-087), and nontraumatic coma (080-081). The exposure of interest was neighborhood SES, measured by the area deprivation index (ADI), which uses socioeconomic indicators, such as educational attainment, unemployment, infrastructure access, and income, to estimate area-level socioeconomic deprivation at the level of census block groups. Patients were grouped into high, middle, and low neighborhood-level SES based on ADI percentiles. Adjustment covariates included age, comorbidity burden, race/ethnicity, individual SES, and sex. RESULTS: After exclusions, 905,784 patients were included in the mortality analysis and 915,993 were included in the readmission analysis. After adjustment for age, sex, race/ethnicity, comorbidity burden, and individual SES, patients from low SES neighborhoods had higher 30-day mortality rates compared with patients from high SES neighborhoods for all disease categories except for multiple sclerosis: magnitudes of the effect ranged from an adjusted odds ratio of 2.46 (95% CI 1.60-3.78) for the nontraumatic coma group to 1.23 (95% CI 1.19-1.28) for the stroke group. After adjustment, no significant differences in readmission rates were observed for any of the groups. DISCUSSION: Neighborhood SES is strongly associated with 30-day mortality for many common neurologic conditions even after accounting for baseline comorbidity burden and individual SES. Strategies to improve health equity should explicitly consider the effect of neighborhood environments on health outcomes.
 Anti-glycolipid antibodies have been reported to play pathogenic roles in peripheral inflammatory neuropathies, such as Guillain-Barré syndrome. On the other hand, the role in multiple sclerosis (MS), inflammatory demyelinating disease in the central nervous system (CNS), is largely unknown, although the presence of anti-glycolipid antibodies was reported to differ among MS patients with relapsing-remitting (RR), primary progressive (PP), and secondary progressive (SP) disease courses. We investigated whether the induction of anti-glycolipid antibodies could differ among experimental MS models with distinct clinical courses, depending on induction methods. Using three mouse strains, SJL/J, C57BL/6, and A.SW mice, we induced five distinct experimental autoimmune encephalomyelitis (EAE) models with myelin oligodendrocyte glycoprotein (MOG)(35-55), MOG(92-106), or myelin proteolipid protein (PLP)(139-151), with or without an additional adjuvant curdlan injection. We also induced a viral model of MS, using Theiler's murine encephalomyelitis virus (TMEV). Each MS model had an RR, SP, PP, hyperacute, or chronic clinical course. Using the sera from the MS models, we quantified antibodies against 11 glycolipids: GM1, GM2, GM3, GM4, GD3, galactocerebroside, GD1a, GD1b, GT1b, GQ1b, and sulfatide. Among the MS models, we detected significant increases in four anti-glycolipid antibodies, GM1, GM3, GM4, and sulfatide, in PLP(139-151)-induced EAE with an RR disease course. We also tested cellular immune responses to the glycolipids and found CD1d-independent lymphoproliferative responses only to sulfatide with decreased interleukin (IL)-10 production. Although these results implied that anti-glycolipid antibodies might play a role in remissions or relapses in RR-EAE, their functional roles need to be determined by mechanistic experiments, such as injections of monoclonal anti-glycolipid antibodies.
 Multiple sclerosis (MS) is an autoimmune disease driven by lymphocyte activation against myelin autoantigens in the central nervous system leading to demyelination and neurodegeneration. The deoxyribonucleoside salvage pathway with the rate-limiting enzyme deoxycytidine kinase (dCK) captures extracellular deoxyribonucleosides for use in intracellular deoxyribonucleotide metabolism. Previous studies have shown that deoxyribonucleoside salvage activity is enriched in lymphocytes and required for early lymphocyte development. However, specific roles for the deoxyribonucleoside salvage pathway and dCK in autoimmune diseases such as MS are unknown. Here we demonstrate that dCK activity is necessary for the development of clinical symptoms in the MOG(35-55) and MOG(1-125) experimental autoimmune encephalomyelitis (EAE) mouse models of MS. During EAE disease, deoxyribonucleoside salvage activity is elevated in the spleen and lymph nodes. Targeting dCK with the small molecule dCK inhibitor TRE-515 limits disease severity when treatments are started at disease induction or when symptoms first appear. EAE mice treated with TRE-515 have significantly fewer infiltrating leukocytes in the spinal cord, and TRE-515 blocks activation-induced B and T cell proliferation and MOG(35-55) -specific T cell expansion without affecting innate immune cells or naïve T and B cell populations. Our results demonstrate that targeting dCK limits symptoms in EAE mice and suggest that dCK activity is required for MOG(35-55) -specific lymphocyte activation-induced proliferation.
 Experimental autoimmune encephalomyelitis (EAE) is an induced autoimmune disease widely used as an animal model for multiple sclerosis, which is mainly characterized by demyelination, axonal loss, as well as neurodegeneration of central nervous system (CNS). T-helper (Th) 17 cell that generate interleukin-17 (IL-17) plays a key role in its pathogenesis. Their activity and differentiation are tightly regulated by some cytokines and transcription factors. Certain microRNAs (miRNAs) are involved in the pathogenesis of various autoimmune disorders, including EAE. Our research detected a novel miRNA that can regulate EAE. According to the results, during EAE, the expression of miR-485 notably lowered, and STAT3 was significantly increased. It was discovered that miR-485 knockdown in vivo upregulated Th17-associated cytokines and aggravated EAE, while the overexpressed miR-485 down-regulated Th17-associated cytokines and mitigated EAE. The up-regulation of miRNA-485 in vitro inhibited Th17-associated cytokines expression within EAE CD4+ T cells. Furthermore, as revealed by target prediction and dual-luciferase reporter assays, miR-485 directly targets STAT3, a gene that encodes a protein responsible for Th17 generation. Overall, miR-485 exert vital functions in Th17 generation and EAE pathogenesis.
 INTRODUCTION: The objective was to assess the immunogenicity and effectiveness of vaccines against SARSCoV-2 in multiple sclerosis (MS) patients included in the Argentinean MS registry. METHODS: A prospective cohort study between May and December 2021. The primary outcome was immunogenicity and effectiveness of vaccines during a three-month follow-up. Immunogenicity was evaluated based on detection of total antibodies (Ab) against spike protein and neutralizing Ab in serum 4 weeks after the second vaccine dose. A positive COVID-19 case was defined according to Argentinean Ministry of Health. RESULTS: 94 patients were included, mean age: 41.7 ± 12.1 years. Eighty (85.1%) had relapsing remitting multiple sclerosis (RRMS); 30 (31.9%) were under fingolimod treatment. The Sputnik V vaccine was the first dose in 33 (35.1%), and AstraZeneca in 61 (64.9%). In 60 (63.8%), the vaccine elicited a specific humoral response. Immunological response according to the vaccination schemes showed no qualitative differences (p = 0.45). Stratified analysis according to the MS treatment showed that a significantly smaller number of subjects developed antibodies against spike antigen among those that were on ocrelizumab compared to other groups (p = 0.001), while a reduced number of patients under ocrelizumab where evaluated (n = 7). This was also observed for neutralizing antibodies in the ocrelizumab group (p < 0.001). During the three-month follow-up, two individuals were diagnosed with COVID-19. CONCLUSION: We found that MS patients that received Sputnik V or AstraZeneca vaccines for SARS-CoV-2 developed a serological response with no differences between the vaccines used.
 Mesenchymal stem cells (MSCs) are a type of versatile adult stem cells present in various organs. These cells give rise to extracellular vesicles (EVs) containing a diverse array of biologically active elements, making them a promising approach for therapeutics and diagnostics. This article examines the potential therapeutic applications of MSC-derived EVs in addressing neurodegenerative disorders such as Alzheimer's disease (AD), multiple sclerosis (MS), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD). Furthermore, the present state-of-the-art for MSC-EV-based therapy in AD, HD, PD, ALS, and MS is discussed. Significant progress has been made in understanding the etiology and potential treatments for a range of neurodegenerative diseases (NDs) over the last few decades. The contents of EVs are carried across cells for intercellular contact, which often results in the control of the recipient cell's homeostasis. Since EVs represent the therapeutically beneficial cargo of parent cells and are devoid of many ethical problems connected with cell-based treatments, they offer a viable cell-free therapy alternative for tissue regeneration and repair. Developing innovative EV-dependent medicines has proven difficult due to the lack of standardized procedures in EV extraction processes as well as their pharmacological characteristics and mechanisms of action. However, recent biotechnology and engineering research has greatly enhanced the content and applicability of MSC-EVs.
 CONTEXT: Serum neurofilament light chain (sNfL) levels are biomarkers of neuroaxonal injury in multiple neurological diseases. OBJECTIVE: Given the paucity of data on the distribution of sNfL levels in the general population, in the present study we identified predictors of sNfL levels in a community setting and investigated the association between diabetes and sNfL. METHODS: sNfL levels were measured in 2070 people aged 20 to 75 years from the general US population (275 with and 1795 without diabetes) that participated in the 2013-2014 cycle of the National Health and Nutrition Examination Survey. We evaluated the association between diabetes and sNfL levels after adjustment for age, sex, race-ethnicity, alcohol use, and kidney function using a multivariable linear regression model. Cognitive function was evaluated in a subset of participants aged 60 to 75 years using the Consortium to Establish a Registry for Alzheimer's Disease-Word Learning test, the Animal Fluency test, and the Digit Symbol Substitution test. RESULTS: The weighted prevalence of diabetes was 10.4% (95% CI, 9.0-11.9). In each age stratum, patients with diabetes exhibited higher sNfL levels compared with nondiabetic participants. Age, proportion of males, prevalence of diabetes, and homeostatic model of insulin resistance increased progressively across quartiles of sNfL levels in the overall population, whereas estimated glomerular filtration rate (eGFR) showed an opposite trend. In the multivariable model, age, sex, eGFR, alcohol use and diabetes were significantly associated with sNfL levels. Moreover, higher sNfL levels were associated with worse performance in all 3 cognitive function tests. CONCLUSION: Diabetes is associated with higher sNfL. Further large-scale and prospective studies are needed to replicate our results and evaluate the ability of sNfL to predict the incidence of neuropathy and dementia in this patient population.
 BACKGROUND: The most common non-traumatic neurological disease in young- and middle-aged adults is multiple sclerosis (MS), leading to central nervous system (CNS) atrophy and neurological disorders with loss of myelin and axonal degeneration. Due to the inadequate efficiency of common treatments, some natural products with antioxidant properties such as Carvacrol have been considered. OBJECTIVE: the present study aimed to investigate carvacrol's anti-inflammatory and therapeutic effects on MS symptoms in healthy and experimental autoimmune encephalomyelitis (EAE) induced female Lewis rats. METHODS: The study was performed in three groups of Lewis rats: control group, EAE model, and EAE treated with carvacrol (carvacrol-treated group). The treatment group received 25 mg/kg of carvacrol intraperitoneally daily. Histologic examination and expression analysis of pro-inflammatory genes (Interleukin-1 and 17 (IL-1 and IL-17), Nuclear Factor Kappa B Cells (NF-κB) and Tumor Necrosis Factor-α (TNF-α)), myelin repair, and also regeneration genes (Myelin basic protein (MBP), Oligodendrocyte Transcription Factor 2 (OLIG2) and Platelet-Derived Growth Factor Receptor α (PDGFR-α)) were carried out. Gene studies, Hematoxylin and Eosin (H&E), and Luxol fast blue stain were performed in the lumbar region of the spinal cord. RESULTS: The EAE clinical scores in the carvacrol-treated group were lower than in untreated rats (P < 0.001). The expression of two genes, IL-17 and MBP, was confirmed using fluorescence immunohistochemistry (FIHC). A significant decrease was observed in NF-κB and IL-17, and IL-1 gene expression. The MBP and OLIG2 gene expression was increased in the carvacrol-treated group (p < 0.001). In EAE, PDGFR-α expression increased about four times. However, carvacrol administration did not affect PDGFR-α and TNF-α gene expression. In this treatment, H&E staining of spinal cord regions showed a significant decrease in inflammatory cell infiltration. Moreover, immunostaining analysis demonstrated a considerable increase in MBP and a reduction in IL-17 secretion. CONCLUSION: The results showed that carvacrol administration reduces the entry of inflammatory cells into the CNS by stimulating myelination-related processes employing increasing the expression of genes involved in myelin repair and reducing the expression of inflammatory genes. Our findings confirm that carvacrol improves the clinical and pathological symptoms of EAE through its therapeutic and modification properties as a potential adjunctive therapy and needs to be studied more.
 BACKGROUND AND PURPOSE: Epstein-Barr virus (EBV) is implicated in multiple sclerosis (MS) risk; evidence for other herpesviruses is inconsistent. Here, we test blood markers of infection with human herpesvirus 6 (HHV-6), varicella zoster virus (VZV), and cytomegalovirus (CMV) as risk factors for a first clinical diagnosis of central nervous system demyelination (FCD) in the context of markers of EBV infection. METHODS: In the Ausimmune case-control study, cases had an FCD, and population controls were matched on age, sex, and study region. We quantified HHV-6- and VZV-DNA load in whole blood and HHV-6, VZV, and CMV antibodies in serum. Conditional logistic regression tested associations with FCD risk, adjusting for Epstein-Barr nuclear antigen (EBNA) IgG, EBV-DNA load, and other covariates. RESULTS: In 204 FCD cases and 215 matched controls, only HHV-6-DNA load (positive vs. negative) was associated with FCD risk (adjusted odds ratio = 2.20, 95% confidence interval = 1.08-4.46, p = 0.03). Only EBNA IgG and HHV-6-DNA positivity were retained in a predictive model of FCD risk; the combination had a stronger association than either alone. CMV-specific IgG concentration modified the association between an MS risk-related human leucocyte antigen gene and FCD risk. Six cases and one control had very high HHV-6-DNA load (>1.0 × 10(6) copies/mL). CONCLUSIONS: HHV-6-DNA positivity and high load (possibly due to inherited HHV-6 chromosomal integration) were associated with increased FCD risk, particularly in association with markers of EBV infection. With growing interest in prevention/management of MS through EBV-related pathways, there should be additional consideration of the role of HHV-6 infection.
 BACKGROUND: The SARS-CoV-2 Omicron variant appears to cause milder infections, however, its capacity for immune evasion and high transmissibility despite vaccination remains a concern, particularly in immunosuppressed patients. Herein, we investigate the incidence and risk factors for COVID-19 infection in vaccinated adult patients with Multiple Sclerosis (MS), Aquaporin-4-antibody Neuromyelitis Optica Spectrum Disorder (AQP4-Ab NMOSD), and Myelin Oligodendrocyte Glycoprotein-antibody associated disease (MOGAD) during the Omicron subvariant BA.1/2 wave in Singapore. METHODS: This was a prospective observational study conducted at the National Neuroscience Institute, Singapore. Only patients who had at least two doses of mRNA vaccines were included. Data on demographics, disease characteristics, COVID-19 infections and vaccinations, and immunotherapies were collected. SARS-CoV-2 neutralising antibodies were measured at various time points after vaccination. RESULTS: Two hundred and one patients were included; 47 had COVID-19 infection during the study period. Multivariable logistic regression revealed that receipt of a third SARS-CoV-2 mRNA vaccination (V3) was protective against COVID-19 infection. No particular immunotherapy group increased the risk of infection, however, Cox proportional-hazards regression showed that patients on anti-CD20s and sphingosine-1-phosphate modulators (S1PRMs) had a shorter time to infection after V3, compared to those on other immunotherapies or not on immunotherapy. CONCLUSIONS: The Omicron subvariant BA.1/2 is highly infectious in patients with central nervous system inflammatory diseases; three doses of mRNA vaccination improved protection. However, treatment with anti-CD20s and S1PRMs predisposed patients to earlier infection. Future studies are required to determine the protective efficacy of newer bivalent vaccines that target the Omicron (sub)variant, especially in immunocompromised patients.
 Immune cell function is critically dependent on precise control over transcriptional output from the genome. In this respect, integration of environmental signals that regulate gene expression, specifically by transcription factors, enhancer DNA elements, genome topography and non-coding RNAs (ncRNAs), are key components. The first three have been extensively investigated. Even though non-coding RNAs represent the vast majority of cellular RNA species, this class of RNA remains historically understudied. This is partly because of a lag in technological and bioinformatic innovations specifically capable of identifying and accurately measuring their expression. Nevertheless, recent progress in this domain has enabled a profusion of publications identifying novel sub-types of ncRNAs and studies directly addressing the function of ncRNAs in human health and disease. Many ncRNAs, including circular and enhancer RNAs, have now been demonstrated to play key functions in the regulation of immune cells and to show associations with immune-mediated diseases. Some ncRNAs may function as biomarkers of disease, aiding in diagnostics and in estimating response to treatment, while others may play a direct role in the pathogenesis of disease. Importantly, some are relatively stable and are amenable to therapeutic targeting, for example through gene therapy. Here, we provide an overview of ncRNAs and review technological advances that enable their study and hold substantial promise for the future. We provide context-specific examples by examining the associations of ncRNAs with four prototypical human autoimmune diseases, specifically rheumatoid arthritis, psoriasis, inflammatory bowel disease and multiple sclerosis. We anticipate that the utility and mechanistic roles of these ncRNAs in autoimmunity will be further elucidated in the near future.
 BACKGROUND: Central nervous system inflammatory demyelinating diseases (CNSIDDs) have notable interracial heterogeneity. The epidemiology of CNSIDDs in Thailand, a mainland Southeast Asian country, is unknown. OBJECTIVES: To determine the cumulative incidence, point prevalence, and disease burden of neuromyelitis optica spectrum disorder (NMOSD) and other CNSIDDs in Thailand using population-based data of Chumphon. METHODS: Searching for CNSIDD patients at a public secondary care hospital in Chumphon, the only neurology center in the province, from January 2016 to December 2021 was implemented using relevant ICD-10-CM codes. All diagnoses were individually ascertained by a retrospective chart review. Cumulative incidence, point prevalence, attack rate, mortality rate, and disability-adjusted life years (DALYs) were calculated. RESULTS: Aquaporin 4-IgG-positive NMOSD was the most prevalent CNSIDD in the Thai population at 3.08 (1.76-5.38) per 100,000 persons. The prevalence of multiple sclerosis (MS) followed at 0.77 (0.26-2.26) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) at 0.51(0.14-1.87) per 100,000 adults. In the pediatric population, the incidence of acute disseminated encephalomyelitis was 0.28 (0.08-1.02) per 100,000 persons/year. Among other idiopathic demyelinating diseases, idiopathic optic neuritis had the highest incidence at 0.58 (0.24-0.92) per 100,000 persons/year, followed by acute transverse myelitis at 0.44 (0.14-0.74). Idiopathic demyelinating brainstem syndrome was also observed at 0.04 (0.01-0.25) per 100,000 persons/year. Although most had a fair recovery, disability was worst among NMOSD patients with DALYs of 3.61 (3.00-4.36) years per 100,000 persons. Mortality rate was the highest in NMOSD as well. CONCLUSION: CNSIDDs are rare diseases in Thailand. The prevalence is comparable to that of East Asian populations. A nationwide CNSIDDs registry would better elaborate the epidemiology of these diseases.
 The exact mechanisms of the evolution of multiple sclerosis are still unknown. At the same time, the development in C57BL/6 mice of experimental autoimmune encephalomyelitis (EAE, simulating human multiple sclerosis) happens as a result of the violation of bone marrow hematopoietic stem cell differentiation profiles integrated with the production of toxic auto-antibodies splitting the basic myelin protein, myelin oligodendrocyte glycoprotein (MOG), histones, and DNA. It has been shown that IgGs from the plasma of healthy humans and autoimmune patients oxidize many different compounds due to their peroxidase (H(2)O(2)-dependent) and oxidoreductase (H(2)O(2)-independent) activities. Here, we first analyzed the changes in the relative catalase activity of IgGs from C57BL/6 mice blood plasma over time at different stages of the EAE development (onset, acute, and remission phases). It was shown that the catalase activity of IgGs of 3-month-old mice is, on average, relatively low (k(cat) = 40.7 min(-1)), but it increases during 60 days of spontaneous development of EAE 57.4-fold (k(cat) = 2.3 × 10(3) min(-1)). The catalase activity of antibodies increases by a factor of 57.4 by 20 days after the immunization of mice with MOG (k(cat) = 2.3 × 10(3) min(-1)), corresponding to the acute phase of EAE development, and 52.7-fold by 60 days after the treatment of mice with a DNA-histone complex (k(cat) = 2.1 × 10(3) min(-1)). It is the acceleration of the EAE development after the treatment of mice with MOG that leads to the increased production of lymphocytes synthesizing antibodies with catalase activity. All data show that the IgGs' catalase activity can play an essential role in reducing the H(2)O(2) concentration and protecting mice from oxidative stress.
 BACKGROUND: As far as 80% of people diagnosed with multiple sclerosis (MS) experience disabling symptoms in the course of the disease, such as spasticity and neuropathic pain. As first-line symptomatic therapy is associated with important adverse reactions, cannabinoids have become increasingly popular among patients with MS. This review intends to provide an overview of the evidence of the role of cannabinoids in treating symptoms related to MS and to encourage further research on this matter. AREAS OF UNCERTAINTY: To date, the evidence supporting the role of cannabis and its derivatives in alleviating the MS-related symptoms comes only from studies on experimental models of demyelination. To the best of our knowledge, relatively few clinical trials inquired about the therapeutic effects of cannabinoids on patients with MS, with variable results. DATA SOURCES: We conducted a literature search through PubMed and Google Scholar from the beginning until 2022. We included articles in English describing the latest findings regarding the endocannabinoid system, the pharmacology of cannabinoids, and their therapeutic purpose in MS. RESULTS: Evidence from preclinical studies showed that cannabinoids can limit the demyelination process, promote remyelination, and have anti-inflammatory properties by reducing immune cell infiltration of the central nervous system in mice with experimental autoimmune encephalomyelitis. Moreover, it has been established that experimental autoimmune encephalomyelitis mice treated with cannabinoids experienced a significant reduction of symptoms and slowing of the disease progression. Given the complexity of human immune and nervous systems, cannabinoids did not have the anticipated effects on human subjects. However, data obtained from clinical trials showed some beneficial results of cannabinoids as a single or as add-on therapy in reducing the spasticity and pain related to MS. CONCLUSION: Considering their various mechanisms of action and good tolerability, cannabinoids remain an interesting therapy for spasticity and chronic pain related to MS.
 BACKGROUND AND OBJECTIVES: The B cell-depleting anti-CD20 antibody ocrelizumab (OCR) effectively reduces MS disease activity and slows disability progression. Given the role of B cells as antigen-presenting cells, the primary goal of this study was to evaluate the effect of OCR on the T-cell receptor repertoire diversity. METHODS: To examine whether OCR substantially alters the molecular diversity of the T-cell receptor repertoire, deep immune repertoire sequencing (RepSeq) of CD4(+) and CD8(+) T-cell receptor β-chain variable regions was performed on longitudinal blood samples. The IgM and IgG heavy chain variable region repertoire was also analyzed to characterize the residual B-cell repertoire under OCR treatment. RESULTS: Peripheral blood samples for RepSeq were obtained from 8 patients with relapsing MS enrolled in the OPERA I trial over a period of up to 39 months. Four patients each were treated with OCR or interferon β1-a during the double-blind period of OPERA I. All patients received OCR during the open-label extension. The diversity of the CD4(+)/CD8(+) T-cell repertoires remained unaffected in OCR-treated patients. The expected OCR-associated B-cell depletion was mirrored by reduced B-cell receptor diversity in peripheral blood and a shift in immunoglobulin gene usage. Despite deep B-cell depletion, longitudinal persistence of clonally related B-cells was observed. DISCUSSION: Our data illustrate that the diversity of CD4(+)/CD8(+) T-cell receptor repertoires remained unaltered in OCR-treated patients with relapsing MS. Persistence of a highly diverse T-cell repertoire suggests that aspects of adaptive immunity remain intact despite extended anti-CD20 therapy. TRIAL REGISTRATION INFORMATION: This is a substudy (BE29353) of the OPERA I (WA21092; NCT01247324) trial. Date of registration, November 23, 2010; first patient enrollment, August 31, 2011.
 BACKGROUND: Fabry disease is an inherited metabolic disorder with various symptoms. Neurological manifestations are small fiber neuropathy, cerebral white matter lesions (WML), megadolicho basilar artery, and stroke. The relevance of the D313Y variant in the galactosidase alpha gene is controversially discussed. OBJECTIVES: We aimed at elucidating the implications of this differential diagnosis of multiple sclerosis (MS), focussing on the analysis of WML over time and correlations with other markers. METHODS: We reviewed retrospectively the clinical, laboratory, and magnetic resonance imaging data of 21 carriers of the D313Y variant at a single German outpatient clinic for MS between 2004 and 2021. RESULTS: In our cohort (15 females, 6 males), mean age at diagnosis was 44.1 ± 16.3 years, and mean follow-up duration was 3.1 ± 3.9 years. WML were rated on both, the Fazekas scale and the age-related white matter changes rating scale, and were of variable interindividual extent. Follow-up imaging showed virtually no progress. WML did not correlate with the severity of clinical findings or lysoGb3 levels. Symptomatic carriers of the variant are characterized by an almost complete lack of internal organ manifestations and laboratory findings, usually associated with Fabry disease. CONCLUSION: WML in carriers of the D313Y variant do not seem to be suitable for assessing or predicting the (para-) clinical status. Concerning MS patients, the variant and its clinical signs can be a differential diagnosis, but also a co-factor. Imaging and cerebrospinal fluid findings facilitate the distinction between both entities.
 Multiple sclerosis (MS) is a chronic disease and one of the leading causes of disability in young adults. The current study aims to investigate the pathogenesis of MS via studying the regulatory role of novel lncRNA MAGI2-AS3 in miR-374b-5p and their downstream targets PTEN/AKT/IRF-3/IFN-β and the relationship of this pathway with disease severity. Moreover, it aims to assess the role of MAGI2-AS3/miR-374b-5p as diagnostic and/or prognostic biomarkers for MS. Overall, 150 contributors were recruited: 100 patients with MS and 50 healthy volunteers. Gene expression of MAGI2-AS3, miR-374b-5p, PTEN, AKT, and IRF-3 were assessed using RT-qPCR, and IFN-β was measured by ELISA. Compared with the healthy control group, serum MAGI2-AS3 and PTEN were downregulated in MS patients, whereas miR-374b-5p, PI3K, AKT, IRF-3, and IFN-β were upregulated in MS patients. Furthermore, MAGI2-AS3 was downregulated, while miR-374b-5p was upregulated in MS patients with an expanded disability status scale (EDSS) ≥3.5, compared to patients with an EDSS <3.5. Receiver-operating-characteristic curve analysis revealed that MAGI2-AS3 and miR-374b-5p can be used in the diagnosis of MS. Remarkably, multivariate logistic analysis revealed that MAGI2-AS3, miR-374b-5p, PTEN, and AKT act as independent variables in MS. Moreover, MAGI2-AS3 was directly correlated with PTEN and inversely correlated with miR-374b-5p, AKT, and EDSS. Regarding miR-374b-5p, it was positively correlated with AKT and EDSS. In conclusion, the study showed for the first time that the crosstalk between MAGI2-AS3 and miR-374b-5p could affect the AKT/IRF3/IFN-β axis in MS. Interestingly, MAGI2-AS3 and miR-374b-5p could be genetic noninvasive biomarkers for MS.
 BACKGROUND: Several reports have been documented in possible association with the administration of different severe acute respiratory coronavirus 2 (SARS-CoV-2) vaccines and central nervous system (CNS)demyelinating disorders, specifically post mRNA vaccines. We report twelve cases of developing Multiple sclerosis (MS) or Neuromyelitis Optica spectrum disorders (NMOSD) following neither the first nor second dose of inactivated or viral vector COVID-19 vaccine. METHODS: We retrospectively compiled twelve patients' medical information with a new onset of MS or NMOSD in their first six weeks following a COVID-19 vaccine. RESULTS: We report twelve cases of MS (n = 9), clinically isolated syndrome (CIS)(n = 1), and NMOSD (n = 2) following COVID-19 inactivated vaccines (n = 11) or viral vector vaccines (n = 1), within some days following either the first (n = 3), second dose (n = 8), or third dose (n = 1). Their median age was 33.3 years, ranging from 19 to 53 years. Ten were women (83 %). All patients fully (n = 5) or partially (n = 2) recovered after receiving 3 doses of Corticosteroids. Common medications were Natalizumab, Teriflunomide, Dimethyl fumarate, and Rituximab. Also, Interferon beta 1-a was administered to one patient with severe symptoms of numbness. CONCLUSION: Our case series identifies the Sinopharm BBIBP-CorV and the AstraZeneca AZD1222 vaccines as potential triggers for CNS demyelinating diseases. Vaccine administration routines are not affected by these rare and coincidental events. However, these manifestations are not deniable and require serious attention. Further investigations are needed to clarify the actual mechanisms and real associations.
 The central nervous system (CNS) exploits anticipatory (APAs) and compensatory (CPAs) postural adjustments to maintain the balance. The postural adjustments comprising stability of the center of mass (CoM) and the pressure distribution of the body influence each other if there is a lack of performance in either of them. Any predictable or sudden perturbation may pave the way for the divergence of CoM from equilibrium and inhomogeneous pressure distribution of the body. Such a situation is often observed in the daily lives of Multiple Sclerosis (MS) patients due to their poor APAs and CPAs and induces their falls. The way of minimizing the risk of falls in neurological patients is by utilizing perturbation-based rehabilitation, as it is efficient in the recovery of the balance disorder. In light of the findings, we present the design, implementation, and experimental evaluation of a novel 3 DoF parallel manipulator to treat the balance disorder of MS. The robotic platform allows angular motion of the ankle based on its anthropomorphic freedom. Moreover, the end-effector endowed with upper and lower platforms is designed to evaluate both the pressure distribution of each foot and the CoM of the body, respectively. Data gathered from the platforms are utilized to both evaluate the performance of the patients and used in high-level control of the robotic platform to regulate the difficulty level of tasks. In this study, kinematic and dynamic analyses of the robot are derived and validated in the simulation environment. Low-level control of the first prototype is also successfully implemented through the PID controller. The capacity of each platform is evaluated with a set of experiments considering the assessment of pressure distribution and CoM of the foot-like objects on the end-effector. The experimental results indicate that such a system well-address the need for balance skill training and assessment through the APAs and CPAs.
 BACKGROUND: Evidence indicates a strong link between Zika virus (ZikV) and neurological complications. Acute myelitis, optic neuritis, polyneuropathy, and encephalomyelitis that mimic inflammatory idiopathic demyelination disorders (IIDD) after ZikV infection have been reported in Brazil. OBJECTIVE: The present study aims to investigate the possible occurrence of molecular mimicry between ZikV antigens and Multiple Sclerosis (MS) autoantigens, the most frequent IIDD of the central nervous system (CNS). METHODS: A retrospective cohort study with 305 patients admitted due to suspected arbovirus infection in Rio de Janeiro was performed, all subjects were submitted to neurological examination, and a biological sample was collected for serologic and molecular diagnostic. Bioinformatics tools were used to analyze the peptides shared between ZikV antigens and MS autoantigens. RESULTS: Of 305 patients, twenty-six were positive for ZikV and 4 presented IDD patterns found in MS cases. Sequence homology comparisons by bioinformatics approach between NS5 ZikV and PLP MS protein revealed a homology of 5/6 consecutive amino acids (CSSVPV/CSAVPV) with 83% identity, deducing a molecular mimicry. Analysis of the 3D structures revealed a similar conformation with alpha helix presentation. CONCLUSIONS: Molecular mimicry between NS5 Zika virus antigen and PLP MS autoantigens emerge as a possible mechanism for IDD spectrum in genetically susceptible individuals.
 Optic neuritis (ON) is one of the most frequently seen neuro-ophthalmic causes of vision loss worldwide. Typical ON is often idiopathic or seen in patients with multiple sclerosis, which is well described in the landmark clinical trial, the Optic Neuritis Treatment Trial (ONTT). However, since the completion of the ONTT, there has been the discovery of aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies, which are biomarkers for neuromyelitis optica spectrum disorder (NMOSD) and MOG antibody-associated disease (MOGAD), respectively. These disorders are associated with atypical ON that was not well characterised in the ONTT. The severity, rate of recurrence and overall outcome differs in these two entities requiring prompt and accurate diagnosis and management. This review will summarise the characteristic neuro-ophthalmological signs in NMOSD and MOGAD, serological markers and radiographic findings, as well as acute and long-term therapies used for these disorders.
 BACKGROUND AND OBJECTIVES: Some disease-modifying treatments impair response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines in multiple sclerosis (MS), potentially increasing the risk of breakthrough infections. We aimed to investigate longitudinal SARS-CoV-2 antibody dynamics and memory B cells after 2 and 3 messenger RNA (mRNA) vaccine doses and their association with the risk of COVID-19 in patients with MS on different treatments over 1 year. METHODS: Prospective observational cohort study in patients with MS undergoing SARS-CoV-2 mRNA vaccinations. Antispike (anti-S) immunoglobulin G (IgG) titers were measured by chemiluminescence microparticle immunoassay. Frequencies of spike-specific memory B cells were measured on polyclonal stimulation of peripheral blood mononuclear cells and screening of secreted antibodies by ELISA. RESULTS: We recruited 120 patients with MS (58 on anti-CD20 antibodies, 9 on sphingosine 1-phosphate (S1P) receptor modulators, 15 on cladribine, 24 on teriflunomide (TFL), and 14 untreated) and collected 392 samples up to 10.8 months after 2 vaccine doses. When compared with untreated patients, anti-CD20 antibodies (β = -2.07, p < 0.001) and S1P modulators (β = -2.02, p < 0.001) were associated with lower anti-S IgG, while TFL and cladribine were not. Anti-S IgG decreased with months since vaccine (β = -0.14, p < 0.001), independently of treatments. Within anti-CD20 patients, anti-S IgG remained higher in those with greater baseline B-cell counts and were not influenced by postvaccine anti-CD20 infusions. Anti-S IgG increase after a 3rd vaccine was mild on anti-CD20 and S1P modulators. Spike-specific memory B-cell responses were weaker on S1P modulators and anti-CD20 than on TFL and influenced by postvaccine anti-CD20 infusions. The frequency of breakthrough infections was comparable between DMTs, but the risk of COVID-19 was predicted by the last measured anti-S IgG titer before infection (OR = 0.56, 95% CI = 0.37-0.86, p = 0.008). DISCUSSION: Postvaccine anti-S IgG titers decrease over time regardless of MS treatment and are associated with breakthrough COVID-19. Both humoral and specific memory B-cell responses are diminished on S1P modulators. Within anti-CD20-treated patients, B-cell count at first vaccine determines anti-S IgG production, whereas postvaccine anti-CD20 infusions negatively affect spike-specific memory B cells.
 Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by focal inflammatory lesions and prominent demyelination. Even though the currently available therapies are effective in treating the initial stages of disease, they are unable to halt or reverse disease progression into the chronic progressive stage. Thus far, no repair-inducing treatments are available for progressive MS patients. Hence, there is an urgent need for the development of new therapeutic strategies either targeting the destructive immunological demyelination or boosting endogenous repair mechanisms. Using in vitro, ex vivo, and in vivo models, we demonstrate that selective inhibition of phosphodiesterase 4 (PDE4), a family of enzymes that hydrolyzes and inactivates cyclic adenosine monophosphate (cAMP), reduces inflammation and promotes myelin repair. More specifically, we segregated the myelination-promoting and anti-inflammatory effects into a PDE4D- and PDE4B-dependent process respectively. We show that inhibition of PDE4D boosts oligodendrocyte progenitor cells (OPC) differentiation and enhances (re)myelination of both murine OPCs and human iPSC-derived OPCs. In addition, PDE4D inhibition promotes in vivo remyelination in the cuprizone model, which is accompanied by improved spatial memory and reduced visual evoked potential latency times. We further identified that PDE4B-specific inhibition exerts anti-inflammatory effects since it lowers in vitro monocytic nitric oxide (NO) production and improves in vivo neurological scores during the early phase of experimental autoimmune encephalomyelitis (EAE). In contrast to the pan PDE4 inhibitor roflumilast, the therapeutic dose of both the PDE4B-specific inhibitor A33 and the PDE4D-specific inhibitor Gebr32a did not trigger emesis-like side effects in rodents. Finally, we report distinct PDE4D isoform expression patterns in human area postrema neurons and human oligodendroglia lineage cells. Using the CRISPR-Cas9 system, we confirmed that pde4d1/2 and pde4d6 are the key targets to induce OPC differentiation. Collectively, these data demonstrate that gene specific PDE4 inhibitors have potential as novel therapeutic agents for targeting the distinct disease processes of MS.
 OBJECTIVE: Percutaneous radiofrequency rhizotomy is a common procedure for trigeminal neuralgia (TN) that creates thermocoagulative lesions in the trigeminal ganglion. Lesioning parameters for the procedure are left to the individual surgeon's discretion, and published guidance is primarily anecdotal. The purpose of this work was to assess the role of lesioning temperature on long-term surgical outcomes. METHODS: This was a retrospective analysis of patients who underwent percutaneous radiofrequency rhizotomy from 2009 to 2020. Patient data, including demographics, disease presentation, surgical treatment, and outcomes, were collected from medical records. The primary endpoint was the recurrence of TN pain. Univariate and multivariate Cox proportional hazards regressions were used to assess the impact of chosen covariates on pain-free survival. RESULTS: A total of 280 patients who had undergone 464 procedures were included in the analysis. Overall, roughly 80% of patients who underwent rhizotomy would have a recurrence within 10 years. Lower lesion temperature was predictive of longer periods without pain recurrence (HR 1.05, p < 0.001). The inclusion of lesion time, postoperative numbness, prior history of radiofrequency rhizotomy, surgeon, and multiple sclerosis as confounding variables did not affect the hazard ratio or the statistical significance of this finding. Postoperative numbness and the absence of multiple sclerosis were significant protective factors in the model. CONCLUSIONS: The study findings suggest that lower lesion temperatures and, separately, postoperative numbness result in improved long-term outcomes for patients with TN who undergo percutaneous radiofrequency rhizotomies. Given the limitations of retrospective analysis, the authors suggest that a prospective multisite clinical trial testing lesion temperatures would provide definitive guidance on this issue with specific recommendations about the number needed to treat and trial design.
 BACKGROUND/AIM: Tau is a microtubule-associated protein involved in the assembly and stabilization of microtubules. In human medicine, hyperphosphorylation of tau is associated with microtubule instability and is considered to play a role in the progression of multiple sclerosis (MS). MS is an autoimmune neurological disease that shares many characteristics, including pathological mechanisms, with canine meningoencephalitis of unknown etiology (MUE). With this background, this study investigated the presence of hyperphosphorylated tau in dogs with MUE and experimental autoimmune encephalomyelitis (EAE). MATERIALS AND METHODS: In total, eight brain samples were examined from two neurologically normal dogs, three dogs with MUE, and three canine EAE models. Anti-(phospho-S396) tau antibody was used for immunohisto-chemistry, which stained hyperphosphorylated tau. RESULTS: In normal brain tissues, hyperphosphorylated tau was not found. In all the dogs with EAE and one of the dogs with MUE, immunoreactivity for S396 p-tau was observed in glial cell cytoplasm and the background in the periphery of the inflammatory lesion. CONCLUSION: These results suggest for the first time that tau pathology may be involved in the progression of neuroinflammation in dogs, similar to that in human MS.
 BACKGROUND: Long-term data on the effectiveness and safety of the booster dose of anti-SARS-CoV-2 vaccines in people affected by multiple sclerosis (pwMS) are lacking, hence a retrospective monocentric study exploring these issues was undertaken. MATERIALS AND METHODS: PwMS who had received the booster dose of anti-COVID19 mRNA vaccines (either Comirnaty or Spikevax) according to the national regulation were included. The occurrence of adverse events or disease reactivation and SARS-CoV-2 infection were recorded up to last follow-up. Factors predictive of COVID-19 were explored using logistic regression analyses. A two-tailed p-value <0.05 was considered significant. RESULTS: One hundred and fourteen pwMS were included: 80 females (70%); median age at the booster dose 42 years (range 21 - 73); 106/114 patients (93%) were receiving a disease-modifying treatment at vaccination. The median follow-up after the booster dose was 6 (range 2 - 7) months. Adverse events were experienced in 58% of the patients, being mild to moderate in most cases; 4 reactivations of MS were observed, two of which occurring within 4 weeks after the booster. SARS-CoV-2 infection was reported in 24/114 (21%) cases, occurring a median of 74 days (5-162) after the booster dose and requiring hospitalisation in 2 patients. Six cases received direct antiviral drugs. Age at vaccination and time between the primary vaccination cycle and the booster dose were independently and inversely associated with the risk of COVID-19 (HR 0.95 and 0.98, respectively). CONCLUSIONS: The administration of the booster dose in pwMS showed an overall good safety profile and protected 79% of the patients from SARS-CoV-2 infection. The observed association between the risk of infection after the booster dose and both younger age at vaccination and shorter interval period to the booster dose suggest that unobserved confounders, possibly including behavioural and social factors, play a relevant role in determining the individual propensity to get infected with COVID-19.
 Multiple sclerosis (MS) is an autoimmune disease affecting the CNS and occurring far more prevalently in women than in men. In both MS and its animal models, sex hormones play important immunomodulatory roles. We have previously shown that experimental autoimmune encephalomyelitis (EAE) affects the hypothalamic-pituitary-gonadal axis in rats of both sexes and induces an arrest in the estrous cycle in females. To investigate the gonadal status in female rats with EAE, we explored ovarian morphometric parameters, circulating and intraovarian sex steroid levels, and the expression of steroidogenic machinery components in the ovarian tissue. A prolonged state of diestrus was recorded during the peak of EAE, with maintenance of the corpora lutea, elevated intraovarian progesterone levels, and increased gene and protein expression of StAR, similar to the state of pseudopregnancy. The decrease in CYP17A1 protein expression was followed by a decrease in ovarian testosterone and estradiol levels. On the contrary, serum testosterone levels were slightly increased. With unchanged serum estradiol levels, these results point at extra-gonadal sites of sex steroid biosynthesis and catabolism as important regulators of their circulating levels. Our study suggests alterations in the function of the female reproductive system during central autoimmunity and highlights the bidirectional relationships between hormonal status and EAE.
 BACKGROUND: Overweight and obesity increase multiple sclerosis (MS) susceptibility, disease severity, and disability progression. Kynurenine pathway (KP) dysregulation is present in overweight and obesity, and in MS. Since the effect of overweight and obesity on KP dysregulation in persons with MS (pwMS) remains to be established, this study primarily aims to explore the effect of overweight and obesity on the serum KP metabolic profile in pwMS. METHODS: This cross-sectional study represents a secondary analysis of a randomized clinical trial at Valens rehabilitation clinic, Switzerland. Registration was performed on 22 April 2020 at clinicaltrials.gov (NCT04356248, https://clinicaltrials.gov/ct2/show/NCT04356248). The first participant was enrolled on 13 July 2020. Based on body mass index (BMI), 106 MS inpatients (Expanded Disability Status Scale (EDSS) score ≤ 6.5) were dichotomised to a lean group (LG, BMI < 25 kg/m(2)), and an overweight/obese group (OG, BMI ≥ 25 kg/m(2)). Targeted metabolomics (LC-MS/MS) was performed to determine serum concentrations of tryptophan (TRP), KP downstream metabolites, and neopterin (Neopt). Correlations between BMI, kynurenine-to-TRP ratio (KTR), and serum concentrations of TRP, KP downstream metabolites, and Neopt were calculated. ANCOVA was used to determine differences in KTR, and serum concentrations of TRP, KP downstream metabolites and Neopt between OG and LG, and across MS phenotypes. RESULTS: Higher BMI correlated with higher KTR (r = 0.425, p <0.001) and serum concentrations of most KP downstream metabolites, but not with EDSS score. Higher KTR (r = 0.470, p < .001) and serum concentrations of most KP downstream metabolites correlated with a higher serum concentration of Neopt. The OG (n = 44, 59% female, 51.68 (9.98) years, EDSS: 4.71 (1.37)) revealed higher KTR (0.026 (0.007) vs. 0.022 (0.006), p=.001) and serum concentrations of most KP downstream metabolites than the LG (n = 62, 71% female, 48.37 (9.63) years, EDSS: 4.60 (1.29)). KP metabolic profiles did not differ between MS phenotypes. CONCLUSION: Overweight and obesity are associated with a systemic elevation of KP metabolic flux and an accumulation of most KP downstream metabolites in pwMS. Further research is needed to clarify if KP involvement serves as a mechanism linking overweight and obesity with symptom expression, disease severity, and disability progression in pwMS.
 Microtubule-associated protein Tau is primarily expressed in axons of neurons, but also in Olig2-positive oligodendrocytes in adult rodent and monkey brains. In this study, we sought to determine at what cell stage Tau becomes expressed in the oligodendrocyte lineage. We performed immunostaining of adult mouse brain sections using well-known markers of oligodendrocyte lineage and found that Tau is expressed in mature oligodendrocytes, but not in oligodendrocyte progenitors and immature pre-oligodendrocytes. We also investigated Tau expression in developing mouse brain. Surprisingly, Tau expression occurred after the peak of myelination and even exceeded GSTπ expression, which has been considered as a marker of myelinating oligodendrocytes. These results suggest Tau as a novel marker of oligodendrocyte maturation. We then investigated whether Tau is important for oligodendrocyte development and/or myelination and how Tau changes in demyelination. First, we found no changes in myelination and oligodendrocyte markers in Tau knockout mice, suggesting that Tau is dispensable. Next, we analyzed the proteolipid protein 1 transgenic model of Pelizaeus-Merzbacher disease, which is a rare leukodystrophy. In hemizygous transgenic mice, the number of Tau-positive cells were significantly increased as compared with wild type mice. These cells were also positive for Olig2, CC1, and GSTπ, but not PDGFRα and GPR17. In stark contrast, the expression level of Tau, as well as GSTπ, was dramatically decreased in the cuprizone-induced model of multiple sclerosis. Taken together, we propose Tau as a new marker of oligodendrocyte lineage and for investigating demyelination lesions.
 Blood-brain barrier (BBB) breakdown and immune cell infiltration into the central nervous system (CNS) are early hallmarks of multiple sclerosis (MS). High numbers of CD8(+) T cells are found in MS lesions, and antigen (Ag) presentation at the BBB has been proposed to promote CD8(+) T cell entry into the CNS. Here, we show that brain endothelial cells process and cross-present Ag, leading to effector CD8(+) T cell differentiation. Under physiological flow in vitro, endothelial Ag presentation prevented CD8(+) T cell crawling and diapedesis resulting in brain endothelial cell apoptosis and BBB breakdown. Brain endothelial Ag presentation in vivo was limited due to Ag uptake by CNS-resident macrophages but still reduced motility of Ag-specific CD8(+) T cells within CNS microvessels. MHC class I-restricted Ag presentation at the BBB during neuroinflammation thus prohibits CD8(+) T cell entry into the CNS and triggers CD8(+) T cell-mediated focal BBB breakdown.
 CXC chemokine receptor6 (CXCR6)-based immunotherapy plays a significant role in autoimmune diseases, however, little is known about possible small compounds that inhibit pathogenic CXCR6(+) T cells for treating multiple sclerosis (MS). Baicalein, a flavonoid isolated from Scutellarin baicalensis (Huang Qin), was shown to exert therapeutic effects on MS, but the underlying mechanisms are largely unknown. In the current study, we found that baicalein inhibited Th1 and Th17 differentiation in vitro. Oral administration of baicalein (25 mg/kg) significantly reduced the disease severity and the infiltration process, decreased the extent of demyelination in EAE, and selectively blocked IL-17A production and specific antibodies (IgG and IgG(3)) in MOG(35-55)-induced specific immune responses. In addition, the expression of CD4 cell effectors (CD44(hi)CD62L(low)) and pathogenic Th17 cells was decreased by baicalein treatment. Furthermore, baicalein treatment largely decreased CXCR6(+) CD4 and CD8 cells and prominently inhibited CXCR6(+) Th17 cells in EAE. Taken together, the findings of this study suggest for the first time that baicalein may ameliorate EAE by suppressing pathogenetic CXCR6(+) CD4 cells.
 BACKGROUND AND OBJECTIVES: Neurodegeneration and astrocytic activation are pathologic hallmarks of progressive multiple sclerosis (MS) and can be quantified by serum neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP). We investigated sNfL and sGFAP as tools for stratifying patients with progressive MS based on progression and disease activity status. METHODS: We leveraged our Comprehensive Longitudinal Investigation of MS at the Brigham and Women's Hospital (CLIMB) natural history study, which includes clinical, MRI data and serum samples collected over more than 20 years. We included patients with MS with a confirmed Expanded Disability Status Scale (EDSS) score ≥3 that corresponds with our classifier for patients at high risk of underlying progressive pathology. We analyzed sNfL and sGFAP within 6 months from the confirmed EDSS score ≥3 corresponding with our baseline visit. Patients who further developed 6-month confirmed disability progression (6mCDP) were classified as progressors. We further stratified our patients into active/nonactive based on new brain/spinal cord lesions or relapses in the 2 years before baseline or during follow-up. Statistical analysis on log-transformed sGFAP/sNfL assessed the baseline association with demographic, clinical, and MRI features and associations with future disability. RESULTS: We included 257 patients with MS who had an average EDSS score of 4.0 and a median follow-up after baseline of 7.6 years. sNfL was higher in patients with disease activity in the 2 years before baseline (adjusted β = 1.21; 95% CI 1.04-1.42; p = 0.016), during the first 2 years of follow-up (adjusted β = 1.17; 95% CI = 1.01-1.36; p = 0.042). sGFAP was not increased in the presence of disease activity. Higher sGFAP levels, but not sNfL levels, were associated with higher risk of 6mCDP (adjusted hazard ratio [HR] = 1.71; 95% CI = 1.19-2.45; p = 0.004). The association was stronger in patients with low sNfL (adjusted HR = 2.44; 95% CI 1.32-4.52; p = 0.005) and patients who were nonactive in the 2 years prior or after the sample. DISCUSSION: Higher levels of sGFAP correlated with subsequent progression, particularly in nonactive patients, whereas sNfL reflected acute disease activity in patients with MS at high risk of underlying progressive pathology. Thus, sGFAP and sNfL levels may be used to stratify patients with progressive MS for clinical research studies and clinical trials and may inform clinical care.
 Multiple sclerosis (MS) is a complex and multifactorial neurodegenerative disease with unknown etiology, MS is featured by multifocal demyelinated lesions distributed throughout the brain. It is assumed to result from an interaction between genetic and environmental factors, including nutrition. Therefore, different therapeutic approaches are aiming to stimulate remyelination which could be defined as an endogenous regeneration and repair of myelin in the central nervous system. Carvedilol is an adrenergic receptor antagonist. Alpha lipoic acid (ALA) is a well-known antioxidant. Herein, we investigated the remyelination potential of Carvedilol or ALA post-Cuprizone (CPZ) intoxication. Carvedilol or ALA (20 mg/kg/d) was administrated orally for two weeks at the end of the five weeks of CPZ (0.6%) administration. CPZ provoked demyelination, enhanced oxidative stress, and stimulated neuroinflammation. Histological investigation of CPZ-induced brains showed obvious demyelination in the corpus callosum (CC). Both Carvedilol and ALA demonstrated remyelinating activities, with corresponding upregulation of the expression of MBP and PLP, the major myelin proteins, downregulation of the expression of TNF-α and MMP-9, and decrement of serum IFN-γ levels. Moreover, both Carvedilol and ALA alleviated oxidative stress, and ameliorated muscle fatigue. This study highlights the neurotherapeutic potential of Carvedilol or ALA in CPZ-induced demyelination, and offers a better model for the exploring of neuroregenerative strategies. The current study is the first to demonstrate a pro-remyelinating activity for Carvedilol, as compared to ALA, which might represent a potential additive benefit in halting demyelination and alleviating neurotoxicity. However, we could declare that Carvedilol showed a lower neuroprotective potential than ALA.
 It remains uncertain how brain glycosaminoglycans (GAGs) contribute to the progression of inflammatory disorders like multiple sclerosis (MS). We investigated here neuroinflammation-mediated changes in GAG composition and metabolism using the mouse model of experimental autoimmune encephalomyelitis (EAE) and sham-immunized mice as controls. Cerebellum, mid- and forebrain at different EAE phases were investigated using gene expression analysis (microarray and RT-qPCR) as well as HPLC quantification of CS and hyaluronic acid (HA). The cerebellum was the most affected brain region showing a downregulation of Bcan, Cspg5, and an upregulation of Dse, Gusb, Hexb, Dcn and Has2 at peak EAE. Upregulation of genes involved in GAG degradation as well as synthesis of HA and decorin persisted from onset to peak, and diminished at remission, suggesting a severity-related decrease in CS and increments in HA. Relative disaccharide quantification confirmed a 3.6 % reduction of CS-4S at peak and a normalization during remission, while HA increased in both phases by 26.1 % and 17.6 %, respectively. Early inflammatory processes led to altered GAG metabolism in early EAE stages and subsequent partially reversible changes in CS-4S and in HA. Targeting early modifications in CS could potentially mitigate progression of EAE/MS.
 BACKGROUND: Adequate response to the SARS-CoV-2 vaccine represents an important treatment goal in caring for patients with multiple sclerosis (MS) during the ongoing COVID-19 pandemic. Previous data so far have demonstrated lower spike-specific IgG responses following two SARS-CoV-2 vaccinations in MS patients treated with sphingosine-1-phosphate (S1P) receptor modulators and anti-CD20 monoclonal antibodies (mAb) compared to other disease modifying therapies (DMTs). It is unknown whether subsequent vaccinations can augment antibody responses in these patients. OBJECTIVES: The goal of this observational study was to determine the effects of a third SARS-CoV-2 vaccination on antibody and T cell responses in MS patients treated with anti-CD20 mAb or S1P receptor modulators. METHODS: Vaccine responses in patients treated with anti-CD20 antibodies (ocrelizumab and ofatumumab) or S1P receptor modulators (fingolimod and siponimod) were evaluated before and after third SARS-CoV-2 vaccination as part of an ongoing longitudinal study. Total spike protein and spike receptor binding domain (RBD)-specific IgG responses were measured by Luminex bead-based assay. Spike-specific CD4+ and CD8+ T cell responses were measured by activation-induced marker expression. RESULTS: MS patients and healthy controls were enrolled before and following SARS-CoV-2 vaccination. A total of 31 MS patients (n = 10 ofatumumab, n = 13 ocrelizumab, n = 8 S1P) and 10 healthy controls were evaluated through three SARS-CoV-2 vaccinations. Compared to healthy controls, total spike IgG was significantly lower in anti-CD20 mAb-treated patients and spike RBD IgG was significantly lower in anti-CD20 mAb and S1P-treated patients following a third vaccination. While seropositivity was 100% in healthy controls after a third vaccination, total spike IgG and spike RBD IgG seropositivity were lower in ofatumumab (60% and 60%, respectively), ocrelizumab (85% and 46%, respectively), and S1P-treated patients (100% and 75%, respectively). Longer treatment duration, including prior treatment history, appeared to negatively impact antibody responses. Spike-specific CD4+ and CD8+ T cell responses were well maintained across all groups following a third vaccination. Finally, immune responses were also compared in patients who were vaccinated prior to or following ofatumumab treatment. Antibody responses were significantly higher in those patients who received their primary SARS-CoV-2 vaccination prior to initiating ofatumumab treatment. CONCLUSIONS: This study adds to the evolving understanding of SARS-CoV-2 vaccine responses in people with MS treated with disease-modifying therapies (DMTs) known to suppress humoral immunity. Our findings provide important information for optimizing vaccine immunity in at-risk MS patient populations.
 Pathogenic Th17 cells play a key role in the pathogenesis of many autoimmune diseases. Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is the commonly used animal model for human MS and is characterized by autoreactive CD4(+)T cells attacking autoantigens in the CNS and causing myelin sheath damage. Although the recombinant BTN2A2-IgG2aFc (BTN2A2-Ig) fusion protein has been shown to inhibit T cell functions in vitro, it's unclear whether BTN2A2-Ig affects pathogenic Th17 cells and EAE development. We show here that BTN2A2-Ig protein attenuates established EAE, as compared with control Ig protein treatment. This is associated with reduced activation and proliferation of T cells in BTN2A2-Ig-treated EAE mice. Furthermore, BTN2A2-Ig protein inhibits the differentiation of CD4 naïve T cells into pathogenic Th17 cells and reduces the expression levels of Th1/Th17 cytokines and the Th1/Th17 pathway related genes and proteins but increases the expression levels of Th2-related genes and proteins. Our studies not only provide new insights into the mechanisms by which BTN2A2-Ig affects T cells, but also have the potential to provide a new strategy to treat MS and other autoimmune diseases.
 IMPORTANCE: Differential diagnosis of patients with seronegative demyelinating central nervous system (CNS) disease is challenging. In this regard, evidence suggests that immunoglobulin (Ig) A plays a role in the pathogenesis of different autoimmune diseases. Yet little is known about the presence and clinical relevance of IgA antibodies against myelin oligodendrocyte glycoprotein (MOG) in CNS demyelination. OBJECTIVE: To investigate the frequency of MOG-IgA and associated clinical features in patients with demyelinating CNS disease and healthy controls. DESIGN, SETTING, AND PARTICIPANTS: This longitudinal study comprised 1 discovery and 1 confirmation cohort derived from 5 centers. Participants included patients with suspected or confirmed demyelinating diseases and healthy controls. MOG-IgA, MOG-IgG, and MOG-IgM were measured in serum samples and cerebrospinal fluid (CSF) of patients, who were assessed from September 2012 to April 2022. MAIN OUTCOMES AND MEASURES: Frequency and clinical features of patients who were seropositive for MOG-IgA and double-seronegative for aquaporin 4 (AQP4) IgG and MOG-IgG. RESULTS: After the exclusion of 5 participants with coexisting AQP4-IgG and MOG-IgA, MOG-IgG, and/or MOG-IgM, 1339 patients and 110 healthy controls were included; the median follow-up time was 39 months (range, 0-227 months). Of included patients with isolated MOG-IgA, 11 of 18 were female (61%), and the median age was 31.5 years (range, 3-76 years). Among patients double-seronegative for AQP4-IgG and MOG-IgG (1126/1339; 84%), isolated MOG-IgA was identified in 3 of 50 patients (6%) with neuromyelitis optica spectrum disorder, 5 of 228 patients (2%) with other CNS demyelinating diseases, and 10 of 848 patients (1%) with multiple sclerosis but in none of the healthy controls (0/110). The most common disease manifestation in patients seropositive for isolated MOG-IgA was myelitis (11/17 [65%]), followed by more frequent brainstem syndrome (7/16 [44%] vs 14/75 [19%], respectively; P = .048), and infrequent manifestation of optic neuritis (4/15 [27%] vs 46/73 [63%], respectively; P = .02) vs patients with MOG-IgG. Among patients fulfilling 2017 McDonald criteria for multiple sclerosis, MOG-IgA was associated with less frequent CSF-specific oligoclonal bands (4/9 [44%] vs 325/351 [93%], respectively; P < .001) vs patients with multiple sclerosis who were MOG-IgG/IgA seronegative. Further, most patients with isolated MOG-IgA presented clinical attacks after recent infection or vaccination (7/11 [64%]). CONCLUSION AND RELEVANCE: In this study, MOG-specific IgA was identified in a subgroup of patients who were double-seronegative for AQP4-/MOG-IgG, suggesting that MOG-IgA may be a novel diagnostic biomarker for patients with CNS demyelination.
 AIMS: Demyelination affects the propogation of neuronal action potential by slowing down the progression. This process results in a neuro-impairment like Multiple Sclerosis (MS). Evidence show that MS also contributes to involvement of the autonomic system. In the molecular approach to this involvement, we aimed to observe muscarinic ACh receptor 2-3 (mAChR2-3), and inwardly rectifying potassium channel 3.1 (Kir3.1) immunoreactivities on the brainstem, vagus nerve, and heart under cuprizone model. MAIN METHODS: Wistar albino rats were randomly divided into 8 groups; duplicating 4 groups as male and female: control groups (n = 3 +3), Cuprizone groups (n = 12 +12), sham groups (n = 4 +4), and carboxy-methyl-cellulose groups (n = 3 +3). Cuprizone-fed rats underwent demyelination via Luxol fast blue (LFB) staining of the hippocampus (Gyrus dentatus and Cornu Ammonis) and cortex. Immunohistochemistry analysis followed to the pathologic measurement of the brainstem, vagus nerve, and heart for mAChR2, mAChR3 and Kir3.1 proteins KEY FINDINGS: A significant demyelination was observed in the hippocampus and cortex tissues of rats in the female and male cuprizone groups. Myelin basic protein immunoreactivity demonstrated that cuprizone groups, in both males and females, had down-regulation in the hippocampus and cortex areas. The weights of the cuprizone-fed rats significantly decreased over six weeks. Dilated blood vessels and neuronal degeneration were severe in the hippocampus and cortex of the cuprizone groups. In the female cuprizone group, expression of mAChR2 and mAChR2 was significantly increased in the brainstem, atrium/ventricle of heart, and left/right sections of vagus nerve. Kir3.1 channels were also up-regulated in the left vagus nerve and heart sections of the female cuprizone group SIGNIFICANCE: Especially in our data where female-based significant results were obtained reveal that demyelination may lead to significant mAChR2, mAChR3 and Kir3.1 changes in brainstem, vagus nerve, and heart. A high immunoreactive response to demyelination at cholinergic centers may be a new target.
 BACKGROUND AND OBJECTIVES: Kappa free light chains (KFLC) seem to efficiently diagnose MS. However, extensive cohort studies are lacking to establish consensus cut-offs, notably to rule out non-MS autoimmune CNS disorders. Our objectives were to (1) determine diagnostic performances of CSF KFLC, KFLC index, and KFLC intrathecal fraction (IF) threshold values that allow us to separate MS from different CNS disorder control populations and compare them with oligoclonal bands' (OCB) performances and (2) to identify independent factors associated with KFLC quantification in MS. METHODS: We conducted a retrospective multicenter study involving 13 French MS centers. Patients were included if they had a noninfectious and nontumoral CNS disorder, eligible data concerning CSF and serum KFLC, albumin, and OCB. Patients were classified into 4 groups according to their diagnosis: MS, clinically isolated syndrome (CIS), other inflammatory CNS disorders (OIND), and noninflammatory CNS disorder controls (NINDC). RESULTS: One thousand six hundred twenty-one patients were analyzed (675 MS, 90 CIS, 297 OIND, and 559 NINDC). KFLC index and KFLC IF had similar performances in diagnosing MS from nonselected controls and OIND (p = 0.123 and p = 0.991 for area under the curve [AUC] comparisons) and performed better than CSF KFLC (p < 0.001 for all AUC comparisons). A KFLC index of 8.92 best separated MS/CIS from the entire nonselected control population, with better performances than OCB (p < 0.001 for AUC comparison). A KFLC index of 11.56 best separated MS from OIND, with similar performances than OCB (p = 0.065). In the multivariate analysis model, female gender (p = 0.003), young age (p = 0.013), and evidence of disease activity (p < 0.001) were independent factors associated with high KFLC index values in patients with MS, whereas MS phenotype, immune-modifying treatment use at sampling, and the FLC analyzer type did not influence KFLC index. DISCUSSION: KFLC biomarkers are efficient tools to separate patients with MS from controls, even when compared with other patients with CNS autoimmune disorder. Given these results, we suggest using KFLC index or KFLC IF as a criterion to diagnose MS. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that KFLC index or IF can be used to differentiate patients with MS from nonselected controls and from patients with other autoimmune CNS disorders.
 Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). While most of the current treatment strategies focus on immune cell regulation, except for the drug siponimod, there is no therapeutic intervention that primarily aims at neuroprotection and remyelination. Recently, nimodipine showed a beneficial and remyelinating effect in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Nimodipine also positively affected astrocytes, neurons, and mature oligodendrocytes. Here we investigated the effects of nimodipine, an L-type voltage-gated calcium channel antagonist, on the expression profile of myelin genes and proteins in the oligodendrocyte precursor cell (OPC) line Oli-Neu and in primary OPCs. Our data indicate that nimodipine does not have any effect on myelin-related gene and protein expression. Furthermore, nimodipine treatment did not result in any morphological changes in these cells. However, RNA sequencing and bioinformatic analyses identified potential micro (mi)RNA that could support myelination after nimodipine treatment compared to a dimethyl sulfoxide (DMSO) control. Additionally, we treated zebrafish with nimodipine and observed a significant increase in the number of mature oligodendrocytes (* p≤ 0.05). Taken together, nimodipine seems to have different positive effects on OPCs and mature oligodendrocytes.
 BACKGROUND: Sphingosine-one phosphate receptor (S1PR) modulation inhibits S1PR1-mediated lymphocyte migration, lesion formation and positively-impacts on active multiple sclerosis (MS). These S1PR modulatory drugs have different: European Union use restrictions, pharmacokinetics, metabolic profiles and S1PR receptor affinities that may impact MS-management. Importantly, these confer useful properties in dealing with COVID-19, anti-viral drug responses and generating SARS-CoV-2 vaccine responses. OBJECTIVE: To examine the biology and emerging data that potentially underpins immunity to the SARS-CoV-2 virus following natural infection and vaccination and determine how this impinges on the use of current sphingosine-one-phosphate modulators used in the treatment of MS. METHODS: A literature review was performed, and data on infection, vaccination responses; S1PR distribution and functional activity was extracted from regulatory and academic information within the public domain. OBSERVATIONS: Most COVID-19 related information relates to the use of fingolimod. This indicates that continuous S1PR1, S1PR3, S1PR4 and S1PR5 modulation is not associated with a worse prognosis following SARS-CoV-2 infection. Whilst fingolimod use is associated with blunted seroconversion and reduced peripheral T-cell vaccine responses, it appears that people on siponimod, ozanimod and ponesimod exhibit stronger vaccine-responses, which could be related notably to a limited impact on S1PR4 activity. Whilst it is thought that S1PR3 controls B cell function in addition to actions by S1PR1 and S1PR2, this may be species-related effect in rodents that is not yet substantiated in humans, as seen with bradycardia issues. Blunted antibody responses can be related to actions on B and T-cell subsets, germinal centre function and innate-immune biology. Although S1P1R-related functions are seeming central to control of MS and the generation of a fully functional vaccination response; the relative lack of influence on S1PR4-mediated actions on dendritic cells may increase the rate of vaccine-induced seroconversion with the newer generation of S1PR modulators and improve the risk-benefit balance IMPLICATIONS: Although fingolimod is a useful asset in controlling MS, recently-approved S1PR modulators may have beneficial biology related to pharmacokinetics, metabolism and more-restricted targeting that make it easier to generate infection-control and effective anti-viral responses to SARS-COV-2 and other pathogens. Further studies are warranted.
 INTRODUCTION: Among the most frequent demyelinating autoimmune disorders of the central nervous system (CNS) is multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is used as an animal model of multiple sclerosis. Berberine is an alkaloid found in some medicinal plants with anti-inflammatory effects. METHODS: C57BL/6 female mice were used and divided into three groups: (1) The control group received PBS, (2) the low-dose treatment group received 10 mg/kg of berberine, and (3) The high-dose treatment group received 30 mg/kg of berberine. Myelin Oligodendrocyte Glycoprotein and complete Freund's adjuvant were subcutaneously administered to induce EAE. Mice were given intraperitoneal injections of pertussis toxin on the day of immunization and 2 days later. Histological studies showed low lymphocyte infiltration and demyelination of CNS in the treated groups. RESULTS: The clinical scores of the treatment group with low-dose berberine (T1: 2 ± 0.13) and high-dose berberine (T2: 1.5 ± 0.14) were significantly (p < .001) lower than the control group (CTRL: 4.5 ± 0.13). Treatment groups decreased pro-inflammatory cytokines (IFN-γ, TNF-α, interleukin [IL]-17) (p < .001) as well as increased anti-inflammatory cytokine expression (IL-4, IL-10, IL-27, IL-33, IL-35, TGF-β) (p < .01) when compared to the CTRL group. Treatment groups with berberine reduced expression of the Th1 and Th17 cytokines and transcription factors (p < .001) and increased expression of transcription factors and Th2 and Treg cytokines (p < .01) in contrast to CTRL group. CONCLUSION: Berberine appears to have a protective effect on disease development and alleviating disease status in EAE, which appears to be due to the cell expansion and function of Treg and Th2 cells in addition to berberine's anti-inflammatory properties.

 BACKGROUND AND OBJECTIVES: Epstein-Barr virus (EBV) is a ubiquitous herpesvirus that establishes lifelong latency in memory B cells and has been identified as a major risk factor of multiple sclerosis (MS). B cell depletion therapies have disease-modifying benefit in MS. However, it is unclear whether this benefit is partly attributable to the elimination of EBV(+) B cells. Currently, there are no EBV-specific antiviral therapies available for targeting EBV latent infection in MS and limited experimental models to study EBV in MS. METHODS: In this study, we describe the establishment of spontaneous lymphoblastoid cell lines (SLCLs) generated ex vivo with the endogenous EBV of patients with MS and controls and treated with either an Epstein-Barr virus nuclear antigen 1 (EBNA1) inhibitor (VK-1727) or cladribine, a nucleoside analog that eliminates B cells. RESULTS: We showed that a small molecule inhibitor of EBNA1, a critical regulator of the EBV life cycle, blocks the proliferation and metabolic activity of these SLCLs. In contrast to cladribine, a highly cytotoxic B cell depleting therapy currently used in MS, the EBNA1 inhibitor VK-1727 was cytostatic rather than cytotoxic and selective for EBV(+) cells, while having no discernible effects on EBV(-) cells. We validate that VK-1727 reduces EBNA1 DNA binding at known viral and cellular sites by ChIP-qPCR. DISCUSSION: This study shows that patient-derived SLCLs provide a useful tool for interrogating the role of EBV(+) B cells in MS and suggests that a clinical trial testing the effect of EBNA1 inhibitors in MS may be warranted.
 CD4(+) T helper 17 (T(H)17) cells protect barrier tissues but also trigger autoimmunity. The mechanisms behind these opposing processes remain unclear. Here, we found that the transcription factor EGR2 controlled the transcriptional program of pathogenic T(H)17 cells in the central nervous system (CNS) but not that of protective T(H)17 cells at barrier sites. EGR2 was significantly elevated in myelin-reactive CD4(+) T cells from patients with multiple sclerosis and mice with autoimmune neuroinflammation. The EGR2 transcriptional program was intricately woven within the T(H)17 cell transcriptional regulatory network and showed high interconnectivity with core T(H)17 cell-specific transcription factors. Mechanistically, EGR2 enhanced T(H)17 cell differentiation and myeloid cell recruitment to the CNS by upregulating pathogenesis-associated genes and myelomonocytic chemokines. T cell-specific deletion of Egr2 attenuated neuroinflammation without compromising the host's ability to control infections. Our study shows that EGR2 regulates tissue-specific and disease-specific functions in pathogenic T(H)17 cells in the CNS.
 The proinflammatory microRNA-155 (miR-155) is highly expressed in the serum and CNS lesions of patients with multiple sclerosis (MS). Global knockout (KO) of miR-155 in mice confers resistance to a mouse model of MS, experimental autoimmune encephalomyelitis (EAE), by reducing the encephalogenic potential of CNS-infiltrating Th17 T cells. However, cell-intrinsic roles for miR-155 during EAE have not been formally determined. In this study, we use single-cell RNA sequencing and cell-specific conditional miR-155 KOs to determine the importance of miR-155 expression in distinct immune cell populations. Time-course single-cell sequencing revealed reductions in T cells, macrophages, and dendritic cells (DCs) in global miR-155 KO mice compared with wild-type controls at day 21 after EAE induction. Deletion of miR-155 in T cells, driven by CD4 Cre, significantly reduced disease severity similar to global miR-155 KOs. CD11c Cre-mediated deletion of miR-155 in DCs also resulted in a modest yet significant reduction in the development of EAE, with both T cell- and DC-specific KOs showing a reduction in Th17 T cell infiltration into the CNS. Although miR-155 is highly expressed in infiltrating macrophages during EAE, deletion of miR-155 using LysM Cre did not impact disease severity. Taken together, these data show that although miR-155 is highly expressed in most infiltrating immune cells, miR-155 has distinct roles and requirements depending on the cell type, and we have demonstrated this using the gold standard conditional KO approach. This provides insights into which functionally relevant cell types should be targeted by the next generation of miRNA therapeutics.
 OBJECTIVE: Currently, there are no data available on SARS-CoV-2 vaccine responses in pediatric-onset multiple sclerosis (POMS), and little is known about the course of SARS-CoV-2 infection in this age group. We therefore investigated humoral immune responses after COVID-19 vaccination and/or infection in POMS. METHODS: We retrospectively analyzed seroconversion rates and SARS-CoV-2-specific antibody levels in 30 POMS and one pediatric CIS patient treated with no disease-modifying therapy (no DMT), immunomodulatory DMT (IM-DMT), or immunosuppressive DMT (IS-DMT) from two Austrian MS centers. RESULTS: The median age at MS onset was 15.39 years (interquartile range [IQR]: 1.97). The median age at the first COVID-19 vaccination was 17.43 years (IQR: 2.76). After two vaccine doses, seroconversion (≥0.8 BAU/ml) was reached in 25 of 28 patients (89.3%). All patients with no DMT or IM-DMT generated robust immune responses to vaccination (seroconversion: no DMT: 6/6, IM-DMT: 7/7 [100%]; median titers: no DMT: 2075 BAU [IQR: 1268.50], IM-DMT: 2500 BAU [IQR: 0]). In the IS-DMT group, seroconversion was achieved in 12 of 14 patients (80%), and median titers were 50.8 BAU (IQR 254.63). Titers were significantly higher in no DMT versus IS-DMT (P = 0.012) and in IM-DMT versus IS-DMT (P = 0.001). Infection with SARS-CoV-2 occurred in 11 of 31 patients, and symptoms were mild in all cases. One relapse occurred after infection, but no relapses were documented after vaccination. CONCLUSIONS: Generally, mRNA vaccinations were well tolerated in POMS patients with and without DMT. Immune response was significantly reduced in patients treated with IS-DMT. No unexpected adverse events or relapses related to vaccinations were observed.
 Multiple sclerosis (MS) is an autoimmune disease characterized by autoreactive immune cells damaging myelinated nerves, impairing brain function. Treatments aim for tolerance induction to reeducate the immune system to recognize myelin as "self" rather than "foreign." As peripheral immune tolerance is primarily mediated by regulatory T cells (T(regs)), we developed a therapy to support T(reg) expansion and activity in vivo. To target, engage, and activate myelin-specific T(regs), we designed a biodegradable microparticle (MP) loaded with rapamycin and functionalized with a biased interleukin-2 (IL-2) fusion protein and a major histocompatibility complex (MHC) class II loaded with a myelin peptide. These tolerogenic MPs (Tol-MPs) were validated in vitro and then evaluated in a mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Tol-MPs promoted sustained disease reversal in 100% of mice and full recovery in 38% of mice with symptomatic EAE. Tol-MPs are a promising platform for treatment of autoimmune diseases.
 To better understand the impact of gut dysbiosis on four autoimmune diseases [Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS)], this review investigated the altered gut bacteria in each disease and the shared ones among the four diseases. The enriched gut bacteria shared by three of the four autoimmune diseases were Streptococcus, Prevotella, and Eggerthella, which are associated with autoantibody production or activation of Th17 cells in immune-related diseases. On the other hand, Faecalibacterium comprises depleted gut bacteria shared by patients with SLE, MS, and SS, which is associated with various anti-inflammatory activities. The indexes of gut dysbiosis, defined as the number of altered gut bacterial taxa divided by the number of studies in SLE, MS, RA, and SS, were 1.7, 1.8, 0.7, and 1.3, respectively. Interestingly, these values presented a positive correlation trend with the standardized mortality rates -2.66, 2.89, 1.54, and 1.41, respectively. In addition, shared altered gut bacteria among the autoimmune diseases may correlate with the prevalence of polyautoimmunity in patients with SLE, SS, RA, and MS, that is, 41 percent, 32.6 percent, 14 percent, and 1-16.6 percent, respectively. Overall, this review suggests that gut dysbiosis in autoimmune diseases may be closely related to the failure of the gut immune system to maintain homeostasis.
 BACKGROUND: Neuromyelitis Optica Spectrum Disorder (NMOSD) is a rare neuroinflammatory disease characterized by recurrent relapses. The most common signs are myelitis and optic neuritis. It can also present by cerebral or brain stem syndromes. There are still many challenges in its diagnosis and treatment, and long-term follow-up studies are needed to see the disease course over time. METHODS: We established an electronic registration system of NMOSD patients starting from October 2015 in Kashani hospital, Isfahan, Iran. Every suspected patient was documented and included in the follow-up system to survey their disease course. Anti-aquaporine 4 (AQP4) antibody checked for all by cell-based assay method. All information such as demographic and clinical data and laboratory and MRI findings were documented. Participants were followed up for any relapses, new paraclinical tests and drug changes. This study is based on the definite NMOSD cases (according to the 2015 criteria) characteristics and clinical course during 7 years of registration. RESULTS: The study included 173 NMOSD cases and 56 ones were seropositive for AQP4 Ab. Their mean age was 40.02±11.11 years (45.78 in the seropositive group). The mean age at disease onset was about 30.16 years. The mean time of follow-up by our registration system is 55.84 ± 18.94 months (54.82 months in seropositive ones). The annual relapse rate is estimated as 0.47±0.36. Long extended transvers myelitis (LETM) was present in the baseline MRI of 77 patients (44.5%), while 32 of them did not show any related clinical symptoms. 124 patients revealed an abnormality in the first brain MRI. 27 individuals suffer hypothyroidism as the most common comorbid disease. The disease seems to be more prevalent in the west and southwest areas of Isfahan province. CONCLUSION: The mean age of onset is higher than Multiple Sclerosis (MS) patients, but there are notable pediatric cases too. It should also be noticed that cervical LETM can be asymptomatic at first. Brain MRI abnormalities are frequently observed. The disease is more prevalent in the geographical areas where showing high MS prevalence.
 BACKGROUND/OBJECTIVE: Serum neurofilament light chain (sNfL) is a specific biomarker of neuronal damage. Elevated sNfL levels have been reported in numerous neurologic diseases in adults, whereas data on sNfL in the pediatric population are incomplete. The aim of this study was to investigate sNfL levels in children with various acute and chronic neurologic disorders and describe the age dependence of sNfL from infancy to adolescence. METHODS: The total study cohort of this prospective cross-sectional study consisted of 222 children aged from 0 to 17 years. Patients' clinical data were reviewed and patients were assigned to the following groups: 101 (45.5%) controls, 34 (15.3%) febrile controls, 23 (10.4%) acute neurologic conditions (meningitis, facial nerve palsy, traumatic brain injury, or shunt dysfunction in hydrocephalus), 37 (16.7%) febrile seizures, 6 (2.7%) epileptic seizures, 18 (8.1%) chronic neurologic conditions (autism, cerebral palsy, inborn mitochondrial disorder, intracranial hypertension, spina bifida, or chromosomal abnormalities), and 3 (1.4%) severe systemic disease. sNfL levels were measured using a sensitive single-molecule array assay. RESULTS: There were no significant differences in sNfL levels between controls, febrile controls, febrile seizures, epileptic seizures, acute neurologic conditions, and chronic neurologic conditions. In children with severe systemic disorders, by far the highest NfL levels were found with an sNfL of 429 pg/ml in a patient with neuroblastoma, 126 pg/ml in a patient with cranial nerve palsy and pharyngeal Burkitt's lymphoma, and 42 pg/ml in a child with renal transplant rejection. The relationship between sNfL and age could be described by a second order polynomial with an R(2) of 0.153 with a decrease of sNfL by 3.2% per year from birth to age 12 years and thereafter an increase by 2.7% per year until age 18 years. CONCLUSIONS: In this study cohort, sNfL levels were not elevated in children with febrile or epileptic seizures, or various other neurologic diseases. Strikingly high sNfL levels were detected in children with oncologic disease or transplant rejection. A biphasic sNfL age-dependency was documented, with highest levels in infancy and late adolescence and the lowest levels in middle school age.
 B cells play a key mechanistic role in the pathogenesis of multiple sclerosis (MS), a chronic neurological disease of the central nervous system with an autoimmune etiology. B cells contribute to disease initiation and progression by acting as professional antigen-presenting cells as well as via secreting autoantibodies and proinflammatory cytokines. We have recently shown that the polyglutamine protein ataxin-1, which was first linked to the movement disorder spinocerebellar ataxia type 1, also acts as a master regulator of B-cell functions in the context of central nervous system autoimmunity. In fact, ataxin-1-deficient mice display an aggravated manifestation of the MS disease model experimental autoimmune encephalomyelitis along with aberrant B-cell functions. Consistent with this scenario, transcriptomic analysis of Atxn1-null B cells highlighted distinct genetic signatures involved in cell activation, proliferation and antigen presentation. To further characterize the role of ataxin-1, we profiled the noncoding transcriptome controlled by ataxin-1 in the B-cell compartment upon an encephalitogenic challenge. We show that two specific classes of noncoding RNAs, namely, processed pseudogenes and intergenic long noncoding RNAs, are differentially regulated along disease. Furthermore, pathway and protein network analyses on their putative protein-coding gene targets found a significant enrichment in ontologies related to cell mitosis, together with molecular processes relevant to MS such as chitin metabolism. Altogether, these findings shed light on the possible contribution of noncoding RNAs to B-cell biology and MS pathogenesis, and further establish the immunomodulatory role of ataxin-1 in autoimmune demyelination.
 Multiple Sclerosis (MS) is a chronic autoimmune inflammatory disorder of the central nervous system (CNS). Current therapies mainly target inflammatory processes during acute stages, but effective treatments for progressive MS are limited. In this context, astrocytes have gained increasing attention as they have the capacity to drive, but also suppress tissue-degeneration. Here we show that astrocytes upregulate the immunomodulatory checkpoint molecule PD-L1 during acute autoimmune CNS inflammation in response to aryl hydrocarbon receptor and interferon signaling. Using CRISPR-Cas9 genetic perturbation in combination with small-molecule and antibody-mediated inhibition of PD-L1 and PD-1 both in vivo and in vitro, we demonstrate that astrocytic PD-L1 and its interaction with microglial PD-1 is required for the attenuation of autoimmune CNS inflammation in acute and progressive stages in a mouse model of MS. Our findings suggest the glial PD-L1/PD-1 axis as a potential therapeutic target for both acute and progressive MS stages.
 In Covid-19 and autoimmune patients, there are several similarities revealed in the immune responses (Liu et al., 2021; Woodruff et al., 2020). Earlier, we firstly detected a truncated (48 kDa) form of the unconventional Myosin 1C (48/Myo1C) in a fraction of proteins soluble in 10% 2,2,2-trichloroacetic acid (TCA). These proteins were obtained from blood serum of patients with autoimmune diseases, such as multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis (Kit et al., 2018). Here, we demonstrated that content of 48/Myo1C was also elevated in blood serum of the severe Covid-19 patients. Whereas in blood of 28 clinically healthy human individuals regularly tested for Covid-19 infection, the amount of this protein was undetectable or very low, in blood of 16 of 28 patients hospitalized with severe course of this disease, its amount was significantly increased. Dexamethasone, steroid hormone which is widely used for treatment of severe Covid-19 patients, induced time-dependent elevation of the 48/Myo1C in blood of such patients. The 48/Myo1C dose-dependently suppressed the viability of anti-CD3-activated lymphocytes of human peripheral blood. Recently, we used affinity chromatography on the magnetic poly(glycidyl-methacrylate) (mag-PGMA-NH(2)) microparticles functionalized with Myo1C and MALDI-TOF mass spectrometry with molecular modeling in silico in order to identify potential molecular partners of the 48/Myo1C. It was found that 48/Myo1C might bind to component 3 of the complement system and the anti-thrombin-III (Starykovych et al., 2021). Thus, the mechanisms of the pathogenic action of truncated form of Myo1C in severe COVID-19 patients may involve a suppression of the immune cells, as well as modulation of complement and coagulation cascades.
 CD4(+) T cells, specifically Th cells (Th1 and Th17) and regulatory T cells (Tregs), play a pivotal role in the pathogenesis of multiple sclerosis (MS), a demyelinating autoimmune disease of the CNS. STAT3 inhibitors are potential therapeutic targets for several immune disorders. In this study, we investigated the role of a well-known STAT3 inhibitor, S3I-201, in experimental autoimmune encephalomyelitis (EAE), a model of MS. Following induction of EAE, mice were intraperitoneally administered S3I-201 (10 mg/kg) each day, beginning on day 14 and continuing till day 35 and were evaluated for clinical signs. Flow cytometry was used to investigate further the effect of S3I-201 on Th1 (IFN-γ, STAT1, pSTAT1, and T-bet), Th17 (IL-17A, STAT3, pSTAT3, and RORγt), and regulatory T cells (Treg, IL-10, TGF-β1, and FoxP3) expressed in splenic CD4(+) T cells. Moreover, we analyzed the effects of S3I-201 on mRNA and protein expression of IFN-γ, T-bet, IL-17A, STAT1, STAT3, pSTAT1, pSTAT3, RORγ, IL-10, TGF-β1, and FoxP3 in the brains of EAE mice. The severity of clinical scores decreased in S3I-201-treated EAE mice compared to vehicle-treated EAE mice. S3I-201 treatment significantly decreased CD4(+)IFN-γ(+), CD4(+)STAT1(+), CD4(+)pSTAT1(+), CD4(+)T-bet(+), CD4(+)IL-17A(+), CD4(+)STAT3(+), CD4(+)pSTAT3(+), and CD4(+)RORγt(+) and increased CD4(+)IL-10(+), CD4(+)TGF-β1(+), and CD4(+)FoxP3(+) in the spleens of EAE mice. Additionally, S3I-201 administration in EAE mice significantly decreased the mRNA and protein expression of Th1 and Th17 and increased those of Treg. These results suggest that S3I-201 may have novel therapeutic potential against MS.
 We recently discovered a (to our knowledge) new neuroimmune interaction named the gateway reflex, in which the activation of specific neural circuits establishes immune cell gateways at specific vessel sites in organs, leading to the development of tissue-specific autoimmune diseases, including a multiple sclerosis (MS) mouse model, experimental autoimmune encephalomyelitis (EAE). We have reported that peripheral-derived myeloid cells, which are CD11b+MHC class II+ and accumulate in the fifth lumbar (L5) cord during the onset of a transfer model of EAE (tEAE), play a role in the pain-mediated relapse via the pain-gateway reflex. In this study, we investigated how these cells survive during the remission phase to cause the relapse. We show that peripheral-derived myeloid cells accumulated in the L5 cord after tEAE induction and survive more than other immune cells. These myeloid cells, which highly expressed GM-CSFRα with common β chain molecules, grew in number and expressed more Bcl-xL after GM-CSF treatment but decreased in number by blockade of the GM-CSF pathway, which suppressed pain-mediated relapse of neuroinflammation. Therefore, GM-CSF is a survival factor for these cells. Moreover, these cells were colocalized with blood endothelial cells (BECs) around the L5 cord, and BECs expressed a high level of GM-CSF. Thus, GM-CSF from BECs may have an important role in the pain-mediated tEAE relapse caused by peripheral-derived myeloid cells in the CNS. Finally, we found that blockade of the GM-CSF pathway after pain induction suppressed EAE development. Therefore, GM-CSF suppression is a possible therapeutic approach in inflammatory CNS diseases with relapse, such as MS.
 BACKGROUND AND OBJECTIVES: Inflammasomes are involved in the pathogenesis of different neuroimmune and neurodegenerative diseases, including multiple sclerosis (MS). In a previous study by our group, the nucleotide-binding oligomerization domain, leucine-rich repeat receptor and pyrin-domain-containing 3 (NLRP3) inflammasome was reported to be associated with the response to interferon-beta in MS. Based on recent data showing the potential for the oral therapy fingolimod to inhibit NLRP3 inflammasome activation, here we investigated whether fingolimod could also be implicated in the response to this therapy in patients with MS. METHODS: NLRP3 gene expression levels were measured by real-time PCR in peripheral blood mononuclear cells at baseline and after 3, 6, and 12 months in a cohort of patients with MS treated with fingolimod (N = 23), dimethyl fumarate (N = 21), and teriflunomide (N = 21) and classified into responders and nonresponders to the treatment according to clinical and radiologic criteria. In a subgroup of fingolimod responders and nonresponders, the percentage of monocytes with an oligomer of ASC was determined by flow cytometry, and the levels of interleukin (IL)-1β, IL-18, IL-6, tumor necrosis factor (TNF)α, and galectin-3 were quantified by ELISA. RESULTS: NLPR3 expression levels were significantly increased in fingolimod nonresponders after 3 (p = 0.03) and 6 months (p = 0.008) of treatment compared with the baseline but remained similar in responders at all time points. These changes were not observed in nonresponders to the other oral therapies tested. The formation of an oligomer of ASC in monocytes after lipopolysaccharide and adenosine 5'-triphosphate stimulation was significantly decreased in responders (p = 0.006) but increased in nonresponders (p = 0.0003) after 6 months of fingolimod treatment compared with the baseline. Proinflammatory cytokine release from stimulated peripheral blood mononuclear cells was comparable between responders and nonresponders, but galectin-3 levels on cell supernatants, as a marker of cell damage, were significantly increased in fingolimod nonresponders (p = 0.02). DISCUSSION: The differential effect of fingolimod on the formation of an inflammasome-triggered ASC oligomer in monocytes between responders and nonresponders could be used as a response biomarker after 6 months of fingolimod treatment and suggests that fingolimod may exert their beneficial effects by reducing inflammasome signaling in a subset of patients with MS.
 Multiple sclerosis (MS), a distinct autoimmune neuroinflammatory disorder, affects millions of people worldwide, including Saudi Arabia. Changes in the gut microbiome are linked to the development of neuroinflammation via mechanisms that are not fully understood. Prebiotics and probiotics in camel milk that has been fermented have a variety of health benefits. In this study, Bacillus amyloliquefaciens-supplemented camel milk (BASY) was used to assess its preventive effect on MS symptoms in a myelin oligodendrocyte glycoprotein (MOG)-immunized C57BL6J mice model. To this end, MOG-induced experimental autoimmune encephalomyelitis (EAE) was established and the level of disease index, pathological scores, and anti-inflammatory markers of BASY-treated mice using macroscopic and microscopic examinations, qPCR and immunoblot were investigated. The results demonstrate that BASY significantly reduced the EAE disease index, increased total microbial load (2.5 fold), and improved the levels of the short-chain fatty acids propionic, butyric and caproic acids in the diseased mice group. Additionally, myeloperoxidase (MPO) proinflammatory cytokines (IL-1β, IL-6, IL-17, TNF-α) and anti-inflammatory cytokines (TGF-β) were regulated by BASY treatment. Significant suppression of MPO and VCAM levels were noticed in the BASY-treated group (from 168 to 111 µM and from 34 to 27 pg/mL, respectively), in comparison to the EAE group. BASY treatment significantly reduced the expression of inflammatory cytokines, inflammatory progression related transcripts, and inflammatory progression protein markers. In conclusion, BASY significantly reduced the symptoms of EAE mice and may be used to develop a probiotic-based diet to promote host gut health. The cumulative findings of this study confirm the significant neuroprotection of BASY in the MOG-induced mice model. They could also suggest a novel approach to the treatment of MS-associated disorders.
 BACKGROUND: There is limited and inconsistent information on the prevalence of cognitive impairment in neuromyelitis optica spectrum disorders (NMOSD). OBJECTIVE: To assess cognitive performance and changes over time in NMOSD. METHODS: This study included data from 217 aquaporin-4-IgG-seropositive (80%) and double-seronegative NMOSD patients. Cognitive functions measured by Symbol Digit Modalities Test (SDMT), Paced Auditory Serial-Addition Task (PASAT), and/or Multiple Sclerosis Inventory Cognition (MuSIC) were standardized against normative data (N = 157). Intraindividual cognitive performance at 1- and 2-year follow-up was analyzed. Cognitive test scores were correlated with demographic and clinical variables and assessed with a multiple linear regression model. RESULTS: NMOSD patients were impaired in SDMT (p = 0.007), MuSIC semantic fluency (p < 0.001), and MuSIC congruent speed (p < 0.001). No significant cognitive deterioration was found at follow-up. SDMT scores were related to motor and visual disability (p(Bon) < 0.05). No differences were found between aquaporin-4-IgG-seropositive and double-seronegative NMOSD. CONCLUSIONS: A subset of NMOSD patients shows impairment in visual processing speed and in semantic fluency regardless of serostatus, without noticeable changes during a 2-year observation period. Neuropsychological measurements should be adapted to physical and visual disabilities.
 BACKGROUND: CSF free light chains help diagnose multiple sclerosis, but no data is available on the Asian population. Our objective was to study the diagnostic utility of CSF free light chains for diagnosing multiple sclerosis in Indian patients. METHODS: Prospective multicentric case-control study. Cases included those who were tested for oligoclonal bands and fulfilled the modified McDonald criteria 2017 for multiple sclerosis and clinically isolated syndromes. Those tested for oligoclonal bands (OCB) but with other diagnoses- inflammatory and non-inflammatory were included as controls. Clinical details were collected from electronic medical records. CSF and serum kappa and lambda free light chains were measured, apart from oligoclonal bands, immunoglobulin, and albumin in paired serum and CSF samples. RESULTS: There were 70 patients (31 cases and 39 controls). The mean age was 43.41(SD 16.073) years, and 43(61.4%) were females. CSF kappa showed highest specificity 97.4%, at a cut off 2.06 mg/L (sensitivity 71%) and highest sensitivity 90.3%, at a cut off 0.47 mg/L (specificity 79.5%). Best balance of sensitivity and specificity for CSF kappa was seen at a cut-off of ≥ 0.63 mg/L {sensitivity 87·1 (CI - 70.17-96.37), and specificity 87·18 (CI -72.57-95.70)}. The ratio of Kappa/lambda showed highest specificity of 100%(similar to OCB) with a sensitivity of 71% at a cut off of 1.72. The ratio of sum of kappa and lambda light chains, and Qalb (∑CSF FLC/Qalb), showed the highest specificity (94.87%)among the blood brain barrier corrected ratios. CONCLUSION: This study showed that the diagnostic utility of CSF kappa was comparable to OCB to diagnose multiple sclerosis in sensitivity, but not specificity, so can be a screening test before testing for OCB in our population.
 BACKGROUND AND OBJECTIVE: In people with multiple sclerosis (pwMS), concern for potential disease exacerbation or triggering of other autoimmune disorders contributes to vaccine hesitancy. We assessed the humoral and T-cell responses to SARS-CoV-2 after mRNA vaccination, changes in disease activity, and development of antibodies against central or peripheral nervous system antigens. METHODS: This was a prospective 1-year longitudinal observational study of pwMS and a control group of patients with other inflammatory neurologic disorders (OIND) who received an mRNA vaccine. Blood samples were obtained before the first dose (T1), 1 month after the first dose (T2), 1 month after the second dose (T3), and 6 (T4), 9 (T5), and 12 (T6) months after the first dose. Patients were assessed for the immune-specific response, annualized relapse rate (ARR), and antibodies to onconeuronal, neural surface, glial, ganglioside, and nodo-paranodal antigens. RESULTS: Among 454 patients studied, 390 had MS (22 adolescents) and 64 OIND; the mean (SD) age was 44 (14) years; 315 (69%) were female; and 392 (87%) were on disease-modifying therapies. Antibodies to the receptor-binding domain were detected in 367 (86%) patients at T3 and 276 (83%) at T4. After a third dose, only 13 (22%) of 60 seronegative patients seroconverted, and 255 (92%) remained seropositive at T6. Cellular responses were present in 381 (93%) patients at T3 and in 235 (91%) patients at T6 including all those receiving anti-CD20 therapies and in 79% of patients receiving fingolimod. At T3 (429 patients) or T6 (395 patients), none of the patients had developed CNS autoantibodies. Seven patients had neural antibodies that were already present before immunization (3 adult patients with MS had MOG-IgG, 2 with MG and 1 with MS had neuronal cell surface antibodies [unknown antigen], and 1 with MS had myelin antibody reactivity [unknown antigen]. Similarly, no antibodies against PNS antigens were identified at T3 (427 patients). ARR was lower in MS and not significantly different in patients with OIND. Although 182 (40%) patients developed SARS-CoV-2 infection, no cases of severe COVID-19 or serious adverse events occurred. DISCUSSION: In this study, mRNA COVID-19 vaccination was safe and did not exacerbate the autoimmune disease nor triggered neural autoantibodies or immune-mediated neurologic disorders. The outcome of patients who developed SARS-CoV-2 infection was favorable.
 BACKGROUND: Observational studies showed renal function had associations with Alzheimer's disease (AD), Parkinson's disease (PD), Lewy body dementia (LBD) and multiple sclerosis (MS). However, it is unknown whether these associations are causal. METHODS: We use a two-sample Mendelian randomization (MR) analysis to investigate causal relationships between renal function and 6 neurodegenerative diseases (NDDs): AD (including familial AD), PD, LBD, frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and MS. Blood urea nitrogen (BUN), chronic kidney disease (CKD) and estimated glomerular filtration rate (eGFR) were used to measure renal function. The inverse-variance weighted (IVW) was the predominant estimation method. The results were further validated using sensitivity analysis (i.e. MR Egger regression, Cochran Q statistic of IVW, and leave-one-out method). RESULTS: There was no indication of any causative relationship of BUN, CKD, or eGFR with AD, familial AD, PD, LBD, FTD and ALS (all P values >0.05). The IVW analysis demonstrated a causal relationship between eGFR and MS [odds ratio (OR), 4.89; 95% confidence interval (CI), 1.43 to 16.71; P = 0.01] that was not verified in the MR-Egger and weighted median (all P values >0.05). However, no causal association of MS with BUN (OR, 0.91; 95% CI, 0.40-2.07; P = 0.82) and CKD (OR,1.04; 95% CI, 0.88-1.23; P = 0.66) was found. There was no single SNP that affects the overall trend. CONCLUSIONS: Our study showed that reduced eGFR was related to MS. The value of this study is that it provides a direction for further research on the relationship between reduced eGFR and MS.
 VLCFAs (very-long-chain fatty acids) are the most abundant fatty acids in myelin. Hence, during demyelination or aging, glia are exposed to higher levels of VLCFA than normal. We report that glia convert these VLCFA into sphingosine-1-phosphate (S1P) via a glial-specific S1P pathway. Excess S1P causes neuroinflammation, NF-κB activation, and macrophage infiltration into the CNS. Suppressing the function of S1P in fly glia or neurons, or administration of Fingolimod, an S1P receptor antagonist, strongly attenuates the phenotypes caused by excess VLCFAs. In contrast, elevating the VLCFA levels in glia and immune cells exacerbates these phenotypes. Elevated VLCFA and S1P are also toxic in vertebrates based on a mouse model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE). Indeed, reducing VLCFA with bezafibrate ameliorates the phenotypes. Moreover, simultaneous use of bezafibrate and fingolimod synergizes to improve EAE, suggesting that lowering VLCFA and S1P is a treatment avenue for MS.
 Glial cells play an essential role in the complex function of the nervous system. In particular, astrocytes provide nutritive support for neuronal cells and are involved in regulating synaptic transmission. Oligodendrocytes ensheath axons and support information transfer over long distances. Microglial cells constitute part of the innate immune system in the brain. Glial cells are equipped with the glutamate-cystine-exchanger xCT (SLC7A11), the catalytic subunit of system xc-, and the excitatory amino acid transporter 1 (EAAT1, GLAST) and EAAT2 (GLT-1). Thereby, glial cells maintain balanced extracellular glutamate levels that enable synaptic transmission and prevent excitotoxic states. Expression levels of these transporters, however, are not fixed. Instead, expression of glial glutamate transporters are highly regulated in reaction to the external situations. Interestingly, such regulation and homeostasis is lost in diseases such as glioma, (tumor-associated) epilepsy, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis or multiple sclerosis. Upregulation of system xc- (xCT or SLC7A11) increases glutamate export from the cell, while a downregulation of EAATs decreases intracellular glutamate import. Occurring simultaneously, these reactions entail excitotoxicity and thus harm neuronal function. The release of glutamate via the antiporter system xc- is accompanied by the import of cystine-an amino acid essential in the antioxidant glutathione. This homeostasis between excitotoxicity and intracellular antioxidant response is plastic and off-balance in central nervous system (CNS) diseases. System xc- is highly expressed on glioma cells and sensitizes them to ferroptotic cell death. Hence, system xc- is a potential target for chemotherapeutic add-on therapy. Recent research reveals a pivotal role of system xc- and EAAT1/2 in tumor-associated and other types of epilepsy. Numerous studies show that in Alzheimer's disease, amyotrophic lateral sclerosis and Parkinson's disease, these glutamate transporters are dysregulated-and disease mechanisms could be interposed by targeting system xc- and EAAT1/2. Interestingly, in neuroinflammatory diseases such as multiple sclerosis, there is growing evidence for glutamate transporter involvement. Here, we propose that the current knowledge strongly suggest a benefit from rebalancing glial transporters during treatment.
 Accumulating evidence highlights the pathogenetic role of human endogenous retroviruses (HERVs) in eliciting and maintaining multiple sclerosis (MS). Epigenetic mechanisms, such as those regulated by TRIM 28 and SETDB1, are implicated in HERV activation and in neuroinflammatory disorders, including MS. Pregnancy markedly improves the course of MS, but no study explored the expressions of HERVs and of TRIM28 and SETDB1 during gestation. Using a polymerase chain reaction real-time Taqman amplification assay, we assessed and compared the transcriptional levels of pol genes of HERV-H, HERV-K, HERV-W; of env genes of Syncytin (SYN)1, SYN2, and multiple sclerosis associated retrovirus (MSRV); and of TRIM28 and SETDB1 in peripheral blood and placenta from 20 mothers affected by MS; from 27 healthy mothers, in cord blood from their neonates; and in blood from healthy women of child-bearing age. The HERV mRNA levels were significantly lower in pregnant than in nonpregnant women. Expressions of all HERVs were downregulated in the chorion and in the decidua basalis of MS mothers compared to healthy mothers. The former also showed lower mRNA levels of HERV-K-pol and of SYN1, SYN2, and MSRV in peripheral blood. Significantly lower expressions of TRIM28 and SETDB1 also emerged in pregnant vs. nonpregnant women and in blood, chorion, and decidua of mothers with MS vs. healthy mothers. In contrast, HERV and TRIM28/SETDB1 expressions were comparable between their neonates. These results show that gestation is characterized by impaired expressions of HERVs and TRIM28/SETDB1, particularly in mothers with MS. Given the beneficial effects of pregnancy on MS and the wealth of data suggesting the putative contribution of HERVs and epigenetic processes in the pathogenesis of the disease, our findings may further support innovative therapeutic interventions to block HERV activation and to control aberrant epigenetic pathways in MS-affected patients.
 IMPORTANCE: Natalizumab cessation is associated with a risk of rebound disease activity. It is important to identify the optimal switch disease-modifying therapy strategy after natalizumab to limit the risk of severe relapses. OBJECTIVES: To compare the effectiveness and persistence of dimethyl fumarate, fingolimod, and ocrelizumab among patients with relapsing-remitting multiple sclerosis (RRMS) who discontinued natalizumab. DESIGN, SETTING, AND PARTICIPANTS: In this observational cohort study, patient data were collected from the MSBase registry between June 15, 2010, and July 6, 2021. The median follow-up was 2.7 years. This was a multicenter study that included patients with RRMS who had used natalizumab for 6 months or longer and then were switched to dimethyl fumarate, fingolimod, or ocrelizumab within 3 months after natalizumab discontinuation. Patients without baseline data were excluded from the analysis. Data were analyzed from May 24, 2022, to January 9, 2023. EXPOSURES: Dimethyl fumarate, fingolimod, and ocrelizumab. MAIN OUTCOMES AND MEASURES: Primary outcomes were annualized relapse rate (ARR) and time to first relapse. Secondary outcomes were confirmed disability accumulation, disability improvement, and subsequent treatment discontinuation, with the comparisons for the first 2 limited to fingolimod and ocrelizumab due to the small number of patients taking dimethyl fumarate. The associations were analyzed after balancing covariates using an inverse probability of treatment weighting method. RESULTS: Among 66 840 patients with RRMS, 1744 had used natalizumab for 6 months or longer and were switched to dimethyl fumarate, fingolimod, or ocrelizumab within 3 months of natalizumab discontinuation. After excluding 358 patients without baseline data, a total of 1386 patients (mean [SD] age, 41.3 [10.6] years; 990 female [71%]) switched to dimethyl fumarate (138 [9.9%]), fingolimod (823 [59.4%]), or ocrelizumab (425 [30.7%]) after natalizumab. The ARR for each medication was as follows: ocrelizumab, 0.06 (95% CI, 0.04-0.08); fingolimod, 0.26 (95% CI, 0.12-0.48); and dimethyl fumarate, 0.27 (95% CI, 0.12-0.56). The ARR ratio of fingolimod to ocrelizumab was 4.33 (95% CI, 3.12-6.01) and of dimethyl fumarate to ocrelizumab was 4.50 (95% CI, 2.89-7.03). Compared with ocrelizumab, the hazard ratio (HR) of time to first relapse was 4.02 (95% CI, 2.83-5.70) for fingolimod and 3.70 (95% CI, 2.35-5.84) for dimethyl fumarate. The HR of treatment discontinuation was 2.57 (95% CI, 1.74-3.80) for fingolimod and 4.26 (95% CI, 2.65-6.84) for dimethyl fumarate. Fingolimod use was associated with a 49% higher risk for disability accumulation compared with ocrelizumab. There was no significant difference in disability improvement rates between fingolimod and ocrelizumab. CONCLUSION AND RELEVANCE: Study results show that among patients with RRMS who switched from natalizumab to dimethyl fumarate, fingolimod, or ocrelizumab, ocrelizumab use was associated with the lowest ARR and discontinuation rates, and the longest time to first relapse.
 BACKGROUND: Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that may lead to progressive disability. Here, we explored the behavioral pattern and the role of vasculature especially PDGFRB+ pericytes/ perivascular cells, in MS pathogenesis. METHODS: We have evaluated vascular changes in two different experimental allergic encephalomyelitis (EAE) mice models (MOG and PLP-induced). PDGFRB+ cells demonstrated distinct and different behavioral patterns. In both models, fibrosis formation was detected via collagen, fibronectin, and extracellular matrix accumulation. RESULTS: The PLP-induced animal model revealed that fibrosis predominantly occurs in perivascular locations and that PDGFRB+ cells are accumulated around vessels. Also, the expression of fibrotic genes and genes coding extracellular matrix (ECM) proteins are upregulated. Moreover, the perivascular thick wall structures in affected vessels of this model presented primarily increased PDGFRB+ cells but not NG2+ cells in the transgenic NG2-DsRed transgenic animal model. On the other hand, in MOG induced model, PDGFRB+ perivascular cells were accumulated at the lesion sites. PDGFRB+ cells colocalized with ECM proteins (collagen, fibronectin, and lysyl oxidase L3). Nevertheless, both MOG and PLP-immunized mice showed increasing EAE severity, and disability parallel with enhanced perivascular cell accumulation as the disease progressed from earlier (day 15) to later (day 40). CONCLUSION: As a result, we have concluded that PDGFRB+ perivascular cells may be participating in lesion progression and as well as demonstrating different responses in different EAE models.
 BACKGROUND: Neurodegenerative diseases are among the most prevalent and devastating neurological disorders, with few effective prevention and treatment strategies. We aimed to integrate genetic and proteomic data to prioritize drug targets for neurodegenerative diseases. METHODS: We screened human proteomes through Mendelian randomization to identify causal mediators of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, frontotemporal dementia, and Lewy body dementia. For instruments, we used brain and blood protein quantitative trait loci identified from one genome-wide association study with 376 participants and another with 3301 participants, respectively. Causal associations were subsequently validated by sensitivity analyses and colocalization. The safety and druggability of identified targets were also evaluated. RESULTS: Our analyses showed targeting BIN1, GRN, and RET levels in blood as well as ACE, ICA1L, MAP1S, SLC20A2, and TOM1L2 levels in brain might reduce Alzheimer's disease risk, while ICA1L, SLC20A2, and TOM1L2 were not recommended as prioritized drugs due to the identified potential side effects. Brain CD38, DGKQ, GPNMB, and SEC23IP were candidate targets for Parkinson's disease. Among them, GPNMB was the most promising target for Parkinson's disease with their causal relationship evidenced by studies on both brain and blood tissues. Interventions targeting FCRL3, LMAN2, and MAPK3 in blood and DHRS11, FAM120B, SHMT1, and TSFM in brain might affect multiple sclerosis risk. The risk of amyotrophic lateral sclerosis might be reduced by medications targeting DHRS11, PSMB3, SARM1, and SCFD1 in brain. CONCLUSIONS: Our study prioritized 22 proteins as targets for neurodegenerative diseases and provided preliminary evidence for drug development. Further studies are warranted to validate these targets.
 Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is an extremely rare hereditary cerebral small vessel disease caused by homozygous or compound heterozygous mutations in the gene coding for high-temperature requirement A serine peptidase 1 (HtrA1). Given the rare nature of the disease, delays in diagnosis and misdiagnosis are not uncommon. In this article, we reported the first case of CARASIL from Saudi Arabia with a novel homozygous variant c.1156C>T in exon 7 of the HTRA1 gene. The patient was initially misdiagnosed with primary progressive multiple sclerosis and treated with rituximab. CARASIL should be considered in the differential diagnosis of patients with suspected atypical progressive multiple sclerosis who have additional signs such as premature scalp alopecia and low back pain with diffuse white matter lesions in brain MRI. Genetic testing is important to confirm the diagnosis.
 INTRODUCTION: Concern of a correlation between disease relapse in patients with acquired demyelinating disorders of central nervous system (CNS) and SARS-CoV2 vaccines has been raised. In this single center study, we retrospectively evaluated safety of SARS-CoV2 vaccination and COVID-19 short-term outcome in pediatric acquired demyelinating disorders of CNS. MATERIALS AND METHODS: Patients with multiple sclerosis (MS), myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) and neuromyelitis optica spectrum disorder (NMOSD) with disease onset before 18 years of age were included. Demographic and clinical data, and information regarding previous SARS-CoV-2 infection and vaccination were collected. RESULTS: We included nine patients with MOGAD. Six patients received SARS-CoV2 vaccination and complained pain at injection site while only one had fever and fatigue. Median follow-up was 28 weeks (range 20-48). Seven patients had COVID-19 occurring with mild flu-like symptoms and median follow-up was 28 weeks (range 24-34). Nobody had disease relapse. Five patients with NMOSD were included. All patients received SARS-CoV2 vaccination (BNT162b2-Pfizer-BioNTech). The median follow-up was 20 weeks (range 14-24) and only two patients complained pain at injection site, fever and fatigue. Three patients had also COVID-19 with mild flu-like symptoms, despite two of them being under immunosuppressive treatment. Lastly, forty-three patients with MS were included. 35 out of 43 received SARS-CoV2 vaccination with a median follow-up of 24 weeks (range 8-36). Fourteen patients had no side effects, while 21 complained mild side effects (mainly pain at injection site) and one experienced a disease relapse with complete recovery after steroid therapy. At vaccination, all but one were under treatment. Sixteen patients had COVID-19 occurring with mild symptoms. DISCUSSION: COVID-19 outcome was good although many patients were under immunosuppressive treatment. Vaccine-related side effects were frequent but were mild and self-limited. Only one MS patient had a post-vaccination relapse with complete recovery after steroid therapy. In conclusion, our data support the safety of SARS-CoV-2 vaccines in pediatric MS, MOGAD and NMOSD.
 BACKGROUND: Tumour necrosis factor (TNF) is a pleiotropic cytokine and master regulator of the immune system. It acts through two receptors resulting in often opposing biological effects, which may explain the lack of therapeutic potential obtained so far in multiple sclerosis (MS) with non-receptor-specific anti-TNF therapeutics. Under neuroinflammatory conditions, such as MS, TNF receptor-1 (TNFR1) is believed to mediate the pro-inflammatory activities associated with TNF, whereas TNF receptor-2 (TNFR2) may instead induce anti-inflammatory effects as well as promote remyelination and neuroprotection. In this study, we have investigated the therapeutic potential of blocking TNFR1 whilst simultaneously stimulating TNFR2 in a mouse model of MS. METHODS: Experimental autoimmune encephalomyelitis (EAE) was induced with myelin oligodendrocyte glycoprotein (MOG(35-55)) in humanized TNFR1 knock-in mice. These were treated with a human-specific TNFR1-selective antagonistic antibody (H398) and a mouse-specific TNFR2 agonist (EHD2-sc-mTNF(R2)), both in combination and individually. Histopathological analysis of spinal cords was performed to investigate demyelination and inflammatory infiltration, as well as axonal and neuronal degeneration. Retinas were examined for any protective effects on retinal ganglion cell (RGC) degeneration and neuroprotective signalling pathways analysed by Western blotting. RESULTS: TNFR modulation successfully ameliorated symptoms of EAE and reduced demyelination, inflammatory infiltration and axonal degeneration. Furthermore, the combinatorial approach of blocking TNFR1 and stimulating TNFR2 signalling increased RGC survival and promoted the phosphorylation of Akt and NF-κB, both known to mediate neuroprotection. CONCLUSION: These results further support the potential of regulating the balance of TNFR signalling, through the co-modulation of TNFR1 and TNFR2 activity, as a novel therapeutic approach in treating inflammatory demyelinating disease.
 Multiple sclerosis (MS) is a severe autoimmune disease leading to demyelination, followed by consequent axonal degeneration, causing sensory, motor, cognitive, and visual symptoms. Experimental autoimmune encephalomyelitis (EAE) is the most well-studied animal model of MS. Most current MS treatments are not completely effective, and severe side effects remain a great challenge. In this study, we report the therapeutic efficacy of PD98059, a potent mitogen-activated protein kinase inhibitor, on proteolipid protein (PLP)(139-151)-induced EAE in SJL/J mice. Following the induction of EAE, mice were intraperitoneally treated with PD98059 (5 mg/kg for 14 days) daily from day 14 to day 28. This study investigated the effects of PD98059 on C-C motif chemokine receptor 6 (CCR6), CD14, NF-κB p65, IκBα, GM-CSF, iNOS, IL-6, TNF-α in CD45R(+) B lymphocytes using flow cytometry. Furthermore, we analyzed the effect of PD98059 on CCR6, CD14, NF-κB p65, GM-CSF, iNOS, IL-6, and TNF-α mRNA and protein expression levels using qRT-PCR analysis in brain tissues. Mechanistic investigations revealed that PD98059-treated in mice with EAE had reduced CD45R(+)CCR6(+), CD45R(+)CD14(+), CD45R(+)NF-κB p65(+), CD45R(+)GM-CSF(+), CD45R(+)iNOS(+), CD45R(+)IL-6(+), and CD45R(+)TNF-α(+) cells and increased CD45R(+)IκBα(+) cells compared with vehicle-treated control mice in the spleen. Moreover, downregulation of CCR6, CD14, NF-κB p65, GM-CSF, iNOS, IL-6, and TNF-α mRNA expression level was observed in PD98059-treated mice with EAE compared with vehicle-treated control mice in the brain tissue. The results of this study demonstrate that PD98059 modulates inflammatory mediators through multiple cellular mechanisms. The results of this study suggest that PD98059 may be pursued as a therapeutic agent for the treatment of MS.
 Autoreactive T cells, particularly those characterized by a Th17 phenotype, exert significant influence on the pathogenesis of multiple sclerosis (MS). The present study aimed to elucidate the impact of individual and combined administration of vitamin A and D on neuroinflammation, and microRNAs (miRNAs) involved in T helper (Th)17 development, utilizing a murine model of experimental autoimmune encephalomyelitis (EAE). EAE was induced in C57BL/6 mice, and 3 days prior to immunization, intraperitoneal injections of vitamins A and D or their combination were administered. Th17 cell percentages were determined in splenocytes utilizing intracellular staining and flow cytometry. Furthermore, the expression of Ror γ-t, miR-98-5p and Let-7a-5p, was measured in both splenocytes and spinal cord tissues using RT-PCR. Treatment with vitamin A and D resulted in a reduction in both disease severity in EAE mice. Treated mice showed a decreased frequency of Th17 cells and lower expression levels of IL17 and Ror γ-t in splenocytes and spinal cord. The spinal cord tissues and splenocytes of mice treated with vitamins A, D, and combined A+D showed a significant upregulation of miR-98-5p and Let-7a-5p compared to the EAE group. Statistical analysis indicated a strong negative correlation between miR-98-5p and Let-7a-5p levels in splenocytes and Ror-t expression. Our findings indicate that the administration of vitamins A and D exerts a suppressive effect on neuroinflammation in EAE that is associated with a reduction in the differentiation of T cells into the Th17 phenotype and is mediated by the upregulation of miR-98-5p and Let-7a-5p, which target the Ror γ-t.
 BACKGROUND: Increasing evidence suggests that gut dysbiosis can directly or indirectly affect the immune system through the brain-gut axis and play a role in the occurrence and development of Multiple sclerosis (MS). Oxymatrine (OMAT) has been shown to ameliorate the symptoms of MS in the classical experimental autoimmune encephalomyelitis (EAE) model of MS, but whether its therapeutic role is through the correction of gut dysbiosis, is unclear. METHODS: The effects of OMAT on intestinal flora and short-chain fatty acids in EAE model mice were evaluated by 16S rRNA sequencing and GC-MS/MS, respectively, and the function change of the blood-brain barrier and intestinal epithelial barrier was further tested by immunohistochemical staining, Evans Blue leakage detection, and RT-qPCR. RESULTS: The alpha and beta diversity in the feces of EAE mice were significantly different from that of the control group but recovered substantially after OMAT treatment. Besides, the OMAT treatment significantly affected the gut functional profiling and the abundance of genes associated with energy metabolism, amino acid metabolism, the immune system, infectious diseases, and the nervous system. OMAT also decreased the levels of isobutyric acid and isovaleric acid in EAE mice, which are significantly related to the abundance of certain gut microbes and were consistent with the reduced expression of TNF-a, IL-6, and IL-1b. Furthermore, OMAT treatment significantly increased the expression of ZO-1 and occludin in the brains and colons of EAE mice and decreased blood-brain barrier permeability. CONCLUSION: OMAT may alleviate the clinical and pathological symptoms of MS by correcting dysbiosis, restoring gut ecological and functional microenvironment, and inhibiting immune cell-mediated inflammation to remodel the brain-gut axis.
 Demyelinating disorders are among the most common and debilitating diseases in neurology. Canavan disease (CD) is a lethal demyelinating disease caused by mutation of the aspartoacylase (ASPA) gene, which leads to the accumulation of its substrate N-acetyl-l-aspartate (NAA), and consequently demyelination and vacuolation in the brain. In this study, hypoimmunogenic human induced pluripotent stem cell (iPSC)-derived oligodendrocyte progenitor cells (OPC) are developed from a healthy donor as an "off-the-shelf" cell therapy. Hypoimmunogenic iPSCs are generated through CRISPR/Cas9 editing of the human leukocyte antigen (HLA) molecules in healthy donor-derived iPSCs and differentiated into OPCs. The OPCs are engrafted into the brains of CD (nur7) mice and exhibit widespread distribution in the brain. The engrafted OPCs mature into oligodendrocytes that express the endogenous wildtype ASPA gene. Consequently, the transplanted mice exhibit elevated human ASPA expression and enzymatic activity and reduced NAA level in the brain. The transplanted OPCs are able to rescue major pathological features of CD, including defective myelination, extensive vacuolation, and motor function deficits. Moreover, the hypoimmunogenic OPCs exhibit low immunogenicity both in vitro and in vivo. The hypoimmunogenic OPCs can be used as "off-the-shelf" universal donor cells to treat various CD patients and many other demyelinating disorders, especially autoimmune demyelinating diseases, such as multiple sclerosis.
 Tumefactive multiple sclerosis comprises a rare subset of multiple sclerosis that often poses a diagnostic challenge to physicians. It is unique in its presentation as a solitary lesion, usually larger than 2 cm, with surrounding vasogenic edema, commonly mimicking a primary intracranial malignancy. We present a case of a 25-year-old female with no significant past medical history who presented to our institution with homonymous superior quadrantanopia. During her admission, she underwent a magnetic resonance imaging (MRI) of the brain, which revealed a large lesion in the left temporal area surrounded by marked edema. A thorough workup revealed a diagnosis of tumefactive multiple sclerosis. Subsequently, she was initiated on intravenous immunoglobulin rather than stress dose steroids, given the concern for a superimposed infection. Interestingly, the patient had a paradoxical progression of her symptoms as well as expansion of the vasogenic edema on a repeat MRI. In our case, we highlight the key differences in tumefactive multiple sclerosis diagnosis and management.
 Multiple sclerosis has been established as an inflammatory disease of the central nervous system. Many aspects of the pathophysiology are still unknown and it is presently unclear how different treatments affect the immunopathology of multiple sclerosis. In this study, we explored cytokines discriminating between individuals with multiple sclerosis and healthy controls and then how these cytokines were affected by treatment intervention with autologous haematopoietic stem cell transplantation or intrathecal rituximab. CSF from individuals with multiple sclerosis and healthy controls were analysed with a proximity extension assay to simultaneously determine the level of 92 cytokines and other inflammation-related proteins. In total, CSF from 158 multiple sclerosis patients and 53 healthy controls were analysed. Sixty-four patients with relapsing-remitting multiple sclerosis and 27 with progressive multiple sclerosis took part in a cross-sectional study and underwent lumbar puncture on a single occasion. Forty-five patients with relapsing-remitting multiple sclerosis were treated with autologous haematopoietic stem cell transplantation and underwent lumbar puncture at baseline and then at follow-up visits made at 1-, 2- and 5 years. Twenty-two patients with progressive multiple sclerosis were treated with intrathecal rituximab and followed with lumbar punctures at baseline and then at follow-up visits made at 3-, 6- and 12 months. Of the 92 studied cytokines, 16 were found to be altered in multiple sclerosis and 11 were decreased after treatment with autologous haematopoietic stem cell transplantation. None of the studied cytokines was affected by treatment with intrathecal rituximab for progressive multiple sclerosis. Some proteins were highly associated with each other. Therefore, a cluster analysis was made and then the highest-ranked protein from the four highest-ranked clusters was used for the subsequent analyses. CCL3, IL-12B, CXCL10 and IL-8 discriminated between multiple sclerosis patients and controls, but only IL-12B differed between patients with relapsing-remitting and progressive multiple sclerosis. The CSF concentrations of CCL3, IL-12B and CXCL10 were decreased after autologous haematopoietic stem cell transplantation, whereas IL-8 appeared to be unaffected by this intervention. High concentrations of IL-8 were associated with worse outcome in both treatment groups. Overall, the results suggest a profound effect of autologous haematopoietic stem cell transplantation on the inflammatory milieu of the CSF in multiple sclerosis.

 The course of pediatric-onset multiple sclerosis and adult multiple sclerosis shows some clinical differences. The rate of having a second attack after the first clinical event is 80% in children and around 45% in adults but the time to the second event is similar in all age groups. The pediatric group usually has a more aggressive onset than adults. On the other hand, a higher rate of complete recovery is observed in pediatric-onset multiple sclerosis after the first clinical event compared to the adult group. Despite a highly active initial disease course, pediatric-onset multiple sclerosis patients show a slower increase in disability than patients with adult-onset disease. This is thought to be due to greater remyelination capacity and plasticity of the developing brain. The management of pediatric-onset multiple sclerosis includes safety issues as well as effective disease control. In the pediatric-onset multiple sclerosis group, similar to adult multiple sclerosis, injectable treatments have been used for many years with reasonable efficacy and safety. Since 2011, oral treatments and then infusion treatments have been approved and used effectively in adult multiple sclerosis and have gradually entered clinical use in the pediatric-onset multiple sclerosis group. However, clinical trials are fewer, smaller, and include shorter follow-up due to the much lower prevalence of pediatric-onset multiple sclerosis than adult multiple sclerosis. This is particularly important in the era of recent disease-modifying treatments. This review of the literature presents existing data on the safety and efficacy of fingolimod, pointing to a relatively favorable profile.
 Registries have the potential to tackle some of the current limitations in determining the long-term impact of multiple sclerosis. Online assessments using patient-reported outcomes can streamline follow-up enabling large-scale, long-term, cost-effective, home-based, and patient-focused data collection. However, registry data are sparsely sampled and the sensitivity of patient-reported outcomes relative to clinician-reported scales is unknown, making it hard to fully leverage their unique scope and scale to derive insights. This retrospective and prospective cohort study over 11 years involved 15 976 patients with multiple sclerosis from the United Kingdom Multiples Sclerosis Register. Primary outcomes were changes in two patient-reported outcomes: Multiple Sclerosis Impact Scale motor component, and Multiple Sclerosis Walking Scale. First, we investigated their validity in measuring the impact of physical disability in multiple sclerosis, by looking at their sensitivity to disease subtype and duration. We grouped the available records (91 351 for Multiple Sclerosis Impact Scale motor and 68 092 for Multiple Sclerosis Walking Scale) by these two factors, and statistically compared the resulting groups using a novel approach based on Monte Carlo permutation analysis that was designed to cope with the intrinsic sparsity of registry data. Next, we used the patient-reported outcomes to draw novel insights into the developmental time course of subtypes; in particular, the period preceding the transition from relapsing to progressive forms. We report a robust main effect of disease subtype on the patient-reported outcomes and interactions of disease subtype with duration (all P < 0.0001). Specifically, patient-reported outcomes worsen with disease duration for all subtypes (all P < 0.0001) apart from benign multiple sclerosis (Multiple Sclerosis Impact Scale motor: P = 0.796; Multiple Sclerosis Walking Scale: P = 0.983). Furthermore, the patient-reported outcomes of each subtype are statistically different from those of the other subtypes at all time bins (Multiple Sclerosis Impact Scale motor: all P < 0.05; Multiple Sclerosis Walking Scale: all P < 0.01) except when comparing relapsing-remitting multiple sclerosis with benign multiple sclerosis and primary progressive multiple sclerosis with secondary progressive multiple sclerosis. Notably, there were statistically significant differences between relapsing-remitting and progressive subtypes at disease onset. Critically, the patient-reported outcomes are sensitive to future transitions to progressive subtypes, with individuals who transition presenting with higher patient-reported outcomes in their relapsing-remitting phase compared to individuals who don't transition since onset (all P < 0.0001). Patient-reported outcomes capture different patterns of physical worsening over disease length and across subtypes; therefore, they are a valid tool to measure the physical impact of multiple sclerosis over the long-term and cost-effectively. Furthermore, more advanced physical disability manifests years before clinical detection of progressive subtypes, adding evidence to the presence of a multiple sclerosis prodrome.
 BACKGROUND: Differences in pain between subtypes of multiple sclerosis are understudied. OBJECTIVE: To compare the prevalence of pain, and the association between pain and: (a) pain interference and (b) social participation in people with relapsing-remitting multiple sclerosis and progressive multiple sclerosis. METHODS: Participants completed the McGill Pain Questionnaire Short-Form-2, Pain Effects Scale and Ability to Participate in Social Roles and Activities-V2.0 questionnaires. We tested the association between multiple sclerosis subtype, pain severity, and pain interference/social participation using quantile regression. RESULTS: Of 231 participants (relapsing-remitting multiple sclerosis: 161, progressive multiple sclerosis: 70), 82.3% were women. The prevalence of pain was 95.2%, of more than mild pain was 38.1%, and of pain-related limitations was 87%; there were no differences between multiple sclerosis subtypes. Compared to participants with relapsing-remitting multiple sclerosis, those with progressive multiple sclerosis reported higher pain interference (mean (standard deviation) Pain Effects Scale; progressive multiple sclerosis: 15[6.0] vs relapsing-remitting multiple sclerosis: 13[5], p = 0.039) and lower social participation (Ability to Participate in Social Roles and Activities T-scores 45[9.0] vs 48.3[8.9], p = 0.011). However, on multivariable analysis accounting for age, physical disability, mood/anxiety and fatigue, multiple sclerosis subtype was not associated with differences in pain interference or social participation. CONCLUSIONS: Pain was nearly ubiquitous. Over one-third of individuals with relapsing-remitting multiple sclerosis and progressive multiple sclerosis reported pronounced pain, although this did not differ by multiple sclerosis subtype.
 Clinical observations suggest that the prevalence of autoimmune diseases is changing over time. Both autoimmune liver diseases and multiple sclerosis have shown a significant increase in the last decades. Although the coexistence of autoimmune diseases within individuals and families is a common phenomenon, the extent to which liver disease and multiple sclerosis co-occur is not clear. Case reports and few studies have reported the possible coexistence of multiple sclerosis with thyroid diseases, inflammatory bowel disease, psoriasis, and rheumatoid arthritis. It is unknown whether there is a definite association between multiple sclerosis and autoimmune liver diseases. We reviewed the literature to summarize the available studies on the association between different autoimmune liver diseases (autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis) and treated or untreated multiple sclerosis.
 Multiple sclerosis is a chronic inflammatory and demyelinating disease of the central nervous system, usually seen in young adults. Early onset of multiple sclerosis at age younger than 18 years is called paediatric multiple sclerosis. Unlike adult multiple sclerosis, paediatric multiple sclerosis causes morbidity at earlier ages and often progresses in a relapsing-remitting form. Although fingolimod is an effective drug used as a disease-modifiying therapy agent in relapsing-remitting paediatric multiple sclerosis patients, it can cause dysryhthmia in the early period after first dose. Our first case is a 14-year-old girl with relapsing-remitting paediatric multiple sclerosis patients who was started to take fingolimod treatment. In the fifth hour of the follow-up, asymptomatic bradycardia was seen and the electrocardiogram was consistent with first-degree atrioventricular block. Her rhythm got spontaneously normal after 12 hours. Second case was 13 years old girl. Steroid treatment was started after her first paediatric multiple sclerosis attack. Despite treatment, she had a second attack 2 weeks after the first attack. Therefore, the neurologist switched to fingolimod therapy. Second-degree atrioventriculer block developed after 4 hours from the initiation of therapy. After 8 hours, rhythm regressed to first-degree atrioventricular block then returned to normal up to 13th hours of follow up. The aim of this article is to draw attention to dysrhythmia side effect of fingolimod which can be fatal. Therefore, the clinician must take precautions. Close cardiac rhythm monitoring is mandatory after the initiation fingolimod theraphy.
 Remyelination failure is one of the main characteristics of multiple sclerosis and is potentially correlated with disease progression. Previous research has shown that the extracellular matrix is associated with remyelination failure because remodeling of the matrix often fails in both chronic and progressive multiple sclerosis. Fibronectin aggregates are assembled and persistently exist in chronic multiple sclerosis, thus inhibiting remyelination. Although many advances have been made in the mechanisms and treatment of multiple sclerosis, it remains very difficult for drugs to reach pathological brain tissues; this is due to the complexity of brain structure and function, especially the existence of the blood-brain barrier. Therefore, herein, we review the effects of fibronectin aggregates on multiple sclerosis and the efficacy of different forms of drug delivery across the blood-brain barrier in the treatment of this disease.
 Cognitive impairment occurs in 40-65% of persons with multiple sclerosis and may be related to alterations in glutamatergic and GABAergic neurotransmission. Therefore, the aim of this study was to determine how glutamatergic and GABAergic changes relate to cognitive functioning in multiple sclerosis in vivo. Sixty persons with multiple sclerosis (mean age 45.5 ± 9.6 years, 48 females, 51 relapsing-remitting multiple sclerosis) and 22 age-matched healthy controls (45.6 ± 22.0 years, 17 females) underwent neuropsychological testing and MRI. Persons with multiple sclerosis were classified as cognitively impaired when scoring at least 1.5 standard deviations below normative scores on ≥30% of tests. Glutamate and GABA concentrations were determined in the right hippocampus and bilateral thalamus using magnetic resonance spectroscopy. GABA-receptor density was assessed using quantitative [(11)C]flumazenil positron emission tomography in a subset of participants. Positron emission tomography outcome measures were the influx rate constant (a measure predominantly reflecting perfusion) and volume of distribution, which is a measure of GABA-receptor density. Twenty persons with multiple sclerosis (33%) fulfilled the criteria for cognitive impairment. No differences were observed in glutamate or GABA concentrations between persons with multiple sclerosis and healthy controls, or between cognitively preserved, impaired and healthy control groups. Twenty-two persons with multiple sclerosis (12 cognitively preserved and 10 impaired) and 10 healthy controls successfully underwent [(11)C]flumazenil positron emission tomography. Persons with multiple sclerosis showed a lower influx rate constant in the thalamus, indicating lower perfusion. For the volume of distribution, persons with multiple sclerosis showed higher values than controls in deep grey matter, reflecting increased GABA-receptor density. When comparing cognitively impaired and preserved patients to controls, the preserved group showed a significantly higher volume of distribution in cortical and deep grey matter and hippocampus. Positive correlations were observed between both positron emission tomography measures and information processing speed in the multiple sclerosis group only. Whereas concentrations of glutamate and GABA did not differ between multiple sclerosis and control nor between cognitively impaired, preserved and control groups, increased GABA-receptor density was observed in preserved persons with multiple sclerosis that was not seen in cognitively impaired patients. In addition, GABA-receptor density correlated to cognition, in particular with information processing speed. This could indicate that GABA-receptor density is upregulated in the cognitively preserved phase of multiple sclerosis as a means to regulate neurotransmission and potentially preserve cognitive functioning.
 BACKGROUND AND OBJECTIVE: As an essential but not specific marker of multiple sclerosis, oligoclonal bands are bands displayed by electrophoretic separation technique. Detection method evolves from conventional protein electrophoresis to isoelectric focusing electrophoresis. This article aims to review the role of oligoclonal bands in the diagnosis of multiple sclerosis and other neuroimmunological diseases. METHODS: The search engine PubMed (https://www.ncbi.nlm.nih.gov/pmc/) was used to research the keywords: "blood brain barrier", "blood brain barrier permeability", "detection methods", "multiple sclerosis" and "oligoclonal bands". A narrative review was conducted to literature findings from 1937 to 2021. KEY CONTENT AND FINDINGS: We first introduced the history of oligoclonal bands and its detection techniques. Next, the interpretation of different results of oligoclonal bands and the clinical implication, especially the value for the diagnosis of multiple sclerosis were discussed. Then the different prevalence of oligoclonal bands in multiple sclerosis between eastern and western countries and its occurrence rate in other neuroimmunological diseases were reviewed. Finally, we discussed the detection methods of blood brain barrier permeability and intrathecal immunoglobulin synthesis. It reveals that comprehensive analysis of oligoclonal bands, blood-brain barrier permeability and intrathecal synthesis of immunoglobulin provides valuable supporting information for the diagnosis of multiple sclerosis and other neuroimmunological diseases. CONCLUSIONS: This review discusses the comprehensive application of oligoclonal bands in multiple sclerosis and other neuroimmunological diseases.
 This study aimed to compare sensory processing skills and occupational performance between participants with multiple sclerosis and healthy controls. Eighty participants were enrolled in this study, 40 with multiple sclerosis and 40 with healthy controls. Participants were between 18 and 65 years of age and asked to complete the Adult Sensory Profile, and Canadian Occupational Performance Measure. The findings of the study revealed that participants with multiple sclerosis had a lower ability to register sensory input, a higher sensory sensitivity, and avoidance, as well as lower levels of performance and satisfaction in their daily occupations, compared to the healthy controls (p < 0.05). People with multiple sclerosis often experience difficulties with sensory processing and occupational performance in daily life. More research and practice are needed on the role of sensory processing and occupational performance in daily life in people with multiple sclerosis.
 Multiple sclerosis is a multifactorial chronic inflammatory disease of the central nervous system that leads to demyelination and neuronal cell death, resulting in functional disability. Remyelination is the natural repair process of demyelination, but it is often incomplete or fails in multiple sclerosis. Available therapies reduce the inflammatory state and prevent clinical relapses. However, therapeutic approaches to increase myelin repair in humans are not yet available. The substance cytidine-5'-diphosphocholine, CDP-choline, is ubiquitously present in eukaryotic cells and plays a crucial role in the synthesis of cellular phospholipids. Regenerative properties have been shown in various animal models of diseases of the central nervous system. We have already shown that the compound CDP-choline improves myelin regeneration in two animal models of multiple sclerosis. However, the results from the animal models have not yet been studied in patients with multiple sclerosis. In this review, we summarise the beneficial effects of CDP-choline on biolipid metabolism and turnover with regard to inflammatory and regenerative processes. We also explain changes in phospholipid and sphingolipid homeostasis in multiple sclerosis and suggest a possible therapeutic link to CDP-choline.
 BACKGROUND: Multiple sclerosis is a leading cause of non-traumatic neurological disability among young adults worldwide. Prior studies have identified modifiable risk factors for multiple sclerosis in cohorts of White ethnicity, such as infectious mononucleosis, smoking, and obesity during adolescence/early adulthood. It is unknown whether modifiable exposures for multiple sclerosis have a consistent impact on risk across ethnic groups. AIM: To determine whether modifiable risk factors for multiple sclerosis have similar effects across diverse ethnic backgrounds. METHODS: We conducted a nested case-control study using data from the UK Clinical Practice Research Datalink. Multiple sclerosis cases diagnosed from 2001 until 2022 were identified from electronic healthcare records and matched to unaffected controls based on year of birth. We used stratified logistic regression models and formal statistical interaction tests to determine whether the effect of modifiable risk factors for multiple sclerosis differed by ethnicity. RESULTS: We included 9662 multiple sclerosis cases and 118,914 age-matched controls. The cohort was ethnically diverse (MS: 277 South Asian [2.9%], 251 Black [2.6%]; Controls: 5043 South Asian [5.7%], 4019 Black [4.5%]). The age at MS diagnosis was earlier in the Black (40.5 [SD 10.9]) and Asian (37.2 [SD 10.0]) groups compared with White cohort (46.1 [SD 12.2]). There was a female predominance in all ethnic groups; however, the relative proportion of males was higher in the South Asian population (proportion of women 60.3% vs 71% [White] and 75.7% [Black]). Established modifiable risk factors for multiple sclerosis-smoking, obesity, infectious mononucleosis, low vitamin D, and head injury-were consistently associated with multiple sclerosis in the Black and South Asian cohorts. The magnitude and direction of these effects were broadly similar across all ethnic groups examined. There was no evidence of statistical interaction between ethnicity and any tested exposure, and no evidence to suggest that differences in area-level deprivation modifies these risk factor-disease associations. These findings were robust to a range of sensitivity analyses. CONCLUSIONS AND RELEVANCE: Established modifiable risk factors for multiple sclerosis are applicable across diverse ethnic backgrounds. Efforts to reduce the population incidence of multiple sclerosis by tackling these risk factors need to be inclusive of people from diverse ethnicities.
 Multiple sclerosis is a frequent condition where the diagnosis relies on clinical presentation, neurologic examination, cerebro spinal fluid markers, and diagnostic imaging tests; however, atypical variants of the disease can lead to misdiagnosis in some scenarios. Herein, we describe a case of a 24-year-old patient with multiple sclerosis with megacystic plaques, in which appropriate interpretation of the imaging findings lead to a proper diagnosis and treatment.
 Over the last few decades, the incidence of multiple sclerosis has increased as society's dietary habits have switched from a whole foods approach to a high fat, high salt, low dietary fiber, and processed food diet, termed the "Western diet." Environmental factors, such as diet, could play a role in the pathogenesis of multiple sclerosis due to gut microbiota alterations, gut barrier leakage, and subsequent intestinal inflammation that could lead to exacerbated neuroinflammation. This mini-review explores the gut microbiome alterations of various dietary strategies that improve upon the "Western diet" as promising alternatives and targets to current multiple sclerosis treatments. We also provide evidence that gut microbiome modulation through diet can improve or exacerbate clinical symptoms of multiple sclerosis, highlighting the importance of including gut microbiome analyses in future studies of diet and disease.
 Multiple sclerosis is a highly complex and heterogeneous disease. At the onset it often presents as a clinically isolated syndrome. Thereafter relapses are followed by periods of remissions, but eventually, most patients develop secondary progressive multiple sclerosis. It is widely accepted that autoantibodies are important to the pathogenesis of multiple sclerosis, but hitherto it has been difficult to identify the target of such autoantibodies. As an alternative strategy, cell-based methods of detecting autoantibodies have been developed. The objective of this study was to explore differences in the binding of antibodies from sera and CSF of multiple sclerosis patients and controls to oligodendroglial and neuronal cell-lines, related to antibody type, immunoglobulin (IgG/IgM), matrix (serum/CSF) and disease course. The oligodendroglial and neuronal cell-lines were expanded in tissue culture flasks and transferred to 96-well plates at a concentration of 50 000 cells/well followed by fixation and blocking with bovine serum albumin. Sera and CSF samples, from healthy controls and multiple sclerosis patients, were incubated with the fixed cells. Epitope binding of immunoglobulins (IgG and IgM) in sera and CSF was detected using biotinylated anti-human IgM and IgG followed by avidin conjugated to horseradish peroxidase. Horseradish peroxidase activity was detected with 3,3',5,5'-tetramethylbenzidine substrate. Serum from 76 patients and 30 controls as well as CSF from 62 patients and 32 controls were investigated in the study. The binding was similar between clinically isolated syndrome patients and controls, whereas the largest differences were observed between secondary progressive multiple sclerosis patients and controls. Antibodies from multiple sclerosis patients (all disease course combined) bound more to all investigated cell-lines, irrespectively of matrix type, but binding of immunoglobulin G from CSF to human oligodendroglioma cell-line discriminated best between multiple sclerosis patients and controls with a sensitivity of 93% and a specificity of 96%. The cell-based enzyme linked immunosorbent assay (ELISA) was able to discriminate between multiple sclerosis patients and controls with a high degree of accuracy. The disease course was the major determinant for the antibody binding.
 Cerebral cortical inflammation and neurodegeneration are hallmark pathological features of multiple sclerosis that contribute to irreversible neurological disability. While the reason for nerve cell death is unknown, the pathogenic inflammatory role of infiltrating lymphocytes is likely an important contributor. The nuclear receptor-related factor 1 counteracts inflammation in animal models of multiple sclerosis, and protects against neuronal loss in other neurodegenerative disorders, but its expression in post-mortem multiple sclerosis tissue is not known. This study aims to investigate the nuclear receptor-related factor 1 expression in multiple sclerosis motor cortex and evaluate its relationship with motor cortical pathology. To accomplish this, an autopsy cohort of pathologically confirmed multiple sclerosis (n = 46), and control (n = 11) cases was used, where the nuclear receptor-related factor 1 expression was related to neuronal and lymphocytic densities. Motor cortical nuclear receptor-related factor 1 was overexpressed in multiple sclerosis compared to control cases. Increased nuclear receptor-related factor 1 expression positively associated with neuronal densities, especially when present in nucleus of neurons, and associated with decreased CD8+ cytotoxic lymphocyte density. Our findings expand the current knowledge on nuclear receptor-related factor 1 in neurological diseases, and support the hypothesis that nuclear receptor-related factor 1 may play a dual neuroprotective role in multiple sclerosis by influencing inflammatory and neurodegenerative processes. Future studies elucidating the influence of nuclear receptor-related factor 1 on these processes in multiple sclerosis may cast light onto novel targets that may be modulated to alter clinical outcome.
 Multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system (CNS). Historically, research on MS has focused on White persons with MS. This preponderance of representation has important possible implications for minority populations with MS, from developing effective therapeutic agents to understanding the role of unique constellations of social determinants of health. A growing body of literature involving persons of historically underrepresented races and ethnicities in the field of multiple sclerosis is assembling. Our purpose in this narrative review is to highlight two populations in the United States: Black and Hispanic persons with multiple sclerosis. We will review the current understanding about the patterns of disease presentation, genetic considerations, response to treatment, roles of social determinants of health, and healthcare utilization. In addition, we explore future directions of inquiry as well as practical methods of meeting these challenges.
 Simultaneous occurrence of multiple sclerosis (MS) and ulcerative colitis (UC) is seldom encountered by clinicians and poses unique challenges. The sphingosine-1-phosphate receptor modulator ozanimod has been recently approved for UC. Ozanimod can be used in such scenarios where it can treat both conditions, reducing the need for multiple targeted therapies. We report the first case of successfully treated multiple sclerosis and UC with ozanimod.
 More than 2 million people live with multiple sclerosis worldwide and the prevalence has been increasing over time. Patients living with multiple sclerosis often explore diet and lifestyle interventions as a means of managing their symptoms and reducing reliance on medication; yet, these approaches are rarely discussed with their physicians. Currently, there is a lack of evidence on when to stop disease-modifying therapies (DMT), and recent research showed no statistically significant difference in the time between relapses when comparing participants who stopped DMT to those who did not, especially over the age of 45. This case report presents 2 patients with multiple sclerosis who made an informed decision to stop their DMT medications and have been managing their condition with a whole food plant-based diet and a healthy lifestyle approach. Over the period of 5 to 6 years since stopping the medications, each patient only had 1 multiple sclerosis flare-up to date. In the report, the focus is on the impact of diet on multiple sclerosis. It adds to currently available literature and encourages further research in the field of managing multiple sclerosis with lifestyle interventions.
 Behcet's disease is a chronic polysymptomatic systemic vasculitis disorder of unknown etiology characterized by several clinical manifestations in multiple organ systems. Involvement of the nervous system occurs in ∼9% of patients with Behcet's disease (ranging from 3 to 30%). Neuro-Behcet's disease is a great masquerader of multiple sclerosis. Diagnosing this disorder might be challenging, especially in a patient who does not fulfill the criteria of Behcet's disease while having a neurological presentation. We report a case of neuro-Behcet's disease who was misdiagnosed as having multiple sclerosis for many years and started on unnecessary disease-modifying therapy for multiple sclerosis. A thorough history, physical examination, and systematic investigations are mandatory to differentiate between these two conditions. Our case presentation raises awareness of the importance of differentiating between these two conditions since the consequences of misdiagnosis are catastrophic. The main challenges differentiating between multiple sclerosis and neuro-Behcet's are clinical and paraclinical, including neuroimaging.
 PURPOSE OF REVIEW: This review summarizes the pathophysiology and potential therapeutic options for treatment of multiple sclerosis, a common neuronal demyelinating disorder affecting 2.2 million people worldwide. As an autoimmune disorder, multiple sclerosis is associated with neuroinflammation and increased permeability of the blood-brain barrier (BBB), although the cause linking multiple sclerosis with compromised barrier function remains ill-defined. It has been previously shown that coagulation factors, including thrombin and fibrin, exacerbate the inflammatory processes and permeability of the BBB. RECENT FINDINGS: Increased levels of the coagulation factor (F) XII have been found in patients presenting with relapsing-remitting multiple sclerosis, with a deleterious role for FXII being validated in murine model of multiple sclerosis, experimental autoimmune encephalitis (EAE). Recent work has uncovered a role for the major substrate activated by FXII and thrombin, FXI, in the disorder of EAE. The study found that pharmacological targeting of FXI decreased clinical symptoms, lymphocyte invasion, and white matter destruction in a multiple sclerosis model. SUMMARY: This review emphasizes the role of FXII and FXI in regulating barrier function and the immune response in neuroinflammation. These new findings broaden the potential for therapeutic utility of FXI inhibitors beyond thrombosis to include neuroinflammatory diseases associated with compromised BBB function, including multiple sclerosis.
 Multiple sclerosis is a chronic autoimmune disease of the central nervous system and is generally considered to be a non-traumatic, physically debilitating neurological disorder. In addition to experiencing motor disability, patients with multiple sclerosis also experience a variety of non-motor symptoms, including cognitive deficits, anxiety, depression, sensory impairments, and pain. However, the pathogenesis and treatment of such non-motor symptoms in multiple sclerosis are still under research. Preclinical studies for multiple sclerosis benefit from the use of disease-appropriate animal models, including experimental autoimmune encephalomyelitis. Prior to understanding the pathophysiology and developing treatments for non-motor symptoms, it is critical to characterize the animal model in terms of its ability to replicate certain non-motor features of multiple sclerosis. As such, no single animal model can mimic the entire spectrum of symptoms. This review focuses on the non-motor symptoms that have been investigated in animal models of multiple sclerosis as well as possible underlying mechanisms. Further, we highlighted gaps in the literature to explain the non-motor aspects of multiple sclerosis in experimental animal models, which will serve as the basis for future studies.
 BACKGROUND: Fatigue is associated with reduced quality of life and social participation, and poor employment outcomes. However, most studies examining fatigue are limited by small sample sizes or short follow-up periods. OBJECTIVE: To characterize the natural history of fatigue. METHODS: The North American Research Committee on Multiple Sclerosis Registry participants with ≥7 years of longitudinal data between 2004 and 2019 and a relapsing disease course were included. A subset of participants enrolled within 5 years of diagnosis was identified. The Fatigue Performance Scale assessed fatigue and ≥1-point increase in Fatigue Performance Scale sustained at the next survey defined fatigue worsening. RESULTS: Of 3057 participants with longitudinal data, 944 were within 5 years of multiple sclerosis diagnosis. Most participants (52%) reported fatigue worsening during follow-up. Median time to fatigue worsening ranged from 3.5 to 5 years at lower levels of index fatigue. Fatigue worsening was associated with lower annual income, increasing disability, lower initial fatigue level, taking injectable disease-modifying therapies and increasing depression levels in the relapsing multiple sclerosis participants. CONCLUSION: Most multiple sclerosis participants early in their disease suffer from fatigue and at least half reported fatigue worsening over time. Understanding factors associated with fatigue may help to identify populations most at risk of fatigue worsening will be informative for the overall management of patients with multiple sclerosis.

 We report a case of intermediate uveitis in the setting of both systemic sarcoidosis and multiple sclerosis. A 68-year-old female was diagnosed with bilateral granulomatous intermediate uveitis and cystoid macular edema. Initial systemic work-up was unrevealing. The uveitis was treated successfully with local corticosteroid injections. Eighteen months after presentation, the patient developed new systemic symptoms. Additional testing revealed systemic lymphadenopathy, with biopsy showing non-caseating granulomas, leading to a diagnosis of sarcoidosis. However, MRI of the brain and spinal cord along with cerebrospinal fluid analysis was consistent with MS. The management of the uveitis and systemic inflammation was co-managed by ophthalmology, neurology, and rheumatology, and eventually controlled with leflunomide and rituximab. Patients can rarely have co-existing systemic sarcoidosis and multiple sclerosis. Although challenging to diagnose, radiographic findings and cerebrospinal fluid analysis can be helpful to differentiate multiple sclerosis and neurosarcoidosis. Management of these patients requires coordination between multiple specialties.
 In the last two years, a new severe acute respiratory syndrome coronavirus (SARS-CoV) infection has spread worldwide leading to the death of millions. Vaccination represents the key factor in the global strategy against this pandemic, but it also poses several problems, especially for vulnerable people such as patients with multiple sclerosis. In this review, we have briefly summarized the main findings of the safety, efficacy, and acceptability of Coronavirus Disease 2019 (COVID-19) vaccination for multiple sclerosis patients. Although the acceptability of COVID-19 vaccines has progressively increased in the last year, a small but significant part of patients with multiple sclerosis still has relevant concerns about vaccination that make them hesitant about receiving the COVID-19 vaccine. Overall, available data suggest that the COVID-19 vaccination is safe and effective in multiple sclerosis patients, even though some pharmacological treatments such as anti-CD20 therapies or sphingosine l-phosphate receptor modulators can reduce the immune response to vaccination. Accordingly, COVID-19 vaccination should be strongly recommended for people with multiple sclerosis and, in patients treated with anti-CD20 therapies and sphingosine l-phosphate receptor modulators, and clinicians should evaluate the appropriate timing for vaccine administration. Further studies are necessary to understand the role of cellular immunity in COVID-19 vaccination and the possible usefulness of booster jabs. On the other hand, it is mandatory to learn more about the reasons why people refuse vaccination. This would help to design a more effective communication campaign aimed at increasing vaccination coverage among vulnerable people.

 Remyelination biology and the therapeutic potential of restoring myelin sheaths to prevent neurodegeneration and disability in multiple sclerosis (MS) has made considerable gains over the past decade with many regeneration strategies undergoing tested in MS clinical trials. Animal models used to investigate oligodendroglial responses and regeneration of myelin vary considerably in the mechanism of demyelination, involvement of inflammatory cells, neurodegeneration and capacity for remyelination. The investigation of remyelination in the context of aging and an inflammatory environment are of considerable interest for the potential translation to progressive multiple sclerosis. Here we review how remyelination is assessed in mouse models of demyelination, differences and advantages of these models, therapeutic strategies that have emerged and current pro-remyelination clinical trials.
 Multiple sclerosis is an inflammatory degenerative condition of the central nervous system that may result in debilitating disability. Several studies over the past twenty years suggest that multiple sclerosis manifests with a rapid, more disabling disease course among individuals identifying with Black or Latin American ethnicity relative to those of White ethnicity. However, very little is known about immunologic underpinnings that may contribute to this ethnicity-associated discordant clinical severity. Given the importance of B cells to multiple sclerosis pathophysiology, and prior work showing increased antibody levels in the cerebrospinal fluid of Black-identifying, compared to White-identifying multiple sclerosis patients, we conducted a cohort study to determine B cell subset dynamics according to both self-reported ethnicity and genetic ancestry over time. Further, we determined relationships between ethnicity, ancestry, and neuron-binding IgG levels. We found significant associations between Black ethnicity and elevated frequencies of class-switched B cell subsets, including memory B cells; double negative two B cells; and antibody-secreting cells. The frequencies of these subsets positively correlated with West African genetic ancestry. We also observed significant associations between Black ethnicity and increased IgG binding to neurons. Our data suggests significantly heightened T cell-dependent B cell responses exhibiting increased titres of neuron-binding antibodies among individuals with multiple sclerosis identifying with the Black African diaspora. Factors driving this immunobiology may promote the greater demyelination, central nervous system atrophy and disability more often experienced by Black-, and Latin American-identifying individuals with multiple sclerosis.
 BACKGROUND: Multiple sclerosis is a neuro-inflammatory disease that affects adults and children and causes somatic and cognitive symptoms. Diagnosis after the first clinical symptoms is challenging, involves laboratory and magnetic resonance imaging work-up and is often inconclusive unless subsequent clinical attacks occur. Neurofilament light chains are structural proteins within neurons. Levels of this marker in cerebrospinal fluid, plasma and serum are consistently higher in patients with an initial clinical demyelinating attack that later go on to develop multiple sclerosis. Evidence concerning serum levels of this biomarker in children with multiple sclerosis is scarce. Our aim is to review and analyze the evidence available for patients with multiple sclerosis, under the age of 18. METHODS: We conducted a systematic search of PubMed/Medline, Embase, Cochrane Database, and ProQuest. Human studies that provided data on serum levels of Neurofilament light chains in pediatric patients with MS, measured at the time of the first demyelinating attack and before treatment were included in meta-analysis. RESULTS: Three studies satisfied the inclusion criteria. 157 pediatric patients with multiple sclerosis and 270 hospital-based controls that did not present with this condition were included in the analysis. A fixed effects meta-analysis showed that the standardized mean difference between patients and controls is 1.82, with a 95% confidence interval of [1.56-2.08]. CONCLUSION: Pediatric patients with multiple sclerosis show higher levels of serum neurofilament light chains at their first clinical demyelinating attack compared to pediatric hospital-based controls.
 Insomnia is a common complaint for adults with multiple sclerosis and can severely impact health-related quality of life. Point prevalence estimates of insomnia are, however, difficult to determine in this population due to the use of different measurement tools as well as the highly variable clinical presentation of multiple sclerosis. This review consolidates the current evidence base to provide a global estimate of insomnia disorders and symptoms in multiple sclerosis, with consideration of both measurement and sample issues. A comprehensive review of the PUBMED, EMBASE, PsycINFO and CINAHL databases from database inception until January 31st(,) 2023 identified 1649 records, of which 34 (7636 participants total) were eligible for inclusion. Findings were meta-analysed using a random-effects model. Estimates based on self-reported symptoms (52%, CI: 44%-59%) were significantly higher than those obtained by diagnostic tools (22%, CI: 16%-29%). Gender was identified as a potential moderator, with women more likely to report insomnia than men. One in two adults with multiple sclerosis endorse symptoms of poor sleep quality and daytime sleepiness, with 1 in 5 diagnosed with an insomnia disorder. Future research is needed to enhance understanding of these comorbid conditions, including the trajectory of insomnia with disease progression. PROSPERO registration number CRD42021281524.
 We used network analysis to identify subtypes of relapsing-remitting multiple sclerosis subjects based on their cumulative signs and symptoms. The electronic medical records of 113 subjects with relapsing-remitting multiple sclerosis were reviewed, signs and symptoms were mapped to classes in a neuro-ontology, and classes were collapsed into sixteen superclasses by subsumption. After normalization and vectorization of the data, bipartite (subject-feature) and unipartite (subject-subject) network graphs were created using NetworkX and visualized in Gephi. Degree and weighted degree were calculated for each node. Graphs were partitioned into communities using the modularity score. Feature maps visualized differences in features by community. Network analysis of the unipartite graph yielded a higher modularity score (0.49) than the bipartite graph (0.25). The bipartite network was partitioned into five communities which were named fatigue, behavioral, hypertonia/weakness, abnormal gait/sphincter, and sensory, based on feature characteristics. The unipartite network was partitioned into five communities which were named fatigue, pain, cognitive, sensory, and gait/weakness/hypertonia based on features. Although we did not identify pure subtypes (e.g., pure motor, pure sensory, etc.) in this cohort of multiple sclerosis subjects, we demonstrated that network analysis could partition these subjects into different subtype communities. Larger datasets and additional partitioning algorithms are needed to confirm these findings and elucidate their significance. This study contributes to the literature investigating subtypes of multiple sclerosis by combining feature reduction by subsumption with network analysis.
 Amantadine is an N-methyl-d-aspartate receptor agonist with secondary dopaminergic activity that is used to treat Parkinson's disease-related dyskinesia and to treat fatigue in multiple sclerosis. It is primarily renally excreted and so impaired kidney function prolongs its half-life and may lead to toxicity. We describe a woman with multiple sclerosis taking amantadine who developed acute renal impairment, which triggered florid visual hallucinations that resolved on stopping the medication.
 [This corrects the article DOI: 10.3389/fgene.2023.1076421.].

 Multiple sclerosis features complex pathological changes in grey matter that begin early and eventually lead to diffuse atrophy. Novel approaches to image grey-matter microstructural alterations in vivo are highly sought after and would enable more sensitive monitoring of disease activity and progression. This cross-sectional study aimed to assess the sensitivity of high-gradient diffusion MRI for microstructural tissue damage in cortical and deep grey matter in people with multiple sclerosis and test the hypothesis that reduced cortical cell body density is associated with cortical and deep grey-matter volume loss. Forty-one people with multiple sclerosis (age 24-72, 14 females) and 37 age- and sex-matched healthy controls were scanned on a 3 T Connectom MRI scanner equipped with 300 mT/m gradients using a multi-shell diffusion MRI protocol. The soma and neurite density imaging model was fitted to high-gradient diffusion MRI data to obtain estimates of intra-neurite, intra-cellular and extra-cellular signal fractions and apparent soma radius. Cortical and deep grey-matter microstructural imaging metrics were compared between multiple sclerosis and healthy controls and correlated with grey-matter volume, clinical disability and cognitive outcomes. People with multiple sclerosis showed significant cortical and deep grey-matter volume loss compared with healthy controls. People with multiple sclerosis showed trends towards lower cortical intra-cellular signal fraction and significantly lower intra-cellular and higher extra-cellular signal fractions in deep grey matter, especially the thalamus and caudate, compared with healthy controls. Changes were most pronounced in progressive disease and correlated with the Expanded Disability Status Scale, but not the Symbol Digit Modalities Test. In multiple sclerosis, normalized thalamic volume was associated with thalamic microstructural imaging metrics. Whereas thalamic volume loss did not correlate with cortical volume loss, cortical microstructural imaging metrics were significantly associated with thalamic volume, and not with cortical volume. Compared with the short diffusion time (Δ = 19 ms) achievable on the Connectom scanner, at the longer diffusion time of Δ = 49 ms attainable on clinical scanners, multiple sclerosis-related changes in imaging metrics were generally less apparent with lower effect sizes in cortical and deep grey matter. Soma and neurite density imaging metrics obtained from high-gradient diffusion MRI data provide detailed grey-matter characterization beyond cortical and thalamic volumes and distinguish multiple sclerosis-related microstructural pathology from healthy controls. Cortical cell body density correlates with thalamic volume, appears sensitive to the microstructural substrate of neurodegeneration and reflects disability status in people with multiple sclerosis, becoming more pronounced as disability worsens.
 [This corrects the article DOI: 10.3389/fneur.2022.830057.].
 Physical rehabilitation and physical activity are known non-pharmacological methods of treating multiple sclerosis. Both lead to an improvement in physical fitness in patients with movement deficits while improving cognitive function and coordination. These changes occur through the induction of brain plasticity. This review presents the basics of the induction of brain plasticity in response to physical rehabilitation. It also analyzes the latest literature evaluating the impact of traditional physical rehabilitation methods, as well as innovative virtual reality-based rehabilitation methods, on the induction of brain plasticity in patients with multiple sclerosis.
 Multiple sclerosis is a tissue-specific autoimmune disease of the central nervous system in which the antigen(s) remains elusive. Antibodies targeting the flotillin-1/2 complex have been described in 1-2% of the patients in a recent study. Other candidate antigens as anoctamin-2 or neurofascin-155 have been previously described in multiple sclerosis patients, although their clinical relevance remains uncertain. Our study aims to analyse the frequency and clinical relevance of antibodies against neurofascin-155, anoctamin-2 and flotillin-1/2 complex in multiple sclerosis. Serum (n = 252) and CSF (n = 50) samples from 282 multiple sclerosis patients were included in the study. The control group was composed of 260 serum samples (71 healthy donors and 189 with other neuroinflammatory disorders). Anti-flotillin-1/2, anti-anoctamin-2 and anti-neurofascin-155 antibodies were tested by cell-based assays using transfected cells. We identified six multiple sclerosis patients with antibodies against the flotillin-1/2 complex (2.1%) and one multiple sclerosis patient with antibodies against anoctamin-2 (0.35%). All multiple sclerosis patients were negative for anti-neurofascin-155 antibodies. Three of the anti-flotillin-1/2 positive patients showed anti-flotillin-1/2 positivity in other serum samples extracted at different moments of their disease. Immunoglobulin G subclasses of anti-flotillin-1/2 antibodies were predominantly one and three. We confirm that antibodies targeting the flotillin-1/2 complex are present in a subgroup of patients with multiple sclerosis. Further studies are needed to understand the clinical and pathological relevance of anti-flotillin-1/2 autoantibodies in multiple sclerosis.
 Cognitive impairment and sexual dysfunction are common symptoms in persons with Multiple Sclerosis (MS). The present study focuses on the relationship between these two dimensions by means of a specific assessment commonly used in clinical practice with this population. Fifty-five persons with a diagnosis of MS underwent specific cognitive tests and answered clinical questionnaires. Two cognitive tests, one for memory (the Selective Reminding Test), and one for attention (the Symbol Digit Modalities Test), were administered together with two tests for executive functions (the D-KEFS Sorting Test and Stroop Test). Two self-report questionnaires to investigate clinical, psychological and sexual features (the Beck Depression Inventory-II and Self-perception of Cognition in Multiple Sclerosis and Multiple Sclerosis Intimacy and Sexuality Questionnaire-19), were also administered. The main result highlights that sexual difficulties are associated with cognitive deficits, particularly with executive disorders, but not with memory and attention. Furthermore, sexual difficulties are better explained when depression symptoms are also taken into account. This study disentangles the interaction between sexual dysfunction, cognitive impairment and depression in persons with MS by emphasising the role of very high cognitive processing (i.e., executive functioning) in determining human behaviour.
 BACKGROUND/OBJECTIVE: Multiple Sclerosis is a common demyelinating disease of the central nervous system. Several studies suggested a link between vitamin D deficiency and multiple sclerosis disease activity, which can be evaluated by magnetic resonance imaging. Thereby, the main objective of the following scoping review is to summarize the magnetic resonance imaging findings assessing the probable effects of vitamin D on MS disease activity. METHODOLOGY: PRISMA checklist for systematic reviews and meta-analyses was employed to structure this review. Literature was searched for observational and clinical studies tackling the given matter using several search engines including PubMed, CORE, and Embase. Data was extracted in a systematic manner, and the articles meeting the inclusion criteria were quality-assessed by Jadad scale for randomized clinical trials (RCTs) and Newcastle-Ottawa scale for observational studies. RESULTS: A total of 35 articles were included. Twenty-one (60%) studies noted a statistically significant association between vitamin D and Multiple Sclerosis MRI-detected disease activity. MRI-detected features involved lower contrast-enhancing T1 lesions, lower hyperintense T2 lesions, and a decrease in lesions volume. On the other hand, 40% (14 articles) of the articles did not detect any significant effect of vitamin D on Multiple Sclerosis disease activity. Due to the heterogeneity of the studies involved, meta-analysis was not employed in the given review. DISCUSSION/CONCLUSION: There was an abundance in the number of research studies investigating the relationship between vitamin D and Multiple Sclerosis while highlighting the significant role of MRI in assessing the activity of the disease. Numerous studies found that higher serum vitamin D levels are associated with decreased new active cortical and subcortical lesions and lower lesions volume. These findings highlight the importance of imaging modalities in the various aspects of neurological diseases and encourage further research to focus on the preventive effects of vitamin D on MS patients.
 An erratum was issued for: Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis. The citation was updated. The citation was updated from: de Paula Faria, D., Cristiano Real, C., Estessi de Souza, L., Teles Garcez, A., Navarro Marques, F. L., Buchpiguel, C. A. Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis. J. Vis. Exp. (168), e62094, doi:10.3791/62094 (2021). to: de Paula Faria, D., Real, C.C., Estessi de Souza, L., Teles Garcez, A., Navarro Marques, F. L., Buchpiguel, C. A. Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis. J. Vis. Exp. (168), e62094, doi:10.3791/62094 (2021).
 Multiple sclerosis (MS) frequently affects women of childbearing age, and an increasing number of disease-modifying therapies are available. However, a consequence of this is that women and clinicians face complex shared decisions surrounding disease-modifying therapy use in pregnancy and postpartum. It has been suggested that there are both knowledge and communication gaps that need to be addressed in order to improve outcomes for women with MS desiring a pregnancy. Existing pregnancy studies are subject to limitations including selection bias and missing data; however, when these are combined with clinical expertise, consensus guidelines can be developed and used as a framework to support this complex decision-making process. This commentary paper aims to provide a practical and evidence-based overview of the safety of disease-modifying therapies and symptomatic drug therapies during pregnancy and breastfeeding, along with highlighting where insufficient data exist to guide practice.
 Black Americans with multiple sclerosis (MS) experience higher levels of disease-related disability compared to White Americans (Marrie et al., 2006). Comorbidities such as depression and anxiety, which are underdiagnosed and undertreated in this population, negatively impact quality of life and treatment outcomes for people living with multiple sclerosis (plwMS) (D'Alisa et al., 2006; Marrie et al., 2009; Stepleman et al., 2014). Acts of discrimination toward Black Americans is associated with stress, which is a contributing factor for depression (Carter, 2017; Nadimpalli, 2015; Williams and Mohammed, 2009). This study compared the severity of multiple sclerosis symptoms amongst Black Americans and White Americans, and whether worsened MS symptoms in Black Americans are associated with increased experiences of discrimination. Data was analyzed from 143 plwMS in the Stress Indicators in Minorities with Multiple Sclerosis (SiMMS) study. Using the Mann-Whitney U test, significant differences were found on the NIH Emotional Distress - Anxiety measure (U = 1466.500, p = 0.045) and NIH Sleep Disturbance measure (U = 1467.000, p = 0.044) between the Black participant and the White participant groups. Discrimination was significantly correlated with both NIH Emotional Distress - Anxiety (r = 0.677, p < .001) and NIH Sleep Disturbance (r = 0.446, p = .007) in Black MS individuals. Additionally, several physiological condition and psychological outcome measures were correlated with the NIH Emotional Distress - Anxiety and NIH Sleep Disturbance measures. This study contributes to literature highlighting the negative impacts of discrimination and race related stress on the physical and mental health of Black Americans.
 OBJECTIVES: We describe the development of Your Multiple Sclerosis Questionnaire and present the real-world usability testing results of Your Multiple Sclerosis Questionnaire. METHODS: The Your Multiple Sclerosis Questionnaire tool was developed in four stages to collect feedback from people living with MS (plwMS), patient organizations, and clinicians on content, format, and applicability. To assess its usability, 13 clinicians across 7 countries completed an online survey after using the tool with plwMS in a total of 261 consultations from September, 2020 to July, 2021. RESULTS: The initial Your Multiple Sclerosis Questionnaire version was based on findings from previous research developing MSProDiscuss™, a clinician-completed tool. Subsequently, insights from plwMS obtained during cognitive debriefing, patient councils and advisory boards led to changes including the addition of mood and sexual problems and the definition of relapse. All 13 clinicians completed the individual survey, whereas 10 clinicians completed the final survey. Clinicians "strongly agreed" or "agreed" that Your Multiple Sclerosis Questionnaire was easy to use and understand (98.5%; 257/261 patient consultations). The clinicians were willing to use the tool again with the same patient (98.1%; 256/261 patient consultations). All clinicians who completed the final survey (100%; 10/10) reported the tool to have a positive influence on their clinical practice, helped patients engage with their MS, facilitated discussion with patients, and complemented neurological assessment. CONCLUSION: Your Multiple Sclerosis Questionnaire benefits both plwMS and clinicians by facilitating a structured discussion and engaging the plwMS to self-monitor and self-manage. Your Multiple Sclerosis Questionnaire is compatible with telemedicine practice and integration of the tool into electronic health records would enable tracking of the disease evolution and individual monitoring of MS symptoms over time.
 OBJECTIVE: Most multiple sclerosis patients have urological complications such as lower urinary tract symptoms. This study was conducted to evaluate the prevalence of these symptoms and whether they result in a urological evaluation. METHODS: A cross-sectional study of 517 multiple sclerosis patients at Tehran's referral multiple sclerosis center and neurology clinics between 2018 and 2022 was performed. Data were collected through interviews after patients completed informed consent forms. Urological examinations, including urine analysis and ultrasonography, were evaluated as final assessments. The data were analyzed using descriptive and inferential statistical tests in Statistical Package for Social Science. RESULTS: Among all participants, the prevalence of lower urinary tract symptoms was 73% (n = 384), with urgency (44.8% n = 232) being the most common symptom. The prevalence of intermittency was significantly higher among women (p = 0.004). There was no gender-significant difference in terms of the prevalence of other symptoms (p > 0.050). Lower urinary tract symptoms were significantly correlated with age, clinical course, disease duration, and disability (p < 0.001). Additionally, 37.3% and 18.7% of patients with lower urinary tract symptoms, as well as 17.9% and 37.5% of patients with multiple sclerosis attacks, respectively, had undergone urine analysis and ultrasonography. CONCLUSION: Multiple sclerosis patients rarely undergo urological evaluations during the course of their disease. Proper assessment is essential as these symptoms are among the most detrimental manifestations of this disease.
 BACKGROUND: Adherence to home-based exercise programs can be improved by determining the factors associated with exercise adoption and maintenance in patients with multiple sclerosis. However, the factors that influence adherence to home-based exercise have been poorly studied among patients with multiple sclerosis in Saudi Arabia. This study aimed to examine predictors of adherence to home-based exercise programs among patients with multiple sclerosis in Saudi Arabia. METHODS: This was a cross-sectional observational study. A total of forty individuals (mean age = 38.65 ± 8.16 years) diagnosed with multiple sclerosis participated in the study. Outcome measures were self-reported exercise adherence, the Arabic version of exercise self-efficacy, the Arabic version of patient-determined disease steps, and the Arabic version of the fatigue severity scale. All outcome measures were assessed at baseline, except for self-reported adherence to exercise, which was measured after 2 weeks. RESULTS: Our results showed that the adherence to home-based exercise programs was significantly positively correlated with exercise self-efficacy and negatively correlated with fatigue and disability. Exercise self-efficacy (β = 0.62, p < 0.01) and fatigue (β = -0.24, p = 0.04) were significant predictors of adherence to home-based exercise programs. CONCLUSION: These findings suggest that exercise self-efficacy and fatigue should be considered by physical therapists when designing a tailored exercise program for patients with multiple sclerosis. This may facilitate greater adherence to the home-based exercise programs and improve functional outcomes.
 KEY CLINICAL MESSAGE: Malignancies were reported in some studies following taking Fingolimod. We reported a case of bladder lymphoma after taking Fingolimod. Physicians should consider the carcinogenic effects of Fingolimod in long-term use and replace it with safer medicines. ABSTRACT: Fingolimod is a medication with a potential cure to control multiple sclerosis (MS) relapses. Here we describe a 32-year-old woman with relapsing-remitting multiple sclerosis who developed bladder lymphoma induced by long-term use of Fingolimod. Physicians should consider the carcinogenic effects of Fingolimod in long-term use and replace it with safer medicines.
 Multiple sclerosis has a highly variable course and disabling symptoms even in absence of associated imaging data. This clinical-radiological paradox has motivated functional studies with particular attention to the resting-state networks by functional MRI. The EEG microstates analysis might offer advantages to study the spontaneous fluctuations of brain activity. This analysis investigates configurations of voltage maps that remain stable for 80-120 ms, termed microstates. The aim of our study was to investigate the temporal dynamic of microstates in patients with multiple sclerosis, without reported cognitive difficulties, and their possible correlations with clinical and neuropsychological parameters. We enrolled fifty relapsing-remitting multiple sclerosis patients and 24 healthy subjects, matched for age and sex. Demographic and clinical data were collected. All participants underwent to high-density EEG in resting-state and analyzed 15 min free artefact segments. Microstates analysis consisted in two processes: segmentation, to identify specific templates, and back-fitting, to quantify their temporal dynamic. A neuropsychological assessment was performed by the Brief International Cognitive Assessment for Multiple Sclerosis. Repeated measures two-way ANOVA was run to compare microstates parameters of patients versus controls. To evaluate association between clinical, neuropsychological and microstates data, we performed Pearsons' correlation and stepwise multiple linear regression to estimate possible predictions. The alpha value was set to 0.05. We found six templates computed across all subjects. Significant differences were found in most of the parameters (global explained variance, time coverage, occurrence) for the microstate Class A (P < 0.001), B (P < 0.001), D (P < 0.001), E (P < 0.001) and F (P < 0.001). In particular, an increase of temporal dynamic of Class A, B and E and a decrease of Class D and F were observed. A significant positive association of disease duration with the mean duration of Class A was found. Eight percent of patients with multiple sclerosis were found cognitive impaired, and the multiple linear regression analysis showed a strong prediction of Symbol Digit Modalities Test score by global explained variance of Class A. The EEG microstate analysis in patients with multiple sclerosis, without overt cognitive impairment, showed an increased temporal dynamic of the sensory-related microstates (Class A and B), a reduced presence of the cognitive-related microstates (Class D and F), and a higher activation of a microstate (Class E) associated to the default mode network. These findings might represent an electrophysiological signature of brain reorganization in multiple sclerosis. Moreover, the association between Symbol Digit Modalities Test and Class A may suggest a possible marker of overt cognitive dysfunctions.
 While conventional magnetic resonance imaging (MRI) is central to the evaluation of patients with multiple sclerosis, its role in detecting the pathophysiology underlying neurodegeneration is more limited. One of the common outcome measures for progressive multiple sclerosis trials, atrophy on brain MRI, is non-specific and reflects end-stage changes after considerable neurodegeneration has occurred. Identifying biomarkers that identify processes underlying neurodegeneration before it is irreversible and that reflect relevant neurodegenerative pathophysiology is an area of significant need. Accumulating evidence suggests that oxidative stress plays a major role in the pathogenesis of multiple neurodegenerative diseases, including multiple sclerosis. Imaging markers related to inflammation, myelination, and neuronal integrity have been areas of advancement in recent years but oxidative stress has remained an area of unrealized potential. In this article we will begin by reviewing the role of oxidative stress in the pathogenesis of multiple sclerosis. Chronic inflammation appears to be directly related to the increased production of reactive oxygen species and the effects of subsequent oxidative stress appear to be amplified by aging and accumulating disease. We will then discuss techniques in development used in the assessment of MS as well as other models of neurodegenerative disease in which oxidative stress is implicated. Multiple blood and CSF markers of oxidative stress have been evaluated in subjects with MS, but non-invasive imaging offers major upside in that it provides real-time assessment within the brain.

 INTRODUCTION: Much of the current literature on treatment patterns and disability progression in multiple sclerosis (MS) does not distinguish between the relapsing-remitting and progressive subtypes (including primary [PPMS] and secondary progressive MS [SPMS]), or between active/nonactive disease. Current treatment options for progressive MS are limited, with only one approved product for PPMS and none specifically for nonactive SPMS. Here we report treatment patterns, disability progression, and unmet needs among patients with active and nonactive PPMS and SPMS. METHODS: The annual, cross-sectional survey from the Adelphi Disease Specific Program was used to collect physician-reported data on US adult patients with PPMS and SPMS, including active and nonactive disease. Treatment patterns (including the proportion of patients who were untreated with a disease-modifying therapy [DMT]), disability progression, and unmet need are described from 2016 to 2021. RESULTS: Data were collected for 2067 patients with progressive MS (PPMS, 1583; SPMS, 484). A substantial proportion of patients were untreated across all groups, and this was highest for nonactive PPMS (~ 43%). The proportion of untreated patients generally declined over time but remained high in 2018-2021 (~ 10-38%). Among treated patients, the proportion receiving infusions increased over time to ~ 34-46%, largely driven by ocrelizumab use after approval. Disability progression was reported for most patients (> 50%), including many who were receiving a DMT. Across all disease subtypes, when physicians were asked about the greatest unmet need with current DMTs, they most frequently cited effectiveness (~ 63-87%), and specifically slowing disease progression (~ 32-59%). CONCLUSIONS: This analysis of physician-reported data reveals that patients with progressive MS, particularly those with nonactive disease, frequently remain untreated or continue to decline despite treatment with available DMTs. Thus there is an enduring need for safe and effective treatments for this underserved population.
 In multiple sclerosis (MS), progression independent of new focal inflammation may commence shortly after disease onset, and it is increasingly revealed that the risk of disability accrual is reduced by early use of high-efficacy disease-modifying therapies (HE-DMTs). People with aggressive MS may therefore benefit from early treatment with autologous haematopoietic stem cell transplantation (AHSCT), a procedure inducing maximal immunosuppression followed by immune reconstitution, demonstrated to be superior to DMTs in one randomized clinical trial. However, in current practice prior failure to HE-DMTs is typically required to establish the indication for AHSCT. In the present article, the available evidence on the potential role of AHSCT as first-line treatment in aggressive MS and the rationale for its early use will be summarized. Proposed definitions of aggressive MS that could help identifying MS patients eligible for early treatment with AHSCT will also be discussed.
 Teriflunomide is a once-daily oral immunomodulatory disease-modifying treatment for multiple sclerosis (MS). Skin reactions are an infrequent side effect of teriflunomide. Here, we present the case of a 52-year-old female patient with ankylosing spondylitis who was consulted for demyelinating lesions and limb weakness. She was diagnosed with multiple sclerosis and started treatment with teriflunomide. Palmoplantar pustular psoriasis developed after three weeks of treatment initiation. It is a rare side effect related to teriflunomide.

 [This corrects the article DOI: 10.3389/fneur.2023.1158487.].
 BACKGROUND: Primary-progressive multiple sclerosis (PPMS) and relapsing-remitting multiple sclerosis (RRMS) are two frequent multiple sclerosis (MS) subtypes that involve 10%-15% of patients. PPMS progresses slowly and is diagnosed later in life. Both subtypes are influenced by genetic and environmental factors such as smoking, obesity, and vitamin D insufficiency. Although there is no cure, ocrelizumab can reduce symptoms and delay disease development. RRMS is an autoimmune disease that causes inflammation, demyelination, and disability. Early detection, therapy, and lifestyle changes are critical. This study delves into genetics, immunology, biomarkers, neuroimaging, and the usefulness of ocrelizumab in the treatment of refractory patients of PPMS. METHOD: In search of published literature providing up-to-date information on PPMS and RRMS, this review conducted numerous searches in databases such as PubMed, Google Scholar, MEDLINE, and Scopus. We looked into genetics, immunology, biomarkers, current breakthroughs in neuroimaging, and the role of ocrelizumab in refractory cases. RESULTS: Our comprehensive analysis found considerable advances in genetics, immunology, biomarkers, neuroimaging, and the efficacy of ocrelizumab in the treatment of refractory patients. CONCLUSION: Early detection, timely intervention, and the adoption of lifestyle modifications play pivotal roles in enhancing treatment outcomes. Notably, ocrelizumab has demonstrated potential in symptom control and mitigating the rate of disease advancement, further underscoring its clinical significance in the management of MS.
 Ocrelizumab is a medication used in the management and treatment of primary progressive and relapsing multiple sclerosis. It is in the anti-CD20 monoclonal antibody class of medications. This activity describes the indications, action, and contraindications for ocrelizumab as a valuable agent in multiple sclerosis management. This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., administration, contraindications, monitoring, toxicity) pertinent for interprofessional team members in the care of patients with multiple sclerosis.

 Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) with a profound neurodegenerative component early in the disease pathogenesis. Age is a factor with a well-described effect on the primary disease phenotype, namely, the relapsing-remitting vs. the primary progressive disease. Moreover, aging is a prominent factor contributing to the transition from relapsing-remitting MS (RRMS) to secondary progressive disease. However, sex also seems to, at least in part, dictate disease phenotype and evolution, as evidenced in humans and in animal models of the disease. Sex-specific gene expression profiles have recently elucidated an association with differential immunological signatures in the context of experimental disease. This review aims to summarize current knowledge stemming from experimental autoimmune encephalomyelitis (EAE) models regarding the effects of sex, either independently or as a factor combined with aging, on disease phenotype, with relevance to the immune system and the CNS.
 OBJECTIVE: The purpose of the study was to understand how people with multiple sclerosis experience dual-tasking situations in their everyday lives. METHODS: Focus groups involving a total of 11 individuals with multiple sclerosis (eight females and three males) participated in this qualitative inquiry. Participants were asked open-ended questions focused on the nature of and consequences around dual tasking when standing or walking. Reflexive thematic analysis was employed to examine the data. RESULTS: Three themes were generated from the data: (a) Life Is a Dual Task, (b) The Social Divide, and (c) Sacrifices for Stability. CONCLUSIONS: This study highlights the significance and impact of dual tasking on the lived experience of adults with multiple sclerosis, furthering the need to more fully examine this phenomenon and potentially improve fall-prevention interventions and facilitate community participation.
 OBJECTIVE: Research directly examining brain tissue has played an important role in understanding the pathology and pathogenesis of multiple sclerosis (MS) and other diseases of the central nervous system. Such research relies heavily on donations of post-mortem brain tissue yet little is known about the attitudes of people with multiple sclerosis (MS) about brain donation. We aimed to assess the attitudes of people with MS toward brain donation, their preferences related to discussions of brain donation, and factors associated with attitudes toward brain donation including sociodemographic and clinical characteristics, health literacy and religiosity. METHODS: In a cross-sectional study, we surveyed participants in the North American Research Committee on Multiple Sclerosis (NARCOMS) Registry regarding their attitudes toward brain donation, reasons for participating or not participating in brain donation, and related communication preferences. We used multivariable logistic regression analyses to test factors associated with attitudes regarding brain donation. RESULTS: Most of the 4,520 participants were women (80.8%), self-identified as white (88.1%), with a post-secondary education, functional health literacy and moderate-severe disability. Sixty-two percent of participants would consider brain donation. Factors associated with considering brain donation included female gender, having a post-secondary education, being physically active, having moderate-severe disability and more comorbidities, and alcohol intake. Seventy-five percent of participants indicated that they preferred to receive information regarding brain donations from physicians. CONCLUSION: Two-thirds of people with MS would consider brain donation. People with MS desire to hear about brain donation from their health care providers rather than other sources.
 Objective To compare the initial presentation, clinical features, disease courses, and radiological parameters between familial multiple sclerosis (fMS) and sporadic multiple sclerosis (sMS) to determine if the two represent distinct clinical entities. Methods This retrospective study was conducted at the Neurology Clinic at Kocaeli University Hospital. Records of 114 fMS and 150 sMS patients, aged 18-65, diagnosed based on either the Poser criteria or the McDonald 2001 criteria were analyzed. Radiological data and Expanded Disability Status Scale (EDSS) evaluations were conducted by a specialist neurologist. Variables included age at MS onset, first symptoms, relapses, EDSS scores at diagnosis and last examination, and MRI findings. Statistical Package for the Social Sciences (IBM SPSS Statistics for Windows, IBM Corp., Version 28, Armonk, NY) was utilized for data analysis. Results Both fMS and sMS groups were comparable in age (43.55±12.50 and 42.35±10.61 years, respectively) and gender distribution (females: fMS 71.9%, sMS 71.3%). No significant difference was noted regarding disease onset age (fMS 29.83±10.77, sMS 30.42±9.7). Age of onset, final EDSS, and relapse rate didn't significantly vary among sMS, fMS with first-degree relatives having MS (fMS(1)), and fMS with second or third-degree relatives having MS (fMS(2)). The fMS group showed a significantly higher incidence of initial spinal cord lesions on MRI compared to the sMS group (38.6% vs. 17.3%; p<0.001). Within the fMS group, the presence of spinal cord lesions on initial MRI correlated with a higher relapse rate and elevated initial and final EDSS scores. Conclusion Despite overarching similarities between fMS and sMS, spinal cord lesions' prevalence and implications in fMS may point to a genetic underpinning warranting in-depth exploration.
 Cognitive impairment is a prevalent and debilitating symptom of multiple sclerosis (MS) but is not routinely addressed in clinical care. The Brief Cognitive Assessment for Multiple Sclerosis (BICAMS) was developed in 2012 to screen and monitor MS patients’ cognition. This systematic review and meta-analysis aimed to identify, synthesise, and critically appraise current BICAMS’ international validations. The literature search was conducted using PubMed, PsycINFO and Web of Science electronic databases in August 2022. Quantitative, peer-reviewed adult studies, which followed the BICAMS international validation protocol and were published in English, were included. The search identified a total of 203 studies, of which 26 were eligible for inclusion. These reported a total of 2833 adults with MS and 2382 healthy controls (HC). The meta-analysis showed that BICAMS identified impaired cognitive functioning in adults with MS compared to HC for all three subtests: information processing speed (g = 0.854, 95% CI = 0.765, 0.944, p < 0.001), immediate verbal recall (g = 0.566, 95% CI = 0.459, 0.673, p < 0.001) and immediate visual recall (g = 0.566, 95% CI = 0.487, 0.645, p < 0.001). Recruitment sites and strategies limit the generalisability of results. BICAMS is a valid and feasible international MS cognitive assessment.
 [This corrects the article DOI: 10.3389/fpsyg.2022.1028814.].
 MS (Multiple sclerosis) associated uveitis used to have limited phenotypes. Bilateral exudative retinal detachment has never been recognized as a pattern of MS-associated uveitis. We are reporting a patient with multiple sclerosis who presented initially with the usual pattern of intermediate uveitis and later developed bilateral exudative retinal detachment.
 This review summarizes the cellular and molecular underpinnings of autoimmune demyelinating optic neuritis (ADON), a common sequela of multiple sclerosis and other demyelinating diseases. We further present nutritional interventions tested for people with multiple sclerosis focusing on strategies that have shown efficacy or associations with disease course and clinical outcomes. We then close by discuss the potential dietary guidance for preventing and/or ameliorating ADON.


 Patients with vertigo and facial nerve palsy as initial symptoms are rarely diagnosed with multiple sclerosis. A 43-year-old woman presented to our department with symptoms of vertigo and right facial nerve palsy (Yanagihara 16-point system [total score, 40] or House- Brackmann grade IV [obvious facial weakness]). On the day of the visit, she presented with right eye abduction, left eye adduction, and complaints of diplopia. Based on magnetic resonance imaging findings, she was diagnosed with clinically isolated syndrome, which is an early manifestation of multiple sclerosis. She was treated with intravenous methylprednisolone. Otolaryngologists often suspect Hunt's syndrome in patients who present with facial nerve palsy combined with vertigo. However, herein, we report our experience with an extremely rare case of a patient with atypical nystagmus symptoms, eye movement disorder, and diplopia secondary to facial palsy and vertigo, who presented with a clinical course different from that of Hunt's syndrome.
 BACKGROUND: Medication satisfaction is a patient-reported outcome which could show medication adherence. The aim of this study was to determine Iranian MS patients' satisfaction with Disease Modifying Therapies (DMTs). METHODS: A standardized questionnaire was developed using Treatment Satisfaction Questionnaire for Medication (TSQM). The online link was released on IMSS (Iranian Multiple Sclerosis Society) social media channel, accessible to 4272 MS patients totally. RESULTS: Three hundred and ninety-four patients participated in our survey with 324 females, 70 males and an F/M ratio of 4.6:1. The most frequent DMTs used were interferon-beta (IFNβ) followed by rituximab. The mean effectiveness and global satisfaction scores were significantly higher for injectable DMTs, while the convenience score was significantly higher for oral DMTs. Mean effectiveness and side-effect scores were significantly higher in the Tysabri group and convenience score was significantly higher in the fingolimod group while global satisfaction was higher in the IFNβ group. CONCLUSION: The global satisfaction and effectiveness were significantly higher with injectable DMTs while the convenience score was significantly higher with oral DMTs.
 Natalizumab is an FDA-approved monoclonal antibody approved for the treatment of multiple sclerosis and Crohn's disease. The drug was originally approved to treat multiple sclerosis in 2004, but after reported cases of death due to progressive multifocal leukoencephalopathy during treatment with natalizumab, the FDA removed the drug from the market. However, in 2006, the FDA reintroduced the drug when multiple protests by those with multiple sclerosis advocated for the use of natalizumab in conjunction with the establishment of an advisory committee that would monitor those on natalizumab. This activity outlines the indications, mechanism of action, methods of administration, important adverse effects, contraindications, monitoring, and toxicity of natalizumab so that providers can direct patient therapy to optimal outcomes for MS patients.
 Many biological markers have been explored in multiple sclerosis (MS) to better quantify disease burden and better evaluate response to treatments, beyond clinical and MRI data. Among these, neurofilament light chain (Nf-L), although non-specific for this disease and found to be increased in other neurological conditions, has been shown to be the most promising biomarker for assessing axonal damage in MS, with a definite role in predicting the development of MS in patients at the first neurological episode suggestive of MS, and also in a preclinical phase. There is strong evidence that Nf-L levels are increased more in relapsing versus stable MS patients, and that they predict future disease evolution (relapses, progression, MRI measures of activity/progression) in MS patients, providing information on response to therapy, helping to anticipate clinical decisions in patients with an apparently stable evolution, and identifying patient non-responders to disease-modifying treatments. Moreover, Nf-L can contribute to the better understanding of the mechanisms of demyelination and axonal damage in adult and pediatric MS. A fundamental requirement for its clinical use is the accurate standardization of normal values, corrected for confounding factors, in particular age, sex, body mass index, and presence of comorbidities. In this review, a guide is provided to update clinicians on the use of Nf-L in clinical activity.
 OBJECTIVE: Over the last few decades clinicians have become aware that cognitive impairment might be a major cause of disability, loss of employment and poor quality of life in patients suffering from multiple sclerosis [MS].The impact of disease modifying therapies [DMTs] on cognition is still a matter of debate. Theoretically, DMTs could exert a substantial beneficial effect by means of reducing neuroinflammation and brain atrophy, which are established correlates of cognitive dysfunction. The aim of the study was to review the evidence concerning the effect of DMTs on cognitive functions. METHODS: PubMed, Scopus, and the European Committee for Treatment and Research in Multiple Sclerosis [ECTRIMS] Library were searched for articles concerning the pediatric and adult populations of patients with multiple sclerosis, including clinical trials and RWD, where psychometric results were analyzed as secondary or exploratory endpoints. RESULTS: We reviewed a total of 44 studies that were found by our search strategy, analyzed the psychological tests that were applied, the length of the follow-up, and possible limitations. We pointed out the difficulties associated with assessing of DMTs' effects on cognitive functions, and pitfalls in cognitive tools used for evaluating of MS patients. CONCLUSION: There is a need to highlight this aspect of MS therapies, and to collect adequate data to make informed therapeutic decisions, to improve our understanding of MS-related cognitive dysfunction and provide new therapeutic targets.
 Geographical variations in the incidence and prevalence of multiple sclerosis have been reported globally. Latitude as a surrogate for exposure to ultraviolet radiation but also other lifestyle and environmental factors are regarded as drivers of this variation. No previous studies evaluated geographical variation in the risk of secondary progressive multiple sclerosis, an advanced form of multiple sclerosis which is characterised by steady accrual of irreversible disability. We evaluated differences in the risk of secondary progressive multiple sclerosis in relation to latitude and country of residence, modified by high-to-moderate-efficacy immunotherapy in a geographically diverse cohort of patients with relapsing-remitting multiple sclerosis. The study included relapsing-remitting multiple sclerosis patients from the global MSBase registry with at least one recorded assessment of disability. Secondary progressive multiple sclerosis was identified as per clinician diagnosis. Sensitivity analyses used the operationalised definition of secondary progressive multiple sclerosis and the Swedish decision tree algorithm. A proportional hazards model was used to estimate the cumulative risk of secondary progressive multiple sclerosis by country of residence (latitude), adjusted for sex, age at disease onset, time from onset to relapsing-remitting phase, disability (Multiple Sclerosis Severity Score) and relapse activity at study inclusion, national multiple sclerosis prevalence, government health expenditure, and proportion of time treated with high-to-moderate-efficacy disease-modifying therapy. Geographical variation in time from relapsing-remitting phase to secondary progressive phase of multiple sclerosis was modelled through a proportional hazards model with spatially correlated frailties. We included 51126 patients (72% female) from 27 countries. The median survival time from relapsing-remitting phase to secondary progressive multiple sclerosis among all patients was 39 (95% confidence interval: 37 to 43) years. Higher latitude (median hazard ratio = 1.21, 95% credible interval [1.16, 1.26]), higher national multiple sclerosis prevalence (1.07 [1.03, 1.11]), male sex (1.30 [1.22, 1.39]), older age at onset (1.35 [1.30, 1.39]), higher disability (2.40 [2.34, 2.47]) and frequent relapses (1.18 [1.15, 1.21]) at inclusion were associated with increased hazard of secondary progressive multiple sclerosis. Higher proportion of time on high-to-moderate-efficacy therapy substantially reduced the hazard of secondary progressive multiple sclerosis (0.76 [0.73, 0.79]) and reduced the effect of latitude (interaction: 0.95 [0.92, 0.99]). At the country-level, patients in Oman, Kuwait, and Canada had higher risks of secondary progressive multiple sclerosis relative to the other studied regions. Higher latitude of residence is associated with a higher probability of developing secondary progressive multiple sclerosis. High-to-moderate-efficacy immunotherapy can mitigate some of this geographically co-determined risk.
 BACKGROUND: Multiple sclerosis is the most important cause of non-injury-related disability in young adults. The disease has unknown causes and distresses and affects daily activities. While therapeutic interventions mainly focus on body function and structure to reduce impairment, Cognitive Orientation to Daily Occupational Performance (CO-OP) is a cognitive approach that provides intervention at the level of activity and participation. PURPOSE: We aim to examine the effects of CO-OP approach on fatigue, quality of life, occupational performance, and satisfaction in people living with multiple sclerosis; and to examine whether they could transfer strategies and skills learned during CO-OP to untrained goals. METHODS: A pre-post design was used. Assessment tools included Montreal Cognitive Assessment, Multiple Sclerosis Impact Scale, Fatigue Impact Scale and the Canadian Occupational Performance Measure. Six individuals living with multiple sclerosis participated in 10 CO-OP sessions twice a week. The sessions were held in an environment of the participants' choice, along with an extra session added to determine the goals. The study was registered in the ethics committee of University of Social Welfare and Rehabilitation Sciences (IR.USWR.REC.1399.089). RESULTS: The performance improved (2-point positive change) in 12 out of 18 trained goals and in three out of six untrained goals (self-report). The improvement was maintained at a 3-month follow-up assessment. There was a statistically significant difference in Canadian Occupational Performance Measure (χ(2)  = 11.565, p = 0.003 same for performance and satisfaction scores), Fatigue Impact Scale (χ(2)  = 7.000, p = 0.030), and Multiple Sclerosis Impact Scale scores over time (χ(2)  = 9.478, p = 0.009) respectively. CONCLUSION: The CO-OP approach has the potential to improve daily activity performance, reduce pain, and improve the quality of life for people living with multiple sclerosis. A definitive randomised controlled trial is required.
 Seventy-year-old male with primary progressive multiple sclerosis that had a severe episode of oropharyngeal dysphagia following initiation of carbamazepine. He was being treated for trigeminal neuralgia. Four days after discontinuation of carbamazepine resulted in a complete resolution of the patient's dysphagia, and he returned to baseline.
 Timely diagnosis of secondary progressive multiple sclerosis (SPMS) represents a clinical challenge. The Frailty Index, a quantitative frailty measure, and the Neurophysiological Index, a combined measure of sensorimotor cortex inhibitory mechanism parameters, have recently emerged as promising tools to support SPMS diagnosis. The aim of this study was to explore the possible relationship between these two indices in MS. MS participants underwent a clinical evaluation, Frailty Index administration, and neurophysiological assessment. Frailty and Neurophysiological Index scores were found to be higher in SPMS and correlated with each other, thus suggesting that they may capture similar SPMS-related pathophysiological mechanisms.
 From the perspective of precision medicine, the challenge for the future is to improve the accuracy of diagnosis, prognosis, and prediction of therapeutic responses through the identification of biomarkers. In this framework, the omics sciences (genomics, transcriptomics, proteomics, and metabolomics) and their combined use represent innovative approaches for the exploration of the complexity and heterogeneity of multiple sclerosis (MS). This review examines the evidence currently available on the application of omics sciences to MS, analyses the methods, their limitations, the samples used, and their characteristics, with a particular focus on biomarkers associated with the disease state, exposure to disease-modifying treatments (DMTs), and drug efficacies and safety profiles.
 The phenotypes of B lineage cells that produce oligoclonal IgG in multiple sclerosis have not been unequivocally determined. Here, we utilized single-cell RNA-seq data of intrathecal B lineage cells in combination with mass spectrometry of intrathecally synthesized IgG to identify its cellular source. We found that the intrathecally produced IgG matched a larger fraction of clonally expanded antibody-secreting cells compared to singletons. The IgG was traced back to two clonally related clusters of antibody-secreting cells, one comprising highly proliferating cells, and the other consisting of more differentiated cells expressing genes associated with immunoglobulin synthesis. These findings suggest some degree of heterogeneity among cells that produce oligoclonal IgG in multiple sclerosis.
 We describe the case of a young woman affected by debilitating chorea and rapidly progressive cognitive decline. While her original diagnosis was multiple sclerosis, we performed a full instrumental and genetic assessement, though which we identified multiple genetic variants, including a novel variant of the APP gene. We propose some possible mechanisms by which such variants may contribute to neuroinflammation and ultimately lead to this devastating clinical course.


 Emodin, a substance extracted from herbs such as rhubarb, has a protective effect on the central nervous system. However, the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown. In this study, a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis, and the rats were intraperitoneally injected with emodin (20 mg/kg/d) from the day of immune induction until they were sacrificed. In this model, the nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and the microglia exacerbated neuroinflammation, playing an important role in the development of multiple sclerosis. In addition, silent information regulator of transcription 1 (SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator (PGC-1α) was found to inhibit activation of the NLRP3 inflammasome, and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis. Furthermore, treatment with emodin decreased body weight loss and neurobehavioral deficits, alleviated inflammatory cell infiltration and demyelination, reduced the expression of inflammatory cytokines, inhibited microglial aggregation and activation, decreased the levels of NLRP3 signaling pathway molecules, and increased the expression of SIRT1 and PGC-1α. These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis, possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation. These findings provide experimental evidence for treatment of multiple sclerosis with emodin, enlarging the scope of clinical application for emodin.
 Cognitive functioning may account for minimal levels (i.e., 5%-14%) of variance of performance validity test (PVT) scores in clinical examinees. The present study extended this research twofold: (a) by determining the variance cognitive functioning explains within three distinct PVTs (b) in a sample of patients with multiple sclerosis (pwMS). Seventy-five pwMS (M(age) = 48.50, 70.6% female, 80.9% White) completed the Victoria Symptom Validity Test (VSVT), Word Choice Test (WCT), Dot Counting Test (DCT), and three objective measures of working memory, processing speed, and verbal memory as part of clinical neuropsychological assessment. Regression analyses in credible groups (ns ranged from 54 to 63) indicated that cognitive functioning explained 24% to 38% of the variance in logarithmically transformed PVT variables. Variance from cognitive testing differed across PVTs: verbal memory significantly influenced both VSVT and WCT scores; working memory influenced VSVT and DCT scores; and processing speed influenced DCT scores. The WCT appeared least related to cognitive functioning of the included PVTs. Alternative plausible explanations, including the apparent domain/modality specificity hypothesis of PVTs versus the potential sensitivity of these PVTs to neurocognitive dysfunction in pwMS were discussed. Continued psychometric investigations into factors affecting performance validity, especially in multiple sclerosis, are warranted.
 Anti-NMDA receptor (Anti-NMDAR) encephalitis is an autoimmune disease that presents with diverse symptoms. Since literature is scarce on the overlap with multiple sclerosis (MS), this report aims to elucidate the distinctive clinical presentation and diagnostic challenges of anti-NMDAR encephalitis in MS patients. A 73-year-old woman with secondary progressive multiple sclerosis, after experiencing status epilepticus and subsequent non-convulsive status epilepticus, presented with neuropsychiatric symptoms and autonomic nervous dysfunction. Notably, the patient had not received any immunomodulatory therapy. The clinical picture together with diagnostics (MRI, EEG, cerebro-spinal fluid) let us suspect HSV-meningoencephalitis and empirically treat the patient with IV acyclovir. Due to a lack of clinical improvement, we reconsidered the diagnosis and found the diagnostic criteria for autoimmune encephalitis to be met. Antibodies in blood and CSF were positive and we diagnosed the patient with anti-NMDAR encephalitis. The patient responded well to IV prednisolone treatment, leading to a stable outcome in a six-month follow-up. This case highlights the difficulties in diagnosing anti-NMDAR encephalitis in patients with multiple sclerosis. The presence of epileptic seizures can serve as a crucial diagnostic indicator to distinguish between an MS relapse and an overlapping disease. Compared to patients with other demyelinating diseases, patients with overlapping MS appear to have a higher risk of motor seizures.
 PURPOSE: Caregivers of people with Multiple sclerosis (MS) face various challenges in the occupations of daily lives. We investigated the effect of an online occupational therapy program on the mastery and performance in caregivers of people with MS. METHOD: In a single-blind randomized controlled trial twenty-four eligible caregivers of people with MS participated in the control and an occupational therapy group program. Caregivers completed The Canadian Occupational Performance Measure (COPM) and the Relative Mastery Scale (RMS) before and after the intervention and one-month later. FINDINGS: The level of performance, satisfaction and mastery were significantly improved in the intervention group after the intervention (p<.001) and there were significant differences in performance and satisfaction scores between the groups (p<.001). IMPLICATIONS: Online Occupational therapy shows promising results in facilitating the adaptation process and improving caregivers' performance and satisfaction levels.IMPLICATIONS FOR REHABILITATIONCaregivers of people with multiple sclerosis face various challenges when engaging in their daily occupations.Managing the challenges faced by caregivers as essential members of the treatment team contributes to improving their performance level in daily occupations and can finally enhance the quality of treatment interventions for patients.Online delivery can overcome caregivers' time constraints for attendance in the treatment centers for training.Online occupational therapy can enhance mastery, occupational performance level, and satisfaction, and is recommended for caregivers of people with multiple sclerosis.
 Multiple sclerosis is an autoimmune inflammatory disease that affects the central nervous system through chronic demyelination and loss of oligodendrocytes. Since the relapsing-remitting form is the most prevalent, relapse-reducing therapies are a primary choice for specialists. Universal Immune System Simulator is an agent-based model that simulates the human immune system dynamics under physiological conditions and during several diseases, including multiple sclerosis. In this work, we extended the UISS-MS disease layer by adding two new treatments, i.e., cladribine and ocrelizumab, to show that UISS-MS can be potentially used to predict the effects of any existing or newly designed treatment against multiple sclerosis. To retrospectively validate UISS-MS with ocrelizumab and cladribine, we extracted the clinical and MRI data from patients included in two clinical trials, thus creating specific cohorts of digital patients for predicting and validating the effects of the considered drugs. The obtained results mirror those of the clinical trials, demonstrating that UISS-MS can correctly simulate the mechanisms of action and outcomes of the treatments. The successful retrospective validation concurred to confirm that UISS-MS can be considered a digital twin solution to be used as a support system to inform clinical decisions and predict disease course and therapeutic response at a single patient level.
 BACKGROUND: A number of recent studies have shown that the intestinal microbiome, part of the brain-gut axis, is implicated in the pathophysiology of multiple sclerosis. An essential part of this axis, is the intestinal barrier and gastrointestinal disorders with intestinal barrier dysregulation appear to be linked to CNS demyelination, and hence involved in the etiopathogenesis of multiple sclerosis (MS). OBJECTIVE: The aim of this study was to evaluate the integrity of the intestinal barrier in patients with clinically definite multiple sclerosis (CDMS) and clinically isolated syndrome (CIS) using two serum biomarkers, claudin-3 (CLDN3), a component of tight epithelial junctions, and intestinal fatty acid binding protein (I-FABP), a cytosolic protein in enterocytes. METHODS: Serum levels of CLDN3 in 37 MS patients and 22 controls, and serum levels of I-FABP in 46 MS patients and 51 controls were measured using commercial ELISA kits. Complete laboratory tests excluded the presence of gluten-related disorders in all subjects. Thirty MS patients received either disease-modifying drugs (DMD), immunosuppression (IS) or corticosteroid treatment. RESULTS: CLDN3 levels were only significantly higher in the MS patients treated with DMD or IS compared to the control group (P=0.006). There were no differences in I-FABP serum levels between the groups. Serum CLDN3 levels did not correlate with serum I-FABP levels in CDMS, in CIS patients or controls. CONCLUSIONS: In multiple sclerosis patients, the intestinal epithelium may be impaired with increased permeability, but without significant enterocyte damage characterized by intracellular protein leakage. Based on our data, CLDN3 serum levels appear to assess intestinal dysfunction in MS patients but mainly in treated ones.
 Multiple sclerosis is a chronic central nervous system demyelinating disease whose onset and progression are driven by a combination of immune dysregulation, genetic predisposition, and environmental factors. The activation of microglia and astrocytes is a key player in multiple sclerosis immunopathology, playing specific roles associated with anatomical location and phase of the disease and controlling demyelination and neurodegeneration. Even though reactive microglia can damage tissue and heighten deleterious effects and neurodegeneration, activated microglia also perform neuroprotective functions such as debris phagocytosis and growth factor secretion. Astrocytes can be activated into pro-inflammatory phenotype A1 through a mechanism mediated by activated neuroinflammatory microglia, which could also mediate neurodegeneration. This A1 phenotype inhibits oligodendrocyte proliferation and differentiation and is toxic to both oligodendrocytes and neurons. However, astroglial activation into phenotype A2 may also take place in response to neurodegeneration and as a protective mechanism. A variety of animal models mimicking specific multiple sclerosis features and the associated pathophysiological processes have helped establish the cascades of events that lead to the initiation, progression, and resolution of the disease. The colony-stimulating factor-1 receptor is expressed by myeloid lineage cells such as peripheral monocytes and macrophages and central nervous system microglia. Importantly, as microglia development and survival critically rely on colony-stimulating factor-1 receptor signaling, colony-stimulating factor-1 receptor inhibition can almost completely eliminate microglia from the brain. In this context, the present review discusses the impact of microglial depletion through colony-stimulating factor-1 receptor inhibition on demyelination, neurodegeneration, astroglial activation, and behavior in different multiple sclerosis models, highlighting the diversity of microglial effects on the progression of demyelinating diseases and the strengths and weaknesses of microglial modulation in therapy design.
 BACKGROUND: The relationship between being overweight during early life and disease course in multiple sclerosis (MS) is unresolved. We investigated the association between being overweight or obese during early life (childhood and adolescence) and MS case status, age of first symptom onset and onset type in people with MS (pwMS) of the same birth year. METHODS: We enrolled 363 PwMS and 125 healthy controls (HC) from Project Y, a Dutch population-based cross-sectional cohort study including all PwMS born in 1966 and age and sex-matched HC. The associations between weight during childhood and adolescence (non-overweight vs. overweight or obese) and MS, age at symptom onset and onset type (relapsing vs. progressive) were assessed using logistic and linear regressions. In addition, sex-separated associations were explored. RESULTS: Being overweight or obese during childhood (OR = 2.82, 95% CI 1.17-6.80) and adolescence (OR = 2.45, 95% CI 1.13-5.34) was associated with developing MS. Furthermore, being overweight or obese during adolescence was associated with a younger age of onset (β = -0.11, p = 0.041). Of all 47 patients with a primary progressive (PP) onset type, only one patient (2.1%) was overweight or obese during childhood, whereas 45 patients with a relapsing remitting (RR) onset (14.3%) were overweight or obese during childhood (PP vs. RR p = 0.017; PP vs. HC p = 0.676; RR vs. HC, p = 0.015). However, using logistic regression analysis we did not find evidence of a significant association. CONCLUSION: In a nationwide population-based birth year cohort, being overweight or obese during childhood or adolescence is associated with MS prevalence and an earlier age of onset, but does not seem to associate with the type of onset.
 BACKGROUND: Although there is emerging evidence that aerobic training improves walking capacity in persons with multiple sclerosis (MS), data are limited about the potential benefits of Nordic walking (NW) for this population. This study evaluates the effectiveness of outdoor NW training on walking capacity and related quality of life for people with MS compared with cycloergometer and treadmill aerobic training. METHODS: A single-blinded (evaluator), randomized, 2-arm clinical trial was designed. RESULTS: A total of 57 patients with MS (38 women and 19 men; mean ± SD age, 51.98 ± 9.93 years; mean ± SD disease duration, 14.75 ± 8.52 years) were included. Both therapeutic modalities improved walking distance as measured by the 6-Minute Walk Test after the training period. The NW group showed significant improvement on the physical and emotional subscales of the Multiple Sclerosis Quality of Life-54 compared with the cycloergometer and treadmill group, which showed improvement only on the physical subscale. CONCLUSIONS: Both training modalities proved to be of equal benefit in improving the walking capacity of people with MS, but outdoor NW training also seems to have a beneficial effect on the emotional component of health-related quality of life.
 BACKGROUND: Alemtuzumab is an effective therapy for relapsing multiple sclerosis. Autoimmune thyroid events are a common adverse event. OBJECTIVE: Describe endocrine and multiple sclerosis outcomes over 6 years for alemtuzumab-treated relapsing multiple sclerosis patients in the phase 3 CARE-MS I, II, and extension studies who experienced adverse thyroid events. METHODS: Endocrine and multiple sclerosis outcomes were evaluated over 6 years. Thyroid event cases, excluding those pre-existing or occurring after Year 6, were adjudicated retrospectively by expert endocrinologists independently of the sponsor and investigators. RESULTS: Thyroid events were reported for 378/811 (46.6%) alemtuzumab-treated patients. Following adjudication, endocrinologists reached consensus on 286 cases (75.7%). Of these, 39.5% were adjudicated to Graves' disease, 2.5% Hashimoto's disease switching to hyperthyroidism, 15.4% Hashimoto's disease, 4.9% Graves' disease switching to hypothyroidism, 10.1% transient thyroiditis, and 27.6% with uncertain diagnosis; inclusion of anti-thyroid antibody status reduced the number of uncertain diagnoses. Multiple sclerosis outcomes of those with and without thyroid events were similar. CONCLUSION: Adjudicated thyroid events occurring over 6 years for alemtuzumab-treated relapsing multiple sclerosis patients were primarily autoimmune. Thyroid events were considered manageable and did not affect disease course. Thyroid autoimmunity is a common but manageable adverse event in alemtuzumab-treated relapsing multiple sclerosis patients.ClinicalTrials.gov Registration Numbers: CARE-MS I (NCT00530348); CARE-MS II (NCT00548405); CARE-MS Extension (NCT00930553).

 Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease that commonly results in nontraumatic disability in young adults. The characteristic pathological hallmark of MS is damage to myelin, oligodendrocytes, and axons. Microglia provide continuous surveillance in the CNS microenvironment and initiate defensive mechanisms to protect CNS tissue. Additionally, microglia participate in neurogenesis, synaptic refinement, and myelin pruning through the expression and release of different signaling factors. Continuous activation of microglia has been implicated in neurodegenerative disorders. We first review the lifetime of microglia, including the origin, differentiation, development, and function of microglia. We then discuss microglia participate in the whole processes of remyelination and demyelination, microglial phenotypes in MS, and the NF-κB/PI3K-AKT signaling pathway in microglia. The damage to regulatory signaling pathways may change the homeostasis of microglia, which would accelerate the progression of MS.
 Multiple sclerosis (MS) is the most frequent inflammatory and demyelinating disease of the Central Nervous System (CNS). Significant progress has been made during recent years in preventing relapses by using systemic immunomodulatory or immunosuppressive therapies. However, the limited effectiveness of such therapies for controlling the progressive disease course indicates there is a continuous disease progression independent of relapse activity which may start very early during the disease course. Dissecting the underlying mechanisms and developing therapies for preventing or stopping this disease progression represent, currently, the biggest challenges in the field of MS. Here, we summarize publications of 2022 which provide insight into susceptibility to MS, the basis of disease progression and features of relatively recently recognized distinct forms of inflammatory/demyelinating disorders of the CNS, such as myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).
 INTRODUCTION: The associations between multiple sclerosis (MS) and altered intestinal microbiomes have clinicians considering the use of fecal microbiota transplantation (FMT). Animal data suggests that administering FMT from people with MS into healthy mice results in a microbiome with decreased abundance of Sutterella, reduced anti-inflammatory signals, increase in inflammation and experimental autoimmune encephalomyelitis (EAE). Animal studies that administered FMT (from normal healthy donors) into mice resulted in slowing down EAE development relieving symptoms, improving BBB integrity and restoration of microbiota diversity. Human studies indicated clinical benefits of FMT (from healthy donors) in people with MS including: improved intestinal motility and motor ability which lasted at least for the duration of the studies, ranging from 2 to 15 years. AREAS COVERED: The authors discuss the efficacy and safety of FMT in treatment of experimental MS in animals and humans with MS. A literature search was performed via PubMed (up to July 2023), using the key words: multiple sclerosis, fecal microbiota transplantation, microbiome. EXPERT OPINION: Limited associative data do not provide an understanding of role of FMT in the treatment for MS. Until appropriately designed randomized comparative trials which are underway, are completed, we cannot recommend routine use of FMT in people with MS.
 BACKGROUND: Previous research has shown that users of complementary and alternative medicine (CAM) among persons with multiple sclerosis are more likely to be women and to have a higher level of education compared with nonusers. This qualitative study was performed to explore the motivations linked to CAM use among highly educated women with multiple sclerosis. METHODS: The study was based on a phenomenological approach, and 8 semistructured, in-depth qualitative interviews were performed. Data were transcribed verbatim and analyzed through meaning condensation and identification of recurring themes. RESULTS: Regarding the informants' motivations for CAM use, 3 main themes emerged: (1) Self-reliance is essential in disease management, (2) conventional health care lacks a holistic approach, and (3) personal experience is the primary guide. CONCLUSIONS: The interviewees wanted approaches to health care that supported their desire to actively participate in the management of their disease. They were critical of the conventional health care system, and they emphasized the importance of letting their own personal experiences, as well as those of others, guide their decisions.
 INTRODUCTION: Based on theoretical models, physical activity has been introduced as a promoting method to mitigate the disease severity, fatigue and relapse rate in multiple sclerosis. The primary objective of the study was to investigate the relation between self-reported physical activity level and disease severity, fatigue and relapse rate in persons with relapsing remitting multiple sclerosis (RRMS). METHODS: A survey was offered to persons with RRMS from March 2019 to August 2021 (n = 253). Physical activity level, fatigue and disease severity were determined using the Godin Leisure-Time Questionnaire (GLTEQ), the Patient Determined Disease Steps (PDDS) scale and the Fatigue Scale for Motor and Cognitive Functions (FSMC). Additionally, participants' relapse rate was recorded. RESULTS: Bivariate correlations revealed an inverse relation between physical activity level and PDDS (ρ = -0.279; p < 0.001) as well as between physical activity and FSMC (r = -0.213, p < 0.001), but not between physical activity and relapse rate (r = 0.033, p > 0.05). Multiple linear regression analyses explained 12.6% and 5.2% of the variance of PDDS and FSMC. CONCLUSION: Our findings confirm a relation between self-reported physical activity, disease severity and fatigue in persons with RRMS. However, self-reported physical activity level does not seem to affect the annualised relapse rate.
 Cerebrospinal fluid (CSF) soluble CD27 (sCD27) is a sensitive biomarker of intrathecal inflammation. Although generally considered a biomarker of T cell activation, CSF sCD27 has been shown to correlate with biomarkers of B cell activity in multiple sclerosis. We analyzed CSF from 40 patients with relapsing-remitting multiple sclerosis (RRMS) and nine symptomatic controls using flow cytometry and multiplex electrochemiluminescence immunoassays. CSF sCD27 levels were increased in RRMS and correlated with IgG index, soluble B cell maturation antigen, cell count, B cell frequency and CD8(+) T cell frequency. We provide new data indicating that CSF sCD27 is associated with CD8(+) T cells and B cells in RRMS.
 Ocrelizumab is a humanized monoclonal antibody against the B-lymphocyte antigen CD20 and the only approved treatment option in primary progressive multiple sclerosis. Herpesvirus-related infections like cytomegalovirus (CMV) infections are common in patients receiving ocrelizumab, whereas gastrointestinal side effects with inflammatory bowel disease (IBD) like esophagitis or colitis are very rare. This case report describes the challenging clinical, endoscopic, and histologic features of an ocrelizumab-induced colitis overlapping with CMV infection and their disadvantageous interaction with the underlying multiple sclerosis.
 Uhthoff’s phenomenon (also known as Uhthoff sign or Uhthoff syndrome) is described as temporary, short-lived (less than 24 hours), and stereotyped worsening of neurological function among multiple sclerosis patients in response to increases in core body temperature. This phenomenon is named after Wilhelm Uhthoff, a German ophthalmologist who described it. In 1890, Uhthoff first described exercise-induced amblyopia in multiple sclerosis patients.  In 1961, this phenomenon was given his surname, Uhthoff’s Phenomenon (UP), by G. Ricklefs. In four out of 100 MS patients, Uhthoff observed the appearance of reversible optic symptoms induced by an increase in body temperature, “marked deterioration of visual acuity during physical exercise and exhausting”. Subsequent observations have shown that the same physiological mechanism responsible for visual dysfunction in the setting of heat exposure, is responsible for a variety of other neurological symptoms experienced by multiple sclerosis (MS) patients. When Uhthoff studied this phenomenon, exercise was thought to be the etiology, and the significance of elevation in body temperature escaped his notice. Six decades later in 1950, the hot bath test was developed based on this phenomenon and was used as a diagnostic test for multiple sclerosis. By 1980, with the advancement in neuroimaging, the hot bath test began to be replaced by other diagnostic tests such as MRI and cerebrospinal fluid analysis because of its unspecific nature and potential complications. The temporary worsening of neurological function in response to heat exposure affects the physical and cognitive function of multiple sclerosis patients and interfere with their activities of daily life and functional capacity. This worsening needs to be differentiated from a true relapse or exacerbation of MS. An understanding of this phenomenon and its pathophysiology, therefore, is essential for recognition and appropriate treatment.
 Our registry-based cross-sectional study covered 27,508 PwMS in Tehran with a point incidence rate and prevalence of 7.87 and 194.62 per 100,000 in 2021, respectively. We found that the incidence and prevalence of MS in Tehran are still on an upward trend which requires general attention and measures to overcome. The proportion of men with a family history of MS was significantly higher. Whilst IMSS deals with economic difficulties, it continues to collect new PwMS to reach regional-level coverage in Tehran for better MS care services.
 Chronic fatigue is a common symptom in people with multiple sclerosis (PwMS) and presents as a reversible motor and cognitive impairment with reduced motivation and a desire to rest. The presentation of fatigue symptomatology in PwMS can be spontaneous or induced by mental or physical activity, temperature and humidity fluctuations, acute infections, and even food ingestion. Even though the exacerbation of fatigue symptomatology due to heat reaction is well established, the role of environmental temperature (ambient temperature and relative humidity) is not yet fully understood, and there is not enough systematic evidence regarding its effect. In this article, we present our opinion (based on the current literature and clinical experience) regarding the role of environmental temperature in the manifestation of fatigue symptomatology in PwMS.
 Radiologically isolated syndrome is characterised by central nervous system white-matter hyperintensities highly suggestive of multiple sclerosis in individuals without a neurological history of clinical demyelinating episodes. It probably represents the pre-symptomatic phase of clinical multiple sclerosis but is poorly understood. This mini review summarises our current knowledge regarding advanced imaging techniques in radiologically isolated syndrome that provide insights into its pathobiology and prognosis. The imaging covered will include magnetic resonance imaging-derived markers of central nervous system volumetrics, connectivity, and the central vein sign, alongside optical coherence tomography-related metrics.
 INTRODUCTION: Multiple sclerosis (MS) is a persistent neurological condition impacting the central nervous system (CNS). The precise cause of multiple sclerosis is still uncertain; however, it is thought to arise from a blend of genetic and environmental factors. MS diagnosis includes assessing medical history, conducting neurological exams, performing magnetic resonance imaging (MRI) scans, and analyzing cerebrospinal fluid. While there is currently no cure for MS, numerous treatments exist to address symptoms, decelerate disease progression, and enhance the quality of life for individuals with MS. METHODS: This paper introduces a novel machine learning (ML) algorithm utilizing decision trees to address a key objective: creating a predictive tool for assessing the likelihood of MS development. It achieves this by combining prevalent demographic risk factors, specifically gender, with crucial immunogenetic risk markers, such as the alleles responsible for human leukocyte antigen (HLA) class I molecules and the killer immunoglobulin-like receptors (KIR) genes responsible for natural killer lymphocyte receptors. RESULTS: The study included 619 healthy controls and 299 patients affected by MS, all of whom originated from Sardinia. The gender feature has been disregarded due to its substantial bias in influencing the classification outcomes. By solely considering immunogenetic risk markers, the algorithm demonstrates an ability to accurately identify 73.24% of MS patients and 66.07% of individuals without the disease. DISCUSSION: Given its notable performance, this system has the potential to support clinicians in monitoring the relatives of MS patients and identifying individuals who are at an increased risk of developing the disease.
 BACKGROUND: A limited subgroup of multiple sclerosis (MS) patients present with a long-term disease evolution characterized by a limited disease progression, known as benign MS (BMS). Chitinase 3-like-1 (CHI3L1) levels are sensitive to inflammatory processes and may play a role in the pathogenesis of MS. In this observational, cross-sectional study, we aimed to evaluate the implications of serum CHI3L1 and inflammatory cytokines in BMS patients treated with interferon β-1b for over a decade. METHODS: We collected serum samples from 17 BMS patients and 17 healthy controls (HC) to measure serum CHI3L1 levels and a Th17 panel of inflammatory cytokines. Serum levels of CHI3L1 were analysed using the sandwich ELISA method and the Th17 panel was assessed using the multiplex XMap technology on a Flexmap 3D Analyzer. RESULTS: Serum CHI3L1 levels did not differ significantly from HC. We identified a positive correlation between CHI3L1 levels and relapses during treatment. CONCLUSIONS: Our findings suggest that there are no differences in serum CHI3L1 levels between BMS patients and HC. However, serum CHI3L1 levels are sensitive to clinical inflammatory activity and may be associated with relapses in BMS patients.
 BACKGROUND: Patients with multiple sclerosis (MS) experience disabilities which significantly affect their quality of life (QOL) and mental health. Mood disorders and depressive symptoms are one of the most common psychiatric conditions in MS patients. This study aimed to evaluate the level of QOL in MS patients and to assess the influence of depressive symptoms and physical disability on QOL. METHODS: This prospective and observational study was conducted among 100 MS patients (mean age of 36.23 ± 11.77) recruited from the Lower Silesian Unit of the Polish Association for Multiple Sclerosis. This study used a questionnaire designed by the authors, which contained questions about sociodemographic and clinical data, as well as the following standardized questionnaires: the Activities of Daily Living questionnaire (ADL), the Instrumental Activities of Daily Living questionnaire (IADL), the Expanded Disability Status Scale (EDSS), the Beck Depression Inventory (BDI) and Multiple Sclerosis International Quality of Life Questionnaire (MusiQOL). RESULTS: The average EDSS score among patients was 3.13 ± 2.38 points. More than half of the respondents (68%) suffered from depression of varying severity. The univariate linear regression models showed that the independent (p < 0.05) QOL predictors (total MusiQOL) were as follows: the number of complaints, IADL results, BDI results, EDSS score, higher education, and material status >2000 PLN. In addition, the multiple linear regression model showed that the BDI result was a significant predictor of QOL (p < 0.005). CONCLUSION: Depressive symptoms significantly affect the QOL of MS patients.
 B cell clonal expansion and cerebrospinal fluid (CSF) oligoclonal IgG bands are established features of the immune response in multiple sclerosis (MS). Clone-specific IgG1 monoclonal recombinant antibodies (rAbs) derived from MS patient CSF plasmablasts bound to conformational proteolipid protein 1 (PLP1) membrane complexes and, when injected into mouse brain with human complement, recapitulated histologic features of MS pathology: oligodendrocyte cell loss, complement deposition, and CD68+ phagocyte infiltration. Conformational PLP1 membrane epitopes were complex and governed by the local cholesterol and glycolipid microenvironment. Antibodies against conformational PLP1 membrane complexes targeted multiple surface epitopes, were enriched within the CSF compartment, and were detected in most MS patients but not in inflammatory and non-inflammatory neurologic controls. CSF PLP1 complex antibodies provide a pathogenic autoantibody biomarker specific for MS.

 Multiple sclerosis is a chronic autoimmune demyelinating disease of the central nervous system and is difficult to diagnose in early stages. Without homeostatic control, urine was reported to have the ability to accumulate early changes in the body. We expect that urinary proteome can reflect early changes in the nervous system. The early urinary proteome changes in a most employed multiple sclerosis rat model (experimental autoimmune encephalomyelitis) were analysed to explore early urinary candidate biomarkers, and early treatment of methylprednisolone was used to evaluate the therapeutic effect. Twenty-five urinary proteins were altered at day 7 when there were no clinical symptoms and obvious histological changes. Fourteen were reported to be differently expressed in the serum/cerebrospinal fluid/brain tissues of multiple sclerosis patients or animals such as angiotensinogen and matrix metallopeptidase 8. Functional analysis showed that the dysregulated proteins were associated with asparagine degradation, neuroinflammation and lipid metabolism. After the early treatment of methylprednisolone, the incidence of encephalomyelitis in the intervention group was only 1/13. This study demonstrates that urine may be a good source of biomarkers for the early detection of multiple sclerosis. These findings may provide important information for early diagnosis and intervention of multiple sclerosis in the future.
 Juvenile multiple sclerosis (JMS) is a rare but significant subtype of multiple sclerosis (MS) that affects a small percentage of patients under the age of 10 and 3-5% of all MS patients. Despite its rarity, JMS poses unique challenges in terms of diagnosis, treatment, and management, as it can significantly impact a child or adolescent's physical, cognitive, and emotional development. JMS presents with a varying spectrum of signs and symptoms such as coordination difficulties and permanent cognitive dysfunctions and may include atypical clinical features such as seizures, acute disseminated encephalomyelitis, and optic neuritis, making diagnostic evaluations challenging. Whilst the biology of JMS shares similarities with adult-onset MS, there exist notable distinctions in disease progression, clinical manifestations, and ultimate prognoses. The International Pediatric MS Study Group (IPMSSG) was founded in 2005 to improve understanding of JMS, but there remains a lack of knowledge and guidelines on the management of this condition. This review summarizes the current knowledge on JMS, including its epidemiology, clinical presentations, diagnostic challenges, current treatment options, and outcomes. Current treatment options for JMS include disease-modifying therapies, but JMS can also result in impaired quality of life and psychiatric comorbidity, highlighting the need for comprehensive care for affected children. Through gathering and analyzing scattered studies and recent updates on JMS, the authors aim to address the gaps in current knowledge on JMS and provide an improved understanding of appropriate care for affected children. By doing so, this review hopes to contribute to improving the quality of life and outcomes for JMS patients.
 Introduction: Cognitive impairment is a debilitating symptom in people with multiple sclerosis (MS). Most of the neuropsychological tasks have little resemblance to everyday life. There is a need for ecologically valid tools for assessing cognition in real-life functional contexts in MS. One potential solution would involve the use of virtual reality (VR) to exert finer control over the task presentation environment; however, VR studies in the MS population are scarce. Objectives: To explore the utility and feasibility of a VR program for cognitive assessment in MS. Methods: A VR classroom embedded with a continuous performance task (CPT) was assessed in 10 non-MS adults and 10 people with MS with low cognitive functioning. Participants performed the CPT with distractors (i.e., WD) and without distractors (i.e., ND). The Symbol Digit Modalities Test (SDMT), California Verbal Learning Test-II (CVLT-II), and a feedback survey on the VR program was administered. Results: People with MS exhibited greater reaction time variability (RTV) compared to non-MS participants, and greater RTV in both WD and ND conditions was associated with lower SDMT. Conclusions: VR tools warrant further research to determine their value as an ecologically valid platform for assessing cognition and everyday functioning in people with MS.

 BACKGROUND AND PURPOSE: Fibroblast growth factors and receptors (FGFR) have been shown to modulate inflammation and neurodegeneration in multiple sclerosis (MS). The selective FGFR inhibitor infigratinib has been shown to be effective in cancer models. Here, we investigate the effects of infigratinib on prevention and suppression of first clinical episodes of myelin oligodendrocyte glycoprotein (MOG)(35-55) -induced experimental autoimmune encephalomyelitis (EAE) in mice. EXPERIMENTAL APPROACH: The FGFR inhibitor infigratinib was given over 10 days from the time of experimental autoimmune encephalomyelitis induction or the onset of symptoms. The effects of infigratinib on proliferation, cytotoxicity and FGFR signalling proteins were studied in lymphocyte cell lines and microglial cells. KEY RESULTS: Administration of infigratinib prevented by 40% and inhibited by 65% first clinical episodes of the induced experimental autoimmune encephalomyelitis. In the spinal cord, infiltration of lymphocytes and macrophages/microglia, destruction of myelin and axons were reduced by infigratinib. Infigratinib enhanced the maturation of oligodendrocytes and increased remyelination. In addition, infigratinib resulted in an increase of myelin proteins and a decrease in remyelination inhibitors. Further, lipids associated with neurodegeneration such as lysophosphatidylcholine and ceramide were decreased as were proliferation of T cells and microglial cells. CONCLUSION AND IMPLICATIONS: This proof of concept study demonstrates the therapeutic potential of targeting FGFRs in a disease model of multiple sclerosis. Application of oral infigratinib resulted in anti-inflammatory and remyelinating effects. Thus, infigratinib may have the potential to slow disease progression or even to improve the disabling symptoms of multiple sclerosis.
 PURPOSE: Investigations of the hemodynamic changes of the venous system in patients with multiple sclerosis (MS) have shown contradictory results. Herein, the biomechanical parameters of the internal jugular vein (IJV) and common carotid artery (CCA) of MS patients were extracted and compared to healthy individuals. METHODS: B-mode and Doppler sequential ultrasound images of 64 IJVs and CCAs of women including 22 healthy individuals, 22 relapsing-remitting multiple sclerosis (RRMS) patients, and 20 primary-progressive multiple sclerosis (PPMS) patients were recorded and processed. The biomechanical parameters of the IJV and the CCA walls during three cardiac cycles were calculated. RESULTS: The IJV maximum and minimum pressures were higher in the MS patients than in the healthy subjects, by 31% and 19% in RRMS patients and 39% and 24% in PPMS patients. The venous wall thicknesses in RRMS and PPMS patients were 51% and 60% higher than in healthy subjects, respectively. IJV distensibility in RRMS and PPMS patients was 70% and 75% lower, and compliance was 40% and 59% lower than in healthy subjects. The maximum intima-media thicknesses of the CCAs were 38% and 24%, and the minimum intima-media thicknesses were 27% and 23% higher in RRMS and PPMS patients than in healthy individuals, respectively. The shear modulus of CCA walls in RRMS and PPMS patients was 17% and 31%, and the radial elastic moduli were 47% and 9% higher than in healthy individuals. CONCLUSION: Some physical and biomechanical parameters of the CCA and IJV showed significant differences between MS patients and healthy individuals.
 People with multiple sclerosis (pwMS) have an increased risk of infection. As disease-modifying therapies (DMTs) and other treatments may interact with the immune system, there may be concerns about vaccine efficacy and safety. Therefore, it is important to evaluate possible interactions between DMTs and vaccines. The fumarates, dimethyl fumarate, diroximel fumarate, and monomethyl fumarate, are approved for the treatment of relapsing multiple sclerosis. This review assesses the evidence on vaccine response in pwMS treated with fumarates, with a particular focus on COVID-19 vaccines. Treatment with fumarates does not appear to result in blunting of humoral responses to vaccination; for COVID-19 vaccines, particularly RNA-based vaccines, evidence indicates antibody responses similar to those of healthy recipients. While data on the effect of fumarates on T-cell responses are limited, they do not indicate any significant blunting. COVID-19 vaccines impart a similar degree of protection against severe COVID-19 infection for pwMS on fumarates as in the general population. Adverse reactions following vaccination are generally consistent with those observed in the wider population; no additional safety signals have emerged in those on fumarates. Additionally, no increase in relapse has been observed in pwMS following vaccination. In pwMS receiving fumarates, vaccination is generally safe and elicits protective immune responses.
 BACKGROUND: Multiple sclerosis is a progressive degenerative disorder that frequently involves the development of physical and emotional changes, including loss of limb function or sensitivity, sexual dysfunction, and cognitive and mood alterations. It is likely that these alterations lead to changes in body aspects. However, knowledge about body image perception in multiple sclerosis is lacking. PURPOSE: The present study investigated the relationship between body image perception and its correlation with a disability, neuropsychiatric symptoms, and self-esteem. METHODS: A total of 100 outpatients with relapsing-remitting multiple sclerosis underwent neurological assessment using the Expanded Disability Status Scale. Participants also completed the Body Image Scale (BIS), Rosenberg Self-Esteem Scale (RSES), and Symptom Checklist-90-Revised (SCL-90-R). RESULTS: We found a significant positive correlation between body image and disability (r = 0.21; p = 0.03), body image and self-esteem (r = -0.52; p < 0.001), body image and somatization (r = 0.44; p < 0.001), body image and depression (r = 0.57; p < 0.001), and body image and anxiety (r = 0.5; p < 0.001). CONCLUSIONS: The body is considered one of the main parts of a person's identity. Dissatisfaction with one's own body changes the general evaluation of the "self". The body image construct has important health outcomes and should be studied more in patients with multiple sclerosis.
 CD8+ T cells outnumber CD4+ cells in multiple sclerosis lesions associated with disease progression, but the pathogenic role and antigenic targets of these clonally expanded effectors are unknown. Based on evidence that demyelination is necessary but not sufficient for disease progression in multiple sclerosis (MS), we previously hypothesized that CNS-infiltrating CD8+ T cells specific for neuronal antigens directly drive the axon and neuron injury that leads to cumulative neurologic disability in MS patients. We now show that demyelination induced expression of MHC class I on neurons and axons and resulted in presentation of a neuron-specific neoantigen (synapsin promoter-driven chicken ovalbumin) to antigen-specific CD8+ T cells (anti-ovalbumin OT-I transgenic T cells). These neuroantigen-specific effectors surveilled the CNS in the absence of demyelination but were not retained. However, upon induction of demyelination via cuprizone intoxication, neuroantigen-specific CD8+ T cells proliferated, accumulated in the CNS, and damaged neoantigen-expressing neurons and axons. We further report elevated neuronal expression of MHC class I and β2-microglobulin transcripts and protein in gray matter and white matter tracts in tissue from patients with MS. These findings support a pathogenic role for autoreactive anti-axonal and anti-neuronal CD8+ T cells in MS progression.
 BACKGROUND: Multiple sclerosis (MS) as a complex neurological abnormality is marked with loss of myelin and axons due to chronic inflammatory and autoimmune responses. The modulatory properties of the low dose radiation (LDR) on inflammatory and immune responses have well known. OBJECTIVE: The current research aimed to assess the impacts of LDR on the disability in patients suffering from MS. MATERIAL AND METHODS: This experimental pilot study was done on 10 patients with secondary progressive multiple sclerosis (SPMS). After magnetic resonance imaging, the SPMS patients were treated by LDR at a daily dose of 2 Gray for 5 consecutive days (totally 10 Gray dose) using a linear accelerator. The extent of the disability was evaluated one week after the completion of radiotherapy using expanded disability status scale (EDSS). RESULTS: After receiving radiotherapy, the patients had a feeling of wellbeing of some sort. The mean of EDSS was significantly reduced after radiotherapy compared with before irradiation (7.4±0.45 vs 6.35±1.18; P<0.017). EDSS more decreased in younger SPMS patients (P=0.0001), and in the women after LDR (P=0.027). CONCLUSION: Radiotherapy can reduce fatigue and EDSS in patients with SPMS. The age and gender of patients may influence the LDR efficacy.
 Multiple sclerosis is a demyelinating disease of the central nervous system. It contributes to a variety of symptoms affecting different areas of the body. The primary care NP must be familiar with the disease, therapies, and social impact to provide proper care to affected patients.
 BACKGROUND: Up to 70% of people with multiple sclerosis (MS) experience cognitive difficulties. Cognitive rehabilitation is a type of therapy that helps manage cognitive problems. OBJECTIVE: The Cognitive Rehabilitation for Attention and Memory in MS (CRAMMS) trial showed some evidence of effectiveness of cognitive rehabilitation in improving cognitive function, with some participants benefitting more than others. We therefore conducted a secondary analysis of the CRAMMS data to understand who benefits most. METHODS: We grouped baseline data into four categories of possible predictors. We used regression models to identify specific factors/characteristics that could predict the likelihood that an individual will benefit from cognitive rehabilitation. RESULTS: The models predicted whether a participant improved or did not improve in neuropsychological function following cognitive rehabilitation in up to 86% of participants. Results suggest that younger participants with medium to high education, diagnosed with relapsing-remitting multiple sclerosis (RRMS) and primary-progressive multiple sclerosis (PPMS) who have not experienced any recent relapses, with mild to moderate cognitive difficulties were most likely to benefit from cognitive rehabilitation. CONCLUSION: We can predict which participants are most likely to demonstrate significant improvements in neuropsychological function following group-based cognitive rehabilitation. Clinically, this allows us to optimise limited neuropsychology resources by offering such cognitive rehabilitation to those most likely to benefit.
 Objective: Retinal neuronal and vascular changes have been observed in multiple sclerosis (MS) patients. The aim of this review was to highlight the most current optical coherence tomography (OCT) and optical coherence tomography angiography (OCT-A) data in MS and to provide information about the possibility of using OCT / OCT-A parameters as biomarkers for screening, diagnosis and monitoring of MS. Methods: To carry out this review, a meticulous literature search was undergone on PubMed between 2014 and the present day, using the following terms: "multiple", "sclerosis", "optical", "coherence", "tomography" and "angiography". Additional studies were found via references, being chosen according to relevance. Results: Retinal nerve fiber layer (RNFL) and ganglion cell layer (GCL) were significantly lower in MS patients compared to controls, and correlated with clinical and paraclinical variables, such as visual function, disability, and magnetic resonance imaging (MRI). Retinal capillary plexuses could be higher, lower or the same, and the best OCT-A microvasculature parameter for the detection of MS was the superficial capillary plexus (SCP). The reduced retinal vessel density (VD) was correlated with the disability in MS. Conclusions: OCT and OCT-A parameters could improve the development of retinal biomarkers for screening, early diagnosis and monitoring the disease progression of MS, and they could improve the development of potential future therapies that could slow or stop the course of this incurable disease. Abbreviations: DCP = deep capillary plexus; EDSS = Expanded Disability Status Scale; GCC = ganglion cell complex; GCL = ganglion cell layer; MRI = magnetic resonance imaging; MS = Multiple sclerosis; OCT = optical coherence tomography; OCT-A = optical coherence tomography angiography; ON = optic neuritis; RNFL = retinal nerve fiber layer; SCP = superficial capillary plexus; VD = vessel density.
 BACKGROUND AND PURPOSE: Multiple sclerosis (MS) has a high incidence of debilitating spasticity. Central Nervous System (CNS) intrafusal settings have an impact on spasticity level. Mechanoreceptors of the Peripheral Nervous System (PNS) communicate monosynaptically with the central nervous system (CNS). This case series assesses feasibility of multimodal treatment of individuals with MS using a direct current electrical stimulation (DC) to influence mechanoreceptors. CASE DESCRIPTION AND INTERVENTION: Seven MS diagnosed participants with Expanded Disability Status Scale (EDSS) = 6.0-8.0 completed 18 visits over 6 weeks of using DC combined with neuromuscular reeducation. Design included pre-, post- outcome measures of EDSS, 12-item MS Walking Scale (MSWS-12), Range of Motion (ROM), Manual Muscle Testing (MMT), Modified Ashworth Test (MAT), Timed 25-Foot walk (T25WT), Timed Up and Go (TUG) and the Multiple Sclerosis Impact Scale-29 (MSIS-29). OUTCOME: 125 out of a possible 126 visits were completed, demonstrating a high level of tolerance. Individual results included trends towards improvement in spasticity and agonists. DISCUSSION: This case series design of seven heterogenous subjects with MS is a low sample size for statistical analysis and should be considered a pilot. The study demonstrates a high level of feasibility and possible correlations to consider. Further research is warranted.
 Cognitive impairment in multiple sclerosis (MS) affects approximately 40-70% of patients and can have varying degrees of severity. Even mild cognitive impairment can impact on quality of life and productivity. Despite this, patients are not routinely screened or monitored for cognitive impairment in Australia due to a range of issues, with time and space being the main limiting factors. This Australian multidisciplinary perspective provides recommendations on cognition management in Australia. It gives a broad overview of cognition in MS, advice on the screening and monitoring tools available to clinicians, and strategies that can be implemented in clinics to help monitor for cognitive impairment in patients with MS. We suggest a routine baseline assessment and multidomain cognitive battery in regular intervals; a change should trigger a thorough investigation of the cause.
 This study aimed to assess the effects of the immunomodulator thymulin, a thymic peptide with anti-inflammatory effects, and peroxiredoxin 6 (Prdx6), an antioxidant enzyme with dual peroxidase and phospholipase A2 activities, on the blood‒brain barrier (BBB) condition and general health status of animals with relapsing-remitting experimental autoimmune encephalomyelitis (EAE), which is a model of multiple sclerosis in humans. Both thymulin and Prdx6 significantly improved the condition of the BBB, which was impaired by EAE induction, as measured by Evans blue dye accumulation, tight-junction protein loss in brain tissue, and lymphocyte infiltration through the BBB. The effect was associated with significant amelioration of EAE symptoms. Thymulin treatment was accompanied by a decrease in immune cell activation as judged by interleukin-6, -17, and interferon-gamma cytokine levels in serum and NF-kappaB cascade activation in splenocytes of mice with EAE. Prdx6 did not induce significant immunomodulatory effects but abruptly decreased EAE-induced NOX1 and NOX4 gene expression in brain tissue, which may be one of the possible mechanisms of its beneficial effects on BBB conditions and health status. The simultaneous administration of thymulin and Prdx6 resulted in complete symptomatic restoration of mice with EAE. The results demonstrate prospective strategies for multiple sclerosis treatment.
 Psychological resilience is one of the most important factors that help a person adapt to the difficulties of life. The present study aimed to examine the role of psychological resilience in the social and professional functioning of patients with multiple sclerosis (MS), diabetes mellitus, and rheumatoid arthritis (RA). A total of 301 individuals (58.8% female) participated in the study. Approximately 44% of participants were diagnosed with diabetes, 28% with rheumatoid arthritis, and around 25% with multiple sclerosis. Two psychometric measures were used to achieve the objectives of the present study: the Psychological Resilience Scale and the Performance of Social and Occupational Functions Scale. Regression analyses were used to examine the amount of variance predicted by psychological resilience in terms of the following variables of social and professional functions: relationships, communication, social activities, entertainment activities, life skills, employment-based job functions, and unemployment-based job functions. Results revealed that psychological resilience positively predicted social and occupational functions among all illnesses. Resilience best predicted social and professional functions among MS patients, followed by diabetes patients and RA patients. These findings highlight the role of psychological resilience in improving the social and occupational performance of patients with chronic illnesses and the positive relationship between employment and resilience.
 Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare genetic disorder due to a NOTCH 3 mutation on chromosome 19 resulting in a small vessel disease that may mimic many other neurological disorders like migraine, stroke, transient ischaemic attack (TIA), dementia and psychiatric illnesses. The disease is confirmed by genetic testing and other investigations like MRI and skin biopsy are also helpful. Here, we present a 43-year-old male with a confirmed CADASIL through genetic testing, who was initially diagnosed as having multiple sclerosis due to recurrent attacks of focal neurological deficits in the form of weakness and vertigo and other progressive features like mental slowing and difficulties in performing the usual tasks at work, He had a strong family history of neurological illnesses from his mother's side that made us think of an alternative diagnosis.
 BACKGROUND AND OBJECTIVES: The current clinical course descriptors of multiple sclerosis (MS) include a combination of clinical and magnetic resonance imaging (MRI) features. Recently there has been a growing call to base these descriptors more firmly on biological mechanisms. We investigated the implications of proposing a new mechanism-driven framework for describing MS. METHODS: In a web-based survey, multiple stakeholders rated the need to change current MS clinical course descriptors, the definitions of disease course and their value in clinical practice and related topics. RESULTS: We received 502 responses across 49 countries. In all, 77% of the survey respondents supported changing the current MS clinical course descriptors. They preferred a framework that informs treatment decisions, aids the design and conduct of clinical trials, allows patients to understand their disease, and links disease mechanisms and clinical expression of disease. Clinical validation before dissemination and ease of communication to patients were rated as the most important aspects to consider when developing any new framework for describing MS. CONCLUSION: A majority of MS stakeholders agreed that the current MS clinical course descriptors need to change. Any change process will need to engage a wide range of affected stakeholders and be guided by foundational principles.
 Multiple sclerosis (MS) is an autoimmune demyelinating disorder that disproportionately affects middle-aged women, and is capable of resulting in severe disability. However, the use of disease-modifying therapies has profoundly contributed to the improvement in the morbidity of the disorder. Diroximel fumarate (DRF) is a second-generation drug that has seen success in the treatment of relapsing-remitting MS (RRMS). While its relatively mild side effects of gastrointestinal discomfort are known, the less common complications are often missed in clinical settings. This includes a resulting susceptibility to opportunistic infections. In this case report, we describe a patient who experienced lymphopenia, recurrent yeast infections, and labial shingles while on the medication. This case highlights the side effects and the rare complications of the immunomodulator, DRF.
 Multiple sclerosis (MS) is a chronic, neurodegenerative, inflammatory condition usually associated with physical disability. Clinical care has been skewed toward the physical manifestations of the disease, yet a range of silent symptoms occurs including the cognitive aspects of MS. In a 2018 meeting of MS in the 21st Century (MS21), an international steering committee comprising both specialists and patient experts recognised that the 'invisible symptoms' of MS pose a significant challenge to patient engagement. These findings prompted the European Charcot Foundation (ECF) MS21 symposium (2020), where a panel consisting of two leading MS clinicians and an MS patient expert (who were all members of the MS21 steering group) gathered to discuss the impact of cognitive impairment on the everyday lives of people with MS.The perspectives and experiences of the panellists are summarised in this paper. The key points raised were that (1) the cognitive manifestations of MS are under-recognised and have consequently been undermanaged from a clinical perspective and (2) cognitive impairment due to MS has a significant impact upon daily living and patient quality of life. During discussions about how these challenges can be addressed, the panel advocated for an improvement in education about cognitive symptoms for people living with MS and healthcare professionals (HCPs) to raise awareness about this aspect of MS. Furthermore, the panel emphasised the importance of open and proactive communication between HCPs and their patients with MS about cognitive symptoms to reduce the stigma attached to these symptoms. In the opinion of the panel, future clinical trials which include cognitive outcomes as key endpoints are needed. Reflecting this point, cognitive impairment in MS care also needs to be treated as an important disease symptom, as is done with physical symptoms of the disease. Implementing early and routine cognition screening and promoting measures for protecting cognition to people living with MS, such as cognitive rehabilitation and a 'brain-healthy' lifestyle, are actions which can drive forward the recognition of cognitive impairment as a care priority.If prioritised as highly as physical disability in both the MS care and clinical drug development setting, and proactively discussed in conversations between HCPs and patients with MS, the 'invisibility' of cognitive impairment in MS can be lifted and a better quality of life can be promoted for people living with MS.



 Driven by the limitations and obstacles of the available approaches and medications for multiple sclerosis (MS) that still cannot treat the disease, but only aid in accelerating the recovery from its attacks, the use of naturally occurring molecules as a potentially safe and effective treatment for MS is being explored in model organisms. MS is a devastating disease involving the brain and spinal cord, and its symptoms vary widely. Multiple molecular pathways are involved in the pathogenesis of the disease. The present review showcases the recent advancements in harnessing nature's resources to combat MS. By deciphering the molecular pathways involved in the pathogenesis of the disease, a wealth of potential therapeutic agents is uncovered that may revolutionize the treatment of MS. Thus, a new hope can be envisioned in the future, aiming at paving the way toward identifying novel safe alternatives to improve the lives of patients with MS.
 A link between neurodegenerative diseases and infections has been previously reported. However, it is not clear to what extent such link is caused by confounding factors or to what extent it is intimately connected with the underlying conditions. Further, studies on the impact of infections on mortality risk following neurodegenerative diseases are rare. We analysed two data sets with different characteristics: (i) a community-based cohort from the UK Biobank with 2023 patients with multiple sclerosis, 2200 patients with Alzheimer's disease, 3050 patients with Parkinson's disease diagnosed before 1 March 2020 and 5 controls per case who were randomly selected and individually matched to the case; (ii) a Swedish Twin Registry cohort with 230 patients with multiple sclerosis, 885 patients with Alzheimer's disease and 626 patients with Parkinson's disease diagnosed before 31 December 2016 and their disease-free co-twins. The relative risk of infections after a diagnosis of neurodegenerative disease was estimated using stratified Cox models, with adjustment for differences in baseline characteristics. Causal mediation analyses of survival outcomes based on Cox models were performed to assess the impact of infections on mortality. Compared with matched controls or unaffected co-twins, we observed an elevated infection risk after diagnosis of neurodegenerative diseases, with a fully adjusted hazard ratio (95% confidence interval) of 2.45 (2.24-2.69) for multiple sclerosis, 5.06 (4.58-5.59) for Alzheimer's disease and 3.72 (3.44-4.01) for Parkinson's disease in the UK Biobank cohort, and 1.78 (1.21-2.62) for multiple sclerosis, 1.50 (1.19-1.88) for Alzheimer's disease and 2.30 (1.79-2.95) for Parkinson's disease in the twin cohort. Similar risk increases were observed when we analysed infections during the 5 years before diagnosis of the respective disease. Occurrence of infections after diagnosis had, however, relatively little impact on mortality, as mediation of infections on mortality (95% confidence interval) was estimated as 31.89% (26.83-37.11%) for multiple sclerosis, 13.38% (11.49-15.29%) for Alzheimer's disease and 18.85% (16.95-20.97%) for Parkinson's disease in the UK Biobank cohort, whereas it was 6.56% (-3.59 to 16.88%) for multiple sclerosis, -2.21% (-0.21 to 4.65%) for Parkinson's disease and -3.89% (-7.27 to -0.51%) for Alzheimer's disease in the twin cohort. Individuals with studied neurodegenerative diseases display an increased risk of infections independently of genetic and familial environment factors. A similar magnitude of risk increase is present prior to confirmed diagnosis, which may indicate a modulating effect of the studied neurological conditions on immune defences.
 BACKGROUNDS AND AIMS: Patients with multiple sclerosis (pwMS) need self-management (SM) skills to manage their symptoms and problems. An essential step to SM improvement is accurate SM assessment using valid and reliable instruments. The aim of this study was to evaluate the psychometric properties of the Persian version of the Multiple Sclerosis Self-Management Scale-Revised (MSSMS-R). METHODS: This cross-sectional methodological study was conducted from December 2021 to June 2022. The face, content, and construct‎ validity of MSSMS-R were evaluated. Construct validity was evaluated through confirmatory factor analysis (CFA) and evaluating convergent and discriminant‎ validity using the data obtained from 210 randomly selected MS patients. The reliability of the scale was also evaluated through the test-retest stability and the internal consistency evaluation methods. RESULTS: The face validity was confirmed and the content validity ratio and index values of all items were more than 0.62 and 0.79, respectively. CFA revealed the acceptable construct validity of the scale after omitting items 21 and 22. In convergent and discriminant validity evaluation, the total score of MSSMS-R had significant positive correlation with the total mean scores of the Multiple Sclerosis Self-Efficacy Scale (r = 0.36; p < 0.001) and the physical health composite‎ (r = 0.31; p < 0.001) and the mental health composite‎ (r = 0.39; p < 0.001) dimensions of the 54-item Multiple Sclerosis Quality of Life scale ‎and significant inverse correlation with the total mean score of the Beck Depression Inventory (r = -0.28; p < 0.001). The Cronbach's alpha values of the scale and its subscales were 0.86 and 0.65-0.90 and their test-retest intraclass correlation coefficients were 0.97 and 0.95-0.99, respectively. CONCLUSION: The Persian MSSMS-R is a valid and reliable scale and can be used in future studies for SM assessment among pwMS.
 The programmed cell death protein 1/programmed cell death ligand 1 axis plays an important role in the adaptive immune system and has influence on neoplastic and inflammatory diseases, while its role in multiple sclerosis is unclear. Here, we aimed to analyse expression patterns of programmed cell death protein 1 and programmed cell death ligand 1 on peripheral blood mononuclear cells and their soluble variants in multiple sclerosis patients and controls, to determine their correlation with clinical disability and disease activity. In a cross-sectional study, we performed in-depth flow cytometric immunophenotyping of peripheral blood mononuclear cells and analysed soluble programmed cell death protein 1 and programmed cell death ligand 1 serum levels in patients with relapsing-remitting multiple sclerosis and controls. In comparison to control subjects, relapsing-remitting multiple sclerosis patients displayed distinct cellular programmed cell death protein 1/programmed cell death ligand 1 expression patterns in immune cell subsets and increased soluble programmed cell death ligand 1 levels, which correlated with clinical measures of disability and MRI activity over time. This study extends our knowledge of how programmed cell death protein 1 and programmed cell death ligand 1 are expressed in the membranes of patients with relapsing-remitting multiple sclerosis and describes for the first time the elevation of soluble programmed cell death ligand 1 in the blood of multiple sclerosis patients. The distinct expression pattern of membrane-bound programmed cell death protein 1 and programmed cell death ligand 1 and the correlation between soluble programmed cell death ligand 1, membrane-bound programmed cell death ligand 1, disease and clinical factors may offer therapeutic potential in the setting of multiple sclerosis and might improve future diagnosis and clinical decision-making.
 The effects of probiotics have mostly been shown to be favorable on measures of anxiety and stress. More recent experiments indicate single- and multi-strain probiotics in treating motor- related diseases. Initial studies in patients with Parkinson's disease and Prader-Willi syndrome are concordant with this hypothesis. In addition, probiotics improved motor coordination in normal animals and models of Parkinson's disease, multiple sclerosis, and spinal cord injury as well as gripstrength in hepatic encephalopathy. Further studies should delineate the most optimal bacterial profile under each condition.

 Polygenic risk scores aggregate an individual's burden of risk alleles to estimate the overall genetic risk for a specific trait or disease. Polygenic risk scores derived from genome-wide association studies of European populations perform poorly for other ancestral groups. Given the potential for future clinical utility, underperformance of polygenic risk scores in South Asian populations has the potential to reinforce health inequalities. To determine whether European-derived polygenic risk scores underperform at multiple sclerosis prediction in a South Asian-ancestry population compared with a European-ancestry cohort, we used data from two longitudinal genetic cohort studies: Genes & Health (2015-present), a study of ∼50 000 British-Bangladeshi and British-Pakistani individuals, and UK Biobank (2006-present), which is comprised of ∼500 000 predominantly White British individuals. We compared individuals with and without multiple sclerosis in both studies (Genes & Health: N (Cases) = 42, N (Control) = 40 490; UK Biobank: N (Cases) = 2091, N (Control) = 374 866). Polygenic risk scores were calculated using clumping and thresholding with risk allele effect sizes obtained from the largest multiple sclerosis genome-wide association study to date. Scores were calculated with and without the major histocompatibility complex region, the most influential locus in determining multiple sclerosis risk. Polygenic risk score prediction was evaluated using Nagelkerke's pseudo-R (2) metric adjusted for case ascertainment, age, sex and the first four genetic principal components. We found that, as expected, European-derived polygenic risk scores perform poorly in the Genes & Health cohort, explaining 1.1% (including the major histocompatibility complex) and 1.5% (excluding the major histocompatibility complex) of disease risk. In contrast, multiple sclerosis polygenic risk scores explained 4.8% (including the major histocompatibility complex) and 2.8% (excluding the major histocompatibility complex) of disease risk in European-ancestry UK Biobank participants. These findings suggest that polygenic risk score prediction of multiple sclerosis based on European genome-wide association study results is less accurate in a South Asian population. Genetic studies of ancestrally diverse populations are required to ensure that polygenic risk scores can be useful across ancestries.
 BACKGROUND: Several observational studies have explored the relationships between multiple sclerosis (MS) and breast cancer; however, whether an association exists remains unknown. METHODS: We conducted a meta-analysis of observational studies and Mendelian randomization (MR) based on genetic variants to identify the relationship between MS and breast cancer. The observational studies were searched from PubMed, Embase, Web of Science, and Scopus to assess the relationship between MS and breast cancer from inception to 07 Nov 2022. Moreover, we explored the association between genetically pre-disposed MS and breast cancer risk based on an MR study. The summary analysis for MS from two separate databases [International Multiple Sclerosis Genetics Consortium (IMSGC), FinnGen] and the summary analysis for breast cancer from Breast Cancer Association Consortium. RESULTS: Fifteen cohort studies involving 173,565 female MS patients were included in this meta-analysis. The correlation between MS and breast cancer was not statistically significant [relative ratio (RR) = 1.08, 95% confidence interval (CI) = 0.99-1.17]. In the MR analysis, we did not observe causal associations of genetically determined MS with breast cancer and its subtypes from both the IMSGC and FinnGen datasets. CONCLUSION: The meta-analysis of observational and MR based on genetic variants does not support the correlation between MS and breast cancer.
 Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) is a rare neuro-ophthalmological condition in which there is ocular motility impairment characterized by bilateral adduction deficiencies, bilateral abducting nystagmus, and exotropia in primary gaze, and is often associated with multiple sclerosis (MS). This report describes a young female who presented with sudden onset of binocular diplopia and alternating exotropia for two days duration, which was associated with a history of intermittent headaches for one year before presenting complaints. Examination revealed alternating exotropia on the primary gaze with bilateral limitation of adduction and bilateral nystagmus on abduction. Other ocular and neurological examinations were unremarkable. Neuroimaging showed multiple white matter lesions that were consistent with demyelinating disease. Her symptoms completely resolved after the initiation of intravenous corticosteroid therapy. However, she developed left upper limb numbness four months later, and a repeat magnetic resonance imaging (MRI) of the brain showed the presence of multiple new brain lesions. Subsequently, she was diagnosed with MS and started on immunotherapy. Her symptoms resolved, with no residual ophthalmoplegia or any neurological symptoms.
 BACKGROUND: The Berg Balance Scale (BBS) is one of the most used tools to quantify balance in Persons with Multiple Sclerosis, a population at high risk of falling. AIM: To evaluate the measurement characteristics of the BBS in Multiple Sclerosis through Rasch analysis. DESIGN: Retrospective study. SETTING: Outpatients in three Italian Rehabilitation centers. POPULATION: Eight hundred and fourteen persons with Multiple Sclerosis able to stand independently for more than 3 s. METHODS: The sample (N = 1,220) was split into one validating (B1) and three confirmatory subsamples. Following the Rasch analysis performed on B1, the item estimates were exported and anchored to the three confirmatory subsamples. After obtaining the same final solution across all samples, we studied the convergent and discriminant validity of the final BBS-MS using the EDSS, the ABC scale, and the number of falls. RESULTS: The base analysis on the B1 subsample failed the monotonicity, local independence, and unidimensionality requirements and did not fit the Rasch model. After grouping locally dependent items, the BBS-MS fitted the model (χ(2)(8) = 23.8; p = 0.003) and satisfied all requirements for adequate internal construct validity (ICV). However, it was mistargeted to the sample, given the striking prevalence of higher scores (targeting index 1.922) with a distribution-independent Person Separation Index sufficient for individual measurements (0.962). The B1 item estimates were anchored to the confirmatory samples with confirmation of adequate fit (χ(2) = [19.0, 22.8], value of ps = [0.015, 0.004]) and satisfaction of all ICV requirements for all subsamples. The final BBS-MS directly correlated with the ABC scale (rho = 0.523) and inversely with EDSS (rho = -0.573). The BBS-MS estimates significantly differed across groups according to the pre-specified hypotheses (between the three EDSS groups, between the ABC cut-offs, distinguishing 'fallers' vs. 'non-fallers', and between the 'low' vs. 'moderate' vs. 'high' levels of physical functioning; and, finally, between 'no falls' vs. 'one or more falls'). CONCLUSION: This study supports the internal construct validity and reliability of the BBS-MS in an Italian multicentre sample of persons with Multiple Sclerosis. However, as the scale is slightly mistargeted to the sample, it represents a candidate tool to assess balance, mainly in more disabled people with an advanced walking disability.
 BACKGROUND: Multiple sclerosis profoundly affects the sexual aspects of patients' life, especially in women. Various coping strategies are used by women with multiple sclerosis to overcome, tolerate, or minimize these sexual effects. The present study aimed to assess the relationship between sexual satisfaction, sexual intimacy, and coping strategies in women with multiple sclerosis. METHODS: This cross-sectional study was performed on a sample of 122 married women who were members of Iran's MS society in Tehran, Iran. The study was conducted from December 2018 to September 2019. Data were collected using the Index of Sexual Satisfaction (ISS), the Sexual Intimacy Questionnaire (SIQ), and the Folkman and Lazarus Coping Strategies Questionnaire. Frequency, percentage, mean and standard deviation were used to explore the observations. Independent t-test and logistic regression were applied to analyze the data using the SPSS-23. RESULTS: The majority (n = 71, 58.2%) used an emotion-focused coping strategy with the highest score for the escape-avoidance subscale [mean (SD): 13.29 (5.40)]. However, 41.8% of the patients (n = 51) used a problem-focused coping strategy with the highest score for the positive reappraisal strategy subscale [mean (SD): 10.50 (4.96)]. The sexual satisfaction in women with problem-focused coping strategies was significantly higher than women who used emotion-focused coping strategies (95.6 vs. 84.71, P-value = 0.001). There was a negative association between sexual intimacy and higher emotion-focused coping strategy (OR = 0.919, 95% CI 0.872-0.968, P = 0.001). CONCLUSIONS: Problem-focused coping strategy in women with multiple sclerosis increases sexual satisfaction, while the emotion-focused coping strategy has a significant negative relationship with sexual intimacy.
 BACKGROUND: Oral cladribine (OC) is approved for the treatment of highly active relapsing multiple sclerosis. Postmarketing safety assessments have reported rare, but occasionally severe cases of liver injury in temporal association with OC, with pathophysiologic mechanisms still unknown. In the only detailed case report on this topic, idiosyncratic drug-induced liver injury (iDILI) during OC treatment was well characterised for the first time, but occurred in the context of prior high-dose steroid exposure. Although high-dose steroids are known to induce iDILI in patients with multiple sclerosis with a delay of up to 12 weeks, OC was assumed to be the culprit agent for observed liver injury and the role of steroid exposure was not further investigated. CASE: Herein, we describe a case of a 35-year-old women treated with high-dose oral prednisolone during the first treatment cycle OC and subsequently developed iDILI. A causality assessment of the role of prednisolone and OC was performed using the updated Roussel Uclaf Causality Assessment Method which also included a negative re-exposure test for OC during the second OC treatment cycle 1 year later. CONCLUSION: Our observations suggest that prednisolone or interactions between prednisolone and OC are more likely to foster development of iDILI rather than OC treatment itself.
 BACKGROUND: Sleep disorders are common in patients with multiple sclerosis and have a bidirectional interplay with fatigue and depression. OBJECTIVE: To evaluate the effect of treatment with oral dimethyl fumarate on the quality of sleep in relapsing-remitting multiple sclerosis. METHODS: This was a multicentre observational study with 223 relapsing-remitting multiple sclerosis subjects starting treatment with dimethyl fumarate (n=177) or beta interferon (n=46). All patients underwent subjective (Pittsburgh Sleep Quality Index) and objective (wearable tracker) measurements of quality of sleep. Fatigue, depression, and quality of life were also investigated and physical activity was monitored. RESULTS: Patients treated with dimethyl fumarate had significant improvement in the quality of sleep as measured with the Pittsburgh Sleep Quality Index (p<0.001). At all-time points, no significant changes in Pittsburgh Sleep Quality Index score were observed in the interferon group. Total and deep sleep measured by wearable tracker decreased at week 12 with both treatments, then remained stable for the total study duration. Depression significantly improved in patients treated with dimethyl fumarate. No significant changes were observed in mobility, fatigue and quality of life. CONCLUSION: In patients with relapsing-remitting multiple sclerosis, the treatment with dimethyl fumarate was associated with improvements in patient-reported quality of sleep. Further randomised clinical trials are needed to confirm the benefits of long-term treatment with dimethyl fumarate.
 BACKGROUND: Functional connectome fingerprinting can identify individuals based on their functional connectome. Previous studies relied mostly on short intervals between fMRI acquisitions. OBJECTIVE: This cohort study aimed to determine the stability of connectome-based identification and their underlying signatures in patients with multiple sclerosis and healthy individuals with long follow-up intervals. METHODS: We acquired resting-state fMRI in 70 patients with multiple sclerosis and 273 healthy individuals with long follow-up times (up to 4 and 9 years, respectively). Using functional connectome fingerprinting, we examined the stability of the connectome and additionally investigated which regions, connections and networks supported individual identification. Finally, we predicted cognitive and behavioural outcome based on functional connectivity. RESULTS: Multiple sclerosis patients showed connectome stability and identification accuracies similar to healthy individuals, with longer time delays between imaging sessions being associated with accuracies dropping from 89% to 76%. Lesion load, brain atrophy or cognitive impairment did not affect identification accuracies within the range of disease severity studied. Connections from the fronto-parietal and default mode network were consistently most distinctive, i.e., informative of identity. The functional connectivity also allowed the prediction of individual cognitive performances. CONCLUSION: Our results demonstrate that discriminatory signatures in the functional connectome are stable over extended periods of time in multiple sclerosis, resulting in similar identification accuracies and distinctive long-lasting functional connectome fingerprinting signatures in patients and healthy individuals.
 BACKGROUND: The effects of socio-economic status on mortality in patients with multiple sclerosis is not well known. The objective was to examine mortality due to multiple sclerosis according to socio-economic status. METHODS: A retrospective observational cohort design was used with recruitment from 18 French multiple sclerosis expert centers participating in the Observatoire Français de la Sclérose en Plaques. All patients lived in metropolitan France and had a definite or probable diagnosis of multiple sclerosis according to either Poser or McDonald criteria with an onset of disease between 1960 and 2015. Initial phenotype was either relapsing-onset or primary progressive onset. Vital status was updated on January 1st 2016. Socio-economic status was measured by an ecological index, the European Deprivation Index and was attributed to each patient according to their home address. Excess death rates were studied according to socio-economic status using additive excess hazard models with multidimensional penalised splines. The initial hypothesis was a potential socio-economic gradient in excess mortality. FINDINGS: A total of 34,169 multiple sclerosis patients were included (88% relapsing onset (n = 30,083), 12% progressive onset (n = 4086)), female/male sex ratio 2.7 for relapsing-onset and 1.3 for progressive-onset). Mean age at disease onset was 31.6 (SD = 9.8) for relapsing-onset and 42.7 (SD = 10.8) for progressive-onset. At the end of follow-up, 1849 patients had died (4.4% for relapsing-onset (n = 1311) and 13.2% for progressive-onset (n = 538)). A socio-economic gradient was found for relapsing-onset patients; more deprived patients had a greater excess death rate. At thirty years of disease duration and a year of onset of symptoms of 1980, survival probability difference (or deprivation gap) between less deprived relapsing-onset patients (EDI = -6) and more deprived relapsing-onset patients (EDI = 12) was 16.6% (95% confidence interval (CI) [10.3%-22.9%]) for men and 12.3% (95%CI [7.6%-17.0%]) for women. No clear socio-economic mortality gradient was found in progressive-onset patients. INTERPRETATION: Socio-economic status was associated with mortality due to multiple sclerosis in relapsing-onset patients. Improvements in overall care of more socio-economically deprived patients with multiple sclerosis could help reduce these socio-economic inequalities in multiple sclerosis-related mortality. FUNDING: This study was funded by the ARSEP foundation "Fondation pour l'aide à la recherche sur la Sclérose en Plaques" (Grant Reference Number 1122). Data collection has been supported by a grant provided by the French State and handled by the "Agence Nationale de la Recherche," within the framework of the "Investments for the Future" programme, under the reference ANR-10-COHO-002, Observatoire Français de la Sclérose en Plaques (OFSEP).
 Those of African American or Latin American descent have been demonstrated to have more severe clinical presentations of multiple sclerosis (MS) than non-Latin American White people with MS. Concurrently, radiological burden of disease on magnetic resonance imaging (MRI) in African Americans with MS has also been described as being more aggressive. Here, we review MRI studies in diverse racial and ethnic groups (adult and pediatric) investigating lesion burden, inflammation, neurodegeneration, and imaging response to disease modifying therapy. We also discuss why such disparities may exist beyond biology, and how future studies may provide greater insights into underlying differences.
 BACKGROUND: Multiple sclerosis (MS) management varies markedly between different countries of the Middle East and North Africa (MENA) region based on the availability and accessibility of disease-modifying therapies (DMTs). OBJECTIVE: To evaluate the accessibility to DMTs in each MENA country, identify barriers to treatment and make recommendations for improved access to DMTs across the region. METHODS: This is a descriptive, survey-based study whereby we extracted data collected, between October 2019 and April 2020, for countries in the MENA region by the Multiple Sclerosis International Federation (MSIF) through their Atlas of MS survey. RESULTS: 16 out of 19 countries in the MENA region were included in this study. Sudan and Syria did not have any originator DMTs approved. Interferons were the most widely low-efficacy originator approved DMTs. Three countries did not have any high efficacy DMTs approved. Moreover, follow-on DMTs were approved in half (50%) of the countries. Cost of treatment was the most important barrier, reported in nearly half (47%) of the MENA countries. CONCLUSION: Although most MENA countries have access to DMTs, more than half of countries report problems with treatment continuation, highlighting the need for a targeted regional strategy to address the variations in access to MS treatments.
 BACKGROUND: The COVID-19 pandemic has underlined the need to evaluate cognitive profile via videoconferencing (teleneuropsychology, TeleNP) as a suitable alternative to face-to-face assessment (F-F). OBJECTIVE: To evaluate the feasibility and the reliability of Rao's Brief Repeatable Battery of Neuropsychological Tests (R-BRB) remote administration in people with multiple sclerosis (PwMS). METHODS: Sixty PwMS underwent R-BRB in two conditions: F-F and TeleNP, 1 month apart. RESULTS: Cognitive test performance was similar, regardless of the administration type, but visuospatial test performance was better in F-F. CONCLUSION: These data suggest that TeleNP is feasible and highly reliable in MS clinical practice.
 PURPOSE: The aim of the present study was to adapt and validate the Speech Pathology-Specific Questionnaire for Persons with Multiple Sclerosis (SMS) into the Greek language. METHOD: The study sample consisted of 124 people with multiple sclerosis (PwMS) and 50 healthy controls (HCs). All PwMS underwent cognitive assessment using the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS). Both PwMS and HCs completed the SMS, the Eating Assessment tool (EAT-10), the Voice Handicap Index (VHI), and the Stroke and Aphasia Quality of Life Scale-39 (SAQOL-39). RESULT: Significant difference was found between PwMS and HCs for the EAT-10, SAQOL-39, the total SMS, and the SMS subscales. Discriminant validity analyses revealed a statistically significant difference between PwMS and HCs for the total and subscales SMS. Convergent validity analyses between the total SMS and the SMS subscales, and scores on the BICAMS, EAT-10, SAQOL-39, and VHI in PwMS were significantly correlated, with exception of the SMS Speech/Voice with the Symbol Digit Modalities Test (SDMT) and the Greek Verbal Learning Test-II (GVLT-II). Scores on the EAT-10, SAQOL-39, and VHI in PwMS were also correlated with the total SMS and the SMS subscales in PwMS, HCs, and the total sample. Construct validity analyses revealed that the total SMS and the SMS subscales were significantly correlated with the Expanded Disability Status Scale (EDSS) and years of education, while no associations were found with regards to age, MS subtype (relapsing-remitting MS [RRMS] vs progressive MS [PMS]), disease duration, or sex. The internal consistency of all items was excellent in PwMS and the total sample (Cronbach's alpha was >0.7 after deletion of one item), with the exception of two items, which still fell within the acceptable range (>0.6) for PwMS and the total sample. CONCLUSION: The Greek version of the SMS is a reliable and valid patient-reported outcome measure to assess speech-language and swallowing pathology related symptoms in PwMS, and can be used for research and clinical purposes.
 A benign form of multiple sclerosis (BMS) is not easily diagnosed, but changes of the retinal ganglion cell layer-inner plexiform layer (GCL-IPL) and retinal nerve fiber layer (RNFL) may be sensitive to the disease. The aim of this study was to use optical coherence tomography (OCT) to investigate longitudinal changes of GCL-IPL and RNFL in BMS. Eighteen patients with BMS and 22 healthy control (HC) subjects were included, with a mean follow-up period of 32.1 months in BMS and 34.3 months in HC. Mean disease duration in BMS was 23.3 years, with 14 patients left untreated. Unilateral optic neuritis (ON) was found in eight patients. Non-ON eyes showed thinner GCL-IPL layer in the BMS group relative to HC (p < 0.001). The thinning rate of GCL-IPL in non-ON BMS, however, was -0.19 ± 0.15 µm/year vs. 0 ± 0.11 µm/year for HC (p = 0.573, age-adjusted). Thinning rate of RNFL in non-ON BMS was -0.2 ± 0.27 µm/year vs. -0.05 ± 0.3 µm/year for HC (p = 0.454, age adjusted). Conclusions: Thinning rate of the GCL-IPL and RNFL in BMS is similar to the healthy population but differs from the thinning rate in relapsing-remitting MS, presenting a non-invasive OCT-based criterion for assessing a benign course in multiple sclerosis.
 BACKGROUND: Multiple sclerosis (MS), one of the main neurological causes of disability seen at young ages, affects the quality of life of patients. Studies on which dietary pattern or consumption of food groups may have an impact on quality of life for MS patients are insufficient. The study was conducted to determine the relationship between adherence to Mediterranean diet and consumption levels of food groups on quality of life in multiple sclerosis patients. METHODS: This study was conducted with 95 patients, 76 females and 19 males, aged 18-65 years, who had been diagnosed with MS for at least 2 years and did not have any other chronic disease. Food Frequency Questionnaire, Mediterranean Diet Adherence Screener (MEDAS), Expanded Disability Status Scale (EDSS) and Multiple Sclerosis Quality of Life-54 Instrument (MS-QoL-54) used as tools. Data were analyzed by SPSS 25.0. RESULTS: Adherence to the Mediterranean diet was associated with EDSS and physical and mental quality of life parameters (CPH and CMH), independent of progression. It was associated with EDSS and CMH in progressive MS. A statistically significant negative weak correlation was found between daily milk and oilseed consumption and EDSS. Daily fruit consumption was associated with CMH, and vegetable consumption was associated with both CPH and CMH. CONCLUSIONS: The Mediterranean diet may be an effective nutritional model in MS patients and may be related to the disability level and quality of life of the patients. Some food groups can be associated with the quality of life and disability level of MS patients.
 Multiple sclerosis (MS) is a chronic, debilitating condition affecting many African people. However, the management of MS in Africa is often inadequate, and there is a need to improve the care and support provided to patients. This paper aims to identify the challenges and opportunities in navigating the journey of MS management in Africa. MS management's main challenges in Africa include a lack of awareness and education about the disease, limited access to diagnostic tools and treatments, and inadequate care coordination. However, by increasing awareness and education about MS, improving access to diagnostic tools and treatments, fostering multidisciplinary collaborations, encouraging and supporting research on MS in Africa, and collaborating with regional and international organizations to share knowledge and resources, it is possible to improve the management of the disease and improve the lives of those affected by MS in Africa. This paper concludes that improving the management of MS in Africa requires a concerted effort from all stakeholders, including healthcare professionals, policymakers, and international organizations. Collaboration and sharing of knowledge and resources are crucial to ensure that patients receive the best possible care and support.
 INTRODUCTION: To describe the parainfectious or postinfectious effects of COVID-19 infection on the first demyelinating presentation of Multiple Sclerosis and tumefactive demyelinating lesion (TDL) developing with Longitudinally Extensive Transverse Myelitis (LETM). METHODS: We present six patients who presented with a first CNS demyelination event or whose demyelinating lesions had aggravated after COVID-19 infection between May and December 2020. Nasopharyngeal swab SARS-CoV-2 PCR positivity was detected in five cases and cerebrospinal fluid (CSF) PCR was positive in one. The symptoms, neurological signs, radiological and CSF findings of the cases were examined. RESULTS: A 24-year-old woman presented with LETM aggravated by COVID-19, accompanied by a newly developed open-ring enhanced TDL. Four patients were diagnosed with the first presentation of MS, and one presented with clinically isolated syndrome according to the McDonald 2017 criteria. The interval between SARS-CoV-2 infection and the onset of clinical symptoms ranged from 4-93 days. All of the cases present with pyramidal or brain stem findings and have high brain and/or spinal MRI load. This suggests the moderate activity of CNS demyelinating disease after COVID-19 infection. CONCLUSIONS: Based on this case series, all these first demyelinating events suggested that COVID-19 infection might trigger or exacerbate CNS demyelinating disease. SARS-CoV-2 plays a role in the clinical onset of Multiple Sclerosis. Active delayed demyelination developed within the first three months. This can be explained by COVID-triggered neuroimmune response that had been latent, and the initiation of the active disease process began with triggering or aggravation of the lesions in MRI. Multiple Sclerosis should be maintained during the COVID-19 pandemic.
 BACKGROUND: Restless Legs Syndrome is a sleep-related sensorimotor disorder with a higher prevalence in Multiple Sclerosis (MS) patients than in the general population. Our aim was to determine the prevalence of RLS in a group of relapsing-remittent multiple sclerosis (RRMS) patients, and to investigate whether RLS is associated with MS-related disability, sleep quality, mood disorders and fatigue. METHODS: In this retrospective, mono-centric, observational study, 92 RRMS patients were recruited (median age 46.5 years, 68.5% female patients). Data on MS clinical and radiological variables were collected. Patients underwent a subjective evaluation with standardized questionnaires on sleep fatigue and mood, which were evaluated by an expert neurologists specialized in sleep disorders about the occurrence of RLS. RESULTS: Prevalence of RLS in our sample was of 47.8%. Patients with RLS had a significantly higher rate of worse sleep quality and fatigue, compared to non RLS subjects (respectively 56.8% vs. 35.4%, p=0.04 and 54.4% vs 22.7%, p=0.002). Univariate analysis showed that RLS was significantly more frequent in fatigued patients (66.7% vs 38.5% RLS- patients, p=0.009). Multivariate analysis showed that fatigue correlated with MS-related disability (OR 1.556, p=0.011), poor sleep quality (OR 1.192, p 0.036), and mood disorders (OR 1.096, p 0.046). RLS appears to independently increase the risk of fatigue of 50%, without reaching clear statistical significance (OR 1.572, p 0,0079). CONCLUSION: Our study confirms the high prevalence of RLS in patients with multiple sclerosis and highlights the potential impact of RLS on fatigue and its strict interaction with sleep quality.
 BACKGROUND: Black and Hispanic patients with multiple sclerosis (MS) have been shown to accumulate greater multiple sclerosis-associated disability (MSAD) than White patients. Disparities in social determinants of health (SDOH) among these groups have also been reported. OBJECTIVE: To determine the extent to which associations of race and ethnicity with MSAD may be attributable to differences in SDOH. METHODS: Retrospective chart analysis of patients at an academic MS center grouped by self-identified Black (n = 95), Hispanic (n = 93), and White (n = 98) race/ethnicity. Individual patient addresses were geocoded and matched with neighborhood-level area deprivation index (ADI) and social vulnerability index (SVI). RESULTS: Average Expanded Disability Status Scale (EDSS) scores at last-recorded evaluations of White patients (1.7 ± 2.0) were significantly lower than Black (2.8 ± 2.4, p = 0.001) and Hispanic (2.6 ± 2.6, p = 0.020) patients. Neither Black race nor Hispanic ethnicity was significantly associated with EDSS in multivariable linear regression models that included individual-level SDOH indicators and either ADI or SVI. CONCLUSION: Black race and Hispanic ethnicity are not significantly associated with EDSS in models that include individual and neighborhood-level SDOH indicators. Further research should elucidate mechanisms by which structural inequities affect MS disease course.
 A 54-year-old woman with multiple sclerosis treated with interferon-β (IFN-β)-1b for 15 years presented with sustained hypertension (240/124 mmHg) and retinal bleeding. She had proteinuria, anemia, thrombocytopenia, elevated serum creatinine levels, and haptoglobin depletion. Intravenous nicardipine stabilized her blood pressure, but her renal function and platelet count deteriorated. The initial disintegrin-like metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13) activity was 28% of normal without its inhibitor. The subsequent peripheral appearance of schistocytes suggested thrombotic microangiopathy (TMA). After IFN-β-1b cessation, the platelet count increased, and the blood pressure stabilized. The ADAMTS13 activity normalized, although the creatinine level did not. TMA may develop after the long-term use of IFN-β without adverse events.
 OBJECTIVE: Our aim was to determine whether serum C-X-C motif chemokine 5 (CXCL5) may serve as a diagnostic biomarker for relapsing-remitting multiple sclerosis (RRMS) as well as a marker that can be used to predict treatment response. METHODS: CXCL5 levels were measured by ELISA in sera of 20 RRMS patients under fingolimod treatment, 10 neuromyelitis optica spectrum disorder (NMOSD) patients, 15 RRMS patients presenting predominantly with spinal cord and optic nerve attacks (MS-SCON), and 14 healthy controls. RESULTS: Fingolimod treatment significantly reduced CXCL5 levels. CXCL5 levels were comparable among NMOSD and MS-SCON patients. CONCLUSION: Fingolimod might regulate the innate immune system. Serum CXCL5 measurement does not differentiate between RRMS and NMOSD.
 The immense neuroinflammation induced by multiple sclerosis (MS) promotes a favorable environment for ischemic stroke (IS) development, making IS a deadly complication of MS. The overlapping inflammation in MS and IS is a prelude to the vascular pathology, and an inherent cell death mechanism that exacerbates neurovascular unit (NVU) impairment in the disease progression. Despite this consequence, no therapies focus on reducing IS incidence in patients with MS. To this end, the preclinical and clinical evidence we review here argues for cell-based regenerative medicine that will augment the NVU dysfunction and inflammation to ameliorate IS risk.
 Multiple sclerosis (MS) is the most frequent neurological disease in young adults, with the greatest incidence between age of 30 and 35 years. Sexual dysfunctions (SDs) are frequent, but are often underestimated in patients with MS, and can have a significantly high impact on patient's quality of life. Aim of this review is to summarize sexual dysfunctions in male and female MS patients and to illustrate current and emerging therapeutic options for treatment.
 Magnetic resonance imaging (MRI) of the brain is commonly used to detect where chronic and active lesions are in multiple sclerosis (MS). MRI is also extensively used as a tool to calculate and extrapolate brain health by way of volumetric analysis or advanced imaging techniques. In MS patients, psychiatric symptoms are common comorbidities, with depression being the main one. Even though these symptoms are a major determinant of quality of life in MS, they are often overlooked and undertreated. There has been evidence of bidirectional interactions between the course of MS and comorbid psychiatric symptoms. In order to mitigate disability progression in MS, treating psychiatric comorbidities should be investigated and optimized. New research for the prediction of disease states or phenotypes of disability have advanced, primarily due to new technologies and a better understanding of the aging brain.
 Health literacy has been identified as key to improving patient outcomes and is particularly important for patients facing chronic illnesses such as multiple sclerosis (MS). Low health literacy rates can negatively impact communication between healthcare providers and patients and is associated with poor health outcomes. It is critical to raise awareness of conversational techniques to healthcare providers that can support more effective communication with patients. In this podcast article, nurse practitioners discuss multimodal strategies that enable appropriate conversations to meet patients' needs through the following four techniques: patient-centric language, teach-back, open-ended questions, and active listening and paraphrasing. These techniques are incorporated into example patient-provider conversations to demonstrate their effectiveness in clinical practice. Comprehensive patient conversations and optimizing patient interactions builds a trustworthy foundation for shared decision-making to improve health literacy and outcomes in patients with MS. Podcast Discussion (mp4 37425 KB).
 BACKGROUND: Although the relationships among physical disability, mood disorders, and pain are well described in multiple sclerosis (MS), little is known about whether those symptoms are associated with sleep disturbances. METHODS: Forty-six patients with MS experiencing pain participated. Sleep was indirectly measured by assessing rest-activity rhythm via actigraphy: interdaily stability, intradaily variability, and relative amplitude. Pain was assessed using visual and verbal analog scales, mood by the Beck Depression Inventory and Symptom Checklist-90, and physical disability by the Expanded Disability Status Scale. RESULTS: Incorporating mood, pain, and physical disability into 1 regression model resulted in a significant association with interdaily stability. CONCLUSIONS: Compared with intradaily variability and relative amplitude, interdaily stability seems to be the most vulnerable actigraphy variable for mood disturbances, pain, and physical disabilities.
 OBJECTIVES: This study assessed the prevalence of restless leg syndrome (RLS) among patients with multiple sclerosis (pwMS) and the association between RLS and MS disease duration, sleep disturbance, and daytime fatigue. METHODS: In this cross-sectional study, we interviewed 123 patients via phone calls using preset questionnaires containing the International Restless Legs Syndrome Study Group (IRLSSG) diagnostic criteria, Pittsburgh Sleep Quality Index (PSQI), and Fatigue Severity Scale (FSS) diagnostic criteria validated in both Arabic and English. The prevalence of RLS in MS was compared to a group of healthy controls. RESULTS: The prevalence of RLS in pwMS, defined by meeting all four requirements included in the IRLSSG diagnostic criteria, was 30.3% compared to 8.3% in the control group. About 27.3% had mild RLS, 36.4% presented with moderate, and the remaining had severe or very severe symptoms. Patients with MS who experience RLS had a 2.8 times higher risk of fatigue compared to pwMS without RLS. pwMS with RLS had worse sleep quality, with a mean difference of 0.64 in the global PSQI score. Sleep disturbance and latency had the most significant impact on sleep quality. CONCLUSION: The prevalence of RLS among MS patients was significantly higher compared to the control group. We recommend educating neurologists and general physicians to increase their awareness of the increasing prevalence of RLS and its association with fatigue and sleep disturbance in patients with MS.
 There is a growing need to better understand the risk of malignancy in the multiple sclerosis (MS) population, particularly given the relatively recent and widespread introduction of immunomodulating disease modifying therapies (DMTs). Multiple sclerosis disproportionately affects women, and the risk of gynecological malignancies, specifically cervical pre-cancer and cancer, are of particular concern. The causal relationship between persistent human papillomavirus (HPV) infection and cervical cancer has been definitively established. To date, there is limited data on the effect of MS DMTs on the risk of persistent HPV infection and subsequent progression to cervical pre-cancer and cancer. This review evaluates the risk of cervical pre-cancer and cancer in women with MS, including the risk conferred by DMTs. We examine additional factors, specific to the MS population, that alter the risk of developing cervical cancer including participation in HPV vaccination and cervical screening programs.
 BACKGROUND: Multiple sclerosis (MS) is recognized as the most prevalent autoimmune abnormality of the CNS. T1WI, T2WI, and FLAIR are limited in the quantification of tissue damage and detection of tissue alterations in white and grey matter in MS. This study aimed to the evaluation of changes in DTI indices in these patients at the thalamus and basal ganglia. METHODS: 30 relapsing-remitting MS (RRMS) cases and 30 normal individuals were included. Conventional MRI (T2, FLAIR) was acquired to confirm NAGM in MS patients. A T1 MPRAGE protocol was used to normalize DTI images. FSL, SPM, and Explore DTI software were employed to reach Mean Diffusivities (MD), Axial Diffusivities (AD), Fractional anisotropy (FA), and Radial Diffusivity (RD) at the thalamus and the basal ganglia. RESULTS: The FA and RD of the thalamus were decreased in healthy controls compared to MS cases (0.319 vs. 0.296 and 0.0009 vs. 0.0006, respectively) (P < 0.05). The AD value in the thalamus and the FA value in the caudate nucleus were significantly lower in MS cases than in controls (0.0009 vs. 0.0011 and 0.16 vs. 0.18, respectively) (P < 0.05). MD values in the thalamus or basal ganglia were not significantly different between groups. CONCLUSIONS: DTI measures including FA, RD, and AD have a good diagnostic performance in detecting microstructural changes in the normal-appearing thalamus in cases with RRMS while they had no significant relationship with clinical signs in terms of EDSS. AVAILABILITY OF DATA AND MATERIAL: Not applicable.
 Ocrelizumab is a recombinant humanized monoclonal antibody selectively targeting CD20-expressing B cells. The effect of ocrelizumab on primary progressive multiple sclerosis (PPMS) has been evaluated during phase 3 trials that enrolled patients under 55 years with a maximum Expanded Disability Status Scale (EDSS) of 6.5. However, little is known on older disabled patients with longer disease duration. We aimed to assess the clinical effectiveness of ocrelizumab in PPMS patients out of the ORATORIO eligibility criteria. This multicenter retrospective study collected data about the effectiveness of ocrelizumab in PPMS patients who received treatment between May 2017 and June 2022 in the Italian MS centers contributing to the Italian MS Registry who adhered to the Compassionate Use Program. The confirmed EDSS worsening (CEW) (defined as either a ≥ 1-point or ≥ 2-point increase in EDSS score from baseline that was confirmed at T12 and T24) was calculated. At the date of data extraction, out of 887 PPMS patients who had received ocrelizumab, 589 (mean age 49.7 ± 10.7 years, 242 (41.1%) females) were enrolled. The mean follow-up period was 41.3 ± 12.3 months. A total of 149 (25.3%) received ocrelizumab according to the ORATORIO criteria (ORATORIO group) and 440 (74.7%) outside the ORATORIO criteria (non-ORATORIO group). No differences in terms of cumulative probabilities of 12 and 24 months of CEW of ≤ 1 point were found between ORATORIO and non-ORATORIO groups. Cox regression analyses showed that age older than 65 years (HR 2.51, 25% CI 1.07-3.65; p = 0.01) was associated with higher risk of CEW at 24 months. Patients not responding to ORATORIO criteria for reimbursability may benefit from ocrelizumab treatment, as disease activity, disease duration, and EDSS seem to not impact the disability outcome. Our results may suggest to extend the possible use of this powerful agent in selected patients under the age of 65 years.
 Emergence of a definitive link between Epstein-Barr virus (EBV) and multiple sclerosis has provided an impetus to develop immune-based therapies to target EBV-infected B cells. Initial studies with autologous EBV-specific T-cell therapy demonstrated that this therapy is safe with minimal side effects and more importantly multiple patients showed both symptomatic and objective neurological improvements including improved quality of life, reduction of fatigue and reduced intrathecal IgG production. These observations have been successfully extended to an 'off-the-shelf' allogeneic EBV-specific T-cell therapy manufactured using peripheral blood lymphocytes of healthy seropositive individuals. This adoptive immunotherapy has also been shown to be safe with encouraging clinical responses. Allogeneic EBV T-cell therapy overcomes some of the limitations of autologous therapy and can be rapidly delivered to patients with improved therapeutic potential.
 OBJECTIVE: The study aimed to investigate the effect of exercise on immune cell count and cell mechanical properties in people with multiple sclerosis (pwMS) on different disease-modifying treatments (DMT) vs. healthy controls (HCs). METHODS: A cohort of 16 HCs and 45 pwMS, including patients with lymphopenia (alemtuzumab and fingolimod) as well as increased lymphocyte counts (natalizumab), was evaluated for exercise-mediated effects on immune cell counts and lymphocyte deformability. As exercise paradigms, climbing stairs at normal speed or as fast as possible and cycling were used, while blood samples were collected before, immediately, and 20 as well as 60 min post-exercise. Immune cell subtypes and lymphocyte deformability were analyzed using multicolor flow cytometry and real-time deformability cytometry. RESULTS: An increase in lymphocytes and selected subsets was observed following exercise in HCs and all pwMS on different DMTs. Patients with lymphopenia exhibited an increase in absolute lymphocyte counts and immune cell subsets till just below or into the reference range. An increase above the upper limit of the reference range was detected in patients on natalizumab. Exercise-induced alterations were observable even in low and more pronounced in high-intensity physical activities. Lymphocyte deformability was found to be only mildly affected by the investigated exercise regimes. CONCLUSION: People with multiple sclerosis (PwMS) treated with alemtuzumab, fingolimod, and natalizumab respond to acute exercise with a comparable temporal pattern characterized by the increase of immune cell subsets as HCs. The magnitude of response is influenced by exercise intensity. Exercise-mediated effects should be considered when interpreting laboratory values in patients on immunomodulatory therapy. The impact of exercise on biophysical properties should be further elucidated.
 Multiple sclerosis (MS) is a neurological chronic disease with autoimmune demyelinating lesions and one of the most common disability causes in young adults. People with MS (PwMS) experience cognitive impairments (CIs) and clinical evidence shows their presence during all MS stages even in the absence of other symptoms. Cognitive rehabilitation (CR) aims at reducing CI and improving PwMS' awareness of cognitive difficulties faced in their daily living. More defined cognitive profiles, easier treatment access and the need to transfer intervention effects into everyday life activities are aims of utmost relevance for CR in MS. Currently, advanced technologies may pave the way to rethink CR in MS to address the priority of more personalized and effective, accessible and ecological interventions. For this purpose, digital twins, tele-cognitive-rehabilitation and metaverse are the main candidate digital ingredients. Based on scientific evidences, we propose digital twin technology to enhance MS cognitive phenotyping; tele-cognitive-rehabilitation to make feasible the cognitive intervention access to a larger number of PwMS; and metaverse to represent the best choice to train real-world dual- and multi-tasking deficits in virtual daily life environments. Moreover, multi-domain high-frequency big-data collected through tele-cognitive-assessment, tele-cognitive-rehabilitation, and metaverse may be merged to refine artificial intelligence algorithms and obtain increasingly detailed patient's cognitive profile in order to enhance intervention personalization. Here, we present how these digital ingredients and their integration could be crucial to address the current and future needs of CR facilitating the early detection of subtle CI and the delivery of increasingly effective treatments.
 BACKGROUND: Neuromyelitis Optica Spectrum Disorder (NMOSD) is an inflammatory disease of the central nervous system. The study aimed to characterize the neuropsychological profile of NMOSD by comparing them with multiple sclerosis (MS) patients and healthy controls. METHOD: Sixty-four participants were included:19 NMOSD, 27 MS, and 18 healthy controls. The neuropsychological protocol included the Portuguese version of Montreal Cognitive Assessment, the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS), Verbal Fluency (phonemic and semantic), the Hospital Anxiety and Depression Scale, and the Expanded Disability Status Scale for clinical groups. RESULTS: NMOSD patients had significant lower cognitive performance when compared to HC mainly in information processing speed, concentration, language processing, and in executive functions (cognitive flexibility, sustained, and divided attention). No significant differences were observed between NMOSD and MS patients. Three predictors for cognitive impairment, according to BICAMS criteria, were found: depression, disease duration, and the level of disability. CONCLUSION: The neuropsychological profile found in the present study for NMOSD is consistent with the previous findings. Information regarding the predictors of cognitive impairment in both diseases and their different associations are important for future research and for guiding interventions more suitable for the neuropsychological needs of affected patients.
 Glatiramer is an immunomodulator used in the treatment and management of multiple sclerosis. Its mechanism is not clearly understood, but it appears to work by altering the immune processes responsible for MS. This activity reviews the indications, contraindications, mechanism of action, adverse events, and other key elements of glatiramer therapy and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes for patients with multiple sclerosis.
 In the early stages of multiple sclerosis (MS), there are currently no sensitive assessments to evaluate complex motor functions. The countermovement jump (CMJ), a high-challenge task in form of a maximal vertical bipedal jump, has already been investigated as a reliable assessment in healthy subjects for lower extremity motor function. The aim was to investigate whether it is possible to use CMJ to identify subthreshold motor deficits in people with multiple sclerosis (pwMS). All participants (99 pwMS and 33 healthy controls) performed three maximal CMJs on a force plate. PwMS with full motor function and healthy controls (HC) did not differ significantly in age, disease duration, Body Mass Index and the Expanded Disability Scale Score. In comparison to HC, pwMS with full motor function demonstrated a significantly decreased CMJ performance in almost all observed kinetic, temporal and performance parameters (p < 0.05). With increasing disability in pwMS, it was also observed that jump performance decreased significantly. This study showed that the CMJ, as a high challenge task, could detect motor deficits in pwMS below the clinical threshold of careful neurological examination. Longitudinal studies are pending to evaluate whether the CMJ can be used as a standardized measure of disease progression.
 Multiple sclerosis is a degenerative inflammatory disease that causes different musculoskeletal problems. Its impact has led to the study of treatment alternatives such as the use of invasive physiotherapy. In this study, we analyze the effects of ultrasound-guided percutaneous neuromodulation to a 51-year-old man suffering from multiple sclerosis and an associated hemiparesis in the left upper limb. A dry needling needle was placed in contact with the median nerve under ultrasound guidance and 10 trains of 10 seconds of electrostimulation with a frequency of 10 Hz and an impulse width of 240 µs were applied, with 10 seconds of pause between them. There was a significant improvement in the grip strength immediately after the treatment which increased progressively at 24 hours and at 4 days follow-up. There was also an improvement in the hand function, with a decrease in the time necessary to perform the 9 Hole Peg Test immediately after the treatment, which was maintained at 24 hours and at 4 days follow-up. Future studies with larger samples are needed to further test the effects of this invasive physiotherapy technique as well as its possible applications to other neurological conditions.
 Balance impairment is frequent in people with multiple sclerosis (pwMS) and affects risk of falls and quality of life. By using inertial measurement units (IMUs) on the Single Leg Stance Test (SLS) we aimed to discriminate healthy controls (HC) from pwMS and detect differences in balance endurance and quality. Thirdly, we wanted to test the correlation between instrumented SLS parameters and self-reported measures of gait and balance. Fifty-five pwMS with mild (EDSS<4) and moderate disability (EDSS≥4) and 20 HC performed the SLS with 3 IMUs placed on the feet and sacrum and filled the Twelve Item Multiple Sclerosis Walking Scale (MSWS-12) questionnaire. A linear mixed model was used to compare differences in the automated balance measures. Balance duration was significantly longer in HC compared to pwMS (p < 0.001) and between the two disability groups (p < 0.001). Instrumented measures identified that trunk stability (normalized mediolateral and antero-posterior center of mass stability) had the strongest association with disability (R(2) marginal 0.30, p < 0.001) and correlated well with MSWS-12 (R = 0.650, p < 0.001). PwMS tended to overestimate own balance compared to measured balance duration. The use of both self-reported and objective assessments from IMUs can secure the follow-up of balance in pwMS.
 Multiple sclerosis (MS) is a neuroinflammatory disease with limited therapeutic effects, eventually developing into handicap. Seeking novel therapeutic strategies for MS is timely important. Active autophagy/mitophagy could mediate neurodegeneration, while its roles in MS remain controversial. To elucidate the exact roles of autophagy/mitophagy and reveal its in-depth regulatory mechanisms, we conduct a systematic literature study and analyze the factors that might be responsible for divergent results obtained. The dynamic change levels of autophagy/mitophagy appear to be a determining factor for final neuron fate during MS pathology. Excessive neuronal autophagy/mitophagy contributes to neurodegeneration after disease onset at the active MS phase. Reactive nitrogen species (RNS) serve as key regulators for redox-related modifications and participate in autophagy/mitophagy modulation in MS. Nitric oxide ((•)NO) and peroxynitrite (ONOO(-)), two representative RNS, could nitrate or nitrosate Drp1/parkin/PINK1 pathway, activating excessive mitophagy and aggravating neuronal injury. Targeting RNS-mediated excessive autophagy/mitophagy could be a promising strategy for developing novel anti-MS drugs. In this review, we highlight the important roles of RNS-mediated autophagy/mitophagy in neuronal injury and review the potential therapeutic compounds with the bioactivities of inhibiting RNS-mediated autophagy/mitophagy activation and attenuating MS progression. Overall, we conclude that reactive nitrogen species could be promising therapeutic targets to regulate autophagy/mitophagy for multiple sclerosis treatment.
 Multiple sclerosis (MS) is one of the most common inflammatory neurological diseases which leads to a highly heterogeneous set of symptoms and signs due to the differential involvement of the motor, sensory, visual, and autonomic systems [...].
 INTRODUCTION: Rituximab (RTX) is considered a potential therapeutic option for relapsing-remitting (RRMS) and progressive forms (PMS) of multiple sclerosis (MS). The main objective of this work was to investigate the effectiveness and safety of rituximab in MS. PATIENTS AND METHODS: Observational multicenter study of clinical and radiological effectiveness and safety of rituximab in RRMS and PMS. RESULTS: A total of 479 rituximab-treated patients were included in 12 Spanish centers, 188 RRMS (39.3%) and 291 (60.7%) PMS. Despite standard treatment, the annualized relapse rate (ARR) the year before RTX was 0.63 (SD: 0.8) and 156 patients (41%) had at least one gadolinium-enhanced lesion (GEL) on baseline MRI. Mean EDSS had increased from 4.3 (SD: 1.9) to 4.8 (SD: 1.7) and almost half of the patients (41%) had worsened at least one point. After a median follow-up of 14.2 months (IQR: 6.5-27.2), ARR decreased by 85.7% (p < 0.001) and GEL by 82.9%, from 0.41 to 0.07 (p < 0.001). A significant decrease in EDSS to 4.7 (p = 0.046) was observed after 1 year of treatment and this variable remained stable during the second year of therapy. There was no evidence of disease activity in 68% of patients. Infusion-related symptoms were the most frequent side effect (19.6%) and most were mild. Relevant infections were reported only in 18 patients (including one case of probable progressive multifocal leukoencephalopathy). CONCLUSION: Rituximab could be an effective and safe treatment in RRMS, including aggressive forms of the disease. Some selected PMS patients could also benefit from this treatment.
 Multiple sclerosis is characterised by the chronic inflammatory destruction of myelinated axons in the central nervous system. Several ideas have been put foward to clarify the roles of the peripheral immune system and neurodegenerative events in such destruction. Yet, none of the resulting models appears to be consistent with all the experimental evidence. They also do not answer the question why MS is exclusively seen in humans, how Epstein-Barr virus contributes to its development but does not immediately trigger it, and why optic neuritis is such a frequent early manifestation in MS. Here we describe a scenario for the development of MS that unifies existing experimental evidence as well as answer the above questions. We propose that all manifestions of MS are caused by a series of unfortunate events that usually unfold over a longer period of time after a primary EBV infection and involves periodic weakening of the blood-brain barrier, antibody-mediated CNS disturbances, accumulation of the oligodendrocyte stress protein αB-crystallin and self-sustaining inflammatory damage.
 Multiple sclerosis (MS) is a neuroinflammatory disorder damaging structural connectivity. Natural remodeling processes of the nervous system can, to some extent, restore the damage caused. However, there is a lack of biomarkers to evaluate remodeling in MS. Our objective is to evaluate graph theory metrics (especially modularity) as a biomarker of remodeling and cognition in MS. We recruited 60 relapsing-remitting MS and 26 healthy controls. Structural and diffusion MRI, plus cognitive and disability evaluations, were done. We calculated modularity and global efficiency from the tractography-derived connectivity matrices. Association of graph metrics with T2 lesion load, cognition, and disability was evaluated using general linear models adjusting for age, gender, and disease duration wherever applicable. We showed that MS subjects had higher modularity and lower global efficiency compared with controls. In the MS group, modularity was inversely associated with cognitive performance but positively associated with T2 lesion load. Our results indicate that modularity increase is due to the disruption of intermodular connections in MS because of the lesions, with no improvement or preserving of cognitive functions.
 Multiple sclerosis (MS) is a chronic, immune-mediated, neurodegenerative condition of the central nervous system, with distinct challenges due to its heterogeneous presentation, prognostic uncertainty, and variable clinical course of neurological and non-neurological symptoms and disability. Although there have been significant advances in management of MS, many patients experience disability progression. Despite MS being a frequent cause of neurological disability, particularly in young persons, involvement of palliative care physicians in the care of patients with MS has been limited. This article provides ten tips for palliative clinicians for caring for patients with MS and their care partners.
 PURPOSE: To explore the lived experience of physical exertion for persons living with advanced multiple sclerosis (MS). METHOD: An interpretive (hermeneutic) phenomenological approach was undertaken with 8 persons living with advanced MS. Interviews were conducted with exploratory questions that explored participants' experiences of physical exertion. Data was analysed using phenomenological methods and the findings presented as hermeneutic stories. RESULTS: Participants conveyed physical exertion as a means of influencing their connection with the world. Interpretation identified four subthemes; Lived Body, Sense of Self, Purpose of exertion, and Attributes of the World and an overarching superordinate theme Body-World engagement. Hermeneutic stories illuminated the intertwined relationship between the themes and the idiographic nature of physical exertion. CONCLUSION: The experience of physical exertion was meaningfully related to participants' sense of self, agency, and 'being in the world'.
 Sleepiness is a frequent and underrecognized symptom in neurological disorders, that impacts functional outcomes and quality of life. Multiple and potentially additive factors might contribute to sleepiness in neurological disorders, including sleep quality alterations, circadian rhythm disorders, drugs, and sleep disorders including sleep apnea or central disorders of hypersomnolence. Physician awareness of the possible symptoms of hypersomnolence, and associated causes is of crucial importance to allow proper identification and treatment of underlying causes. This review first provides a brief overview on clinical aspects of excessive daytime sleepiness, and diagnosis tools, then examines its frequency and mechanisms in various neurological disorders, including neurodegenerative disorders, multiple sclerosis, autoimmune encephalitis, epilepsy, and stroke.
 INTRODUCTION: Multiple sclerosis (MS) is an autoimmune disease affecting the central nervous system. Monoclonal antibodies (mAbs) have shown efficacy in reducing MS relapse rates, disease progression, and brain lesion activity. AREAS COVERED: This article reviews the literature on the use of mAbs for the treatment of MS, including their mechanisms of action, clinical trial data, safety profiles, and long-term outcomes. The review focuses on the three main categories of mAbs used in MS: alemtuzumab, natalizumab, and anti-CD20 drugs. A literature search was conducted using relevant keywords and guidelines and reports from regulatory agencies were reviewed. The search covered studies published from inception to 31 December 2022. The article also discusses the potential risks and benefits of these therapies, including their effects on infection rates, malignancies, and vaccination efficacy. EXPERT OPINION: Monoclonal antibodies have revolutionized the treatment of MS, but safety concerns must be considered, particularly with regards to infection rates, malignancy risk, and vaccination efficacy. Clinicians must weigh the potential benefits and risks of mAbs on an individual patient basis, taking into account factors such as age, disease severity, and comorbidities. Ongoing monitoring and surveillance are essential to ensure the long-term safety and effectiveness of monoclonal antibody therapies in MS.
 There are several case reports describing a temporal correlation between the first clinical manifestation of multiple sclerosis (MS) and the occurrence of relapses with vaccination against SARS-CoV-2. Here we report a case of a 33-year-old male who developed partial right upper and lower extremities numbness 2 weeks after receiving Johnson & Johnson's Janssen COVID-19 vaccine. The brain MRI performed during diagnostics in the Department of Neurology detected several demyelinating lesions, one with enhancement. Oligoclonal bands were present in the cerebrospinal fluid. The patient was treated with high-dose glucocorticoid therapy with improvement and the diagnosis of MS was made. It seems plausible that the vaccination revealed the underlying autoimmune condition. Cases like the one we reported here are rare, and-based on current knowledge-the benefits of vaccination against SARS-CoV-2 far outweigh the potential risks.
 Teriflunomide is an oral disease-modifying therapy for relapsing-remitting multiple sclerosis patients. A decline in physical and cognitive functions, which negatively impacts their quality of life (QoL), is observed in relapsing-remitting multiple sclerosis patients. The aim of this study was to characterise adult Portuguese relapsing-remitting multiple sclerosis patients treated with teriflunomide in routine clinical practice concerning their quality of life, comorbidities, treatment effectiveness, satisfaction, compliance and safety. TeriLIVE-QoL was a multicentre, non-interventional, prospective cohort study that collected demographic and clinical characteristics, patient-reported outcomes and adverse events from patients treated with teriflunomide of 14 mg over 2 years. Notably, around 18 months of this period occurred during the COVID-19 pandemic. Of the 99 participants, 25% were treatment-naïve. Annualised relapse rate and the score for the Hospital Anxiety and Depression Scale decreased after 1 (p = 0.01) and 2 years of treatment (p < 0.001), respectively. Convenience (p = 0.001), effectiveness (p = 0.002) and global satisfaction scores (p < 0.001) presented high values (up to 95.6) and continued to improve along the study. Treatment persistence was 77%, and compliance reached 82% 2 years after initiation. Three patients experienced serious adverse events. TeriLIVE-QoL provides real-world evidence of clinical effectiveness, high treatment satisfaction, consistent safety and improved psychiatric outcomes, associated with elevated treatment persistence and compliance in patients treated with teriflunomide.iance reached 82% 2 years after initiation. Three patients experienced serious adverse events.
 BACKGROUND: Impaired manual dexterity is frequent and disabling in patients with multiple sclerosis (MS), affecting activities of daily living and quality of life. OBJECTIVE: To develop a new immersive virtual-reality (VR) headset-based dexterity training to improve impaired manual dexterity in persons with MS (pwMS) while being feasible and usable in a home-based setting. METHODS: The training intervention was tailored to the specific group of pwMS by implementing a simple and intuitive application with regard to hardware and software. To be efficacious, the training intervention covers the main functions of the hands and arm relevant for use in everyday life. RESULTS: Taking clinical, feasibility, usability as well as technical aspects with regard to hardware and software into account, six different training exercises using hand tracking technology were developed on the Meta quest 2 using Unity. CONCLUSION: We report the developmental process of a new immersive virtual VR headset-based dexterity training for pwMS implementing clinical and technical aspects. Good feasibility, usability, and patient satisfaction was already shown in a feasibility study qualifying this training intervention for further efficacy trials.
 Multiple sclerosis (MS) can progress with neurodegeneration as a consequence of chronic inflammatory mechanisms that drive neural cell loss and/or neuroaxonal dystrophy in the central nervous system. Immune-mediated mechanisms can accumulate myelin debris in the disease extracellular milieu during chronic-active demyelination that can limit neurorepair/plasticity and experimental evidence suggests that potentiated removal of myelin debris can promote neurorepair in models of MS. The myelin-associated inhibitory factors (MAIFs) are integral contributors to neurodegenerative processes in models of trauma and experimental MS-like disease that can be targeted to promote neurorepair. This review highlights the molecular and cellular mechanisms that drive neurodegeneration as a consequence of chronic-active inflammation and outlines plausible therapeutic approaches to antagonize the MAIFs during the evolution of neuroinflammatory lesions. Moreover, investigative lines for translation of targeted therapies against these myelin inhibitors are defined with an emphasis on the chief MAIF, Nogo-A, that may demonstrate clinical efficacy of neurorepair during progressive MS.
 In recent years, epidemiological and genetic studies have shown an association between autoimmune diseases and psychosis. The question arises whether patients with schizophrenia are more likely to develop multiple sclerosis (MS) later in life. It is well known that the immune system plays an important role in the etiopathogenesis of both disorders. Immune disturbances may be similar or very different in terms of different types of immune responses, disturbed myelination, and/or immunogenetic predispositions. A psychotic symptom may be a consequence of the MS diagnosis itself or a separate entity. In this review article, we discussed the timing of onset of psychotic symptoms and MS and whether the use of corticosteroids as therapy for acute relapses in MS is unfairly neglected in patients with psychiatric comorbidities. In addition, we discussed that the anti-inflammatory potential of antipsychotics could be useful and should be considered, especially in the treatment of psychosis that coexists with MS. Autoimmune disorders could precipitate psychotic symptoms, and in this context, autoimmune psychosis must be considered as a persistent symptomatology that requires continuous and specific treatment.
 The fluid compartment surrounding the central nervous system (CNS) is a unique source of immune cells capable of reflecting the pathophysiology of neurologic diseases. While human clinical and experimental studies often employ cerebrospinal fluid (CSF) analysis, assessment of CSF in animal models of disease are wholly uncommon, particularly in examining the cellular component. Barriers to routine assessment of CSF in animal models of multiple sclerosis (MS) include limited sample volume, blood contamination, and lack of feasible longitudinal approaches. The few studies characterizing CSF immune cells in animal models of MS are largely outdated, but recent work employing transcriptomics have been used to explore new concepts in CNS inflammation and MS. Absence of extensive CSF data from rodent and other systems has curbed the overall impact of experimental models of MS. Future approaches, including examination of CSF myeloid subsets, single cell transcriptomics incorporating antigen receptor sequencing, and use of diverse animal models, may serve to overcome current limitations and provide critical insights into the pathogenesis of, and therapeutic developments for, MS.
 Multiplex arrays designed for enzyme-linked immunosorbent assays (ELISAs) are robust and cost-effective for profiling biomarkers. Identification of relevant biomarkers in biological matrices or fluids helps in the understanding of disease pathogenesis. Here, we describe a sandwich ELISA-based multiplex assay to assess growth factor and cytokine levels in cerebrospinal fluid (CSF) samples derived from multiple sclerosis patients, amyotrophic lateral sclerosis patients, and control subjects without any neurological disorder. Results indicate that multiplex assay designed for the sandwich ELISA method is a unique, robust, and cost-effective method for profiling growth factors and cytokines present in CSF samples.
 Multiple sclerosis (MS) is a chronic demyelinating and neurodegenerative disease that affects the central nervous system. MS is a heterogeneous disorder of multiple factors that are mainly associated with the immune system including the breakdown of the blood-brain and spinal cord barriers induced by T cells, B cells, antigen presenting cells, and immune components such as chemokines and pro-inflammatory cytokines. The incidence of MS has been increasing worldwide recently, and most therapies related to its treatment are associated with the development of several secondary effects, such as headaches, hepatotoxicity, leukopenia, and some types of cancer; therefore, the search for an effective treatment is ongoing. The use of animal models of MS continues to be an important option for extrapolating new treatments. Experimental autoimmune encephalomyelitis (EAE) replicates the several pathophysiological features of MS development and clinical signs, to obtain a potential treatment for MS in humans and improve the disease prognosis. Currently, the exploration of neuro-immune-endocrine interactions represents a highlight of interest in the treatment of immune disorders. The arginine vasopressin hormone (AVP) is involved in the increase in blood-brain barrier permeability, inducing the development and aggressiveness of the disease in the EAE model, whereas its deficiency improves the clinical signs of the disease. Therefore, this present review discussed on the use of conivaptan a blocker of AVP receptors type 1a and type 2 (V1a and V2 AVP) in the modulation of immune response without completely depleting its activity, minimizing the adverse effects associated with the conventional therapies becoming a potential therapeutic target in the treatment of patients with multiple sclerosis.
 BACKGROUND: Cognitive dysfunctions are often presented as a symptom in multiple sclerosis which is associated with both structural and functional imapirments of neuronal networks in the brain. OBJECTIVE: The aim of the study was to evaluate the influence of dysability, duration and type of disesase on cognitive functions in multiple sclerosis patients. METHODS: This study included 60 MS patients treated at the Department of Neurology, Clinical Center University of Sarajevo. Inclusion criteria were clinically definite diagnosis of multiple sclerosis, 18 years of age or older and were able to give written informed consent. Cognitive function was evaluated by the Montreal Cognitive Assessment (MoCa) screening test. Mann-Whitney and Kruskal-Wallis test were used for comparisons between clinical characteristics and MoCa test scores. RESULTS: Out of 63.33% of patients had EDSS <=4.5. Disease lasted longer than 10 years in 30% of patients. 80% had relapsing-remitting MS and 20% had secondary progressive MS. 84,2 % of patients with EDSS ≤ 4.5 had cognitive dysfunction. Higher disability (rho=0,306, p<0,05), progressive type of disease (rho=0,377, p< 0,01) and longer disease duration (rho=0,282, p<0,05) were associated with worse overall cognitive functions. Level of disability showed statistical significant correlation with the executive functions and language domains of cognition (p<0.01). Longer disease duration was significant correlated with executive functions (p<0,01) and language domains (p<0,01), while progressive type of disease was signifacant correlated only with executive functions domain (p<0,01). MoCa score variables did not show a statistically significant difference in relation to the number of relapses per year and the use of imunoterapy. Statistically significant negative correlation was obtained between executive functions domain and level of disability, disease duration and progressive type of disease, while language domain significantly correlated only with disability level and progressive type of disease. CONCLUSION: High percentage of MS patients has cognitive impairment. Patients with higher disability were presented with lower cognitive abilities, especially in executive functions and language domains. Higher frequency of cognitive impairment were presented in progessive forms of disaese and longer disease duration with strong influence on executive functions domains of cognition.
 Although the understanding of secondary progressive multiple sclerosis (SPMS) is evolving, early detection of relapse-independent progression remains difficult. This is further complicated by superimposed relapses and compensatory mechanisms that allow for silent progression. The term relapsing multiple sclerosis (RMS) subsumes relapsing-remitting multiple sclerosis (RRMS) and SPMS with relapses. The latter is termed 'active' SPMS, for which disease-modifying therapies (DMTs) approved for either RMS or active SPMS can be used. However, the level of evidence supporting efficacy and safety in SPMS differs between drugs approved for RMS and SPMS. Our review aims to identify current evidence from published clinical trials and European public assessment reports from the marketing authorization procedure on the efficacy, especially on progression, of DMTs approved for RMS and SPMS. To identify relevant evidence, a literature search has been conducted and European public assessment reports of DMTs approved for RMS have been screened for unpublished data specific to SPMS. Only two clinical trials demonstrated a significant reduction in disability progression in SPMS study populations: the EXPAND study for siponimod, which included a typical SPMS population, and the European study for interferon (IFN)-beta 1b s.c., which included patients with very early and active SPMS. Both DMTs also achieved significant reductions in relapse rates. Ocrelizumab, cladribine, ofatumumab, and ponesimod are all approved for RMS - ocrelizumab, ofatumumab, and ponesimod based on an RMS study, cladribine based on an RRMS study. Data on efficacy in SPMS are only available from post hoc analyses of very small subgroups, representing only up to 15% of the total study population. For these DMTs, approval for RMS, including active SPMS, was mainly based on the assumption that the reduction in relapse rate observed in patients with RRMS can also be applied to SPMS. Based on that, the potential of these drugs to reduce relapse-independent progression remains unclear.
 OBJECTIVE: To examine the association between physical activity (PA) and quality of life (QOL) in persons newly diagnosed with multiple sclerosis (MS) who have been under-represented in MS research. DESIGN: Cross-sectional study with secondary data analysis. SETTING: General community. PARTICIPANTS: The study included 152 persons newly diagnosed with MS (ie, diagnosed with MS within the past 2 years) aged 18 and older (N=152). MAIN OUTCOME MEASURES: Participants completed the Godin Leisure-Time Exercise Questionnaire to measure PA. QOL, disability status, fatigue, mood, and comorbidity were assessed using the 12-Item Short Form Survey (SF-12), Patient Determined Disease Steps, Hamburg Quality of Life Questionnaire Multiple Sclerosis, and comorbidity questionnaire. RESULTS: The bivariate correlations indicated that PA was significantly and positively associated with the physical component of QOL (ie, SF-12 PCS) (r=0.46). The stepwise multiple linear regression analysis indicated PA as associated with SF-12 PCS (β=0.43, R(2)=0.17) when solely included in the model. After controlling for fatigue, mood, disability status, and comorbidity as covariates (R(2)=0.63), the association between PA and SF-12 PCS was still statistically significant, but attenuated in magnitude (β=0.11). CONCLUSIONS: This study observed that PA was significantly associated with the physical component of QOL in persons newly diagnosed with MS, even after controlling for covariates. The findings underscore the importance of developing behavior change interventions targeting PA while addressing the roles of fatigue and disability status for enhancing the physical component of QOL of this MS subpopulation.
 OBJECTIVE: This study examined the prevalence and correlates of depression, anxiety, insomnia, and dysmenorrhea in stressed fingolimod-treated women with multiple sclerosis. METHODS: This cross-sectional study recruited female patients diagnosed with multiple sclerosis and stress from Al-Bashir Hospital in Jordan. Depression was assessed by the Patient Health Questionnaire (PHQ-9); anxiety by the Generalized Anxiety Disorder (GAD-7) scale; insomnia by the Insomnia Severity Index (ISI-A) scale; and dysmenorrhea severity by a measure assessing working ability, location, intensity, days of pain, and miscellaneous dysmenorrhea symptoms (WaLIDD). RESULTS: A total of 129 patients were recruited for the study. Severe depression was reported in 55.8%, severe anxiety in 62.0%, severe insomnia in 36.4%, and severe dysmenorrhea in 23.3%. Multivariate analyses revealed that depressive symptoms were associated with dysmenorrhea (OR = 3.55, 95% CI = 1.56-8.12, p = 0.003); anxiety symptoms with "not using dysmenorrhea analgesics" (OR = 2.74, 95% CI = 1.16-6.46, p = 0.02) and dysmenorrhea symptoms (OR = 4.74, 95% CI = 1.94-11.59, p = 0.001); insomnia symptoms with age above 30 years (OR = 4.34, 95% CI = 1.64-11.51, p = 0.003); and dysmenorrhea symptoms with the presence of chronic diseases (OR = 4.21, 95% CI = 1.28-13.92, p = 0.02), anxiety symptoms (OR = 3.03, 95% CI = 1.18-7.73, p = 0.02), and insomnia symptoms (OR = 3.00, 95% CI = 1.18-7.64, p = 0.02). CONCLUSION: Stressed women with multiple sclerosis in Jordan experience high rates of depression, anxiety, insomnia, and dysmenorrhea; characteristics related to these conditions have been determined, which may help clinicians to identify those at risk. Longitudinal studies are needed to determine the causal nature of these associations."
 BACKGROUND: Teriflunomide is a first-line oral immunomodulatory agent approved in China for the treatment of relapsing multiple sclerosis. OBJECTIVE: To compare the treatment outcomes of teriflunomide and no disease-modifying therapy (DMT) treatment (in first year) in multi-center real-world Chinese multiple sclerosis patients. DESIGN: Retrospective study. METHODS: This study was conducted in five tertiary hospitals in different geographical regions of China. We collected clinical data of patients treated with teriflunomide and no DMT treatment (in first year) between 1 January 2017 and 31 August 2021. The effectiveness of teriflunomide was described. Potential factors influencing the effectiveness of teriflunomide were investigated. RESULTS: A total of 372 patients treated with teriflunomide and 148 no DMT treatment patients were included. A total of 292 patients were treated with teriflunomide for at least 6 months, described as a stable teriflunomide cohort. The annualized relapse rate was significantly lower in the stable teriflunomide cohort than in the no DMT treatment cohort (0.23 ± 0.47 versus 0.87 ± 0.67, p < 0.001). The mean Expanded Disability Status Scale (EDSS) score of the stable teriflunomide cohort (1.77 ± 1.62) was slightly different from that of the no DMT treatment cohort (2.09 ± 2.00). A previous annualized relapse rate of ⩾1, a previous EDSS score of ⩾2, and a long disease duration of ⩾5 years were associated with better clinical effectiveness. CONCLUSION: Teriflunomide is associated with a lower relapse rate and less disability accumulation in Chinese patients with multiple sclerosis.
 Baclofen, a racemic γ-aminobutyric acid B receptor agonist, is commonly used for the management of multiple sclerosis-related spasticity but is associated with frequent dosing and poor tolerability. Arbaclofen, the active R-enantiomer of baclofen, exhibits 100- to 1000-fold greater specificity for the γ-aminobutyric acid B receptor compared with the S-enantiomer and ∼5-fold greater potency compared with racemic baclofen. Arbaclofen extended-release tablets allow a dosing interval of 12 h and have shown a favourable safety and efficacy profile in early clinical development. A 12-week, randomized, placebo-controlled Phase 3 trial in adults with multiple sclerosis-related spasticity demonstrated that arbaclofen extended-release 40 mg/day significantly reduced spasticity symptoms compared with placebo and was safe and well tolerated. The current study is an open-label extension of the Phase 3 trial designed to evaluate the long-term safety and efficacy of arbaclofen extended-release. In a 52-week, open-label, multicentre study, adults with a Total Numeric-transformed Modified Ashworth Scale score ≥2 in the most affected limb received oral arbaclofen extended-release titrated over 9 days up to 80 mg/day based on tolerability. The primary objective was assessment of arbaclofen extended-release safety and tolerability. Secondary objectives included an assessment of efficacy using the Total Numeric-transformed Modified Ashworth Scale-most affected limb, the Patient Global Impression of Change and Expanded Disability Status Scale. Of 323 patients enrolled, 218 (67.5%) completed 1 year of treatment. Most patients (74.0%) achieved an arbaclofen extended-release maintenance dose of 80 mg/day. At least one treatment-emergent adverse event was reported by 278 patients (86.1%). The most common adverse events were [n patients (%)]: urinary tract disorder [112 (34.7)], muscle weakness [77 (23.8)], asthenia [61 (18.9)], nausea [70 (21.7)], dizziness [52 (16.1)], somnolence [41 (12.7)], vomiting [29 (9.0)], headache [24 (7.4)] and gait disturbance [20 (6.2)]. Most adverse events were of mild-moderate severity. Twenty-eight serious adverse events were reported. One death occurred during the study, a myocardial infarction that was considered by investigators as unlikely to be related to treatment. Overall, 14.9% of patients discontinued due to adverse events, primarily muscle weakness, multiple sclerosis relapse, asthenia and nausea. Evidence of improvement in multiple sclerosis-related spasticity was observed across arbaclofen extended-release dosages. Arbaclofen extended-release treatment (up to 80 mg/day) was well tolerated and reduced symptoms of spasticity in adult patients with multiple sclerosis for 1 year. Clinical Trial Identifier: ClinicalTrials.gov, NCT03319732.
 INTRODUCTION: Multiple sclerosis is a chronic inflammatory autoimmune demyelinating disease that secondarily leads to the axonal loss and associated brain atrophy. Disease-modifying drugs (DMDs) have previously been studied for their ability to affect specific immunity. This study investigates the effect of interferon beta-1a (INF) and glatiramer acetate (GA) administration on changes in innate immunity cell populations. METHODS: Sixty Caucasian female patients with relapsing-remitting multiple sclerosis undergo blood sample testing for 15 blood parameters at baseline, 1M, 3M and 6M after treatment by GA or IFN (started as their first line DMD). RESULTS: A statistically significant difference in the change after 6 months was found in the parameter monocytes (relative count) in the group of patients treated with IFN. The median increase was 27.8%. Changes in many of the other 15 parameters studied were 10-20%. CONCLUSION: Innate immunity has long been neglected in MS immunopathology. The findings of this study show that innate immunity cells, especially monocytes may contribute significantly to MS immunopathology.
 Fingolimod has been used for about ten years to treat multiple recurrent sclerosis. It has been reported that Fingolimod causes an elevation in liver enzymes. In this case report, the clinical and laboratory parameters improved after discontinuation of the drug. However, there is no publication in the literature regarding acute liver failure and liver transplantation following Fingolimod treatment. In this article, we presented a 33 - year - old female patient who developed acute liver failure and underwent liver transplantation after Fingolimod treatment for recurrent multiple sclerosis.
 BACKGROUND: Optic neuritis (ON) is one of the main neuro-ophthalmic presentations of multiple sclerosis (MS), and it causes optic nerve atrophy and axonal loss. However, so far, there is no effective treatment to improve long-term outcomes. METHODS: In a double-blind placebo-controlled randomized clinical trial, 50 patients with MS-related ON were allocated into two arms (24 in the control group and 26 in the intervention group) receiving either 25000IU retinyl palmitate or an identical placebo for six months. Visual evoked potential (VEP), visual acuity, and the retinal nerve fiber layer (RNFL) thickness were evaluated and compared before and after the treatment. RESULTS: RNFL thickness reduction in the affected eyes at sixth month compared to the baseline were 14.81 and 19.46 μm, in the intervention and control groups, respectively (P=0.017). However, VitA therapy did not affect visual acuity and VEP. CONCLUSION: Vitamin A supplementation in the patients with acute ON in MS could lessen optic nerve axonal loss.
 BACKGROUND: Patients with multiple sclerosis (MS) should have magnetic resonance imaging evaluation regularly. They will experience anxiety before this examination. We conducted this study to evaluate the validity and reliability of emotions and attitudes towards MRI" (MRI-EMA). METHODS: One hundred-nine patients with MS were asked to fill the valid and reliable Persian version of Beck Anxiety Inventory (BAI), and MRI-EMA, questionnaires. Two weeks later, twenty cases were asked to fill the questionnaire again to assess reliability. The intra-class correlation coefficient (ICC) and Cronbach's alpha analysis were used. The correlation coefficient between BAI and MRI-EMA was calculated. Five neurologists assessed content validity by content validity ratio (CVR) and content validity index (CVI). RESULTS: The mean age was 37.2±1.2 years and 77% were females. CVI and CVR for all questions were 100%. The correlation coefficient between BAI and MRI-EMA was r=0.1, P=0.1 and only fear of MRI subscale was significantly correlated with BAI. The ICC of all questions was between 0.79 and 0.98. CONCLUSION: Patients with MS have to be routinely screened with MRI which provides anxiety for them. Considering MRI related anxiety is crucial for these cases. The Persian version of the MRI-EMA questionnaire is a valid and reliable instrument for measuring MRI related anxiety in patients with multiple sclerosis.
 Neuroglial cells, and especially astrocytes, constitute the most varied group of central nervous system (CNS) cells, displaying substantial diversity and plasticity during development and in disease states. The morphological changes exhibited by astrocytes during the acute and chronic stages following CNS injury can be characterized more precisely as a dynamic continuum of astrocytic reactivity. Different subpopulations of reactive astrocytes may be ascribed to stages of degenerative progression through their direct pathogenic influence upon neurons, neuroglia, the blood-brain barrier, and infiltrating immune cells. Multiple sclerosis (MS) constitutes an autoimmune demyelinating disease of the CNS. Despite the previously held notion that reactive astrocytes purely form the structured glial scar in MS plaques, their continued multifaceted participation in neuroinflammatory outcomes and oligodendrocyte and neuronal function during chronicity, suggest that they may be an integral cell type that can govern the pathophysiology of MS. From a therapeutic-oriented perspective, astrocytes could serve as key players to limit MS progression, once the integral astrocyte-MS relationship is accurately identified. This review aims toward delineating the current knowledge, which is mainly focused on immunomodulatory therapies of the relapsing-remitting form, while shedding light on uncharted approaches of astrocyte-specific therapies that could constitute novel, innovative applications once the role of specific subgroups in disease pathogenesis is clarified.
 Multiple sclerosis is a chronic demyelinating disease of the central nervous system and long-term disabling. Different disease-modifying treatments are available. These patients, despite being generally young, have high comorbidity and risk of polymedication due to their complex symptomatology and disability. OBJECTIVE PRIMARY: To determine the type of disease-modifying treatment in patients seen in Spanish hospital pharmacy departments. SECONDARY OBJECTIVES: To determine concomitant treatments, determine the prevalence of polypharmacy, identify the prevalence of interactions and analyse pharmacotherapeutic complexity. METHOD: Observational, cross-sectional, multicentre study. All patients with a diagnosis of multiple sclerosis and active disease-modifying treatment who were seen in outpatient clinics or day hospitals during the second week of February 2021 were included. Modifying treatment, comorbidities and concomitant treatments were collected to determine multimorbidity pattern, polypharmacy, pharmacotherapeutic complexity (Medication Regimen Complexity Index) and drug-drug interactions. RESULTS: 1,407 patients from 57 centres in 15 autonomous communities were included. The most frequent form of disease presentation was the relapsing remitting form (89.3%). The most prescribed disease-modifying treatment was dimethyl fumarate (19.1%), followed by teriflunomide (14.0%). Of the parenteral disease-modifying treatments, the two most prescribed were glatiramer acetate and natalizumab with 11.1% and 10.8%. 24.7% of the patients had one comorbidity and 39.8% had at least 2 comorbidities. 13.3% belonged to at least one of the defined patterns of multimorbidity and 16.5% belonged to 2 or more patterns. The concomitant treatments prescribed were psychotropic drugs (35.5%); antiepileptic drugs (13.9%) and antihypertensive drugs and drugs for cardiovascular pathologies (12.4%). The presence of polypharmacy was 32.7% and extreme polypharmacy 8.1%. The prevalence of interactions was 14.8%. Median pharmacotherapeutic complexity was 8.0 (IQR: 3.3 -- 15.0). CONCLUSIONS: We have described the disease-modifying treatment of patients with multiple sclerosis seen in Spanish pharmacy services and characterised concomitant treatments, the prevalence of polypharmacy, interactions, and their complexity.
 OBJECTIVES: Multiple sclerosis (MS) is among the most prevalent chronic immune-mediated inflammatory diseases. If MS onset is under 18, it is defined as pediatric-onset MS (POMS). This study aimed to determine the clinical and epidemiological aspects of POMS. MATERIALS & METHODS: This population-based study was conducted in East-Azerbaijan (EA) province and concerned POMS patients. The data concerning almost all of the POMS patients of the province was gathered from the only MS registry center in the university hospital of the Tabriz University of Medical Sciences by the end of 2017. The diagnosis of patients was based on McDonald's criteria. RESULTS: Out of 2976 total cases of MS, eighty-five (2.85%) were POMS. The overall regional prevalence of POMS was 11.67 per 100,000 (95% CI:9.43-11.43). Sixty-seven cases were female (prevalence: 18.94 per 100,000 [95% CI:14.91-24.07], and eighteen were male (prevalence: 4.80 per 100,000 [95% CI:3.03-7.62]. The crude regional incidence in 2017 was 1.37/100,000 (95% CI:0.74-2.55). The mean age of onset was 15.81±1.33 years, with a minimum age of 12. 71.76% of the patients were diagnosed in the 16- or 17-years old age group. 7.05% had a positive family history, and 87.5% of the patients diagnosed the disease promptly. The most common first clinical presentations were blurred vision (43.75%), sensory (28.12%), cerebellar (15.62%), and brainstem (9.37%) symptoms. CONCLUSION: POMS is not a rare condition, and it mainly affects females. POMS prevalence increases significantly after age 15 years old, and the first manifestation of the disease is usually blurred vision.
 Quantifying the relationship between the brain's functional activity patterns and its structural backbone is crucial when relating the severity of brain pathology to disability in multiple sclerosis (MS). Network control theory (NCT) characterizes the brain's energetic landscape using the structural connectome and patterns of brain activity over time. We applied NCT to investigate brain-state dynamics and energy landscapes in controls and people with MS (pwMS). We also computed entropy of brain activity and investigated its association with the dynamic landscape's transition energy and lesion volume. Brain states were identified by clustering regional brain activity vectors, and NCT was applied to compute the energy required to transition between these brain states. We found that entropy was negatively correlated with lesion volume and transition energy, and that larger transition energies were associated with pwMS with disability. This work supports the notion that shifts in the pattern of brain activity in pwMS without disability results in decreased transition energies compared to controls, but, as this shift evolves over the disease, transition energies increase beyond controls and disability occurs. Our results provide the first evidence in pwMS that larger lesion volumes result in greater transition energy between brain states and decreased entropy of brain activity.
 Purpose: Falls are a major issue for people with neurological conditions, and the evaluation of falls prevention interventions is of high priority. To date, the views of patient groups regarding outcomes of importance have been largely overlooked. The purpose of this study was to explore outcomes of interest among people with Multiple Sclerosis (MS), Parkinson's disease (PD) and stroke upon completion of falls prevention interventions to inform the development of a core outcome set (COS).Materials and methods: Five online focus groups and one semi-structured interview were conducted among people with PD (n = 10), MS (n = 7), and post-stroke (n = 3), one of whom also had PD. Transcripts were analysed using reflexive thematic analysis.Results: Four themes were developed; (1) Fall events are not homogeneous, (2) Exercise-based programmes are beneficial but falls services are not meeting user needs, (3) Programme success beyond the reduction in falls, and (4) Acquisition of skills to self-manage falls beyond the life of the programme.Conclusions: This study presents new perspectives across patient groups regarding important outcomes upon completion of falls prevention interventions. Taken together with the findings of a literature review, this data will inform the development of a COS.Implications for rehabilitationPeople with multiple sclerosis, Parkinson's disease and stroke consider the success of a falls prevention intervention to be dependent on improvements across a wide range of outcomes.The design and implementation of falls prevention interventions should align with patient preferences.Clinicians and researchers should consider the use of multidomain interventions to facilitate improvements in the desired outcomes of patients.
 A prodrome is an early set of symptoms, which indicates the onset of a disease; these symptoms are often non-specific. Prodromal phases are now recognized in multiple central nervous system diseases. The depth of understanding of the prodromal phase varies across diseases, being more nascent for multiple sclerosis for example, than for Parkinson disease or Alzheimer's disease. Key challenges when identifying the prodromal phase of a disease include the lack of specificity of prodromal symptoms, and consequent need for accessible and informative biomarkers. Further, heterogeneity of the prodromal phase may be influenced by age, sex, genetics and other poorly understood factors. Nonetheless, recognition that an individual is in the prodromal phase of disease offers the opportunity for earlier diagnosis and with it the opportunity for earlier intervention.
 Multiple sclerosis is a chronic demyelinating disease of the central nervous system and long-term disabling. Different disease-modifying treatments are available. These patients, despite being generally young, have high comorbidity and risk of polymedication due to their complex symptomatology and disability. OBJECTIVE PRIMARY: To determine the type of disease-modifying treatment in patients seen in Spanish hospital pharmacy departments. SECONDARY OBJECTIVES: to determine concomitant treatments, determine the prevalence of polypharmacy, identify the prevalence of interactions and analyze pharmacotherapeutic complexity. METHOD: Observational, cross-sectional, multicentre study. All patients with a diagnosis of multiple sclerosis and active disease-modifying treatment who were seen in outpatient clinics or day hospitals during the second week of February 2021 were included. Modifying treatment, comorbidities and concomitant treatments were collected to determine multimorbidity pattern, polypharmacy, pharmacotherapeutic complexity (Medication Regimen Complexity Index) and drug-drug interactions. RESULTS: 1407 patients from 57 centres in 15 autonomous communities were included. The most frequent form of disease presentation was the relapsing remitting form (89.3%). The most prescribed disease-modifying treatment was dimethyl fumarate (19.1%), followed by teriflunomide (14.0%). Of the parenteral disease-modifying treatments, the two most prescribed were glatiramer acetate and natalizumab with 11.1% and 10.8%. 24.7% of the patients had 1 comorbidity and 39.8% had at least 2 comorbidities. 13.3% belonged to at least one of the defined patterns of multimorbidity and 16.5% belonged to 2 or more patterns. The concomitant treatments prescribed were psychotropic drugs (35.5%); antiepileptic drugs (13.9%) and antihypertensive drugs and drugs for cardiovascular pathologies (12.4%). The presence of polypharmacy was 32.7% and extreme polypharmacy 8.1%. The prevalence of interactions was 14.8%. Median pharmacotherapeutic complexity was 8.0 (IQR: 3.3-15.0). CONCLUSIONS: We have described the disease-modifying treatment of patients with multiple sclerosis seen in Spanish pharmacy services and characterized concomitant treatments, the prevalence of polypharmacy, interactions, and their complexity.
 OBJECTIVE: The potential of magnetization transfer imaging (MTI) and diffusion tensor imaging (DTI) for the detection and evolution of new multiple sclerosis (MS) lesions was analyzed. METHODS: Nineteen patients with MS obtained conventional MRI, MTI, and DTI examinations bimonthly for 12 months and again after 24 months at 1.5 T MRI. MTI was acquired with balanced steady-state free precession (bSSFP) in 10 min (1.3 mm(3) isotropic resolution) yielding both magnetization transfer ratio (MTR) and quantitative magnetization transfer (qMT) parameters (pool size ratio (F), exchange rate (kf), and relaxation times (T1/T2)). DTI provided fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD). RESULTS: At the time of their appearance on MRI, the 21 newly detected MS lesions showed significantly reduced MTR/F/kf and prolonged T1/T2 parameters, as well as significantly reduced FA and increased AD/MD/RD. Significant differences were already observed for MTR 4 months and for qMT parameters 2 months prior to lesions' detection on MRI. DTI did not show any significant pre-lesional differences. Slightly reversed trends were observed for most lesions up to 8 months after their detection for qMT and less pronounced for MTR and three diffusion parameters, while appearing unchanged on MRI. CONCLUSIONS: MTI provides more information than DTI in MS lesions and detects tissue changes 2 to 4 months prior to their appearance on MRI. After lesions' detection, qMT parameter changes promise to be more sensitive than MTR for the lesions' evolutional assessment. Overall, bSSFP-based MTI adumbrates to be more sensitive than MRI and DTI for the early detection and follow-up assessment of MS lesions. CLINICAL RELEVANCE STATEMENT: When additionally acquired in routine MRI, fast bSSFP-based MTI can complement the MRI/DTI longitudinal lesion assessment by detecting MS lesions 2-4 months earlier than with MRI, which could implicate earlier clinical decisions and better follow-up/treatment assessment in MS patients. KEY POINTS: • Magnetization transfer imaging provides more information than DTI in multiple sclerosis lesions and can detect tissue changes 2 to 4 months prior to their appearance on MRI. • After lesions' detection, quantitative magnetization transfer changes are more pronounced than magnetization transfer ratio changes and therefore promise to be more sensitive for the lesions' evolutional assessment. • Balanced steady-state free precession-based magnetization transfer imaging is more sensitive than MRI and DTI for the early detection and follow-up assessment of multiple sclerosis lesions.
 BACKGROUND: Multiple Sclerosis (MS), a chronic disease of the central nervous system (CNS), affects functional ability and quality of life (QoL). Depression, fatigue, and disability status are among the many factors that have been shown to impact QoL in people with MS, but the extent to which MS-related cognitive impairment is related to QoL is understudied in the literature. OBJECTIVE: The purpose of this study was to determine relevant predictors of QoL from a wide list of symptoms including physical disability, and a multi-dimensional computerized cognitive assessment battery (CAB), depression, fatigue, and demographic variables (including employment status). In addition, the unique predictive power of cognitive impairment on QoL was explored in relation to other common factors of disease impact. METHODS: 171 people with MS (PwMS) were evaluated with a computerized assessment battery (CAB), EDSS examination, and validated Patient Reported Outcome (PRO) measures (Multiple Sclerosis Impact Scale, MSIS-29; Beck Depression Inventory - Second Edition BDI-2; and the Modified Fatigue Impact Scale, MFIS). RESULTS: 171 PwMS were included [Age: 46.02 years ± 9.85, 124 (72.5%) female]. Depression and fatigue scores were highly correlated with MSIS-29. EDSS, unemployment, memory, executive functioning, and motor skills were moderately correlated with MSIS-29. Predictors of QoL were EDSS, depression, fatigue, executive functioning, and attention. Attention and executive functioning were predictive of QoL even after controlling for demographic variables, fatigue, depression, and physical disability status. CONCLUSION: Findings indicate the need for comprehensive and quantified evaluation of all factors associated with disease burden, which will ultimately serve to improve the QoL in PwMS through more targeted and patient-centered care.
 Sleep disturbance is common in people with multiple sclerosis and may worsen fatigue; however, the assessment of sleep-fatigue relationships varies across studies. To better understand sleep-fatigue relationships in this population, we conducted a systematic review and random effects meta-analyses for the associations between fatigue and 10 sleep variables: Sleep-disordered breathing, daytime sleepiness, sleep quality, insomnia, restless legs, number of awakenings, sleep efficiency, sleep latency, sleep duration, and wake after sleep onset. Of the 1062 studies screened, 46 met inclusion criteria and provided sufficient data for calculating Hedges' g. Study quality was assessed using the Newcastle-Ottawa Scale. Sample characteristics did not differ between the 10 analyses. Results indicated that sleep quality and insomnia (assessed via self-report or diagnostic criteria) were strongly associated with fatigue (all gs ≥ 0.80 and all ps < .001). In contrast, the number of awakenings and sleep duration (assessed objectively) were not significantly associated with fatigue. Remaining sleep variables yielded moderate, significant effects. Most effects did not vary based on study quality or sample demographics. Results highlight that insomnia and perceptions of poor sleep have a stronger link than objective sleep duration to fatigue in multiple sclerosis and may represent a more effective target for intervention.
 BACKGROUND: There is significant inconsistency regarding the prevalence rate of depression and anxiety among people with multiple sclerosis (MS) in Iran. We sought to conduct this comprehensive meta-analysis to assess the prevalence of depression and anxiety in Iranian multiple sclerosis patients. METHODS: A systematic search was conducted on 14 March 2023 in PubMed/MEDLINE, Web of Science, Scopus, Embase, and Iranian national databases. All studies assessing the prevalence of depression and anxiety among Iranian people with MS were included. We used the NEWCASTLE-OTTAWA tool for quality assessment. We pooled the prevalence of individual studies using the random effect model. RESULTS: Our systematic search showed 23 articles that meet the eligibility criteria. Most of the included studies were cross-sectional. The most used questionnaire to assess depression and anxiety were Beck Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS), respectively. The overall prevalence of depression and anxiety among Iranian people with MS was 47% (95%CI: 39%-55%%, I2 =94%) and 51% (95%CI: 36%-66%%, I2 =97%), respectively. The results of subgroup and meta-regression analyses showed assessment scale used and the province was significantly associated with the prevalence of the outcomes. Tehran had the most studies published on this topic. The prevalence of depression and anxiety was highest in Kermanshah province. The funnel plot and Egger's regression test did not show a significant source of funnel plot asymmetry for depression (p-value = 0.8138), and anxiety (p-value = 0.8259). CONCLUSION: Our study indicates that a significant proportion of people with MS in Iran are affected by depression and anxiety.
 Real-world evidence in multiple sclerosis (MS) is limited by the availability of data elements in individual real-world datasets. We introduce a novel, growing database which links administrative claims and medical records from an MS patient management system, allowing for the complete capture of patient profiles. Using the AOK PLUS sickness fund and the Multiple Sclerosis Documentation System MSDS(3D) from the Center of Clinical Neuroscience (ZKN) in Germany, a linked MS-specific database was developed (MSDS-AOK PLUS). Patients treated at ZKN and insured by AOK PLUS were recruited and asked for informed consent. For linkage, insurance IDs were mapped to registry IDs. After the deletion of insurance IDs, an anonymized dataset was provided to a university-affiliate, IPAM e.V., for further research applications. The dataset combines a complete record of patient diagnoses, treatment, healthcare resource use, and costs (AOK PLUS), with detailed clinical parameters including functional performance and patient-reported outcomes (MSDS(3D)). The dataset currently captures 500 patients; however, is actively expanding. To demonstrate its potential, we present a use case describing characteristics, treatment, resource use, and costs of a patient subsample. By linking administrative claims to clinical information in medical charts, the novel MSDS-AOK PLUS database can increase the quality and scope of real-world studies in MS.
 BACKGROUND: Multiple sclerosis (MS) is characterized by inflammation, demyelination and axonal degeneration. Oxidative stress (OS) plays a significant role in the pathogenesis of the disease. The aim of the study was to examine the association between OS and smoking on the MS development. METHODS: The study included 175 patients with relapsing-remitting multiple sclerosis (RRMS) (76 males, 99 females) and 254 healthy subjects (81 males and 173 females). Oxidative stress biomarkers in serum, Total Antioxidant Status (TAS) and Total Oxidative Status (TOS) were determined spectrophotometrically. Oxidative Stress Index (OSI) was calculated as the ratio of TOS and TAS. Urinary 8-oxo7,8-dihydro-2'-deoxyguanosine were determined by HPLC-MS/MS and expressed as 8-oxodG/creatinine. RESULTS: In females with RRMS were higher TOS, OSI and 8-oxodG/creatinine than in females in control group. The group of males with RRMS had lower level of TAS than the males in control group. Higher levels of 8-oxodG/creatinine was obtained in active, passive and former smokers with RRMS than in control group with the same exposition to tobacco smoke. Independent predictors of MS are passive smoking, increased OSI and increased levels of urinary 8-oxodG/creatinine. CONCLUSIONS: Our results demonstrate that the OS parameters should be included in the assessment of the risk for MS development. Due to the more sensitivity to oxidative stress, females may be at higher risk of MS development. This data indicates the importance of introducing the antioxidant therapy as a complementary treatment in patients with RRMS.
 Big conductance calcium-activated (BK) channel openers can inhibit pathologically driven neural hyperactivity to control symptoms via hyperpolarizing signals to limit neural excitability. We hypothesized that BK channel openers would be neuroprotective during neuroinflammatory, autoimmune disease. The neurodegenerative disease was induced in a mouse experimental autoimmune encephalomyelitis model with translational value to detect neuroprotection in multiple sclerosis. Following the treatment with the BK channel openers, BMS-204253 and VSN16R, neuroprotection was assessed using subjective and objective clinical outcomes and by quantitating spinal nerve content. Treatment with BMS-204253 and VSN16R did not inhibit the development of relapsing autoimmunity, consistent with minimal channel expression via immune cells, nor did it change leukocyte levels in rodents or humans. However, it inhibited the accumulation of nerve loss and disability as a consequence of autoimmunity. Therefore, in addition to symptom control, BK channel openers have the potential to save nerves from excitotoxic damage and could be useful as either stand-alone neuroprotective agents or as add-ons to current disease-modifying treatments that block relapsing MS but do not have any direct neuroprotective activity.
 Multiple sclerosis (MS) is a chronic autoimmune disease that impacts the central nervous system and can result in disability. Although the prevalence of MS has increased in India, diagnosis and treatment continue to be difficult due to several factors. The present study examines the difficulties in detecting and treating multiple sclerosis in India. A lack of MS knowledge among healthcare professionals and the general public, which delays diagnosis and treatment, is one of the significant issues. Inadequate numbers of neurologists and professionals with knowledge of MS management also exacerbate the situation. In addition, MS medications are expensive and not covered by insurance, making them inaccessible to most patients. Due to the absence of established treatment protocols and standards for MS care, India's treatment techniques vary. In addition, India's population diversity poses unique challenges regarding genetic variations, cellular and molecular abnormalities, and the potential for differing treatment responses. MS is more difficult to accurately diagnose and monitor due to a lack of specialized medical supplies and diagnostic instruments. Improved awareness and education among healthcare professionals and the general public, as well as the development of standardized treatment regimens and increased investment in MS research and infrastructure, are required to address these issues. By addressing these issues, it is anticipated that MS diagnosis and treatment in India will improve, leading to better outcomes for those affected by this chronic condition.
 Multiple sclerosis is a chronic neuroinflammatory disorder characterized by demyelination, oligodendrocyte damage/loss and neuroaxonal injury in the context of immune cell infiltration in the central nervous system. No neuroprotective therapy is available to promote the survival of oligodendrocytes and protect their myelin processes in immune-mediated demyelinating diseases. Pro-inflammatory CD4 Th17 cells can interact with oligodendrocytes in multiple sclerosis and its animal model, causing injury to myelinating processes and cell death through direct contact. However, the molecular mechanisms underlying the close contact and subsequent detrimental interaction of Th17 cells with oligodendrocytes remain unclear. In this study we used single cell RNA sequencing, flow cytometry and immunofluorescence studies on central nervous system tissue from multiple sclerosis subjects, its animal model and controls to characterize the expression of cell adhesion molecules by mature oligodendrocytes. We found that a significant proportion of human and murine mature oligodendrocytes express melanoma cell adhesion molecule and activated leukocyte cell adhesion molecule in multiple sclerosis, in experimental autoimmune encephalomyelitis and in controls, although their regulation differs between human and mouse. We observed that exposure to pro-inflammatory cytokines or to human activated T cells are associated with a marked downregulation of the expression of melanoma cell adhesion molecule but not of activated leukocyte cell adhesion molecule at the surface of human primary oligodendrocytes. Furthermore, we used in vitro live-imaging, immunofluorescence, and flow cytometry to determine the contribution of these molecules to Th17-polarized cell adhesion and cytotoxicity towards human oligodendrocytes. Silencing and blocking activated leukocyte cell adhesion molecule but not melanoma cell adhesion molecule limited prolonged interactions between human primary oligodendrocytes and Th17-polarized cells, resulting in decreased adhesion of Th17-polarized cells to oligodendrocytes and conferring significant protection of oligodendrocytic processes. In conclusion, we showed that human oligodendrocytes express melanoma and activated leukocyte cell adhesion molecules, which are differently modulated by inflammation and T cell contact. We found that activated leukocyte cell adhesion molecule is a ligand for Th17-polarized cells, contributing to their capacity to adhere and induce damage to human oligodendrocytes, and therefore could represent a relevant target for neuroprotection in multiple sclerosis.
 Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a poorly understood chronic illness with many case definitions that disagree on key symptoms, including hypersensitivities to noise and lights. The aim of the current study was to understand the prevalence rates and characteristics of these symptoms amongst people with ME/CFS and to compare them to people with another chronic illness, multiple sclerosis (MS). International datasets consisting of 2,240 people with either ME/CFS or MS have completed the DePaul Symptom Questionnaire (DSQ) and the Short Form Health Survey Questionnaire (SF-36). Hypersensitivities to noise and lights were indicated from items on the DSQ, and participants were analyzed against DSQ and SF-36 subscales through a multivariate analysis of covariance. There were significantly higher percentages of people with hypersensitivities in the ME/CFS sample compared to the MS sample. Regardless of illness, participants that exhibited both hypersensitivities reported greater symptomology than those without hypersensitivities. Healthcare providers and researchers should consider these symptoms when developing treatment plans and evaluating ME/CFS case diagnostic criteria.
 Blood-based biomarkers can be economic and easily accessible tools for monitoring and predicting disease activity in multiple sclerosis. The objective of this study was to determine the predictive value of a multivariate proteomic assay for concurrent and future microstructural/axonal brain pathology in a longitudinal study of a heterogeneous group of people with multiple sclerosis. A proteomic analysis was obtained on serum samples from 202 people with multiple sclerosis (148 relapsing-remitting and 54 progressive) at baseline and 5-year follow-up. The concentration of 21 proteins related to multiple pathways of multiple sclerosis pathophysiology was derived using Proximity Extension Assay on the Olink platform. Patients were imaged on the same 3T MRI scanner at both timepoints. Тhe rate of whole brain, white matter and grey matter atrophy over the 5-year follow-up was determined using the multi-timepoint Structural Image Evaluation, using Normalisation, of Atrophy algorithms. Lesion burden measures were also assessed. The severity of microstructural axonal brain pathology was quantified using diffusion tensor imaging. Fractional anisotropy and mean diffusivity of normal-appearing brain tissue, normal-appearing white matter, grey matter, T2 and T1 lesions were calculated. Age, sex and body mass index-adjusted step-wise regression models were used. Glial fibrillary acidic protein was the most common and highest-ranked proteomic biomarker associated with greater concurrent microstructural central nervous system alterations (P < 0.001). The rate of whole brain atrophy was associated with baseline levels of glial fibrillary acidic protein, protogenin precursor, neurofilament light chain and myelin oligodendrocyte (P < 0.009), whereas grey matter atrophy was associated with higher baseline neurofilament light chain, higher osteopontin and lower protogenin precursor levels (P < 0.016). Higher baseline glial fibrillary acidic protein level was a significant predictor of future severity of the microstructural CNS alterations as measured by normal-appearing brain tissue fractional anisotropy and mean diffusivity (standardized β = -0.397/0.327, P < 0.001), normal-appearing white matter fractional anisotropy (standardized β = -0.466, P < 0.0012), grey matter mean diffusivity (standardized β = 0.346, P < 0.011) and T2 lesion mean diffusivity (standardized β = 0.416, P < 0.001) at the 5-year follow-up. Serum levels of myelin-oligodendrocyte glycoprotein, neurofilament light chain, contactin-2 and osteopontin proteins were additionally and independently associated with worse concomitant and future axonal pathology. Higher glial fibrillary acidic protein levels were associated with future disability progression (Exp(B) = 8.65, P = 0.004). Multiple proteomic biomarkers are independently associated with greater severity of axonal brain pathology as measured by diffusion tensor imaging in multiple sclerosis. Baseline serum glial fibrillary acidic protein levels can predict future disability progression.
 Almost three million individuals suffer from multiple sclerosis (MS) throughout the world, a demyelinating disease in the nervous system with increased prevalence over the last five decades, and is now being recognized as one significant etiology of cognitive loss and dementia. Presently, disease modifying therapies can limit the rate of relapse and potentially reduce brain volume loss in patients with MS, but unfortunately cannot prevent disease progression or the onset of cognitive disability. Innovative strategies are therefore required to address areas of inflammation, immune cell activation, and cell survival that involve novel pathways of programmed cell death, mammalian forkhead transcription factors (FoxOs), the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), and associated pathways with the apolipoprotein E (APOE-ε4) gene and severe acute respiratory syndrome coronavirus (SARS-CoV-2). These pathways are intertwined at multiple levels and can involve metabolic oversight with cellular metabolism dependent upon nicotinamide adenine dinucleotide (NAD+). Insight into the mechanisms of these pathways can provide new avenues of discovery for the therapeutic treatment of dementia and loss in cognition that occurs during MS.
 Introduction: Multiple sclerosis (MS) is an autoimmune, chronic, inflammatory and demyelinating disease that affects the Central Nervous System (CNS). It is the most common disabling neurological disease in young patients not caused by traumatic shock. Depending on how symptoms appear and how often they occur, there are different subtypes of MS. One of them is the relapsing-remitting phenotype (R-R), which the symptoms appear in the form of isolated outbreaks which, little by little, are causing the increase of the disease and its sequelae. MS encompasses a wide variety of symptoms, including possible cognitive impairment. In the literature there is no clear methodology and a defined and structured consensus to carry out neuropsychological rehabilitation processes in this group.Aim: This study aims to review and synthesize the available scientific evidence about the neuropsychological intervention on cognitive impairment of people with multiple sclerosis, relapsing-remitting subtype.Methods: Keywords for database search (Pubmed and Wos) were established, as well as inclusion and exclusion criteria. Then, the articles were selected according to inclusion and exclusion criteria; methodological quality criteria were applied. Articles published in the last 10 years were included.Results: Fifteen articles that met the established criteria were selected. Most of these studies identify as effective their cognitive rehabilitation programs, some of them showed changes in neural structures after rehabilitation.Discussion: It seems that cognitive rehabilitation is effective in influencing cognitive deterioration in R-R MS. This highlights the importance of neuropsychological evaluation and intervention from the early stages of the disease.
 Patients with multiple sclerosis (MS) experience various physical symptoms and psychosocial problems that disrupt their normal life, and adapting to these conditions is vital for them. Many factors that serve as facilitators of and barriers to achieving adjustment should be identified to be able to help the patients. This study was conducted to explain the experiences of patients with MS regarding the facilitators of and barriers to adjustment using conventional content analysis. The participants consisted of 18 patients, one nurse, one physician, and one patient companion, who were selected from the Multiple Sclerosis Clinic of BouAli, northern Iran, through purposive sampling. Data were collected through individual, in-depth, and semi-structured interviews and analyzed using the method recommended by Elo and Kyngäs (2008). The data analysis generated five subcategories as facilitators and five subcategories as barriers. The subcategories of facilitators included family's appropriate behavior with the patient, occupation, studying and information gathering, religious beliefs, and turning attitude into disease simplification and optimism. The subcategories of barriers were concerns about the uncertain future of the disease, physicians' poor communication and behavior, society's poor attitude, economic problems, and unsatisfactory support by the government and insurance companies. The results showed that a set of individual, environmental, and social factors serves as facilitators of or barriers to the process of adjustment to MS in patients. Gaining knowledge about these factors in congruence with the sociocultural context of the society, as derived from people's real experiences, can help healthcare staff and the family of these patients provide more efficient assistance to the patients for achieving adjustment earlier.
 To investigate cognitive reserve as a possible moderator in the relationship between fatigue and depressive symptoms in persons with multiple sclerosis (PwMS). Fifty-three PwMS (37 female; mean age, 52.66; mean education, 14.81) completed comprehensive neuropsychological testing and psychosocial questionnaires assessing the perceived effects of fatigue (Fatigue Impact Scale) and depressive symptoms (Beck Depression Inventory-Fast Screen). Cognitive reserve (CR) was operationalized as Fixed CR and Malleable CR. Fixed CR was quantified as the standardized mean of years of education and a vocabulary-based estimate of premorbid intelligence. Malleable CR was quantified as the standardized mean of cognitive exertion, exercise, and socializing items from the Cognitive Health Questionnaire. Regressions on depressive symptoms examining fatigue, both conceptualizations of CR, and their interactions were explored. A Bonferroni correction was used; results were considered significant at an alpha level of p < .01. The interactions between fatigue and both conceptualizations of CR were significant, p = .005 (Fixed CR); p = .004 (Malleable CR). Simple effects tests revealed that fatigue only predicted depressive symptoms in PwMS with low Fixed CR or low Malleable CR (p's < .001), and not in those with high Fixed or high Malleable CR (p > .01). Cognitive reserve moderated the relationship between fatigue and depressive symptoms in PwMS. Specifically, fatigue does not appear to influence depression in PwMS with high cognitive reserve. Having higher cognitive reserve (either Fixed or Malleable) may reduce the likelihood that fatigue will lead to depressive symptoms in MS.

 By applying the acetyl-CoA-carboxylase inhibitors soraphen A (SorA) and coenzyme A (CoA) ex vivo, we aimed to reduce proinflammatory cytokine release by PBMCs and increase anti-inflammatory cytokine levels, thereby demonstrating a possible application of those pathways in future multiple sclerosis (MS) therapy. In a prospective exploratory monocentric study, we analysed cytokine production by PBMCs treated with SorA (10 or 50 nM) and CoA (600 μM). Thirty-one MS patients were compared to 18 healthy age-matched controls. We demonstrated the immunomodulatory potential of SorA and CoA in targeting the immune function of MS patients, with an overall reduction of cytokines except of IL-2, IL-6 and IL-10.
 Multiple Sclerosis (MS) causes a variety of symptoms in speech production, such as more frequent pauses and an increase in the duration of pauses in the speech. However, there is almost no data on whether the disease affects speech fluency in other ways, such as changes in the frequency of disfluencies in speech. The main question of this study is the following: if we examine speech fluency in speech tasks requiring different cognitive load, will there be a difference between patients and controls? Twenty people with relapsing-remitting MS (3 men and 17 women) and 20 age- and education-matched control speakers (4 men and 16 women) participated in the study. Speech samples were recorded with each participant in three speech tasks: 1) spontaneous narratives about their own lives, 2) narratives about their previous day, and 3) narrative recalls based on a heard text. In the speech samples, pauses and disfluencies were annotated and the duration of pauses was measured. Then, the frequency of pauses and disfluencies were calculated and the types of disfluencies were examined. The results show that there are differences in the frequency and duration of pauses between people with MS and controls. However, there were no significant differences in the frequency of disfluencies between the groups. The same types of disfluencies occurred in the same frequency in both groups. The results help to better understand the speech production processes in MS.
 Remyelination relies on the repair of damaged myelin sheaths, involving microglia cells, oligodendrocyte precursor cells (OPCs), and mature oligodendrocytes. This process drives the pathophysiology of autoimmune chronic disease of the central nervous system (CNS), multiple sclerosis (MS), leading to nerve cell damage and progressive neurodegeneration. Stimulating the reconstruction of damaged myelin sheaths is one of the goals in terms of delaying the progression of MS symptoms and preventing neuronal damage. Short, noncoding RNA molecules, microRNAs (miRNAs), responsible for regulating gene expression, are believed to play a crucial role in the remyelination process. For example, studies showed that miR-223 promotes efficient activation and phagocytosis of myelin debris by microglia, which is necessary for the initiation of remyelination. Meanwhile, miR-124 promotes the return of activated microglia to the quiescent state, while miR-204 and miR-219 promote the differentiation of mature oligodendrocytes. Furthermore, miR-138, miR-145, and miR-338 have been shown to be involved in the synthesis and assembly of myelin proteins. Various delivery systems, including extracellular vesicles, hold promise as an efficient and non-invasive way for providing miRNAs to stimulate remyelination. This article summarizes the biology of remyelination as well as current challenges and strategies for miRNA molecules in potential diagnostic and therapeutic applications.
 The use of high-efficacy disease-modifying therapies (DMTs) early in the course of multiple sclerosis (MS) has been shown to improve clinical outcomes and is becoming an increasingly popular treatment strategy. As a result, monoclonal antibodies, including natalizumab, alemtuzumab, ocrelizumab, ofatumumab, and ublituximab, are frequently used for the treatment of MS in women of childbearing age. To date, only limited evidence is available on the use of these DMTs in pregnancy. We aim to provide an updated overview of the mechanisms of action, risks of exposure and treatment withdrawal, and pre-conception counseling and management during pregnancy and post-partum of monoclonal antibodies in women with MS. Discussing treatment options and family planning with women of childbearing age is essential before commencing a DMT in order to make the most suitable choice for each individual patient.
 Diffusion tensor imaging (DTI) showed its adequacy in evaluating the normal-appearing white matter (NAWM) and lesions in the brain that are difficult to evaluate with routine clinical magnetic resonance imaging (MRI) in multiple sclerosis (MS). Recently, MRI systems have been developed with regard to software and hardware, leading to different proposed diffusion analysis methods such as diffusion tensor imaging, q-space imaging, diffusional kurtosis imaging, neurite orientation dispersion and density imaging, and axonal diameter measurement. These methods have the ability to better detect in vivo microstructural changes in the brain than DTI. These different analysis modalities could provide supplementary inputs for MS disease characterization and help in monitoring the disease's progression as well as treatment efficacy. This paper reviews some of the recent diffusion MRI methods used for the assessment of MS in vivo.
 OBJECTIVE: The time perspective of individuals with chronic disease is a little-studied parameter. Our aim is to examine multiple sclerosis (MS) patients' time perspective and factors that may affect time perspective and to research the correlation of past, present, and future perspectives. METHODS: Demographic characteristics, the Zimbardo Time Perspective Inventory (ZTPI) score, and the expanded disability status scale score were recorded. Overall, 50 with MS were included in the study. RESULTS: We found that there was a significant difference between present-fatalistic (x=3.18), and present-hedonistic (x=3.49), (p=0.017); also between present-fatalistic (x=3.18), and future (x=3.57), (p=0.011). There was no significant difference in ZTPI scores between gender, place of residence, marital status, number of attacks, or education level. CONCLUSION: MS patients focus mostly on the hedonistic dimension of the life than the fatalistic one in present time. We concluded that patients with MS focused mostly on the future. We found that our patients' present-fatalistic scores were lower, and the future was higher time perspective dimension.
 Prostate cancer (PCa) risk in patients with multiple sclerosis (MS) remains to be elucidated. The present study conducted a meta-analysis to assess the relationship between MS and PCa. PubMed, EMBASE, Web of Science, and Cochrane Library databases were searched to identify studies on the PCa risk in patients with MS up to September 2022. A random effects meta-analyses model was performed to estimate the relative risk (RR) and the 95% confidence intervals (CI). All eight studies involving 210,943 patients with MS were identified and included in the meta-analysis. The present study revealed that there was no significant association between MS and the risk of PCa (RR=0.78, 95% CI: 0.56-1.08, P<0.0001). Subgroup analyses verified this conclusion when stratified by regions. However, after adjusting for potential confounders, the findings suggested conflicting results. The current evidence shows that compared with the population control, patients with MS have no relationship with PCa risk and further large samples and long-term trials are needed to verify these results.
 The French Multiple Sclerosis Association offers a psychological helpline for people with this disease, their families, friends and caregivers. Two clinical psychologists answer this toll-free number, which is accessible seven days a week at set times. They offer callers active listening and adapted support, particularly after the announcement of the medical diagnosis and/or in times of difficulty. The space thus created for discussion allows them to address emotional or personal aspects, material situations, as well as questions and problems associated with the experience of the disease.
 INTRODUCTION: Multiple sclerosis (MS) is a chronic inflammatory, demyelinating, and neurodegenerative condition affecting the central nervous system (CNS). Although therapeutic approaches have become available over the last 20 years that markedly slow the progression of disease, there is no cure for MS. Furthermore, the capacity to repair existing CNS damage caused by MS remains very limited. AREAS COVERED: Several animal models are widely used in MS research to identify potential druggable targets for new treatment of MS. In this review, we look at targets identified since 2019 in studies using these models, and their potential for effecting a cure for MS. EXPERT OPINION: Refinement of therapeutic strategies targeting key molecules involved in the activation of immune cells, cytokine, and chemokine signaling, and the polarization of the immune response have dominated recent publications. While some progress has been made in identifying effective targets to combat chronic demyelination and neurodegeneration, much more work is required. Progress is largely limited by the gaps in knowledge of how the immune system and the nervous system interact in MS and its animal models, and whether the numerous targets present in both systems respond in the same way in each system to the same therapeutic manipulation.
 The blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) represent two complex structures protecting the central nervous system (CNS) against potentially harmful agents and circulating immune cells. The immunosurveillance of the CNS is governed by immune cells that constantly patrol the BCSFB, whereas during neuroinflammatory disorders, both BBB and BCSFB undergo morphological and functional alterations, promoting leukocyte intravascular adhesion and transmigration from the blood circulation into the CNS. Multiple sclerosis (MS) is the prototype of neuroinflammatory disorders in which peripheral T helper (Th) lymphocytes, particularly Th1 and Th17 cells, infiltrate the CNS and contribute to demyelination and neurodegeneration. Th1 and Th17 cells are considered key players in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis. They can actively interact with CNS borders by complex adhesion mechanisms and secretion of a variety of molecules contributing to barrier dysfunction. In this review, we describe the molecular basis involved in the interactions between Th cells and CNS barriers and discuss the emerging roles of dura mater and arachnoid layer as neuroimmune interfaces contributing to the development of CNS inflammatory diseases.
 The immunoprotective role of pregnancy in multiple sclerosis (MS) has been known for decades. Conversely, there has been rich debate on the topic of breastfeeding and disease activity in MS. In clinical practice, women are often offered to restart their disease-modifying drug (DMD) soon after delivery to maintain their relapse risk protection. Limited available information about peri-partum DMD safety can discourage women to choose breastfeeding, despite the World Health Organization's recommendation to breastfeed children for the first 6 months of life exclusively. New evidence is emerging about the protective role of exclusive breastfeeding on relapse rate. Research studies shed light on the hormonal and immunological mechanisms driving the risk of relapses during pregnancy and postpartum. Finally, case reports, real-world data, and clinical trials are increasing our knowledge of the safety of DMDs for the fetus and infant. While some DMDs must be avoided, others may be considered in highly active pregnant or lactating women with MS. This mini-review conveys recent evidence regarding the protective role of exclusive breastfeeding in MS and offers clinicians practical considerations for a patient-tailored approach.
 BACKGROUND: Social support is crucial for persons with multiple sclerosis (MS). We sought to analyze differences in perceived social support in persons with MS vs controls; to study associations between perceived social support, clinical measures, and health-related quality of life (HRQOL) variables in persons with MS; and to establish a predictive value of perceived social support for HRQOL. METHODS: We studied 151 persons with MS (mean ± SD: age, 42.01 ± 9.97 years; educational level, 14.05 ± 3.26 years) and 89 controls (mean ± SD: age, 41.46 ± 12.25 years; educational level, 14.60 ± 2.44 years) using the Medical Outcomes Study Social Support Survey (MOS-SSS), Expanded Disability Status Scale, Fatigue Severity Scale, Beck Depression Inventory, and Multiple Sclerosis International Quality of Life (MusiQoL) questionnaire. Parametric and nonparametric statistical methods were used accordingly; P < .05. RESULTS: Persons with MS exhibited lower scores on the MOS-SSS's overall support index (t(238) = -1.98, P = .04) and on each functional subscale (t(238) = -2.56 to -2.19, P < .05). No significant differences were found on the social support structural component (P > .05). Significant associations were observed between social support and depression and fatigue (r = -0.20 to -0.29, P < .05) and with MusiQoL dimensions (r = -0.18 to 0.48, P < .05). Multiple regression analysis showed all 4 tested models contributed to HRQOL-explained variance (41%-47%). The emotional/informational support model explained the most HRQOL variability (47%). CONCLUSIONS: Persons with MS perceived reduced social support, presenting lower functional scores than controls. Perceived social support proved to be a predictor of HRQOL. These findings should be considered during therapeutic treatment.

 Current treatment for Multiple Sclerosis (MS) consists of a multidisciplinary approach including disease-modifying therapies. The response to treatment is heterogeneous, representing a crucial challenge in the classification of patients. Metabolomics is an innovative tool that can identifies biomarkers/predictors of treatment response. We aimed to evaluate plasma metabolic changes in a group of naïve Relapsing-Remitting MS patients starting Fingolimod treatment, to find specific metabolomic features that predict the therapeutic response as well as the possible side effects. The study included 42 Relapsing-Remitting MS blood samples, of which 30 were classified as responders after two years of FINGO treatment, whereas 12 patients were Not-Responders. For fifteen patients, samples were collected at four time points: before starting the therapy; at six months after the initiation; at twelve months after; and at twenty-four months after initiation. The serum was analysed through Nuclear Magnetic Resonance and multivariate and univariate statistical analysis. Considering the single comparison between each time point, it was possible to identify a set of metabolites changing their concentrations based on the drug intake. FINGO influences aminoacidic and energy metabolisms and reduces oxidative stress and the activity of the immune system, both typical features of MS.
 BACKGROUND: Multiple sclerosis (MS) is a common debilitating neurologic disease that affects mostly young women. This review provides an overview of research on the psychosocial impact of parental MS on children to inform clinicians and support people with MS considering parenthood. METHODS: A systematic review of the literature was performed by searching the MEDLINE, PsycINFO, and PSYNDEX databases. We included quantitative and mixed-method studies assessing psychosocial outcomes of children with a parent with MS. Studies were screened for eligibility and evaluated for risk of bias. RESULTS: We screened 608 references, assessed 72 studies in full-text, and included 28 studies in this review. Most of the studies reported on psychosocial adjustment processes, with most results suggesting negative consequences, including difficulties with mood, behavior, or social interaction. Several studies also described associations between children with a parent with MS and increased incidences of psychiatric disorders. Nevertheless, some studies claimed that children with a parent with MS were not more likely to have psychosocial problems compared with children without a parent with MS. A few studies indicated probable positive effects of parental MS, eg potentially increased social competence. Other investigated outcomes were children's coping skills, early childhood development, body image, and effects on education, and these were unaffected or only slightly affected by having a parent with MS. CONCLUSIONS: Having a parent with MS has a relevant effect on children. However, the heterogeneous nature and varying quality of the included studies limit the interpretability of these findings. Further research is needed to provide robust evidence.
 OBJECTIVE: The function of Th17 cells in the neuroinflammatory process in multiple sclerosis (MS) has been previously clarified. It has been suggested that Quercetin can influence MS due to a variety of anti-inflammatory effects. The present study aimed to examine in vitro immunomodulatory aspects of Quercetin Penta Acetate as a modified compound on Th17 cells of MS patients and also to compare its effects with Quercetin. MATERIALS AND METHODS: In this experimental study, peripheral blood mononuclear cell (PBMCs) were isolated and stained with CFSE then, half-maximal inhibitory concentration (IC(50)) values were determined using different doses and times for Quercetin Penta Acetate, and Methyl Prednisolone Acetate. Th17 cell proliferation was analyzed by flow cytometry and the expression levels of IL-17 and RORc genes were assessed by real-time polymerase chain reaction (PCR) method. RESULTS: The results showed that IL-17 gene expression was inhibited by Quercetin Penta Acetate (P=0.0081), but Quercetin Penta Acetate did not have a significant inhibitory effect on Th17 cells proliferation (P= 0.59) and RORc gene expression (P=0.1), compared to Quercetin. CONCLUSION: Taken together, our results showed some immunomodulatory aspects of Quercetin Penta Acetate on Th17 cells are more effective than Quercetin and it could be considered in the treatment of MS.
 OBJECTIVE: Multiple sclerosis (MS) is a debilitating inflammatory and neurodegenerative disease which commonly involves cognitive dysfunction. Magnetic resonance imaging (MRI) studies have shown that patients with MS (pwMS) have diffuse patterns of brain atrophy, however, the relationship between the presentation of cognitive dysfunction and brain tissue loss remains understudied. Given the integral function of thalamus as a central nervous system relay center and its involvement in various brain circuits, thalamic atrophy may play a key role in the development and progression of cognitive dysfunction. The purpose of this study is to examine the relationship between cognitive impairment in pwMS and thalamic atrophy. METHODS: A total of 121 pwMS who had neuropsychological testing and quantitative MRI within 1 year of each were retrospectively identified. Grouped LASSO linear regression with 10-fold cross validation was used to estimate each neuropsychological test score with thalamic volume as the focal predictor and all other demographic and MRI metrics as covariates. RESULTS: Rates of impairment ranged from 19% to 44%. Results showed notable associations between thalamic volume and Symbol Digit Modalities Test (β = 0.11), Brief Visuospatial Memory Test, delayed (β = 0.12), California Verbal Learning Test, delayed and total (β = 0.24 and β = 0.15 respectively), and Trail Making Test Part A (β = -0.01), after adjusting for covariates. CONCLUSIONS: These findings demonstrate an independent association between thalamic volumes and processing speed and memory performance, after accounting for demographic, clinical, and other MRI variables, among pwMS.

 BACKGROUND: Due to the invariably progressive nature of multiple sclerosis (MS) and the high economic burden of chronic diseases, this study was performed to estimate the economic burden of MS medications in Iran. METHODS: The present research is a descriptive study performed using comprehensive national data of Iran's Health Insurance Organization (IHIO). The timeframe for study was 2011-2019. In order to calculate the economic burden of MS medications, the cost of illness (COI) method based on the prevalence approach was used. In this study, economic burden estimation was performed according to available data on medication costs. Data mining was also used to perform different stages of study. RESULTS: The number of patients receiving MS medications covered by IHIO has increased from 19,367 in 2011 to 50,642 in 2019. The economic burden of MS medications of patients covered by the IHIO increased from $81 million to $96 million between 2011 and 2019, respectively. Among the 9 medications studied, Interferon accounted for a very high share of costs in all years. The cost per patient receiving medication has also increased from $7,000 in 2011 to $18,000 in 2019. CONCLUSION: Calculations of the economic burden of MS medications in Iran showed an upward trend during the 9 years of the study, which due to the increasing number of patients in Iran, the arrival of new medications and also the increase in prices.
 Neurodegenerative diseases, featured by progressive loss of structure or function of neurons, are considered incurable at present. Movement disorders like tremor and postural instability, cognitive or behavioral disorders such as memory impairment are the most common symptoms of them and the growing patient population of neurodegenerative diseases poses a serious threat to public health and a burden on economic development. Hence, it is vital to prevent the occurrence of the diseases and delay their progress. Vitamin D can be transformed into a hormone in vivo with both genomic and non-genomic actions, exerting diverse physiological effects. Cumulative evidence indicates that vitamin D can ameliorate neurodegeneration by regulating pertinent molecules and signaling pathways including maintaining Ca(2+) homeostasis, reducing oxidative stress, inhibiting inflammation, suppressing the formation and aggregation of the pathogenic protein, etc. This review updates discoveries of molecular mechanisms underlying biological functions of vitamin D in neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and vascular dementia. Clinical trials investigating the influence of vitamin D supplementation in patients with neurodegenerative diseases are also summarized. The synthesized information will probably provoke an enhanced understanding of the neuroprotective roles of vitamin D in the nervous system and provide therapeutic options for patients with neurodegenerative diseases in the future.
 BACKGROUND: Patients with multiple sclerosis (MS) often experience balance issues during physical activities. Traditional rehabilitation exercises such as stretching, resistance, and aerobic training have been found to be effective, but can be repetitive and tedious, leading to reduced patient motivation and adherence. Furthermore, direct supervision by a therapist is not always possible. METHODS: The aim of this study was to develop and evaluate the effectiveness of a virtual training program incorporating visual feedback from the Kinect® sensor in male patients with multiple sclerosis. Forty-five participants, with an age range of 22-56 years (mean age = 39), were randomly assigned to one of three equal groups, including two experimental groups and one control group. The experimental groups participated in eight-week exercise interventions, with each session lasting 20 to 30 min and occurring three times per week. In contrast, the control group received no interventions. Within the experimental groups, one was exposed to conventional balance exercises, whereas the other engaged in the proposed virtual training program. Both of these groups undertook three balance exercises, namely the single-foot stance, lunge maneuvers, and arm/leg stretching routines. The assessment encompassed diverse facets of balance, including parameters of 10 Meter Walk Time, Berg Balance Scale, Static Balance Score, and Time-Up and Go Scale, as well as the quality of life, gauged through the Multiple Sclerosis Quality of Life (MSQOL)-54 Questionnaire. The effect of test variables was investigated using analysis of covariance (ANCOVA), while the independent samples t-test was used to check for significant differences among the groups. The effects of the groups were compared using a paired samples t-test. RESULTS: The findings revealed that both rehabilitation programs positively affected the dependent variables compared to the control group. However, the significant difference between the pre-test and post-test scores of the experimental groups indicated the effectiveness of the proposed program compared to the traditional method. CONCLUSIONS: Entertaining virtual training programs utilizing visual feedback can be effective for rehabilitating patients with MS. The proposed method enables patients to perform rehabilitation exercises at home with high motivation, while accurate information about the treatment process are provided to the therapist.
 PURPOSE: Despite typically more pronounced cognitive and mental health issues in progressive disease courses of multiple sclerosis (PMS), rehabilitation research in this subgroup is rare. The efficacy of two non-pharmacological interventions with positive results from prior investigations was therefore examined in PMS specifically. METHODS: Persons with PMS (pwPMS) received either computerized cognitive training (BrainStim), standardized cognitive-behavioral group sessions (Metacognitive Training [MaTiMS]), or a combination of both in an ambulatory setting. Neuropsychological assessment was conducted before and after the four-week intervention. RESULTS: 37 participants (13 with primary/24 with secondary PMS, mean(age) = 52.87, SD(age) = 7.11, mean(EDSS) = 4.02, SD(EDSS) = 1.35) entered analyses. The BrainStim group improved in immediate and delayed verbal memory, recognition, verbal working memory, and perceived cognitive deficits while experiencing increased anxiety post-intervention. MaTiMS participants reported high program satisfaction and less cognitive difficulties at retest. The Combination group performed better in immediate and delayed verbal memory, and in information processing speed after training. Descriptive data further indicated positive effects on anxiety and depression in the MaTiMS and Combination group. CONCLUSIONS: While objective cognitive performance improved when explicitly trained, psychoeducative sessions contributed to subjective mental health. The combination of both approaches is thus suggested, considering the specific needs of pwPMS treated in an ambulatory setting.
 BACKGROUND AND PURPOSE: Sarcoidosis is a granulomatous disease of unknown etiology affecting the central nervous system in up to 15% of the patients. Diagnosis of neurosarcoidosis is very challenging due to the heterogeneity of its clinical manifestation. This study intended to evaluate the distribution of cerebral lesion sites and the potential presence of specific lesion clusters in neurosarcoidosis patients using voxel-based lesion symptom mapping (VLSM). METHODS: Patients with neurosarcoidosis were retrospectively identified and included between 2011 and 2022. Cerebral lesion sites were correlated voxel-wise with presence and absence of neurosarcoidosis using non-parametric permutation test. Multiple sclerosis patients served as controls for the VLSM-analysis. RESULTS: Thirty-four patients (mean age 52 ± 15 years) of whom 13 were diagnosed with possible, 19 with probable and 2 with confirmed neurosarcoidosis were identified. Lesion overlap of neurosarcoidosis patients demonstrated a distribution of white matter lesions in all brain areas, with a periventricular predilection similar to multiple sclerosis. In contrast to multiple sclerosis controls, no propensity for lesions in proximity of the corpus callosum was observed. Neurosarcoidosis lesions appeared smaller and lesion volume was lower in the neurosarcoidosis cohort. The VLSM analysis showed minor associations between neurosarcoidosis and damaged voxels in the bilateral frontobasal cortex. CONCLUSIONS: The VLSM analysis yielded significant associations in the bilateral frontal cortex, suggesting that leptomeningeal inflammatory disease with following cortical involvement is a quite specific feature in neurosarcoidosis. Lesion load was lower in neurosarcoidosis than in multiple sclerosis. However, no specific pattern of subcortical white matter lesions in neurosarcoidosis was revealed.
 OBJECTIVES: When a married family member suffers from multiple sclerosis (MS), the collective physical and psychosocial well-being of the family is impacted and much of the burden is on the healthier spouse. The purpose of the present study was to determine the contribution of psychosocial support from spouses, friends, and others in overall family functioning in respect of Iranian patients with MS, considering the mediating role of spiritual experiences and moral foundations. METHODS: Spouses of patients with MS were chosen through the judgmental sampling method. The research instruments comprised the Family Assessment Device, Social Support Appraisals Scale, Daily Spiritual Experience Scale, and Moral Foundations Questionnaire. Data analysis was done through the path analysis technique. RESULTS: The subjects comprised 220 spouses of MS patients. We found a significant relationship between family support path and overall functioning mediated by the variable 'spiritual experiences', the root mean square error of approximation (RMSEA) value being < 0.001. Similarly, the relationship between spiritual experiences and moral foundations had a significant effect on overall family functioning (RMSEA < 0.001). After eliminating insignificant relationships and estimating fit indicators, the modified (adjusted) model indicated goodness of fit with data. CONCLUSIONS: This study found, for the first time in the Iranian community, a significant effect of family support focused on spouses of MS patients compared to the support from friends and others, with regard to family functioning. The mediating roles of spiritual experiences and moral foundations were confirmed. Further studies are suggested to delve into the role of family support for MS patients in developing countries.
 BACKGROUND: Multiple Sclerosis lesions in the brain and spinal cord can lead to different symptoms, including cognitive and mood changes. In this study we explore the temporal relationship between early microstructural changes in subcortical volumes and cognitive and emotional function in a longitudinal cohort study of patients with relapsing-remitting Multiple Sclerosis. METHODS: In vivo imaging in forty-six patients with relapsing-remitting Multiple Sclerosis was performed annually over 3 years magnetic resonance imaging. Microstructural changes were estimated in subcortical structures using the free water fraction, a diffusion-based MRI metric. In parallel, patients were assessed with the Hospital Anxiety and Depression Scale amongst other tests. Predictive structural equation modeling was set up to further explore the relationship between imaging and the assessment scores. In a general linear model analysis, the cohort was split into patients with higher and lower depression scores. RESULTS: Nearly all subcortical diffusion microstructure estimates at the baseline visit correlate with the depression score at the 2 years follow-up. The predictive nature of baseline free water estimates and depression subscores after 2 years are confirmed in the predictive structural equation modeling analysis with the thalamus showing the greatest effect size. The general linear model analysis shows patterns of MRI free water differences in the thalamus and amygdala/hippocampus area between participants with high and low depression score. CONCLUSIONS: Our data suggests a relationship between higher levels of free-water in the subcortical structures in an early stage of Multiple Sclerosis and depression symptoms at a later stage of the disease.
 Multiple Sclerosis (MS) is a chronic demyelinating and neurodegenerative disease of the central nervous system, with a variety of symptoms and uncertain course. It affects multiple facets of everyday life and since it results to some degree of disability, MS may cause deterioration of quality of life, both in mental and physical health. In this study, we investigated the role of demographic, clinical and, mostly, personal and psychological factors related to physical health quality of life (PHQOL). Our sample consisted of 90 patients with definite MS and the instruments used were: MSQoL-54 for PHQOL, DSQ-88 and LSI for the assessment of defense styles and mechanisms, BDI-II for depression, STAI for anxiety, SOC-29 as a measure of sense of coherence and FES for family relations. Important personality factors affecting PHQOL were the maladaptive and the self-sacrificing defense styles, the defense mechanisms of displacement and reaction formation, sense of coherence, while from the family environment, conflict affected PHQOL negatively and expressiveness positively. However, in the regression analysis none of these factors were found to be important. Multiple regression analysis showed the major impact of depression in PHQOL (negative correlation. Moreover, the fact that a person receives disability allowance, the number of the children, disability status and the event of a relapse in the current year, were also important negative factors for PHQOL. After a step-wise analysis, in which BDI and employment status were excluded, the most important variables were EDSS, SOC and relapse during the past year. This study confirms the hypothesis that psychological parameters play an important role in PHQOL and highlights the importance of the assessment of every PwMS by mental health professionals, as a routine. Not only psychiatric symptoms but also psychological parameters should be searched out in order to determine in which way each individual adjusts to the illness, thus impacting his PHQOL. As a result, targeted interventions, in personal or group level, or even in the family may enhance their QOL.
 Objective: The aim of this study was to evaluate the association between changes in the autonomic control of cardiorespiratory system induced by walk tests and outcome measures in people with Multiple Sclerosis (pwMS). Methods: Electrocardiogram (ECG) recordings of 148 people with Relapsing-Remitting MS (RRMS) and 58 with Secondary Progressive MS (SPMS) were acquired using a wearable device before, during, and after walk test performance from a total of 386 periodical clinical visits. A subset of 90 participants repeated a walk test at home. Various MS-related symptoms, including fatigue, disability, and walking capacity were evaluated at each clinical visit, while heart rate variability (HRV) and ECG-derived respiration (EDR) were analyzed to assess autonomic nervous system (ANS) function. Statistical tests were conducted to assess differences in ANS control between pwMS grouped based on the phenotype or the severity of MS-related symptoms. Furthermore, correlation coefficients (r) were calculated to assess the association between the most significant ANS parameters and MS-outcome measures. Results: People with SPMS, compared to RRMS, reached higher mean heart rate (HRM) values during walk test, and larger sympathovagal balance after test performance. Furthermore, pwMS who were able to adjust their HRM and ventilatory values, such as respiratory rate and standard deviation of the ECG-derived respiration, were associated with better clinical outcomes. Correlation analyses showed weak associations between ANS parameters and clinical outcomes when the Multiple Sclerosis phenotype is not taken into account. Blunted autonomic response, in particular HRM reactivity, was related with worse walking capacity, yielding r = 0.36 r = 0.29 (RRMS) and r > 0.5 (SPMS). A positive strong correlation r > 0.7 r > 0.65 between cardiorespiratory parameters derived at hospital and at home was also found. Conclusion: Autonomic function, as measured by HRV, differs according to MS phenotype. Autonomic response to walk tests may be useful for assessing clinical outcomes, mainly in the progressive stage of MS. Participants with larger changes in HRM are able to walk longer distance, while reduced ventilatory function during and after walk test performance is associated with higher fatigue and disability severity scores. Monitoring of disorder severity could also be feasible using ECG-derived cardiac and respiratory parameters recorded with a wearable device at home.
 Purpose: The aim of this study was to assess the reliability and validity of the Arabic version of the patient-specific functional scale (PSFS-Ar) in patients with multiple sclerosis (MS) disorder. Materials and Methods: Reliability and validity were examined in patients with multiple sclerosis using a longitudinal cohort study design. One hundred (N = 100) patients with MS were recruited to examine the PSFS-Ar, test-retest reliability (using the interclass correlation coefficient model 2,1 (ICC(2,1))), construct validity (using the hypothesis testing method), and floor-ceiling effect. Results: A total of 100 participants completed the PSFS-Ar (34% male, 66% female). The PSFS-Ar showed an excellent test-retest reliability score (ICC(2,1) = 0.87; 95% confidence interval, 0.75-0.93). The SEM of the PSFS-Ar was 0.80, while the MDC(95) was 1.87, indicating an acceptable measurement error. The construct validity of the PSFS-Ar was 100% correlated with the predefined hypotheses. As hypothesized, the correlation analysis revealed positive correlations between the PSFS-Ar and the RAND-36 domains of physical functioning (0.5), role limitations due to physical health problems (0.37), energy/fatigue (0.35), and emotional well-being (0.19). There was no floor or ceiling effect in this study. Conclusions: The study results showed that the PSFS-Ar is a self-reported outcome measure that is useful for detecting specific functional difficulties in patients with multiple sclerosis. Patients are able to express and report a variety of functional limitations easily and effectively, as well as to measure their response to physical therapy. The PSFS-Ar is, therefore, recommended for use in Arabic-speaking countries for clinical practice and research for patients with multiple sclerosis.
 INTRODUCTION: Increasingly, dietary improvements have been shown to have positive associations with health outcomes in people with multiple sclerosis (pwMS). However, adhering to a MS-specific or high-quality diet may be a challenge. We therefore assessed the level of diet-adherence necessary to improve health outcomes of depression, fatigue, and disability. METHODS: Data from an international population of pwMS followed over 7.5 years (n = 671) were analyzed. Self-reported diet quality via diet habits questionnaire (DHQ), and adherence to six MS-diets [Ashton Embry Best Bet, McDougall, Overcoming MS (OMS), Paleolithic (Paleo), Swank, and Wahls] were queried at two timepoints. Four levels of diet adherence were assessed: non-adherence at either timepoint; ceased at second timepoint; commenced at second timepoint; and ongoing at both timepoints. Associations between adherence to OMS and high-quality diet (DHQ score > median) with depression, fatigue, and disability, were assessed by log-binomial regression models adjusted for confounders. RESULTS: Forty-two percent of pwMS reported ongoing-adherence to a MS-diet at both timepoints, OMS (33%), Swank (4%), Wahls (1.5%), other (<1%). Of these, only OMS-diet adherence was analyzed for associations due to data availability. Ongoing-adherence to the OMS-diet or a high-quality diet, was associated with lower depression compared to non-adherence [OMS: Risk ratios (RR) = 0.80, p = 0.021; DHQ: RR = 0.78, p = 0.009] and ceased-adherence (OMS: RR = 0.70, p = 0.008; DHQ: RR = 0.70, p = 0.010), respectively. Ongoing-adherence to OMS-diet was associated with lower fatigue (RR = 0.71, p = 0.031) and lower severe disability (RR = 0.43, p = 0.033) compared to ceased-adherence. CONCLUSION: Results suggest potential benefits of adherence to the OMS- or a high-quality diet on MS health outcomes, with ongoing-adherence likely best. Diet modification and maintenance may serve as a point of intervention to manage MS symptoms, especially depression, in pwMS.
 Magnetic resonance imaging (MRI) of focal or diffuse myelin damage or remyelination may provide important insights into disease progression and potential treatment efficacy in multiple sclerosis (MS). We performed post-mortem MRI and histopathological myelin measurements in seven progressive MS cases to evaluate the ability of three myelin-sensitive MRI scans to distinguish different stages of MS pathology, particularly chronic demyelinated and remyelinated lesions. At 3 Tesla, we acquired two different myelin water imaging (MWI) scans and magnetisation transfer ratio (MTR) data. Histopathology included histochemical stainings for myelin phospholipids (LFB) and iron as well as immunohistochemistry for myelin proteolipid protein (PLP), CD68 (phagocytosing microglia/macrophages) and BCAS1 (remyelinating oligodendrocytes). Mixed-effects modelling determined which histopathological metric best predicted MWF and MTR in normal-appearing and diffusely abnormal white matter, active/inactive, inactive, remyelinated and ischemic lesions. Both MWI measures correlated well with each other and histology across regions, reflecting the different stages of MS pathology. MTR data showed a considerable influence of components other than myelin and a strong dependency on tissue storage duration. Both MRI and histology revealed increased myelin densities in inactive compared with active/inactive lesions. Chronic inactive lesions harboured single scattered myelin fibres indicative of low-level remyelination. Mixed-effects modelling showed that smaller differences between white matter areas were linked to PLP densities and only to a small extent confounded by iron. MWI reflects differences in myelin lipids and proteins across various levels of myelin densities encountered in MS, including low-level remyelination in chronic inactive lesions.
 BACKGROUND: cladribine tablets is a highly effective option for the treatment of relapsing-remitting multiple sclerosis (RRMS). OBJECTIVE: to evaluate the effectiveness of cladribine in a real-world setting. METHODS: this prospective real-world study consecutively screened all RRMS patients from seven different MS centers in Sicily (Italy), who completed the 2-year treatment course of cladribine tablets in the period between 11th March 2019 and 31st October 2021. Data about Expanded Disability Status Scale (EDSS), relapses, previous treatments, adverse events (AEs) and magnetic resonance imaging (MRI) were collected. Patients who were previously treated with other DMTs were further stratified in moderately active treatment (MAT) and highly active treatment (HAT) patients. RESULTS: a total of 217 patients, (70% women, with mean age of 38.4 ± 11.3 years), were enrolled. Fifty patients (23.0%) were naïve to treatment and 167 (77%) switched from another disease modifying therapies. After the second year of treatment, about 80% of were EDSS progression free, 88% remained relapse-free at T24, and 48% of patients were MRI activity-free. Kaplan Meier analyses showed significant differences between MT and HAT in terms of time to first clinical relapse (HR: 2.43, IC 1.02 - 5.76; p=0.04), time to the first new T1-gadolinium enhancing lesion (HR: 3.43, IC 1.35 - 8.70; p= 0.009) and time to MRI worsening (HR: 2.42, IC 1.15 - 5.09; p= 0.02). CONCLUSION: this study confirmed that cladribine is an effective treatment for MS, in particular in naïve patients and in those who have switched from MATs.
 Multiple sclerosis (MS) is a chronic inflammatory disease that damages the myelin sheath around the axons of the central nervous system. While there are periods of inflammation and remyelination in MS, the latter can sometimes be insufficient and lead to the formation of lesions in the brain and spinal cord. Environmental factors such as vitamin D deficiency, viral or bacterial infections, tobacco smoking, and anxiety have been shown to play a role in the development of MS. Dysbiosis, where the composition of the microbiome changes, may also be involved in the pathogenesis of MS by affecting the gut's microbial population and negatively impacting the integrity of the epithelia. While the cause of MS remains unknown, genetic susceptibility, and immunological dysregulation are believed to play a key role in the development of the disease. Further research is needed to fully understand the complex interplay between genetic, environmental, and microbial factors in the pathogenesis of MS.
 BACKGROUND: Urinary incontinence (UI) and fecal incontinence (FI) are challenging manifestations of multiple sclerosis (MS) that have historically been treated with limited success. Sacral neuromodulation (SNM) has provided successful resolution of UI and FI in the general population and in patients with neurologic conditions, including MS. We report on 6 patients with MS-related incontinence treated successfully with SNM and review the literature. METHODS: Medical records were reviewed retrospectively to identify patients with MS seeking treatment for incontinence. Six patients were identified, and each is presented with follow-up assessment of the severity of UI or FI. RESULTS: All 6 individuals with MS had severe incontinence that had been refractory to therapies that included medications and pelvic floor physical therapy. Five patients reported severe UI and 2 patients reported severe FI. Each patient was successfully treated with SNM, with large reductions of incontinence scores and improved quality of life. CONCLUSIONS: In this case series, SNM was effective as a treatment for UI and FI among patients with MS. These findings confirm other published series that have reported the success of SNM in patients with MS with incontinence. Sacral neuromodulation should be considered as a potential treatment option for patients with MS and UI and/or FI.
 Cladribine tablets (Mavenclad(®)) were approved by the European Union in 2017 as high-efficacy therapy for highly active relapsing-remitting multiple sclerosis. In Israel, Mavenclad(®) was approved in 2018. Real-life experience has confirmed the efficacy of cladribine tablets over at least 4 years from the initial course. During the last years, several questions were raised concerning the management of people with MS who show disease activity during years 3 and 4 post-cladribine initiation and what treatment decisions are needed beyond year 4. A few expert boards have tried to provide insight based on research data and to suggest recommendations on the therapeutic dilemmas and treatment decisions with cladribine. However, there is currently no widely accepted consensus about these issues. The vast clinical experience gained in Israel in the past 5 years in several MS centers across the country allows for a broad perspective of the outcomes with long-term cladribine use. This article summarizes previously published recent recommendations and describes the insights of Israeli neurology key opinion leaders that convened for an advisory board meeting on January 29th, 2023, with the aim of reaching a consensus regarding cladribine long-term treatment and follow-up.
 Objective: The objective of the current study is to investigate how Big Five personality traits could predict the risk of multiple sclerosis (MS) diagnosis in 7 years. Methods: A binary logistic regression was used to analyze data from 17,791 participants who responded to questions at Wave 3 (collected between 2011 to 2012) and Wave 10 (collected between 2018 to 2019) using a binary logistic regression from UKHLS with a mean age of 47.01 (S.D. = 16.31) years old with 42.62% males. Results: The current study found that Openness (OR = 0.68, p < 0.01, 95% C.I. (0.51, 0.89)) and Conscientiousness (OR = 0.70, p < 0.05, 95% C.I. (0.52, 0.93)) are positively associated with a reduced risk of MS diagnosis in 7 years. Conclusion: Health professionals can use findings from the current study as evidence for developing tools for assessing the risk of MS, and providing interventions for people who may be at high risk of MS based on their personality traits.
 BACKGROUND: In patients with multiple sclerosis (MS), relapses and disability progression have been associated with decreased health-related quality of life (HRQoL). METHODS: PROTYS, a prospective, multicentre, single-arm, observational study in seven Swiss MS centres, evaluated correlations between change in disability status (measured through the Expanded Disability Status Scale (EDSS)) and HRQoL changes (measured through the global Multiple Sclerosis International Quality of Life (MusiQoL) index questionnaire) in 35 patients with relapsing remitting MS on natalizumab for 1 year. In addition, several other scales were also used, such as: Multiple Sclerosis Intimacy and Sexuality Questionnaire-19, EuroQoL-5 Dimension, and Fatigue Scale of Motor and Cognitive Function. A post hoc analysis further assessed the association between HRQoL changes after 1 year and the MusiQoL subscores and other patient-reported outcome (PRO) measures. RESULTS: At 1 year, patients were categorised into 'EDSS improved' (6/35), 'EDSS stable' (28/35) and 'EDSS worsened' (1/35). Mean disability scores decreased for 'EDSS improved' and 'EDSS stable' but increased for 'EDSS worsened'. Mean MusiQoL index score for 'EDSS improved' increased from 61.2 at baseline to 66.3 at 1 year, while the 'EDSS stable' group increased from 67.9 to 70.8. No meaningful statistical relationship was observed between EDSS group and changes in MusiQoL score. For the post hoc analysis, patients were categorised in 'MusiQoL improved' (n=21) and 'MusiQoL worsened' (n=14) groups. MusiQoL subscores for 'symptoms,' 'psychological well-being' and 'activities of daily living', as well as scores for several related PRO measures, correlated with improvement of the MusiQoL global index. There was no correlation between the changes in MusiQoL global index and EDSS score. CONCLUSIONS: Natalizumab treatment for 1 year resulted in either improved or stable EDSS status in most patients, and although no significant relationship was observed between global HRQoL change and EDSS change, several domains of HRQoL seemed to improve with natalizumab treatment. TRIAL REGISTRATION NUMBER: NCT02386566.
 Ferroptosis is an iron- and lipid peroxidation (LPO)-mediated programmed cell death type. Recently, mounting evidence has indicated the involvement of ferroptosis in neurodegenerative diseases, especially in Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and so on. Treating ferroptosis presents opportunities as well as challenges for neurodegenerative diseases. This review provides a comprehensive overview of typical features of ferroptosis and the underlying mechanisms that contribute to its occurrence, as well as their implications in the pathogenesis and advancement of major neurodegenerative disorders. Meanwhile, we summarize the utilization of ferroptosis inhibition in both experimental and clinical approaches for the treatment of major neurodegenerative disorders. In addition, we specifically summarize recent advances in developing therapeutic means targeting ferroptosis in these diseases, which may guide future approaches for the effective management of these devastating medical conditions.
 BACKGROUND: Multiple sclerosis (MS) is an immune-mediated disease that has been related to several risk factors such as various viral infections. We carried out this study in order to establish a relationship between COVID-19 infection and MS severity. METHODS: In a case-control study, we recruited patients with relapsing-remitting multiple sclerosis (RRMS). Patients were divided into two groups based on positive COVID-19 PCR at the end of the enrollment phase. Each patient was prospectively followed for 12 months. Demographical, clinical, and past medical history were collected during routine clinical practice. Assessments were performed every six months; MRI was performed at enrollment and 12 months later. RESULTS: Three hundred and sixty-two patients participated in this study. MS patients with COVID-19 infection had significantly higher increases in the number of MRI lesions (p: 0.019, OR(CI): 6.37(1.54-26.34)) and EDSS scores (p: 0.017), but no difference was found in total annual relapses or relapse rates. COVID-19 infections were positively correlated with EDSS progression (p: 0.02) and the number of new MRI lesions (p: 0.004) and predicted the likelihood of the number of new MRI lesions by an odds of 5.92 (p: 0.018). CONCLUSION: COVID-19 may lead to higher disability scores in the RRMS population and is associated with developing new Gd-enhancing lesions in MRI imaging. However, no difference was observed between the groups regarding the number of relapses during follow-up.
 In multiple sclerosis (MS), activation of the astrocytes and microglia induces a cascading inflammatory response. Overexpression of the aquaporin 4 (AQP4) in the glia is a trigger for this reaction. This study aimed to block AQP4 by injecting TGN020 to alleviate the symptoms of MS. Total of 30 male mice were randomly divided into control (intact), cuprizone model of MS (fed with 0.2% cuprizone for 35 days), and TGN020-treated (received daily intraperitoneal injections of 200 mg/kg TGN020 with cuprizone intake) groups. Astrogliosis, M1-M2 microglia polarization, NLRP3 inflammasome activation, and demyelination were investigated in the corpus callosum by immunohistochemistry, real-time PCR, western blot, and luxol fast blue staining. The Rotarod test was performed for a behavior assessment. AQP4 inhibition caused a significant decrease in the expression of the astrocyte-specific marker, GFAP. It also changed the microglia polarization from M1 to M2 indicated by a significant downregulation of iNOS, CD86, MHC-ІІ, and upregulation of arginase1, CD206, and TREM-2. In addition, western blot data showed a significant decrease in the NLRP3, caspase1, and IL-1b proteins in the treatment group, which indicated inflammasome inactivation. The molecular changes following the TGN020 injection resulted in remyelination and motor recovery enhancement in the treatment group. In conclusion, the results draw the attention to the role of AQP4 in the cuprizone model of MS.

 Neurodegenerative disorders are characterized by the progressive dysfunction and death of selectively vulnerable neuronal populations, often associated with the accumulation of aggregated host proteins. Sustained brain inflammation and hyperactivation of inflammasome complexes have been increasingly demonstrated to contribute to neurodegenerative disease progression. Here, we review molecular mechanisms leading to inflammasome assembly in neurodegeneration. We focus primarily on four degenerative brain disorders in which inflammasome hyperactivation has been well documented: Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and the spectrum of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). We discuss shared and divergent principles of inflammasome assembly across these disorders, and underscore the differences between neurodegeneration-associated inflammasome activation pathways and their peripheral-immune counterparts. We examine how aberrant assembly of inflammasome complexes may amplify pathology in neurodegeneration, including misfolded protein aggregation, and highlight prospects for neurotherapeutic interventions based on targeting inflammasome pathways.
 BACKGROUND: A growing body of evidence has been paid to the cognitive impairment in patients with multiple sclerosis (MS). However, studies concerning cognitive functions in MS have also yielded conflicting results. This study investigates the attention and inhibitory control functions in patients with MS and their relationship with other clinical features, such as depression and fatigue in these patients. METHODS: Participants included 80 patients with MS and 60 healthy controls. The attention and inhibitory control, fatigue, and psychiatric screening in all subjects were studied, respectively with the Integrated Visual and Auditory Continuous Performance Test (IVA-CPT), Fatigue Severity Scale (FSS), and the Hospital Anxiety and Depression Scale (HADS). RESULTS: Patients with MS performed the IVA-CPT task more poorly than the healthy control group (p < 0.001). However, multiple regression analysis did not show any significant relationship between disease duration, FSS, and HADS on attention and inhibitory control. CONCLUSION: Inhibitory control and attention are significantly impaired in patients with MS. Finding the basics of cognitive deficits in MS have potentially important clinical implications for developing better cognitive rehabilitation strategies.

 Multiple sclerosis is an autoimmune disease of the central nervous system. Yet, the autoimmune targets are still undefined. The extracellular e1 sequence of KCNJ10, the inwardly rectifying potassium channel 4.1, has been subject to fierce debate for its role as a candidate autoantigen in multiple sclerosis. Inwardly rectifying potassium channel 4.1 is expressed in the central nervous system but also in peripheral tissues, raising concerns about the central nervous system-specificity of such autoreactivity. Immunization of C57Bl6/J female mice with the e1 peptide (amino acids 83-120 of Kir4.1) induced anti-e1 immunoglobulin G- and T-cell responses and promoted demyelinating encephalomyelitis with B cell central nervous system enrichment in leptomeninges and T cells/macrophages in central nervous system parenchyma from forebrain to spinal cord, mostly in the white matter. Within our cohort of multiple sclerosis patients (n = 252), 6% exhibited high anti-e1 immunoglobulin G levels in serum as compared to 0.7% in the control cohort (n = 127; P = 0.015). Immunolabelling of inwardly rectifying potassium channel 4.1-expressing white matter glia with the anti-e1 serum from immunized mice increased during murine autoimmune neuroinflammation and in multiple sclerosis white matter as compared with controls. Strikingly, the mouse and human anti-e1 sera labelled astrocytoma cells when N-glycosylation was blocked with tunicamycin. Western blot confirmed that neuroinflammation induces Kir4.1 expression, including its shorter aglycosylated form in murine experimental autoencephalomyelitis and multiple sclerosis. In addition, recognition of inwardly rectifying potassium channel 4.1 using mouse anti-e1 serum in Western blot experiments under unreduced conditions or in cells transfected with the N-glycosylation defective N104Q mutant as compared to the wild type further suggests that autoantibodies target an e1 conformational epitope in its aglycosylated form. These data highlight the e1 sequence of inwardly rectifying potassium channel 4.1 as a valid central nervous system autoantigen with a disease/tissue-specific post-translational antigen modification as potential contributor to autoimmunity in some multiple sclerosis patients.
 BACKGROUND: This is an open-label, single-arm, single-center pilot study using 7-Tesla in vivo proton magnetic resonance spectroscopy ((1)H MRS) to measure brain cortical glutathione concentration at baseline before and during the use of oral fumarates as a disease-modifying therapy for multiple sclerosis. The primary endpoint of this research was the change in prefrontal cortex glutathione concentration relative to a therapy-naïve baseline after one year of oral fumarate therapy. METHODS: Brain glutathione concentrations were examined by (1)H MRS in single prefrontal and occipital cortex cubic voxels (2.5 × 2.5 × 2.5 cm(3)) before and during initiation of oral fumarate therapy (120 mg b.i.d. for 7 days and 240 mg b.i.d. thereafter). Additional measurements of related metabolites glutamate, glutamine, myoinositol, total N-acetyl aspartate, and total choline were also acquired in voxels centered on the same regions. Seven relapsing-remitting multiple sclerosis patients (4 f / 3 m, age range 28-50 years, mean age 40 years) naïve to fumarate therapy were scanned at pre-therapy baseline and after 1, 3, 6 and 12 months of therapy. A group of 8 healthy volunteers (4 f / 4 m, age range 33-48 years, mean age 41 years) was also scanned at baseline and Month 6 to characterize (1)H-MRS measurement reproducibility over a comparable time frame. RESULTS: In the multiple sclerosis cohort, general linear models demonstrated a significant positive linear relationship between prefrontal glutathione and time either linearly across all time points (+0.05 ± 0.02 mM/month, t(27) = 2.6, p = 0.02) or specifically for factor variable Month 12 (+0.6 ± 0.3 mM/12 months, t(24) = 2.2, p = 0.04) relative to baseline. No such effects of time on glutathione concentration were demonstrated in the occipital cortex or in the healthy volunteer group. Changes in occipital total choline were further observed in the multiple sclerosis cohort as well as prefrontal total choline and occipital glutamine and myoinositol in the control cohort throughout the study duration. CONCLUSIONS: While the open-label single-arm pilot study design and abbreviated control series cannot support firm conclusions about the influence of oral fumarate therapy independent of test-retest factors or normal biological variation in a state of either health or disease, these results do justify further investigation at a larger scale into the potential relationship between prefrontal cortex glutathione increases and oral fumarate therapy in relapsing-remitting multiple sclerosis.
 Multiple sclerosis and the major sporadic neurogenerative disorders, amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer disease are considered to have both genetic and environmental components. Advances have been made in finding genetic predispositions to these disorders, but it has been difficult to pin down environmental agents that trigger them. Environmental toxic metals have been implicated in neurological disorders, since human exposure to toxic metals is common from anthropogenic and natural sources, and toxic metals have damaging properties that are suspected to underlie many of these disorders. Questions remain, however, as to how toxic metals enter the nervous system, if one or combinations of metals are sufficient to precipitate disease, and how toxic metal exposure results in different patterns of neuronal and white matter loss. The hypothesis presented here is that damage to selective locus ceruleus neurons from toxic metals causes dysfunction of the blood-brain barrier. This allows circulating toxicants to enter astrocytes, from where they are transferred to, and damage, oligodendrocytes, and neurons. The type of neurological disorder that arises depends on (i) which locus ceruleus neurons are damaged, (ii) genetic variants that give rise to susceptibility to toxic metal uptake, cytotoxicity, or clearance, (iii) the age, frequency, and duration of toxicant exposure, and (iv) the uptake of various mixtures of toxic metals. Evidence supporting this hypothesis is presented, concentrating on studies that have examined the distribution of toxic metals in the human nervous system. Clinicopathological features shared between neurological disorders are listed that can be linked to toxic metals. Details are provided on how the hypothesis applies to multiple sclerosis and the major neurodegenerative disorders. Further avenues to explore the toxic metal hypothesis for neurological disorders are suggested. In conclusion, environmental toxic metals may play a part in several common neurological disorders. While further evidence to support this hypothesis is needed, to protect the nervous system it would be prudent to take steps to reduce environmental toxic metal pollution from industrial, mining, and manufacturing sources, and from the burning of fossil fuels.
 BACKGROUND: We aimed to determine the proportion of highly active multiple sclerosis patients under high-efficacy therapies (HETs) achieve no evidence of disease activity-3 (NEDA-3) at 1 and 2 years, and to identify factors associated with failing to meet no evidence of disease activity 3 at 2 years. METHODS: This retrospective cohort study based on Argentina Multiple Sclerosis patient registry (RelevarEM), includes highly active multiple sclerosis patients who received HETs. RESULTS: In total, 254 (78.51%) achieved NEDA-3 at year 1 and 220 (68.12%) achieved NEDA-3 at year 2. Patients who achieved NEDA-3 at 2 years had a shorter duration of multiple sclerosis (p < 0.01) and a shorter time between first treatment and current treatment (p = 0.01). Early high-efficacy strategy patients reached NEDA-3 more frequently (p < 0.01). Being a naïve patient (odds ratio: 3.78, 95% confidence interval 1.50-9.86, p < 0.01) was an independent predictor to reach NEDA-3 at 2 years. No association was found between type of HETs and NEDA-3 at 2 years when adjusted for potential confounders (odds ratio: 1.73; 95% confidence interval 0.51-6.06, p 0.57). CONCLUSION: We found a high proportion of patients who achieved NEDA-3 at 1 and 2 years. Early high-efficacy strategy patients had a higher probability of achieving NEDA-3 at 2 years.
 PURPOSE: This study examined the bivariate association between fatigue and depression symptoms and physical activity behavior in persons with multiple sclerosis (MS). METHODS: The sample of adults with MS completed the Fatigue Severity Scale (FSS) and the Hospital Anxiety and Depression Scale (HADS) and wore a waist mounted accelerometer during waking hours for 7 days. We categorized participants as having elevated fatigue and depression based on cut-points for the FSS (i.e., 4+ as indicative of severe fatigue) and the HADS (i.e., 8+ as indicative of elevated depressive symptoms). We used a two-way multivariate analysis of variance (MANOVA) to examine the contribution of fatigue and depression to volume and pattern of sedentary, light (LPA) and moderate-to-vigorous physical activity (MVPA). RESULTS: Results indicated no bivariate association between fatigue and depression and measures of physical activity behavior. The MANOVA indicated there was a significant association between fatigue and MVPA (F = 2.30, p = 0.032) and steps/day (F = 13.6, p < 0.001), independent of depression symptoms. There was no association between depression symptoms and physical activity behavior. CONCLUSIONS: This study demonstrated an interrelation between fatigue symptoms and MVPA and steps/day in MS, independent of depression symptoms, and this should be considered in the future design and delivery of physical activity interventions in MS.IMPLICATIONS FOR REHABILIATIONFatigue and depression are prevalent and burdensome symptoms of multiple sclerosis (MS).These symptoms can collectively worsen psychological and functional outcomes in MS.Fatigue symptoms may impact ambulatory physical activity to a greater degree than depression symptom status in persons with MS.Fatigue is an important consideration when designing behavior change interventions targeted at promoting physical activity in persons with MS.
 Autoimmune disorders (AIDs) are known to be associated with intracranial aneurysms; however, the coexistence of dual AIDs is a rare entity. Perioperative neuroanesthetic management of aneurysmal subarachnoid hemorrhage (aSAH) is typically complicated and challenging in such patients. In this report, we describe the successful management of a case of aSAH complicated by coexistent multiple sclerosis and systemic lupus erythematosus. A multidisciplinary team approach is warranted to manage such complicated cases.
 (1) Background: Multiple sclerosis (MS) is an auto-immune, chronic, neuroinflammatory, demyelinating disease that affects mainly young patients. This progressive inflammatory process causes the chronic loss of brain tissue and results in a deterioration in quality of life. To monitor neuroinflammatory process activity and predict the further development of disease, it is necessary to find a suitable biomarker that could easily be used. In this research, we verify the usability of choroid plexus (CP) volume, a new MS biomarker, in the monitoring of the progression of multiple sclerosis disease. (2) Methods: A single-center, prospective study with three groups of patients was conducted based on the following groups: MS patients who received experimental cellular therapy (Treg), treatment-naïve MS patients and healthy controls. (3) Results: This study concludes that there is a correlation between the CPV/TIV (choroid plexus/total intracranial volume) ratio and the progress of multiple sclerosis disease-patients with MS (MS + Treg) had larger volumes of choroid plexuses. CPV/TIV ratios in MS groups were constantly and significantly growing. In the Treg group, patients with relapses had larger plexuses in comparison to the group with no relapses of MS. A similar correlation was observed for the GD+ group (patients with postcontrast enhancing plaques) compared against the non-GD group (patients without postcontrast enhancing plaques). (4) Conclusion: Choroid plexus volume, due to its immunological function, correlates with the inflammatory process in the central nervous system. We consider it to become a valuable radiological biomarker of MS activity.
 INTRODUCTION: Multiple sclerosis (MS) is a progressive disease with a fluctuating and unpredictable course that has no curative treatment at present. One of its main characteristics is the variety of signs and symptoms that produce a high percentage of patients who present alterations in balance and gait during the development of the disease, decreased muscle strength, spasticity, or decreased pimax. Rehabilitative therapy, especially physiotherapy, is the main course of the treatment of these alterations using reflex locomotion and the Bobath concept as a form of kinesitherapy that activates the preorganized circuits of the central nervous system. OBJECTIVE: The objective of this study is to evaluate the reflex locomotion and Bobath concept effects on balance, spasticity, reaction time, respiratory parameters, and lacrimal biomolecular markers. METHODS AND ANALYSIS: This is a randomized controlled trial on the effectiveness of two neurorehabilitation techniques in patients with multiple sclerosis conducted at the University of Salamanca. The research will take place at the Faculty of Nursing and Physiotherapy, University of Salamanca. The study will be conducted from June 2023 to June 2024. The reflex locomotion group will receive individual sessions of therapy (n = 27), and the Bobath concept group (n = 27) will receive the same number of sessions. Both groups will receive two sessions per week for 12 months. The measurement variables will be the Berg Balance Scale, the Tardieu Scale, the Cognitfit Program, Maximum Inspiratory Pressure, and Lacrimal Biomarkers. ETHICS AND DISSEMINATION: This study has been approved by the Ethics Committee of the University of Salamanca on March 2023 (ref: 896). LIMITATIONS: The main limitations of this study are the selection and number of patients, the delay in implementing the therapy within the initially scheduled period, inadequate sample collection, and inadequate sample processing. TRIAL REGISTRATION NUMBER: ClinicalTrials.gov; identifier: NCT05558683.
 The clinical-radiological and biological overlap of the spectrum of pediatric demyelinating disorders makes the diagnostic process of a child with an acquired demyelinating syndrome truly challenging. We present a 9-year-old girl with subacute symptoms of severe decrease in bilateral visual acuity and gait ataxia. An urgent MRI showed inflammatory-demyelinating lesions affecting the periaqueductal gray matter, the cerebellar hemispheres, the area postrema as well as both optic nerves and chiasm. Likewise, multisegmental involvement of the cervical and dorsal spinal cord was found, with short and peripheral lesions. Anti myelin oligodendrocyte glycoprotein (MOG) antibodies (Abs) were positive in cerebrospinal fluid (CSF) and weakly in serum. Oligoclonal bands (OB) were positive in CSF. Based on all this, the diagnosis of MOG antibody disease (MOGAD) with a neuromyelitis optica spectrum disorder (NMOSD)-like picture was made. Given the good clinical and radiological recovery after the acute phase treatment, and that anti MOG Abs became negative, it was decided to keep the patient without specific treatment. However, during follow-up, while the patient was asymptomatic, a control brain MRI showed the appearance of new lesions with morphology and topography suggestive of multiple sclerosis (MS). This, added to the presence of OB, made the diagnosis of pediatric-onset MS (POMS) likely. Immunosuppressive treatment was restarted with a good response since then. Unlike adult-onset MS, children with POMS may usually not have entirely typical clinical and radiological features at presentation. In many cases, the time factor and close clinical and radiological monitoring could be critical to make an accurate diagnosis.
 INTRODUCTION: Multiple sclerosis is a chronic disease that profoundly impacts the patient's life. This study investigates the effectiveness of cognitive behavioral group therapy on psycho-social and emotional adaptability and cognitive flexibility in patients with multiple sclerosis in Hamedan city. METHODS: The current study was semi-experimental and was designed with a pretest-posttest and follow-up with a control group. The statistical population included all people suffering from MS who referred to the MS association in Hamedan, Iran, in 2022, among whom 30 people were selected by sampling and randomly assigned to two experimental and control groups (each group of 15 people). The experimental group received cognitive behavioral intervention during eight sessions of 90 min weekly. The control group did not receive any interventions. The subjects were re-evaluated after 2 months for follow-up. The data were collected using a psycho-social adaptability with illness scale questionnaire, Bell's emotional adjustment questionnaire, and cognitive flexibility inventory questionnaire. The data were analyzed using variance analysis with repeated measurements using SPSS-21 software. RESULTS: The results revealed that the cognitive behavioral therapy intervention significantly impacted the improvement of psycho-social and emotional adaptability and cognitive flexibility compared to the control group. This impact persisted until the follow-up stage. CONCLUSION: Cognitive behavioral therapy removes cognitive barriers related to attitude and self-management by increasing the information, which improves psycho-social and emotional adaptability, cognitive flexibility, and, consequently, self-care behaviors.
 BACKGROUND: Multiple sclerosis (MS) is accompanied by many health-related issues. This study aimed to evaluate the anthropometric indices, nutrient intakes and health-related characteristics of MS patients as well as their possible correlations. METHODS: This cross-sectional study was performed on 283 MS patients in Shiraz, Iran, during 2018-2019. Body mass index (BMI) and body composition were measured for each participant. A food frequency questionnaire was used to determine the patients' nutrient intakes. The level of fatigue, disability and quality of life of the individuals were assessed by the modified fatigue impact scale (MFIS), the expanded disability status scale and the multiple sclerosis quality of life-54 questionnaires, respectively. RESULTS: The results revealed that 43.11% of the patients were overweight or obese, and their %body fat (%BF) was 35.65 ± 7.63. Besides, intakes of vitamins A, E, D, folic acid, calcium, zinc and magnesium were significantly lower than recommendations in both genders, and sodium intake was significantly higher than the tolerable upper intake level in females. A significant positive linear correlation was observed between MFIS and BMI (r = 0.12, P = 0.045). Significant positive correlations were also found between psychosocial subscale of MFIS and both of %BF (r = 0.12, P = 0.049) and visceral fat area (r = 0.14, P = 0.02). Unexpectedly, the patients' quality of life showed significant negative correlations with fat free mass and skeletal muscle mass. CONCLUSION: Being overweight, having a high %BF and poor nutrient intakes are common among MS patients. Improving the patients' lifestyle and dietary intake is recommended to reduce fatigue and increase their life quality.
 BACKGROUND: Natalizumab is a highly effective monoclonal antibody for the treatment of multiple sclerosis (MS), which can diffuse in different anatomical compartments, including cerebrospinal fluid (CSF) and milk. OBJECTIVES: Starting from incidental detection of natalizumab in the CSF of MS patients, the objective of this study was to develope a flow-cytometry-based assay and apply it to quantify natalizumab in body fluids, including milk collected from nursing patients over 180 days and in patients with neutralizing antibodies against natalizumab. METHODS: CSF, milk and sera samples from patients with multiple sclerosis were tested by flow-cytometry for binding to a VLA-4 expressing cell line or to a control cell line. A standard curve was prepared by incubating the same cells with natalizumab at 50 μg/ml and serially diluted to 0.005 ng/ml. Binding specificity was confirmed using an anti-natalizumab neutralizing antibody. RESULTS: Our assay was sensitive enough to detect natalizumab in CSF, with a lower detection limit of 1.5 ng/ml. Neutralizing antibodies against natalizumab inhibited binding to the cell line. In breastmilk, the peak concentration was observed during the first 2 weeks after infusion and the average concentration over the observation time was 173.3 ng/ml, with a trend toward increased average milk concentration over subsequent administrations. CONCLUSION: Routine use of such an assay would enable a better understanding of the safety of therapeutic antibody administration during pregnancy and lactation.
 BACKGROUND AND PURPOSE: disease-modifying treatments (DMT) for Multiple Sclerosis (MS) have expanded in recent years making the shared-decision process challenging. Moreover, no head-to-head studies are available within the first-line options. Our aim is to compare therapeutic persistence within first-line DMT: teriflunomide (TER), dimethyl fumarate (DMF), and injectable drugs (INJ) in a real-world setting. METHODS: Retrospective observational study analyzing diagnosed with Relapsing-Remitting Multiple Sclerosis (RRMS) who started DMT between January 2015 and April 2022 (TER=117, DMF=117, INJ=123). Clinical, radiological, and demographic variables were collected. The primary outcome was the median time to discontinuation of any DMT. Dropout was defined as discontinuation for 6 months for any reason. RESULTS: Of the total of 357 patients, 155 withdraw with a median time-to-discontinuation of 1.427 years (IQR 2.410). The discontinuation rate was higher in the injectable group, 49.6%; compared to teriflunomide 40.2%, and dimethyl fumarate 39.8% (p = 0.201). The most frequent reason of discontinuation differs within groups (lack of efficacy in TER, 63.8%, and adverse effects in DMF and INJ (40.4% and 40.9% respectively). No difference in persistence was observed between DMT (p = 0.30). After 2018 there has been a tendency to treat in a quick and early manner (lower EDSS; relapse rate and number of naïve patients), statistically significant for TER (p = 0.005, p = 0.010, and p = 0.045). CONCLUSIONS: Our study demonstrated no differences in persistence between the actual first-line DMT in a real-world setting, although a trend to favor oral-DMT was seen. Reasons for discontinuation differs within groups.
 PURPOSE: Spasticity is common in multiple sclerosis (MS), often leading to functional limitations and disability. We developed a conceptual model of spasticity in MS integrating expert opinion, recent literature, and experiences of clinicians and people with MS spasticity. METHODS: A conceptual model was developed based on a targeted literature review of articles published between 2014 and 2019, followed by input from clinicians, then input from participants with MS spasticity. Multidisciplinary experts on spasticity provided guidance at each step. RESULTS: Key concepts of the integrated spasticity conceptual model included: moderators; triggers; modifiers; treatment; objective manifestations; subjective experience; physical, functional, social, and emotional/psychological impacts; and long-term consequences. Participants with MS spasticity most frequently endorsed spasms, tightness, and pain as descriptors of spasticity. Some participants with MS spasticity had difficulty distinguishing spasticity from other MS symptoms (e.g. muscle weakness). Some triggers, emotional/psychological impacts, and long-term consequences of spasticity reported by participants with MS spasticity were not previously identified in the published literature. CONCLUSIONS: This conceptual model of spasticity, integrating published literature with the experience of clinicians, people with MS spasticity, and experts, demonstrates the complex, multidimensional nature of MS spasticity. This model may be used to improve clinician-patient dialogue, research, and patient care.
 Therapy for relapsing-remitting multiple sclerosis (MS) has advanced dramatically despite incomplete understanding of the cause of the condition. Current treatment involves inducing broad effects on immune cell populations with consequent off-target side effects, and no treatment can completely prevent disability progression. Further therapeutic advancement will require a better understanding of the pathobiology of MS. Interest in the role of Epstein-Barr virus (EBV) in multiple sclerosis has intensified based on strong epidemiological evidence of an association between EBV seroprevalence and MS. Hypotheses proposed to explain the biological relationship between EBV and MS include molecular mimicry, EBV immortalised autoreactive B cells and infection of glial cells by EBV. Examining the interaction between EBV and immunotherapies that have demonstrated efficacy in MS offers clues to the validity of these hypotheses. The efficacy of B cell depleting therapies could be consistent with a hypothesis that EBV-infected B cells drive MS; however, loss of T cell control of B cells does not exacerbate MS. A number of MS therapies invoke change in EBV-specific T cell populations, but pathogenic EBV-specific T cells with cross-reactivity to CNS antigen have not been identified. Immune reconstitution therapies induce EBV viraemia and expansion of EBV-specific T cell clones, but this does not correlate with relapse. Much remains unknown regarding the role of EBV in MS pathogenesis. We discuss future translational research that could fill important knowledge gaps.
 BACKGROUND: People with multiple sclerosis (PwMS) suffer from some comorbidities, including physical and psychiatric disorders, low quality of life (QoL), hormonal dysregulation, and hypothalamic-pituitary-adrenal axis dysfunction. The current study aimed to investigate the effects of eight weeks of tele-yoga and tele-Pilates on the serum levels of prolactin and cortisol and selected physical and psychological factors. METHODS: Forty-five females with relapsing remitting multiple sclerosis, based on age (18-65), expanded disability status scale (0-5.5), and body mass index (20-32), were randomly assigned to tele-Pilates, tele-yoga, or control groups (n = 15). Serum blood samples and validated questionnaires were collected before and after interventions. RESULTS: Following online interventions, there was a significant increase in the serum levels of prolactin (p = 0.004) and a significant decrease in cortisol (p = 0.04) in the time × group interaction factors. In addition, significant improvements were observed in depression (p = 0.001), physical activity levels (p < 0.001), QoL (p ≤ 0.001), and the speed of walking (p < 0.001). CONCLUSION: Our findings suggest that tele-yoga and tele-Pilates training could be introduced as patient-friendly, non-pharmacological, add-on therapeutic methods for increasing prolactin and decreasing cortisol serum levels and achieving clinically relevant improvements in depression, walking speed, physical activity level, and QoL in female MS patients.



 BACKGROUND: The impact of microRNAs (miRNAs) on the differentiation and function of inflammatory cells is well-established. MiRNAs play a crucial role in modulating the expression of pro-inflammatory genes in neuronal cells as well. With this knowledge in mind, our study aimed to explore the relationship between the expression of miRNAs and inflammatory markers in the cerebrospinal fluid (CSF) of patients diagnosed with multiple sclerosis (MS). By investigating this relationship, we aimed to gain insights into the potential involvement of miRNAs in the regulation of inflammation in the context of MS. MATERIALS AND METHODS: The expression levels of miRNA-21, miRNA-155, and miRNA-182 in cerebrospinal fluid (CSF) samples from multiple sclerosis (MS) patients and controls were determined by RT-PCR. CSF levels of the inflammatory cytokines IL-1β, IL-6, and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA). In addition, high-sensitivity C-reactive protein (hs-CRP) levels were measured by quantitative turbidimetry. RESULTS: The expression levels of microRNAs and inflammatory factors were found to be significantly higher in the CSF of MS patients compared to controls (P < 0.05). Receiver operating characteristics (ROC) analysis revealed that miRNA-21, miRNA-182, and miRNA-155 had a high area under the curve (AUC) in discriminating MS patients, with AUC values of 0.97 (P < 0.0001) for miRNA-21, 0.97 (P < 0.0001) for miRNA-182, and 0.96 (P < 0.0001) for miRNA-155. Notably, CSF miRNA-155 showed the highest accuracy in correctly diagnosing MS. Furthermore, a statistically significant relationship was observed between inflammatory cytokines and miRNA-21, miRNA-155 and miRNA-182. CONCLUSION: Our results demonstrated that cerebrospinal fluid (CSF) levels of IL-1β, IL-6, TNF-α, hs-CRP and specific miRNAs serve as biomarkers for assessing central nervous system (CNS) inflammation and neurodegenerative processes in patients with multiple sclerosis (MS).
 Lhermitte's sign (also known as Lhermitte's phenomenon or the barber chair phenomenon) is the term used that describes a transient sensation of an electric shock that extends down the spine and extremities upon flexion and/or movement of the neck. It was first described by Marie and Chatelin in 1917, but was erroneously first credited to Babinski and Dubois, and thenafter credited to Jean Jaque Lhermitte through the seminal paper Les douleurs à type de décharge électrique consécutives à la flexion céphalique dans la sclérose en plaques: Un cas de forme sensitive de la sclérose multiple (1924) by Lhermitte et al. and Gutre. Lhermitte described this phenomenon in patients with multiple sclerosis and other spinal cord diseases. It was then further hypothesized that it resulted from irritation and inflammation of the spinal cord, likely in the posterior and lateral columns. Lhermitte's sign is also classified as one of the paroxysmal pain syndromes of multiple sclerosis, a chronic, predominantly immune-mediated disease of the central nervous system. It is among the most common causes of neurological disability in young adults globally. It can cause many other neurological clinical symptoms, including mononuclear painful visual loss, spinal cord hemiparesis, mono/paraparesis, hypoesthesia, dysesthesia, paraesthesia, urinary and/or sphincter dysfunction, diplopia, oscillopsia, vertigo, gait ataxia, dysmetria, intentional/postural tremor, facial paresis, faciobrachial–crural hemiparesis, and faciobrachial–crural hemihypesthesia. Lhermitte's sign should not be confused with the Uhthoff phenomenon, another finding in multiple sclerosis patients that is defined by heat sensitivity after prolonged heat exposure, saunas, and hot tubs. 
 Memory deficits are common in patients with dementia, such as Alzheimer's disease, but also in patients with other neurological and psychiatric disorders, such as brain injury, multiple sclerosis, ischemic stroke and schizophrenia. Memory loss affects patients' functionality and, by extension, their quality of life. Non-invasive brain training methods, such as EEG neurofeedback, are used to address cognitive deficits and behavioral changes in dementia and other neurological disorders by training patients to alter their brain activity via operant activity. In this review paper, we analyze various protocols of EEG neurofeedback in memory rehabilitation in patients with dementia, multiple sclerosis, strokes and traumatic brain injury. The results from the studies show the effectiveness of the ΕΕG-NFB method in improving at least one cognitive domain, regardless of the number of sessions or the type of protocol applied. In future research, it is important to address methodological weaknesses in the application of the method, its long-term effects as well as ethical issues.

 OBJECTIVES: To evaluate the diffusion kurtosis and susceptibility change in the U-fiber region of patients with relapsing-remitting multiple sclerosis (pwRRMS) and their correlations with cognitive status and degeneration. MATERIALS AND METHODS: Mean kurtosis (MK), axial kurtosis (AK), radial kurtosis (RK), kurtosis fractional anisotropy (KFA), and the mean relative quantitative susceptibility mapping (mrQSM) values in the U-fiber region were compared between 49 pwRRMS and 48 healthy controls (HCs). The U-fiber were divided into upper and deeper groups based on the location. The whole brain volume, gray and white matter volume, and cortical thickness were obtained. The correlations between the mrQSM values, DKI-derived metrics in the U-fiber region and clinical scale scores, brain morphologic parameters were further investigated. RESULTS: The decreased MK, AK, RK, KFA, and increased mrQSM values in U-fiber lesions (p < 0.001, FDR corrected), decreased RK, KFA, and increased mrQSM values in U-fiber non-lesions (p = 0.034, p < 0.001, p < 0.001, FDR corrected) were found in pwRRMS. There were differences in DKI-derived metrics and susceptibility values between the upper U-fiber region and the deeper one for U-fiber non-lesion areas of pwRRMS and HCs (p < 0.05), but not for U-fiber lesions in DKI-derived metrics. The DKI-derived metrics and susceptibility values were widely related with cognitive tests and brain atrophy. CONCLUSION: RRMS patients show abnormal diffusion kurtosis and susceptibility characteristics in the U-fiber region, and these underlying tissue abnormalities are correlated with cognitive deficits and degeneration. CLINICAL RELEVANCE STATEMENT: The macroscopic and microscopic tissue damages of U-fiber help to identify cognitive impairment and brain atrophy in multiple sclerosis and provide underlying pathophysiological mechanism. KEY POINTS: • Diffusion kurtosis and susceptibility changes are present in the U-fiber region of multiple sclerosis. • There are gradients in diffusion kurtosis and susceptibility characteristics in the U-fiber region. • Tissue damages in the U-fiber region are correlated with cognitive impairment and brain atrophy.
 OBJECTIVE: We examined the total number of comorbid conditions as a correlate of physical function in persons with multiple sclerosis (MS). We further identified the presence of common comorbid conditions and examined physical function outcomes based on presence or absence of the comorbid conditions in persons with MS. DESIGN: Cross-sectional, comparative study. SETTING: University-based laboratory. PARTICIPANTS: Two hundred seven persons with MS (N=207) completed the study. MAIN OUTCOME MEASURES: Participants provided demographic, clinical, and comorbidity information. Participants then completed the 6-minute walk (6MW), timed 25-foot walk (T25FW), timed Up and Go (TUG), and short physical performance battery (SPPB). INTERVENTIONS: Not applicable. RESULTS: The number of comorbid conditions was associated with 6MW, T25FW, TUG, and SPPB scores (all P≤.001). Persons with MS who had hypertension performed worse on the 6MW, T25FW, TUG, and SPPB than persons without hypertension. Persons who had osteoarthritis performed worse on the 6MW, T25FW, and SPPB than persons without osteoarthritis. CONCLUSIONS: The results demonstrate that persons who report more comorbid conditions have worse physical function, and this may largely be associated with hypertension or osteoarthritis. There are opportunities for the design of behavioral interventions that target physical activity and/or diet for improving physical function via comorbid conditions in persons with MS.
 PURPOSE: The main aim of the study was to compare the effectiveness of the dietary patterns studied in the context of multiple sclerosis (MS), including anti-inflammatory, Mediterranean diet (MD), Mediterranean-DASH intervention for neurodegenerative delay (MIND), intermittent fasting (IF), gluten-free and ketogenic diets. In addition, another aim was to verify or otherwise the efficacy of other alternative dietary models, which include the Paleo diet, the Wahls diet, the McDougall diet and the Swank diet. Whether and to what extent the use of different dietary regimens can affect the course and reduction of individual MS symptoms was also examined. The advantages and disadvantages of selected diets and dietary patterns in the context of MS are discussed. VIEWS: Autoimmune diseases are estimated to affect more than 3% of the world's people, the majority of whom are of working age. Therefore, delaying the first manifestation of the disease, reducing the number of relapses and alleviating symptoms are particularly welcome developments. In addition to finding effective pharmacotherapy, high hopes for patients lie in nutritional prevention and diet therapy. For years the medical literature has discussed supporting the treatment of diseases caused by an impairment of the body's immune system with the help of nutrition. CONCLUSIONS: An appropriate and balanced diet can be extremely helpful in improving the condition and well-being of patients with MS, and effectively support drug therapy.
 Research shows that patients can have values and use practices that are different from those envisioned by technology developers. Using sociomaterialism as an analytical lens, we show how patients negotiated with digital self-monitoring in the context of a scientific study. Our paper draws on interviews with 26 patients with the chronic neurological disease multiple sclerosis (MS) who were invited to use an activity tracker and a self-monitoring app for a period of 12 months as part of their everyday life. Our study aims to fill a gap: relatively little is known about how digital self-monitoring becomes materialized in the everyday lives of patients with chronic diseases. We show that patients engaged in digital self-monitoring because they are eager to participate in research to contribute knowledge that will benefit the larger community of patients rather than to improve their personal self-management. Although respondents adhered to digital self-monitoring during the study, it is not self-evident that they would do so for private self-monitoring purposes. It became clear that respondents did not necessarily perceive digital self-monitoring as useful for their self-management practices due to their established knowledge and routines. Moreover, respondents referred to the inconvenience of having to perform self-monitoring tasks and the emotional burden of being reminded of the MS because of the digital self-monitoring. We conclude by indicating what could be considered when designing scientific studies, including the suitability of conventional study designs for evaluating technologies used daily by patients and the challenge of integrating patients' experiential knowledge into scientific practices.
 To date, the relationship between central hallmarks of multiple sclerosis (MS), such as white matter (WM)/cortical demyelinated lesions and cortical gray matter atrophy, remains unclear. We investigated the interplay between cortical atrophy and individual lesion-type patterns that have recently emerged as new radiological markers of MS disease progression. We employed a machine learning model to predict mean cortical thinning in whole-brain and single hemispheres in 150 cortical regions using demographic and lesion-related characteristics, evaluated via an ultrahigh field (7 Tesla) MRI. We found that (i) volume and rimless (i.e., without a "rim" of iron-laden immune cells) WM lesions, patient age, and volume of intracortical lesions have the most predictive power; (ii) WM lesions are more important for prediction when their load is small, while cortical lesion load becomes more important as it increases; (iii) WM lesions play a greater role in the progression of atrophy during the latest stages of the disease. Our results highlight the intricacy of MS pathology across the whole brain. In turn, this calls for multivariate statistical analyses and mechanistic modeling techniques to understand the etiopathogenesis of lesions.
 The aim of the retrospective study was to compare the immunophenotyping of T-lymphocytes, B-lymphocytes, and natural killer cells before the administration of the first and the second dose of ocrelizumab in 22 patients with multiple sclerosis in a three-year period (2019-2021) at the Department of Neurology of the University Hospital of Split. The values of cell immunophenotyping and protein electrophoresis, as well as laboratory parameters, were investigated. There was no significant decrease in serum albumin and globulins before the second dose of ocrelizumab (p > 0,05). A decrease in the number of T-lymphocytes before administration of the second dose of ocrelizumab was observed, but without statistical significance (p = 0.274). Significant depletion occurred in median CD19+ B-lymphocytes (p < 0.001) before the intake of the second dose of ocrelizumab confirming the primary action of ocrelizumab on the B cell lineage.
 This review aimed to elucidate protein biomarkers in body fluids, such as blood and cerebrospinal fluid (CSF), to identify those that may be used for early diagnosis of multiple sclerosis (MS), prediction of disease activity, and monitoring of treatment response among MS patients. The potential biomarkers elucidated in this review include neurofilament proteins (NFs), glial fibrillary acidic protein (GFAP), leptin, brain-derived neurotrophic factor (BDNF), chitinase-3-like protein 1 (CHI3L1), C-X-C motif chemokine 13 (CXCL13), and osteopontin (OPN), with each biomarker playing a different role in MS. GFAP, leptin, and CHI3L1 levels were increased in MS patient groups compared to the control group. NFs are the most studied proteins in the MS field, and significant correlations with disease activity, future progression, and treatment outcomes are evident. GFAP CSF level shows a different pattern by MS subtype. Increased concentration of CHI3L1 in the blood/CSF of clinically isolated syndrome (CIS) is an independent predictive factor of conversion to definite MS. BDNF may be affected by chronic progression of MS. CHI3L1 has potential as a biomarker for early diagnosis of MS and prediction of disability progression, while CXCL13 has potential as a biomarker of prognosis of CIS and reflects MS disease activity. OPN was an indicator of disease severity. A periodic detailed patient evaluation should be performed for MS patients, and broadly and easily accessible biomarkers with higher sensitivity and specificity in clinical settings should be identified.
 Sexuality is an integral part of our existence. Multiple Sclerosis (MS) can complicate the lifelong course of sexual development and the ways in which one defines and expresses sexuality. Unfortunately, these issues are not adequately addressed by the health professionals involved in the rehabilitation process. Present research attempts to study the effect that can arise on the sexual and relational satisfaction of couples having a partner with MS after the implementation of a sexual rehabilitation program. 60 couples where one partner has MS and the other does not, were divided into three groups and accepted the PLISSIT (PLISSIT stands for Permission, Limited Information, Specific Suggestions, Intensive Therapy) sexual rehabilitation program as follows: Group a (n = 40, control group) completed self-referencing questionnaires at three times (initial measurement, after 10 weeks and 6 months later), group b (n = 40) did 10 weeks of sexual counselling and completed the same questionnaires at the same times and group c (n = 40) followed the PLISSIT programme and was evaluated in the same way at the same times. The implementation of PLISSIT improved Sexual Dysfunction (SD) levels, increased sexual satisfaction between partners along with general relational satisfaction. PLISSIT can be used by professionals involved in the management of the disease as a comprehensive psychosexual rehabilitation program for MS patients and their partners.
 Multiple sclerosis (MS) is an immune-driven disease that affects the central nervous system and is characterized by acute-on-chronic demyelination attacks. It is a major cause of global neurological disability, and its prevalence has increased in the United States. Conceptual understandings of MS have evolved over time, including the identification of B cells as key factors in its pathophysiology. The foundation of MS management involves preventing flares so as to avoid long-term functional decline. Treatments may be categorized into low-, middle-, and high-efficacy medications based on their efficacy in relapse prevention. With 24 FDA-approved treatments for MS, individual therapy is chosen based on distinct mechanisms and potential side effects. This review provides a detailed update on the epidemiology, diagnosis, treatment advances, and major ongoing research investigations in MS.
 BACKGROUND: Hereditary angioedema is a rare hereditary and potentially life-threatening disorder characterized by recurrent attacks of cutaneous and submucosal swelling. In spite of the advances made in terms of pathophysiology, underlying mechanisms are not fully clear and this, in turn, hinders the development of effective therapies. Currently, on demand treatment is considered first-class, with few cost-effective, long-term prophylactic options. CASE PRESENTATION: Here we describe the case of a 34-year-old man diagnosed with hereditary angioedema at the age of 10, who used to suffer several angioedema attacks per month. He was given prophylactic treatment with antifibrinolytic agents and androgens without improvement. Moreover, he was treated with plasma-derived C1-INH concentrate or icatibant for on-demand treatment of moderate and severe angioedema attacks. At the age of 33, after suffering sudden vision loss and lower limb paresthesia, he was studied and diagnosed with multiple sclerosis. Teriflunomide was administered at a dosage of 14 mg/day. Angioedema attacks disappeared 40 days after starting treatment. CONCLUSION: Thus, we suggest considering the pathophysiologic mechanisms on which teriflunomide could be active and consider this drug carefully as an option for prophylaxis purposes. Yet, its effectiveness on this condition should be further studied. LEARNING POINTS: Underlying mechanisms in hereditary angioedema lack clarity and hence hinder the development of effective therapies.On-demand treatment of hereditary angioedema is considered first class, with few cost-effective, long-term prophylactic options.The mechanisms of action and effectiveness of teriflunomide on hereditary angioedema should be studied further.
 Treatment options for multiple sclerosis (MS) are now numerous, but it is unclear which Disease-Modifying Treatment (DMT) is the optimal choice for a given patient. Treatment switches are common, both because of side effects and because of lack of efficacy. There are few data available on the treatment courses of patients newly diagnosed with MS in the current DMT era. All patients newly diagnosed with MS in 2012-2018 at North Karelia Central Hospital were identified (N = 55), and those with complete follow-up data available (N = 43) were included. The minimum follow-up from diagnosis was 44 months with a maximum of 9 years. Seven patients (16%) had no DMT at any time during the follow-up. Treatment was most often initiated with interferon or glatiramer acetate (69%), but 72% of these treatments were discontinued. After cladribine, teriflunomide and fingolimod showed the best treatment persistence. Patients who experienced their first MS symptoms at ≥40 years of age all continued with their initial treatment category until the end of the follow-up. In a third of the patients who had received a DMT, at the end of the follow-up, the treatment had been escalated to fingolimod, cladribine or natalizumab. Only 13 patients (28%) continued with their initial DMT until the end of the follow-up.
 Dimethyl fumarate (DMF) is a widely used oral disease-modifying therapy for multiple sclerosis (MS). Its efficacy and safety profiles are supported by over a decade of experience. Differences exist between Asia and Europe/United States in the prevalence and characteristics of MS; most data for DMF are derived from populations outside Asia. DMF was recently (2021) approved for use in China. The objectives of this review were to evaluate the evidence for DMF's profile, to provide an update to healthcare providers on current knowledge surrounding its use and to assess the relevance of existing data to use in China. This study used a modified Delphi method based on the insights of a scientific Steering Committee (SC), with a structured literature review conducted to assess the data of DMF. The literature review covered all papers in English (from 01 January 2011 to 21 February 2022) that include 'dimethyl fumarate' and 'multiple sclerosis', and their MeSH terms, on PubMed, supplemented by EMBASE and Citeline searches. Papers were categorized by topic and assessed for relevance and quality, before being used to formulate statements summarizing the literature on each subject. SC members voted on/revised statements, requiring ⩾80% agreement and ⩽10% disagreement for inclusion. Statements not reaching this level were discussed further until agreement was reached or until there was agreement to remove the statement. A total of 1030 papers were retrieved and used to formulate the statements and evidence summaries considered by the SC members. A total of 45 statements were agreed by the SC members. The findings support the positive efficacy and safety profile of DMF in treating patients with MS. Limited Chinese patient data are an ongoing consideration; however, based on current evidence, the statements are considered applicable to both the global and Chinese populations. DMF is a valuable addition to address unmet MS treatment needs in China. Registration: Not applicable.
 BACKGROUND: Cognitive impairment (CI) is a prevalent and debilitating manifestation of multiple sclerosis (MS); however, it is not included in the widely used concept of No Evidence of Disease Activity (NEDA-3). We expanded the NEDA-3 concept to NEDA-3 + by encompassing CI assessed through the Symbol Digit Modality Test (SDMT) and evaluated the effect of teriflunomide on NEDA3 + in patients treated in a real-world setting. The value of NEDA-3 + in predicting disability progression was also assessed. METHODS: This 96-weeks observational study enrolled patients already on treatment with teriflunomide for ≥ 24 weeks. The predictiveness of NEDA-3 and NEDA-3 + at 48 weeks on the change in motor disability at 96 weeks was compared through a two-sided McNemar test. RESULTS: The full analysis set (n = 128; 38% treatment naïve) featured relatively low level of disability (baseline EDSS = 1.97 ± 1.33). NEDA-3 and NEDA-3 + statuses were achieved by 82.8% and 64.8% of patients, respectively at 48 weeks vs. baseline, and by 57.0% and 49.2% of patients, respectively at 96 weeks vs. baseline. All patients except one were free of disability progression at Week 96, and NEDA-3 and NEDA-3 + were equally predictive. Most patients were free of relapse (87.5%), disability progression (94.5%) and new MRI activity (67.2%) comparing 96 weeks with baseline. SDMT scores were stable in patients with baseline score ˃35 and improved significantly in those with baseline score ≤ 35. Treatment persistence was high (81.0% at Week 96). CONCLUSION: Teriflunomide confirmed its real-world efficacy and was found to have a potentially beneficial effect on cognition.

 BACKGROUND: Evidence of the benefits of dance for people with Parkinson disease is well established, but only recently has dance been investigated for people with multiple sclerosis (MS). The purpose of this review was to identify and evaluate the feasibility and effectiveness of dance interventions to improve functional, psychosocial, and participation outcomes in people with MS. METHODS: Eight databases and gray literature sources were searched from inception to March 2022. Quantitative, mixed-methods, and qualitative studies evaluating dance interventions for adults with MS were included. Included studies were critically appraised using the Mixed Methods Appraisal Tool, and results were analyzed through a parallel-results convergent synthesis. RESULTS: Thirteen studies were included, with a total of 174 participants. Various dance genres were investigated, and only 1 mild adverse event was reported. Four to 12 weeks of twice-weekly, 60-minute dance sessions were feasible in those with mild to moderate relapsing-remitting MS. Positive effects were identified mainly in motor outcomes, with qualitative themes indicating psychological and social benefits. CONCLUSIONS: A variety of dance interventions are likely feasible and potentially beneficial for people with mild to moderate relapsing-remitting MS, but studies were generally of low-moderate quality. High-quality studies are needed to determine the effectiveness of dance interventions for people with MS, including those with progressive forms of MS and higher levels of disability.
 In accordance with European regulation, medicines containing a new active substance to treat neurodegenerative diseases as well as autoimmune and other immune dysfunctions must be approved by the European Medicines Agency (EMA) through the centralized procedure before they can be marketed. However, after EMA approval, each country is responsible for national market access, following the assessment performed by health technology assessment (HTA) bodies with regard to the therapeutic value. This study aims to provide a comparative analysis of HTA recommendations issued by three EU countries (France, Germany, and Italy) for new drugs for multiple sclerosis (MS) following EMA approval. In the reference period, we identified 11 medicines authorized in Europe for MS, including relapsing forms of MS (RMS; n = 4), relapsing-remitting MS (RRMS; n = 6), secondary progressive MS (SPMS; n = 1), and the primary progressive form (PPMS; n = 1). We found no agreement on the therapeutic value (in particular, the "added value" compared to the standard of care) of the selected drugs. Most evaluations resulted in the lowest score ("additional benefit not proven/no clinical improvement"), underlining the need for new molecules with better efficacy and safety profiles for MS, especially for some forms and clinical settings.
 Diffusion-weighted imaging has been applied to investigate alterations in multiple sclerosis (MS). In the last years, advanced diffusion models were used to identify subtle changes and early lesions in MS. Among these models, neurite orientation dispersion and density imaging (NODDI) is an emerging approach, quantifying specific neurite morphology in both grey (GM) and white matter (WM) tissue and increasing the specificity of diffusion imaging. In this systematic review, we summarized the NODDI findings in MS. A search was conducted on PubMed, Scopus, and Embase, which yielded a total number of 24 eligible studies. Compared to healthy tissue, these studies identified consistent alterations in NODDI metrics involving WM (neurite density index), and GM lesions (neurite density index), or normal-appearing WM tissue (isotropic volume fraction and neurite density index). Despite some limitations, we pointed out the potential of NODDI in MS to unravel microstructural alterations. These results might pave the way to a deeper understanding of the pathophysiological mechanism of MS. EVIDENCE LEVEL: 2. TECHNICAL EFFICACY: Stage 3.
 The hallmarks of Parkinson's disease (PD) include the loss of dopaminergic neurons and formation of Lewy bodies, whereas multiple sclerosis (MS) is an autoimmune disorder with damaged myelin sheaths and axonal loss. Despite their distinct etiologies, mounting evidence in recent years suggests that neuroinflammation, oxidative stress, and infiltration of the blood-brain barrier (BBB) all play crucial roles in both diseases. It is also recognized that therapeutic advances against one neurodegenerative disorder are likely useful in targeting the other. As current drugs in clinical settings exhibit low efficacy and toxic side effects with long-term usages, the use of natural products (NPs) as treatment modalities has attracted growing attention. This mini-review summarizes the applications of natural compounds to targeting diverse cellular processes inherent in PD and MS, with the emphasis placed on their neuroprotective and immune-regulating potentials in cellular and animal models. By reviewing the many similarities between PD and MS and NPs according to their functions, it becomes evident that some NPs studied for one disease are likely repurposable for the other. A review from this perspective can provide insights into the search for and utilization of NPs in treating the similar cellular processes common in major neurodegenerative diseases.
 Proteinase-activated receptor-2 (PAR2), which modulates inflammatory responses, is elevated in the central nervous system (CNS) in multiple sclerosis (MS) and in its murine model, experimental autoimmune encephalomyelitis (EAE). In PAR2-null mice, disease severity of EAE is markedly diminished. We therefore tested whether inhibiting PAR2 activation in vivo might be a viable strategy for the treatment of MS. Using the EAE model, we show that a PAR2 antagonist, the pepducin P2pal-18S, attenuates EAE progression by affecting immune cell function. P2pal-18S treatment markedly diminishes disease severity and reduces demyelination, as well as the infiltration of T-cells and macrophages into the CNS. Moreover, P2pal-18S decreases GM-CSF production and T cell activation in cultured splenocytes and prevents macrophage polarization in vitro. We conclude that PAR2 plays a key role in regulating neuroinflammation in EAE and that PAR2 antagonists represent promising therapeutic agents for treating MS and other neuroinflammatory diseases. Significance Statement Proteinase-activated receptor-2 (PAR2) modulates inflammatory responses and is increased in multiple sclerosis (MS) lesions. We show that the PAR2 antagonist P2pal-18S reduces disease in the murine EAE model of MS by inhibiting T cell and macrophage activation and infiltration into the CNS, making it a potential treatment for MS.
 BACKGROUND: Cognitive impairment is a disabling and underestimated consequence of multiple sclerosis (MS), with multiple determinants that are poorly understood. OBJECTIVES: We explored predictors of MS-related processing speed impairment (PSI) and age-related mild cognitive impairment (MCI) and hypothesized that cardiorespiratory fitness and corticospinal excitability would predict these impairments. METHODS: We screened 73 adults with MS (53 females; median [range]: Age 48 [21-70] years, EDSS 2.0 [0.0-6.5]) for PSI and MCI using the Symbol Digit Modalities Test and Montréal Cognitive Assessment, respectively. We identified six persons with PSI (No PSI, n = 67) and 13 with MCI (No MCI, n = 60). We obtained clinical data from medical records and self-reports; used transcranial magnetic stimulation to test corticospinal excitability; and assessed cardiorespiratory fitness using a graded maximal exercise test. We used receiver operator characteristic (ROC) curves to discern predictors of PSI and MCI. RESULTS: Interhemispheric asymmetry of corticospinal excitability was specific for PSI, while age was both sensitive and specific for MCI. MS-related PSI was also associated with statin prescriptions, while age-related MCI was related to progressive MS and GABA agonist prescriptions. Cardiorespiratory fitness was associated with neither PSI nor MCI. DISCUSSION: Corticospinal excitability is a potential marker of neurodegeneration in MS-related PSI, independent of age-related effects on global cognitive function. Age is a key predictor of mild global cognitive impairment. Cardiorespiratory fitness did not predict cognitive impairments in this clinic-based sample of persons with MS.
 Viral infections have been suspected of being involved in the pathogenesis of certain autoimmune diseases for many years. Epstein-Barr virus (EBV), a DNA virus belonging to the Herpesviridae family, is thought to be associated with the onset and/or the progression of multiple sclerosis (MS), systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome and type 1 diabetes. The lifecycle of EBV consists of lytic cycles and latency programmes (0, I, II and III) occurring in infected B-cells. During this lifecycle, viral proteins and miRNAs are produced. This review provides an overview of the detection of EBV infection, focusing on markers of latency and lytic phases in MS. In MS patients, the presence of latency proteins and antibodies has been associated with lesions and dysfunctions of the central nervous system (CNS). In addition, miRNAs, expressed during lytic and latency phases, may be detected in the CNS of MS patients. Lytic reactivations of EBV can occur in the CNS of patients as well, with the presence of lytic proteins and T-cells reacting to this protein in the CNS of MS patients. In conclusion, markers of EBV infection can be found in MS patients, which argues in favour of a relationship between EBV and MS.
 People with multiple sclerosis (pwMS) report many different visual complaints, but not all of them are well understood. Decline in visual, visuoperceptual and cognitive functions do occur in pwMS, but it is unclear to what extend those help us understand visual complaints. The purpose of this cross-sectional study was to explore the relation between visual complaints and decline in visual, visuoperceptual and cognitive functions, to optimize care for pwMS. Visual, visuoperceptual and cognitive functions of 68 pwMS with visual complaints and 37 pwMS with no or minimal visual complaints were assessed. The frequency of functional decline was compared between the two groups and correlations were calculated between visual complaints and the assessed functions. Decline in several functions occurred more frequently in pwMS with visual complaints. Visual complaints may be an indication of declined visual or cognitive functioning. However, as most correlations were not significant or weak, we cannot infer that visual complaints are directly related to functions. The relationship may be indirect and more complex. Future research could focus on the overarching cognitive capacity that may contribute to visual complaints. Further research into these and other explanations for visual complaints could help us to provide appropriate care for pwMS.
 With a rapidly aging global population and improvement of outcomes with newer multiple sclerosis (MS)-specific disease-modifying therapies (DMTs), the epidemiology of MS has shifted to an older than previously described population, with a peak prevalence of the disease seen in the 55-65 years age group. Changes in the pathophysiology of MS appear to be age-dependent. Several studies have identified a consistent phase of disability worsening around the fifth decade of life. The latter appears to be independent of prior disease duration and inflammatory activity and concomitant to pathological changes from acute focal active demyelination to chronic smoldering plaques, slow-expanding lesions, and compartmentalized inflammation within the central nervous system (CNS). On the other hand, decreased CNS tissue reserve and poorer remyelinating capacity with aging lead to loss of relapse recovery potential. Aging with MS may imply longer exposure to DMTs, although treatment efficacy in patients >55 years has not been evaluated in pivotal randomized controlled trials and appears to decrease with age. Older individuals are more prone to adverse effects of DMTs, an important aspect of treatment individualization. Aging with MS also implies a higher global burden of comorbid illnesses that contribute to overall impairments and represent a crucial confounder in interpreting clinical worsening. Discontinuation of DMTs after age 55, when no evidence of clinical or radiological activity is detected, is currently under the spotlight. In this review, we will discuss the impact of aging on MS pathobiology, the effect of comorbidities and other confounders on clinical worsening, and focus on current therapeutic considerations in this age group.
 BACKGROUND: Besides disease-modifying therapies, various pharmacologic agents are frequently prescribed to people with multiple sclerosis (MS) for symptom treatment and for comorbid conditions. The present study aims to investigate the types and frequencies of agents prescribed to people with MS in Greece using records from the nationwide digital prescription database. METHODS: Prescription records for 21,218 people (65.9% women) with MS were included in the study. The criterion for study inclusion was a minimum of 3 months of continuous prescription of an agent. Identified treatments were further examined by age group. RESULTS: Antispasticity agents (17.5%) and fampridine (14.5%) were the most regularly prescribed symptomatic medications. Antihypertensives (21.1%) and drugs for affective disorders, including antidepressants (36.1%) and anxiolytics (16.2%), were the most frequently prescribed medications for comorbid conditions. Antidepressants were prescribed at almost equally high rates among individuals older than 40 years. Hypertension was one of the leading comorbidities among the study sample, with rates rising significantly after age 40 years and plateauing after age 60 years. Polypharmacy was observed in 22.5% of the study sample, with a higher incidence among people with MS older than 60 years (46.98%). CONCLUSIONS: Agents prescribed for the treatment of disease symptoms and other medical conditions are expected to positively affect quality of life in people with MS. However, polypharmacy seems to be particularly high, especially in the aged population. The potential implications of polypharmacy in the disease course should further be explored.
 OBJECTIVE: To summarize recent evidence about ovarian reserve markers in women affected by multiple sclerosis (MS) compared with healthy controls, as women with MS seem to be characterized by lower anti-Müllerian hormone (AMH) levels. METHODS: The research was conducted using PubMed (MEDLINE), Scopus, ClinicalTrial.gov, OVID and Cochrane Library from inception of each database to June 30, 2022. Studies comparing ovarian reserve markers between women with MS and healthy controls were considered eligible for inclusion. The primary outcome was serum AMH (ng/mL) levels. Results were reported as pooled odds ratio (OR) for categorical outcomes and as mean difference (MD) for continuous variables, with their 95% confidence intervals (CIs). The random effect model of DerSimonian and Laird was adopted for all analyses. A P-value less than 0.05 was considered significant. RESULTS: Serum AMH circulating levels were not significantly different (MD -0.25, 95% CI -0.83 to 0.32; P = 0.390), as well as blood levels of follicle-stimulating hormone or ovarian volume. However, antral follicle count (AFC) and estradiol blood levels were significantly lower, and luteinizing hormone (LH) levels were significantly higher in women with MS than in controls. CONCLUSION: A significant difference in AFC, estradiol and LH levels was observed, but not for AMH levels.
 BACKGROUND: Multiple sclerosis (MS) is a chronic, autoimmune, neurodegenerative disorder affecting over 2.9 million people worldwide. First line care revolves around disease modifying therapy and supporting people living with MS to manage their disease. Early management often sees lifestyle modification as people living with MS try to gain a sense of control. Lifestyle management is an evolving area of care with variable strength of evidence for different lifestyle factors. OBJECTIVE: To explore factors that impact on the self-management of MS with a socio-ecological focus. METHODS: A scoping review following the Joanna Briggs Institute guidelines for a systematic search was conducted across six databases with 9241 articles identified and 51 included in the review. The results were analysed in conjunction with the socio-ecological model considering the categories: individual, interpersonal, organisational, community, and public policy. RESULTS: A map of health behaviour (lifestyle) factors extending across all levels of the socio-ecological model revealed a complex web of pathways to behavioural patterns impacting MS self-management. Factors followed a cascading effect towards either of two key principles: (1) self-identity or (2) accessibility. These principles in-turn impact on an individual's self-efficacy, and hence, effectiveness of MS self-management strategies. CONCLUSIONS: MS care is highly individualised to the personal context and circumstances of the individual, with consideration towards suitable management strategies required. Healthcare professionals must consider these lifestyle influences and coordinate an approach to assisting people living with MS to self-manage their disease in relation to their personal circumstances. Person-centred care addressing both barriers and motivators to health behaviour changes is key to effective MS self-management.
 INTRODUCTION: Poorly developed patient-reported outcome measures (PROs) risk type-II errors (i.e. false negatives) in clinical trials, resulting in erroneous failure to achieve trial endpoints. Validity is a fundamental requirement of fit-for-purpose PROs, with the main determinant of validity being the PROs items, i.e. content validity. Here, we sought to identify fatigue PRO instruments used in multiple sclerosis (MS) studies and to assess the extent to which their development satisfied current content validity standards. METHODS: We searched Embase(®) and Medline(®) for MS studies using fatigue-based PROs. Abstracts were screened, PROs identified, and their relevant development papers assessed against seven Consensus Standards for Measurement Instruments (COSMIN) criteria for content development. RESULTS: From 3814 abstracts, 18 fatigue PROs met our inclusion criteria. Most PROs did not satisfy at least one COSMIN content validity standard. Frequent omissions during PRO development include: clearly defined constructs; conceptual frameworks; qualitative research in representative samples; and literature reviews. PRO development quality has improved significantly since FDA guidance was published (U = 10.0, p = 0.02). However, scatterplots and correlations between PRO COSMIN scores and citation frequency (rho = - 0.62) and clinical trials usage (rho =  + 0.18) implied that PRO quality is unrelated to choice. COSMIN scores implied that the Fatigue Symptoms and Impact Questionnaire-Relapsing Multiple Sclerosis (FSIQ-RMS) and Neurological Fatigue Index-Multiple Sclerosis (NFI-MS) had the strongest evidence for adequate content validity. CONCLUSION: Most existing fatigue PROs do not meet COSMIN content validity requirements. Although two PROs scored well on aggregate (NFI-MS and FSIQ-RMS), our subsequent evaluation of the item sets that generated their scores implied that both PROs have weaker content validity than COSMIN suggests. This indicates that COSMIN criteria require further development, and raises significant concerns about how we have measured one of the most common and burdensome MS symptoms. A detailed head-to-head psychometric evaluation is needed to determine the impact of different PRO development qualities and the implications of the problems implied by our analyses, on measurement performance.
 INTRODUCTION: Vortioxetine is a multimodal antidepressant drug that has been reported to have a positive impact on cognition, social function, and fatigue. Nevertheless, it has not been widely studied. Our objective was to explore the effects of vortioxetine on these and other parameters in patients with multiple sclerosis (MS) and depression. PATIENTS AND METHODOLOGY: This observational case series study included patients with MS and depression who received treatment with vortioxetine for at least 6 months. The patient history of depression and depressive symptoms was assessed. A neuropsychiatric evaluation was carried out using different scales, both before and after treatment. RESULTS: Of the 25 patients who enrolled in the study, 17 completed the treatment. Significant improvements were observed in health status (EQ-5D; p = 0.002), mood (Beck's Depression Inventory, BDI-II; p = 0.006), anxiety (State-Trait Anxiety Inventory, STAI-State; p = 0.021, and STAI-Trait; p = 0.011), and in the general health test (Short Form Health Survey, SF-36) for the vitality (p = 0.028) and mental health (p = 0.025) domains of the patients who completed the treatment. However, no statistically significant differences were observed in the cognitive tests related to attention, information processing speed, or fatigue. CONCLUSION: In this population, vortioxetine treatment was effective in reducing the symptoms of depression and improving anxiety, vitality, and mental health. In contrast, it did not produce any improvement in cognition or fatigue but an increase in sample size would be necessary to confirm these results.
 Myelin oligodendrocyte glycoprotein (MOG) is expressed on the outermost layer of the myelin sheath in the central nervous system. Recently, the clinical concept of MOG antibody-associated disease (MOGAD) was established based on the results of human MOG-transfected cell-based assays which can detect conformation-sensitive antibodies against MOG. In this review, we summarized the pathological findings of MOGAD and discussed the issues that remain unresolved. MOGAD pathology is principally inflammatory demyelination without astrocyte destruction, characterized by perivenous demyelination previously reported in acute disseminated encephalomyelitis and by its fusion pattern localized in both the white and gray matter, but not by radially expanding confluent demyelination typically seen in multiple sclerosis (MS). Some of demyelinating lesions in MOGAD show severe loss of MOG staining compared with those of other myelin proteins, suggesting a MOG-targeted pathology in the disease. Perivascular cuffings mainly consist of macrophages and T cells with CD4-dominancy, which is also different from CD8+ T-cell-dominant inflammation in MS. Compared to aquaporin 4 (AQP4) antibody-positive neuromyelitis optica spectrum disorders (NMOSD), perivenous complement deposition is less common, but can be seen on myelinated fibers and on myelin degradation products within macrophages, resembling MS Pattern II pathology. Thus, the pathogenetic contribution of complements in MOGAD is still debatable. Together, these pathological features in MOGAD are clearly different from those of MS and AQP4 antibody-positive NMOSD, suggesting that MOGAD is an independent autoimmune demyelinating disease entity. Further research is needed to clarify the exact pathomechanisms of demyelination and how the pathophysiology relates to the clinical phenotype and symptoms leading to disability in MOGAD patients.
 BACKGROUND: MS is a chronic inflammatory neurological and immune-mediated disease of multifactorial etiology. Ultra-processed foods (UPFs) have been generally considered unhealthy due to their poor nutritional value. Emerging evidence suggests that factors other than their nutritional content may play an additional role toward chronic inflammation. AIM: To investigate the potential association of UPF consumption and MS severity in a group of MS Italian consecutive patients. METHODS: Demographic (age, sex, marital status, educational level), neurological (EDSS, MSSS), and nutritional (anthropometric measures, dietary habits) information were collected. Physical activity and smoking habits were also investigated. Food items were grouped according to the NOVA classification. Patients were classified in two groups based on MS severity ("mild" and "moderate to high"). RESULTS: Higher UPF consumption was associated with moderate-to-high MS severity compared to lower consumption in both the unadjusted model (OR = 2.28, 95% CI: 1.04-5.01) and after adjustment for potential background (OR = 2.46, 95% CI: 1.04-5.83) and clinical confounding factors (OR = 2.97, 95% CI: 1.13-7.77). CONCLUSIONS: Although these results are only preliminary and hypothesis generating, it is important to explore how various aspects of the diet may relate to MS severity in order to identify the best strategy to support MS patients over the disease course.
 BACKGROUND: There is limited evidence and lack of guidelines for diagnostic laboratory evaluation of patients with possible multiple sclerosis (MS). OBJECTIVE: To survey neurologists on their practice of laboratory testing in patients with possible MS. METHODS: An online survey was developed to query the frequency of serum and cerebrospinal fluid (CSF) studies ordered in the routine evaluation of patients with possible MS, and in three hypothetical clinical cases. Non-MS specialist neurologists who evaluate patients for MS in their practice were invited to participate by MedSurvey (a medical market research company). RESULTS: The survey was completed by 190 neurologists. A mean of 17.2 (SD: 17.0) tests in serum and CSF were reported "always" ordered in the evaluation of patients with possible MS. CSF oligoclonal bands was the most frequently selected ("always" among 73.7% of participants). Antinuclear antibody (43.2%), erythrocyte sedimentation rate (34.2%), and thyroid stimulating hormone (31.6%) were also among the most frequently ordered. DISCUSSION: Extensive laboratory evaluations are often completed in the evaluation of possible MS. However, many of these tests have poor specificity and false positive results could yield unnecessary increased costs, diagnostic delay, and potentially misdiagnosis. Further research is needed to identify optimal laboratory approaches for possible MS.
 BACKGROUND: The two main phenotypes of multiple sclerosis (MS), primary progressive (PPMS) and relapsing Onset (ROMS), show clinical and demographic differences suggesting possible differential risk mechanisms. Understanding the heritable features of these phenotypes could provide aetiological insight. OBJECTIVES: To evaluate the magnitude of familial components in PPMS and ROMS and to estimate the heritability of disease phenotypes. METHODS: We used data from 25,186 MS patients of Nordic ancestry from the Swedish MS Registry between 1987 and 2019 with known disease phenotype (1593 PPMS and 16,718 ROMS) and 251,881 matched population-based controls and 3,364,646 relatives of cases and controls. Heritability was calculated using threshold-liability models. For familial odds ratios (ORs), logistic regression with robust sandwich estimator was utilized. RESULTS: The OR of MS diagnosis in those with a first-degree family member with ROMS was 7.00 and 8.06 in those with PPMS. The corresponding ORs for having a second-degree family member with ROMS was 2.16 and 2.18 in PPMS. The additive genetic effect in ROMS was 0.54 and 0.22 in PPMS. CONCLUSION: Risk of MS increases by several folds in those with a relative with MS. The likelihood of developing either disease phenotype appears independent of genetic predisposition.
 Over the past three years, humanity faced the abrupt spread of COVID-19, responsible for a worldwide health crisis. Initially, it was believed that individuals with chronic disorders, including multiple sclerosis, were more likely to be infected and suffer a worse degree of COVID-19 disease. Therefore, data with regard to COVID-19 disease outcomes in these populations may provide additional insight with regard to the management of chronic diseases during viral pandemics. The objective of this study is to evaluate COVID-19 disease course in people with multiple sclerosis (PwMS) during the COVID-19 pandemic in Greece and explore the impact of vaccination in the outcome of SARS-CoV-2 infection in this population. Anonymized data, extracted from nationwide administrative records between February 2020 and December 2021, were retrospectively analyzed in order to identify PwMS with SARS-CoV-2 infection. Demographic data, as well as data regarding COVID-19 infection and vaccination, were additionally collected. The study sample included 2351 PwMS (65.1% females, 51.2% unvaccinated at the time of infection). A total of 260 PwMS were hospitalized, while 25 PwMS died from COVID-19 disease and its complications. Older age, male sex and the presence of comorbidities were independently associated with a higher probability of hospitalization. The risk of hospitalization was decreased in PwMS receiving some disease-modifying treatments. Anti-CD20s demonstrated high odds ratios without reaching statistical significance. Regarding fatal outcome, only age reached statistical significance. Vaccination provided a significant protective effect against hospitalization but did not exhibit a statistically significant effect on mortality.
 Background Multiple sclerosis (MS) is a chronic autoimmune disease caused by multiple factors. It can lead to many physical and mental symptoms. Fatigue is one of the most commonly mentioned complaints among MS patients that can affect their quality of life. Physical activity has many benefits for the physical and mental health of patients with MS. Aim To assess the role of exercise on fatigue among patients with multiple sclerosis and identify the relationship between depression, sleep quality, sociodemographic variables, and fatigue. Methods This is an analytical cross-sectional study based on a sample size of 235 patients recruited from the MS clinic at King Fahad Hospital (KFH) in Madinah. The outcome of the study was fatigue among MS patients. Data were collected through telephone calls from February to May 2022 using a structured questionnaire and scales, such as the Godin Leisure-Time Exercise Questionnaire (GLTEQ), Modified Fatigue Impact Scale (MFIS), Patient Health Questionnaire (PHQ2), and Pittsburgh Sleep Quality Index (PSQI). Data were analyzed through SPSS version 20 (IBM Corp., Armonk, NY, USA). The correlation coefficient (r), Chi-square tests, and simple and multiple logistic regression were used as found appropriate. Results Out of the total samples, 37.4% were male and 62.6% were female. The median age of patients was 36 years. The prevalence of fatigue was 37% among patients, with a reported median fatigue score of 26. It was found that 63% of the patients were physically inactive; 32.2% were overweight, 14.2% were obese; 63.8% of patients had poor sleep quality. The fatigue score was negatively correlated with the GLTEQ score, but the results were not significant (r=-0.066; P-value (level of significance)=0.335). Nonetheless, a moderately significant correlation was observed between the MFIS and PSQI and MFIS and PHQ2 (r=0.505, P=<0.001 and r=0.520, P=<0.001, respectively). The Chi-square test showed a significant association between fatigue and progressive types of MS, the primary progressive MS (PPMS), secondary progressive MS (SPMS), and relapsing-remitting MS (RRMS) (odds ratio (OR)=4.4; 95% confidence interval (CI): 2.1-8.9), P=<0.001). Depressed patients were 9.7 times more likely to develop fatigue compared to non-depressed patients (P=<0.001). Those with poor sleep quality were 4.6 times more likely to develop fatigue compared to those with good sleep quality (P=<0.001). Fifty-six percent of fatigue among MS patients were predicted by low income, progressive types, unemployment, obesity, depression, and poor sleep quality. Conclusion Fatigue is a major complaint among MS patients. Most of the patients were found to be physically inactive, depressed, and have poor sleep quality. This study found an association between physical inactivity and fatigue, but the results were not significant. There was a significant association between sociodemographic factors like low income and unemployment, poor sleep quality, obesity, progressive types of MS, depression, and fatigue. Encouraging exercise practice and implementing a regular exercise program are needed, along with weight management plans. Further studies and psychological support meetings are required, with the importance of a holistic approach to patient care.

 WHAT IS THIS SUMMARY ABOUT? Previous studies have shown that people living with multiple sclerosis (MS) treated with cladribine tablets have fewer relapses (where new symptoms occur or existing symptoms get worse for 24 hours or more) and delayed disability progression (slowing down of the disease getting worse). The CLASSIC-MS study looked at the long-term effectiveness of treatment with cladribine tablets in people living with MS who had taken part in the original CLARITY and CLARITY Extension clinical studies. WHAT WERE THE RESULTS? Results showed that people treated with cladribine tablets maintained their mobility (the ability to move freely) for longer and experienced other positive effects long after their treatment ended, including being less likely to need further treatment for their MS. WHAT DO THE RESULTS MEAN? The results obtained from CLASSIC-MS show that the benefits of taking cladribine tablets carry on even when patients stop taking the treatment. Clinical Trial Registration: NCT03961204 (CLASSIC-MS) (ClinicalTrials.gov).
 OBJECTIVES: The development of new drugs for the treatment of progressive multiple sclerosis (MS) highlights the need for new prognostic biomarkers. Phase-rim lesions (PRLs) have been proposed as markers of progressive disease but are difficult to identify and quantify. Previous studies have identified T1-hypointensity in PRLs. The aim of this study was to compare the intensity profiles of PRLs and non-PRL white-matter lesions (nPR-WMLs) on three-dimensional T1-weighted turbo field echo (3DT1TFE) MRI. We then evaluated the performance of a derived metric as a surrogate for PRLs as potential markers for risk of disease progression. METHODS: This study enrolled a cohort of relapsing-remitting (n = 10) and secondary progressive MS (n = 10) patients for whom 3 T MRI was available. PRLs and nPR-WMLs were segmented, and voxel-wise normalized T1-intensity histograms were analyzed. The lesions were divided equally into training and test datasets, and the fifth-percentile (p5)-normalized T1-intensity of each lesion was compared between groups and used for classification prediction. RESULTS: Voxel-wise histogram analysis showed a unimodal histogram for nPR-WMLs and a bimodal histogram for PRLs with a large peak in the hypointense limit. Lesion-wise analysis included 1075 nPR-WMLs and 39 PRLs. The p5 intensity of PRLs was significantly lower than that of nPR-WMLs. The T1 intensity-based PRL classifier had a sensitivity of 0.526 and specificity of 0.959. CONCLUSIONS: Profound hypointensity on 3DT1TFE MRI is characteristic of PRLs and rare in other white-matter lesions. Given the widespread availability of T1-weighted imaging, this feature might serve as a surrogate biomarker for smoldering inflammation. CLINICAL RELEVANCE STATEMENT: Quantitative analysis of 3DT1TFE may detect deeply hypointense voxels in multiple sclerosis lesions, which are highly specific to PRLs. This could serve as a specific indicator of smoldering inflammation in MS, aiding in early detection of disease progression. KEY POINTS: • Phase-rim lesions (PRLs) in multiple sclerosis present a characteristic T1-hypointensity on 3DT1TFE MRI. • Intensity-normalized 3DT1TFE can be used to systematically identify and quantify these deeply hypointense foci. • Deep T1-hypointensity may act as an easily detectable, surrogate marker for PRLs.




 A library of queuine analogues targeting the modification of tRNA isoacceptors for Asp, Asn, His and Tyr catalysed by queuine tRNA ribosyltransferase (QTRT, also known as TGT) was evaluated in the treatment of a chronic multiple sclerosis model: murine experimental autoimmune encephalomyelitis. Several active 7-deazaguanines emerged, together with a structure-activity relationship involving the necessity for a flexible alkyl chain of fixed length.
 Children and adolescents with early onset autoimmune diseases have a different seasonality of month of birth than the general population. This pattern is consistent with an infection during pregnancy affecting the fetus or an infection immediately after birth that act as early triggers of the autoimmune diseases. We present data supporting the use of Rotavirus vaccinations in the reduction of incidence of childhood T1D and propose further investigations into whether other anti-virus vaccinations may reduce the burden of other autoimmune diseases such as multiple sclerosis, atopic dermatitis, psoriasis and subtypes of rheumatoid arthritis, Hashimoto thyroiditis.
 BACKGROUND: Sexual dysfunction (SD) is common in women with multiple sclerosis (MS) and affects their quality of life. OBJECTIVES: The primary aim is to assess their expectations concerning SD management. The secondary aim is to identify if expectations were associated with specific patient's characteristics. METHODS: All women with MS who underwent a urodynamic assessment in a neuro-urology clinic and had a standardized assessment of SD expectations between June 2020 and November 2022 were retrospectively screened. Demographic data and assessment of bladder, bowel, and sexual dysfunctions with validated questionnaires were collected. RESULTS: One hundred and sixty-seven patients were included in the study (mean age 47.9 ± 12.5 years). Expectations on SD information or management were reported by 112 (67.1%) patients. Interest in SD information and management was less frequent after menopause (56% vs 80%, p = 0.004), and in those with EDSS>6 (49% vs 74%, p = 0.03) and progressive type of MS (54% vs 71% p = 0.003). In multivariate analysis, the progressive type of MS was the only criterion related to a lack of interest (OR=2.9 IC95% [1.09; 7.72]). CONCLUSIONS: Women with MS have high expectations on treatment and information about SD. A systematic screening of SD expectations should be encouraged.
 Multiple Sclerosis (MS) is a chronic inflammatory, autoimmune disease of the Central Nervous System with a vast spectrum of clinical phenotypes. A major aspect of its clinical presentation is cerebellar ataxia where physiotherapy and treatment modalities play a significant role on its management. This systematic review aims to investigate the physiotherapeutic rehabilitation techniques regarding the management of cerebellar ataxia due to MS and secondary to stratify each protocol as part of a multi structural personalized rehabilitation approach based on the gravity of the symptoms. A Pubmed Medline, Scopus and Web of Science research was performed using the corresponding databases. The results were screened by the authors in pairs. In our study, six (6) non-pharmacological interventional protocols, 3 Randomized Controlled Trials and 3 pilot studies, were included with a total of 145 MS patients. Physiotherapeutic techniques, such as NDT-Bobath, robotic and visual biofeedback re-education protocols and functional rehabilitation techniques were included. In most cases cerebellar ataxic symptoms were decreased post-treatment. The overall quality of the studies included was of moderate level (level B). Rehabilitation in cerebellar ataxia due to MS should be based on multicentric studies with the scope of adjusting different types of treatments and physiotherapeutic techniques based on the severity of the symptom.
 Epidemiologic studies on the risk of multiple sclerosis (MS) or demyelinating events associated with anti-tumor necrosis factor alpha (TNFαalpha;) use among patients with rheumatic diseases or inflammatory bowel diseases have shown conflicting results. Causal directed acyclic graphs (cDAGs) are useful tools for understanding the differing results and identifying the structure of potential contributing biases. Most of the available literature on cDAGs uses language that might be unfamiliar to clinicians. This article demonstrates how cDAGs can be used to determine whether there is a confounder, a mediator or collider-stratification bias and when to adjust for them appropriately. We also use a case study to show how to control for potential biases by drawing a cDAG depicting anti-TNFαalpha; use and its potential to contribute to MS onset. Finally, we describe potential biases that might have led to contradictory results in previous studies that examined the effect of anti-TNFαalpha; and MS, including confounding, confounding by contraindication, and bias due to measurement error. Clinicians and researchers should be cognizant of confounding, confounding by contraindication, and bias due to measurement error when reviewing future studies on the risk of MS or demyelinating events associated with anti-TNFαalpha;use. cDAGs are a useful tool for selecting variables and identifying the structure of different biases that can affect the validity of observational studies.
 Intestinal microbiota can influence the phenotype and function of immune cell responses through the dissemination of bacterial antigens or metabolites. Diet is one of the major forces shaping the microbiota composition and metabolism, contributing to host homeostasis and disease susceptibility. Currently, nutrition is a complementary and alternative approach to the management of metabolic and neurological diseases and cancer. However, the knowledge of the exact mechanism of action of diet and microbiota on the gut-brain communication is only developing in recent years. Here, we reviewed the current knowledge on the effect of diet and microbiota on the gut-brain axis in patients with two different central nervous system diseases, multiple sclerosis and stroke. We have also highlighted the open questions in the field that we believe are important to address to gain a deeper understanding of the mechanisms by which diet can directly or indirectly affect the host via the microbiota. We think this will open up new approaches to the treatment, diagnosis, and monitoring of various diseases.
 BACKGROUND: Multiple sclerosis (MS) is a progressive and neurodegenerative disease of the central nervous system. Its symptoms vary greatly, which makes its diagnosis complex, expensive, and time-consuming. One of its most prevalent symptoms is muscle fatigue. It occurs in about 92% of patients with MS (PwMS) and is defined as a decrease in maximal strength or energy production in response to contractile activity. This article aims to compare the behavior of a healthy control (HC) with that of a patient with MS before and after muscle fatigue. METHODS: For this purpose, a static baropodometric test and a dynamic electromyographic analysis are performed to calculate the area of the stabilometric ellipse, the remitting MS (RMS) value, and the sample entropy (SampEn) of the signals, as a proof of concept to explore the feasibility of this test in the muscle fatigue quantitative analysis; in addition, the statistical analysis was realized to verify the results. RESULTS: According to the results, the ellipse area increased in the presence of muscle fatigue, indicating a decrease in postural stability. Likewise, the RMS value increased in the MS patient and decreased in the HC subject and the opposite behavior in the SampEn was observed in the presence of muscle fatigue. CONCLUSION: Thus, this study demonstrates that SampEn is a viable parameter to estimate muscle fatigue in PwMS and other neuromuscular diseases.
 Multiple sclerosis (MS) is a chronic autoimmune disease characterized by inflammation, demyelination of axons, and oligodendrocyte loss in the central nervous system. This leads to neurological dysfunction, including hand impairment, which is prevalent among patients with MS. However, hand impairment is the least targeted area for neurorehabilitation studies. Therefore, this study proposes a novel approach to improve hand functions compared to current strategies. Studies have shown that learning new skills in the motor cortex (M1) can trigger the production of oligodendrocytes and myelin, which is a critical mechanism for neuroplasticity. Transcranial direct current stimulation (tDCS) has been used to enhance motor learning and function in human subjects. However, tDCS induces non-specific effects, and concurrent behavioral training has been found to optimize its benefits. Recent research indicates that applying tDCS during motor learning can have priming effects on the long-term potentiation mechanism and prolong the effects of motor training in health and disease. Therefore, this study aims to assess whether applying repeated tDCS during the learning of a new motor skill in M1 can be more effective in improving hand functions in patients with MS than current neurorehabilitation strategies. If this approach proves successful in improving hand functions in patients with MS, it could be adopted as a new approach to restore hand functions. Additionally, if the application of tDCS demonstrates an accumulative effect in improving hand functions in patients with MS, it could provide an adjunct intervention during rehabilitation for these patients. This study will contribute to the growing body of literature on the use of tDCS in neurorehabilitation and could have a significant impact on the quality of life of patients with MS.
 Multiple sclerosis (MS) is an immune system-mediated neurodegenerative disease. Recent studies suggest that viral agents, especially the Epstein Barr virus (EBV), are etiological agents for MS. The roles of other viruses in MS have been investigated. Studies have shown an increase in the level of antibodies against bovine leukemia virus (BLV) in patients with MS. In this regard, our study aimed to examine the presence of BLV DNA in peripheral blood mononuclear cells (PBMCs) of MS patients in Iran. In this cross-sectional study, the presence of BLV in 109 Iranian MS patients and 60 healthy controls was evaluated. The isolated PBMCs were used for DNA extraction and PCR, using specific primers for two distinct genes. The mean age of the participants was 39 ± 9.5 years, and 27 (24.77%) of them were male. Clinical evaluation of these patients showed the most frequent MS type to be relapsing-remitting MS (RRMS) (71; 65.14%). BLV evaluation did not show any BLV DNA presence in the PBMCs of individuals in either the MS or healthy control groups. Therefore, our study showed no evidence of BLV infection in Iranian MS patients.
 BACKGROUND AND OBJECTIVES: Medical science needs to further elucidate the role of ultraviolet radiation (UVR), geographic latitude, and the role of vitamin D in the autoimmune disease multiple sclerosis (MS). We separated several papers into categories out of the thousands published and used their conclusions to explore the relationship between UVR and MS. RELEVANCE: MS is increasing in incidence, particularly in women where MS is two to three times that in men and particularly severe in African Americans. METHODS: We collected UVR data at our observatory in Central Maine and calculated the average coefficient of variation (CV(UVR)) for each month for 15 years (2007-2021, inclusive). RESULTS: The month of conception (MOC) is more important than the month of birth (MOB) in explaining how UVR triggers the variable genetic predisposition to MS. We hypothesize that the rapidly increasing CV(UVR) is important in preventing an increase in the activity of the vitamin D receptor (VDR) from August to December, which then requires a higher intensity of UVR later in life to suppress the immune system, therefore predisposing to more MS. LIMITATIONS: One observatory at about 44° latitude. CONCLUSIONS: While variation in UVR is important at the MOC if UVR exceeds a threshold (e.g., if the sunspot number equals or is greater than 90, usually at a solar cycle MAX, or at elevations above approximately 3,000 feet above sea level), the MS mitigating vitamin D-VDR mechanism is overwhelmed and the genotoxic effects of higher-intensity UVR promote MS in those with a genetic predisposition. WHAT IS NEW IN THIS RESEARCH: This paper offers a new concept in MS research.
 The link between Epstein-Barr virus (EBV) and multiple sclerosis (MS) has puzzled researchers since it was first discovered over 40 years ago. Until that point, EBV was primarily viewed as a cancer-causing agent, but the culmination of evidence now shows that EBV has a pivotal role in development of MS. Early MS disease is characterised by episodic neuroinflammation and focal lesions in the central nervous system (CNS) that over time develop into progressive neurodegeneration and disability. Risk of MS is vanishingly low in EBV seronegative individuals, history of infectious mononucleosis (acute symptomatic primary infection with EBV) significantly increases risk and elevated antibody titres directed against EBV antigens are well-characterised in patients. However, the underlying mechanism - or mechanisms - responsible for this interplay remains to be fully elucidated; how does EBV-induced immune dysregulation either trigger or drive MS in susceptible individuals? Furthermore, deep understanding of virological and immunological events during primary infection and long-term persistence in B cells will help to answer the many questions that remain regarding MS pathogenesis. This review discusses the current evidence and mechanisms surrounding EBV and MS, which have important implications for the future of MS therapies and prevention.
 OBJECTIVE: Executive functioning (EF) can be one of the earliest, despite under-detected, impaired cognitive domains in patients with multiple sclerosis (pwMS). However, it is still not clear the role of EF on verbal fluency tests given the presence of information processing speed (IPS) deficits in pwMS. METHOD: Performance of a group of 43 pwMS without IPS impairment as measured with the Symbol Digit Modalities Test (SDMT) and a group of 32 healthy controls (HC) was compared on the Phonemic and Semantic Fluency Tests. For each group, we scored the number of words generated (i) in the early time interval (i.e., first 15 sec, semi-automatic process) and (ii) in the late time interval (i.e., from 15 to 60 sec, controlled process). RESULTS: Globally, pwMS produced significantly fewer words than HC on the Phonemic but not on the Semantic Fluency Test. Crucially, in the Phonemic Fluency Test pwMS generated significantly fewer words than HC in the late time interval, whereas no significant difference between the two groups emerged in the early time interval. CONCLUSIONS: These findings suggest that executive dysfunction is the core element on the Phonemic Fluency Test also in pwMS and it deserves attention in both research and clinical practice.
 Multiple sclerosis (MS) is an immune-inflammatory disease that attacks and damages myelinated axons in the central nervous system (CNS) and causes nontraumatic neurological impairment in young people. Historically, Lidwina of Schiedam documented the first MS case. After that, Augustus d'Este wrote for years about how his MS symptoms worsened. Age, sex, genetics, environment, smoking, injuries, and infections, including herpes simplex and rabies, are risk factors for MS. According to epidemiology, the average age of onset is between 20 and 40 years. MS is more prevalent in women and is common in Europe and America. As diagnostic methods and criteria change, people with MS may be discovered at earlier and earlier stages of the disease. MS therapy has advanced dramatically due to breakthroughs in our knowledge of the disease's etiology and progression. Therefore, the efficacy and risk of treatment medications increased exponentially. Management goals include reducing lesion activity and avoiding secondary progression. Current treatment approaches focus on managing acute episodes, relieving symptoms, and reducing biological activity. Disease-modifying drugs such as fingolimod, interferon-beta, natalizumab, and dimethyl fumarate are the most widely used treatments for MS. For proof of the efficacy and safety of these medications, investigations in the real world are necessary.
 BACKGROUND: Children with the chronic disease multiple sclerosis (MS) report lower health-related quality of life (HRQOL) compared with children who experience transient illness. The relationship between an MS diagnosis and the HRQOL of affected children is mediated by parental HRQOL. Interventions to improve the HRQOL of children with MS should, therefore, include parents of affected children. METHODS: We performed a configurative review for improvements in the HRQOL of children facing diseases similar to MS and their parents. We used the generated concepts to form theories. Next, we performed qualitative interviews with clinicians who care for children with MS to characterize overlap between the proposed theories and usual care. Finally, we generated recommendations for improving the HRQOL of children with MS and their parents. RESULTS: We theorize that the HRQOL of children with MS and their parents may be improved by strengthening self-concept, hope, and knowledge. Qualitative interviews with 7 clinicians who care for children with MS revealed no common psychosocial care protocol. The interviews did, however, reveal sources of psychosocial care that overlap with the proposed theories and barriers to optimizing such care. CONCLUSIONS: Grounded in theory and clinically oriented practice, recommendations to improve the HRQOL of children with MS and their parents are to implement standardized screening, pool provider counseling strategies, create computer applications with psychosocial interventions, promote age-appropriate education resources, and secure positions for MS specialists.
 BACKGROUND: Multiple sclerosis (MS) is a neurodegenerative disorder. Individuals with MS frequently present symptoms such as functional disability, obesity, and anxiety and depression. Axonal demyelination can be observed and implies alterations in mitochondrial activity and increased inflammation associated with disruptions in glutamate neurotransmitter activity. In this context, the ketogenic diet (KD), which promotes the production of ketone bodies in the blood [mainly β-hydroxybutyrate (βHB)], is a non-pharmacological therapeutic alternative that has shown promising results in peripheral obesity reduction and central inflammation reduction. However, the association of this type of diet with emotional symptoms through the modulation of glutamate activity in MS individuals remains unknown. AIM: To provide an update on the topic and discuss the potential impact of KD on anxiety and depression through the modulation of glutamate activity in subjects with MS. DISCUSSION: The main findings suggest that the KD, as a source of ketone bodies in the blood, improves glutamate activity by reducing obesity, which is associated with insulin resistance and dyslipidemia, promoting central inflammation (particularly through an increase in interleukins IL-1β, IL-6, and IL-17). This improvement would imply a decrease in extrasynaptic glutamate activity, which has been linked to functional disability and the presence of emotional disorders such as anxiety and depression.
 (1) Background: Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease. Fatigue is a prevalent and debilitating symptom that significantly impacts the quality of life of these patients. A relationship between personality traits and fatigue in MS has been hypothesized but not clearly defined. (2) Methods: A literature search was carried out from databases up to April 2023 for studies correlating personality traits and fatigue in patients suffering from MS. (3) Results: A total of ten articles was included; most of the studies depict a neuroticism-fatigue correlation; however, they were not consistent in terms of the fatigue, personality, and covariate assessments. (4) Conclusions: The clinical and methodological heterogeneity of the included studies prevented us from drawing any firm conclusion on the link between personality traits and fatigue in MS. Several models of personality and different fatigue assessments have been found. Despite this, a common pathway shows that the neuroticism trait or similar personality patterns has a role in fatigue diagnosis. This may be a useful target to improve the quality of life and enhance the modification of the disease treatment results. Further homogeneous and longitudinal studies are needed.
 Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by inflammation and neurodegeneration. Current research suggests that diet may influence disease course, severity of symptoms, and quality of life in MS patients. The ketogenic diet (KD) has been used for more than a century as a therapeutic approach for various medical conditions. It was originally developed in the 1920s as a treatment option for epilepsy, and especially in the last 30 years, has gained popularity for its potential benefits in a variety of neurological conditions other than epilepsy. This prompted us to perform a literature survey regarding the effect of KD on the onset and progression of MS. The here reviewed 15 original research articles including in vitro, preclinical, and clinical studies provide evidence for the safety and feasibility of the KD in MS, showing potential neuroprotective effects and positive impacts on cellular metabolism and disease outcome. Since the literature is limited and most studies were conducted with low numbers of MS patients and rather exploratory in nature, further studies with larger cohorts are needed to gain a better understanding of the mechanisms by which the improvements of the MS disease course are achieved.
 BACKGROUND: We compared the characteristics, comorbidities, and complications in spinal deformity patients with and without multiple sclerosis (MS) undergoing primary lumbar spine fusion. METHODS: We used the Nationwide Inpatient Sample (NIS) from 2003 to 2014, International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis and procedure codes to create experimental MS (842 patients) and non-MS control (165,726 patients) cohorts undergoing primary lumbar spine fusion. Characteristics, comorbidities, and complications in spinal deformity patients with and without MS were evaluated using univariate and bivariate analysis. RESULTS: MS spinal deformity patients undergoing primary lumbar spine fusion were younger, more likely to be female and more likely to undergo surgery at urban teaching hospitals. They also exhibited higher rates of depression and lower rates of diabetes without chronic complications, hypertension, and renal failure. However, no significant differences were found in mortality or total perioperative complication rates between MS and nonMS patients. CONCLUSION: We found that MS versus non-MS patients undergoing primary lumbar fusion for spinal deformity were younger, more likely to be female and had higher rates of depression but lower rates of diabetes, hypertension, and renal failure. Notably, both groups experienced comparable mortality and perioperative complication rates.
 Multiple sclerosis (MS) is a demyelinating, degenerating disorder of the central nervous system (CNS) that is accompanied by mitochondria energy production failure. A loss of myelin paired with a deficit in energy production can contribute to further neurodegeneration and disability in patients in MS. Mitochondria are essential organelles that produce adenosine triphosphate (ATP) via oxidative phosphorylation in all cells in the CNS, including neurons, oligodendrocytes, astrocytes, and immune cells. In the context of demyelinating diseases, mitochondria have been shown to alter their morphology and undergo an initial increase in metabolic demand. This is followed by mitochondrial respiratory chain deficiency and abnormalities in mitochondrial transport that contribute to progressive neurodegeneration and irreversible disability. The current methodologies to study mitochondria are limiting and are capable of providing only a partial snapshot of the true mitochondria activity at a particular timepoint during disease. Mitochondrial functional studies are mostly performed in cell culture or whole brain tissue, which prevents understanding of mitochondrial pathology in distinct cell types in vivo. A true understanding of cell-specific mitochondrial pathophysiology of MS in mouse models is required. Cell-specific mitochondria morphology, mitochondria motility, and ATP production studies in animal models of MS will help us understand the role of mitochondria in the normal and diseased CNS. In this review, we present currently used methods to investigate mitochondria function in MS mouse models and discuss the current advantages and caveats with using each technique. In addition, we present recently developed mitochondria transgenic mouse lines expressing Cre under the control of CNS specific promoters to relate mitochondria to disease in vivo.
 Interferon (IFN)-β is the first-line disease management choice in multiple sclerosis (MS) with profound effects; however, in up to 50% of patients, clinical response does not occur. Ascertaining the responding state, need a long-term clinical follow-up, and this may lead to delay in use of other effective medications. IFN-induced cascade and its regulation is considered to play a major role in MS. Adenosine deaminase, RNA-specific (ADAR) dysregulation is important to IFN signaling pathway as an activity suppressor. Hence, we investigated the expression of ADAR and its single nucleotide variants of rs2229857 association with response to IFN-β in relapsing-remitting MS patients. mRNA levels and genotyping of rs2229857 in 167 MS patients were investigated via SYBR Green real-time (RT)-quantitative polymerase chain reaction and high-resolution melting RT PCR, respectively. The allele-A in rs2229857 and higher expression of ADAR were associated with poor response to IFN-β. Two response groups were significantly different in terms of annualized relapse rate, first symptoms, first extended disability status scale (EDSS), current EDSS, and the MS severity score. According to this study's findings, assessment of transcript levels and also variants in ADAR may be useful in identifying patients' response to IFN-β before starting treatment. Further investigations are needed to determine the potency of ADAR to be a predictive biomarker in drug responsiveness.
 BACKGROUND: Progression Independent of Relapse Activity (PIRA) is heterogeneously described in patients with multiple sclerosis (MS) regarding the frequency and nature of PIRA. This systematic review was conducted to characterise and define the elements of PIRA. METHOD: This systematic review was conducted and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A systematic search was conducted of the databases Embase, Medline, Cochrane Central Register of Controlled Trials, Scopus, Web of Science, ClinicalTrials.gov and Google Scholar. RESULTS: 5,812 studies were identified by the initial search. 13 studies satisfied the inclusion criteria and were included in the systematic review. PIRA definitions varied considerably between studies. In the context of these variable definitions, along with other methodological differences relating to disease modifying therapy (DMT) use and follow-up duration, the reported proportion of patients experiencing PIRA varied from 4% to 24%. CONCLUSIONS: The currently available research supports the presence of PIRA in relapsing MS. Based on review of the existing literature, we propose a definition of PIRA that is clinically relevant and minimises confounding from inclusion of patients who have reached the secondary progressive phase of the disease.
 Climate change is contributing to increasingly hazardous tropical cyclones that endanger persons living in susceptible coastal and island communities. People living with chronic illness, including multiple sclerosis (MS), face unique challenges and vulnerabilities when exposed to hurricane hazards. Disaster and emergency preparedness requires a customized approach that considers the necessary adaptations to accommodate the mobility, self-care, sensory, cognitive, and communication impairments of persons living with MS. Related considerations include the potential for worsening neurologic signs and symptoms during and after a catastrophic storm. The impact of emotional and financial stresses, as well as disruptions in health care delivery, on this population are also key concerns. This paper addresses the challenges faced by individuals with MS in advance of, during, and in the aftermath of extreme storms. We propose new guidelines on how health care professionals can assist persons with MS when creating tailored disaster readiness and response plans.
 Multiple sclerosis (MS) and myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) share the symptom of fatigue, and might even coexist together. Specifically focusing on genetics, pathophysiology, and neuroimaging data, the authors discuss an overview of the parallels, correlation, and differences in fatigue between MS and ME/CFS along with ME/CFS presence in MS. Studies have revealed that the prefrontal cortex and basal ganglia regions, which are involved in fatigue regulation, have similar neuroimaging findings in the brains of people with both MS and ME/CFS. Additionally, in both conditions, genetic factors have been implicated, with particular genes known to enhance susceptibility to MS and CFS. Management approaches for fatigue in MS and ME/CFS differ based on the underlying factors contributing to fatigue. The authors also focus on the recent updates and the relationship between MS and sleep disorders, including restless legs syndrome, focusing on pathophysiology and therapeutic approaches. Latest therapeutic approaches like supervised physical activity and moderate-intensity exercises have shown better outcomes.
 This Summary of Research summarizes a previously published discussion between people with multiple sclerosis (PwMS) and their caregivers and healthcare professionals (HCPs) about how to include caregivers in consultations and decisions about multiple sclerosis (MS) care. The aim of the discussion was to help HCPs to understand differences in these relationships so they can adapt the style of consultations to support everyone.
 BACKGROUND AND INTRODUCTION: Federated learning (FL) has been widely employed for medical image analysis to facilitate multi-client collaborative learning without sharing raw data. Despite great success, FL's applications remain suboptimal in neuroimage analysis tasks such as lesion segmentation in multiple sclerosis (MS), due to variance in lesion characteristics imparted by different scanners and acquisition parameters. METHODS: In this work, we propose the first FL MS lesion segmentation framework via two effective re-weighting mechanisms. Specifically, a learnable weight is assigned to each local node during the aggregation process, based on its segmentation performance. In addition, the segmentation loss function in each client is also re-weighted according to the lesion volume for the data during training. RESULTS: The proposed method has been validated on two FL MS segmentation scenarios using public and clinical datasets. Specifically, the case-wise and voxel-wise Dice score of the proposed method under the first public dataset is 65.20 and 74.30, respectively. On the second in-house dataset, the case-wise and voxel-wise Dice score is 53.66, and 62.31, respectively. DISCUSSIONS AND CONCLUSIONS: The Comparison experiments on two FL MS segmentation scenarios using public and clinical datasets have demonstrated the effectiveness of the proposed method by significantly outperforming other FL methods. Furthermore, the segmentation performance of FL incorporating our proposed aggregation mechanism can achieve comparable performance to that from centralized training with all the raw data.
 Multiple sclerosis (MS) is an autoimmune-mediated demyelinating disease of the central nervous system. The main pathological features are inflammatory reaction, demyelination, axonal disintegration, reactive gliosis, etc. The etiology and pathogenesis of the disease have not been clarified. The initial studies believed that T cell-mediated cellular immunity is the key to the pathogenesis of MS. In recent years, more and more evidence has shown that B cells and their mediated humoral immune and innate immune cells (such as microglia, dendritic cells, macrophages, etc.) also play an important role in the pathogenesis of MS. This article mainly reviews the research progress of MS by targeting different immune cells and analyzes the action pathways of drugs. The types and mechanisms of immune cells related to the pathogenesis are introduced in detail, and the mechanisms of drugs targeting different immune cells are discussed in depth. This article aims to clarify the pathogenesis and immunotherapy pathway of MS, hoping to find new targets and strategies for the development of therapeutic drugs for MS.
 BACKGROUND: Apathy is relatively frequent and significantly associated with clinical and cognitive outcomes in Multiple Sclerosis (MS), even if previous research has produced mixed results. This varied picture could be due to most studies treating apathy as a unitary construct, despite the evidence showing that apathy is a multifaceted syndrome including three different sub-domains (i.e., cognitive, affective, and behavioral). This study aims to investigate the neuropsychological correlates of apathy fractionated into its three sub-domains in participants with MS. METHODS: Eighty-five participants with MS underwent a comprehensive neuropsychological battery. The severity of apathy symptoms was assessed by the self-report version of the Apathy Evaluation Scale. RESULTS: Correlational analysis showed that cognitive apathy sub-domain scores had a high correlation with the performances obtained at cognitive tests tapping into inhibitory control (i.e., IML and Strop test-interference task), whereas the affective apathy sub-domain scores had a high correlation with the performances obtained at cognitive test tapping into the use of executive functions in visuospatial abilities (i.e., Clock Drawing Test). Moreover, linear regression analysis results showed that the cognitive apathy sub-domain scores predicted executive functioning domain scores and that the cognitive and affective apathy sub-domains scores predicted visuospatial abilities domain scores. CONCLUSION: These results confirm that apathy is a multidimensional concept with important neuropsychological correlates, visible only when it is fractionated into its sub-domains.
 INTRODUCTION: Intermittent fasting (IF) has become a popular dietary pattern for adults with multiple sclerosis (MS), and initial studies in animal models and human trials indicate promising results for improving symptoms and slowing disease progression. Most studies published to date have focused on alternate day fasting or fasting mimicking diets including a 5:2 pattern, in which participants greatly restrict calorie intake on two non-consecutive days and eat regularly on other days; however, time restricted eating (TRE) may be equally effective for improving symptoms and may lead to better long term adherence due to its focus only on the time of day in which calories are consumed with no restriction on number of calories or types of food consumed. METHODS: The purpose of this pilot study was to determine the feasibility and acceptability of a TRE intervention in adults with relapsing remitting MS (RRMS). Participants (n = 12) were instructed to eat all food within an 8-h window every day and fast the remaining 16 h for 8 weeks. RESULTS: The eating pattern was determined to be feasible based on retention rates (n = 11; 92%) and acceptable based on participant feedback. DISCUSSION: Exploratory results of changes in cognition, pain, and fatigue, indicate that further study of TRE in this population is warranted. CLINICAL TRIAL REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT04389970; NCT04389970.
 (1) Background: Multiple Sclerosis (MS) is a chronic, progressive, immune-mediated disorder that affects the Central Nervous System and is the most common cause of non-traumatic neurological disability in young adults. The study aimed to assess the levels of stress, resilience, well-being, sleep quality, and fatigue in Israeli people with MS (PwMS), and to examine the associations between these factors and the sociodemographic and clinical characteristics. These factors had never before been studied in conjunction in PwMS, nor had they been systematically addressed in Israel, the unique geopolitical situation of which may pose unique challenges. (2) Methods: This was a survey-based, cross-sectional study conducted through an Internet platform. (3) Results: Israeli PwMS who participated in the study were experiencing relatively high levels of stress and low resilience, poor sleep quality, and severe fatigue. The analysis revealed significant associations between resilience and stress, well-being, and anxiety, as well as stress and well-being, resilience, sleep quality, fatigue, and Clinically Isolated Syndrome (CIS). (4) Conclusions: the Israeli PwMS who participated in the study were experiencing higher levels of stress, lower resilience and worse sleep quality than PwMS in other countries, as compared to results previously reported in literature. The findings of this study ought to serve as a call to action for the MS care providers in Israel and warrant further research into the possible causes of the phenomenon and strategies to address it.
 Fatigue is a prevalent symptom experienced by individuals diagnosed with multiple sclerosis (MS), which greatly affects their daily activities and causes frustration and depression, thus affecting their lives and society. This can be prevented through the use of medicines such as L-carnitine and modafinil. The study aimed to examine the effect of L-carnitine and modafinil on fatigue and which one is better for MS patients. This was a clinical trial. This clinical trial was conducted in cooperation between Al-Kut University College and an MS consultant at Al-Zahraa Teaching Hospital in addition to the private neurological clinic from October 1, 2022, to March 15, 2023. Forty participants were split into two groups; both of which were almost identical characteristics regarding age, disease duration, and degree of fatigue. Group I (n = 20): relapsing-remitting MS patients with fatigue received modafinil. Group II (n = 20): relapsing-remitting MS patients with fatigue received L-carnitine. Fatigue was evaluated according to the Modified Fatigue Impact Scale (MFIS). The statistical work was done in SPSS (IBM Corp., Chicago, IL, USA, version 24). P values were calculated by the t-test. Significant data have P = 0.05. After 2 months of treatment, the results show a significant decrease in MFIS in both groups with a higher reduction in patients who use L-carnitine. Both modafinil and L-carnitine show a significant influence on fatigue in MS patients, and these effects are more in L-carnitine.


 Mycobacterium abscessus infections have been reported as adverse events related to medical tourism. We report M. abscessus meningitis in a patient who traveled from Colorado, USA, to Mexico to receive intrathecal stem cell injections as treatment for multiple sclerosis. We also review the management of this challenging central nervous system infection.
 BACKGROUND: Radiologically isolated syndrome (RIS) describes asymptomatic individuals with incidental radiologic abnormalities suggestive of multiple sclerosis (MS). Much of RIS literature is about adult-onset cases. Treatment of RIS is controversial, especially in pediatric age, but early treatment in selected patients might improve long-term outcomes. CASE PRESENTATION: We report a single RIS patient who followed up for 18 years in our MS center. At first, she was only monitored with follow-up MRIs. Then, as the lesion load increased, she was treated with a first-line disease-modifying treatment (DMT) reaching MRI stability. CONCLUSION: This report highlights how treatment can be an appropriate choice in pediatric forms of RIS.
 We discuss a case of a 53-year-old woman with multiple sclerosis on monthly ofatumumab injections, who was infected with SARS-CoV-2 with persistent fevers for seven weeks. She was hospitalized for fever with diagnostic workup being unremarkable with negative SARS-CoV-2 IgM and undetectable nucleocapsid IgG antibodies four weeks out from the initial infection, indicating she may not have mounted an appropriate immune response to the infection. Patients on immunosuppression therapy may have a prolonged course of disease given that medications such as ofatumumab can take up to 24 weeks of B-cell recovery post-treatment discontinuation and a longer road to recovery.
 BACKGROUND: Relapse risk after delivery is increased in women with active multiple sclerosis (MS), the best strategy to reduce it is unknown. We aimed to assess the association of four different postpartum strategies with relapses during the first 6 months post partum. METHODS: This cohort study includes data prospectively collected through structured telephone interviews from the German Multiple Sclerosis and Pregnancy Registry. Pregnancies with active MS (fingolimod or natalizumab treatment OR relapse within 1 year before pregnancy) and postpartum follow-up of ≥6 months were included. We compared four strategies: (1) intention to breastfeed exclusively without disease-modifying therapy (DMT) (exclusive breast feeding ≥2 months or switching to non-exclusive/weaning within 2 weeks after a relapse during the first 2 months), (2) early treatment with natalizumab/fingolimod and (3) other DMT initiated within 6 weeks post partum before a relapse. If women did not or only partially breastfed, or started DMT≤6 weeks after delivery after a relapse or later, we assumed (4) no-DMT-no-exclusive- breastfeeding-strategy. Main outcome was time to postpartum MS relapses. RESULTS: In 867 women with 911 pregnancies, most (n=416) intended to breastfeed exclusively or had no-DMT-no-exclusive-breastfeeding-strategy (n=290); fewer started fingolimod (n=38), natalizumab (n=74) or another DMT (n=93) early. Recurrent time-to-event analysis showed a statistically significant reduction in relapse hazard only with the natalizumab/fingolimod-strategy as of months 3-4 post partum compared with intention-to-breastfeed-exclusively-strategy. The very early relapse risk was highest in no-DMT-no-exclusive-breastfeeding-strategy. CONCLUSION: In active MS, an early postpartum treatment strategy should be determined well before delivery. Natalizumab/fingolimod-strategy reduced postpartum relapse hazard from month 3, but none diminished the early postpartum relapse hazard.
 PURPOSE: In this review, we have highlighted a new class of drugs, Bruton's tyrosine kinase (BTK) inhibitors, and summarized the results of recent clinical trials in the treatment of multiple sclerosis. VIEWS: Multiple sclerosis (MS) is considered an autoimmune disease of the central nervous system, in which B-lymphocytes and myeloid cells, such as macrophages and microglia, play an important role in the pathogenesis. B-cells induce pathological processes by presenting autoantigens to T-lymphocytes, secreting pro-inflammatory cytokines, and forming ectopic lymphoid follicle-shaped clusters. Accordingly, the activation of microglia contributes to the development of chronic inflammation due to the production of chemokines, cytokines, reactive oxygen, and nitrogen species. BTK is an enzyme important in the activation and function of both B-lymphocytes and microglia. The demand for highly effective and well-tolerated drugs still remains at all stages of MS despite the availability of a number of effective drugs against the disease. Thus, in recent years BTK inhibitors have been the newest approach in the treatment of MS, since they affect the leading links of the pathogenesis of this disease and are able to pass through the blood-brain barrier. CONCLUSIONS: The study of new mechanisms of the development of MS continues in combination with the elaboration of new treatment methods, i.e., Bruton's tyrosine kinase inhibitors. The review provided the analysis of core studies evaluating the safety and efficacy of these drugs. In the future, positive results of these studies will be able to greatly expand the therapy for various forms of MS.
 PURPOSE: To ascertain the feasibility and acceptability of delivering a job retention vocational rehabilitation intervention [MSVR] for people with multiple sclerosis (pwMS) in a community setting. Secondary objectives included determining whether MSVR was associated with changes in quality of life, fatigue, mood, cognition, workplace accommodations, work instability, work self-efficacy, and goal attainment. METHODS: Single-centre mixed-methods feasibility case series. RESULTS: 15 pwMS and three employers received 8.36 (SD = 4.48) and 1.94 (SD = 0.38) hours of MSVR respectively over three months. The intervention predominantly addressed managing cognition, fatigue, and negotiating reasonable accommodations. Four healthcare professionals were recruited to clarify clinical information.The intervention was feasible to deliver, and there was a significant positive impact on goal attainment immediately following MSVR (t(14) = 7.44, p = .0001, d = 1.9), and at months 3 (t(13) = 4.81, p = .0001, d = 1.28), 6 (t(11) = 4.45, p = .001, d = 1.28), and 12 (t(9) = 5.15, p = .001, d = -2.56). There was no impact on quality of life, fatigue, mood, cognition, workplace accommodations, work instability, and work self-efficacy. In post-intervention interviews, participants reported that MSVR was acceptable. Four themes were derived regarding the context, employer engagement, empowerment through knowledge, and intervention components and attributes. CONCLUSION: It was feasible and acceptable to deliver MSVR. Participants better understood their MS, became more confident managing problems at work and attained their work-related goals.IMPLICATIONS FOR REHABILITATIONPeople with multiple sclerosis (MS) experience problems at work because of the interaction between symptoms and environmental factors (e.g., co-workers' attitudes).Vocational rehabilitation for people with MS and their employers should be tailored in terms of content and intensity.People with MS can be empowered at work by learning about MS and how their symptoms fluctuate over time.Understanding legal responsibilities and examples of accommodations at work can be beneficial for employers.
 AIM: Synthetic MRI (SyMRI) works on the MDME sequence, which acquires the relaxation properties of the brain and helps to measure the accurate tissue properties in 6 minutes. The aim of this study was to evaluate the synthetic MRI (SyMRI)-generated myelin (MyC) to white matter (WM) ratio, the WM fraction (WMF), MyC partial maps performing normative brain volumetry to investigate MyC loss in multiple sclerosis (MS) patients with white-matter hyperintensites (WMHs) and non-MS patients with WMHs in a clinical setting. MATERIALS AND METHODS: Synthetic MRI images were acquired from 15 patients with MS, and from 15 non-MS patients on a 3T MRI scanner (Discovery MR750w; GE Healthcare; Milwaukee, USA) using MAGiC, a customized version of SyntheticMR's SyMRI® IMAGE software marketed by GE Healthcare under a license agreement. Fast multi-delay multi-echo acquisition was performed with a 2D axial pulse sequence with different combinations of echo time (TEs) and saturation delay times. The total image acquisition time was 6 minutes. SyMRI image analysis was done using SyMRI software (SyMRI Version: 11.3.6; Synthetic MR, Linköping, Sweden). SyMRI data were used to generate the MyC partial maps and WMFs to quantify the signal intensities of test group and control group, andcontrol group , and their mean values were recorded. All patients also underwent conventional diffusion-weighted imaging, i.e., T1w and T2w imaging. RESULTS: The results showed that the WMF was significantly lower in the test group than in the control group (38.8% vs 33.2%, p < 0.001). The Mann-Whitney U nonparametric t-test revealed a significant difference in the mean myelin volume between the test group and the control group (158.66 ± 32.31 vs. 138.29 ± 29.28, p = 0.044). Also, there were no significant differences in the gray matter fraction and intracranial volume between the test group and the control group. CONCLUSIONS: We observed MyC loss in test group using quantitative SyMRI. Thus, myelin loss in MS patients can be quantitatively evaluated using SyMRI.
 BACKGROUND: Multiple sclerosis (MS) is the most prevalent neurological disease among young adults. Because of the chronic nature of this disease, it is important to assess quality of life in these patients. The Multiple Sclerosis Quality of Life -29 (MSQOL-29) questionnaire which contains two main scales, Physical Health Composite (PHC) and Mental Health Composite (MHC), has been designed for this goal. The purpose of the present study is to translate and validate a Persian version of MSQOL-29 (P-MSQOL-29). METHODS: Using the forward-backward translation method, a panel of experts established the content validity of P-MSQOL-29. It was then administered to 100 patients with MS who also completed the Short Form-12 (SF-12) questionnaire. Cronbach's alpha was used to assess the internal consistency of P-MSQOL-29. Spearman's correlation coefficient was used to analyze the concurrent validity when correlating the items of P-MSQOL-29 to SF-12. RESULTS: Mean (Standard Deviation) of PHC and MHC for all patients was 51 (16.4), and 58 (23), respectively. Cronbach's alpha was 0.7 for PHC and 0.9 for MHC. Thirty patients completed the questionnaire again after 3-4 weeks, Intraclass Correlation Coeffiecient (ICC) was 0.80 for PHCs and 0.85 for MHCs (both P values < 0.01). A moderate to high correlation was detected between MHC/PHC and the corresponding scales of SF-12 (MHC with Mental Component Score: ρ = 0.55; PHC with Physical Component Score: ρ = 0.77; both P values < 0.01). CONCLUSION: P-MSQOL-29 is a valid and reliable questionnaire and can be used for assessing quality of life in patients with MS.
 Autoimmune thyroid disease (AITD) is the most common adverse effect in alemtuzumab (ALZ) treated relapsing-remitting (RR) multiple sclerosis (MS) patients. The objective of this prospective study was to analyze the occurrence, timing of onset, clinical course, and laboratory characteristics of AITD post-ALZ. We evaluated 35 RRMS patients treated with ALZ at a single academic MS center; clinical and laboratory data were collected before ALZ initiation and thereafter quarterly on follow-up with a median of 43.5 months. Seventeen out of 31 patients (54.8%) with no prior history of thyroid dysfunction developed AITD with a mean onset of 19.4 months ± 10.2 (SD) after the first ALZ cycle; Graves' disease (GD) (n = 9); hypothyroidism with positive stimulating thyrotropin receptor antibodies (TRAb) (n = 1); Hashimoto thyroiditis (HT) (n = 6); HT with hypothyroidism (n = 1). Interestingly, seven of nine (77.7%) GD patients showed a fluctuating course. Three out of four patients with preexisting thyroid disease remained stable, whereas one with prior HT and hypothyroidism developed fluctuating GD. All patients with GD commenced antithyroid drugs (ATDs); five continued on "block and replace" treatment; one required radioactive iodine, and one total thyroidectomy. Our analysis showed earlier onset of ALZ-induced AITD in comparison to most other ALZ cohorts; overall, these patients required complex therapeutic approaches of the AITD. We observed a higher rate of fluctuating GD, with earlier onset and lower remission rate than previously reported, which in the majority of patients required prolonged "block and replace" therapy in the minimum dose of each therapeutic agent or more definitive interventions.
 BACKGROUND: Ambulatory impairment is a common and complex manifestation of multiple sclerosis (MS), and longitudinal patterns are not well understood. OBJECTIVE: To characterize longitudinal walking speed trajectories in a general MS patient population and in those with early disease (⩽ 5 years from onset), identify subgroups with similar patterns, and examine associations with individual attributes. METHODS: Using a retrospective cohort study design, latent class growth analysis was applied to longitudinal timed 25-foot walk (T25-FW) data from 7683 MS patients, to determine T25-FW trajectories. Associations were evaluated between trajectory assignment and individual attributes. Analyses were repeated for 2591 patients with early disease. RESULTS: In the general patient population, six trajectories were discerned, ranging from very minimal to very high impairment at baseline, with variability in impairment accrual. The clusters with moderate to very high walking impairment were associated with being female, older and Black American, longer symptom duration, progressive course, and depressive symptoms. In the early disease subset, eight trajectories were discerned that included two subgroups that rapidly accrued impairment. CONCLUSION: We identified novel subgroups of MS patients will distinct long-term T25-FW trajectories. These results underscore that socially disadvantaged and economically marginalized MS patients are the most vulnerable for severe ambulatory impairment.
 BACKGROUND: Hearing can be impaired in many neurological conditions and can even represent a forme fruste of specific disorders. Auditory function can be measured by either subjective or objective tests. Objective tests are more useful in identifying which auditory pathway (superior or inferior) is most affected by disease. The inner ear's perilymphatic fluid communicates with the cerebrospinal fluid (CSF) via the cochlear aqueduct representing a window from which pathological changes in the contents of the CSF due to brain inflammation could, therefore, spread to and cause inflammation in the inner ear, damaging inner hair cells and leading to hearing impairment identifiable on tests of auditory function. METHODS: A systematic review of the literature was performed, searching for papers with case-control studies that analyzed the hearing and migraine function in patients with neuro-inflammatory, neurodegenerative disorders. With data extracted from these papers, the risk of patients with neurological distortion product otoacoustic emission (DPOAE) was then calculated. RESULTS: Patients with neurological disorders (headache, Parkinson's disease, and multiple sclerosis) had a higher risk of having peripheral auditory deficits when compared to healthy individuals. CONCLUSION: Existing data lend credence to the hypothesis that inflammatory mediators transmitted via fluid exchange across this communication window, thereby represents a key pathobiological mechanism capable of culminating in hearing disturbances associated with neuroimmunological and neuroinflammatory disorders of the nervous system.
 BACKGROUND: Self-concept change may impact psychological wellbeing and functioning in people with MS (pwMS). However, the extent and nature of change in self-concept that pwMS experience is poorly understood, owing to the lack of quantitative measures available to assess this construct. OBJECTIVE: To examine the factor structure, validity, and internal consistency of the newly developed Multiple Sclerosis Self-Concept Change Scale (MSSCCS). METHODS: Items measuring self-concept change were created, reviewed by a panel of experts and pre-tested in a sample of 135 pwMS. A revised list of 51 items were then administered to 1307 pwMS (80.3% female; Age M = 59.21 years, SD = 11.40), together with measures of disease impact and psychosocial functioning. RESULTS: Exploratory factor analysis using principal axis factor extraction in 643 randomly selected participants yielded 23-items measuring 5 latent factors for the final MSSCCS. Confirmatory factor analysis involving the remaining participants supported the 5-factor model, as well as a 2nd order model of "global change". Internal consistency of the total scale was good (α = 0.89). The MSSCCS also demonstrated evidence of concurrent and construct validity. CONCLUSION: The MSSCCS is a reliable and valid assessment, which may assist in enhancing understanding of self-concept change in pwMS.
 BACKGROUND: The prevalence and functional burden of the chronic demyelinating disease multiple sclerosis (MS) are well documented; however, little is known about the initial clinical course of alertness, sleep, cognitive, and psychological symptoms. OBJECTIVES: This exploratory, prospective, longitudinal study multidimensionally investigated the development and progression of alertness, sleep, fitness to drive, and psychological symptoms in the first year after de novo MS diagnosis. METHODS: Twenty-five people with MS (pwMS) were assessed cognitively, psychologically, and using polysomnography soon after diagnosis and one year later, with outcomes compared to matched healthy controls. RESULTS: In the early stage of the disease, psychological symptoms of pwMS were comparable with those of controls, and patient conditions did not deteriorate within the first disease year. A small percentage of pwMS experienced increased levels of anxiety and depression after diagnosis. Alertness, sustained attention, and fitness to drive were comparable between both groups, and fatigue levels remained low over the course of the year. CONCLUSIONS: This study highlights patient experiences within the initial clinical course of MS in a small group of patients. Further research is needed to understand the progression of symptoms and impairments in MS over a longer period and in different stages of the disease.
 BACKGROUND: Ofatumumab (OFA) is a fully human anti-CD20 monoclonal antibody administered with a 20 mg subcutaneous monthly dosing regimen. METHODS: Inclusion criteria were patients: 1) aged 18-55; 2) with a confirmed diagnosis of relapsing Multiple Sclerosis (RMS), per the revised 2010 McDonald criteria; 2) who started OFA according to Italian Medicines Agency prescription rules and within 12 months from the RMS diagnosis; 3) naïve to any disease-modifying therapy. The primary outcome was to offer an overview of cellular subsets of RMS naïve patients (time 0) and then after 4 weeks (time 1) and 12 weeks (time 2) on therapy with OFA in a real-world setting. RESULTS: Fifteen patients were enrolled. CD3+ T cell frequencies were higher at time 1 (%80.4, SD 7.7) and time 2 (%82.6, SD 5.8) when compared to time 0 (%72.4, SD 9.8), p = .013. B naïve cells were barely detectable in the OFA group at time 1 (%0.4, SD 0.5) and 2 (%1.4, SD 2.9) when com- pared to time 0 (%11.5, SD 3.8), p < .001. CONCLUSION: The progressive and increasing use of anti-CD20 drugs imposes the need for larger, pro- spective, real-world, long-term studies to characterize further immunophenotypes of patients with RMS treated with OFA.
 BACKGROUND: Advances in treatments for Multiple Sclerosis (MS) have resulted in a growing number of aging individuals with MS. Research has shown that perceived social support has protective effects against age-related cognitive decline but no study to date has examined the relationship between perceived social support and cognition in older adults with MS. The current study addressed this gap in knowledge examining the association between perceived social support and cognition in older adults with and without MS. METHODS: Participants were older adults with MS (n = 67, mean age = 64.75 years;%female =  64.2) and controls (n = 71, mean age = 68.25 years;%female = 57.7) Linear regression models examined the associations of total and domain scores of perceived social support with cognition in the entire sample, and then stratified by group status. RESULTS: Analyses revealed that total perceived social support, emotional/informational support, and positive social interaction were associated with cognition in the total sample. In stratified analyses, emotional/informational support was significantly associated with cognition in the MS group; however, this association became insignificant when analyses adjusted for depressive symptoms. Positive social interaction was significantly associated with cognition in the control group. Notably, this association remained significant even after adjusting for depressive symptoms. CONCLUSION: These findings suggest that distinct dimensions of perceived social support may have differential relationships with cognitive function in older adults with MS and healthy controls.
 BACKGROUND AND PURPOSE: In multiple sclerosis (MS), brain atrophy measurements have emerged as an important biomarker reflecting neurodegeneration and disability progression. However, due to several potential confounders, investigation of brain atrophy in clinical routine and even in controlled clinical studies can be challenging. The aim of this study was to investigate the short-term dynamics of brain atrophy development after initiation of disease-modifying therapy (DMT) in a "real-world setting." METHODS: In this retrospective study, we included MS patients starting DMT (natalizumab, fingolimod, dimethyl fumarate, or interferon-ß1a) or without DMT, availability of a baseline MRI, and two annual follow-up scans on the same MRI system. Two-timepoint percentage brain volume changes (PBVCs) were calculated. RESULTS: Fifty-five MS patients (12 patients starting DMT with natalizumab, 7 fingolimod, 14 dimethyl fumarate, 11 interferon-ß1a, and 11 patients without DMT) were included. We found the highest PBVCs in the first 12 months after initiation of natalizumab treatment. Furthermore, the PBVCs in our study were very much comparable to the results observed by other groups, as well as for fingolimod, dimethyl fumarate, and interferon-ß1a. CONCLUSION: We found PBVCs that are comparable to the results of previous studies, suggesting that brain atrophy, assessed on 3D MRI data sets acquired on the same 3T MRI, provides a robust MS biomarker.
 BACKGROUND: Considering that brain activity involves communication between millions of neurons in a complex network, nonlinear analysis is a viable tool for studying electroencephalography (EEG). The main objective of this review was to collate studies that utilized chaotic measures and nonlinear dynamical analysis in EEG of multiple sclerosis (MS) patients and to discuss the contributions of chaos theory techniques to understanding, diagnosing, and treating MS. METHODS: Using the preferred reporting items for systematic reviews and meta-analysis (PRISMA), the databases EbscoHost, IEEE, ProQuest, PubMed, Science Direct, Web of Science, and Google Scholar were searched for publications that applied chaos theory in EEG analysis of MS patients. RESULTS: A bibliographic analysis was performed using VOSviewer software keyword co-occurrence analysis indicated that MS was the focus of the research and that research on MS diagnosis has shifted from conventional methods, such as magnetic resonance imaging, to EEG techniques in recent years. A total of 17 studies were included in this review. Among the included articles, nine studies examined resting-state, and eight examined task-based conditions. CONCLUSION: Although nonlinear EEG analysis of MS is a relatively novel area of research, the findings have been demonstrated to be informative and effective. The most frequently used nonlinear dynamics analyses were fractal dimension, recurrence quantification analysis, mutual information, and coherence. Each analysis selected provided a unique assessment to fulfill the objective of this review. While considering the limitations discussed, there is a promising path forward using nonlinear analyses with MS data.
 Multiple Sclerosis (MS) is a complex neurological disorder that involves demyelination, lesions and atrophy in both white and gray matter. Such changes in the central nervous system are diagnostic in MS and has a strong relationship with both physical and cognitive symptoms. As a result, magnetic resonance imaging (MRI) scans as a metric of brain atrophy have emerged as an important outcome measure in MS studies. Recently, research has begun to focus on the contribution of aging to the structural changes in the brain associated with MS; prompting questions about whether there is an amplifying effect of aging superimposed on MS-related brain atrophy. To examine current evidence of how the brain ages in individuals with MS, a systematic review of the literature was performed. Specific questions were focused on how aging affects gray and white matter structure, whether patterns of brain atrophy differ in younger and older cohorts and if there are structural differences in the brain as a function of sex in aging people with MS. This review considered studies that used MRI to examine the effects of aging in adults with MS. Twenty-one studies met eligibility criteria. Findings across these studies revealed that gray matter atrophy was more pronounced in older adults with MS, particularly in subcortical regions such as the thalamus; that the rates of atrophy were similar but varied by region for younger and older cohorts; and that males may experience more brain atrophy than females. Further studies that use multimodal MRI acquisition methods are needed to capture changes in both males and females over time, particularly in middle to older adulthood.
 Alzheimer's disease (AD) and multiple sclerosis (MS) are two CNS disorders affecting millions of people, for which no cure is available. AD is usually diagnosed in individuals age 65 and older and manifests with accumulation of beta amyloid in the brain. MS, a demyelinating disorder, is most commonly diagnosed in its relapsing-remitting (RRMS) form in young adults (age 20-40). The lack of success in a number of recent clinical trials of immune- or amyloid-targeting therapeutics emphasizes our incomplete understanding of their etiology and pathogenesis. Evidence is accumulating that infectious agents such as viruses may contribute either directly or indirectly. With the emerging recognition that demyelination plays a role in risk and progression of AD, we propose that MS and AD are connected by sharing a common environmental factor (a viral infection such as HSV-1) and pathology (demyelination). In the viral DEmyelinating Neurodegenerative Trigger (vDENT) model of AD and MS, the initial demyelinating viral (e.g., HSV-1) infection provokes the first episode of demyelination that occurs early in life, with subsequent virus reactivations/demyelination and associated immune/inflammatory attacks resulting in RRMS. The accumulating damage and/or virus progression deeper into CNS leads to amyloid dysfunction, which, combined with the inherent age-related defects in remyelination, propensity for autoimmunity, and increased blood-brain barrier permeability, leads to the development of AD dementia later in life. Preventing or diminishing vDENT event(s) early in life, thus, may have a dual benefit of slowing down the progression of MS and reducing incidence of AD at an older age.
 INTRODUCTION: Multiple sclerosis (MS) is one of the most common autoimmune diseases worldwide, and various autoimmune comorbidities have been reported with MS. The aim of this study was to estimate the prevalence of autoimmune disease comorbidity in patients with MS and their relatives in a Polish population. MATERIAL AND METHODS: In this retrospective multicentre study, we investigated a group of patients with MS, and their relatives, in terms of age, gender, and the presence of simultaneous autoimmune diseases such as Graves's Disease, Hashimoto's thyroiditis, type 1 diabetes mellitus, myasthenia gravis, psoriasis, ulcerative enteritis, Crohn's Disease, coeliac disease, rheumatoid arthritis, autoimmune hepatitis and systemic lupus erythematous. RESULTS: This study included 381 patients with MS, of whom 52.23% were women. 27 patients (7.09%) had at least one autoimmune disease. The most common comorbidity was Hashimoto's thyroiditis (14 patients). 77 patients (21.45%) had relatives with an autoimmune disease, of which the most common was Hashimoto's thyroiditis. CONCLUSIONS: Our study revealed that the probability of autoimmune diseases co-occurring in patients with MS, and in their relatives, is higher and we found the greatest risk to be for Hashimoto's thyroiditis.
 BACKGROUND: Caregivers of persons with multiple sclerosis (MS) report high levels of distress. The National Comprehensive Cancer Network Distress Thermometer (DT) is used extensively with patients with cancer and their caregivers but has not been tested in nononcology caregivers. The purpose of this study was to examine the psychometric properties and clinical utility of the barometer portion of the DT in caregivers of persons with MS. METHODS: A secondary analysis was performed of data from a randomized trial comparing the effectiveness of 2 interventions aimed at reducing psychological outcomes associated with caregiving. The DT and the 4-item Patient-Reported Outcomes Measurement Information System Anxiety and Depression scales, which were administered at baseline, were used for all analyses. Construct validity (known groups) and convergent validity (interscale correlations) were evaluated. Receiver operating characteristic curve analysis was used to evaluate clinical diagnostic test evaluation. RESULTS: The DT had good construct validity supported by strong correlations for known-groups analyses and good convergent validity (r = 0.70-0.72). The DT also demonstrated good discrimination for anxiety (area under the curve [AUC] = 0.83) and depression (AUC = 0.80). The optimal screening cut point on the DT was 4 for anxiety and 5 for depression. CONCLUSIONS: The barometer portion of the DT demonstrates good psychometric properties and clinical utility in caregivers of persons with MS. This is the first examination of the DT in MS care partners.
 Multiple sclerosis (MS) is a complicated condition in which the immune system attacks myelinated axons in the central nervous system (CNS), destroying both myelin and axons to varying degrees. Several environmental, genetic, and epigenetic factors influence the risk of developing the disease and how well it responds to treatment. Cannabinoids have recently sparked renewed interest in their therapeutic applications, with growing evidence for their role in symptom control in MS. Cannabinoids exert their roles through the endogenous cannabinoid (ECB) system, with some reports shedding light on the molecular biology of this system and lending credence to some anecdotal medical claims. The double nature of cannabinoids, which cause both positive and negative effects, comes from their actions on the same receptor. Several mechanisms have been adopted to evade this effect. However, there are still numerous limitations to using cannabinoids to treat MS patients. In this review, we will explore and discuss the molecular effect of cannabinoids on the ECB system, the various factors that affect the response to cannabinoids in the body, including the role of gene polymorphism and its relation to dosage, assessing the positive over the adverse effects of cannabinoids in MS, and finally, exploring the possible functional mechanism of cannabinoids in MS and the current and future progress of cannabinoid therapeutics.
 The coagulation-inflammation interplay has recently been identified as a critical risk factor in the early onset of multiple sclerosis (MS), and antibodies against coagulation components have been recognized as contributing factors to thrombotic and inflammatory signaling pathways in diseases with overlapping symptoms to MS, paving the way for further research into their effects on MS pathology. The current study aimed to enlighten the role of IgG antibodies against coagulation components by performing a preclinical study, analyzing the astrocytic activation by purified IgG antibodies derived from 15 MS patients, and assessing their possible pro-inflammatory effects using a bead-based multiplexed immunoassay system. The results were compared with those obtained following astrocyte treatment with samples from 14 age- and gender-matched healthy donors, negative for IgG antibody presence. Serum samples collected from 167 MS patients and 40 age- and gender-matched controls were also analyzed for pro- and anti-inflammatory factors. According to our results, astrocytic activation in response to IgG treatment caused an upregulation of various pro-inflammatory factors, including cytokines, chemokines, and interleukins. Conversely, in serum samples from patients and controls, the pro-inflammatory factors did not differ significantly; medication may lower the levels in patients. Our findings suggest that antibodies may function as effectors in neuroinflammation and serve as targets for new treatments that eventually benefit novel therapeutic approaches.
 BACKGROUND: Multiple sclerosis (MS) causes motor, cognitive, and sensory impairments that result in injurious falls. Current fall risk measures in MS (ie, forward walking [FW] speed and balance) are limited in their sensitivity. Backward walking (BW) velocity is a sensitive marker of fall risk and correlates with information processing speed (IPS) and visuospatial memory (VSM) in persons with MS. Backward walking is a complex motor task that requires increased cognitive demands, which are negatively affected by MS; however, whether cognitive function modifies the sensitivity of BW as a fall risk assessment in MS remains unknown. This study examines the influence of cognition on the relationship between BW and falls in persons with MS. METHODS: Measures of BW, FW, IPS, VSM, and retrospective falls were collected. Hierarchical regression tested moderation and included an interaction term predicting number of falls. Covariates for all analyses included age and disease severity. RESULTS: Thirty-eight persons with MS participated. Although BW, IPS, and covariates significantly predicted the number of falls (R (2) = 0.301; P = .016), there was no evidence of moderation. Backward walking, VSM, and covariates also significantly predicted number of falls (R (2) = 0.332, P = .008), but there was no evidence of moderation. The FW models generated comparable results. CONCLUSIONS: The relationship between BW velocity and falls was not conditional on IPS or VSM in this sample. Larger-scale studies examining additional cognitive domains commonly affected by MS and prospective falls are needed to characterize neurobiological processes relevant to BW and its clinical application in the assessment of fall risk.
 (1) Background: Multiple sclerosis (MS) is an immune system disease in which myelin in the nervous system is affected. This abnormal immune system mechanism causes physical disabilities and cognitive impairment. Functional magnetic resonance imaging (fMRI) is a common neuroimaging technique used in studying MS. Computational methods have recently been applied for disease detection, notably graph theory, which helps researchers understand the entire brain network and functional connectivity. (2) Methods: Relevant databases were searched to identify articles published since 2000 that applied graph theory to study functional brain connectivity in patients with MS based on fMRI. (3) Results: A total of 24 articles were included in the review. In recent years, the application of graph theory in the MS field received increased attention from computational scientists. The graph-theoretical approach was frequently combined with fMRI in studies of functional brain connectivity in MS. Lower EDSSs of MS stage were the criteria for most of the studies (4) Conclusions: This review provides insights into the role of graph theory as a computational method for studying functional brain connectivity in MS. Graph theory is useful in the detection and prediction of MS and can play a significant role in identifying cognitive impairment associated with MS.
 We aimed to investigate the extent of alterations in the pro/antioxidant balance in the blood of patients with relapsing-remitting multiple sclerosis (RRMS) in relation to drug-modified therapy, gender, disability score, and disease duration. 161 patients (67 men and 94 women, aged 24-69 years, median 43.0) and 29 healthy individuals (9 men and 20 women, aged 25-68 years, median 41.0) were included in the study. We measured the activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) as well as the concentration of interleukin-6 (IL-6), lipid peroxidation parameters (LPO), total oxidant status (TOS), and total antioxidant capacity (TAS). The activity of SOD did not show any significant differences between patients with RRMS and the control group in our study. In contrast, significant decreased GPx activity and increased CAT activity was observed in the blood of patients with RRMS compared to the control group. Additionally, the activity of CAT was influenced by gender and the use of disease-modifying therapies. Disease-modifying therapies also affected the concentration of TOS, TAS, and LPO. Our studies indicated that enhancing GPx activity may be more beneficial to providing potential therapeutic strategies aimed at modulating antioxidant defenses to mitigate oxidative stress in this disease.
 BACKGROUND: The frequency of bowel symptoms (BSs) is still a matter for debate in multiple sclerosis (MS) patients. However, BSs have been shown to cause significant distress. Our study aimed to (i) investigate the frequency of BSs, particularly those that are not managed, (ii) identify potential predictors for help-seeking care for patients with BSs, and (iii) evaluate the ability of the Neurogenic Bowel Dysfunction (NBD) score to screen for BSs. METHOD: Three hundred sixty-nine MS patients completed a cross-sectional demographic and clinical survey of MS and BSs and their management. RESULTS: BSs were reported by 47.7% of MS patients. Eighty-eight percent of MS patients had a very minor-minor Neurogenic Bowel Disorder (NBD) score and 12% had a moderate-severe NBD score. Forty-one percent of patients did not report their BS to a healthcare provider, mainly because they preferred not to talk about the problem. BS duration was the only significant predictor of help-seeking for BS management. Female sex, visual impairment, a digestive history, and longer MS duration were good predictors of BSs. Patients with BSs (86%) were correctly identified with an NBD score >2. CONCLUSION: BSs are under-detected in MS populations. This is partially related to non-declaration by patients. Targeting BSs using the NBD score is a good way to increase reporting.
 This paper proposes a deep learning model based on an artificial neural network with a single hidden layer for predicting the diagnosis of multiple sclerosis. The hidden layer includes a regularization term that prevents overfitting and reduces the model complexity. The purposed learning model achieved higher prediction accuracy and lower loss than four conventional machine learning techniques. A dimensionality reduction method was used to select the most relevant features from 74 gene expression profiles for training the learning models. The analysis of variance test was performed to identify the statistical difference between the mean of the proposed model and the compared classifiers. The experimental results show the effectiveness of the proposed artificial neural network.
 BACKGROUND: Social participation levels of individuals with Multiple Sclerosis (iwMS) are lower than those of healthy individuals. OBJECTIVE: This study aimed to evaluate to which extent the walking capacity, balance, and fear of falling (FoF) affect the community integration levels of iwMS. METHODS: Thirty-nine iwMS were evaluated for their participation levels [The Community Integration Questionnaire (CIQ)], walking capacity [The Six-Minute Walk Test (6MWT)], balance [Kinesthetic Ability Trainer (SportKAT®)], and FoF [The Modified Falls Efficacy Scale (MFES)]. Correlation and regression analyses were performed to detect the effects of SportKAT®, 6MWT, and MFES on CIQ. RESULTS: CIQ scores were significantly correlated with 6MWT (p = .043) and MFES (p = .005) scores, while CIQ was not related with static (for two feet test p = .356, for right single-leg stance test p = .412, for left single-leg stance test p = .730) and dynamic balance (for clockwise test p = .097, for counterclockwise test p = .540) measured with the SportKAT®. It was found that CIQ could be predicted by 6MWT and MFES at the level of 16% and 25%, respectively. CONCLUSION: FoF and walking capacity are associated with community integration in iwMS. Therefore, physiotherapy and rehabilitation programs of iwMS should be combined with treatment goals to increase community integration, balance, and gait and decrease the disability and FoF from an early stage. Comprehensive studies examining other factors that may impact participation in iwMS with different levels of disability are needed.
 INTRODUCTION: Immunoablative therapy followed by autologous hematopoietic stem cell transplantation (AHSCT) is one of the possible disease-modifying therapies (DMTs) for patients with multiple sclerosis (MS). In this case series, we would like to present six patients with MS, who underwent AHSCT as the first-line DMT. CASE REPORTS: Six MS patients with a rapid progression of disability with or without relapses underwent AHSCT as the first-line DMT at the University Hospital Ostrava between 2018 and 2021. The conditioning regimens for AHSCT used were a medium-intensity regime BEAM (Carmustine, Etoposid, Cytarabin, Melphalan) and low-intensity regime based on Cyclophosphamide. Four out of six patients showed some disability progression after AHSCT, so the rapid progression of MS was just slowed down by AHSCT. One patient developed activity on magnetic resonance imaging three months after AHSCT, and two experienced mild relapses during the follow-up period. None of our patients developed grade 4 non-hematological toxicity; all infections were mild. In one patient, an allergic reaction probably to dimethyl sulfoxide was observed. CONCLUSION: Our case series of 6 patients shows that AHSCT is a promising therapeutic approach to slow down the rapid progression of clinical disability in MS patients with a good safety profile.
 BACKGROUND: Although studies regarding multiple sclerosis (MS) and olfactory dysfunction (OD) have been previously described and summarized, there is not a sole review of longitudinal studies regarding the matter. This review examines the existing literature investigating MS and its effect on olfaction. In addition, the role of OD in the diagnosis and prognosis of MS is explored. METHODS: A scoping review of the literature was performed covering longitudinal studies investigating MS and OD. Systematic searches of PubMed, Google Scholar, Web of Science, Embase, PsycInfo, Cumulative Index to Nursing and Allied Health Literature, AgeLine, and MEDLINE were performed using terms that encompassed MS and olfaction. The aim of this review was to build on the existing literature by summarizing only findings that were demonstrated longitudinally. RESULTS: Of 6938 articles identified from the search, 9 met the inclusion criteria: longitudinal observation of relapsing-remitting or progressive MS. Olfaction was measured and scored using various testing arrays, and these scores were then correlated with a multitude of clinical markers. Across all studies, patients with MS demonstrated increased OD. Longitudinally, 2 contrasting patterns were identified: (1) clinical markers of acute inflammation correlated with an increased odor threshold and (2) clinical markers of neurodegeneration, or progression of disease, correlated with a decreased ability to discriminate and identify odors. CONCLUSIONS: These studies suggest that olfaction is a dynamic, dependent variable of neurodegeneration, correlating with inflammation and clinical markers. This opens the door for future exploration of olfaction's relationship with MS diagnosis, characterization, and therapeutic response.
 BACKGROUND: Sexual dysfunction (SD) is a common complaint among multiple sclerosis (MS) patients with a significant impact on the quality of life (QoL) of afflicted couples. The purpose of this study was to determine sexual satisfaction (SS) in the spouses of MS patients and its impact on the QoL. METHODS: A total of 214 spouses of MS patients were enrolled in this cross-sectional study. They completed the Larson Sexual Satisfaction Questionnaire and SF-8 Health Survey. RESULTS: The mean ± SD age of the spouses was 39.8 ± 9.7 years, and the duration of MS was 5 years or less in most of their partners. The mean ± SD score of QoL was 71.0 ± 20.3 (out of 100), and the mean SS score was 89.2 ± 18.6 (out of 125), showing moderate satisfaction. The highest score was among male spouses younger than 40 years old. The SS scores were also lower among female spouses. In the final model, it was found that SD, psychiatric symptoms, cognitive impairment, and the level of disability of patients were independent explanatory factors for the SS of their spouses. CONCLUSION: The findings supported the role of SS in the QoL of spouses of MS patients. Therefore, the attention of physicians to this hidden aspect of the life of MS patients is crucial.
 INTRODUCTION: Various inflammatory diseases have been associated with the administration of various vaccines. Several reports have associated vaccine administration with the demyelinating diseases of the central nervous system (CNS). However, no clear or strong scientific evidence exists to support the association of vaccine administration with the onset of demyelinating diseases. Some CNS demyelination diseases such as acute disseminated encephalomyelitis (ADEM) and neuromyelitis optica spectrum disorders (NMOSD) were reported following the administration of COVID-19 vaccines. In this study, new onset multiple sclerosis (MS) following COVID-19 vaccine administration was reported. METHODS: In this longitudinal observational case-control study, a total of 65 participants were studied, who were divided into two groups. Group A included 32 MS patients who were diagnosed post-COVID-19 vaccine administration and group B included 33 participants who received COVID-19 vaccines and did not develop MS. Group B was used as a control. The Chi-square test and logistic regression analysis were carried out using Statistical Product and Service Solutions (SPSS) (IBM SPSS Statistics for Windows, Armonk, NY) software. RESULTS: Univariate and multivariate logistic regression analysis was performed and a significant correlation between the risk factors and the development of MS post-COVID-19 vaccination was identified. CONCLUSION: The risk factors, identified in this study, can be used as significant independent predictors for developing MS post-COVID-19 vaccinations.
 INTRODUCTION: Multiple sclerosis (MS), a non-contagious and chronic disease of the central nervous system, is an unpredictable and indirectly inherited disease affecting different people in different ways. Using Omics platforms genomics, transcriptomics, proteomics, epigenomics, interactomics, and metabolomics database, it is now possible to construct sound systems biology models to extract full knowledge of the MS and recognize the pathway to uncover the personalized therapeutic tools. METHODS: In this study, we used several Bayesian Networks in order to find the transcriptional gene regulation networks that drive MS disease. We used a set of BN algorithms using the R add-on package bnlearn. The BN results underwent further downstream analysis and were validated using a wide range of Cytoscape algorithms, web based computational tools and qPCR amplification of blood samples from 56 MS patients and 44 healthy controls. The results were semantically integrated to improve understanding of the complex molecular architecture underlying MS, distinguishing distinct metabolic pathways and providing a valuable foundation for the discovery of involved genes and possibly new treatments. RESULTS: Results show that the LASP1, TUBA1C, and S100A6 genes were most likely playing a biological role in MS development. Results from qPCR showed a significant increase (P < 0.05) in LASP1 and S100A6 gene expression levels in MS patients compared to that in controls. However, a significant down regulation of TUBA1C gene was observed in the same comparison. CONCLUSION: This study provides potential diagnostic and therapeutic biomarkers for enhanced understanding of gene regulation underlying MS.
 BACKGROUND: The objective of this study was to understand the uptake of hemopoietic stem cell transplantation (HSCT) in neuroimmunological disorders like multiple sclerosis (MS). METHOD: An independent University affiliated research organization conducted a global online survey of people having had HSCT, examining demographics, treatment protocol, and effectiveness. RESULTS: Of 271 participants, useful data were available in 223; women aged 35-54 accounted for 73.5%. Most had a household income greater than US$50,000, and the majority of participants were from Australia and the United States. Nearly 94.6% of people suffer from MS. Most had their treatment in Russia (38.7%) and 78.1% had nonmyeloablative transplants. Nearly half of the participants spent between US$50,000 to US$74,999. There were 54.5% of neurologists who did not support their patients having HSCT. Around 85.5% of participants believed HSCT helped them manage their disease from weeks to years after transplantation, and treatment was recommended by 9.5% of participants. The average reduction in Expanded Disability Status Score after transplantation was 1.2 (95% CI: 0.97-1.41; N = 197; p < 0.01; t: 10.7, df: 196). CONCLUSION: Participants were supportive of HSCT despite the costs and would recommend it to others. The data suggest some benefit in minimizing disability in MS and provides justification for large randomized controlled trials.
 OBJECTIVE: To report for the first time an Italian epidemiological analysis of the prevalence of multiple sclerosis (MS) in patients with endometriosis (EMS), through the study of the endometriosis population of our referral center; to analyze the clinical profile and perform a laboratory analysis to examine the immune profile and the possible correlation to other autoimmune diseases of the enrolled patients. METHODS: We evaluated 1652 women registered with EMS in the University of Naples Federico II and retrospectively searched patients with a co-diagnosis of MS. Clinical features of both conditions were recorded. Serum autoantibody and immune profiles were analyzed. RESULTS: 9 out of 1652 patients presented a co-diagnosis of EMS and MS (9/1652 = 0.005%). Clinically, EMS and MS presented in mild forms. Hashimoto's thyroiditis was found in two patients (2/9). Even if not statistically significant, a trend of variation in CD4- CD8 T lymphocytes and of B cells were found. CONCLUSION: Our findings suggest an increased risk of MS in women with EMS. However, large-scale prospective studies are needed.
 Multiple sclerosis (MS) represents the most common acquired demyelinating disorder of the central nervous system (CNS). Its pathogenesis, in parallel with the well-established role of mechanisms pertaining to autoimmunity, involves several key functions of immune, glial and nerve cells. The disease's natural history is complex, heterogeneous and may evolve over a relapsing-remitting (RRMS) or progressive (PPMS/SPMS) course. Acute inflammation, driven by infiltration of peripheral cells in the CNS, is thought to be the most relevant process during the earliest phases and in RRMS, while disruption in glial and neural cells of pathways pertaining to energy metabolism, survival cascades, synaptic and ionic homeostasis are thought to be mostly relevant in long-standing disease, such as in progressive forms. In this complex scenario, many mechanisms originally thought to be distinctive of neurodegenerative disorders are being increasingly recognized as crucial from the beginning of the disease. The present review aims at highlighting mechanisms in common between MS, autoimmune diseases and biology of neurodegenerative disorders. In fact, there is an unmet need to explore new targets that might be involved as master regulators of autoimmunity, inflammation and survival of nerve cells.
 WHAT IS THIS SUMMARY ABOUT? People with multiple sclerosis (shortened to MS) who are taking cladribine tablets may have concerns about whether they can be vaccinated against COVID-19. This summary details the findings from a previously published article, in which an international committee of 10 MS experts developed recommendations to answer some important questions about COVID-19 vaccines in people with MS (including relapsing-remitting or active secondary progressive disease) taking cladribine tablets. WHAT WERE THE RESULTS? The committee identified 13 recommendations, which were all agreed upon by at least three-quarters (75%) of the 38 voting MS experts. Generally, they recommended that people with MS taking cladribine tablets should be vaccinated for COVID-19 as soon as possible, because the vaccine is thought to be both safe and effective, and vaccine responses were not likely to be affected by cladribine tablets. WHAT DO THE RESULTS MEAN? Overall, people with MS taking cladribine tablets should receive the COVID-19 vaccine to protect themselves, unless advised differently by their healthcare provider.
 BACKGROUND: Misdiagnosis of multiple sclerosis (MS) is common and can have harmful effects on patients and healthcare systems. Identification of factors associated with misdiagnosis may aid development of prevention strategies. OBJECTIVE: To identify clinical and radiological predictors of MS misdiagnosis. METHODS: We retrospectively reviewed medical records of all patients who were referred to Johns Hopkins MS Center from January 2018 to June 2019. Patients who carried a diagnosis of MS were classified as correctly diagnosed or misdiagnosed with MS by the Johns Hopkins clinician. Demographics, clinical, laboratory, and radiologic data were collected. Differences between the two groups were evaluated, and a regression model was constructed to identify predictors of misdiagnosis. RESULTS: Out of 338 patients who were previously diagnosed with MS, 41 (12%) had been misdiagnosed. An alternative diagnosis was confirmed in 28 (68%) of the misdiagnosed patients; cerebrovascular disease was the most common alternate diagnosis. Characteristics associated with misdiagnosis were female sex (odds ratio (OR): 5.81 (95% confidence interval (CI): 1.60, 21.05)) and non-specific brain magnetic resonance imaging (MRI) lesions (OR: 7.66 (3.42, 17.16)). CONCLUSION: Misdiagnosis is a frequent problem in MS care. Non-specific brain lesions were the most significant predictor of misdiagnosis. Interventions aimed to reduce over-reliance on imaging findings and misapplication of the McDonald criteria may prevent MS misdiagnosis.
 INTRODUCTION: Observational studies suggested that diabetes mellitus [type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM)], multiple sclerosis (MS), and migraine are associated with Alzheimer's disease (AD). However, the causal link has not been fully elucidated. Thus, we aim to assess the causal link between T1DM, T2DM, MS, and migraine with the risk of AD using a two-sample Mendelian randomization (MR) study. METHODS: Genetic instruments were identified for AD, T1DM, T2DM, MS, and migraine respectively from genome-wide association study. MR analysis was conducted mainly using the inverse-variance weighted (IVW) method. RESULTS: The result of IVW method demonstrated that T2DM is causally associated with risk of AD (OR: 1.237, 95% CI: 1.099-1.391, P: 0.0003). According to the IVW method, there is no causal association between TIDM, MS, migraine, and the risk of AD (all p value > 0.05). Here we show, there is a causal link between T2DM and the risk of AD. CONCLUSION: These findings highlight the significance of active monitoring and prevention of AD in T2DM patients. Further studies are required to actively search for the risk factors of T2DM combined with AD, explore the markers that can predict T2DM combined with AD, and intervene and treat early.
 Introduction Multiple sclerosis (MS) is one of the most prevalent disorders of the central nervous system (CNS), and it can be observed in the field of radiological cross-sectional magnetic resonance imaging (MRI). The prevalence of MS in Saudi Arabia has increased as compared to the past few years. MRI is the gold standard non-invasive modality of choice in MS diagnosis according to the National Multiple Sclerosis Society (NMSS), New York City. This study aimed to highlight the significance of using diffusion-weighted images (DWIs) and the use of contrast media in the MS protocol, as well as the importance of identifying the suitable time of imaging after contrast enhancement to detect active lesions. Methods A retrospective cross-sectional study was conducted of 100 MS patients with an age range of 17 to 56 years. The data set included 41 active cases and 59 inactive cases. All patients had an MRI standard protocol of both the brain and spine in addition to DWI sequence and contrast agent (CA) injection, with images taken in early and delayed time. Results Of the patients, 71% were female and 29% were male. Active MS disease was more significant at younger ages than at older ages. Active lesions were significantly enhanced in delayed contrast images and showed high signal intensity in both the DWI and apparent diffusion coefficient (ADC) map, while inactive lesions showed no enhancement after contrast injection and showed an iso-signal intensity in both the DWI and ADC map. Conclusion The use of CA has developed over the years in the diagnosis of MS patients. In this study, the relationship between active lesions, DWI, and delayed contrast enhancement is very strong. In future research, we recommend adding a DWI sequence for the suspected active MS spine lesions in addition to delayed enhancement time in active MS after contrast injection to increase MRI sensitivity toward active MS lesions of the brain and spinal cord as well.
 Multiple sclerosis is a neurological disorder categorized by inflammatory processes with a high prevalence worldwide. It affects both motor and sensory pathways and is also associated with the visual pathway. Fingolimod is a commonly used drug for relapsing-remitting multiple sclerosis. It is a sphingosine 1-phosphate modulator acting on its receptors for immune cell accumulation, neuronal function, embryological development, vascular permeability, smooth muscle cell function, and endothelial barrier maintenance. This review aims to understand the processes, mechanisms, risks, and management of fingolimod-associated macular edema. Due to the anti-inflammatory properties of fingolimod, it decreases various cytokines, including interleukin (IL)-1B and IL-6, spike wave, and spike amplitude, in electrophysiological activities and decreases insoluble receptors for advanced glycation end product ligand. A daily dosage of 0.5 mg of fingolimod has an increased association with macular edema. The serious adverse events of fingolimod are lymphopenia, cardiovascular events, ocular events, and carcinoma. Fingolimod decreases brain volume and increases vascular permeability, resulting in increased macular volume and damage to the blood-retinal barrier, which causes an increased risk for macular edema. Cystoid macular edema is more common in older individuals suffering from comorbidities affecting the retina, such as diabetes, or those undergoing ophthalmological surgeries. This review also highlights the importance of regular ophthalmology examinations on patients consuming fingolimod both in the initial stages and chronic use. The treatment options for macular edema include nonsteroidal anti-inflammatory drugs, acetazolamide, triamcinolone, ketorolac, corticosteroids, and intravitreal procedures.
 AIM AND BACKGROUND: Multiple sclerosis (MS) is a long-course incurable disease as well as an unknown prognosis causing patients to experience a variety of psychological outcomes. Meanwhile, inability to control the disease-related uncertainty leads to the use of maladaptive coping strategies, causing more psychological distress. This study investigated the effectiveness of intervention focused on the intolerance of uncertainty on psychological distress and quality of life in MS patients. MATERIALS AND METHODS: This research adopted a true experimental design. All phases of the study were conducted online due to the COVID-19 pandemic during 2021 in Tehran. The statistical population of the study was purposefully selected from among MS patients and was randomly assigned to three groups of 20: IU intervention and two control groups (cognitive behavioral therapy (CBT) and treatment as usual (TAU) groups). The study included pre-test, post-test, and follow-up stages. The outcome measures of the study included the Depression Anxiety Stress Scale (DASS-21) as well as Multiple Sclerosis Quality of Life-54 (MSQoL-54). Mixed analysis of variance was used to analyze the data. RESULTS: The results showed that IU intervention compared to CBT, is more effective on psychological distress (depression P = 0.006, anxiety P = 0.01, and stress P = 0.01) and quality of life (P = 0.001) in MS patients. Nonetheless, IU-focused intervention is more effective than TAU on psychological distress (depression P = 0.0001, anxiety P = 0.0001, stress P = 0.0001) as well as quality of life (P = 0.0001) in these patients. CONCLUSIONS: IU-based intervention can reduce psychological distress and improve quality of life of MS patients. Accepting uncertainty can reduce the anxiety and stress of MS patients which can increase the quality of life of these patients.
 BACKGROUND: Fatigue affects 60-90% of people with multiple sclerosis (MS). It reduces quality of life and the ability to work. The cause of fatigue in MS remains unknown. Several disease-modifying treatments (DMTs) slow the disease process in relapsing MS by suppressing neuroinflammation. We aimed to investigate if treatment with a DMT is associated with lower rates of fatigue. METHODS: In this cross-sectional study of the MS population in three counties in Norway, we used the Fatigue Scale for Motor and Cognitive Functions (FSMC) and the Hospital Anxiety and Depression Scale (HADS) to assess patient-reported fatigue, anxiety and depression. Clinical data were retrieved from the electronic patient record system. We categorized DMTs as high-efficacy therapy or moderate-efficacy therapy. High-efficacy drugs included fingolimod, natalizumab, ocrelizumab, rituximab, alemtuzumab, daclizumab, and autologous hematopoietic stem cell transplantation. Moderate-efficacy drugs included interferons, glatiramer acetate, dimethyl fumarate, and teriflunomide. We included persons with relapsing MS only. RESULTS: Of 1142 patients, 80% had fatigue. Fifty-six percent of the patients were on DMTs (25% on moderate-efficacy treatment and 30% on high-efficacy treatment), 18% had discontinued treatment and 26% had never received any DMT. Sex, level of disability as measured by the Multiple Sclerosis Severity Score, anxiety and depression were independently associated with fatigue. Moderate-efficacy treatment was associated with less fatigue, but not after adjustment for other variables. There was no association between high-efficacy treatment and fatigue. CONCLUSION: We found no independent relationship between the use of disease-modifying treatment and fatigue in MS.
 BACKGROUND: Backward walking training (BWT) can have a positive effect on balance, gait, and functional mobility in neurological diseases; however, the effectiveness of BWT has not been examined in multiple sclerosis (MS). Therefore, the study aimed to investigate the effects of BWT on balance, gait, and functional mobility in people with MS (PwMS). METHOD: Nineteen PwMS were randomly allocated to either the experimental group (n=10) and the control group (n=9). The experimental group received BWT in addition to conventional walking training (CWT) while the control group only received CWT. Both groups performed training three times a week for 8 weeks. Participants were assessed with the Berg Balance Scale (BBS), four square step test (FSST), activities-specific balance confidence scale (ABC), timed 25-foot walk test (T25FW), dynamic gait index (DGI), 3-meter backward walk test (3MBWT), Multiple Sclerosis Walking Scale-12 (MSWS-12), and timed up and go test (TUG) before and after training. RESULTS: After training, both groups showed significant improvements on the T25FW, and TUG (p<0.05) while only the experimental group showed significant improvements on the BBS, FSST, ABC, DGI, 3MBWT, and MSWS-12 (p<0.05). The experimental group significantly improved more than the control group in all outcomes (p<0.05) except for the T25FW (p=0.202). CONCLUSION: BWT in addition to CWT is an effective way to improve balance, gait, and functional mobility for PwMS. These results suggest that BWT may be a potentially useful treatment approach when added to CWT in the rehabilitation of MS.
 PURPOSE: This study was conducted to evaluate the reliability and validity of the Fullerton Advanced Balance Scale (FAB) in people with Multiple Sclerosis (PwMS). METHODS: A total of 65 people with multiple sclerosis, Expanded Disability Status Scale (EDSS) ranging from 1 to 5.5, were included in the study. Test-retest reliability, intra-rater, inter-rater reliability, and internal consistency (item-total score correlation, Cronbach's alpha coefficient) were investigated to examine the reliability of FAB. In the intra-rater and inter-rater reliability analysis, the FAB application of 34 patients, whose initial evaluation was gathered, was video-recorded and re-watched by two physiotherapists at different times and scored. For the Validity of FAB, concurrent validity with criterion validity; construct validity with hypothesis testing were calculated. Convergent validity was assessed for correlations with EDDS, Dynamic Gait Index (DGI), and Timed Up and Go Test (TUG). RESULTS: Test-retest reliability of FAB Intraclass Correlation Coefficient (ICC) values was excellent (ICC= 0.994, p < 0.001). While the intra-rater reliability (ICC=0.986, p < 0.001) and inter-rater reliability (ICC=0.985, p < 0.001) of the FAB were calculated at an excellent level. Cronbach's alpha value was determined to perfect correlation. (Cronbach's alpha coefficient: 0.929). FAB had an excellent correlation with BBS (0.919 (p < 0.001). For convergent validity of FAB, EDSS (r=-0.885, p < 0.001), TUG (r=-0.833, p < 0.001), and DGI (r = 0.916, p < 0.001), it was determined that the scale had convergent validity. CONCLUSION: The FAB proved to be a reliable and valid in PwMS. The study showed that the FAB could be applied regardless of the physiotherapists' clinical experiences. It has been determined that the scale can be used in PwMS with a wide EDSS score. Considering the inter-rater and intra-rater reliability results, it is thought that the FAB is also suitable for use in the online environment.
 PURPOSE: Lifestyle/dietetic habits play an important role in the development and progression of multiple sclerosis (MS) disease. Here, we examine the basic pathomechanisms underlying intestinal and brain barrier modifications in MS and consider diets and dietary supplementations proposed over time to complement pharmacological therapies for improving disease outcome both in adults and in children. METHODS: Scoping literature search about evidence-based findings in MS-related gut-brain axis (GBA) pathophysiology and nutritional issues at all ages. FINDINGS: Data show that (1) no universal best diet exists, (2) healthy/balanced diets are, however, necessary to safeguard the adequate intake of all essential nutrients, (3) diets with high intakes of fruits, vegetables, whole grains, and lean proteins that limit processed foods, sugar, and saturated fat appear beneficial for their antioxidant and anti-inflammatory properties and their ability to shape a gut microbiota that respects the gut and brain barriers, (4) obesity may trigger MS onset and/or its less favorable course, especially in pediatric-onset MS. Vitamin D and polyunsaturated fatty acids are the most studied supplements for reducing MS-associated inflammation. CONCLUSIONS: Pending results from other and/or newer approaches targeting the GBA (e.g., pre- and probiotics, engineered probiotics, fecal-microbiota transplantation), accurate counseling in choosing adequate diet and maintaining physical activity remains recommended for MS prevention and management both in adults and children.
 The term "neurodegenerative diseases" (NDs) identifies a group of heterogeneous diseases characterized by progressive loss of selectively vulnerable populations of neurons, which progressively deteriorates over time, leading to neuronal dysfunction. Protein aggregation and neuronal loss have been considered the most characteristic hallmarks of NDs, but growing evidence confirms that significant dysregulation of innate immune pathways plays a crucial role as well. NDs vary from multiple sclerosis, in which the autoimmune inflammatory component is predominant, to more "classical" NDs, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and spinal muscular atrophy. Of interest, many of the clinical differences reported in NDs seem to be closely linked to sex, which may be justified by the significant changes in immune mechanisms between affected females and males. In this review, we examined some of the most studied NDs by looking at their pathogenic and phenotypical features to highlight sex-related discrepancies, if any, with particular interest in the individuals' responses to treatment. We believe that pointing out these differences in clinical practice may help achieve more successful precision and personalized care.


 Higher-order DNA structure and gene expression are governed by epigenetic processes like DNA methylation and histone modifications. Abnormal epigenetic mechanisms are known to contribute to the emergence of numerous diseases, including cancer. Historically, the chromatin abnormalities were only considered to be limited to discrete DNA sequences and were thought to be associated with rare genetic syndrome however, recent discoveries have pointed to genome-wide level changes in the epigenetic machinery which has contributed to a better knowledge of the mechanisms underlying developmental and degenerative neuronal problems associated with diseases such as Parkinson's disease, Huntington's disease, Epilepsy, Multiple sclerosis, etc. In the given chapter we describe the epigenetic alterations seen in various neurological disorders and further discuss the influence of these epigenetic changes on developing novel therapies.
 ISSUE ADDRESSED: Evaluated the impact of the Understanding Multiple Sclerosis (MS) massive open online course, which was intended to increase understanding and awareness about MS, on self-reported health behaviour change 6 months after course completion. METHODS: Observational cohort study evaluating precourse(baseline) and postcourse (immediately postcourse and six-month follow-up) survey data. The main study outcomes were self-reported health behaviour change; change type; and measurable improvement. We also collected participant characteristic data (eg, age, physical activity). We compared participants who reported health behaviour change at follow-up to those who did not and compared those who improved to those who did not using χ(2) and t tests. Participant characteristics, change types and change improvement were described descriptively. Consistency between changes reported immediately postcourse and at the 6-month follow-up was assessed using χ(2) tests and textual analysis. RESULTS: N = 303 course completers were included in this study. The study cohort included MS community members (eg, people with MS, healthcare providers) and nonmembers. N = 127 (41.9%) reported behaviour change in ≥1 area at follow-up. Of these, 90 (70.9%) reported a measured change, and of these, 57 (63.3%) showed improvement. The most reported change types were knowledge, exercise/physical activity and diet. N = 81 (63.8% of those reporting a change) reported a change in both immediately and 6 months after course completion, with 72.0% of those that described both changes giving similar responses each time. CONCLUSION: Understanding MS encourages health behaviour change among course completers up to 6 months after course completion. SO WHAT?: An online education intervention can effectively encourage health behaviour change over a 6-month follow-up period, suggesting a transition from acute change to maintenance. The primary mechanisms underpinning this effect are information provision, including both scientific evidence and lived experience, and goal-setting activities and discussions.
 [This corrects the article DOI: 10.3389/fncel.2023.1207540.].
 BACKGROUND: The Multiple Sclerosis Resiliency Scale (MSRS) was designed to assess factors connected to resilience when facing MS-related challenges. Although the MSRS has demonstrated good internal consistency and construct validity, its test-retest reliability has yet to be established. Identifying the minimal detectable change (MDC) of the scale will also improve its utility as an outcome measure for resilience-based interventions. This study aimed to determine the test-retest reliability and MDC of the MSRS. METHODS: Participants were 62 persons with MS who completed the MSRS twice, with a mean ± SD of 16.60 ± 3.97 days (range, 14-30 days) between assessments. Test-retest reliability was evaluated using a 2-way, random-effects, single-measurement intraclass correlation coefficient (ICC), with agreement between time 1 and time 2 visualized with a Bland-Altman plot. The MDC was calculated using the standard error of measurement with a 95% CI. RESULTS: At time 1, the mean ± SD MSRS score was 77.19 ± 11.97 (range, 45.83-97.00); at time 2, the mean ± SD score was 76.38 ± 12.75 (range, 46-98). The MSRS total score had good test-retest reliability (ICC = 0.88), with the subscale ICCs ranging from 0.77 (MS Peer Support) to 0.93 (Spirituality). The MDC for the total score was 11.95. CONCLUSIONS: These findings suggest that the MSRS has good test-retest reliability and that persons with MS with a difference of 12 points or more between assessments have experienced a reliable change. The results support the utility of the MSRS as a potential outcome measure for MS-related resilience.
 Objectives: As part of the CLARION study: (1) characterize the incidence of severe infections, herpes zoster, and malignancies in patients newly initiating cladribine or fingolimod for relapsing multiple sclerosis (MS); (2) estimate the incidence of severe lymphopenia among cladribine users; and (3) describe prior/subsequent disease-modifying therapy (DMT) in both cohorts.Methods: Patients were identified from seven participating MS registries/data sources. The incidence rate (IR) of each outcome per 1000 patient-years and its 95% confidence interval (95%CI) were estimated for cohorts using Poisson regression.Results: By cut-off date (01-April-2020), 742 cladribine and 867 fingolimod users were included. Mean follow-up was ∼1 year. The IR for severe infections from all contributing sources (except Denmark) was: cladribine, 7.37 (2.76,19.6); fingolimod, 6.55 (2.46,17.4). The corresponding IR for herpes zoster was 5.51 (1.78,17.1) and 3.27 (0.82,13.1), respectively, while values for opportunistic infections were 0 (0,6.76) and 1.63 (0.23,11.6), respectively. There were no events of progressive multifocal leukoencephalopathy in either cohort. The IR of severe lymphopenia was 63.9 (40.7,100.1) in 349 cladribine users from contributing sources. The IR of malignancies (cut-off date 01-April-2022) was 3.55 (1.59,7.90) for the cladribine cohort (N = 1035) and 3.55 (1.48,8.52) for the fingolimod cohort (N = 843) from three MS registries/data sources. In the combined data sources, 36.8% of cladribine and 27.4% of fingolimod users were DMT-naïve; after initiation of study treatment, 2.5% and 20.2% switched to another DMT, respectively.Conclusion: No new safety signal was observed in patients treated with cladribine tablets, although results are limited by a relatively short duration of follow-up.
 BACKGROUND: This study evaluates the real-world safety and discontinuation rate of Zadiva(®) (generic product of dimethyl fumarate (DMF)) in Iranian patients with relapsing-remitting multiple sclerosis (RRMS), supplementing existing clinical evidence from randomized controlled trials. METHODS: This retrospective observational study evaluated the real-world safety and discontinuation rate of DMF in RRMS patients from Amir A'lam referral hospital's neurology clinic. Data on safety, discontinuation rate, and clinical disease activity were collected retrospectively. The study aimed to assess the discontinuation rate, safety, and reasons for discontinuation, as well as the number of patients experiencing a relapse, MRI activity, and EDSS scores. RESULTS: In total, 142 RRMS patients receiving DMF were included in the study, with 15 discontinuing treatment due to adverse events, lack of efficacy, or pregnancy. Notably, a significant reduction in relapse rates was observed, with 90.8% of patients remaining relapse-free throughout the study period. After 1 year of treatment with Zadiva(®), only 17.6% of patients experienced MRI activity, whereas the EDSS score remained stable. CONCLUSIONS: This study provides important real-world data on the safety and tolerability of Zadiva(®) in RRMS patients. The results indicate that Zadiva(®) is generally well tolerated and safe, with a low discontinuation rate due to adverse events or lack of efficacy. These findings suggest that Zadiva(®) is an effective and safe treatment option for RRMS patients in real-world practice.
 Since the beginning of the mass immunization of patients with multiple sclerosis (MS), many data on the efficacy and safety of COVID-19 vaccines have been produced. Considering that MS is an autoimmune disease and that some disease-modifying therapies (DMTs) could decrease the antibody response against COVID-19 vaccines, we carried out this retrospective study with the aim to evaluate the safety of these vaccines in terms of AEFI occurrence and the antibody response after MS patients had received the third dose. Two hundred and ten patients (64.8% female; mean age: 46 years) received the third dose of the mRNA-based COVID-19 vaccine and were included in the study. Third doses were administered from October 2021 to January 2022. The majority of patients (n = 193) were diagnosed with RRMS and EDSS values were ≤3.0 in 72.4% of them. DMTs most commonly used by included patients were interferon Beta 1-a, dimethyl fumarate, natalizumab and fingolimod. Overall, 160 patients (68.8% female) experienced 294 AEFIs, of which about 90% were classified as short-term, while 9.2% were classified as long-term. The most commonly reported following the booster dose were pain at the injection site, flu-like symptoms, headache, fever and fatigue. Regarding the immune response, consistently with literature data, we found that patients receiving ocrelizumab and fingolimod had lower IgG titer than patients receiving other DMTs.
 BACKGROUND: Treatment decisions for multiple sclerosis (MS) are influenced by many factors such as disease symptoms, comorbidities, and tolerability. OBJECTIVE: To determine how much relapsing MS patients were willing to accept the worsening of certain aspects of their MS in return for improvements in symptoms or treatment convenience. METHODS: A web-based discrete choice experiment (DCE) was conducted in patients with relapsing MS. Multinomial logit models were used to estimate relative attribute importance (RAI) and to quantify attribute trade-offs. RESULTS: The DCE was completed by 817 participants from the US, the UK, Poland, and Russia. The most valued attributes of MS therapy to participants were effects on physical fatigue (RAI = 22.3%), cognitive fatigue (RAI = 22.0%), relapses over 2 years (RAI = 20.7%), and MS progression (RAI = 18.4%). Participants would accept six additional relapses in 2 years and a decrease of 7 years in time to disease progression to improve either cognitive or physical fatigue from "quite a bit of difficulty" to "no difficulty." CONCLUSION: Patients strongly valued improving cognitive and physical fatigue and were willing to accept additional relapses or a shorter time to disease progression to have less fatigue. The impact of fatigue on MS patients' quality of life should be considered in treatment decisions.
 The etiology of Multiple Sclerosis (MS) remains undetermined. Its pathogenic risk factors are thought to play a negligible role individually in the development of the disease, instead assuming a pathogenic role when they interact with each other. Unfortunately, the statistical weighting of this pathogenic role in predicting MS risk is currently elusive, preventing clinical and health insurance applications. Here, we aim to develop a population-based multi-criterial model for weighting biological risk factors in MS; also, to calculate the individual MS risk value useful for health insurance application. Accordingly, among 596 MS patients retrospectively assessed at the time of diagnosis, the value of vitamin D < 10 nm/L, BMI (Body Mass Index) < 15 Kg/m(2) and >30 Kg/m(2), female sex, degree of family kinship, and the range of age at onset of 20-45 years were considered as biological risk factors for MS. As a result, in a 30-year-old representative patient having a BMI of 15 and second degree of family kinship for MS, the major developmental contributor for disease is the low vitamin D serum level of 10 nm/L, resulting in an MS risk of 0.110 and 0.106 for female and male, respectively. Furthermore, the Choquet integral applied to uncertain variables, such as biological risk factors, evidenced the family kinship as the main contributor, especially if coincident with the others, to the MS risk. This model allows, for the first time, for the risk stratification of getting sick and the application of the health insurance in people at risk for MS.
 BACKGROUND: Cognitive impairment is present in 40-65% of patients with multiple sclerosis (pwMS). Objectively measured cognitive performance often does not match patients' subjective perception of their own performance. OBJECTIVE: We aimed to compare cognitive performance and subjective perception of cognitive deficits between pwMS and healthy controls (HCs), as well as the accuracy of subjective perception. METHODS: In total, 54 HC and 112 pwMS (relapsing-remitting, RRMS, and progressive PMS) underwent neuropsychological evaluation and completed perceived deficit, fatigue, and anxiety-depression scales. Participants were classified according to their consistency between subjective self-evaluation of cognitive abilities and objective cognitive performance to assess accuracy. Regression models were used to compare cognitive performance between groups and explore factors explaining inaccuracy in the estimation of cognitive performance. RESULTS: PMS showed greater and more widespread cognitive differences with HC than RRMS. No differences were found between pwMS and HC in the perception of deficit. PMS had higher ratios of overestimators. In explaining inaccuracy, fatigue and cognitive preservation were found to be risk factors for underestimation, whereas physical disability and cognitive impairment were risk factors for overestimation. CONCLUSION: PwMS have metacognitive knowledge impairments. This study provides new information about metacognition, data on the prevalence of impairments over a relatively large sample of PwMS, and new insights into factors explaining it. Anosognosia, related to cognitive impairment, may be present in pwMS. Fatigue is a key factor in underestimating cognition.
 [This corrects the article DOI: 10.4103/1673-5374.363188].
 BACKGROUND: Multiple sclerosis (MS) remains a highly unpredictable disease. Many hope that fluid biomarkers may contribute to better stratification of disease, aiding the personalisation of treatment decisions, ultimately improving patient outcomes. OBJECTIVE: The objective of this study was to evaluate the predictive value of CSF brain-specific proteins from early in the disease course of MS on long term clinical outcomes. METHODS: In this study, 34 MS patients had their CSF collected and stored within 5 years of disease onset and were then followed clinically for at least 15 years. CSF concentrations of 64 brain-specific proteins were analyzed in the 34 patient CSF, as well as 19 age and sex-matched controls, using a targeted liquid-chromatography tandem mass spectrometry approach. RESULTS: We identified six CSF brain-specific proteins that significantly differentiated MS from controls (p < 0.05) and nine proteins that could predict disease course over the next decade. CAMK2A emerged as a biomarker candidate that could discriminate between MS and controls and could predict long-term disease progression. CONCLUSION: Targeted approaches to identify and quantify biomarkers associated with MS in the CSF may inform on long term MS outcomes. CAMK2A may be one of several candidates, warranting further exploration.
 BACKGROUND: Relapsing-remitting multiple sclerosis (RRMS) affects predominantly young women within reproductive years. As an increased risk of relapses is known to occur during the post-partum period, it is important to consider treatment options. AIM: Evaluate the effects of intravenous immunoglobulins (IVIg) to prevent post-partum relapses. METHODS: We prospectively followed 198 pregnant female RRMS patients, 67 treated with IVIg during pregnancy and the three months post-partum, and 131 untreated patients that served as controls. RESULTS: During the pre-gestation year, 41.4% were treated with immunomodulatory drugs, and 28.3% experienced a relapse. During pregnancy and the post-partum period, the number of relapsing patients significantly decreased in the IVIg group (37.3%, 10.4%, 8.9%, respectively, p = 0.0003), while no significant change was observed in the untreated group (23.7%, 17.6%, and 22.1%). During the three-month post-partum period, there were only mild and moderate relapses in the IVIg group, while in the untreated group, there were also severe relapses. Stepwise logistic regression that assessed the relation between three-month post-partum relapse and explanatory variables demonstrated that untreated patients had increased risk for post-partum relapse (odds ratio = 4.6, 95% CI [1.69, 12.78], p = 0.033). CONCLUSIONS: IVIg treatment proved efficient to reduce the rate and severity of relapses during pregnancy and the three-month post-partum.
 BACKGROUND: Employment deterioration is common in people with multiple sclerosis (PwMS). Clinicians often learn of job loss after its occurrence, leaving no opportunity for preventive measures. OBJECTIVES: Identify which neuropsychological measures discriminate between healthy volunteers (HVs) and employed/disabled PwMS at baseline and predict work deterioration over 2 years. METHODS: We examined 198 PwMS with computerized tests such as the Processing Speed Test (PST) and conventional tests such as the Symbol-Digit Modalities Test (SDMT), administered at baseline. Employment was assessed via Buffalo Vocational Monitoring Survey. Univariate and regression analyses identified significant predictors of PwMS categorized as work-stable versus work-deteriorated status. RESULTS: PwMS were impaired on all baseline assessments relative to HVs (p's < 0.001). Post hoc analyses showed that employed PwMS and HVs performed similarly and better than work-disabled PwMS. At the univariate level, both PST and SDMT discriminated between work-deteriorated and work-stable PwMS (p's < 0.01). The logistic regression model accounting for all measures retained PST and the computerized Walking Speed Test. PwMS with increased negative work events had lower PST (p < 0.001), SDMT (p < 0.001), and BVMT-R (p < 0.01) scores than stable PwMS. The related regression model retained PST and BVMT-R (p < 0.001). CONCLUSION: Cognition, as measured by the PST and BVMT-R, are predictive of job deterioration in PwMS and may be a useful screening tool to identify those at high risk of unemployment.
 BACKGROUND: Interdisciplinary therapies for the management of people with multiple sclerosis (MS) are underappreciated. There is an urgent need to introduce music therapy (MT), either alone or in combination with physical therapy (PT), into clinical practice to achieve synergy with disease-modifying therapies. A holistic approach to rehabilitation for people with MS may mitigate symptoms and reduce polypharmacy, potentially lowering health care costs. RESULTS: As MS progresses, patients experience a range of worsening symptoms, and many develop psychosocial comorbidities. As disease-modifying therapies delay disability progression, nonpharmacologic treatments become increasingly important. The main aim of PT is to improve or maintain patients' functional mobility, strength, and flexibility. Because it targets multiple functions, MT can help improve functional and psychosocial domains and may be a valuable intervention to help patients achieve the physical, cognitive, and emotional goals of PT. Exploratory studies showed that MT, alone or in combination with PT, can lead to functional improvements in mobility, balance, gait, and fatigue. Similar to PT, MT also has benefits in improving fine motor skills, cognition, learning, and memory and in providing emotional support. CONCLUSIONS: Both MT and PT have the potential to improve overall well-being and health-related quality of life in physically active patients with MS, and MT can provide added emotional support for those who are less able to engage in physical activity. However, MT is not typically a part of standard of care, and PT visits are limited. Nevertheless, interdisciplinary therapies should be incorporated into clinical practice.
 BACKGROUND: Epidemiologic studies have established obesity as a risk factor for multiple sclerosis (MS). These studies relied on body-mass index (BMI) and body size silhouettes as the primary measures of obesity. Unfortunately, the causal mechanisms through which obesity confers MS risk are not yet known. OBJECTIVES: To investigate the causal effects of multiple specific measures of body fat on MS risk in populations of European descent, using Mendelian randomization (MR). METHODS: MR is a genetic instrumental variable analysis utilizing genome-wide association (GWA) summary statistics to infer causality between phenotypes. MR analyses were performed to investigate the relationships between seven measures of body fat (BMI, waist-hip ratio, visceral adipose tissue [VAT], subcutaneous adipose tissue, and arm-, leg-, and trunk-fat to total body fat ratio) and MS risk. RESULTS: Only BMI and VAT were significantly associated with MS risk in separate MR analyses (β(BMI)=0.27, p(BMI)<0.001; β(VAT)=0.28, p(VAT)=0.006). High correlation between BMI and VAT instruments suggest that two-sample MR associations for BMI and VAT likely capture the same causal mechanisms. CONCLUSIONS: BMI and VAT were causally associated with MS risk in European populations, though their effects do not appear independent, suggesting overlap in the role of overall body mass and visceral obesity in MS pathogenesis.
 INTRODUCTION: Extensive human and animal research shows that exercise has beneficial effects on multiple clinical outcomes for patients suffering from multiple sclerosis (MS). This research was conducted to examine the effect of aerobic exercise with probiotic consumption on the myelination of nerve fibers in a cuprizone-induced demyelination mouse model of MS. METHODS: Rats exposed to cuprizone (CPZ) for 13 weeks were subjected to motor and balance tests in week 5. They (5 people in each group) were assigned to five groups of control (C), MS, MS with exercise (MS+Exe), MS with probiotic (MS+Pro), and MS with probiotic and exercise (MS+Pro+Exe) randomly. The exercise groups conducted aerobic exercises 5 days a week for 60 days. The rats received probiotics by gavage. Performance and balance tests were repeated when the eight-week protocol of exercise and probiotic consumption was finished. One day after these interventions, they were sacrificed to undergo biochemical and molecular biology assays. RESULTS: The results showed that Myelin basic protein (MBP) was increased in the MS+Pro+Exe, MS+Pro, and MS+Exe compared to the MS group (P<0.05).The nestin mRNA showed an increase in MS+Pro+Exe, MS+Exe, and MS+Pro groups compared to the MS group, but this increase was not significant in MS+Pro+Exe and MS+Exe groups compared to the control and MS groups (P>0.05). CONCLUSION: According to the results, lifestyle interventions can effectively alleviate demyelinating-inflammatory processes that happen in the brains of MS patients.
 Multiple sclerosis (MS) is a chronic neurological disorder characterized by inflammation in the central nervous system (CNS) that leads to neurodegeneration. The clinical course is highly variable, but its prevalence is rising worldwide, partly thanks to novel disease-modifying therapies. Additionally, the lifespan of people with MS is increasing, and for this reason, it is fundamental to have a multidisciplinary approach to MS. MS may be associated with cardiovascular diseases (CVD), but there is scarce attention on this issue. In particular, CNS is essential in regulating the autonomic system and heart activity. Moreover, cardiovascular risk factors show a higher prevalence in MS patients. On the other hand, conditions like Takotsubo syndrome are rare complications of MS. The parallelism between MS and myocarditis is also interesting. Finally, cardiac toxicity represents a not infrequent adverse reaction to MS drugs. This narrative review aims to provide an overview of cardiovascular complications in MS and their management to prompt further clinical and pre-clinical research on this topic.
 The maintenance of adequate blood supply and vascular integrity is fundamental to ensure cerebral function. A wide range of studies report vascular dysfunction in white matter dementias, a group of cerebral disorders characterized by substantial white matter damage in the brain leading to cognitive impairment. Despite recent advances in imaging, the contribution of vascular-specific regional alterations in white matter dementia has been not extensively reviewed. First, we present an overview of the main components of the vascular system involved in the maintenance of brain function, modulation of cerebral blood flow and integrity of the blood-brain barrier in the healthy brain and during aging. Second, we review the regional contribution of cerebral blood flow and blood-brain barrier disturbances in the pathogenesis of three distinct conditions: the archetypal white matter predominant neurocognitive dementia that is vascular dementia, a neuroinflammatory predominant disease (multiple sclerosis) and a neurodegenerative predominant disease (Alzheimer's). Finally, we then examine the shared landscape of vascular dysfunction in white matter dementia. By emphasizing the involvement of vascular dysfunction in the white matter, we put forward a hypothetical map of vascular dysfunction during disease-specific progression to guide future research aimed to improve diagnostics and facilitate the development of tailored therapies.
 BACKGROUND: Oceania is a continent, covering more than 8 million km(2), with a population of more than 44 million people. In different countries landing in Oceania, various prevalence of MS has been reported, so we designed this systematic review and meta-analysis to estimate the pooled prevalence of MS in Oceania. METHODS: We systematically searched PubMed, Scopus, EMBASE, Web of Science, and Google Scholar. We also searched references of included studies, and conference abstracts. The search was done on January 1, 2023, by two independent researchers. We extracted the name of the first author, country, publication year, prevalence period, number of study participants, total female and male population, disease duration, type of MS, mean duration of the disease, mean age at disease onset, mean Expanded Disability Status Scale (EDSS), and total female and male patients with MS. RESULTS: A literature search revealed 81,044 records; after deleting duplicates, 38,260 records remained. One hundred and six full texts were evaluated, and finally, seventeen studies remained for systematic review. Most studies were done in Newcastle; eight studies were done in 1961, 8 in 1981, 2 in 1996, and 2 in 2001. In all other years, only one study was done. The pooled prevalence of MS in 1961 in Oceania was estimated as 19.85/100,000 (I(2)=70.3%, p=0.001). The pooled prevalence of MS in 1981 in Oceania was estimated as 39.07/100,000 (I(2) =88%, p=0.001). CONCLUSIONS: The result of this systematic review and meta-analysis shows that the prevalence of MS has increased dramatically during the timespan in Oceania.

 BACKGROUND: Acquired pendular nystagmus is most often seen in patients with demyelinating disease. Although it is often bilateral, rare cases may be monocular. There is paucity of data on the spectrum of clinical presentation, underlying mechanism, and response to treatment in patients with monocular pendular nystagmus. METHODS: Retrospective case series of patients with monocular pendular nystagmus seen in 2 tertiary neuro-ophthalmology clinics between January 2019 and June 2022. All patients underwent a complete neuro-ophthalmological assessment and MRI. RESULTS: We describe 5 patients (3 women) aged 31-49 with monocular pendular nystagmus. All had a diagnosis of multiple sclerosis. Three patients had horizontal and 2 had vertical pendular nystagmus. The Snellen visual acuity in the eye with pendular nystagmus varied from 20/20 to 20/200. Two patients were asymptomatic and 3 suffered visually debilitating oscillopsia. Treatment response was available for 2 patients, both of which responded well to treatment with memantine. The pendular nystagmus was observed in the eye with worse visual acuity in 4 of 5 cases (80%). Three patients had bilateral pontine lesions, and 2 had unilateral pontine lesion ipsilateral to the side of nystagmus. CONCLUSIONS: Monocular pendular nystagmus in adults is seen most often in patients with multiple sclerosis. Asymmetry in brainstem lesions and afferent visual input may be the culprit. Treatment with memantine may result in significant improvement in symptomatic patients.
 The c-Jun amino terminal kinases (JNKs) regulate transcription, and studies suggest they contribute to neuropathology in the EAE model of MS. To examine the role of the JNK3 isoform, we compared EAE in JNK3 null mice to wild type (WT) littermates. Although disease severity was similar in female mice, in male JNK3 null mice the day of onset and time to reach 100% incidence occurred sooner, and disease severity was increased. While glial activation in spinal cord was similar, white matter lesions were increased in JNK3 null mice. These results suggest JNK3 normally limits EAE disease in a sex-dependent manner.

 A healthy gut flora contains a diverse and stable commensal group of microorganisms, whereas, in disease conditions, there is a shift toward pathogenic microbes, termed microbial dysbiosis. Many studies associate microbial dysbiosis with neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Multiple sclerosis (MS), and Amyotrophic lateral sclerosis (ALS). Although, an overall comparative analysis of microbes and their metabolic involvement in these diseases is still lacking. In this study, we have performed a comparative analysis of microbial composition changes occurring in these four diseases. Our research showed a high resemblance of microbial dysbiosis signatures between AD, PD, and MS. However, ALS appeared dissimilar. The most common population of microbes to show an increase belonged to the phyla, Bacteroidetes, Actinobacteria, Proteobacteria, and Firmicutes. Although, Bacteroidetes and Firmicutes were the only phyla that showed a decrease in their population. The functional analysis of these dysbiotic microbes showed several potential metabolic links which can be involved in the altered microbiome-gut-brain axis in neurodegenerative diseases. For instance, the microbes with elevated populations lack pathways for synthesizing SCFA acetate and butyrate. Also, these microbes have a high capacity for producing L-glutamate, an excitatory neurotransmitter and precursor of GABA. Contrastingly, Tryptophan and histamine have a lower representation in the annotated genome of elevated microbes. Finally, the neuroprotective compound spermidine was less represented in elevated microbes' genomes. Our study provides a comprehensive catalog of potential dysbiotic microbes and their metabolic involvement in neurodegenerative disorders, including AD, PD, MS, and ALS.
 Hippocampal area CA2 plays a critical role in social recognition memory and has unique cellular and molecular properties that distinguish it from areas CA1 and CA3. In addition to having a particularly high density of interneurons, the inhibitory transmission in this region displays two distinct forms of long-term synaptic plasticity. Early studies on human hippocampal tissue have reported unique alteration in area CA2 with several pathologies and psychiatric disorders. In this review, we present recent studies revealing changes in inhibitory transmission and plasticity of area CA2 in mouse models of multiple sclerosis, autism spectrum disorder, Alzheimer's disease, schizophrenia and the 22q11.2 deletion syndrome and propose how these changes could underly deficits in social cognition observed during these pathologies.
 BACKGROUND: Faulty dietary habits and overnutrition are prevalent among Egyptian patients with multiple sclerosis (MS) who do not receive nutrition care as part of treatment. Thus, this study was conducted to identify the effect of nutrition counseling on the nutritional status of patients with MS. This endeavor might provide evidence for the value of counseling in such a setting and advance the integration of nutrition counseling into the routine management of patients with MS. METHODS: A single-blinded, parallel-randomized controlled clinical trial was conducted at Kasr Alainy MS Unit on 120 eligible patients with MS from September 2019 to February 2020. Patients were randomly allocated to either the nutrition counseling intervention group (IG) or the control group (CG). Allocation concealment was performed by using sequentially numbered opaque sealed envelopes. All patients were assessed initially and complied with the Kasr Alainy MS Unit standard management protocol for the study period. Only patients in the IG underwent initial nutrition counseling sessions followed by a monthly evaluation. All patients were assessed at the end of the 3-month follow-up period. Sociodemographic data were gathered through a structured interview. Nutritional status was assessed anthropometrically and via 24-h recall. The 2 groups were compared initially and at the end of the follow-up. Both intention-to-treat and per-protocol analyses were conducted. RESULTS: At baseline assessment, the prevalence of overweight and obesity was 31.7% and 32.5%, respectively, and the mean body mass index was 27.7 ± 5.7 kg/m(2). Mean waist circumference was 93.5 ± 11.9 and 99.2 ± 13.1 cm for males and females, respectively. Approximately 27.3% of males and 83.9% of females showed abdominal obesity. After 3 months of counseling, weight, body mass index, waist circumference, nutrient intake and adequacy significantly improved in the IG (p < 0.05). CONCLUSION: Nutrition counseling significantly improved anthropometric measurements, dietary habits, nutrient intake and adequacy. TRIAL REGISTRATION: The study was registered on ClinicalTrial.gov and was given a code (NCT04217564).
 BACKGROUND AND OBJECTIVES: To evaluate the factors determining the final clinical phenotype after an initial isolated attack of optic neuritis (ON). ON could be an isolated event or the initial presentation of a chronic neuroimmunological condition. METHODS: This was a retrospective analysis of patients presenting to University Hospitals Cleveland Medical Center for an initial, isolated attack of ON. Final clinical phenotypes were idiopathic ON, multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein associated disease (MOGAD), or secondary ON (e.g. neurosarcoidosis). Several potential predictors at the time of initial presentation were compared among the different phenotypes to determine early predictors. Categorical variables were compared using Pearson χ2 or Fisher's exact test, and continuous variables were compared using independent t-test. RESULTS: Sixty-four patients met criteria (average age 41.3 ± 13.3, 78.1% females). Average time to final diagnosis was 8.3 months, and average follow-up was 47 months. The final phenotypes were MS (22, 34%), idiopathic ON (14, 22%), MOGAD (11, 17%), NMOSD (10, 16%), and secondary ON (7, 11%). White race, unilateral ON, short segment hyperintensity on orbital MRI, classical demyelination on brain MRI, and not requiring PLEX were associated with MS. Older age, poor steroid responsiveness, and requiring PLEX were associated with NMOSD. African American race, bilateral ON, papillitis on fundoscopy, long segment hyperintensity on orbital MRI, and normal brain MRI were associated with MOGAD. Normal or thinned retinal nerve fiber layer on OCT, short segment hyperintensity on orbital MRI, and normal brain MRI were associated with idiopathic ON. CONCLUSION: The final clinical phenotype may be predictable at the time of initial ON presentation. This requires a careful evaluation of patient demographics, treatment response, funduscopic findings, OCT, and orbital and brain MRIs. Utilizing early predictors in clinical practice could better inform prognosis and management decisions.
 Patients with multiple sclerosis consistently show widespread changes in functional connectivity. Yet, alterations are heterogeneous across studies, underscoring the complexity of functional reorganization in multiple sclerosis. Here, we aim to provide new insights by applying a time-resolved graph-analytical framework to identify a clinically relevant pattern of dynamic functional connectivity reconfigurations in multiple sclerosis. Resting-state data from 75 patients with multiple sclerosis (N = 75, female:male ratio of 3:2, median age: 42.0 ± 11.0 years, median disease duration: 6 ± 11.4 years) and 75 age- and sex-matched controls (N = 75, female:male ratio of 3:2, median age: 40.2 ± 11.8 years) were analysed using multilayer community detection. Local, resting-state functional system and global levels of dynamic functional connectivity reconfiguration were characterized using graph-theoretical measures including flexibility, promiscuity, cohesion, disjointedness and entropy. Moreover, we quantified hypo- and hyper-flexibility of brain regions and derived the flexibility reorganization index as a summary measure of whole-brain reorganization. Lastly, we explored the relationship between clinical disability and altered functional dynamics. Significant increases in global flexibility (t = 2.38, P(FDR) = 0.024), promiscuity (t = 1.94, P(FDR) = 0.038), entropy (t = 2.17, P(FDR) = 0.027) and cohesion (t = 2.45, P(FDR) = 0.024) were observed in patients and were driven by pericentral, limbic and subcortical regions. Importantly, these graph metrics were correlated with clinical disability such that greater reconfiguration dynamics tracked greater disability. Moreover, patients demonstrate a systematic shift in flexibility from sensorimotor areas to transmodal areas, with the most pronounced increases located in regions with generally low dynamics in controls. Together, these findings reveal a hyperflexible reorganization of brain activity in multiple sclerosis that clusters in pericentral, subcortical and limbic areas. This functional reorganization was linked to clinical disability, providing new evidence that alterations of multilayer temporal dynamics play a role in the manifestation of multiple sclerosis.
 Multiple sclerosis (MS) primarily affects adult females. However, in the last decades, rising incidence and prevalence have been observed for demographic extremes, such as pediatric-onset MS (POMS; occurring before 18 years of age) and late-onset MS (corresponding to an onset above 50 years). These categories show peculiar clinical-pathogenetic characteristics, aging processes and disease courses, therapeutic options, and unmet needs. Nonetheless, several open questions are still pending. POMS patients display an important contribution of multiple genetic and environmental factors such as EBV, while in LOMS, hormonal changes and pollution may represent disease triggers. In both categories, immunosenescence emerges as a pathogenic driver of the disease, particularly for LOMS. In both populations, patient and caregiver engagement are essential from the diagnosis communication to early treatment of disease-modifying therapy (DMTs), which in the elderly population appears more complex and less proven in terms of efficacy and safety. Digital technologies (e.g., exergames and e-training) have recently emerged with promising results, particularly in treating and following motor and cognitive deficits. However, this offer seems more feasible for POMS, being LOMS less familiar with digital technology. In this narrative review, we discuss how the aging process influences the pathogenesis, disease course, and therapeutic options of both POMS and LOMS. Finally, we evaluate the impact of new digital communication tools, which greatly interest the current and future management of POMS and LOMS patients.
 BACKGROUND: Some multiple sclerosis (MS) disease-modifying therapies (DMTs) impair responses to vaccines, emphasizing the importance of understanding COVID-19 vaccine immune responses in people with MS (PwMS) receiving different DMTs. METHODS: This prospective, open-label observational study enrolled 45 participants treated with natalizumab (n = 12), ocrelizumab (n = 16), fumarates (dimethyl fumarate or diroximel fumarate, n = 11), or interferon beta (n = 6); ages 18-65 years inclusive; stable on DMT for at least 6 months. Responder rates, anti-SARS-CoV-2 spike receptor-binding domain IgG (anti-RBD) geometric mean titers (GMTs), antigen-specific T cells, and vaccination-related adverse events were evaluated at baseline and 8, 24, 36, and 48 weeks after first mRNA-1273 (Moderna) dose. RESULTS: At 8 weeks post vaccination, all natalizumab-, fumarate-, and interferon beta-treated participants generated detectable anti-RBD IgG titers, compared to only 25% of the ocrelizumab cohort. At 24 and 36 weeks post vaccination, natalizumab-, fumarate-, and interferon beta-treated participants continued to demonstrate detectable anti-RBD IgG titers, whereas participants receiving ocrelizumab did not. Anti-RBD GMTs decreased 81.5% between 8 and 24 weeks post vaccination for the non-ocrelizumab-treated participants, with no significant difference between groups. At 36 weeks post vaccination, ocrelizumab-treated participants had higher proportions of spike-specific T cells compared to other treatment groups. Vaccine-associated side effects were highest in the ocrelizumab arm for most symptoms. CONCLUSIONS: These results suggest that humoral response to mRNA-1273 COVID-19 vaccine is preserved and similar in PwMS treated with natalizumab, fumarate, and interferon beta, but muted with ocrelizumab. All DMTs had preserved T cell response, including the ocrelizumab cohort, which also had a greater risk of vaccine-related side effects.
 BACKGROUND: Several studies demonstrated the association between tobacco smoking and higher risk and increased progression of multiple sclerosis (MS). Data about the effect of smoking during the recovery from MS attacks is limited. Furthermore, different types of tobacco exposures such as water pipe and passive smoking are not well assessed separately. So this study evaluated the effect of different types of smokes, cigarette and water pipe as well as passive smoking on the function recovery of relapsing-remitting MS (RRMS) attacks METHODS: This cohort study evaluated the adult patients with RRMS and Expanded Disability Status Scale (EDSS) < 5 in the attack phase. Patients were divided into two groups: smokers and non-smokers. The smokers included those who use cigarette, water pipe as well as passive smokers as subgroups for more analyses later. EDSS was monitored after relapse and two months after relapse. Change of EDSS considered as the criteria for functional recovery. The correlation between the amount of consumption and disability level was assessed among smokers by Pearson's correlation test. While, the difference of EDSS between smoker and non-smoker were assessed by Independent samples T-test. RESULTS: 142 patients were evaluated. 79 (55.6%) were smokers (43% male) while 63 (44.4%) were non-smokers (36.5% male). There was a statistically significant difference in change of EDSS between smoker and non-smoker groups, which change of EDSS was higher in non-smoker (-2.62 ± 0.90 non-smoker vs. -1.75 ± 0.76 smoker, P < 0.001). Also, only there was a significantly lesser decline in EDSS after two months in the cigarette smokers in subgroups analyses (P < 0.001). A correlation analysis revealed a significant positive correlation between the number per day of cigarette smoking and EDSS after relapse (r = 0.3, P = 0.03) and a significant positive correlation between minutes per month of smoking of water pipe and EDSS two months after relapse (r = ‎0.6‎‎, P > 0.001). CONCLUSION: Tobacco smoking especially cigarette smoking is associated with a negative effect on recovery from the attack in patients with RRMS.
 BACKGROUND: Contrast-enhancing (CE) lesions are an important finding on brain magnetic resonance imaging (MRI) in patients with multiple sclerosis (MS) but can be missed easily. Automated solutions for reliable CE lesion detection are emerging; however, independent validation of artificial intelligence (AI) tools in the clinical routine is still rare. METHODS: A three-dimensional convolutional neural network for CE lesion segmentation was trained externally on 1488 datasets of 934 MS patients from 81 scanners using concatenated information from FLAIR and T1-weighted post-contrast imaging. This externally trained model was tested on an independent dataset comprising 504 T1-weighted post-contrast and FLAIR image datasets of MS patients from clinical routine. Two neuroradiologists (R1, R2) labeled CE lesions for gold standard definition in the clinical test dataset. The algorithmic output was evaluated on both patient- and lesion-level. RESULTS: On a patient-level, recall, specificity, precision, and accuracy of the AI tool to predict patients with CE lesions were 0.75, 0.99, 0.91, and 0.96. The agreement between the AI tool and both readers was within the range of inter-rater agreement (Cohen's kappa; AI vs. R1: 0.69; AI vs. R2: 0.76; R1 vs. R2: 0.76). On a lesion-level, false negative lesions were predominately found in infratentorial location, significantly smaller, and at lower contrast than true positive lesions (p < 0.05). CONCLUSIONS: AI-based identification of CE lesions on brain MRI is feasible, approaching human reader performance in independent clinical data and might be of help as a second reader in the neuroradiological assessment of active inflammation in MS patients. CRITICAL RELEVANCE STATEMENT: Al-based detection of contrast-enhancing multiple sclerosis lesions approaches human reader performance, but careful visual inspection is still needed, especially for infratentorial, small and low-contrast lesions.
 AIM: This study aimed to explain the experiences of individuals with multiple sclerosis (MS) about the collaborative care programme. DESIGN: This qualitative study was conducted from July 2021 to March 2022. METHODS: We conducted this study with individuals with MS who participated in the collaborative care programme in Hamadan, Iran. A purposive sampling with maximum variety was applied to recruit patients until data saturation. Eventually, 18 patients consented and were interviewed using a semi-structured interview guide. The transcriptions of audio-checked interviews were analysed using a conventional content analysis approach of Graneheim and Lundman by MAXQDA 10, 2010 edition. RESULTS: The study identified three main categories. that emerged from the participants' experiences of collaborative care: the 'Beginning of Communication', which included two subcategories, 'Introduction and Acquaintance with Each Other' and 'Formation of Trust'; 'Mutual Interaction', which included three subcategories, 'Dialogue', 'Mutual Goal Setting' and 'Mutual Agreement of Care Solutions'; and 'Exchange of Targeted Behaviors', which included six categories, Implementation of Strategies for 'Nutritional Behaviors', 'Sleep and Rest', 'Constipation Relief', 'Promotion of Physical Activity and Exercise', 'Fatigue Reduction' and 'Stress Management'. CONCLUSIONS: The findings highlight the statistically significant role of collaborative care in MS management. Utilizing these research findings can update the development of interventions based on collaborative care, which can provide appropriate support to individuals with MS. PATIENT OR PUBLIC CONTRIBUTION: Individuals with multiple sclerosis.
 BACKGROUND: Neurodegeneration leads to continuous accumulation of disability in progressive Multiple Sclerosis (MS). Exercise is considered to counteract disease progression, but little is known on the interaction between fitness, brain networks and disability in MS. OBJECTIVE: The aim of this study to explore functional and structural brain connectivity and the interaction between fitness and disability based on motor and cognitive functional outcomes in a secondary analysis of a randomised, 3-month, waiting group controlled arm ergometry intervention in progressive MS. METHODS: We modelled individual structural and functional brain networks based on magnetic resonance imaging (MRI). We used linear mixed effect models to compare changes in brain networks between the groups and explore the association between fitness, brain connectivity and functional outcomes in the entire cohort. RESULTS: We recruited 34 persons with advanced progressive MS (pwMS, mean age 53 years, females 71%, mean disease duration 17 years and an average walking restriction of < 100 m without aid). Functional connectivity increased in highly connected brain regions of the exercise group (p = 0.017), but no structural changes (p = 0.817) were observed. Motor and cognitive task performance correlated positively with nodal structural connectivity but not nodal functional connectivity. We also found that the correlation between fitness and functional outcomes was stronger with lower connectivity. CONCLUSIONS: Functional reorganisation seems to be an early indicator of exercise effects on brain networks. Fitness moderates the relationship between network disruption and both motor and cognitive outcomes, with growing importance in more disrupted brain networks. These findings underline the need and opportunities associated with exercise in advanced MS.
 PURPOSE: To explore quantitative and qualitative features of anomia in participants with left-hemisphere stroke, Parkinson's disease, or multiple sclerosis. MATERIALS AND METHODS: This descriptive cross-sectional study compares signs of anomia within and across participants (n = 87), divided into four groups; moderate to severe anomia after stroke (MSAS, n = 19), mild anomia after stroke (MAS, n = 22), PD (n = 19) and MS (n = 27). Aspects analysed include naming accuracy and speed, the nature of incorrect responses, semantic and phonemic verbal fluency, information content in re-telling, and the relationship between test results and self-reports on word-finding difficulties and communicative participation. RESULTS: All groups had impaired verbal fluency, prolonged response times and reduced information content in re-telling. The MSAS group had significantly more signs of anomia than the other groups. Results from the other groups overlapped on a MAS-PD-MS continuum. Both semantically and phonologically incorrect responses were common in the stroke groups, while semantically incorrect ones predominated in the PD and MS groups. All four groups reported a similar negative impact on self-perceived communicative participation. Correlations between self-reports and test results were inconsistent. CONCLUSIONS: Anomia features have quantitative and qualitative similarities and differences across neurological conditions.
 PURPOSE: It is known that clinical Pilates improves strength, core stability, balance, gait, fatigue, and quality of life (QOL) in patients with multiple sclerosis (PwMS). On the other hand, there is insufficient information about whether similar benefits can be achieved with Pilates-based telerehabilitation (Pilates-TR). We aimed to investigate the effects of Pilates-TR on physical performance and QOL in PwMS. METHODS: Thirty PwMS were recruited and randomly allocated into two groups. The Pilates-TR group received Pilates-TR via videoconferences three days per week during six weeks at home. The control group (CG) was a waitlist with no Pilates-TR treatment. Physical performance measures included extremity muscle strength, core endurance and power, balance, gait analysis, and functional exercise capacity. In addition, fatigue and QOL were evaluated. RESULTS: Extremity muscle strength, core endurance and power, balance, walking speed, cadence, distance, functional exercise capacity, and QOL were improved after Pilates-TR (p < 0.05). Fatigue level and the effects of fatigue on functions decreased in Pilates-TR, while fatigue level increased in CG (p < .05). The CG showed no changes in any other measurements (p > .05). CONCLUSION: Pilates-TR was effective in improving physical performance and QOL in PwMS. Pilates-TR can be recommended as an effective option, especially for patients with barriers to reaching the clinic.Trial registration: ClinicalTrials.gov (NCT04838886)IMPLICATIONS FOR REHABILITATIONPilates-based telerehabilitation (Pilates-TR) is an effective means of improving muscle strength, core stability, balance, walking, functional exercise capacity, and fatigue in patients with multiple sclerosis (PwMS).Pilates-TR seems like an appropriate option for improving both the mental and physical dimensions of quality of life in PwMS.Clinicians can safely use Pilates-TR to increase physical performance and quality of life in PwMS who have limitations to participate in clinical Pilates for various reasons.
 BACKGROUND: Although disease-modifying therapies (DMTs) in multiple sclerosis (MS) are known to target the immune system, mechanisms of action, efficacy, safety, and tolerability profiles differ. The long-term impact of DMTs on the immune system and its relation to infectious complications is still poorly understood. OBJECTIVES: To analyze the effect of DMTs on serum immunoglobulin (Ig) levels under consideration of patient demographics and therapy duration. DESIGN: We included 483 patients on DMTs, 69 patients without DMTs, and 51 controls in this retrospective cross-sectional study. METHODS: IgG, IgM, and IgG subclass 1-4 levels of patients with MS under treatment with DMTs were compared with treatment naive MS patients and controls by multivariate linear regression. Further, Ig levels stratified by DMTs were analyzed regarding therapy duration. RESULTS: MS patients treated with fingolimod (FG), natalizumab, and B-cell depleting therapies (BCDT) demonstrated significantly lower IgG and IgM levels than healthy controls after a median treatment of 37, 31, and 23 months, respectively (p < 0.05). Treatment with dimethyl fumarate (DMF) and teriflunomide was associated with lower IgG, but not IgM levels. DMF and BCDT were also associated with lower IgG1 levels, while FG led to a reduction of IgG2. Treatment with interferon-beta (IFN) and glatiramer acetate (GA) had no impact on Ig levels. Analysis of subgroups by linear regression also showed a time-dependent decrease of Igs levels in patients treated with BCDT with a median annual reduction of IgG of 3.2% and IgM of 6.2%. CONCLUSION: Treatment with DMTs, except GA and IFN, was associated with a decrease in Ig levels. DMTs differed in the extent of decreasing Ig levels but also in their differential effects on Ig subclasses. Monitoring of Ig levels should be considered in patients on long-term treatment with DMTs, particularly those on BCDT, to identify patients at risk of low immunoglobulin levels.
 INTRODUCTION: Tuberous sclerosis complex (TSC) is an autosomal dominant neurocutaneous disease with central nervous system (CNS) involvement. Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS characterized by symptomatic episodes that occur months or years apart and affect different anatomic locations. In the absence of symptomatic episodes, radiologically isolated syndrome (RIS) could be diagnosed. Here, we report the case of a 10-year-old boy followed-up for TSC and diagnosed with RIS after a routine neuroimaging assessment. CASE DESCRIPTION: The patient was diagnosed with TSC after seizure onset at the age of 4 years. The follow-up magnetic resonance imaging (MRI) showed multiple asymptomatic demyelinating lesions. Brain and spinal cord MRI was performed after 2 months and showed additional lesions in the right frontal white matter and left cerebral peduncle, the latter with contrast enhancement. Therefore, he received a diagnosis of RIS. Visual evoked potentials were normal. Cerebrospinal fluid examination showed oligoclonal bands. The search for AQP4-IgG and MOG-IgG antibodies was negative. He was treated with interferon beta-1a. Six months later, follow-up MRI revealed no new demyelinating lesions and resolution of contrast enhancement. CONCLUSION: To the best of our knowledge, this is the third reported patient presenting a co-occurrence of TSC and demyelinating disease. Although we cannot state if the described comorbidity is casual or not, some clinical and preclinical data suggest that the mTOR complex might be the link between TSC and demyelinating disease.
 PURPOSE: To assess dysarthric disorders in multiple sclerosis (MS) patients in comparison with healthy individuals and MS patients without dysarthria depending on the patient's sex, age, and the type of text read using an objective tool. METHODS: The study was carried out in a group of 72 persons, including 24 with MS presenting dysarthria (study group) and 24 healthy individuals (healthy control group), and 24 with MS without dysarthria (MS control group). Performance (reading) time was evaluated by means of an objective tool created for the purpose of the analysis. RESULTS: The study showed significant statistical differences in the analyzed performance time of: poetry reading, prose reading, and completing a diction exercise, among persons with MS from the study group presenting dysarthria and both control groups (p < 0.05). It took more time to read the poem, and prose and to perform a diction exercise in the study group with dysarthria than in both control groups (with no significant differences between the two) Similarly, the comparison between the groups in terms of sex and age showed disturbances in the above-mentioned parameter in the study group. What was not demonstrated were significant differences in the evaluated speech parameters depending on both sex and age separately in the group of MS patients with dysarthria, and both control groups (p < 0.05). CONCLUSION: The objective tool created for the purpose of speech analysis is useful in detecting discrepancies in performance (reading) time among MS patients with dysarthria, and healthy individuals, as well as patients with MS without dysarthria and can be used in clinical practice for diagnostic purposes, however, further research is essential to complete its validation.
 BACKGROUND: Rehabilitation of Multiple Sclerosis (MS) is associated with various clinical, social and economic outcomes. We aimed to evaluate the cost-utility of MS multidisciplinary rehabilitation in Iran. RESEARCH DESIGN AND METHODS: An economic evaluation was conducted using a Markov model designed to reflect the natural course of the disease and interventions. Parameters and variables were extracted from available evidence, and costs and outcomes were calculated from the social perspective. The base-case analysis considered a 5-year time horizon. Costs were estimated based on approved national standards for MS rehabilitation. Sensitivity analyses were also performed. RESULTS: The average cost of the rehabilitation strategy was higher compared to the non-rehabilitation strategy, but it resulted in higher quality-adjusted life years (QALYs) values. The incremental cost-effectiveness ratio (ICER) was found to be $2,845.8 per QALY, indicating that the rehabilitation strategy is cost-effective. In the deterministic sensitivity analysis, extending the time horizon to 10 years made the rehabilitation strategy a dominant choice. Probabilistic sensitivity analysis results were consistent with the base-case findings. CONCLUSIONS: The MS multidisciplinary rehabilitation proved to be a cost-effective strategy; however, the results were sensitive to the input values of the model. Increasing the time horizon increased the probability of rehabilitation being cost-effective.
 Multiple sclerosis (MS) is an autoimmune, demyelinating disorder of the central nervous system (CNS) affecting approximately 2.5 million people worldwide. The mechanisms underlying the pathogenesis of MS are still only partially elucidated. Galectins are a family of β-galactoside-binding lectins that are involved in the regulation of immune and inflammatory responses and have been shown to exert a role in the maintenance of central nervous system (CNS) homeostasis. There has been an increasing interest in the role of galectin-3 in neuroinflammation and neurodegeneration. In the current study, we have evaluated the expression levels of galectin-3 in different cellular populations involved in the etiopathogenesis of MS. We have observed dramatically higher transcriptomic levels of galectin-3 in encephalitogenic CD4+ T cells in a preclinical model of MS, the MOG-induced experimental allergic encephalomyelitis (EAE). Also, significantly higher levels of galectin-3 were found in microglial cells, astrocytes, and oligodendrocytes isolated from the spinal cord of EAE mice, as well as in human MS-related white matter lesions. Modular co-expression analysis revealed that galectin-3 is co-expressed with genes involved in the regulation of microglia, cytokine production, and chemotaxis. This is the first comprehensive analysis of the expression of galectin-3 in MS, further strengthening its potential pathogenetic role in the etiopathogenesis of this CNS autoimmune disorder.
 Multiple sclerosis (MS) is a chronic autoimmune and demyelinating disease of the central nervous system (CNS) which leads to focal demyelinated lesions in the brain and spinal cord. Failure of remyelination contributes to chronic disability in young adults. Characterization of events occurring during the demyelination and remyelination processes and those of which subsequently limit remyelination or contribute to demyelination can provide the possibility of new therapies development for MS. Most of the currently available therapies and investigations modulate immune responses and mediators. Since most therapeutic strategies have unsatisfied outcomes, developing new therapies that enhance brain lesion repair is a priority. A close look at cellular and chemical components of MS lesions will pave the way to a better understanding of lesions pathology and will provide possible opportunities for repair strategies and targeted pharmacotherapy. This review summarizes the lesion components and features, particularly the detrimental elements, and discusses the possibility of suggesting new potential targets as therapies for demyelinating diseases like MS.
 PURPOSE: Multiple sclerosis (MS) is a disease that progresses not only with demyelination but also with neurodegeneration. One of the goals of drug treatment in MS is to prevent neurodegeneration. Cortical thickness (CT), sulcal depth (SD), and local gyrification index (LGI) are indicators related to neurodegeneration. The aim of this study is to investigate changes in CT, SD, and LGI in patients with relapsing-remitting MS (RRMS). METHODS: T1 images of 74 RRMS patients and 65 healthy controls were used. T1 hypointense areas in RRMS patients were corrected using fully automated methods. CT, SD, and LGI were calculated for each patient. RESULTS: RRMS patients showed widespread cortical thinning, especially in bilateral temporoparietal areas, decreased SD in bilateral supramarginal gyrus, superior temporal gyrus, postcentral gyrus, and transverse temporal gyrus, and decreased LGI, especially in the left posterior cingulate gyrus and insula. The decrease in cortical thickness was associated with the number of attacks and lesion volume. EDSS was related to CT in the right lingual, inferior temporal, and fusiform gyrus. The LGI was correlated with T2 lesion volume in bilateral insula, with EDSS in the right insula and transverse and superior temporal gyri, and with the number of attacks in the right paracentral gyrus and pre-cuneus. However, SD did not show any correlation with EDSS, T2 lesion volume, or the number of attacks. CONCLUSION: Our results demonstrate widespread cortical thinning, decreased sulcal depth in local areas, and decreased gyrification in folds in RRMS patients, which are related to clinical parameters.
 Multiple sclerosis (MS) is a dysimmune and neurodegenerative disease of the central nervous system that continues to be one of the main causes of non-traumatic disability in young people despite the recent availability of highly effective drugs. Exercise-based interventions seem to have a positive impact on the course of the disease although pathophysiological mechanisms responsible for this benefit remain unclear. This is a longitudinal study to examine the effects of a short-term training program on neurofilament plasma levels, a biomarker of axonal destruction, measured using the ultrasensitive single molecule array (SiMoA). Eleven patients completed a 6-week supervised resistance-training program of 18 sessions that consisted of 3 sets of 8-10 repetitions of 7 exercises. Median plasma neurofilament levels significantly decreased from baseline (6.61 pg/ml) to 1 week after training intervention (4.44 pg/ml), and this effect was maintained after 4 weeks of detraining (4.38 pg/ml). These results suggest a neuroprotective effect of resistance training in this population and encourage us to investigate further the beneficial impact of physical exercise and to emphasize the importance of lifestyle in MS.
 Despite the global decline in the standardized mortality rate of multiple sclerosis (MS), recent research on MS patient survival, especially in Taiwan, remains limited. This study aimed to investigate survival, mortality causes, and associated factors among MS patients in Taiwan. The Taiwan National Health Insurance Research Database was used as the primary data source, and a Cox proportional hazard model was employed to estimate and analyze factors related to survival. We analyzed data from 1444 MS patients diagnosed between 2000 and 2018. Age at diagnosis was positively correlated with the risk of death. Among the 190 patients who died, the leading causes of disease-related deaths were nervous system diseases (n = 83, 43.68%), followed by respiratory system diseases and certain infectious and parasitic diseases. The 8-, 13-, and 18-year survival rates for MS patients were 0.97, 0.91, and 0.81, respectively. This study highlights that the MS patient's socioeconomic status, environmental factors, comorbidity severity, and related medical variables were not significantly associated with survival.
 This study aimed to identify the clinical significance of iron rim lesions (IRLs) in distinguishing multiple sclerosis (MS) from other central nervous system (CNS) demyelinating diseases, determine the relationship between IRLs and disease severity, and understand the long-term dynamic changes in IRLs in MS. We retrospectively evaluated 76 patients with CNS demyelinating diseases. CNS demyelinating diseases were classified into three groups: MS (n = 30), neuromyelitis optica spectrum disorder (n = 23), and other CNS demyelinating diseases (n = 23). MRI images were obtained using conventional 3T MRI including susceptibility-weighted imaging. Sixteen of 76 patients (21.1%) had IRLs. Of the 16 patients with IRLs, 14 were in the MS group (87.5%), indicating that IRLs were significantly specific for MS. In the MS group, patients with IRLs had a significantly higher number of total WMLs, experienced more frequent recurrence, and were treated more with second-line immunosuppressive agents than were patients without IRLs. In addition to IRLs, T1-blackhole lesions were observed more frequently in the MS group than in the other groups. IRLs are specific for MS and could represent a reliable imaging biomarker to improve the diagnosis of MS. Additionally, the presence of IRLs seems to reflect more severe disease progression in MS.
 BACKGROUND: It is recommended that patients taking immunosuppressive anti-CD20 monoclonal antibodies (mAbs) receive pneumococcal vaccinations before their first dose to ensure optimal immune response. An initial medication use evaluation reviewed adherence to Centers for Disease Control and Prevention (CDC) pneumococcal immunization recommendations at the study site, and room for improvement was identified. The nursing team implemented workflow changes to increase nursing involvement in vaccination coordination, education, tracking, and administration. We sought to evaluate the impact of a nursing intervention on optimal pneumococcal vaccination administration rates in patients receiving anti-CD20 mAbs at a multiple sclerosis (MS) center. METHODS: We performed a single-center, retrospective, pre/post medication use evaluation. Inclusion criteria were older than 18 years with a diagnosis of MS and received their first anti-CD20 mAb infusion at the study site during the preintervention or postintervention time frame. RESULTS: We included 406 and 73 patients in the preintervention and postintervention studies, respectively. The nursing intervention significantly improved the percentage of patients receiving optimal pneumococcal vaccination before their first infusion from 58% to 84% and significantly reduced the number with unknown vaccination status from 17% to 3%. Patients who received optimal follow-up vaccination with 23-valent pneumococcal polysaccharide vaccine after optimal 13-valent pneumococcal conjugate vaccine administration improved from 9% to 56%. CONCLUSIONS: A nursing team intervention improved adherence to CDC pneumococcal immunization recommendations for patients receiving anti-CD20 mAb therapy. This project highlights the value of interdisciplinary team collaboration between health system specialty pharmacies and specialized nursing teams in the care of patients with MS.
 BACKGROUND: Previous studies have demonstrated different MRI characteristics in Asian and Western patients with multiple sclerosis (MS). However, the number of studies performed on Thai patients is still limited. Furthermore, these studies were conducted before the revision of the McDonald criteria in 2017. METHODS: A retrospective descriptive study was performed on Thai patients diagnosed with MS, according to the McDonald criteria (2017), in a tertiary care hospital in Thailand. RESULTS: Thirty-two patients were included (twenty-seven female and five male patients). The mean age was 37.8 years. Most (28 patients) had relapsing remitting MS. Brain MRIs were available for all 32 patients, all of which showed abnormalities. The most common locations were the periventricular regions (78.1%), juxtacortical regions (75%) and deep white matter (62.5%). Dawson's fingers were identified in 20 patients (62.5%). Tumefactive MS was noted in two patients. Gadolinium-enhancing brain lesions were noted in nine patients (28.1%). Optic nerve lesions were found in seven patients. Six of the seven patients showed short segmental lesions with predominant posterior-half involvement. Spinal MRIs were available for 26 patients, with abnormalities detected in 23. Most (11 patients) had lesions both in the cervical and in the thoracic spinal cord. In total, 22 patients (95.7%) showed lesions at the periphery, most commonly at the lateral column. Fifteen patients showed lesions shorter than three vertebral segments (65.2%). Enhancing spinal lesions were noted in 14 patients. Dissemination in space was fulfilled in 31 patients (96.9%). CONCLUSION: Some of the MRI findings in our study were similar to those of previous studies in Thailand and Asia, emphasizing the difference between Asian and Western MS.
 Purpose: Drug repurposing is an approach successfully used for discovery of new therapeutic applications for the existing drugs. The current study was aimed to use the combination of in silico methods to identify FDA-approved drugs with possible S1P(1) agonistic activity useful in multiple sclerosis (MS). Methods: For this, a 3D-QSAR model for the known 21 S1P(1) agonists were generated based on 3D-QSAR approach and used to predict the possible S1P(1) agonistic activity of FDA-approved drugs. Then, the selected compounds were screened by docking into S1P(1) and S1P(3) receptors to select the S1P(1) potent and selective compounds. Further evaluation was carried out by molecular dynamics (MD) simulation studies where the S1P(1) binding energies of selected compounds were calculated. Results: The analyses resulted in identification of cobicistat, benzonatate and brigatinib as the selective and potent S1P(1) agonists with the binding energies of -85.93, -69.77 and -67.44 kcal. mol(-1), calculated using MM-GBSA algorithm based on 50 ns MD simulation trajectories. These values are better than that of siponimod (-59.35 kcal mol(-1)), an FDA approved S1P(1) agonist indicated for MS treatment. Furthermore, similarity network analysis revealed that cobicistat and brigatinib are the most structurally favorable compounds to interact with S1P(1). Conclusion: The findings in this study revealed that cobicistat and brigatinib can be evaluated in experimental studies as potential S1P(1) agonist candidates useful in the treatment of MS.
 PURPOSE: A systematic review and meta-analysis was conducted to investigate changes in retinal and choroidal microvasculature in patients with multiple sclerosis (MS) using optical coherence tomography angiography (OCTA). METHODS: PubMed and Google Scholar were searched for studies that compared retinal and choroidal microvasculature between MS and healthy controls (HC) with OCTA. MS patients were divided into 2 groups: MS with (MSON) or without optic neuritis (MSNON). RESULTS: Totally, 13 studies including 996 MS eyes and 847 HC eyes were included. Compared with the HC, the vessel density of the whole superficial vascular complex (SVC) was reduced by 2.27% and 4.30% in the MSNON and MSON groups, respectively. The peripapillary vessel density was 2.28% lower and 4.96% lower in the MSNON and MSON groups, respectively, than in the HC. Furthermore, the MSON group had significant lower vessel density of the SVC (mean difference [MD] = -2.17%, P < 0.01) and lower peripapillary vessel density (MD = -2.02%, P = 0.02) than the MSNON group. No significant difference was found in the deep vascular complex or choriocapillaris densities among MSNON, MSON or HC groups (P > 0.05). Meta-regression analyses suggested that illness duration and the Expanded Disability Status Scale scores of MS patients were possible sources of heterogeneity (P < 0.05). CONCLUSION: The retinal SVC and peripapillary vessel density decreased significantly in MS eyes, especially in eyes with optic neuritis. Retinal microvasculature is a potential biomarker of disease progression in MS.
 INTRODUCTION AND IMPORTANCE: Intracranial germinomas are germ cell tumors that commonly develop in the pineal or neurohypophysis regions. As ectopic germinomas are rarely observed within the cerebrum and are associated with atypical image findings, diagnosis is challenging. CASE PRESENTATION: A 14-year-old boy was admitted to our hospital with complaints of vomiting and headache. Gadolinium-enhanced magnetic resonance imaging revealed ring-enhancing lesions in his left frontal lobe and basal ganglia. Susceptibility-weighted imaging indicated that the subependymal veins passing through the lesion centers were engorged, while electrophoretic analysis of cerebrospinal fluid identified oligoclonal bands (OCBs); both were typical of multiple sclerosis (MS). Tumor biopsy revealed many cells with atypical mitotic figures and nuclear enlargements, suggesting malignant disease. As the tumor rapidly proliferated, we opted for surgical excision of the lesions. Histopathological analyses revealed "two-cell patterns" characteristic of germinoma. Immunohistochemistry was positive for placental alkaline phosphatase and c-KIT. The definitive diagnosis was germinoma. After chemoradiotherapy, the patient was discharged without neurological deficits. CLINICAL DISCUSSION: OCBs and several magnetic resonance imaging features (including open ring enhancement, T2 hypointense rims, mild mass effects, mild perilesional edema, peripheral restriction around the lesion, and vessel-like structures running through the lesion center) are useful diagnostic signs for the radiological discrimination of MS from germinoma. However, owing to these factors, some cases are difficult to diagnose. CONCLUSION: Our case report of an unusual ectopic cerebral germinoma illustrates the difficulty of distinguishing it from MS. Therefore, we recommend proper tissue sampling in such cases, especially in adolescent patients, to make definitive germinoma diagnoses.
 INTRODUCTION: Persons with multiple sclerosis (MS) frequently report pain that negatively affects their quality of life. Evidence linking pain and corticospinal excitability in MS is sparse. We aimed to (1) examine differences in corticospinal excitability in MS participants with and without pain and (2) explore predictors of pain. METHODS: Sixty-four participants rated their pain severity on a visual analog scale (VAS). Transcranial magnetic stimulation (TMS) and validated clinical instruments characterized corticospinal excitability and subjective disease features like mood and fatigue. We retrieved information on participants' prescriptions and disability status from their clinical records. RESULTS: Fifty-five percent of participants reported pain that affected their daily functioning. Persons with pain had significantly greater fatigue and lower area under the excitatory motor evoked potential (MEP) recruitment curve (eREC AUC), a measure of total corticospinal excitability. After controlling for age, disability status, and pain medications, increased fatigue and decreased eREC AUC together explained 40% of the variance in pain. DISCUSSION: Pain in MS is multifactorial and relates to both greater fatigue and lesser corticospinal excitability. Future work should better characterize relationships between these outcomes to develop targeted pain interventions such as neuromodulation. SUMMARY: We examined pain in MS. Individuals with pain had higher fatigue and lower corticospinal excitability than those without pain. These outcomes significantly predicted self-reported pain.
 OBJECTIVES: This study aims to identify the factors associated with pain and neuropathic pain (NP) in patients with multiple sclerosis (MS) and to determine the relationship between pain and NP with disability, functionality, activities of daily living, fatigue, mood, and quality of life (QoL). PATIENTS AND METHODS: Between July 2017 and October 2017, a total of 100 adult patients with MS (18 males, 82 females; mean age: 35.3±9.9 years; range, 19 to 71 years) were included. All patients were evaluated in terms of pain and NP. Patients with and without pain, and patients with and without NP were compared in terms of sociodemographic characteristics, disease data, disability, functionality, daily living activities, fatigue severity, mood, and QoL using various scales. RESULTS: A total of 62% of the patients had pain. Pain was found to be associated with low education level (p=0.014), increased fatigue (p<0.001), depressive mood (p<0.001) and lower QoL (p<0.001). A total of 29.03% of patients with pain had NP. Patients with NP had a greater pain intensity (p<0.001) and fatigue (p=0.002) and lower QoL (p=0.011). The number of patients who received the correct treatment for their symptoms was low. CONCLUSION: Pain and NP should be better investigated and treated by physicians, as these symptoms are common in MS and adversely affect the QoL and social relations of affected patients and reduce their productivity.
 BACKGROUND: Various relaxation procedures have been proposed to reduce fatigue in multiple sclerosis (MS). However, it is unknown, which type of relaxation has the largest effect on fatigue reduction and on autonomic nervous system (ANS) activity. OBJECTIVE: We aimed to compare two biofeedback-supported relaxation exercises: a deep breathing (DB) exercise and progressive muscle relaxation (PMR), which may ameliorate MS fatigue and alter ANS activity. METHODS: We performed a single-blind randomized clinical trial, introducing MS patients (n = 34) to the DB or PMR exercise. We first tested cardiovagal integrity, reflected by changes in heart rate variability (HRV) in response to DB. Participants then performed a fatigue-inducing vigilance task, followed by the DB or PMR. State fatigue was recorded consecutively at baseline, after the vigilance task, and after the relaxation exercise, along with HRV reflecting ANS activity. RESULTS: Only patients assigned to the PMR group experienced a significant drop in fatigue, whereas both relaxation exercises changed ANS activity. MS patients showed the expected autonomic response during the cardiovagal reflex test. The vigilance task elevated short-term feelings of fatigue and significantly reduced HRV parameters of parasympathetic activity. Trait fatigue was negatively correlated with HRV during the second half of the vigilance task. CONCLUSION: PMR alleviates short-term feelings of fatigue in persons with MS. The vigilance task in combination with HRV measurements may be helpful for evaluating relaxation procedures as a treatment of fatigue. Hereby, future studies should ensure longer and more frequent relaxation exercises and focus on patients with weak to moderate fatigue. TRIAL REGISTRATION: Trial Registry: DRKS00024358.
 BACKGROUND: Previous cohort studies evaluating the performances of the McDonald criteria suffered from bias regarding real-life conditions. We aimed to evaluate the probability of diagnosing relapsing-remitting multiple sclerosis (MS) at several timepoints from the first medical evaluation and the gain in time-to-diagnosis with the 2017 McDonald criteria compared with the 2001, 2005 and 2010 versions in real life. METHODS: Patients with a first demyelinating event suggestive of MS between 2002 and 2020 were included in the ReLSEP, an exhaustive and prospectively incremented registry of MS patients in North-Eastern France. We estimated the probability of being positive at the first medical evaluation and at five timepoints according to the four versions of criteria using Kaplan-Meier estimators and Cox models. RESULTS: A total of 2220 patients were followed up for a median of 7.1 years. At baseline, 31.7%, 32.1%, 36.6% and 54.0% of patients, respectively, fulfilled the 2001, 2005, 2010 and 2017 McDonald criteria. Using the 2017 criteria, the gain in time-to-diagnosis was 3.7 months compared with the 2010 criteria. The presence of intrathecal synthesis of immunoglobulin G in the McDonald 2017 criteria led to a 1.8-month reduction in median time-to-diagnosis compared to a version of McDonald 2017 without this criteria. CONCLUSIONS: In real-life, the 2017 McDonald criteria revision undoubtedly shortened time-to-diagnosis.
 BACKGROUND AND GOAL: In vivo characterization of brain lesion types in multiple sclerosis (MS) has been an ongoing challenge. Based on verified texture analysis measures from clinical magnetic resonance imaging (MRI), this study aimed to develop a method to identify two extremes of brain MS lesions that were approximately severely demyelinated (sDEM) and highly remyelinated (hREM), and compare them in terms of common clinical variables. METHOD: Texture analysis used an optimized gray-level co-occurrence matrix (GLCM) method based on FLAIR MRI from 200 relapsing-remitting MS participants. Two top-performing metrics were calculated: texture contrast and dissimilarity. Lesion identification applied a percentile approach according to texture values calculated: ≤ 25 percentile for hREM and ≥75 percentile for sDEM. RESULTS: The sDEM had a greater total normalized volume yet smaller average size, and worse MRI texture than hREM. In lesion distribution mapping, the two lesion types appeared to overlap largely in location and were present the most in the corpus callosum and periventricular regions. Further, in sDEM, the normalized volume was greater and in hREM, the average size was smaller in men than women. There were no other significant results in clinical variable-associated analyses. CONCLUSION: Percentile statistics of competitive MRI texture measures may be a promising method for probing select types of brain MS lesion pathology. Associated findings can provide another useful dimension for improved measurement and monitoring of disease activity in MS. The different characteristics of sDEM and hREM between men and women likely adds new information to the literature, deserving further confirmation.
 BACKGROUND/AIMS: Multiple sclerosis (MS) is an inflammatory disease characterized by the demyelination of primarily the central nervous system. Diffuse esophageal spasm (DES) and achalasia are both disorders of esophageal peristalsis which cause clinical symptoms of dysphagia. Mechanisms involving dysfunction of the pre- and post-ganglionic nerve fibers of the myenteric plexus have been proposed. We sought to determine whether MS confers an increased risk of developing achalasia or DES. METHODS: Cohort analysis was done using the Explorys database. Univariate logistic regression was performed to determine the odds MS confers to each motility disorder studied. Comparison of proportions of dysautonomia comorbidities was performed among the cohorts. Patients with a prior diagnosis of diabetes mellitus, chronic Chagas' disease, opioid use, or CREST syndrome were excluded from the study. RESULTS: Odds of MS patients developing achalasia or DES were (OR, 2.09; 95% CI, 1.73-2.52; P < 0.001) and (OR, 3.15; 95% CI, 2.89-3.42; P < 0.001), respectively. In the MS/achalasia cohort, 27.27%, 18.18%, 9.09%, and 45.45% patients had urinary incontinence, gastroparesis, impotence, and insomnia, respectively. In the MS/DES cohort, 35.19%, 11.11%, 3.70%, and 55.56% had these symptoms. In MS patients without motility disorders, 12.64%, 0.79%, 2.21%, and 21.85% had these symptoms. CONCLUSIONS: Patients with MS have higher odds of developing achalasia or DES compared to patients without MS. MS patients with achalasia or DES have higher rates of dysautonomia comorbidities. This suggests that these patients have a more severe disease phenotype in regards to the extent of neuronal degradation and demyelination causing the autonomic dysfunction.
 Multiple sclerosis (MS) is an autoimmune demyelinating disease that often initially presents with optic neuritis (ON). Little is known about the demographic factors and familial histories that may be associated with the development of MS after a diagnosis of ON. We utilised a nationwide database to characterise specific potential drivers of MS following ON as well as analyse barriers to healthcare access and utilisation. The All of Us database was queried for all patients who were diagnosed with ON and for all patients diagnosed with MS after an initial diagnosis of ON. Demographic factors, family histories, and survey data were analysed. Multivariable logistic regression was performed to analyse the potential association between these variables of interest with the development of MS following a diagnosis of ON. Out of 369,297 self-enrolled patients, 1,152 were identified to have a diagnosis of ON, while 152 of these patients were diagnosed with MS after ON. ON patients with a family history of obesity were more likely to develop MS (obesity odd ratio: 2.46; p < .01). Over 60% of racial minority ON patients reported concern about affording healthcare compared with 45% of White ON patients (p < .01). We have identified a possible risk factor of developing MS after an initial diagnosis of ON as well as alarming discrepancies in healthcare access and utilisation for minority patients. These findings bring attention to clinical and socioeconomic risk factors for patients that could enable earlier diagnosis and treatment of MS to improve outcomes, particularly in racial minorities.
 Background and Purpose: Evidence has emerged for an association between degenerative disc disease (DDD) and multiple sclerosis (MS). The purpose of the current study is to determine the presence and extent of cervical DDD in young patients (age <35) with MS, an age cohort that is less well studied for these changes. Methods: Retrospective chart review of consecutive patients aged <35 referred from the local MS clinic who were MRI scanned between May 2005 and November 2014. 80 patients (51 female and 29 male) with MS of any type ranging between 16 and 32 years of age (average 26) were included. Images were reviewed by 3 raters and assessed for presence and extent of DDD, as well as cord signal abnormalities. Interrater agreement was assessed using Kendall's W and Fleiss' Kappa statistics. Results: Substantial to very good interrater agreement was observed using our novel DDD grading scale. At least some degree of DDD was found in over 91% of patients. The majority scored mild (grade 1, 30-49%) to moderate (grade 2, 39-51%) degenerative changes. Cord signal abnormality was seen in 56-63%. Cord signal abnormality, when present, occurred exclusively at degenerative disc levels in only 10-15%, significantly lower than other distributions (P < .001 for all pairwise comparisons). Conclusions: MS patients demonstrate unexpected cervical DDD even at a young age. Future study is warranted to investigate the underlying etiology, such as altered biomechanics. Furthermore, cord lesions were found to occur independently of DDD.
 Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease, characterised by the demyelination of neurons in the central nervous system. Whilst it is unclear what precisely leads to MS, it is believed that genetic predisposition combined with environmental factors plays a pivotal role. It is estimated that close to half the disease risk is determined by genetic factors. However, the risk of developing MS cannot be attributed to genetic factors alone, and environmental factors are likely to play a significant role by themselves or in concert with host genetics. Epstein-Barr virus (EBV) infection is the strongest known environmental risk factor for MS. There has been increasing evidence that leaves little doubt that EBV is necessary, but not sufficient, for developing MS. One plausible explanation is EBV may alter the host immune response in the presence of MS risk alleles and this contributes to the pathogenesis of MS. In this review, we discuss recent findings regarding how EBV infection may contribute to MS pathogenesis via interactions with genetic risk loci and discuss possible therapeutic interventions.
 INTRODUCTION: Increasing migration, due to wars, is one of the environmental factors in the etiology of multiple sclerosis. This study aims to compare demographic and clinical features of immigrant and local MS patients, as well as relapses during pregnancy and postpartum in female patients. METHOD: Immigrant (Group 1) and local (Group 2) MS patients were evaluated between January 2019 - September 2020 retrospectively. Below-mentioned data of two groups were recorded and compared: i) demographic data, ii) cerebrospinal fluid (CSF) and magnetic resonance imaging (MRI) findings, iii) MS subtypes, iv) expanded disability status scores (EDSS), v) the time between first two relapses, vi) comorbidities, vii) treatment, viii) age of migration and country of origin, ix) pregnancy, x) relapse during pregnancy, xi) birth number, xii) breastfeeding, xiii) postpartum relapses. RESULTS: Both of the groups were composed of 34 MS patients (in total n=68). Gender distribution, mean age, MS subtypes, the time between first two relapses, disease duration, EDSS, CSF findings and comorbidities were similar between groups. Symptom of onset was predominantly sensory in both groups. Local patients had more cervical lesions and higher lesion load (p=0.003, p=0.006). 20.6% of migrant MS patients were untreated, all local patients were on treatment. Rates of injection and infusion therapies were similar, the rate of receiving oral therapy was higher in the second group. Clinical features and fertility status of female patients were similar. CONCLUSION: According to the study no differences were preseentpresent between immigrant and local MS patients except for MRI lesion load and treatment parameters. The language barrier and irregular follow-ups were the major problems in treatment management.
 BACKGROUND: Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. Diagnosis is based on the 2017 revised McDonald criteria. Unmatched oligoclonal bands (OCB) within the CSF (i.e. positive OCB) can substitute for dissemination in time by magnetic resonance imaging (MRI). Simonsen et al. (2020) claimed a raised (>0.7) immunoglobulin G (IgG) index could replace OCB status. This study aimed to establish the diagnostic utility of IgG index for MS in the population served by The Walton Centre NHS Foundation Trust (WCFT) a neurology and neurosurgery hospital, and to derive a population-based IgG index reference interval. METHODS: OCB results from the laboratory information system (LIS) were collated from November 2018 to 2021. Final diagnosis and medication history was obtained from the electronic patient record. Exclusions were made based on age (<18 years) at the time of lumbar puncture (LP) disease-modifying treatment prior to LP, unknown IgG index and unclear OCB patterns. RESULTS: 935 of 1101 results remained following exclusions. 226 (24.2%) had a diagnosis of MS, 212 (93.8%) were OCB positive and 165 (73.0%) had a raised IgG index. The diagnostic specificity of a raised IgG index was calculated at 90.3% compared to 86.9% for positive OCB. 386 results with negative OCB were used to establish the IgG index reference interval (0.36-0.68) at 95th percentiles. CONCLUSION: This study provides evidence that IgG index should not replace OCB in the diagnosis of MS. >0.7 is an appropriate cut-off to define a raised IgG index for the patient population.
 INTRODUCTION: The study aims to evaluate the concentration of IgG antibodies against the receptor-binding domain of the SARS-CoV-2 spike1 protein (S1RBD) in BNT162b2- vaccinated relapsing-remitting multiple sclerosis (RRMS) individuals receiving disease-modifying treatments (DMTs). METHODS: Serum from 126 RRMS volunteers was collected 3 months after the administration of the second dose of the Pfizer-BioNTech BNT162b2 vaccine. Additional samples were analyzed after the administration of the booster dose in fingolimod- treated MS. Anti-S1RBD IgG antibody concentrations were quantified using the ABBOTT SARS-CoV-2 IgG II Quant assay. RESULTS: Anti-S1RBD IgG antibody concentrations in RRMS individuals receiving natalizumab, interferons, teriflunomide, and dimethyl fumarate showed no significant difference to those in healthy controls. However, fingolimod-treated MS individuals showed a marked inability to produce SARS-CoV-2- specific antibodies (p < 0.0001). Furthermore, a booster dose was not able to elicit the production of IgG antibodies in a large portion of matched individuals. DISCUSSION: A possible explanation for the altered immune response in fingolimod- treated MS individuals could be due to the medication inhibiting the circulation of lymphocytes, and possibly in turn inhibiting antibody production. Overall, patients on DMTs are generally of no disadvantage toward mounting an immune response against the vaccine. Nevertheless, further studies require evaluating non-humoral immunity against SARS-CoV-2 following vaccination, as well as the suitability of such vaccinations on patients treated with fingolimod.
 Multiple sclerosis (MS) is an inflammatory disease characterized by demyelination and axonal degeneration affecting the central nervous system. Among the genetic factors suggested to be associated with this disease are polymorphisms to the vitamin D receptor (VDR) gene. We tested the hypothesis that polymorphisms in the vitamin D receptor (VDR) gene are associated with MS. The aim of the study was to investigate the relationship of MS with the VDR gene Fok-I, Bsm-I and Taq-I polymorphisms among the Turkish population. This study contains 271 MS patients and 203 healthy controls. Genomic DNA was isolated from the samples and the VDR gene Fok-I, Bsm-I and Taq-I polymorphism regions were amplified by polymerase chain reaction (PCR). The PCR products were digested, and the genotypes were determined based on size of digested PCR products. Our results demonstrate associations between MS and the distribution of the VDR gene Fok-I T/T polymorphism genotype in a dominant model, VDR gene Fok-I T allele frequency, distribution of VDR gene Taq-I C/C polymorphism genotype in a dominant model and VDR gene Taq-I C allele frequency (Pearson test, p<0.05). However, there was no association between MS and the VDR gene Bsm-I polymorphisms for the genotype distribution (Pearson test, p>0.05) or allele frequency (Pearson test, p>0.05). Fok-I and Taq-I VDR gene polymorphisms are significantly associated with MS in dominant, homozygote and heterozygote inheritance models among the Turkish population.
 BACKGROUND: Management of multiple sclerosis (MS) requires a high level of communication between health care professionals (HCPs) and people with MS (pwMS) including profound investigation and discussion of symptoms to identify therapeutic needs. For treatment decisions, monitoring of disease activity is important, in this respect self-monitoring devices and apps, as well as magnetic resonance imaging are important tools. METHODS: MS Perspectives is a cross-sectional online survey conducted in Germany which was designed to collect data, among others, on the communication between pwMS and HCPs regarding treatment goals, symptom assessment, usage of devices and apps to self-monitor health functions, as well as to identify patients' attitude toward the role of magnetic resonance imaging (MRI). Between December 2021 and February 2022, 4,555 pwMS completed the survey. RESULTS: In total, 63.7% of participants reported that treatment goals have been discussed with their HCPs. Symptoms worsening in the past 12 months independent of relapses was more often reported by pwMS than inquired by HCPs, according to patients' report. Devices or apps for health monitoring were used by less than half of participants. Frequency of MRI controls was much lower in participants with longer compared to shorter disease duration (47.5 vs. 86.3%). The proportion of patients with annual or semiannual scans was highest among pwMS receiving infusion therapy (93.5%), followed by oral medication (82.5%) and injectables (73.4%), and lowest for pwMS without immunotherapy (58.2%). CONCLUSION: MS Perspectives identified a rather low patient involvement regarding treatment goals and symptom assessment in clinical practice. Regarding this and our findings for health self-monitoring and MRI usage, strategies for improving patient-HCP communication and disease monitoring may be considered.
 Based on the results of the pivotal CLARITY study, cladribine tablets were approved for use in the European Union in 2017 as a high-efficacy therapy for highly active relapsing-remitting multiple sclerosis (MS). Cladribine tablets are used as an induction therapy: half of the total dose is given in year 1 and the other half in year 2. In the CLARITY Extension trials, repeating the dose routinely in years 3 and 4, was not associated with significantly improved disease control. However, there is very limited evidence on how to manage people with MS (pwMS) beyond year 4, which is increasingly important because more and more patients are now ≥ 4 years after cladribine treatment. Overall, postapproval data show that treatment with two cladribine cycles effectively controls disease activity in the long term. However, there is general agreement that some pwMS with suboptimal response could benefit from retreatment. This study reviews the practical aspects of using cladribine tablets, summarizes the evidence from clinical trials and real-world studies on the safety and efficacy of cladribine, and proposes a treatment algorithm developed by expert consensus for pwMS previously treated with cladribine. In brief, we propose that additional courses of cladribine tablets should be considered in patients with minimal (no relapses, 1-2 new lesions) or moderate (1 relapse, 3-4 new lesions) disease activity, while significant disease activity (> 1 relapse, > 3 new lesions) or progression should warrant a switch to another high-efficacy treatment (HET). More evidence is needed to improve the treatment guidelines for pwMS who previously received cladribine.
 Theory of Mind (ToM), the ability to understand and attribute mental states to ourselves and others, could be impaired in Multiple Sclerosis (MS), a neurodegenerative disease affecting young adults. Considering that ToM is strictly connected to Quality of Life (QoL) in MS and that could enhance the social support network -which is particularly important for this population-, we aimed to design and implement a novel ToM rehabilitation training. To make the training as much ecological as possible, we have devised a protocol enhancing ToM through stimuli depicting real-world conditions (video-clips taken from cinema movies, literary fictions, and audio voices). We test training's effect on both cognitive and affective components of ToM in a sample of 13 subjects, randomly assigned to the ToM training Group and to the Control Group. The following ToM tasks were administered: the Reading the Mind in the Eyes (RMET), the Strange Stories task, the Faux Pas Task and the False Belief First- and Second - Order Task (FB II and III order). We also administered a psycho-behavioral assessment through the Toronto Alexithymia Scale (TAS-20). Results show that our novel ToM training is useful in enhancing ToM abilities measured by the following tasks: the RMET (affective task, p = 0.015) and the FB II-order task (FB, cognitive task, p = 0.032). Our ToM training had also a significant effect on the total score of the TAS-20 Scale (p = 0.018) and on its "Difficulty Describing Feelings subscale" (p = 0.018), indicating a reduction of the alexithymia traits. Future works with larger samples could investigate the ToM training effectiveness in a more representative MS populations.

 Polypharmacy (intake of ≥5 drugs) is an important issue for patients with chronic diseases such as multiple sclerosis (MS). We aimed to assess the prevalence of polypharmacy with regard to the severity of anxiety/depression and to comorbidities. Therefore, 374 MS patients from two German neurological sites were examined for drug burden, comorbidities, disability level and psychopathological measures capturing depression and anxiety using the Hospital Anxiety and Depression Scale (HADS-A and HADS-D). We found that patients with a higher HADS-D score take more medication (r = 0.217, p < 0.001). Furthermore, patients with higher depression severity were more likely to show polypharmacy (p < 0.001). These differences were not significant for anxiety. (p = 0.413). Regarding the frequency of ≥1 comorbidities, there were no significant differences between patients with different HADS-A (p = 0.375) or HADS-D (p = 0.860) severity levels, whereas the concrete number of comorbidities showed a significant positive linear correlation with HADS-A (r = 0.10, p = 0.045) and HADS-D scores (r = 0.19, p < 0.001). In conclusion, symptoms of depression pose a relevant issue for MS patients and are correlated with polypharmacy and comorbidities. Anxiety is not correlated with polypharmacy but with the frequency of several comorbidity groups in MS patients.
 Multiple sclerosis (MS) is a demyelinating and neurodegenerative disease of the central nervous system. It affects young people, and a considerable percentage of patients need the help of a wheelchair in 15 years of evolution. Currently, there is not a specific technique for the diagnosis of MS. The detection of oligoclonal IgG bands (OIgGBs) is the most sensitive assay for it, but it is not standardizable, only reference laboratories develop it, and uses cerebrospinal fluid. To obtain this sample, a lumbar puncture is necessary, an invasive proceeding with important side effects. It is important to develop and implement standard assays to obtain a rapid diagnosis because the earlier the treatment, the better the evolution of the disease. There are numerous modifying disease therapies, which delay the progression of the disease, but they have important side effects, and a considerable percentage of patients give up the treatment. In addition, around 40% of MS patients do not respond to the therapy and the disease progresses. Numerous researches have been focused on the characterization of predictive biomarkers of response to treatment, in order to help physicians to decide when to change to a second-line treatment, and then the best therapeutic option. Here, we review the new biomarkers for the diagnosis and response to treatment in MS. We draw attention in a new assay, the detection of serum IgM to phosphatidylcholine, that showed a similar sensitivity as OIgGBs and predicts the response to disease modifying treatments.
 BACKGROUND: Dimethyl fumarate (DMF) depletes CD8+ and CD4+ T cells, and cases of herpes zoster (HZ) in patients with multiple sclerosis (MS) on DMF have been documented. OBJECTIVES: To evaluate lymphocyte subsets in patients with MS who developed HZ on DMF (Tecfidera) compared to matched controls who did not develop HZ. METHODS: We used linear mixed-effects models to test for differences in white blood cell count, lymphocyte percentage, absolute lymphocyte count, CD3+ percentage, absolute CD3+ count, CD4+ percentage, absolute CD4+ count, CD8+ percentage, absolute CD8+ count, and CD4+:CD8+ ratio over time in HZ and non-HZ groups. RESULTS: Eighteen patients developed HZ while on DMF. The linear mixed-effects model for CD4+:CD8+ ratio showed a significant difference between the HZ and non-HZ groups (p = 0.033). CD4+:CD8+ ratio decreased over time in the HZ group and increased over time in the non-HZ group. CONCLUSION: Patients with MS who develop HZ while on DMF have high CD4+:CD8+ ratios, suggesting an imbalance of CD4+ and CD8+ cells that may put a patient at risk for developing HZ while on DMF. This result emphasizes the need for lymphocyte subset monitoring (including CD4+:CD8+ ratios) on DMF, as well as vaccination prior to DMF initiation.
 A systematic review was employed utilizing Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, to analyze all primary clinical data on the efficacy of spinal cord stimulation (SCS) in the treatment of multiple sclerosis (MS) induced spasticity. Databases include: Embase, PubMed, Scopus, Cochrane, and Web of Science. The review included case series, case studies, and clinical trials. Outcomes of interest were spasticity reduction. Grading of Recommendations Assessment, Development and Evaluation criteria was utilized to grade the certainty of evidence. Five hundred thirty-two articles were retrieved following database systematic review. One hundred eighty-eight articles were removed as duplicates utilizing the "Detect Duplicates" function on Rayyan.ai. A further 344 articles were excluded following abstract and title appraisal. As a result, 16 articles were subjected to full text appraisal. The dates of publication ranged from 1973 to 2019. Although a unique modality, there is not enough evidence to support the employment of SCS over current medical standard of care. Further high-quality randomized control trials are required to elucidate SCS's role in MS induced spasticity algorithm.
 BACKGROUND: Brain connectome fingerprinting is progressively gaining ground in the field of brain network analysis. It represents a valid approach in assessing the subject-specific connectivity and, according to recent studies, in predicting clinical impairment in some neurodegenerative diseases. Nevertheless, its performance, and clinical utility, in the Multiple Sclerosis (MS) field has not yet been investigated. METHODS: We conducted the Clinical Connectome Fingerprint (CCF) analysis on source-reconstructed magnetoencephalography signals in a cohort of 50 subjects: twenty-five MS patients and twenty-five healthy controls. RESULTS: All the parameters of identifiability, in the alpha band, were reduced in patients as compared to controls. These results implied a lower similarity between functional connectomes (FCs) of the same patient and a reduced homogeneity among FCs in the MS group. We also demonstrated that in MS patients, reduced identifiability was able to predict, fatigue level (assessed by the Fatigue Severity Scale). CONCLUSION: These results confirm the clinical usefulness of the CCF in both identifying MS patients and predicting clinical impairment. We hope that the present study provides future prospects for treatment personalization on the basis of individual brain connectome.
 INTRODUCTION: Visual evoked potentials (VEPs) are a non-invasive technique routinely used in clinical and preclinical practice. Discussion about inclusion of VEPs in McDonald criteria, used for Multiple Sclerosis (MS) diagnosis, increased the importance of VEP in MS preclinical models. While the interpretation of the N1 peak is recognized, less is known about the first and second positive VEP peaks, P1 and P2, and the implicit time of the different segments. Our hypothesis is that P2 latency delay describes intracortical neurophysiological dysfunction from the visual cortex to the other cortical areas. METHODS: In this work, we analyzed VEP traces that were included in our two recently published papers on Experimental Autoimmune Encephalomyelitis (EAE) mouse model. Compared with these previous publications other VEP peaks, P1 and P2, and the implicit time of components P1-N1, N1-P2 and P1-P2, were analyzed in blind. RESULTS: Latencies of P2, P1-P2, P1-N1 and N1-P2 were increased in all EAE mice, including group without N1 latency change delay at early time points. In particular, at 7 dpi the P2 latency delay change was significantly higher compared with N1 latency change delay. Moreover, new analysis of these VEP components under the influence of neurostimulation revealed a decrease in P2 delay in stimulated animals. DISCUSSION: P2 latency delay, P1-P2, P1-N1, and N1-P2 latency changes which reflect intracortical dysfunction, were consistently detected across all EAE groups before N1 change. Results underline the importance of analyzing all VEP components for a complete overview of the neurophysiological visual pathway dysfunction and treatment efficacy.
 BACKGROUND: Patients diagnosed as having multiple sclerosis (MS) experience a wide range of symptoms requiring pharmacologic management, and many do not achieve adequate symptom control. The purpose of this study was to evaluate the role of medical cannabis (MC) as part of a comprehensive treatment plan for patients with MS. METHODS: A retrospective medical record review of 141 patients with MS receiving MC for symptom management was conducted. Data were collected for up to 4 follow-up appointments after initiation of MC. Outcomes included changes in MS symptoms, medication changes, adverse events, and changes in cognition and mobility. RESULTS: Patients experienced extensive MS symptom improvement after initiation of MC, with alleviation of pain (72% of patients) and spasticity (48% of patients) and improvement in sleep (40% of patients) the most common. There was a significant reduction in concomitant opioid use after initiating MC as evidenced by a significant decrease in daily morphine milligram equivalents among patients prescribed opioid analgesics (P = .01). Decreases in muscle relaxant use and benzodiazepine use did not reach significance (P > .05). The most common adverse reaction to MC was fatigue (11% of patients). CONCLUSIONS: In many patients with MS, MC was well tolerated, eased pain and spasticity, improved sleep and other symptoms, and reduced use of concomitant opioid analgesics. Prospective studies are needed to further investigate the role of MC in the treatment of patients with MS.
 Physical capacity provides a link between disease or impairment and limitations in activity; in multiple sclerosis (MS), it is limited and decreased. The aim of this study was to study the effects of exercise and transcranial direct current stimulation (tDCS) on the left dorsolateral prefrontal cortex area in MS patients with fatigue and an impaired gait ability. A cross-over design was carried out on fifteen patients with two disability associations, but three were excluded. Before and after each intervention, the 6 min walk test (6MWT) and the 2 min walk test (2MWT) were used to assess walking ability and the Modified Fatigue Impact Scale (MFIS) was used to assess fatigue. A total of twelve patients were enrolled (48.0 median age, Kurtzke Disability Scale (EDSS) 3.66 ± 1.3): five females and seven males. After the application of the exercise program, significant improvements were observed in the 6MWT (p < 0.001, g = 0.159) and 2MWT (p < 0.001, g = 0.182). Furthermore, fatigue was significantly reduced after the application of the exercise program (p < 0.05, g = 0.742) and after tDCS (p < 0.05, g = 0.525). We could consider therapeutic exercise in the future to improve the walking ability and fatigue in MS patients. Furthermore, tDCS did not exert a significant improvement in walking ability, but it appeared to influence fatigue. Clinical trial registration code: ACTRN12622000264785.
 INTRODUCTION: Contribution of MAPK14 in the pathogenesis of multiple sclerosis (MS) has been proposed by several studies. Long non-coding RNA (lncRNA) have been suggested to be functionally linked with Mitogen-activated protein kinase 14 (MAPK14). METHODS: Expression levels of MAPK14 and its associated lncRNAs were measured in the circulation of MS patients compared with control subjects. RESULTS: Expression levels of NORAD and RAD51-AS1 were higher in total patients compared with controls (Expression ratio (95% CI) = 1.4 (1.04-1.89), P value = 0.015 and Expression ratio (95% CI) = 1.91 (1.43-2.6), P value = 0.0001, respectively). Conversely, ZNRD1ASP was under-expressed in cases compared with controls (Expression ratio (95% CI) = 0.61 (0.41-0.8), P value = 0.0005). In spite of the observed abnormal expression levels of these lncRNAs in the circulation of MS patients, their expressions were not correlated with Expanded Disability Status Scale (EDSS) score, disease duration or age at disease onset. CONCLUSION: To sum up, the current investigation shows dysregulation of MAPK14-related lncRNAs in MS patients.
 PURPOSE: This study aimed to (1) evaluate in patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) the presence of sleep disorders such as hypersomnia, fatigue, risk of apnea, and the presence of restless legs syndrome/Willis-Ekbom disease (RLS/WED); (2) evaluate quality of sleep in patients with MS and NMOSD; and (3) correlate them with clinical and imaging data. METHODS: The study was cross-sectional and was carried out in the sector of demyelinating diseases of the neurology service of HUGV-UFAM, Manaus, Brazil, from January 2017 to December 2020. RESULTS: Our sample consisted of 60 patients, 41 with MS and 19 with NMOSD. We found that patients with MS and NMOSD have poor sleep quality (65%) and hypersomnia (53% in MS; 47% in NMOSD), but low risk of apnea by STOP-BANG. The frequency of RLS/WE found was 14% in MS, and 5% in NMOSD. No correlation existed between sleep quality, number of relapses, and sleep quality for the Expanded Disability Status Scale (EDSS), i.e., fatigue/illness duration. CONCLUSION: Patients with MS and NMOSD have poor sleep quality, excessive sleepiness, and are at low risk for OSA, yet the frequency of RLS/WED is like that of the general population. There does not seem to be a significant difference between these sleep disorders in these demyelinating diseases of the CNS.
 OBJECTIVE: This study examined the relationships among functional outcomes and performance on standard-length and abbreviated cognitive screening measures for multiple sclerosis (MS). METHOD: 72 adults with MS underwent neurological examination and cognitive screening. They completed standard-length and abbreviated versions of tests from the Minimal Assessment of Cognitive Function in MS (MACFIMS), the abbreviated aMACFIMS, and the Brief International Cognitive Assessment for MS (BICAMS). Functional outcomes included neurological disability, physical and psychological dysfunction, and employment status. RESULTS: Concordance of impairment classifications was examined between standard-length and abbreviated tests using logistic regression and ROC curve analyses. Overall, the abbreviated test versions showed a broad range of concordance with impairment classifications made using the full-length tests. Processing speed was the strongest correlate of neurological disability and employment status; immediate recall was the strongest predictor of subjective physical dysfunction. Test performance provided unique value toward predicting neurological disability and employment status, but not physical and psychological dysfunction. CONCLUSIONS: The findings replicate some support for abbreviated tests in MS assessment, although caveats regarding loss of validity associated with abbreviation remain. The findings extend prior research showing that abbreviated tests of processing speed and immediate recall can provide unique predictive information regarding objective functional outcomes.
 BACKGROUND AND PURPOSE: Aim of this study was to evaluated anxiety, depression, and possible negative implications on work activities during the Sars-CoV-2 pandemic, in a group of Multiple Sclerosis (MS) patients at risk of flu-like syndrome (FLS) compared with FLS- free treatments. METHODS: The present study included patients treated with interferon-ß (IFNß), glatiramer, and natalizumab for at least one year. Collected data included the diagnosis of COVID-19 infection, Beck Depression Inventory-II (BDI-II), Beck Anxiety Inventory (BAI), together with questions about FLS, change in work habits, use of antipyretics, anxiety, and depression. RESULTS: 100 patients were included in the study. Six patients in IFNß and 5 in the natalizumab group had a confirmed COVID-19 infection. 68% in the IFNß patients reported FLS and only one reported an increase in flu-like frequency during the pandemic; 14% reported lower compliance with treatment, and 40% reported uptake of antipyretics several times. Only one IFNß patient reported having lost more working days than the previous year. The average BAI (p = 0.039) was higher in natalizumab group. Correcting these data by age, sex and EDSS to a multivariate analysis we did not find any statistically significant difference in terms of BAI and BDI-II between the three treatment groups. CONCLUSIONS: FLS were not perceived as COVID19-like symptoms but as expected by traditional pharmacological treatments indeed. These data suggest that IFNß can be used safely.
 Multiple sclerosis (MS) is a condition that affects the veins and small blood vessels. Previous research suggests that individuals with MS have an increased risk of vascular events and higher mortality rates. However, the relationship between MS and cerebral small vessel disease (CSVD) remains uncertain. This study aims to investigate the association between MS and lacunes. A prospective observational study was conducted, including a total of 112 participants, of which 46 had MS and 66 had CSVD. All participants underwent an MRI scan and a battery of neurological functional assessments. The presence of definite lacunes and black holes was determined through the analysis of T2-weighted, T1-weighted, and FLAIR images. The occurrence of lacunes in MS patients was found to be 19.6%. Notably, the duration of MS was identified as the sole risk factor for the development of lacune lesions in MS patients [odds ratio (OR) = 1.3, 95% confidence interval (CI) = 1.1-1.6, p = 0.008]. Comparatively, MS patients with lacunes exhibited a higher frequency of attacks and larger volumes of T2 lesions compared to MS patients without lacunes. Further analysis using receiver operating characteristic (ROC) curves showed that lacune lesions had limited ability to discriminate between MS and CSVD when disease duration exceeded 6 years. The presence of small arterial lesions in the brain of individuals with MS, along with the duration of the disease, contributes to the development of lacunes in MS patients.
 Background: Research in telerehabilitation (TR) in neurology tends to focus on patients with low to moderate disability. For neurology patients with severe mobility limitations, TR can help to enable rehabilitation for people whose mobility limitations make it difficult for them to access rehabilitation facilities. The aim of this study is to evaluate the interest of people with neurological disability caused by multiple sclerosis (MS) in TR services. Methods: This electronic survey targeted individuals with MS, specifically those with a higher level of disability. Results: A total of 355 patients with MS (155 with severe disabilities) participated in this study. There was no difference in interest in rehabilitation between people with mild-to-moderate and severe disabilities (p = 0.1258, confidence interval [CI] = 95%). However, we found a higher interest in upper limb exercises (p = 0.0006, CI = 95%) and balance training (p = 0.0000, CI = 95%) among people with higher disability. Conclusion: The results of this study may help to improve the planning and targeting of TR interventions, where a different focus of intervention is appropriate for patients with different levels of disability. This may enable TR to be maximally tailored to patient capabilities and current greatest limitations. For example, for people with severe disabilities, it is appropriate to focus on training the upper limb function to maintain self-sufficiency and implement interventions to prevent falls.
 BACKGROUND: Multiple sclerosis (MS) is a progressive neurodegenerative disease characterized by axonal degeneration and demyelination. Changes in gait, related to joint kinematics and kinetics, especially at the ankle and knee, have been observed in people with MS (pwMS). Muscle coactivation plays an important role in joint stabilization; however, excessive coactivation may interfere with gait. The aim of this study was to analyze the differences in muscle activation during gait in pwMS compared to healthy individuals. METHODS: A cross-sectional study was conducted involving pwMS and healthy controls. Surface electromyography was used to record muscle activity during gait. The main outcome measures were the coactivation index (CI) and the area under the curve (AUC), which were calculated for several pairs of lower extremity muscles. RESULTS: Nine pwMS and nine healthy controls were included. When comparing the MS group to the control group, the AUC was significantly higher in the lateral gastrocnemius (p = 0.023) and the CI for the lateral gastrocnemius-anterior tibialis (p = 0.022) and gluteus maximus-lateral gastrocnemius (p = 0.047). CONCLUSION: Mildly affected pwMS have altered muscle coactivation patterns during gait, especially in the most affected limb. The results highlight the importance of muscle coactivation in pwMS and its possible role in the early detection of gait abnormalities.
 INTRODUCTION: Machine learning (ML) has great potential for using health data to predict clinical outcomes in individual patients. Missing data are a common challenge in training ML algorithms, such as when subjects withdraw from a clinical study, leaving some samples with missing outcome labels. In this study, we have compared three ML models to determine whether accounting for label uncertainty can improve a model's predictions. METHODS: We used a dataset from a completed phase-III clinical trial that evaluated the efficacy of minocycline for delaying the conversion from clinically isolated syndrome to multiple sclerosis (MS), using the McDonald 2005 diagnostic criteria. There were a total of 142 participants, and at the 2-year follow-up 81 had converted to MS, 29 remained stable, and 32 had uncertain outcomes. In a stratified 7-fold cross-validation, we trained three random forest (RF) ML models using MRI volumetric features and clinical variables to predict the conversion outcome, which represented new disease activity within 2 years of a first clinical demyelinating event. One RF was trained using subjects with the uncertain labels excluded (RF(exclude)), another RF was trained using the entire dataset but with assumed labels for the uncertain group (RF(naive)), and a third, a probabilistic RF (PRF, a type of RF that can model label uncertainty) was trained on the entire dataset, with probabilistic labels assigned to the uncertain group. RESULTS: Probabilistic random forest outperformed both the RF models with the highest AUC (0.76, compared to 0.69 for RF(exclude) and 0.71 for RF(naive)) and F1-score (86.6% compared to 82.6% for RF(exclude) and 76.8% for RF(naive)). CONCLUSION: Machine learning algorithms capable of modeling label uncertainty can improve predictive performance in datasets in which a substantial number of subjects have unknown outcomes.
 BACKGROUND: This study evaluates and describes the pattern of services provided for people living with multiple sclerosis (MS) in a local area as a starting point for a more global assessment. METHODS: A health care ecosystem approach has been followed using an internationally standardized service classification instrument-the Description and Evaluation of Services and DirectoriEs for Long Term Care (DESDE-LTC)-to identify and describe all services providing care to people with MS in the Australian Capital Territory, Australia. Available services were classified according to the target population into those specifically dedicated to people living with MS and those providing general neurologic services, both public and private, and across both social and health sectors. RESULTS: A limited range of services was available. There were no local facilities providing or coordinating multidisciplinary integrated care specific to people with MS. Subspecialty services specific to MS were limited in number (6 of the 28 services), and use of specialist services provided in neighboring states was frequently reported. Overall, very few services were provided outside the core health sector (4%). CONCLUSIONS: The provision of care to people living with MS in the Australian Capital Territory is fragmented and relies heavily on generic neurology services in the public and private sectors. More widespread use of the DESDE-LTC as a standardized method of service classification in MS will facilitate comparison with other local areas, allow monitoring of changes over time, and permit comparison with services provided for other health conditions (eg, dementia, mental disorders).
 Hippocampus demyelinating lesions in multiple sclerosis (MS) have been frequently observed in ex vivo histopathological studies; however, they are difficult to image and quantify in vivo. Diffusion tensor imaging (DTI) and T2 mapping could potentially detect such regional in vivo changes if acquired with sufficient spatial resolution. The goal here was to evaluate whether there are focal hippocampal abnormalities in 43 MS patients (35 relapsing-remitting, eight secondary progressive) with and without cognitive impairment (CI) versus 43 controls using high-resolution 1 mm isotropic DTI, as well as complementary methods of T2-weighted and T2 mapping at 3 T. Abnormal hippocampus regions were identified voxel-by-voxel by using mean diffusivity (MD)/T2 thresholds and avoiding voxels attributed to cerebrospinal fluid. When compared with controls, averaged left/right whole hippocampus MD was higher in both MS groups, while lower fractional anisotropy (FA) and volume, and higher T2 relaxometry and T2-weighted signal values, were only significant in CI MS. The hippocampal MD and T2 images/maps were not uniformly affected and focal regions of elevated MD/T2 were evident in MS patients. Both CI and not CI MS groups showed greater proportional areas of the hippocampus with elevated MD, whereas only the CI group showed a greater proportional area of elevated T2 relaxation times or T2-weighted signal. Higher T2 relaxometry and T2-weighted signal values of elevated regions correlated with greater disability and whole hippocampus FA negatively correlated with physical fatigue. High-resolution hippocampus DTI and T2 mapping with less partial volume effects showed whole hippocampus abnormalities with regional elevations of MD/T2 in MS, which could be interpreted as potentially from demyelination, neuron loss, and/or inflammation, and which overall were more extensive in the hippocampus of patients with larger total brain lesion volumes and CI.
 Background: Neurological disorders with dyskinesia would seriously affect older people's daily activities, which is not only associated with the degeneration or injury of the musculoskeletal or the nervous system but also associated with complex linkage between them. This study aims to review the relationship between motor performance and cortical activity of typical older neurological disorder patients with dyskinesia during walking and balance tasks. Methods: Scopus, PubMed, and Web of Science databases were searched. Articles that described gait or balance performance and cortical activity of older Parkinson's disease (PD), multiple sclerosis, and stroke patients using functional near-infrared spectroscopy were screened by the reviewers. A total of 23 full-text articles were included for review, following an initial yield of 377 studies. Results: Participants were mostly PD patients, the prefrontal cortex was the favorite region of interest, and walking was the most popular test motor task, interventional studies were four. Seven studies used statistical methods to interpret the relationship between motor performance and cortical activation. The motor performance and cortical activation were simultaneously affected under difficult walking and balance task conditions. The concurrent changes of motor performance and cortical activation in reviewed studies contained the same direction change and different direction change. Conclusion: Most of the reviewed studies reported poor motor performance and increased cortical activation of PD, stroke and multiple sclerosis older patients. The external motor performance such as step speed were analyzed only. The design and results were not comprehensive and profound. More than 5 weeks walking training or physiotherapy can contribute to motor function promotion as well as cortices activation of PD and stroke patients. Thus, further study is needed for more statistical analysis on the relationship between motor performance and activation of the motor-related cortex. More different type and program sports training intervention studies are needed to perform.
 INTRODUCTION: Ofatumumab (Kesimpta™) is a s.c. applicable anti-CD20 antibody, which has been used in Germany since 2021 for the treatment of relapsing multiple sclerosis (RMS). The self-application offers a high degree of independence from intravenous forms of application with highly effective immunotherapy. In this study we recorded the patient-centered experience in 99 out of 127 patients who were adjusted to the drug by us. The aim was to investigate the tolerability and acceptance from the patient's perspective. METHODS: Data collection was carried out using doctor documentation, questionnaires and telephone interviews. RESULTS: The cohort consists of 127 patients. The patients received 2.8 (± SD 1.7) pre-therapies. The mean duration of therapy with Ofatumumab was 9.8 months (± SD 3.5). Structured data were collected from 99 patients. 23% of patients had no side effects during initial application. 19% rated the side effects as "very mild" and 18% as "mild". In addition to chills/fever (48%), headache (46%), limb pain (45%) and "other symptoms" (19%) also occurred. For subsequent injections, 72% of patients reported no side effects. 87% of patients found handling the medication "very easy". There was one relapse event during therapy. CONCLUSION: Our study shows that Ofatumumab is well accepted and tolerated by patients. There was one relapse event during the observation period. The side effects are mild and occur during initial application. No increased tendency to infection could be observed. The data suggest that Ofatumumab is also an effective and safe treatment option for patients with relapsing remitting multiple sclerosis in real-world use.
 INTRODUCTION: Multiple sclerosis (MS) is mainly diagnosed in women of reproductive age. However, there is a paucity of guidelines jointly prepared by neurologists and gynaecologists on managing women with MS and the desire for motherhood. Therefore, in this review we propose recommendations for such cases, with an particular focus on those requiring assisted reproductive techniques (ART). METHODS: A group of seven MS experts (4 neurologists and 3 gynaecologists) came together for three discussion sessions to achieve consensus. RESULTS: The recommendations reported here focus on the importance of early preconception counselling, the management of disease-modifying therapies before and during ART procedures, important considerations for women with MS regarding ART (intrauterine insemination, in vitro fertilisation and oocyte cryopreservation) and the paramount relevance of multidisciplinary units to manage these patients. CONCLUSIONS: Early preconception consultations are essential to individualising pregnancy management in women with MS, and an early, well-planned, spontaneous pregnancy should be the aim whenever possible. The management of women with MS and the desire for motherhood by multidisciplinary units is warranted to ensure appropriate guidance through the entire pregnancy.
 Multiple sclerosis (MS) and its preclinical models are characterized by marked changes in neuroplasticity, including excitatory/inhibitory imbalance and synaptic dysfunction that are believed to underlie the progressive cognitive impairment (CI), which represents a significant clinical hallmark of the disease. In this study, we investigated several parameters of neuroplasticity in the hippocampus of the experimental autoimmune encephalomyelitis (EAE) SJL/J mouse model, characterized by rostral inflammatory and demyelinating lesions similar to Relapsing-Remitting MS. By combining morphological and molecular analyses, we found that the hippocampus undergoes extensive inflammation in EAE-mice, more pronounced in the CA3 and dentate gyrus (DG) subfields than in the CA1, associated with changes in GABAergic circuitry, as indicated by the increased expression of the interneuron marker Parvalbumin selectively in CA3. By laser-microdissection, we investigated the impact of EAE on the alternative splicing of Arhgef9, a gene encoding a post-synaptic protein playing an essential role in GABAergic synapses and whose mutations have been related to CI and epilepsy. Our results indicate that EAE induces a specific increase in inclusion of the alternative exon 11a only in the CA3 and DG subfields, in line with the higher local levels of inflammation. Consistently, we found a region-specific downregulation of Sam68, a splicing-factor that represses this splicing event. Collectively, our findings confirm a regionalized distribution of inflammation in the hippocampus of EAE-mice. Moreover, since neuronal circuit rearrangement and dynamic remodeling of structural components of the synapse are key processes that contribute to neuroplasticity, our study suggests potential new molecular players involved in EAE-induced hippocampal dysfunction.
 OBJECTIVES: In this study, the effect of sleep disturbance on the quality of life in MS patients and its relationship between demographic and clinical characteristics of the patients were investigated. METHODS: 67 MS patients and 51 healthy individuals were included in our study. The patient group consisted of 43 women and 24 men. The control group consisted of 32 women and 19 men. Demographic and clinical characteristics of the patients; age, gender, duration of illness, annual number of attacks, treatments, and medical history were recorded and neurological examinations of all patients were performed and disability was determined for each patient with Kurtzke's expanded disability status scale (EDSS). Evaluations were made using demographic data, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, Expanded Disability Status Scale (EDSS), Fatigue Severity Scale, Hospital Anxiety and Depression Scale, Berlin Questionnaire and Multiple Sclerosis Quality of Life (MSYK) - 54 Instrument. RESULTS: We found that the quality of life was significantly impaired in MS patients compared to healthy controls (p < 0.001). And we found that this was related to the presence of progressive MS and chronic fatigue among the clinical features of the patient, sleep-disordered breathing among sleep disorders, poor sleep quality, comorbid anxiety and depression (p = 0.001, p:0.009, p = 0.022, p = 0.007, p < 0.001 and p = 0.001, respectively). CONCLUSION: All these findings show that sleep disorders in patients with MS are a condition that should be questioned and treated in the follow up of the disease, otherwise it may affect the quality of life of patients negatively.
 INTRODUCTION: In STRIVE, natalizumab treatment demonstrated effectiveness in clinical, magnetic resonance imaging (MRI), and patient-reported outcomes (PROs) in patients with early relapsing-remitting multiple sclerosis (RRMS). This post hoc analysis examined the effectiveness and safety of natalizumab in patients who self-identified as either Black/African American (AA) or Hispanic/Latino. METHODS: Clinical, MRI, and PROs were assessed for the Black/AA subgroup (n = 40) and compared with the non-Hispanic White subgroup (n = 158). As a result of the very small sample size, outcomes for the Hispanic/Latino subgroup (n = 18) were assessed separately, including a sensitivity analysis with Hispanic/Latino patients who completed the 4-year study on natalizumab. RESULTS: Clinical, MRI, and PROs were comparable between the Black/AA and non-Hispanic White subgroups except for MRI outcomes at year 1. A higher proportion of non-Hispanic White than Black/AA patients achieved MRI no evidence of disease activity (NEDA; 75.4% vs. 50.0%, p = 0.0121) and no new or newly enlarging T2 lesions (77.6% vs. 50.0%, p = 0.0031) at year 1; these differences were not observed in years 2-4 of the study. For the Hispanic/Latino subgroup in the intent-to-treat population, 46.2% and 55.6% achieved NEDA at years 1 and 2; 66.7% and 90.0% achieved clinical NEDA at years 3 and 4. Annualized relapse rate was reduced by 93.0% at year 1 versus the year before natalizumab initiation; this reduction was maintained throughout the study. Over 4 years, 37.5-50.0% of patients had a clinically meaningful improvement in their Symbol Digit Modalities Test score, and 81.8-100.0% and 90.9-100.0% had stable/improved Multiple Sclerosis Impact Scale-29 physical and psychological scores, respectively. Similar results were observed in the sensitivity analysis with Hispanic/Latino subgroup of the 4-year natalizumab completers. CONCLUSION: These results highlight the effectiveness and safety of natalizumab in patients with early RRMS who self-identified as Black/AA or Hispanic/Latino. CLINICALTRIALS: GOV: NCT01485003.
 INTRODUCTION: Multiple sclerosis (MS) causes a progressive disability, which substantially impacts the quality of life (QoL). Health interventions that meet the needs and demands of people with MS are essential to minimize QoL impairment. Expert patient programs (EPPs) facilitate health-related empowerment through peer learning. Based on a previous focus group study, we designed an EPP for MS coordinated by nursing professionals for implementation in the different MS reference units of Catalonia (Southwestern Europe). This study aims to evaluate the effects on quality of life, disease-related knowledge, and self-management related to the health process of the participants of the Expert Patient Program Catalonia™ for people with multiple sclerosis (EPPC-MS). METHODS: Pre-post intervention multicenter clinical study involving 12 groups of 12 participants: six groups including relapsing and six groups including progressive MS patients, with 144 participants from 7 MS reference units from all over Catalonia, organized in six teams. The intervention will consist of nine telematic learning peer-led sessions (one weekly session). The expert patient (EP) leading the sessions will be an individual with MS with disease-related knowledge, who will be further trained by nurses to lead the sessions. Study variables will be measured before and immediately after the intervention and 6 and 12 months after the end of the sessions and will include: QoL, emotional impact, activation of the person, MS-related knowledge, fatigue, habits and lifestyles, health services use, and program-related experience. Baseline characteristics considered will be sociodemographic data, date of MS diagnosis and type, family history, and treatment characteristics. Variables related to disease follow-up will be new relapses and characteristics and changes in the ongoing treatment. The number of sessions attended will also be collected. Study variables will be analyzed using a pre-post comparison. DISCUSSION: Peer-led learning programs led by EP help empower people with chronic conditions and offer them tools to improve their autonomy and QoL. This study's intervention will be performed remotely, offering advantages both for people with chronic conditions and the healthcare system regarding the facilitation of family and work conciliation, saving time, simplifying attendance to meetings, lowering costs, and using fewer material resources. TRIAL REGISTRATION: NCT04988880 on September 22, 2021.
 [This corrects the article DOI: 10.1177/20552173221132469.].
 OBJECTIVE: In this study we aim to determine seasonal patterns underlying optic neuritis (ON) onset that may provide valuable epidemiologic information and help delineate causative or protective factors. DESIGN: Single-centre retrospective chart review. METHODS: A database search of centralized electronic health records was completed using diagnostic codes employed at the Ottawa Eye Institute for data collection. Charts were reviewed for documentation supporting a diagnosis of ON falling into the following categories: multiple sclerosis ON and clinically isolated syndrome ON, myelin oligodendrocyte glycoprotein ON, neuromyelitis optica ON, and idiopathic ON. Date of onset, biological sex, and age were extracted from each chart. Data were analyzed for calculation of frequency by season and overall pooled seasonal trends of all cases of ON. RESULTS: From the 218 included patients with ON, there was no statistically significant seasonal correlation. The overall trend of ON was lowest in winter and spring (22% and 23%, respectively) and highest in summer and fall (28% and 27% respective). Divided further, multiple sclerosis ON or clinically isolated syndrome ON rates (n = 144) were lowest in the spring (21%) and highest in fall (29%); myelin oligodendrocyte glycoprotein ON rates (n = 25) were lowest in winter (16%) and highest in summer and fall (both at 32%); neuromyelitis optica ON rates (n = 16) were lowest in fall (12.5%) and highest in winter and summer (both at 31.25%); and idiopathic ON rates (n = 33) were lowest in fall (18%) and highest in spring (33%). CONCLUSIONS: The overall ON seasonal trend appears to have a predilection for the summer and fall months, which may be explained by warmer weather and viral infections as risk factors for multiple sclerosis relapse during those seasons.
 Given the aging population, with a peak age-specific prevalence that is shifting beyond the age of 50, several women currently living with MS are very close to menopause. Menopause is usually characterized by several specific symptoms with adverse impacts on different aspects of a woman's quality of life, such as fatigue, and cognitive, mood and bladder disorders, which overlap with symptoms of MS. Generally, after this biological transition, women with MS appear to be subject to less inflammatory activity. However, several studies have reported an increase of disability accumulation after menopause, suggesting that it is a turning point to a more progressive phase of the disease. This may be attributable to the hormonal and immunological changes associated with menopause, with several effects on neuroinflammation and neurodegeneration increasing due to the immunosenescence of aging. This review summarizes the hormonal and immunological changes associated with menopause, detailing the effects on MS symptoms, outcomes, and the aging process. Furthermore, possible interventions to improve patients' quality of life are evaluated. In fact, it is increasingly necessary to improve the global management of MS women, as well as their lives, at this multifaceted turning point.
 Recent data on the distribution and influence of copper, zinc and cadmium in glial cells are summarized. This review also examines the relationship between those metals and their role in neurodegenerative diseases like Alzheimer disease, multiple sclerosis, Parkinson disease and Amyotrophic lateral sclerosis, which have become a great challenge for today's physicians. The studies suggest that among glial cells, iron has the highest concentration in oligodendrocytes, copper in astrocytes and zinc in the glia of hippocampus and cortex. Previous studies have shown neurotoxic effects of copper, iron and manganese, while zinc can have a bidirectional effect, i.e., neurotoxic but also neuroprotective effects depending on the dose and disease state. Recent data point to the association of metals with neurodegeneration through their role in the modulation of protein aggregation. Metals can accumulate in the brain with aging and may be associated with age-related diseases.
 BACKGROUND: Fatigue is one of the most common symptoms in patients with multiple sclerosis (MS). Furthermore, measuring its effects on patients in daily life is challenging. This study aimed to discover the association between relapsing-remitting MS (RRMS) patients' disability, fatigue, and accelerometer-measured physical activity. METHODS: A total of 41 patients with RRMS with an Expanded Disability Status Scale (EDSS) level of 0-5.5 and 20 healthy controls completed the Modified Fatigue Impact Scale (MFIS) and the Fatigue Severity Scale (FSS) questionnaires. The EDSS was evaluated for all patients with RRMS, and all participants performed the MS Functional Composite (MSFC) test and six-min walk test and wore an accelerometer for seven days. RESULTS: Patients with an EDSS level of 0-2.5 were found to have higher fatigue levels (p < 0.001) than healthy controls but lower levels than patients with an EDSS level of 3-5.5 (p < 0.001). A significant correlation was found to exist between fatigue and disability level measured by the EDSS (EDSS/FSS, r=0.750/p=0.001; EDSS/MFIS, r=0.661/p=0.001) and with the MSFC test in the patient group (MSFC/FSS, r = -0.350 p=0.025; MSFC/MFIS, r = -0.423/p=0.007). Total daily activity correlated with fatigue as measured by the FSS (MVPS/FSS r = -0.357/p=0.028, step count/FSS r = -0.463/p=0.003), but no correlation was found between the EDSS or the MSFC. CONCLUSION: A lower disability rate, better physical condition, and higher daily-living activity were found to predict lower fatigue levels.
 OBJECTIVE: To summarize the available literature and provide an overview of in utero exposure to maternal multiple sclerosis (MS) and the influence on offspring health outcomes. METHODS: We conducted a systematic review by searching Embase, Medline and PubMed.gov databases, and we used covidence.org to conduct a thorough sorting of the articles into three groups; 1) women with MS and the influence on birth outcomes; 2) women with MS treated with disease-modifying therapy (DMT) during pregnancy and the influence on birth outcomes; and 3) women with MS and the influence on long-term health outcomes in the children. RESULTS: In total, 22 cohort studies were identified. Ten studies reported on MS without DMT and compared with a control group without MS, and nine studies on women with MS and DMT prior to or during pregnancy met the criteria. We found only four studies reporting on long-term child health outcomes. One study had results belonging to more than one group. CONCLUSION: The studies pointed towards an increased risk of preterm birth and small for gestational age among women with MS. In terms of women with MS treated with DMT prior to or during pregnancy, no clear conclusions could be reached. The few studies on long-term child outcomes all had different outcomes within the areas of neurodevelopment and psychiatric impairment. In this systematic review, we have highlighted the research gaps on the impact of maternal MS on offspring health.
 History is full of women who made enormous contributions to science. While there is little to no imbalance at the early career stage, a decreasing proportion of women is found as seniority increases. In the multiple sclerosis (MS) field, 44% of first authors and only 35% of senior authors were female. So, in this review, we highlight ground-breaking research done by women in the field of MS, focusing mostly on their work as principal investigators. MS is an autoimmune disorder of the central nervous system (CNS), with evident paradigm shifts in the understating of its pathophysiology. It is known that the immune system becomes overactivated and attacks myelin sheath surrounding axons. The resulting demyelination disrupts the communication signals to and from the CNS, which causes unpredictable symptoms, depending on the neurons that are affected. Classically, MS was reported to cause mostly physical and motor disabilities. However, it is now recognized that cognitive impairment affects more than 50% of the MS patients. Another shifting paradigm was the involvement of gray matter in MS pathology, formerly considered to be a white matter disease. Additionally, the identification of different T cell immune subsets and the mechanisms underlying the involvement of B cells and peripheral macrophages provided a better understanding of the immunopathophysiological processes present in MS. Relevantly, the gut-brain axis, recognized as a bi-directional communication system between the CNS and the gut, was found to be crucial in MS. Indeed, gut microbiota influences not only different susceptibilities to MS pathology, but it can also be modulated in order to positively act in MS course. Also, after the identification of the first microRNA in 1993, the role of microRNAs has been investigated in MS, either as potential biomarkers or therapeutic agents. Finally, concerning MS therapeutical approaches, remyelination-based studies have arisen on the spotlight aiming to repair myelin loss/neuronal connectivity. Altogether, here we emphasize the new insights of remarkable women that have voiced the impact of cognitive impairment, white and gray matter pathology, immune response, and that of the CNS-peripheral interplay on MS diagnosis, progression, and/or therapy efficacy, leading to huge breakthroughs in the MS field.
 BACKGROUND: Multiple sclerosis (MS) is often diagnosed in women of childbearing age (WCBA), with a mean age of onset of 30 years. Women with MS have long been cautioned to carefully plan their pregnancies and, traditionally, disease-modifying therapies (DMTs) have not been recommended for use in patients engaged in family planning. In 2020, the United States Food and Drug Administration (FDA) approved a label update for interferon beta (IFN ß) by adding new safety data on pregnancy and breastfeeding. Because current management guidelines do not yet reflect the recent label update, a panel of neurology experts from Iraq decided to discuss the potential need for changes in treatment strategies in Iraq. METHODS: A panel of experts consisting of 8 neurologists from Iraq and one international neurology expert from Germany convened to develop an expert opinion that would provide practical guidance for the pharmacological management of WCBA with MS in Iraq. They considered the latest label update and relevant published literature, along with local clinical practice and available resources. RESULTS: Interferon and Glatiramer acetate have no evidence of harm during pregnancy. IFN β can be continued safely through pregnancy. Switching treatment during pregnancy is generally not recommended. Short-term intravenous methylprednisolone can be used to treat disabling relapses. CONCLUSION: Given the complexity of managing MS in pregnant women, it is the opinion of the expert panel that family planning should be discussed early in the disease course, planned pregnancy should be encouraged, and open communication with patient for her treatment decisions is paramount. Patients who are engaged in family planning are no longer discouraged from treatment with some of the currently available DMTs.


 AIM OF THE STUDY: Amino acid metabolism is crucial for regulating immune responses and can be monitored in blood serum samples. This study aimed to analyse serum amino acid profiles in people with multiple sclerosis (pwMS), taking into account differences depending on the disease outcomes. CLINICAL RATIONALE FOR THE STUDY: Serum amino acid profiling is a promising, reproducible and minimally invasive technology, available at different stages of the disease, enabling the search for a specific biomarker to differentiate MS clinical outcomes. MATERIAL AND METHODS: The serum concentrations of 29 amino acids were determined using high-performance liquid chromatography mass spectrometry. RESULTS: A total of 121 pwMS (41 relapsing-remitting MS-RRMS; 55 secondary progressive MS - SPMS; and 25 primary progressive MS-RRMS) with a median Expanded Disability Status Scale (EDSS) score of 6 and 53 healthy controls (HCs) were included. We found significantly higher serum total amino acids concentrations in pwMS compared to HCs. Serum concentrations of arginine, 1-methyl-L-histidine and proline were higher in pwMS, while circulating citrulline, α-aminobutyric acid and tryptophan were lower in pwMS. We observed significant differences in serum total amino acids concentrations depending on MS type, with the highest level in the PPMS group and the lowest in the RRMS group. We found significantly higher serum levels of beta-aminoisobutyric acid in PPMS patients compared to those with RRMS and SPMS, and significantly higher serum levels of aspartic acid in PPMS patients compared to RRMS patients. From visual inspection, no trend was observed in total amino acids concentration with respect to the EDSS score. When analysing serum total amino acids concentration in pwMS with EDSS ≤ 5 compared to those with EDSS > 5, no significant differences were found. CONCLUSIONS AND CLINICAL IMPLICATIONS: Amino acid metabolism is altered in pwMS and depends on the clinical type of the disease. Further studies are needed to determine whether serum metabolomic profiling of amino acids may have an application in the search for clinical phenotype-specific MS biomarkers.
 OBJECTIVES: Central fatigue is one of the most common symptoms in multiple sclerosis (MS). It has a profound impact on quality of life and a negative effect on cognition. Despite its widespread impact, fatigue is poorly understood and very difficult to measure. Whilst the basal ganglia has been implicated in fatigue the nature of its role and involvement with fatigue is still unclear. The aim of the present study was to establish the role of the basal ganglia in MS fatigue using functional connectivity measures. METHODS: The present study examined the functional connectivity (FC) of the basal ganglia in a functional MRI study with 40 female participants with MS (mean age = 49.98 (SD = 9.65) years) and 40 female age-matched (mean age = 49.95 (SD = 9.59) years) healthy controls (HC). To measure fatigue the study employed the subjective self-report Fatigue Severity Scale and a performance measure of cognitive fatigue using an alertness-motor paradigm. To distinguish physical and central fatigue force measurements were also recorded. RESULTS: The results suggest that decreased local FC within the basal ganglia plays a key role in cognitive fatigue in MS. Increased global FC between the basal ganglia and the cortex may sub serve a compensatory mechanism to reduce the impact of fatigue in MS. CONCLUSION: The current study is the first to show that basal ganglia functional connectivity is associated with both subjective and objective fatigue in MS. In addition, the local FC of the basal ganglia during fatigue inducing tasks could provide a neurophysiological biomarker of fatigue.
 The purpose of this study is to investigate the role of psychological flexibility in mediating the beneficial effects of resilience on distress and quality of life (QoL) in people with MS (PwMS). The psychological flexibility framework underpinning acceptance and commitment therapy (ACT) was used to conceptualise psychological flexibility. A total of 56 PwMS completed an online survey that assessed global psychological flexibility and each of its six core sub-processes, resilience, distress, mental and physical health QoL, socio-demographics, and illness variables. Mediation analyses showed that, as hypothesised, higher levels of global psychological flexibility and its sub-processes were associated with increases in the positive impacts of resilience on distress and mental and physical health QoL via a mediational mechanism. These findings suggest that psychological flexibility skills build resilience capacities in PwMS. The psychological flexibility framework offers an ACT-based intervention pathway to build resilience and enhance mental health and QoL in PwMS.
 Here, we offer a roadmap for what might be studied next in understanding how EBV triggers MS. We focus on two areas: The first area concerns the molecular mechanisms underlying how clonal antibody in the CSF emanates in widespread molecular mimicry to key antigens in the nervous system including GlialCAM, a protein associated with chloride channels. A second and equally high priority in the roadmap concerns various therapeutic approaches that are related to blocking the mechanisms whereby EBV triggers MS. Therapies deserving of attention include clinical trials with antivirals and the development of 'inverse' vaccines based on nucleic acid technologies to control or to eradicate the consequences of EBV infection. High enthusiasm is given to continuation of ongoing clinical trials of cellular adoptive therapy to attack EBV-infected cells. Clinical trials of vaccines to EBV are another area deserving attention. These suggested topics involving research on mechanism, and the design, implementation and performance of well-designed trials are not intended to be an exhaustive list. We have splendid tools available to our community of medical scientists to tackle how EBV triggers MS and then to perhaps change the world with new therapies to potentially eradicate MS, as we have done with nearly complete success for poliomyelitis.
 The neurodegenerative and inflammatory illnesses of amyotrophic lateral sclerosis and multiple sclerosis were once thought to be completely distinct entities that did not share any remarkable features, but new research is beginning to reveal more information about their similarities and differences. Here, we review some of the pathophysiological features of both diseases and their experimental models: RNA-binding proteins, energy balance, protein transportation, and protein degradation at the molecular level. We make a thorough analysis on TDP-43 and hnRNP A1 dysfunction, as a possible common ground in both pathologies, establishing a potential link between neurodegeneration and pathological immunity. Furthermore, we highlight the putative variations that diverge from a common ground in an atemporal course that proposes three phases for all relevant molecular events.
 The world witnessed much research fund allocation on the COVID-19 outbreak's epidemiology, pathology, impact on lifestyles, social behaviours and treatment possibilities. The highly contagious nature of the disease compelled scientific communities and related organisations to hasten vaccine development and supplies. Well-timed international collaborations resulted in quicker development of varied forms of vaccines against COVID-19. Prospective observational studies and systematic reviews on vaccine trials reported their safety and efficacies. Nevertheless, post-marketing surveillance is quintessential to ascertain such safety and efficacy claims. There have been scattered reports lately of several adverse temporal events, such as haematological, immunological and neurological untoward occurrences following COVID-19 inoculation. There is a growing piece of evidence of the impact of COVID vaccination on patients with neurological-neuroimmunological disorders. Here two unrelated cases of neurological deficits post-COVID vaccination are reported. One was an incidence of Acute Disseminated Encephalomyelitis, while the other was an acute exacerbation of Multiple Sclerosis following vaccination. Ayurvedic treatments were effective in either of these conditions. Case series and case reports shall judiciously add information to vaccine safety data and acknowledge the necessity of clinician approval, based on detailed individualised assessments before mass vaccination.
 This paper offers new insights into the promotion of the Exercise is Medicine (EIM) framework for mental illness and chronic disease. Utilising the Syndemics Framework, which posits mental health conditions as corollaries of social conditions, we argue that medicalized exercise promotion paradigms both ignore the social conditions that can contribute to mental illness and can contribute to mental illness via discrimination and worsening self-concept based on disability. We first address the ways in which the current EIM framework may be too narrow in scope in considering the impact of social factors as determinants of health. We then consider how this narrow scope in combination with the emphasis on independence and individual prescriptions may serve to reinforce stigma and shame associated with both chronic disease and mental illness. We draw on examples from two distinct research projects, one on exercise interventions for depression and one on exercise interventions for multiple sclerosis (MS), in order to consider ways to improve the approach to exercise promotion for these and other, related populations.
 BACKGROUND: Although effective contraception is strongly recommended during the therapy of women with multiple sclerosis (MS) with some immunomodulatory drugs, unplanned pregnancies still occur. Adequate medication management is essential to avoid foetal harm in the event of an unplanned pregnancy. OBJECTIVE: The aim was to screen for medications used in women of childbearing age with MS that may pose a risk of side effects on foetal development. METHODS: Sociodemographic, clinical and medication data were collected from 212 women with MS by structured interviews, clinical examinations and medical records. Using the databases from Embryotox, Reprotox, the Therapeutic Goods Administration and on the German summaries of product characteristics, we assessed whether the taken drugs were potentially harmful regarding the foetal development. RESULTS: The majority of patients (93.4%) were taking one or more drugs for which a possible harmful effect on the foetus is indicated in at least one of the four databases used. This proportion was even higher in patients who used hormonal contraceptives (birth control pills or vaginal rings) (PwCo, n = 101), but it was also quite high in patients who did not use such contraceptives (Pw/oCo, n = 111) (98.0% and 89.2%, respectively). PwCo were significantly more likely to take five or more medications with potential foetal risk according to at least one database than Pw/oCo (31.7% versus 6.3%). PwCo were also more severely disabled (average Expanded Disability Status Scale score: 2.8 versus 2.3) and more frequently had comorbidities (68.3% versus 54.1%) than Pw/oCo. CONCLUSION: Data on the most commonly used drugs in MS therapy were gathered to study the risk of possible drug effects on foetal development in female MS patients of childbearing age. We found that the majority of drugs used by patients with MS are rated as having a potential risk of interfering with normal foetal development. More effective contraception and special pregnancy information programmes regarding the therapy management during pregnancy should be implemented to reduce potential risks to mother and child. PLAIN LANGUAGE SUMMARY: Use of drugs not recommended during pregnancy by women with multiple sclerosis Introduction: Patients with multiple sclerosis (MS) often have to take different drugs simultaneously. During the therapy with some immunomodulatory drugs, effective contraception is strongly recommended. Nevertheless, unplanned pregnancies occur regularly in women with MS.Methods: Here, we investigated whether the 212 patients included in this study were taking drugs with known possibility of harm to the development of an unborn child. This was done using four different drug databases.Results: A subset of 111 patients was not taking hormonal contraceptives (birth control pills or vaginal rings). Of those, 99 patients were taking at least one drug that is not recommended during pregnancy according to at least one of the four databases. Most of the medications taken have the potential to affect normal foetal development.Conclusion: To ensure safe use of medications, the patients should be reminded of the importance of effective contraception.
 PURPOSE: People with multiple sclerosis (pwMS) want disease-specific dietary advice to reduce the confusion around diet. This study used co-design principles to develop an online nutrition education program for pwMS. METHODS: Mixed-methods (multiphase sequential design). Phase 1: online survey (n = 114 pwMS) to explore preferred content and characteristics of a nutrition program and develop a draft program. Phase 2: feedback on the draft program from stakeholders (two meetings; n = 10 pwMS and multiple sclerosis (MS) health professionals) and pwMS (two workshops; n = 6) to produce a full program prototype. Phase 3: cognitive interviews (n = 8 pwMS plus 1 spouse) to explore acceptability and ease of comprehension of one module of the program, analysed using deductive content analysis. RESULTS: Preferred topics were included in the program, which were further developed with consumer feedback. Cognitive interviews produced four themes: (1) positive and targeted messaging to motivate behaviour change; (2) "not enough evidence" is not good enough; (3) expert advice builds in credibility; and (4) engaging and appropriate online design elements are crucial. CONCLUSIONS: Positive language appears to improve motivation to make healthy dietary changes and engagement with evidence-based nutrition resources. To ensure acceptability, health professionals can use co-design to engage consumers when developing resources for pwMS.IMPLICATIONS FOR REHABILITATIONCo-designed nutrition education programs can help people achieve high-quality diets in line with recommendations, but very few programs exist for people with multiple sclerosis (MS), and none were co-designedThe participatory research in this study was instrumental in ensuring that important information regarding program acceptability was identifiedCo-design can ensure that the language is appropriate for the target audience, and positive language appeared to improve motivation in people with MS to engage with the online nutrition education programWhere practical and feasible, health professionals should collaborate with MS consumers when developing resources, and use positive, empowering language.
 Thymic and bone marrow outputs were evaluated in 13 sequential samples of 68 multiple sclerosis patients who initiated alemtuzumab and were clinically followed for 48 months. Three months after alemtuzumab infusions, the levels of new T lymphocytes were significantly reduced, but progressively increased reaching the highest values at 36 months, indicating the remarkable capacity of thymic function recovery. Newly produced B cells exceeded baseline levels as early as 3 months after alemtuzumab initiation. Heterogeneous patterns of new T- and B-cell recovery were identified, but without associations with age, sex, previous therapies, development of secondary autoimmunity or infections, and disease re-emergence. Trial registration version 2.0-27/01/2016.
 Fingolimod is a multiple sclerosis disease-modifying therapy which sequestrates lymphocytes in the lymph nodes, thereby reducing peripheral blood lymphocytes. Cryptococcal infection is an important adverse effect which should be recognised. We report a case of cutaneous and central nervous system infection who presented with isolated cutaneous symptoms in the absence of neurological or systemic manifestations.
 The frequency of switches between Disease Modifying Therapies (DMTs) in Multiple Sclerosis (MS) has increased considerably over previous years. Between fingolimod and anti-CD20 therapies, a 1-month washout period is usually recommended. However, disease reactivations are frequent after fingolimod (Fg) cessation. Using a retrospective observational monocentric exposed/non-exposed cohort study, we investigated the efficacy and the safety of a shorter washout period (WP) between Fg and anti-CD20. We compared two groups: 25 patients with a short WP (<21 days) and 20 patients with a longer WP (>21 days). We observed no reactivation during WP in patients with a short WP against a relapse in 55% of patients in the longer group. Moreover, clinical and biological safety was excellent. Based on these findings, we recommend a shorter WP between fingolimod and anti-CD20 therapies in MS.
 Existing methods for fitting continuous time Markov models (CTMM) in the presence of covariates suffer from scalability issues due to high computational cost of matrix exponentials calculated for each observation. In this article, we propose an optimization technique for CTMM which uses a stochastic gradient descent algorithm combined with differentiation of the matrix exponential using a Padé approximation. This approach makes fitting large scale data feasible. We present two methods for computing standard errors, one novel approach using the Padé expansion and the other using power series expansion of the matrix exponential. Through simulations, we find improved performance relative to existing CTMM methods, and we demonstrate the method on the large-scale multiple sclerosis NO.MS data set.
 The gut microbiota plays a key role in the function of the host immune system and neuroimmune diseases. Alterations in the composition of the gut microbiota can lead to pathology and altered formation of microbiota-derived components and metabolites. A series of neuroimmune diseases, such as myasthenia gravis (MG), multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSDs), Guillain-Barré syndrome (GBS), and autoimmune encephalitis (AIE), are associated with changes in the gut microbiota. Microecological therapy by improving the gut microbiota is expected to be an effective measure for treating and preventing some neuroimmune diseases. This article reviews the research progress related to the roles of gut microbiota and fecal microbiota transplantation (FMT) in neuroimmune diseases.
 INTRODUCTION: Plasma exchange (PE) is widely used in many immune-based neurological diseases. Our aim is to analyze characteristics of PE in neurological patients at the Clinical Center of Montenegro. METHODS: Our study involved neurological patients treated with PE between January 2020 and April 2022. RESULTS: In total, 246 PEs were performed in 43 patients. We divided patients into 4 groups according to indications. In 8/9 multiple sclerosis (MS) patients a decrease of Expanded Dysability Status Scale at least 0.5 was verified. In 14/20 Guillain Barre syndrome patients reduction of Hughes was observed. Four patients with myasthenia gravis (MG) were treated with PE. The most heterogeneous group (4) consisted of patients in whom the mechanism of disease development is assumed to be immune system dysregulation. Fourteen patients had any adverse event. CONCLUSION: Our results show that PE is widely used and safe in the treatment of neurological diseases.
 KEY CLINICAL MESSAGE: According to this report, a biopsy revealed a diagnosis of neurosarcoidosis in a patient with a history of MS. The development of the disease can be slowed down by early diagnosis and appropriate treatment. ABSTRACT: Neurosarcoidosis is a rare type of sarcoidosis that affects the central nervous system (CNS). Herein, we present a case of neurosarcoidosis with a history of multiple sclerosis (MS). Based on the pathological findings of the biopsy, a diagnosis of neurosarcoidosis was established. The administration of appropriate treatment at an early stage can assist in decelerating its progression.
 The myosin superfamily is a group of molecular motors. Autoimmune diseases are characterized by dysregulation or deficiency of the immune tolerance mechanism, resulting in an immune response to the human body itself. The link between myosin and autoimmune diseases is much more complex than scientists had hoped. Myosin itself immunization can induce experimental autoimmune diseases of animals, and myosins were abnormally expressed in a number of autoimmune diseases. Additionally, myosin takes part in the pathological process of multiple sclerosis, Alzheimer's disease, Parkinson's disease, autoimmune myocarditis, myositis, hemopathy, inclusion body diseases, etc. However, research on myosin and its involvement in the occurrence and development of diseases is still in its infancy, and the underlying pathological mechanisms are not well understood. We can reasonably predict that myosin might play a role in new treatments of autoimmune diseases.




 INTRODUCTION: Reliable measurement of disability in multiple sclerosis (MS) using a comprehensive, patient self-reported scale, such as the World Health Organization Disability Assessment Schedule (WHODAS) 2.0, would be of clinical and research benefit. METHODS: In the Trajectories of Outcome in Neurological Conditions-MS study, WHODAS 2.0 (WHODAS-36 items for working, WHODAS-32 items if not working, WHODAS-12 items short-form) was examined using Rasch analysis in 5809 people with MS. RESULTS: The 36- and 32-item parallel forms, and the cognitive and physical domains, showed reliability consistent with individual or group use. The 12-item short-form is valid for group use only. Interval level measurement for parametric statistics can be derived from all three scales which showed medium to strong effect sizes for discrimination across characteristics such as age, subtype, and disease duration. Smallest detectable difference for each scale was < 6 on the standardised metric of 0-100 so < 6% of the total range. There was no substantial differential item functioning (DIF) by age, gender, education, working full/part-time, or disease duration; the finding of no DIF for time or sample supports the use of WHODAS 2.0 for longitudinal studies, with the 36- and 32-item versions and the physical and cognitive domains valid for individual patient follow-up. CONCLUSIONS: Disability in MS can be comprehensively measured at interval level by the WHODAS 2.0, and validly monitored over time. Routine use of this self-reported measure in clinical and research practice would give valuable information on the trajectories of disability of individuals and groups.
 BACKGROUND: Spinal cord (SC) lesions have been associated with unfavourable clinical outcomes in multiple sclerosis (MS). However, the relation of whole SC lesion number (SCLN) and volume (SCLV) to the future occurrence and type of confirmed disability accumulation (CDA) remains largely unexplored. METHODS: In this monocentric retrospective study, SC lesions were manually delineated. Inclusion criteria were: age between 18 and 60 years, relapsing-remitting MS, disease duration under 2 years and clinical follow-up of 5 years. The first CDA event after baseline, determined by a sustained increase in the Expanded Disability Status Scale over 6 months, was classified as either progression independent of relapse activity (PIRA) or relapse-associated worsening (RAW). SCLN and SCLV were compared between different (sub)groups to assess their prospective value. RESULTS: 204 patients were included, 148 of which had at least one SC lesion and 59 experienced CDA. Patients without any SC lesions experienced significantly less CDA (OR 5.8, 95% CI 2.1 to 19.8). SCLN and SCLV were closely correlated (r(s)=0.91, p<0.001) and were both significantly associated with CDA on follow-up (p<0.001). Subgroup analyses confirmed this association for patients with PIRA on CDA (34 events, p<0.001 for both SC lesion measures) but not for RAW (25 events, p=0.077 and p=0.22). CONCLUSION: Patients without any SC lesions are notably less likely to experience CDA. Both the number and volume of SC lesions on MRI are associated with future accumulation of disability largely independent of relapses.
 OBJECTIVES: Fatigue in multiple sclerosis (MS) is a frequent and invalidating symptom, which can be relieved by non-invasive neuromodulation, which presents only negligible side effects. A 5-day transcranial direct-current stimulation, 15 min per day, anodically targeting the somatosensory representation of the whole body against a larger occipital cathode was efficacious against MS fatigue (fatigue relief in multiple sclerosis, Faremus treatment). The present proof-of-concept study tested the working hypothesis that Faremus S1 neuromodulation modifies the homology of the dominant and non-dominant corticospinal (CST) circuit recruitment. METHODS: CST homology was assessed via the Fréchet distance between the morphologies of motor potentials (MEPs) evoked by transcranial magnetic stimulation in the homologous left- and right-hand muscles of 10 fatigued MS patients before and after Faremus. RESULTS: In the absence of any change in MEP features either as differences between the two body sides or as an effect of the treatment, Faremus changed in physiological direction the CST's homology. Faremus effects on homology were more evident than recruitment changes within the dominant and non-dominant sides. CONCLUSIONS: The Faremus-related CST changes extend the relevance of the balance between hemispheric homologs to the homology between body sides. With this work, we contribute to the development of new network-sensitive measures that can provide new insights into the mechanisms of neuronal functional patterning underlying relevant symptoms.
 BACKGROUND AND AIMS: Relapses are an important clinical feature of multiple sclerosis (MS) that result in temporary negative changes in quality of life (QoL), measured by health state utilities (HSUs) (disutilities). We aimed to quantify disutilities of relapse in relapsing remitting MS (RRMS), secondary progressive MS (SPMS), and relapse onset MS [ROMS (including both RRMS and SPMS)] and examine these values by disability severity using four multi-attribute utility instruments (MAUIs). METHODS: We estimated (crude and adjusted and stratified by disability severity) disutilities (representing the mean difference in HSUs of 'relapse' and 'no relapse' groups as well as 'unsure' and 'no relapse' groups) in RRMS (n = 1056), SPMS (n = 239), and ROMS (n = 1295) cohorts from the Australian MS Longitudinal Study's 2020 QoL survey, using the EQ-5D-5L, AQoL-8D, EQ-5D-5L-Psychosocial, and SF-6D MAUIs. RESULTS: Adjusted mean overall disutilities of relapse in RMSS/SPMS/ROMS were - 0.101/- 0.149/- 0.129 (EQ-5D-5L), - 0.092/- 0.167/- 0.113 (AQoL-8D), - 0.080/- 0.139/- 0.097 (EQ-5D-5L-Psychosocial), and - 0.116/- 0.161/- 0.130 (SF-6D), approximately 1.5 times higher in SPMS than in RRMS, in all MAUI. All estimates were statistically significant and/or clinically meaningful. Adjusted disutilities of RRMS and ROMS demonstrated a U-shaped relationship between relapse disutilities and disability severity. Relapse disutilities were higher in 'severe' disability than 'mild' and 'moderate' in the SPMS cohort. CONCLUSION: MS-related relapses are associated with substantial utility decrements. As the type and severity of MS influence disutility of relapse, the use of disability severity and MS-type-specific disutility inputs is recommended in future health economic evaluations of MS. Our study supports relapse management and prevention as major mechanisms to improve QoL in people with MS.
 BACKGROUND: Previous studies have shown that CD134 (OX40) co-stimulation is involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) models and the antigen is expressed within multiple sclerosis lesions in humans. OX40 (CD134) is thought to be a secondary co-stimulatory immune checkpoint molecule that is expressed by T cells. This study aimed to evaluate the mRNA expression of OX40 and its serum levels in the peripheral blood of patients with Multiple Sclerosis (MS) or Neuromyelitis Optica (NMO). METHODS: Patients with MS (n = 60), NMO (n = 20), and 20 healthy subjects were recruited from Sina Hospital, Tehran, Iran. The diagnoses were confirmed by a specialist in clinical neurology. Peripheral venous blood was obtained from all subjects, and mRNA quantification of OX40 was conducted using real-time PCR. Serum samples were also obtained and the concentration of OX40 was determined using an enzyme-linked immunosorbent assay (ELISA). RESULTS: There was a significant correlation between the mRNA expression and serum levels of OX40 and disability as assessed using the expanded disability status scale (EDSS) in the patients with MS, but not in the patients with NMO. Expression of OX40 mRNA was significantly higher in the peripheral blood of MS patients compared to healthy individuals and NMO patients (*P < 0.05). In addition, serum OX40 concentrations were also significantly higher in patients with MS patients compared with healthy subjects (9.08 ± 2.48 vs. 1.49 ± 0.54 ng/ml; P = 0.041). CONCLUSIONS: It appears that an increased expression of OX40 may be associated with the hyperactivation of T cells in patients with MS, and this may play a role in the pathogenesis of the disease.
 BACKGROUND: Although there is evidence that shows worse cognitive functioning in male patients with multiple sclerosis (MS), the role of brain pathology in this context is under-investigated. OBJECTIVE: To investigate sex differences in cognitive performance of MS patients, in the context of brain pathology and disease burden. METHODS: Brain MRI, neurological examination, neuropsychological assessment (Brief International Cognitive Assessment in MS-BICAMS, and Paced Auditory Verbal Learning Test-PASAT), and patient-reported outcome questionnaires were performed/administered in 1052 MS patients. RESULTS: Females had higher raw scores in the Symbol Digit Modalities Test (SDMT) (57.0 vs. 54.0; p < 0.001) and Categorical Verbal Learning Test (CVLT) (63.0 vs. 57.0; p < 0.001), but paradoxically, females evaluated their cognitive performance by MS Neuropsychological Questionnaire as being worse (16.6 vs 14.5, p = 0.004). Females had a trend for a weaker negative correlation between T2 lesion volume and SDMT ([Formula: see text] = - 0.37 in females vs. - 0.46 in men; interaction p = 0.038). On the other hand, women had a trend for a stronger correlation between Brain Parenchymal Fraction (BPF) and a visual memory test (Spearman's [Formula: see text] = 0.31 vs. 0.21; interaction p = 0.016). All these trends were not significant after correction for false discovery rate. CONCLUSIONS: Although, females consider their cognition as worse, males had at a group level slightly worse verbal memory and information processing speed. However, the sex differences in cognitive performance were smaller than the variability of scores within the same sex group. Brain MRI measures did not explain the sex differences in cognitive performance among MS patients.
 BACKGROUND: Our study investigated the rate of breakthrough SARS-CoV-2 infection and clinical outcomes in a cohort of multiple sclerosis (MS) patients who were treated with the anti-CD20 monoclonal antibody (Ab), ocrelizumab, before first, second and third BNT162b2 mRNA vaccinations. To correlate clinical outcomes with the humoral and cellular response. METHODS: The study was a prospective non-randomised controlled multicentre trial observational study. Participants with a diagnosis of MS who were treated for at least 12 months with ocrelizumab prior to the first BNT162b2 mRNA vaccination were prospectively followed up from January 2021 to June 2022. RESULTS: Out of 54 participants, 32 (59.3%) developed a positive SARS-CoV-2 PCR test in the study period. Mild infection was observed in all infected participants. After the third vaccination, the non-infected participants had higher mean Ab levels compared to the infected participants (54.3 binding antibody unit (BAU)/mL vs 26.5 BAU/mL, p=0.030). The difference in reactivity between spike-specific CD4(+) and CD8(+) T lymphocytes in the two groups was not significant. CONCLUSION AND RELEVANCE: The study results demonstrate rates of 59% in breakthrough infections after the third SARS-CoV-2 mRNA vaccination in ocrelizumab-treated patients with MS, without resulting in critical disease courses. These findings suggest the need for continuous development of prophylactic treatments when proved important in the protection of severe breakthrough infection.
 Progressive multiple sclerosis (PMS) is currently diagnosed retrospectively. Here, we work toward a set of biomarkers that could assist in early diagnosis of PMS. A selection of cerebrospinal fluid metabolites (n = 15) was shown to differentiate between PMS and its preceding phenotype in an independent cohort (AUC = 0.93). Complementing the classifier with conformal prediction showed that highly confident predictions could be made, and that three out of eight patients developing PMS within three years of sample collection were predicted as PMS at that time point. Finally, this methodology was applied to PMS patients as part of a clinical trial for intrathecal treatment with rituximab. The methodology showed that 68% of the patients decreased their similarity to the PMS phenotype one year after treatment. In conclusion, the inclusion of confidence predictors contributes with more information compared to traditional machine learning, and this information is relevant for disease monitoring.
 BACKGROUND: Cognitive impairment (CI) may be present in people with multiple sclerosis (PwMS) in different stages of the disease, as well as in PwMS with various degrees of disability. This study aimed to investigate cognitive decline over a period of 12 months and to examine an association between cognition and the disability in PwMS, also over a period of 12 months. METHODS: The Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) battery was used, containing the Symbol Digit Modalities Test (SDMT), the Categorical Verbal Learning Test (CVLT), and the Brief Visuospatial Memory Test-Revised (BVMT-R). The Expanded Disability Status Scale (EDSS), Timed 25-Foot Walk (T25FW), and 9-Hole Peg Test (9-HPT) were used to assess the degree of disability. For the analysis of cognitive decline over the period of 12 months, Wilcoxon signed-rank test (paired sample t-test) was used. For the correlation between cognition and disability, Spearman's correlation test was used. RESULTS: We observed statistically meaningful difference only in one measure of cognition (CVLT), not the other two (SDMT and BVMT-R). SDMT significantly correlated with methods assessing the degree of disability in both time points. In the second examination, we observed a correlation between BICAMS and 9-HPT. Similarly, SDMT and BVMT-R also correlated with EDSS. CONCLUSION: To investigate the cognitive decline in PwMS, a longer period of time probably should have been chosen. EDSS is commonly used to monitor disease progression, but it does not include the evaluation of various parameters, such as cognition or upper limb function. Its use with the 9-HPT and cognitive tests may represent a more reliable and comprehensive assessment of a patient's clinical condition.
 Multiple sclerosis (MS), neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) are inflammatory diseases of the central nervous system (CNS) with a multifactorial aetiology. Environmental factors are important for their development and microorganisms could play a determining role. They can directly damage the CNS, but their interaction with the immune system is even more important. The possible mechanisms involved include molecular mimicry, epitope spreading, bystander activation and the dual cell receptor theory. The role of Epstein-Barr virus (EBV) in MS has been definitely established, since being seropositive is a necessary condition for the onset of MS. EBV interacts with genetic and environmental factors, such as low levels of vitamin D and human endogenous retrovirus (HERV), another microorganism implicated in the disease. Many cases of onset or exacerbation of neuromyelitis optica spectrum disorder (NMOSD) have been described after infection with Mycobacterium tuberculosis, EBV and human immunodeficiency virus; however, no definite association with a virus has been found. A possible role has been suggested for Helicobacter pylori, in particular in individuals with aquaporin 4 antibodies. The onset of MOGAD could occur after an infection, mainly in the monophasic course of the disease. A role for the HERV in MOGAD has been hypothesized. In this review, we examined the current understanding of the involvement of infectious factors in MS, NMO and MOGAD. Our objective was to elucidate the roles of each microorganism in initiating the diseases and influencing their clinical progression. We aimed to discuss both the infectious factors that have a well-established role and those that have yielded conflicting results across various studies.
 INTRODUCTION: Dysphagia as a consequence of Multiple Sclerosis (MS) puts individuals at higher risk of dehydration, malnutrition, and aspiration pneumonia. This study intended to investigate the effects of a combined program of neuromuscular electrical stimulation (NMES) and conventional swallowing therapy to improve swallow safety and efficiency, oral intake, and physical, emotional and functional impacts of dysphagia in people with dysphagia and MS. METHODS: In this single case experimental study with ABA design, two participants with dysphagia caused by MS underwent 12 sessions therapy during 6 weeks following a baseline of 4 evaluation sessions. They were evaluated 4 more times in the follow-up phase after therapy sessions. Scores of Mann Assessment of Swallowing Ability (MASA), DYsphagia in MUltiple Sclerosis (DYMUS), and timed test of swallowing capacity were obtained at baseline, during treatment, and in the follow-up phases. The Dysphagia Outcome and Severity Scale (DOSS) based on videofluoroscopic swallow studies, Persian-Dysphagia Handicap Index (Persian-DHI), and Functional Oral Intake Scale (FOIS) were also completed before and after treatment. Visual analysis and Percentage of Non-Overlapping Data (PND) were calculated. RESULTS: MASA, DYMUS, FOIS, and DHI scores indicated significant improvement in both participants. Although the scores of the timed test of swallowing capacity in participant 1 (B.N) and DOSS in participant 2(M.A) showed no changes, considerable improvements including reducing the amount of residue and the number of swallows required to clear bolus were seen in the post-treatment videofluoroscopic records of both participants. DISCUSSION/CONCLUSION: NMES in conjunction with conventional dysphagia therapy based on motor learning principles could improve the swallowing function and decrease disabling effects of dysphagia on different aspects of life in participants with dysphagia caused by MS.
 Nervous system disorders may be accompanied by gastrointestinal (GI) dysfunction. Brain lesions may be responsible for GI problems such as decreased peristalsis (e.g., lesions in the basal ganglia, pontine defecation center/Barrington's nucleus), decreased abdominal strain (e.g., lesions in the parabrachial nucleus), hiccupping and vomiting (e.g., lesions in the area postrema), and appetite loss (e.g., lesions in the hypothalamus). Decreased peristalsis also may be caused by lesions of the spinal long tracts or the intermediolateral nucleus projecting to the myenteric plexus. This review addresses GI dysfunction caused by multiple sclerosis, neuromyelitis optica spectrum disorder, and myelin oligodendrocyte glycoprotein-associated disorder. Neuro-associated GI dysfunction may develop concurrently with brain or spinal cord dysfunction or may predate it. Collaboration between gastroenterologists and neurologists is highly desirable when caring for patients with GI dysfunction related to nervous system disorders, particularly since patients with these symptoms may visit a gastroenterologist prior to the establishment of a neurological diagnosis.
 Neurodegeneration occurs early in the multiple sclerosis (MS) disease course and is an important driver of permanent disability. Current immunomodulatory therapies do not directly target neuronal health; thus, there is a critical need to develop neuroprotective strategies in MS. Outcome measures in clinical trials primarily evaluate disease activity and clinical disability scores rather than measures of neurodegeneration. The visual system provides a noninvasive correlate of brain atrophy and neuronal function through structural and functional exams. Furthermore, optic nerve axons and their respective neuronal cell bodies in the retina, in addition to their synaptic input to the thalamus, provide a distinct anatomy to investigate neurodegenerative processes. This review discusses the utility of the visual system as an early output measure of neurodegeneration in MS as well as an important platform to evaluate neuroprotective strategies in preclinical models.
 In the long-term management of a degenerative illness there is a risk that the approach we take to treatment can be characterized by therapeutic inertia (TI). With no evidence of disease progression clinicians can be reluctant to make a change to treatment regimes. This can lead to less choice and suboptimal outcomes for people with multiple sclerosis. The risk of TI is however greater when clinicians have an aversion to ambiguity and a low tolerance for uncertainty. (1) This article is an art-based inquiry into the possibility of TI in decision making when the advice from my neurologist was to stick with the treatment unless something goes wrong. (2) Through a unique process of rusting an existing canvas, the article reveals that the phrase, unless something goes wrong, is an expression of openness to uncertainty and ambiguity. (3) Art making offers the artist an opportunity to lean into and grow and capacity for tolerating uncertainty and ambiguity, thereby minimizing the risk of TI.
 Rehabilitation via virtual reality (VR) training tools allows repetitive, intensive, and task-specific practice in a controlled and safe environment. Our goal was to develop and validate a novel immersive VR system based on the practice of real-life activities in a kitchen environment in people with multiple sclerosis (pwMS) with upper-limb dysfunction. The novel immersive VR kitchen application includes several tasks, i.e., tidying up the kitchen, preparing a hamburger and soup meal, and dish washing. Following the development phase, the system was tested for an 8-week intervention period on a small sample of pwMS suffering from upper-limb dysfunction. The Suitability Evaluation Questionnaire for VR systems served as the primary outcome. The scores for enjoyment, sense of comfort with the system, feelings of success and control, realism, easy-to-understand instructions, assists in rehabilitation therapy, were between 4.0 and 4.6, indicating a high satisfaction. The scores for eye discomfort, dizziness, nausea, and disorientation during practice were between 2.8 and 1.3, indicating a low-to-moderate interference of the system. The virtual kitchen training system is feasible and safe for upper-limb training in pwMS and paves the way for future RCTs to examine the benefits of the system compared with standard care, thus improving the functionality of the upper limbs in pwMS.
 BACKGROUND: People with multiple sclerosis (MS) have been coping with high levels of stress during the ongoing coronavirus pandemic, affecting their employment, physical, and mental health, and overall life satisfaction. OBJECTIVE: This study evaluated constructs of the stress-appraisal-coping theory and positive person-environment factors as predictors of subjective well-being for adults with MS. METHOD: Participants included 477 adults with MS recruited through the National Multiple Sclerosis Society. Hierarchical regression analysis was used to determine the incremental variance in subjective well-being accounted for by demographic covariates, functional disability, perceived stress, stress appraisal, coping styles, and positive person-environment contextual factors. RESULTS: Positive stress appraisal and coping flexibility were significantly associated with subjective well-being at the bivariate correlation level and at the step they were entered into the regression model. Marital status, household income, functional disability, perceived stress, hope, core self-evaluations, and social support were significant predictors in the final model, accounting for 60% of the variance in subjective well-being scores (R² = .60, f² = 1.48; large effect size). CONCLUSIONS: Findings from this study support a stress management and well-being model based on constructs of Lazarus and Folkman's stress-appraisal-coping theory and positive person-environment contextual factors, which can inform the development of theory-driven and empirically supported stress management and well-being interventions for people with MS during the ongoing global health crisis. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 Multiple sclerosis (MS) is a chronic autoimmune disease where activated immune cells can attack oligodendrocytes causing damage to the myelin sheath. Several molecular mechanisms are responsible for the auto-activation of immune cells such as RNA interference (RNAi) through microRNAs (miRNAs or miRs). In the present study, the role of miR-155 in regulating CD8(+) T-cell activity in patients with relapsing-remitting multiple sclerosis (RRMS) was investigated, in terms of its migratory functions with regard to intracellular adhesion molecule-1 (ICAM1) and integrin subunit β2 (ITGB2), and its cytotoxic proteins, perforin and granzyme B. Gene expression of miR-155, ICAM1, ITGB2, perforin and granzyme B was evaluated following epigenetic modulations using reverse transcription-quantitative polymerase chain reaction in CD8(+) T-cells isolated from blood samples of patients with RRMS and compared to healthy controls. The ectopic expression of miR-155 resulted in a persistent downregulation in all genes of interest related to CD8(+) T-cell activation that were positively correlated with the Expanded Disability Status Scale of patients. The present study revealed the interplay between miR-155, ICAM1, and ITGB2, shedding light on their beneficial use as possible therapeutic regulators and diagnostic biomarkers of disease. Moreover, epigenetic modulations enhancing the efficacy of disease-modifying therapies (DMTs) may be employed as personalized therapy, to decrease the side effects of DMTs and improve the outcomes of patients.
 BACKGROUND: Multiple sclerosis (MS) is an autoimmune disease that is often treated with multiple medications. Managing multiple medications, also known as polypharmacy, can be challenging for persons with MS. Toolkits are instructional resources designed to promote behaviour change. Toolkits may support medication self-management for adults with MS, as they have been useful in other populations with chronic conditions. OBJECTIVE: The main purpose of this review was to identify and summarize medication self-management toolkits for MS, as related to the design, delivery, components, and measures used to evaluate implementation and/or outcomes. METHODS: A scoping review was conducted following guidelines by JBI. Articles were included if they focused on adults (18 years or older) with MS. RESULTS: Six articles reporting on four unique toolkits were included. Most toolkits were technology-based, including mobile or online applications, with only one toolkit being paper-based. The toolkits varied in type, frequency, and duration of medication management support. Varying outcomes were also identified, but there were improvements reported in symptom management, medication adherence, decision-making, and quality of life. The six studies were quantitative in design, with no studies exploring the user experience from a qualitative or mixed-methods design. CONCLUSIONS: There is limited research on medication self-management toolkits among adults with MS. Future development, implementation, and evaluation mixed-methods research are needed to explore user experiences and overall design of toolkits.



 PURPOSE: Multiple sclerosis (MS) is a chronic condition linked to a wide range of psychological difficulties. While traditional cognitive behavioural therapy has been studied extensively with people with MS, much less is known about more recent "third wave" approaches. METHODS: A scoping review was carried out by performing a systematic search across MEDLINE Complete, PsycINFO, CINAHL, Academic Search Ultimate, and Cochrane Library up to January 2022. RESULTS: From an initial return of 8306 citations, 35 studies were included, 20 of which were randomised controlled trials (RCTs). These showed that four third wave approaches have been investigated with people with MS to date: acceptance and commitment therapy (ACT), dialectical behaviour therapy (DBT), mindfulness-based stress reduction (MBSR), and mindfulness-based cognitive therapy (MBCT). MBSR and MBCT may be helpful to address a range of psychological difficulties up to three months post-intervention. However, MS-specific adaptations may be required, and more evidence is needed on longer-term effectiveness. Limited evidence is also available for DBT and ACT, but additional research is warranted before any recommendation can be made. CONCLUSIONS: As third wave approaches keep being refined, further more rigorous investigations are needed to implement them to the benefit of people with MS. Implications for RehabilitationMultiple sclerosis is linked to a wide range of psychological difficulties in adults.Little is currently known on third wave psychotherapies for people with MS.Mindfulness-based stress reduction and mindfulness-based cognitive therapy may be helpful to address a wide range of difficulties in MS.Specific adaptations may be needed to deliver suitable therapies to people with MS.Additional research is warranted to build on preliminary findings for DBT and ACT.



 BACKGROUND: Multiple sclerosis (MS) is a chronic neuroinflammatory disease affecting about 2.8 million people worldwide. Disease course after the most common diagnoses of relapsing-remitting multiple sclerosis (RRMS) and clinically isolated syndrome (CIS) is highly variable and cannot be reliably predicted. This impairs early personalized treatment decisions. OBJECTIVES: The main objective of this study was to algorithmically support clinical decision-making regarding the options of early platform medication or no immediate treatment of patients with early RRMS and CIS. DESIGN: Retrospective monocentric cohort study within the Data Integration for Future Medicine (DIFUTURE) Consortium. METHODS: Multiple data sources of routine clinical, imaging and laboratory data derived from a large and deeply characterized cohort of patients with MS were integrated to conduct a retrospective study to create and internally validate a treatment decision score [Multiple Sclerosis Treatment Decision Score (MS-TDS)] through model-based random forests (RFs). The MS-TDS predicts the probability of no new or enlarging lesions in cerebral magnetic resonance images (cMRIs) between 6 and 24 months after the first cMRI. RESULTS: Data from 65 predictors collected for 475 patients between 2008 and 2017 were included. No medication and platform medication were administered to 277 (58.3%) and 198 (41.7%) patients. The MS-TDS predicted individual outcomes with a cross-validated area under the receiver operating characteristics curve (AUROC) of 0.624. The respective RF prediction model provides patient-specific MS-TDS and probabilities of treatment success. The latter may increase by 5-20% for half of the patients if the treatment considered superior by the MS-TDS is used. CONCLUSION: Routine clinical data from multiple sources can be successfully integrated to build prediction models to support treatment decision-making. In this study, the resulting MS-TDS estimates individualized treatment success probabilities that can identify patients who benefit from early platform medication. External validation of the MS-TDS is required, and a prospective study is currently being conducted. In addition, the clinical relevance of the MS-TDS needs to be established.
 BACKGROUND AND AIMS: Educational self-management interventions (SMI) have an important role in improving symptom management, preventing relapse of multiple sclerosis (MS) and promoting quality of life (QoL) of these patients; since there is little knowledge about overall effectiveness of MS self-management programs and which types of SMI improves the outcomes, this research aims to assess the efficacy of structured SMI in improving health outcomes in people with MS (PwMS) by synthesizing and compare outcomes from related randomized controlled trials. METHODS: In the present systematic review protocol, the keywords related to self-management and MS will be searched in electronic databases including (PubMed, Web of Science, Scopus, EMBASE, Cochrane Central Register of Controlled Trials [CENTRAL]), gray literature resources and key journals from 2000 to July 2023. Research-related articles will be collected and after removing duplicate articles, will be included in the study. In the screening step, titles and abstracts of articles will be reviewed and after deleting irrelevant articles, the full text of related articles will be evaluated independently by two researchers and data will be extracted from final articles and the findings will be categorized in an extraction table. Risk of bias will be assessed by using the Cochrane collaboration's tool. If possible, the data will be analyzed using random effect models and the statistical analysis will be performed using STATA software (version 14.2) developed by StataCorp. DISCUSSION: Comparative effectiveness of SMI is currently unknown. We will analyze outcome measures used to assess effectiveness of self-management education in improving QoL, depression, self-efficacy, pain, and fatigue. These findings will help identify the most promising components of SMIs, guiding targeted interventions for specific subpopulations, and facilitating the design of better interventions.
 BACKGROUND AND PURPOSE: In relapsing-remitting multiple sclerosis (RRMS), analyses from observational studies comparing dimethyl fumarate (DMF) and teriflunomide showed conflicting results. We aimed to compare the effectiveness of DMF and teriflunomide in a real-world setting, where both drugs are licensed as first-line therapies for RRMS. METHODS: We included all patients who initiated DMF or teriflunomide between 2013 and 2022, listed in the Swiss National Treatment Registry. Coarsened exact matching was applied using age, gender, disease duration, baseline Expanded Disability Status Scale (EDSS) score, time since last relapse, and relapse rate in the previous year as matching variables. Time to relapse and time to 12-month confirmed EDSS worsening were compared using Cox proportional hazard models. RESULTS: In total, 2028 patients were included in this study, of whom 1498 were matched (DMF: n = 1090, 69.6% female, mean age 45.1 years, median EDSS score 2.0; teriflunomide: n = 408, 68.9% female, mean age 45.1 years, median EDSS score 2.0). Time to relapse and time to EDSS worsening was longer in the DMF than the teriflunomide group (hazard ratio 0.734, p = 0.026 and hazard ratio 0.576, p = 0.003, respectively). CONCLUSION: Analysis of real-world data showed that DMF treatment was associated with more favorable outcomes than teriflunomide treatment.
 INTRODUCTION: People with multiple sclerosis (pwMS) may suffer from some degree of impaired social cognition (SC), the process that integrates the mental operations underlying social interactions. SC is still not clearly characterized in the early stages of MS, and it is not defined whether SC is independent of cognitive impairment. METHODS: In this cross-sectional study, we aimed to compare SC measures in a population of early (≤5 years) relapsing-remitting MS (RRMS) with an age, sex, and education-matched control group. All participants performed a clinical and a comprehensive neuropsychological assessment. SC evaluation included assessment of facial emotion recognitionn by the Emotion Recognition Task, affective theory of mind (ToM) by the Reading the Mind in the eyes Test (RMET) and cognitive ToM by the Faux Pas test (FPT). Depression, anxiety, fatigue, and quality of life were also assessed. We included 38 pwMS (mean age 34.8 ± 8.7, 78.9% female sex, mean disease duration 1.9±1.3 years) and 38 healthy controls (mean age 34.9 ± 8.4, 81.6% female sex). RESULTS: Altered social cognition was present in 34.2% of pwMS. Participants with MS performed worse than controls on measures of cognitive ToM, and affective ToM. There were no differences regarding FER. Cognitive ToM and FER correlated with cognitive functions, but no correlation was found between affective ToM and cognitive tests. The only clinical factor associated with altered SC was poor quality of life. CONCLUSIONS: Social cognition impairment is already present in a significant percentage of early RRMS patients, namely ToM deficits. While cognitive ToM and FER appears to correlate with impaired cognitive results, affective ToM is likely independent of other cognitive functions.
 PURPOSE: To our knowledge, no studies compared the video-clinician-based tools and patient-reported questionnaires in assessing gait and balance in people with MS (pwMS). The present study investigated the correlation and agreement between video-clinician-based objective measurement tools and patient-reported outcome measures (PROMs) in gait and balance evaluation. METHODS: A prospective cross-sectional study was conducted with 55 pwMS. Video analysis-based gait was evaluated by the Tinetti Gait Assessment (TGA), Gait Assessment and Intervention Tool (GAIT), and Functional Ambulation Classification Scale (FACS) by the clinician. Participants' self-reported gait and balance were assessed with the Multiple Sclerosis Walking Scale-12 (MSWS-12) and Activity-Specific Balance Confidence Scale (ABC). RESULTS: There was a moderate positive correlation between ABC with TGA and FACS (r(1): 0.552, r(2): 0.510, p < 0.001). ABC was strongly correlated with GAIT (r: - 0.652, p < 0.001). A moderate positive correlation was observed between MSWS-12 with TGA and FACS (r(1): - 0.575, r(2): - 0.524, p < 0.001). In addition, there was a strong positive correlation between MSWS-12 and GAIT (r: - 0.652, p < 0.001). Clinician-rated tools and PROMs were within the agreement limits regarding the unstandardized beta values p < 0.001). CONCLUSIONS: Clinician-based gait and balance tools demonstrate consistent results with PROMs in pwMS. Considering the low cost and practical use of PROMs, in cases where video-based clinician-based measurements cannot be provided (time, space, and technical inadequacies), questionnaires can provide concordant results at moderate and severe levels compared with objective tools.
 PURPOSE: Treatment of patients with relapsing-remitting multiple sclerosis (RRMS) in Poland begins with first-line therapy; however, the treatment often fails. The aim of this study was to investigate the course of first-line treatment in patients who, despite experiencing an active course of the disease, did not receive more efficacious treatment due to the existing criteria in the drug program. METHODS: The study included 139 patients from 45 treatment centers. Medical data concerning the course of treatment were collected with the use of specific forms. RESULTS: The most frequently used drugs were β-interferons, and treatment was initiated with these drugs in most cases; however, administration of dimethyl fumarate was also common. The median treatment duration was 30.9 months, with the longest treatment duration observed for β-interferons. The most common reason for therapy switching or termination was treatment failure. CONCLUSIONS: First-line therapy in the studied population was based mainly on β-interferons and dimethyl fumarate. For most medications, the discontinuation of therapy or drug switching were very common and the main reason was total or partial treatment failure. These observations suggest the need for earlier implementation of more effective treatment, based on drugs with high efficacy, in the study population.
 BACKGROUND: Approximately two-thirds of patients with multiple sclerosis (MS) complain different degrees of balance dysfunction, but some of them are able to withstand considerable disease burden without an overt balance impairment. Here, we tested the hypothesis that brain and cognitive reserve lessen the effect of MS-related tissue damage on balance control. METHODS: We measured the postural sway of 148 patients and 74 sex- and age-matched healthy controls by force platform under different conditions reflecting diverse neuro-pathological substrates of balance dysfunction: eyes opened (EO), eyes closed (EC), and while performing the Stroop test, i.e., dual-task (DT). Lesion volumes on T2-hyperintense and T1-hypointense sequences, and normalized brain volume provided estimations of MS-related tissue damage in patients with MS. Hierarchical linear regressions explored the protective effect against the MS-related tissue damage of intracranial volume and educational attainment (proxies for brain and cognitive reserve, respectively) on balance. RESULTS: Larger intracranial volume and high educational attainment mitigated the detrimental effect of MS-related tissue damage on postural sway under EO (adjusted-R(2)=0.20 and 0.27, respectively, p<0.01) and DT (adjusted-R(2)=0.22 and 0.30, respectively, p<0.06) conditions. Neither educational level nor brain size was associated with postural sway under EC condition. CONCLUSION: Our findings suggest a protective role of brain and cognitive reserve even on balance, an outcome that relies on both motor control and higher order processing resources. The lack of a protective effect on postural sway under EC condition confirms that this latter outcome is closer associated with spinal cord rather than brain damage.
 Multiple sclerosis (MS) is the most common disabling neurological disease characterized by chronic inflammation and neuronal cell viability impairment. Based on previous studies reporting that adiponectin exhibits neuroprotective effects in some models of neurodegenerative diseases, we analyzed the effects of AdipoRon treatment, alone or in combination with the cerebrospinal fluid of patients with MS (MS-CSF), to verify whether this adipokine acts on the basal neuronal cellular processes. To this aim, SH-SY5Y and U-87 cells (models of neuronal and glial cells, respectively) were exposed to MS-CSF alone or in co-treatment with AdipoRon. The cell viability was determined via MTT assay, and the possible underlying mechanisms were investigated via the alterations of oxidative stress and inflammation. MTT assay confirmed that AdipoRon alone did not affect the viability of both cell lines; whereas, when used in combination with MS-CSF, it reduces MS-CSF inhibitory effects on the viability of both SH-SY5Y and U-87 cell lines. In addition, MS-CSF treatment causes an increase in pro-inflammatory cytokines, whereas it determines the reduction in anti-inflammatory IL-10. Interestingly, the co-administration of AdipoRon counteracts the MS-CSF-induced production of pro-inflammatory cytokines, whereas it determines an enhancement of IL-10. In conclusion, our data suggest that AdipoRon counteracts the cytotoxic effects induced by MS-CSF on SH-SY5Y and U-87 cell lines and that one of the potential molecular underlying mechanisms might occur via reduction in oxidative stress and inflammation. Further in vivo and in vitro studies are essential to confirm whether adiponectin could be a neuro-protectant candidate against neuronal cell injury.
 Primary headaches are known to be associated with multiple sclerosis (MS), but previous studies concerning this relationship are not conclusive. Nowadays, there are no studies assessing the prevalence of headaches in Polish MS patients. The aim of the study was to assess the prevalence and characterise headaches in MS patients treated with disease-modifying therapies (DMTs). In a cross-sectional study of 419 consecutive RRMS patients, primary headaches were diagnosed according to the International Classification of Headache Disorders (ICHD-3) criteria. Primary headaches were observed in 236 (56%) of RRMS patients, with a higher prevalence in women (ratio of 2:1). The most common was migraine 174 (41%) (migraine with aura 80 (45%), migraine without aura 53 (30%), and probable migraine without aura 41 (23%); less frequent was tension-type headache 62 (14%). Female sex was a risk factor for migraines but not for tension-type headaches (p = 0.002). Migraines mostly started before MS onset (p = 0.023). Migraine with aura was associated with older age, longer disease duration (p = 0.028), and lower SDMT (p = 0.002). Longer DMT time was associated with migraine (p = 0.047), particularly migraine with aura (p = 0.035). Typical for migraine with aura were headaches during clinical isolated syndrome (CIS) (p = 0.001) and relapses (p = 0.025). Age and type of CIS, oligoclonal band presence, family MS history, EDSS, 9HTP, T25FW, and type of DMT did not correlate with headache. Headaches are present in more than half of MS patients treated with DMTs; migraines occur almost three times more frequently than tension-type headaches. Migraines with aura headaches during CIS and relapses are typical. Migraine in MS patients had high severity and typical migraine characteristics. DMTs had no correlation with the presence or type of headache.
 BACKGROUND: TNF-dependent synaptotoxicity contributes to the neuronal damage occurring in patients with Multiple Sclerosis (pwMS) and its mouse model Experimental Autoimmune Encephalomyelitis (EAE). Here, we investigated miR-142-3p, a synaptotoxic microRNA induced by inflammation in EAE and MS, as a potential downstream effector of TNF signalling. METHODS: Electrophysiological recordings, supported by molecular, biochemical and histochemical analyses, were performed to explore TNF-synaptotoxicity in the striatum of EAE and healthy mice. MiR-142 heterozygous (miR-142 HE) mice and/or LNA-anti miR-142-3p strategy were used to verify the TNF-miR-142-3p axis hypothesis. The cerebrospinal fluid (CSF) of 151 pwMS was analysed to evaluate possible correlation between TNF and miR-142-3p levels and their impact on clinical parameters (e.g. progression index (PI), age-related clinical severity (gARMSS)) and MRI measurements at diagnosis (T0). RESULTS: High levels of TNF and miR-142-3p were detected in both EAE striatum and MS-CSF. The TNF-dependent glutamatergic alterations were prevented in the inflamed striatum of EAE miR-142 HE mice. Accordingly, TNF was ineffective in healthy striatal slices incubated with LNA-anti miR- 142-3p. However, both preclinical and clinical data did not validate the TNF-miR-142-3p axis hypothesis, suggesting a permissive neuronal role of miR-142-3p on TNF-signalling. Clinical data showed a negative impact of each molecule on disease course and/or brain lesions and unveiled that their high levels exert a detrimental synergistic effect on disease activity, PI and white matter lesion volume. CONCLUSION: We propose miR-142-3p as a critical modulator of TNF-mediated neuronal toxicity and suggest a detrimental synergistic action of these molecules on MS pathology.
 INTRODUCTION: Interferon beta (IFN beta) preparations are an established group of drugs used for immunomodulation in patients with multiple sclerosis (MS). Subcutaneously (sc) applied interferon beta-1a (IFN beta-1a sc) has been in continuous clinical use for 25 years as a disease-modifying treatment. AREAS COVERED: Based on data published since 2018, we discuss recent insights from analyses of the pivotal trial PRISMS and its long-term extension as well as from newer randomized studies with IFN beta-1a sc as the reference treatment, the use of IFN beta-1a sc across the patient life span and as a bridging therapy, recent data regarding the mechanisms of action, and potential benefits of IFN beta-1a sc regarding vaccine responses. EXPERT OPINION: IFN beta-1a sc paved the way to effective immunomodulatory treatment of MS, enabled meaningful insights into the disease process, and remains a valid therapeutic option in selected vulnerable MS patient groups.
 BACKGROUND: Thalamic volume (TV) is a sensitive biomarker of disease burden of injury in multiple sclerosis (MS) and appears to reflect overall lesion loads. Ibudilast showed significant treatment effect on brain atrophy and magnetization transfer ratio (MTR) of normal-appearing brain tissue but not in new/enlarging T2 lesion in the SPRINT-MS randomized clinical trial. OBJECTIVE: To evaluate the effect of ibudilast on thalamic tissue integrity and volume in the SPRINT-MS. METHODS: A total of 255 participants with progressive MS were randomized to oral ibudilast or placebo, and thalamic MTR and normalized TV over 96 weeks were quantified. Mixed-effect modeling assessed treatment effects on the thalamic MTR and TV, separately. Similarly, the measures were compared between the participants with confirmed disability progression (CDP). RESULTS: Ibudilast's treatment effect was observed compared to placebo for thalamic MTR (p = 0.03) but not for TV (p = 0.68) while TV correlated with T2 lesion volume (p < 0.001). CDP associated with thalamic MTR (p = 0.04) but not with TV (p = 0.7). CONCLUSION: Ibudilast showed an effect on thalamic MTR, which was associated with CDP, suggesting a clinically relevant effect on thalamic tissue integrity. However, the treatment effect was not observed in TV, suggesting that thalamic atrophy is more closely associated with global inflammatory activity than local tissue integrity. CLINICALTRIALS.GOV: NCT01982942.
 BACKGROUND: We investigated sex-related differences in upper limb motor performance tested with the 9-Hole Peg Test (9HPT) in healthy controls (HC) and multiple sclerosis (MS) patients and their MRI substrates. MATERIALS AND METHODS: We enrolled 94 HC and 133 MS patients, who underwent neurological examination, 9HPT and brain 3T MRI, with sequences for regional grey matter volume (GMV), white matter (WM) fractional anisotropy (FA) and resting state (RS) functional connectivity (FC) analysis. Associations between MRI variables and 9HPT performance were analyzed with general linear models. RESULTS: 9HPT performance was better in HC vs MS patients, and in female vs male HC. Regional GMV analysis showed: associations between better 9HPT performance and higher GMV in motor and cognitive cortical areas in HC, with stronger positive correlations in females vs males. In MS, worse 9HPT performance correlated with lower volume in motor and cognitive areas. Sex-related differences were minimal and mostly found in cerebellar areas. WM FA analysis disclosed neither associations with 9HPT performance in HC, nor sex-related differences in MS. RS FC analysis showed: in the sensorimotor network, stronger associations of RS FC with 9HPT performance in female vs male HC and no sex-related differences in MS; in the cerebellar network, no sex-related differences in HC but stronger negative correlation in left cerebellum in male vs female MS patients. CONCLUSIONS: Sex influences 9HPT performance in HC, mainly through differences in volume and RS FC of motor and cognitive areas. Sex-related effects on motor performance become secondary but still present in MS.
 BACKGROUND: The research involving vascular comorbidity in people with multiple sclerosis (MS) could be advanced through investigations applying measurements of vascular function such as pulse wave velocity or flow mediated dilation as mechanistic endpoints in the study of physical comorbidity management in MS across the lifespan. We conducted a scoping review of research on vascular function parameters and outcomes in MS and developed a research agenda for future inquiry. METHODS: We searched PubMed from inception through February 2023 for articles involving relevant central and peripheral vascular function data or correlates of vascular function (arterial stiffness, endothelial function, blood pressure parameters, etc.) in conjunction with relevant outcomes (walking function, cognition, etc.) in MS. Studies were limited to English-language and primary research articles. RESULTS: Our search and subsequent screening identified 10 relevant articles. Four papers focused on arterial stiffness and reported pulse wave velocity and arterial compliance in MS compared with controls. Two papers focused on endothelial function and reported flow-mediated dilation in MS compared with controls. There was evidence that arterial stiffness and endothelial function were associated with cognition and disease progression in MS, respectively. One paper reported that physical activity was associated with arterial stiffness in MS. There was one protocol paper examining the effect of a home-based exercise program on markers of subclinical atherosclerosis; however, the results are unpublished, and there was no literature beyond this surrounding the impact of lifestyle behavior (e.g., diet) or exercise interventions on vascular function. CONCLUSION: There is emerging evidence for vascular dysfunction in MS, and this is associated with cognition and disease progression; we know very little about approaches for managing vascular dysfunction in MS. To that end, we offer an agenda for research on measurements and outcomes of vascular function in relation to MS and disease attributes, along with proposed mechanisms and lifestyle changes that could aid in managing vascular dysfunction.
 BACKGROUND: Patients with multiple sclerosis (MS) frequently switch their Disease-Modifying Agents (DMA) for effectiveness and safety concerns. This study aimed to develop and compare the random forest (RF) machine learning (ML) model with the logistic regression (LR) model for predicting DMA switching among MS patients. METHODS: This retrospective longitudinal study used the TriNetX data from a federated electronic medical records (EMR) network. Between September 2010 and May 2017, adults (aged ≥18) MS patients with ≥1 DMA prescription were identified, and the earliest DMA date was assigned as the index date. Patients prescribed any DMAs different from their index DMAs were considered as treatment switch. . The RF and LR models were built with 72 baseline characteristics and trained with 70% of the randomly split data after up-sampling. Area Under the Curves (AUC), accuracy, recall, G-measure, and F-1 score were used to evaluate the model performance. RESULTS: In this study, 7258 MS patients with ≥1 DMA were identified. Within two years, 16% of MS patients switched to a different DMA. The RF model obtained significantly better discrimination than the LR model (AUC = 0.65 vs. 0.63, p < 0.0001); however, the RF model had a similar predictive performance to the LR model with respect to F- and G-measures (RF: 72% and 73% vs. LR: 72% and 73%, respectively). The most influential features identified from the RF model were age, type of index medication, and year of index. CONCLUSIONS: Compared to the LR model, RF performed better in predicting DMA switch in MS patients based on AUC measures; however, judged by F- and G-measures, the RF model performed similarly to LR. Further research is needed to understand the role of ML techniques in predicting treatment outcomes for the decision-making process to achieve optimal treatment goals.
 BACKGROUND: Low vitamin D levels may synergize with changing levels of the vitamin D binding protein (DBP) to precipitate in the development and clinical progression of multiple sclerosis (MS). In this study, this hypothesis was explored in groups of Kuwaiti healthy controls and patients with different clinical phenotypes of MS. METHODS: Fasting serum concentrations of 25-hydroxyvitamin D [25(OH)D] and DBP were measured in 146 healthy controls and 195 patients with MS. The latter were classified according to the duration, type, and onset of the disease and the mode of treatment. Factors such as relapse/remitting, and the use of nutritional supplements were also considered. RESULTS: The DBP levels were significantly lower in the patients than in the controls. This was more evident in newly diagnosed drug-naïve patients than in those patients with more established MS. MS status and severity were negatively impacted by concurrently low levels of 25(OH)D and DBP. This was most clearly expressed in drug-naïve patients and in those with a disease in relapse. It was also established that the 25(OH)D level had a significant positive correlation with the duration of the disease. CONCLUSION: Lower levels of 25(OH)D and DBP appear to have a synergistic effect on MS status. This was most clearly demonstrated in patients who were newly diagnosed (drug-naïve) and in those patients who were in relapse.
 BACKGROUND: Toxoplasma gondii, an obligate intracellular parasite, is prevalent in various mammalian species, as well as certain avian, reptilian, and cold-blooded organisms. While immunocompetent individuals generally remain asymptomatic, immunocompromised individuals may experience severe and life-threatening conditions. Multiple sclerosis (MS), a chronic autoimmune disease affecting the central nervous system (CNS), is characterized by inflammation, demyelination, and axonal damage. Despite extensive research, the etiology and pathogenesis of MS remain incompletely understood. Given the strong affinity of T. gondii for the CNS, researchers have explored the potential association between T. gondii and autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes, and MS. This study aimed to investigate the possible relationship between MS and T. gondii. METHODS: A population-based incident cohort of MS patients in Sivas, Turkey, was used to randomly select MS patients. Age- and sex-matched controls were also randomly selected from the general population. A total of 182 MS patients and 182 controls were included in the study. Clinical and socio-demographic variables were recorded using a structured questionnaire. Blood samples were collected from MS patients, and Toxoplasma IgG and IgM antibodies were measured using the enzyme-linked immunosorbent assay technique. RESULTS: Anti-Toxoplasma IgG antibodies were detected in 78 cases (42.9%) and 73 controls (40.1%) (p>0.05). Age, female sex, and consumption of raw meat were identified as risk factors for toxoplasmosis in both MS patients and controls. CONCLUSION: In contrast to previous studies, this study did not find a significant difference in T. gondii seropositivity between the control group and MS patients. Further investigations are recommended to elucidate the precise relationship between MS patients and T. gondii.
 BACKGROUND: Little is known about the prevalence and clinical characteristics of tremors in patients with multiple sclerosis (MS), their associated clinical disability, and their impact on quality of life (QoL). OBJECTIVE: This study aimed to investigate the frequency and types of tremors in patients with relapsing remitting MS (RRMS) in remission, and their impact on patients' QoL. METHODS: A total of 250 patients with RRMS in remission were examined for tremors. All patients were assessed using the Expanded Disability Status Scale (EDSS). Patients with tremors underwent further assessment using the Fahn-Tolosa-Marin Tremor Rating Scale (FTMTRS), the Beck Depression Inventory (BDI), the Montreal Cognitive Assessment (MoCA) scale, and the Short Form 36 Health Survey Questionnaire (SF-36). Brain MRI was obtained for a subgroup of patients. RESULTS: Tremors were detected in 36 patients (14.4%) and were associated with significantly worse EDSS scores, BDI (P = 0.021), MoCA, most SF-36 domains, higher total and last year relapses (P < 0.001) and longer disease duration (P = 0.027). Patients with tremors showed higher lesion load (P = 0.007), more infratentorial (P ≤ 0.001), cerebellar and diencephalic lesions (P = 0.024), and cortical atrophy (P = 0.012). Total FTMTRS was significantly correlated to age, EDSS, and physical functioning. Dystonia was associated with tremors in 17 patients (6.8% of total RRMS patients and 47.2% of patients with tremors). CONCLUSION: The current study confirms the common occurrence of tremors and their subtypes among patients with RRMS with mild disability and demonstrates their association with increased disability and impaired QoL.
 INTRODUCTION: Mortality is an important feature of the natural history of multiple sclerosis (MS). We report the mortality of all individuals with MS in Iceland, identified in a nationwide population-based study. PATIENTS AND METHODS: The results are based on a prevalence cohort and an incidence cohort. The prevalence cohort consisted of all patients with MS (n = 526) living in Iceland on the 31 December 2007. The incidence cohort consisted of all residents of Iceland (n = 222) diagnosed with MS during 2002 to 2007. Mortality was determined by following both the incidence cohort (from diagnosis) and the prevalence cohort (from the prevalence day) until death or 31 December 2020. The mortality, associated with MS, was compared with that expected in the Icelandic population (standardized mortality ratio (SMR)). RESULTS: (a) Prevalence cohort (n = 526). The mean follow up was 12.0 years (range 0.3-13.0). The SMR was 1.6 (95% confidence interval (CI) 1.3-2.0). (b) Incidence cohort (n = 222). The mean follow up was 15.4 years (range 3.7-18.5). The SMR was 1.2 (95% CI 0.6-2.2). CONCLUSION: During the follow-up period, there was a substantial increase in mortality among the patients with MS, compared with the general population. There was no increase in mortality among the incidence cohort, when followed for up to 18.5 years following diagnosis.
 INTRODUCTION: Conventional MRI is routinely used for the characterization of pathological changes in multiple sclerosis (MS), but due to its lack of specificity is unable to provide accurate prognoses, explain disease heterogeneity and reconcile the gap between observed clinical symptoms and radiological evidence. Quantitative MRI provides measures of physiological abnormalities, otherwise invisible to conventional MRI, that correlate with MS severity. Analyzing quantitative MRI measures through machine learning techniques has been shown to improve the understanding of the underlying disease by better delineating its alteration patterns. METHODS: In this retrospective study, a cohort of healthy controls (HC) and MS patients with different subtypes, followed up 15 years from clinically isolated syndrome (CIS), was analyzed to produce a multi-modal set of quantitative MRI features encompassing relaxometry, microstructure, sodium ion concentration, and tissue volumetry. Random forest classifiers were used to train a model able to discriminate between HC, CIS, relapsing remitting (RR) and secondary progressive (SP) MS patients based on these features and, for each classification task, to identify the relative contribution of each MRI-derived tissue property to the classification task itself. RESULTS AND DISCUSSION: Average classification accuracy scores of 99 and 95% were obtained when discriminating HC and CIS vs. SP, respectively; 82 and 83% for HC and CIS vs. RR; 76% for RR vs. SP, and 79% for HC vs. CIS. Different patterns of alterations were observed for each classification task, offering key insights in the understanding of MS phenotypes pathophysiology: atrophy and relaxometry emerged particularly in the classification of HC and CIS vs. MS, relaxometry within lesions in RR vs. SP, sodium ion concentration in HC vs. CIS, and microstructural alterations were involved across all tasks.
 BACKGROUND: Caring for patients with multiple sclerosis (MS) imposes a great burden on caregivers and affects their lives in various aspects. This study aimed to evaluate the psychometric properties of Persian version of 22-item Zarit Burden Interview (ZBI-22) among family caregivers of patients with MS. METHODS: This methodological study was conducted in Fars province, southern of Iran. For this purpose, 120 family caregivers were recruited to participate in the study from January to March 2022. Zarit Burden Interview (ZBI) was translated into Persian through forward-backward method. Face and content validity were assessed. Construct validity was assessed using exploratory factor analyses (EFA), and its reliability was assessed by measuring internal consistency and testretest stability. RESULTS: According to face validity, the impact scores of all items were more than 1.5. Content validity ratio and content validity index values of all 22 items were 0.64-1 and 0.82-1, respectively. The scalelevel CVI/Ave was 0.97. Based on the results of factor analysis, five factors with eigenvalues more than 1 were extracted, which altogether explained 62.62% of the total variance of ZBI score. Among 22 items, one item was deleted during EFA validity assessment. Factor loading values ranged from 0.40 to 0.88. The reliability of the scale was confirmed (total Cronbach's alpha of the ZBI = 0.88). Moreover, testretest stability assessment revealed no significant difference between test and retest scores (P > 0.05). The intraclass correlation (ICC) for the ZBI and ICCs among its factors were 0.88 and 0.6-0.86, respectively. CONCLUSION: The Persian version of five-factor structure ZBI can be a valid and reliable scale, and it can be used to assess caregiver burden among family caregivers of patients with MS in Iran.
 INTRODUCTION: Although many lesion-based MRI biomarkers in multiple sclerosis (MS) patients were investigated, none of the previous studies dealt with the signal intensity variations (SIVs) of MS lesions. In this study, the SIVs of MS lesions on direct myelin imaging and standard clinical sequences as possible MRI biomarkers for disability in MS patients were assessed. METHODS: Twenty seven MS patients were included in this prospective study. IR-UTE, FLAIR, and MPRAGE sequences were employed on a 3T scanner. Regions of interest (ROIs) were manually drawn within the MS lesions, and the cerebrospinal fluid (CSF) and signal intensity ratios (SIR) were calculated from the derived values. Variations coefficients were determined from the standard deviations (Coeff 1) and the absolute differences (Coeff 2) of the SIRs. Disability grade was assessed by the expanded disability status scale (EDSS). Cortical/gray matter, subcortical, infratentorial, and spinal lesions were excluded. RESULTS: The mean diameter of the lesions was 7.8 ± 1.97 mm, while the mean EDSS score was 4.5 ± 1.73. We found moderate correlations between the EDSS and Coeff 1 and 2 on IR-UTE and MPRAGE images. Accordingly, Pearson's correlations on IR-UTE were R = 0.51 (p = 0.007) and R = 0.49 (p = 0.01) for Coeff 1 and 2, respectively. For MPRAGE, Pearson's correlations were R = 0.5 (p = 0.008) and R = 0.48 (p = 0.012) for Coeff 1 and 2, respectively. For FLAIR, only poor correlations could be found. CONCLUSION: The SIVs of MS lesions on IR-UTE and MPRAGE images, assessed by Coeff 1 and 2, could be used as novel potential MRI biomarkers for patients' disability.
 OBJECTIVE: The literature that has examined healthcare access and needs of the multiple sclerosis (MS) population is limited. Currently, no research has engaged healthcare providers delivering services to this population to examine their perspectives on the provision of MS care in Canada. We aimed to summarize what good MS care should look like according to Canadian healthcare providers working with people with MS, and to identify the supports and resources required, within their care setting, to enable this standard of care. METHODS: A qualitative descriptive approach was taken to analyze data from participants who responded to additional open-ended survey questions, within a larger "MS Models of Care Survey" targeting Canadian healthcare providers working with persons with MS. RESULTS: Currently, a gap exists between what healthcare providers working with persons with MS believe MS care should encompass and what they are able to offer. Participants emphasized that their MS clinics are currently understaffed and patient-to-provider ratios are high, leaving very little time to address the array of healthcare concerns their patients present with. The healthcare providers overwhelmingly described that moving toward multidisciplinary team-based MS care that includes appropriate numbers of MS-trained neurologists, nurses, physiotherapists, occupational therapists, and mental health providers working within one location would be their prioritized approach to comprehensively managing MS care. This model of care enables all professionals to effectively coordinate care and use their time efficiently by only focusing on their area of expertise, all while meeting the needs of their patient in one setting, reducing wait-times and improving overall care. CONCLUSION: To meet the care needs of Canadians with MS, the healthcare system must consider standardizing and funding multidisciplinary team-based MS clinics, comparable to Stroke units, which continue to show favorable health outcomes after years of implementation.
 BACKGROUND: Consumer-grade fitness trackers offer exciting opportunities to study persons with chronic diseases in greater detail and in their daily-life environment. However, attempts to bring fitness tracker measurement campaigns from tightly controlled clinical environments to home settings are often challenged by deteriorating study compliance or by organizational and resource limitations. OBJECTIVES: By revisiting the study design and patient-reported experiences of a partly remote study with fitness trackers (BarKA-MS study), we aimed to qualitatively explore the relationship between overall study compliance and scalability. On that account, we aimed to derive lessons learned on strengths, weaknesses, and technical challenges for the conduct of future studies. METHODS: The two-phased BarKA-MS study employed Fitbit Inspire HR and electronic surveys to monitor physical activity in 45 people with multiple sclerosis in a rehabilitation setting and in their natural surroundings at home for up to 8 weeks. We examined and quantified the recruitment and compliance in terms of questionnaire completion and device wear time. Furthermore, we qualitatively evaluated experiences with devices according to participants' survey-collected reports. Finally, we reviewed the BarKA-MS study conduct characteristics for its scalability according to the Intervention Scalability Assessment Tool checklist. RESULTS: Weekly electronic surveys completion reached 96%. On average, the Fitbit data revealed 99% and 97% valid wear days at the rehabilitation clinic and in the home setting, respectively. Positive experiences with the device were predominant: only 17% of the feedbacks had a negative connotation, mostly pertaining to perceived measurement inaccuracies. Twenty-five major topics and study characteristics relating to compliance were identified. They broadly fell into the three categories: "effectiveness of support measures", "recruitment and compliance barriers", and "technical challenges". The scalability assessment revealed that the highly individualized support measures, which contributed greatly to the high study compliance, may face substantial scalability challenges due to the strong human involvement and limited potential for standardization. CONCLUSION: The personal interactions and highly individualized participant support positively influenced study compliance and retention. But the major human involvement in these support actions will pose scalability challenges due to resource limitations. Study conductors should anticipate this potential compliance-scalability trade-off already in the design phase.
 OBJECTIVE: To determine the clinical and MRI characteristics of multiple sclerosis (MS) in the children and adolescents. MATERIAL & METHODS: In this cross-sectional study, information of 95 MS patients was obtained from the Iranian MS registry. Disease characteristics and imaging data were collected using medical records. RESULTS: Ninety-five patients including 64 female and 31 male subjects with mean age of 13.97±2.4 years (range, 8-18) years were enrolled. The most frequent signs and symptoms were ophthalmic symptoms (n=61, 64.2%), brainstem signs (n=44, 46.3%), cerebellar signs (n=32, 33.6%) and pyramidal signs (n=26, 27.3%). Blurred vision (n=21, 34.4%) was the most common ophthalmic symptom and ataxia (n=24, 75%) the most prevalent cerebellar sign. The most common brainstem signs/symptoms were motor symptoms and vertigo (each n=14, 31.8%) and the most common pyramidal sign/symptom was right upper monoparesis (n=14, 23.3%). Active demyelinating lesions were reported in brain MRI of all patients, mostly appeared as periventricular (n=91, 95.8%) and pericallosal (n=55, 57.9%) lesions. Acute demyelinating spinal lesions were presented in 38 patients (51.3%) with a prominent involvement of the cervical spine (n=33, 86.8%). CONCLUSION: In our study, the most frequent signs and symptoms were eye symptoms, brainstem signs, cerebellar signs and pyramidal signs, respectively. Moreover, our results showed that MRI plays a critical role in the diagnostic evaluation of MS in children with presence of brain lesions in all patients and spinal lesion in a considerable portion of patients.
 BACKGROUND: People with multiple sclerosis (MS) are living longer but not necessarily better lives, and this portends reduced health-related quality of life (HRQOL). Physical activity (PA) may be a correlate of HRQOL for people with MS. We examined differences in HRQOL and PA between older adults with and without MS to determine whether PA is associated with HRQOL and whether it accounts for group differences in HRQOL. METHODS: Thirty-one older adults with MS and 30 age- and sex-matched controls without MS completed the 36-Item Short Form Health Survey (SF-36) and the Godin Leisure-Time Exercise Questionnaire (GLTEQ). Data were analyzed using the Baron and Kenny approach for examining PA via the GLTEQ as a mediator of group differences in HRQOL. RESULTS: The MS group had significantly lower component scores on the SF-36 and the GLTEQ than the control group. The GLTEQ scores were correlated with SF-36 physical component scores (r = 0.52), whereas the correlation with mental component scores (r = 0.23) was small and nonsignificant. Group assignment initially explained 31% of the variance in physical component scores (β = 0.55) and adding GLTEQ to the model accounted for an additional 12% of the variance in physical component scores. Thus, group (β = 0.42) and GLTEQ (β = 0.37) were both significant correlates of physical component scores. The group effect was modestly attenuated with the addition of GLTEQ in step 2 (step 1 β = 0.55; step 2 β = 0.42) and indicated partial rather than full mediation. CONCLUSIONS: These results provide cross-sectional support for future research examining approaches to increase PA to possibly improve the physical component of HRQOL in older adults with MS.
 We conducted a retrospective analysis on multiple sclerosis (MS) patients with perceived cognitive decline and long disease duration to investigate early predictors of future cognitive impairment (CI) and motor disability. Sixty-five patients complaining of cognitive decline were assessed with an extensive neuropsychological battery at the last clinical follow-up and classified as mildly impaired, severely impaired, and cognitively spared based on the results. Motor disability was assessed with EDSS, MSSS, and ARMSS. Baseline demographic, clinical, and imaging parameters were retrospectively collected and inserted in separate multivariate regression models to investigate the predictive power of future impairment. Twenty-one patients (32.3%) showed no CI, seventeen (26.2%) showed mild CI, and twenty-seven (41.5%) showed severe CI. Older and less educated patients with higher EDSS, longer disease duration, and higher white matter lesion load (WMLL) at diagnosis (particularly with cerebellar involvement) were more likely to develop CI after a mean follow-up from diagnosis of 16.5 ± 6.9 years. DMT exposure was protective. The multivariate regression analyses confirmed WMLL, disease duration, and educational levels as the parameters with significant predictive value for future CI (R2 adjusted: 0.338 p: 0.001). Older patients with progressive phenotype both at diagnosis and T1 were more likely to be not fully ambulatory at T1 (R2 adjusted: 0.796 p: 0.0001). Our results further expand knowledge on early predictors of cognitive decline and evolution over time.
 OBJECTIVES: While patients with concomitant trigeminal neuralgia (TN) and multiple sclerosis (MS) are understood to experience a more intractable pain phenotype, whether TN pain outcomes differ by the presenting MS subtype is not well characterized. This study's objective is to compare post-operative pain and numbness outcomes following microvascular decompression (MVD) in TN patients with either relapsing-remitting MS (RRMS) or progressive MS. METHODS: We retrospectively reviewed all TN patients who underwent MVDs at our institution from 2007 to 2020. Of the 1044 patients reviewed, 45 (4.3%) patients with MS were identified. Patient demographics, procedural characteristics, and post-operative pain and numbness scores were recorded and compared. Factors associated with pain recurrence were assessed using survival analyses and multivariate regressions. RESULTS: Of the resulting 45 MS patients, 34 (75.6%) patients presented with the RRMS subtype, whereas 11 (24.4%) patients exhibited progressive MS. Using an adjusted multivariate ordinal regression, the subtype of MS was not significantly associated with the Barrow Neurological Institute (BNI) pain score at final follow-up. Using a Kaplan-Meier survival analysis and a multivariate Cox proportional hazards regression, respectively, RRMS was significantly associated with a shorter post-operative pain-free interval (p = 0.04) as well as a greater risk for pain recurrence (p = 0.02). CONCLUSIONS: Although the degree of pain at final follow-up may not differ, RRMS patients are at increased risk for pain recurrence following MVD for TN. These results align with a growing understanding that neuroinflammation may play a significant role in TN pain.
 INTRODUCTION: Understanding alterations to brain anatomy and cognitive function associated with neurodegenerative diseases remains a challenge for neuroscience today. In experimental neuroscience, several computerised tests have been developed to contribute to our understanding of neural networks involved in cognition. The Attention Network Test (ANT) enables us to measure the activity of 3 attentional networks (alertness, orienting, and executive function). OBJECTIVES: The main aim of this review is to describe all the anatomical and functional alterations found in diverse neurological diseases using the ANT. MATERIAL AND METHODS: We collected studies published since 2010 in the PubMed database that employed the ANT in different neurological diseases. Thirty-two articles were obtained, addressing multiple sclerosis, epilepsy, and Parkinson's disease, among other disorders. CONCLUSIONS: Some of the anatomical structures proposed in the 3 attentional networks model were confirmed. The most relevant structures in the alertness network are the prefrontal cortex, parietal region, thalamus, and cerebellum. The thalamus is also relevant in the orienting network, together with posterior parietal regions. The executive network does not depend exclusively on the prefrontal cortex and anterior cingulate cortex, but also involves such subcortical structures as the basal ganglia and cerebellum and their projections towards the entire cortex.
 This chapter describes ex vivo isolation of human T cells and of naïve splenocytes respectively collected from multiple sclerosis patients and healthy controls and experimental autoimmune encephalomyelitis-affected mice. After the magnetic sorting of naïve and activated T helper lymphocytes, we provide details about the cell cultures to measure the interaction with extracellular matrix proteins using standard cell invasion or hand-made in vitro assays, upon different stimuli, through Toll-like receptor(s) ligands, T-cell activators, and cell adhesion molecules modulators. Finally, we describe the methods to harvest and recover T cells to evaluate the properties associated with their trafficking ability.
 High carrier prevalence of STAT3 SH2 domain somatic mutations was recently discovered in CD8+ T cells. We found these low-allele-fraction clones in 26% of donors, without difference between multiple sclerosis (MS) patients and controls. Here we tested whether anti-viral antibodies associate with the carriership of these mutant clones. We compared antibody responses against common viruses in mutation carriers vs. non-carriers. Plasma samples of 152 donors (92 MS patients, 60 controls) were analyzed for antibodies against cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus-6A and parvovirus B19. The mutation carrier status associated with EBV VCA IgG level (p = 0.005) and remained significant after logistic regression (p = 0.036). This association was contributed similarly by MS patients and controls. These results suggest that EBV contributes to the generation or growth of these clones. The pathogenic role of the STAT3 mutant clones in MS is presently unclear, but their detailed characterization warrants further study.
 BACKGROUND AND OBJECTIVE: Fatigability is a distinct construct from fatigue that has been reported to contribute to activity limitations in people with multiple sclerosis (PwMS). Identifying predictors of performance and perceived fatigability may guide the development of interventions to mitigate fatigability. This study investigated predictors of performance and perceived fatigability among PwMS. METHODS: PwMS (N = 51) completed self-report measures of demographics, clinical history, symptoms severity (Modified Fatigue Impact Scale), and functioning (PROMIS Physical Function and PROMIS Cognitive Function Abilities). Performance fatigability measures included Ambulatory Fatigue Index (AFI), Deceleration Index (DI), and Distance Walking Index (DWI). Perceived fatigability measures included Pittsburgh Fatigability Scale (PFS), Perceived Physical Exertion, and Perceived Fatigue Intensity. Performance and perceived fatigability measures were calculated based on the Timed 25-Foot Walk Test and the 6-Minute Walk Test. RESULTS: Multivariable linear regression analyses indicated that PROMIS Cognitive Function was a significant independent predictor of performance fatigability measured with AFI (β = -0.515, p = 0.007), DI (β = -0.511, p = 0.008), and DWI (β = -0.516, p = 0.007). Regarding perceived fatigability, PROMIS Pain Intensity predicted Perceived Fatigue Intensity (β = 0.325, p = 0.035). PROMIS Physical Function predicted PFS Mental fatigability (β = -0.503, p < 0.001). PROMIS Physical Function (β = -0.619, p < 0.001) and Cognitive Function (β = -0.249, p = 0.037) predicted PFS Physical fatigability. CONCLUSIONS: Preliminary findings suggest that self-reported functioning levels, including physical and perceived cognitive function, are potential predictors of performance and perceived fatigability in MS. Notably, perceived fatigue impact showed no association with performance or perceived fatigability. Future studies are warranted to confirm and extend our findings.
 BACKGROUND: Successful translation of evidence-based exercise training interventions from research to clinical practice depends on the balance of treatment fidelity and adaptability when delivering the exercise program across settings. The current paper summarizes fidelity of study design, provider training, and intervention delivery strategies from best practice recommendations, and reports challenges experienced and adaptations instrumented by behavioral coaches delivering the multi-site Supervised versus Telerehabilitation Exercise Programs for Multiple Sclerosis (STEP for MS) Trial. METHODS: Using a reflexive thematic analysis approach, open-ended survey questions were analyzed to explore experiences of behavioral coaches, transcripts from team meetings among behavioral coaches, and notes from audits of one-on-one sessions between behavioral coaches and participants. RESULTS: Themes related to the fidelity of study design and delivery of the STEP for MS Trial included adaptations to the intervention itself (e.g., completion of virtual supervised exercise sessions with behavioral coaches in place of face-to-face sessions during COVID-19 pandemic restrictions), modification of exercise equipment, and adjustments of program delivery. The adjustments of program delivery reported by behavioral coaches included increasing program fit, maintaining engagement, and addressing participant safety concerns; however, these adaptations did not jeopardize the content of the essential elements of the program model. CONCLUSIONS: The current paper demonstrates that when best practice recommendations are implemented, it is possible to address challenges to study design and evidence-based intervention delivery in ways that adaptations to overcome real-world obstacles can be accomplished without compromising fidelity.
 Atrophy related to multiple sclerosis (MS) has been found at the early stages of the disease. However, the archetype dynamic trajectories of the neurodegenerative process, even prior to clinical diagnosis, remain unknown. We modeled the volumetric trajectories of brain structures across the entire lifespan using 40,944 subjects (38,295 healthy controls and 2649 MS patients). Then, we estimated the chronological progression of MS by assessing the divergence of lifespan trajectories between normal brain charts and MS brain charts. Chronologically, the first affected structure was the thalamus, then the putamen and the pallidum (around 4 years later), followed by the ventral diencephalon (around 7 years after thalamus) and finally the brainstem (around 9 years after thalamus). To a lesser extent, the anterior cingulate gyrus, insular cortex, occipital pole, caudate and hippocampus were impacted. Finally, the precuneus and accumbens nuclei exhibited a limited atrophy pattern. Subcortical atrophy was more pronounced than cortical atrophy. The thalamus was the most impacted structure with a very early divergence in life. Our experiments showed that lifespan models of most impacted structures could be an important tool for future preclinical/prodromal prognosis and monitoring of MS.
 BACKGROUND: Longitudinal studies of health-related quality of life (HRQoL) in multiple sclerosis (MS) are limited. Most have examined average changes within the population, rather than dynamic changes within individuals. OBJECTIVE: To assess the between- and within-individual association between depression, anxiety, fatigue, cognition, physical functioning, and physical comorbidities and HRQoL. METHODS: Adults with MS underwent physical and cognitive assessments and reported symptoms of fatigue (Daily Fatigue Impact Scale), depression and anxiety (Hospital Anxiety and Depression Scale (HADS)), and HRQoL (RAND-36) annually (n = 4 visits). We evaluated associations of elevated symptoms of anxiety (HADS-A) and depression (HADS-D), fatigue, physical function (timed-walk and nine-hole peg test), cognitive function and comorbidity count with physical (PCS-36) and mental (MCS-36) HRQoL using multivariable linear models-estimating between-person and within-person effects. RESULTS: Of 255 participants with MS enrolled, 81.6% were women. After adjustment, within-person increases in depression and fatigue were associated with decreases in physical HRQoL. Increases in depression, anxiety, and comorbidity count were associated with decreases in mental HRQoL. CONCLUSIONS: Within-person increases in symptoms of depression, anxiety and fatigue, and comorbidity count are associated with HRQoL decreases among adults with MS, highlighting the potential magnitude of individual benefit of intervention for these symptoms.
 According to current knowledge, the etiopathogenesis of multiple sclerosis (MS) is complex, involving genetic background as well as several environmental factors that result in dysimmunity in the central nervous system (CNS). MS is an immune-mediated, inflammatory neurological disease affecting the CNS. As part of its attack on the axons of the CNS, MS witnesses varying degrees of myelin and axonal loss. A total of about 20 disease-modifying therapies (DMTs) are available today that, both in clinical trials and in real-world studies, reduce disease activity, such as relapses, magnetic resonance imaging lesions, and disability accumulation. Currently, the world is facing an outbreak of the new coronavirus disease 2019 (COVID-19), which originated in Wuhan, Hubei Province, China, in December 2019 and spread rapidly around the globe. Viral infections play an important role in triggering and maintaining neuroinflammation through direct and indirect mechanisms. There is an old association between MS and viral infections. In the context of MS-related chronic inflammatory damage within the CNS, there has been concern regarding COVID-19 worsening neurological damage. A high rate of disability and increased susceptibility to infection have made MS patients particularly vulnerable. In addition, DMTs have been a concern during the pandemic since many DMTs have immunosuppressive properties. In this article, we discuss the impact of DMTs on COVID-19 risks and the effect of DMTs on COVID-19 vaccination efficacy and outcome in MS patients.
 Multiple sclerosis is a chronic demyelinating disease with different disease phenotypes. The current FDA-approved disease-modifying therapeutics (DMTs) cannot cure the disease, but only alleviate the disease progression. While the majority of patients respond well to treatment, some of them are suffering from rapid progression. Current drug delivery strategies include the oral, intravenous, subdermal, and intramuscular routes, so these drugs are delivered systemically, which is appropriate when the therapeutic targets are peripheral. However, the potential benefits may be diminished when these targets sequester behind the barriers of the central nervous system. Moreover, systemic drug administration is plagued with adverse effects, sometimes severe. In this context, it is prudent to consider other drug delivery strategies improving their accumulation in the brain, thus providing better prospects for patients with rapidly progressing disease course. These targeted drug delivery strategies may also reduce the severity of systemic adverse effects. Here, we discuss the possibilities and indications for reconsideration of drug delivery routes (especially for those "non-responding" patients) and the search for alternative drug delivery strategies. More targeted drug delivery strategies sometimes require quite invasive procedures, but the potential therapeutic benefits and reduction of adverse effects could outweigh the risks. We characterized the major FDA-approved DMTs focusing on their therapeutic mechanism and the potential benefits of improving the accumulation of these drugs in the brain.
 BACKGROUND: Remote ischemic conditioning (RIC), exposure of body parts to brief periods of circulatory occlusion and reperfusion, has been shown to improve cardiovascular responses to exercise in healthy individuals but its effects in people with MS are unknown. OBJECTIVE: This study aimed to assess the effect of RIC on heart rate responses to walking in people with MS. DESIGN: Double blind randomized controlled trial. SETTING: Multiple sclerosis clinic of tertiary care center teaching hospital in the United Kingdom. METHODS: Three cycles of RIC were delivered by occluding the upper arm with a blood pressure cuff inflated to a pressure of 30 mmHg above the systolic blood pressure. In the sham group, the blood pressure cuff was inflated to 30 mmHg below diastolic blood pressure. Heart rate responses to the 6-minute walk test (6MWT), the tolerability of RIC using a numerical rating scale for discomfort (0-10), and adverse events were studied. RESULTS: Seventy-five participants (RIC -38 and Sham-37) completed the study. RIC was well tolerated. Compared to sham, RIC significantly decreased the rise in heart rate (P = 0.04) and percentage of predicted maximum heart rate (P = 0.016) after the 6MWT. CONCLUSION: RIC was well tolerated and improved the heart rate response to walking in people with MS. Further studies on RIC in the management of MS are needed.
 BACKGROUND: People with moderate to severe multiple sclerosis (MS) and their family care partners do not engage in sufficient physical activity (PA) for health benefits. Dyadic PA interventions need to be developed to benefit each individual and the dyad. The objective of this study was to engage expert stakeholders in prioritizing and refining key intervention content, delivery methods, and the practical/logistical aspects of a dyadic PA intervention for persons with MS and their care partners. METHODS: Thirty-two stakeholders (14 clinicians, 11 people with MS, 5 MS care partners, and 2 representatives of organizations that provide support services for people with MS and/or MS care partners) completed 2 rounds of a modified e-Delphi survey. In round 1, participants rated items across 3 domains: key intervention content (n = 8), delivery methods (n = 9), and practical/logistical aspects (n = 4). Participants contributed additional ideas about these domains, which were incorporated into round 2. Items that did not reach consensus in round 1 were forwarded to round 2 for rerating. Data were analyzed using descriptive statistics and content analysis. RESULTS: A 24-item list of recommendations was generated, including ensuring that presentation of the intervention content encouraged lifestyle activities in addition to exercise, using videoconferencing rather than teleconferencing as a delivery platform, and stressing the importance of flexibility during the support calls. CONCLUSIONS: Feedback will be used to improve the quality of the intervention. The next step in this line of research involves evaluating the refined intervention in a pilot feasibility trial.
 The treatment strategy in relapsing multiple sclerosis (RMS) is a complex decision requiring individualization of treatment sequences to maximize clinical outcomes. Current local and international guidelines do not provide specific recommendation on the use of immune reconstitution therapy (IRT) as alternative to continuous immunosuppression in the management of RMS. The objective of the program was to provide consensus-based expert opinion on the optimal use of IRT in the management of RMS. A Delphi method was performed from May 2022 to July 2022. Nineteen clinical assertions were developed by a scientific committee and sent to 14 French clinical experts in MS alongside published literature. Two consecutive reproducible anonymous votes were conducted. Consensus on recommendations was achieved when more than 75% of the respondents agreed or disagreed with the clinical assertions. After the second round, consensus was achieved amongst 16 out of 19 propositions: 13 clinical assertions had a 100% consensus, 3 clinical assertions a consensus above 75% and 3 without consensus. Expert-agreed consensus is provided on topics related to the benefit of the early use of IRT from immunological and clinical perspectives, profiles of patients who may benefit most from the IRT strategy (e.g. patients with family planning, patient preference and lifestyle requirements). These French expert consensuses provide up-to-date relevant guidance on the use of IRT in clinical practice. The current program reflects status of knowledge in 2022 and should be updated in timely manner when further clinical data in IRT become available.
 Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system. Spontaneous restoration of myelin after demyelination occurs, but its efficiency declines during disease progression. Efficient myelin repair requires fine-tuning inflammatory responses by brain-resident microglia and infiltrating macrophages. Accordingly, promising therapeutic strategies aim at controlling inflammation to promote remyelination. Polysialic acid (polySia) is a polymeric glycan with variable chain lengths, presented as a posttranslational modification on select protein carriers. PolySia emerges as a negative regulator of inflammatory microglia and macrophage activation and has been detected on oligodendrocyte precursors and reactive astrocytes in multiple sclerosis lesions. As shown recently, polySia-modified proteins can also be released by activated microglia, and the intrinsically released protein-bound and exogenously applied free polySia were equally able to attenuate proinflammatory microglia activation via the inhibitory immune receptor Siglec-E. In this study, we explore polySia as a candidate substance for promoting myelin regeneration by immunomodulation. Lysophosphatidylcholine-induced demyelination of organotypic cerebellar slice cultures was used as an experimental model to analyze the impact of polySia with different degrees of polymerization (DP) on remyelination and inflammation. In lysophosphatidylcholine-treated cerebellar slice cultures, polySia-positive cells were abundant during demyelination but largely reduced during remyelination. Based on the determination of DP24 as the minimal polySia chain length required for the inhibition of inflammatory BV2 microglia activation, pools with short and long polySia chains (DP8-14 and DP24-30) were generated and applied to slice cultures during remyelination. Unlike DP8-14, treatment with DP24-30 significantly improved remyelination, increased arginase-1-positive microglia ratios, and reduced the production of nitric oxide in wildtype, but not in Siglec-E-deficient slice cultures. In vitro differentiation of oligodendrocytes was not affected by DP24-30. Collectively, these results suggest a beneficial effect of exogenously applied polySia DP24-30 on remyelination by Siglec-E-dependent microglia regulation.
 BACKGROUND: Apathy is common in multiple sclerosis (MS) and neurological disease, but its presence and underlying brain mechanisms in older adults with MS (OAMS) have not been evaluated. OBJECTIVE: Examine apathy and its association with caudate nuclei volume in OAMS and controls. We hypothesized that compared to controls, OAMS would demonstrate: a) greater apathy; b) stronger associations between apathy and caudate nuclei volumes. METHODS: OAMS (n = 67, mean age = 64.55 ± 3.89) and controls (n = 74, mean age = 69.04 ± 6.32) underwent brain MRI, cognitive assessment, psychological, and motoric testing. Apathy was assessed through the apathy subscale of the 30-item Geriatric Depression Scale. RESULTS: OAMS reported greater apathy compared to controls (β = 0.281, p = 0.004). Adjusted moderation analyses revealed a significantly stronger association between caudate volume and apathy (left: B = -1.156, p = 0.039, right: B = -1.163, p = 0.040) among OAMS compared to controls. Conditional effects revealed that in adjusted models, lower volume of both the left (b = -0.882, p = 0.037) and right (b = -0.891, p = 0.038) caudate nuclei was significantly associated with greater apathy only among OAMS. CONCLUSION: Caudate nuclei, which are susceptible to adverse MS effects and implicated in mediating cognitive and motor function, may influence the presence and severity of apathy in OAMS.
 Glatiramer acetate (GA) is a widely used immune-modulating drug in relapsing multiple sclerosis (MS). Although a few cases of drug-induced liver injury during GA therapy have been reported earlier, herein we present the case of a 43-year-old woman with relapsing MS who experienced acute liver failure after GA therapy, ultimately leading to liver transplant.
 INTRODUCTION: Different disease-modifying therapies (DMTs) have been developed to slow down the progression of pediatric multiple sclerosis (MS). Teriflunomide is one such DMT that has recently been approved for use in pediatric MS in the European Union. AREAS COVERED: The article provides an introduction to the mechanism of action of teriflunomide, reviews the clinical trials conducted on the safety and efficacy of the drug, and the optimal dosing and monitoring strategies. EXPERT OPINION: Teriflunomide is an oral medication that has shown promise in improving outcomes for pediatric MS patients, including reduced relapse rates and improved quality of life. However, more research is needed to determine its long-term safety in pediatric patients. As MS often presents with an aggressive course in children, the choice of disease-modifying treatment should be carefully evaluated, with a preference for second-line therapy. Despite the potential benefits of teriflunomide, changes in clinical practice may be hindered by factors such as cost and physician familiarity with alternative treatments. Longer-term studies and biomarker identification are areas for improvement, but the future of research in this area holds promise for the continued development and refinement of disease-modifying therapies and more personalized, targeted treatments for pediatric MS patients.
 Multiple sclerosis (MS) is a neuroinflammatory disease of the central nervous system (CNS). Although classically considered a demyelinating disease, neuroaxonal injury occurs in both the acute and chronic phases and represents a pathologic substrate of disability not targeted by current therapies. Nitric oxide (NO) generated by CNS macrophages and microglia contributes to neuroaxonal injury in all phases of MS, but candidate therapies that prevent NO-mediated injury have not been identified. Here, we demonstrate that the multifunctional protein glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is robustly nitrosylated in the CNS in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. GAPDH nitrosylation is blocked in vivo with daily administration of CGP3466b, a CNS-penetrant compound with an established safety profile in humans. Consistent with the known role of nitrosylated GAPDH (SNO-GAPDH) in neuronal cell death, blockade of SNO-GAPDH with CGP3466b attenuates neurologic disability and reduces axonal injury in EAE independent of effects on the immune system. Our findings suggest that SNO-GAPDH contributes to neuroaxonal injury during neuroinflammation and identify CGP3466b as a candidate neuroprotective therapy in MS.
 Drug development for multiple sclerosis (MS) clinical management focuses on both neuroprotection and repair strategies, and is challenging due to low permeability of the blood-brain barrier, off-target distribution, and the need for high doses of drugs. The changes in the extracellular matrix have been documented in MS patients. It has been shown that the expression of nidogen-1 increases in MS lesions. Laminin forms a stable complex with nidogen-1 through a heptapeptide which was selected to target the lesion area in this study. Here we showed that the peptide binding was specific to the injured area following lysophosphatidylcholine (LPC) induced demyelination. In vivo data showed enhanced delivery of the peptide-functionalized gold nanoparticles (Pep-GNPs) to the lesion area. In addition, Pep-GNPs administration significantly enhanced myelin content and reduced astrocyte/microglia activation. Results demonstrated the possibility of using this peptide to target and treat lesions in patients suffering from MS.
 BACKGROUND: Despite the 2017 revisions to the McDonald criteria, diagnosing primary progressive multiple sclerosis (PPMS) remains challenging. To improve clinical practice, we aimed to identify frequent diagnostic challenges in a real-world setting and associate these with the performance of the 2010 and 2017 PPMS diagnostic McDonald criteria. METHODS: We retrospectively recorded clinical, radiological and laboratory characteristics at time of diagnosis from designated PPMS patient files. Possible complicating factors were recorded such as confounding comorbidity, signs indicative of alternative diagnoses, possible earlier relapses, and/or incomplete diagnostic workup (no cerebrospinal fluid examination and/or MRI brain and spinal cord). We calculated the percentages of patients fulfilling the 2010 and 2017 McDonald criteria after censoring patients with these complicating factors. RESULTS: A total of 322 designated PPMS patients were included. Of all participants, we found that n=28/322 had confounding comorbidity and/or signs indicative of alternative diagnoses, n=103/294 had possible initial relapsing and/or uncertainly progressive phenotypes, and n=73/191 received an incomplete diagnostic work-up. When applying the 2010 and 2017 diagnostic PPMS McDonald criteria on n=118 cases with a full diagnostic workup and a primary progressive disease course without a better alternative explanation, these were met by 104/118 (88.1%) and 98/118 remaining patients (83.1%), respectively (p=0.15). CONCLUSION: Accurate interpretation of the initial clinical course, consideration of alternative diagnoses, and a full diagnostic workup are the cornerstones of a PPMS diagnosis. When these conditions are met, the 2010 and 2017 McDonald criteria for PPMS perform similarly, emphasizing the importance of their appropriate application in clinical practice.
 PURPOSE: Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory demyelinating lesions in the white matter of the central nervous system. Myocyte enhancer factor 2 (MEF2) family genes play important roles in the immune response. This study focuses on the relationship between MEF2 family gene polymorphisms and MS. METHODS: A total of 174 MS patients and 120 healthy controls were recruited. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to analyze the gene polymorphisms of MEF2D and MEF2C. In addition, peripheral blood was collected and leukocytes were isolated. The transcription level of MEF2D in the two groups of samples was detected with quantitative real time polymerase chain reaction (qRT-PCR). RESULTS: We found that the C allele frequency and CC genotype frequency of rs2274316 in MEF2D were significantly higher in MS patients. The C allele and CT genotype distribution for rs3790455 were significantly more frequent in MS patients. Female patients showed higher CC genotype frequency of rs2274316. The genotype frequency distribution of rs2274316 and rs3790455 were not related to onset age and phenotype of MS patients. In addition, this study also proved that MEF2D was significantly overexpressed in the peripheral blood leukocytes of MS patients. The transcription level of MEF2D was significantly higher in patients with CC genotype of rs2274316. CONCLUSION: These findings suggest rs2274316 and rs3790455 of MEF2D gene are potential genetic risk factors for MS in Chinese population. The transcription level of MEF2D is also associated with susceptibility to MS and MEF2D gene polymorphisms.
 PURPOSE: The macular ganglion cell layer (mGCL) is a strong potential biomarker of axonal degeneration in multiple sclerosis (MS). For this reason, this study aims to develop a computer-aided method to facilitate diagnosis and prognosis in MS. METHODS: This paper combines a cross-sectional study of 72 MS patients and 30 healthy control subjects for diagnosis and a 10-year longitudinal study of the same MS patients for the prediction of disability progression, during which the mGCL was measured using optical coherence tomography (OCT). Deep neural networks were used as an automatic classifier. RESULTS: For MS diagnosis, greatest accuracy (90.3%) was achieved using 17 features as inputs. The neural network architecture comprised the input layer, two hidden layers and the output layer with softmax activation. For the prediction of disability progression 8 years later, accuracy of 81.9% was achieved with a neural network comprising two hidden layers and 400 epochs. CONCLUSION: We present evidence that by applying deep learning techniques to clinical and mGCL thickness data it is possible to identify MS and predict the course of the disease. This approach potentially constitutes a non-invasive, low-cost, easy-to-implement and effective method.
 BACKGROUND: Percutaneous tibial nerve stimulation (PTNS) is widely used in the treatment of neurogenic detrusor overactivity (NDO) in multiple sclerosis (MS); however, controlled studies are still lacking.Objective:: To assess effectiveness of PTNS in MS patients with NDO unresponsive to pharmacological and behavioural therapies. METHODS: MS patients with NDO were enrolled. Inclusion criteria were NDO not responding to pharmacological and behavioural therapies. Exclusion criteria were the presence of relevant comorbidities and urinary tract infections. Patients were evaluated using 3-day bladder diaries and validated questionnaires at baseline, after 4 weeks of educational therapy and after 12 PTNS sessions. The primary outcome measure was the percentage of patients considered responders after the behavioural therapy and after the PTNS in a historical controlled fashion (definition of 'responder' was reduction ⩾50% of urgency episodes). RESULTS: A total of 33 patients (26 women, 7 men) were enrolled. Two patients dropped out for reasons not related to the protocol. Two out of 31 patients (6.5%) and 21/29 (72.4%) were considered responders at visits 1 and 2, respectively. In PTNS responders, a statistically significant improvement in both bladder diary results and standardized questionnaire scores was recorded, compared with that obtained with behavioural therapy alone. No serious adverse events were reported. CONCLUSION: This historically controlled study suggests that PTNS may be effective in improving NDO in MS patients.
 People with multiple sclerosis (PWMS) are at high risk of being affected by the disruption of health services that occurred during the COVID-19 pandemic months. The aim of this study was to evaluate the effect of the pandemic on the health outcomes of PWMS. PWMS and MS-free residing in Piedmont (north-west of Italy) were identified from electronic health records and linked with the regional COVID-19 database, the hospital-discharge database, and the population registry. Both cohorts (9333 PWMS and 4,145,856 MS-free persons) were followed-up for access to swab testing, hospitalisation, access to the Intensive Care Unit (ICU), and death from 22 February 2020 to 30 April 2021. The relationship between the outcomes and MS was evaluated using a logistic model, which was adjusted for potential confounders. The rate of swab testing was higher in PWMS, but the positivity to infection was similar to that of MS-free subjects. PWMS had a higher risk of hospitalisation (OR = 1.74; 95% IC, 1.41-2.14), admission to ICU (OR = 1.79; 95% IC, 1.17-2.72), and a slight, albeit not statistically significant, increase in mortality (OR = 1.28; 95% IC, 0.79-2.06). Compared to the general population PWMS with COVID-19 had an increased risk of hospitalization and admission to the ICU; the mortality rate did not differ.
 Relapsing-remitting multiple sclerosis (RRMS) is the most prevalent MS subtype. Ample evidence has indicated that long noncoding RNAs (lncRNAs) are crucial players in autoimmune and inflammatory disorders. This study investigated the expression of lnc-EGFR, SNHG1, and lincRNA-Cox2 in RRMS patients during active relapses and in remission. Additionally, the expression of FOXP3, a master transcription factor for regulatory T cells, and NLRP3-inflammasome-related genes were determined. Relationships between these parameters and MS activity and annualized relapse rate (ARR) were also evaluated. The study included 100 Egyptian participants: 70 RRMS patients (35 during relapse and 35 in remission) and 30 healthy controls. RRMS patients showed significant downregulation of lnc-EGFR and FOXP3 and dramatic upregulation of SNHG1, lincRNA-Cox2, NLRP3, ASC, and caspase-1 compared to controls. Lower serum TGF-β1 and elevated IL-1β levels were observed in RRMS patients. Notably, patients during relapses displayed more significant alterations than those in remission. Lnc-EGFR was positively correlated with FOXP3 and TGF-β1 and negatively correlated with ARR, SNHG1, lincRNA-Cox2, and NLRP3 inflammasome components. Meanwhile, SNHG1 and lincRNA-Cox2 were positively correlated with ARR, NLRP3, ASC, caspase-1, and IL-1β. Excellent diagnostic performance for lnc-EGFR, FOXP3, and TGF-β1 was demonstrated, while all biomarkers exhibited strong prognostic potential for predicting relapses. Finally, the differential expression of lnc-EGFR, SNHG1, and lincRNA-Cox2 in RRMS patients, especially during relapses, suggests their involvement in RRMS pathogenesis and activity. Correlation between their expression and ARR implies relationships to disease progression. Our findings also highlight their promising roles as biomarkers for RRMS.
 INTRODUCTION: Functional neurological symptoms (FNS) in multiple sclerosis (MS) have shown to be underinvestigated even though neurological diseases such as MS represent a risk factor for developing FNS. Comorbidity of FNS and MS can produce high personal and social costs since FNS patients have high healthcare utilization costs and a quality of life at least as impaired as in patients with disorders with underlying structural pathology. This study aims to assess comorbid FNS in patients with MS (pwMS) and investigate whether FNS in pwMS are associated with poorer health-related quality of life and work ability. METHODS: Newly admitted patients (234) with MS were studied during their stay at Kliniken Schmieder, a neurological rehabilitation clinic in Konstanz, Germany. The degree to which the overall clinical picture was explained by MS pathology was rated by neurologists and allied health practitioners on a five-point Likert scale. Additionally, neurologists rated each symptom reported by the patients. Health-related quality of life was assessed using a self-report questionnaire and work ability was assessed using the mean number of hours worked per day and information regarding disability pension as reported by patients. RESULTS: In 55.1% of cases, the clinical picture was completely explained by structural pathology due to MS. 17.1% of pwMS presented an overall clinical picture half or less of which could be explained by underlying structural pathology. PwMS with a higher comorbid FNS burden had a lower health-related quality of life and reported fewer working hours per day than pwMS with symptoms explained by structural pathology. Furthermore, pwMS with a full disability pension had a higher comorbid FNS burden than pwMS with no or partial disability pension. DISCUSSION: These results show that FNS should be addressed diagnostically and therapeutically since such symptoms are an important comorbidity in MS that is related to poorer health-related quality of life and lower work ability.
 PURPOSE: Brain MRI with high spatial resolution allows for a more detailed delineation of multiple sclerosis (MS) lesions. The recently developed deep learning-based reconstruction (DLR) technique enables image denoising with sharp edges and reduced artifacts, which improves the image quality of thin-slice 2D MRI. We, therefore, assessed the diagnostic value of 1 mm-slice-thickness 2D T2-weighted imaging (T2WI) with DLR (1 mm T2WI with DLR) compared with conventional MRI for identifying MS lesions. METHODS: Conventional MRI (5 mm T2WI, 2D and 3D fluid-attenuated inversion recovery) and 1 mm T2WI with DLR (imaging time: 7 minutes) were performed in 42 MS patients. For lesion detection, two neuroradiologists counted the MS lesions in two reading sessions (conventional MRI interpretation with 5 mm T2WI and MRI interpretations with 1 mm T2WI with DLR). The numbers of lesions per region category (cerebral hemisphere, basal ganglia, brain stem, cerebellar hemisphere) were then compared between the two reading sessions. RESULTS: For the detection of MS lesions by 2 neuroradiologists, the total number of detected MS lesions was significantly higher for MRI interpretation with 1 mm T2WI with DLR than for conventional MRI interpretation with 5 mm T2WI (765 lesions vs. 870 lesions at radiologist A, < 0.05). In particular, of the 33 lesions in the brain stem, radiologist A detected 21 (63.6%) additional lesions by 1 mm T2WI with DLR. CONCLUSION: Using the DLR technique, whole-brain 1 mm T2WI can be performed in about 7 minutes, which is feasible for routine clinical practice. MRI with 1 mm T2WI with DLR enabled increased MS lesion detection, particularly in the brain stem.
 INTRODUCTION: Multiple sclerosis (MS) is a progressive neurodegenerative disorder affecting motor and nonmotor function including physical and cognitive decline, fatigue, anxiety, and depression. Qigong is a mind-body self-care practice with the potential to address MS symptoms. Publicly available community qigong classes may provide opportunities for people with MS to access qigong, but little is known about the risks and benefits. A mixed methods study of community qigong was conducted for people with MS. In this article, the results of this qualitative analysis to identify benefits and challenges faced by people with MS attending community qigong classes were presented. METHODS: Qualitative data were collected from an exit survey of 14 study participants with MS who enrolled in a pragmatic trial of community qigong classes for 10 weeks. Participants were new to community-based classes offered but some had experience with qigong/tai chi/other martial arts or yoga. Data were analyzed using reflexive thematic analysis. RESULTS AND DISCUSSION: Seven common themes were identified from this analysis: (1) physical function, (2) motivation/energy, (3) learning, (4) dedicating time for self, (5) meditation/centering/focus, (6) relaxation/stress relief, and (7) psychological/psychosocial. These themes reflected both positive and negative experiences with community qigong classes and home practice. Self-reported benefits centered around improved flexibility, endurance, energy, and focus; stress relief; and psychological/psychosocial benefits. Challenges included physical discomfort including short-term pain, balance difficulty, and heat intolerance. CONCLUSION: The qualitative findings provide evidence to support qigong as a self-care practice that may benefit people with MS. The challenges identified in the study will help to inform future clinical trials of qigong for MS. TRIAL REGISTRATION: ClinicalTrials.gov (CTR#: NCT04585659).
 INTRODUCTION: Overactive bladder (OAB) is one of the most common complications in patients with multiple sclerosis (MS). Choosing the effective treatment is very important in improving their quality of life (QOL). Therefore, the aim of this study was to compare solifenacin (SS) and posterior tibial nerve stimulation (PTNS) treatment effects in the MS Patients with OAB. MATERIALS AND METHODS: In total, 70 MS patients suffering from OAB enrolled in this clinical trial study. Patients with a score of at least 3 according to the OAB questionnaire were randomly divided into two groups (35 patients in each group). In one group, patients received SS (5 mg daily for 4 weeks and 10 mg/day for another 8 weeks) and in a second group, patients were treated by PTNS (12 weekly session, 30 min). RESULTS: The mean (SD) age of patients participating in this study was 39.82 (9.088) and 42.41 (9.175) years for the SS group and the PTNS group, respectively. Patients in both groups showed statistically significant improvements in urinary incontinence, micturition, and daytime frequency (p < 0.001). Patients in the SS group had a better response for urinary incontinence after 12 weeks compared to the PTNS group. Also, patients in the SS group reported higher satisfaction and less daytime frequency compared to the PTNS group. CONCLUSION: SS and PTNS were effective for improving the OAB symptoms in patients with MS. However, patients demonstrated a better experience with SS in terms of daytime frequency, urinary incontinence, and treatment satisfaction rate.
 BACKGROUND: The imaging g-ratio, estimated from axonal volume fraction (AVF) and myelin volume fraction (MVF), is a novel biomarker of microstructural tissue integrity in multiple sclerosis (MS). OBJECTIVE: To assess axonal and myelin changes and their inter-relationship as measured by g-ratio in the optic radiations (OR) in people with MS (pwMS) with and without previous optic neuritis (ON) compared to healthy controls (HC). METHODS: Thirty pwMS and 17 HCs were scanned on a 3Tesla Connectom scanner. AVF and MVF, derived from a multi-shell diffusion protocol and macromolecular tissue volume, respectively, were measured in normal-appearing white matter (NAWM) and lesions within the OR and used to calculate imaging g-ratio. RESULTS: OR AVF and MVF were decreased in pwMS compared to HC, and in OR lesions compared to NAWM, whereas the g-ratio was not different. Compared to pwMS with previous ON, AVF and g-ratio tended to be higher in pwMS without prior ON. AVF and MVF, particularly in NAWM, were positively correlated with retinal thickness, which was more pronounced in pwMS with prior ON. CONCLUSION: Axonal measures reflect microstructural tissue damage in the OR, particularly in the setting of remote ON, and correlate with established metrics of visual health in MS.
 Multiple sclerosis (MS) is an autoimmune disease involving demyelination and axonal damage in the central nervous system (CNS). In this study, we investigated pathological changes in the lumbar spinal cord of C57BL/6 mice induced with progressive experimental autoimmune encephalomyelitis (EAE) disease using 9.4-T magnetic resonance imaging (MRI). Multiparametric MRI measurements including MR spectroscopy, diffusion tensor imaging (DTI) and volumetric analyses were applied to detect metabolic changes in the CNS of EAE mice. Compared with healthy mice, EAE mice showed a significant reduction in N-acetyl aspartate and increases in choline, glycine, taurine and lactate. DTI revealed a significant reduction in fractional anisotropy and axial diffusivity and an increase in radial diffusivity in the lumbar spinal cord white matter (WM), while in the grey matter (GM), fractional anisotropy increased. High-resolution structural imaging also revealed lumbar spinal cord WM hypertrophy and GM atrophy. Importantly, these MRI changes were strongly correlated with EAE disease scoring and pathological changes in the lumbar (L2-L6), particularly WM demyelination lesions and aggregation of immune cells (microglia/macrophages and astrocytes) in this region. This study identified changes in MRI biomarker signatures that can be useful for evaluating the efficacy of novel drugs using EAE models in vivo.
 Multiple sclerosis (MS) is characterized by a compromised blood-brain barrier (BBB) resulting in central nervous system (CNS) entry of peripheral lymphocytes, including T cells and B cells. While T cells have largely been considered the main contributors to neuroinflammation in MS, the success of B cell depletion therapies suggests an important role for B cells in MS pathology. Glial cells in the CNS are essential components in both disease progression and recovery, raising the possibility that they represent targets for B cell functions. Here, we examine astrocyte and microglia responses to B cell depleting treatments in an animal model of MS, experimental autoimmune encephalomyelitis (EAE). B cell depleted EAE animals had markedly reduced disease severity and myelin damage accompanied by reduced microglia and astrocyte reactivity 20 days after symptom onset. To identify potential initial mechanisms mediating functional changes following B cell depletion, astrocyte and microglia transcriptomes were analyzed 3 days following B cell depletion. In control EAE animals, transcriptomic analysis revealed astrocytic inflammatory pathways were activated and microglial influence on neuronal function were inhibited. Following B cell depletion, initial functional recovery was associated with an activation of astrocytic pathways linked with restoration of neurovascular integrity and of microglial pathways associated with neuronal function. These studies reveal an important role for B cell depletion in influencing glial function and CNS vasculature in an animal model of MS.
 INTRODUCTION: Several studies have described prognostic value of serum neurofilament light chain (sNfL) at the group level in relapsing multiple sclerosis (RMS) patients. Here, we aimed to explore the temporal association between sNfL and development of subclinical disease activity as assessed by magnetic resonance imaging (MRI) at the group level and evaluate the potential of sNfL as a biomarker for capturing subclinical disease activity in individual RMS patients. METHODS: In the 12-week APLIOS study, patients (N = 284) received subcutaneous ofatumumab 20 mg. Frequent sNfL sampling (14 time points over 12 weeks) and monthly MRI scans enabled key analyses including assessment of the group-level temporal relationship of sNfL levels with on-study subclinical development of gadolinium-enhancing (Gd +)T1 lesions. Prognostic value of baseline sNfL ("high" vs. "low") level for subsequent on-study clinical relapse or Gd + T1 activity was assessed. Individual patient-level development of on-study Gd + T1 lesions was compared across three predictors: baseline Gd + T1 lesion number, baseline sNfL ("high" vs. "low"), and time-matched sNfL. RESULTS: In patients developing Gd + T1 lesions at week 4 (absent at baseline), sNfL levels increased during the month preceding the week-4 MRI scan and then gradually decreased back to baseline. High versus low baseline sNfL conferred increased risk of subsequent on-study clinical relapse or Gd + T1 activity (HR, 2.81; p < 0.0001) in the overall population and, notably, also in the patients without baseline Gd + T1 lesions (HR, 2.48; p = 0.0213). Individual patient trajectories revealed a marked difference in Gd + T1 lesions between patients with the ten highest vs. lowest baseline sNfL levels (119 vs. 19 lesions). Prognostic value of baseline or time-matched sNfL for on-study Gd + T1 lesions was comparable to that of the number of baseline MRI Gd + T1 lesions. CONCLUSIONS: sNfL measurement may have utility in capturing and monitoring subclinical disease activity in RMS patients. sNfL assessments could complement regular MRI scans and may provide an alternative when MRI assessment is not feasible. CLINICALTRIALS: GOV: NCT03560739. CLASSIFICATION OF EVIDENCE: This study provides class I evidence that serum neurofilament light may be used as a biomarker for monitoring subclinical disease activity in relapsing multiple sclerosis patients, as shown by its elevation in the weeks preceding the development of new gadolinium-enhancing T1 lesion activity.
 BACKGROUND: Currently, there are conflicting reports on the associations between Toxoplasma gondii infection and multiple sclerosis (MS) in humans. In the present study, a case-control study was carried out to assess associations between seropositivity to T. gondii infection and MS. METHODS: This case-control study was carried out on 200 MS patients (cases) attended in Sina Hospital affiliated to Tehran University of Medical Sciences, Tehran, Iran, and 200 healthy subjects from the general population of the same city, March to July 2017. Blood samples were collected from individuals and were examined using Enzyme-linked immunosorbent assay (ELISA) for the presence of T. gondii IgG antibodies and the IgG-positive samples were further analyzed for specific anti-T. gondii IgM. RESULTS: The overall seroprevalence of anti-T. gondii IgG was 44.2% (177/400) in 121 (60.5%) sera of the 200 MS patients (cases) and 56 (28.0%) sera of the 200 controls (OR = 3.94; 95% CI: 2.59-5.99; P < 0.001). Seroprevalence of T. gondii infection in MS patients increased significantly with increasing of age (P < 0.001). In the control group, no statistically significant differences were seen between the seroprevalence of T. gondii infection in various age groups (P = 0.858). Moreover, no statistically significant relationships were reported between the seropositivity to T. gondii and the sex for the cases and controls (P>0.05). Anti-T. gondii IgM antibodies were not detected in anti-T. gondii IgG positive patients. CONCLUSION: T. gondii infection might be a probability risk factor for MS. However, further studies are necessary to describe clearly the roles of T. gondii infection in MS.
 BACKGROUND AND PURPOSE: Urinary incontinence is a common symptom in people with multiple sclerosis. The primary aim was to investigate feasibility of telerehabilitation-based pelvic floor muscle training (Tele-PFMT) and compare its effects on leakage episodes and pad usage with home exercise-based pelvic floor muscle training (Home-PFMT) and control groups. METHODS: Forty-five people with multiple sclerosis with urinary incontinence were randomized into 3 groups. Tele-PFMT and Home-PFMT groups followed the same protocol for 8 weeks, but Tele-PFMT performed exercises 2 sessions/week under a physiotherapist's supervision. The control group did not receive any specific treatment. Assessments were made at baseline, weeks 4, 8, and 12. Primary outcome measures were feasibility (compliance to exercise, patient satisfaction, and number of participants included in the study), number of leakage episodes, and pad usage. Secondary outcomes included severity of urinary incontinence and overactive bladder symptoms, sexual function, quality of life, anxiety, and depression. RESULTS: Participant eligibility rate was 19%. Patient satisfaction and compliance to exercise were significantly higher in Tele-PFMT than in Home-PFMT (P < 0.05). No significant differences in the change of leakage episodes and pad usage were found between Tele-PFMT and Home-PFMT. No significant differences in secondary outcomes were found between PFMT groups. Participants in both the Tele-PFMT and Home-PFMT groups had significantly better scores for some measures of urinary incontinence, and overactive bladder and quality of life in compared with the control group. DISCUSSION AND CONCLUSIONS: Tele-PFMT was feasible and acceptable in people with multiple sclerosis, and this mode of delivery was associated with greater exercise compliance and satisfaction compared with Home-PFMT. However, Tele-PFMT did not exhibit superiority in terms of leakage episodes and pad usage compared with Home-PFMT. A large trial comparing Home-PFMT and Tele-PFMT is warranted.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content, available at: http://links.lww.com/JNPT/A440).
 BACKGROUND: The purpose of this study was to investigate the efficacy and safety of Jollab monzej (JMZ), a Traditional Persian compound medicine, on multiple sclerosis-related fatigue (MSRF). METHODS: We did a double-blind randomized controlled phase3 clinical trial on the JMZ syrup in fifty-six relapsing-remitting MS (RRMS) patients aged 18-55 years with moderate to severe fatigue using the Expanded Disability Status Scale (EDSS) score ≤ 6. We randomly assigned (1;1) participants to the JMZ syrup or placebo (syrup) groups treated for one month. Participants, investigators, and assessors were unaware of the assignments. The primary outcome was changes in the fatigue score on the Fatigue Severity Scale (FSS), at baseline and one month after treatment using the intention-to-treat (ITT) analysis. The secondary outcomes were changes in the score of Visual Analogue Scale (VAS), Beck Depression Inventory (BDI), and Pittsburgh Sleep Quality Index (PSQI). Outcomes were measured at baseline, one month after treatment, and 2-week follow-up. Safety was detected in all participants. RESULTS: We randomly assigned 56 participants to the JMZ group (n=28) and placebo group (n=28). Fatigue scores significantly changed in both groups; however, the JMZ group had a greater reduction in FSS score in the ITT analysis. The adjusted mean difference was 8.80 (Confidence interval (CI) 95%, 2.90-14.70, P = 0.00). The mean difference of VAS, BDI, and global PSQI scores were statistically significant (P=0.01, P₌0.00, P₌0.01; respectively). Regarding safety, mild adverse events (AEs) were reported. CONCLUSION: The results of our study revealed that the administration of JMZ syrup alleviated MSRF and also could improve depression and sleep disorders.
 BACKGROUND: Ofatumumab has demonstrated superior efficacy and favorable safety for up to 2.5 years versus teriflunomide in relapsing multiple sclerosis (RMS). OBJECTIVE: Further characterize efficacy and safety of ofatumumab in RMS. METHODS: Efficacy set: patients randomized to ofatumumab/teriflunomide in ASCLEPIOS I/II (core). Safety set: patients who received ⩾ 1 dose of ofatumumab in ASCLEPIOS I/II, APLIOS, APOLITOS (all core), or ALITHIOS (umbrella open-label extension). Patients received continuous ofatumumab or were newly switched from teriflunomide. Data cut-off: 25 September 2021. RESULTS: In the efficacy set (n = 1882), the continuous ofatumumab group had a low annualized relapse rate (ARR 0.05 (95% confidence interval: 0.04-0.07)), low numbers of gadolinium-enhancing (Gd+) T1 lesions (0.01 lesions/scan) and fewer new/enlarging T2 lesions (annualized rate 0.08). Overall, 78.8% met three-parameter "no evidence of disease activity" criteria through 4 years. Switching from teriflunomide led to reduced ARR, risk of confirmed disability worsening (CDW), new/enlarging T2 lesions, Gd+ T1 lesions, and serum neurofilament light chain. In the continuous and newly switched ofatumumab groups, cumulative 3- and 6-month CDW rates remained low. In the safety set (n = 1969), the most frequently reported adverse events were infections and infestations (58.35%). No new safety signals were identified. CONCLUSION: Ofatumumab has a favorable longer-term benefit-risk profile in RMS. TRIAL REGISTRY: ALITHIOS (NCT03650114): https://clinicaltrials.gov/ct2/show/NCT03650114.
 Background: It has been suggested that nutrition might contribute to multiple sclerosis etiology (MS). Aim: This case-control study aimed to determine the role of food habits and dietary patterns in preventing or developing MS in a multicenter study in Iran (Tehran and Shiraz). Methods: In this study, food intake of (106 patients with relapsing/remitting MS (RRMS) and 72 healthy controls in Tehran) and (75 patients with relapsing/remitting MS (RRMS) and 72 healthy controls in Shiraz) were collected using a validated semi-quantitative food frequency questionnaire. Dietary patterns were extracted using factor analysis. The association between dietary patterns and the risk of MS was analyzed by Logistic regression. Results: Two major dietary patterns were extracted: the "healthy" and the "unhealthy" patterns. After adjustment for potential confounders, in Tehran city, subjects in the highest tertile of the unhealthy dietary pattern score had greater odds of having MS, compared with those in the lowest tertile (OR: 2.16; 95% CI: [1.95-2.41]; p for trend  =  0.01). In Shiraz city, subjects in the highest tertile of the unhealthy dietary pattern score had greater odds with MS than those in the lowest tertile (OR: 3.08; 95% CI: [1.27-7.38]; p for trend  =  0.01). However, in both groups, no significant association was found between healthy dietary pattern and MS risk. Conclusions: Adherence to unhealthy dietary pattern may increase the risk of MS in Iran. The results can be used for developing interventions that aim to promote healthy eating for preventing MS.

 BACKGROUND: Disease-modifying therapies (DMTs) for people with multiple sclerosis (pwMS) may decrease vaccine effectiveness. We aimed to explore the association between various DMTs and the risk for breakthrough COVID-19. METHODS: Population-based data from Clalit Health Services, Israel's largest healthcare organization, were used. PwMS treated with DMTs without prior COVID-19 were followed from the commencement of the mass vaccination campaign in December 2020. The end of follow-up was at the time of COVID-19 infection, the receipt of a third vaccine dose or until the end of August 2021. Time-dependent multivariate Cox proportional hazard models were used to estimate hazard ratios for COVID-19 according to vaccination, DMT, age, gender, disability and comorbidities. RESULTS: 2511 PwMS treated with DMTs were included (Age: 46.2 ± 14.6, 70% Female, EDSS: 3.0 ± 2.1). Of whom, 2123 (84.5%) received 2 vaccine doses. On multivariate models that included all pwMS, vaccination was protective (HR = 0.41, P < 0.001). On multivariate models that included only fully vaccinated pwMS cladribine, ocrelizumab, S1P receptor modulators and natalizumab were associated with breakthrough COVID-19 (HR = 6.1, 4.7, 3.7 and 3.3; P = 0.004, 0.008, 0.02 and 0.05, respectively). On multivariate models that included unvaccinated and fully vaccinated pwMS on each DMT separately, a protective trend was noted for vaccination on all DMTs (0.09 < HR < 0.65), except for cladribine (HR = 1.1). This protective trend was not statistically significant on ocrelizumab, S1P receptor modulators and natalizumab. COVID-19 among pwMS was generally mild. Only 2 vaccinated pwMS had a severe infection with eventual recovery. CONCLUSIONS: Vaccination effectively protects pwMS from COVID-19. An increased risk of breakthrough infection was noted on high-efficacy DMTs, however COVID-19 after vaccination was usually mild.
 BACKGROUND AND OBJECTIVE: Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune condition, which can lead to significant disability, and up to 3%-5% of the cases have a pediatric onset. There are limited studies to guide physicians in disease-modifying treatment (DMT) choices for children with NMOSD. METHODS: This retrospective cohort study evaluated children with NMOSD cases followed at 12 clinics in the US Network of Pediatric MS Centers. Cases were classified as aquaporin-4 antibody positive (AQP4+) and double seronegative (DS) when negative for AQP4+ and for myelin oligodendrocyte glycoprotein (MOG) antibody. The effect of initial DMTs including rituximab, mycophenolate, azathioprine, and IV immunoglobulin (IVIg) on the annualized relapse rate (ARR) was assessed by negative binomial regression. Time to disability progression (EDSS score increase ≥1.0 point) was modeled with a Cox proportional-hazards model. RESULTS: A total of 91 children with NMOSD were identified: 77 AQP4+ and 14 DS (85.7% females; 43.2% White and 46.6% African American). Eighty-one patients were started on a DMT, and 10 were treatment naive at the time of the analysis. The ARR calculated in all serogroups was 0.25 (95% CI 0.13-0.49) for rituximab, 0.33 (95% CI 0.19-0.58) for mycophenolate, 0.40 (95% CI 0.13-1.24) for azathioprine, and 0.54 (95% CI 0.28-1.04) for IVIg. The ARR in the AQP4+ subgroup was 0.28 (95% CI 0.14-0.55) for rituximab, 0.39 (95% CI 0.21-0.70) for mycophenolate, 0.41 (95% CI 0.13-1.29) for azathioprine, and 0.54 (95% CI 0.23-1.26) for IVIg. The ARR in the treatment-naive group was 0.97 (95% CI 0.58-1.60) in all serogroups and 0.91 (95% CI 0.53-1.56) in the AQP4+ subgroup. None of the initial DMT had a statistically significant effect on EDSS progression. DISCUSSION: The use of DMTs, particularly rituximab, is associated with a lowered annualized relapse rate in children with NMOSD AQP4+. CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that use of disease-modifying treatments is associated with a lowered annualized relapse rate in children with NMOSD AQP4+.
 BACKGROUND: Recent evidence has shown a significant association between menopause and multiple sclerosis (MS) progression. This study investigated the possible role of menopause in influencing MS from clinical and neuroradiological perspectives. Notably, the possible association between menopause and brain atrophy has been evaluated. MATERIALS AND METHODS: This study included women with MS whose ages ranged from 45 to 55 years. Demographic and clinical characteristics were collected, and the reproductive phase was defined as non-menopausal or menopausal based on the final menstrual period. Thus, MS activity over the past year was reported as the annualised relapse rate (ARR), and MRI activity (defined as new T2 lesions and/or the presence of gadolinium-enhancing lesions at the last MRI assessment in comparison with the MRI performed within the previous 12 months) were compared between non-menopausal women (non-MW) and menopausal women (MW). Volume measurements of the whole brain (WB), white matter (WM), grey matter (GM), and cortical GM were estimated using the SIENAX software, and the possible relationship with menopausal status was assessed by regression analysis. RESULTS: The study included 147 women with MS. Eighty-four (57.1%) were MW, with a mean age of 48.5 ± 4.3 years at menopause onset and a mean duration of menopause of 4.1 ± 1.1 years. When compared for ARR, MW reported a lower rate than the non-MW (ARR of 0.29 ± 0.4 vs. 0.52 ± 0.5; p < 0.01). MRI activity was observed in 13.1% of MW and 20.6% of non-MW (p = 0.03). Lower cortical GM volumes (578.1 ± 40.4 mL in MW vs. 596.9 ± 35.8 mL in non-MW; p < 0.01) have also been reported. Finally, multivariate analysis showed a significant association of lower ARR (p = 0.001) and cortical GM volume (p = 0.002) with menopausal status after correction for chronological age and other variables. DISCUSSION: Menopause may be an adverse prognostic factor of MS. Our preliminary results suggest that menopause may facilitate cortical GM atrophy, probably due to a decline in the neuroprotective effects of estrogen, with negative effects on MS evolution.
 High-dose intravenous steroid treatment (HDIST) represents the first choice of treatment for multiple sclerosis (MS) relapses. Chronic oral glucocorticoid (GC) administration correlates with bone loss whereas data regarding HDIST in MS are still conflicting. Twenty-five newly diagnosed MS patients (NDMSP) (median age: 37 years) were prospectively studied for the effects of HDIST on bone mineral density (BMD) and bone metabolism. Patients received 1000 mg methylprednisolone intravenously every day for 5 days followed by oral prednisolone tapering over 21 days. Bone metabolism indices were determined prior to GC, on days 2, 4, 6, and 90, and at months 6, 12, 18, and 24 post GC therapy. Femoral, lumbar-spine BMD, and whole-body measurement of adipose/lean tissue were assessed prior to GC-administration and then every six months. Ten patients completed the study. N-terminal-propeptide-procollagen-type-1 and bone-specific alkaline phosphatase showed a significant increase at day-90 (p < 0.05). A transient non-significant fall of BMD was observed at 6 months after GC-administration, which subsequently appeared to be restored. We conclude that HDIST seems not to have long-term negative effects on BMD, while the observed transient increase of bone formation markers probably indicates a high bone turnover phase to GC-administration. Additional prospective studies with larger sample size are needed.
 Diagnostic and prognostic markers are necessary to help in patient diagnosis and the prediction of future clinical events or disease progression. As promising biomarkers of selected diseases, the free light chains (FLCs) κ and λ were considered. Measurements of FLCs are currently used in routine diagnostics of, for example, multiple myeloma, and the usefulness of FLCs as biomarkers of monoclonal gammopathies is well understood. Therefore, this review focuses on the studies concerning FLCs as new potential biomarkers of other disorders in which an inflammatory background has been observed. We performed a bibliometric review of studies indexed in MEDLINE to assess the clinical significance of FLCs. Altered levels of FLCs were observed both in diseases strongly connected with inflammation such as viral infections, tick-borne diseases or rheumatic disorders, and disorders that are moderately associated with immune system reactions, e.g., multiple sclerosis, diabetes, cardiovascular disorders and cancers. Increased concentrations of FLCs appear to be a useful prognostic marker in patients with multiple sclerosis or tick-borne encephalitis. Intensive synthesis of FLCs may also reflect the production of specific antibodies against pathogens such as SARS-CoV-2. Moreover, abnormal FLC concentrations might predict the development of diabetic kidney disease in patients with type 2 diabetes. Markedly elevated levels are also associated with increased risk of hospitalization and death in patients with cardiovascular disorders. Additionally, FLCs have been found to be increased in rheumatic diseases and have been related to disease activity. Furthermore, it has been suggested that inhibition of FLCs would reduce the progression of tumorigenesis in breast cancer or colitis-associated colon carcinogenesis. In conclusion, abnormal levels of κ and λ FLCs, as well as the ratio of κ:λ, are usually the result of disturbances in the synthesis of immunoglobulins as an effect of overactive inflammatory reactions. Therefore, it seems that κ and λ FLCs may be significant diagnostic and prognostic biomarkers of selected diseases. Moreover, the inhibition of FLCs appears to be a promising therapeutical target for the treatment of various disorders where inflammation plays an important role in the development or progression of the disease.
 BACKGROUND: Preliminary dietary intervention trials with the low-saturated fat (Swank) and modified Paleolithic elimination (Wahls) diets have shown favorable effects on fatigue among people with multiple sclerosis (MS); however, their impact on metabolic health is unknown. OBJECTIVE: To evaluate the impact of the Swank and Wahls diets on markers of metabolic health and to determine the association and mediation effect between changes in metabolic health and perceived fatigue among people with relapsing-remitting MS (RRMS). METHODS: As part of a randomized parallel-arm trial, vital signs, blood metabolic biomarkers, and the fatigue scale for motor and cognitive functions (FSMC) were collected from participants with relapsing-remitting MS (n = 77) at four study visits spaced 12 weeks apart: (1) run-in, (2) baseline, (3) 12-weeks, and (4) 24-weeks. Participants followed their usual diet at run-in, then were randomized at baseline to either the Swank or Wahls diets and followed for 24 weeks. RESULTS: Both groups had significant reductions in weight, body mass index (BMI), total cholesterol, and low-density lipoprotein (LDL) at 12- and 24-weeks compared to respective baseline values (p ≤ 0.04 for all). The Swank group also had a significant reduction in high-density lipoprotein (HDL) at 12- and 24-weeks (p = 0.0001 and p = 0.02, respectively), while the Wahls group had significant reductions in diastolic blood pressure (DBP). In addition, both groups had significant reductions in FSMC total perceived fatigue and the motor and cognitive fatigue subscales at 12- and 24-weeks (p ≤ 0.01 for all); however, change in the cognitive subscale was not significant at 12-weeks in the Swank group (p = 0.06). Furthermore, the favorable effects, of both diets, on markers of metabolic health were not associated with and did not mediate the effect of the diets on perceived fatigue (p > 0.05 for all). CONCLUSION: Both diets lead to significant reductions in perceived fatigue, weight, BMI, total cholesterol, and LDL, but the significant reductions in perceived fatigue were independent of changes in markers of metabolic health.
 BACKGROUND: Caesarean section (CS) may affect the risk of developing multiple sclerosis (MS) in the offspring, possibly through changes in gut microbiota composition, but findings from previous studies are inconsistent. We investigated whether birth by CS was associated with the risk of adult-onset MS. METHODS: We conducted a prospective population-based cohort study, including all individuals born in Norway between 1967 and 2003, using the Medical Birth Registry of Norway linked with the Norwegian Multiple Sclerosis Registry and Biobank. The follow-up was until 2021. We used multivariable Cox models to estimate HRs for MS risk with 95% CIs. RESULTS: Among 2 046 637 individuals in the cohort, 4954 MS cases were identified. Being born by CS was associated with a modest increase in MS risk (HR=1.18, 95% CI 1.05 to 1.32). In the sibling-matched analysis, we found no association between CS and MS risk. We found an interaction between CS and gestational age (p=0.03): CS was associated with an increased risk of MS in individuals born preterm (HR=1.62, 95% CI 1.18 to 2.24), whereas there was no association in individuals born at term (HR=1.13, 95% CI 0.99 to 1.27). In a subgroup analysis of individuals born in 1988 and onwards, emergency CS was related to an elevated MS risk (HR=1.40, 95% CI 1.07 to 1.83), whereas planned CS was not (HR: 1.10, 95% CI 0.77 to 1.58). CONCLUSIONS: CS was associated with a modestly higher risk of developing MS. However, the stronger associations seen in subgroups who likely experienced a more complicated pregnancy/delivery may point to confounding underlying these associations.
 OBJECTIVE: In this study, we aimed to investigate the effects of non-invasive brain stimulation (NIBS) on cognitive and motor functions in patients with multiple sclerosis (pwMS). METHODS: A literature search was performed in the Cochrane Library, Embase, PubMed, Web of Science, Medline, CNKI, and Wan fang. The time interval used for database construction was up to December 2022, and the language was not limited. The collected trials were subsequently screened, the data were extracted, the quality was evaluated, and the effect sizes were computed using STATA/MP Version 13 for outcome analysis. Standard mean difference (SMD) and 95% confidence interval (CI) were calculated for domain of interest. RESULTS: In total, 17 articles that examined 364 patients with multiple sclerosis were included in this analysis. Non-invasive brain stimulation did not improve the overall cognitive function [SMD = 0.18, 95% CI (-0.32, 0.69), P = 0.475] but helped improve motor function in patients [SMD = 0.52, 95% CI (0.19, 0.85), P = 0.002]. Moreover, this study specifically indicated that non-invasive brain stimulation improved alerting [SMD = 0.68, 95% CI (0.09, 1.26), P = 0.02], whereas non-invasive brain stimulation intervention improved motor function in patients aged <45 years [SMD = 0.67, 95% CI (0.23, 1.10), P = 0.003] and in patients with expanded disability status scale scores (EDSS) <3.5 [SMD = 0.82, 95% CI (0.22, 1.42), P = 0.007]. In particular, NIBS contributed to the improvement of spasticity in pwMS [SMD = 0.68, 95% CI (0.13, 1.23), P = 0.015]. CONCLUSION: These results of this present study provide evidence that non-invasive brain stimulation could improve alertness in pwMS. Furthermore, NIBS may help pwMS with motor function and those who are under 45 years of age or with EDSS < 3.5 improve their motor function. For the therapeutic use of NIBS, we recommend applying transcranial magnetic stimulation as an intervention and located on the motor cortex M1 according to the subgroup analysis of motor function. These findings warrant verification. SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42022301012.
 An NAD(+)-dependent deacetylase called Sirtuin 3 (Sirt3) is involved in the metabolic processes of the mitochondria, including energy generation, the tricarboxylic acid cycle, and oxidative stress. Sirt3 activation can slow down or prevent mitochondrial dysfunction in response to neurodegenerative disorders, demonstrating a strong neuroprotective impact. The mechanism of Sirt3 in neurodegenerative illnesses has been elucidated over time; it is essential for neuron, astrocyte, and microglial function, and its primary regulatory factors include antiapoptosis, oxidative stress, and the maintenance of metabolic homeostasis. Neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS), may benefit from a thorough and in-depth investigation of Sirt3. In this review, we primarily cover Sirt3's role and its regulation in the nerve cells and the connection between Sirt3 and neurodegenerative disorders.
 PURPOSE: The purpose of this study was to compare the performance of three magnetic resonance imaging (MRI) reading methods in the follow-up of patients with multiple sclerosis (MS). MATERIALS AND METHODS: This retrospective study included patients with MS who underwent two brain follow-up MRI examinations with three-dimensional fluid-attenuated inversion recovery (FLAIR) sequences between September 2016 and December 2019. Two neuroradiology residents independently reviewed FLAIR images using three post-processing methods including conventional reading (CR), co-registration fusion (CF), and co-registration subtraction with color-coding (CS), while being blinded to all data but FLAIR images. The presence and number of new, growing, or shrinking lesions were compared between reading methods. The reading time, reading confidence, and inter- and intra-observer agreements were also assessed. An expert neuroradiologist established the standard of reference. Statistical analyses were corrected for multiple testing. RESULTS: A total of 198 patients with MS were included. There were 130 women and 68 men, with a mean age of 41 ± 12 (standard deviation) years (age range: 21-79 years). Using CS and CF, more patients were detected with new lesions compared to CR (93/198 [47%] and 79/198 [40%] vs. 54/198 [27%], respectively; P < 0.01). The median number of new hyperintense FLAIR lesions detected was significantly greater using CS and CF compared to CR (2 [Q1, Q3: 0, 6] and 1 [Q1, Q3: 0, 3] vs. 0 [Q1, Q3: 0, 1], respectively; P < 0.001). The mean reading time was significantly shorter using CS and CF compared to CR (P < 0.001), with higher confidence in readings and higher inter- and intra-observer agreements. CONCLUSION: Post-processing tools such as CS and CF substantially improve the accuracy of follow-up MRI examinations in patients with MS while reducing reading time and increasing readers' confidence and reproducibility.
 Extracellular vesicles are secreted by a wide variety of cells, and their primary functions include intercellular communication, immune responses, human reproduction, and synaptic plasticity. Their molecular cargo reflects the physiological processes that their cells of origin are undergoing. Thus, many studies have suggested that extracellular vesicles could be a promising biomarker tool for many diseases, mainly due to their biological relevance and easy accessibility to a broad range of body fluids. Moreover, since their biological composition leads them to cross the blood-brain barrier bidirectionally, growing evidence points to extracellular vesicles as emerging mirrors of brain diseases processes. In this regard, this review explores the biogenesis and biological functions of extracellular vesicles, their role in different physiological and pathological processes, their potential in clinical practice, and the recent outstanding studies about the role of exosomes in major human brain diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), or brain tumors.
 The circadian rhythm is a nearly 24-h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple-system atrophy, focusing on research published in the last 3 years.
 Multiple sclerosis (MS) is a chronic neuroinflammatory and neurodegenerative disease of the central nervous system (CNS). The etiology of MS is not well understood, but it's likely one of the genetic and environmental factors. Approximately 85% of patients have relapsing-remitting MS (RRMS), while 10-15% have primary progressive MS (PPMS). Epstein-Barr virus (EBV) and Human herpesvirus 6 (HHV-6), members of the human Herpesviridae family, are strong candidates for representing the macroenvironmental factors associated with MS) pathogenesis. Antigenic mimicry of EBV involving B-cells has been implicate in MS risk factors and concomitance of EBV and HHV-6 latent infection has been associated to inflammatory MS cascade. To verify the possible role of EBV and HHV-6 as triggering or aggravating factors in RRMS and PPMS, we compare their frequency in blood samples collected from 166 MS patients. The presence of herpes DNA was searched by real-time PCR (qPCR). The frequency of EBV and HHV-6 in MS patients were 1.8% (3/166) and 8.9% (14/166), respectively. Among the positive patients, 100% (3/3) EBV and 85.8% (12/14) HHV-6 are RRMS and 14.4% (2/14) HHV-6 are PPMS. Detection of EBV was 1.2% (2/166) and HHV-6 was 0.6% (1/166) in blood donors. About clinical phenotype of these patients, incomplete multifocal myelitis, and optic neuritis were the main CNS manifestations. These are the first data about concomitant infection of these viruses in MS patients from Brazil. Up to date, our findings confirm a higher prevalence in female with MS and a high frequency of EBV and HHV-6 in RRMS patients.
 Background: Mesenchymal stem cell-derived neural progenitor cell (MSC-NP) therapy is an experimental approach to treat multiple sclerosis. The influence of MSC-NPs on microglial activation was investigated. Methods: Microglia were stimulated in the presence of MSC-NP-conditioned media, and proinflammatory or proregenerative marker expression was assessed by quantitative PCR and ELISA. Results: Microglia stimulated in the presence of MSC-NP-conditioned media displayed reduced expression of proinflammatory markers including CCL2, increased expression of proregenerative markers and reduced phagocytic activity. The paracrine effects of MSC-NPs from multiple donors correlated with TGF-β3 gene expression and was reversed by TGF-β signaling inhibition. Conclusion: MSC-NPs promote beneficial microglial polarization through secreted factors. This study suggests that microglia are a potential therapeutic target of MSC-NP cell therapy.
 BACKGROUND: Although multiple sclerosis (MS) Intimacy and Sexuality Questionnaire-19 (MSISQ-19) is a widely applied tool, no unique definition of sexual dysfunction (SD) based on its score exists. OBJECTIVE: To explore the impact of different MSISQ-19 cut-offs on SD prevalence and associated risk factors, providing relevant information for its application in research and clinical settings. METHODS: After defining SD according to two different MSISQ-19 cut-offs in 1155 people with MS (pwMS), we evaluated SD prevalence and association with sociodemographic and clinical features, mood status and disability via logistic regression. RESULTS: Depending on the chosen cut-off, 45% to 54% of pwMS reported SD. SD defined as MSISQ-19 score >30 was predicted by age (OR=1.01, p=0.047), cognition (OR=0.96, p=0.004) and anxiety (OR=1.03, p=0.019). SD defined as a score >3 on any MSISQ-19 item was predicted by motor disability (OR=1.12, p=0.003) and cognition (OR= 0.96, p=0.002). CONCLUSION: Applying different MSISQ-19 cut-offs influences both the estimated prevalence and the identification of risk factors for SD, a finding that should be considered during study planning and data interpretation. Preserved cognition exerts a protective effect towards SD regardless from the specific study setting, representing a key point for the implementation of preventive and therapeutic strategies.

 The T2-fluid attenuated inversion recovery (FLAIR) mismatch sign has been suggested as an imaging marker of isocitrate dehydrogenase-mutant 1p/19q non-codeleted gliomas with 100% specificity. Tumefactive demyelination is a common mimic of neoplasm that has led to unnecessary biopsies and even resections. We report a case of tumefactive multiple sclerosis in a 46-year-old male without prior symptomatic demyelinating episodes that demonstrates the T2-FLAIR mismatch sign. Our findings suggest the T2-FLAIR mismatch sign should not be used as a differential feature between glioma and tumefactive demyelination. Because typical isocitrate dehydrogenase-mutant 1p/19q non-codeleted gliomas typically do not demonstrate significant enhancement, such diagnosis should be reserved when post-contrast images are unavailable.
 Neurodegenerative diseases, including Alzheimer disease, Parkinson disease, amyotrophic lateral sclerosis, and multiple sclerosis, are chronic disorders of the CNS that are characterized by progressive neuronal dysfunction. These diseases have diverse clinical and pathological features and their pathogenetic mechanisms are not yet fully understood. Currently, widely accepted hypotheses include the accumulation of misfolded proteins, oxidative stress from reactive oxygen species, mitochondrial dysfunction, DNA damage, neurotrophin dysfunction, and neuroinflammatory processes. In the CNS of patients with neurodegenerative diseases, a variety of abnormally phosphorylated proteins play important roles in pathological processes such as neuroinflammation and intracellular accumulation of β-amyloid plaques and tau. In recent years, the roles of abnormal tyrosine phosphorylation of intracellular signaling molecules regulated by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs) in neurodegenerative diseases have attracted increasing attention. Here, we summarize the roles of signaling pathways related to protein tyrosine phosphorylation in the pathogenesis of neurodegenerative diseases and the progress of therapeutic studies targeting PTKs and PTPs that provide theoretical support for future studies on therapeutic strategies for these devastating and important neurodegenerative diseases.
 BACKGROUND: Vitamin D insufficiency is associated with risk of multiple sclerosis (MS) relapse; whether supplementation influences prognosis is unknown. The Vitamin D to Ameliorate MS (VIDAMS) trial aimed to determine if high dose (5000 International Units (IU)/day) versus low dose (600 IU/day) vitamin D(3,) added to daily glatiramer acetate (GA), reduced the risk of clinical relapse in people with established relapsing remitting MS (RRMS) over 96 weeks. METHODS: VIDAMS is a randomised, phase 3, double-blind, multi-centre, controlled trial conducted at sixteen neurology clinics in the United States. Participants with MAGNIMS 2010 RRMS, aged 18-50 years, with recent disease activity were eligible to enroll if they had an Expanded Disability Status Scale score ≤4.0; minimum serum 25-hydroxyvitamin D level of 15 ng/ml within 30 days of screening; and average ≤ 1000 IU supplemental vitamin D(3) daily in the 90 days prior to screening. Of 203 screened, 183 were eligible for the 30-day run-in to assess GA adherence, after which 172 were randomised 1:1 to low dose vitamin D(3) (LDVD) or high dose vitamin D(3) (HDVD), and were followed every 12 weeks for 96 weeks. The primary outcome was the proportion that experienced a confirmed relapse and analyses used Kaplan Meier and Cox proportional hazards models. 165 participants returned for ≥1 follow-up visit and were included in the primary and safety analyses; 140 completed a week 96 visit. This study was registered with ClinicalTrials.gov, NCT01490502. FINDINGS: Between March 22, 2012 and March 8, 2019, 172 participants were enrolled and randomised (83 LDVD, 89 HDVD) and differed at baseline only in gender and race: more males received HDVD (31%) than LDVD (16%), and fewer Black participants received HDVD (12%) than LDVD (22%). Among 165 participants with at least one follow-up visit, the proportion experiencing confirmed relapse did not differ between LDVD and HDVD [at 96 weeks: 32% vs. 34%, p = 0.60; hazard ratio (HR): 1.17 (0.67, 2.05), p = 0.57]. There was no hypercalcaemia. Three participants developed nephrolithiasis or ureterolithiasis (1 in the LDVD and 2 in the HDVD group). Two were possibly related to study drug; and one was presumed related to concomitant treatment with topiramate for migraine. INTERPRETATION: VIDAMS provides evidence that HDVD supplementation, added to GA, does not reduce the risk of clinical relapse in people with RRMS. Taken together with the null findings of previous trials, these results suggest that prescribing higher doses of vitamin D for purposes of modifying the RRMS course may not be beneficial. FUNDING: This investigation was supported by a grant from the National Multiple Sclerosis Society (RG 4407A2/1). Teva Neuroscience, Inc. provided Copaxone (GA) for the duration of the trial.
 Magnetic resonance imaging (MRI) is the most sensitive technique for detecting inflammatory demyelinating lesions in multiple sclerosis (MS) and plays a crucial role in diagnosis and monitoring treatment effectiveness, and for predicting the disease course. In clinical practice, detection of MS lesions is mainly based on T2-weighted and contrast-enhanced T1-weighted sequences. Contrast-enhancing lesions (CEL) on T1-weighted sequences are related to (sub)acute inflammation, while new or enlarging T2 lesions reflect the permanent footprint from a previous acute inflammatory demyelinating event. These two types of MRI features provide redundant information, at least in regular monitoring of the disease. Due to the concern of gadolinium deposition after repetitive injections of gadolinium-based contrast agents (GBCAs), scientific organizations and regulatory agencies in Europe and North America have proposed that these contrast agents should be administered only if clinically necessary. In this article, we provide data on the mode of action of GBCAs in MS, the indications of the use of these agents in clinical practice, their value in MS for diagnostic, prognostic, and monitoring purposes, and their use in specific populations (children, pregnant women, and breast-feeders). We discuss imaging strategies that achieve the highest sensitivity for detecting CELs in compliance with the safety regulations established by different regulatory agencies. Finally, we will briefly discuss some alternatives to the use of GBCA for detecting blood-brain barrier disruption in MS lesions. CLINICAL RELEVANCE STATEMENT: Although use of GBCA at diagnostic workup of suspected MS is highly valuable for diagnostic and prognostic purposes, their use in routine monitoring is not mandatory and must be reduced, as detection of disease activity can be based on the identification of new or enlarging lesions on T2-weighted images. KEY POINTS: • Both the EMA and the FDA state that the use of GBCA in medicine should be restricted to clinical scenarios in which the additional information offered by the contrast agent is required. • The use of GBCA is generally recommended in the diagnostic workup in subjects with suspected MS and is generally not necessary for routine monitoring in clinical practice. • Alternative MRI-based approaches for detecting acute focal inflammatory MS lesions are not yet ready to be used in clinical practice.
 AIMS: During pregnancy, fetal cells can migrate to the mother via blood circulation. A percentage of these cells survive in maternal tissues for decades generating a population of fetal microchimeric cells (fMCs), whose biological role is unclear. The aim of this study was to investigate the association between the sex of offspring, an indirect marker of fMCs, and magnetic resonance imaging (MRI) features in women with multiple sclerosis (MS). METHODS: We recruited 26 nulliparous MS patients (NPp), 20 patients with at least one male son (XYp), and 8 patients with only daughters (XXp). Each patient underwent brain MR scan to acquire 3D-T2w FLAIR FatSat and 3D-T1w FSPGR/TFE. Lesion Segmentation Tool (LST) and FreeSurfer were used to obtain quantitative data from MRI. Additional data were collected using medical records. Multiple regression models were applied to evaluate the association between sex of offspring and MS data. RESULTS: Comparing NPp and XXp, we found that NPp had larger 4th ventricle volume (2.02 ± 0.59 vs. 1.70 ± 0.41; p = 0.022), smaller left entorhinal volume (0.55 ± 0.17 vs. 0.68 ± 0.25; p = 0.028), and lower thickness in the following cortical areas: left paracentral (2.34 ± 0.16 vs. 2.39 ± 0.17; p = 0.043), left precuneus (2.27 ± 0.11 vs. 2.34 ± 0.16; p = 0.046), right lateral occipital (2.14 ± 0.11 vs. 2.25 ± 0.08; p = 0.006). NPp also had lower thickness in left paracentral cortex (2.34 ± 0.16 vs. 2.46 ± 0.17; p = 0.004), left precalcarine cortex (1.64 ± 0.14 vs. 1.72 ± 0.12; p = 0.041), and right paracentral cortex (2.34 ± 0.17 vs. 2.42 ± 0.14; p = 0.015) when compared to XYp. Comparing XYp and XXp, we found that XYp had higher thickness in left cuneus (1.80 ± 0.14 vs. 1.93 ± 0.10; p = 0.042) and left pericalcarine areas (1.59 ± 0.19 vs. 1.72 ± 0.12; p = 0.032) and lower thickness in right lateral occipital cortex (2.25 ± 0.08 vs. 2.18 ± 0.13; p = 0.027). DISCUSSION: Our findings suggested an association between the sex of offspring and brain atrophy. Considering the sex of offspring as an indirect marker of fMCs, we speculated that fMCs could accumulate in different brain areas modulating MS neuropathological processes.
 The central nervous system (CNS) is the most complex system in human body, and there is often a lack of effective treatment strategies for the disorders related with CNS. Natural compounds with multiple pharmacological activities may offer better options because they have broad cellular targets and potentially produce synergic and integrative effects. Bryostatin-1 is one of such promising compounds, a macrolide separated from marine invertebrates. Bryostatin-1 has been shown to produce various biological activities through binding with protein kinase C (PKC). In this review, we mainly summarize the pharmacological effects of bryostatin-1 in the treatment of multiple neurological diseases in preclinical studies and clinical trials. Bryostatin-1 is shown to have great therapeutic potential for Alzheimer's disease, multiple sclerosis, fragile X syndrome, stroke, traumatic brain injury, and depression. It exhibits significant rescuing effects on the deficits of spatial learning, cognitive function, memory and other neurological functions caused by diseases, producing good neuroprotective effects. The promising neuropharmacological activities of bryostatin-1 suggest that it is a potential candidate for the treatment of related neurological disorders although there are still some issues needed to be addressed before its application in clinic.
 Neuroinflammation is associated with disorders of the nervous system, and it is induced in response to many factors, including pathogen infection, brain injury, toxic substances, and autoimmune diseases. Astrocytes and microglia have critical roles in neuroinflammation. Microglia are innate immune cells in the central nervous system (CNS), which are activated in reaction to neuroinflammation-inducing factors. Astrocytes can have pro- or anti-inflammatory responses, which depend on the type of stimuli presented by the inflamed milieu. Microglia respond and propagate peripheral inflammatory signals within the CNS that cause low-grade inflammation in the brain. The resulting alteration in neuronal activities leads to physiological and behavioral impairment. Consequently, activation, synthesis, and discharge of various pro-inflammatory cytokines and growth factors occur. These events lead to many neurodegenerative conditions, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis discussed in this study. After understanding neuroinflammation mechanisms and the involvement of neurotransmitters, this study covers various drugs used to treat and manage these neurodegenerative illnesses. The study can be helpful in discovering new drug molecules for treating neurodegenerative disorders.
 Optical coherence tomography (OCT) is a non-invasive tool to measure thickness of various layers of retina. Recently, retinal nerve fibre layer (RNFL) and ganglion cell and inner plexiform layer (GCIP) thinning has been observed in OCT in patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), This study compared OCT profile, along with visual acuity (VA), color vision (CV), contrast saturation (CS) and visual evoked potentials (VEP) in two main cohorts of MS and NMOSD and with controls, during acute episode of optic neuritis (ON), at 3 and 6 months. We found that changes of ON were present in 75% of MS eyes and in 45% of NMOSD patients. Of these, subclinical involvement was present in 56.25% of MS eyes and only in 5% of NMOSD eyes suggesting frequent subclinical involvement in the former. Mean RNFL was 95.23 ± 15.53 in MS and 66.14 ± 43.73 in NMOSD after 6 months of ON episode. Thinning of NQ and IQ was observed in NMOSD eyes in the immediate period after ON attack. At 6 months relative sparing of RNFL in TQ was observed in NMOSD ON eyes and MS ON showed predilection for involvement of TQ.
 INTRODUCTION: Isolated Clinical Syndrome (ACS) refers to the first clinical event with characteristics suggestive of multiple sclerosis (MS). CLINICAL CASE: We report the case of a previously healthy 8-year-old male patient hospitalized for altered gait with suspicion of transverse myelitis. Spinal MRI was performed showing evidence of hyperintense D3-D5 lesion in T2. He receives treatment with intravenous corticosteroid therapy and with the result of oligoclonal bands in serum and CSF, a diagnosis of ACS is made. CONCLUSION: The objective is to describe a rare form of manifestation of demyelinating disease in pediatric age and to assess the importance of timely diagnosis and treatment.




 In 2010, the FDA approved the administration of FTY720, S1P lipid mediator, as a therapy to treat relapsing forms of multiple sclerosis. FTY720 was found to sequester pro-inflammatory lymphocytes within the lymph node, preventing them from causing injury to the central nervous system due to inflammation. Studies harnessing the anti-inflammatory properties of FTY720 as a pro-regenerative strategy in wound healing of muscle, bone and mucosal injuries are currently being performed. This in-depth review discusses the current regenerative impact of FTY720 due to its anti-inflammatory effect stratified into an assessment of wound regeneration in the muscular, skeletal, and epithelial systems. The regenerative effect of FTY720 in vivo was characterized in three animal models, with differing delivery mechanisms emerging in the last 20 years. In these studies, local delivery of FTY720 was found to increase pro-regenerative immune cell phenotypes (neutrophils, macrophages, monocytes), vascularization, cell proliferation and collagen deposition. Delivery of FTY720 to a localized wound environment demonstrated increased bone, muscle, and mucosal regeneration through changes in gene and cytokine production primarily by controlling the local immune cell phenotypes. These changes in gene and cytokine production reduced the inflammatory component of wound healing and increased the migration of pro-regenerative cells (neutrophils and macrophages) to the wound site. The application of FTY720 delivery using a biomaterial has demonstrated the ability of local delivery of FTY720 to promote local wound healing leveraging an immunomodulatory mechanism.
 BACKGROUND: Granulocyte-macrophage colony stimulating factor (GM-CSF) is a pro-inflammatory cytokine secreted by various immune cells. Several studies have demonstrated an expansion of GM-CSF producing T cells in the blood or CSF of people with MS (pwMS). However, whether this equates to greater concentrations of circulating cytokine remains unknown as quantification is difficult with traditional assays. OBJECTIVE: To determine whether GM-CSF can be quantified and whether GM-CSF levels are elevated in pwMS. METHODS: We employed Single Molecule Array (Simoa) to measure GM-CSF in both CSF and blood. We then investigated relationships between GM-CSF levels and measures of blood-CSF-barrier integrity. RESULTS: GM-CSF was quantifiable in all samples and was significantly higher in the CSF of pwMS compared with controls. No association was found between CSF GM-CSF levels and Q-Albumin - a measure of blood-CSF-barrier integrity. CSF GM-CSF correlated with measures of intrathecal inflammation, and these relationships were greater in primary progressive MS compared with relapsing-remitting MS. CONCLUSION: GM-CSF levels are elevated specifically in the CSF of pwMS. Our results suggest that elevated cytokine levels may reflect (at least partial) intrathecal production, as opposed to simple diffusion across a dysfunctional blood-CSF-barrier.


 BACKGROUND: Pseudocystic inflammatory demyelinating lesions (PIDLs) are poorly described in MS and might represent a diagnostic challenge. OBJECTIVES: We described the clinical, radiological, pathological, and follow-up characteristics of 13 PIDL in 9 MS patients. METHODS: We constituted a single-center retrospective case series of PIDLs in MS, defined on MRI as expansive cyst-like lesions, with a fluid-signal content, and a diameter of 1 cm or more. RESULTS: PIDL often occurred at first event (56%), were often asymptomatic (69%), and encircled by a hypo-T2 diffusion-restricted rim and a thin ring-like gadolinium enhancement (100%) on magnetic resonance imaging (MRI). Associated typical MS lesions were constant. Biopsies from two PIDLs displayed classical features of active MS, except for unusual edema. CONCLUSION: PIDLs are clinically unremarkable and associated with a good outcome. Their easily recognizable MRI features could help avoid biopsy.
 BACKGROUND: Pediatric forms of multiple sclerosis are more active than those in adults. Yet, the effectiveness of different therapeutic approaches is not well studied in this population. Our objective was to compare the effectiveness of the early use of high efficacy therapies (HETs) with the effectiveness of moderate efficacy therapies (METs) in children with MS. METHODS: This observational study included patients diagnosed with pediatric MS, at 4 hospital centers in France, during a 10-year period. METs included: interferon β-1a, glatiramer acetate, dimethyl fumarate, teriflunomide; HETs included: fingolimod, natalizumab, ocrelizumab, alemtuzumab. The primary endpoint was the occurrence of a new relapse, the secondary endpoint was EDSS worsening. RESULTS: Sixty-four patients were included in the analysis (80% women; mean age 15.5 years, 81% treated with MET) with a median follow-up of 22.5 months. At baseline, 52 patients were on MET (interferon β-1a, glatiramer acetate, dimethyl fumarate, teriflunomide) and 12 patients were on HET (natalizumab, ocrelizumab). The cumulative probability of being relapse-free at 6.5 years was 23.3% on MET, vs 90.9% on HET (p = 0.013). The cumulative probability of no EDSS worsening did not differ between the 2 groups. CONCLUSION: Patients starting with METs had much higher clinical disease activity than those starting early with HETs. Rapid initiation of more aggressive treatment may allow better disease control; however, the data on EDSS worsening are not conclusive.
 BACKGROUND AND PURPOSE: The validity, reliability, and longitudinal performance of the Patient-Determined Disease Steps (PDDS) scale is unknown in people with multiple sclerosis (MS) with mild to moderate disability. We aimed to examine the psychometric properties and longitudinal performance of the PDDS. METHODS: We included relapsing-remitting MS patients with an Expanded Disability Status Scale (EDSS) score of less than 4. Validity and test-retest reliability was examined. Longitudinal data were analysed with mixed-effect modelling and Cohen's kappa for concordance in confirmed disability progression (CDP). RESULTS: We recruited a total of 1093 participants, of whom 904 had complete baseline data. The baseline correlation between PDDS and EDSS was weak (ρ = 0.45, p < 0.001). PDDS had stronger correlations with patient-reported outcomes (PROs). Conversely, EDSS had stronger correlations with age, disease duration, Kurtzke's functional systems and processing speed test. PDDS test-retest reliability was good to excellent (concordance correlation coefficient = 0.73-0.89). Longitudinally, PDDS was associated with EDSS, age and depression. A higher EDSS score was associated with greater PDSS progression. The magnitude of these associations was small. There was no concordance in CDP as assessed by PDDS and EDSS. CONCLUSION: The PDDS has greater correlation with other PROs but less correlation with other MS-related outcome measures compared to the EDSS. There was little correlation between PDDS and EDSS longitudinally. Our findings suggest that the PDDS scale is not interchangeable with the EDSS.
 DISCLAIMER: In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. PURPOSE: This study evaluated patient-reported outcomes (PROs) and pharmacist actions for patients on disease-modifying therapies (DMTs) for multiple sclerosis (MS) through health-system specialty pharmacies (HSSPs). METHODS: A multisite, prospective cohort study of patients utilizing an HSSP for DMT fulfillment was performed. Primary outcomes were affirmative answers to PRO questions regarding impacted productivity, hospitalization, and relapse and pharmacist actions. Rates of pharmacist action were reported as the number of person-years of treatment per action. Univariate and multivariate logistic regression were used to evaluate the association between each PRO and covariates, including the number of pharmacist actions performed, age, sex, insurance, site, and route of administration. RESULTS: The 968 patients included had 10,562 fills and 6,946 PRO assessments. The most common PRO was impacted productivity (14.6%). Pharmacists performed 3,683 actions, most commonly general medication education (42.6%) and safety (33.3%). Rates of general medication education and nonfinancial coordination of care actions were similar across medication classes; other pharmacist actions varied by medication class. Insurance type was significantly associated with reporting impacted productivity; patients with Medicare and Medicaid were 2.2 and 3.1 times more likely to have reported impacted productivity, respectively (P < 0.001) than commercially insured patients. Patients who reported impacted productivity had more pharmacist actions (P < 0.001). CONCLUSION: Patients on DMTs through an HSSP reported low rates of impacted productivity, relapse, and hospitalization due to MS, although patients with noncommercial insurance were more likely to have impacted productivity. Patients reporting impacted productivity and those taking certain DMTs may require more frequent pharmacist actions.
 BACKGROUND: Cladribine is an oral disease-modifying drug authorized by the European Medicine Agency for the treatment of highly active relapsing multiple sclerosis (MS). OBJECTIVES: To provide real-world evidence of cladribine's effectiveness and safety in people with MS (pwMS). METHODS: A retrospective observational multi-center, multi-national study of pwMS who were started on cladribine tablets in ten centers from five European countries. RESULTS: We identified 320 pwMS treated with cladribine tablets. The most common comorbidities were arterial hypertension and depression. Three patients had resolved hepatitis B infection, while eight had positive Quantiferon test prior to cladribine commencement. There were six pwMS who had malignant diseases, but all were non-active. During year 1, 91.6% pwMS did not have EDSS worsening, 86.9% were relapse-free and 72.9% did not have MRI activity. During the second year, 90.2% did not experience EDSS worsening, 86.5% were relapse-free and 75.5% did not have MRI activity. NEDA-3 was present in 58.0% pwMS in year 1 and in 54.2% in year 2. In a multivariable logistic regression model age positively predicted NEDA-3 in year 1. The most common adverse events were infections and skin-related adverse events. Lymphopenia was noted in 54.7% of pwMS at month 2 and in 35.0% at month 6. Two pwMS had a newly discovered malignant disease, one breast cancer, and one melanoma, during the first year of treatment. CONCLUSION: Our real-world data on the effectiveness and safety of cladribine tablets are comparable to the pivotal study and other real-world data with no new safety signals.
 BACKGROUND: Evusheld (EVS) was authorized by FDA and EMA as pre-exposure prophylaxis (PrEP) in people at high risk of severe Covid-19 outcomes, including people with Multiple Sclerosis (pwMS) on B-cell depleting (BCD) therapies-such as Ocrelizumab (OCR). In this population, no data on possible adverse drug reactions (ADRs) to EVS, B-lymphocytes (CD20 +) counts pre- and post-EVS injection, and comparison of percentage increase of IgG antibodies directed against SARS-CoV-2 trimeric spike protein (anti-TSP IgG) post-EVS and Covid-19 vaccine was available. The aim of this study was to better characterize the efficacy and safety profile of EVS in pwMS on BCD agents. METHODS: 17 pwMS on OCR agreed to receive EVS as PrEP for Covid-19. Sera samples were collected before the first dose of Covid-19 vaccine (T0), 4 weeks after the second dose (T1), 4 weeks after third dose (T2), immediately before (T3) and 4 weeks after (T4) EVS. RESULTS: Covid-19 vaccine ADRs were mild-to-moderate, whereas no ADRs were reported after EVS injection. A significant increase of anti-TSP IgG was found only at T0-T1 (Z = -3.059, p = .002) and T3-T4 (Z = -3.621, p < .001) time-points. The median percentage increase between T3-T4 was significantly higher with respect to the T0-T1(Z = -3.296, p = .001) and T1-T2 (Z = -3.059, p = .002) time-points. CONCLUSIONS: These results further support EVS safety and efficacy in boosting anti-TSP IgG titers in pwMS on OCR, with a statistically greater increase than that observed after completion of a full Covid-19 vaccine cycle, plus a booster dose.
 BACKGROUND: Comorbidity is a current area of interest in multiple sclerosis (MS) and is essential for multidisciplinary management. Although recent studies suggest that patients with MS have an elevated risk of developing inflammatory bowel diseases (IBD), this systematic review and meta-analysis aimed to estimate the overall risk of developing ulcerative colitis (UC), specifically in patients with MS. METHODS: In 2021, a comprehensive literature search was performed on PubMed, Scopus, Embase, and Web of Science to identify studies investigating the association between UC and MS. The selected papers were utilized to estimate the associations, risk ratios (RRs), and a 95% confidence interval (CI). RESULTS: The analysis revealed a slightly elevated risk of UC incidence in patients with MS compared to controls, but this finding was not statistically significant (RR: 1.27 [95% CI: 0.96-1.67]). In contrast, the study found that patients with UC have a significantly higher risk of developing MS than controls (RR: 1.66 [95% CI: 1.15-2.40]). CONCLUSION: Our findings highlight that the presence of UC increases the risk of developing MS by more than 50%, whereas the presence of MS does not increase the risk of UC occurrence. These results underscore the importance of considering the potential development of UC in the clinical management and early diagnosis of patients with MS, as it may contribute to better therapeutic outcomes.
 INTRODUCTION: The objective of the study was to investigate long-term food intake patterns and establish possible associations between the inferred dietary habits and levels of reported symptoms among people with multiple sclerosis (MS) in Denmark. METHODS: The present study was designed as a prospective cohort study. Participants were invited to register daily food intake and MS symptoms and were observed during a period of 100 days. Dropout and inclusion probabilities were addressed using generalized linear models. Dietary clusters were identified among 163 participants using hierarchical clustering on principal component scores. Associations between the dietary clusters and the levels of self-assessed MS symptoms were estimated using inverse probability weighting. Furthermore, the effect of a person's position on the first and second principal dietary component axis on symptom burden was investigated. RESULTS: Three dietary clusters were identified: a Western dietary cluster, a plant-rich dietary cluster and a varied dietary cluster. Analyses further indicated a vegetables-fish-fruit-whole grain axis and a red-meat-processed-meat axis. The plant-rich dietary cluster showed reduction in symptom burden in nine pre-defined MS symptoms compared to the Western dietary cluster (between 19 and 90% reduction). This reduction was significant for pain and bladder dysfunction as well as across all nine symptoms (pooled p value = 0.012). Related to the two dietary axes, high intake of vegetables resulted in 32-74% reduction in symptom burden compared to low levels of vegetable intake. Across symptoms, this was significant (pooled p value = 0.015), also regarding walking difficulty and fatigue. CONCLUSIONS: Three dietary clusters were identified. Compared to levels of self-assessed MS-related symptoms, and adjusted for potential confounders, the results suggested less symptom burden with increased intake of vegetables. Although the research design limits the possibilities of establishing causal inference, the results indicate that general guidelines for healthy diet may be relevant as a tool in coping with MS symptoms.
 Multiple sclerosis (MS) is associated with an impaired immune system that severely affects the spinal cord and brain, and which is marked by progressive inflammatory demyelination. Patients with MS may benefit from exercise training as a suggested course of treatment. The most commonly used animal models of studies on MS are experimental autoimmune/allergic encephalomyelitis (EAE) models. The present review intends to concisely discuss the interventions using EAE models to understand the effectiveness of exercise as treatment for MS patients and thereby provide clear perspective for future research and MS management. For the present literature review, relevant published articles on EAE animal models that reported the impacts of exercise on MS, were extracted from various databases. Existing literature support the concept that an exercise regimen can reduce the severity of some of the clinical manifestations of EAE, including neurological signs, motor function, pain, and cognitive deficits. Further results demonstrate the mechanisms of EAE suppression with information relating to the immune system, demyelination, regeneration, and exercise in EAE. The role for neurotrophic factors has also been investigated. Analyzing the existing reports, this literature review infers that EAE is a suitable animal model that can help researchers develop further understanding and treatments for MS. Besides, findings from previous animal studies supports the contention that exercise assists in ameliorating MS progression.
 BACKGROUND: People with multiple sclerosis (MS) who use a wheelchair or scooter full-time fall frequently; however, fall prevention programming that meets the unique needs of this population is limited. This study examined the preliminary efficacy of a group-based online fall prevention and management intervention designed specifically for people with MS. METHODS: This pre/post intervention, mixed-methods study included people with MS who used a wheelchair or scooter full-time, experienced at least 1 fall within the past year, and transferred independently or with minimal or moderate assistance. Participants engaged in a 6-week, online, individualized, multicomponent fall prevention and management intervention: Individualized Reduction of Falls-Online (iROLL-O). RESULTS: No statistically significant change in fall incidence occurred after iROLL-O. However, fear of falling significantly decreased (P < .01) and knowledge related to fall management (P = .04) and fall prevention and management (P = .03) significantly improved. Qualitative results indicated that participants valued the opportunity for peer learning and iROLL-O's attention to diverse influences on fall risk. CONCLUSIONS: This study is the first to examine the preliminary efficacy of an online fall prevention and management intervention for people with MS who use a wheelchair or scooter full-time. iROLL-O has promise, and participants found it valuable. Further efforts are needed to retain iROLL-O participants with lower confidence and functional mobility, and more research is needed to investigate the impact of the intervention on key outcomes over time.
 PURPOSE OF THE STUDY: Calreticulin is an endoplasmic reticulum chaperone protein, which is involved in protein folding and in peptide loading of major histocompatibility complex class I molecules together with its homolog calnexin. Mutated calreticulin is associated with a group of hemopoietic disorders, especially myeloproliferative neoplasms. Currently only the cellular immune response to mutated calreticulin has been described, although preliminary findings have indicated that antibodies to mutated calreticulin are not specific for myeloproliferative disorders. These findings have prompted us to characterize the humoral immune response to mutated calreticulin and its chaperone homologue calnexin. PATIENTS AND METHODS: We analyzed sera from myeloproliferative neoplasm patients, healthy donors and relapsing-remitting multiple sclerosis patients for the occurrence of autoantibodies to wild type and mutated calreticulin forms and to calnexin by enzyme-linked immunosorbent assay. RESULTS: Antibodies to mutated calreticulin and calnexin were present at similar levels in serum samples of myeloproliferative neoplasm and multiple sclerosis patients as well as healthy donors. Moreover, a high correlation between antibodies to mutated calreticulin and calnexin was seen for all patient and control groups. Epitope binding studies indicated that cross-reactive antibodies bound to a three-dimensional epitope encompassing a short linear sequence in the C-terminal of mutated calreticulin and calnexin. CONCLUSION: Collectively, these findings indicate that calreticulin mutations may be common and not necessarily lead to onset of myeloproliferative neoplasm, possibly due to elimination of cells with mutations. This, in turn, may suggest that additional molecular changes may be required for development of myeloproliferative neoplasm.
 BACKGROUND: Vocal disorders are frequent in people with multiple sclerosis (MS). Cognitive impairment, fatigue, depression, and other clinical characteristics can be associated with treatment effectiveness in rehabilitation. Finding baseline characteristics that identify those who are responding to treatment can help the clinical decision-making process, which can then help improve the effectiveness of voice treatment. We developed a model to identify factors associated with treatment-related improvement on voice intensity in people with MS. METHODS: Data are from a randomized controlled trial of the effects of voice therapy. Forty-four people with MS were enrolled and randomized to receive Lee Silverman Voice Treatment LOUD, specifically addressing voice intensity, or conventional speech-therapy group. Voice intensity (dB) was measured during monologue before and after treatment and was used to differentiate those who responded (posttreatment voice intensity > 60 dB) from those who did not. Possible associated factors were cognitive impairment, fatigue, depression, disability, and disease duration. Associations were assessed by univariate logistic regression and univariate and multivariate linear regressions. RESULTS: Mean ± SD monologue voice intensity is improved in the whole sample (before rehabilitation: 51.8 ± 4.2 dB; and after rehabilitation 57.0 ± 6.5 dB; P < .001), and 11 people with MS (27.5%) responded to treatment. Specificity of treatment was associated with the return to normal voice intensity (OR, 14.28; 95% CI, 12.17-309.56) and we found a linear association between voice improvement and the specificity of treatment (6.65 [SE = 1.54] dB; P < .05). Moreover, the analysis revealed a nonlinear association between improvement and fatigue, suggesting increased benefits for people with MS with moderate fatigue. Other factors were not significantly associated with treatment effectiveness. CONCLUSIONS: Moderate fatigue and the specificity of the intervention seem to be key factors associated with clinically relevant improvement in voice intensity even in people with MS with a high level of disability and long disease duration.
 INTRODUCTION: LEMVIDA is a real-world prospective study of 3-year follow-up on quality of life of patients with multiple sclerosis (MS) receiving alemtuzumab in Spain. METHODS: This is an interim analysis evaluating the baseline characteristics of patients who started alemtuzumab between October 2016-September 2018. For 3 additional subanalysis patients were categorised by baseline EDSS score; time of alemtuzumab initiation during the recruitment period (cohort 1: October 2016-March 2017, cohort 2: April-September 2017, cohort 3: October 2017-March 2018 and cohort 4: April-September 2018); and the presence of highly active MS criteria. RESULTS: 161 patients were analysed: 67.1% female, age 38.7 ± 9.4 years, MS duration 8.5 ± 6.0 years, EDSS 3.3 ± 1.7 and number of relapses in the previous 2 years 1.8 ± 1.3. 48.3% of patients presented gadolinium-enhanced (Gd+) lesions (mean: 5.2 ± 6.9) and 63.1% had received prior treatment with fingolimod or natalizumab. Baseline EDSS scores and number of Gd+ lesions were higher in cohort 1 than in cohort 4 (4.1 ± 1.8 vs 3.2 ± 1.7; P = .040 and 10.9 ± 11.9 vs 4.5 ± 5.7; P = .020). The frequency of prior treatment with fingolimod and natalizumab was lower in cohort 4 (60.6%) than in cohort 1 (70.6%) (comparison between groups not analysed). CONCLUSIONS: Unlike phase 3 studies of alemtuzumab, the patients included in LEMVIDA are older, have a longer duration of MS, higher disability and have received previous immunosuppressants. However, throughout the recruitment period, there is a tendency towards an early beginning of treatment with alemtuzumab, probably due to the evidence of higher effectiveness in the early stages of MS.
 BACKGROUND: Although the necessity of upper limb (UL) (dys)function assessment in people with Multiple Sclerosis (pwMS) has been demonstrated in recent years, this is still neglected at an early-stage. OBJECTIVE: The aim of our study was to comprehensively examine bilateral UL in early-stage pwMS who are thought to have no or minimal involvement in activities of daily living for the UL. METHODS: UL muscle strength, sensation and dexterity of 44 pwMS (EDSS score<4, disease duration<5 years, who did not report problems in daily living activities specifically for the UL) were evaluated bilaterally and compared with 44 healthy controls (HC). The relationship between UL function and muscle strength, sensation, cognitive function, fatigue, mood status, participation, EDSS, and disease duration were examined. The results of the outcome measures evaluating the UL function objectively and subjectively were analyzed. RESULTS: Muscle strength, sensation and dexterity were similar in the dominant and nondominant extremities of pwMS and were affected compared to HC. A fair relationship was found between UL function and proximal muscle strength, fatigue, cognitive function, home participation and EDSS. According to the cut-off value (18 s) of Nine Hole Peg Test, only 9.09% of pwMS was unaffected, but 79.54% of affected pwMS had a full ABILHAND score. CONCLUSION: Early-stage pwMS are unaware of the dysfunction since their UL involvement does not affect their daily living activities yet. Patient-reported outcome measures such as ABILHAND can be misleading and have a ceiling effect in the early-stage of the disease. Objective functional evaluations reveal that UL capacity is affected from the early period. Even if pwMS do not report UL involvement, clinicians and researchers should evaluate UL function and include it in the treatment program from an early-stage to prevent further disease burden.
 PURPOSE: Ganglion cell layer thickness (GCLT)-to-total macular thickness (MT) is a new parameter that has not been studied in multiple sclerosis (MS) before. The current study aims to reveal the status of the GCLT-to-MT ratio in MS and its role in supporting the diagnosis of MS. METHODS: In this retrospective and cross sectional study, the medical records of the MS patients between January 2016 and December 2021 were reviewed. Age-sex matched healthy control group was generated. Demographic and clinical data recorded. All participants were examined using a spectral-domain optic coherence tomography (OCT) device. Retinal layers, choroidal thickness (CT) was recorded. GCLT-to-MT ratio was calculated. RESULTS: A total of 74 eyes of 37 MS (9 male,28 female) patients and 82 eyes of 41 control (13 male, 28 female) were included in the study. The mean age was 37 ± 9.0 (years) in MS group. The MS patients and the control group were compared in terms of OCT parameters, CT was thicker at all regions in MS patients (p < 0.001). Macular thickness, GCLT, and inner plexiform layer thickness (IPLT) were thinner than the control group (p < 0.05). For distinguishing MS patients from healthy subjects, AUROC values for central GCLT/MT, temporal GCLT/MT, superior GCLT/MT, nasal GCLT/MT, and inferior GCLT/MT were 0.717, 0.689, 0.694, 0.733, and 0.740, respectively. CONCLUSIONS: In conclusion MT, GCLT, and IPLT thickness were thinner in MS patients, regardless of optic neuritis. The AUROC values of GCLT/MT were high and GCLT/MT ratio may be a helpful modality in demonstrating retinal neurodegeneration in MS patients.
 Multiple sclerosis (MS) is a neuroinflammatory demyelinating disease, mediated by pathogenic T helper 17 (Th17) cells. However, the therapeutic effect is accompanied by the fluctuation of the proportion and function of Th17 cells, which prompted us to find the key regulator of Th17 differentiation in MS. Here, we demonstrated that the triggering receptor expressed on myeloid cells 2 (TREM-2), a modulator of pattern recognition receptors on innate immune cells, was highly expressed on pathogenic CD4-positive T lymphocyte (CD4(+) T) cells in both patients with MS and experimental autoimmune encephalomyelitis (EAE) mouse models. Conditional knockout of Trem-2 in CD4(+) T cells significantly alleviated the disease activity and reduced Th17 cell infiltration, activation, differentiation, and inflammatory cytokine production and secretion in EAE mice. Furthermore, with Trem-2 knockout in vivo experiments and in vitro inhibitor assays, the TREM-2/zeta-chain associated protein kinase 70 (ZAP70)/signal transducer and activator of transcription 3 (STAT3) signal axis was essential for Th17 activation and differentiation in EAE progression. In conclusion, TREM-2 is a key regulator of pathogenic Th17 in EAE mice, and this sheds new light on the potential of this therapeutic target for MS.
 OBJECTIVE: To determine the COVID-19 vaccine uptake among people with multiple sclerosis (pwMS) compared to the general population in Croatia. METHODS: Data from all pwMS entered in the MS Base register until March 24th, 2022 were extracted including age, sex, MS phenotype, disease-modifying therapy (DMT), and date of COVID-19 vaccination. Data on the general population of Croatia were obtained from the vaccination register of the Croatian Institute of Public Health. RESULTS: 64.4% pwMS were fully COVID-19 vaccinated which was comparable to 66.3% of the general population. More pwMS were fully vaccinated in the age group 20-24 (74.1% vs 51.7%), and fewer pwMS were fully vaccinated in the age group 65-69 (33.3% vs 80.4%) compared to the general population of the same age group, respectively. PwMS who received at least one dose of any COVID-19 vaccine were older (40.5 vs 37.6 years, p = 0.01), had higher EDSS (2.0 vs 1.0, p = 0.025), and had longer disease duration (6.39 vs 5.35 years, p = 0.02), were more likely to have progressive disease course (p = 0.049) and were on high efficacy DMTs (p = 0.045) compared to unvaccinated pwMS. Longer disease duration positively predicted vaccine uptake. CONCLUSION: Croatia has suboptimal COVID-19 vaccination uptake without a significant difference between the general population and pwMS.
 PURPOSE: Multiple sclerosis (MS) is an inflammatory neurodegenerative disease of the central nervous system. Recent evidence suggests that degeneration of the inner layers of the retina occurs in MS. This study aimed to examine whether there are outer retinal changes in patients living with MS. DESIGN: This was a single center, cross-sectional study. PARTICIPANTS: Sixteen patients with MS and 25 controls (volunteers without diagnosed MS) were recruited for the study. METHODS: We acquired volumetric spectral domain-OCT scans of the macula and a circular scan around the optic nerve head (ONH). We also captured adaptive optics (AO) images at 0° (centered on the foveola), 2°, 4°, and 6° temporal to the fovea. MAIN OUTCOME MEASURES: We calculated the thickness of the different retinal layers in the macula and around the ONH using the inbuilt software of the OCT. We evaluated changes in cone photoreceptors by calculating cone density and spacing by the inbuilt AO automatic segmentation algorithm with manual correction. We compared patients with and without optic neuritis and controls. RESULTS: We found significant thinning of the inner retina and a thickening of the outer retina in the eye with a history of optic neuritis (eyes of patients with MS with a history of optic neuritis; mean difference [MD]: -11.13 ± 3.61 μm, P = 0.002 and MD: 2.86 ± 0.89 μm, P = 0.001; respectively). We did not observe changes in retinal layers without optic neuritis in eyes of patients with MS without a history of optic neuritis. However, regional differences were detected in the peripapillary retinal nerve fiber layer. Analyzing AO images revealed a significantly lower cone outer-segment density at all eccentricities in all patients compared with control eyes (P < 0.05), independent of optic neuritis history. CONCLUSIONS: Our results showed that all MS cases were associated with decreased cone densities. Future longitudinal studies will help to elucidate whether this is a specific and sensitive method to detect and monitor the development and progression of MS. FINANCIAL DISCLOSURES: Proprietary or commercial disclosure may be found after the references.
 BACKGROUND: Takotsubo syndrome (TTS) is mainly characterized by chest pain, left ventricular dysfunction, ST-segment deviation on electrocardiogram (ECG) and elevated troponins in the absence of obstructive coronary artery disease. Diagnostic features include left ventricular systolic dysfunction shown on transthoracic echocardiography (TTE) with wall motion abnormalities, generally with the typical "apical ballooning" pattern. In very rare cases, it involves a reverse form which is characterized by basal and mid-ventricular severe hypokinesia or akinesia, and sparing of the apex. TTS is known to be triggered by emotional or physical stressors. Recently, multiple sclerosis (MS) has been described as a potential trigger of TTS, especially when lesions are located in the brainstem. CASE SUMMARY: We herein report the case of a 26-year-old woman who developed cardiogenic shock due to reverse TTS in the setting of MS. After being admitted for suspected MS, the patient presented with rapidly deteriorating clinical condition, with acute pulmonary oedema and hemodynamic collapse, requiring mechanical ventilation and aminergic support. TTE found a severely reduced left ventricular ejection fraction (LVEF) of 20%, consistent with reverse TTS (basal and mid ventricular akinesia, apical hyperkinesia). Cardiac magnetic resonance imaging (MRI) performed 4 days later showed myocardial oedema in the mid and basal segments on T2-weighted imaging, with partial recovery of LVEF (46%), confirmed the diagnosis of TTS. In the meantime, the suspicion of MS was also confirmed, based on cerebral MRI and cerebral spinal fluid analyses, with a final diagnosis of reverse TTS induced by MS. High-dose intravenous corticotherapy was initiated. Subsequent evolution was marked by rapid clinical improvement, as well as normalization of LVEF and segmental wall-motion abnormalities. CONCLUSION: Our case is an example of the brain-heart relationship: it shows how neurologic inflammatory diseases can trigger a cardiogenic shock due to TTS, with potentially serious outcomes. It sheds light on the reverse form, which, although rare, has already been described in the setting of acute neurologic disorders. Only a handful of case reports have highlighted MS as a trigger of reverse TTS. Finally, through an updated systematic review, we highlight the unique features of patients with reversed TTS triggered by MS.
 Botulinum toxin type A (BoNT-A) is the treatment of choice for focal spasticity, with a concomitant effect on pain reduction and improvement of quality of life (QoL). Current evidence of its efficacy is based mainly on post stroke spasticity. This study aims to clarify the role of BoNT-A in the context of non-stroke spasticity (NSS). We enrolled 86 patients affected by multiple sclerosis, spinal cord injury, and traumatic brain injury with clinical indication to perform BoNT-A treatment. Subjects were evaluated before injection and after 1, 3, and 6 months. At every visit, spasticity severity using the modified Ashworth scale, pain using the numeric rating scale, QoL using the Euro Qol Group EQ-5D-5L, and the perceived treatment effect using the Global Assessment of Efficacy scale were recorded. In our population BoNT-A demonstrated to have a significant effect in improving all the outcome variables, with different effect persistence over time in relation to the diagnosis and the number of treated sites. Our results support BoNT-A as a modifier of the disability condition and suggest its implementation in the treatment of NSS, delivering a possible starting point to generate diagnosis-specific follow-up programs. CLINICAL TRIAL IDENTIFIER: NCT04673240.
 Objective: Studies on the relationship between depression and cognition on patients with multiple sclerosis (MS) are inconsistent and it is not clear whether higher depression levels are associated with impairment of specific cognitive domains or processes. This meta-analytic study aimed at evaluating the possible association between depressive symptomatology and performance on cognitive tests assessing several cognitive domains (global cognition, attention, processing speed, verbal, spatial and working memory, verbal fluency, inhibitory control, set-shifting) in individuals living with MS. Method: The literature search on three electronic databases yielded 5402 studies (4333 after the duplicates removal); after the evaluation of titles, abstracts full-text articles, 37 studies were included in the meta-analytic study. A random-effect model meta-analysis was performed and mean weighted effect sizes (ESs) were calculated using Hedges' g. Results: Small ESs were found for the relationship between depression and verbal memory (g = 0.25, p < 0.001), spatial memory (g = 0.23, p < 0.001), verbal fluency (g = 0.26, p < 0.001), and inhibitory control (g = 0.32, p = 0.003). Medium ESs were found for the relationship between depression and global cognition (g = 0.46, p < 0.001), attention (g = 0.43, p < 0.001), processing speed (g = 0.47, p < 0.001) and working memory (g = 0.38, p = 0.037). The relationship between set-shifting abilities and depression was not significant (g = 0.39, p = 0.095). Conclusions: Results suggest that patients with MS and higher levels of depressive symptomatology may also show more difficulties in several aspects of cognition, especially those needed to retain, respond, and process information in one's environment, and to those needed be adequately stimulated in processing relevant information.
 BACKGROUND: The association of multiple sclerosis (MS) with joint diseases has been established. However, the impact of MS on postoperative outcomes following total joint arthroplasty (TJA) remains controversial. Therefore, a systematic review of the literature is warranted to ascertain the relationship between MS and adverse outcomes post-TJA. METHODS: A systematic literature search of PubMed, Embase, Scopus, and the Cochrane Library from inception to 1 March 2023 was conducted to identify observational studies comparing post-TJA outcomes in MS and non-MS patients. Two investigators independently screened titles, abstracts, and full-text articles for eligibility. A random-effects model was used to calculate odds ratios (OR), mean differences (MD), and corresponding 95% confidence intervals (CI). RESULTS: Seven retrospective cohort studies published between 2018 and 2022 met the inclusion criteria. Patients with MS had a higher risk of medical, surgical, and overall complications than patients without MS. Similarly, the MS group was more likely to experience an extended hospital stay, non-home discharge, and revision surgery compared to the control group. Joint infection and implant instability were also more common in patients with MS. CONCLUSION: Although TJA may benefit MS patients, current evidence suggests that their postoperative outcomes may be inferior to those of non-MS patients. Thus, orthopaedic surgeons should inform MS patients of potential risks and perform preoperative optimization individually when considering elective arthroplasty.
 Immunoglobulin gamma (IgG) oligoclonal bands (OCB) in the cerebrospinal fluid (CSF) are absent in a small group of multiple sclerosis (MS) patients. According to previous research, OCB-negative MS patients differ genetically but not clinically from OCB-positive MS patients. However, whether OCB-negative MS is a unique immunological and clinical entity remains unclear. The absence of OCB poses a significant challenge in diagnosing MS. (1) Objective: The objective of this study was twofold: (1) to determine the prevalence of OCB-negative MS patients in the Uppsala region, and (2) to assess the frequency of misdiagnosis in this patient group. (2) Methods: We conducted a retrospective study using data from the Swedish MS registry (SMSreg) covering 83% of prevalent MS cases up to 20 June 2020 to identify all MS patients in the Uppsala region. Subsequently, we collected relevant information from the medical records of all OCB-negative MS cases, including age of onset, gender, presenting symptoms, MRI features, phenotype, Expanded Disability Status Scale (EDSS) scores, and disease-modifying therapies (DMTs). (3) Results: Out of 759 MS patients identified, 69 had an OCB-negative MS diagnosis. Upon re-evaluation, 46 patients had a typical history and MRI findings of MS, while 23 had unusual clinical and/or radiologic features. An alternative diagnosis was established for the latter group, confirming the incorrectness of the initial MS diagnosis. The average EDSS score was 2.0 points higher in the MS group than in the non-MS group (p = 0.001). The overall misdiagnosis rate in the cohort was 33%, with 22% of misdiagnosed patients having received DMTs. (4) Conclusions: Our results confirm that the absence of OCB in the CSF should raise suspicion of possible misdiagnosis in MS patients and prompt a diagnostic reassessment.
 Multiple sclerosis (MS) is an autoimmune demyelinating neurodegenerative disease of the central nervous system (CNS) due to injury of the myelin sheath by immune cells. The clotting factor fibrinogen is involved in the pathogenesis of MS by triggering microglia and the progress of neuroinflammation. Fibrinogen level is correlated with MS severity; consequently, inhibition of the fibrinogen cascade may reduce MS neuropathology. Thus, this review aimed to clarify the potential role of fibrinogen in the pathogenesis of MS and how targeting of fibrinogen affects MS neuropathology. Accumulation of fibrinogen in the CNS may occur independently or due to disruption of blood-brain barrier (BBB) integrity in MS. Fibrinogen acts as transduction and increases microglia activation which induces the progression of inflammation, oxidative stress, and neuronal injury. Besides, brain fibrinogen impairs the remyelination process by inhibiting the differentiation of oligodendrocyte precursor cells. These findings proposed that fibrinogen is associated with MS neuropathology through interruption of BBB integrity, induction of neuroinflammation, and demyelination with inhibition of the remyelination process by suppressing oligodendrocytes. Therefore, targeting of fibrinogen and/or CD11b/CD18 receptors by metformin and statins might decrease MS neuropathology. In conclusion, inhibiting the expression of CD11b/CD18 receptors by metformin and statins may decrease the pro-inflammatory effect of fibrinogen on microglia which is involved in the progression of MS.
 BACKGROUND: Impairment of higher language functions associated with natural spontaneous speech in multiple sclerosis (MS) remains underexplored. OBJECTIVES: We presented a fully automated method for discriminating MS patients from healthy controls based on lexical and syntactic linguistic features. METHODS: We enrolled 120 MS individuals with Expanded Disability Status Scale ranging from 1 to 6.5 and 120 age-, sex-, and education-matched healthy controls. Linguistic analysis was performed with fully automated methods based on automatic speech recognition and natural language processing techniques using eight lexical and syntactic features acquired from the spontaneous discourse. Fully automated annotations were compared with human annotations. RESULTS: Compared with healthy controls, lexical impairment in MS consisted of an increase in content words (p = 0.037), a decrease in function words (p = 0.007), and overuse of verbs at the expense of noun (p = 0.047), while syntactic impairment manifested as shorter utterance length (p = 0.002), and low number of coordinate clause (p < 0.001). A fully automated language analysis approach enabled discrimination between MS and controls with an area under the curve of 0.70. A significant relationship was detected between shorter utterance length and lower symbol digit modalities test score (r = 0.25, p = 0.008). Strong associations between a majority of automatically and manually computed features were observed (r > 0.88, p < 0.001). CONCLUSION: Automated discourse analysis has the potential to provide an easy-to-implement and low-cost language-based biomarker of cognitive decline in MS for future clinical trials.
 BACKGROUND: New interventions for multiple sclerosis (MS) commonly require a demonstration of cost-effectiveness using health-related quality of life (HRQoL) utility values. The EQ-5D is the utility measure approved for use in the UK NHS funding decision-making. There are also MS-specific utility measures - e.g., MS Impact Scale Eight Dimensions (MSIS-8D) and MSIS-8D-Patient (MSIS-8D-P). OBJECTIVES: Provide EQ-5D, MSIS-8D and MSIS-8D-P utility values from a large UK MS cohort and investigate their association with demographic/clinical characteristics. METHODS: UK MS Register data from 14,385 respondents (2011 to 2019) were analysed descriptively and using multivariable linear regression, with self-report Expanded Disability Status Scale (EDSS) scores. RESULTS: The EQ-5D and MSIS-8D were both sensitive to differences in demographic/clinical characteristics. An inconsistency found in previous studies whereby mean EQ-5D values were higher for an EDSS score of 4 rather than 3 was not observed. Similar utility values were observed between MS types at each EDSS score. Regression showed EDSS score and age were associated with utility values from all three measures. CONCLUSIONS: This study provides generic and MS-specific utility values for a large UK MS sample, with the potential for use in cost-effectiveness analyses of treatments for MS.
 OBJECTIVE: Fatigue in multiple sclerosis (MS) is common, burdensome, and usually assessed by self-report measures. This retrospective data analysis of the twice-daily Alertness test (Test battery of Attentional Performance) examined the extent to which this assessment procedure is associated with MS-related fatigue. METHOD: Two-hundred and thirteen German inpatients (136 women) aged 18-69 years with predominantly relapsing MS (72.8%) were included. Based on reaction time (RT) differences between morning tonic alertness (8:30-11:00 a.m.) and afternoon tonic alertness (3:00-4:30 p.m.), patients were divided into an "improver," "maintainer," or "decliner" group. Multinomial logistic regression (MLR) was calculated to predict the likelihood of belonging to one of these performance groups, taking into account cognitive fatigue (Fatigue Scale of Motor and Cognition, FSMCcog), disease severity (Expanded Disability Status Scale, EDSS), depression (Center for Epidemiologic Studies Depression Scale, CES-D), gender, and tonic alertness (a.m.). RESULTS: The final MLR model (R2 = .30) included tonic alertness (a.m.) (<.001), FSMCcog (.008), EDSS (.038), CES-D (.161), and gender (.057). Using this model, correct assignment to alertness performance groups was 56.8%. Tonic alertness (p.m.) demonstrated the greatest potential for differentiation among the three performance groups (<.001). CONCLUSIONS: These results show a relationship between subjective fatigue and tonic alertness. However, other variables also contribute to this association, suggesting that the RT differences between twice-daily measures of tonic alertness is not related to increased subjective fatigue in a substantial number of pwMS, which diminishes the diagnostic value. Further studies including relevant variables such as sleepiness are urgently needed.
 BACKGROUND: Spasticity is a common symptom of multiple sclerosis (MS) which affects mobility. Dry Needling (DN) has shown a reduction in spasticity in neuromuscular conditions such as stroke and spinal cord injury although the mechanism of action is still unclear. In spastic individuals, the Rate-Dependent Depression (RDD) of the H reflex is decreased as compared to controls and analyzing the effects of DN in the RDD may help to understand its mechanism of action. OBJECTIVE: To evaluate the effect of Dry Needling on spasticity measured by the Rate-dependent Depression (RDD) of the H reflex in an MS patient. METHODS: Three time points were evaluated: Pre-intervention (T1), Post-intervention assessments were carried out in the seventh week at two-time points: Before DN (T2) and After DN (T3). Main outcomes included the RDD and latency of the H reflex in the lower limbs at stimulation frequencies of 0.1, 1, 2, and 5 Hz in a five consecutive pulses protocol. RESULTS: An impairment of the RDD of the H reflex at frequencies ≥1 Hz was found. Statistically significant differences were found when comparing the mean RDD of the H reflex in Pre-intervention compared to Post-intervention at 1, 2, and 5 Hz stimulation frequencies. Mean latencies were statistically lower when comparing Pre- vs Post-intervention. CONCLUSION: Results suggest a partial reduction in spasticity represented by decrease of the excitability of the neural elements involved in the RDD of the H reflex following DN. The RDD of the H reflex could be implemented as an objective tool to monitor changes in spasticity in larger DN trials.
 BACKGROUND: Multiple sclerosis (MS) and cerebral small vessel disease (CSVD) are relatively common radiological entities that occasionally necessitate differential diagnosis. PURPOSE: To investigate the differences in magnetic resonance imaging (MRI) signal intensity (SI) between MS and CSVD related white matter lesions. MATERIAL AND METHODS: On 1.5-T and 3-T MRI scanners, 50 patients with MS (380 lesions) and 50 patients with CSVD (395 lesions) were retrospectively evaluated. Visual inspection was used to conduct qualitative analysis on diffusion-weighted imaging (DWI)_b1000 to determine relative signal intensity. The thalamus served as the reference for quantitative analysis based on SI ratio (SIR). The statistical analysis utilized univariable and multivariable methods. There were analyses of patient and lesion datasets. On a dataset restricted by age (30-50 years), additional evaluations, including unsupervised fuzzy c-means clustering, were performed. RESULTS: Using both quantitative and qualitative features, the optimal model achieved a 100% accuracy, sensitivity, and specificity with an area under the curve (AUC) of 1 in patient-wise analysis. With an AUC of 0.984, the best model achieved a 94% accuracy, sensitivity, and specificity when using only quantitative features. The model's accuracy, sensitivity, and specificity were 91.9%, 84.6%, and 95.8%, respectively, when using the age-restricted dataset. Independent predictors were T2_SIR_max (optimal cutoff=2.1) and DWI_b1000_SIR_mean (optimal cutoff=1.1). Clustering also performed well with an accuracy, sensitivity, and specificity of 86.5%, 70.6%, and 100%, respectively, in the age-restricted dataset. CONCLUSION: SI characteristics derived from DWI_b1000 and T2-weighted-based MRI demonstrate excellent performance in differentiating white matter lesions caused by MS and CSVD.
 BACKGROUND: Many factors are believed to be positively associated with the incidence of relapses in people with multiple sclerosis (MS), including infections. However, their role is still controversial. We aimed to investigate whether symptomatic infections in people with MS increase the risk of relapse in the short, medium, or long term. MATERIALS AND METHODS: We enrolled consecutive patients with relapsing MS (RMS) from October to December 2018. From enrolment up to September 2020, an online questionnaire investigating the occurrence of infections was sent via WhatsApp(®) monthly to the enrolled patients, while in-person visits were performed every six months. When patients complained of symptoms compatible with relapses, they attended an extra in-person visit. RESULTS: We enrolled 155 patients with RMS, and 88.38% of patients were treated with disease-modifying therapies. In the dataset, 126,381 total patient days, 78 relapses, and 1202 infections were recorded over a period of about 2 years. No increased risk of relapse after clinically manifest infections was found in the short-, medium-, or long-term period. No correlation was found between all infections and the number of relapses (p = 0.212). The main analyses were repeated considering only those infections that had at least two of the following characteristics: duration of infection ≥ 4 days, body temperature > 37° Celsius, and the use of drugs (antibiotics and/or antivirals), and no significant associations were observed. CONCLUSIONS: No associations between infections and relapses were observed, likely suggesting that disease-modifying therapies may protect against the risk of relapse potentially triggered by infections.
 INTRODUCTION: Early identification of patients at high risk of progression could help with a personalised treatment strategy. Magnetic resonance imaging (MRI) measures have been proposed to predict long-term disability in multiple sclerosis (MS), but a reliable predictor that can be easily implemented clinically is still needed. AIM: Assess MRI measures during the first 5 years of the MS disease course for the ability to predict progression at 10+ years. METHODS: Eighty-two MS patients (53 females), with ≥10 years of clinical follow-up and having two MRI scans, were included. Clinical data were obtained at baseline, follow-up and at ≥10 years. White matter lesion (WML) counts and volumes, and four linear brain sizes were measured on T2/FLAIR 'Fluid-Attenuated-Inversion-Recovery' and T1-weighted images. RESULTS: Baseline and follow-up inter-caudate diameter (ICD) and third ventricular width (TVW) measures correlated positively with Expanded Disability Status Scale, ≥10 or more of WMLs showed a high sensitivity in predicting progression, at ≥10 years. A steeper rate of lesion volume increase was observed in subjects converting to secondary progressive MS. The sensitivity and specificity of both ICD and TVW, to predict disability at ≥10 years were 60% and 64%, respectively. CONCLUSION: Despite advances in brain imaging and computerised volumetric analysis, ICD and TVW remain relevant as they are simple, fast and have the potential in predicting long-term disability. However, in this study, despite the statistical significance of these measures, the clinical utility is still not reliable.
 INTRODUCTION: This study aimed to compare the neuroaxonal damage of the optic nerve and retina in multiple sclerosis (MS) patients with and without overactive bladder (OAB). PATIENTS AND METHODS: We included patients with MS, divided into two groups, based on the severity of OAB symptoms, as evaluated by the OAB-V8 questionnaire. The groups were compared in terms of each dial of the Expanded Disability Status Scale (EDSS), best-corrected visual acuity, intraocular pressure, peripapillary retinal nerve fiber layer (pRNFL) thickness, macular thickness, and macular ganglion cell-inner plexiform layer (mGCIPL) thickness. RESULTS: The study involved a total of 120 eyes, 78 eyes from 43 female patients, and 42 from 22 male patients. There were 86 eyes (Group 1) with OAB-V8 score under 8 and there were 34 eyes (Group 2) with OAB-V8 score of 8 or over. EDSS median value was 1 (0-2) for Group 1 and 2 (0.8-3.3) for Group 2 (p=0.004). A comparison of pRNFL thicknesses showed statistically significant lower average, superior, and inferior median values in Group 2. A comparison of mGCIPL thicknesses showed statistically significant lower values in Group 2 for superior, superonasal, inferotemporal, and superotemporal quadrants CONCLUSION: This study revealed, for MS patients without optic neuritis attacks, there was a higher incidence of OAB when the EDSS score was higher. There was a statistically significant relationship between the existence of OAB and thinning in both mGCIPL and pRNFL. The most relevant factor for OAB was found to be pRFNL inferior quadrant thinning.
 BACKGROUND: A compelling body of evidence implicates cigarette smoking and lung inflammation in Multiple Sclerosis (MS) susceptibility and progression. Previous studies have reported epigenetic age (DNAm age) acceleration in blood immune cells and in glial cells of people with MS (pwMS) compared to healthy controls (HC). OBJECTIVES: We aimed to examine biological ageing in lung immune cells in the context of MS and smoking. METHODS: We analyzed age acceleration residuals in lung bronchoalveolar lavage (BAL) cells, constituted of mainly alveolar macrophages, from 17 pwMS and 22 HC in relation to smoking using eight DNA methylation-based clocks, namely AltumAge, Horvath, GrimAge, PhenoAge, Zhang, SkinBlood, Hannum, Monocyte clock as well as two RNA-based clocks, which capture different aspects of biological ageing. RESULTS: After adjustment for covariates, five epigenetic clocks showed significant differences between the groups. Four of them, Horvath (P(adj) = 0.028), GrimAge (P(adj) = 4.28 × 10(-7)), SkinBlood (P(adj) = 0.001) and Zhang (P(adj) = 0.02), uncovered the sole effect of smoking on ageing estimates, irrespective of the clinical group. The Horvath, SkinBlood and Zhang clocks showed a negative impact of smoking while GrimAge detected smoking-associated age acceleration in BAL cells. On the contrary, the AltumAge clock revealed differences between pwMS and HC and indicated that, in the absence of smoking, BAL cells of pwMS were epigenetically 5.4 years older compared to HC (P(adj) = 0.028). Smoking further affected epigenetic ageing in BAL cells of pwMS specifically as non-smoking pwMS exhibited a 10.2-year AltumAge acceleration compared to pwMS smokers (P(adj) = 0.0049). Of note, blood-derived monocytes did not show any MS-specific or smoking-related AltumAge differences. The difference between BAL cells of pwMS smokers and non-smokers was attributable to the differential methylation of 114 AltumAge-CpGs (P(adj) < 0.05) affecting genes involved in innate immune processes such as cytokine production, defense response and cell motility. These changes functionally translated into transcriptional differences in BAL cells between pwMS smokers and non-smokers. CONCLUSIONS: BAL cells of pwMS display inflammation-related and smoking-dependent changes associated to epigenetic ageing captured by the AltumAge clock. Future studies examining potential confounders, such as the distribution of distinct BAL myeloid cell types in pwMS compared to control individuals in relation to smoking may clarify the varying performance and DNAm age estimations among epigenetic clocks.
 AIMS: Fibroblast growth factor (FGF) signalling is dysregulated in multiple sclerosis (MS) and other neurological and psychiatric conditions, but there is little or no consensus as to how individual FGF family members contribute to disease pathogenesis. Lesion development in MS is associated with increased expression of FGF1, FGF2 and FGF9, all of which modulate remyelination in a variety of experimental settings. However, FGF9 is also selectively upregulated in major depressive disorder (MDD) prompting us to speculate it may also have a direct effect on neuronal function and survival. METHODS: Transcriptional profiling of myelinating cultures treated with FGF1, FGF2 or FGF9 was performed and the effects of FGF9 on cortical neurons investigated using a combination of transcriptional, electrophysiological and immunofluorescence microscopic techniques. The in vivo effects of FGF9 were explored by stereotactic injection of adeno-associated viral (AAV) vectors encoding either FGF9 or EGFP into the rat motor cortex. RESULTS: Transcriptional profiling of myelinating cultures after FGF9 treatment revealed a distinct neuronal response with a pronounced downregulation of gene networks associated with axonal transport and synaptic function. In cortical neuronal cultures, FGF9 also rapidly downregulated expression of genes associated with synaptic function. This was associated with a complete block in the development of photo-inducible spiking activity, as demonstrated using multi-electrode recordings of channel rhodopsin-transfected rat cortical neurons in vitro and ultimately, neuronal cell death. Overexpression of FGF9 in vivo resulted in rapid loss of neurons and subsequent development of chronic grey matter lesions with neuroaxonal reduction and ensuing myelin loss. CONCLUSIONS: These observations identify overexpression of FGF9 as a mechanism by which neuroaxonal pathology could develop independently of immune-mediated demyelination in MS. We suggest targeting neuronal FGF9-dependent pathways may provide a novel strategy to slow if not halt neuroaxonal atrophy and loss in MS, MDD and potentially other neurodegenerative diseases.
 BACKGROUND: The hippocampus is a clinically relevant region where neurogenesis and neuroplasticity occur throughout the whole lifespan. Neuroinflammation and cardiorespiratory fitness (CRF) may influence hippocampal integrity by modulating the processes promoting neurogenesis and neuroprotection that contribute to the preservation of functions. This study aimed to investigate the effects of neuroinflammation and CRF on hippocampal volume in multiple sclerosis (MS) patients with relapsing-remitting (RR) and progressive (P) clinical phenotypes. The influence of neuroinflammation and CRF on brain, grey matter (GM) and thalamic volumes was also assessed to determine whether the effects were specific for the hippocampus. METHOD: Brain 3T structural MRI scans and maximum oxygen consumption (VO(2)max), a proxy of CRF, were acquired from 81 MS patients (27 RR and 54 P) and 45 age-matched and sex-matched healthy controls. T2-hyperintense white matter lesion volume (T2-LV) and choroid plexuses volume (CPV) were quantified as neuroinflammatory measures. Associations of demographic, clinical, neuroinflammatory and CRF measures with normalised brain, GM, hippocampal and thalamic volumes in relapsing-remitting MS (RRMS) and progressive MS patients were assessed using Shapley and best subset selection regression. RESULTS: For most volumetric measures, the largest portions of variance were explained by T2-LV (variable importance (VI)=9.4-39.4) and CPV (VI=4.5-26.2). VO(2)max explained the largest portion of variance of normalised hippocampal volume only in RRMS patients (VI=16.9) and was retained as relevant predictor (standardised β=0.374, p=0.023) with T2-LV (standardised β=-0.330, p=0.016). CONCLUSIONS: A higher CRF may play a specific neuroprotective role on MS patients' hippocampal integrity, but only in the RR phase of the disease.
 BACKGROUND AND OBJECTIVES: Disability and cognitive impairment are known to be related to brain atrophy in multiple sclerosis (MS), but 3D-T1 imaging required for brain volumetrics is often unavailable in clinical protocols, unlike 3D-FLAIR. Here our aim was to investigate whether brain volumes derived from 3D-FLAIR images result in similar associations with disability and cognition in MS as do those derived from 3D-T1 images. METHODS: 3T-MRI scans of 329 MS patients and 76 healthy controls were included in this cross-sectional study. Brain volumes were derived using FreeSurfer on 3D-T1 and compared with brain volumes derived with SynthSeg and SAMSEG on 3D-FLAIR. Relative agreement was evaluated by calculating the intraclass correlation coefficient (ICC) of the 3D-T1 and 3D-FLAIR volumes. Consistency of relations with disability and average cognition was assessed using linear regression, while correcting for age and sex. The findings were corroborated in an independent validation cohort of 125 MS patients. RESULTS: The ICC between volume measured with FreeSurfer and those measured on 3D-FLAIR for brain, ventricle, cortex, total deep gray matter and thalamus was above 0.74 for SAMSEG and above 0.91 for SynthSeg. Worse disability and lower average cognition were similarly associated with brain (adj. R(2) = 0.24-0.27, p < 0.01; adj. R(2) = 0.26-0.29, p < 0.001) ventricle (adj. R(2) = 0.27-0.28, p < 0.001; adj. R(2) = 0.19-0.20, p < 0.001) and deep gray matter volumes (adj. R(2) = 0.24-0.28, p < 0.001; adj. R(2) = 0.27-0.28, p < 0.001) determined with all methods, except for cortical volumes derived from 3D-FLAIR. DISCUSSION: In this cross-sectional study, brain volumes derived from 3D-FLAIR and 3D-T1 show similar relationships to disability and cognitive dysfunction in MS, highlighting the potential of these techniques in clinical datasets.
 BACKGROUND: Neurosarcodosis is one of the most frequent differential diagnoses of multiple sclerosis (MS) and requires central nervous system (CNS) biopsy to establish definite diagnosis according to the latest consensus diagnostic criteria. We here analyzed diagnostic values of basic cerebrospinal fluid (CSF) parameters to distinguish neurosarcoidosis from MS without CNS biopsy. METHODS: We retrospectively assessed clinical, radiological and laboratory data of 27 patients with neurosarcoidosis treated at our center and compared following CSF parameters with those of 138 patients with relapsing-remitting MS: CSF white cell count (WCC), CSF/serum albumin quotient (Q(alb)), intrathecal production of immunoglobulins including oligoclonal bands (OCB), MRZ reaction, defined as a polyspecific intrathecal production of IgG reactive against ≥2 of 3 the viruses measles (M), rubella (R), and zoster (Z) virus, and CSF lactate levels. Additional inflammatory biomarkers in serum and/or CSF such as neopterin, soluble interleukin-2 receptor (sIL-2R) and C-reactive protein (CRP) were assessed. RESULTS: There was no significant difference in the frequency of CSF pleocytosis, but a CSF WCC > 30/μl was more frequent in patients with neurosarcoidosis. Compared to MS, patients with neurosarcoidosis showed more frequently an increased Q(alb) and CSF lactate levels as well as increased serum and CSF levels of sIL-2R, but a lower frequency of intrathecal IgG synthesis and positive MRZ reaction. Positive likelihood ratio (PLR) of single CSF parameters indicating neurosarcoidosis was highest, if (a) CSF WCC was >30/μl (PLR 7.2), (b) Q(alb) was >10 × 10(-3) (PLR 66.4), (c) CSF-specific OCB were absent (PLR 11.5), (d) CSF lactate was elevated (PLR 23.0) or (e) sIL-2R was elevated (PLR>8.0). The combination of (a) one of three following basic CSF parameters, i.e., (a.1.) CSF WCC >30/ul, or (a.2.) Q(Alb) >10 × 10(-3), or (a.3.) absence of CSF-specific OCB, and (b) absence of positive MRZ reaction showed the best diagnostic accuracy (sensitivity and specificity each >92%; PLR 12.8 and NLR 0.08). CONCLUSION: Combined evaluation of basic CSF parameters and MRZ reaction is powerful in differentiating neurosarcoidosis from MS, with moderate to severe pleocytosis and Q(Alb) elevation and absence of intrathecal IgG synthesis as useful rule-in parameters and positive MRZ reaction as a rule-out parameter for neurosarcoidosis.
 BACKGROUND: Spinal cord lesions in multiple sclerosis (MS) are an important contributor to disability. Knowledge on the effect of disease-modifying treatment (DMT) on spinal lesion formation in MS is sparse, as cord outcome measures are seldom included in MS treatment trials. We aim to investigate whether intermediate- or high-efficacy DMTs (i/hDMT) can reduce spinal lesion formation, compared with low-efficacy DMTs (lDMT) and/or no treatment. METHODS: Relapse-onset MS patients with ≥2 spinal MRIs (interval >3 months and <10 years) were retrospectively identified. The i/hDMT-group was defined as patients who were treated with i/hDMTs during ≥90% of spinal MRI follow-up time. Controls received lDMTs and/or no treatment ≥90% of follow-up duration. In a secondary analysis, only patients using lDMT for ≥90% of follow-up were considered controls. Patients were matched using propensity-scores. Cox proportional hazards models were used to estimate the risk of new spinal lesions. RESULTS: 323 patients had ≥2 spinal cord MRIs. 49 satisfied i/hDMT and 168 control group criteria. 34 i/hDMT patients were matched to 83 controls. Patients in the i/hDMT-group were significantly less likely to develop new cord lesions at follow-up (HR 0.29 [0.12-0.75], p = 0.01). When the i/hDMT-group was matched to only controls using lDMT ≥90% of follow-up time (n = 17 and n = 25, respectively), there was no statistically significant difference (HR 1.01 [0.19-5.24], p = 0.99). CONCLUSION: Treatment with intermediate- or high-efficacy DMTs reduces the risk of new spinal cord lesions compared with matched patients receiving no treatment and/or lDMTs. No conclusions could be drawn on whether i/hDMTs provide a larger risk reduction compared to only lDMTs (control group receiving lDMTs ≥90% of follow-up time).
 BACKGROUND: Multiple sclerosis (MS) is an autoimmune central nervous system (CNS) disorder indicated by demyelination, chronic inflammation, and neuronal destruction. Regional demyelination, inflammation responses, scar development, and various axonal damage are pathological characteristics of MS. Curcumin is a hydrophobic polyphenol extracted from the rhizome of the turmeric plant. In addition to anti-inflammatory effects, beneficial therapeutic effects such as antioxidant, anti-cancer and nerve protection have also been seen from this compound. The purpose of the current investigation was to provide light on the potential benefits of Curcumin in treating experimental autoimmune encephalomyelitis (EAE), the animal model of MS. METHODS AND RESULTS: in Female C57BL/6 mice were used to induce EAE through myelin oligodendroglial glycoprotein (MOG). Curcumin doses of 100 and 200 mg/kg were administered orally in the treatment groups starting on the first day of EAE induction. Brains and splenocytes were extracted from euthanized animals on day 25 following EAE induction. Demyelination and leukocyte infiltration, proliferation, cytokine, and gene expression profiles were assessed. Our findings demonstrate that both low and high doses of Curcumin decreased the progression of EAE. Histological analyses revealed low infiltration of leukocytes into the CNS. Curcumin therapy enhanced Th2 and Treg cell secretion of IL-4, IL-10, and TGF-β although considerably decreasing IFN-γ and TNF-α. Curcumin-induced Th2 and Treg cell cytokine production and transcription factor gene expression (IL-13, GATA3, STAT6 and IL-35, CTLA4, Foxp3) and anti-inflammatory cytokines (IL-27, IL-33). CONCLUSION: Overall, these findings provide additional evidence that Curcumin can slow disease development and alleviate symptoms in EAE through stimulating Treg and Th2 cell polarization. They support Curcumin's potential therapeutic role in MS.
 BACKGROUND: Tremor affects up to 25%-58% in multiple sclerosis (MS) population. Deep-brain stimulation (DBS) of the ventral-intermediate nucleus (VIM) of the thalamus is considered as a potential option following medical treatments. Long term DBS efficacy is not well known in these patients with a poor outcome mostly related to disease progression. OBJECTIVE: To report a large and retrospective study of thalamic DBS in MS tremor. METHODS: We conducted a large and retrospective study of patients with MS disabling and pharmacologically resistant upper limb tremor, who underwent thalamic DBS procedure from January 1992 to January 2015 in University Hospital of Henri Mondor, France. Demographic data, clinical assessment and activity daily living were collected. A three-month and twelve-month post-operative assessment with clinical and functional rating scales have been achieved, as well as long term follow-up for most patients. RESULTS: One hundred and four patients underwent DBS procedure. There were 71 female (68%) and 33 male (32%). At three-month post-operative assessment, 64% patients were improved clinically and functionally. Among these, 93% of patients kept a good efficacy at one-year post-operative assessment. Mean duration of follow-up for these patients was 6 years. CONCLUSION: We described a long-term sustained clinical and functional improvement in this large and retrospective report of thalamic DBS. This neuromodulation approach could be a therapeutic option for all severe upper extremity refractory tremor in MS patients.
 BACKGROUND: Multiple Sclerosis (MS) is a chronic disease with a high prevalence of neuropsychiatric symptoms. Mindfulness is a practice that encourages individuals to cultivate a present-focused, acceptance-based approach for managing psychological distress. Its positive effect on MS has been demonstrated, but learning such technique is expensive and time-consuming. In this study, we investigated the feasibility and efficacy of an 8-week, at-home, smart-device aided mindfulness program in a cohort of MS patients. Specifically, we explored the role of a brain-sensing headband providing real-time auditory feedback as supportive tool for meditation exercises. METHODS: The study included two visits, one at baseline and another after the mindfulness program. We measured adherence to the proposed mindfulness treatment and its effect on questionnaires investigating different psychological domains, cognition, fatigue, quality of life and quantitative EEG parameters. All participants received a smart biofeedback device to be used during the therapeutic program consisting of daily meditative exercises. RESULTS: Twenty-nine patients were recruited for the present study. Among them, 27 (93%) completed the entire program and 17 (63%) completed more than 80% of the scheduled sessions. We observed a statistically significant reduction of the Ruminative Response Scale score and a significant increase of the Digit Span Backward. Regarding neurophysiological data, we found a significant reduction of the whole-scalp beta and parieto-occipital theta power post intervention. CONCLUSION: Our results show that an at-home, smart-device aided mindfulness program is feasible for people with MS. The efficacy in terms of reappraisals of stress, cognitive and emotional coping responses is also supported by our neurophysiological data. Further studies are warranted to better explore the role of such approaches in managing the psychological impact of MS diagnosis.
 BACKGROUND: We recently reported in a phase-III, randomized controlled trial that a behavioral intervention based on social cognitive theory (SCT) and delivered through the Internet using e-learning approaches increased device-measured minutes/day of moderate-to-vigorous physical activity (MVPA) over a 6-month period among persons with multiple sclerosis (MS). OBJECTIVE: This planned tertiary outcome paper examined SCT variables as mediators of the behavioral intervention effect on change in device-measured minutes/day of MVPA. METHOD: Persons with MS (N = 318) were randomized into behavioral intervention (n = 159) or attention/social contact control (n = 159) conditions. The conditions were administered over a 6-month period via an Internet website and supported with behavioral coaching by persons who were uninvolved in screening, recruitment, random assignment, and outcome assessments. We collected MVPA and SCT data before and after the 6-month period. The data analysis involved linear mixed modeling on MVPA and SCT outcomes followed by latent change score modeling for examining SCT variables as mediators of the intervention effect on change in MVPA. RESULTS: The linear mixed model indicated statistically significant group by time interactions on device-measured minutes/day of MVPA and scores from SCT measures of exercise self-efficacy, barriers self-efficacy, goal setting, and planning. The effect of the intervention on device-measured minutes/day of MVPA was mediated by the SCT variable of exercise self-efficacy based on the statistical significance of the Wald z-score for the indirect effect in the latent change score model. CONCLUSIONS: This study provides evidence for exercise self-efficacy as a SCT mediator of the behavioral intervention effect on device-measured minutes/day of MVPA in persons with MS.
 PURPOSE: COB-MS is an eight-session, Cognitive Occupation-Based programme for people with both MS and cognitive difficulty - designed to enhance cognition and daily functioning, through a combination of goal-setting, cognitive strategy engagement, group activities, home-practice activities and one-on-one sessions. This research aims to investigate the acceptability of COB-MS from the perspective of people living with MS, as well as the occupational therapists who facilitated the programme. MATERIALS AND METHODS: Two content analyses were conducted on interview data from (n = 11) COB-MS participants and (n = 8) COB-MS facilitators. Thematic analysis was also conducted on the participant interview data. RESULTS: Through a, primary, content analysis, participants reported that the COB-MS provided both a positive experience and quality resources. Qualitative improvement and utilisation of their learning beyond completion of the intervention were also identified. Four themes were identified via, secondary, thematic analysis: (1) Group interaction within COB-MS was vital; (2) Online COB-MS had positive and negative effects on participation; (3) COB-MS as a provider of clarity; and (4) Using learned strategies after the completion of COB-MS. Recommendations for future administration are provided. CONCLUSIONS: Findings suggest COB-MS acceptability, as well as appropriateness and feasibility, indicative of progression to a definitive trial in future research. TRIAL REGISTRATION: ISRCTN: ISRCTN11462710. Registered on 9 September 2019.
 OBJECTIVE: We aimed to synthesize all available observational studies and clinical trials of rituximab to estimate the safety and efficacy of this monoclonal antibody in people with multiple sclerosis (MS). METHODS: The four databases including PubMed, Scopus, Embase, and Web of Science were comprehensively searched in April 2022. We defined PICO as follows. Problem or study population (P): patients with MS; intervention (I): Rituximab; comparison (C): none; outcome (O): efficacy and safety. RESULTS: After two-step screening, a total of 27 studies entered into our qualitative and quantitative synthesis. Our analysis showed a significant decrease in EDSS score in all patients with MS after treatment (SMD: - 0.44, 95% CI - 0.85, - 0.03). In addition, the ARR was reduced after using rituximab compared to the pre-treatment period (SMD: - 0.65, 95% CI - 1.55, 0.24) but it was not significant. The most common side effect after rituximab with a pooled prevalence of 28.63% (95% CI 16.61%, 42.33%). Furthermore, the pooled prevalence of infection was 24% in patients with MS (95% CI 13%, 36%). In the end, the pooled prevalence of malignancies after rituximab treatment was 0.39% (95% CI 0.02%, 1.03%). CONCLUSION: Our findings illustrated an acceptable safety for this treatment. However, further studies with randomized design, long follow-up, and large sample sizes are needed to confirm the safety and efficacy of rituximab in patients with MS.
 BACKGROUND: Blood-brain barrier dysfunction in active multiple sclerosis (MS) lesions leads to pathological changes in the cerebrospinal fluid (CSF). This study aimed to investigate the possible association between routine CSF findings, especially CSF chloride, at the time of the first lumbar puncture and the relapse risk and disability progression of relapsing-remitting MS (RRMS). METHODS: This retrospective study included 77 patients with RRMS at the MS Center of our institution from January 2012 to December 2020. The Anderson and Gill (AG) model and Spearman correlation analysis were used to explore predictors of relapse and disability during follow-up. RESULTS: In the multivariate AG model, patients with elevated CSF chloride level (hazard ratio [HR], 1.1; 95% confidence interval [CI]: 1.06-1.22; p = 0.001) had a high risk of MS relapse. Using median values of CSF chloride (123.2 mmol/L) as a cut-off, patients with CSF chloride level ≥ 123.2 mmol/L had a 120% increased relapse risk compared with those with CSF chloride level < 123.2 mmol/L (HR = 2.20; 95% CI: 1.19-4.05; p = 0.012). CONCLUSIONS: Elevated CSF chloride levels might be a biologically unfavorable predictive factor for disease relapse in RRMS.
 OBJECTIVE: In spite of the advances in therapeutic modalities, morbidity, due to multiple sclerosis (MS), still remains high. Therefore, a large body of research is endeavouring to discover or develop novel therapies with improved efficacy for treating MS patients. In the present study, we examined the immunomodulatory effects of apigenin (Api) on peripheral blood mononuclear cells (PBMCs) isolated from MS patients. We also developed an acetylated form of Api (apigenin- 3-acetate) to improve In its blood-brain barrier (BBB) permeability. Additionally, we compared its anti-inflammatory properties to original Api and methyl-prednisolone-acetate (a standard therapy), as a potential option in treating MS patients. MATERIALS AND METHODS: The current study was an experimental-interventional research. The half maximal inhibitory concentration (IC(50)) values for apigenin-3-acetate, apigenin, and methyl-prednisolone-acetate were determined in healthy volunteers' PBMCs (n=3). Gene expressions of T-box transcription factor (TBX21 or T-bet) and IFN-γ, as well as proliferation of T cells isolated from MS patients' PBMCs (n=5), were examined in co-cultures of apigenin-3-acetate, Api and methyl-prednisolone-acetate after 48 hours of treatment, using quantitative reverse transcription polymerase chain reaction (qRT-PCR). RESULTS: Our findings showed that apigenin-3-acetate, apigenin, and methyl-prednisolone-acetate at concentrations of 80, 80, and 2.5 M could inhibit Th1 cell proliferation after 48 hours (P=0.001, P=0.036, and P=0.047, respectively); they also inhibited T-bet (P=0.015, P=0.019, and P=0.022) and interferon-γ (IFN-γ) gene expressions (P=0.0001). CONCLUSION: Our findings suggested that Api may have anti-inflammatory properties, possibly by inhibiting proliferation of IFN-producing Th1 cells. Moreover, comparative immunomodulatory effects were found for the acetylated version of apigenin-3-acetate versus Api and methyl-prednisolone-acetate.
 This study aimed to determine whether peripapillary retinal nerve fiber layer (pRNFL) and ganglion cell-inner plexiform layer (GCIPL) thickness thresholds for single-time-point swept-source optical coherence tomography (SS-OCT) measures can differentiate the clinical outcomes of treatment-naïve people with multiple sclerosis (pwMS). A total of 275 patients with the clinically isolated syndrome (n = 23), benign MS (n = 8), relapsing-remitting MS (n = 185), secondary progressive MS (n = 28), primary progressive MS (n = 31), and with no history of optic neuritis were included. The mean Expanded Disability Status Scale (EDSS) score was 3.0 ± 1.6. The cut-off values of pRNFL (87 µm and 88 µm) and GCIPL (70 µm) thicknesses have been adopted from previous studies using spectral-domain OCT. PwMS with pRNFL ≤87 µm and ≤88 µm had a longer disease duration, more advanced disability, and more frequently progressive MS variants compared to those with greater pRNFL thicknesses. In distinguishing pwMS with disability greater than or equal to the mean EDSS score (EDSS ≥ 3) from those with less severe disability, GCIPL thickness <70 µm had the highest sensitivity, while pRNFL thickness ≤87 µm had the greatest specificity. The optimal cut-off values differentiating patients with EDSS ≥ 3 from those with less severe disability was 63 µm for GCIPL thickness and 93.5 µm for pRNFL thickness. In conclusion, pRNFL and GCIPL thickness thresholds for single-time-point SS-OCT measurements may be helpful in differentiating the disability status of treatment-naïve pwMS.
 BACKGROUND: Gait variability in people with multiple sclerosis (PwMS) reflects disease progression or may be used to evaluate treatment response. To date, marker-based camera systems are considered as gold standard to analyze gait impairment in PwMS. These systems might provide reliable data but are limited to a restricted laboratory setting and require knowledge, time, and cost to correctly interpret gait parameters. Inertial mobile sensors might be a user-friendly, environment- and examiner-independent alternative. The purpose of this study was to evaluate the validity of an inertial sensor-based gait analysis system in PwMS compared to a marker-based camera system. METHODS: A sample N = 39 PwMS and N = 19 healthy participants were requested to repeatedly walk a defined distance at three different self-selected walking speeds (normal, fast, slow). To measure spatio-temporal gait parameters (i.e., walking speed, stride time, stride length, the duration of the stance and swing phase as well as max toe clearance), an inertial sensor system as well as a marker-based camera system were used simultaneously. RESULTS: All gait parameters highly correlated between both systems (r > 0.84) with low errors. No bias was detected for stride time. Stance time was marginally overestimated (bias = -0.02 ± 0.03 s) and gait speed (bias = 0.03 ± 0.05 m/s), swing time (bias = 0.02 ± 0.02 s), stride length (0.04 ± 0.06 m), and max toe clearance (bias = 1.88 ± 2.35 cm) were slightly underestimated by the inertial sensors. DISCUSSION: The inertial sensor-based system captured appropriately all examined gait parameters in comparison to a gold standard marker-based camera system. Stride time presented an excellent agreement. Furthermore, stride length and velocity presented also low errors. Whereas for stance and swing time, marginally worse results were observed.
 BACKGROUND: Chronic diseases affect the lives of the patient and caregiver. Caring for a patient with a chronic psychiatric illness, such as bipolar disorder, is a stressful and challenging activity. Caregivers of severe psychiatric patients are the primary victims of violence by patients. Caring for these patients can be very stressful for the caregiver to the extent of experiencing post-traumatic stress symptoms. This study compares the frequency of trauma exposure and PTSD in the caregivers of patients with bipolar disorder type 1(BD-1), bipolar disorder type 1, comorbid post-traumatic stress disorder (BD-1+PTSD), and multiple sclerosis (MS).The MS group served as the control group. METHODS: This cross-sectional study with convenient sampling was conducted at three hospitals in Tehran, Iran, from April 2020 to January 2022. One hundred eighty caregivers answered a clinical demographic questionnaire. We then used the Trauma History Questionnaire (THQ) to assess the frequency of exposure to different types of trauma. Then, the Persian version of the SCID-5, a valid and reliable instrument for psychiatric diagnoses, was used to diagnose PTSD. Chi-square was used for analyzing data. RESULTS: Exposure to trauma has a significant difference between the groups. BD-1 + PTSD patients' caregivers were exposed to more physical assaults than others (P < 0.0001) There was a significant difference between sexual harassment in the MS group (P = 0.010). There was a significant difference between the three groups in the development of PTSD (P = 0.003). PTSD prevalence in the BD-1 + PTSD caregiver group is more than in other groups. In the caregivers of BD-1+PTSD, the caregiving experience caused traumatic exposure and the development of PTSD in all caregivers. CONCLUSION: This study shows that the prevalence of exposure to traumatic events and PTSD is higher in the caregivers of BD-1 patients, especially if the patient has comorbid PTSD. Detecting these symptoms early and using intervention can make the caregiving burden more tolerable.
 INTRODUCTION: The subventricular zone (SVZ) represents one of the main adult brain neurogenesis niche. In-vivo imaging of SVZ is very challenging and little is known about MRI correlates of SVZ macro- and micro-structural injury in multiple sclerosis (MS) patients. METHODS: The aim of the present study is to evaluate differences in terms of volume and microstructural changes [as assessed with the novel Spherical Mean Technique (SMT) model, evaluating: Neurite Signal fraction (INTRA); Extra-neurite transverse (EXTRATRANS) and mean diffusivity (EXTRAMD)] in SVZ between relapsing-remitting (RR) or progressive (P) MS patients and healthy controls (HC). We are also going to explore whether SVZ microstructural injury correlate with caudate (a nucleus that is in the vicinity of the SVZ) or thalamus (another well-defined grey matter area which is further from SVZ than caudate) volume and clinical disability. Clinical and brain MRI data were prospectively acquired from 20 HC, 101 RRMS, and 50 PMS patients. Structural and diffusion metrics inside the global SVZ, normal appearing (NA-) SVZ, caudate and thalamus were collected. RESULTS: We found a statistically significant difference between groups in terms of NA-SVZ EXTRAMD (PMS>RRMS>HC; p = 0.002), EXTRATRANS (PMS>RRMS>HC; p<0.0001), and INTRA (HC>RRMS>PMS; p = 0.009). Multivariable models showed that NA-SVZ metrics significantly predicted caudate (R (2) = 0.21, p < 0.0001), but not thalamus, atrophy. A statistically significant correlation between EXTRAMD and EXTRATRANS of the NA-SVZ and EDSS (r=0.25, p=0.003 and r=0.24, p = 0.003, respectively) was found. These findings were confirmed in analyses restricted to RRMS, but not to PMS patients. DISCUSSION: In conclusion, the microstructural damage we observed within the NA-SVZ of MS patients - reflecting higher free water content (higher EXTRAMD), cytoarchitecture disruption and astrogliosis (higher EXTRATRANS and lower INTRA) - was more evident in the progressive as compared to the relapsing phases of MS. These abnormalities were significantly associated with a more pronounced caudate atrophy and higher clinical disability scores. Our findings may support the neuroprotective role of SVZ in MS patients.
 BACKGROUND: Diagnosis of multiple sclerosis (MS) is established on criteria according to clinical and radiological manifestation. Cerebrospinal fluid (CSF) analysis is an important part of differential diagnosis of MS and other inflammatory processes in the central nervous system (CNS). METHODS: In total, 242 CSF samples were collected from patients undergoing differential MS diagnosis because of the presence of T2-hyperintensive lesions on brain MRI. The non-MS patients were subdivided into systemic inflammatory diseases with CNS involvement (SID) or cerebrovascular diseases (CVD) or other non-inflammatory diseases (NID). All samples were analyzed for the presence of oligoclonal bands and ELISA was performed for detection of: INF gamma, IL-6, neurofilaments light chain (NF-L), GFAP, CHI3L1, CXCL13, and osteopontin. RESULTS: The level of IL-6 (p = 0.024), osteopontin (p = 0.0002), and NF-L (p = 0.002) was significantly different among groups. IL-6 (p = 0.0350) and NF-L (p = 0.0015) level was significantly higher in SID compared to NID patients. A significantly higher level of osteopontin (p = 0.00026) and NF-L (p = 0.002) in MS compared to NID population was noted. ROC analysis found weak diagnostic power for osteopontin and NFL-L. CONCLUSIONS: The classical and non-standard markers of inflammatory process and neurodegeneration do not allow for sufficient differentiation between MS and non-MS inflammatory CNS disorders. Weak diagnostic power observed for the osteopontin and NF-L needs to be further investigated.
 BACKGROUND: Late-onset multiple sclerosis (LOMS) is most commonly defined as the onset of the disease's presentations at age 50 or older. There is still much to discover about the radiological features of LOMS. The current study aims to assess the imaging features of LOMS, as well as the correlation between these findings and the clinical characteristics of these patients. METHOD: This study was conducted following the PRISMA statement. A systematic search was conducted through PubMed, Scopus, and EMBASE databases to identify the studies that have applied magnetic-resonance imaging (MRI) or other imaging methods to investigate the radiological findings, as well as the relationship between them and clinical findings of LOMS patients. The risk of bias was assessed using the Joanna Briggs Institute (JBI) checklists. Meta-analysis was conducted using the third version of the compressive meta-analysis software (CMA3). RESULTS: Our search identified 753 unique titles. Among them, 15 studies, including seven case-control, five case-series, and three cross-sectional studies, met the eligibility criteria. According to the quantitative synthesis, brain lesions were detected among 72.2% of LOMS patients (4 studies; 95% CI: 67.0% - 93.1%). In the context of spinal lesions, overall spinal cord involvement was 64.0% (8 studies; 95% CI: 42.5% - 81.1%). Based on the available evidence, supratentorial involvement was found in 82.7% of cases (3 studies; 95% CI: 17.4% - 99.1%), juxtacortical involvement in 34.1% (3 studies; 95% CI: 26.4% - 42.7%), infratentorial involvement in 51.3% (4 studies; 95% CI: 32.1% - 70.1%), and cerebellar involvement in 18.5% (3 studies; 95% CI: 13.9% - 24.1%). CONCLUSION: Based on the neuroimaging findings, we found that, given the heterogeneity of MS, LOMS patients have a high rate of spinal cord lesions and supratentorial involvement. The limited available evidence suggests that Barkhof criteria are the best compromise for the diagnosis of LOMS. There is still a need for future studies.
 Smoking is associated with an increased risk of multiple sclerosis (MS), and smoking and early menopause are related to poor outcomes in MS. Smoking is also associated with early menopause. To explore this intricate relationship between smoking status, age at menopause and disease course in MS, 137 women with MS and 396 age-matched controls were included in this case-control study. Age at menopause (median 49.0 vs. 50.0 years; p = 0.79) and smoking status (40.3% vs. 47.6%; p = 0.15) were similar among MS and control women. Relapsing MS onset was earlier in ever-smoker women with early menopause compared to the rest of the women (median 30.4 vs. 37.0 years; p = 0.02) and also compared to ever-smoker women with normal age at menopause (median 30.4 vs. 41.0 years; p = 0.008) and never-smoker women with early menopause (median 30.4 vs. 41.5 years; p = 0.004). Progressive MS onset was also earlier in ever-smoker women with early menopause compared to ever-smoker women with normal age at menopause (median 41.1 vs. 49.4 years; p = 0.05) and never-smoker women with early menopause (median 41.1 vs. 50.1 years; p = 0.12). Our results suggest that smoking and menopause associate with MS disease course, including the onset of relapsing and progressive MS in women.
 BACKGROUND: Multiple sclerosis, a chronic inflammatory disease in young and middle-aged adults, is one of the leading causes of non-traumatic disability in adults. Diet is known to have an important role in the modulating inflammatory processes and influencing molecular pathways. PURPOSE: This study aims to examine the association of the inflammatory capacity of diet measured by DII with MS in Jordan. METHODS: This prevalent case-control study included participants of both sexes, aged between 20 and 60 years. The cases (n = 541) had a confirmed diagnosis of prevalent Multiple Sclerosis (MS) in the previous 3 years, and controls (n = 607) were apparently healthy individuals matched on sex and age (42 ± 4 years). A validated Arabic food frequency questionnaire (FFQ) was utilized to obtain estimated dietary intake. Dietary data from the FFQ were analyzed using ESHA's Food Processor(®) nutrition analysis software, and the results were used to calculate the DII scores. Logistic regression analyses, controlling for covariates such as age, sex, body mass index, and smoking status, were used to measure the association between DII score and MS outcomes. RESULTS: Cases represent a mixed sample of MS phenotypes and controls were comparable on age and sex. However, controls tended to be taller, lighter, had a lower BMI, and had a lower smoking rate. After controlling for age, BMI, sex, and smoking status, there was a consistent increase in MS risk according to DII score, with a 10-fold increase in odds in quartile 4 vs. quartile 1 [OR(quartile 4vs1) = 10.17 (95% CI: 6.88; 15.04)]. For each point increase in DII score, there was nearly a doubling of odds [OR(1) = 1.75 (95% CI: 1.59; 1.92)]. Individual nutrients and food values aligned according to their contribution to the DII score calculations. CONCLUSION: The findings of this study, obtained in MS patients with varied illness duration over the previous 3 years, are consistent with an association between the overall inflammatory potential of diet and MS odds. Our findings among MS participants showed a significantly more pro-inflammatory DII scores than age- and sex-matched controls. Our results also suggest that MS group had a diet rich in pro-inflammatory foods and nutrients.
 BACKGROUND: COVID-19 pandemic has affected the management of multiple sclerosis (MS). OBJECTIVE: To explore the impact of COVID-19 on healthcare delivery to people with MS and the subsequent recovery of the system. METHODS: In this population-based study in the Campania Region (Italy), we included people with MS across pre-COVID-19, lockdown, pre-vaccination, and vaccination periods. Differences in continuous outcomes between periods were explored using linear mixed models (annualized hospitalization rate (AHR) and adherence measured as medication possession ratio (MPR)). Differences in disease-modifying treatment (DMT) prescription rates (first DMT prescription, any DMT switch, switch from platform to highly effective DMT, and combination of first DMT prescription and any DMT switch) were assessed using an interrupted time series design. RESULTS: Compared with pre-COVID-19, AHR decreased during the lockdown (Coeff = 0.64;95%CI = -0.69, -0.59; p < 0.01), and remained lower during pre-vaccination and vaccination periods. Adherence decreased during pre-vaccination (Coeff = -0.04;95%CI = -0.05, -0.03; p < 0.01) and vaccination periods (Coeff = -0.07;95%CI = -0.08, -0.07; p < 0.01). After the lockdown, there was an increase in any DMT switch (IRR 2.05 95%CI 1.38,3.05; p < 0.01), in switch from platform to highly effective DMTs (IRR 4.45;95%CI 2.48,8.26; p < 0.01) and in first DMT prescriptions (IRR 2.48;95%CI 1.64,3.74; p < 0.01). CONCLUSIONS: DMT prescriptions quickly returned to pre-pandemic levels, reflecting good health system recovery. However, adherence has remained lower than the past, as from suboptimal care. Assessing long-term COVID-19 impact on MS healthcare is warranted.
 BACKGROUND: Multiple sclerosis (MS) is an autoimmune inflammatory disease of the central nervous system that causes the damage to the myelin sheath as well as axonal degeneration. Individuals with MS appear to have changes in the numbers and functions of T-cell subsets, leading to an immunological imbalance accompanied by enhanced autoreactivity. In previous preclinical studies, (2 S,3 S,4R)-1-O-(α-D-Galactopyranosyl)-N-tetracosanoyl-2-amino-1,3,4-nonanetriol (OCH), a synthetic analog of α-galactosylceramide stimulatory for invariant NKT (iNKT) cells, has shown therapeutic or disease-preventive immunoregulatory effects in autoimmune disease models such as experimental autoimmune encephalomyelitis (EAE). OBJECTIVES: This study is the first-in-human study of oral OCH to evaluate the pharmacokinetics and to examine the effects on immune cells as well as related gene expression profiles. METHODS: Fifteen healthy volunteers and 13 MS patients who met the study criteria were enrolled. They were divided into five cohorts and received oral administration of various doses of granulated powder of OCH (0.3-30 mg), once per week for 4 or 13 weeks. Plasma OCH concentrations were measured by high-performance liquid chromatography. Frequencies of lymphocyte subsets in peripheral blood were evaluated by flow cytometry, and microarray analysis was performed to determine OCH-induced changes in gene expression. RESULTS: Oral OCH was well tolerated, and its bioavailability was found to be sufficient. Six hours after a single dose of OCH, increased frequencies of Foxp3(+) regulatory T-cells were observed in some cohorts of healthy subjects and MS patients. Furthermore, gene expression analysis demonstrated an upregulation of several immunoregulatory genes and downregulation of pro-inflammatory genes following OCH administration. CONCLUSION: This study has demonstrated immunomodulatory effects of the iNKT cell-stimulatory drug OCH in human. Safety profiles together with the presumed anti-inflammatory effects of oral OCH encouraged us to conduct a phase II trial.
 INTRODUCTION/OBJECTIVES: Multiple sclerosis (MS) leads to physical and cognitive disability, which in turn impacts the socioeconomic status of the individual. The altered socioeconomic trajectory combined with the critical role of aging in MS progression could potentially lead to pronounced differences between MS patients and the general population. Few nations have the ability to connect long-term clinical and socioeconomic data at the individual level, and Denmark's robust population-based registries offer unique insights. This study aimed to examine the socioeconomic aspects of elderly Danish MS patients in comparison to matched controls from the general population. METHODS: A nationwide population-based study in Denmark was conducted, comprising all living MS patients aged 50 years or older as of 1 January 2021. Patients were matched 1:10 based on sex, age, ethnicity, and residence with a 25% sample of the total Danish population. Demographic and clinical information was sourced from the Danish Multiple Sclerosis Registry, while socioeconomic data were derived from national population-based registries containing details on education, employment, social services, and household characteristics. Univariate comparisons between MS patients and matched controls were then carried out. RESULTS: The study included 8,215 MS patients and 82,150 matched individuals, with a mean age of 63.4 years (SD: 8.9) and a 2:1 female-to-male ratio. For those aged 50-64 years, MS patients demonstrated lower educational attainment (high education: 28.3 vs. 34.4%, P < 0.001) and fewer received income from employment (46.0 vs. 78.9%, P < 0.001), and working individuals had a lower annual income (48,500 vs. 53,500€, P < 0.001) in comparison to the controls. Additionally, MS patients within this age group were more likely to receive publicly funded practical assistance (14.3 vs. 1.6%, P < 0.001) and personal care (10.5 vs. 0.8%, P < 0.001). Across the entire population, MS patients were more likely to live alone (38.7 vs. 33.8%, P < 0.001) and less likely to have one or more children (84.2 vs. 87.0%, P < 0.001). CONCLUSION: MS presents significant socioeconomic challenges among the elderly population, such as unemployment, reduced income, and increased dependence on social care. These findings underscore the pervasive impact of MS on an individual's life course, extending beyond the clinical symptoms of cognitive and physical impairment.
 BACKGROUND AND OBJECTIVES: alemtuzumab is a monoclonal anti-CD52 antibody acting on B and T cells in highly active multiple sclerosis (MS). We analyzed changes in lymphocyte subsets after alemtuzumab administration in relation to disease activity and autoimmune adverse events. METHODS: lymphocyte subset counts were assessed longitudinally using linear mixed models. Subset counts at baseline and during follow-up were correlated with relapse rate, adverse events, or magnetic resonance (MRI) activity. RESULTS: we recruited 150 patients followed for a median of 2.7 years (IQR: 1.9-3.7). Total lymphocytes, CD4, CD8, and CD20 significantly decreased in all patients over 2 years (p < 0.001). Previous treatment with fingolimod increased the risk of disease activity and adverse events (p = 0.029). We found a higher probability of disease reactivation in males and in patients with over three active lesions at baseline. Higher EDSS scores at baseline and longer disease duration predicted the switch to other treatments after alemtuzumab. DISCUSSION AND CONCLUSIONS: Our real-world study supports data from clinical trials in which lymphocyte subsets were not useful for predicting disease activity or autoimmune disease during treatment. The early use of an induction therapy such as alemtuzumab in patients with a lower EDSS score and short history of disease could mitigate the risk of treatment failure.
 BACKGROUND: Focal inflammatory disease activity in relapsing-remitting multiple sclerosis (RRMS) diminishes with increasing age. Here we use patient-level data from randomised controlled trials (RCTs) of natalizumab treatment in RRMS to investigate the association of age and inflammatory disease activity. METHODS: We used patient-level data from the AFFIRM (natalizumab vs placebo in relapsing-remitting MS, NCT00027300) and SENTINEL (natalizumab plus interferon beta vs interferon beta in relapsing remitting MS, NCT00030966) RCTs. We determined the proportion of participants developing new T2 lesions, contrast-enhancing lesions (CELs) and relapses over 2 years of follow-up as a function of age, and investigated the association of age with time to first relapse using time-to-event analyses. RESULTS: At baseline, there were no differences between age groups in T2 lesion volume and number of relapses in the year before inclusion. In SENTINEL, older participants had a significantly lower number of CELs. During both trials, the number of new CELs and the proportion of participants developing new CELs were significantly lower in older age groups. The number of new T2 lesions and the proportion of participants with any radiological disease activity during follow-up were also lower in older age groups, especially in the control arms. CONCLUSIONS: Older age is associated with a lower prevalence and degree of focal inflammatory disease activity in treated and untreated RRMS. Our findings inform the design of RCTs, and suggest that patient age should be taken into consideration when deciding on immunomodulatory treatment in RRMS.
 BACKGROUND: Alemtuzumab (ALZ) is a humanized monoclonal antibody approved for the treatment of patients with highly active relapsing-remitting multiple sclerosis (RRMS) administered in two annual courses. The objective of this study was to describe the effectiveness and safety data of ALZ and to report the health resource utilization in patients receiving this treatment. METHODS: In this retrospective, non-interventional study, information was retrieved from patients' medical charts at one center in Spain. Included patients were ≥18 years old, and ALZ treatment was initiated between 1 March 2015 and 31 March 2019, according to routine clinical practice and local labeling. RESULTS: Of 123 patients, 78% were women. The mean (standard deviation, SD) age of patients at diagnosis was 40.3 (9.1) years, and the mean time since diagnosis was 13.8 (7.3) years. Patients were previously treated with a median (interquartile range; IQR) number of two (2.0-3.0) disease-modifying treatments (DMTs). Patients were treated with ALZ for a mean (SD) of 29.7 (13.8) months. ALZ reduced the annualized relapse rate (ARR) (1.5 before vs. 0.05 after; p < 0.001) and improved the median EDSS (4.63 before vs. 4.00 after; p < 0.001). Most (90.2%) patients were relapse-free while receiving ALZ. The mean number of gadolinium-enhancing [Gd+] T1 lesions was reduced (1.7 before vs. 0.1 after; p < 0.001), and the mean number of T2 hyperintense lesions was maintained (35.7 before vs. 35.4 after; p = 0.392). A total of 27 (21.9%) patients reported 29 autoimmune diseases: hyperthyroidism (12), hypothyroidism (11), idiopathic thrombocytopenic purpura (ITP) (3), alopecia areata (1), chronic urticaria (1), and vitiligo (1). The mean number of health resources (outpatient visits, emergency room visits, hospital admissions, and tests performed in the hospital) used while patients were treated with ALZ progressively decreased from year 1 to year 4, except for a slight increase at year 2 of outpatient visits. CONCLUSION: The ReaLMS study provides real-world evidence that ALZ can promote clinical and magnetic resonance imaging disease remission, as well as disability improvement in patients with MS, despite several prior DMT failures. The ALZ safety profile was consistent with data available from clinical trials and other real-world studies. Healthcare resource use was reduced throughout the treatment period.
 Multiple sclerosis (MS) is a chronic, progressive neurological disease involving neuroinflammation, neurodegeneration, and demyelination. Cladribine tablets are approved for immune reconstitution therapy in patients with highly active relapsing-remitting MS based on favorable efficacy and tolerability results from the CLARITY study that have been confirmed in long-term extension studies. The approved 4-year dosing regimen foresees a cumulative dose of 3.5 mg/kg administered in two cycles administered 1 year apart, followed by 2 years of observation. Evidence on managing patients beyond year 4 is scarce; therefore, a group of 10 neurologists has assessed the available evidence and formulated an expert opinion on management of the growing population of patients now completing the approved 4-year regimen. We propose five patient categories based on response to treatment during the first 4-year regimen, and corresponding management pathways that envision close monitoring with clinical visits, magnetic resonance imaging (MRI) and/or biomarkers. At the first sign of clinical or radiological disease activity, patients should receive a highly effective disease-modifying therapy, comprising either a full cladribine regimen as described in regulatory documents (cumulative dose 7.0 mg/kg) or a comparably effective treatment. Re-treatment decisions should be based on the intensity and timing of onset of disease activity, clinical and radiological assessments, as well as patient eligibility for treatment and treatment preference.
 In vivo induction of antigen (Ag)-specific regulatory T cells (Treg) is considered the holy grail of therapeutic strategies for restoring tolerance in autoimmunity. Unfortunately, in the autoimmune disease multiple sclerosis, an effective and durable therapy targeting the diverse repertoire of emerging Ags without compromising the patient's natural immunity has remained elusive. To address this deficiency, we have developed an Ag-specific adeno-associated virus (AAV) immunotherapy that will restore tolerance in a Treg-dependent manner. Using multiple strains of mice with different genetic and immunological backgrounds, we demonstrate that a liver directed AAV vector expressing a single transgene can prevent experimental autoimmune encephalomyelitis from developing and effectively mitigate pre-existing or established disease that was induced by one or more auto-reactive myelin oligodendrocyte glycoprotein-derived peptides. Overall, the results suggests that AAV can efficiently restore Ag-specific immune tolerance to an immunogenic protein that is neither restricted by the major histocompatibility complex haplotype, nor by the specific antigenic epitope(s) presented. These findings may pave the way for developing a comprehensive Ag-specific immunotherapy that does not require prior knowledge of the specific immunogenic epitopes and that may prove to be universally applicable to all MS patients, and adaptable for other autoimmune diseases.
 PURPOSE: The purpose of this study was to determine the demographic and clinical patterns of optic neuritis (ON) in patients presenting to a tertiary health-care institute and to study the incidence of multiple sclerosis (MS), magnetic resonance imaging features in varied ON, treatment outcome, and prognosis. METHODS: A retrospective analysis of patients with first episode of ON presenting to a tertiary care center during the period from March 2013 to March 2021 was done. Details of ocular examination were retrieved from medical records and statistically analyzed. RESULTS: Three hundred and fifty-four participants with ON were included in this study. The mean age was 40.25 ± 12.2 years. The male: female ratio was 1:1.35. 48.1% had visual acuity of <3/60. Based on clinical presentation, papillitis was seen in 31.5% of subjects, neuroretinitis in 24.1%, and retrobulbar neuritis in 44.4%. Based on etiology, 79.6% were idiopathic, 1.8% presented with infectious ON, and 9.26% were associated with demyelinating disease (MS). CONCLUSION: Females were predominantly affected. Idiopathic ON formed the major subset etiologically. Sixty-six percent had visual recovery of 6/18 or better following corticosteroid therapy. 9.2% revealed multiple intracranial lesions on neuroimaging, suggesting high association with MS. Therefore, early diagnosis, vigilant monitoring of steroid therapy, and regular follow-up screening for MS remain the mainstay of management in ON.

 BACKGROUND: Anti-CD20 is a highly effective therapy for multiple sclerosis (MS), a disease with multiple abnormalities in function of B and T cells and innate immune cells. Anti-CD20 therapy depletes B cells, which alters antibody production and has diverse effects on B cell immunity. These changes potentially affect immunity beyond B cells in MS. OBJECTIVE: Determine if anti-CD20 therapy effects non-B cell, as well as B cell, gene expression, and serum protein levels. METHODS: Samples were collected from 10 healthy controls and from clinically stable relapsing-remitting MS - 10 untreated, 9 interferon-β-treated, and 15 ocrelizumab-treated patients were studied before, and 2  weeks and 6  months after, the first anti-CD20 infusion. Peripheral blood mononuclear cells (PBMC) were analyzed with sensitive, 135,000-transcript RNA expression microarrays, using stringent criteria. Gene expression was compared to 43 MS-relevant serum immune and neurotrophic proteins, using multiplex protein assays. RESULTS: Anti-CD20 therapy reduced expression of 413 total genes and 185 B-cell-regulated genes at 2  weeks vs. pre-therapy. Expression of 19 (15%) of these B cell genes returned toward baseline by 6  months, including genes for the B cell activation protein, CD79A, and for immunoglobulin A, D, and G heavy chains. Expression pathways for Th17 and CD4 regulatory T-cell (Treg) development, differentiation, and proliferation also quieted. In contrast, expression increased in Th1 and myeloid cell antiviral, pro-inflammatory, and toll-like receptor (TLR) gene pathways. CONCLUSION: These findings have clinical implications. B cell gene expression diminishes 2  weeks after anti-CD20 antibody infusion, but begins to rebound by 6  months. This suggests that the optimum time for vaccination is soon before reinfusion of anti-CD20 therapy. In addition, at 6  months, there is enhanced Th1 cell gene expression and induction of innate immune response genes and TLR expression, which can enhance anti-viral and anti-tumor immunity. This may compensate for diminished B cell gene expression after therapy. These data suggest that anti-CD20 therapy has dynamic effect on B cells and causes a compensatory rise in Th1 and myeloid immunity.
 OBJECTIVE: To characterize patterns of prescription opioid use among individuals with multiple sclerosis (MS) and identify risk factors associated with chronic use. DESIGN: Retrospective longitudinal cohort study examining US Department of Veterans Affairs electronic medical record data of Veterans with MS. The annual prevalence of prescription opioid use by type (any, acute, chronic, incident chronic) was calculated for each study year (2015-2017). Multivariable logistic regression was used to identify demographics and medical, mental health, and substance use comorbidities in 2015-2016 associated with chronic prescription opioid use in 2017. SETTING: US Department of Veterans Affairs, Veteran's Health Administration. PARTICIPANTS: National sample of Veterans with MS (N=14,974). MAIN OUTCOME MEASURE: Chronic prescription opioid use (≥90 days). RESULTS: All types of prescription opioid use declined across the 3 study years (chronic opioid use prevalence=14.6%, 14.0%, and 12.2%, respectively). In multivariable logistic regression, prior chronic opioid use, history of pain condition, paraplegia or hemiplegia, post-traumatic stress disorder, and rural residence were associated with greater risk of chronic prescription opioid use. History of dementia and psychotic disorder were both associated with lower risk of chronic prescription opioid use. CONCLUSION: Despite reductions over time, chronic prescription opioid use remains common among a substantial minority of Veterans with MS and is associated with multiple biopsychosocial factors that are important for understanding risk for long-term use.
 INTRODUCTION: The presence of focal cortical and white matter damage in patients with multiple sclerosis (pwMS) might lead to specific alterations in brain networks that are associated with cognitive impairment. We applied microstructure-weighted connectomes to investigate (i) the relationship between global network metrics and information processing speed in pwMS, and (ii) whether the disruption provoked by focal lesions on global network metrics is associated to patients' information processing speed. MATERIALS AND METHODS: Sixty-eight pwMS and 92 healthy controls (HC) underwent neuropsychological examination and 3T brain MRI including multishell diffusion (dMRI), 3D FLAIR, and MP2RAGE. Whole-brain deterministic tractography and connectometry were performed on dMRI. Connectomes were obtained using the Spherical Mean Technique and were weighted for the intracellular fraction. We identified white matter lesions and cortical lesions on 3D FLAIR and MP2RAGE images, respectively. PwMS were subdivided into cognitively preserved (CPMS) and cognitively impaired (CIMS) using the Symbol Digit Modalities Test (SDMT) z-score at cut-off value of -1.5 standard deviations. Statistical analyses were performed using robust linear models with age, gender, and years of education as covariates, followed by correction for multiple testing. RESULTS: Out of 68 pwMS, 18 were CIMS and 50 were CPMS. We found significant changes in all global network metrics in pwMS vs HC (p < 0.05), except for modularity. All global network metrics were positively correlated with SDMT, except for modularity which showed an inverse correlation. Cortical, leukocortical, and periventricular lesion volumes significantly influenced the relationship between (i) network density and information processing speed and (ii) modularity and information processing speed in pwMS. Interestingly, this was not the case, when an exploratory analysis was performed in the subgroup of CIMS patients. DISCUSSION: Our study showed that cortical (especially leukocortical) and periventricular lesions affect the relationship between global network metrics and information processing speed in pwMS. Our data also suggest that in CIMS patients increased focal cortical and periventricular damage does not linearly affect the relationship between network properties and SDMT, suggesting that other mechanisms (e.g. disruption of local networks, loss of compensatory processes) might be responsible for the development of processing speed deficits.



 BACKGROUND: Clinical observation has revealed that multiple sclerosis (MS) and autoimmune thyroid disease (AITD) are strongly correlated. The aim of this study was to explore the shared molecular causes of MS and AITD, and to conduct drug rearrangement on this basis, search for comorbidity drugs and feasible drugs for mutual reference between the two diseases. METHODS: Based on genome-wide association study (GWAS) data and transcriptome data, susceptibility genes and differentially expressed genes related to MS and AITD were identified by bioinformatics analysis. Pathway enrichment, gene ontology (GO), protein-protein interaction analysis, and gene-pathway network analysis of the above genes were performed to identify a common target pool, including common genes, common hub genes, and common pathways, and to explore the specific pathogenesis of the two diseases, respectively. Drugs that target the common pathways/genes were identified through the Comparative Toxicogenomics Database (CTD), DrugBank database, and Drug-Gene Interaction (DGI) Database. Common hub genes were compared with the target genes of drugs approved for treating MS/AITD and drugs under investigation identified by DrugBank and ClinicalTrials, respectively. RESULTS: We identified a pool of shared targets containing genes and pathways, including 46 common genetic susceptibility pathways and 9 common differentially expressed pathways, including JAK-STAT signaling pathway, Th17 cell differentiation, Th1 and Th2 cell differentiation, PD-L1 expression and PD-1 checkpoint pathway in cancer, etc. In addition, a total of 29 hub genes, including TYK2, JAK1, STAT3, IL2RA, HLA-DRB1, and TLR3, were identified. Drugs approved for treating MS or AITD, such as methylprednisolone, cyclophosphamide, glatiramer, natalizumab, and methimazole, can target the shared genes and pathways, among which methylprednisolone and cyclophosphamide have been shown to be beneficial for the treatment of the two diseases, indicating that these drugs have the potential to become a priority in the treatment of comorbidities. Moreover, drugs targeting multiple common genes and pathways, including tacrolimus, deucravacitinib, and nivolumab, were identified as potential drugs for the treatment of MS, AITD, and their comorbidities. CONCLUSION: We observed that T-cell activation-related genes and pathways play a major role in the pathogenesis of both MS and AITD, which may be the molecular basis of the comorbidity. Moreover, we identified a variety of drugs which may be used as priority or potential treatments for comorbidities.
 INTRODUCTION: Many studies have investigated pregnancy in women with multiple sclerosis (MS). However, no study has measured prenatal healthcare utilization in women with MS or adherence to follow-up recommendations to improve antenatal care quality. A better knowledge of the quality of antenatal care in women with MS would help identify and better support women with insufficient follow-up. Our objective was to measure the level of compliance to prenatal care recommendations in women with MS using data from the French National Health Insurance Database. METHODS: This retrospective cohort study included all pregnant women with MS who gave live birth in France between 2010 and 2015. Using the French National Health Insurance Database, follow-up visits with gynecologists, midwives, and general practitioners (GPs) were identified, as well as ultrasound exams and laboratory tests. Based on the Adequacy of Prenatal Care Use and Content and Timing of care in Pregnancy indices, a new tool adapted to the French recommendations was developed to measure and classify the antenatal care trajectory (adequate or inadequate). Explicative factors were identified using multivariate logistic regression models. A random effect was included because women may have had more than one pregnancy during the study period. RESULTS: In total, 4,804 women with MS (N = 5,448 pregnancies ending in live births) were included. When considering only visits with gynecologists/midwives, 2,277 pregnancies (41.8%) were considered adequate. When adding visits with GP, their number increased to 3,646 (66.9%). Multivariate models showed that multiple pregnancy and higher medical density were associated with better adherence to follow-up recommendations. Conversely, adherence was lower in 25-29-year-old and >40-year-old women, in women with very low income, and agricultural and self-employed workers. No visits, ultrasound exams, and laboratory tests were recorded in 87 pregnancies (1.6%). In 50% of pregnancies, women had at least one visit with a neurologist during the pregnancy, and women restarted disease-modifying therapy (DMT) within 6 months after delivery in 45.9% of pregnancies. DISCUSSION: Many women consulted their GP during pregnancy. This could be linked to a low density of gynecologists but may also reflect the preferences of women. Our findings can help adapt recommendations and healthcare providers' practices according to the women's profiles.

 Background: Both greater retinal neurodegenerative pathology and greater cardiovascular burden are seen in people with multiple sclerosis (pwMS). Studies also describe multiple extracranial and intracranial vascular changes in pwMS. However, there have been few studies examining the neuroretinal vasculature in MS. Our aim is to determine differences in retinal vasculature between pwMS and healthy controls (HCs) and to determine the relationship between retinal nerve fiber layer (RNFL) thickness and retinal vasculature characteristics. Methods: A total of 167 pwMS and 48 HCs were scanned using optical coherence tomography (OCT). Earlier OCT scans were available for 101 pwMS and 35 HCs for an additional longitudinal analysis. Segmentation of retinal vasculature was performed in a blinded manner in MATLAB's optical coherence tomography segmentation and evaluation GUI (OCTSEG) software. Results: PwMS has fewer retinal blood vessels when compared to HCs (35.1 vs. 36.8, p = 0.017). Over the 5.4 year follow up, and when compared to HCs, pwMS has a significant decrease in number of retinal vessels (average loss of -3.7 p = 0.007). Moreover, the total vessel diameter in pwMS does not change when compared to the increase in vessel diameter in the HCs (0.06 vs. 0.3, p = 0.017). Only in pwMS is there an association between lower RNFL thickness and fewer retinal vessel number and smaller diameter (r = 0.191, p = 0.018 and r = 0.216, p = 0.007). Conclusions: Over 5 years, pwMS exhibit significant retinal vascular changes that are related to greater atrophy of the retinal layers.
 Multiple sclerosis (MS) and inflammatory bowel disease (IBD) are autoimmune disorders characterized by inflammatory episodes affecting the brain and the gastrointestinal (GI) tract, respectively. The frequent association between MS and IBD suggests that both conditions may share common pathogenic mechanisms. However, different responses to biological therapies indicate differences in immune mechanisms of inflammation. Anti-CD20 therapies are high efficacy treatments increasingly used to control inflammatory bursts in MS, but they may alter GI homeostasis and promote the development of bowel inflammation in susceptible individuals. This review analyzes the mechanistic association between immunity in MS and IBD, the effect of anti-CD20 therapies on the gut microenvironment, and provides recommendations for early detection and management of GI toxicities in the context of B-cell depletion in MS patients.
 Vascular function is worse in multiple sclerosis (MS) than healthy controls perhaps based on differences in aerobic fitness. We compared carotid-femoral pulse wave velocity (cfPWV) and augmentation index (AIx75) between MS and controls while accounting for aerobic fitness. Aerobic fitness was measured as peak oxygen consumption on a recumbent stepper. cfPWV and AIx75 were measured using applanation tonometry. Persons with MS demonstrated lower aerobic fitness and higher cfPWV, but no difference in AIx75 compared with controls. The difference in cfPWV remained statistically significant after controlling for aerobic fitness, suggesting that arterial stiffness might reflect underlying pathophysiology processes of MS.
 Epstein-Barr virus (EBV), a causative agent for several types of lymphomas and mucosal cancers, is a human lymphotropic herpesvirus with the capacity to establish lifelong latent infection. More than 90% of the human population worldwide is infected. The primary infection is usually asymptomatic in childhood, whereas infectious mononucleosis (IM) is common when the infection occurs in adolescence. Primary EBV infection, with or without IM, or reactivation of latent infection in immunocompromised individuals have been associated with a wide range of neurologic conditions, such as encephalitis, meningitis, acute disseminated encephalomyelitis, and cerebellitis. EBV is also involved in malignant lymphomas in the brain. An increasing number of reports on EBV-related disorders of the central nervous system (CNS) including the convincing association with multiple sclerosis (MS) have put in focus EBV-related conditions beyond its established link to malignancies. In this review, we present the clinical manifestations of EBV-related CNS-disorders, put them in the context of known EBV biology and focus on available treatment options and future therapeutic approaches.
 We investigated the impact of dimethyl fumarate (DMF), an oral therapy for relapsing multiple sclerosis (MS), on blood microRNA (miRNA) signatures and neurofilament light (NFL) levels. DMF normalized miR-660-5p and modulated various miRNAs associated with the NF-kB pathway. These alterations reached a peak 4-7 months after treatment. Notably, particular miRNAs correlated with high or low NFL levels, implying their potential role as markers of treatment efficacy. Our findings broaden the understanding of DMF's immunomodulatory effects and may aid in predicting treatment responses.
 Cytokines and receptors of the IL-1 family are key mediators in innate immune and inflammatory reactions in physiological defensive conditions, but are also significantly involved in immune-mediated inflammatory diseases. Here, we will address the role of cytokines of the IL-1 superfamily and their receptors in neuroinflammatory and neurodegenerative diseases, in particular Multiple Sclerosis and Alzheimer's disease. Notably, several members of the IL-1 family are present in the brain as tissue-specific splice variants. Attention will be devoted to understanding whether these molecules are involved in the disease onset or are effectors of the downstream degenerative events. We will focus on the balance between the inflammatory cytokines IL-1β and IL-18 and inhibitory cytokines and receptors, in view of future therapeutic approaches.
 Genome-wide association studies (GWAS) map genetic associations of complex traits with precision limited to a linkage disequilibrium group. To translate GWAS results into new understanding of disease mechanisms, individual causative polymorphisms and their target genes should be identified. CRISPR/Cas9 genome editing can be used to create isogenic cell lines bearing alternative genotypes of candidate single-nucleotide polymorphisms to test their causality and to reveal gene targets. An intergenic polymorphism rs12946510 is associated with multiple sclerosis, inflammatory bowel disease and asthma. We created sublines of the T-helper cell line bearing alternative genotypes of rs12946510 and showed that its risk ("T") allele is associated with lower expression of IKZF3 and ORMDL3 genes and reduced cell activation. Our editing procedure can become an effective tool for discovering new genes involved in pathogenesis of complex diseases.
 The blood platelet plays an important role but often remains under-recognized in several vascular complications and associated diseases. Surprisingly, platelet hyperactivity and hyperaggregability have often been considered the critical risk factors for developing vascular dysfunctions in several neurodegenerative diseases (NDDs) like Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. In addition, platelet structural and functional impairments promote prothrombotic and proinflammatory environment that can aggravate the progression of several NDDs. These findings provide the rationale for using antiplatelet agents not only to prevent morbidity but also to reduce mortality caused by NDDs. Therefore, we thoroughly review the evidence supporting the potential pleiotropic effects of several novel classes of synthetic antiplatelet drugs, that is, cyclooxygenase inhibitors, adenosine diphosphate receptor antagonists, protease-activated receptor blockers, and glycoprotein IIb/IIIa receptor inhibitors in NDDs. Apart from this, the review also emphasizes the recent developments of selected natural antiplatelet phytochemicals belonging to key classes of plant-based bioactive compounds, including polyphenols, alkaloids, terpenoids, and flavonoids as potential therapeutic candidates in NDDs. We believe that the broad analysis of contemporary strategies and specific approaches for plausible therapeutic treatment for NDDs presented in this review could be helpful for further successful research in this area.
 In addition to disease-associated microglia (DAM), microglia with MHC-II and/or IFN-I signatures may form additional pathogenic subsets that are relevant to neurodegeneration. However, the significance of such MHC-II and IFN-I signatures remains elusive. We demonstrate here that these microglial subsets play intrinsic roles in orchestrating neurotoxic properties of neurotoxic Eomes(+) Th cells under the neurodegeneration-associated phase of experimental autoimmune encephalomyelitis (EAE) that corresponds to progressive multiple sclerosis (MS). Microglia acquire IFN-signature after sensing ectopically expressed long interspersed nuclear element-1 (L1) gene. Furthermore, ORF1, an L1-encoded protein aberrantly expressed in the diseased central nervous system (CNS), stimulated Eomes(+) Th cells after Trem2-dependent ingestion and presentation in MHC-II context by microglia. Interestingly, administration of an L1 inhibitor significantly ameliorated neurodegenerative symptoms of EAE concomitant with reduced accumulation of Eomes(+) Th cells in the CNS. Collectively, our data highlight a critical contribution of new microglia subsets as a neuroinflammatory hub in immune-mediated neurodegeneration.
 The complement system is implicated in a broad range of neuroinflammatory disorders such as Alzheimer's disease (AD) and multiple sclerosis (MS). Consequently, measuring complement levels in biofluids could serve as a potential biomarker for these diseases. Indeed, complement levels are shown to be altered in patients compared to controls, and some studies reported a correlation between the level of free complement in biofluids and disease progression, severity or the response to therapeutics. Overall, they are not (yet) suitable as a diagnostic tool due to heterogeneity of reported results. Moreover, measurement of free complement proteins has the disadvantage that information on their origin is lost, which might be of value in a multi-parameter approach for disease prediction and stratification. In light of this, extracellular vesicles (EVs) could provide a platform to improve the diagnostic power of complement proteins. EVs are nanosized double membrane particles that are secreted by essentially every cell type and resemble the (status of the) cell of origin. Interestingly, EVs can contain complement proteins, while the cellular origin can still be determined by the presence of EV surface markers. In this review, we summarize the current knowledge and future opportunities on the use of free and EV-associated complement proteins as biomarkers for neuroinflammatory and neurodegenerative disorders.

 BACKGROUND/OBJECTIVES: Serum proteomic analysis of deeply-phenotyped samples, biological pathway modeling and network analysis were performed to elucidate the inflammatory and neurodegenerative processes of multiple sclerosis (MS) and identify sensitive biomarkers of MS disease activity (DA). METHODS: Over 1100 serum proteins were evaluated in >600 samples from three MS cohorts to identify biomarkers of clinical and radiographic (gadolinium-enhancing lesions) new MS DA. Protein levels were analyzed and associated with presence of gadolinium-enhancing lesions, clinical relapse status (CRS), and annualized relapse rate (ARR) to create a custom assay panel. RESULTS: Twenty proteins were associated with increased clinical and radiographic MS DA. Serum neurofilament light chain (NfL) showed the strongest univariate correlation with radiographic and clinical DA measures. Multivariate modeling significantly outperformed univariate NfL to predict gadolinium lesion activity, CRS and ARR. DISCUSSION: These findings provide insight regarding correlations between inflammatory and neurodegenerative biomarkers and clinical and radiographic MS DA. FUNDING: Octave Bioscience, Inc (Menlo Park, CA).
 Dimethyl fumarate (DMF) is an FDA-approved drug for treating relapsing-remitting multiple sclerosis; but it is susceptible to sublimation leading to its loss during processing. Cocrystals can protect against thermal energy via the interaction of DMF with a coformer via weak forces of interaction. With this hypothesis, we have, for the first time, prepared DMF cocrystals using the solvent evaporation method using coformers like citric acid and succinic acid screened by in-silico predictions and hydrogen bonding properties. Analysis using infra-red (IR), powder x-ray diffraction (PXRD), thermogravimetric analysis (TGA), differential scanning calorimetry (DSC), and sublimation evaluation characterized cocrystals and their thermostability. Comparative analysis of the release profile has been done by dissolution and pharmacokinetic study of DMF and its cocrystals. The cocrystals have improved thermal stability and better pharmacological activities than DMF. In the safety and efficacy evaluation of the formulated cocrystals, they were found to be non-cytotoxic, antioxidant, and inhibiting IL-6 and TNF-α in PBMC induced by lipopolysaccharide (LPS). We have obtained cocrystals of DMF with improved thermal stability and better pharmacological activities than DMF.
 The complicated multiple sclerosis (MS) can exhibit subacute sight deterioration and can lead to total deprivation of vision. In the current work, we explored the therapeutic outcome of Cathepsin B inhibitor (CA-074) against retinopathy and optic neuritis (ON) caused by experimental autoimmune encephalomyelitis (EAE) induced by proteolipid protein peptide (PLP) in female SJL/J mice. A daily dose of 10 mg/kg CA-074 was administered to the EAE mice intraperitoneally for 14 days from day 14 post-immunization until day 28. The Western blot and immunofluorescence analyses show inflammation in the optic nerve through the elevation of iNOS and NFkB markers in EAE mice. Optic neuritis was reported which is a consequence of demyelination and axon injury, estimated with the reduction in myelin basic protein (MBP). The glial fibrillary acidic protein (GFAP) expression level was found to be elevated in the retina of EAE mice which confirmed the retinopathy. The administration of CA-074 ameliorated optic neuritis and retinopathy by reducing inflammation. The treatment with CA-074 also reduced the demyelination and axonal injuries in the EAE mice. The findings of this study have shown the protective effect of CA-074 in the case of retinopathy and ON inflicted by EAE in SJL/J mice.
 Frequent use of hormones and drugs may be associated with side-effects. Recent studies have shown that probiotics have effects on the prevention and treatment of immune-related diseases. Limosilactobacillus reuteri (L. reuteri) had regulatory effects on intestinal microbiota, host epithelial cells, immune cells, cytokines, antibodies (Ab), toll-like receptors (TLRs), tryptophan (Try) metabolism, antioxidant enzymes, and expression of related genes, and exhibits antibacterial and anti-inflammatory effects, leading to alleviation of disease symptoms. Although the specific composition of the cell-free supernatant (CFS) of L. reuteri has not been clarified, its efficacy in animal models has drawn increased attention to its potential use. This review summarizes the effects of L. reuteri on intestinal flora and immune regulation, and discusses the feasibility of its application in atopic dermatitis (AD), asthma, necrotizing enterocolitis (NEC), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS), and provides insights for the prevention and treatment of immune-related diseases.
 Community-based palliative care is defined as palliative care delivered outside of the hospital and outpatient clinics. These settings include the home, nursing homes, day programs, volunteer organizations, and support groups. There is strong evidence outside of the neuropalliative context that community-based palliative care can reduce hospital costs and admissions at the end of life. Research that focuses on specialized community-based palliative care for neurologic disease have similar findings, although with significant variability across conditions and geographic locations. Several of these studies have investigated home-based care for neurologic conditions including dementia, Parkinson's disease, multiple sclerosis, brain tumors, and motor neuron disease. Other work has focused on incorporating palliative care models into the treatment of patients with neurologic diseases within nursing home settings. Similar to nonneurologic community-based palliative care, little has been published on patient and caregiver quality-of-life outcomes in such models of care, although the emerging data are generally positive. Future studies should explore how best to provide comprehensive, cost-effective, scalable, and replicable models of community-based neuropalliative care, patient and caregiver outcomes in such models, and how care can be adapted between and within specific patient populations and healthcare systems.
 BACKGROUND: The traditional paper and pencil method for EDSS calculation (pEDSS) is the cornerstone of multiple sclerosis practice; however, it requires an expert for an accurate calculation, and it takes a lot of time to perform the function scores. A new algorithmic approach (aEDSS) has been developed for easier and faster assessment. OBJECTIVE: To determine if using aEDSS can achieve good inter-rater agreement and save time compared to pEDSS. SUBJECTS AND METHODS: This study was conducted on 200 MS patients; EDSS was performed twice for each patient by two neurologists on the same day; one used the pEDSS, and the other used the aEDSS in a random order to test the inter-rater agreement regarding functional system scores and the final EDSS score and to detect the difference in the time needed for calculation between both methods. RESULTS: The new algorithmic approach achieved excellent agreement with the traditional method (Kappa > 0.81) with a shorter calculation time (16 ± 2.67 min for aEDSS vs 31 ± 4.3 min for pEDSS, P < 0.0001). CONCLUSION: The new algorithmic approach could represent a suitable alternative to the traditional method, making EDSS calculation easier and faster.
 BACKGROUND: Evobrutinib is an oral, central nervous system (CNS)-penetrant and highly selective covalent Bruton's tyrosine kinase inhibitor under clinical development for patients with relapsing multiple sclerosis (RMS). OBJECTIVE: To investigate the effect of evobrutinib on immune responses in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccinated patients with RMS from a Phase II trial (NCT02975349). METHODS: A post hoc analysis of patients with RMS who received evobrutinib 75 mg twice daily and SARS-CoV-2 vaccines during the open-label extension (n = 45) was conducted. Immunoglobulin (Ig)G anti-S1/S2-specific SARS-CoV-2 antibodies were measured using an indirect chemiluminescence immunoassay. RESULTS: In the vaccinated subgroup, mean/minimum evobrutinib exposure pre-vaccination was 105.2/88.7 weeks. In total, 43 of 45 patients developed/increased S1/S2 IgG antibody levels post-vaccination; one patient's antibody response remained negative post-vaccination and the other had antibody levels above the upper limit of detection, both pre- and post-vaccination. Most patients (n = 36/45), regardless of pre-vaccination serostatus, had a 10-100-fold increase of antibody levels pre- to post-vaccination. Antibody levels post-booster were higher versus post-vaccination. CONCLUSION: These results suggest evobrutinib, an investigational drug with therapeutic potential for patients with RMS, acts as an immunomodulator, that is, it inhibits aberrant immune cell responses in patients with RMS, while responsiveness to foreign de novo and recall antigens is maintained.
 BACKGROUND: Alemtuzumab (ALZ) is an immune reconstitution therapy for treating relapsing-remitting multiple sclerosis (RRMS). However, ALZ increases the risk of secondary autoimmune diseases (SADs). OBJECTIVE: We explored whether the detection of autoimmune antibodies (auto-Abs) could predict the development of SADs. METHODS: We included all patients with RRMS in Sweden who initiated ALZ treatment (n = 124, 74 female subjects) from 2009 to 2019. The presence of auto-Abs was determined in plasma samples obtained at the baseline and at 6, 12, and 24 months of follow-up, as well as in a subgroup of patients (n = 51), it was determined in plasma samples obtained at the remaining 3-month intervals up to 24 months. Monthly blood tests, urine tests, and the assessment of clinical symptoms were performed for monitoring safety including that of SADs. RESULTS: Autoimmune thyroid disease (AITD) developed in 40% of patients, within a median follow-up of 4.5 years. Thyroid auto-Abs were detected in 62% of patients with AITD. The presence of thyrotropin receptor antibodies (TRAbs) at the baseline increased the risk of AITD by 50%. At 24 months, thyroid auto-Abs were detected in 27 patients, and 93% (25/27) developed AITD. Among patients without thyroid auto-Abs, only 30% (15/51) developed AITD (p < 0.0001). In the subgroup of patients (n = 51) with more frequent sampling for auto-Abs, 27 patients developed ALZ-induced AITD, and 19 of them had detectable thyroid auto-Abs prior to the AITD onset, with a median interval of 216 days. Eight patients (6.5%) developed non-thyroid SAD, and none had detectable non-thyroid auto-Abs. CONCLUSION: We conclude that monitoring thyroid auto-Abs, essentially TRAbs, may improve the surveillance of AITD associated with ALZ treatment. The risk for non-thyroid SADs was low, and monitoring non-thyroid auto-Abs did not seem to provide any additional information for predicting non-thyroid SADs.




 Objective: The purpose of this literature review article is to provide a synthesis of recent research focused on the use of 3 techniques to evaluate MS-related fatigue: electroencephalography [EEG], transcranial direct-current stimulation (tDSC), and transcranial- magnetic stimulation (TMS). Method: We performed a literature search in the Cumulative Index to Nursing and Allied Health Literature (CINAHL, EBSCOhost), MEDLINE (OVID), APA PsycInfo (OVID), Scopus (Elsevier), and Web of Science (Clarivate) databases, limited to 2015 and after. Results: Our review revealed that fatigue in MS patients can be quantified and predicted using electrophysiological techniques. Such techniques, which yield objective data, are historically assessed in relation to subjective data, or perceived fatigue. We identified studies using EEG, TMS, and/or tDCS to study fatigue in people with MS. In total, 220 records were identified with 19 studies meeting inclusion criteria. Quality appraisal revealed that the level of evidence was generally graded "good". Conclusions: Despite the heterogenous nature of reviewed the studies and selected the varied self-report fatigue measures, our literature synthesis suggests promise for the use of EEG, TMS, and/or tDCS approaches in more accurately assessing fatigue in people with MS. Further research is needed in this arena.
 BACKGROUND: Whether progression independent of relapse activity (PIRA) heralds earlier onset of secondary progressive multiple sclerosis (SPMS) and more rapid accumulation of disability during SPMS remains to be determined. We investigated the association between early PIRA, relapse-associated worsening (RAW) of disability and time to SPMS, subsequent disability progression and their response to therapy. METHODS: This observational cohort study included patients with relapsing-remitting multiple sclerosis (RRMS) from the MSBase international registry across 146 centres and 39 countries. Associations between the number of PIRA and RAW during early multiple sclerosis (MS) (the initial 5 years of MS onset) were analysed with respect to: time to SPMS using Cox proportional hazards models adjusted for disease characteristics; and disability progression during SPMS, calculated as the change of Multiple Sclerosis Severity Scores over time, using multivariable linear regression. RESULTS: 10 692 patients met the inclusion criteria: 3125 (29%) were men and the mean MS onset age was 32.2 years. A higher number of early PIRA (HR=1.50, 95% CI 1.28 to 1.76, p<0.001) and RAW (HR=2.53, 95% CI 2.25 to 2.85, p<0.001) signalled a higher risk of SPMS. A higher proportion of early disease-modifying therapy exposure (per 10%) reduced the effect of early RAW (HR=0.94, 95% CI 0.89 to 1.00, p=0.041) but not PIRA (HR=0.97, 95% CI 0.91 to 1.05, p=0.49) on SPMS risk. No association between early PIRA/RAW and disability progression during SPMS was found. CONCLUSIONS: Early disability increase during RRMS is associated with a greater risk of SPMS but not the rate of disability progression during SPMS. The deterioration associated with early relapses represents a potentially treatable risk factor of SPMS. TRIAL REGISTRATION NUMBER: Australian New Zealand Clinical Trials Registry (ACTRN12605000455662).
 BACKGROUND: Network-based measures are emerging MRI markers in multiple sclerosis (MS). We aimed to identify networks of white (WM) and grey matter (GM) damage that predict disability progression and cognitive worsening using data-driven methods. METHODS: We analysed data from 1836 participants with different MS phenotypes (843 in a discovery cohort and 842 in a replication cohort). We calculated standardised T1-weighted/T2-weighted (sT1w/T2w) ratio maps in brain GM and WM, and applied spatial independent component analysis to identify networks of covarying microstructural damage. Clinical outcomes were Expanded Disability Status Scale worsening confirmed at 24 weeks (24-week confirmed disability progression (CDP)) and time to cognitive worsening assessed by the Symbol Digit Modalities Test (SDMT). We used Cox proportional hazard models to calculate predictive value of network measures. RESULTS: We identified 8 WM and 7 GM sT1w/T2w networks (of regional covariation in sT1w/T2w measures) in both cohorts. Network loading represents the degree of covariation in regional T1/T2 ratio within a given network. The loading factor in the anterior corona radiata and temporo-parieto-frontal components were associated with higher risks of developing CDP both in the discovery (HR=0.85, p<0.05 and HR=0.83, p<0.05, respectively) and replication cohorts (HR=0.84, p<0.05 and HR=0.80, p<0.005, respectively). The decreasing or increasing loading factor in the arcuate fasciculus, corpus callosum, deep GM, cortico-cerebellar patterns and lesion load were associated with a higher risk of developing SDMT worsening both in the discovery (HR=0.82, p<0.01; HR=0.87, p<0.05; HR=0.75, p<0.001; HR=0.86, p<0.05 and HR=1.27, p<0.0001) and replication cohorts (HR=0.82, p<0.005; HR=0.73, p<0.0001; HR=0.80, p<0.005; HR=0.85, p<0.01 and HR=1.26, p<0.0001). CONCLUSIONS: GM and WM networks of microstructural changes predict disability and cognitive worsening in MS. Our approach may be used to identify patients at greater risk of disability worsening and stratify cohorts in treatment trials.
 BACKGROUND AND PURPOSE: Understanding predictors of changes in employment status among people living with multiple sclerosis (MS) can assist health care providers to develop appropriate work retention/rehabilitation programs. We aimed to model longitudinal transitions of employment status in MS and estimate the probabilities of retaining employment status or losing or gaining employment over time in individuals with a first clinical diagnosis of central nervous system demyelination (FCD). METHODS: This prospective cohort study comprised adults (aged 18-59 years) diagnosed with FCD (n = 237) who were followed for more than 11 years. At each review, participants were assigned to one of three states: unemployed, part-time, or full-time employed. A Markov multistate model was used to examine the rate of state-to-state transitions. RESULTS: At the time of FCD, participants with full-time employment had an 89% chance of being in the same state over a 1-year period, but this decreased to 42% over the 10-year follow-up period. For unemployed participants, there was a 92% likelihood of remaining unemployed after 1 year, but this probability decreased to 53% over 10 years. Females, those who progressed to clinically definite MS, those with a higher relapse count, and those with a greater level of disability were at increased risk of transitioning to a deteriorated employment state. In addition, those who experienced clinically significant fatigue over the follow-up period were less likely to gain employment after being unemployed. CONCLUSIONS: In our FCD cohort, we found a considerable rate of employment transition during the early years post-diagnosis. Over more than a decade of follow-up post-FCD, we found that females and individuals with a greater disability and a higher relapse count are at higher risk of losing employment.
 AIMS: Multiple sclerosis treatment strategies are changing in the Czech Republic. According to data from 2013-2021, the proportion of patients starting high-efficacy disease-modifying therapies is increasing. In this survey, we describe the actual data trends in multiple sclerosis (MS) patients beginning their first disease‑modifying therapies (DMTs) from 2013 to 2021. The secondary objective was to present the history, data collection, and scientific potential of the Czech National MS registry (ReMuS). METHODS: First, using descriptive statistics, we analysed the data for patients starting their first DMTs, either platform (including dimethyl fumarate) or high-efficacy DMTs (HE-DMTs), for each successive year. Second, a detailed description of the history, data collection, completeness, quality optimising procedures, and legal policies of ReMuS is provided. RESULTS: Based on the dataset from December 31, 2021, the total number of monitored patients with MS in ReMuS increased from 9,019 in 2013 (referred from 7 of 15 MS centres) to 12,940 in 2016 (referred from all 15 Czech MS centres) to 17,478 in 2021. In these years, the percentage of patients treated with DMTs in the registry ranged from 76 to 83%, but the proportion of patients treated with HE-DMTs changed from 16.2% in 2013 to 37.1% in 2021. During the follow-up period, a total of 8,491 treatment-naive patients received DMTs. The proportion of patients (all MS phenotypes) starting HE-DMTs increased from 2.1% in 2013 to 18.5% in 2021. CONCLUSION: Patient registries, including ReMuS, provide an essential quality data source, especially in light of the increasing percentage of patients on HE-DMTs. Although early initiation of HE-DMT can provide considerable benefits, it also carries greater potential risks. Consistent long-term follow-up of patients in real‑world clinical practice, which only registries allow, is therefore crucial to evaluate the efficacy and safety of therapeutic strategies, for epidemiological research and to assist decision making by healthcare providers and regulatory bodies.
 BACKGROUND: Results from observational studies indicate an association between circulating levels of mammalian target of rapamycin (mTOR)-dependent circulating proteins and the risk of multiple sclerosis (MS). However, a causal association has not been fully elucidated. Mendelian randomization (MR) is used to overcome limitations inherent to observational studies, assess the causal association, and minimize bias due to confounding and reverse causation. METHODS: To explore the causal association between seven mTOR-dependent proteins (AKT, RP-S6K, eIF4E-BP, eIF4A, eIF4E, eIF4G, and PKC-α) and MS, we obtained summary statistics from the genome-wide association study (GWAS) meta-analysis of the International Multiple Sclerosis Genetics Consortium (47,429 patients and 68,374 controls) and the INTERVAL study (genetic associations with 2994 plasma proteins from 3301 healthy individuals). MR analyses were conducted using inverse variance weighted, weighted median estimator, and MR-Egger regression methods/models. Sensitivity analyses were performed to ensure the reliability of the findings. Single nucleotide polymorphisms (SNPs) that are independent (r(2) < 0.01) and strongly associated to minerals (p < 1e(-5)) were selected as instrumental variables. RESULTS: The results of the MR analyses revealed that among the seven mTOR-dependent proteins selected for study, the circulating level of PKC-α (odds ratio [OR] 0.90, 95% confidence interval [CI] 0.82-0.98; P = 0.017) and RP-S6K (OR 1.12, 95% CI 1.00-1.25; P = 0.045) were associated with MS risk and that there was no sign of pleiotropy or heterogeneity. PKC-α was negatively related to MS, while RP-S6K was positively related to MS. No significant causation was found between the other proteins studied (AKT, eIF4E-BP, eIF4A, eIF4E, eIF4G) and MS. CONCLUSION: Molecules in the mTOR signaling pathway may bidirectionally regulate the occurrence and development of MS. PKC-α is a protective factor, while RP-S6K is a risk factor. Further explorations of pathways underlying the association between mTOR-dependent proteins and MS are required. PKC-α and RP-S6K might be used as future therapeutic targets for screening high-risk individuals and potentially improving opportunities for targeted prevention strategies.
 Cyclophosphamide is a medication primarily used in the management and treatment of neoplasms, including multiple myeloma, sarcoma, and breast cancer. Cyclophosphamide is a nitrogen mustard that exerts its anti-neoplastic effects through alkylation. This activity reviews the indications, contraindications, mechanism of action, and other key factors of cyclophosphamide as a valuable agent in the treatment and management of neoplastic diseases by an interprofessional team. There is also a discussion of cyclophosphamide use in the management of severe multiple sclerosis.
 Stem cells have been the subject of research for years due to their enormous therapeutic potential. Most neurological diseases such as multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD) are incurable or very difficult to treat. Therefore new therapies are sought in which autologous stem cells are used. They are often the patient's only hope for recovery or slowing down the progress of the disease symptoms. The most important conclusions arise after analyzing the literature on the use of stem cells in neurodegenerative diseases. The effectiveness of MSC cell therapy has been confirmed in ALS and HD therapy. MSC cells slow down ALS progression and show early promising signs of efficacy. In HD, they reduced huntingtin (Htt) aggregation and stimulation of endogenous neurogenesis. MS therapy with hematopoietic stem cells (HSCs) inducted significant recalibration of pro-inflammatory and immunoregulatory components of the immune system. iPSC cells allow for accurate PD modeling. They are patient-specific and therefore minimize the risk of immune rejection and, in long-term observation, did not form any tumors in the brain. Extracellular vesicles derived from bone marrow mesenchymal stromal cells (BM-MSC-EVs) and Human adipose-derived stromal/stem cells (hASCs) cells are widely used to treat AD. Due to the reduction of Aβ42 deposits and increasing the survival of neurons, they improve memory and learning abilities. Despite many animal models and clinical trial studies, cell therapy still needs to be refined to increase its effectiveness in the human body.
 BACKGROUND: Cognitive dysfunction and brain atrophy are both common in progressive multiple sclerosis (MS) but are seldom examined comprehensively in clinical trials. Antioxidant treatment may affect the neurodegeneration characteristic of progressive MS and slow its symptomatic and radiographic correlates. OBJECTIVES: This study aims to evaluate cross-sectional associations between cognitive battery components of the Brief International Cognitive Assessment for Multiple Sclerosis with whole and segmented brain volumes and to determine if associations differ between secondary progressive (SPMS) and primary progressive (PPMS) MS subtypes. DESIGN: The study was based on a baseline analysis from a multi-site randomized controlled trial of the antioxidant lipoic acid in veterans and other people with progressive MS (NCT03161028). METHODS: Cognitive batteries were conducted by trained research personnel. MRIs were processed at a central processing site for maximum harmonization. Semi-partial Pearson's adjustments evaluated associations between cognitive tests and MRI volumes. Regression analyses evaluated differences in association patterns between SPMS and PPMS cohorts. RESULTS: Of the 114 participants, 70% had SPMS. Veterans with MS made up 26% (n = 30) of the total sample and 73% had SPMS. Participants had a mean age of 59.2 and sd 8.5 years, and 54% of them were women, had a disease duration of 22.4 (sd 11.3) years, and had a median Expanded Disability Status Scale of 6.0 (with an interquartile range of 4.0-6.0, moderate disability). The Symbol Digit Modalities Test (processing speed) correlated with whole brain volume (R = 0.29, p = 0.01) and total white matter volume (R = 0.33, p < 0.01). Both the California Verbal Learning Test (verbal memory) and Brief Visuospatial Memory Test-Revised (visual memory) correlated with mean cortical thickness (R = 0.27, p = 0.02 and R = 0.35, p < 0.01, respectively). Correlation patterns were similar in subgroup analyses. CONCLUSION: Brain volumes showed differing patterns of correlation across cognitive tasks in progressive MS. Similar results between SPMS and PPMS cohorts suggest combining progressive MS subtypes in studies involving cognition and brain atrophy in these populations. Longitudinal assessment will determine the therapeutic effects of lipoic acid on cognitive tasks, brain atrophy, and their associations.
 INTRODUCTION: Fingolimod is the first oral immunomodulatory treatment used as secondary care therapy in the treatment of multiple sclerosis for the last 10 years. The objective of our study is to reveal the experiences of the first generic fingolimod active ingredient treatment in different centers across Turkey. METHOD: The first generic fingolimod efficacy and safety data of patients followed-up in 29 different clinical multiple sclerosis units in Turkey were analyzed retrospectively. Data regarding efficacy and safety of the patients were transferred to the data system both before the treatment and on the 6th, 12(th) and 24(th) month following the treatment. The data were analyzed using the IBM SPSS 20.00. P value of <0.05 was considered to be statistically significant. RESULTS: A total of 508 multiple sclerosis patients, 331 of whom were women, were included in the study. Upon comparing the Expanded Disability Status values before and after the treatment, a significant decrease was observed, especially at month 6 and thereafter. Since bradycardia occurred in 11 of the patients (2.3%), the first dose had to be longer than 6 hours. During the observation of the first dose, no issues that could prevent the use of the drug occured. Side effects were seen in 49 (10.3%) patients during the course of fingolimod treatment. Respectively, the most frequent side effects were bradycardia, hypotension, headache, dizziness and tachycardia. CONCLUSION: The observed results regarding efficacy and safety were similar to clinical trial data in the literature and real life data in terms of the first equivalent with fingolimod active ingredient.
 BACKGROUND: We aim to evaluate whether fertility, pregnancy, delivery and breastfeeding have been actually improving in women with multiple sclerosis (MS), compared with general population, and in relation to treatment features. METHODS: We included 2018-2020 population-level healthcare data on women with MS living in the Campania region (Italy). Fertility, pregnancy and delivery outcomes were obtained from Certificate of Delivery Assistance; breastfeeding was collected up to 6 months after delivery by trained personnel. RESULTS: Out of 2748 women with MS in childbearing age, 151 women delivered 156 babies. Fertility rate was 0.58 live births per woman with MS, compared with 1.29 in Campania region and 1.25 in Italy. Disease-modifying treatment (DMT) continuation during pregnancy was associated with lower birth weight (coeff -107.09; 95% CI -207.91 to -6.26; p=0.03). Exposure to DMTs with unknown/negative effects on pregnancy was associated with birth defects (OR 8.88; 95% CI 1.35 to 58.41; p=0.02). Birth defects occurred in pregnancies exposed to dimethyl fumarate (2/21 exposed pregnancies), fingolimod (1/11 exposed pregnancies) and natalizumab (2/30 exposed pregnancies). After delivery, 18.8% of women with MS were escalated of DMT efficacy, while 50.7% started on same/similar-efficacy DMTs, and 30.5% did not receive DMT. The probability of breastfeeding was higher in women who were treated with breastfeeding-safe DMTs (OR 5.57; 95% CI 1.09 to 28.55; p=0.03). CONCLUSIONS: Fertility rate in women with MS remains below the general population. Family planning and subsequent DMT decisions should aim to achieve successful pregnancy, delivery and breastfeeding outcomes, while controlling disease activity.
 INTRODUCTION: Dimethyl fumarate (DMF) showed favorable benefit-risk in patients with relapsing-remitting multiple sclerosis (MS) in phase 3 DEFINE and CONFIRM trials and in the ENDORSE extension study. Disease activity can differ in younger patients with MS compared with the overall population. METHODS: Randomized patients received DMF 240 mg twice daily or placebo (PBO; years 0-2 DEFINE/CONFIRM), then DMF (years 3-10; continuous DMF/DMF or PBO/DMF; ENDORSE); maximum follow-up (combined studies) was 13 years. This integrated post hoc analysis evaluated safety and efficacy of DMF in a subgroup of young adults aged 18-29 years. RESULTS: Of 1736 patients enrolled in ENDORSE, 125 were young adults, 86 treated continuously with DMF (DMF/DMF) and 39 received delayed DMF (PBO/DMF) in DEFINE/CONFIRM. Most (n = 116 [93%]) young adults completed DMF treatment in DEFINE/CONFIRM. Median (range) follow-up time in ENDORSE was 6.5 (2.0-10.0) years. Young adults entering ENDORSE who had been treated with DMF in DEFINE/CONFIRM had a model-based Annualized Relapse Rate (ARR; 95% CI) of 0.24 (0.16-0.35) vs. 0.56 (0.35-0.88) in PBO patients. ARR remained low in ENDORSE: 0.07 (0.01-0.47) at years 9-10 (DMF/DMF group). At year 10 of ENDORSE, EDSS scores were low in young adults: DMF/DMF, 1.9 (1.4); PBO/DMF, 2.4 (1.6). At ~ 7 years, the proportion of young adults with no confirmed disability progresion was 81% for DMF/DMF and 72% for PBO/DMF. Patient-reported outcomes (PROs) (SF-36 and EQ-5D) generally remained stable during ENDORSE. The most common adverse events (AEs) in young adults during ENDORSE were MS relapse (n = 53 [42%]). Most AEs were mild (n = 20 [23.3%], n = 7 [17.9%]) to moderate (n = 45 [52.3%], n = 23 [59.0%]) in the DMF/DMF and PBO/DMF groups, respectively. The most common serious AE (SAE) was MS relapse (n = 19 [15%]). CONCLUSION: The data support a favorable benefit-risk profile of DMF in young adults, as evidenced by well-characterized safety, sustained efficacy, and stable PROs. CLINICAL TRIAL INFORMATION: Clinical trials.gov, DEFINE (NCT00420212), CONFIRM (NCT00451451), and ENDORSE (NCT00835770).
 Multiple sclerosis (MS) is a central nervous system (CNS) disease with complicated etiology. Multifocal demyelination and invasion of inflammatory cells are its primary pathological features. Fasudil has been confirmed to improve experimental autoimmune encephalomyelitis (EAE), an animal model of MS. However, Fasudil is accompanied by several shortcomings in the clinical practice. Hydroxyfasudil is a metabolite of Fasudil in the body with better pharmaceutical properties. Therefore, we attempted to study the influence of Hydroxyfasudil upon EAE mice. The results demonstrated that Hydroxyfasudil relieved the symptoms of EAE and the associated pathological damage, reduced the adhesion molecules and chemokines, decreased the invasion of peripheral immune cells. Simultaneously, Hydroxyfasudil modified the rebalance of peripheral T cells. Moreover, Hydroxyfasudil shifted the M1 phenotype to M2 polarization, inhibited inflammatory signaling cascades as well as inflammatory factors, and promoted anti-inflammatory factors in the CNS. In the end, mice in the Hydroxyfasudil group expressed more tight junction proteins, indirectly indicating that the blood-brain barrier (BBB) was protected. Our results indicate that Hydroxyfasudil may be a prospective treatment for MS.
 BACKGROUND: We analysed the COMparison Between All immunoTherapies for Multiple Sclerosis (NCT03193866), a Swedish nationwide observational study in relapsing-remitting multiple sclerosis (RRMS), to identify trajectories of processing speed and physical disability after disease-modulating therapy (DMT) start. METHODS: Using a group-modelling approach, we assessed trajectories of processing speed with oral Symbol Digit Modalities Test (SDMT) and physical disability with Expanded Disability Status Scale, from first DMT start among 1645 patients with RRMS followed during 2011-2022. We investigated predictors of trajectories using group membership as a multinomial outcome and calculated conditional probabilities linking membership across the trajectories. RESULTS: We identified 5 stable trajectories of processing speed: low SDMT scores (mean starting values=29.9; 5.4% of population), low/medium (44.3; 25.3%), medium (52.6; 37.9%), medium/high (63.1; 25.8%) and high (72.4; 5.6%). We identified 3 physical disability trajectories: no disability/stable (0.8; 26.8%), minimal disability/stable (1.6; 58.1%) and moderate disability (3.2; 15.1%), which increased to severe disability. Older patients starting interferons were more likely than younger patients starting rituximab to be on low processing speed trajectories. Older patients starting teriflunomide, with more than one comorbidity, and a history of pain treatment were more likely to belong to the moderate/severe physical disability trajectory, relative to the no disability one. There was a strong association between processing speed and physical disability trajectories. CONCLUSIONS: In this cohort of actively treated RRMS, patients' processing speed remained stable over the years following DMT start, whereas patients with moderate physical disability deteriorated in physical function. Nevertheless, there was a strong link between processing speed and disability after DMT start.
 BACKGROUND: interleukin 23 (IL-23) is an important factor involved in the survival and proliferation of T helper 17 cells (Th17), known for their implication in multiple sclerosis (MS). By contrast, IL-27 regulates and modulates the function of T lymphocytes, in particular as a suppressor of Th17 differentiation. The aims of the study were i) to test the association of cytokines with the clinical and genetic characteristics in each of the multiple sclerosis groups (CIS - clinically isolated syndrome, RRMS - relapsing-remitting MS and SPMS - Secondary progressive MS) and ii) to evaluate the association between serum levels of IL-23 and IL-27 with T4730C (IL-27), A964G (IL-27) and R381Q (IL-23) gene polymorphisms in RRMS patients. METHODS: Blood samples were obtained from 82 patients diagnosed with MS under treatment with glatiramer acetate (GA), interferon beta (IFN) 1 A and 1 B. IL-23 and IL-27 serum concentrations were measured by enzyme-linked immunosorbant assay (ELISA). Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used in order to determine the genotypes for R381Q (IL-23) polymorphisms, T4730C (IL-27) and A964G (IL-27). RESULTS: Patients with SPMS, RRMS and CIS respectively differed significantly regarding age distribution (p = 0.003) but the studied MS groups were similar regarding age at disease onset (p = 0.528) and treatment type (p = 0.479). A significant increase of mean serum IL-27 was noticed in cases with early onset (age at disease onset <28 years) of RRMS (mean difference: 4.2 pg/ml, 95% CI: 0.8-5.3 pg/ml), compared to cases with later onset of RRMS (age at disease onset ≥28 years). RRMS patients with wild GG genotype of R381Q (IL-23) showed a significant increase of mean serum IL-23 than patients with variant AG genotype (mean difference: 115.1 pg/ml, 95% CI: 8.6-221.6 pg/ml). A trend for a higher increase in means of serum IL-23 (p = 0.086) was observed in RRMS patients carriers of AA genotype of A964G (IL-27) polymorphism in comparison with patients with AG or GG genotypes. We found no significant monotonic correlation of IL-27, IL-23 serum levels with age at disease onset (years) and duration of disease (p > 0.05) in the CIS and SPMS group respectively but a significant correlation between IL-23 and the duration of disease-modifying treatment was noticed only in the SPMS group. CONCLUSIONS: The results of the current study suggest an association between IL-23 levels and the R381Q gene polymorphism and also a relationship between IL-27 serum levels and early age at disease onset in RRMS patients.
 BACKGROUND AND PURPOSE: A systematic review and meta-analysis was performed of the outcome of Coronavirus disease 2019 (COVID-19) infection in patients with multiple sclerosis (MS) who received disease-modifying therapies (DMTs). METHODS: Relevant studies published before November 2022 in the PubMed, Cochrane Library, Chinese National Knowledge Infrastructure, and Web of Science databases were retrieved using the following search expression: ("multiple sclerosis" OR "MS") AND ("DMT" OR "disease modifying therapies") AND ("COVID-19"). Two authors independently screened the articles and extracted the data. Qualitative analyses and a meta-analysis constituted 22 of the 794 retrieved articles. Differences in the hospitalization and mortality rates were used as the main measures of efficacy, and the meta-analysis was performed using RevMan software. RESULTS: 22 clinical trials were selected. The hospitalization rate was lower in the 3,216 patients who received DMTs than in the 774 patients who did not receive any treatment, with a moderate effect size of 0.43 (p<0.00001). The mortality rate was also lower among patients with MS treated using DMTs than in controls (odds ratio [OR]=0.19, 95% confidence interval [CI]=0.13-0.27, p<0.00001). The hospitalization rates for COVID-19 infection in patients with MS treated with anti-CD20 therapy also increased markedly (OR=3.32, 95% CI=2.63-4.20, p<0.00001). However, there was no significant difference between patients with MS who did and did not receive DMTs. CONCLUSIONS: In summary, the application of DMTs was found to be valuable for patients with MS infected with COVID-19. However, more clinical studies are needed to determine the use of anti-CD20 drugs in patients with MS during the COVID-19 pandemic.
 BACKGROUND: Previous studies attempted to define the best threshold for κ free light chains (κFLC) index, confirming higher sensitivity (Se) but less specificity (Sp) compared with IgG oligoclonal bands (OCB) for the diagnosis of MS. OBJECTIVE: To evaluate the diagnostic accuracy of different κFLC index intervals in a miscellaneous cohort of neurological patients, proposing a procedural flowchart for MS diagnosis. METHODS: We analyzed data from 607 patients diagnosed with MS (179), CIS (116), other inflammatory (94) or non-inflammatory neurological diseases (218). Measures of diagnostic accuracy were reported for different potential thresholds of κFLC index, and for IgG OCB and IgG index. Binary logistic regression was to used to calculate the odds of being diagnosed with MS based on each increase of κFLC index. RESULTS: CSF IgG OCB showed 72.2% Se (CI 95% 68.4-75.7) and 95.2% Sp (CI 95% 93.1-96.7) in discriminating between MS/CIS and controls, with an AUC of 0.84 (CI 95% 0.80-0.87). The highest diagnostic accuracy was reported for κFLC index cut-off of 5.0 (Se = 85.4%, Sp = 90.4%, AUC = 0.88), while a threshold of 11.0 exhibited higher Sp (95.5%, 95% CI 93.1-97.1) than IgG OCB. AUCs for all thresholds between 4.25 and 6.6 were not significantly different from each other, but were significantly higher than the AUC of IgG OCB (p < 0.05). The odds of being diagnosed with MS/CIS increased by 17.1% for each unit increase of κFLC index (OR = 1.17; 95% CI 1.12-1.23; p < 0.001). CONCLUSION: κFLC index performed better than CSF IgG OCB in supporting the diagnosis of MS/CIS, with the advantage of being a cost-effective and quantitative analysis.
 BACKGROUND AND PURPOSE: Hybrid immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develops from a combination of natural infection and vaccine-generated immunity. Multiple sclerosis (MS) disease-modifying therapies (DMTs) have the potential to impact humoral and cellular immunity induced by SARS-CoV-2 vaccination and infection. The aims were to compare antibody and T-cell responses after SARS-CoV-2 mRNA vaccination in persons with MS (pwMS) treated with different DMTs and to assess differences between naïvely vaccinated pwMS and pwMS with hybrid immunity vaccinated following a previous SARS-CoV-2 infection. METHODS: Antibody and T-cell responses were determined in pwMS at baseline and 4 and 12 weeks after the second dose of SARS-CoV-2 vaccination in 143 pwMS with or without previous SARS-CoV-2 infection and 40 healthy controls (HCs). The MS cohort comprised natalizumab (n = 22), dimethylfumarate (n = 23), fingolimod (n = 38), cladribine (n = 30), alemtuzumab (n = 17) and teriflunomide (n = 13) treated pwMS. Immunoglobulin G antibody responses to SARS-CoV-2 antigens were measured using a multiplex bead assay and FluoroSpot was used to assess T-cell responses (interferon γ and interleukin 13). RESULTS: Humoral and T-cell responses to vaccination were comparable between naïvely vaccinated HCs and pwMS treated with natalizumab, dimethylfumarate, cladribine, alemtuzumab and teriflunomide, but were suppressed in fingolimod-treated pwMS. Both fingolimod-treated pwMS and HCs vaccinated following a previous SARS-CoV-2 infection had higher antibody levels 4 weeks after vaccination compared to naïvely vaccinated individuals. Antibody and interferon γ levels 12 weeks after vaccination were positively correlated with time from last treatment course of cladribine. CONCLUSION: These findings are of relevance for infection risk mitigation and for vaccination strategies amongst pwMS undergoing DMT.
 Neuroinflammation can be triggered by microbial products disrupting immune regulation. In this study, we investigated the levels of IgG1, IgG2, IgG3, and IgG4 subclasses against the heat shock protein (HSP)70(533-545) peptide and lipopentapeptide (MAP_Lp5) derived from Mycobacterium avium subsp. paratuberculosis (MAP) in the blood samples of Japanese and Italian individuals with relapsing remitting multiple sclerosis (MS). Additionally, we examined the impact of this peptide on MOG-induced experimental autoimmune encephalomyelitis (EAE). A total of 130 Japanese and 130 Italian subjects were retrospectively analyzed using the indirect ELISA method. Furthermore, a group of C57BL/6J mice received immunization with the MAP_HSP70(533-545) peptide two weeks prior to the active induction of MOG(35-55) EAE. The results revealed a significantly robust antibody response against MAP_HSP70(533-545) in serum of both Japanese and Italian MS patients compared to their respective control groups. Moreover, heightened levels of serum IgG4 antibodies specific to MAP antigens were correlated with the severity of the disease. Additionally, EAE mice that were immunized with MAP_HSP70(533-545) peptide exhibited more severe disease symptoms and increased reactivity of MOG(35-55)-specific T-cell compared to untreated mice. These findings provide evidence suggesting a potential link between MAP and the development or exacerbation of MS, particularly in a subgroup of MS patients with elevated serum IgG4 levels.
 INTRODUCTION: Cognitive impairment represents one of the most hidden and disabling clinical aspects of multiple sclerosis (MS). In this regard, the major challenges are represented by the need for a comprehensive and standardised cognitive evaluation of each patient, both at disease onset and during follow-up, and by the lack of clear-cut data on the effects of treatments. In the present review, we summarize the current evidence on the effects of the available oral disease-modifying treatments (DMTs) on cognitive outcome measures. MATERIALS AND METHODS: In this systematised review, we extract all the studies that reported longitudinally acquired cognitive outcome data on oral DMTs in MS patients. RESULTS: We found 29 studies that evaluated at least one oral DMT, including observational studies, randomised controlled trials, and their extension studies. Most of the studies (n = 20) evaluated sphingosine-1-phosphate (S1P) modulators, while we found seven studies on dimethyl fumarate, six on teriflunomide, and one on cladribine. The most frequently used cognitive outcome measures were SDMT and PASAT. Most of the studies reported substantial stability or mild improvement in cognitive outcomes in a short-time follow-up (duration of most studies ≤2 years). A few studies also reported MRI measures of brain atrophy. CONCLUSION: Cognitive outcomes were evaluated only in a minority of prospective studies on oral DMTs in MS patients with variable findings. More solid and numerous data are present for the S1P modulators. A standardised cognitive evaluation remains a yet unmet need to better clarify the possible positive effect of oral DMTs on cognition.
 INTRODUCTION: Fabry disease (FD) can be undiagnosed in the context of multiple sclerosis (MS) due to similar clinical and paraclinical features. Our study aimed to determine the prevalence (and the necessity of screening) of FD among patients with possible or definite MS. METHODS: In this prospective monocentric observational study, we included consecutive patients enrolled between May 2017 and May 2019 after the first clinical event suggestive of MS. All patients underwent FD screening using dried blood spots in a stepwise manner combining genetic and enzyme testing. Patients were followed until May 2022. RESULTS: We included 160 patients (73.1% female, mean age 33.9 years). The 2017 revised McDonald's criteria for definite MS were fulfilled by 74 (46.3%) patients at the time of study recruitment and 89 (55.6%) patients after 3-5 years of follow-up. None of the patients had a pathogenic GLA variant, and four (2.5%) had a variant of unknown significance (p.A143T, p.S126G, 2 × p.D313Y). In two of these patients, the intrathecal synthesis of oligoclonal bands was absent, and none had hyperproteinorachia or pleocytosis in cerebrospinal fluid. Detailed examination of FD organ manifestations revealed only discrete ocular and kidney involvement in two patients. CONCLUSION: The prevalence of FD in the population of suspected or definite MS patients does not appear to be high. Our results do not support routine FD screening in all patients with a possible diagnosis of MS, but there is an urgent need to search for red flags and include FD in the differential diagnosis of MS.
 BACKGROUND: We clinically evaluated the quality of white matter lesions (WML) of the cerebrum on 3D inversion recovery ultrashort echo time (IR-UTE) magnetic resonance imaging (MRI) in multiple sclerosis (MS) patients. METHODS: Forty-nine patients with MS were included in this study. A 3T MRI scanner was used. Two radiologists (readers) evaluated the quality of WML on IR-UTE images using a three-point Likert scale (1-good quality, 2-moderate quality, 3-insufficient quality). They also rated other WML-related factors potentially influencing WML quality using another three-point Likert scale (1-no/minor impact, 2-moderate impact, 3-high impact). Another reader rated the presence of WML on IR-UTE to evaluate the diagnostic value (right/false positive and false negative) of IR-UTE in detecting WML. Signal intensity ratios (SIRs) derived from WML signal intensities and WML sizes were also determined and analyzed. RESULTS: Two hundred and seventy-five MS lesions were evaluated. 87% of the lesions were rated Likert 1 on IR-UTE (P<0.01). WML rated Likert 2 and 3 presented near the grey matter (GM) in 58% of the cases (n=21), with 14 lesions being ≤2 mm (P=0.03). 62.5% of the WML rated Likert 2/3 were in the temporal lobe (P=0.02). The mean SIR of WML on IR-UTE was 1.14±0.22, while the mean SIR on fluid-attenuated inversion recovery (FLAIR) was 6.97±1.88. There was no significant correlation of SIRs between IR-UTE and FLAIR (R=0.14, P=0.245). 92.4% of the WML were correctly detected on IR-UTE (n=254). 19 out of the 21 false positive/negative rated WML were located near the GM or in the temporal lobe. WML presented 7.7% smaller in mean on IR-UTE compared to FLAIR. Factors affecting WML quality with a moderate or high impact (Likert 2 and 3) were not found. CONCLUSIONS: Most WML are clearly detectable on IR-UTE sequences. The main limitations are WML in the temporal lobe and near the GM.
 OBJECTIVE: Assess patient characteristics, healthcare resource utilization (HCRU), and relapses in patients with multiple sclerosis (MS) who switched to teriflunomide from other disease-modifying therapies (DMTs). METHODS: Retrospective study of US Merative™ MarketScan(®) claims database (Jan 1, 2012-July 31, 2020,) including HIPAA-compliant, deidentified data. Patients ≥18 years with MS diagnosis (based on ICD-9/ICD-10 codes), receiving ≥1 DMT prior to teriflunomide and ≥12 months continuous enrollment pre and post index (date of teriflunomide initiation). Outcomes included inpatient and emergency room claims coinciding with MS diagnosis, MS-related healthcare costs, and annualized relapse rates (ARRs) (indirectly assessed using hospitalization/outpatient claims and steroid use coinciding with MS diagnosis). RESULTS: The analyzed cohort (N=2016) was primarily female (79%); age (mean ± standard deviation) 51.4 ± 9.3 years; MS duration 4.7±2.8 years (at index). The majority (89.2%) were treated with one DMT before switching to teriflunomide. Use of outpatient services (event rate/100 person-years) increased post vs pre index; however, MRI visits significantly reduced over the same period (both P<0.0001). Costs for MS-specific outpatient visits decreased by $371 per patient per year (PPPY) after switching to teriflunomide. Despite an increase in use post index (0.024 to 0.033 rate/100 person-years; P<0.0001), costs for MS-specific laboratory services reduced (pre-index: $271 vs $248 PPPY post-index; P=0.02). Fewer patients had relapses after switching (pre-index: n=417 [20.7%]; post-index: n=333 [16.5%]). ARR was significantly lower after switching (pre-index: 0.269 vs post-index: 0.205; P=0.000). CONCLUSION: Switching to teriflunomide from existing DMTs in patients with relapsing MS resulted in a reduction in outpatient HCRU in this analysis of US claims data. The real-world effectiveness of teriflunomide was generally consistent with efficacy reported in clinical trials, showing a reduction in relapse following a switch to teriflunomide.
 BACKGROUND: Patients with multiple sclerosis (MS) suffer from repetitive neurological deterioration, while anxiety may play a significant role in the disease's progression. OBJECTIVE: To explore the prevalence of anxiety in MS and to investigate the risk factors related to anxiety in MS patients. METHODS: An analysis of four databases, PubMed, Web of Science, EMBASE, and Cochrane Library, has been conducted to determine the prevalence or risk factors for anxiety in MS published before May 2021. RESULTS: In total, 32 studies were found to be eligible. Anxiety prevalence was estimated to be 36% based on the pooled estimates [the 95% confidence interval (CI) = [0.30-0.42], I (2) = 98.4%]. Significant risk factors for developing of anxiety were as follows: age at survey [the weighted mean difference (WMD) = 0.96, 95% CI = [0.86-1.06], I (2) = 43.8%], female [the odd ratio (OR) = 1.78, 95% CI = [1.38-2.30], I (2) = 0%], living together (OR 2.83, 95% CI = [1.74-4.59], I (2) = 0%), past psychiatric history (OR 2.42, 95% CI = [1.56-3.75], I (2) = 0%), depression (OR 7.89, 95% CI = [3.71-16.81], I (2) = 0%), not taking MS medication (OR 2.33, 95% CI = [1.29-4.21], I (2) = 77.8%), relapsing-remitting MS (RRMS) (OR 1.50, 95% CI = [0.94-2.37], I (2) = 53.5%), and baseline Expanded Disability Status Scale (EDSS) (OR 0.84, 95% CI = [0.48-1.21], I (2) = 62.2%). CONCLUSION: An estimated 36% of people with MS suffer from anxiety. And anxiety rates in MS patients are significantly associated with age, gender, living together, prior psychiatric history, depression, drug compliance, RRMS, and baseline EDSS. SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=287069, identifier CRD42021287069.
 BACKGROUND: Excessive daytime sleepiness (EDS) in multiple sclerosis (MS) can be a significant source of disability. Despite this, its prevalence as a patient-reported outcome in this condition has not been well established, and its causes are not well understood. METHODS: We prospectively assessed EDS as part of an observational study for patients referred for diagnostic neuro-ophthalmological testing. EDS was evaluated by the Epworth Sleepiness Scale (ESS), and visual data were also collected as part of a research protocol. Analysis with patient data was performed following the exclusion of patients with known primary sleep disorders. RESULTS: A total of 69 patients with MS were included in the analysis. The mean ESS was 6.5 with a SD of 4.3. ESS ≥ 10 was present in 23% of the cohort even in the presence of minimal mean neurological disability (Patient Determined Disease Steps (PDDS) = 1.5). The ESS score was not associated with age, sex, disease-related disability, retinal nerve fiber layer (RNFL), or optic neuritis (ON), but displayed an association with visual dysfunction. CONCLUSIONS: There is an increased prevalence of EDS in MS. The increased values of the ESS are not explained by other sleep disorders, suggesting separate mechanisms. Further study of the underlying mechanisms is warranted.
 BACKGROUND: STRIVE was a prospective, 4-year, multicenter, observational, open-label, single-arm study of natalizumab treatment in anti-JC virus antibody-negative patients with early relapsing-remitting multiple sclerosis (RRMS). OBJECTIVE: Study objectives examined the effects of natalizumab on cognitive processing speed, confirmed disability improvement (CDI), and patient-reported outcomes (PROs). METHODS: Clinical and PRO secondary endpoints were assessed annually over 4 years in STRIVE. The Symbol Digit Modalities Test (SDMT) was used as a measure of cognitive processing speed. PROs were assessed using the Multiple Sclerosis Impact Score (MSIS-29) and the Work Productivity and Activity Impairment Questionnaire (WPAI). RESULTS: At all four annual assessments, the proportion of patients in the intent-to-treat (ITT) population (N = 222) who exhibited clinically meaningful improvement in their SDMT score from baseline (i.e., change ≥ 4 points) ranged from 41.9 to 54.0%. The cumulative probability of CDI at 4 years in patients in the ITT population with a baseline Expanded Disability Status Scale score ≥ 2 (N = 133) was 43.9%. Statistically significant reductions in the mean change from screening in the MSIS-29 physical and psychological scores, indicating improved quality of life, were observed over all 4 years (P ≤ 0.0012 for all). A statistically significant decrease from screening in the impact of MS on regular activities, signifying an improvement in this WPAI measure, was also observed over all 4 years of the study. CONCLUSION: These results further extend our knowledge of the effectiveness, specifically regarding improvements in cognitive processing speed, disability and PROs, of long-term natalizumab treatment in early RRMS patients. CLINICALTRIALS: GOV: NCT01485003 (5 December 2011).
 BACKGROUND: Relapses in multiple sclerosis (MS) patients are usually defined as subacute clinical symptoms that last for at least 24 h. To validate a clinical relapse on magnetic resonance imaging (MRI), an anatomically fitting lesion with gadolinium enhancement in the central nervous system (CNS) would be mandatory. The aim of this study was to validate clinical relapses in regard to the concomitant detection of active, anatomically fitting MRI lesions. METHODS: We performed a retrospective analysis of 199 MS patients with acute relapse who had received an MRI scan before the initiation of methylprednisolone (MPS) therapy. Clinical data and MRIs were systematically reanalyzed by correlating clinical symptoms with their anatomical representation in the CNS. Patients were then categorized into subgroups with a clinical-radiological match (group 1) or clinical-radiological mismatch (group 2) between symptoms and active, topographically fitting lesions and further analyzed in regard to clinical characteristics. RESULTS: In 43% of our patients, we observed a clinical-radiological mismatch (group 2). Further analysis of patient characteristics showed that these patients were significantly older at the time of relapse. MS patients in group 2 also showed a significantly longer disease duration and significantly more previous relapses when compared to group 1. Comparing symptom clusters, the appearance of motor dysfunction during the current relapse was significantly more frequent in group 2 than in group 1. The overall dose of MPS treatment was significantly lower in group 2 than in group 1 with a similar treatment response in both groups. CONCLUSIONS: The substantial clinical-radiological mismatch during acute relapse in our study could be explained by several factors, including a psychosomatic component or disturbance of network connectivity. Alternatively, secondary progression or a diffuse neuro-inflammatory process might cause clinical symptoms, especially in older patients with a longer disease duration. As a consequence, treatment of clinical relapses and the definition of breakthrough disease should be reconsidered in regard to combined clinical and MRI criteria and/or additional biomarkers. Further studies are necessary to address the contribution of diffuse neuro-inflammation to the clinical presentation of symptoms.
 BACKGROUND AND AIMS: Multiple sclerosis (MS) is a chronic disease characterized by axonal damage, demyelination, inflammation, oxidative stress, and immune cell infiltration. This disease is the first cause of nontraumatic disability in young adults leading to a decline in patients' quality of life. Patients with MS may also suffer from gastrointestinal symptoms due to the disease or prescription drugs. Unfortunately, no treatment for MS has been discovered yet, and prescribed drugs can only help control its clinical course. Interestingly, recent animal studies have shown positive effects of ginger administration in the MS model. Therefore, we aim to determine the effect of ginger supplementation on neurofilament light chain, matrix metalloproteinase-9, interleukin-17, nitric oxide, complete and differential blood counts, disability status, quality of life, gastrointestinal symptoms, and body mass index (BMI) in MS patients. METHODS: This study is a double-blind randomized controlled trial. Fifty-two patients with relapsing-remitting MS will be assigned to intervention and control groups using stratified permuted block randomization. The intervention and control groups will take 1500 mg/day ginger and placebo (as corn) supplements for 12 weeks, respectively. All outcomes will be assessed before and after the trial. Serum concentrations of neurofilament light chain, matrix metalloproteinase-9, and interleukin-17 will be measured by enzyme-linked immunosorbent assay. Nitric oxide serum levels will be detected using colorimetry. Complete and differential blood counts will be assessed by an automated hematology analyzer. Disability status, quality of life, and gastrointestinal symptoms will be evaluated by the Expanded Disability Status Scale, MS Impact Scale, and Visual Analog Scale, respectively. BMI will be calculated by dividing weight in kilograms by height in meters squared. Potential side effects of ginger supplementation will also be closely monitored during the study. TRIAL REGISTRATION: This protocol was registered at the Iranian Registry of Clinical Trials (www.irct.ir) under the registration number IRCT20180818040827N3.
 INTRODUCTION: Antibodies to cell surface proteins of astrocytes have been described in chronic inflammatory demyelinating disorders (CIDD) of the central nervous system including multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Our aim was to identify novel anti-astrocyte autoantibodies in relapsing remitting MS (RRMS) patients presenting predominantly with spinal cord and optic nerve attacks (MS-SCON). METHODS: Sera of 29 MS-SCON patients and 36 healthy controls were screened with indirect immunofluorescence to identify IgG reacting with human astrocyte cultures. Putative target autoantigens were investigated with immunoprecipitation (IP) and liquid chromatography-mass/mass spectrometry (LC-MS/MS) studies using cultured human astrocytes. Validation of LC-MS/MS results was carried out by IP and ELISA. RESULTS: Antibodies to astrocytic cell surface antigens were detected in 5 MS-SCON patients by immunocytochemistry. LC-MS/MS analysis identified chloride intracellular channel protein-1 (CLIC1) as the single common membrane antigen in 2 patients with MS-SCON. IP experiments performed with the commercial CLIC1 antibody confirmed CLIC1-antibody. Home made ELISA using recombinant CLIC1 protein as the target antigen identified CLIC1 antibodies in 9/29 MS-SCON and 3/15 relapsing inflammatory optic neuritis (RION) patients but in none of the 30 NMOSD patients, 36 RRMS patients with only one or no myelitis/optic neuritis attacks and 36 healthy controls. Patients with CLIC1-antibodies showed trends towards exhibiting reduced disability scores. CONCLUSION: CLIC1-antibody was identified for the first time in MS and RION patients, confirming once again anti-astrocytic autoimmunity in CIDD. CLIC1-antibody may potentially be utilized as a diagnostic biomarker for differentiation of MS from NMOSD.
 BACKGROUND: Changes in brain connectivity occur in patients with multiple sclerosis (MS), even in patients under disease-modifying therapies. Using magnetic resonance imaging (MRI) to asses patients treated with disease-modifying therapies, such as natalizumab, can elucidate the mechanisms involved in clinical deterioration in MS. OBJECTIVES: To evaluate differences in resting-state functional connectivity among MS patients treated with natalizumab, MS patients not treated with natalizumab, and controls. DESIGN: Single-center retrospective cross-sectional study. METHODS: Twenty-three MS patients being treated with natalizumab were retrospectively compared with 23 MS patients who were naïve for natalizumab, and were using first-line medications (interferon-β and/or glatiramer acetate), and 17 gender- and age-matched control subjects. The MS patient groups were also matched for time since diagnosis and hyperintense lesion volume on FLAIR. All participants underwent brain MRI using a 3 Tesla scanner. Independent component analysis and dual regression were used to identify resting-state functional connectivity using the FMRIB Software Library. RESULTS: In comparison to controls, the MS patients treated with natalizumab presented decreased connectivity in the left orbitofrontal cortex, in the anterior cingulate and orbitofrontal cortex network. The patients not treated with natalizumab presented increased connectivity in the secondary visual, sensorimotor, and ventral attention networks in comparison to controls.Compared to patients treated with natalizumab, the patients not using natalizumab presented increased connectivity in the left Heschl's gyrus and in the right superior frontal gyrus in the ventral attention network. CONCLUSION: Differences in brain connectivity between MS patients not treated with natalizumab, healthy controls, and patients treated with natalizumab may be secondary to suboptimal neuronal compensation due to prior less efficient treatments, or due to a compensation in response to maladaptive plasticity.
 BACKGROUND: Spasticity affects 54% of multiple sclerosis (MS) patients at disease onset, but this rate gradually increases with disease progression. Spasticity does not fully respond to standard treatment in one-third of the patients. OBJECTIVE: Our systematic review and meta-analysis assessed whether add-on nabiximols, can improve MS-associated refractory spasticity. METHODS: The systematic literature search was performed in Web of Science, MEDLINE, Scopus, CEN- TRAL, and Embase, on 15/10/2021, without restrictions. We included in the review blinded, randomized, placebo-controlled trials evaluating the efficacy of nabiximols in adult MS patients with refractory spas- ticity, by comparison with placebo. The primary outcome was responder rate by spasticity numerical rat- ing scale (NRS). Secondary outcomes were spasticity-related parameters. We used random effect models to calculate odds ratios (OR) or mean differences and the corresponding 95% CI. Bias-factors were as- sessed with Cochrane risk of bias tool (RoB2). (PROSPERO ID: CRD42021282177). RESULTS: We identified 9 eligible articles, of which 7 (1128 patients) were included in the meta-analysis. The spasticity numerical rating scale (NRS) was significantly higher in the nabiximols group than in the placebo group (OR 2.41 (95% CI 1.39; 4.18)). Secondary outcomes were in accordance with our primary results. At least some concerns were detected in the risk of bias analysis. CONCLUSION: Our results indicate that nabiximols is efficient in MS associated spasticity, refractory to standard treatment and it may be considered as add-on symptomatic therapy. Nevertheless, further studies are needed to establish the optimal treatment protocol - dose, duration, moment of initiation, disease type.
 PURPOSE: Sexual motives are major determinants of sexual behaviour. It has been known that sexual motives may vary according to circumstances. Multiple sclerosis (MS) is a chronic disease causing a broad range of symptoms and disabilities, that often interfere with sexual activities. We aimed to investigate the sexual motives in persons with MS. PATIENTS AND METHODS: Cross-sectional study in 157 persons with MS and 157 controls matched for age, gender, relationship, duration of relationship and educational status via propensity score matching. The Reasons for Having Sex (YSEX) questionnaire assessed the proportion with which a person had engaged in sexual intercourse for each of 140 distinct motives to have sex. Estimated mean differences in scores for four primary factors (Physical, Goal attainment, Emotional, Insecurity) and 13 sub-factors, and sexual satisfaction and importance of sex were calculated as Average Treatment Effect of the Treated using 99% confidence intervals. RESULTS: Persons with MS reported a lower proportion of engaging in sex compared with the controls for the factors Physical (-0.29), Emotional (-0.23) and Insecurity (-0.10); and for the physical sub-factors Pleasure (-0.48), Experience seeking (-0.32), Stress reduction (-0.24), and Physical desirability (-0.16), the emotional sub-factors Love and commitment (-0.27) and Expression (-0.17), and the insecurity sub-factor Self-esteem boost (-0.23). In the control group seven of the top 10 sexual motives were physical versus five in the MS group. The importance of sex was lower in the MS group (-0.68). CONCLUSION: Findings of this controlled cross-sectional study suggest a reduction in the number of sexual motives in persons with MS, especially of physical motives related to pleasure and experience seeking. Health care professionals may consider assessing sexual motivation when dealing with persons with MS who suffer from decreased sexual desire or another sexual dysfunction.
 Introduction: This study aimed to assess the prognostic role of visual evoked potentials (VEPs) of the non-neuritic eye at the diagnosis of multiple sclerosis (MS). Patients and methods: We enrolled 181 MS patients (62% females, mean age at diagnosis: 38 years, standard deviation: 12) at the time of the first diagnostic work-up, including VEPs. We collected P100 latency and N75-P100 amplitude of non-neuritic eyes at diagnosis, and then we calculated the mean values in 127 patients with no history of optic neuritis (ON) or considered the unaffected eye in the remaining. At last follow-up (minimum: one year), disability was evaluated according to MS Severity Score or MSSS (median: 2.44, range: 0.18-9.63). Statistical analysis included Mann-Whitney descriptive analysis, Spearman correlation for independent samples, and linear regression for significant predictors of MSSS. Results: 38/181 patients had P100 latency >115 ms, and 63/181 showed N75-P100 amplitude < 5 microV in the unaffected eyes at MS diagnosis. At last follow-up, MSSS correlated with P100 latency (rho = 0.21, p = 0.004) and N75-P100 amplitude (rho = 0.19, p = 0.009) collected at diagnosis. P100 latency (not N75-P100 amplitude) resulted in a predictor for disability over time (MSSS) in the regression model (along with age at onset, MS course, and disease-modifying treatments). Conclusions: Our study showed a prognostic value of VEPs in clinically unaffected eyes at MS diagnosis to predict future disability, independently from a history of ON.
 Progressive multiple sclerosis (MS) is a chronic disease with a unique pattern, which is histologically classified into the subpial type 3 lesions in the autopsy. The lesion is also homologous to that of cuprizone (CPZ) toxin-induced animal models of demyelination. Aberration of the tryptophan (TRP)-kynurenine (KYN) metabolic system has been observed in patients with MS; nevertheless, the KYN metabolite profile of progressive MS remains inconclusive. In this study, C57Bl/6J male mice were treated with 0.2% CPZ toxin for 5 weeks and then underwent 4 weeks of recovery. We measured the levels of serotonin, TRP, and KYN metabolites in the plasma and the brain samples of mice at weeks 1, 3, and 5 of demyelination, and at weeks 7 and 9 of remyelination periods by ultra-high-performance liquid chromatography with tandem mass spectrometry (UHPLC-MS/MS) after body weight measurement and immunohistochemical analysis to confirm the development of demyelination. The UHPLC-MS/MS measurements demonstrated a significant reduction of kynurenic acid, 3-hydoxykynurenine (3-HK), and xanthurenic acid in the plasma and a significant reduction of 3-HK, and anthranilic acid in the brain samples at week 5. Here, we show the profile of KYN metabolites in the CPZ-induced mouse model of demyelination. Thus, the KYN metabolite profile potentially serves as a biomarker of progressive MS and thus opens a new path toward planning personalized treatment, which is frequently obscured with immunologic components in MS deterioration.
 BACKGROUND: People with multiple sclerosis (MS) are susceptible to severe COVID-19 outcomes. They were included as a priority group for the Australian COVID-19 vaccine roll-out in early 2021. However, vaccine hesitancy remains a complex barrier to vaccination in this population group, which may be partly related to disease relapse concerns following COVID-19 vaccination. This study examined the COVID-19 vaccination status, intent, hesitancy, and disease-related beliefs in people with MS. METHODS: An online survey was conducted with people with MS receiving care at two Australian health services between September and October 2021. It collected sociodemographic and disease-specific characteristics and responses to validated scales that assessed vaccine hesitancy and general and MS-related vaccine beliefs. RESULTS: Of the 281 participants [mean age 47.7 (SD 12.8) years; 75.8% females], most (82.9%) had received at least one COVID-19 vaccine dose. Younger participants were less likely to be vaccinated, as were those within 1-5 years of disease duration. After controlling for age, disease duration was not associated with vaccination status. Unvaccinated participants were more likely to report less willingness to receive the COVID-19 vaccine, higher vaccine complacency and lower vaccine confidence, greater MS-related vaccine complacency, and higher MS and treatment interaction concerns. CONCLUSIONS: People with MS reported a high vaccination rate, despite general and MS-specific COVID-19 vaccine concerns. Greater MS-specific concerns were reported by those who indicated that their MS was not well-controlled and their MS impacted their daily activities. By understanding the factors that influence vaccine hesitancy and their interplay with MS disease course and treatment concerns, this can inform tailored interventions and educational messages to address these concerns in people with MS. Clinicians, governments, and community organisations are key partners in delivering these interventions and messages, as ongoing booster doses are needed for this vulnerable population.
 BACKGROUND AND AIMS: Multiple sclerosis (MS) is associated with osteoporosis, possibly due to neurological disability and decreased calcium intake. The objective of this study was to evaluate the efficacy of a personalized nutritional advice program by a dietitian compared to the delivery of a standard advice form to optimize dietary calcium intake in outpatients with MS. METHODS: We performed a randomized, controlled, parallel trial comparing the efficacy of a personalized dietary advice (PDA) program to standard advice form (SAF) to increase daily calcium intake in MS patients. The study population was composed by patients with relapsing-remitting MS aged 18-69 years old. PDA program consisted in dietary advice delivered by a dietitian at baseline, 1 month, and 3 months. Calcium and nutrient intake in patients from both groups was evaluated at baseline and 6 months using a dietary survey. RESULTS: Of the 194 patients screened for inclusion, 182 patients were included (79% female, median age of 42 years, and median EDSS of 2.0), and randomized to SAF (n = 92) or PDA (n = 90). At 6 months, median calcium intake increased by 241 mg/day in the PDA group and decreased by 120 mg/day in the SAF group (p < 0.0001). However, the median calcium intake was 947 mg/day in the SAF group and 778 mg/day in the PDA group at baseline (p = 0.0077), potentially favoring the effect of dietary advice. Complementary analyses focusing on patients with insufficient calcium intakes at baseline revealed comparable values in both groups (p = 0.69). Of those, patients included in the PDA group obtained significantly higher calcium intakes at 6 months than patients from the SAF group (p = 0.0086) independently of EDSS, PASAT, HADS and EQ-5D scores. CONCLUSION: This work shows the efficacy of dietary management based on personalized advice program over 3 months to durably increase calcium consumption in MS patients with insufficient calcium intake. CLINICAL TRIAL REGISTRATION: clinicaltrials.gov, identifier NCT02664623.
 INTRODUCTION: Adherence to disease-modifying therapies is key for achieving optimal outcomes in multiple sclerosis (MS). Diroximel fumarate (DRF) is an oral fumarate approved for treatment of relapsing forms of MS. It has the same pharmacologically active metabolite as dimethyl fumarate (DMF) and similar efficacy and safety profiles, but with demonstrated fewer gastrointestinal (GI) related adverse events (AEs). There are limited data characterizing persistence and adherence to DRF in the real world. METHODS: This retrospective analysis of the AcariaHealth Specialty Pharmacy Program included patients with MS initiating DRF from 1 December 2019 to 30 January 2021. This analysis evaluated persistence, measured as proportion of patients remaining on therapy; discontinuation rate due to GI AEs; and adherence measured by proportion of days covered (PDC). RESULTS: Overall, 1143 patients were included; 433 (37.9%) patients had been treated with prior DMF and switched to DRF. Persistence was high in both groups: the estimated proportion of patients remaining on DRF at 16 months was 82.3% [95% confidence internal (CI) 77.2-86.3%], and 90.1% (95% CI 82.2-94.6%) in the DMF to DRF group. Fifty-two (4.5%) patients overall and 15 (3.5%) in the DMF switch subgroup discontinued DRF due to GI AEs. Mean PDC was 90.8% (95% CI 89.2-92.5%), and 85.4% (95% CI 83.3-87.4%) of patients achieved PDC ≥ 80% in the overall population. In the DMF to DRF group, mean PDC was 90.7% (95% CI 88.0-93.5%), and 84.8% (95% CI 81.4-88.1%) of patients achieved PDC ≥ 80%. CONCLUSION: In this analysis of  > 1000 patients treated with DRF in real-world clinical practice, overall persistence at 16 months was high, treatment discontinuation due to GI AEs was low, and patients were highly adherent to therapy. Of 433 patients who switched from DMF to DRF, most (> 90%) were able to tolerate and persist on DRF after switching. Graphical abstract available for this article.
 Despite being a common issue in people with multiple sclerosis (pwMS), sexual dysfunction is still underinvestigated. This work aims to assess the potential determinants of sexual dysfunction in pwMS by considering its relationship with disease severity (in terms of global disability), illness perception, and depressive symptoms. In this multicenter study, 1010 pwMS responded to an online survey. A serial mediation model considering negative illness perception and depressive symptoms as mediators of the relationship between disease severity and sexual dysfunction was conducted using the SPSS PROCESS Macro with bias-corrected bootstrapping (5000 samples). Disease severity exerts an indirect effect on sexual dysfunction via illness perception, both independently and through depressive symptoms. However, the results indicated that illness perception plays a more crucial role in sexual dysfunction in pwMS with mild disability than in pwMS with moderate-severe disability. This study suggests that higher disability increases its magnitude by enhancing negative illness perception, that, in turn, affects sexual dysfunction both directly and through depressive symptoms, especially in pwMS with mild disability. Modulating the effect of illness perception by favoring adaptive coping strategies might represent a valid approach to mitigate sexual dysfunction symptoms in MS.
 Multiple sclerosis (MS) is a neurodegenerative disease characterized by neuronal and synaptic loss, resulting in an imbalance of excitatory and inhibitory synaptic transmission and potentially cognitive impairment. Current methods for measuring the excitation/inhibition (E/I) ratio are mostly invasive, but recent research combining neurocomputational modeling with measurements of local field potentials has indicated that the slope with which the power spectrum of neuronal activity captured by electro- and/or magnetoencephalography rolls off, is a non-invasive biomarker of the E/I ratio. A steeper roll-off is associated with a stronger inhibition. This novel method can be applied to assess the E/I ratio in people with multiple sclerosis (pwMS), detect the effect of medication such as benzodiazepines, and explore its utility as a biomarker for cognition. We recruited 44 healthy control subjects and 95 pwMS who underwent resting-state magnetoencephalographic recordings. The 1/f spectral slope of the neural power spectra was calculated for each subject and for each brain region. As expected, the spectral slope was significantly steeper in pwMS treated with benzodiazepines (BZDs) compared to pwMS not receiving BZDs (p = .01). In the sub-cohort of pwMS not treated with BZDs, we observed a steeper slope in cognitively impaired pwMS compared to cognitively preserved pwMS (p = .01) and healthy subjects (p = .02). Furthermore, we observed a significant correlation between 1/f spectral slope and verbal and spatial working memory functioning in the brain regions located in the prefrontal and parietal cortex. In this study, we highlighted the value of the spectral slope in MS by quantifying the effect of benzodiazepines and by putting it forward as a potential biomarker of cognitive deficits in pwMS.
 BACKGROUND: In the United States, health insurance coverage and quality mediate access to health care, a key social determinant of health. OBJECTIVE: To perform a scoping review regarding the impact of insurance coverage and benefit design on health care access and both clinical and quality of life outcomes in people with MS (pwMS). METHODS: Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines were followed. A literature search was conducted from January 2010 to February 2022. Included studies were in English, peer-reviewed, US-based, and evaluated elements of insurance and their relationship with access and quality outcomes for adult pwMS. RESULTS: Our search identified 1619 articles, of which 32 met inclusion criteria. Privately insured pwMS were more likely to be on disease-modifying therapy (DMT). Increased out-of-pocket spending was associated with lower DMT adherence and greater discontinuation rates. Access to specialty pharmacy programs was associated with improved DMT adherence. CONCLUSION: Health insurance coverage and design strongly influences health care for pwMS in the United States and may be a modifiable social determinant of health. Increased pharmaceutical cost-sharing is associated with declines in DMT utilization and adherence. Further study is needed to better characterize the impacts of other core elements of health insurance, including prior authorization requirements and step therapy.
 The symptoms of multiple sclerosis (MS) frequently include fatigue, depression, and neurogenic lower urinary tract symptoms (LUTS), causing severe burdens on affected individuals. The relationships between these symptoms have not been intensively researched and there are no studies on the detailed influence of the different neurogenic LUTS. We aimed to investigate the relationships between fatigue, depression, and neurogenic LUTS as recorded in bladder diaries by persons with MS. We analyzed the bladder diaries of 274 people and their scores on the Fatigue Scale for Motor and Cognitive Functions and the Centre for Epidemiologic Studies Depression Scale (German version). The neurogenic LUTS were defined as urgency, reduced voided volume, increased standardized voiding frequency, nocturia, and urinary incontinence. Those suffering from incontinence, nocturia, reduced voided volume, or urgency had higher fatigue scores compared to those without these symptoms. Those with nocturia showed significantly higher scores for depression. The severity of urgency and voided volume had the greatest effect on the severity of individuals' fatigue and depression levels. With increasing urgency, the risk of clinically significant fatigue and depression was expected to increase. Urgency and voided volume correlated most with fatigue and depression. A prospective longitudinal study investigating fatigue/depression after the successful treatment of neurogenic LUTS is needed to clarify causality and offer possible treatment options for fatigue and depression.
 PURPOSE: The objective was to compare the risk of malignancies in real-world settings between exclusive immunosuppressant (IS) and immunomodulator (IM) use in multiple sclerosis (MS). METHODS: A nested case-control study was designed within a new-user cohort of all patients with MS who initiated a first IM or IS between 2008 and 2014, and without cancer history, using the information of the SNDS nationwide French claims database. Incident cancer cases were matched with up to six controls on year of birth, sex, initiation date, and disease risk score of cancer. A conditional logistic regression (odds ratio [95% confidence interval]) was used to compare exclusive IS versus IM use during follow-up and according to three use durations. RESULTS: From 28 720 newly treated patients with MS, 407 incident cancers were observed during the follow-up with 2324 matched controls. A significant increase in cancer risk was observed for IS compared with IM (1.36 [1.05, 1.77]), with similar increases for the first 2 years of use but not for ≥2 years (1.06 [0.65, 1.75]). Similar increase was also observed for IS with indications other than MS (1.37 [1.04, 1.81]) but not for IS indicated only in MS (1.03 [0.45, 2.34]). CONCLUSIONS: Compared with IM, a 37% increase in cancer risk was observed for IS with indications other than MS and used for a short duration (≤2 years) but not for IS indicated only in MS. The absence of risk for prolonged exposure of IS with indications other than MS is not in favor of a causal relation with these drugs.
 BACKGROUND: The influence of diet quality on multiple sclerosis (MS) progression or inflammatory activity is not well understood. METHODS: Study participants with MS from the AusLong cohort, were followed annually (10 years, n = 223 post-onset). At baseline, 5 and 10-year reviews, indices of dietary quality - the Australian Recommended Food Score (ARFS) and Diet Quality Tracker (DQT) - were calculated from self-reported dietary intake data of the preceding 12 months (Food Frequency Questionnaire, Dietary Questionnaire for Epidemiological Studies v2). Associations were examined between measures of dietary quality with measures of MS progression and inflammatory activity hazard of relapse, annualised disability progression (Expanded Disability Status Scale, EDSS) and Magnetic Resonance Imaging (MRI) outcomes. MRI outcomes included fluid-attenuated inversion recovery (FLAIR, T2 MRI) lesion volume and black hole volume (T1 MRI) in the juxtacortical, periventricular, and infratentorial regions of the brain, as well as total calculated from the sum of the three regions. RESULTS: A higher diet quality (at least with the ARFS) was associated with lower FLAIR lesion volume in the periventricular region only (highest vs lowest quartile: β=-1.89,95%CI=-3.64, -0.13, p = 0.04, periventricular FLAIR region median (IQR) for 5-year review: 4.41 (6.06) and 10-year review: 4.68 (7.27)). Associations with black hole lesion volume, hazard of relapse, and annualised EDSS progression, lacked in significance and/or dose-dependency. CONCLUSION: We found evidence that diet quality may have a role in modulating one aspect of MS inflammatory activity (periventricular MRI FLAIR lesion volume), but not other MRI and clinical outcome measures.
 Multiple sclerosis (MS) is a chronic, autoimmune condition that primarily affects the myelin sheath covering the neurons of the central nervous system, including those of the brain and spinal cord. Although the etiology is not completely understood, various factors, such as genetic infections and environmental background, play a role in the pathogenesis. Repeated active episodes of MS characterized with marked inflammation results in the scarring of particular nerve segments, and eventually results in functional impairment over a period of time. Based on the clinical course of the disease, four clinical types of MS have been identified, with the relapsing-remitting type being the commonest. MS is known to occur more commonly in females in the age group of 20-40 years. Dysarthria, fatigue, muscle spasm, and numbness are the common presenting symptoms of MS. Diagnosis is generally achieved with MRI brain scans, showing demyelination plaques and lumbar puncture. Treatment of MS's acute phase includes high doses of corticosteroids; whereas preventive treatment of MS includes the prescription of immunosuppressive therapy, including biologics. A large group of MS patients present with oral manifestations, including dysphagia, dysarthria, temporomandibular joint (TMJ) disturbances, facial palsy, and chronic periodontal diseases. Other typical oral manifestations seen in MS patients include trigeminal neuralgia, paresthesia, or orofacial pain. Dental treatment and following drug prescription needs to be tailored to each patient, as there is a possibility of drug interactions. This paper presents a comprehensive, updated review of MS, with emphasis on oral manifestations and dental considerations. Additionally, it presents a case of a 40-year-old female diagnosed with MS that was presented to a dental hospital. The report discusses the oral manifestations and dental management.
 INTRODUCTION: Prior research has demonstrated that early treatment with high-efficacy disease-modifying therapies (DMTs), including ocrelizumab (OCR), can reduce relapses and delay disease progression among persons with multiple sclerosis (pwMS) compared with escalation from low-/moderate-efficacy DMTs. However, there is a lack of research examining the impact of early use of OCR on real-world clinical and economic outcomes. This study aimed to evaluate differences in events often associated with a relapse (EOAR) as well as non-DMT healthcare resource use (HCRU) and costs among pwMS who received OCR as a first-line treatment compared with later-line treatment after diagnosis. METHODS: Newly diagnosed adult pwMS were selected from deidentified Optum Market Clarity claims data (study period: January 1, 2015-June 30, 2021). All pwMS were required to have initiated OCR after diagnosis and have 12 months of continuous eligibility prior to diagnosis. The index date was the date of initiation of the first-line DMT after diagnosis. pwMS who initiated OCR as first-line (1L OCR cohort) or a second- or later-line treatment (2L + OCR cohort) were matched 1:1 based on length of continuous eligibility after the first-line DMT and weighted using stabilized inverse probability of treatment. In the follow-up period, differences in outcomes, including annualized EOAR, non-DMT HCRU and costs, were evaluated for pwMS in the 1L vs. 2L + OCR cohorts. RESULTS: The sample included 748 pwMS. During the follow-up period, pwMS in the 1L OCR cohort had a significantly lower annual rate of EOAR compared with pwMS in the 2L + OCR cohort (0.37 vs. 0.56; difference: 0.20 [95% CI 0.08, 0.32]). pwMS in the 1L OCR cohort had a significantly lower probability of any hospitalization within 1 year, fewer non-DMT outpatient visits and lower all-cause and MS-related, non-DMT costs compared with pwMS in the 2L + OCR cohort. CONCLUSIONS: First-line initiation OCR was associated with improvements in clinical and non-DMT economic outcomes compared with later-line initiation of OCR, suggesting that early initiation may benefit both patients and the healthcare system.
 BACKGROUND: Dysarthria is one of the most frequent communication disorders in patients with Multiple Sclerosis (MS), with an estimated prevalence of around 50%. However, it is unclear if there is a relationship between dysarthria and the severity or duration of the disease. OBJECTIVE: Describe the speech pattern in MS, correlate with clinical data, and compare with controls. METHODS: A group of MS patients (n = 73) matched to healthy controls (n = 37) by sex and age. Individuals with neurological and/or systemic conditions that could interfere with speech were excluded. MS group clinical data were obtained through the analysis of medical records. The speech assessment consisted of auditory-perceptual and speech acoustic analysis, from recording the following speech tasks: phonation and breathing (sustained vowel/a/); prosody (sentences with different intonation patterns) and articulation (diadochokinesis; spontaneous speech; diphthong/iu/repeatedly). RESULTS: In MS, 72.6% of the individuals presented mild dysarthria, with alterations in speech subsystems: phonation, breathing, resonance, and articulation. In the acoustic analysis, individuals with MS were significantly worse than the control group (CG) in the variables: standard deviation of the fundamental frequency (p = 0.001) and maximum phonation time (p = 0.041). In diadochokinesis, individuals with MS had a lower number of syllables, duration, and phonation time, but larger pauses per seconds, and in spontaneous speech, a high number of pauses were evidenced as compared to CG. Correlations were found between phonation time in spontaneous speech and the Expanded Disability Status Scale (EDSS) (r = - 0.238, p = 0.043) and phonation ratio in spontaneous speech and EDSS (r = -0.265, p = 0.023), which indicates a correlation between the number of pauses during spontaneous speech and the severity of the disease. CONCLUSION: The speech profile in MS patients was mild dysarthria, with a decline in the phonatory, respiratory, resonant, and articulatory subsystems of speech, respectively, in order of prevalence. The increased number of pauses during speech and lower rates of phonation ratio can reflect the severity of MS.
 BACKGROUND: Pregnancy has been observed to reduce the frequency of relapses in Multiple Sclerosis (MS) patients, but the relapse risk tends to increase during the early post-partum period. Increased pre- and post-partum disease activity may predict a poor long-term prognosis. This study aimed to evaluate the correlation between magnetic resonance imaging (MRI) activity during the year before pregnancy and long-term clinically meaningful worsening in Expanded Disability Status Scale (EDSS). METHODS: This observational, retrospective, case-control study included 141 pregnancies in 99 females with MS. Statistical analyses were used to evaluate the correlation between MRI activity during the year pre-pregnancy and post-partum clinical worsening during a 5-year follow-up. Clustered logistic regression was used to investigate the predictors of 5-year clinically meaningful worsening in EDSS (lt-EDSS). RESULTS: We found a significant correlation between an active MRI pre-pregnancy and lt-EDSS (p = 0.0006). EDSS pre-pregnancy and lt-EDSS were also significantly correlated (p = 0.043). Using a multivariate model, we predicted which females would not experience long-term clinical deterioration by a stable MRI pre-pregnancy (92.7% specificity; p = 0.004). CONCLUSIONS: An active MRI pre-conception is a strong predictor of lt-EDSS and a higher annual relapse rate during the follow-up period, regardless of whether the female had clinical evidence of disease activity prior to conception and delivery. Optimizing disease control and achieving imaging stability prior to conception may reduce the risk of long-term clinical deterioration.
 PURPOSE: Co-design has previously been used to design custom assistive devices, involving the end user in the process to ensure the device meets their needs. From devices previously created, designs could be re-used and modified to meet variations in the needs of other individuals with similar clinical needs. This service evaluation explored the re-usability of a holder for helping administer the spray medication Sativex, for individuals with multiple sclerosis. METHODS: This evaluation was conducted in a UK based Rehabilitation Engineering NHS department. Five individuals who were currently prescribed Sativex trialled the device and provided feedback to further customise the device. Questionnaires evaluated the satisfaction and impact of the devices provided. The resources to provide the devices were calculated. RESULTS: Three of the five individuals who trialled the Sativex spray holder were using long term. Modifications to the shape of the holder were made due to differences in hand strength and dexterity from the initial user. Results indicated high satisfaction with the device and service provided, with improvements in the individuals' competence, adaptability and self-esteem. The mean cost of providing and modifying the device was £78.62. CONCLUSIONS: The previously co-designed Sativex spray holder was used by other individuals, demonstrating how a co-design framework can be used to identify user needs and modifications to previous designs and then implement design changes. The wider use of the device helped off-set the initial costs associated with co-designing devices. Further work is required to explore how other devices could be modified to meet individual needs.IMPLICATIONS FOR REHABILITATIONA previously co-designed assistive device was re-used and modified to accommodate for variation's in the different needs of individual users, for example due to differences in hand strength and dexterity.Through utilising a robust framework to identify user needs, deviations from the original design were identified and implemented. This improved the cost-effectiveness associated with co-designing custom assistive devices, off-setting the initial high cost associated with producing a custom device.There are secondary benefits to initially co-designing devices within healthcare settings beyond the initial user through re-using and modifying devices.
 INTRODUCTION: This study assessed the cost-effectiveness of ozanimod compared with commonly used disease-modifying therapies (DMTs) for relapsing-remitting multiple sclerosis (RRMS). METHODS: Annualized relapse rate (ARR) and safety data were obtained from a network meta-analysis (NMA) of clinical trials of RRMS treatments including ozanimod, fingolimod, dimethyl fumarate, teriflunomide, interferon beta-1a, interferon beta-1b, and glatiramer acetate. ARR-related number needed to treat (NNT) relative to placebo and annual total MS-related healthcare costs was used to estimate the incremental annual cost per relapse avoided with ozanimod vs each DMT. ARR and adverse event (AE) data were combined with drug costs and healthcare costs to manage relapses and AEs in order to estimate annual cost savings with ozanimod vs other DMTs, assuming a 1 million USD fixed treatment budget. RESULTS: Treatment with ozanimod was associated with lower incremental annual healthcare costs to avoid a relapse, ranging from $843,684 vs interferon beta-1a (30 μg; 95% confidence interval [CI] - $1,431,619, - $255,749) to $72,847 (95% CI - $153,444, $7750) vs fingolimod. Compared with all other DMTs, ozanimod was associated with overall healthcare cost savings ranging from $8257 vs interferon beta-1a (30 μg) to $2178 vs fingolimod. Compared with oral DMTs, ozanimod was associated with annual cost savings of $6199 with teriflunomide 7 mg, $4737 with teriflunomide 14 mg, $2178 with fingolimod, and $2793 with dimethyl fumarate. CONCLUSION: Treatment with ozanimod was associated with substantial reductions in annual drug costs and total MS-related healthcare costs to avoid relapses compared with other DMTs. In the fixed-budget analysis, ozanimod demonstrated a favorable cost-effective profile relative to other DMTs.
 INTRODUCTION: S1P(1) receptor modulators (S1P(1)-RM) are oral disease-modifying therapies (DMTs) for multiple sclerosis (MS). Several authorities have raised doubts that S1P(1)-RM are responsible for an increased risk of melanoma in patients with MS. We studied the in vitro effects of S1P(1)-RM on different melanoma cell lines to compare the effect of available S1P(1)-RM on the proliferation of human melanoma cells. METHODS: Four S1P(1)-RM were studied which are currently approved for managing MS, namely fingolimod (Gilenya(®)), siponimod (Mayzent(®)), ozanimod (Zeposia(®)), and ponesimod (Ponvory(®)). We tested these four drugs at different concentrations, including therapeutic doses (0.5, 1.6, 5.5, 18, and 60 µM), on human melanoma cell lines (501Mel cells, 1205LU cells, and M249R cells) to analyze in vitro cell proliferation monitored with the IncuCyte ZOOM live cell microscope (Essen Bioscience). RESULTS: At therapeutic doses, median confluence increased overall for all lineages: + 122% for ozanimod (p < 0.001), + 71% for ponesimod (p < 0.001), + 67% for siponimod (NS), and + 41% for fingolimod (p = 0.094). Ozanimod- and ponesimod-treated cells increased confluency in 501Mel, 1205LU, and M249R cell lines (p < 0.001). CONCLUSION: These data suggest an increased proliferation of various melanoma cell lines with S1P(1)-RM treatments used at therapeutic concentrations for patients with MS and should raise the question of increased dermatologic surveillance.
 BACKGROUND: Intrathecal clonal expansion of antibody-producing plasma cells in multiple sclerosis (MS) perpetuates central nervous system injury and is associated with active demyelination. Immunoglobulin G (IgG) effector functions are modulated by linked N-glycan structures. The aim of the study was to detect potential differences in N-glycosylation of IgG in serum and cerebrospinal fluid (CSF) and total sera proteins between people with MS and those in whom the diagnosis of MS was excluded. Furthermore, we investigated the association with standard laboratory biomarkers of intrathecal inflammation as well as clinical and neuroradiological disease activity. METHODS: This cross-sectional study included patients with suspected demyelinating disease. MS diagnosis was based on the 2017 McDonald criteria and controls were patients with excluded MS diagnosis. N-glycans were compared with Expanded Disability Status Scale (EDSS), magnetic resonance imaging (MRI) markers of disease activity and biomarkers of intrathecal inflammation (cell count, CSF-IgG concentration, percentage of intrathecal IgG, oligoclonal bands (OCB), virus-specific antibody index (MRZH reaction)). RESULTS: Differences between groups were observed only in the CSF-IgG N-glycome. In MS, the presence of bisecting N-acetylglucosamine (Padj=2.63E-05) and monogalactosylation (Padj=1.49E-06) were more abundant and associated with positive OCBs. N-glycans monogalactosylated at the α6 arm FA2[6]G1 (r = 0.56) and FA2[6]BG1 (r = 0.45) correlated with percentage of intrathecal IgG, but not total CSF-IgG. This trait was also more abundant in MRZH positive people with MS who had higher MRI lesion load (P = 0.018) but unrelated to active lesions or EDSS. CONCLUSIONS: More abundant monogalactosylation of intrathecally synthesized IgG is the most prominent trait in MS and is associated with higher MRI lesion load.
 BACKGROUND: Ocrelizumab is a humanized anti-CD20 antibody that has been approved for the treatment of patients with multiple sclerosis (MS). Real-world data in the Middle East is very limited. OBJECTIVES: To describe the effectiveness and safety of ocrelizumab treatment in MS patients in a real clinical setting. METHODS: This is an observational, registry-based study. MS patients who were treated with ocrelizumab and completed at least one-year follow-up post-treatment were included. Baseline clinical and radiological characteristics were collected before ocrelizumab initiation. The relapse rate, disability measures, magnetic resonance image (MRI) activity (new T2 lesions and/or GD+ enhancing T1 lesions), and adverse events (AE) at the last follow-up visits were assessed. RESULTS: Data from 447 patients were analyzed, of which 260 (58.2%) were females. The mean age and mean disease duration were 37.39 ± 11.61 and 9.38 ± 7.57 years respectively. Most of the cohort was of a relapsing form (74.3%; n = 332), whereas active secondary and primary progressive forms represented 15.4% (n = 69) and 10.3% (n = 46) respectively. In the relapsing cohort, Ocrelizumab was prescribed in 162 (48.8%) patients due to highly active disease, and in 99 (29.8%) patients due to disease breakthrough while on prior therapies. In the last follow-up visits, most of the relapsing cohort was relapse-free (95.8% vs. 27.4%; p <0.001), had no evidence of MRI activity (3.6% vs. 67.5%; p <0.001) while EDSS score was stable (1.80+1.22 vs. 1.87+1.16; p < 0.104) when compared to baseline. NEDA-3 was achieved in 302 (91%) of RRMS patients. Confirmed disability progression was 27.5% and 23.9% in SPMS and PPMS respectively. Adverse events were observed in 139 (31.1%); infusion reactions and infections represented the most. CONCLUSION: This study showed that ocrelizumab is an effective and safe treatment for MS patients in a real clinical setting similar to what was observed in clinical trials.
 BACKGROUND: Multiple sclerosis (MS) is a progressively debilitating neurologic disease that poses significant costs to the healthcare system and workforce. OBJECTIVE: To evaluate the impact of MS disease progression on societal costs and quality of life (QoL) using data from the German NeuroTransData (NTD) MS registry. METHODS: Cross-sectional cohort study. The cost cohort included patients with MS disability assessed using Expanded Disability Status Scale (EDSS) in 2019 while the QoL cohort included patients assessed using EDSS and EuroQol-5 Dimension 5-Levels between 2009 and 2019. Direct and indirect medical, and non-medical resource use was quantified and costs derived from public sources. RESULTS: Within the QoL cohort (n = 9821), QoL worsened with increasing EDSS. Within the cost cohort (n = 7286), increasing resource use with increasing EDSS was observed. Societal costs per patient, excluding or including disease-modifying therapies, increased from €5694 or €19,315 at EDSS 0 to 3.5 to €25,419 or €36,499 at EDSS 4 to 6.5, and €52,883 or €58,576 at EDSS 7 to 9.5. In multivariate modeling, each 0.5-step increase in EDSS was significantly associated with increasing costs, and worsening QoL. CONCLUSION: This study confirms the major socioeconomic burden associated with MS disability progression. From a socioeconomic perspective, delaying disability progression may benefit patients and society.
 BACKGROUND: Alpha calcitonin gene-related peptide (aCGRP), neuropeptide Y (NPY), and substance P (SP) are neuropeptides that have emerged recently as potent immunomodulatory factors with potential as novel biomarkers and therapeutic targets in multiple sclerosis (MS). OBJECTIVE: The study aimed to detect serum levels of aCGRP, NPY, and SP in MS patients versus healthy controls and their association with disease activity and severity. METHODS: Serum levels were measured in MS patients and age and sex-matched healthy controls using ELISA. RESULTS: We included 67 MS patients: 61 relapsing-remitting MS (RR-MS) and 6 progressive MS (PR-MS), and 67 healthy controls. Serum NPY level was found to be lower in MS patients than in healthy controls (p<0.001). Serum aCGRP level was higher in PR-MS compared to RR-MS (p=0.007) and healthy controls (p=0.001), and it positively correlated with EDSS (r=0.270, p=0.028). Serum NPY level was significantly higher in RR-MS and PR-MS than in healthy controls (p<0.001 and p=0.001, respectively), and it was lower in patients with mild or moderate/severe disease than in healthy controls (p<0.001). Significant inverse correlations were found between SP level and MS disease duration (r= -0.279, p=0.022) and duration of current DMT (r=-0.315, p=0.042). CONCLUSION: Lower serum levels of NPY were revealed in MS patients compared to healthy controls. Since serum levels of aCGRP are significantly associated with disease activity and severity, it is a potential disease progression marker.



 BACKGROUND: The role of vaccine-mediated inflammation in exacerbating multiple sclerosis (MS) is a matter of debate. OBJECTIVE: In this cross-sectional study, we compared the cerebrospinal fluid (CSF) inflammation associated with MS relapses or anti-COVID-19 mRNA vaccinations in relapsing-remitting multiple sclerosis (RRMS). METHODS: We dosed CSF cytokines in 97 unvaccinated RRMS patients with clinical relapse within the last 100 days. In addition, we enrolled 29 stable RRMS and 24 control patients receiving COVID-19 vaccine within the last 100 days. RESULTS: In RRMS patients, a negative association was found between relapse distance and the CSF concentrations of the pro-inflammatory cytokines interleukin (IL)-2 (beta = -0.265, p = 0.016), IL-6 (beta = -0.284, p = 0.01), and IL-17 (beta = -0.224, p = 0.044). Conversely, vaccine distance positively correlated with a different set of cytokines including IL-12 (beta = 0.576, p = 0.002), IL-13 (beta = 0.432, p = 0.027), and IL-1ra (beta = 0.387, p = 0.05). These associations were significant also considering other clinical characteristics. No significant associations emerged between vaccine distance and CSF molecules in the control group. CONCLUSION: Vaccine for COVID-19 induces a central inflammatory response in RRMS patients that is qualitatively different from that associated with disease relapse.
 Some of the greatest challenges in medicine are the neurodegenerative diseases (NDs), which remain without a cure and mostly progress to death. A companion study employed a toolkit methodology to document 2001 plant species with ethnomedicinal uses for alleviating pathologies relevant to NDs, focusing on its relevance to Alzheimer's disease (AD). This study aimed to find plants with therapeutic bioactivities for a range of NDs. 1339 of the 2001 plant species were found to have a bioactivity from the literature of therapeutic relevance to NDs such as Parkinson's disease, Huntington's disease, AD, motor neurone diseases, multiple sclerosis, prion diseases, Neimann-Pick disease, glaucoma, Friedreich's ataxia and Batten disease. 43 types of bioactivities were found, such as reducing protein misfolding, neuroinflammation, oxidative stress and cell death, and promoting neurogenesis, mitochondrial biogenesis, autophagy, longevity, and anti-microbial activity. Ethno-led plant selection was more effective than random selection of plant species. Our findings indicate that ethnomedicinal plants provide a large resource of ND therapeutic potential. The extensive range of bioactivities validate the usefulness of the toolkit methodology in the mining of this data. We found that a number of the documented plants are able to modulate molecular mechanisms underlying various key ND pathologies, revealing a promising and even profound capacity to halt and reverse the processes of neurodegeneration.
 A central issue in regenerative medicine is understanding the mechanisms that regulate the self-renewal of endogenous stem cells in response to injury and disease. Interferons increase hematopoietic stem cells during infection by activating STAT1, but the mechanisms by which STAT1 regulates intrinsic programs in neural stem cells (NSCs) during neuroinflammation is less known. Here we explored the role of STAT1 on NSC self-renewal. We show that overexpressing Stat1 in NSCs derived from the subventricular zone (SVZ) decreases NSC self-renewal capacity while Stat1 deletion increases NSC self-renewal, neurogenesis, and oligodendrogenesis in isolated NSCs. Importantly, we find upregulation of STAT1 in NSCs in a mouse model of multiple sclerosis (MS) and an increase in pathological T cells expressing IFN-γ rather than interleukin 17 (IL-17) in the cerebrospinal fluid of affected mice. We find IFN-γ is superior to IL-17 in reducing proliferation and precipitating an abnormal NSC phenotype featuring increased STAT1 phosphorylation and Stat1 and p16(ink4a) gene expression. Notably, Stat1(-/-) NSCs were resistant to the effect of IFN-γ. Lastly, we identified a Stat1-dependent gene expression profile associated with an increase in the Sox9 transcription factor, a regulator of self-renewal. Stat1 binds and transcriptionally represses Sox9 in a transcriptional luciferase assay. We conclude that Stat1 serves as an inducible checkpoint for NSC self-renewal that is upregulated during chronic brain inflammation leading to decreased self-renewal. As such, Stat1 may be a potential target to modulate for next generation therapies to prevent progression and loss of repair function in NSCs/neural progenitors in MS.
 In general, individuals who are lesbian, gay, bisexual, transgender, queer or questioning, plus other identities (LGBTQ+) living with multiple sclerosis (MS) have less favorable healthcare experiences and poorer overall health than cisgendered heterosexual individuals. They may experience further challenges in addition to managing their MS, including psychological or emotional problems, and an increased risk of comorbid diseases and substance abuse. Transgender individuals specifically face additional unique challenges, including high rates of mental health distress and effects from long-term exogenous hormone use and gender affirmation surgery. These findings highlight disparities in both quality of care and health outcomes of LGBTQ+ individuals. Unmet needs and drivers of these disparities relate to a lack of inclusivity in healthcare environments, poor communication between healthcare professionals (HCPs) and LGBTQ+ patients, inadequate HCP knowledge of LGBTQ+ health issues, and gaps in research into the impact of sexual orientation and gender identity in MS. Although data are limited, recommendations to improve the experience and care of LGBTQ+ individuals with MS include increasing HCP awareness of the challenges LGBTQ+ individuals face and provision of inclusive care, with the overarching goal for HCPs to be allies to the LGBTQ+ community. Improvements may be achieved through diversity and cultural awareness training of HCPs on sexual orientation and gender identity, and ensuring a friendly, open, and supportive healthcare environment. Use of sensitive and gender-neutral language by HCPs, representation of LGBTQ+ individuals in patient materials, and access to LGBTQ+ MS support groups are also recommended. HCPs should aim to integrate discussion of sexual orientation and gender identity and sexual and mental health into routine assessments and collaborate with other HCPs as needed. By addressing the challenges and unmet needs of LGBTQ+ individuals with MS, this should help resolve disparities in their quality of care and improve their overall health.
 T cell-driven autoimmune responses are subject to striking sex-dependent effects. While the contributions of sex hormones are well-understood, those of sex chromosomes are meeting with increased appreciation. Here, we outline what is known about the contribution of sex chromosome-linked factors to experimental autoimmune encephalomyelitis (EAE), a mouse model that recapitulates many of the T cell-driven mechanisms of multiple sclerosis (MS) pathology. Particular attention is paid to the KDM family of histone demethylases, several of which - KDM5C, KDM5D and KDM6A - are sex chromosome encoded. Finally, we provide evidence that functional inhibition of KDM5 molecules can suppress interferon (IFN)γ production from murine male effector T cells, and that an increased ratio of inflammatory Kdm6a to immunomodulatory Kdm5c transcript is observed in T helper 17 (Th17) cells from women with the autoimmune disorder ankylosing spondylitis (AS). Histone lysine demethlyases thus represent intriguing targets for the treatment of T cell-driven autoimmune disorders.
 The occurrence of B cell aggregates within the central nervous system (CNS) has prompted the investigation of the potential sources of pathogenic B cell and T cell responses in a subgroup of secondary progressive multiple sclerosis (MS) patients. Nevertheless, the expression profile of molecules associated with these aggregates and their role in aggregate development and persistence is poorly described. Here, we focused on the expression pattern of osteopontin (OPN), which is a well-described cytokine, in MS brain tissue. Autopsied brain sections from MS cases with and without B cell pathology were screened for the presence of CD20(+) B cell aggregates and co-expression of OPN. To demonstrate the effect of OPN on B cells, flow cytometry, ELISA and in vitro aggregation assays were conducted using the peripheral blood of healthy volunteers. Although OPN was expressed in MS brain tissue independent of B cell pathology, it was also highly expressed within B cell aggregates. In vitro studies demonstrated that OPN downregulated the co-stimulatory molecules CD80 and CD86 on B cells. OPN-treated B cells produced significantly lower amounts of IL-6. However, OPN-treated B cells also exhibited a higher tendency to form homotypic cell aggregates in vitro. Taken together, our data indicate a conflicting role of OPN in modulating B cell responses.
 BACKGROUND AND PURPOSE: <p>Neuro&shy;fibromatosis type 1 (NF1) is a rare, auto&shy;somal dominant multisystemic disease. The NF1 gene is localized on chromosome 17q11.2. Patients with NF1 have different clinical presentations and comorbidities. The aim of the present study is to determine the novel mutations and neurological comorbidities of NF1.</p>. METHODS: <p>Patients who were diagnosed with NF1 by clinical criteria of the National Institutes of Health were included in the study. After a detailed examination, the NF1 gene was analysed with the help of next generation sequencing technology from pe&shy;ripheral blood samples via MiSeq (Illu&shy;mina, USA). Bioinformatic analyzes were per&shy;for&shy;med to evaluate the clinical sig&shy;ni&shy;fi&shy;cance of the detected variants via the in&shy;ternational databanks in accordance with the ACMG (American College of Medical Ge&shy;netics) guide&shy;line. In addition, cerebral-spinal MRI, cerebral angiography, and ENMG exa&shy;mi&shy;na&shy;tions were performed if deemed necessary.</p>. RESULTS: <p>Twenty patients (12 female, 8 male) were included in the study. The mean age was 25.8&plusmn;10 (10-56) years. Previously defined 13 different pathogenic mutations according to the ACMG criteria were identified in 18 patients. Also, two novel mutations were detected in 2 cases. Moreover, neurological comorbidities (moyamoya disease, multiple sclerosis, Charcot Marie Tooth Type 1A) were found in 3 patients with NF1.</p>. CONCLUSION: <p>In the present study two novel mutations and three different neurological comorbidities were identified in NF1.</p>.
 Multiple Sclerosis (MS) is a chronic autoimmune-mediated demyelinating disease of the central nervous system (CNS) that might be triggered by aberrant epigenetic changes in the genome. DNA methylation is the most studied epigenetic mechanism that participates in MS pathogenesis. However, the overall methylation level in the CNS of MS patients remains elusive. We used direct long-read nanopore DNA sequencing and characterized the differentially methylated genes in the brain from mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. We identified 163 hypomethylated promoters and 327 hypermethylated promoters. These genomic alterations were linked to various biological processes including metabolism, immune responses, neural activities, and mitochondrial dynamics, all of which are vital for EAE development. Our results indicate a great potential of nanopore sequencing in identifying genomic DNA methylation in EAE and provide important guidance for future studies investigating the MS/EAE pathology.
 Reelin was originally identified as a regulator of neuronal migration and synaptic function, but its non-neuronal functions have received far less attention. Reelin participates in organ development and physiological functions in various tissues, but it is also dysregulated in some diseases. In the cardiovascular system, Reelin is abundant in the blood, where it contributes to platelet adhesion and coagulation, as well as vascular adhesion and permeability of leukocytes. It is a pro-inflammatory and pro-thrombotic factor with important implications for autoinflammatory and autoimmune diseases such as multiple sclerosis, Alzheimer's disease, arthritis, atherosclerosis, or cancer. Mechanistically, Reelin is a large secreted glycoprotein that binds to several membrane receptors, including ApoER2, VLDLR, integrins, and ephrins. Reelin signaling depends on the cell type but mostly involves phosphorylation of NF-κB, PI3K, AKT, or JAK/STAT. This review focuses on non-neuronal functions and the therapeutic potential of Reelin, while highlighting secretion, signaling, and functional similarities between cell types.
 BACKGROUND AND PURPOSE: (11) C-Methionine (MET)-PET is a useful tool in neuro-oncology. This study aimed to examine whether a combination of diagnostic variables associated with MET uptake could help distinguish between brain lesions that are often difficult to discriminate in conventional CT and MRI. METHODS: MET-PET was assessed in 129 patients with glioblastoma multiforme, primary central nervous lymphoma, metastatic brain tumor, tumefactive multiple sclerosis, or radiation necrosis. The accuracy of the differential diagnosis was analyzed using five diagnostic characteristics in combination: higher maximum standardized uptake value (SUV) of MET in the lesion/the mean normal cortical SUV of MET ratio, overextension beyond gadolinium, peripheral pattern indicating abundant MET accumulation in the peripheral region, central pattern denoting abundant MET accumulation in the central region, and dynamic-up suggesting increased MET accumulation during dynamic study. The analysis was conducted on sets of two of the five brain lesions. RESULTS: Significant differences in the five diagnostic traits were observed among the five brain lesions, and differential diagnosis could be achieved by combining these diagnostic features. The area under the curve between each set of two of the five brain lesions using MET-PET features ranged from .85 to 1.0. CONCLUSIONS: According to the findings, combining the five diagnostic criteria could help with the differential diagnosis of the five brain lesions. MET-PET is an auxiliary diagnostic technique that could help in distinguishing these five brain lesions.
 Advent of the acute respiratory coronavirus SARS-CoV-2 has resulted in the search for novel antiviral agents and in the repurposing of existing agents with demonstrated efficacy against other known coronaviruses in the search for an agent with antiviral activity for use during the COVID-19 pandemic. Adamantanes including amantadine, rimantadine, and memantine have well-established benefit in the treatment of neurodegenerative diseases including Parkinson's disease (PD), Alzheimer's disease (AD) and fatigue related to Multiple sclerosis (MS) all of which are known comorbidities related to COVID-19 Moreover, results of basic pharmacological studies both in vitro and in vivo reveal that amantadine has the potential to inhibit SARS-CoV-2 via down-regulation of host-cell proteases resulting in impaired viral genome release into the host cell and via amantadine's property as an NMDA receptor antagonist resulting in the prevention of the acute lung injury and respiratory distress that is characteristic of COVID-19. Cases suggestive of COVID-19 prophylaxis have been reported in patients with PD or MS or severe cognitive impairment treated in all cases for several months with an adamantane [amantadine or memantine] who were subsequently infected with SARS-CoV-2 confirmed by RT-PCR, and, in all cases, no signs of infectious disease were encountered. Amantadine is effective for the treatment of fatigue in MS and for the neurological complications of Traumatic Brain Injury (TBI).
 Embelin (EMB) (2,5-Dihydroxy-3-undecyl-1,4-benzoquinone) is a natural benzoquinone extracted mainly from Embelia ribes (ER) and appear as vivid orange dots beneath the fruit's pericarp. It is being used to treat various diseases since ancient times in India. It has been ascribed as one of the 32 ayurvedic drugs of national importance in the National Medicinal Plant Board set up by the Government of India under the Ministry of Indian System of Medicine and Homeopathy. Embelin prevents neuronal oxidative damage by decreasing the peroxidation of lipids. Along with having antioxidant properties, it also prevents the production of amyloid-protein-related fibrils and blocks the progression of inflammatory cascades. Due to embelin's ability to cross the blood-brain barrier, its neuroprotective effects have been studied in the past using in vitro models of neuronal disorders such as convulsion and epilepsy, Alzheimer's disease, anxiety and depression, traumatic brain injury, cerebral ischemia, Huntington's disease, and multiple sclerosis. In addition to its neuroprotective effects, its role as an antitubercular, anti-cancer, antioxidant, astringent, anti-inflammatory, anti-bacterial, contraceptive, carminative, diuretic, and anthelmintic agent has also been studied. With docking studies and recent advancements in formulations of embelin including polyethylene and embelin micelles and embelin noisome preparations, embelin can prove to be a promising compound for its therapeutic actions in a wide range of diseases and disorders. The findings of docking studies suggest the binding ability of embelin to be similar to the standard drug in their respective disorders. In this review and docking analysis, we bring an outline of scientific evidence concerning the neuroprotective actions of embelin, still, further research is required for its prospective as a chief compound in clinical approaches.
 Since 1997, when the first case of autoimmune hyperthyroidism induced by Interferon (IFN)-β1b therapy was described, we know about the risk of thyroid dysfunction related to this treatment, particularly in patients with preexisting thyroid autoimmune disorders (AITD). A 60-year-old female, with a 15-year history of euthyroid autoimmune thyroiditis and a 3-year history of Multiple Sclerosis (MS), was admitted to our department for the evaluation of hyperthyroidism. Twenty months before, she had started specific immunomodulant IFN-β1a therapy (30 μg/week). At the first visit, the patient complained tachycardia, weight loss, blurry vision with swollen eyes and excessive lacrimation; thyroid tests showed hyperthyroidism with positive TSH-receptor-autoantibodies. Further evaluation with orbit Magnetic Resonance Imaging (MRI) revealed bilaterally mild enlargement of the extraocular muscles, supporting the suspect of Graves' ophthalmopathy (GO). To our knowledge, this is the first report of Graves' disease (GD) and ophthalmopathy associated with IFN-β1a treatment in a patient with MS. Furthermore, this case could open new interesting knowledge behind GD immunopathogenesis.
 BACKGROUND: Computerized training in persons with multiple sclerosis (PwMS) seems to enhance working memory (WM)/information processing (IP), but factors associated with the efficacy of the treatment have not been sufficiently explored. Objective: To identify clinical and radiological characteristics associated with positive WM/IP training responses. METHODS: Radiological and neuropsychological assessments were carried out on a sample of 35 PwMs who were divided into "WM/IP-impaired" and "WM/IP-preserved." All participants underwent adaptive n-back training for 10 days and were assessed post-training. Between-group differences ("WM/IP-impaired" vs. "WM/IP-preserved") in training-induced cognitive improvement were assessed and exploratory correlational/ regression-based methods were employed to assess the relationship between cognitive improvement and clinical and radiological variables. RESULTS: All PwMS exhibited WM/IP benefits after training, but those with preserved WM/IP functions showed greater positive effects as well as transfer effects to other WM/IP tests when compared to the impaired group. Additional analyses revealed that positive response to treatment was associated with WM/IP baseline capabilities and greater gray matter volume (GMVOL) in relevant areas such as the thalamus. CONCLUSIONS: Restorative cognitive training is suitable to improve cognition in PwMS but its effective outcome differs depending on the baseline WM/IP capabilities and GMVOL.
 The recruitment of T-cells to tissues and their retention there are essential processes in the pathogenesis of many autoimmune and inflammatory diseases. The mechanisms regulating these processes have become better understood over the past three decades and are now recognised to involve temporally and spatially specific interactions between cell adhesion molecules. These include integrins, which are heterodimeric molecules that mediate in-to-out and out-to-in signalling in T-cells, other leukocytes, and most other cells of the body. Integrin signalling contributes to T-cell circulation through peripheral lymph nodes, immunological synapse stability and function, extravasation at the sites of inflammation, and T-cell retention at these sites. Greater understanding of the contribution of integrin signalling to the role of T-cells in autoimmune and inflammatory diseases has focused much attention on the development of therapeutics that target T-cell integrins. This literature review describes the structure, activation, and function of integrins with respect to T-cells, then discusses the use of integrin-targeting therapeutics in inflammatory bowel disease, multiple sclerosis, and psoriasis. Efficacy and safety data from clinical trials and post-marketing surveillance are presented for currently approved therapeutics, therapeutics that have been withdrawn from the market, and novel therapeutics currently in clinical trials. This literature review will inform the reader on the current means of targeting T-cell integrins in autoimmune and inflammatory diseases, as well as recent developments in the field.
 BACKGROUND: Poor sleep is common in multiple sclerosis (MS) and may impact daily functioning. The extent to which disease-modifying therapies (DMTs) contribute to sleep outcomes is under-examined. OBJECTIVE: To compare the effects of DMTs on sleep outcomes in an Australian cohort of people with MS and investigate associations between DMT use and beliefs about sleep problems and daily functioning (social functioning and activity engagement). METHODS: Sleep outcomes were assessed using the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale. DMT use and functioning were self-reported. RESULTS: Of 1,715 participants, 64% used a DMT. No differences in sleep outcomes were detected between participants who did and did not use DMTs, the type of DMT used (lower vs higher efficacy, interferon-β vs other DMTs), the timing of administration, or adherence to standard administration recommendations. Beliefs that DMT use worsened sleep were associated with poorer sleep quality and perceptions that sleep problems interfered with daily functioning. CONCLUSION: The use of a DMT does not appear to affect self-reported sleep outcomes in people with MS. However, beliefs that DMT use makes sleep worse were associated with poorer sleep quality and increased interference in daily functioning, suggesting a need for education to diminish negative perceptions of DMT use.
 Natalizumab is a well-established disease-modifying therapy used in active multiple sclerosis (MS). The most serious adverse event is progressive multifocal leukoencephalopathy. For safety reasons, hospital implementation is mandatory. The SARS-CoV-2 pandemic has deeply affected hospital practices leading French authorities to temporarily authorize to administer the treatment at home. The safety of natalizumab home administration should be assessed to allow ongoing home infusion. The aim of the study is to describe the procedure and assess the safety in a home infusion natalizumab model. Patients presenting relapsing-remitting MS treated by natalizumab for over two years, non-exposed to John Cunningham Virus (JCV) and living in the Lille area (France) were included from July 2020 to February 2021 to receive natalizumab infusion at home every four weeks for 12 months. Teleconsultation occurrence, infusion occurrence, infusion cancelling, JCV risk management, annual MRI completion were analyzed. The number of teleconsultations allowing infusion was 365 (37 patients included in the analysis), all home infusions were preceded by a teleconsultation. Nine patients did not complete the one-year home infusion follow-up. Two teleconsultations canceled infusions. Two teleconsultations led to a hospital visit to assess a potential relapse. No severe adverse event was reported. All 28 patients who have completed the follow-up benefited from biannual hospital examination and JCV serologies and annual MRI. Our results suggested that the established home natalizumab procedure was safe using the university hospital home-care department. However, the procedure should be evaluated using home-based services outside the university hospital.
 Plexin-B1 is a receptor for the cell surface semaphorin, Sema4D. This signaling system has been implicated in a variety of human diseases, including cancer, multiple sclerosis and osteoporosis. While inhibitors of the Plexin-B1:Sema4D interaction have been previously reported, understanding their mechanism has been hindered by an incomplete structural view of Plexin-B1. In this study, we have raised and characterized a pair of nanobodies that are specific for mouse Plexin-B1 and which inhibit the binding of Sema4D to mouse Plexin-B1 and its biological activity. Structural studies of these nanobodies reveal that they inhibit the binding of Sema4D in an allosteric manner, binding to epitopes not previously reported. In addition, we report the first unbound structure of human Plexin-B1, which reveals that Plexin-B1 undergoes a conformational change on Sema4D binding. These changes mirror those seen upon binding of allosteric peptide modulators, which suggests a new model for understanding Plexin-B1 signaling and provides a potential innovative route for therapeutic modulation of Plexin-B1.
 Epstein-Barr virus (EBV) is an oncogenic virus infecting more than 95% of the world's population. After primary infection-responsible for infectious mononucleosis in young adults-the virus persists lifelong in the infected host, especially in memory B cells. Viral persistence is usually without clinical consequences, although it can lead to EBV-associated cancers such as lymphoma or carcinoma. Recent reports also suggest a link between EBV infection and multiple sclerosis. In the absence of vaccines, research efforts have focused on virological markers applicable in clinical practice for the management of patients with EBV-associated diseases. Nasopharyngeal carcinoma is an EBV-associated malignancy for which serological and molecular markers are widely used in clinical practice. Measuring blood EBV DNA load is additionally, useful for preventing lymphoproliferative disorders in transplant patients, with this marker also being explored in various other EBV-associated lymphomas. New technologies based on next-generation sequencing offer the opportunity to explore other biomarkers such as the EBV DNA methylome, strain diversity, or viral miRNA. Here, we review the clinical utility of different virological markers in EBV-associated diseases. Indeed, evaluating existing or new markers in EBV-associated malignancies or immune-mediated inflammatory diseases triggered by EBV infection continues to be a challenge.
 INTRODUCTION AND IMPORTANCE: Superior mesenteric artery syndrome (SMAS) is a rare but severe condition characterized by acute angulation of the aortomesenteric axis. It can result in compression and obstruction of the third part of the duodenum leading to life-threatening dilation and perforation of the proximal duodenum and stomach. PRESENTATION OF CASE: We report a rare case of a patient with postural abnormality secondary to multiple sclerosis and a borderline but normal aortomesenteric axis who developed SMAS following a paraesophageal hernia repair with Nissen fundoplication complicated by massive gastric dilation and perforation secondary due to a closed-loop-like foregut obstruction. The patient was managed with emergent damage control surgery and washout with delayed duodenojejunostomy for SMAS. CLINICAL DISCUSSION: SMAS with partial obstruction can mimic common complications after Nissen fundoplication such as gas-bloat syndrome. SMAS with complete obstruction is a life-threatening surgical emergency. Postoperative weight loss, large hiatal hernia reduction, gas-bloat syndrome and postural changes in this patient may have contributed to an altered aortomesenteric axis and promoted the development of SMAS. Identifying possible predisposing factors should heighten vigilance and prompt radiological evaluation and surgical management to prevent life-threatening complications. CONCLUSION: SMAS after Nissen fundoplication is a potentially life-threatening complication that presents with non-specific symptoms mimicking common complications like gas-bloat syndrome. A high index of suspicious should prompt early radiological evaluation in patients with predisposing factors.
 PURPOSE: Optic neuritis, defined as inflammation of the optic nerve, is the most common optic neuropathy affecting adults. Various studies in Southeast Asia have shown that the clinical profile of optic neuritis might differ in these regions from that reported in the western literature. Through this study, we evaluate the clinical profile of pediatric optic neuritis (PON) in the Indian population. METHODS: This was a hospital-based prospective observational study. Patients with optic neuritis younger than 16 years who attended the neuro-ophthalmology clinic from May 2016 to April 2017 were included in the study. RESULTS: This study included 54 eyes of 38 patients. The mean age of presentation was 10.6 years. Unilateral disease (58%) was found to be more common, and a slight female preponderance (58%) was noted. The most common feature was visual loss (96.3%). Pupillary light reflex abnormality was seen in most patients. Fundus examination revealed disk edema (77.7%) to be the most common feature. Neuroimaging was performed in 34 patients, and multiple sclerosis was diagnosed in four patients. At 3 months follow-up after treatment, 89% of eyes had best correct visual acuity of 6/9 or better (P < 0.001). CONCLUSION: In our study, we found the clinical profile of PON to be similar to that seen in western studies as well as those done previously in the Indian population, although with a few differences.
 The human brain is populated by perivascular T cells with a tissue-resident memory T (T(RM))-cell phenotype, which in multiple sclerosis (MS) associate with lesions. We investigated the transcriptional and functional profile of freshly isolated T cells from white and gray matter. RNA sequencing of CD8(+) and CD4(+) CD69(+) T cells revealed T(RM)-cell signatures. Notably, gene expression hardly differed between lesional and normal-appearing white matter T cells in MS brains. Genes up-regulated in brain T(RM) cells were MS4A1 (CD20) and SPP1 (osteopontin, OPN). OPN is also abundantly expressed by microglia and has been shown to inhibit T cell activity. In line with their parenchymal localization and the increased presence of OPN in active MS lesions, we noticed a reduced production of inflammatory cytokines IL-2, TNF, and IFNγ by lesion-derived CD8(+) and CD4(+) T cells ex vivo. Our study reports traits of brain T(RM) cells and reveals their tight control in MS lesions.
 Teriflunomide and its prodrug, leflunomide, are disease-modifying medications used to treat relapsing-remitting multiple sclerosis (RRMS) and rheumatoid arthritis (RA), respectively. Peripheral neuropathy is a rare side effect associated with both medications, although the incidence rate and exact pathological mechanism remain unknown. We present a retrospective case series of three patients with RRMS, who developed painful small fiber neuropathy at various timeframes (<6 months, one year, and four years, respectively) while on teriflunomide treatment (14 mg/day); we also engage in a literature review of small and large fiber neuropathy associated with teriflunomide and leflunomide use. All three patients developed small fiber neuropathy following teriflunomide exposure. Laboratory workup was negative for metabolic, infectious, vitamin deficiency-related, and autoimmune etiologies, except for one patient who had chronic metabolic syndromes (impaired glucose, hyperlipidemia) before medication intake. However, the patient developed neuropathy following teriflunomide treatment. Electrophysiological findings were negative for large fiber neuropathy in all three patients with positive skin biopsy, with reduced epidermal nerve fiber density (ENFD) in two of the three patients. Teriflunomide was discontinued in all cases, after which symptoms stabilized. Current literature on leflunomide supports a direct neurotoxic effect or buildup of toxic intermediates from uridine synthesis inhibition. Cessation of teriflunomide use in the described cases resulted in symptom stabilization. Early recognition and treatment may lead to good clinical outcomes in these patients.

 BACKGROUND: In the demyelinating disease multiple sclerosis (MS), chronic-active brain inflammation, remyelination failure and neurodegeneration remain major issues despite immunotherapy. While B cell depletion and blockade/sequestration of T and B cells potently reduces episodic relapses, they act peripherally to allow persistence of chronic-active brain inflammation and progressive neurological dysfunction. N-acetyglucosamine (GlcNAc) is a triple modulator of inflammation, myelination and neurodegeneration. GlcNAc promotes biosynthesis of Asn (N)-linked-glycans, which interact with galectins to co-regulate the clustering/signaling/endocytosis of multiple glycoproteins simultaneously. In mice, GlcNAc crosses the blood brain barrier to raise N-glycan branching, suppress inflammatory demyelination by T and B cells and trigger stem/progenitor cell mediated myelin repair. MS clinical severity, demyelination lesion size and neurodegeneration inversely associate with a marker of endogenous GlcNAc, while in healthy humans, age-associated increases in endogenous GlcNAc promote T cell senescence. OBJECTIVES AND METHODS: An open label dose-escalation mechanistic trial of oral GlcNAc at 6 g (n = 18) and 12 g (n = 16) for 4 weeks was performed in MS patients on glatiramer acetate and not in relapse from March 2016 to December 2019 to assess changes in serum GlcNAc, lymphocyte N-glycosylation and inflammatory markers. Post-hoc analysis examined changes in serum neurofilament light chain (sNfL) as well as neurological disability via the Expanded Disability Status Scale (EDSS). RESULTS: Prior to GlcNAc therapy, high serum levels of the inflammatory cytokines IFNγ, IL-17 and IL-6 associated with reduced baseline levels of a marker of endogenous serum GlcNAc. Oral GlcNAc therapy was safe, raised serum levels and modulated N-glycan branching in lymphocytes. Glatiramer acetate reduces T(H)1, T(H)17 and B cell activity as well as sNfL, yet the addition of oral GlcNAc dose-dependently lowered serum IFNγ, IL-17, IL-6 and NfL. Oral GlcANc also dose-dependently reduced serum levels of the anti-inflammatory cytokine IL-10, which is increased in the brain of MS patients. 30% of treated patients displayed confirmed improvement in neurological disability, with an average EDSS score decrease of 0.52 points. CONCLUSIONS: Oral GlcNAc inhibits inflammation and neurodegeneration markers in MS patients despite concurrent immunomodulation by glatiramer acetate. Blinded studies are required to investigate GlcNAc's potential to control residual brain inflammation, myelin repair and neurodegeneration in MS.
 Optic neuritis (ON) is the most common cause of subacute optic neuropathy in young adults. Although most cases of optic neuritis (ON) are classified as typical, meaning idiopathic or associated with multiple sclerosis, there is a growing understanding of atypical forms of optic neuritis such as antibody mediated aquaporin-4 (AQP4)-IgG neuromyelitis optica spectrum disorder (NMOSD) and the recently described entity, myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD). Differentiating typical ON from atypical ON is important because they have different prognoses and treatments. Findings of atypical ON, including severe vision loss with poor recovery with steroids or steroid dependence, prominent optic disc edema, bilateral vision loss, and childhood or late adult onset, should prompt serologic testing for AQP4-IgG and MOG-IgG. Although the traditional division of typical and atypical ON can be helpful, it should be noted that there can be severe presentations of otherwise typical ON and mild presentations of atypical ON that blur these traditional lines. Rare causes of autoimmune optic neuropathies, such as glial fibrillary acidic protein (GFAP) and collapsin response-mediator protein 5 (CRMP5) autoimmunity also should be considered in patients with bilateral painless optic neuropathy associated with optic disc edema, especially if there are other accompanying suggestive neurologic symptoms/signs. Typical ON usually recovers well without treatment, though recovery may be expedited by steroids. Atypical ON is usually treated with intravenous steroids, and some forms, such as NMOSD, often require plasma exchange for acute attacks and long-term immunosuppressive therapy to prevent relapses. Since treatment is tailored to the cause of the ON, elucidating the etiology of the ON is of the utmost importance.
 Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) that causes progressive neurological disability in most patients due to neurodegeneration. Activated immune cells infiltrate the CNS, triggering an inflammatory cascade that leads to demyelination and axonal injury. Non-inflammatory mechanisms are also involved in axonal degeneration, although they are not fully elucidated yet. Current therapies focus on immunosuppression; however, no therapies to promote regeneration, myelin repair, or maintenance are currently available. Two different negative regulators of myelination have been proposed as promising targets to induce remyelination and regeneration, namely the Nogo-A and LINGO-1 proteins. Although Nogo-A was first discovered as a potent neurite outgrowth inhibitor in the CNS, it has emerged as a multifunctional protein. It is involved in numerous developmental processes and is necessary for shaping and later maintaining CNS structure and functionality. However, the growth-restricting properties of Nogo-A have negative effects on CNS injury or disease. LINGO-1 is also an inhibitor of neurite outgrowth, axonal regeneration, oligodendrocyte differentiation, and myelin production. Inhibiting the actions of Nogo-A or LINGO-1 promotes remyelination both in vitro and in vivo, while Nogo-A or LINGO-1 antagonists have been suggested as promising therapeutic approaches for demyelinating diseases. In this review, we focus on these two negative regulators of myelination while also providing an overview of the available data on the effects of Nogo-A and LINGO-1 inhibition on oligodendrocyte differentiation and remyelination.
 Adipose tissue-derived mesenchymal stem cells (ASCs) are adult stem cells, endowed with self-renewal, multipotent capacities, and immunomodulatory properties, as mesenchymal stem cells (MSCs) from other origins. However, in a pathological context, ASCs like MSCs can exhibit pro-inflammatory properties and attract inflammatory immune cells at their neighborhood. Subsequently, this creates an inflammatory microenvironment leading to ASCs' or MSCs' dysfunctions. One such example is given by obesity where adipogenesis is impaired and insulin resistance is initiated. These opposite properties have led to the classification of MSCs into two categories defined as pro-inflammatory ASC1 or anti-inflammatory ASC2, in which plasticity depends on the micro-environmental stimuli. The aim of this review is to (i) highlight the pathogenic role of ASCs during obesity and obesity-related inflammatory diseases, such as rheumatoid arthritis, multiple sclerosis, psoriasis, inflammatory bowel disease, and cancer; and (ii) describe some of the mechanisms leading to ASCs dysfunctions. Thus, the role of soluble factors, adhesion molecules; TLRs, Th17, and Th22 cells; γδ T cells; and immune checkpoint overexpression will be addressed.
 OBJECTIVE: To examine the efficacy of Speed of Processing Training (SOPT) in improving everyday functional outcomes in persons with multiple sclerosis (MS). DESIGN: Randomized controlled trial. SETTING: A nonprofit rehabilitation research institution and the community. PARTICIPANTS: In total, 60 participants with MS with impaired processing speed were randomly assigned to SOPT (n=33) or an active control group (n=27). INTERVENTION: SOPT, a restorative computerized cognitive intervention involving 10 treatment sessions consisting of visual tasks designed to improve speed and accuracy of information processing MAIN OUTCOME MEASURES: Outcomes included performance on the Timed Instrumental Activities of Daily Living (TIADL) and self-report of functional behavior, quality of life, and affect. RESULTS: The treatment group showed improvement in the total TIADL score and 2 subtests compared with the active control group. Participants in the treatment group who demonstrated improved cognitive performance after the intervention also showed improved performance on one TIADL subtest. Quality of life, affective symptomatology, and self-reported functional status were not changed after the intervention. CONCLUSIONS: Improvement in underlying cognitive or perceptual deficits is thought to promote recovery and everyday performance as per the restorative approach to cognitive rehabilitation. However, this study showed only selected improvements in everyday functional outcomes for persons with MS.
 BACKGROUND: Promotion of myelin repair in the context of demyelinating diseases such as multiple sclerosis (MS) still represents a clinical unmet need, given that this disease is not only characterized by autoimmune activities but also by impaired regeneration processes. Hence, this relates to replacement of lost oligodendrocytes and myelin sheaths-the primary targets of autoimmune attacks. Endogenous remyelination is mainly mediated via activation and differentiation of resident oligodendroglial precursor cells (OPCs), whereas its efficiency remains limited and declines with disease progression and aging. Teriflunomide has been approved as a first-line treatment for relapsing remitting MS. Beyond its role in acting via inhibition of de novo pyrimidine synthesis leading to a cytostatic effect on proliferating lymphocyte subsets, this study aims to uncover its potential to foster myelin repair. METHODS: Within the cuprizone mediated de-/remyelination model teriflunomide dependent effects on oligodendroglial homeostasis and maturation, related to cellular processes important for myelin repair were analyzed in vivo. Teriflunomide administration was performed either as pulse or continuously and markers specific for oligodendroglial maturation and mitochondrial integrity were examined by means of gene expression and immunohistochemical analyses. In addition, axon myelination was determined using electron microscopy. RESULTS: Both pulse and constant teriflunomide treatment efficiently boosted myelin repair activities in this model, leading to accelerated generation of oligodendrocytes and restoration of myelin sheaths. Moreover, teriflunomide restored mitochondrial integrity within oligodendroglial cells. CONCLUSIONS: The link between de novo pyrimidine synthesis inhibition, oligodendroglial rescue, and maintenance of mitochondrial homeostasis appears as a key for successful myelin repair and hence for protection of axons from degeneration.
 There is clearly an unmet need for more effective and safer treatments for multiple sclerosis (MS). Our previous studies showed a significant therapeutic effect of matrine, a monomer of traditional herbal medicine, on experimental autoimmune encephalomyelitis (EAE) mice. To explore the mechanism of matrine action, we used 16S rRNA sequencing technology to determine the gut microbes in matrine-treated EAE mice and controls. The concentrations of short-chain fatty acids (SCFAs) were then tested by metabonomics. Finally, we established pseudo-sterile mice and transplanted into them fecal microbiota, which had been obtained from the high-dose matrine-treated EAE mice to test the effects of matrine. The results showed that matrine could restore the diversity of gut microbiota and promote the production of SCFAs in EAE mice. Transplantation of fecal microbiota from matrine-treated mice significantly alleviated EAE severity, reduced CNS inflammatory infiltration and demyelination, and decreased the level of IL-17 but increased IL-10 in sera of mice. In conclusion, matrine treatment can regulate gut microbiota and metabolites and halt the progression of MS.
 BACKGROUND: Exercise and self-awareness are popular in the management of people with MS (pwMS). The combination of these techniques for diminishing mental and cognitive imparements doesn't apply. Since the capacity to monitor one's mind and maintain balance and efficient mobility is fundamental for carrying out the daily affairs of pwMS, in this study we assess the effect of Pilates Suspension with Self-awareness on Gait and Metacognition of pwMS. We also evaluate whether metacognition is trainable and, if so, which component of self-awareness (mental and physical) would be instrumental in this improvement. METHOD: Twenty-four female PwMS who scored 2-6.5 on the EDSS were homogeneously divided into two intervention groups [one received pilates suspension training (PST) with Benson relaxation (PSBR), and the other received PST with Jacobson's progressive muscle relaxation (PSJR)] and one control group for 7 consecutive weeks. Relaxation training was used as a means to self-awareness. Due to the coronavirus pandemic around the world during the research process, baseline and postintervention tests and training sessions were held online. Dynamic Gait Index (DGI) and Metacognition Questionnaire-30 (MCQ-30), outcome measures were collected before and after the intervention. RESULTS: Analysis of group data revealed significant improvement between baseline and intervention phases for Dynamic Gate Index (p = 0.002 for Benson relaxation and p = 0.001 for Jacobson's progressive muscle) and Metacognition Questionnaire-30 (p = 0.02 for Benson relaxation and p = 0.002 for Jacobson's progressive muscle). CONCLUSIONS: With regard to multidimensional disorders of pwMS, a combined training protocol is recommended for pwMS.
 PURPOSE: To analyse the clinical characteristics of adult patients with pars planitis (PP-IU), non-pars planitis (NPP-IU) and multiple sclerosis-associated intermediate uveitis (MS-IU) and distinguish between groups. METHODS: Seventy-three adult patients with intermediate uveitis (IU) reviewed retrospectively and divided as PP-IU, NPP-IU and MS-IU according to 'The standardization of uveitis nomenclature working group classification criteria.' Demographic and clinical characteristics, OCT and fluorescein angiography (FA) findings, complications and treatments were recorded. RESULTS: A total of 134 eyes of 73 patients were included, and 42 of the patients were classified as PP-IU, 12 as NPP-IU, and 19 as MS-IU. If a patient presenting with blurred vision, or tent-shaped vitreous band/snowballs/snowbank on examination, or vascular leakage on FA and accompanying neurological symptoms, the frequency of demyelinating plaque detection on cranial MRI and the risk of MS-IU increased. Mean BCVA was increased from 0.22 ± 0.30 logMAR to 0.19 ± 0.31 logMAR (p = 0.021). Gender, initial BCVA, snowbank formation, disc oedema and periphlebitis on examination, and disc leakage/occlusion on FA were found predictive of decreased BCVA at final visit (p < 0.05). CONCLUSIONS: The clinical features of these three groups are similar, some features that can guide the differential diagnosis. It may be recommended to periodically evaluate "suspicious" patients with MRI for MS.
 INTRODUCTION: Siponimod, a potent and selective sphingosine-1-phosphate (S1P(1,5)) agonist, is the only therapeutic agent that has shown efficacy against disability progression, decline in cognitive processing speed, total brain volume loss, gray matter atrophy and signs of demyelination in patients with secondary progressive multiple sclerosis (SPMS). Although the pathophysiology of progression in SPMS and primary progressive MS (PPMS) is thought to be similar, fingolimod, the prototype S1P(1,3,45) agonist, failed to show efficacy against disability progression in PPMS. Differentiating siponimod from fingolimod at the level of their central effects is believed to be the key to a better understanding of the underlying characteristics that could make siponimod uniquely efficacious in progressive MS (PMS). METHODS: Here, we compared the central vs. peripheral dose-dependent drug exposures for siponimod and fingolimod in healthy mice and mice with experimental autoimmune encephalomyelitis (EAE). RESULTS: Siponimod treatment achieved dose-dependent efficacy and dose-proportional increases in steady-state drug blood levels, with a central nervous system (CNS)/blood drug-exposure ratio ((CNS/blood)DER) of ~ 6 in both healthy and EAE mice. In contrast, fingolimod treatments achieved dose-proportional increases in fingolimod and fingolimod-phosphate blood levels, with respective (CNS/blood)DER that were markedly increased (≥ threefold) in EAE vs. healthy mice. CONCLUSION: If proven to have translational value, these observations would suggest that (CNS/blood)DER may be a key differentiator for siponimod over fingolimod for clinical efficacy in PMS.
 Neurological disorders are recognized as major causes of death and disability worldwide. Because of this, they represent one of the largest public health challenges. With awareness of the massive burden associated with these disorders, came the recognition that treatment options were disproportionately scarce and, oftentimes, ineffective. To address these problems, modern research is increasingly looking into novel, more effective methods to treat neurological patients; one of which is cell-based therapies. In this review, we present a critical analysis of the features, challenges, and prospects of one of the stem cell types that can be employed to treat numerous neurological disorders-mesenchymal stem cells (MSCs). Despite the fact that several studies have already established the safety of MSC-based treatment approaches, there are still some reservations within the field regarding their immunocompatibility, heterogeneity, stemness stability, and a range of adverse effects-one of which is their tumor-promoting ability. We additionally examine MSCs' mechanisms of action with respect to in vitro and in vivo research as well as detail the findings of past and ongoing clinical trials for Parkinson's and Alzheimer's disease, ischemic stroke, glioblastoma multiforme, and multiple sclerosis. Finally, this review discusses prospects for MSC-based therapeutics in the form of biomaterials, as well as the use of electromagnetic fields to enhance MSCs' proliferation and differentiation into neuronal cells.
 BACKGROUND: Neurological diseases such as Alzheimer's disease and Parkinson's disease (AD, PD), acute ischemic stroke (AIS), and multiple sclerosis (MS) are thought to be deeply affected by changes in the pathophysiological processes of neurons. As new peptides, it was aimed to evaluate the level of adropin and MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) and its possible relationship with NSE (neuron-specific enolase) and NF-L (neurofilament light chain) in terms of neuronal interaction. METHODS: This study was conducted with 32 patients from each subgroup and group-appropriate controls. Disease identifiers and hemogram/biochemical parameters specific to the groups of participants were obtained. Additionally, plasma adropin, MOTS-c, NSE, and NF-L levels were evaluated by the ELISA method. RESULTS: Plasma adropin levels were decreased in the AD group and decreased in MOTS-c, AIS, and AD groups compared to the control (p < 0.05). Similar values were found in the MS group compared to its control (p > 0.05). In correlation analysis of these markers with laboratory parameters, while platelet and cholesterol levels were negatively correlated with adropin levels; platelet, lymphocyte, and triglyceride levels were positively correlated with MOTS-c (p < 0.05). CONCLUSION: This study provides new information about adropin may be potentially important markers in AD and MOTS-C in AIS and AD. Future studies are needed to examine the relationship between changes in metabolic profiles and these peptides.
 BACKGROUND: In relapsing-remitting multiple sclerosis (RRMS), cortical grey matter pathology relevantly contributes to long-term disability. Still, diffuse cortical inflammation cannot be detected with conventional MRI. OBJECTIVE: We aimed to assess microstructural damage of cortical grey matter over time and the relation to clinical disability as well as relapse activity in patients with RRMS using multiparametric quantitative (q)MRI techniques. METHODS: On 40 patients with RRMS and 33 age-matched and sex-matched healthy controls, quantitative T1, T2, T2* and proton density (PD) mapping was performed at baseline and follow-up after 2 years. Cortical qMRI parameter values were extracted with the FreeSurfer software using a surface-based approach. QMRI parameters, cortical thickness and white matter lesion (WML) load, as well as Expanded Disability Status Scale (EDSS) and relapse rate, were compared between time points. RESULTS: Over 2 years, significant increases of T1 (p≤0.001), PD (p≤0.001) and T2 (p=0.005) values were found in the patient, but not in the control group. At decreased relapse rate over time (p=0.001), cortical thickness, WML volume and EDSS remained unchanged. CONCLUSION: Despite clinical stability, cortical T1, T2 and PD values increased over time, indicating progressive demyelination and increasing water content. These parameters represent promising surrogate parameters of diffuse cortical inflammation in RRMS.
 The lack of interpretability of deep learning reduces understanding of what happens when a network does not work as expected and hinders its use in critical fields like medicine, which require transparency of decisions. For example, a healthy vs pathological classification model should rely on radiological signs and not on some training dataset biases. Several post-hoc models have been proposed to explain the decision of a trained network. However, they are very seldom used to enforce interpretability during training and none in accordance with the classification. In this paper, we propose a new weakly supervised method for both interpretable healthy vs pathological classification and anomaly detection. A new loss function is added to a standard classification model to constrain each voxel of healthy images to drive the network decision towards the healthy class according to gradient-based attributions. This constraint reveals pathological structures for patient images, allowing their unsupervised segmentation. Moreover, we advocate both theoretically and experimentally, that constrained training with the simple Gradient attribution is similar to constraints with the heavier Expected Gradient, consequently reducing the computational cost. We also propose a combination of attributions during the constrained training making the model robust to the attribution choice at inference. Our proposition was evaluated on two brain pathologies: tumors and multiple sclerosis. This new constraint provides a more relevant classification, with a more pathology-driven decision. For anomaly detection, the proposed method outperforms state-of-the-art especially on difficult multiple sclerosis lesions segmentation task with a 15 points Dice improvement.
 Since its first description over a century ago, neurodegenerative diseases (NDDs) have impaired the lives of millions of people worldwide. As one of the major threats to human health, NDDs are characterized by progressive loss of neuronal structure and function, leading to the impaired function of the CNS. While the precise mechanisms underlying the emergence of NDDs remains elusive, association of neuroinflammation with the emergence of NDDs has been suggested. The immune system is tightly controlled to maintain homeostatic milieu and failure in doing so has been shown catastrophic. Here, we review current concepts on the cellular and molecular drivers responsible in the induction of neuroinflammation and how such event further promotes neuronal damage leading to neurodegeneration. Experimental data generated from cell culture and animal studies, gross and molecular pathologies of human CNS samples, and genome-wide association study are discussed to provide deeper insights into the mechanistic details of neuroinflammation and its roles in the emergence of NDDs.

 Autoimmune diseases develop due to self-tolerance failure in recognizing self and non-self-antigens. Several factors play a role in inducing autoimmunity, including genetic and environmental elements. Several studies demonstrated the causative role of viruses; however, some studies showed the preventive effect of viruses in the development of autoimmunity. Neurological autoimmune diseases are classified based on the targets of autoantibodies, which target intracellular or extracellular antigens rather than neurons. Several theories have been hypothesized to explain the role of viruses in the pathogenesis of neuroinflammation and autoimmune diseases. This study reviewed the current data on the immunopathogenesis of viruses in autoimmunity of the nervous system.
 Digital Twin (DT) is a novel concept that may bring a paradigm shift for precision medicine. In this study we demonstrate a DT application for estimating the age of onset of disease-specific brain atrophy in individuals with multiple sclerosis (MS) using brain MRI. We first augmented longitudinal data from a well-fitted spline model derived from a large cross-sectional normal aging data. Then we compared different mixed spline models through both simulated and real-life data and identified the mixed spline model with the best fit. Using the appropriate covariate structure selected from 52 different candidate structures, we augmented the thalamic atrophy trajectory over the lifespan for each individual MS patient and a corresponding hypothetical twin with normal aging. Theoretically, the age at which the brain atrophy trajectory of an MS patient deviates from the trajectory of their hypothetical healthy twin can be considered as the onset of progressive brain tissue loss. With a 10-fold cross validation procedure through 1000 bootstrapping samples, we found the onset age of progressive brain tissue loss was, on average, 5-6 years prior to clinical symptom onset. Our novel approach also discovered two clear patterns of patient clusters: earlier onset vs. simultaneous onset of brain atrophy.
 Myeloid-derived suppressor cells (MDSCs), a heterogeneous cell population that consists of mostly immature myeloid cells, are immunoregulatory cells mainly characterized by their suppressive functions. Emerging findings have revealed the involvement of MDSCs in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). MS is an autoimmune and degenerative disease of the central nervous system characterized by demyelination, axon loss, and inflammation. Studies have reported accumulation of MDSCs in inflamed tissues and lymphoid organs of MS patients and EAE mice, and these cells display dual functions in EAE. However, the contribution of MDSCs to MS/EAE pathogenesis remains unclear. This review aims to summarize our current understanding of MDSC subsets and their possible roles in MS/EAE pathogenesis. We also discuss the potential utility and associated obstacles in employing MDSCs as biomarkers and cell-based therapies for MS.

 We describe the case of a 48-year-old woman presenting with a two-year history of progressive left hemibody-weakness associated with frequent falls, speech difficulties and cognitive dysfunction. Her clinical examination was noticeable for subcortical frontal-predominant cognitive impairment, asymmetrical spastic paraparesis, pseudobulbar findings and delayed horizontal saccade initiation with head-trust phenomenon. Apart from brain atrophy in excess for her age group, the patient's initial cranial-spinal MRI appearances were unremarkable.

 BACKGROUND: Social support is a protective factor against cognitive decline in the general population. However, the relationship between social support and cognitive functioning among persons with multiple sclerosis (MS) is not well understood. OBJECTIVE: The present study aimed to investigate the associations between different aspects of social support and cognitive performance among persons with MS. METHODS: A volunteer sample of 60 persons with MS completed the Medical Outcomes Study Support Social Survey 5-item short form (MSSS-5) and the Social Network Index (SNI). Cognitive functioning was assessed through a virtually-administered neuropsychological battery. Multiple linear regressions were conducted to examine the associations between social support measures and cognitive performance. RESULTS: In models adjusting for level of premorbid functioning, both perceived social support (i.e., to what extent one receives assistance from their social network; p = .002) and total size of social network (i.e., total number of people one regularly talks to; p = .002) were significant predictors of processing speed/executive functioning with moderate effect sizes. However, when we accounted for employment status in a post hoc analysis, the association between social network size and processing speed/executive functioning became statistically insignificant, while the relationship between perceived social support and processing speed/executive functioning remained significant (p = .002). CONCLUSIONS: Greater perceived social support is associated with better performance on processing speed/executive functioning measures among persons with MS, independent of effects from premorbid functioning and employment status. Maintaining a strong social support network may be an important factor in optimizing cognitive health in MS.

 Immune tolerance deletes or suppresses autoreactive lymphocytes and is established at multiple levels during the development, activation and effector phases of T and B cells. These mechanisms are cell-intrinsically programmed and critical in preventing autoimmune diseases. We have witnessed the existence of another type of immune tolerance mechanism that is shaped by lifestyle choices, such as diet, microbiome and microbial metabolites. Short-chain fatty acids (SCFAs) are the most abundant microbial metabolites in the colonic lumen and are mainly produced by the microbial fermentation of prebiotics, such as dietary fiber. This review focuses on the preventive and immunomodulatory effects of SCFAs on autoimmunity. The tissue- and disease-specific effects of dietary fiber, SCFAs and SCFA-producing microbes on major types of autoimmune diseases, including type I diabetes, multiple sclerosis, rheumatoid arthritis and lupus, are discussed. Additionally, their key regulatory mechanisms for lymphocyte development, tissue barrier function, host metabolism, immunity, autoantibody production, and inflammatory effector and regulatory lymphocytes are discussed. The shared and differential effects of SCFAs on different types and stages of autoimmune diseases are discussed.
 OBJECTIVE: To examine the extent to which three sociobehavioral proxies of cognitive reserve-years of education, education quality, and cognitive enrichment-differ in their prediction of cognitive performance among Black and White people with MS (PwMS). METHODS: 82 PwMS (Black n = 41, White n = 41) underwent a neurological examination and a neuropsychological evaluation that included tests of word recognition (Wechsler Test of Adult Reading) as well as measures of verbal memory, visuospatial memory, and processing speed (the Brief International Cognitive Assessment for MS; BICAMS). Participants rated their lifetime engagement in various cognitively-enriching activities (Cognitive Reserve Scale). RESULTS: For the full sample, education quality and cognitive enrichment were more strongly associated with cognitive performance than were years of education. Cognitive enrichment was not associated with cognitive performance among participants with high education quality. In contrast, among participants with low education quality, cognitive enrichment was strongly associated with cognitive performance, suggesting that high engagement in cognitively-enriching activities provided similar protection to high education quality. Furthermore, among Black participants, cognitive enrichment and educational quality moderated the relationship between disability level and cognitive performance. In contrast, among White participants, cognitive enrichment did not provide additional protection beyond the buffering effect of education quality. CONCLUSIONS: PwMS can successfully build reserve through multiple routes, including formal education or informal cognitive enrichment. Treatment for MS should incorporate cognitively-enriching activities to build resilience against cognitive decline, particularly for members of marginalized racial/ethnic groups, who are at greatest risk for poor health outcomes, and for whom years of education may not best reflect education quality.
 BACKGROUND: Fatigue is a disabling symptom of multiple sclerosis. Its biological causes are still poorly understood. Several years ago, we proposed that fatigue might be the subjective representation of inflammatory processes. An important step for a straight-forward evaluation of our model would be to show that the level of fatigue is associated with vagal activation. The heart rate is under partial control of the vagus nerve. Using power spectrum analysis allows to separate, at least partly, sympathetic and parasympathetic impact on heart rate variability. METHODS: This narrative review summarizes the evidence for heart rate variability changes in MS patients, their relationship with fatigue and disease course. To do this, we conducted a literature search, including 45 articles relevant to the topic treated in this review. RESULTS: We illustrate that (1) inflammation leads to a change in cardiac behavior during acute and chronic phases, both in animals and in humans; (2) MS patients show changes of heart rate variability (HRV) that resemble those during acute and chronic inflammation due to multiple causes; (3) existing evidence favors a set of specific predictions about fatigue and parallel HRV changes; and (4) that MS-related brainstem lesions or neurological impairments do not completely explain HRV changes, leaving enough place for an explanatory relation between HRV and fatigue. DISCUSSION: We discuss the results of this review in relation to our model of fatigue and propose several observational and experimental studies that could be conducted to gain a better insight into whether fatigue and HRV can be interpreted as a common pathway, both reflecting activated autoimmune processes in MS patients.

 Baclofen is used to treat muscle spasticity; it is FDA-approved for managing reversible spasticity, particularly for the relief of flexor spasms, clonus, and concomitant pain, common sequelae of spinal cord lesions, and multiple sclerosis. Baclofen also has several off-label uses. This activity outlines the indications, mechanism of action, safe administration, adverse effects, contraindications, toxicology, and monitoring of the broad array of physiological possibilities when using baclofen in the clinical setting.

 Autoimmune neuroinflammatory diseases are a group of disorders resulting from abnormal immune responses in the nervous system, causing inflammation and tissue damage. The interleukin (IL) family of cytokines, especially IL-1, IL-6, and IL-17, plays a critical role in the pathogenesis of these diseases. IL-1 is involved in the activation of immune cells, production of pro-inflammatory cytokines, and promotion of blood-brain barrier breakdown. IL-6 is essential for the differentiation of T cells into Th17 cells and has been implicated in the initiation and progression of neuroinflammation. IL-17 is a potent pro-inflammatory cytokine produced by Th17 cells that plays a crucial role in recruiting immune cells to sites of inflammation. This review summarizes the current understanding of the roles of different interleukins in autoimmune neuroinflammatory diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, neuromyelitis optica, and autoimmune encephalitis, and discusses the potential of targeting ILs as a therapeutic strategy against these diseases. We also highlight the need for further research to better understand the roles of ILs in autoimmune neuroinflammatory diseases and to identify new targets for treating these debilitating diseases.
 BACKGROUND: Neurodegeneration in multiple sclerosis (MS) affects the visual system but dynamics and pathomechanisms over several years especially in primary progressive MS (PPMS) are not fully understood. METHODS: We assessed longitudinal changes in visual function, retinal neurodegeneration using optical coherence tomography, MRI and serum NfL (sNfL) levels in a prospective PPMS cohort and matched healthy controls. We investigated the changes over time, correlations between outcomes and with loss of visual function. RESULTS: We followed 81 patients with PPMS (mean disease duration 5.9 years) over 2.7 years on average. Retinal nerve fibre layer thickness (RNFL) was reduced in comparison with controls (90.1 vs 97.8 µm; p<0.001). Visual function quantified by the area under the log contrast sensitivity function (AULCSF) remained stable over a continuous loss of RNFL (0.46 µm/year, 95% CI 0.10 to 0.82; p=0.015) up until a mean turning point of 91 µm from which the AULCSF deteriorated. Intereye RNFL asymmetry above 6 µm, suggestive of subclinical optic neuritis, occurred in 15 patients and was related to lower AULCSF but occurred also in 5 out of 44 controls. Patients with an AULCSF progression had a faster increase in Expanded Disability Status Scale (beta=0.17/year, p=0.043). sNfL levels were elevated in patients (12.2 pg/mL vs 8.0 pg/mL, p<0.001), but remained stable during follow-up (beta=-0.14 pg/mL/year, p=0.291) and were not associated with other outcomes. CONCLUSION: Whereas neurodegeneration in the anterior visual system is already present at onset, visual function is not impaired until a certain turning point. sNfL is not correlated with structural or functional impairment in the visual system.
 INTRODUCTION: Chronic disorders commonly require long-term therapies. Medication non-adherence can cause major morbidity and mortality in chronic illness individuals, as well as increase the financial burden on the healthcare system. It is considered that patients who adhere to their treatment may improve their quality of life (QoL). There is a scarcity of updated comprehensive data on medication adherence among Saudi patients with neurological disorders. Therefore, this study aimed to assess the medication adherence status among individuals with neurological conditions and its association with QoL. METHOD: A cross-sectional questionnaire-based study was conducted. The study included subjects individuals who have neurological conditions aged at least 18 from different regions of Saudi Arabia. The questionnaire measured medication adherence by using the 10-item version of the Medication Adherence Report Scale (MARS-10, ©Professor Rob Horne). The QoL was measured by employing validated Euro Quality of Life 5-dimension scale (EQ-5D). RESULTS: A total of 370 participants were included. Respondents aged 18 to 35 years represented 62.4% of the sample. More than half of the participants were females (65.7%). The most frequently reported chronic conditions were migraine (29.2%), epilepsy (20.8%), and multiple sclerosis (20.5%). The reliability of the EQ-5D questionnaire was acceptable (Cronbach's alpha = 0.764). In general, more than half of the participants indicated that had problems due to pain/discomfort (60.3%) and anxiety/depression (62.2%). The most common pattern of non-adherence was taking the medication only when a patient needed it followed by avoiding taking the medication as possible. Non-adherence to medications was less prevalent among participants with epilepsy (68.8%) and multiple sclerosis (65.8%). On the other hand, medication adherence was higher among respondents with migraine compared to participants without the condition (86.1% vs 73.7%, p = 0.009). A significantly lower proportion of participants who had some or extreme problems with self-care were non-adherent to medications compared to those who had no problems (68.1% vs 80.3%, respectively, p = 0.016). Results of the regression analysis showed that participants with epilepsy and multiple sclerosis were less likely to be non-adherence to medications. Furthermore, respondents with moderate and severe problems in self-care were less likely to be non-adherent. CONCLUSION: It was found that more than half of the participants had problems regarding their QoL due to pain/discomfort and anxiety/depression. The most prevalent pattern of non-adherence was taking the medication only when needed. Participants with epilepsy and multiple sclerosis were less likely to be non-adherent to medications. Furthermore, respondents with moderate and severe problems in self-care were less likely to be non-adherent. We recommend serial studies on the issue should be conducted to gather more evidence regarding this topic.
 INTRODUCTION: Development and worsening of most common neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, have been associated with COVID-19 However, the mechanisms associated with neurological symptoms in COVID-19 patients and neurodegenerative sequelae are not clear. The interplay between gene expression and metabolite production in CNS is driven by miRNAs. These small non-coding molecules are dysregulated in most common neurodegenerative diseases and COVID-19. METHODS: We have performed a thorough literature screening and database mining to search for shared miRNA landscapes of SARS-CoV-2 infection and neurodegeneration. Differentially expressed miRNAs in COVID-19 patients were searched using PubMed, while differentially expressed miRNAs in patients with five most common neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis) were searched using the Human microRNA Disease Database. Target genes of the overlapping miRNAs, identified with the miRTarBase, were used for the pathway enrichment analysis performed with Kyoto Encyclopedia of Genes and Genomes and Reactome. RESULTS: In total, 98 common miRNAs were found. Additionally, two of them (hsa-miR-34a and hsa-miR-132) were highlighted as promising biomarkers of neurodegeneration, as they are dysregulated in all five most common neurodegenerative diseases and COVID-19. Additionally, hsa-miR-155 was upregulated in four COVID-19 studies and found to be dysregulated in neurodegeneration processes as well. Screening for miRNA targets identified 746 unique genes with strong evidence for interaction. Target enrichment analysis highlighted most significant KEGG and Reactome pathways being involved in signaling, cancer, transcription and infection. However, the more specific identified pathways confirmed neuroinflammation as being the most important shared feature. DISCUSSION: Our pathway based approach has identified overlapping miRNAs in COVID-19 and neurodegenerative diseases that may have a valuable potential for neurodegeneration prediction in COVID-19 patients. Additionally, identified miRNAs can be further explored as potential drug targets or agents to modify signaling in shared pathways. Graphical AbstractShared miRNA molecules among the five investigated neurodegenerative diseases and COVID-19 were identified. The two overlapping miRNAs, hsa-miR-34a and has-miR-132, present potential biomarkers of neurodegenerative sequelae after COVID-19. Furthermore, 98 common miRNAs between all five neurodegenerative diseases together and COVID-19 were identified. A KEGG and Reactome pathway enrichment analyses was performed on the list of shared miRNA target genes and finally top 20 pathways were evaluated for their potential for identification of new drug targets. A common feature of identified overlapping miRNAs and pathways is neuroinflammation. AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; COVID-19, coronavirus disease 2019; HD, Huntington's disease; KEGG, Kyoto Encyclopedia of Genes and Genomes; MS, multiple sclerosis; PD, Parkinson's disease.


 Clinical and neuroscientific studies suggest a link between psychological stress and reduced brain health in health and neurological disease but it is unclear whether mediating pathways are similar. Consequently, we applied an arterial-spin-labeling MRI stress task in 42 healthy persons and 56 with multiple sclerosis, and investigated regional neural stress responses, associations between functional connectivity of stress-responsive regions and the brain-age prediction error, a highly sensitive machine learning brain health biomarker, and regional brain-age constituents in both groups. Stress responsivity did not differ between groups. Although elevated brain-age prediction errors indicated worse brain health in patients, anterior insula-occipital cortex (healthy persons: occipital pole; patients: fusiform gyrus) functional connectivity correlated with brain-age prediction errors in both groups. Finally, also gray matter contributed similarly to regional brain-age across groups. These findings might suggest a common stress-brain health pathway whose impact is amplified in multiple sclerosis by disease-specific vulnerability factors.
 BACKGROUND: Emotional competencies (i.e., understanding emotions in self and others) are crucial for psychological well-being and successful social interaction. However, despite the deficits in psychological well-being and social interaction among individuals with multiple sclerosis (MS), emotional competencies have not been broadly investigated in MS. The present study: (1) compared emotional competencies between persons with MS and (a) previously published norms for the general population and (b) persons with major depressive disorder; and (2) investigated the association between emotional competencies and symptoms of insomnia, depression, fatigue, and paresthesia in persons with MS. METHODS: The sample of 1135 persons with MS (mean age: 34.6 years; 81.1% female; median EDSS: 2; range: 0 - 5) self-rated emotional competencies and symptoms of insomnia, symptoms of depression, fatigue, and paresthesia. Data on emotional competencies of historical samples (general population: N = 622; mean age: 22.0 years; 61% females; outpatients with major depressive disorders (MDD); N = 50; mean age: 42.46 years; 68% females) were used for comparison. RESULTS: Persons with MS reported lower levels of emotional competencies than both the general population (t (1, 1756) = 55.18, p < 0.001, d = 1.66; large effect size) and outpatients with MDD (t (1, 1183) = 3.48, p <0.001, d = 0.50; medium effect size). Among persons with MS, lower levels of emotional competencies were associated with higher MS-related symptoms of insomnia(r = - 0.24; p < 0.001), depression (r = - 0.42; p < 0.001), fatigue (r = - 0.31; p < 0.001), and paresthesia (r = - 0.18; p < 0.001). CONCLUSIONS: Persons with MS reported significantly lower scores for emotional competencies when compared with the general population and outpatients with MDD. Further, lower scores for emotional competencies were associated with typical MS-related symptoms of insomnia, depression, fatigue and paresthesia. These findings suggest that emotional competencies may be an important target for intervention in persons with MS.
 PURPOSE: The effects of physical activity on health are well-established for chronic diseases such as multiple sclerosis (MS), Alzheimer's disease (AD), and ischaemic heart disease (IHD). However, sustaining physical activity in everyday life is difficult. Lifeworld knowledge can help qualify interventions aimed at resolving this public health issue, but there is a gap in regard to synthesized research on peoples' experiences with integrating and sustaining physical activity. Hence, the purpose of this review is to explore and present the available evidence on experiences with integrating and sustaining physical activity in a lived life with MS, AD, and IHD. METHODS: We conducted a scoping review with qualitative analysis and narrative syntheses in accordance with PRISMA-ScR. Based on SPIDER we ran a systematic search in Cinahl, Embase, Medline, and PsychInfo for primary qualitative research papers published until December 2022. RESULTS: 43 papers were included. A thematic content analysis found that individuals who have MS, AD or IHD find integrating and sustaining physical activity in everyday life meaningful on several levels: Physical activity can facilitate meaningful movement with outcomes of physical, psychosocial, and existential importance. CONCLUSION: The research literature presents a meaning to physical activity that extends the idea of physical fitness to one of existential movement and personal growth. In addition, our review finds that people are more likely to integrate and sustain physical activity if they feel acknowledged, supported and believe that physical activity has a meaningful purpose reflecting their sense of self. Taking a more person-centred approach in rehabilitative care might help qualify the content of physical activity in terms of integration into everyday life, but more research is needed on how to implement a person-centred approach in practice.IMPLICATIONS FOR REHABILITATIONThe research literature presents an experiential meaning to physical activity that extends the idea of physical fitness to one of more existential movement and personal growth.To ensure the integration of physical activity in people's everyday life, future rehabilitation interventions might benefit from adapting a more person-centred approach.People are more likely to sustain physical activity when they feel acknowledged, supported through social relationships, can access activities adapted to their specific needs and preferences, and believe that physical activity has a meaningful purpose reflecting their sense of self.
 INTRODUCTION: It is known that multiple sclerosis (MS) often coexists with other autoimmune diseases. Hence, autoantibody (auto-Ab) tests may prove useful in the differential diagnosis of MS. The objectives of this study were to: (a) investigate the prevalence of auto-Ab positivity at the beginning of the MS diagnostic process; (b) assess whether Auto-Ab+ and Auto-Ab- patients differ in baseline clinical, laboratory, and radiological parameters; and (c) investigate the prognostic value during a two-year follow-up period. MATERIAL AND METHODS: This retrospective study consisted of 450 patients aged between 18 and 55 years. All patients underwent a wide range of auto-Ab tests, anti-nuclear antibody (ANA) tests in particular. The expanded disability status scale (EDSS) scores of the patients were recorded at the time of diagnosis and at the end of a two-year follow-up period. RESULTS: The mean age of the 212 patients, 148 (69.8%) female and 64 (30.2%) male, included in the study sample was 37 ± 10.83 years. The rate of relapsing cases was 84% (178). Oligoclonal band (OCB) was positive in 142 (86.6%) of the 164 tested cases. At least one of the auto-Ab tests was positive in 51 (24.1%) of the cases. ANA test was positive in 21 (9.9%) cases. There was no significant difference between patients with at least one positive auto-Ab test and without any positive auto-Ab test and between ANA-positive and ANA-negative patients in terms of age, gender, clinical features of MS, presence of brain stem lesion, presence of spinal lesion, OCB positivity, level of clinical improvement after the first pulse steroid treatment, family history, presence of comorbidity, presence of autoimmune disease, or EDSS scores recorded at the end of the two-year follow-up period (p > 0.05). CONCLUSIONS: Our study findings revealed that Auto-Ab positivity was more common in MS patients than in the general population. However, given their limited contribution to the diagnosis and differential diagnosis of MS with no effect on the prognostic process, auto-Ab tests should be requested only in the event of accompanying autoimmune disease symptoms, and in cases where the diagnosis of MS may be suspected.
 Objectives: To evaluate the efficacy of dietary modifications based on complementary and alternative Iranian medicine (CAIM) in patients with secondary-progressive multiple sclerosis (SPMS). Design: In this randomized controlled trial, 70 SPMS patients were randomized to receive either a moderate-nature diet based on Persian medicine (as intervention) or usual diet plus health-related diet recommendations (as control) for 2 months. Serum high-sensitivity C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), Expanded Disability Status Scale (EDSS), Modified Fatigue Impact Scale (MFIS), State-Trait Anxiety Inventory (STAI), Global Pain Scale (GPS), Gastrointestinal Symptom Rating Scale (GSRS), anthropometric measurements, and quality of life (QOL) were assessed at baseline and end of trial. Analysis of covariance was performed, and the results were adjusted for potential confounders using SPSS v.14. Results: All participants completed the study for 2 months. There were significant improvements across the mean changes of hs-CRP (-0.1 ± 0.2 mg/L for intervention vs. -0.01 ± 0.13 mg/L for control; p(adjusted) = 0.012), MFIS (-11.0 ± 11.8 vs. -0.7 ± 9.9; p(adjusted) <0.001), GSRS (-19.9 ± 16.3 to 1.2 ± 17.5; p(adjusted) <0.001), GPS (p(adjusted) = 0.032), and QOL (p(adjusted) <0.05). No significant difference was observed across the ESR, EDSS, STAI, and anthropometric measurements. Conclusion: Dietary modifications based on CAIM may improve inflammation and clinical manifestations in SPMS patients. Nonetheless, further trials are required to confirm these findings. Clinical Trial Registration number: IRCT20181113041641N2.
 Mongolia is located at 45° north latitude in the center of the Asian continent, and about 80% of the territory is at 1000 m above sea level. Epidemiologically, multiple sclerosis (MS) has not been investigated in Mongolia, although there have been a few MS case reports. We investigated the characteristics of MS in Mongolia for the first time, focusing on the association between MS-related parameters and depression levels. We initiated cross-sectional analyses, using data from 27 MS patients aged 20 to 60 years in Ulaanbaatar, Mongolia. The patients completed a questionnaire on their lifestyles and clinical information. We classified the MS patients on the basis of disability levels using the expanded disability status scale (EDSS) scores: 11.1% mild disability and 88.9% moderate to severe disability (median EDSS score, 5.5). We also classified the patients on the basis of depression levels using the 9-item patient health questionnaire (PHQ-9) scores: 44.4% mild depression, 40.7% moderate depression, and 14.8% severe depression (mean PHQ-9's score, 9.96 ± 5.05). We used multivariate logistical regression analyses to identify predictors of EDSS or PHQ-9 scores. Disability levels were associated with vision and balance problems. Depression levels were associated with corticosteroid treatment; no patients were treated with disease-modifying drugs (DMDs). The odds ratios for disease onset age and treatment duration were associated with EDSS scores. In conclusion, MS onset age and treatment duration were independent predicting factors influencing the level of disability. Appropriate DMD treatment would lower the disability and depression levels.
 BACKGROUND AND OBJECTIVES: Acute COVID-19 infection has been associated with neurological involvement. We report a case series of newly diagnosed patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) developed in a short period of time after acute COVID-19 infection. METHODS: New MS patients developing initial symptoms shortly after an acute COVID-19 infection were diagnosed based on the 2017 McDonald Criteria [Garcia-Ramos et al. in Cells, 2021]. The patients diagnosed with NMOSD met the 2015 International Panel criteria for the diagnosis of NMOSD (IPDN) [Thompson et al. in Lancet Neurol 17:162-173, 2018]. RESULTS FROM THE MS PATIENT GROUP: Ten patients were included who had developed initial MS symptoms after COVID-19 infection. Gender distribution was equal (50% male). The mean age was 28 (range 17-39) years. Average time to neurological presentation was between 2 and 6 weeks following acute COVID-19 infection. Partial transverse myelitis was the initial presentation in 40% of the cases, and 60% of patients had spinal cord lesions present at the moment of diagnosis. All patients showed enhancing lesions on brain magnetic resonance imaging (MRI). The presence of cerebrospinal fluid (CSF) oligoclonal bands was found in all six tested cases. The majority of patients (80%) were unvaccinated for COVID-19. The two vaccinated patients had received two doses of the monovalent COVID-19 messenger ribonucleic acid (mRNA) (Pfizer Biotech) vaccine and no booster, a year prior to contracting COVID-19. RESULTS FROM THE NMOSD GROUP: Two patients with NMOSD were included. Positive aquoporin-4 protein antibody (AQP-4 Ab) was detected in serum in both cases [one Enzyme Linked immunosorbent assay (ELISA) and one cell based]. Both patients had mild COVID-19 infection prior to presentation, initial neurologic symptoms presented between 3 and 6 weeks after COVID-19 infection. Neither patients were vaccinated. Both responded partially to steroids, one developed a relapse 40 days after diagnosis. CONCLUSION: COVID-19 infection has been linked to several neurological and immune-driven conditions. This study suggests that in susceptible individuals, acute COVID-19 infection may act as a trigger for developing MS and NMOSD.
 Changes is lymphocyte subpopulations in peripheral blood have been proposed as biomarkers for evaluation of disease activity in multiple sclerosis (MS). Serum neurofilament light chain (sNfL) is a biomarker reflecting neuro-axonal injury in MS that could be used to monitor disease activity, response to drugs and to prognosticate disease course. Here we show a moderate correlation between sNfL and lymphocyte cell subpopulations, and our data furthermore suggest that sNfL and specific immune cell subpopulations together could predict future disease worsening in MS.
 INTRODUCTION: Multiple sclerosis (MS) is a chronic autoimmune-mediated demyelinating disease of the central nervous system (CNS). A clinical presentation of the disease is highly differentiated even from the earliest stages of the disease. The application of stratifying tests in clinical practice would allow for improving clinical decision-making including a proper assessment of treatment benefit/risk balance. METHODS: This prospective study included patients with MS diagnosed up to 1 year before recruitment. We analyzed serum biomarkers such as CXCL13, CHI3L1, OPN, IL-6, and GFAP and neurofilament light chains (NfLs); brain MRI parameters of linear atrophy such as bicaudate ratio (BCR), third ventricle width (TVW); and information processing speed were measured using the Symbol Digit Modalities Test (SDMT) during the 2 years follow-up. RESULTS: The study included a total of 50 patients recruited shortly after the diagnosis of MS diagnosis (median 0 months; range 0-11 months), and the mean time of observation was 28 months (SD = 4.75). We observed a statistically significant increase in the EDSS score (Wilcoxon test: Z = 3.06, p = 0.002), BCR (Wilcoxon test: Z = 4.66, p < 0.001), and TVW (Wilcoxon test: Z = 2.84, p = 0.005) after 2 years of disease. Patients who had a significantly higher baseline level of NfL suffered from a more severe disease course as per the EDSS score (Mann-Whitney U-test: U = 107, Z = -2,74, p = 0.006) and presence of relapse (Mann-Whitney U-test: U = 188, Z = -2.01, p = 0.044). In the logistic regression model, none of the parameters was a significant predictor for the achieving of no evidence of disease activity status (NEDA). In the model considering all assessed parameters, only the level of NfL had a significant impact on disease progression, measured as the increase in EDSS (logistic regression: β = 0.002, p = 0.017). CONCLUSION: We confirmed that NfL levels in serum are associated with more active disease. Moreover, we found that TVW at the time of diagnosis was associated with an impairment in cognitive function measured by information processing speed at the end of the 2-year observation. The inclusion of serum NfL and TVW assessment early in the disease may be a good predictor of disease progression independent of NEDA.
 Multiple Sclerosis (MS) is a prevalent inflammatory disease in which the immune system plays an essential role in the damage, inflammation, and demyelination of central nervous system neurons (CNS). The cannabinoid receptor type 2 (CB(2)) agonists possess anti-inflammatory effects against noxious stimuli and elevate the neuronal survival rate. We attempted to analyze the protective impact of low doses of β-Caryophyllene (BCP) in experimental autoimmune encephalomyelitis (EAE) mice as a chronic MS model. Immunization of female C57BL/6 mice was achieved through two subcutaneous injections into different areas of the hind flank with an emulsion that consisted of myelin Myelin oligodendrocyte glycoprotein (MOG)(35-55) (150 µg) and complete Freund's adjuvant (CFA) (400 µg) with an equal volume. Two intraperitoneal (i.p.) injections of pertussis toxin (300 ng) were performed on the animals on day zero (immunizations day) and 48 h (2nd day) after injection of MOG + CFA. The defensive effect of low doses of BCP (2.5 and 5 mg/kg/d) was investigated in the presence and absence of a CB(2) receptor antagonist (1 mg/kg, AM630) in the EAE model. We also examined the pro/anti-inflammatory cytokine levels and the polarization of brain microglia and spleen lymphocytes in EAE animals. According to our findings, low doses of BCP offered protective impacts in the EAE mice treatment in a CB2 receptor-dependent way. In addition, according to results, BCP decreased the pathological and clinical defects in EAE mice via modulating adaptive (lymphocytes) and innate (microglia) immune systems from inflammatory phenotypes (M(1)/Th(1)/Th(17)) to anti-inflammatory (M(2)/Th(2)/T(reg)) phenotypes. Additionally, BCP elevated the anti-inflammatory cytokine IL-10 and reduced blood inflammatory cytokines. BCP almost targeted the systemic immune system more than the CNS immune system. Thus, a low dose of BCP can be suggested as a therapeutic effect on MS treatment with potent anti-inflammatory effects and possibly lower toxicity.
 BACKGROUND: Fatigue is the most common symptom associated with multiple sclerosis (MS). Fatigue as a risk factor for injurious falls and frequency of falls is understudied. Falling recurrently is associated with injurious falls which may lead to reduced functional independence and poor quality of life of people with MS. Identifying contributors of recurrent falls and injurious falls is clinically useful to develop effective interventions. OBJECTIVE: To investigate the associations between fatigue impact and frequency of falls and injurious falls in people with MS. METHODS: Fifty-one participants completed the Modified Fatigue Impact Scale (MFIS) and a survey of number of falls and injurious falls during the past year. Logistic regression analyses were conducted to investigate whether scores on the MFIS (Total, Physical, Cognitive, and Psychosocial) predicted odds of being a recurrent faller (> 2 falls) or infrequent faller (1- 2 falls) versus a non-faller, and odds of experiencing an injurious fall (yes/no). The analyses were adjusted for demographic and clinical characteristics and common symptoms of MS (depression, cognition, pain, and sleep disturbance). RESULTS: Higher MFIS Total score was associated with higher odds of infrequent falls (OR = 1.07, 95% CI, 1.00 - 1.15, p = 0.05) and recurrent falls (OR = 1.10, 95% CI, 1.00 - 1.20, p = 0.04) relative to not falling in the past year. Higher scores on the MFIS Physical subscale were significantly associated with high odds of infrequent falls (OR = 1.15, 95% CI, 1.02 - 1.30, p = 0.03) and recurrent falls (OR = 1.19, 95% CI, 1.02 - 1.39, p = 0.03). MFIS Psychosocial subscale was significantly associated with higher odds of infrequent falls (OR = 2.01, 95% CI, 1.14 - 3.53, p = 0.02). MFIS Total and MFIS Cognitive subscale were significantly associated with higher odds of injurious falls (OR = 1.11, 95% CI, 1.00 - 1.23, p = 0.04) and (OR = 1.28, 95% CI, 1.02 - 1.60, p = 0.04), respectively. CONCLUSION: The findings indicated self-reported fatigue impact and its specific domains were associated with an increased risk of falling and injurious falls. Further studies using prospective falls assessment and longitudinal evaluation of fatigue are warranted to extend our findings.
 INTRODUCTION: The polyspecific intrathecal immune response (PSIIR), aka MRZ reaction (M = measles, R = rubella, Z = zoster, optionally Herpes simplex virus, HSV) is defined as intrathecal immunoglobulin synthesis (IIS) for two or more unrelated viruses. Although an established cerebrospinal fluid (CSF) biomarker for multiple sclerosis (MS), a chronic autoimmune-inflammatory neurological disease (CAIND) of the central nervous system (CNS) usually starting in young adulthood, the full spectrum of CAINDs with a positive PSIIR remains ill defined. METHODS: In this retrospective, cross-sectional study, patients with CSF-positive oligoclonal bands (OCB) and - to enrich for non-MS diagnoses - aged ≥50 years were enrolled. RESULTS: Of 415 with PSIIR testing results (MRZ, HSV optional), 76 were PSIIR-positive. Of these, 25 (33%) did not meet the diagnostic criteria for MS spectrum diseases (MS-S) comprising clinically or radiologically isolated syndrome (CIS/RIS) or MS. PSIIR-positive non-MS-S phenotypes were heterogenous with CNS, peripheral nerve and motor neuron involvement and often defied unequivocal diagnostic classification. A rating by neuroimmunology experts suggested non-MS CAINDs in 16/25 (64%). Long-term follow-up available in 13 always showed a chronically progressive course. Four of five responded to immunotherapy. Compared to MS-S patients, non-MS CAIND patients showed less frequent CNS regions with demyelination (25% vs. 75%) and quantitative IgG IIS (31% vs. 81%). MRZ-specific IIS did not differ between both groups, while additional HSV-specific IIS was characteristic for non-MS CAIND patients. DISCUSSION: In conclusion, PSIIR positivity occurs frequently in non-MS-S patients ≥50 years. Although sometimes apparently coincidental, the PSIIR seems to represent a suitable biomarker for previously unnoticed chronic neurologic autoimmunities, which require further characterization.
 In many countries, the COVID-19 pandemic led to healthcare reorganization limiting access to diagnostic or therapeutic procedures for chronically-ill patients. In this article, we describe the psychological consequences and coping strategies of several groups of chronically-ill patients. During the cross-sectional survey conducted in 2020, we enrolled 398 patients with four different chronic conditions (psoriasis, multiple sclerosis, and patients who have undergone a kidney transplant or received dialysis). The study sample was examined regarding the experienced stress levels (Perceived Stress Scale) and coping strategies (Brief-COPE). All four groups of patients most commonly declared using problem-focused coping strategies and least commonly reported the use of avoidant coping. Higher levels of perceived stress strongly correlated with self-blaming. The participants who declared previous psychiatric treatment or psychotherapy were more likely to use self-blaming, behavioral disengagement, substance use, and avoidant coping, while previous psychotherapy additionally correlated with emotion-focused coping. Group comparison identifies patients with a chronic neurological disease, such as multiple sclerosis, at higher risk of a less beneficial coping profile than kidney transplant recipients. Further focus on education and early interventions in at-risk individuals is needed, and widely targeted mental health programs are indicated in order to improve the mental health of patients suffering from chronic diseases.
 BACKGROUND: Balance training interventions with a gradual progression of difficulty and highly challenging tasks designed specifically for people with multiple sclerosis (MS) are rare. The objective was to adapt a balance training intervention originally developed for Parkinson's disease through a co-design process and then conduct a pilot trial in MS to evaluate the feasibility of a large, full-scale study. METHODS: Twelve people with MS with mild to moderate overall MS-disability were included in this single-group feasibility trial. Participants received one-hour training sessions twice or three times weekly for 10 weeks. The assessment included tests of physical and cognitive functioning and patient-reported quality of life-related outcomes. Data on feasibility aspects were collected at baseline and follow-up assessments and three times during the intervention period to inform the recruitment process, as well as to monitor retention and inclusion rates, study procedures, intervention delivery, and dynamic changes in the selected potential outcome measures. Progression criteria were used to determine whether to proceed to a full-scale trial. Descriptive statistics were used to present the data. RESULTS: Out of six progression criteria, only retention and attendance at training sessions were not met. Reasons reported for not completing the intervention period mainly depended on external circumstances beyond the control of the study. In contrast, study procedures, intervention delivery, and intervention content (progression, adjustment, and control of challenge level of exercises) were considered feasible for a future, full-scale trial. The Mini-BESTest, which was used for the assessment of balance control, was considered suitable as the primary outcome in a full-scale trial with no ceiling or floor effects. Further, the Mini-BESTest showed a positive trend in outcome response with a median difference of 3.5 points between baseline and follow-up assessments. The power calculation performed suggests a feasible number of participants for recruitment. CONCLUSIONS: Overall trial aspects and intervention delivery were deemed feasible for a full-scale trial, but adjustments are needed to increase retention and attendance.
 OBJECTIVE: This systematic review aimed to identify the prevalence of CAM use in patients with neurological disorders, and also to know most frequent types of CAM used. METHODS: Five databases: PubMed, Science Direct, EBSCO, Latindex and Scielo (in English and Spanish) were searched from January 2010 to May 2021. Only original cross-sectional, retrospective and cohort studies were included, whose primary objective was to describe the frequency of CAM use in neurological disorders and/or the related factors to its use in adults. Based on the data, a descriptive analysis was performed, covering the characteristics of studies, measuring methods, prevalence, types and related factors. To control the risk of bias, a quality assessment of each study was performed using STROBE checklist. RESULTS: For the final analysis, 40 studies were included. Most common pathologies observed in the studies were multiple sclerosis, headache, stroke, Parkinson and epilepsy. The STROBE score of studies ranged from 13 to 22 points, with an average of 18.2. Prevalence of CAM use was highly variable from one study to another (16% in stroke patients, to 100% in amyotrophic lateral sclerosis or spinal cord injury patients). Biological therapies (dietary supplements and herbal medicine) were the most commonly CAM types used. The associated factors identified were female sex, an age between 40 and 50 years, and higher socioeconomic level. Not all studies investigated about the results of CAMs but these ranged from 35% to more than 80% of reporting positive effects. CONCLUSIONS: The prevalence of CAM use in neurological diseases is highly variable (16%-100%); the most used type of CAM was biological therapies and the associated factors were female sex, age between 40 and 50 years old and high socioeconomic level.


 [This corrects the article DOI: 10.7759/cureus.32695.].

 Neurodegenerative diseases are age-related, multifactorial, and complicated conditions that affect the nervous system. In most cases, these diseases may begin with an accumulation of misfolded proteins rather than decay before they develop clinical symptoms. The progression of these diseases can be influenced by a number of internal and external factors, including oxidative damage, neuro-inflammation, and the accumulation of misfolded amyloid proteins. Astrocytes, with the highest abundance among the cells of the mammalian central nervous system, perform several important activities, such as maintaining brain homeostasis and playing a role in the neurodegenerative condition onset and progress. Therefore, these cells have been considered to be potential targets for managing neurodegeneration. Curcumin, with multiple special properties, has been effectively prescribed to manage various diseases. It has hepato-protective, anti-carcinogenic, cardio-protective, thrombo-suppressive, anti-inflammatory, chemo-therapeutic, anti-arthritic, chemo-preventive, and anti-oxidant activities. In the current review, the effects of curcumin on astrocytes in common neurodegenerative conditions, such as Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease, and Parkinson's disease, are discussed. Hence, it can be concluded that astrocytes play a critical role in neurodegenerative diseases, and curcumin is able to directly modulate astrocyte activity in neurodegenerative diseases.
 Methylprednisolone is an FDA-approved medication for the management and treatment of allergic conditions, arthritis, asthma exacerbations, long-term asthma maintenance, acute exacerbation of multiple sclerosis, and as an anti-inflammatory and immunosuppressive agent. It is in the systemic corticosteroid class of medications. This activity outlines the indications, action, and contraindications for methylprednisolone as a valuable agent in treating many endocrine, inflammatory, immunologic, hematologic, and respiratory disorders.
 BACKGROUND AND PURPOSE: There is growing evidence that dietary modification can improve clinical manifestations in multiple sclerosis (MS) patients. This study aimed to assess the impact of synbiotics and anti-inflammatory-antioxidant-rich diet on fatigue, pain, gut and bladder status, and sexual function in patients with progressive forms of MS. MATERIALS AND METHODS: In this single-center, single-blind, randomized, controlled clinical trial, seventy participants with three forms of progressive MS (primary-progressive, secondary-progressive, and progressive-relapsing) were randomly assigned to receive either synbiotics supplement and anti-inflammatory-antioxidant-rich diet or a placebo along with their usual diet for a duration of four months. Modified fatigue impact scale (MFIS), global pain scale (GPS), bladder control scale (BLCS), bowel control scale (BWCS), and sexual satisfaction scale (SSS) were assessed at baseline and at the end of the trial. RESULTS: Sixty-nine participants successfully completed the trial, resulting in a 98% adherence rate to the diet, and no reports of serious side effects. Significant mean changes were observed in fatigue (Δ for experimental group = -10.5 ± 10.8 vs. Δ for control group = -0.08 ± 4.1; P < 0.001), pain (-14.1 ± 19.0 vs. 0.9 ± 10.3; P < 0.001), bladder (-0.76 ± 2.1 vs. 0.3 ± 1.1; P = 0.013) and bowel (-6.6 ± 3.2 vs. -0.05 ± 2.3; P < 0.001) control, as well as sexual function (-1.0 ± 2.3 vs. 0.51 ± 0.21; P < 0.001). CONCLUSION: The anti-inflammatory-antioxidant-rich diet and synbiotics co-supplementation demonstrated improvements in fatigue, pain, sexual function, and bowel/bladder status among patients with progressive MS.
 BACKGROUND: Fatigue is a disabling symptom of multiple sclerosis (MS). The lack of effective therapeutics has promoted the development of cognitive behavioural therapy (CBT)-based fatigue management programmes. However, their efficacy does not sustain over time. We proposed to test the long-term effectiveness of a 6-week fatigue programme supplemented with four booster sessions ('FACETS+') in patients with relapsing remitting MS (RRMS) and fatigue. METHODS: This multicentre, randomised, controlled, open-label, parallel-group trial versus standard care enrolled patients with RRMS and fatigue. Participants were randomised to either FACETS+ plus standard care or standard care alone. The primary outcome measure was fatigue impact (Modified Fatigue Impact Scale (MFIS) at 12 months) based on intention-to-treat analyses. RESULTS: From May 2017 to September 2020, 162 patients were screened; 105 were randomly assigned to FACETS+ (n=57) or standard care (n=48) and 88 completed the primary outcome assessment for the MFIS. At month 12, participants showed improved MFIS compared with baseline in the intervention group (mean difference (MD)=14.0 points; (95% CI 6.45 to 21.5)) and the control group (MD=6.1 points; (95% CI -0.30 to 12.5)) with a significant between-group difference in favour of the intervention group (adjusted MD=7.89 points; (95% CI 1.26 to 14.52), standardised effect size=0.52, p=0.021). No trial-related serious adverse events were reported. CONCLUSIONS: A 6-week CBT-based programme with four booster sessions is superior to standard care alone to treat MS-related fatigue in the long term (12 months follow-up). The results support the use of the FACETS+ programme for the treatment of MS-related fatigue. TRIAL REGISTRATION NUMBER: NCT03758820.
 Multiple sclerosis (MS) is a progressive, demyelinating neurodegenerative disease of the central nervous system. MS is immune-mediated and leads to disability especially in young adults. Even though 18 MS therapy drugs were approved, they slightly inhibit disease progression and do not induce regeneration and repair in the nervous system. Mesenchymal stromal cells (MSCs) have emerged as a new therapeutic modality in regenerative medicine and tissue engineering due to their immunomodulation and bio regenerative properties. We have designed a randomized, controlled clinical trial to assess safety and possible efficacy of MSC application in MS patients. Twenty-one MS patients were enrolled. Patients were allocated in two distinct groups: treatment group, which received systemic transplantation of autologous bone marrow-derived MSCs, and control group, which received placebo at the first injections. Patients in control group received MSCs at the second injection while the treatment group received placebo. All the patients were followed for 18 months. Follow-ups included regular visits, laboratory evaluation, and imaging analysis. Control patients received MSCs six month after treatment group. No severe immediate or late adverse events were observed in both groups after interventions. We did not find any significant differences in the rate of relapses, Expanded Disability Status Scale (EDSS) score, cognitive condition, Magnetic Resonance Imaging (MRI) findings, or any biomarkers of cerebrospinal fluid between the two groups and in each group before and after cell infusion. Transplantation of autologous bone marrow-derived mesenchymal stromal cells is safe and feasible. The efficacy of transplantation of these cells should be evaluated through designing randomized clinical trials with larger sample sizes, different administration routes, other cell types (allogeneic adipose derived MSCs, allogeneic Wharton's jelly derived MSCs …), repeated injections, and longer follow-up periods.
 Cladribine tablets (CladT) is a highly active oral disease-modifying therapy (DMT) for the management of relapsing multiple sclerosis (RMS). CladT acts as an immune reconstitution therapy, in that two short courses of treatment 1 year apart have been shown to suppress disease activity for a prolonged period in most patients, without need for continued DMT. Each course of CladT induces a profound reduction in B lymphocytes that recovers over months, and serious lymphopenia (Grade 3-4) is uncommon. Smaller reductions in levels of T lymphocytes occur slightly later: on average, these remain within the normal range and repopulate progressively. A larger effect occurs on CD8 vs. CD4 cells. Reactivation of latent or opportunistic infections (e.g. varicella zoster, tuberculosis) is mostly associated with very low lymphocyte counts (< 200/mm(3)). Screening and managing pre-existing infections, vaccinating non-exposed patients and delaying the 2nd year of treatment with CladT to allow lymphocytes to recover to > 800/mm(3) (if necessary) are important for avoiding infections and higher-grade lymphopenia. There was no demonstrable or apparent effect of CladT on the efficacy of vaccinations, including against Covid-19. Adverse events consistent with drug-induced liver injury (DILI) represent a rare but potentially serious complication of CladT therapy in spontaneous adverse event reporting; patients should be screened for liver dysfunction before starting treatment. Ongoing hepatic monitoring is not required, but CladT must be withdrawn if signs and symptoms of DILI develop. There was a numerical imbalance for malignancies when comparing cladribine to placebo in the clinical programme, particularly in short-term data, but recent evidence shows that the risk of malignancy with CladT is similar to the background rate in the general population and to that with other DMTs. Overall, CladT is well tolerated with a favorable safety profile appropriate for the management of RMS.
 BACKGROUND: Multiple sclerosis (MS) is a common neurological disease affecting the optic nerve, directly or indirectly, through transsynaptic axonal degeneration along the visual pathway. New ophthalmological tools, arguably the most important being optical coherence tomography (OCT), could prove paramount in redefining MS diagnoses and shaping their follow-up protocols, even when the optic nerve is not involved. METHODS: A prospective clinical study was conducted. In total, 158 eyes from patients previously diagnosed with relapsing remitting MS (RRMS)-with or without optic neuritis (ON), clinically isolated syndrome (CIS) with or without ON, and healthy controls were included. Each patient underwent an ophthalmologic exam and OCT evaluation for both eyes (a posterior pole analysis (PPA) and the optic nerve head radial circle protocol (ONH-RC)). RESULTS: The macular retinal thickness (the 4 × 4, respectively, 2 × 2 grid) and thickness of the peripapillary retinal nerve fiber layer (pRNFL) were investigated. Various layers of the retina were also compared. Our study observed significant pRNFL thinning in the RRMS eyes compared to the control group, the pRNFL atrophy being more severe in the RRMS-ON eyes than the RRMS-NON eyes. In the ON group, the macular analysis showed statistically significant changes in the RRMS-ON eyes when compared only to the CIS-ON eyes, regarding decreases in the inner plexiform layer (IPL) thickness and inner nuclear layer (INL) on the central 2 × 2 macular grid. The neurodegenerative process affected both the inner retina and pRNFL, with clinical damage appearing for the latter in the following order: CIS-NON, CIS-ON, RRMS-NON, and RRMS-ON. In the presence of optic neuritis, SMRR patients presented an increase in their outer retina thickness compared to CIS patients. CONCLUSIONS: To differentiate the MS patients from the CIS patients, in the absence of optic neuritis, OCT Posterior Pole Analysis could be a useful tool when using a central 2 × 2 sectors macular grid. Retinal changes in MS seem to start from the fovea and spread to the posterior pole. Finally, MS could lead to alterations in both the inner and outer retina, along with pRNFL.
 We investigated the influence of post-traumatic growth (PTG) and mental health (MH) on multiple sclerosis (MS) caregivers' uses of coping strategies and identified biopsychosocial predictors of proactive or reactive coping. The Short Form Health Survey (SF-12), General Health Questionnaire (GHQ-28), Post-Traumatic Growth Inventory (PGI-21), Brief COPE Questionnaire (COPE-28), and Multidimensional Scale of Perceived Social Support (MSPSS) were used to evaluate 209 caregivers. Higher PTG was related to greater use of emotional support, positive reframing, religion, active coping, instrumental support, planning, denial, self-distraction, self-blaming, and venting. Better MH was associated with greater use of acceptance, while behavioral disengagement and self-distraction were associated with poorer MH. The PTG dimensions relating to others and new possibilities, SF-12 dimensions of physical and emotional roles as well as partnership, not living with the patient, and significant others' social support were predictors of proactive coping. Reactive coping was positively predicted by the PTG dimension relating to others, depression, vitality, other than partner relation, and physical role, and negatively predicted by mental health level and emotional role. In summary, higher MH was associated with proactive coping strategies, whereas post-traumatic growth was related to the use of a wide range of proactive coping as well as reactive coping strategies.
 OBJECTIVES: To compare the signal alterations of amide proton transfer (APT), apparent diffusion coefficient (ADC), and fractional anisotropy (FA) in white matter (WM) lesions in multiple sclerosis (MS), compared with healthy controls (HCs), and to investigate the relationships between these changes and clinical measurements such as serum neurofilament light chain (sNfL). MATERIALS AND METHODS: Twenty-nine patients with relapsing-remitting MS (21 females and 8 males) and 30 HCs (23 females and 7 males) were recruited. APT-weighted (APTw) and diffusion tensor imaging (DTI) data were acquired using a 3.0-T magnetic resonance system. APTw and DTI images were registered to FLAIR-SPIR images and assessed by two neuroradiologists. MTRasym (3.5 ppm), ADC, FA values for MS and HC are calculated using mean values from all regions of interest (ROI). The ROI criteria were: (1) for MS patients, ROI were defined as MS lesions, and each lesion was identified. (2) The WM around each HC's lateral ventricle (frontal lobe, parietal lobe, and centrum semiovale) was assessed bilaterally. The diagnostic efficacy of MTRasym (3.5 ppm), ADC, and FA in the lesions of MS patients was compared using receiver operating characteristic (ROC) curve analysis. The associations between MTRasym (3.5 ppm), ADC, and FA values and the clinical measurements were investigated further. RESULTS: The MTRasym (3.5 ppm) and ADC values of brain lesions were increased, while FA values were decreased in patients with MS. The diagnostic area under curve (AUC) of MTRasym (3.5 ppm), ADC, and FA value was 0.891 (95% CI: 0.813, 0.970), 0.761 (95% CI: 0.647, 0.875) and 0.970 (95% CI: 0.924, 1.0), respectively. sNfL was considerably positively correlated with MTRasym (3.5 ppm) (P = 0.043, R = 0.38) and disease durations were significantly negatively correlated with FA (P = 0.046, R = -0.37). CONCLUSION: Amide proton transfer-weighted (APTw) and DTI are potential imaging methods for assessing brain lesions in patients with MS at the molecular and microscopic levels, respectively. The association between APTw, DTI parameters and clinical factors implies that they may play a role in disease damage monitoring.
 A personalized approach is strongly advocated for treatment selection in Multiple Sclerosis patients due to the high number of available drugs. Machine learning methods proved to be valuable tools in the context of precision medicine. In the present work, we applied machine learning methods to identify a combined clinical and genetic signature of response to fingolimod that could support the prediction of drug response. Two cohorts of fingolimod-treated patients from Italy and France were enrolled and divided into training, validation, and test set. Random forest training and robust feature selection were performed in the first two sets respectively, and the independent test set was used to evaluate model performance. A genetic-only model and a combined clinical-genetic model were obtained. Overall, 381 patients were classified according to the NEDA-3 criterion at 2 years; we identified a genetic model, including 123 SNPs, that was able to predict fingolimod response with an AUROC= 0.65 in the independent test set. When combining clinical data, the model accuracy increased to an AUROC= 0.71. Integrating clinical and genetic data by means of machine learning methods can help in the prediction of response to fingolimod, even though further studies are required to definitely extend this approach to clinical applications.
 INTRODUCTION: Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS with an autoimmune pathogenesis. Over the years, numerous disease-modifying therapies (DMTs) have proven effective in disease control; to date, there is a need to identify a personalized treatment effective in ensuring disease-free status or no evidence of disease activity (NEDA). OBJECTIVE: identify clinical, demographic and treatment approach characteristics that affect the maintenance of NEDA-3 and the occurrence of clinical relapses during a 6-years follow-up. MATERIALS AND METHOD: a retrospective study was conducted on a cohort of MS patients followed up with six-year period. All participants were treated with first- or second-line MS drugs.Clinical relapse, NEDA-3 at 6 years and sustained EDSS were assessed as disease activity outcomes. Patients with follow-up of less than 6 years and insufficient clinical and radiological data were excluded from the study. RESULTS: Two-hundred-eighty naive patients (mean age was 49.8 years, SD ± 11.35 years, 23-76, F/M 182/98), with MS were followed up for 6 years.The mean age at diagnosis was 34.3 years (SD ±11.5, 14-62 years), the mean EDSS score at the onset was 1.9 (±1.3), 76.8% of patients had an EDSS below or equal to 2.5 at diagnosis.In the cohort 37 (13.2%) directly received second-line treatment, 243 (86.8%) received first-line drugs.The analysis showed that second-line treatment from beginning had a protective effect for the achievement of NEDA-3 (p = 0.029), on the prevention of clinical relapse (p = 0.018) and on number of relapses (p = 0.010); this finding was confirmed by logistic regression analysis (p = 0.04) and Kaplan-Meier analysis (p = 0.034). CONCLUSION: The results of this study demonstrate the efficacy of targeted and early intervention so as to act in the right time window, ensuring a favorable outcome in both clinical and radiological terms; this could be decisive in reducing clinical relapse, disease progression and related disability. Therefore, prescribing highly effective drug in the early stages of the disease represents a leading strategy with the most favorable cost-benefit ratio.
 INTRODUCTION: Abnormal lung function in people with multiple sclerosis (PwMS) could be considered as the result of muscle weakness or MS-specific structural central nervous system (CNS) abnormalities as a precipitant factor for the worsening of motor impairment or cognitive symptoms. METHODS: This is a cross-sectional observational study in PwMS. Forced spirometry was conducted, and normative metrics of forced vital capacity (FVC), forced expiratory volume in the first second (FEV(1)), and the relation FEV1/FVC were calculated. Qualitative and quantitative brain magnetic resonance imaging (MRI) examinations were carried out. RESULTS: A total of 371 PwMS were included in the study. Of those, 196 (53%) had RRMS, 92 (25%) SPMS, and 83 (22%) PPMS. Low FVC and FEV(1) was present in 16 (8%), 16 (19%), and 23 (25%) of the patients in the RRMS, PPMS, and SPMS, respectively. PwMS with T2-FLAIR lesions involving the corpus callosum (CC) had a significantly higher frequency of abnormally low FVC and FEV(1) (OR 3.62; 95% CI 1.33-9.83; p = 0.012) than patients without lesions in that region. This association remained significant in the RRMS group (OR 10.1; 95% CI 1.3-67.8; p 0.031) when the model excluded PPMS and SPMS. According to our study, for every increase of 1 z score of FVC, we observed an increase of 0.25 cm(3) of hippocampal volume (β 0.25; 95% CI 0.03-0.47; p 0.023) and 0.43 cm(3) of left hippocampus volume (β 0.43; 95% CI 0.16-0.71; p 0.002). CONCLUSIONS: We observed an incremental prevalence of abnormally low pulmonary function tests that parallels a sequence from more early relapsing courses to long-standing progressive courses (RRMS to PPMS or SPMS).
 Patients suffering from neuro-inflammatory diseases such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) remain vulnerable to COVID-19. We investigated the risk of COVID-19 in MS and NMOSD patients over time, considering the impact of disease-modifying treatments (DMTs), vaccinations, and the spread of new SARS-CoV-2 variants. We retrospectively collected clinical information regarding all MS and NMOSD consecutive patients seen at the Neurocenter of Southern Switzerland. Logistic regression was used to test variables (age, sex, vaccination status, DMT at vaccination, DMT at infection, disease course, disability scores, prevalent SARS-CoV-2 variant) for association with COVID-19 risk and severe outcome (hospitalization or death). We included 352 individuals in this study; 315 (89.5%) received ≥1 dose of SARS-CoV-2 mRNA-vaccine, and 134 (38.1%) experienced COVID-19 between March 2020 and August 2022. COVID-19 risk decreased in vaccinated patients (OR = 0.10, 95% CI = 0.05-0.20, p < 0.001) and increased in anti-CD20 therapies (OR = 2.26, 95% CI = 1.28-4.00, p = 0.005). Anti-CD20 treatment was associated with severe COVID-19 (OR = 27.41, 95% CI = 3.68-204.25, p = 0.001), whereas Omicron infections were milder compared to Alpha infections (OR = 0.03, 95% CI = 0.01-0.35, p = 0.006). We confirmed a protective effect of mRNA vaccines on COVID-19 risk, which is impaired by anti-CD20 treatment. We provided evidence for milder COVID-19 with the Omicron SARS-CoV-2 variant, which should not, however, discourage vaccinations.
 BACKGROUND: Gait initiation (GI) is an important functional task related to balance and gait performance. In addition, it has predictive importance for falls and postural instability in patient with multiple sclerosis (MS). However, it is uncertain how GI is affected in patients in the early stage of MS (Expanded Disability Status Scale (EDSS) ≤3). In this study, it was aimed to investigate the anticipatory postural adjustments (APAs), posterior center of pressure (COPap) displacement, and spatiotemporal variability during GI in patients with and without functional loss in the early stage of MS. METHODS: Forty-four participants (31 MS patients and 13 healthy subjects) involved in this prospective cross-sectional study were divided into three groups: Group-I: Patients without functional loss (EDSS 0 to 1.5) (n = 14), Group-II: Patients with functional loss (EDSS 2 to 3) (n = 17) and Group-III: Healthy subjects (n = 13). Electromyographic activity of the bilateral tibialis anterior (TA) and gastrocnemius medialis (GM) and COPap displacement were recorded during the postural phase of GI. Additionally, spatiotemporal parameters were recorded within the first three steps, and the coefficient of variation was calculated with 40 walks for variability. RESULTS: There were significant differences in the Kruskal-Wallis tests of variables (p<0.05). Group-I demonstrated smaller APAs magnitudes in TA [stance (p = 0.01), swing (p = 0.01)], GM of swing limb (p<0.0001), and smaller COPap displacement (p<0.0001) compared to group-III. Group-II demonstrated smaller APAs magnitudes in all muscles (p<0.0001) compared to group-III and the smallest COPap displacement (p<0.0001). Group-I showed a significant increase in stride width variability compared to group-III (p = 0.01). Group-II showed a significant increase in several variabilities [first stride length (p<0.0001), second stride time (p<0.0001), first double support time (p<0.0001), stride width (p<0.0001)] compared to group-III. CONCLUSION: Patients in the early stage of MS had impairment in both the postural and locomotor phases of GI with more obvious in the patients with functional loss. The results indicate that MS patients without functional loss have difficulty initiating gait. Although there is no functional loss, the patients have a risk of falls, postural instability, and gait impairment due to their inability to initiate gait effectively. As a result, rehabilitation is necessary even if there is no functional loss in patients with MS.
 Neural stem and precursor cells (NPCs) build and regenerate the central nervous system (CNS) by maintaining their pool (self-renewal) and differentiating into neurons, astrocytes, and oligodendrocytes (multipotency) throughout life. This has inspired research into pro-regenerative therapies that utilize transplantation of exogenous NPCs or recruitment of endogenous adult NPCs for CNS regeneration and repair. Recent advances in single-cell RNA sequencing and other "omics" have revealed that NPCs express not just traditional progenitor-related genes, but also genes involved in immune function. Here, we review how NPCs exert immunomodulatory function by regulating the biology of microglia, immune cells that are present in NPC niches and throughout the CNS. We discuss the role of transplanted and endogenous NPCs in regulating microglia fates, such as survival, proliferation, migration, phagocytosis and activation, in the developing, injured and degenerating CNS. We also provide a literature review on NPC-specific mediators that are responsible for modulating microglia biology. Our review highlights the immunomodulatory properties of NPCs and the significance of these findings in the context of designing pro-regenerative therapies for degenerating and diseased CNS.
 Recombinant antibody fragments are promising alternatives to full-length immunoglobulins, creating big opportunities for the pharmaceutical industry. Nowadays, antibody fragments such as antigen-binding fragments (Fab), single-chain fragment variable (scFv), single-domain antibodies (sdAbs), and bispecific antibodies (bsAbs) are being evaluated as diagnostics or therapeutics in pre-clinical models and in clinical trials. Immunotherapy approaches, including passive transfer of protective antibodies, have shown therapeutic efficacy in several animal models of Alzheimer ́s disease(AD), Parkinson ́s disease (PD), frontotemporal dementia (FTD), Huntington ́s disease (HD), transmissible spongiform encephalopathies (TSEs) and multiple sclerosis (MS). There are various antibodies approved by the Food and Drug Administration (FDA) for treating multiple sclerosis and two amyloid beta-specific humanized antibodies, Aducanumab and Lecanemab, for AD. Our previous review summarized data on recombinant antibodies evaluated in pre-clinical models for immunotherapy of neurodegenerative diseases. Here, we explore recent studies in this fascinating research field, give an update on new preventive and therapeutic applications of recombinant antibody fragments for neurological disorders and discuss the potential of antibody fragments for developing novel approaches for crossing the blood-brain barrier (BBB) and targeting cells and molecules of interest in the brain.
 Air pollution is recognized as a significant public health problem and is associated with illnesses of the central nervous system (CNS) as well as neuroinflammation and neuropathology. Air pollution may cause chronic brain inflammation, white matter abnormalities, and microglia activation, which increases the risk of autism spectrum disorders, neurodegenerative disorders, stroke, and multiple sclerosis (MS). Methods: A literature review was done on "PubMed, EMBASE and Web of Science" on the relationship of air pollution with MS and stroke, using the keywords "air pollution" OR "pollution"; "ambient air pollution," "particulate matter, ozone, black carbon" AND "stroke" OR "cerebrovascular diseases," "multiple sclerosis," "neuroinflammation," or "neurodegeneration." Results: We first identified 128 articles and their related websites, of which 44 articles were further selected for analysis mainly based on study relevance, study quality and reliability, and date of publication. Further studies on air pollution and its adverse effects on the CNS are needed. The findings of such studies will support the development of appropriate preventive measures in the future.
 A 44-year-old female patient with multiple sclerosis (MS) treated with ocrelizumab was hospitalized with SARS-CoV-2 pneumonia three times over the course of five months, eventually expiring. Viral sequencing of samples from her first and last admissions suggests a single persistent SARS-CoV-2 infection. We hypothesize that her immunocompromised state, due to MS treatment with an immunosuppressive monoclonal antibody, prevented her from achieving viral clearance.
 In this study, the researchers aimed to investigate the effects of pelvic floor muscle training (PFMT) applied with telerehabilitation on urinary symptoms, quality of life, and subjective perception of improvement and satisfaction in multiple sclerosis (MS) patients having lower urinary tract symptoms. Patients were randomly divided into PFMT (n:21) and control (n:21) groups. The PFMT group received PFMT via telerehabilitation for 8 weeks and lifestyle advice, while the control group received only lifestyle advice. Although lifestyle advice alone was not effective, PFMT applied with telerehabilitation was an effective method in the management of lower urinary tract symptoms in MS patients. PFMT applied with telerehabilitation can be considered as an alternative method.
 BACKGROUND AND OBJECTIVE: Reports of fundus fluorescein angiography (FFA) in active multiple sclerosis (MS) have shown peripheral perivenous sheathing. We sought to assess the feasibility of ultra-widefield (UWF) FFA and optical coherence tomography (OCT) in assessing the peripheral retina in MS. MATERIALS AND METHODS: Participants with MS and healthy controls underwent bilateral UWF fundus photography and FFA. Swept-source OCTs were captured centrally, peripherally, and to delineate any abnormalities visualized. RESULTS: We recruited five people with relapsing remitting MS, with a mean age of 36.9 (± 9.9), mean disease duration of 11 years (± 6.3), and a median expanded disability status score of 0.75 (0 to 2.5). In all MS participants, the disease was not active clinically or radiologically. Using UWF-FFA and OCT, we did not detect clear evidence of peripheral retinal abnormalities, which is consistent with the participants having inactive MS. CONCLUSION: A pilot study using UWF-FFA and peripheral OCT to examine the retina in MS suggests that it may be useful to perform a larger prospective longitudinal study to establish its potential as a monitor of disease activity. [Ophthalmic Surg Lasers Imaging Retina 2023;54:xx-xx.].
 The influence of environmental factors on the development of autoimmune disease is being broadly investigated to better understand the multifactorial nature of autoimmune pathogenesis and to identify potential areas of intervention. Areas of particular interest include the influence of lifestyle, nutrition, and vitamin deficiencies on autoimmunity and chronic inflammation. In this review, we discuss how particular lifestyles and dietary patterns may contribute to or modulate autoimmunity. We explored this concept through a spectrum of several autoimmune diseases including Multiple Sclerosis (MS), Systemic Lupus Erythematosus (SLE) and Alopecia Areata (AA) affecting the central nervous system, whole body, and the hair follicles, respectively. A clear commonality between the autoimmune conditions of interest here is low Vitamin D, a well-researched hormone in the context of autoimmunity with pleiotropic immunomodulatory and anti-inflammatory effects. While low levels are often correlated with disease activity and progression in MS and AA, the relationship is less clear in SLE. Despite strong associations with autoimmunity, we lack conclusive evidence which elucidates its role in contributing to pathogenesis or simply as a result of chronic inflammation. In a similar vein, other vitamins impacting the development and course of these diseases are explored in this review, and overall diet and lifestyle. Recent work exploring the effects of dietary interventions on MS showed that a balanced diet was linked to improvement in clinical parameters, comorbid conditions, and overall quality of life for patients. In patients with MS, SLE and AA, certain diets and supplements are linked to lower incidence and improved symptoms. Conversely, obesity during adolescence was linked with higher incidence of MS while in SLE it was associated with organ damage. Autoimmunity is thought to emerge from the complex interplay between environmental factors and genetic background. Although the scope of this review focuses on environmental factors, it is imperative to elaborate the interaction between genetic susceptibility and environment due to the multifactorial origin of these disease. Here, we offer a comprehensive review about the influence of recent environmental and lifestyle factors on these autoimmune diseases and potential translation into therapeutic interventions.
 INTRODUCTION: Fatigue is the most common and disabling symptom in multiple sclerosis (MS), being reported by 55% to 78% of patients with multiple sclerosis (PwMS). Etiology of MS-related fatigue remains poorly understood but an increased neuromuscular fatigability (i.e., greater loss of torque during exercise) could contribute to this phenomenon. This study aims to characterize the correlates of MS-related fatigue in PwMS using a comprehensive group of physiological and psychosocial measures, with a particular focus on fatigability. METHODS: Forty-two relapsing-remitting PwMS and 20 healthy subjects (HS) were recruited. PwMS were assigned in two groups (high [HF] and low [LF] fatigue) based on two fatigue questionnaires (Fatigue Severity Scale and Modified Fatigue Impact Scale). The main outcomes of this study are derived from incremental cycling completed to task failure (i.e., inability to pedal around 60 rotations per minute). Maximal voluntary contraction (MVC), rating of perceived exertion (RPE), central and peripheral parameters measured using transcranial magnetic and peripheral nerve stimulation were assessed in the knee extensor muscles before, during and after the fatiguing task. Other potential correlates of fatigue were also tested. RESULTS: MVC torque decreased to greater extent for the HF group than LF group after the third common stage of the incremental fatiguing exercise (-15.7 ± 6.6 % vs -5.9 ± 13.0 %, p < 0.05), and this occurred concurrently with a higher RPE for HF (11.8 ± 2.5 vs 9.3 ± 2.6, p < 0.05). Subjective parameters (depression, quality of life) were worse for HF compared to LF and HS (p < 0.001). Moreover, MVC torque loss at the final common stage and maximal heart rate explained 29% of the variance of the MFIS. CONCLUSIONS: These results provide novel insight into the relationship between MS-related fatigue and fatigability among PwMS. HF group exhibited greater performance fatigability, likely contributing to a higher perceived exertion than LF when measured during a dynamic task.
 Background and objective: Multiple sclerosis is a chronic neurological disease causing debilitating physical symptoms and a reduced quality of life, which incurs staggering costs of treatment not only to patients and their family but also to the healthcare system. Thus, getting familiar with the prevalence of this disease is considered essential for developing screening programs. Method:This is a descriptive analytical cross-sectional study. Samples were chosen via the census sampling method. The investigation was based on data provided by the unit of special diseases of Kermanshah University of Medical Sciences. Data were collected via a predesigned checklist and further analyzed by SPSS 24 software. Results:A total of 1426 patients who developed MS between 2009 and 2019 and had archived medical files in the center of special diseases of Kermanshah medical sciences were studied. Among all MS participants, the ratio of female to male participants was 1.5:1, and 52.14% (n=747) of all studied patients were persons aged over 60 years. Discussion and conclusion:Based on our findings and patients' data provided by the center of special diseases of Kermanshah University of Medical Sciences, it can be stated that Kermanshah is one of the regions with a high prevalence of MS. This necessitates intervention by the healthcare system of Kermanshah province for screening and controlling the disease.
 Retinal layer thickness is an important bio-marker for people with multiple sclerosis (PwMS). In clinical practice, retinal layer thickness changes in optical coherence tomography (OCT) are widely used for monitoring multiple sclerosis (MS) progression. Recent developments in automated retinal layer segmentation algorithms allow cohort-level retina thinning to be observed in a large study of PwMS. However, variability in these results make it difficult to identify patient-level trends; this prevents patient specific disease monitoring and treatment planning using OCT. Deep learning based retinal layer segmentation algorithms have achieved state-of-the-art accuracy, but the segmentation is performed on each individual scan without utilizing longitudinal information, which can be important in reducing segmentation error and reveal subtle changes in retinal layers. In this paper, we propose a longitudinal OCT segmentation network which achieves more accurate and consistent layer thickness measurements for PwMS.
 Brain morphometric alterations involve multiple brain regions on progression of the disease in multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) and exhibit age-related degenerative changes during the pathological aging. Recent advance in brain morphometry as measured using MRI have leveraged Person-Based Similarity Index (PBSI) approach to assess the extent of within-diagnosis similarity or heterogeneity of brain neuroanatomical profiles between individuals of healthy populations and validate in neuropsychiatric disorders. Brain morphometric changes throughout the lifespan would be invaluable for understanding regional variability of age-related structural degeneration and the substrate of inflammatory demyelinating disease. Here, we aimed to quantify the neuroanatomical profiles with PBSI measures of cortical thickness (CT) and subcortical volumes (SV) in 263 MS, 207 NMOSD, and 338 healthy controls (HC) from six separate central datasets (aged 11-80). We explored the between-group comparisons of PBSI measures, as well as the advancing age and sex effects on PBSI measures. Compared to NMOSD, MS showed a lower extent of within-diagnosis similarity. Significant differences in regional contributions to PBSI score were observed in 29 brain regions between MS and NMOSD (P < 0.05/164, Bonferroni corrected), of which bilateral cerebellum in MS and bilateral parahippocampal gyrus in NMOSD represented the highest divergence between the two patient groups, with a high similarity effect within each group. The PBSI scores were generally lower with advancing age, but their associations showed different patterns depending on the age range. For MS, CT profiles were significantly negatively correlated with age until the early 30 s (ρ = -0.265, P = 0.030), while for NMOSD, SV profiles were significantly negatively correlated with age with 51 year-old and older (ρ = -0.365, P = 0.008). The current study suggests that PBSI approach could be used to quantify the variation in brain morphometric changes in CNS inflammatory demyelinating disease, and exhibited a greater neuroanatomical heterogeneity pattern in MS compared with NMOSD. Our results reveal that, as an MR marker, PBSI may be sensitive to distribute the disease-associated grey matter diversity and complexity. Disease-driven production of regionally selective and age stage-dependency changes in the neuroanatomical profile of MS and NMOSD should be considered to facilitate the prediction of clinical outcomes and assessment of treatment responses.
 BACKGROUND: Cladribine belongs to the group of disease-modifying therapies (DMTs) used to treat multiple sclerosis (MS). According to the highlights of a meeting held by the Pharmacovigilance Risk Assessment Committee (PRAC) on 14 January 2022, cladribine may be associated with the occurrence of liver injury, and thus liver function monitoring is recommended. OBJECTIVES AND METHODS: Using data from the European spontaneous reporting database (EudraVigilance-EV), we aimed to describe the main characteristics of Individual Case Safety Reports (ICSRs) reporting cases of hepatobiliary disorders related to cladribine. The reporting odds ratio (ROR) was calculated to provide the probability of reporting hepatobiliary ICSRs among DMTs used to treat MS. RESULTS: Overall, 118 ICSRs described the occurrence of cladribine-induced hepatobiliary ADRs. The majority of the ICSRs reported ADRs that were classified as serious (93%), and the outcome was mostly reported as "unknown" (50.8%). The most reported hepatobiliary disorders were drug-induced liver injury, abnormal hepatic function, ALT increases, liver disorders, hepatic failure, jaundice, lymphocyte count decreases, hepatotoxicity and hypertransaminasemia. The majority of cladribine-induced hepatic ADRs occurred in female patients belonging to the age group of 18-65 years. CONCLUSION: Considering the seriousness of cladribine-induced hepatic ADRs, a close monitoring of patients receiving this drug is highly recommended. In this context, further pharmacovigilance studies evaluating the hepatic safety profile of cladribine are strongly needed.
 OBJECTIVES: Ocrelizumab demonstrated significant clinical benefit for the treatment of relapsing (RMS) and primary progressive (PPMS) multiple sclerosis (MS), an incurable disease characterized by disability progression. This study evaluated the clinical and economic impact of ocrelizumab relative to current clinical practice, including other disease-modifying therapies (DMT), available in Portugal. METHODS: Markov models for MS were adapted to estimate the impact of ocrelizumab across three patient populations: treatment-naïve RMS, previously treated RMS, and PPMS. Health states were defined according to the Expanded Disability Status Scale. For RMS, the model further captured the occurrence of relapses and progression to secondary progressive multiple sclerosis (SPMS). A lifetime time-horizon and Portuguese societal perspective were adopted. RESULTS: For RMS patients, ocrelizumab was estimated to maximize the expected time (years) without progression to SPMS (10.50) relative to natalizumab (10.10), dimethyl fumarate (8.64), teriflunomide (8.39), fingolimod (8.38), interferon β-1a (8.33) and glatiramer acetate (8.18). As the most effective option, with quality-adjusted life year (QALY) gains between 0.3 and 1.2, ocrelizumab was found to be cost-saving relative to natalizumab and fingolimod, and presented incremental cost-effectiveness ratios (ICER) below €16,720/QALY relative to the remaining DMT. For PPMS patients, the ICER of ocrelizumab versus best supportive care was estimated at €78,858/QALY. CONCLUSIONS: Ocrelizumab provides important health benefits for RMS and PPMS patients, comparing favourably with other widely used therapies. In RMS, ocrelizumab was revealed to be either cost-saving or have costs-per-QALY likely below commonly accepted cost-effectiveness thresholds. In PPMS, ocrelizumab fills a clear clinical gap in the current clinical practice. Overall, ocrelizumab is expected to provide good value for money in addressing the need of MS patients.
 BACKGROUND: Disease-modifying therapies (DMTs) in multiple sclerosis (MS) can be classified according to the efficacy in which they prevent inflammatory activity. To date, there are limited data regarding the use of high-efficacy treatments (HETs) in Latin America (LATAM). We aimed to analyze the use of HETs in Argentina, focusing on the clinical and sociodemographic characteristics of the patients who use these treatments and the changes in the trend of use over the years. METHODS: A retrospective cohort study was done using the Argentina MS patient registry, RelevarEM. Patients diagnosed with relapsing-remitting MS (RRMS) according to validated diagnostic criteria and under treatment with natalizumab, alemtuzumab, cladribine, rituximab or ocrelizumab were included. RESULTS: Out of 2450 RRMS patients under a DMT, 462 (19%) were on HETs. One third of those patients (35%) received HETs as the first treatment. The most frequent reason for switching to HETs was treatment failure to previous DMT (77%). The time from MS diagnosis to the first HET in treatment-naive patients was less than one year (IQR: 0-1 year) and in treatment-experienced patients it was 5 years (IQR: 3-9 years). Between 2015 and 2017 (P1), 729 patients included in RelevarEM started a new treatment, of which 85 (11.65%) were HETs. Between 2018 and 2020 (P2), 961 patients included in RelevarEM started a new treatment, of which 284 (29.55%) were HETs. When comparing P2 with P1, a significant increase in the use of HETs was observed (p < 0.01). The most frequently used HETs were alemtuzumab (50.59%) in P1, and cladribine (45.20%) in P2. CONCLUSION: The demographic and clinical characteristics of patients under HET in Argentina were identified. Based on a real-world setting, we found a significant trend towards and a rapid increase in the use of HETs in clinical practice in patients with RRMS.
 IMPORTANCE: There is a lack of validated biomarkers for disability progression independent of relapse activity (PIRA) in multiple sclerosis (MS). OBJECTIVE: To determine how serum glial fibrillary acidic protein (sGFAP) and serum neurofilament light chain (sNfL) correlate with features of disease progression vs acute focal inflammation in MS and how they can prognosticate disease progression. DESIGN, SETTING, AND PARTICIPANTS: Data were acquired in the longitudinal Swiss MS cohort (SMSC; a consortium of tertiary referral hospitals) from January 1, 2012, to October 20, 2022. The SMSC is a prospective, multicenter study performed in 8 centers in Switzerland. For this nested study, participants had to meet the following inclusion criteria: cohort 1, patients with MS and either stable or worsening disability and similar baseline Expanded Disability Status Scale scores with no relapses during the entire follow-up; and cohort 2, all SMSC study patients who had initiated and continued B-cell-depleting treatment (ie, ocrelizumab or rituximab). EXPOSURES: Patients received standard immunotherapies or were untreated. MAIN OUTCOMES AND MEASURES: In cohort 1, sGFAP and sNfL levels were measured longitudinally using Simoa assays. Healthy control samples served as the reference. In cohort 2, sGFAP and sNfL levels were determined cross-sectionally. RESULTS: This study included a total of 355 patients (103 [29.0%] in cohort 1: median [IQR] age, 42.1 [33.2-47.6] years; 73 female patients [70.9%]; and 252 [71.0%] in cohort 2: median [IQR] age, 44.3 [33.3-54.7] years; 156 female patients [61.9%]) and 259 healthy controls with a median [IQR] age of 44.3 [36.3-52.3] years and 177 female individuals (68.3%). sGFAP levels in controls increased as a function of age (1.5% per year; P < .001), were inversely correlated with BMI (-1.1% per BMI unit; P = .01), and were 14.9% higher in women than in men (P = .004). In cohort 1, patients with worsening progressive MS showed 50.9% higher sGFAP levels compared with those with stable MS after additional sNfL adjustment, whereas the 25% increase of sNfL disappeared after additional sGFAP adjustment. Higher sGFAP at baseline was associated with accelerated gray matter brain volume loss (per doubling: 0.24% per year; P < .001) but not white matter loss. sGFAP levels remained unchanged during disease exacerbations vs remission phases. In cohort 2, median (IQR) sGFAP z scores were higher in patients developing future confirmed disability worsening compared with those with stable disability (1.94 [0.36-2.23] vs 0.71 [-0.13 to 1.73]; P = .002); this was not significant for sNfL. However, the combined elevation of z scores of both biomarkers resulted in a 4- to 5-fold increased risk of confirmed disability worsening (hazard ratio [HR], 4.09; 95% CI, 2.04-8.18; P < .001) and PIRA (HR, 4.71; 95% CI, 2.05-9.77; P < .001). CONCLUSIONS AND RELEVANCE: Results of this cohort study suggest that sGFAP is a prognostic biomarker for future PIRA and revealed its complementary potential next to sNfL. sGFAP may serve as a useful biomarker for disease progression in MS in individual patient management and drug development.
 BACKGROUND: CombiRx was a randomized, double-blind, placebo-controlled phase 3 trial in treatment-naive relapsing-remitting multiple sclerosis (RRMS) patients randomized to intramuscular interferon beta-1a (IM IFN beta-1a), glatiramer acetate (GA), or both therapies. OBJECTIVE: This analysis investigated changes in serum neurofilament light-chain (sNfL) levels in response to treatment and assessed baseline sNfL as a predictor of relapse. METHODS: RRMS patients treated with IM IFN beta-1a 30 µg weekly + placebo (n = 159), GA 20 mg/mL daily + placebo (n = 172), or IM IFN beta-1a + GA (n = 344) were included. A linear mixed model compared sNfL values over time. Cox regression models analyzed baseline sNfL and gadolinium-enhancing (Gd+) lesions as predictors of relapse. RESULTS: In all treatment arms, the proportion of patients with sNfL ≥16 pg/mL decreased significantly from baseline to 6 months and was maintained at 36 months. A significantly higher percentage of patients with both baseline sNfL ≥16 pg/mL and ≥1 Gd+ lesion experienced relapses within 90 days compared to patients with sNfL <16 pg/mL and/or no Gd+ lesions. CONCLUSION: sNfL levels were reduced within 6 months and remained low at 36 months. Results suggest that the combination of lesion activity and sNfL was a stronger predictor of relapse than either factor alone.
 Disability accrual is mainly driven by progression independent of relapse activity, which is present even in early stages of relapsing-remitting multiple sclerosis (RRMS) and sometimes overlooked. This multicenter, non-interventional study evaluated whether patient-reported outcomes measures (PROMs) could capture disability in 189 early-stage RRMS patients (mean age: 36.1 ± 9.4 years, 71.4% female, mean disease duration: 1.4 ± 0.8 years, median EDSS: 1.0). The 9-Hole Peg Test (9-HPT), NeuroQoL Upper Extremity (NeuroQoL-UE), Timed 25-Foot Walk (T25-FW), Multiple Sclerosis Walking Scale (MSWS-12), Symbol Digit Modalities Test (SDMT), and Perceived Deficits Questionnaire (PDQ-5) were used to assess hand function, gait, and cognition, respectively. These functions were at least mildly affected in this early-stage population, finding significant correlations between PROMs and clinical assessments. PROMs could enable early-stage RRMS patients to communicate their perceived disability in different domains, assisting clinicians in disease monitoring and decision making.
 Myelination depends on the maintenance of oligodendrocytes that arise from oligodendrocyte precursor cells (OPCs). We show that OPC-specific proliferation, morphology, and BMAL1 are time-of-day dependent. Knockout of Bmal1 in mouse OPCs during development disrupts the expression of genes associated with circadian rhythms, proliferation, density, morphology, and migration, leading to changes in OPC dynamics in a spatiotemporal manner. Furthermore, these deficits translate into thinner myelin, dysregulated cognitive and motor functions, and sleep fragmentation. OPC-specific Bmal1 loss in adulthood does not alter OPC density at baseline but impairs the remyelination of a demyelinated lesion driven by changes in OPC morphology and migration. Lastly, we show that sleep fragmentation is associated with increased prevalence of the demyelinating disorder multiple sclerosis (MS), suggesting a link between MS and sleep that requires further investigation. These findings have broad mechanistic and therapeutic implications for brain disorders that include both myelin and sleep phenotypes.
 Fampridine (dalfampridine) is used to improve walking in people who have multiple sclerosis (a disease in which the nerves do not function properly and may cause weakness, numbness, loss of muscle coordination and problems with vision, speech and bladder control). Measurement of fampridine plasma concentrations is not practical at sites lacking the facilities to prepare and process blood samples. A dried blood spot (DBS) sampling method, in which a few drops of blood, drawn by lancet from the finger, are applied onto specially manufactured absorbent filter paper, can be used as an alternative to plasma monitoring and would allow for simplified sample storage and transport. Using blood samples from pharmacokinetic studies, an ultra-high performance liquid chromatography assay method for quantification of fampridine in DBS is developed and validated for specificity, selectivity, accuracy, precision, reproducibility and stability. Method was specific and selective relative to endogenous compounds, with required process efficiency, and no matrix effect. Inaccuracy and precision for intra-day and inter-day analyses were tested at all concentrations. Quantification of fampridine in DBS assay was not affected by blood deposit volume and punch position within spot, and hematocrit level had a limited but acceptable effect on measurement accuracy. Fampridine was stable for at least 2 months at room temperature. The correlation between DBS and plasma concentrations with an average blood-to-plasma ratio is determined. DBS sampling is a simple and practical method for monitoring fampridine concentrations. The method is completely validated as per ICH guidelines and extended to the in vivo determination of fampridine in male albino rats.
 BACKGROUND AND PURPOSE: Data on disease-modifying therapy (DMT) exposure throughout pregnancy in patients with multiple sclerosis are scarce. In this analysis, we assessed pregnancy and fetal outcomes following maternal glatiramer acetate (GA) exposure in all three trimesters among cases reported between 1997 and 2020. METHODS: Pregnancy reports of maternal in utero exposure to 20 and 40 mg/mL GA in all three trimesters from 1997 to 2020 were eligible. Both prospective pregnancy data, reported prior to knowledge of pregnancy outcome, and retrospective data were included. The primary endpoint was major congenital malformations (MCMs) based on the European Surveillance of Congenital Anomalies and Twins (EUROCAT) classification. Additional endpoints included fetal death, preterm birth, and low birth weight. The MCM rate was compared to the EUROCAT background rate. RESULTS: A total of 618 GA-exposed pregnancies in all three trimesters resulted in 634 fetuses, including 14 twin pregnancies. One fetal death was reported. All 414 fetuses with data reported prior to knowledge of pregnancy outcome (prospective data) were live births and no fetal death was reported. Preterm birth was reported in 23/213 (10.8%) pregnancies with known gestational age. Low birth weight was reported in 13/203 (6.4%) infants with known birth weight. The prevalence of MCM in prospective live births ranged from 2.2% to 2.4%, which was similar to background rates (2.1%-3.0%). The frequency of these pregnancy and infant outcomes was comparable across GA doses. CONCLUSIONS: In utero exposure to 20 and 40 mg/mL GA in three trimesters of pregnancy does not appear to be related to adverse pregnancy or infant outcomes.
 BACKGROUND: Monoaminergic network dysfunction may have a role in multiple sclerosis (MS) fatigue pathogenesis. OBJECTIVE: To investigate modifications of fatigue severity and resting state (RS) functional connectivity (FC) in monoaminergic networks of 45 fatigued MS patients after different symptomatic treatments. METHODS: Patients were randomly, blindly assigned to fampridine (n = 15), amantadine (n = 15) or placebo (n = 15) treatment and underwent clinical and 3T-MRI evaluations at baseline (t0) and week 4 (w4), i.e. after four weeks of treatment. Fifteen healthy controls (HC) were enrolled. Dopamine-, noradrenaline- and serotonin-related RS FC was assessed by PET-guided constrained independent component analysis. RESULTS: At t0, MS patients showed widespread monoamine-related RS FC abnormalities. At w4, fatigue scores decreased in all groups (p = range < 0.001-0.002). Concomitantly, fampridine and amantadine patients showed increased insular RS FC in dopamine-related and noradrenaline-related networks (p < 0.001, uncorrected). Amantadine patients also showed increased RS FC of anterior cingulate cortex in dopamine-related and noradrenaline-related networks (p < 0.001, uncorrected). Placebo patients showed increased precuneus/middle cingulate RS FC in the noradrenaline-related network (p < 0.001, uncorrected). In fampridine and placebo patients, just tendencies towards correlations between RS FC and fatigue modifications were found. CONCLUSIONS: In MS patients, specific RS FC modifications in PET-guided monoaminergic networks were observed, concomitantly with fatigue improvements following treatment. TRIAL REGISTRATION NUMBER: EudraCT 2010-023678-38.
 The neuroprotective role of 5-hydroxymethyl-2-furfural (5-HMF) has been demonstrated in a variety of neurological diseases. The aim of this study is to investigate the effect of 5-HMF on multiple sclerosis (MS). IFN-γ-stimulated murine microglia (BV2 cells) are considered a cell model of MS. With 5-HMF treatment, microglial M1/2 polarization and cytokine levels are detected. The interaction of 5-HMF with migration inhibitory factor (MIF) is predicted using online databases. The experimental autoimmune encephalomyelitis (EAE) mouse model is established, followed by a 5-HMF injection. The results show that 5-HMF facilitates IFN-γ-stimulated microglial M2 polarization and attenuates the inflammatory response. According to the network pharmacology and molecular docking results, 5-HMF has a binding site for MIF. Further results show that blocking MIF activity or silencing CD74 enhances microglial M2 polarization, reduces inflammatory activity, and prevents ERK1/2 phosphorylation. 5-HMF inhibits the MIF-CD74 interaction by binding to MIF, thereby inhibiting microglial M1 polarization and enhancing the anti-inflammatory response. 5-HMF ameliorates EAE, inflammation, and demyelination in vivo. In conclusion, our research indicates that 5-HMF promotes microglial M2 polarization by inhibiting the MIF-CD74 interaction, thereby attenuating inflammation and demyelination in EAE mice.
 Neurological disorders are the major cause of disability, leading to a decrease in quality of life by impairing cognitive, sensorimotor, and motor functioning. Several factors have been proposed in the pathogenesis of neurobehavioral changes, including nutritional, environmental, and genetic predisposition. Vitamin D (VD) is an environmental and nutritional factor that is widely distributed in the central nervous system's subcortical grey matter, neurons of the substantia nigra, hippocampus, thalamus, and hypothalamus. It is implicated in the regulation of several brain functions by preserving neuronal structures. It is a hormone rather than a nutritional vitamin that exerts a regulatory role in the pathophysiology of several neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and multiple sclerosis. A growing body of epidemiological evidence suggests that VD is critical in neuronal development and shows neuroprotective effects by influencing the production and release of neurotrophins, antioxidants, immunomodulatory, regulation of intracellular calcium balance, and direct effect on the growth and differentiation of nerve cells. This review provides up-to-date and comprehensive information on vitamin D deficiency, risk factors, and clinical and preclinical evidence on its relationship with neurological disorders. Furthermore, this review provides mechanistic insight into the implications of vitamin D and its deficiency on the pathogenesis of neurological disorders. Thus, an understanding of the crucial role of vitamin D in the neurobiology of neurodegenerative disorders can assist in the better management of vitamin D-deficient individuals.
 INTRODUCTION: Machine learning (ML) is an established technique that uses sets of training data to develop algorithms and perform data classification without using human intervention/supervision. This study aims to determine how functional and anatomical brain connectivity (FC and SC) data can be used to classify voiding dysfunction (VD) in female MS patients using ML. METHODS: Twenty-seven ambulatory MS individuals with lower urinary tract dysfunction were recruited and divided into two groups (Group 1: voiders [V, n = 14]; Group 2: VD [n = 13]). All patients underwent concurrent functional MRI/urodynamics testing. RESULTS: Best-performing ML algorithms, with highest area under the curve (AUC), were partial least squares (PLS, AUC = 0.86) using FC alone and random forest (RF) when using SC alone (AUC = 0.93) and combined (AUC = 0.96) as inputs. Our results show 10 predictors with the highest AUC values were associated with FC, indicating that although white matter was affected, new connections may have formed to preserve voiding initiation. CONCLUSIONS: MS patients with and without VD exhibit distinct brain connectivity patterns when performing a voiding task. Our results demonstrate FC (grey matter) is of higher importance than SC (white matter) for this classification. Knowledge of these centres may help us further phenotype patients to appropriate centrally focused treatments in the future.
 Vitamin D is a secosteroid hormone that is highly involved in bone health. Mounting evidence revealed that, in addition to the regulation of mineral metabolism, vitamin D is implicated in cell proliferation and differentiation, vascular and muscular functions, and metabolic health. Since the discovery of vitamin D receptors in T cells, local production of active vitamin D was demonstrated in most immune cells, addressing the interest in the clinical implications of vitamin D status in immune surveillance against infections and autoimmune/inflammatory diseases. T cells, together with B cells, are seen as the main immune cells involved in autoimmune diseases; however, growing interest is currently focused on immune cells of the innate compartment, such as monocytes, macrophages, dendritic cells, and natural killer cells in the initiation phases of autoimmunity. Here we reviewed recent advances in the onset and regulation of Graves' and Hashimoto's thyroiditis, vitiligo, and multiple sclerosis in relation to the role of innate immune cells and their crosstalk with vitamin D and acquired immune cells.
 Interleukin (IL)-10 is a main player in peripheral immune tolerance, the physiological mechanism preventing immune reactions to self/harmless antigens. Here, we investigate IL-10-induced molecular mechanisms generating tolerogenic dendritic cells (tolDC) from monocytes. Using genomic studies, we show that IL-10 induces a pattern of accessible enhancers exploited by aryl hydrocarbon receptor (AHR) to promote expression of a set of core genes. We demonstrate that AHR activity occurs downstream of IL-10 signaling in myeloid cells and is required for the induction of tolerogenic activities in DC. Analyses of circulating DCs show that IL-10/AHR genomic signature is active in vivo in health. In multiple sclerosis patients, we instead observe significantly altered signature correlating with functional defects and reduced frequencies of IL-10-induced-tolDC in vitro and in vivo. Our studies identify molecular mechanisms controlling tolerogenic activities in human myeloid cells and may help in designing therapies to re-establish immune tolerance.
 BACKGROUND: Cladribine is a useful therapeutic option in RRMS with moderate to high disease activity. Its oral formulation and tolerability make it a useful alternative to infusion therapies. Cladribine is known to deplete CD19(+) B lymphocytes, but its effect on immunoglobulin subsets is unclear. OBJECTIVE: To identify whether cladribine therapy in pwMS reduces immunoglobulin subset levels as a surrogate marker of infection risk. METHODS: A 'real-world' retrospective analysis of 341 pwMS presenting to a single tertiary centre between March 2017 and July 2021. Differences in immunoglobulin levels between cladribine, other disease-modifying therapies and no active treatment were assessed using a univariate ANOVA. RESULTS: Three hundred and forty-one patients had immunoglobulin levels assessed, with 29 patients treated with cladribine. The mean IgG, IgM and IgA levels on cladribine therapy were 10.44 ± 0.40, 0.99 ± 0.09 and 2.04 ± 0.18 g/L respectively. These were not significantly different from patients not on active treatment. There was a statistically significant reduction in IgG and IgM levels for patients treated with ocrelizumab (9.37 ± 0.19 and 0.68 ± 0.04 g/L) and natalizumab (8.72 ± 0.53 and 0.69 ± 0.12 g/L) compared to patients not on treatment. CONCLUSION: Cladribine therapy for RRMS was not associated with immunoglobulin subset deficiencies. This is contrasted to ocrelizumab and natalizumab which demonstrate significant reductions in both IgG and IgM levels.
 INTRODUCTION: Immune medications affect antibody responses to SARS-CoV-2 vaccination in adults with neuroinflammatory disorders, but little is known about antibody responses in children with neuroinflammation and on immune treatments. Here we measure antibody levels in response to SARS-CoV-2 vaccination in children receiving anti-CD20 monoclonal antibodies, or fingolimod. METHODS: Children under 18 years of age with pediatric-onset neuroinflammatory disorders who received at least two mRNA vaccines were included. Plasma samples were assayed for SARS-CoV-2 antibodies (spike, spike receptor binding domain-RBD, nucleocapsid) and neutralization antibodies. RESULTS: Seventeen participants with pediatric onset neuroinflammatory diseases were included: 12 multiple sclerosis, one neuromyelitis optica spectrum disorder, two MOG-associated disease, and two autoimmune encephalitis. Fourteen were on medications (11 on CD20 monoclonal antibodies-mAbs, one on fingolimod, one on steroids, one on intravenous immunoglobulin) and three were untreated. Nine patients also had pre-vaccination samples available. All participants had seropositivity to spike or spike RBD antibodies except for those receiving CD20 mAbs. However, this proportion was higher in children than in an adult MS patient cohort. The most significant contributor to antibody levels was duration of DMT. CONCLUSION: SARS-CoV-2 antibodies are decreased in children on CD20 monoclonal antibodies than on other treatments. Treatment duration associated with vaccination responses.
 BACKGROUND: An association between certain immunomodulatory therapies (rituximab, ipilimumab, and other immune checkpoint inhibitors) and inflammatory (non-ischemic and non-infectious) colitis in oncologic and non-oncologic patient populations is well documented in the medical literature. OBJECTIVE: The purpose of this case series is to describe adverse event reports of new onset, inflammatory colitis in association with ocrelizumab in patients with multiple sclerosis submitted to U.S. Food and Drug Administration (FDA) or published in the medical literature. METHODS: The FDA Adverse Event Reporting System (FAERS) and medical literature were searched. RESULTS: A review of postmarketing cases from FAERS and published medical literature identified 38 cases consistent with inflammatory, non-ischemic, and non-infectious colitis in association with ocrelizumab. The median time-to-onset was 8 months. Cases were reported using the following diagnostic terms: Crohn's disease (13), unspecified colitis (11), microscopic colitis (5), ulcerative colitis (5), medication-induced colitis (3), and autoimmune colitis (2). CONCLUSIONS: This case series highlights ocrelizumab induced immune-mediated colitis that can be clinically severe and potentially life-threatening. Based on the findings of this review, the ocrelizumab Prescribing Information was amended to include immune-mediated colitis in the Warnings and Precautions section.
 Multiple sclerosis (MS) is a chronic neurodegenerative disease that affects the central nervous system (CNS). Currently, MS treatment is limited to several Food and Drug Administration (FDA)- and European Medicines Agency (EMA)-approved medications that slow disease progression by immunomodulatory action. Fingolimod and siponimod have similar mechanisms of action, and consequently, their therapeutic effects may be comparable. However, while fingolimod is mainly used for relapsing-remitting MS (RRMS), siponimod, according to EMA label, is recommended for active secondary progressive MS (SPMS). Clinicians and scientists are analysing whether patients can switch from fingolimod to siponimod and identifying the advantages or disadvantages of such a switch from a therapeutic point of view. In this review, we aim to discuss the therapeutic effects of these two drugs and the advantages/disadvantages of switching treatment from fingolimod to siponimod in patients with the most common forms of MS, RRMS and SPMS.
 The metabolic needs of the premature/premyelinating oligodendrocytes (pre-OLs) and mature oligodendrocytes (OLs) are distinct. The metabolic control of oligodendrocyte maturation from the pre-OLs to the OLs is not fully understood. Here, we show that the terminal maturation and higher mitochondrial respiration in the OLs is an integrated process controlled through pyruvate dehydrogenase complex (Pdh). Combined bioenergetics and metabolic studies show that OLs show elevated mitochondrial respiration than the pre-OLs. Our signaling studies show that the increased mitochondrial respiration activity in the OLs is mediated by the activation of Pdh due to inhibition of the pyruvate dehydrogenase kinase-1 (Pdhk1) that phosphorylates and inhibits Pdh activity. Accordingly, when Pdhk1 is directly expressed in the pre-OLs, they fail to mature into the OLs. While Pdh converts pyruvate into the acetyl-CoA by its oxidative decarboxylation, our study shows that Pdh-dependent acetyl-CoA generation from pyruvate contributes to the acetylation of the bHLH family transcription factor, oligodendrocyte transcription factor 1 (Olig1) which is known to be involved in the OL maturation. Pdh inhibition via direct expression of Pdhk1 in the pre-OLs blocks the Olig1-acetylation and OL maturation. Using the cuprizone model of demyelination, we show that Pdh is deactivated during the demyelination phase, which is however reversed in the remyelination phase upon cuprizone withdrawal. In addition, Pdh activity status correlates with the Olig1-acetylation status in the cuprizone model. Hence, the Pdh metabolic node activation allows a robust mitochondrial respiration and activation of a molecular program necessary for the terminal maturation of oligodendrocytes. Our findings open a new dialogue in the developmental biology that links cellular development and metabolism. These findings have far-reaching implications in the development of therapies for a variety of demyelinating disorders including multiple sclerosis.
 Remyelination failure is considered a major obstacle in treating chronic-progressive multiple sclerosis (MS). Studies have shown blockage in the differentiation of resident oligodendrocyte progenitor cells (OPC) into myelin-forming cells, suggesting that pushing OPC into a differentiation program might be sufficient to overcome remyelination failure. Others stressed the need for a permissive environment to allow proper activation, migration, and differentiation of OPC. PD0325901, a MAPK/ERK inhibitor, was previously shown to induce OPC differentiation, non-specific immunosuppression, and a significant therapeutic effect in acute demyelinating MS models. We examined PD0325901 effects in the chronically inflamed central nervous system. Treatment with PD0325901 induced OPC differentiation into mature oligodendrocytes with high morphological complexity. However, treatment of Biozzi mice with chronic-progressive experimental autoimmune encephalomyelitis with PD0325901 showed no clinical improvement in comparison to the control group, no reduction in demyelination, nor induction of OPC migration into foci of demyelination. PD0325901 induced a direct general immunosuppressive effect on various cell populations, leading to a diminished phagocytic capability of microglia and less activation of lymph-node cells. It also significantly impaired the immune-modulatory functions of OPC. Our findings suggest OPC regenerative function depends on a permissive environment, which may include pro-regenerative inflammatory elements. Furthermore, they indicate that maintaining a delicate balance between the pro-myelinating and immune functions of OPC is of importance. Thus, the highly complex mission of creating a pro-regenerative environment depends upon an appropriate immune response controlled in time, place, and intensity. We suggest the need to employ a multi-systematic therapeutic approach, which cannot be achieved through a single molecule-based therapy.
 BACKGROUND: In high-income countries, four anti-CD20 monoclonal antibodies (mAbs) are used or in the pipeline for relapsing MS: ocrelizumab, ofatumumab (both registered), ublituximab (awaiting registration) and rituximab (off-label). List prices differ significantly between registered and off-label drugs. OBJECTIVE: Comparing differences in benefits between anti-CD20 mAbs from a health-economic and societal perspective. METHODS: To reflect lifetime use of DMTs, we used a treatment-sequence model to compare ocrelizumab/ofatumumab and eight other drug classes in terms of health (lifetime relapses, time to Expanded Disability Status Scale [EDSS] 6, lifetime quality-adjusted life years) and cost-effectiveness (net health benefit). To become cost-effective compared to ocrelizumab, we modelled the list price of ublituximab and desired effect on EDSS progression of rituximab. RESULTS: Although drug sequences with ocrelizumab in first- and second-line were more cost-effective than ofatumumab, our probabilistic analysis suggests this outcome was very uncertain. To be more cost-effective than ocrelizumab, ublituximab needs to be about 25% cheaper whilst rituximab needs to equal the effect on disability progression seen with first-line treatments. CONCLUSIONS: Our model showed no clear difference in cost-effectiveness between ocrelizumab and ofatumumab. Hence, prescribing the least costly anti-CD20 mAb can democratise MS care without a loss in health benefits.
 Cognitive difficulties are reported in up to 60% of people with MS (pwMS). There is often a discrepancy between self-reported cognitive difficulties and performance on cognitive assessments. Some of this discrepancy can be explained by depression and fatigue. Pre-MS cognitive abilities may be another important variable in explaining differences between self-reported and assessed cognitive abilities. PwMS with high estimated premorbid cognitive functioning (ePCF) may notice cognitive difficulties in daily life whilst performing within the average range on cognitive assessments. We hypothesised that, taking into account depression and fatigue, ePCF would predict (1) differences between self-reported and assessed cognitive abilities and (2) performance on cognitive assessments. We explored whether ePCF predicted (3) self-reported cognitive difficulties. Eighty-seven pwMS completed the Test of Premorbid Functioning (TOPF), the Brief International Cognitive Assessment for MS (BICAMS), self-report measures of cognitive difficulty (MS Neuropsychological Questionnaire; MSNQ), fatigue (MS Fatigue Impact Scale; MFIS) and depression (Hospital Anxiety and Depression Scale; HADS). Results revealed that, taking into account covariates, ePCF predicted (1) differences between self-reported and assessed cognitive abilities, p < .001 (model explained 29.35% of variance), and (2) performance on cognitive assessments, p < .001 (model explained 46.00% of variance), but not (3) self-reported cognitive difficulties, p = .545 (model explained 35.10% of variance). These results provide new and unique insights into predictors of the frequently observed discrepancy between self-reported and assessed cognitive abilities for pwMS. These findings have important implications for clinical practice, including the importance of exploring premorbid factors in self-reported experience of cognitive difficulties.
 Multiple sclerosis (MS) is the most prevalent demyelinating disease of the central nervous system, characterized by myelin destruction, axonal degeneration, and progressive loss of neurological functions. Remyelination is considered an axonal protection strategy and may enable functional recovery, but the mechanisms of myelin repair, especially after chronic demyelination, remain poorly understood. Here, we used the cuprizone demyelination mouse model to investigate spatiotemporal characteristics of acute and chronic de- and remyelination and motor functional recovery following chronic demyelination. Extensive remyelination occurred after both the acute and chronic insults, but with less robust glial responses and slower myelin recovery in the chronic phase. Axonal damage was found at the ultrastructural level in the chronically demyelinated corpus callosum and in remyelinated axons in the somatosensory cortex. Unexpectedly, we observed the development of functional motor deficits after chronic remyelination. RNA sequencing of isolated brain regions revealed significantly altered transcripts across the corpus callosum, cortex and hippocampus. Pathway analysis identified selective upregulation of extracellular matrix/collagen pathways and synaptic signaling in the chronically de/remyelinating white matter. Our study demonstrates regional differences of intrinsic reparative mechanisms after a chronic demyelinating insult and suggests a potential link between long-term motor function alterations and continued axonal damage during chronic remyelination. Moreover, the transcriptome dataset of three brain regions and over an extended de/remyelination period provides a valuable platform for a better understanding of the mechanisms of myelin repair as well as the identification of potential targets for effective remyelination and neuroprotection for progressive MS.
 Introduction: A rapid and reliable detection of glial fibrillary acidic protein (GFAP) in biological samples could assist in the diagnostic evaluation of neurodegenerative disorders. Sensitive assays applicable in the routine setting are needed to validate the existing GFAP tests. This study aimed to develop a highly sensitive and clinically applicable microfluidic immunoassay for the measurement of GFAP in blood. Methods: A microfluidic GFAP assay was developed and validated regarding its performance. Subsequently, serum and cerebrospinal fluid (CSF) of Alzheimer's disease (AD), Multiple Sclerosis (MS) and control patients were analyzed with the established assay, and levels were compared to the commercial GFAP Simoa discovery kit. Results: The developed GFAP assay showed a good performance with a recovery of 85% of spiked GFAP in serum and assay variations below 15%. The established assay was highly sensitive with a calculated lower limit of quantification and detection of 7.21 pg/mL and 2.37 pg/mL, respectively. GFAP levels were significantly increased in AD compared to control patients with advanced age (p = 0.002). However, GFAP levels revealed no significant increase in MS compared to control patients in the same age range (p = 0.140). Furthermore, serum GFAP levels evaluated with the novel microfluidic assay strongly correlated with Simoa concentrations (r = 0.88 (95% CI: 0.81-0.93), p < 0.0001). Conclusion: We successfully developed a sensitive and easy-to-use microfluidic assay to measure GFAP in blood. Furthermore, we could confirm previous findings of elevated GFAP levels in AD by applying the assay in a cohort of clinically characterized patients.
 Failure of the immune system to discriminate myelin components from foreign antigens plays a critical role in the pathophysiology of multiple sclerosis. In fact, the appearance of anti-myelin autoantibodies, targeting both proteins and glycolipids, is often responsible for functional alterations in myelin-producing cells in this disease. Nevertheless, some of these antibodies were reported to be beneficial for remyelination. Recombinant human IgM22 (rHIgM22) binds to myelin and to the surface of O4-positive oligodendrocytes, and promotes remyelination in mouse models of chronic demyelination. Interestingly, the identity of the antigen recognized by this antibody remains to be elucidated. The preferential binding of rHIgM22 to sulfatide-positive cells or tissues suggests that sulfatide might be part of the antigen pattern recognized by the antibody, however, cell populations lacking sulfatide expression are also responsive to rHIgM22. Thus, we assessed the binding of rHIgM22 in vitro to purified lipids and lipid extracts from various sources to identify the antigen(s) recognized by this antibody. Our results show that rHIgM22 is indeed able to bind both sulfatide and its deacylated form, whereas no significant binding for other myelin sphingolipids has been detected. Remarkably, binding of rHIgM22 to sulfatide in lipid monolayers can be positively or negatively regulated by the presence of other lipids. Moreover, rHIgM22 also binds to phosphatidylinositol, phosphatidylserine and phosphatidic acid, suggesting that not only sulfatide, but also other membrane lipids might play a role in the binding of rHIgM22 to oligodendrocytes and to other cell types not expressing sulfatide.
 Opportunistic viral infections of the central nervous system represent a significant cause of morbidity and mortality among an increasing number of immunocompromised patients. Since antiviral treatments are usually poorly effective, the prognosis generally relies on the ability to achieve timely immune reconstitution. Hence, strategies aimed at reinvigorating antiviral immune activity have recently emerged. Among these, virus-specific T-cells are increasingly perceived as a principled and valuable tool to treat opportunistic viral infections. Here we briefly discuss how to develop and select virus-specific T-cells, then review their main indications in central nervous system infections, including progressive multifocal leukoencephalopathy, CMV infection, and adenovirus infection. We also discuss their potential interest in the treatment of progressive multiple sclerosis, or EBV-associated central nervous system inflammatory disease. We finish with the key future milestones of this promising treatment strategy.
 Acthar(®) Gel (repository corticotropin injection [RCI]) is a naturally sourced complex mixture of adrenocorticotropic hormone analogs and other pituitary peptides used to treat patients with serious and rare inflammatory and autoimmune conditions. This narrative review summarizes the key clinical and economic findings among 9 indications: infantile spasms (IS), multiple sclerosis (MS) relapses, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), dermatomyositis and polymyositis (DM/PM), ocular inflammatory diseases (primarily uveitis and severe keratitis), symptomatic sarcoidosis, and proteinuria in nephrotic syndrome (NS). Key studies of clinical efficacy and healthcare resource utilization and cost from 1956 to 2022 are discussed. Evidence supports the efficacy of RCI across all 9 indications. RCI is recommended as first-line treatment for IS and is associated with improved outcomes for the other 8 indications, including increased recovery rates in MS relapse; improved disease control in RA, SLE, and DM/PM; real-world effectiveness in patients with uveitis and severe keratitis; improved lung function and reduced corticosteroid use in symptomatic sarcoidosis; and increased rates of partial remission of proteinuria in NS. For many indications, RCI may improve clinical outcomes during exacerbations or when conventional treatments have failed to show a benefit. RCI is also associated with a reduction in the use of biologics, corticosteroids, and disease-modifying antirheumatic drugs. Economic data suggest RCI is a cost-effective, value-based treatment option for MS relapse, RA, and SLE. Other economic benefits have been demonstrated for IS, MS relapses, RA, SLE, and DM/PM, including reduced hospitalizations, lengths of stay, inpatient and outpatient services, and emergency department visits. RCI is considered safe and effective and features economic benefits for numerous indications. Its ability to control relapse and disease activity makes RCI an important nonsteroid treatment option that could help preserve functioning and well-being among patients with inflammatory and autoimmune conditions.
 Although immunodeficient patients are less prone to develop Coronavirus disease 2019 (COVID-19)-mediated cytokine storm, secondary infections can cause serious complications in this vulnerable population. They are more likely to develop opportunistic infections that can mimic the symptoms of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Herein, we presented a 27-year-old male patient of SARS-CoV-2 infection, who was complicated with Pneumocystis jirovecii pneumonia (PJP), following treatment with rituximab. First, he was hospitalized for 5 days with fever, cough, and dyspnea due to COVID-19 infection, and treated with remdesivir and glucocorticoid. Then, he has been referred to our center with cough, dyspnea, body pain, and fever. Due to persistent fever, the progression of pulmonary lesions, and reduced oxygen saturation, we began treatment with piperacillin + tazobactam, vancomycin, and levofloxacin. Nevertheless, the patient's fever did not stop after the aforementioned empiric treatment and his condition got worse and he was admitted to the intensive care unit. The result of BAL fluid, tested for P. jirovecii by RT-PCR, turned out to be positive. Therefore, we started trimethoprim-sulfamethoxazole and dexamethasone, which improved his condition. We hope this article helps clinicians consider causes other than COVID-19, especially opportunistic infections such as PJP, in patients with respiratory symptoms and fever.
 BACKGROUND: Multiple Sclerosis (MS) is a chronic and progressive neurological autoimmune disease currently affecting 250,000 individuals in Germany. Patients suffering from the disease can be severely impaired in their day-to-day activities. BRISA is a digital app specifically designed to help MS patients monitor their disease by regularly tracking symptoms. Lengthy and time-consuming questionnaires for patient-reported outcomes (PRO) are the standard method to assess the patients' current condition. Here, we examine whether simplified versions of these questionnaires can provide comparable information regarding individual symptom presentations in BRISA users. METHODS: 828 users were included in the analysis. Patients who provided onboarding information and answered at least one questionnaire and the corresponding simplified smiley symptoms assessment were included. Correlation of questionnaire and symptom scores was calculated using Pearson's correlation. RESULTS: Our analysis cohort predominantly consisted of female, 26-55-year-olds. Relapsing-remitting MS (RRMS) was the most common MS type recorded. Most patients were diagnosed 2-5 years ago. Questionnaires regarding fatigue and vision impairment were among the most answered, those regarding bowel movement and sexual satisfaction received fewest responses. Overall, the scores from questionnaires and symptoms correlated positively. Scoring correlation could also be shown across the subgroups divided by gender, age groups, type of MS, and time since diagnosis of the disease. CONCLUSION: Scores recorded from traditional PRO questionnaires can be reflected more easily as a trend in a simplified scale using smileys. Nevertheless, traditional questionnaires are needed to also maintain a more objective assessment. In conclusion, the patient will benefit most from an adaptive combination of regular traditional PRO questionnaire assessments and simplified symptom recording.
 BACKGROUND: Real-world evidence on experience and satisfaction of ofatumumab as a treatment option for relapsing multiple sclerosis (RMS) is limited. OBJECTIVE: To present cumulative responses from a questionnaire related to first-hand experience of treating physicians on handling and convenience of ofatumumab therapy along with concerns related to COVID-19. METHODS: PERITIA was a multicentre survey conducted to collect responses from the ASCLEPIOS I/II trial investigators from Europe via an online questionnaire. RESULTS: Forty-six physicians (Germany, n = 14; Spain, n = 12; Portugal, n = 10; Italy, n = 10) completed the survey. Overall, 43% of the physicians considered the benefit-risk ratio of ofatumumab as very good. Over 93% were in favour of ofatumumab self-administration at home and the majority (83%) believed it to be completely true that self-administration of ofatumumab eases the burden for patients in terms of time. All investigators would like to potentially use anti-CD20 therapy as a long-term strategy. Even during the COVID-19 pandemic, physicians were in favour of a self-administration of MS therapy at home over other anti-CD20 therapy infusions. CONCLUSION: European neurologists who were part of this survey considered the benefit-risk-ratio of ofatumumab as favourable and the monthly self-administered subcutaneous injections offering convenience for patients in the clinical practice.
 (1) Background: Early disability accrual in RRMS patients is frequent and is associated with worse long-term prognosis. Correctly identifying the patients that present a high risk of early disability progression is of utmost importance, and may be aided by the use of predictive biomarkers. (2) Methods: We performed a prospective cohort study that included newly diagnosed RRMS patients, with a minimum follow-up period of one year. Biomarker samples were collected at baseline, 3-, 6- and 12-month follow-ups. Disability progression was measured using the EDSS-plus score. (3) Results: A logistic regression model based on baseline and 6-month follow-up sNfL z-scores, RNFL and GCL-IPL thickness and BREMSO score was statistically significant, with χ2(4) = 19.542, p < 0.0001, R2 = 0.791. The model correctly classified 89.1% of cases, with a sensitivity of 80%, a specificity of 93.5%, a positive predictive value of 85.7% and a negative predictive value of 90.62%. (4) Conclusions: Serum biomarkers (adjusted sNfL z-scores at baseline and 6 months) combined with OCT metrics (RNFL and GCL-IPL layer thickness) and the clinical score BREMSO can accurately predict early disability progression using the EDSS-plus score for newly diagnosed RRMS patients.
 BACKGROUND: Multiple sclerosis (MS) is a degenerative disease with typical onset between 20 and 50 years of age. An increase in MS cases has been found in the adolescent US population. Adolescents require fine motor manipulation skills for their functional and academic performance. Deficits in the major components of manipulation skills may result in insufficient function. This study examined the 2-point, 3-point, and lateral pinch strength of adolescents diagnosed as having MS. METHODS: Seventy-four adolescents, 37 with a diagnosis of relapsing-remitting MS and a control group of 37 age-matched peers, participated in this study. Data on 2-point, 3-point, and lateral pinch strength in both hands were collected using a pinch meter. Analyses of covariance were used to describe differences across the 2 groups, and effect sizes (Cohen d) were calculated by finding the mean difference between the study groups divided by the pooled SD. RESULTS: A significant difference was found in the 2-point pinch strength of the right hand of participants with pediatric MS compared with age- and sex-matched control participants. There were no significant differences in 2-point pinch strength of the left hand or in 3-point or lateral pinch strength of the right and left hands. CONCLUSIONS: Pinch grasp strength was differentially affected in adolescents with MS. Pinch strength should be assessed and considered in adolescents with MS for a better understanding of their functional performance of fine motor tasks in activities of daily living and academics.
 Primary hyperparathyroidism (PHPT) often leads to neurological or psychiatric disorders, thus mimicking different diseases. Here we present a 77-years old man visited in the Emergency Department complaining for fatigue, multiple falls, nausea, anorexia, and constipation. Symptoms were rapidly worsening, and on admission he appeared sleepy, responsive to verbal stimulus, disoriented, dehydrated, unable to maintain upright position. He suffered from mild, relapsing and remitting Multiple Sclerosis (MS) since the age of 45, at that moment not requiring treatment. The laboratory tests displayed severe hypercalcemia (16.8 mg/dL), slightly decreased level of serum phosphorus (2.8 mg/dL), very high levels of parathyroid hormone (PTH) (508 pg/mL). A parathyroid mass (35x21x32 mm) in left paratracheal position was found with Computed Tomography (CT) of the neck. After correcting hypercalcemia, he was operated on day 18, thus confirming the parathyroid adenoma, that was successfully removed. One month later, the patient was completely well, and able to walk without any help, like three months before. The lab tests' values obtained during the control visit showed complete normalization of calcium-phosphate metabolism. Diabetes, too, was going better, allowing a reduction in metformin dosage. At the best of our knowledge this is the first described case of a clinically significant overlapping between symptoms due to a long-lasting mild MS and an unrecognized, severe, PHPT. This case underlines the importance of a thorough metabolic evaluation of each patient presenting worsening of his neuromuscular and/or neuropsychiatric condition, even when previously known to be affected by a defined neurologic or psychiatric disease.
 This case illustrates two diagnostic challenges for clinicians: the rarely described sixteen syndrome and the relationship between tumour necrosis factor (TNF)-alpha inhibitors and central demyelination. Sixteen syndrome affects horizontal eye movements and the facial nerve bilaterally reflecting a lesion in the posterior pontine tegmentum, adjacent to the fourth ventricle. Given its rarity and complexity of clinical signs, this syndrome risks misdiagnosis and mismanagement. The relationship between TNF-alpha inhibitors and demyelination is a complex issue in which causality is yet to be established. This diagnostic challenge poses a management dilemma for clinicians.
 BACKGROUND: Attenuation in post-vaccination SARS-CoV-2 humoral responses has been demonstrated in people treated with either anti-CD20 therapies or sphingosine-1-phosphate (S1P) receptor modulators. In the setting of disease modifying therapy (DMT) use, humoral response may not correlate with effective immunity, and analysis of vaccine-mediated SARS-CoV-2-specific memory T-cell responses is crucial. While vaccination in patients treated with anti-CD20 agents leads to deficient antibody production, emerging data from live cell assays suggests intact T-cell responses to vaccination. We evaluated post-vaccination SARS-CoV-2 T-cell receptor (TCR) repertoires in DMT-treated patients using the ImmunoSeq(R) assay, an assay that does not require live cells. METHODS: Adults 18-80 years old without prior COVID-19, with neuroimmune conditions, who had been vaccinated with two doses of Pfizer-BioNTech or Moderna mRNA vaccines at least 3 weeks and up to 6 months prior, were recruited. Whole blood was obtained for immunosequencing, and matched serum was obtained for humoral analysis. Immunosequencing of the CDR3 regions of human TCRβ chains was completed using the immunoSEQR Assay (Adaptive Biotechnologies). TCR sequences were mapped across a set of TCR sequences reactive to SARS-CoV-2. Clonal diversity (breadth) and frequency (depth) of TCRs specific to SARS-CoV-2 spike protein were calculated and relationships with clinical variables were assessed. RESULTS: Forty patients were recruited into the study, aged 25-77, and 27 female. 37 had MS, 2 had neuromyelitis optica spectrum disorder (NMOSD), and 1 had hypophysitis. Subjects treated with anti-CD20 agents and S1P receptor modulators had severely attenuated humoral responses, but SARS-CoV-2-spike-specific TCR clonal depth and breadth were robust across all treatment classes except S1P modulators. No spike-specific or non-spike-specific SARS-CoV-2-associated TCRs were found in those treated with S1P modulators (p = 0.002 for both breadth and depth). Subjects treated with fumarates exhibited somewhat lower spike TCR breadth than subjects treated with other or no DMTs (median 2.27 × 10^-5 for fumarates and 4.96 × 10^-5 for all others, p = 0.008), but no statistically significant difference was demonstrated with spike TCR depth. No other significant associations with DMT type were found. We found no significant correlations between depth or breadth and age, duration of treatment, type of vaccination, or time interval since vaccination. CONCLUSION: This is the first study to characterize post-vaccination SARS-CoV-2 TCR repertoires in DMT-treated individuals. We demonstrated a dichotomous response to SARS-CoV-2 vaccination in anti-CD20-treated patients, with severely attenuated humoral response but intact TCR depth and breadth. It is unclear to what degree each arm of the adaptive immune system impacts post-vaccine immunity, both from the standpoint of incidence of post-vaccine infections and that of infection severity, and further clinical studies are necessary. S1P modulator-treated subjects exhibited both severely attenuated humoral responses and absent spike-specific TCR depth and breadth, information which is crucial for counseling of patients on these agents. Our methodology can be used in larger studies to determine the benefit of repeated vaccination doses, including those that are modified to better target modern or seasonal variants, without the use of live cell assays.
 Provided herein are novel carboxylic acid-containing indanyl compounds as S1P5 modulators, pharmaceutical compositions, use of such compounds in treating neurodegenerative diseases, particularly Alzheimer's disease and multiple sclerosis, and processes for preparing such compounds.





 BACKGROUND: We aimed to describe the severity of the changes in brain diffusion-based connectivity as multiple sclerosis (MS) progresses and the microstructural characteristics of these networks that are associated with distinct MS phenotypes. METHODS: Clinical information and brain MRIs were collected from 221 healthy individuals and 823 people with MS at 8 MAGNIMS centres. The patients were divided into four clinical phenotypes: clinically isolated syndrome, relapsing-remitting, secondary progressive and primary progressive. Advanced tractography methods were used to obtain connectivity matrices. Then, differences in whole-brain and nodal graph-derived measures, and in the fractional anisotropy of connections between groups were analysed. Support vector machine algorithms were used to classify groups. RESULTS: Clinically isolated syndrome and relapsing-remitting patients shared similar network changes relative to controls. However, most global and local network properties differed in secondary progressive patients compared with the other groups, with lower fractional anisotropy in most connections. Primary progressive participants had fewer differences in global and local graph measures compared with clinically isolated syndrome and relapsing-remitting patients, and reductions in fractional anisotropy were only evident for a few connections. The accuracy of support vector machine to discriminate patients from healthy controls based on connection was 81%, and ranged between 64% and 74% in distinguishing among the clinical phenotypes. CONCLUSIONS: In conclusion, brain connectivity is disrupted in MS and has differential patterns according to the phenotype. Secondary progressive is associated with more widespread changes in connectivity. Additionally, classification tasks can distinguish between MS types, with subcortical connections being the most important factor.
 IMPORTANCE: Radiologically isolated syndrome (RIS) represents the earliest detectable preclinical phase of multiple sclerosis (MS) punctuated by incidental magnetic resonance imaging (MRI) white matter anomalies within the central nervous system. OBJECTIVE: To determine the time to onset of symptoms consistent with MS. DESIGN, SETTING, AND PARTICIPANTS: From September 2017 to October 2022, this multicenter, double-blind, phase 3, randomized clinical trial investigated the efficacy of teriflunomide in delaying MS in individuals with RIS, with a 3-year follow-up. The setting included referral centers in France, Switzerland, and Turkey. Participants older than 18 years meeting 2009 RIS criteria were randomly assigned (1:1) to oral teriflunomide, 14 mg daily, or placebo up to week 96 or, optionally, to week 144. INTERVENTIONS: Clinical, MRI, and patient-reported outcomes (PROs) were collected at baseline and yearly until week 96, with an optional third year in the allocated arm if no symptoms have occurred. MAIN OUTCOMES: Primary analysis was performed in the intention-to-treat population, and safety was assessed accordingly. Secondary end points included MRI outcomes and PROs. RESULTS: Among 124 individuals assessed for eligibility, 35 were excluded for declining to participate, not meeting inclusion criteria, or loss of follow-up. Eighty-nine participants (mean [SD] age, 37.8 [12.1] years; 63 female [70.8%]) were enrolled (placebo, 45 [50.6%]; teriflunomide, 44 [49.4%]). Eighteen participants (placebo, 9 [50.0%]; teriflunomide, 9 [50.0%]) discontinued the study, resulting in a dropout rate of 20% for adverse events (3 [16.7%]), consent withdrawal (4 [22.2%]), loss to follow-up (5 [27.8%]), voluntary withdrawal (4 [22.2%]), pregnancy (1 [5.6%]), and study termination (1 [5.6%]). The time to the first clinical event was significantly extended in the teriflunomide arm compared with placebo, in both the unadjusted (hazard ratio [HR], 0.37; 95% CI, 0.16-0.84; P = .02) and adjusted (HR, 0.28; 95% CI, 0.11-0.71; P = .007) analysis. Secondary imaging end point outcomes including the comparison of the cumulative number of new or newly enlarging T2 lesions (rate ratio [RR], 0.57; 95% CI, 0.27-1.20; P = .14), new gadolinium-enhancing lesions (RR, 0.33; 95% CI, 0.09-1.17; P = .09), and the proportion of participants with new lesions (odds ratio, 0.72; 95% CI, 0.25-2.06; P = .54) were not significant. CONCLUSION AND RELEVANCE: Treatment with teriflunomide resulted in an unadjusted risk reduction of 63% and an adjusted risk reduction of 72%, relative to placebo, in preventing a first clinical demyelinating event. These data suggest a benefit to early treatment in the MS disease spectrum. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03122652.
 The present study is aimed at determining the effect of cigarette smoking (CS) on serum uric acid (UA) levels quantitatively before and after smoking cessation among people with MS (pwMS). Additionally, a possible correlation between UA levels and both disability progression and disease severity was also investigated. A retrospective cross-sectional study was conducted using the Nottingham University Hospitals MS Clinics database. It involves 127 people with definite MS recorded when reporting the latest smoking status and the clinical diagnosis. All necessary demographics and clinical characteristics were collected. We found that smoker pwMS had significantly lower serum UA levels than non-smoker pwMS (p-value = 0.0475), and this reduction was recovered after smoking cessation (p-value = 0.0216). However, the levels of disability or disease severity were not correlated with the levels of serum UA in current smoker pwMS, measured by the expanded disability status scale (EDSS; r = -0.24; p-value = 0.38), multiple sclerosis impact scale 29 (MSIS-29; r = 0.01; p-value = 0.97) and MS severity score (MSSS; r = -0.16; p-value = 0.58), respectively. Our result suggests that the reduction in UA levels is more likely a consequence of oxidative stress triggered by many risk factors, including CS, and could be considered a potential indicator of smoking cessation. In addition, the absence of a correlation between UA levels and disease severity and disability suggests that UA is not an optimal biomarker for disease severity and disability prediction among current smoker, ex-smoker or non-smoker pwMS.
 OBJECTIVES: To evaluate compliance with the available recommendations, we assessed the current clinical practice of imaging in the evaluation of multiple sclerosis (MS). METHODS: An online questionnaire was emailed to all members and affiliates. Information was gathered on applied MR imaging protocols, gadolinium-based contrast agents (GBCA) use and image analysis. We compared the survey results with the Magnetic Resonance Imaging in MS (MAGNIMS) recommendations considered as the reference standard. RESULTS: A total of 428 entries were received from 44 countries. Of these, 82% of responders were neuroradiologists. 55% performed more than ten scans per week for MS imaging. The systematic use of 3 T is rare (18%). Over 90% follow specific protocol recommendations with 3D FLAIR, T2-weighted and DWI being the most frequently used sequences. Over 50% use SWI at initial diagnosis and 3D gradient-echo T1-weighted imaging is the most used MRI sequence for pre- and post-contrast imaging. Mismatches with recommendations were identified including the use of only one sagittal T2-weighted sequence for spinal cord imaging, the systematic use of GBCA at follow-up (over 30% of institutions), a delay time shorter than 5 min after GBCA administration (25%) and an inadequate follow-up duration in pediatric acute disseminated encephalomyelitis (80%). There is scarce use of automated software to compare images or to assess atrophy (13% and 7%). The proportions do not differ significantly between academic and non-academic institutions. CONCLUSIONS: While current practice in MS imaging is rather homogeneous across Europe, our survey suggests that recommendations are only partially followed. CLINICAL RELEVANCE STATEMENT: Hurdles were identified, mainly in the areas of GBCA use, spinal cord imaging, underuse of specific MRI sequences and monitoring strategies. This work will help radiologists to identify the mismatches between their own practices and the recommendations and act upon them. KEY POINTS: • While current practice in MS imaging is rather homogeneous across Europe, our survey suggests that available recommendations are only partially followed. • Several hurdles have been identified through the survey that mainly lies in the areas of GBCA use, spinal cord imaging, underuse of specific MRI sequences and monitoring strategies.
 Background: Research on employee care partners of patients with multiple sclerosis (MS) is limited. Objectives: The clinical and economic impact on employee care partners was evaluated by MS disease severity. Methods: Employees with spouses/domestic partners with MS from the Workpartners database (Jan. 1, 2010-Dec. 31, 2019) were eligible if: spouse/partner had at least 3 MS-related (ICD-9-CM/ICD-10-CM:340.xx/G35) inpatient/outpatient/disease-modifying therapy claims within 1 year (latest claim = index date); 6-month pre-index/1-year post-index enrollment; and age 18 to 64 years. Employee care partners' demographic/clinical characteristics and direct/indirect costs were compared across predetermined MS severity categories. Logistic and generalized linear regression modeled the costs. Results: Among 1041 employee care partners of patients with MS, 358 (34.4%) patients had mild MS, 491 (47.2%) moderate, and 192 (18.4%) severe. Mean (standard error [SE]) employee care partner age was 49.0 (0.5) for patients with mild disease, 50.5 (0.4) for moderate, 51.7 (0.6) for severe; percent female care partners was 24.6% [2.3%] mild, 19.8% [1.8%] moderate, 27.6% [3.2%] severe; and mean care partner Charlson Comorbidity Index scores 0.28 (0.05) mild, 0.30 (0.04) moderate, 0.27 (0.06) severe. More care partners of patients with moderate/severe vs mild MS had hyperlipidemia (32.6%/31.8% vs 21.2%), hypertension (29.5%/29.7% vs 19.3%), gastrointestinal disease (20.8%/22.9% vs 13.1%), depression (9.2%/10.9% vs 3.9%), and anxiety 10.6%/8.9% vs 4.2%). Adjusted mean medical costs were greater for employee care partners of patients with moderate vs mild/severe disease (P<.001). Pharmacy costs (SE) were lower for employee care partners of mild vs severe/moderate patients (P<.005). Sick leave costs (SE) were greater for employee care partners of mild/severe vs moderate patients (P<.05). Discussion: Employee care partners of patients with moderate/severe vs mild MS had more comorbidities (ie, hypertension, gastrointestinal disease, depression, and anxiety) and higher pharmacy costs. Employee care partners of patients with moderate vs mild/severe MS had higher medical and lower sick leave costs. Treatment strategies that improve patient outcomes may reduce employee care partner burden and lower costs for employers in some instances. Conclusions: Comorbidities and direct/indirect costs of employees whose spouses/partners have MS were considerable and varied with MS severity.
 BACKGROUND: Multiple sclerosis (MS) is an autoimmune disease characterized by chronic, progressive neurodegeneration of the central nervous system (CNS), and it is the most common inflammatory neurological disease affecting young adults. Given the chronic, progressive nature of the disease, psychiatric disorders are more prevalent among these patients, as reported in the literature; however, data in Saudi Arabia are limited. This study aimed to estimate the prevalence of major depression and generalized anxiety disorder in patients with MS and their association with different patient demographics. METHODS: This was a cross-sectional, multicentered study that included adult patients with MS from 30 June 2021 to 30 June 2022. Participants were interviewed in person and asked to complete a survey that included general demographics, the Patient Health Questionnaire-9 (PHQ-9), and the Generalized Anxiety Disorder-7 (GAD-7) questionnaire. Other variables related to the patients' conditions, such as MS type and Expanded Disability Status Scale (EDSS) score, were collected from the patient's electronic records. Descriptive statistics were performed, and associations were made using the chi-square, Fisher's exact, and analysis of variance tests, as appropriate. RESULTS: A total of 192 participants were included in this study. Based on a cutoff score of >10 on the GAD-7 and PHQ-9 scales, the prevalence of generalized anxiety disorder was 26.1% (50), with the majority of participants having minimal anxiety (40%); meanwhile, the prevalence of major depression was 42.7% (n = 82), and most of them had mild depression (30%). Female participants scored significantly higher compared to men on the GAD-7 scale (p = 0.0376), but not on the PHQ-9 scale (p = 0.1134). In addition, no statistically significant association was detected between functional disability (EDSS score) and prevalence of anxiety and depression. CONCLUSION: This study demonstrated a high prevalence of generalized anxiety disorder and major depression among patients with MS compared with that in the general population, with women being more affected. As these comorbid disorders could negatively affect the disease course, screening is of paramount significance.
 BACKGROUND: Treatment with cladribine tablets, a high-efficacy disease-modifying therapy (DMT), has been available in England since 2017 for patients with highly active relapsing multiple sclerosis (MS). Real-world data on treatment completion, persistence and switching in patients treated with cladribine tablets are beginning to emerge, but only small single and multicentre cohorts have reported so far. This longitudinal retrospective observational study (CLARENCE) evaluated a large cohort (>1900) of patients with highly active relapsing MS, receiving cladribine tablets across England, to determine rates of treatment completion, persistence and switching in the real world. METHODS: Using data obtained from Blueteq® forms, a compulsory requirement for DMT reimbursement in England, we evaluated rates of treatment completion (defined as the proportion of patients who received the full 2-year course of cladribine tablets), treatment persistence (defined as the proportion of patients who did not switch and/or discontinue treatment before receiving the full 2-year course) and treatment switch (defined as the proportion of patients who switched treatment from cladribine tablets to another DMT at any point after their first course). The change in Expanded Disability Status Scale (EDSS) score between Years 1 and 2 of treatment was also determined. All data were analysed descriptively. RESULTS: Blueteq® forms were completed for 1934 MS patients treated with cladribine tablets; of these patients, 691 (36%) were treatment naïve. The median EDSS score (range) at treatment initiation with cladribine tablets was 2.5 (0, 8.5). At time of analysis (September 2021, last follow-up point), a total of 1020 (53%) patients had completed the full 2-year course of cladribine tablets. At the same time point, 1762 (91%) patients were considered as treatment persistent (i.e., the patient had completed either 1 course of tablets with <18 months of follow-up data or the full 2-year course of cladribine tablets). Overall, 78 (4%) patients switched to another DMT at any point after their first course, which included 33 (1.7%) patients who switched after completing the full 2-year course. In terms of their disability, 469 (84%) patients had stable EDSS scores between Years 1 and 2 of treatment. CONCLUSION: In this large real-world study of patients receiving cladribine tablets across England, high rates of treatment persistence and low rates of switching were observed, with only 1.7% of patients receiving the full 2-year course and switching treatment. The majority (84%) of evaluable patients showed stable disability between Years 1 and 2 of treatment. These findings complement earlier data from clinical trials and real-world studies, confirming the effectiveness of cladribine tablets for patients with highly active relapsing MS.
 PURPOSE: The present research translated and validated the Persian version of the Everyday Memory Questionnaire-Revised (EMQ-R) in patients with multiple sclerosis (MS). METHODS: A two-step study was performed in the current work. First, the scale was translated and culturally adopted to Persian. In the second step, the translated questionnaire was presented to 150 patients with MS and 50 individuals in the control group. Then, construct validity (factor analysis and clinical validity) and reliability measures (test-retest reliability and internal consistency) were computed for this questionnaire. RESULTS: Patients with MS obtained higher scores in EMQ-R than the control group (p < .001). The findings of the Kaiser-Meyer-Olkin and Bartlett test approved the sampling adequacy for computing the factor analysis (p < .001). The accuracy of the three-dimensional structure was confirmed by confirmatory factor analysis (CFA). Findings of test-retest (ICC = .95, 95%CI .91-.98, p < .001) and internal consistency revealed a satisfactory value (α = .95, p < .001). CONCLUSIONS: Satisfactory findings for construct validity and high values for reliability revealed that the Persian version of EMQ-R is a reliable and valid scale to measure the everyday memory of patients with MS in the cognitive assessments of this group.IMPLICATIONS FOR REHABILITATIONPersian EMQ-R is a valid, reliable, fast, and easy to administer tool for evaluating the beliefs and insights of patients suffering from MS or other clinical conditions about their cognitive dysfunctions, in day-to-day lives with some differentiation between memory and attentional difficulties. This questionnaire can be a practical clinical tool for the assessment of the cognitive deficits, which might not be detected via formal neuropsychological assessments, and could be a valuable scale to measure the effects of treatment approaches to level up memory function in a way that could be generalized to daily life performance.
 BACKGROUND: A substantial autonomic nervous system (ANS) dysfunction has been described in multiple sclerosis (MS) and recently, also in neuromyelitis optica spectrum disorder (NMOSD). The prevalence of ANS symptoms contributes to the chronic symptom burden in both diseases. The aim of our study was to assess ANS dysfunction in people with (pw) NMOSD and MS, using the Composite Autonomic Symptom Score-31 (COMPASS-31), and additionally, to evaluate if ANS dysfunction have impact on the quality of life of these patients. METHODS: We conducted cross-sectional study at three national referral neurological clinics in Serbia, Croatia, and Montenegro. A total of 180 consecutive subjects, 80 pwNMOSD and 100 pwMS, followed-up at these clinics, were enrolled in the study. Subjects included in the study completed: the validated versions of the COMPASS-31 and the Multiple Sclerosis Quality of Life-54 (MSQoL-54), and the Beck Depression Inventory (BDI). RESULTS: This study demonstrated that the total COMPASS-31 score > 0.0, implicating the presence of ANS dysfunction, was detected in almost all NMOSD and MS study participants tested (80/80, and 97/100, respectively). Our findings showed that autonomic symptom burden was statistically significantly correlated with decreased quality of life, in both NMOSD and MS cohorts. The independent predictors of the better quality of life in pwNMOSD were lower autonomic burden, particularly the absence of the orthostatic intolerance (p = 0.005), along with lower EDSS and BDI score (p ≤ 0.001). Similarly, in pwMS, independent predictors were EDSS, BDI, orthostatic intolerance, and the total COMPASS-31 (p ≤ 0.001). CONCLUSION: Our study demonstrated that a significant proportion of persons with both NMOSD and MS have considerable dysautonomic symptom burden which is correlated with the decreased quality of life. Further investigations are warranted in order to optimize treatment interventions in MS and NMOSD.
 OBJECTIVES: To investigate the effects of noninvasive brain stimulation (NIBS) on spasticity in people with multiple sclerosis (PwMS). LITERATURE SURVEY: We searched PubMed, SCOPUS, MEDLINE, REHABDATA, PEDro, CINAHL, AMED, and Web of Science until December 2022. METHODOLOGY: Studies were selected if they included PwMS, using transcranial direct current stimulation (tDCS) or repetitive transcranial magnetic stimulation (rTMS) as a main intervention, and the study was a randomized controlled trial (RCT) including at least one outcome measure evaluating spasticity. Two researchers individually screened the selected studies. The study's quality was assessed using the Cochrane Collaborations tool. The researchers decided that the meta-analysis was not possible because the treatment interventions varied among the selected studies. SYNTHESIS: In total, 147 studies were reviewed. Of them, nine studies met the eligibility criteria and included 193 PwMS (mean age = 43.25), 54.4% of whom were females. Eight studies considered "high" quality and one considered "moderate" quality. Seven studies that used rTMS demonstrated a significant decrease in spasticity in PwMS after the intervention. The remaining studies that provided tDCS did not show meaningful effects. CONCLUSIONS: The evidence for the influences of rTMS on spasticity in PwMS is promising. The evidence for the impact of tDCS on spasticity in PwMS was limited. Further RCTs with long-term follow-ups are encouraged. This article is protected by copyright. All rights reserved.
 BACKGROUND: The purpose of this study was to identify differences in community mobility in adults with multiple sclerosis (MS) at various ambulation levels. METHODS: Seventy-one adults with MS completed a survey about their mobility impairment and avoidance of challenging mobility tasks. Individuals were categorized as having mild, moderate, or severe gait impairment. RESULTS: Participants across the different functional groups significantly differed in perceived ambulation disability, fatigue impact, falls efficacy, quality of life, challenges with dual-tasking, and self-efficacy for community mobility. There were no significant differences between the mild and moderate gait impairment groups in crossing a busy street or going out in different ambient conditions. Significant differences were found between those with mild impairment and those with severe impairment in avoidance of various terrain elements, heavy manual doors, postural transitions, attentional situations, and crowded places. The only environmental dimension that significantly differed across all 3 groups was carrying 2 or more items, in which avoidance increased as ambulation worsened. CONCLUSIONS: Avoidance behavior for particular environmental features can begin relatively early in the disease process. This underscores the need to further study mobility differences, community ambulation, and participation restrictions in adults with MS.
 Neuromyelitis optica (NMO), also known as Devic's disease, is a chronic inflammatory disorder of the optic nerve and the spinal cord. Similar to multiple sclerosis, it has a relapsing and remitting characteristic. The disease is characterized by optic neuritis and longitudinal extensive inflammation of the spinal cord. Magnetic resonance imaging (MRI) is the modality of choice for this disorder. The serological examination also shows the presence of aquaporin-4 (AQP4) autoantibodies. MRI shows longitudinal extensive transverse myelitis and signs of optic neuritis such as inflammation of the optic nerve. The treatment is based on intravenous corticosteroids with or without plasmapheresis. The current case is a 25-year-old African American male patient who presented with multiple sclerosis-like symptoms (i.e., optic neuritis and transverse myelitis) but turned out to have NMO. Serological examination reveals the absence of AQP4 autoantibodies. A radiological examination showed swelling in the cervical cord. This case report strongly focuses on the radiological findings of NMO.
 BACKGROUND: tumefactive multiple sclerosis (TmMS) is a rare subtype of a demyelinating disease that develops over time. Cases of hyperacute presentations mimicking cerebrovascular disorders have been reported; however, detailed clinical and demographic data are lacking. METHODS: this study aimed to systematically review the literature on tumefactive demyelinating disorders presenting as strokes. After screening the PubMed, PubMed Central, and Web of Science databases, 39 articles describing 41 patients were identified, including 2 historical patients from our center. RESULTS: 23 (53.4%) patients were diagnosed with multiple sclerosis variants (vMS), 17 (39.5%) with inflammatory demyelinating variants (vInf), and 3 with tumors; however, only 43.5% of cases were verified histologically. In subgroup analysis, vMS differed from vInf in several aspects. Inflammatory cerebral spinal fluid parameters, including pleocytosis, proteinorachia was more commonly observed in vInf [11 (64.7%) vs. 1 (5.2%), P = 0.001 and 13/17 (76.4%) vs. 6/23 (31.5%), P = 0.02] than that in vMS. Neurological deterioration and fatal outcomes were more commonly observed in vInf [13/17 (76.4%) vs. 7/23 (30.4%), P = 0.003, and 11/17 (64.7%) vs. 0/23 (0%), P = 0.0001] than that in vMS. CONCLUSIONS: Clinicodemographic data might aid in recognizing different subtypes of TmMS and warrant consideration of unconventional therapies because outcomes may be poor in the vInf of TmMS.
 BACKGROUND: We carried out the current study to compare COVID-19-related hospitalization and mortality rates between people living with multiple sclerosis (PLWMS) and MS-free controls from the Isfahan general population. METHOD: In this retrospective population-based study, we used available data from four datasets of Isfahan University of Medical Sciences from January 1, 2020, to August 22, 2021. Data on all PLWMS, SARS-CoV-2 polymerase chain reaction (PCR) and rapid antigen test, hospitalization, and death were included. We compared the odds of COVID-19-related hospitalization and mortality between PLWMS and the control group before and after adjustment for age and sex. We categorized all people into young (18-49 years) and old age (50-79 years) groups and compared the hospitalization rate between people with and without MS. RESULTS: In total, 829 PLWMS and 2494 MS-free controls with confirmed COVID-19 were included. Hospitalization rates among PLWMS and MS-free controls were 16.2% and 16.5% (crude OR= 0.978, 95%CI: 0.79, 1.21). In the adjusted model, PLWMS with COVID-19 had 56% increased odds of hospitalization (OR=1.56, 95%CI: 1.23, 1.97). During follow-up, there were 11 (1.3%) and 49 (2%) COVID-19-related deaths among PLWMS and MS-free controls, respectively. No significant difference between people with and without MS in COVID-19-related mortality rate was observed (crude OR= 0.678, 95%CI: 0.351, 1.31; adjusted OR=2.013, 95%CI: 0.95, 4.26). We found increased odds of hospitalization in young PLWMS compared to those without MS at the same age (OR=1.699, 95%CI: 1.289, 2.240). But, no difference between older people with and without MS was detected (OR=1.005, 95%CI: 0.662, 1.524). CONCLUSION: This study revealed higher odds of hospitalization and mortality due to COVID-19 among PLWMS in comparison to age- and sex-matched controls from the general population. Nevertheless, it remains unclear whether the elevated odds are directly associated with MS itself or if they are influenced by factors such as rituximab using, comorbidity, and disease severity.
 BACKGROUND AND PURPOSE: Multicenter study designs involving a variety of MRI scanners have become increasingly common. However, these present the issue of biases in image-based measures due to scanner or site differences. To assess these biases, we imaged 11 volunteers with multiple sclerosis (MS) with scan and rescan data at four sites. METHODS: Images were acquired on Siemens or Philips scanners at 3 Tesla. Automated white matter lesion detection and whole-brain, gray and white matter, and thalamic volumetry were performed, as well as expert manual delineations of T1 magnetization-prepared rapid acquisition gradient echo and T2 fluid-attenuated inversion recovery lesions. Random-effect and permutation-based nonparametric modeling was performed to assess differences in estimated volumes within and across sites. RESULTS: Random-effect modeling demonstrated model assumption violations for most comparisons of interest. Nonparametric modeling indicated that site explained >50% of the variation for most estimated volumes. This expanded to >75% when data from both Siemens and Philips scanners were included. Permutation tests revealed significant differences between average inter- and intrasite differences in most estimated brain volumes (P < .05). The automatic activation of spine coil elements during some acquisitions resulted in a shading artifact in these images. Permutation tests revealed significant differences between thalamic volume measurements from acquisitions with and without this artifact. CONCLUSION: Differences in brain volumetry persisted across MR scanners despite protocol harmonization. These differences were not well explained by variance component modeling; however, statistical innovations for mitigating intersite differences show promise in reducing biases in multicenter studies of MS.
 BACKGROUND: Paramagnetic rim lesions (PRLs) are associated with chronic inflammation in multiple sclerosis (MS). 7-Tesla (7T) magnetic resonance imaging (MRI) can evaluate the integrity of the blood-brain barrier (BBB) in addition to the tissue myelination status and cell loss. PURPOSE: To use MRI metrics to investigate underlying physiology and clinical importance of PRLs. STUDY TYPE: Prospective. SUBJECTS: Thirty-six participants (mean-age 47, 23 females, 13 males) of mixed MS subtypes. FIELD STRENGTH/SEQUENCE: 7T, MP2RAGE, MULTI-ECHO 3D-GRE, FLAIR. ASSESSMENT: Lesion heterogeneity; longitudinal changes in lesion counts; comparison of T1, R2*, and χ; association between baseline lesion types and disease progression (2-3 annual MRI visits with additional years of annual clinical follow-up). STATISTICAL TESTS: Two-sample t-test, Wilcoxon Rank-Sum test, Pearson's chi-square test, two-group comparison with linear-mixed-effect model, mixed-effect ANOVA, logistic regression. P-values <0.05 were considered significant. RESULTS: A total of 58.3% of participants had at least one PRL at baseline. Higher male proportion in PRL+ group was found. Average change in PRL count was 0.20 (SD = 2.82) for PRLs and 0.00 (SD = 0.82) for mottled lesions. Mean and median pre-/post-contrast T1 were longer in PRL+ than in PRL-. No differences in mean χ were seen for lesions grouped by PRL (P = 0.310, pre-contrast; 0.086, post-contrast) or PRL/M presence (P = 0.234, pre-contrast; 0.163, post-contrast). Median χ were less negative in PRL+ and PRL/M+ than in PRL- and PRL/M-. Mean and median pre-/post-contrast R2* were slower in PRL+ compared to PRL-. Mean and median pre-/post-contrast R2* were slower in PRL/M+ than in PRL/M-. PRL presence at baseline was associated with confirmed EDSS Plus progression (OR 3.75 [1.22-7.59]) and PRL/M+ at baseline with confirmed EDSS Plus progression (OR 3.63 [1.14-7.43]). DATA CONCLUSION: Evidence of BBB breakdown in PRLs was not seen. Quantitative metrics confirmed prior results suggesting greater demyelination, cell loss, and possibly disruption of tissue anisotropy in PRLs. EVIDENCE LEVEL: 2 TECHNICAL EFFICACY: Stage 2.
 BACKGROUND: Compared to the general population, persons with multiple sclerosis (MS) are at increased risk of suffering from major depressive disorder (MDD). Repetitive Transcranial Magnetic Stimulation (rTMS) was used successfully to treat individuals with MDD. Here, we conducted a randomized clinical trial and pilot study, and tested the effectiveness of rTMS adjuvant to a standard pharmacological treatment among persons with MS, compared to a sham condition. MATERIALS AND METHODS: A total of 40 persons with MS (mean age: 32 years; 42.5% females; median EDSS score: 4) and with moderate to severe symptoms of depression were randomly assigned to the rTMS or to the rTMS sham condition, always as adjuvant intervention to the standard treatment with sertraline, a selective serotonin reuptake inhibitor (SSRI). rTMS consisted of 10 sessions each of 37.5 min; the sham condition was identical to the active condition except for the absence of rTMS stimuli. At the beginning and two weeks after the end of the study, participants reported on their fatigue, while experts rated the severity of participants' depressive symptoms (Montgomery-Asberg Depression Rating Scale; MADRS), cognitive performance (Montreal Cognitive Assessment; MoCA), and degree of disability (Expanded Disability Status Scale; EDSS). RESULTS: Data were analyzed per intent-to-treat. Scores for depression, fatigue, and EDSS declined significantly over time (large effect sizes), but more so in the rTMS condition than in the sham condition (large effect sizes for the time by group-interactions). Compared to the sham condition, scores for depression were significantly lower in the rTMS condition. Scores for cognition improved over time in both study conditions (large effect size). CONCLUSION: Compared to a sham condition, adjuvant rTMS to a standard pharmacological treatment ameliorated typical MS-related symptoms (depression; fatigue; EDSS scores). Results from this pilot study suggested that rTMS might be routinely applied in persons with MS displaying symptoms of depression and fatigue.
 BACKGROUND: Patient-reported outcomes (PROs) are increasingly associated with concurrent and future impairments in persons with multiple sclerosis (pwMS). The structural and pathological relationships with PROs in pwMS have not been elucidated. METHODS: One hundred and forty-two pwMS and 47 healthy controls (HCs) were scanned using 3T MRI and completed a PRO questionnaire named Lifeware(®) that outlines the physical and psychosocial abilities. Beck's Depression Inventory (BDI) assessed levels of depression. T1- and T2-lesion volume, volumes of the whole brain (WBV), gray matter (GMV), white matter (WMV) and lateral ventricle (LVV) were derived using JIM and SIENAX software. Additional deep GM (DGMV) and nuclei-specific volumes of the thalamus, caudate, globus pallidus, putamen, and hippocampus were calculated using FIRST. Ordinal regression models adjusted for age and depression and mediation analyses were used. RESULTS: When compared to HCs, pwMS reported significantly greater limitations in mobility domains, including standing up from low seat (p < 0.001), climbing flight of stairs (p < 0.001), lower limb limitation (p < 0.001), limitations in bladder continence (p = 0.001) and fatigability (p < 0.001). Patient-reported limitations related to lower extremity function were explained by age, BDI, and all DGM nuclei volumes (p < 0.029). No such relationships were seen in the HCs. Fatiguability and the extent of life satisfaction were only related to depression (BDI p < 0.001) and not associated with any MRI-based outcomes. Most relationships between structural pathology and PROs were mediated by BDI scores (p < 0.001). In the pwMS group, there were no significant differences in any MRI-based brain volumes between the levels of reported life satisfaction. CONCLUSION: PRO measures of lower extremity limitations were associated with DGM structures and DGM-specific nuclei. These findings promote the relevance of measuring DGM structures as measures directly related to subjective well-being and walking limitations. Depression is a significant mediator of PROs and in particular of life satisfaction.
 BACKGROUND: The RebiSmart(®) electromechanical autoinjector supports people living with relapsing multiple sclerosis (MS) with their adherence to treatment with subcutaneous interferon beta-1a (sc IFN β-1a; Rebif(®)), a well-established and effective therapy. We report on the validation of the next-generation device, RebiSmart 3.0, tailored to meet patients' changing needs. METHODS: To conclude a series of formative usability studies, a final formative study of an updated prototype version of the RebiSmart electromechanical autoinjector was conducted to identify the device's strengths, potential device-related use errors, opportunities for improvement, and to inform device safety. The findings were incorporated into the next-generation device, RebiSmart 3.0, which was then evaluated in a summative usability study involving 45 participants. The study consisted of evaluation activities - use scenarios and knowledge tasks - designed to validate mitigations to reduce the risks of not successfully completing critical tasks for successful administration of medication. During each evaluation activity, observations (including use errors, instances of moderator assistance, close calls, and difficulties) were recorded, focusing on the potential for serious harm arising from not completing critical tasks. Participants then provided their subjective assessment of RebiSmart 3.0 as part of a user needs survey that assessed device usability and design. RESULTS: Regarding critical tasks, main findings were failure to inspect/dispose of the cartridge and not washing hands or disinfecting the injection site. These issues could be readily overcome by modifying future training. In the subjective assessment, 43 out of 45 participants considered the updated device safe to use as-is. In the user needs survey, overall, the participants rated the device positively. CONCLUSION: Findings validate the safety of use of the next-generation device, RebiSmart 3.0, through a comprehensive evaluation of use scenarios and knowledge tasks by the study participants, who provided positive ratings of the device in the user needs survey.
 BACKGROUND: Treatment for multiple sclerosis (MS), a chronic inflammatory disease of the central nervous system, has changed drastically in the last thirty years. Several different disease-modifying therapies are now available, with off-label use of the B-cell-depleting antibody rituximab becoming an increasingly popular choice, as more and more studies report on its effectiveness. OBJECTIVES: To summarize the current state of evidence for rituximab as a treatment for relapsing-remitting MS (RRMS). METHODS: A structured literature search was conducted in PubMed, focusing on peer-reviewed studies of adult populations with RRMS. Ongoing trials with rituximab in MS were identified through Clinicaltrials.gov and additional references were identified through review articles. FINDINGS: Despite promising results for rituximab as a treatment of MS, the market-authorization holder switched focus from rituximab and discontinued the industry-sponsored trials programme. However, several observational studies, smaller clinical trials, and one large investigator-initiated randomized-controlled trial have continued to report fewer clinical relapses, fewer contrast-enhancing lesions on magnetic resonance imaging, and better drug survival with rituximab, compared with MS-approved alternatives. CONCLUSIONS: Rituximab should be considered as both a first-line and second-line therapy option for most MS patients with active, non-progressive disease. However, as an off-label therapy for MS, regulatory approval remains a barrier for wider adoption in many countries.
 Health Locus of control (LOC) refers to one's beliefs regarding control over one's health. This study aimed to determine the relationship between LOC on clinical and psychosocial aspects associated with multiple sclerosis (MS). 5059 participants with MS completed a questionnaire pack including the Multidimensional Health Locus of Control Scale. Associations between LOC and sociodemographic (age, gender, educational level) and clinical variables (duration, disability, depression, anxiety, self-efficacy, QoL) were explored. LOC was found to be significantly associated with all of the clinical variables and age, but not gender or educational level. When controlling for level of disability, Chance (CLOC) was associated with higher self-efficacy, lower anxiety and higher QoL than Powerful Others (PLOC), while Internal (ILOC) had no association. The proportion with ILOC preference was lower in increased disability. In MS, believing that health is controlled mainly by chance confers the most benefit with regard to quality of life. There is prima-facie evidence that LOC preference changes with MS progression, in a pattern that is protective against psychological distress.
 BACKGROUND: The structural changes associated with cognitive performance in older people with multiple sclerosis (PwMS; age ≥ 50 years old) remain unknown. OBJECTIVE: To determine the relationship between whole-brain (WBV), thalamus as the largest deep gray matter nuclei, and cortex-specific volume measurements with both cognitive impairment and numerical performance in older PwMS. The main hypothesis is that cognitive impairment (CI) in older PwMS is explained by cortical thinning in addition to global and thalamic neurodegenerative changes. METHODS: A total of 101 older PwMS underwent cognitive and neuroimaging assessment. Cognitive assessment included tests established as sensitive in MS samples (Minimal Assessment of Cognitive Function in MS; MACFIMS), as well as those tests often utilized in Alzheimer's dementia studies (Wechsler's Memory Scale, Boston Naming Test, Visual Motor Integration and language). Cognitive impairment (CI) was based on -1.5 standard deviations in at least 2 cognitive domains (executive function, learning and memory, spatial processing, processing speed and working memory and language) when compared to healthy controls. WBV and thalamic volume were calculated using SIENAX/FIRST and cortical thickness using FreeSurfer. Differences in cortical thickness between CI and cognitively preserved (CP) were determined using age, sex, education, depression and WBV-adjusted analysis of covariance (ANCOVA). The relationship between domain-specific cognitive performance and cortical thickness was analyzed by linear regression models adjusted for age, sex, education, depression, WBV and thalamic volume. Benjamini-Hochberg-adjusted p-values lower than 0.05 were considered significant. RESULTS: The average age of the study population was 62.6 (5.9) years old. After adjustment, CI PwMS had significantly thinner left fusiform (p = 0.0003), left inferior (p = 0.0032), left transverse (p = 0.0013), and bilateral superior temporal gyri (p = 0.002 and p = 0.0011) when compared to CP PwMS. After adjusting for age, sex, education, depression WBV, and thalamic volume, CI status was additionally predicted by the thickness of the left fusiform (p = 0.001) and left cuneus gyri (p = 0.004). After the adjustment, SDMT scores were additionally associated with left fusiform gyrus (p < 0.001) whereas letter-based verbal fluency performance with left pars opercularis gyrus (p < 0.001). CONCLUSION: In addition to global and thalamic neurodegenerative changes, the presence of CI in older PwMS is additionally explained by the thickness of multiple cortical regions.
 PURPOSE OF REVIEW: A variety of neurological complications have been reported following the widespread use of the COVID-19 vaccines which may lead to vaccine hesitancy and serve as a major barrier to the public health aim of achieving protective herd immunity by vaccination. In this article, we review the available evidence regarding these neurological adverse events reported, to provide clarity regarding the same so that unfounded fears maybe put to rest. RECENT FINDINGS: There is a greater than expected occurrence of severe neurological adverse events such as cortical sinus venous thrombosis, Bell's palsy, transverse myelitis, and Guillain-Barré syndromes along with other common effects such as headaches following different kinds of COVID-19 vaccination. Precipitation of new onset demyelinating brain lesions with or without detection of specific antibodies and worsening of pre-existing neurological disorders (like epilepsy, multiple sclerosis) are also a matter of great concern though no conclusive evidence implicating the vaccines is available as of now. The COVID-19 pandemic is far from being over. Till such time that a truly effective anti-viral drug is discovered, or an appropriate therapeutic strategy is developed, COVID-appropriate behavior and highly effective mass vaccination remain the only weapons in our armamentarium to fight this deadly disease. As often occurs with most therapeutic means for the treatment and prevention of any disease, vaccination against COVID-19 has its hazards. These range from the most trivial ones like fever, local pain and myalgias to several potentially serious cardiac and neurological complications. The latter group includes conditions like cerebral venous thrombosis (curiously often with thrombocytopenia), transverse myelitis and acute inflammatory demyelinating polyneuropathy amongst others. Fortunately, the number of reported patients with any of these serious complications is far too low for the total number of people vaccinated. Hence, the current evidence suggests that the benefits of vaccination far outweigh the risk of these events in majority of the patients. As of now, available evidence also does not recommend withholding vaccination in patients with pre-existing neurological disorders like epilepsy and MS, though adenoviral vaccines should be avoided in those with history of thrombotic events.
 Preventing relapse of myelin oligodendrocyte glycoprotein-immunoglobulin G-associated disease (MOGAD) with steroids and immunosuppressants is sometimes difficult. There is no standard treatment for refractory cases. We present the case of a 17-year-old female patient with longitudinally extensive myelitis, asymptomatic bilateral optic neuritis, and positive serum MOG-IgG. While taking steroids and several immunosuppressants during the following 14 months, she suffered from two symptomatic relapses in the cerebrum and spinal cord, and multiple asymptomatic relapses in the cerebrum. The patient was negative for MOG-IgG at the second relapse of myelitis. Subcutaneous ofatumumab has suppressed relapse for 13 months. Ofatumumab can be considered a therapeutic option for refractory MOGAD.
 BACKGROUND: Nearly 1 million Americans are living with multiple sclerosis (MS) and 30-50% will experience memory dysfunction. It remains unclear whether this memory dysfunction is due to overall white matter lesion burden or damage to specific neuroanatomical structures. Here we test if MS memory dysfunction is associated with white matter lesions to a specific brain circuit. METHODS: We performed a cross-sectional analysis of standard structural images and verbal memory scores as assessed by immediate recall trials from 431 patients with MS (mean age 49.2 years, 71.9% female) enrolled at a large, academic referral center. White matter lesion locations from each patient were mapped using a validated algorithm. First, we tested for associations between memory dysfunction and total MS lesion volume. Second, we tested for associations between memory dysfunction and lesion intersection with an a priori memory circuit derived from stroke lesions. Third, we performed mediation analyses to determine which variable was most associated with memory dysfunction. Finally, we performed a data-driven analysis to derive de-novo brain circuits for MS memory dysfunction using both functional (n = 1000) and structural (n = 178) connectomes. RESULTS: Both total lesion volume (r = 0.31, p < 0.001) and lesion damage to our a priori memory circuit (r = 0.34, p < 0.001) were associated with memory dysfunction. However, lesion damage to the memory circuit fully mediated the association of lesion volume with memory performance. Our data-driven analysis identified multiple connections associated with memory dysfunction, including peaks in the hippocampus (T = 6.05, family-wise error p = 0.000008), parahippocampus, fornix and cingulate. Finally, the overall topography of our data-driven MS memory circuit matched our a priori stroke-derived memory circuit. CONCLUSIONS: Lesion locations associated with memory dysfunction in MS map onto a specific brain circuit centered on the hippocampus. Lesion damage to this circuit fully mediated associations between lesion volume and memory. A circuit-based approach to mapping MS symptoms based on lesions visible on standard structural imaging may prove useful for localization and prognosis of higher order deficits in MS.


 Persons with MS have the highest unemployment rates compared to other chronic diseases. We want to develop a MS Toolkit with several aids for persons with MS to help them gain a sustainable employment with sufficient and permanent attention and guidance for the daily obstacles in the workplace. Therefore, the opportunities and bottlenecks were mapped through a survey with persons with MS and employers, a diary and expert interviews. There were 3 major problems identified: Persons with MS find it difficult to ask for help in time; they have little or no concrete knowledge about who they can turn to for support and healthcare professionals do not always possess the expertise to guide their patients through problems experienced on the work floor. These problems were used as fundaments in a cocreation session to create the content of the MS Toolkit: a screening tool and dashboard. The screening tool ensures an annual reflection of the work situation. The dashboard links each problem to the most appropriate service.

 Multiple sclerosis (MS) is considered an inflammatory and neurodegenerative disease of the central nervous system, typically resulting in significant neurological disability that worsens over time. While considerable progress has been made in defining the immune system's role in MS pathophysiology, the contribution of intrinsic CNS-cell dysfunction remains unclear. Here, we generated the largest reported collection of iPSC lines from people with MS spanning diverse clinical subtypes and differentiated them into glia-enriched cultures. Using single-cell transcriptomic profiling, we observed several distinguishing characteristics of MS cultures pointing to glia-intrinsic disease mechanisms. We found that iPSC-derived cultures from people with primary progressive MS contained fewer oligodendrocytes. Moreover, iPSC-oligodendrocyte lineage cells and astrocytes from people with MS showed increased expression of immune and inflammatory genes that match those of glial cells from MS postmortem brains. Thus, iPSC-derived MS models provide a unique platform for dissecting glial contributions to disease phenotypes independent of the peripheral immune system and identify potential glia-specific targets for therapeutic intervention.
 PURPOSE OF REVIEW: The association of multiple sclerosis (MS) with depression has been well documented; however, it frequently remains undiagnosed, untreated, or undertreated, with consequences to the person, family, and economy. The aim of this study was to determine the quality, scope, and consistency of available guidelines and consensus statements to guide clinicians managing people with comorbid MS and depression. RECENT FINDINGS: Based on our systematic search of the literature, 6 guidelines and consensus statements met the inclusion criteria. Of these, 4 presented recommendations on depression screening in MS and 5 offered recommendations for treatment. Despite most guidelines presenting evidence-based recommendations, they were generally of low-quality evidence overall. Inconsistencies identified across guidelines and consensus statements included variations in recommendation for routine screening and which screening tool to use. Most guidelines lacked detail, often referring to general population guidelines without describing to what extent they can be applied to people with MS. SUMMARY: The findings of this review highlight the need to develop high-quality, comprehensive clinical practice guidelines with clear recommendations that can be globally implemented by healthcare clinicians working with people with MS.
 PURPOSE: Multiple sclerosis (MS) is a clinically heterogeneous disease. Biomarkers that can assess pathological processes that are unseen with conventional imaging remain an unmet need in MS disease management. Motor evoked potentials (MEPs) could be such a biomarker. To determine and follow longitudinal MEP reliability and correlations with clinical measures in MS patients. METHODS: This is a single-center study in alemtuzumab-treated MS patients to evaluate temporal reliability of MEPs, identify MEP minimum detectible differences, and explore correlations with existing clinical scales. Ten MS patients recently treated with alemtuzumab were evaluated every 6 months over 3 years. Clinical evaluations consisted of expanded disability status scale, timed 25-foot walk, 6-minute walk, and nine-hole peg test. MEPs were measured twice, 2 weeks apart, every 6 months. RESULTS: Eight patients completed all 3 years of study. The intraclass correlation coefficient for MEP parameters ranged from 0.76 to 0.98. TA latency and amplitude with facilitation significantly and strongly correlated with all clinical measures, whereas the MEP duration modestly correlated. Biceps latency with facilitation significantly and moderately correlated with 9-hole peg test. Longitudinal correlations demonstrated good predictive values for either clinical deterioration or improvement. CONCLUSIONS: MEPs have excellent intrapatient and intrarater reliability, and TA MEPs significantly and strongly correlated with expanded disability status scale, 6-minute walk, and timed 25-foot walk, whereas biceps MEPs significantly and moderately correlated with nine-hole peg test. Further studies using larger cohorts of MS patients are indicated. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, Identifier: NCT02623946.
 BACKGROUND: Cannabidiol (CBD) is one of the main phytocannabinoids found in Cannabis sativa. In contrast to Δ9-tetrahydrocannabinol, it has a low affinity for cannabinoid receptors CB1 and CB2, thereby it does not induce significant psychoactive effects. However, CBD may interact with other receptors, including peroxisome proliferator-activated receptor gamma (PPARγ). CBD is a PPARγ agonist and changes its expression. There is considerable evidence that CBD's effects are mediated by its interaction with PPARγ. So, we reviewed studies related to the interaction of CBD and PPARγ. METHODS: In this comprehensive literature review, the term 'cannabidiol' was used in combination with the following keywords including 'PPARγ', 'Alzheimer's disease', 'Parkinson's disease', 'seizure', 'multiple sclerosis', 'immune system', 'cardiovascular system', 'cancer', and 'adipogenesis'. PubMed, Web of Science, and Google Scholar were searched until December 20, 2022. A total of 78 articles were used for the reviewing process. RESULTS: CBD, via activation of PPARγ, promotes significant pharmacological effects. The present review shows that the effects of CBD on Alzheimer's disease and memory, Parkinson's disease and movement disorders, multiple sclerosis, anxiety and depression, cardiovascular system, immune system, cancer, and adipogenesis are mediated, at least in part, via PPARγ. CONCLUSION: CBD not only activates PPARγ but also affects its expression in the body. It was suggested that the late effects of CBD are mediated via PPARγ activation. We suggested that CBD's chemical structure is a good backbone for developing new dual agonists. Combining it with other chemicals enhances their biological effectiveness while reducing their dosage. The present study indicated that PPARγ is a key target for CBD, and its activation by CBD should be considered in all future studies.
 BACKGROUND:  Differential diagnosis of non-compressive cervical myelopathy encompasses a broad spectrum of inflammatory, infectious, vascular, neoplastic, neurodegenerative, and metabolic etiologies. Although the speed of symptom onset and clinical course seem to be specific for certain neurological diseases, lesion pattern on MR imaging is a key player to confirm diagnostic considerations. METHODS:  The differentiation between acute complete transverse myelitis and acute partial transverse myelitis makes it possible to distinguish between certain entities, with the latter often being the onset of multiple sclerosis. Typical medullary MRI lesion patterns include a) longitudinal extensive transverse myelitis, b) short-range ovoid and peripheral lesions, c) polio-like appearance with involvement of the anterior horns, and d) granulomatous nodular enhancement prototypes. RESULTS AND CONCLUSION:  Cerebrospinal fluid analysis, blood culture tests, and autoimmune antibody testing are crucial for the correct interpretation of imaging findings. The combination of neuroradiological features and neurological and laboratory findings including cerebrospinal fluid analysis improves diagnostic accuracy. KEY POINTS:   · The differentiation of medullary lesion patterns, i. e., longitudinal extensive transverse, short ovoid and peripheral, polio-like, and granulomatous nodular, facilitates the diagnosis of myelitis.. · Discrimination of acute complete and acute partial transverse myelitis makes it possible to categorize different entities, with the latter frequently being the overture of multiple sclerosis (MS).. · Neuromyelitis optica spectrum disorders (NMOSD) may start as short transverse myelitis and should not be mistaken for MS.. · The combination of imaging features and neurological and laboratory findings including cerebrospinal fluid analysis improves diagnostic accuracy.. · Additional brain imaging is mandatory in suspected demyelinating, systemic autoimmune, infectious, paraneoplastic, and metabolic diseases..
 Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is a murine model for multiple sclerosis. This model is characterized by chronic and progressive demyelination, leading to impairment of motor function and paralysis. While the outcomes of the disease, including impaired motor function and immunological changes, are well-characterized, little is known about the impact of EAE on the electrophysiology of the motor and sensory systems. In this study, we assessed evoked potentials as a quantitative marker for in vivo monitoring of nervous system damage. Motor-evoked potentials (MEPs) and sensory-evoked potentials (SEPs) were first standardized in naïve C57BL mice and studied thoroughly in EAE mice. The duration of MEPs and the number of connotative potentials increased significantly alongside an increase in temporal SEP amplitudes. Moreover, a new SEP wave was identified in naïve animals, which significantly increased in MOG-induced EAE animals with no or mild symptoms (clinical score 0-2, 0-5 scale). This wave occurred ∼25 milliseconds poststimulation, thus named p25. P25 was correlated with increased vocalization and was also reduced in amplitude following treatment with morphine. As the EAE score progressed (clinical score 3-4, 0-5 scale), the amplitude of MEPs and SEPs decreased drastically. Our results demonstrate that desynchronized neural motor activity, along with hypersensitivity in the early stages of EAE, leads to a complete loss of motor and sensory functions in the late stages of the disease. The findings also suggest an increase in p25 amplitude before motor deficits appear, indicating SEP as a predictive marker for disease progression. PERSPECTIVE: This article assesses p25, a new sensory electrophysiology wave that correlates with pain-related behavior in MOG-induced EAE mice and appears prior to the clinical symptoms. Motor electrophysiology correlates with traditional motor behavior scoring and histology.
 3-O-sulfogalactosylceramide (sulfatide) constitutes a class of sphingolipids that comprise about 4% of myelin lipids in the central nervous system. Previously, our group characterized a mouse with sulfatide's synthesizing enzyme, cerebroside sulfotransferase (CST), constitutively disrupted. Using these mice, we demonstrated that sulfatide is required for establishment and maintenance of myelin, axoglial junctions, and axonal domains and that sulfatide depletion results in structural pathologies commonly observed in Multiple Sclerosis (MS). Interestingly, sulfatide is reduced in regions of normal appearing white matter (NAWM) of MS patients. Sulfatide reduction in NAWM suggests depletion occurs early in disease development and consistent with functioning as a driving force of disease progression. To closely model MS, an adult-onset disease, our lab generated a "floxed" CST mouse and mated it against the PLP-creERT mouse, resulting in a double transgenic mouse that provides temporal and cell-type specific ablation of the Cst gene (Gal3st1). Using this mouse, we demonstrate adult-onset sulfatide depletion has limited effects on myelin structure but results in the loss of axonal integrity including deterioration of domain organization accompanied by axonal degeneration. Moreover, structurally preserved myelinated axons progressively lose the ability to function as myelinated axons, indicated by the loss of the N1 peak. Together, our findings indicate that sulfatide depletion, which occurs in the early stages of MS progression, is sufficient to drive the loss of axonal function independent of demyelination and that axonal pathology, which is responsible for the irreversible loss of neuronal function that is prevalent in MS, may occur earlier than previously recognized.
 Microglia, being the primary immune cells of the central nervous system (CNS), are responsible for pathological inflammatory demyelination in multiple sclerosis (MS). It has been demonstrated that AXL, one of the receptor tyrosine kinases, could alleviate the inflammatory response of microglia. However, the specific mechanism remains unclear. Herein, we explored the role of AXL in the autophagy of microglia and its effect on the experimental autoimmune encephalomyelitis (EAE) model. We revealed that knockout of AXL in BV2 microglia significantly promoted the expression of phosphorylated-PI3K/p-AKT/p-mTOR while significantly inhibiting LC3-Ⅱ/Beclin1. Similarly, autophagy was significantly inhibited in the AXL(-/-) mice. Knockout of AXL induced serious symptoms, infiltration of inflammatory cells, and demyelination changes, manifesting as the upregulation of pro-inflammatory factors TNF-α and IL-6 and downregulation of anti-inflammatory factors TGF-β and IL-10. In conclusion, this study substantiated that autophagy induced by AXL inhibited the inflammatory response of microglia and alleviated symptoms of EAE. Autophagy activation was mediated by the PI3K/AKT/mTOR signaling pathway.
 BACKGROUND: Few data exist on how ofatumumab treatment impacts SARS-CoV-2 booster vaccination response. METHODS: KYRIOS is an ongoing prospective open-label multicenter study on the response to initial and booster SARS-CoV-2 mRNA vaccination before or during ofatumumab treatment in relapsing MS patients. The results on the initial vaccination cohort have been published previously. Here, we describe 23 patients who received their initial vaccination outside of the study but booster vaccination during the study. Additionally, we report the booster results of two patients in the initial vaccination cohort. The primary endpoint was SARS-CoV-2-specific T-cell response at month 1. Furthermore, serum total and neutralizing antibodies were measured. RESULTS: The primary endpoint was reached by 87.5% of patients with booster before (booster cohort 1, N = 8) and 46.7% of patients with booster during ofatumumab treatment (booster cohort 2, N = 15). Seroconversion rates for neutralizing antibodies increased from 87.5% at baseline to 100.0% at month 1 in booster cohort 1 and from 71.4% to 93.3% in booster cohort 2. Of note, 3 of 4 initially seronegative patients in booster cohort 2 and one seronegative patient in the initial vaccination cohort seroconverted after the booster during ofatumumab treatment. CONCLUSIONS: Booster vaccinations increase neutralizing antibody titers in ofatumumab-treated patients. A booster is recommended in ofatumumab-treated patients.
 Objective: This study was designed to compare object relations and anger control between MS patients and normal individuals. Method : The present study was a cross-sectional case-control study with two groups: the case group (patients with MS) and the control group (normal controls without MS). 80 patients and 80 healthy individuals were selected according to the inclusion and exclusion criteria using a simple random sampling method. The research's data collection tool was a three-part questionnaire consisting of demographic information, the Bell Object Relations and the Reality Testing Inventory (BORRTI) and the State-Trait Anger Expression Inventory 2 (STAXI-2). The data were analyzed by the SPSS software version 26 using descriptive and analytical statistics (stepwise regression). Results: The results showed that in terms of object relations, there was no significant difference between the two groups except in alienation of relations (P = 0.035). The results also showed that in general, there was no statistically significant difference between the anger index of the group of MS patients and the normal controls. However, 12.8% of MS patients were significantly different in state of anger, trait anger and anger control compared to normal individuals. This difference was especially higher in angry temperament (P = 0.025) and the anger expression-in (P = 0.04). Conclusion: Although patients with MS were not significantly different from healthy individuals in terms of intrapsychic and interpersonal functions in the context of object relations and anger management, it seems that more complex and multifaceted explanations lie in the results that need further research.
 BACKGROUND: Inflammation, myelin loss, astrocytosis, and microgliosis are pathological signs of the autoimmune and demyelinating disease known as multiple sclerosis (MS). Axonal and neuronal degenerations have basic molecular pathways. The remyelination process can be influenced by the secretome of mesenchymal stem cells due to their capacity for immunomodulation, differentiation, and neuroprotection. Microglial cells are divided into two subgroups: M1 and M2 phenotypes. A crucial component of the microglial function is the colony stimulating factor 1 receptor (CSF1R). We aimed to evaluate the immunomodulating effects of secretome and conditioned serum on the microglial phenotypes and improvement of demyelination in a cuprizone model of MS. METHODS: The study used 48 male C57BL/6 mice, which were randomly distributed into 6 subgroups (n=8), i.e., control, cuprizone, MSC (confluency 40% and 80%) secretome group, and blood derived conditioned serum (autologous and humanized). The animals were fed with 0.2% cuprizone diet for 12 weeks. Supplements were injected into the lateral tail vein using a 27-gauge needle every 3 days 500 μl per injection. RESULTS: At 14 days after transplantation, animals from each group were sacrificed and analyzed by Real time PCR. The results showed that the administration of MSC secretome can efficiently reduce expression of pro-inflammatory cytokines (IL-1, IL6 and TNF-α) in the corpus callosum; also, conditioned serum downregulated IL-1. Moreover, the oligodendrocyte-specific gene was upregulated by secretome and conditioned serum treatment. Also, the expression of microglial- specific gene was reduced after treatment. CONCLUSIONS: These findings demonstrated that the secretome isolated from MSCs used as a therapy decreased and increased the M1 and M2 levels, respectively, to control neuroinflammation in CPZ mice. In conclusion, the current study showed the viability of devising a method to prepare suitable MSCs and secreted factor to cure neurodegenerative diseases, as well as the capability of regulating MSC secretome patterns by manipulating the cell density.
 A growing body of evidence has demonstrated an intricate association between inflammatory bowel disease (IBD) and neurodegenerative conditions, expanding beyond previous foci of comorbidities between IBD and mood disorders. These new discoveries stem from an improved understanding of the gut-microbiome-brain axis: specifically, the ability of the intestinal microbiota to modulate inflammation and regulate neuromodulatory compounds. Clinical retrospective studies incorporating large sample sizes and population-based cohorts have demonstrated and confirmed the relevance of IBD and chronic neurodegeneration in clinical medicine. In this review, we expound upon the current knowledge on the gut-microbiome-brain axis, highlighting several plausible mechanisms linking IBD with neurodegeneration. We also summarize the known associations between IBD with Parkinson disease, Alzheimer disease, vascular dementia and ischemic stroke, and multiple sclerosis in a clinical context. Finally, we discuss the implications of an improved understanding of the gut-microbiome-brain axis in preventing, diagnosing, and managing neurodegeneration among IBD and non-IBD patients.
 Here, prostaglandin D(2)-glycerol ester (PGD(2)-G) was selected to target neuroinflammation. As PGD(2)-G is reported to have a short plasmatic half-life, we propose to use lipid nanocapsules (LNC) as vehicle to safely transport PGD(2)-G to the central nervous system (CNS). PGD(2)-G-loaded LNC (PGD(2)-G-LNC) reduced pro-inflammatory cytokine expression in activated microglial cells, even so after crossing a primary olfactory cell monolayer. A single nasal administration of PGD(2)-G-LNC in lipopolysaccharide (LPS)-treated mice reduced pro-inflammatory cytokine expression in the olfactory bulb. Coating LNC's surface with a cell-penetrating peptide, transactivator of transcription (TAT), increased its accumulation in the brain. Although TAT-coated PGD(2)-G-LNC modestly exerted its anti-inflammatory effect in a mouse model of multiple sclerosis similar to free PGD(2)-G after nasal administration, TAT-coated LNC surprisingly reduced the expression of pro-inflammatory chemokines in the CNS. These data propose LNC as an interesting drug delivery tool and TAT-coated PGD(2)-G-LNC remains a good candidate, in need of further work.
 Multiple sclerosis (MS) predominantly affects women of fertile age. Various aspects of MS could impact on fertility, such as sexual dysfunction, endocrine alterations, autoimmune imbalances, and disease-modifying therapies (DMTs). The proportion of women with MS (wMS) requesting infertility management and assisted reproductive technology (ART) is increasing over time. In this review, we report on data regarding ART in wMS and address safety issues. We also discuss the clinical aspects to consider when planning a course of treatment for infertility, and provide updated recommendations to guide neurologists in the management of wMS undergoing ART, with the goal of reducing the risk of disease activation after this procedure. According to most studies, there is an increase in relapse rate and magnetic resonance imaging activity after ART. Therefore, to reduce the risk of relapse, ART should be considered in wMS with stable disease. In wMS, especially those with high disease activity, fertility issues should be discussed early as the choice of DMT, and fertility preservation strategies might be proposed in selected cases to ensure both disease control and a safe pregnancy. For patients with stable disease taking DMTs compatible with pregnancy, treatment should not be interrupted before ART. If the ongoing therapy is contraindicated in pregnancy, then it should be switched to a compatible therapy. Prior to beginning fertility treatments in wMS, it would be reasonable to assess vitamin D serum levels, thyroid function and its antibody serum levels; start folic acid supplementation; and ensure smoking and alcohol cessation, adequate sleep, and food hygiene. Cervico-vaginal swabs for Ureaplasma urealyticum, Mycoplasma hominis, and Chlamydia trachomatis, as well as serology for viral hepatitis, HIV, syphilis, and cytomegalovirus, should be performed. Steroids could be administered under specific indications. Although the available data do not clearly show a definite raised relapse risk associated with a specific ART protocol, it seems reasonably safe to prefer the use of gonadotropin-releasing hormone (GnRH) antagonists for ovarian stimulation. Close clinical and radiological monitoring is reasonably recommended, particularly after hormonal stimulation and in case of pregnancy failure.
 BACKGROUND: Currently, two major magnetic resonance (MR) vendors provide commercial 7‑T scanners that are approved by the Food and Drug Administration (FDA) for clinical application. There is growing interest in ultrahigh-field MRI because of the improved clinical results in terms of morphological detail, as well as functional and metabolic imaging capabilities. MATERIALS AND METHODS: The 7‑T systems benefit from a higher signal-to-noise ratio, which scales supralinearly with field strength, a supralinear increase in the blood oxygenation level dependent (BOLD) contrast for functional MRI and susceptibility weighted imaging (SWI), and the chemical shift increases linearly with field strength with consequently higher spectral resolution. RESULTS: In multiple sclerosis (MS), 7‑T imaging enables visualization of cortical lesions, the central vein sign, and paramagnetic rim lesions, which may be beneficial for the differential diagnosis between MS and other neuroinflammatory diseases in challenging and inconclusive clinical presentations and are seen as promising biomarkers for prognosis and treatment monitoring. The recent development of high-resolution proton MR spectroscopic imaging in clinically reasonable scan times has provided new insights into tumor metabolism and tumor grading as well as into early metabolic changes that may precede inflammatory processes in MS. This technique also improves the detection of epileptogenic foci in the brain. Multi-nuclear clinical applications, such as sodium imaging, have shown great potential for the evaluation of repair tissue quality after cartilage transplantation and in the monitoring of newly developed cartilage regenerative drugs for osteoarthritis. CONCLUSION: For special clinical applications, such as SWI in MS, MR spectroscopic imaging in tumors, MS and epilepsy, and sodium imaging in cartilage repair, 7T may become a new standard.
 Either optic neuritis (neuropathy) or hypopituitarism has been known to occur separately after COVID-19 vaccination. In this report, we describe the rare combination of hypophysitis and optic neuritis which occurred after COVID-19 vaccination. A 74-year-old woman began to have thirst, polydipsia, and polyuria, and was diagnosed as central diabetes insipidus 1 month after the fourth COVID-19 mRNA vaccine. Head magnetic resonance imaging (MRI) disclosed the thickened pituitary stalk and enlarged pituitary gland with high contrast enhancement as well as the absence of high-intensity signals in the posterior pituitary lobe on the T1-weighted image, leading to the diagnosis of lymphocytic hypophysitis. She was well with desmopressin nasal spray until further 2 months later, when she developed bilateral optic neuritis, together with gait disturbance, intention tremor of the upper extremities, urinary retention, constipation, abnormal sensation in the distal part of the lower extremities, and moderate hemiplegia on the left side. Autoantibodies, including anti-aquaporin 4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG), were all negative. She showed multifocal spinal cord lesions on MRI and oligoclonal bands in the cerebrospinal fluid obtained by spinal tap, and so underwent steroid pulse therapy with methylprednisolone in the tentative diagnosis of multiple sclerosis, resulting in visual acuity recovery and alleviation of neurological symptoms. In the literature review, the combination of optic neuritis and hypophysitis, mostly with diabetes insipidus, was reported in 15 patients as case reports before the years of COVID-19 pandemic. The COVID-19 vaccination would trigger the onset of hypophysitis and optic neuritis in this patient.
 BACKGROUND: Multiple sclerosis (MS) typically presents in young adulthood. Recent data show the highest prevalence of MS in people aged 55 to 64 years; however, there are limited studies of this population. METHODS: Administrative US claims data from IBM-Truven MarketScan commercial and Medicare databases (2011-2017) were analyzed. People with MS 50 years or older were assigned to the aging MS cohort (n = 10,746). The matched controls were people 50 years or older without MS (n = 10,746). Multivariable models compared outcomes between groups. RESULTS: Infections were more frequent in the aging MS cohort vs matched controls (61% vs 45%; P < .0001); urinary tract, acute upper respiratory tract, and herpes zoster were the most frequent infection types. Malignancy rates were 20% for both groups (P = .8167); skin, breast, and prostate malignancies were the most frequent types. Skilled nursing facilities (aging MS cohort, 12%; matched controls, 3%; P < .0001) and MRI (aging MS cohort, 87%; matched controls, 37%; P < .0001) were used more frequently in the aging MS cohort; brain and spine were the most frequent types of MRI in the aging MS cohort. Time to first cane/walker or wheelchair use was shorter in the aging MS cohort (cane/walker use: HR, 2.1; 95% CI, 1.9-2.3; P < .0001; wheelchair use: HR, 6.9; 95% CI, 6.0-8.1; P < .0001). CONCLUSIONS: In people 50 years or older, measures typically associated with worse health primarily resulted from having MS rather than being a consequence of aging alone.
 This research aimed to assess gray matter (GM), white matter (WM), lesions of multiple sclerosis (MS) and the therapeutic effect using diffusion kurtosis imaging (DKI). From January 2018 to October 2019, 78 subjects (48 of MS and 30 of health) perform routine MR scan and DKI of cervical spinal cord. The MS patients were divided into 2 groups according to the presence or absence of T2 hyperintensity. DKI-metrics were measured in the lesions, normal-appearing GM and WM. Significant differences were detected in DKI metrics between MS and healthy (P < .05) and between patients with cervical spinal cord T2-hyperintense and without T2-hyperintense (P < .001). Compared to healthy, GM-mean kurtosis (MK), GM-radial kurtosis, and WM-fractional anisotropy, WM-axial diffusion were statistically reduced in patients without T2-hyperintense (P < .05). Significant differences were observed in DKI metrics between patients with T2-hyperintense after therapy (P < .05), as well as GM-MK and WM-fractional anisotropy, WM-axial diffusion in patients without T2-hyperintense (P < .05); Expanded Disability Status Scale was correlated with MK values, as well as Expanded Disability Status Scale scores and MK values after therapy. Our results indicate that DKI-metrics can detect and quantitatively evaluate the changes in cervical spinal cord micropathological structure.
 OBJECTIVE: This study aimed to investigate the impact of six weeks of at-home sensory-motor exercises on balance and fatigue levels in women with multiple sclerosis, a progressive autoimmune disease affecting the central nervous system. MS symptoms can significantly reduce quality of life. DESIGN: In this Quasi-Experimental Study, 26 MS female patients aged 20-40 with an EDSS of 0-4 were randomly assigned to control and experimental groups. The experimental group performed sensory-motor exercises for six weeks, three sessions a week and for one hour at home. Balance and fatigue were evaluated with Sharpened-Romberg tests (for Static Balance), a 6-step test of Get-Up and Go (for Dynamic Balance) and a Fatigue Severity Scale (FSS). At the end of the sixth week, these tests were re-evaluated like the pre-test stage. RESULTS: Experimental group showed better static balance and FSS than control group, but no difference in dynamic balance. CONCLUSIONS: Considering the outbreak of Covid-19 and the resultant lockdown, the importance of exercise and physical activities in patients with MS, and the positive effects of sensory-motor exercises at home in the present study, these kinds of sensory-motor workouts are highly recommended to improve balance and reduce the fatigue in MS patients.
 INTRODUCTION: The Central Vein Sign (CVS) has been suggested as a potential biomarker to improve diagnostic specificity in multiple sclerosis (MS). Nevertheless, the impact of comorbidities on CVS performance has been poorly investigated so far. Despite the similar features shared by MS, migraine and Small Vessel Disease (SVD) at T2-weighted conventional MRI sequences, ex-vivo studies demonstrated their heterogeneous histopathological substrates. If in MS, inflammation, primitive demyelination and axonal loss coexist, in SVD demyelination is secondary to ischemic microangiopathy, while the contemporary presence of inflammatory and ischemic processes has been suggested in migraine. The aims of this study were to investigate the impact of comorbidities (risk factors for SVD and migraine) on the global and subregional assessment of the CVS in a large cohort of MS patients and to apply the Spherical Mean Technique (SMT) diffusion model to evaluate whether perivenular and non-perivenular lesions show distinctive microstructural features. METHODS: 120 MS patients stratified into 4 Age Groups performed 3T brain MRI. WM lesions were classified in "perivenular" and "non-perivenular" by visual inspection of FLAIR(*) images; mean values of SMT metrics, indirect estimators of inflammation, demyelination and fiber disruption (EXTRAMD: extraneurite mean diffusivity, EXTRATRANS: extraneurite transverse diffusivity and INTRA: intraneurite signal fraction, respectively) were extracted. RESULTS: Of the 5303 lesions selected for the CVS assessment, 68.7% were perivenular. Significant differences were found between perivenular and non-perivenular lesion volume in the whole brain (p < 0.001) and between perivenular and non-perivenular lesion volume and number in all the four subregions (p < 0.001 for all). The percentage of perivenular lesions decreased from youngest to oldest patients (79.7%-57.7%), with the deep/subcortical WM of oldest patients as the only subregion where the number of non-perivenular was higher than the number of perivenular lesions. Older age and migraine were independent predictors of a higher percentage of non-perivenular lesions (p < 0.001 and p = 0.013 respectively). Whole brain perivenular lesions showed higher inflammation, demyelination and fiber disruption than non perivenular lesions (p = 0.001, p = 0.001 and p = 0.02 for EXTRAMD, EXTRATRANS and INTRA respectively). Similar findings were found in the deep/subcortical WM (p = 0.001 for all). Compared to non-perivenular lesions, (i) perivenular lesions located in periventricular areas showed a more severe fiber disruption (p = 0.001), (ii) perivenular lesions located in juxtacortical and infratentorial regions exhibited a higher degree of inflammation (p = 0.01 and p = 0.05 respectively) and (iii) perivenular lesions located in infratentorial areas showed a higher degree of demyelination (p = 0.04). DISCUSSION: Age and migraine have a relevant impact in reducing the percentage of perivenular lesions, particularly in the deep/subcortical WM. SMT may differentiate perivenular lesions, characterized by higher inflammation, demyelination and fiber disruption, from non perivenular lesions, where these pathological processes seemed to be less pronounced. The development of new non-perivenular lesions, especially in the deep/subcortical WM of older patients, should be considered a "red flag" for a different -other than MS- pathophysiology.
 Data on how retinal structural and vascular parameters jointly influence the diagnostic performance of detection of multiple sclerosis (MS) patients without optic neuritis (MSNON) are lacking. To investigate the diagnostic performance of structural and vascular changes to detect MSNON from controls, we performed a cross-sectional study of 76 eyes from 51 MS participants and 117 eyes from 71 healthy controls. Retinal macular ganglion cell complex (GCC), retinal nerve fiber layer (RNFL) thicknesses, and capillary densities from the superficial (SCP) and deep capillary plexuses (DCP) were obtained from the Cirrus AngioPlex. The best structural parameter for detecting MS was compensated RNFL from the optic nerve head (AUC = 0.85), followed by GCC from the macula (AUC = 0.79), while the best vascular parameter was the SCP (AUC = 0.66). Combining structural and vascular parameters improved the diagnostic performance for MS detection (AUC = 0.90; p<0.001). Including both structure and vasculature in the joint model considerably improved the discrimination between MSNON and normal controls compared to each parameter separately (p = 0.027). Combining optical coherence tomography (OCT)-derived structural metrics and vascular measurements from optical coherence tomography angiography (OCTA) improved the detection of MSNON. Further studies may be warranted to evaluate the clinical utility of OCT and OCTA parameters in the prediction of disease progression.
 BACKGROUND: Melatonin is a neurohormone secreted predominantly by the pineal gland that is demonstrated to be associated with the pathogenesis of multiple sclerosis (MS). This research desires to evaluate the tolerability and beneficial effects of exogenous melatonin supplementations in patients with MS. METHODS: This study was executed following the PRISMA 2020 statement. Both observational and interventional studies which reported the clinical effectiveness and/or safety of melatonin supplementation in patients with MS were included in this systematic review. Ovid, PubMed, Scopus, Embase, and Web of Science databases were searched and the risk of bias in included studies was assessed using the Joanna Briggs Institute (JBI) critical appraisal tools based on study design. RESULTS: Out of 1304 results of database searches, finally, 14 articles, including 7 randomized controlled trials (RCTs), 6 case-control studies, and one quasi-experimental study, were included based on the full-text review. Included phenotypes of MS were mostly relapsing-remitting MS (RRMS) (in 11 studies); it was secondary progressive MS (SPMS) in only one study, and two other studies had a mixture of the different phenotypes. The course of treatment with melatonin supplementation was between 2 weeks and 12 months. There were no substantial safety issues. Although melatonin was associated with enhanced oxidative stress and inflammation status, concerning the clinical benefits, limited studies suggested improvements in sleep conditions, cognitive outcomes, and fatigue in MS. DISCUSSION: There are insufficient data to support the regular melatonin prescription in MS. Limitations such as the small number of included studies, the diversity of the dosage, route, and duration of melatonin administration, and the diversity of assessment tests lead to unconvincing findings in this study. There is a need for future studies to achieve a comprehensive judgment on this subject.
 Bruton's tyrosine kinase (BTK) is an emerging target in multiple sclerosis (MS). Alongside its role in B cell receptor signaling and B cell development, BTK regulates myeloid cell activation and inflammatory responses. Here we demonstrate efficacy of BTK inhibition in a model of secondary progressive autoimmune demyelination in Biozzi mice with experimental autoimmune encephalomyelitis (EAE). We show that late in the course of disease, EAE severity could not be reduced with a potent relapse inhibitor, FTY720 (fingolimod), indicating that disease was relapse-independent. During this same phase of disease, treatment with a BTK inhibitor reduced both EAE severity and demyelination compared to vehicle treatment. Compared to vehicle treatment, late therapeutic BTK inhibition resulted in fewer spinal cord-infiltrating myeloid cells, with lower expression of CD86, pro-IL-1β, CD206, and Iba1, and higher expression of Arg1, in both tissue-resident and infiltrating myeloid cells, suggesting a less inflammatory myeloid cell milieu. These changes were accompanied by decreased spinal cord axonal damage. We show similar efficacy with two small molecule inhibitors, including a novel, highly selective, central nervous system-penetrant BTK inhibitor, GB7208. These results suggest that through lymphoid and myeloid cell regulation, BTK inhibition reduced neurodegeneration and disease progression during secondary progressive EAE.
 BACKGROUND: Dimethyl fumarate (DMF) is a methyl ester of fumaric acid and has been approved for treating multiple sclerosis (MS) and psoriasis due to anti-inflammatory effect. There is a close association between platelets and the pathogenesis of MS. Whether DMF affects platelet function remains unclear. Our study intends to evaluate DMF's effect on platelet function. METHODS: Washed human platelets were treated with different concentrations of DMF (0, 50, 100 and 200 μM) at 37 °C for 1 h followed by analysis of platelet aggregation, granules release, receptors expression, spreading and clot retraction. In addition, mice received intraperitoneal injection of DMF (15 mg/kg) to assess tail bleeding time, arterial and venous thrombosis. RESULTS: DMF significantly inhibited platelet aggregation and the release of dense/alpha granules in response to collagen-related peptide (CRP) or thrombin stimulation dose-dependently without altering the expression of platelet receptors α(IIbβ3), GPIbα, and GPVI. In addition, DMF-treated platelets presented significantly reduced spreading on collagen or fibrinogen and thrombin-mediated clot retraction along with the decreased phosphorylation of c-Src and PLCγ2. Moreover, administration of DMF into mice significantly prolonged the tail bleeding time and impaired arterial and venous thrombus formation. Furthermore, DMF reduced the generation of intracellular reactive oxygen species and calcium mobilization, and inhibited NF-κB activation and the phosphorylation of ERK1/2, p38 and AKT. CONCLUSION: DMF inhibits platelet function and arterial/venous thrombus formation. Considering the presence of thrombotic events in MS, our study indicates that DMF treatment for patients with MS might obtain both anti-inflammatory and anti-thrombotic benefits.
 Autophagy comprises a growing range of cellular pathways, which occupy central roles in response to energy deprivation, organelle turnover and proteostasis. Over the years, autophagy has been increasingly linked to governing several aspects of immunity, including host defence against various pathogens, unconventional secretion of cytokines and antigen presentation. While canonical autophagy-mediated antigen processing in thymic epithelial cells supports the generation of a self-tolerant CD4(+) T cell repertoire, mounting evidence suggests that deregulated autophagy pathways contribute to or sustain autoimmune responses. In animal models of multiple sclerosis (MS), non-canonical autophagy pathways such as microtubule-associated protein 1 A/1 B-light chain 3 (LC3)-associated phagocytosis can contribute to major histocompatibility complex (MHC) class II presentation of autoantigen, thereby amplifying autoreactive CD4(+) T cell responses. In systemic lupus erythematosus (SLE), increased type 1 interferon production is linked to excessive autophagy in plasmacytoid dendritic cells (DCs). In rheumatoid arthritis (RA), autophagy proteins contribute to pathological citrullination of autoantigen. Immunotherapies effective in autoimmune diseases modulate autophagy functions, and strategies harnessing autophagy pathways to restrain autoimmune responses have been developed. This review illustrates recent insights in how autophagy, distinct autophagy pathways and autophagy protein functions intersect with the evolution and progression of autoimmune diseases, focusing on MS, SLE and RA.
 AIMS: The neuropeptide galanin is a widely distributed neurotransmitter/neuromodulator that regulates a variety of physiological processes and also participates in the regulation of stress responses. The aims of the present study were to investigate the expression of galanin receptors (GalR1, GalR2, GalR3) in the spinal cords in a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE) using qPCR analysis and to determine GalR1 cellular localization (oligodendrocytes, microglia, astrocytes, ependymal cells, and endothelial cells in the capillaries) by immunohistochemistry. METHODS: Twelve samples from the EAE group and 14 samples from the control group were analyzed. Spinal cords samples were obtained at the peak of the EAE disease. RESULTS: The GalR1 mRNA level was significantly decreased in the EAE mice compared with the controls (P=0.016), whereas the mRNA levels of GalR2 and GalR3 were not significantly different for the EAE and the control mice. No significant correlations were found between the severity of the EAE disease and the mRNA levels of GalR1, GalR2 and GalR3. Immunochemical detection of the GalR1 revealed its expression in the ependymal and endothelial cells. Additionally, a weak GalR1 immunoreactivity was occasionally detected in the oligodendrocytes. CONCLUSION: This study provides additional evidence of galanin involvement in EAE pathophysiology, but this has to be further investigated.
 Despite protection from severe COVID-19 courses through vaccinations, some people with multiple sclerosis (PwMS) are vaccination-hesitant due to fear of post-vaccination side effects/increased disease activity. The aim was to reveal the frequency and predictors of post-SARS-CoV-2-vaccination relapses in PwMS. This prospective, observational study was conducted as a longitudinal Germany-wide online survey (baseline survey and two follow-ups). Inclusion criteria were age ≥18 years, MS diagnosis, and ≥1 SARS-CoV-2 vaccination. Patient-reported data included socio-demographics, MS-related data, and post-vaccination phenomena. Annualized relapse rates (ARRs) of the study cohort and reference cohorts from the German MS Registry were compared pre- and post-vaccination. Post-vaccination relapses were reported by 9.3% PwMS (247/2661). The study cohort's post-vaccination ARR was 0.189 (95% CI: 0.167-0.213). The ARR of a matched unvaccinated reference group from 2020 was 0.147 (0.129-0.167). Another reference cohort of vaccinated PwMS showed no indication of increased post-vaccination relapse activity (0.116; 0.088-0.151) compared to pre-vaccination (0.109; 0.084-0.138). Predictors of post-vaccination relapses (study cohort) were missing immunotherapy (OR = 2.09; 1.55-2.79; p < 0.001) and shorter time from the last pre-vaccination relapse to the first vaccination (OR = 0.87; 0.83-0.91; p < 0.001). Data on disease activity of the study cohort in the temporal context are expected for the third follow-up.
 Neurological disorders such as stroke, multiple sclerosis, as well as the neurodegenerative diseases Parkinson's or Alzheimer's disease are accompanied or even powered by danger associated molecular patterns (DAMPs), defined as endogenous molecules released from stressed or damaged tissue. Besides protein-related DAMPs or "alarmins", numerous nucleic acid DAMPs exist in body fluids, such as cell-free nuclear and mitochondrial DNA as well as different species of extracellular RNA, collectively termed as self-extracellular nucleic acids (SENAs). Among these, microRNA, long non-coding RNAs, circular RNAs and extracellular ribosomal RNA constitute the majority of RNA-based DAMPs. Upon tissue injury, necrosis or apoptosis, such SENAs are released from neuronal, immune and other cells predominantly in association with extracellular vesicles and may be translocated to target cells where they can induce intracellular regulatory pathways in gene transcription and translation. The majority of SENA-induced signaling reactions in the brain appear to be related to neuroinflammatory processes, often causally associated with the onset or progression of the respective disease. In this review, the impact of the diverse types of SENAs on neuroinflammatory and neurodegenerative diseases will be discussed. Based on the accumulating knowledge in this field, several specific antagonistic approaches are presented that could serve as therapeutic interventions to lower the pathological outcome of the indicated brain disorders.
 BACKGROUND: Strategies recommended to decrease the risk of infection associated with the use of multiple sclerosis disease-modifying treatments include screening and immunization against common viral infections such as varicella-zoster (VZV) and hepatitis B (HBV). However, the data concerning the durability of those vaccine responses and the need for re-test is scarce. OBJECTIVES: We aimed to evaluate HBV and VZV seroprotection loss in MS patients under DMT. METHODS: We conducted a cohort study including patients with basal seroprotective titers against HBV/VZV viruses and a subsequent serology performed at least 3 months apart. We evaluated predictors of seroprotection loss through a binary regression. RESULTS: HBV seroprotection loss occurred in one-fifth of patients in a median interval of 21.3 months. Anti-CD20 treatment (OR 8.559 95%CI 3.467- 21.130, p < 000.1), age at last serology higher or equal to 55 years (OR 7.506, 95% CI 2.473-22.786, p < 0.001) and basal HBsAb titer (OR 0.992, 95%CI 0.987 -0.996, p=0.001) increase the risk of seroprotection loss. VZV seroprotection loss occurred rarely in a median interval of 21.3 months. We could not identify any factor associated with an increased risk of VZV seroprotection loss. CONCLUSIONS: Anti-CD20 drugs are associated with a loss of seroprotection against HBV in a short-interval follow-up.
 Introduction: The interactions between Diabetes Mellitus type II (DMII) and Multiple Sclerosis (MS) lead to higher levels of fatigue, higher risk of physical disability, faster cognitive decline, and in general a lower quality of life and a higher frequency of depression compared to the general population. All of the above accelerate the disability progression of patients with MS, reduce the patients' functional capacity, and further increase their psychological and economic burden. Methods: This systematic review and meta-analysis aims to calculate the prevalence of DMII in the MS population. Following PRISMA guidelines, a thorough search of the Medline Pubmed, Cochrane Library, and Scopus databases was performed, focusing on the frequency of DMII in the MS population. Results: A total of 19 studies were included in the synthesis. The results of the main meta-analysis of random effects using R studio 3.3.0 for Windows and the Meta r package showed that the prevalence of DMII in the MS population is 5% (95% CI [0.03, 0.07], 19 studies, I(2) = 95%, p(Q) < 0.001). Additional subgroup analysis based on region showed a difference of 4.4% (I(2) = 95.2%, p(Q) < 0.001), p(subgroupdifference) = 0.003) between European and non-European participants, while demographic- and MS-specific characteristic (EDSS, Disease Duration) did not seem to affect the prevalence of DMII in the MS population (p = 0.30, p = 0.539, p = 0.19, p = 0.838). No publication bias was discovered (Egger's p test value: 0.896). Conclusions: Even though the prevalence of DMII in the MS population is lower than 10% (the reported prevalence of DMII in the general population) the interactions between the two conditions create significant challenges for MS patients, their caregivers, and physicians. DΜΙΙ should be systematically recorded in the case of MS patients to clearly delineate any potential relationship between the two conditions. Additionally, more structured studies investigating the interactions of MS and DMΙΙ as well as the direction of the causation between those two conditions are necessary in order to gain a deeper insight into the nature of the interaction between MS and DMII.
 The imbalance in the concentration of metallic nanoparticles has been demonstrated to play an important role in multiple sclerosis (MS), which may impact cognition. Biomarkers are needed to provide insights into the pathogenesis and diagnosis of MS. They can be used to gain a better understanding of cognitive decline in people with MS (pwMS). In this study, we investigated the relationship between the blood concentration of metallic nanoparticles (blood nanoparticles) and cognitive performance in pwMS. First, four mL blood samples, clinical characteristics, and cognitive performance were obtained from 21 pwMS. All participants had relapse-remitting MS, with a score of ≤4.5 points in the expanded disability status scale. They were relapse-free in the three previous months from the day of collection and had no orthopedic, muscular, cardiac, and cerebellar diseases. We quantified the following metallic nanoparticles: aluminum, chromium, copper, iron, magnesium, nickel, zinc, and total concentration. Cognitive performance was measured by mini-mental state examination (MMSE) and the symbol digit modalities test (SDMT). Pearson's and Spearman's correlation coefficients and stepwise linear regression were calculated to assess the relationship between cognitive performance and blood nanoparticles. We found that better performance in SDMT and MMSE was related to higher total blood nanoparticles (r = 0.40; p < 0.05). Also, better performance in cognitive processing speed and attention (SDMT) and mental state (MMSE) were related to higher blood iron (r = 0.44; p < 0.03) and zinc concentrations (r = 0.41; p < 0.05), respectively. The other metallic nanoparticles (aluminum, chromium, copper, magnesium, and nickel) did not show a significant relationship with the cognitive parameters (p > 0.05). Linear regression estimated a significant association between blood iron concentration and SDMT performance. In conclusion, blood nanoparticles are related to cognitive performance in pwMS. Our findings suggest that the blood concentration of metallic nanoparticles, particularly the iron concentration, is a promising biomarker for monitoring cognitive impairment in pwMS.
 INTRODUCTION: Cognitive impairment is a common feature of multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). However, there is a lack of population-based study of dementia risk in these disorders. In the present study, the risk of dementia in MS and NMOSD patients in Republic of Korea was estimated. METHODS: Data analyzed in this study were obtained from the Korean National Health Insurance Service (KNHIS) database between January 2010 and December 2017. The study included 1,347 MS patients and 1,460 NMOSD patients ≥40 years of age who had not been diagnosed with dementia within 1 year prior to the index date. Matched controls were selected based on age, sex, and the presence of hypertension, diabetes mellitus, or dyslipidemia. RESULTS: In MS and NMOSD patients, the risk of developing any dementia [adjusted hazard ratio (aHR) = 2.34; 95% confidence interval (CI) = 1.84-2.96 and aHR = 2.19; 95% CI = 1.61-3.00, respectively], Alzheimer's disease [AD; aHR = 2.23; 95% confidence interval (CI) = 1.70-2.91 and aHR = 1.99; 95% CI = 1.38-2.88, respectively], and vascular dementia (aHR = 3.75; 95% CI = 1.91-7.35 and aHR = 3.21; 95% CI = 1.47-7.02, respectively) was higher compared with the matched controls. NMOSD patients had a lower risk of any dementia and AD compared with MS patients after adjusting for age, sex, income, hypertension, diabetes, and dyslipidemia (aHR = 0.67 and 0.62). CONCLUSION: The risk of dementia increased in MS and NMOSD patients and dementia risk was higher in MS than in NMOSD.
 Fatigue is frequently reported by patients with multiple sclerosis, aquaporin-4-antibody neuromyelitis optica spectrum disorder and myelin-oligodendrocyte-glycoprotein antibody disease; thus they could share a similar pathophysiological mechanism. In this cross-sectional cohort study, we assessed the association of fatigue with resting-state functional MRI, diffusion and structural imaging measures across these three disorders. Sixteen patients with multiple sclerosis, 17 with aquaporin-4-antibody neuromyelitis optica spectrum disorder and 17 with myelin-oligodendrocyte-glycoprotein antibody disease assessed, outside of relapses, at the Oxford Neuromyelitis Optica Service underwent Modified Fatigue Impact Scale, Hospital Anxiety and Depression Scale and Expanded Disability Status Scale scoring. A 3T brain and spinal cord MRI was used to derive cortical, deep grey and white matter volumetrics, lesions volume, fractional anisotropy, brain functional connectivity metrics, cervical spinal cord cross-sectional area, spinal cord magnetic transfer ratio and average functional connectivity between the ventral and the dorsal horns of the cervical cord. Linear relationships between MRI measures and total-, cognitive- and physical-fatigue scores were assessed. All analyses were adjusted for correlated clinical regressors. No significant differences in baseline clinical characteristics, fatigue, depression and anxiety questionnaires and disability measures were seen across the three diseases, except for older age in patients with aquaporin-4-antibody neuromyelitis optica spectrum disorder (P = 0.0005). In the total cohort, median total-fatigue score was 35.5 (range 3-72), and 42% of patients were clinically fatigued. A positive correlation existed between the total-fatigue score and functional connectivity of the executive/fronto-temporal network in the in left middle temporal gyrus (P = 0.033) and between the physical-fatigue score and functional connectivity of the sensory-motor network (P = 0.032) in both pre- and post-central gyri. A negative relationship was found between the total-fatigue score and functional connectivity of the salience network (P = 0.023) and of the left fronto-parietal network (P = 0.026) in the right supramarginal gyrus and left superior parietal lobe. No clear relationship between fatigue subscores and the average functional connectivity of the spinal cord was found. Cognitive-fatigue scores were positively associated with white matter lesion volume (P = 0.018) and negatively associated with white matter fractional anisotropy (P = 0.032). Structural, diffusion and functional connectivity alterations were not influenced by the disease group. Functional and structural imaging metrics associated with fatigue relate to brain rather than spinal cord abnormalities. Salience and sensory-motor networks alterations in relation to fatigue might indicate a disconnection between the perception of the interior body state and activity and the actual behavioural responses and performances (reversible or irreversible). Future research should focus on functional rehabilitative strategies.
 Upper limb intention tremor in persons with multiple sclerosis (pwMS) affects the ability to perform activities of daily life and is difficult to treat. The study investigated the effect of peripheral upper limb cooling on tremor severity and functional performance in MS patients with intention tremor. In experiment 1, 17 patients underwent two 15 min cooling conditions for the forearm (cold pack and cryomanchet) and one control condition. In experiment 2, 22 patients underwent whole arm cooling for 15 min using multiple cold packs. In both experiments, patients were tested at four time points (pre- and post-0, -25 and -50 min cooling) on unilateral tasks of the Test Evaluant les Membres supérieurs des Personnes Agées (TEMPA), Fahn's tremor rating scale (FTRS), Nine Hole Peg Test (NHPT). In experiment 1, the mean FTRS ranged from 13.2 to 14.1 across conditions. A two-way ANOVA showed mainly time effects, showing that cooling the forearm significantly reduced the FTRS, the performance on the NHPT, and three out of four items of the TEMPA, mostly independent of the cooling modality. In experiment 2, the mean FTRS was 13.1. A repeated measures ANOVA showed that cooling the whole arm reduced the FTRS and time needed to execute two out of four items of the TEMPA. These effects occurred immediately after cooling lasting at least 25 min. Cooling the whole upper limb led to a clinically noticeable effect on tremor severity and improved functional performance, which was pronounced during the first half-hour after cooling.
 Bullous pemphigoid (BP) is the most prevalent autoimmune vesiculobullous skin illness that tends to affect the elderly. Growing evidence has hinted a correlation between BP and neurological diseases. However, existing observational studies contained inconsistent results, and the causality and direction of their relationship remain poorly understood. To assess the causal relationship between BP and neurological disorders, including Alzheimer's disease (AD), multiple sclerosis (MS), Parkinson's disease (PD), and stroke. A bidirectional two-sample Mendelian randomization (MR) adopted independent top genetic variants as instruments from the largest accessible genome-wide association studies (GWASs), with BP (n = 218 348), PD (n = 482 730), AD (n = 63 926), stroke (n = 446 696), and MS (n = 115 803). Inverse variance weighted (IVW), MR-Egger, weighted mode methods, weighted median, and simple mode were performed to explore the causal association. Multiple sensitivity analyses, MR-Pleiotropy Residual Sum and Outlier (PRESSO) was used to evaluate horizontal pleiotropy and remove outliers. With close-to-zero effect estimates, no causal impact of BP on the risk of the four neurological diseases was discovered. However, we found that MS was positively correlated with higher odds of BP (OR = 1.220, 95% CI: 1.058-1.408, p = 0.006), while no causal associations were observed between PD (OR = 0.821, 95% CI: 0.616-1.093, p = 0.176), AD (OR = 1.066, 95% CI: 0.873-1.358, p = 0.603), stroke (OR = 0.911, 95% CI: 0.485-1.713, p = 0.773) and odds of BP. In summary, no causal impact of BP on the risk of PD, AD, MS and stroke was detected in our MR analysis. However, reverse MR analysis identified that only MS was positively correlated with higher odds of BP, but not PD, AD and stroke.
 Differentiating multiple sclerosis (MS) from other relapsing inflammatory autoimmune diseases of the central nervous system such as neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is crucial in clinical practice. The differential diagnosis may be challenging but making the correct ultimate diagnosis is critical, since prognosis and treatments differ, and inappropriate therapy may promote disability. In the last two decades, significant advances have been made in MS, NMOSD, and MOGAD including new diagnostic criteria with better characterization of typical clinical symptoms and suggestive imaging (magnetic resonance imaging [MRI]) lesions. MRI is invaluable in making the ultimate diagnosis. An increasing amount of new evidence with respect to the specificity of observed lesions as well as the associated dynamic changes in the acute and follow-up phase in each condition has been reported in distinct studies recently published. Additionally, differences in brain (including the optic nerve) and spinal cord lesion patterns between MS, aquaporin4-antibody-positive NMOSD, and MOGAD have been described. We therefore present a narrative review on the most relevant findings in brain, spinal cord, and optic nerve lesions on conventional MRI for distinguishing adult patients with MS from NMOSD and MOGAD in clinical practice. In this context, cortical and central vein sign lesions, brain and spinal cord lesions characteristic of MS, NMOSD, and MOGAD, optic nerve involvement, role of MRI at follow-up, and new proposed diagnostic criteria to differentiate MS from NMOSD and MOGAD were discussed.
 INTRODUCTION: One of the most debilitating problems encountered by people with multiple sclerosis (MS) is the loss of balance and coordination. Our study aimed to comprehensively evaluate the effectiveness of one year of Tai-chi exercise in patients with MS using both subjective and objective methods, including posturography. METHODS: This was a single-group longitudinal one-year study performed from the 1st of January 2019 to the 1st of January 2020. The primary outcomes of interest were the Mini-Balance Evaluation Systems Test (Mini-BESTest) and static posturography measures as objective methods to detect subtle changes associated with postural control/balance impairment. Secondary outcomes were measures of depression, anxiety, cognitive performance, and quality of life. All objective and subjective parameters were assessed four times: at baseline, and after three, six and 12 months of regular Tai-chi training. The difference was calculated as a subtraction of baseline values from every timepoint value for each measurement. If the normality test was passed, parametric one-sample t-test was used, if failed, Wilcoxon signed ranks test was used to test the difference between the baseline and each timepoint. Alpha was set to 0.017 using Bonferroni correction for multiple comparisons. RESULTS: Out of 25 patients with MS enrolled, 15 women with MS (mean age 44.27 years) were included for statistical analyses after completing the 12-month program. After 12 months, significant improvements were found in all objective balance and gait tests: Mini-BESTest (p<0.001), static posturography measures (total area of the centre of foot pressure - TA; p = 0.015), 25 Feet Walk Test (25FWT; p = 0.001), anxiety (Beck Anxiety Inventory - BAI; p = 0.005) and cognition tests (Paced Auditory Serial Addition Test - PASAT; p = 0.003). Measures of depression (Beck Depression Inventory - BDI; p = 0.071), cognition (Symbol Digit Modalities Test - SDMT; p = 0.079), and health-related quality of life (European Quality of Life 5-Dimensions Questionnaire - EQ-5D-5L; p = 0.095) showed a trend of improvement but were not significant, which could be the result of a small sample and increased bias due the type II error. CONCLUSION: According to these preliminary results, this study indicates the possible beneficial effects of long-term Tai-chi training on patients with MS. Although these findings need to be confirmed by further studies with a larger sample of participants of both genders and require more rigorous randomized controlled trials (RCT) design, our findings support the recommendation of regular and long-term Tai-chi exercise in patients with MS. GOV IDENTIFIER (RETROSPECTIVELY REGISTERED): NCT05474209.
 Motor neuron disorders can be thought of as residing on a spectrum, whether upper motor neurons, lower motor neurons, or both are affected. Motor neuron diseases include amyotrophic lateral sclerosis (affects both upper and lower motor neurons), primary lateral sclerosis (affects upper motor neurons), progressive muscular atrophy (affects lower motor neurons ), progressive bulbar palsy (affects lower motor neurons), spinal muscular atrophy (affects lower motor neurons), and post-polio syndrome (affects lower motor neurons). Motor neuron disease is used interchangeably with amyotrophic lateral sclerosis (ALS) as ALS is the most common adult-onset presentation of this disease.  ALS is a neurodegenerative disorder leading to weakness of bulbar, thoracic, limb, and abdominal muscles with sparing of sensory function. Death usually occurs within two to five years from respiratory failure. Roughly 85 to 90% of ALS cases are sporadic, with about 10% being of familial origin. According to the 2014 US Census data, the prevalence of ALS was 5 per 100,000 people.  Though there is variation in clinical presentation, the majority of the patients present with asymmetric limb weakness (80%) or bulbar dysfunction (20%). Bulbar dysfunction can manifest as dysphagia (trouble swallowing) and dysarthria (trouble speaking). There is progressive spread to other areas of the body with accompanying upper motor neuron and lower motor neuron findings. Upper motor findings include spasticity, hyperactive reflexes, and a positive Babinski sign. Lower motor neuron signs include muscle atrophy, weakness, flaccid paralysis, absent reflexes, fasciculations, and fibrillations.  Patients can also display changes in behavior due to frontotemporal dysfunction, and about 15% of patients develop frontotemporal dementia. Some patients may also present with Pseudobulbar affect, which is dysregulation of emotional responses as exhibited by excessive laughter or crying. Many other neurological disorders such as strokes, Alzheimer’s disease, and multiple sclerosis also present with pseudobulbar affect. Once the diagnosis of ALS is suspected, electrodiagnostic testing is needed. Electrodiagnostic testing assesses the integrity of lower motor neurons and is crucial to diagnosing motor neuron disease as oftentimes, neuroimaging, and laboratory studies are normal. Nerve conduction studies (NCS) and needle electromyography (EMG)  are important for supporting the diagnosis of ALS and ruling out other potential mimics of the disease. Some disorders that can mimic motor neuron disease are multifocal motor neuropathy with conduction block, chronic inflammatory demyelinating polyradiculoneuropathy, central nervous system tumors, multiple sclerosis, and polyradiculopathy, among others.  It is important to rule out such mimics with NCS and needle EMG as the treatment regimens and prognosis differ among the varying disorders. Since the prognosis of ALS is poor, it is imperative to accurately diagnose the disorder to appropriately manage the associated symptoms involved and develop a treatment plan.
 BACKGROUND: Cone contrast threshold testing (CCT) provides quantitative measurements of color and contrast function to reveal changes in vision quality that are not standard endpoints in clinical trials. We utilize CCT to measure visual function in patients with multiple sclerosis (MS), age-related macular degeneration (AMD), epiretinal membrane (ERM), and retinal vein occlusion (RVO). METHODS: Retrospective data was gathered from 237 patients of the Gavin Herbert Eye Institute. Subjects included 17 patients with MS, 45 patients with AMD, 41 patients with ERM, 11 patients with RVO, and 123 healthy controls. Patients underwent the primary measurement outcome, CCT testing, as well as Sloan visual acuity test and spectral domain optical coherence tomography during normal care. RESULTS: Color and contrast deficits were present in MS patients regardless of history of optic neuritis. AMD with intermediate or worse disease demonstrated reduced CCT scores. All 3 stages of ERM demonstrated cone contrast deficits. Despite restoration of visual acuity, RVO-affected eyes demonstrated poorer CCT performance than unaffected fellow eyes. CONCLUSIONS: CCT demonstrates color and contrast deficits for multiple retinal diseases with differing pathophysiology. Further prospective studies of CCT in other disease states and with larger samples sizes is warranted.
 The eye and the brain are the best investigated immune privileged sites for T cell mediated autoimmune diseases, with several experimental animal models in multiple species like experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune uveitis (EAU). It was difficult to explain autoimmunity to antigens which are sequestered behind blood-organ barriers since those barriers can only be passed by already activated lymphocytes. Antigen-specific lymphocytes must therefore be activated outside of the immune privileged target organs by crossreactivity of immune receptors to similar antigens, designated as "antigenic mimicry". Crossreactivity as the basic mechanism for antigenic mimicry is generally important for the immune recognition of a huge variety of different antigens with a comparably restricted number of T cell receptors and antibodies. Here, various T cell mimotopes are discussed that can induce autoimmune diseases or immune tolerance or both. Mimotopes are antigenic epitopes with similarity to different, unrelated antigens that are not distinguished by T cell receptors. Finally, the role of the microbiome is touched briefly, it is suspected to provide many mimotopes for T cell responses that, however, are very difficult to define due to the enormous size, and individual variability of our microbiome and virome.
 BACKGROUND: Fatigue, one of the most common symptoms in patients with multiple sclerosis (MS), severely impairs quality of life and the ability to work or perform activities of daily living. Real-world data on fatigue in MS can help inform healthcare decisions and identify care gaps. We identified fatigue in patients with MS, using existing codes for fatigue and proxies of fatigue in healthcare claims database records and characterized cohorts with and without markers of fatigue who had been prescribed disease-modifying therapies for MS (MS-DMTs). METHODS: In this cohort study, we retrospectively analyzed Optum's de-identified Clinformatics® Data Mart database from 1 January 2015 to 31 December 2019. The index date was defined as the first prescription record date for any MS-DMT during the study identification period. Included patient records were from adults (≥18 years) with ≥2 MS diagnosis claims listed within 12 months prior to the index date. Patients had ≥1 claim for any MS-DMT during the identification period (1 January 2016-31 December 2018), continuous enrollment in a health plan with medical and pharmacy benefits for 12 months before the index date (assessment one), and 12 months following the index date or to end of data availability (assessment two). After exploratory analyses, we applied the following definition to sort patient records into two cohorts according to presence or absence of markers of fatigue: ≥1 diagnosis (International Classification of Diseases, Ninth/Tenth Revisions code) claim for fatigue or ≥2 claims for stimulant drugs or ≥2 procedure claims for a sleep study or ≥2 pharmacy claims for sleep aid drugs; we used the broadest definition of fatigue so meeting any of these criteria qualified patients with MS as having fatigue. To minimize assessment one differences in selected patient characteristics between cohorts, we applied 1:1 propensity score matching with age, sex, US geographic region, and Charlson Comorbidity Index score as covariates. We analyzed demographic data, markers of fatigue, comorbidities at assessment one, and physical disabilities and neurologic impairment at assessment two. RESULTS: Of 4077 patient records that met the eligibility criteria, 1976 had markers of fatigue. The propensity score-matched cohorts included 1519 patients each with and without fatigue. Assessment one comorbidities including anxiety (25.3% vs 10.5%; P<0.0001), arthritis (17.6% vs 12.9%; P = 0.0003), depression (15.0% vs 3.5%; P<0.0001), and gastrointestinal disorders (20.3% vs 14.2%; P<0.0001) were significantly more prevalent in the cohort with markers of fatigue at assessment one compared with those without fatigue. At assessment two, the cohort with baseline fatigue upon initial assessment was more likely to have indication of physical impairments (spasticity [63.5% vs 35.8%; P<0.0001], bladder dysfunction [37.8% vs 24.0%; P<0.0001], cognitive/behavioral dysfunction [27.0% vs 18.6%; P<0.0001]), neurologic impairments (pain [59.1% vs 44.0%; P<0.0001], depression [29.2% vs 9.9%; P<0.0001], and sensory disturbances [54.2% vs 36.7%; P<0.0001]), compared with the cohort without markers of fatigue at assessment one. CONCLUSIONS: In our analysis, patients with MS and fatigue were more likely to have comorbidities at assessment one and to develop physical disabilities and neurologic impairments at assessment two. Appropriate identification of patients with MS and fatigue may facilitate targeted care interventions to a group of patients at higher risk for disease progression and disability.
 INTRODUCTION: Depression, fatigue, and anxiety are three common clinical comorbidities of multiple sclerosis (MS). We investigated the role of physical activity (PA) level and body mass index (BMI) as modifiable lifestyle factors in these three comorbidities. METHODS: A cross-sectional study was conducted in the MS specialist clinic of Sina Hospital, Tehran, Iran. Demographic and clinical data were collected. BMI was categorized in accordance with the WHO's standard classification. Physical activity (PA) level and sitting time per day were obtained using the short form of the International Physical Activity Questionnaire (IPAQ-SF). Fatigue, anxiety, and depression scores were measured using the Persian version of the Fatigue Severity Scale (FSS), Beck Anxiety Inventory (BAI), and Beck's Depression Inventory II (BDI-II) questionnaires, respectively. The correlation between the metabolic equivalent of tasks (MET), BMI, and daily sitting hours with depression, anxiety, and fatigue were checked using the linear regression test. The normal BMI group was considered a reference, and the difference in quantitative variables between the reference and the other groups was assessed using an independent sample t-test. Physical activity was classified with tertiles, and the difference in depression, anxiety, and fatigue between the PA groups was evaluated by a one-way ANOVA test. RESULTS: In total, 85 MS patients were recruited for the study. The mean ± SD age of the participants was 39.07 ± 8.84 years, and 72.9% (n: 62) of them were female. The fatigue score was directly correlated with BMI (P: 0.03; r: 0.23) and sitting hours per day (P: 0.01; r: 0.26) and indirectly correlated with PA level (P < 0.01; r: -0.33). Higher depression scores were significantly correlated with elevated daily sitting hours (P: 0.01; r: 0.27). However, the correlation between depression with PA and BMI was not meaningful (p > 0.05). Higher anxiety scores were correlated with BMI (P: 0.01; r: 0.27) and lower PA (P: 0.01; r: -0.26). The correlation between anxiety and sitting hours per day was not significant (p > 0.05). Patients in the type I obesity group had significantly higher depression scores than the normal weight group (23.67 ± 2.30 vs. 14.05 ± 9.12; P: 0.001). Fatigue (32.61 ± 14.18 vs. 52.40 ± 12.42; P: <0.01) and anxiety (14.66 ± 9.68 vs. 27.80 ± 15.48; P: 0.01) scores were significantly greater among participants in the type II obesity group in comparison with the normal weight group. Fatigue (P: 0.01) and anxiety (P: 0.03) scores were significantly different in the three levels of PA, but no significant difference was found in the depression score (P: 0.17). CONCLUSION: Our data suggest that a physically active lifestyle and being in the normal weight category are possible factors that lead to lower depression, fatigue, and anxiety in patients with MS.
 Sarcoidosis is a multi-organ systemic disease that presents with several clinical manifestations, and patients can develop neurologic complications. Neurosarcoidosis may be life-threatening; therefore, early recognition and treatment are key. Here, we present a case of a 55-year-old African American male who presented with a complaint of dizziness and left-sided weakness; he ultimately received a diagnosis of neurosarcoidosis after elaborate radiographic investigations and bladder mass biopsy. Neurosarcoidosis remains a diagnostic dilemma as it can clinically and radiographically mimic multiple conditions including multiple sclerosis, central nervous system lymphoma, multiple myeloma, and progressive multifocal leukoencephalopathy.


 Melanosis of the urinary bladder is an extremely rare benign condition in which melanin deposits occur in the urothelial and stromal cells. We report such a case in which melanosis of the urinary bladder was detected in a 55-year-old woman with known multiple sclerosis during an extended workup due to urinary urgency complaints. The findings were confirmed by biopsy.
 BACKGROUND AND OBJECTIVES: Ocrelizumab and rituximab are monoclonal antibodies targeting the CD20 marker on B lymphocytes. The enhanced efficacy of B lymphocyte depleting therapies poses a greater risk of decreased immunoglobulin (Ig) levels. The rate and risk factors of hypogammaglobulinemia in MS and NMOSD patients treated with anti-CD20 therapies are unknown. METHODS: A retrospective study was conducted among patients who received anti-CD20 therapy for the treatment of MS, NMOSD, and other related neurological disorders. The goal was to determine the incidence and risk factors of hypogammaglobulinemia and serious infections in patients receiving ocrelizumab versus rituximab. The secondary goals were to determine the rates of lymphopenia, neutropenia, and early B cell repopulation among patients on anti-CD20 therapy. RESULTS: Overall, 184 patients (mean age 48.4 ± 13.7, 66.8% female) met inclusion criteria; 152 patients received ocrelizumab and 32 patients received rituximab. A total of 22 patients (12%) developed hypogammaglobulinemia. Patients who developed hypogammaglobulinemia were more likely to have been ≥50 years of age (p = .0275) with lower baseline IgG (p = .001) and IgA (p = .0038) levels. Serious infections were observed in 21 patients (11%) and seen more commonly in those that developed total lymphopenia (<1.0 × 109/L) and had longer duration of B-cell therapy. Multivariate analysis identified age ≥ 50 years, white race, and rituximab as independent predictors of hypogammaglobulinemia, and absolute lymphopenia as an independent risk factor for serious infections. DISCUSSION: Among patients receiving anti-CD20 therapy, 12% of patients experienced hypogammaglobulinemia which was seen more commonly in white patients, at least 50 years old, with lower baseline IgG and IgA levels and in those treated with rituximab. Serious infections were seen more commonly in patients with total lymphopenia and longer exposure to anti-CD20 therapy.
 OBJECTIVES: To report pregnancy outcomes among multiple sclerosis (MS) patients treated with disease-modifying therapies (DMTs). METHODS: We performed a retrospective chart review of articles published from June 1996 to May 2023. Additional information was acquired from the drug registries of individual pharmaceutical companies. A comparison was also made with pregnancy data of the general population using the World Health Organization database. Summary analysis was achieved using R statistical software (v3.6), and the overall prevalence of outcomes was estimated using a random effects model. RESULTS: A meta-analysis of 44 studies was conducted. Dimethyl fumarate had the highest prevalence of premature births at 0.6667% (SD:0.5236-0.7845). The highest rates of stillbirths and infant deaths (perinatal and neonatal) were observed with interferons at 0.004% (SD:0.001-0.010) and 0.009% (SD:0.005-0.0015), respectively. Cladribine had the majority of ectopic pregnancies (0.0234%, SD:0.0041-1217), while natalizumab had the highest prevalence of spontaneous abortions (0.1177%, SD:0.0931-0.1477) and live birth defects (0.0755%, SD:0.0643-0.0943).None of the outcomes were significantly different from those of the general population (p > 0.05), except ectopic pregnancy and spontaneous abortion (p < 0.001), where the odds were 0.665 (0.061-0.886) and 0.537(0.003-0.786), respectively. The pooled prevalence of MS relapses was 221% for a single episode (SD:0.001-0.714), 0.075% for more than one episode (SD:0.006-0.167), and 0.141% for at least one episode requiring steroids (SD:0.073-0.206) none of these reached clinical significance. CONCLUSION: Existing research suggests that DMT use in MS patients during pregnancy is generally considered safe. This study supports their utilization on a case-by-case basis. However, further primary research on this topic with clinical trials is warranted.
 Interferons are currently used clinically to treat viral infections such as hepatitis C, cancers including non-Hodgkin’s lymphoma, and autoimmune diseases such as multiple sclerosis. This activity outlines the different types of interferons, namely interferon alpha, beta, and gamma. It discusses the pharmacological properties of different interferons, their medical uses, methods of administration, potential adverse effects, and other properties. It also highlights the important role that providers play in terms of correctly administering and dosing interferon medication, regularly monitoring patients for adverse effects, and counseling patients on the importance of medication adherence.

 INTRODUCTION: Brain atrophy is a critical biomarker of disease progression and treatment response in neurodegenerative diseases such as multiple sclerosis (MS). Confounding factors such as inconsistent imaging acquisitions hamper the accurate measurement of brain atrophy in the clinic. This study aims to develop and validate a robust deep learning model to overcome these challenges; and to evaluate its impact on the measurement of disease progression. METHODS: Voxel-wise pseudo-atrophy labels were generated using SIENA, a widely adopted tool for the measurement of brain atrophy in MS. Deformation maps were produced for 195 pairs of longitudinal 3D T1 scans from patients with MS. A 3D U-Net, namely DeepBVC, was specifically developed overcome common variances in resolution, signal-to-noise ratio and contrast ratio between baseline and follow up scans. The performance of DeepBVC was compared against SIENA using McLaren test-retest dataset and 233 in-house MS subjects with MRI from multiple time points. Clinical evaluation included disability assessment with the Expanded Disability Status Scale (EDSS) and traditional imaging metrics such as lesion burden. RESULTS: For 3 subjects in test-retest experiments, the median percent brain volume change (PBVC) for DeepBVC and SIENA was 0.105 vs. 0.198% (subject 1), 0.061 vs. 0.084% (subject 2), 0.104 vs. 0.408% (subject 3). For testing consistency across multiple time points in individual MS subjects, the mean (± standard deviation) PBVC difference of DeepBVC and SIENA were 0.028% (± 0.145%) and 0.031% (±0.154%), respectively. The linear correlation with baseline T2 lesion volume were r = -0.288 (p < 0.05) and r = -0.249 (p < 0.05) for DeepBVC and SIENA, respectively. There was no significant correlation of disability progression with PBVC as estimated by either method (p = 0.86, p = 0.84). DISCUSSION: DeepBVC is a deep learning powered brain volume change estimation method for assessing brain atrophy used T1-weighted images. Compared to SIENA, DeepBVC demonstrates superior performance in reproducibility and in the context of common clinical scan variances such as imaging contrast, voxel resolution, random bias field, and signal-to-noise ratio. Enhanced measurement robustness, automation, and processing speed of DeepBVC indicate its potential for utilisation in both research and clinical environments for monitoring disease progression and, potentially, evaluating treatment effectiveness.
 BACKGROUND: To assign a course of secondary progressive multiple sclerosis (MS) (SPMS) may be difficult and the proportion of persons with SPMS varies between reports. An objective method for disease course classification may give a better estimation of the relative proportions of relapsing-remitting MS (RRMS) and SPMS and may identify situations where SPMS is under reported. MATERIALS AND METHODS: Data were obtained for 61,900 MS patients from MS registries in the Czech Republic, Denmark, Germany, Sweden, and the United Kingdom (UK), including date of birth, sex, SP conversion year, visits with an Expanded Disability Status Scale (EDSS) score, MS onset and diagnosis date, relapses, and disease-modifying treatment (DMT) use. We included RRMS or SPMS patients with at least one visit between January 2017 and December 2019 if ≥ 18 years of age. We applied three objective methods: A set of SPMS clinical trial inclusion criteria ("EXPAND criteria") modified for a real-world evidence setting, a modified version of the MSBase algorithm, and a decision tree-based algorithm recently published. RESULTS: The clinically assigned proportion of SPMS varied from 8.7% (Czechia) to 34.3% (UK). Objective classifiers estimated the proportion of SPMS from 15.1% (Germany by the EXPAND criteria) to 58.0% (UK by the decision tree method). Due to different requirements of number of EDSS scores, classifiers varied in the proportion they were able to classify; from 18% (UK by the MSBase algorithm) to 100% (the decision tree algorithm for all registries). Objectively classified SPMS patients were older, converted to SPMS later, had higher EDSS at index date and higher EDSS at conversion. More objectively classified SPMS were on DMTs compared to the clinically assigned. CONCLUSION: SPMS appears to be systematically underdiagnosed in MS registries. Reclassified patients were more commonly on DMTs.
 PURPOSE: Multiple sclerosis (MS) is a neurological disease that is chronic, progressive characterized by symptoms of relapsing fatigue and pain. Despite evidence supporting the use of physical activity (PA) for MS symptom management, low rates of PA participation are observed. Previous research suggests exercise-related cognitive errors (ECEs) can deter and decrease PA participation. The purpose of this study was to examine whether ECEs and self-regulatory efficacy for MS symptom control predict important behavior-related outcomes for MS self-management (dependent variables: PA, maladaptive behavioral responses to illness, and perceived walking impairment). METHOD: Adults with MS (N = 110; aged 18 and over, with a patient-determined disease steps score of six or less) completed the following validated questionnaires: ECEs, MS symptom control self-efficacy, self-report moderate to vigorous physical activity, behavioral responses to illness, and perceived walking impairment. RESULTS: ECEs significantly predicted behavioral responses to illness (β = .459, p < .01) and perceived walking impairment (β = .279, p < .01). The interaction between ECEs and self-regulatory efficacy significantly predicted all three dependent variables (βs ranged from .155 to .263, ps < .05). CONCLUSION: This is the first study to demonstrate associations between ECEs and different illness- and mobility-related perceptions for persons with MS. Findings suggested that self-regulatory efficacy to manage MS symptoms varied based on low, moderate, or high levels of ECEs. Disability status is not easily modifiable; targeting social cognitions, like self-regulatory efficacy or ECEs, may be a promising way to promote PA for MS self-management. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 Multiple sclerosis (MS) is a life-threading disease that poses a great threat to the human being lifestyle. Having said extensive research in the realm of underlying mechanisms and treatment procedures, no definite remedy has been found. Over the past decades, many medicines have been disclosed to alleviate the symptoms and marking of MS. Meanwhile, the substantial efficacy of herbal medicines including curcumin must be underscored. Accumulated documents demonstrated the fundamental role of curcumin in the induction of the various signaling pathways. According to evidence, curcumin can play a role in mitochondrial dysfunction and apoptosis, autophagy, and mitophagy. Also, by targeting the signaling pathways AMPK, PGC-1α/PPARγ, and PI3K/Akt/mTOR, curcumin interferes with the metabolism of MS. The anti-inflammatory, antioxidant, and immune regulatory effects of this herbal compound are involved in its effectiveness against MS. Thus, the present review indicates the molecular and metabolic pathways associated with curcumin's various pharmacological actions on MS, as well as setting into context the many investigations that have noted curcumin-mediated regulatory effects in MS.
 Behavioral aspects and underlying pathology of attention deficit in multiple sclerosis (MS) remain unknown. This study aimed to clarify impairment of attention and its relationship with MS-related fatigue. Thirty-four relapse-remitting MS (RRMS), 35 secondary-progressive MS (SPMS) and 45 healthy controls (HC) were included. Results of psychophysics tasks (attention network test (ANT) and Posner spatial cueing test) and fatigue assessments (visual analogue scale and modified fatigue impact scale (MFIS)) were compared between groups. In ANT, attentional network effects were not different between MS phenotypes and HC. In Posner task, RRMS or SPMS patients did not benefit from valid cues unlike HC. RRMS and SPMS patients had less gain in exogenous trials with 62.5 ms cue-target interval time (CTIT) and endogenous trials with 250 ms CTIT, respectively. Total MFIS was the predictor of gain in 250 ms endogenous blocks and cognitive MFIS predicted orienting attentional effect. Executive attentional effect in RRMS patients with shorter disease duration and orienting attentional effect in longer diagnosed SPMS were correlated with MFIS scores. The pattern of attention deficit in MS differs between phenotypes. Exogenous attention is impaired in RRMS patients while SPMS patients have deficit in endogenous attention. Fatigue trait predicts impairment of endogenous and orienting attention in MS.
 Low pH stress and its influence on antibody binding is a common consideration among chemists, but is only recently emerging as a consideration in Immunological studies. Antibody characterizations in Multiple Sclerosis (MS), an autoimmune disease of the Central Nervous System (CNS) has revealed that antibodies in the cerebrospinal fluid (CSF) of patients with Multiple Sclerosis bind to myelin-related and non-myelin antigen targets. Many laboratories have used molecular biology techniques to generate recombinant human antibodies (rhAbs) expressed by individual B cells from healthy donors and patients with systemic autoimmune disease to identify antigen targets. This approach has been adapted within the Neuroimmunology research community to investigate antigen targets of individual B cells in the CSF of MS patients. Our laboratory determines which antibodies to clone based on their immunogenetics and this method enriches for cloning of rhAbs that bind to neurons. However, newer technologies to assist in purification of these rhAbs from culture supernatants use an acidic elution buffer which may enhance low pH stress on the antibody structure. Our laboratory routinely uses a basic elution buffer to purify rhAbs from culture supernatants to avoid low pH stress to the antibody structure. Our goal was to investigate whether acidic elution of our rhAbs using Next Generation Chromatography would impact the rhAbs' ability to bind neurons. The limited data presented here for two neuron-binding rhAbs tested indicated that acidic elution buffers used during rhAb purification impacted the ability of rhAbs with low CDR3 charge to maintain binding to neuronal targets. Reproducibility in a larger panel of rhAbs and factors underlying these observations remain untested.
 OBJECTIVE: Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system, resulting in a range of potential motor and cognitive impairments. The latter can affect both executive functions that orchestrate general goal-directed behavior and social cognitive processes that support our ability to interact with others and maintain healthy interpersonal relationships. Despite a long history of research into the cognitive symptoms of MS, it remains uncertain if social cognitive disruptions occur independently of, or reflect underlying disturbances to, more foundational executive functions. The present preregistered study investigated this directly. METHOD: Employing an experimental design, we administered a battery of computerized tasks online to a large sample comprising 134 individuals with MS and 134 age- and sex-matched healthy controls (HCs). Three tasks measured elements of executive function (working memory, response inhibition, and switching) and two assessed components of social cognition disrupted most commonly in MS (emotion perception and theory of mind). RESULTS: Individuals with MS exhibited poorer working memory (d = .31), response inhibition (d = -.26), emotion perception (d = .32), and theory of mind (d = .35) compared with matched HCs. Furthermore, exploratory mediation analyses revealed that working memory performance accounted for approximately 20% of the group differences in both measures of social cognition. CONCLUSIONS: Disruptions to working memory appear to serve as one of the mechanisms underpinning disturbances to social cognition in MS. Future research should examine if the benefits of cognitive rehabilitation programs that incorporate working memory training transfer to these social cognitive processes. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 Afferent and efferent visual dysfunction are prominent features of multiple sclerosis (MS). Visual outcomes have been shown to be robust biomarkers of the overall disease state. Unfortunately, precise measurement of afferent and efferent function is typically limited to tertiary care facilities, which have the equipment and analytical capacity to make these measurements, and even then, only a few centers can accurately quantify both afferent and efferent dysfunction. These measurements are currently unavailable in acute care facilities (ER, hospital floors). We aimed to develop a moving multifocal steady-state visual evoked potential (mfSSVEP) stimulus to simultaneously assess afferent and efferent dysfunction in MS for application on a mobile platform. The brain-computer interface (BCI) platform consists of a head-mounted virtual-reality headset with electroencephalogram (EEG) and electrooculogram (EOG) sensors. To evaluate the platform, we recruited consecutive patients who met the 2017 MS McDonald diagnostic criteria and healthy controls for a pilot cross-sectional study. Nine MS patients (mean age 32.7 years, SD 4.33) and ten healthy controls (24.9 years, SD 7.2) completed the research protocol. The afferent measures based on mfSSVEPs showed a significant difference between the groups (signal-to-noise ratio of mfSSVEPs for controls: 2.50 ± 0.72 vs. MS: 2.04 ± 0.47) after controlling for age (p = 0.049). In addition, the moving stimulus successfully induced smooth pursuit movement that can be measured by the EOG signals. There was a trend for worse smooth pursuit tracking in cases vs. controls, but this did not reach nominal statistical significance in this small pilot sample. This study introduces a novel moving mfSSVEP stimulus for a BCI platform to evaluate neurologic visual function. The moving stimulus showed a reliable capability to assess both afferent and efferent visual functions simultaneously.
 Virchow-Robin spaces (VRS) have been associated with neurodegeneration and neuroinflammation. However, it remains uncertain to what degree non-dilated or dilated VRS reflect specific features of neuroinflammatory pathology. Thus, we aimed at investigating the clinical relevance of VRS as imaging biomarker in multiple sclerosis (MS) and to correlate VRS to their histopathologic signature. In a cohort study comprising 205 MS patients (including a validation cohort) and 30 control subjects, we assessed the association of non-dilated and dilated VRS to clinical and magnetic resonance imaging (MRI) out-comes. Brain blocks from 6 MS patients and 3 non-MS controls were histopathologically processed to correlate VRS to their tissue substrate. The count of dilated centrum semiovale VRS was associated with increased T1 and T2 lesion volumes. There was no systematic spatial colocalization of dilated VRS with MS lesions. At tissue level, VRS mostly corresponded to arteries and were not associated with MS pathological hallmarks. Interestingly, dilated VRS in MS were associated with signs of small vessel disease. Contrary to prior beliefs, these observations suggest that VRS in MS do not associate with accumulation of immune cells. But instead, these findings indicate vascular pathology as a driver and/or consequence of neuroinflammatory pathology for this imaging feature.
 Trigeminal neuralgia is a heterogeneous disorder with likely multifactorial and complex etiology; however, trigeminal nerve demyelination and injury is observed in almost all patients with trigeminal neuralgia. The current management strategies for trigeminal neuralgia primarily involve anticonvulsants and surgical interventions, neither of which directly address demyelination, the pathological hallmark of trigeminal neuralgia and treatments targeting demyelination are not available. Demyelination of the trigeminal nerve has been historically considered a secondary effect of vascular compression, and as a result, trigeminal neuralgia is not recognized nor treated as a primary demyelinating disorder. In this article, we review the evolution of our understanding of trigeminal neuralgia and provide evidence to propose its potential categorization, at least in some cases, as a primary demyelinating disease by discussing its course and similarities to multiple sclerosis, the most prevalent central nervous system demyelinating disorder. This proposed categorization may provide a basis in investigating novel treatment modalities beyond the current medical and surgical interventions, emphasizing the need for further research into demyelination of the trigeminal sensory pathway in trigeminal neuralgia. PERSPECTIVE: This article proposes trigeminal neuralgia as a demyelinating disease, supported by histological, clinical, and radiological evidence. Such categorization offers a plausible explanation for controversies surrounding trigeminal neuralgia. This perspective holds potential for future research and developing therapeutics targeting demyelination in the condition.
 OBJECTIVE: This paper provided an updated quantitative synthesis of physical activity levels in persons with multiple sclerosis (MS) compared with controls and other clinical populations. DESIGN: A systematic search through PubMed, Scopus, and PsycINFO was conducted for articles published between August, 2016 and July, 2022. Articles that included a group comparison of at least one measurement of physical activity between adults with MS and controls or other clinical populations were included in the meta-analysis. RESULTS: Twenty-four studies met the inclusion criteria and yielded a total of 119 comparisons. There was a moderate difference in physical activity levels between persons with MS and controls (effect size [ES] = -0.56,p < 0.01), but no significant difference between persons with MS and other clinical populations (ES = 0.01,p = 0.90). The pooled ESs comparing MS with controls (Q104 = 457.9,p < 0.01) as well as with clinical populations (Q13 = 108.4,p < 0.01) were heterogeneous. Moderating variables included sex, disability status, measurement method, outcome, intensity, and application of an MS-specific cut-point. CONCLUSION: Physical activity levels remain significantly lower in persons with MS compared with controls, but the magnitude of difference has become smaller over the past decade. There is a need for continued development of effective physical activity programs that can reach the greater community with MS.
 OBJECTIVE: Although language is often considered to be largely intact in multiple sclerosis (MS), word-finding difficulties are a common complaint. Recent work suggests that declines in language are not solely the result of motoric and cognitive slowing that is most strongly associated with MS. Network science approaches have been effectively used to examine network structure as it relates to clinical conditions, aging, and language. The present study utilizes a network science approach to investigate whether individuals with MS exhibit less interconnected and resilient semantic networks compared to age-matched neurotypical peers. METHOD: We used semantic fluency data from 89 participants with MS and 88 neurotypical participants to estimate and analyze the semantic network structure for each participant group. Additionally, we conducted a percolation analysis to examine the resilience of each network. RESULTS: Network measures showed that individuals with MS had lower local and global clustering coefficients, longer average shortest path lengths, and higher modularity values compared to neurotypical peers. Small-worldness, network portrait divergence measures, and community detection analyses were consistent with these results and indicated that macroscopic properties of the two networks differed and that the semantic network for individuals with MS was more fractured than the neurotypical peer network. Moreover, a spreading activation simulation and percolation analysis suggested that the semantic networks of individuals with MS are less flexible and activation degrades faster than those of age-matched neurotypical participants. CONCLUSIONS: These differing semantic network structures suggest that language retrieval difficulties in MS partially result from decline in language-specific factors. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 In this paper, we explore the characteristics of cognitive dysfunction in patients with schizophrenia complicated with metabolic syndrome (MS), and to explore the effects of psychological intervention on MS and cognitive function changes in patients with schizophrenia, and to provide theoretical basis for early intervention of MS. 159 patients with schizophrenia were retrospectively analyzed and divided into 2 groups according to whether they were accompanied by MS. (41 cases), the second group was not MS. (118 cases). Results shows PANSS total score as (53.72 ± 5.03), positive symptom score (12.39 ± 2.68), negative symptom score (14.94 ± 3.27), general pathological score (26.27 ± 3.63). In MS group,Verbal fluency (16.69 ± 1.27), symbol coding (30.46 ± 2.55), number sequence (15.21 ± 1.84), spatial span (10.14 ± 0.68), continuous operation (16.72 ± 1.34), verbal memory (16.72 ± 1.34), and visual memory (14.24 ± 1.26), all indicators were significantly lower than those of non-MS group. The cognitive impairment of schizophrenia patients with multiple sclerosis is more severe than that of schizophrenia patients without multiple sclerosis. Increasing psychological intervention can effectively improve the therapeutic effect and cognitive function of schizophrenia patients. Early identification and intervention of MS in the clinical treatment of schizophrenia is particularly important.
 Although B cells are implicated in multiple sclerosis (MS) pathophysiology, a predictive or diagnostic autoantibody remains elusive. Here, the Department of Defense Serum Repository (DoDSR), a cohort of over 10 million individuals, was used to generate whole-proteome autoantibody profiles of hundreds of patients with MS (PwMS) years before and subsequently after MS onset. This analysis defines a unique cluster of PwMS that share an autoantibody signature against a common motif that has similarity with many human pathogens. These patients exhibit antibody reactivity years before developing MS symptoms and have higher levels of serum neurofilament light (sNfL) compared to other PwMS. Furthermore, this profile is preserved over time, providing molecular evidence for an immunologically active prodromal period years before clinical onset. This autoantibody reactivity was validated in samples from a separate incident MS cohort in both cerebrospinal fluid (CSF) and serum, where it is highly specific for patients eventually diagnosed with MS. This signature is a starting point for further immunological characterization of this MS patient subset and may be clinically useful as an antigen-specific biomarker for high-risk patients with clinically- or radiologically-isolated neuroinflammatory syndromes.
 BACKGROUND: Atrophy related to Multiple Sclerosis (MS) has been found at the early stages of the disease. However, the archetype dynamic trajectories of the neurodegenerative process, even prior to clinical diagnosis, remain unknown. METHODS: We modeled the volumetric trajectories of brain structures across the entire lifespan using 40944 subjects (38295 healthy controls and 2649 MS patients). Then, we estimated the chronological progression of MS by assessing the divergence of lifespan trajectories between normal brain charts and MS brain charts. RESULTS: Chronologically, the first affected structure was the thalamus, then the putamen and the pallidum (3 years later), followed by the ventral diencephalon (7 years after thalamus) and finally the brainstem (9 years after thalamus). To a lesser extent, the anterior cingulate gyrus, insular cortex, occipital pole, caudate and hippocampus were impacted. Finally, the precuneus and accumbens nuclei exhibited a limited atrophy pattern. CONCLUSION: Subcortical atrophy was more pronounced than cortical atrophy. The thalamus was the most impacted structure with a very early divergence in life. It paves the way toward utilization of these lifespan models for future preclinical/prodromal prognosis and monitoring of MS.
 BACKGROUND: Infections, early life exposures and the microbiome have been associated with the aetiology of multiple sclerosis (MS). Data on any possible roles of antibiotics is scarce and conflicting. OBJECTIVE: The objective of this study was to investigate associations between outpatient systemic antibiotic exposure and the risk of MS in a nationwide case-control setting. METHODS: Patients with MS were identified from the nation MS registry and their exposure to antibiotics was compared with that of persons without MS, provided by the national census authority. Antibiotic exposure was investigated using the national prescription database and analyzed by Anatomical Therapeutic Chemical (ATC) category. RESULTS: Among the 1830 patients with MS and 12765 control persons, there were no associations between exposure to antibiotics in childhood (5-9 years) or adolescence (10-19 years) and the subsequent risk of MS. There was also no association between antibiotic exposure 1-6 years before disease onset and the risk of MS, save for exposure to fluoroquinolones in women (odds ratio: 1.28; 95% confidence interval: 1.03, 1.60; p = 0.028) which is probably associated with the increased infection burden in the MS prodrome. CONCLUSION: Use of systemic prescription antibiotics was not associated with subsequent MS risk.
 BACKGROUND: Backward walking (BW) interventions have improved gait and balance in persons with stroke, cerebral palsy, and Parkinson disease but have not been studied in persons with multiple sclerosis (MS). We examined the feasibility of a BW intervention and how it affected strength, balance, and gait vs forward walking (FW) in persons with MS. METHODS: Sixteen persons with MS with a Patient-Determined Disease Steps (PDDS) scale score of 3 to 5 (gait impairment-late cane) were randomized to the FW (n = 8) or BW (n = 8) group. Participants did 30 minutes of FW or BW on a treadmill 3 times per week for 8 weeks (24 visits). Enrollment, adherence rate, and safety were tracked. The Timed Up and Go test, Six-Spot Step Test, single-leg stance, and abbreviated Activities-specific Balance Confidence scale were used to measure balance. Hip and knee flexion and extension strength (isometric peak torque), gait speed, and spatiotemporal gait parameters were measured. A 2×2 factorial multivariate analysis of covariance was used to examine changes in strength, balance, and gait, with the PDDS scale score as the covariate. RESULTS: Treatment adherence rate was 99.7%, with no safety concerns. After controlling for baseline differences in disability (PDDS scale score; P = .041), the BW group improved dominant hip flexion strength preintervention to postintervention compared with the FW group (F (1,13) = 9.03; P = .010). No other significant differences were seen between groups. CONCLUSIONS: This was the first study to look at BW as an intervention in persons with MS. Based on its feasibility, safety, and significant finding, BW should be studied in a larger, definitive trial in the future.
 Neurodegenerative diseases are highly prevalent but poorly understood, and with few treatment options despite decades of intense research, attention has recently shifted toward other mediators of neurological disease that may present future targets for therapeutic research. One such mediator is the gut microbiome, which communicates with the brain through the gut-brain axis and has been implicated in various neurological disorders. Alterations in the gut microbiome have been associated with numerous neurological and other diseases, and restoration of the dysbiotic gut has been shown to improve disease conditions. One method of restoring a dysbiotic gut is via fecal microbiota transplantation (FMT), recolonizing the "diseased" gut with normal microbiome. Fecal microbiota transplantation is a treatment method traditionally used for Clostridium difficile infections, but it has recently been used in neurodegenerative disease research as a potential treatment method. This review aims to present a summary of neurodegenerative research that has used FMT, whether as a treatment or to investigate how the microbiome influences pathogenesis.
 BACKGROUND: Relapsing multiple sclerosis (MS) is an inflammatory, demyelinating, neurodegenerative disease of the central nervous system that causes episodes of neurological dysfunction (relapse) alternating with variable intervals of stability. Disease-modifying therapies (DMTs) aim to reduce the rate of relapse and slow disease progression in people with MS, particularly in those with relapsing MS. Ofatumumab is a fully human anti-CD20 monoclonal antibody approved to treat patients with relapsing forms of MS. This study describes the demographics, clinical characteristics, and prior DMT use of patients with at least one ofatumumab prescription claim following approval by the United States (US) Food and Drug Administration (FDA). Understanding ofatumumab utilization patterns and patient characteristics can help define the journey of patients with MS and aid future clinical decision-making. METHODS: This retrospective study is based on data from IQVIA's Longitudinal Prescription Data (LRx) and Medical Claims (Dx) databases in the US, collected between August 01, 2019 and May 31, 2021. The index date was defined as the date of the first ofatumumab prescription. The pre-index period was defined as the 12 months prior to the index date. Adult patients (aged ≥18 years) with a diagnosis of MS and at least one prescription for ofatumumab between August 2020 and May 2021 in the LRx database were included. Only patients with at least one medical claim in the Dx database and a diagnosis of MS 24 months prior to the index date were included. Descriptive analyses were conducted 3, 6, and 9 months after FDA approval. RESULTS: Overall, 3,600 patients with a prescription for ofatumumab were identified in the LRx claims database, and 2,101 patients remained in the study after inclusion and exclusion criteria had been applied. At the 9-month post-approval time point, patients with ofatumumab claims were characterized as primarily female (74%) and middle-aged (median age: 48 years); two-thirds (64.7%) had a mild MS disability level. Patients were otherwise generally healthy with limited comorbid conditions. Most patients (81.7%) in the study did not experience relapse during the pre-index period. DMT-naïve patients who were prescribed ofatumumab at 3, 6, and 9 months post-approval accounted for 46.9%, 54.8%, and 58.4% of the study population, respectively. Over time, this increase in DMT-naïve ofatumumab initiators was statistically significant (p = 0.0003). Among patients who had been treated with DMTs during the previous year, most had taken them orally (50.6%), some had received them via intravenous infusion (32.2%), and some via subcutaneous/intramuscular injection (21.1%). Intravenous ocrelizumab was the most common DMT switch observed (n = 205, 23.4%) among these patients. CONCLUSION: This real-world study is the first to describe patients treated with ofatumumab since FDA approval during the COVID-19 pandemic. The majority of patients in this study were middle-aged women with mild MS symptoms. Ofatumumab was increasingly used as a first-line DMT. Additionally, a number of patients aged ≥55 years (beyond the trial population) used ofatumumab, which may suggest expanding clinician confidence in the safety and clinical utility of ofatumumab therapy. However, future long-term observational studies are needed to confirm these results.
 Gait speed is frequently the primary efficacy endpoint in clinical trials of interventions targeting mobility in people with multiple sclerosis (MS). However, it is unclear whether increased gait speed is a meaningful outcome for people living with MS. The purpose of this study was to identify the most important aspects of mobility for people with MS and physical therapists and to explore how patients and clinicians perceive whether physical therapy has been effective. Forty-six people with MS and 23 physical therapy clinicians participated in a focus group, one-on-one interview, or electronic survey. The focus group and interview data were transcribed and coded to identify themes. Free-text survey responses were also coded, and multiple-choice options were analyzed for frequency. Among people with MS, falls and difficulties getting out into the community were identified as highly important mobility limitations. Clinicians also identified falls and safety as a priority. Walking speed was infrequently described as a problem, and although gait speed is often measured by clinicians, improving gait speed is rarely a treatment goal. Despite their emphasis on safety, clinicians lacked certainty about how to objectively measure improvements in safety. People with MS evaluated physical therapy effectiveness based on the ease by which they can do things and acknowledged that "not getting worse" is a positive outcome. Clinicians evaluated effectiveness based on the amount of change in objective outcome measures and by patient and caregiver reports of improved function. These findings indicate that gait speed is not of major importance to people with MS or physical therapy clinicians. People with MS want to be able to walk further and without an assistive device, and they want to avoid falls. Clinicians want to maximize safety while improving functional ability. Clinicians and patients may differ in their expected outcomes from physical therapy.
 (1) Background: Multiple sclerosis (MS), a chronic progressive neurological disorder which affects the central nervous system (CNS), can result in disorders of all the functions controlled by the CNS: motor, sensory, cognitive and emotional. Physical therapy (PT), conducted through proprioceptive neuromuscular facilitation (PNF) techniques, can be customized to the individual patient's needs and has the potential to improve the patient's evolution. This study aims to establish if PT based on PNF techniques has a beneficial role in MS treatment. (2) Methods: We performed a prospective study on 40 patients who were diagnosed with MS and previously treated only with MS drug treatment (DT). These patients have participated in a PT program throughout one year. At the beginning and at the end of our study, after one year, we have assessed the following parameters: timed walk for 25 feet (Timed 25-Foot Walk test- T25FW test), dexterity of the upper limbs (9-Hole Peg Test-9HPT), disability level (Expanded Disability Status Scale-EDSS) and cognitive function (Paced Auditory Serial Addition Test-PASAT. (3) Results: In subjects in the early stages of MS, lower limb mobility improved significantly, T25FW decreasing from 6.46 to 5.80 (p < 0.001) and upper limb ability increased significantly in the dominant hand, 9HPT decreasing from 17.73 to 16.97 (p = 0.006) and not significantly in the non-dominant hand, 9HPT decreasing from 17.73 to 17.50 (p = 0.255). Furthermore, among these subjects, cognitive performance improved; their PASAT increased from 52.14 to 54.14 (p = 0.036), while the level of disability of these subjects improved only slightly, the EDSS scale evolving from 3.08 to 2.91 (p = 0.650). (4) Conclusions: In patients with early forms of MS, combining DT with a PT program based on PNF techniques results in: regaining muscle strength in the lower limbs, improving coordination while walking, correcting dexterity in the upper limbs and increasing the ability to concentrate.
 BACKGROUND: Cladribine tablets and fingolimod have similar marketing authorisations in Europe for the treatment of patients with highly active relapsing multiple sclerosis (HA-RMS). In the absence of direct head-to-head studies, real-world data are important to assess the comparative effectiveness of these oral disease-modifying therapies (DMTs). The primary objective of the present study was to compare relapse rates between patients who received either cladribine tablets or fingolimod. METHODS: This multicentre retrospective study conducted in the United Kingdom and Germany assessed non-inferiority in relapse rates of cladribine tablets versus fingolimod in HA-RMS patients over a 12-month period. Eligible patients who initiated treatment with cladribine tablets or fingolimod at least 12 months prior to the screening date were sampled consecutively until the target sample size was reached. Patients were censored at discontinuation of study treatment, commencement of another DMT, death, loss to follow-up, or at 12 months post-baseline, whichever happened earliest. The primary analytic timeframe for physician-confirmed relapse outcomes was the study effectiveness period (nine months of follow-up after an initial 12 weeks of treatment). Propensity score analysis was applied based on the inverse probability of treatment weighting approach. RESULTS: The primary analytic cohort consisted of 1,095 HA-RMS patients: 610 (55.7%) receiving cladribine tablets and 485 (44.3%) receiving fingolimod. Fewer patients discontinued cladribine tablets and/or switched to another DMT compared with fingolimod (0.2% versus 3.5%, respectively). The primary endpoint, adjusted annualised relapse rate (ARR), was 0.10 (95% confidence interval [CI]: 0.07-0.14) for cladribine tablets and 0.14 (95% CI: 0.10-0.20) for fingolimod. The adjusted ARR ratio of cladribine tablets versus fingolimod was 0.68 (95% CI: 0.42-1.11). Given the entire 95% CI was less than the non-inferiority margin of 1.2, cladribine tablets was non-inferior to fingolimod. CONCLUSIONS: In this real-world retrospective cohort study, cladribine tablets demonstrated comparable effectiveness to fingolimod at one year following treatment initiation. The full treatment dosage of cladribine tablets is completed over two years and so these results may be conservative.
 BACKGROUND: While kappa free light chain (KFLC) index has become a useful diagnostic biomarker in multiple sclerosis (MS), its prognostic properties are less explored. B cells play a crucial role in MS pathogenesis, but the impact from increased intrathecal production of immunoglobulins and KFLC remains to be determined. Recently, it has become evident that insidious worsening is not confined to progressive MS but is also common in relapsing-remitting MS (RRMS), a feature known as progression independent of relapse activity (PIRA). METHODS: We retrospectively identified 131 patients with clinically isolated syndrome or early RRMS who had determined KFLC index as part of their diagnostic workup. Demographic and clinical data were extracted from the Swedish MS registry. Associations of baseline KFLC index with evidence of disease activity (EDA) and PIRA were investigated in multivariable cox proportional hazards regression models. RESULTS: KFLC index was significantly higher in PIRA (median 148.5, interquartile range [IQR] 106.9-253.5) compared with non-PIRA (78.26, IQR 28.93-186.5, p = 0.009). In a multivariable cox regression model adjusted for confounders, KFLC index emerged as an independent risk factor for PIRA (adjusted hazard ratio [aHR] 1.005, 95% confidence interval [CI] 1.002-1.008, p = 0.002). Dichotomized by the cut-off value KFLC index > 100, patients with KFLC index > 100 had an almost fourfold increase in the risk for developing PIRA. KFLC index was also predictive of evidence of disease activity during follow-up. CONCLUSIONS: Our data indicate that high KFLC index at baseline is predictive of PIRA, EDA-3, and overall worse prognosis in MS.
 Over the last two decades, neuroimmunologic disorders of childhood have been increasingly described, phenotyped, and treated. These disorders remain rare in the general population and while sharing common therapeutic interventions due to their immune pathophysiology, are heterogeneous with regard to presentation and risk of recurrence. As such, the impact of these disorders on the developing brain has come into the forefront of emerging research in pediatric neuroimmunology. Investigations into the singular impact of monophasic disease on long-term development and the impact of early and aggressive disease-modifying therapy in relapsing conditions are quickly becoming areas of ripe investigation as the field's most optimal way to treat and monitor these conditions over time. Although critically important in evaluating the developing brain, research has been heterogeneous among these diseases and limited by small cohort size. This narrative review details the role of common neuroimmunologic disorders in long-term neurological and cognitive outcomes in children as they develop.
 BACKGROUND: Choroid plexus (CP) volume has been recently proposed as a proxy for brain neuroinflammation in multiple sclerosis (MS). PURPOSE: To develop and validate a fast automatic method to segment CP using routinely acquired brain T1-weighted and FLAIR MRI. STUDY TYPE: Retrospective. POPULATION: Fifty-five MS patients (33 relapsing-remitting, 22 progressive; mean age = 46.8 ± 10.2 years; 31 women) and 60 healthy controls (HC; mean age = 36.1 ± 12.6 years, 33 women). FIELD STRENGTH/SEQUENCE: 3D T2-weighted FLAIR and 3D T1-weighted gradient echo sequences at 3.0 T. ASSESSMENT: Brain tissues were segmented on T1-weighted sequences and a Gaussian Mixture Model (GMM) was fitted to FLAIR image intensities obtained from the ventricle masks of the SIENAX. A second GMM was then applied on the thresholded and filtered ventricle mask. CP volumes were automatically determined and compared with those from manual segmentation by two raters (with 3 and 10 years' experience; reference standard). CP volumes from previously published automatic segmentation methods (freely available Freesurfer [FS] and FS-GMM) were also compared with reference standard. Expanded Disability Status Scale (EDSS) score was assessed within 3 days of MRI. Computational time was assessed for each automatic technique and manual segmentation. STATISTICAL TESTS: Comparisons of CP volumes with reference standard were evaluated with Bland Altman analysis. Dice similarity coefficients (DSC) were computed to assess automatic CP segmentations. Volume differences between MS and HC for each method were assessed with t-tests and correlations of CP volumes with EDSS were assessed with Pearson's correlation coefficients (R). A P value <0.05 was considered statistically significant. RESULTS: Compared to manual segmentation, the proposed method had the highest segmentation accuracy (mean DSC = 0.65 ± 0.06) compared to FS (mean DSC = 0.37 ± 0.08) and FS-GMM (0.58 ± 0.06). The percentage CP volume differences relative to manual segmentation were -0.1% ± 0.23, 4.6% ± 2.5, and -0.48% ± 2 for the proposed method, FS, and FS-GMM, respectively. The Pearson's correlations between automatically obtained CP volumes and the manually obtained volumes were 0.70, 0.54, and 0.56 for the proposed method, FS, and FS-GMM, respectively. A significant correlation between CP volume and EDSS was found for the proposed automatic pipeline (R = 0.2), for FS-GMM (R = 0.3) and for manual segmentation (R = 0.4). Computational time for the proposed method (32 ± 2 minutes) was similar to the manual segmentation (20 ± 5 minutes) but <25% of the FS (120 ± 15 minutes) and FS-GMM (125 ± 15 minutes) methods. DATA CONCLUSION: This study developed an accurate and easily implementable method for automatic CP segmentation in MS using T1-weighted and FLAIR MRI. EVIDENCE LEVEL: 1 TECHNICAL EFFICACY: Stage 4.
 Alzheimer's disease (AD), the leading cause of dementia, is a growing health issue with very limited treatment options. To meet the need for novel therapeutics, existing drugs with additional preferred pharmacological profiles could be recruited. This strategy is known as 'drug repurposing'. Here, we describe dimethyl fumarate (DMF), a drug approved to treat multiple sclerosis (MS), to be tested as a candidate for other brain diseases. We used an APP-transgenic model (APPtg) of senile β-amyloidosis mice to further investigate the potential of DMF as a novel AD therapeutic. We treated male and female APPtg mice through drinking water at late stages of β-amyloid (Aβ) deposition. We found that DMF treatment did not result in modulating effects on Aβ deposition at this stage. Interestingly, we found that glutathione-modified DMF interacts with the ATP-binding cassette transporter ABCC1, an important gatekeeper at the blood-brain and blood-plexus barriers and a key player for Aβ export from the brain. Our findings suggest that ABCC1 prevents the effects of DMF, which makes DMF unsuitable as a novel therapeutic drug against AD. The discovered effects of ABCC1 also have implications for DMF treatment of multiple sclerosis.
 Proton magnetic resonance spectroscopy ((1)H-MRS) is an advanced method of examining metabolic profiles. The present study aimed to assess in vivo metabolite levels in areas of normal-appearing grey (thalamus) and white matter (centrum semiovale) using (1)H-MRS in patients with clinically isolated syndrome (CIS) suggestive of multiple sclerosis and compare them to healthy controls (HCs). Data from 35 patients with CIS (CIS group), of which 23 were untreated (CIS-untreated group) and 12 were treated (CIS-treated group) with disease-modifying-therapies (DMTs) at the time of (1)H-MRS, and from 28 age- and sex-matched HCs were collected using a 3.0 T MRI and single-voxel (1)H-MRS (point resolved spectroscopy sequence; repetition time, 2,000 msec; time to echo, 35 msec). Concentrations and ratios of total N-acetyl aspartate (tNAA), total creatine (tCr), total choline (tCho), myoinositol, glutamate (Glu), glutamine (Gln), Glu + Gln (Glx) and glutathione (Glth) were estimated in the thalamic-voxel (th) and centrum semiovale-voxel (cs). For the CIS group, the median duration from the first clinical attack to (1)H-MRS was 102 days (interquartile range, 89.5.-131.5). Compared with HCs, significantly lower Glx(cs) (P=0.014) and ratios of tCho/tCr(th) (P=0.026), Glu/tCr(cs) (P=0.040), Glx/tCr(cs) (P=0.004), Glx/tNAA(th) (P=0.043) and Glx/tNAA(cs) (P=0.015) were observed in the CIS group. No differences in tNAA levels were observed between the CIS and the HC groups; however, tNAA(cs) was higher in the CIS-treated than in the CIS-untreated group (P=0.028). Compared with those in HC group, decreased Glu(cs) (P=0.019) and Glx(cs) levels (P=0.014) and lower ratios for tCho/tCr(th) (P=0.015), Gln/tCr(th) (P=0.004), Glu/tCr(cs) (P=0.021), Glx/tCr(th) (P=0.041), Glx/tCr(cs) (P=0.003), Glx/tNAA(th) (P=0.030) and Glx/tNAA(cs) (P=0.015) were found in the CIS-untreated group. The present findings showed alterations in the normal-appearing grey and white matter of patients with CIS; moreover, the present results suggested an early indirect treatment effect of DMTs on the brain metabolic profile of these patients.
 BACKGROUND: Clinical and radiological signs of recurring disease activity (RDA) have been described in patients with multiple sclerosis (pwMS) after discontinuation of fingolimod (FGL). OBJECTIVE: To describe frequency, severity and potential risk factors for RDA after FGL discontinuation in a large real-world cohort of pwMS. METHODS: Post-FGL RDA was defined as evidence of clinical and/or radiological activity within 6 months after FGL discontinuation. Relapses with Expanded Disability Status Scale increase ⩾2 points and/or magnetic resonance imaging (MRI) activity with at least five cerebral gadolinium-enhancing lesions and/or ⩾6 cerebral new T2 lesions were defined as severe recurring disease activity (sRDA). Using a multivariate logistic model, we explored the influence of age, disease duration, sex, clinical, and MRI activity under FGL on the occurrence of RDA. RESULTS: We identified 110 pwMS who discontinued FGL. Thirty-seven (33.6%) developed post-FGL RDA and 13 (11.8%) also fulfilled criteria for sRDA. Younger age at diagnosis [odds ratio (OR) = 1.10, p < 0.01], shorter disease duration (OR = 1.17, p < 0.01), and MRI activity under FGL (OR = 2.92, p = 0.046) were independent risk factors for the occurrence of post-FGL RDA. CONCLUSION: Individual risk assessment and optimal treatment sequencing can help to minimize the risk of post-FGL RDA. Early switch to highly effective disease-modifying therapy might reduce occurrence of post-FGL RDA.
 BACKGROUND: Conventional gadolinium (Gd)-enhanced MRI is currently used for stratifying the lesion activity of multiple sclerosis (MS) despite limited correlation with disability and disease activity. The stratification of MS lesion activity needs further improvement to better support clinics. PURPOSE: To investigate if the novel proton exchange rate (k (ex) ) MRI combined with quantitative susceptibility mapping (QSM) may help to further stratify non-enhanced (Gd-negative) MS lesions. MATERIALS AND METHODS: From December 2017 to December 2020, clinically diagnosed relapsing-remitting MS patients who underwent MRI were consecutively enrolled in this IRB-approved retrospective study. The customized MRI protocol covered conventional T(2)-weighted, T(2)-fluid-attenuated-inversion-recovery, pre- and post-contrast T(1)-weighted imaging, and quantitative sequences, including k (ex) MRI based on direct-saturation removed omega plots and QSM. Each MS lesion was evaluated based on its Gd-enhancement as well as its susceptibility and k (ex) elevation compared to the normal appearing white matter. The difference and correlation concerning lesion characteristics and imaging contrasts were analyzed using the Mann-Whitney U test or Kruskal-Wallis test, and Spearman rank analysis with p < 0.05 considered significant. RESULTS: A total of 322 MS lesions from 30 patients were identified with 153 Gd-enhanced and 169 non-enhanced lesions. We found that the k (ex) elevation of all lesions significantly correlated with their susceptibility elevation (r = 0.30, p < 0.001). Within the 153 MS lesions with Gd-enhancement, ring-enhanced lesions showed higher k (ex) elevation than the nodular-enhanced ones' (p < 0.001). Similarly, lesions with ring-hyperintensity in QSM also had higher k (ex) elevation than the lesions with nodular-QSM-hyperintensity (p < 0.001). Of the 169 Gd-negative lesions, three radiological patterns were recognized according to lesion manifestations on the k (ex) map and QSM images: Pattern I (k (ex) (+) and QSM(+), n = 114, 67.5%), Pattern II (only k (ex) (+) or QSM(+), n = 47, 27.8%) and Pattern III (k (ex) (-) and QSM(-), n = 8, 4.7%). Compared to Pattern II and III, Pattern I had higher k (ex) (p < 0.001) and susceptibility (p < 0.05) elevation. The percentage of Pattern I of each subject was negatively correlated with the disease duration (r = -0.45, p = 0.015). CONCLUSION: As a potential imaging biomarker for inflammation due to oxidative stress, in vivo k (ex) MRI combined with QSM is promising in extending the clinical classification of MS lesions beyond conventional Gd-enhanced MRI.
 INTRODUCTION: Over the years, disease registers have been increasingly considered a source of reliable and valuable population studies. However, the validity and reliability of data from registers may be limited by missing data, selection bias or data quality not adequately evaluated or checked. This study reports the analysis of the consistency and completeness of the data in the Italian Multiple Sclerosis and Related Disorders Register. METHODS: The Register collects, through a standardized Web-based Application, unique patients. Data are exported bimonthly and evaluated to assess the updating and completeness, and to check the quality and consistency. Eight clinical indicators are evaluated. RESULTS: The Register counts 77,628 patients registered by 126 centres. The number of centres has increased over time, as their capacity to collect patients. The percentages of updated patients (with at least one visit in the last 24 months) have increased from 33% (enrolment period 2000-2015) to 60% (enrolment period 2016-2022). In the cohort of patients registered after 2016, there were ≥ 75% updated patients in 30% of the small centres (33), in 9% of the medium centres (11), and in all the large centres (2). Clinical indicators show significant improvement for the active patients, expanded disability status scale every 6 months or once every 12 months, visits every 6 months, first visit within 1 year and MRI every 12 months. CONCLUSIONS: Data from disease registers provide guidance for evidence-based health policies and research, so methods and strategies ensuring their quality and reliability are crucial and have several potential applications.
 BACKGROUND: Fatigue is a particularly debilitating symptom for people with multiple sclerosis (MS). Although personality traits and MS have been studied, interoception and emotional susceptibility and their links to fatigue have not yet been explored. METHODS: Study participants provided demographic information and completed standardized patient-reported outcomes of walking function, physical activity, subjective fatigue, interoceptive awareness, and emotional susceptibility. A subset of participants participated in semistructured interviews discussing fatigue, body sensations, emotions, and their effects on exercise. Quantitative data were analyzed using multiple regression. Qualitative data were analyzed using thematic analysis. RESULTS: Mean ± SD Fatigue Severity Scale scores (5.0 ± 1.3) indicated that fatigue was a problematic symptom. Mean ± SD Multidimensional Assessment of Interoceptive Awareness, Version 2 (2.8 ± 0.6) and Emotional Susceptibility Scale (3.0 ± 1.0) scores indicated lower levels of interoceptive awareness and emotional susceptibility. Quantitative data indicated no relationship between fatigue and interoceptive awareness (β = -0.20; P = .88) and emotional susceptibility (β = 0.03; P = .83), and neither were these related to physical activity (β = -0.07; P = .64). Qualitative themes indicated strong fatigue experiences involving the whole body and individual limbs, anger and frustration, and effects on physical activity. CONCLUSIONS: Physically active people with MS report strong sensations of fatigue closely linked to frustration and helplessness. There was agreement between qualitative and quantitative assessments of fatigue but dissonance regarding interoceptive awareness and physical activity. The practice of clinicians, particularly those involved with facilitating or planning physical activity for persons with MS, would benefit from these findings about fatigue.
 Tools for monitoring daily physical activity (PA) are desired by persons with multiple sclerosis (MS). However, current research-grade options are not suitable for longitudinal, independent use due to their cost and user experience. Our objective was to assess the validity of step counts and PA intensity metrics derived from the Fitbit Inspire HR, a consumer-grade PA tracker, in 45 persons with MS (Median age: 46, IQR: 40-51) undergoing inpatient rehabilitation. The population had moderate mobility impairment (Median EDSS 4.0, Range 2.0-6.5). We assessed the validity of Fitbit-derived PA metrics (Step count, total time in PA, time in moderate to vigorous PA (MVPA)) during scripted tasks and free-living activity at three levels of data aggregation (minute, daily, and average PA). Criterion validity was assessed though agreement with manual counts and multiple methods for deriving PA metrics via the Actigraph GT3X. Convergent and known-groups validity were assessed via relationships with reference standards and related clinical measures. Fitbit-derived step count and time in PA, but not time in MVPA, exhibited excellent agreement with reference measures during scripted tasks. During free-living activity, step count and time in PA correlated moderately to strongly with reference measures, but agreement varied across metrics, data aggregation levels, and disease severity strata. Time in MVPA weakly agreed with reference measures. However, Fitbit-derived metrics were often as different from reference measures as reference measures were from each other. Fitbit-derived metrics consistently exhibited similar or stronger evidence of construct validity than reference standards. Fitbit-derived PA metrics are not equivalent to existing reference standards. However, they exhibit evidence of construct validity. Consumer-grade fitness trackers such as the Fitbit Inspire HR may therefore be suitable as a PA tracking tool for persons with mild or moderate MS.
 BACKGROUND AND OBJECTIVES: Some patients with multiple sclerosis (MS) receiving ocrelizumab (OCR) report worsening symptoms toward the end of the 6-month infusion cycle ('wearing off'). The objective of our study was to comprehensively assess changes in symptom burden across 2 consecutive OCR infusion cycles. METHODS: SYMptom Burden on Ocrelizumab, a Longitudinal Study (SymBOLS; NCT04855617) was an investigator-initiated, 2-center study of patients with MS starting or receiving OCR. Patients' symptoms were assessed with NeuroQoL short forms, SymptoMScreen, and Work Productivity and Activity Impairment Questionnaire at the start-cycle, mid-cycle, and end-cycle time points in each of the 2 infusion cycles. Symptom scores at the 3 time points within each cycle were compared with repeated-measures ANOVA or the Friedman rank-sum test for non-normal variables. The proportions of patients with a meaningful symptomatic change from the start to the end of each infusion cycle were calculated, and patients whose symptoms improved, worsened, and stayed the same from the start to the end of the cycle were compared with respect to demographic and clinical characteristics. RESULTS: One hundred three patients with MS provided longitudinal data for analyses (mean age [SD]: 46.7 [12.2] years, 68% female, 33% non-White, disease duration: 15.5 [5] years, 41% with the Extended Disability Status Scale score >3). On a group level, NeuroQoL and SymptoMScreen scores mostly remained stable or even improved slightly toward the end of each cycle. On an individual level, symptoms remained unchanged across either cycle for most patients, and meaningful symptom worsening from the start to the end of the cycle was no more common than improvement. Meaningful change in symptoms in both cycles was very rare and generally in the direction of improvement toward the end cycle. Despite the lack of evidence for symptom worsening with a longer time from infusion, 54% of patients endorsed feeling of "wearing off" at least sometimes, most commonly as an increase in fatigue. DISCUSSION: Our prospective study failed to uncover evidence for the worsening of symptoms with a longer time from OCR infusion. These findings cast doubt on the existence of wearing off as a physiologic phenomenon in OCR-treated patients with MS. The perception of wearing off is likely the result of natural fluctuations in MS symptoms and attribution bias.
 INTRODUCTION: Multiple sclerosis (MS) clinical trials have included low numbers of patients from racial and ethnic minority populations; therefore, it is uncertain whether differences exist in response to disease-modifying therapies. We evaluated the real-world safety and effectiveness of dimethyl fumarate (DMF) treatment over 5 years in four patient cohorts: Black, non-Black, Hispanic, and non-Hispanic people with relapsing-remitting MS. METHODS: ESTEEM is an ongoing, 5-year, multinational, prospective study evaluating the long-term safety and effectiveness of DMF in people with MS. The analysis included patients newly prescribed DMF in routine practice at 393 sites globally. RESULTS: Overall, 5251 patients were analyzed (220 Black, 5031 non-Black; 105 Hispanic, 5146 non-Hispanic). Median (min-max) months of follow-up was 32 (0-72) for Black, 29 (1-77) for Hispanic, and 41 (0-85) for both the non-Black and non-Hispanic populations. In total, 39 (18%) Black and 29 (28%) Hispanic patients reported adverse events leading to treatment discontinuation versus 1126 (22%) non-Black and 1136 (22%) non-Hispanic patients; gastrointestinal disorders were the most common in all subgroups. Median lymphocyte counts decreased by 37% in Black, 40% in non-Black, 10% in Hispanic, and 39% in non-Hispanic patients in the first year, then remained stable and above the lower limit of normal in most patients. Annualized relapse rates (ARRs) (95% confidence intervals) up to 5 years were 0.054 (0.038-0.078) for Black, 0.077 (0.072-0.081) for non-Black, 0.069 (0.043-0.112) for Hispanic, and 0.076 (0.072-0.081) for non-Hispanic populations, representing reductions of 91-92% compared with ARR 12 months before study entry (all p < 0.0001). CONCLUSION: The safety profile of DMF in these subgroups was consistent with the overall ESTEEM population. Relapse rates remained low in Black and Hispanic patients, and consistent with non-Black and non-Hispanic patients. These data demonstrate a comparable real-world treatment benefit of DMF in Black and Hispanic patients. TRIAL REGISTRATION: ClinicalTrials.gov identifier NCT02047097.
 INTRODUCTION: Inconvenient administration and side effects of some disease-modifying therapies (DMTs) for relapsing multiple sclerosis (RMS) can deter adherence. We evaluated treatment satisfaction with cladribine tablets (CladT) for RMS in the Arabian Gulf. METHODS: This was a non-interventional, multicentre, prospective observational study in non-pregnant/lactating adults (aged ≥ 18 years) with RMS eligible for 1st treatment with CladT (EU labelling). The primary outcome was overall treatment satisfaction at 6 months (Treatment Satisfaction Questionnaire for Medication [TSQM]-14, v. 1.4), Global Satisfaction subscale. Secondary endpoints were TSQM-14 scores for convenience, satisfaction with side effects and satisfaction with effectiveness. Patients provided written informed consent. RESULTS: Of 63 patients screened, 58 received CladT and 55 completed the study. Mean age was 33 ± 9 years; mean weight 73 ± 17 kg; 31% male/69% female; mostly from the United Arab Emirates (52%) or Kuwait (30%). All had RMS (mean 0.9 ± 1.1 relapses in the past year), mean Expanded Disability Status Scale (EDSS) 1.4 ± 1.2; 36% were DMT-naïve. Mean [95% CI] score was high for overall treatment satisfaction (77.8 [73.0-82.6]), ease of use (87.4 [83.7-91.0]), tolerability (94.2 [91.0-97.3]) and effectiveness (76.2 [71.6-80.7]). Scores were similar irrespective of DMT history, age, gender, relapse history or EDSS. No relapses or serious treatment-emergent adverse events (TEAE) occurred. Two severe TEAE occurred (fatigue, headache) and 16% reported lymphopenia (two cases of grade 3 lymphopenia). Absolute lymphocyte counts at baseline and 6 months were 2.2 ± 0.8 × 10(9)/L and 1.3 ± 0.3 × 10(9)/L, respectively. CONCLUSIONS: Treatment satisfaction, ease of use, tolerability and patient-perceived effectiveness for CladT were high, irrespective of baseline demographics, disease characteristics and prior treatment.
 BACKGROUND: Resourceful endpoints of axonal loss are needed to predict the course of multiple sclerosis (MS). Corneal confocal microscopy (CCM) can detect axonal loss in patients with clinically isolated syndrome and established MS, which relates to neurological disability. OBJECTIVE: To assess corneal axonal loss over time in relation to retinal atrophy, and neurological and radiological abnormalities in MS. METHODS: Patients with relapsing-remitting (RRMS) (n = 68) or secondary progressive MS (SPMS) (n = 15) underwent CCM and optical coherence tomography. Corneal nerve fibre density (CNFD-fibres/mm(2)), corneal nerve branch density (CNBD-branches/mm(2)), corneal nerve fibre length (CNFL-mm/mm(2)) and retinal nerve fibre layer (RNFL-μm) thickness were quantified along with neurological and radiological assessments at baseline and after 2 years of follow-up. Age-matched, healthy controls (n = 20) were also assessed. RESULTS: In patients with RRMS compared with controls at baseline, CNFD (p = 0.004) and RNFL thickness (p < 0.001) were lower, and CNBD (p = 0.003) was higher. In patients with SPMS compared with controls, CNFD (p < 0.001), CNFL (p = 0.04) and RNFL thickness (p < 0.001) were lower. For identifying RRMS, CNBD had the highest area under the receiver operating characteristic (AUROC) curve (0.99); and for SPMS, CNFD had the highest AUROC (0.95). At follow-up, there was a further significant decrease in CNFD (p = 0.04), CNBD (p = 0.001), CNFL (p = 0.008) and RNFL (p = 0.002) in RRMS; in CNFD (p = 0.04) and CNBD (p = 0.002) in SPMS; and in CNBD (p = 0.01) in SPMS compared with RRMS. Follow-up corneal nerve loss was greater in patients with new enhancing lesions and optic neuritis history. CONCLUSION: Progressive corneal and retinal axonal loss was identified in patients with MS, especially those with more active disease. CCM may serve as an imaging biomarker of axonal loss in MS.
 BACKGROUND: Current therapeutic strategies in multiple sclerosis (MS) target neurodegeneration. However, the integration of atrophy measures into the clinical scenario is still an unmet need. PURPOSE: To compare methods for whole-brain and gray matter (GM) atrophy measurements using the Italian Neuroimaging Network Initiative (INNI) dataset. STUDY TYPE: Retrospective (data available from INNI). POPULATION: A total of 466 patients with relapsing-remitting MS (mean age = 37.3 ± 10 years, 323 women) and 279 healthy controls (HC; mean age = 38.2 ± 13 years, 164 women). FIELD STRENGTH/SEQUENCE: A 3.0-T, T1-weighted (spin echo and gradient echo without gadolinium injection) and T2-weighted spin echo scans at baseline and after 1 year (170 MS, 48 HC). ASSESSMENT: Structural Image Evaluation using Normalization of Atrophy (SIENA-X/XL; version 5.0.9), Statistical Parametric Mapping (SPM-v12); and Jim-v8 (Xinapse Systems, Colchester, UK) software were applied to all subjects. STATISTICAL TESTS: In MS and HC, we evaluated the intraclass correlation coefficient (ICC) among FSL-SIENA(XL), SPM-v12, and Jim-v8 for cross-sectional whole-brain and GM tissue volumes and their longitudinal changes, the effect size according to the Cohen's d at baseline and the sample size requirement for whole-brain and GM atrophy progression at different power levels (lowest = 0.7, 0.05 alpha level). False discovery rate (Benjamini-Hochberg procedure) correction was applied. A P value <0.05 was considered statistically significant. RESULTS: SPM-v12 and Jim-v8 showed significant agreement for cross-sectional whole-brain (ICC = 0.93 for HC and ICC = 0.84 for MS) and GM volumes (ICC = 0.66 for HC and ICC = 0.90) and longitudinal assessment of GM atrophy (ICC = 0.35 for HC and ICC = 0.59 for MS), while no significant agreement was found in the comparisons between whole-brain and GM volumes for SIENA-X/XL and both SPM-v12 (P = 0.19 and P = 0.29, respectively) and Jim-v8 (P = 0.21 and P = 0.32, respectively). SPM-v12 and Jim-v8 showed the highest effect size for cross-sectional GM atrophy (Cohen's d = -0.63 and -0.61). Jim-v8 and SIENA(XL) showed the smallest sample size requirements for whole-brain (58) and GM atrophy (152), at 0.7 power level. DATA CONCLUSION: The findings obtained in this study should be considered when selecting the appropriate brain atrophy pipeline for MS studies. EVIDENCE LEVEL: 4. TECHNICAL EFFICACY: Stage 1.
 BACKGROUND: B cells can be enriched within meningeal immune-cell aggregates of multiple sclerosis (MS) patients, adjacent to subpial cortical demyelinating lesions now recognized as important contributors to progressive disease. This subpial demyelination is notable for a 'surface-in' gradient of neuronal loss and microglial activation, potentially reflecting the effects of soluble factors secreted into the CSF. We previously demonstrated that MS B-cell secreted products are toxic to oligodendrocytes and neurons. The potential for B-cell-myeloid cell interactions to propagate progressive MS is of considerable interest. METHODS: Secreted products of MS-implicated pro-inflammatory effector B cells or IL-10-expressing B cells with regulatory potential were applied to human brain-derived microglia or monocyte-derived macrophages, with subsequent assessment of myeloid phenotype and function through measurement of their expression of pro-inflammatory, anti-inflammatory and homeostatic/quiescent molecules, and phagocytosis (using flow cytometry, ELISA and fluorescently-labeled myelin). Effects of secreted products of differentially activated microglia on B-cell survival and activation were further studied. FINDINGS: Secreted products of MS-implicated pro-inflammatory B cells (but not IL-10 expressing B cells) substantially induce pro-inflammatory cytokine (IL-12, IL-6, TNFα) expression by both human microglia and macrophage (in a GM-CSF dependent manner), while down-regulating their expression of IL-10 and of quiescence-associated molecules, and suppressing their myelin phagocytosis. In contrast, secreted products of IL-10 expressing B cells upregulate both human microglia and macrophage expression of quiescence-associated molecules and enhance their myelin phagocytosis. Secreted factors from pro-inflammatory microglia enhance B-cell activation. INTERPRETATION: Potential cross-talk between disease-relevant human B-cell subsets and both resident CNS microglia and infiltrating macrophages may propagate CNS-compartmentalized inflammation and injury associated with MS disease progression. These interaction represents an attractive therapeutic target for agents such as Bruton's tyrosine kinase inhibitors (BTKi) that modulate responses of both B cells and myeloid cells. FUNDING: Stated in Acknowledgments section of manuscript.
 Pioneering advancements in optical coherence tomography (OCT) have facilitated the discernment of peripapillary hyper-reflective ovoid mass-like structures (PHOMS), prevalent neuro-ophthalmological findings associated with an array of ophthalmic conditions, such as optic disc drusen (ODD), papilledema, myopic/tilted optic discs, non-arteritic anterior ischemic optic neuropathy (NA-AION), and optic neuritis. Despite an expanding corpus of research, numerous inquiries persist concerning their clinical significance, correlations with ocular afflictions, and prognostic implications. This comprehensive review endeavors to impart an in-depth comprehension of PHOMS, encompassing facets like conceptualization, detection, pathogenesis, and associations with diverse ophthalmic conditions. Furthermore, we underscore several unresolved quandaries and suggest prospective avenues for future exploration.
 BACKGROUND: The management of neurodegenerative diseases can be frustrating for clinicians, given the limited progress of conventional medicine in this context. AIM: For this reason, a more comprehensive, integrative approach is urgently needed. Among various emerging focuses for intervention, the modulation of central nervous system energetics, oxidative stress, and inflammation is becoming more and more promising. METHOD: In particular, electrons leakage involved in the mitochondrial energetics can generate reactive oxygen-free radical-related mitochondrial dysfunction that would contribute to the etiopathology of many disorders, such as Alzheimer's and other dementias, Parkinson's disease, multiple sclerosis, stroke, and amyotrophic lateral sclerosis (ALS). RESULTS: In this context, using agents, like acetyl L-carnitine (ALCAR), provides mitochondrial support, reduces oxidative stress, and improves synaptic transmission. CONCLUSION: This narrative review aims to update the existing literature on ALCAR molecular profile, tolerability, and translational clinical potential use in neurodegeneration, focusing on ALS.
 Anti-myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG) associated disorder (MOGAD) is an immune-mediated central nervous system (CNS) inflammatory demyelinating disorder that has been widely recognized in recent years. It is distinct from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), which are separate disease spectrums. Here we report the case of a 5-year-old boy who was admitted for 3 days with fever, headache, and vomiting. Magnetic resonance imaging revealed abnormal hyperintensity in the left thalamus and positive serum IgM for M. pneumoniae. After treatment with azithromycin, the headache gradually disappeared, but paralysis and urinary retention occurred on the 6th day after admission. MRI re-examination showed that the original abnormal signal in the left thalamus was significantly weakened, but new abnormal signals appeared in the brain and cerebrospinal cord, and the serum MOG-IgG was positive. After treatment, the child has fully recovered and is still receiving follow-up care. We believe that this is a case of MOGAD in a child with a biphasic ADEM phenotype secondary to M. pneumoniae infection, which has potential value in elucidating the pathophysiology of MOGAD.
 In the context of autoimmunity, myeloid cells of the central nervous system (CNS) constitute an ontogenically heterogeneous population that includes yolk sac-derived microglia and infiltrating bone marrow-derived cells (BMC). We previously identified a myeloid cell subset in the brain and spinal cord that expresses the surface markers CD88 and CD317 and is associated with the onset and persistence of clinical disease in the murine model of the human CNS autoimmune disorder, experimental autoimmune encephalomyelitis (EAE). We employed an experimental platform utilizing single-cell transcriptomic and epigenomic profiling of bone marrow-chimeric mice to categorically distinguish BMC from microglia during CNS autoimmunity. Analysis of gene expression and chromosomal accessibility identified CD88(+)CD317(+) myeloid cells in the CNS of EAE mice as originating from BMC and microglia. Interestingly, each cell lineage exhibited overlapping and unique gene expression patterns and transcription factor motifs that allowed their segregation. Our observations will facilitate determining pathogenic contributions of BMC and microglia in CNS autoimmune disease. Ultimately, this agnostic characterization of myeloid cells will be required for devising disease stage-specific and tissue-specific interventions for CNS inflammatory and neurodegenerative disorders.
 OBJECTIVES: Intra-individual variability (IIV), measured across repeated response times (RT) during continuous psychomotor tasks, is an early marker of cognitive change in the context of neurodegeneration. To advance IIV towards broader application in clinical research, we evaluated IIV from a commercial cognitive testing platform and compared it to the calculation approaches used in experimental cognitive studies. METHODS: Cognitive assessment was administered in participants with multiple sclerosis (MS) during the baseline of an unrelated study. Cogstate was used for computer-based measures providing three timed-trial tasks measuring simple (Detection; DET) and choice (Identification; IDN) RT and working memory (One-Back; ONB). IIV for each task was automatically output by the program (calculated as a log(10)-transformed standard deviation or "LSD"). We calculated IIV from the raw RTs using coefficient of variation (CoV), regression-based, and ex-Gaussian methods. The IIV from each calculation was then compared by rank across participants. RESULTS: A total of n = 120 participants with MS aged 20-72 (Mean ± SD, 48.99 ± 12.09) completed the baseline cognitive measures. For each task, the interclass correlation coefficient was generated. Each ICC showed that LSD, CoV, ex-Gaussian, and regression methods clustered strongly (Average ICC for DET: 0.95 with 95% CI [0.93, 0.96]; Average ICC for IDN: 0.92 with 95% CI [0.88 to 0.93]; Average ICC for ONB: 0.93 with 95% CI [0.90 to 0.94]). Correlational analyses indicated the strongest correlation between LSD and CoV for all tasks (rs ≥ 0.94). CONCLUSION: The LSD was consistent with research-based methods for IIV calculations. These findings support the use of LSD for the future measurement of IIV for clinical studies.
 BACKGROUND: The Patient-Determined Disease Steps (PDDS) scale is a patient-reported measure of disability used by at least 3 North American multiple sclerosis (MS) registries. We conducted a systematic review of the psychometric properties of the PDDS scale as part of a harmonization effort related to disability measures used in MS registries. METHODS: We searched the EMBASE, Ovid Medline, Scopus, Cochrane Database of Systematic Reviews, CENTRAL, CINAHL Plus, and ClinicalTrials.gov databases from database inception through July 28, 2020. Two reviewers independently screened abstracts and full-text reports for study inclusion and data extraction and assessed study quality and risk of bias. We included studies that assessed the validity or reliability of the PDDS scale. We conducted a meta-analysis to quantitatively summarize the findings. RESULTS: From the 2476 abstracts screened, 234 articles underwent full-text review, of which 5 met the inclusion criteria. These studies assessed criterion validity, construct validity, and test-retest reliability. In all studies, criterion validity was assessed by correlating the PDDS scale score with the Expanded Disability Status Scale score (pooled r = 0.73; 95% CI, 0.66-0.79). Test-retest reliability was high (pooled intraclass correlation coefficient = 0.96; 95% CI, 0.92-0.99). CONCLUSIONS: In this systematic review, the PDDS scale demonstrated criterion and construct validity for assessing disability in individuals with MS who have mild to moderate disabilities. This review also supports the test-retest reliability of the PDDS scale, although further studies with larger samples are needed.
 Multiple-surface segmentation in optical coherence tomography (OCT) images is a challenging problem, further complicated by the frequent presence of weak image boundaries. Recently, many deep learning-based methods have been developed for this task and yield remarkable performance. Unfortunately, due to the scarcity of training data in medical imaging, it is challenging for deep learning networks to learn the global structure of the target surfaces, including surface smoothness. To bridge this gap, this study proposes to seamlessly unify a U-Net for feature learning with a constrained differentiable dynamic programming module to achieve end-to-end learning for retina OCT surface segmentation to explicitly enforce surface smoothness. It effectively utilizes the feedback from the downstream model optimization module to guide feature learning, yielding better enforcement of global structures of the target surfaces. Experiments on Duke AMD (age-related macular degeneration) and JHU MS (multiple sclerosis) OCT data sets for retinal layer segmentation demonstrated that the proposed method was able to achieve subvoxel accuracy on both datasets, with the mean absolute surface distance (MASD) errors of 1.88 ± 1.96μm and 2.75 ± 0.94μm, respectively, over all the segmented surfaces.
 Neurodegenerative diseases (NDDs) form a heterogeneous, widespread group of disorders, generally characterized by progressive cognitive decline and neuropsychiatric disturbances. One of the abilities that seems particularly vulnerable to the impairments in neurodegenerative diseases is the capability to manage one's personal finances. Indeed, people living with neurodegenerative diseases were shown to consistently present with more problems on performance-based financial tasks than healthy individuals. While objective, performance-based tasks provide insight into the financial competence of people living with neurodegenerative diseases in a controlled, standardized setting; relatively little can be said, based on these tasks, about their degree of success in dealing with the financial demands, issues, or questions of everyday life (i.e., financial performance). The aim of this systematic review is to provide an overview of the literature examining self and informant reports of financial performance in people living with neurodegenerative diseases. In total, 22 studies were included that compared the financial performance of people living with mild cognitive impairment (MCI), Alzheimer's disease (AD), Parkinson's disease, or multiple sclerosis to a (cognitively) normal control group. Overall, the results indicate that people living with neurodegenerative diseases are more vulnerable to impairments in financial performance than cognitively normal individuals and that the degree of reported problems seems to be related to the severity of cognitive decline. As the majority of studies however focused on MCI or AD and made use of limited assessment methods, future research should aim to develop and adopt more comprehensive assessments to study strengths and weaknesses in financial performance of people living with different neurodegenerative diseases.
 Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system, characterized by chronic, inflammatory, demyelinating, and neurodegenerative processes. MS management relies on disease-modifying drugs that suppress/modulate the immune system. Cladribine tablets (CladT) have been approved by different health authorities for patients with various forms of relapsing MS. The drug has been demonstrated to deplete CD4(+) and CD8(+) T-cells, with a higher effect described in the former, and to decrease total CD19(+), CD20(+), and naive B-cell counts. COVID-19 is expected to become endemic, suggesting its potential infection risk for immuno-compromised patients, including MS patients treated with disease-modifying drugs. We report here the available data on disease-modifying drug-treated-MS patients and COVID-19 infection and vaccination, with a focus on CladT. MS patients treated with CladT are not at higher risk of developing severe COVID-19. While anti-SARS-CoV-2 vaccination is recommended in all MS patients with guidelines addressing vaccination timing according to the different disease-modifying drugs, no vaccination timing restrictions seem to be necessary for cladribine, based on its mechanism of action and available evidence. Published data suggest that CladT treatment does not impact the production of anti-SARS-CoV-2 antibodies after COVID-19 vaccination, possibly due to its relative sparing effect on naïve B-cells and the rapid B-cell reconstitution following treatment. Slightly lower specific T-cell responses are likely not impacting the risk of breakthrough COVID-19. It could be stated that cladribine's transient effect on innate immune cells likely contributes to maintaining an adequate first line of defense against the SARS-CoV-2 virus.
 3-O-sulfogalactosylceramide, or sulfatide, is a prominent myelin glycosphingolipid reduced in the normal appearing white matter (NAWM) in Multiple Sclerosis (MS), indicating that sulfatide reduction precedes demyelination. Using a mouse model that is constitutively depleted of sulfatide, we previously demonstrated that sulfatide is essential during development for the establishment and maintenance of myelin and axonal integrity and for the stable tethering of certain myelin proteins in the sheath. Here, using an adult-onset depletion model of sulfatide, we employ a combination of ultrastructural, immunohistochemical and biochemical approaches to analyze the consequence of sulfatide depletion from the adult CNS. Our findings show a progressive loss of axonal protein domain organization, which is accompanied by axonal degeneration, with myelin sparing. Similar to our previous work, we also observe differential myelin protein anchoring stabilities that are both sulfatide dependent and independent. Most notably, stable anchoring of neurofascin155, a myelin paranodal protein that binds the axonal paranodal complex of contactin/Caspr1, requires sulfatide. Together, our findings show that adult-onset sulfatide depletion, independent of demyelination, is sufficient to trigger progressive axonal degeneration. Although the pathologic mechanism is unknown, we propose that sulfatide is required for maintaining myelin organization and subsequent myelin-axon interactions and disruptions in these interactions results in compromised axon structure and function.
 Microglia are the resident immune cells of the central nervous system, playing a role in the inflammatory process development and resolution, presenting two main phenotypes, pro-inflammatory M1, and anti-inflammatory M2. Therapies affecting the microglia phenotype may be beneficial in treating inflammatory neurodegenerative diseases. In our experiments, we used the animal multiple sclerosis model, experimental allergic encephalomyelitis (EAE). Rats were treated during the pre- or symptomatic phase of the disease with cyclophosphamide, followed by hematopoietic stem cell transplantation, and with/without post-transplantation cyclophosphamide. Our study aimed to analyze the microglia phenotype in animals subjected to this treatment. The number of M1 cells in the spinal cord, and inducible nitric oxide synthase (iNOS) levels in the brain were similar in all experimental groups. The differences were observed in M2 cells number and arginase 1 (Arg1) levels, which were decreased in EAE animals, and increased after treatment in the symptomatic phase of EAE, and in the pre-symptomatic phase, but only with post-transplantation cyclophosphamide. Analysis of gene expression in the brain showed decreased iNOS expression in EAE animals treated in the symptomatic phase of EAE and no differences in Arg1 expression. Results indicate that treatment applied to experimental animals influences the microglia phenotype, promoting differentiation towards M2 cells.
 Significance: Central nervous system (CNS) diseases are disorders of the brain and/or spinal cord and include neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Nuclear factor erythroid 2-related factor 2 (NRF2) is a transcription factor belonging to the cap-n-collar family that harbors a unique basic leucine zipper motif and plays as a master regulator of homeostatic responses. Recent Advances: Kelch-like ECH-associated protein 1 (KEAP1) is an adaptor of the Cullin3 (CUL3)-based ubiquitin E3 ligase that enhances the ubiquitylation of NRF2, which promotes the degradation of NRF2 to suppress its transcriptional activity in the absence of stress. Cysteine residues of KEAP1 are modified under stress conditions, and NRF2 degradation is attenuated, allowing it to accumulate and induce the expression of target genes. This regulatory system is referred to as the KEAP1-NRF2 system and plays a central role in protecting cells against various stresses. NRF2 also negatively regulates the expression of inflammatory cytokine and chemokine genes and suppresses pathological inflammation. As oxidative stress, inflammation, and proteostasis are known to contribute to neurodegenerative diseases, the KEAP1-NRF2 system is an attractive target for the treatment of these diseases. Critical Issues: In mouse models of neurodegenerative diseases, Nrf2 depletion exacerbates symptoms and enhances oxidative damage and inflammation in the CNS. In contrast, chemical or genetic NRF2 activation improves these symptoms. Indeed, the NRF2-activating chemical dimethyl fumarate is now widely used for the clinical treatment of MS. Future Directions: The KEAP1-NRF2 system is a promising therapeutic target for neurodegenerative diseases.
 OBJECTIVE: To evaluate the influence of transfer quality and demographics on fear of falling (FOF) among full-time wheelchair users. DESIGN: Secondary data analysis. SETTING: University research laboratory and community, United States. PARTICIPANTS: Ninety-six individuals (N=96) living with multiple sclerosis or spinal cord injury who use a manual or power scooter full time with median age of 54.00 years (interquartile range, 29.00 years), and median duration of health condition of 19.50 years (interquartile range, 23.00 years) were included. Fifty-two participants (54%) were manual wheelchair users. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Demographics information included age, sex, duration of health condition, height, weight, body mass index, and wheelchair type. To assess transfer quality, the Transfer Assessment Instrument versions 3.0 and 4.0 were used. The Spinal Cord Injury Falls Concern Scale was used to quantify FOF. Stepwise linear regression analysis was conducted to examine factors influencing FOF. RESULTS: Participant's age, sex, duration of health condition, wheelchair type, and transfer quality were associated with FOF. The regression analysis indicated transfer quality (β=-0.25, P<.01) and wheelchair type (manual wheelchair, β=- 0.32, P<.01) were significant predictors of FOF, R(2)=20% (F=11.19; P<.01). CONCLUSIONS: Compared with manual wheelchair users, power wheelchair/scooter users with poor transfer quality reported higher levels of FOF. Clinicians and researchers working with wheelchair users should emphasize quality of transfers and consider the type of wheelchair while developing interventions to reduce FOF in this population. Further longitudinal prospective studies on modifiable factors associated with FOF among full-time wheelchair users are warranted.
 Demyelination in the central nervous system (CNS) is a hallmark of many neurodegenerative diseases such as multiple sclerosis (MS) and others. Here, we studied astrocytes during de- and remyelination in the cuprizone mouse model. To this end, we exploited the ribosomal tagging (RiboTag) technology that is based on Cre-mediated cell type-selective HA-tagging of ribosomes. Analyses were performed in the corpus callosum of GFAP-Cre(+/-) Rpl22(HA/wt) mice 5 weeks after cuprizone feeding, at the peak of demyelination, and 0.5 and 2 weeks after cuprizone withdrawal, when remyelination and tissue repair is initiated. After 5 weeks of cuprizone feeding, reactive astrocytes showed inflammatory signatures with enhanced expression of genes that modulate leukocyte migration (Tlr2, Cd86, Parp14) and they produced the chemokine CXCL10, as verified by histology. Furthermore, demyelination-induced reactive astrocytes expressed numerous ligands including Cx3cl1, Csf1, Il34, and Gas6 that act on homeostatic as well as activated microglia and thus potentially mediate activation and recruitment of microglia and enhancement of their phagocytotic activity. During early remyelination, HA-tagged cells displayed reduced inflammatory response signatures, as indicated by shutdown of CXCL10 production, and enhanced expression of osteopontin (SPP1) as well as of factors that are relevant for tissue remodeling (Timp1), regeneration and axonal repair. During late remyelination, the signatures shifted towards resolving inflammation by active suppression of lymphocyte activation and differentiation and support of glia cell differentiation. In conclusion, we detected highly dynamic astroglial transcriptomic signatures in the cuprizone model, which reflects excessive communication among glia cells and highlights different astrocyte functions during neurodegeneration and regeneration.
 INTRODUCTION: Natalizumab is a biologic drug for relapsing-remitting multiple sclerosis that may induce the generation of anti-drug antibodies in some patients. Anti-natalizumab antibodies (ANA) increase the risk of adverse events and reduce efficacy, being useful biomarkers for monitoring treatment response. METHODS: Retrospective observational study including MS patients treated with natalizumab that experienced infusion-related events (IRE) or disease exacerbations (DE). ANA were tested by Elisa including a screening and a confirmation assay. Patients were further classified as transient (one positive result) or persistent (two or more positive results) ANA. RESULTS: A total of 1251 MS patients were included and 153 (12.3%) had ANA with at least one single point determination, which were more frequent among patients with IRE compared to those with DE (21,6% vs.10.8%) during the first six infusions. Two or more determinations ANA were performed in 184 patients, being 31.5% permanently positive and 7.1% transiently positive. Interestingly, 26.1% of patients that experienced DE had persistent ANA, while 2.6% were transient. In contrast, 43% of patients with IRE had persistent ANA, and 9.3% had transient antibodies. Patients with persistent antibodies had more frequently high levels at the first sampling compared to patients with transient ANA. CONCLUSION: Real-world evidence shows that the presence of ANA is behind an important percentage of patients treated with natalizumab that experience IRE, as well as DE but in a lower degree. These findings support the need to systematically evaluate ANA towards a personalized management of these patients to avoid undesired complications.
 GABA and GABA(A)-receptors (GABA(A)-Rs) play major roles in neurodevelopment and neurotransmission in the central nervous system (CNS). There has been a growing appreciation that GABA(A)-Rs are also present on most immune cells. Studies in the fields of autoimmune disease, cancer, parasitology, and virology have observed that GABA-R ligands have anti-inflammatory actions on T cells and antigen-presenting cells (APCs), while also enhancing regulatory T cell (Treg) responses and shifting APCs toward anti-inflammatory phenotypes. These actions have enabled GABA(A)-R ligands to ameliorate autoimmune diseases, such as type 1 diabetes (T1D), multiple sclerosis (MS), and rheumatoid arthritis, as well as type 2 diabetes (T2D)-associated inflammation in preclinical models. Conversely, antagonism of GABA(A)-R activity promotes the pro-inflammatory responses of T cells and APCs, enhancing anti-tumor responses and reducing tumor burden in models of solid tumors. Lung epithelial cells also express GABA-Rs, whose activation helps maintain fluid homeostasis and promote recovery from injury. The ability of GABA(A)-R agonists to limit both excessive immune responses and lung epithelial cell injury may underlie recent findings that GABA(A)-R agonists reduce the severity of disease in mice infected with highly lethal coronaviruses (SARS-CoV-2 and MHV-1). These observations suggest that GABA(A)-R agonists may provide off-the-shelf therapies for COVID-19 caused by new SARS-CoV-2 variants, as well as novel beta-coronaviruses, which evade vaccine-induced immune responses and antiviral medications. We review these findings and further advance the notions that (1) immune cells possess GABA(A)-Rs to limit inflammation in the CNS, and (2) this natural "braking system" on inflammatory responses may be pharmacologically engaged to slow the progression of autoimmune diseases, reduce the severity of COVID-19, and perhaps limit neuroinflammation associated with long COVID.
 INTRODUCTION: Five to eight percent of the world population currently suffers from at least one autoimmune disorder. Despite multiple immune modulatory therapies for autoimmune demyelinating diseases of the central nervous system, these treatments can be limiting for subsets of patients due to adverse effects and expense. To circumvent these barriers, we investigated a nutritional intervention in mice undergoing experimental autoimmune encephalomyelitis (EAE), a model of autoimmune-mediated demyelination that induces visual and motor pathologies similar to those experienced by people with multiple sclerosis (MS). METHODS: EAE was induced in female and male mice and the impact of limiting dietary carbohydrates by feeding a ketogenic diet (KD) enriched in medium chain triglycerides (MCTs), alpha-linolenic acid (an omega-3 fatty acid), and fiber was evaluated in both a preventive regimen (prior to immunization with MOG antigen) and an interventional regimen (following the onset of symptoms). Motor scores were assigned daily and visual acuity was measured using optokinetic tracking. Immunohistochemical analyses of optic nerves were done to assess inflammatory infiltrates and myelination status. Fatty acid and cytokine profiling from blood were performed to evaluate systemic inflammatory status. RESULTS: The KD was efficacious when fed as a preventive regimen as well as when initiated as an interventional regimen following symptom onset. The KD minimally impacted body weight during the experimental time course, increased circulating ketones, prevented motor and ocular deficits, preserved myelination of the optic nerve, and reduced infiltration of immune cells to optic nerves. The KD also increased anti-inflammatory-associated omega-3 fatty acids in the plasma and reduced select cytokines in the circulation associated with EAE-mediated pathological inflammation. DISCUSSION: In light of ongoing clinical trials using dietary strategies to treat people with MS, these findings support that a KD enriched in MCTs, omega-3 fatty acids, and fiber promotes a systemic anti-inflammatory milieu and ameliorates autoimmune-induced demyelinating visual and motor deficits.
 BACKGROUND: In clinical practice, females with MS often report menstrually-related symptom fluctuations. Hypothetically, use of oral contraceptives (OCs) could reduce these fluctuations, particularly continuous OCs (11+ weeks of consistent exogenous hormones followed by 1 week placebo). OBJECTIVES: To prospectively capture (1) whether neurologic and generalized symptoms vary with menstrual cycle phase and (2) whether type of contraception impacts symptom fluctuations. METHODS: In this two-center pilot study, females with MS and a regular menstrual cycle prospectively tracked their menstrual cycles and completed symptom surveys for up to 6 months. Participants were categorized as 1) users of oral contraceptives, either a) cyclic or b) continuous, or 2) endogenously cycling, either c) hormonal intrauterine device (IUD) users or d) "none users" (e.g. no hormonal contraception; included condoms, copper IUD, tubal ligation, "fertility awareness methods"). There was no correction for multiple analyses. RESULTS: Altogether, 47/70 participants (67%) provided >4 weeks of data and were included in the analyses. Mean (SD) age was 35.0 (0.9) years, median (IQR) EDSS was 1.5 (1-2) and mean (SD) SymptoMScreen score was 10.4 (9.6). For endogenously cycling patients (IUD and none users), fatigue (MFIS) was lower in the perimenstrual period than in the luteal period (p < 0.05). For continuous OC users, variability in symptoms was lower than for endogenously cycling females (MFIS: p < 0.01; Daily Hassles, from Uplift & Hassles Survey: p < 0.05) or cyclic OC users (MFIS: p < 0.001). CONCLUSIONS: In this pilot study, symptom severity did not definitively fluctuate in relationship to the menstrual cycle in endogenously cycling participants. However, fatigue and daily hassles were less variable for participants using continuous OC than for cyclic OC users or no-OC users. Future confirmatory studies are warranted to further examine whether contraceptive choice can be leveraged to manage symptom fluctuation in cycling females with MS. Such studies could enroll larger cohorts over fewer cycles or employ incentivization and hormonal measurements to enhance participant retention and statistical power.


 Baclofen is FDA-approved and primarily used as an antispasmodic agent and muscle relaxant. It is utilized as an adjunct in treating painful muscle spasticity, clonus, and rigidity caused by spinal-cord related diseases such as multiple sclerosis, cerebral palsy, or spinal cord injury. It is most often administered as an oral medication, but in severe or chronic cases, and can also be delivered centrally using an implantable intrathecal pump. Chronic use of baclofen can result in withdrawal when abruptly discontinued. Baclofen overdose or withdrawal can be life-threatening. This review summarizes the clinical toxicity of baclofen, baclofen withdrawal, and acute management principles.
 Multiple sclerosis (MS) is an immune-mediated inflammatory demyelinating disease of the central nervous system, resulting in loss of oligodendrocytes, astroglial scarring, and axonal injury (end-stage). Disease-modifying drugs help minimize long-term disability for people with MS by decreasing CNS inflammation, reducing the frequency and severity of acute attacks, delaying disease progression, and improving the overall quality of life. This activity covers cladribine, an established oral chemotherapy agent that the FDA recently approved for relapsing MS.
 The clinical characteristics of three types of optic neuritis (double seronegative optic neuritis; DN-ON, Neuromyelitis optica spectrum disorder-related optic neuritis; NMOSD-ON, and multiple sclerosis-related optic neuritis; MS-ON) were examined in order to identify factors that may affect good visual recovery in Thai patients. The study included patients diagnosed with three types of optic neuritis at Rajavithi Hospital between 2011 and 2020. Visual acuity at the end of 12 months was used as the treatment outcome. Multiple logistic regression analysis was used to evaluate potential predictors of good visual recovery. Of the 76 patients, 61 had optic neuritis, with DN-ON as the most common subtype (52.6%). MS-ON patients were significantly younger (28.3 ± 6.6 years, p = 0.002) and there was a female predominance in all subgroups (p = 0.076). NMOSD-ON patients had a significantly higher proportion of poor baseline VA (p < 0.001). None of the NMOSD-ON patients achieved 0.3 logMAR visual recovery in the 12-month period (p = 0.022). A delay in treatment with intravenous methylprednisolone (IVMP) for more than 7 days increased the risk of failure to gain 0.3 logMAR visual recovery by five times (OR 5.29, 95% CI 1.359-20.616, p = 0.016), with NMOSD-ON as the strongest predictor (OR 10.47, 95% CI; 1.095-99.993, p = 0.041). Early treatment with intravenous methylprednisolone may be important for achieving at least 0.3 logMAR visual recovery in Thai patients with optic neuritis.
 BACKGROUND: Optic neuritis (ON) is an inflammatory disease of optic nerve. The distinct etiologies of ON significantly influence its clinical manifestation, neuroimaging findings, and visual outcomes. However, the clinical characteristics might be influenced by the racial differences. The purpose of this study is to investigate the clinical characteristics of various types of ON at a Taiwanese tertiary center. METHODS: This cohort study analyzed 163 patients who received treatment and continued following-up for ON between 2015 and 2022. We selected patients who had been tested for anti-aquaporin-4 antibody (AQP4-Ab) and anti-myelin oligodendrocyte glycoprotein antibody (MOG-Ab). The participants were classified into four groups on the basis of their etiologies, specifically (1) multiple sclerosis (MS)-related, (2) AQP4-Ab-positive, (3) MOG-Ab-positive, or (4) idiopathic ON. The researchers recorded the patients' clinical characteristics, treatment course, magnetic resonance imaging and optical coherence tomography (OCT) findings, and visual outcomes. RESULTS: MOG-Ab-positive group had higher percentages of disk swelling and pain with eye movement. Long optic nerve and perineural enhancement are the hallmarks of MOG-Ab-related ON. The ON relapse rate was higher in AQP4-Ab-positive group. Although members of AQP4-Ab-positive group received immediate steroid pulse therapy, these patients experienced the worst visual outcomes. Moreover, a thinner retinal nerve fiber layer (RNFL) was noted in AQP4-Ab-positive group. MS group had a higher incidence of extra-optic nerve lesions. Multivariate regression identified pretreatment visual acuity and RNFL thickness as the important factors affecting visual outcomes. CONCLUSIONS: This cohort study identified the clinical features of different types of ON. Patients with AQP4-Ab-positive ON had poorer visual outcomes, which may be attributed to multiple relapses and profound nerve damage, as revealed by OCT findings. Patients with MOG-Ab-positive ON displayed long optic nerve enhancement but had more favorable prognoses. Thus, antibody-based classification facilitates treatment and prognosis in ON.

 BACKGROUND: In recent years, the ability of conventional magnetic resonance imaging (MRI), including T(1) contrast-enhanced (CE) MRI, to monitor high-efficacy therapies and predict long-term disability in multiple sclerosis (MS) has been challenged. Therefore, non-invasive methods to improve MS lesions detection and monitor therapy response are needed. METHODS: We studied the combined cuprizone and experimental autoimmune encephalomyelitis (CPZ-EAE) mouse model of MS, which presents inflammatory-mediated demyelinated lesions in the central nervous system as commonly seen in MS patients. Using hyperpolarized (13)C MR spectroscopy (MRS) metabolic imaging, we measured cerebral metabolic fluxes in control, CPZ-EAE and CPZ-EAE mice treated with two clinically-relevant therapies, namely fingolimod and dimethyl fumarate. We also acquired conventional T(1) CE MRI to detect active lesions, and performed ex vivo measurements of enzyme activities and immunofluorescence analyses of brain tissue. Last, we evaluated associations between imaging and ex vivo parameters. RESULTS: We show that hyperpolarized [1-(13)C]pyruvate conversion to lactate is increased in the brain of untreated CPZ-EAE mice when compared to the control, reflecting immune cell activation. We further demonstrate that this metabolic conversion is significantly decreased in response to the two treatments. This reduction can be explained by increased pyruvate dehydrogenase activity and a decrease in immune cells. Importantly, we show that hyperpolarized (13)C MRS detects dimethyl fumarate therapy, whereas conventional T(1) CE MRI cannot. CONCLUSIONS: In conclusion, hyperpolarized MRS metabolic imaging of [1-(13)C]pyruvate detects immunological responses to disease-modifying therapies in MS. This technique is complementary to conventional MRI and provides unique information on neuroinflammation and its modulation.
 BACKGROUND: Multiple sclerosis (MS) is a chronic autoimmune inflammatory, demyelinating, and neurodegenerative disease affecting young adults. People with MS are highly interested in engaging in physical symptom management and decision-making but are often not actively engaged in symptom management discussions. Research examining the benefit of shared decision-making in the management of physical MS symptoms is sparse. OBJECTIVES: This study aimed to identify and synthesize the evidence on the use of shared decision-making in physical MS symptom management. DESIGN: This study is a systematic review of published evidence on the use of shared decision-making in physical MS symptom management. DATA SOURCES AND METHODS: MEDLINE, CINAHL, EMBASE, and CENTRAL databases were searched in April 2021, June 2022, and April 2, 2023, for primary, peer-reviewed studies of shared decision-making in the management of MS physical symptoms. Citations were screened, data extracted, and study quality assessed according to Cochrane guidelines for systematic reviews, including risk of bias assessment. Statistical synthesis of the included study results was not appropriate; results were summarized in a nonstatistical manner using the vote-counting method to estimate beneficial versus harmful effects. RESULTS: Of 679 citations, 15 studies met the inclusion criteria. Six studies addressed shared decision-making in the management of pain, spasms, neurogenic bladder, fatigue, gait disorder, and/or balance issues, and nine studies addressed physical symptoms in general. One study was a randomized controlled trial; most studies were observational studies. All study results and study author conclusions indicated that shared decision-making is important to the effective management of physical MS symptoms. No study results suggested that shared decision-making was harmful or delayed the management of physical MS symptoms. CONCLUSION: Reported results consistently indicate that shared decision-making is important in effective MS symptomatic care. Further rigorous randomized controlled trials are warranted to investigate the effectiveness of shared decision-making associated with MS physical symptomatic care. REGISTRATION: PROSPERO: CRD42023396270.
 BACKGROUND: There is limited knowledge about T cell responses in patients with multiple sclerosis (MS) after 3 doses of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mRNA vaccine. OBJECTIVES: Assess the SARS-CoV-2 spike antibody and T cell responses in MS patients and healthy controls (HCs) after 2 doses (2-vax) and 3 doses (3-vax) of SARS-CoV-2 mRNA vaccination. METHODS: We studied seroconversion rates and T cell responses by flow cytometry in HC and MS patients on fingolimod or ocrelizumab. RESULTS: After 2-vax, 8/33 (24.2%) patients in ocrelizumab group, 5/7 (71.4%) in fingolimod group, and 29/29 (100%) in HC group (P = 5.7 × 10(-11)) seroconverted. After 3-vax, 9/22 (40.9%) patients in ocrelizumab group, 19/21 (90.5%) in fingolimod group, and 7/7 (100%) in HC group seroconverted (P = 0.0003). The percentage of SARS-CoV-2 peptide reactive total CD4+ T cells increased in HC and ocrelizumab group but not in fingolimod group after 2-vax and 3-vax (P < 0.0001). The percentage of IFNγ and TNFα producing total CD4+ and CD8+ T cells increased in fingolimod group as compared to HC and ocrelizumab group after 2-vax and 3-vax (P < 0.0001). CONCLUSIONS: MS patients on ocrelizumab and fingolimod had attenuated humoral responses, but preserved cytokine producing T cell responses compared to HCs after SARS-CoV-2 mRNA vaccination. CLINICAL TRIALS REGISTRATION: NCT05060354.
 Nogo receptor 1 is the high affinity receptor for the potent myelin-associated inhibitory factors that make up part of the inflammatory extracellular milieu during experimental autoimmune encephalomyelitis. Signalling through the Nogo receptor 1 complex has been shown to be associated with axonal degeneration in an animal model of multiple sclerosis, and neuronal deletion of this receptor homologue, in a disease specific manner, is associated with preserving axons even in the context of neuroinflammation. The local delivery of Nogo receptor(1-310)-Fc, a therapeutic fusion protein, has been successfully applied as a treatment in animal models of spinal cord injury and glaucoma. As multiple sclerosis and experimental autoimmune encephalomyelitis exhibit large numbers of inflammatory cell infiltrates within the CNS lesions, we utilized transplantable haematopoietic stem cells as a cellular delivery method of the Nogo receptor(1-310)-Fc fusion protein. We identified CNS-infiltrating macrophages as the predominant immune-positive cell type that overexpressed myc-tagged Nogo receptor(1-310)-Fc fusion protein at the peak stage of experimental autoimmune encephalomyelitis. These differentiated phagocytes were predominant during the extensive demyelination and axonal damage, which are associated with the engulfment of the protein complex of Nogo receptor(1-310)-Fc binding to myelin ligands. Importantly, mice transplanted with haematopoietic stem cells transduced with the lentiviral vector carrying Nogo receptor(1-310)-Fc and recovered from the peak of neurological decline during experimental autoimmune encephalomyelitis, exhibiting axonal regeneration and eventual remyelination in the white matter tracts. There were no immunomodulatory effects of the transplanted, genetically modified haematopoietic stem cells on immune cell lineages of recipient female mice induced with experimental autoimmune encephalomyelitis. We propose that cellular delivery of Nogo receptor(1-310)-Fc fusion protein through genetically modified haematopoietic stem cells can modulate multifocal experimental autoimmune encephalomyelitis lesions and potentiate neurological recovery.
 OBJECTIVE: Due to the growing complexity in monitoring and treatment of many disorders, disease-specific care and research networks offer patients certified healthcare. However, the networks' ability to provide health services close to patients' homes usually remains vague. Digital Health Technologies (DHTs) help to provide better care, especially if implemented in a targeted manner in regions undersupplied by specialised networks. Therefore, we used a car travel time-based isochrone approach to identify care gaps using the example of the neuroinflammation-focused German healthcare and research networks for multiple sclerosis (MS), myasthenia gravis (MG), myositis and immune-mediated neuropathy. METHODS: Excellence centres were mapped, and isochrones for 30, 60, 90 and 120 minutes were calculated. The resulting geometric figures were aggregated and used to mask the global human settlement population grid 2019 to estimate German inhabitants that can reach centres within the given periods. RESULTS: While 96.48% of Germans can drive to an MS-focused centre within one hour, coverage is lower for the rare disease networks for MG (48.3%), myositis (43.1%) and immune-mediated neuropathy (56.7%). Within 120 minutes, more than 80% of Germans can reach a centre of any network. Besides the generally worse covered rural regions such as North-Eastern Germany, the rare disease networks also show network-specific regional underrepresentation. CONCLUSION: An isochrone-based approach helps identify regions where specialised care is hard to reach, which might be especially troublesome in the case of an often disabled patient collective. Patient care could be improved by focusing deployments of disease-specific DHTs on these areas.
 MYD88 mutation status is assessed in the evaluation of CNS lymphoma since the mutation MYD88 L265P is highly predictive of this disease. However, whether the MYD88 L265P mutation may lead to other diseases outside of malignancy is not well understood. Here we describe two patients with the MYD88 L265P mutation in the CSF with no additional evidence of neoplastic disease but were found to have two distinct neurologic autoimmune conditions (anti-GFAP astrocytopathy and multiple sclerosis). These cases suggest this activating mutation may predispose certain patients to autoimmune conditions and may have future therapeutic implications.
 BACKGROUND: This study aimed to evaluate short- and long-term humoral and T-cell-specific immune responses to SARS-CoV-2 vaccines in patients with multiple sclerosis (MS) treated with different disease-modifying therapies (DMTs). METHODS: Single-center observational longitudinal study including 102 patients with MS who consecutively received vaccination against SARS-CoV-2. Serum samples were collected at baseline and after receiving the second dose of the vaccine. Specific Th1 responses following in vitro stimulation with spike and nucleocapsid peptides were analyzed by quantifying levels of IFN-γ. Serum IgG-type antibodies against the spike region of SARS-CoV-2 were studied by chemiluminescent microparticle immunoassay. RESULTS: Patients undergoing fingolimod and anti-CD20 therapies had a markedly lower humoral response than those treated with other DMTs and untreated patients. Robust antigen-specific T-cell responses were detected in all patients except those treated with fingolimod, who had lower IFN-γ levels than those treated with other DMTs (25.8 pg/mL vs. 868.7 pg/mL, p = 0.011). At mid-term follow-up, a decrease in vaccine-induced anti-SARS-CoV-2 IgG antibodies was observed in all subgroups of patients receiving DMTs, although most patients receiving induction DMTs or natalizumab and non-treated patients remained protected. Cellular immunity was maintained above protective levels in all DMT subgroups except the fingolimod subgroup. CONCLUSIONS: SARS-CoV-2 vaccines induce robust and long-lasting humoral and cell-mediated specific immune responses in most patients with MS.
 Remyelination is a key repair process that ensures neurons remain protected following injury. This process is mediated by remyelinating oligodendrocytes in vertebrates, however, similarly to other neurobiological processes, the rate and efficiency of remyelination decreases across age and under pathological conditions. This has largely been attributed to two main contributors: 1) decreased exogenous signals supporting remyelination; and 2) aging of precursor cells that no longer differentiate into remyelinating oligodendrocytes. Here we discuss a key paper by Ruckh et al. (2012) who presented novel evidence that exposure to soluble bloodstream factors of young mice significantly rescues remyelination in old mice following a demyelinating insult. In this paper, a parabiosis approach was used where young and old mice were surgically joined for three weeks before and then left as a pair throughout the experiment. Ruckh and colleagues also offer novel insight into the role played by immune system cells, specifically macrophages, in clearance of myelin debris, a further contributor to remyelination. This paper is a good tool to expose undergraduate neuroscience students to basic molecular processes underlying conduction and transmission, helping them link cellular and network components. It also offers a platform for introducing the practicalities of in vivo research and debating ethical controversies that arise in animal research.
 In contrast to conventional dendritic cells (cDCs) that are constantly exposed to microbial signals at anatomical barriers, cDCs in systemic lymphoid organs are sheltered from proinflammatory stimulation in the steady state but respond to inflammatory signals by gaining specific immune functions in a process referred to as maturation. Recent findings show that, during maturation, a population of systemic tolerogenic cDCs undergoes an acute tumor necrosis factor α (TNFα)-mediated cell death, resulting in the loss of tolerance-inducing capacity. This tolerogenic cDC population is restored upon return to the homeostatic baseline. We propose that such a dynamic reshaping of cDC populations becomes the foundation of a novel framework for maintaining tolerance at the steady state while being conducive to unhampered initiation of immune responses under proinflammatory conditions.

 Neuroinflammation plays a critical role in the pathological process of multiple neurological disorders and pathological pain conditions. GPR109A, a Gi protein-coupled receptor, has emerged as an important therapeutic target for controlling inflammation in various tissues and organs. In this review, we summarized current data about the role of GPR109A in neuroinflammation. Specifically, we focused on the pharmacological features of GPR109A and signaling pathways used by GPR109A to ameliorate neuroinflammation and symptoms in Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, and pathological pain conditions.
 Dexamethasone has a wide variety of uses in the medical field. As a treatment, dexamethasone has been useful in treating acute exacerbation of multiple sclerosis, allergies, cerebral edema, inflammation, and shock. Patients with COVID-19, asthma, atopic and contact dermatitis, and drug hypersensitivity reactions have benefited from dexamethasone. Clinicians use it as a diagnostic agent for Cushing disease. This activity will highlight the mechanism of action, adverse event profile, FDA-approved and off-label uses, administration, dosing, contraindications, pharmacodynamics, pharmacokinetics, monitoring parameters, and relevant interactions of dexamethasone pertinent for interprofessional team members using dexamethasone for any of its intended indications.

 The announcement of multiple sclerosis is likely to turn a person's life and plans upside down. Many questions then arise, particularly concerning rights and available assistance. Faced with the multitude of existing organizations and mechanisms, caregivers can direct the patient to a social service assistant. This person will be able to advise and accompany the patient in his or her efforts.

 IL-17-blocking antibodies have shown little clinical effect in some autoimmune diseases such as multiple sclerosis. In this issue of Immunity, Luo et al. demonstrate that SHP2-Act1 complexes can mediate autonomous IL-17R signaling in the absence of the IL-17 ligand itself.
 The second messenger, cyclic adenosine monophosphate (cAMP), is a master regulator of signal transduction that maintains cell homeostasis. A fine balance between cAMP synthesis by adenylyl cyclase and degradation by phosphodiesterases (PDEs) underpins receptor-specific responses. As multiple receptors rely on cAMP for signaling, PDEs shape three-dimensional, localized gradients of the cyclic nucleotide to drive appropriate signaling cascades. Of the 11 PDE families, PDE4, which comprises long, short, and supershort isoforms and a dead-short isoform, is of great interest due to its implication in disease. Aberrant PDE4 expression and post-translational modifications are hallmarks of several clinical indications for which curative treatment is not yet available. While some PDE4-specific small molecule inhibitors directed against the active site are approved for clinical use, they are limited by severe side effects owing to the high degree of conservation of the catalytic domain between over 20 unique isoforms. Some attempts to use the different modular structure that exists between long and shorter isoforms are now bearing success. However, these inhibitors are exclusively aimed at PDE4 long isoforms, which have been the focus of the majority of research in this area. Here, we have summarised literature on the lesser-studied short PDE4 isoforms and provide a record of the discovery, regulation, and disease relevance of this class of enzymes that represent an untapped target for specific inhibition in the future.
 IMPORTANCE: Proposed biosimilar natalizumab (biosim-NTZ) PB006 is the first biosimilar monoclonal antibody therapy developed for multiple sclerosis (MS) treatment. OBJECTIVE: To evaluate matching efficacy, safety, and immunogenicity between biosim-NTZ and reference natalizumab (ref-NTZ) in patients with relapsing-remitting MS (RRMS). DESIGN, SETTING, AND PARTICIPANTS: The Antelope trial was a phase 3, parallel-group, randomized, active-controlled study, conducted between October 2019 and March 2021, with last patient follow-up visit on August 23, 2021. The study took place in 48 centers in 7 countries. Of 531 patients with RRMS aged 18 to 60 years screened, 266 were excluded before randomization in line with study criteria. Eligible participants had 1 or more documented relapse within the previous year and either 1 or more gadolinium-enhancing T1-weighted or 9 or more T2-weighted brain lesions, Kurtzke Expanded Disability Status Scale score of 0 to 5.0 (inclusive), and John Cunningham virus index of 1.5 or less at screening. One patient withdrew consent before dosing. INTERVENTIONS: Intravenous infusions every 4 weeks of biosim-NTZ, 300 mg, or ref-NTZ, 300 mg (1:1 randomization), from week 0 to week 44 (end-of-study visit: week 48). At week 24, the ref-NTZ group was rerandomized and 30 patients were switched to biosim-NTZ for the remainder of the study. MAIN OUTCOMES AND MEASURES: The primary end point was the cumulative number of new active lesions on magnetic resonance imaging (new gadolinium-enhancing T1-weighted lesions and new/enlarging T2-weighted lesions without double counting) over 24 weeks. Additional end points included further magnetic resonance imaging parameters, annualized relapse rate, and Kurtzke Expanded Disability Status Scale score. Safety, tolerability, and immunogenicity assessments included adverse events, laboratory evaluations, and positivity for anti-John Cunningham virus antibodies and antinatalizumab antibodies. RESULTS: A total of 264 participants (mean [SD] age, 36.7 [9.38] years; 162 [61.4%] female) received treatment with biosim-NTZ (n = 131) or ref-NTZ (n = 133). At week 24, the model-based mean difference in cumulative number of new active lesions between biosim-NTZ and ref-NTZ treatment groups was 0.17 (least square means [SE]: biosim-NTZ, 0.34 [0.34]; ref-NTZ, 0.45 [0.28]; 95% CI, -0.61 to 0.94 within the prespecified margins of ±2.1). No significant differences between treatment groups were observed across secondary efficacy end points, safety, tolerability, or immunogenicity assessments. CONCLUSIONS AND RELEVANCE: Biosim-NTZ matched ref-NTZ in efficacy, safety, and immunogenicity for patients with RRMS in the tested setting. This phase 3 trial supports proposed biosim-NTZ as a biosimilar alternative to ref-NTZ for treating RRMS. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04115488.
 OBJECTIVES: Neurofilament light chain (NfL) has emerged as a promising biomarker for detecting and monitoring axonal injury. Until recently, NfL could only be reliably measured in cerebrospinal fluid, but digital single molecule array (Simoa) technology has enabled its precise measurement in blood samples where it is typically 50-100 times less abundant. We report development and multi-center validation of a novel fully automated digital immunoassay for NfL in serum for informing axonal injury status. METHODS: A 45-min immunoassay for serum NfL was developed for use on an automated digital analyzer based on Simoa technology. The analytical performance (sensitivity, precision, reproducibility, linearity, sample type) was characterized and then cross validated across 17 laboratories in 10 countries. Analytical performance for clinical NfL measurement was examined in individual patients with relapsing remitting multiple sclerosis (RRMS) after 3 months of disease modifying treatment (DMT) with fingolimod. RESULTS: The assay exhibited a lower limit of detection (LLoD) of 0.05 ng/L, a lower limit of quantification (LLoQ) of 0.8 ng/L, and between-laboratory imprecision <10 % across 17 validation sites. All tested samples had measurable NfL concentrations well above the LLoQ. In matched pre-post treatment samples, decreases in NfL were observed in 26/29 RRMS patients three months after DMT start, with significant decreases detected in a majority of patients. CONCLUSIONS: The sensitivity characteristics and reproducible performance across laboratories combined with full automation make this assay suitable for clinical use for NfL assessment, monitoring in individual patients, and cross-comparisons of results across multiple sites.
 Neurological and psychiatric disorders are considered to reflect distinct underlying pathogenic entities. However, the extent to which they share genetic influences remains unclear. Here, we performed a comprehensive analysis of GWAS data, involving nearly 1 million cases across ten neurological diseases and ten psychiatric disorders, to compare their common genetic risk and biological underpinnings. Using complementary statistical tools, we demonstrate extensive genetic overlap across the disorders, with varying degrees of genetic correlations. In particular, migraine, essential tremor, stroke and multiple sclerosis were genetically correlated with several psychiatric disorders. Biological interrogation indicated heterogenous biological processes associated with neurological diseases, while psychiatric disorders consistently implicated neuronal biology. Altogether, the study demonstrates that neurological and psychiatric disorders are not genetically disparate, but share key etiological aspects, which have important implications for disease classification, clinical practice, and genomic precision medicine.
 BACKGROUND: Currently, no tests can definitively diagnose and distinguish neuromyelitis optica spectrum disorder (NMOSD) from multiple sclerosis (MS). METHODS: Initially, cerebrospinal fluid (CSF) proteomics were employed to uncover the novel biomarkers that differentiate NMOSD from MS into cohorts of 10 MS and 10 NMOSD patients. Subsequently, screening biomarkers were validated using an enzyme-linked immunosorbent assay method and CSF and serum samples from 20 MS patients, 20 NMOSD patients, 20 non-inflammatory neurological controls, and 20 healthy controls. RESULTS: In study cohort, insulin-like growth factor-binding protein 7 (IGFBP7) and lysosome-associated membrane glycoprotein 2 (LAMP2) were screened. In validation cohort, serum and CSF IGFBP7 not only exhibited higher levels in MS and NMOSD patients than controls, but also had greatest area under the curve (AUC, above or equal to 0.8) in MS and NMOSD diagnoses. Serum IGFBP7 (0.945) and CSF IGFBP7 (0.890) also had the greatest AUCs for predicting MS progression, while serum LAMP2 had a moderate curve (0.720). CONCLUSIONS: IGFBP7 was superior in diagnosing MS and NMOSD, and IGFBP7 and serum LAMP2 performed exceptionally well in predicting the MS progression. These results offered reasons for further investigations into the functions of IGFBP7 and LAMP2 in MS and NMOSD.
 G-protein coupled receptors (GPCR) regulate 3',5'-cyclic adenosine monophosphate (cAMP) levels in T cells. cAMP as ubiquitous second messenger is crucial for adequate physiology of T cells by mediating effector T cell (Teff) function as well as regulatory T cell (Treg)-mediated immunosuppression. Several GPCRs have been identified to be crucial for Teff and Treg function. However, the role of the orphan, constitutively active Gs-coupled GPCR GPR52 is unknown. Here we show that GPR52 regulates cAMP levels in T cells but does not affect T cell function. We found that stimulation of transfected HEK cells or primary T cells with a GPR52 agonist results in a rise of intracellular cAMP. However, neither Gpr52 deficiency nor pharmacological modulation of GPR52 by antagonists or agonists affected T cell activation, differentiation, and proliferation or Treg-mediated immunosuppression. Moreover, Gpr52 deletion did not modify the clinical disease course of experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that a modulation of cAMP levels in T cells does not inevitably result in altered T cell function. While we could not identify an obvious role of GPR52 in in vitro T cell assays and in vivo CNS autoimmunity, it might regulate T cell function in a different context or affect the function of other GPR52-expressing cells.
 PURPOSE: Individuals with multiple sclerosis (MS) are at an increased fall risk due to motor and cognitive dysfunction. Our past studies suggest that backward walking (BW) velocity predicts fall risk; however, specific cognitive domains associated with BW velocity remain understudied. The goal of this study was to determine the specific contributions of cognitive functioning to BW velocity in persons with MS. We hypothesized that better visuospatial memory, verbal immediate recall, and faster information processing speed would contribute to faster BW velocity, and deficits in these domains would partially account for disease severity-related impairment in BW velocity. METHODS: Participants completed demographic questionnaires, walking tests, and cognitive assessments. Applied structural equation modeling was used to test our hypothesized model of competing cognitive mediators. Within the model, disease severity was a predictor of BW via three intercorrelated cognitive mediators. RESULTS: Participants included 39 individuals with relapsing-remitting MS. Results indicated that 35.3% of the significant total effect of disease severity on BW was accounted for by specific cognitive deficits. Verbal immediate recall had the largest contribution, followed by visuospatial memory and information processing speed. CONCLUSIONS: When examining the unique effects of cognitive domains on disease severity-related deficits in BW, a meaningful source of impairment related to visuospatial memory and verbal immediate recall was demonstrated. Considering the utility of BW velocity as a predictor of falls, these results highlight the importance of assessing cognition when evaluating fall risk in MS. Cognitive-based intervention studies investigating fall prevention may find BW as a more specific and sensitive predictor of fall risk than forward walking.
 INTRODUCTION: Regular exercise is beneficial for people with Multiple Sclerosis (MS), regardless of disability level. The previously reported differential effect of COVID-19-related lockdowns on exercise levels in this population remains unexplained. We examined effects of lockdowns on exercise in Australians with MS according to disability levels, lockdown severity and health technology use. METHODS: A cross-sectional survey of people with MS in Australia (22 April-23 September 2021) collected demographic and clinical information as well as exercise patterns before and during lockdowns. Mann-Whitney was used to compare ordinal data and Likelihood Ratio to compare dichotomous data. RESULTS: 151 people completed the survey. 72.2% had mild disability and 25.2% moderate disability. Extended lockdowns were associated with significantly decreased sedentary behaviour (31.5% to 25.9%) but also with decreased exercise frequency in frequent exercisers (≥3 times/week; 53.7% to 22.2%). The latter occurred significantly more in those with mild disability (-22.7%) than with moderate disability (-3.5%). More people with mild disability walked for exercise pre-pandemic (LR 8.6, p=.004) and during lockdowns (LR 6.6, p=.010). Walking during lockdowns was positively associated with working from home. People with moderate disability were more likely to engage in home exercise both pre-pandemic (LR 5.5, p=.019) and during lockdown (LR 5.2, p=.023). Engagement in home exercise rose for both groups during lockdowns and was facilitated by on-line exercise classes. CONCLUSION: Lockdowns differentially affected exercise patterns according to disability level. The proportion of people achieving exercise recommendations decreased more in those with mild but not moderate disability. Incidental physical activity was disproportionately impacted in people with moderate disability.
 BACKGROUND: There is some evidence that sleep patterns and psychological health have worsened in the general population as a result of the COVID-19-pandemic. Persons with multiple sclerosis (MS) represent a particularly vulnerable population for COVID-19 infections and effects of restrictions. The present study investigated whether insomnia and depressive symptoms, as well as other MS-related symptoms (i.e. fatigue and paresthesia), changed from before to during the COVID-19-pandemic among persons with diagnosed MS. METHOD: A sample of 90 Iranian females with MS (mean age; 37.62 years; median EDSS score: 2.5) completed a series of self-rating scales at two time points: Nine months before the COVID-19 outbreak in May 2019 (baseline) and then again during the COVID-19 pandemic in May 2020 (study end). Self-rating questionnaires covered sociodemographic and disease-related information, insomnia, depressive symptoms, fatigue, and paresthesia. RESULTS: Depressive symptoms increased over time with a significant p-value and medium effect size. Symptoms of insomnia increased over time (significant p-value, but small effect size), while no significant changes were observed in fatigue and paresthesia (very small effect sizes). The only predictor for insomnia during the COVID-19 pandemic was insomnia before the COVID-19 pandemic; the only predictor for depressive symptoms during the COVID-19 pandemic was insomnia before the COVID-19 pandemic. CONCLUSIONS: Overall, the COVID-19 pandemic and its related social restrictions had significant effects on symptoms of depression and insomnia in this sample of Iranian women with MS, but had no effect on fatigue and paresthesia.
 Multiple sclerosis (MS) is an autoimmune disorder characterized by demyelination and neurodegeneration in the central nervous system (CNS); severe symptoms lead MS patients to use complementary treatments. Ketogenic diet (KD) shows wide neuroprotective effects, but the precise mechanisms underlying the therapeutic activity of KD in MS are unclear. The present study established a continuous 24 days experimental autoimmune encephalomyelitis (EAE) mouse model with or without KD. The changes in motor function, pathological hallmarks of EAE, the status of microglia, neuroinflammatory response and intracellular signaling pathways in mice were detected by the rotarod test, histological analysis, real-time PCR (RT-PCR) and western blotting. Our results showed that KD could prevent motor deficiency, reduce clinical scores, inhibit demyelination, improve pathological lesions and suppress microglial activation in the spinal cord of EAE mice. Meanwhile, KD shifted microglial polarization toward the protective M2 phenotype and modified the inflammatory milieu by downregulating the production of pro-inflammatory cytokines, including TNF-α, IL-1β and IL-6, as well as upregulating the release of anti-inflammatory cytokines such as TGF-β. Furthermore, KD decreased the expression levels of CCL2, CCR2, CCL3, CCR1, CCR5, CXCL10 and CXCR3 in the spinal cord and spleen with reduced monocyte/macrophage infiltration in the CNS. In addition, KD inhibits NLRP3 activation in the microglia, as revealed by the significantly decreased co-expression of NLRP3(+) and Iba-1(+) in the KD + EAE group. Further studies demonstrated that KD suppresses inflammatory response and M1 microglial polarization by inhibiting the TLR4/MyD88/NF-κB/NLRP3 pathway, the JAK1/STAT1 pathway, HDAC3 and P2X7R activation, as well as up-regulation of JAK3/STAT6.
 BACKGROUND: Race and ancestry influence the course of multiple sclerosis (MS). OBJECTIVES: Explore clinical characteristics of MS and neuromyelitis optica spectrum disorder (NMOSD) in Asian American patients. METHODS: Chart review was performed for 282 adults with demyelinating disease who self-identified as Asian at a single North American MS center. Demographics and clinical characteristics were compared to non-Asian MS patients and by region of Asian ancestry. RESULTS: Region of ancestry was known for 181 patients. Most (94.7%) preferred English, but fewer East Asian patients did (80%, p = 0.0001). South Asian patients had higher neighborhood household income (p = 0.002). Diagnoses included MS (76.2%) and NMOSD (13.8%). More patients with NMOSD than MS were East and Southeast Asian (p = 0.004). For MS patients, optic nerve and spinal cord involvement were similar across regions of ancestry. Asian MS patients were younger at symptom onset and diagnosis than non-Asian MS patients. MS Severity Scale scores were similar to non-Asian MS patients but worse among Southeast Asians (p = 0.006). CONCLUSIONS: MS severity was similar between Asian American patients and non-Asian patients. Region of ancestry was associated with differences in sociodemographics and MS severity. Further research is needed to uncover genetic, socioeconomic, or environmental factors causing these differences.
 OBJECTIVE: Multiple Sclerosis (MS) is a degenerative disease of the CNS characterized by inflammation, demyelination, and axonal damage. It has been hypothesized that hypoxia plays a role in the pathogenesis of MS. This study was undertaken to investigate the reproducibility of non-invasively measured cortical microvascular hemoglobin oxygenation (S(t) O(2) ) using frequency domain near-infrared spectroscopy (fdNIRS), investigate its temporal pattern of hypoxia in people with MS (pwMS), and its relationship with neurocognitive function and mood. METHODS: We investigated the reproducibility of fdNIRS measurements. We measured cortical hypoxia in pwMS, and the relationships between S(t) O(2) , neurocognitive function, fatigue, and measures of physical disability. Furthermore, we cataloged the temporal pattern of S(t) O(2) measured at 1-week intervals for 4 weeks, and at 8 weeks and ~1 year. RESULTS: We show that fdNIRS parameters were highly reproducible in 7 healthy control participants measured over 6 days (p>0.05). There was low variability between and within subjects. In line with our previous findings, we show that 33% of pwMS (n=88) have cortical microvascular hypoxia. Over 8 weeks and at ~1 year, S(t) O(2) values for normoxic and hypoxic groups did not change significantly. There was no significant association between cognitive function and S(t) O(2) . This conclusion should be revisited as only a small proportion of the RRMS group (21%) was cognitively impaired. INTERPRETATION: fdNIRS parameters have high reproducibility and repeatability, and we have demonstrated that hypoxia in MS is a chronic condition, lasting at least a year. The results show a weak relationship between cognitive functioning and oxygenation indicating future study is required. This article is protected by copyright. All rights reserved.
 Iron is an essential element involved in a multitude of bodily processes. It is tightly regulated, as elevated deposition in tissues is associated with diseases such as multiple sclerosis (MS). Iron accumulation in the central nervous system (CNS) of MS patients is linked to neurotoxicity through mechanisms including oxidative stress, glutamate excitotoxicity, misfolding of proteins, and ferroptosis. In the past decade, the combination of MRI and histopathology has enhanced our understanding of iron deposition in MS pathophysiology, including in the pro-inflammatory and neurotoxicity of iron-laden rims of chronic active lesions. In this regard, iron accumulation may not only have an impact on different CNS-resident cells but may also promote the innate and adaptive immune dysfunctions in MS. Although there are discordant results, most studies indicate lower levels of iron but higher amounts of the iron storage molecule ferritin in the circulation of people with MS. Considering the importance of iron, there is a need for evidence-guided recommendation for dietary intake in people living with MS. Potential novel therapeutic approaches include the regulation of iron levels using next generation iron chelators, as well as therapies to interfere with toxic consequences of iron overload including antioxidants in MS.
 INTRODUCTION: Multiple sclerosis neuropsychological questionnaire (MSNQ) is a brief questionnaire useful for screening patient's and informant's self-perception of cognitive dysfunctions in daily life activities. Our study aims to evaluate the MSNQ validity in Huntington's disease (HD) mutation carriers and to correlate MSNQ scores with neurological, cognitive, and behavioral variables. METHODS: The study was conducted on a sample of 107 subjects from presymptomatic to the middle stage of HD recruited at LIRH Foundation and C.S.S. Mendel Institute in Rome. Unified Huntington's Disease Rating Scale (UHDRS), an internationally standardized and validated scale, was used to evaluate motor, functional cognitive, and behavioral domains. RESULTS: Our results showed that in HD subjects, MSNQ has a unidimensional factor structure. Correlational analyses indicated a good correlation between the MSNQ-patient version (MSNQ-p) and clinical variables, specifically with cognitive dysfunction and behavioral alterations. Moreover, higher scores in MSNQ-p were associated with higher motor disease and functional impairment showing that patients in advanced stage of HD perceive a greater cognitive impairment. These results confirm the questionnaire's reliability. CONCLUSIONS: The present study demonstrates the validity and adaptability of MSNQ in the HD population proposing it as a cognitive tool during routine clinical follow-ups, although further research is needed to determine an optimal cut-off score for this measure.
 Multiple sclerosis (MS) is a chronic and progressive autoimmune disease of the central nervous system (CNS), with both genetic and environmental factors contributing to the pathobiology of the disease. Although HLA genes have emerged as the strongest genetic factor linked to MS, consensus on the environmental risk factors is lacking. Recently, the gut microbiota has garnered increasing attention as a potential environmental factor in MS, as mounting evidence suggests that individuals with MS exhibit microbial dysbiosis (changes in the gut microbiome). Thus, there has been a strong emphasis on understanding the role of the gut microbiome in the pathobiology of MS, specifically, factors regulating the gut microbiota and the mechanism(s) through which gut microbes may contribute to MS. Among all factors, diet has emerged to have the strongest influence on the composition and function of gut microbiota. As MS patients lack gut bacteria capable of metabolizing dietary phytoestrogen, we will specifically discuss the role of a phytoestrogen diet and phytoestrogen metabolizing gut bacteria in the pathobiology of MS. A better understanding of these mechanisms will help to harness the enormous potential of the gut microbiota as potential therapeutics to treat MS and other autoimmune diseases.
 Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by inflammation, demyelination, gliosis, and neuronal loss. Pathologically, perivascular lymphocytic infiltrates, and macrophages produce degradation of myelin sheaths that surround neurons. Neurological symptoms vary and can include vision impairment, numbness and tingling, focal weakness, bladder and bowel incontinence, and cognitive dysfunction. Symptoms vary depending on lesion location. Clinical symptoms characterized by acute relapses typically first develop in young adults. A gradually progressive course then ensues with permanent disability in 10 to 15 years. MS groups into seven categories based on disease course: 1) Relapsing-remitting (RR): 70 to 80% of MS patients demonstrate an initial onset characterized by a relapsing-remitting (RR) course, demonstrating the following neurologic presentation: New or recurrent neurological symptoms consistent with MS. Symptoms last 24 to 48 hours. They develop over days to weeks. 2) Primary progressive (PP): 15 to 20% of patients present with a gradual deterioration from the onset, with an absence of relapses. 3) Secondary progressive (SP): this is characterized by a more gradual neurologic deterioration after an initial RR course. Superimposed relapses can be a feature of this clinical course, as well, although this is not a mandatory feature. 4) Progressive-relapsing (PR) MS: in 5% of patients, a gradual deterioration with superimposed relapses occurs. The following three categories are sometimes included in the spectrum of MS: 5) Clinically isolated syndrome (CIS): often classified as a single episode of inflammatory CNS demyelination. 6) Fulminant: characterized by severe MS with multiple relapses and rapid progression towards disability. 7) Benign: a clinical course characterized by an overall mild disability. Relapses are rare. When discussing MS, clinicians most often describe the RR course, considering its high prevalence amongst affected patients. Relapses often recover either partially or completely over weeks and months, frequently without treatment. Over time, residual symptoms from relapses without complete recovery accumulate and contribute to general disability. The diagnosis of RR MS is made with at least two CNS inflammatory events. Although different diagnostic criteria have been used for MS, the general principle of diagnosing the RR course has involved establishing episodes separated in "time and space." This means that episodes must be separated in time and affect different locations of the CNS. Making the diagnosis of MS expeditiously allows for the early and effective institution of disease-modifying therapy. Treatment aims at decreasing relapses and MRI activity. Long-term therapy aims at reducing the risk of permanent disability.
 INTRODUCTION: Systemic prolactin levels have been found to increase in 19 patients diagnosed with neuromyelitis optica spectrum disorders (NMOSD). However, the relationship between plasma prolactin levels and clinical manifestations in NMOSD patients remains unclear. METHODS: This cross-sectional study was conducted as part of a Registered Cohort Study of Inflammatory Demyelination Disease (NCT04386018). A total of 95 patients diagnosed with central nervous system demyelinating diseases and 43 healthy controls were recruited between May 2020 and February 2022 at the First Affiliated Hospital of Fujian Medical University. Plasma samples were collected from all participants and analyzed for prolactin levels using electrochemiluminescence immunoassay. The study aimed to investigate the correlation between plasma prolactin levels and clinical features in patients with central nervous system demyelinating diseases. RESULTS: Plasma prolactin levels in NMOSD patients were significantly higher than those in multiple sclerosis/myelin oligodendrocyte glycoprotein antibody-associated diseases patients and controls (p<0.05, respectively), and were found to be correlated with disease activity, sensory abnormalities, thoracic spinal cord lesions, and MR lesion enhancement (p<0.05). A total of 16.28% of NMOSD patients exhibited macroprolactinemia. However, there was no correlation found between macroprolactin levels and disease activity (p>0.05). CONCLUSION: Prolactin may play a role in the pro-inflammatory regulation mechanism of NMOSD.
 Dietary green tea epigallocatechin-3-gallate (EGCG) could attenuate experimental autoimmune encephalomyelitis via the modification of the balance of CD4(+) T helper (Th) cells. Moreover, EGCG administration in vitro has a direct impact on the regulatory cytokines and differentiation of CD4(+) T cells. Here, we aim to determine whether EGCG directly affects the cell division and progression in naive CD4(+) T cells. We first investigate the effect of EGCG on naïve CD4(+) T cell division and progression in vitro. An integrated analysis of network pharmacology and molecular docking was utilized to further identify the targets of EGCG for T cell-mediated autoimmune diseases and multiple sclerosis (MS). EGCG treatment prevented naïve CD4(+) T cells from progressing through the cell cycle when stimulated with anti-CD3/CD28 antibodies. This was achieved by increasing the proportion of cells arrested in the G0/G1 phase by 8.6% and reducing DNA synthesis activity by 51% in the S phase. Furthermore, EGCG treatment inhibited the expression of cyclins (cyclin D1, cyclin D3, cyclin A, and cyclin B1) and CDKs (CDK2 and CDK6) during naïve CD4(+) T cell activation in response to anti-CD3/CD28 stimulation. However, EGCG inhibited the decrease of P27(Kip1) (CDKN1B) during naïve CD4(+) T cell activation, whereas it inhibited the increase of P21(Cip1) (CDKN1A) expression 48 h after mitogenic stimulation. The molecular docking analysis confirmed that these proteins (CD4, CCND1, and CDKN1A) are the primary targets for EGCG, T cell-mediated autoimmune diseases, and MS. Finally, target enrichment analysis indicated that EGCG may affect the cell cycle, T cell receptor signaling pathway, Th cell differentiation, and NF-κB signaling pathway. These findings reveal a crucial role of EGCG in the division and progression of CD4(+) T cells, and underscore other potential targets of EGCG in T cell-mediated autoimmune diseases such as MS.
 The C-X-C motif ligand 16, or CXCL16, is a chemokine that belongs to the ELR - CXC subfamily. Its function is to bind to the chemokine receptor CXCR6, which is a G protein-coupled receptor with 7 transmembrane domains. The CXCR6/CXCL16 axis has been linked to the development of numerous autoimmune diseases and is connected to clinical parameters that reflect disease severity, activity, and prognosis in conditions such as multiple sclerosis, autoimmune hepatitis, rheumatoid arthritis, Crohn's disease, and psoriasis. CXCL16 is expressed in various immune cells, such as dendritic cells, monocytes, macrophages, and B cells. During autoimmune diseases, CXCL16 can facilitate the adhesion of immune cells like monocytes, T cells, NKT cells, and others to endothelial cells and dendritic cells. Additionally, sCXCL16 can regulate the migration of CXCR6-expressing leukocytes, which includes CD8(+) T cells, CD4(+) T cells, NK cells, constant natural killer T cells, plasma cells, and monocytes. Further investigation is required to comprehend the intricate interactions between chemokines and the pathogenesis of autoimmune diseases. It remains to be seen whether the CXCR6/CXCL16 axis represents a new target for the treatment of these conditions.
 BACKGROUND: Reports suggest a potential association between coronavirus disease 2019 (COVID-19) vaccines and acute central nervous system (CNS) inflammation. OBJECTIVE: The main objective of this study is to describe features of acute CNS inflammation following COVID-19 vaccination. METHODS: A retrospective observational cohort study was performed at the BARLO MS Centre in Toronto, Canada. Clinicians reported acute CNS inflammatory events within 60 days after a COVID-19 vaccine from March 2021 to August 2022. Clinical characteristics were evaluated. RESULTS: Thirty-eight patients (median age 39 (range: 20-82) years; 60.5% female) presented within 0-55 (median 15) days of a receiving a COVID-19 vaccine and were diagnosed with relapsing remitting multiple sclerosis (MS) (n = 16), post-vaccine transverse myelitis (n = 7), clinically isolated syndrome (n = 5), MS relapse (n = 4), tumefactive demyelination (n = 2), myelin oligodendrocyte glycoprotein antibody disease (n = 1), neuromyelitis optica spectrum disorder (n = 1), chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (n = 1) and primary autoimmune cerebellar ataxia (n = 1). Twenty-two received acute treatment and 21 started disease-modifying therapy. Sixteen received subsequent COVID-19 vaccination, of which 87.5% had no new or worsening neurological symptoms. CONCLUSION: To our knowledge, this is the largest study describing acute CNS inflammation after COVID-19 vaccination. We could not determine whether the number of inflammatory events was higher than expected.
 Introduction: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system characterized by neuroinflammation leading to demyelination. The associated symptoms lead to a devastating decrease in quality of life. The cannabinoids and their derivatives have emerged as an encouraging alternative due to their management of symptom in MS. Objective: The aim of the study was to investigate the mechanism of action of cannabidiol (CBD), a nonpsychoactive cannabinoid, on molecular and cellular events associated with leukocyte recruitment induced by experimental autoimmune encephalomyelitis (EAE). Materials and Methods: C57BL/6 female mice were randomly assigned to the four experimental groups: C (control group), CBD (cannabidiol-treated group, 5 mg/kg i.p.; 14 days), EAE (experimental autoimmune encephalomyelitis-induced group), and EAE+CBD (experimental autoimmune encephalomyelitis-induced plus cannabidiol-treated group). Results: The results indicated that 5 mg/kg of CBD injected intraperitoneally between the 1st and 14th days of EAE could reduce the leukocyte rolling and adhesion into the spinal cord microvasculature as well cellular tissue infiltration. These results were supported by a decreased mRNA expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the spinal cord. Conclusion: Purified CBD reduces in vivo VCAM and ICAM-mediated leukocyte recruitment to the spinal cord microvasculature at EAE peak disease.
 B cells contribute to the pathogenesis of both cellular- and humoral-mediated central nervous system (CNS) inflammatory diseases through a variety of mechanisms. In such conditions, B cells may enter the CNS parenchyma and contribute to local tissue destruction. It remains unexplored, however, how infection and autoimmunity drive transcriptional phenotypes, repertoire features, and antibody functionality. Here, we profiled B cells from the CNS of murine models of intracranial (i.c.) viral infections and autoimmunity. We identified a population of clonally expanded, antibody-secreting cells (ASCs) that had undergone class-switch recombination and extensive somatic hypermutation following i.c. infection with attenuated lymphocytic choriomeningitis virus (rLCMV). Recombinant expression and characterisation of these antibodies revealed specificity to viral antigens (LCMV glycoprotein GP), correlating with ASC persistence in the brain weeks after resolved infection. Furthermore, these virus-specific ASCs upregulated proliferation and expansion programs in response to the conditional and transient induction of the LCMV GP as a neo-self antigen by astrocytes. This class-switched, clonally expanded, and mutated population persisted and was even more pronounced when peripheral B cells were depleted prior to autoantigen induction in the CNS. In contrast, the most expanded B cell clones in mice with persistent expression of LCMV GP in the CNS did not exhibit neo-self antigen specificity, potentially a consequence of local tolerance induction. Finally, a comparable population of clonally expanded, class-switched, and proliferating ASCs was detected in the cerebrospinal fluid of relapsing multiple sclerosis (RMS) patients. Taken together, our findings support the existence of B cells that populate the CNS and are capable of responding to locally encountered autoantigens.
 Demyelinating disorders of the central nervous system (CNS) occur when myelin and oligodendrocytes are damaged or lost. Remyelination and regeneration of oligodendrocytes can be achieved from endogenous oligodendrocyte precursor cells (OPCs) that reside in the adult CNS tissue. Using a cuprizone mouse model of demyelination, we show that infusion of fractalkine (CX3CL1) into the demyelinated murine brain increases de novo oligodendrocyte formation and enhances remyelination in the corpus callosum and cortical gray matter. This is achieved by increased OPC proliferation in the cortical gray matter as well as OPC differentiation and attenuation of microglia/macrophage activation both in corpus callosum and cortical gray matter. Finally, we show that activated OPCs and microglia/macrophages express fractalkine receptor CX3CR1 in vivo, and that in OPC-microglia co-cultures fractalkine increases in vitro oligodendrocyte differentiation by modulating both OPC and microglia biology. Our results demonstrate a novel pro-regenerative role of fractalkine in a demyelinating mouse model.
 PURPOSE: Quantitative magnetization transfer (QMT) using selective inversion recovery (SIR) can quantify the macromolecular-to-free proton pool size ratio (PSR), which has been shown to relate closely with myelin content. Currently clinical applications of SIR have been hampered by long scan times. In this work, the acceleration of SIR-QMT using CS-SENSE (compressed sensing SENSE) was systematically studied. THEORY AND METHODS: Phantoms of varied concentrations of bovine serum albumin and human scans were first conducted to evaluate the SNR, precision of SIR-QMT parameters, and scan time. Based on these results, an optimized CS-SENSE factor of 8 was determined and the test-retest repeatability was further investigated. RESULTS: A whole-brain SIR imaging of 6 min can be achieved. Bland-Altman analyses indicated excellent agreement between the test and retest sessions with a difference in mean PSR of 0.06% (and a difference in mean R(1f) of -0.001 s(-1) ). In addition, the assessment of the intraclass correlation coefficient (ICC) revealed high reliability in nearly all the white matter and gray matter regions. In white matter regions, the ICC was 0.93 (95% confidence interval [CI]: 0.88-0.96, p < 0.001) for PSR, and 0.90 (95% CI: 0.83-0.94, p < 0.001) for R(1f) . In gray matter, ICC was 0.84 (95% CI: 0.66-0.93, p < 0.001) in PSR, and 0.98 (95% CI: 0.95-0.99, p < 0.001) for R(1f) . The method also showed excellent capability to detect focal lesions in multiple sclerosis. CONCLUSION: Rapid, reliable, and sensitive whole-brain SIR imaging can be achieved using CS-SENSE, which is expected to significantly promote widespread clinical translation.
 INTRODUCTION: Multiple sclerosis (MS) is characterized by a wide range of disabling symptoms, including cognitive dysfunction, fatigue, depression, anxiety, pain, and sleep difficulties. The current study aimed to examine real-time associations between non-cognitive and cognitive symptoms (latter measured both objectively and subjectively in real-time) using smartphone-administered ecological momentary assessment (EMA). METHODS: Forty-five persons with MS completed EMA four times per day for 3 weeks. For each EMA, participants completed mobile versions of the Trail-Making Test part B (mTMT-B) and a finger tapping task, as well as surveys about symptom severity. Multilevel models were conducted to account for within-person and within-day clustering. RESULTS: A total of 3,174 EMA sessions were collected; compliance rate was 84%. There was significant intra-day variability in mTMT-B performance (p < 0.001) and levels of self-reported fatigue (p < 0.001). When participants reported depressive symptoms that were worse than their usual levels, they also performed worse on the mTMT-B (p < 0.001), independent of upper extremity motor functioning. Other self-reported non-cognitive symptoms were not associated with real-time performance on the mTMT-B [p > 0.009 (Bonferroni-corrected)]. In contrast, when self-reported fatigue (p < 0.001), depression (p < 0.001), anxiety (p < 0.001), and pain (p < 0.001) were worse than the individual's typical levels, they also reported more severe cognitive dysfunction at the same time. Further, there was a statistical trend that self-reported cognitive dysfunction (not mTMT-B performance) predicted one's self-reported sense of accomplishment in real-time. DISCUSSION: The current study was the first to identify divergent factors that influence subjectively and objectively measured cognitive functioning in real time among persons with MS. Notably, it is when symptom severity was worse than the individual's usual levels (and not absolute levels) that led to cognitive fluctuations, which supports the use of EMA in MS symptom monitoring.
 Triggering receptor expressed on myeloid cell 2 (TREM2) signaling often drives opposing effects in traumatic versus demyelinating CNS disorders. Here, we identify two distinct phenotypes of microglia and infiltrating myeloid populations dependent on TREM2 expression levels at the acute stage and elucidate how they mediate the opposing effects of TREM2 in spinal cord injury (SCI) versus multiple sclerosis animal models (experimental autoimmune encephalomyelitis [EAE]). High TREM2 levels sustain phagocytic microglia and infiltrating macrophages after SCI. In contrast, moderate TREM2 levels sustain immunomodulatory microglia and infiltrating monocytes in EAE. TREM2-ablated microglia (purine-sensing phenotype in SCI and reduced immunomodulatory phenotype in EAE) drive transient protection at the acute stage of both disorders, whereas reduced phagocytic macrophages and lysosome-activated monocytes lead to contrasting neuroprotective and demyelinating effects in SCI versus EAE, respectively. Our study provides comprehensive insights into the complex roles of TREM2 in myeloid populations across diverse CNS disorders, which has crucial implications in devising TREM2-targeting therapeutics.
 BACKGROUND: Alzheimer's disease (AD) and Multiple sclerosis (MS) lead to neurodegenerative processes negatively affecting millions of people worldwide. Their treatment is still difficult and practically incomplete. One of the most commonly used drugs against these neurodegenerative diseases is 4-aminopyridine. However, its use is confined by the high toxicity. OBJECTIVES: The aim of this work is to obtain new peptide derivatives of 4-aminopyridine with decreased toxicity compared to 4-aminopyridine. METHODS: Synthesis was conducted in solution using a consecutive condensation approach. The new derivatives were characterized by melting points, NMR, and Mass spectra. Important ADME (absorption, distribution, metabolism, and excretion) properties have been studied in silico using ACD/Percepta v.2020.2.0 software. Acute toxicity was determined in mice according to a Standard protocol. All new derivatives were tested in vitro for cytotoxic activity in a panel of human (HEP-G2, BV-173) and murine (NEURO 2A) tumor cell lines via a standard MTT-based colorimetric method. β-secretase inhibitory activity was determined by applying the fluorescent method. RESULTS: New derivatives of 4-aminopyridine containing analogues of the β-secretase inhibitory peptide (Boc-Val-Asn-Leu-Ala-OH) were obtained. The in vivo toxicity of the tested compounds was found to be as high as 1500 mg/kg. Cell toxicity screening against tumor cell lines of different origins showed negligible growth-inhibitory effects of all investigated 4-aminopyridine analogues. CONCLUSION: Synthesis of new peptide derivatives of 4-aminopyridine is reported. Acute toxicity studies revealed a ca. 150 times lower toxicity of the new compounds as compared to 4-aminopyridine that may be ascribed to their peptide fragment.
 Atopic dermatitis (AD) is a Th(2)-driven inflammatory skin disease that has been associated with other autoimmune illnesses (AI) and has a well-known predisposition to infection with herpes simplex virus infection. Yet, few studies have evaluated the association between atopic dermatitis, autoimmune illness, and other human herpes virus (HHV) infections such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV). We aimed to evaluate the association between AD, specific AIs, CMV, and EBV in a random sample of the Optum Clinformatics Data Mart database, a US administrative claims database. AD was defined based on ICD diagnostic codes. Patients with AD were exact matched to those without AD on sex, age at enrollment, time observed in the dataset and census division. Our outcomes of interest were rheumatoid arthritis (RA), Crohn's disease (CD), ulcerative colitis (UC), multiple sclerosis (MS), CMV, and EBV infection as defined by specific ICD codes. Logistic regression models were used to examine the association between AD and our outcomes of interest [odds ratio (95% confidence intervals)]. Our full cohort included 40,141,017 patients. In total, 601,783 patients with AD were included. As expected, patients with AD had a higher prevalence of asthma and seasonal allergies versus controls. Individuals with AD have an increased risk of EBV, CMV, RA, CD, UC, and MS. While we cannot demonstrate a causal association, the observed associations between AD and AI may be in part mediated by these types of HHV (i.e., CMV and EBV), a finding that merits further study.
 Multiple sclerosis (MS), a T-cell-mediated autoimmune disease that affects the central nervous system (CNS), is characterized by white matter demyelination, axon destruction, and oligodendrocyte degeneration. Ivermectin, an anti-parasitic drug, has anti-inflammatory, anti-tumor, and antiviral properties. However, to date, there are no in-depth studies on the effect of ivermectin on the function effector of T cells in murine experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Here, we conducted in vitro experiments and found that ivermectin inhibited the proliferation of total T cells (CD3(+)) and their subsets (CD4(+) and CD8(+) T cells) as well as T cells secreting the pro-inflammatory cytokines IFN-γ and IL-17A; ivermectin also increased IL-2 production and IL-2Rα (CD25) expression, which was accompanied by an increase in the frequency of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg). Importantly, ivermectin administration reduced the clinical symptoms of EAE mice by preventing the infiltration of inflammatory cells into the CNS. Additional mechanisms showed that ivermectin promoted Treg cells while inhibiting pro-inflammatory Th1 and Th17 cells and their IFN-γ and IL-17 secretion; ivermectin also upregulated IL-2 production from MOG(35-55)-stimulated peripheral lymphocytes. Finally, ivermectin decreased IFN-γ and IL-17A production and increased IL-2 level, CD25 expression, and STAT5 phosphorylation in the CNS. These results reveal a previously unknown etiopathophysiological mechanism by which ivermectin attenuates the pathogenesis of EAE, indicating that it may be a promising option for T-cell-mediated autoimmune diseases such as MS.
 OBJECTIVE: To examine the evidence regarding the potential of hybrid functional electrical stimulation (FES) cycling for improving cardiorespiratory fitness for people with a mobility disability related to a central nervous system (CNS) disorder. DATA SOURCES: Nine electronic databases: MEDLINE, EMBASE, Web of Science, CINAHL, PsycInfo, SPORTDiscus, Pedro, Cochrane, and Scopus, were searched from inception until October 2022. STUDY SELECTION: Search terms included multiple sclerosis, spinal cord injury (SCI), stroke, Parkinson's disease, cerebral palsy, synonyms of FES cycling, arm crank ergometry (ACE) or hybrid exercise, and V̇o(2). All experimental studies, including randomized controlled trials that included an outcome measure related to peak or sub-maximal V̇o(2) were eligible. DATA EXTRACTION: From a total of 280 articles, 13 were studies included. The Downs and Black Checklist was used to assess study quality. Random effects (Hedges' g) meta-analyses were undertaken to determine whether there were differences in V̇o(2peak) during acute bouts of hybrid FES cycling vs other modes of exercise and changes resulting from longitudinal training. DATA SYNTHESIS: During acute bouts of exercise, hybrid FES cycling was moderately more effective than ACE (effect size [ES] of 0.59 (95% CI 0.15-1.02, P=.008) in increasing V̇o(2peak) from rest. There was a large effect on the increase of V̇o(2peak) from rest for hybrid FES cycling compared with FES cycling (ES of 2.36 [95% CI 0.83-3.40, P=.003]). Longitudinal training with hybrid FES cycling showed a significant improvement in V̇o(2peak) from pre to post intervention with a large, pooled ES of 0.83 (95% CI 0.24-1.41, P=.006). CONCLUSIONS: Hybrid FES cycling produced higher V̇o(2peak) compared with ACE or FES cycling during acute bouts of exercise. Hybrid FES cycling can improve cardiorespiratory fitness in people with SCI. Additionally, there is emerging evidence that hybrid FES cycling might increase aerobic fitness in people with mobility disability related to CNS disorders.
 Virtual Reality (VR) has emerged as a new safe and efficient tool for the rehabilitation of many childhood and adulthood illnesses. VR-based therapies have the potential to improve both motor and functional skills in a wide range of age groups through cortical reorganization and the activation of various neuronal connections. Recently, the potential for using serious VR-based games that combine perceptual learning and dichoptic stimulation has been explored for the rehabilitation of ophthalmological and neurological disorders. In ophthalmology, several clinical studies have demonstrated the ability to use VR training to enhance stereopsis, contrast sensitivity, and visual acuity. The use of VR technology provides a significant advantage in training each eye individually without requiring occlusion or penalty. In neurological disorders, the majority of patients undergo recurrent episodes (relapses) of neurological impairment, however, in a few cases (60-80%), the illness progresses over time and becomes chronic, consequential in cumulated motor disability and cognitive deficits. Current research on memory restoration has been spurred by theories about brain plasticity and findings concerning the nervous system's capacity to reconstruct cellular synapses as a result of interaction with enriched environments. Therefore, the use of VR training can play an important role in the improvement of cognitive function and motor disability. Although there are several reviews in the community employing relevant Artificial Intelligence in healthcare, VR has not yet been thoroughly examined in this regard. In this systematic review, we examine the key ideas of VR-based training for prevention and control measurements in ocular diseases such as Myopia, Amblyopia, Presbyopia, and Age-related Macular Degeneration (AMD), and neurological disorders such as Alzheimer, Multiple Sclerosis (MS) Epilepsy and Autism spectrum disorder. This review highlights the fundamentals of VR technologies regarding their clinical research in healthcare. Moreover, these findings will raise community awareness of using VR training and help researchers to learn new techniques to prevent and cure different diseases. We further discuss the current challenges of using VR devices, as well as the future prospects of human training.
 One third of patients with multiple sclerosis (MS) suffered from depressive symptoms. The pathogenesis of depression in MS patients has been related to innate immune activation in certain regions of the brain such as hippocampus. However, pharmacotherapy lacks sufficient evidence for beneficial effects on depression in MS patients, urging for a novel treatment modality for this mental disorder. Treatment effects of rTMS on depression/anxiety-like behaviors in mice with experimental autoimmune encephalomyelitis (EAE) were assessed by behavioral tests. The role of innate immune response was examined by RNA sequencing, quantitative RT-PCR, and immunofluorescence techniques. Depressive symptom severity and astroglial activation in patients with MS were assessed by Beck Depression Inventory and serum glial fibrillary acidic protein (GFAP), respectively. EAE mice displayed depression/anxiety-like behaviors, which were ameliorated by rTMS. Transcriptome and gene-specific expression analysis of the hippocampus showed significant reduction in transcript levels associated with neurotoxic reactive astrocytes in EAE mice after rTMS treatment. This was confirmed by immunofluorescence studies. Complement component 3d, a marker of neurotoxic reactive astrocytes, was highly expressed in EAE hippocampus, but was reduced to a basal level after rTMS treatment. In patients with MS, astroglial activation, indicated by serum GFAP levels, was significantly elevated in those with moderate or major depressive symptoms. These findings support that the suppression of neurotoxic reactive astrocytes might be a potential target for treatment of depression in patients with MS, and suggest the potential of using rTMS as a potential therapeutic treatment for this disorder.
 The most recent and non-invasive approach for studying early-stage biomarkers is liquid biopsy. This implies the extraction and analysis of non-solid biological tissues (serum, plasma, saliva, urine, and cerebrospinal fluid) without undergoing invasive procedures to determine disease prognosis. Liquid biopsy can be used for the screening of several components, such as extracellular vesicles, microRNAs, cell-free DNA, cell-free mitochondrial and nuclear DNA, circulating tumour cells, circulating tumour DNA, transfer RNA, and circular DNA or RNA derived from body fluids. Its application includes early disease diagnosis, the surveillance of disease activity, and treatment response monitoring, with growing evidence for validating this methodology in cancer, liver disease, and central nervous system (CNS) disorders. This review will provide an overview of mentioned liquid biopsy components, which could serve as valuable biomarkers for the evaluation of complex neurological conditions, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, epilepsy, stroke, traumatic brain injury, CNS tumours, and neuroinfectious diseases. Furthermore, this review highlights the future directions and potential limitations associated with liquid biopsy.
 Acute disseminated encephalomyelitis is an immune mediated inflammatory-demyelinizing disease that usually manifests after infection or vaccination in school-age children. It typically presents a prodromal phase with flu-like symptoms, followed by a phase with varied clinical symptoms, neuro-ophthalmological alterations such as ophthalmoplegia or optic neuritis may occur. The differential diagnosis includes tumor, vascular, infectious, inflammatory and demyelinating diseases. Diagnosis is based on the clinical history and the characteristics of brain magnetic resonance imaging, the gold standard test. The study of the cerebrospinal fluid can help to guide the clinical picture. The prognosis is favorable, with an excellent response to corticosteroids and immunoglobulins, with minimal long-term sequelae in most cases. We report the case of an 8-year-old male with acute demyelinating disease due to adenovirus whose manifestation was an eight-and-a-half syndrome.
 INTRODUCTION: Coronavirus disease 2019 (COVID-19) is the biggest health challenge of recent times. Studies so far reveal that vaccination is the only way to prevent this pandemic. There may be factors that decrease or increase vaccine effectiveness. In multiple sclerosis (MS), some of these factors may cause changes in the effectiveness of the vaccine, depending on the nature of the disease and disease-modifying treatments (DMT). In this study, we aimed to investigate the relationship between antibody titer and smoking in non-treated and DMT-treated MS patients who received inactivated vaccine (Sinovac) and messenger RNA BNT162b2 (BioNTech) mRNA vaccines. METHOD: Vaccine antibody responses were measured between 4-12 weeks after two doses of inactivated vaccine and mRNA vaccines. Patients were separated into 6 groups as: patients with MS without treatment PwMS w/o T, ocrelizumab, fingolimod, interferons (interferon beta-1a and interferon beta-1b), dimethyl fumarate, and teriflunomide. Antibody titers of smokers and non-smokers were compared for both vaccines and for each group. RESULTS: The study included 798 patients. In the mRNA vaccine group, smokers (n=148; 2982±326 AU/mL) had lower antibody titers compared to the non-smokers (n=244; 5903±545 AU/mL) in total (p=0.020). In the inactivated vaccine group, no significant difference was detected between smokers (n=136; 383±51 AU/mL) and non-smokers (n=270; 388±49 AU/mL) in total (p=0.149). In both vaccine groups, patients receiving ocrelizumab and fingolimod had lower antibody titers than those receiving other DMTs or PwMS w/o T. In untreated MS patients, antibody levels in smokers were lower than in non-smokers in the mRNA vaccine group. No difference was found between antibody levels of smokers and non-smokers in any of the inactivated vaccine groups. CONCLUSION: Ocrelizumab and fingolimod have lower antibody levels than PwMS w/o T or other DMTs in both mRNA and inactivated vaccine groups. Smoking decreases antibody levels in the mRNA vaccine group, while it has no effect in the inactivated vaccine group.
 BACKGROUND: Non-invasive brain stimulation (NIBS) has demonstrated mixed effects on the clinical symptoms of multiple sclerosis. This systematic review and meta-analysis aimed to evaluate the effects of NIBS techniques on the most common symptoms of MS. METHODS: A literature search was performed until October 2022 which included randomized controlled trials and quasi-experimental studies that used sham-controlled NIBS in patients with MS. We calculated the Hedge's effect sizes of each domain of interest and their 95% confidence intervals (95% CIs) and performed random effects meta-analyses. RESULTS: A total of 49 studies were included in the systematic review (944 participants). Forty-four eligible studies were included for quantitative analysis, of which 33 applied transcranial direct current stimulation (tDCS), 9 transcranial magnetic stimulation (TMS), and 2 transcranial random noise stimulation (tRNS). We found a significant decrease in fatigue (ES:  - 0.86, 95% CI:  - 1.22 to - 0.51, p < 0.0001), pain (ES: - 1.91, 95% CI, - 3.64 to - 0.19, p=  0.03) and psychiatric symptoms (ES: - 1.44, 95% CI - 2.56 to - 0.32, p = 0.01) in favor of tDCS compared with the sham. On the other hand, there was no strong evidence showing tDCS effectiveness on motor performance and cognition (ES: - 0.03, 95% CI - 0.35 to 0.28, p = 0.83 and ES: 0.71, 95% CI, - 0.09 to 1.52, p = 0.08, respectively). Regarding TMS, we found a significant decrease in fatigue (ES: - 0.45, 95% CI: - 0.84 to -0.07, p = 0.02) and spasticity levels (ES: - 1.11, 95% CI: - 1.48 to - 0.75, p < 0.00001) compared to the sham. However, there was no strong evidence of the effectiveness of TMS on motor performance (ES: - 0.39, 95% CI - 0.95 to 0.16, p = 0.16). Finally, there was no significant evidence showing the effectiveness of tRNS on fatigue levels (ES: - 0.28, 95% CI: - 1.02 to 0.47, p = 0.46) and cognitive improvement (ES: - 0.04, 95% CI: - 0.6, 0.52, p = 0.88) compared with the sham. CONCLUSIONS: Overall, most studies have investigated the effects of tDCS on MS symptoms, particularly fatigue. The symptom that most benefited from NIBS was fatigue, while the least to benefit was motor performance. In addition, we found that disability score was associated with fatigue improvement. Thus, these findings support the idea that NIBS could have some promising effects on specific MS symptoms. It is also important to underscore that studies are very heterogeneous regarding the parameters of stimulation, and this may also have influenced the effects on some specific behavioral domains.
 BACKGROUND: Reduced physical activity is a worldwide challenge in individuals with multiple sclerosis (MS). The aim of this systematic review and meta-analysis was to identify devise-measured effects of physical activity, exercise and physiotherapy-interventions on step count and intensity level of physical activity in individuals with MS. METHODS: A systematic search of the databases of PubMed (including Medline), Scopus, CINHAL and Web of Science was carried out to retrieve studies published in the English language from the inception to the first of May 2023. All trials concerning the effectiveness of different types of exercise on step count and intensity level in people with MS were included. The quality of the included studies and their risk of bias were critically appraised using The modified consolidated standards of reporting trials and the Cochrane Risk of Bias tool, respectively. The pooled standardized mean difference (SMD) and 95% CI of the step-count outcome and moderate to vigorous intensity level before versus after treatment were estimated in both Intervention and Control groups using the random effect model. The Harbord test were used to account for heterogeneity between studies and assess publication bias, respectively. Further sensitivity analysis helped with the verification of the reliability and stability of our review results. RESULTS: A total of 8 randomized clinical trials (involving 919 individuals with MS) were included. The participants (including 715 (77.8%) female and 204 (22.2%) male) had been randomly assigned to the Intervention (n = 493) or Control group (n = 426). The pooled mean (95% CI) age and BMI of participants were 49.4 years (95% CI: 47.4, 51.4 years) and 27.7 kg/m(2) (95% CI: 26.4, 29 kg/m(2)), respectively. In terms of the comparison within the Intervention and the Control groups before and after the intervention, the results of the meta-analysis indicate that the pooled standardized mean difference (SMD) for step-count in the Intervention group was 0.56 (95% CI: -0.42, 1.54), while in the Control group it was 0.12 (95% CI: -0.05, 0.28). Furthermore, there was no significant difference in the pooled SMD of step-count in the physical activity Intervention group compared to the Controls after the intervention (pooled standard mean difference = 0.19, 95% CI: -0.36,0.74). Subgroup analysis on moderate to vigorous intensity level of physical activity revealed no significant effect of the physical activity intervention in the Intervention group compared to the Control group after the intervention, or within groups before and after the intervention. Results of meta regression showed that age, BMI, duration of disease and Expanded Disability Status Scale (EDSS) score were not the potential sources of heterogeneity (all p > 0.05). Data on the potential harms of the interventions were limited. CONCLUSION: The results of this meta-analysis showed no significant differences in step count and moderate to vigorous physical activity level among individuals with MS, both within and between groups receiving physical activity interventions. More studies that objectively measure physical activity are needed. SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/prospero/, identifier: CRD42022343621.
 Neurodegenerative diseases are prevalent and currently incurable conditions that progressively impair cognitive, behavioral, and psychiatric functions of the central or peripheral nervous system. Fibrinogen, a macromolecular glycoprotein, plays a crucial role in the inflammatory response and tissue repair in the human body and interacts with various nervous system cells due to its unique molecular structure. Accumulating evidence suggests that fibrinogen deposits in the brains of patients with neurodegenerative diseases. By regulating pathophysiological mechanisms and signaling pathways, fibrinogen can exacerbate the neuro-pathological features of neurodegenerative diseases, while depletion of fibrinogen contributes to the amelioration of cognitive function impairment in patients. This review comprehensively summarizes the molecular mechanisms and biological functions of fibrinogen in central nervous system cells and neurodegenerative diseases, including Alzheimer's disease, Multiple Sclerosis, Parkinson's disease, Vascular dementia, Huntington's disease, and Amyotrophic Lateral Sclerosis. Additionally, we discuss the potential of fibrinogen-related treatments in the management of neurodegenerative disorders.
 Autoimmune diseases are conditions in which the immune system mistakenly targets and damages healthy tissue in the body. In recent decades, the incidence of autoimmune diseases has increased, resulting in a significant disease burden. The current autoimmune therapies focus on targeting inflammation or inducing immunosuppression rather than addressing the underlying cause of the diseases. The activity of metabolic pathways is elevated in autoimmune diseases, and metabolic changes are increasingly recognized as important pathogenic processes underlying these. Therefore, metabolically targeted therapies may represent an important strategy for treating autoimmune diseases. This review provides a comprehensive overview of the evidence surrounding glucose metabolic reprogramming and its potential applications in drug discovery and development for autoimmune diseases, such as type 1 diabetes, multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis, and systemic sclerosis.

 Progressive multifocal leukoencephalopathy (PML) is a neurological condition caused by the JC virus. PML is a demyelinating disease preferentially affecting the central nervous system. In most individuals, it remains a latent infection however, it is particularly virulent in patients with immunosuppressive conditions such as AIDS, post solid organ and bone marrow transplant recipients, malignancies, and chronic inflammatory conditions. It has also been known to cause disease in patients who receive antiretroviral therapy as therapy can incite immune reconstitution. These cases of PML are termed PML- IRIS. Certain monoclonal antibodies, specifically, natalizumab used in the treatment of multiple sclerosis can also cause PML. It is an important differential to be considered when assessing neurological symptoms in patients with these specific risk factors.
 Tizanidine is an FDA-approved drug for managing spasticity. It is a centrally acting alpha-2 receptor agonist. Tizanidine effectively works with spasticity caused by multiple sclerosis, an acquired brain injury, or a spinal cord injury. It has also been shown to be clinically effective in managing patients suffering from chronic neck and lumbosacral neuralgia with a myofascial component to their pain and regional musculoskeletal pain syndromes. It is also prescribed off-label for migraine headaches, insomnia, and as an anticonvulsant. Tizanidine can also be applied as part of a detoxification therapy regimen in patients exhibiting analgesic rebound headaches to assist with analgesic withdrawal. This activity outlines the indications, mechanism of action, methods of administration, significant adverse effects, toxicity, and monitoring, of tizanidine so providers can direct patient therapy as part of the inter-professional team.
 Myoclonus is defined as rapid, brief, jerky, or shock-like movements involving muscle or group of muscles. Among all hyperkinetic movement disorders, myoclonus is considered to be the most rapid and brief. When caused by sudden muscle contractions, it is known as 'positive myoclonus', while a brief loss of muscular tone results in 'negative myoclonus' such as in asterixis. Myoclonus is classified in different ways according to its physiology, anatomical site of origin, and etiology. As with most movement disorders, myoclonus can be focal, multifocal, segmental, or generalized. Myoclonus is one of the signs in a wide variety of nervous system disorders such as dystonia, multiple sclerosis, Parkinson's disease, Creutzfeldt-Jakob disease (CJD), serotonin toxicity, Huntington disease, subacute sclerosing panencephalitis, Alzheimer's disease, and Gaucher disease.
 The Berg Balance Scale is a test used to assess functional balance. It was created by Katherine Berg in 1989 to evaluate balance ability in the elderly, with the initial target population having an average age of 73. It evaluates both dynamic and static balance through 14 tasks regarding mobility. In the beginning, it was mostly used to assess stroke patients; however, this test has shown high validity and reliability in various patient populations, including neurological conditions such as Parkinson disease, multiple sclerosis, traumatic brain injury, and acquired conditions as lower extremity amputees.  The scale has been useful in predicting the risk of falls and outcomes and even assessing the length of stay at inpatient rehabilitation. It is a short test that can be performed relatively quickly under different environments. 
 Neurodegenerative disorders are among the most common life-threatening disorders among the elderly worldwide and are marked by neuronal death in the brain and spinal cord. Several studies have demonstrated the beneficial role of dietary fatty acids in different brain disorders. This is due to their neurotrophic, antioxidant, and anti-inflammatory properties. Furthermore, extensive evidence shows that an unbalanced intake of certain dietary fatty acids increases the risk of neuropsychiatric diseases. Several research has been done on erucic acid, an ingestible omega-9 fatty acid that is found in Lorenzo's oil. Erucic acid was previously thought to be a natural toxin because of its negative effects on heart muscle function and hepatic steatosis, but it has been discovered that erucic acid is regularly consumed in Asian countries through the consumption of cruciferous vegetables like mustard and rapeseed oil with no evidence of cardiac harm. Erucic acid can also be transformed into nervonic acid, a crucial element of myelin. Therefore, erucic acid may have remyelinating effects, which may be crucial for treating different demyelinating conditions. Also, erucic acid exerts antioxidant and anti-inflammatory effects, suggesting its possible therapeutic role in different neurodegenerative disorders. Considering the fruitful effects of this compound, this article reviews the probable role of erucic acid as a pharmacological agent for treating and managing different neurodegenerative disorders.
 Since their original discovery, type I interferons (IFN-Is) have been closely associated with antiviral immune responses. However, their biological functions go far beyond this role, with balanced IFN-I activity being critical to maintain cellular and tissue homeostasis. Recent findings have uncovered a darker side of IFN-Is whereby chronically elevated levels induce devastating neuroinflammatory and neurodegenerative pathologies. The underlying causes of these 'interferonopathies' are diverse and include monogenetic syndromes, autoimmune disorders, as well as chronic infections. The prominent involvement of the CNS in these disorders indicates a particular susceptibility of brain cells to IFN-I toxicity. Here we will discuss the current knowledge of how IFN-Is mediate neurotoxicity in the brain by analyzing the cell-type specific responses to IFN-Is in the CNS, and secondly, by exploring the spectrum of neurological disorders arising from increased IFN-Is. Understanding the nature of IFN-I neurotoxicity is a crucial and fundamental step towards development of new therapeutic strategies for interferonopathies.
 BACKGROUND: People living with multiple sclerosis (MS) and other disorders treated with immunomodulatory therapies remain concerned about suboptimal responses to coronavirus disease 2019 (COVID-19) vaccines. Important questions persist regarding immunological response to third vaccines, particularly with respect to newer virus variants. The objective of this study is to evaluate humoral and cellular immune responses to a third COVID-19 vaccine dose in people on anti-CD20 therapy and sphingosine 1-phosphate receptor (S1PR) modulators, including Omicron-specific assays. METHODS: This is an observational study evaluating immunological responses to third COVID-19 vaccine dose in participants treated with anti-CD20 agents, S1PR modulators, and healthy controls. Neutralizing antibodies against USA-WA1/2020 (WA1) and B.1.1.529 (BA.1) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were measured before and after third vaccine. Groups were compared by one-way ANOVA with Tukey multiple comparisons. Cellular responses to spike peptide pools generated from WA1 and BA.1 were evaluated. Pre-post comparisons were made by Wilcoxon paired t-tests, inter-cohort comparisons by Mann-Whitney t-test. RESULTS: This cohort includes 25 participants on anti-CD20 therapy, 12 on S1PR modulators, and 14 healthy controls. Among those on anti-CD20 therapy, neutralizing antibodies to WA1 were significantly reduced compared to healthy controls (ID50% GM post-vaccination of 8.1 ± 2.8 in anti-CD20 therapy group vs 452.6 ± 8.442 healthy controls, P < 0.0001) and neutralizing antibodies to BA.1 were below the threshold of detection nearly universally. However, cellular responses, including to Omicron-specific peptides, were not significantly different from controls. Among those on S1PR modulators, neutralizing antibodies to WA1 were detected in a minority, and only 3/12 had neutralizing antibodies just at the limit of detection to BA.1. Cellular responses to Spike antigen in those on S1PR modulators were reduced by a factor of 100 compared to controls (median 0.0008% vs. 0.08%, p < 0.001) and were not significantly "boosted" by a third injection. CONCLUSIONS: Participants on anti-CD20 and S1PR modulator therapies had impaired antibody neutralization capacity, particularly to BA.1, even after a third vaccine. T cell responses were not affected by anti-CD20 therapies, but were nearly abrogated by S1PR modulators. These results have clinical implications warranting further study.
 The identification of prognostic markers in early multiple sclerosis (MS) is challenging and requires reliable measures that robustly predict future disease trajectories. Ideally, such measures should make inferences at the individual level to inform clinical decisions. This study investigated the prognostic value of longitudinal structural networks to predict five-year EDSS progression in patients with relapsing-remitting MS (RRMS). We hypothesized that network measures, derived from magnetic resonance imaging (MRI), outperform conventional MRI measurements at identifying patients at risk of developing disability progression. This longitudinal, multicentre study within the Magnetic Resonance Imaging in MS (MAGNIMS) network included 406 patients with RRMS (mean age = 35.7 ± 9.1 years) followed up for five years (mean follow-up = 5.0 ± 0.6 years). Expanded Disability Status Scale (EDSS) was determined to track disability accumulation. A group of 153 healthy subjects (mean age = 35.0 ± 10.1 years) with longitudinal MRI served as controls. All subjects underwent MRI at baseline and again one year after baseline. Grey matter (GM) atrophy over one year and white matter (WM) lesion load were determined. A single-subject brain network was reconstructed from T1-weighted scans based on GM atrophy measures derived from a statistical parameter mapping (SPM)-based segmentation pipeline. Key topological measures, including network degree, global efficiency and transitivity, were calculated at single-subject level to quantify network properties related to EDSS progression. Areas under receiver operator characteristic (ROC) curves were constructed for GM atrophy, WM lesion load and the network measures, and comparisons between ROC curves were conducted. The applied network analyses differentiated patients with RRMS who experience EDSS progression over five years through lower values for network degree [H(2)=30.0, p<0.001] and global efficiency [H(2)=31.3, p<0.001] from healthy controls but also from patients without progression. For transitivity, the comparisons showed no difference between the groups (H(2)= 1.5, p=0.474). Most notably, changes in network degree and global efficiency were detected independent of disease activity in the first year. The described network reorganization in patients experiencing EDSS progression was evident in the absence of GM atrophy. Network degree and global efficiency measurements demonstrated superiority of network measures in the ROC analyses over GM atrophy and WM lesion load in predicting EDSS worsening (all p-values < 0.05). Our findings provide evidence that GM network reorganization over one year discloses relevant information about subsequent clinical worsening in RRMS. Early GM restructuring towards lower network efficiency predicts disability accumulation and outperforms conventional MRI predictors.


 Trigeminal neuralgia, or tic douloureux, clinically presents as a unilateral paroxysmal, stabbing, intense pain of the face, lasting for seconds but occurring frequently. Alternative causes including multiple sclerosis or mass of the brainstem or cranial nerves must be ruled out. Medical treatment, most commonly with carbamazepine, remains an effective first-line treatment. Ultimately, if medical management becomes refractory or symptoms progressive, then procedural and surgical options including microvascular decompression, stereotactic radiosurgery, radiofrequency thermocoagulation, and others should be considered. Most notably, microvascular decompression, as in this case, can be considered with an 85%-95% initial success rate.
 Chronic olfactory dysfunction after SARS-CoV-2 infection occurs in approximately 10% of patients with COVID-19-induced anosmia, and it is a growing public health concern. A regimen of olfactory training and anti-neuroinflammatory therapy with co-ultramicronized palmitoylethanolamide with luteolin (um-PEA-LUT) has shown promising results in clinical trials; however, approximately 15% of treated patients do not achieve full recovery of a normal olfactory threshold, and almost 5% have no recovery. Disease-modifying therapies (DMTs), which are used to treat autoimmune neuroinflammation in multiple sclerosis (MS), have not been studied for treating persistent inflammation in refractory post-COVID-19 smell disorder. This study evaluated COVID-19-related smell loss and MS-related smell loss, comparing the responses to different therapies. Forty patients with MS and 45 reporting post-COVID-19 olfactory disorders were included in the study. All patients underwent nasal endoscopy and were evaluated by using validated Sniffin' Sticks testing. The patients with long COVID were treated for three months with um-PEA-LUT plus olfactory training. The patients with MS were treated with DMTs. Olfactory functions before and after treatment were analyzed in both groups. At the experimental endpoint, 13 patients in the COVID-19 group treated with um-PEA-LUT had residual olfactory impairment versus 10 patients in the MS group treated with DMTs. The severity of the persistent olfactory loss was lower in the MS group, and the patients with MS treated with IFN-beta and glatiramer acetate had the preservation of olfactory function. These data provide a rationale for considering prospective trials investigating the efficacy of DMTs for post-COVID-19 olfactory disorders that are refractory to um-PEA-LUT with olfactory training. This study is the first to consider the role of DMT in treating refractory post-viral olfactory loss in patients with long COVID.
 INTRODUCTION: Limited data exist on brain MRI enhancement in myelin-oligodendrocyte-glycoprotein (MOG) antibody-associated disease (MOGAD) and differences from aquaporin-4-IgG-positive-neuromyelitis-optica-spectrum-disorder (AQP4+NMOSD), and multiple sclerosis (MS). METHODS: In this retrospective observational study, we identified 122 Mayo Clinic MOGAD patients (1 January 1996-1 July 2020) with cerebral attacks. We explored enhancement patterns using a discovery set (n=41). We assessed enhancement frequency and Expanded Disability Status Scale scores at nadir and follow-up in the remainder (n=81). Two raters assessed T1-weighted-postgadolinium MRIs (1.5T/3T) for enhancement patterns in MOGAD, AQP4+NMOSD (n=14) and MS (n=26). Inter-rater agreement was assessed. Leptomeningeal enhancement clinical correlates were analysed. RESULTS: Enhancement occurred in 59/81 (73%) MOGAD cerebral attacks but did not influence outcome. Enhancement was often patchy/heterogeneous in MOGAD (33/59 (56%)), AQP4+NMOSD (9/14 (64%); p=0.57) and MS (16/26 (62%); p=0.63). Leptomeningeal enhancement favoured MOGAD (27/59 (46%)) over AQP4+NMOSD (1/14 (7%); p=0.01) and MS (1/26 (4%); p<0.001) with headache, fever and seizures frequent clinical correlates. Ring enhancement favoured MS (8/26 (31%); p=0.006) over MOGAD (4/59 (7%)). Linear ependymal enhancement was unique to AQP4+NMOSD (2/14 (14%)) and persistent enhancement (>3 months) was rare (0%-8%) across all groups. Inter-rater agreement for enhancement patterns was moderate. CONCLUSIONS: Enhancement is common with MOGAD cerebral attacks and often has a non-specific patchy appearance and rarely persists beyond 3 months. Leptomeningeal enhancement favours MOGAD over AQP4+NMOSD and MS.
 The aim of this study was to perform a genome-wide expression analysis of whole-blood samples from people with optic neuritis (ON) and to determine differentially expressed mRNAs compared to healthy control subjects. The study included eight people with acute ON and six healthy control subjects. Gene expression was analyzed using DNA microarrays for whole-human-genome analysis, which contain 54,675 25-base pairs. The additional biostatistical analysis included gene ontology analysis and gene set enrichment analysis (GSEA). Quantitative RT-PCR (qPCR) was used to confirm selected differentially expressed genes. In total, 722 differently expressed genes were identified, with 377 exhibiting increased, and 345 decreased, expression. Gene ontology analysis and GSEA revealed that protein phosphorylation and intracellular compartment, apoptosis inhibition, pathways involved in cell cycles, T and B cell functions, and anti-inflammatory central nervous system (CNS) pathways are implicated in ON pathology. qPCR confirmed the differential expression of eight selected genes, with SLPI, CR3, and ITGA4 exhibiting statistically significant results. In conclusion, whole-blood gene expression analysis showed significant differences in the expression profiles of people with ON compared to healthy control subjects. Additionally, pathways involved in T cell regulation and anti-inflammatory pathways within CNS were identified as important in the early phases of MS.
 L-Azetidine-2-carboxylic acid (AZE) is a non-protein amino acid that shares structural similarities with its proteogenic L-proline amino acid counterpart. For this reason, AZE can be misincorporated in place of L-proline, contributing to AZE toxicity. In previous work, we have shown that AZE induces both polarization and apoptosis in BV2 microglial cells. However, it is still unknown if these detrimental effects involve endoplasmic reticulum (ER) stress and whether L-proline co-administration prevents AZE-induced damage to microglia. Here, we investigated the gene expression of ER stress markers in BV2 microglial cells treated with AZE alone (1000 µM), or co-treated with L-proline (50 µM), for 6 or 24 h. AZE reduced cell viability, nitric oxide (NO) secretion and caused a robust activation of the unfolded protein response (UPR) genes (ATF4, ATF6, ERN1, PERK, XBP1, DDIT3, GADD34). These results were confirmed by immunofluorescence in BV2 and primary microglial cultures. AZE also altered the expression of microglial M1 phenotypic markers (increased IL-6, decreased CD206 and TREM2 expression). These effects were almost completely prevented upon L-proline co-administration. Finally, triple/quadrupole mass spectrometry demonstrated a robust increase in AZE-bound proteins after AZE treatment, which was reduced by 84% upon L-proline co-supplementation. This study identified ER stress as a pathogenic mechanism for AZE-induced microglial activation and death, which is reversed by co-administration of L-proline.
 Multiple sclerosis is an autoimmune-mediated myelin damage disorder in the central nervous system that is widespread among neurological patients. It has been demonstrated that several genetic and epigenetic factors control autoimmune encephalomyelitis (EAE), a murine model of MS, through CD4+ T-cell population quantity. Alterations in the gut microbiota influence neuroprotectiveness via unexplored mechanisms. In this study, the ameliorative effect of Bacillus amyloliquefaciens fermented in camel milk (BEY) on an autoimmune-mediated neurodegenerative model using myelin oligodendrocyte glycoprotein/complete fraud adjuvant/pertussis toxin (MCP)-immunized C57BL6j mice is investigated. Anti-inflammatory activity was confirmed in the in vitro cell model, and inflammatory cytokines interleukins IL17 (from EAE 311 to BEY 227 pg/mL), IL6 (from EAE 103 to BEY 65 pg/mL), IFNγ (from EAE 423 to BEY 243 pg/mL) and TGFβ (from EAE 74 to BEY 133 pg/mL) were significantly reduced in BEY-treated mice. The epigenetic factor miR-218-5P was identified and confirmed its mRNA target SOX-5 using in silico tools and expression techniques, suggesting SOX5/miR-218-5p could serve as an exclusive diagnostic marker for MS. Furthermore, BEY improved the short-chain fatty acids, in particular butyrate (from 0.57 to 0.85 µM) and caproic (from 0.64 to 1.33 µM) acids, in the MCP mouse group. BEY treatment significantly regulated the expression of inflammatory transcripts in EAE mice and upregulated neuroprotective markers such as neurexin (from 0.65- to 1.22-fold) (p < 0.05), vascular endothelial adhesion molecules (from 0.41- to 0.76-fold) and myelin-binding protein (from 0.46- to 0.89-fold) (p < 0.03). These findings suggest that BEY could be a promising clinical approach for the curative treatment of neurodegenerative diseases and could promote the use of probiotic food as medicine.
 BACKGROUND: People with chronic neurological diseases, such as Parkinson's Disease (PD) and Multiple Sclerosis (MS), often present postural disorders and a high risk of falling. When difficulties in achieving outpatient rehabilitation services occur, a solution to guarantee the continuity of care may be telerehabilitation. This study intends to expand the scope of our previously published research on the impact of telerehabilitation on quality of life in an MS sample, testing the impact of this type of intervention in a larger sample of neurological patients also including PD individuals on postural balance. METHODS: We included 60 participants with MS and 72 with PD. All enrolled subjects were randomized into two groups: 65 in the intervention group and 67 in the control group. Both treatments lasted 30-40 sessions (5 days/week, 6-8 weeks). Motor, cognitive, and participation outcomes were registered before and after the treatments. RESULTS: All participants improved the outcomes at the end of the treatments. The study's primary outcome (Mini-BESTest) registered a greater significant improvement in the telerehabilitation group than in the control group. CONCLUSIONS: Our results demonstrated that non-immersive virtual reality telerehabilitation is well tolerated and positively affects static and dynamic balance and gait in people with PD and MS.
 Myelin basic protein (MBP) is one of the key structural elements of the myelin sheath and has autoantigenic properties in multiple sclerosis (MS). Its intracellular interaction network is still partially deconvoluted due to the unfolded structure, abnormally basic charge, and specific cellular localization. Here we used the fusion protein of MBP with TurboID, an engineered biotin ligase that uses ATP to convert biotin to reactive biotin-AMP that covalently attaches to nearby proteins, to determine MBP interactome. Despite evident benefits, the proximity labeling proteomics technique generates high background noise, especially in the case of proteins tending to semi-specific interactions. In order to recognize unique MBP partners, we additionally mapped protein interaction networks for deaminated MBP variant and cyclin-dependent kinase inhibitor 1 (p21), mimicking MBP in terms of natively unfolded state, size and basic amino acid clusters. We found that in the plasma membrane region, MBP is colocalized with adhesion proteins occludin and myelin protein zero-like protein 1, solute carrier family transporters ZIP6 and SNAT1, Eph receptors ligand Ephrin-B1, and structural components of the vesicle transport machinery-synaptosomal-associated protein 23 (SNAP23), vesicle-associated membrane protein 3 (VAMP3), protein transport protein hSec23B and cytoplasmic dynein 1 heavy chain 1. We also detected that MBP potentially interacts with proteins involved in Fe(2+) and lipid metabolism, namely, ganglioside GM2 activator protein, long-chain-fatty-acid-CoA ligase 4 (ACSL4), NADH-cytochrome b5 reductase 1 (CYB5R1) and metalloreductase STEAP3. Assuming the emerging role of ferroptosis and vesicle cargo docking in the development of autoimmune neurodegeneration, MBP may recruit and regulate the activity of these processes, thus, having a more inclusive role in the integrity of the myelin sheath.
 Due to the limitations of culture techniques, the lung in a healthy state is traditionally considered to be a sterile organ. With the development of non-culture-dependent techniques, the presence of low-biomass microbiomes in the lungs has been identified. The species of the lung microbiome are similar to those of the oral microbiome, suggesting that the microbiome is derived passively within the lungs from the oral cavity via micro-aspiration. Elimination, immigration, and relative growth within its communities all contribute to the composition of the lung microbiome. The lung microbiome is reportedly altered in many lung diseases that have not traditionally been considered infectious or microbial, and potential pathways of microbe-host crosstalk are emerging. Recent studies have shown that the lung microbiome also plays an important role in brain autoimmunity. There is a close relationship between the lungs and the brain, which can be called the lung-brain axis. However, the problem now is that it is not well understood how the lung microbiota plays a role in the disease-specifically, whether there is a causal connection between disease and the lung microbiome. The lung microbiome includes bacteria, archaea, fungi, protozoa, and viruses. However, fungi and viruses have not been fully studied compared to bacteria in the lungs. In this review, we mainly discuss the role of the lung microbiome in chronic lung diseases and, in particular, we summarize the recent progress of the lung microbiome in multiple sclerosis, as well as the lung-brain axis.

 Monitoring of clinical trials is a fundamental process required by regulatory agencies. It assures the compliance of a center to the required regulations and the trial protocol. Traditionally, monitoring teams relied on extensive on-site visits and source data verification. However, this is costly, and the outcome is limited. Thus, central statistical monitoring (CSM) is an additional approach recently embraced by the International Council for Harmonisation (ICH) to detect problematic or erroneous data by using visualizations and statistical control measures. Existing implementations have been primarily focused on detecting inlier and outlier data. Other approaches include principal component analysis and distribution of the data. Here we focus on the utilization of comparisons of centers to the Grand mean for different model types and assumptions for common data types, such as binomial, ordinal, and continuous response variables. We implement the usage of multiple comparisons of single centers to the Grand mean of all centers. This approach is also available for various non-normal data types that are abundant in clinical trials. Further, using confidence intervals, an assessment of equivalence to the Grand mean can be applied. In a Monte Carlo simulation study, the applied statistical approaches have been investigated for their ability to control type I error and the assessment of their respective power for balanced and unbalanced designs which are common in registry data and clinical trials. Data from the German Multiple Sclerosis Registry (GMSR) including proportions of missing data, adverse events and disease severity scores were used to verify the results on Real-World-Data (RWD).
 Multiple sclerosis (MS) is inflammatory demyelinating and neurodegenerative disease of the central nervous system (CNS) with autoimmune mechanism of development. The study of the neuroimmune interactions is one of the most developing directions in the research of the pathogenesis of MS. The influence of biogenic amines on the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and MS was shown by the modulation of subsets of T-helper cells and B-cells, which plays a crucial role in the autoimmunity of the CNS. However, along with T- and B-cells the critical involvement of mononuclear phagocytes such as dendritic cells, macrophages, and monocytes in the development of neuroinflammation also was shown. It was demonstrated that the activation of microglial cells (resident macrophages of the CNS) could initiate the neuroinflammation in the EAE, suggesting their role at an early stage of the disease. In contrast, monocytes, which migrate from the periphery into the CNS through the blood-brain barrier, mediate the effector phase of the disease and cause neurological disability in EAE. In addition, the clinical efficacy of the therapy with depletion of the monocytes in EAE was shown, suggesting their crucial role in the autoimmunity of the CNS. Biogenic amines, such as epinephrine, norepinephrine, dopamine, and serotonin are direct mediators of the neuroimmune interaction and may affect the pathogenesis of EAE and MS by modulating the immune cell activity and cytokine production. The anti-inflammatory effect of targeting the biogenic amines receptors on the pathogenesis of EAE and MS by suppression of Th17- and Th1-cells, which are critical for the CNS autoimmunity, was shown. However, the latest data showed the potential ability of biogenic amines to affect the functions of the mononuclear phagocytes and their involvement in the modulation of neuroinflammation. This article reviews the literature data on the role of monocytes in the pathogenesis of EAE and MS. The data on the effect of targeting of biogenic amine receptors on the function of monocytes are presented.
 The effective treatment of central nervous system (CNS) disorders such as multiple sclerosis (MS) has been challenging due to the limited ability of therapeutic agents to cross the blood-brain barrier (BBB). In this study, we investigated the potential of nanocarrier systems to deliver miR-155-antagomir-teriflunomide (TEF) dual therapy to the brain via intranasal (IN) administration to manage MS-associated neurodegeneration and demyelination. Our results showed that the combinatorial therapy of miR-155-antagomir and TEF loaded in nanostructured lipid carriers (NLCs) significantly increased brain concentration and improved targeting potential. The novelty of this study lies in the use of a combinatorial therapy approach of miR-155-antagomir and TEF loaded in NLCs. This is a significant finding, as the effective delivery of therapeutic molecules to the CNS has been a challenge in treating neurodegenerative disorders. Additionally, this study sheds light on the potential use of RNA-targeting therapies in personalized medicine, which could revolutionize the way CNS disorders are managed. Furthermore, our findings suggest that nanocarrier-loaded therapeutic agents have great potential for safe and economical delivery in treating CNS disorders. Our study provides novel insights into the effective delivery of therapeutic molecules via the IN route for managing neurodegenerative disorders. In particular, our results demonstrate the potential of delivering miRNA and TEF via the intranasal route using the NLC system. We also demonstrate that the long-term use of RNA-targeting therapies could be a promising tool in personalized medicine. Importantly, using a cuprizone-induced animal model, our study also investigated the effects of TEF-miR155-antagomir-loaded NLCs on demyelination and axonal damage. Following six weeks of treatment, the TEF-miR155-antagomir-loaded NLCs potentially lowered the demyelination and enhanced the bioavailability of the loaded therapeutic molecules. Our study is a paradigm shift in delivering miRNAs and TEF via the intranasal route and highlights the potential of this approach for managing neurodegenerative disorders. In conclusion, our study provides critical insights into the effective delivery of therapeutic molecules via the IN route for managing CNS disorders, and especially MS. Our findings have significant implications for the future development of nanocarrier-based therapies and personalized medicine. Our results provide a strong foundation for further studies and the potential to develop safe and economic therapeutics for CNS disorders.
 Neuroinflammation is one of the common features in most neurological diseases including multiple sclerosis (MScl) and neurodegenerative diseases such as Alzheimer's disease (AD). It is associated with local brain inflammation, microglial activation, and infiltration of peripheral immune cells into cerebrospinal fluid (CSF) and the central nervous system (CNS). It has been shown that the diversity of phenotypic changes in monocytes in CSF relates to neuroinflammation. It remains to be investigated whether these phenotypic changes are associated with functional or metabolic alteration, which may give a hint to their function or changes in cell states, e.g., cell activation. In this article, we investigate whether major metabolic pathways of blood monocytes alter after exposure to CSF of healthy individuals or patients with AD or MScl. Our findings show a significant alteration of the metabolism of monocytes treated with CSF from patients and healthy donors, including higher production of citric acid and glutamine, suggesting a more active glycolysis and tricarboxylic acid (TCA) cycle and reduced production of glycine and serine. These alterations suggest metabolic reprogramming of monocytes, possibly related to the change of compartment (from blood to CSF) and/or disease-related. Moreover, the levels of serine differ between AD and MScl, suggesting different phenotypic alterations between diseases.
 BACKGROUND: For patients with multiple sclerosis (MS), both structure and microvasculature alterations in the inner retina have been investigated in several studies. However, little is known about the alterations in the outer retina and choroid. Hence, this study aimed to assess the outer retinal and choroidal changes in patients with MS with no history of optic neuritis (ON). METHODS: Patients with MS and healthy control participants were enrolled in this cross-sectional study. Quantitative analyses were performed using swept source optical coherence tomography and swept source optical coherence tomography angiography images to assess outer retina thickness (ORT) and choroid thickness (CT), vessel density (VD) of choriocapillaris, and choroidal vascularity index (CVI), which were then compared between the groups. RESULTS: A total of 37 participants with MS (72 eyes) and 74 healthy control participants (148 eyes) were included in this study. Compared with healthy controls, patients with MS with no history of ON showed reduced VD of the choriocapillaris and CVI. There was no significant difference in ORT and CT between 2 groups. Meanwhile, in patients with MS, no correlation between OCTA parameters and expanded disability status scale score were found in this study. CONCLUSIONS: Our study indicates that patients with MS with no history of optical neuritis have reduced choriocapillaris vessel density and decreased choroidal vascularity index without detectable alteration in outer retina thickness and choroid thickness. The findings complement the outer retinal and choroidal component of MS, providing deeper insight into the pathophysiology of MS.
 INTRODUCTION: Routinely assessing exercise levels during clinical visits may be a starting point for clinicians to support physical activity in persons with multiple sclerosis (MS). OBJECTIVE: To evaluate the feasibility and findings of routinely implementing a self-reported physical activity vital sign during clinical visits. DESIGN: Retrospective database review. SETTING: Outpatient academic MS center. PATIENTS: All adult patients of our MS center with confirmed MS presenting for an in-person or telemedicine clinic visit with a physician or nurse practitioner. INTERVENTIONS: None. MAIN MEASURE(S): A standard physical activity vital sign representing minutes per week of moderate-to-vigorous exercise was collected. Percentage of persons with MS with a recorded physical activity vital sign was retrospectively evaluated along with demographic characteristics and key findings. RESULTS: Ninety-three percent of patients with MS at our center had a physical activity vital sign recorded in at least one visit, and 86% at the most recent visit. Of 1560 patients with a recorded physical activity vital sign, 24.3% of patients were consistently active (≥150 min/week of exercise), 20.8% were consistently inactive (0 min/week), and the remaining 54.9% were inconsistently active. The physical activity vital sign was inversely associated with BMI (p < .001) and 25-foot walk test times (p < .001), but not associated with biological sex or age. CONCLUSIONS: Approximately a quarter of patients with MS with a documented physical activity vital sign met national aerobic exercise guidelines of 150 min/week per the U.S. Department of Health and Human Services. Routine implementation of the physical activity vital sign at our MS center was feasible and helped identify inactive patients who may benefit from physical activity counseling.
 BACKGROUND: Cognitive behavioural therapy (CBT) reduces multiple sclerosis (MS)-related fatigue. Implementation of face-to-face CBT is hindered by limited treatment capacity and traveling distances to treatment locations. OBJECTIVE: Evaluate whether blended CBT (online treatment modules supported with guidance by a therapist) is non-inferior to face-to-face CBT in reducing fatigue severity in severely fatigued patients with MS. METHOD: A non-inferiority multicentre randomized clinical trial, in which 166 patients with MS were allocated to either face-to-face or blended CBT. Primary outcome was fatigue severity assessed with the Checklist Individual Strength fatigue subscale directly post-treatment (week 20). Mixed model analysis was used by a statistician blinded for allocation to determine between-group differences post-treatment. The upper limit of the 95% confidence interval (CI) was compared to a pre-specified non-inferiority margin of 5.32. RESULTS: Blended CBT (N = 82) was non-inferior to face-to-face CBT (N = 84) (B = 1.70, 95% CI: -1.51 to 4.90). Blended CBT significantly reduced therapist time (B = -187.1 minutes, 95% CI: 141.0-233.3). Post hoc analysis showed more improvement (B = -5.35, 95% CI: -9.22 to -1.48) when patients received their preferred treatment. No harm related to treatment was reported. DISCUSSION: Blended CBT is an efficient alternative to face-to-face CBT. Offering the preferred CBT format may optimize treatment outcome.
 PURPOSE: Just noticeable difference for interaural time difference (JND-ITD) is a sensitive test to detect silent lesions and neural asynchrony along the auditory pathways among individuals with multiple sclerosis (MS), but it has not been studied with brainstem functional system scores (BFSS) and expanded disability status scale (EDSS). The study aims to assess the usefulness of JND-ITD thresholds in individuals with MS and relate to brainstem magnetic resonance imaging (MRI) lesions, BFSS, and disability (EDSS). METHOD: Standard group comparison design was adapted to compare the JND-ITD thresholds between individuals with MS (n = 45) and age and gender-matched healthy participants (n = 45). All participants underwent case history, neurological examination including BFSS and EDSS scoring, MRI brain imaging, minimental state examination, routine audiological evaluation, and ITD testing for high-pass filtered noise stimuli. RESULTS: Of the 36 MS participants with abnormal JND-ITD thresholds, 22 (48.9%) participants could not identify maximum JND-ITD values (1,280 μs) in the ITD task. Abnormal JND-ITDs thresholds (139-1,280 μs) were obtained in 14 (31.11%) participants with MS. The JND-ITD thresholds were significantly different between the healthy and MS group. No significant association was found between the presence of ITD abnormality with the presence of brainstem lesions (MRI) and brainstem dysfunction (BFSS). Also, this study did not find any relationship between JND-ITD thresholds with disability (EDSS). CONCLUSIONS: This study supports the findings that JND-ITD for high-pass filtered noise is a sensitive test to detect lesions along the auditory system. Even though JND-ITD thresholds did not relate with BFSS and EDSS scores, JND-ITD abnormalities can be of great value in identifying lesions along the auditory system, especially in the early stages of MS, when clinical neurological examination does not show any signs of brainstem dysfunction, disability, and MRI without any lesions in the brain.
 BACKGROUND AND PURPOSE: The symptom of fatigue impairs function in people with multiple sclerosis (MS). Choosing appropriate measures to assess fatigue is challenging. The purpose of this article is to report the findings of a systematic review of patient-reported fatigue measures for people with MS. METHODS: PubMed, CINAHL, and Embase databases were searched through January 2020 using terms related to fatigue and MS. Studies were included if the sample size was 30 or more or smaller samples if adequately powered, and if information about measurement characteristics (ie, test-retest reliability, content validity, responsiveness, interpretability, or generalizability) of the measure(s) could be extracted. Study quality was appraised with the 2-point COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN) checklist. Data about measurement characteristics, psychometrics, and clinical utility were extracted and results were synthesized. RESULTS: Twenty-four articles met inclusion criteria with information about 17 patient-reported fatigue measures. No studies had critical methodologic flaws. Measurement characteristic data were not available for all measures. Clinical utility varied in time to complete and fatigue domains assessed. DISCUSSION AND CONCLUSIONS: Five measures had data pertaining to all properties of interest. Of these, only the Modified Fatigue Impact Scale (MFIS) and Fatigue Severity Scale (FSS) had excellent reliability, responsiveness data, no notable ceiling/floor effects, and high clinical utility. We recommend the MFIS for comprehensive measurement and the FSS for screening of subjective fatigue in people with MS.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A443).
 INTRODUCTION: The rapid pace of research in the field of Artificial Intelligence in medicine has associated risks for near-term AI. Ethical considerations of the use of AI in medicine remain a subject of much debate. Concurrently, the Involvement of People living with disease and the Public (PPI) in research is becoming mandatory in the EU and UK. The goal of this research was to elucidate the important values for our relevant stakeholders: People with MS, Radiologists, neurologists, Registered Healthcare Practitioners and Computer Scientists concerning AI in radiology and synthesize these in an ethical matrix. METHODS: An ethical matrix workshop co-designed with a patient expert. The workshop yielded a survey which was disseminated to the professional societies of the relevant stakeholders. Quantitative data were analysed using the Pingouin 0.53 python package. Qualitative data were examined with word frequency analysis and analysed for themes with grounded theory with a patient expert. RESULTS: 184 participants were recruited, (54, 60, 17, 12, 41 respectively). There were significant (p < 0.00001) differences in age, gender and ethnicity between groups. Key themes emerging from our results were the importance fast and accurate results, explanations over model performance and the significance of maintaining personal connections and choice. These themes were used to construct the ethical matrix. CONCLUSION: The ethical matrix is a useful tool for PPI and stakeholder engagement with particular advantages for near-term AI in the pandemic era. IMPLICATIONS FOR PRACTICE: We have produced an ethical matrix that allows for the inclusion of stakeholder opinion in medical AI research design.
 BACKGROUND: The extent of cortical pathology is an important determinant of multiple sclerosis (MS) severity. Cortical demyelination and neurodegeneration are related to inflammation of the overlying leptomeninges, a more inflammatory CSF milieu and with parenchymal microglia and astroglia activation. These are all components of the compartmentalised inflammatory response. Compartmentalised inflammation is a feature of progressive MS, which is not targeted by disease modifying therapies. Complement is differentially expressed in the MS CSF and complement, and complement receptors, are associated with demyelination and neurodegeneration. METHODS: To better understand if complement activation in the leptomeninges is associated with underlying cortical demyelination, inflammation, and microglial activation, we performed a neuropathological study of progressive MS (n = 22, 14 females), neuroinflammatory (n = 8), and non-neurological disease controls (n = 10). We then quantified the relative extent of demyelination, connective tissue inflammation, complement, and complement receptor positive microglia/macrophages. RESULTS: Complement was elevated at the leptomeninges, subpial, and within and around vessels of the cortical grey matter. The extent of complement C1q immunoreactivity correlated with connective tissue infiltrates, whilst activation products C4d, Bb, and C3b associated with grey matter demyelination, and C3a receptor 1+ and C5a receptor 1+ microglia/macrophages closely apposed C3b labelled cells. The density of C3a receptor 1+ and C5a receptor 1+ cells was increased at the expanding edge of subpial and leukocortical lesions. C5a receptor 1+ cells expressed TNFα, iNOS and contained puncta immunoreactive for proteolipid protein, neurofilament and synaptophysin, suggesting their involvement in grey matter lesion expansion. INTERPRETATION: The presence of products of complement activation at the brain surfaces, their association with the extent of underlying pathology and increased complement anaphylatoxin receptor positive microglia/macrophages at expanding cortical grey matter lesions, could represent a target to modify compartmentalised inflammation and cortical demyelination.
 OBJECTIVE: Prediction of disease progression is challenging in multiple sclerosis (MS) as the sequence of lesion development and retention of inflammation within a subset of chronic lesions is heterogeneous among patients. We investigated the sequence of lesion-related regional structural disconnectivity across the spectrum of disability and cognitive impairment in MS. METHODS: In a full cohort of 482 patients, the Expanded Disability Status Scale was used to classify patients into (i) no or mild vs (ii) moderate or severe disability groups. In 363 out of 482 patients, Quantitative Susceptibility Mapping was used to identify paramagnetic rim lesions (PRL), which are maintained by a rim of iron-laden innate immune cells. In 171 out of 482 patients, Brief International Cognitive Assessment was used to identify subjects with cognitive impairment. Network Modification Tool was used to estimate the regional structural disconnectivity due to MS lesions. Discriminative event-based modeling was applied to investigate the sequence of regional structural disconnectivity due to all representative lesions across the spectrum of disability and cognitive impairment. RESULTS: Structural disconnection in the ventral attention and subcortical networks was an early biomarker of moderate or severe disability. The earliest biomarkers of disability progression were structural disconnections due to PRL in the motor-related regions. Subcortical structural disconnection was an early biomarker of cognitive impairment. INTERPRETATION: MS lesion-related structural disconnections in the subcortex is an early biomarker for both disability and cognitive impairment in MS. PRL-related structural disconnection in the motor cortex may identify the patients at risk for moderate or severe disability in MS.
 OBJECTIVE: The purpose of this study was to evaluate the extent to which treatment effect on magnetic resonance imaging (MRI)-derived measures of brain atrophy and focal lesions can mediate, at the trial level, the treatment effect on cognitive outcomes in multiple sclerosis (MS). METHODS: We collected all published randomized clinical trials in MS lasting at least 2 years and including as end points: active MRI lesions (defined as new/enlarging T2 lesions), brain atrophy (defined as a change in brain volume between month 12 and month 24), and change in cognitive performance (assessed by the Paced Auditory Serial Addition Test [PASAT]). Relative reductions were used to quantify the treatment effect on MRI markers (lesions and atrophy), whereas the standardized mean difference (Hedges g) between baseline and follow-up cognitive assessment was used to quantify the treatment effects on cognition. A linear regression, weighted for trial size, was used to assess the relationship between the treatment effects on MRI markers and cognition. RESULTS: Fourteen trials including more than 8,813 patients with MS were included in the meta-regression. Treatment effect on cognition was strongly associated with the treatment effect on brain atrophy (R(2)  = 0.79, p < 0.001), but was not correlated with the treatment effect on active MRI lesions (R(2)  = 0.16, p = 0.14). INTERPRETATION: Results reported here suggest that brain atrophy, a well-established MRI marker in MS clinical trials, can be used as a main outcome for clinical trials with drugs targeting cognitive impairment and neurodegeneration. ANN NEUROL 2023.
 Multiple sclerosis (MS), a neuroinflammation that results in neurodegeneration, is the most prevalent central nervous system inflammatory disease in young people. A diet rich in antioxidants is known to decrease the production/activity of pro-inflammatory cytokines and have a positive impact on the prognosis of MS. The purpose of this study was to assess if dietary antioxidant capacity is related to Expanded Disability Status Scale (EDSS) scores in patients with MS. Patients with MS (n=220; 137 women and 83 men) were asked to complete a questionnaire on diet. According to the EDSS score, patients were split into two groups (group 1: EDSS ≤5 and group 2: EDSS >5). Analyzed risk variables were antioxidant levels and demographic data. A nutritional database tool (BeBiS 4 software, Germany) created for the evaluation of Turkish foods was used to examine the questionnaire findings. Age, vitamin A, retinol, vitamin D, vitamin E, and vitamin C were significantly different between groups (P<0.05). The levels of vitamins A, D, E, C, and retinol were significantly correlated, according to Pearson's correlation analysis. Receiver operator characteristic curve analysis revealed that vitamin A, vitamin D, and vitamin C levels were discriminating variables in group 2 patients (EDSS >5). The current study has shown that antioxidant levels obtained by EDSS may be useful in determining illness severity and treatment success of patients with MS. Further clinical trials have been initiated in MS patients with more effective antioxidants.
 In this project, the possibility of drug delivery application of three anti-Multiple sclerosis (MS) agents (containing diroximel fumarate (DXF), dimethyl fumarate (DMF), and mono methyl fumarate (MMF)) by using some heteroatom decorated graphitic carbonitride (g-C(3)N(4)) (as nano-sized carriers) have been systematically investigated. The results of the study have indicated that As-g-C(3)N(4) QD is not a suitable candidate for drug delivery (at least in the cases of DMF, and DXF drugs); while, it would be an accurate semiconductor sensor for selective detection of each mentioned agents. Also, the use of the P-doped as well as pristine g-C(3)N(4) QD could lead to weak electronic signals with relatively same values (in electronvolts). It means that P-g-C(3)N(4), and g-C(3)N(4) QDs are not good sensors for detection of each of the three considered drugs. However, those two sorbents would be suitable carriers for delivering of all three mentioned pharmaceuticals.
 BACKGROUND: Multiple sclerosis (MS) comparative effectiveness research needs to go beyond average treatment effects (ATEs) and post-host subgroup analyses. OBJECTIVE: This retrospective study assessed overall and patient-specific effects of dimethyl fumarate (DMF) versus teriflunomide (TERI) in patients with relapsing-remitting MS. METHODS: A novel precision medicine (PM) scoring approach leverages advanced machine learning methods and adjusts for imbalances in baseline characteristics between patients receiving different treatments. Using the German NeuroTransData registry, we implemented and internally validated different scoring systems to distinguish patient-specific effects of DMF relative to TERI based on annualized relapse rates, time to first relapse, and time to confirmed disease progression. RESULTS: Among 2791 patients, there was superior ATE of DMF versus TERI for the two relapse-related endpoints (p = 0.037 and 0.018). Low to moderate signals of treatment effect heterogeneity were detected according to individualized scores. A MS patient subgroup was identified for whom DMF was more effective than TERI (p = 0.013): older (45 versus 38 years), longer MS duration (110 versus 50 months), not newly diagnosed (74% versus 40%), and no prior glatiramer acetate usage (35% versus 5%). CONCLUSION: The implemented approach can disentangle prognostic differences from treatment effect heterogeneity and provide unbiased patient-specific profiling of comparative effectiveness based on real-world data.
 BACKGROUND AND PURPOSE: Individuals with multiple sclerosis (MS) frequently report low physical activity and psychosocial support due to concerns with transportation, time, finances, access to services, and lack of caregiver support. These barriers can be addressed by online group interventions; however, utility of such programs in individuals with MS has not been examined yet. The purpose of this retrospective study was, therefore, to (a) investigate the feasibility, safety, and outcomes of a virtual group exercise program in individuals with MS, and (b) explore the participant perceptions after the program. METHODS: Retrospective data from the medical records of 17 individuals with MS (mean [SD] age = 53.5 [12.3] years, body mass index = 28.2 [7.2]) who completed the virtual 13-week group exercise program, pre- and posttraining functional status questionnaires, and the end-of-program feedback were extracted. The exercise program included aerobic, resistance, balance, and flexibility training components recommended for people with MS. Feasibility, safety, outcomes, and participant perceptions were determined by adherence to the prescribed daily exercise dosage, number of adverse events, within-group differences in self-reported functional status, and thematic analysis of the participant feedback, respectively. RESULTS: Participants were adherent (79%), reported minimal adverse effects, and demonstrated significant changes (P < 0.05) in functional status posttraining. Several themes on the perceived barriers, facilitators, and suggestions for improvement were identified. DISCUSSION AND CONCLUSIONS: A virtual 13-week group exercise program can be feasible, safe, effective, and well received by individuals with MS. Future research should investigate the dose-response effectiveness of telehealth and compare various telehealth models of exercise training using large randomized controlled trials.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1 available at: http://links.lww.com/JNPT/A434, which demonstrates an overview of the study).
 BACKGROUND: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system and a leading cause of neurological disability in young adults. Clinical presentation and disease course are highly heterogeneous. Typically, disease progression occurs over time and is characterized by the gradual accumulation of disability. The risk of developing MS is driven by complex interactions between genetic and environmental factors, including the gut microbiome. How the commensal gut microbiota impacts disease severity and progression over time remains unknown. METHODS: In a longitudinal study, disability status and associated clinical features in 60 MS patients were tracked over 4.2 ± 0.97 years, and the baseline fecal gut microbiome was characterized via 16S amplicon sequencing. Progressor status, defined as patients with an increase in Expanded Disability Status Scale (EDSS), were correlated with features of the gut microbiome to determine candidate microbiota associated with risk of MS disease progression. RESULTS: We found no overt differences in microbial community diversity and overall structure between MS patients exhibiting disease progression and non-progressors. However, a total of 45 bacterial species were associated with worsening disease, including a marked depletion in Akkermansia , Lachnospiraceae, and Oscillospiraceae , with an expansion of Alloprevotella , Prevotella-9 , and Rhodospirillales . Analysis of the metabolic potential of the inferred metagenome from taxa associated with progression revealed a significant enrichment in oxidative stress-inducing aerobic respiration at the expense of microbial vitamin K (2) production (linked to Akkermansia ), and a depletion in SCFA metabolism (linked to Lachnospiraceae and Oscillospiraceae ). Further, statistical modeling demonstrated that microbiota composition and clinical features were sufficient to robustly predict disease progression. Additionally, we found that constipation, a frequent gastrointestinal comorbidity among MS patients, exhibited a divergent microbial signature compared with progressor status. CONCLUSIONS: These results demonstrate the utility of the gut microbiome for predicting disease progression in MS. Further, analysis of the inferred metagenome revealed that oxidative stress, vitamin K (2) and SCFAs are associated with progression.
 PURPOSE: Adherence to disease-modifying therapies (DMTs) in multiple sclerosis (MS) is a complex and multidimensional phenomenon. Identifying the predictors of therapeutic adherence in MS will guide the design of interventions to improve health outcomes. Our aim was to assess the degree of adherence to pharmacological treatments, assess the relationship between patient-related factors and pharmacological adherence and to identify predictors of adherence to pharmacological treatments in patients with MS in Spain. PATIENTS AND METHODS: A cross-sectional nationwide study was carried out in Spain between December 2020 and September 2021. The web-based evaluation protocol consisted of a self-questionnaire survey designed ad hoc and the application of validated questionnaires to assess adherence, as well as beliefs about medication and quality of life. Predictor variables of adherence to MS treatment were assessed using multivariate analysis. RESULTS: A total of 152 patients with MS participated (mean age: 44 years; 64% were female; and 78% had relapsing-remitting MS). Seventy-three percent of the patients reported being adherent to their pharmacological treatment for MS. Forgetfulness was the most common cause of non-adherence. Necessity beliefs and concerns beliefs were not statistically associated with adherence. The adherent group shows statistically significant better levels of quality of life in the cognitive function subscale than the non-adherent participants (p=0.040). Role limitations-emotional, emotional well-being and overall quality of life were not significantly associated with adherence. Predictors with a statistical association with adherence to treatment were years of education (OR=0.79; 95% CI: 0.65-0.96; p=0.020) and intravenous treatment (OR=3.17; 95% CI: 1.07-9.45; p=0.038). CONCLUSION: We found an adequate adherence to pharmacological treatment. Low education and intravenous treatment were significant predictors of adherence to DMTs.
 The human gastrointestinal tract is home to trillions of microorganisms-collectively referred to as the gut microbiome-that maintain a symbiotic relationship with their host. This diverse community of microbes grows and changes as we do, with developmental, lifestyle, and environmental factors all shaping microbiome community structure. Increasing evidence suggests this relationship is bidirectional, with the microbiome also influencing host physiological processes. For example, changes in the gut microbiome have been shown to alter neurodevelopment and have lifelong effects on the brain and behavior. Age-related changes in gut microbiome composition have also been linked to inflammatory changes in the brain, perhaps increasing susceptibility to neurological disease. Indeed, associations between gut dysbiosis and many age-related neurological diseases-including Parkinson's disease, Alzheimer's disease, multiple sclerosis, and amyotrophic lateral sclerosis-have been reported. Further, microbiome manipulation in animal models of disease highlights a potential role for the gut microbiome in disease development and progression. Although much remains unknown, these associations open up an exciting new world of therapeutic targets, potentially allowing for improved quality of life for a wide range of patient populations.
 BACKGROUND: Despite the extensive research in recent years, the current treatment modalities for neurological disorders are suboptimal. Curcumin, a polyphenol found in Curcuma genus, has been shown to mitigate the pathophysiology and clinical sequalae involved in neuroinflammation and neurodegenerative diseases. METHODS: We searched PubMed database for relevant publications on curcumin and its uses in treating neurological diseases. We also reviewed relevant clinical trials which appeared on searching PubMed database using 'Curcumin and clinical trials'. RESULTS: This review details the pleiotropic immunomodulatory functions and neuroprotective properties of curcumin, its derivatives and formulations in various preclinical and clinical investigations. The effects of curcumin on neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), brain tumors, epilepsy, Huntington's disorder (HD), ischemia, Parkinson's disease (PD), multiple sclerosis (MS), and traumatic brain injury (TBI) with a major focus on associated signalling pathways have been thoroughly discussed. CONCLUSION: This review demonstrates curcumin can suppress spinal neuroinflammation by modulating diverse astroglia mediated cascades, ensuring the treatment of neurological disorders.
 The present disclosure relates to p38α mitogen-activated protein kinase inhibitors, pharmaceutical compositions thereof, and the use of the p38α mitogen-activated protein kinase inhibitors and pharmaceutical compositions thereof for treating various diseases such as cancer, rheumatoid arthritis, amyotrophic lateral sclerosis, cystic fibrosis, cardiovascular disease, multiple sclerosis, inflammatory bowel disease, chronic obstructive pulmonary disease (COPD), asthma, COVID-19, acute respiratory distress syndrome (ARDS), and acute lung injury (ALI).
 Microglia are resident macrophages of the central nervous system that have key functions in its development, homeostasis and response to damage and infection. Although microglia have been increasingly implicated in contributing to the pathology that underpins neurological dysfunction and disease, they also have crucial roles in neurological homeostasis and regeneration. This includes regulation of the maintenance and regeneration of myelin, the membrane that surrounds neuronal axons, which is required for axonal health and function. Myelin is damaged with normal ageing and in several neurodegenerative diseases, such as multiple sclerosis and Alzheimer disease. Given the lack of approved therapies targeting myelin maintenance or regeneration, it is imperative to understand the mechanisms by which microglia support and restore myelin health to identify potential therapeutic approaches. However, the mechanisms by which microglia regulate myelin loss or integrity are still being uncovered. In this Review, we discuss recent work that reveals the changes in white matter with ageing and neurodegenerative disease, how this relates to microglia dynamics during myelin damage and regeneration, and factors that influence the regenerative functions of microglia.
 BACKGROUND: Receiving the diagnosis of a motor neurodegenerative condition (MNDC) can be a life-changing experience. Although several studies of individuals' experiences have indicated dissatisfaction with aspects of how an MNDC diagnosis was communicated, few studies have addressed doctors' experiences of breaking bad news for these conditions, especially from a qualitative perspective. This study explored UK neurologists' lived experience of delivering an MNDC diagnosis. METHODS: Interpretative phenomenological analysis was used as the overarching method. Eight consultant neurologists working with patients with MNDCs took part in individual, semi-structured interviews. RESULTS: Two themes were constructed from the data: 'Meeting patients' emotional and information needs at diagnosis: a balancing act between disease, patient and organization-related factors', and 'Empathy makes the job harder: the emotional impact and uncovered vulnerabilities associated with breaking bad news'. Breaking the news of an MNDC diagnosis was challenging for participants, both in terms of achieving a patient-centred approach and in terms of dealing with their own emotions during the process. CONCLUSIONS: Based on the study's findings an attempt to explain sub-optimal diagnostic experiences documented in patient studies was made and how organizational changes can support neurologists with this demanding clinical task was discussed.
 L-serine is a non-essential amino acid that plays a vital role in protein synthesis, cell proliferation, development, and sphingolipid formation in the central nervous system. It exerts its effects through the activation of glycine receptors and upregulation of PPAR-γ, resulting in neurotransmitter synthesis, neuroprotection, and anti-inflammatory effects. L-serine shows potential as a protective agent in various neurological diseases and neurodegenerative disorders. Deficiency of L-serine and its downstream products has been linked to severe neurological deficits. Despite its crucial role, there is limited understanding of its mechanistic production and impact on glial and neuronal cells. Most of the focus has been on D-serine, the downstream product of L-serine, which has been implicated in a wide range of neurological diseases. However, L-serine is approved by FDA for supplemental use, while D-serine is not. Hence, it is imperative that we investigate the wider effects of L-serine, particularly in relation to the pathogenesis of several neurological deficits that, in turn, lead to diseases. This review aims to explore current knowledge surrounding L-serine and its potential as a treatment for various neurological diseases and neurodegenerative disorders.
 INTRODUCTION: Myelin-oligodendrocyte glycoprotein antibody (MOG)-associated disorder (MOGAD) is a recently identified immune-mediated inflammatory disorder of the central nervous system (CNS). The significance of oligoclonal bands (OCBs) is not fully elucidated. This study investigated the clinical differences between patients with MOGAD who tested positive or negative for OCBs. METHODS: The study was conducted on 23 patients with MOG-IgG-seropositivity who presented with central nervous system (CNS) symptoms. The patients were screened and divided into OCB-positive (n=10) and OCB-negative (n=13) groups, and their demographic, clinical, and magnetic resonance imaging (MRI) features were compared. RESULTS: The results revealed that patients with OCB-positivity had a significantly higher frequency of relapse, and their IgG index was significantly higher. DISCUSSION: OCBs were common in MOGAD met the consensus criteria. The study concluded that careful treatment decision-making is necessary in MOG antibody-positive cases with OCB-positivity.
 Macrophages can be characterized as a very multifunctional cell type with a spectrum of phenotypes and functions being observed spatially and temporally in various disease states. Ample studies have now demonstrated a possible causal link between macrophage activation and the development of autoimmune disorders. How these cells may be contributing to the adaptive immune response and potentially perpetuating the progression of neurodegenerative diseases and neural injuries is not fully understood. Within this review, we hope to illustrate the role that macrophages and microglia play as initiators of adaptive immune response in various CNS diseases by offering evidence of: (1) the types of immune responses and the processes of antigen presentation in each disease, (2) receptors involved in macrophage/microglial phagocytosis of disease-related cell debris or molecules, and, finally, (3) the implications of macrophages/microglia on the pathogenesis of the diseases.
 There is increasing evidence that viral infections are the source/origin of various types of encephalitis, encephalomyelitis, and other neurological and cognitive disorders. While the involvement of certain viruses, such as the Nipah virus and measles virus, is known, the mechanisms of neural invasion and the factors that trigger intense immune reactions are not fully understood. Based on recent publications, this review discusses the role of the immune response, interactions between viruses and glial cells, and cytokine mediators in the development of inflammatory diseases in the central nervous system. It also highlights the significant gaps in knowledge regarding these mechanisms.
 Neurodegenerative disorders are characterized by complex multifactorial pathogeneses, thus posing a challenge for standard therapeutic approaches that tend to focus only on one underlying disease aspect. For systemically administered drugs, the blood-brain barrier (BBB) is yet another major obstacle to overcome. In this context, naturally occurring extracellular vesicles (EVs) with intrinsic ability to cross the BBB have been investigated as therapeutics for various diseases, including Alzheimer's and Parkinson's diseases. EVs are cell-derived, lipid membrane-enclosed vesicles carrying a broad spectrum of biologically active molecules, which play a crucial role in intercellular communication. In a therapeutic context, mesenchymal stem cell (MSC)-derived EVs are in the spotlight because they reflect the therapeutic properties of their parental cells and, thus, hold promise as independent cell-free therapeutics. On the other hand, EVs can be used as drug delivery vehicles by modifying their surface or content, e.g., by decorating the surface with brain-specific ligands or loading the EVs with therapeutic RNAs or proteins, thus further enhancing the EV's targeting and therapeutic potency, respectively. Although EVs have been deemed safe for use in humans, some obstacles remain that prevent their progression into clinics. This review scrutinizes the promises and challenges of EV-based treatments for neurodegenerative disorders.
 OBJECTIVE: To learn the mechanisms between gut microbiome and the autoimmunity benefits on Traditional Chinese Medicine (TCM) in central nervous system (CNS), we investigated the neuro-protection effects and gut mircobiota changes of Heshouwu () on experimental autoimmune encepha-lomyelitis (EAE), an animal model of multiple sclerosis (MS). METHODS: Mice were randomly divided into four groups: EAE mice (control phosphate-buffered saline group), 50 mg·kg·d Heshouwu ()-treated EAE mice, 100 mg·kg·d Heshouwu ()-treated EAE mice, and 200 mg·kg·d Heshouwu ()-treated EAE mice. The spinal cords were stained with hematoxylin and eosin (HE) and luxol fast blue for evaluating inflammatory infiltration and demyelination. The percentages of granulocyte macrophage-colony stimulating factor (GM-CSF)+CD4+, interleukin 17 (IL-17)+CD4+, Foxp3 CD4+, and interferon-γ (IFN-γ)+CD4+ T cells in the inguinal lymph nodes (LNs) and brain were determined by flow cytometry analysis. 16S rRNA gene sequencing was employed to analyze the changes in gut microbiota. RESULTS: We found that Heshouwu () alleviated the disease severity and neuropathology of EAE as evaluated by clinical and histopathologyical scores. Heshouwu () increased the diversity and abundance of the gut microbiota, and decreased / ratio (F/B ratio). Heshouwu () also decreased the concentrations of IL-10, and IL-21 and increase the levels of GM-CSF, IL-17A, IL-17F and IL-22 in serum of EAE mice. Moreover, Heshouwu () modulated the T cell responses by inhibiting Th17 cells and restoring Treg cells in the small intestine lymphoid tissues and inguinal lymph nodes. Microbiota-depleted mice receiving Heshouwu ()-treated fecal microbiota trans-plantation had lower disease severity, neuropathology scores and alleviation of Th17/Treg imbalance compared to ad libitum group. CONCLUSIONS: Our findings suggested that the vital neuro-protection role of Heshouwu () (TCM) in immunomodulation effects partly by regulations of gut microbiome.
 INTRODUCTION: Extracellular vesicles (EVs) are one of the crucial means of intercellular communication, which takes many different forms. They are heterogeneous, secreted by a range of cell types, and can be generally classified into microvesicles and exosomes depending on their location and function. Exosomes are small EVs with diameters of about 30-150 nm and diverse cell sources. METHODS: The MEDLINE/PubMed database was reviewed for papers written in English and publication dates of recent years, using the search string "Exosome" and "Neurodegenerative diseases." RESULTS: The exosomes have attracted interest as a significant biomarker for a better understanding of disease development, gene silencing delivery, and alternatives to stem cell-based therapy because of their low-invasive therapeutic approach, repeatable distribution in the central nervous system (CNS), and high efficiency. Also, they are nanovesicles that carry various substances, which can have an impact on neural plasticity and cognitive functioning in both healthy and pathological circumstances. Therefore, exosomes are conceived as nanovesicles containing proteins, lipids, and nucleic acids. However, their composition varies considerably depending on the cells from which they are produced. CONCLUSION: In the present review, we discuss several techniques for the isolation of exosomes from different cell sources. Furthermore, reviewing research on exosomes' possible functions as carriers of bioactive substances implicated in the etiology of neurodegenerative illnesses, we further examine them. We also analyze the preclinical and clinical research that shows exosomes to have therapeutic potential.
 High mobility group box 1 (HMGB1) is a ubiquitous and highly conserved non-histone DNA-binding protein with different biological functions according to its subcellular localization. It is widely believed that HMGB1, which is released into the extracellular space, plays a key role in the inflammatory response. In recent years, numerous studies have shown that the development of various neurological diseases such as epilepsy, Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), cerebrovascular disease and traumatic brain injury (TBI) are inextricably linked to inflammation. We will review the mechanisms of HMGB1 and its receptors in nervous system inflammation to provide a basis for further development of new HMGB1-based therapies.
 BACKGROUND: Recently, an association between painful tonic spasms (PTS) and Neuromyelitis Optica Spectrum Disorder (NMOSD) was established. OBJECTIVE: To describe the clinical characteristics of PTS in NMOSD based on a video recording and to provide a literature review on the topic. METHODS: We report a case of a 38 years-old woman with a diagnosis of NMOSD and positive aquaporin-4 IgG antibody status who developed PTS five weeks after an episode of longitudinal extensive transverse myelitis (LETM). RESULTS: Repetitive, brief, and painful episodes of muscle contraction were observed on the patient's left hand, spreading to the left arm, and then extending to the four limbs. While pregabalin and topiramate had no influence on these episodes, the patient responded to carbamazepine (CBZ), without symptom recurrence after one year. CONCLUSIONS: PTS in association with LETM can be considered typical for NMOSD. Although the exact mechanism is unknown, ephaptic transmission after spinal cord damage and excitatory soluble factors released during acute inflammation responses are sought to be involved. Symptomatic treatment with CBZ achieved remission of spams in our case.

 The importance of B cells in multiple sclerosis (MS) has been demonstrated through the advent of B-cell-depleting anti-CD20 antibody therapies. Ofatumumab is the first fully human anti-CD20 monoclonal antibody (mAb) developed and tested for subcutaneous (SC) self-administration at monthly doses of 20 mg, and has been approved in the US, UK, EU, and other regions and countries worldwide for the treatment of relapsing MS. The development goal of ofatumumab was to obtain a highly efficacious anti-CD20 therapy, with a safety and tolerability profile that allows for self-administration by MS patients at home and a positive benefit-risk balance for use in the broad relapsing MS population. This development goal was enabled by the unique binding site, higher affinity to B cells, and higher potency of ofatumumab compared to previous anti-CD20 mAbs; these properties of ofatumumab facilitate rapid B-cell depletion and maintenance with a low dose at a low injection volume (20 mg/0.4 ml). The high potency in turn enables the selective targeting of B cells that reside in the lymphatic system via subcutaneous (SC) administration. Through a comprehensive dose-finding program in two phase 2 studies (one intravenous and one SC) and model simulations, it was found that safety and tolerability can be further improved, and the risk of systemic injection-related reactions (IRRs) minimized, by avoiding doses ≥ 30 mg, and by reaching initial and rapid B-cell depletion via stepwise weekly administration of ofatumumab at Weeks 0, 1, and 2 (instead of a single high dose). Once near-complete B-cell depletion is reached, it can be maintained by monthly doses of 20 mg/0.4 ml. Indeed, in phase 3 trials (ASCLEPIOS I/II), rapid and sustained near-complete B-cell depletion (largely independent of body weight, race and other factors) was observed with this dosing regimen, which resulted in superior efficacy of ofatumumab versus teriflunomide on relapse rates, disability worsening, neuronal injury (serum neurofilament light chain), and imaging outcomes. Likely due to its fully human nature, ofatumumab has a low immunogenic risk profile-only 2 of 914 patients receiving ofatumumab in ASCLEPIOS I/II developed anti-drug antibodies-and this may also underlie the infrequent IRRs (20% with ofatumumab vs. 15% with the placebo injection in the teriflunomide arm) that were mostly (99.8%) mild to moderate in severity. The overall rates of infections and serious infections in patients treated with ofatumumab were similar to those in patients treated with teriflunomide (51.6% vs. 52.7% and 2.5% vs. 1.8%, respectively). The benefit-risk profile of ofatumumab was favorable compared to teriflunomide in the broad RMS population, and also in the predefined subgroups of both recently diagnosed and/or treatment-naïve patients, as well as previously disease-modifying therapy-treated patients. Interim data from the ongoing extension study (ALITHIOS) have shown that long-term treatment with ofatumumab up to 4 years is well-tolerated in RMS patients, with no new safety risks identified. In parallel to the phase 3 trials in which SC administration was carried out with a pre-filled syringe, an autoinjector pen for more convenient self-administration of the ofatumumab 20 mg dose was developed and is available for use in clinical practice.
 The differential diagnosis of abdominal cramping accompanied by nausea and vomiting is overwhelmingly broad. It demands a finely detailed history to further tease out an etiology as well as directed treatments. In addition to infectious and neurologic causes of said symptoms, it is important to remember potential chemical causes responsible for clinical pictures featuring abdominal cramping, nausea, and vomiting. In 2004, a peculiar syndrome of vomiting associated with chronic cannabis use appeared in the literature with the curious historical qualifier that symptoms seemed to be relieved with hot showering or bathing. This syndrome came to be known as cannabinoid hyperemesis syndrome (CHS). With the increasing use of cannabis among all manner of age groups, especially recreationally among adolescents as well as medically for use as an antiemetic in chemotherapy-induced vomiting, appetite stimulant in those with cachexia, and analgesic (e.g., for peripheral neuropathies) and as an antispasmodic in multiple sclerosis, it is important to recognize this phenomenon’s risk factors and presentation in both emergency and primary care.
 Diffusion magnetic resonance imaging offers unique in vivo sensitivity to tissue microstructure in brain white matter, which undergoes significant changes during development and is compromised in virtually every neurological disorder. Yet, the challenge is to develop biomarkers that are specific to micrometer-scale cellular features in a human MRI scan of a few minutes. Here we quantify the sensitivity and specificity of a multicompartment diffusion modeling framework to the density, orientation and integrity of axons. We demonstrate that using a machine learning based estimator, our biophysical model captures the morphological changes of axons in early development, acute ischemia and multiple sclerosis (total N=821). The methodology of microstructure mapping is widely applicable in clinical settings and in large imaging consortium data to study development, aging and pathology.
 Ferroptosis is a distinct type of regulated cell death characterized by iron overload and lipid peroxidation. Ferroptosis is regulated by numerous factors and controlled by several mechanisms. This cell death type has a relationship with the immune system, which may be regulated by damage-associated molecular patterns. Ferroptosis participates in the progression of autoimmune diseases, including autoimmune hepatitis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, multiple sclerosis, Parkinson's Disease, psoriasis and insulin-dependent diabetes mellitus. The present review summarizes the role of ferroptosis in autoimmune disorders and discusses ferroptosis as a potential therapeutic target for autoimmune disease.
 Astrocytes, an integral component of the central nervous system (CNS), contribute to the maintenance of physiological homeostasis through their roles in synaptic function, K(+) buffering, blood-brain barrier (BBB) maintenance, and neuronal metabolism. Reactive astrocytes refer to astrocytes undergoing morphological, molecular and functional remodelling in response to pathological stimuli. The activation and differentiation of astrocytes are implicated in the pathogenesis of multiple neurodegenerative diseases. However, there are still controversies regarding their subset identification, function and nomenclature in neurodegeneration. In this review, we revisit the multidimensional roles of reactive astrocytes in Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS). Furthermore, we propose a precise linkage between astrocyte subsets and their functions based on single-cell sequencing analyses.
 Prednisone is a synthetic, anti-inflammatory glucocorticoid that derives from cortisone. It is biologically inert and converted to prednisolone in the liver. Prednisone is an FDA-approved, delayed-release corticosteroid indicated as an anti-inflammatory or immunosuppressive agent to treat a broad range of diseases, including immunosuppressive/endocrine, rheumatic, collagen, dermatologic, allergic states, ophthalmic, respiratory, hematologic, neoplastic, edematous, gastrointestinal, acute exacerbations of multiple sclerosis, and as an anti-inflammatory and an antineoplastic agent. Prednisone is a corticosteroid (cortisone-like medicine or steroid). It works on the immune system to help relieve swelling, redness, itching, and allergic reactions. This activity will also highlight the mechanism of action, adverse event profile, and other key factors (e.g., dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the interprofessional team who are involved in the administration of prednisone to patients.
 A 22-year-old male was referred from the medicine department with the chief complaint of double vision for 2 months. The patient had suffered from dengue viral hemorrhagic encephalitis for 2 months for which intensive medical care was given. On ocular examination, both eyes (OU) showed limited adduction with contralateral abducting nystagmus on attempted horizontal gaze. Magnetic resonance imaging of brain showed pontine and midbrain hemorrhages which involved the region of medial longitudinal fasciculus and caused bilateral internuclear ophthalmoplegia (INO). Bilateral INO is very rare and most commonly caused by multiple sclerosis. The presentation of dengue fever causing midbrain and pontine hemorrhages which resulted in bilateral INOs has not been previously reported, to our knowledge.
 An intention, rubral, cerebellar, or course tremor is defined as a rhythmic, oscillatory, and high amplitude tremor during a directed and purposeful motor movement, worsening before reaching the target. It is due to cerebellar dysfunction. It can affect precision in coordinated movements of speech muscles and limbs. The cerebellum, along with its sensory-motor white matter tracts, is responsible for motor coordination, posture and balance. The feedback mechanisms between the cerebellum, the cortex, and the brainstem become impaired, leading to kinetic errors, more prominent in fine motor skill tasks.  Intention tremor was first described by Jean-Martin Charcot in 1868, who noticed that multiple sclerosis (MS) patients could be differentiated from Parkinson disease (PD) patients by the type of tremor they present. MS is the most common cause of intention tremor. MS patients had intention tremors along with nystagmus and scanning speech, bearing his name as the Charcot's triad.
 A structured health care transition is essential for adolescents with chronic disease to ensure continuity of care without treatment lapse. Though rare, multiple sclerosis is diagnosed in children and adolescents and these patients will eventually require transition to adult care in late adolescence and early adulthood. Some barriers to transition include limited independence of the adolescent, fear of an unknown adult care model, and difficulty ending close relationships with longstanding pediatric providers. For optimal success, transition planning should be started in the early teenage years, and graduated independence and self-management skills should be fostered over time. Providers should also be aware of the developmental evolution of adolescents when assessing transition readiness and should screen for barriers during routine clinic visits to ensure that these are addressed prior to the time of transfer.
 Disease-modifying therapies remain an important unmet medical need in many neurological diseases. However, recent advances in novel therapies, such as antisense oligonucleotides, antibodies, and enzyme supplementation have significantly improved the prognosis and delayed time until relapse of various neurological diseases. Nusinersen used for spinal muscular atrophy and patisiran for transthyretin-mediated familial amyloid polyneuropathy significantly suppress disease progression and prolong longevity. Antibodies against the CD antigen, interleukin, or complement significantly lessen the time until relapse of multiple sclerosis or neuromyelitis optica. Administration of antibodies has expanded for treatment of migraine and neurodegenerative diseases such as Alzheimer's disease. Therefore, a paradigm shift is being observed in therapeutic strategies for many neurological diseases, many of which are typically considered "intractable."
 Interferons are glycoproteins that have antiviral, antiproliferative, and immunomodulatory functions. They are used widely for the treatment of many conditions like Hepatitis C, cancers, and immune-mediated disorders like multiple sclerosis. Interferon was discovered by Issacs and Lindenmann in 1957 while studying the phenomenon of virus interference. The FDA approved the use of interferon-alpha-2a and alpha-2b for the treatment of hairy cell leukemia in 1986. As time progressed, the use of interferons (IFN) has expanded to include a broad spectrum of conditions. However, their use correlates with numerous adverse effects like fatigue, influenza-like syndrome, toxicities related to the central nervous system, the gastrointestinal tract, endocrine system, and cardiovascular, renal, and musculoskeletal systems. Ikebe and associates made the first report of ocular toxicity of IFN therapy in 1990 in a 39-year-old patient who developed retinal hemorrhages and cotton wool spots after receiving intravenous IFN. 
 IMPORTANCE: Multiple sclerosis (MS) is an immune-mediated neurological disorder that affects nearly one million people in the United States. Up to 50% of patients with MS experience depression. OBJECTIVE: To investigate how white matter network disruption is related to depression in MS. DESIGN: Retrospective case-control study of participants who received research-quality 3-tesla neuroimaging as part of MS clinical care from 2010-2018. Analyses were performed from May 1 to September 30, 2022. SETTING: Single-center academic medical specialty MS clinic. PARTICIPANTS: Participants with MS were identified via the electronic health record (EHR). All participants were diagnosed by an MS specialist and completed research-quality MRI at 3T. After excluding participants with poor image quality, 783 were included. Inclusion in the depression group ( MS+Depression ) required either: 1) ICD-10 depression diagnosis (F32-F34.*); 2) prescription of antidepressant medication; or 3) screening positive via Patient Health Questionnaire-2 (PHQ-2) or -9 (PHQ-9). Age- and sex-matched nondepressed comparators ( MS-Depression ) included persons with no depression diagnosis, no psychiatric medications, and were asymptomatic on PHQ-2/9. EXPOSURE: Depression diagnosis. MAIN OUTCOMES AND MEASURES: We first evaluated if lesions were preferentially located within the depression network compared to other brain regions. Next, we examined if MS+Depression patients had greater lesion burden, and if this was driven by lesions specifically in the depression network. Outcome measures were the burden of lesions (e.g., impacted fascicles) within a network and across the brain. Secondary measures included between-diagnosis lesion burden, stratified by brain network. Linear mixed-effects models were employed. RESULTS: Three hundred-eighty participants met inclusion criteria, (232 MS+Depression: age[SD]=49[12], %females=86; 148 MS-Depression: age[SD]=47[13], %females=79). MS lesions preferentially affected fascicles within versus outside the depression network (β=0.09, 95% CI=0.08-0.10, P<0.001). MS+Depression had more white matter lesion burden (β=0.06, 95% CI=0.01-0.10, P=0.015); this was driven by lesions within the depression network (β=0.02, 95% CI 0.003-0.040, P=0.020). CONCLUSIONS AND RELEVANCE: We provide new evidence supporting a relationship between white matter lesions and depression in MS. MS lesions disproportionately impacted fascicles in the depression network. MS+Depression had more disease than MS-Depression, which was driven by disease within the depression network. Future studies relating lesion location to personalized depression interventions are warranted. KEY POINTS: Question: Are white matter lesions that impact fascicles connecting a previously-described depression network associated with depression in patients with multiple sclerosis (MS)?Findings: In this retrospective, case-control study of patients with MS including 232 patients with depression and 148 nondepressed MS comparators, patients with MS had more disease within the depression network, irrespective of depression diagnosis. Patients with depression had more disease than those without depression, which was driven by disease within the depression network specifically.Meaning: Lesion location and burden may contribute to depression comorbidity in MS.
 Emotionalism can develop following a range of neurological disorders; however the aetiology of emotionalism is still unclear. To identify anatomical, neuropsychological and psychological predictors and correlates of emotionalism across neurological disorders: stroke, Parkinson's disease, multiple sclerosis, traumatic brain injury, Alzheimer's disease, vascular dementia and amyotrophic lateral sclerosis. To explore if these predictors and correlates of emotionalism differ across neurological disorders. A comprehensive systematic search was completed of four databases: MEDLINE, CINAHL Complete, PsycINFO and EMBASE. Methodological quality was assessed using the Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies and each study was graded according to the level of evidence using the Scottish Intercollegiate Guidelines Network. Fifty papers (participants N = 1922) were included. 25 studies were rated as "Fair," 21 "Good" and 4 "Poor." The review identified predictors and correlates found in several neurological disorder such as bulbar networks, serotonergic pathways, genetics and female gender. Multiple studies across diseases (stroke, MS, ALS) indicate emotionalism is associated with cognitive impairment, especially frontal deficits. Due to the disproportionate number of studies identified across neurological disorders, it is difficult to draw definitive answers. Further research is required across neurological disorders to explore similarities and differences in anatomical, neuropsychological and psychological predictors and correlates.
 Stimulation of remyelination is critical for the treatment of multiple sclerosis (MS) to alleviate symptoms and protect the myelin sheath from further damage. The current study aimed to investigate the possible therapeutic effects of combining vitamin D3 (Vit D3) and siponimod (Sipo) on enhancing remyelination and modulating microglia phenotypes in the cuprizone (CPZ) demyelination mouse model. The study was divided into two stages; demyelination (first 5 weeks) and remyelination (last 4 weeks). In the first 5 weeks, 85 mice were randomly divided into two groups, control (n = 20, standard rodent chow) and CPZ (n = 65, 0.3% CPZ mixed with chow for 6 weeks, followed by 3 weeks of standard rodent chow). At week 5, the CPZ group was re-divided into four groups (n = 14) for remyelination stages; untreated CPZ (0.2 ml of CMC orally), CPZ+Vit D3 (800 IU/kg Vit D3 orally), CPZ+Sipo (1.5 mg/kg Sipo orally), and CPZ+Vit D3 (800 IU/kg Vit D3) + Sipo (1.5 mg/kg Sipo orally). Various behavioral tasks were performed to evaluate motor performance. Luxol Fast Blue (LFB) staining, the expression level of myelin basic protein (MBP), and M1/M2 microglia phenotype genes were assessed in the corpus callosum (CC). The results showed that the combination of Vit D3 and Sipo improved behavioral deficits, significantly promoted remyelination, and modulated expression levels of microglia phenotype genes in the CC at early and late remyelination stages. These results demonstrate for the first time that a combination of Vit D3 and Sipo can improve the remyelination process in the cuprizone (CPZ) mouse model by attenuating the M1 microglia phenotype. This may help to improve the treatment of MS patients.
 Neuroimmune-triggered neuroinflammation of the central nervous system is emerging as an important aetiopathogenic factor for multiple neurological disorders, including depression, dementia, Alzheimer's disease, multiple sclerosis and others. Tryptophan metabolism via the kynurenic pathway, which is initiated by the indoleamine-2,3-dioxygenase (IDO-1) enzyme, is a key regulator of the neuroimmune system and its associated neuroinflammatory effects. As discussed in this review, targeting the production of immunopathic and potentially neurotoxic kynurenine metabolites by inhibitory downregulation of IDO-1 may prove a viable target against inflammation-induced neurological conditions, particularly depression and dementia.
 Pneumonia is an infection of lung parenchyma caused by a variety of pathogens such as bacteria, viruses, fungi, and parasites. One type of bacteria includes Chlamydia species. These species consist of C. pneumoniae, C. psittaci, and C. trachomatis, which are obligate intracellular bacterial pathogens. They frequently infect the respiratory tract in humans. Most of the respiratory tract infections (about 70%) caused by C. pneumoniae are asymptomatic or only with mild symptoms, but a minority (30%) of them are responsible for more severe respiratory illnesses such as community-acquired pneumonia (CAP) with atypical symptoms, bronchitis and upper respiratory tract infections (URTIs). In addition, C. pneumoniae is involved not only in respiratory infections but also in the pathogenesis of multiple inflammatory conditions including chronic obstructive pulmonary disease (COPD), asthma, lung cancer, neurological disorders such as Alzheimer disease, multiple sclerosis, and schizophrenia as well as atherosclerosis and arthritis. Thus, the clinician must be able to promptly recognize, evaluate, and treat this condition to avoid its complications.  The following activity will provide an overview of the etiology, clinical features, evaluation, and approach to the management of a patient with chlamydial pneumonia.
 NLRX1 is a member of the of the Nod-like receptor (NLR) family, and it represents a unique pattern recognition molecule (PRM) as it localizes to the mitochondrial matrix in resting conditions. Over the past fifteen years, NLRX1 has been proposed to regulate multiple cellular processes, including antiviral immunity, apoptosis, reactive oxygen species (ROS) generation and mitochondrial metabolism. Similarly, in vivo models have shown that NLRX1 was associated with the control of a number of diseases, including multiple sclerosis, colorectal cancer and ischemia-reperfusion injury. This apparent versatility in function hinted that a common and general overarching role for NLRX1 may exist. Recent evidence has suggested that NLRX1 controls mitophagy through the detection of a specific "danger signal", namely the defective import of proteins into mitochondria, or mitochondrial protein import stress (MPIS). In this review article, we propose that mitophagy regulation may represent the overarching process detected by NLRX1, which could in turn impact on a number of diseases if dysfunctional.
 AIMS: Neuroinflammation might be involved in the degeneration and progression of Amyotrophic Lateral Sclerosis (ALS). Here, we studied the role of the circulating lymphocytes in ALS, in particular the NK cells. We focused on the relationship between blood lymphocytes, ALS clinical subtype and disease severity. SUBJECTS AND METHODS: Blood samples were collected from 92 patients with sporadic ALS, 21 patients with Primary Lateral Sclerosis (PLS) and 37 patients affected by primary progressive multiple sclerosis (PPMS) with inactive plaques. Blood was taken from ALS and controls at the time of diagnosis/referral. Circulating lymphocytes were analyzed by flow cytometry with specific antibodies. Values were expressed as absolute number (n°/µl) of viable lymphocytes subpopulations in ALS were compared with controls. Multivariable analysis was made using site of onset, gender changes in ALSFRS-R and disease progression rate (calculated as ΔFS score). RESULTS: Age at onset was 65y (58-71) in ALS (spinal 67.4%; bulbar, 32.6%), 57y (48-78) in PLS and 56y (44-68) PPMS. Absolute blood levels of the lymphocytes in the different cohorts were within normal range. Furthermore, while levels of lymphocytes T and B were not different between disease groups, NK cells were increased in the ALS cohort (ALS = 236 [158-360] vs. Controls = 174[113-240], p < 0.001). In ALS, blood levels of NK cells were not related with the main clinical-demographic variables, including the rate of disease progression. Multivariable analysis suggested that male gender and bulbar onset were independently associated with a risk of high blood NK cells levels. CONCLUSIONS: We show that blood NK cells are selectively increased in ALS, though their level appear unaffected in patients with an estimated rapidly progressing disease. Being of a male gender and with a bulbar onset seems to confer higher susceptibility to have increased NK lymphocytes levels at diagnosis/referral. Our experiments provides a further clear-cut evidence of the role of the NK lymphocytes as a significant player in ALS pathogenesis.
 Neurodegenerative diseases are characterized by neuroinflammation, neuronal depletion and oxidative stress. They coincide with subtle chronic or flaring inflammation, sometimes escalating with infiltrations of the immune system cells in the inflamed parts causing mild to severe or even lethal damage. Thus, neurodegenerative diseases show all features of autoimmune diseases. Prevalence of neurodegenerative diseases has dramatically increased in recent decades and unfortunately, the therapeutic efficacy and safety profile of available drugs is moderate. The beneficial effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) polyunsaturated fatty acids (omega-3 PUFAs) are nowadays highlighted by a plethora of studies. They play a role in suppression of inflammation, gene expression, cellular membrane fluidity/permeability, immune functionality and intracellular/exocellular signaling. The role of omega-6 polyunsaturated fatty acids, such as linoleic acid (LA), gamma linolenic acid (GLA), and arachidonic acid (AA), on neuroprotection is controversial, as some of these agents, specifically AA, are proinflammatory, whilst current data suggest that they may have neuroprotective properties as well. This review provides an overview of the existing recent clinical studies with respect to the role of omega-3 and omega-6 PUFAs as therapeutic agents in chronic, inflammatory, autoimmune neurodegenerative diseases as well as the dosages and the period used for testing.
 INTRODUCTION: Over the past few years, the deep learning community has developed and validated a plethora of tools for lesion detection and segmentation in Multiple Sclerosis (MS). However, there is an important gap between validating models technically and clinically. To this end, a six-step framework necessary for the development, validation, and integration of quantitative tools in the clinic was recently proposed under the name of the Quantitative Neuroradiology Initiative (QNI). AIMS: Investigate to what extent automatic tools in MS fulfill the QNI framework necessary to integrate automated detection and segmentation into the clinical neuroradiology workflow. METHODS: Adopting the systematic Cochrane literature review methodology, we screened and summarised published scientific articles that perform automatic MS lesions detection and segmentation. We categorised the retrieved studies based on their degree of fulfillment of QNI's six-steps, which include a tool's technical assessment, clinical validation, and integration. RESULTS: We found 156 studies; 146/156 (94%) fullfilled the first QNI step, 155/156 (99%) the second, 8/156 (5%) the third, 3/156 (2%) the fourth, 5/156 (3%) the fifth and only one the sixth. CONCLUSIONS: To date, little has been done to evaluate the clinical performance and the integration in the clinical workflow of available methods for MS lesion detection/segmentation. In addition, the socio-economic effects and the impact on patients' management of such tools remain almost unexplored.
 INTRODUCTION: The humanized anti-α4 integrin blocking antibody natalizumab (NTZ) is an effective treatment for relapsing-remitting multiple sclerosis (RRMS) that is associated with the risk of progressive multifocal leukoencephalopathy (PML). While extended interval dosing (EID) of NTZ reduces the risk for PML, the minimal dose of NTZ required to maintain its therapeutic efficacy remains unknown. OBJECTIVE: Here we aimed to identify the minimal NTZ concentration required to inhibit the arrest of human effector/memory CD4(+) T cell subsets or of PBMCs to the blood-brain barrier (BBB) under physiological flow in vitro. RESULTS: Making use of three different human in vitro BBB models and in vitro live-cell imaging we observed that NTZ mediated inhibition of α4-integrins failed to abrogate T cell arrest to the inflamed BBB under physiological flow. Complete inhibition of shear resistant T cell arrest required additional inhibition of β2-integrins, which correlated with a strong upregulation of endothelial intercellular adhesion molecule (ICAM)-1 on the respective BBB models investigated. Indeed, NTZ mediated inhibition of shear resistant T cell arrest to combinations of immobilized recombinant vascular cell adhesion molecule (VCAM)-1 and ICAM-1 was abrogated in the presence of tenfold higher molar concentrations of ICAM-1 over VCAM-1. Also, monovalent NTZ was less potent than bivalent NTZ in inhibiting T cell arrest to VCAM-1 under physiological flow. In accordance with our previous observations ICAM-1 but not VCAM-1 mediated T cell crawling against the direction of flow. CONCLUSION: Taken together, our in vitro observations show that high levels of endothelial ICAM-1 abrogate NTZ mediated inhibition of T cell interaction with the BBB. EID of NTZ in MS patients may thus require consideration of the inflammatory status of the BBB as high levels of ICAM-1 may provide an alternative molecular cue allowing for pathogenic T cell entry into the CNS in the presence of NTZ.
 BACKGROUND: Myelopathies require prompt etiologic diagnosis. We aimed to identify a specific myelopathy diagnosis in cases of suspected myelitis to highlight clinicoradiologic differences. METHODS: In this retrospective, single-centre cohort of subjects with suspected myelitis referred to London Multiple Sclerosis (MS) Clinic between 2006 and 2021, we identified those with MS and reviewed the remaining charts for etiologic diagnosis based on clinical, serologic, and imaging details. RESULTS: Of 333 included subjects, 318/333 (95.5%) received an etiologic diagnosis. Most (274/333, 82%) had MS or clinically isolated syndrome. Spinal cord infarction (n = 10) was the commonest non-inflammatory myelitis mimic characterized by hyperacute decline (n = 10/10, 100%), antecedent claudication (n = 2/10, 20%), axial owl/snake eye (n = 7/9, 77%) and sagittal pencillike (n = 8/9, 89%) MRI patterns, vertebral artery occlusion/stenosis (n = 4/10, 40%), and concurrent acute cerebral infarct (n = 3/9, 33%). Longitudinal lesions were frequent in aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) (n = 7/7, 100%) and myelin oligodendrocyte glycoprotein-IgG-associated disorder (MOGAD) (n = 6/7, 86%), accompanied by bright spotty (n = 5/7, 71%) and central-grey-restricted (n = 4/7, 57%) T2-lesions on axial sequences, respectively. Leptomeningeal (n = 4/4, 100%), dorsal subpial (n = 4/4, 100%) enhancement, and positive body PET/CT (n = 4/4, 100%) aided the diagnosis of sarcoidosis. Spondylotic myelopathies had chronic sensorimotor presentations (n = 4/6, 67%) with relative bladder sparing (n = 5/6, 83%), localizable to sites of disc herniation (n = 6/6, 100%). Metabolic myelopathies showed dorsal column or inverted 'V' sign (n = 2/3, 67%) MRI T2-abnormality with B12 deficiency. CONCLUSIONS: Although no single feature reliably confirms or refutes a specific myelopathy diagnosis, this study highlights patterns that narrow the differential diagnosis of myelitis and facilitate early recognition of mimics.
 BACKGROUND: Neuromyelitis optica spectrum disorders (NMOSD) is an autoimmune demyelinating disease, leading recurrently relapses and severe disability. There is a need for new biomarkers to meet clinical needs in diagnosis and monitoring. METHODS: Through liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) analysis, brain lesions from NMO animal models were analyzed to identify potential biomarkers. Then, we assessed the levels of serum glial fibrillary acidic protein (sGFAP), neurofilament light chain (sNfL), Tau protein (sTau) and Ubiquitin C-terminal hydrolase L1 (sUCHL1) using an ultrasensitive single molecule array (Simoa) of AQP4-IgG + NMOSD patients, myelin oligodendrocyte glycoprotein antibody-associated disorder (MOGAD) patients, multiple sclerosis (MS) patients and healthy controls (HCs). Additionally, we further explored the early diagnosis value of these proteins. RESULTS: There were 72 differentially expressed proteins between the NMO and control groups. NfL abundance was elevated when GFAP, UCHL1, and Tau abundance was decreased in the NMO group. Then, we observed that the sGFAP and sUCHL1 levels in patients with NMOSD in the early stage were significantly increased compared to those in control participants. Combined ROCs of the sGFAP, sNfL, and sUCHL1 levels to better predict NMOSD with relapse stages was optimal. Notably, univariate and multivariate analyses demonstrated that the sGFAP and sNfL levels were higher in patients with brain lesions, while the sUCHL1 levels were higher in those with spinal cord lesions during recent relapse. CONCLUSIONS: These findings suggested that sGFAP, sNfL, and sUCHL1 displayed good diagnostic performance in AQP4-IgG + NMOSD and could be novel candidates for early discrimination.
 OBJECTIVE: To identify the burden of hospitalization and common primary admitting diagnoses among MS patients in the United States (US). BACKGROUND: The burden of hospitalizations and conditions leading to hospitalizations in MS patients in the US has not been well described. DESIGN/METHODS: Using the Nationwide Inpatient Sample for 2001-2010, all patients with principal or secondary diagnosis of MS were identified, and the principal admitting diagnoses were compared with that of non-MS patients. Trends in hospitalizations were studied in specific age groups (1-9 yrs, 10-19 yrs, 20-29 yrs, 30-39 yrs, 40-49 yrs, 50-59 yrs, 60-69 yrs,70-79 yrs, 80-84 yrs and ≥85 yrs), and population level rates were obtained and compared with non-MS patients to obtain rate ratios (RR) and odds ratios (OR). RESULTS: A total of 1,240,410 MS patients were identified representing 4 out of every 1000 US hospital admissions, with an estimated female/male ratio of 2.72/1. The median age for MS hospitalizations was 53 years (Interquartile range=18). The majority of all MS hospitalizations occurred in the 30-69-year age bracket (82.17 %). The average length of in-patient hospital stays for MS patients compared to the non-MS population was 5.8 vs. 4.5 days (p < 0.001), and more MS patients had Medicare insurance (50.36 % vs. 42.24 %, p < 0.001). Overall, conditions such as urinary tract infections (UTI) - (RR11.43, p < 0.001), septicemia (RR8.53, p < 0.001), pneumonia (RR2.84, p < 0.001), chronic skin ulcers (RR20.64, p < 0.001), and lower limb and femoral neck fractures (RR2.86, p < 0.001) were present with increased frequency among MS patients. Patterns of comorbidity varied markedly by age group. The estimated average annual in-hospital charges adjusted to 2010 dollars for all MS inpatient hospitalizations was 3 billion U.S. dollars. CONCLUSIONS: Patients with MS are admitted into hospital at a younger age, are hospitalized longer and consume more Medicare resources than the similar patients without MS in the general population. Infections account for a large proportion of MS-associated hospitalizations, from young adulthood onward. These findings are particularly significant in light of the increasing availability of disease modifying therapies with more potent immunosuppressive properties, as well as the accumulating data that systemic infection can drive MS relapses.
 BACKGROUND: Neurodegenerative diseases (NDs) impose significant financial and healthcare burden on populations all over the world. The prevalence and incidence of NDs have been observed to increase dramatically with age. Hence, the number of reported cases is projected to increase in the future, as life spans continues to rise. Despite this, there is limited effective treatment against most NDs. Interferons (IFNs), a family of cytokines, have been suggested as a promising therapeutic target for NDs, particularly IFN-α, which governs various pathological pathways in different NDs. OBJECTIVE: This systematic review aimed to critically appraise the currently available literature on the pathological role of IFN-α in neurodegeneration/NDs. METHODS: Three databases, Scopus, PubMed, and Ovid Medline, were utilized for the literature search. RESULTS: A total of 77 journal articles were selected for critical evaluation, based on the inclusion and exclusion criteria. The studies selected and elucidated in this current systematic review have showed that IFN-α may play a deleterious role in neurodegenerative diseases through its strong association with the inflammatory processes resulting in mainly neurocognitive impairments. IFN-α may be displaying its neurotoxic function via various mechanisms such as abnormal calcium mineralization, activation of STAT1-dependent mechanisms, and increased quinolinic acid production. CONCLUSION: The exact role IFN-α in these neurodegenerative diseases have yet to be determine due to a lack in more recent evidence, thereby creating a variability in the role of IFN-α. Future investigations should thus be conducted, so that the role played by IFN-α in neurodegenerative diseases could be delineated.
 Occupational injuries and toxicant exposures lead to the development of neuroinflammation by activating distinct mechanistic signaling cascades that ultimately culminate in the disruption of neuronal function leading to neurological and neurodegenerative disorders. The entry of toxicants into the brain causes the subsequent activation of glial cells, a response known as 'reactive gliosis'. Reactive glial cells secrete a wide variety of signaling molecules in response to neuronal perturbations and thus play a crucial role in the progression and regulation of central nervous system (CNS) injury. In parallel, the roles of protein phosphorylation and cell signaling in eliciting neuroinflammation are evolving. However, there is limited understanding of the molecular underpinnings associated with toxicant- or occupational injury-mediated neuroinflammation, gliosis, and neurological outcomes. The activation of signaling molecules has biological significance, including the promotion or inhibition of disease mechanisms. Nevertheless, the regulatory mechanisms of synergism or antagonism among intracellular signaling pathways remain elusive. This review highlights the research focusing on the direct interaction between the immune system and the toxicant- or occupational injury-induced gliosis. Specifically, the role of occupational injuries, e.g., trips, slips, and falls resulting in traumatic brain injury, and occupational toxicants, e.g., volatile organic compounds, metals, and nanoparticles/nanomaterials in the development of neuroinflammation and neurological or neurodegenerative diseases are highlighted. Further, this review recapitulates the recent advancement related to the characterization of the molecular mechanisms comprising protein phosphorylation and cell signaling, culminating in neuroinflammation.
 OBJECTIVES: Evaluate the performance of a deep learning (DL)-based model for multiple sclerosis (MS) lesion segmentation and compare it to other DL and non-DL algorithms. METHODS: This ambispective, multicenter study assessed the performance of a DL-based model for MS lesion segmentation and compared it to alternative DL- and non-DL-based methods. Models were tested on internal (n = 20) and external (n = 18) datasets from Latin America, and on an external dataset from Europe (n = 49). We also examined robustness by rescanning six patients (n = 6) from our MS clinical cohort. Moreover, we studied inter-human annotator agreement and discussed our findings in light of these results. Performance and robustness were assessed using intraclass correlation coefficient (ICC), Dice coefficient (DC), and coefficient of variation (CV). RESULTS: Inter-human ICC ranged from 0.89 to 0.95, while spatial agreement among annotators showed a median DC of 0.63. Using expert manual segmentations as ground truth, our DL model achieved a median DC of 0.73 on the internal, 0.66 on the external, and 0.70 on the challenge datasets. The performance of our DL model exceeded that of the alternative algorithms on all datasets. In the robustness experiment, our DL model also achieved higher DC (ranging from 0.82 to 0.90) and lower CV (ranging from 0.7 to 7.9%) when compared to the alternative methods. CONCLUSION: Our DL-based model outperformed alternative methods for brain MS lesion segmentation. The model also proved to generalize well on unseen data and has a robust performance and low processing times both on real-world and challenge-based data. CLINICAL RELEVANCE STATEMENT: Our DL-based model demonstrated superior performance in accurately segmenting brain MS lesions compared to alternative methods, indicating its potential for clinical application with improved accuracy, robustness, and efficiency. KEY POINTS: • Automated lesion load quantification in MS patients is valuable; however, more accurate methods are still necessary. • A novel deep learning model outperformed alternative MS lesion segmentation methods on multisite datasets. • Deep learning models are particularly suitable for MS lesion segmentation in clinical scenarios.
 Multiple sclerosis (MS) is an autoimmune inflammatory disease of the central nervous system characterized by motor deficits, cognitive impairment, fatigue, pain, and sensory and visual dysfunction. CD40, highly expressed in B cells, plays a significant role in MS pathogenesis. The experimental autoimmune encephalomyelitis (EAE) mouse model of MS has been well established, as well as its relevance in MS patients. This study aimed to evaluate the therapeutic potential of DAPTA, a selective C-C chemokine receptor 5 (CCR5) antagonist in the murine model of MS, and to expand the knowledge of its mechanism of action. Following the induction of EAE, DAPTA was administrated (0.01 mg/kg, i.p.) daily from day 14 to day 42. We investigated the effects of DAPTA on NF-κB p65, IκBα, Notch-1, Notch-3, GM-CSF, MCP-1, iNOS, and TNF-α in CD40(+) spleen B cells using flow cytometry. Furthermore, we also analyzed the effect of DAPTA on NF-κB p65, IκBα, Notch-1, Notch-3, GM-CSF, MCP-1, iNOS, and TNF-α mRNA expression levels using qRT-PCR in brain tissue. EAE mice treated with DAPTA showed substantial reductions in NF-κB p65, Notch-1, Notch-3, GM-CSF, MCP-1, iNOS, and TNF-α but an increase in the IκBα of CD40(+) B lymphocytes. Moreover, EAE mice treated with DAPTA displayed decreased NF-κB p65, Notch-1, Notch-3, GM-CSF, MCP-1, iNOS, and TNF-α and but showed increased IκBα mRNA expression levels. This study showed that DAPTA has significant neuroprotective potential in EAE via the downregulation of inflammatory mediators and NF-κB/Notch signaling. Collectively, DAPTA might have potential therapeutic targets for use in MS treatment.
 Background: Glatiramer acetate (GA) is a well-established treatment option for patients with clinically isolated syndrome and relapsing-remitting multiple sclerosis (MS) with few side effects. The double transgenic mouse model spontaneous opticospinal encephalomyelitis (OSE), based on recombinant myelin oligodendrocyte glycoprotein(35-55) reactive T and B cells, mimicks features of chronic inflammation and degeneration in MS and related disorders. Here, we investigated the effects of prophylactic GA treatment on the clinical course, histological alterations and peripheral immune cells in OSE. Objective: To investigate the effects of prophylactic glatiramer acetate (GA) treatment in a mouse model of spontaneous opticospinal encephalomyelitis (OSE). Methods: OSE mice with a postnatal age of 21 to 28 days without signs of encephalomyelitis were treated once daily either with 150 µg GA or vehicle intraperitoneally (i. p.). The animals were scored daily regarding clinical signs and weight. The animals were sacrificed after 30 days of treatment or after having reached a score of 7.0 due to animal care guidelines. We performed immunohistochemistry of spinal cord sections and flow cytometry analysis of immune cells. Results: Preventive treatment with 150 µg GA i. p. once daily significantly reduced clinical disease progression with a mean score of 3.9 ± 1.0 compared to 6.2 ± 0.7 in control animals (p < 0.01) after 30 d in accordance with positive effects on weight (p < 0.001). The immunohistochemistry showed that general inflammation, demyelination or CD11c(+) dendritic cell infiltration did not differ. There was, however, a modest reduction of the Iba1(+) area (p < 0.05) and F4/80(+) area upon GA treatment (p < 0.05). The immune cell composition of secondary lymphoid organs showed a trend towards an upregulation of regulatory T cells, which lacked significance. Conclusions: Preventive treatment with GA reduces disease progression in OSE in line with modest effects on microglia/macrophages. Due to the lack of established prophylactic treatment options for chronic autoimmune diseases with a high risk of disability, our study could provide valuable indications for translational medicine.
 BACKGROUND: Many clinical trials use patient-reported outcome (PRO) measures, which can influence treatment decision-making, drug approval and label claims. Given that many PRO measure options exist, and there are conceptual and contextual complexities with PRO measurement, we aimed to evaluate how and why specific PRO measures have been selected for pivotal multiple sclerosis (MS) clinical trials. Specifically, we aimed to identify the reasons documented for PRO measure selection in contemporary phase III MS disease-modifying treatment (DMT) clinical trials. METHODS: We searched for phase III clinical trials of MS DMTs published between 2015 and 2021 and evaluated trial protocols, or primary publications where available, for PRO measure selection information. Specifically, we examined study documents for their clarification of clinical concepts measured, definitions of concepts measured, explanations of which PRO measures were considered, why specific PRO measures were chosen, and trade-offs in PRO measure selection. RESULTS: We identified 1705 abstracts containing 61 unique phase III MS DMT clinical trials. We obtained and examined 27/61 trial protocols. Six protocols were excluded: four contained no mention of PRO measures and two contained redacted sections preventing adequate assessment, leaving 21 protocols for assessment. For the remaining 34 trials (61-27), we retrieved 31 primary publications; 15 primary publications mentioned the use of a PRO measure. None of the 36 clinical trials that mentioned the use of PRO measures (21 protocols and 15 primary publications) documented clear PRO or clinical outcome assessment (COA) measurement strategies, provided clear justifications for PRO selection, or reasons why specific PRO measures were selected when alternatives existed. CONCLUSION: PRO measure selection for clinical trials is not evidence-based or underpinned by structured systematic approaches. This represents a critical area for study design improvement as PRO measure results directly affect patient care, PRO measurement has conceptual and contextual complexities, and there is a wide range of options when selecting a PRO measure. We recommend trial designers use formal approaches for PRO measure selection to ensure PRO measurement-based decisions are optimised. We provide a simple, logical, five-stage approach for PRO measure selection in clinical trials.
 Dysfunctional immune cells participate in the pathogenesis of a variety of autoimmune diseases, although the specific mechanisms remain elusive and effective clinical interventions are lacking. Recent research on immune checkpoint molecules has revealed significant expression of T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) on the surfaces of various immune cells. These include different subsets of T cells, macrophages, dendritic cells, natural killer cells, and mast cells. Further investigation into its protein structure, ligands, and intracellular signaling pathway activation mechanisms has found that TIM-3, by binding with different ligands, is involved in the regulation of crucial biological processes such as proliferation, apoptosis, phenotypic transformation, effector protein synthesis, and cellular interactions of various immune cells. The TIM-3-ligand axis plays a pivotal role in the pathogenesis of numerous conditions, including autoimmune diseases, infections, cancers, transplant rejection, and chronic inflammation. This article primarily focuses on the research findings of TIM-3 in the field of autoimmune diseases, with a special emphasis on the structure and signaling pathways of TIM-3, its types of ligands, and the potential mechanisms implicated in systemic lupus erythematosus, multiple sclerosis, rheumatoid arthritis, as well as other autoimmune diseases and chronic inflammation. The latest research results in the field of immunology suggest that TIM-3 dysfunction affects various immune cells and participates in the pathogenesis of diseases. Monitoring the activity of its receptor-ligand axis can serve as a novel biological marker for disease clinical diagnosis and prognosis evaluation. More importantly, the TIM-3-ligand axis and the downstream signaling pathway molecules may become key targets for targeted intervention treatment of autoimmune-related diseases.
 Transverse myelitis is a noncompressive myelopathy of inflammatory origin. The causes are broad, ranging from infective or toxic to immuno-mediated etiology. They can be manifestations of systemic diseases, such as sarcoidosis and systemic lupus erythematous, or phenotypes of neuroinflammation; in a portion of cases, the etiology remains unknown, leading to the designation idiopathic. The clinical presentation of transverse myelitis depends on the level of spinal cord damage and may include sensorimotor deficits and autonomic dysfunction. The age of onset of the disorder can impact the symptoms and outcomes of affected patients, with differences in manifestation and prognosis between children and adults. Spinal cord magnetic resonance imaging and cerebrospinal fluid examination are the main diagnostic tools that can guide clinicians in the diagnostic process, even though the search for antibodies that target the structural components of the neural tissue (anti-aquaporin4 antibodies and anti-myelin-oligodendrocyte antibodies) helps in the distinction among the immune-mediated phenotypes. Management and outcomes depend on the underlying cause, with different probabilities of relapse according to the phenotypes. Hence, immunosuppression is often recommended for the immune-mediated diseases that may have a higher risk of recurrence. Age at onset has implications for the choice of treatment.
 T follicular helper (Tfh) cells are heterogeneous and mainly characterized by expressing surface markers CXCR5, ICOS, and PD-1; cytokine IL-21; and transcription factor Bcl6. They are crucial for B-cell differentiation into long-lived plasma cells and high-affinity antibody production. T follicular regulatory (Tfr) cells were described to express markers of conventional T regulatory (Treg) cells and Tfh cells and were able to suppress Tfh-cell and B-cell responses. Evidence has revealed that the dysregulation of Tfh and Tfr cells is positively associated with the pathogenic processes of autoimmune diseases. Herein, we briefly introduce the phenotype, differentiation, and function of Tfh and Tfr cells, and review their potential roles in autoimmune diseases. In addition, we discuss perspectives to develop novel therapies targeting Tfh/Tfr balance.
 A 69-year-old woman with progressive short-term memory deficits was diagnosed with Alzheimer disease (MMSE 26/30, CDR 0.5) and underwent PET using 18 F-PBR06, a second-generation 18-kDa translocator protein ligand, targeting brain microglia and astrocytes. SUV and voxel-by-voxel binding potential maps (using simplified reference tissue method and a cerebellar pseudo-reference region) were generated. Images showed evidence of increased glial activation in biparietal cortices (including bilateral precuneus and posterior cingulate gyri) and bilateral frontal cortices. After 6 years of clinical follow-up, patient progressed to moderate cognitive impairment (CDR 2.0) and required assistance for activities of daily living.
 Vocal cord paralysis refers to the immobility of the vocal cord, while vocal cord paresis refers to the impaired mobility of the vocal cord. Both can be due to processes intrinsically affecting the vocal cord itself (scarring, tumor, etc.), due to cranial neuropathies of the nerves providing vocal cord mobility [the vagus nerve, the recurrent laryngeal nerve (RLN), and the superior laryngeal nerve (SLN)], central neurologic problems [stroke, tumor, multiple sclerosis (MS), etc.], or systemic disease [amyotrophic lateral sclerosis (ALS), Guillain-Barre syndrome, etc.]. Vocal cord paralysis is most commonly unilateral, and this is discussed in detail in another StatPearls article. Here we will concentrate on the rarer bilateral vocal cord paralysis. The vocal cords serve two functions: production of voice (phonation) and protection of the lower airways via glottic competence. The presentation and symptoms will depend upon the underlying etiology of the bilateral paralysis and the resultant position of the vocal cords. If the cords are paralyzed in a more median position, stridor and breathing symptoms may predominate (or the patient may be asymptomatic) while the voice may be normal, and no aspiration events will occur. If the vocal cords are paralyzed in a more lateral position, the airway will be widely patent and unable to close. This may present with significant voice complaints of breathiness and potential aspiration or choking, but with far fewer breathing or stridor complaints. Management will similarly depend on the underlying etiology and vocal cord position, as well as the overall prognosis of the patient.
 Finland is a relatively small genetic isolate with a genetically non-homogenous population. Available Finnish data on neuroepidemiology of adult-onset disorders are limited, and this paper describes the conclusions that can be drawn and their implications. Apparently, Finnish people have a (relatively) high risk of developing Unverricht-Lundborg disease (EPM1), Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), Spinal muscular atrophy, Jokela type (SMAJ) and adult-onset dystonia. On the other hand, some disorders, such as Friedreich's ataxia (FRDA) and Wilson's disease (WD), are almost absent or completely absent in the population. Valid and timely data concerning even many common disorders, such as stroke, migraine, neuropathy, Alzheimer's disease and Parkinson's disease, are unavailable, and there are virtually no data on many less-common neurological disorders, such as neurosarcoidosis or autoimmune encephalitides. There also appear to be marked regional differences in the incidence and prevalence of many diseases, suggesting that non-granular nationwide data may be misleading in many cases. Concentrated efforts to advance neuroepidemiological research in the country would be of clinical, administrative and scientific benefit, but currently, all progress is blocked by administrative and financial obstacles.
 BACKGROUND: Nursing home residents face many barriers to accessing specialist physician outpatient care. However, little data exists on how specialty care use changes when individuals transition to a nursing home in the US. METHODS: We studied specialist outpatient visits for new long-term care (LTC) residents within 1 year before and after their transition to nursing home residence using the Minimum Data Set v3.0 (MDS) and a 20% sample of Medicare fee-for-service claims in 2014-2018. To focus on residents requiring specialty care at baseline, we limited the cohort to residents with specialty care in the 13-24 months before LTC transition. We then measured the proportion of residents receiving at least one visit in the 12 months before the transition and the 12 months after the transition. We also examined subgroups of residents with a prior diagnosis likely requiring long-term specialty care (e.g., multiple sclerosis). Finally, we examined whether there was continuity of care within the same specialty care provider. RESULTS: Among 39,288 new LTC transitions identified in 2016-2017, 17,877 (45.5%) residents had a prior specialist visit 13-24 months before the transition. Among them, the proportion of residents with specialty visits decreased consistently in all specialties in the 12 months after the transition, ranging from a relative decrease of 14.4% for orthopedics to 67.9% for psychiatry. The relative decrease among patients with a diagnosis likely requiring specialty care ranged from 0.9% for neurology in patients with multiple sclerosis to 67.1% for psychiatry in patients with severe mental illness. Among residents who continued visiting a specialist, 78.9% saw the same provider as before the transition. CONCLUSIONS: The use of specialty care falls significantly after patients transition to a nursing home. Further research is needed to understand what drives this drop in use and whether interventions, such as telemedicine can ameliorate potential barriers to specialty care.
 An imbalance of oxy-inflammation status has been involved in axonal damage and demyelination in multiple sclerosis (MS). The aim of this study was to investigate the efficacy of an antioxidant treatment (calcium disodium ethylenediaminetetracetic acid-EDTA) chelation therapy associated with a micronutrient complex in MS patients. A total of 20 MS patients and 20 healthy subjects, enrolled as a control group (CTR), were recruited. We measured the plasma ROS production and total antioxidant capacity (TAC) by a direct assessment using Electron Paramagnetic Resonance; activities of the antioxidant system (thiols' redox status and enzymes); and the urinary presence of biomarkers of oxidative stress by immunoenzymatic assays. We also evaluated the levels of inflammation by plasmatic cytokines (TNFα, IL-1β, and IL-6) and assessed the sICAM levels, as well as the nitric oxide (NO) catabolism and transthyretin (TTR) concentration. Comparing CTR and MS, in the latter ROS production, oxidative damage, inflammatory biomarkers, and NO metabolite concentrations results were significantly higher, while TAC was significantly lower. Treatment in MS induced significant (p < 0.05) down-regulating of pro-inflammatory sICAM1, TNF-α, IL6, as well as biomarkers of lipid peroxidation and DNA damage production. The protective effect exhibited may occur by decreasing ROS production and increasing antioxidant capacity, turning into a more reduced thiols' status.
 OBJECTIVE: To determine early magnetic resonance imaging (MRI) features of new multiple sclerosis (MS) lesions that will develop into paramagnetic rim lesions (PRLs), which have been associated with progressive tissue injury in MS. METHODS: New contrast-enhancing lesions observed on routine clinical MRI were imaged at 7 T within 4 weeks of observation, and 3 and 6 months later. The 6-month MRI was used to classify PRL status (PRL or non-PRL). The relationship between early lesion characteristics and subsequent PRL status was assessed using generalized linear mixed effects models. Random forest classification was performed to classify early predictors of subsequent PRL status. RESULTS: From 93 contrast-enhancing lesions in 23 MS patients, 37 lesions developed into a PRL. In lesions that developed into PRLs compared with those that did not, the average lesion T(1) on the initial 7 T MRI was 1994 ms compared with 1,670 ms (p-value <0.001), and the average volume was 168.7 mL compared with 44 mL (p-value <0.001) in lesions that did not. These volume differences were also found on 3 T scans (p-value <0.001), and for intensity-normalized T(1) -w (p-value = 0.011) and fluid-attenuated inversion recovery (p-value = 0.005). The area under the receiver operating characteristic curve for the random forest classification with leave-one-out cross-validation was found to be 0.86 using initial 7 T features. INTERPRETATION: New MS lesions that evolve into PRLs can be identified early in lesion evolution. These findings suggest that biological mechanisms underlying PRL development begin early, which has important implications for clinical trials targeting PRLs development and subsequent therapeutics. ANN NEUROL 2023.

 OBJECTIVE: The study aimed to investigate the physical performance, gait, balance, falls efficacy, and step reaction time in individuals with MS. METHODS: A total of 60 individuals (30 individuals with MS and 30 age and sex-matched healthy controls) were enrolled. Individuals' physical performance was evaluated with the Timed Up and Go Test (TUG) and Five-Times-Sit-to-Stand Test (FTSTS). Activities-specific Balance Confidence (ABC) Scale, 12-item Multiple Sclerosis Walking Scale (MSWS-12v2) and Falls Efficacy Scale International (FES-I) were used to assess the balance, gait and fall efficacy of the participants. Individuals' step reaction time (SRT) was calculated with video-based software. The time between the step command and the first contact of the foot with the ground in the first step was recorded. RESULTS: The mean age of the individuals with MS and the control group was 38.5 ± 9.4 years and 33.9 ± 11.7 years, respectively. Significant differences existed between the groups in SRT, FES-I, ABC, and FTSTS (p < 0.05). There was no significant correlation between SRT with any other parameter (p > 0.05). TUG was moderately correlated with MSWS-12 and FES-I (r(1) =0.426, r(2) =0.495, p < 0.05). Besides, there was a moderate correlation between ABC with TUG and FTSTS (r(1) =-0.605, r(2) =-0.468, p < 0.05). A high degree correlation was found between MSWS-12 with FES-I and ABC (r(1) =0.843, r(2) =-0.834, p < 0.05). CONCLUSION: Individuals with MS have decreased SRTs. However, this condition was not found to be related to physical performance. Further studies should focus on the association of SRT with cognitive and psychosocial parameters.
 OBJECTIVE: Wheat has become a main staple globally. We studied the effect of defined pro-inflammatory dietary proteins, wheat amylase trypsin inhibitors (ATI), activating intestinal myeloid cells via toll-like receptor 4, in experimental autoimmune encephalitis (EAE), a model of multiple sclerosis (MS). DESIGN: EAE was induced in C57BL/6J mice on standardised dietary regimes with defined content of gluten/ATI. Mice received a gluten and ATI-free diet with defined carbohydrate and protein (casein/zein) content, supplemented with: (a) 25% of gluten and 0.75% ATI; (b) 25% gluten and 0.19% ATI or (c) 1.5% purified ATI. The effect of dietary ATI on clinical EAE severity, on intestinal, mesenteric lymph node, splenic and central nervous system (CNS) subsets of myeloid cells and lymphocytes was analysed. Activation of peripheral blood mononuclear cells from patients with MS and healthy controls was compared. RESULTS: Dietary ATI dose-dependently caused significantly higher EAE clinical scores compared with mice on other dietary regimes, including on gluten alone. This was mediated by increased numbers and activation of pro-inflammatory intestinal, lymph node, splenic and CNS myeloid cells and of CNS-infiltrating encephalitogenic T-lymphocytes. Expectedly, ATI activated peripheral blood monocytes from both patients with MS and healthy controls. CONCLUSIONS: Dietary wheat ATI activate murine and human myeloid cells. The amount of ATI present in an average human wheat-based diet caused mild intestinal inflammation, which was propagated to extraintestinal sites, leading to exacerbation of CNS inflammation and worsening of clinical symptoms in EAE. These results support the importance of the gut-brain axis in inflammatory CNS disease.
 BACKGROUND: Great advances have been made in the field of multiple sclerosis (MS) therapy due to the publication of numerous randomised clinical trials (RCTs). In this study, we carried out a critical appraisal of phase III RCTs of disease-modifying therapies (DMTs) for MS published after 2010, intending to identify critical areas of improvement. METHODS: We performed a systematic search of published RCTs on MS from January 2010 until December 2021. RCTs were assessed using an ad-hoc tool. This tool was developed based on existing generic methodological instruments and MS-specific guidelines and methodological papers. It included 14 items grouped in 5 domains: methodological quality, adequacy and measurement of outcomes, adverse event reporting, applicability and relevance of results, and transparency and conflict of interest. RESULTS: We identified 31 phase III RCTs. Most of them were fully compliant in terms of sample size (87%), randomisation (68%), blinding (61%), participant selection (68%), adverse event reporting (84%) and clinical relevance (52%). Only a few were compliant in terms of participant description (6%), comparison (42%), attrition bias (26%), adequacy of outcome measures (26%), applicability (23%), transparency (36%) and conflict of interest (6%). None were compliant in terms of analysis and reporting of outcomes. The most common limitations related to the absence of comorbidity data, unjustified use of placebo, inadequacy of outcomes design and absence of protocol and/or prospective registration. CONCLUSIONS: RCTs for DMTs in MS have relevant and frequent limitations. These should be addressed to enhance their quality, transparency and external validity.
 BACKGROUND: There is strong evidence for the benefits of exercise for people with Multiple Sclerosis (MS), however, up to 80% of people with MS report experiencing exacerbated symptoms with elevated body temperatures. A range of cooling garments to assist people with MS manage symptoms of heat sensitivity have been investigated. Therefore, the aim of this systematic review was to assess the effect of cooling garments to improve physical function in people with MS, and to determine any associated physiological and perceptual responses. METHOD: A systematic review adhering to the PRISMA guidelines was performed. The eligibility criteria required investigations to have conducted a randomized controlled trial or cross-over study to assess the effect of a cooling garment to improve physical function, or a related physiological or perceptual measure, in people with MS. RESULTS: Thirteen empirical studies were identified, compromising of acute cross-over designs (61.5%), longitudinal parallel group designs (23.1%) or a combination of both (15.4%). The studies included 384 participants with MS with an expanded disability status scale range of 1-7.5. Garments included liquid-perfused cooling vests/tops/hoods (50.0%), phase-change cooling vests (38.9%), a cooling thigh-cuff (5.6%) and a palm cooling device (5.6%). The cooling garments were effective at improving walking capacity and functional mobility, and some studies demonstrated improvements in muscular strength and balance, but not manual dexterity. The garments also resulted in improved core temperature, skin temperature, thermal sensation and subjective fatigue. Improvements occurred in temperate and warm conditions, and both with and without an exercise stimulus. DISCUSSION: Cooling garments can improve physical function for people with MS. Since none of the cooling garments caused harm, and no particular cooling garment could be identified as being superior, people with MS should experiment with different cooling garments to determine their preference, and industry should focus on cooling garments that are effective, accessible and user-friendly.
 INTRODUCTION: The retina, a window into the brain, allows for the investigation of many disease-associated inflammatory and neurodegenerative changes affecting the central nervous system (CNS). Multiple sclerosis (MS), an autoimmune disease targeting the CNS, typically impacts on the visual system including the retina. Hence, we aimed to establish innovative functional retinal measures of MS-related damage, e.g., spatially resolved non-invasive retinal electrophysiology, backed by established morphological retinal imaging markers, i.e., optical coherence tomography (OCT). METHODS: 20 healthy controls (HC) and 37 people with MS [17 without history of optic neuritis (NON) and 20 with (HON) history of optic neuritis] were included. In this work, we differentially assessed photoreceptor/bipolar cells (distal retina) and retinal ganglion cell (RGC, proximal retina) function besides structural assessment (OCT). We compared two multifocal electroretinography-based approaches, i.e., the multifocal pattern electroretinogram (mfPERG) and the multifocal electroretinogram to record photopic negative response (mfERG (PhNR) ). Structural assessment utilized peripapillary retinal nerve fiber layer thickness (pRNFL) and macular scans to calculate outer nuclear thickness (ONL) and macular ganglion cell inner plexiform layer thickness (GCIPL). One eye was randomly selected per subject. RESULTS: In NON, photoreceptor/bipolar cell layer had dysfunctional responses evidenced by reduced mfERG (PhNR) -N1 peak time of the summed response, but preserved structural integrity. Further, both NON and HON demonstrated abnormal RGC responses as evidenced by the photopic negative response of mfERG (PhNR) (mfPhNR) and mfPERG indices (P < 0.05). Structurally, only HON had thinned retina at the level of RGCs in the macula (GCIPL, P < 0.01) and the peripapillary area (pRNFL, P < 0.01). All three modalities showed good performance to differentiate MS-related damage from HC, 71-81% area under curve. CONCLUSION: In conclusion, while structural damage was evident mainly for HON, functional measures were the only retinal read-outs of MS-related retinal damage that were independent of optic neuritis, observed for NON. These results indicate retinal MS-related inflammatory processes in the retina prior to optic neuritis. They highlight the importance of retinal electrophysiology in MS diagnostics and its potential as a sensitive biomarker for follow-up in innovative interventions.
 Epidemiological studies have demonstrated that Epstein-Barr virus (EBV) is a known etiologic risk factor, and perhaps prerequisite, for the development of MS. EBV establishes life-long latent infection in a subpopulation of memory B cells. Although the role of memory B cells in the pathobiology of MS is well established, studies characterizing EBV-associated mechanisms of B cell inflammation and disease pathogenesis in EBV (+) B cells from MS patients are limited. Accordingly, we analyzed spontaneous lymphoblastoid cell lines (SLCLs) from multiple sclerosis patients and healthy controls to study host-virus interactions in B cells, in the context of an individual's endogenous EBV. We identify differences in EBV gene expression and regulation of both viral and cellular genes in SLCLs. Our data suggest that EBV latency is dysregulated in MS SLCLs with increased lytic gene expression observed in MS patient B cells, especially those generated from samples obtained during "active" disease. Moreover, we show increased inflammatory gene expression and cytokine production in MS patient SLCLs and demonstrate that tenofovir alafenamide, an antiviral that targets EBV replication, decreases EBV viral loads, EBV lytic gene expression, and EBV-mediated inflammation in both SLCLs and in a mixed lymphocyte assay. Collectively, these data suggest that dysregulation of EBV latency in MS drives a pro-inflammatory, pathogenic phenotype in memory B cells and that this response can be attenuated by suppressing EBV lytic activation. This study provides further support for the development of antiviral agents that target EBV-infection for use in MS.
 Black and Hispanic American patients frequently develop earlier onset of multiple sclerosis (MS) and a more severe disease course that can be resistant to disease modifying treatments. The objectives were to identify differential methylation of genomic DNA (gDNA) associated with disease susceptibility and treatment responses in a cohort of MS patients from underrepresented minority populations. Patients with MS and controls with non-inflammatory neurologic conditions were consented and enrolled under an IRB-approved protocol. Approximately 64% of donors identified as Black or African American and 30% as White, Hispanic-Latino. Infinium MethylationEPIC bead arrays were utilized to measure epigenome-wide gDNA methylation of whole blood. Data were analyzed in the presence and absence of adjustments for unknown covariates in the dataset, some of which corresponded to disease modifying treatments. Global patterns of differential methylation associated with MS were strongest for those probes that showed relative demethylation of loci with lower M values. Pathway analysis revealed unexpected associations with shigellosis and amoebiasis. Enrichment analysis revealed an over-representation of probes in enhancer regions and an under-representation in promoters. In the presence of adjustments for covariates that included disease modifying treatments, analysis revealed 10 differentially methylated regions (DMR's) with an FDR <1E-77. Five of these genes (ARID5B, BAZ2B, RABGAP1, SFRP2, WBP1L) are associated with cancer risk and cellular differentiation and have not been previously identified in MS studies. Hierarchical cluster and multi-dimensional scaling analysis of differential DNA methylation at 147 loci within those DMR's was sufficient to differentiate MS donors from controls. In the absence of corrections for disease modifying treatments, differential methylation in patients treated with dimethyl fumarate was associated with immune regulatory pathways that regulate cytokine and chemokine signaling, axon guidance, and adherens junctions. These results demonstrate possible associations of gastrointestinal pathogens and regulation of cellular differentiation with MS susceptibility in our patient cohort. This work further suggests that analyses can be performed in the presence and absence of corrections for immune therapies. Because of their high representation in our patient cohort, these results may be of specific relevance in the regulation of disease susceptibility and treatment responses in Black and Hispanic Americans.
 Altered expression of multiple miRNAs was found to be extensively involved in the pathogenesis of different neurological disorders including Alzheimer's disease, Parkinson's disease, stroke, epilepsy, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington's disease. One of the biggest concerns within gene-based therapy is the delivery of the therapeutic microRNAs to the intended place, which is obligated to surpass the biological barriers without undergoing degradation in the bloodstream or renal excretion. Hence, the delivery of modified and unmodified miRNA molecules using excellent vehicles is required. In this light, mesenchymal stem cells (MSCs) have attracted increasing attention. The MSCs can be genetically modified to express or overexpress a particular microRNA aimed with promote neurogenesis and neuroprotection. The current review has focused on the therapeutic capabilities of microRNAs-overexpressing MSCs to ameliorate functional deficits in neurological conditions.
 Ozonolysis is a widely used and practical synthetic technique for the deconstructive oxidation of olefins using ozone. While there are numerous ozonolysis reactions that give a myriad of products and functionalities, almost all of them involve scission at the olefin double bond. Using ozone as a constructive reagent rather than a deconstructive one would open new domains of chemical reactivity and amplify molecular complexity in synthetic methodology. Here we report the use of primary ozonides as preparative synthetic intermediates for a safe and green olefin syn-dihydroxylation reaction. Furthermore, we have demonstrated this method using a continuous flow reactor that virtually eliminates peroxide accumulation and extended these applications towards the synthesis of pharmaceutically relevant small molecules such as guaifenesin, the active ingredient in Mucinex, and a precursor to ponesimod, a drug to treat multiple sclerosis.

 Initial studies suggested that the fluctuations in the quantity, variety, and composition of the gut microbiota can significantly affect disease processes. This change in the gut microbiota causing negative health benefits was coined dysbiosis. Initial research focused on gastrointestinal illnesses. However, the gut microbiome was found to affect more than just gastrointestinal diseases. Numerous studies have proven that the gut microbiome can influence neuropsychiatric diseases such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis.
 Spinal cord injury (SCI), in addition to motor and sensory problems, may also lead to autonomic dysfunction. Postural orthostatic tachycardia syndrome (POTS) is one of them and has often been reported in traumatic brain injuries, multiple sclerosis, and other spinal cord pathologies. However, there is not much data on POTS in SCI even in extensive databases. We present a case of an adolescent female with paraplegia due to traumatic SCI. During her tilt table training, she started having episodes of sinus tachycardia associated with fatigue, dizziness, headache, palpitations, and presyncope with no orthostatic hypotension, after achieving 60 degrees of head tilt. After ruling out the common causes of tachycardia and syncope, a diagnosis of POTS was established. With pharmacologic and non-pharmacological measures, including metoprolol, increased fluid intake, and compression stockings, her symptoms resolved, and she was able to continue rehabilitation.

 A selection of drugs and vaccines newly available in Switzerland is reviewed. Shingrix: recombinant shingles vaccine recommended for all patients ≥65 years and some immunosuppressed patients. Nirmaltrevir/ritonavir: oral treatment of SARS-CoV-2 with a high potential of drug-drug interactions. Tixagevimab/cilgavimab: antibody combination for pre-exposure prophylaxis of SARS-CoV-2 in subjects without vaccine response or contraindication to vaccine. Cabotegravir/rilpivirine: 1st long-acting injectable treatment for HIV. Imvanex: monkeypox vaccine for subjects most at risk. Tezepelumab: first-in-class treatment for severe asthma. Eptinezumab: another anti-CGRP antibody for the prevention of migraine. Ponesimod: multiple sclerosis treatment with the advantage of a shorter half-life than fingolimod or ozanimod.
 Neutrophils are the first cells to be recruited to sites of acute inflammation and contribute to host defense through phagocytosis, degranulation and neutrophil extracellular traps (NETs). Neutrophils are rarely found in the brain because of the highly selective blood-brain barrier (BBB). However, several diseases disrupt the BBB and cause neuroinflammation. In this regard, neutrophils and NETs have been visualized in the brain after various insults, including traumatic (traumatic brain injury and spinal cord injury), infectious (bacterial meningitis), vascular (ischemic stroke), autoimmune (systemic lupus erythematosus), neurodegenerative (multiple sclerosis and Alzheimer's disease), and neoplastic (glioma) causes. Significantly, preventing neutrophil trafficking into the central nervous system or NET production in these diseases alleviates brain pathology and improves neurocognitive outcomes. This review summarizes the major studies on the contribution of NETs to central nervous system (CNS) disorders.
 Optic neuritis is an inflammatory demyelinating disorder that primarily affects the optic nerve and is often associated with multiple sclerosis. While it is rare for optic neuritis to be accompanied by autoimmune encephalitis, it can occur in some cases. A 65-year-old woman with bipolar disorder presented with a progressively altered mentality. Magnetic resonance imaging of the brain showed no definite abnormal findings. Electroencephalography revealed nonconvulsive status epilepticus. Cerebrospinal fluid study and autoimmune and paraneoplastic encephalitis antibodies were negative. The patient was diagnosed with seronegative autoimmune encephalitis and treated with methylprednisolone, intravenous immunoglobulin, and rituximab. Her condition gradually improved except for persistent blindness on the left side. This case highlights the importance of considering autoimmune encephalitis even in the absence of identifiable pathogenic antibodies when clinical manifestations and response to immunotherapy support such a diagnosis.
 The clinical significance of Epstein-Barr virus (EBV) cannot be understated. Not only does it infect approximately 90% of the world's population, but it is also associated with numerous pathologies. Diseases linked to this virus include hematologic malignancies such as diffuse large B-cell lymphoma, Hodgkin lymphoma, Burkitt lymphoma, primary CNS lymphoma, and NK/T-cell lymphoma, epithelial malignancies such as nasopharyngeal carcinoma and gastric cancer, autoimmune diseases such as multiple sclerosis, Graves' disease, and lupus. While treatment for these disease states is ever evolving, much work remains to more fully elucidate the relationship between EBV, its associated disease states, and their treatments. This paper begins with an overview of EBV latency and latency-associated proteins. It will then review EBV's contributions to select hematologic malignancies with a focus on the contribution of latent proteins as well as their associated management.
 Altered expression of vacuole membrane protein 1 (VMP1) has recently been observed in the context of multiple sclerosis and Parkinson’s disease (PD). However, how changes in VMP1 expression may impact pathogenesis has not been explored. Here, we report that genetic deletion of VMP1 from a monocytic cell line resulted in increased NLRP3 inflammasome activation and release of proinflammatory molecules. Examination of the VMP1 dependent changes in these cells revealed that VMP1 deficiency led to decreased SERCA activity and increased intracellular [Ca (2+) ]. We also observed calcium overload in mitochondria in VMP1 depleted cells, which was associated with mitochondrial dysfunction and release of mitochondrial DNA into the cytoplasm and the extracellular environment. Autophagic defects were also observed in VMP1 depleted macrophages. Collectively, these studies reveal VMP1 as a negative regulator of inflammatory responses, and we postulate that decreased expression of VMP1 can aggravate the inflammatory sequelae associated with neurodegenerative diseases like PD.
 Immune globulin G (IgG) is a normal component of breastmilk. Data from 2 mothers indicate that IgG concentrations in milk are normal or higher and IgM levels in milk are normal or lower during intravenous immunoglobulin (IVIG) therapy. The antibacterial activity of milk in these women was normal. There appears to be an emerging consensus that intravenous immune globulin is the treatment of choice for postpartum mothers with multiple sclerosis who are breastfeeding,[1-4] although one retrospective study failed to find a decrease in relapse rate among mothers who received IgG postpartum.[5] Rare cases of transient rash have been reported in breastfed infants during maternal IVIG therapy. No special precautions are required during breastfeeding.
 Aging is a major risk factor for several neurodegenerative diseases and is associated with cognitive decline. In addition to affecting neuronal function, the aging process significantly affects the functional phenotype of the glial cell compartment, comprising oligodendrocyte lineage cells, astrocytes, and microglia. These changes result in a more inflammatory microenvironment, resulting in a condition that is favorable for neuron and synapse loss. In addition to facilitating neurodegeneration, the aging glial cell population has negative implications for central nervous system remyelination, a regenerative process that is of particular importance to the chronic demyelinating disease multiple sclerosis. This review will discuss the changes that occur with aging in the three main glial populations and provide an overview of the studies documenting the impact these changes have on remyelination.
 OBJECTIVES: To achieve consensus on the performance, interpretation and reporting of MS imaging according to up-to-date guidelines using the Peer Learning Methodology. MATERIALS AND METHODS: We utilized the Peer Learning Methodology to engage our clinical and radiology colleagues, review the current guidelines, acheive consensus on imaging techniques and reporting standards. After implementing changes, we collected radiologist feedback on the impact of the optimized images on their interpretation. RESULTS: Survey responders indicated a strong preference for the new protocol in terms of overall image quality, individual lesions conspicuity and confidence in the ability to detect an MS lesion. The new protocol was preferred for both MS diagnosis and MS surveillance in 25 of 28 responses. CONCLUSION: The Peer Learning Methodology is an effective tool to standardize and improve MR imaging quality, interpretation and reporting for Multiple Sclerosis in accordance with current guidelines.
 Myelin is a modified cell membrane that forms a multilayer sheath around the axon. It retains the main characteristics of biological membranes, such as lipid bilayer, but differs from them in several important respects. In this review, we focus on aspects of myelin composition that are peculiar to this structure and differentiate it from the more conventional cell membranes, with special attention to its constituent lipid components and several of the most common and important myelin proteins: myelin basic protein, proteolipid protein, and myelin protein zero. We also discuss the many-fold functions of myelin, which include reliable electrical insulation of axons to ensure rapid propagation of nerve impulses, provision of trophic support along the axon and organization of the unmyelinated nodes of Ranvier, as well as the relationship between myelin biology and neurologic disease such as multiple sclerosis. We conclude with a brief history of discovery in the field and outline questions for future research.
 Transverse myelitis (TM) is a rare, acquired focal inflammatory disorder often presenting with rapid onset weakness, sensory deficits, and bowel/bladder dysfunction. Generally occurring independently; often as a complication of infection; however, it may also exist as part of a continuum of other neuro-inflammatory disorders. Some of the included continua are acute disseminated encephalomyelitis, multiple sclerosis, neuromyelitis optica spectrum disorder, and acute flaccid myelitis. TM generally occurs at the spinal cord at any level, but most commonly affects the thoracic region. The disorder transverses the spinal cord causing bilateral deficiencies. However, there may only be partial or asymmetric involvement. The duration of this disease may be as little as 3 to 6 months or may become permanently debilitating. At peak deficit, 50% of patients are complete paraplegic with virtually all of the patients having a degree of bladder/bowel dysfunction. Approximately 33% of patients recover with little to no lasting deficits, 33% have a moderate degree of permanent disability, and 33% are permanently disabled.
 Standardized or simulated patients (SPs) have become an essential aspect of medical education. They date back to the 1960s when Dr. Howard Barrows of the University of Southern California first utilized them to simulate multiple sclerosis patients and trained them to evaluate learners as well. Dr. Paula Stillman of the University of Arizona is identified as another early user of SPs, training actors in the 1970s to portray mothers of child patients to assist students with acquiring appropriate histories. She is also cited as one of the first to use ‘standardized actors’ to teach physical exam and direct students on how to perform aspects of the physical correctly. Building upon these successes, SPs have slowly been embraced in the medical education community, especially at the undergraduate level, where they are utilized for formative assessment in the form of the Objective Structured Clinical Exam (OSCE) and the summative evaluation in the form of the USMLE Step 2 CS. SPs have also been utilized in graduate medical education in more formative roles and have been applied to other medical disciplines, including nursing, physical therapy, and respiratory therapy. The flexibility of SPs in their ability to be utilized in multiple disciplines and multiple education levels and its superiority in the development of learner interpersonal skills all serve to emphasize the importance of having a strong standardized patient program.
 Over the last decade, our understanding of spliceosome structure and function has significantly improved, refining the study of the impact of dysregulated splicing on human disease. As a result, targeted splicing therapeutics have been developed, treating various diseases including spinal muscular atrophy and Duchenne muscular dystrophy. These advancements are very promising and emphasize the critical role of proper splicing in maintaining human health. Herein, we provide an overview of the current information on the composition and assembly of early splicing complexes-commitment complex and pre-spliceosome-and their association with human disease.
 (1) Background: Even though music therapy is acknowledged to have positive benefits in neurology, there is still a lack of knowledge in the literature about the applicability of music treatments in clinical practice with a neurological population using wearable devices. (2) Methods: a systematic review was conducted following PRISMA 2020 guidelines on the 29 October 2022, searching in five databases: PubMed, PEDro, Medline, Web of Science, and Science Direct. (3) Results: A total of 2964 articles were found, including 413 from PubMed, 248 from Web of Science, 2110 from Science Direct, 163 from Medline, and none from PEDro. Duplicate entries, of which there were 1262, were eliminated. In the first screening phase, 1702 papers were screened for title and abstract. Subsequently, 1667 papers were removed, based on population, duplicate, outcome, and poor study design. Only 15 studies were considered after 35 papers had their full texts verified. Results showed significant values of spatiotemporal gait parameters in music-based therapy rhythmic auditory stimulation (RAS), including speed, stride length, cadence, and ROM. (4) Conclusions: The current findings confirm the value of music-based therapy RAS as a favorable and effective tool to implement in the health care system for the rehabilitation of patients with movement disorders.
 Autoimmune diseases (AIDs) are the consequence of a breach in immune tolerance, leading to the inability to sufficiently differentiate between self and non-self. Immune reactions that are targeted towards self-antigens can ultimately lead to the destruction of the host's cells and the development of autoimmune diseases. Although autoimmune disorders are comparatively rare, the worldwide incidence and prevalence is increasing, and they have major adverse implications for mortality and morbidity. Genetic and environmental factors are thought to be the major factors contributing to the development of autoimmunity. Viral infections are one of the environmental triggers that can lead to autoimmunity. Current research suggests that several mechanisms, such as molecular mimicry, epitope spreading, and bystander activation, can cause viral-induced autoimmunity. Here we describe the latest insights into the pathomechanisms of viral-induced autoimmune diseases and discuss recent findings on COVID-19 infections and the development of AIDs.
 Natural therapeutic microorganisms provide a potent alternative healthcare treatment nowadays, with the potential to prevent several human diseases. These health-boosting living organisms, probiotics mostly belong to Gram-positive bacteria such as Lactobacillus, Bifidobacterium, Streptococcus, Saccharomyces, Bacillus and Enterococcus. Initiated almost a century ago, the probiotic application has come a long way. The present review is focused on the potential therapeutic role of probiotics in ameliorating multiple infections, such as upper respiratory tract infections and viral respiratory infections, including COVID-19; liver diseases and hepatic encephalopathy; neurological and psychiatric disorders; autoimmune diseases, particularly rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis. Apart from these, the therapeutic exacerbations of probiotics in urinary tract infections have been extremely promising, and several approaches are reviewed and presented here. We also present upcoming and new thrust areas where probiotic therapeutic interventions are showing promising results, like faecal microbial transplant and vaginal microbial transplant.
 Sphingosine 1-phosphate lyase (SPL) is the terminal enzyme that controls the degradation of the bioactive lipid sphingosine 1-phosphate (S1P) within an interconnected sphingolipid metabolic network. The unique metabolic position of SPL in maintaining S1P levels implies SPL could be an emerging new therapeutic target. Over the past decade, an evolving effort has been made to unravel the role of SPL in the nervous system; however, to what extent SPL influences the developing and mature nervous system through altering S1P biosynthesis remains opaque. While congenital SPL deletion is associated with deficits in the developing nervous system, the loss of SPL activity in adults appears to be neuroprotective in acquired neurological disorders. The controversial findings concerning SPL's role in the nervous system are further constrained by the current genetic and pharmacological tools. This review attempts to focus on the multi-faceted nature of SPL function in the mammalian nervous systems, implying its dichotomy in the developing and adult central nervous system (CNS). This article also highlights SPL is emerging as a therapeutic molecule that can be selectively targeted to modulate S1P for the treatment of acquired neurodegenerative diseases, raising new questions for future investigation. The development of cell-specific inducible conditional SPL mutants and selective pharmacological tools will allow the precise understanding of SPL's function in the adult CNS, which will aid the development of a new strategy focusing on S1P-based therapies for neuroprotection.
 Autoimmune diseases (AIDs) are poorly understood clinical syndromes due to breakdown of immune tolerance towards specific types of self-antigens. They are generally associated with an inflammatory response mediated by lymphocytes, autoantibodies or both. Ultimately, chronic inflammation culminates in tissue damages and clinical manifestations. AIDs affect 5% of the world population, and they represent the main cause of fatality in young to middle-aged females. In addition, the chronic nature of AIDs has a devastating impact on the patient's quality of life. It also places a heavy burden on the health care system. Establishing a rapid and accurate diagnosis is considered vital for an ideal medical management of these autoimmune disorders. However, for some AIDs, this task might be challenging. Vibrational spectroscopies, and more particularly Fourier-transform infrared (FTIR) spectroscopy, have emerged as universal analytical techniques with promising applications in the diagnosis of various types of malignancies and metabolic and infectious diseases. The high sensitivity of these optical sensing techniques and their minimal requirements for test reagents qualify them to be ideal analytical techniques. The aim of the current review is to explore the potential applications of FTIR spectroscopy in the diagnosis and management of most common AIDs. It also aims to demonstrate how this technique has contributed to deciphering the biochemical and physiopathological aspects of these chronic inflammatory diseases. The advantages that can be offered by this optical sensing technique over the traditional and gold standard methods used in the diagnosis of these autoimmune disorders have also been extensively discussed.
 Regulatory B cells (Bregs) are immunosuppressive cells that support immunological tolerance by the production of interleukin (IL)-10, IL-35, and transforming growth factor β (TGF-β). Bregs arise from different developmental stages in response to inflammatory stimuli. In that regard, mounting evidence points towards a direct influence of gut microbiota on mucosal B cell development, activation, and regulation in health and disease. While an increasing number of diseases are associated with alterations in gut microbiome (dysbiosis), little is known about the role of microbiota on Breg development and induction in neuroinflammatory disorders. Notably, gut-originating, IL-10- and immunoglobulin A (IgA)-producing regulatory plasma cells have recently been demonstrated to egress from the gut to suppress inflammation in the central nervous system (CNS) raising fundamental questions about the triggers and functions of mucosal-originating Bregs in systemic inflammation. Advancing our understanding of regulatory B cells in neuroinflammatory diseases could lead to novel therapeutic approaches. Here, we summarize main aspects about regulatory B cell differentiation and functions and evidence about their involvement in neuroinflammatory diseases. Further, we highlight current data of gut-originating regulatory B cells and their microbial interactions and discuss future microbiota-/regulatory B cell-targeted therapies in immune-mediated diseases. This article is protected by copyright. All rights reserved.
 Neurofilaments (NFs) are not only important for axonal integrity and nerve conduction in large myelinated axons but they are also thought to be crucial for receptor and synaptic functioning. Therefore, NFs may play a critical role in cognitive functions, as cognitive processes are known to depend on synaptic integrity and are modulated by dopaminergic signaling. Here, we present a theory-driven interdisciplinary approach that NFs may link inflammation, neurodegeneration, and cognitive functions. We base our hypothesis on a wealth of evidence suggesting a causal link between inflammation and neurodegeneration and between these two and cognitive decline (see Fig. 1), also taking dopaminergic signaling into account. We conclude that NFs may not only serve as biomarkers for inflammatory, neurodegenerative, and cognitive processes but also represent a potential mechanical hinge between them, moreover, they may even have predictive power regarding future cognitive decline. In addition, we advocate the use of both NFs and MRI parameters, as their synthesis offers the opportunity to individualize medical treatment by providing a comprehensive view of underlying disease activity in neurological diseases. Since our society will become significantly older in the upcoming years and decades, maintaining cognitive functions and healthy aging will play an important role. Thanks to technological advances in recent decades, NFs could serve as a rapid, noninvasive, and relatively inexpensive early warning system to identify individuals at increased risk for cognitive decline and could facilitate the management of cognitive dysfunctions across the lifespan.
 Central nervous system (CNS) diseases are currently a major challenge in medicine. One reason is the presence of the blood-brain barrier, which is a significant limitation for currently used medicinal substances that are characterized by a high molecular weight and a short half-life. Despite the application of nanotechnology, there is still the problem of targeting and the occurrence of systemic toxicity. Viral vectors and virus-like particles (VLPs) may provide a promising solution to these challenges. Their small size, biocompatibility, ability to carry medicinal substances, and specific targeting of neural cells make them useful in research when formulating a new generation of biological carriers. Additionally, the possibility of genetic modification has the potential for gene therapy. Among the most promising viral vectors are adeno-associated viruses, adenoviruses, and retroviruses. This is due to their natural tropism to neural cells, as well as the possibility of genetic and surface modification. Moreover, VLPs that are devoid of infectious genetic material in favor of increasing capacity are also leading the way for research on new drug delivery systems. The aim of this study is to review the most recent reports on the use of viral vectors and VLPs in the treatment of selected CNS diseases.
 An unmet clinical goal in demyelinating pathologies is to restore the myelin sheath prior to neural degeneration. N-acetylaspartate (NAA) is an acetylated derivative form of aspartate, abundant in the healthy brain but severely reduced during traumatic brain injury and in patients with neurodegenerative pathologies. How extracellular NAA variations impact the remyelination process and, thereby, the ability of oligodendrocytes to remyelinate axons remains unexplored. Here, we evaluated the remyelination properties of the oligodendroglial (OL) mouse cell line Oli-neuM under different concentrations of NAA using a combination of biochemical, qPCR, immunofluorescence assays, and in vitro engagement tests, at NAA doses compatible with those observed in healthy brains and during brain injury. We observed that oligodendroglia cells respond to decreasing levels of NAA by stimulating differentiation and promoting gene expression of myelin proteins in a temporally regulated manner. Low doses of NAA potently stimulate Oli-neuM to engage with synthetic axons. Furthermore, we show a concentration-dependent expression of specific histone deacetylases essential for MBP gene expression under NAA or Clobetasol treatment. These data are consistent with the idea that oligodendrocytes respond to lowering the NAA concentration by activating the remyelination process via deacetylase activation.
 BACKGROUND: Progressive multifocal leukoencephalopathy (PML), an important identified risk for natalizumab, has been described for standard interval dosing (SID; dosing interval every-4-weeks). Information on PML with natalizumab extended interval dosing (EID; dosing interval >every-4-weeks) in the US and the rest of the world (ROW) is limited. RESEARCH DESIGN AND METHODS: A retrospective analysis of patient demographics, risk factors, clinical characteristics, and clinical outcomes was conducted on confirmed natalizumab EID and SID PML cases evaluated from Biogen pharmacovigilance systems. RESULTS: Of 857 confirmed natalizumab PML cases, EID and SID accounted for 7.5% and 92.5%, respectively (US: 12.9% and 87.1%; ROW: 5.4% and 94.6%). PML risk factors included anti-JCV index > 1.5 (US: EID, 56.7% and SID, 12.8%; ROW: EID, 44.1% and SID, 21.0%), mean duration of natalizumab treatment (US: 90.0 and 70.2 months; ROW: 54.1 and 49.8 months), and prior immunosuppressive therapy (US: 20.0% and 21.7%; ROW:11.8% and 18.0%). In the EID and SID groups, 68.8% and 76.0% of patients, respectively, were alive at up to 2 years after diagnosis. CONCLUSIONS: This analysis provides insights on PML in patients receiving natalizumab that extend current knowledge, particularly regarding PML in patients receiving natalizumab EID, which can be built upon in the future.
 Biomodulina T (InmunyVital®) is a thymic factor that modulates immune response and inflammation. Biomodulina T stimulates the differentiation, maturation and proliferation of T cells. Additionally, Biomodulina T improves the ability of T cells to produce cytokines, therefore enhancing T lymphocyte function. Biomodulina T stimulates the thymus gland and, thus, promotes the recovery of normal thymus size in children with thymic hypoplasia and restores the functions of immunosenescent T cells in aging people. In 1984 Rodriguez Martin RR established the laboratory of Biomodulators, where he created and developed an immunomodulatory thymic factor that he named "Biomodulina T." The biological activity of Biomodulina T was demonstrated in several studies. An extensive series of preclinical toxicological studies were conducted and these studies demonstrated that Biomodulina T is an active and safe thymic factor. Clinical trials were conducted with Biomodulina T in patients with immunodeficiency and infections, autoimmune diseases, older adults with recurrent respiratory infections, and cancer. In 1994, we obtained the approval of Biomodulina T as an immunomodulatory drug. This article identifies the milestones involved in the development of Biomodulina T. Since its discovery more than 35 years ago, reports show that Biomodulina T is a modulator of immune response and inflammation that is very useful for restoring the immune system in young and elderly people with immunodeficiencies, autoimmune diseases, and infections. Biomodulina T is also useful as an immunotherapeutic agent for improving immune responses in cancer and vaccines, for reversing immunosenescence and for improving healthspan in aging.
 Compelling evidence has shown that interferon (IFN)-γ has dual effects in multiple sclerosis and in its animal model of experimental autoimmune encephalomyelitis (EAE), with results supporting both a pathogenic and beneficial function. However, the mechanisms whereby IFN-γ may promote neuroprotection in EAE and its effects on central nervous system (CNS)-resident cells have remained an enigma for more than 30 years. In this study, the impact of IFN-γ at the peak of EAE, its effects on CNS infiltrating myeloid cells (MC) and microglia (MG), and the underlying cellular and molecular mechanisms were investigated. IFN-γ administration resulted in disease amelioration and attenuation of neuroinflammation associated with significantly lower frequencies of CNS CD11b(+) myeloid cells and less infiltration of inflammatory cells and demyelination. A significant reduction in activated MG and enhanced resting MG was determined by flow cytometry and immunohistrochemistry. Primary MC/MG cultures obtained from the spinal cord of IFN-γ-treated EAE mice that were ex vivo re-stimulated with a low dose (1 ng/ml) of IFN-γ and neuroantigen, promoted a significantly higher induction of CD4(+) regulatory T (Treg) cells associated with increased transforming growth factor (TGF)-β secretion. Additionally, IFN-γ-treated primary MC/MG cultures produced significantly lower nitrite in response to LPS challenge than control MC/MG. IFN-γ-treated EAE mice had a significantly higher frequency of CX3CR1(high) MC/MG and expressed lower levels of program death ligand 1 (PD-L1) than PBS-treated mice. Most CX3CR1(high)PD-L1(low)CD11b(+)Ly6G(-) cells expressed MG markers (Tmem119, Sall2, and P2ry12), indicating that they represented an enriched MG subset (CX3CR1(high)PD-L1(low) MG). Amelioration of clinical symptoms and induction of CX3CR1(high)PD-L1(low) MG by IFN-γ were dependent on STAT-1. RNA-seq analyses revealed that in vivo treatment with IFN-γ promoted the induction of homeostatic CX3CR1(high)PD-L1(low) MG, upregulating the expression of genes associated with tolerogenic and anti-inflammatory roles and down-regulating pro-inflammatory genes. These analyses highlight the master role that IFN-γ plays in regulating microglial activity and provide new insights into the cellular and molecular mechanisms involved in the therapeutic activity of IFN-γ in EAE.
 BACKGROUND: Hopelessness is a risk factor for depression and suicide. There is little information on this phenomenon among patients with relapsing-remitting multiple sclerosis (RRMS), one of the most common causes of disability and loss of autonomy in young adults. The aim of this study was to assess state hopelessness and its associated factors in early-stage RRMS. METHODS: A multicenter, non-interventional study was conducted. Adult patients with a diagnosis of RRMS, a disease duration ≤ 3 years, and an Expanded Disability Status Scale (EDSS) score of 0-5.5 were included. The State-Trait Hopelessness Scale (STHS) was used to measure patients´ hopelessness. A battery of patient-reported and clinician-rated measurements was used to assess clinical status. A multivariate logistic regression analysis was conducted to determine the association between patients' characteristics and state hopelessness. RESULTS: A total of 189 patients were included. Mean age (standard deviation-SD) was 36.1 (9.4) years and 71.4% were female. Median disease duration (interquartile range-IQR) was 1.4 (0.7, 2.1) years. Symptom severity and disability were low with a median EDSS (IQR) score of 1.0 (0, 2.0). A proportion of 65.6% (n=124) of patients reported moderate-to-severe hopelessness. Hopelessness was associated with older age (p=0.035), depressive symptoms (p=<0.001), a threatening illness perception (p=0.001), and psychological and cognitive barriers to workplace performance (p=0.029) in the multivariate analysis after adjustment for confounders. CONCLUSION: Hopelessness was a common phenomenon in early-stage RRMS, even in a population with low physical disability. Identifying factors associated with hopelessness may be critical for implementing preventive strategies helping patients to adapt to the new situation and cope with the disease in the long term.
 BACKGROUND: Fatigue is one of the most frequent symptoms in persons with multiple sclerosis (pwMS) and impacts health-related quality of life (HRQoL). A multidisciplinary rehabilitation approach is recommended for the treatment of fatigue in pwMS. However, high-quality evidence exists only for unimodal interventions, such as physical therapies/exercise or energy/fatigue management programmes. The primary objective of the current study was to test the hypothesis that a combination of inpatient energy management education (IEME) and high-intensity interval training (HIIT) is superior to a combination of progressive muscle relaxation (PMR) and moderate continuous training (MCT) for improving HRQoL at 6-month follow-up in fatigued pwMS. METHODS: A randomized (1:1) controlled superiority trial with fatigued pwMS >18 years of age, with Expanded Disability Status Scale (EDSS) score ≤6.5, recruited at the Valens clinic, Switzerland. Participants in the experimental group performed IEME twice and HIIT 3 times per week and those in the usual care group performed PMR twice and MCT 3 times per week, during a 3-week inpatient rehabilitation stay. Primary outcome was HRQoL (Physical and Mental Component Scales of the Medical Outcome Study 36-item Short Form Health Survey (SF-36)), assessed at entry to the clinic (T(0)), after 3 weeks' rehabilitation (T(1)) and 4 (T(2)) and 6 (T(3)) months after T(0). Secondary outcomes included SF-36 subscales, fatigue (Fatigue Scale for Motor and Cognitive Functions (FSMC)), mood (Hospital Anxiety and Depression Scale (HADS)), self-efficacy for performing energy conservation strategies (Self-Efficacy for Performing Energy Conservation Strategies Assessment (SEPECSA)), self-perceived competence in activities of daily living (Occupational Self Assessment (OSA)) and cardiorespiratory fitness (peak oxygen consumption (VȮ(2peak))). Data were analysed using a mixed model for repeated measures approach. RESULTS: A total of 106 pwMS (age (years): 49.75 (9.87), 66% female, EDSS: 4.64 (1.32)) were recruited. There were no significant group × time interaction effects in the primary and secondary outcomes. There were significant between-group differences in the pairwise comparisons of the group × time interaction in favour of the IEME + HIIT group at: (i) T(1) in cardiorespiratory fitness (p = 0.011) and SEPECSA (p = 0.032); (ii) T(2) in SF-36 mental health subscale (p = 0.022), HADS anxiety subscale (p = 0.014) and SEPECSA (p = 0.040); (iii) T(3) in SF-36 physical functioning subscale (p = 0.012) and SEPECSA (p = 0.003). CONCLUSION: IEME + HIIT was not superior to PMR + MCT regarding the effects on HRQoL (SF-36 Physical and Mental Component Scales) at 6-month follow-up in pwMS. However, there were significant between-group differences in favour of IEME + HIIT in physical functioning and mental health (SF-36 subscales), anxiety (HADS), cardiorespiratory fitness (VȮ(2peak)) and self-efficacy (SEPECSA) at different measurement time-points that need to be considered in clinical practice.
 The present study aimed to investigate the effects of 8-week of coenzyme Q10 (CoQ10) supplementation alone or combined with concurrent training (CT) on functional capacity, serum brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in multiple sclerosis (MS) patients. Our hypothesis is that CT promotes improvements in the studied outcomes with higher results for the combination of CT and CoQ10. Randomized placebo-controlled trial. Twenty-eight patients with MS were randomly divided into 4 groups: CT+placebo, CT+CoQ10, CoQ10 and placebo. CT involved two resistance training sessions and one aerobic training session per week. CoQ10 was supplemented with 200 mg daily. Serum levels of BDNF, NGF and functional tests [timed up and go (TUG), 6-min walk (6MW), chest press, lateral pull down, leg extension, and lying leg curls one repetition maximum] were measured before and after the intervention period. CT+placebo and CT+CoQ10 significantly improved performance in TUG, 6MW, chest press, lateral pull down, leg extension, and lying leg curls, with superior results to both CoQ10 and placebo groups. Changes in TUG for CT+placebo were significantly higher than CT+CoQ10 (p<0.05). There were no significant differences in NGF and BDNF among the four groups (p >0.05). CT improves physical abilities in patient with MS, regardless CoQ10 supplementation. CT should be recommended for MS patients to increase functional capacity, but there seems to be no benefit in supplementing CoQ10.
 Ca(2+) signaling is one of the essential signaling systems for T lymphocyte activation, the latter being an essential step in the pathogenesis of autoimmune diseases such as multiple sclerosis (MS). Store-operated Ca(2+) entry (SOCE) ensures long lasting Ca(2+) signaling and is of utmost importance for major downstream T lymphocyte activation steps, e.g. nuclear localization of the transcription factor 'nuclear factor of activated T cells' (NFAT). 2-Methoxyestradiol (2ME2), an endogenous metabolite of estradiol (E2), blocks nuclear translocation of NFAT. The likely underlying mechanism is inhibition of SOCE, as shown for its synthetic sulfamate ester analogue 2-ethyl-3-sulfamoyloxy-17β-cyanomethylestra-1,3,5(10)-triene (STX564). Here, we demonstrate that another synthetic bis-sulfamoylated 2ME2 derivative, 2-methoxyestradiol-3,17-O,O-bis-sulfamate (2-MeOE2bisMATE, STX140), an orally bioavailable, multi-targeting anticancer agent and potent steroid sulfatase (STS) inhibitor, antagonized SOCE in T lymphocytes. Downstream events, e.g. secretion of the pro-inflammatory cytokines interferon-γ and interleukin-17, were decreased by STX140 in in vitro experiments. Remarkably, STX140 dosed in vivo completely blocked the clinical disease in both active and transfer experimental autoimmune encephalomyelitis (EAE) in Lewis rats, a T cell-mediated animal model for MS, at a dose of 10 mg/kg/day i.p., whereas neither 2ME2 nor Irosustat, a pure STS inhibitor, showed any effect. The STS inhibitory activity of STX140 is therefore not responsible for its activity in this model. Taken together, inhibition of SOCE by STX140 resulting in full antagonism of clinical symptoms in EAE in the Lewis rat, paired with the known excellent bioavailability and pharmaceutical profile of this drug, open potentially new therapeutic avenues for the treatment of MS.
 Background: People with chronic illnesses have increased morbidity and mortality associated with COVID-19 infection. The influence of a person's serious and/or comorbid chronic illness on COVID-19 vaccine uptake is not well understood. Aim: To undertake an in-depth exploration of factors influencing COVID-19 vaccine uptake among those with various serious and/or chronic diseases in the Australian context, using secondary data analysis of a survey study. Methods: Adults with cancer, diabetes and multiple sclerosis (MS) were recruited from 10 Australian health services to undertake a cross-sectional online survey (30 June to 5 October 2021) about COVID-19 vaccine uptake, vaccine hesitancy, confidence and complacency and disease-related decision-making impact. Free-text responses were invited regarding thoughts and feelings about the interaction between the participant's disease, COVID-19, and vaccination. Qualitative thematic analysis was undertaken using an iterative process and representative verbatim quotes were chosen to illustrate the themes. Results: Of 4683 survey responses (cancer 3560, diabetes 842, and MS 281), 1604 (34.3%) included free-text comments for qualitative analysis. Participants who provided these were significantly less likely to have received a COVID-19 vaccination than those who did not comment (72.4% and 86.2%, respectively). People with diabetes were significantly less likely to provide free-text comments than those with cancer or MS (29.0%, 35.1% and 39.9%, respectively). Four key themes were identified from qualitative analysis, which were similar across disease states: (1) having a chronic disease heightened perceived susceptibility to and perceived severity of COVID-19; (2) perceived impact of vaccination on chronic disease management and disease-related safety; (3) uncertain benefits of COVID-19 vaccine; and (4) overwhelming information overload disempowering patients. Conclusions: This qualitative analysis highlights an additional layer of complexity related to COVID-19 vaccination decision making in people with underlying health conditions. Appreciation of higher susceptibility to severe COVID-19 outcomes appears to be weighed against uncertain impacts of the vaccine on the progression and management of the comorbid disease. Interactions by clinicians addressing individual factors may alleviate concerns and maximise vaccine uptake in people with significant underlying health conditions.
 Long-term cognitive dysfunction, or "chemobrain", has been observed in cancer patients treated with chemotherapy. Mitoxantrone (MTX) is a topoisomerase II inhibitor that binds and intercalates with DNA, being used in the treatment of several cancers and multiple sclerosis. Although MTX can induce chemobrain, its neurotoxic mechanisms are poorly studied. This work aimed to identify the adverse outcome pathways (AOPs) activated in the brain upon the use of a clinically relevant cumulative dose of MTX. Three-month-old male CD-1 mice were given a biweekly intraperitoneal administration of MTX over the course of three weeks until reaching a total cumulative dose of 6 mg/kg. Controls were given sterile saline in the same schedule. Two weeks after the last administration, the mice were euthanized and their brains removed. The left brain hemisphere was used for targeted profiling of the metabolism of glutathione and the right hemisphere for an untargeted metabolomics approach. The obtained results revealed that MTX treatment reduced the availability of cysteine (Cys), cysteinylglycine (CysGly), and reduced glutathione (GSH) suggesting that MTX disrupts glutathione metabolism. The untargeted approach revealed metabolic circuits of phosphatidylethanolamine, catecholamines, unsaturated fatty acids biosynthesis, and glycerolipids as relevant players in AOPs of MTX in our in vivo model. As far as we know, our study was the first to perform such a broad profiling study on pathways that could put patients given MTX at risk of cognitive deficits.
 The imbalance between pathogenic and protective T cell subsets is a cardinal feature of autoimmune disorders such as multiple sclerosis (MS). Emerging evidence indicates that endogenous and dietary-induced changes in fatty acid metabolism have a major impact on both T cell fate and autoimmunity. To date, however, the molecular mechanisms that underlie the impact of fatty acid metabolism on T cell physiology and autoimmunity remain poorly understood. Here, we report that stearoyl-CoA desaturase-1 (SCD1), an enzyme essential for the desaturation of fatty acids and highly regulated by dietary factors, acts as an endogenous brake on regulatory T-cell (Treg) differentiation and augments autoimmunity in an animal model of MS in a T cell-dependent manner. Guided by RNA sequencing and lipidomics analysis, we found that the absence of Scd1 in T cells promotes the hydrolysis of triglycerides and phosphatidylcholine through adipose triglyceride lipase (ATGL). ATGL-dependent release of docosahexaenoic acid enhanced Treg differentiation by activating the nuclear receptor peroxisome proliferator-activated receptor gamma. Our findings identify fatty acid desaturation by SCD1 as an essential determinant of Treg differentiation and autoimmunity, with potentially broad implications for the development of novel therapeutic strategies and dietary interventions for autoimmune disorders such as MS.
 Chemical exchange saturation transfer (CEST) sensitively detects molecular alterations in the brain, such as relayed nuclear Overhauser effect (rNOE) CEST contrast at -3.5 ppm representing aliphatic protons in both lipids and proteins, and CEST contrast at 3.5 ppm correlating with amide proton in proteins. Myelin is rich in lipids and proteins, and therefore CEST can be explored as a biomarker for myelin pathology, which could contribute to the diagnosis and prognosis of multiple sclerosis (MS). In the current study, we investigate the specificity of aliphatic rNOE and the amide pool in myelin detection using the cuprizone (CPZ) mouse model, which recapitulates the demyelination and remyelination of MS. In this study, preclinical 3T MRI was performed in 19 male C57BL/6 mice. Mice in the normal control (NC) group (n = 9) were fed a normal diet for the whole course, while mice in the CPZ group (n = 10) were fed with CPZ for 10 weeks, followed by 4 weeks with a normal diet. The CEST contrast of rNOE (-3.5 ppm) and amide (3.5 ppm) in brain regions of the corpus callosum (CC) and the caudate putamen were compared. Statistical differences between the groups were calculated using two-way ANOVA. We observed significantly decreased rNOE (NC: 4.85% ± 0.09%/s vs. CPZ: 3.88% ± 0.18%/s, p = 0.007) and amide pool (NC: 3.20% ± 0.10%/s vs. CPZ: 2.46% ± 0.16%/s, p = 0.02) in the CC after 8 weeks on CPZ diet (p < 0.05). Moreover, the rNOE in the CPZ group recovered to a level comparable with the NC group at week 14 (p = 0.39), while amide remained at a level as low as that for the NC group (p = 0.051). Significant rNOE and amide changes, validated by immunohistochemistry results for demyelination and remyelination, demonstrate the huge potential of CEST for revealing myelin pathology, which has implications for MS identification at the clinical field strength of 3T.
 OBJECTIVE: MOG antibodies (MOG-Ab) distinguish multiple sclerosis (MS) from MOG-associated disease (MOGAD) in most cases. However, studies analyzing MOG-Ab at the time of a first demyelinating event suggestive of MS in adults are lacking. We aimed to 1) evaluate the prevalence of MOG-Ab in a first demyelinating event suggestive of MS, and 2) compare clinical and paraclinical features between seropositive (MOG-Ab+) and seronegative (MOG-Ab-) patients. METHODS: 630 adult patients with available serum samples obtained within 6 months from the first event were included. MOG-Ab were analyzed using a live cell-based assay. Statistical analyses included parametric and non-parametric tests, logistic regression and survival models. RESULTS: MOG-Ab were positive in 17/630 (2.7%). 14/17 (82.4%) MOG-Ab+ patients presented with optic neuritis (ON) compared to 227/613 (37.0%) MOG-Ab-, p=0.009. CSF-restricted oligoclonal bands (CSF-OBs) were found in 2/16 (12.5%) MOG-Ab+ vs. 371/601 (61.7%) MOG-Ab-, p<0.001. Baseline brain magnetic resonance imaging (MRI) was normal in 9/17 (52.9%) MOG-Ab+ vs. 153/585 (26.2%) MOG-Ab-, p=0.029. Absence of CSF-OBs and ON at onset were independently associated with MOG-Ab positivity: Odds-Ratios (OR) 9.03; 95%Confidence Interval (95%CI) 2.04-53.6, p=0.009, and 4.17; 95%CI 1.15-19.8, p=0.042, respectively. 22.9% (95%CI 0.0-42.7) of MOG-Ab+ patients compared to 67.6% (95%CI 63.3-71.3) of MOG-Ab- fulfilled McDonald 2017 criteria at 5 years (log-rank p=0.003). INTERPRETATION: MOG-Ab are infrequent in adults with a first demyelinating event suggestive of MS. However, based on our results, we suggest determining these antibodies, as long as the brain MRI is not suggestive of MS. This article is protected by copyright. All rights reserved.
 Emerging evidence have shown the importance of gut microbiota in regulating brain functions. The diverse molecular mechanisms involved in cross-talk between gut and brain provide insight into importance of this communication in maintenance of brain homeostasis. It has also been observed that disturbed gut microbiota contributes to neurological diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis and aging. Recently, gut microbiome-derived exosomes have also been reported to play an essential role in the development and progression of neurodegenerative diseases and could thereby act as a therapeutic target. Further, pharmacological interventions including antibiotics, prebiotics and probiotics can influence gut microbiome-mediated management of neurological diseases. However, extensive research is warranted to better comprehend this interconnection in maintenance of brain homeostasis and its implication in neurological diseases. Thus, the present review is aimed to provide a detailed understanding of gut-brain axis followed by possibilities to target the gut microbiome for improving neurological health.
 The role of inflammation in nervous system injury and disease is attracting increased attention. Much of that research has focused on microglia in the central nervous system (CNS) and macrophages in the peripheral nervous system (PNS). Much less attention has been paid to the roles played by neutrophils. Neutrophils are part of the granulocyte subtype of myeloid cells. These cells, like macrophages, originate and differentiate in the bone marrow from which they enter the circulation. After tissue damage or infection, neutrophils are the first immune cells to infiltrate into tissues and are directed there by specific chemokines, which act on chemokine receptors on neutrophils. We have reviewed here the basic biology of these cells, including their differentiation, the types of granules they contain, the chemokines that act on them, the subpopulations of neutrophils that exist, and their functions. We also discuss tools available for identification and further study of neutrophils. We then turn to a review of what is known about the role of neutrophils in CNS and PNS diseases and injury, including stroke, Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, spinal cord and traumatic brain injuries, CNS and PNS axon regeneration, and neuropathic pain. While in the past studies have focused on neutrophils deleterious effects, we will highlight new findings about their benefits. Studies on their actions should lead to identification of ways to modify neutrophil effects to improve health.
 Advancing age is a major risk factor of Alzheimer's disease (AD). The worldwide prevalence of AD is approximately 50 million people, and this number is projected to increase substantially. The molecular mechanisms underlying the aging-associated susceptibility to cognitive impairment in AD are largely unknown. As a hallmark of aging, cellular senescence is a significant contributor to aging and age-related diseases including AD. Senescent neurons and glial cells have been detected to accumulate in the brains of AD patients and mouse models. Importantly, selective elimination of senescent cells ameliorates amyloid beta and tau pathologies and improves cognition in AD mouse models, indicating a critical role of cellular senescence in AD pathogenesis. Nonetheless, the mechanisms underlying when and how cellular senescence contributes to AD pathogenesis remain unclear. This review provides an overview of cellular senescence and discusses recent advances in the understanding of the impact of cellular senescence on AD pathogenesis, with brief discussions of the possible role of cellular senescence in other neurodegenerative diseases including Down syndrome, Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis.
 The immune system is embedded in a network of regulatory systems to keep homeostasis in case of an immunologic challenge. Neuroendocrine immunologic research revealed several aspects of these interactions over the past decades, e.g. between the autonomic nervous system and the immune system. This review will focus on evidence revealing the role of the sympathetic nervous system (SNS) in chronic inflammation, like colitis, multiple sclerosis, systemic sclerosis, lupus erythematodes, and arthritis with a focus on animal models supported by human data. A theory of the contribution of the SNS in chronic inflammation will be presented that spans these disease entities. One major finding is the biphasic nature of the sympathetic contribution to inflammation with proinflammatory effects until the point of disease outbreak and mainly anti-inflammatory influence thereafter. Since sympathetic nerve fibers are lost from sites of inflammation during inflammation, local cells and immune cells achieve the capability to endogenously produce catecholamines to fine-tune the inflammatory response independent of brain control. On a systemic level, it has been shown across models that the SNS is activated in inflammation as opposed to the parasympathetic nervous system. Permanent overactivity of the SNS contributes many of the known disease sequelae. One goal of neuroendocrine immune research is defining new therapeutic targets. In this respect, it will be discussed that at least in arthritis, it might be beneficial to support β-adrenergic and inhibit α-adrenergic activity besides restoring autonomic balance. Overall, in the clinical setting we now need controlled interventional studies to successfully translate the theoretical knowledge into benefits for patients.
 Retinal Optical Coherence Tomography (OCT) allows the non-invasive direct observation of the central nervous system, enabling the measurement and extraction of biomarkers from neural tissue that can be helpful in the assessment of ocular, systemic and Neurological Disorders (ND). Deep learning models can be trained to segment the retinal layers for biomarker extraction. However, the onset of ND can have an impact on the neural tissue, which can lead to the degraded performance of models not exposed to images displaying signs of disease during training. We present a fully automatic approach for the retinal layer segmentation in multiple neurodegenerative disorder scenarios, using an annotated dataset of patients of the most prevalent NDs: Alzheimer's disease, Parkinson's disease, multiple sclerosis and essential tremor, along with healthy control patients. Furthermore, we present a two-part, comprehensive study on the effects of ND on the performance of these models. The results show that images of healthy patients may not be sufficient for the robust training of automated segmentation models intended for the analysis of ND patients, and that using images representative of different NDs can increase the model performance. These results indicate that the presence or absence of patients of ND in datasets should be taken into account when training deep learning models for retinal layer segmentation, and that the proposed approach can provide a valuable tool for the robust and reliable diagnosis in multiple scenarios of ND.
 INTRODUCTION: Prospective data on the risk of hepatitis B reactivation (HBVr) among patients with resolved HBV infection undergoing anti-CD20 antibodies monotherapy is scarce. We aimed to assess the risk of HBVr in patients with resolved HBV infection treated with rituximab or ocrelizumab in monotherapy for multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD) without antiviral prophylaxis. METHODS: HEBEM is a prospective study that included all consecutive adults HBsAg-negative/anti-HBc-positive who initiated anti-CD20 antibodies for MS or NMOSD at Cemcat. Inclusion criteria encompassed undetectable HBV-DNA, absence of other immunosuppressants or antiviral therapy. Every 6 months HBsAg, ALT and HBV-DNA were performed to rule out HBVr (defined by 2-log increase in HBV-DNA or seroconversion to HBsAg+). RESULTS: From August/2019 to August/2022, 540 subjects initiated anti-CD20 antibodies, 28 (5.2%) were anti-HBc-positive and were included. Twenty-two received rituximab and 6 ocrelizumab. The majority (89.3%) had previously received ≥ 1 immunomodulatory drug, with corticosteroids (82.1%) and interferon (42.9%) as the most common. At inclusion, all presented normal transaminases and undetectable HBV-DNA. Median anti-HBs levels were 105.5 mIU/mL (IQR 0-609). Median follow-up was 3.1 years (2.1-4.0). Median number of cycles of anti-CD20 antibodies was 6 (3-7), with a cumulative dose of 8.5 g (5.8-11.2) of rituximab and 3 g (1.8-3.8) of ocrelizumab. Neither cases of HBVr nor changes in anti-HBs titers were observed per 83.6 patient-years treated with monotherapy with anti-CD20 antibodies. CONCLUSIONS: In this cohort of patients with MS or NMOSD and resolved HBV infection, anti-CD20 monotherapy was not associated with detectable risk of HBV reactivation despite the lack of antiviral prophylaxis.
 BACKGROUND: Neurodegenerative procedures include a large spectrum of disorders with diverse pathological features and clinical manifestations, such as Alzheimer's Disease (AD), Parkinson's disease (PD), Multiple sclerosis, and Amyotrophic lateral sclerosis (ALS). Neurodegenerative diseases (NDs) are indicated by progressive loss of neurons and cognitive function, which is associated with free radical formation, extra and intercellular accumulation of misfolded proteins, oxidative stress, mitochondrial and neurotrophins dysfunction, bioenergetic impairment, inflammation, and apoptotic cell death. Boswellic acid is a pentacyclic triterpene molecule of plant origin that has been applied for treating several inflammatory disorders. Numerous studies have also investigated its' therapeutic potential against multiple NDs. OBJECTIVE: In this article, we aim to review the neuroprotective effects of boswellic acid on NDs and the related mechanisms of action. METHODS: The databases of PubMed, Google Scholar, Web of Sciences, and Scopus were searched to find studies that reported the effects of boswellic acid on NDs without time limits. Review articles, letters, editorials, unpublished data, and articles not published in the English language were not included in the study Results: Overall, 17 studies were included in the present study (8 NDs in general, 5 AD, 3 PD, and 1 ALS). According to the reports, boswellic acid exerts anti-inflammatory, antioxidant, anti-apoptotic, and neuromodulatory effects against NDs. Boswellic acid decreases Tau phosphorylation and amyloid-β (Aβ) generation in AD. This substance also protects nigrostriatal dopaminergic neurons and improves motor impairments in PD and modulates neurotransmitters, decreases the demyelination region, and improves behavioral functions in ALS. CONCLUSION: Due to the significant effects of boswellic acid in NDs, more clinical studies are necessary to evaluate the pharmacokinetics of this substance because it seems that boswellic acid can be used as a complementary or alternative treatment in patients with NDs.
 BACKGROUND: Some neurodegenerative diseases have an element of neuroinflammation that is triggered by viral nucleic acids, resulting in the generation of type I interferons. In the cGAS-STING pathway, microbial and host-derived DNA bind and activate the DNA sensor cGAS, and the resulting cyclic dinucleotide, 2'3-cGAMP, binds to a critical adaptor protein, stimulator of interferon genes (STING), which leads to activation of downstream pathway components. However, there is limited work demonstrating the activation of the cGAS-STING pathway in human neurodegenerative diseases. METHODS: Post-mortem CNS tissue from donors with multiple sclerosis (n = 4), Alzheimer's disease (n = 6), Parkinson's disease (n = 3), amyotrophic lateral sclerosis (n = 3) and non-neurodegenerative controls (n = 11) were screened by immunohistochemistry for STING and relevant protein aggregates (e.g., amyloid-β, α-synuclein, TDP-43). Human brain endothelial cells were cultured and stimulated with the STING agonist palmitic acid (1-400 μM) and assessed for mitochondrial stress (release of mitochondrial DNA into cytosol, increased oxygen consumption), downstream regulator factors, TBK-1/pIRF3 and inflammatory biomarker interferon-β release and changes in ICAM-1 integrin expression. RESULTS: In neurodegenerative brain diseases, elevated STING protein was observed mainly in brain endothelial cells and neurons, compared to non-neurodegenerative control tissues where STING protein staining was weaker. Interestingly, a higher STING presence was associated with toxic protein aggregates (e.g., in neurons). Similarly high STING protein levels were observed within acute demyelinating lesions in multiple sclerosis subjects. To understand non-microbial/metabolic stress activation of the cGAS-STING pathway, brain endothelial cells were treated with palmitic acid. This evoked mitochondrial respiratory stress up to a ~2.5-fold increase in cellular oxygen consumption. Palmitic acid induced a statistically significant increase in cytosolic DNA leakage from endothelial cell mitochondria (Mander's coefficient; p < 0.05) and a significant increase in TBK-1, phosphorylated transcription factor IFN regulatory factor 3, cGAS and cell surface ICAM. In addition, a dose response in the secretion of interferon-β was observed, but it failed to reach statistical significance. CONCLUSIONS: The histological evidence shows that the common cGAS-STING pathway appears to be activated in endothelial and neural cells in all four neurodegenerative diseases examined. Together with the in vitro data, this suggests that the STING pathway might be activated via perturbation of mitochondrial stress and DNA leakage, resulting in downstream neuroinflammation; hence, this pathway may be a target for future STING therapeutics.
 INTRODUCTION: The 18-kDa translocator protein (TSPO) is increasingly recognized as a molecular target for PET imaging of inflammatory responses in various central nervous system (CNS) disorders. However, the reported sensitivity and specificity of TSPO PET to identify brain inflammatory processes appears to vary greatly across disorders, disease stages, and applied quantification methods. To advance TSPO PET as a potential biomarker to evaluate brain inflammation and anti-inflammatory therapies, a better understanding of its applicability across disorders is needed. We conducted a transdiagnostic systematic review and meta-analysis of all in vivo human TSPO PET imaging case-control studies in the CNS. Specifically, we investigated the direction, strength, and heterogeneity associated with the TSPO PET signal across disorders in pre-specified brain regions, and explored the demographic and methodological sources of heterogeneity. METHODS: We searched for English peer-reviewed articles that reported in vivo human case-control TSPO PET differences. We extracted the demographic details, TSPO PET outcomes, and technical variables of the PET procedure. A random-effects meta-analysis was applied to estimate case-control standardized mean differences (SMD) of the TSPO PET signal in the lobar/whole-brain cortical grey matter (cGM), thalamus, and cortico-limbic circuitry between different illness categories. Heterogeneity was evaluated with the I(2) statistic and explored using subgroup and meta-regression analyses for radioligand generation, PET quantification method, age, sex, and publication year. Significance was set at the False Discovery Rate (FDR)-corrected P < 0.05. RESULTS: 156 individual case-control studies were included in the systematic review, incorporating data for 2381 healthy controls and 2626 patients. 139 studies documented meta-analysable data and were grouped into 11 illness categories. Across all the illness categories, we observed a significantly higher TSPO PET signal in cases compared to controls for the cGM (n = 121 studies, SMD = 0.358, P(FDR) < 0.001, I(2) = 68%), with a significant difference between the illness categories (P = 0.004). cGM increases were only significant for Alzheimer's disease (SMD = 0.693, P(FDR) < 0.001, I(2) = 64%) and other neurodegenerative disorders (SMD = 0.929, P(FDR) < 0.001, I(2) = 73%). Cortico-limbic increases (n = 97 studies, SMD = 0.541, P < 0.001, I(2) = 67%) were most prominent for Alzheimer's disease, mild cognitive impairment, other neurodegenerative disorders, mood disorders and multiple sclerosis. Thalamic involvement (n = 79 studies, SMD = 0.393, P < 0.001, I(2) = 71%) was observed for Alzheimer's disease, other neurodegenerative disorders, multiple sclerosis, and chronic pain and functional disorders (all P(FDR) < 0.05). Main outcomes for systemic immunological disorders, viral infections, substance use disorders, schizophrenia and traumatic brain injury were not significant. We identified multiple sources of between-study variance to the TSPO PET signal including a strong transdiagnostic effect of the quantification method (explaining 25% of between-study variance; V(T)-based SMD = 0.000 versus reference tissue-based studies SMD = 0.630; F = 20.49, df = 1;103, P < 0.001), patient age (9% of variance), and radioligand generation (5% of variance). CONCLUSION: This study is the first overarching transdiagnostic meta-analysis of case-control TSPO PET findings in humans across several brain regions. We observed robust increases in the TSPO signal for specific types of disorders, which were widespread or focal depending on illness category. We also found a large and transdiagnostic horizontal (positive) shift of the effect estimates of reference tissue-based compared to V(T)-based studies. Our results can support future studies to optimize experimental design and power calculations, by taking into account the type of disorder, brain region-of-interest, radioligand, and quantification method.
 The emergence of new digital technologies has enabled a new way of doing research, including active collaboration with the public ('citizen science'). Innovation in machine learning (ML) and natural language processing (NLP) has made automatic analysis of large-scale text data accessible to study individual perspectives in a convenient and efficient fashion. Here we blend citizen science with innovation in NLP and ML to examine (1) which categories of life events persons with multiple sclerosis (MS) perceived as central for their MS; and (2) associated emotions. We subsequently relate our results to standardized individual-level measures. Participants (n = 1039) took part in the 'My Life with MS' study of the Swiss MS Registry which involved telling their story through self-selected life events using text descriptions and a semi-structured questionnaire. We performed topic modeling ('latent Dirichlet allocation') to identify high-level topics underlying the text descriptions. Using a pre-trained language model, we performed a fine-grained emotion analysis of the text descriptions. A topic modeling analysis of totally 4293 descriptions revealed eight underlying topics. Five topics are common in clinical research: 'diagnosis', 'medication/treatment', 'relapse/child', 'rehabilitation/wheelchair', and 'injection/symptoms'. However, three topics, 'work', 'birth/health', and 'partnership/MS' represent domains that are of great relevance for participants but are generally understudied in MS research. While emotions were predominantly negative (sadness, anxiety), emotions linked to the topics 'birth/health' and 'partnership/MS' was also positive (joy). Designed in close collaboration with persons with MS, the 'My Life with MS' project explores the experience of living with the chronic disease of MS using NLP and ML. Our study thus contributes to the body of research demonstrating the potential of integrating citizen science with ML-driven NLP methods to explore the experience of living with a chronic condition.
 Multiple sclerosis (MS) involves the infiltration of autoreactive T cells into the CNS, yet we lack a comprehensive understanding of the signaling pathways that regulate this process. Here, we conducted a genome-wide in vivo CRISPR screen in a rat MS model and identified 5 essential brakes and 18 essential facilitators of T cell migration to the CNS. While the transcription factor ETS1 limits entry to the CNS by controlling T cell responsiveness, three functional modules, centered around the adhesion molecule α4-integrin, the chemokine receptor CXCR3 and the GRK2 kinase, are required for CNS migration of autoreactive CD4(+) T cells. Single-cell analysis of T cells from individuals with MS confirmed that the expression of these essential regulators correlates with the propensity of CD4(+) T cells to reach the CNS. Our data thus reveal key regulators of the fundamental step in the induction of MS lesions.
 OBJECTIVE: To investigate the serologic response, predictors of response, and clinical outcomes associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination and infection in ozanimod-treated participants with relapsing multiple sclerosis (RMS) from DAYBREAK. METHODS: DAYBREAK (ClinicalTrials.gov-NCT02576717), an open-label extension study of oral ozanimod 0.92 mg, enrolled participants aged 18-55 years with RMS who completed phase 1-3 ozanimod trials. Participants who were fully vaccinated against SARS-CoV-2 with mRNA or non-mRNA vaccines, were unvaccinated, and/or had COVID-19-related adverse events (AEs, with or without vaccination) and postvaccination serum samples were included (n = 288). Spike receptor binding domain (RBD) antibody levels (seroconversion: ≥0.8 U/mL) and serologic evidence of SARS-CoV-2 infection (nucleocapsid IgG: ≥1 U/mL) were assessed (Roche Elecsys/Cobas e411 platform). RESULTS: In fully vaccinated participants (n = 148), spike RBD antibody seroconversion occurred in 90% (n = 98/109) of those without serologic evidence of prior SARS-CoV-2 exposure (100% [n = 80/80] seroconversion after mRNA vaccination) and in 100% (n = 39/39) of participants with serologic evidence of viral exposure. mRNA vaccination predicted higher spike RBD antibody levels, whereas absolute lymphocyte count (ALC), age, body mass index, and sex did not. COVID-19-related AEs were reported in 10% (n = 15/148) of fully vaccinated participants-all were nonserious and not severe; all participants recovered. INTERPRETATION: Most ozanimod-treated participants with RMS mounted a serologic response to SARS-CoV-2 vaccination and infection, regardless of participant characteristics or ALC levels. In this analysis, all COVID-19-related AEs post-full vaccination in participants taking ozanimod were nonserious and not severe.
 BACKGROUND: Multiple sclerosis (MS) is a chronic autoimmune and neuroinflammatory disease of the central nervous system characterized by peripheral activation of immune-inflammatory pathways which culminate in neurotoxicity causing demyelination of central neurons. Nonetheless, the pathophysiology of relapsing-remitting MS (RRMS)-related chronic fatigue, depression, anxiety, cognitive impairments, and autonomic disturbances is not well understood. OBJECTIVES: The current study aims to delineate whether the remitted phase of RRMS is accompanied by activated immune-inflammatory pathways and if the latter, coupled with erythron variables, explain the chronic fatigue and mood symptoms due to RRMS. MATERIAL AND METHODS: We recruited 63 MS patients, 55 in the remitted phase of RRMS and 8 with secondary progressive MS, and 30 healthy controls and assessed erythron variables, and used a bio-plex assay to measure 27 serum cytokines. RESULTS: A significant proportion of the MS patients (46%) displayed activation of the immune-inflammatory response (IRS) and compensatory immune response (CIRS) systems, and T helper (Th)1 and Th17 cytokine profiles. Remitted RRMS patients showed increased chronic fatigue, depression, anxiety, physiosomatic, autonomic, and insomnia scores, which could partly be explained by M1 macrophage, Th1, Th-17, growth factor, and CIRS activation, as well as aberrations in the erythron including lowered hematocrit and hemoglobin levels. CONCLUSIONS: Around 50% of remitted RRMS patients show activation of immune-inflammatory pathways in association with mood and chronic-fatigue-like symptoms. IRS and CIRS activation as well as the aberrations in the erythron are new drug targets to treat chronic fatigue and affective symptoms due to MS.
 Vitamin D plays an important role in calcium homeostasis and many cellular processes. Although vitamin D supplements are widely recommended for community-dwelling adults, definitive data on whether these supplements benefit clinically important skeletal and extraskeletal outcomes have been conflicting. Although observational studies on effects of vitamin D on musculoskeletal and extraskeletal outcomes may be confounded by reverse causation, randomized controlled studies (RCTs) and Mendelian randomization (MR) studies can help to elucidate causation. In this review, we summarize the recent findings from large RCTs and/or MR studies of vitamin D on bone health and risk of fractures, falls, cancer, and cardiovascular disease, disorders of the immune system, multiple sclerosis, and mortality in community-dwelling adults. The primary analyses indicate that vitamin D supplementation does not decrease bone loss, fractures, falls, cancer incidence, hypertension, or cardiovascular risk in generally healthy populations. Large RCTs and meta-analyses suggest an effect of supplemental vitamin D on cancer mortality. The existence of extraskeletal benefits of vitamin D supplementations are best documented for the immune system especially in people with poor vitamin D status, autoimmune diseases, and multiple sclerosis. Accumulating evidence indicates that vitamin D may reduce all-cause mortality. These findings, in mostly vitamin D-replete populations, do not apply to older adults in residential communities or adults with vitamin D deficiency or osteoporosis. The focus of vitamin D supplementation should shift from widespread use in generally healthy populations to targeted vitamin D supplementation in select individuals, good nutritional approaches, and elimination of vitamin D deficiency globally. © 2023 American Society for Bone and Mineral Research (ASBMR).
 Social media and internet platforms have become significant drivers of mass-information. Highly publicized events, such as John McCain's announcement of his glioblastoma diagnosis, often drive national public interest in medical topics. Improved understanding of the temporality of interest spikes as well as the nature of the information that garners attention from outside the medical community can help inform ways in which the medical community can boost awareness of (and interest in) the field of neurosurgery. We utilized the "explore topics" feature on Google Trends to obtain web, news, and YouTube search data from May 1, 2015, to May 1, 2019 for the terms "glioblastoma," "brain tumor," "stroke," and "multiple sclerosis" to identify periods of visibly increased search interest. Search results for "glioblastoma" showed significantly elevated average interest during the period of July 3-23, 2017, as compared to that generated since this specific time period (42.6 vs. 8.73, P<0.001). This increased search activity therefore directly correlated with John McCain's public announcement of his glioblastoma diagnosis, and a similar search interest spike was evident using the search term "brain tumor" (87.3 vs. 64.2, P<0.001). Search results for "multiple sclerosis" showed - as a result of the online buzz created by Selma Blair's battle with the disease - significantly elevated average interest from October 8, 2018, to October 28, 2018, and February 11, 2019, to March 3, 2019, when compared to the average interest of the remaining time (59 vs. 40.16, P<0.001 and 69 vs. 40.16, P<0.001). Finally, there were no corresponding elevations in YouTube search interest for any of the terms associated with increased interest on Google Trends. Following major events related to the neurological disease of public figures there is an expected rise in Google search interest relevant to these topics. Our findings suggest that there is an optimal window of approximately 2 weeks following each of these events for activist and clinical groups to publicize their desired message, and for the field of neurosurgery and neurological science to increase public awareness regarding specific diseases, with a regression to baseline interest by 4 months following the event.
 BACKGROUND: The 30-second Chair Stand Test (30s-CST) and Modified Four Square Step Test (mFSST) are used to determine the functional status of individuals with multiple sclerosis (MS). No other studies have demonstrated the reliability and validity of the 30s-CST and mFSST. PURPOSE: To identify the test-retest reliability, concurrent validity and the known-group validity of the 30s-CST and mFSST in persons with MS. METHODS: A total of 64 persons with MS were enrolled. 30s-CST, mFSST, Timed Up and Go Test (TUG) and Five Times Sit to Stand (FTST) tests were performed. 30s-CST and mFSST were conducted again one-hour later. RESULTS: The mean age of the persons with MS were 37.9±11.3 years. The test-retest reliability of the 30s-CST and mFSST were excellent (ICC(30s-CST) = 0.974, 95%CI: 0.95-0.98; ICC(mFSST) = 0.992, 95%CI: 0.98-0.99). The 30s-CST was strongly correlated with FTST and TUG (r(1) = -0.871, p(1) = 0.0001; r(2) = -0.741,p(2) = 0.0001). There was a strong relationship between mFSST with TUG and FTST (r(1) = 0.781,p(1) = 0.0001;r(2) = 0.788,p(2) = 0.0001). The SEM(95) and MDC(95) values of the 30s-CST and mFSST were 0.41/1.13 and 0.34/0.94, respectively. Besides, there were significant differences between the persons with or without fall history in 30s-CST (MD: 1.66, CI: 0.27 to 3.05, p = .019) and mFSST CST (MD:-2.70, CI: -4.73 to -0.67, p = .010) performances. CONCLUSION: The 30s-CST and mFSST are both valid and reliable in mildly-disabled individuals with MS.
 Magnetic resonance imaging (MRI) is of exceptional importance in the diagnostics and monitoring of multiple sclerosis (MS); however, a close interdisciplinary cooperation between neurologists in private practice, (neuro)radiological practices, hospitals or specialized MS centers is only rarely established. In particular, there is a lack of standardized MRI protocols for image acquisition as well as established quality parameters, which guarantee the comparability of MRI records; however, this is a fundamental prerequisite for an effective application of MRI in the treatment of MS patients, e.g., for making the diagnosis or treatment monitoring. To address these challenges a group of neurologists and (neuro)radiologists developed a consensus proposal for standardization of image acquisition, interpretation and transmission of results and for improvement in interdisciplinary cooperation. This pilot project in the metropolitan area of Essen used a modified Delphi process and was based on the most up to date scientific knowledge. The recommendation takes the medical, economic, temporal and practical aspects of MRI in MS into consideration. The model of interdisciplinary cooperation between radiologists and neurologists with the aim of a regional standardization of MRI could serve as an example for other regions of Germany in order to optimize MRI for MS.
 In this study, we sought to create a database summarizing the expression of human endogenous retroviruses (HERVs) in various human cancers. HERVs are suitable therapeutic targets due to their abundance in the human genome, overexpression in various malignancies, and involvement in various cancer pathways. We identified articles on HERVs from PubMed and then prescreened and automatically categorized them using the portable document format (PDF) data extractor (PDE) R package. We discovered 196 primary research articles with HERV expression data from cancer tissues or cancer cell lines. HERV RNA and protein expression was reported in brain, breast, cervical, colorectal, endocrine, gastrointestinal, kidney/renal/pelvis, liver, lung, genital, oral cavity, pharynx, ovary, pancreas, prostate, skin, testicular, urinary/bladder, and uterus cancers, leukemias, lymphomas, and myelomas. Additionally, we discovered reports of HERV RNA-only overexpression in soft tissue cancers including heart, thyroid, bone, and joint cancers. The CancerHERVdb database is hosted in the form of interactive visualizations of the expression data and a summary data table at https://erikstricker.shinyapps.io/cancerHERVdb/. The user can filter the findings according to cancer type, HERV family, HERV gene, or a combination thereof and easily export the results with the corresponding reference list. In our report, we provide examples of potential uses of the CancerHERVdb, such as identification of cancers suitable for off-target treatment with the multiple sclerosis-associated retrovirus (MSRV)-Env-targeting antibody GNbAC1 (now named temelimab) currently in phase 2b clinical trials for multiple sclerosis or the discovery of cancers overexpressing HERV-H long terminal repeat-associating 2 (HHLA2), a newly emerging immune checkpoint. In summary, the CancerHERVdb allows cross-study comparisons, encourages data exploration, and informs about potential off-target effects of HERV-targeting treatments. IMPORTANCE Human endogenous retroviruses (HERVs), which in the past have inserted themselves in various regions of the human genome, are to various degrees activated in virtually every cancer type. While a centralized naming system and resources summarizing HERV levels in cancers are lacking, the CancerHERVdb database provides a consolidated resource for cross-study comparisons, data exploration, and targeted searches of HERV activation. The user can access data extracted from hundreds of articles spanning 25 human cancer categories. Therefore, the CancerHERVdb database can aid in the identification of prognostic and risk markers, drivers of cancer, tumor-specific targets, multicancer spanning signals, and targets for immune therapies. Consequently, the CancerHERVdb database is of direct relevance for clinical as well as basic research.
 PURPOSE: Although articulatory impairment represents distinct speech characteristics in most neurological diseases affecting movement, methods allowing automated assessments of articulation deficits from the connected speech are scarce. This study aimed to design a fully automated method for analyzing dysarthria-related vowel articulation impairment and estimate its sensitivity in a broad range of neurological diseases and various types and severities of dysarthria. METHOD: Unconstrained monologue and reading passages were acquired from 459 speakers, including 306 healthy controls and 153 neurological patients. The algorithm utilized a formant tracker in combination with a phoneme recognizer and subsequent signal processing analysis. RESULTS: Articulatory undershoot of vowels was presented in a broad spectrum of progressive neurodegenerative diseases, including Parkinson's disease, progressive supranuclear palsy, multiple-system atrophy, Huntington's disease, essential tremor, cerebellar ataxia, multiple sclerosis, and amyotrophic lateral sclerosis, as well as in related dysarthria subtypes including hypokinetic, hyperkinetic, ataxic, spastic, flaccid, and their mixed variants. Formant ratios showed a higher sensitivity to vowel deficits than vowel space area. First formants of corner vowels were significantly lower for multiple-system atrophy than cerebellar ataxia. Second formants of vowels /a/ and /i/ were lower in ataxic compared to spastic dysarthria. Discriminant analysis showed a classification score of up to 41.0% for disease type, 39.3% for dysarthria type, and 49.2% for dysarthria severity. Algorithm accuracy reached an F-score of 0.77. CONCLUSIONS: Distinctive vowel articulation alterations reflect underlying pathophysiology in neurological diseases. Objective acoustic analysis of vowel articulation has the potential to provide a universal method to screen motor speech disorders. SUPPLEMENTAL MATERIAL: https://doi.org/10.23641/asha.23681529.
 CD8+ lymphocytes are adaptive immunity cells with the particular function to directly kill the target cell following antigen recognition in the context of MHC class I. In addition, CD8+ T cells may release pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), and a plethora of other cytokines and chemoattractants modulating immune and inflammatory responses. A role for CD8+ T cells has been suggested in aging and several diseases of the central nervous system (CNS), including Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, limbic encephalitis-induced temporal lobe epilepsy and Susac syndrome. Here we discuss the phenotypic and functional alterations of CD8+ T cell compartment during these conditions, highlighting similarities and differences between CNS disorders. Particularly, we describe the pathological changes in CD8+ T cell memory phenotypes emphasizing the role of senescence and exhaustion in promoting neuroinflammation and neurodegeneration. We also discuss the relevance of trafficking molecules such as selectins, mucins and integrins controlling the extravasation of CD8+ T cells into the CNS and promoting disease development. Finally, we discuss how CD8+ T cells may induce CNS tissue damage leading to neurodegeneration and suggest that targeting detrimental CD8+ T cells functions may have therapeutic effect in CNS disorders.
 BACKGROUND: There is a need in Relapsing-Remitting Multiple Sclerosis (RRMS) treatment for biomarkers that monitor neuroinflammation, neurodegeneration, treatment response, and disease progression despite treatment. OBJECTIVE: To assess the value of serum glial fibrillary acidic protein (sGFAP) as a biomarker for clinical disease progression and brain volume measurements in natalizumab-treated RRMS patients. METHODS: sGFAP and neurofilament light (sNfL) were measured in an observational cohort of natalizumab-treated RRMS patients at baseline, +3, +12, and +24 months and at the last sample follow-up (median 5.17 years). sGFAP was compared between significant clinical progressors and non-progressors and related to magnetic resonance imaging (MRI)-derived volumes of the whole brain, ventricle, thalamus, and lesion. The relationship between sGFAP and sNfL was assessed. RESULTS: A total of 88 patients were included, and 47.7% progressed. sGFAP levels at baseline were higher in patients with gadolinium enhancement (1.3-fold difference, p = 0.04) and decreased in 3 months of treatment (adj. p < 0.001). No association was found between longitudinal sGFAP levels and progressor status. sGFAP at baseline and 12 months was significantly associated with normalized ventricular (positively), thalamic (negatively), and lesion volumes (positively). Baseline and 12-month sGFAP predicted annualized ventricle volume change rate after 1 year of treatment. sGFAP correlated with sNfL at baseline (p < 0.001) and last sample follow-up (p < 0.001) but stabilized earlier. DISCUSSION: sGFAP levels related to MRI markers of neuroinflammation and neurodegeneration.
 We present the case of a 21 year-old woman with newly diagnosed relapsing-remitting multiple sclerosis who is given a single dose of ocrelizumab and placed on moderate-dose steroids with subsequent development of hepatic failure who goes on to develop highly fulminant systemic and central nervous system (CNS) aspergillosis. Ocrelizumab has no documented association with aspergillus infection, and moderate-dose steroids less often lead to such fulminant disease, but liver failure is associated with often-fatal aspergillus infection. We emphasize that liver failure is an underrecognized immune dysregulated state that predisposes to bacterial and fungal infections and suggest changes in diagnostic reasoning that could be considered in patients with multiple modalities of immunosuppression.
 Multiple sclerosis (MS) is the most common causes of non-traumatic disability in young adults worldwide. MS pathophysiologies include the formation of inflammatory lesions, axonal damage and demyelination, and blood brain barrier (BBB) disruption. Coagulation proteins, including factor (F)XII, can serve as important mediators of the adaptive immune response during neuroinflammation. Indeed, plasma FXII levels are increased during relapse in relapsing-remitting MS patients, and previous studies showed that reducing FXII levels was protective in a murine model of MS, experimental autoimmune encephalomyelitis (EAE). Our objective was to determine if pharmacological targeting of FXI, a major substrate of activated FXII (FXIIa), improves neurological function and attenuates CNS damage in the setting of EAE. EAE was induced in male mice using murine myelin oligodendrocyte glycoprotein peptides combined with heat-inactivated Mycobacterium tuberculosis and pertussis toxin. Upon onset of symptoms, mice were treated every other day intravenously with anti-FXI antibody, 14E11, or saline. Disease scores were recorded daily until euthanasia for ex vivo analyses of inflammation. Compared to the vehicle control, 14E11 treatment reduced the clinical severity of EAE and total mononuclear cells, including CD11b(+)CD45(high) macrophage/microglia and CD4(+) T cell numbers in brain. Following pharmacological targeting of FXI, BBB disruption was reduced, as measured by decreased axonal damage and fibrin(ogen) accumulation in the spinal cord. These data demonstrate that pharmacological inhibition of FXI reduces disease severity, immune cell migration, axonal damage, and BBB disruption in mice with EAE. Thus, therapeutic agents targeting FXI and FXII may provide a useful approach for treating autoimmune and neurologic disorders.
 INTRODUCTION: The brain myelin and neurons destruction in multiple sclerosis may be associated with the production of neuroinflammatory cells (macrophages, astrocytes, T-lymphocytes) of pro-inflammatory cytokines and free radicals. The age-associated changes of the above cells can influence on the response of nervous system cells to toxic damaging and regulatory factors of humoral/endocrine nature, in particular pineal hormone melatonin. The study aim was (1) to evaluate changes of the brain macrophages, astrocytes, T-cells, neural stem cells, neurons, and central nervous system (CNS) functioning in the neurotoxin cuprizone-treated mice of different age; and (2) to assess in such mice the effects of exogenous melatonin and possible courses of its action. METHODS: A toxic demyelination and neurodegeneration model was induced in 129/Sv mice aged 3-5 and 13-15 months by adding cuprizone neurotoxin to their food for 3 weeks. From the 8th day of the cuprizone treatment, melatonin was injected intraperitoneally at 6 p.m. daily, at a dose of 1 mg/kg. The brain GFPA + -cells were evaluated by immunohistochemical method, the proportion of CD11b+, CD3+CD11b+, CD3+, CD3+CD4+, CD3+CD8+, Nestin+-cells was determined via flow cytometry. Macrophage activity was evaluated by their ability to phagocytose latex beads Morphometric analysis of the brain neurons and the behavioral reactions ("open field" and rotarod tests) were performed. To assess the involvement of the bone marrow and thymus in the action of melatonin, the amount of granulocyte/macrophage colony-forming cells (GM-CFC), and blood monocytes and thymic hormone thymulin were evaluated. RESULTS AND DISCUSSION: The numbers of the GFAP+-, CD3+-, CD3+CD4+, CD3+CD8+, CD11b+, CD3+CD11b+, Nestin+-cells and macrophages phagocytic latex beads and malondialdehyde (MDA) content were increased in the brain of young and aging mice under cuprizone influence. The proportion of undamaged neurons within the brain, motor, affective, and exploratory activities, and muscle tone decreased in mice of both ages. Introducing melatonin to mice of any age reduced the number of GFAP+-, CD3+- cells and their subpopulations, macrophage activation, and MDA content. At the same time, the percentage of brain neurons that were unchanged increased as the number of Nestin+ cells decreased. The behavioral responses were also improved. Besides, the number of bone marrow GM-CFC and the blood level of monocytes and thymulin increased. The effects of both neurotoxin and melatonin on the brain astrocytes, macrophages T-cells, and immune system organs as well as the structure and functioning of neurons were more pronounced in the young mice. CONCLUSION: We have observed the involvement of the astrocytes, macrophages, T-cells, neural stem cells, and neurons in the brain reaction of mice different age after administration of neurotoxin cuprizone and melatonin. The brain cell composition reaction has the age features. The neuroprotective effects of melatonin in cuprizone-treated mice have been realized through an improvement of the brain cell composition and oxidative stress factors and functioning of bone marrow and thymus.
 INTRODUCTION: Natalizumab, a therapy for relapsing-remitting multiple sclerosis (RRMS), is associated with a risk of progressive multifocal leukoencephalopathy (PML). Over the last several years, practitioners have used off-label extended interval dosing (EID) of natalizumab to reduce PML risk, despite the absence of a large-scale efficacy evaluation. METHODS: We conducted a retrospective, multicenter cohort study among adults with RRMS receiving stable standard interval dosing (SID), defined as a ≥ 12-month consecutive period of ≥ 11 natalizumab infusions/year in France. We compared the 12-month risk difference of remaining relapse-free (primary endpoint) between patients who switched to EID (≤ 9 natalizumab infusions) and those who remained on SID, with a noninferiority margin of - 11%. We used propensity score methods such as inverse probability treatment weighting (IPTW) and 1:1 propensity score matching (PSM). Secondary endpoints were annualized relapse rate, disease progression, and safety. RESULTS: Baseline characteristics were similar between patients receiving EID (n = 147) and SID (n = 156). The proportion of relapse-free patients 12 months postbaseline was 142/147 in the EID (96.6%) and 144/156 in the SID group (92.3%); risk difference (95% CI) 4.3% (- 1.3 to 9.8%); p < 0.001 for non-inferiority. There were no significant differences between relapse rates (0.043 vs. 0.083 per year, respectively; p = 0.14) or Expanded Disability Status Scale mean scores (2.43 vs. 2.72, respectively; p = 0.18); anti-JC virus index values were similar (p = 0.23); and no instances of PML were reported. The comparisons using IPTW (n = 306) and PSM (n = 204) were consistent. CONCLUSION: These results support the pertinence of using an EID strategy for RRMS patients treated with natalizumab. CLINICAL TRIALS: gov identifier (NCT04580381).
 BACKGROUNDWhile B cell depletion is associated with attenuated antibody responses to SARS-CoV-2 mRNA vaccination, responses vary among individuals. Thus, elucidating the factors that affect immune responses after repeated vaccination is an important clinical need.METHODSWe evaluated the quality and magnitude of the T cell, B cell, antibody, and cytokine responses to a third dose of BNT162b2 or mRNA-1273 mRNA vaccine in patients with B cell depletion.RESULTSIn contrast with control individuals (n = 10), most patients on anti-CD20 therapy (n = 48) did not demonstrate an increase in spike-specific B cells or antibodies after a third dose of vaccine. A third vaccine elicited significantly increased frequencies of spike-specific non-naive T cells. A small subset of B cell-depleted individuals effectively produced spike-specific antibodies, and logistic regression models identified time since last anti-CD20 treatment and lower cumulative exposure to anti-CD20 mAbs as predictors of those having a serologic response. B cell-depleted patients who mounted an antibody response to 3 vaccine doses had persistent humoral immunity 6 months later.CONCLUSIONThese results demonstrate that serial vaccination strategies can be effective for a subset of B cell-depleted patients.FUNDINGThe NIH (R25 NS079193, P01 AI073748, U24 AI11867, R01 AI22220, UM 1HG009390, P01 AI039671, P50 CA121974, R01 CA227473, U01CA260507, 75N93019C00065, K24 AG042489), NIH HIPC Consortium (U19 AI089992), the National Multiple Sclerosis Society (CA 1061-A-18, RG-1802-30153), the Nancy Taylor Foundation for Chronic Diseases, Erase MS, and the Claude D. Pepper Older Americans Independence Center at Yale (P30 AG21342).
 BACKGROUND: Although vaccination against SARS-CoV-2 is recommended prior to introducing anti-CD20 therapies, limited data are available regarding the evolution of post-vaccinal immunity. METHODS: This retrospective study compared anti-Spike antibody titres at 6 and 12 months from SARS-CoV-2 vaccination between patients vaccinated before switching to anti-CD20 ('Switch') and two control groups: (1) patients vaccinated under disease-modifying therapies (DMTs) other than fingolimod and anti-CD20 ('Other DMTs'); (2) patients vaccinated on anti-CD20 ('Anti-CD20'). Anti-Spike-specific T-cell responses were compared between 'Switch' and 'Anti-CD20' groups. RESULTS: Fifty-three patients were included in the 'Switch' group, 54 in the 'Other DMTs' group and 141 in the 'Anti-CD20' group. At 6 months, in the subset of patients who received a booster dose, the 'Switch' group had lower anti-Spike titres compared with the 'Other DMTs' group (median 241.0 IQR (88.0; 504.0) BAU/mL vs 2034 (1155; 4634) BAU/mL, p<0.001), and less patients in the 'Switch' group reached the protective threshold of 264 BAU/mL. The 'Switch' group had higher anti-Spike titres than the 'Anti-CD20' group (7.5 (0.0; 62.1) BAU/mL, p=0.001). Anti-Spike titres were not different between the 'Switch' and 'Other DMTs' groups before booster administration. These results were similar at 12 months. Spike-specific T-cell positivity was similar between the 'Switch' and 'Anti-CD20' groups at 6 and 12 months (60.4% vs 61.0%, p=0.53, and 79.4% vs 87.5%, p=0.31, respectively). CONCLUSIONS: Despite a primary vaccination performed before the first anti-CD20 cycle, our results suggest weaker immune responses at 6 and 12 months and decreased booster efficacy after introducing anti-CD20. Patients vaccinated prior to anti-CD20 introduction might falsely be considered as fully protected by vaccination.
 OBJECTIVES: Define the concept of cerebral microbleeds (CMBs) and describe the most useful MRI sequences for detecting this finding. Review the entities that most frequently present with CMBs and that may benefit from the use of susceptibility-weighted imaging (SWI) sequences. CONCLUSIONS: SWI is a useful MRI sequence for the detection and characterization of microhemorrhages, venous structures and other sources of susceptibility in imaging. SWI is particularly sensitive to local magnetic field inhomogeneities generated by certain substances and is superior to T2* GRE sequences for this assessment. CMBs may be seen in different neurologic conditions, in certain infrequent clinical contexts and have a key role as a biomarker status in gliomas (ITTS) and as a marker of inflammatory activity in multiple sclerosis.
 The sphingosine-1-phosphate (S1P) pathway remains an active area of research for drug discovery because S1P modulators are effective medicine for autoimmune diseases such as multiple sclerosis and ulcerative colitis. As such, other nodes in the pathway can be probed for alternative therapeutic candidates. As S1P elicits its function in an 'outside-in' fashion, targeting the transporter, Spns2, which is upstream of the receptors, is of great interest. To support our medicinal chemistry campaign to inhibit S1P transport, we developed a mammalian cell-based assay. In this protocol, Spns2 inhibition is assessed by treating HeLa, U-937, and THP-1 cells with inhibitors and S1P exported in the extracellular milieu is quantified by LC-MS/MS. Our studies demonstrated that the amount of S1P in the media in inversely proportional to inhibitor concentration. The details of our investigations are described herein.
 Cannabis, commonly known as marijuana, is used by at least 18% of the United States (US) population, which makes it the most commonly used federally illegal drug in the United States. It is widely used for recreational purposes, while its therapeutic benefits have been extensively explored in the US. For several years, cannabis has been used for the treatment of diverse health conditions, including pain management, anti-inflammatory effects, and spasticity associated with multiple sclerosis and other neurodegenerative diseases. However, cannabis use has been associated with some acute and chronic adverse effects. This review sheds light on gastrointestinal disorders, gastroesophageal reflux disease, pancreatitis, and peptic ulcer disease that have been associated with cannabis use.
 Catatonia, a neuropsychiatric syndrome characterized by psychomotor and behavioral symptoms, can be associated with various underlying conditions, including demyelinating diseases such as multiple sclerosis. This paper presents a case study of a 47-year-old female with recurrent catatonic relapses and an underlying demyelinating disease. The patient exhibited symptoms of confusion, decreased oral intake, and difficulty with movement and speech. Neurological examinations, brain imaging, and laboratory tests were conducted to evaluate the etiology and guide treatment. The patient showed improvement with lorazepam and electroconvulsive therapy (ECT). However, relapses occurred after the abrupt withdrawal of medication. The case study highlights the potential connection between demyelinating diseases and catatonia and emphasizes the importance of considering demyelinating diseases in the workup, treatment, and relapse prevention of catatonia. Further research is needed to explore the mechanisms underlying the relationship between demyelination and catatonia and to investigate how different etiologies may impact the recurrence rates of catatonic episodes.
 Neuroinflammation is both cause and effect of many neurodegenerative disorders. Activation of astrocytes and microglia leads to the release of cytokines and reactive oxygen species followed by blood-brain barrier leakage and neurotoxicity. Transient neuroinflammation is considered to be largely protective, however, chronic neuroinflammation contributes to the pathology of Alzheimer's disease, multiple sclerosis, traumatic brain injury, and many more. In this study, we focus on the aspect of cytokine-induced neuroinflammation in human microglia and astrocytes. Here we show by mRNA and protein analysis that cytokines, released not only by microglia but also by astrocytes, lead to a circuit of proinflammatory activation. Moreover, we present how the natural compound resveratrol can stop the circuit of proinflammatory activation and facilitate return to resting conditions. These results will contribute to distinguishing between the causes and the effects of neuroinflammation, a better understanding of underlying mechanisms, and potential treatment options.
 Microglia exhibit diverse phenotypes in various central nervous system disorders and metabolic pathways exert crucial effects on microglial activation and effector functions. Here, we discovered two novel distinct microglial clusters, functionally associated with enhanced phagocytosis (PEMs) and myelination (MAMs) respectively, in human patients with multiple sclerosis by integrating public snRNA-seq data. Microglia adopt a PEMs phenotype during the early phase of demyelinated lesions, predominated in pro-inflammatory responses and aggravated glycolysis, while MAMs mainly emerged during the later phase, with regenerative signatures and enhanced oxidative phosphorylation. In addition, microglial triggering receptor expressed on myeloid cells 2 (Trem2) was greatly involved in the phenotype transition in demyelination, but not indispensable for microglia transition toward PEMs. Rosiglitazone could promote microglial phenotype conversion from PEMs to MAMs, thus favoring myelin repair. Taken together, these findings provide insights into therapeutic interventions targeting immunometabolism to switch microglial phenotypes and facilitate regenerative capacity in demyelination.
 The modified Ashworth scale is the most universally accepted clinical tool used to measure the increase of muscle tone. Spasticity was defined by Jim Lance in 1980, as a velocity-dependent increase in muscle stretch reflexes associated with increased muscle tone as a component of upper motor neuron syndrome. Spasticity has a wide range of etiologies, including brain injury, stroke, cerebral palsy, multiple sclerosis, trauma, and spinal cord injury. In a study looking at the prevalence of spasticity in stroke populations, 42.6% of stroke patients developed spasticity, and severe spasticity occurred in 15.6% of patients. Another study looking at the prevalence of spasticity in cerebral palsy found spastic subtypes in 90% of the patients studied. The impact of severe spasticity on a patient’s life is far-reaching, affecting everything from activities of daily living to mental health and even income. On the other hand, spasticity can be helpful in patients with weak limbs, especially in the lower extremities, by enabling the patient to transfer or ambulate with less assistance.  For these reasons, the assessment of spasticity is important so that practitioners can determine if their treatment therapies are effective. 
 Neurodegenerative disorders (NDs) are progressive morbidities that represent a serious health issue in the aging world population. There is a contemporary upsurge in worldwide interest in the area of traditional remedies and phytomedicines are widely accepted by researchers due to their health-promoted effects and fewer side effects. Hesperidin, a flavanone glycoside present in the peels of citrus fruits, possesses various biological activities including anti-inflammatory and antioxidant actions. In various preclinical studies, hesperidin has provided significant protective actions in a variety of brain disorders such as Alzheimer's disease, epilepsy, Parkinson's disease, multiple sclerosis, depression, neuropathic pain, etc. as well as their underlying mechanisms. The findings indicate that the neuroprotective effects of hesperidin are mediated by modulating antioxidant defence activities and neural growth factors, diminishing apoptotic and neuro-inflammatory pathways. This review focuses on the potential role of hesperidin in managing and treating diverse brain disorders.
 OBJECTIVES: Vaccination against SARS-CoV-2 is considered beneficial by the majority, but side effects occur in some cases. RESULTS AND CONCLUSIONS: We report on a 28-year-old female who developed fever within 3 days of an initial dose with a vector-based SARS-CoV-2 vaccine. Eight days after vaccination, she developed paresthesias and dysesthesias of all four limbs. Cerebral imaging showed two non-specific and non-enhancing lesions in the left white matter. Cerebrospinal fluid (CSF) studies revealed pleocytosis of 82/3 cells. Examination for multiple sclerosis, neuromyelitis optica, acute, demyelinating encephalomyelitis, and Guillain-Barre syndrome was negative. She received steroids, which resulted in complete resolution of the neurological abnormalities. In summary, SARS-CoV-2 vaccination can occasionally be complicated by an inflammatory CSF syndrome, which resolves on administration of steroids.

 Niacin (vitamin B3) is an essential nutrient that treats pellagra, and prior to the advent of statins, niacin was commonly used to counter dyslipidemia. Recent evidence has posited niacin as a promising therapeutic for several neurological disorders. In this review, we discuss the biochemistry of niacin, including its homeostatic roles in NAD(+) supplementation and metabolism. Niacin also has roles outside of metabolism, largely through engaging hydroxycarboxylic acid receptor 2 (Hcar2). These receptor-mediated activities of niacin include regulation of immune responses, phagocytosis of myelin debris after demyelination or of amyloid beta in models of Alzheimer's disease, and cholesterol efflux from cells. We describe the neurological disorders in which niacin has been investigated or has been proposed as a candidate medication. These are multiple sclerosis, Alzheimer's disease, Parkinson's disease, glioblastoma and amyotrophic lateral sclerosis. Finally, we explore the proposed mechanisms through which niacin may ameliorate neuropathology. While several questions remain, the prospect of niacin as a therapeutic to alleviate neurological impairment is promising.
 BACKGROUND AND OBJECTIVE: Prognostication is the process of predicting a patient's likely outcome from their medical condition, and consists of determining both how well and how long a patient may live. There are few disease-specific prognostic tools to estimate a patient's individualized prognosis in terms of symptom burden and mortality. Here we summarize relevant literature on prognosis in four progressive neurologic diseases-dementia, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis-as well as on best practices on communicating prognosis with patients and care partners. METHODS: We conducted a PubMed search for terms including "prognosis", "mortality" and "prognostic indicators" in addition to specific diseases, and for terms including "prognosis AND communication". Only English-language papers were included in this review. The time frame of our literature search was 1965 through March 1, 2023. KEY CONTENT AND FINDINGS: There is some literature to help clinicians in predicting disease progression and survival. These include both general factors (e.g., age, medical co-morbidities) and diseasespecific factors (e.g., postural instability in Parkinson's disease). There is also literature on communication of prognosis in neurologic and non-neurologic disease which demonstrates that many patients and care partners prefer to hear prognosis early after diagnosis and to have prognosis discussed as a roadmap of disease. CONCLUSIONS: More work is needed to develop tools for individualized prognostication and communication for patients with neurologic disease. While there is limited literature on disease-specific prognostic models, existing literature combined with palliative care approaches may improve prognostic guidance for patients.
 The amount of cladribine in milk is low with oral doses of 10 to 20 mg daily used in multiple sclerosis. Data in one patient indicates that the drug is rapidly eliminated over 24 hours and undetectable at 48 hours after a dose. Manufacturers recommend a 7-day (Europe) or 10-day (US) abstinence period. Chemotherapy may adversely affect the normal microbiome and chemical makeup of breastmilk.[1] Women who receive chemotherapy during pregnancy are more likely to have difficulty nursing their infant.[2]

 Tissue macrophages, including microglia, are notoriously resistant to genetic manipulation. Here, we report the creation of Adeno-associated viruses (AAV) variants that efficiently and widely transduce microglia and tissue macrophages in vivo following intravenous delivery, with transgene expression of up to 80%. We use this technology to demonstrate manipulation of microglia gene expression and microglial ablation, thereby providing invaluable research tools for the study of these important cells.
 In recent years the definition of neuromyelitis optica (NMO), or Devic disease, has been expanded as a specific antibody was discovered in the serum of affected patients. Because of this, the term neuromyelitis optica spectrum disorder (NMOSD) is now used to include optic neuritis with spinal cord manifestations and include other neurologic disorders associated with the serum aquaporin-4 immunoglobulin G antibodies (AQP4-IgG).  NMO was first described by Dr. Eugene Devic, who in 1894 described a patient with optic neuritis with accompanying neuromuscular manifestations. That same year, Fernand Gault, who was Devic’s student, published his doctoral thesis presenting a literature review of previous medical cases, including the clinicopathological findings of Dr. Devic’s case.  For years, multiple sclerosis (MS) was the most prevalent identifiable cause of optic neuritis. Recent discoveries have highlighted rarer, more sinister manifestations of optic neuritis such as NMOSD and myelin oligodendrocyte glycoprotein (MOG), which necessitate additional evaluation and treatment.
 Human endogenous retroviruses (ERVs) are ancestorial retroviral elements that were integrated into our genome through germline infections and insertions during evolution. They have repeatedly been implicated in the aetiology and pathophysiology of numerous human disorders, particularly in those that affect the central nervous system. In addition to the known association of ERVs with multiple sclerosis and amyotrophic lateral sclerosis, a growing number of studies links the induction and expression of these retroviral elements with the onset and severity of neurodevelopmental and psychiatric disorders. Although these disorders differ in terms of overall disease pathology and causalities, a certain degree of (subclinical) chronic inflammation can be identified in all of them. Based on these commonalities, we discuss the bidirectional relationship between ERV expression and inflammation and highlight that numerous entry points to this reciprocal sequence of events exist, including initial infections with ERV-activating pathogens, exposure to non-infectious inflammatory stimuli, and conditions in which epigenetic silencing of ERV elements is disrupted.
 OBJECTIVE: Among persons with immune-mediated inflammatory diseases (IMIDs) who received SARS-CoV-2 vaccines, we compared postvaccine antibody responses and IMID disease activity/states. DESIGN: Single-centre prospective cohort study. SETTING: Specialty ambulatory clinics in central Canada. PARTICIPANTS: People with inflammatory arthritis (n=78; 77% rheumatoid arthritis), systemic autoimmune rheumatic diseases (n=84; 57% lupus), inflammatory bowel disease (n=93; 43% Crohn's) and multiple sclerosis (n=72; 71% relapsing-remitting) (female 79.4%, white 84.7%, mean (SD) age 56.0 (14.3) years) received COVID-19 vaccinations between March 2021 and September 2022. PRIMARY OUTCOME: Postvaccination anti-spike, anti-receptor binding domain (anti-RBD) and anti-nucleocapsid (anti-NC) IgG antibodies tested by multiplex immunoassays compared across vaccine regimens and with responses in 370 age-matched and sex-matched vaccinated controls. SECONDARY OUTCOMES: COVID-19 infection and self-reported IMID disease activity/state. RESULTS: Most (216/327, 66.1%) received homologous messenger RNA (mRNA) (BNT162b2 or mRNA1273) vaccines, 2.4% received homologous ChAdOx1 and 30.6% received heterologous vaccines (23.9% ChAdOx1/mRNA, 6.4% heterologous mRNA) for their first two vaccines (V1, V2). Seroconversion rates were 52.0% (91/175) for post-V1 anti-spike and 58.9% (103/175) for anti-RBD; 91.5% (214/234) for post-V2 anti-spike and 90.2% (211/234) for anti-RBD; and were lower than controls (post-V2 anti-spike 98.1% (360/370), p<0.0001). Antibody titres decreased 3 months after V2 but increased 1 month after the third vaccine (V3) and 1 month after the fourth vaccine (V4) (BAU/mL median (IQR), anti-spike 1835 (2448) 1 month post-V2, 629.1 (883.4) 3 months post-V2, 4757.5 (7033.1) 1 month post-V3 and 4356.0 (9393.4) 1 month post-V4; anti-RBD 1686.8 (2199.44) 1 month post-V2, 555.8 (809.3) 3 months post-V2, 4280.3 (6380.6) 1 month post-V3 and 4792.2 (11 673.78) 1 month post-V4). If primed with a vector vaccine, an mRNA vaccine increased antibody titres to those comparable to homologous mRNA vaccines. Anti-RBD and anti-spike titres were higher in anti-NC seropositive (n=31; 25 participants) versus seronegative samples (BAU/mL median (IQR) anti-RBD 11 755.3 (20 373.1) vs 1248.0 (53 278.7); anti-spike 11 254.4 (15 352.6) vs 1313.1 (3106.6); both p<0.001). IMID disease activity/state and rates of self-reported moderate or severe IMID flare were similar across vaccinations. CONCLUSION: Heterologous COVID-19 vaccination improves seroconversion rates following a vector vaccine and does not lead to IMID disease flare. IMIDs benefit from at least three vaccines.
 BACKGROUND: For patients with idiopathic or multiple sclerosis (MS)-associated optic neuritis (ON), the largest multicenter clinical trial (Optic Neuritis Treatment Trial [ONTT]) showed excellent visual outcomes and baseline high-contrast visual acuity (HCVA) was the only predictor of HCVA at 1 year. We aimed to evaluate predictors of long-term HCVA in a modern, real-world population of patients with ON and compare with previously published ONTT models. METHODS: We performed a retrospective, longitudinal, observational study at the University of Michigan and the University of Calgary evaluating 135 episodes of idiopathic or MS-associated ON in 118 patients diagnosed by a neuro-ophthalmologist within 30 days of onset (January 2011-June 2021). Primary outcome measured was HCVA (Snellen equivalents) at 6-18 months. Multiple linear regression models of 107 episodes from 93 patients assessed the association between HCVA at 6-18 months and age, sex, race, pain, optic disc swelling, symptoms (days), viral illness prodrome, MS status, high-dose glucocorticoid treatment, and baseline HCVA. RESULTS: Of the 135 acute episodes (109 Michigan and 26 Calgary), median age at presentation was 39 years (interquartile range [IQR], 31-49 years), 91 (67.4%) were women, 112 (83.0%) were non-Hispanic Caucasians, 101 (75.9%) had pain, 33 (24.4%) had disc edema, 8 (5.9%) had a viral prodrome, 66 (48.9%) had MS, and 62 (46.6%) were treated with glucocorticoids. The median (IQR) time between symptom onset and diagnosis was 6 days (range, 4-11 days). The median (IQR) HCVA at baseline and at 6-18 months were 20/50 (20/22, 20/200) and 20/20 (20/20, 20/27), respectively; 62 (45.9%) had better than 20/40 at baseline and 117 (86.7%) had better than 20/40 at 6-18 months. In linear regression models (n = 107 episodes in 93 patients with baseline HCVA better than CF), only baseline HCVA (β = 0.076; P = 0.027) was associated with long-term HCVA. Regression coefficients were similar and within the 95% confidence interval of coefficients from published ONTT models. CONCLUSIONS: In a modern cohort of patients with idiopathic or MS-associated ON with baseline HCVA better than CF, long-term outcomes were good, and the only predictor was baseline HCVA. These findings were similar to prior analyses of ONTT data, and as a result, these are validated for use in conveying prognostic information about long-term HCVA outcomes.
 BACKGROUND: In the field of neurorehabilitation, robot-assisted therapy (RAT) and virtual reality (VR) have so far shown promising evidence on multiple motor and functional outcomes. The related effectiveness on patients' health-related quality of life (HRQoL) has been investigated across neurological populations but still remains unclear. The present study aimed to systematically review the studies investigating the effects of RAT alone and with VR on HRQoL in patients with different neurological diseases. METHODS: A systematic review of the studies evaluating the impact of RAT alone and combined with VR on HRQoL in patients affected by neurological diseases (i.e., stroke, multiple sclerosis, spinal cord injury, Parkinson's Disease) was conducted according to PRISMA guidelines. Electronic searches of PubMed, Web of Science, Cochrane Library, CINAHL, Embase, and PsychINFO (2000-2022) were performed. Risk of bias was evaluated through the National Institute of Health Quality Assessment Tool. Descriptive data regarding the study design, participants, intervention, rehabilitation outcomes, robotic device typology, HRQoL measures, non-motor factors concurrently investigated, and main results were extracted and meta-synthetized. RESULTS: The searches identified 3025 studies, of which 70 met the inclusion criteria. An overall heterogeneous configuration was found regarding the study design adopted, intervention procedures and technological devices implemented, rehabilitation outcomes (i.e., related to both upper and lower limb impairment), HRQoL measures administered, and main evidence. Most of the studies reported significant effects of both RAT and RAT plus VR on patients HRQoL, whether they adopted generic or disease-specific HRQoL measures. Significant post-intervention within-group changes were mainly found across neurological populations, while fewer studies reported significant between-group comparisons, and then, mostly in patients with stroke. Longitudinal investigations were also observed (up to 36 months), but significant longitudinal effects were exclusively found in patients with stroke or multiple sclerosis. Finally, concurrent evaluations on non-motor outcomes beside HRQoL included cognitive (i.e., memory, attention, executive functions) and psychological (i.e., mood, satisfaction with the treatment, device usability, fear of falling, motivation, self-efficacy, coping, and well-being) variables. CONCLUSIONS: Despite the heterogeneity observed among the studies included, promising evidence was found on the effectiveness of RAT and RAT plus VR on HRQoL. However, further targeted short- and long-term investigations, are strongly recommended for specific HRQoL subcomponents and neurological populations, through the adoption of defined intervention procedures and disease-specific assessment methodology.
 INTRODUCTION: Lhermitte's phenomenon (LP) is a transient shock-like sensation that radiates down the spine into the extremities, usually with neck flexion. The potential efficacy and tolerability of various symptomatic therapies in the management of LP have not been systematically reviewed previously. METHOD: A systematic review was conducted using PubMed, EMBASE, and the Cochrane Library from inception to August 2022 for peer-reviewed articles describing the treatment of patients with Lhermitte's phenomenon. The review adheres to the PRISMA guidelines and was registered on PROSPERO. RESULTS: This systematic review included sixty-six articles, which included 450 patients with LP. Treatment of the underlying cause varied by aetiology. Whilst LP is most commonly considered in the context of structural pathology of the cervical cord, medication-induced LP was a common theme in the literature. The most common cause of medication-induced LP was platinum-based chemotherapy agents such as cisplatin and oxaliplatin. In medication-induced LP, symptoms typically resolved with cessation of the causative agent. Non-pharmacological treatment options were associated with mild-moderate symptomatic improvement. The most commonly used agents to treat patients with LP were carbamazepine and gabapentin, which resulted in variable degrees of symptomatic benefit. CONCLUSIONS: No randomised studies currently exist to support the use of symptomatic therapies to treat LP. Observational data suggest that some therapies may yield a symptomatic benefit in the management of LP. However, this systematic review identified a significant paucity of evidence in the literature, which suggests that further controlled studies are needed to investigate the optimal management of this common neurologic phenomenon.
 The vitamin D/Vitamin D receptor (VDR) axis is crucial for human health as it regulates the expression of genes involved in different functions, including calcium homeostasis, energy metabolism, cell growth and differentiation, and immune responses. In particular, the vitamin D/VDR complex regulates genes of both innate and adaptive immunity. Autoimmune diseases are believed to arise from a genetic predisposition and the presence of triggers such as hormones and environmental factors. Among these, a role for Vitamin D and molecules correlated to its functions has been repeatedly suggested. Four single nucleotide polymorphisms (SNPs) of the VDR gene, ApaI, BsmI, TaqI, and FokI, in particular, have been associated with autoimmune disorders. The presence of particular VDR SNP alleles and genotypes, thus, was observed to modulate the likelihood of developing diverse autoimmune conditions, either increasing or reducing it. In this work, we will review the scientific literature suggesting a role for these different factors in the pathogenesis of autoimmune conditions and summarize evidence indicating a possible VDR SNP involvement in the onset of these diseases. A better understanding of the role of the molecular mechanisms linking Vitamin D/VDR and autoimmunity might be extremely useful in designing novel therapeutic avenues for these disorders.
 The aim was to evaluate the performance of the latest quantitative marker for intrathecal IgG synthesis and to compare it with other established markers used for the same purpose. We retrospectively applied Auer's and Reiber's intrathecal IgG synthesis formulae in a cohort of 372 patients under investigation for central nervous system demyelination who had undergone lumbar puncture and oligoclonal bands (OCBs) detection for demonstrating intrathecal IgG synthesis. A ROC analysis revealed Auer's formula had lower sensitivity (68%) compared to Reiber's formula (83%) and IgG index (89%), in our cohort of patients that exhibited normal to mildly elevated albumin quotients (4.48 ± 3.93). By excluding possible sources of errors, we assume that Auer's formula is less sensitive than other established tools for the "prediction" of the detection of OCBs in routine cerebrospinal fluid (CSF) analyses due to the mathematical model used. Given the ability of Reiber's hyperbolic formula to describe the blood-CSF IgG distribution across a wide range of blood-brain barrier functionality, its use and the use of similar formulae are recommended for the discrimination between CNS-derived and blood-derived molecules in clinical laboratories.
 BACKGROUND: Anti-CD20 agents are commonly used in MS, NMOSD, and MOGAD. Few studies have compared strategies to address hypogammaglobulinemia. OBJECTIVE: To compare strategies to manage secondary hypogammaglobulinemia in neuroimmunology patients, including reducing anti-CD20 dose and dosing frequency, IVIG/SCIG, anti-CD20 cessation, and DMT switches. METHODS: All MS, NMOSD, and MOGAD patients at our institution with hypogammaglobulinemia on anti-CD20 agents from 2001 to 2022 were analyzed. The median change in IgG, infection frequency, and infection severity before and after the treatment was calculated. RESULTS: In total, 257 patients were screened, and 30 had a treatment for hypogammaglobulinemia. IVIG/SCIG yielded the largest increase in IgG per year (674.0 mg/dL), followed by B-cell therapy cessation (34.7 mg/dL), and DMT switch (5.9 mg/dL). Dose reduction had the largest decrease in yearly infection frequency (2.7 fewer infections), followed by IVIG/SCIG (2.5 fewer), DMT switch (2 fewer), and reduced dosing frequency (0.5 fewer). Infection grade decreased by 1.9 for reduced dosing frequency (less severe infections), by 1.3 for IVIG/SCIG, and by 0.6 for DMT switch. CONCLUSION: This data suggests that IVIG/SCIG may yield the greatest recovery in IgG while also reducing infection frequency and severity. Stopping anti-CD20 therapy and/or switching DMTs also increase IgG and may lower infection risk.
 The implantation of oligodendrocyte precursor cells may be a useful therapeutic strategy for targeting remyelination. However, it is yet to be established how these cells behave after implantation and whether they retain the capacity to proliferate or differentiate into myelin-forming oligodendrocytes. One essential issue is the creation of administration protocols and determining which factors need to be well established. There is controversy around whether these cells may be implanted simultaneously with corticosteroid treatment, which is widely used in many clinical situations. This study assesses the influence of corticosteroids on the capacity for proliferation and differentiation and the survival of human oligodendroglioma cells. Our findings show that corticosteroids reduce the capacity of these cells to proliferate and to differentiate into oligodendrocytes and decrease cell survival. Thus, their effect does not favour remyelination; this is consistent with the results of studies with rodent cells. In conclusion, protocols for the administration of oligodendrocyte lineage cells with the aim of repopulating oligodendroglial niches or repairing demyelinated axons should not include corticosteroids, given the evidence that the effects of these drugs may undermine the objectives of cell transplantation.
 BACKGROUND: As operative techniques and implant design have evolved over time, total hip arthroplasty (THA) is increasingly being carried out for patients with neurological impairment. This patient group places unique surgical challenges to the arthroplasty surgeon, which may include contractures, instability, and altered muscular tone. The purpose of this systematic review is to report the patient outcomes, complications, and implant survival following THA for patients with neurological conditions affecting the hip. Thus, we aim to support orthopaedic surgeon decision-making when considering and planning THA for these patients. METHODS: A systematic review was performed as per Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines using the PubMed/Medline OVID, Cochrane, and Embase databases. All studies reporting the outcomes of THA in the neurological population which met defined inclusion criteria were included. RESULTS: From an initial screen of 1820 studies, 45 studies with a total of 36,251 THAs were included in the final selection. All 45 studies reported complication rates, with controls included in 16 for comparison. High complication rates were observed following THA in the neurologically impaired population, most notably dislocation with observed rates up to 10.6%. An improvement was noted in all 36 studies (1811 THAs) which reported upon patient-reported outcomes. CONCLUSIONS: THA may be beneficial in the selected patients with neurological conditions, to reduce pain and improve function. There is an increased risk of complications which require careful consideration when planning the operation and open discussion with prospective patients and caregivers before proceeding with surgery.
 OBJECTIVE: To investigate the prevalence of sexual dysfunction (SD) and depression in patients with neuromyelitis optica (NMO), a demyelinating disorder of the central nervous system. METHODS: A total of 110 NMO patients and 112 healthy individuals were included as a control group, and their SD was assessed using the Female Sexual Function Inventory (FSFI) and the International Index of Erectile Function (IIEF) for women and men, respectively. The FSFI categorizes female sexual dysfunction into six subscores, including libido, arousal, lubrication, orgasm, sexual satisfaction, and pain, while the IIEF categorizes male sexual dysfunction into five subscores, including sexual desire, erection, orgasm, intercourse satisfaction, and overall satisfaction. RESULTS: SD was prevalent among NMO patients, with 78% of female patients and 63.2% of male patients reporting SD in at least one subscore. The severity of the disease, as measured by the Expanded Disability Status Scale (EDSS), was found to be significantly correlated with SD in all subscores, while the duration of the disease was only correlated with the overall satisfaction subscore in men and the pain subscore in women. Furthermore, SD was found to be significantly correlated with depression in these patients. CONCLUSION: The study highlights the importance of addressing SD and depression in NMO patients, as they adversely affect the quality of life. The findings suggest that the physical aspects of SD are mostly affected by the severity of the disease, while psychological aspects are highly correlated with the chronicity of the disease.
 INTRODUCTION: Recombinant monoclonal antibodies (mAbs) are highly selective and effective biologicals with proven utility as therapeutics. mAbs have demonstrated substantial promise in the treatment of several central nervous system diseases. AREAS COVERED: Databases including PubMed and Clinicaltrials.gov were used to identify clinical studies of mAbs involving patients with neurological disorders. This manuscript reviews the current status and recent advances in the development and engineering of therapeutic blood-brain barrier (BBB)-crossing mAbs and their potential in treatment of central nervous system diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), brain tumors, and neuromyelitis optica spectrum disorder (NMSOD). In addition, the clinical implications of recently developed monoclonal antibodies are also discussed, along with the strategies to enhance their BBB permeability. The adverse events associated with the administration of monoclonal antibodies are also presented in the manuscript. EXPERT OPINION: There is growing evidence that supports the therapeutic utility of monoclonal antibodies in central nervous system and neurodegenerative diseases. Several studies have offered evidence of clinical efficacy in AD through use of anti-amyloid beta antibodies and anti-tau passive immunotherapy-based strategies. Additionally, ongoing research trials have produced promising findings for the treatment of brain tumors and NMSOD.
 The specialized nurse in MS is a new profession practiced in MS clinics and outpatients specialized coordination structures. She is part of a specialized multi-professional team. The nurse must master a broad knowledge of the disease and the treatments. Have skills in therapeutic education, communication and coordination. She has a detailed knowledge of the resources of the care offer. The MS nurse thus participates in the assessment of the patient's needs for the implementation of a personalized care plan combining response to medical, paramedical, psychological and social needs.
 BACKGROUND: MS is deeply impacted by social factors, such as access to health services, support from official and unofficial sources, and social welfare, which are also thought to contribute to the quality of life of MS patients. The purpose of this study is to examine the quality of life and to analyse the psychosocial challenges of MS patients in North Cyprus and Germany. METHODS: This study was designed with a cross-sectional and comparative research method. The personal information form and the WHO Quality of Life Scale Short Form were used. A total sixty-eight participants joined the study: 35 German patients and 33 Turkish Cypriot patients. Researchers collected the data by face-to-face interviews between December 2021 and March 2022. The majority of MS patients were females average age was 49.48 years old. RESULTS: In general, the two populations had comparable total sub-dimension scores of quality of life. However, only environment sub-dimension score has significant difference between Germany (x̄ =70.04) and North Cyprus (x̄ =55.87). Perceived opportunities for accessing medication, physiotherapy, and psychological support, as well as the opportunity to receive psychological support after the time of diagnosis were considered greater in the German group compared to the Turkish Cypriot one. CONCLUSION: Findings from this cross-sectional research demonstrate significant differences in services provided, particularly in the psychosocial domain, between those in Germany and those in Cyprus. Consequently, all parties in both countries (governments, families, health workers, social workers and people with MS) should cooperate to improve social support mechanisms. Moreover, it is needed better access to health services in Northern Cyprus.
 Epstein-Barr virus (EBV) infection is associated with a variety of the autoimmune diseases. There is apparently no unified model for the role of EBV in autoimmune diseases. In this article, the development of autoimmune diseases is proposed as a simple two-step process: specific autoimmune initiators may cause irreversible changes to genetic materials that increase autoimmune risks, and autoimmune promoters promote autoimmune disease formation once cells are susceptible to autoimmunity. EBV has several types of latencies including type III latency with higher proliferation potential. EBV could serve as autoimmune initiators for some autoimmune diseases. At the same time, EBV may play a promotional role in majority of the autoimmune diseases by repeated replenishment of EBV type III latency cells and inflammatory cytokine productions in persistent stage. The type III latency cells have enhanced capacity as antigen-presenting cells that would facilitate the development of both B and T cell-mediated autoimmunity. The repeated cytokine productions are achieved by the repeated infection of naive B-lymphocytes and proliferation of type III latency cells that produce inflammatory cytokines. Presentation of viral or self-antigens by EBV type III latency B lymphocytes may promote autoreactive B cell and T cell proliferation, which can be amplified by type III latency cells-mediated cytokines productions. Different autoimmune diseases may require different kinds of pathogenic immune cells and/or specific cytokines. Frequency of the replenishment of EBV type III latency cells may determine the specific effect of the promoter functions. A specific initiator plus EBV-mediated common promoter function may lead to development of a specific autoimmune disease and link EBV-infection to a variety of autoimmunity.
 Microglia, the resident immune cells of the central nervous system, play a critical role in maintaining brain homeostasis. However, in neurodegenerative conditions, microglial cells undergo metabolic reprogramming in response to pathological stimuli, including Aβ plaques, Tau tangles, and α-synuclein aggregates. This metabolic shift is characterized by a transition from oxidative phosphorylation (OXPHOS) to glycolysis, increased glucose uptake, enhanced production of lactate, lipids, and succinate, and upregulation of glycolytic enzymes. These metabolic adaptations result in altered microglial functions, such as amplified inflammatory responses and diminished phagocytic capacity, which exacerbate neurodegeneration. This review highlights recent advances in understanding the molecular mechanisms underlying microglial metabolic reprogramming in neurodegenerative diseases and discusses potential therapeutic strategies targeting microglial metabolism to mitigate neuroinflammation and promote brain health. Microglial Metabolic Reprogramming in Neurodegenerative Diseases This graphical abstract illustrates the metabolic shift in microglial cells in response to pathological stimuli and highlights potential therapeutic strategies targeting microglial metabolism for improved brain health.
 BACKGROUND: Early and effective treatment of central nervous system (CNS) inflammatory disorders is vital to reduce neurologic morbidity and improve long-term outcomes in affected children. Rituximab is a B-cell-depleting monoclonal antibody whose off-label use for these disorders is funded in the province of Alberta, Canada, by the Short-Term Exceptional Drug Therapy (STEDT) program. This study describes the use of rituximab for pediatric CNS inflammatory disorders in Alberta. METHODS: Rituximab applications for CNS inflammatory indications in patients <18 years of age were identified from the STEDT database between January 1, 2012, and December 31, 2019. Patient information was linked to other provincial datasets including the Discharge Abstract Database, Pharmaceutical Information Network, and Provincial Laboratory data. Analysis was descriptive. RESULTS: Fifty-one unique rituximab applications were identified, of which 50 were approved. New applications increased from one in 2012 to a high of 12 in 2018. The most common indication was autoimmune encephalitis without a specified antibody (n = 16, 31%). Most children were approved for a two-dose (n = 33, 66%) or four-dose (n = 16, 32%) induction regimen. Physician-reported outcomes were available for 24 patients, of whom 14 (58%) were felt to have fully met outcome targets. CONCLUSION: The use of rituximab for pediatric CNS inflammatory disorders has increased, particularly for the indication of autoimmune encephalitis. This study identified significant heterogeneity in dosing practices and laboratory monitoring. Standardized protocols for the use of rituximab in these disorders and more robust outcome reporting will help better define the safety and efficacy of rituximab in this population.
 When sojourners visit to high altitude, various symptoms may appear in the body including gastrointestinal symptoms such as poor appetite or nausea, vomiting, and incapacitating. The gastrointestinal tract is a key organ involved in the development of acute mountain sickness (AMS). The intestinal epithelial lining is covered by mucus layer. Mucosal barrier is considered as first line of protection of the gut wall which not only helps in lubricating and facilitating progression of bolus but also protects intestinal epithelial lining. Gut microbes play a major role in alterations of mucus barrier and may have important role in curtailing gastrointestinal symptoms at high altitude. In our previous study, we have reported ~ 17% decrease in Akkermansia muciniphila bacteria under hypobaric hypoxia exposure in Sprague-Dawley rats. A. muciniphila is a mucin-degrading bacterium. Its presence in the human intestine is inversely associated to a number of diseases. A. muciniphila is found in the mucus layer, where it helps to maintain intestinal integrity and protects from various inflammatory diseases. Hypoxia decreases A. muciniphila bacterium in gut leading to gastrointestinal barrier injury. It could be an important probiotic that may have physiological benefits in high-altitude hypoxia induced clinical scenarios. A large-scale clinical experiments, production feasibility, and regulatory clearances need to be resolved to develop it as next generation probiotic. In this review, we have searched various databases including PubMed and Google Scholar with keywords Akkermansia muciniphila, A. muciniphila, human physiology, etc. to comprehensively highlight the importance of this gut bacterium. KEY POINTS: • High-altitude hypoxia leads to gastrointestinal barrier injury. • Hypoxia decreases Akkermansia muciniphila bacterium in gut. • A. muciniphila as probiotic may help to maintain intestinal integrity.
 Oxidative stress is heavily involved in several pathological features of Multiple Sclerosis (MS), such as myelin destruction, axonal degeneration, and inflammation. Different therapies have been shown to reduce the oxidative stress that occurs in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). Some of these therapies are transcranial magnetic stimulation (TMS), extra virgin olive oil (EVOO) and S-allyl cysteine (SAC). This study aims to test the antioxidant effect of these three therapies, to compare the efficacy of SAC versus TMS and EVOO, and to analyze the effect of combining SAC + TMS and SAC and EVOO. Seventy Dark Agouti rats were used, which were divided into Control group; Vehicle group; Mock group; SAC; EVOO; TMS; SAC + EVOO; SAC + TMS; EAE; EAE + SAC; EAE + EVOO; EAE + TMS; EAE + SAC + EVOO; EAE + SAC + TMS. The TMS consisted of an oscillatory magnetic field in the form of a sine wave with a frequency of 60 Hz and an amplitude of 0.7mT (EL-EMF) applied for two hours in the morning, once a day, five days a week. SAC was administered at a dose of 50 mg/kg body weight, orally daily, five days a week. EVOO represented 10% of their calorie intake in the total standard daily diet of rats AIN-93G. All treatments were maintained for 51 days. TMS, EVOO and SAC, alone or in combination, reduce oxidative stress, increasing antioxidant defenses and also lowering the clinical score. Combination therapies do not appear to be more potent than individual therapies against the oxidative stress of EAE or its clinical symptoms.
 Spinal cord MRI is not routinely performed for multiple sclerosis (MS) monitoring. Here, we explored whether spinal cord MRI activity offers any added value over brain MRI activity for clinical outcomes prediction in MS. This is a retrospective, monocentric study including 830 MS patients who underwent longitudinal brain and spinal cord MRI [median follow-up 7 years (range: < 1-26)]. According to the presence (or absence) of MRI activity defined as at least one new T2 lesion and/or gadolinium (Gd) enhancing lesion, each scan was classified as: (i) brain MRI negative/spinal cord MRI negative; (ii) brain MRI positive/spinal cord MRI negative; (iii) brain MRI negative/spinal cord MRI positive; (iv) brain MRI positive/spinal cord MRI positive. The relationship between such patterns and clinical outcomes was explored by multivariable regression models. When compared with the presence of brain MRI activity alone: (i) Gd + lesions in the spine alone and both in the brain and in the spinal cord were associated with an increased risk of concomitant relapses (OR = 4.1, 95% CI 2.4-7.1, p < 0.001 and OR = 4.9, 95% CI 4.6-9.1, p < 0.001, respectively); (ii) new T2 lesions at both locations were associated with an increased risk of disability worsening (HR = 1.4, 95% CI = 1.0-2.1, p = 0.05). Beyond the presence of brain MRI activity, new spinal cord lesions are associated with increased risk of both relapses and disability worsening. In addition, 16.1% of patients presented asymptomatic, isolated spinal cord activity (Gd + lesions). Monitoring MS with spinal cord MRI may allow a more accurate risk stratification and treatment optimization.
 BACKGROUND: Cladribine was approved for the treatment of multiple sclerosis (MS). Real-world data is very limited. OBJECTIVES: To study the effectiveness and the safety of Cladribine treatment in only one group of MS patients after treatment with Cladribine for two years. METHODS: This observational, longitudinal prospective study. Eligible subjects were relapsing remitting MS patients who had at least two-year follow-up after Cladribine treatment. The primary endpoint was the proportion of relapse free patients. Secondary endpoints were ARR, change in EDSS scores, the proportion of patients with CDP, MRI activity, and NEDA-3 status, also the rate of occurrence of AEs. Patients were assessed for primary and secondary endpoints at the end of two years of follow-up. RESULTS: Of a total of seventy-two patients, 59 (81.9 %) were females, mean age of 36.32 + 10.06 years old, mean disease duration 7.21 + 6.19. Most patients (n = 32; 44.4 %) were naïve to any treatment. Forty patients (55.6 %) completed two courses of treatment. The primary endpoint showed that most of our cohort was relapse free (85 % versus 25 %; P < 0.001), Secondary endpoints showed that ARR was significantly reduced 0.15 + 0.36 versus 0.85 + 0.53; P < 0.01). Most of the cohort 90 % have no progression of disability. Few subjects had new T2 lesions (7.5 % versus 70.8 %; P < 0.001 and gadolinium enhancement 5 % versus 66.7 %; P < 0.001) in MRI compared to baseline. No evidence of disease activity 3 (NEDA-3) was achieved in 30 (75 %) patients. It was achieved in 87.5 % of naive patients versus 66.7 % in patients who received prior disease modification drugs before Cladribine initiation. Infections 6 (n = 6; 8.4 %) lymphocytopenia (n = 3; 4.2 %), and elevated liver enzymes (n = 1; 1.4 %) were reported. CONCLUSION: Cladribine treatment reduced significantly relapse rate and MRI activity. It was safe and tolerable. Early initiation of cladribine is associated with favorable outcomes.
 Modern data often take the form of a multiway array. However, most classification methods are designed for vectors, i.e., 1-way arrays. Distance weighted discrimination (DWD) is a popular high-dimensional classification method that has been extended to the multiway context, with dramatic improvements in performance when data have multiway structure. However, the previous implementation of multiway DWD was restricted to classification of matrices, and did not account for sparsity. In this paper, we develop a general framework for multiway classification which is applicable to any number of dimensions and any degree of sparsity. We conducted extensive simulation studies, showing that our model is robust to the degree of sparsity and improves classification accuracy when the data have multiway structure. For our motivating application, magnetic resonance spectroscopy (MRS) was used to measure the abundance of several metabolites across multiple neurological regions and across multiple time points in a mouse model of Friedreich's ataxia, yielding a four-way data array. Our method reveals a robust and interpretable multi-region metabolomic signal that discriminates the groups of interest. We also successfully apply our method to gene expression time course data for multiple sclerosis treatment. An R implementation is available in the package MultiwayClassification at http://github.com/lockEF/MultiwayClassification.
 BACKGROUND: Simultaneous comparisons of multiple disease-modifying therapies for relapsing-remitting multiple sclerosis (RRMS) over an extended follow-up are lacking. Here we emulate a randomised trial simultaneously comparing the effectiveness of six commonly used therapies over 5 years. METHODS: Data from 74 centres in 35 countries were sourced from MSBase. For each patient, the first eligible intervention was analysed, censoring at change/discontinuation of treatment. The compared interventions included natalizumab, fingolimod, dimethyl fumarate, teriflunomide, interferon beta, glatiramer acetate and no treatment. Marginal structural Cox models (MSMs) were used to estimate the average treatment effects (ATEs) and the average treatment effects among the treated (ATT), rebalancing the compared groups at 6-monthly intervals on age, sex, birth-year, pregnancy status, treatment, relapses, disease duration, disability and disease course. The outcomes analysed were incidence of relapses, 12-month confirmed disability worsening and improvement. RESULTS: 23 236 eligible patients were diagnosed with RRMS or clinically isolated syndrome. Compared with glatiramer acetate (reference), several therapies showed a superior ATE in reducing relapses: natalizumab (HR=0.44, 95% CI=0.40 to 0.50), fingolimod (HR=0.60, 95% CI=0.54 to 0.66) and dimethyl fumarate (HR=0.78, 95% CI=0.66 to 0.92). Further, natalizumab (HR=0.43, 95% CI=0.32 to 0.56) showed a superior ATE in reducing disability worsening and in disability improvement (HR=1.32, 95% CI=1.08 to 1.60). The pairwise ATT comparisons also showed superior effects of natalizumab followed by fingolimod on relapses and disability. CONCLUSIONS: The effectiveness of natalizumab and fingolimod in active RRMS is superior to dimethyl fumarate, teriflunomide, glatiramer acetate and interferon beta. This study demonstrates the utility of MSM in emulating trials to compare clinical effectiveness among multiple interventions simultaneously.
 Neurodegeneration is a condition of the central nervous system (CNS) characterized by loss of neural structures and function. The most common neurodegenerative disorders (NDDs) include Alzheimer's disease (AD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), multiple sclerosis (MS), motor neuron disorders, psychological disorders, dementia with vascular dementia (VaD), Lewy body dementia (DLB), epilepsy, cerebral ischemia, mental illness, and behavioral disorders. CREB (cAMP-response element-binding protein) represent a nuclear protein that regulates gene transcriptional activity. The primary focus of the review pertains to the exploration of CREB expression and activation within the context of neurodegenerative diseases, specifically in relation to the phosphorylation and dephosphorylation events that occur within the CREB signaling pathway under normal physiological conditions. The findings mentioned have contributed to the elucidation of the regulatory mechanisms governing CREB activity. Additionally, they have provided valuable insights into the potential mediation of diverse biological processes, such as memory consolidation and neuroprotective effects, by various related studies. The promotion of synaptic plasticity and neurodevelopment in the central nervous system through the targeting of CREB proteins has the potential to contribute to the prevention or delay of the onset of neurodegenerative disorders. Multiple drugs have been found to initiate downstream signaling pathways, leading to neuroprotective advantages in both animal model studies and clinical trials. The clinical importance of the cAMP-response element-binding protein (CREB) is examined in this article, encompassing its utility as both a predictive/prognostic marker and a target for therapeutic interventions.
 Recent evidence suggests that misfolding, clumping, and accumulation of proteins in the brain may be common causes and pathogenic mechanism for several neurological illnesses. This causes neuronal structural deterioration and disruption of neural circuits. Research from various fields supports this idea, indicating that developing a single treatment for several severe conditions might be possible. Phytochemicals from medicinal plants play an essential part in maintaining the brain's chemical equilibrium by affecting the proximity of neurons. Matrine is a tetracyclo-quinolizidine alkaloid derived from the plant Sophora flavescens Aiton. Matrine has been shown to have a therapeutic effect on Multiple Sclerosis, Alzheimer's disease, and various other neurological disorders. Numerous studies have demonstrated that matrine protects neurons by altering multiple signalling pathways and crossing the blood-brain barrier. As a result, matrine may have therapeutic utility in the treatment of a variety of neurocomplications. This work aims to serve as a foundation for future clinical research by reviewing the current state of matrine as a neuroprotective agent and its potential therapeutic application in treating neurodegenerative and neuropsychiatric illnesses. Future research will answer many concerns and lead to fascinating discoveries that could impact other aspects of matrine.
 Toll-like receptors (TLRs) are a family of pattern recognition receptors (PRRs) that are ubiquitously expressed in the human body. They protect the brain and central nervous system from self and foreign antigens/pathogens. The immune response elicited by these receptors culminates in the release of cytokines, chemokines, and interferons causing an inflammatory response, which can be both beneficial and harmful to neurodevelopment. In addition, the detrimental effects of TLR activation have been implicated in multiple neurodegenerative diseases such as Alzheimer's, multiple sclerosis, etc. Many studies also support the theory that cytokine imbalance may be involved in schizophrenia, and a vast amount of literature showcases the deleterious effects of this imbalance on cognitive performance in the human population. In this review, we examine the current literature on TLRs, their potential role in the pathogenesis of schizophrenia, factors affecting TLR activity that contribute towards the risk of schizophrenia, and lastly, the role of TLRs and their impact on cognitive performance in schizophrenia.
 Prohibitin 1 (PHB1) and prohibitin 2 (PHB2) are proteins that are nearly ubiquitously expressed. They are localized in mitochondria, cytosol and cell nuclei. In the healthy CNS, they occur in neurons and non-neuronal cells (oligodendrocytes, astrocytes, microglia, and endothelial cells) and fulfill pivotal functions in brain development and aging, the regulation of brain metabolism, maintenance of structural integrity, synapse formation, aminoacidergic neurotransmission and, probably, regulation of brain action of certain hypothalamic-pituitary hormones.With regard to the diseased brain there is increasing evidence that prohibitins are prominently involved in numerous major diseases of the CNS, which are summarized and discussed in the present review (brain tumors, neurotropic viruses, Alzheimer disease, Down syndrome, Fronto-temporal and vascular dementia, dementia with Lewy bodies, Parkinson disease, Huntington disease, Multiple sclerosis, Amyotrophic lateral sclerosis, stroke, alcohol use disorder, schizophrenia and autism). Unfortunately, there is no PHB-targeted therapy available for any of these diseases.
 The immune system is deeply involved in autoimmune diseases of the central nervous system (CNS), such as multiple sclerosis, N-methyl-d-aspartate (NMDA) receptor encephalitis, and narcolepsy. Additionally, the immune system is involved in various brain diseases including cerebral infarction and neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). In particular, reports related to T cells are increasing. T cells may also play important roles in brain deterioration and dementia that occur with aging. Our understanding of the role of immune cells in the context of the brain has been greatly improved by the use of acute ischemic brain injury models. Additionally, similar neural damage and repair events are shown to occur in more chronic brain neurodegenerative brain diseases. In this review, we focus on the role of T cells, including CD4(+) T cells, CD8(+) T cells and regulatory T cells (Tregs) in cerebral infarction and neurodegenerative diseases.
 The deimination or citrullination of arginine residues in the polypeptide chain by peptidylarginine deiminase 4 alters the charge state of the polypeptide chain and affects the function of proteins. It is one of the main ways of protein post-translational modifications to regulate its function. Peptidylarginine deiminase 4 is widely expressed in multiple tissues and organs of the body, especially the central nervous system, and regulates the normal development of organisms. The abnormal expression and activation of peptidylarginine deiminase 4 is an important pathological mechanism for the occurrence and development of central nervous system diseases such as multiple sclerosis, Alzheimer's disease, cerebral ischemia reperfusion injury, and glioblastoma.

 Neurobiomarkers have attracted significant attention over the last ten years. One promising biomarker is the neurofilament light chain protein (NfL). Since the introduction of ultrasensitive assays, NfL has been developed into a widely used axonal damage marker of relevance to the diagnosis, prognostication, follow-up, and treatment monitoring of a range of neurological disorders, including multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. The marker is increasingly used clinically, as well as in clinical trials. Even if we have validated precise, sensitive, and specific assays for NfL quantification in both cerebrospinal fluid and blood, there are analytical, as well as pre- and post-analytical aspects of the total NfL testing process, including biomarker interpretation, to consider. Although the biomarker is already in use in specialised clinical laboratory settings, a more general use requires some further work. In this review, we provide brief basic information and opinions on NfL as a biomarker of axonal injury in neurological diseases and pinpoint additional work needed to facilitate biomarker implementation in clinical practice.
 Neuroactive steroids can be synthetic or endogenous molecules produced by neuronal and glial cells and peripheral glands. Examples include estrogens, testosterone, progesterone and its reduced metabolites such as 5α-dihydro-progesterone and allopregnanolone. Steroids produced by neurons and glia target the nervous system and are called neurosteroids. Progesterone and analog molecules, known as progestogens, have been shown to exhibit neurotrophic, neuroprotective, antioxidant, anti-inflammatory, glial modulatory, promyelinating, and remyelinating effects in several experimental models of neurodegenerative and injury conditions. Pleiotropic mechanisms of progestogens may act synergistically to prevent neuron degeneration, astrocyte and microglial reactivity, reducing morbidity and mortality. The aim of this review is to summarize the significant findings related to the actions of progesterone and other progestogens in experimental models and epidemiological and clinical trials of some of the most prevalent and debilitating chronic neurodegenerative disorders, namely, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. We evaluated progestogen alterations under pathological conditions, how pathology modifies their levels, as well as the intracellular mechanisms and glial interactions underlying their neuroprotective effects. Furthermore, an analysis of the potential of natural progestogens and synthetic progestins as neuroprotective and regenerative agents, when administered as hormone replacement therapy in menopause, is also discussed.
 BACKGROUND: Western lifestyle has been associated with an increase in relapsing-remitting multiple sclerosis (RRMS). In mice, dietary wheat amylase-trypsin inhibitors (ATIs) activate intestinal myeloid cells and augment T cell-mediated systemic inflammation. OBJECTIVE: The aim of this study was to assess whether a wheat- and thus ATI-reduced diet might exert beneficial effects in RRMS patients with modest disease activity. METHODS: In this 6-month, crossover, open-label, bicentric proof-of-concept trial, 16 RRMS patients with stable disease course were randomized to either 3 months of a standard wheat-containing diet with consecutive switch to a > 90% wheat-reduced diet, or vice versa. RESULTS: The primary endpoint was negative, as the frequency of circulating pro-inflammatory T cells did not decrease during the ATI-reduced diet. We did, however, observe decreased frequencies of CD14(+) CD16(++) monocytes and a concomitant increase in CD14(++) CD16(-) monocytes during the wheat-reduced diet interval. This was accompanied by an improvement in pain-related quality of life in health-related quality of life assessed (SF-36). CONCLUSION: Our results suggest that the wheat- and thus ATI-reduced diet was associated with changes in monocyte subsets and improved pain-related quality of life in RRMS patients. Thus, a wheat (ATI)-reduced diet might be a complementary approach accompanying immunotherapy for some patients. REGISTRATION: German Clinical Trial Register (No. DRKS00027967).
 Autoimmune diseases are heterogeneous pathologies characterized by a breakdown of immunological tolerance to self, resulting in a chronic and aberrant immune response to self-antigens. The scope and extent of affected tissues can vary greatly per autoimmune disease and can involve multiple organs and tissue types. The pathogenesis of most autoimmune diseases remains unknown but it is widely accepted that a complex interplay between (autoreactive) B and T cells in the context of breached immunological tolerance drives autoimmune pathology. The importance of B cells in autoimmune disease is exemplified by the successful use of B cell targeting therapies in the clinic. For example, Rituximab, a depleting anti-CD20 antibody, has shown favorable results in reducing the signs and symptoms of multiple autoimmune diseases, including Rheumatoid Arthritis, Anti-Neutrophil Cytoplasmic Antibody associated vasculitis and Multiple Sclerosis. However, Rituximab depletes the entire B cell repertoire, leaving patients susceptible to (latent) infections. Therefore, multiple ways to target autoreactive cells in an antigen-specific manner are currently under investigation. In this review, we will lay out the current state of antigen-specific B cell inhibiting or depleting therapies in the context of autoimmune diseases.
 Vitamin D deficiency is relatively common, and its management in patients with sarcoidosis is challenging due to the risk of hypercalcaemia. Our patient had an autologous stem cell transplant for multiple sclerosis and was given high-dose vitamin D concurrently with immunosuppressive therapy. The patient subsequently presented with symptomatic hypercalcaemia and an acute kidney injury. A clinical and biochemical recovery was reached by withdrawing vitamin D and administering intravenous fluids. Interestingly, new evidence suggests that activated vitamin D can actually dampen the inflammatory process in sarcoidosis, and this was reflected in a reduction of our patient's serological markers of sarcoidosis activity. One large study found no significant risk of hypercalcaemia when low doses of vitamin D were used in sarcoidosis. Where indicated, and until clear guidelines are established, we suggest using low doses of vitamin D with cautious monitoring of calcium and renal function.
 BACKGROUND: Farnesol (FOL) prevents the onset of experimental autoimmune encephalitis (EAE), a murine model of multiple sclerosis (MS). OBJECTIVE: We examined the transcriptomic profile of the brains of EAE mice treated with daily oral FOL using next-generation sequencing (RNA-seq). METHODS: Transcriptomics from whole brains of treated and untreated EAE mice at the peak of EAE was performed. RESULTS: EAE-induced mice, compared to naïve, healthy mice, overall showed increased expression in pathways for immune response, as well as an increased cytokine signaling pathway, with downregulation of cellular stress proteins. FOL downregulates pro-inflammatory pathways and attenuates the immune response in EAE. FOL downregulated the expression of genes involved in misfolded protein response, MAPK activation/signaling, and pro-inflammatory response. CONCLUSION: This study provides insight into the molecular impact of FOL in the brain and identifies potential therapeutic targets of the isoprenoid pathway in MS patients.
 PURPOSE OF REVIEW: To summarize the current evidence on the associations between autoimmune neurological diseases (e.g., multiple sclerosis, myasthenia gravis) and sleep disturbances (e.g., insomnia, parasomnias), as well as to review the main characteristics of sleep disorders with an immune-related pathophysiology (e.g., narcolepsy, anti-IgLON5 disease). RECENT FINDINGS: An immune-mediated damage of the areas in the central nervous system that control sleep and wake functions (e.g., hypothalamus, brainstem) can lead to sleep disorders and sleep symptoms. Sleep disturbances are the reason to seek for medical attention in certain neuroimmunological conditions (e.g., narcolepsy, anti-IgLON5 disease) where sleep-related alterations are the main clinical feature. The assessment of sleep-related symptomatology and disorders should be included in the routine evaluation of patients with autoimmune neurological diseases. Clinicians should be aware of the typical clinical presentation of certain neuroimmunological disorders mainly affecting sleep.
 This article reviews the role of neuronal activity in myelin regeneration and the related neural signaling pathways. The article points out that neuronal activity can stimulate the formation and regeneration of myelin, significantly improve its conduction speed and neural signal processing ability, maintain axonal integrity, and support axonal nutrition. However, myelin damage is common in various clinical diseases such as multiple sclerosis, stroke, dementia, and schizophrenia. Although myelin regeneration exists in these diseases, it is often incomplete and cannot promote functional recovery. Therefore, seeking other ways to improve myelin regeneration in clinical trials in recent years is of great significance. Research has shown that controlling neuronal excitability may become a new intervention method for the clinical treatment of demyelinating diseases. The article discusses the latest research progress of neuronal activity on myelin regeneration, including direct or indirect stimulation methods, and the related neural signaling pathways, including glutamatergic, GABAergic, cholinergic, histaminergic, purinergic and voltage-gated ion channel signaling pathways, revealing that seeking treatment strategies to promote myelin regeneration through precise regulation of neuronal activity has broad prospects.
 Painful tonic spasms initially described in association with multiple sclerosis are actually more common in patients with neuromyelitis optica spectrum disorder. Characterized by fierce pain and tonic posture of limbs, painful tonic spasms are common in patients during the recovery phase after the first episode of myelitis. A 68-year-old man presented with painful tonic spasm after 2 months of diagnosis of neuromyelitis optica spectrum disorder. Eventual use of eslicarbazepine resulted in significant control of spasms. Early recognition of painful tonic spasms and appropriate therapeutic medications can significantly decrease the impact it can have on the quality of life among neuromyelitis optica spectrum disorder patients.
 Neurological disease is characterized the by dysfunction of specific neuroanatomical regions. To determine whether region-specific vulnerabilities have a transcriptional basis at cell-type-specific resolution, we analyzed gene expression in mouse oligodendrocytes across various brain regions. Oligodendrocyte transcriptomes cluster in an anatomical arrangement along the rostrocaudal axis. Moreover, regional oligodendrocyte populations preferentially regulate genes implicated in diseases that target their region of origin. Systems-level analyses identify five region-specific co-expression networks representing distinct molecular pathways in oligodendrocytes. The cortical network exhibits alterations in mouse models of intellectual disability and epilepsy, the cerebellar network in ataxia, and the spinal network in multiple sclerosis. Bioinformatic analyses reveal potential molecular regulators of these networks, which were confirmed to modulate network expression in vitro in human oligodendroglioma cells, including reversal of the disease-associated transcriptional effects of a pathogenic Spinocerebellar ataxia type 1 allele. These findings identify targetable region-specific vulnerabilities to neurological disease mediated by oligodendrocytes.
 T helper 17 cells are thought to significantly contribute to the neuroinflammation process during neurogenerative diseases via their signature cytokine, interleukin (IL)-17. Recently, an emerging key role of IL-17 and its receptors has been documented in inflammatory and autoimmune diseases. The clinical studies conducted on patients with neurodegenerative disease have also shown an increase in IL-17 levels in serum as well as cerebrospinal fluid samples. Therapeutic targeting of either IL-17 receptors or direct IL-17 neutralizing antibodies has shown a promising preclinical and clinical proof of concept for treating chronic autoimmune neurodegenerative diseases such as multiple sclerosis. Thus, IL-17 and its receptors have a central role in regulation of neuroinflammation and can be considered as one of the major therapeutic targets in chronic neuroinflammatory diseases.

 Normal aging leads to myelin alternations in the rhesus monkey dorsolateral prefrontal cortex (dlPFC), which are often correlated with cognitive impairment. It is hypothesized that remyelination with shorter and thinner myelin sheaths partially compensates for myelin degradation, but computational modeling has not yet explored these two phenomena together systematically. Here, we used a two-pronged modeling approach to determine how age-related myelin changes affect a core cognitive function: spatial working memory. First we built a multicompartment pyramidal neuron model fit to monkey dlPFC data, with axon including myelinated segments having paranodes, juxtaparanodes, internodes, and tight junctions, to quantify conduction velocity (CV) changes and action potential (AP) failures after demyelination and subsequent remyelination in a population of neurons. Lasso regression identified distinctive parameter sets likely to modulate an axon's susceptibility to CV changes following demyelination versus remyelination. Next we incorporated the single neuron results into a spiking neural network model of working memory. While complete remyelination nearly recovered axonal transmission and network function to unperturbed levels, our models predict that biologically plausible levels of myelin dystrophy, if uncompensated by other factors, can account for substantial working memory impairment with aging. The present computational study unites empirical data from electron microscopy up to behavior on aging, and has broader implications for many demyelinating conditions, such as multiple sclerosis or schizophrenia.
 Orphan receptors constitute a historically varied subsection of a superfamily of nuclear receptors. Nuclear receptors regulate gene expression in response to ligand signals and are particularly alluring therapeutic targets for chronic illnesses. Neuroinflammation and neurodegenerative diseases have been linked to these orphan nuclear receptors. Preclinical and clinical evidence suggests that orphan receptors could serve as future targets in neuroinflammation, such as Parkinson's disease (PD), Alzheimer's Disease (AD), Huntington's Disease (HD), Multiple Sclerosis (MS), and Cerebral Ischemia. Given the therapeutic relevance of certain orphan receptors in a variety of disorders, their potential in neuroinflammation remains unproven. There is substantial evidence that ligand-activated transcription factors have great promise for preventing neurodegenerative and neurological disorders, with certain orphan nuclear receptors i.e., PPARγ, NR4As, and orphan GPCRs holding particularly high potential. Based on previous findings, we attempted to determine the contribution of PPAR, NR4As, and orphan GPCRs-regulated neuroinflammation to the pathogenesis of these disorders and their potential to become novel therapeutic targets.

 The year 2022 was marked by the development of numerous new treatments for refractory myasthenia gravis. The link between epilepsy and cerebrovascular disorder was studied and lamotrigine discovered to be the optimal treatment choice for epilepsy secondary to stroke to prevent mortality on patient of 45 years and older. New randomized study finally demonstrated the utility of thrombectomy in selected patients with basilar artery occlusion. The causal relationship between Epstein-Barr infection and multiple sclerosis has been proved thanks to a large cohort study. A new possibility of subcutaneous continuous levodopa administration gave promising result. Finally, numerous studies confirmed the efficacy and excellent tolerability of anti-CGRP antibodies.
 Recently, a rising interest is given to neuroimmune communication in physiological and neuropathological conditions. Meningeal immunity is a complex immune environment housing different types of immune cells. Here, we focus on meningeal T cells, possibly the most explored aspect of neuro-immune cell interactions. Emerging data have shown that meningeal T cells play a crucial role in the pathogenesis of several neurodegenerative disorders, including multiple sclerosis, Alzheimer's, Parkinson's, and Huntington's diseases. This review highlights how meningeal T cells may contribute to immune surveillance of the central nervous system (CNS) and regulate neurobehavioral functions through the secretion of cytokines. Overall, this review assesses the recent knowledge of meningeal T cells and their effects on CNS functioning in both health and disease conditions and the underlying mechanisms.

 Multiple sclerosis is a demyelinating disease of the central nervous system characterized by the loss of the myelin sheath-the nonconductive membrane surrounding neuronal axons. Demyelination interrupts neuronal transmission, which can impair neurological pathways and present a variety of neurological deficits. Prolonged demyelination can damage neuronal axons resulting in irreversible neuronal damage. Efforts have been made to identify agents that can promote remyelination. However, the assessment of remyelination that new therapies promote can be challenging. The method described in this chapter addresses this challenge by using isobaric C13-histidine as a tag for monitoring its incorporation into myelin proteins and thus monitoring the remyelination process.
 BACKGROUND: Peptidyl arginine deiminase IV (PADI4, also called PAD4), a Ca(2+)-dependent posttranslational modification enzyme, catalyzes the conversion of arginine residues to non-coded citrulline residues. Dysregulation of PADI4 is involved in a variety of diseases including rheumatoid arthritis (RA), multiple sclerosis (MS), Alzheimer's disease (AD) and many kinds of malignant tumors. OBJECTIVE: The roles of PADI4 in different tumors and the underlying molecular mechanisms are presented in this article. RESULTS: PADI4-mediated citrullination is associated with either transcriptional activation or repression in different contexts. Abnormal expression of PADI4 exists in a variety of malignant tumors and affects tumor progression and metastasis. Epithelial-to-mesenchymal transition (EMT), apoptosis, and neutrophil extracellular traps (NETs) may be the underlying molecular mechanisms. CONCLUSION: PADI4 plays crucial role in the occurrence, development, and metastasis of tumors, and PADI4 may be an effective biomarker for cancer prognosis and a potential target for cancer treatment.
 Neurodegenerative diseases (NDDs) and neuropsychiatric disorders (NPDs) are two common causes of death in elderly people, which includes progressive neuronal cell death and behavioral changes. NDDs include Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, and motor neuron disease, characterized by cognitive defects and memory impairment, whereas NPDs include depression, seizures, migraine headaches, eating disorders, addictions, palsies, major depressive disorders, anxiety, and schizophrenia, characterized by behavioral changes. Mounting evidence demonstrated that NDDs and NPDs share an overlapping mechanism, which includes post-translational modifications, the microbiota-gut-brain axis, and signaling events. Mounting evidence demonstrated that various drug molecules, namely, natural compounds, repurposed drugs, multitarget directed ligands, and RNAs, have been potentially implemented as therapeutic agents against NDDs and NPDs. Herein, we highlighted the overlapping mechanism, the role of anxiety/stress-releasing factors, cytosol-to-nucleus signaling, and the microbiota-gut-brain axis in the pathophysiology of NDDs and NPDs. We summarize the therapeutic application of natural compounds, repurposed drugs, and multitarget-directed ligands as therapeutic agents. Lastly, we briefly described the application of RNA interferences as therapeutic agents in the pathogenesis of NDDs and NPDs. Neurodegenerative diseases and neuropsychiatric diseases both share a common signaling molecule and molecular phenomenon, namely, pro-inflammatory cytokines, γCaMKII and MAPK/ERK, chemokine receptors, BBB permeability, and the gut-microbiota-brain axis. Studies have demonstrated that any alterations in the signaling mentioned above molecules and molecular phenomena lead to the pathophysiology of neurodegenerative diseases, namely, Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, and neuropsychiatric disorders, such as bipolar disorder, schizophrenia, depression, anxiety, autism spectrum disorder, and post-traumatic stress disorder.
 Neurodegenerative and mental disorders are a public health burden with pharmacological treatments of limited efficacy. Organoselenium compounds are receiving great attention in medicinal chemistry mainly because of their antioxidant and immunomodulatory activities, with a multi-target profile that can favor the treatment of multifactorial diseases. Therefore, the purpose of this review is to discuss recent preclinical studies about organoselenium compounds as therapeutic agents for the management of mental (e.g., depression, anxiety, bipolar disorder, and schizophrenia) and neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis). We have summarized around 70 peer-reviewed articles from 2016 to the present that used in silico, in vitro, and/or in vivo approaches to assess the neuropharmacology of selenium- containing compounds. Among the diversity of organoselenium molecules investigated in the last five years, diaryl diselenides, Ebselen-derivatives, and Se-containing heterocycles are the most representative. Ultimately, this review is expected to provide disease-oriented information regarding the neuropharmacology of organoselenium compounds that can be useful for the design, synthesis, and pharmacological characterization of novel bioactive molecules that can potentially be clinically viable candidates.
 The microbiome is a complex micro-ecosystem that provides the host with pathogen defense, food metabolism, and other vital processes. Alterations of the microbiome (dysbiosis) have been linked with a number of diseases such as cancers, multiple sclerosis (MS), Alzheimer's disease, etc. Generally, differential abundance testing between the healthy and patient groups is performed to identify important bacteria (enriched or depleted in one group). However, simply providing a singular species of bacteria to an individual lacking that species for health improvement has not been as successful as fecal matter transplant (FMT) therapy. Interestingly, FMT therapy transfers the entire gut microbiome of a healthy (or mixture of) individual to an individual with a disease. FMTs do, however, have limited success, possibly due to concerns that not all bacteria in the community may be responsible for the healthy phenotype. Therefore, it is important to identify the community of microorganisms linked to the health as well as the disease state of the host. Here we applied topic modeling, a natural language processing tool, to assess latent interactions occurring among microbes; thus, providing a representation of the community of bacteria relevant to healthy vs. disease state. Specifically, we utilized our previously published data that studied the gut microbiome of patients with relapsing-remitting MS (RRMS), a neurodegenerative autoimmune disease that has been linked to a variety of factors, including a dysbiotic gut microbiome. With topic modeling we identified communities of bacteria associated with RRMS, including genera previously discovered, but also other taxa that would have been overlooked simply with differential abundance testing. Our work shows that topic modeling can be a useful tool for analyzing the microbiome in dysbiosis and that it could be considered along with the commonly utilized differential abundance tests to better understand the role of the gut microbiome in health and disease. AUTHOR SUMMARY: Trillion of bacteria (microbiome) living in and on the human body play an important role in keeping us healthy and an alteration in their composition has been linked to multiple diseases such as cancers, multiple sclerosis (MS), and Alzheimer's. Identifying specific bacteria for targeted therapies is crucial, however studying individual bacteria fails to capture their interactions within the microbial community. The relative success of fecal matter transplants (FMTs) from healthy individual(s) to patients and the failure of individual bacterial therapy suggests the importance of the microbiome community in health. Therefore, there is a need to develop tools to identify the communities of microbes making up the healthy and disease state microbiome. Here we applied topic modeling, a natural language processing tool, to identify microbial communities associated with relapsing-remitting MS (RRMS). Specifically, we show the advantage of topic modeling in identifying the bacterial community structure of RRMS patients, which includes previously reported bacteria linked to RRMS but also otherwise overlooked bacteria. These results reveal that integrating topic modeling with traditional approaches improves the understanding of the microbiome in RRMS and it could be employed with other diseases that are known to have an altered microbiome.

 The lack of standardization and consistency of acquisition is a prominent issue in magnetic resonance (MR) imaging. This often causes undesired contrast variations in the acquired images due to differences in hardware and acquisition parameters. In recent years, image synthesis-based MR harmonization with disentanglement has been proposed to compensate for the undesired contrast variations. The general idea is to disentangle anatomy and contrast information from MR images to achieve cross-site harmonization. Despite the success of existing methods, we argue that major improvements can be made from three aspects. First, most existing methods are built upon the assumption that multi-contrast MR images of the same subject share the same anatomy. This assumption is questionable, since different MR contrasts are specialized to highlight different anatomical features. Second, these methods often require a fixed set of MR contrasts for training (e.g., both T1-weighted and T2-weighted images), limiting their applicability. Lastly, existing methods are generally sensitive to imaging artifacts. In this paper, we present Harmonization with Attention-based Contrast, Anatomy, and Artifact Awareness (HACA3), a novel approach to address these three issues. HACA3 incorporates an anatomy fusion module that accounts for the inherent anatomical differences between MR contrasts. Furthermore, HACA3 can be trained and applied to any combination of MR contrasts and is robust to imaging artifacts. HACA3 is developed and evaluated on diverse MR datasets acquired from 21 sites with varying field strengths, scanner platforms, and acquisition protocols. Experiments show that HACA3 achieves state-of-the-art harmonization performance under multiple image quality metrics. We also demonstrate the versatility and potential clinical impact of HACA3 on downstream tasks including white matter lesion segmentation for people with multiple sclerosis and longitudinal volumetric analyses for normal aging subjects. Code is available at https://github.com/lianruizuo/haca3.
 BACKGROUND: MS severity may be affected by genetic, patient-related, disease-related and environmental factors. Socioeconomic status, including income and healthcare access, amongst others, may also have a role in affecting diagnostic delay or therapy prescription. In Chile, two main healthcare systems exist, public-healthcare and private-healthcare, nonetheless universal care laws (e.g., access to High Efficacy Therapy-HET), including both systems, have been recently enacted for people with MS. OBJECTIVE: To assess the role of Socioeconomic Conditions (SEC), clinical variables and public health policies on the impact of disease severity of MS patients in Chile. METHODS: Multicentric, observational, cross-sectional study including patients from two reference centres (1 national reference centre from the private-health system and 1 regional reference centre from the public-health system). SEC and clinical variables included healthcare insurance (private or public), subclassification of health insurance according to monthly income, sex, age at onset, diagnostic delay, disease duration, diagnosis before HET law (as a proxy of HET delay), and current HET treatment. Progression Index (PI), EDSS ≥6.0 and Progressive MS diagnosis were used as outcome measures. Multivariable binary logistic regression was performed. RESULTS: We included 604 patients (460 private-health, 144 public-health), 67% women, 100% white/mestizo, 88% RRMS, mean age 42±12 years, mean age at onset 32±11 years, mean disease duration 10±6 years, median diagnostic delay 0 (0-34) years, 86% currently receiving any DMT, 55% currently receiving HET, median EDSS at last visit of 2.0 (0-10), and median PI 0.17 (0-4.5). Lower monthly income was associated with higher EDSS and higher PI. In the multivariable analysis, public-healthcare (OR 10.2), being diagnosed before HET-law (OR 4.89), longer diagnostic delay (OR 1.26), and older age at onset (OR 1.05) were associated with a higher risk of PI>0.2, while current HET (OR 0.39) was a protective factor. Diagnosis before HET-law (OR 7.59), public-healthcare (OR 6.49), male sex (OR 2.56), longer disease duration (OR 1.2) and older age at onset (OR 1.1) were associated with a higher risk of Progressive MS. Public-healthcare (OR 5.54), longer disease duration (OR 1.14) and older age at onset (OR 1.08) were associated with a higher risk of EDSS ≥6.0 while current treatment with HET had a trend as being a protective factor (OR 0.44, p = 0.05). CONCLUSION: MS severity is impacted by non-modifiable factors such as sex and age at onset. Interventions focused on shortening diagnostic delay and encouraging early access to high-efficacy therapies, as well as initiatives that may reduce the disparities inherent to lower socioeconomic status, may improve outcomes in people with MS.
 BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has affected the mental health, sleep and quality of life, especially in individuals with chronic disease. Therefore, the purpose of this systematic review and meta-analysis was to investigate the impact of the COVID-19 pandemic on neuropsychiatric disorders (depression, anxiety, stress), sleep disorders (sleep quality, insomnia) and quality of life in individuals with Parkinson's disease (PD), Multiple Sclerosis (MS) and Alzheimer's disease (AD) compared to healthy controls. METHODS: Seven databases (Medline, Embase, ScienceDirect, Web of Science, The Cochrane Library, Scielo and Lilacs) were searched between March 2020 and December 2022. Observational studies (i.e., cross-sectional, case-control, cohort) were included. GRADE approach was used to assess the quality of evidence and strength of the recommendation. Effect size was calculated using standardized mean differences (SMD; random effects model). A customized Downs and Black checklist was used to assess the risk of bias. RESULTS: Eighteen studies (PD = 7, MS = 11) were included. A total of 627 individuals with PD (healthy controls = 857) and 3923 individuals with MS (healthy controls = 2432) were analyzed. Twelve studies (PD = 4, MS = 8) were included in the meta-analysis. Individuals with PD had significantly elevated levels of depression (very low evidence, SMD = 0.40, p = 0.04) and stress (very low evidence, SMD = 0.60, p < 0.0001). There was no difference in anxiety (p = 0.08). Individuals with MS had significantly higher levels of depression (very low evidence, SMD = 0.73, p = 0.007) and stress (low evidence, SMD = 0.69, p = 0.03) and low quality of life (very low evidence, SMD = 0.77, p = 0.006). There was no difference in anxiety (p = 0.05) and sleep quality (p = 0.13). It was not possible to synthesize evidence in individuals with AD and sleep disorder (insomnia). CONCLUSION: In general, the COVID-19 pandemic negatively impacted individuals with PD and MS. Individuals with PD showed significantly higher levels of depression and stress; and individuals with MS presented significantly higher depression and stress levels, as well as significantly lower quality of life when compared to healthy controls. Further studies are needed to investigate the impact of the COVID-19 pandemic in individuals with AD.
 Multiple sclerosis (MS) is a chronic disease that is characterized by demyelination and neuronal damage. Experimental autoimmune encephalomyelitis (EAE) mice are used to model the disease progression of MS and mirror MS-like pathology. Previous researches have confirmed that inhibition of NLRP3 inflammasome significantly alleviated the severity of EAE mice and the demyelination of spinal cord, but its effect on neuronal damage and oligodendrocyte loss in the brain remains unclear. In this study, female C57BL/6 mice were immunized with MOG35-55 and PTX to establish experimental autoimmune encephalomyelitis (EAE) model. MCC950, a selective NLRP3 inflammasome inhibitor, was used to investigate the effect of NLRP3 inflammasome on the pathological changes and glial cell activation in the brain of EAE mice by immunohistochemistry. Our results demonstrated that MCC950 ameliorated the neuronal damage, demyelination, and oligodendrocyte loss in the brain of EAE mice. This protective effect of MCC950 may be attributed to its ability to suppress the activation of glial cells and prevents microglia polarization to M1 phenotype. Our work indicates that inhibition of NLRP3 inflammasome has the therapeutic effects of neuroprotection through immunomodulation and is a promising therapeutic strategy for MS.
 Failed regeneration of myelin around neuronal axons following central nervous system damage contributes to nerve dysfunction and clinical decline in various neurological conditions, for which there is an unmet therapeutic demand. Here, we show that interaction between glial cells - astrocytes and mature myelin-forming oligodendrocytes - is a determinant of remyelination. Using in vivo/ ex vivo/ in vitro rodent models, unbiased RNA sequencing, functional manipulation, and human brain lesion analyses, we discover that astrocytes support the survival of regenerating oligodendrocytes, via downregulation of the Nrf2 pathway associated with increased astrocytic cholesterol biosynthesis pathway activation. Remyelination fails following sustained astrocytic Nrf2 activation in focally-lesioned male mice yet is restored by either cholesterol biosynthesis/efflux stimulation, or Nrf2 inhibition using the existing therapeutic Luteolin. We identify that astrocyte-oligodendrocyte interaction regulates remyelination, and reveal a drug strategy for central nervous system regeneration centred on targeting this interaction.
 Neurodegenerative diseases represent a growing burden on healthcare systems worldwide. Mesenchymal stem cells (MSCs) have shown promise as a potential therapy due to their neuroregenerative, neuroprotective, and immunomodulatory properties, which are, however, linked to the bioactive substances they release, collectively known as secretome. This paper provides an overview of the most recent research on the safety and efficacy of MSC-derived secretome and extracellular vesicles (EVs) in clinical (if available) and preclinical models of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, Huntington's disease, acute ischemic stroke, and spinal cord injury. The article explores the biologically active substances within MSC-secretome/EVs, the mechanisms responsible for the observed therapeutic effects, and the strategies that may be used to optimize MSC-secretome/EVs production based on specific therapeutic needs. The review concludes with a critical discussion of current clinical trials and a perspective on potential future directions in translating MSC-secretome and EVs into the clinic, specifically regarding how to address the challenges associated with their pharmaceutical manufacturing, including scalability, batch-to-batch consistency, adherence to Good Manufacturing Practices (GMP) guidelines, formulation, and storage, along with quality controls, access to the market and relative costs, value for money and impact on total expenditure.
 Cholesterol is a key component of the cell membrane that impacts the permeability, fluidity, and functions of membrane-bound proteins. It also participates in synaptogenesis, synaptic function, axonal growth, dendrite outgrowth, and microtubule stability. Cholesterol biosynthesis and metabolism are in balance in the brain. Its metabolism in the brain is mediated mainly by CYP46A1 or cholesterol 24-hydroxylase. It is responsible for eliminating about 80% of the cholesterol excess from the human brain. CYP46A1 converts cholesterol to 24S-hydroxycholesterol (24HC) that readily crosses the blood-brain barrier and reaches the liver for the final elimination process. Studies show that cholesterol and 24HC levels change during neurological diseases and conditions. So, it was hypothesized that inhibition or activation of CYP46A1 would be an effective therapeutic strategy. Accordingly, preclinical studies, using genetic and pharmacological interventions, assessed the role of CYP46A1 in main neurodegenerative disorders such as Parkinson's disease, Huntington's disease, Alzheimer's disease, multiple sclerosis, spinocerebellar ataxias, and amyotrophic lateral sclerosis. In addition, its role in seizures and brain injury was evaluated. The recent development of soticlestat, as a selective and potent CYP46A1 inhibitor, with significant anti-seizure effects in preclinical and clinical studies, suggests the importance of this target for future drug developments. Previous studies have shown that both activation and inhibition of CYP46A1 are of therapeutic value. This article, using recent studies, highlights the role of CYP46A1 in various brain diseases and insults.
 INTRODUCTION: Neurological diseases are the leading cause of disability and the second leading cause of death worldwide. Physical and psychological pain, despair, and disconnection with the environment are observed after the diagnosis of numerous neurological processes, particularly neurodegenerative diseases. DEVELOPMENT: A higher risk of suicide is observed in patients with such common neurological diseases as epilepsy, migraine, and multiple sclerosis, as well as in those with such degenerative disorders as Alzheimer disease, Huntington disease, amyotrophic lateral sclerosis, and Parkinson's disease. In most cases, suicidal ideation appears in the early stages after diagnosis, in the presence of disabling symptoms, and/or in patients with psychiatric comorbidities (often associated with these neurological diseases). CONCLUSIONS: Effective suicide prevention in this population group requires assessment of the risk of suicide mainly in newly diagnosed patients, in patients showing unmistakable despair or disabling symptoms, and in patients presenting psychiatric comorbidities (especially depressive symptoms). It is essential to train specialists to detect warning signs in order that they may adopt a suitable approach and determine when psychiatric assessment is required.
 BACKGROUND: Turning during walking is a relevant and common everyday movement and it depends on a correct top-down intersegmental coordination. This could be reduced in several conditions (en bloc turning), and an altered turning kinematics has been linked to increased risk of falls. Smartphone use has been associated with poorer balance and gait; however, its effect on turning-while-walking has not been investigated yet. This study explores turning intersegmental coordination during smartphone use in different age groups and neurologic conditions. OBJECTIVE: This study aims to evaluate the effect of smartphone use on turning behavior in healthy individuals of different ages and those with various neurological diseases. METHODS: Younger (aged 18-60 years) and older (aged >60 years) healthy individuals and those with Parkinson disease, multiple sclerosis, subacute stroke (<4 weeks), or lower-back pain performed turning-while-walking alone (single task [ST]) and while performing 2 different cognitive tasks of increasing complexity (dual task [DT]). The mobility task consisted of walking up and down a 5-m walkway at self-selected speed, thus including 180° turns. Cognitive tasks consisted of a simple reaction time test (simple DT [SDT]) and a numerical Stroop test (complex DT [CDT]). General (turn duration and the number of steps while turning), segmental (peak angular velocity), and intersegmental turning parameters (intersegmental turning onset latency and maximum intersegmental angle) were extracted for head, sternum, and pelvis using a motion capture system and a turning detection algorithm. RESULTS: In total, 121 participants were enrolled. All participants, irrespective of age and neurologic disease, showed a reduced intersegmental turning onset latency and a reduced maximum intersegmental angle of both pelvis and sternum relative to head, thus indicating an en bloc turning behavior when using a smartphone. With regard to change from the ST to turning when using a smartphone, participants with Parkinson disease reduced their peak angular velocity the most, which was significantly different from lower-back pain relative to the head (P<.01). Participants with stroke showed en bloc turning already without smartphone use. CONCLUSIONS: Smartphone use during turning-while-walking may lead to en bloc turning and thus increase fall risk across age and neurologic disease groups. This behavior is probably particularly dangerous for those groups with the most pronounced changes in turning parameters during smartphone use and the highest fall risk, such as individuals with Parkinson disease. Moreover, the experimental paradigm presented here might be useful in differentiating individuals with lower-back pain without and those with early or prodromal Parkinson disease. In individuals with subacute stroke, en bloc turning could represent a compensative strategy to overcome the newly occurring mobility deficit. Considering the ubiquitous smartphone use in daily life, this study should stimulate future studies in the area of fall risk and neurological and orthopedic diseases. TRIAL REGISTRATION: German Clinical Trials Register DRKS00022998; https://drks.de/search/en/trial/DRKS00022998.
 Quantitative diffusion MRI (dMRI) is a promising technique for evaluating the spinal cord in health and disease. However, low signal-to-noise ratio (SNR) can impede interpretation and quantification of these images. The purpose of this study is to evaluate several dMRI denoising approaches on their ability to improve the quality, reliability, and accuracy of quantitative diffusion MRI of the spinal cord. We evaluate three denoising approaches (Non-Local Means, Marchenko-Pastur PCA, and a newly proposed Patch2Self algorithm) and conduct five experiments to validate the denoising performance on clinical-quality and commonly-acquired dMRI acquisitions: 1) a phantom experiment to assess denoising error and bias; 2) a multi-vendor, multi-acquisition open experiment for both qualitative and quantitative evaluation of noise residuals; 3) a bootstrapping experiment to estimate uncertainty of parametric maps; 4) an assessment of spinal cord lesion conspicuity in a multiple sclerosis group; and 5) an evaluation of denoising for advanced parametric multi-compartment modeling. We find that all methods improve signal-to-noise ratio and conspicuity of MS lesions in individual diffusion weighted images (DWIs), but MPPCA and Patch2Self excel at improving the quality and intra-cord contrast of diffusion weighted images - removing signal fluctuations due to thermal noise while improving precision of estimation of diffusion parameters even with very few DWIs (i.e., 16-32) typical of clinical acquisitions. These denoising approaches hold promise for facilitating reliable diffusion observations and measurements in the spinal cord to investigate biological and pathological processes.
 KEY CLINICAL MESSAGE: In MS patients, especially those frail or malnourished, combining home-based exercise twice weekly with essential amino acids and vitamin D may improve body composition, strength, and physical performance, enabling long-term functional improvements. ABSTRACT: Multiple sclerosis (MS) is associated with reduced bone and muscle strength and function. We aimed to investigate the effectiveness of a 24-week intervention in a 57-year-old frail female with MS. The participant completed a 2×/week exercise intervention and ingested 2×/day a supplement containing 7.5 g essential amino acids and 500 IU cholecalciferol. Body composition, 6-m gait speed (GS), handgrip strength (HGS), 30-sec arm-curl test (30ACT), 6-min walking test (6MWT), 30-sec chair-stand test (30CST), and plasma concentrations of 25-hydroxyvitamin D(3) [25(OH)D(3)], insulin-like growth factor 1 (IGF-1), and amino acids were assessed at baseline, and at Weeks 12 and 24. Plasma 25(OH)D(3) increased from 23.2 to 41.3 ng/mL and IGF-1 from 131.6 to 140.7 ng/mL from baseline to post-intervention. BMI, total lean tissue mass (LTM), fat mass, bone mineral content, and the sum of 17 amino acids increased by 3.8, 1.0, 3.5, 0.2, and 19%, respectively, at Week 24. There were clinically significant increases in regional LTM (6.9% arms and 6.3% legs) and large increases in GS (67.3%), dominant HGS (31.5%), non-dominant HGS (11.8%), dominant 30ACT (100%), non-dominant 30ACT (116.7%), 6MWT (125.6%), and 30CST (44.4%). The current intervention was effective in improving components of physical fitness and body composition in a female with MS.
 The metabolism of L-tryptophan (TRP) regulates homeostasis, immunity, and neuronal function. Altered TRP metabolism has been implicated in the pathophysiology of various diseases of the central nervous system. TRP is metabolized through two main pathways, the kynurenine pathway and the methoxyindole pathway. First, TRP is metabolized to kynurenine, then kynurenic acid, quinolinic acid, anthranilic acid, 3-hydroxykynurenine, and finally 3-hydroxyanthranilic acid along the kynurenine pathway. Second, TRP is metabolized to serotonin and melatonin along the methoxyindole pathway. In this review, we summarize the biological properties of key metabolites and their pathogenic functions in 12 disorders of the central nervous system: schizophrenia, bipolar disorder, major depressive disorder, spinal cord injury, traumatic brain injury, ischemic stroke, intracerebral hemorrhage, multiple sclerosis, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. Furthermore, we summarize preclinical and clinical studies, mainly since 2015, that investigated the metabolic pathway of TRP, focusing on changes in biomarkers of these neurologic disorders, their pathogenic implications, and potential therapeutic strategies targeting this metabolic pathway. This critical, comprehensive, and up-to-date review helps identify promising directions for future preclinical, clinical, and translational research on neuropsychiatric disorders.
 Originating from slow irreversible and progressive loss and dysfunction of neurons and synapses in the nervous system, neurodegenerative diseases (NDDs) affect millions of people worldwide. Common NDDs include Parkinson's disease, Alzheimer's disease multiple sclerosis, Huntington's disease, and amyotrophic lateral sclerosis. Currently, no sensitive biomarkers are available to monitor the progression and treatment response of NDDs or to predict their prognosis. Exosomes (EXOs) are small bilipid layer-enclosed extracellular vesicles containing numerous biomolecules, including proteins, nucleic acids, and lipids. Recent evidence indicates that EXOs are pathogenic participants in the spread of neurodegenerative diseases, contributing to disease progression and spread. EXOs are also important tools for diagnosis and treatment. Recently, studies have proposed exosomal microRNAs (miRNAs) as the targets for therapies or biomarkers of NDDs. In this review, we outline the latest research on the roles of exosomal miRNAs in NDDs and their applications as potential diagnostic and therapeutic biomarkers, targets, and drugs for NDDs.
 Over the past few decades, the application of mesenchymal stem cells has captured the attention of researchers and practitioners worldwide. These cells can be obtained from practically every tissue in the body and are used to treat a broad variety of conditions, most notably neurological diseases such as Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. Studies are still being conducted, and the results of these studies have led to the identification of several different molecular pathways involved in the neuroglial speciation process. These molecular systems are closely regulated and interconnected due to the coordinated efforts of many components that make up the machinery responsible for cell signaling. Within the scope of this study, we compared and contrasted the numerous mesenchymal cell sources and their cellular features. These many sources of mesenchymal cells included adipocyte cells, fetal umbilical cord tissue, and bone marrow. In addition, we investigated whether these cells can potentially treat and modify neurodegenerative illnesses.
 Cellular and mitochondrial membrane phospholipids provide the substrate for synthesis and release of prostaglandins in response to certain chemical, mechanical, noxious and other stimuli. Prostaglandin D(2), prostaglandin E(2), prostaglandin F(2α), prostaglandin I(2) and thromboxane-A(2) interact with five major receptors (and their sub-types) to elicit specific downstream cellular and tissue actions. In general, prostaglandins have been associated with pain, inflammation, and edema when they are present at high local concentrations and involved on a chronic basis. However, in acute settings, certain endogenous and exogenous prostaglandins have beneficial effects ranging from mediating muscle contraction/relaxation, providing cellular protection, regulating sleep, and enhancing blood flow, to lowering intraocular pressure to prevent the development of glaucoma, a blinding disease. Several classes of prostaglandins are implicated (or are considered beneficial) in certain central nervous system dysfunctions (e.g., Alzheimer's, Parkinson's, and Huntington's diseases; amyotrophic lateral sclerosis and multiple sclerosis; stroke, traumatic brain injuries and pain) and in ocular disorders (e.g., ocular hypertension and glaucoma; allergy and inflammation; edematous retinal disorders). This review endeavors to address the physiological/pathological roles of prostaglandins in the central nervous system and ocular function in health and disease, and provides insights towards the therapeutic utility of some prostaglandin agonists and antagonists, polyunsaturated fatty acids, and cyclooxygenase inhibitors.
 Both schizophrenia (SZ) and multiple sclerosis (MS) affect millions of people worldwide and impose a great burden on society. Recent studies indicated that MS elevated the risk of SZ and vice versa, whereas the underlying pathological mechanisms are still obscure. Considering that fecal microbiota played a vital role in regulating brain functions, the fecal microbiota and serum cytokines from 90 SZ patients and 71 age-, gender-, and BMI-matched cognitively normal subjects (referred as SZC), 22 MS patients and 33 age-, gender-, and BMI-matched healthy subjects (referred as MSC) were analyzed. We found that both diseases demonstrated similar microbial diversity and shared three differential genera, including the down-regulated Faecalibacterium, Roseburia, and the up-regulated Streptococcus. Functional analysis indicated that the three genera were involved in pathways such as "carbohydrate metabolism" and "amino acid metabolism." Moreover, the variation patterns of serum cytokines associated with MS and SZ patients were a bit different. Among the six cytokines perturbed in both diseases, TNF-α increased, while IL-8 and MIP-1α decreased in both diseases. IL-1ra, PDGF-bb, and RANTES were downregulated in MS patients but upregulated in SZ patients. Association analyses showed that Faecalibacterium demonstrated extensive correlations with cytokines in both diseases. Most notably, Faecalibacterium correlated negatively with TNF-α. In other words, fecal microbiota such as Faecalibacterium may contribute to the coexistence of MS and SZ by regulating serum cytokines. Our study revealed the potential roles of fecal microbiota in linking MS and SZ, which paves the way for developing gut microbiota-targeted therapies that can manage two diseases with a single treat.
 Exosomal microRNAs (miRNAs) are emerging diagnostic biomarkers for neurodegenerative diseases. In this study, we aimed to detect relapsing-remitting multiple sclerosis (RRMS)-specific miRNAs in cerebrospinal fluid (CSF) and serum exosomes with diagnostic potential. One ml of CSF and serum sample were collected from each of the 30 untreated RRMS patients and healthy controls (HCs). A panel of 18 miRNAs affecting inflammatory responses was applied, and qRT-PCR was conducted to detect differentially expressed exosomal miRNAs in CSF and serum of RRMS patients. We identified that 17 out of 18 miRNAs displayed different patterns in RRMS patients compared to HCs. Let-7 g-5p, miR-18a-5p, miR-145-5p, and miR-374a-5p with dual pro-inflammatory and anti-inflammatory actions and miR-150-5p and miR-342-3p with anti-inflammatory action were significantly upregulated in both CSF and serum-derived exosomes of RRMS patients compared to corresponding HCs. Additionally, anti-inflammatory miR-132-5p and pro-inflammatory miR-320a-5p were significantly downregulated in both CSF and serum-derived exosomes of RRMS patients compared to HCs. Ten of 18 miRNAs were differentially expressed in CSF and serum exosomes of the patients. Furthermore, miR-15a-5p, miR-19b-3p, and miR-432-5p were upregulated, and miR-17-5p was downregulated only in CSF exosomes. Interestingly, U6 housekeeping gene was differentially expressed in CSF and serum exosomes, in both RRMS and HCs. As the first report describing CSF exosomal miRNAs expression profile compared to that of serum exosomes in untreated RRMS patients, we showed that CSF and serum exosomes are not identical in terms of biological compounds and display different patterns in miRNAs and U6 expression.
 Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by debilitating fatigue that profoundly impacts patients' lives. Diagnosis of ME/CFS remains challenging, with most patients relying on self-report, questionnaires, and subjective measures to receive a diagnosis, and many never receiving a clear diagnosis at all. In this study, a single-cell Raman platform and artificial intelligence are utilized to analyze blood cells from 98 human subjects, including 61 ME/CFS patients of varying disease severity and 37 healthy and disease controls. These results demonstrate that Raman profiles of blood cells can distinguish between healthy individuals, disease controls, and ME/CFS patients with high accuracy (91%), and can further differentiate between mild, moderate, and severe ME/CFS patients (84%). Additionally, specific Raman peaks that correlate with ME/CFS phenotypes and have the potential to provide insights into biological changes and support the development of new therapeutics are identified. This study presents a promising approach for aiding in the diagnosis and management of ME/CFS and can be extended to other unexplained chronic diseases such as long COVID and post-treatment Lyme disease syndrome, which share many of the same symptoms as ME/CFS.
 BACKGROUND: Evidence shows that genetic factors play important roles in the severity of coronavirus disease 2019 (COVID-19). Sulfatase modifying factor 1 (SUMF1) gene is involved in alveolar damage and systemic inflammatory response. Therefore, we speculate that it may play a key role in COVID-19. RESULTS: We found that rs794185 was significantly associated with COVID-19 severity in Chinese population, under the additive model after adjusting for gender and age (for C allele = 0.62, 95% CI = 0.44-0.88, P = 0.0073, logistic regression). And this association was consistent with this in European population Genetics Of Mortality In Critical Care (GenOMICC: OR for C allele = 0.94, 95% CI = 0.90-0.98, P = 0.0037). Additionally, we also revealed a remarkable association between rs794185 and the prothrombin activity (PTA) in subjects (P = 0.015, Generalized Linear Model). CONCLUSIONS: In conclusion, our study for the first time identified that rs794185 in SUMF1 gene was associated with the severity of COVID-19.
 BACKGROUND: The Processing Speed Test (PST), a validated iPad®-based cognitive screening test for MS, has been applied to the cognitive assessment of Japanese MS patients using US normative data. METHODS: To develop PST normative data from Japanese healthy volunteers and compare the PST score distribution between Japanese and US healthy volunteers, 254 healthy Japanese-speaking volunteers were enrolled and stratified by age (20-65 years). Potential participants with a Mini-Mental State Examination score < 27 were excluded. PST raw scores (total correct) were from the Japan cohort and compared with age-restricted US normative data and propensity score-matched data created by matching sex, age, and educational level from a published study of 428 healthy participants. PST score distributions and standardized z-scores were compared using t-test and Kolmogorov-Smirnov test statistics. RESULTS: The mean age of the Japan cohort was 44.1 years. The PST scores of Japanese volunteers were significantly different from those of the age-restricted (mean ± SD 61.8 ± 10.1 vs 53.7 ± 10.8; p < 0.001) and the propensity score-matched US cohort (62.1 ± 10.1 vs 53.3 ± 10.6; p < 0.001). CONCLUSION: Regression analyses centered on US normative data could underestimate disease severity in Japanese MS patients, suggesting that separate normative data should be considered for each population sample.
 Hemorrhage in the setting of myelitis is rarely seen in clinical practice. We report a series of 3 women aged 26, 43, and 44 years, who presented with acute hemorrhagic myelitis within 4 weeks of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Two required intensive care, and 1 had severe disease with multiorgan failure. Serial MRI of the spine demonstrated T2-weighted hyperintensity with T1-weighted postcontrast enhancement in the medulla and cervical spine (patient 1) and thoracic spine (patients 2 and 3). Hemorrhage was identified on precontrast T1-weighted, susceptibility-weighted, and gradient echo sequences. Distinct from typical inflammatory or demyelinating myelitis, clinical recovery was poor in all cases, with residual quadriplegia or paraplegia, despite immunosuppression. These cases highlight that although hemorrhagic myelitis is rare, it can occur as a post/parainfectious complication of SARS-CoV-2 infection.
 BACKGROUND: Neurological diseases frequently affect sexual activity, and the resulting sexual dysfunction can cause much distress for patients. However, despite the importance of such complaints, neurologists frequently do not ask patients about their sexual symptoms or how their neurological illness and medications are affecting their sexual health. This study aimed to identify these difficulties as well as potential obstructions to conversations for addressing sexual dysfunction in patients with neurological diseases. METHODS: This cross-sectional study was performed by sending invitation letters and questionnaires to registered neurologists in Saudi Arabia. The questionnaire was constructed to determine the possibility of discussing sexual activities and function with patients with neurological diseases and the possible obstacles neurologists face in this regard. Statistical analyses were performed using the Statistical Package of Social Sciences (SPSS) program version 25, and p-values of <0.05 were considered statistically significant. RESULTS: A total of 258 of 750 neurologists (34.4%) returned the survey, of which 252 had completed the entire survey; therefore, their responses were considered suitable for further analysis. The majority of the respondents (63.1%) seldom discussed sexuality with their patients, more than half of the participants never discussed sexuality with female patients, and patients aged 60 years or older. The most commonly reported barriers were the lack of spontaneous communication by patients regarding their sexual problems (82.1%), insufficient consultation time (60.7%), and barriers based on language/culture/religion (53.6%). The majority of the respondents (61.9%) expressed the need for training on discussing sexuality as a measure that may enhance the discussion of sexual life with patients. Most of the respondents (92.9%) considered the patients responsible for bringing up problems in their sexual functioning during a patient interview. CONCLUSION: Sexual dysfunction is rarely discussed with patients showing neurological diseases, particularly with female patients. This is due to the patient's inability to articulate their sexual problems freely as well as a lack of consultation time. Training on discussing sexuality may enhance the discussion of sexual life with patients.
 BACKGROUND: High self-esteem can help people with disabilities overcome barriers and improve their mental health and well-being. This study sought to examine self-esteem levels among Saudis with physical disabilities based on socio-economic factors. It also aimed to determine the minimum weekly duration of physical activity performed by participants and examine its effects, along with those of other socio-economic factors, on participants' self-esteem. METHODS: A participant sample (N = 582) consisting of Saudi individuals aged 33.78 ± 9.81 years with physical disabilities (males, n = 289; females, n = 293) was recruited to participate in this study. Levels of self-esteem were measured using the Arabic version of the Rosenberg Self-Esteem Scale. RESULTS: Compared to women, men demonstrated significantly higher levels of overall self-esteem, positive feelings, and negative feelings (p < 0.01). The respondents' average levels of overall self-esteem (p < 0.001), positive feelings (p < 0.01), and negative feelings (p < 0.001) also varied by type of physical disability. Wheelchair-using participants had the highest values for self-esteem and positive feelings; cane-using participants or those who did not use mobility aids had the lowest values. Weighted least squares regression showed that weekly physical activity was the factor that most affected self-esteem (β = 0.002), followed by education level (β = 0.115), then type of mobility device used (β = -0.07). CONCLUSION: Increased weekly physical activity, higher education levels, and the use of mobility aids were the factors likely to improve the self-esteem of Saudis with physical disabilities.
 AMPA receptors are glutamate-gated ion channels, present in a wide range of neuron types and in glial cells. Their main role is to mediate fast excitatory synaptic transmission, and therefore, they are critical for normal brain function. In neurons, AMPA receptors undergo constitutive and activity-dependent trafficking between the synaptic, extrasynaptic and intracellular pools. The kinetics of AMPA receptor trafficking is crucial for the precise functioning of both individual neurons and neural networks involved in information processing and learning. Many of the neurological diseases evoked by neurodevelopmental and neurodegenerative malfunctions or traumatic injuries are caused by impaired synaptic function in the central nervous system. For example, attention-deficit/hyperactivity disorder (ADHD), Alzheimer's disease (AD), tumors, seizures, ischemic strokes, and traumatic brain injury are all characterized by impaired glutamate homeostasis and associated neuronal death, typically caused by excitotoxicity. Given the important role of AMPA receptors in neuronal function, it is not surprising that perturbations in AMPA receptor trafficking are associated with these neurological disorders. In this book chapter, we will first introduce the structure, physiology and synthesis of AMPA receptors, followed by an in-depth description of the molecular mechanisms that control AMPA receptor endocytosis and surface levels under basal conditions or synaptic plasticity. Finally, we will discuss how impairments in AMPA receptor trafficking, particularly endocytosis, contribute to the pathophysiology of various neurological disorders and what efforts are being made to therapeutically target this process.
 The modulation of macrophage phenotype from a pro-inflammatory to an anti-inflammatory state holds therapeutic potential in the treatment of inflammatory disease. We have previously shown that arginase-2 (Arg2), a mitochondrial enzyme, is a key regulator of the macrophage anti-inflammatory response. Here, we investigate the therapeutic potential of Arg2 enhancement via target site blockers (TSBs) in human macrophages. TSBs are locked nucleic acid antisense oligonucleotides that were specifically designed to protect specific microRNA recognition elements (MREs) in human ARG2 3' UTR mRNA. TSBs targeting miR-155 (TSB-155) and miR-3202 (TSB-3202) MREs increased ARG2 expression in human monocyte-derived macrophages. This resulted in decreased gene expression and cytokine production of TNF-α and CCL2 and, for TSB-3202, in an increase in the anti-inflammatory macrophage marker, CD206. Proteomic analysis demonstrated that a network of pro-inflammatory responsive proteins was modulated by TSBs. In silico bioinformatic analysis predicted that TSB-3202 suppressed upstream pro-inflammatory regulators including STAT-1 while enhancing anti-inflammatory associated proteins. Proteomic data were validated by confirming increased levels of sequestosome-1 and decreased levels of phosphorylated STAT-1 and STAT-1 upon TSB treatment. In conclusion, upregulation of Arg2 by TSBs inhibits pro-inflammatory signaling and is a promising novel therapeutic strategy to modulate inflammatory signaling in human macrophages.

 The central nervous system (CNS) has long been considered an immune-privileged site, with minimal interaction between immune cells, particularly of the adaptive immune system. Previously, the presence of immune cells in this organ was primarily linked to events involving disruption of the blood-brain barrier (BBB) or inflammation. However, current research has shown that immune cells are found patrolling CNS under homeostatic conditions. Specifically, T cells of the adaptive immune system are able to cross the BBB and are associated with ageing and cognitive impairment. In addition, T-cell infiltration has been observed in pathological conditions, where inflammation correlates with poor prognosis. Despite ongoing research, the role of this population in the ageing brain under both physiological and pathological conditions is not yet fully understood. In this review, we provide an overview of the interactions between T cells and other immune and CNS parenchymal cells, and examine the molecular mechanisms by which these interactions may contribute to normal brain function and the scenarios in which disruption of these connections lead to cognitive impairment. A comprehensive understanding of the role of T cells in the ageing brain and the underlying molecular pathways under normal conditions could pave the way for new research to better understand brain disorders.
 Previous evidences show that Musculin (Msc), a repressor member of basic helix-loop-helix transcription factors, is responsible in vitro for the low responsiveness of human Th17 cells to the growth factor IL-2, providing an explanation for Th17 cells rarity in inflammatory tissue. However, how and to what extent Musculin gene can regulate the immune response in vivo in an inflammatory context is still unknown. Here, exploiting two animal models of inflammatory diseases, the Experimental Autoimmune Encephalomyelitis (EAE) and the dextran sodium sulfate (DSS)-induced colitis, we evaluated the effect of Musculin gene knock-out on clinical course, performing also a deep immune phenotypical analysis on T cells compartment and an extended microbiota analysis in colitis-sick mice. We found that, at least during the early phase, Musculin gene has a very marginal role in modulating both the diseases. Indeed, the clinical course and the histological analysis showed no differences between wild type and Msc knock-out mice, whereas immune system appeared to give rise to a regulatory milieu in lymph nodes of EAE mice and in the spleen of DSS colitis-sick mice. Moreover, in the microbiota analysis, we found irrelevant differences between wild type and Musculin knock-out colitis-sick mice, with a similar bacterial strains' frequency and diversity after the DSS treatment. This work strengthened the idea of a negligible Msc gene involvement in these models.
 INTRODUCTION: Aerobic exercise has been shown to modify Alzheimer pathology in animal models, and in patients with multiple sclerosis to reduce neurofilament light (NfL), a biomarker of neurodegeneration. OBJECTIVE: To investigate whether a 16-week aerobic exercise program was able to reduce serum NfL in patients with mild Alzheimer's disease (AD). METHODS: This is a secondary analysis of data from the multi-center Preserving Cognition, Quality of Life, Physical Health, and Functional Ability in Alzheimer's disease: The Effect of Physical Exercise (ADEX) study. Participants were randomized to 16 weeks of moderate intensity aerobic exercise or usual care. Clinical assessment and measurement of serum NfL was done at baseline and after the intervention. RESULTS: A total of 136 participants were included in the analysis. Groups were comparable at baseline except for APOEε4 carriership which was higher in the usual care group (75.3 versus 60.2%; p = 0.04). There was no effect of the intervention on serum NfL [intervention: baseline NfL (pg/mL) 25.76, change from baseline 0.87; usual care: baseline 27.09, change from baseline -1.16, p = 0.09]. CONCLUSION: The findings do not support an effect of the exercise intervention on a single measure of neurodegeneration in AD. Further studies are needed using other types and durations of exercise and other measures of neurodegeneration. CLINICAL TRIAL REGISTRATION: clinicaltrials.gov, identifier NCT01681602.
 BACKGROUND: At the moment, the possible options for the management of cognitive dysfunctions in patients with MS (pMS) are pharmacological interventions, cognitive rehabilitation (CR), and physical exercise. However, worldwide, multimodal programs are infrequently applied in pMS and CR is not easily accessible through the National Health System as MR. OBJECTIVE: The aim of the study is to explore if the combination of motor and cognitive rehabilitation may favor better outcomes on cognitive efficiency compared to separate trainings. METHODS: Forty-eight pMS were submitted to detailed neuropsychological and motor assessments, before (T0) and after (T1) having performed one of three rehabilitation conditions (two cognitive trainings/week-Reha1; one cognitive and one motor training/week-Reha2; two motor trainings/week-Reha3, for 12 weeks); they were randomly assigned to one condition or another. The CR was focused on memory functioning and performed with the Rehacom program. RESULTS: No significant differences in age, sex, education, and disease course were found between the three groups (sig. > .05). Reha1 patients increased only their cognitive performance, and Reha3 only increased their motor performance, while Reha2 increased both cognitive and motor performances. This benefit was also confirmed by the cognitive efficiency expressed by the Cognitive Impairment Index. CONCLUSIONS: These data confirm that to include cognitive training within rehabilitation programs may induce important benefits in pMS. Furthermore, pMS seem to benefit from a combined approach (cognitive and motor) more than from CR and motor rehabilitation separately (ClinicalTrial.gov ID: NCT05462678; 14 July 2022, retrospectively registered).
 The objective of this study is to examine IL-11-induced mechanisms of inflammatory cell migration to the central nervous system (CNS). We report that IL-11 is produced at highest frequency by myeloid cells among the peripheral blood mononuclear cell (PBMC) subsets. Patients with relapsing-remitting multiple sclerosis (RRMS) have an increased frequency of IL-11(+) monocytes, IL-11(+) and IL-11R(+) CD4(+) lymphocytes, and IL-11R(+) neutrophils in comparison to matched healthy controls. IL-11(+) and granulocyte-macrophage colony-stimulating factor (GM-CSF)(+) monocytes, CD4(+) lymphocytes, and neutrophils accumulate in the cerebrospinal fluid (CSF). The effect of IL-11 in-vitro stimulation, examined using single-cell RNA sequencing, revealed the highest number of differentially expressed genes in classical monocytes, including up-regulated NFKB1, NLRP3, and IL1B. All CD4(+) cell subsets had increased expression of S100A8/9 alarmin genes involved in NLRP3 inflammasome activation. In IL-11R(+)-sorted cells from the CSF, classical and intermediate monocytes significantly up-regulated the expression of multiple NLRP3 inflammasome-related genes, including complement, IL18, and migratory genes (VEGFA/B) in comparison to blood-derived cells. Therapeutic targeting of this pathway with αIL-11 mAb in mice with RR experimental autoimmune encephalomyelitis (EAE) decreased clinical scores, CNS inflammatory infiltrates, and demyelination. αIL-11 mAb treatment decreased the numbers of NFκBp65(+), NLRP3(+), and IL-1β(+) monocytes in the CNS of mice with EAE. The results suggest that IL-11/IL-11R signaling in monocytes represents a therapeutic target in RRMS.
 Klotho, a gene found on chromosome 13q12, is involved in a variety of processes and signaling pathways in the human body related to vitamin D metabolism; cardiovascular, renal, musculoskeletal, and skin diseases; and cancer biology. However, more importantly, it has been linked to beneficial effects related to anti-aging. The levels of soluble Klotho in the blood have been found to decline with age, increasing the risk of age-related diseases. When the Klotho gene was silenced or defective, it caused a shorter lifespan. However, when the gene was overexpressed, it resulted in a longer lifespan. Klotho has positive benefits on the neurological system by causing a higher representation of useful longevity genes, preventing further neuronal damage, and offering neuroprotection. Thus, it has the potential to become a new treatment for many age-related diseases that cause dementia, including multiple sclerosis, Alzheimer's disease, and Parkinson's disease. In this review, we discuss the mechanisms of Klotho's benefits and roles on various organ systems, specifically on nervous system disorders that lead to dementia.
 CCL13/MCP-4 belongs to the CC chemokine family, which induces chemotaxis in many immune cells. Despite extensive research into its function in numerous disorders, a thorough analysis of CCL13 is not yet accessible. The role of CCL13 in human disorders and existing CCL13-focused therapies are outlined in this study. The function of CCL13 in rheumatic diseases, skin conditions, and cancer is comparatively well-established, and some studies also suggest that it may be involved in ocular disorders, orthopedic conditions, nasal polyps, and obesity. We also give an overview of research that found very little evidence of CCL13 in HIV, nephritis, and multiple sclerosis. Even though CCL13-mediated inflammation is frequently linked to disease pathogenesis, it's fascinating to note that in some conditions, like primary biliary cholangitis (PBC) and suicide, it might even act as a preventative measure.
 Cannabidiol (CBD) is one of the major phytocannabinoids present in the cannabis plant, with no acute psychotropic effects and a favorable safety and abuse liability profile. Animal and limited controlled human studies have demonstrated CBD to have analgesic, anxiolytic, anti-inflammatory, antipsychotic, and anticonvulsant effects, to name a few possible indications. There is growing evidence for the use of CBD to treat neurological disorders such as epilepsy, multiple sclerosis, Parkinson's disease, and Alzheimer's disease. It has been suggested that CBD improves cognition and neurogenesis. Cognitive impairment is associated with numerous disorders and can involve deficits in learning, memory, executive functioning, and attention. The purpose of this review will be to evaluate the available preclinical and clinical data on CBD for the treatment of the cognitive impairment associated with several disorders including schizophrenia, epilepsy, Alzheimer's disease, and others. Preclinical, but not clinical, studies found evidence for an improvement in cognitive performance after treatment with CBD. More research is needed to determine whether CBD can be effectively used as a monotherapy to treat cognitive dysfunction. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 Wobbly hedgehog syndrome (WHS) has been long considered to be a myelin disease primarily affecting the four-toed hedgehog. In this study, we have shown for the first time that demyelination is accompanied by extensive remyelination in WHS. However, remyelination is not enough to compensate for the axonal degeneration and neuronal loss, resulting in a progressive neurodegenerative disease reminiscent of progressive forms of multiple sclerosis (MS) in humans. Thus, understanding the pathological features of WHS may shed light on the disease progression in progressive MS and ultimately help to develop therapeutic strategies for both diseases. HIGHLIGHTS: Wobbly hedgehog syndrome (WHS) is a progressive neurodegenerative disease.Spongy degeneration of the brain and spinal cord is the diagnostic feature of WHS.WHS affected brain and spinal cord show extensive demyelination and remyelination.Axonal degeneration is accompanied by loss of neurons in WHS.
 Alzheimer's Disease (AD) is a debilitating disease that leads to severe cognitive impairment and functional decline. The role of tau hyperphosphorylation and amyloid plaque deposition in the pathophysiology of AD has been well described; however, neuroinflammation and oxidative stress related to sustained microglial activation is thought to play a significant role in the disease process as well. NRF-2 has been identified in modulating the effects of inflammation and oxidative stress in AD. Activation of NRF-2 leads to an increased production of antioxidant enzymes, including heme oxygenase, which has been shown to have protective effects in neurodegenerative disorders such as AD. Dimethyl fumarate and diroximel fumarate (DMF) have been approved for the use in relapsing-remitting multiple sclerosis. Research indicates that they can modulate the effects of neuroinflammation and oxidative stress through the NRF-2 pathway, and as such, could serve as a potential therapeutic option in AD. We propose a clinical trial design that could be used to assess DMF as a treatment option for AD.
 Susac syndrome is a rare autoimmune vasculopathy involving the small precapillary arterioles of the brain, retina, and inner ear. It is characterized by a triad of symptoms: encephalopathy, visual disturbances due to obstruction of retinal artery branches, and sensorineural hearing loss. The study aimed to review the current medical knowledge on Susac syndrome and present our clinical experience regarding this disease entity. The paper also presents a case of a 25-year-old patient who was diagnosed with Susac&apos;s syndrome based on the clinical picture and the results of additional tests. This syndrome should be considered in the differential diagnosis of multiple sclerosis and other multifocal lesions of the central nervous system because early diagnosis of the disease and immunosuppressive treatment significantly alleviates its course and improves the prognosis.
 Interferons were repeatedly used in the therapy of COVID-19 due to their antiviral effects. Three recently published randomized controlled clinical phase III trials (WHO SOLIDARITY, ACTT-3, and SPRINTER) missed their primary objectives, i.e., a significant therapeutic effect of interferons was not demonstrated in these studies. In only one randomized controlled phase III trial (TOGETHER), a significant reduction in the hospitalization rate was revealed. Our study analyzes these findings, gives possible explanations for the failure of interferons, provides a proposal on how these agents could be successfully used, and also highlights the limitations of their employment in COVID-19. Interferons are apparently beneficial only if the patients are in the early stage of this disease and when they are usually not hospitalized, i.e., if the patients do not require oxygen support and/or if corticosteroids are not yet indicated. Furthermore, a higher dosage than the one used in the long-term treatment of multiple sclerosis with interferon beta or of chronic viral hepatitis with interferon alpha or lambda should be employed to achieve a better therapeutic effect in COVID-19.
 Adalimumab (Humira) is a human monoclonal antibody that belongs to the tumor necrosis factor (TNF) alpha antagonist class of medications. Central Nervous System (CNS) demyelination is a rare side effect of adalimumab, and only a few cases have been reported in the literature of patients who developed multiple sclerosis or other demyelinating patterns after using adalimumab. In this report, we present a case of CNS demyelination in a patient with rheumatoid arthritis that developed a few months after using adalimumab. Performing brain MRI for asymptomatic individuals prior to initiating anti-TNF alpha agents to exclude a pre-existing demyelinating disease may be worthwhile. Routine brain MRI for monitoring and surveillance may facilitate detecting cases early and avoid the development of permanent neurological disability. Further studies are needed to clarify the neurological safety of anti-TNF alpha agents.
 Biotin (vitamin H or vitamin B7) is a B-complex vitamin that acts as an essential coenzyme for five carboxylases: pyruvate carboxylase, 3-methylcrotonyl-CoA carboxylase, propionyl-CoA carboxylase, and coenzyme for acetyl-CoA carboxylases 1 and 2. These carboxylases help in several chemical processes in the cell, including gluconeogenesis, amino acid metabolism, and fatty acid synthesis. The Food and Nutrition Board of the Institute of Medicine recommends a daily dietary intake of 30 mcg/day to maintain good health. Biotin deficiency is very rare in those who take in a normal balanced diet. Mammals obtain biotin from food. Foods rich in biotin are egg yolk, liver, cereals (wheat, oats), vegetables (spinach, mushrooms), and rice. Dairy items and breast milk also contain biotin. Besides, gut micro bacteria can produce biotin. The average dietary intake of biotin in the western population is approximately 35 to 70 mcg/day.  Nominal biotin deficiency has been noted in pregnant and lactating women, but its clinical significance is unknown. Biotin supplements are available in the market for improvement in nail, hair, and skin health, but there is no robust evidence available. Taking biotin supplements can interfere with some laboratory tests resulting in false-positive and false-negative results. There are studies reporting the efficacy of high-dose biotin in some neurological conditions, such as multiple sclerosis; however, the underlying mechanism is uncertain.
 Myeloperoxidase (MPO) plays a key role in human antimicrobial system by oxidizing vital molecules of microorganisms in phagolysosomes through produced hypochlorous acid (HOCl). However, MPO can be released outside the phagocyte and produces reactive intermediates leading to tissue damage. MPO, as a local mediator of tissue damage, has been associated with inflammatory diseases such as renal injury, multiple sclerosis, cardiovascular and neurodegenerative diseases. Therefore, the enzyme currently draws attention as a potential therapeutic target. In this study, isomeric 1,3-dihydro-2H-benzo[d]imidazole-2-thione derivatives having amide, hydrazide and hydroxamic acid groups either on nitrogen or on sulphur atom were designed and their inhibitory activity was determined on chlorination and peroxidation cycles of MPO. Among the compounds, 2-(2-thioxo-2,3-dihydro-1H-benzo[d]imidazole-1-yl)acetohydrazide(C19) was found as the most active inhibitor on both cycles.
 The metabolic activity of all the micro-organism composing the human microbiome interacts with the host metabolism contributing to human health and disease in a way that is not fully understood. Here, we introduce STELLA, a computational method to derive the spectrum of metabolites associated with the microbiome of an individual. STELLA integrates known information on metabolic pathways associated with each bacterial species and extracts from these the list of metabolic products of each singular reaction by means of automatic text analysis. By comparing the result obtained on a single subject with the metabolic profile data of a control set of healthy subjects, we are able to identify individual metabolic alterations. To illustrate the method, we present applications to autism spectrum disorder and multiple sclerosis.
 Microglia are the specialized macrophages of the central nervous system and play an important role in neural circuit development, modulating neurotransmission, and maintaining brain homeostasis. Microglia in normal brain is quiescent and show ramified morphology with numerous branching processes. They constantly survey their surrounding microenvironment through the extension and retraction of their processes and interact with neurons, astrocytes, and blood vessels using these processes. Microglia respond quickly to any pathological event in the brain by assuming ameboid morphology devoid of branching processes and restore homeostasis. However, when there is chronic inflammation, microglia may lose their homeostatic functions and secrete various proinflammatory cytokines and mediators that initiate neural dysfunction and neurodegeneration. In this article, we review the role of microglia in the normal brain and in various pathological brain conditions, such as Alzheimer's disease and multiple sclerosis. We describe strategies to manipulate microglia, focusing on depletion, repopulation, and replacement, and we discuss their therapeutic potential.
 Energy-restricted diet is a specific dietary regimen, including the continuous energy-restricted diet and the intermittent energy-restricted diet. It has been proven effective not only to reduce weight and extend the lifespan in animal models, but also to regulate the development and progression of various neurological diseases such as epilepsy, cerebrovascular diseases (stroke), neurodegenerative disorders (Alzheimer's disease and Parkinson's disease) and autoimmune diseases (multiple sclerosis). However, the mechanism in this field is still not clear and a systematic neurological summary is still missing. In this review, we first give a brief summary of the definition and mainstream strategies of energy restrictions. We then review evidence about the effects of energy-restricted diet from both animal models and human trials, and update the current understanding of mechanisms underlying the biological role of energy-restricted diet in the fight against neurological diseases. Our review thus contributes to the modification of dietary regimen and the search for special diet mimics.
 OBJECTIVES: Susac syndrome is a rare autoimmune endotheliopathy involving the brain, retina, and inner ear. Olfactory dysfunction is a common early manifestation of several central nervous system diseases, including neurodegenerative diseases and autoimmune-mediated diseases such as Multiple Sclerosis. While the literature is abundant about the Susac syndrome classic triad of encephalopathy, branch retinal artery occlusion, and low-frequency sensorineural hearing loss, little is known about the extent of olfactory sense involvement. METHODS: Using the Sniffin' Sticks test, this study evaluated olfactory function (identification and threshold) in ten recovering Susac syndrome patients under our clinic surveillance with a median of 3.1 (SD=1.53) years post-disease onset. RESULTS: olfactory assessment by threshold and odor identification were within the normal range. No differences between recovering Susac syndrome patients to standard norms of odor identification and threshold were found. CONCLUSIONS: Our findings do not support olfactory dysfunction in Susac syndrome and thereby, do not support olfactory assessment as a reliable biomarker for this condition.
 Endoplasmic reticulum (ER) luminal Ca(2+) is vital for the function of the ER and regulates many cellular processes. Calreticulin is a highly conserved, ER-resident Ca(2+) binding protein and lectin-like chaperone. Over four decades of studying calreticulin demonstrate that this protein plays a crucial role in maintaining Ca(2+) supply under different physiological conditions, in managing access to Ca(2+) and how Ca(2+) is used depending on the environmental events and in making sure that Ca(2+) is not misused. Calreticulin plays a role of ER luminal Ca(2+) sensor to manage Ca(2+) -dependent ER luminal events including maintaining interaction with its partners, Ca(2+) handling molecules, substrates and stress sensors. The protein is strategically positioned in the lumen of the ER from where the protein manages access to and distribution of Ca(2+) for many cellular Ca(2+) -signalling events. The importance of calreticulin Ca(2+) pool extends beyond the ER and includes influence of cellular processes involved in many aspects of cellular pathophysiology. Abnormal handling of the ER Ca(2+) contributes to many pathologies from heart failure to neurodegeneration and metabolic diseases.
 Vasculitis in neurosarcoidosis is rare, with only a few cases reported in the literature. We report the clinical observation of a 51-year-old patient with no previous medical history, who was admitted to the emergency department due to sudden onset confusion, fever, sweating, weakness, and headaches. The first brain scan was normal, but a further biological exam with a lumbar puncture revealed lymphocytic meningitis. A complementary cerebral MRI revealed abnormalities in the white matter signal, suggestive of multiple sclerosis, with petechial hemorrhagic foci associated with leptomeningeal involvement and cerebral vasculitis. Thoraco-abdomino-pelvic computed tomography revealed hilar and mediastinal lymphadenopathy, as well as lymph nodes in the lower cervical region. A biopsy of the lymph nodes confirmed the presence of non-caseating granulomatous inflammation consistent with sarcoidosis. High-dose corticosteroid therapy was initiated with good clinical outcomes. Cerebral vasculitis in neurosarcoidosis is rare but can lead to neurological complications requiring long-term multidisciplinary management.
 GPR15 is a G protein-coupled receptor involved in immune disorders such as human immunodeficiency virus-induced enteropathy, multiple sclerosis, and colitis. Yet, the important endocytosis mechanism of GPR15 remained unclear. This study determined the participation of endocytic machinery proteins, including Gα proteins, G protein-coupled receptor kinases (GRKs), protein kinase C, arrestins, clathrin, caveolin, and dynamin in GPR15 internalization. The results demonstrate that GPR15 internalization is moderately dependent on GRKs and clathrin, and highly dependent on caveolin and dynamin. Moreover, a bystander arrestin recruitment assay showed that GPR15 recruits arrestin-3 to the cell membrane upon agonist stimulation, although GPR15 internalizes in an arrestin-independent manner. Overall, our study provides novel insights into β-arrestin recruitment and receptor internalization mechanisms for the recently deorphanized GPR15.
 FOXP3 (+) regulatory T cells (Treg) depend on exogenous IL-2 for their survival and function, but circulating levels of IL-2 are low, making it unclear how Treg access this critical resource in vivo . Here, we show that Treg use heparanase (HPSE) to access IL-2 sequestered by heparan sulfate (HS) within the extracellular matrix (ECM) of inflamed central nervous system tissue. HPSE expression distinguishes human and murine Treg from conventional T cells and is regulated by the availability of IL-2. HPSE (-/-) Treg have impaired stability and function in vivo , including the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. Conversely, endowing Treg with HPSE enhances their ability to access HS-sequestered IL-2 and their tolerogenic function in vivo . Together, these data identify novel roles for HPSE and the ECM in immune tolerance, providing new avenues for improving Treg-based therapy of autoimmunity. ONE-SENTENCE SUMMARY: Regulatory T cells use heparanase to strip IL-2 bound to extracellular matrix within inflamed tissues, thereby supporting their homeostasis and function.
 Optic neuritis (ON) often occurs at the presentation of multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD). The recommended treatment of high-dose corticosteroids for ON is based on a North American study population, which did not address treatment timing or antibody serostatus. The Acute Optic Neuritis Network (ACON) presents a global, prospective, observational study protocol primarily designed to investigate the effect of time to high-dose corticosteroid treatment on 6-month visual outcomes in ON. Patients presenting within 30 days of the inaugural ON will be enrolled. For the primary analysis, patients will subsequently be assigned into the MS-ON group, the aquapotin-4-IgG positive ON (AQP4-IgG+ON) group or the MOG-IgG positive ON (MOG-IgG+ON) group and then further sub-stratified according to the number of days from the onset of visual loss to high-dose corticosteroids (days-to-Rx). The primary outcome measure will be high-contrast best-corrected visual acuity (HC-BCVA) at 6 months. In addition, multimodal data will be collected in subjects with any ON (CIS-ON, MS-ON, AQP4-IgG+ON or MOG-IgG+ON, and seronegative non-MS-ON), excluding infectious and granulomatous ON. Secondary outcomes include low-contrast best-corrected visual acuity (LC-BCVA), optical coherence tomography (OCT), magnetic resonance imaging (MRI) measurements, serum and cerebrospinal fluid (CSF) biomarkers (AQP4-IgG and MOG-IgG levels, neurofilament, and glial fibrillary protein), and patient reported outcome measures (headache, visual function in daily routine, depression, and quality of life questionnaires) at presentation at 6-month and 12-month follow-up visits. Data will be collected from 28 academic hospitals from Africa, Asia, the Middle East, Europe, North America, South America, and Australia. Planned recruitment consists of 100 MS-ON, 50 AQP4-IgG+ON, and 50 MOG-IgG+ON. This prospective, multimodal data collection will assess the potential value of early high-dose corticosteroid treatment, investigate the interrelations between functional impairments and structural changes, and evaluate the diagnostic yield of laboratory biomarkers. This analysis has the ability to substantially improve treatment strategies and the accuracy of diagnostic stratification in acute demyelinating ON. TRIAL REGISTRATION: ClinicalTrials.gov, identifier: NCT05605951.
 BACKGROUND: Economic burden studies can provide insights into the drivers leading to increasing healthcare costs. It can also provide a more holistic view of how diseases impact the welfare of patients and their families. Having concrete estimates of the economic burden across multiple diseases can help policymakers determine which diseases are economically more burdensome. This study aimed to review and summarise comprehensively economic burden studies across multiple diseases in the Nordic countries between 2000 and 2020. METHODS: According to the 2020 PRISMA statement, a systematic literature review was conducted in PubMed, CINAHL, Academic Search Premier and Global Health databases using key terms related to the economic burden of any disease in Denmark, Finland, Greenland, Iceland, Norway and Sweden. Grey literature was also reviewed. RESULTS: A total of 10,050 potential titles and abstracts were identified and screened, and 254 full-text papers that met the inclusion criteria were evaluated by two independent reviewers. Of these, 119 articles were included in a qualitative synthesis. Twenty-nine had clearly defined comparison groups, thus able to attribute the costs to the disease. Large variations concerning methodology and cost components were noted. Across diseases, the economic burden ranged from EUR 1668 per patient annually for chronic obstructive pulmonary disease to EUR 93,041 for multiple sclerosis. However, estimates varied widely, even within each disease. CONCLUSIONS: Our review highlights the need for more comparable economic burden studies. Future studies should focus on applying robust methodology and homogeneous cost-reporting methods to inform policymakers about which diseases are economically more burdensome.
 BACKGROUND: Post-COVID syndrome is a severe long-term complication of COVID-19. Although fatigue and cognitive complaints are the most prominent symptoms, it is unclear whether they have structural correlates in the brain. We therefore explored the clinical characteristics of post-COVID fatigue, describe associated structural imaging changes, and determine what influences fatigue severity. METHODS: We prospectively recruited 50 patients from neurological post-COVID outpatient clinics (age 18-69 years, 39f/8m) and matched non-COVID healthy controls between April 15 and December 31, 2021. Assessments included diffusion and volumetric MR imaging, neuropsychiatric, and cognitive testing. At 7.5 months (median, IQR 6.5-9.2) after the acute SARS-CoV-2 infection, moderate or severe fatigue was identified in 47/50 patients with post-COVID syndrome who were included in the analyses. As a clinical control group, we included 47 matched multiple sclerosis patients with fatigue. FINDINGS: Our diffusion imaging analyses revealed aberrant fractional anisotropy of the thalamus. Diffusion markers correlated with fatigue severity, such as physical fatigue, fatigue-related impairment in everyday life (Bell score) and daytime sleepiness. Moreover, we observed shape deformations and decreased volumes of the left thalamus, putamen, and pallidum. These overlapped with the more extensive subcortical changes in MS and were associated with impaired short-term memory. While fatigue severity was not related to COVID-19 disease courses (6/47 hospitalised, 2/47 with ICU treatment), post-acute sleep quality and depressiveness emerged as associated factors and were accompanied by increased levels of anxiety and daytime sleepiness. INTERPRETATION: Characteristic structural imaging changes of the thalamus and basal ganglia underlie the persistent fatigue experienced by patients with post-COVID syndrome. Evidence for pathological changes to these subcortical motor and cognitive hubs provides a key to the understanding of post-COVID fatigue and related neuropsychiatric complications. FUNDING: Deutsche Forschungsgemeinschaft (DFG) and German Ministry of Education and Research (BMBF).
 The sigma-1 receptor is a 223 amino acid-long protein with a recently identified structure. The sigma-2 receptor is a genetically unrelated protein with a similarly shaped binding pocket and acts to influence cellular activities similar to the sigma-1 receptor. Both proteins are highly expressed in neuronal tissues. As such, they have become targets for treating neurological diseases, including Alzheimer's disease (AD), Huntington's disease (HD), Parkinson's disease (PD), multiple sclerosis (MS), Rett syndrome (RS), developmental and epileptic encephalopathies (DEE), and motor neuron disease/amyotrophic lateral sclerosis (MND/ALS). In recent years, there have been many pre-clinical and clinical studies of sigma receptor (1 and 2) ligands for treating neurological disease. Drugs such as blarcamesine, dextromethorphan and pridopidine, which have sigma-1 receptor activity as part of their pharmacological profile, are effective in treating multiple aspects of several neurological diseases. Furthermore, several sigma-2 receptor ligands are under investigation, including CT1812, rivastigmine and SAS0132. This review aims to provide a current and up-to-date analysis of the current clinical and pre-clinical data of drugs with sigma receptor activities for treating neurological disease.

 BACKGROUND: To what extent retinal atrophy in neurodegenerative diseases reflects the severity and/or the chronicity of brain pathology or is a local independent phenomenon remains to be clarified. Moreover, whether retinal atrophy has a clinical (diagnostic and prognostic) value in these diseases remains unclear. OBJECTIVE: To add light on the pathological significance and clinical value of retinal atrophy in patients with amyotrophic lateral sclerosis (ALS) and Kennedy's disease (KD). METHODS: Thirty-five ALS, thirty-seven KD, and forty-nine age-matched healthy controls (HC) were included in a one-year longitudinal study. Spectrum-domain optical coherence tomography (OCT) was performed at study entry (T0) and after 12 months (T1). Disease duration and functional rating scale (FRS) for ALS and KD patients were correlated to retinal thicknesses. RESULTS: Compared to HC, peripapillary retinal nerve fiber layer (pRNFL) thickness was significantly thinner in both ALS (p = 0.034) and KD (p = 0.003). pRNFL was thinner in KD compared to ALS, but the difference was not significant. In KD, pRNFL atrophy significantly correlated with both disease severity (r = 0.296, p = 0.035) and disease duration (r = - 0.308, p = 0.013) while no significant correlation was found in ALS (disease severity: r = 0.147, p = 0.238; disease duration: r = - 0.093, p = 0.459). During the follow-up, pRNFL thickness remained stable in KD while significantly decreased in ALS (p = 0.043). CONCLUSIONS: Our study provides evidence of retinal atrophy in both ALS and KD and suggests that retinal thinning is a primary local phenomenon in motoneuron diseases. The clinical value of pRNFL atrophy in KD is worthy of further investigation.
 Chitinase-3-like protein 1 (CHI3L1) is a secreted glycoprotein characterized by its ability to regulate multiple biological processes, such as the inflammatory response and gene transcriptional signaling activation. Abnormal CHI3L1 expression has been associated with multiple neurological disorders and serves as a biomarker for the early detection of several neurodegenerative diseases. Aberrant CHI3L1 expression is also reportedly associated with brain tumor migration and metastasis, as well as contributions to immune escape, playing important roles in brain tumor progression. CHI3L1 is synthesized and secreted mainly by reactive astrocytes in the central nervous system. Thus, targeting astrocytic CHI3L1 could be a promising approach for the treatment of neurological diseases, such as traumatic brain injury, ischemic stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, and glioma. Based on current knowledge of CHI3L1, we assume that it acts as a molecule mediating several signaling pathways driving the initiation and progression of neurological disorders. This narrative review is the first to introduce the potential roles of astrocytic CHI3L1 in neurological disorders. We also equally explore astrocytic CHI3L1 mRNA expression under physiological and pathological conditions. Inhibiting CHI3L1 and disrupting its interaction with its receptors through multiple mechanisms of action are briefly discussed. These endeavors highlight the pivotal roles of astrocytic CHI3L1 in neurological disorders and could contribute to the development of effective inhibitors based on the strategy of structure-based drug discovery, which could be an attractive therapeutic approach for neurological disease treatment.
 Neuroinflammation plays a fundamental role in the development and progression of neurodegenerative diseases. It could therefore be said that neuroinflammation in neurodegenerative pathologies is not a consequence but a cause of them and could represent a therapeutic target of neuronal degeneration. CX3CL1 and several proteases (ADAMs/MMPs) are strongly involved in the inflammatory pathways of these neurodegenerative pathologies with multiple effects. On the one hand, ADAMs have neuroprotective and anti-apoptotic effects; on the other hand, they target cytokines and chemokines, thus causing inflammatory processes and, consequently, neurodegeneration. CX3CL1 itself is a cytokine substrate for the ADAM, ADAM17, which cleaves and releases it in a soluble isoform (sCX3CL1). CX3CL1, as an adhesion molecule, on the one hand, plays an inhibiting role in the pro-inflammatory response in the central nervous system (CNS) and shows neuroprotective effects by binding its membrane receptor (CX3CR1) present into microglia cells and maintaining them in a quiescent state; on the other hand, the sCX3CL1 isoform seems to promote neurodegeneration. In this review, the dual roles of CX3CL1 and ADAMs/MMPs in different neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (MH), and multiple sclerosis (MS), are investigated.
 The purpose of this study was to develop and test a 3D multi-parameter MR fingerprinting (MRF) method for brain imaging applications. The subject cohort included 5 healthy volunteers, repeatability tests done on 2 healthy volunteers and tested on two multiple sclerosis (MS) patients. A 3D-MRF imaging technique capable of quantifying T (1) , T (2) and T (1ρ) was used. The imaging sequence was tested in standardized phantoms and 3D-MRF brain imaging with multiple shots (1, 2 and 4) in healthy human volunteers and MS patients. Quantitative parametric maps for T (1) , T (2) , T (1ρ) , were generated. Mean gray matter (GM) and white matter (WM) ROIs were compared for each mapping technique, Bland-Altman plots and intra-class correlation coefficient (ICC) were used to assess repeatability and Student T-tests were used to compare results in MS patients. Standardized phantom studies demonstrated excellent agreement with reference T (1) /T (2/) T (1ρ) mapping techniques. This study demonstrates that the 3D-MRF technique is able to simultaneously quantify T (1) , T (2) and T (1ρ) for tissue property characterization in a clinically feasible scan time. This multi-parametric approach offers increased potential to detect and differentiate brain lesions and to better test imaging biomarker hypotheses for several neurological diseases, including MS.
 Lipids are essential structural and functional components of the central nervous system (CNS). Sphingolipids are ubiquitous membrane components which were discovered in the brain in the late 19(th) century. In mammals, the brain contains the highest concentration of sphingolipids in the body. Sphingosine 1-phosphate (S1P) derived from membrane sphingolipids evokes multiple cellular responses which, depending on its concentration and localization, make S1P a double-edged sword in the brain. In the present review we highlight the role of S1P in brain development and focus on the often contrasting findings regarding its contributions to the initiation, progression and potential recovery of different brain pathologies, including neurodegeneration, multiple sclerosis (MS), brain cancers, and psychiatric illnesses. A detailed understanding of the critical implications of S1P in brain health and disease may open the door for new therapeutic options. Thus, targeting S1P-metabolizing enzymes and/or signaling pathways might help overcome, or at least ameliorate, several brain illnesses.
 There is an urgent need for therapies that target the multicellular pathology of central nervous system (CNS) disease. Modified, nonanticoagulant heparins mimic the heparan sulfate glycan family and are known regulators of multiple cellular processes. In vitro studies have demonstrated that low sulfated modified heparin mimetics (LS-mHeps) drive repair after CNS demyelination. Herein, we test LS-mHep7 (an in vitro lead compound) in experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination. In EAE, LS-mHep7 treatment resulted in faster recovery and rapidly reduced inflammation which was accompanied by restoration of animal weight. LS-mHep7 treatment had no effect on remyelination or on OLIG2 positive oligodendrocyte numbers within the corpus callosum in the cuprizone model. Further in vitro investigation confirmed that LS-mHep7 likely mediates its pro-repair effect in the EAE model by sequestering inflammatory cytokines, such as CCL5 which are upregulated during immune-mediated inflammatory attacks. These data support the future clinical translation of this next generation modified heparin as a treatment for CNS diseases with active immune system involvement.
 Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been implicated in numerous chronic inflammatory diseases, including multiple sclerosis (MS). GM-CSF impacts multiple properties and functions of myeloid cells via species-specific mechanisms. Therefore, we assessed the effect of GM-CSF on different human myeloid cell populations found in MS lesions: monocyte-derived macrophages (MDMs) and microglia. We previously reported a greater number of interleukin (IL)-15(+) myeloid cells in the brain of patients with MS than in controls. Therefore, we investigated whether GM-CSF exerts its deleterious effects in MS by increasing IL-15 expression on myeloid cells. We found that GM-CSF increased the proportion of IL-15(+) cells and/or IL-15 levels on nonpolarized, M1-polarized and M2-polarized MDMs from healthy donors and patients with MS. GM-CSF also increased IL-15 levels on human adult microglia. When cocultured with GM-CSF-stimulated MDMs, activated autologous CD8(+) T lymphocytes secreted and expressed significantly higher levels of effector molecules (e.g. interferon-γ and GM-CSF) compared with cocultures with unstimulated MDMs. However, neutralizing IL-15 did not attenuate enhanced effector molecule expression on CD8(+) T lymphocytes triggered by GM-CSF-stimulated MDMs. We showed that GM-CSF stimulation of MDMs increased their expression of CD80 and ICAM-1 and their secretion of IL-6, IL-27 and tumor necrosis factor. These molecules could participate in boosting the effector properties of CD8(+) T lymphocytes independently of IL-15. By contrast, GM-CSF did not alter CD80, IL-27, tumor necrosis factor and chemokine (C-X-C motif) ligand 10 expression/secretion by human microglia. Therefore, our results underline the distinct impact of GM-CSF on human myeloid cells abundantly present in MS lesions.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune condition that is associated with severe disability. Approximately 40% of individuals are misdiagnosed with multiple sclerosis (MS) or other diseases. We aimed to define factors that influence the misdiagnosis of people with NMOSD and provide strategies for reducing error rates. METHODS: A retrospective study was performed involving all people with a confirmed diagnosis of NMOSD within a single academic institution. Comprehensive clinical timelines were constructed for each individual that included presenting symptoms, provider type and timing of evaluations, aquaporin 4-IgG (AQP4) results, and MRI scans. Two-sample comparisons of continuous and categorial variables were performed for people accurately diagnosed with NMOSD and those originally misdiagnosed with another medical condition. A subanalysis of only AQP4-IgG positive people was also performed. RESULTS: The study cohort included 199 people fulfilling International Panel criteria for NMOSD with 71 people (62 female; mean age at first symptom presentation (standard deviation (SD)) = 32.8 years (y) (SD 16.1)) being initially misdiagnosed and 128 people (106 female; 41.14y (SD 15.41)) who were accurately diagnosed. Of the 199 people with NMOSD, 166 had a positive serostatus. Identified factors associated with misdiagnosis, regardless of AQP4-IgG serostatus, were the presence of protracted nausea/vomiting/hiccups without any accompanying neurological symptoms, 23 (32.4%) versus 16 (12.5%) (p = 0.001), a longer median (range) time to see a neuroimmunology specialist 4.2y (0.14-31.8) versus 0.5y (0.0-21.2) (p<0.0001), and a delay in acquiring an MRI study, 4.7y (0.0-27.3) versus 0.3y (0.0-20.2) (p<0.0001). A greater proportion of people misdiagnosed were identified with a negative live-cell based AQP4-IgG serum test result, 13/13 (100%) versus 22/114 (19.3%) (p<0.0001). Additionally, the mean (SD) time between a first negative and successive live-cell based AQP4-IgG positive test result was greater for people misdiagnosed with another condition, 3.9y (SD 5.0) versus 1.5y (SD 2.1) (p = 0.01). Although not significant between groups, a rash was also reported in 63/199 people with NMOSD, with 31/63 having an anti-nuclear antibody titer ≥ 1:160. CONCLUSION: Defined factors can help guide both generalists and specialists in the pursuit of strategies aimed at efficiently diagnosing those with NMOSD such that effective care can be delivered.
 OBJECTIVE: To estimate the cost-effectiveness of single-use hydrophilic-coated intermittent catheters (HCICs) versus single-use uncoated intermittent catheters (UICs) for urinary catheterization. METHODS: The evaluation took a UK national health service (NHS) perspective. The population of interest were people using intermittent catheters, with either a spinal cord injury or multiple sclerosis. A Markov model was developed that estimated costs and clinical evidence over the lifetime of a hypothetical cohort and applied health-related quality-of-life estimates. Model inputs were sourced from published evidence, including a network meta-analysis to inform the treatment effect (reduction in catheter-associated urinary tract infections [CAUTIs]), and were supported by expert opinion. The model outputs included per-patient lifetime costs, quality-adjusted life years (QALYs), and the incremental cost effectiveness ratio (ICER). Event counts were also produced. RESULTS: Using HCICs instead of UICs could prevent seven CAUTI events per patient over a lifetime horizon (1.8 requiring secondary care). Overall, lifetime use of HCICs is £3,183 more expensive than use of UICs per patient. However, for these additional costs, 0.55 QALYs are gained. The ICER is £5,755 per additional QALY gained. Key drivers of the model results were identified and subject to sensitivity analyses. The results were found to be robust to parameter uncertainty. CONCLUSION: HCICs are likely to be a cost-effective alternative to UICs, a result driven by substantial reductions in the number of CAUTIs. Their adoption across clinical practice could avoid a substantial number of infections, freeing up resources in the NHS and reducing antibiotic use in urinary catheter users.
 BACKGROUND: Leptomeningeal contrast enhancement (LME) on T2-weighted Fluid-Attenuated Inversion Recovery (T2-FLAIR) MRI is a reported marker of leptomeningeal inflammation, which is known to be associated with progression of multiple sclerosis (MS). However, this MRI approach, as typically implemented on clinical 3-tesla (T) systems, detects only a few enhancing foci in ~25% of patients and has thus been criticized as poorly sensitive. PURPOSE: To compare an optimized 3D real-reconstruction inversion recovery (Real-IR) MRI sequence on a clinical 3 T scanner to T2-FLAIR for prevalence, characteristics, and clinical/radiological correlations of LME. MATERIALS AND METHODS: We obtained 3D T2-FLAIR and Real-IR scans before and after administration of standard-dose gadobutrol in 177 scans of 154 participants (98 women, 64%; mean ± SD age: 49 ± 12 years), including 124 with an MS-spectrum diagnosis, 21 with other neurological and/or inflammatory disorders, and 9 without neurological history. We calculated contrast-to-noise ratios (CNR) in 20 representative LME foci and determined association of LME with cortical lesions identified at 7 T (n = 19), paramagnetic rim lesions (PRL) at 3 T (n = 105), and clinical/demographic data. RESULTS: We observed focal LME in 73% of participants on Real-IR (70% in established MS, 33% in healthy volunteers, P < 0.0001), compared to 33% on T2-FLAIR (34% vs. 11%, P = 0.0002). Real-IR showed 3.7-fold more LME foci than T2-FLAIR (P = 0.001), including all T2-FLAIR foci. LME CNR was 2.5-fold higher by Real-IR (P < 0.0001). The major determinant of LME status was age. Although LME was not associated with cortical lesions, the number of PRL was associated with the number of LME foci on both T2-FLAIR (P = 0.003) and Real-IR (P = 0.0003) after adjusting for age, sex, and white matter lesion volume. CONCLUSIONS: Real-IR a promising tool to detect, characterize, and understand the significance of LME in MS. The association between PRL and LME highlights a possible role of the leptomeninges in sustaining chronic inflammation.
 BACKGROUND: Ketogenic diets (KDs) are safe and tolerable in people with multiple sclerosis (MS). While many patient-reported and clinical benefits are noted, the sustainability of these diets outside of a clinical trial is unknown. AIMS: Evaluate patient perceptions of the KD following intervention, determine the degree of adherence to KDs post-trial, and examine what factors increase the likelihood of KD continuation following the structured diet intervention trial. METHODS: Sixty-five subjects with relapsing MS previously enrolled into a 6-month prospective, intention-to-treat KD intervention. Following the 6-month trial, subjects were asked to return for a 3-month post-study follow-up, at which time patient reported outcomes, dietary recall, clinical outcome measures, and laboratory values were repeated. In addition, subjects completed a survey to evaluate sustained and attenuated benefits following completion of the intervention phase of the trial. RESULTS: Fifty-two subjects (81%) returned for the 3-month post-KD intervention visit. Twenty-one percent reported continued adherence to a strict KD and an additional 37% reported adhering to a liberalized, less restrictive form of the KD. Those subjects with greater reductions in body mass index (BMI) and fatigue at 6-months on-diet were more likely to continue on KD following trial completion. Using intention-to-treat analysis, patient-reported and clinical outcomes at 3-months post-trial remained significantly improved from baseline (pre-KD), though the degree of improvement was slightly attenuated relative to outcomes at 6-months on KD. Regardless of diet type following the KD intervention, dietary patterns shifted toward greater protein and polyunsaturated fats and less carbohydrate/added sugar consumption. CONCLUSIONS: Following the 6-month KD intervention study, the majority of subjects elected to continue on KD, though many pursued a more liberal limit for carbohydrate restriction. Those who experienced a greater reduction in BMI or fatigue were more likely to continue with strict KD. The 6-month KD intervention induced persistent changes to dietary habits in the months following study completion. TRIAL REGISTRATION INFORMATION: Registered on Clinicaltrials.gov under registration number NCT03718247, posted on Oct 24, 2018. First patient enrollment date: Nov 1, 2018. Link: https://clinicaltrials.gov/ct2/show/NCT03718247?term=NCT03718247&amp;draw=2&amp;rank=1.
 Overall mental health depends in part on the blood-brain barrier, which regulates nutrient transfer in-and-out of the brain and its central nervous system. Lactoferrin, an innate metal-transport protein, synthesized in the substantia nigra, particularly in dopaminergic neurons and activated microglia is vital for brain physiology. Lactoferrin rapidly crosses the blood-brain barrier via receptor-mediated transcytosis and accumulates in the brain capillary endothelial cells. Lactoferrin receptors are additionally present on glioma cells, brain micro-vessels, and neurons. As a regulator of neuro-redox, microglial lactoferrin is critical for protection/repair of neurons and healthy brain function. Iron imbalance and oxidative stress are common among patients with neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease, dementia, depression, and multiple sclerosis. As an endogenous iron-chelator, lactoferrin prevents iron accumulation and dopamine depletion in Parkinson's disease patients. Oral lactoferrin supplementation could modulate the p-Akt/PTEN pathway, reduce Aβ deposition, and ameliorate cognitive decline in Alzheimer's disease. Novel lactoferrin-based nano-therapeutics have emerged as effective drug-delivery systems for clinical management of neurodegenerative disorders. Recent emergence of the Coronavirus disease-2019 (COVID-19) pandemic, initially considered a respiratory illness, demonstrated a broader virulence spectrum with the ability to cross the blood-brain barrier and inflict a plethora of neuropathological manifestations in the brain - the Neuro-COVID-19. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections are widely reported in Parkinson's disease, Alzheimer's disease, dementia, and multiple sclerosis patients with aggravated clinical outcomes. Lactoferrin, credited with several neuroprotective benefits in the brain could serve as a potential adjuvant in the clinical management of Neuro-COVID-19.
 BACKGROUND: Osteopontin, an extracellular matrix protein involved in bone remodeling, tissue repair and inflammation, has previously been associated with increased inflammation and neurodegeneration in multiple sclerosis (MS), promoting a worse disease course. Osteopontin is also likely involved in acute MS relapses. METHODS: In 47 patients with relapsing-remitting MS, we explored the correlation between the time elapsed between the last clinical relapse and lumbar puncture, and the cerebrospinal fluid (CSF) levels of osteopontin and a group of inflammatory cytokines and adipokines such as resistin, plasminogen activator inhibitor-1, osteoprotegerin, interleukin (IL)-1β, IL-2, IL-6 and IL-1 receptor antagonist (IL-1ra). We also analyzed the correlations between CSF levels of osteopontin and the other CSF molecules considered. RESULTS: Osteopontin CSF concentrations were higher in patients with a shorter time interval between the last clinical relapse and CSF withdrawal. In addition, CSF levels of osteopontin were positively correlated with the proinflammatory cytokines IL-2 and IL-6 and negatively correlated with the anti-inflammatory molecule IL-1ra. CONCLUSIONS: Our results further suggest the role of osteopontin in acute MS relapses showing that, in proximity to relapses, osteopontin expression in CSF may be increased along with other proinflammatory mediators and correlated with decreased concentrations of anti-inflammatory molecules.
 BACKGROUND: There has been considerable interest in statins due to their pleiotropic effects beyond their lipid-lowering properties. Many of these pleiotropic effects are predominantly ascribed to Rho small guanosine triphosphatases (Rho GTPases) proteins. We aimed to genetically investigate the role of lipids and statin interventions on multiple sclerosis (MS) risk and severity. METHOD: We employed two-sample Mendelian randomization (MR) to investigate: (1) the causal role of genetically mimic both cholesterol-dependent (via low-density lipoprotein cholesterol (LDL-C) and cholesterol biosynthesis pathway) and cholesterol-independent (via Rho GTPases) effects of statins on MS risk and MS severity, (2) the causal link between lipids (high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG)) levels and MS risk and severity; and (3) the reverse causation between lipid fractions and MS risk. We used summary statistics from the Global Lipids Genetics Consortium (GLGC), eQTLGen Consortium and the International MS Genetics Consortium (IMSGC) for lipids, expression quantitative trait loci and MS, respectively (GLGC: n = 188,577; eQTLGen: n = 31,684; IMSGC (MS risk): n = 41,505; IMSGC (MS severity): n =7,069). RESULTS: The results of MR using the inverse variance weighted method show that genetically predicted RAC2, a member of cholesterol-independent pathway, (OR 0.86 (95% CI 0.78 to 0.95), p-value 3.80E-03) is implicated causally in reducing MS risk. We found no evidence for the causal role of LDL-C and the member of cholesterol biosynthesis pathway on MS risk. MR results also show that lifelong higher HDL-C (OR 1.14 (95% CI 1.04 to1.26), p-value 7.94E-03) increase MS risk but TG was not. Furthermore, we found no evidence for the causal role of lipids and genetically mimicked statins on MS severity. There is no evidence of reverse causation between MS risk and lipids. CONCLUSION: Evidence from this study suggests that RAC2 is a genetic modifier of MS risk. Since RAC2 has been reported to mediate some of the pleiotropic effects of statins, we suggest that statins may reduce MS risk via a cholesterol-independent pathway (i.e., RAC2-related mechanism(s)). MR analyses also support a causal effect of HDL-C on MS risk.
 Relapsing-remitting multiple sclerosis (RRMS) is an autoimmune neurological disease and is the most common subtype of MS. In addition, it is associated with the development of depression and anxiety. To date, depressive- and anxiety-like behaviours were only studied using models of progressive MS, which causes severe motor alterations. Thus, we sought to standardise the depressive and anxiety-like behaviours in an RRMS model induced by experimental autoimmune encephalomyelitis (RR-EAE) in mice. The RR-EAE model was induced in C57BL/6 female mice using myelin oligodendrocyte glycoprotein (MOG35-55) antigen and Quillaja saponin (Quil A) as an adjuvant. The immunisation of RR-EAE did not induce locomotor alteration but caused relapsing-remitting induction of clinical scores in mice until 35 post-immunization (p.i.). Also, increased levels of tumour necrosis factor alpha (TNF-α), astrocyte marker (GFAP), and microglial markers (IBA-1) were detected in the prefrontal cortex at 35 p.i. of RR-EAE. In the open field test, RR-EAE mice showed decreased time spent at the centre and sniffing behaviour (at days 21 and 34 p.i.). Also, on day 35 p.i. the RR-EAE group spent less time in the open arms and had decreased open-arm entries compared to control mice in the elevated plus maze (EPM) test, confirming the anxiety-like behaviour. At day 36° p.i. in the tail suspension test, mice showed depression-like behaviour with decreased latency time and increased immobility time. Thus, the RR-EAE model mimics the neuroinflammatory and behavioural features of the RRMS, including depression- and anxiety-like symptoms.
 Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a rare chronic central-nervous-system inflammatory disorder that became known only recently, and the pathogenesis of CLIPPERS remains poorly understood. This report presents clinical and radiological features of a rare case: a young female patient who rapidly died of suspected CLIPPERS. Helpful multiparametric MRI diagnostic criteria are proposed that can help discriminate CLIPPERS from non-CLIPPERS pathologies. We reviewed clinical history, symptoms, quantitative data from brain multiparametric MRI before and after treatment, and histopathological data. Perfusion-weighted imaging revealed a decrease in regional cerebral blood flow by 31% and in cerebral blood volume by 64%, with a moderate increase in transit time and in time to peak by up to 23% in affected pontine and cerebral white matter. As estimated by diffusion tensor imaging, there was elevated density of tracts (n/mm(2)) and a decrease of fraction anisotropy (×10(-3) mm/s(2)) in the patient's pons as compared to a healthy control: density of tracts = 13.5 vs 12.4 and fraction anisotropy = 0.32 vs 0.45, respectively. Macromolecular proton fraction values proved to be reduced (15.8% and 14.5% in the control, respectively) in the patient's cerebral peduncles by 3% and in the pons by 4.1% and in a periventricular white matter lesion by 6.4% (11.3% in the normal-looking contralateral hemisphere). Based on our findings, we argue that quantitative MRI techniques may be a valuable source of biomarkers and reliable diagnostic criteria and can shed light on the pathogenesis and exact nosological position of this disorder.

 A large number of causative agents can result in spinal cord disorders in the tropics including etiologies similar to those of temperate regions such as trauma, spinal bone and disc lesions, tumors, epidural abscess, and congenital malformations. Yet infectious and nutritional disorders differ in their higher prevalence in tropical regions including Pott's disease; brucellosis; neuroborreliosis; various parasitic diseases such as schistosomiasis, neurocysticercosis, and eosinophilic meningitis. Notably, the retrovirus HTLV-1 is the causeof tropical spastic paraparesis/paraplegia or TSP. Nutritional causes of TSP include vitamin B and folate deficiencies, while endemic clusters of konzo and tropical ataxic myeloneuropathy occur in Africa, along with malnutrition and excessive consumption of cyanide-containing bitter cassava. Other toxic etiologies of TSP include lathyrism and fluorosis. Nutritional forms of myelopathy are associated often with optic and sensory neuropathy, hence the name tropical myeloneuropathies. Acute transverse myelopathy, seen in association with vaccination, infections, and fibrocartilaginous embolism of the nucleus pulposus, can be ubiquitous. Multiple sclerosis and optic myelopathy occur in the tropics but with lesser prevalence than in temperate regions. The advent of modern imaging in the tropics, including computed tomography and magnetic resonance imaging, has allowed better diagnosis and treatment of these conditions that are a frequent cause of death and disability. This chapter provides an overview of TSP emphasizing the most common causes with clues to diagnosis and effective therapy.
 Crystallization has revolutionized the field of solid-state formulations by modulating the physiochemical and release profile of active pharmaceutical ingredients (APIs). Dimethyl fumarate (DF), an FDA-approved first-line drug for relapsing-remitting multiple sclerosis, has a sublimation problem, leading to loss of the drug during its processing. To tackle this problem, DF cocrystal has been prepared by using solvent evaporation technique using nicotinamide as a coformer, which has been chosen based on in silico predictions and their ability to participate in hydrogen bonding. Fourier transform infrared (FT-IR), powder X-ray diffraction (PXRD), thermogravimetric analysis (TGA), differential scanning calorimetry (DSC), and sublimation analysis have characterized the cocrystal and its thermostability. Comparative analysis of the release profile has been done by the dissolution and pharmacokinetic study of DF and its cocrystal. Formulated cocrystal is noncytotoxic, antioxidant and inhibits interleukin-6 and tissue necrosis factor-α in peripheral blood mononuclear cells induced by lipopolysaccharide. We have obtained a thermostable cocrystal of DF with a similar physicochemical and release profile to that of DF. The formulated cocrystal also provides a gastroprotective effect which helps counterbalance the adverse effects of DF by reducing lipid peroxidation and total nitrite levels.
 As a rapidly growing field, microbiota research offers novel approaches to promoting ocular health and treating major retinal diseases, such as glaucoma. Gut microbiota changes throughout life; however, certain patterns of population changes have been increasingly associated with specific diseases. It has been well established that disrupted microbiome contributes to central nervous system diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, and glioma, suggesting that it could play a prominent role in neurodegenerative diseases. This review summarizes the progress in identifying significant microbe changes in patients with glaucoma by compiling studies completed in insolation that underlines the association between the microbiota and disease progression. Among pathways of interest, the finding of increased Firmicutes/Bacteroidetes ratio in patients with primary open-angled glaucoma links the increased taurocholic acid and decreased glutathione to a negative impact on retinal ganglion cell survival. Connecting these microbes to specific metabolites sheds light on the pathogenic mechanism and novel treatment strategies. In summary, the current review is intended to synthesize the findings of several studies investigating the effects of shifting bacterial population in retinal diseases, particularly glaucoma, to identify the current direction of treatment development and help direct future endeavors.
 A large number of observational studies have highlighted the prevalence rates of vitamin D insufficiency and deficiency in many populations including pregnant women. Vitamin D is well known to have a crucial role in differentiation and proliferation, as well as neurotrophic and neuroprotective actions in the brain. It has been observed that this micronutrient can modulate neurotransmission and synaptic plasticity. Recent results from animal and epidemiological studies indicated that maternal vitamin D deficiency is associated with a wide range of neurobiological diseases including autism, schizophrenia, depression, multiple sclerosis and developmental defects. The aim of this review is to summarize the current state of knowledge on the effect of maternal vitamin D deficiency on brain functions and development.
 Digital Health Technologies (DHTs) such as connected sensors offer particular promise for improving data collection and patient empowerment in neurology research and care. This study analyzed the recent evolution of the use of DHTs in trials registered on ClinicalTrials.gov for four chronic neurological disorders: epilepsy, multiple sclerosis, Alzheimer's, and Parkinson's disease. We document growth in the collection of both more established digital measures (e.g., motor function) and more novel digital measures (e.g., speech) over recent years, highlighting contexts of use and key trends.
 Dimension reduction tools preserving similarity and graph structure such as t -SNE and UMAP can capture complex biological patterns in high-dimensional data. However, these tools typically are not designed to separate effects of interest from unwanted effects due to confounders. We introduce the partial embedding (PARE) framework, which enables removal of confounders from any distance-based dimension reduction method. We then develop partial t -SNE and partial UMAP and apply these methods to genomic and neuroimaging data. Our results show that the PARE framework can remove batch effects in single-cell sequencing data as well as separate clinical and technical variability in neuroimaging measures. We demonstrate that the PARE framework extends dimension reduction methods to highlight biological patterns of interest while effectively removing confounding effects.
 Elderly patients have greater morbidity and mortality associated with falls versus their younger peers. Estimates are that greater than 30% of individuals over the age of 65 and approximately 50% of individuals over the age of 85 will fall each year. Approximately 12 to 42% of those who fall will have an injury. Further, once individuals fall, they are 50% more likely to have a second fall. In this population, a fall is associated with restricted mobility, a decline in activities of daily living (ADLs), hip fracture and other musculoskeletal injuries, dehydration, pneumonia, and long-term hospitalization. Moreover, a fear of falling compromises the patient’s independence and mobility, affecting overall physical and mental health. Fortunately, many falls are preventable using appropriate screening modalities and prevention interventions. Falls are often multi-factorial, considering there is usually a disturbance in gait and balance. Some causes include sarcopenia, muscle atrophy and imbalance, improper bio-mechanics, poor-blood pressure control, home environment, and polypharmacy. The pathologies on this list can be identified through screening modalities. One screening modality that can be used in many different settings such as outpatient primary care, inpatient hospital ward, or physical therapy office is the Tinetti gait and balance assessment, also known as the performance-oriented mobility assessment (POMA). This test is useful because it can be applied to different patient populations, including the elderly, patients with Parkinson disease or multiple sclerosis, traumatic brain injury (TBI), and stroke patients. The test assesses a patient’s balance and gait using a standardized scoring system.
 After a standard subcutaneous dose of peginterferon beta-1a, the amount of peginterferon beta 1a in milk is miniscule. In addition, because interferon is poorly absorbed orally, it is not likely to reach the bloodstream of the infant. Polyethylene glycol is not excreted into breastmilk.[1] Many women have breastfed while taking conventional interferon beta-1a and a few with peginterferon beta-1a with no adverse infant effects reported. The Multiple Sclerosis Centre of Excellence on Reproduction and Child Health considers interferon beta to be "moderately safe" to use during breastfeeding,[2] and a French consensus group of neurologists concluded that interferon beta can be used during breastfeeding.[3] No special precautions appear to be required during breastfeeding while using peginterferon beta.
 The optic tract is a bundle of nerve fibers that serves to carry visual information from the optic chiasm to the left and right lateral geniculate bodies as a part of the visual pathway. The visual pathway refers to the series of cells and synapses that transmit visual signals from the environment to the brain for processing. This pathway begins with light striking the specialized nerve cells of the retina, which convert photons of light into electrochemical signals. Neural signals travel primarily through the retinal layers to the optic nerve (cranial nerve II, or CN II), optic chiasm, optic tract, lateral geniculate bodies, and visual cortex in the brain’s occipital lobe. Each optic tract carries one half of the visual field, consisting of afferent (sensory) information from temporal hemi-retinal fibers ipsilaterally and nasal hemi-retinal fibers contralaterally. The left optic tract is responsible for the right visual field, and the right optic tract corresponds to the left visual field. Both optic tracts serve as clinically relevant structures in the evaluation of visual deficits, particularly in cases of homonymous hemianopsia. Lesions may impact other physiologic processes that are dependent on visual input to one or both optic tracts, including pupillary light reflex, accommodation reflex, and circadian rhythms. The neuroanatomy of the optic tract is relevant in cases of stroke, infiltrative tumors, encephalitis, multiple sclerosis, congenital anomalies of the brain development or function, and neurosurgery.
 Numerous studies in humans and animals hypothesize that gut microbiota dysbiosis is involved in the development of behavioral and neurological diseases such as depression, autism spectrum disorder, Parkinson disease, multiple sclerosis, stroke and Alzheimer's disease. Some of the most salient works so far regarding the brain-gut axis are mentioned below. The current knowledge on the impact of gut microbiota on nervous system diseases is far from being directly used for pharmacologic or nutritional advice toward restoration of normal bodily functions. It seems that a more comprehensive approach should be followed so that the individual effect of each kind of intervention on the patient's somatic or psychological status is determined. Future research must address global need for regimens which could reestablish normal composition of gut microorganisms after each neuropsychological disorder.

 The CC chemokine receptor 6 (CCR6) is a G protein-coupled receptor (GPCR) involved in a wide range of biological processes. When CCR6 binds to its sole ligand CCL20, a signaling network is produced. This pathway is implicated in mechanisms related to many diseases, such as cancer, psoriasis, multiple sclerosis, HIV infection or rheumatoid arthritis. The CCR6/CCL20 axis plays a fundamental role in immune homeostasis and activation. Th17 cells express the CCR6 receptor and inflammatory cytokines, including IL-17, IL-21 and IL-22, which are involved in the spread of inflammatory response. The CCL20/CCR6 mechanism plays a crucial role in the recruitment of these pro-inflammatory cells to local tissues. To date, there are no drugs against CCR6 approved, and the development of small molecules against CCR6 is complicated due to the difficulty in screenings. This review highlights the potential as a therapeutic target of the CCR6 receptor in numerous diseases and the importance of the development of antibodies against CCR6 that could be a promising alternative to small molecules in the treatment of CCR6/CCL20 axis-related pathologies.
 No information is available on the clinical use of alemtuzumab during breastfeeding. Because alemtuzumab is a large protein molecule with a molecular weight of 145,454 Da, the amount in milk is likely to be very low. It is also likely to be partially destroyed in the infant's gastrointestinal tract and absorption by the infant is probably minimal. Until more data become available, alemtuzumab should be used with caution or avoided in nursing mothers during treatment for multiple sclerosis, especially while nursing a newborn or preterm infant.[1-5] Waiting for at least 2 weeks postpartum to resume therapy may minimize transfer to the infant.[5] The manufacturer recommends that women not breastfeed during treatment and for at least 3 months following the last dose.
 Anthraquinones constitute an important class of compounds with wide applications. The solubility of derivatives at 298.15 K was discussed in ethanol-water solution and at atmospheric pressure, the solubility of 1-amino-4-hydroxy-9,10-anthraquinone (AHAQ) in binary solvents (ethanol-water combinations) was determined. Colour strength and fastening properties depend upon the kind and position of a hydrophobic group connected to the phenoxy ring of Anthraquinone moiety. There is a continuing interest in the creation of novel anthraquinone derivatives with biological activities since they have demonstrated potential for treating multiple sclerosis. For this purpose, by utilizing voltammetric and absorption studies, interactions of various derivatives with calf thymus DNA (ct-DNA) and the cationic surfactant cetyltrimethylammoniumbromide (CTAB) were examined. Here prominent Hydrophobic interaction and electron transfer resulting in binding to CTAB micelles were observed. The polarity index of the media was assessed and associated with the electrochemical parameters. The medicinal behaviour of Anthraquinone derivatives was a result of electron transfer reactions with DNA. UV-Visible and fluorescence properties were due to the transitions between n* and π* orbitals. Large absorption band with low dichroic ratio was characteristic of various derivatives of Anthraquinone. Presence of -NH group proves various derivatives remarkable calorimetric and anionic sensors.
 INTRODUCTION: Pegylated interferon lambda substantially reduced the risk of COVID-19-related hospitalizations or emergency room visits in a recent phase 3, multi-center, randomized, double-blind, placebo-controlled study of high-risk, non-hospitalized adult patients with SARS-CoV-2 infection compared to treatment with placebo. AREAS COVERED: Interferons are a family of signaling molecules produced as part of the innate immune response to viral infections. The administration of exogenous interferon may limit disease progression in patients with COVID-19. EXPERT OPINION: Interferons have been used to treat viral infections, including hepatitis B and hepatitis C, and malignancies such as non-Hodgkin's lymphoma, as well as the autoimmune condition multiple sclerosis. This manuscript examines what is known about the role of interferon lambda in the treatment of COVID-19, including potential limitations, and explores how this approach may be used in the future.
 Receptor-interacting serine/threonine kinase 2 (RIPK2) is a vital immunomodulator that plays critical roles in nucleotide-binding oligomerization domain 1 (NOD1), NOD2, and Toll-like receptors (TLRs) signaling. Stimulated NOD1 and NOD2 interact with RIPK2 and lead to the activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPK), followed by the production of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-12/23. Defects in NOD/RIPK2 signaling are associated with numerous inflammatory diseases, including asthma, sarcoidosis, inflammatory bowel disease (Crohn's disease and ulcerative colitis), multiple sclerosis, and Blau syndrome. As RIPK2 is a crucial element of innate immunity, small molecules regulating RIPK2 functions are attractive to establish novel immunotherapies. The increased interest in developing RIPK2 inhibitors has led to the clinical investigations of novel drug candidates. In this review, we attempt to summarize recent advances in the development of RIPK2 inhibitors and degraders.
 Synovitis-acne-pustulosis-hyperostosis-osteitis (SAPHO) syndrome is a rare disease with an unknown entity that affects the skin and the peripheral and/or axial joints. Here, we report on a patient with SAPHO syndrome complicated by lesions of the central nervous system who was successfully treated with brodalumab, an IL-17 receptor blocker. He had been suffering from arthralgia in the wrists and knees as well as axial symptoms such as back pain and assimilation of cervical vertebrae. He had been treated with corticosteroid, salazosulfapyridine, methotrexate, and bisphosphonate; however, his peripheral and axial articular manifestation were intractable. Recently, biologics predominantly targeting TNF-α is employed for difficult-to-treat SAPHO cases; however, he had been complicated with the lesions of the central nervous system resembling multiple sclerosis (MS), an inflammatory demyelinating disorder in the central nervous system, for which application of TNF-α inhibitor is contraindicated. Alternatively, brodalumab was administered , which promptly ameliorated the articular manifestations without aggravating the lesions of the central nervous system. We propose that this type of IL-17 blockade could be an alternative therapy for DMARDs-resistant SAPHO syndrome.
 Astrocytes (ASTs) and oligodendroglial lineage cells (OLGs) are major macroglial cells in the central nervous system. ASTs communicate with each other through connexin (Cx) and Cx-based network structures, both of which allow for quick transport of nutrients and signals. Moreover, ASTs interact with OLGs through connexin (Cx)-mediated networks to modulate various physiological processes in the brain. In this article, following a brief description of the infrastructural basis of the glial networks and exocrine factors by which ASTs and OLGs may crosstalk, we focus on recapitulating how the interactions between these two types of glial cells modulate myelination, and how the AST-OLG interactions are involved in protecting the integrity of the blood-brain barrier (BBB) and regulating synaptogenesis and neural activity. Recent studies further suggest that AST-OLG interactions are associated with myelin-related diseases, such as multiple sclerosis. A better understanding of the regulatory mechanisms underlying AST-OLG interactions may inspire the development of novel therapeutic strategies for related brain diseases.
 Damage or microstructural alterations of the white matter can cause dysfunction of the intrinsic neural networks in a condition termed as white matter disease (WMD). Frequently detected on brain computed tomography and magnetic resonance imaging scans, WMD is commonly presented in inflammatory demyelinating diseases like multiple sclerosis (MS) and vascular diseases such as cerebral small vessel disease (CSVD). Prevention of MS and CSVD progression requires early treatments with drastically different medications and approaches, as such, early and accurate diagnosis of WMD, derived from vascular or demyelinating etiologies, is of paramount importance. However, the clinical and imaging similarities between MS, especially during the early stage, and CSVD, pose a significant dilemma in differentiating these two conditions. In this review, we attempt to summarize and contrast the distinguishing features of MS and CSVD for aiding accurate diagnosis to ensure timely corresponding management in the early stages of MS and CSVD.
 Neuroprotection is one of the important protection methods against neuronal cells and tissue damage caused by neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and multiple sclerosis. Various bioactive compounds produced by medicinal plants can potentially treat central nervous system (CNS) disorders. Apart from these resources, endophytes also produce diverse secondary metabolites capable of protecting the CNS. The bioactive compounds produced by endophytes play essential roles in enhancing the growth factors, antioxidant defence functions, diminishing neuroinflammatory, and apoptotic pathways. The efficacy of compounds produced by endophytic fungi was also evaluated by enzymes, cell lines, and in vivo models. Acetylcholine esterase (AChE) inhibition is frequently used to assess in vitro neuroprotective activity along with cytotoxicity-induced neuronal cell lines. Some of drugs, such as tacrine, donepezil, rivastigmine, galantamine, and other compounds, are generally used as reference standards. Furthermore, clinical trials are required to confirm the role of these natural compounds in neuroprotection efficacy and evaluate their safety profile. This review illustrates the production of various bioactive compounds produced by endophytic fungi and their role in preventing neurodegeneration.
 The inflammasome is a multiprotein complex that is responsible for mounting an innate immune response through the activation of caspase-1 and the cleavage of interleukin-1β. This multiprotein complex plays an important role in a variety of central nervous system (CNS) diseases and conditions such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, and traumatic brain injury, among others. Here we describe methodological procedures to carry out immunoblotting and immunohistochemical techniques used to study inflammasome signaling in CNS tissues (brain and spinal cord).
 Isolated abducens nerve palsy is a rare presentation in women during pregnancy. When an abducens nerve palsy is elicited in a pregnant woman, work-up should start with labs and neuroimaging to rule out mechanical and organic causes such as tumors, preeclampsia, and multiple sclerosis. This case report highlights a 35-year-old woman, gravida 1, para 0, who was sent to the local medical center by her ophthalmologist at 37 weeks of gestation due to a left-sided headache and blurry vision. Upon admission, work-up was negative for preeclampsia. Tick-borne disease panel and lumbar puncture were unrevealing. No other mechanical or lab abnormalities were elicited. Magnetic resonance venography revealed a diminutive left transverse sinus, left sigmoid sinus, and left internal jugular vein in comparison with the right, indicating a possible congenital variant. Labor was induced to see if this would alleviate the patient's abducens nerve palsy. After induction of labor and initiation of dexamethasone, the patient's sixth cranial nerve palsy began to improve.
 BACKGROUND: Differentiating foot drop due to upper motor neuron (UMN) lesions from that due to lower motor neuron lesions is crucial to avoid unnecessary surgery or surgery at the wrong location. Electrodiagnostic (EDX) studies are useful in evaluating patients with spastic foot drop (SFD). OBSERVATIONS: Among 16 patients with SFD, the cause was cervical myelopathy in 5 patients (31%), cerebrovascular accident in 3 (18%), hereditary spastic paraplegia in 2 (12%), multiple sclerosis in 2 (12%), chronic cerebral small vessel disease in 2 (12%), intracranial meningioma in 1 (6%), and diffuse brain injury in 1 (6%). Twelve patients (75%) had weakness of a single leg, whereas 2 others (12%) had bilateral weakness. Eleven patients (69%) had difficulty walking. The deep tendon reflexes of the legs were hyperactive in 15 patients (94%), with an extensor plantar response in 9 patients (56%). Twelve patients (75%) had normal motor and sensory conduction, 11 of whom had no denervation changes of the legs. LESSONS: This study is intended to raise awareness among surgeons about the clinical features of SFD. EDX studies are valuable in ruling out peripheral causes of foot drop, which encourages diagnostic investigation into a UMN source for the foot drop.
 Immune-mediated inflammatory diseases (IMIDs) consist of a common and clinically diverse group of diseases. Despite remarkable progress in the past two decades, no remission is observed in a large number of patients, and no effective treatments have been developed to prevent organ and tissue damage. Brain-derived neurotrophic factor precursor (proBDNF) and receptors, such as p75 neurotrophin receptor (p75(NTR)) and sortilin, have been proposed to mediate intracellular metabolism and mitochondrial function to regulate the progression of several IMIDs. Here, the regulatory role of proBDNF and its receptors in seven typical IMIDs, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, allergic asthma, type I diabetes, vasculitis, and inflammatory bowel diseases, was investigated.
 Multiple sclerosis (MS) is an autoimmune disease associated with inflammatory demyelination in the central nervous system (CNS). Autologous hematopoietic cell transplantation (HCT) is under investigation as a promising therapy for treatment-refractory MS. Here we identify a reactive myeloid state in chronic experimental autoimmune encephalitis (EAE) mice and MS patients that is surprisingly associated with neuroprotection and immune suppression. HCT in EAE mice leads to an enhancement of this myeloid state, as well as clinical improvement, reduction of demyelinated lesions, suppression of cytotoxic T cells, and amelioration of reactive astrogliosis reflected in reduced expression of EAE- associated gene signatures in oligodendrocytes and astrocytes. Further enhancement of myeloid cell incorporation into the CNS following a modified HCT protocol results in an even more consistent therapeutic effect corroborated by additional amplification of HCT-induced transcriptional changes, underlining myeloid-derived beneficial effects in the chronic phase of EAE. Replacement or manipulation of CNS myeloid cells thus represents an intriguing therapeutic direction for inflammatory demyelinating disease.
 Acute disseminated encephalomyelitis (ADEM) is a monophasic condition characterized by inflammation of the central nervous system. Besides multiple sclerosis, optic neuropathy, acute transverse myelitis, and neuromyelitis optica spectrum disorder, ADEM is a primary inflammatory demyelinating disorder of the central nervous system. It is estimated that approximately three-quarters of cases of encephalomyelitis occur after an infection or immunization, where the onset of neurological disease is coincident with a febrile event. Here, we report an 80-year-old woman with coronavirus disease pneumonia who developed sudden onset of decreased level of consciousness, focal seizure, and right-side weakness. Magnetic resonance imaging (MRI) of the brain showed a multifocal hemorrhagic lesion with surrounding edema, suggesting ADEM. An electroencephalogram (EEG) revealed moderate generalized encephalopathy. The patient received alternating pulse steroids with plasma exchange for five days. Subsequently, her Glasgow coma scale score continued to decrease, and thus, she required inotropic support until she expired.
 Functional Electrical Stimulation (FES) has been used to support mobility for people with upper motor neuron conditions such as stroke and multiple sclerosis for over 25 years. Recent development and publication of clinical practice guidelines (CPGs) provide evidence to guide clinical decision making for application of FES to improve mobility. Understanding key barriers to the implementation of these CPGs is a critical initial step necessary to create tailored knowledge translation strategies. A public involvement and engagement consultation was conducted with international stakeholders including researchers, clinicians and engineers working with FES to inform implementation strategies for CPG use internationally. Reflexive thematic analysis of the consultation transcripts revealed themes including inconsistent use of CPGs, barriers to implementation such as limited access to FES and low clinician confidence, and the need for a tiered education approach with ongoing support. Insights derived from this consultation will inform the development of knowledge translation strategies to support the next steps to implementing FES use for mobility.
 Emerging evidence is encouraging and suggests that a substantial proportion of patients without antibody responses (due to anti-CD20 therapy or other etiologies) to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) vaccines develop T cell responses. However, antigen-specific T cellular responses are notoriously difficult to assess clinically, given the lack of such assays under satisfactory CAP/CLIA regulation, and the laborious nature of the flow cytometric assessment. To evaluate the ability to apply a clinically feasible assay to measure T cellular responses to SARS-CoV-2 mRNA vaccination, we compared flow cytometric and enzyme-linked immunosorbent assay (ELISA) based assays in 24 participants treated with anti-CD20 therapy. T cellular activation (CD69 + CD137+ surface expression, i.e., activation induced markers [AIM]) and intracellular interferon gamma (INFγ) production via flow cytometry was compared to plasma Interferon Gamma Release Assay (IGRA) via ELISA. Plasma INFγ production measured by IGRA correlated with the percent of INFγ-producing AIM positive T cells, supporting the use of IGRA assay as a robust assessment of T cellular response to the SARS-CoV-2 vaccine for B-cell depleted patients that is clinically feasible, time efficient, and cost effective.
 BACKGROUND: Evidence on SARS-CoV-2 mRNA vaccination under siponimod treatment is rare. METHODS: AMA-VACC is a prospective, open-label clinical study on SARS-CoV-2 mRNA vaccination during ongoing siponimod treatment (cohort 1), during siponimod interruption (cohort 2), or during treatment with other disease-modifying therapies or without therapy (cohort 3). SARS-CoV-2-specific antibodies and T-cell reactivity were measured six months after the initial vaccination and one month after the booster. RESULTS: 41 patients were recruited into cohort 1 (n = 17), cohort 2 (n = 4), and cohort 3 (n = 20). Seroconversion for SARS-CoV-2 neutralizing antibodies was reached by 50.0%, 100.0%, and 90.0% of patients at month 6 and by 81.3%, 100.0%, and 100.0% one month after booster (cohorts 1, 2, and 3, respectively). Antibody levels in cohort 1 increased after the booster compared to month 6 but remained lower compared to cohorts 2 and 3. T-cell responses were seen in 28.5%, 25.0%, and 73.7% at month 6 and in 28.6%, 50.0%, and 83.3% after the booster (cohorts 1, 2, and 3, respectively). In cohort 1, the extent of T-cell response was lower at month 6 compared to cohorts 2 and 3 but reached almost similar levels after the booster. CONCLUSIONS: The antibody and T-cell responses support SARS-CoV-2 (booster) vaccines in siponimod-treated patients.
 Proline isomerization, the process of interconversion between the cis- and trans-forms of proline, is an important and unique post-translational modification that can affect protein folding and conformations, and ultimately regulate protein functions and biological pathways. Although impactful, the importance and prevalence of proline isomerization as a regulation mechanism in biological systems have not been fully understood or recognized. Aiming to fill gaps and bring new awareness, we attempt to provide a wholistic review on proline isomerization that firstly covers what proline isomerization is and the basic chemistry behind it. In this section, we vividly show that the cause of the unique ability of proline to adopt both cis- and trans-conformations in significant abundance is rooted from the steric hindrance of these two forms being similar, which is different from that in linear residues. We then discuss how proline isomerization was discovered historically followed by an introduction to all three types of proline isomerases and how proline isomerization plays a role in various cellular responses, such as cell cycle regulation, DNA damage repair, T-cell activation, and ion channel gating. We then explore various human diseases that have been linked to the dysregulation of proline isomerization. Finally, we wrap up with the current stage of various inhibitors developed to target proline isomerases as a strategy for therapeutic development.
 BACKGROUND: Due to the demographic development and improved treatment options, the role of comorbidities is of increasing importance in the medical care of people with MS (pwMS). A higher risk of osteoporosis is well known in chronic autoimmune diseases, and is also described in MS. While there are several screening guidelines in the elderly or in patients with rheumatoid arthritis, there are no generally accepted recommendations when to perform bone mineral testing in pwMS under the age of 65 years. We aimed to determine risk factors of osteoporosis in pwMS and to develop a risk score which can be applied in daily clinical routine. METHODS: Densitometry (hip and lumbar spine) was performed in 159 pwMS aged ≤65 years and in 81 age- and sex-matched healthy controls (HC). Osteoporosis was defined according to WHO criteria as a bone density 2.5 standard deviation or more below the mean of young adults. Risk factors were identified by logistic regression analysis. RESULTS: Osteoporosis occurred more frequently in postmenopausal pwMS and male pwMS as compared to HC. Besides age, sex, menopausal status in females, body-mass-index and smoking, a higher degree of disability - as assessed by the Expanded Disability Status Scale - was identified as MS specific risk factor for osteoporosis, whereas the cumulative glucocorticoid dose was not associated with osteoporosis risk. Based on these risk factors, we developed an MS-specific risk score which allows to estimate the individual probability of osteoporosis. CONCLUSION: This risk score enables individual screening recommendation for pwMS and, subsequently, early prevention of osteoporosis which probably should result in reduction of fractures and morbidity.
 The cytokine TNF signals via two distinct receptors, TNF receptor 1 (TNFR1) and TNFR2, and is a central mediator of various immune-mediated diseases. Indeed, TNF-neutralizing biologic drugs have been in clinical use for the treatment of many inflammatory pathological conditions, including various rheumatic diseases, for decades. TNF has pleiotropic effects and can both promote and inhibit pro-inflammatory processes. The integrated net effect of TNF in vivo is a result of cytotoxic TNFR1 signalling and the stimulation of pro-inflammatory processes mediated by TNFR1 and TNFR2 and also TNFR2-mediated anti-inflammatory and tissue-protective activities. Inhibition of the beneficial activities of TNFR2 might explain why TNF-neutralizing drugs, although highly effective in some diseases, have limited benefit in the treatment of other TNF-associated pathological conditions (such as graft-versus-host disease) or even worsen the pathological condition (such as multiple sclerosis). Receptor-specific biologic drugs have the potential to tip the balance from TNFR1-mediated activities to TNFR2-mediated activities and enable the treatment of diseases that do not respond to current TNF inhibitors. Accordingly, a variety of reagents have been developed that either selectively inhibit TNFR1 or selectively activate TNFR2. Several of these reagents have shown promise in preclinical studies and are now in, or approaching, clinical trials.
 Published observational studies have revealed the connection between neurodegenerative disorders and inflammatory bowel disease (IBD), whereas the causal association remains largely unclear. Our study aims to assess the causality and identify the shared genetic architecture between neurodegenerative disorders and IBD. Two-sample Mendelian randomization analyses were performed to assess the causality between IBD and neurodegenerative disorders (amyotrophic lateral sclerosis [ALS], Alzheimer's disease [AD], Parkinson's disease [PD], and multiple sclerosis [MS]). Shared genetic loci, functional interpretation, and transcriptomic profiles were further investigated in ALS and IBD. We identified that genetic predisposition to IBD was suggestively associated with lower odds of ALS (odds ratio [OR] 0.96, 95% confidence interval [CI] 0.94 to 0.99). In contrast, IBD was not genetically associated with an increased risk of AD, PD, or MS (and vice versa). Two shared genetic loci (rs6571361 and rs7154847) were derived, and SCFD1, G2E3, and HEATR5A were further identified as novel risk genes with enriched functions related to membrane trafficking. G2E3 was differentially expressed and significantly correlated with SCFD1 in patients with ALS or IBD. Our study reveals the suggestively protective role of IBD on ALS, and does not support the causality of AD, PD, or MS on IBD (and vice versa). Our findings indicate possible shared genetic architecture and pathways between ALS and IBD. These results provide insights into the pathogenesis and therapeutics of IBD and neurodegenerative disorders.
 Neuroimmune diseases are a group of disorders that occur due to the dysregulation of both the nervous and immune systems, and these illnesses impact tens of millions of people worldwide. However, patients who suffer from these debilitating conditions have very few FDA-approved treatment options. Neuroimmune crosstalk is important for controlling the immune system both centrally and peripherally to maintain tissue homeostasis. This review aims to provide readers with information on how natural products modulate neuroimmune crosstalk and the therapeutic implications of natural products, including curcumin, epigallocatechin-3-gallate (EGCG), ginkgo special extract, ashwagandha, Centella asiatica, Bacopa monnieri, ginseng, and cannabis to mitigate the progression of neuroimmune diseases, such as Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease, depression, and anxiety disorders. The majority of the natural products based clinical studies mentioned in this study have yielded positive results. To achieve the expected results from natural products based clinical studies, researchers should focus on enhancing bioavailability and determining the synergistic mechanisms of herbal compounds and extracts, which will lead to the discovery of more effective phytomedicines while averting the probable negative effects of natural product extracts. Therefore, future studies developing nutraceuticals to mitigate neuroimmune diseases that incorporate phytochemicals to produce synergistic effects must analyse efficacy, bioavailability, gut-brain axis function safety, chemical modifications, and encapsulation with nanoparticles.
 STUDY DESIGN: A retrospective case-control study. OBJECTIVE: To differentiate neurodegenerative diseases from compressive cervical myelopathy (CCM) using motor evoked potentials (MEPs). SUMMARY OF BACKGROUND DATA: When considering surgery for CCM, it may be necessary to differentiate the condition from a neurodegenerative disease. METHODS: A total of 30 healthy volunteers, 52 typical CCM patients with single-level compression of the spinal cord at C4-5 or C5-6, seven patients with amyotrophic lateral sclerosis (ALS), and 12 patients with demyelinating disease of the central nervous system (DDC), including 11 patients with multiple sclerosis and one patient with neuromyelitis optica spectrum disorder, formed our study population. MEPs were recorded from the bilateral abductor digiti minimi (ADM) and abductor hallucis (AH) muscles using transcranial magnetic stimulation and electrical stimulation of the ulnar and tibial nerves. Central motor conduction time (CMCT), peripheral conduction time, amplitude of MEPs, and frequency of F-waves were evaluated. Receiver operating characteristic (ROC) curve analysis was used to determine the cut-off value for distinguishing between CCM and ALS. RESULTS: Significant differences were observed in the amplitude of MEPs and frequency of F-waves evoked by peripheral nerve stimulation between patients with CCM and ALS. The MEP amplitude of AH was more accurate in differentiating between the two diseases compared to ADM (cut-off value, 11.2mV, sensitivity, 87.5%; specificity, 85.7%). All seven patients with ALS showed reduced frequency of F waves from ADM or AH, but none of the healthy volunteers or patients with other diseases demonstrated this finding. Moreover, there were no significant differences between CCM and DDC in any of the assessments. CONCLUSION: The amplitude of MEPs and frequency of F waves evoked by peripheral nerve stimulation could be helpful in differentiating ALS from CCM.
 Masitinib is an orally acceptable tyrosine kinase inhibitor that is currently investigated under clinical trials against cancer, asthma, Alzheimer's disease, multiple sclerosis and amyotrophic lateral sclerosis. A recent study confirmed the anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) activity of masitinib through inhibition of the main protease (M(pro)) enzyme, an important pharmacological drug target to block the replication of the coronavirus. However, due to the adverse effects and lower potency of the drug, there are opportunities to design better analogues of masitinib. Herein, we substituted the N-methylpiperazine group of Masitinib with different chemical moieties and evaluated their drug-likeness and toxicities. The filtered analogues were subjected to molecular docking studies which revealed that the analogues with substituents methylamine in M10 (CID10409602), morpholine in M23 (CID59789397) and 4-methylmorpholine in M32 (CID143003625) have a stronger affinity to the drug receptor compared to masitinib. The molecular dynamics (MD) simulation analysis reveals that the identified analogues alter the mobility, structural compactness, accessibility to solvent molecules, and the number of hydrogen bonds in the native target enzyme. These structural alterations can help explain the inhibitory mechanisms of these analogues against the target enzyme. Thus, our studies provide avenues for the design of new masitinib analogues as the SARS-CoV-2 M(pro) inhibitors.
 Resveratrol is known to exhibit neuroprotective effects in many neurological disorders via autophagy modulation. However, controversial results have been reported about the therapeutic potential of resveratrol and the implication of autophagy in demyelinating diseases. This study aimed to evaluate the autophagic changes in cuprizone-intoxicated C57Bl/6 mice and explore the effect of autophagy activation by resveratrol on the demyelination and remyelination processes. Mice were fed with chow containing 0.2% cuprizone for 5 weeks, followed by a cuprizone-free diet for 2 weeks. Resveratrol (250 mg/kg/day) and/or chloroquine (an autophagy inhibitor; 10 mg/kg/day) were given for 5 weeks starting from the third week. At the end of the experiment, animals were tested on rotarod and then sacrificed for biochemical assessment, luxol fast blue (LFB) staining, and transmission electron microscopy (TEM) imaging of the corpus callosum. We observed that cuprizone-induced demyelination was associated with impaired degradation of autophagic cargo, induction of apoptosis, and manifest neurobehavioral disturbances. Oral treatment with resveratrol promoted motor coordination and improved remyelination with regular compacted myelin in most axons without a significant impact on myelin basic protein (MBP) mRNA expression. These effects are mediated, at least in part, via activating autophagic pathways that may involve SIRT1/FoxO1 activation. This study verified that resveratrol dampens cuprizone-induced demyelination, and partially enhances myelin repair through modulation of the autophagic flux, since interruption of the autophagic machinery by chloroquine reversed the therapeutic potential of resveratrol.
 OBJECTIVE: To determine the effectiveness of telehealth interventions in reducing community falls risk or rates compared to equivalent in-person interventions in adults with neurological conditions. DATA SOURCES: Eight electronic databases, trial registries and search engines were searched for the concepts 'falls', 'neurological conditions', and 'telehealth', limited to English language, from inception until August 2022. REVIEW METHODS: Search for original research where the intervention was delivered via synchronous videoconferencing with the aim of reducing falls and falls-related outcomes. Screening and risk of bias assessment were completed by two independent researchers. Outcome data included falls rates, falls-related outcomes, safety, feasibility, and acceptability. Risk of bias was assessed using the ROB-2 and ROBINS-I tools. Quality of evidence was rated with the grading of recommendations, assessment, development and evaluation (GRADE) approach. RESULTS: Seventeen studies with 581 participants were included; six were randomised controlled trials. Risk of bias ranged from low to high. Only one study (n = 76) reported falls and did not find differences between telehealth and in-person physiotherapy. There was low-quality evidence that telehealth interventions improve balance outcomes more than face-to-face interventions (pooled between-group mean difference 2.48 Berg Balance Scale units, 95%CI 0.77 to 4.20). Fear of falling was not different between intervention delivery modes. CONCLUSION: Findings suggest that telehealth delivered falls prevention interventions are safe, feasible and acceptable in community-dwelling adults with neurological conditions, however, data related to effectiveness in reducing falls is limited. Low-quality evidence suggests that telehealth may deliver similar or better outcomes for standing balance in this population.PROSPERO Registration: (CRD42021240167).
 BACKGROUND: Cognitive dysfunction is a pervasive symptom of multiple sclerosis (MS). Correlational evidence on the relationships between physical activity, sedentary behavior, and cognition has been mixed and limited to a few activity measures. The collinearity of accelerometry-based metrics has precluded an assessment of the full activity spectrum. Here, we aimed to examine the rich set of activity measures using analytic approaches suitable for collinear metrics. We investigated the combination of physical activity, sedentary, and clinicodemographic measures that explain the most variance in composite scores of working memory/processing speed, visual memory, and verbal memory. METHODS: We analyzed baseline accelerometry and neuropsychological data (n = 80) from a randomized controlled trial of pedometer tracking. Using partial least squares regression (PLSR), we built three models to predict latent scores on the three domains of cognition using 12 activity metrics, sex, education, and Expanded Disability Status Scale (EDSS) scores. Significance was assessed using linear regression models with model component scores as predictors and cognitive composites as outcomes. RESULTS: The latent component was significant for working memory/processing speed but was not significant for visual memory and verbal memory after Bonferroni correction. Working memory/processing speed was positively associated with average kilocalories, moderate-to-vigorous physical activity (MVPA), steps, and sex (i.e., higher scores in males) and negatively related to duration of long sedentary bouts and EDSS. CONCLUSIONS: These findings suggest that increasing overall energy expenditure through walking and MVPA, while decreasing prolonged sedentary time may positively benefit working memory/processing speed in people with MS. TRIAL REGISTRATION: This RCT #NCT03244696 was registered on Clinicaltrials.gov (https://www. CLINICALTRIALS: gov/ct2/show/NCT03244696).
 It was shown that the spontaneous development of experimental encephalomyelitis (EAE) in C57BL/6 mice occurs due to changes in the profile of bone marrow stem cells differentiation. This leads to the appearance of lymphocytes producing antibodies-abzymes that hydrolyze DNA, myelin basic protein (MBP), and histones. The activity of abzymes in the hydrolysis of these auto-antigens slowly but constantly increases during the spontaneous development of EAE. Treatment of mice with myelin oligodendrocyte glycoprotein (MOG) leads to a sharp increase in the activity of these abzymes with their maximum at 20 days (acute phase) after immunization. In this work, we analyzed changes in the activity of IgG-abzymes hydrolyzing (pA)(23), (pC)(23), (pU)(23), and six miRNAs (miR-9-5p, miR-219a-5p, miR-326, miR-155-5p, miR-21-3p, and miR-146a-3p) before and after mice immunization with MOG. Unlike abzymes hydrolyzing DNA, MBP, and histones, the spontaneous development of EAE leads not to an increase but to a permanent decrease of IgGs activity of hydrolysis of RNA-substrates. Treatment of mice with MOG resulted in a sharp but transient increase in the activity of antibodies by day 7 (onset of the disease), followed by a sharp decrease in activity 20-40 days after immunization. A significant difference in the production of abzymes against DNA, MBP, and histones before and after mice immunization with MOG with those against RNAs may be since the expression of many miRNAs decreased with age. This can lead to a decrease in the production of antibodies and abzymes that hydrolyze miRNAs with age mice.
 INTRODUCTION: Whole-body cryotherapy (WBC) is a controlled exposure of the whole body to cold to gain health benefits. In recent years, data on potential applications of WBC in multiple clinical settings have emerged. SOURCES OF DATA: PubMed, EBSCO and Clinical Key search using keywords including terms 'whole body', 'cryotherapy' and 'cryostimulation'. AREAS OF AGREEMENT: WBC could be applied as adjuvant therapy in multiple conditions involving chronic inflammation because of its potent anti-inflammatory effects. Those might include systemic inflammation as in rheumatoid arthritis. In addition, WBC could serve as adjuvant therapy for chronic inflammation in some patients with obesity. AREAS OF CONTROVERSY: WBC probably might be applied as an adjuvant treatment in patients with chronic brain disorders including mild cognitive impairment and general anxiety disorder and in patients with depressive episodes and neuroinflammation reduction as in multiple sclerosis. WBC effects in metabolic disorder treatment are yet to be determined. WBC presumably exerts pleiotropic effects and therefore might serve as adjuvant therapy in multi-systemic disorders, including myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). GROWING POINTS: The quality of studies on the effects of WBC in the clinical setting is in general low; hence, randomized controlled trials with adequate sample size and longer follow-up periods are needed. AREAS ARE TIMELY FOR DEVELOPING RESEARCH: Further studies should examine the mechanism underlying the clinical efficacy of WBC. Multiple conditions might involve chronic inflammation, which in turn could be a potential target of WBC. Further research on the application of WBC in neurodegenerative disorders, neuropsychiatric disorders and ME/CFS should be conducted.
 OBJECTIVE: Certain neurologic diseases have been noted to vary by season, and this is important for understanding disease mechanisms and risk factors, but seasonality has not been systematically examined across the spectrum of neurologic disease, and methodologic guidance is also lacking. METHODS: Using nationally representative data from the National Inpatient Sample, a stratified 20% sample of all non-federal acute care hospitalizations in the United States, we calculated the monthly rate of hospitalization for 14 neurologic diseases from 2016 to 2018. For each disease, we assessed seasonality of hospitalization using chi-squared, Edward, and Walter-Elwood tests and seasonal time series regression models. Statistical tests were adjusted for multiple hypothesis testing using Bonferroni correction. RESULTS: Meningitis, encephalitis, ischemic stroke, intracerebral hemorrhage, Guillain-Barre syndrome, and multiple sclerosis had statistically significant seasonality according to multiple methods of testing. Subarachnoid hemorrhage, status epilepticus, myasthenia gravis, and epilepsy had significant seasonality according to Edwards and Walter-Elwood tests but not chi-square tests. Seasonal time series regression illustrated seasonal variation in all 14 diseases of interest, but statistical testing for seasonality within these models using the Kruskal-Wallis test only achieved statistical significance for meningitis. INTERPRETATION: Seasonal variation is present across the spectrum of acute neurologic disease, including some conditions for which seasonality has not previously been described, and can be examined using multiple different methods. ANN NEUROL 2023;93:743-751.
 PURPOSE: The US Food and Drug Administration (FDA) Amendments Act of 2007 authorized the FDA to require risk evaluation and mitigation strategy (REMS) programs for drugs with important safety concerns. REMS can have elements to assure safe use (ETASU), such as patient registries, dispensing restrictions, and physician training and certification requirements. We aimed to understand physician experiences with and perceptions of a selection of ETASU REMS. METHODS: Physicians prescribing 1 of 4 ETASU REMS-covered drugs: natalizumab, riociguat, sodium oxybate, and vigabatrin. STUDY DESIGN: Descriptive phenomenological study based on semi-structured phone interviews. DATA COLLECTION/EXTRACTION METHODS: Qualitative content analysis to summarize physician responses to open-ended questions. RESULTS: Of 31 physicians (14 female), 6 prescribed riociguat, 6 vigabatrin, 7 sodium oxybate, and 12 natalizumab (5 for Crohn's disease, 7 for multiple sclerosis), most demonstrated good understanding of the rationale for and requirements of the ETASU REMS but believed that the programs had limited effect on clinical practice. Some physicians reported that the ETASU REMS made them more comfortable with prescribing covered drugs due to heightened oversight, facilitated discussions about treatment, and were likely more beneficial for non-specialists. Concerns were raised about the administrative effort needed to comply with the programs and the potential misuse of patient health information transmitted to manufacturers. CONCLUSIONS: Physicians are generally aware of ETASU REMS and get reassurance from the additional oversight, but the programs can be better integrated into clinical workflows and can be designed to better protect patient health information.
 In the central nervous system (CNS) there are a greater number of glial cells than neurons (between five and ten times more). Furthermore, they have a greater number of functions (more than eight functions). Glia comprises different types of cells, those of neural origin (astrocytes, radial glia, and oligodendroglia) and differentiated blood monocytes (microglia). During ontogeny, neurons develop earlier (at fetal day 15 in the rat) and astrocytes develop later (at fetal day 21 in the rat), which could indicate their important and crucial role in the CNS. Analysis of the phylogeny reveals that reptiles have a lower number of astrocytes compared to neurons and in humans this is reversed, as there have a greater number of astrocytes compared to neurons. These data perhaps imply that astrocytes are important and special cells, involved in many vital functions, including memory, and learning processes. In addition, astrocytes are involved in different mechanisms that protect the CNS through the production of antioxidant and anti-inflammatory proteins and they clean the extracellular environment and help neurons to communicate correctly with each other. The production of inflammatory mediators is important to prevent changes in brain homeostasis. On the contrary, excessive, or continued production appears as a characteristic element in many diseases, such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and in neurodevelopmental diseases, such as bipolar disorder, schizophrenia, and autism. Furthermore, different drugs and techniques have been developed to reverse oxidative stress and/or excess of inflammation that occurs in many CNS diseases, but much remains to be investigated. This review attempts to highlight the functional relevance of astrocytes in normal and neuropathological conditions by showing the molecular and cellular mechanisms of their role in the CNS.
 Exosomes are spherical lipid bilayer vesicles composed of lipids, proteins and nucleic acids that deliver signaling molecules through a vesicular transport system to regulate the function and morphology of target cells, thereby involving in a variety of biological processes, such as cell apoptosis or proliferation, and cytokine production. In the past decades, there are emerging evidence that exosomes play pivotal roles in the pathological mechanisms of several autoimmune diseases (ADs), including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes mellitus (T1DM), Sjogren's syndrome (SS), multiple sclerosis (MS), inflammatory bowel disease (IBD). systemic sclerosis (SSc), etc. Several publications have shown that exosomes are involved in the pathogenesis of ADs mainly through intercellular communication and by influencing the response of immune cells. The level of exosomes and the expression of nucleic acids can reflect the degree of disease progression and are excellent biomarkers for ADs. In addition, exosomes have the potential to be used as drug carriers thanks to their biocompatibility and stability. In this review, we briefly summarized the current researches regarding the biological functions of exosomes in ADs, and provided an insight into the potential of exosomes as biomarkers and therapeutic delivery for these diseases.
 First described in 1875 by Wilhelm Heinrich Erb and Carl Friedrich Otto Westphal, the deep tendon reflex (DTR) is essential in examining and diagnosing neurologic disease. Deep tendon reflexes or, more accurately, the 'muscle stretch reflex' can aid in evaluating neurologic disease affecting afferent nerves, spinal cord synaptic connections, motor nerves, and descending motor pathways. Proper technique and interpretation of results are crucial in achieving a proper distinction between upper and lower motor neuron pathologic processes such as multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), spinal cord injuries, and spinal muscular atrophies, with the presence of hyporeflexia or hyperreflexia considered a 'hard sign' of neurologic dysfunction. There are five primary deep tendon reflexes: biceps, brachioradialis, triceps, patellar, and ankle. Biceps Reflex: Muscle involved: biceps brachii. Nerve supply: musculocutaneous. Segmental innervation: C5-C6. Brachioradialis Reflex: Muscle involved: brachioradialis. Nerve supply: radial. Segmental innervation: C5-C6. Triceps Reflex: Muscle involved: triceps brachii. Nerve supply: radial . Segmental innervation: C7-C8. Patellar Reflex (knee-jerk): Muscle involved: quadriceps femoris. Nerve supply: femoral. Segmental innervation: L2-L4. Achilles Reflex (ankle-jerk): Muscles involved: gastrocnemius, soleus. Nerve supply: tibial. Segmental innervation: S1-S2. To provide a standard scale for evaluating deep tendon reflexes, in 1993, the National Institute of Neurological Disorders and Stroke (NINDS) proposed a grading scale from 0 to 4. This scale has been validated and is universally accepted. NINDS grading of deep tendon reflexes. 0: Reflex absent. 1: Reflex small, less than normal, includes a trace response or a response brought out only with reinforcement. 2: Reflex in the lower half of a normal range. 3: Reflex in the upper half of a normal range. 4: Reflex enhanced, more than normal, includes clonus if present, which optionally can be noted in an added verbal description of the reflex. In some instances, a plus sign (+) is written after the number. When discussing DTRs, adding or omitting a plus sign does not change the meaning of the reflex grade observed.  What is 'normal' typically depends on the patient's history and past documented reflex grade. Abnormality is suggested when asymmetric reflexes are found. Once the examiner obtains a reflex on one side, they should test the same reflex on the opposite side for comparison.
 The role of Akkermansia muciniphila, one of the most abundant microorganisms of the intestinal microbiota, has been studied extensively in metabolic diseases, such as obesity and diabetes. It is considered a next-generation probiotic microorganism. Although its mechanism of action has not been fully elucidated, accumulating evidence indicates the important role of A. muciniphila in brain functions via the gut-brain axis and its potential as a therapeutic target in various neuropsychiatric disorders. However, only a limited number of studies, particularly clinical studies, have directly assessed the therapeutic effects of A. muciniphila interventions in these disorders. This is the first review to discuss the comprehensive mechanism of A. muciniphila in the gut-brain axis via the protection of the intestinal mucosal barrier and modulation of the immune system and metabolites, such as short-chain fatty acids, amino acids, and amino acid derivatives. Additionally, the role of A. muciniphila and its therapeutic potential in various neuropsychiatric disorders, including Alzheimer's disease and cognitive deficit, amyotrophic lateral sclerosis, Parkinson's disease, and multiple sclerosis, have been discussed. The review suggests the potential role of A. muciniphila in healthy brain functions.
 ETHNOPHARMACOLOGICAL RELEVANCE: Rhizomes of Panax japonicus (RPJ), a traditional herbal medicine, was used for treating arthritis and physical weakness in China from the Ming dynasty. Triterpene saponins are the main bioactive components of RPJ. In this work, for the first time, we evaluate the therapeutic effect of the total saponin from RPJ (TSPJ) on experimental autoimmune encephalomyelitis (EAE) mice induced by myelin oligodendrocyte glycoprotein (MOG) (35-55), a commonly used animal model of Multiple sclerosis (MS). AIM OF THE STUDY: To evaluate the therapeutic effect of TSPJ on EAE and explored its possible underlying mechanisms. MATERIALS AND METHODS: EAE was induced by MOG (35-55). Mice were administrated with TSPJ (36.5 mg/kg, 73 mg/kg) and prednisone acetate (positive control) orally once daily up to 28 days postimmunization, and their neurological deficit was scored. Hematoxylin and Eosin (HE), Luxol Fast Blue (LFB), and transmission electron microscopy (TEM) were carried out to evaluate the EAE-induced pathological changes in the brain and spinal cord. IL-17a and Foxp3 levels in central nervous system (CNS)were evaluated by immunohistochemical staining. The changes in IL-1β, IL-6, and TNF-α levels in serum and CNS were measured with ELISA. Quantitative reverse transcription PCR (qRT-PCR) was used to access mRNA expression in CNS of the above indices. The percentages of Th1, Th2, Th17and Treg cells in spleen were determined by Flow Cytometry (FCM). Furthermore, 16S rDNA sequencing was used to detect the intestinal flora of mice in each group. In vitro studies, lipopolysaccharides (LPS)-induced BV2 microglia cells were used and the expression of TLR4, MyD88, p65, and p-p65 in cells was detected by Western blot. RESULTS: TSPJ treatment significantly alleviated neurological impairment caused by EAE. Histological examination confirmed the protective effects of TSPJ on myelin sheath and the reduction of inflammatory cell infiltration in the brain and spinal cord of EAE mice. TSPJ notably downregulated the ratio of IL-17a/Foxp3 at protein and mRNA levels in CNS, as well as Th17/Treg and Th1/Th2 cell ratios in the spleen of EAE mice. The levels of TNF-α, IL-6, and IL-1β in CNS and peripheral serum also decreased post-TSPJ treatment. In vitro, TSPJ suppressed LPS-induced production of inflammatory factors in BV2 cells via TLR4-MyD88-NF-κB signaling pathway. More importantly, TSPJ interventions altered the composition of gut microbiota and restored the ratio of Firmicutes to Bacteroidetes in EAE mice. Furthermore, Spearman's correlation analysis revealed that a relationship existed between statistically significantly altered genera and CNS inflammatory indices. CONCLUSION: Our results demonstrated TSPJ had therapeutic effects on EAE. Its anti-neuroinflammation property in EAE was related to modulating gut microbiota and inhibiting TLR4-MyD88-NF-κB signaling pathway. Our study indicated that TSPJ may be a potential candidate for the treatment of MS.
 The gut microbiota (GM) plays an important role in the physiology and pathology of the host. Microbiota communicate with different organs of the organism by synthesizing hormones and regulating body activity. The interaction of the central nervous system (CNS) and gut signaling pathways includes chemical, neural immune and endocrine routes. Alteration or dysbiosis in the gut microbiota leads to different gastrointestinal tract disorders that ultimately impact host physiology because of the abnormal microbial metabolites that stimulate and trigger different physiologic reactions in the host body. Intestinal dysbiosis leads to a change in the bidirectional relationship between the CNS and GM, which is linked to the pathogenesis of neurodevelopmental and neurological disorders. Increasing preclinical and clinical studies/evidence indicate that gut microbes are a possible susceptibility factor for the progression of neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS) and autism spectrum disorder (ASD). In this review, we discuss the crucial connection between the gut microbiota and the central nervous system, the signaling pathways of multiple biological systems and the contribution of gut microbiota-related neurological disorders.
 A previously healthy 2-year-old boy presented with a left sixth cranial nerve palsy. There was a family history of multiple sclerosis and optic neuritis. Neuroimaging showed multiple foci of T2/FLAIR hyperintense signal abnormality in both cerebral hemispheres and in the brainstem. The initial diagnosis was suspicious for demyelinating disease. However, there was no clinical improvement after a course of corticosteroids, and there was no change in his follow-up MRI. He later developed bilateral sixth nerve palsies, with esotropia addressed with bilateral medial rectus botulinum toxin injections. A brain biopsy was planned. However, his 3-month-old sister was separately admitted for fever and pancytopenia. She had markedly elevated ferritin, D-dimer, triglycerides, sIL-2R, CXCL9, and IL-18 and low fibrinogen. Her bone marrow biopsy showed hemophagocytosis. Genetic testing of both siblings revealed biallelic mutations in the PRF1 locus. The final diagnosis of familial hemophagocytic lymphohistiocytosis Type 2 was made. Both siblings underwent chemotherapy. The boy's sixth nerve palsies and MRI abnormalities resolved. Both siblings then went on to undergo bone marrow transplant.
 OBJECTIVE: To investigate relationships between serum neurofilament light chain (sNfL), ubiquitin C-terminal hydrolase L1 (sUCHL1), tau (sTau) and glial fibrillary acidic protein (sGFAP) levels and disease activity/disability in neuromyelitis optica spectrum disorder (NMOSD), and the effects of inebilizumab on these biomarkers in N-MOmentum. METHODS: N-MOmentum randomised participants to receive inebilizumab or placebo with a randomised controlled period (RCP) of 28 weeks and an open-label follow-up period of ≥2 years. The sNfL, sUCHL1, sTau and sGFAP were measured using single-molecule arrays in 1260 scheduled and attack-related samples from N-MOmentum participants (immunoglobulin G (IgG) autoantibodies to aquaporin-4-positive, myelin oligodendrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy donors and patients with relapsing-remitting multiple sclerosis). RESULTS: The concentration of all four biomarkers increased during NMOSD attacks. At attack, sNfL had the strongest correlation with disability worsening during attacks (Spearman R(2)=0.40; p=0.01) and prediction of disability worsening after attacks (sNfL cut-off 32 pg/mL; area under the curve 0.71 (95% CI 0.51 to 0.89); p=0.02), but only sGFAP predicted upcoming attacks. At RCP end, fewer inebilizumab-treated than placebo-treated participants had sNfL>16 pg/mL (22% vs 45%; OR 0.36 (95% CI 0.17 to 0.76); p=0.004). CONCLUSIONS: Compared with sGFAP, sTau and sUCHL1, sNfL at attack was the strongest predictor of disability worsening at attack and follow-up, suggesting a role for identifying participants with NMOSD at risk of limited post-relapse recovery. Treatment with inebilizumab was associated with lower levels of sGFAP and sNfL than placebo. TRIAL REGISTRATION NUMBER: NCT02200770.
 IMPORTANCE: Scientific literature is sparse about the association of vaccination with the onset of multiple sclerosis (MS) flare-ups. Immunization by vaccines of the entire population is crucially important for public health. OBJECTIVE: To evaluate the risk of hospitalization for severe MS flare-ups after vaccination in patients with MS. DESIGN, SETTING, PARTICIPANTS: This cohort study included patients diagnosed with MS between January 1, 2007, and December 31, 2017, who were included in the System of National Health Databases, a national health claims database in France. In a nested case-crossover analysis, cases were defined by vaccine exposure prior to the onset of hospitalization due to an MS flare-up, and flare-up rates were compared with those that occurred prior to vaccine exposure in up to 4 control time windows immediately preceding the at-risk time window (ie, the MS flare-up) for each patient. Data were analyzed from January 2022 to December 2022. EXPOSURE: Receipt of at least 1 vaccination, including the diphtheria, tetanus, poliomyelitis, pertussis, or Haemophilus influenzae (DTPPHi) vaccine, influenza vaccine, and pneumococcal vaccine, during follow-up. MAIN OUTCOMES AND MEASURES: The primary outcome was the risk of hospitalization for an MS flare-up after receipt of a vaccine. Adjusted odds ratios (AORs) and 95% CIs were derived using conditional logistic regression to measure the risk of hospitalization for an MS flare-up associated with vaccination. RESULTS: A total of 106 523 patients constituted the MS cohort (mean [SD] age, 43.9 [13.8] years; 76 471 females [71.8%]; 33 864 patients [31.8%] had incident MS and 72 659 patients [68.2%] had prevalent MS) and were followed up for a mean (SD) of 8.8 (3.1) years. Of these patients, 35 265 (33.1%) were hospitalized for MS flare-ups during the follow-up period for a total of 54 036 MS-related hospitalizations. The AORs of hospitalization for an MS flare-up and vaccine exposure in the 60 days prior to the flare-up were 1.00 (95% CI, 0.92-1.09) for all vaccines, 0.95 (95% CI, 0.82-1.11) for the DTPPHi, 0.98 (95% CI, 0.88-1.09) for the influenza vaccine, and 1.20 (95% CI, 0.94-1.55) for the pneumococcal vaccine. CONCLUSIONS AND RELEVANCE: A nationwide study of the French population found no association between vaccination and the risk of hospitalization due to MS flare-ups. However, considering the number of vaccine subtypes available, further studies are needed to confirm these results.
 Microglia are resident immune cells in the central nervous system. During the pathogenesis of Alzheimer's disease, stimulatory factors continuously act on the microglia causing abnormal activation and unbalanced phenotypic changes; these events have become a significant and promising area of research. In this review, we summarize the effects of microglial polarization and crosstalk with other cells in the central nervous system in the treatment of Alzheimer's disease. Our literature search found that phenotypic changes occur continuously in Alzheimer's disease and that microglia exhibit extensive crosstalk with astrocytes, oligodendrocytes, neurons, and penetrated peripheral innate immune cells via specific signaling pathways and cytokines. Collectively, unlike previous efforts to modulate microglial phenotypes at a single level, targeting the phenotypes of microglia and the crosstalk with other cells in the central nervous system may be more effective in reducing inflammation in the central nervous system in Alzheimer's disease. This would establish a theoretical basis for reducing neuronal death from central nervous system inflammation and provide an appropriate environment to promote neuronal regeneration in the treatment of Alzheimer's disease.
 Astrocytes are the most abundant glial cell type in the brain, where they participate in various homeostatic functions. Transcriptomically, diverse astrocyte subpopulations play distinct roles during development and disease progression. However, the biochemical identification of astrocyte subtypes, especially by membrane surface protein glycosylation, remains poorly investigated. Protein tyrosine phosphatase receptor type zeta (PTPRZ) is a highly expressed membrane protein in CNS glia cells that can be modified with diverse glycosylation, including the unique HNK-1 capped O-mannosyl (O-Man) core M2 glycan mediated by brain-specific branching enzyme GnT-IX. Although PTPRZ modified with HNK-1 capped O-Man glycans (HNK-1-O-Man(+) PTPRZ) is increased in reactive astrocytes of demyelination model mice, whether such astrocytes emerge in a broad range of disease-associated conditions or are limited to conditions associated with demyelination remains unclear. Here, we show that HNK-1-O-Man(+) PTPRZ localizes in hypertrophic astrocytes of damaged brain areas in patients with multiple sclerosis. Furthermore, we show that astrocytes expressing HNK-1-O-Man(+) PTPRZ are present in two demyelination mouse models (cuprizone-fed mice and a vanishing white matter disease model), while traumatic brain injury does not induce glycosylation. Administration of cuprizone to Aldh1l1-eGFP and Olig2(KICreER/+) ;Rosa26(eGFP) mice revealed that cells expressing HNK-1-O-Man(+) PTPRZ are derived from cells in the astrocyte lineage. Notably, GnT-IX but not PTPRZ mRNA was up-regulated in astrocytes isolated from the corpus callosum of cuprizone model mice. These results suggest that the unique PTPRZ glycosylation plays a key role in the patterning of demyelination-associated astrocytes.
 Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and multiple sclerosis (MS) are two complex and multifactorial diseases whose patients experience persistent fatigue, cognitive impairment, among other shared symptoms. The onset of these diseases has also been linked to acute herpesvirus infections or their reactivations. In this work, we re-analyzed a previously-described dataset related to IgG antibody responses to 6 herpesviruses (CMV - cytomegalovirus; EBV - Epstein-Barr virus; HHV6 - human herpesvirus-6; HSV1 and HSV2 - herpes simplex virus-1 and -2, respectively; VZV - varicella-zoster virus) from the United Kingdom ME/CFS biobank. The primary goal was to report the underlying symptomology and its association with herpesvirus IgG antibodies using data from 4 disease-trigger-based subgroups of ME/CFS patients (n = 222) and patients with MS (n = 46). The secondary objective was to assess whether serological data could distinguish ME/CFS and its subgroup from MS using a SuperLearner (SL) algorithm. There was evidence for a significant negative association between temporary eye insight disturbance and CMV antibody concentrations and for a significant positive association between bladder problems and EBV antibody concentrations in the MS group. In the ME/CFS or its subgroups, the most significant antibody-symptom association was obtained for increasing HSV1 antibody concentration and brain fog, a finding in line with a negative impact of HSV1 exposure on cognitive outcomes in both healthy and disease conditions. There was also evidence for a higher number of significant antibody-symptom associations in the MS group than in the ME/CFS group. When we combined all the serological data in an SL algorithm, we could distinguish three ME/CFS subgroups (unknown disease trigger, non-infection trigger, and an infection disease trigger confirmed in the lab at the time of the event) from the MS group. However, we could not find the same for the remaining ME/CFS group (related to an unconfirmed infection disease). In conclusion, IgG antibody data explains more the symptomology of MS patients than the one of ME/CFS patients. Given the fluctuating nature of symptoms in ME/CFS patients, the clinical implication of these findings remains to be determined with a longitudinal study. This study is likely to ascertain the robustness of the associations during natural disease course.
 BACKGROUND: Neurodegenerative diseases (NDs) have posed significant challenges to public health, and it is crucial to understand their mechanisms in order to develop effective therapeutic strategies. Recent studies have highlighted the potential role of selenium in ND pathogenesis, as it plays a vital role in maintaining cellular homeostasis and preventing oxidative damage. However, a comprehensive analysis of the association between selenium and NDs is still lacking. METHOD: Five public databases, namely PubMed, Web of Science, EMBASE, Cochrane and Clinical Trials, were searched in our research. Random model effects were chosen, and Higgins inconsistency analyses (I(2)), Cochrane's Q test and Tau2 were calculated to evaluate the heterogeneity. RESULT: The association of selenium in ND patients with Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD) was studied. A statistically significant relationship was only found for AD patients (SMD = -0.41, 95% CI (-0.64, -0.17), p < 0.001), especially for erythrocytes. However, no significant relationship was observed in the analysis of the other four diseases. CONCLUSION: Generally, this meta-analysis indicated that AD patients are strongly associated with lower selenium concentrations compared with healthy people, which may provide a clinical reference in the future. However, more studies are urgently needed for further study and treatment of neurodegenerative diseases.
 In sporadic amyotrophic lateral sclerosis (sALS), IL-17A- and granzyme-positive cytotoxic T lymphocytes (CTL), IL-17A-positive mast cells, and inflammatory macrophages invade the brain and spinal cord. In some patients, the disease starts following a trauma or a severe infection. We examined cytokines and cytokine regulators over the disease course and found that, since the early stages, peripheral blood mononuclear cells (PBMC) exhibit increased expression of inflammatory cytokines IL-12A, IFN-γ, and TNF-α, as well as granzymes and the transcription factors STAT3 and STAT4. In later stages, PBMCs upregulated the autoimmunity-associated cytokines IL-23A and IL-17B, and the chemokines CXCL9 and CXCL10, which attract CTL and monocytes into the central nervous system. The inflammation is fueled by the downregulation of IL-10, TGFβ, and the inhibitory T-cell co-receptors CTLA4, LAG3, and PD-1, and, in vitro, by stimulation with the ligand PD-L1. We investigated in two sALS patients the regulation of the macrophage transcriptome by dimethyl fumarate (DMF), a drug approved against multiple sclerosis and psoriasis, and the cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway inhibitor H-151. Both DMF and H-151 downregulated the expression of granzymes and the pro-inflammatory cytokines IL-1β, IL-6, IL-15, IL-23A, and IFN-γ, and induced a pro-resolution macrophage phenotype. The eicosanoid epoxyeicosatrienoic acids (EET) from arachidonic acid was anti-inflammatory in synergy with DMF. H-151 and DMF are thus candidate drugs targeting the inflammation and autoimmunity in sALS via modulation of the NFκB and cGAS/STING pathways.

 Intermittent fasting, which includes periods of fasting and nutrition, has been considered a dietary approach for weight loss and metabolic health improvement. However, its potential benefits in autoimmune diseases have not been widely studied. This study aims to review the existing studies on the role and effects of intermittent fasting on autoimmune diseases. A comprehensive search was conducted on electronic databases such as PubMed, Scopus, Embase, and Web of Science, and relevant studies were included based on inclusion criteria. Studies show that intermittent fasting may have beneficial effects on various autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, and systemic lupus erythematosus, by reducing inflammatory markers, modulating the immune system, altering and improving gut microbiota, and enhancing cellular repair mechanisms through autophagy. However, evidence regarding the effects of intermittent fasting on other autoimmune diseases such as multiple sclerosis, systemic lupus erythematosus, thyroid diseases, and psoriasis is limited and inconclusive. Nevertheless, further research is needed to determine optimal intermittent fasting guidelines and its long-term effects on autoimmune diseases. Overall, this literature review proves intermittent fasting may be a promising dietary intervention for managing autoimmune diseases.
 INTRODUCTION: Cholesterol homeostasis is critical for normal brain function. It is tightly controlled by various biological elements. ATP-binding cassette transporter A1 (ABCA1) is a membrane transporter that effluxes cholesterol from cells, particularly astrocytes, into the extracellular space. The recent studies pertaining to ABCA1's role in CNS disorders were included in this study. AREAS COVERED: In this comprehensive literature review, preclinical and human studies showed that ABCA1 has a significant role in the following diseases or disorders: Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, neuropathy, anxiety, depression, psychosis, epilepsy, stroke, and brain ischemia and trauma. EXPERT OPINION: ABCA1 via modulating normal and aberrant brain functions such as apoptosis, phagocytosis, BBB leakage, neuroinflammation, amyloid β efflux, myelination, synaptogenesis, neurite outgrowth, and neurotransmission promotes beneficial effects in aforementioned diseases. ABCA1 is a key molecule in the CNS. By boosting its expression or function, some CNS disorders may be resolved. In preclinical studies, liver X receptor agonists have shown promise in treating CNS disorders via ABCA1 and apoE enhancement.
 Sleep-wake cycle disorders are an important symptom of many neurological diseases, including Parkinson's disease, Alzheimer's disease, and multiple sclerosis. Circadian rhythms and sleep-wake cycles play a key role in maintaining the health of organisms. To date, these processes are still poorly understood and, therefore, need more detailed elucidation. The sleep process has been extensively studied in vertebrates, such as mammals and, to a lesser extent, in invertebrates. A complex, multi-step interaction of homeostatic processes and neurotransmitters provides the sleep-wake cycle. Many other regulatory molecules are also involved in the cycle regulation, but their functions remain largely unclear. One of these signaling systems is epidermal growth factor receptor (EGFR), which regulates the activity of neurons in the modulation of the sleep-wake cycle in vertebrates. We have evaluated the possible role of the EGFR signaling pathway in the molecular regulation of sleep. Understanding the molecular mechanisms that underlie sleep-wake regulation will provide critical insight into the fundamental regulatory functions of the brain. New findings of sleep-regulatory pathways may provide new drug targets and approaches for the treatment of sleep-related diseases.
 Chiari malformation type I (CM-I) is a group of deformities in the posterior fossa and hindbrain, including the pons, cerebellum, and medulla oblongata. Paroxysmal pruritus in CM-I has been reported only once before in the literature. This study was a cross-sectional study over 12 months at a tertiary care pediatric hospital involving children aged one to 18 years with CM-I presenting with paroxysmal itching. Three patients with CM-I presented with severe episodes of paroxysmal itching. Patient 3 was started on carbamazepine therapy for seizures, and incidentally, his itching subsided. The pruritus of neuropathic etiology has been reported to be associated with syringomyelia, spongiform encephalopathies, autoimmune disorders like multiple sclerosis, patients with end-stage renal failure on dialysis, and neoplasms. Antihistamines and antiallergics are ineffective in treating these patients, reiterating a central mechanism for pruritus. At present, no drugs have been approved for the treatment of neuropathic pruritus specifically. The commonly used treatments for neuropathic itch are antiseizure medications, tricyclic antidepressants, gabapentinoids, ketamine, and oral kappa opioids, including butorphanol and difelikefalin. Better structured prospective studies are needed to analyze the prevalence and scales to assess disability caused due to neuropathic itch in CM and may enhance understanding in this area.
 Patients experience existential themes as pivotal in their lives, in order to be able to live with a severe, chronic illness; however, physicians report a hesitative approach to existential communication. The current study investigated Nordic patients' experiences of existential communication with their physicians related to the treatment of multiple sclerosis or chronic pain. Semi-structured interviews with 23 patients were analyzed following Interpretative Phenomenological Analysis. Physicians focusing on medical aspects at the expense of psychological and existential aspects of being ill was experienced by patients as challenging their treatment and well-being. For making a shared decision with the physician on their treatment, patients needed a transition from being dependent to being autonomous. A holding environment and existential communication about transitional objects such as relationships with something bigger than themselves, as nature or religion, supported this autonomy. The analysis showed that existential communication not only supported patients in developing and regaining autonomy but also functioned as a moderator for illness-related distress, as a prevention of withdrawal from treatment, and as significant for patients in relation to living with chronic illness. Further education in existential communication is desirable, to support physicians integrating existential dimensions in consultations and shared decision-making with patients suffering from a severe, chronic illness.
 Accelerometers provide an opportunity to expand standing balance assessments outside of the laboratory. The purpose of this narrative review is to show that accelerometers are accurate, objective, and accessible tools for balance assessment. Accelerometry has been validated against current gold standard technology, such as optical motion capture systems and force plates. Many studies have been conducted to show how accelerometers can be useful for clinical examinations. Recent studies have begun to apply classification algorithms to accelerometry balance measures to discriminate populations at risk for falls. In addition to healthy older adults, accelerometry can monitor balance in patient populations such as Parkinson's disease, multiple sclerosis, and traumatic brain injury. The lack of software packages or easy-to-use applications have hindered the shift into the clinical space. Lack of consensus on outcome metrics has also slowed the clinical adoption of accelerometer-based balance assessments. Future studies should focus on metrics that are most helpful to evaluate balance in specific populations and protocols that are clinically efficacious.
 Dialectical behavior therapy (DBT) has been found to be an efficacious treatment for disorders characterized by high levels of emotional instability. In view of the multifaceted applications of DBT and the extent to which mental disorders can incapacitate cognitive functions, the current systematic review aimed to investigate the effect of DBT in strengthening cognitive functions across various mental health conditions. Original research studies employing both experimental and quasi-experimental designs were included in the review. The literature search was done using different electronic databases, from the first available literature until June 2022, that covered an approximate period of ten years. Joanna Briggs Institute checklist was used to assess the methodological rigor of the studies. Twelve studies conducted on adolescents with emotional dysregulation, and adults with borderline personality disorder, bipolar disorder, attention deficit hyperactivity disorder, and multiple sclerosis were selected. Results indicate that DBT has the potential to improve key cognitive functions such as attention, memory, fluency, response inhibition, planning, set shifting, tolerance for delayed rewards and time perception, as assessed by neuropsychological tests, self-report of cognitive functions, and neuroimaging techniques. Considering the review's findings that showcase the effectiveness of DBT in fostering improvements in cognitive functions, DBT may possibly be chosen as a preferred treatment to ensure that patients reach optimal levels of cognitive functioning. Limitations include lack of sufficient studies encompassing all the common mental health conditions, usage of neuroimaging techniques as only an indirect measure of cognitive functioning and nuances related to the quality of individual studies.
 Transient ischemic attack (TIA) has gained significant attention recently due to the increased incidence of subsequent stroke. However, there are many nonvascular clinical mimics of TIA, creating a need for improved biomarkers to identify a vascular origin. Following the recent approval of ultra-high field (UHF) 7T MRI in clinical practice, several clinical studies have highlighted its added utility in neuroimaging compared to lower-field 1.5T and 3T MRI, particularly in epilepsy and multiple sclerosis. Our case series of three patients with TIA illustrates that 7T MRI can depict small areas of intracortical microhemorrhages and microinfarctions, which could not be resolved with 3T or 1.5T MRI. There are currently no reports of intracortical localization of microhemorrhages in patients with TIA. This discovery may enhance our understanding and characterization of cerebrovascular abnormalities in TIAs. In addition, UHF imaging could potentially be utilized to distinguish transient neurological episodes secondary to cerebrovascular events from other differential considerations. Our cases highlight the underestimation of imaging abnormalities in cases of TIA and support the potential expanded application of clinical 7T to assess patients with TIA. Future studies are necessary at 7T redundant to determine the true incidence of such lesions in TIA and to examine the correlation between cortical microhemorrhages and subsequent ischemic stroke, hemorrhagic events, and neurocognitive impairment.
 Statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) reduce plasma cholesterol and improve endothelium-dependent vasodilation, inflammation, and oxidative stress. The effect of statins on the central nervous system (CNS), particularly on cognition and neurological disorders such as cerebral ischemic stroke, multiple sclerosis (MS), and Alzheimer's disease (AD), has received increasing attention in recent years, both within the scientific community and in the media. This review aims to provide an updated discussion on the effects of statins on the differentiation and function of various nervous system cells, including neurons and glial cells. Additionally, the mechanisms of action and how different types of statins enter the CNS will be discussed.
 Familial Mediterranean fever (FMF) is a rare autoinflammatory disorder characterized mainly by recurrent self-limited episodes of fever and polyserositis. FMF-related neurologic complication is an old debate, and the correlation between FMF and demyelinating disorders has been a matter of dispute for a long time. Few reports demonstrated a relationship between FMF and multiple sclerosis; however, the existence of a causal relationship between FMF and demyelinating disorders is still a puzzle. This report presents the first case of transverse myelitis following FMF attacks in which neurologic manifestations were resolved using colchicine treatment. Due to relapses of FMF, which were accompanied by transverse myelitis, rituximab was administered, which resulted in stabilizing disease activity. Accordingly, in the case of colchicine-resistant FMF and FMF-related demyelinating conditions, rituximab could be considered as a potential therapeutic option to alleviate both polyserositis and demyelinating manifestations.
 The ketogenic diet (KD) was initially used in 1920 for drug-resistant epileptic patients. From this point onward, ketogenic diets became a pivotal part of nutritional therapy research. To date, KD has shown therapeutic potential in many pathologies such as Alzheimer's disease, Parkinson's disease, autism, brain cancers, and multiple sclerosis. Although KD is now an adjuvant therapy for certain diseases, its effectiveness as an antitumor nutritional therapy is still an ongoing debate, especially in Neuroblastoma. Neuroblastoma is the most common extra-cranial solid tumor in children and is metastatic at initial presentation in more than half of the cases. Although Neuroblastoma can be managed by surgery, chemotherapy, immunotherapy, and radiotherapy, its 5-year survival rate in children remains below 40%. Earlier studies have proposed the ketogenic diet as a possible adjuvant therapy for patients undergoing treatment for Neuroblastoma. In this study, we seek to review the possible roles of KD in the treatment of Neuroblastoma.
 In the COVID-19 pandemic era, antibody testing against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has proven an invaluable tool and herein we highlight some of the most useful clinical and/or epidemiological applications of humoral immune responses recording. Anti-spike circulating IgGs and SARS-CoV-2 neutralizing antibodies can serve as predictors of disease progression or disease prevention, whereas anti-nucleocapsid antibodies can help distinguishing infection from vaccination. Also, in the era of immunotherapies we address the validity of anti-SARS-CoV-2 antibody monitoring post-infection and/or vaccination following therapies with the popular anti-CD20 monoclonals, as well as in the context of various cancers or autoimmune conditions such as rheumatoid arthritis and multiple sclerosis. Additional crucial applications include population immunosurveillance, either at the general population or at specific communities such as health workers. Finally, we discuss how testing of antibodies in cerebrospinal fluid can inform us on the neurological complications that often accompany COVID-19.
 Volvulus occurs when a loop of intestine twists around itself and the mesentery that supplies it, causing a bowel obstruction. Symptoms include abdominal distension, pain, vomiting, constipation, and bloody stools. The onset of symptoms may be insidious or sudden. The mesentery becomes so tightly twisted that blood supply is cut off, resulting in bowel ischemia. Pain may be significant and fever may develop.  Risk factors for volvulus include intestinal malrotation, Hirschsprung disease, an enlarged colon, pregnancy, and abdominal adhesions. A higher incidence of volvulus is also noticed among hospitalized patients with neuropsychiatric disorders such as Parkinson's disease, multiple sclerosis, etc.  High fiber diet, chronic constipation with chronic use of laxatives and/or enema, and associated myopathy like Duchene muscular dystrophy, etc. are also associated with an increased risk of sigmoid volvulus. In adults, the sigmoid colon and cecum are the most commonly affected. On the contrary, splenic flexure is least prone to volvulus. In children, the small intestine and stomach are more commonly involved. Diagnosis is mainly clinical, however, characteristic radiological findings on plain radiograph, ultrasound, and upper GI series help in differentiating from other differentials.  The present article will cover volvulus in adults with specific differences from midgut volvulus in children. However, a detailed discussion of malrotation and midgut volvulus is beyond the scope of this article. Sigmoidoscopy or a barium enema can be attempted as an initial treatment for sigmoid volvulus. However, due to the high risk of recurrence, bowel resection with anastomosis within two days is generally recommended. If the bowel is severely twisted or the blood supply is cut off, emergent surgery is required. In a cecal volvulus, part of the bowel is usually removed. If the cecum is still healthy, it may be returned and sutured in place. However, conservative treatment in both cases is associated with high rates of recurrence.
 Epilepsy is a common neurological disease affecting 50 million individuals worldwide, and some forms of epilepsy do not respond to available treatments. Overactivation of the glutamate pathway and excessive entrance of calcium ions into neurons are proposed as the biochemical mechanisms behind epileptic seizures. However, the overactivation of neurons has also been associated with other neurodegenerative diseases (NDDs), such as Alzheimer's, Parkinson's, Huntington's, and multiple sclerosis. The most widely used food ingredient, monosodium glutamate (MSG), increases the level of free glutamate in the brain, putting humans at risk for NDDs and epilepsy. Glutamate is a key neurotransmitter that activates nerve cells. MSG acts on glutamate receptors, specifically NMDA and AMPA receptors, leading to an imbalance between excitatory glutamate and inhibitory GABA neurotransmission. This imbalance can cause hyperexcitability of neurons and lead to epileptic seizures. Overuse of MSG causes neuronal cells to become overexcited, which in turn leads to an increase in the flow of Ca2+ and Na+ ions, mutations, and upregulation in the enzymes superoxide dismutase 1 (SOD-1) and TDP43, all of which contribute to the development of NDDs. While TDP43 and SOD-1 protect cells from damage, a mutation in their genes makes the proteins unprotective and cause neurodegeneration. Yet to what extent mutant SOD1 and TDP43 aggregates contribute to neurotoxicity is generally unknown. This study is focused on neuroprotective herbal medications that can pass the blood-brain barrier and cure MSG-induced NDDs and the factors that influence MSG-induced glutaminergic, astrocyte, and GABAergic neuron abnormalities causing neurodegeneration.
 Recent research in neuroimmunology has revolutionized our understanding of the intricate interactions between the immune system and the central nervous system (CNS). The CNS, an "immune-privileged organ", is now known to be intimately connected to the immune system through different cell types and cytokines. While type 2 immune responses have traditionally been associated with allergy and parasitic infections, emerging evidence suggests that these responses also play a crucial role in CNS homeostasis and disease pathogenesis. Type 2 immunity encompasses a delicate interplay among stroma, Th2 cells, innate lymphoid type 2 cells (ILC2s), mast cells, basophils, and the cytokines interleukin (IL)-4, IL-5, IL-13, IL-25, TSLP and IL-33. In this review, we discuss the beneficial and detrimental roles of type 2 immune cells and cytokines in CNS injury and homeostasis, cognition, and diseases such as tumors, Alzheimer's disease and multiple sclerosis.
 Delayed-release dimethyl fumarate (DMF), Tecfidera((®)), is approved globally for treating relapsing-remitting multiple sclerosis. The disposition of DMF was determined in humans after administration of a single oral dose of [(14)C]DMF, and the total recovery was estimated to be between 58.4% to 75.0%, primarily through expired air.The absorption of [(14)C]DMF-derived radioactivity was rapid, with Tmax at 1h postdose. Glucose was the predominant circulating metabolite, accounting for ∼60% of the total extractable radioactivity. Cysteine and N-acetylcysteine conjugates of mono- or di-methyl succinate were found to be the major urinary metabolites.In vitro studies showed that [(14)C]DMF was mainly metabolised to MMF, and fumarase exclusively converted fumaric acid to malic acid and did not catalyse the conversion of fumaric acid esters to malic acid. DMF was observed to bind with human serum albumin through Michael addition to the Cys-34 residue when exposed to human plasma.These findings indicate that DMF undergoes metabolism via hydrolysis, GSH conjugation, and the TCA cycle, leading to the formation of citric acid, CO(2), and water. These ubiquitous and well-conserved metabolism pathways minimise the risk of drug-drug interactions and reduce variability related to pharmacogenetics and ethnicity.
 Crocus sativus L. (saffron) is widely used as a traditional spice for flavoring, coloring and medicinal purposes. As a traditional Chinese herb, saffron promotes blood circulation, removes blood stasis, cools and detoxifies the blood, relieves depression and calms the mind. According to modern pharmacological studies, the active constituents of saffron, including crocetin, safranal and crocus aldehyde, exhibit antioxidant, anti-inflammatory, mitochondrial function-improving and antidepressant effects. Thus, saffron has the potential to treat neurodegenerative diseases (NDs) associated with oxidative stress, inflammation and impaired mitochondrial function, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis and cerebral ischemia. The present article provides a review of the pharmacological effects of saffron and its constituents in terms of neuroprotective effects, including antioxidant and anti-inflammatory effects and the improvement of mitochondrial dysfunction, as well as their clinical application in treating NDs.
 The process of ageing is characteristic of multicellular organisms associated with late stages of the lifecycle and is manifested through a plethora of phenotypes. Its underlying mechanisms are correlated with age-dependent diseases, especially neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and multiple sclerosis (MS) that are accompanied by social and financial difficulties for patients. Over time, people not only become more prone to neurodegeneration but they also lose the ability to trigger pivotal restorative mechanisms. In this review, we attempt to present the already known molecular and cellular hallmarks that characterize ageing in association with their impact on the central nervous system (CNS)'s structure and function intensifying possible preexisting pathogenetic conditions. A thorough and elucidative study of the underlying mechanisms of ageing will be able to contribute further to the development of new therapeutic interventions to effectively treat age-dependent manifestations of neurodegenerative diseases.
 HCN4 channels are considered to be a promising target for cardiac pathologies, epilepsy, and multiple sclerosis. However, there are no subtype-selective HCN channel blockers available, and only a few compounds are reported to display subtype preferences, one of which is EC18 (cis-1). Herein, we report the optimized synthetic route for the preparation of EC18 and its evaluation in three different pharmacological models, allowing us to assess its activity on cardiac function, thalamocortical neurons, and immune cells.
 Delivering customer-centric product presentations for biotherapeutics, such as monoclonal antibodies (mAbs), represents a long-standing and paramount area of engagement for pharmaceutical scientists. Activities include improving experience with the dosing procedure, reducing drug administration-related expenditures, and ultimately shifting parenteral treatments outside of a controlled healthcare institutional setting. In times of increasingly cost-constrained markets and reinforced with the coronavirus pandemic, this discipline of "Product Optimization" in healthcare has gained momentum and changed from a nice-to-have into a must. This review summarizes latest trends in the healthcare ecosystem that inform key strategies for developing customer-centric products, including the availability of a wider array of sustainable drug delivery options and treatment management plans that support dosing in a flexible care setting. Three disease area archetypes with varying degree of implementation of customer-centric concepts are introduced to highlight relevant market differences and similarities. Namely, rheumatoid arthritis and inflammatory bowel disease, multiple sclerosis, and oncology have been chosen due to differences in the availability of subcutaneously dosed and ready-to-use self-administration products for mAb medicines and their follow-on biologics. Different launch scenarios are described from a manufacturer's perspective highlighting the necessity of platform approaches. To unfold the full potential of customer-centric care, value-based healthcare provider reimbursement schemes that incentivize the efficiency of care need to be broadly implemented.
 Interleukin-4 (IL-4) is a pleiotropic cytokine mainly known for its role in type 2 immunity. Therapies antagonizing or blocking IL-4 activity have been developed to counteract diseases such as atopic dermatitis and asthma. In contrast, other disorders experimentally benefit from IL-4-related effects and IL-4 recently demonstrated beneficial activity in experimental stroke, spinal cord injury and the animal model of multiple sclerosis. To exploit IL-4-related activity for therapeutic concepts, current experimental efforts include modifying the pathway without inducing type 2 immune response and targeting of the cytokine to specific tissues. Here, we review different activities of IL-4 as well as therapeutic strategies.
 The use of in silico trials is expected to play an increasingly important role in the development and regulatory evaluation of new medical products. Among the advantages that in silico approaches offer, is that they permit testing of drug candidates and new medical devices using virtual patients or computational emulations of preclinical experiments, allowing to refine, reduce or even replace time-consuming and costly benchtop/in vitro/ex vivo experiments as well as the involvement of animals and humans in in vivo studies. To facilitate and widen the adoption of in silico trials, InSilicoTrials Technologies has developed a cloud-based platform, hosting healthcare simulation tools for different bench, preclinical and clinical evaluations, and for diverse disease areas. This paper discusses four use cases of in silico trials performed using the InSilicoTrials.com platform. The first application illustrates how in silico approaches can improve the early preclinical assessment of drug-induced cardiotoxicity risks. The second use case is a virtual reproduction of a bench test for the safety assessment of transcatheter heart valve substitutes. The third and fourth use cases are examples of virtual patients generation to evaluate treatment effects in multiple sclerosis and prostate cancer patients, respectively.
 There are several autoimmune and rheumatic diseases affecting different organs of the human body. Multiple sclerosis (MS) mainly affects brain, rheumatoid arthritis (RA) mainly affects joints, Type 1 diabetes (T1D) mainly affects pancreas, Sjogren's syndrome (SS) mainly affects salivary glands, while systemic lupus erythematosus (SLE) affects almost every organ of the body. Autoimmune diseases are characterized by production of autoantibodies, activation of immune cells, increased expression of pro-inflammatory cytokines, and activation of type I interferons. Despite improvements in treatments and diagnostic tools, the time it takes for the patients to be diagnosed is too long, and the main treatment for these diseases is still non-specific anti-inflammatory drugs. Thus, there is an urgent need for better biomarkers, as well as tailored, personalized treatment. This review focus on SLE and the organs affected in this disease. We have used the results from various rheumatic and autoimmune diseases and the organs involved with an aim to identify advanced methods and possible biomarkers to be utilized in the diagnosis of SLE, disease monitoring, and response to treatment.
 The effects of the hepatitis C virus (HCV) on the nervous system have been primarily reported with a pathology of the peripheral nervous system through the involvement of a vasculitic process via cryoglobulinemia. A review of the recent literature reinforced the likely association between chronic HCV infection and transverse myelitis (TM), but the causal relationship remains elusive. Here, we present a rare case of acute TM developing over the course of days from symptom onset and a concomitant new diagnosis of HCV infection. A 31-year-old male with a medical history of stimulant use disorder with intravenous methamphetamine use presented to the hospital for acute bilateral leg weakness. The weakness was predominantly in his thighs and later progressed to his calves over the course of days. He denied urinary or fecal incontinence; however, on hospital day two, he developed acute urinary retention requiring the insertion of a Foley catheter. An initial MRI of the spine revealed an intramedullary T2 hyperintense signal at the lower thoracic cord concerning for TM, multiple sclerosis, ischemia, or neoplasm. MRI of the brain was unremarkable. Lumbar puncture results also displayed no abnormalities. HCV screening should be considered in all patients who develop acute neurological deficits that are not otherwise explained, such as TM, given the significant morbidity associated with delayed treatment.
 Akkermansia muciniphila is a mucin-degrading bacterium of the intestinal niche, exerting beneficial effects on the host metabolic profile. Accumulating evidence indicated Akkermansia as a promising therapeutic probiotic against metabolic disorders such as obesity, type 2 diabetes and cardiovascular diseases. However, in specific intestinal microenvironments, its excessive enrichment may be not beneficial. Conditions like inflammatory bowel disease (IBD), Salmonella typhimurium infection or post-antibiotic reconstitution may not benefit from Akkermansia supplementation. Furthermore, using Akkermansia in patients with endocrine and gynecological disorders-such as polycystic ovary syndrome (PCOS) or endometriosis-that have a higher risk of developing IBD, should be critically evaluated. In addition, a cautionary note comes from the neurological field, as the gut microbiota of patients suffering from Parkinson's disease or multiple sclerosis exhibits a characteristic signature of Akkermansia municiphila abundance. Overall, considering these controversial points, the use of Akkermansia should be evaluated on an individual basis, avoiding risking unexpected effects.
 Metalloproteinase-9 (MMP-9) is one of the most strongly expressed matrix metalloproteinases (MMPs) in the brain. The MMP-9 activity in the brain is strictly regulated, and any disruptions in this regulation contribute to a development of many disorders of the nervous system including multiple sclerosis, brain strokes, neurodegenerative disorders, brain tumors, schizophrenia, or Guillain-Barré syndrome. This article discusses a relationship between development of the nervous system diseases and the functional single nucleotide polymorphism (SNP) at position -1562C/T within the MMP-9 gene. A pathogenic influence of MMP-9-1562C/T SNP was observed both in neurological and psychiatric disorders. The presence of the allele T often increases the activity of the MMP-9 gene promoter and consequently the expression of MMP-9 when compared to the allele C. This leads to a change in the likelihood of an occurrence of diseases and modifies the course of certain brain diseases in humans, as discussed below. The presented data indicates that the MMP-9-1562C/T functional polymorphism influences the course of many neuropsychiatric disorders in humans suggesting a significant pathological role of the MMP-9 metalloproteinase in pathologies of the human central nervous system.
 Interleukin-17A plays a crucial role in multiple sclerosis and other autoimmune diseases. Although the link between IL-17 and disease activity has been clearly demonstrated, the precise function of this cytokine remains elusive. Here, we investigated the function of astrocyte-targeted IL-17A production in GF/IL-17 transgenic mice during EAE. In particular, IL-17A is important during disease induction. In mice with transgenic IL-17A production, disease occurs earlier and peak disease is more severe, whereas remission is unimpaired. IL-17A synthesis is associated with increased infiltration of granulocytes into the CNS and microglial activation. Moreover, IL-17A synthesis allows induction of MOG-EAE without the additional administration of the co-adjuvant pertussis toxin. Examination of double transgenic GF/IL-17 2D2 mice revealed that, in addition, local IL-17A production facilitates spontaneous infiltration of immune cells into the CNS in mice expressing a MOG-specific T-cell receptor. Overall, we provide evidence for a crucial effect of IL-17A in the induction phase of EAE, facilitating the infiltration of granulocytes and autoreactive T-cells into the CNS.
 Hemiplegic migraine (HM) is a rare, heterogenous form of migraine characterized by unilateral weakness. This motor aura can present with reversible visual, sensory, and language deficits. HM can be difficult to diagnose due to overlapping presentation with other complex conditions such as multiple sclerosis, seizure disorders, and transient ischemic attack (TIA). We describe a case of a 40-year-old female with asymptomatic COVID-19 infection who presented after a motor vehicle collision caused by HM consistent with left-sided weakness and loss of consciousness. To date, this is the first description of a patient with known complex migraines to have a motor vehicle collision as a result of HM. The risk of HM-associated neurologic symptoms while driving poses a significant public safety concern. We suggest driving restrictions be considered in patients with HM when migraine aura is present. This case presents support to examine active infection with SARS-CoV-2 as a trigger for HM.
 INTRODUCTION: The pathogenesis of neuropsychiatric systemic lupus erythematosus (NPSLE) is widely unknown, and the role of autoantibodies is still undetermined. METHODS: To identify brain-reactive autoantibodies possibly related to NPSLE, immunofluorescence (IF) and transmission electron microscopy (TEM) on rat and human brains were performed. ELISA was used to reveal the presence of known circulating autoantibodies, while western blot (WB) was applied to characterize potential unknown autoantigen(s). RESULTS: We enrolled 209 subjects, including patients affected by SLE (n=69), NPSLE (n=36), Multiple Sclerosis (MS, n=22), and 82 age- and gender-matched healthy donors (HD). Autoantibody reactivity by IF was observed in almost the entire rat brain (cortex, hippocampus, and cerebellum) using sera from NPSLE and SLE patients and was virtually negative in MS and HD. NPSLE showed higher prevalence (OR 2.4; p = 0.047), intensity, and titer of brain-reactive autoantibodies than SLE patients. Most of the patient sera with brain-reactive autoantibodies (75%) also stained human brains. Double staining experiments on rat brains mixing patients' sera with antibodies directed against neuronal (NeuN) or glial markers showed autoantibody reactivity restricted to NeuN-containing neurons. Using TEM, the targets of brain-reactive autoantibodies were located in the nuclei and, to a lesser extent, in the cytoplasm and mitochondria. Given the high degree of colocalization between NeuN and brain-reactive autoantibodies, we assumed NeuN was a possible autoantigen. However, WB analysis with HEK293T cell lysates expressing or not expressing the gene encoding for NeuN protein (RIBFOX3) showed that patients' sera carrying brain-reactive autoantibodies did not recognize the NeuN corresponding band size. Among the panel of NPSLE-associated autoantibodies (e.g., anti-NR2, anti-P-ribosomal protein, antiphospholipid) investigated by ELISA assay, only the anti-β2-glycoprotein-I (aβ2GPI) IgG was exclusively found in those sera containing brain-reactive autoantibodies. CONCLUSION: In conclusion, SLE and NPSLE patients possess brain-reactive autoantibodies but with higher frequency and titers found in NPSLE patients. Although many target antigens of brain-reactive autoantibodies are still undetermined, they likely include β2GPI.
 INTRODUCTION: Patients with MS are MRI scanned continuously throughout their disease course resulting in a large manual workload for radiologists which includes lesion detection and size estimation. Though many models for automatic lesion segmentation have been published, few are used broadly in clinic today, as there is a lack of testing on clinical datasets. By collecting a large, heterogeneous training dataset directly from our MS clinic we aim to present a model which is robust to different scanner protocols and artefacts and which only uses MRI modalities present in routine clinical examinations. METHODS: We retrospectively included 746 patients from routine examinations at our MS clinic. The inclusion criteria included acquisition at one of seven different scanners and an MRI protocol including 2D or 3D T2-w FLAIR, T2-w and T1-w images. Reference lesion masks on the training (n = 571) and validation (n = 70) datasets were generated using a preliminary segmentation model and subsequent manual correction. The test dataset (n = 100) was manually delineated. Our segmentation model https://github.com/CAAI/AIMS/ was based on the popular nnU-Net, which has won several biomedical segmentation challenges. We tested our model against the published segmentation models HD-MS-Lesions, which is also based on nnU-Net, trained with a more homogenous patient cohort. We furthermore tested model robustness to data from unseen scanners by performing a leave-one-scanner-out experiment. RESULTS: We found that our model was able to segment MS white matter lesions with a performance comparable to literature: DSC = 0.68, precision = 0.90, recall = 0.70, f1 = 0.78. Furthermore, the model outperformed HD-MS-Lesions in all metrics except precision = 0.96. In the leave-one-scanner-out experiment there was no significant change in performance (p < 0.05) between any of the models which were only trained on part of the dataset and the full segmentation model. CONCLUSION: In conclusion we have seen, that by including a large, heterogeneous dataset emulating clinical reality, we have trained a segmentation model which maintains a high segmentation performance while being robust to data from unseen scanners. This broadens the applicability of the model in clinic and paves the way for clinical implementation.
 The aryl hydrocarbon receptor (AHR) is a sensor of low-molecular-weight molecule signals that originate from environmental exposures, the microbiome, and host metabolism. Building upon initial studies examining anthropogenic chemical exposures, the list of AHR ligands of microbial, diet, and host metabolism origin continues to grow and has provided important clues as to the function of this enigmatic receptor. The AHR has now been shown to be directly involved in numerous biochemical pathways that influence host homeostasis, chronic disease development, and responses to toxic insults. As this field of study has continued to grow, it has become apparent that the AHR is an important novel target for cancer, metabolic diseases, skin conditions, and autoimmune disease. This meeting attempted to cover the scope of basic and applied research being performed to address possible applications of our basic knowledge of this receptor on therapeutic outcomes.
 BACKGROUND: Although the beneficial role of training and the use of some antioxidants in physiological and psychological disorders in autoimmune diseases has been reported, the simultaneous effect of aerobic training (AT) and royal jelly (RJ) with different doses is not well understood. The present study aimed to investigate the impact of AT and RJ on inflammatory factors in the hippocampus, as well as depression and anxiety in the experimental autoimmune encephalomyelitis (EAE). METHODS: Sprague-Dawley rats with EAE were assigned to seven groups: (1) EAE without any other intervention (EAE); (2) sham, receiving normal saline (Sh); (3) 50 mg/kg RJ (RJ50); (4) 100 mg/kg RJ (RJ100); (5) AT; (6) AT + RJ50; and (7) AT + RJ100. In addition, a healthy control group was assessed. RESULTS: EAE significantly increased interleukin 17 (IL-17), transforming growth factor-β (TGF-β) gene expression and immobilization time as well as anxiety and depression indices, and significantly decreased interleukin 10 (IL-10), compared to the control group. AT decreased significantly IL-17, TGF-β gene expression and immobilization time as well as anxiety and depression indices, while it significantly increased IL-10, compared to the EAE group. RJ50 and RJ100 decreased significantly IL-17, IL-23 gene expression, anxiety and depression indices, and significantly increased IL-10 compared to the EAE group. AT + RJ50 and AT + RJ100 significantly decreased IL-17, IL-23, and TGF-β and as well as anxiety and depression indices while significantly increasing IL-10 compared to the EAE group. The effects of AT + RJ100 on significant decreasing IL-17, IL-23, anxiety and depression and increasing TGF-β, IL-10 were more favorable than RJ50. CONCLUSION: AT and RJ improved inflammatory and regulatory factors of autoimmunity and reduced anxiety and depression. The RJ combined with AT induced additive effects while using RJ100 was more favorable than RJ50.
 Although there is a substantial amount of data on the clinical characteristics, diagnostic criteria, and pathogenesis of myelin oligodendrocyte glycoprotein (MOG) autoantibody-associated disease (MOGAD), there is still uncertainty regarding the MOG protein function and the pathogenicity of anti-MOG autoantibodies in this disease. It is important to note that the disease characteristics, immunopathology, and treatment response of MOGAD patients differ from those of anti-aquaporin 4 antibody-positive neuromyelitis optica spectrum disorders (NMOSDs) and multiple sclerosis (MS). The clinical phenotypes of MOGAD are varied and can include acute disseminated encephalomyelitis, transverse myelitis, cerebral cortical encephalitis, brainstem or cerebellar symptoms, and optic neuritis. The frequency of optic neuritis suggests that the optic nerve is the most vulnerable lesion in MOGAD. During the acute stage, the optic nerve shows significant swelling with severe visual symptoms, and an MRI of the optic nerve and brain lesion tends to show an edematous appearance. These features can be alleviated with early extensive immune therapy, which may suggest that the initial attack of anti-MOG autoantibodies could target the structures on the blood-brain barrier or vessel membrane before reaching MOG protein on myelin or oligodendrocytes. To understand the pathogenesis of MOGAD, proper animal models are crucial. However, anti-MOG autoantibodies isolated from patients with MOGAD do not recognize mouse MOG efficiently. Several studies have identified two MOG epitopes that exhibit strong affinity with human anti-MOG autoantibodies, particularly those isolated from patients with the optic neuritis phenotype. Nonetheless, the relations between epitopes on MOG protein remain unclear and need to be identified in the future.
 Watershed strokes have been described previously as ischemic strokes located in vulnerable border zones between brain tissue supplied by the anterior, posterior, and middle cerebral arteries in the distal junction between two non-anastomotic arterial territories. Ischemic strokes in border zones are well-recognized entities and well-described in terms of imaging features, but the pathophysiological mechanism of brain injury production is not fully defined. Border zone ischemia is caused by cerebral hypoperfusion through decreased cerebral blood flow and arterial embolism in unstable atheroma plaque. It is often difficult to say which mechanisms are fully responsible for producing cerebral ischemic lesions. This review aimed to highlight the imaging aspect of watershed strokes and to correlate the clinical characteristics of this type of stroke with the diagnostic algorithm for optimal therapeutic management. Neurologists should promptly recognize this type of stroke and investigate its etiology in the shortest possible time.
 T cells are essential for a healthy life, performing continuously: immune surveillance, recognition, protection, activation, suppression, assistance, eradication, secretion, adhesion, migration, homing, communications, and additional tasks. This paper describes five aspects of normal beneficial T cells in the healthy or diseased brain. First, normal beneficial T cells are essential for normal healthy brain functions: cognition, spatial learning, memory, adult neurogenesis, and neuroprotection. T cells decrease secondary neuronal degeneration, increase neuronal survival after central nervous system (CNS) injury, and limit CNS inflammation and damage upon injury and infection. Second, while pathogenic T cells contribute to CNS disorders, recent studies, mostly in animal models, show that specific subpopulations of normal beneficial T cells have protective and regenerative effects in several neuroinflammatory and neurodegenerative diseases. These include Multiple Sclerosis (MS), Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis (ALS), stroke, CNS trauma, chronic pain, and others. Both T cell-secreted molecules and direct cell-cell contacts deliver T cell neuroprotective, neuroregenerative and immunomodulatory effects. Third, normal beneficial T cells are abnormal, impaired, and dysfunctional in aging and multiple neurological diseases. Different T cell impairments are evident in aging, brain tumors (mainly Glioblastoma), severe viral infections (including COVID-19), chronic stress, major depression, schizophrenia, Parkinson's disease, Alzheimer's disease, ALS, MS, stroke, and other neuro-pathologies. The main detrimental mechanisms that impair T cell function are activation-induced cell death, exhaustion, senescence, and impaired T cell stemness. Fourth, several physiological neurotransmitters and neuropeptides induce by themselves multiple direct, potent, beneficial, and therapeutically-relevant effects on normal human T cells, via their receptors in T cells. This scientific field is called "Nerve-Driven Immunity". The main neurotransmitters and neuropeptides that induce directly activating and beneficial effects on naïve normal human T cells are: dopamine, glutamate, GnRH-II, neuropeptide Y, calcitonin gene-related peptide, and somatostatin. Fifth, "Personalized Adoptive Neuro-Immunotherapy". This is a novel unique cellular immunotherapy, based on the "Nerve-Driven Immunity" findings, which was recently designed and patented for safe and repeated rejuvenation, activation, and improvement of impaired and dysfunctional T cells of any person in need, by ex vivo exposure of the person's T cells to neurotransmitters and neuropeptides. Personalized adoptive neuro-immunotherapy includes an early ex vivo personalized diagnosis, and subsequent ex vivo → in vivo personalized adoptive therapy, tailored according to the diagnosis. The Personalized Adoptive Neuro-Immunotherapy has not yet been tested in humans, pending validation of safety and efficacy in clinical trials, especially in brain tumors, chronic infectious diseases, and aging, in which T cells are exhausted and/or senescent and dysfunctional.
 INTRODUCTION: Neuromyelitis optica spectrum disorders (NMOSD) is an autoimmune, inflammatory disease of the central nervous system affecting the optic nerves and spinal cord. Most NMOSD patients have autoantibodies against the astrocyte water channel protein aquaporin-4 (AQP4). Eculizumab treatment is used effectively and safely in AQP4-IgG+ NMOSD. Our study evaluated the prognosis and outcomes of all clinical trial (PREVENT) patients from Turkey who received eculizumab treatment for AQP4-IgG+ NMOSD. METHOD: Clinical and demographic data of all patients enrolled in the PREVENT and OLE clinical trial in Turkey were analyzed during the study period and after the study ended. Clinical follow-up results were recorded in detail in patients who had to discontinue eculizumab treatment. RESULTS: The study included 10 patients who participated in PREVENT and OLE. Seven patients completed the studies, three patients did not continue the study and were switched to other treatments. Only one of the seven patients was able to continue treatment after eculizumab was approved in AQP4-IgG+NMOSD. The other six patients could not continue treatment due to reimbursement conditions. Four of the six patients who could not continue eculizumab treatment experienced early relapse (within the first three months after stopping the drug). All of these patients had high disease activity before eculizumab and had never relapsed under eculizumab treatment over the long term. CONCLUSION: Eculizumab was used effectively and safely in Turkish AQP4-IgG+NMOSD patients with high disease activity. Disease reactivation and relapse may occur after discontinuation of eculizumab treatment in patients with a long-term stable course. In these cases, close monitoring for disease reactivation is recommended.
 Therapeutic plasma exchange (TPE) is used for drug-resistant neuroimmunological disorders, but its mechanism of action remains poorly understood. We therefore prospectively explored changes in soluble, humoral, and cellular immune components associated with TPE. We included ten patients with neurological autoimmune disorders that underwent TPE and assessed a panel of clinically relevant pathogen-specific antibodies, total serum immunoglobulin (Ig) levels, interleukin-6 (IL-6, pg/mL), C-reactive protein (CRP, mg/dL), procalcitonin (PCT, µg/L) and major lymphocyte subpopulations (cells/µL). Blood was collected prior to TPE (pre-TPE, baseline), immediately after TPE (post-TPE), as well as five weeks (follow-up1) and 130 days (follow-up2) following TPE. Pathogen-specific antibody levels were reduced by -86% (p < 0.05) post-TPE and recovered to 55% (follow-up1) and 101% (follow-up2). Ig subclasses were reduced by -70-89% (p < 0.0001) post-TPE with subsequent complete (IgM/IgA) and incomplete (IgG) recovery throughout the follow-ups. Mean IL-6 and CRP concentrations increased by a factor of 3-4 at post-TPE (p > 0.05) while PCT remained unaffected. We found no alterations in B- and T-cell populations. No adverse events related to TPE occurred. TPE induced a profound but transient reduction in circulating antibodies, while the investigated soluble immune components were not washed out. Future studies should explore the effects of TPE on particular cytokines and assess inflammatory lymphocyte lineages to illuminate the mode of action of TPE beyond autoantibody removal.
 PURPOSE: Hyperreflective foci are poorly understood transient elements seen on optical coherence tomography (OCT) of the retina in both healthy and diseased eyes. Systematic studies may benefit from the development of automated tools that can map and track such foci. The outer nuclear layer (ONL) of the retina is an attractive layer in which to study hyperreflective foci as it has no fixed hyperreflective elements in healthy eyes. In this study, we intended to evaluate whether automated image analysis can identify, quantify and visualize hyperreflective foci in the ONL of the retina. METHODS: This longitudinal exploratory study investigated 14 eyes of seven patients including six patients with optic neuropathy and one with mild non-proliferative diabetic retinopathy. In total, 2596 OCT B-scan were obtained. An image analysis blob detector algorithm was used to detect candidate foci, and a convolutional neural network (CNN) trained on a manually labelled subset of data was then used to select those candidate foci in the ONL that fitted the characteristics of the reference foci best. RESULTS: In the manually labelled data set, the blob detector found 2548 candidate foci, correctly detecting 350 (89%) out of 391 manually labelled reference foci. The accuracy of CNN classifier was assessed by manually splitting the 2548 candidate foci into a training and validation set. On the validation set, the classifier obtained an accuracy of 96.3%, a sensitivity of 88.4% and a specificity of 97.5% (AUC 0.989). CONCLUSION: This study demonstrated that automated image analysis and machine learning methods can be used to successfully identify, quantify and visualize hyperreflective foci in the ONL of the retina on OCT scans.
 Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis (MS), spinal cord injury (SCI), and amyotrophic lateral sclerosis (ALS), are characterized by acute or chronic progressive loss of one or several neuronal subtypes. However, despite their increasing prevalence, little progress has been made in successfully treating these diseases. Research has recently focused on neurotrophic factors (NTFs) as potential regenerative therapy for neurodegenerative diseases. Here, we discuss the current state of knowledge, challenges, and future perspectives of NTFs with a direct regenerative effect in chronic inflammatory and degenerative disorders. Various systems for delivery of NTFs, such as stem and immune cells, viral vectors, and biomaterials, have been applied to deliver exogenous NTFs to the central nervous system, with promising results. The challenges that currently need to be overcome include the amount of NTFs delivered, the invasiveness of the delivery route, the blood-brain barrier permeability, and the occurrence of side effects. Nevertheless, it is important to continue research and develop standards for clinical applications. In addition to the use of single NTFs, the complexity of chronic inflammatory and degenerative diseases may require combination therapies targeting multiple pathways or other possibilities using smaller molecules, such as NTF mimetics, for effective treatment.
 Neurodegenerative diseases (NDs) affect 15% of the world's population and are becoming an increasingly common cause of morbidity and mortality worldwide. Circadian rhythm disorders (CRDs) have been reported to be involved in the pathogenic regulation of various neurologic diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis and amyotrophic lateral sclerosis. Proteomic technology is helpful to explore treatment targets for CRDs in patients with NDs. Here, we review the key differentially expressed (DE) proteins identified in previous proteomic studies investigating NDs, CRDs and associated models and the related pathways identified by enrichment analysis. Furthermore, we summarize the advantages and disadvantages of the above studies and propose new proteomic technologies for the precise study of circadian disorder-mediated regulation of ND pathology. This review provides a theoretical and technical reference for the precise study of circadian disorder-mediated regulation of ND pathology.
 Neurodegenerative diseases (NDs) such as Alzheimer's, Parkinson's, Multiple Sclerosis, Hereditary Spastic Paraplegia, and Amyotrophic Lateral Sclerosis have emerged as the most dreaded diseases due to a lack of precise diagnostic tools and efficient therapies. Despite the fact that the contributing factors of NDs are still unidentified, mounting evidence indicates the possibility that genetic and cellular changes may lead to the significant production of abnormally misfolded proteins. These misfolded proteins lead to damaging effects thereby causing neurodegeneration. The association between Neurite outgrowth factor (Nogo) with neurological diseases and other peripheral diseases is coming into play. Three isoforms of Nogo have been identified Nogo-A, Nogo-B and Nogo-C. Among these, Nogo-A is mainly responsible for neurological diseases as it is localized in the CNS (Central Nervous System), whereas Nogo-B and Nogo-C are responsible for other diseases such as colitis, lung, intestinal injury, etc. Nogo-A, a membrane protein, had first been described as a CNS-specific inhibitor of axonal regeneration. Several recent studies have revealed the role of Nogo-A proteins and their receptors in modulating neurite outgrowth, branching, and precursor migration during nervous system development. It may also modulate or affect the inhibition of growth during the developmental processes of the CNS. Information about the effects of other ligands of Nogo protein on the CNS are yet to be discovered however several pieces of evidence have suggested that it may also influence the neuronal maturation of CNS and targeting Nogo-A could prove to be beneficial in several neurodegenerative diseases.
 Metal homeostasis is critical to normal neurophysiological activity. Metal ions are involved in the development, metabolism, redox and neurotransmitter transmission of the central nervous system (CNS). Thus, disturbance of homeostasis (such as metal deficiency or excess) can result in serious consequences, including neurooxidative stress, excitotoxicity, neuroinflammation, and nerve cell death. The uptake, transport and metabolism of metal ions are highly regulated by ion channels. There is growing evidence that metal ion disorders and/or the dysfunction of ion channels contribute to the progression of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Therefore, metal homeostasis-related signaling pathways are emerging as promising therapeutic targets for diverse neurological diseases. This review summarizes recent advances in the studies regarding the physiological and pathophysiological functions of metal ions and their channels, as well as their role in neurodegenerative diseases. In addition, currently available metal ion modulators and in vivo quantitative metal ion imaging methods are also discussed. Current work provides certain recommendations based on literatures and in-depth reflections to improve neurodegenerative diseases. Future studies should turn to crosstalk and interactions between different metal ions and their channels. Concomitant pharmacological interventions for two or more metal signaling pathways may offer clinical advantages in treating the neurodegenerative diseases.
 Wnt/β-catenin (WβC) signaling pathway is an important signaling pathway for the maintenance of cellular homeostasis from the embryonic developmental stages to adulthood. The canonical pathway of WβC signaling is essential for neurogenesis, cell proliferation, and neurogenesis, whereas the noncanonical pathway (WNT/Ca(2+) and WNT/PCP) is responsible for cell polarity, calcium maintenance, and cell migration. Abnormal regulation of WβC signaling is involved in the pathogenesis of several neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and spinal muscular atrophy (SMA). Hence, the alteration of WβC signaling is considered a potential therapeutic target for the treatment of neurodegenerative disease. In the present review, we have used the bibliographical information from PubMed, Google Scholar, and Scopus to address the current prospects of WβC signaling role in the abovementioned neurodegenerative diseases.
 Small intestinal bacterial overgrowth (SIBO) is defined as an increase in the bacterial content of the small intestine above normal values. The presence of SIBO is detected in 33.8% of patients with gastroenterological complaints who underwent a breath test, and is significantly associated with smoking, bloating, abdominal pain, and anemia. Proton pump inhibitor therapy is a significant risk factor for SIBO. The risk of SIBO increases with age and does not depend on gender or race. SIBO complicates the course of a number of diseases and may be of pathogenetic significance in the development of their symptoms. SIBO is significantly associated with functional dyspepsia, irritable bowel syndrome, functional abdominal bloating, functional constipation, functional diarrhea, short bowel syndrome, chronic intestinal pseudo-obstruction, lactase deficiency, diverticular and celiac diseases, ulcerative colitis, Crohn's disease, cirrhosis, metabolic-associated fatty liver disease (MAFLD), primary biliary cholangitis, gastroparesis, pancreatitis, cystic fibrosis, gallstone disease, diabetes, hypothyroidism, hyperlipidemia, acromegaly, multiple sclerosis, autism, Parkinson's disease, systemic sclerosis, spondylarthropathy, fibromyalgia, asthma, heart failure, and other diseases. The development of SIBO is often associated with a slowdown in orocecal transit time that decreases the normal clearance of bacteria from the small intestine. The slowdown of this transit may be due to motor dysfunction of the intestine in diseases of the gut, autonomic diabetic polyneuropathy, and portal hypertension, or a decrease in the motor-stimulating influence of thyroid hormones. In a number of diseases, including cirrhosis, MAFLD, diabetes, and pancreatitis, an association was found between disease severity and the presence of SIBO. Further work on the effect of SIBO eradication on the condition and prognosis of patients with various diseases is required.
 BACKGROUND: Myeloid cells, including monocytes, macrophages, microglia, dendritic cells and neutrophils are a part of innate immunity, playing a major role in orchestrating innate and adaptive immune responses. Microglia are the resident myeloid cells of the central nervous system, and many Alzheimer's disease (AD) risk loci are found in or near genes that are highly or sometimes uniquely expressed in myeloid cells. Similarly, inflammatory bowel disease (IBD) loci are also enriched for genes expressed by myeloid cells. However, the extent to which there is overlap between the effects of AD and IBD susceptibility loci in myeloid cells remains poorly described, and the substantial IBD genetic maps may help to accelerate AD research. METHODS: Here, we leveraged summary statistics from large-scale genome-wide association studies (GWAS) to investigate the causal effect of IBD (including ulcerative colitis and Crohn's disease) variants on AD and AD endophenotypes. Microglia and monocyte expression Quantitative Trait Locus (eQTLs) were used to examine the functional consequences of IBD and AD risk variants enrichment in two different myeloid cell subtypes. RESULTS: Our results showed that, while PTK2B is implicated in both diseases and both sets of risk loci are enriched for myeloid genes, AD and IBD susceptibility loci largely implicate distinct sets of genes and pathways. AD loci are significantly more enriched for microglial eQTLs than IBD. We also found that genetically determined IBD is associated with a lower risk of AD, which may driven by a negative effect on the accumulation of neurofibrillary tangles (beta=-1.04, p=0.013). In addition, IBD displayed a significant positive genetic correlation with psychiatric disorders and multiple sclerosis, while AD showed a significant positive genetic correlation with amyotrophic lateral sclerosis. CONCLUSION: To our knowledge, this is the first study to systematically contrast the genetic association between IBD and AD, our findings highlight a possible genetically protective effect of IBD on AD even if the majority of effects on myeloid cell gene expression by the two sets of disease variants are distinct. Thus, IBD myeloid studies may not help to accelerate AD functional studies, but our observation reinforces the role of myeloid cells in the accumulation of tau proteinopathy and provides a new avenue for discovering a protective factor.
 A large and growing body of research suggests that the skin plays an important role in regulating total body sodium, challenging traditional models of sodium homeostasis that focused exclusively on blood pressure and the kidney. In addition, skin sodium may help to prevent water loss and facilitate macrophage-driven antimicrobial host defence, but may also trigger immune dysregulation via upregulation of proinflammatory markers and downregulation of anti-inflammatory processes. We performed a systematic search of PubMed for published literature on skin sodium and disease outcomes and found that skin sodium concentration is increased in patients with cardiometabolic conditions including hypertension, diabetes and end-stage renal disease; autoimmune conditions including multiple sclerosis and systemic sclerosis; and dermatological conditions including atopic dermatitis, psoriasis and lipoedema. Several patient characteristics are associated with increased skin sodium concentration including older age and male sex. Animal evidence suggests that increased salt intake results in higher skin sodium levels; however, there are conflicting results from small trials in humans. Additionally, limited data suggest that pharmaceuticals such as diuretics and sodium-glucose co-transporter-2 inhibitors approved for diabetes, as well as haemodialysis may reduce skin sodium levels. In summary, emerging research supports an important role for skin sodium in physiological processes related to osmoregulation and immunity. With the advent of new noninvasive magnetic resonance imaging measurement techniques and continued research on skin sodium, it may emerge as a marker of immune-mediated disease activity or a potential therapeutic target.

 BACKGROUND: Depression has a major impact on the disease burden of multiple sclerosis (MS). Analyses of overlapping MS and depression risk factors [smoking, vitamin D (25-OH-VD) and Epstein-Barr virus (EBV) infection] and sex, age, disease characteristics and neuroimaging features associated with depressive symptoms in early MS are scarce. OBJECTIVES: To assess an association of MS risk factors with depressive symptoms within the German NationMS cohort. DESIGN: Cross-sectional analysis within a multicenter observational study. METHODS: Baseline data of n = 781 adults with newly diagnosed clinically isolated syndrome or relapsing-remitting MS qualified for analysis. Global and region-specific magnetic resonance imaging (MRI)-volumetry parameters were available for n = 327 patients. Association of demographic factors, MS characteristics and risk factors [sex, age, smoking, disease course, presence of current relapse, expanded disability status scale (EDSS) score, fatigue (fatigue scale motor cognition), 25-OH-VD serum concentration, EBV nuclear antigen-1 IgG (EBNA1-IgG) serum levels] and depressive symptoms (Beck Depression Inventory-II, BDI-II) was tested as a primary outcome by multivariable linear regression. Non-parametric correlation and group comparison were performed for associations of MRI parameters and depressive symptoms. RESULTS: Mean age was 34.3 years (95% confidence interval: 33.6-35.0). The female-to-male ratio was 2.3:1. At least minimal depressive symptoms (BDI-II > 8) were present in n = 256 (32.8%), 25-OH-VD deficiency (<20 ng/ml) in n = 398 (51.0%), n = 246 (31.5%) participants were smokers. Presence of current relapse [coefficient (c) = 1.48, p = 0.016], more severe fatigue (c = 0.26, p < 0.0001), lower 25-OH-VD (c = -0.03, p = 0.034) and smoking (c = 0.35, p = 0.008) were associated with higher BDI-II scores. Sex, age, disease course, EDSS, month of visit, EBNA1-IgG levels and brain volumes at baseline were not. CONCLUSION: Depressive symptoms need to be assessed in early MS. Patients during relapse seem especially vulnerable to depressive symptoms. Contributing factors such as fatigue, vitamin D deficiency and smoking, could specifically be targeted in future interventions and should be investigated in prospective studies.

 Magnetic nanoparticles possess unique properties distinct from other types of nanoparticles developed for biomedical applications. Their unique magnetic properties and multifunctionalities are especially beneficial for central nervous system (CNS) disease therapy and diagnostics, as well as targeted and personalized applications using image-guided therapy and theranostics. This review discusses the recent development of magnetic nanoparticles for CNS applications, including Alzheimer's disease, Parkinson's disease, epilepsy, multiple sclerosis, and drug addiction. Machine learning (ML) methods are increasingly applied towards the processing, optimization and development of nanomaterials. By using data-driven approach, ML has the potential to bridge the gap between basic research and clinical research. We review ML approaches used within the various stages of nanomedicine development, from nanoparticle synthesis and characterization to performance prediction and disease diagnosis.
 Naltrexone is a mu-opioid receptor antagonist with a long half-life compared with naloxone. Both of these drugs, along with others, were developed with the intention of reversing the effects of opioid abuse or toxicity. Evidence has also shown that naltrexone has a benefit in preventing relapse by reducing opioid cravings and reducing symptoms of opioid withdrawal. The benefits of this drug were not only shown with opioid abuse. In 1984 this drug was also approved for alcohol abuse. Naltrexone has been proven to decrease alcohol relapse by decreasing the craving. Apart from these approved indications for the use of naltrexone, with time, it has been seen that this drug has a benefit in treating chronic pain. A number of studies have shown the benefits of this drug with inflammatory bowel disease, fibromyalgia, multiple sclerosis, diabetic neuropathy, and complex regional pain syndrome, among others. More studies are needed to approve this medication for specific chronic pain conditions.
 Neurorehabilitation is now one of the most exciting areas in neuroscience. Recognition that the central nervous system (CNS) remains plastic through life, new understanding of skilled behaviors (skills), and novel methods for engaging and guiding beneficial plasticity combine to provide unprecedented opportunities for restoring skills impaired by CNS injury or disease. The substrate of a skill is a distributed network of neurons and synapses that changes continually through life to ensure that skill performance remains satisfactory as new skills are acquired, and as growth, aging, and other life events occur. This substrate can extend from cortex to spinal cord. It has recently been given the name "heksor." In this new context, the primary goal of rehabilitation is to enable damaged heksors to repair themselves so that their skills are once again performed well. Skill-specific practice, the mainstay of standard therapy, often fails to optimally engage the many sites and kinds of plasticity available in the damaged CNS. New noninvasive technology-based interventions can target beneficial plasticity to critical sites in damaged heksors; these interventions may thereby enable much wider beneficial plasticity that enhances skill recovery. Targeted-plasticity interventions include operant conditioning of a spinal reflex or corticospinal motor evoked potential (MEP), paired-pulse facilitation of corticospinal connections, and brain-computer interface (BCI)-based training of electroencephalographic (EEG) sensorimotor rhythms. Initial studies in people with spinal cord injury, stroke, or multiple sclerosis show that these interventions can enhance skill recovery beyond that achieved by skill-specific practice alone. After treatment ends, the repaired heksors maintain the benefits.
 The levels of interferon beta-1a in breastmilk are minuscule. In addition, because interferon is poorly absorbed orally, it is not likely to reach the bloodstream of the infant. Many women have breastfed while taking interferon beta-1a with no adverse infant effects reported. Interferon beta is generally considered safe by most experts and appears to be one of the preferred disease-modifying agents for treating multiple sclerosis during breastfeeding.[1-5] No special precautions appear to be required during breastfeeding while using interferon beta and breastfeeding can resume immediately after injection.[6]
 Protein phosphatase 2A (PP2A) is a serine-threonine phosphatase that plays an important role in the regulation of cell proliferation and signal transduction. The catalytic activity of PP2A is integral in the maintenance of physiological functions which gets severely impaired in its absence. PP2A plays an essential role in the activation, differentiation, and functions of T cells. PP2A suppresses Th1 cell differentiation while promoting Th2 cell differentiation. PP2A fosters Th17 cell differentiation which contributes to the pathogenesis of systemic lupus erythematosus (SLE) by enhancing the transactivation of the Il17 gene. Genetic deletion of PP2A in Tregs disrupts Foxp3 expression due to hyperactivation of mTORC1 signaling which impairs the development and immunosuppressive functions of Tregs. PP2A is important in the induction of Th9 cells and promotes their antitumor functions. PP2A activation has shown to reduce neuroinflammation in a mouse model of experimental autoimmune encephalomyelitis (EAE) and is now used to treat multiple sclerosis (MS) clinically. In this review, we will discuss the structure and functions of PP2A in T cell differentiation and diseases and therapeutic applications of PP2A-mediated immunotherapy.
 MicroRNAs (miRNAs) are crucial post-transcriptional regulators of gene expression in ubiquitous biological processes, including immune-related pathways. This review focuses on the miR-183/96/182 cluster (miR-183C), which contains three miRNAs, miR-183, -96, and -182, having almost identical seed sequences with minor differences. The similarity among seed sequences allows these three miRNAs to act cooperatively. In addition, their minor differences permit them to target distinct genes and regulate unique pathways. The expression of miR-183C was initially identified in sensory organs. Subsequently, abnormal expression of miR-183C miRNAs in various cancers and autoimmune diseases has been reported, implying their potential role in human diseases. The regulatory effects of miR-183C miRNAs on the differentiation and function of both innate and adaptive immune cells have now been documented. In this review, we have discussed the complex role of miR-183C in the immune cells in both normal and autoimmune backgrounds. We highlighted the dysregulation of miR-183C miRNAs in several autoimmune diseases, including systemic lupus erythematosus (SLE), multiple sclerosis (MS), and ocular autoimmune disorders, and discussed the potential for utilizing miR-183C as biomarkers and therapeutic targets of specific autoimmune diseases.
 Nucleoside-based drugs, recognized as purine or pyrimidine analogs, have been potent therapeutic agents since their introduction in 1950, deployed widely in the treatment of diverse diseases such as cancers, myelodysplastic syndromes, multiple sclerosis, and viral infections. These antimetabolites establish complex interactions with cellular molecular constituents, primarily via activation of phosphorylation cascades leading to consequential interactions with nucleic acids. However, the therapeutic efficacy of these agents is frequently compromised by the development of drug resistance, a continually emerging challenge in their clinical application. This comprehensive review explores the mechanisms of resistance to nucleoside-based drugs, encompassing a wide spectrum of phenomena from alterations in membrane transporters and activating kinases to changes in drug elimination strategies and DNA damage repair mechanisms. The critical analysis in this review underlines complex interactions of drug and cell and also guides towards novel therapeutic strategies to counteract resistance. The development of targeted therapies, novel nucleoside analogs, and synergistic drug combinations are promising approaches to restore tumor sensitivity and improve patient outcomes.
 Marijuana, also known as cannabis, is a psychoactive drug that comes from the Cannabis plant. Marijuana can be smoked, vaporized, or consumed through edibles in a variety of ways. Perception changes, changes in mood, and problems with coordination are all possible side effects. Marijuana is used for both recreational and medical purposes to treat a variety of health conditions. The literature review on the effects of marijuana on the human body has increased in recent years as more states legalize its use. It is important to investigate the benefits and harmful effects of marijuana on individuals due to the widespread use of cannabis-derived substances like marijuana for medical, recreational, and combined purposes. The paper will review different aspects of marijuana in 4 main domains. A thorough discussion of marijuana's definition, history, mechanism of action, pharmacokinetics, and effects on human cells will be given in the first domain. The second domain will concentrate on marijuana's negative effects, while the third domain will look at marijuana's possible positive impacts, such as its usage in controlling multiple sclerosis, treating obesity, lowering social anxiety, and managing pain. The fourth domain will concentrate on marijuana's effects on anxiety, educational attainment, and social consequences. Additionally, this paper also will provide a highlight of the history of marijuana use and governmental legislation, both of which play a significant role in determining how the public views marijuana. In conclusion, this paper provides a comprehensive review of marijuana's effects, which may be of interest to a large readership. This review adds to the continuing discussion about the use of marijuana by analyzing the data that is currently available about the possible advantages and disadvantages of marijuana usage.
 Inflammasome molecules make up a family of receptors that typically function to initiate a proinflammatory response upon infection by microbial pathogens. Dysregulation of inflammasome activity has been linked to unwanted chronic inflammation, which has also been implicated in certain autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, type 1 diabetes, systemic lupus erythematosus, and related animal models. Classical inflammasome activation-dependent events have intrinsic and extrinsic effects on both innate and adaptive immune effectors, as well as resident cells in the target tissue, which all can contribute to an autoimmune response. Recently, inflammasome molecules have also been found to regulate the differentiation and function of immune effector cells independent of classical inflammasome-activated inflammation. These alternative functions for inflammasome molecules shape the nature of the adaptive immune response, that in turn can either promote or suppress the progression of autoimmunity. In this review we will summarize the roles of inflammasome molecules in regulating self-tolerance and the development of autoimmunity.
 Approximately half of the brain's circuits are involved in vision and control of eye movements. Therefore, visual dysfunction is a common symptom of concussion, the mildest form of traumatic brain injury (TBI). Photosensitivity, vergence dysfunction, saccadic abnormalities, and distortions in visual perception have been reported as vision-related symptoms following concussion. Impaired visual function has also been reported in populations with a lifetime history of TBI. Consequently, vision-based tools have been developed to detect and diagnose concussion in the acute setting, and characterize visual and cognitive function in those with a lifetime history of TBI. Rapid automatized naming (RAN) tasks have provided widely accessible and quantitative measures of visual-cognitive function. Laboratory-based eye tracking approaches demonstrate promise in measuring visual function and validating results from RAN tasks in patients with concussion. Optical coherence tomography (OCT) has detected neurodegeneration in patients with Alzheimer's disease and multiple sclerosis and may provide critical insight into chronic conditions related to TBI, such as traumatic encephalopathy syndrome. Here, we review the literature and discuss the future directions of vision-based assessments of concussion and conditions related to TBI.
 BACKGROUND: During the Covid-19 health crisis, telerehabilitation provided a solution to ensure the continuity of care. Since then, it has been offered as an alternative to face-to-face rehabilitation in chronic conditions. Data measuring satisfaction are essential to adapt and increase the effectiveness of this type of programme. AIM AND SCOPE: This research focused on determining the most significant determinants of participant satisfaction in a telerehabilitation programme. METHODS: We conducted a retrospective study by analysing the satisfaction questionnaire used from the start of the programme. RESULT: Two hundred and ten (210) participants completed the programme; 180 questionnaires were filled in and 175 analyzed of which 70 with chronic low back pain (CLBP), 59 for multiple sclerosis (MS) and 22 with parkinson's disease (PD). Satisfaction was high for all participants (scoring out of 10, mean = 8.22 sd = 1.53), but the determinants reported for the three main conditions involved in the programme differed. Main determinant was "benefice" for CLBP (p = 1.23e-05), "home exercises adapted" for MS (p = 0.000679) and "interest in staying at home" for PD (p = 1.84e-05). CONCLUSION: Depending on the context of the condition/disease, the drivers of satisfaction were not identical. Knowledge of these determinants will allow us to further improve the programme. However, some unresolved questions remain regarding the place of therapists, their role and the skills required for a successful telerehabilitation programme. Further studies are required to understand the impact.
 Numerous studies have been published about the implication of the neurotrophin brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the pathogenesis of several neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, Multiple Sclerosis and motor neuron disease. BDNF activates the TrkB receptor with high potency and specificity, promoting neuronal survival, differentiation and synaptic plasticity. Based on the main structural characteristics of LM22A-4, a previously published small molecule that acts as activator of the TrkB receptor, we have designed and synthesized a small data set of compounds. The lead idea for the design of the new compounds was to modify the third position of the LM22A-4, by introducing different substitutions in order to obtain compounds which will have not only better physicochemical properties but selective activity as well. ADME and toxicity profiles of molecules have been evaluated as well as their biological properties through the TrkB receptor and affinity to promote neurite differentiation.
 The intestinal barrier, which primarily consists of a mucus layer, an epithelial barrier, and a gut vascular barrier, has a crucial role in health and disease by facilitating nutrient absorption and preventing the entry of pathogens. The intestinal barrier is in close contact with gut microbiota on its luminal side and with enteric neurons and glial cells on its tissue side. Mounting evidence now suggests that the intestinal barrier is compromised not only in digestive disorders, but also in disorders of the central nervous system (CNS), such as Parkinson's disease, autism spectrum disorder, depression, multiple sclerosis, and Alzheimer's disease. After providing an overview of the structure and functions of the intestinal barrier, we review existing preclinical and clinical studies supporting the notion that intestinal barrier dysfunction is present in neurological, neurodevelopmental, and psychiatric disorders. On the basis of this evidence, we discuss the mechanisms that possibly link gut barrier dysfunction and CNS disorders and the potential impact that evaluating enteric barriers in brain disorders could have on clinical practice, in terms of novel diagnostic and therapeutic strategies, in the near future.
 PURPOSE OF REVIEW: Optical coherence tomography angiography (OCTA) is a novel, noninvasive imaging technique, which provides depth resolved visualization of microvasculature of the retina and choroid. Although OCTA has been widely used for the evaluation of a number of retinal diseases, its use in the field of neuro-ophthalmology has been less studied. In this review, we provide an update on the utility of OCTA in neuro-ophthalmic conditions. RECENT FINDINGS: Peripapillary and macular microvasculature analyses have indicated that OCTA can be a promising tool for early detection of a number of neuro-ophthalmic diseases, differential diagnosis, and monitoring of disease progression. Recent studies have demonstrated that structural and functional impairment can develop at early stages in some conditions such as in multiple sclerosis and Alzheimer's disease even in the absence of overt clinical symptoms. Furthermore, this dye-less technique can be a valuable adjunct tool in the detection of complications commonly seen in some congenital entities such optic disc drusen. SUMMARY: Since its introduction, OCTA has emerged as an important imaging approach shedding light on unrevealed pathophysiological mechanisms of several ocular diseases. The use of OCTA as a biomarker in the field of neuro-ophthalmology has recently gained considerable attention with studies supporting its role in clinical setting while larger studies are warranted for correlating these findings with traditional diagnostic procedures and clinical features and outcomes.
 Immunosensors are a special class of biosensors that employ specific antibodies for biorecognition of the target analyte. Immunosensors that target disease biomarkers may be exploited as tools for disease diagnosis and/or follow-up, offering several advantages over conventional analytical techniques, such as rapid and easy analysis of patients' samples at the point-of-care. Autoimmune diseases have been increasingly prevalent worldwide in recent years, while the COVID-19 pandemic has also been associated with autoimmunity. Consequently, demand for tools enabling the early and reliable diagnosis of autoimmune diseases is expected to increase in the near future. To this end, interest in immunosensors targeting autoimmune disease biomarkers, mainly, various autoantibodies and specific pro-inflammatory proteins (e.g., specific cytokines), has been rekindled. This review article presents most of the immunosensors proposed to date as potential tools for the diagnosis of various autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, and multiple sclerosis. The signal transduction and the immunoassay principles of each immunosensor have been suitably classified and are briefly presented along with certain sensor elements, e.g., special nano-sized materials used in the construction of the immunosensing surface. The main concluding remarks are presented and future perspectives of the field are also briefly discussed.
 Neurological disorders affect the nervous system. Biochemical, structural, or electrical abnormalities in the spinal cord, brain, or other nerves lead to different symptoms, including muscle weakness, paralysis, poor coordination, seizures, loss of sensation, and pain. There are many recognized neurological diseases, like epilepsy, Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), stroke, autosomal recessive cerebellar ataxia 2 (ARCA2), Leber's hereditary optic neuropathy (LHON), and spinocerebellar ataxia autosomal recessive 9 (SCAR9). Different agents, such as coenzyme Q10 (CoQ10), exert neuroprotective effects against neuronal damage. Online databases, such as Scopus, Google Scholar, Web of Science, and PubMed/MEDLINE were systematically searched until December 2020 using keywords, including review, neurological disorders, and CoQ10. CoQ10 is endogenously produced in the body and also can be found in supplements or foods. CoQ10 has antioxidant and anti-inflammatory effects and plays a role in energy production and mitochondria stabilization, which are mechanisms, by which CoQ10 exerts its neuroprotective effects. Thus, in this review, we discussed the association between CoQ10 and neurological diseases, including AD, depression, MS, epilepsy, PD, LHON, ARCA2, SCAR9, and stroke. In addition, new therapeutic targets were introduced for the next drug discoveries.
 We set out to describe in detail the afferent neuro-ophthalmological complications that have been reported in association with coronavirus disease 2019 (COVID-19) infection. We describe and elaborate on mechanisms of disease, including para-infectious inflammation, hypercoagulability, endothelial damage, and direct neurotropic viral invasion. Despite global vaccination programs, new variants of COVID-19 continue to pose an international threat, and patients with rare neuro-ophthalmic complications are likely to continue to present for care.Afferent complications from COVID-19 include homonymous visual field loss, with or without higher cortical visual syndromes, resulting from stroke, intracerebral hemorrhage, or posterior reversible leukoencephalopathy. Optic neuritis has frequently been reported, sometimes along with acute disseminated encephalomyelopathy, often in association with either myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) or less commonly aquaporin-4 seropositivity or in newly diagnosed multiple sclerosis. Ischemic optic neuropathy has rarely been reported. Papilledema, resulting either from venous sinus thrombosis or idiopathic intracranial hypertension in the setting of COVID-19, has also been described.Observed afferent neuro-ophthalmic associations need to be confirmed though larger comparative studies. Meanwhile, the range of possible complications should be recognized by neurologists and ophthalmologists alike, to facilitate faster diagnosis and treatment of both COVID-19 and its neuro-ophthalmic manifestations.
 BACKGROUND: Systematic reviews, i.e., research summaries that address focused questions in a structured and reproducible manner, are a cornerstone of evidence-based medicine and research. However, certain systematic review steps such as data extraction are labour-intensive which hampers their applicability, not least with the rapidly expanding body of biomedical literature. OBJECTIVE: To bridge this gap, we aimed at developing a data mining tool in the R programming environment to automate data extraction from neuroscience in vivo publications. The function was trained on a literature corpus (n=45 publications) of animal motor neuron disease studies and tested in two validation corpora (motor neuron diseases, n=31 publications; multiple sclerosis, n=244 publications). RESULTS: Our data mining tool Auto-STEED (Automated and STructured Extraction of Experimental Data) was able to extract key experimental parameters such as animal models and species as well as risk of bias items such as randomization or blinding from in vivo studies. Sensitivity and specificity were over 85 and 80%, respectively, for most items in both validation corpora. Accuracy and F-scores were above 90% and 0.9 for most items in the validation corpora. Time savings were above 99%. CONCLUSIONS: Our developed text mining tool Auto-STEED is able to extract key experimental parameters and risk of bias items from the neuroscience in vivo literature. With this, the tool can be deployed to probe a field in a research improvement context or to replace one human reader during data extraction resulting in substantial time-savings and contribute towards automation of systematic reviews. The function is available on Github.
 The Cannabinoid (CB) signalling cascade is widely located in the human body and is associated with several pathophysiological processes. The endocannabinoid system comprises cannabinoid receptors CB1 and CB2, which belong to G-protein Coupled Receptors (GPCRs). CB1 receptors are primarily located on nerve terminals, prohibiting neurotransmitter release, whereas CB2 are present predominantly on immune cells, causing cytokine release. The activation of CB system contributes to the development of several diseases which might have lethal consequences, such as CNS disorders, cancer, obesity, and psychotic disorders on human health. Clinical evidence revealed that CB1 receptors are associated with CNS ailments such as Alzheimer's disease, Huntington's disease, and multiple sclerosis, whereas CB2 receptors are primarily connected with immune disorders, pain, inflammation, etc. Therefore, cannabinoid receptors have been proved to be promising targets in therapeutics and drug discovery. Experimental and clinical outcomes have disclosed the success story of CB antagonists, and several research groups have framed newer compounds with the binding potential to these receptors. In the presented review, we have summarized variously reported heterocycles with CB receptor agonistic/antagonistic properties against CNS disorders, cancer, obesity, and other complications. The structural activity relationship aspects have been keenly described along with enzymatic assay data. The specific outcomes of molecular docking studies have also been highlighted to get insights into the binding patterns of the molecules to CB receptors.
 INTRODUCTION: Plasmapheresis is a well-recognized treatment for autoimmune neurological diseases in Japan. However, the practice varies depending on the facility, and the actual treatment conditions are unclear. METHODS: To clarify real-world conditions, a prospective observational study was conducted on patients with neurological diseases who were scheduled to receive plasmapheresis. A dataset was analyzed that included 887 treatments from 210 patients with myasthenia gravis (MG), multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and other diseases for 82, 30, 24, and 74 patients, respectively. RESULTS: The types of plasmapheresis performed included immunoadsorption plasmapheresis, plasma exchange, and double filtration plasmapheresis with 620, 213, and 54 treatments, respectively. Approximately, 60% of the treatments were performed using peripheral blood access alone. Non-serious adverse events were observed in 10 patients. CONCLUSIONS: A statistically significant improvement was observed after plasmapheresis in patients with MG, MS, and NMOSD. These were evaluated using the modified Rankin Scale.
 Ethical concerns have been raised about the practice of using teriflunomide, an oral licensed disease-modifying therapy, as an active comparator in phase 3 multiple sclerosis (MS) trials. The assumption is based on the perceived low efficacy of teriflunomide as judged by its effect on relapses and focal MRI activity. However, when you look beyond focal inflammation, teriflunomide has a robust impact on disability progression and a similar effect to the anti-CD20 monoclonal antibody therapies on slowing down the accelerated brain volume loss associated with MS. Teriflunomide is also more effective when used second or third line. The other classes of disease-modifying therapies have problems with their use as active comparators in clinical trials. Using a non-inferiority or equivalence trial design has its own unique set of regulatory and ethical challenges and is not necessarily a solution. There are also economic, altruistic and pragmatic reasons for continuing to use teriflunomide as an active comparator in MS clinical trials. An online survey indicates that the majority of the MS community feels it is still ethical to randomise subjects to teriflunomide and that procedures can be put in place to protect trial subjects randomised to teriflunomide. Therefore, we still have equipoise, and teriflunomide comparator trials are ethical.
 Cannabis is one of the world's oldest cultivated plants and the most commonly used recreational drug worldwide. The plant relevant for medicinal use is Cannabis sativa that has two pharmacologically active ingredients - delta-9-tetrahydrocannabinol that is psychoactive and cannabidiol that does not have psychotropic activity. The policy tapestry of Cannabis has undergone a significant change in the past few decades worldwide. Different countries have diverse policies, ranging from classifying use of Cannabis as illicit, to legalization of its use, both for medicinal and recreational purposes. Cannabis products are approved for use, for instance, in multiple sclerosis and Dravet syndrome (US Food Drug and Administration). Against this backdrop, we find that the knowledge foundations for use of Cannabis in clinical trials in India are still evolving. Conducting ethical research within a clinical trials framework is essential to understand dosing, formulation, shelf life, drug-drug interaction, tolerability, and safety before establishing its utility for various indications. In the absence of guidelines or a regulatory framework for conduct of these studies, the various Institutional Ethics Committees (IECs), which are responsible for reviewing projects related to Cannabis, face unique challenges with respect to the basic requirements. The principal investigators (PIs) are equally strained to find local guidance, recommendations, and literature in support of their application to the respective IEC, thus leading to an impasse and delay in initiating the proposed clinical studies with Cannabis. The present article addresses considerations, questions, and issues that affect the conduct of these clinical studies and recommends mandatory documents and some suggested guidelines for use by both PIs and IECs to take studies with Cannabis forward until such time that an interdisciplinary regulatory framework is firmed up by regulatory authority.
 PURPOSE OF REVIEW: Neuromyelitis optica spectrum disorder (NMOSD) is a rare but highly disabling disease of the central nervous system. Unlike multiple sclerosis, disability in NMOSD occurs secondary to relapses that, not uncommonly, lead to blindness, paralysis, and death. Recently, newer, targeted immunotherapies have been trialed and are now in the treatment arsenal. We have endeavoured to evaluate the current state of NMOSD therapeutics. RECENT FINDINGS: This review provides a pragmatic evaluation of recent clinical trials and post-marketing data for rituximab, inebilizumab, satralizumab, eculizumab, and ravalizumab, contrasted to older agents. We also review contemporary issues such as treatment in the context of SARS-CoV2 infection and pregnancy. There has been a dramatic shift in NMOSD morbidity and mortality with earlier and improved disease recognition, diagnostic accuracy, and the advent of more effective, targeted therapies. Choosing a maintenance therapy remains nuanced depending on patient factors and accessibility. With over 100 putative agents in trials, disease-free survival is now a realistic goal for NMOSD patients.
 Interferons play a critical role in the innate immune response against several infections and play a key role in the control of a variety of viral and bacterial infectious diseases such as hepatitis, covid-19, cancer, and multiple sclerosis. Therefore, natural or synthetic IFN production is important and had three common methods, including bacterial fermentation, animal cell culture, and recombinant nucleic acid technology. However, the safety, purity, and accuracy of the most preferred INF production systems have not been extensively studied. This study provides a comprehensive comparative overview of interferon production in various systems that include viral, bacterial, yeast, and mammalian. We aim to determine the most efficient, safe, and accurate interferon production system available in the year 2023. The mechanisms of artificial interferon production were reviewed in various organisms, and the types and subtypes of interferons produced by each system were compared. Our analysis provides a comprehensive overview of the similarities and differences in interferon production and highlights the potential for developing new therapeutic strategies to combat infectious diseases. This review article offers the diverse strategies used by different organisms in producing and utilizing interferons, providing a framework for future research into the evolution and function of this critical immune response pathway.
 INTRODUCTION: Medical image segmentation is an important tool for doctors to accurately analyze the volume of brain tissue and lesions, which is important for the correct diagnosis of brain diseases. However, manual image segmentation methods are time-consuming, subjective and lack of repeatability, it needs to develop automatic and reliable methods for image segmentation. METHODS: Magnetic Resonance Imaging (MRI), a non-invasive imaging technique, is commonly used to detect, characterize and quantify tissues and lesions in the brain. Partial volume effect, gray scale in homogeneity, and lesions presents a great challenge for automatic medical image segmentation methods. So, the paper is dedicated to address the impact of partial volume effect and multiple sclerosis lesions on the segmentation accuracy in MRI. The objective function of the improved model and the post-processing method of lesion filling are researched based on the fuzzy clustering space and energy model. RESULTS: In particular, an energy-minimized segmentation algorithm is proposed. Through experimental verification, the AR-FCM algorithm can better overcome the problem of low segmentation accuracy of the RFCM algorithm for tissue boundary voxels and improve the segmentation accuracy of this algorithm. Meanwhile, a multi-channel input energy-minimization segmentation method with lesion filling and anatomical mapping is further proposed. DISCUSSION: The feasibility of the lesion filling strategy using post-processing can be confirmed and the segmentation accuracy is increased by comparison experiments.
 OBJECTIVE: Well-being and quality of life can vary independently of disease. Instruments measuring well-being and quality of life are commonly used in neurology, but there has been little investigation into the extent in which they accurately measure wellbeing/quality of life or if they merely reflect a diseased state of an individual. DESIGN: Systematic searches, thematic analysis and narrative synthesis were undertaken. Individual items from instruments represented in ≥ 5 publications were categorised independently, without prior training, by five neurologists and one well-being researcher, as relating to 'disease-effect' or 'Well-being' with a study-created instrument. Items were additionally categorised into well-being domains. DATA SOURCES: MEDLINE, EMBASE, EMCARE and PsycINFO from 1990 to 2020 were performed, across the 13 most prevalent neurological diseases. RESULTS: 301 unique instruments were identified. Multiple sclerosis had most unique instruments at 92. SF-36 was used most, in 66 studies. 22 instruments appeared in ≥ 5 publications: 19/22 'well-being' outcome instruments predominantly measured disease effect (Fleiss kappa = .60). Only 1/22 instruments was categorised unanimously as relating to well-being. Instruments predominantly measured mental, physical and activity domains, over social or spiritual. CONCLUSIONS: Most neurological well-being or quality-of-life instruments predominantly measure disease effect, rather than disease-independent well-being. Instruments differed widely in well-being domains examined.
 Over the last two decades, haematopoietic stem cell transplantation (HSCT) has been explored as a potential therapeutic strategy for autoimmune diseases refractory to conventional treatments, including neurological disorders. Although both autologous (AHSCT) and allogeneic HSCT (allo-HSCT) were investigated, AHSCT was preferentially developed due to a more favourable safety profile compared to allo-HSCT. Multiple sclerosis (MS) represents the most frequent neurological indication for AHSCT, but increasing evidence on the potential effectiveness of transplant in other autoimmune neurological diseases is emerging, although with a risk-benefit ratio overall more uncertain than in MS. In the present work, the rationale for the use of HSCT in neurological diseases and the experimental models that prompted its clinical application will be briefly covered. Case series and prospective studies exploring the use of HSCT in autoimmune diseases other than MS will be discussed, covering both frequent and rare neurological disorders such as myasthenia gravis, myopathies, and stiff-person syndrome. Finally, an updated summary of ongoing and future studies focusing on this issue will be provided.
 Numerous studies suggest that neutrophils might have a crucial role in the pathogenesis of systemic autoimmune diseases through neutrophil extracellular trap (NET) formation, production of pro-inflammatory cytokines, and organ destruction. NET components that are released into extracellular spaces can be considered autoantigens, which contribute to causing a break in self-tolerance. Subsequently, this leads to the development of autoimmune responses in predisposed individuals. Additionally, an imbalance between NET formation and NET degradation may prolong immune system contact with these modified autoantigens and enhance NET-induced tissue damage. In this review, we discuss the generation and clearance of the NET, as well as the role of NETosis in the pathogenesis of autoimmune disorders, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), multiple sclerosis (MS), psoriasis, antiphospholipid syndrome (APS), and Type-1 diabetes mellitus (T1DM).
 Key biomarkers such as Brain Derived Neurotrophic Factor (BDNF) and Neurofilament light chain (NfL) play important roles in the development and progression of many neurological diseases, including multiple sclerosis, Alzheimer's disease, and Parkinson's disease. In these clinical conditions, the underlying biomarker processes are markedly heterogeneous. In this context, robust biomarker discovery is of critical importance for screening, early detection, and monitoring of neurological diseases. The difficulty of directly identifying biochemical processes in the central nervous system (CNS) is challenging. In recent years, biomarkers of CNS inflammatory response have been identified in various body fluids such as blood, cerebrospinal fluid, and tears. Furthermore, biotechnology and nanotechnology have facilitated the development of biosensor platforms capable of real-time detection of multiple biomarkers in clinically relevant samples. Biosensing technology is approaching maturity and will be deployed in communities, at which point screening programs and personalized medicine will become a reality. In this multidisciplinary review, our goal is to highlight clinical and current technological advances in the development of multiplex-based solutions for effective diagnosis and monitoring of neuroinflammatory and neurodegenerative diseases. The trend in the detection if BDNF and NfL.
 Regulatory T cells (Treg) maintain immune homeostasis due to their anti-inflammatory functions. They can be generated either centrally in the thymus or in peripheral organs. Metabolites such as short-chain fatty acids produced by intestinal microbiota can induce peripheral Treg differentiation, by activating G-protein-coupled-receptors like GPR109A. In this study, we identified a novel role for GPR109A in thymic Treg development. We found that Gpr109a(-/-) mice had increased Treg under basal conditions in multiple organs compared with WT mice. GPR109A was not expressed on T cells but on medullary thymic epithelial cells (mTECs), as revealed by single-cell RNA sequencing in both mice and humans and confirmed by flow cytometry in mice. mTECs isolated from Gpr109a(-/-) mice had higher expression of autoimmune regulator (AIRE), the key regulator of Treg development, while the subset of mTECs that did not express Gpr109a in the WT displayed increased Aire expression and also enhanced signaling related to mTEC functionality. Increased thymic Treg in Gpr109a(-/-) mice was associated with protection from experimental autoimmune encephalomyelitis, with ameliorated clinical signs and reduced inflammation. This work identifies a novel role for GPR109A and possibly the gut microbiota, on thymic Treg development via its regulation of mTECs.
 BACKGROUND: Current practice in health technology assessment (HTA) of pharmaceuticals conducts cost-effectiveness analyses (CEAs) based on a static price or the estimated price at market launch. Recent publications suggest incorporating dynamic pricing. To test the feasibility and importance of including dynamic pricing, we compared the standard static approach to four dynamic scenarios by replicating US-based HTA evaluations with dynamic pricing inputs. METHODS: The four case examples included omalizumab (Xolair(®)) for the treatment of allergic asthma, elagolix (Orilissa(®)) for the treatment of endometriosis, ocrelizumab (Ocrevus(®)) for the treatment of primary progressive multiple sclerosis (PPMS), and dupilumab (Dupixent(®)) for the treatment of atopic dermatitis (AD). The primary outcome was the relative percentage change in incremental cost-effectiveness ratios (ICERs) per quality-adjusted life-year (QALY) for two dynamic pricing scenarios versus static pricing. Secondary outcomes included the absolute difference in ICERs versus base-case and an assessment of decision uncertainty. RESULTS: Base-case ICERs were $327,000, $102,000, $700,000, and $102,000 for allergic asthma, endometriosis, PPMS, and AD, respectively. Across scenarios and case examples, the range of ICERs versus base-case varied from decreases of 56% to increases of 232%. The absolute difference in ICERs versus base-case ranged from decreases of $120,000 to increases of $758,000. Conclusions on cost effectiveness were altered in 2/16 scenarios across the four case examples. CONCLUSIONS: Given the decision context that US payers face, with prices varying over time, findings suggest further research to reduce uncertainty around price trajectories, as well as conducting or updating multiple assessments over the lifecycle of pharmaceutical products.
 AIMS: To evaluate the validity of recorded chronic disease diagnoses in Icelandic healthcare registries. METHODS: Eight different chronic diseases from multiple sub-specialties of medicine were validated with respect to accuracy, but not to timeliness. For each disease, 30 patients with a recorded diagnosis and 30 patients without the same diagnosis were randomly selected from >80,000 participants in the iStopMM trial, which includes 54% of the Icelandic population born before 1976. Each case was validated by chart review by physicians using predefined criteria. RESULTS: The overall accuracy of the chronic disease diagnoses was 96% (95% CI 94-97%), ranging from 92 to 98% for individual diseases. After weighting for disease prevalence, the accuracy was estimated to be 98.5%. The overall positive predictive value (PPV) of chronic disease diagnosis was 93% (95% CI 89-96%) and the overall negative predictive value (NPV) was 99% (95% CI 96-100%). There were disease-specific differences in validity, most notably multiple sclerosis, where the PPV was 83%. Other disorders had PPVs between 93 and 97%. The NPV of most disorders was 100%, except for hypertension and heart failure, where it was 97 and 93%, respectively. Those who had the registered chronic disease had objective findings of disease in 96% of cases. CONCLUSIONS: When determining the presence of chronic disease, diagnosis data from the Icelandic healthcare registries has a high PPV, NPV and accuracy. Furthermore, most diagnoses can be confirmed by objective findings such as imaging or blood testing. These findings can inform the interpretation of studies using diagnostic data from the Icelandic healthcare registries.
 INTRODUCTION: This study aims to explore the clinical features and prognostic factors for relapse of acute disseminated encephalomyelitis (ADEM) in adults. MATERIAL AND METHODS: 56 patients with ADEM were retrospectively analyzed. The epidemiological characteristics, clinical manifestations, laboratory features, magnetic resonance imaging (MRI), treatment and prognosis data of these patients were analyzed using the χ(2) test for categorical variables and Mann-Whitney U-test for continuous variables. Then, the clinical characteristics and recurrence factors were summarized. RESULTS: 56 patients with ADEM, based on the criteria of the International Pediatric Multiple Sclerosis Study Group, were recruited to the study. Among these patients, 31 were male and 25 were female. Furthermore, 13 patients had multiphasic ADEM, and 29 patients (52%) had definite incentive factors before onset. The commonest presenting symptoms and signs were fever (36%), disturbance of consciousness (52%), mental disorder (38%), seizure (14%), headache and dizziness (43%), optic neuritis (34%), autonomic nervous system symptoms (43%), limb paralysis or abnormal sensation (73%), and unilateral or bilateral pyramidal tract signs (48%). Inflammatory changes in the cerebrospinal fluid were prominent. MRI T2-weighted and fluid-attenuated inversion recovery images displayed multiple or large flaky high signals, and the lesions were usually different in the number and distribution of these lesions. Intravenous corticosteroids and/or immunoglobulin were still important treatments in the acute phase. After treatment, 38 patients completely recovered, 9 patients had neurologic deficits, and 9 patients died. CONCLUSIONS: ADEM in adults is not uncommon, its clinical features are complex and varied, and some of these are multiphasic. There may be some potential clinical predictors at first onset.
 Cannabinoids are active substances present in plants of the Cannabis genus. Both the Food and Drug Administration (FDA) and European Medicines Agency (EMA) have approved several medicinal products containing natural cannabinoids or their synthetic derivatives for the treatment of drug-resistant epilepsy, nausea and vomiting associated with cancer chemotherapy, anorexia in AIDS patients, and the alleviation of symptoms in patients with multiple sclerosis. In fact, cannabinoids constitute a broad group of molecules with a possible therapeutic potential that could be used in the management of much more diseases than mentioned above; therefore, multiple preclinical and clinical studies on cannabinoids have been carried out in recent years. Danio rerio (zebrafish) is an animal model that has gained more attention lately due to its numerous advantages, including easy and fast reproduction, the significant similarity of the zebrafish genome to the human one, simplicity of genetic modifications, and body transparency during the early stages of development. A number of studies have confirmed the usefulness of this model in toxicological research, experiments related to the impact of early life exposure to xenobiotics, modeling various diseases, and screening tests to detect active substances with promising biological activity. The present paper focuses on the current knowledge of the endocannabinoid system in the zebrafish model, and it summarizes the results and observations from studies investigating the pharmacological effects of natural and synthetic cannabinoids that were carried out in Danio rerio. The presented data support the notion that the zebrafish model is a suitable animal model for use in cannabinoid research.
 In this paper we describe and validate a longitudinal method for whole-brain segmentation of longitudinal MRI scans. It builds upon an existing whole-brain segmentation method that can handle multi-contrast data and robustly analyze images with white matter lesions. This method is here extended with subject-specific latent variables that encourage temporal consistency between its segmentation results, enabling it to better track subtle morphological changes in dozens of neuroanatomical structures and white matter lesions. We validate the proposed method on multiple datasets of control subjects and patients suffering from Alzheimer's disease and multiple sclerosis, and compare its results against those obtained with its original cross-sectional formulation and two benchmark longitudinal methods. The results indicate that the method attains a higher test-retest reliability, while being more sensitive to longitudinal disease effect differences between patient groups. An implementation is publicly available as part of the open-source neuroimaging package FreeSurfer.
 Kombucha is a fermented, acidic beverage that dates back thousands of years as a remedy for various health problems in East Asia. Due to its health benefits, kombucha has gained popularity and attracted the attention of both consumers and researchers. The health benefits of kombucha are predominantly attributed to its bioactive compounds that have antioxidant, antimicrobial, probiotic, and other positive effects owing to fermentation. Many factors such as the type of the substrate used, the symbiotic culture of the bacterial yeast composition, and fermentation conditions influence the extent of these properties. This review focuses on recent developments regarding the bioactive constituents of kombucha and its potential health benefits (antimicrobial, antioxidant, antidiabetic, hepatoprotective effects) as well as its impact on multiple sclerosis, nephrotoxicity, gastric ulceration and gut microbiota. Additionally, the composition of kombucha, alternative uses of its biofilm, and potential toxicity are also discussed. Kombucha is a healthy and safe beverage with multiple health benefits that are primarily related to the presence of bacteria, yeasts, and other bioactive constituents. Moreover, kombucha has been suggested as a potential source of probiotics and eco-friendly materials (kombucha-derived bacterial cellulose) for several industries including food and textile.
 INTRODUCTION: The C1236T, G2677T/A, and C3435T variants of the ABCB1 gene alter the functioning of P-glycoprotein and the transport of endogenous and exogenous substances across the blood-brain barrier, and act as risk factors for some neurodegenerative diseases. This study aimed to determine the association between demyelinating disease and the C1236T, G2677T/A, and C3435T variants of ABCB1 and its haplotypes and combinations of genotypes. METHODS: Polymerase chain reaction with restriction fragment length polymorphism analysis (PCR-RFLP) and Sanger sequencing were used to genotype 199 patients with demyelinating disease and 200 controls, all Mexicans of mixed race; frequencies of alleles, genotypes, haplotypes, and genotype combinations were compared between patients and controls. We conducted a logistic regression analysis and calculated chi-square values and 95% confidence intervals (CI); odds ratios (OR) were calculated to evaluate the association with demyelinating disease. RESULTS: The TTT and CGC haplotypes were most frequent in both patients and controls. The G2677 allele was associated with demyelinating disease (OR: 1.79; 95% CI, 1.12-2.86; P =  .015), as were the genotypes GG2677 (OR: 2.72; 95% CI, 1.11-6.68; P =  .025) and CC3435 (OR: 1.82; 95% CI, 1.15-2.90; P =  .010), the combination GG2677/CC3435 (OR: 2.02; 95% CI, 1.17-3.48; P =  .010), and the CAT haplotype (OR: 0.21; 95% CI, 0.05-0.66; P =  .001). TTTTTT carriers presented the earliest age of onset (23.0 ± 7.7 years, vs 31.6 ± 10.7; P =  .0001). CONCLUSIONS: The GG2677/CC3435 genotype combination is associated with demyelinating disease in this sample, particularly among men, who may present toxic accumulation of P-glycoprotein substrates. In our study, the G2677 allele of ABCB1 may differentially modulate age of onset of demyelinating disease in men and women.
 The intricate interplay between gut microbes and the onset of experimental autoimmune encephalomyelitis (EAE) remains poorly understood. Here, we uncover remarkable similarities between CD4(+) T cells in the spinal cord and their counterparts in the small intestine. Furthermore, we unveil a synergistic relationship between the microbiota, particularly enriched with the tryptophan metabolism gene EC:1.13.11.11, and intestinal cells. This symbiotic collaboration results in the biosynthesis of kynurenic acid (KYNA), which modulates the recruitment and aggregation of GPR35-positive macrophages. Subsequently, a robust T helper 17 (Th17) immune response is activated, ultimately triggering the onset of EAE. Conversely, modulating the KYNA-mediated GPR35 signaling in Cx3cr1(+) macrophages leads to a remarkable amelioration of EAE. These findings shed light on the crucial role of microbial-derived tryptophan metabolites in regulating immune responses within extraintestinal tissues.
 OBJECTIVES: To evaluate clinical characteristics, imaging features and etiological profile of Radiologically Isolated Syndrome (RIS) along with clinical and radiological follow-up. METHODS: Demographic, clinical and radiological data of patients younger than 18 years fulfilling the criteria for RIS were retrospectively analyzed. RIS was defined by the detection of lesions meeting the revised 2010 McDonald Criteria for dissemination in space on magnetic resonance imaging (MRI) in the absence of any symptoms of demyelinating disease or an alternative cause for the MRI findings. RESULTS: There were total 69 patients (38 girls, 31 boys). The median age at index MRI was 15.7 years, and median follow-up time was 28 months. The most common reason for neuroimaging was headache (60.9%). A first clinical event occurred with median 11 months in 14/69 (20%) of cases. Those with oligoclonal bands (OCB) in cerebrospinal fluid (CSF) and follow-up longer than 3 years were more likely to experience a clinical event (p<0.05): 25% of those with OCB manifested clinical symptoms within the first year and 33.3% within the first two years compared to 6.3% and 9.4%, respectively in those without OCB. Radiological evolution was not associated with any variables: age, sex, reason for neuroimaging, serum 25-hydroxyvitamin D level, elevated IgG index, OCB positivity, total number and localization of lesions, presence of gadolinium enhancement, achievement of 2005 criteria for DIS and duration of follow-up. CONCLUSION: Children and adolescents with RIS and CSF OCB should be followed-up for at least 3 years in order to detect any clinical symptoms suggestive of a demyelinating event. Because disease-modifying treatments are not approved in RIS and no consensus report justifies their use especially in pediatric RIS, close follow-up of OCB-positive patients is needed for early recognition of any clinical event and timely initiation of specific treatment.
 Toll-like receptor 9 (TLR9) can participate in the signal transduction of activated immune cells and induce myelitis and other autoimmune diseases. The effector molecule fibrin-like protein 2 (Fgl2) plays a role in regulating the body's autoimmune signaling pathway. They both have the conditions for the treatment of this disease target. The objective of this work was to investigate the effect of Fgl2 on the expression of DNA receptor TLR9 in autoimmune myelitis. 140 rats were randomly divided into a normal control group, an autoimmune myelitis group, a low-dose Fgl2 group, a middle-dose Fgl2 group, a higher-dose Fgl2 group, a high-dose Fgl2 group, and a methylprednisolone group. Different injection methods were used in each group. The changes of rat behavior and disease were recorded, and brain and spinal cord tissue slices were made for observation. The results showed that in the high dose Fgl2 group, the incidence of disease was 15 %, the nerve injury score was 1.0 ± 0.15, the body weight change was -5.8 ± 1.24 g, the number of spinal cord tissue injury was 1.82 ± 0.44, the number of TLR9 positive cells in the brain tissue was 7.53 ± 1.84, and the number of TLR9 positive cells in spinal cord tissue was 5.02 ± 1.81. These indexes were lower than those in other Fgl2 groups and significantly lower than those in autoimmune myelitis group (P < 0.05). The average incubation period of the disease was 13.66 ± 0.41 days, which was significantly higher than that of the autoimmune myelitis group (P < 0.05). It can be observed that TLR9 signaling pathway played an important role in the occurrence and development of autoimmune myelitis. With the increase of Fgl2 dose, the number of TLR9 positive cells decreased gradually. Fgl2 treatment can reduce the expression of inflammatory factors and the severity of dysfunction in autoimmune myelitis, inhibit the expression of TLR9, and improve the condition of autoimmune myelitis.
 OBJECTIVE: To describe demographic, clinical, and radiographic features of tumefactive demyelination (TD) and identify factors associated with severe attacks and poor outcomes. METHODS: Retrospective review of TD cases seen at Mayo Clinic, 1990-2021. RESULTS: Of 257 patients with TD, 183/257 (71%) fulfilled the 2017 multiple sclerosis (MS) McDonald criteria at the last follow-up, 12/257 (5%) had myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), 0 had aquaporin-4-IgG seropositive neuromyelitis optic spectrum disorders (AQP4+ NMOSD), and 62/257 (24%) were cryptogenic. Onset before age 18 was present in 18/257 (7%). Female to male ratio was 1.3:1. Cerebrospinal fluid oligoclonal (CSF) bands were present in 95/153 (62%). TD was the first demyelinating attack in 176/257 (69%). At presentation, 59/126 (47%) fulfilled Barkhof criteria for dissemination in space, 59/100 (59%) had apparent diffusion coefficient (ADC) restriction, and 57/126 (45%) had mass effect. Despite aggressive clinical presentation at onset, 181/257 (70%) of patients remained fully ambulatory (Expanded Disability Status Scale [EDSS] ≤4) after a 3.0-year median follow-up duration. Severe initial attack-related disability (EDSS ≥4) was more common in patients with motor symptoms (81/143 vs. 35/106, p < 0.0001), encephalopathy (20/143 vs. 2/106, p < 0.0001) and ADC restriction on initial MRI (42/63 vs. 15/33, p = 0.04). Poor long-term outcome (EDSS ≥4) was more common in patients with older onset age (41.9 ± 15 vs. 36.8 ± 15.6, p = 0.02) and motor symptoms at onset (49/76 vs. 66/171, p < 0.0001). INTERPRETATION: Most TD patients should be considered part of the MS spectrum after excluding MOGAD and NMOSD. Motor symptoms and older age at presentation portend a poor outcome.
 Previous data have suggested an antiviral effect of teriflunomide, including against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the agent underlying the ongoing COVID-19 pandemic. We undertook an in vitro investigation to evaluate the inhibitory activity of teriflunomide against SARS-CoV-2 in a cell-based assay. Teriflunomide was added to Vero (kidney epithelial) cells that had been infected with SARS-CoV-2. A nucleocapsid immunofluorescence assay was performed to examine viral inhibition with teriflunomide and any potential cytotoxic effect. The 50% effective concentration (EC(50)) for teriflunomide against SARS-CoV-2 was 15.22 μM. No cytotoxicity was evident for teriflunomide in the Vero cells (i.e., the 50% cytotoxic concentration [CC(50)] was greater than the highest test concentration of 100 μM). The data were supported by additional experiments using other coronaviruses and human cell lines. In the SARS-CoV-2-infected Vero cells, the prodrug leflunomide had an EC(50) of 16.49 μM and a CC(50) of 54.80 μM. Our finding of teriflunomide-mediated inhibition of SARS-CoV-2 infection at double-digit micromolar potency adds to a growing body of evidence for a broad-ranging antiviral effect of teriflunomide.
 OBJECTIVE: To search for and critically appraise the psychometric quality of patient-reported outcome measures (PROMs) developed or validated in optic neuritis, in order to support high-quality research and care. METHODS: We systematically searched MEDLINE(Ovid), Embase(Ovid), PsycINFO(Ovid) and CINAHLPlus(EBSCO), and additional grey literature to November 2021, to identify PROM development or validation studies applicable to optic neuritis associated with any systemic or neurologic disease in adults. We included instruments developed using classic test theory or Rasch analysis approaches. We used established quality criteria to assess content development, validity, reliability, and responsiveness, grading multiple domains from A (high quality) to C (low quality). RESULTS: From 3142 screened abstracts we identified five PROM instruments potentially applicable to optic neuritis: three differing versions of the National Eye Institute (NEI)-Visual Function Questionnaire (VFQ): the 51-item VFQ; the 25-item VFQ and a 10-item neuro-ophthalmology supplement; and the Impact of Visual Impairment Scale (IVIS), a constituent of the Multiple Sclerosis Quality of Life Inventory (MSQLI) handbook, derived from the Functional Assessment of Multiple Sclerosis (FAMS). Psychometric appraisal revealed the NEI-VFQ-51 and 10-item neuro module had some relevant content development but weak psychometric development, and the FAMS had stronger psychometric development using Rasch Analysis, but was only somewhat relevant to optic neuritis. We identified no content or psychometric development for IVIS. CONCLUSION: There is unmet need for a PROM with strong content and psychometric development applicable to optic neuritis for use in virtual care pathways and clinical trials to support drug marketing authorisation.



 Neurodegeneration is a multifactorial process that involves multiple mechanisms. Examples of neurodegenerative diseases are Parkinson's disease, multiple sclerosis, Alzheimer's disease, prion diseases such as Creutzfeldt-Jakob's disease, and amyotrophic lateral sclerosis. These are progressive and irreversible pathologies, characterized by neuron vulnerability, loss of structure or function of neurons, and even neuron demise in the brain, leading to clinical, functional, and cognitive dysfunction and movement disorders. However, iron overload can cause neurodegeneration. Dysregulation of iron metabolism associated with cellular damage and oxidative stress is reported as a common event in several neurodegenerative diseases. Uncontrolled oxidation of membrane fatty acids triggers a programmed cell death involving iron, ROS, and ferroptosis, promoting cell death. In Alzheimer's disease, the iron content in the brain is significantly increased in vulnerable regions, resulting in a lack of antioxidant defenses and mitochondrial alterations. Iron interacts with glucose metabolism reciprocally. Overall, iron metabolism and accumulation and ferroptosis play a significant role, particularly in the context of diabetes-induced cognitive decline. Iron chelators improve cognitive performance, meaning that brain iron metabolism control reduces neuronal ferroptosis, promising a novel therapeutic approach to cognitive impairment.
 IMPORTANCE: Laminin-332 is an important component of the basement membrane. Recently, autoantibodies to Laminin-332 have been described in several autoimmune diseases. Many of these autoimmune diseases have a high incidence of malignancy. The importance of Laminin-332 autoantibodies and its relationship to malignancy is highlighted by using Laminin-332 Pemphigoid (LM-332Pg) as a prototype. OBJECTIVE: To identify several autoimmune diseases that have autoantibodies to Laminin-332 present, and to determine the prevalence of malignancy in them. Using Laminin-332 Pemphigoid (LM-332Pg) as a prototype, to compare clinical profiles of LM-332Pg patients with and without cancer. By identifying the temporal detection of cancer, can the influence of autoantibodies to Laminin-332 on prognosis be determined. EVIDENCE REVIEW: A literature search was conducted to identify autoimmune and inflammatory diseases in which autoantibodies to Laminin-332 were present. Subsequently, the rate of malignancy in these autoimmune diseases was determined. A search for publications on LM-332Pg patients to determine cancer rates and clinical outcomes to examine if a relationship can be proposed, was performed. FINDINGS: Autoantibodies to Laminin-332 were detected in recent studies of systemic lupus erythematosus (SLE), psoriasis, bronchiolitis obliterans (BO), graft-vs-host disease (GVH), bullous pemphigoid (BP), lichen planus (LP), epidermolysis bullosa acquisita (EBA), and membranous glomerulonephropathy (MGN). A high incidence of cancer rate was reported in these autoimmune diseases including primary Sjögren's syndrome (pSS), systemic sclerosis (SS), dermatomyositis (DM), multiple sclerosis (MS), immune thrombocytopenia purpura (ITP), and rheumatoid arthritis (RA). Data analysis demonstrated that LM-332Pg patients had a higher risk of developing ovarian, uterine, lung, gastric cancers and leukemia. The incidence for breast cancer was lower, when compared with global cancer rates. Patients diagnosed with cancer after the presence of LM-332Pg had higher rates of mortality and lower rates of remission, compared to those diagnosed with cancer prior to the discovery/diagnosis of LM-332Pg. When studied, levels of Laminin-332 autoantibodies correlated with the presence or absence of malignancy. CONCLUSIONS AND RELEVANCE: Preliminary analysis suggests that autoantibodies to Laminin-332 are present in multiple autoimmune diseases, which also have a high incidence of malignancy. Detailed analysis of available data highlights that patients who developed LM-332Pg after cancer was diagnosed, had a more favorable prognosis, compared to patients who developed cancer when LM-332Pg was previously present. Preliminary data would suggest that autoantibodies to Laminin-332 could serve as an important biomarker in certain patients, for correlation with possible incidence of malignancy.
 The complement system is an essential component of the innate immune response and plays a vital role in host defense and inflammation. Dysregulation of the complement system, particularly involving the anaphylatoxin C5a and its receptors (C5aR1 and C5aR2), has been linked to several autoimmune diseases, indicating the potential for targeted therapies. C5aR1 and C5aR2 are seven-transmembrane receptors with distinct signaling mechanisms that play both partially overlapping and opposing roles in immunity. Both receptors are expressed on a broad spectrum of immune and non-immune cells and are involved in cellular functions and physiological processes during homeostasis and inflammation. Dysregulated C5a-mediated inflammation contributes to autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, epidermolysis bullosa acquisita, antiphospholipid syndrome, and others. Therefore, targeting C5a or its receptors may yield therapeutic innovations in these autoimmune diseases by reducing the recruitment and activation of immune cells that lead to tissue inflammation and injury, thereby exacerbating the autoimmune response. Clinical trials focused on the inhibition of C5 cleavage or the C5a/C5aR1-axis using small molecules or monoclonal antibodies hold promise for bringing novel treatments for autoimmune diseases into practice. However, given the heterogeneous nature of (systemic) autoimmune diseases, there are still several challenges, such as patient selection, optimal dosing, and treatment duration, that require further investigation and development to realize the full therapeutic potential of C5a receptor inhibition, ideally in the context of a personalized medicine approach. Here, we aim to provide a brief overview of the current knowledge on the function of C5a receptors, the involvement of C5a receptors in autoimmune disorders, the molecular mechanisms underlying C5a receptor-mediated autoimmunity, and the potential for targeted therapies to modulate their activity.
 The role of NLRP3 inflammasome in innate immunity is newly recognized. The NLRP3 protein is a family of nucleotide-binding and oligomerization domain-like receptors as well as a pyrin domain-containing protein. It has been shown that NLRP3 may contribute to the development and progression of a variety of diseases, such as multiple sclerosis, metabolic disorders, inflammatory bowel disease, and other auto-immune and auto-inflammatory conditions. The use of machine learning methods in pharmaceutical research has been widespread for several decades. An important objective of this study is to apply machine learning approaches for the multinomial classification of NLRP3 inhibitors. However, data imbalances can affect machine learning. Therefore, a synthetic minority oversampling technique (SMOTE) has been developed to increase the sensitivity of classifiers to minority groups. The QSAR modelling was performed using 154 molecules retrieved from the ChEMBL database (version 29). The accuracy of the multiclass classification top six models was found to fall within ranges of 0.99 to 0.86, and log loss ranges of 0.2 to 2.3, respectively. The results showed that the receiver operating characteristic curve (ROC) plot values significantly improved when tuning parameters were adjusted and imbalanced data was handled. Moreover, the results demonstrated that SMOTE offers a significant advantage in handling imbalanced datasets as well as substantial improvements in overall accuracy of machine learning models. The top models were then used to predict data from unseen datasets. In summary, these QSAR classification models exhibited robust statistical results and were interpretable, which strongly supported their use for rapid screening of NLRP3 inhibitors.
 Objective: Emotional disturbances are the most common mental health problems in different populations and societies. We intend to provide the latest evidence related to the effectiveness of Acceptance and Commitment Therapy (ACT) on depression and anxiety by reviewing systematic review and meta-analysis studies published in the last three years. Method : PubMed and Google Scholar databases were systematically searched between January 1, 2019 and November 25, 2022 with relevant keywords for English systematic review and meta-analysis articles reviewing the utilization of ACT to reduce anxiety and depression symptoms. Results: 25 articles were included in our study: 14 systematic review and meta-analysis studies and 11 systematic reviews. These studies have investigated the effects of ACT on depression and anxiety in populations of children or adults, mental health patients, patients with different cancers or multiple sclerosis, people with audiological problems, parents or caregivers of children with mental or physical illnesses as well as normal people. Furthermore, they have examined the effects of ACT in individual, group, Internet, computerized, or combined delivery formats. Most of the reviewed studies reported significant effect sizes (small to large effect sizes) of ACT, regardless of the delivery method, compared to passive (placebo, waitlist) and active (treatment as usual and other psychological interventions except cognitive behavioral therapy (CBT)) controls for depression and anxiety. Conclusion: Recent literature mainly agrees on the small to moderate effect sizes of ACT on depression and anxiety symptoms in different populations.
 Aging causes considerable changes in the nervous system, inducing progressive and long-lasting loss of physiological integrity and synaptic plasticity, leading to impaired brain functioning. These age-related changes quite often culminate in behavioral dysfunctions, such as impaired cognition, which can ultimately result in various forms of neurodegenerative disorders. Still, little is known regarding the effects of aging on behavior. Moreover, the identification of factors involved in regenerative plasticity, in both the young and aged brain, is scarce but crucial from a regenerative point of view and for our understanding on the mechanisms that control the process of normal aging. Recently, we have identified the iron-trafficking protein lipocalin-2 (LCN2) as novel regulator of animal behavior and neuronal plasticity in the young adult brain. On the other hand, others have proposed LCN2 as a biological marker for disease progression in neurodegenerative disorders such as Alzheimer's disease and multiple sclerosis. Still, and even though LCN2 is well accepted as a regulator of neural processes in the healthy and diseased brain, its contribution in the process of normal aging is not known. Here, we performed a broad analysis on the effects of aging in mice behavior, from young adulthood to middle and late ages (2-, 12-, and 18-months of age), and in the absence of LCN2. Significant behavioral differences between aging groups were observed in all the dimensions analyzed and, in mice deficient in LCN2, aging mainly reduced anxiety, while sustained depressive-like behavior observed at younger ages. These behavioral changes imposed by age were further accompanied by a significant decrease in cell survival and neuronal differentiation at the hippocampus. Our results provide insights into the role of LCN2 in the neurobiological processes underlying brain function and behavior attributed to age-related changes.
 Activating Transcription Factor 3 (ATF3) is upregulated in reaction to several cellular stressors found in a wide range of pathological conditions to coordinate a transcriptional response. ATF3 was first implicated in the transcriptional reaction to axotomy when its massive upregulation was measured in sensory and motor neuron cell bodies following peripheral nerve injury. It has since been shown to be critical for successful axon regeneration in the peripheral nervous system and a promising target to mitigate regenerative failure in the central nervous system. However, much of the research to date has focused on ATF3's function in neurons, leaving the expression, function, and therapeutic potential of ATF3 in glia largely unexplored. In the immunology literature ATF3 is seen as a master regulator of the innate immune system. Specifically, in macrophages following pathogen or damage associated molecular pattern receptor activation and subsequent cytokine release, ATF3 upregulation abrogates the inflammatory response. Importantly, ATF3 upregulation is not exclusively due to cellular stress exposure but has been achieved by the administration of several small molecules. In the central nervous system, microglia represent the resident macrophage population and are therefore of immediate interest with respect to ATF3 induction. It is our perspective that the potential of inducing ATF3 expression to dampen inflammatory microglial phenotype represents an unexplored therapeutic target and may have synergistic benefits when paired with concomitant neuronal ATF3 upregulation. This would be of particular benefit in pathologies that involve both detrimental inflammation and neuronal damage including spinal cord injury, multiple sclerosis, and stroke.
 BACKGROUND: Role of radiosurgical lesioning in functional disorders has been restricted because of development of deep brain stimulation (DBS) techniques. However, many elderly patients with comorbidities and coagulation abnormalities may not be eligible for DBS. Radiosurgical lesioning may be a good alternative in such cases. The objective of the study was to review the role of radiosurgical lesioning for functional targets in common functional disorders. MATERIALS AND METHODS: Literature reports pertaining to common disorders were reviewed. Disorders included are tremors (essential tremors, tremor-dominant Parkinson's disease [PD], multiple sclerosis [MS] related refractory tremors), Parkinson's disease (for rigidity, bradykinesia, drug-induced dyskinesias), dystonia, and obsessive-compulsive disorder (OCD). RESULTS: The most commonly performed procedure was ventral intermediate nucleus (VIM) lesioning for essential tremors and tremor-dominant PD, with about 90% patients demonstrating improvement. Intractable OCD with 60% responders is a promising indication. Other disorders are less commonly treated, with dystonia being the least commonly treated entity. Subthalamic nucleus (STN) and globus pallidus interna/posteroventral pallidum (GPi) lesioning are very rarely reported, and the available literature suggests caution due to high rates of adverse effects. CONCLUSIONS: Outcomes for radiosurgical lesioning for essential tremors (VIM) and OCD (anterior limb of internal capsule [ALIC]) are encouraging. Radiosurgical lesioning offers a lower immediate risk profile in patient population with several comorbidities; however, long-term adverse effects due to radiation are a concern, especially for STN and GPi lesioning.
 BACKGROUND: Statistical monitoring involves the review of prospective study data collected in participating sites to detect intra/inter patients and sites inconsistencies. We report methods and results of statistical monitoring in a phase IV clinical trial. METHOD: PRO-MSACTIVE is a study evaluating ocrelizumab in active relapsing multiple sclerosis (RMS) patients in France. Specific statistical methods (volcano plots, mahalanobis distance, funnel plot …) have been applied to a SDTM database to detect potential issues. R-Shiny application was developed to generate an interactive web application in order to ease site and/or patients identification during statistical data review meetings. RESULTS: The PRO-MSACTIVE study enrolled 422 patients in 46 centers between July 2018 and August 2019. Three data review meetings were held between April and October 2019 and 14 standard and planned tests were run on study data, with a total of 15 (32.6%) sites identified as needing review or investigation. Overall 36 findings were identified during the meetings: duplicate records, outliers, inconsistent delays between dates. CONCLUSION: Statistical monitoring is useful to identify unusual or clustered data patterns that might be revealing issues that could impact the data integrity and/or may potentially impact patients' safety. With anticipated and appropriate interactive data visualization, early signals can easily be identified or reviewed by the study team and appropriate actions be set up and assigned to the most appropriate function for a close follow-up and resolution. Interactive statistical monitoring is time consuming to initiate using R-Shiny, but is time saving after the 1st data review meeting (DRV).(ClinicalTrials.gov identifier: NCT03589105; EudraCT identifier: 2018-000780-91).
 Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies specific to self-molecules in the nucleus, cytoplasm, and cell surface. The diversity of serologic and clinical manifestations observed in SLE patients challenges the development of diagnostics and tools for monitoring disease activity. Elevated type I interferon signature (IFN- I) in SLE leads to dysregulation of innate and adaptive immune function, resulting in autoantibodies production. The most common method to determine IFN-I signature is measuring the gene expression of several IFN-α-inducible genes (IFIGs) in blood samples and calculating a score. Optimal selection of IFIGs improves the sensitivity, specificity, and accuracy of the diagnosis of SLE. We describe the mechanisms of the immunopathogenesis of IFN-I signature (IFNα production) and its clinical consequences in SLE. In addition, we explore the association between IFN-I signature, the presence of autoantibodies, disease activity, medical therapy, and ethnicity. We discuss the presence of IFN-I signature in some patients with other autoimmune diseases, including rheumatoid arthritis, systemic and multiple sclerosis, Sjogren's syndrome, and dermatomyositis. Prospective studies are required to assess the role of IFIG and the best combination of IFIGs to monitor SLE disease activity and drug treatments.
 Pituitary adenylate cyclase activating polypeptide (PACAP) is a conserved neuropeptide, which confers diverse anti-aging endocrine and paracrine/autocrine effects, including anti-apoptotic, anti-inflammatory and antioxidant action. The results of the in vivo and in vitro experiments show that increasing emphasis is being placed on the diagnostic/prognostic biomarker potential of this neuropeptide in a wide array of age-related diseases. After the initial findings regarding the presence and alteration of PACAP in different body fluids in physiological processes, an increasing number of studies have focused on the changes of its levels in various pathological conditions associated with advanced aging. Until 2016 - when the results of previous human studies were reviewed - a vast majority of the studies had dealt with age-related neurological diseases, like cerebrovascular and neurodegenerative diseases, multiple sclerosis, as well as some other common diseases in elderly such as migraine, traumatic brain injury and post-traumatic stress disorder, chronic hepatitis and nephrotic syndrome. The aim of this review is to summarize the old and the new results and highlight those 'classical' and emerging clinical fields in which PACAP may become subject to further investigation as a diagnostic and/or prognostic biomarker in age-related diseases.
 BACKGROUND: Percutaneous rhizotomy of the trigeminal nerve is a common surgery to manage medically refractory trigeminal neuralgia. Traditionally, these procedures have been performed based on anatomic landmarks with fluoroscopic guidance. Augmented reality (AR) relays virtual content on the real world and has the potential to improve localization of surgical targets based on preoperative imaging. OBJECTIVE: To study the potential application and benefits of AR as an adjunct to traditional fluoroscopy-guided glycerol rhizotomy (GR). METHODS: We used traditional fluoroscopy-guided percutaneous GR technique as previously described, performed under general anesthesia. Anatomic registration to the Medivis SurgicalAR system was performed based on the patient's preoperative computerized tomography, and the surgeon was equipped with the system's AR goggles. AR was used as an adjunct to fluoroscopy for trajectory planning to place a spinal needle into the medial aspect of the foramen ovale. RESULTS: A 50-year-old woman with multiple sclerosis-related right-sided classical trigeminal neuralgia had persistent pain, refractory to medications, previous gamma knife stereotactic radiosurgery, and percutaneous radiofrequency rhizotomy performed elsewhere. The patient underwent AR-assisted fluoroscopy-guided percutaneous GR. The needle was placed into the right trigeminal cistern within seconds. She was discharged home after a few hours of observation with no complications and reported pain relief. CONCLUSION: AR-assisted percutaneous rhizotomy may enhance the learning curve of these types of procedures and decrease surgery duration and radiation exposure. This allowed rapid and correct placement of a spinal needle through the foramen ovale.
 Paraquat (PQ) is the most important cationic bipyridyl herbicide in the agricultural industry, which is very toxic to humans and animals and causes disruption in many organs, mainly in the lungs. Dimethyl fumarate (DMF) is an immune-modulating drug used in the treatment of multiple sclerosis and psoriasis shows antioxidant, anti-inflammatory, and antifibrotic effects. In this study, the ameliorative effects of DMF (10, 30 and 100 mg/kg, orally) on PQ (30 mg/kg) model of lung damage were evaluated in male mice. DMF was given daily for 7 days and PQ was administrated in the fourth day in a single dose. On the eighth day, the animals were sacrificed, and their lung tissue were removed. The results indicated that DMF can ameliorate PQ-induced the significant increase in lung index, hydroxyproline, as well as TBARS, TGF-β, NF-κB and decrease in the amount of total thiol, catalase, glutathione peroxidase, superoxide dismutase, Nrf-2, and INF-γ. The histopathological results confirmed indicated findings. The results showed that the protective effect of DMF on PQ-induced toxicity is mediated through antioxidant, anti-inflammatory and antifibrotic activities.
 Significance: Central nervous system (CNS) diseases are disorders of the brain and/or spinal cord and include neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). NF-E2-related factor 2 (NRF2) is a transcription factor belonging to the cap-n-collar (CNC) family that harbors a unique basic leucine zipper motif and plays as a master regulator of homeostatic responses. Recent Advances: Kelch-like ECH-associated protein 1 (KEAP1) is an adaptor of the Cullin3 (CUL3)-based ubiquitin E3 ligase that enhances the ubiquitylation of NRF2, which promotes the degradation of NRF2 to suppress its transcriptional activity in the absence of stress. Cysteine residues of KEAP1 are modified under stress conditions, and NRF2 degradation is attenuated, allowing it to accumulate and induce the expression of target genes. This regulatory system is referred to as the KEAP1-NRF2 system and plays a central role in protecting cells against various stresses. NRF2 also negatively regulates the expression of inflammatory cytokine and chemokine genes and suppresses pathological inflammation. As oxidative stress, inflammation, and proteostasis are known to contribute to neurodegenerative diseases, the KEAP1-NRF2 system is an attractive target for the treatment of these diseases. Critical Issues: In mouse models of neurodegenerative diseases, Nrf2 depletion exacerbates symptoms and enhances oxidative damage and inflammation in the CNS. In contrast, chemical or genetic NRF2 activation improves these symptoms. Indeed, the NRF2-activating chemical dimethyl fumarate (DMF) is now widely used for the clinical treatment of MS. Future Directions: The KEAP1-NRF2 system is a promising therapeutic target for neurodegenerative diseases.
 Gait and balance disorders are common signs in several neurodegenerative diseases such as Parkinson's disease, atypical parkinsonism, idiopathic normal pressure hydrocephalus, cerebrovascular disease, dementing disorders and multiple sclerosis. According to each condition, patients present with different gait and balance alterations depending on the structural and functional brain changes through the disease course. In this review, we will summarize the main clinical characteristics of gait and balance disorders in the major neurodegenerative conditions, providing an overview of the significant structural and functional MRI brain alterations underlying these deficits. We also will discuss the role of neurorehabilitation strategies in promoting brain plasticity and gait/balance improvements in these patients.
 Immune cell trafficking is a complex and tightly regulated process that is indispensable for the body's fight against pathogens. However, it is also increasingly acknowledged that dysregulation of cell trafficking contributes to the pathogenesis of immune-mediated inflammatory diseases (IMIDs) in gastroenterology and hepatology, such as inflammatory bowel disease and primary sclerosing cholangitis. Moreover, altered cell trafficking has also been implicated as a crucial step in the immunopathogenesis of other IMIDs, such as rheumatoid arthritis and multiple sclerosis. Over the past few years, a central role of the gut in mediating these disorders has progressively emerged, and the partly microbiota-driven imprinting of particular cell trafficking phenotypes in the intestine seems to be crucially involved. Therefore, this Review highlights achievements in understanding immune cell trafficking to, within and from the intestine and delineates its consequences for immune-mediated pathology along the gut-liver, gut-joint and gut-brain axes. We also discuss implications for current and future therapeutic approaches that specifically interfere with homing, retention, egress and recirculation of immune cells.
 A 68-year-old female with past medical history of hypertension, hyperlipidemia, multiple sclerosis, diverticulitis, and tobacco use presented with 1 day of atypical chest pain after a recent diverticulitis flare. Initial workup was notable for a normal electrocardiogram but elevated high sensitivity troponin T (616 ng/L). Due to persistent symptoms, the patient was given antiplatelet therapy and taken urgently to the catheterization lab where she was found to have complete occlusion of an anomalous right coronary artery branching off the mid-left anterior descending artery. Angioplasty was performed with a drug-eluting stent and her symptoms resolved. The patient recovered well and was discharged on appropriate medical therapy. This case demonstrates a case of acute coronary syndrome in an extremely rare coronary congenital abnormality. Further research is needed on when to be suspicious for coronary anomalies on patients presenting with myocardial infarction.
 Ras-homologous (Rho) guanosine triphosphatases (GTPases) are considered a central player in regulating various biological processes, extending to immune regulation. Perturbations in Rho GTPase signalling have been implicated in immune-related dysregulation, contributing to the development of autoimmunity. This study presents a scientometric analysis exploring the interlink between the Rho GTPase signalling system and autoimmunity, while also delving into the trends of past studies. A total of 967 relevant publications from 1990 to 2023 were retrieved from the Web of Science Core Collection database after throrough manual filtering of irrelevant articles. The findings show an upward trajectory in publications related to this field since 2006. Over the past three decades, the United States of America (41.68%) emerged as the primary contributor in advancing our understanding of the association between the Rho GTPase signalling system and autoimmunity. Research in autoimmunity has mainly centered around therapeutic interventions, with an emphasis on studying leukocyte (macrophage) and endothelial remodelling. Interestingly, within the domains of multiple sclerosis and rheumatoid arthritis, the current focus has been directed towards comprehending the role of RhoA, Rac1, and Cdc42. Notably, certain subfamilies of Rho (such as RhoB and RhoC), Rac (including Rac2 and RhoG), Cdc42 (specifically RhoJ), and other atypical Rho GTPases (like RhoE and RhoH) consistently demonstrating compelling link with autoimmunity, but still warrants emphasis in the future study. Hence, strategic manipulation of the Rho signalling system holds immense promise as a pivotal approach to addressing the global challenge of autoimmunity.
 Multiple sclerosis (MS) is one of the most common autoimmune diseases of central nervous system (CNS) demyelination. Experimental autoimmune encephalomyelitis (EAE) is the most classic animal model for simulating the onset of clinical symptoms in MS. Previous research has reported the anti-inflammatory effects of artemisinin on autoimmune diseases. In our study, we identified a novel small molecule, TPN10518, an artemisinin derivative, which plays a protective role on the EAE model. We found that TPN10518 reduced CNS inflammatory cell infiltration and alleviated clinical symptoms of EAE. In addition, TPN10518 downregulated the production of Th1 and Th17 cells in vivo and in vitro, and decrease the levels of related chemokines. RNA-seq assay combined with the experimental results demonstrated that TPN10518 lowered the mRNA and protein levels of the AP1 subunits c-Fos and c-Jun in EAE mice. It was further confirmed that TPN10518 was dependent on AP1 to inhibit the differentiation of Th1 and Th17 cells. The results suggest that TPN10518 reduces the production of Th1 and Th17 cells through inhibition of AP1 to alleviate the severity of EAE disease. It is expected to be a potential drug for the treatment of MS.
 Experimental autoimmune encephalomyelitis (EAE) is an animal model of central nervous system (CNS) autoimmunity. It is most commonly used to mimic aspects of multiple sclerosis (MS), a demyelinating disorder of the human brain and spinal cord. The innate immune response displays one of the core pathophysiological features linked to both the acute and chronic stages of MS. Hence, understanding and targeting the innate immune response is essential. Microglia and other CNS resident MUs, as well as infiltrating myeloid cells, diverge substantially in terms of both their biology and their roles in EAE. Recent advances in the field show that antigen presentation, as well as disease-propagating and regulatory interactions with lymphocytes, can be attributed to specific myeloid cell types and cell states in EAE lesions, following a distinct temporal pattern during disease initiation, propagation and recovery. Furthermore, single-cell techniques enable the assessment of characteristic proinflammatory as well as beneficial cell states, and identification of potential treatment targets. Here, we discuss the principles of EAE induction and protocols for varying experimental paradigms, the composition of the myeloid compartment of the CNS during health and disease, and systematically review effects on myeloid cells for therapeutic approaches in EAE.
 Fatigue, characterised by lack of energy, mental exhaustion and poor muscle endurance which do not recover following a period of rest, is a common characteristic symptom of several conditions and negatively impacts the quality of life of those affected. Fatigue is often a symptom of concern for people suffering from conditions such as fibromyalgia, chronic fatigue syndrome, cancer, and multiple sclerosis. Vitamins and minerals, playing essential roles in a variety of basic metabolic pathways that support fundamental cellular functions, may be important in mitigating physical and mental fatigue. Several studies have examined the potential benefits of nutrients on fatigue in various populations. The current review aimed to gather the existing literature exploring different nutrients' effects on fatigue. From the searches of the literature conducted in PubMed, Ovid, Web of Science, and Google scholar, 60 articles met the inclusion criteria and were included in the review. Among the included studies, 50 showed significant beneficial effects (p < 0.05) of vitamin and mineral supplementation on fatigue. Altogether, the included studies investigated oral or parenteral administration of nutrients including Coenzyme Q10, L-carnitine, zinc, methionine, nicotinamide adenine dinucleotide (NAD), and vitamins C, D and B. In conclusion, the results of the literature review suggest that these nutrients have potentially significant benefits in reducing fatigue in healthy individuals as well as those with chronic illness, both when taken orally and parenterally. Further studies should explore these novel therapies, both as adjunctive treatments and as sole interventions.
 The myelin sheath facilitates signal conduction along axons in white matter tracts, and when disrupted, can result in significant functional deficits. Demyelination, observed in diseases like multiple sclerosis and optic neuritis, are associated with neural degeneration, however the extent of this damage on upstream circuitry is not well understood. Here we use the MBP-iCP9 mouse model to induce selective oligodendrocyte ablation in the optic nerve at P14 via a chemical inducer of dimerization (CID), resulting in partial demyelination of retinal ganglion cell (RGC) axons with minimal inflammation after two weeks. Oligodendrocyte loss reduced axon diameter and altered compound action potential waveforms, blocking conduction in the slowest-conducting axon populations. Demyelination resulted in disruptions to the normal composition of the retina, including reduced density of RBPMS+, Brn3a+, and OFF-transient RGCs, thinning of the IPL, and reduced density of displaced amacrine cells. The INL and ONL were unaffected by oligodendrocyte loss, suggesting that demyelination-induced deficits in this model are specific to the IPL and GCL. These results show that a partial demyelination of a subpopulation of RGC axons disrupts optic nerve function and affects the organization of the retinal network. This study highlights the significance of myelination in maintaining upstream neural connectivity and provides support for targeting neuronal degeneration in treatments of demyelinating diseases.
 Rheumatoid arthritis (RA), multiple sclerosis (MS), type 1 diabetes (T1D), and celiac disease (CD), are strongly associated with susceptible HLA class II haplotypes. The peptide-binding pockets of these molecules are polymorphic, thus each HLA class II protein presents a distinct set of peptides to CD4(+) T cells. Peptide diversity is increased through post-translational modifications, generating non-templated sequences that enhance HLA binding and/or T cell recognition. The high-risk HLA-DR alleles that confer susceptibility to RA are notable for their ability to accommodate citrulline, promoting responses to citrullinated self-antigens. Likewise, HLA-DQ alleles associated with T1D and CD favor the binding of deamidated peptides. In this review, we discuss structural features that promote modified self-epitope presentation, provide evidence supporting the relevance of T cell recognition of such antigens in disease processes, and make a case that interrupting the pathways that generate such epitopes and reprogramming neoepitope-specific T cells are key strategies for effective therapeutic intervention.
 INTRODUCTION: Spinal dural arterio-venous fistula (SDAVF) is a rare and underdiagnosed cause of myelopathy which can result in a devastating neurological outcome if not properly managed. CASE DESCRIPTION: We report a case of SDAVF in a middle-aged man with gradual progressively deteriorating myelopathy and associated symptoms. This was first managed as demyelinating disease but was refractory to steroid therapy. Vigilant review of his spinal magnetic resonance imaging (MRI) scans showed dilated perimedullary veins, suspicious for SDAVF. The diagnosis was confirmed with catheter angiography. Neurological symptoms resolved after surgical treatment. DISCUSSION: SDAVF can closely mimic demyelinating conditions such as transverse myelitis or multiple sclerosis. MRI finding of dilated perimedullary veins can be subtle and masked in the late stage, posing a diagnostic challenge for physicians. It is potentially curable after timely treatment. CONCLUSION: Clinicians should maintain a high level of suspicion for SDAVF and actively review all available radiological imaging for clues, particularly when there is a lack of response to treatment for other causes of myelopathy. LEARNING POINTS: Spinal dural arterio-venous fistula (SDAVF) can have clinical and radiological features similar to those of demyelinating disease, often causing a diagnostic dilemma for physicians. Neurological sequalae can be devastating if left untreated.Clinicians should be aware of this rare yet important differential diagnosis for myelopathy and its classic MRI findings (spinal cord oedema and dilated perimedullary veins).The gold standard for diagnosis is catheter spinal angiography. Treatment options include endovascular embolization and surgical ligation of the fistula.
 Nervonic acid, a 24-carbon fatty acid with only one double bond at the 9th carbon (C24:1n-9), is abundant in the human brain, liver, and kidney. It not only functions in free form but also serves as a critical component of sphingolipids which participate in many biological processes such as cell membrane formation, apoptosis, and neurotransmission. Recent studies show that nervonic acid supplementation is not only beneficial to human health but also can improve the many medical conditions such as neurological diseases, cancers, diabetes, obesity, and their complications. Nervonic acid and its sphingomyelins serve as a special material for myelination in infants and remyelination patients with multiple sclerosis. Besides, the administration of nervonic acid is reported to reduce motor disorder in mice with Parkinson's disease and limit weight gain. Perturbations of nervonic acid and its sphingolipids might lead to the pathogenesis of many diseases and understanding these mechanisms is critical for investigating potential therapeutic approaches for such diseases. However, available studies about this aspect are limited. In this review, relevant findings about functional mechanisms of nervonic acid have been comprehensively and systematically described, focusing on four interconnected functions: cellular structure, signaling, anti-inflammation, lipid mobilization, and their related diseases.
 Neuromyelitis optica spectrum disorders (NMOSD) comprise a group of autoimmune inflammatory demyelinating diseases of the central nervous system that manifest as optic neuritis and transverse myelitis. Its manifestation in the form of optic neuritis makes early diagnosis difficult because neuroimaging of the spinal cord is not a part of the routine examination algorithm for such patients. This article presents the results of a comprehensive ophthalmological examination of 4 patients (8 eyes) diagnosed with NMSOD. Optic neuritis was the disease debut in 3 patients and had 1-2 relapses, in all cases partial optic atrophy with moderate to severe loss of visual function occurred. The clinical picture was characterized by a pronounced heterogeneity in terms of both ophthalmological symptoms, and accession of neurological disorders. Treatment of NMOSD requires differential diagnosis with multiple sclerosis, which depends on the awareness of specialists and the inclusion of antibody titers to aquaporin-4 and myelin oligodendrocyte glycoprotein into the examination algorithm of patients with optical neuritis.
 INTRODUCTION: Acute transverse myelitis (ATM) is a term that encompasses a wide range of etiologies from immune-mediated to infectious. Management and prognosis differ for each specific etiology, and thus determining the disease-specific diagnosis of ATM is crucial. AREAS COVERED: The distinguishing clinical, radiologic, serologic, and cerebrospinal fluid features for common etiologies of ATM, such as multiple sclerosis, aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and spinal cord sarcoidosis, are covered. Acute flaccid myelitis variant of ATM is also explored. Red flags suggesting ATM mimics are briefly reviewed. Management of ATM in this review mainly focuses on treatment for immune-mediated causes and is divided into acute treatment, preventive treatment for certain etiologies, and supportive management. Although maintenance attack-prevention treatment for immune-mediated ATM is mainly guided by observational studies and expert opinion, clinical trials have been completed in AQP4+NMOSD and are underway in MOGAD to help provide solid evidence for treatment efficacy. EXPERT OPINION: The term ATM should be replaced by a disease-specific diagnosis to direct management. Discovery of disease-associated antibodies has changed the landscape of ATM diagnosis and allowed research on disease mechanisms. Translating our knowledge on pathophysiology into targeted therapy with monoclonal antibodies has provided new treatment options for patients.
 Disease modifying drugs and biologics used to treat autoimmune diseases, although promising, are non-curative. As the field moves towards development of new approaches to treat autoimmune disease, antigen-specific therapies immunotherapies (ASITs) have emerged. Despite clinical approval of ASITs for allergies, clinical trials using soluble ASITs for autoimmunity have been largely unsuccessful. A major effort to address this shortcoming is the use of biomaterials to harness the features unique to specific delivery routes. This review focuses on biomaterials being developed for delivery route-specific strategies to induce antigen-specific responses in autoimmune diseases such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis, and celiac disease. We first discuss the delivery strategies used in ongoing and completed clinical trials in autoimmune ASITs. Next, we highlight pre-clinical biomaterial approaches from the most recent 3 years in the context of these same delivery route considerations. Lastly, we provide discussion on the gaps remaining in biomaterials development and comment on the need to consider delivery routes in the process of designing biomaterials for ASITs.
 Human urinary proteins are a goldmine of natural proteins a feature that simplifies their translation to biologics. Combining this goldmine together with the ligand-affinity-chromatography (LAC) purification method, proved a winning formula in their isolation. LAC specificity, efficiency, simplicity and inherent indispensability in the search for predictable and unpredictable proteins, is superior to other separation techniques. Unlimited amounts of recombinant cytokines and monoclonal antibodies (mAb) accelerated the "triumph". My approach concluded 35 years of worldwide pursuit for Type I IFN receptor (IFNAR2) and advanced the understanding of the signal transduction of this Type of IFN. TNF, IFNγ and IL-6 as baits enabled the isolation of their corresponding soluble receptors and N-terminal amino acid sequence of the isolated proteins facilitated the cloning of their cell surface counterparts. IL-18, IL-32, and heparanase as the baits yielded the corresponding unpredictable proteins: the antidote IL-18 Binding Protein (IL-18BP), the enzyme Proteinase 3 (PR3) and the hormone Resistin. IFNβ proved beneficial in Multiple Sclerosis and is a blockbuster drug, Rebif(®). TNF mAbs translated into Remicade(®) to treat Crohn's disease. Enbrel(®) based on TBPII is for Rheumatoid Arthritis. Both are blockbusters. Tadekinig alfa™, a recombinant IL-18BP, is in phase III clinical study for inflammatory and autoimmune diseases. Seven years of continuous compassionate use of Tadekinig alfa™ in children born with mutations (NLRC4, XIAP) proved life-saving and is an example of tailored made medicine. IL-18 is a checkpoint biomarker in cancer and IL-18BP is planned recently to target cytokine storms resulting from CAR-T treatment and in COVID 19.
 Cannabidiol (CBD) is the main non-psychotropic cannabinoid derived from cannabis (Cannabis sativa L., fam. Cannabaceae). CBD has received approval by the Food and Drug Administration (FDA) and European Medicines Agency (EMA) for the treatment of seizures associated with Lennox-Gastaut syndrome or Dravet syndrome. However, CBD also has prominent anti-inflammatory and immunomodulatory effects; evidence exists that it could be beneficial in chronic inflammation, and even in acute inflammatory conditions, such as those due to SARS-CoV-2 infection. In this work, we review available evidence concerning CBD's effects on the modulation of innate immunity. Despite the lack so far of clinical studies, extensive preclinical evidence in different models, including mice, rats, guinea pigs, and even ex vivo experiments on cells from human healthy subjects, shows that CBD exerts a wide range of inhibitory effects by decreasing cytokine production and tissue infiltration, and acting on a variety of other inflammation-related functions in several innate immune cells. Clinical studies are now warranted to establish the therapeutic role of CBD in diseases with a strong inflammatory component, such as multiple sclerosis and other autoimmune diseases, cancer, asthma, and cardiovascular diseases.
 Neuroinflammation is a common event in degenerative diseases of the central and peripheral nervous system, triggered by alterations in the immune system or inflammatory cascade. The pathophysiology of these disorders is multifactorial, whereby the therapy available has low clinical efficacy. This review propounds the relationship between the deregulation of T helper cells and hypoxia, mainly Th17 and HIF-1α molecular pathways, events that are involved in the occurrence of the neuroinflammation. The clinical expression of neuroinflammation is included in prevalent pathologies such as multiple sclerosis, Guillain-Barré syndrome, and Alzheimer's disease, among others. In addition, therapeutic targets are analyzed in relation to the pathways that induced neuroinflammation.
 The gut microbiota and its derived metabolites greatly impact the host immune system, both innate and adaptive responses. Gut dysbiosis and altered levels of microbiota-derived metabolites have been described in several immune-related and immune-mediated diseases such as intestinal bowel disease, multiple sclerosis, or colorectal cancer. Gut microbial-derived metabolites are synthesized from dietary compounds ingested by the host or host-produced metabolites, and additionally, some bacterial products can be synthesized de novo. In this review, we focus on the two first metabolites families including short-chain fatty acids, indole metabolites, polyamines, choline-derived compounds, and secondary bile acids. They all have been described as immunoregulatory molecules that specifically affect the adaptive immune system and T helper 17 and regulatory T cells. We discuss the mechanisms of action and the consequences in health and diseases related to these gut microbial-derived metabolites. Finally, we propose that the exogenous administration of these molecules or other compounds that bind to their immunoregulatory receptors in a homologous manner could be considered therapeutic approaches.
 Autoimmune diseases (ADs) are chronic pathologies generated by the loss of immune tolerance to the body's own cells and tissues. There is growing recognition that RNA-binding proteins (RBPs) critically govern immunity in healthy and pathological conditions by modulating gene expression post-transcriptionally at all levels: nuclear mRNA splicing and modification, export to the cytoplasm, as well as cytoplasmic mRNA transport, storage, editing, stability, and translation. Despite enormous efforts to identify new therapies for ADs, definitive solutions are not yet available in many instances. Recognizing that many ADs have a strong genetic component, we have explored connections between the molecular biology and the genetics of RBPs in ADs. Here, we review the genetics and molecular biology of RBPs in four major ADs, multiple sclerosis (MS), type 1 diabetes mellitus (T1D), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). We anticipate that gaining insights into the genetics and biology of ADs can facilitate the discovery of new therapies. This article is categorized under: RNA in Disease and Development > RNA in Disease.
 BACKGROUND: Efforts to understand how treatments affect patients and society have broadened the criteria that health technology assessment (HTA) organizations apply to value assessments. We examined whether HTA agencies in eight countries consider treatment novelty in methods and deliberations. METHODS: We defined a novel pharmaceutical product to be one that offers a new approach to treatment (e.g., new mechanism of action), addresses an unmet need (e.g., targets a rare condition without effective treatments), or has a broader impact beyond what is typically measured in an HTA. We reviewed peer-reviewed publications and technical guidance materials from HTA organizations in Australia, Canada, England, France, The Netherlands, Norway, Sweden, and the United States (US). In addition, we explored how HTA organizations integrated novelty considerations into deliberations and recommendations related to two newer therapies-voretigene neparvovec for an inherited retinal disorder and ocrelizumab for multiple sclerosis. RESULTS: None of the HTA organizations acknowledge treatment novelty as an explicit value criterion in their assessments of pharmaceutical products. However, drugs that have novel characteristics are given special consideration, particularly when they address an unmet need. Several organizations document a willingness to expend more resources and accept greater evidence uncertainty for such treatments. Qualitative deliberations about the additional unquantified potential benefits of treatment may also influence HTA recommendations. CONCLUSION: Major HTA organizations do not recognize novelty as an explicit value criterion, although drugs with novel characteristics may receive special consideration. There is an opportunity for organizations to codify their approach to evaluating novelty in value assessment.
 Intravascular endothelial hyperplasia is a benign soft tissue mass rarely reported in the foot. Advanced imaging and confirming a benign diagnosis are critical for any soft tissue mass. This paper identifies 2 patients that developed intravascular endothelial hyperplasia tumors which required surgical excision. A 17-year-old male patient presented to clinic complaining of a painful bump to the arch of his right foot which he related to an injury 9 months prior. Magnetic resonance imaging of the right foot revealed a mass within the plantar subcutaneous fat that was serpiginous in nature similar to adjacent branching vessels favoring a low-flow vascular malformation. A 38-year-old female with Multiple Sclerosis presented with complaints of persistent symptoms of pain to the 1(st) interspace, difficult ambulation and neuritis. Ultrasound and MRI observed solid, multilobulated mass, with internal vascular malformation, MRI describing intrinsic involvement along the abductor musculature and flexor tendons. Both lesions were surgically excised and sent for pathology. Pathology report indicated a diagnosis of intravascular papillary endothelial hyperplasia or Masson's tumor in both cases. Pathology diagnosis of intravascular papillary endothelial hyperplasia is generally good with wide resection leading to low recurrence rates. Both patients in the current study have progressed postoperatively with resolution of symptoms and without recurrence.
 INTRODUCTION: Coronavirus disease 2019 (COVID-19) has been recently associated with infarction of the central splenium of the corpus callosum. These are described as cytotoxic lesions, and imaging rarely reveals enhancement. They have not been described in the body or head of the corpus callosum. Few diseases affect the corpus callosum, but the most common include multiple sclerosis, aquaporin-4 disease, and Susac syndrome. There is also emerging literature on Mild Encephalopathy with Reversible Splenial lesions associated with central and not basal lesions. The reason for the location of these lesions in acute COVID-19 infection is unknown. CASE REPORT: A 22-year-old female presented to the ED for altered mental status after being found down. A brief history review indicated that the patient had been altered for 2-3 days before being found naked and covered in her own feces and urine by her family after they had not heard from her. As she lived alone, a clear history of the events preceding her admission remains unclear. On initial assessment, the patient was found to be somnolent and nonverbal, though she could follow simple commands. On admission, testing for SARS CoV-2 RNA PCR was positive. Patient was admitted to the hospital for further work up to determine the cause of the altered mental status. CONCLUSION: We present a new case of a young woman who developed a central splenium lesion during acute COVID-19 infection and explain the predilection for the callosum in these patients, as well as literature to show that COVID-19 was most likely the cause.
 Calcium is imperative in maintaining a quality life, particularly during later ages. Its deficiency results in a wide range of metabolic disorders such as dental changes, cataracts, alterations in brain function, and osteoporosis. These deficiencies are more pronounced in females due to increased calcium turnover throughout their life cycle, especially during pregnancy and lactation. Vitamin D perform a central role in the metabolism of calcium. Recent scientific interventions have linked calcium with an array of metabolic disorders in females including hypertension, obesity, premenstrual dysphoric disorder, polycystic ovary syndrome (PCOS), multiple sclerosis, and breast cancer. This review encompasses these female metabolic disorders with special reference to calcium and vitamin D deficiency. This review article aims to present and elaborate on available data regarding the worldwide occurrence of insufficient calcium consumption in females and allied health risks, to provide a basis for formulating strategies and population-level scientific studies to adequately boost calcium intake and position where required.
 Liver fibrosis is a typical pathological state/stage involved in most chronic liver diseases and its persistence results in cirrhosis. Inflammasomes are cytoplasmic sensors that induce inflammation in response to stress. Glibenclamide (GLB) is an USFDA-approved drug for type 2 diabetes and is reported to possess anti-inflammatory activity by inhibiting inflammatory cytokines. Dimethyl fumarate (DMF) is an USFDA-approved drug for multiple sclerosis and has been reported to activate the Nrf2/ARE pathway to maintain the cellular antioxidant balance. A total of 36 rats were randomized into six groups (n = 6 each). The rats were injected with thioacetamide (TAA) 200 mg/kg, intraperitoneally every third day for eight consecutive weeks to induce liver fibrosis and oral treatment of GLB 0.5 mg/kg/day and DMF 25 mg/kg/day, and their combinations were provided for the last four consecutive weeks. Treatment with GLB, DMF, and GLB+DMF significantly protected against TAA-mediated oxidative stress and inflammatory conditions by improving hepatic function test, triglycerides, hydroxyproline, and histopathological alterations, by inhibiting the NLRP3 inflammasome signaling and fibrogenic markers, and by activating Nrf2/ARE pathway in Wistar rats. The present results suggest that simultaneous Nrf2/ARE activation and NLRP3 inflammasome inhibition could significantly contribute to developing a novel therapy for patients with liver fibrosis.
 There is growing evidence that the long noncoding RNAs (lncRNAs) contribute to the pathogenesis of various neurodegenerative diseases such as multiple sclerosis (MS). The role of lncRNAs nuclear repressor of NFAT (NRON) and Taurine up-regulated 1 (TUG1) in the inflammatory processes occurring in the experimental autoimmune encephalomyelitis (EAE) model of MS is yet to be investigated. Transcript levels of NRON and TUG1 in acute and chronic phases of EAE and cultured macrophages as well as the correlation between NRON and TUG1 expression with inflammatory cytokines, were evaluated in this study. EAE experimental model was induced in female C57BL/6 mice with subcutaneous injection of MOG(35-55/)CFA. Mice were scored for 28 days and then sacrificed. The expression of lncRNAs TUG1 and NRON in lumbar spinal cords, activated and controlled macrophages as well as the expression of IL-1, IL-6, and CDe-3 inflammatory cytokines, were assayed by real-time RT-PCR. The lncRNAs TUG1 and NRON were significantly down-regulated in lumbar spinal cords tissues in the acute phase of EAE compared to the control group. TUG1 and NRON were significantly down-regulated in macrophages treated with 10 ng lipopolysaccharide (LPS) compared to the control macrophages. A negative correlation was identified between NRON and TUG1 expression and IL-1, IL-6, and CDe-3 inflammatory cytokines. The present study demonstrates the dysregulation of lncRNAs TUG1 and NRON in spinal cord tissue lesions of EAE and activated macrophages, pointing to their potential role in the pathogenesis of EAE.
 Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune disorder that was first described in the late 1800s as a variant of multiple sclerosis (MS). However, it has recently been categorized, as a disease, especially with the discovery of aquaporin-4 (AQP4-Ab) and myelin oligodendrocyte glycoprotein antibodies (MOG-Ab). Unfortunately, patient presentation is not always clear, and NMOSD may initially be diagnosed as an alternative neurological disease. We present a 58-year-old woman who was hospitalized several times for what was initially perceived as a pontine stroke. However, given worsening symptoms, serologic testing confirmed AQP4-Ab positivity and, subsequently, the NMOSD diagnosis. In addition to the case report, a systematic literature review was performed to identify NMOSD cases initially misdiagnosed as stroke. Publications were selected and curated in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Six NMOSD patients were initially thought to have had acute strokes. However, steady progression and/or the recurrence of symptoms suggested that further investigations with neuroimaging studies and serological immune assays were necessary to exclude alternative etiologies. Notably, the age at onset in all cases was significantly more advanced than patients with typical NMOSD presentations (median age 32-41). In conclusion, the NMOSD diagnosis should be considered in cases with atypical stroke-like presentations, particularly those of later onset (defined as equal to or greater than 50 years of age). This is important as early recognition and treatment with immune therapies can improve functional outcomes.
 BACKGROUND: Neuropathic pain is caused by a neurological injury or disease and can have a significant impact on people's daily lives. Studies have shown that neuropathic pain is commonly associated with neurodegenerative diseases. In recent years, there has been a lot of literature on the relationship between neuropathic pain and neurodegenerative diseases. However, bibliometrics is rarely used in analyzing the general aspects of studies on neuropathic pain in neurodegenerative diseases. METHODS: The bibliometric analysis software CiteSpace and VOSviewer were used to analyze the knowledge graph of 387 studies in the Science Citation Index Expanded of the Web of Science Core Collection Database. RESULTS: We obtained 2,036 documents through the search, leaving 387 documents after culling. 387 documents were used for the data analysis. The data analysis showed that 330 papers related to neuropathic pain in neurodegenerative diseases were published from 2007-2022, accounting for 85.27% of all published literature. In terms of contributions to the scientific study of neuropathic pain, the United States is in the top tier, with the highest number of publications, citations, and H-indexes. CONCLUSION: The findings in our study may provide researchers with useful information about research trends, frontiers, and cooperative institutions. Multiple sclerosis, Parkinson's disease, and Alzheimer's disease are the three most studied neurodegenerative diseases. Among the pathological basis of neurodegenerative diseases, microglia-regulated neuroinflammation is a hot research topic. Deep brain stimulation and gamma knife radiosurgery are two popular treatments.
 Although microvascular decompression (MVD) is a reliable treatment for trigeminal neuralgia (TN), neurosurgeons sometimes encounter patients whose symptoms do not improve postoperatively or who experience good treatment efficacy but develop other sensory disturbances. This study aims to objectively identify changes in nerve fibers before and after surgery by MRI and to clarify the relationship between the changes and residual postoperative symptoms. We retrospectively analyzed data from 36 consecutive patients who underwent MVD for classical TN at our hospital between November 2019 and November 2020. Cases that fulfilled the diagnostic criteria for multiple sclerosis were excluded. We confirmed the changes on the brainstem side of the trigeminal nerve preoperatively and at seven days postoperatively using 3D T2-SPACE MRI, in which the patients were divided into three groups: preoperative T2 high intensity positive (A), postoperative T2 high intensity positive (B), and no T2 high-intensity region (C). The primary outcome measures were therapeutic efficacy and frequency of postoperative numbness. The results of MVD surgery were evaluated one year postoperatively. The percentage of cases in which treatment outcomes were rated as excellent or good at one year: group A: 0 (0%), group B: 6 (100%), and group C: 25 (96.2%) (p < 0.05); the frequency of numbness: 2 (50%) in group A, 3 (50%) in group B, and 1 (3.8%) in group C, indicating significant differences between the three groups (p < 0.05). 3D T2-SPACE MRI sequences can be used to identify changes in trigeminal nerve fibers before and after MVD, which might correlate with eventual residual symptoms.
 Royal jelly is a yellowish to white gel-like substance that is known as a "superfood" and consumed by queen bees. There are certain compounds in royal jelly considered to have health-promoting properties, including 10-hydroxy-2-decenoic acid and major royal jelly proteins. Royal jelly has beneficial effects on some disorders such as cardiovascular disease, dyslipidemia, multiple sclerosis, and diabetes. Antiviral, anti-inflammatory, antibacterial, antitumor, and immunomodulatory properties have been ascribed to this substance. This chapter describes the effects of royal jelly on COVID-19 disease.
 The first commercially available 7-T MRI scanner (Magnetom Terra) was approved by the FDA in 2017 for clinical imaging of the brain and knee. Following initial protocol development and sequence optimization efforts in volunteers, we now routinely use the 7-T system, in combination with an FDA-approved 1-channel transmit/32-channel receive array head coil, for brain MRI examinations in clinical patients. The ultra-highfield strength of 7-T MRI has the advantages of improved spatial resolution, increased SNR, and increased CNR, but also introduces an array of new technical challenges. This Clinical Perspective describes our institutional experience in the use of the commercially available 7-T MRI scanner for routine brain imaging in clinical patients. We discuss specific clinical indications where 7-T MRI may be useful for brain imaging, including brain tumor evaluation with possible perfusion imaging and/or spectroscopy, radiotherapy planning; multiple sclerosis or other demyelinating diseases; Parkinson disease and guidance of deep brain stimulator placement; high-detail intracranial MRA and vessel wall imaging; pituitary pathology; and epilepsy. For these various indications, we present detailed protocols, including sequence parameters. We also explore implementation challenges (including artifacts, safety, and side effects) and potential solutions.
 Chronic pain conditions create major financial and emotional burdens that can be devastating for individuals and society. One primary source of pain is arthritis, a common inflammatory disease of the joints that causes persistent pain in affected people. The main objective of pharmacological treatments for either rheumatoid arthritis (RA) or osteoarthritis (OA) is to reduce pain. Non-steroidal anti-inflammatory drugs, opioids, and opioid antagonists have each been considered in the management of chronic pain in arthritis patients. Naltrexone is an oral-activated opioid antagonist with biphasic dose-dependent pharmacodynamic effects. The molecule acts as a competitive inhibitor of opioid receptors at high doses. However, naltrexone at low doses has been shown to have hormetic effects and provides relief for chronic pain conditions such as fibromyalgia, multiple sclerosis (MS), and inflammatory bowel disorders. Current knowledge of naltrexone suggests that low-dose treatments may be effective in the treatment of pain perception in chronic inflammatory conditions observed in patients with either RA or OA. In this review, we evaluated the therapeutic benefits of low-dose naltrexone (LDN) on arthritis-related pain conditions.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a demyelinating syndrome of the central nervous system. A tremendous amount of literature on NMOSD has been published. This study aimed to perform a bibliometric analysis of the publications on NMOSD and show its hotspots and development trends. METHODS: We used the Web of Science Core Collection as a database and searched the literature published between 2002 and 2022. CiteSpace, VOSviewer, online bibliometric platform, and R-bibliometrix were used to conduct bibliometric analysis and network visualization, including the number of publications, citations, countries/regions, institutions, journals, authors, references, and keywords. RESULTS: A total of 3,057 publications on NMOSD were published in 198 journals by 200 authors at 200 institutions from 93 countries/regions. The United States published the most literature and made great contributions to this field. The Mayo Clinic was the institution with the largest number of publications. The journal with the most publications was Multiple Sclerosis and Related Disorders, and the most co-cited journal was Neurology. The author with the most publications was Fujihara, K., while the most frequently co-cited author was Wingerchuk, DM. The current research hotspots may be focused on "efficacy," "multicenter," "interleukin-6 receptor blockade," "safety," "azathioprine," "tolerance," and "adult". CONCLUSION: This study was the first bibliometric analysis of publications on the NMOSD field, visualizing its bibliometric characteristics and gaining insight into the direction, hotspots, and development of global NMOSD research, which may provide helpful information for researchers. Future research hotspots might be conducting randomized controlled trials on targeted immunotherapy in the NMOSD field.
 Understanding the diagnostic goal of medical reports is valuable information for understanding patient flows. This work focuses on extracting the reason for taking an MRI scan of Multiple Sclerosis (MS) patients using the attached free-form reports: Diagnosis, Progression or Monitoring. We investigate the performance of domain-dependent and general state-of-the-art language models and their alignment with domain expertise. To this end, eXplainable Artificial Intelligence (XAI) techniques are used to acquire insight into the inner workings of the model, which are verified on their trustworthiness. The verified XAI explanations are then compared with explanations from a domain expert, to indirectly determine the reliability of the model. BERTje, a Dutch Bidirectional Encoder Representations from Transformers (BERT) model, outperforms RobBERT and MedRoBERTa.nl in both accuracy and reliability. The latter model (MedRoBERTa.nl) is a domain-specific model, while BERTje is a generic model, showing that domain-specific models are not always superior. Our validation of BERTje in a small prospective study shows promising results for the potential uptake of the model in a practical setting.
 Acrolein, a highly reactive unsaturated aldehyde, is a ubiquitous environmental pollutant that seriously threatens human health and life. Due to its high reactivity, cytotoxicity and genotoxicity, acrolein is involved in the development of several diseases, including multiple sclerosis, neurodegenerative diseases such as Alzheimer's disease, cardiovascular and respiratory diseases, diabetes mellitus and even the development of cancer. Traditional tobacco smokers and e-cigarette users are particularly exposed to the harmful effects of acrolein. High concentrations of acrolein have been found in both mainstream and side-stream tobacco smoke. Acrolein is considered one of cigarette smoke's most toxic and harmful components. Chronic exposure to acrolein through cigarette smoke has been linked to the development of asthma, acute lung injury, chronic obstructive pulmonary disease (COPD) and even respiratory cancers. This review addresses the current state of knowledge on the pathological molecular mechanisms of acrolein in the induction, course and development of lung diseases and cancers in smokers.
 Demyelination is a hallmark of multiple sclerosis, leukoencephalopathies, cerebral vasculopathies, and several neurodegenerative diseases. The cuprizone mouse model is widely used to simulate demyelination and remyelination occurring in these diseases. Here, we present a high-resolution single-nucleus RNA sequencing (snRNA-seq) analysis of gene expression changes across all brain cells in this model. We define demyelination-associated oligodendrocytes (DOLs) and remyelination-associated MAFB(hi) microglia, as well as astrocytes and vascular cells with signatures of altered metabolism, oxidative stress, and interferon response. Furthermore, snRNA-seq provides insights into how brain cell types connect and interact, defining complex circuitries that impact demyelination and remyelination. As an explicative example, perturbation of microglia caused by TREM2 deficiency indirectly impairs the induction of DOLs. Altogether, this study provides a rich resource for future studies investigating mechanisms underlying demyelinating diseases.
 Dynamic loads have short and long-term effects in the rehabilitation of lower limb joints. However, an effective exercise program for lower limb rehabilitation has been debated for a long time. Cycling ergometers were instrumented and used as a tool to mechanically load the lower limbs and track the joint mechano-physiological response in rehabilitation programs. Current cycling ergometers apply symmetrical loading to the limbs, which may not reflect the actual load-bearing capacity of each limb, as in Parkinson's and Multiple Sclerosis diseases. Therefore, the present study aimed to develop a new cycling ergometer capable of applying asymmetric loads to the limbs and validate its function using human tests. The instrumented force sensor and crank position sensing system recorded the kinetics and kinematics of pedaling. This information was used to apply an asymmetric assistive torque only to the target leg using an electric motor. The performance of the proposed cycling ergometer was studied during a cycling task at three different intensities. It was shown that the proposed device reduced the pedaling force of the target leg by 19% to 40%, depending on the exercise intensity. This reduction in pedal force caused a significant reduction in the muscle activity of the target leg (p < 0.001), without affecting the muscle activity of the non-target leg. These results demonstrated that the proposed cycling ergometer device is capable of applying asymmetric loading to lower limbs, and thus has the potential to improve the outcome of exercise interventions in patients with asymmetric function in lower limbs.
 P2X7R, which is a member of the purinergic P2 receptor family, is widely expressed in many immune cells, such as macrophages, lymphocytes, monocytes, and neutrophils. P2X7R is upregulated in response to proinflammatory stimulation, which is closely related to a variety of inflammatory diseases. The inhibition of P2X7 receptors has resulted in the elimination or reduction of symptoms in animal models of arthritis, depression, neuropathic pain, multiple sclerosis, and Alzheimer's disease. Therefore, the development of P2X7R antagonists is of great significance for the treatment of various inflammatory diseases. This review classifies the reported P2X7R antagonists according to their different cores, focuses on the structure-activity relationship (SAR) of the compounds, and analyzes some common substituents and strategies in the design of lead compounds, with the hope of providing valuable information for the development of new and efficient P2X7R antagonists.
 The gut-brain axis augments the bidirectional communication between the gut and brain and modulates gut homeostasis and the central nervous system through the hypothalamic-pituitary-adrenal axis, enteroendocrine system, neuroendocrine system, inflammatory and immune pathways. Preclinical and clinical reports showed that gut dysbiosis might play a major regulatory role in neurological diseases such as epilepsy, Parkinson's, multiple sclerosis, and Alzheimer's disease. Epilepsy is a chronic neurological disease that causes recurrent and unprovoked seizures, and numerous risk factors are implicated in developing epilepsy. Advanced consideration of the gut-microbiota-brain axis can reduce ambiguity about epilepsy pathology, antiepileptic drugs, and effective therapeutic targets. Gut microbiota sequencing analysis reported that the level of Proteobacteria, Verrucomicrobia, Fusobacteria, and Firmicutes was increased and the level of Actinobacteria and Bacteroidetes was decreased in epilepsy patients. Clinical and preclinical studies also indicated that probiotics, ketogenic diet, faecal microbiota transplantation, and antibiotics can improve gut dysbiosis and alleviate seizure by enhancing the abundance of healthy biota. This study aims to give an overview of the connection between gut microbiota, and epilepsy, how gut microbiome changes may cause epilepsy, and whether gut microbiome restoration could be used as a treatment for epilepsy.
 BACKGROUND: General practitioners are well positioned to contribute to the pharmacovigilance of medical cannabis via the general practice electronic medical record (EMR). The aim of this research is to interrogate de-identified patient data from the Patron primary care data repository for reports of medicinal cannabis to ascertain the feasibility of using EMRs to monitor medicinal cannabis prescribing in Australia. METHODS: EMR rule-based digital phenotyping of 1 164 846 active patients from 109 practices was undertaken to investigate reports of medicinal cannabis use from September 2017 to September 2020. RESULTS: Eighty patients with 170 prescriptions of medicinal cannabis were identified in the Patron repository. Reasons for prescription included anxiety, multiple sclerosis, cancer, nausea, and Crohn's disease. Nine patients showed symptoms of a possible adverse event, including depression, motor vehicle accident, gastrointestinal symptoms, and anxiety. CONCLUSIONS: The recording of medicinal cannabis effects in the patient EMR provides potential for medicinal cannabis monitoring in the community. This is especially feasible if monitoring were to be embedded into general practitioner workflow.
 The brain-gut axis forms a bidirectional communication system between the gastrointestinal (GI) tract and cognitive brain areas. Disturbances to this system in disease states such as inflammatory bowel disease have consequences for neuronal activity and subsequent cognitive function. The gut-microbiota-brain axis refers to the communication between gut-resident bacteria and the brain. This circuits exists to detect gut microorganisms and relay information to specific areas of the central nervous system (CNS) that in turn, regulate gut physiology. Changes in both the stability and diversity of the gut microbiota have been implicated in several neuronal disorders, including depression, autism spectrum disorder Parkinson's disease, Alzheimer's disease and multiple sclerosis. Correcting this imbalance with medicinal herbs, the metabolic products of dysregulated bacteria and probiotics have shown hope for the treatment of these neuronal disorders. In this review, we focus on recent advances in our understanding of the intricate connections between the gut-microbiota and the brain. We discuss the contribution of gut microbiota to neuronal disorders and the tangible links between diseases of the GI tract with cognitive function and behaviour. In this regard, we focus on irritable bowel syndrome (IBS) given its strong links to brain function and anxiety disorders. This adds to the growing body of evidence supporting targeted therapeutic strategies to modulate the gut microbiota for the treatment of brain/mental-health-related disease.
 Sphingosine-1-phosphate (S1P) is generated intracellularly and, when transported to the extracellular compartment, predominantly signals through S1P receptors. The S1P signalling pathway has been implicated in the pathophysiology of neurological injury following aneurysmal subarachnoid haemorrhage (aSAH). In this review, we bring together all the available data regarding the role of S1P in neurological injury following aSAH. There is agreement in the literature that S1P increases in the cerebrospinal fluid following aSAH and leads to cerebral artery vasospasm. On the other hand, the role of S1P in the parenchyma is less clear cut, with different studies arguing for beneficial and deleterious effects. A parsimonious interpretation of this apparently conflicting data is presented. We discuss the potential of S1P receptor modulators, in clinical use for multiple sclerosis, to be repurposed for aSAH. Finally, we highlight the gaps in our knowledge of S1P signalling in humans, the clinical challenges of targeting the S1P pathway after aSAH and other research priorities.
 CNS inflammation triggers activation of the integrated stress response (ISR). We previously reported that prolonging the ISR protects remyelinating oligodendrocytes and promotes remyelination in the presence of inflammation (Chen et al., eLife , 2021). However, the exact mechanisms through which this occurs remain unknown. Here, we investigated whether the ISR modulator Sephin1 in combination with the oligodendrocyte differentiation enhancing reagent bazedoxifene (BZA) is able to accelerate remyelination under inflammation, and the underlying mechanisms mediating this pathway. We find that the combined treatment of Sephin1 and BZA is sufficient to accelerate early-stage remyelination in mice with ectopic IFN-γ expression in the CNS. IFN-γ, which is a critical inflammatory cytokine in multiple sclerosis (MS), inhibits oligodendrocyte precursor cell (OPC) differentiation in culture and triggers a mild ISR. Mechanistically, we further show that BZA promotes OPC differentiation in the presence of IFN-γ, while Sephin1 enhances the IFN-γ-induced ISR by reducing protein synthesis and increasing RNA stress granule formation in differentiating oligodendrocytes. Finally, the ISR suppressor 2BAct is able to partially lessen the beneficial effect of Sephin1 on disease progression, in an MS mouse model of experimental autoimmune encephalitis (EAE). Overall, our findings uncover distinct mechanisms of action of BZA and Sephin1 on oligodendrocyte lineage cells under inflammatory stress, suggesting that a combination therapy may effectively promote restoring neuronal function in MS patients.
 The purpose of this paper is to confirm previous reports that identified magnetization transfer (MT) as an inherent driver of longitudinal relaxation in brain tissue by asserting a substantial difference between the $T_1$ relaxation times of the free and the semi-solid spin pools. Further, we aim to identify an avenue towards the quantification of these relaxation processes on a voxel-by-voxel basis in a clinical imaging setting, i.e. with a nominal resolution of 1mm isotropic and full brain coverage in 12min. To this end, we optimized a hybrid-state pulse sequence for mapping the parameters of an unconstrained MT model. We scanned 4 people with relapsing-remitting multiple sclerosis (MS) and 4 healthy controls with this pulse sequence and estimated $T_1^f \approx 1.90$s and $T_1^s \approx 0.327$s for the free and semi-solid spin pool of healthy WM, respectively, confirming previous reports and questioning the commonly used assumptions $T_1^s = T_1^f$ or $T_1^s = 1$s. Further, we estimated a fractional size of the semi-solid spin pool of $m_0^s \approx 0.202$, which is larger than previously assumed. An analysis of $T_1^f$ in normal appearing white matter revealed statistically significant differences between individuals with MS and controls. In conclusion, we confirm that longitudinal spin relaxation in brain tissue is dominated by MT and that the hybrid state facilitates a voxel-wise fit of the unconstrained MT model, which enables the analysis of subtle neurodegeneration.
 Necroptosis, a regulated form of cell death, is involved in the genesis and development of various life-threatening diseases, including cancer, neurological disorders, cardiac myopathy, and diabetes. Necroptosis initiates with the formation and activation of a necrosome complex, which consists of RIPK1, RIPK2, RIPK3, and MLKL. Emerging studies has demonstrated the regulation of the necroptosis cell death pathway through the implication of numerous post-translational modifications, namely ubiquitination, acetylation, methylation, SUMOylation, hydroxylation, and others. In addition, the negative regulation of the necroptosis pathway has been shown to interfere with brain homeostasis through the regulation of axonal degeneration, mitochondrial dynamics, lysosomal defects, and inflammatory response. Necroptosis is controlled by the activity and expression of signaling molecules, namely VEGF/VEGFR, PI3K/Akt/GSK-3β, c-Jun N-terminal kinases (JNK), ERK/MAPK, and Wnt/β-catenin. Herein, we briefly discussed the implication and potential of necrosome activation in the pathogenesis and progression of neurological manifestations, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, traumatic brain injury, and others. Further, we present a detailed picture of natural compounds, micro-RNAs, and chemical compounds as therapeutic agents for treating neurological manifestations.
 BACKGROUND: Apart from reducing the circulating LDL-c and the number of cardiovascular cases as well as fatalities, statins have auxiliary non-lipid-related or cholesterol independent effects, the pleiotropic effects. The aim of the present review is to understand the pleotropic effects of statins. MAIN BODY: Cardiovascular disease (CVD) is presently the major cause of patient misery as well as mortality among non-communicable diseases (NCDs) in the world. Despite the fact that statins are the most extensively affirmed, prescribed and evidence-based lipid-lowering medicine worldwide that curtail low density lipoprotein cholesterol (LDL-c) levels and the number of cardiovascular cases as well as deaths, statins also elicit auxiliary non-lipid-related or cholesterol independent effects, the pleiotropic effects. Improved endothelial function, significantly lowered oxidative stress, atherosclerotic plaque stabilization, immunomodulatory, cessation of vascular smooth muscle proliferation, effects on bone metabolism, anti-inflammatory, antithrombotic effects, and reduced risk of dementia are among these pleotropic effects. Statins have also been explored for its uses in life threatening diseases like cancer and inflammatory bowel disease. They have been demonstrated to revamp vascular tone. Many research and review articles have been thoroughly studied for this systematic review. CONCLUSIONS: Statins have not only shown to be benefitial in lowering the levels of LDL-C but have also been established to be advantageous in the treatment of cancer, neurological conditions like dementia, multiple sclerosis, inflammatory bowel disease. Future high-quality trials are needed to include statins in the treatment of these conditions as per guidelines.
 Autoimmune diseases are characterized by the recognition of self-antigens by the immune system, which leads to inflammation and tissue damage. B cells are directly and indirectly involved in the pathophysiology of autoimmunity, both via antigen-presentation to T cells and production of proinflammatory cytokines and/or autoantibodies. Consequently, B lineage cells have been identified as therapeutic targets in autoimmune diseases. B cell depleting strategies have proven beneficial in the treatment of rheumatoid arthritis (RA), systemic lupus erythematous (SLE), ANCA-associated vasculitis (AAV), multiple sclerosis (MS), and a wide range of other immune-mediated inflammatory diseases (IMIDs). However, not all patients respond to treatment or may not reach (drug-free) remission. Moreover, B cell depleting therapies do not always target all B cell subsets, such as short-lived and long-lived plasma cells. These cells play an active role in autoimmunity and in certain diseases their depletion would be beneficial to achieve disease remission. In the current review article, we provide an overview of novel strategies to target B lineage cells in autoimmune diseases, with the focus on rheumatic diseases. Both advanced therapies that have recently become available and more experimental treatments that may reach the clinic in the near future are discussed.
 T2 mapping from 2D proton density and T2-weighted images (PD-T2) using Bloch equation simulations can be time consuming and introduces a latency between image acquisition and T2 map production. A fast T2 mapping reconstruction method is investigated and compared with a previous modeling approach to reduce computation time and allow inline T2 maps on the MRI console. Brain PD-T2 images from five multiple sclerosis patients were used to compare T2 map reconstruction times between the new subtraction method and the Euclidean norm minimization technique. Bloch equation simulations were used to create the lookup table for decay curve matching in both cases. Agreement of the two techniques used Bland-Altman analysis for investigating individual subsets of data and all image points in the five volumes (meta-analysis). The subtraction method resulted in an average reduction of computation time for single slices from 134 s (minimization method) to 0.44 s. Comparing T2 values between the subtraction and minimization methods resulted in a confidence interval ranging from -0.06 to 0.06 ms (95% of values were within ± 0.06 ms between the techniques). Using identical reconstruction code based on the subtraction method, inline T2 maps were produced from PD-T2 images directly on the scanner console. The excellent agreement between the two methods permits the subtraction technique to be interchanged with the previous method, reducing computation time and allowing inline T2 map reconstruction based on Bloch simulations directly on the scanner.
 Myelin oligodendrocyte glycoprotein-immunoglobulin G (IgG)-associated optic neuritis has been established as a new entity of immune-mediated optic neuropathy. Patients usually present with recurrent optic neuritis, often bilaterally with initially severe vision loss and optic disc edema. However, in contrast to aquaporin 4-IgG-seropositive neuromyelitis optica spectrum disorder, visual recovery tends to be more favorable, with good response to steroid treatment. Another important differential diagnosis of myelin oligodendrocyte glycoprotein-IgG--associated optic neuritis is multiple sclerosis. Close monitoring for signs of relapse and long-term immunosuppression may be considered to maintain optimal visual function. The diagnosis can be made on the basis of the presence of a specific, usually serological, antibody against myelin oligodendrocyte glycoprotein (IgG; cell-based assay), and a demyelinating event (optic neuritis, myelitis, brainstem syndrome, or cortical lesions with seizures). The clinical spectrum of this newly recognized inflammatory demyelinating disease is expanding rapidly. We briefly review the epidemiological characteristics, clinical manifestations, diagnostic considerations, and treatment options of myelin oligodendrocyte glycoprotein-IgG-associated optic neuritis.
 PURPOSE: Peer-based interventions are increasingly popular and cost-effective therapeutic opportunities to support others experiencing similar life circumstances. However, little is known about the similarities and differences among peer-based interventions and their outcomes for people with neurological conditions. This scoping review aims to describe and compare the characteristics of existing peer-based interventions for adults with common neurological conditions. MATERIALS AND METHODS: We searched MEDLINE, CINAHL, PsychInfo, and Embase for research on peer-based interventions for individuals with brain injury, Parkinson's, multiple sclerosis, spinal cord injury, and stroke up to June 2019. The search was updated in March 2021. Fifty-three of 2472 articles found were included. RESULTS: Characteristics of peer-based intervention for this population vary significantly. They include individual and group-based formats delivered in-person, by telephone, or online. Content varied from structured education to tailored approaches. Participant outcomes included improved health, confidence, and self-management skills; however, these varied based on the intervention model. CONCLUSION: Various peer-based interventions exist, each with its own definition of what it means to be a peer. Research using rigorous methodology is needed to determine the most effective interventions. Clear definitions of each program component are needed to better understand the outcomes and mechanism of action within each intervention.IMPLICATIONS FOR REHABILITATIONRehabilitation services can draw on various peer support interventions to add experiential knowledge and support based on shared experience to enhance outcomes.Fulfilling the role of peer mentor may be beneficial and could be encouraged as part of the rehabilitation process for people with SCI, TBI, Stroke, PD, or MS.In planning peer-based interventions for TBI, Stroke, SCI, PD, and MS populations, it is important to clearly define intervention components and evaluate outcomes to measure the impact of the intervention.
 In multiple sclerosis (MS), microglia and macrophages within the central nervous system (CNS) play an important role in determining the balance between myelin repair and demyelination/neurodegeneration. Phagocytic and regenerative functions of these CNS innate immune cells support remyelination, whereas chronic and maladaptive inflammatory activation promotes lesion expansion and disability, particularly in the progressive forms of MS. No currently approved drugs convincingly target microglia and macrophages within the CNS, contributing to the critical lack of therapies promoting remyelination and slowing progression in MS. Here, we found that the protein kinase C (PKC)-modulating drug bryostatin-1 (bryo-1), a CNS-penetrant compound with an established human safety profile, produces a shift in microglia and CNS macrophage transcriptional programs from pro-inflammatory to regenerative phenotypes, both in vitro and in vivo. Treatment of microglia with bryo-1 prevented the activation of neurotoxic astrocytes while stimulating scavenger pathways, phagocytosis, and secretion of factors that promote oligodendrocyte differentiation. In line with these findings, systemic treatment with bryo-1 augmented remyelination following a focal demyelinating injury in vivo. Our results demonstrate the potential of bryo-1 and functionally related PKC modulators as myelin regenerative and neuroprotective agents in MS and other neurologic diseases through therapeutic targeting of microglia and CNS-associated macrophages. ONE SENTENCE SUMMARY: PKC modulation in CNS innate immune cells favors the activation of a beneficial phenotype that promotes myelin regeneration and neuroprotection.
 OBJECTIVE: This study evaluated the volume of thickened dura mater lesions and their impact on clinical findings in immune-mediated hypertrophic pachymeningitis (HP). METHODS: The volume of contrast-enhanced dura mater on magnetic resonance imaging was evaluated using the imaging feature quantification system in 19 patients with immune-mediated HP, including 12 with antineutrophil cytoplasmic antibody-related, 4 with IgG4-related, and 3 with idiopathic HP, as well as 10 with multiple sclerosis (MS) as controls. The implications of HP volume on neurological manifestations and cerebrospinal fluid (CSF) laboratory markers were statistically analyzed in patients with immune-mediated HP. RESULTS: The volumes of the contrast-enhanced dura mater in the convexity, cranial fossa, and tentorium cerebelli were significantly higher in patients with immune-mediated HP than in those with MS. Among patients with immune-mediated HP, those with cranial nerve (CN) VIII neuropathy had a significantly higher volume of the contrast-enhanced dura mater in the cranial fossa than those without CN VIII neuropathy. The volume of the contrast-enhanced dura mater in the tentorium cerebelli was positively correlated with CSF protein levels. CONCLUSION: Quantification of the thickened dura mater is useful for elucidating the relationship with the clinical findings in immune-mediated HP. Thickened dura mater lesions in the cranial fossa may be implicated in the development of CN VIII neuropathy. The enlargement of HP lesions in the tentorium cerebelli can increase CSF protein levels.
 TRPM7, a TRP channel with ion conductance and kinase activities, has emerged as an attractive drug target for immunomodulation. Reverse genetics and cell biological studies have already established a key role for TRPM7 in the inflammatory activation of macrophages. Advancing TRPM7 as a viable molecular target for immunomodulation requires selective TRPM7 inhibitors with in vivo tolerability and efficacy. Such inhibitors have the potential to interdict inflammatory cascades mediated by systemic and tissue-specialized macrophages. FTY720, an FDA-approved drug for multiple sclerosis inhibits TRPM7. However, FTY720 is a prodrug and its metabolite, FTY720-phosphate, is a potent agonist of sphingosine 1-phosphate (S1P) receptors. In this study, we tested non-phosphorylatable FTY720 analogs, which are inert against S1PRs and well tolerated in vivo , for activity against TRPM7 and tissue bioavailability. Using patch clamp electrophysiology, we show that VPC01091.4 and AAL-149 block TRPM7 current at low micromolar concentrations. In culture, they act directly on macrophages to blunt LPS-induced inflammatory cytokine expression, an effect that is predominantly but not solely mediated by TRPM7. We found that VPC01091.4 has significant and rapid accumulation in the brain and lungs, along with direct anti-inflammatory action on alveolar macrophages and microglia. Finally, using a mouse model of endotoxemia, we show VPC01091.4 to be an efficacious anti-inflammatory agent that arrests systemic inflammation in vivo . Together, these findings identify novel small molecule inhibitors that allow TRPM7 channel inhibition independent of S1P receptor targeting. These inhibitors exhibit potent anti-inflammatory properties that are mediated by TRPM7 and likely other molecular targets that remain to be identified.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a neuroimmune disease, i.e. under constant research. The aim of this bibliometric study is to perform a bibliometric indicator analysis of the worldwide academic production of NMOSD during the period 2017-2021. METHODS: A bibliographic search was assessed in the Scopus database to identify NMOSD-related articles published during the period 2017-2021. Collected publications were exported and analyzed in Scival (Elsevier). Bibliographic data were described through absolute values and percentages in descriptive tables. VOSviewer was used to visualize collaborative networks. RESULTS: A total of 1920 documents were collected, and the highest percentage of these belonged to the area of neurology. Friedemann Paul was the author with the highest scientific production, but Brian Weinshenker had the greatest impact worldwide. Three of the institutions with the highest production were North American. Multiple sclerosis and related disorders were the journal with the highest production of publications. Most papers were published in Q1 or Q2 journals. CONCLUSION: NMOSD-related articles are mostly published in first and second quartile journals, which would reflect a high interest of the scientific community. Publications with international collaboration reported a higher impact. Although African and South American regions have considerable prevalence of this disease, they do not have institutions with high productivity developing research on this disease.
 Tolerogenic dendritic cells (tolDCs) are a promising strategy to treat autoimmune diseases since they have the potential to re-educate and modulate pathological immune responses in an antigen-specific manner and, therefore, have minimal adverse effects on the immune system compared to conventional immunosuppressive treatments. TolDC therapy has demonstrated safety and efficacy in different experimental models of autoimmune disease, such as multiple sclerosis (MS), type 1 diabetes (T1D), and rheumatoid arthritis (RA). Moreover, data from phase I clinical trials have shown that therapy with tolDCs is safe and well tolerated by MS, T1D, and RA patients. Nevertheless, various parameters need to be optimized to increase tolDC efficacy. In this regard, one important parameter to be determined is the most appropriate route of administration. Several delivery routes, such as intravenous, subcutaneous, intraperitoneal, intradermal, intranodal, and intraarticular routes, have been used in experimental models as well as in phase I clinical trials. This review summarizes data obtained from preclinical and clinical studies of tolDC therapy in the treatment of MS, T1D, and RA and their animal models, as well as data from the context of cancer immunotherapy using mature peptide-loaded DC, and data from in vivo cell tracking experiments, to define the most appropriate route of tolDC administration in relation to the most feasible, safest, and effective therapeutic use.
 BACKGROUND: Thalamic pain syndrome (TPS) is an enigmatic and rare condition. Thalamic pain syndrome is under the umbrella of central pain syndrome, which is classically associated with multiple sclerosis, spinal cord injury, postamputation, epilepsy, stroke, tumor, and Parkinson's disease. The mainstay treatment of TPS is polypharmacy. There is uncertainty about the intermediate options to manage medication-resistant TPS before resorting to invasive, and often expensive, intracranial therapies. Stellate ganglion block (SGB) has shown promise in reducing TPS symptoms of the upper extremity and face following a thalamic ischemic event. AIMS: Discuss the effect and potential utility of SGB on ipsilateral headache, facial, and upper extremity neuropathic pain due to thalamic malignancies. MATERIALS AND METHODS: A review of two patient records that underwent SGB for treatment of TPS of oncologic origin. RESULTS: We present two cases of the successful use of SGB for the treatment of oncologic-related TPS for patients who had failed other conservative pharmacologic measures. DISCUSSION: Chronic pain is a complex experience that often simultaneously involves psychosocial, neuropathic, and nociceptive constituents. Among advanced cancer patients, factors such as an individual's spirituality, psychological stressors, and views on their mortality add layers of intricacy in addressing their pain. While TPS has been characterized in both stroke populations and oncologic populations, the treatment of SGB for pain relief in TPS has been limited to the stroke population. Repeated SGB worked to alleviate the ipsilateral headache, facial, and upper extremity pain in these two patients. The benefits of utilization of SGB, with the possibility of pain relief, within the thalamic malignancy population cannot be understated. CONCLUSION: In summary, ultrasound-guided SGB may be considered in patients with TPS due to thalamic cancer, before pursuing more invasive intracranial surgeries to treat pain.
 Inflammasome complexes and their integral receptor proteins have essential roles in regulating the innate immune response and inflammation at the post-translational level. Yet despite their protective role, aberrant activation of inflammasome proteins and gain of function mutations in inflammasome component genes seem to contribute to the development and progression of human autoimmune and autoinflammatory diseases. In the past decade, our understanding of inflammasome biology and activation mechanisms has greatly progressed. We therefore provide an up-to-date overview of the various inflammasomes and their known mechanisms of action. In addition, we highlight the involvement of various inflammasomes and their pathogenic mechanisms in common autoinflammatory, autoimmune and neurodegenerative diseases, including atherosclerosis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, Alzheimer's disease, Parkinson's disease, and multiple sclerosis. We conclude by speculating on the future avenues of research needed to better understand the roles of inflammasomes in health and disease.
 Intrathecal therapy began to emerge in the late 1970s when the World Health Organization (WHO) placed attention on a more careful treatment of cancer pain. Later on, the interest in the use of intrathecal catheters for intrathecal administrations of drugs increased after the clinical demonstration of the efficacy of intrathecal morphine. In 1978, indeed, Wang et al. and later, Ventafridda et al. demonstrated that subarachnoid injections of morphine attenuated pain in patients with cancer. The next step was the intrathecal administration of morphine through implantable reservoirs. The first to describe the use of an implantable pump for the administration of intrathecal drugs was Onofrio, in 1981, followed by several clinical cases and several clinical investigations. With proven efficacy, intrathecal therapy quickly came into use for the management of intractable pain for both cancer and non-cancerous pain. An intrathecal catheter can also be used to prevent post-dural puncture headache (PDPH) following an accidental dural puncture during epidural anesthesia (e.g., in parturients). Through this approach, the catheter can be used to provide analgesia (local anesthetics) and gets removed after at least 24 hours. Finally, since 1984, intrathecal therapy has also been used for severe spasticity in individuals affected by multiple sclerosis (MS), spinal cord injury (SCI), cerebral palsy (CP), and in patients with acquired brain injury (stroke). In the management of spasticity, baclofen is the recommended pharmacological treatment of choice. Attempts have also been made to use intrathecal baclofen for the treatment of tetanus spasticity. In summary: The advantages of intrathecal therapy include better analgesia with fewer side effects and a lower dose of drugs administered as the drug is taken directly to the receptors with a good impact on severe spasticity in adults and children. The disadvantages include the risks associated with the procedure, infections, side effects of the drugs administered, and costs.
 Ubiquitously expressed in mammalian cells, the Kelch-like ECH-associated protein 1 (Keap1)-NF erythroid 2-related factor 2 (Nrf2) complex forms the evolutionarily conserved antioxidation system to tackle oxidative stress caused by reactive oxygen species. Reactive oxygen species, generated as byproducts of cellular metabolism, were identified as essential second messengers for T cell signaling, activation, and effector responses. Apart from its traditional role as an antioxidant, a growing body of evidence indicates that Nrf2, tightly regulated by Keap1, modulates immune responses and regulates cellular metabolism. Newer functions of Keap1 and Nrf2 in immune cell activation and function, as well as their role in inflammatory diseases such as sepsis, inflammatory bowel disease, and multiple sclerosis, are emerging. In this review, we highlight recent findings about the influence of Keap1 and Nrf2 in the development and effector functions of adaptive immune cells, that is, T cells and B cells, and discuss the knowledge gaps in our understanding. We also summarize the research potential and targetability of Nrf2 for treating immune pathologies.
 The S1P1 receptor is the target of four marketed drugs for the treatment of multiple sclerosis and ulcerative colitis. Targeting an S1P exporter, specifically Spns2, that is "upstream" of S1P receptor engagement is an alternate strategy that might recapitulate the efficacy of S1P receptor modulators without cardiac toxicity. We recently reported the first Spns2 inhibitor SLF1081851 (16d) that has modest potency with in vivo activity. To develop more potent compounds, we initiated a structure-activity relationship study that identified 2-aminobenzoxazole as a viable scaffold. Our studies revealed SLB1122168 (33p), which is a potent inhibitor (IC(50) = 94 ± 6 nM) of Spns2-mediated S1P release. Administration of 33p to mice and rats resulted in a dose-dependent decrease in circulating lymphocytes, a pharmacodynamic indication of Spns2 inhibition. 33p provides a valuable tool compound to explore both the therapeutic potential of targeting Spns2 and the physiologic consequences of selective S1P export inhibition.
 Cannabis belongs to the family Cannabaceae, and phytocannabinoids are produced by the Cannabis sativa L. plant. A long-standing debate regarding the plant is whether it contains one or more species. Phytocannabinoids are bioactive natural products found in flowers, seeds, and fruits. They can be beneficial for treating human diseases (such as multiple sclerosis, neurodegenerative diseases, epilepsy, and pain), the cellular metabolic process, and regulating biological function systems. In addition, several phytocannabinoids are used in various therapeutic and pharmaceutical applications. This study provides an overview of the different sources of phytocannabinoids; further, the biosynthesis of bioactive compounds involving various pathways is elucidated. The structural classification of phytocannabinoids is based on their decorated resorcinol core and the bioactivities of naturally occurring cannabinoids. Furthermore, phytocannabinoids have been studied in terms of their role in animal models and antimicrobial activity against bacteria and fungi; further, they show potential for therapeutic applications and are used in treating various human diseases. Overall, this review can help deepen the current understanding of the role of biotechnological approaches and the importance of phytocannabinoids in different industrial applications.
 Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. In addition to distinct clinical, radiological, and immunological features, the infectious prodrome is more commonly reported in MOGAD (37-70%) than NMOSD (15-35%). Interestingly, pediatric MOGAD is not more aggressive than adult-onset MOGAD, unlike in multiple sclerosis (MS), where annualized relapse rates are three times higher in pediatric-onset MS. MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). MOGAD lesions show a perivenous confluent pattern around the small veins, lacking the radiological central vein sign. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help differentiate MOG antibody-producing plasma cells in the peripheral blood. Neuroinflammatory biomarkers (such as MBP, sNFL, GFAP, Tau) in MOGAD support that most axonal damage happens in the initial attack, whereas relapses are associated with increased myelin damage.
 Chronic inflammation driven by proinflammatory cytokines (TNFα, IL-1β, IL-6, etc.), and nitric oxide (NO) plays an important role in the pathogenesis of several autoimmune, inflammatory as well as neurodegenerative disorders like rheumatoid arthritis, multiple sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, etc. Therefore, identification of nontoxic anti-inflammatory drugs may be beneficial for these autoimmune, inflammatory and neurodegenerative disorders. Cinnamein, an ester derivative of cinnamic acid and benzyl alcohol, is used as a flavoring agent and for its antifungal and antibacterial properties. This study underlines the importance of cinnamein in inhibiting the induction of proinflammatory molecules in RAW 264.7 macrophages and primary mouse microglia and astrocytes. Stimulation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and interferon γ (IFNγ) led to marked production of NO. However, cinnamein pretreatment significantly inhibited LPS- and IFNγ-induced production of NO in RAW 264.7 macrophages. Cinnamein also reduced the mRNA expression of inducible nitric oxide synthase (iNOS) and TNFα in RAW cells. Accordingly, LPS and viral double-stranded RNA mimic polyinosinic: polycytidylic acid (polyIC) stimulated the production of TNFα, IL-1β and IL-6 in primary mouse microglia, which was inhibited by cinnamein pretreatment. Similarly, cinnamein also inhibited polyIC-induced production of TNFα and IL-6 in primary mouse astrocytes. These results suggest that cinnamein may be used to control inflammation in different autoimmune, inflammatory and neurodegenerative disorders.
 INTRODUCTION: The neural control of the immune system by the nervous system is critical to maintaining immune homeostasis, whose disruption may be an underlying cause of several diseases, including cancer, multiple sclerosis, rheumatoid arthritis, and Alzheimer's disease. METHODS: Here we studied the role of vagus nerve stimulation (VNS) on gene expression in peripheral blood mononuclear cells (PBMCs). Vagus nerve stimulation is widely used as an alternative treatment for drug-resistant epilepsy. Thus, we studied the impact that VNS treatment has on PBMCs isolated from a cohort of existing patients with medically refractory epilepsy. A comparison of genome-wide changes in gene expression was made between the epilepsy patients treated and non-treated with vagus nerve stimulation. RESULTS: The analysis showed downregulation of genes related to stress, inflammatory response, and immunity, suggesting an anti-inflammatory effect of VNS in epilepsy patients. VNS also resulted in the downregulation of the insulin catabolic process, which may reduce circulating blood glucose. DISCUSSION: These results provide a potential molecular explanation for the beneficial role of the ketogenic diet, which also controls blood glucose, in treating refractory epilepsy. The findings indicate that direct VNS might be a useful therapeutic alternative to treat chronic inflammatory conditions.
 Therapeutic plasma exchange (TPE) is an efficient extracorporeal blood purification technique to remove circulating autoantibodies and other pathogenic substances. Its mechanism of action in immune-mediated neurological disorders includes immediate intravascular reduction of autoantibody concentration, pulsed induction of antibody redistribution, and subsequent immunomodulatory changes. Conventional TPE with 1 to 1.5 total plasma volume (TPV) exchange is a well-established treatment in Guillain-Barre Syndrome, Chronic Inflammatory Demyelinating Polyradiculoneuropathy, Neuromyelitis Optica Spectrum Disorder, Myasthenia Gravis and Multiple Sclerosis. There is insufficient evidence for the efficacy of so-called low volume plasma exchange (LVPE) (<1 TPV exchange) implemented either by the conventional or by a novel nanomembrane-based TPE in these neurological conditions, including their impact on conductivity and neuroregenerative recovery. In this narrative review, we focus on the role of nanomembrane-based technology as an alternative LVPE treatment option in these neurological conditions. Nanomembrane-based technology is a promising type of TPE, which seems to share the basic advantages of the conventional one, but probably with fewer adverse effects. It could play a valuable role in patient management by ameliorating neurological symptoms, improving disability, and reducing oxidative stress in a cost-effective way. Further research is needed to identify which patients benefit most from this novel TPE technology.
 A major therapeutic goal in demyelinating diseases, such as Multiple Sclerosis, is to improve remyelination, thereby restoring effective axon conduction and preventing neurodegeneration. In the adult central nervous system (CNS), parenchymal oligodendrocyte progenitor cells (pOPCs) and, to a lesser extent, pre-existing oligodendrocytes (OLs) and oligodendrocytes generated from neural stem cells (NSCs) in the sub-ventricular zone (SVZ) are capable of forming new myelin sheaths. Due to their self-renewal capabilities and the ability of their progeny to migrate widely within the CNS, NSCs represent an additional source of remyelinating cells that may be targeted to supplement repair by pOPCs. However, in demyelinating disorders and disease models, the NSC contribution to myelin repair is modest and most evident in regions close to the SVZ. We hypothesized that NSC-derived cells may compete with OPCs to remyelinate the same axons, with pOPCs serving as the primary remyelinating cells due to their widespread distribution within the adult CNS, thereby limiting the contribution of NSC-progeny. Here, we have used a dual reporter, genetic fate mapping strategy, to characterize the contribution of pOPCs and NSC-derived OLs to remyelination after cuprizone-induced demyelination. We confirmed that, while pOPCs are the main remyelinating cells in the corpus callosum, NSC-derived cells are also activated and recruited to demyelinating lesions. Blocking pOPC differentiation genetically, resulted in a significant increase in the recruitment NSC-derived cells into the demyelinated corpus callosum and their differentiation into OLs. These results strongly suggest that pOPCs and NSC-progeny compete to repair white matter lesions. They underscore the potential significance of targeting NSCs to improve repair when the contribution of pOPCs is insufficient to affect full remyelination.
 Autoimmune diseases comprise a very heterogeneous group of disorders characterized by disruptive immune responses against self-antigens, chronic morbidity and increased mortality. The incidence and prevalence of major autoimmune conditions are particularly high in the western world, at northern latitudes, and in industrialized countries. This study will mainly focus on five major autoimmune conditions, namely type 1 diabetes, multiple sclerosis, inflammatory bowel diseases, rheumatoid arthritis, and autoimmune thyroid disorders. Epidemiological and experimental evidence suggests a protective role of sunlight exposure on the etiology of major autoimmune conditions mediated by the endogenous production of vitamin D and nitric oxide. A historical perspective shows how the rise of anthropogenic air pollutants is temporally associated with dramatic increases in incidence of these conditions. The scattering caused by ambient particulate matter and the presence of tropospheric ozone can reduce the endogenous production of vitamin D and nitric oxide, which are implicated in maintaining the immune homeostasis. Air pollutants have direct detrimental effects on the human body and are deemed responsible of an increasingly higher portion of the annual burden of human morbidity and mortality. Air pollution contributes in systemic inflammation, activates oxidative pathways, induces epigenetic alterations, and modulates the function and phenotype of dendritic cells, Tregs, and T-cells. In this review, we provide epidemiological and mechanistic insights regarding the role of UV-mediated effects in immunity and how anthropic-derived air pollution may affect major autoimmune conditions through direct and indirect mechanisms.
 We have previously identified an immune modulating peptide, termed FhHDM-1, within the secretions of the liver fluke, Fasciola hepatica, which is sufficiently potent to prevent the progression of type 1 diabetes and multiple sclerosis in murine models of disease. Here, we have determined that the FhHDM-1 peptide regulates inflammation by reprogramming macrophage metabolism. Specifically, FhHDM-1 switched macrophage metabolism to a dependence on oxidative phosphorylation fuelled by fatty acids and supported by the induction of glutaminolysis. The catabolism of glutamine also resulted in an accumulation of alpha ketoglutarate (α-KG). These changes in metabolic activity were associated with a concomitant reduction in glycolytic flux, and the subsequent decrease in TNF and IL-6 production at the protein level. Interestingly, FhHDM-1 treated macrophages did not express the characteristic genes of an M2 phenotype, thereby indicating the specific regulation of inflammation, as opposed to the induction of an anti-inflammatory phenotype per se. Use of an inactive derivative of FhHDM-1, which did not modulate macrophage responses, revealed that the regulation of immune responses was dependent on the ability of FhHDM-1 to modulate lysosomal pH. These results identify a novel functional association between the lysosome and mitochondrial metabolism in macrophages, and further highlight the significant therapeutic potential of FhHDM-1 to prevent inflammation.
 The SARS-coronavirus-2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19), has spread worldwide and caused a global health emergency. SARS-CoV-2 is a coronaviridae virus that infects target cells by interacting with the plasma membrane-expressed angiotensin-converting enzyme 2 (ACE2) via the S1 component of the S protein. Effective host immune response to SARS-CoV-2 infection, which includes both innate and adaptive immunity, is critical for virus management and elimination. The intensity and outcome of COVID-19 may be related to an overabundance of pro-inflammatory cytokines, which results in a "cytokine storm" and acute respiratory distress syndrome. After SARS-CoV-2 infection, the immune system's hyperactivity and production of autoantibodies may result in autoimmune diseases such as autoimmune hemolytic anemia, autoimmune thrombocytopenia, Guillain-Barré syndrome, vasculitis, multiple sclerosis, pro-thrombotic state, and diffuse coagulopathy, as well as certain autoinflammatory conditions such as Kawasaki disease in children. We have reviewed the association between COVID-19 and autoimmune disorders in this article.
 Neurodegenerative diseases are caused by progressive degeneration of the central nervous system (CNS)'s neuronal structure. Well-known diseases in this category include Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS), which are also addressed in this study. The CNS appears to be a complex dynamic system, whose parameters change during the disease due to neuronal damage, resulting in various symptoms. Since the change in dynamic behavior is due to the neurons' death and change in neurons' connectivity, brain images of the affected areas appear to provide a good understanding of this change. This work attempts to focus on brain magnetic resonance images (MRI) and examine the effect of neuronal loss on the images. To this end, the complex features of these images, including 2D and Higuchi's fractal dimensions (HFD), correlation dimension (CD), largest Lyapunov exponent (LLE), and approximate entropy (ApEn) were calculated. Despite small differences in numerical values (0.01-0.35), these values differ significantly. This shows that the brain dynamic system behaves and functions differently in the disease state, which is clear in the behavior of global features. These three diseases have the same functional pattern, and this study seems to have captured the roots of these seemingly variant diseases.
 Brain disorders are currently one of the world's most serious and difficult health issues. These brain disorders are accountable for a massive number of morbidities and mortalities around the world. The current treatments of these disorders are frequently accompanied by severe side effects and cause a detrimental effect on health. Recently, plant flavonoids have sparked a surge in public and scientific attention because of their alleged health-promoting impact and almost no adverse repercussions. Also, scientific research has shown that phytochemicals possess numerous neuroprotective properties under in vivo and in vitro conditions. Chrysin is a therapeutic phytochemical that falls under the class of flavonoids based on its structure. The biological activities and pharmacological effects of chrysin include anticancer, antioxidant, and anti-inflammatory activities as well as amyloidogenic and neurotrophic effects. These therapeutic abilities of chrysin are attributed to its structural diverseness arising in ring-A and lack of oxygenation in B and C rings. Several studies have highlighted the rising significance of chrysin in a variety of brain illnesses, like Alzheimer's disease, Parkinson's disease, depression, anxiety, brain tumours, epilepsy, multiple sclerosis, traumatic brain injury, spinal cord injury, and ischemic stroke. This study depicts the relationship of chrysin with different brain-related disorders and discusses the mechanisms responsible for the potential role of chrysin as a pharmacological agent for the treatment and management of different brain disorders based on the results of several preclinical studies and taking into account the therapeutic effects of the compound.
 Oral cholera vaccine is one of the key interventions used in our fight to end the longest pandemic of our time, cholera. The immune response conferred by the currently available cholera vaccines, as measured by serum antibody levels, is variable amongst its recipients. We undertook a genome wide association study (GWAS) on antibody response to the cholera vaccine; globally, the first GWAS on cholera vaccine response. We identified three clusters of bi-allelic SNPs, in high within-cluster linkage disequilibrium that were moderately (p < 5 × 10(-6)) associated with antibody response to the cholera vaccine and mapped to chromosomal regions 4p14, 4p16.1 and 6q23.3. Intronic SNPs of TBC1D1 comprised the cluster on 4p14, intronic SNPs of TBC1D14 comprised that on 4p16.1 and SNPs upstream of TNFAIP3 formed the cluster on 6q23.3. SNPs within and around these clusters have been implicated in immune cell function and immunological aspects of autoimmune or infectious diseases (e.g., diseases caused by Helicobacter pylori and malarial parasite). 6q23.3 is a prominent region harbouring many loci associated with immune related diseases, including multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus, as well as IL2 and INFα response to a smallpox vaccine. The gene clusters identified in this study play roles in vesicle-mediated pathway, autophagy and NF-κB signaling. No significant effect of O blood group on antibody response to the cholera vaccine was observed in this study.
 Lymphocytes are key players in the pathogenesis of multiple sclerosis and a distinct target of several immunomodulatory treatment strategies. In this study, we aim to evaluate the effect of various pre-analytic conditions on immune cell counts to conclude the relevance for clinical implications. Twenty healthy donors were assessed for the effects of distinct storage temperatures and times after blood draws, different durations of tourniquet application, body positions and varying aspiration forces during blood draws. Immune cell frequencies were analyzed using multicolor flowcytometry. While storage for 24 h at 37 °C after blood draws was associated with significantly lower cell counts, different durations of tourniquet application, body positions and varying aspirations speeds did not have significant impacts on the immune cell counts. Our data suggest that immune cell counts are differently affected by pre-analytic conditions being more sensitive to storage temperature. Pre-analytic conditions should be carefully considered when interpreting the laboratory values of immune cell subpopulations.
 Neuroinflammation has been implicated in the initiation and progression of several central nervous system (CNS) disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, ischemic stroke, traumatic brain injury, spinal cord injury, viral encephalitis, and bacterial encephalitis. Microglia and astrocytes are essential in neural development, maintenance of synaptic connections, and homeostasis in a healthy brain. The activation of astrocytes and microglia is a defense mechanism of the brain against damaged tissues and harmful pathogens. However, their activation triggers neuroinflammation, which can exacerbate or induce CNS injury. Non-coding RNAs (ncRNAs) are functional RNA molecules that lack coding capabilities but can actively regulate mRNA expression and function through various mechanisms. ncRNAs are highly expressed in astrocytes and microglia and are potential mediators of neuroinflammation. We reviewed the recent research progress on the role of miRNAs, lncRNAs, and circRNAs in regulating neuroinflammation in various CNS diseases. Understanding how these ncRNAs affect neuroinflammation will provide important therapeutic insights for preventing and managing CNS dysfunction.
 BACKGROUND: Mechanical insufflation/exsufflation (MI-E) devices are often prescribed to patients with inefficient cough and recurrent infections, but their use in the home setting is not well characterized. OBJECTIVE: The objective of this study was to report a real-life experience and identify factors that are associated with home MI-E use in adult patients. METHODS: This is a cross-sectional observational study of adult subjects with neurological disease using MI-E at home for more than 3 months. RESULTS: A total of 43 patients were included. Median age (interquartile range) was 48 (31-64) years. The most common diagnosis was muscular dystrophy (n = 15), followed by multiple sclerosis (n = 7) and amyotrophic lateral sclerosis (n = 7). 24 subjects (56%) reported using the MI-E at least once weekly. Based on device data downloads, the median objective use was 23% of days analysed (approximately 2 times per week). The vast majority (94%) of all participants reported using the device at least daily during an infectious episode, while 62% reported having used the device in emergency situations such as bronchoaspiration. Reported use correlated well with objective use (r = 0.82). Most subjects reported an improvement in their respiratory health (64%) and were satisfied with the device (78%). Higher reported and objective use were associated with increased symptoms (p = 0.001) and higher satisfaction with the device (p = 0.008). We found no association between frequency of use and baseline cough peak flow (CPF), bulbar impairment, non-invasive ventilation use, living environment, or supervised administration. CONCLUSION: Regular home MI-E use was associated with greater symptom burden and overall satisfaction with the device and was not influenced by baseline CPF. Patients without substantial bronchorrhea might not use the MI-E regularly but might still need to use the device at home during acute events. Therefore, familiarity with the MI-E via appropriate and repeated practical training is crucial.
 Toxic air pollutants are one of the most agent that have many acute, chronic and non-communicable diseases (NCDs) on human health under long or short-term exposure has been raised from the past to the present. The aim of this study was investigation effect of long-term exposure to toxic air pollutants on the increased risk of malignant brain tumors. Databases used to for searched were the PubMed, Web of Science, Springer and Science Direct (Scopus) and Google Scholar. 71 papers based on abstract and article text filtered. In the end after sieve we selected 7 papers. Identify all relevant studies published 1970-2022. The literature showed that exposure to toxic air pollutants and their respiration can cause disorders in different parts of the brain by transmission through the circulatory system and other mechanisms. Various unpleasant abnormalities are caused by the inhalation of toxic air pollutants in the human body that some of the most common of them include chronic lung disease, coronary heart disease and heart attacks, strokes and brain diseases (Parkinson's, Alzheimer's and multiple Sclerosis), cancers (liver, blood, prostate and brain) and eventually death. According to the finding brain health and proper functioning can be easily disrupted by various genetic or external factors such as air pollution, causing a wide range of abnormalities in the brain and malignant brain tumors. The results of this study showed that reducing the concentration of toxic pollutants in the air, that exposure to them play an increasing role in the development of brain diseases can slow down the process of abnormalities in the brain and will have significant impacts on reducing the number of people affected by them.
 Epigallocatechin-3-gallate (EGCG), a polyphenolic moiety found in green tea extracts, exhibits pleiotropic bioactivities to combat many diseases including neurological ailments. These neurological diseases include Alzheimer's disease, multiple sclerosis, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. For instance, in the case of Alzheimer's disease, the formation of a β-sheet in the region of the 10th-21st amino acids was significantly reduced in EGCG-induced oligomeric samples of Aβ40. Its interference induces the formation of Aβ structures with an increase in intercenter-of-mass distances, reduction in interchain/intrachain contacts, reduction in β-sheet propensity, and increase in α-helix. Besides, numerous neurotropic viruses are known to instigate or aggravate neurological ailments. It exerts an effect on the oxidative damage caused in neurodegenerative disorders by acting on GSK3-β, PI3K/Akt, and downstream signaling pathways via caspase-3 and cytochrome-c. EGCG also diminishes these viral-mediated effects, such as EGCG delayed HSV-1 infection by blocking the entry for virions, inhibitory effects on NS3/4A protease or NS5B polymerase of HCV and potent inhibitor of ZIKV NS2B-NS3pro/NS3 serine protease (NS3-SP). It showed a reduction in the neurotoxic properties of HIV-gp120 and Tat in the presence of IFN-γ. EGCG also involves numerous viral-mediated inflammatory cascades, such as JAK/STAT. Nonetheless, it also inhibits the Epstein-Barr virus replication protein (Zta and Rta). Moreover, it also impedes certain viruses (influenza A and B strains) by hijacking the endosomal and lysosomal compartments. Therefore, the current article aims to describe the importance of EGCG in numerous neurological diseases and its inhibitory effect against neurotropic viruses.
 BACKGROUND: Many studies have shown an association between COVID-19 and autoimmune diseases (ADs). Studies on COVID-19 and ADs have also increased significantly, but there is no bibliometric analysis to summarize the association between COVID-19 and ADs. The purpose of this study was to perform a bibliometric and visual analysis of published studies related to COVID-19 and ADs. METHODS: Based on the Web of Science Core Collection SCI-Expanded database, we utilize Excel 2019 and visualization analysis tools Co-Occurrence13.2 (COOC13.2), VOSviewer, CiteSpace, and HistCite for analysis. RESULTS: A total of 1736 related kinds of papers were included, and the number of papers presented an overall increasing trend. The country/region with the most publications is the USA, the institution is the Harvard Medical School, the author is Yehuda Shoenfeld from Israel, and the journal is Frontiers in Immunology. Research hotspots include immune responses (such as cytokines storm), multisystem ADs (such as systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis), treatment modalities (such as hydroxychloroquine, rituximab), vaccination and autoimmune mechanisms (such as autoantibodies, molecular mimicry). The future research direction may be the mechanisms and treatment ideas of the association between ADs and COVID-19 (such as NF-κB, hyperinflammation, antiphospholipid antibodies, neutrophil extracellular traps, granulocyte-macrophage colony-stimulating factor), other cross-diseases of COVID-19 and ADs (such as inflammatory bowel disease, chronic mucocutaneous candidiasis, acute respiratory distress syndrome). CONCLUSION: The growth rate of publications regarding ADs and COVID-19 has risen sharply. Our research results can help researchers grasp the current status of ADs and COVID-19 research and find new research directions in the future.
 S100B is a calcium-binding protein mainly concentrated in astrocytes in the nervous system. Its levels in biological fluids are recognized as a reliable biomarker of active neural distress, and more recently, mounting evidence points to S100B as a Damage-Associated Molecular Pattern molecule, which, at high concentration, triggers tissue reactions to damage. S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease. In addition, in experimental models of diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, multiple sclerosis, traumatic and vascular acute neural injury, epilepsy, and inflammatory bowel disease, alteration of S100B levels correlates with the occurrence of clinical and/or toxic parameters. In general, overexpression/administration of S100B worsens the clinical presentation, whereas deletion/inactivation of the protein contributes to the amelioration of the symptoms. Thus, the S100B protein may be proposed as a common pathogenic factor in different disorders, sharing different symptoms and etiologies but appearing to share some common pathogenic processes reasonably attributable to neuroinflammation.
 Mitochondrial dysfunction is reiteratively involved in the pathogenesis of diverse neurodegenerative diseases. Current in vitro and in vivo approaches support that mitochondrial dysfunction is branded by several molecular and cellular defects, whose impact at different levels including the calcium and iron homeostasis, energetic balance and/or oxidative stress, makes it difficult to resolve them collectively given their multifactorial nature. Mitochondrial transfer offers an overall solution since it contains the replacement of damage mitochondria by healthy units. Therefore, this review provides an introducing view on the structure and energy-related functions of mitochondria as well as their dynamics. In turn, we summarize current knowledge on how these features are deregulated in different neurodegenerative diseases, including frontotemporal dementia, multiple sclerosis, amyotrophic lateral sclerosis, Friedreich ataxia, Alzheimer´s disease, Parkinson´s disease, and Huntington's disease. Finally, we analyzed current advances in mitochondrial transfer between diverse cell types that actively participate in neurodegenerative processes, and how they might be projected toward developing novel therapeutic strategies.
 BACKGROUND: Nuclear factor erythroid 2-related factor 2 (Nrf2) is a classical nuclear transcription factor that regulates the system's anti-oxidative stress response. The activation of Nrf2 induces the expression of antioxidant proteins and improves the system's anti-oxidative stress ability. Accumulating evidence suggests that Nrf2-centered signaling pathways may be a key pharmacological target for the treatment of neurodegenerative diseases (NDDs). However, phytochemicals as new therapeutic agents against NDDs have not been clearly delineated. PURPOSE: To review the therapeutic effects of phytochemical ingredients on NDDs by activating Nrf2 and reducing oxidative stress injury. METHODS: A comprehensive search of published articles was performed using various literature databases including PubMed, Google Scholar, and China National Knowledge Infrastructure. The search terms included "Nrf2", "phytochemical ingredients", "natural bioactive agents", "neurodegenerative diseases", "Antioxidant", "Alzheimer's disease", "Parkinson's disease", "Huntington's disease", "amyotrophic lateral sclerosis" "multiple sclerosis", "toxicity", and combinations of these keywords. A total of 769 preclinical studies were retrieved until August 2022, and we included 39 of these articless on phytochemistry, pharmacology, toxicology and other fields. RESULTS: Numerous in vivo and in vitro studies showed that phytochemical ingredients could act as an Nrf2 activator in the treatment of NDDs through the antioxidant defense mechanism. These phytochemical ingredients, such as salidroside, naringenin, resveratrol, sesaminol, ellagic acid, ginsenoside Re, tanshinone I, sulforaphane, curcumin, naringin, tetramethylpyrazine, withametelin, magnolol, piperine, and myricetin, had the potential to improve Nrf2 signaling, thereby combatting NDDs. CONCLUSION: As Nrf2 activators, phytochemical ingredients may provide a novel potential strategy for the treatment of NDDs. Here, we reviewed the interaction between phytochemical ingredients, Nrf2, and its antioxidant damaging pathway in NDDs and explored the advantages of phytochemical ingredients in anti-oxidative stress, which provides a reliable basis for improving the treatment of NDDs. However, further clinical trials are needed to determine the safety and efficacy of Nrf2 activators for NDDs.
 INTRODUCTION: Systemic sclerosis (SSc) is a rare chronic autoimmune disease characterized by diffuse fibrosis of the skin and internal organs and vascular abnormalities. The etiology and physiopathology are complex due to the heterogeneity of its overall clinical presentation. Arsenic trioxide (ATO) has been proven to be effective against SSc, sclerodermatous Graft-versus-Host Disease, multiple sclerosis, Crohn's disease or systemic lupus erythematosus animal models and has demonstrated promising effects in human clinical trials. Its efficacy was shown to be related at least in part to the generation of Reactive Oxygen Species (ROS) and the selective deletion of activated immune cells and fibroblasts. However, ATO can induce some adverse effects that must be considered, especially when used for the treatment of a chronic disease. METHODS: We evaluate here, in vitro and in a mouse model of SSc, the improved efficacy of ATO when associated with a Fenton-like divalent cation, namely copper chloride (CuCl(2)), also known to trigger the production of ROS. RESULTS: In preliminary experiments in vitro, ATO 1 µM + CuCl(2) 0.5 µM increased ROS production and increased apoptosis of NIH 3T3 murine fibroblasts compared to 1 µM ATO alone. In vivo, in the HOCl-induced mouse model of SSc, co-treatment with ATO 2.5 μg/g + CuCl(2) 0.5 μg/g significantly alleviated clinical signs such as the thickening of the skin (p<0.01) and cutaneous fibrosis, in a manner equivalent to treatment with ATO 5 µg/g. Our results provide evidence that co-treatment with ATO 2.5 μg/g + CuCl(2) 0.5 μg/g decreases the number of B cells and the activation of CD4(+) T lymphocytes. The co-treatment substantially blocks the NRF2 signaling pathway, increases H2O2 production and results in the improvement of the health status of mice with experimental SSc. CONCLUSION: In conclusion, copper combined with ATO treatment halved the concentration of ATO needed to obtain the same effect as a high dose of ATO alone for the treatment of SSc mice. The strategy of using lower doses of drugs with different mechanisms of action in combination has many potential advantages, the first being to lessen the potential side effects induced by ATO, a drug with side effects quickly increased with dosage.
 OBJECTIVE: Evaluation of serum neurofilament light chain (sNfL), measured using high-throughput assays on widely accessible platforms in large, real-world MS populations, is a critical step for sNfL to be utilized in clinical practice. METHODS: Multiple Sclerosis Partners Advancing Technology and Health Solutions (MS PATHS) is a network of healthcare institutions in the United States and Europe collecting standardized clinical/imaging data and biospecimens during routine clinic visits. sNfL was measured in 6974 MS and 201 healthy control (HC) participants, using a high-throughput, scalable immunoassay. RESULTS: Elevated sNfL levels for age (sNfL-E) were found in 1238 MS participants (17.8%). Factors associated with sNfL-E included male sex, younger age, progressive disease subtype, diabetes mellitus, impaired renal function, and active smoking. Higher body mass index (BMI) was associated with lower odds of elevated sNfL. Active treatment with disease-modifying therapy was associated with lower odds of sNfL-E. MS participants with sNfL-E exhibited worse neurological function (patient-reported disability, walking speed, manual dexterity, and cognitive processing speed), lower brain parenchymal fraction, and higher T2 lesion volume. Longitudinal analyses revealed accelerated short-term rates of whole brain atrophy in sNfL-E participants and higher odds of new T2 lesion development, although both MS participants with or without sNfL-E exhibited faster rates of whole brain atrophy compared to HC. Findings were consistent in analyses examining age-normative sNfL Z-scores as a continuous variable. INTERPRETATION: Elevated sNfL is associated with clinical disability, inflammatory disease activity, and whole brain atrophy in MS, but interpretation needs to account for comorbidities including impaired renal function, diabetes, and smoking.
 BACKGROUND AND OBJECTIVE: Tolebrutinib is a covalent inhibitor of Bruton's tyrosine kinase, an enzyme expressed in B lymphocytes and myeloid cells including microglia, which are thought to be major drivers of inflammation in multiple sclerosis. This excretion balance and metabolism study evaluated the metabolite profile of tolebrutinib in healthy male volunteers. METHODS: Six healthy volunteers received a 60-mg oral dose of [(14)C]-tolebrutinib, and metabolite profiling of (14)C-labeled metabolites was performed using a combination of liquid chromatography, mass spectrometry, and radioactivity assay methods. RESULTS: Tolebrutinib was rapidly and completely absorbed from the gastrointestinal tract, followed by rapid and extensive metabolism. Excretion via feces was the major elimination pathway of the administered radioactivity (78%). Tolebrutinib was highly metabolized, with 19 metabolites identified in human plasma. Phase 1 biotransformations were primarily responsible for the circulating metabolites in plasma. Seven metabolites that achieved exposure in plasma similar to or higher than the parent compound were characterized biochemically for inhibition of Bruton's tyrosine kinase activity. Metabolite M8 exceeded the exposure threshold of 10% (18%) of the total radioactivity but had little if any pharmacological activity. Metabolite M2 (4% of circulating radioactivity) retained the ability to irreversibly and potently inhibit Bruton's tyrosine kinase in vitro, similar to the parent compound. Tolebrutinib and metabolite M2 had short (3.5-h) half-lives but durable pharmacodynamic effects as expected for an irreversible antagonist. CONCLUSIONS: Tolebrutinib was extensively metabolized to multiple metabolites. The hydroxylated metabolite M2 demonstrated similar inhibitory potency toward Bruton's tyrosine kinase as the parent compound. Both tolebrutinib and metabolite M2 likely contributed to pharmacological activity in vivo.
 PURPOSE: There is little representative evidence for the German rehabilitation system on occupational reintegration after medical rehabilitation. For persons who have undergone rehabilitation on behalf of the German Pension Insurance (GPI) due to a neurological disease, it is therefore important to determine (a) what socio-medical risks exist prior to rehabilitation, (b) how well persons were able to participate in working life after rehabilitation, and (c) what conditions determine the work participation. METHODS: The study is conducted on the basis of the GPI's database of rehabilitation statistics. Included were all persons, who completed medical rehabilitation in 2016 due to a neurological disease. The analyses were carried out for the entire group and also in a differentiated manner for the 2 main diseases, cerebrovascular diseases (CD) and multiple sclerosis (MS). Work participation was operationalized both via a monthly status variable until 24 months after rehabilitation and as a rate of all persons who were employed at the 12 and 24 months follow up and in the 3 months before, respectively. To analyse the factors influencing stable work participation, multiple logistic regression models with stepwise inclusion were calculated separately for the rates after 12 and 24 months. RESULTS: A total of 42,230 data sets were included in the analysis (CD: n=18,368, 44%; MS: n=6,343, 15%). Patients with neurological diseases were 50 years old on average, 43% were female. We found that approximately15% of patients reported no absenteeism, whereas 17% stated an absence leave of six months or more in the year prior to rehabilitation. Mental and cardiovascular comorbidity was documented in 31 and 44% of the cases respectively. Nearly 48% of patients with CD returned to work two years after rehabilitation. For MS patients, the percentage was slightly higher at 54%. The amount of sick leave of the rehabilitated individual, their gross/net income prior to rehabilitation as well their work capacity prior to admission were the three strongest influencing factors on their return to the labour market. CONCLUSION: About half of all persons with neurological diseases return to sustainable work after medical rehabilitation in Germany. The amount of sick leave and the income before rehabilitation are determining factors as to whether the person will return to work. The analysis provides representative data on occupational reintegration after medical rehabilitation due to a neurological disease for the first time.
 OBJECTIVE: Relapses in patients with relapsing-remitting multiple sclerosis (RRMS) are typically treated with high-dose corticosteroids including methylprednisolone. However, high-dose corticosteroids are associated with significant adverse effects, can increase the risk for other morbidities, and often do not impact disease course. Multiple mechanisms are proposed to contribute to acute relapses in RRMS patients, including neuroinflammation, fibrin formation and compromised blood vessel barrier function. The protein C activator, E-WE thrombin is a recombinant therapeutic in clinical development for its antithrombotic and cytoprotective properties, including protection of endothelial cell barrier function. In mice, treatment with E-WE thrombin reduced neuroinflammation and extracellular fibrin formation in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE). We therefore tested the hypothesis that E-WE thrombin could reduce disease severity in a relapsing-remitting model of EAE. METHODS: Female SJL mice were inoculated with proteolipid protein (PLP) peptide and treated with E-WE thrombin (25 µg/kg; iv) or vehicle at onset of detectable disease. In other experiments, E-WE thrombin was compared to methylprednisolone (100 mg/kg; iv) or the combination of both. RESULTS: Compared to vehicle, administration of E-WE thrombin significantly improved disease severity of the initial attack and relapse and delayed onset of relapse as effectively as methylprednisolone. Both methylprednisolone and E-WE thrombin reduced demyelination and immune cell recruitment, and the combination of both treatments had an additive effect. CONCLUSION: The data presented herein demonstrate that E-WE thrombin is protective in mice with relapsing-remitting EAE, a widely used model of MS. Our data indicate that E-WE thrombin is as effective as high-dose methylprednisolone in improving disease score and may exert additional benefit when administered in combination. Taken together, these data suggest that E-WE thrombin may be an effective alternative to high-dose methylprednisolone for managing acute MS attacks.
 Poor dynamic balance and impaired gait adaptation to different contexts are hallmarks of people with neurological disorders (PwND), leading to difficulties in daily life and increased fall risk. Frequent assessment of dynamic balance and gait adaptability is therefore essential for monitoring the evolution of these impairments and/or the long-term effects of rehabilitation. The modified dynamic gait index (mDGI) is a validated clinical test specifically devoted to evaluating gait facets in clinical settings under a physiotherapist's supervision. The need of a clinical environment, consequently, limits the number of assessments. Wearable sensors are increasingly used to measure balance and locomotion in real-world contexts and may permit an increase in monitoring frequency. This study aims to provide a preliminary test of this opportunity by using nested cross-validated machine learning regressors to predict the mDGI scores of 95 PwND via inertial signals collected from short steady-state walking bouts derived from the 6-minute walk test. Four different models were compared, one for each pathology (multiple sclerosis, Parkinson's disease, and stroke) and one for the pooled multipathological cohort. Model explanations were computed on the best-performing solution; the model trained on the multipathological cohort yielded a median (interquartile range) absolute test error of 3.58 (5.38) points. In total, 76% of the predictions were within the mDGI's minimal detectable change of 5 points. These results confirm that steady-state walking measurements provide information about dynamic balance and gait adaptability and can help clinicians identify important features to improve upon during rehabilitation. Future developments will include training of the method using short steady-state walking bouts in real-world settings, analysing the feasibility of this solution to intensify performance monitoring, providing prompt detection of worsening/improvements, and complementing clinical assessments.
 Kinins are endogenous peptides that belong to the kallikrein-kinin system, which has been extensively studied for over a century. Their essential role in multiple physiological and pathological processes is demonstrated by activating two transmembrane G-protein-coupled receptors, the kinin B(1) and B(2) receptors. The attention is mainly given to the pathological role of kinins in pain transduction mechanisms. In the past years, a wide range of preclinical studies has amounted to the literature reinforcing the need for an updated review about the participation of kinins and their receptors in pain disorders. Here, we performed an extensive literature search since 2004, describing the historical progress and the current understanding of the kinin receptors' participation and its potential therapeutic in several acute and chronic painful conditions. These include inflammatory (mainly arthritis), neuropathic (caused by different aetiologies, such as cancer, multiple sclerosis, antineoplastic toxicity and diabetes) and nociplastic (mainly fibromyalgia) pain. Moreover, we highlighted the pharmacological actions and possible clinical applications of the kinin B(1) and B(2) receptor antagonists, kallikrein inhibitors or kallikrein-kinin system signalling pathways-target molecules in these different painful conditions. Notably, recent findings sought to elucidate mechanisms for guiding new and better drug design targeting kinin B(1) and B(2) receptors to treat a disease diversity. Since the kinin B(2) receptor antagonist, Icatibant, is clinically used and well-tolerated by patients with hereditary angioedema gives us hope kinin receptors antagonists could be more robustly tested for a possible clinical application in the treatment of pathological pains, which present limited pharmacology management.
 Astrocytes constitute the parenchymal border of the blood-brain barrier (BBB), modulate the exchange of soluble and cellular elements, and are essential for neuronal metabolic support. Thus, astrocytes critically influence neuronal network integrity. In hypoxia, astrocytes upregulate a transcriptional program that has been shown to boost neuroprotection in several models of neurological diseases. We investigated transgenic mice with astrocyte-specific activation of the hypoxia-response program by deleting the oxygen sensors, HIF prolyl-hydroxylase domains 2 and 3 (Phd2/3). We induced astrocytic Phd2/3 deletion after onset of clinical signs in experimental autoimmune encephalomyelitis (EAE) that led to an exacerbation of the disease mediated by massive immune cell infiltration. We found that Phd2/3-ko astrocytes, though expressing a neuroprotective signature, exhibited a gradual loss of gap-junctional Connexin-43 (Cx43), which was induced by vascular endothelial growth factor-alpha (Vegf-a) expression. These results provide mechanistic insights into astrocyte biology, their critical role in hypoxic states, and in chronic inflammatory CNS diseases.
 BACKGROUND: Serum levels of neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) reflect the disease activity and disability in central nervous system (CNS) demyelinating diseases. However, the clinical significance of NfL and GFAP in idiopathic transverse myelitis (iTM), an inflammatory spinal cord disease with unknown underlying causes, remains unclear. This study aimed to investigate NfL and GFAP levels in iTM and their association with the clinical parameters compared with those in TM with disease-specific antibodies such as anti-aquaporin 4 or myelin oligodendrocyte glycoprotein antibodies (sTM). METHODS: We collected serum and clinical data of 365 patients with CNS inflammatory diseases from 12 hospitals. The serum NfL and GFAP levels were measured in patients with iTM (n = 37) and sTM (n = 39) using ultrasensitive single-molecule array assays. Regression analysis was performed to investigate the associations between serum levels of NfL and GFAP and the clinical parameters such as higher EDSS scores (EDSS ≥ 4.0). RESULTS: Mean NfL levels were not significantly different between iTM (50.29 pg/ml) and sTM (63.18 pg/ml) (p = 0.824). GFAP levels were significantly lower in iTM (112.34 pg/ml) than in sTM (3814.20 pg/ml) (p = 0.006). NfL levels correlated with expanded disability status scale (EDSS) scores in sTM (p = 0.001) but not in iTM (p = 0.824). Disease duration also correlated with higher EDSS scores in sTM (p = 0.017). CONCLUSION: NfL levels and disease duration correlated with EDSS scores in sTM, and GFAP levels could be a promising biomarker to differentiate iTM from sTM.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a rare chronic neuroinflammatory autoimmune condition. Since the onset of the COVID-19 pandemic, there have been reports of NMOSD clinical manifestations following both SARS-CoV-2 infections and COVID-19 vaccinations. OBJECTIVE: This study aims to systematically review the published literature of NMOSD clinical manifestations associated with SARS-CoV-2 infections and COVID-19 vaccinations. METHODS: A Boolean search of the medical literature was conducted between December 1, 2019 to September 1, 2022, utilizing Medline, Cochrane Library, Embase, Trip Database, Clinicaltrials.gov, Scopus, and Web of Science databases. Articles were collated and managed on Covidence(®) software. The authors independently appraised the articles for meeting study criteria and followed PRISMA guidelines. The literature search included all case reports and case series that met study criteria and involved NMOSD following either the SARS-CoV-2 infection or the COVID-19 vaccination. RESULTS: A total of 702 articles were imported for screening. After removing 352 duplicates and 313 articles based on exclusion criteria, 34 articles were analyzed. A total of 41 cases were selected, including 15 patients that developed new onset NMOSD following a SARS-CoV-2 infection, 21 patients that developed de novo NMOSD following COVID-19 vaccination, 3 patients with known NMOSD that experienced a relapse following vaccination, and 2 patients with presumed Multiple Sclerosis (MS) that was unmasked as NMOSD post-vaccination. There was a female preponderance of 76% among all NMOSD cases. The median time interval between the initial SARS-CoV-2 infection symptoms and NMOSD symptom onset was 14  days (range 3-120  days) and the median interval between COVID-19 vaccination and onset of NMO symptoms was 10  days (range 1 to 97  days). Transverse myelitis was the most common neurological manifestation in all patient groups (27/41). Management encompassed acute treatments such as high dose intravenous methylprednisolone, plasmapheresis, and intravenous immunoglobulin (IVIG) and maintenance immunotherapies. The majority of patients experienced a favorable outcome with complete or partial recovery, but 3 patients died. CONCLUSION: This systematic review suggests that there is an association between NMOSD and SARS-CoV-2 infections and COVID-19 vaccinations. This association requires further study using quantitative epidemiological assessments in a large population to better quantify the risk.
 PURPOSE: [(18)F]3F4AP is a novel PET radiotracer that targets voltage-gated potassium (K(+)) channels and has shown promise for imaging demyelinated lesions in animal models of neurological diseases. This study aimed to evaluate the biodistribution, safety, and radiation dosimetry of [(18)F]3F4AP in healthy human volunteers. METHODS: Four healthy volunteers (2 females) underwent a 4-h dynamic PET scan from the cranial vertex to mid-thigh using multiple bed positions after administration of 368 ± 17.9 MBq (9.94 ± 0.48 mCi) of [(18)F]3F4AP. Volumes of interest for relevant organs were manually drawn guided by the CT, and PET images and time-activity curves (TACs) were extracted. Radiation dosimetry was estimated from the integrated TACs using OLINDA software. Safety assessments included measuring vital signs immediately before and after the scan, monitoring for adverse events, and obtaining a comprehensive metabolic panel and electrocardiogram within 30 days before and after the scan. RESULTS: [(18)F]3F4AP distributed throughout the body with the highest levels of activity in the kidneys, urinary bladder, stomach, liver, spleen, and brain and with low accumulation in muscle and fat. The tracer cleared quickly from circulation and from most organs. The clearance of the tracer was noticeably faster than previously reported in nonhuman primates (NHPs). The average effective dose (ED) across all subjects was 12.1 ± 2.2 μSv/MBq, which is lower than the estimated ED from the NHP studies (21.6 ± 0.6 μSv/MBq) as well as the ED of other fluorine-18 radiotracers such as [(18)F]FDG (~ 20 μSv/MBq). No differences in ED between males and females were observed. No substantial changes in safety assessments or adverse events were recorded. CONCLUSION: The biodistribution and radiation dosimetry of [(18)F]3F4AP in humans are reported for the first time. The average total ED across four subjects was lower than most (18)F-labeled PET tracers. The tracer and study procedures were well tolerated, and no adverse events occurred.
 Parkinson's disease (PD) is a neurodegenerative disease characterized by the pathological loss of nigrostriatal dopaminergic neurons, which causes an insufficient release of dopamine (DA) and then induces motor and nonmotor symptoms. Hyperoside (HYP) is a lignan component with anti-inflammatory, antioxidant, and neuroprotective effects. In this study, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its active neurotoxic metabolite 1-methyl-4-phenylpyridinium ion (MPP(+)) were used to induce dopaminergic neurodegeneration. The results showed that HYP (100 µg/mL) reduced MPTP-mediated cytotoxicity of SH-SY5Y cells in vitro, and HYP [25 mg/(kg d)] alleviated MPTP-induced motor symptoms in vivo. HYP treatment reduced the contents of nitric oxide (NO), H(2)O(2), and malondialdehyde (MDA), as well as the mitochondrial damage of dopaminergic neurons, both in vitro and in vivo. Meanwhile, HYP treatment elevated the levels of neurotrophic factors such as glial cell line-derived neurotrophic factor, brain-derived neurotrophic factor, and recombinant cerebral dopamine neurotrophic factor in vivo, but not in vitro. Finally, Akt signaling was activated after the administration of HYP in MPP(+)/MPTP-induced dopaminergic neurodegeneration. However, the blockage of the Akt pathway with Akt inhibitor did not abolish the neuroprotective effect of HYP on DA neurons. These results showed that HYP protected the dopaminergic neurons from the MPP(+)- and MPTP-induced injuries, which did not rely on the Akt pathway.
 BACKGROUND: IgG antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) define a subset of associated disorders (myelin oligodendrocyte glycoprotein associated disorders (MOGAD)) that can have a relapsing course. However, information on relapse predictors is scarce. The utility of retesting MOG-IgG over time and measuring their titres is uncertain. We aimed to evaluate the clinical relevance of longitudinal MOG-IgG titre measurement to predict relapses in patients with MOGAD. METHODS: In this retrospective multicentre Italian cohort study, we recruited patients with MOGAD and available longitudinal samples (at least one >3 months after disease onset) and tested them with a live cell-based assay with endpoint titration (1:160 cut-off). Samples were classified as 'attack' (within 30 days since a disease attack (n=59, 17%)) and 'remission' (≥31 days after attack (n=295, 83%)). RESULTS: We included 102 patients with MOGAD (57% adult and 43% paediatric) with a total of 354 samples (83% from remission and 17% from attack). Median titres were higher during attacks (1:1280 vs 1:640, p=0.001). Median onset titres did not correlate with attack-related disability, age or relapses. Remission titres were higher in relapsing patients (p=0.02). When considering the first remission sample available for each patient, titres >1:2560 were predictors of relapsing course in survival (log rank, p<0.001) and multivariate analysis (p<0.001, HR: 10.9, 95% CI 3.4 to 35.2). MOG-IgG seroconversion to negative was associated with a 95% relapse incidence rate reduction (incidence rate ratio: 0.05, p<0.001). CONCLUSIONS: Persistent MOG-IgG positivity and high remission titres are associated with an increased relapse risk. Longitudinal MOG-IgG titres could be useful to stratify patients to be treated with long term immunosuppression.
 INTRODUCTION: A subcutaneous (SC) formulation of natalizumab has been recently authorised for multiple sclerosis patients. This study aimed to assess the implications of the new SC formulation, and to compare the annual treatment costs of SC versus intravenous (IV) natalizumab therapy from both the Spanish healthcare system (direct health cost) and the patient (indirect cost) perspectives. METHODS: A patient care pathway map and a cost-minimisation analysis were developed to estimate SC and IV natalizumab annual costs over a 2-year time horizon. Considering the patient care pathway and according to natalizumab experience (IV) or estimation (SC), a national expert panel involving neurologists, pharmacists, and nurses provided information/data regarding resource consumption for drug and patient preparation, administration, and documentation. One hour of observation was applied to the first six (SC) or 12 (IV) doses, and 5 min for successive doses. The Day hospital (infusion suite) facilities at a reference hospital were considered for IV administrations and the first six SC injections. For successive SC injections, either a reference hospital or regional hospital in a consulting room was considered. Productivity time associated with travel (56 min to reference hospital, 24 min to regional hospital) and waiting time pre- and post-treatment (SC 15 min, IV 25 min) were assessed for patients and caregivers (accompanying 20% of SC and 35% of IV administrations). National salaries for healthcare professionals were used for cost estimation (€, year 2021). RESULTS: At years 1 and 2, total time and cost savings (excluding drug acquisition cost) per patient, driven by saving on administration and patient and caregiver productivity for SC at a reference hospital versus IV at a reference hospital, were 116 h (a reduction of 54.6%) and €3682.82 (a reduction of 66.2%). In the case of natalizumab SC at a regional hospital, the total time and cost saving were 129 h (a reduction of 60.6%) and €3883.47 (a reduction of 69.8%). CONCLUSIONS: Besides the potential benefits of convenient administration and improving work-life balance, as suggested by the expert panel, natalizumab SC was associated with cost savings for the healthcare system by avoiding drug preparation, reducing administration time, and freeing up infusion suite capacity. Additional cost savings could be derived with regional hospital administration of natalizumab SC by reducing productivity loss.
 OBJECTIVE: To examine the anti-inflammatory effect of grape seed extract (GSE) in animal and cellular models and explore its mechanism of action. METHODS: This study determined the inhibitory effect of GSE on macrophage inflammation and Th1 and Th17 polarization in vitro. Based on the in vitro results, the effects and mechanisms of GSE on multiple sclerosis (MS)-experimental autoimmune encephalomyelitis (EAE) mice model were further explored. The C57BL/6 mice were intragastrically administered with 50 mg/kg of GSE once a day from the 3rd day to the 27th day after immunization. The activation of microglia, the polarization of Th1 and Th17 and the inflammatory factors such as tumor necrosis factor- α (TNF- α), interleukin-1 β (IL-1 β), IL-6, IL-12, IL-17 and interferon-γ (IFN-γ) secreted by them were detected in vitro and in vivo by flow cytometry, enzyme linked immunosorbent assay (ELISA), immunofluorescence staining and Western blot, respectively. RESULTS: GSE reduced the secretion of TNF-α, IL-1 β and IL-6 in bone marrow-derived macrophages stimulated by lipopolysaccharide (P<0.01), inhibited the secretion of TNF-α, IL-1 β, IL-6, IL-12, IL-17 and IFN-γ in spleen cells of EAE mice immunized for 9 days (P<0.05 or P<0.01), and reduced the differentiation of Th1 and Th17 mediated by CD3 and CD28 factors (P<0.01). GSE significantly improved the clinical symptoms of EAE mice, and inhibited spinal cord demyelination and inflammatory cell infiltration. Peripherally, GSE downregulated the expression of toll-like-receptor 4 (TLR4) and Rho-associated kinase (ROCKII, P<0.05 or P<0.01), and inhibited the secretion of inflammatory factors (P<0.01 or P<0.05). In the central nervous system, GSE inhibited the infiltration of CD45(+)CD11b(+) and CD45(+)CD4(+) cells, and weakened the differentiation of Th1 and Th17 (P<0.05). Moreover, it reduced the secretion of inflammatory factors (P<0.01), and prevented the activation of microglia (P<0.05). CONCLUSION: GSE had a beneficial effect on the pathogenesis and progression of EAE by inhibiting inflammatory response as a potential drug and strategy for the treatment of MS.
 METHODS: We searched PubMed, Cochrane Library, and Epistemonikos to identify systematic reviews and meta-analysis (SRs). We searched for neurological diseases and psychiatric disorders, including Alzheimer's disease (AD), attention deficit hyperactivity disorder (ADHD), amyotrophic lateral sclerosis (ALS), autism spectrum disorder (ASD), anorexia nervosa (AN), bipolar disorder (BD), eating disorder (ED), generalized anxiety disorder (GAD), major depressive disorder (MDD), multiple sclerosis (MS), obsessive compulsive disorder (OCD), Parkinson's disease (PD), posttraumatic stress disorder (PTSD), spinal cord injury (SCI), schizophrenia, and stroke. We used A Measurement Tool to Assess Systematic Reviews (AMSTAR-2) to evaluate the quality of included SRs. We also created an evidence map showing the role of gut microbiota in neurological diseases and the certainty of the evidence. RESULTS: In total, 42 studies were included in this evidence mapping. Most findings were obtained from observational studies. According to the AMSTAR-2 assessment, 21 SRs scored "critically low" in terms of methodological quality, 16 SR scored "low," and 5 SR scored "moderate." A total of 15 diseases have been investigated for the potential association between gut microbiome alpha diversity and disease, with the Shannon index and Simpson index being the most widely studied. A total of 12 diseases were investigated for potential link between beta diversity and disease. At the phylum level, Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, and Verrucomicrobia were more researched. At the genus level, Prevotella, Coprococcus, Parabacteroides, Phascolarctobacterium, Escherichia Shigella, Alistipes, Sutteralla, Veillonella, Odoribacter, Faecalibacterium, Bacteroides, Bifidobacterium, Dialister, and Blautia were more researched. Some diseases have been found to have specific flora changes, and some diseases have been found to have common intestinal microbiological changes. CONCLUSION: We found varied levels of evidence for the associations between gut microbiota and neurological diseases; some gut microbiota increased the risk of neurological diseases, whereas others showed evidence of benefit that gut microbiota might be promising therapeutic targets for such diseases.
 The retina and the optic nerve are considered extensions of the central nervous system (CNS) and thus can serve as the window for evaluation of CNS disorders. Spectral domain optical coherence tomography (OCT) allows for detailed evaluation of the retina and the optic nerve. OCT can non-invasively document changes in single retina layer thickness and structure due to neuronal and retinal glial cells (RGC) modifications in systemic and local inflammatory and neurodegenerative diseases. These can include evaluation of retinal nerve fibre layer and ganglion cell complex, hyper-reflective retinal spots (HRS, sign of activated microglial cells in the retina), subfoveal neuroretinal detachment, disorganization of the inner retinal layers (DRIL), thickness and integrity of the outer retinal layers and choroidal thickness. This review paper will report the most recent data on the use of OCT as a non invasive imaging biomarker for evaluation of the most common systemic neuroinflammatory and neurodegenerative/neurocognitive disorders in the adults and in paediatric population. In the adult population the main focus will be on diabetes mellitus, multiple sclerosis, optic neuromyelitis, neuromyelitis optica spectrum disorders, longitudinal extensive transverse myelitis, Alzheimer and Parkinson diseases, Amyotrophic lateral sclerosis, Huntington's disease and schizophrenia. In the paediatric population, demyelinating diseases, lysosomal storage diseases, Nieman Pick type C disease, hypoxic ischaemic encephalopathy, human immunodeficiency virus, leukodystrophies spinocerebellar ataxia will be addressed.
 Myalgic encephalitis/chronic fatigue syndrome, an intractable disease characterized by profound fatigue, sleep disturbance, cognitive impairment, and orthostatic intolerance, among other features, often occurs after infectious episodes. Patients experience various types of chronic pain; however, post-exertional malaise is the most significant feature, which requires pacing. In this article, I summarize the current diagnostic and therapeutic approaches and describe recent biological research in this domain.
 Obesity-induced chronic inflammation has been linked to several autoimmune diseases, including rheumatoid arthritis, type 1 diabetes, and multiple sclerosis. The underlying mechanisms are not yet fully understood, but it is believed that chronic inflammation in adipose tissue can lead to the production of pro-inflammatory cytokines and chemokines, which can trigger immune responses and contribute to the development of autoimmune diseases. However, the underlying mechanisms that lead to the infiltration of immune cells into adipose tissue are not fully understood. In this study, we observed a time-dependent response to a high-fat diet in the liver and epididymal white adipose tissue using gene set enrichment analysis. Our findings revealed a correlation between early abnormal innate immune responses in the liver and late inflammatory response in the adipose tissue, that eventually leads to systemic inflammation. Specifically, our data suggest that the dysregulated NADH homeostasis in the mitochondrial matrix, interacting with the mitochondrial translation process, could serve as a sign marking the transition from liver inflammation to adipose tissue inflammation. Taken together, our study provides valuable insights into the molecular mechanisms underlying the development of chronic inflammation and associated autoimmune diseases in obesity.
 The Australian rainforest is a rich source of medicinal plants that have evolved in the face of dramatic environmental challenges over a million years due to its prolonged geographical isolation from other continents. The rainforest consists of an inherent richness of plant secondary metabolites that are the most intense in the rainforest. The search for more potent and more bioavailable compounds from other plant sources is ongoing, and our short review will outline the pathways from the discovery of bioactive plants to the structural identification of active compounds, testing for potency, and then neuroprotection in a triculture system, and finally, the validation in an appropriate neuro-inflammatory mouse model, using some examples from our current research. We will focus on neuroinflammation as a potential treatment target for neurodegenerative diseases including multiple sclerosis (MS), Parkinson's (PD), and Alzheimer's disease (AD) for these plant-derived, anti-inflammatory molecules and highlight cytokine suppressive anti-inflammatory drugs (CSAIDs) as a better alternative to conventional nonsteroidal anti-inflammatory drugs (NSAIDs) to treat neuroinflammatory disorders.
 Controlling CD4(+) immune cell infiltration of the brain is a leading aim in designing therapeutic strategies for a range of neuropathological disorders such as multiple sclerosis, Alzheimer's disease, and depression. CD4(+) T cells are a highly heterogeneous and reprogrammable family, which includes various distinctive cell types such as Th17, Th1, and Treg cells. Interestingly Th17 and Treg cells share a related transcriptomic profile, where the TGFβ-SMADS pathway plays a fundamental role in regulating the differentiation of both of these cell types. However, Th17 could be highly pathogenic and was shown to promote inflammation in various neuropathological disorders. Conversely, Treg is anti-inflammatory and is known to inhibit Th17. It could be noticed that Th17 frequencies of infiltration of the blood-brain barrier in various neurological disorders are significantly upregulated. However, Treg infiltration numbers are significantly low. The reasons behind these contradicting observations are still unknown. In this perspective, we propose that the difference in the T-cell receptor repertoire diversity, diapedesis pathways, chemokine expression, and mechanical properties of these two cell types could be contributing to answering this intriguing question.
 BACKGROUND: Nabiximols is a commercially available cannabinoid buccal spray containing 2.7 mg Δ9-tetrahydrocannabinol (THC) and 2.5 mg cannabidiol (CBD) per spray. It is approved by Health Canada for adults with cancer pain or spasticity/neuropathic pain related to multiple sclerosis. Despite a lack of published studies regarding the use of nabiximols in children, it is being used in clinical practice for indications of pain, nausea/vomiting, and spasticity. OBJECTIVE: To describe the use of nabiximols in children. METHODS: This retrospective single-cohort study involved hospitalized pediatric patients who received at least 1 dose of nabiximols between January 2005 and August 2018. Descriptive statistical analyses were performed. RESULTS: A total of 34 patients were included. The median age was 14 (range 0.6-18) years, and 11 patients (32%) were admitted under the oncology service. The median dose of nabiximols was 1.9 (range 0.3-10.8) sprays per day, and the median duration was 3.8 (range 1-213) days. Nabiximols was most commonly used to treat pain and nausea/vomiting and was most frequently prescribed by pain specialists. Perceived effectiveness was documented in 17 (50%) of the cases, with variable results being reported. The most commonly reported adverse effects were drowsiness and tachycardia (3/34, 9%, for each). CONCLUSION: In this study, nabiximols was prescribed for children in all age groups, for a variety of conditions, but most commonly for pain and nausea/vomiting. Further study, in the form of a large, prospective randomized controlled trial with clearly defined efficacy and safety end points for nausea/vomiting and/or pain, is needed to determine whether nabiximols is effective and safe in children.
 BACKGROUND AND OBJECTIVES: Although the association between multiple sclerosis and trigeminal neuralgia (TN) is well established, little is known about TN pain characteristics and postoperative pain outcomes after microvascular decompression (MVD) in patients with TN and other autoimmune diseases. In this study, we aim to describe presenting characteristics and postoperative outcomes in patients with concomitant TN and autoimmune disease who underwent an MVD. METHODS: A retrospective review of all patients who underwent an MVD at our institution between 2007 and 2020 was conducted. The presence and type of autoimmune disease were recorded for each patient. Patient demographics, comorbidities, clinical characteristics, postoperative Barrow Neurological Institute (BNI) pain and numbness scores, and recurrence data were compared between groups. RESULTS: Of the 885 patients with TN identified, 32 (3.6%) were found to have concomitant autoimmune disease. Type 2 TN was more common in the autoimmune cohort (P = .01). On multivariate analysis, concomitant autoimmune disease, younger age, and female sex were found to be significantly associated with higher postoperative BNI score (P = .04, <0.001, and <0.001, respectively). In addition, patients with autoimmune disease were more likely to experience significant pain recurrence (P = .009) and had shorter time to recurrence on Kaplan-Meier analysis (P = .047), although this relationship was attenuated on multivariate Cox proportional hazards regression. CONCLUSION: Patients with concomitant TN and autoimmune disease were more likely to have Type 2 TN, had worse postoperative BNI pain scores at the final follow-up after MVD, and were more likely to experience recurrent pain than patients with TN alone. These findings may influence postoperative pain management decisions for these patients and support a possible role for neuroinflammation in TN pain.
 BACKGROUND: The aim of this study was to analyze the relationship between extent, severity (stage), and rate of progression (grade) of periodontitis with systemic diseases as well as smoking using a large database. METHODS: Patients' records identified in the BigMouth Dental Data Repository with a periodontal diagnosis based on the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions were evaluated. Patients were further categorized based on extent, severity, and rate of progression. Data were extracted from patients' electronic health records including demographic characteristics, dental procedural codes, and self-reported medical conditions, as well as the number of missing teeth. RESULTS: A total of 2069 complete records were ultimately included in the analysis. Males were more likely to have generalized periodontitis and stage III or IV periodontitis. Older individuals were more likely diagnosed with grade B and stage III or IV periodontitis. Individuals with generalized disease, grade C, and stage IV demonstrated a significantly higher number of missing teeth. Higher numbers of tooth loss reported during supportive periodontal treatment were noted in generalized disease and stage IV periodontitis. Multiple sclerosis and smoking were significantly associated with grade C periodontitis. CONCLUSIONS: Within the limitations of this retrospective study that utilized the BigMouth dental data repository, smokers were significantly associated with rapid progression of periodontitis (grade C). Gender, age, number of missing teeth, and number of tooth loss during supportive periodontal treatment were associated with disease characteristics.
 Topographic mapping of neural circuits is fundamental in shaping the structural and functional organization of brain regions. This developmentally important process is crucial not only for the representation of different sensory inputs but also for their integration. Disruption of topographic organization has been associated with several neurodevelopmental disorders. The aim of this review is to highlight the mechanisms involved in creating and refining such well-defined maps in the brain with a focus on the Eph and ephrin families of axon guidance cues. We first describe the transgenic models where ephrin-A expression has been manipulated to understand the role of these guidance cues in defining topography in various sensory systems. We further describe the behavioral consequences of lacking ephrin-A guidance cues in these animal models. These studies have given us unexpected insight into how neuronal activity is equally important in refining neural circuits in different brain regions. We conclude the review by discussing studies that have used treatments such as repetitive transcranial magnetic stimulation (rTMS) to manipulate activity in the brain to compensate for the lack of guidance cues in ephrin-knockout animal models. We describe how rTMS could have therapeutic relevance in neurodevelopmental disorders with disrupted brain organization.
 Inflammatory bowel disease (IBD) is a widespread autoimmune disease that may even be life-threatening. IBD is divided into two major subtypes: ulcerative colitis and Crohn's disease. Interleukin (IL)-35 and IL-37 are anti-inflammatory cytokines that belong to IL-12 and IL-1 families, respectively. Their recruitment relieves inflammation in various autoimmune diseases, including psoriasis, multiple sclerosis, rheumatoid arthritis, and IBD. Regulatory T cells (Tregs) and regulatory B cells (Bregs) are the primary producers of IL-35/IL-37. IL-35 and IL-37 orchestrate the regulation of the immune system through two main strategies: Blocking nuclear transcription factor kappa-B (NF-kB) and mitogen-activated protein kinase (MAPK) signaling pathways or promoting the proliferation of Tregs and Bregs. Moreover, IL-35 and IL-37 can also inhibit inflammation by adjusting the T helper (Th)17/Treg ratio balance. Among the anti-inflammatory cytokines, IL-35 and IL-37 have significant potential to reduce intestinal inflammation. Therefore, administering IL-35/IL-37-based drugs or blocking their inhibitor microRNAs could be a promising approach to alleviate IBD symptoms. Overall, in this review article, we summarized the therapeutic application of IL-35 and IL-37 in both human and experimental models of IBD. Also, it is hoped that this practical information will reach beyond IBD therapy and shed some light on treating all intestinal inflammations.
 Neurological diseases are recognized as major causes of disability and mortality worldwide. Due to the dynamic progress of diseases such as Alzheimer's disease (AD), Parkinson's Disease (PD), Schizophrenia, Depression, and Multiple Sclerosis (MD), scientists are mobilized to look for new and more effective methods of interventions. A growing body of evidence suggests that inflammatory processes and an imbalance in the composition and function of the gut microbiome, which play a critical role in the pathogenesis of various neurological diseases and dietary interventions, such as the Mediterranean diet the DASH diet, or the ketogenic diet can have beneficial effects on their course. The aim of this review was to take a closer look at the role of diet and its ingredients in modulating inflammation associated with the development and/or progression of central nervous system diseases. Presented data shows that consuming a diet abundant in fruits, vegetables, nuts, herbs, spices, and legumes that are sources of anti-inflammatory elements such as omega-3 fatty acids, polyphenols, vitamins, essential minerals, and probiotics while avoiding foods that promote inflammation, create a positive brain environment and is associated with a reduced risk of neurological diseases. Personalized nutritional interventions may constitute a non-invasive and effective strategy in combating neurological disorders.
 Vitamin D plays an active role beyond mineral metabolism and skeletal health, including regulation of the immune system. Vitamin D deficiency is widely prevalent, and observational studies link low vitamin D status to a risk of infections and auto-immune disorders. Reports indicate an inverse relationship between vitamin D status and such conditions. This review details vitamin D signalling interactions with the immune system and provides experimental and clinical evidence evaluating vitamin D status, vitamin D supplementation and host susceptibility to infections, inflammation and auto-immunity. The published literature including related reviews, systematic reviews, meta-analyses, randomised controlled trials (RCTs), observational studies and basic science reports have been synthesised. Meta-analyses of observational studies have demonstrated a link between low vitamin D status and risk of acute respiratory infections, COVID-19 disorders, multiple sclerosis, type 1 diabetes (T1DM), inflammatory bowel disease (IBD), systemic lupus erythematosus and other auto-immune disorders. Observational studies suggest that vitamin D supplementation may protect against several infectious and auto-immune conditions. Meta-analyses of RCTs had mixed results, demonstrating a small protective role for vitamin D supplementation against acute respiratory infections, especially in those with vitamin D deficiency and children, and providing modest benefits for the management of T1DM and IBD. Vitamin D status is inversely associated with the incidence of several infectious and auto-immune conditions. Supplementation is recommended for those with vitamin D deficiency or at high risk of deficiency, and it might provide additional benefit in acute respiratory infections and certain auto-immune conditions.
 Neurodegenerative diseases (NDs) are sporadic maladies that affect patients' lives with progressive neurological disabilities and reduced quality of life. Neuroinflammation and oxidative reaction are among the pivotal factors for neurodegenerative conditions, contributing to the progression of NDs, such as Parkinson's disease (PD), Alzheimer's disease (AD), multiple sclerosis (MS) and Huntington's disease (HD). Management of NDs is still less than optimum due to its wide range of causative factors and influences, such as lifestyle, genetic variants, and environmental aspects. The neuroprotective and anti-neuroinflammatory activities of Moringa oleifera have been documented in numerous studies due to its richness of phytochemicals with antioxidant and anti-inflammatory properties. This review highlights up-to-date research findings on the anti-neuroinflammatory and neuroprotective effects of M. oleifera, including mechanisms against NDs. The information was gathered from databases, which include Scopus, Science Direct, Ovid-MEDLINE, Springer, and Elsevier. Neuroprotective effects of M. oleifera were mainly assessed by using the crude extracts in vitro and in vivo experiments. Isolated compounds from M. oleifera such as moringin, astragalin, and isoquercitrin, and identified compounds of M. oleifera such as phenolic acids and flavonoids (chlorogenic acid, gallic acid, ferulic acid, caffeic acid, kaempferol, quercetin, myricetin, (-)-epicatechin, and isoquercitrin) have been reported to have neuropharmacological activities. Therefore, these compounds may potentially contribute to the neuroprotective and anti-neuroinflammatory effects. More in-depth studies using in vivo animal models of neurological-related disorders and extensive preclinical investigations, such as pharmacokinetics, toxicity, and bioavailability studies are necessary before clinical trials can be carried out to develop M. oleifera constituents into neuroprotective agents.
 BACKGROUND: Microvascular decompressions (MVDs) are effective open-surgical procedures for trigeminal neuralgia (TN). Intraoperative management of compressive veins may include either venous transposition or coagulation. Although both are generally considered safe, which technique results in optimal postoperative outcomes remains unclear. OBJECTIVE: To compare postoperative pain and numbness outcomes after an MVD in patients with TN of exclusive venous compression. METHODS: We retrospectively reviewed all patients with TN who underwent MVDs at our institution from 2007 to 2020. Patients with TN of pure venous compression were identified using MRI imaging, which was subsequently confirmed intraoperatively. Patient demographics, procedural characteristics, and postoperative pain and numbness scores were recorded and compared. Factors associated with pain recurrence were assessed using survival analyses and multivariate regressions. RESULTS: We identified 181 patients who presented with TN of pure venous compression. Using a multivariate linear regression, adjusted for age, sex, and presence of multiple sclerosis, use of venous transposition vs coagulation was not significantly associated with the Barrow Neurological Institute pain score at final follow-up, although venous transposition was significantly predictive of a worse postoperative Barrow Neurological Institute numbness score ( P = .003). Using a Kaplan-Meier survival analysis and a multivariate Cox proportional hazards regression, respectively, venous transposition was significantly associated with faster ( P = .01) as well as higher risk for pain recurrence ( P = .01). CONCLUSION: The use of venous coagulation during an MVD is associated with better postoperative pain and numbness outcomes. The results of our study may help inform preoperative patient counseling and surgical management for TN cases that involve pure venous compression.
 OBJECTIVES: Since the beginning of its use for the prevention of tuberculosis (TB) in 1921, other uses of BCG (Bacillus Calmette-Guérin) have been proposed, particularly in the treatment of malignant solid tumors, multiple sclerosis, and other autoimmune diseases. Its beneficial impact on other infections, by nontuberculous mycobacteria, and by viruses, has been more often studied in recent years, especially after the introduction of the concept of trained immunity. The present study's objective was to review the possible indications of BCG and the immunological rationale for these indications. DATA SOURCE: Non-systematic review carried out in the PubMed, SciELO and Google Scholar databases, using the following search terms: "BCG" and "history", "efficacy", "use", "cancer", "trained immunity", "other infections", "autoimmune diseases". DATA SYNTHESIS: There is epidemiological evidence that BCG can reduce overall child morbidity/mortality beyond what would be expected from TB control. BCG is able to promote cross-immunity with nontuberculous mycobacteria and other bacteria. BCG promotes in vitro changes that increase innate immune response to other infections, mainly viral ones, through mechanisms known as trained immunity. Effects on cancer, except bladder cancer, and on autoimmune and allergic diseases are debatable. CONCLUSIONS: Despite evidence obtained from in vitro studies, and some epidemiological and clinical evidence, more robust evidence of in vivo efficacy is still needed to justify the use of BCG in clinical practice, in addition to what is recommended by the National Immunization Program for TB prevention and bladder cancer treatment.
 Rheumatoid arthritis (RA) as a chronic inflammatory disorder affects around 1% of the world population. Fibroblast-like synoviocyte (FLS), one of the main cells in RA pathogenesis is characterized by hyperproliferation and resistance to apoptosis resulting to synovial hyperplasia. Dimethyl fumarate (DMF) has been licensed for the treatment of multiple sclerosis (MS) and psoriasis; however, its role in RA is unknown. DMF has immunomodulatory properties and may be considered as therapeutic approach in RA treatment. In this study, we aimed to investigate the effect of DMF on controlling FLS-mediated synovial inflammation and joint destruction in RA. FLSs were isolated from synovial tissues of 8 patients with RA and treated with DMF. Apoptosis rate was analyzed by Annexin V-FITC. Cell proliferation was measured by carboxyfluorescein succinimidyl ester (CFSE) dye. The matrix metalloproteinase 3 (MMP3) and NF-кB pathway protein (p65) mRNA expression were evaluated by RT-PCR. Also, the IL-6 production and lactate release were measured in FLS supernatant. DMF treatment decreased the cell proliferation and increased apoptosis in a dose dependent manner. DMF-treated FLS showed a reduction in IL-6 and lactate release. Moreover, it was revealed that DMF inhibited the expression of p65 and MMP3. Our data demonstrate that DMF treatment suppresses the aggressive and inflammatory features of RA FLSs. Our Results suggest that DMF might be expected to be evaluated as a therapy for RA.
 This study was conducted to demonstrate the possible protective and therapeutic effects of naringenin, an estrogenically effective flavonoid, in experimental autoimmune encephalomyelitis (EAE), which is the rodent model of multiple sclerosis. For this purpose, 50 12-week-old C57BL6 male mice were divided into five groups; control, naringenin, EAE, prophylactic naringenin + EAE, and EAE + therapeutic naringenin. The EAE model was induced with myelin oligodendrocyte glycoprotein((35-55)), and naringenin (50 mg/kg) was administered by oral gavage. The prophylactic and therapeutic effects of naringenin were examined according to clinical, histopathological, immunohistochemical, electron microscopic, and RT-PCR (aromatase, 3βHSD, estrogen receptors, and progesterone receptor expression) parameters. The acute EAE model was successfully induced, along with its clinical and histopathological findings. RT-PCR showed that expression of aromatase, 3βHSD, estrogen receptor-β, and progesterone receptor gene decreased, while estrogen receptor-α increased after EAE induction. Electron microscopic analysis showed mitochondrial damage and degenerative changes in myelinated axons and neurons in EAE, which could be behind the downregulation in the expressions of neurosteroid enzymes. Aromatase immunopositivity rates also decreased in EAE, while estrogen receptor α and β, and progesterone receptor immunopositivity rates increased. Naringenin improved aromatase immunopositivity rates and gene expression in both prophylactic and therapeutic use. Clinical and histopathological findings revealed that EAE findings were alleviated in both prophylactic and therapeutic groups, along with significantly decreased inflammatory cell infiltrations in the white matter of the spinal cords. In conclusion, naringenin could provide long-term beneficial effects even in prophylactic use due to stimulating aromatase expression, but it could not prevent or eliminate the EAE model's lesions completely.
 Since the discovery of the mechanosensitive Piezo1 channel in 2010, there has been a significant amount of research conducted to explore its regulatory role in the physiology and pathology of various organ systems. Recently, a growing body of compelling evidence has emerged linking the activity of the mechanosensitive Piezo1 channel to health and disease of the central nervous system. However, the exact mechanisms underlying these associations remain inadequately comprehended. This review systematically summarizes the current research on the mechanosensitive Piezo1 channel and its implications for central nervous system mechanobiology, retrospects the results demonstrating the regulatory role of the mechanosensitive Piezo1 channel on various cell types within the central nervous system, including neural stem cells, neurons, oligodendrocytes, microglia, astrocytes, and brain endothelial cells. Furthermore, the review discusses the current understanding of the involvement of the Piezo1 channel in central nervous system disorders, such as Alzheimer's disease, multiple sclerosis, glaucoma, stroke, and glioma.
 Royal jelly (RJ), a highly nutritious natural product, has gained recognition for its remarkable health-promoting properties, leading to its widespread use in the pharmaceutical, food, and cosmetic industries. Extensive investigations have revealed that RJ possesses a broad spectrum of therapeutic effects, including anti-inflammatory, antioxidant, antitumor, anti-aging, and antibacterial activities. Distinctive among bee products, RJ exhibits a significantly higher water and relatively lower sugar content. It is characterized by its substantial protein content, making it a valuable source of this essential macronutrient. Moreover, RJ contains a diverse array of bioactive substances, such as lipids, phenolic compounds, flavonoids, organic acids, minerals, vitamins, enzymes, and hormones. This review aims to provide an overview of current research on the bioactive components present in RJ and their associated health-promoting qualities. According to existing literature, these bioactive substances hold great potential as alternative approaches to enhancing human health. Notably, this review emphasizes the anti-inflammatory properties of RJ, particularly in relation to inflammatory diseases, such as multiple sclerosis (MS), rheumatoid arthritis (RA), and inflammatory bowel diseases (IBD). Furthermore, we delve into the antitumor and antioxidant activities of RJ, aiming to deepen our understanding of its biological functions. By shedding light on the multifaceted benefits of RJ, this review seeks to encourage its utilization and inspire further investigation in this field.
 OBJECTIVE: Modern clinical rehabilitation practice aligned to the International Classification of Functioning, Disability and Health and the Convention on the Rights of Persons with Disabilities highlights the importance of attention to participation in the rehabilitation formulation. This systematic review investigates the efficacy of rehabilitation interventions evaluated in common neurological disorders reported to influence participation outcomes. DATA SOURCES: PubMed, Web of Science and PsycINFO databases were searched from inception to 25 April 2023. Only randomised controlled trials were considered for inclusion. REVIEW METHODS: The data were extracted by two independent reviewers in the following categories: characteristics of the included study publications, description of intervention and outcome measures. RESULTS: A total of 1248 unique article records were identified through the databases. Twenty-eight randomized controlled trials were included with 15 publications having participation as a primary outcome measure. Articles were related to multiple sclerosis (N = 4), spinal cord injury (N = 2), stroke (N = 16) and traumatic brain injury (N = 6). Four publications showed significant differences in pre- and post-intervention within experimental groups. All four articles described participation as primary outcome measure. CONCLUSION: There is a limited evidence of the identified rehabilitation interventions to improve participation in common neurological conditions. However, there was a paucity of articles involving individual with Parkinson's disease that met the inclusion criteria.
 Type-B monoamine oxidase inhibitors, encompassing selegiline, rasagiline, and safinamide, are available to treat Parkinson's disease. These drugs ameliorate motor symptoms and improve motor fluctuation in the advanced stages of the disease. There is also evidence supporting the benefit of type-B monoamine oxidase inhibitors on non-motor symptoms of Parkinson's disease, such as mood deflection, cognitive impairment, sleep disturbances, and fatigue. Preclinical studies indicate that type-B monoamine oxidase inhibitors hold a strong neuroprotective potential in Parkinson's disease and other neurodegenerative diseases for reducing oxidative stress and stimulating the production and release of neurotrophic factors, particularly glial cell line-derived neurotrophic factor, which support dopaminergic neurons. Besides, safinamide may interfere with neurodegenerative mechanisms, counteracting excessive glutamate overdrive in basal ganglia motor circuit and reducing death from excitotoxicity. Due to the dual mechanism of action, the new generation of type-B monoamine oxidase inhibitors, including safinamide, is gaining interest in other neurological pathologies, and many supporting preclinical studies are now available. The potential fields of application concern epilepsy, Duchenne muscular dystrophy, multiple sclerosis, and above all, ischemic brain injury. The purpose of this review is to investigate the preclinical and clinical pharmacology of selegiline, rasagiline, and safinamide in Parkinson's disease and beyond, focusing on possible future therapeutic applications.
 JC polyomavirus (JCV) establishes an asymptomatic latent and/or persistent infection in most of the adult population. However, in immunocompromised individuals, JCV can cause a symptomatic infection of the brain, foremost progressive multifocal leukoencephalopathy (PML). In the last two decades, there has been increasing concern among patients and the medical community as PML was observed as an adverse event in individuals treated with modern (selective) immune suppressive treatments for various immune-mediated diseases, especially multiple sclerosis (MS). It became evident that this devastating complication also needs to be considered beyond the patient populations historically at risk, including those with hematological malignancies or HIV-infected individuals.We review the clinical presentation of PML, its variants, pathogenesis, and current diagnostic approaches. We further discuss the need to validate JCV-directed interventions and highlight current management strategies based on early diagnosis and restoring JCV-specific cellular immunity, which is crucial for viral clearance and survival. Lastly, we discuss the importance of biomarkers for diagnosis and response to therapy, instrumental in defining sensitive study endpoints for successful clinical trials of curative or preventive therapeutics.Advances in understanding PML pathophysiology, host and viral genetics, and diagnostics, in conjunction with novel immunotherapeutic approaches indicate that the time is right to design and carry out definitive trials to develop preventive options and curative therapy for JCV-associated diseases.
 PURPOSE: A Clinical Practice Guideline (CPG) is required to provide guidance on optimal service delivery for Functional Electrical Stimulation (FES) to support upright mobility in people living with mobility difficulties due to an upper motor neuron lesion, such as stroke or multiple sclerosis. A modified Delphi consensus study was used to provide expert consensus on best practice. METHODS: A Steering Group supported the recruitment of an Expert Panel, which included a range of stakeholders who participated in up to three survey rounds. In each round, panelists were asked to rate their agreement with draft statements about best practice using a 6-point Likert scale and add free text to explain their answer. Statements that achieved over 75% agree/strongly agree on the Likert scale were included in the CPG. Those that did not were revised based on free text comments and proposed in the next survey round. RESULTS: The first round included 82 statements with seven substatements. Sixty-five people (84% response rate) completed survey round 1 leading to 62 statements and four substatements being accepted. Fifty-six people responded to survey round 2, and consensus was achieved for all remaining statements. CONCLUSION: The accepted statements are included within the CPG and provide recommendations about who can benefit from FES and how they can be optimally supported through FES service provision. As such the CPG will support advocacy for, and optimal design of, FES services.
 Serum/glucocorticoid-regulated kinase 1 (SGK1), a member of the serine/threonine protein kinase gene family, is primarily regulated by serum and glucocorticoids. SGK1 is involved in the development of tumors and fibrotic diseases. However, relatively little research has been conducted on their role in immune and inflammatory diseases. SGK1 may act as a pivotal immune regulatory gene by modulating immune cells (e.g., T cells, macrophages, dendritic cells, and neutrophils) and functions and is involved in the pathogenesis of some immune and inflammatory diseases, such as inflammatory bowel disease, multiple sclerosis, allergic diseases, sepsis, and major depressive disorder. This review aims to provide an overview of the latest research focusing on the immune and inflammatory regulatory roles of SGK1 and provide new insights into diagnostic and therapeutic approaches for immune and inflammatory diseases.
 Gut microbiota can interact with the immune system through its metabolites. Short-chain fatty acids (SCFAs), as one of the most abundant metabolites of the resident gut microbiota play an important role in this crosstalk. SCFAs (acetate, propionate, and butyrate) regulate nearly every type of immune cell in the gut's immune cell repertoire regarding their development and function. SCFAs work through several pathways to impose protection towards colonic health and against local or systemic inflammation. Additionally, SCFAs play a role in the regulation of immune or non-immune pathways that can slow the development of autoimmunity either systematically or in situ. The present study aims to summarize the current knowledge on the immunomodulatory roles of SCFAs and the association between the SCFAs and autoimmune disorders such as celiac disease (CD), inflammatory bowel disease (IBD), rheumatoid arthritis (RA), multiple sclerosis (MS), systemic lupus erythematosus (SLE), type 1 diabetes (T1D) and other immune-mediated diseases, uncovering a brand-new therapeutic possibility to prevent or treat autoimmunity.
 INTRODUCTION: Processing speed is defined as the ability to quickly process information, which is generally considered as one of the affected cognitive functions of multiple sclerosis and schizophrenia. Paper-pencil type tests are traditionally used in the assessment of processing speed. However, these tests generally need to be conducted under the guidance of clinicians in a specific environment, which limits their application in cognitive assessment or training in daily life. Therefore, this paper proposed an intelligent evaluation method of processing speed to assist clinicians in diagnosis. METHODS: We created an immersive virtual street embedded with Stroop task (VR-Street). The behavior and performance information was obtained by performing the dual-task of street-crossing and Stroop, and a 50-participant dataset was established with the label of standard scale. Utilizing Pearson correlation coefficient to find the relationship between the dual-task features and the cognitive test results, and an intelligent evaluation model was developed using machine learning. RESULTS: Statistical analysis showed that all Stroop task features were correlated with cognitive test results, and some behavior features also showed correlation. The estimated results showed that the proposed method can estimate the processing speed score with an adequate accuracy (mean absolute error of 0.800, relative accuracy of 0.916 and correlation coefficient of 0.804). The combination of Stroop features and behavior features showed better performance than single task features. DISCUSSION: The results of this work indicates that the dual-task design in this study better mobilizes participants' attention and cognitive resources, and more fully reflects participants' cognitive processing speed. The proposed method provides a new opportunity for accurate quantitative evaluation of cognitive function through virtual reality.
 Human mesenchymal stromal cells (hMSCs) are mechanically sensitive undergoing phenotypic alterations when subjected to shear stress, cell aggregation, and substrate changes encountered in 3D dynamic bioreactor cultures. However, little is known about how bioreactor microenvironment affects the secretion and cargo profiles of hMSC-derived extracellular vesicles (EVs) including the subset, "exosomes", which contain therapeutic proteins, nucleic acids, and lipids from the parent cells. In this study, bone marrow-derived hMSCs were expanded on 3D Synthemax II microcarriers in the PBS mini 0.1L Vertical-Wheel bioreactor system under variable shear stress levels at 25, 40, and 64 RPM (0.1-0.3 dyn/cm(2)). The bioreactor system promotes EV secretion from hMSCs by 2.5-fold and upregulates the expression of EV biogenesis markers and glycolysis genes compared to the static 2D culture. The microRNA cargo was also altered in the EVs from bioreactor culture including the upregulation of miR-10, 19a, 19b, 21, 132, and 377. EV protein cargo was characterized by proteomics analysis, showing upregulation of metabolic, autophagy and ROS-related proteins comparing with 2D cultured EVs. In addition, the scalability of the Vertical-Wheel bioreactor system was demonstrated in a 0.5L bioreactor, showing similar or better hMSC-EV secretion and cargo content compared to the 0.1L bioreactor. This study advances our understanding of bio-manufacturing of stem cell-derived EVs for applications in cell-free therapy towards treating neurological disorders such as ischemic stroke, Alzheimer's disease, and multiple sclerosis.
 Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) is an essential regulator of the inflammatory process and immune response. In innate immunity, the NOD-RIPK2 signaling axis is an important pathway that directly mediates inflammation and immune response. In adaptive immunity, RIPK2 may affect T cell proliferation, differentiation and cellular homeostasis thereby involving T cell-driven autoimmunity, but the exact mechanism remains unclear. Recent advances suggest a key role of RIPK2 in diverse autoimmune diseases (ADs) such as inflammatory bowel diseases, rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and Behcet's disease. This review aims to provide valuable therapeutic direction for ADs by focusing on the function and modulation of RIPK2 in innate and adaptive immunity, its involvement with various ADs and the application of RIPK2-related drugs in ADs. We raise the notion that drug targeting RIPK2 could be a promising therapeutic strategy for the treatment of ADs, though much work remains to be done for clinical application.
 Many studies have shown that gut microbiota is closely related to autoimmune diseases (ADs). Studies on gut microbiota and ADs have also increased significantly, but no bibliometric analysis has summarized the association between gut microbiota and ADs. This study aimed to conduct a bibliometric and visual analysis of published studies on gut microbiota and ADs. Based on the Web of Science Core Collection SCI-expanded database, we utilize Excel 2019 and visualization analysis tools VOSviewer and co-occurrence13.2 (COOC13.2) for analysis. A total of 2516 related kinds of literature were included, and the number of papers presented an overall increasing trend. The country/region with the most publications is the USA, the institution is the Harvard Medical School, and the author is Mikael Knip from the USA. Hot research areas include intestinal regulation (such as dysbiosis, short chain fatty acids, and probiotics), multisystem ADs (such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease), and immune-related cells (such as T cells, and dendritic cells). Psoriasis, dysbiosis, autoimmune liver disease, and fecal microbiota transplantation may be the future research direction. Our research results can help researchers grasp the current status of ADs and gut microbiota research and find new research directions in the future.
 Oligodendrocytes are highly specialized glial cells characterized by their production of multilayer myelin sheaths that wrap axons to speed up action potential propagation. It is due to their specific role in supporting axons that impairment of myelin structure and function leads to debilitating symptoms in a wide range of degenerative diseases, including Multiple Sclerosis and Leukodystrophies. It is known that myelin damage can be receptor-mediated and recently oligodendrocytes have been shown to express Ca(2+) -permeable Transient Receptor Potential Ankyrin-1 (TRPA1) channels, whose activation can result in myelin damage in ischemia. Here, we show, using organotypic cortical slice cultures, that TRPA1 activation, by TRPA1 agonists JT010 and Carvacrol for varying lengths of time, induces myelin damage. Although TRPA1 activation does not appear to affect oligodendrocyte progenitor cell number or proliferation, it prevents myelin formation and after myelination causes internodal shrinking and significant myelin degradation. This does not occur when the TRPA1 antagonist, A967079, is also applied. Of note is that when TRPA1 agonists are applied for either 24 h, 3 days or 7 days, axon integrity appears to be preserved while mature myelinated oligodendrocytes remain but with significantly shortened internodes. These results provide further evidence that TRPA1 inhibition could be protective in demyelination diseases and a promising therapy to prevent demyelination and promote remyelination.
 Neuropathic pain arises from injuries to the nervous system. It affects 20% of the adult US population and poses a major socioeconomic burden yet remains exceedingly difficult to treat. Current therapeutic approaches have limited efficacy and a large side effect profile that impedes their ability to treat neuropathic pain effectively. Preclinical research over the last 30 yr has established the critical role that pro-inflammatory neuro-immune cell interactions have in the development and maintenance of neuropathic pain arising from various etiologies. Pro-inflammatory neuro-immune cell interactions also underlie the development of adverse side effects of opioids and the loss of their efficacy to treat pain. Evidence from work in our lab and others in preclinical animal models have shown that signaling from the bioactive sphingolipid, sphingosine-1-phosphate (S1P), through the S1P receptor subtype 1 (S1PR1) modulates neuro-immune cell interactions. Here, we discuss how targeting S1P/S1PR1 signaling with S1PR1 antagonists already Food and Drug Administration-approved or in clinical trials for multiple sclerosis can provide a viable pharmacotherapeutic approach to reduce neuro-immune cell inflammatory signaling and potentially treat patients suffering neuropathic pain and the adverse effects of opioids.
 Artemisinin and its derivatives, since their discovery by professor Tu Youyou in the early 1970s, have been the bedrock for the management of malaria globally. Recent works have implied that they could be used to manage other diseases including neurodegenerative disorders. Neurodegenerative disorders mainly occur in the adult population resulting from a progressive deterioration of neuronal structures. These include Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Multiple sclerosis (MS), among others. The PI3K/Akt signaling pathway plays a significant role in the central nervous system. It has been investigated extensively for its role in central nervous system physiological processes such as cell survival, autophagy, neuronal proliferation, and synaptic plasticity. Therefore, the modulation of this pathway will be crucial in the management of neurodegenerative disorders. This review seeks to compile most of the research findings on the possible neuroprotective role of artemisinins with special emphasis on their modulatory role on the PI3k/Akt pathway. A literature survey was conducted on PubMed, EBSCO, Web of Science, and EMBASE using the keyword artemisinins, and a total of 10,281 articles were retrieved from 1956 to 2022. Among these, 120 articles were examined using Mesh words like PI3k/Akt, neurodegeneration, and neuroinflammation coupled with boolean operators. Most research revealed that artemisinins could help neurodegenerative disorders by modulating the PI3k/Akt with subsequent inhibition of oxidative stress, neuroinflammation, and apoptosis. This paper illustrates that artemisinins could be repurposed as a neuroprotective agent.
 Profiling performance in the physiological domains underpinning upper limb function (such as strength, sensation, coordination) provides insight into an individual's specific impairments. This compliments the traditional medical 'diagnosis' model that is currently used in contemporary medicine. From an initial battery of 13 tests in which data were collected across the adult lifespan (n = 367, 20-95 years) and in those with neurological conditions (specifically, multiple sclerosis (n = 40), Parkinson's disease (n = 34), and stroke (n = 50)), six tests were selected to comprise a core upper limb physiological profile assessment (PPA). This comprised measures of handgrip strength, simple reaction time, finger dexterity, tactile sensation, bimanual coordination, and a functional task. Individual performance in each of these tests can be compared to a reference population score (devised from our database of healthy individuals aged under 60 years), informing the researcher or clinician how to best direct an intervention or treatment for the individual based on their specific impairment(s). Lastly, a composite score calculated from the average performance across the six tests provides a broad overview of an individual's overall upper limb function. Collectively, the upper limb PPA highlights specific impairments that are prevalent within distinct pathologies and reveals the magnitude of upper limb motor impairment specific to each condition.
 The purpose of the current study was to develop deep learning-regularized, single-step quantitative susceptibility mapping (QSM) quantification, directly generating QSM from the total phase map. A deep learning-regularized, single-step QSM quantification model, named SS-POCSnet, was trained with datasets created using the QSM synthesis approach in QSM reconstruction challenge 2.0. In SS-POCSnet, a data fidelity term based on a single-step model was iteratively applied that combined the spherical mean value kernel and dipole model. Meanwhile, SS-POCSnet regularized susceptibility maps, avoiding underestimating susceptibility values. We evaluated the SS-POCSnet on 10 synthetic datasets, 24 clinical datasets with lesions of cerebral microbleed (CMB) and calcification, and 10 datasets with multiple sclerosis (MS).On synthetic datasets, SS-POCSnet showed the best performance among the methods evaluated, with a normalized root mean squared error of 37.3% ± 4.2%, susceptibility-tuned structured similarity index measure of 0.823 ± 0.02, high-frequency error norm of 37.0 ± 5.7, and peak signal-to-noise ratio of 42.8 ± 1.1. SS-POCSnet also reduced the underestimations of susceptibility values in deep brain nuclei compared with those from the other models evaluated. Furthermore, SS-POCSnet was sensitive to CMB/calcification and MS lesions, demonstrating its clinical applicability. Our method also supported variable imaging parameters, including matrix size and resolution. It was concluded that deep learning-regularized, single-step QSM quantification can mitigate underestimating susceptibility values in deep brain nuclei.
 The prevalence of autoimmune diseases (ADs) worldwide has rapidly increased over the past few decades. Thus, in addition to the classical risk factors for ADs, such as genetic polymorphisms, infections and smoking, environmental triggers have been considered. Recent sequencing-based approaches have revealed that patients with extra-intestinal ADs, such as multiple sclerosis, rheumatoid arthritis, type 1 diabetes and systemic lupus erythematosus, have distinct gut microbiota compositions compared to healthy controls. Faecal microbiota transplantation or inoculation with specific microbes in animal models of ADs support the hypothesis that alterations of gut microbiota influence autoimmune responses and disease outcome. Here, we describe the compositional and functional changes in the gut microbiota in patients with extra-intestinal AD and discuss how the gut microbiota affects immunity. Moreover, we examine how the gut microbiota might be modulated in patients with ADs as a potential preventive or therapeutic approach.
 Alterations in the nuclear retinoid X receptor (RXRs) signalling have been implicated in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, stroke, multiple sclerosis and glaucoma. Single nucleotide polymorphisms (SNPs) are the main cause underlying single nucleic acid variations which in turn determine heterogeneity within various populations. These genetic polymorphisms have been suggested to associate with various degenerative disorders in population-wide analysis. This bioinformatics study was designed to investigate, search, retrieve and identify deleterious SNPs which may affect the structure and function of various RXR isoforms through a computational and molecular modelling approach. Amongst the 1,813 retrieved SNPs several were found to be deleterious with rs140464195_G139R, rs368400425_R358W and rs368586400_L383F RXRα mutant variants being the most detrimental ones causing changes in the interatomic interactions and decreasing the flexibility of the mutant proteins. Molecular genetics analysis identified seven missense mutations in RXRα/β/γ isoforms. Two novel mutations SNP IDs (rs1588299621 and rs1057519958) were identified in RXRα isoform. We used several in silico prediction tools such as SIFT, PolyPhen, I-Mutant, Protein Variation Effect Analyzer (PROVEAN), PANTHER, SNP&Go, PhD-SNP and SNPeffect to predict pathogenicity and protein stability associated with RXR mutations. The structural assessment by DynaMut tool revealed that hydrogen bonds were affected along with hydrophobic and carbonyl interactions resulting in reduced flexibility at the mutated residue positions but ultimately stabilizing the molecule as a whole. Summarizing, analysis of the missense mutations in RXR isoforms showed a mix of conclusive and inconclusive genotype-phenotype correlations suggesting the use of sophisticated computational analysis tools for studying RXR variants.Communicated by Ramaswamy H. Sarma.
 B cells play a crucial role in antigen presentation, antibody production and pro-/anti-inflammatory cytokine secretion in adaptive immunity. Several translational factors including transcription factors and cytokines participate in the regulation of B cell development, with the cooperation of epigenetic regulations. Autoimmune diseases are generally characterized with autoreactive B cells and high-level pathogenic autoantibodies. The success of B cell depletion therapy in mouse model and clinical trials has proven the role of B cells in pathogenesis of autoimmune diseases. The failure of B cell tolerance in immune checkpoints results in accumulated autoreactive naïve B (B(N)) cells with aberrant B cell receptor signaling and dysregulated B cell response, contributing to self-antibody-mediated autoimmune reaction. Dysregulation of translational factors and epigenetic alterations in B cells has been demonstrated to correlate with aberrant B cell compartment in autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, primary Sjögren's syndrome, multiple sclerosis, diabetes mellitus and pemphigus. This review is intended to summarize the interaction of translational factors and epigenetic regulations that are involved with development and differentiation of B cells, and the mechanism of dysregulation in the pathogenesis of autoimmune diseases.
 BACKGROUND AND PURPOSE: This study was undertaken to retrospectively compare rates of John Cunningham virus (JCV) seroconversion in natalizumab-treated patients before and during COVID-19-related community restrictions. Natalizumab is highly effective therapy for relapsing-remitting multiple sclerosis. Prolonged exposure to natalizumab in JCV-positive patients can cause progressive multifocal leukoencephalopathy, a potentially fatal brain infection. Serial assessment of JCV status is required for patients receiving natalizumab. METHODS: Patients receiving natalizumab at the Royal Melbourne Hospital were assessed for change in JCV serostatus and duration of exposure to natalizumab in two discrete time periods: from 1 February 2012 until 1 February 2017 ("pre-COVID"; n = 128) and from 1 April 2020 until 12 October 2022 ("COVID"; n = 214). A Poisson regression model adjusted for age at natalizumab commencement and sex was used to model seroconversion rate between the two time periods. RESULTS: The pre-COVID JCV seroconversion rate among natalizumab-treated patients at the Royal Melbourne Hospital was 9.08%. Conversely, we found a precipitous decline in JCV seroconversion during COVID lockdown. Annualized seroconversion during COVID-19-related restrictions was 2.01%. The annualized seroconversion rate was 4.7 times higher during the pre-COVID-19 period (95% confidence interval = 2.96-7.45, p < 0.0001) compared to the annualized seroconversion rate during COVID lockdown. Males had a 2× higher rate of seroconversion compared to females. CONCLUSIONS: JCV seroconversion among natalizumab-treated patients was markedly lower during COVID-19-related community restrictions. Restrictions observed in Melbourne were among the longest and most comprehensive implemented worldwide. This suggests the presence of modifiable risk factors that could lower rates of JCV seroconversion among natalizumab-treated patients.
 Experimental autoimmune encephalomyelitis (EAE) is a mouse model that can be used to investigate aetiology, pathogenesis, and treatment approaches for multiple sclerosis (MS). A novel integrated bioinformatics approach was used to understand the involvement of differentially expressed genes (DEGs) in the spleen of EAE mice through data mining of existing microarray and RNA-seq datasets. We screened differentially expressed mRNAs using mRNA expression profile data of EAE spleens taken from Gene Expression Omnibus (GEO). Functional and pathway enrichment analyses of DEGs were performed by Database for Annotation, Visualization, and Integrated Discovery (DAVID). Subsequently, the DEGs-encoded protein-protein interaction (PPI) network was constructed. The 784 DEGs in GSE99300 A.SW PP-EAE mice spleen mRNA profiles, 859 DEGs in GSE151701 EAE mice spleen mRNA profiles, and 646 DEGs in GSE99300 SJL/J PP-EAE mice spleen mRNA profiles were explored. Functional enrichment of 55 common DEGs among 3 sub-datasets revealed several immune-related terms, such as neutrophil extravasation, leucocyte migration, antimicrobial humoral immune response mediated by an antimicrobial peptide, toll-like receptor 4 bindings, IL-17 signalling pathway, and TGF-beta signalling pathway. In the screening of 10 hub genes, including MPO, ELANE, CTSG, LTF, LCN2, SELP, CAMP, S100A9, ITGA2B, and PRTN3, and in choosing and validating the 5 DEGs, including ANK1, MBOAT2, SLC25A21, SLC43A1, and SOX6, the results showed that SLC43A1 and SOX6 were significantly decreased in EAE mice spleen. Thus this study offers a list of genes expressed in the spleen that might play a key role in the pathogenesis of EAE.
 BACKGROUND: Electroacupuncture (EA) is given to assist in the treatment of MS, which is an effective therapeutic method. However, the therapy mechanism of EA related to stem cells in the treatment of MS is not yet known. In this study, we used a classic animal model of multiple sclerosis: experimental autoimmune encephalomyelitis (EAE) to evaluate the therapeutic effect of EA at Zusanli (ST36) acupoint in EAE and shed light on its potential roles in the effects of stem cells in vivo. METHODS: The EAE animal models were established. From the first day after immunization, EAE model mice received EA at ST36 acupoint, named the EA group. The weight and clinical score of the three groups were recorded for 28 days. The demyelination, inflammatory cell infiltration, and markers of neural stem cells (NSCs), hematopoietic stem cells (HSCs), and mesenchymal stem cells (MSCs) were compared. RESULTS: We showed that EAE mice treated with EA at ST36 acupoint, were suppressed in demyelination and inflammatory cell infiltration, and thus decreased clinical score and weight loss and mitigated the development of EAE when compared with the EAE group. Moreover, our data revealed that the proportions of NSCs, HSCs, and MSCs increased in the EA group compared with the EAE group. CONCLUSIONS: Our study suggested that EA at ST36 acupoint was an effective nonpharmacological therapeutic protocol that not only reduced the CNS demyelination and inflammatory cell infiltration in EAE disease but also increased the proportions of various stem cells. Further study is necessary to better understand how EA at the ST36 acupoint affects EAE.
 An accumulating body of evidence suggests that the bacterium Akkermansia muciniphila exhibits positive systemic effects on host health, mainly by improving immunological and metabolic functions, and it is therefore regarded as a promising potential probiotic. Recent clinical and preclinical studies have shown that A. muciniphila plays a vital role in a variety of neuropsychiatric disorders by influencing the host brain through the microbiota-gut-brain axis (MGBA). Numerous studies observed that A. muciniphila and its metabolic substances can effectively improve the symptoms of neuropsychiatric disorders by restoring the gut microbiota, reestablishing the integrity of the gut mucosal barrier, regulating host immunity, and modulating gut and neuroinflammation. However, A. muciniphila was also reported to participate in the development of neuropsychiatric disorders by aggravating inflammation and influencing mucus production. Therefore, the exact mechanism of action of A. muciniphila remains much controversial. This review summarizes the proposed roles and mechanisms of A. muciniphila in various neurological and psychiatric disorders such as depression, anxiety, Parkinson's disease, Alzheimer's disease, multiple sclerosis, strokes, and autism spectrum disorders, and provides insights into the potential therapeutic application of A. muciniphila for the treatment of these conditions.
 BACKGROUND AND OBJECTIVES: The influence of prior stereotactic radiosurgery (SRS) on outcomes of subsequent microvascular decompression (MVD) for patients with trigeminal neuralgia (TN) is not well understood. To directly compare pain outcomes in patients undergoing primary MVD vs those undergoing MVD with a history of 1 prior SRS procedure. METHODS: We retrospectively reviewed all patients undergoing MVD at our institution from 2007 to 2020. Patients were included if they underwent primary MVD or had a history of SRS alone before MVD. Barrow Neurological Institute (BNI) pain scores were assigned at preoperative and immediate postoperative time points and at every follow-up appointment. Evidence of pain recurrence was recorded and compared via Kaplan-Meier analysis. Multivariate Cox proportional hazards regression was used to identify factors associated with worse pain outcomes. RESULTS: Of patients reviewed, 833 met our inclusion criteria. Thirty-seven patients were in the SRS alone before MVD group, and 796 patients were in the primary MVD group. Both groups demonstrated similar preoperative and immediate postoperative BNI pain scores. There were no significant differences between average BNI at final follow-up between the groups. Multiple sclerosis (hazard ratio (HR) = 1.95), age (HR = 0.99), and female sex (HR = 1.43) independently predicted increased likelihood of pain recurrence on Cox proportional hazards analysis. SRS alone before MVD did not predict increased likelihood of pain recurrence. Furthermore, Kaplan-Meier survival analysis demonstrated no relationship between a history of SRS alone and pain recurrence after MVD (P = .58). CONCLUSION: SRS is an effective intervention for TN that may not worsen outcomes for subsequent MVD in patients with TN.
 Retinal complications in patients with inflammatory optic neuritis (ON) are generally related to post-infectious neuroretinitis and are considered uncommon in autoimmune/demyelinating ON, whether isolated or caused by multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD). More recently, however, cases with retinal complications have been reported in subjects positive for myelin oligodendrocyte glycoprotein (MOG) antibodies. We report a 53-year-old woman presenting with severe bilateral ON associated with a focal area of paracentral acute middle maculopathy (PAMM) in one eye. Visual loss recovered remarkably after high-dose intravenous corticosteroid treatment and plasmapheresis, but the PAMM lesion remained visible on both optical coherence tomography and angiography as an ischaemic lesion affecting the middle layers of the retina. The report emphasises the possible occurrence of retinal vascular complications in MOG-related optic neuritis, an important addition to the diagnosis of, and possible differentiation from, MS-related or NMOSD-related ON.
 Different psychological chronic pain treatments benefit some individuals more than others. Understanding the factors that are associated with treatment response-especially when those factors differ between treatments-may inform more effective patient-treatment matching. This study aimed to identify variables that moderate treatment response to 4 psychological pain interventions in a sample of adults with low back pain or chronic pain associated with multiple sclerosis, spinal cord injury, acquired amputation, or muscular dystrophy (N = 173). The current study presents the results from secondary exploratory analyses using data from a randomized controlled clinical trial which compared the effects of 4 sessions of cognitive therapy (CT), hypnosis focused on pain reduction (HYP), hypnosis focused on changing pain-related cognitions and beliefs (HYP-CT), and a pain education control condition (ED). The analyses tested the effects of 7 potential treatment moderators. Measures of primary (pain intensity) and secondary (pain interference, depression severity) outcome domains were administered before and after the pain treatments, and potential moderators (catastrophizing, hypnotizability, and electroencephalogram (EEG)-assessed oscillation power across five bandwidths) were assessed at pre-treatment. Moderator effects were tested fitting regression analyses to pre- to post-treatment changes in the three outcome variables. The study findings, while preliminary, support the premise that pre-treatment measures of hypnotizability and EEG brain activity predict who is more (or less) likely to respond to different psychological pain treatments. If additional research replicates the findings, it may be possible to better match patients to their more individually suitable treatment, ultimately improving pain treatment outcomes. PERSPECTIVE: Pre-treatment measures of hypnotizability and EEG-assessed brain activity predicted who was more (or less) likely to respond to different psychological pain treatments. If these findings are replicated in future studies, they could inform the development of patient-treatment matching algorithms.
 BACKGROUND: To investigate the association of optic neuritis (ON) after the COVID-19 vaccines. METHODS: Cases of ON from Vaccine Adverse Event Reporting System (VAERS) were collected and divided into the prepandemic, COVID-19 pandemic, and COVID-19 vaccine periods. Reporting rates were calculated based on estimates of vaccines administered. Proportion tests and Pearson χ2 test were used to determine significant differences in reporting rates of ON after vaccines within the 3 periods. Kruskal-Wallis testing with Bonferroni-corrected post hoc analysis and multivariable binary logistic regression was used to determine significant case factors such as age, sex, concurrent multiple sclerosis (MS) and vaccine manufacturer in predicting a worse outcome defined as permanent disability, emergency room (ER) or doctor visits, and hospitalizations. RESULTS: A significant increase in the reporting rate of ON after COVID-19 vaccination compared with influenza vaccination and all other vaccinations (18.6 vs 0.2 vs 0.4 per 10 million, P < 0.0001) was observed. However, the reporting rate was within the incidence range of ON in the general population. Using self-controlled and case-centered analyses, there was a significant difference in the reporting rate of ON after COVID-19 vaccination between the risk period and control period (P < 0.0001). Multivariable binary regression with adjustment for confounding variables demonstrated that only male sex was significantly associated with permanent disability. CONCLUSIONS: Some cases of ON may be temporally associated with the COVID-19 vaccines; however, there is no significant increase in the reporting rate compared with the incidence. Limitations of this study include those inherent to any passive surveillance system. Controlled studies are needed to establish a clear causal relationship.
 Perivascular spaces (PVS) and their enlargement (EPVS) have been gaining interest as EPVS can be visualized non-invasively by magnetic resonance imaging (MRI) when viewing T-2-weighted images. EPVS are most commonly observed in the regions of the basal ganglia and the centrum semiovale; however, they have also been identified in the frontal cortex and hippocampal regions. EPVS are known to be increased in aging and hypertension, and are considered to be a biomarker of cerebral small vessel disease (SVD). Interest in EPVS has been significantly increased because these PVS are now considered to be an essential conduit necessary for the glymphatic pathway to provide the necessary efflux of metabolic waste. Metabolic waste includes misfolded proteins of amyloid beta and tau that are known to accumulate in late-onset Alzheimer's disease (LOAD) within the interstitial fluid that is delivered to the subarachnoid space and eventually the cerebral spinal fluid (CSF). The CSF acts as a sink for accumulating neurotoxicities and allows clinical screening to potentially detect if LOAD may be developing early on in its clinical progression via spinal fluid examination. EPVS are thought to occur by obstruction of the PVS that associates with excessive neuroinflammation, oxidative stress, and vascular stiffening that impairs flow due to a dampening of the arterial and arteriolar pulsatility that aids in the convective flow of the metabolic debris within the glymphatic effluxing system. Additionally, increased EPVS has also been associated with Parkinson's disease and non-age-related multiple sclerosis (MS).
 BACKGROUND: Highly proliferating cells, such as cancer cells, are in high demand of pyrimidine nucleotides for their proliferation, accomplished by de novo pyrimidine biosynthesis. The human dihydroorotate dehydrogenase (hDHODH) enzyme plays a vital role in the ratelimiting step of de novo pyrimidine biosynthesis. As a recognised therapeutic target, hDHODH plays a significant role in cancer and other illness. OBJECTIVE: In the past two decades, small molecules as inhibitors hDHODH enzyme have drawn much attention as anticancer agents, and their role in rheumatoid arthritis (RA), and multiple sclerosis (MS). METHODS: In this review, we have compiled patented hDHODH inhibitors published between 1999 and 2022 and discussed the development of hDHODH inhibitors as anticancer agents. DISCUSSION: Therapeutic potential of small molecules as hDHODH inhibitors for the treatment of various diseases, such as cancer, is very well recognised. Human DHODH inhibitors can rapidly cause intracellular uridine monophosphate (UMP) depletion to produce starvation of pyrimidine bases. Normal cells can better endure a brief period of starvation without the side effects of conventional cytotoxic medication and resume synthesis of nucleic acid and other cellular functions after inhibition of de novo pathway using an alternative salvage pathway. Highly proliferative cells such as cancer cells do not endure starvation because they are in high demand of nucleotides for cell differentiation, which is fulfilled by de novo pyrimidine biosynthesis. In addition, hDHODH inhibitors produce their desired activity at lower doses rather than a cytotoxic dose of other anticancer agents. Thus, inhibition of de novo pyrimidine biosynthesis will create new prospects for the development of novel targeted anticancer agents, which ongoing preclinical and clinical experiments define. CONCLUSION: Our work brings together a comprehensive review of the role of hDHODH in cancer, as well as various patents related to the hDHODH inhibitors and their anticancer and other therapeutic potential. This compiled work will guide researchers in pursuing the most promising drug discovery strategies against the hDHODH enzyme as anticancer agents.
 The airway epithelium is exposed to numerous external irritants including infectious agents, environmental allergens, and atmospheric pollutants, releasing epithelial cytokines including thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 and initiating downstream type 2 (IL-4, IL-13, and IL-5) and IgE-driven pathways. These pathways trigger the initiation and progression of allergic airway diseases, including chronic rhinosinusitis with nasal polyps (CRSwNP), allergic rhinitis (AR), and allergic asthma. However, the use of biological agents that target downstream cytokines, such as IL-5, IL-4, and IL-13 receptors and IgE, might not be sufficient to manage some patients successfully. Instead of blocking downstream cytokines, targeting upstream epithelial cytokines has been proposed to address the complex immunologic networks associated with allergic airway diseases. Osteopontin (OPN), an extracellular matrix glyco-phosphoprotein, is a key mediator involved in Th1-related diseases, including systemic lupus erythematosus, multiple sclerosis, inflammatory bowel disease, and rheumatoid arthritis. Emerging evidence, including ours, indicates that epithelial-cell-derived OPN also plays an essential role in Th2-skewed airway diseases, including CRSwNP, AR, and allergic asthma involving the Th17 response. Therefore, we reviewed the current knowledge of epithelial-cell-derived OPN in the pathogenesis of three type-2-biased airway diseases and provided a direction for its future investigation and clinical relevance.
 Therapies that target the multicellular pathology of central nervous system (CNS) disease/injury are urgently required. Modified non-anticoagulant heparins mimic the heparan sulphate (HS) glycan family and have been proposed as therapeutics for CNS repair since they are effective regulators of numerous cellular processes. Our in vitro studies have demonstrated that low-sulphated modified heparan sulphate mimetics (LS-mHeps) drive CNS repair. However, LS-mHeps are derived from pharmaceutical heparin purified from pig intestines, in a supply chain at risk of shortages and contamination. Alternatively, cellular synthesis of heparin and HS can be achieved using mammalian cell multiplex genome engineering, providing an alternative source of recombinant HS mimetics (rHS). TEGA Therapeutics (San Diego) have manufactured rHS reagents with varying degrees of sulphation and we have validated their ability to promote repair in vitro using models that mimic CNS injury, making comparisons to LS-mHep7, a previous lead compound. We have shown that like LS-mHep7, low-sulphated rHS compounds promote remyelination and reduce features of astrocytosis, and in contrast, highly sulphated rHS drive neurite outgrowth. Cellular production of heparin mimetics may, therefore, offer potential clinical benefits for CNS repair.
 Sphingosine-1-phosphate receptor 1 (S1PR1) is recognized as a novel therapeutic and diagnostic target in neurological disorders. We recently transferred the S1PR1 radioligand [(11)C]CS1P1 into clinical investigation for multiple sclerosis. Herein, we reported the design, synthesis and evaluation of novel F-18 S1PR1 radioligands. We combined the structural advantages of our two lead S1PR1 radioligands and synthesized 14 new S1PR1 compounds, then performed F-18 radiochemistry on the most promising compounds. Compound 6h is potent (IC(50) = 8.7 nM) and selective for S1PR1. [(18)F]6h exhibited a high uptake in macaque brain (SUV > 3.0) and favorable brain washout pharmacokinetics in positron emission tomography (PET) study. PET blocking and displacement studies confirmed the specificity of [(18)F]6h in vivo. Radiometabolite analysis confirmed no radiometabolite of [(18)F]6h entered into the brain to confound the PET measurement. In summary, [(18)F]6h is a promising radioligand to image S1PR1 and worth translational clinical investigation for humans with brain disorders.
 BACKGROUND: Immediately after spinal trauma, immune cells, and proinflammatory cytokines infiltrate the spinal cord and disrupt the focal microenvironment, which impedes axon regeneration and functional recovery. Previous studies have reported that regulatory T cells (Tregs) enter the central nervous system and exert immunosuppressive effects on microglia during multiple sclerosis and stroke. However, whether and how Tregs interact with microglia and modulate injured microenvironments after spinal cord injury (SCI) remains unknown. METHOD: Regulatory T cells spatiotemporal characteristics were analyzed in a mouse contusion SCI model. Microglia activation status was evaluated by immunostaining and RNA sequencing. Cytokine production in injured spinal cord was examined using Luminex. The role of STAT3 in Treg-microglia crosstalk was investigated in a transwell system with isolated Tregs and primary microglia. RESULTS: Regulatory T cells infiltration of the spinal cord peaked on day 7 after SCI. Treg depletion promoted microglia switch to a proinflammatory phenotype. Inflammation-related genes, such as ApoD, as well as downstream cytokines IL-6 and TNF-α were upregulated in microglia in Treg-depleted mice. STAT3 inhibition was involved in Treg-microglia crosstalk, and STAT3 chemical blockade improved function recovery in Treg-depleted mice. CONCLUSION: Our results suggest that Tregs promote functional recovery after SCI by alleviating microglia inflammatory reaction via STAT3.
 White-matter brain abnormalities have been found across a variety of psychiatric disorders. The extent of white matter pathology is proposed to be predictive of the severity of anxiety disorders. However, it is still unknown whether disruptions of white matter integrity precede, and are sufficient to give rise to, the behavioural symptoms. Interestingly, mood disturbances feature prominently in central demyelinating diseases such as multiple sclerosis. It is unclear whether the greater frequency of neuropsychiatric symptoms is linked to underlying neuropathology. In this study, we characterised male and female Tyro3 knockout (KO) mice using a variety of behavioural paradigms. Anxiety-related behaviours were assessed with the elevated-plus maze and light-dark box. Fear memory processing was assessed using fear conditioning and extinction paradigms. Finally, we assessed immobility time in the Porsolt swim test as a measure of depression-related behavioural despair. Surprisingly, loss of Tyro3 did not lead to manifestation of major shifts in baseline behaviour. We noted significant differences in habituation to novel environments and post-conditioning freezing levels of female Tyro3 KO mice, which are consistent with the female bias in anxiety disorders and could be indicative of maladaptive stress-responses. This study has demonstrated that white matter pathology related to a loss of Tyro3 is associated with pro-anxiety behavioural responses of female mice. Future studies could probe their contribution to increased risk for neuropsychiatric disorders when combined with stressful triggering events.
 Chemokines modulate the immune response by regulating the migration of immune cells. They are also known to participate in such processes as cell-cell adhesion, allograft rejection, and angiogenesis. Chemokines interact with two different subfamilies of G protein-coupled receptors: conventional chemokine receptors and atypical chemokine receptors. Here, we focused on the former one which has been linked to many inflammatory diseases, including: multiple sclerosis, asthma, nephritis, and rheumatoid arthritis. Available crystal and cryo-EM structures and homology models of six chemokine receptors (CCR1 to CCR6) were described and tested in terms of their usefulness in structure-based drug design. As a result of structure-based virtual screening for CCR2 and CCR3, several new active compounds were proposed. Known inhibitors of CCR1 to CCR6, acquired from ChEMBL, were used as training sets for two machine learning algorithms in ligand-based drug design. Performance of LightGBM was compared with a sequential Keras/TensorFlow model of neural network for these diverse datasets. A combination of structure-based virtual screening with machine learning allowed to propose several active ligands for CCR2 and CCR3 with two distinct compounds predicted as CCR3 actives by all three tested methods: Glide, Keras/TensorFlow NN, and LightGBM. In addition, the performance of these three methods in the prediction of the CCR2/CCR3 receptor subtype selectivity was assessed.
 Cerium oxide nanoparticles (nano-series) are used as catalysts in industrial applications due to their free radical scavenging properties. Given that free radicals play an essential role in the pathology of many neurological diseases, we investigated the use of nanocrystals as a potential therapeutic agent for oxidative damage. This project synthesized nano-series from a new and environmentally friendly bio-pathway. Investigation of cerium nitrate in culture medium containing inoculated Lactobacillus acidophilus strain before incubation produces nano-series. Loaded with glatiramer acetate (GA) was formed by coating carboxymethylcellulose (CMC) and CeO(2). FE-SEM analysis showed nano-series in the 9-11 nm range, spherical shape, and uniform particle size distribution. Cubic nanoparticles containing anti-multiple sclerosis (anti-Ms) treatment called GA were used. Glycerol monostearate (GMS) was used as a fat base, and evening primrose extract was used as an anti-inflammatory in cubosomes. Design-Expert® software was used to study the effects of different formulation factors on the properties of GA-loaded cubic dispersions. Thirty GA-labeled cubic dispersions were prepared with GA-labeled carboxymethylcellulose and evaluated in vitro. The results showed an average nano-series size of 89.02 and a zeta potential of -49.9. Cubosomes containing GA-CMC/CeO(2) showed a stable release profile for 180 min. The results showed that cubosomes containing GA-CMC/CeO(2) could be a promising drug carrier with normal release behavior.
 Hyperexcitability-induced neuronal damage plays a role both in epilepsy as well as in inflammatory brain diseases such as multiple sclerosis (MS) and as such represents an important disease pathway which potentially can be targeted to mitigate neuronal damage. Dimethyl fumarate (DMF) and its pharmacologically active metabolite monomethyl fumarate (MMF) are FDA-approved therapeutics for MS, which can induce immunosuppressive and antioxidant pathways, and their neuroprotective capacity has been demonstrated in other preclinical neurological disease models before. In this study, we used an unbiased proteomic approach to identify potential new targets upon the treatment of MMF in glio-neuronal hippocampal cultures. MMF treatment results in induction of antioxidative (HMOX1, NQO1) and anaplerotic metabolic (GAPDH, PC) pathways, which correlated with reduction in ROS production, increased mitochondrial NADH-redox index and decreased NADH pool, independent of glutathione levels. Additionally, MMF reduced glycolytic capacity indicating individual intra-cellular metabolic programs within different cell types. Furthermore, we demonstrate a neuroprotective effect of MMF upon hyperexcitability in vitro (low magnesium model), where MMF prevents glio-neuronal death via reduced ROS production. These results highlight MMF as a potential new therapeutic opportunity in hyperexcitability-induced neurodegeneration.
 BACKGROUND: Immunotherapy is nowadays considered a mainstay of cancer treatment, dramatically affecting the disease-free survival rate in several aggressive malignancies. Unfortunately, cancer immunotherapy can also trigger life-threatening autoimmune neurological complications named "neurological adverse effects" (NAEs). NAEs can affect both the central nervous system (CNS), as in ipilimumab-related aseptic meningitis, and the peripheral nervous system (PNS), as in nivolumab-induced myasthenia gravis. CURRENT EVIDENCE: The incidence of NAEs is highly variable, ranging from 2 to 4% using checkpoint inhibitors to 50% using blinatumomab. Looking at these numbers, it appears clear that neurologists will soon be called more and more frequently to decide upon the best therapeutic strategy for a patient receiving immunotherapy and experiencing a NAE. Most of them can be treated or reverted withholding the offending drug and adding IVIg, plasmapheresis, or steroids to the therapy. Sometimes, however, for oncological reasons, immunotherapy cannot be stopped so the neurologist needs to know what countermeasures have proven most effective. Moreover, patients with a pre-existing autoimmune neurological disease (AID), such as myasthenia gravis or multiple sclerosis, might need immunotherapy during their life, risking a severe worsening of their symptoms. In that setting, the neurologist needs to properly counsel patients about the risk of a therapy-related relapse. CONCLUSION: In this article, we describe the most frequently reported NAEs and aim to give neurologists a practical overview on how to deal with them.
 Neurodegenerative diseases refer to a group of neurological disorders as a consequence of various destructive illnesses, that predominantly impact neurons in the central nervous system, resulting in impairments in certain brain functions. Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, and other neurodegenerative disorders represent a major risk to human health. In order to optimize structural and functional recovery, reconstructive methods integrate many approaches now, to address the complex and multivariate pathophysiology of neurodegenerative disorders. Stem cells, with their unique property of regeneration, offer new possibilities in regenerative and reconstructive medicine. Concurrently, there is an important role for natural products in controlling many health sufferings and they can delay or even prevent the onset of various diseases. In addition, due to their therapeutic properties, they have been used as neuroprotective agents to treat neurodegenerative disorders. After decades of intensive research, scientists made advances in treating these disorders so far, but current therapies are still not capable of preventing the illnesses from progressing. Therefore, in this review, we focused on a new perspective combining stem cells and natural products as an innovative therapy option in the management of neurodegenerative diseases.
 Oxidative stress plays a vital role in the pathophysiology of most neurodegenerative diseases such as Parkinson's disease (PD). The Keap1-Nrf2-ARE pathway, one of the internal defense mechanisms, curbs the reactive oxygen species (ROS) generated in the cellular environment. The pathway leads to the expression of antioxidant genes such as HO-1, GCLC, and NQO1, which act as cellular redox switches and protect the cellular environment. Keap1, the negative regulator of Nrf2, is a potential therapeutic target for treating age-related neurodegenerative diseases. Tecfidera (Dimethyl fumarate), used in the intervention for relapsing multiple sclerosis, is the only commercial drug known to regulate the Nrf2 function. Here, we have identified a repurposing drug, chlorhexidine (LBP125), through ligand-based pharmacophore development and screening against the DrugBank, as a potential inhibitor of the β-propeller domain of Keap1 (Keap1-DC). Chlorhexidine, an antimicrobial agent, is widely used as a mouthwash, skin cleanser, and intervening bacterial infection during childbirth. The biochemical assay confirmed a significant binding affinity of 30 µM and competitively inhibited the Nrf2 peptide interaction. Moreover, chlorhexidine also exerts cytoprotection in a neurotoxic cell model of PD through Keap1-Nrf2 disruption leading to nuclear translocation of Nrf2 and expression of downstream genes, HO-1, and NQO1. Hence, the chemical scaffold of chlorhexidine is a potential lead to develop new chemical libraries with drug-like properties for treating PD.Communicated by Ramaswamy H. Sarma.
 Rare diseases (RDs) may affect individuals in small numbers, but they have a significant impact on a global scale. Accurate diagnosis of RDs is challenging, and there is a severe lack of drugs available for treatment. Pharmaceutical companies have shown a preference for drug repurposing from existing drugs developed for other diseases due to the high investment, high risk, and long cycle involved in RD drug development. Compared to traditional approaches, knowledge graph embedding (KGE) based methods are more efficient and convenient, as they treat drug repurposing as a link prediction task. KGE models allow for the enrichment of existing knowledge by incorporating multimodal information from various sources. In this study, we constructed RDKG-115, a rare disease knowledge graph involving 115 RDs, composed of 35,643 entities, 25 relations, and 5,539,839 refined triplets, based on 372,384 high-quality literature and 4 biomedical datasets: DRKG, Pathway Commons, PharmKG, and PMapp. Subsequently, we developed a trimodal KGE model containing structure, category, and description embeddings using reverse-hyperplane projection. We utilized this model to infer 4199 reliable new inferred triplets from RDKG-115. Finally, we calculated potential drugs and small molecules for each of the 115 RDs, taking multiple sclerosis as a case study. This study provides a paradigm for large-scale screening of drug repurposing and discovery for RDs, which will speed up the drug development process and ultimately benefit patients with RDs. The source code and data are available at https://github.com/ZhuChaoY/RDKG-115.
 Theiler's murine encephalomyelitis virus (TMEV) causes a chronic demyelinating disease similar to multiple sclerosis in mice. Although sialic acids have been shown to be essential for TMEV attachment to the host, the surface receptor has not been identified. While type I interferons play a pivotal role in the elimination of the chronic infectious Daniel (DA) strain, the role of plasmacytoid dendritic cells (pDCs) is controversial. We herein found that TMEV binds to conventional DCs but not to pDCs. A glycomics analysis showed that the sialylated N-glycan fractions were lower in pDCs than in conventional DCs, indicating that pDCs are not susceptible to TMEV infection due to the low levels of sialic acid. TMEV capsid proteins contain an integrin recognition motif, and dot blot assays showed that the integrin proteins bind to TMEV and that the viral binding was reduced in the desialylated α(X) β(2) . α(X) β(2) protein suppressed TMEV replication in vivo, and TMEV co-localized with integrin α(M) at the cell membrane and TLR 3 in the cytoplasm, suggesting that α(M) serves as the viral attachment and entry. These results show that the chronic encephalomyelitis virus utilizes sialylated integrins as cell surface receptors, leading to cellular tropism to evade pDC activation.
 Glaucoma is a leading cause of permanent blindness worldwide and is characterized by neurodegeneration linked to progressive retinal ganglion cell (RGC) death, axonal damage, and neuroinflammation. Glutamate excitotoxicity mediated through N-methyl-D-aspartate (NMDA) receptors plays a crucial role in glaucomatous RGC loss. Sphingosine 1-phosphate receptors (S1PRs) are important mediators of neurodegeneration and neuroinflammation in the brain and the retina. Siponimod is an immunomodulatory drug for multiple sclerosis and is a selective modulator of S1PR subtypes 1 and 5 and has been shown to have beneficial effects on the central nervous system (CNS) in degenerative conditions. Our previous study showed that mice administered orally with siponimod protected inner retinal structure and function against acute NMDA excitotoxicity. To elucidate the molecular mechanisms behind these protective effects, we investigated the inflammatory pathways affected by siponimod treatment in NMDA excitotoxicity model. NMDA excitotoxicity resulted in the activation of glial cells coupled with upregulation of the inflammatory NF-kB pathway and increased expression of TNFα, IL1-β, and IL-6. Siponimod treatment significantly reduced glial activation and suppressed the pro-inflammatory pathways. Furthermore, NMDA-induced activation of NLRP3 inflammasome and upregulation of neurotoxic inducible nitric oxide synthase (iNOS) were significantly diminished with siponimod treatment. Our data demonstrated that siponimod induces anti-inflammatory effects via suppression of glial activation and inflammatory singling pathways that could protect the retina against acute excitotoxicity conditions. These findings provide insights into the anti-inflammatory effects of siponimod in the CNS and suggest a potential therapeutic strategy for neuroinflammatory conditions.
 Astrocytes are diverse brain cells that form large networks communicating via gap junctions and chemical transmitters. Despite recent advances, the functions of astrocytic networks in information processing in the brain are not fully understood. In culture, brain slices, and in vivo, astrocytes, and neurons grow in tight association, making it challenging to establish whether signals that spread within astrocytic networks communicate with neuronal groups at distant sites, or whether astrocytes solely respond to their local environments. A multi-electrode array (MEA)-based device called AstroMEA is designed to separate neuronal and astrocytic networks, thus allowing to study the transfer of chemical and/or electrical signals transmitted via astrocytic networks capable of changing neuronal electrical behavior. AstroMEA demonstrates that cortical astrocytic networks can induce a significant upregulation in the firing frequency of neurons in response to a theta-burst charge-balanced biphasic current stimulation (5 pulses of 100 Hz × 10 with 200 ms intervals, 2 s total duration) of a separate neuronal-astrocytic group in the absence of direct neuronal contact. This result corroborates the view of astrocytic networks as a parallel mechanism of signal transmission in the brain that is separate from the neuronal connectome. Translationally, it highlights the importance of astrocytic network protection as a treatment target.
 Glatiramer is the active portion of the drug, glatiramer acetate. The drug is undetectable in most women and appears in only low amounts for up to 3 hours in others. Furthermore, the oral absorption by the breastfed infant is estimated to be less than 3%, except perhaps in neonates.[1] Follow-up of infants indicates that maternal use of glatiramer acetate does not appear to cause any adverse effects in breastfed infants. Glatiramer acetate is generally considered safe by most experts and appears to be one of the preferred disease-modifying agents for treating multiple sclerosis during breastfeeding.[2-9] No special precautions appear to be required during breastfeeding while using glatiramer and breastfeeding can resume immediately after injection.[10]
 Amyloids are misfolded proteins that aggregate into fibrillar structures, the accumulation of which is associated with the pathogenesis of many neurodegenerative diseases, such as Alzheimer's disease (AD). Early, sensitive detection of these misfolded aggregates is of great interest to the field, as amyloid deposition begins well before the presentation of clinical symptoms. Thioflavin-S (ThS) is a fluorescent probe commonly used to detect amyloid pathology. Protocols for ThS staining vary, but they often use high staining concentrations followed by differentiation, which causes varying levels of non-specific staining and potentially leaves more subtle amyloid deposition unidentified. In this study, we developed an optimized ThS staining protocol for the sensitive detection of β-amyloids in the widely used 5xFAD Alzheimer's mouse model. Controlled dye concentrations together with fluorescence spectroscopy and advanced analytical methods enabled not only the visualization of plaque pathology, but also the detection of subtle and widespread protein misfolding throughout the 5xFAD white matter and greater parenchyma. Together, these findings demonstrate the efficacy of a controlled ThS staining protocol and highlight the potential use of ThS for the detection of protein misfolding that precedes clinical manifestation of disease.
 OBJECTIVES: Clinical inertia, or therapeutic inertia (TI), is the medical behavior of not initiating or intensifying treatment when recommended by clinical recommendations. To our knowledge, our survey is the first to assess TI around psoriatic arthritis (PsA). METHODS: 825 French rheumatologists were contacted via email between January and March 2021 and invited to complete an online questionnaire consisting of seven clinical vignettes: five cases ("oligoarthritis", "enthesitis", "polyarthritis", "neoplastic history", "cardiovascular risk") requiring treatment OPTImization, and two "control" cases (distal interphalangeal arthritis, atypical axial involvement) not requiring any change of treatment-according to the most recent PsA recommendations. Rheumatologists were also questioned about their routine practice, continuing medical education, and perception of PsA. RESULTS: 101 rheumatologists completed this OPTI'PsA survey. Almost half the respondents (47%) demonstrated TI on at least one of the five vignettes that warranted treatment optimization. The complex profiles inducing the most TI were "oligoarthritis" and "enthesitis" with 20% and 19% of respondents not modifying treatment, respectively. Conversely, clinical profiles for which there was the least uncertainty ("polyarthritis in relapse", "neoplastic history" and "cardiovascular risk") generated less TI with 11%, 8% and 6% of respondents, respectively, choosing not to change the current treatment. CONCLUSION: The rate of TI we observed for PsA is similar to published data for other chronic diseases such as diabetes, hypertension, gout, or multiple sclerosis. Our study is the first to show marked clinical inertia in PsA, and further research is warranted to ascertain the reasons behind this inertia.
 A healthy brain is protected by the blood-brain barrier (BBB), which is formed by the endothelial cells that line brain capillaries. The BBB plays an extremely important role in supporting normal neuronal function by maintaining the homeostasis of the brain microenvironment and restricting pathogen and toxin entry to the brain. Dysfunction of this highly complex and regulated structure can be life threatening. BBB dysfunction is implicated in many neurological diseases such as stroke, Alzheimer's disease, multiple sclerosis, and brain infections. Among other mechanisms, inflammation and/or flow disturbances are major causes of BBB dysfunction in neurological infections and diseases. In particular, in ischaemic stroke, both inflammation and flow disturbances contribute to BBB disruption, leading to devastating consequences. While a transient or minor disruption to the barrier function could be tolerated, chronic or a total breach of the barrier can result in irreversible brain damage. It is worth noting that timing and extent of BBB disruption play an important role in the process of any repair of brain damage and treatment strategies. This review evaluates and summarises some of the latest research on the role of the BBB during neurological disease and infection with a focus on the effects of inflammation and flow disturbances on the BBB. The BBB's crucial role in protecting the brain is also the bottleneck in central nervous system drug development. Therefore, innovative strategies to carry therapeutics across the BBB and novel models to screen drugs, and to study the complex, overlapping mechanisms of BBB disruption are urgently needed.
 BACKGROUND AND PURPOSE: Differentiating between peripheral and central aetiologies can be challenging in patients with acute vertigo, given substantial symptom overlap. A detailed clinical history and focused physical eye movement examination such as the HINTS eye examination appear to be the most reliable approach to identify acute cerebellar/brainstem stroke, outperforming even acute brain imaging. We have observed, however, that isolated vertigo of central cause may be accompanied by acute truncal ataxia, in the absence of nystagmus. METHODS: We explored the frequency of ataxia without concurrent nystagmus in a cross section of patients with acute vertigo who presented to the emergency department at two centres in Argentina (Group A) and the UK (Group B). Patients underwent detailed clinical neuro-otological assessments (Groups A and B), which included instrumented head impulse testing and oculography (Group B). RESULTS: A total of 71 patients in Group A and 24 patients in Group B were included in this study. We found acute truncal ataxia-without nystagmus-in 15% (n = 14) of our overall cohort. Lesions involved stroke syndromes affecting the posterior inferior cerebellar artery, anterior inferior cerebellar artery, and superior cerebellar artery, thalamic stroke, cerebral hemisphere stroke, multiple sclerosis, and a cerebellar tumour. Additional oculomotor deficits did not reliably identify a central cause in these individuals, even with oculography. CONCLUSIONS: We have identified a significant subpopulation of patients with acute vertigo in whom the current standard approaches such as the HINTS examination that focus on oculomotor assessment may not be applicable, highlighting the need for a formal assessment of gait in this setting.
 Central nervous system virus infections are a major cause of morbidity and mortality worldwide and a significant global public health concern. As in many tissues, inflammation and immune responses in the brain, despite their protective roles, can also be harmful. Control of brain inflammation is important in many neurological diseases from encephalitis to multiple sclerosis and neurogenerative disease. The suppressors of cytokine signaling (SOCS) proteins are a key mechanism controlling inflammatory and immune responses across all tissues including the brain. Using a mouse model system, we demonstrate that lack of SOCS4 results in changes in the pathogenesis and clinical outcome of a neurotropic virus infection. Relative to wild-type mice, SOCS4-deficient mice showed accelerated clearance of virus from the brain, lower levels of persisting viral RNA in the brain, increased neuroinflammation and more severe neuropathology. We conclude that, in the mouse brain, SOCS4 is a vital regulator of antiviral immunity that mediates the critical balance between immunopathology and virus persistence.
 OBJECTIVES: Uncertainty regarding the legitimacy of functional neurological disorder (FND) remains among some health care professionals. Despite treatment guidelines and consensus recommendations, variability in clinical practice referral decisions persists. Evidence from other conditions suggests such clinical decision making is impacted by practitioners' implicit and explicit attitudes. We aimed to identify whether health care professionals hold implicit and/or explicit attitudes about the legitimacy of FND and whether these attitudes are associated with referral decision making. DESIGN/METHODS: We included 66 health care professionals who work with people with neurological conditions: n = 37 medical doctors, mainly neurologists (n = 18) and psychiatrists (n = 10), and n = 29 doctoral level practitioner psychologists. Participants completed an Implicit Association Test (IAT), Implicit Relational Assessment Procedure (IRAP), a referral decision-making vignette task and self-report measures of explicit attitudes on FND-legitimacy, therapeutic optimism and clinician confidence. Multiple Sclerosis (MS) was used as a comparator condition. RESULTS: Participants self-reported strong explicit FND-legitimate and MS-legitimate attitudes but demonstrated an implicit FND-illegitimate/MS-legitimate bias. Deeper examination provided by the IRAP data indicated pro-FND-legitimate attitudes, but no bias for or against FND-illegitimate-contrasting the pro-MS-legitimate, anti-MS-illegitimate attitudes for the comparator condition. Attitudes about FND-illegitimacy were negatively associated with likelihood of referral to physical interventions such as physiotherapy. Medical doctors had lower treatment optimism and stronger explicit attitudes that FND is illegitimate than psychologists. CONCLUSIONS: At an implicit level, clinicians are uncertain about the illegitimacy of FND, and such attitudes are associated with lower likelihood of referral to physiotherapy in particular. Improved education on FND among health care professionals is indicated.
 Despite advances in the treatment of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and other common autoimmune neuropathies (AN), still-many patients with these diseases do not respond satisfactorily to the available treatments. Repurposing of disease-modifying therapies (DMTs) from other autoimmune conditions, particularly multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD), is a promising strategy that may accelerate the establishment of novel treatment choices for AN. This approach appears attractive due to homologies in the pathogenesis of these diseases and the extensive post-marketing experience that has been gathered from treating MS and NMOSD patients. The idea is also strengthened by a number of studies that explored the efficacy of DMTs in animal models of AN but also in some CIDP patients. We here review the available preclinical and clinical data of approved MS therapeutics in terms of their applicability to AN, especially CIDP. Promising therapeutic approaches appear to be B cell-directed and complement-targeting strategies, such as anti-CD20/anti-CD19 agents, Bruton's tyrosine kinase inhibitors and anti-C5 agents, as they exert their effects in the periphery. This is a major advantage because, in contrast to MS, their action in the periphery is sufficient to exert significant immunomodulation.
 Aim: Vitamin D deficiency is a prevalent condition among the general population, all around the world. Vitamin D deficiency is defined as serum levels of 25-hydroxy vitamin D lower than 20 ng/ml (50 nmol/ml). It is a known actor in the skeletal system through the regulation of calcium and phosphate metabolism and bone mineralization. Still, the role of vitamin D as an immunomodulator is yet to be acknowledged by healthcare practitioners as a cause, precipitating factor, and contributor to a variety of diseases. Vitamin D is shown to be an actor in multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus, and irritable bowel syndrome. Fibromyalgia syndrome (FMS) is a chronic disorder associated with a severe pain that can affect a patient's musculoskeletal system, daily routine, and mood. The clinical presentation encapsulates other disorders such as lethargy and sleep problems, brain fog and other cognitive issues, and physical and psychiatric symptoms. Methods: We have used PubMed and ResearchGate in the reviewing process of our paper. We tried to address as many topics as we judged to be adequate and relevant for the practicing clinicians. Results: Management of fibromyalgia syndrome is both nonpharmacologic and pharmacologic, which are provided in a stepwise fashion. Yet, the management of FMS remains a challenge, heeding a multidisciplinary approach. Among the dietary interventions, we chose vitamin D and its effects on FMS. Literature shows that supplementation improves pain caused by fibromyalgia syndrome, yet specific recommendations are still to be created. Conclusions: We call on all the relevant governmental bodies, public health experts and health policy makers, healthcare practitioners, and the civil society to use novel data related to fibromyalgia syndrome, and in a broader perspective, the integral role of vitamin D.
 The American College of Radiology has published appropriateness criteria to help guide when to use MRI. Many health insurance carriers use proprietary clinical guidelines for prior authorization of imaging studies. The purpose of this study was to compare the specific criteria in those guidelines, for neck pain both with and without radicular symptoms. An online search was conducted to identify the guidelines for authorization of cervical spine MRI used by the largest commercial insurance carriers in the United States by market share. Guidelines were analyzed for neck pain with and without radiculopathy. Cervical trauma, myelopathy, infection, neoplasm, multiple sclerosis, and postprocedural care were excluded. The remaining criteria were broken down into categories including clinical symptoms, conservative therapy, other required radiologic studies, and clinical re-evaluation. Individual criteria within each of the categories were compared. After evaluation of the top 56 insurance companies in the United States, 30 companies using four main utilization management companies remained for analysis. After direct comparison of publicly available guidelines documents, notable discrepancies existed between the four companies in all subcategories analyzed. In addition, varying amounts of evidence-based literature was identified to support criteria requirements for prior authorization. This study demonstrates that the guidelines used by private health insurance companies for cervical MRI authorization in the setting of neck pain with and without cervical radiculopathy are inconsistent and use objective measures that have not been validated in the literature. We think this warrants additional scrutiny and investigation.
 OBJECTIVE: To summarize the measurement properties (reliability, validity, and responsiveness) and the clinical utility of measurement tools used in telerehabilitation in individuals with neurological conditions. DESIGN: Systematic review. SUBJECTS: Individuals with neurological conditions. INTERVENTION: Not applicable. MAIN MEASURES: The methodological quality of the studies using the COSMIN Risk of Bias Checklist, the quality of the measurement properties using the criteria for good measurement properties, and the clinical utility of the measurements using the Tyson & Connell scale. RESULTS: From the 22,188 identified studies, 47 were included. Forty-three measurement tools were identified. The main modes of administration were telephone and videoconference. Studies involved mostly individuals with stroke, multiple sclerosis, and Alzheimer's disease. Criterion validity and reliability were the most investigated measurement properties. None of the tools had their responsiveness investigated. Twenty-two measurement tools have at least one measurement property evaluated as "sufficient" in a study with appropriate methodological quality ("very good" or "adequate"). Nineteen measurement tools showed adequate clinical utility. Eight measurement tools, investigated in individuals with stroke, spinal cord injury or Alzheimer's disease, all administered by telephone, were recommended. CONCLUSION: The present results can be used to assist in choosing appropriate measurement tools, both in research and clinical practice, during telerehabilitation in individuals with neurological conditions. Measurement error, content validity, structural validity, and responsiveness need to be further investigated. In addition, the measurement properties of tools used in telerehabilitation in other neurological conditions, such as Huntington's disease, should also be investigated. REGISTRATION NUMBER: CRD42021257662.
 This article reviews recent developments in the application of cell-free DNA-based liquid biopsies to neurological diseases. Over the past few decades, an explosion of interest in the use of accessible biofluids to identify and track molecular disease has revolutionized the fields of oncology, prenatal medicine and others. More recently, technological advances in signal detection have allowed for informative analysis of biofluids that are typically sparse in cells and other circulating components, such as CSF. In parallel, advancements in epigenetic profiling have allowed for novel applications of liquid biopsies to diseases without characteristic mutational profiles, including many degenerative, autoimmune, inflammatory, ischaemic and infectious disorders. These events have paved the way for a wide array of neurological conditions to benefit from enhanced diagnostic, prognostic, and treatment abilities through the use of liquid biomarkers: a 'liquid biopsy' approach. This review includes an overview of types of liquid biopsy targets with a focus on circulating cell-free DNA, methods used to identify and probe potential liquid biomarkers, and recent applications of such biomarkers to a variety of complex neurological conditions including CNS tumours, stroke, traumatic brain injury, Alzheimer's disease, epilepsy, multiple sclerosis and neuroinfectious disease. Finally, the challenges of translating liquid biopsies to use in clinical neurology settings-and the opportunities for improvement in disease management that such translation may provide-are discussed.
 Magnetic resonance imaging (MRI) is a diagnostic technique useful for noninvasive visualization of organs and soft tissue structures. The ability to evaluate for structural integrity lends MRI for imaging the neural axis and large joints of the musculoskeletal system where it was used most heavily during its infancy. Since that time, MR's scope and application have broadened significantly and now encompasses abdominopelvic and cardiac imaging. Clinicians frequently order MRI to characterize soft tissue and osseous lesions or masses. In some cases, the varying MRI sequences can determine the composition of these abnormalities. For example, MRI elastography can diagnose and surveil hepatic fibrosis sparing the patient from an invasive and repetitive biopsy. MR angiography, using both contrast-enhanced and non-contrast techniques, can diagnose vascular occlusive disease and stenosis. Faster scan times and gating techniques minimizing cardiac and respiratory motion make MRI a useful non-invasive tool for cardiac evaluations of structure, function, and myocardial perfusion. A major advantage of MRI is the ability to produce high-quality images with superior soft-tissue contrast without using ionizing radiation. The magnet generates images based on the specific and unique magnetic properties of the tissues driven by the spin properties of hydrogen molecules. This makes MRI especially useful to evaluate "high radiation risk" patients like pregnant women and children. MRI is also valuable for patients with chronic conditions requiring routine imaging surveillance, such as multiple sclerosis and inflammatory bowel diseases. MRI does not exist without hazard – the magnetic field can be dangerous and strict parameters are in place to ensure patient safety. Pre- imaging screening protocols are in place to assess the patient’s risk factors ranging from occupational exposures to surgically implanted devices determined to be incompatible with the magnetic field. Though many of the newer generation implanted devices are MR compatible, it is crucial to consult with both the radiologist and MR technologists. The magnetic field can alter implanted devices and result in loss of function, positioning, and temperature changes. Additionally, while some prosthetic devices- like heart valves, stents, and artificial joints- are MR safe, they may cause signal artifacts that limit the diagnostic quality of the exam. While in no way all-inclusive, this article provides information for clinicians to consider when ordering MR imaging.
 Autoimmune diseases are a heterogeneous group of diseases with an unclear aetiology. Genome-wide association studies (GWAS) and meta-analysis are inefficient in identifying shared variants. This study aims to identify shared genetic susceptibility for seven autoimmune diseases using sum of powered score (SPU) tests. GWAS summary statistics datasets of seven autoimmune diseases were downloaded from Open Targets Genetics, Dryad and International Multiple Sclerosis Genetics Consortium (IMSGC). The MTaSPUs was applied to confirm common single-nucleotide polymorphisms (SNP), MTaSPUsSet and aSPUs were performed to identify potential shared genes, and MTaSPUsPath was conducted to explore biological functions based on Kyoto encyclopedia of genes and genomes (KEGG) biological pathways. The MTaSPUs test found 104 pleiotropic SNPs (P < 1.19 × 10(-6)) in our study. The 38 of these SNPs were associated with at least one trait in the original GWAS study. A total of 56 genes associated with at least one trait (P < 4.98 × 10(-6)) were recognized by aSPUs test. The 45 potential pleiotropic genes (P < 4.98 × 10(-6)) were significant in MTaSPUsSet test. By aggregating results of aSPUs test and MTaSPUsSet test, we ascertained 38 pleiotropic genes. The 10 of these 38 pleiotropic genes have been reported in previous studies, while the remaining 28 genes were newly discovered. These 38 genes were matched in 14 significant KEGG pathways. We found new variants linked with complicated illnesses derived from several GWAS datasets using the SPU testing technique. The discovery of pleiotropic genes and shared pathways may aid in the development of common treatment approaches for autoimmune disorders.

 Histones play vital roles in chromatin function and gene transcription; however, they are very harmful in the intercellular space because they stimulate systemic inflammatory and toxic responses. Myelin basic protein (MBP) is the major protein of the axon myelin-proteolipid sheath. Antibodies-abzymes with various catalytic activities are specific features of some autoimmune diseases. IgGs against individual histones (H2A, H1, H2B, H3, and H4) and MBP were isolated from the blood of experimental-autoimmune-encephalomyelitis-prone C57BL/6 mice by several affinity chromatographies. These Abs-abzymes corresponded to various stages of EAE development: spontaneous EAE, MOG, and DNA-histones accelerated the onset, acute, and remission stages. IgGs-abzymes against MBP and five individual histones showed unusual polyreactivity in the complex formation and enzymatic cross-reactivity in the specific hydrolysis of the H2A histone. All the IgGs of 3-month-old mice (zero time) against MBP and individual histones demonstrated from 4 to 35 different H2A hydrolysis sites. The spontaneous development of EAE over 60 days led to a significant change in the type and number of H2A histone hydrolysis sites by IgGs against five histones and MBP. Mice treatment with MOG and the DNA-histone complex changed the type and number of H2A hydrolysis sites compared to zero time. The minimum number (4) of different H2A hydrolysis sites was found for IgGs against H2A (zero time), while the maximum (35) for anti-H2B IgGs (60 days after mice treatment with DNA-histone complex). Overall, it was first demonstrated that at different stages of EAE evolution, IgGs-abzymes against individual histones and MBP could significantly differ in the number and type of specific sites of H2A hydrolysis. The possible reasons for the catalytic cross-reactivity and great differences in the number and type of histone H2A cleavage sites were analyzed.
 BACKGROUND: Advance care planning (ACP) is influenced by several factors (e.g., patient's readiness to engage, clinician's skills, and the cultural environment). Availability of reliable and valid self-reported measures of the ACP domains is crucial, including cross-cultural equivalence. AIM: To culturally adapt into Italian the 19-item Quality of Communication (QOC) and the 4-item ACP Engagement (4-item ACP-E) questionnaires. METHODS: We translated and culturally adapted the two questionnaires and produced a significant other (SO) version of the QOC (QOC-SO). Each questionnaire was field tested via cognitive interviews with users: nine patients (QOC, 4-item ACP-E) and three SOs (QOC-SO) enrolled at three palliative care services. RESULTS: We made minor changes to 5/19 QOC items, to improve clarity and internal consistency; we changed the response option 'didn't do' into 'not applicable'. Finally, we slightly revised the QOC to adapt it to the paper/electronic format. QOC debriefing revealed that the section on end of life was emotionally challenging for both patients and SOs. We simplified the 4-item ACP-E layout, added a sentence in the introduction, and revised the wording of one item, to improve coherence with the Italian ACP legislation. ACP-E debriefing did not reveal any major issue. CONCLUSIONS: Results were satisfactory in terms of semantic, conceptual and normative equivalence of both questionnaires. Acceptability was satisfactory for the 4-item ACP-E, while findings of the QOC cognitive debriefing informed a major amendment of a pilot trial protocol on ACP in multiple sclerosis (ConCure-SM): use of the interviewer version only, in an adaptive form. Psychometric testing of both questionnaires on a large, independent sample will follow.
 BACKGROUND: Few studies documented the potential association between vaccination and the risk of central demyelination (CD). Specifically, anti-hepatitis B and anti-human papillomavirus (HPV) vaccines have been the subject of distrust with regard to their implication to trigger CD. METHODS: From a systematic national registry, patients with first signs of CD (cases) were identified and documented for their exposure to vaccination up to 24 months before the first signs occurred. This exposure was compared to that of a representative sample of general practice patients without a history of CD, randomly selected from a national registry (referents). CD cases were 2:1 matched on age, sex, index date (ID), and region of residence. Vaccines against influenza, HPV, hepatitis B and diphtheria-tetanus-pertussis-poliomyelitis-haemophilus (DTPPHae) were considered. Associations between vaccination and CD were assessed using multivariate conditional logistic regressions, controlled for confounding factors. FINDINGS: 564 CD cases were matched to 1,128 randomly selected referents (age range: 2-79 years old). Overall, 123 (22%) CD cases and 320 (28%) referents had received at least one vaccine within 24 months before ID. Adjusted odds ratios (ORs) for any vaccination were 0.69, 95% confidence interval (CI) [0.54-0.88] with respect to any CD first signs, 0.68 [0.51-0.90] for myelitis and 0.70 [0.42-1.17] for optic neuritis. Adjusted ORs for any CD first signs were 1.02 [0.71-1.47] for influenza vaccine (administered in 9.6% of cases and 10.4% of referents) and 0.72 [0.53-0.99] for DTPPHae vaccine (administered in 10.8% of cases and 14.5% of referents). Vaccines against hepatitis B and HPV were only administered in 1.1% and 1.2% of cases and in 2.9% and 3.2% of referents respectively, which statistically explained the point estimates < 1 (ORs of 0.39 [0.16-0.94] and of 0.32 [0.13-0.80]). INTERPRETATION: No increased risk of CD incidence was observed amongst vaccinated patients. Lower rates of vaccination against hepatitis B and HPV observed in patients with CD compared to referents may be due to the reluctance of physicians to vaccinate patients considered at risk of CD.
 Histones have vital roles in chromatin functioning and gene transcription. At the same time, they are pernicious in intercellular space because they stimulate systemic inflammatory and toxic responses. Myelin basic protein (MBP) is the major protein of the axon myelin-proteolipid sheath. Antibody-abzymes with various catalytic activities are specific features of some autoimmune diseases. IgGs against five individual histones (H2B, H1, H2A, H3, and H4) and MBP were isolated from the blood of experimental autoimmune encephalomyelitis-prone C57BL/6 mice by affinity chromatography. Abzymes corresponding to various stages of EAE development, including spontaneous EAE, myelin oligodendrocyte glycoprotein (MOG)- and DNA-histone complex-accelerated onset, as well as acute and remission stages, were analyzed. IgG-abzymes against MBP and five individual histones showed unusual polyreactivity in complex formation and enzymatic cross-reactivity in the specific hydrolysis of H2B histone. All IgGs against MBP and individual histones in 3-month-old mice (zero time) demonstrated from 4 to 11 different H2B hydrolysis sites. Spontaneous development of EAE during 60 days led to a significant change in the type and number of H2B hydrolysis sites by IgGs against the five histones and MBP. Mouse treatment with MOG and DNA-histone complex changed the type and number of H2B hydrolysis sites compared to zero time. The minimum number (3) of different H2B hydrolysis sites was found for IgGs against H3 20 days after mouse immunization with DNA-histone complex, whereas the maximum number (33) for anti-H2B IgGs was found 60 days after mouse treatment with DNA-histone complex. Overall, this is the first study to demonstrate that at different stages of EAE evolution, IgG-abzymes against five individual histones and MBP could significantly differ in the specific sites and number of H2B hydrolysis sites. Possible reasons for the catalytic cross-reactivity and significant differences in the number and type of histone H2B cleavage sites were analyzed.
 BACKGROUND: Omega-3 polyunsaturated fatty acids are known to be associated with numbers of health benefits, and which can be uptake from fish. The aim of this study was to evaluate the current evidence of associations between consumption of fish and diverse health outcomes. Here, we performed an umbrella review to summarize the breadth, strength, and validity of the evidence derived from meta-analyses and systematic reviews of fish consumption on all health outcomes. METHODS: The methodological quality of the included meta-analyses and the quality of the evidence were assessed by the Assessment of Multiple Systematic Reviews (AMSTAR) and the grading of recommendations, assessment, development, and evaluation (GRADE) tools, respectively. The umbrella review identified 91 meta-analyses with 66 unique health outcomes, of which 32 outcomes were beneficial, 34 showed nonsignificant associations and only one was harmful (myeloid leukemia). RESULTS: A total of 17 beneficial associations [all-cause mortality, prostate cancer mortality, cardiovascular disease (CVD) mortality, esophageal squamous cell carcinoma (ESCC), glioma, non-Hodgkin lymphoma (NHL), oral cancer, acute coronary syndrome (ACS), cerebrovascular disease, metabolic syndrome, age-related macular degeneration (AMD), inflammatory bowel disease (IBD), Crohn's disease (CD), triglycerides, vitamin D, high-density lipoprotein (HDL)-cholesterol, and multiple sclerosis (MS)], and eight nonsignificant associations [colorectal cancer (CRC) mortality, esophageal adenocarcinoma (EAC), prostate cancer, renal cancer, ovarian cancer, hypertension, ulcerative colitis (UC), and rheumatoid arthritis (RA)] were evaluated as moderate/high quality of evidence. According to dose-response analyses, consumption of fish, especially fatty types, seems generally safe at one-two servings per week and could exert protective effects. CONCLUSIONS: Fish consumption is often associated with a variety of health outcomes, both beneficial and harmless, but only about 34% of the associations were graded as based on a moderate/high quality of evidence, and additional multicenter high quality randomized controlled trials (RCTs) with a large sample size are needed to verify these findings in the future.
 We sought to assess the impact of 4-Methylhistamine (4-MeH), a specific agonist targeting the Histamine H4 Receptor (H4R), on the progression of experimental autoimmune encephalomyelitis (EAE) and gain insight into the underlying mechanism. EAE is a chronic autoimmune, inflammatory, and neurodegenerative disease of the central nervous system (CNS) characterized by demyelination, axonal damage, and neurodegeneration. Over the past decade, pharmacological research into the H4R has gained significance in immune and inflammatory disorders. For this study, Swiss Jim Lambert EAE mice were treated with 4-MeH (30 mg/kg/day) via intraperitoneal administration from days 14 to 42, and the control group was treated with a vehicle. Subsequently, we evaluated the clinical scores. In addition, flow cytometry was employed to estimate the impact of 4-Methylhistamine (4-MeH) on NF-κB p65, GM-CSF, MCP-1, IL-6, and TNF-α within CD19(+) and CXCR5(+) spleen B cells. Additionally, we investigated the effect of 4-MeH on the mRNA expression levels of Nf-κB p65, Gmcsf, Mcp1, Il6, and Tnfα in the brain of mice using RT-PCR. Notably, the clinical scores of EAE mice treated with 4-MeH showed a significant increase compared with those treated with the vehicle. The percentage of cells expressing CD19(+)NF-κB p65(+), CXCR5(+)NF-κB p65(+), CD19(+)GM-CSF(+), CXCR5(+)GM-CSF(+), CD19(+)MCP-1(+), CXCR5(+)MCP-1(+), CD19(+)IL-6(+), CXCR5(+)IL-6(+), CD19(+)TNF-α(+), and CXCR5(+)TNF-α(+) exhibited was more pronounced in 4-MeH-treated EAE mice when compared to vehicle-treated EAE mice. Moreover, the administration of 4-MeH led to increased expression of NfκB p65, Gmcsf, Mcp1, Il6, and Tnfα mRNA in the brains of EAE mice. This means that the H4R agonist promotes pro-inflammatory mediators aggravating EAE symptoms. Our results indicate the harmful role of H4R agonists in the pathogenesis of MS in an EAE mouse model.
 Optic neuritis (ON) admits diverse differential diagnoses. Petzold proposed diagnostic criteria for ON in 2022, although real-world application of these criteria is missing. We conducted a retrospective review of patients with ON. We classified patients into definite or possible ON, and into groups A (typical neuritis), B (painless), or C (binocular) and estimated the frequency of etiologies for each group. We included 77 patients, with 62% definite and 38% possible ON. CRION and NMOSD-AQP4 negative-ON were less commonly seen in definite ON. Application of the 2022 criteria revealed a lower-than-expected frequency of definite ON, particularly for seronegative non-MS causes.
 Theiler's murine encephalomyelitis virus (TMEV) is the causative agent of TMEV-induced demyelinating disease (TMEV-IDD); a well-established animal model for the chronic progressive form of human multiple sclerosis (MS). In susceptible mice with an inadequate immune response, TMEV-IDD is triggered by virus persistence and maintained by a T cell mediated immunopathology. OT-mice are bred on a TMEV-resistant C57BL/6 background and own predominantly chicken ovalbumin (OVA)-specific populations of CD8(+) T cells (OT-I) or CD4(+) T cells (OT-II), respectively. It is hypothesized that the lack of antigen specific T cell populations increases susceptibility for a TMEV-infection in OT-mice on a TMEV-resistant C57BL/6 background. OT-I, OT-II, and C57BL/6 control mice were infected intracerebrally with the TMEV-BeAn strain. Mice were scored weekly for clinical disease and after necropsy, histological and immunohistochemical evaluation was performed. OT-I mice started to develop progressive motor dysfunction between 7 and 21 days post infection (dpi), leading up to hind limb paresis and critical weight loss, which resulted in euthanasia for humane reasons between 14 and 35 dpi. OT-I mice displayed a high cerebral virus load, an almost complete absence of CD8(+) T cells from the central nervous system (CNS) and a significantly diminished CD4(+) T cell response. Contrarily, only 60% (12 of 20) of infected OT-II mice developed clinical disease characterized by mild ataxia. 25% of clinically affected OT-II mice (3 of 12) made a full recovery. 5 of 12 OT-II mice with clinical disease developed severe motor dysfunction similar to OT-I mice and were euthanized for humane reasons between 13 and 37 dpi. OT-II mice displayed only low virus-immunoreactivity, but clinical disease correlated well with severely reduced infiltration of CD8(+) T cells and the increased presence of CD4(+) T cells in the brains of OT-II mice. Though further studies are needed to reveal the underlying pathomechanisms following TMEV infection in OT mice, findings indicate an immunopathological process as a main contributor to clinical disease in OT-II mice, while a direct virus-associated pathology may be the main contributor to clinical disease in TMEV-infected OT-I mice.
 Schizophrenia is a psychiatric disorder that affects around 1% of the population in widespread populations, with severe cases leading to long-term hospitalization and necessitation of lifelong treatment. Recent studies on schizophrenia have highlighted the involvement of inflammatory and immunoregulatory mechanisms with the onset of symptoms, and the usage of anti-inflammatory treatments are being tested against periods of rapid psychosis. In the central nervous system, microglia are the innate immune population which are activated in response to a wide range of physical and psychological stress factors and produce proinflammatory mediators such as cytokines. Microglial activation and neuroinflammation has been associated to numerous psychiatric disorders including schizophrenia, especially during psychotic episodes. Thus, novel treatments which dampen microglial activation may be of great relevance in the treatment of psychiatric disorders. Fingolimod (FTY720) is a drug used as an immunosuppressive treatment to multiple sclerosis. Recent clinical trials have focused on FTY720 as a treatment for the behavioral symptoms in schizophrenia. However, the mechanisms of Fingolimod in treating the symptoms of schizophrenia are not clear. In this study we use a recently developed neuroinflammatory psychosis model in mice: cuprizone short-term exposure, to investigate the effects of FTY720 administration. FTY720 administration was able to completely alleviate methamphetamine hypersensitivity caused by cuprizone exposure. Moreover, administration of FTY720 improved multiple measures of neuroinflammation (microglial activation, cytokine production, and leucocyte infiltration). In conclusion, our results highlight the future use of FTY720 as a direct anti-inflammatory treatment against microglial activation and psychosis.
 Brain MR images are the most suitable method for detecting chronic nerve diseases such as brain tumors, strokes, dementia, and multiple sclerosis. They are also used as the most sensitive method in evaluating diseases of the pituitary gland, brain vessels, eye, and inner ear organs. Many medical image analysis methods based on deep learning techniques have been proposed for health monitoring and diagnosis from brain MRI images. CNNs (Convolutional Neural Networks) are a sub-branch of deep learning and are often used to analyze visual information. Common uses include image and video recognition, suggestive systems, image classification, medical image analysis, and natural language processing. In this study, a new modular deep learning model was created to retain the existing advantages of known transfer learning methods (DenseNet, VGG16, and basic CNN architectures) in the classification process of MR images and eliminate their disadvantages. Open-source brain tumor images taken from the Kaggle database were used. For the training of the model, two types of splitting were utilized. First, 80% of the MRI image dataset was used in the training phase and 20% in the testing phase. Secondly, 10-fold cross-validation was used. When the proposed deep learning model and other known transfer learning methods were tested on the same MRI dataset, an improvement in classification performance was obtained, but an increase in processing time was observed.
 Research describing patients using medicinal cannabis and its effectiveness is lacking. We aimed to describe adults with non-cancer diagnoses who are prescribed medicinal cannabis via a retrospective medical record review and assess its effectiveness and safety. From 157 Australian records, most were female (63.7%; mean age 63.0 years). Most patients had neurological (58.0%) or musculoskeletal (24.8%) conditions. Medicinal cannabis was perceived beneficial by 53.5% of patients. Mixed-effects modelling and post hoc multiple comparisons analysis showed significant changes overtime for pain, bowel problems, fatigue, difficulty sleeping, mood, quality of life (all p < 0.0001), breathing problems (p = 0.0035), and appetite (p = 0.0465) Symptom Assessment Scale scores. For the conditions, neuropathic pain/peripheral neuropathy had the highest rate of perceived benefit (66.6%), followed by Parkinson's disease (60.9%), multiple sclerosis (60.0%), migraine (43.8%), chronic pain syndrome (42.1%), and spondylosis (40.0%). For the indications, medicinal cannabis had the greatest perceived effect on sleep (80.0%), followed by pain (51.5%), and muscle spasm (50%). Oral oil preparations of balanced delta-9-tetrahydrocannabinol/cannabidiol (average post-titration dose of 16.9 mg and 34.8 mg per day, respectively) were mainly prescribed. Somnolence was the most frequently reported side effect (21%). This study supports medicinal cannabis' potential to safely treat non-cancer chronic conditions and indications.
 The patient was a 17-year-old girl with transient right-sided weakness and dysesthesia associated with headache and nausea. Head magnetic resonance imaging (MRI) revealed white matter lesions confined to the left hemisphere. Initially, multiple sclerosis was suspected, and methylprednisolone (mPSL) pulse therapy was administered, followed by fingolimod hydrochloride. However, on day 267, the patient again experienced transient hypesthesia. Cranial MRI showed expansion of the highly infiltrated areas of the left hemisphere on fluid-attenuated inversion recovery (FLAIR) and T2 weighted image, accompanied by edema. Multiple contrasting areas were also observed. Susceptibility-weighted imaging demonstrated several streaks and some corkscrew-like appearances with low signals from the white matter to the cortex, suggestive of occluded or dilated collateral vessels. Multiple dotted spots indicating cerebral microbleeds (MBs) were also observed. A brain biopsy revealed lymphocytic, non-granulomatous inflammation in and around the vessels. Vascular occlusion and perivascular MBs were prevalent. The patient was diagnosed with relapsing primary angiitis of the central nervous system (PACNS), and immunosuppressive treatment was initiated, mPSL 1000 mg/day pulse therapy. The patient's clinical symptoms and neuroradiological abnormalities gradually improved. She is now receiving oral prednisolone (6 mg/day) and mycophenolate mofetil (1750 mg/day). This case corresponds to unilateral relapsing, which has recently been reported as a specific clinicopathological subtype of PACNS.
 4-aminopyridine (4AP) is a potassium (K (+) ) channel blocker used clinically to improve walking in people with multiple sclerosis (MS). 4AP binds to exposed K (+) channels in demyelinated axons, reducing the leakage of intracellular K (+) and enhancing impulse conduction. Multiple derivatives of 4AP capable of blocking K (+) channels have been reported including three radiolabeled with positron emitting isotopes for imaging demyelinated lesions using positron emission tomography (PET). Here, we describe 3-fluoro-5-methylpyridin-4-amine (5Me3F4AP), a novel K (+) channel blocker with potential application in PET. 5Me3F4AP has comparable potency to 4AP and the PET tracer 3-fluoro-4-aminopyridine (3F4AP). Compared to 3F4AP, 5Me3F4AP is more lipophilic (logD = 0.664 ± 0.005 vs. 0.414 ± 0.002) and slightly more basic (p K (a) = 7.46 ± 0.01 vs . 7.37 ± 0.07). In addition, 5Me3F4AP appears to be more permeable to an artificial brain membrane and more stable towards oxidation by the cytochrome P450 enzyme family 2 subfamily E member 1 (CYP2E1), responsible for the metabolism of 4AP and 3F4AP. Taken together, 5Me3F4AP has promising properties for PET imaging warranting additional investigation. SIGNIFICANCE STATEMENT: The PET tracer [ (18) F]3-fluoro-4-aminopyridine ([ (18) F]3F4AP) binds to K (+) channels in demyelinated axons and has shown promise for imaging demyelinated lesions in animal models. However, its use in humans may be compromised due to rapid metabolism. Thus, a novel 3F4AP derivative amenable to labeling with fluorine-18 was designed and evaluated in vitro . The results indicate that 5-methyl-3F4AP exhibits high binding affinity, good physicochemical properties and slower oxidation by CYP2E1 than 3F4AP, making it a promising candidate for further PET studies.
 INTRODUCTION: General practitioners (GPs) play a crucial role in the early management and treatment of the comorbidities and complications experienced by people with disability. However, GPs experience multiple constraints, including limited time and disability-related expertise. Knowledge gaps around the health needs of people with disability as well as the frequency and extent of their engagement with GPs mean evidence to inform practice is limited. Using a linked dataset, this project aims to enhance the knowledge of the GP workforce by describing the health needs of people with disability. METHODS AND ANALYSIS: This project is a retrospective cohort study using general practice health records from the eastern Melbourne region in Victoria, Australia. The research uses Eastern Melbourne Primary Health Network (EMPHN)-owned de-identified primary care data from Outcome Health's POpulation Level Analysis and Reporting Tool (POLAR). The EMPHN POLAR GP health records have been linked with National Disability Insurance Scheme (NDIS) data. Data analysis will involve comparisons across disability groups and the rest of the population to explore utilisation (eg, frequency of visits), clinical and preventative care (eg, cancer screening, blood pressure readings) and health needs (eg, health conditions, medications). Initial analyses will focus on NDIS participants as a whole and NDIS participants whose condition is either an acquired brain injury, stroke, spinal cord injury, multiple sclerosis or cerebral palsy, as classified by the NDIS. ETHICS AND DISSEMINATION: Ethics approval was obtained from the Eastern Health Human Research Ethics Committee (E20/001/58261), and approval for the general collection, storage and transfer of data was from the Royal Australian College of General Practitioners National Research Ethics and Evaluation Committee (protocol ID: 17-088). Dissemination mechanisms will include the engagement of stakeholders through reference groups and steering committees, as well as the production of research translation resources in parallel with peer-reviewed publications and conference presentations.
 Myeloperoxidase (MPO) is a highly oxidative, pro-inflammatory enzyme involved in post-myocardial infarction (MI) injury and is a potential therapeutic target. While multiple MPO inhibitors have been developed, the lack of an imaging reporter to select appropriate patients and assess therapeutic efficacy has hampered clinical development. Thus, a translational imaging method to detect MPO activity non-invasively would help to better understand the role MPO plays in MI and facilitate novel therapy development and clinical validation. Interestingly, many MPO inhibitors affect both intracellular and extracellular MPO, but previous MPO imaging methods can only report extracellular MPO activity. In this study, we found that an MPO-specific PET imaging agent ((18)F-MAPP) can cross cell membranes to report intracellular MPO activity. We showed that (18)F-MAPP can track the treatment effect of an MPO inhibitor (PF-2999) at different doses in experimental MI. The imaging results were corroborated by ex vivo autoradiography and gamma counting data. Furthermore, extracellular and intracellular MPO activity assays revealed that (18)F-MAPP imaging can report the changes induced by PF-2999 on both intracellular and extracellular MPO activities. These findings support (18)F-MAPP as a translational candidate to noninvasively report MPO activity and accelerate drug development against MPO and other related inflammatory targets.

 OBJECTIVES: The aim of the study was to study the demographical, clinical, radiological features, and outcome of anti-myelin oligodendrocyte glycoprotein (MOG) antibody spectrum disorder and compare these features with patients negative for anti-MOG antibody. MOG antibody-associated disease (MOGAD) and aquaporin-4 (AQP4) antibody-related diseases are immunologically distinct pathologies. Our aim was to compare the clinical and radiological features of MOG antibody-related diseases with AQP4 antibody-related diseases and seronegative demyelinating diseases (Non-multiple sclerosis). MATERIALS AND METHODS: This was a prospective and cohort study conducted at an apex tertiary care institute in the northern part of India from Jan 2019 to May 2021. We compared clinical, laboratory, and radiological findings of patients with MOGAD, AQP4 antibody-related diseases, and seronegative demyelinating disease. RESULTS: There were a total of 103 patients - 41 patients of MOGAD, 37 patients of AQP4 antibody-related diseases and 25 seronegative demyelinating disease. Bilateral optic neuritis was the most frequent phenotype in patients with MOGAD (18/41) whereas myelitis was the most common phenotype in the AQP4 (30/37) and seronegative groups (13/25). Cortical, juxtacortical lesions, anterior segment optic neuritis, optic sheath enhancement, and conus involvement in myelitis were radiological findings that separated MOGAD from AQP4 related diseases. Nadir Expanded Disability Status Scale (EDSS) and visual acuity were similar across the groups. Last follow-up EDSS was significantly better in the MOG antibody group as compared to AQP4 antibody group (1 [0-8] vs. 3.5 [0-8]; P = 0.03). Encephalitis, myelitis, and seizures were more common in the younger population (<18 vs. >18 years) in MOGAD (9 vs. 2, P = 0.001; 9 vs. 7, P = 0.03; 6 vs. 0, P = 0.001). CONCLUSION: We identified several clinical and radiological features that can help physicians to distinguish MOGAD from AQP4-immunoglobulin G+neuromyelitis optica spectrum disorder. Differentiation is vital as treatment response might vary among both groups.
 Hyperactive sphingosine 1-phosphate (S1P) signaling is associated with a poor prognosis of triple-negative breast cancer (TNBC). Despite recent evidence that links the S1P receptor 1 (S1P1) to TNBC cell survival, its role in TNBC invasion and the underlying mechanisms remain elusive. Combining analyses of human TNBC cells with zebrafish xenografts, we found that phosphorylation of S1P receptor 1 (S1P1) at threonine 236 (T236) is critical for TNBC dissemination. Compared to luminal breast cancer cells, TNBC cells exhibit a significant increase of phospho-S1P1 T236 but not the total S1P1 levels. Misexpression of phosphorylation-defective S1P1 T236A (alanine) decreases TNBC cell migration in vitro and disease invasion in zebrafish xenografts. Pharmacologic disruption of S1P1 T236 phosphorylation, using either a pan-AKT inhibitor (MK2206) or an S1P1 functional antagonist (FTY720, an FDA-approved drug for treating multiple sclerosis), suppresses TNBC cell migration in vitro and tumor invasion in vivo. Finally, we show that human TNBC cells with AKT activation and elevated phospho-S1P1 T236 are sensitive to FTY720-induced cytotoxic effects. These findings indicate that the AKT-enhanced phosphorylation of S1P1 T236 mediates much of the TNBC invasiveness, providing a potential biomarker to select TNBC patients for the clinical application of FTY720.
 BACKGROUND: Immune-mediated inflammatory diseases (IMIDs) are likely to complicate maternal health. However, literature data on patients with IMIDs undergoing pregnancy is scarce and often overlooks the impact of comorbidities. METHODS: We investigated 12 selected IMIDs: psoriasis, inflammatory bowel disease, rheumatoid arthritis, spondyloarthritis, multiple sclerosis, systemic lupus erythematosus, psoriatic arthritis, antiphospholipid syndrome, Sjögren's syndrome, vasculitis, sarcoidosis, systemic sclerosis. We characterized patients with IMIDs prior to pregnancy (IMIDs group) based on pregnancy/maternal characteristics, comorbidities, and pre-pregnancy/prenatal immunomodulatory medications (IMMs) prescription patterns. We 1:1 propensity score matched the IMIDs cohort with people who had no IMID diagnoses prior to pregnancy (non-IMIDs cohort). Outcome measures were preterm birth (PTB), low birth weight (LBW), small for gestational age (SGA), and cesarean section. FINDINGS: The prevalence rate of pregnancy occurring with people with a previous IMID diagnosis has doubled in the past ten years. We identified 5,784 patients with IMIDs. 17% of the IMIDs group had at least one prenatal IMM prescription. Depending on the type of IMM, from 48% to 70% of the patients taking IMMs before pregnancy continued them throughout pregnancy. Patients with IMIDs had similar but slightly increased risks of PTB (Relative risk (RR)=1·1[1·0, 1·3]), LBW (RR=1·2 [1·0,1·4]), SGA (RR=1·1 [1·0,1·2]), and cesarean section (RR=1·1 [1·1,1·2]) compared to a matched cohort of people without IMIDs. Out of the 12 selected IMIDs, three for PTB, one for LBW, two for SGA, and six for cesarean section had results supporting increased risk. INTERPRETATION: The association between IMIDs and the increased risk of adverse pregnancy outcomes depend on both the nature of the IMID and the presence of comorbidities. FUNDING: NIH.
 Neurodegenerative diseases are caused by the gradual loss of neurons' function. These neurological illnesses remain incurable, and current medicines only alleviate the symptoms. Given the social and economic burden caused by the rising frequency of neurodegenerative diseases, there is an urgent need for the development of appropriate therapeutics. Natural compounds are gaining popularity as alternatives to synthetic drugs due to their neuroprotective properties and higher biocompatibility. While natural compounds' therapeutic effects for neurodegenerative disease treatment have been investigated in numerous in vitro and in vivo studies, only few have moved to clinical trials. This article provides the first systematic review of the clinical trials evaluating natural compounds' safety and efficacy for the treatment of the five most prevalent neurodegenerative disorders: Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington's disease.
 Ferroptosis is a type of regulated cell death characterized by intracellular accumulation of iron and reactive oxygen species, inhibition of system Xc-, glutathione depletion, nicotinamide adenine dinucleotide phosphate oxidation and lipid peroxidation. Since its discovery and characterization in 2012, many efforts have been made to reveal the underlying mechanisms, modulating compounds, and its involvement in disease pathways. Ferroptosis inducers include erastin, sorafenib, sulfasalazine and glutamate, which, by inhibiting system Xc-, prevent the import of cysteine into the cells. RSL3, statins, Ml162 and Ml210 induce ferroptosis by inhibiting glutathione peroxidase 4 (GPX4), which is responsible for preventing the formation of lipid peroxides, and FIN56 and withaferin trigger GPX4 degradation. On the other side, ferroptosis inhibitors include ferrostatin-1, liproxstatin-1, α-tocopherol, zileuton, FSP1, CoQ10 and BH4, which interrupt the lipid peroxidation cascade. Additionally, deferoxamine, deferiprone and N-acetylcysteine, by targeting other cellular pathways, have also been classified as ferroptosis inhibitors. Increased evidence has established the involvement of ferroptosis in distinct brain diseases, including Alzheimer's, Parkinson's and Huntington's diseases, amyotrophic lateral sclerosis, multiple sclerosis, and Friedreich's ataxia. Thus, a deep understanding of how ferroptosis contributes to these diseases, and how it can be modulated, can open a new window of opportunities for novel therapeutic strategies and targets. Other studies have shown a sensitivity of cancer cells with mutated RAS to ferroptosis induction and that chemotherapeutic agents and ferroptosis inducers synergize in tumor treatment. Thus, it is tempting to consider that ferroptosis may arise as a target mechanistic pathway for the treatment of brain tumors. Therefore, this work provides an up-to-date review on the molecular and cellular mechanisms of ferroptosis and their involvement in brain diseases. In addition, information on the main ferroptosis inducers and inhibitors and their molecular targets is also provided.
 BACKGROUND AND AIM: Calprotectin (CLP) is a heterodimeric complex formed by two S100 proteins (S100A8/A9), which plays a pivotal role in innate immunity. Due to its intrinsic cytotoxic and proinflammatory properties, CLP controls cell differentiation, proliferation and NETosis and has been associated with a wide range of rheumatic diseases. Our review summarizes the widespread interest in circulating CLP (cCLP) as a biomarker of neutrophil-related inflammation, in autoimmune rheumatic disease (ARD) and non-ARD. METHODS: A thorough literature review was performed using PubMed and EMBASE databases searching for circulating calprotectin and synonyms S100A8/A9, myeloid-related protein 8/14 (MRP8/MRP14), calgranulin A/B and L1 protein in addition to specific ARDs and autoimmune non-rheumatic diseases. We selected only English-language articles and excluded abstracts without the main text. RESULTS: High cCLP serum levels are associated with worse structural outcomes in rheumatoid arthritis and to a lesser extent, in spondyloarthritis. In addition, cCLP can predict disease relapse in some autoimmune diseases including systemic lupus erythematosus (SLE), anti-neutrophil cytoplasmic antibodies-associated vasculitis (AAV) and some severe manifestations of connective tissue diseases, such as glomerulonephritis in SLE, AAV, juvenile idiopathic arthritis, adult-onset Still's disease and lung fibrosis in systemic sclerosis. Therefore, cCLP levels enable the identification of patients who need an accurate and tight follow-up. The clinical usefulness of cCLP as an inflammatory marker has been suggested for inflammatory/autoimmune non-rheumatic diseases, and especially for the monitoring of the inflammatory bowel diseases patients. Currently, there are only a few studies that evaluated the cCLP efficacy as a clinical biomarker in inflammatory/autoimmune non-rheumatic diseases with controversial results. Future studies are warranted to better clarify the role of cCLP in relation to the disease severity in myasthenia gravis, multiple sclerosis, chronic inflammatory demyelinating polyneuropathy, Graves' orbitopathy, autoimmune bullous diseases and uveitis. CONCLUSION: Our literature review supports a relevant role of cCLP as potential prognostic biomarker mirroring local or systemic inflammation, especially in chronic inflammatory rheumatic diseases.
 OBJECTIVES: The aim of this study was to assess the cognitive abilities of people with spinal cord injury (SCI) using the Edinburgh Cognitive and Behavior Amyotrophic Lateral Sclerosis Screen (ECAS), a tool designed for testing cognition in individuals with limited hand motor function. The impact of cognitive dysfunction on quality of life was also assessed. METHODS: Forty-one patients with SCI were assessed using ECAS, the brief version of the World Health Organisation Quality of Life questionnaire (WHOQOL-BREF), and the Spinal Cord Independence Measure. RESULTS: Overall, 28 of the 41 participants scored below the cut-off threshold for normal population in ECAS. The domains affected were language, 63%; memory, 51%; executive function, 44%; verbal fluency, 44%; and visuospatial skills, 24%. On multiple regression analysis, the ECAS total score moderately strongly explained the variance in the WHOQOL-BREF psychological (β = 0.428, t = 2.958, P = 0.005) and environmental (β = 0.411, t = 2.819, P = 0.008) domains. ECAS memory scores independently influenced WHOQOL-BREF physical (β = 0.398, t = 2.67, P = 0.011) and environmental (β = 0.37, t = 2.697, P = 0.010) domains. WHOQOL-BREF psychological scores were significantly influenced by ECAS executive scores (β = 0.415, t = 2.85, P = 0.007), whereas the social domain was not significantly influenced by ECAS scores. CONCLUSIONS: It was feasible to use ECAS in individuals with SCI. Cognitive ability influenced the quality of life of people with SCI.
 BACKGROUND: The N-MOmentum trial investigated safety and efficacy of inebilizumab in participants with neuromyelitis optica spectrum disorder (NMOSD). OBJECTIVE: Evaluate the attack identification process and adjudication committee (AC) performance in N-MOmentum. METHODS: Adults (n = 230) with NMOSD and Expanded Disability Status Scale score ⩽8 were randomized (3:1) to inebilizumab 300 mg or placebo. The randomized controlled period was 28 weeks or until adjudicated attack. Attacks were adjudicated according to 18 predefined criteria. Magnetic resonance imaging (MRI) and biomarker (serum glial fibrillary acidic protein [sGFAP]) analyses were performed. RESULTS: A total of 64 participant-reported neurological events occurred; 51 (80%) were investigator-determined to be attacks. The AC confirmed 43 of the investigator-determined attacks (84%). There was high inter- and intra-AC-member agreement. In 25/64 events (39%) and 14/43 AC-adjudicated attacks (33%), MRI was reviewed during adjudication. Retrospective analysis revealed new domain-specific T1 and T2 MRI lesions in 90% of adjudicated attacks. Increased mean sGFAP concentrations (>2-fold change) from baseline were observed in 56% of adjudicated attacks versus 14% of investigator-determined attacks rejected by the AC and 31% of participant-reported events determined not to be attacks. CONCLUSION: AC adjudication of NMOSD attacks according to predefined criteria appears robust. MRI lesion correlates and sGFAP elevations were found in most adjudicated attacks.
 ETHNOPHARMACOLOGICAL RELEVANCE: Wuzi Yanzong Pill (WYP) is a classic traditional Chinese medicine (TCM) formula that is used for reproductive system diseases. Previous studies showed that WYP had a preventive effect on the development of neural tube defects (NTDs) induced by all-trans retinoic acid (atRA) in mice. AIM OF THE STUDY: This study aimed to determine the optimal combination of main monomer components in WYP on preventing NTDs and to understand the underlying mechanism. MATERIALS AND METHODS: An optimal combination was made from five representative components in WYP including hyperoside, acteoside, schizandrol A, kaempferide and ellagic acid by orthogonal design method. In a mouse model of NTDs induced by intraperitoneal injection of atRA, pathological changes of neural tube tissues were observed by Hematoxylin & Eosin (HE) staining, neural tube epithelial cells apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), protein changes related to apoptosis, anti-apoptosis, and antioxidant factors were detected with Western blot. Potential targets and mechanisms of monomer compatibility group (MCG) acting on NTDs were analyzed by bioinformatics. RESULTS: Treatment with different combinations of WYP bioactive ingredients resulted in varying decreases in the incidence of NTDs in mice embryos. The combination of MCG15 (200 mg/kg of hyperoside, 100 mg/kg of acteoside, 10 mg/kg of schizandrol A, 100 mg/kg of kaempferide and 1 mg/kg of ellagic acid) showed the most significant reduction in NTD incidence. Mechanistically, MCG15 inhibited apoptosis and oxidative stress, as evidenced by reduced TUNEL-positive cells, downregulation of caspase-9, cleaved caspase-3, Bad, and Bax, and upregulation of Bcl-2, as well as decreased MDA and increased SOD, CAT, GSH, HO-1, and GPX1 levels. Bioinformatics analysis showed that MCG15 acted on the PI3K/Akt signaling pathway, which was confirmed by Western blot analysis showing increased expression of p-PI3K, p-Akt/Akt, and Nrf2 related indicators. CONCLUSION: We have identified an optimal combination of five bioactive components in WYP (MCG15) that prevented NTDs in mice embryos induced by atRA by activating the PI3K/Akt signaling pathway and inhibiting apoptosis and oxidative stress.
 AIMS: Pyroptosis is a unique pro-inflammatory form of programmed cell death which plays a critical role in promoting the pathogenesis of multiple inflammatory and autoimmune diseases. However, the current drug that is capable of inhibition pyroptosis has not been translated successfully in the clinic, suggesting a requirement for drug screening in depth. METHODS: We screened more than 20,000 small molecules and found D359-0396 demonstrates a potent anti-pyroptosis and anti-inflammation effect in both mouse and human macrophage. In vivo, EAE (a mouse model of MS) and septic shock mouse model was used to investigate the protective effect of D359-0396. In vitro experiments we used LPS plus ATP/nigericin/MSU to induce pyroptosis in both mouse and human macrophage, and finally the anti-pyroptosis function of D359-0396 was assessed. RESULTS: Our findings show that D359-0396 is well-tolerated without remarkable disruption of homeostasis. Mechanistically, while D359-0396 is capable of inhibiting pyroptosis and IL-1β release in macrophages, this process depends on the NLRP3-Casp1-GSDMD pathway rather than NF-κB, AIM2 or NLRC4 inflammasome signaling. Consistently, D359-0396 significantly suppresses the oligomerization of NLRP3, ASC, and the cleavage of GSDMD. In vivo, D359-0396 not only ameliorates the severity of EAE (a mouse model of MS), but also exhibits a better therapeutic effect than teriflunomide, the first-line drug of MS. Similarly, D359-0396 treatment also significantly protects mice from septic shock. CONCLUSION: Our study identified D359-0396 as a novel small-molecule with potential application in NLRP3-associated diseases.
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) diagnostic criteria for inflammatory demyelinating central nervous system diseases included symptomatic narcolepsy; however, no relevant case-control studies exist. We aimed to examine the relationship among cerebrospinal fluid orexin-A (CSF-OX) levels, cataplexy and diencephalic syndrome; determine risk factors for low-and-intermediate CSF-OX levels (≤200 pg/mL) and quantify hypothalamic intensity using MRI. METHODS: This ancillary retrospective case-control study included 50 patients with hypersomnia and 68 controls (among 3000 patients) from Akita University, the University of Tsukuba and community hospitals (200 facilities). Outcomes were CSF-OX level and MRI hypothalamus-to-caudate-nucleus-intensity ratio. Risk factors were age, sex, hypersomnolence and MRI hypothalamus-to-caudate-nucleus-intensity ratio >130%. Logistic regression was performed for the association between the risk factors and CSF-OX levels ≤200 pg/mL. RESULTS: The hypersomnia group (n=50) had significantly more cases of NMOSD (p<0.001), diencephalic syndrome (p=0.006), corticosteroid use (p=0.011), hypothalamic lesions (p<0.023) and early treatment (p<0.001). No cataplexy occurred. In the hypersomnia group, the median CSF-OX level was 160.5 (IQR 108.4-236.5) pg/mL and median MRI hypothalamus-to-caudate-nucleus-intensity ratio was 127.6% (IQR 115.3-149.1). Significant risk factors were hypersomnolence (adjusted OR (AOR) 6.95; 95% CI 2.64 to 18.29; p<0.001) and MRI hypothalamus-to-caudate-nucleus-intensity ratio >130% (AOR 6.33; 95% CI 1.18 to 34.09; p=0.032). The latter was less sensitive in predicting CSF-OX levels ≤200 pg/mL. Cases with MRI hypothalamus-to-caudate-nucleus-intensity ratio >130% had a higher rate of diencephalic syndrome (p<0.001, V=0.59). CONCLUSIONS: Considering orexin as reflected by CSF-OX levels and MRI hypothalamus-to-caudate-nucleus-intensity ratio may help diagnose hypersomnia with diencephalic syndrome.
 INTRODUCTION: B-cell-depleting agents have been widely used for neuromyelitis optica spectrum disorder (NMOSD) and MOG-associated diseases (MOGAD), but no consensus exists on the optimal dose and frequency of treatment administration. The aim of our study was to evaluate the effect of a Rituximab (RTX) personalized treatment approach based on CD27-positive B-cell monitoring on efficacy, safety, and infusion rates. METHODS: This is a retrospective, uncontrolled, single-center study including patients with NMOSD and MOGAD treated with RTX at a tertiary multiple sclerosis center at the San Luigi University Hospital, Orbassano, Italy. All the patients were treated with RTX induction, followed by maintenance infusion at the dosage of 1000 mg according to cell repopulation: initially according to total CD19-positive B-cell monitoring (> 0.1% of lymphocytes), and subsequently according to CD27-positive B-cell repopulation (> 0.05% of lymphocytes for the first 2 years, and subsequently > 0.1%). NMOSD and MOGAD activity was assessed as clinical or MRI activity. All patients were screened of the occurrence of severe adverse events (AEs). RESULTS: A total of 19 patients were included in the analysis. Median follow-up was 7.64 years (range 3.09-16.25). The annualized relapse rate (ARR) 1 year before RTX start was 2.37 [Standard deviation (SD), 1.34] and decreased to 0.08 (SD 0.11) in the subsequent years after RTX initiation. ARR did not differ before and after start of CD27 monitoring. Median inter-dose time was 8.80 (range 5.78-14.23) before CD27 monitoring and 15.93 months (range 8.56-35.37) after CD27 monitoring (p < 0.001). We observed no AEs. CONCLUSION: Our findings suggest that in our cohort CD27-positive B-cell-based RTX reinfusion regimen was able to reduce the number of RTX reinfusions relative to CD19-positive B-cell monitoring, with comparable efficacy and safety profile. In order to achieve an even more individualized and effective treatment, the FCGR3A genetic polymorphisms could be evaluated when assessing RTX efficacy.
 BACKGROUND: Immune checkpoint inhibitor (ICI) therapies may cause unpredictable and potentially severe autoimmune toxicities termed immune-related adverse events (irAEs). Because T cells mediate ICI effects, T cell profiling may provide insight into the risk of irAEs. Here we evaluate a novel metric-the T-cell tolerant fraction-as a predictor of future irAEs. METHODS: We examined T-cell receptor beta (TRB) locus sequencing from baseline pretreatment samples from an institutional registry and previously published studies. For each patient, we used TRB sequences to calculate the T-cell tolerant fraction, which was then assessed as a predictor of future irAEs (classified as Common Terminology Criteria for Adverse Event grade 0-1 vs grade ≥2). We then compared the tolerant fraction to TRB clonality and diversity. Finally, the tolerant fraction was assessed on (1) T cells enriched against napsin A, a potential autoantigen of irAEs; (2) thymic versus peripheral blood T cells; and (3) TRBs specific for various infections and autoimmune diseases. RESULTS: A total of 77 patients with cancer (22 from an institutional registry and 55 from published studies) receiving ICI therapy (43 CTLA4, 19 PD1/PDL1, 15 combination CTLA4+PD1/PDL1) were included in the study. The tolerant fraction was significantly lower in cases with clinically significant irAEs (p<0.001) and had an area under the receiver operating curve (AUC) of 0.79. The tolerant fraction was lower for each ICI treatment category, reaching statistical significance for CTLA4 (p<0.001) and demonstrating non-significant trends for PD1/PDL1 (p=0.21) and combination ICI (p=0.18). The tolerant fraction for T cells enriched against napsin A was lower than other samples. The tolerant fraction was also lower in thymic versus peripheral blood samples, and lower in some (multiple sclerosis) but not other (type 1 diabetes) autoimmune diseases. In our study cohort, TRB clonality had an AUC of 0.62, and TRB diversity had an AUC of 0.60 for predicting irAEs. CONCLUSIONS: Among patients receiving ICI, the baseline T-cell tolerant fraction may serve as a predictor of clinically significant irAEs.
 PURPOSE: Observational studies have reported that autoimmune diseases are closely related to sarcopenia, but the causalities of autoimmune diseases with sarcopenia have not been established. We conducted this Mendelian randomization (MR) study to reveal the causal associations of overall autoimmune disease and five common autoimmune diseases with sarcopenia-related traits. METHODS: The publicly available summary-level data of autoimmune diseases and three sarcopenia-related traits were used for analysis. The causal effects of autoimmune diseases on sarcopenia-related traits were first identified in discovery samples using the inverse-variance-weighted method as the primary method, and the robustness of results was examined by additional sensitivity analyses. Replication MR analyses were then conducted using replication samples of five autoimmune diseases. Finally, the possibility of reverse causation was assessed by reverse MR analyses. RESULTS: In both the discovery and replication samples, we identified potential causal effects of rheumatoid arthritis (RA) on appendicular lean mass (ALM) and low grip strength (OR = 0.979, 95% CI: 0.964-0.995 for ALM; OR = 1.042, 95% CI: 1.013-1.072 for low grip strength), but not on walking pace. We also found that inflammatory bowel disease (IBD) and type 1 diabetes (T1D) were only causally negatively associated with ALM in the discovery stage (OR = 0.986, 95% CI: 0.974-0.999 for IBD; OR = 0.987, 95% CI: 0.975-0.999 for T1D), whereas systemic lupus erythematosus, multiple sclerosis, and overall autoimmune disease were not associated with any of the three sarcopenia-related traits. Additionally, reverse MR analysis only found an association between walking pace and overall autoimmune disease, but this association did not remain in the weighted-median method. CONCLUSION: This study demonstrates that RA is causally associated with low grip strength and reduced ALM, and that IBD and T1D may be causally negatively related to ALM.
 Changes in myelination are a cardinal feature of brain development and the pathophysiology of several central nervous system diseases, including multiple sclerosis and dementias. Advanced magnetic resonance imaging (MRI) methods have been developed to probe myelin content through the measurement of myelin water fraction (MWF). However, the prolonged data acquisition and post-processing times of current MWF mapping methods pose substantial hurdles to their clinical implementation. Recently, fast steady-state MRI sequences have been implemented to produce high-spatial resolution whole-brain MWF mapping within ∼20 min. Despite the subsequent significant advances in the inversion algorithm to derive MWF maps from steady-state MRI, the high-dimensional nature of such inversion does not permit further reduction of the acquisition time by data under-sampling. In this work, we present an unprecedented reduction in the computation (∼30 s) and the acquisition time (∼7 min) required for whole-brain high-resolution MWF mapping through a new Neural Network (NN)-based approach, named NN-Relaxometry of Extremely Under-SamplEd Data (NN-REUSED). Our analyses demonstrate virtually similar accuracy and precision in derived MWF values using NN-REUSED compared to results derived from the fully sampled reference method. The reduction in the acquisition and computation times represents a breakthrough toward clinically practical MWF mapping.
 BACKGROUND: Spasticity is a pathophysiological outcome of impaired muscle motor activity, primarily the muscle tone. Muscle tone problems are signs of several neurological conditions, such as multiple sclerosis, movement disorders, spine damage, stroke, and traumatic brain injury. Antispasticity therapeutics belong to a class of treatments that restore motor function and muscle tone. There are several routes of therapeutic administration of antispastic medications; among them, the oral drug delivery system plays a significant role. OBJECTIVE: The purpose of the study was to present a complete synthesis of the scientific evidence on the safety and efficacy of antispasticity medicines used orally for the management of nonprogressive neurological disorders. MATERIALS AND METHODS: In order to carry out a comprehensive meta-analysis, the most pertinent scientific studies on the use of oral antispasticity medications to treat non-progressive neurological illnesses were identified. A search was conducted across a number of databases, including SciELO, Cochrane Central Register of Controlled Trials (CENTRAL), and PubMed. MedCalc statistical software was used to perform a meta-analysis in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards for odds ratio across the studies, relative risk, and risk factor analysis. RESULTS: In the present study, a total of 252 original records were retrieved from different predefined databases on oral antispasticity drugs and their association with non-progressive neurological disorders. After several screening steps, 12 studies were found to be eligible for meta-analysis. These studies represented different antispasticity therapeutics that were administered via the oral route. Based on the meta-analysis, oral antispasticity drugs were found to be moderately effective (P < 0.001). CONCLUSION: The findings of the meta-analysis showed that the interventions of tizanidine, diazepam, dantrolene, baclofen, and gabapentin were more effective in tackling spasticity than the control. Therefore, in the treatment of non-progressive neurological diseases, oral antispasticity medications are only modestly effective.
 BACKGROUND: Intrathecal baclofen therapy can substantially improve symptoms in most patients with severe spasticity due to traumatic spinal cord injury, multiple sclerosis, or cerebral paresis. To the best of our knowledge, decompression surgeries at the intrathecal catheter insertion site in patients with a preexisting intrathecal pump for drug delivery have not been reported. CASE PRESENTATION: We report the case of a 61-year-old Japanese man with lumbar spinal stenosis who underwent intrathecal baclofen therapy. We performed decompression for lumbar spinal stenosis at the intrathecal catheter insertion site during intrathecal baclofen therapy. The yellow ligament was removed by partial resection of the lamina under a microscope to avoid damage to the intrathecal catheter. The dura mater was distended. No obvious cerebrospinal fluid leakage was observed. Postoperatively, lumbar spinal stenosis symptoms improved, and spasticity remained well controlled with intrathecal baclofen therapy. CONCLUSIONS: This is the first reported case of lumbar spinal stenosis decompression at an intrathecal catheter insertion site during intrathecal baclofen therapy. Preoperative preparation is necessary, as the intrathecal catheter may be replaced during surgery. We performed surgery without removing or replacing the intrathecal catheter, taking care not to damage the spinal cord by migrating the intrathecal catheter.
 BACKGROUND: Over the past few years, mesenchymal stromal cells (MSCs) have attracted a great deal of scientific attention owing to their promising results in the treatment of incurable diseases. However, there are several concerns about their possible side effects after direct cell transplantation, including host immune response, time-consuming cell culture procedures, and the dependence of cell quality on the donor, which limit the application of MSCs in clinical trials. On the other hand, it is well accepted that the beneficial effects of MSCs are mediated by secretome rather than cell replacement. MSC secretome refers to a variety of bioactive molecules involved in different biological processes, specifically neuro-regeneration. MAIN BODY: Due to the limited ability of the central nervous system to compensate for neuronal loss and relieve disease progress, mesenchymal stem cell products may be used as a potential cure for central nervous system disorders. In the present study, the therapeutic effects of MSC secretome were reviewed and discussed the possible mechanisms in the three most prevalent central nervous system disorders, namely Alzheimer's disease, multiple sclerosis, and Parkinson's disease. The current work aimed to help discover new medicine for the mentioned complications. CONCLUSION: The use of MSC-derived secretomes in the treatment of the mentioned diseases has encouraging results, so it can be considered as a treatment option for which no treatment has been introduced so far.
 INTRODUCTION: This study aimed to assess the predictive role of blood markers in neuromyelitis optica spectrum disorders (NMOSD). METHODS: Data from patients with NMOSD, multiple sclerosis (MS), and healthy individuals were retrospectively collected in a 1:1:1 ratio. The expanded disability status scale (EDSS) score was used to assess the severity of the NMOSD upon admission. Receiver operating characteristic (ROC) curve analysis was used to distinguish NMOSD patients from healthy individuals, and active NMOSD from remitting NMOSD patients. Binary logistic regression analysis was used to evaluate risk factors that could be used to predict disease recurrence. Finally, Wilcoxon signed-rank test or matched-sample t-test was used to analyze the differences between the indicators in the remission and active phases in the same NMOSD patient. RESULTS: Among the 54 NMOSD patients, neutrophil count, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) (platelet × NLR) were significantly higher than those of MS patients and healthy individuals and positively correlated with the EDSS score of NMOSD patients at admission. PLR can be used to simultaneously distinguish between NMOSD patients in the active and remission phase. Eleven (20.4%) of the 54 patients had recurrence within 12 months. We found that monocyte-to-lymphocyte ratio (MLR) (AUC = 0.76, cut-off value = 0.34) could effectively predict NMOSD recurrence. Binary logistic regression analysis showed that a higher MLR at first admission was the only risk factor for recurrence (p = 0.027; OR = 1.173; 95% CI = 1.018-1.351). In patients in the relapsing phase, no significant changes in monocyte and lymphocyte count was observed from the first admission, whereas patients in remission had significantly higher levels than when they were first admitted. CONCLUSION: High PLR is a characteristic marker of active NMOSD, while high MLR is a risk factor for disease recurrence. These inexpensive indicators should be widely used in the diagnosis, prognosis, and judgment of treatment efficacy in NMOSD.
 Introduction: Dimethyl fumarate (DMF) is FDA-approved for use in patients with relapsing multiple sclerosis, and it processes neuroprotection in several experimental settings; however, its impact on combating Huntington's disease (HD) remains elusive. This study aimed to explore the role of DMF post-treatment on HD mediated endoplasmic reticulum (ER) stress response in a selective striatal degeneration HD model. Methods: Rats, exposed to 3-nitropropionic acid, were either left untreated or post-treated with DMF for 14 days. Results and Discussion: DMF reduced locomotion deficits in both the open field and beam walk paradigms, boosted the striatal dopamine (DA) content, improved its architecture at the microscopic level, and hindered astrogliosis. Mechanistically, DMF limited the activation of two of the ER stress arms in the striatum by reducing p-IRE1α, p-JNK, and p-PERK protein expressions besides the CHOP/GADD153 content. Downstream from both ER stress arms' suppression, DMF inhibited the intrinsic apoptotic pathway, as shown by the decrease in Bax and active caspase-3 while raising Bcl-2. DMF also decreased oxidative stress markers indicated by a decline in both reactive oxygen species and malondialdehyde while boosting glutathione. Meanwhile, it enhanced p-AKT to activate /phosphorylate mTOR and stimulate the CREB/BDNF/TrkB trajectory, which, in a positive feedforward loop, activates AKT again. DMF also downregulated the expression of miRNA-634, which negatively regulates AKT, to foster survival kinase activation. Conclusion: This study features a focal novel point on the DMF therapeutic ability to reduce HD motor manifestations via its ability to enhance DA and suppress the IRE1α/JNK and PERK/CHOP/GADD153 hubs to inhibit the mitochondrial apoptotic pathway through activating the AKT/mTOR and BDNF/TrkB/AKT/CREB signaling pathways and abating miRNA-634 and oxidative stress.
 Microinflammation enhances the permeability of specific blood vessel sites through an elevation of local inflammatory mediators, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α. By a two-dimensional immunohistochemistry analysis of tissue sections from mice with experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), we previously showed that pathogenic immune cells, including CD4(+) T cells, specifically accumulate and cause microinflammation at the dorsal vessels of the fifth lumbar cord (L5), resulting in the onset of disease. However, usual pathological analyses by using immunohistochemistry on sections are not effective at identifying the microinflammation sites in organs. Here, we developed a new three-dimensional visualization method of microinflammation using luminescent gold nanoclusters (AuNCs) and the clear, unobstructed brain/body imaging cocktails and computational analysis (CUBIC) tissue-clearing method. Our protocol is based on the detection of leaked AuNCs from the blood vessels due to an enhanced vascular permeability caused by the microinflammation. When we injected ultrasmall coordinated Au(13) nanoclusters intravenously (i.v.) to EAE mice, and then subjected the spinal cords to tissue clearing, we detected Au signals leaked from the blood vessels at L5 by light sheet microscopy, which enabled the visualization of complex tissue structures at the whole organ level, consistent with our previous report that microinflammation occurs specifically at this site. Our method will be useful to specify and track the stepwise development of microinflammation in whole organs that is triggered by the recruitment of pathogenic immune cells at specific blood vessels in various inflammatory diseases.
 Bidirectional communication between central nervous system (CNS) and intestine is mediated by nerve, endocrine, immune and other pathways in gut-brain axis. Many diseases of CNS disturb the homeostasis of intestine and gut microbiota. Similarly, the dysbiosis of intestinal and gut microbiota also promotes the progression and deterioration of CNS diseases. IL-23/IL-17 axis is an important inflammatory axis which is widely involved in CNS diseases such as experimental autoimmune encephalomyelitis (EAE), multiple sclerosis (MS), and ischemic stroke (IS). Attributing to the long anatomically distances between ischemic brain and gut, previous studies on IL-23/IL-17 axis in IS are rarely focused on intestinal tissues. However, recent studies have found that IL-17(+)T cells in CNS mainly originate from intestine. The activation and migration of IL-17(+)T cells to CNS is likely to be affected by the altered intestinal homeostasis. These studies promoted the attention of IL-23/IL-17 axis and gut-brain axis. IS is difficult to treat because of its extremely complex pathological mechanism. This review mainly discusses the relationship between IL-23/IL-17 axis and IS from the perspective of gut-brain axis. By analyzing the immune pathways in gut-brain axis, the activation of IL-23/IL-17 axis, the roles of IL-23/IL-17 axis in gut, CNS and other systems after stoke, this review is expected to provide new enlightenments for the treatment strategies of IS. This article is part of the Special Issue on "Microbiome & the Brain: Mechanisms & Maladies".
 OBJECTIVE: The study aimed to assess the prevalence, clinical characteristics, and therapeutic outcomes of the central nervous system (CNS) demyelinating disease in a large cohort of primary Sjögren's syndrome (pSS). METHODS: This is an explorative cross-sectional study of patients with pSS seen in the departments of rheumatology, otorhinolaryngology, or neurology of a tertiary university center between January 2015 and September 2021. RESULTS: In a cohort of 194 pSS patients, 22 patients had a CNS manifestation. In this CNS group, 19 patients had a lesion pattern suggestive of demyelination. While there were no obvious differences in the patients' epidemiological disposition or rate of other extraglandular manifestations, the CNS group differed from the remaining patients with pSS by having less glandular manifestations but a higher seroprevalence for anti-SSA/Ro antibodies. Notably, patients with CNS manifestations were often diagnosed with multiple sclerosis (MS) and treated as such, although age and disease course were atypical of MS. Many first-line MS agents were ineffective in these "MS look-alikes"; however, the disease course was benign with B-cell-depleting agents. CONCLUSION: Neurological symptoms of pSS are common and clinically manifest mainly as myelitis or optic neuritis. Notably, in the CNS, the pSS phenotype can overlap with MS. The prevailing disease is crucial since it has a major impact on the long-term clinical outcome and the choice of disease-modifying agents. Although our observations neither confirm pSS as a more appropriate diagnosis nor rule out simple comorbidity, physicians should consider pSS in the extended diagnostic workup of CNS autoimmune diseases.
 SARS-CoV-2 virus has attracted a lot of attention globally due to the autoimmune and inflammatory processes that were observed during the development of Covid-19 disease. Excessive activation of immune response and triggering of autoantibodies synthesis as well as an excessive synthesis of inflammatory cytokines and the onset of cytokine storm has a vital role in the disease outcome and the occurring autoimmune complications. This scenario is reminiscent of infiltration of lymphocytes and monocytes in specific organs and the increased production of autoantibodies and chemoattractants noted in other inflammatory and autoimmune diseases. The main goal of this study is to investigate the complex inflammatory processes that occur in Covid-19 disease and to find similarities with other inflammatory diseases such as multiple sclerosis (MS), acute respiratory distress syndrome (ARDS), rheumatoid arthritis (RA) and Kawasaki syndrome to advance existing diagnostic and therapeutic protocols. The therapy with Interferon-gamma (IFN-γ) and the use of S1P receptor modulators showed promising results. However, there are many unknowns about these mechanisms and possible novel therapies. Therefore, the inflammation and autoimmunity triggered by Covid-19 should be further investigated to improve existing diagnostic procedures and therapeutic protocols for Covid-19.
 Promoting myelination capacity of endogenous oligodendrocyte precursor cells (OPCs) is a promising therapeutic approach for CNS demyelinating disorders such as Multiple Sclerosis (MS). To aid in the discovery of myelination-promoting compounds, we generated a genome-engineered human pluripotent stem cell (hPSC) line that consists of three reporters: identification-and-purification tag, GFP, and secreted-NanoLuc, driven by the endogenous PDGFRA, PLP1, and MBP genes, respectively. Using this cell line, we established a high-throughput drug screening platform and performed a small-molecule screen, which identified at least two myelination-promoting small-molecule (Ro1138452 and SR2211) that target prostacyclin (IP) receptor and retinoic acid receptor-related orphan receptor γ (RORγ), respectively. Single-cell-transcriptomic analysis of differentiating OPCs treated with these molecules further confirmed that they promote oligodendrocyte differentiation and revealed several pathways that are potentially modulated by them. The molecules and their target pathways provide promising targets for the possible development of remyelination-based therapy for MS and other demyelinating disorders.
 Objective: To identify and summarize data that describe the impact of effectively treating major depressive disorder (MDD) on the severity or risk of serious comorbidities. Data Sources: MEDLINE, Embase, PsycINFO, Cochrane Database of Systematic Reviews, and several congresses were searched. Searches included terms related to MDD, randomized controlled trials (RCTs), and physical comorbidities and were restricted to English-language publications. Searches were conducted in November 2019 for the previous 2 years for conference proceedings; no date restriction was applied to the database searches. Study Selection: Included studies were RCTs or meta-analyses that assessed depression therapies. Studies were required to report a statistically significant improvement in depression scores as well as the concurrent impact on comorbidities. A total of 1,997 articles were initially identified for screening. Data Extraction: Two investigators extracted data and assessed study quality. Results: A total of 30 studies, including 24 RCTs (N = 6,333) and 6 meta/pooled analyses of RCTs, were included. Findings in several comorbidity categories were mixed; for example, in half (4 of 8) of the identified studies in people with cardiovascular disease and depression, individuals who received treatment leading to reduced depressive symptoms compared with a control arm also had a significantly decreased incidence of cardiovascular events or significantly improved cardiac disease symptom/severity scores compared with controls. Significant improvements in comorbid disease severity observed alongside improvements in depressive symptoms were also noted in studies of comorbid Parkinson's disease, multiple sclerosis, chronic pain and fibromyalgia, and chronic obstructive pulmonary disease. Conclusions: Effective treatment of MDD may lead to a reduction in the severity of certain serious comorbidities. These results highlight the importance of appropriate and timely treatment of MDD.
 Over the last century, there has been a gradual but sustained increase in life expectancy globally. A consequence of increased life expectancy is an associated rise in the prevalence of agerelated chronic debilitating neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease, Huntington's disease, and multiple sclerosis. These disorders, which are generally characterised by the loss of motor/sensory neurons and cognitive decline, have continued to confound researchers who are working tirelessly to define their pathogenetic mechanisms and develop effective therapies. In the last few years, there has been increasing evidence of the existence of a relationship between energy metabolism and neurodegeneration, with reports that type 2 diabetes mellitus increases the risk of AD. Evidence from preclinical and epidemiologic studies has associated dysmetabolism and dysmetabolic syndromes with the development of neurodegenerative changes. More recently, diabetes mellitus and energy dysmetabolism have been linked to the aetiopathogenesis of AD. Moreover, metabolic hormones, including ghrelin, leptin, insulin, and insulin-like growth factor (IGF)-1, have been reported to play key roles in the regulation of neuronal injury and loss in neurodegenerative diseases like AD. In this narrative review, we examine the current scientific evidence regarding the role of dysmetabolism (including diabetes mellitus and metabolic syndrome) in AD and how it impacts disease progression and the development of novel therapies in AD.
 The effectiveness of cerebellar repetitive transcranial magnetic stimulation (rTMS) on motor dysfunction in patients with neurological disorders has received increasing attention because of its potential for neuromodulation. However, studies on the neuromodulatory effects, parameters, and safety of rTMS implementation in the cerebellum to alleviate motor dysfunction are limited. This systematic review aimed to evaluate the effectiveness and safety of cerebellar rTMS treatment for motor dysfunction caused by neurological disorders and to review popular stimulation parameters. Five electronic databases-Medline, Web of Science, Scopus, Cochrane Library, and Embase-were searched for relevant research published from inception to July 2022. All randomized controlled trials (RCTs) that reported the effects of cerebellar rTMS combined with behavioral rating scales on motor dysfunction were eligible for enrollment. Additionally, reference lists of the enrolled studies were manually checked. Among 1156 articles screened, 21 RCTs with 666 subjects were included. rTMS conducted on the cerebellum showed an improvement in stroke (spasticity, balance, and gait), cervical dystonia, Parkinson's disease (tremor), cerebellar ataxia, and essential tremor but not in multiple sclerosis. The 8-shaped coil with a diameter of 70 mm was determined as the most common therapeutic choice. None of the studies reported severe adverse events except mild side effects in three. Therefore, rTMS appears to be a promising and safe technique for the treatment of motor dysfunction, targeting the cerebellum to induce motor behavioral improvement. Further rigorous RCTs, including more samples and longer follow-up periods, are required to precisely explore the effective stimulation parameters and possible mechanisms.
 The human receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is a critical necroptosis regulator implicated in cancer, psoriasis, ulcerative colitis, rheumatoid arthritis, Alzheimer's disease, and multiple sclerosis. Currently, there are no specific RIPK1 antagonists in clinical practice. In this study, we took a target-based computational approach to identify blood-brain-barrier-permeable potent RIPK1 ligands with novel chemotypes. Using molecular docking, we virtually screened the Marine Natural Products (MNP) library of 14,492 small molecules. Initial 18 hits were subjected to detailed ADMET profiling for bioavailability, brain penetration, druglikeness, and toxicities and eventually yielded 548773-66-6 as the best ligand. RIPK1 548773-66-6 binding was validated through duplicated molecular dynamics (MD) simulations where the co-crystallized ligand L8D served as a reference. Trajectory analysis indicated negligible Root-Mean-Square-Deviations (RMSDs) of the best ligand 548773-66-6 relative to the protein backbone: 0.156 ± 0.043 nm and 0.296 ± 0.044 nm (mean ± standard deviations) in two individual simulations. Visual inspection confirmed that 548773-66-6 occupied the RIPK1 ligand-binding pocket associated with the kinase activation loop. Further computations demonstrated consistent hydrogen bond interactions of the ligand with the residue ASP156. Binding free energy estimation also supported stable interactions of 548773-66-6 and RIPK1. Together, our in silico analysis predicted 548773-66-6 as a novel ligand for RIPK1. Therefore, 548773-66-6 could be a viable lead for inhibiting necroptosis in central nervous system inflammatory disorders.Communicated by Ramaswamy H. Sarma.
 The Human Leukocyte Antigen (HLA) locus associates with a variety of complex diseases, particularly autoimmune and inflammatory conditions. The HLA-DR15 haplotype, for example, confers the major risk for developing Multiple Sclerosis in Caucasians, pinpointing an important role in the etiology of this chronic inflammatory disease of the central nervous system. In addition to the protein-coding variants that shape the functional HLA-antigen-T cell interaction, recent studies suggest that the levels of HLA molecule expression, that are epigenetically controlled, also play a role in disease development. However, deciphering the exact molecular mechanisms of the HLA association has been hampered by the tremendous genetic complexity of the locus and a lack of robust approaches to investigate it. Here, we developed a method to specifically enrich the genomic DNA from the HLA class II locus (chr6:32,426,802-34,167,129) and proximal promoters of 2,157 immune-relevant genes, utilizing the Agilent RNA-based SureSelect Methyl-Seq Capture related method, followed by sequencing to detect genetic and epigenetic variation. We demonstrated successful simultaneous detection of the genetic variation and quantification of DNA methylation levels in HLA locus. Moreover, by the detection of differentially methylated positions in promoters of immune-related genes, we identified relevant pathways following stimulation of cells. Taken together, we present a method that can be utilized to study the interplay between genetic variance and epigenetic regulation in the HLA class II region, potentially, in a wide disease context.
 BACKGROUND AND OBJECTIVES: A hematopoietic stem cell transplant (HSCT) includes a conditioning regimen which may cause unwanted metabolic changes. We analyzed the changes in electrolytes, glucose, urea, and glomerular filtration rate in patients with multiple sclerosis (MS) who underwent an autologous HSCT employing the "Mexican method." PATIENTS AND METHODS: Serum and urinary electrolytes, blood glucose, creatinine, uric acid, and estimated glomerular filtration rate (eGFR) were prospectively assessed on days -11, -9, and 0 in a group of 75 patients with MS receiving an autologous HSCT employing the "Mexican method," which includes high doses of both cyclophosphamide (Cy, 200 mg/kg) and rituximab (1000 mg). RESULTS: The median age of the patients was 46 years, with a range of 20-65. Baseline data were defined at day -11 of the HSCT. There were significant changes in serum and urinary electrolytes, which diminished substantially after the delivery of high-dose Cy; 12 patients (16%) developed hyponatremia and 2 had hyponatremia-induced seizures, which resulted in hospital admissions. A comparison of baseline blood metabolites with those obtained after the full Cy dosage (day 0) revealed a significant increase in blood glucose and uric acid levels with an associated decrease in serum calcium, sodium, and potassium levels. The salient findings were drug-induced hyponatremia and hyperglycemia. CONCLUSION: Significant changes in serum electrolytes, blood glucose, creatinine, uric acid, and estimated glomerular filtration rate (eGFR) were observed in patients given autologous HSCT for MS employing high-dose Cy. Some of these changes may have clinical consequences, mainly those derived from iatrogenic hyponatremia. No evidence of damage to renal function was observed at day 0.
 Secondary demyelinating diseases comprise a wide spectrum group of pathological conditions and may either be attributed to a disorder primarily affecting the neurons or axons, followed by demyelination, or to an underlying condition leading to secondary damage of the myelin sheath. In the elderly, primary demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis, are relatively uncommon. However, secondary causes of CNS demyelination may often occur and in this case, extensive diagnostic workup is usually needed. Infectious, postinfectious, or postvaccinal demyelination may be observed, attributed to age-related alterations of the immune system in this population. Osmotic disturbances and nutritional deficiencies, more commonly observed in the elderly, may lead to conditions such as pontine/extrapontine myelinolysis, Wernicke encephalopathy, and demyelination of the posterior columns of the spinal cord. The prevalence of malignancies is higher in the elderly, sometimes leading to radiation-induced, immunotherapy-related, or paraneoplastic CNS demyelination. This review intends to aid clinical neurologists in broadening their diagnostic approach to secondary CNS demyelinating diseases in the elderly. Common clinical conditions leading to secondary demyelination and their clinical manifestations are summarized here, while the current knowledge of the underlying pathophysiological mechanisms is additionally presented.
 Soma and neurite density image (SANDI) is an advanced diffusion magnetic resonance imaging biophysical signal model devised to probe in vivo microstructural information in the gray matter (GM). This model requires acquisitions that include b values that are at least six times higher than those used in clinical practice. Such high b values are required to disentangle the signal contribution of water diffusing in soma from that diffusing in neurites and extracellular space, while keeping the diffusion time as short as possible to minimize potential bias due to water exchange. These requirements have limited the use of SANDI only to preclinical or cutting-edge human scanners. Here, we investigate the potential impact of neglecting water exchange in the SANDI model and present a 10-min acquisition protocol that enables to characterize both GM and white matter (WM) on 3 T scanners. We implemented analytical simulations to (i) evaluate the stability of the fitting of SANDI parameters when diminishing the number of shells; (ii) estimate the bias due to potential exchange between neurites and extracellular space in such reduced acquisition scheme, comparing it with the bias due to experimental noise. Then, we demonstrated the feasibility and assessed the repeatability and reproducibility of our approach by computing microstructural metrics of SANDI with AMICO toolbox and other state-of-the-art models on five healthy subjects. Finally, we applied our protocol to five multiple sclerosis patients. Results suggest that SANDI is a practical method to characterize WM and GM tissues in vivo on performant clinical scanners.
 Shikonin, the primary active compound found in the rhizome of the traditional Chinese medicinal herb known as "ZiCao", exhibits a diverse range of pharmacological effects. This drug has a wide range of uses, including as an anti-inflammatory, antioxidant, and anti-cancer agent. It is also effective in promoting wound healing and treating autoimmune diseases such as multiple sclerosis, diabetes, asthma, systemic lupus erythematosus, inflammatory bowel disease, psoriasis, and rheumatoid arthritis. Although shikonin has a wide range of applications, its mechanisms are still not fully understood. This review article provides a comprehensive overview of the recent advancements in the use of shikonin for the treatment of immune-related diseases. The article also delves into the anti-inflammatory and immunoregulatory mechanisms of shikonin and offers insights into the inflammation and immunopathogenesis of related diseases. Overall, this article serves as a valuable resource for researchers and clinicians working in this field. These findings not only provide significant new information on the effects and mechanisms of shikonin but also establish a foundation for the development of clinical applications in treating autoimmune diseases.
 The therapeutic success and widespread approval of genetically engineered T cells for a variety of hematologic malignancies spurred the development of synthetic cell-based immunotherapies for CNS lymphoma, primary brain tumors, and a growing spectrum of nononcologic disease conditions of the nervous system. Chimeric antigen receptor effector T cells bear the potential to deplete target cells with higher efficacy, better tissue penetration, and greater depth than antibody-based cell depletion therapies. In multiple sclerosis and other autoimmune disorders, engineered T-cell therapies are being designed and currently tested in clinical trials for their safety and efficacy to eliminate pathogenic B-lineage cells. Chimeric autoantibody receptor T cells expressing a disease-relevant autoantigen as cell surface domains are designed to selectively deplete autoreactive B cells. Alternative to cell depletion, synthetic antigen-specific regulatory T cells can be engineered to locally restrain inflammation, support immune tolerance, or efficiently deliver neuroprotective factors in brain diseases in which current therapeutic options are very limited. In this article, we illustrate prospects and bottlenecks for the clinical development and implementation of engineered cellular immunotherapies in neurologic diseases.
 BACKGROUND: Non-invasive neuromodulation using translingual neurostimulation (TLNS) has been shown to advance rehabilitation outcomes, particularly when paired with physical therapy (PT). Together with motor gains, patient-reported observations of incidental improvements in cognitive function have been noted. Both studies in healthy individuals and case reports in clinical populations have linked TLNS to improvements in attention-related cognitive processes. We investigated if the use of combined TLNS/PT would translate to changes in objective neurophysiological cognitive measures in a real-world clinical sample of patients from two separate rehabilitation clinics. METHODS: Brain vital signs were derived from event-related potentials (ERPs), specifically auditory sensation (N100), basic attention (P300), and cognitive processing (N400). Additional analyses explored the attention-related N200 response given prior evidence of attention effects from TLNS/PT. The real-world patient sample included a diverse clinical group spanning from mild-to-moderate traumatic brain injury (TBI), stroke, Multiple Sclerosis (MS), Parkinson's Disease (PD), and other neurological conditions. Patient data were also acquired from a standard clinical measure of cognition for comparison. RESULTS: Results showed significant N100 variation between baseline and endpoint following TLNS/PT treatment, with further examination showing condition-specific significant improvements in attention processing (i.e., N100 and N200). Additionally, CogBAT composite scores increased significantly from baseline to endpoint. DISCUSSION: The current study highlighted real-world neuromodulation improvements in neurophysiological correlates of attention. Overall, the real-world findings support the concept of neuromodulation-related improvements extending beyond physical therapy to include potential attention benefits for cognitive rehabilitation.
 When stopping a closing door or catching an object, humans process the motion of inertial objects and apply reactive limb force over short period to interact with them. One way in which the visual system processes motion is through extraretinal signals associated with smooth pursuit eye movements (SPEMs). We conducted three experiments to investigate how SPEMs contribute to anticipatory and reactive hand force modulation when interacting with a virtual object moving in the horizontal plane. We hypothesized that SPEM signals are critical for timing motor responses, anticipatory control of hand force, and task performance. Participants held a robotic manipulandum and attempted to stop an approaching simulated object by applying a force impulse (area under force-time curve) that matched the object's virtual momentum upon contact. We manipulated the object's momentum by varying either its virtual mass or its speed under free gaze or constrained gaze conditions. We examined gaze variables, the timing of hand motor responses, anticipatory force control, and overall task performance. Our results show that when participants were fixated at a designated location instead of following objects with SPEM, anticipatory modulation of hand force before contact decreased. However, constraining gaze by asking participants to fixate did not seem to affect the timing of the motor response or the task performance. Together, these results suggest that SPEMs may be important for anticipatory control of hand force before contact and may also play a critical role in anticipatory stabilization of limb posture when humans interact with moving objects.NEW & NOTEWORTHY We show for the first time that smooth pursuit eye movements (SPEMs) play a role in the modulation of anticipatory control of hand force to stabilize posture against contact forces. SPEMs are critical for tracking moving objects, facilitate processing motion of moving objects, and are impacted during aging and in many neurological disorders, such as Alzheimer's disease and multiple sclerosis. These results provide a novel basis to probe how changes in SPEMs could contribute to deficient limb motor control in older adults and patients with neurological disorders.
 Neuro-imaging has given urologists a new tool to investigate the neural control of the lower urinary tract. Using functional magnetic resonance imaging (fMRI), it is now possible to understand which areas of the brain contribute to the proper function of the storage and voiding of the lower urinary tract. This field of research has evolved from simple anatomical descriptions to elucidating the complex micturition network. A keyword search of the Medline database was conducted by two reviewers for relevant studies from January 1, 2010, to August 2022. Of 2047 peer-reviewed articles, 49 are included in this review. In the last decade, a detailed understanding of the brain-bladder network has been described, elucidating a dedicated network, as well as activated areas in the brainstem, cerebellum, and cortex that share reproducible connectivity patterns. Research has shown that various urological diseases can lead to specific changes in this network and that therapies used by urologists to treat lower urinary tract symptoms (LUTS) are also able to modify neuronal activity. This represents a set of potential new therapeutic targets for the management of the lower urinary tract symptoms (LUTS). fMRI technology has made it possible to identify subgroups of responders to various treatments (biofeedback, anticholinergic, neuromodulation) and predict favourable outcomes. Lastly, this breakthrough understanding of neural control over bladder function has led to treatments that directly target brain regions of interest to improve LUTS. One such example is the use of non-invasive transcranial neuromodulation to improve voiding symptoms in individuals with multiple sclerosis.
 Macrophages play a crucial role in, the currently uncurable, chronic rejection of transplants. In rodent transplantation models, inhibition of the RhoA/Rock pathway disrupts actin-related functions of macrophages, preventing them from entering the graft, and reducing vessel occlusion, fibrosis, and chronic rejection. Among RhoA/Rock inhibitors that inhibit chronic rejection in mouse transplantation are Y27632, Fingolimod, and Rezurock. In a mouse model, Rezurok is more effective in preventing fibrosis and less effective in preventing vessel occlusion than Y27632 or Fingolimod. Fingolimod is FDA-approved for treating multiple sclerosis (MS) and Rezurock for chronic graft versus host disease (GVHD). Still, none had been tested for chronic rejection in humans. To explain the differences in the anti-chronic rejection properties of Y27632, Fingolimod, and Rezurock, we compared the transcriptome profile of mouse macrophages treated with these compounds separately. Treatment with Y27632 or Fingolimod downregulated GTPase and actin pathways involved in cell migration. Rezurock downregulated genes related to fibrosis, such as PTX3, CCR2, CCL2, cell cycle, DNA replication, adaptive immune response, and organelle assembly, while Fingolimod also specifically downregulated NOTCH1 at mRNA . The result of this study not only uncovers which pathways are shared or specific for these drugs but will help in the development of macrophage pathway-targeted therapies in human transplantation, MS, and GVHD. Because macrophages are the major players in immune response, tissue regeneration, renewal, and homeostasis, and development of many diseases, including cancer, the data compiled here will help in designing novel or improved therapies in many clinical applications.
 In the last few decades, there has been a growing interest in Bruton's tyrosine kinase (BTK) and the compounds that target it. BTK is a downstream mediator of the B-cell receptor (BCR) signaling pathway and affects B-cell proliferation and differentiation. Evidence demonstrating the expression of BTK on the majority of hematological cells has led to the hypothesis that BTK inhibitors (BTKIs) such as ibrutinib can be an effective treatment for leukemias and lymphomas. However, a growing body of experimental and clinical data has demonstrated the significance of BTK, not just in B-cell malignancies, but also in solid tumors, such as breast, ovarian, colorectal, and prostate cancers. In addition, enhanced BTK activity is correlated with autoimmune disease. This gave rise to the hypothesis that BTK inhibitors can be beneficial in the therapy of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), multiple sclerosis (MS), Sjögren's syndrome (SS), allergies, and asthma. In this review article, we summarize the most recent findings regarding this kinase as well as the most advanced BTK inhibitors that have been developed to date and their clinical applications mainly in cancer and chronic inflammatory disease patients.
 Background: The pharmacological activity of dimethyl fumarate (DMF) in treating psoriasis and multiple sclerosis (MS) is not fully understood. DMF is hydrolysed to monomethyl fumarate (MMF) in vivo, which is believed to account for the therapeutic effects of DMF. However, previous studies have provided evidence that DMF also enters the circulation. Given that DMF is short-lived in the blood, whether DMF has a therapeutic impact is still unclear. Methods: Lipopolysaccharide (LPS)-mediated RAW264.7 cell activation was used as a model of inflammation to explore the anti-inflammatory effects of short-term DMF exposure in vitro. Whole blood LPS stimulation assay was applied to compare the anti-inflammatory effects of DMF and MMF in vivo. Griess assay was performed to examined nitrite release. The expression of pro-inflammatory cytokines and transcription factors were measured by quantitative PCR (qPCR), ELISA and Western blot. Depletion of intracellular glutathione (GSH) was evaluated by Ellman's assay. Luciferase reporter assays were performed to evaluate DMF effects on Nrf2-ARE pathway activation, promoter activity of Nfkbiz and mRNA stability of Nfkbiz. Binding of STAT3 to the IκBζ promoter were examined using Chromatin immunoprecipitation (ChIP) assay. Results: Short-term exposure to DMF significantly inhibited the inflammatory response of RAW264.7 cells and suppressed LPS-induced IκBζ expression. Importantly, oral DMF but not oral MMF administration significantly inhibited IκBζ transcription in murine peripheral blood cells. We demonstrated that the expression of IκBζ is affected by the availability of intracellular GSH and regulated by the transcription factor Nrf2 and STAT3. DMF with strong electrophilicity can rapidly deplete intracellular GSH, activate the Nrf2-ARE pathway, and inhibit the binding of STAT3 to the IκBζ promoter, thereby suppressing IκBζ expression in macrophages. Conclusion: These results demonstrate the rapid anti-inflammatory effects of DMF in macrophages, providing evidence to support the direct anti-inflammatory activity of DMF.
 BACKGROUND: Trigeminal neuralgia (TN) is a neuropathic pain that affects one or more branches of the trigeminal nerve. Surgical options after pharmacological failure are Microvascular Decompression (MVD) or percutaneous procedures, which include Balloon Compression (PBC). This study aims to describe pain outcomes and complications after PBC and MVD procedures for patients with trigeminal neuralgia. METHODS: We performed a systematic review and meta-analysis on PubMed, EMBASE, LILACS, and Web of Science databases up to April 2022, following PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and meta-Analysis). Articles that separately describe pain outcome for MVD and PBC were included. MINORS tool was used for bias assessment. Meta-analysis results are presented in forest plot and funnel plot. RESULTS: 853 studies were assessed for screening, and 11 studies met the inclusion criteria for this review. A total of 1046 patients underwent PBC and 1324 underwent MVD. The subgroup analysis for patients without multiple sclerosis shows that MVD was associated with lower number of patients with pain than PBC, with an OR value of 0.54 (95 % CI 0.34-0.84). All other analyses evidenced a tendency for better outcomes after the MVD procedure, but with no statistically significant difference. CONCLUSION: Considering short and long pain relief, recurrence of pain and total complications for MVD and PBC, our study found that MVD is the best surgical option available for trigeminal neuralgia.
 Recently, it has been described that innate immune cells such as monocytes, macrophages, and natural killer cells can develop a non-specific immune response induced by different stimuli, including lipopolysaccharides, Mycobacterium bovis Bacillus Calmette-Guérin, and oxidized low-density lipoprotein. This non-specific immune response has been named "trained immunity," whose mechanism is essential for host defense and vaccine response, promoting better infection control. However, limited information about trained immunity in other non-infectious diseases, such as autoimmune illness, has been reported. The complexity of autoimmune pathology arises from dysfunctions in the innate and adaptive immune systems, triggering different clinical outcomes depending on the disease. Nevertheless, T and B cell function dysregulation is the most common characteristic associated with autoimmunity by promoting the escape from central and peripheral tolerance. Despite the importance of adaptative immunity to autoimmune diseases, the innate immune system also plays a prominent and understudied role in these pathologies. Accordingly, epigenetic and metabolic changes associated with innate immune cells that undergo a trained process are possible new therapeutic targets for autoimmune diseases. Even so, trained immunity can be beneficial or harmful in autoimmune diseases depending on several factors associated with the stimuli. Here, we reviewed the role of trained immunity over the innate immune system and the possible role of these changes in common autoimmune diseases, including Systemic Lupus Erythematosus, Rheumatoid Arthritis, Multiple Sclerosis, and Type 1 Diabetes.
 Dimethyl fumarate (DMF), a therapeutic agent for relapsing-remitting multiple sclerosis, has cytoprotective and antioxidant effects. Ferroptosis, a pathological cell death process, is recently shown to play a vital part in ischemia-reperfusion injury (IRI). This study aimed to unveil the suppressive role of DMF on ferroptosis in liver IRI. The anti-ferroptosis effect of DMF on hepatic IRI was investigated using a liver IRI mouse model and a hypoxia-reoxygenation injury (HRI) model in alpha mouse liver (AML12) cells. Serum transaminase concentrations reflected liver function. Hematoxylin and eosin staining was used to assess liver damage. Cell viability was evaluated utilizing the CCK-8 assay. Malondialdehyde (MDA), the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, and BODIPY 581/591C11 were measured to estimate the injury caused by lipid peroxidation. Western blotting and real-time polymerase chain reaction (RT-PCR) were performed to explore the underlying molecular mechanisms. We demonstrated the anti-ferroptosis effects of DMF both in vivo and in vitro. DMF treatment ameliorated hepatic IRI. KEGG enrichment analysis and transmission electron microscopy revealed a close relationship between ferroptosis and liver IRI. Furthermore, DMF protected against HRI by inhibiting ferroptosis via activating the nuclear factor E2-related factor 2 (NRF2) pathway. Interestingly, NRF2 knockdown notably decreased the expression of SLC7A11 and HO-1 and blocked the anti-ferroptosis effects of DMF. DMF inhibits ferroptosis by activating the NRF2/SLC7A11/HO-1 axis and exerts a protective effect against hepatic IRI.
 PURPOSE: This retrospective study investigates oral health and oral care in patients with neurodegenerative and cerebrovascular diseases (CVDs) treated in a dental facility for people with disabilities. METHODS: Oral health indices decayed, missing, and filled teeth (DMFT), periodontal screening index (PSI), treatment spectrum, and oral hygiene were evaluated in 152 patients with multiple sclerosis, Parkinson's disease, dementia, and CVD and 30 controls. Regression analyses identified group differences and influencing factors on DMFT. RESULTS: Patients with neurodegenerative or CVD had a significantly higher DMFT (21.2 ± 5.8 vs. 18.3 ± 5.9), more decayed teeth (4.3 ± 4.8 vs. 1 ± 1.9), fewer filled teeth (7.9 ± 5.5 vs. 11 ± 5.6), and a higher number of surgical (39.5% vs. 20%) treatments but significantly less conservative (49.3% vs. 73.3%) and prosthetic (15.1% vs. 56.7%) treatments than the control group (p< 0.05). The frequency of toothbrushing and the use of an electric toothbrush were related to lower DMFT in patients with neurodegenerative and CVD. Smoking was associated with higher DMFT. CONCLUSIONS: Poor oral health was found in all individuals with disabilities, suggesting that limitations in oral care attributed to aging and neurological disorders negatively affect oral health. Oral rehabilitation of patients with disabilities requires awareness of oral health limitations and early intervention through dental care. Implications for rehabilitationPoor oral health and oral hygiene is common among older people with disabilities.To optimize oral rehabilitation of patients with disabilities, early intervention, individualized treatment plans and an adapted time frame for dental treatment are required.Education of dentists, caregivers, and family members is essential for oral rehabilitation and improvement of oral hygiene in patients with disabilities.
 INTRODUCTION: Currently, clinical trials of DMTs strive to determine their effect on neuroinflammation and neurodegeneration. We aimed to determine the impact of currently used DMTs on brain atrophy and disability in RRMS. The main goal of this review is to evaluate the neuroprotective potential of MS therapy and assess its impact on disability. METHODS: We performed a systematic analysis of clinical trials that used brain atrophy as an outcome or performed post hoc analysis of volumetric MRI parameters to assess the neuroprotective potential of applied therapies. Trials between 2008 and 2019 that included published results of brain parenchymal fraction (BPF) change and brain volume loss (BVL) in the period from baseline to week 96 or longer were considered. RESULTS: Twelve from 146 clinical trials met the inclusion criteria and were incorporated into the analysis. DMTs that presented a large reduction in BVL also exhibited robust effects on clinical disability worsening, e.g., alemtuzumab with a 42% risk reduction in 6-month confirmed disability accumulation (p = 0.0084), ocrelizumab with a 40% risk reduction in 6-month confirmed disability progression (p = 0.003), and other DMTs (cladribine and teriflunomide) with moderate influence on brain atrophy were also associated with a marked impact on disability worsening. Dimethyl fumarate (DEFINE) and fingolimod (FREEDOMS I) initially exhibited significant effect on BVL; however, this effect was not confirmed in further clinical trials: CONFIRM and FREEDOMS II, respectively. Peg-IFN-β1a shows a modest effect on BVL and disability worsening. CONCLUSION: Our results show that BVL in one of the components of clinical disability worsening, together with other variables (lesion volume and annualized relapse rate). Standardization of atrophy measurement technique as well as harmonization of disability worsening and progression criteria in further clinical trials are of utmost importance as they enable a reliable comparison of neuroprotective potential of DMTs.
 OBJECTIVES: The objective of this study was to investigate the needs of carers of patients suffering from chronic diseases. MATERIAL AND METHODS: The present study is a mixed approach, quantitative and qualitative. The study population consisted of 560 caregivers of patients with chronic diseases. The data collection was done with an improvised needs survey questionnaire, which included 57 questions. The questionnaire surveyed carers 'financial needs, social needs, psychological needs, and patients' education needs. The Cronbach-a index of the Patient Needs Survey was 0.956 and that of caregivers was 0.965. Carers' burden of care was assessed with The Zarit Burden Interview scale. The statistical analysis of the data was done with the statistical program IBM SPSS for Windows version 26.0. RESULTS: The main diseases of the patients were chronic renal failure (22.6%), multiple sclerosis (19%), cancer (19%), diabetes mellitus (7.1%), dementia (6%), and chronic obstructive pulmonary disease (6%). The majority of patients (82.1%) had health problems for more than 24 months. Caregivers provided 12.5 ± 8.3 h of daycare and cared for patients for more than 24 months (73.2%). Caregivers seek information from health professionals (4.41 ± 1.2), need more information (4.11 ± 1.4), feel stressed about the role of caregiver (3.91 ± 1.3), time available for vacation is limited (3.89 ± 1.4), time available for entertainment is limited (3.80 ± 1.3) and they feel intimidated with the role of carer (3.76 ± 1.3). The caregivers' charge was 42.4 ± 19.6. Most caregivers reported moderate to severe burdens. CONCLUSION: Caregivers experience a lack of clear and comprehensible information about the treatment that caring patients receive, as well as a lack of ongoing care from health professionals.
 BACKGROUND/AIM: Fingolimod is a sphingosine-1-phosphate receptor modulator that prevents lymphocytes egress from lymphoid organs. It has been used as a disease-modifying drug for human multiple sclerosis and has shown better therapeutic effects than other conventional therapies. Therefore, this study was performed to obtain preclinical data of fingolimod in dogs. MATERIALS AND METHODS: Nine laboratory Beagle dogs were used and randomized into three groups for pharmacokinetics (PK) and pharmacodynamics (PD). The dogs were administered once with a low-dose (0.01 mg/kg, n=3), medium-dose (0.05 mg/kg, n=3), and high-dose (0.1 mg/kg, n=3) of fingolimod, orally. Samples were collected serially at predetermined time points, and whole blood fingolimod concentrations were measured using high-performance liquid chromatography-mass spectrometry. Differential counts of leukocytes over time were determined to identify immune cells' response to fingolimod. RESULTS: Regarding PK, the concentration of fingolimod in the blood increased in a dose-dependent manner, but it was not proportional. Regarding PD, the number of lymphocytes significantly decreased compared to baseline in all dose groups (low-dose, p=0.0002; medium-dose, p<0.0001; high-dose, p=0.0012). Eosinophils were significantly reduced in low- (p=0.0006) and medium- (p=0.0006) doses, and neutrophils were also significantly reduced in medium-(p=0.0345) and high- (p=0.0016) doses. CONCLUSION: This study provides the basis for future clinical applications of fingolimod in dogs with immune-mediated diseases, such as meningoencephalitis of unknown etiology.
 Despite the anatomical separation, strong evidence suggested a bidirectional association between gut microbiota and central nervous system. Cross-talk between gut microbiota and brain has an important role in the pathophysiology of neurodegenerative disorders and regenerative processes. However, choosing the appropriate probiotics and combination therapy of probiotics to provide a synergistic effect is very crucial. In the present study, we investigated the effect of Lactobacillus casei (L. casei) and Bifidobacterium breve (B. breve) on alternation performance, oxidant/antioxidant biomarkers, the extent of demyelination, and the expression level of HO-1, Nrf-2, Olig2, MBP, PDGFRα, and BDNF in cuprizone (CPZ)-induced demyelination model of rat corpus callosum. In order to induce this model, rats received oral administration of CPZ 0.6% w/w in corn oil for 28 days. Then, L. casei, B. breve, or their combinations were orally administrated for 28 days. Y maze test was performed to investigate the alternation performance. Oxidant/antioxidant biomarkers were determined by colorimetric methods. Extent of demyelination was investigated using FluoroMyelin staining. The genes' expression levels of antioxidant and myelin lineage cells were assessed by quantitative real time PCR. The results showed the probiotics supplementation significantly improve the alternation performance and antioxidant capacity in demyelinated corpus callosum. Interestingly, B. breve supplementation alleviated demyelination and oxidative stress levels more than the administration of L. casei alone or the combination of two probiotics. These observations suggest that B. breve could provide a supplementary strategy for the treatment of multiple sclerosis by increasing antioxidant capacity and remyelination.
 Granulomatous meningoencephalitis (GME) and necrotizing encephalitides (NE) are the most common immune-mediated inflammatory diseases of the central nervous system in dogs. Activation of the fibrinolytic system in multiple sclerosis, a similar immune-mediated disease affecting the central nervous system in humans, seems to be related to disease progression. The aim of this study was to identify fibrin/fibrinogen and D-dimer deposition, as well as presence of intravascular thrombosis (IVT) in brains of dogs with a diagnosis of GME or NE. Immunohistochemical studies using antibodies against fibrin/fibrinogen and D-dimers were performed. Statistical analyses were performed to determine whether there were differences in the presence and location of fibrin/fibrinogen, D-dimers deposits, and IVT between GME and NE. Samples from sixty-four dogs were included in the study: 32 with a diagnosis of GME and 32 with a diagnosis of NE. Fibrin/fibrinogen depositions were detected in all samples and d-dimers were detected in 43/64 samples. IVT was present in 29/64 samples, with a significantly higher score in samples from dogs with NE than in samples from dogs with GME (P = 0.001). These data support hemostatic system activation in both diseases, especially NE. This finding might be related to the origin of the necrotic lesions seen in NE, which could represent chronic ischemic lesions. Further studies are needed to investigate the association between vascular lesions and the histopathological differences between GME and NE and the hemostatic system as a potential therapeutic target.
 B cells expressing the transcription factor T-bet are found to have a protective role in viral infections, but are also considered major players in the onset of different types of autoimmune diseases. Currently, the exact mechanisms driving such 'atypical' memory B cells to contribute to protective immunity or autoimmunity are unclear. In addition to general autoimmune-related factors including sex and age, the ways T-bet(+) B cells instigate autoimmune diseases may be determined by the close interplay between genetic risk variants and Epstein-Barr virus (EBV). The impact of EBV on T-bet(+) B cells likely relies on the type of risk variants associated with each autoimmune disease, which may affect their differentiation, migratory routes and effector function. In this hypothesis-driven review, we discuss the lines of evidence pointing to such genetic and/or EBV-mediated influence on T-bet(+) B cells in a range of autoimmune diseases, including systemic lupus erythematosus (SLE) and multiple sclerosis (MS). We provide examples of how genetic risk variants can be linked to certain signaling pathways and are differentially affected by EBV to shape T-bet(+) B-cells. Finally, we propose options to improve current treatment of B cell-related autoimmune diseases by more selective targeting of pathways that are critical for pathogenic T-bet(+) B-cell formation.
 Autoimmune diseases are complex, chronic inflammatory conditions initiated by the loss of immunological tolerance to self-antigens. Nowadays, there is no effective and useful therapy for autoimmune diseases, and the existing medications have some limitations due to their nonspecific targets and side effects. During the last few decades, it has been established that mesenchymal stem cells (MSCs) have immunomodulatory functions. It is proposed that MSCs can exert an important therapeutic effect on autoimmune disorders. In parallel with these findings, several investigations have shown that MSCs alleviate autoimmune diseases. Intriguingly, the results of studies have demonstrated that the effective roles of MSCs in autoimmune diseases do not depend on direct intercellular communication but on their ability to release a wide spectrum of paracrine mediators such as growth factors, cytokines and extracellular vehicles (EVs). EVs that range from 50 to 5,000 nm were produced by almost any cell type, and these nanoparticles participate in homeostasis and intercellular communication via the transfer of a broad range of biomolecules such as modulatory proteins, nucleic acids (DNA and RNA), lipids, cytokines, and metabolites. EVs derived from MSCs display the exact properties of MSCs and can be safer and more beneficial than their parent cells. In this review, we will discuss the features of MSCs and their EVs, EVs biogenesis, and their cargos, and then we will highlight the existing discoveries on the impacts of EVs from MSCs on autoimmune diseases such as multiple sclerosis, arthritis rheumatic, inflammatory bowel disease, Type 1 diabetes mellitus, systemic lupus erythematosus, autoimmune liver diseases, Sjögren syndrome, and osteoarthritis, suggesting a potential alternative for autoimmune conditions therapy.
 BACKGROUND: Frailty is an intermediate and reversible geriatric syndrome that often precedes dependence. Therefore, its identification is essential to prevent dependence. Several molecules have been proposed as biomarkers of frailty, but none of them have reached clinical practice. Recently, circular RNAs have emerged as new non-coding RNAs. Their regulatory role together with their high stability in biofluids makes them good candidates as biomarkers for various processes, but, to date, no study has characterized the expression of circRNA in frailty. RESULTS: We studied RNA from leukocytes of 35 frails and 35 robust individuals. After RNA-Sequencing, circRNA detection was performed by CIRI2 and Circexplorer2 and differential expression analysis by DESeq2. Validation was performed by Quantitative-PCR. Linear Discriminant Analysis was performed to determine the best circRNA combination to discriminate frail from robust. In addition, CircRNA candidates were studied in 13 additional elder donors before and after a 3-month physical intervention. We found 89 differentially expressed circRNAs (p-value<0.05, FC>|1.5|) with frailty. Upregulation of hsa_circ_0007817, hsa_circ_0101802 and hsa_circ_0060527 in frail individuals was validated. The combination of hsa_circ_0079284, hsa_circ_0007817 and hsa_circ_0075737 levels showed a great biomarker value with a 95.9% probability of correctly classifying frail and robust individuals. Moreover, hsa_circ_0079284 levels decreased after physical intervention in concordance with an improvement in frailty scores. CONCLUSIONS: This work describes for the first time a different expression pattern of circular RNA (circRNAs) between frail and robust individuals. Moreover, the level of some circRNAs is modulated after a physical intervention. These results suggest that they could be used as minimally invasive biomarkers of frailty.
 Copper deficiency can present as myelopathy by the manifestation of sensory ataxia, secondary to demyelination of the posterior cords of the spinal cord, accompanied by cytopenia, mainly anemia, and leukopenia. Case series study of three patients with myelopathy due to copper deficiency, diagnosed and managed from 2020 to 2022 in a highly complex university hospital in Colombia. Regarding gender, two cases were female patients. The age range was between 57 and 68 years. In all three cases serum copper levels were decreased, and in two of these, different causes of myelopathy affecting the posterior cords of the spinal cord were ruled out, such as vitamin B12, vitamin E and folic acid deficiency, tabes dorsalis, myelopathy due to human immunodeficiency virus, multiple sclerosis and infection by the human lymphotropic virus type I and II, among others. However, at the moment of the myelopathy diagnosis, one patient had vitamin B12 deficiency associated with copper insufficiency. All three cases presented sensory ataxia, and in two, paraparesis was the initial motor deficit. The diagnostic approach must include copper levels assessment in every case of patients with chronic gastrointestinal pathology, chronic diarrhea, malabsorption syndrome, or significant reduction in dietary intake; and the development of neurological symptoms that may suggest cord involvement. It has been reported that a delay in diagnosis can lead to poor neurological outcomes.
 c-Jun activation domain binding protein-1 (JAB1) is a multifunctional regulator that plays vital roles in diverse cellular processes. It regulates AP-1 transcriptional activity and also acts as the fifth component of the COP9 signalosome complex. While JAB1 is considered an oncoprotein that triggers tumor development, recent studies have shown that it also functions in neurological development and disorders. In this review, we summarize the general features of the JAB1 gene and protein, and present recent updates on the regulation of JAB1 expression. Moreover, we also highlight the functional roles and regulatory mechanisms of JAB1 in neurodevelopmental processes such as neuronal differentiation, synaptic morphogenesis, myelination, and hair cell development and in the pathogenesis of some neurological disorders such as Alzheimer's disease, multiple sclerosis, neuropathic pain, and peripheral nerve injury. Furthermore, current challenges and prospects are discussed, including updates on drug development targeting JAB1.
 The term neuronutrition has been proposed as part of nutritional neuroscience, studying the effects of various dietary components on behavior and cognition. Other researchers underline that neuronutrition includes the use of various nutrients and diets to prevent and treat neurological disorders. The aim of this narrative review was to explore the current understanding of the term neuronutrition as the key concept for brain health, its potential molecular targets, and perspectives of its nutritional approach to the prevention and treatment of Alzheimer's and Parkinson's diseases, multiple sclerosis, anxiety, depressive disorders, migraine, and chronic pain. Neuronutrition can be defined as a part of neuroscience that studies the influence of various aspects of nutrition (nutrients, diet, eating behavior, food environment, etc.) on the development of nervous disorders and includes nutrition, clinical dietetics, and neurology. There is evidence that the neuronutritional approach can influence neuroepigenetic modifications, immunological regulation, metabolic control, and behavioral patterns. The main molecular targets in neuronutrition include neuroinflammation, oxidative/nitrosative stress and mitochondrial dysfunction, gut-brain axis disturbance, and neurotransmitter imbalance. To effectively apply neuronutrition for maintaining brain health, a personalized approach is needed, which includes the adaptation of the scientific findings to the genetic, biochemical, psycho-physiological, and environmental features of each individual.
 Stimulator of Interferon Genes (STING) is a crucial protein that controls the immune system's reaction to bacterial and viral infections. As a pattern-recognition receptor, STING is found in immune cells as well as in neurons and glia in the enteric nervous system (ENS). Recent studies have linked STING to the pathogenesis of several neurological disorders like multiple sclerosis (MS), Alzheimer's disease (AD), and gastrointestinal disorders, including irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), which are characterized by chronic inflammation and dysregulation of the enteric nervous system (ENS) in the digestive tract. STING plays a crucial role in the pathway that induces the production of interferon in response to viral infection in the central nervous system (CNS). A new study by Dharshika et al. in the current issue of Neurogastroenterology and Motility has demonstrated distinct roles for STING in enteric neurons and glia, namely activation of STING leads to IFN-β production in enteric neurons but not in glia and reducing STING activation in enteric glia does not modulate the severity of Dextran sulfate sodium (DSS) colitis or subsequent loss of enteric neurons. Rather, the role of STING in enteric glia is related to enhancing autophagy. STING can influence gastrointestinal motility and barrier function and therefore be involved in the pathophysiology of IBS and IBD. This mini review highlights the current knowledge of STING in the pathophysiology of CNS and gastrointestinal diseases as well as these newly uncovered roles STING in enteric neurons and glia.
 Increasing evidence indicates that cellular identity can be reduced to the distinct gene regulatory networks controlled by transcription factors (TFs). However, redundancy exists in these states as different combinations of TFs can induce broadly similar cell types. We previously demonstrated that by overcoming gene silencing, it is possible to deterministically reprogram human pluripotent stem cells directly into cell types of various lineages. In the present study we leverage the consistency and precision of our approach to explore four different TF combinations encoding astrocyte identity, based on previously published reports. Analysis of the resulting induced astrocytes (iAs) demonstrated that all four cassettes generate cells with the typical morphology of in vitro astrocytes, which expressed astrocyte-specific markers. The transcriptional profiles of all four iAs clustered tightly together and displayed similarities with mature human astrocytes, although maturity levels differed between cells. Importantly, we found that the TF cassettes induced iAs with distinct differences with regards to their cytokine response and calcium signaling. In vivo transplantation of selected iAs into immunocompromised rat brains demonstrated long term stability and integration. In conclusion, all four TF combinations were able to induce stable astrocyte-like cells that were morphologically similar but showed subtle differences with respect to their transcriptome. These subtle differences translated into distinct differences with regards to cell function, that could be related to maturation state and/or regional identity of the resulting cells. This insight opens an opportunity to precision-engineer cells to meet functional requirements, for example, in the context of therapeutic cell transplantation.
 OBJECTIVE: To determine the prevalence of restless leg syndrome in patients with spinal cord injury using a consensus criterion. METHODS: The cross-sectional study was conducted from November 29, 2018, to February 28, 2021 at the departments of Neurology and Orthopaedic Surgery, King Edward Medical University, Mayo Hospital, Lahore, Pakistan, and comprised patients of either gender aged 18-80 years having spinal cord injuries. All the patients were interviewed using a 10-item questionnaire, and were assessed using the five-point consensus criteria of the International Restless Leg Syndrome Study Group. Data was analysed using SPSS 20. RESULTS: Of the 253 patients, 128(50.6%) were males and 125(49.4%) were females. The overall mean age was 38.6±14.2 years. Restless leg syndrome was present in 116(45.8%) patients, and 64(55.2%) of them were males (p>0.05). The mean duration of the symptoms was 18.9±16.9 months. Causes of spinal cord injury included metastasis 28(11.1%) multiple sclerosis 32(12.6%), neuromyelitis optica spectrum disorders 68(26.9%), tuberculous spondylitis 85(33.6%), trauma 24(9.5%) and viral myelitis 16(6.3%). CONCLUSIONS: Restless leg syndrome was prevalent in less than half the patients having spinal cord injury. It was more prevalent in males compared to females, but the difference was not significant.
 Global and regional trends of population aging spotlight major public health concerns. As one of the most common adverse prognostic factors, advanced age is associated with a remarkable incidence risk of many non-communicable diseases, affecting major organ systems of the human body. Age-dependent factors and molecular processes can change the nervous system's normal function and lead to neurodegenerative disorders. Oxidative stress results from of a shift toward reactive oxygen species (ROS) production in the equilibrium between ROS generation and the antioxidant defense system. Oxidative stress and neuroinflammation caused by Amyloid-ß protein deposition in the human brain are the most likely pathogenesis of Alzheimer's disease (AD). Walnut extracts could reduce Amyloid-ß fibrillation and aggregation, indicating their beneficial effects on memory and cognition. Walnut can also improve movement disabilities in Parkinson's disease due to their antioxidant and neuroprotective effect by reducing ROS and nitric oxide (NO) generation and suppressing oxidative stress. It is noteworthy that Walnut compounds have potential antiproliferative effects on Glioblastoma (the most aggressive primary cerebral neoplasm). This effective therapeutic agent can stimulate apoptosis of glioma cells in response to oxidative stress, concurrent with preventing angiogenesis and migration of tumor cells, improving the quality of life and life expectancy of patients with glioblastoma. Antioxidant Phenolic compounds of the Walnut kernel could explain the significant anti-convulsion ability of Walnut to provide good prevention and treatment for epileptic seizures. Moreover, the anti-inflammatory effect of Walnut oil could be beneficial in treating multiple sclerosis. In this study, we review the pharmaceutical properties of Walnut in age-related neurological disorders.
 Autoimmune diseases (AIDs) are caused by the loss of self-tolerance and destruction of tissues by the host's immune system. Several antigen-specific immunotherapies, focused on arresting the autoimmune attack, have been tested in clinical trials with discouraging results. Therefore, there is a need for innovative strategies to restore self-tolerance safely and definitively in AIDs. We previously demonstrated the therapeutic efficacy of phosphatidylserine (PS)-liposomes encapsulating autoantigens in experimental type 1 diabetes and multiple sclerosis. Here, we show that PS-liposomes can be adapted to other autoimmune diseases by simply replacing the encapsulated autoantigen. After administration, they are distributed to target organs, captured by phagocytes and interact with several immune cells, thus exerting a tolerogenic and immunoregulatory effect. Specific PS-liposomes demonstrate great preventive and therapeutic efficacy in rheumatoid arthritis and myasthenia gravis. Thus, this work highlights the therapeutic potential of a platform for several autoimmunity settings, which is specific, safe, and with long-term effects.
 Magnetic resonance imaging (MRI) plays an increasingly important role in the diagnosis and prognosis of neurodegenerative diseases. One field of extensive clinical use of MRI is the accurate and automated classification of degenerative disorders. Most of current classification studies either do not mirror medical practice where patients may exhibit early stages of the disease, comorbidities, or atypical variants, or they are not able to produce probabilistic predictions nor account for uncertainty. Also, the spatial heterogeneity of the brain alterations caused by neurodegenerative processes is not usually considered, despite the spatial configuration of the neuronal loss is a characteristic hallmark for each disorder. In this article, we propose a classification technique that incorporates uncertainty and spatial information for distinguishing between healthy subjects and patients from four distinct neurodegenerative diseases: Alzheimer's disease, mild cognitive impairment, Parkinson's disease, and Multiple Sclerosis. We introduce a spatially informed Bayesian neural network (SBNN) that combines a three-dimensional neural network to extract neurodegeneration features from MRI, Bayesian inference to account for uncertainty in diagnosis, and a spatially informed MRI image using hidden Markov random fields to encode cerebral spatial information. The SBNN model demonstrates that classification accuracy increases up to 25% by including a spatially informed MRI scan. Furthermore, the SBNN provides a robust probabilistic diagnosis that resembles clinical decision-making and can account for the heterogeneous medical presentations of neurodegenerative disorders.
 Manipulation of neural stem cell proliferation and differentiation in the postnatal CNS is receiving significant attention due to therapeutic potential. In the spinal cord, such manipulations may promote repair in conditions such as multiple sclerosis or spinal cord injury, but may also limit excessive cell proliferation contributing to tumours such as ependymomas. We show that when ambient γ-aminobutyric acid (GABA) is increased in vigabatrin-treated or decreased by GAD67 allele haplodeficiency in glutamic acid decarboxylase67-green fluorescent protein (GAD67-GFP) mice of either sex, the numbers of proliferating cells respectively decreased or increased. Thus, intrinsic spinal cord GABA levels are correlated with the extent of cell proliferation, providing important evidence for manipulating these levels. Diazepam binding inhibitor, an endogenous protein that interacts with GABA receptors and its breakdown product, octadecaneuropeptide, which preferentially activates central benzodiazepine (CBR) sites, were highly expressed in spinal cord, especially in ependymal cells surrounding the central canal. Furthermore, animals with reduced CBR activation via treatment with flumazenil or Ro15-4513, or with a G2F77I mutation in the CBR binding site had greater numbers of Ethynyl-2'-deoxyuridine positive cells compared to control, which maintained their stem cell status since the proportion of newly proliferated cells becoming oligodendrocytes or astrocytes was significantly lower. Altering endogenous GABA levels or modulating GABAergic signalling through specific sites on GABA receptors therefore influences NSC proliferation in the adult spinal cord. These findings provide a basis for further study into how GABAergic signalling could be manipulated to enable spinal cord self-regeneration and recovery or limit pathological proliferative activity.
 Sphingosine-1-phosphate receptor (S1PR) signaling regulates diverse pathophysiological processes in the central nervous system. The role of S1PR signaling in neurodegenerative conditions is still largely unidentified. Siponimod is a specific modulator of S1P1 and S1P5 receptors, an immunosuppressant drug for managing secondary progressive multiple sclerosis. We investigated its neuroprotective properties in vivo on the retina and the brain in an optic nerve injury model induced by a chronic increase in intraocular pressure or acute N-methyl-D-aspartate excitotoxicity. Neuronal-specific deletion of sphingosine-1-phosphate receptor (S1PR1) was carried out by expressing AAV-PHP.eB-Cre recombinase under Syn1 promoter in S1PR1(flox/flox) mice to define the role of S1PR1 in neurons. Inner retinal electrophysiological responses, along with histological and immunofluorescence analysis of the retina and optic nerve tissues, indicated significant neuroprotective effects of siponimod when administered orally via diet in chronic and acute optic nerve injury models. Further, siponimod treatment showed significant protection against trans-neuronal degenerative changes in the higher visual center of the brain induced by optic nerve injury. Siponimod treatment also reduced microglial activation and reactive gliosis along the visual pathway. Our results showed that siponimod markedly upregulated neuroprotective Akt and Erk1/2 activation in the retina and the brain. Neuronal-specific deletion of S1PR1 enhanced retinal and dorsolateral geniculate nucleus degenerative changes in a chronic optic nerve injury condition and attenuated protective effects of siponimod. In summary, our data demonstrated that S1PR1 signaling plays a vital role in the retinal ganglion cell and dorsolateral geniculate nucleus neuronal survival in experimental glaucoma, and siponimod exerts direct neuroprotective effects through S1PR1 in neurons in the central nervous system independent of its peripheral immuno-modulatory effects. Our findings suggest that neuronal S1PR1 is a neuroprotective therapeutic target and its modulation by siponimod has positive implications in glaucoma conditions.
 Dipeptidyl peptidase 4 is a serine protease that cleaves X-proline or X-alanine in the penultimate position. Natural substrates of the enzyme are glucagon-like peptide-1, glucagon inhibiting peptide, glucagon, neuropeptide Y, secretin, substance P, pituitary adenylate cyclase-activating polypeptide, endorphins, endomorphins, brain natriuretic peptide, beta-melanocyte stimulating hormone and amyloid peptides as well as some cytokines and chemokines. The enzyme is involved in the maintenance of blood glucose homeostasis and regulation of the immune system. It is expressed in many organs including the brain. DPP4 activity may be effectively depressed by DPP4 inhibitors. Apart from enzyme activity, DPP4 acts as a cell surface (co)receptor, associates with adeosine deaminase, interacts with extracellular matrix, and controls cell migration and differentiation. This review aims at revealing the impact of DPP4 and DPP4 inhibitors for several brain diseases (virus infections affecting the brain, tumours of the CNS, neurological and psychiatric disorders). Special emphasis is given to a possible involvement of DPP4 expressed in the brain.While prominent contributions of extracerebral DPP4 are evident for a majority of diseases discussed herein; a possible role of "brain" DPP4 is restricted to brain cancers and Alzheimer disease. For a number of diseases (Covid-19 infection, type 2 diabetes, Alzheimer disease, vascular dementia, Parkinson disease, Huntington disease, multiple sclerosis, stroke, and epilepsy), use of DPP4 inhibitors has been shown to have a disease-mitigating effect. However, these beneficial effects should mostly be attributed to the depression of "peripheral" DPP4, since currently used DPP4 inhibitors are not able to pass through the intact blood-brain barrier.
 AIM: In the past 5-10 years, there has been a growing number of studies implementing ballistic (i.e. fast) resistance training to improve walking. The aim of this study was to determine whether people with neurological conditions could perform ballistic exercises safely and accurately in their home environment. DESIGN: An observational study of 24 adults with a neurological condition (i.e. stroke, brain injury, multiple sclerosis, and neurosurgical) that limited mobility was carried out. Participants were supervised during seven ballistic exercises over six home-based sessions across three weeks. Safety was determined as the ability to perform the exercise independently. Accuracy was determined as the ability to perform the exercise on pre-determined criteria. RESULTS: The majority of participants had sustained a traumatic brain injury (n = 13) or stroke (n = 9) with a mean age of 38.3 (SD 15.3, range 17-68) years. The mean walking speed was 1.11 (SD 0.29, range 0.53-1.56) m/s. In terms of safety, participants performed the exercises safely 88% of the time, and accurately 49% of the time. Safe completion of each individual exercise ranged initially from 46% to 100% for participants, but accuracy was lower ranging from 17% to 58%. Threshold self-selected walking speeds for optimal sensitivity and specificity for safety ranged from 0.86 to 1.17 m/s and for accuracy ranged from 0.97 to 1.23 m/s. CONCLUSION: Most of the home-based ballistic resistance exercises were safe, but accuracy was low for several of the ballistic resistance exercises. Higher self-selected walking speeds were associated with more accurate performance.
 Background: Neuroinflammatory diseases are progressive leading to loss of function and disability. Although palliative care (PC) utilization has increased globally, it has scarcely increased in neurology. Objectives: To explore PC attitudes and knowledge among patients with neuroinflammatory diseases, such as multiple sclerosis, neuromyelitis optica spectrum disorder, and myelin oligodendrocyte glycoprotein antibody-associated disease. Methods: A cross-sectional 1-year study was conducted using the Palliative Care Knowledge Scale (PaCKS) and the PC Health Information National Trends Survey (HINTS). Murray's transition theory guided this study, which integrates palliative services including decision making, communication, and coordinated care. Results: The majority of study patients were female (69%) (N = 86) and White (79%). Forty-two percent indicated that they had never heard about PC, 46% said that they knew a little bit about PC, and 12% said that they knew a lot about PC. Fifty percent of patients knew the goals of PC and had knowledge about PC services. Forty-four percent to 60% agreed that PC goals include helping friends and family to cope with a patient's illness, offering social and emotional support, and managing pain and other symptoms. Patients who self-reported being familiar with PC performed significantly better on the PaCKS than those unfamiliar with PC (p < 0.001), and those who self-reported moderate or severe memory loss performed significantly worse on the PaCKS than those with mild memory loss (p = 0.027). There was an association between higher education and PC knowledge and between patients' PaCKS scores and their self-reported HINTS PC knowledge. Conclusions: Patients have partial PC knowledge. Patients require education about PC early in their disease along their illness trajectory.
 INTRODUCTION: Chronic diseases represent a huge challenge for the health systems globally due to the rapidly increasing number of patients and their long-term need for healthcare. The purpose of this study was to investigate the needs of patients suffering from chronic diseases. METHODOLOGY: This is a cross-sectional study. The study population consisted of 840 adults with chronic diseases. The data collection was done with an improvised needs survey questionnaire, which included 56 questions. Statistical analyses were performed using IBM SPSS Statistics for Windows, v.25.0, statistical significance being considered at p < 0.05. RESULTS: The main diseases of the patients were chronic renal failure (22.6%), multiple sclerosis (19%), cancer (19%), diabetes mellitus (7.1%), dementia (6%), and chronic obstructive pulmonary disease (6%). The majority of patients (82.1%) were sick for more than 24 months. Patients seek information from health professionals (4.07 ± 1.4), feel tired (4.05 ± 1.4), have to share their feelings with other family members (4.01 ± 1.4), feel anxious about the future (3.94 ± 1.3), and feel out of control (3.80 ± 1.5). CONCLUSIONS: Patients with chronic diseases suffer from numerous physical, mental, emotional, and cognitive problems. Paying attention to the unmet needs of patients could have beneficial effects on both patients and their caregivers.
 Systemic lupus erythematosus (SLE) is an autoimmune disease associated with the production of double-stranded DNA (dsDNA) antibodies and other antibodies that predominantly affects women with a wide range of lesions. Although neuropsychiatric lupus erythematosus (NPSLE), characterized by neuropsychiatric symptoms related to cerebrovascular diseases or depression, ranks high in severity, no specific treatment has been defined. Two-carba cyclic phosphatidic acid (2ccPA), a derivative of cyclic phosphatidic acid, was isolated from the true slime mold Physarum polycephalum in 1992. 2ccPA treatment suppresses neuroinflammation and promotes tissue repair in mouse multiple sclerosis and traumatic brain injury models. In this study, we performed behavioral tests on MRL/lpr mice as an NPSLE model. MRL/lpr mice showed increased depression-like behaviors compared with control mice, which were significantly suppressed by 2ccPA treatment. The expression of CD68, an M1 phenotypic marker of microglia, was significantly elevated in the prefrontal cortex and hippocampus of MRL/lpr mice, which was significantly suppressed by 2ccPA treatment. In contrast, the expression of Arginase1, an M2 phenotypic marker of microglia, was significantly increased by 2ccPA treatment. Compared to control mice, MRL/lpr mice showed higher plasma levels of anti-dsDNA antibodies, which are mainly involved in SLE pathogenesis. 2ccPA treatment decreased these levels in the MRL/lpr mice. These results suggest that 2ccPA treatment suppresses behavioral abnormalities by promoting a microglial phenotypic switch from M1 to M2 in MRL/lpr mice.
 INTRODUCTION: Acute urinary retention (AUR) is one of the most severe symptoms of Benign Prostatic Hyperplasia (BPH). There are some studies in the literature describing the risk factors for the development of AUR in BPH patients. However, the studies that summarize the effect of AUR on Transurethral resection of Prostate (TUR-P) surgery results are limited. The aim of this study is to assess the effect of AUR on TUR-P results. METHODS: Between 2018 and 2020, patients who underwent TUR-P for AUR or lower urinary tract symptoms (LUTS) were included in the study. The inclusion criteria were, men over 50 years old with a BPH diagnosis and who underwent monopolar TUR-P by a single surgeon. The exclusion criteria were; patients who had prostate cancer, multiple sclerosis, or neurogenic bladder were diagnosed or had previous lower urinary tract surgeries such as TUR-P, TUR-Bladder, Urethrotomy, had a chronic indwelling catheter, and patients who did not accept immediate TUR-P and preferred trial without catheter (TWOC) protocol. The age, PSA, prostate volume, pre- and post-operative flow rates, duration of hospitalization, and complications were recorded. Two groups were constituted for comparison such as AUR and Elective Group and p values <0.05 were considered significant. RESULTS: There were 14 and 46 patients for AUR and Elective Groups respectively. The age, pre-operative prostate volume, free and total PSA values, postoperative complication rate, and re-hospitalization rate were significantly higher in the AUR-Group. However, there were no differences between groups in terms of pre-operative medication, duration of hospitalization, and post-operative uroflow maximum flow rate. DISCUSSION: Patients who underwent TUR-P after AUR have a higher risk for complications and re-hospitalization. Care should be taken in these patients and patients should be warned about the risks.
 Vestibular dysfunction is a disturbance of the body's balance system. Etiologies of this disorder are broadly categorized into peripheral and central causes based on the anatomy involved. The symptoms of peripheral and central vestibular dysfunction can overlap, and a comprehensive physical examination can often help differentiate the two. Vestibular disorders usually present acutely, and the most common form of acute peripheral vestibular dysfunction is benign paroxysmal positional vertigo (BPPV). The most common cause of severe central vestibular dysfunction is an ischemic stroke of the posterior fossa, which contains the brainstem and cerebellum. Acute ischemic stroke accounts for up to 25% of patients who present with central vestibular dysfunction. Since acute stroke is treated differently from other causes of disequilibrium, it is essential to recognize this process promptly. Vertebrobasilar artery disease can lead to stroke in 5% of patients, and patients with this condition often present initially with syncopal episodes and/or vestibular dysfunction. The second most common cause of central vestibular dysfunction is a demyelinating disease. Symptoms of vestibular dysfunction include a variety of complaints: vertigo, nausea and vomiting, intolerance to head motion, spontaneous nystagmus, unsteady gait, and postural instability. The prevalence of each of these symptoms varies, and there is no single symptom that is pathognomonic for vestibular dysfunction. The presentation of these symptoms as a cluster should raise the level of clinical suspicion for vestibular dysfunction. A complete history and physical examination is the best way to differentiate peripheral from central vestibular dysfunction. Identifying which type of vestibular dysfunction a patient has is crucial, as this determines the therapeutic approach and the urgency of initiating treatment. The mainstay of treatment for peripheral vestibular disorders is symptomatic therapy, but the treatment for central vestibular dysfunction caused by an ischemic stroke can include emergent intravenous thrombolytic therapy and interventional clot retrieval. Early identification of demyelinating disorders, such as multiple sclerosis, is essential so that treatment can be initiated to prevent the rapid decline and development of disability.  This article will review the epidemiology, history and physical examination, evaluation, differential diagnosis, treatment, complications, and critical points in diagnosing and managing vestibular dysfunction and differentiating peripheral from central vestibular disorders.
 BACKGROUND AND PURPOSE: <p>Using patient registries is essential both in clinical research and in medical practice. Headaches, more specifically migraines are one of the most common complaints that can detract the quality of a patient&rsquo;s life and these complaints also have a significant socio-econo&shy;mic effect. Our goal is to create a national Headache Registry and to also provide the pre-analysis of the registry&rsquo;s database.</p>. METHODS: <p>Our research is based on the national Multiple Sclerosis Registry, which we modified using the latest version of diagnostic criteria published by the International Headache Society. This clinical study contains data collected from patients suffering from migraines and currently receiving care at the Headache Outpatient Department at the Neurologic Clinic of the University of Szeged.</p>. RESULTS: <p>The data of 412 patients (363 wo&shy;men and 49 men) suffering from migraine (migraine without aura: n = 313 and migraine with aura: n = 99) were added to the Headache Registry. The average age of participants was 44.1 &plusmn; 12.5 SD years. Regarding the attributes of migraine headaches we examined the following characteristics: localization, quality and intensity (based on the Visual Analogue Scale) of the pain, frequency (the number of headache days per month), medications (acute or prophylactic), comorbidities (depression, anxiety, hypertension, asthma, epilepsy and others), family history and the occurrence of stroke among patients.</p>. CONCLUSION: <p>Based on international expe&shy;rience, patient registries are the most optimal systems for structured patient mo&shy;nitoring. For high level management and long-term follow up of the patients the application of registries is essential. The registries include the detailed medical history and the diagnostic and therapeutic data of the patients, and they trace the changes during the follow up medical visits. Registries are able to record the entire course of the disease in digital way. The numerous data can be set out any time from the digital database. Extensive spread of patients&rsquo; registries is fundamental not only in every day clinical practice, but also in clinical research.</p>.
 Experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) requires immunization by a MOG peptide emulsified in complete Freund's adjuvant (CFA) containing inactivated Mycobacterium tuberculosis. The antigenic components of the mycobacterium activate dendritic cells to stimulate T-cells to produce cytokines that promote the Th1 response via toll-like receptors. Therefore, the amount and species of mycobacteria present during the antigenic challenge are directly related to the development of EAE. This methods paper presents an alternative protocol to induce EAE in C57BL/6 mice using a modified incomplete Freund's adjuvant containing the heat-killed Mycobacterium avium subspecies paratuberculosis strain K-10. M. paratuberculosis, a member of the Mycobacterium avium complex, is the causative agent of Johne's disease in ruminants and has been identified as a risk factor for several human T-cell-mediated disorders, including multiple sclerosis. Overall, mice immunized with Mycobacterium paratuberculosis showed earlier onset and greater disease severity than mice immunized with CFA containing the strain of M. tuberculosis H37Ra at the same doses of 4 mg/mL. The antigenic determinants of Mycobacterium avium subspecies paratuberculosis (MAP) strain K-10 were able to induce a strong Th1 cellular response during the effector phase, characterized by significantly higher numbers of T-lymphocytes (CD4(+) CD27(+)), dendritic cells (CD11c(+) I-A/I-E(+)), and monocytes (CD11b(+) CD115(+)) in the spleen compared to mice immunized with CFA. Furthermore, the proliferative T-cell response to the MOG peptide appeared to be highest in M. paratuberculosis-immunized mice. The use of an encephalitogen (e.g., MOG35-55) emulsified in an adjuvant containing M. paratuberculosis in the formulation may be an alternative and validated method to activate dendritic cells for priming myelin epitope-specific CD4(+) T-cells during the induction phase of EAE.
 Cyclotides are plant peptides characterized with a head-to-tail cyclized backbone and three interlocking disulfide bonds, known as a cyclic cysteine knot. Despite the variations in cyclotides peptide sequences, this core structure is conserved, underlying their most useful feature: stability against thermal and chemical breakdown. Cyclotides are the only natural peptides known to date that are orally bioavailable and able to cross cell membranes. Cyclotides also display bioactivities that have been exploited and expanded to develop as potential therapeutic reagents for a wide range of conditions (e.g., HIV, inflammatory conditions, multiple sclerosis, etc.). As such, in vitro production of cyclotides is of the utmost importance since it could assist further research on this peptide class, specifically the structure-activity relationship and its mechanism of action. The information obtained could be utilized to assist drug development and optimization. Here, we discuss several strategies for the synthesis of cyclotides using both chemical and biological routes.
 Cyclic nucleotide phosphodiesterases (PDEs) are a superfamily of enzymes that hydrolyse the intracellular second messengers cAMP and cGMP to their inactive forms 5'AMP and 5'GMP. Some members of the PDE family display specificity towards a single cyclic nucleotide messenger, and PDE4, PDE7, and PDE8 specifically hydrolyse cAMP. While the role of PDE4 and its use as a therapeutic target have been well studied, less is known about PDE7 and PDE8. This review aims to collate the present knowledge on human PDE7 and outline its potential use as a therapeutic target. Human PDE7 exists as two isoforms PDE7A and PDE7B that display different expression patterns but are predominantly found in the central nervous system, immune cells, and lymphoid tissue. As a result, PDE7 is thought to play a role in T cell activation and proliferation, inflammation, and regulate several physiological processes in the central nervous system, such as neurogenesis, synaptogenesis, and long-term memory formation. Increased expression and activity of PDE7 has been detected in several disease states, including neurodegenerative diseases such as Parkinson's, Alzheimer's and Huntington's disease, autoimmune diseases such as multiple sclerosis and COPD, and several types of cancer. Early studies have shown that administration of PDE7 inhibitors may ameliorate the clinical state of these diseases. Targeting PDE7 may therefore provide a novel therapeutic strategy for targeting a broad range of disease and possibly provide a complementary alternative to inhibitors of other cAMP-selective PDEs, such as PDE4, which are severely limited by their side-effects.
 INTRODUCTION: Alzheimer's disease (AD) is the most common cause of dementia and is characterized by a progressive deterioration in cognitive function, which typically begins with impairment in memory. Persian clover (Trifolium resupinatum) is an annual plant found in central Asia. Due to its contents (high flavonoid and isoflavones), extensive researches have been done on its therapeutic properties, such as multiple sclerosis (MS) treatment. In this study, we investigate the neuroprotective effects of this plant on Streptozotocin (STZ)-induced AD in rats. MATERIAL AND METHODS: This research aimed to evaluate the neuroprotective effect of Trifolium resupinatum on the spatial learning and memory, superoxide dismutase (SOD), expressions of β amyloid 1-42 (Ab 1-42 ), and b amyloid 1-40 (Ab 1-40 ) in the hippocampus of STZ-induced Alzheimer rats. RESULTS: Our data showed that Trifolium resupinatum extract administration for two weeks before and one week after AD induction significantly improves maze escape latency ( p = 0.027, 0.001 and 0.02 in 100, 200, and 300 mg of the extract, respectively) and maze retention time ( p = 0.003, 0.04 and 0.001 in 100, 200, and 300 mg of the extract, respectively). Also, the administration of this extract significantly increases the SOD levels from 1.72+0.20 to 2.31+0.45 ( p = 0.009), 2.48+0.32 ( p = 0.001) and 2.33+0.32 ( p = 0.007) and decreases the expressions of Ab 1-42 ) ( p = 0.001 in all concentrations of the extract) and Ab 1-40 ) ( p = 0.001 in all concentrations of the extract) in the rat's hippocampus. CONCLUSIONS: This study suggests that the alcoholic extract of Trifolium resupinatum has anti-Alzheimer and neuroprotective effects on rats.
 OBJECTIVE: Group therapy is an intervention that that has been well-studied in patients with medical illness and shown to optimize patients' wellbeing and mental health resource utilization. However, its implementation and effectiveness have not been adequately studied in those with physical disabilities. This review addresses current gaps by synthesizing the literature to examine implementation considerations in the use of psychosocial group therapy for anxiety and depression in individuals with physical disabilities. METHOD: This review adhered to Arksey and O'Malley's methodological framework and the Preferred Reporting Items for Systematic Reviews and Meta-analyses extension for Scoping Reviews Checklist. Studies were identified through MEDLINE, EMBASE, PSYCINFO, and CINAHL. Included studies were qualitative, quantitative, or mixed methods research on participants with a physical disability, and undergoing psychosocial group therapy to address anxiety/depression. RESULTS: Fifty-five studies were included in the review. The most common physical disabilities were multiple sclerosis (n = 31) and Parkinson's disease (n = 13). Group Cognitive Behavioral Therapy was the most commonly used intervention, facilitated by individuals with formal mental health training. A majority of therapy sessions included cohorts of up to 10 patients, and occurred weekly. Almost half of the studies (n = 27) reported high adherence rates (80%-99%), and a large proportion found group therapy led to improvements in their samples on a range of outcomes. CONCLUSION: Group therapies to address anxiety and depression are diverse, widely used, effective, and well-adhered to. This review may help practitioners develop, implement, and evaluate group programming for individuals with physical disabilities to address anxiety and depression. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
 Depression may occur in patients with multiple sclerosis, especially during interferon-β (IFN-β) treatment, and therapy with antidepressants may be necessary. Interactions of IFN-β with antidepressants concerning glia-mediated inflammation have not yet been studied. Primary rat co-cultures of astrocytes containing 5% (M5, consistent with "physiological" conditions) or 30% (M30, consistent with "pathological, inflammatory" conditions) of microglia were incubated with 10 ng/mL amitriptyline or doxepin for 2 h, or with 2000 U/mL IFN-β for 22 h. To investigate the effects of antidepressants on IFN-β treatment, amitriptyline or doxepin was added to IFN-β pre-treated co-cultures. An MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was performed to measure the glial cell viability, immunocytochemistry was performed to evaluate the microglial activation state, and ELISA was performed to measure pro-inflammatory TNF-α and IL-6 cytokine concentrations. Incubation of inflammatory astrocyte-microglia co-cultures with amitriptyline, doxepin or IFN-β alone, or co-incubation of IFN-β pre-treated co-cultures with both antidepressants, significantly reduced the extent of inflammation, with the inhibition of microglial activation. TNF-α and IL-6 levels were not affected. Accordingly, the two antidepressants did not interfere with the anti-inflammatory effect of IFN-β on astrocytes and microglia. Furthermore, no cytotoxic effects on glial cells were observed. This is the first in vitro study offering novel perspectives in IFN-β treatment and accompanying depression regarding glia.
 Neurodegenerative diseases (NDDs) are characterized by the progressive degeneration and/or loss of neurons belonging to the central nervous system, and represent one of the major global health issues. Therefore, a number of immunotherapeutic approaches targeting the non-functional or toxic proteins that induce neurodegeneration in NDDs have been designed in the last decades. In this context, due to unprecedented advances in genetic engineering techniques and molecular farming technology, pioneering plant-based immunogenic antigen expression systems have been developed aiming to offer reliable alternatives to deal with important NDDs, including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Diverse reports have evidenced that plant-made vaccines trigger significant immune responses in model animals, supported by the production of antibodies against the aberrant proteins expressed in the aforementioned NDDs. Moreover, these immunogenic tools have various advantages that make them a viable alternative for preventing and treating NDDs, such as high scalability, no risk of contamination with human pathogens, cold chain free production, and lower production costs. Hence, this article presents an overview of the current progress on plant-manufactured vaccines for NDDs and discusses its future prospects.
 BACKGROUND: Cardiac death caused by malignant arrhythmias is very prevalent. Prolongation of the QT interval is a relevant aspect in arrhythmia mechanisms. Prior studies have revealed that the QTc interval could be shortened by cortisone. Moreover, in an animal model of long QT syndrome, cortisone treatment shortens the ventricular action potential duration. The present study investigated the effect of methylprednisolone (MPS) on the QTc interval in cardiovascularly healthy humans. METHODS: Patients who had just been diagnosed with multiple sclerosis receiving MPS therapy were analysed prospectively. Demographic data, laboratory values, anti-arrhythmic medication and baseline and follow-up ECGs were extracted from the patients' medical records. RESULTS: Seventy-eight patients were included. The mean ± standard deviation age was 47 ± 15 years. The values of the electrolytes were normal. All patients were treated with MPS for 3 or 5 days. The heart rate increased at the beginning of MPS therapy and decreased during the subsequent period. ECG measurements showed that the QTc interval was prolonged at the beginning of MPS therapy and shortened over the course of treatment. The longest QTc intervals were obtained by calculation with Bazett's formula. CONCLUSIONS: In humans, cortisone shortens the QTc interval over time. The analysis indicates a cumulative effect of cortisone that lasts longer. The results of our pilot study reveal that cortisone might be added to therapeutic strategies in patients with long QT syndromes. Further clinical studies have to be carried out to analyze potential clinical options.
 Clinical evidence based on real-world data (RWD) is accumulating exponentially providing larger sample sizes available, which demand novel methods to deal with the enhanced heterogeneity of the data. Here, we used RWD to assess the prediction of cognitive decline in a large heterogeneous sample of participants being enrolled with cognitive stimulation, a phenomenon that is of great interest to clinicians but that is riddled with difficulties and limitations. More precisely, from a multitude of neuropsychological Training Materials (TMs), we asked whether was possible to accurately predict an individual's cognitive decline one year after being tested. In particular, we performed longitudinal modelling of the scores obtained from 215 different tests, grouped into 29 cognitive domains, a total of 124,610 instances from 7902 participants (40% male, 46% female, 14% not indicated), each performing an average of 16 tests. Employing a machine learning approach based on ROC analysis and cross-validation techniques to overcome overfitting, we show that different TMs belonging to several cognitive domains can accurately predict cognitive decline, while other domains perform poorly, suggesting that the ability to predict decline one year later is not specific to any particular domain, but is rather widely distributed across domains. Moreover, when addressing the same problem between individuals with a common diagnosed label, we found that some domains had more accurate classification for conditions such as Parkinson's disease and Down syndrome, whereas they are less accurate for Alzheimer's disease or multiple sclerosis. Future research should combine similar approaches to ours with standard neuropsychological measurements to enhance interpretability and the possibility of generalizing across different cohorts.
 α,β-Unsaturated carbonyls are a common motif in environmental toxins (e.g. acrolein) as well as therapeutic drugs, including dimethylfumarate (DMFU) and monomethylfumarate (MMFU), which are used to treat multiple sclerosis and psoriasis. These compounds form adducts with protein Cys residues as well as other nucleophiles. The specific targets ('adductome') that give rise to their therapeutic or toxic activities are poorly understood. This is due, at least in part, to the absence of antigens or chromophores/fluorophores in these compounds. We have recently reported click-chemistry probes of DMFU and MMFU (Redox Biol., 2022, 52, 102299) that allow adducted proteins to be visualized and enriched for further characterization. In the current study, we hypothesized that adducted proteins could be 'clicked' to agarose beads and thereby isolated for LC-MS analysis of DMFU/MMFU targets in primary human coronary artery smooth muscle cells. We show that the probes react with thiols with similar rate constants to the parent drugs, and give rise to comparable patterns of gene induction, confirming similar biological actions. LC-MS proteomic analysis identified ∼2970 cellular targets of DMFU, ∼1440 for MMFU, and ∼140 for the control (succinate-probe) treated samples. The most extensively modified proteins were galectin-1, annexin-A2, voltage dependent anion channel-2 and vimentin. Other previously postulated DMFU targets, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), cofilin, p65 (RELA) and Keap1 were also identified as adducted species, though at lower levels with the exception of GAPDH. These data demonstrate the utility of the click-chemistry approach to the identification of cellular protein targets of both exogenous and endogenous compounds.
 This study proposed a semisupervised loss function named level-set loss (LSLoss) for cerebral white matter hyperintensities (WMHs) segmentation on fluid-attenuated inversion recovery images. The training procedure did not require manually labeled WMH masks. Our image preprocessing steps included biased field correction, skull stripping, and white matter segmentation. With the proposed LSLoss, we trained a V-Net using the MRI images from both local and public databases. Local databases were the small vessel disease cohort (HKU-SVD, n = 360) and the multiple sclerosis cohort (HKU-MS, n = 20) from our institutional imaging center. Public databases were the Medical Image Computing Computer-assisted Intervention (MICCAI) WMH challenge database (MICCAI-WMH, n = 60) and the normal control cohort of the Alzheimer's Disease Neuroimaging Initiative database (ADNI-CN, n = 15). We achieved an overall dice similarity coefficient (DSC) of 0.81 on the HKU-SVD testing set (n = 20), DSC = 0.77 on the HKU-MS testing set (n = 5), and DSC = 0.78 on MICCAI-WMH testing set (n = 30). The segmentation results obtained by our semisupervised V-Net were comparable with the supervised methods and outperformed the unsupervised methods in the literature.
 MicroRNAs (miRNAs) are non-coding RNAs which are essential post-transcriptional gene regulators in various neuronal degenerative diseases and playact a key role in these physiological progresses. Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, and, stroke, are seriously threats to the life and health of all human health and life kind. Recently, various studies have reported that some various miRNAs can regulate the development of neurodegenerative diseases as well as act as biomarkers to predict these neuronal diseases conditions. Endogenic miRNAs such as miR-9, the miR-29 family, miR-15, and the miR-34 family are generally dysregulated in animal and cell models. They are involved in regulating the physiological and biochemical processes in the nervous system by targeting regulating different molecular targets and influencing a variety of pathways. Additionally, exogenous miRNAs derived from homologous plants and defined as botanmin, such as miR2911 and miR168, can be taken up and transferred by other species to be and then act analogously to endogenic miRNAs to regulate the physiological and biochemical processes. This review summarizes the mechanism and principle of miRNAs in the treatment of some neurodegenerative diseases, as well as discusses several types of miRNAs which were the most commonly reported in diseases. These miRNAs could serve as a study provided some potential biomarkers in neurodegenerative diseases might be an ideal and/or therapeutic targets for neurodegenerative diseases. Finally, the role accounted of the prospective exogenous miRNAs involved in mammalian diseases is described. 1. Listing a large number of neural-related miRNAs and sorting out their pathways. 2. Classify and sort miRNAs according to their mechanism of action. 3. Demonstrating the effects of up-regulation or down-regulation of each miRNAs on the nervous system.
 Destabilization of neural activity caused by failures of homeostatic regulation has been hypothesized to drive the progression of Alzheimer's Disease (AD). However, the underpinning mechanisms that connect synaptic homeostasis and the disease etiology are yet to be fully understood. Here, we demonstrated that neuronal overexpression of Amyloid β (Aβ) causes abnormal histone acetylation in peripheral glia and completely diminishes Presynaptic Homeostatic Potentiation (PHP) at the neuromuscular junction in Drosophila The synaptic deficits caused by Aβ overexpression in motoneurons are associated with motor function impairment at the adult stage. Moreover, we found that a Sphingosine analogue drug, Fingolimod, ameliorates synaptic homeostatic plasticity impairment, abnormal glial histone acetylation, and motor behavior defects in the Aβ models. We further demonstrated that perineurial glial Sphingosine kinase 2 (Sk2) is not only required for PHP, but also plays a beneficial role in modulating PHP in the Aβ models. Glial overexpression of Sk2 rescues PHP, glial histone acetylation, and motor function deficits that are associated with Aβ in Drosophila Finally, we showed that glial overexpression of Sk2 restores PHP and glial histone acetylation in a genetic loss-of-function mutant of the Spt-Ada-Gcn5 Acetyltransferase (SAGA) complex, strongly suggesting that Sk2 modulates PHP through epigenetic regulation. Both male and female animals were used in the experiments and analyses in this study. Collectively, we provided genetic evidence demonstrating that abnormal glial epigenetic alterations in Aβ models in Drosophila are associated with the impairment of PHP and that the Sphingosine signaling pathway displays protective activities in stabilizing synaptic physiology.Significance StatementFingolimod, an oral drug to treat Multiple Sclerosis, is phosphorylated by Sphingosine kinases to generate its active form. It is known that Fingolimod enhances the cognitive function in mouse models of Alzheimer's Disease (AD), but the role of Sphingosine kinases in AD is not clear. We bridge this knowledge gap by demonstrating the relationship between impaired homeostatic plasticity and AD. We show that Sphingosine kinase 2 (Sk2) in glial cells is necessary for homeostatic plasticity and glial Sk2-mediated epigenetic signaling has a protective role in synapse stabilization. Our findings demonstrate the potential of the glial Sphingosine signaling as a key player in glia-neuron interactions during homeostatic plasticity, suggesting it could be a promising target for sustaining synaptic function in AD.
 AIMS: The underlying mechanisms of atrial fibrillation (AF) are largely unknown. Inflammation may underlie atrial remodelling. Autoimmune diseases, related to increased systemic inflammation, may therefore be associated with new-onset AF. METHODS AND RESULTS: Participants from the population-based UK Biobank were screened for rheumatic fever, gastrointestinal autoimmune diseases, autoimmune diseases targeting the musculoskeletal system and connective tissues, and neurological autoimmune diseases. Between 2006 and 2022, participants were followed for incident AF. Cox proportional hazards regression analyses were performed to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) to quantify associations. 494 072 participants free from AF were included (median age 58.0 years, 54.8% women). After a median of 12.8 years, 27 194 (5.5%) participants were diagnosed with new-onset AF. Rheumatic fever without heart involvement (HR, 95% CI: 1.47, 1.26-1.72), Crohn's disease (1.23, 1.05-1.45), ulcerative colitis (1.17, 1.06-1.31), rheumatoid arthritis (1.39, 1.28-1.51), polyarteritis nodosa (1.82, 1.04-3.09), systemic lupus erythematosus (1.82, 1.41-2.35), and systemic sclerosis (2.32, 1.57-3.44) were associated with a larger AF risk. In sex-stratified analyses, rheumatic fever without heart involvement, multiple sclerosis, Crohn's disease, seropositive rheumatoid arthritis, psoriatic and enteropathic arthropathies, systemic sclerosis and ankylosing spondylitis were associated with larger AF risk in women, whereas only men showed a larger AF risk associated with ulcerative colitis. CONCLUSIONS: Various autoimmune diseases are associated with new-onset AF, more distinct in women. Our findings elaborate on the pathophysiological differences in autoimmunity and AF risk between men and women.
 The dysfunction of astrocytes in response to environmental factors contributes to many neurological diseases by impacting neuroinflammation responses, glutamate and ion homeostasis, and cholesterol and sphingolipid metabolism, which calls for comprehensive and high-resolution analysis. However, single-cell transcriptome analyses of astrocytes have been hampered by the sparseness of human brain specimens. Here, we demonstrate how large-scale integration of multi-omics data, including single-cell and spatial transcriptomic and proteomic data, overcomes these limitations. We created a single-cell transcriptomic dataset of human brains by integration, consensus annotation, and analyzing 302 publicly available single-cell RNA-sequencing (scRNA-seq) datasets, highlighting the power to resolve previously unidentifiable astrocyte subpopulations. The resulting dataset includes nearly one million cells that span a wide variety of diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis (MS), epilepsy (Epi), and chronic traumatic encephalopathy (CTE). We profiled the astrocytes at three levels, subtype compositions, regulatory modules, and cell-cell communications, and comprehensively depicted the heterogeneity of pathological astrocytes. We constructed seven transcriptomic modules that are involved in the onset and progress of disease development, such as the M2 ECM and M4 stress modules. We validated that the M2 ECM module could furnish potential markers for AD early diagnosis at both the transcriptome and protein levels. In order to accomplish a high-resolution, local identification of astrocyte subtypes, we also carried out a spatial transcriptome analysis of mouse brains using the integrated dataset as a reference. We found that astrocyte subtypes are regionally heterogeneous. We identified dynamic cell-cell interactions in different disorders and found that astrocytes participate in key signaling pathways, such as NRG3-ERBB4, in epilepsy. Our work supports the utility of large-scale integration of single-cell transcriptomic data, which offers new insights into underlying multiple CNS disease mechanisms where astrocytes are involved.
 High angular resolution diffusion imaging (HARDI) is a promising method for advanced analysis of brain microstructure. However, comprehensive HARDI analysis requires multiple acquisitions of diffusion images (multi-shell HARDI), which is time consuming and often impractical in clinical settings. This study aimed to establish neural network models that can predict new diffusion datasets from clinically feasible brain diffusion MRI for multi-shell HARDI. The development included 2 algorithms: multi-layer perceptron (MLP) and convolutional neural network (CNN). Both followed a voxel-based approach for model training (70%), validation (15%), and testing (15%). The investigations involved 2 multi-shell HARDI datasets: 1) 11 healthy subjects from the Human Connectome Project (HCP); and 2) 10 local subjects with multiple sclerosis (MS). To assess outcomes, we conducted neurite orientation dispersion and density imaging using both predicted and original data and compared their orientation dispersion index (ODI) and neurite density index (NDI) in different brain tissues with 2 measures: peak signal-to-noise ratio (PSNR) and structural similarity index measure (SSIM). Results showed that both models achieved robust predictions, which provided competitive ODI and NDI, especially in brain white matter. The CNN outperformed MLP with the HCP data on both PSNR (p < 0.001) and SSIM (p < 0.01). With the MS data, the models performed similarly. Overall, the optimized neural networks can help generate non-acquired brain diffusion MRI, which will make advanced HARDI analysis possible in clinical practice following further validation. Enabling detailed characterization of brain microstructure will allow enhanced understanding of brain function in both health and disease.
 In 2019, we embarked on a study on the economic burden of multiple sclerosis (MS) in Lebanon, in collaboration with a premier Lebanese MS center. This coincided with a triple disaster in Lebanon, comprising the drastic economic and financial crisis, the COVID-19 pandemic, and the consequences of the explosion of Beirut's port. Specifically, the economic and financial turmoil made the valuation of costs challenging. Researchers could face similar challenges, particularly in low- and middle-income countries (LMICs) where economic crises and recessions are recurrent phenomena. This paper aims to discuss steps taken to overcome the fluctuation of the prices of resources to get a valid valuation of societal costs during times of a financial and economic crisis. In the absence of local costing data and guidelines for conducting cost-of-illness (COI) studies, this paper provides empirical recommendations on the valuation of costs that are particularly relevant in LMICs. We recommend (1) clear reporting and justification of the country-specific context, year of costing, assumptions, data sources, and valuation methods, as well as the indicators used to adjust cost for inflation during different periods of fluctuation of prices; (2) collecting prices of each resource from multiple and various sources; (3) conducting a sensitivity analysis; and (4) reporting costs in local currency and Purchasing Power Parity dollars (PPP$). Precision and transparency in reporting prices of resources and their sources are markers of the reliability of the COI studies.
 Numerous factors can contribute to the development of neurodegenerative disorders (NDs), such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Oxidative stress (OS), a fairly common ND symptom, can be caused by more reactive oxygen species being made. In addition, the pathological state of NDs, which includes a high number of protein aggregates, could make chronic inflammation worse by activating microglia. Carotenoids, often known as "CTs", are pigments that exist naturally and play a vital role in the prevention of several brain illnesses. CTs are organic pigments with major significance in ND prevention. More than 600 CTs have been discovered in nature, and they may be found in a wide variety of creatures. Different forms of CTs are responsible for the red, yellow, and orange pigments seen in many animals and plants. Because of their unique structure, CTs exhibit a wide range of bioactive effects, such as anti-inflammatory and antioxidant effects. The preventive effects of CTs have led researchers to find a strong correlation between CT levels in the body and the avoidance and treatment of several ailments, including NDs. To further understand the connection between OS, neuroinflammation, and NDs, a literature review has been compiled. In addition, we have focused on the anti-inflammatory and antioxidant properties of CTs for the treatment and management of NDs.
 Various laboratories across the world have developed methods to study mitochondrial proteins/markers through extraction of mitochondrial RNA and protein to assess mitophagy/autophagy in Alzheimer's disease and other age-related diseases. Techniques outlined in this article include qRT-PCR, immunoblotting, immunofluorescence, transmission electron microscopy, Seahorse bioanalysis, staining for mitochondrial membrane potential, detection of mitophagy, and mitochondrial functional assays. Most of these techniques have been performed in vitro (in human and mouse neuronal cell lines transfected with mutant amyloid precursor protein or tau protein cDNAs) and in vivo (in brain tissues from different mouse models of Alzheimer's and other neurological diseases). Mitochondrial abnormalities in Alzheimer's disease have taken various forms, including excessive reactive oxygen species production, mitochondrial calcium dyshomeostasis, loss of ATP, defects in mitochondrial dynamics and transport, and mitophagy. Mitochondrial dysfunction is largely involved in aging; age-related diseases such as cancer, diabetes, and obesity; and neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, and others. The goal of this article is to make protocols/methods available to students, scholars, and researchers of mitochondria in order to facilitate future mitochondrial studies. © 2023 Wiley Periodicals LLC. Basic Protocol 1: Analyzing mitochondrial gene expression in mouse brain tissue and HT22 cells by qRT-PCR Basic Protocol 2: Analyzing protein expression in mouse brain tissue and HT22 cells by immunoblotting Basic Protocol 3: Immunofluorescence staining of cells and tissue sections Basic Protocol 4: Staining for mitochondrial membrane potential Basic Protocol 5: Assessing mitochondrial structure by transmission electron microscopy Basic Protocol 6: Methods for detecting mitophagy Basic Protocol 7: Bioenergetics assay via Seahorse Basic Protocol 8: Assays for mitochondrial function.
 BACKGROUND: Neurodegenerative diseases (NDDs) are characterized by progressive neuronal dysfunctionality which results in disability and human life-threatening events. In recent decades, NDDs are on the rise. Besides, conventional drugs have not shown potential effectiveness to attenuate the complications of NDDs. So, exploring novel therapeutic agents is an urgent need to combat such disorders. Accordingly, growing evidence indicates that polyphenols and alkaloids are promising natural candidates, possessing several beneficial pharmacological effects against diseases. Considering the complex pathophysiological mechanisms behind NDDs, Janus kinase (JAK), insulin receptor substrate (IRS), phosphoinositide 3-kinase (PI3K), and signal transducer and activator of transcription (STAT) seem to play critical roles during neurodegeneration/neuroregeneration. In this line, modulation of the JAK/STAT and IRS/PI3K signaling pathways and their interconnected mediators by polyphenols/alkaloids could play pivotal roles in combating NDDs, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), stroke, aging, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), depression and other neurological disorders. PURPOSE: Thus, the present study aimed to investigate the neuroprotective roles of polyphenols/alkaloids as multi-target natural products against NDDs which are critically passing through the modulation of the JAK/STAT and IRS/PI3K signaling pathways. STUDY DESIGN AND METHODS: A systematic and comprehensive review was performed to highlight the modulatory roles of polyphenols and alkaloids on the JAK/STAT and IRS/PI3K signaling pathways in NDDs, according to the PRISMA guideline, using scholarly electronic databases, including Scopus, PubMed, ScienceDirect, and associated reference lists. RESULTS: In the present study 141 articles were included from a total of 1267 results. The results showed that phenolic compounds such as curcumin, epigallocatechin-3-gallate, and quercetin, and alkaloids such as berberine could be introduced as new strategies in combating NDDs through JAK/STAT and IRS/PI3K signaling pathways. This is the first systematic review that reveals the correlation between the JAK/STAT and IRS/PI3K axis which is targeted by phytochemicals in NDDs. Hence, this review highlighted promising insights into the neuroprotective potential of polyphenols and alkaloids through the JAK/STAT and IRS/PI3K signaling pathway and interconnected mediators toward neuroprotection. CONCLUSION: Amongst natural products, phenolic compounds and alkaloids are multi-targeting agents with the most antioxidants and anti-inflammatory effects possessing the potential of combating NDDs with high efficacy and lower toxicity. However, additional reports are needed to prove the efficacy and possible side effects of natural products.
 [This corrects the article DOI: 10.3389/fncel.2023.1205261.].
 BACKGROUND: The neurofilament light chain (NfL) assay is gradually becoming an essential diagnostic tool for the diagnosis of many neurological diseases including amyotrophic lateral sclerosis (ALS). Different methods for the determination of this biomarker in serum have been developed in recent years. METHODS: We measured blood NfL in 429 patients referred to the tertiary ALS center of Montpellier, France using two different ultrasensitive methods (Ella™ and Simoa™) and we compared the clinical performances of these two approaches. We also converted NfL values into age and body mass index-adjusted Z-scores to assess cut-off values of this biomarker in this clinical context. RESULTS: We show comparable diagnostic and prognostic performance of Ella™ and Simoa™ technologies in ALS, with specificities and sensitivities exceeding 80% for both. We propose cut-off values for serum NfL in this clinical context, thus enabling the routine clinical use of this biomarker. CONCLUSION: The use of NfL in routine clinical practice will help predict survival and improve diagnostic accuracy by distinguishing ALS from other neurological diseases and motor neuron disease mimics.
 Siponimod (brand name Mayzent) is a sphingosine-1-phosphate (S1P) receptor modulator used in the treatment and management of relapsing forms of multiple sclerosis (MS) in adults. It works by targeting lymphocytes to decrease the number of circulating cells that are associated with MS symptomatic attacks and disease progression and may also have a direct neuroprotective impact. Siponimod strongly binds to the S1P type 1 and type 5 receptors that are abundantly expressed on lymphocytes and multiple other cell types in the central nervous system (CNS). Off-target interactions and effects on cardiac cells may occur, also. The use of a dose titration schedule is recommended to decrease the risk of bradycardia (see Table 1, Table 2) (1, 2). This medication is approved for multiple forms of relapsing MS (RMS) in the United States (1) and for active, secondary progressive disease in Europe and Canada (2, 3). Siponimod is metabolized by members of the cytochrome P450 family, specifically CYP2C9 and, to a lesser extent CYP3A4. The CYP2C9 gene is polymorphic and activity scores are used to categorize diplotype into phenotype. Decreased CYP2C9 metabolic activity is associated with increased exposure to siponimod and increased risk of adverse effects. Therefore, individuals with the CYP2C9*3/*3 diplotype (activity score = 0) are contraindicated from taking siponimod (1, 2). Individuals with one copy of the no-function *3 allele (diplotype with activity scores of 0.5 or 1.0) are advised to take half the standard maintenance dose (1, 2). Consideration of genotype and activity score is essential for CYP2C9-based siponimod dosing because labeled dose recommendations are not categorized by phenotype. In the US, there is a modified titration schedule for individuals with a CYP2C9*3 allele (Table 1)(1); however, the European prescribing guidelines do not modify the titration schedule for individuals with a single copy of the CYP2C9*3 allele (heterozygous for CYP2C9*3) (Table 2) (2). The Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Association for the Advancement of Pharmacy similarly recommends a 50% reduced maintenance dosage for intermediate metabolizers (IM) (Table 3) (4). It should be noted that dose recommendations in the Siponimod package label are limited to diplotypes consisting of only CYP2C9 *1,*2, and *3 alleles due to lack of clinical data on the impact of other decreased or no-function alleles(1), while other medication and testing guidelines also consider*5, *6, *8, and *11 (5, 6).
 Patients with multiple sclerosis (MS) and spinal cord injury (SCI) commonly sustain central neuropathic pain (NP) and spasticity. Despite a lack of consistent evidence, cannabis-based medicine (CBM) has been suggested as a supplement treatment. We aimed to investigate the effect of CBM on NP and spasticity in patients with MS or SCI. We performed a randomized, double-blinded, placebo-controlled trial in Denmark. Patients aged ≥18 years with NP (intensity >3, ≤9 on a numerical rating scale (NRS0-10) and/or spasticity (>3 on NRS0-10) were randomized to treatment consisting of either delta-9-tetrahydrocannabinol (THC), cannabidiol (CBD), a combination of THC&CBD in maximum doses of 22.5 mg, 45 mg and 22.5/45 mg per day, respectively, or placebo. A baseline registration was performed before randomization. Treatment duration was six weeks followed by a one-week phaseout. Primary endpoints were the intensity of patient-reported NP and/or spasticity. Between February 2019 and December 2021, 134 patients were randomized (MS n = 119, SCI n = 15), where 32 were assigned to THC, 31 to CBD, 31 to THC&CBD, and 40 to placebo. No significant difference was found for: mean pain intensity (THC 0.42 (-0.54-1.38), CBD 0.45 (-0.47-1.38) and THC&CBD 0.16 (-0.75-1.08)), mean spasticity intensity (THC 0.24 (-0.67-1.45), CBD 0.46 (-0.74-1.65), and THC&CBD 0.10 (-1.18-1.39), secondary outcomes (patient global impression of change and quality of life), or any tertiary outcomes. We aimed to include 448 patients in the trial; however, due to COVID-19 and recruitment challenges, fewer were included. Nevertheless, in this four-arm parallel trial, no effect was found between placebo and active treatment with THC or CBD alone or in combination on NP or spasticity in patients with either MS or SCI. The trial was registered with the EU Clinical Trials Register EudraCT (2018-002315-98).
 OBJECTIVES: The very rapidly approved mRNA-based vaccines against SARS-CoV-2 spike glycoprotein, including Pfizer-BioNTech BNT162b2, are effective in protecting from severe coronavirus disease 2019 (COVID-19) in immunocompetent population. However, establishing the duration and identifying correlates of vaccine-induced protection will be crucial to optimise future immunisation strategies. Here, we studied in healthy vaccine recipients and people with multiple sclerosis (pwMS), undergoing different therapies, the regulation of innate immune response by mRNA vaccination in order to correlate it with the magnitude of vaccine-induced protective humoral responses. METHODS: Healthy subjects (n = 20) and matched pwMS (n = 22) were longitudinally sampled before and after mRNA vaccination. Peripheral blood mononuclear cell (PBMC)-associated type I and II interferon (IFN)-inducible gene expression, serum innate cytokine/chemokine profile as well as binding and neutralising anti-SARS-COV-2 antibodies (Abs) were measured. RESULTS: We identified an early immune module composed of the IFN-inducible genes Mx1, OAS1 and IRF1, the serum cytokines IL-15, IL-6, TNF-α and IFN-γ and the chemokines IP-10, MCP-1 and MIG, induced 1 day post second and third BNT162b2 vaccine doses, strongly correlating with magnitude of humoral response to vaccination in healthy and MS vaccinees. Moreover, induction of the early immune module was dramatically affected in pwMS treated with fingolimod and ocrelizumab, both groups unable to induce a protective humoral response to COVID-19 vaccine. CONCLUSION: Overall, this study suggests that the vaccine-induced early regulation of innate immunity is mediated by IFN signalling, impacts on the magnitude of adaptive responses and it might be indicative of vaccine-induced humoral protection.
 Teaching Point: Multiple micronodular pneumocyte hyperplasia (MMPH) is a less-known presentation of tuberous sclerosis complex (TSC) associated lung disease that usually requires no treatment or follow-up imaging.
 Lymphangioleiomyomatosis (LAM) is a multisystem disorder that primarily affects the lung. Tuberous sclerosis complex (TSC) is characterized by multiple benign tumours of the skin, brain, eyes, heart, lung, liver, and kidney. LAM can be either sporadic (sporadic-LAM) or in association with Tuberous Sclerosis (TSC-LAM). Many clinical, radiologic, and pathologic features are shared between TSC and sporadic variants. We present a case admitted at The Indus Hospital Karachi with pneumothorax and multiple manifestations of TSC-LAM.
 Aim: To explore the neuroprotective potential of the secretome (conditioned medium, CM) derived from neurotrophic factors-primed mesenchymal stromal cells (MSCs; primed CM) using an endoplasmic reticulum (ER) stress-induced in vitro model system. Methods: Establishment of ER-stressed in vitro model, immunofluorescence microscopy, real-time PCR, western blot. Results: Exposure of ER-stressed Neuro-2a cells to the primed-CM significantly restored the neurite outgrowth parameters and improved the expression of neuronal markers like Tubb3 and Map2a in them compared with the naive CM. Primed CM also suppressed the induction of apoptotic markers Bax and Sirt1, inflammatory markers Cox2 and NF-κB, and stress kinases such as p38 and SAPK/JNK in the stress-induced cells. Conclusion: The secretome from primed MSCs significantly restored ER stress-induced loss of neuro-regenesis.
 Susceptibility tensor imaging (STI) is an emerging magnetic resonance imaging technique that characterizes the anisotropic tissue magnetic susceptibility with a second-order tensor model. STI has the potential to provide information for both the reconstruction of white matter fiber pathways and detection of myelin changes in the brain at mm resolution or less, which would be of great value for understanding brain structure and function in healthy and diseased brain. However, the application of STI in vivo has been hindered by its cumbersome and time-consuming acquisition requirement of measuring susceptibility induced MR phase changes at multiple head orientations. Usually, sampling at more than six orientations is required to obtain sufficient information for the ill-posed STI dipole inversion. This complexity is enhanced by the limitation in head rotation angles due to physical constraints of the head coil. As a result, STI has not yet been widely applied in human studies in vivo. In this work, we tackle these issues by proposing an image reconstruction algorithm for STI that leverages data-driven priors. Our method, called DeepSTI, learns the data prior implicitly via a deep neural network that approximates the proximal operator of a regularizer function for STI. The dipole inversion problem is then solved iteratively using the learned proximal network. Experimental results using both simulation and in vivo human data demonstrate great improvement over state-of-the-art algorithms in terms of the reconstructed tensor image, principal eigenvector maps and tractography results, while allowing for tensor reconstruction with MR phase measured at much less than six different orientations. Notably, promising reconstruction results are achieved by our method from only one orientation in human in vivo, and we demonstrate a potential application of this technique for estimating lesion susceptibility anisotropy in patients with multiple sclerosis.
 The recent emergence of a causal link between Epstein-Barr virus (EBV) and multiple sclerosis has generated considerable interest in the development of an effective vaccine against EBV. Here we describe a vaccine formulation based on a lymph node targeting Amphiphile vaccine adjuvant, Amphiphile-CpG, admixed with EBV gp350 glycoprotein and an engineered EBV polyepitope protein that includes 20 CD8(+) T cell epitopes from EBV latent and lytic antigens. Potent gp350-specific IgG responses are induced in mice with titers >100,000 in Amphiphile-CpG vaccinated mice. Immunization including Amphiphile-CpG also induces high frequencies of polyfunctional gp350-specific CD4(+) T cells and EBV-specific CD8(+) T cells that are 2-fold greater than soluble CpG and are maintained for >7 months post immunization. This combination of broad humoral and cellular immunity against multiple viral determinants is likely to provide better protection against primary infection and control of latently infected B cells leading to protection against the development of EBV-associated diseases.
 A highly efficient and robust multiple scales in silico protocol, consisting of atomistic Molecular Dynamics (MD), coarse-grain (CG) MD, and constant-pH CG Monte Carlo (MC), has been developed and used to study the binding affinities of selected antigen-binding fragments of the monoclonal antibody (mAbs) CR3022 and several of its here optimized versions against 11 SARS-CoV-2 variants including the wild type. Totally 235,000 mAbs structures were initially generated using the RosettaAntibodyDesign software, resulting in top 10 scored CR3022-like-RBD complexes with critical mutations and compared to the native one, all having the potential to block virus-host cell interaction. Of these 10 finalists, two candidates were further identified in the CG simulations to be the best against all SARS-CoV-2 variants. Surprisingly, all 10 candidates and the native CR3022 exhibited a higher affinity for the Omicron variant despite its highest number of mutations. The multiscale protocol gives us a powerful rational tool to design efficient mAbs. The electrostatic interactions play a crucial role and appear to be controlling the affinity and complex building. Studied mAbs carrying a more negative total net charge show a higher affinity. Structural determinants could be identified in atomistic simulations and their roles are discussed in detail to further hint at a strategy for designing the best RBD binder. Although the SARS-CoV-2 was specifically targeted in this work, our approach is generally suitable for many diseases and viral and bacterial pathogens, leukemia, cancer, multiple sclerosis, rheumatoid, arthritis, lupus, and more.
 BACKGROUND: Differentiating neuromyelitis optica spectrum disorder (NMOSD) from its mimics is crucial to avoid misdiagnosis, especially in the absence of aquaporin-4-IgG. While multiple sclerosis (MS) and myelin oligodendrocyte glycoprotein-IgG associated disease (MOGAD) represent major and well-defined differential diagnoses, non-demyelinating NMOSD mimics remain poorly characterized. METHODS: We conducted a systematic review on PubMed/MEDLINE to identify reports of patients with non-demyelinating disorders that mimicked or were misdiagnosed as NMOSD. Three novel cases seen at the authors' institutions were also included. The characteristics of NMOSD mimics were analyzed and red flags associated with misdiagnosis identified. RESULTS: A total of 68 patients were included; 35 (52%) were female. Median age at symptoms onset was 44 (range, 1-78) years. Fifty-six (82%) patients did not fulfil the 2015 NMOSD diagnostic criteria. The clinical syndromes misinterpreted for NMOSD were myelopathy (41%), myelopathy + optic neuropathy (41%), optic neuropathy (6%), or other (12%). Alternative etiologies included genetic/metabolic disorders, neoplasms, infections, vascular disorders, spondylosis, and other immune-mediated disorders. Common red flags associated with misdiagnosis were lack of cerebrospinal fluid (CSF) pleocytosis (57%), lack of response to immunotherapy (55%), progressive disease course (54%), and lack of magnetic resonance imaging gadolinium enhancement (31%). Aquaporin-4-IgG positivity was detected in five patients by enzyme-linked immunosorbent assay (n = 2), cell-based assay (n = 2: serum, 1; CSF, 1), and non-specified assay (n = 1). CONCLUSIONS: The spectrum of NMOSD mimics is broad. Misdiagnosis frequently results from incorrect application of diagnostic criteria, in patients with multiple identifiable red flags. False aquaporin-4-IgG positivity, generally from nonspecific testing assays, may rarely contribute to misdiagnosis.
 Liver cancer is closely linked to chronic inflammation. While observational studies have reported positive associations between extrahepatic immune-mediated diseases and systemic inflammatory biomarkers and liver cancer, the genetic association between these inflammatory traits and liver cancer remains elusive and merits further investigation. We conducted a two-sample Mendelian randomization (MR) analysis, using inflammatory traits as exposures and liver cancer as the outcome. The genetic summary data of both exposures and outcome were retrieved from previous genome-wide association studies (GWAS). Four MR methods, including inverse-variance-weighted (IVW), MR-Egger regression, weighted-median, and weighted-mode methods, were employed to examine the genetic association between inflammatory traits and liver cancer. Nine extrahepatic immune-mediated diseases, seven circulating inflammatory biomarkers, and 187 inflammatory cytokines were analyzed in this study. The IVW method suggested that none of the nine immune-mediated diseases were associated with the risk of liver cancer, with odds ratios of 1.08 (95% CI 0.87-1.35) for asthma, 0.98 (95% CI 0.91-1.06) for rheumatoid arthritis, 1.01 (95% CI 0.96-1.07) for type 1 diabetes, 1.01 (95% CI 0.98-1.03) for psoriasis, 0.98 (95% CI 0.89-1.08) for Crohn's disease, 1.02 (95% CI 0.91-1.13) for ulcerative colitis, 0.91 (95% CI 0.74-1.11) for celiac disease, 0.93 (95% CI 0.84-1.05) for multiple sclerosis, and 1.05 (95% CI 0.97-1.13) for systemic lupus erythematosus. Similarly, no significant association was found between circulating inflammatory biomarkers and cytokines and liver cancer after correcting for multiple testing. The findings were consistent across all four MR methods used in this study. Our findings do not support a genetic association between extrahepatic inflammatory traits and liver cancer. However, larger-scale GWAS summary data and more genetic instruments are needed to confirm these findings.
 Autophagy serves as a defense mechanism against intracellular pathogens, but several microorganisms exploit it for their own benefit. Accordingly, certain herpesviruses include autophagic membranes into their infectious virus particles. In this study, we analyzed the composition of purified virions of the Epstein-Barr virus (EBV), a common oncogenic γ-herpesvirus. In these, we found several components of the autophagy machinery, including membrane-associated LC3B-II, and numerous viral proteins, such as the capsid assembly proteins BVRF2 and BdRF1. Additionally, we showed that BVRF2 and BdRF1 interact with LC3B-II via their common protein domain. Using an EBV mutant, we identified BVRF2 as essential to assemble mature capsids and produce infectious EBV. However, BdRF1 was sufficient for the release of noninfectious viral envelopes as long as autophagy was not compromised. These data suggest that BVRF2 and BdRF1 are not only important for capsid assembly but together with the LC3B conjugation complex of ATG5-ATG12-ATG15L1 are also critical for EBV envelope release.
 BACKGROUND AND PURPOSE: Longitudinally extensive transverse myelitis (LETM) associated with aquaporin-4 autoantibodies (AQP4-IgG) can cause severe disability. Early diagnosis and prompt treatment are critical to prevent relapses. A novel score is described based on clinical and neuroimaging characteristics that predicts AQP4-IgG positivity in patients with LETM. METHODS: Patients were enrolled both retrospectively and prospectively from multiple Italian centers. Clinical and neuroimaging characteristics of AQP4-IgG positive and negative patients were compared through univariate and multivariate analysis. RESULTS: Sixty-six patients were included. Twenty-seven (41%) were AQP4-IgG positive and median age at onset was 45.5 years (range 19-81, interquartile range 24). Female sex (odds ratio [OR] 17.9, 95% confidence interval [CI] 2.6-381.9; p = 0.014), tonic spasms (OR 45.6, 95% CI 3.1-2197; p = 0.017) and lesion hypointensity on T1-weighted images (OR 52.9, 95% CI 6.8-1375; p = 0.002) were independently associated with AQP4-IgG positivity. The AQP4-IgG positivity in myelitis (AIM) score predicted AQP4-IgG positivity with 85% sensitivity and 95% specificity. Positive and negative likelihood ratios were 16.6 and 0.2 respectively. The inter-rater and intra-rater agreement in the score application were both excellent. CONCLUSIONS: The AIM score predicts AQP4-IgG positivity with good sensitivity and specificity in patients with a first episode of LETM. The score may assist clinicians in early diagnosis and treatment of AQP4-IgG positive LETM.
 Multiple sclerosis (MS) is a neuroinflammatory disease characterized by CD4[Formula: see text] T cell-mediated immune cell infiltration and demyelination in the central nervous system (CNS). The subtypes of CD4[Formula: see text] T cells are T helper cells 1 (Th1), Th2, Th17, and regulatory T cells (Treg), while three other types of cells besides Th2 play a key role in MS and its classic animal model, experimental autoimmune encephalomyelitis (EAE). Tregs are responsible for immunosuppression, while pathogenic Th1 and Th17 cells cause autoimmune-associated demyelination. Therefore, suppressing Th1 and Th17 cell differentiation and increasing the percentage of Treg cells may contribute to the treatment of EAE/MS. Astragali Radix (AR) is a representative medicine with immunoregulatory, anti-inflammatory, antitumor, and neuroprotective effects.The active ingredients in AR include astragalus flavones, polysaccharides, and saponins. In this study, it was found that the total flavonoids of Astragus (TFA) could effectively treat EAE in mice by ameliorating EAE motor disorders, reducing inflammatory damage and demyelination, inhibiting the proportion of Th17 and Th1 cells, and promoting Tregs differentiation by regulating the JAK/STAT and NF[Formula: see text]B signaling pathways. This novel finding may increase the possibility of using AR or TFA as a drug with immunomodulatory effects for the treatment of autoimmune diseases.
 PURPOSE: To compare percutaneous balloon compression (PBC) and radiofrequency thermocoagulation (RFTC) for the treatment of trigeminal neuralgia. METHODS: This was a retrospective single-center analysis of data from 230 patients with trigeminal neuralgia who underwent 202 PBC (46%) and 234 RFTC (54%) from 2002 to 2019. Comparison of demographic data and trigeminal neuralgia characteristics between procedures as well as assessment of 1) initial pain relief by an improved Barrow Neurological Institute (BNI) pain intensity scale of I-III; 2) recurrence-free survival of patients with a follow-up of at least 6 months by Kaplan-Meier analysis; 3) risk factors for failed initial pain relief and recurrence-free survival by regression analysis; and 4) complications and adverse events. RESULTS: Initial pain relief was achieved in 353 (84.2%) procedures and showed no significant difference between PBC (83.7%) and RFTC (84.9%). Patients who suffered from multiple sclerosis (odds ratio 5.34) or had a higher preoperative BNI (odds ratio 2.01) showed a higher risk of not becoming pain free. Recurrence-free survival in 283 procedures was longer for PBC (44%) with 481 days compared to RFTC (56%) with 421 days (p=0.036) but without statistical significance. The only factors that showed a significant influence on longer recurrence-free survival rates were a postoperative BNI ≤ II (P=<0.0001) and a BNI facial numbness score ≥ 3 (p = 0.009). The complication rate of 22.2% as well as zero mortality showed no difference between the two procedures (p=0.162). CONCLUSION: Both percutaneous interventions led to a comparable initial pain relief and recurrence-free survival with a low and comparable probability of complications. An individualized approach, considering the advantages and disadvantages of each intervention, should guide the decision-making process. Prospective comparative trials are urgently needed.
 AIM: Multiple sclerosis (MS) is an autoimmune disease, and its typical characteristics are neuroinflammation and the demyelination of neurons in the central nervous system (CNS). Sterile alpha and TIR motif containing 1 (SARM1) is an essential factor mediating axonal degeneration and SARM1 deletion reduces the neuroinflammation in spinal cord injury. This study aimed to explore the roles of SARM1 and its underlying mechanisms in MS. METHODS: Experimental autoimmune encephalomyelitis (EAE, a model of MS) model was established. Immunostaining, western blot, electron microscope, and HE staining were used to examine the pathological manifestations such as inflammation, demyelination, and neuronal death in SARM1(f/f) EAE mice and SARM1(Nestin) -CKO EAE mice. In addition, RNA-seq, real-time PCR and double-immunostaining were used to examine the underlying mechanism of SARM1 in EAE mice. RESULTS: SARM1 was upregulated in neurons of the spinal cords of EAE mice. SARM1 knockout in CNS ameliorated EAE with less neuroinflammation, demyelination, and dead neurons. Mechanically, SARM1 knockout resulted in the reduction of insulin-like growth factor (IGF)-binding protein 2 (IGFBP2) in neurons of EAE mice, which might inhibit the neuroinflammation through inhibiting NF-κB signaling. Finally, activation of NF-κB partially aggravated the neuroinflammation and demyelination deficits of SARM1(Nestin) -CKO EAE mice. CONCLUSIONS: These results identified the unknown role of SARM1 in the promotion of neuroinflammation and demyelination and revealed a novel drug target pathway of SARM1/IGFBP2/NF-κB for MS.
 Schizophrenia is a multifactorial disorder, the genetic architecture of which remains unclear. Although many studies have examined the etiology of schizophrenia, the gene sets that contribute to its symptoms have not been fully investigated. In this study, we aimed to identify each gene set associated with corresponding symptoms of schizophrenia using the postmortem brains of 26 patients with schizophrenia and 51 controls. We classified genes expressed in the prefrontal cortex (analyzed by RNA-seq) into several modules by weighted gene co-expression network analysis (WGCNA) and examined the correlation between module expression and clinical characteristics. In addition, we calculated the polygenic risk score (PRS) for schizophrenia from Japanese genome-wide association studies, and investigated the association between the identified gene modules and PRS to evaluate whether genetic background affected gene expression. Finally, we conducted pathway analysis and upstream analysis using Ingenuity Pathway Analysis to clarify the functions and upstream regulators of symptom-related gene modules. As a result, three gene modules generated by WGCNA were significantly correlated with clinical characteristics, and one of these showed a significant association with PRS. Genes belonging to the transcriptional module associated with PRS significantly overlapped with signaling pathways of multiple sclerosis, neuroinflammation, and opioid use, suggesting that these pathways may also be profoundly implicated in schizophrenia. Upstream analysis indicated that genes in the detected module were profoundly regulated by lipopolysaccharides and CREB. This study identified schizophrenia symptom-related gene sets and their upstream regulators, revealing aspects of the pathophysiology of schizophrenia and identifying potential therapeutic targets.
 BACKGROUND: People with neuromyelitis optica spectrum disorder (pwNMOSD) experience debilitating neurological attacks, resulting in permanent disability. OBJECTIVE: To evaluate if high-efficacy treatment was better than traditional agents at preventing disease advancement in pwNMOSD. METHODS: A retrospective study of pwNMOSD at one academic center was performed. Timelines were created for treatments subjects were exposed to along with clinical/radiological events related to disease worsening. High-efficacy treatments included eculizumab, inebilizumab, satralizumab, rituximab, ocrelizumab, tocilizumab, and sarilumab while therapies such as azathioprine, methotrexate, cyclophosphamide, and mycophenolate mofetil were classified as traditional agents. Poisson regression and mixed effects logistics models were constructed, and a subject-specific random intercept was used for intrasubject correlation. RESULTS: Of 189 pwNMOSD identified, 161 were aquaporin-4 IgG positive (AQP4 +) with 92 (77 female; median disease duration (MDD) (range) of 6.6 years (y) (1.2-18.6)) exposed only to high-efficacy therapy, 33 (28 female; 10.4 y (0.8-32.7)) only to traditional therapy, and 64 (54 female; 10.8 y (0.7-20.2)) to both. High-efficacy treatments reduced the rate of MRI advancement by 62.4% (95% CrI = [- 86.9%, - 16.8%]), relapses by 99.8% (95% CrI = [- 99.9%, - 99.6%]), and hospitalizations by 99.3% (95% CrI = [- 99.6%, - 98.8%]) when compared to traditional treatments. For AQP4 + subjects, a 655.7-fold increase in the odds of new spinal cord lesion development (95% CrI = [+ 37.4-fold, + 3239.5-fold]) was observed with traditional agents (p < 0.0001). CONCLUSION: High-efficacy treatments maximize opportunity for preventing disease advancement in newly diagnosed and established pwNMOSD.
 Large-scale epidemiological studies suggest that veterans may have poorer physical health than nonveterans, but this has been largely unexamined in post-9/11 veterans despite research indicating their high levels of disability and healthcare utilization. Additionally, little investigation has been conducted on sex-based differences and interactions by veteran status. Notably, few studies have explored veteran physical health in relation to national health guidelines. Self-reported, weighted data were analyzed on post-9/11 U.S. veterans and nonveterans (n = 19,693; 6,992 women, 12,701 men; 15,160 veterans, 4,533 nonveterans). Prevalence was estimated for 24 physical health conditions classified by Healthy People 2020 targeted topic areas. Associations between physical health outcomes and veteran status were evaluated using bivariable and multivariable analyses. Back/neck pain was most reported by veterans (49.3 %), twice that of nonveterans (22.8 %)(p < 0.001). Adjusted odds ratios (AORs) for musculoskeletal and hearing disorders, traumatic brain injury, and chronic fatigue syndrome (CFS) were 3-6 times higher in veterans versus nonveterans (p < 0.001). Women versus men had the greatest adjusted odds for bladder infections (males:females, AOR = 0.08, 95 % CI:0.04-0.18)(p < 0.001), and greater odds than men for multiple sclerosis, CFS, cancer, irritable bowel syndrome/colitis, respiratory disease, some musculoskeletal disorders, and vision loss (p < 0.05). Cardiovascular-related conditions were most prominent for men (p < 0.001). Veteran status by sex interactions were found for obesity (p < 0.03; greater for male veterans) and migraine (p < 0.01; greater for females). Healthy People 2020 targeted topic areas exclude some important physical health conditions that are associated with being a veteran. National health guidelines for Americans should provide greater consideration of veterans in their design.
 BACKGROUND AND PURPOSE: Commercially available tests for Yo antibody detection have low specificity for paraneoplastic cerebellar degeneration (PCD) because these assays use cerebellar degeneration-related protein 2 (CDR2) as the antigen, not CDR2-like (CDR2L). We aimed to test the hypothesis that use of a CDR2L cell-based assay (CBA), as an additional screening technique, would increase the accuracy of Yo-PCD diagnosis. METHODS: An in-house CBA to test for anti-CDR2L antibodies was developed and used to screen sera from 48 patients with confirmed anti-Yo-associated PCD. Fifteen non-Yo PCD patients, 22 patients with ovarian cancer without neurological syndromes, 50 healthy blood donors, 10 multiple sclerosis, 15 Parkinson's disease, and five non-paraneoplastic ataxic patients were included as controls. Sera were also tested by western blot analysis using recombinant CDR2 and CDR2L proteins developed in house, by the commercially available line immunoassays from Ravo Diagnostika and Euroimmun, and by the CDR2 CBA from Euroimmun. RESULTS: The CDR2L CBA identified all 48 patients with Yo-PCD. No CDR2L CBA reaction was observed in any of the control sera. The western blot technique had lower sensitivity and specificity as sera from eight and six of the 48 Yo-PCD patients did not react with recombinant CDR2 or CDR2L, respectively. CONCLUSIONS: The CDR2L CBA is highly reliable for identification of Yo-PCD. Although our findings indicate that, currently, the combination of CDR2 and CDR2L yields the most reliable test results, it remains to be evaluated if a test for single anti-CDR2L positivity will serve as a sufficient biomarker for Yo-PCD diagnosis.
 Vitamin D3 is a secosteroid, broad-spectrum immunomodulatory, antioxidant, and anti-inflammatory hormone produced either by the internal subcutaneous pathway in the presence of ultraviolet B (UVB) rays or by the external pathway in the form of supplements. Vitamin D3 deficiency is a common and reversible contributor to mortality and morbidity among critically ill patients, including Coronavirus Disease 2019 (COVID-19) and other viral infections. The major functions of vitamin D3 are inhibiting the proinflammatory pathways, including nuclear factor kappa B (NF-kB), inflammatory cytokines, such as interleukin-6 (ILs-6), interleukin-18 (ILs-18), and tumour necrosis factor (TNF), preventing the loss of neural sensation in COVID-19, maintaining respiratory homeostasis, and acting as an antiviral, antimalarial, and antihypertensive agent. Vitamin D3 has an important role in reversing the COVID-19 infection in patients who have previously suffered from a neurological disease, such as Alzheimer's disease, Parkinson disease, motor neuron disease, multiple sclerosis, Creutzfeldt-Jakob disease, stroke, cardiovascular problems, headache, sleep-associated disorder, and others. Moreover, vitamin D3 plays a key role in regulating the gene expression of different pro-inflammatory cytokines. In addition to the information provided above, the current review article provides the most recent information on Vitamin D against COVID-19 with comorbid neurological disorders. Furthermore, we present the most recent advancement and molecular mechanism of action of vitamin D3. Diabetes, cardiovascular disease, and neurological disorders are comorbid conditions, and vitamin D3 is a critical regulator of COVID-19 infection during these conditions. In the midst of the COVID-19 epidemic, factors such as sex, latitudes, nutrition, demography, pollution, and gut microbiota warrants for additional research on vitamin D supplements.
 BACKGROUND: walking is crucial for an active and healthy ageing, but the perspectives of individuals living with walking impairment are still poorly understood. OBJECTIVES: to identify and synthesise evidence describing walking as experienced by adults living with mobility-impairing health conditions and to propose an empirical conceptual framework of walking experience. METHODS: we performed a systematic review and meta-ethnography of qualitative evidence, searching seven electronic databases for records that explored personal experiences of walking in individuals living with conditions of diverse aetiology. Conditions included Parkinson's disease, multiple sclerosis, chronic obstructive pulmonary disease, hip fracture, heart failure, frailty and sarcopenia. Data were extracted, critically appraised using the NICE quality checklist and synthesised using standardised best practices. RESULTS: from 2,552 unique records, 117 were eligible. Walking experience was similar across conditions and described by seven themes: (i) becoming aware of the personal walking experience, (ii) the walking experience as a link between individuals' activities and sense of self, (iii) the physical walking experience, (iv) the mental and emotional walking experience, (v) the social walking experience, (vi) the context of the walking experience and (vii) behavioural and attitudinal adaptations resulting from the walking experience. We propose a novel conceptual framework that visually represents the walking experience, informed by the interplay between these themes. CONCLUSION: a multi-faceted and dynamic experience of walking was common across health conditions. Our conceptual framework of the walking experience provides a novel theoretical structure for patient-centred clinical practice, research and public health.
 INTRODUCTION: The aminoadamantanes amantadine and memantine are well known. They mainly act as N-methyl-D-aspartate antagonists. AREAS COVERED: The antiviral drug amantadine moderately ameliorates impaired motor behavior in patients with Parkinson's disease. Memantine provides beneficial effects on memory function in patients with advanced Alzheimer's disease already treated with acetylcholine esterase inhibitors. Both compounds counteract impaired monoamine neurotransmission with associated symptoms, such as depression. They improve vigilance, lack of attention and concentration, fatigue syndromes according to clinical findings in patients with chronic neurodegenerative processes. Their extrasynaptic N-methyl-D-Aspartate receptor blockade weakens a prolonged influx of Ca(2+) ions as the main responsible components of neuronal excitotoxicity. This causes neuronal dying and associated functional deficits. EXPERT OPINION: We suggest aminoadamantanes as future therapies for amelioration of short- and long-term consequences of a COVID 19 infection. Particularly the extended-release amantadine formulations will be suitable. They showed better clinical efficacy compared with the conventional available compounds. Amantadine may particularly be suitable for amelioration of fatigue or chronic exhaustion, memantine for improvement of cognitive deficits. Clinical research in patients, who are affected by the short- and long-term consequences of a COVID 19 infection, is warranted to confirm these still hypothetical putative beneficial effects of aminoadamantanes.
 Curcumin (CUR) is a polyphenol extracted from the rhizome of Curcuma longa that possesses potent anti-inflammatory and antioxidant potential. Despite CUR's numerous beneficial effects on human health, it has limitations, such as poor absorption. Nano-based drug delivery systems have recently been applied to improve CUR's solubility and bioavailability and potentialize its health effects. This review investigated the effects of different CUR-based nanomedicines on inflammatory and immunomodulated diseases. PUBMED, EMBASE, COCHRANE, and GOOGLE SCHOLAR databases were searched, and the Scale for Assessment of Narrative Review Articles (SANRA) was used for quality assessment and PRISMA guidelines. Overall, 66 studies were included comprising atherosclerosis, rheumatoid arthritis (RA), Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), Huntington's disease (HD), inflammatory bowel diseases (IBD), psoriasis, liver fibrosis, epilepsy, and COVID-19. The available scientific studies show that there are many known nanoformulations with curcumin. They can be found in nanosuspensions, nanoparticles, nanoemulsions, solid lipid particles, nanocapsules, nanospheres, and liposomes. These formulations can improve CUR bioavailability and can effectively be used as adjuvants in several inflammatory and immune-mediated diseases such as atheroma plaque formation, RA, dementia, AD, PD, MS, IBD, psoriasis, epilepsy, COVID-19, and can be used as potent anti-fibrotic adjuvants in fibrotic liver disease.
 BACKGROUND: Although Deep Brain Stimulation (DBS) is a safe and proven treatment modality for patients suffering from debilitating movement and neuropsychiatric disorders, it is not free from complications. Management of skin erosion and infection following DBS surgery constitutes a challenge in everyday clinical practice. OBJECTIVES: Skin-related complications were evaluated in patients who underwent DBS surgery due to Parkinson's disease (PD), dystonia, essential tremor (ET), and other indications including Tourette syndrome (TS), Obsessive-Compulsive Disorder (OCD), and epilepsy. METHODS: A retrospective analysis of clinical data was performed on patients who underwent DBS surgery between November 2008 and September 2021 at the Department of Neurosurgery, Institute of Psychiatry and Neurology, Warsaw. RESULTS: 525 patients who underwent 927 DBS leads implantations were included in the analysis. There were 398 patients with PD, 80 with dystonia, 26 with ET, 7 with drug-resistant epilepsy, 5 with Multiple Sclerosis, 4 with Holme's or cerebellar tremor, 3 with TS, and 2 with OCD. 42 patients (8,0%) had 78 skin infection episodes. The overall level of skin erosion was 3,8% (20/525 patients). The risk of developing infection episode was connected with younger age at diagnosis (p = 0.017) and at surgery (p = 0.023), whereas the development of skin erosion was connected with the dystonia diagnosis (p = 0.012). Patients with dystonia showed the highest rate of infections and erosions (11/70 and 7/70 patients retrospectively). DISCUSSION: Postoperative skin complications are a serious side effect of DBS surgery. CONCLUSION: Our study suggests that dystonic patients are at higher risk of developing skin-related complications after DBS surgery.
 INTRODUCTION: The adoption of a Care Pathway (CP) allows the healthcare management of patients suffering from high-epidemiological impact chronic diseases. The continuity of care of these patients is one of the main purposes of the community-based healthcare reform, foreseen in the 6th Mission of the National recovery and resilience plan. Fondazio-ne Ricerca e Salute (ReS) collects and analyses regional CPs approved in Italy, through the Pdta Net database. METHODS: Fondazione ReS has retrieved all the CPs approved by Italian Regions and Autonomous provinces until 12/31/2021 within institutional websites, through specific keywords. The quali- and quantitative analysis of CPs was based on the approving Region, the publication year, the disease (distinguishing between high-epidemiological impact chronic diseases and rare conditions) and clinical area. Following the 5-year experience gained by Fondazione ReS in terms of CPs' aims and organization for the full realization of an evidence-based healthcare of chronic patients, all data collected until 12/31/2021 underwent an in-depth double-blinded quality control. This control was aimed to make the Pdta Net database as representative as possible of the existing documents closest to a real CP. RESULTS: From 2005 to 2021, 729 regional CPs have been approved: 404 on high-impact chronic diseases and 220 on rare conditions. The CPs of chronic diseases, mostly edited by Piemonte (45 CPs), Campania (34) and Toscana (33) Regions, mainly concern on diabetes (19), chronic obstructive pulmonary disease (15), heart failure (13), stroke, multiple sclerosis and colorectal neoplasms (12 each one), breast cancer (11), dementia and chronic kidney disease (10 each one). Most of the CPs on rare diseases have been edited by Regions with an established Rare Disease Network, i.e., Lombardia (125 CPs), Lazio (74) and Toscana (40): neurology (61) and oncology (52) were the most represented clinical areas. CONCLUSIONS: The high number of CPs approved in Italy confirms an increasing interest of the healthcare institutions. The collected CPs show an extreme variety of titles, text structures and disease choices. Given the absence of an institutional observatory and of devotees of shared and harmonized CPs, annually Pdta Net makes available an updated and complete overview of these governance tools, which are essential for the upcoming changes of the Italian national health service.
 The Toulouse-Piéron Cancelation Test (TP) is a classic psychometric tool for the assessment of selective/sustained attention, processing speed and visuo-perceptual abilities. It is commonly used in neurological disorders such as epilepsy, multiple sclerosis or Alzheimer's disease. It encompasses two main indexes: Work-Efficiency (WE) and Dispersion-Index (DI). The aim of this study is to provide normative scores for the TP in a sample of Portuguese healthy adults. The TP was administered to a convenience sample of 357 cognitively-dwelling subjects aged between [45 and 86] years old, following a standard assessment protocol. The normative scores were adjusted for age and education. Education was the main predictor of TP-WE (R(2) = .310), whereas the influence of age on this score was lower (R(2) = .191). These two variables explained 50.1% of the variance of the results. Regarding TP-DI, education was also the main predictor of the results (R(2) = .039), whereas age was responsible for R(2) = .011 and together, they explained 5% of the variance of TP-DI. TP performances are strongly influenced by age and education. This is the first study focused on the establishment of normative data after the age of 45 in the Portuguese population, allowing a reliable assessment in both clinical and research contexts.
 BACKGROUND: The IL-17 (interleukin 17) family consists of six structurally related pro-inflammatory cytokines, namely IL-17A to IL-17F. These cytokines have garnered significant scientific interest due to their pivotal role in the pathogenesis of various diseases. Notably, a specific subset of T-cells expresses IL-17 family members, highlighting their importance in immune responses against microbial infections. INTRODUCTION: IL-17 cytokines play a critical role in host defense mechanisms by inducing cytokines and chemokines, recruiting neutrophils, modifying T-cell differentiation, and stimulating the production of antimicrobial proteins. Maintaining an appropriate balance of IL-17 is vital for overall health. However, dysregulated production of IL-17A and other members can lead to the pathogenesis of numerous inflammatory and autoimmune diseases. METHOD: This review provides a comprehensive overview of the IL-17 family and its involvement in several inflammatory and autoimmune diseases. Relevant literature and research studies were analyzed to compile the data presented in this review. RESULTS: IL-17 cytokines, particularly IL-17A, have been implicated in the development of various inflammatory and autoimmune disorders, including multiple sclerosis, Hashimoto's thyroiditis, systemic lupus erythematosus, pyoderma gangrenosum, autoimmune hepatic disorders, rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis, osteoarthritis, and graft-versus-host disease. Understanding the role of IL-17 in these diseases is crucial for developing targeted therapeutic strategies. CONCLUSION: The significant involvement of IL-17 cytokines in inflammatory and autoimmune diseases underscores their potential as therapeutic targets. Current treatments utilizing antibodies against IL-17 cytokines and IL-17RA receptors have shown promise in managing these conditions. This review consolidates the understanding of IL-17 family members and their roles, providing valuable insights for the development of novel immunomodulators to effectively treat inflammatory and autoimmune diseases.
 Chemokines secreted by dendritic cells (DCs) play a key role in the regulation of inflammation and autoimmunity through chemokine receptors. However, the role of chemokine receptor CXCR1 in inflammation-inducing experimental autoimmune encephalomyelitis (EAE) and acute respiratory distress syndrome (ARDS) remains largely enigmatic. Here we reported that compared with healthy controls, the level of CXCR1 was aberrantly increased in multiple sclerosis (MS) patients. Knockout of CXCR1 not only ameliorated disease severity in EAE mice but also suppressed the secretion of inflammatory factors (IL-6/IL-12p70) production. We observed the same results in EAE mice with DCs-specific deletion of CXCR1 and antibody neutralization of the ligand CXCL5. Mechanically, we demonstrated a positive feedback loop composed of CXCL5/CXCR1/HIF-1α direct regulating of IL-6/IL-12p70 production in DCs. Meanwhile, we found CXCR1 deficiency in DCs limited IL-6/IL-12p70 production and lung injury in LPS-induced ARDS, a disease model caused by inflammation. Overall, our study reveals CXCR1 governs DCs-mediated inflammation and autoimmune disorders and its potential as a therapeutic target for related diseases.
 Traumatic brain injury (TBI) is a debilitating mental condition which causes physical disability and morbidity worldwide. TBI may damage the brain by direct injury that subsequently triggers a series of neuroinflammatory events. The activation of NLRP3 inflammasome and dysregulated host immune system has been documented in various neurological disorders such as TBI, ischemic stroke and multiple sclerosis. The activation of NLRP3 post-TBI increases the production of pro-inflammatory cytokines and caspase-1, which are major drivers of neuroinflammation and apoptosis. Similarly, GSK-3β regulates apoptosis through tyrosine kinase and canonical Wnt signalling pathways. Thus, therapeutic targeting of NLRP3 inflammasome and GSK-3β has emerged as promising strategies for regulating the post-TBI neuroinflammation and neurobehavioral disturbances. In this review, we discuss the identification & development of several structurally diverse and pharmacologically interesting small molecule inhibitors for targeting the NLRP3 inflammasome and GSK-3β in the management of TBI.
 The central nervous system/peripheral nervous system (CNS/PNS) extracellular matrix is a dynamic and highly interactive space-filling, cell-supportive, matrix-stabilising, hydrating entity that creates and maintains tissue compartments to facilitate regional ionic micro-environments and micro-gradients that promote optimal neural cellular activity. The CNS/PNS does not contain large supportive collagenous and elastic fibrillar networks but is dominated by a high glycosaminoglycan content, predominantly hyaluronan (HA) and collagen is restricted to the brain microvasculature, blood-brain barrier, neuromuscular junction and meninges dura, arachnoid and pia mater. Chondroitin sulphate-rich proteoglycans (lecticans) interactive with HA have stabilising roles in perineuronal nets and contribute to neural plasticity, memory and cognitive processes. Hyaluronan also interacts with sialoproteoglycan associated with cones and rods (SPACRCAN) to stabilise the interphotoreceptor matrix and has protective properties that ensure photoreceptor viability and function is maintained. HA also regulates myelination/re-myelination in neural networks. HA fragmentation has been observed in white matter injury, multiple sclerosis, and traumatic brain injury. HA fragments (2 × 10(5)  Da) regulate oligodendrocyte precursor cell maturation, myelination/remyelination, and interact with TLR4 to initiate signalling cascades that mediate myelin basic protein transcription. HA and its fragments have regulatory roles over myelination which ensure high axonal neurotransduction rates are maintained in neural networks. Glioma is a particularly invasive brain tumour with extremely high mortality rates. HA, CD44 and RHAMM (receptor for HA-mediated motility) HA receptors are highly expressed in this tumour. Conventional anti-glioma drug treatments have been largely ineffective and surgical removal is normally not an option. CD44 and RHAMM glioma HA receptors can potentially be used to target gliomas with PEP-1, a cell-penetrating HA-binding peptide. PEP-1 can be conjugated to a therapeutic drug; such drug conjugates have successfully treated dense non-operative tumours in other tissues, therefore similar applications warrant exploration as potential anti-glioma treatments.
 Biomaterials allow for the precision control over the combination and release of cargo needed to engineer cell outcomes. These capabilities are particularly attractive as new candidate therapies to treat autoimmune diseases, conditions where dysfunctional immune cells create pathogenic tissue environments during attack of self-molecules termed self-antigens. Here we extend past studies showing combinations of a small molecule immunomodulator co-delivered with self-antigen induces antigen-specific regulatory T cells. In particular, we sought to elucidate how different ratios of these components loaded in degradable polymer particles shape the antigen presenting cell (APC) -T cell interactions that drive differentiation of T cells toward either inflammatory or regulatory phenotypes. Using rapamycin (rapa) as a modulatory cue and myelin self-peptide (myelin oligodendrocyte glycoprotein- MOG) - self-antigen attacked during multiple sclerosis (MS), we integrate these components into polymer particles over a range of ratios and concentrations without altering the physicochemical properties of the particles. Using primary cell co-cultures, we show that while all ratios of rapa:MOG significantly decreased expression of co-stimulation molecules on dendritic cells (DCs), these levels were insensitive to the specific ratio. During co-culture with primary T cell receptor transgenic T cells, we demonstrate that the ratio of rapa:MOG controls the expansion and differentiation of these cells. In particular, at shorter time points, higher ratios induce regulatory T cells most efficiently, while at longer time points the processes are not sensitive to the specific ratio. We also found corresponding changes in gene expression and inflammatory cytokine secretion during these times. The in vitro results in this study contribute to in vitro regulatory T cell expansion techniques, as well as provide insight into future studies to explore other modulatory effects of rapa such as induction of maintenance or survival cues.
 Interleukin-6 upregulation leads to various acute phase reactions such as local inflammation and systemic inflammation in many diseases like cancer, multiple sclerosis, rheumatoid arthritis, anemia, and Alzheimer's disease stimulating JAK/STAT3, Ras/MAPK, PI3K-PKB/Akt pathogenic pathways. Since no small molecules are available in the market against IL-6 till now, we have designed a class of small bioactive 1,3 - indanedione (IDC) molecules for inhibiting IL-6 using a decagonal approach computational studies. The IL-6 mutations were mapped in the IL-6 protein (PDB ID: 1ALU) from thorough pharmacogenomic and proteomics studies. The protein-drug interaction networking analysis for 2637 FFDA-approved drugs with IL-6 protein using Cytoscape software showed that 14 drugs have prominent interactions with IL-6. Molecular docking studies showed that the designed compound IDC-24 (-11.8 kcal/mol) and methotrexate (-5.20) bound most strongly to the 1ALU south asian population mutated protein. MMGBSA results indicated that IDC-24 (-41.78 kcal/mol) and methotrexate (-36.81 kcal/mol) had the highest binding energy when compared to the standard molecules LMT-28 (-35.87 kcal/mol) and MDL-A (-26.18 kcal/mol). These results we substantiated by the molecular dynamic studies in which the compound IDC-24 and the methotrexate had the highest stability. Further, the MMPBSA computations produced energies of -28 kcal/mol and -14.69 kcal/mol for IDC-24 and LMT-28. KDeep absolute binding affinity computations revealed energies of -5.81 kcal/mol and -4.74 kcal/mol for IDC-24 and LMT-28 respectively. Finally, our decagonal approach established the compound IDC-24 from the designed 1,3-indanedione library and methotrexate from protein drug interaction networking as suitable HITs against IL-6.
 Metabolic syndrome (MetS) is characterized by a constellation of metabolic risk factors, including obesity, hypertriglyceridemia, low high-density lipoprotein (HDL) levels, hypertension, and hyperglycemia, and is associated with stroke and neurodegenerative diseases. This study capitalized on brain structural images and clinical data from the UK Biobank and explored the associations of brain morphology with MetS and brain aging due to MetS. Cortical surface area, thickness, and subcortical volumes were assessed using FreeSurfer. Linear regression was used to examine associations of brain morphology with five MetS components and the MetS severity in a metabolic aging group (N = 23,676, age 62.8 ± 7.5 years). Partial least squares (PLS) were employed to predict brain age using MetS-associated brain morphology. The five MetS components and MetS severity were associated with increased cortical surface area and decreased thickness, particularly in the frontal, temporal, and sensorimotor cortex, and reduced volumes in the basal ganglia. Obesity best explained the variation of brain morphology. Moreover, participants with the most severe MetS had brain age 1-year older than those without MetS. Brain age in patients with stroke (N = 1042), dementia (N = 83), Parkinson's (N = 107), and multiple sclerosis (N = 235) was greater than that in the metabolic aging group. The obesity-related brain morphology had the leading discriminative power. Therefore, the MetS-related brain morphological model can be used for risk assessment of stroke and neurodegenerative diseases. Our findings suggested that prioritizing adjusting obesity among the five metabolic components may be more helpful for improving brain health in aging populations.
 PURPOSE: Low-dose naltrexone (LDN) has increased in popularity as a non-opioid medication that may decrease chronic pain symptoms. LDN is most commonly used to treat fibromyalgia, complex regional pain syndrome (CRPS), and painful diabetic neuropathy. Other studies suggest that LDN provides general symptom reduction in inflammatory conditions such as Crohn's disease and multiple sclerosis. We reviewed our experience with patients to whom we have prescribed LDN to see what types of painful conditions were most responsive to LDN in our patient population. PATIENTS AND METHODS: Charts from patients who came to the Pain Center between 2014 and 2021 were reviewed. RESULTS: Of the n = 137 patients who were prescribed LDN, 44% had no evidence of ever filling the prescription, and 4.4% of the responses were not charted. Of the remaining who took LDN (n = 70), 64% had some relief and were designated as 'Responders'. The most common pain diagnosis was neuropathic pain which, when added to the diagnosis of complex regional pain syndrome, accounted for 51% of responders to LDN. Patients who experienced greater than 50% pain relief from LDN were more likely to have the diagnosis of neuropathic pain or complex regional pain syndrome (p = 0.038, Fisher's Exact Test). There was a significant difference in the diagnosis of patients who responded to LDN. Patients with spondylosis were much less likely to respond to LDN when compared with other diagnoses (p = 0.00435, Chi-Square Test). CONCLUSION: Patients with all types of neuropathic pain, including CRPS, were significantly more likely to have pain relief from LDN than patients with spondylosis (p=0.018). The diagnosis of spondylosis was more often associated with a lack of response to LDN than any other diagnosis. Patients may need to have a trial of several weeks before analgesic effects are seen with LDN.
 The use of terpenoid compounds in different neural-related conditions is becoming useful for several illnesses. Another possible activity of these compounds is the reduction of nervous impairment. Cannabis sativa plants are known for their concentration of two important terpenoids, the delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). CBD and THC have central peripheral activities already described and their usage in different brain diseases, such as Alzheimer's and multiple sclerosis. Aluminum (Al) is known as an important neurotoxic compound, the physiological action of Al is not known already, and in high concentrations can lead to intoxication and cause neurotoxicity. Here we evaluated the potential effect of two different doses of CBD- and THC-rich based oils against Al-induced toxicity, in the zebrafish model. We evaluated behavioral biomarkers of the novel tank test (NTT) and social preference test (SPT), and biochemical markers: the activity of the enzyme acetylcholinesterase (AChE) and the antioxidant enzymes-catalase, superoxide dismutase, and glutathione-S-transferase. CBD- and THC-based oils were able to increase the AChE activity helping the cholinergic nervous system actuate against Al toxicity which was reflected by the behavioral biomarkers changes. We concluded that the oils have a protective effect and might be used with proposals for neurological and antioxidant impairment avoidance caused by Al intoxications.
 Human endogenous retroviruses (HERVs) have evolved from exogenous retroviruses and account for approximately 8% of the human genome. A growing number of findings suggest that the abnormal expression of HERV genes is associated with schizophrenia, multiple sclerosis, endometriosis, breast cancer, bladder cancer and other diseases. HERV-W env (syncytin-1) is a membrane glycoprotein which plays an important role in placental development. It includes embryo implantation, fusion of syncytiotrophoblasts and of fertilized eggs, and immune response. The abnormal expression of syncytin-1 is related to placental development-related diseases such as preeclampsia, infertility, and intrauterine growth restriction, as well as tumors such as neuroblastoma, endometrial cancer, and endometriosis. This review mainly focused on the molecular interactions of syncytin-1 in placental development-related diseases and tumors, to explore whether syncytin-1 can be an emerging biological marker and potential therapeutic target.
 Emerging evidence has shown that leukocyte telomere length (LTL) is associated with various health-related outcomes, while the causality of these associations remains unclear. We performed a systematic review and meta-analysis of current evidence from Mendelian randomization (MR) studies on the association between LTL and health-related outcomes. We searched PubMed, Embase, and Web of Science up to April 2022 to identify eligible MR studies. We graded the evidence level of each MR association based on the results of the main analysis and four sensitive MR methods, MR-Egger, weighted median, MR-PRESSO, and multivariate MR. Meta-analyses of published MR studies were also performed. A total of 62 studies with 310 outcomes and 396 MR associations were included. Robust evidence level was observed for the association between longer LTL and increased risk of 24 neoplasms (the strongest magnitude for osteosarcoma, GBM, glioma, thyroid cancer, and non-GBM glioma), six genitourinary and digestive system outcomes of excessive or abnormal growth, hypertension, metabolic syndrome, multiple sclerosis, and clonal hematopoiesis of indeterminate potential. Robust inverse association was observed for coronary heart disease, chronic kidney disease, rheumatoid arthritis, juvenile idiopathic arthritis, idiopathic pulmonary fibrosis, and facial aging. Meta-analyses of MR studies suggested that genetically determined LTL was associated with 12 neoplasms and 9 nonneoplasm outcomes. Evidence from published MR studies supports that LTL plays a causal role in various neoplastic and nonneoplastic diseases. Further research is required to elucidate the underlying mechanisms and to bring insight into the potential prediction, prevention, and therapeutic applications of telomere length.
 Introduction: Fingolimod is a drug that is used to treat multiple sclerosis (MS). It has pH-dependent solubility and low solubility when buffering agents are present. Multi-spectroscopic and molecular modeling methods were used to investigate the molecular mechanism of Fingolimod interaction with human serum albumin (HSA), and the resulting data were fitted to the appropriate models to investigate the molecular mechanism of interaction, binding constant, and thermodynamic properties. Methods: The interaction of Fingolimod with HSA was investigated in a NaCl aqueous solution (0.1 mM). The working solutions had a pH of 6.5. Data was collected using UV-vis, fluorescence quenching titrations, FTIR, and molecular modeling methods. Results: According to the results of the fluorescence quenching titrations, the quenching mechanism is static. The apparent binding constant value (K(A) = 4.26×10(3)) showed that Fingolimod is a moderate HSA binder. The reduction of the K(A) at higher temperatures could be a result of protein unfolding. Hydrogen bonding and van der Waals interactions are the main contributors to Fingolimod-HSA complex formation. FTIR and CD characterizations suggested a slight decrease in the α-helix and β-sheets of the secondary structure of HSA due to Fingolimod binding. Fingolimod binds to the binding site II, while a smaller tendency to the binding site I was observed as well. The results of the site marker competitive experiment and the thermodynamic studies agreed with the results of the molecular docking. Conclusion: The pharmacokinetic properties of fingolimod can be influenced by its HSA binding. In addition, considering its mild interaction, site II binding drugs are likely to compete. The methodology described here may be used to investigate the molecular mechanism of HSA interaction with lipid-like drugs with low aqueous solubility or pH-dependent solubility.
 BACKGROUND AND PURPOSE: Stiff person syndrome (SPS) spectrum disorders (SPSSD) cause spasms and rigidity throughout different body regions and can be associated with apnea and acute respiratory failure. There are limited data on the prevalence and predictors of respiratory symptoms with spasms (RSwS) in SPSSD. We sought to characterize the spirometry patterns and the frequency and predictors of RSwS in a large SPSSD cohort. METHODS: Participants were recruited from the Johns Hopkins SPS Center between 1997 and 2021, as part of an ongoing, longitudinal observational study. Medical records were reviewed to assess demographics and clinical characteristics. Data were analyzed using descriptive statistics and multivariable logistic regression models. RESULTS: One-hundred ninety-nine participants (mean age = 53.4 ± 13.6 years, median time to diagnosis = 36 [IQR 66] months, 74.9% women, 69.8% White, 62.8% classic SPS phenotype) were included in final analyses; 35.2% of participants reported RSwS, of whom 24.3% underwent spirometry as part of routine clinical care. Obstructive (23.5%) and restrictive (23.5%) patterns were most commonly observed in those with SPSSD. An increasing number of body regions involved predicted the presence of RSwS (odds ratio [OR] = 1.95, 95% confidence interval [CI] = 1.50-2.53); those with ≥5 body regions involved (vs. ≤4) had higher odds (OR = 6.19, 95% CI = 2.81-13.62) of experiencing RSwS in adjusted models. Two patients died from SPSSD-associated respiratory compromise. CONCLUSIONS: RSwS are common in SPSSD and may be predicted by an increasing number of body regions involved by SPSSD. Close clinical monitoring and having a low threshold to obtain spirometry should be considered in people with SPSSD.
 Th1 and Th17 cell migration into the central nervous system (CNS) is a fundamental process in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). Particularly, leptomeningeal vessels of the subarachnoid space (SAS) constitute a central route for T cell entry into the CNS during EAE. Once migrated into the SAS, T cells show an active motility behavior, which is a prerequisite for cell-cell communication, in situ reactivation and neuroinflammation. However, the molecular mechanisms selectively controlling Th1 and Th17 cell trafficking in the inflamed leptomeninges are not well understood. By using epifluorescence intravital microscopy, we obtained results showing that myelin-specific Th1 and Th17 cells have different intravascular adhesion capacity depending on the disease phase, with Th17 cells being more adhesive at disease peak. Inhibition of αLβ2 integrin selectively blocked Th1 cell adhesion, but had no effect on Th17 rolling and arrest capacity during all disease phases, suggesting that distinct adhesion mechanisms control the migration of key T cell populations involved in EAE induction. Blockade of α4 integrins affected myelin-specific Th1 cell rolling and arrest, but only selectively altered intravascular arrest of Th17 cells. Notably, selective α4β7 integrin blockade inhibited Th17 cell arrest without interfering with intravascular Th1 cell adhesion, suggesting that α4β7 integrin is predominantly involved in Th17 cell migration into the inflamed leptomeninges in EAE mice. Two-photon microscopy experiments showed that blockade of α4 integrin chain or α4β7 integrin selectively inhibited the locomotion of extravasated antigen-specific Th17 cells in the SAS, but had no effect on Th1 cell intratissue dynamics, further pointing to α4β7 integrin as key molecule in Th17 cell trafficking during EAE development. Finally, therapeutic inhibition of α4β7 integrin at disease onset by intrathecal injection of a blocking antibody attenuated clinical severity and reduced neuroinflammation, further demonstrating a crucial role for α4β7 integrin in driving Th17 cell-mediated disease pathogenesis. Altogether, our data suggest that a better knowledge of the molecular mechanisms controlling myelin-specific Th1 and Th17 cell trafficking during EAE delevopment may help to identify new therapeutic strategies for CNS inflammatory and demyelinating diseases.
 BACKGROUND: An incomplete spinal cord injury (SCI) refers to remaining sensorimotor function below the injury with the possibility for the patient to regain walking abilities. However, these patients often suffer from diverse gait deficits, which are not objectively assessed in the current clinical routine. Wearable inertial sensors are a promising tool to capture gait patterns objectively and started to gain ground for other neurological disorders such as stroke, multiple sclerosis, and Parkinson's disease. In this work, we present a data-driven approach to assess walking for SCI patients based on sensor-derived outcome measures. We aimed to (i) characterize their walking pattern in more depth by identifying groups with similar walking characteristics and (ii) use sensor-derived gait parameters as predictors for future walking capacity. METHODS: The dataset analyzed consisted of 66 SCI patients and 20 healthy controls performing a standardized gait test, namely the 6-min walking test (6MWT), while wearing a sparse sensor setup of one sensor attached to each ankle. A data-driven approach has been followed using statistical methods and machine learning models to identify relevant and non-redundant gait parameters. RESULTS: Clustering resulted in 4 groups of patients that were compared to each other and to the healthy controls. The clusters did differ in terms of their average walking speed but also in terms of more qualitative gait parameters such as variability or parameters indicating compensatory movements. Further, using longitudinal data from a subset of patients that performed the 6MWT several times during their rehabilitation, a prediction model has been trained to estimate whether the patient's walking speed will improve significantly in the future. Including sensor-derived gait parameters as inputs for the prediction model resulted in an accuracy of 80%, which is a considerable improvement of 10% compared to using only the days since injury, the present 6MWT distance, and the days until the next 6MWT as predictors. CONCLUSIONS: In summary, the work presented proves that sensor-derived gait parameters provide additional information on walking characteristics and thus are beneficial to complement clinical walking assessments of SCI patients. This work is a step towards a more deficit-oriented therapy and paves the way for better rehabilitation outcome predictions.
 BACKGROUND: Ethanol-induced gastric mucosal lesions (EGML) is one of the most common digestive disorders for which current therapies have limited outcomes in clinical practice. Prevotella histicola (P. histicola) has shown probiotic efficacy against arthritis, multiple sclerosis and oestrogen deficiency-induced depression in mice; however, its role in EGML remains unclear in spite of its extensive colonisation of the stomach. Ferroptosis, which is characterised by lipid peroxidation, may be involved in EGML. Herein, we aimed to investigate the effects and underlying mechanism of action of P. histicola on EGML in the ferroptosis-dependent pathway. METHODS: P. histicola was intragastrically administered for a week, and deferoxamine (DFO), a ferroptosis inhibitor, was intraperitoneally injected prior to oral ethanol administration. The gastric mucosal lesions and ferroptosis were assessed via histopathological examinations, quantitative real-time PCR, Western blot, immunohistochemistry and immunofluorescence. RESULTS: P. histicola was originally found to attenuate EGML by reducing histopathological changes and lipid reactive oxygen species (ROS) accumulation. The pro-ferroptotic genes of Transferrin Receptor (TFR1), Solute Carrier Family 39 Member 14 (SLC39A14), Haem Oxygenase-1 (HMOX-1), Acyl-CoA Synthetase Long-chain Family Member 4 (ACSL4), Cyclooxygenase 2 (COX-2) and mitochondrial Voltage-dependent Anion Channels (VDACs) were up-regulated; the anti-ferroptotic System Xc-/Glutathione Peroxidase 4 (GPX4) axis was inhibited after ethanol administration. However, the changes of histopathology and ferroptosis-related parameters induced by ethanol were reversed by DFO. Furthermore, P. histicola treatment significantly downregulated the expression of ACSL4, HMOX-1 and COX-2, as well as TFR1 and SLC39A14, on mRNA or the protein level, while activating the System Xc-/GPX4 axis. CONCLUSIONS: We found that P. histicola reduces ferroptosis to attenuate EGML by inhibiting the ACSL4- and VDAC-dependent pro-ferroptotic pathways and activating the anti-ferroptotic System Xc-/GPX4 axis.
 BACKGROUND: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an uncommon neurological disease affecting the central nervous system (CNS). Numerous neurological disorders, including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), acute transverse myelitis (ATM), and MOGAD, have been reported following the COVID-19 infection during the current COVID-19 pandemic. On the other hand, it has been suggested that patients with MOGAD may be at greater risk for infection (particularly in the current pandemic). OBJECTIVE: In this systematic review, we gathered separately 1) MOGAD cases following COVID-19 infection as well as 2) clinical course of patients with MOGAD infected with COVID-19 based on case reports/series. METHODS: 329 articles were collected from 4 databases. These articles were conducted from inception to March 1(st), 2022. RESULTS: Following the screening, exclusion criteria were followed and eventually, 22 studies were included. In 18 studies, a mean ± SD time interval of 18.6 ± 14.9 days was observed between infection with COVID-19 and the onset of MOGAD symptoms. Symptoms were partially or completely recovered in a mean of 67 days of follow-up.Among 4 studies on MOGAD patients, the hospitalization rate was 25%, and 15% of patients were hospitalized in the intensive care unit (ICU). CONCLUSION: Our systematic review demonstrated that following COVID-19 infection, there is a rare possibility of contracting MOGAD. Moreover, there is no clear consensus on the susceptibility of MOGAD patients to severe COVID-19. However, obtaining deterministic results requires studies with a larger sample size.
 BACKGROUND: Cognitive postscripts of COVID-19, codenamed as 'cognitive COVID' or 'brain fog,' characterized by multidomain cognitive impairments, are now being reckoned as the most devastating sequelae of COVID-19. However, the impact on the already demented brain has not been studied. OBJECTIVE: We aimed to assess the cognitive functioning and neuroimaging following SARS-CoV-2 infection in patients with pre-existing dementia. METHODS: Fourteen COVID-19 survivors with pre-existing dementia (four with Alzheimer's disease, five with vascular dementia, three with Parkinson's disease dementia, and two with the behavioral variant of frontotemporal dementia) were recruited. All these patients had detailed cognitive and neuroimaging evaluations within three months before suffering from COVID-19 and one year later. RESULTS: Of the 14 patients, ten required hospitalization. All developed or increased white matter hyperintensities that mimicked multiple sclerosis and small vessel disease. There was a significant increase in fatigue (p = 0.001) and depression (p = 0.016) scores following COVID-19. The mean Frontal Assessment Battery (p < 0.001) and Addenbrooke's Cognitive Examination (p = 0.001) scores also significantly worsened. CONCLUSION: The rapid progression of dementia, the addition of further impairments/deterioration of cognitive abilities, and the increase or new appearance of white matter lesion burden suggest that previously compromised brains have little defense to withstand a new insult (i.e., 'second hit' like infection/dysregulated immune response, and inflammation). 'Brain fog' is an ambiguous terminology without specific attribution to the spectrum of post-COVID-19 cognitive sequelae. We propose a new codename, i.e. 'FADE-IN MEMORY' (i.e., Fatigue, decreased Fluency, Attention deficit, Depression, Executive dysfunction, slowed INformation processing speed, and subcortical MEMORY impairment).
 Cytotoxic CD8+ T cells contribute to neuronal damage in inflammatory and degenerative CNS disorders, such as multiple sclerosis (MS). The mechanism of cortical damage associated with CD8+ T cells is not well understood. We developed in vitro cell culture and ex vivo brain slice co-culture models of brain inflammation to study CD8+ T cell-neuron interactions. To induce inflammation, we applied T cell conditioned media, which contains a variety of cytokines, during CD8+ T cell polyclonal activation. Release of IFNγ and TNFα from co-cultures was verified by ELISA, confirming an inflammatory response. We also visualized the physical interactions between CD8+ T cells and cortical neurons using live-cell confocal imaging. The imaging revealed that T cells reduced their migration velocity and changed their migratory patterns under inflammatory conditions. CD8+ T cells increased their dwell time at neuronal soma and dendrites in response to added cytokines. These changes were seen in both the in vitro and ex vivo models. The results confirm that these in vitro and ex vivo models provide promising platforms for the study of the molecular details of neuron-immune cell interactions under inflammatory conditions, which allow high-resolution live microscopy and are readily amenable to experimental manipulation.
 Astrocyte activation is associated with neuropathology and the production of tissue inhibitor of metalloproteinase-1 (TIMP1). TIMP1 is a pleiotropic extracellular protein that functions both as a protease inhibitor and as a growth factor. We have previously demonstrated that murine astrocytes that lack expression of Timp1 do not support rat oligodendrocyte progenitor cell (rOPC) differentiation, and adult global Timp1 knockout ( Timp1 (KO) ) mice do not efficiently remyelinate following a demyelinating injury. To better understand the basis of this, we performed unbiased proteomic analyses and identified a fibronectin-derived peptide called anastellin that is unique to the murine Timp1 (KO) astrocyte secretome. Anastellin was found to block rOPC differentiation in vitro and enhanced the inhibitory influence of fibronectin on rOPC differentiation. Anastellin is known to act upon the sphingosine-1-phosphate receptor 1 (S1PR1), and we determined that anastellin also blocked the pro-myelinating effect of FTY720 (or fingolimod) on rOPC differentiation in vitro . Further, administration of FTY720 to wild-type C57BL/6 mice during MOG (35-55) -EAE ameliorated clinical disability while FTY720 administered to mice lacking expression of Timp1 in astrocytes ( Timp1 (cKO) ) had no effect. Analysis of human TIMP1 and fibronectin ( FN1 ) transcripts from healthy and multiple sclerosis (MS) patient brain samples revealed an inverse relationship where lower TIMP1 expression was coincident with elevated FN1 in MS astrocytes. Lastly, we analyzed proteomic databases of MS samples and identified anastellin peptides to be more abundant in the cerebrospinal fluid (CSF) of human MS patients with high versus low disease activity. The prospective role for anastellin generation in association with myelin lesions as a consequence of a lack of astrocytic TIMP-1 production could influence both the efficacy of fingolimod responses and the innate remyelination potential of the the MS brain. SIGNIFICANCE STATEMENT: Astrocytic production of TIMP-1 prevents the protein catabolism of fibronectin. In the absence of TIMP-1, fibronectin is further digested leading to a higher abundance of anastellin peptides that can bind to sphingosine-1-phosphate receptor 1. The binding of anastellin with the sphingosine-1-phosphate receptor 1 impairs the differentiation of oligodendrocytes progenitor cells into myelinating oligodendrocytes in vitro , and negates the astrocyte-mediated therapeutic effects of FTY720 in the EAE model of chronic CNS inflammation. These data indicate that TIMP-1 production by astrocytes is important in coordinating astrocytic functions during inflammation. In the absence of astrocyte produced TIMP-1, elevated expression of anastellin may represent a prospective biomarker for FTY720 therapeutic responsiveness.
 Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorders. The etiology and pathology of AD are complicated, variable, and yet to be completely discovered. However, the involvement of inflammasomes, particularly the NLRP3 inflammasome, has been emphasized recently. NLRP3 is a critical pattern recognition receptor involved in the expression of immune responses and has been found to play a significant role in the development of various immunological and neurological disorders such as multiple sclerosis, ulcerative colitis, gout, diabetes, and AD. It is a multimeric protein which releases various cytokines and causes caspase-1 activation through the process known as pyroptosis. Increased levels of cytokines (IL-1β and IL-18), caspase-1 activation, and neuropathogenic stimulus lead to the formation of proinflammatory microglial M1. Progressive researches have also shown that besides loss of neurons, the pathophysiology of AD primarily includes amyloid beta (Aβ) accumulation, generation of oxidative stress, and microglial damage leading to activation of NLRP3 inflammasome that eventually leads to neuroinflammation and dementia. It has been suggested in the literature that suppressing the activity of the NLRP3 inflammasome has substantial potential to prevent, manage, and treat Alzheimer's disease. The present review discusses the functional composition, various models, signaling molecules, pathways, and evidence of NLRP3 activation in AD. The manuscript also discusses the synthetic drugs, their clinical status, and projected natural products as a potential therapeutic approach to manage and treat NLRP3 mediated AD.
 OBJECTIVE: Atypical Graves' disease (GD) is a common complication in multiple sclerosis (MS) patients treated with alemtuzumab. We present epidemiological, clinical, and biochemical characteristics of alemtuzumab-induced GD. METHOD: Retrospective follow-up study of MS-patients treated with alemtuzumab from 2014 to 2020, including clinical course of GD, pregnancy outcome, and thyroid eye disease (TED). RESULTS: We enrolled 183 of 203 patients (90%, 68% women) treated with alemtuzumab at four hospitals in Norway. Seventy-five (41%) developed thyroid dysfunction, of whom 58 (77%) had GD. Median time from the first dose of alemtuzumab to GD diagnosis was 25 months (range 0-64). Twenty-four of 58 GD patients (41%) had alternating phases of hyper- and hypothyroidism. Thyrotropin receptor antibodies (TRAb) became undetectable in 23 of 58 (40%) and they could discontinue anti-thyroid drug treatment after a median time of 22 (range 2-58) months. Conversely, 26 (44%) had active disease during a median follow-up of 39 months (range 11-72). Two patients (3%) received definitive treatment with radioiodine, six (10%) with thyroidectomy. Nine developed TED (16%), seven had mild and two moderate-to-severe disease. Four patients completed pregnancy, all without maternal or fetal complications. Patients who developed GD had a lower frequency of new MS relapses and MRI lesions than those without. CONCLUSION: GD is a very common complication of alemtuzumab treatment and is characterized by alternating hyper- and hypothyroidism. Both remission rates and the prevalence of TED were lower than those reported for conventional GD. Pregnancies were uncomplicated and GD was associated with a lower risk of subsequent MS activity.
 INTRODUCTION: Objectively measured physical activity (PA) data were collected in the accelerometry sub-study of the UK Biobank. UK Biobank also contains information about MS diagnosis at the time of and after PA collection. This study aims to: 1) Quantify the difference in PA between prevalent MS cases and matched healthy controls; 2) Evaluate the predictive performance of objective PA measures for incident MS cases. METHODS: The first analysis compared eight accelerometer-derived PA summaries between MS patients (N = 316) and matched controls (30 controls for each MS case). The second analysis focused on predicting time to MS diagnosis among participants who were not diagnosed with MS. A total of 19 predictors including eight measures of objective PA were compared using Cox proportional hazards models (number of events = 47; 585,900 person-years of follow-up). RESULTS: In the prevalent MS study, the difference between MS cases and matched controls was statistically significant for all PA summaries (p < 0.001). In the incident MS study, the most predictive variable of progression to MS in univariate Cox regression models was lower age (C = 0.604) and the most predictive PA variable was lower relative amplitude (RA, C = 0.594). A two-stage forward selection using Cox regression resulted in a model with concordance C = 0.693 and four predictors: age (p = 0.015), stroke (p = 0.009), Townsend deprivation index (p = 0.874), and RA (p = 0.004). A model including age, stroke, and RA had a concordance of C = 0.691. CONCLUSIONS: Objective PA summaries were significantly different and consistent with lower activity among study participants who had MS at the time of the accelerometry study. Among individuals who did not have MS, younger age, stroke history, and lower RA were significantly associated with higher risk of a future MS diagnosis.
 microRNAs (miRNAs) play a crucial role in various biological processes, including immune system regulation, such as cell proliferation, tolerance (central and peripheral), and T helper cell development. Dysregulation of miRNA expression and activity can disrupt immune responses and increase susceptibility to neuroimmune disorders. Conversely, miRNAs have been shown to have a protective role in modulating immune responses and preventing autoimmunity. Specifically, reducing the expression of miRNA-128 (miR-128) in an Alzheimer's disease (AD) mouse model has been found to improve cognitive deficits and reduce neuropathology. This comprehensive review focuses on the significance of miR-128 in the pathogenesis of neuroautoimmune disorders, including multiple sclerosis (MS), AD, Parkinson's disease (PD), Huntington's disease (HD), epilepsy, as well as other immune-mediated diseases such as inflammatory bowel disease (IBD) and rheumatoid arthritis (RA). Additionally, we present compelling evidence supporting the potential use of miR-128 as a diagnostic or therapeutic biomarker for neuroimmune disorders. Collectively, the available literature suggests that targeting miR-128 could be a promising strategy to alleviate the behavioral symptoms associated with neuroimmune diseases. Furthermore, further research in this area may uncover new insights into the molecular mechanisms underlying these disorders and potentially lead to the development of novel therapeutic approaches.
 Inflammatory demyelinating disease of the CNS (IDD) is a heterogeneous group of autoimmune diseases, and multiple sclerosis is the most common type. Dendritic cells (DCs), major antigen-presenting cells, have been proposed to play a central role in the pathogenesis of IDD. The AXL(+)SIGLEC6(+) DC (ASDC) has been only recently identified in humans and has a high capability of T cell activation. Nevertheless, its contribution to CNS autoimmunity remains still obscure. Here, we aimed to identify the ASDC in diverse sample types from IDD patients and experimental autoimmune encephalomyelitis (EAE). A detailed analysis of DC subpopulations using single-cell transcriptomics for the paired cerebrospinal fluid (CSF) and blood samples of IDD patients (total n = 9) revealed that three subtypes of DCs (ASDCs, ACY3(+) DCs, and LAMP3(+) DCs) were overrepresented in CSF compared with their paired blood. Among these DCs, ASDCs were also more abundant in CSF of IDD patients than in controls, manifesting poly-adhesional and stimulatory characteristics. In the brain biopsied tissues of IDD patients, obtained at the acute attack of disease, ASDC were also frequently found in close contact with T cells. Lastly, the frequency of ASDC was found to be temporally more abundant in acute attack of disease both in CSF samples of IDD patients and in tissues of EAE, an animal model for CNS autoimmunity. Our analysis suggests that the ASDC might be involved in the pathogenesis of CNS autoimmunity.
 The HLA-DRB1 gene encodes a protein that is essential for the immune system. This gene is important in organ transplant rejection and acceptance, as well as multiple sclerosis, systemic lupus erythematosus, Addison's disease, rheumatoid arthritis, caries susceptibility, and Aspirin-exacerbated respiratory disease. The following Homo sapiens variants were investigated: single-nucleotide variants (SNVs), multi-nucleotide variants (MNVs), and small insertions-deletions (Indels) in the HLA-DRB1 gene via coding and untranslated regions. The current study sought to identify functional variants that could affect gene expression and protein product function/structure. ALL target variants available until April 14, 2022, were obtained from the Single Nucleotide Polymorphism database (dbSNP). Out of all the variants in the coding region, 91 nsSNVs were considered highly deleterious by seven prediction tools and instability index; 25 of them are evolutionary conserved and located in domain regions. Furthermore, 31 indels were predicted as harmful, potentially affecting a few amino acids or even the entire protein. Last, within the coding sequence (CDS), 23 stop-gain variants (SNVs/indels) were predicted as high impact. High impact refers to the assumption that the variant will have a significant (disruptive) effect on the protein, likely leading to protein truncation or loss of function. For untranslated regions, functional 55 single-nucleotide polymorphisms (SNPs), and 16 indels located within microRNA binding sites, furthermore, 10 functionally verified SNPs were predicted at transcription factor-binding sites. The findings demonstrate that employing in silico methods in biomedical research is extremely successful and has a major influence on the capacity to identify the source of genetic variation in diverse disorders. In conclusion, these previously functional identified variants could lead to gene alteration, which may directly or indirectly contribute to the occurrence of many diseases. The study's results could be an important guide in the research of potential diagnostic and therapeutic interventions that require experimental mutational validation and large-scale clinical trials.
 PURPOSE OF REVIEW: Histiocytic disorders, including Erdheim-Chester disease (ECD), Langerhans cell histiocytosis (LCH), and Rosai-Dorfman disease (RDD), are rare neoplasms that may present with a spectrum of neurologic involvement. Diagnostic delay is common due to heterogeneity in presentation and challenging pathology. RECENT FINDINGS: Recent advances in the treatment of these diseases targeted towards mutations in the MAP kinase pathway have led to an improved prognosis in these patients with neurologic involvement. It is critical for clinicians to have a high index of suspicion to allow for early targeted treatment and optimize neurologic outcomes. A systematic approach to diagnosis is presented in this article to allow for accurate diagnosis of these rare diseases.
 BACKGROUND: People diagnosed with neurological pathology may experience gait disorders that affect their quality of life. In recent years, research has been carried out on a variety of exoskeletons in this population. However, the satisfaction perceived by the users of these devices is not known. Therefore, the objective of the present study is to evaluate the satisfaction perceived by users with neurological pathology (patients and professionals) after the use of overground exoskeletons. METHODS: A systematic search of five electronic databases was conducted. In order to be included in this review for further analysis, the studies had to meet the following criteria: [1] the study population was people diagnosed with neurological pathology; [2] the exoskeletons had to be overground and attachable to the lower limbs; and [3]: the studies were to include measures assessing either patient or therapist satisfaction with the exoskeletons. RESULTS: Twenty-three articles were selected, of which nineteen were considered clinical trials. Participants diagnosed with stroke (n = 165), spinal cord injury (SCI) (n = 102) and multiple sclerosis (MS) (n = 68). Fourteen different overground exoskeleton models were analysed. Fourteen different methods of assessing patient satisfaction with the devices were found, and three ways to evaluate it in therapists. CONCLUSION: Users' satisfaction with gait overground exoskeletons in stroke, SCI and MS seems to show positive results in safety, efficacy and comfort of the devices. However, the worst rated aspects and therefore those that should be optimized from the users' point of view are ease of adjustment, size and weight, and ease of use.
 INTRODUCTION: The availability of consumer-facing health technologies for chronic disease management is skyrocketing, yet most are limited by low adoption rates. Improving adoption requires a better understanding of a target population's previous exposure to technology. We propose a low-resource approach of capturing and clustering technology exposure, as a mean to better understand patients and target health technologies. METHODS: Using Multiple Sclerosis (MS) as a case study, we applied exploratory multivariate factorial analyses to survey data from the Swiss MS Registry. We calculated individual-level factor scorings, aiming to investigate possible technology adoption clusters with similar digital behavior patterns. The resulting clusters were transformed using radar and then compared across sociodemographic and health status characteristics. RESULTS: Our analysis included data from 990 respondents, resulting in three clusters, which we defined as the (1) average users, (2) health-interested users, and (3) low frequency users. The average user uses consumer-facing technology regularly, mainly for daily, regular activities and less so for health-related purposes. The health-interested user also uses technology regularly, for daily activities as well as health-related purposes. The low-frequency user uses technology infrequently. CONCLUSIONS: Only about 10% of our sample has been regularly using (adopting) consumer-facing technology for MS and health-related purposes. That might indicate that many of the current consumer-facing technologies for MS are only attractive to a small proportion of patients. The relatively low-resource exploratory analyses proposed here may allow for a better characterization of prospective user populations and ultimately, future patient-facing technologies that will be targeted to a broader audience.
 BACKGROUND: Patients with trigeminal neuralgia (TN) secondary to mass lesions are typically treated by directly addressing the underlying pathology. In cases of TN not alleviated by treatment of the pathology, percutaneous balloon compression (PBC) and glycerol rhizotomy (Gly) are simple and effective ways to alleviate pain. However, there is limited literature on the use of these techniques for patients with TN caused by mass lesions. OBJECTIVE: To describe the use of PBC/Gly to treat mass lesion-related TN. METHODS: We report a retrospective, single-institution, descriptive case series of patients who presented with TN secondary to tumor or mass-like inflammatory lesion from 1999 to 2021. Patients with primary, idiopathic, or multiple sclerosis-related TN were excluded. Outcomes included Barrow Neurological Institute (BNI) pain intensity and hypesthesia scores, pain persistence, and postoperative complications. RESULTS: A total of 459 procedures were identified, of which 16 patients met the inclusion criterion (14 PBC and 2 Gly). Of the 15 patients with tumors, 12 had TN pain despite prior tumor-targeted radiation. Short-term (<3 months) BNI pain intensity improvement occurred in 15 (93.8%) patients. The mean follow-up was 54.4 months. Thirteen (81.3%) patients were pain-free (Barrow Neurological Institute pain intensity scale: IIIa-50%; I-25.0%; II-6.3%) for a mean of 23.8 (range 1-137) months. Ten patients (62.5%) had pain relief for ≥6 months from first procedure. New facial numbness developed immediately postprocedure in 8 (50%) patients. Transient, partial abducens nerve palsy occurred in 1 patient. CONCLUSION: PBC/Gly is an effective option for medically refractory TN in patients with mass-associated TN and is a viable option for repeat treatment.
 Among the subset of T helper cells, Th17 cells are known to play a crucial role in the pathogenesis of various autoimmune disorders, such as psoriasis, rheumatoid arthritis, inflammatory bowel disease, steroid-resistant asthma, and multiple sclerosis. The master transcription factor retinoid-related orphan receptor gamma t (RORγt), a nuclear hormone receptor, plays a vital role in inducing Th17-cell differentiation. Recent findings suggest that metabolic control is critical for Th17-cell differentiation, particularly through the engagement of de novo lipid biosynthesis. Inhibition of lipid biosynthesis, either through the use of pharmacological inhibitors or by the deficiency of related enzymes in CD4(+) T cells, results in significant suppression of Th17-cell differentiation. Mechanistic studies indicate that metabolic fluxes through both the fatty acid and cholesterol biosynthetic pathways are essential for controlling RORγt activity through the generation of a lipid ligand of RORγt. This review highlights recent findings that underscore the significant role of lipid metabolism in the differentiation and function of Th17 cells, as well as elucidating the distinctive molecular pathways that drive the activation of RORγt by cellular lipid metabolism. We further elaborate on a pioneering therapeutic approach for ameliorating autoimmune disorders via the inhibition of RORγt.
 Helicobacter pylori infection consists a high global burden affecting more than 50% of the world's population. It is implicated, beyond substantiated local gastric pathologies, i.e., peptic ulcers and gastric cancer, in the pathophysiology of several neurodegenerative disorders, mainly by inducing hyperhomocysteinemia-related brain cortical thinning (BCT). BCT has been advocated as a possible biomarker associated with neurodegenerative central nervous system disorders such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and/or glaucoma, termed as "ocular Alzheimer's disease". According to the infection hypothesis in relation to neurodegeneration, Helicobacter pylori as non-commensal gut microbiome has been advocated as trigger and/or mediator of neurodegenerative diseases, such as the development of Alzheimer's disease. Among others, Helicobacter pylori-related inflammatory mediators, defensins, autophagy, vitamin D, dietary factors, role of probiotics, and some pathogenetic considerations including relevant involved genes are discussed within this opinion article. In conclusion, by controlling the impact of Helicobacter pylori-related hyperhomocysteinemia on neurodegenerative disorders might offer benefits, and additional research is warranted to clarify this crucial topic currently representing a major worldwide burden.
 Alterations in the gut microbiota, "dysbiosis," have been reported in autoimmune diseases, including multiple sclerosis (MS), and their animal models. Although the animal models were induced by injections of autoantigens with adjuvants, including complete Freund's adjuvant (CFA) and pertussis toxin (PT), the effects of adjuvant injections on the microbiota are largely unknown. We aimed to clarify whether adjuvant injections could affect the microbiota in the ileum and feces. Using 16S rRNA sequencing, we found decreased alpha diversities of the gut microbiota in mice injected with CFA and PT, compared with naïve mice. Overall, microbial profiles visualized by principal component analysis demonstrated dysbiosis in feces, but not in the ileum, of adjuvant-injected mice, where the genera Lachnospiraceae NK4A136 group and Alistipes contributed to dysbiosis. When we compared the relative abundances of individual bacteria, we found changes in 16 bacterial genera in feces and seven genera in the ileum of adjuvant-injected mice, in which increased serum levels of antibody against mycobacteria (a component of CFA) and total IgG2c were correlated with the genus Facklamia. On the other hand, increased IgG1 and IgA concentrations were correlated with the genus Atopostipes. Therefore, adjuvant injections alone could alter the overall microbial profiles (i.e., microbiota) and individual bacterial abundances with altered antibody responses; dysbiosis in animal models could be partly due to adjuvant injections.
 Oxidative stress and neuroinflammation are the main physiopathological changes involved in the initiation and progression of various neurodegenerative disorders or brain injuries. Since the landmark finding reported in 2007 found that hydrogen reduced the levels of peroxynitrite anions and hydroxyl free radicals in ischemic stroke, molecular hydrogen's antioxidative and anti-inflammatory effects have aroused widespread interest. Due to its excellent antioxidant and anti-inflammatory properties, hydrogen therapy via different routes of administration exhibits great therapeutic potential for a wide range of brain disorders, including Alzheimer's disease, neonatal hypoxic-ischemic encephalopathy, depression, anxiety, traumatic brain injury, ischemic stroke, Parkinson's disease, and multiple sclerosis. This paper reviews the routes for hydrogen administration, the effects of hydrogen on the previously mentioned brain disorders, and the primary mechanism underlying hydrogen's neuroprotection. Finally, we discuss hydrogen therapy's remaining issues and challenges in brain disorders. We conclude that understanding the exact molecular target, finding novel routes, and determining the optimal dosage for hydrogen administration is critical for future studies and applications.
 BACKGROUND: In the past two decades, three coronavirus epidemics have been reported. Coronavirus disease 2019 (COVID-19) is caused by a severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2). In most patients, the disease is characterized by interstitial pneumonia, but features can affect other organs. PURPOSE: To document the radiological features of the patients and to perform a narrative review of the literature. MATERIAL AND METHODS: We conducted a retrospective, single-center study on 1060 consecutive hospitalized patients with COVID-19 at our institution. According to the inclusion criteria, we selected patients to be studied in more radiological detail. All images were obtained as per standard of care protocols. We performed a statistic analysis to describe radiological features. We then presented a systematic review of the main and conventional neuroimaging findings in COVID-19. RESULTS: Of 1060 patients hospitalized for COVID-19 disease, 15% (159) met the eligibility criteria. Of these, 16 (10%) did not undergo radiological examinations for various reasons, while 143 (90%) were examined. Of these 143 patients, 48 (33.6%) had positive neuroimaging. We found that the most frequent pathology was acute ischemic stroke (n=16, 33.3%). Much less frequent were Guillain-Barre syndrome (n=9, 18.8%), cerebral venous thrombosis (n=7, 14.6%), encephalitis or myelitis (n=6, 12.5%), intracranial hemorrhage and posterior hemorrhagic encephalopathy syndrome (n=4, 8.3%), exacerbation of multiple sclerosis (n=4, 8.3%), and Miller-Fisher syndrome (n=2, 4.2%). CONCLUSION: Our data are coherent with the published literature. Knowledge of these patterns will make clinicians consider COVID-19 infection when unexplained neurological findings are encountered.
 OBJECTIVE: We investigated the association between distress symptoms (pain, fatigue, depression, anxiety) and work impairment in four patient populations: multiple sclerosis (N = 107), rheumatoid arthritis (N = 40), inflammatory bowel disease (N = 136) and psychiatric disorders (N = 167). METHODS: Four waves of data collection were completed over three years. The relationship between distress symptoms and overall work impairment was evaluated with univariate and multivariable quantile logistic regression at the 25th, 50th and 75th percentiles. Models were fit to participant average scores and change scores on distress symptom measures. Covariates included sociodemographic factors, comorbidity, physical disability and cognitive function. RESULTS: In the primary univariate analyses of overall work impairment at the 50th percentile, greater severity of distress symptoms was associated with greater work impairment: pain (average β = 0.27, p < 0.001; change β = 0.08, p < 0.001), fatigue (average β = 0.21, p < 0.001; change β = 0.09, p < 0.001) depression (average, β = 0.35, p < 0.001; change, β = 0.16, p < 0.001), anxiety (average, β = 0.24, p < 0.001; change, β = 0.08, p < 0 0.01). Findings were similar in multivariable analyses. CONCLUSION: Pain, fatigue, depression, and anxiety symptoms are important determinants of work impairment in persons with immune-mediated diseases and persons with psychiatric disorders. Successful clinical management of these symptoms has potential to improve work-related outcomes across IMIDs.
 Background: Autoimmune diseases can occur at any time in patients with common variable immunodeficiency (CVID). However, the relationship between low immunoglobulin E (IgE) levels and autoimmune diseases in patients with CVID remains poorly understood. Objective: We aimed to determine the relationship between autoimmunity and low IgE in patients with CVID. Methods: This retrospective cohort study was conducted by using data that had been collected from 62 adult patients with CVID between April 2012 and December 2021. Serum basal IgE levels were compared between patients with and patients without autoimmune disease. Results: Overall, 23 of the 62 patients with CVID (37.1%) had at least one autoimmune disease (CVID-O). Autoimmune cytopenias, mainly immune thrombocytopenic purpura, were observed in half of all the patients. Other autoimmune diseases present among the patients included rheumatological diseases, inflammatory bowel diseases, lymphoma, granulomatous lymphocytic interstitial lung disease, autoimmune hepatitis, alopecia, and multiple sclerosis. Serum IgE levels were measured at the time of diagnosis; IgE was undetectable (<2.5 IU/mL) in 82.6% of the patients with CVID-O (n = 19). The median (interquartile range) serum IgE value in the patients with CVID-O was 2 IU/mL (1-16 IU/mL), which was significantly lower than the median serum IgE value in patients with CVID and without autoimmune disease (p < 0.001). Low IgE levels in patients with CVID-O were an independent risk factor for the development of autoimmune disease in patients with CVID (odds ratio 3.081 [95% confidence interval, 1.222-7.771]; p = 0.017). Conclusion: Low serum IgE levels were associated with the development of autoimmune disease in patients with CVID. The monitoring of serum IgE levels in patients with CVID may be useful in the early diagnosis and treatment of autoimmune diseases.
 Cannabis has been used recreationally and medically for centuries, yet research into understanding the mechanisms of its therapeutic effects has only recently garnered more attention. There is evidence to support the use of cannabinoids for the treatment of chronic pain, muscle spasticity, nausea and vomiting due to chemotherapy, improving weight gain in HIV-related cachexia, emesis, sleep disorders, managing symptoms in Tourette syndrome, and patient-reported muscle spasticity from multiple sclerosis. However, tolerance and the risk for cannabis use disorder are two significant disadvantages for cannabinoid-based therapies in humans. Recent work has revealed prominent sex differences in the acute response and tolerance to cannabinoids in both humans and animal models. This review will discuss evidence demonstrating cannabinoid tolerance in rodents, non-human primates, and humans and our current understanding of the neuroadaptations occurring at the cannabinoid type 1 receptor (CB(1)R) that are responsible tolerance. CB(1)R expression is downregulated in tolerant animals and humans while there is strong evidence of CB(1)R desensitization in cannabinoid tolerant rodent models. Throughout the review, critical knowledge gaps are indicated and discussed, such as the lack of a neuroimaging probe to assess CB(1)R desensitization in humans. The review discusses the intracellular signaling pathways that are responsible for mediating CB(1)R desensitization and downregulation including the action of G protein-coupled receptor kinases, β-arrestin2 recruitment, c-Jun N-terminal kinases, protein kinase A, and the intracellular trafficking of CB(1)R. Finally, the review discusses approaches to reduce cannabinoid tolerance in humans based on our current understanding of the neuroadaptations and mechanisms responsible for this process.
 The human gut microbiome contains the largest number of bacteria in the body and has the potential to greatly influence metabolism, not only locally but also systemically. There is an established link between a healthy, balanced, and diverse microbiome and overall health. When the gut microbiome becomes unbalanced (dysbiosis) through dietary changes, medication use, lifestyle choices, environmental factors, and ageing, this has a profound effect on our health and is linked to many diseases, including lifestyle diseases, metabolic diseases, inflammatory diseases, and neurological diseases. While this link in humans is largely an association of dysbiosis with disease, in animal models, a causative link can be demonstrated. The link between the gut and the brain is particularly important in maintaining brain health, with a strong association between dysbiosis in the gut and neurodegenerative and neurodevelopmental diseases. This link suggests not only that the gut microbiota composition can be used to make an early diagnosis of neurodegenerative and neurodevelopmental diseases but also that modifying the gut microbiome to influence the microbiome-gut-brain axis might present a therapeutic target for diseases that have proved intractable, with the aim of altering the trajectory of neurodegenerative and neurodevelopmental diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, autism spectrum disorder, and attention-deficit hyperactivity disorder, among others. There is also a microbiome-gut-brain link to other potentially reversible neurological diseases, such as migraine, post-operative cognitive dysfunction, and long COVID, which might be considered models of therapy for neurodegenerative disease. The role of traditional methods in altering the microbiome, as well as newer, more novel treatments such as faecal microbiome transplants and photobiomodulation, are discussed.
 Dimethyl fumarate (DMF) is an immunomodulatory drug currently approved for the treatment of multiple sclerosis and psoriasis. Its benefits on ischemic stroke outcomes have recently come to attention. To date, only tissue plasminogen activators (tPAs) and clot retrieval methods have been approved by the FDA for the treatment of ischemic stroke. Ischemic conditions lead to inflammation through diverse mechanisms, and recanalization can worsen the state. DMF and the nuclear factor erythroid-derived 2-related factor 2 (Nrf2) pathway it regulates seem to be important in postischemic inflammation, and animal studies have demonstrated that the drug improves overall stroke outcomes. Although the exact mechanism is still unknown, studies indicate that these beneficial impacts are due to the modulation of immune responses, blood-brain barrier permeability, and hemodynamic adjustments. One major component evaluated before, during, and after tPA therapy in stroke patients is blood pressure (BP). Recent studies have found that DMF may impact BP. Both hypotension and hypertension need correction before treatment, which may delay the appropriate intervention. Since BP management is crucial in managing stroke patients, it is important to consider DMF's role in this matter. That being said, it seems further investigations on DMF may lead to an alternative approach for stroke patients. In this article, we discuss the mechanistic roles of DMF and its potential role in stroke based on previously published literature and laboratory findings.
 PURPOSE: 4-Aminopyridine (4AP) is a medication for the symptomatic treatment of multiple sclerosis. Several 4AP-based PET tracers have been developed for imaging demyelination. In preclinical studies, [ (11) C]3MeO4AP has shown promise due to its high brain permeability, high metabolic stability, high plasma availability, and high in vivo binding affinity. To prepare for the translation to human studies, we developed a cGMP-compliant automated radiosynthesis protocol and evaluated the whole-body biodistribution and radiation dosimetry of [ (11) C]3MeO4AP in non-human primates (NHPs). METHODS: Automated radiosynthesis was carried out using a GE TRACERlab FX-C Pro synthesis module. One male and one female adult rhesus macaques were used in the study. A high-resolution CT from cranial vertex to knee was acquired. PET data were collected using a dynamic acquisition protocol with 4 bed positions and 13 passes over a total scan time of ∼150 minutes. Based on the CT and PET images, volumes of interest (VOIs) were manually drawn for selected organs. Non-decay corrected time-activity curves (TACs) were extracted for each VOI. Radiation dosimetry and effective dose were calculated from the integrated TACs using OLINDA software. RESULTS: Fully automated radiosynthesis of [ (11) C]3MeO4AP was achieved with 7.3 ± 1.2 % (n = 4) of non-decay corrected radiochemical yield within 38 min of synthesis and purification time. [ (11) C]3MeO4AP distributed quickly throughout the body and into the brain. The organs with highest dose were the kidneys. The average effective dose of [ (11) C]3MeO4AP was 4.27 ± 0.57 μSv/MBq. No significant changes in vital signs were observed during the scan. CONCLUSION: The cGMP compliant automated radiosynthesis of [ (11) C]3MeO4AP was developed. The whole-body biodistribution and radiation dosimetry of [ (11) C]3MeO4AP was successfully evaluated in NHPs. [ (11) C]3MeO4AP shows lower average effective dose than [ (18) F]3F4AP and similar average effective dose as other carbon-11 tracers.
 INTRODUCTION: The World Health Organization defined electronic health as "the unified usage of information technology and electronic communications in the health sector." In the Kingdom of Saudi Arabia, outpatient encounters were largely shifted to virtual clinics due to the crisis caused by COVID-19. This study aimed to evaluate the neurology consultants', specialists', and residents' experience and perception of utilizing virtual services for neurological assessment in Saudi Arabia. METHODS: This cross-sectional study was conducted by sending an anonymous online survey to neurologists and neurology residents in Saudi Arabia. The survey was developed by the authors and contained three main sections: demographics, subspecialty and years of experience after residency, and virtual clinics during the coronavirus disease 2019 (COVID-19) pandemic. RESULT: A total of 108 neurology-practicing physicians in Saudi Arabia responded to the survey. Overall, 75% experienced virtual clinics, and 61% of them used phones for consultation. In neurology clinical practice, there was a significant difference (P < 0.001) regarding the teleconsultations for follow-up patients compared to the newly referred patients, being more suitable for the follow-up cases. Additionally, most neurology practicing physicians showed more confidence in performing history-taking tasks virtually (82.4%) than in physical examination. However, it was found that consultants were significantly (P < 0.03) more confident to virtually perform the cranial nerve, motor, coordination, and extrapyramidal assessments than the neurology residents. Physicians deemed it more suitable to conduct teleconsultations for patients with headaches and epilepsy than for those with neuromuscular and demyelinating diseases/multiple sclerosis. Furthermore, they agreed that patients' experiences (55.6%) and physicians' acceptance (55.6%) were the two main limitations to implementing virtual clinics. DISCUSSION: This study revealed that neurologists were more confident in performing history-taking in virtual clinics than in physical exams. On the contrary, consultants were more confident in handling the physical examination virtually than the neurology residents. Moreover, the most accepted clinics to be handled electronically were the headache and epilepsy clinics in comparison to the other subspecialties, being mainly diagnosed using history. Further studies with larger sample sizes are warranted to observe the level of confidence in performing different duties in neurology virtual clinics.
 Serum uric acid (SUA), the end product of purine metabolism acts as an antioxidant and is related to oxidative stress. It has been reported that SUA may be involved in the pathogenesis of neurodegenerative diseases including Alzheimer disease, Huntington disease, Parkinson disease, and multiple sclerosis. However, studies evaluating SUA levels in migraine are scarce. This study aimed to explore the relationship between pain characteristics and SUA levels in patients with migraine and compare SUA levels in migraine patients during a headache attack and headache-free period with those control groups. This prospective, cross-sectional study included 78 patients with migraine and 78 healthy subjects who were randomly selected from hospital personnel as the control group. Headache characteristics (duration of attack, pain intensity, and headache frequency) and sociodemographic features were recorded. The SUA level was measured once in the control group and twice in the migraine patients, during the migraine attack and headache-free periods. Although the SUA levels of the migraine group in the headache-free period were higher than those of the control group, the difference was not statistically significant. Gender was not significantly related to the change in SUA levels between the attack and headache-free period. When the correlation between age, duration of migraine, frequency, duration, and intensity of pain was evaluated; the difference between SUA levels in female migraine patients was weakly correlated with headache intensity, whereas male patients had a moderate correlation. ( P < .05; R > 0.250, and R > 0.516, respectively). The difference in SUA level in the migraine attack period compared to the headache-free period showing a positive correlation with pain intensity suggested that SUA may have a role in migraine due to its antioxidant role.
 Multiple sclerosis (MS) treatment has received much attention, yet there is still no certain cure. We herein investigate the therapeutic effect of olean-12-en-28-ol, 3β-pentacosanoate (OPCA) on a preclinical model of MS. First, OPCA was synthesized semisynthetically and characterized. Then, the mice with MOG(35-55)-induced experimental autoimmune/allergic encephalomyelitis (EAE) were given OPCA along with a reference drug (FTY720). Biochemical, cellular, and molecular analyses were performed in serum and brain tissues to measure anti-inflammatory and neuroprotective responses. OPCA treatment protected EAE-induced changes in mouse brains maintaining blood-brain barrier integrity and preventing inflammation. Moreover, the protein and mRNA levels of MS-related genes such as HLD-DR1, CCL5, TNF-α, IL6, and TGFB1 were significantly reduced in OPCA-treated mouse brains. Notably, the expression of genes, including PLP, MBP, and MAG, involved in the development and structure of myelin was significantly elevated in OPCA-treated EAE. Furthermore, therapeutic OPCA effects included a substantial reduction in pro-inflammatory cytokines in the serum of treated EAE animals. Lastly, following OPCA treatment, the promoter regions for most inflammatory regulators were hypermethylated. These data support that OPCA is a valuable and appealing candidate for human MS treatment since OPCA not only normalizes the pro- and anti-inflammatory immunological bias but also stimulates remyelination in EAE.
 The activation of phagocytic cells is a hallmark of many neurological diseases. Imaging them in their 3-dimensional cerebral environment over time is crucial to better understand their role in disease pathogenesis and to monitor their potential therapeutic effects. Phagocytic cells have the ability to internalize metal-based contrast agents both in vitro and in vivo and can thus be tracked by magnetic resonance imaging (MRI) or computed tomography (CT). In this review article, we summarize the different labelling strategies, contrast agents, and in vivo imaging modalities that can be used to monitor cells with phagocytic activity in the central nervous system using MRI and CT, with a focus on clinical applications. Metal-based nanoparticle contrast agents such as gadolinium, gold and iron are ideal candidates for these applications as they have favourable magnetic and/or radiopaque properties and can be fine-tuned for optimal uptake by phagocytic cells. However, they also come with downsides due to their potential toxicity, especially in the brain where they might accumulate. We therefore conclude our review by discussing the pitfalls, safety and potential for clinical translation of these metal-based neuroimaging techniques. Early results in patients with neuropathologies such as multiple sclerosis, stroke, trauma, cerebral aneurysm and glioblastoma are promising. If the challenges represented by safety issues are overcome, phagocytic cells imaging will be a very valuable tool for studying and understanding the inflammatory response and evaluating treatments that aim at mitigating this response in patients with neurological diseases.
 Evobrutinib is a second-generation, highly selective, irreversible Bruton's tyrosine kinase (BTK) inhibitor that has shown efficacy in the autoimmune diseases arthritis and multiple sclerosis. Its development as a positron emission tomography (PET) radiotracer has potential for in vivo imaging of BTK in various disease models including several cancers, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), and lipopolysaccharide (LPS)-induced lung damage. Herein, we report the automated radiosynthesis of [(11) C]evobrutinib using a base-aided palladium-NiXantphos-mediated (11) C-carbonylation reaction. [(11) C]Evobrutinib was reliably formulated in radiochemical yields of 5.5 ± 1.5% and a molar activity of 34.5 ± 17.3 GBq/μmol (n = 12) with 99% radiochemical purity. Ex vivo autoradiography studies showed high specific binding of [(11) C]evobrutinib in HT-29 colorectal cancer mouse xenograft tissues (51.1 ± 7.1%). However, in vivo PET/computed tomography (CT) imaging with [(11) C]evobrutinib showed minimal visualization of HT-29 colorectal cancer xenografts and only a slight increase in radioactivity accumulation in the associated time-activity curves. In preliminary PET/CT studies, [(11) C]evobrutinib failed to visualize either SARS-CoV-2 pseudovirus infection or LPS-induced injury in mouse models. In conclusion, [(11) C]evobrutinib was successfully synthesized by (11) C-carbonylation and based on our preliminary studies does not appear to be a promising BTK-targeted PET radiotracer in the rodent disease models studied herein.
 BACKGROUND AND OBJECTIVES: Neuromyelitis optica spectrum disorder (NMOSD) is a rare debilitating autoimmune disease of the CNS. Three monoclonal antibodies were recently approved as maintenance therapies for aquaporin-4 immunoglobulin G (AQP4-IgG)-seropositive NMOSD (eculizumab, inebilizumab, and satralizumab), prompting the need to consider best practice therapeutic decision-making for this indication. Our objective was to develop validated statements for the management of AQP4-IgG-seropositive NMOSD, through an evidence-based Delphi consensus process, with a focus on recommendations for eculizumab, inebilizumab, and satralizumab. METHODS: We recruited an international panel of clinical experts in NMOSD and asked them to complete a questionnaire on NMOSD management. Panel members received a summary of evidence identified through a targeted literature review and provided free-text responses to the questionnaire based on both the data provided and their clinical experience. Responses were used to generate draft statements on NMOSD-related themes. Statements were voted on over a maximum of 3 rounds; participation in at least 1 of the first 2 rounds was mandatory. Panel members anonymously provided their level of agreement (6-point Likert scale) on each statement. Statements that failed to reach a predefined consensus threshold (≥67%) were revised based on feedback and then voted on in the next round. Final statements were those that met the consensus threshold (≥67%). RESULTS: The Delphi panel comprised 24 experts, who completed the Delphi process in November 2021 after 2 voting rounds. In round 1, 23/25 statements reached consensus and were accepted as final. The 2 statements that failed to reach consensus were revised. In round 2, both revised statements reached consensus. Twenty-five statements were agreed in total: 11 on initiation of or switching between eculizumab, inebilizumab, and satralizumab; 3 on monotherapy/combination therapy; 7 on safety and patient population considerations; 3 on biomarkers/patient-reported outcomes; and 1 on research gaps. DISCUSSION: An established consensus method was used to develop statements relevant to the management of AQP4-IgG-seropositive NMOSD. These international statements will be valuable for informing individualized therapeutic decision-making and could form the basis for standardized practice guidelines.
 Central nervous system glial cells are known to mediate many neurocognitive/neurodegenerative diseases, including Alzheimer's and Parkinson's diseases. Similar glial responses have been recognized as critical factors contributing to the development of diseases in the peripheral nervous system, including various types of peripheral neuropathies, such as peripheral nerve injury-induced neuropathic pain, diabetic neuropathy, and HIV-associated sensory neuropathy. Investigation of the central mechanisms of these peripherally-manifested diseases often requires the examination of spinal cord glial cells at cellular/molecular levels in vitro. When using rodent models to study these diseases, many investigators have chosen to use neonatal cerebral cortices to prepare glial cultures or immortalized cell lines in order to obtain sufficient numbers of cells for assessment. However, differences in responses between cell lines versus primary cultures, neonatal vs. adult cells, and brain vs. spinal cord cells may result in misleading data. Here, we describe a protocol for preparing mixed glial cells from adult mouse spinal cord that can be used for direct in vitro evaluations or further preparation of microglia-enriched and microglia-depleted cells. In this protocol, spinal cord tissue is enzymatically dissociated and adult mixed glial cells are ready to be used between 12 and 14 days after the establishment of the culture. This protocol may be further refined to prepare spinal cord glial cells from spinal cord tissues of adult rats and potentially other species. Mixed glial cultures can be prepared from animals of different strains or post-in vivo manipulations and therefore are suitable for studying a variety of diseases/disorders that involve spinal cord pathological changes, such as amyotrophic lateral sclerosis and multiple sclerosis, as well as toxin-induced changes. © 2023 Wiley Periodicals LLC. Basic Protocol: Preparation of primary mixed glial cell cultures from adult mouse spinal cord tissue.
 BACKGROUND AND OBJECTIVES: The objective of this study was to compare the utilization and costs (total and out-of-pocket) of new-to-market neurologic medications with existing guideline-supported neurologic medications over time. METHODS: We used a healthcare pharmaceutical claims database (from 2001 to 2019) to identify patients with both a diagnosis of 1 of 11 separate neurologic conditions and either a new-to-market medication or an existing guideline-supported medication for that condition. Neurologic conditions included orthostatic hypotension, spinal muscular atrophy, Duchenne disease, Parkinson disease, multiple sclerosis, amyotrophic lateral sclerosis, myasthenia gravis, Huntington disease, tardive dyskinesia, transthyretin amyloidosis, and migraine. New-to-market medications were defined as all neurologic medications approved by the US Food and Drug Administration (FDA) between 2014 and 2018. In each year, we determined the median out-of-pocket and standardized total costs for a 30-day supply of each medication. We also measured the proportion of patients receiving new-to-market medications compared with all medications specific for the relevant condition. RESULTS: We found that the utilization of most new-to-market medications was small (<20% in all but 1 condition), compared with existing, guideline-supported medications. The out-of-pocket and standardized total costs were substantially larger for new-to-market medications. The median (25th percentile, 75th percentile) out-of-pocket costs for a 30-day supply in 2019 were largest for edaravone ($712.8 [$59.8-$802.0]) and eculizumab ($91.1 [$3.0-$3,216.4]). For new-to-market medications, the distribution of out-of-pocket costs was highly variable and the trends over time were unpredictable compared with existing guideline-supported medications. DISCUSSION: Despite the increasing number of FDA-approved neurologic medications, utilization of newly approved medications in the privately insured population remains small. Given the high costs and similar efficacy for most of the new medications, limited utilization may be appropriate. However, for new medications with greater efficacy, future studies are needed to determine whether high costs are a barrier to utilization.
 Potential associations between the risk of neurodegenerative diseases and circulating levels of amino acids have been implied in both experimental research and observational studies. However, because of the confounding and reverse causality, the findings could be biased. We aimed to determine whether circulating amino acid levels have potential effects on the risk of neurodegenerative diseases through a more robust analysis. So, we performed a total of two MR analyses, a discovery two-sample MR analysis, and a replication test, using summary-level genome-wide association study (GWAS) data, both with circulating levels of amino acids as exposure and risk of neurodegenerative diseases as an outcome. The potential causalities between nine amino acids (Glutamine [Glu], Leucine [Leu], Isoleucine [Ile], Phenylalanine [Phe], Valine [Val], Alanine [Ala], Tyrosine [Tyr], Histidine [His], and Glycine [Gly]) and six neurodegenerative disorders (Alzheimer's disease [AD], Parkinson's disease [PD], Multiple sclerosis [MS], Frontotemporal dementia [FTD], Lewy body dementia [DLB], Amyotrophic lateral sclerosis [ALS]) were explored in this study. According to the discovery MR analysis, 1 SD. increase in circulating levels of Gln was genetically determined to result in a 13% lower risk of AD (IVW OR(SD) [95% CI] = 0.872 [0.822, 0.926]; FDR = 7.46 × 10(-5) ) while PD risk was decreased to 63% per SD. increase of circulating Leu levels (IVW OR(SD) [95% CI] = 0.628 [0.467, 0.843]; FDR = 0.021). Results from the replication test provide further evidence of the potential association between circulating Gln levels and AD risk (IVW OR(SD) [95% CI] = 0.094 [0.028, 0.311]; FDR = 9.98 × 10(-4) ). Meanwhile, sensitivity analysis demonstrated that the significant relationships revealed by our two-sample MR outcomes were reliable. Our analyses provided robust evidence of causal associations between circulating levels of Gln and AD risk as well as circulating Leu levels and risk of PD. However, the underlying mechanisms remain to be further investigated.
 Objective To explore the effect of knocking down Rho-associated coiled-coil kinase (ROCK2) gene on the cognitive function of amyloid precursor protein/presenilin-1 (APP/PS1) double transgenic mice and its mechanism. Methods APP/PS1 double transgenic mice were randomly divided into AD model group (AD group), ROCK2 gene knock-down group (shROCK2 group), ROCK2 gene knock-down control group (shNCgroup), and wild-type C57BL/6 mice of the same age served as the wild-type control (WT group). Morris water maze and Y maze were employed to test the cognitive function of mice. Neuron morphology was detected by Nissl staining. Immunofluorescence histochemical staining was used to detect the expression of phosphorylated dynamin-related protein 1 (p-Drp1) and mitochondrial fusion 1 (Mfn1). Western blot analysis was used to detect the expression ROCK2, cleaved-caspase-3 (c-caspase-3), B-cell lymphoma 2 (Bcl2), Bcl2-related protein X (BAX), p-Drp1, mitochondrial fission 1 (Fis1), optic atrophy 1 (OPA1), Mfn1 and Mfn2. Results Compared with AD group mice, the expression of ROCK2 in shROCK2 group mice was significantly reduced; the cognitive function was significantly improved with the number of neurons in the hippocampal CA3 and DG areas increasing, and nissl bodies were deeply stained; the expression of c-caspase-3 and BAX was decreased, while the expression of Bcl2 was increased; the expression of mitochondrial division related proteins p-Drp1 and Fis1 were decreased, while the expression of mitochondrial fusion-related proteins OPA1, Mfn1 and Mfn2 were increased. Conclusion Knock-down of ROCK2 gene can significantly improve the cognitive function and inhibit the apoptosis of nerve cells of APP/PS1 mice. The mechanism may be related to promoting mitochondrial fusion and inhibiting its division.
 In network meta-analysis (NMA), we synthesize all relevant evidence about health outcomes with competing treatments. The evidence may come from randomized clinical trials (RCT) or non-randomized studies (NRS) as individual participant data (IPD) or as aggregate data (AD). We present a suite of Bayesian NMA and network meta-regression (NMR) models allowing for cross-design and cross-format synthesis. The models integrate a three-level hierarchical model for synthesizing IPD and AD into four approaches. The four approaches account for differences in the design and risk of bias (RoB) in the RCT and NRS evidence. These four approaches variously ignoring differences in RoB, using NRS to construct penalized treatment effect priors and bias-adjustment models that control the contribution of information from high RoB studies in two different ways. We illustrate the methods in a network of three pharmacological interventions and placebo for patients with relapsing-remitting multiple sclerosis. The estimated relative treatment effects do not change much when we accounted for differences in design and RoB. Conducting network meta-regression showed that intervention efficacy decreases with increasing participant age. We also re-analysed a network of 431 RCT comparing 21 antidepressants, and we did not observe material changes in intervention efficacy when adjusting for studies' high RoB. We re-analysed both case studies accounting for different study RoB. In summary, the described suite of NMA/NMR models enables the inclusion of all relevant evidence while incorporating information on the within-study bias in both observational and experimental data and enabling estimation of individualized treatment effects through the inclusion of participant characteristics.
 In the central nervous system (CNS), insulin-like growth factor 1 (IGF-1) regulates myelination by oligodendrocyte (ODC) precursor cells and shows anti-apoptotic properties in neuronal cells in different in vitro and in vivo systems. Previous work also suggests that IGF-1 protects ODCs from cell death and enhances remyelination in models of toxin-induced and autoimmune demyelination. However, since evidence remains controversial, the therapeutic potential of IGF-1 in demyelinating CNS conditions is unclear. To finally shed light on the function of IGF1-signaling for ODCs, we deleted insulin-like growth factor 1 receptor (IGF1R) specifically in mature ODCs of the mouse. We found that ODC survival and myelin status were unaffected by the absence of IGF1R until 15 months of age, indicating that IGF-1 signaling does not play a major role in post-mitotic ODCs during homeostasis. Notably, the absence of IGF1R did neither affect ODC survival nor myelin status upon cuprizone intoxication or induction of experimental autoimmune encephalomyelitis (EAE), models for toxic and autoimmune demyelination, respectively. Surprisingly, however, the absence of IGF1R from ODCs protected against clinical neuroinflammation in the EAE model. Together, our data indicate that IGF-1 signaling is not required for the function and survival of mature ODCs in steady-state and disease.
 BACKGROUND: Numerous studies have demonstrated the role of T helper (Th) 17 and T regulatory (reg) cells and pro-inflammatory and anti-inflammatory cytokines related to these cells in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis (EAE). STAT3 is one of the downstream signaling proteins of IL-23, IL-6, and IL-21 that are required for Th17 cells differentiation. STA-21 is a STAT3 inhibitor that functions by inhibiting STAT3 dimerization and binding to DNA impairing the expression of STAT3 target genes including, RORγt, IL-21 and IL-23R that are also required for Th17 cell differentiation. AIM: In this study, we evaluated the effect of STA-21 on EAE Model and investigated how this small molecule can change Th17/Treg balance leading to amelioration of disease. METHODS: After EAE induction and treatment with STA-21, its effects were assessed. Major assays were H&E and LFB staining, Flow cytometric analysis, Reverse transcription-PCR (RT-PCR), and ELISA. RESULTS: STA-21 ameliorated the EAE severity and decreased the EAE inflammation and demyelination. It also decreased STAT3 phosphorylation, the proportion of Th17 cells and the protein level of IL-17. In contrast, the balance of Tregs and the level of anti-inflammatory cytokine, IL-10 increased in STA-21-treated mice. Moreover, STA-21 significantly decreased the expression of Th17 related transcription factors, RORɣt and IL-23R while FOXP3 expression associated with Treg differentiation was increased. CONCLUSION: This study showed that STA-21 has therapeutic effects in EAE by reducing inflammation and shifting inflammatory immune responses to anti-inflammatory and can be used as a suitable treatment strategy for the treatment of EAE. The effectiveness of inhibiting or strengthening the functional cells of the immune system by these small molecules in terms of easy to access, simple construction and inexpensive expansion make them as a suitable tool for the treatment of inflammatory and autoimmune diseases.
 BACKGROUND AND PURPOSE: Population-based studies suggest severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines may trigger neurological autoimmunity including immune-mediated thrombotic thrombocytopenia. Long-term characterization of cases is warranted to facilitate patient care and inform vaccine-hesitant individuals. METHODS: In this single-center prospective case study with a median follow-up of 387 days long-term clinical, laboratory and imaging characteristics of patients with neurological autoimmunity diagnosed in temporal association (≤6 weeks) with SARS-CoV-2 vaccinations are reported. RESULTS: Follow-up data were available for 20 cases (central nervous system demyelinating diseases n = 8, inflammatory peripheral neuropathies n = 4, vaccine-induced immune thrombotic thrombocytopenia n = 3, myositis n = 2, myasthenia n = 1, limbic encephalitis n = 1, giant cell arteritis n = 1). Following therapy, the overall disability level improved (median modified Rankin Scale at diagnosis 3 vs. 1 at follow-up). The condition of two patients worsened despite immunosuppressants possibly related to their autoimmune diagnoses (limbic encephalitis n = 1, giant cell arteritis n = 1). At 12 months' follow-up, 12 patients achieved complete clinical remissions with partial responses in five and stable disease in one case. Correspondingly, autoimmune antibodies were non-detectable or titers had significantly lowered in all, and repeat imaging revealed radiological responses in most cases. Under vigilant monitoring 15 patients from our cohort underwent additional SARS-CoV-2 vaccinations (BNT162b2 n = 12, mRNA-1273 n = 3). Most patients (n = 11) received different vaccines than prior to diagnosis of neurological autoimmunity. Except for one short-lasting relapse, which responded well to steroids, re-vaccinations were well tolerated. CONCLUSIONS: In this study long-term characteristics of neurological autoimmunity encountered after SARS-CoV-2 vaccinations are defined. Outcome was favorable in most cases. Re-vaccinations were well tolerated and should be considered on an individual risk/benefit analysis.
 [This corrects the article DOI: 10.1016/j.radcr.2022.10.043.].


 Epstein-Barr virus (EBV) is a cancer-associated virus that infects more than 90% of adults. Unfortunately, many EBV-driven malignancies, including numerous B cell lymphomas, are highly aggressive and lack acceptable therapeutic outcomes. The concentrations of extracellular purines, namely, ATP and adenosine, are highly dysregulated in the tumor microenvironment and significantly impact the degree of immune responses to the tumor. Additionally, many tumor cells adapt to this dysregulation by overexpressing one or more ectonucleotidases, enzymes that degrade extracellular nucleotides to nucleosides. The degradation of immunostimulatory extracellular ATP to immunosuppressive adenosine through ectonucleotidase activity is one example of tumor cell exploitation of the purinergic signaling pathway. As such, preclinical studies targeting the purinergic signaling pathway have found it to be a promising immunotherapeutic target for the treatment of solid tumors; however, the extent to which purinergic signaling impacts the development and survival of EBV(+) B cell lymphoma remains unstudied. Here, we demonstrate robust ectonucleotidase expression on multiple types of EBV-positive B cell non-Hodgkin lymphoma (NHL). Furthermore, the presence of high concentrations of extracellular ATP resulted in the expression of lytic viral proteins and exhibited cytotoxicity toward EBV(+) B cell lines, particularly when CD39 was inhibited. Inhibition of CD39 also significantly prolonged survival in an aggressive cord blood humanized mouse model of EBV-driven lymphomagenesis and was correlated with an enhanced inflammatory immune response and reduced tumor burden. Taken together, these data suggest that EBV(+) B cell lymphomas exploit ectonucleotidase activity to circumvent ATP-mediated inflammation and cell death. IMPORTANCE EBV is a ubiquitous pathogen responsible for significant global lymphoma burden, including Hodgkin lymphoma, numerous non-Hodgkin B, T, and NK cell lymphomas, and lymphoproliferative disorders. EBV is also associated with epithelial cancers and autoimmune diseases, such as multiple sclerosis. Many of these diseases are highly aggressive and exhibit poor outcomes. As such, new treatments for EBV-driven cancers have the potential to benefit a large number of patients. We use in vitro and in vivo models to demonstrate the therapeutic potential of targeting the purinergic signaling pathway in the context of EBV-driven B cell lymphoma. These findings lend credence to the manipulation of purinergic signaling as a viable therapeutic approach to EBV(+) malignancies and support the feasibility of immunotherapeutic treatments for viral lymphoma.
 At present, a large number of relevant studies have suggested that the changes in gut microbiota are related to the course of nervous system diseases, and the microbiota-gut-brain axis is necessary for the proper functioning of the nervous system. Indole and its derivatives, as the products of the gut microbiota metabolism of tryptophan, can be used as ligands to regulate inflammation and autoimmune response in vivo. In recent years, some studies have found that the levels of indole and its derivatives differ significantly between patients with central nervous system diseases and healthy individuals, suggesting that they may be important mediators for the involvement of the microbiota-gut-brain axis in the disease course. Tryptophan metabolites produced by gut microbiota are involved in multiple physiological reactions, take indole for example, it participates in the process of inflammation and anti-inflammatory effects through various cellular physiological activities mediated by aromatic hydrocarbon receptors (AHR), which can influence a variety of neurological and neuropsychiatric diseases. This review mainly explores and summarizes the relationship between indoles and human neurological and neuropsychiatric disorders, including ischemic stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis, cognitive impairment, depression and anxiety, and puts forward that the level of indoles can be regulated through various direct or indirect ways to improve the prognosis of central nervous system diseases and reverse the dysfunction of the microbiota-gut-brain axis. This article is part of the Special Issue on "Microbiome & the Brain: Mechanisms & Maladies".
 BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a rare, autoimmune disease of the central nervous system that produces acute, unpredictable relapses causing cumulative neurological disability. Satralizumab, a humanized, monoclonal recycling antibody that targets the interleukin-6 receptor, reduced NMOSD relapse risk vs. placebo in two Phase 3 trials: SAkuraSky (satralizumab ± immunosuppressive therapy; NCT02028884) and SAkuraStar (satralizumab monotherapy; NCT02073279). Satralizumab is approved to treat aquaporin-4 IgG-seropositive (AQP4-IgG+) NMOSD. SAkuraBONSAI (NCT05269667) will explore fluid and imaging biomarkers to better understand the mechanism of action of satralizumab and the neuronal and immunological changes following treatment in AQP4-IgG+ NMOSD. OBJECTIVES: SAkuraBONSAI will evaluate clinical disease activity measures, patient-reported outcomes (PROs), pharmacokinetics, and safety of satralizumab in AQP4-IgG+ NMOSD. Correlations between imaging markers (magnetic resonance imaging [MRI] and optical coherence tomography [OCT]) and blood and cerebrospinal fluid (CSF) biomarkers will be investigated. STUDY DESIGN: SAkuraBONSAI is a prospective, open-label, multicenter, international, Phase 4 study that will enroll approximately 100 adults (18-74 years) with AQP4-IgG+ NMOSD. This study includes two patient cohorts: newly diagnosed, treatment-naïve patients (Cohort 1; n = 60); and inadequate responders to recent (<6 months) rituximab infusion (Cohort 2; n = 40). Satralizumab monotherapy (120 mg) will be administered subcutaneously at Weeks 0, 2, 4, and Q4W thereafter for a total of 92 weeks. ENDPOINTS: Disease activity related to relapses (proportion relapse-free, annualized relapse rate, time to relapse, and relapse severity), disability progression (Expanded Disability Status Scale), cognition (Symbol Digit Modalities Test), and ophthalmological changes (visual acuity; National Eye Institute Visual Function Questionnaire-25) will all be assessed. Peri-papillary retinal nerve fiber layer and ganglion cell complex thickness will be monitored using advanced OCT (retinal nerve fiber layer and ganglion cell plus inner plexiform layer thickness). Lesion activity and atrophy will be monitored by MRI. Pharmacokinetics, PROs, and blood and CSF mechanistic biomarkers will be assessed regularly. Safety outcomes include the incidence and severity of adverse events. CONCLUSIONS: SAkuraBONSAI will incorporate comprehensive imaging, fluid biomarker, and clinical assessments in patients with AQP4-IgG+ NMOSD. SAkuraBONSAI will provide new insights into the mechanism of action of satralizumab in NMOSD, while offering the opportunity to identify clinically relevant neurological, immunological, and imaging markers.
 OBJECTIVE: To investigate the clinical manifestations, treatment and prognosis of COVID-19-associated central nervous system (CNS) complications. METHODS: In this single-centre observation study, we recruited patients with COVID-19-associated CNS complications at the neurology inpatient department of the Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen) from Dec 2022 to Feb 2023. Patients were analysed for demographics, clinical manifestations, cerebrospinal fluid properties, electroencephalographic features, neuroimaging characteristics, and treatment outcome. All patients were followed-up at 1 and 2 months after discharge until Apr 2023. RESULTS: Of the 12 patients with COVID-19-associated CNS complications, the CNS symptoms occur between 0 days and 4 weeks after SARS-CoV-2 infection. The most common CNS symptoms were memory deficits (4/12, 33%), Unresponsiveness (4/12, 33%), mental and behavioural disorders (4/12, 33%). Seven of 12 cases can be categorized as probable SARS-CoV-2 encephalitis, and 5 cases can be described as brainstem encephalitis, acute disseminated encephalomyelitis, optic neuritis, multiple sclerosis or tremor probably associated with SARS-CoV-2 infection. Six patients received antiviral therapy, and 11 patients received glucocorticoid therapy, of which 3 patients received human immunoglobulin synchronously. Nine patients recovered well, two patients had residual neurological dysfunction, and one patient passed away from complications associated with tumor. CONCLUSION: In this observational study, we found that the inflammatory or immune-related complications were relatively common manifestations of COVID-19-associated CNS complications, including different phenotypes of encephalitis and CNS inflammatory demyelinating diseases. Most patients recovered well, but a few patients had significant neurological dysfunctions remaining.
 The very-low-calorie KD (VLCKD) is characterized by a caloric intake of under 800 kcal/day divided into less than 50 g/day of carbohydrate (13%) and 1 to 1.5 g of protein/kg of body weight (44%) and 43% of fat. This low carbohydrate intake changes the energy source from glucose to ketone bodies. Moreover, clinical trials have consistently shown a beneficial effect of VLCKD in several diseases, such as heart failure, schizophrenia, multiple sclerosis, Parkinson's, and obesity, among others. The gut microbiota has been associated with the metabolic conditions of a person and is regulated by diet interactions; furthermore, it has been shown that the microbiota has a role in body weight homeostasis by regulating metabolism, appetite, and energy. Currently, there is increasing evidence of an association between gut microbiota dysbiosis and the pathophysiology of obesity. In addition, the molecular pathways, the role of metabolites, and how microbiota modulation could be beneficial remain unclear, and more research is needed. The objective of the present article is to contribute with an overview of the impact that VLCKD has on the intestinal microbiota composition of individuals with obesity through a literature review describing the latest research regarding the topic and highlighting which bacteria phyla are associated with obesity and VLCKD.
 OBJECTIVE: Cognitive-behavioral stress management (CBSM) intervention enhances the psychological status and quality of life in patients with various diseases, such as cancer, human immunodeficiency virus infection, chronic fatigue syndrome, and multiple sclerosis. This multicenter, randomized, controlled study intended to explore the potential benefit of CBSM in ameliorating the anxiety, depression, and quality of life (QoL) in acute myocardial infarction (AMI) patients after percutaneous coronary intervention (PCI). METHODS: A total of 250 AMI patients who received PCI were randomly allocated to the CBSM (N = 125) and control care (CC) (N = 125) groups, and underwent weekly corresponding interventions for 12 weeks. The hospital anxiety and depression scale (HADS), EuroQol 5D (EQ-5D), and EuroQol visual analogue scale (EQ-VAS) scores were evaluated at baseline (M0), month (M)1, M3, and M6. Major adverse cardiovascular events (MACE) were recorded during follow-up. RESULTS: HADS-anxiety score at M1 (P = 0.036), M3 (P = 0.002), and M6 (P = 0.001), as well as anxiety rate at M6 (P = 0.026), was reduced in the CBSM group versus the CC group. HADS-depression score at M3 (P = 0.027) and M6 (P = 0.002), as well as depression rate at M6 (P = 0.013), was decreased in the CBSM group versus the CC group. EQ-5D score at M3 (P = 0.046) and M6 (P = 0.001) was reduced, while EQ-VAS score at M1 (P = 0.037), M3 (P = 0.010), and M6 (P = 0.003) was raised, in the CBSM group versus the CC group. However, accumulating MACE rate did not differ between the two groups (P = 0.360). CONCLUSION: CBSM ameliorates anxiety, depression, and QoL but does not affect MACE in AMI patients after PCI.
 BACKGROUND: Autism spectrum disorder (ASD) is categorized as a neurodevelopmental disorder, presenting with a variety of aetiological and phenotypical features. Ibudilast is known to produce beneficial effects in several neurological disorders including neuropathic pain, multiple sclerosis, etc. by displaying its neuroprotective and anti-inflammatory properties. Here, in our study, the pharmacological outcome of ibudilast administration was investigated in the prenatal valproic acid (VPA)-model of ASD in Wistar rats. METHODS: Autistic-like symptoms were induced in Wistar male pups of dams administered with Valproic acid (VPA) on embryonic day 12.5. VPA-exposed male pups were administered with two doses of ibudilast (5 and10 mg/kg) and all the groups were evaluated for behavioral parameters like social interaction, spatial memory/learning, anxiety, locomotor activity, and nociceptive threshold. Further, the possible neuroprotective effect of ibudilast was evaluated by assessing oxidative stress, neuroinflammation (IL-1β, TNF-α, IL-6, IL-10) in the hippocampus, % area of Glial fibrillary acidic protein (GFAP)-positive cells and neuronal damage in the cerebellum. KEY FINDINGS: Treatment with ibudilast significantly attenuated prenatal VPA exposure associated social interaction and spatial learning/memory deficits, anxiety, hyperactivity, and increased nociceptive threshold, and it decreased oxidative stress markers, pro-inflammatory markers (IL-1β, TNF-α, IL-6), and % area of GFAP-positive cells and restored neuronal damage. CONCLUSIONS: Ibudilast treatment has restored crucial ASD-related behavioural abnormalities, potentially through neuroprotection. Therefore, benefits of ibudilast administration in animal models of ASD suggest that ibudilast may have therapeutic potential in the treatment of ASD.
 OBJECTIVE: We report a case of biopsy-proven giant cell arteritis after an initial presentation of area postrema syndrome. METHODS: A 65-year-old man was evaluated using MRI, temporal artery biopsy, and ultrasound. RESULTS: The patient presented with refractory nausea, vomiting, and hiccups that caused weight loss without any other neurologic or clinical symptoms. His MRI scan 15 days later revealed a hyperintense sign on the area postrema with no abnormal diffusion or contrast enhancement, compatible with isolated area postrema syndrome. An extensive workup for inflammation and other etiologies including neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody disorder, and multiple sclerosis (MS) showed negative results. The patient responded to treatment with methylprednisolone. Two months after the initial clinical manifestation, the patient developed fatigue, headache, and scalp tenderness. He was diagnosed with giant cell arteritis after ultrasonography and biopsy were performed. He responded well to oral glucocorticoids and had only 1 relapse during tapering. He has not had arteritic ischemic optic neuropathy or any new episodes of area postrema syndrome. DISCUSSION: This case demonstrates the importance of expanding the differential diagnosis in patients with area postrema syndrome and no other signs of NMOSD.
 Background and aims: Inflammatory bowel diseases (IBD) are chronic disorders associated with a reduced quality of life, and patients often also suffer from psychiatric comorbidities. Overall, both mood and cognitive disorders are prevalent in chronic organic diseases, especially in the case of a strong immune component, such as rheumatoid arthritis, multiple sclerosis, and cancer. Divergent data regarding the true incidence and prevalence of mental disorders in patients with IBD are available. We aimed to review the current evidence on the topic and the burden of mental illness in IBD patients, the role of the brain-gut axis in their co-existence, and its implication in an integrated clinical management. Methods: PubMed was searched to identify relevant studies investigating the gut-brain interactions and the incidence and prevalence of psychiatric disorders, especially of depression, anxiety, and cognitive dysfunction in the IBD population. Results: Among IBD patients, there is a high prevalence of psychiatric comorbidities, especially of anxiety and depression. Approximately 20-30% of IBD patients are affected by mood disorders and/or present with anxiety symptoms. Furthermore, it has been observed that the prevalence of mental illnesses increases in patients with active intestinal disease. Psychiatric comorbidities continue to be under-diagnosed in IBD patients and remain an unresolved issue in the management of these patients. Conclusions: Psychiatric illnesses co-occurring in IBD patients deserve acknowledgment from IBD specialists. These comorbidities highly impact the management of IBD patients and should be studied as an adjunctive therapeutic target.
 Generative adversarial networks (GANs) are one powerful type of deep learning models that have been successfully utilized in numerous fields. They belong to the broader family of generative methods, which learn to generate realistic data with a probabilistic model by learning distributions from real samples. In the clinical context, GANs have shown enhanced capabilities in capturing spatially complex, nonlinear, and potentially subtle disease effects compared to traditional generative methods. This review critically appraises the existing literature on the applications of GANs in imaging studies of various neurological conditions, including Alzheimer's disease, brain tumors, brain aging, and multiple sclerosis. We provide an intuitive explanation of various GAN methods for each application and further discuss the main challenges, open questions, and promising future directions of leveraging GANs in neuroimaging. We aim to bridge the gap between advanced deep learning methods and neurology research by highlighting how GANs can be leveraged to support clinical decision making and contribute to a better understanding of the structural and functional patterns of brain diseases.
 PURPOSE: Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults with a median overall survival of only 14.6 months despite aggressive treatment. While immunotherapy has been successful in other cancers, its benefit has been proven elusive in GBM, mainly due to a markedly immunosuppressive tumor microenvironment. SARS-CoV-2 has been associated with the development of a pronounced central nervous system (CNS) inflammatory response when infecting different cells including astrocytes, endothelial cells, and microglia. While SARS-CoV2 entry factors have been described in different tissues, their presence and implication on GBM aggressiveness or microenvironment has not been studied on appropriate preclinical models. METHODS: We evaluated the presence of crucial SARS-CoV-2 entry factors: ACE2, TMPRSS2, and NRP1 in matched surgically-derived GBM tissue, cells lines, and organoids; as well as in human brain derived specimens using immunohistochemistry, confocal pixel line intensity quantification, and transcriptome analysis. RESULTS: We show that patient derived-GBM tissue and cell cultures express SARS-CoV2 entry factors, being NRP1 the most crucial facilitator of SARS-CoV-2 infection in GBM. Moreover, we demonstrate that, receptor expression remains present in our GBM organoids, making them an adequate model to study the effect of this virus in GBM for the potential development of viral therapies in the future. CONCLUSION: Our findings suggest that the SARS-CoV-2 virus entry factors are expressed in primary tissues and organoid models and could be potentially utilized to study the susceptibility of GBM to this virus to target or modulate the tumor microenviroment.
 INTRODUCTION: Daily childcare can be challenging for parents with a physical disability who have young children. Occupational therapists are valuable facilitators to family participation. However, occupational therapists have reported significant gaps in knowledge when documenting the parenting role of parents with a physical disability in occupational therapy practice. This study explored and described the parenting assessment methods used with parents with a physical disability in the scientific literature. METHODS: A scoping review was conducted, and search results were reviewed by two separate reviewers. The search strategy was applied to five databases (Embase, CINAHL, MEDLINE, HaPI, PsycInfo). Numerical and thematic analyses were conducted. RESULTS: Four thousand one hundred fifty articles were screened, and 73 relevant scientific articles were included. Seventy-six assessment methods were identified, including 20 assessment instruments with few reported population-specific psychometric studies. Most assessments were conducted via interviews (n = 45), followed by questionnaires (n = 27), and only six were performance based. Parenting practices and experience were the two dimensions most assessed, with little attention given to parenting responsibility. Mothers with multiple sclerosis, spinal cord injury, rheumatoid arthritis, and cerebral palsy were the most assessed. CONCLUSION: Further research is needed to develop specific, multidimensional, and validated parenting assessments for all parents with a physical disability, including performance-based assessments. Formal assessments should be conducted by professionals, including occupational therapists, who have the necessary training.
 Neurological diseases cause physical, psychosocial, and spiritual or existential suffering from the time of their diagnosis. Palliative care focuses on improving quality of life for people with serious illness and their families by addressing this multidimensional suffering. Evidence from clinical trials supports the ability of palliative care to improve patient and caregiver outcomes by the use of outpatient or home-based palliative care interventions for people with motor neuron disease, multiple sclerosis, or Parkinson's disease; inpatient palliative care consultations for people with advanced dementia; telephone-based case management for people with dementia in the community; and nurse-led discussions with decision aids for people with advanced dementia in long-term care. Unfortunately, most people with neurological diseases do not get the support that they need for their palliative care under current standards of healthcare. Improving this situation requires the deployment of routine screening to identify individual palliative care needs, the integration of palliative care approaches into routine neurological care, and collaboration between neurologists and palliative care specialists. Research, education, and advocacy are also needed to raise standards of care.
 Neurogenic detrusor overactivity (NDO) is a complication of multiple sclerosis, spinal cord injury (SCI), stroke, head injury, and other conditions characterized by damage to the upper motor neuronal system. NDO often leads to high bladder pressure that may cause upper urinary tract damage and urinary incontinence (UI). Prior to the use of onabotulinumtoxinA, oral anticholinergics and surgical augmentation cystoplasty were the treatment options. Overactive bladder (OAB) is non-neurogenic and affects a much larger population than NDO. Both NDO and OAB negatively impact patients' quality of life (QOL) and confer high health care utilization burdens. Early positive results from pioneering investigators who injected onabotulinumtoxinA into the detrusor of patients with SCI caught the interest of Allergan, which then initiated collaborative clinical trials that resulted in FDA approval of onabotulinumtoxinA 200U in 2011 for NDO and 100U in 2013 for patients with OAB who inadequately respond to or are intolerant of an anticholinergic. These randomized, double-blind, placebo-controlled trials for NDO showed significant improvements in UI episodes, urodynamic parameters, and QOL; the most frequent adverse events were urinary tract infection (UTI) and urinary retention. Similarly, randomized, double-blind, placebo-controlled trials of onabotulinumtoxinA 100U for OAB found significant improvements in UI episodes, treatment benefit, and QOL; UTI and dysuria were the most common adverse events. Long-term studies in NDO and OAB showed sustained effectiveness and safety with repeat injections of onabotulinumtoxinA, the use of which has profoundly improved the QOL of patients failing anticholinergic therapy and has expanded the utilization of onabotulinumtoxinA into smooth muscle.
 Dysautonomia has substantially impacted acute COVID-19 severity as well as symptom burden after recovery from COVID-19 (long COVID), yet the underlying causes remain unknown. Here, we hypothesized that vagus nerves are affected in COVID-19 which might contribute to autonomic dysfunction. We performed a histopathological characterization of postmortem vagus nerves from COVID-19 patients and controls, and detected SARS-CoV-2 RNA together with inflammatory cell infiltration composed primarily of monocytes. Furthermore, we performed RNA sequencing which revealed a strong inflammatory response of neurons, endothelial cells, and Schwann cells which correlated with SARS-CoV-2 RNA load. Lastly, we screened a clinical cohort of 323 patients to detect a clinical phenotype of vagus nerve affection and found a decreased respiratory rate in non-survivors of critical COVID-19. Our data suggest that SARS-CoV-2 induces vagus nerve inflammation followed by autonomic dysfunction which contributes to critical disease courses and might contribute to dysautonomia observed in long COVID.
 Macrophages are innate immune cells in the organism and can be found in almost tissues and organs. They are highly plastic and heterogeneous cells and can participate in the immune response, thereby playing a crucial role in maintaining the immune homeostasis of the body. It is well known that undifferentiated macrophages can polarize into classically activated macrophages (M1 macrophages) and alternatively activated macrophages (M2 macrophages) under different microenvironmental conditions. The directions of macrophage polarization can be regulated by a series of factors, including interferon, lipopolysaccharide, interleukin, and noncoding RNAs. To elucidate the role of macrophages in various autoimmune diseases, we searched the literature on macrophages with the PubMed database. Search terms are as follows: macrophages, polarization, signaling pathways, noncoding RNA, inflammation, autoimmune diseases, systemic lupus erythematosus, rheumatoid arthritis, lupus nephritis, Sjogren's syndrome, Guillain-Barré syndrome, and multiple sclerosis. In the present study, we summarize the role of macrophage polarization in common autoimmune diseases. In addition, we also summarize the features and recent advances with a particular focus on the immunotherapeutic potential of macrophage polarization in autoimmune diseases and the potentially effective therapeutic targets.
 PURPOSE: To conduct an umbrella review of systematic reviews on functional electrical stimulation (FES) to improve walking in adults with an upper motor neuron lesion. METHODS: Five electronic databases were searched, focusing on the effect of FES on walking. The methodological quality of reviews was evaluated using AMSTAR2 and certainty of evidence was established through the GRADE approach. RESULTS: The methodological quality of the 24 eligible reviews (stroke, n = 16; spinal cord injury (SCI), n = 5; multiple sclerosis (MS); n = 2; mixed population, n = 1) ranged from critically low to high. Stroke reviews concluded that FES improved walking speed through an orthotic (immediate) effect and had a therapeutic benefit (i.e., over time) compared to usual care (low certainty evidence). There was low-to-moderate certainty evidence that FES was no better or worse than an Ankle Foot Orthosis regarding walking speed post 6 months. MS reviews concluded that FES had an orthotic but no therapeutic effect on walking. SCI reviews concluded that FES with or without treadmill training improved speed but combined with an orthosis was no better than orthosis alone. FES may improve quality of life and reduce falls in MS and stroke populations. CONCLUSION: FES has orthotic and therapeutic benefits. Certainty of evidence was low-to-moderate, mostly due to high risk of bias, low sample sizes, and wide variation in outcome measures. Future trials must be of higher quality, use agreed outcome measures, including measures other than walking speed, and examine the effects of FES for adults with cerebral palsy, traumatic and acquired brain injury, and Parkinson's disease.
 Sphingolipidoses are a subcategory of lysosomal storage diseases (LSDs) caused by mutations in enzymes of the sphingolipid catabolic pathway. Like many LSDs, neurological involvement in sphingolipidoses leads to early mortality with limited treatment options. Given the role of myelin loss as a major contributor toward LSD-associated neurodegeneration, we investigated the pathways contributing to demyelination in a CRISPR-Cas9-generated zebrafish model of combined saposin (psap) deficiency. psap knockout (KO) zebrafish recapitulated major LSD pathologies, including reduced lifespan, reduced lipid storage, impaired locomotion and severe myelin loss; loss of myelin basic protein a (mbpa) mRNA was progressive, with no changes in additional markers of oligodendrocyte differentiation. Brain transcriptomics revealed dysregulated mTORC1 signaling and elevated neuroinflammation, where increased proinflammatory cytokine expression preceded and mTORC1 signaling changes followed mbpa loss. We examined pharmacological and genetic rescue strategies via water tank administration of the multiple sclerosis drug monomethylfumarate (MMF), and crossing the psap KO line into an acid sphingomyelinase (smpd1) deficiency model. smpd1 mutagenesis, but not MMF treatment, prolonged lifespan in psap KO zebrafish, highlighting the modulation of acid sphingomyelinase activity as a potential path toward sphingolipidosis treatment.
 Neurodegenerative diseases, in particular for Alzheimer's disease (AD), Parkinson's disease (PD) and Multiple sclerosis (MS), are a category of diseases with progressive loss of neuronal structure or function (encompassing neuronal death) leading to neuronal dysfunction, whereas the underlying pathogenesis remains to be clarified. As the microbiological ecosystem of the intestinal microbiome serves as the second genome of the human body, it is strongly implicated as an essential element in the initiation and/or progression of neurodegenerative diseases. Nevertheless, the precise underlying principles of how the intestinal microflora impact on neurodegenerative diseases via gut-brain axis by modulating the immune function are still poorly characterized. Consequently, an overview of initiating the development of neurodegenerative diseases and the contribution of intestinal microflora on immune function is discussed in this review.
 Osteoclast (OC) abnormalities lead to many osteolytic diseases, such as osteoporosis, inflammatory bone erosion, and tumor-induced osteolysis. Exploring effective strategies to remediate OCs dysregulation is essential. FTY720, also known as fingolimod, has been approved for the treatment of multiple sclerosis and has anti-inflammatory and immunosuppressive effects. Here, we found that FTY720 inhibited osteoclastogenesis and OC function by inhibiting nuclear factor kappa-B (NF-κB) signaling. Interestingly, we also found that FTY720 inhibited osteoclastogenesis by upregulating histone deacetylase 4 (HDAC4) expression levels and downregulating activating transcription factor 4 (ATF4) expression levels. In vivo, FTY720 treatment prevented lipopolysaccharide- (LPS-) induced calvarial osteolysis and significantly reduced the number of tartrate-resistant acid phosphatase- (TRAP-) positive OCs. Taken together, these results demonstrate that FTY720 can inhibit osteoclastogenesis and ameliorate inflammation-induced bone loss. Which may provide evidence of a new therapeutic target for skeletal diseases caused by OC abnormalities.
 CLEC16A is a membrane-associated C-type lectin protein that functions as a E3-ubiquitin ligase. CLEC16A regulates autophagy and mitophagy, and reportedly localizes to late endosomes. GWAS studies have associated CLEC16A SNPs to various auto-immune and neurological disorders, including multiple sclerosis and Parkinson disease. Studies in mouse models imply a role for CLEC16A in neurodegeneration. We identified bi-allelic CLEC16A truncating variants in siblings from unrelated families presenting with a severe neurodevelopmental disorder including microcephaly, brain atrophy, corpus callosum dysgenesis, and growth retardation. To understand the function of CLEC16A in neurodevelopment we used in vitro models and zebrafish embryos. We observed CLEC16A localization to early endosomes in HEK293T cells. Mass spectrometry of human CLEC16A showed interaction with endosomal retromer complex subunits and the endosomal ubiquitin ligase TRIM27. Expression of the human variant leading to C-terminal truncated CLEC16A, abolishes both its endosomal localization and interaction with TRIM27, suggesting a loss-of-function effect. CLEC16A knockdown increased TRIM27 adhesion to early endosomes and abnormal accumulation of endosomal F-actin, a sign of disrupted vesicle sorting. Mutagenesis of clec16a by CRISPR-Cas9 in zebrafish embryos resulted in accumulated acidic/phagolysosome compartments, in neurons and microglia, and dysregulated mitophagy. The autophagocytic phenotype was rescued by wild-type human CLEC16A but not the C-terminal truncated CLEC16A. Our results demonstrate that CLEC16A closely interacts with retromer components and regulates endosomal fate by fine-tuning levels of TRIM27 and polymerized F-actin on the endosome surface. Dysregulation of CLEC16A-mediated endosomal sorting is associated with neurodegeneration, but it also causes accumulation of autophagosomes and unhealthy mitochondria during brain development.
 BACKGROUND: Neurological disorders, such as Alzheimer's disease (AD), comprise a major cause of health-related disabilities in human. However, biomarkers towards pathogenesis or novel targets are still limited. OBJECTIVE: To identify the causality between plasma proteins and the risk of AD and other eight common neurological diseases using a Mendelian randomization (MR) study. METHODS: Exposure data were obtained from a genome-wide association study (GWAS) of 2,994 plasma proteins in 3,301 healthy adults, and outcome datasets included GWAS summary statistics of nine neurological disorders. Inverse variance-weighted MR method as the primary analysis was used to estimate causal effects. RESULTS: Higher genetically proxied plasma myeloid cell surface antigen CD33 level was found to be associated with increased risk of AD (odds ratio [OR] 1.079, 95% confidence interval [CI] 1.047-1.112, p = 8.39×10(-7)). We also discovered the causality between genetically proxied elevated prolactin and higher risk of epilepsy (OR = 1.068, 95% CI = 1.034-1.102; p = 5.46×10(-5)). Negative associations were identified between cyclin-dependent kinase 8 and ischemic stroke (OR = 0.927, 95% CI = 0.896-0.959, p = 9.32×10(-6)), between neuralized E3 ubiquitin-protein ligase 1 and migraine (OR = 0.914, 95% CI = 0.878-0.952, p = 1.48×10(-5)), and between Fc receptor-like protein 4 and multiple sclerosis (MS) (OR = 0.929, 95% CI = 0.897-0.963, p = 4.27×10(-5)). CONCLUSION: The findings identified MR-level protein-disease associations for AD, epilepsy, ischemic stroke, migraine, and MS.
 Over the past few decades, extensive research has shed light on immune alterations and the significance of dysfunctional biological barriers in psychiatric disorders. The leaky gut phenomenon, intimately linked to the integrity of both brain and intestinal barriers, may play a crucial role in the origin of peripheral and central inflammation in these pathologies. Sphingosine-1-phosphate (S1P) is a bioactive lipid that regulates both the immune response and the permeability of biological barriers. Notably, S1P-based drugs, such as fingolimod and ozanimod, have received approval for treating multiple sclerosis, an autoimmune disease of the central nervous system (CNS), and ulcerative colitis, an inflammatory condition of the colon, respectively. Although the precise mechanisms of action are still under investigation, the effectiveness of S1P-based drugs in treating these pathologies sparks a debate on extending their use in psychiatry. This comprehensive review aims to delve into the molecular mechanisms through which S1P modulates the immune system and brain/intestinal barrier functions. Furthermore, it will specifically focus on psychiatric diseases, with the primary objective of uncovering the potential of innovative therapies based on S1P signaling.
 Omega-3 polyunsaturated fatty acids (PUFA) have demonstrated anti-inflammatory properties, while Omega-6 have pro-inflammatory effects, and the balance between the two is an important aspect of healthy nutrition. Over the last 30 years, however, the Western diet has shifted largely from Omega-3 to Omega-6 consumption. Uncontrolled aberrant and chronic inflammation is a leading component of many common diseases, including arthritis, cardiovascular diseases, neurodegenerative diseases, cancer, obesity, autoimmune diseases, and infective diseases. Eicosanoids derived from Omega-6 participate in the inflammatory process, while Omega-3 PUFA have the opposite effect. Many favorable effects of Omega-3 are believed to result from their anti-inflammatory properties, but eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) also have inhibitory effects on immune cells and reduce proinflammatory cytokine release. All these mechanisms can be beneficial in autoimmunity. No effective preventions or definite cures for autoimmune diseases are yet known because pathophysiology is also unclear. Omega-3 fatty acid supplementation is associated with a significant reduction in disease activity in several autoimmune diseases, like type 1 diabetes (T1D), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS). Studies of viral diseases, including COVID-19, show improvement in symptom severity, recovery prognosis, and probability of survival with the use of Omega-3. Finally, the evidence of the beneficial effect of Omega-3 on metabolic diseases associated with aging is persuasive; various studies have demonstrated that their consumption improves lipids, fatty liver disease, obesity, cognitive function, and cardiovascular complications of chronic kidney disease (CKD). Omega-3 PUFA have also been shown to support an anti-inflammatory effect in older age and to have favorable effects on age-related disease's complications, frailty, and mortality. A healthy Omega-6/3 PUFA ratio should be targeted for the modulation of low-grade inflammation, as well as for the prevention of immune dysregulation and complications of uncontrolled inflammation triggered by infections, development, and progression of autoimmune disorders, and the consequences of oxidative stress due to aging. There is still a need for randomized clinical studies to validate current evidence supporting supplementation with correct doses of Omega-3 PUFA in autoimmune and chronic disease prevention.
 Methylglyoxal (MGO) is a highly reactive metabolite generated by glycolysis. Although abnormal accumulation of MGO has been reported in several autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, the role of MGO in autoimmune diseases has not yet been fully investigated. In this study, we found that the intracellular MGO levels increased in activated immune cells, such as microglia and lymphocytes. Treatment with MGO inhibited inflammatory cell accumulation in the spinal cord and ameliorated the clinical symptoms in EAE mice. Further analysis indicated that MGO suppressed M1-polarization of microglia cells and diminished their inflammatory cytokine production. MGO also inhibited the ability of microglial cells to recruit and activate lymphocytes by decreasing chemokine secretion and expression of co-stimulatory molecules. Furthermore, MGO negatively regulated glycolysis by suppressing glucose transporter 1 expression. Mechanically, we found that MGO could activate nuclear factor erythroid 2-related factor 2 (NRF2) pathway and NRF2 could bind to the promoter of IκBζ gene and suppressed its transcription and subsequently pro-inflammatory cytokine production. In conclusion, our results showed that MGO acts as an immunosuppressive metabolite by activating the NRF2-IκBζ.
 Marchiafava Bignami disease (MBD) is a neurological disorder characterized by myelin degeneration and tissue necrosis within the central nervous system. This condition predominantly afflicts individuals with chronic alcohol abuse and malnutrition. The most distinctive pathological feature of MBD is the necrotic degeneration specifically observed in the corpus callosum; however, emerging evidence also indicates the potential involvement of other brain regions. The main pathophysiological mechanisms involve alcohol consumption, which leads to thiamine depletion and disrupts various metabolic pathways. This, in turn, hinders myelin synthesis and impairs signal transmission, resulting in a wide range of symptoms and signs. MBD can manifest in different stages, including acute, subacute, and chronic, each with varying severity. Diagnosing MBD can be challenging due to its presenting symptoms being nonspecific. In the era preceding the development of sophisticated imaging methodologies, the diagnosis of MBD was primarily established through postmortem examination conducted during autopsies. However, with a detailed medical history and imaging modalities such as magnetic resonance imaging (MRI) and computed tomography (CT), it is now possible to diagnose MBD and differentiate it from other diseases with similar clinical presentations. MRI is considered the gold standard for visualizing lesions in the corpus callosum and other affected areas. Also, positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance spectroscopy (MRS) could show brain damage in the corpus callosum associated with MBD. MRI-diffusion-weighted imaging (DWI) detects early lesions, while diffusion tensor imaging (DTI) investigates clinical manifestations and recovery. Poor prognostic indicators for MBD include extensive cerebral cortex involvement and severe disturbances in consciousness. Differential diagnosis involves ruling out other alcohol-related disorders, such as neoplastic conditions, Wernicke's encephalopathy, and multiple sclerosis, among others, through careful evaluation. The therapeutic strategies for the management of MBD are currently lacking definitive establishment; however, available evidence indicates that targeted interventions have the potential to induce amelioration. Corticosteroids offer prospective advantages in addressing brain edema, demyelination, and inflammation; research findings present a heterogeneous outcome pattern. Notably, thiamine treatment reduces the likelihood of unfavorable consequences, particularly when administered promptly, and thus is endorsed as the primary therapeutic approach for MBD. This review will highlight this rare disease that many healthcare providers might not be familiar with. By understanding its clinical presentation, differential diagnosis, imaging, and management, medical providers might better identify and diagnose MBD. Raising awareness about this condition can lead to better prevention, early detection, and timely intervention.
 Neuroinflammation is the precursor for several neurodegenerative diseases (NDDs), such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Targeting neuroinflammation has emerged as a promising strategy to address a wide range of CNS pathologies. These NDDs still present significant challenges in terms of limited and ineffective diagnosis and treatment options, driving the need to explore innovative and novel therapeutic alternatives. Aptamers are single-stranded nucleic acids that offer the potential for addressing these challenges through diagnostic and therapeutic applications. In this review, we summarize diagnostic and therapeutic aptamers for inflammatory biomolecules, as well as the inflammatory cells in NDDs. We also discussed the potential of short nucleotides for Aptamer-Based Targeted Brain Delivery through their unique features and modifications, as well as their ability to penetrate the blood-brain barrier. Moreover, the unprecedented opportunities and substantial challenges of using aptamers as therapeutic agents, such as drug efficacy, safety considerations, and pharmacokinetics, are also discussed. Taken together, this review assesses the potential of aptamers as a pioneering approach for target delivery to the CNS and the treatment of neuroinflammation and NDDs.
 OBIECTIVES: This study aims to prospectively evaluate the frequency and adverse consequences of diagnostic delay and misdiagnosis in a cohort of patients with thrombotic antiphospholipid syndrome (TAPS). In addition, a systematic review of the literature concerning the diagnostic delay and misdiagnosis of TAPS was carried out. METHODS: Patient enrollment occurred between 1999 and 2022. The study group was formed by TAPS patients whose diagnosis was delayed and those who were misdiagnosed. The control group was made up of patients who were timely and correctly diagnosed with TAPS. RESULTS: The literature review showed 42 misdiagnosed patients, 27 of them were in one retrospective cohort study and 15 in 13 case reports. One hundred sixty-one out of 189 patients (85.2%) received a timely, correct diagnosis of TAPS; 28 (14.8%) did not. The number of patients with diagnostic issues was significantly higher for the first period (1999-2010), and the number of patients with a correct diagnosis was significantly higher for the second one (2011-2022). When the clinical and laboratory characteristics of the patients with delayed diagnosis were compared with those with misdiagnosis, there was a significantly higher number of severe adverse consequences characterized by permanent disability or death in the latter group. The two most common types of misdiagnoses were systemic lupus erythematosus (6 cases, 46.1%) and cardiovascular diseases (4 cases, 30.8%). CONCLUSIONS: The study demonstrates that although knowledge about TAPS has improved over time, diagnostic delays and errors remains to be addressed as they are strongly associated to adverse consequences. Key Points •Although knowledge of thrombotic antiphospholipid syndrome has improved over time, it is still limited. •Diagnostic delay and misdiagnosis are still an important issue that remains to be addressed as they are strongly associated to adverse consequences. •The three more frequent misdiagnoses are multiple sclerosis, systemic lupus erythematosus and cardiovascular diseases.
 Introduction Telehealth visits (TH) have become an important pillar of healthcare delivery during the COVID pandemic. No-shows (NS) may result in delays in clinical care and in lost revenue. Understanding the factors associated with NS may help providers take measures to decrease the frequency and impact of NS in their clinics. We aim to study the demographic and clinical diagnoses associated with NS to ambulatory telehealth neurology visits. Methods We conducted a retrospective chart review of all telehealth video visits (THV) in our healthcare system from 1/1/2021 to 5/1/2021 (cross-sectional study). All patients at or above 18 years of age who either had a completed visit (CV) or had an NS for their neurology ambulatory THV were included. Patients having missing demographic variables and not meeting the ICD-10 primary diagnosis codes were excluded. Demographic factors and ICD-10 primary diagnosis codes were retrieved. NS and CV groups were compared using independent samples t-tests and chi-square tests as appropriate. Multivariate regression, with backward elimination, was conducted to identify pertinent variables. Results Our search resulted in 4,670 unique THV encounters out of which 428 (9.2%) were NS and 4,242 (90.8%) were CV. Multivariate regression with backward elimination showed that the odds of NS were higher with a self-identified non-Caucasian race OR = 1.65 (95%, CI: 1.28-2.14), possessing Medicaid insurance OR = 1.81 (95%, CI: 1.54-2.12) and with primary diagnoses of sleep disorders OR = 10.87 (95%, CI: 5.55-39.84), gait abnormalities (OR = 3.63 (95%, CI: 1.81-7.27), and back/radicular pain OR = 5.62 (95%, CI: 2.84-11.10). Being married was associated with CVs OR = 0.74 (95%, CI: 0.59-0.91) as well as primary diagnoses of multiple sclerosis OR = 0.24 (95%, CI: 0.13-0.44) and movement disorders OR = 0.41 (95%, CI: 0.25-0.68). Conclusion Demographic factors, such as self-identified race, insurance status, and primary neurological diagnosis codes, can be helpful to predict an NS to neurology THs. This data can be used to warn providers regarding the risk of NS.
 BACKGROUND: Neuromyelitis optica spectrum disorders (NMOSD) is considered a complex multifactorial disorder. Most cases are sporadic, and familial NMOSD is assumed as a rare occurrence. However, few studies reported familial aggregation of the disorder. OBJECTIVES: To report familial NMOSD cases in Thailand and conduct a systematic review of familial NMOSD. METHODS: A retrospective chart review of familial NMOSD patients at the university hospital was performed. Articles related to "genetic" and "NMOSD" were systematically searched and reviewed. We included NMOSD patients whose one or more relatives were diagnosed with the same disease or multiple sclerosis (MS). Data regarding demographics, clinical features, disease outcomes, and genetic testing were collected and analyzed using descriptive statistics. RESULTS: We identified 6 familial cases from 165 NMOSD cases (3.6%) at our hospital and gathered 77 cases from a systematic review, totaling 83 cases from 40 families. The mean (SD) age at onset was 37.2 (18.0) years. Familial NMOSD involved 1-2 generations with mainly 2 affected individuals. The most common kinship pattern was siblingship in 21 families (52.5%). Initial syndromes were mostly optic neuritis and transverse myelitis. Serum aquaporin-4 IgG was positive in 79.7% of cases. Median number of relapses was 3 (range 1-26). Median expanded disability status scale in the last visit was 2 (range 0-8). Reported human leukocyte antigens (HLA) alleles shared between familial cases were HLA-A*01 and HLA-DRB1*03. CONCLUSION: Familial clustering of NMOSD is more common than would be expected in the general population. The demographic, clinical, and outcome profiles of familial cases were not different from sporadic cases. Certain specific HLA haplotypes were shared among familial cases. Our systematic review highlighted complex genetic predisposition to NMOSD.
 Monoclonal antibodies are immunoglobulins that have a high degree of specificity (mono-specificity) for an antigen or epitope. Monoclonal antibodies are typically derived from a clonal expansion of antibody producing malignant human plasma cells. The initial monoclonal antibodies were created by fusing spleen cells from an immunized mouse with human or mouse myeloma cells (malignant self-perpetuating antibody producing cells), and selecting out and cloning the hybrid cells (hybridomas) that produced the desired antibody reactivity. These initial monoclonal products were mouse antibodies and were very valuable in laboratory and animal research and diagnostic assays, but were problematic as therapeutic agents because of immune reactions to the foreign mouse protein. Subsequently, production of chimeric mouse-human monoclonal antibodies and means of further “humanizing” them and producing fully human recombinant monoclonal antibodies were developed. The conventions used in nomenclature of monoclonal antibodies indicate whether they are mouse dervied (-omab), chimeric (-ximab), humanized (-zumab) or fully human (-umab). Monoclonal antibodies have broad clinical and experimental medical uses. Many of the initial monoclonal antibodies used in clinical medicine were immunomodulatory agents with activity against specific immune cells, such as CD4 or CD3 lymphocytes, which are important in the pathogenesis of rejection after solid organ transplantation. Subsequently, monoclonal antibodies were prepared against specific cytokines (anti-cytokines), which were believed to play a role in cell and tissue damage in immunologically mediated diseases such as rheumatoid arthritis, alkylosing spondylitis, inflammatory bowel disease, multiple sclerosis and psoriasis, among others. In addition, therapeutic monoclonal antibodies were developed, aimed at blocking or inhibiting the activity of specific enzymes, cell surface transporters or signaling molecules and have been used in cancer chemotherapy and to treat severe viral infections. Use of monoclonal antibodies is currently broadening to therapy of other severe, nonmalignant conditions including asthma, atopic dermatitis, migraine headaches, hypercholesterolemia, osteoporosis, bacterial diseases (such as anthrax) and viral infections (such as COVID-19). Thus, the therapeutic monoclonal antibodies do not fall into a single class and have broad therapeutic uses. As of 2022, more than 80 therapeutic monoclonal antibodies have been approved for use in the United States. Monoclonal antibodies are generally well tolerated. Because they are large proteins (typically 150-200,000 daltons in size) they require parenteral, often intravenous, administration. Circulating proteins are metabolized by many cells, but particularly by hepatocytes. Proteins undergo hepatic uptake by endocytosis and are either degraded or recycled to the cell surface for secretion. The hepatic metabolism of antibodies often determines their half-life. Proteins are broken down by cellular proteases into small peptides and amino acids that can used to synthesize other proteins. Metabolism of proteins does not generate toxic intermediates and, therefore, monoclonal antibodies are unlikely to induce drug induced liver injury via production of toxic metabolites. On the other hand, the peptides that are generated by the metabolism of the exogenously administered protein may ultimately be presented as foreign epitopes and generate an immune response. In addition, the primary effect of the monoclonal antibody may generate a response, either immune or otherwise, that leads to an immune mediate hepatic injury. Finally, monoclonal antibodies that suppress the immune system may cause reactivation of latent infections, including tuberculosis, herpes simplex, varicella zoster (shingles) and hepatitis B.
 OBJECTIVE: The pathogenesis of inflammatory bowel disease (IBD) has not been fully uncovered to date. Epstein-Barr-Virus (EBV) infection has recently been associated with the pathogenesis of multiple sclerosis, suggesting a general link between EBV and autoimmune diseases. However, data on an association between EBV and IBD have remained inconclusive. This study aims at evaluating an association between EBV and the development of IBD. METHODS: This retrospective cohort study included 15 931 patients with and 15 931 matched patients without infectious mononucleosis from the Disease Analyzer database (IQVIA) between 2000 and 2018. Incidences of Crohn's disease and ulcerative colitis were evaluated using Cox regression models. RESULTS: Within 5 years of the index date, the cumulative incidence of IBD was 124 and 90 cases per 100 000 person-years among patients with and without infectious mononucleosis, respectively (P = 0.040). In regression analyses, infectious mononucleosis was significantly associated with IBD [hazard ratios (HR), 1.35; 95% confidence interval (CI), 1.01-1.81]. Subgroup analyses revealed an association between infectious mononucleosis and Crohn's disease (HR, 1.93; 95% CI, 1.22-3.05) but not ulcerative colitis (HR, 1.03; 95% CI, 0.70-1.51). This association was strongest in patients between 14 and 20 years (HR, 4.50; 95% CI, 1.55-13.13) and was only observed in females (HR, 2.51; 95% CI, 1.39-4.53). CONCLUSION: Infectious mononucleosis is significantly associated with an increased incidence of Crohn's disease but not ulcerative colitis, especially in young female patients. Our data support the hypothesis of a pathophysiological involvement of EBV in the development of Crohn's disease and should trigger molecular research to further dissect the pathophysiology of IBD.
 BACKGROUND: Acceptance and Commitment Therapy interventions are increasing in use in neurological populations. There is a lack of information on the measures available. PURPOSE: To identify and classify the measures used in Acceptance and Commitment Therapy research studies with adults with acquired neurological conditions. METHODS: PRISMA-ScR guided scoping review. MEDLINE, PsycInfo and CINAHL databases searched (up to date 29/06/2022) with forward and backward searching. All study types included. Extraction of Acceptance and Commitment Therapy process-of-change and health-related outcome measures. Outcomes coded using the Core Outcome Measures in Effectiveness Trials (COMET) taxonomy. RESULTS: Three hundred and thirty three papers found on searching. Fifty four studies included and 136 measurement tools extracted. Conditions included multiple sclerosis, traumatic brain injury and stroke. Thirty-eight studies measured processes of change, with 32 measures extracted. The process measure most often used was the Acceptance and Action Questionnaire (n = 21 studies). One hundred and four health-related outcome measures extracted. Measures exploring quality of life, health status, anxiety and depression occurred most frequently, and were used in all included neurological conditions. COMET domains most frequently coded were emotional functioning/well-being (n = 50), physical functioning (n = 32), role functioning (n = 22) and psychiatric (n = 22). CONCLUSIONS: This study provides a resource to support future identification of candidate measures. This could aid development of a Core Outcome Set to support both research and clinical practice. Further research to identify the most appropriate and relevant targets and tools for use in these populations should include expert consensus, patient, carer and public involvement and psychometric examination of measures.
 Circular RNAs (circRNAs) are a novel class of non-coding RNAs. They are single-stranded RNA transcripts characterized with a closed loop structure making them resistant to degrading enzymes. Recently, circRNAs have been suggested with regulatory roles in gene expression involved in controlling various biological processes. Notably, they have demonstrated abundance, dynamic expression, back-splicing events, and spatiotemporally regulation in the human brain. Accordingly, they are expected to be involved in brain functions and related diseases. Studies in animals and human brain have revealed differential expression of circRNAs in brain compartments. Interestingly, contributing roles of circRNAs in the regulation of central nervous system (CNS) development have been demonstrated in a number of studies. It has been proposed that circRNAs play role in substantial neurological functions like neurotransmitter-associated tasks, neural cells maturation, and functions of synapses. Furthermore, 3 main pathways have been identified in association with circRNAs's host genes including axon guidance, Wnt signaling, and transforming growth factor beta (TGF-β) signaling pathways, which are known to be involved in substantial functions like migration and differentiation of neurons and specification of axons, and thus play role in brain development. In this review, we have an overview to the biogenesis, biological functions of circRNAs, and particularly their roles in human brain development and the pathogenesis of neurodegenerative diseases including Alzheimer's diseases, multiple sclerosis, Parkinson's disease and brain tumors.
 INTRODUCTION: Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing, often debilitating neuroinflammatory disease, whose predominant clinical manifestations are longitudinally extensive transverse myelitis and optic neuritis. About 80% of the patients with an NMOSD phenotype have pathogenic autoantibodies against the astrocyte water channel aquaporin-4 (AQP4-IgG). While therapeutic options for NMOSD have greatly expanded in recent years, well-established biomarkers for prognosis or treatment response are still lacking. Glial fibrillary acidic protein (GFAP) is mainly expressed in astrocytes and can be detected in cerebrospinal fluid (CSF) and blood of patients with NMOSD. AREAS COVERED: Here, we comprehensively review the current knowledge on GFAP as a biomarker in NMOSD. EXPERT OPINION: In patients with AQP4-IgG(+) NMOSD, GFAP levels are elevated in CSF and serum during acute attacks and correlate with disability, consistent with the pathophysiology of this antibody-mediated astrocytopathy. Serum GFAP levels tend to be higher in AQP4-IgG(+) NMOSD than in its differential diagnoses, multiple sclerosis, and myelin oligodendrocyte antibody-associated disease. Importantly, serum GFAP levels in AQP4-IgG(+) NMOSD during remission may be predictive of future disease activity. Serial serum GFAP measurements are emerging as a biomarker to monitor disease activity in AQP4-IgG(+) NMOSD and could have the potential for application in clinical practice.
 OBJECTIVE: Nabiximols is used for treating various symptoms associated with multiple sclerosis (MS). Nabiximols is also being investigated as a potential treatment medication for individuals with cannabis use disorder (CUD). A variety of investigations have shown that, at low doses, nabiximols is overall well tolerated for MS treatment. However, due to tolerance, the management of CUD would likely require much higher doses of nabiximols to be effective. The effects of high doses of nabiximols on clinical laboratory tests remain unclear. Therefore, we investigated the sub-chronic effects of high doses of nabiximols on liver function, renal function, and other routine blood tests in this prospective study. METHODS: We performed a secondary analysis of various blood markers results collected during a double-blind, placebo-controlled randomized clinical trial (Sativex and Behavioral-relapse Prevention Strategy in Cannabis Dependence, NCT01747850, https://clinicaltrials.gov/ct2/show/record/NCT01747850). This trial tested the impact of the 12-week administration of nabiximols with a maximum daily dose of up to 113.4 mg THC/105 mg CBD. RESULTS: The measurements of the various biomarkers were in the normal range during the 12-week time frame. The results indicate an overall good tolerability of high-dose nabiximols on the blood markers measured. CONCLUSION: Our preliminary results suggest that high doses of nabiximols might be well tolerated by individuals with CUD.
 Three-dimensional (3D) cameras used for gait assessment obviate the need for bodily markers or sensors, making them particularly interesting for clinical applications. Due to their limited field of view, their application has predominantly focused on evaluating gait patterns within short walking distances. However, assessment of gait consistency requires testing over a longer walking distance. The aim of this study is to validate the accuracy for gait assessment of a previously developed method that determines walking spatiotemporal parameters and kinematics measured with a 3D camera mounted on a mobile robot base (ROBOGait). Walking parameters measured with this system were compared with measurements with Xsens IMUs. The experiments were performed on a non-linear corridor of approximately 50 m, resembling the environment of a conventional rehabilitation facility. Eleven individuals exhibiting normal motor function were recruited to walk and to simulate gait patterns representative of common neurological conditions: Cerebral Palsy, Multiple Sclerosis, and Cerebellar Ataxia. Generalized estimating equations were used to determine statistical differences between the measurement systems and between walking conditions. When comparing walking parameters between paired measures of the systems, significant differences were found for eight out of 18 descriptors: range of motion (ROM) of trunk and pelvis tilt, maximum knee flexion in loading response, knee position at toe-off, stride length, step time, cadence; and stance duration. When analyzing how ROBOGait can distinguish simulated pathological gait from physiological gait, a mean accuracy of 70.4%, a sensitivity of 49.3%, and a specificity of 74.4% were found when compared with the Xsens system. The most important gait abnormalities related to the clinical conditions were successfully detected by ROBOGait. The descriptors that best distinguished simulated pathological walking from normal walking in both systems were step width and stride length. This study underscores the promising potential of 3D cameras and encourages exploring their use in clinical gait analysis.
 The choroid plexus (ChP) has been suggested as an alternative central nervous system (CNS) entry site for CCR6(+) Th17 cells during the initiation of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS). To advance our understanding of the importance of the ChP in orchestrating CNS immune cell entry during neuroinflammation, we here directly compared the accumulation of CD45(+) immune cell subsets in the ChP, the brain and spinal cord at different stages of EAE by flow cytometry. We found that the ChP harbors high numbers of CD45(int) resident innate but also of CD45(hi) adaptive immune cell subsets including CCR6(+) Th17 cells. With the exception to tissue-resident myeloid cells and B cells, numbers of CD45(+) immune cells and specifically of CD4(+) T cells increased in the ChP prior to EAE onset and remained elevated while declining in brain and spinal cord during chronic disease. Increased numbers of ChP immune cells preceded their increase in the cerebrospinal fluid (CSF). Th17 but also other CD4(+) effector T-cell subsets could migrate from the basolateral to the apical side of the blood-cerebrospinal fluid barrier (BCSFB) in vitro, however, diapedesis of effector Th cells including that of Th17 cells did not require interaction of CCR6 with BCSFB derived CCL20. Our data underscore the important role of the ChP as CNS immune cell entry site in the context of autoimmune neuroinflammation.
 OBJECTIVE: To retrospectively investigate the feasibility and impact on health-related quality of life (HRQoL) of a digital care programme (DCP) designed to guide personalised diet and integrative interventions in a variety of autoimmune diseases and long COVID. METHODS: Adults who participated in the DCP between April 2020 and June 2022, and for whom baseline (BL) and end-of-programme (EOP) Patient-Reported Outcomes Measurement Information System (PROMIS) scores were available, were included in this retrospective study. Changes from BL to EOP were calculated using standardised T-scores. RESULTS: Two hundred two adults between 17 and 82 years old were included. Diagnoses included: rheumatoid arthritis (20.1%); long COVID (14.9%); psoriatic arthritis (10.9%); psoriasis (8.9%); systemic lupus erythematosus (6.4%); inflammatory bowel disease (5.9%); multiple sclerosis (5.9%); ankylosing spondylitis (5.4%) and other (23.3%). On average, individuals entered observations 7.6 times/day on 86% of programme days, attended 14 coach sessions and completed the programme in an average of 17.2 weeks. Statistically significant improvements were seen in all 10 PROMIS domains analysed. Individuals with higher severity of compromise at BL experienced greater average improvements than all-comers in all 10 PROMIS domains included. CONCLUSION: An evidence-based DCP that uses patient data to help identify hidden symptom triggers and guide personalised dietary and other non-pharmacological interventions was associated with a high level of engagement and adherence and statistically significant, clinically meaningful improvements in HRQoL. Those with the least favourable PROMIS scores at BL experienced the greatest improvements.
 Three new phenanthrene derivatives (1, 2, 4), one new fluorenone (3), and four known compounds (5-8) were isolated from the ethyl acetate extract of Dendrobium crumenatum Sw. stems using column chromatography. The chemical structures were elucidated by analysis of spectroscopic data. The absolute configuration of 4 was determined by electronic circular dichroism calculation. We also evaluated the immunomodulatory effects of compounds isolated from D. crumenatum in human peripheral blood mononuclear cells from healthy individuals and those from patients with multiple sclerosis in vitro. Dendrocrumenol B (2) and dendrocrumenol D (4) showed strong immunomodulatory effects on both CD3(+) T cells and CD14(+) monocytes. Compounds 2 and 4 could reduce IL-2 and TNF production in T cells and monocytes that were treated with phorbol-12-myristate-13-acetate and ionomycin (PMA/Iono). Deep immune profiling using high-dimensional single-cell mass cytometry could confirm immunomodulatory effects of 4, quantified by the reduction of activated T cell population under PMA/Iono stimulation, in comparison to the stimulated T cells without treatment.
 BACKGROUND: The anti-CD20 monoclonal antibody ocrelizumab has been widely employed in the treatment of people with multiple sclerosis (pwMS). However, its B-cell-depleting effect may induce a higher risk of infectious events and alterations in the secretion of B-cell-activating factors, such as BAFF, APRIL and CD40L. METHODS: The aim of this study was to investigate plasma BAFF, APRIL and CD40L levels and their relationship with infectious risk in ocrelizumab-treated pwMS at baseline (T0), at 6 months (T6) and at 12 months (T12) after starting the treatment. As a control group, healthy donors (HD) were enrolled too. RESULTS: A total of 38 pwMS and 26 HD were enrolled. At baseline, pwMS showed higher plasma BAFF (p < 0.0001), APRIL (p = 0.0223) and CD40L (p < 0.0001) levels compared to HD. Compared to T0, plasma BAFF levels were significantly increased at both T6 and T12 (p < 0.0001 and p < 0.0001, respectively). Whereas plasma APRIL and CD40L levels were decreased at T12 (p = 0.0003 and p < 0.0001, respectively). When stratifying pwMS according to the development of an infectious event during the 12-month follow-up period in two groups-with (14) and without an infectious event (24)-higher plasma BAFF levels were observed at all time-points; significantly, in the group with an infectious event compared to the group without an infectious event (T0: p < 0.0001, T6: p = 0.0056 and T12: p = 0.0400). Conclusions: BAFF may have a role as a marker of immune dysfunction and of infectious risk.
 BACKGROUND: The frequency and intensity of heat waves have increased and will keep increasing. This meteorological phenomenon, which is considered one of the most dangerous, can affect the entire population, but certain populations are at greater risk. Concretely, elderly people are more prompt to suffer from chronic diseases and therefore to be on medication that can interact with the different temperature-regulating systems of the body. So far, there are no published studies that have analyzed pharmacovigilance databases to characterize the association between specific pharmaceuticals and heat-related adverse reactions. OBJECTIVE: Therefore, in this study, we aimed to investigate the reported cases of heat exhaustion or heat stroke, associated with any drug notified to the European pharmacovigilance database (EudraVigilance). METHOD: The Basque Country Pharmacovigilance Unit selected spontaneous reports recorded in EudraVigilance from January 1, 1995, to January 10, 2022. "Heat Stroke" and "Heat Exhaustion" preferred terms were selected. Non-cases, used as controls, were all the other adverse drug reaction reports recorded in EudraVigilance for the same time period. RESULTS: In total, 469 cases were obtained. Mean age: 49.74 ± 8 years, 62.5% were male, and the majority (94.7%) were considered serious by EU criteria. Fifty-one active substances fulfilled the criteria to generate a signal of disproportionate reporting. CONCLUSIONS: The majority of implicated drugs belong to therapeutic groups that are already mentioned in different heat-illness prevention plans. But we also show that drugs aimed to treat multiple sclerosis and several cytokines were also associated with heat-related adverse effects.
 Endocannabinoids are endogenous lipid signaling mediators that participate in a variety of physiological and pathological processes. 2-Arachidonoylglycerol (2-AG) is the most abundant endocannabinoid and is a full agonist of G-protein-coupled cannabinoid receptors (CB1R and CB2R), which are targets of Δ(9)-tetrahydrocannabinol (Δ(9)-THC), the main psychoactive ingredient in cannabis. While 2-AG has been well recognized as a retrograde messenger modulating synaptic transmission and plasticity at both inhibitory GABAergic and excitatory glutamatergic synapses in the brain, growing evidence suggests that 2-AG also functions as an endogenous terminator of neuroinflammation in response to harmful insults, thus maintaining brain homeostasis. Monoacylglycerol lipase (MAGL) is the key enzyme that degrades 2-AG in the brain. The immediate metabolite of 2-AG is arachidonic acid (AA), a precursor of prostaglandins (PGs) and leukotrienes. Several lines of evidence indicate that pharmacological or genetic inactivation of MAGL, which boosts 2-AG levels and reduces its hydrolytic metabolites, resolves neuroinflammation, mitigates neuropathology, and improves synaptic and cognitive functions in animal models of neurodegenerative diseases, including Alzheimer's disease (AD), multiple sclerosis (MS), Parkinson's disease (PD), and traumatic brain injury (TBI)-induced neurodegenerative disease. Thus, it has been proposed that MAGL is a potential therapeutic target for treatment of neurodegenerative diseases. As the main enzyme hydrolyzing 2-AG, several MAGL inhibitors have been identified and developed. However, our understanding of the mechanisms by which inactivation of MAGL produces neuroprotective effects in neurodegenerative diseases remains limited. A recent finding that inhibition of 2-AG metabolism in astrocytes, but not in neurons, protects the brain from TBI-induced neuropathology might shed some light on this unsolved issue. This review provides an overview of MAGL as a potential therapeutic target for neurodegenerative diseases and discusses possible mechanisms underlying the neuroprotective effects of restraining degradation of 2-AG in the brain.
 The post-vaccination antibody response in patients with immune-mediated neuromuscular diseases under immuno-suppressive therapy has not been sufficiently verified. The Japanese Society of Neurology has stated that coronavirus disease 2019 (COVID-19) vaccination should be given priority in patients with immunotherapy-associated neuromuscular diseases; however, data on antibody production to a novel mRNA vaccine are scarce in these patients. In this study, we aimed to measure residual antibody titers after the second dose and produced antibodies after the third dose of SARS-CoV-2 mRNA vaccine in 25 patients with neuromuscular diseases under immuno-suppressive therapy (disease group). We compared the disease group antibody titers with those of 829 healthy employees in our hospital (control group). The disease group included 17 patients with myasthenia gravis, 4 with multiple sclerosis, 3 with inflammatory muscle disease, and 1 with chronic inflammatory demyelinating polyneuropathies. Seven cases of the disease group showed negative antibody levels (<15.0 s/co) before the third vaccination, and antibody titers in the positive cases ranged from 16.9 to 4,589.0 s/co. Three of the seven antibody-negative cases turned positive after the third vaccination, and all but one of the antibody-positive cases showed a booster effect, with antibody titers after the third dose ranging from 245.1 to 85,374.0 s/co (1.0 to 885.0 times higher than those before vaccination). Although the immune response in the disease group was modest compared to the control group, in which antibody titers after the third vaccination ranged from 67.8 to 150,000 s/co (0.9 to 5,402.1 times higher than those before vaccination), the result indicated that a constant immune response was achieved under immuno-suppressive therapy. Even in the control group, three participants tested negative for residual antibody before the third inoculation, and four of the antibody-positive participants (27.7-24,054.0 s/co) lacked a booster effect after the third vaccination.
 BACKGROUND: Consumption of ultra-processed foods (UPFs) has been linked to risk of chronic diseases, with scant evidence in relation to multiple sclerosis (MS). METHODS: We tested associations between UPF consumption and likelihood of a first clinical diagnosis of central nervous system demyelination (FCD) (267 cases, 508 controls), a common precursor to MS. We used data from the 2003-2006 Ausimmune Study and logistic regression with full propensity score matching for age, sex, region of residence, education, smoking history, body mass index, physical activity, history of infectious mononucleosis, dietary misreporting, and total energy intake. RESULTS: Higher UPF consumption was statistically significantly associated with an increased likelihood of FCD (adjusted odds ratio = 1.08; 95% confidence interval = 1.0,1.15; p = 0.039), representing an 8% increase in likelihood of FCD per one energy-adjusted serving/day of UPFs. CONCLUSION: Higher intakes of UPF were associated with increased likelihood of FCD in this Australian cohort. Nutrition education and awareness of healthy eating patterns may benefit those at high risk of FCD.
 OBJECTIVES: The aim of this study was to assess midterm functional outcomes and complications of robot-assisted laparoscopic cystectomy with non-continent urinary diversion in patients with neurogenic lower urinary tract dysfunction. MATERIALS AND METHODS: We performed a retrospective single center study including all patients who underwent robot-assisted laparoscopic cystectomy with non-continent urinary diversion between January 2008 and December 2018 for neurogenic lower urinary tract dysfunction. Perioperative data, early and late complications, reoperation rate, renal function, and patient satisfaction (PGI-I) were evaluated. RESULTS: One hundred and forty patients were included (70 multiple sclerosis, 37 spinal cord injuries, 33 others) with a median follow-up of 29 months (12-49). The main indication for surgery was an inability to perform intermittent self-catheterization (n = 125, 89%). The early complication rate (<30 days) was 41% (n = 58), including 72% (n = 45) minor complications (Clavien I-II) and 29% (n = 17) major complications (Clavien III-V). Three patients died in the early postoperative period. Late complications appear in 41% (n = 57), with 9% (n = 13) being ureteroileal anastomotic stricture. The overall reintervention rate was 19% (n = 27), mainly for lithiasis surgery. Pre- and postoperative renal function were comparable. Most of patients reported an improvement in their quality of life following their surgery (PGI-I 1-2). CONCLUSION: Robot-assisted laparoscopic cystectomy with non-continent urinary diversion may be of particular interest in patients with neurogenic lower urinary tract dysfunction who are unable to benefit from conservative treatment, as it provides midterm protection of the upper urinary tract and an improvement in quality of life.
 OBJECTIVES: Cognitive and behavioural responses to symptoms can worsen or maintain the severity of symptoms across long-term conditions (LTCs). Although the Cognitive and Behavioural Responses Questionnaire (CBRQ) has been used in research, its original development and psychometric properties as a transdiagnostic measure have not been reported. Our aim was to evaluate the psychometric properties of the CBRQ and a recently proposed short version, across different LTCs. DESIGN: Psychometric validation study. METHODS: Confirmatory factor analysis (CFA) tested the factor structure of the CBRQ in two datasets from the CBRQ's original development; (chronic fatigue syndrome, N = 230; and multiple sclerosis, N = 221) and in additional groups: haemodialysis (N = 174), inflammatory bowel disease (N = 182) and chronic dizziness (N = 185). Scale reliability and construct validity were assessed. The factor structure of the shortened CBRQ (CBRQ-SF) was also assessed. RESULTS: CFA revealed that a 7-or 8-factor structure had generally appropriate fit supporting the originally proposed 7 factors (Fear avoidance, Damage beliefs, Catastrophising, Embarrassment avoidance, Symptom focusing, All-or-nothing behaviour and Avoidance/Resting behaviour). Omega coefficients indicated satisfactory internal reliability. Correlations with related constructs suggested construct validity. The scale appeared sensitive to change. The CBRQ-SF also displayed good psychometric quality, with a better model fit than the CBRQ. CONCLUSIONS: The CBRQ and the shortened version were shown to be reliable and valid at assessing a range of cognitive and behavioural responses to symptoms, highlighting the multi-symptom, transdiagnostic properties of this questionnaire. Further research is necessary to determine the test-retest reliability and sensitivity to change of the CBRQ and CBRQ-SF and a thorough evaluation of the content validity of the items.
 AIMS: To learn about the effect and mechanism of total glucosides of white peony capsule (TGP), on experimental autoimmune encephalomyelitis (EAE), an acknowledged animal model of multiple sclerosis (MS). METHODS: The rat model of EAE was induced by subcutaneous injection with guinea pig spinal cord homogenate. The severity of the disease model was assessed by clinical score, hematoxylin and eosin (H&E) and luxol fast blue (LFB). Immunohistochemical assay was used to observe the types of inflammatory cells and adhesive molecule expression. Enzyme-linked immunosorbent assay (ELISA) was applied to detect content of the stem cell growth factor / mast cell growth factor (scf/MGF), interleukin-6 (IL-6) and IL-2. Immunofluorescence assay was applied to observe the expression of connexin43 (Cx43), glial fibrillary acidic protein (GFAP), connexin47 (Cx47) and the monoclonal antibody anti-adenomatous polyposis coli (APC) clone CC1. RESULTS: Compare with the animals in EAE model group, TGP treated rats (particularly those treated with high doses) showed a significant decrease in morbidity, clinical scores, CNS infiltration of inflammatory cells (including mononuclear macrophages, CD4(+) and CD8(+) T cells) and demyelination. The key adhesion molecule ICAM-1, cytokines IL-2、IL-6 and scf/MGF were significantly decreased with TGP treatment. Oppositely, PD-1, connexin47 in oligodendrocytes and connexin43 in astrocytes were elevated with TGP treatment. CONCLUSION: To sum up, TGP exhibited a significantly prevention and treatment effect on EAE rat model, and this improvement was achieved through a combination way composed of glial and inflammatory cells, junction proteins, various factors including adhesion factors, interleukins and scf/MGF.
 Dimethyl fumarate (DMF) is pharmaceutical activator of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates of many cellular antioxidant response pathways, and has been used to treat inflammatory diseases such as multiple sclerosis. However, DMF has been shown to produce adverse effects on offspring in animal studies and as such is not recommended for use during pregnancy. The goal of this work is to better understand how these adverse effects are initiated and the role of DMF-induced Nrf2 activation during three critical windows of development in embryonic zebrafish (Danio rerio): pharyngula, hatching, and protruding-mouth stages. To evaluate Nrf2 activation, wildtype zebrafish, and mutant zebrafish (nrf2a(fh318/fh318)) embryos with a loss of function mutation in Nrf2a, the co-ortholog to human Nrf2, were treated for 6 h with DMF (0-20 μM) beginning at the pharyngula, hatching, or protruding-mouth stage and assessed for survival and morphology. Nrf2a mutant fish had an increase in survival, however, morphology studies demonstrated Nrf2a mutant fish had more severe deformities occurring with exposures during the hatching stage. To verify Nrf2 cellular localization and downstream impacts on protein-S-glutathionylation in situ, a concentration below the LOAEL was chosen (7 μM) for immunohistochemistry and S-glutathionylation. Embryos were imaged via epifluorescence microscopy studies, the Nrf2a protein in the body tissue was decreased with DMF only when exposed at the hatching stage, while total protein S-glutathionylation was modulated by Nrf2a activity and DMF during the pharyngula and protruding-mouth stage. The pancreatic islet and liver were further analyzed via confocal microscopy. Pancreatic islets and liver also had tissue specific differences with Nrf2a protein expression and protein S-glutathionylation. This work demonstrates how critical windows of exposure and Nrf2a activity may influence toxicity of DMF and highlights tissue-specific changes in Nrf2a protein levels and S-glutathionylation in pancreatic islet and liver during embryonic development.
 The blood-brain barrier (BBB) restricts the access of therapeutic agents to the brain, complicating the treatment of neurological diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), glioma, etc. To overcome this limitation and improve drug delivery to the central nervous system (CNS), the potential of nanocarriers, including lipid-based nanosystems, has been explored. Through active targeting, the surface of the nanocarriers can be modified with ligands that interact with the BBB, enhancing their uptake and penetration across the brain endothelium by different physiological mechanisms, such as receptor- or transporter-mediated transcytosis. This review seeks to provide an overview of active targeting in brain delivery, while highlighting the potential of functionalized lipid nanocarriers to treat brain diseases. Therefore, in the first sections, we discuss the importance of active targeting in CNS drug delivery, present the different ligands commonly used for functionalization, as well as summarize the state of the art of the most recent and relevant studies of surface-modified lipid nanosystems developed for neurological disorders. Lastly, challenges hindering clinical translation are discussed, and critical insights and future perspectives outlined. Although some limitations have been identified, it is expected that in the upcoming years these nanosystems will be an established approach.
 The NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome is a multimeric protein complex that is engaged in the innate immune system and plays a vital role in inflammatory reactions. Activation of the NLRP3 inflammasome and subsequent release of proinflammatory cytokines can be triggered by microbial infection or cellular injury. The NLRP3 inflammasome has been implicated in the pathogenesis of many disorders affecting the central nervous system (CNS), ranging from stroke, traumatic brain injury, and spinal cord injury to Alzheimer's disease, Parkinson's disease, epilepsy, multiple sclerosis, and depression. Furthermore, emerging evidence has suggested that mesenchymal stem cells (MSCs) and their exosomes may modulate NLRP3 inflammasome activation in a way that might be promising for the therapeutic management of CNS diseases. In the present review, particular focus is placed on highlighting and discussing recent scientific evidence regarding the regulatory effects of MSC-based therapies on the NLRP3 inflammasome activation and their potential to counteract proinflammatory responses and pyroptotic cell death in the CNS, thereby achieving neuroprotective impacts and improvement in behavioral impairments.
 BACKGROUND: Substantial evidence suggests that immunoproteasome is implicated in the various neurological diseases such as stroke, multiple sclerosis and neurodegenerative diseases. However, whether the immunoproteasome itself deficiency causes brain disease is still unclear. Therefore, the aim of this study was to explore the contribution of the immunoproteasome subunit low molecular weight protein 2 (LMP2) in neurobehavioral functions. METHODS: Male LMP2 gene completed knockout (LMP2-KO) and littermate wild type (WT) Sprague-Dawley (SD) rats aged 12-month-old were used for neurobehavioral testing and detection of proteins expression by western blotting and immunofluorescence. A battery of neurobehavioral test tools including Morris water maze (MWM), open field maze, elevated plus maze were used to evaluate the neurobehavioral changes in rats. Evans blue (EB) assay, Luxol fast blue (LFB) and Dihydroethidium (DHE) staining were applied to explore the blood-brain barrier (BBB) integrity, brain myelin damage and brain intracellular reactive oxygen species (ROS) levels, respectively. RESULTS: We firstly found that LMP2 gene deletion did not cause significantly difference in rats' daily feeding activity, growth and development as well as blood routine, but it led to metabolic abnormalities including higher levels of low-density lipoprotein cholesterol, uric acid and blood glucose in the LMP2-KO rats. Compared with the WT rats, LMP2-KO rats displayed obviously cognitive impairment and decreased exploratory activities, increased anxiety-like behavior and without strong effects on gross locomotor abilities. Furthermore, multiple myelin loss, increased BBB leakage, downregulation of tight junction proteins ZO-1, claudin-5 and occluding, and enhanced amyloid-β protein deposition were observed in brain regions of LMP2-KO rats. In addition, LMP2 deficiency significantly enhanced oxidative stress with elevated levels of ROS, caused the reactivation of astrocytes and microglials and markedly upregulated protein expression levels of interleukin (IL)-1 receptor-associated kinase 1 (IRAK1), IL-6 and tumor necrosis factor-α (TNF-α) compared to the WT rats, respectively. CONCLUSION: These findings highlight LMP2 gene global deletion causes significant neurobehavioral dysfunctions. All these factors including metabolic abnormalities, multiple myelin loss, elevated levels of ROS, increased BBB leakage and enhanced amyloid-β protein deposition maybe work together and eventually led to chronic oxidative stress and neuroinflammation response in the brain regions of LMP2-KO rats, which contributed to the initial and progress of cognitive impairment.

 Regeneration after a peripheral nerve injury still remains a challenge, due to the limited regenerative potential of axons after injury. While the endocannabinoid system (ECS) has been widely studied for its neuroprotective and analgesic effects, its role in axonal regeneration and during the conditioning lesion remains unexplored. In this study, we observed that a peripheral nerve injury induces axonal regeneration through an increase in the endocannabinoid tone. We also enhanced the regenerative capacity of dorsal root ganglia (DRG) neurons through the inhibition of endocannabinoid degradative enzyme MAGL or a CB1R agonist. Our results suggest that the ECS, via CB1R and PI3K-pAkt pathway activation, plays an important role in promoting the intrinsic regenerative capacity of sensory neurons after injury.

 A 52-year-old woman with multifocal micronodular pneumocyte hyperplasia in bilateral lungs and multiple sclerotic bone lesions (SBLs) visited our hospital. Tuberous sclerosis complex (TSC) was suspected but did not meet the diagnostic criteria. Ten years later, at age 62, the patient developed ureteral cancer. Cisplatin-containing chemotherapy ameliorated ureteral tumor, concomitant with exacerbation of SBLs. It was difficult to distinguish whether the exacerbation of SBLs was due to exacerbation of TSC or bone metastasis of cancer. The administration of cisplatin made the diagnosis even more difficult because its molecular biological effects can exacerbate the complications of TSC.
 INTRODUCTION: Fanconi anemia (FA) is an inherited condition associated with genetic mutations that affect DNA repair proteins. More than 20 genes involved in the FA/BRCA pathway have been implicated in FA, including BRIP1. Tumefactive brain lesions are rare in FA. CASE REPORT: We describe a patient with FA and recurrent tumefactive brain lesions preceded by calcifications on head computed tomography. A biopsy revealed white-matter gliosis with severe vasculopathy. Whole-genome sequencing demonstrated a BRIP1 homozygous variant with a final diagnosis of recurrent tumefactive brain lesions due to BRIP1-associated CNS vasculopathy. Immunosuppressive treatment was ineffective in the present case. CONCLUSIONS: Mechanistically, the specific role of BRIP1 mutation in CNS inflammation and vasculopathy is unclear. However, immunodeficiency disorders can lead to autoimmunity and/or immune dysregulation due to the possible loss or gain of function of components of the immune system.
 BACKGROUND: Anti-NMDAR encephalitis is a leading cause of autoimmune encephalitis in children. Untreated disease can lead to long-term neurological disability. CASE REPORT: We present siblings with pediatric-onset anti-NMDAR encephalitis. One was treated early, while the other's diagnosis and treatment were delayed by several years. Developmental, electrophysiologic, and genetic implications are discussed. CONCLUSION: Anti-NMDAR encephalitis is a severely debilitating disease that often requires prompt initiation and early escalation in treatment. Delayed treatment may lead to irreversible neurological sequalae. Further studies exploring associations between timing and tier of treatment initiation and longitudinal outcomes are needed.
 Amyotrophic lateral sclerosis is a rapidly progressing neurodegenerative disease characterized by the degeneration of motor neurons and loss of various muscular functions. Dyslipidaemia is prevalent in amyotrophic lateral sclerosis with aberrant changes mainly in cholesterol ester and triglyceride. Despite this, little is known about global lipid changes in amyotrophic lateral sclerosis or in relation to disease progression. The present study incorporated a longitudinal lipidomic analysis of amyotrophic lateral sclerosis serum with a comparison with healthy controls using advanced liquid chromatography-mass spectrometry. The results established that diglyceride, the precursor of triglyceride, was enriched the most, while ceramide was depleted the most in amyotrophic lateral sclerosis compared with controls, with the diglyceride species (18:1/18:1) correlating significantly to neurofilament light levels. The prenol lipid CoQ(8) was also decreased in amyotrophic lateral sclerosis and correlated to neurofilament light levels. Most interestingly, the phospholipid phosphatidylethanolamine and its three derivatives decreased with disease progression, in contrast to changes with normal ageing. Unsaturated lipids that are prone to lipid peroxidation were elevated with disease progression with increases in the formation of toxic lipid products. Furthermore, in vitro studies revealed that phosphatidylethanolamine synthesis modulated TARDBP expression in SH-SY5Y neuronal cells. Finally, diglyceride, cholesterol ester and ceramide were identified as potential lipid biomarkers for amyotrophic lateral sclerosis diagnosis and monitoring disease progression. In summary, this study represents a longitudinal lipidomics analysis of amyotrophic lateral sclerosis serum and has provided new insights into multiple pathways of lipid dysregulation in amyotrophic lateral sclerosis.
 The review provides a comprehensive update (previous report: Chen R, Cros D, Curra A, Di Lazzaro V, Lefaucheur JP, Magistris MR, et al. The clinical diagnostic utility of transcranial magnetic stimulation: report of an IFCN committee. Clin Neurophysiol 2008;119(3):504-32) on clinical diagnostic utility of transcranial magnetic stimulation (TMS) in neurological diseases. Most TMS measures rely on stimulation of motor cortex and recording of motor evoked potentials. Paired-pulse TMS techniques, incorporating conventional amplitude-based and threshold tracking, have established clinical utility in neurodegenerative, movement, episodic (epilepsy, migraines), chronic pain and functional diseases. Cortical hyperexcitability has emerged as a diagnostic aid in amyotrophic lateral sclerosis. Single-pulse TMS measures are of utility in stroke, and myelopathy even in the absence of radiological changes. Short-latency afferent inhibition, related to central cholinergic transmission, is reduced in Alzheimer's disease. The triple stimulation technique (TST) may enhance diagnostic utility of conventional TMS measures to detect upper motor neuron involvement. The recording of motor evoked potentials can be used to perform functional mapping of the motor cortex or in preoperative assessment of eloquent brain regions before surgical resection of brain tumors. TMS exhibits utility in assessing lumbosacral/cervical nerve root function, especially in demyelinating neuropathies, and may be of utility in localizing the site of facial nerve palsies. TMS measures also have high sensitivity in detecting subclinical corticospinal lesions in multiple sclerosis. Abnormalities in central motor conduction time or TST correlate with motor impairment and disability in MS. Cerebellar stimulation may detect lesions in the cerebellum or cerebello-dentato-thalamo-motor cortical pathways. Combining TMS with electroencephalography, provides a novel method to measure parameters altered in neurological disorders, including cortical excitability, effective connectivity, and response complexity.
 Utreloxastat (PTC857) is a 15-lipoxygenase inhibitor being developed to treat amyotrophic lateral sclerosis. This first-in-human study investigated the safety and pharmacokinetics of utreloxastat in healthy volunteers (N = 82) in a double-blind, placebo-controlled trial. The effects of a single ascending dose (100-1000 mg), multiple ascending doses (150-500 mg), and food (500 mg) on the pharmacokinetics and safety of utreloxastat were evaluated. Following single doses, the time to maximum plasma concentration (C(max) ) was observed ≈4 hours after dosing and the terminal half-life ranged from 20 to 25.3 hours. The C(max) and area under the concentration-time curve (AUC) increased slightly over dose proportionally. Following multiple doses (once daily/twice daily), the apparent clearance reduced and terminal half-life was ≥33 hours. There was no apparent difference of exposure following morning or evening doses. Varying diets increased the C(max) and AUCs of utreloxastat but did not alter time to C(max) . There were no gender-based differences in exposure. Utreloxastat showed no marked safety signal following single doses up to 1000 mg and multiple doses over 14 days of 500 mg once daily or 250 mg twice daily. The results support further development of utreloxastat for the treatment of patients with amyotrophic lateral sclerosis at a 250-mg twice-daily dose administered with food.
 OBJECTIVES: To determine the association of palliative care for progressive neurologic diseases with patient- and caregiver-centered outcomes. DESIGN: Systematic review and meta-analysis of randomized controlled trials and quasi-experimental studies, including pilot studies. SETTING AND PARTICIPANTS: Adults with progressive neurologic diseases (dementia, multiple sclerosis, Parkinson's disease, motor neuron disease, multiple system atrophy, and progressive supranuclear palsy) and their caregivers. METHODS: MEDLINE, EMBASE, CINAHL PLUS, Cochrane CENTRAL, and PubMed were searched from inception to September 2021. Two reviewers independently screened studies, extracted data, and assessed risk of bias using the Cochrane risk of bias tools. Narrative synthesis was conducted. Patient quality of life (QoL), symptom burden, caregiver burden, and satisfaction with care were meta-analyzed using a random-effects model. RESULTS: Fifteen trials provided data on 3431 patients (mean age, 73.9 years). Compared with usual care, palliative care was statistically significantly associated with lower symptom burden [standardized mean difference (SMD), -0.34 (95% Cl, -0.59 to -0.09)] and higher caregiver satisfaction [SMD, 0.41 (95% Cl, 0.12 to 0.71)] and patient satisfaction [SMD, 0.43 (95% Cl, -0.01 to 0.87)]. However, the associations were not significant after excluding studies with high risk of bias. Insignificant associations of palliative care with caregiver burden [SMD, -0.09 (95% Cl, -0.21 to 0.03)] and patient QoL [SMD, 0.19 (95% Cl, -0.07 to 0.44)] were observed. CONCLUSIONS AND IMPLICATIONS: Palliative care is likely to improve symptom burden and satisfaction with care among patients with progressive neurologic diseases and their caregivers, while its effects on QoL and caregiver burden remains inconclusive. Specific intervention components including interdisciplinary team, palliative care physicians, home visits, and spiritual care appeared to be associated with increased effects on improving palliative outcomes. More rigorous designed studies are warranted to examine the effects of neuropalliative care, effective intervention components, optimal timing, and symptom triggers of palliative care referrals.
 OBJECTIVES: Artificial intelligence (AI) methods can be applied to enhance contrast in diagnostic images beyond that attainable with the standard doses of contrast agents (CAs) normally used in the clinic, thus potentially increasing diagnostic power and sensitivity. Deep learning-based AI relies on training data sets, which should be sufficiently large and diverse to effectively adjust network parameters, avoid biases, and enable generalization of the outcome. However, large sets of diagnostic images acquired at doses of CA outside the standard-of-care are not commonly available. Here, we propose a method to generate synthetic data sets to train an "AI agent" designed to amplify the effects of CAs in magnetic resonance (MR) images. The method was fine-tuned and validated in a preclinical study in a murine model of brain glioma, and extended to a large, retrospective clinical human data set. MATERIALS AND METHODS: A physical model was applied to simulate different levels of MR contrast from a gadolinium-based CA. The simulated data were used to train a neural network that predicts image contrast at higher doses. A preclinical MR study at multiple CA doses in a rat model of glioma was performed to tune model parameters and to assess fidelity of the virtual contrast images against ground-truth MR and histological data. Two different scanners (3 T and 7 T, respectively) were used to assess the effects of field strength. The approach was then applied to a retrospective clinical study comprising 1990 examinations in patients affected by a variety of brain diseases, including glioma, multiple sclerosis, and metastatic cancer. Images were evaluated in terms of contrast-to-noise ratio and lesion-to-brain ratio, and qualitative scores. RESULTS: In the preclinical study, virtual double-dose images showed high degrees of similarity to experimental double-dose images for both peak signal-to-noise ratio and structural similarity index (29.49 dB and 0.914 dB at 7 T, respectively, and 31.32 dB and 0.942 dB at 3 T) and significant improvement over standard contrast dose (ie, 0.1 mmol Gd/kg) images at both field strengths. In the clinical study, contrast-to-noise ratio and lesion-to-brain ratio increased by an average 155% and 34% in virtual contrast images compared with standard-dose images. Blind scoring of AI-enhanced images by 2 neuroradiologists showed significantly better sensitivity to small brain lesions compared with standard-dose images (4.46/5 vs 3.51/5). CONCLUSIONS: Synthetic data generated by a physical model of contrast enhancement provided effective training for a deep learning model for contrast amplification. Contrast above that attainable at standard doses of gadolinium-based CA can be generated through this approach, with significant advantages in the detection of small low-enhancing brain lesions.
 It was recently found that patients with relapsing remitting multiple sclerosis exhibit widespread loss of adenosine-to-inosine (A-to-I) RNA editing, which contributes to the accumulation of immunostimulatory double-stranded Alu RNA in circulating leukocytes and an attendant increase in levels of proinflammatory cytokines (e.g., type I IFNs). A specific Alu RNA (i.e., AluJb RNA) was implicated in activating multiple RNA-sensing pathways and found to be a potent innate immune agonist. Here, we have performed a bioinformatic analysis of A-to-I RNA editing in human melanoma samples and determined that pre-therapy levels of A-to-I RNA editing negatively correlate with survival times, suggesting that an accumulation of endogenous double-stranded Alu RNA might contribute to cancer patient survival. Furthermore, we demonstrated that immunostimulatory Alu RNA can be leveraged pharmacologically for cancer immunotherapy. AluJb RNA was in vitro transcribed and then formulated with endosome-destabilizing polymer nanoparticles to improve intracellular delivery of the RNA and enable activation of RNA-sensing pathways. AluJb RNA/polymer complexes (i.e., Alu-NPs) were engineered to form colloidally stable nanoparticles that exhibited immunostimulatory activity in vitro and in vivo. Finally, the therapeutic potential of Alu-NPs for the treatment of cancer was demonstrated by attenuated tumor growth and prolonged survival in the B16.F10 murine melanoma tumor model. Thus, these data collectively implicate intratumoral Alu RNA as a potentiator of antitumor innate immunity and identify AluJb RNA as a novel nucleic acid immunotherapeutic for cancer. SIGNIFICANCE: Loss of A-to-I editing leads to accumulation of unedited Alu RNAs that activate innate immunity via RNA-sensing pattern recognition receptors. When packaged into endosome-releasing polymer nanoparticles, AluJB RNA becomes highly immunostimulatory and can be used pharmacologically to inhibit tumor growth in mouse melanoma models. These findings identify Alu RNAs as a new class of nucleic acid innate immune agonists for cancer immunotherapy.
 For decades, the hypothesis that brain deposition of the amyloid β protein initiates Alzheimer's disease has dominated research and clinical trials. Targeting amyloid β is starting to produce therapeutic benefit, although whether amyloid-lowering drugs will be widely and meaningfully effective is still unclear. Despite extensive in-vivo biomarker evidence in humans showing the importance of an amyloid cascade that drives cognitive decline, the amyloid hypothesis does not fully account for the complexity of late-life cognitive impairment. Multiple brain pathological changes, inflammation, and host factors of resilience might also be involved in contributing to the development of dementia. This variability suggests that the benefits of lowering amyloid β might depend on how strongly an amyloid pathway is manifest in an individual in relation to other coexisting pathophysiological processes. A new approach to research and treatment, which fully considers the multiple factors that drive cognitive decline, is necessary.
 BACKGROUND/AIM: Several cases of concurrent reduction of expression of polycystin 1 (PKD1) and Tuberous Sclerosis Complex 2 (TSC2) that are contiguous in chromosome 16p13 have been previously reported. This study newly addresses the concurrent reduction of expression of PKD1, TSC2 and NTHL1, which is adjacent to TSC2 and is a tumor suppressor gene. MATERIALS AND METHODS: We investigated the mRNA expression levels of PKD1, TSC2, PKD2, TSC1 and NTHL1 in blood and renal cell carcinoma (RCC) tissues in a proband with autosomal dominant polycystic kidney disease (ADPKD), tuberous sclerosis complex (TSC) and multiple pathologically diverse RCCs, including clear cell, papillary and chromophobe types. Additionally, we investigated germline variants in blood using whole exome sequencing (WES) in the proband and her four siblings. RESULTS: mRNA expression levels of PKD1, TSC2 and NTHL1 were reduced in the proband's blood and RCCs, compared with control groups. WES identified one novel variant with amino acid changes in the PKD1 exon in the three subjects with ADPKD, including the proband. Moreover, two variants in the TSC2 intron specific to the proband were also identified. CONCLUSION: In this study, we report a novel pathogenic variant in the PKD1 exon which likely led to ADPKD, and two variants in the TSC2 intron, which might have led to reduction in the expression of both TSC2 and NTHL1, consequently leading to TSC and multiple pathologically diverse RCCs.
 INTRODUCTION: Impairment in visual and cognitive functions occur in youth with demyelinating disorders such as multiple sclerosis, neuromyelitis optica spectrum disorder, and myelin oligodendrocyte glycoprotein antibody-associated disease. Quantitative behavioral assessment using eye-tracking and pupillometry can provide functional metrics for important prognostic and clinically relevant information at the bedside. METHODS: Children and adolescents diagnosed with demyelinating disorders and healthy, age-matched controls completed an interleaved pro- and anti-saccade task using video-based eye-tracking and underwent spectral-domain optical coherence tomography examination for evaluation of retinal nerve fiber layer and ganglion cell inner plexiform layer thickness. Low-contrast visual acuity and Symbol Digit Modalities Test were performed for visual and cognitive functional assessments. We assessed saccade and pupil parameters including saccade reaction time, direction error rate, pupil response latency, peak constriction time, and peak constriction and dilation velocities. Generalized Estimating Equations were used to examine the association of eye-tracking parameters with optic neuritis history, structural metrics, and visual and cognitive scores. RESULTS: The study included 36 demyelinating disorders patients, aged 8-18 yrs. (75% F; median = 15.22 yrs., SD = 2.8) and 34 age-matched controls (65% F; median = 15.26 yrs., SD = 2.3). Surprisingly, pro- and anti-saccade performance was comparable between patients and controls, whereas pupil control was altered in patients. Oculomotor latency measures were strongly associated with the number of optic neuritis episodes, including saccade reaction time, pupil response latency, and peak constriction time. Peak constriction time was associated with both retinal nerve fiber layer and ganglion cell inner plexiform layer thickness. Pupil response latency and peak constriction time were associated with visual acuity. Pupil velocity for both constriction and dilation was associated with Symbol Digit Modalities Test scores. CONCLUSION: The strong associations between oculomotor measures with history of optic neuritis, structural, visual, and cognitive assessments in these cohorts demonstrates that quantitative eye-tracking can be useful for probing demyelinating injury of the brain and optic nerve. Future studies should evaluate their utility in discriminating between demyelinating disorders and tracking disease progression.
 PURPOSE: To develop a method for rapid sub-millimeter T(1) , T(2) , T2* , and QSM mapping in a single scan using multi-contrast learned acquisition and reconstruction optimization (mcLARO). METHODS: A pulse sequence was developed by interleaving inversion recovery and T(2) magnetization preparations and single-echo and multi-echo gradient echo acquisitions, which sensitized k-space data to T(1) , T(2) , T2* , and magnetic susceptibility. The proposed mcLARO optimized both the multi-contrast k-space under-sampling pattern and image reconstruction based on image feature fusion using a deep learning framework. The proposed mcLARO method with R = 8 under-sampling was validated in a retrospective ablation study and compared with other deep learning reconstruction methods, including MoDL and Wave-MoDL, using fully sampled data as reference. Various under-sampling ratios in mcLARO were investigated. mcLARO was also evaluated in a prospective study using separately acquired conventionally sampled quantitative maps as reference standard. RESULTS: The retrospective ablation study showed improved image sharpness of mcLARO compared to the baseline network without the multi-contrast sampling pattern optimization or image feature fusion module. The under-sampling ratio experiment showed that higher under-sampling ratios resulted in blurrier images and lower precision of quantitative values. The prospective study showed that small or negligible bias and narrow 95% limits of agreement on regional T(1) , T(2) , T2* , and QSM values by mcLARO (5:39 mins) compared to reference scans (40:03 mins in total). mcLARO outperformed MoDL and Wave-MoDL in terms of image sharpness, noise suppression, and artifact removal. CONCLUSION: mcLARO enabled fast sub-millimeter T(1) , T(2) , T2* , and QSM mapping in a single scan.
 INTRODUCTION: Neuropathic pain is a debilitating condition resulting from various etiologies such as diabetes, multiple sclerosis, and infection, and is associated with decreased quality of life, poor health outcomes, and increased economic burden. However, epidemiological studies on neuropathic pain have been largely limited in Vietnam. METHODS: A cross-sectional study was conducted on adult Vietnamese industrial workers across three manufacturing plants. Demographic, socioeconomic, occupational and health data were collected. Prevalence of neuropathic pain was assessed using the Douleur Neuropathique 4 (DN4) scale. Regression modeling was utilized to identify predictors of pain. RESULTS: Among 276 workers, 43.1 and 24.3% reported that they had suffered from spinal pain and osteoarthritis pain, respectively. In terms of work conditions, people maintaining constant posture when working from 30 to 60 min (OR = 3.15, 95% CI = 1.07; 9.29), or over 60 min (OR = 2.59; 95% CI = 1.12; 5.98) had a higher risk of suffering from spinal pain. People who worked in conditions lacking adequate lighting and with exposures to toxic chemicals were also likely to be suffering from osteoarthritis pain with OR = 4.26, 95% CI = 1.02; 17.74 and Coef. = 1.93; 95% CI = 1.49; 2.50, respectively. Regular health examinations and higher expenditure for healthcare were correlated with a lower prevalence of neuropathic pain. DISCUSSION: These results may inform the adoption of pain screening and other programs that increase health care access for this population, as well as more stringent occupational health and safety standards.
 In the area of drug discovery, repurposing strategies represent an approach to discover new uses of approved drugs besides their original indications. We used this approach to investigate the effects of dimethyl fumarate (DMF), a drug approved for relapsing-remitting multiple sclerosis and psoriasis treatment, on early injury associated with diabetic retinopathy (DR). We used an in vivo streptozotocin (STZ)-induced diabetic rat model. Diabetes was induced by a single injection of STZ in rats, and after 1 week, a group of animals was treated with a daily intraperitoneal injection of DMF or a vehicle. Three weeks after diabetes induction, the retinal expression levels of key enzymes involved in DR were evaluated. In particular, the biomarkers COX-2, iNOS, and HO-1 were assessed via Western blot and immunohistochemistry analysis. Diabetic rats showed a significant retinal upregulation of COX-2 and iNOS compared to the retina of normal rats (non-diabetic), and an increase in HO-1 was also observed in the STZ group. This latter result was due to a mechanism of protection elicited by the pathological condition. DMF treatment significantly induced the retinal expression of HO-1 in STZ-induced diabetic animals with a reduction in iNOS and COX-2 retinal levels. Taken together, these results suggested that DMF might be useful to counteract the inflammatory process and the oxidative response in DR. In conclusion, we believe that DMF represents a potential candidate to treat diabetic retinopathy and warrants further in vivo and clinical evaluation.
 INTRODUCTION: Non-compressive myelopathy is a neurological disorder due to pathological processes affecting the spinal cord in the absence of clinical and radiological evidence of spinal cord compression. Two commonly used diagnostic tools for non-compressive myelopathy are somatosensory evoked potentials (SSEPs) and magnetic resonance imaging (MRI). SSEPs are a neurophysiological tool used to assess the functional integrity of the spinal cord. MRI, on the other hand, is the mainstay imaging modality used for identifying compressive lesions and other structural abnormalities in the spinal cord. The aim of this study was to test the diagnostic accuracy of SSEPs versus spine MRI in the diagnosis and assessment of the severity of non-compressive myelopathy using the Modified Japanese Orthopaedic Association (mJOA) clinical severity score. METHODS: Our study included 63 subjects. Whole spine MRI and SSEPs (median and tibial SSEP bilaterally) were done for all subjects; their results were compared according to their relation to the mJOA score and classified into mild, moderate, and severe. The control group was examined to establish normative data for SSEP results and compared with cases. Blood investigations such as complete blood count, thyroid function test, A1C, HIV tests, venereal disease research laboratory test, erythrocyte sedimentation rate, C-reactive protein, and antinuclear antibody tests were done. Blood tests for vitamin B12 levels were done for patients who were suspected of sub-acute combined degeneration of the spinal cord; cerebrospinal fluid (CSF) analysis was done for patients suspected of multiple sclerosis (MS), acute transverse myelitis (ATM), or other inflammatory/infectious diseases. CSF was analyzed for cell count, cytology, protein, and oligoclonal bands (if indicated). RESULTS: No mild categories were registered in this study; 30% of patients were moderate and 70% were severe. Causes for non-compressive myelopathy in this study were hereditary degenerative ataxias in 12 (38.71%), ATM in 8 (25.81%), and MS in 5 (16.13%); other causes included vitamin B12 deficiency in 2 (6.45%), ischemia in 2 (6.45%), and an unknown cause in 2 (6.45%). SSEPs showed abnormal results in all patients (31; 100%) whereas MRI showed abnormality in only seven patients (22.6%). SSEP sensitivity for detecting severe cases was around 63.6% while that for MRI was 27.3%. CONCLUSION: The study concluded that SSEPs were more reliable for the detection of non-compressive myelopathies rather than MRI and correlated better with clinical severity. Performing SSEPs is recommended for all patients with non-compressive myelopathy, especially those with negative imaging.
 FTY720 is an FDA-approved sphingosine derivative drug for the treatment of multiple sclerosis. This compound blocks lymphocyte egress from lymphoid organs and autoimmunity through sphingosine 1-phosphate (S1P) receptor blockage. Drug repurposing of FTY720 has revealed improvements in glucose metabolism and metabolic diseases. Studies also demonstrate that preconditioning with this compound preserves the ATP levels during cardiac ischemia in rats. The molecular mechanisms by which FTY720 promotes metabolism are not well understood. Here, we demonstrate that nanomolar concentrations of the phosphorylated form of FTY720 (FTY720-P), the active ligand of S1P receptor (S1PR), activates mitochondrial respiration and the mitochondrial ATP production rate in AC16 human cardiomyocyte cells. Additionally, FTY720-P increases the number of mitochondrial nucleoids, promotes mitochondrial morphology alterations, and induces activation of STAT3, a transcription factor that promotes mitochondrial function. Notably, the effect of FTY720-P on mitochondrial function was suppressed in the presence of a STAT3 inhibitor. In summary, our results suggest that FTY720 promotes the activation of mitochondrial function, in part, through a STAT3 action.
 Dimethyl fumarate (DMF) is approved as a treatment for multiple sclerosis (MS), however, its mode of action remains unclear. One hypothesis proposes that Michael addition to thiols by DMF, notably glutathione is immunomodulatory. The alternative proposes that monomethyl fumarate (MMF), the hydrolysis product of DMF, is a ligand to the fatty acid receptor GPR109A found in the lysosomes of immune cells. We prepared esters of MMF and macrolides derived from azithromycin, which were tropic to immune cells by virtue of lysosomal trapping. We tested the effects of these substances in an assay of response to Lipopolysaccharide (LPS) in freshly isolated human peripheral blood mononuclear cells (PBMCs). In this system, we observed that the 4'' ester of MMF (compound 2 and 3) reduced levels of Interleukins (IL)-1β, IL-12 and tumor necrosis factor alpha (TNFα) significantly at a concentration of 1 µM, while DMF required about 25 µM for the same effect. The 2' esters of MMF (compound 1 and 2) were, like MMF itself, inactive in vitro. The 4'' ester formed glutathione conjugates rapidly while the 2' conjugates did not react with thiols but did hydrolyze slowly to release MMF in these cells. We then tested the substances in vivo using the imiquimod/isostearate model of psoriasis where the 2' ester was the most active at 0.06-0.12 mg/kg (approximately 0.1 µmol/kg), improving skin score, body weight and cytokine levels (TNFα, IL-17A, IL-17F, IL-6, IL-1β, NLRP3 and IL-23A). In contrast, the thiol reactive 4'' ester was less active than the 2' ester while DMF was ca. 300-fold less active. The thiol reactive 4'' ester was not easily recovered from either plasma or organs while the 2' ester exhibited conventional uptake and elimination. The 2' ester also reduced levels of IL-6 in acute monosodium urate (MSU) induced inflammation. These data suggest that mechanisms that are relevant in vivo center on the release of MMF. Given that GPR109A is localized to the lysosome, and that lysosomal trapping increases 2' ester activity by > 300 fold, these data suggest that GPR109A may be the main target in vivo. In contrast, the effects associated with glutathione (GSH) conjugation in vitro are unlikely to be as effective in vivo due to the much lower dose in use which cannot titrate the more concentrated thiols. These data support the case for GPR109A modulation in autoimmune diseases.
 BACKGROUND: Brain-derived exosomes released into the blood are considered a liquid biopsy to investigate the pathophysiological state, reflecting the aberrant heterogeneous pathways of pathological progression of the brain in neurological diseases. Brain-derived blood exosomes provide promising prospects for the diagnosis of neurological diseases, with exciting possibilities for the early and sensitive diagnosis of such diseases. However, the capability of traditional exosome isolation assays to specifically isolate blood exosomes and to characterize the brain-derived blood exosomal proteins by high-throughput proteomics for clinical specimens from patients with neurological diseases cannot be assured. We report a magnetic transferrin nanoparticles (MTNs) assay, which combined transferrin and magnetic nanoparticles to isolate brain-derived blood exosomes from clinical samples. METHODS: The principle of the MTNs assay is a ligand-receptor interaction through transferrin on MTNs and transferrin receptor on exosomes, and electrostatic interaction via positively charged MTNs and negatively charged exosomes to isolate brain-derived blood exosomes. In addition, the MTNs assay is simple and rapid (< 35 min) and does not require any large instrument. We confirmed that the MTNs assay accurately and efficiently isolated exosomes from serum samples of humans with neurodegenerative diseases, such as dementia, Parkinson's disease (PD), and multiple sclerosis (MS). Moreover, we isolated exosomes from serum samples of 30 patients with three distinct neurodegenerative diseases and performed unbiased proteomic analysis to explore the pilot value of brain-derived blood protein profiles as biomarkers. RESULTS: Using comparative statistical analysis, we found 21 candidate protein biomarkers that were significantly different among three groups of neurodegenerative diseases. CONCLUSION: The MTNs assay is a convenient approach for the specific and affordable isolation of extracellular vesicles from body fluids for minimally-invasive diagnosis of neurological diseases.
 Primary Sjögren's syndrome (pSS) is an autoimmune disease that primarily affects the exocrine glands and is mainly characterized by sicca symptoms of the eyes and mouth. Approximately 30-50% of pSS patients develop systemic multi-organ disorders including malignant lymphoma. The etiology of pSS is not well understood; growing evidence suggests that uncontrolled immune/inflammatory responses, excessive oxidative stress, defected apoptosis, dysregulated autophagy, exosomes, and exogenous virus infections may participate in the pathogenesis of pSS. There is no ideal therapeutic method for pSS; the management of pSS is mainly palliative, which aims to alleviate sicca symptoms. Melatonin, as the main secretory product of the pineal gland, has been evidenced to show various physiological functions, including effects of immunoregulation, capability of antioxidation, moderation of autophagy, suppressive activities of apoptosis, regulative capacity of exosomes, properties of anti-infection, and improvement of sleep. The beneficial effects of melatonin have been already validated in some autoimmune diseases such as multiple sclerosis (MS), type 1 diabetes mellitus (T1DM), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD). However, our previous research firstly revealed that melatonin might inhibit pathogenic responses of peripheral Th17 and double-negative (DN) T cells in pSS. More importantly, melatonin administration alleviated the development of pSS in animal models with reduced infiltrating lymphocytes, improved functional activity of salivary gland, and decreased production of inflammatory factors as well as autoantibodies. Owing to the important biological properties reported in melatonin are characteristics closely related to the treatment of pSS; the potential role and underlying mechanisms of melatonin in the administration of pSS are certainly worth further investigations. Consequently, the aim of this review is to give a deep insight to the therapeutic potency of melatonin for pSS.
 INTRODUCTION: Numerous studies have found an association between autoimmune diseases of the nervous system (ADNS) and schizophrenia (SCZ), but the findings remain controversial. We conducted the first meta-analysis to summarize the current evidence from cohort studies that evaluated the association between ADNS and SCZ. METHODS: PubMed, Web of Science, and Embase were comprehensively searched until May 30, 2022 for articles on the association between ADNS and SCZ. Every included study was reported effect size with 95% CIs for the association between ADNS and SCZ. Meta-regression and subgroup analysis were used to assess the heterogeneity. RESULTS: A total of 8 cohort studies with 12 cohorts were included in the meta-analysis. We observed a significant association between ADNS and SCZ (RR = 1.42; 95%CI, 1.18-1.72). Subgroup analysis showed that the risk of SCZ was significantly increased when ADNS were used as exposure factors (RR = 1.48; 95%CI, 1.15-1.89), whereas with SCZ did not observe an increased risk of subsequent ADNS (RR = 1.33; 95%CI, 0.92-1.92); multiple sclerosis (MS) was positively associated with SCZ (RR = 1.36; 95%CI, 1.12-1.66), but no significant association was found between Guillain-Barre syndrome (GBS) and SCZ (RR = 1.90; 95%CI, 0.87-4.17). Meanwhile, we found location was the source of heterogeneity. LIMITATIONS: High heterogeneity was observed (I(2) = 92.0%), and only English literature was included in the meta-analysis. CONCLUSIONS: We found a positive association between ADNS and SCZ, and the association was different across the different types of ADNS. The results of the study are helpful for clinicians to carry out targeted preventive measures for ADNS and SCZ.
 BACKGROUND AND PURPOSE: The aim was to systematically review the effectiveness and safety of telemedicine combined with usual care (in-person visits) compared to usual care for the therapeutic management and follow-up assessment of neurological diseases. METHODS: The electronic databases MEDLINE, Embase, Web of Science and Cochrane Central Register of Controlled Trials were searched (June 2021). Randomized controlled trials (RCTs) on patients of any age with neurological diseases were considered. Two reviewers screened and abstracted data in duplicate and independently and assessed risk of bias using the Cochrane risk-of-bias tool for randomized trials (RoB 2). When possible, pooled effect estimates were calculated. RESULTS: Of a total of 3018 records initially retrieved, 25 RCTs (n = 2335) were included: 11 (n = 804) on stroke, four (n = 520) on Parkinson's disease, three (n = 110) on multiple sclerosis, two (n = 320) on epilepsy, one (n = 63) on dementia, one (n = 23) on spina bifida, one (n = 40) on migraine, one (n = 22) on cerebral palsy and one (n = 433) on brain damage. Types of telemedicine assessed were online visits (11 studies), tele-rehabilitation (seven studies), telephone calls (three), smartphone apps (two) and online computer software (two). The evidence was quite limited except for stroke. Compared to usual care alone, telemedicine plus usual care was found to improve depressive symptoms, functional status, motor function, executive function, generic quality of life, healthcare utilization and healthy lifestyle in patients in post-stroke follow-up. CONCLUSIONS: Well-designed and executed RCTs are needed to confirm our findings on stroke and to have more scientific evidence available for the other neurological diseases.
 BACKGROUND AND OBJECTIVES: To assess American Academy of Neurology (AAN)-recommended Practice Guidelines (PGs) for equity in gender representation among physician authors. METHODS: This cross-sectional study included AAN-recommended PG publications from January 1, 2015, to December 31, 2020. Author degrees and gender were identified by 2 reviewers using the publication and/or online searches. Gender was determined from pronouns or photographs. Gender representation was compared with Association of American Medical Colleges (AAMC) data on academic neurologists. Data were analyzed using Z tests of 2 proportions and descriptive statistics. RESULTS: AAMC benchmarks report academic women neurologists represented 35% of the specialty in 2015, 38% in 2018, and 39% in 2020. We identified 68 unique PG publications with 709 physician authors, 31% (223) women, 68% (484) men, and 0.3% (2) gender could not be identified. Representation of women physicians was low among PG authors across all benchmarks, significantly so for 2018 and 2020 (p < 0.01). Among physician first authors, women were significantly underrepresented across all benchmarks (18% [12/65], p < 0.01). Representation of women physicians was lower when men physicians were first authors vs women physicians (31% [161/524] vs 43% [50/118], p = 0.02). Among subspecialties with 10+ PGs, women physician authorship was highest in child neurology (48% [57/120]) and lowest in stroke and vascular neurology (16% [18/113]). DISCUSSION: We found that women physicians were underrepresented as authors of AAN-recommended PGs. This suggests a missed opportunity for neurology because PGs that include expertise from women physicians may improve care and translation into practice. In addition, women physicians lose out on professional development from authorship. Further research is needed to understand causality and address gaps.
 OBJECTIVES: This systematic review aimed to evaluate the efficacy of B vitamins and vitamin D therapy in improving the standard treatment of depression and anxiety disorders. We also aimed to gather the evidence supporting the recommendations for supplementation in clinical practice. METHODS: Performed between March 2020 and September 2021, the main inclusion criteria were randomized controlled trials (RCTs), with patients ≥ 18 years old, both sexes, fulfilling target diagnoses of major depressive disorder (MDD), generalized anxiety disorder (GAD), or mild to severe depressive and anxiety symptoms. In addition, the RCTs were included if the scales to assess the severity of the symptoms were standardized rating scales in psychiatric. Trials that reported diagnoses of schizophrenia, perinatal depression, bipolar depression, sleep disorders, eating disorders, cancer, and multiple sclerosis in association with any of the mentioned diagnoses were excluded. RESULTS: We identified 20 RCTs that matched all eligibility criteria, totaling 2,256 subjects, diagnosed with MDD, GAD, and depressive or anxiety symptoms. Supplementation with folic acid or L-methylfolate, B1, B12 or methylcobalamin, and vitamin D (in different doses and study duration) significantly decreased depression score scales by increasing response to standard pharmacological treatment or as monotherapy, including partial or complete remission. As for anxiety symptoms, the availability of results is limited to adjuvant vitamin D therapy. DISCUSSION: B vitamins and vitamin D associated with other compounds also showed significant results, so the improvement in symptoms cannot be attributed strictly to those. Our results suggest that intervention with B vitamins and/or vitamin D may be an effective and well-tolerated adjuvant strategy for improving the symptoms of depression and anxiety, according to the patient's clinical status and nutritional biomarkers.
 Monoclonal antibodies (mAbs) are commonly used biologic drugs for the treatment of diseases such as rheumatoid arthritis, multiple sclerosis, COVID-19 and various cancers. They are produced in Chinese hamster ovary cell lines and are purified via a number of complex and expensive chromatography-based steps, operated in batch mode, that rely heavily on protein A resin. The major drawback of conventional procedures is the high cost of the adsorption media and the extensive use of chemicals for the regeneration of the chromatographic columns, with an environmental cost. We have shown that conventional protein A chromatography can be replaced with a single crystallization step and gram-scale production can be achieved in continuous flow using the template-assisted membrane crystallization process. The templates are embedded in a membrane (e.g., porous polyvinylidene fluoride with a layer of polymerized polyvinyl alcohol) and serve as nucleants for crystallization. mAbs are flexible proteins that are difficult to crystallize, so it can be challenging to determine the optimal conditions for crystallization. The objective of this protocol is to establish a systematic and flexible approach for the design of a robust, economic and sustainable mAb purification platform to replace at least the protein A affinity stage in traditional chromatography-based purification platforms. The procedure provides details on how to establish the optimal parameters for separation (crystallization conditions, choice of templates, choice of membrane) and advice on analytical and characterization methods.
 OBJECTIVES: Mass COVID-19 vaccination commenced in December 2020 in Scotland. Monitoring vaccine safety relies on accurate background incidence rates (IRs) for health outcomes potentially associated with vaccination. This study aimed to quantify IRs in Scotland of adverse events of special interest (AESI) potentially associated with COVID-19 vaccination. STUDY DESIGN AND METHODS: IRs and 95% confidence intervals (CIs) for 36 AESI were calculated retrospectively for the pre-COVID-19 pandemic period (01 January 2015-31 December 2019) and the COVID-19 pandemic period (01 April 2020-30 November 2020), with age-sex stratification, and separately by calendar month and year. Incident cases were determined using International Classification of Diseases-10th Revision (ICD-10)-coded hospitalisations. RESULTS: Prepandemic population-wide IRs ranged from 0.4 (0.3-0.5 CIs) cases per 100,000 person-years (PYRS) for neuromyelitis optica to 478.4 (475.8-481.0 CIs) cases per 100,000 PYRS for acute renal failure. Pandemic population-wide IRs ranged from 0.3 (0.2-0.5 CIs) cases per 100,000 PYRS for Kawasaki disease to 483.4 (473.2-493.7 CIs) cases per 100,000 PYRS for acute coronary syndrome. All AESI IRs varied by age and sex. Ten AESI (acute coronary syndrome, acute myocardial infarction, angina pectoris, heart failure, multiple sclerosis, polyneuropathies and peripheral neuropathies, respiratory failure, rheumatoid arthritis and polyarthritis, seizures and vasculitis) had lower pandemic than prepandemic period IRs overall. Only deep vein thrombosis and pulmonary embolism had a higher pandemic IR. CONCLUSION: Lower pandemic IRs likely resulted from reduced health-seeking behaviours and healthcare provision. Higher IRs may be associated with SARS-CoV-2 infections. AESI IRs will facilitate future vaccine safety studies in Scotland.
 BACKGROUND: Early detection of subclinical injuries can lead to a correct diagnosis and help control the advancement of the condition. This study aims to investigate the presence of subclinical damage and silent progression to the contralateral eye's visual function and structure in patients experiencing their first episode of unilateral optic neuritis (ON). METHODS: Fifty patients with first-onset unilateral ON were enrolled in this study. Based on etiology, they were classified as having neuromyelitis optica spectrum disorder-related ON (NMOSD-ON), myelin oligodendrocyte glycoprotein antibody-associated ON (MOG-ON), idiopathic ON (IDON), or multiple sclerosis-related ON (MS-ON). These cases were followed up for one year to determine whether there was any silent progression of visual function and structure in the contralateral non-ON (NON) eye. A gender- and age-matched healthy control (HC) group was included to compare the differences in visual function and structure between the patients with NON eyes and the HC group. RESULTS: Within two weeks of onset, best-corrected visual acuity (BCVA; P = 0.008), mean deviation (MD) of the visual field (VF) (P = 0.001), and peripapillary retinal nerve fiber layer (pRNFL; P = 0.019) thickness were significantly worse in the NMOSD-NON patients than those in the HC group, while there were no differences in the pRNFL and the ganglion cell-inner plexiform layer (GCIPL) thicknesses and quadrant thicknesses (P > 0.05) of the groups. IDON-NON only showed subclinical damage in VF (P = 0.001) and temporal pRNFL (P = 0.042), while the BCVA, VF, and optic nerve structure (pRNFL, GCIPL) of the MOG-NON patients showed no subclinical damage (P > 0.05). In addition, the one-year follow-up of each NON eye type showed that there was no silent progression in NMOSD-NON, MOG-NON, or IDON-NON. A pairwise comparison of the different types of NON eyes revealed no statistical differences (P > 0.05). CONCLUSION: Among the patients with unilateral ON, NMOSD-NON and IDON-NON resulted in subclinical damage to the visual function and structure of the contralateral eye within two weeks of onset, whereas MOG-NON did not show any subclinical damage to visual function or structure. Furthermore, these subclinical damages did not show any silent progression during the one-year follow-up period.
 Systemic administration of Nogo-A-neutralizing antibody ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. However, the blood-brain barrier (BBB) is a major obstacle limiting the passage of systemically applied antibody to the CNS. To bypass the BBB, in the present study we tested the intranasal route of administration by targeting the olfactory mucosa with the Nogo-A-blocking antibody 11C7 mAb in myelin oligodendrocyte glycoprotein-induced EAE. Antibodies were specifically administered onto the olfactory mucosa using a microcatheter. Antibody distribution was examined in the CNS by ELISA and light-sheet microscopy. The effects of 11C7 mAb on Nogo-A signaling were assessed by Western blotting. EAE-induced deficits were monitored daily. Demyelination was observed on spinal cord histological sections. Gene expression changes were followed by trancriptomic analyses. A sensitive capture ELISA revealed a rapid and widespread distribution of 11C7 mAb in the CNS, including the olfactory bulb, the cerebellum and the lumbar spinal cord, but not in the CSF. Light-sheet microscopy allowed to observe antibody accumulation in the parenchyma, thus demonstrating nose-to-brain transfer of IgG. At the functional level, the widespread penetration of 11C7 mAb in the CNS, including the thoracolumbar spinal cord, resulted in the improvement of motor symptoms and in the preservation of myelin in the spinal cord of EAE mice. This was accompanied by Nogo-A signaling downregulation, as reflected by the decreased level of phosphorylated cofilin observed by Western blotting in the cerebellum. In the brain of EAE score-matched animals, 11C7 modified the expression of genes that can influence neurotransmission and cognitive functions, independently of the demyelination phenotype in the spinal cord. In conclusion, our data show the feasibility of olfactory mucosa-directed administration for the delivery of therapeutic antibodies targeting CNS antigens in EAE mice.
 BACKGROUND: Vitamin D supplementation is associated with a lower incidence of diabetic nephropathy (DN); however, whether this association is causative is uncertain. METHODS: We used two-sample Mendelian randomization to examine the causal influence of vitamin D on diabetic nephropathy in 7,751 individuals with type I diabetes-related nephropathy (T1DN) and 9,933 individuals with type II diabetes-related nephropathy (T2DN). Meanwhile, we repeated some previous studies on the influence of KIM-1 (kidney injury molecule 1) and body mass index (BMI) on DN. Additionally, to test the validity of the instruments variable for vitamin D, we conducted two negative controls Mendelian randomization (MR) on breast and prostate cancer, and a positive control MR on multiple sclerosis. RESULTS: Results of the MR analysis showed that there was no causal association between 25(OH)D with the early/later stage of T1DN (early: OR = 0.903, 95%CI: 0.229 to 3.555; later: OR = 1.213, 95%CI: 0.367 to 4.010) and T2DN (early: OR = 0.588, 95%CI: 0.182 to 1.904; later: OR = 0.904, 95%CI: 0.376 to 2.173), nor with the kidney function of patients with diabetes mellitus: eGFRcyea (creatinine-based estimated GFR) (Beta = 0.007, 95%CI: -0.355 to 0.369)) or UACR (urinary albumin creatinine ratio) (Beta = 0.186, 95%CI: -0.961 to 1.333)). CONCLUSIONS: We found no evidence that Vitamin D was causally associated with DN or kidney function in diabetic patients.
 BACKGROUND: Multiple sclerosis (MS) is characterized by neuroinflammation and demyelination orchestrated by activated neuroglial cells, CNS infiltrating leukocytes, and their reciprocal interactions through inflammatory signals. An inflammatory stimulus triggers inducible nitric oxide synthase (NOS2), a pro-inflammatory marker of microglia/macrophages (MG/Mφ) to catalyze sustained nitric oxide production. NOS2 during neuroinflammation, has been associated with MS disease pathology; however, studies dissecting its role in demyelination are limited. We studied the role of NOS2 in a recombinant β-coronavirus-MHV-RSA59 induced neuroinflammation, an experimental animal model mimicking the pathological hallmarks of MS: neuroinflammatory demyelination and axonal degeneration. OBJECTIVE: Understanding the role of NOS2 in murine-β-coronavirus-MHV-RSA59 demyelination. METHODS: Brain and spinal cords from mock and RSA59 infected 4-5-week-old MHV-free C57BL/6 mice (WT) and NOS2-/- mice were harvested at different disease phases post infection (p.i.) (day 5/6-acute, day 9/10-acute-adaptive and day 30-chronic phase) and compared for pathological outcomes. RESULTS: NOS2 was upregulated at the acute phase of RSA59-induced disease in WT mice and its deficiency resulted in severe disease and reduced survival at the acute-adaptive transition phase. Low survival in NOS2-/- mice was attributed to (i) high neuroinflammation resulting from increased accumulation of macrophages and neutrophils and (ii) Iba1 + phagocytic MG/Mφ mediated-early demyelination as observed at this phase. The phagocytic phenotype of CNS MG/Mφ was confirmed by significantly higher mRNA transcripts of phagocyte markers-CD206, TREM2, and Arg1 and double immunolabelling of Iba1 with MBP and PLP. Further, NOS2 deficiency led to exacerbated demyelination at the chronic phase as well. CONCLUSION: Taken together the results imply that the immune system failed to control the disease progression in the absence of NOS2. Thus, our observations highlight a protective role of NOS2 in murine-β-coronavirus induced demyelination.
 The administration of Ocrevus, an infusion therapy for the treatment of multiple sclerosis, is time and labor intensive, leading to poor patient adherence, treatment delays due to scheduling issues, and significant staff workload. This problem worsened during the COVID-19 pandemic, which created scheduling difficulties due to space restrictions. A US Food and Drug Administration-approved rapid infusion protocol for Ocrevus decreases the infusion time by 1.5 hours per patient. The purpose of this project was to complete a literature review on rapid infusion protocols and analyze the effects of the Ocrevus rapid infusion protocol on 2 outcomes of interest: total visit time and infusion reaction rates. Data were collected using retrospective chart review and analyzed by comparing the results of each outcome to the same data points prior to the implementation of the project. Results found a statistically significant decrease in visit time, with no increase in infusion reaction rates. These findings support the implementation of this rapid Ocrevus infusion protocol in the outpatient setting with the potential to improve patient scheduling, patient satisfaction, and nursing workload, while maintaining patient safety.
 Cholinesterases catalyze the breakdown of the neurotransmitter acetylcholine (ACh), a naturally occurring neurotransmitter, into choline and acetic acid, allowing the nervous system to function properly. In the human body, cholinesterases come in two types, including acetylcholinesterase (AChE; E.C.3.1.1.7) and butyrylcholinesterase (BChE; E.C.3.1.1.8). Both cholinergic enzyme inhibitors are essential in the biochemical processes of the human body, notably in the brain. On the other hand, GSTs are found all across nature and are the principal Phase II detoxifying enzymes in eukaryotes and prokaryotes. Specific isozymes are identified as therapeutic targets because they are overexpressed in various malignancies and may have a role in the genesis of other diseases such as neurological disorders, multiple sclerosis, asthma, and especially cancer cell. Piperazine chemicals have a role in many biological processes and have fascinating pharmacological properties. As a result, therapeutically effective piperazine research is becoming more prominent. Half maximal inhibition concentrations (IC(50) ) of piperazine derivatives were found in ranging of 4.59-6.48 µM for AChE, 4.85-8.35 µM for BChE, and 3.94-8.66 µM for GST. Also, piperazine derivatives exhibited Ki values of 8.04 ± 5.73-61.94 ± 54.56, 0.24 ± 0.03-32.14 ± 16.20, and 7.73 ± 1.13-22.97 ± 9.10 µM toward AChE, BChE, and GST, respectively. Consequently, the inhibitory properties of the AChE/BChE and GST enzymes have been compared to Tacrine (for AChE and BChE) and Etacrynic acid (for GST).
 Antenatal exposures to maternal stress and to particulate matter with an aerodynamic diameter of less than 2.5 μm (PM(2.5)) have been independently associated with developmental outcomes in early infancy and beyond. Knowledge about their joint impact, biological mechanisms of their effects and timing-effects, is still limited. Both PM(2.5) and maternal stress exposure during pregnancy might result in altered patterns of DNA methylation in specific stress-related genes, such as the serotonin transporter gene (SLC6A4 DNAm), that might, in turn, influence infant development across several domains, including bio-behavioral, cognitive and socio-emotional domains. Here, we investigated the independent and interactive influence of variations in antenatal exposures to maternal pandemic-related stress (PRS) and PM(2.5) on SLC6A4 DNAm levels in newborns. Mother-infant dyads (N = 307) were enrolled at delivery during the COVID-19 pandemic. Infants' methylation status was assessed in 13 CpG sites within the SLC6A4 gene's region (chr17:28562750-28562958) in buccal cells at birth and women retrospectively report on PRS. PM(2.5) exposure throughout the entire gestation and at each gestational trimester was estimated using a spatiotemporal model based on residential address. Among several potentially confounding socio-demographic and health-related factors, infant's sex was significantly associated with infants' SLC6A4 DNAm levels, thus hierarchical regression models were adjusted for infant's sex. Higher levels of SLC6A4 DNAm at 6 CpG sites were found in newborns born to mothers reporting higher levels of antenatal PRS and greater PM(2.5) exposure across gestation, while adjusting for infant's sex. These effects were especially evident when exposure to elevated PM(2.5) occurred during the second trimester of pregnancy. Several important brain processes (e.g., synaptogenesis and myelination) occur during mid-pregnancy, potentially making the second trimester a sensitive time window for the effects of stress-related exposures. Understanding the interplay between environmental and individual-level stressors has important implications for the improvement of mother-infant health during and after the pandemic.
 Metformin has been designated as one of the most crucial first-line therapeutic agents in the management of type 2 diabetes mellitus. Primarily being an antihyperglycemic agent, metformin also has a plethora of pleiotropic effects on various systems and processes. It acts majorly by activating AMPK (Adenosine Monophosphate-Activated Protein Kinase) in the cells and reducing glucose output from the liver. It also decreases advanced glycation end products and reactive oxygen species production in the endothelium apart from regulating the glucose and lipid metabolism in the cardiomyocytes, hence minimizing the cardiovascular risks. Its anticancer, antiproliferative and apoptosis-inducing effects on malignant cells might prove instrumental in the malignancy of organs like the breast, kidney, brain, ovary, lung, and endometrium. Preclinical studies have also shown some evidence of metformin's neuroprotective role in Parkinson's disease, Alzheimer's disease, multiple sclerosis and Huntington's disease. Metformin exerts its pleiotropic effects through varied pathways of intracellular signalling and exact mechanism in the majority of them remains yet to be clearly defined. This article has extensively reviewed the therapeutic benefits of metformin and the details of its mechanism for a molecule of boon in various conditions like diabetes, prediabetes, obesity, polycystic ovarian disease, metabolic derangement in HIV, various cancers and aging.
 Repulsive guidance molecule A (RGMa) is an inhibitor of neuronal growth and survival which is upregulated in the damaged central nervous system following acute spinal cord injury (SCI), traumatic brain injury, acute ischemic stroke (AIS), and other neuropathological conditions. Neutralization of RGMa is neuroprotective and promotes neuroplasticity in several preclinical models of neurodegeneration and injury including multiple sclerosis, AIS, and SCI. Given the limitations of current treatments for AIS due to narrow time windows to intervention (TTI), and restrictive patient selection criteria, there is significant unmet need for therapeutic agents that enable tissue survival and repair following acute ischemic damage for a broader population of stroke patients. In this preclinical study, we evaluated whether elezanumab, a human anti-RGMa monoclonal antibody, could improve neuromotor function and modulate neuroinflammatory cell activation following AIS with delayed intervention times up to 24 h using a rabbit embolic permanent middle cerebral artery occlusion model (pMCAO). In two replicate 28-day pMCAO studies, weekly intravenous infusions of elezanumab, over a range of doses and TTIs of 6 and 24 h after stroke, significantly improved neuromotor function in both pMCAO studies when first administered 6 h after stroke. All elezanumab treatment groups, including the 24 h TTI group, had significantly less neuroinflammation as assessed by microglial and astrocyte activation. The novel mechanism of action and potential for expanding TTI in human AIS make elezanumab distinct from current acute reperfusion therapies, and support evaluation in clinical trials of acute CNS damage to determine optimal dose and TTI in humans. A: Ramified/resting astrocytes and microglia in a normal, uninjured rabbit brain. B: Rabbit pMCAO brain illustrating lesion on right side of brain (red), surrounded by penumbra (pink) during acute phase post stroke, with minimal injury to left brain hemisphere. Penumbra characterized by activated astrocytes and microglia (region in crosshair within circle), with upregulation of free and bound RGMa. C: Elezanumab binds to both free and bound RGMa, preventing full activation of astrocytes and microglia. D: Elezanumab is efficacious in rabbit pMCAO with a 4 × larger TTI window vs. tPA (6 vs. 1.5 h, respectively). In human AIS, tPA is approved for a TTI of 3-4.5 h. Elezanumab is currently being evaluated in a clinical Ph2 study of AIS to determine the optimal dose and TTI (NCT04309474).
 [This corrects the article on p. 23 in vol. 60, PMID: 36911568.].
 BACKGROUND: An individual's personal values strongly influence their immediate and long-term decisions. Psychological heterogeneity in clinical trial populations contributes to selection bias and may affect treatment outcomes and inevitably trial results. OBJECTIVES: The objective of this study was to characterize for the first time the main interpersonal values of patients who participated in Phase II and III clinical trials. METHODS: This multicenter observational study included 200 participants from 4 different hospitals who participated in a Phase II or III clinical trial. Patients from different therapeutic areas were included in this study. The patients' interpersonal values were studied using the Survey of Interpersonal Values (SIV). The SIV scale is grouped into six subscales that assess specific personal values: (1) support, the need to be treated with kindness and to receive encouragement from other people; (2) conformity, the extent to which one does what is acceptable and considered socially correct; (3) recognition, the need to be highly regarded and admired, to be considered important and recognized by others; (4) independence, the extent to which individuals feel free to make their own decisions; (5) benevolence, the capacity to understand and show generosity towards the less fortunate; and (6) leadership, the value ascribed to coordinating the work of others, being selected for a leadership position, and being in a position to tell others what to do. The results obtained from the patient population were classified using the following categories: "very high" (P95-P99), "high" (P70-90), "medium" (P35-65) low" (P10-30), or "very low" (P1-5), and subsequently compared with those of the Portuguese normative population. RESULTS: Compared with the normative population, regardless of the patient's underlying disease, the percentile frequency distributions were significantly higher for the independence (p < 0.001) and benevolence (p < 0.001) subscales, and significantly lower for the leadership (p < 0.001) and recognition (p < 0.001) subscales in the patient population. Patient distribution according to underlying disease differed significantly relative differences in distribution relative to the normative population for the majority of subscales. Non-alcoholic steatohepatitis (NASH), heart failure, myocardial infarction, lung cancer, and rheumatoid arthritis patients were those for which the greatest differences were observed across diseases, while stroke, multiple sclerosis, and HIV patients showed the least differences relative to the normative population. CONCLUSIONS: This novel analysis of the interpersonal values of patients that participate in Phase II and III clinical trials revealed that the patients' interpersonal values largely differed from those of the Portuguese normative population. Better understanding the implications of these findings for clinical trial representativeness and outcomes is of crucial importance.
 BACKGROUND AND PURPOSE: Acute flaccid myelitis (AFM) and transverse myelitis (TM) are serious conditions that may be difficult to differentiate, especially at onset of disease. In this study, we compared clinical features of pediatric AFM and TM and evaluated current diagnostic criteria, aiming to improve early and accurate diagnosis. METHODS: Two cohorts of children with enterovirus D68-associated AFM and clinically diagnosed TM were compared regarding presenting clinical features, additional investigations, and outcome. Current diagnostic criteria for AFM and TM were applied to evaluate their specificity. RESULTS: Children with AFM (n = 21) compared to those with TM (n = 36) were younger (median 3 vs. 10 years), more often had a prodromal illness (100% vs. 39%), predominant proximal weakness (69% vs. 17%), and hyporeflexia (100% vs. 44%), and less often had sensory deficits (0% vs. 81%), bowel and/or bladder dysfunction (12% vs. 69%), and hyperreflexia (0% vs. 44%). On magnetic resonance imaging, brainstem involvement was more common in AFM (74% vs. 21%), whereas supratentorial abnormalities were only seen in TM (0% vs. 40%). When omitting the criterion of a sensory level, 11 of 15 (73%) children with AFM fulfilled the diagnostic criteria for TM. Of children with TM, four of 33 (12%) fulfilled the diagnostic criteria for probable/definite AFM. CONCLUSIONS: Although there is considerable overlap between AFM and TM in children, we found important early differentiating clinical and diagnostic features. Meeting diagnostic criteria for AFM in children with TM and vice versa underlines the importance of thorough clinical examination and early and accurate diagnostic studies.
 Multiple sclerosis (MS) is an inflammatory-mediated demyelinating disease of the central nervous system (CNS). Although studies have demonstrated that microglia facilitate remyelination in demyelinating diseases, the underlying mechanisms are still not fully characterized. We found that aryl hydrocarbon receptor (AhR), an environment sensor, was upregulated within the corpus callosum in the cuprizone model of CNS demyelination, and upregulated AhR was mainly confined to microglia. Deletion of AhR in adult microglia inhibited efficient remyelination. Transcriptome analysis using RNA-seq revealed that AhR-deficient microglia displayed impaired gene expression signatures associated with lysosome and phagocytotic pathways. Furthermore, AhR-deficient microglia showed impaired clearance of myelin debris and defected phagocytic capacity. Further investigation of target genes of AhR revealed that spleen tyrosine kinase (SYK) is the downstream effector of AhR and mediated the phagocytic capacity of microglia. Additionally, AhR deficiency in microglia aggravated CNS inflammation during demyelination. Altogether, our study highlights an essential role for AhR in microglial phagocytic function and suggests the therapeutic potential of AhR in demyelinating diseases.
 BACKGROUND: Persons with neuroinflammatory diseases (pwNID) treated with potent immunosuppressives are at risk of severe COVID-19 outcomes and reduced vaccine seroconversion. We aimed at determining the real-world efficacy of tixagevimab and cilgavimab (Evusheld™) in immunosuppressed pwNID in preventing breakthrough COVID-19 infections. METHODS: 31 immunosuppressed pwNID were followed for 6 months after administration of tixagevimab and cilgavimab as a prophylactic COVID-19 medication (January 2022-July 2022). Only pwNID treated with anti-CD20 monoclonal antibodies and sphingosine-1-phosphate modulators were considered eligible for the study. A control group of 126 immunosuppressed pwNID (38 seropositive and 88 seronegative after SARS-CoV-2 vaccination) were included. Breakthrough COVID-19 infections rate and their severity was determined over the follow-up. RESULTS: The pwNID treated with tixagevimab and cilgavimab had more comorbidities when compared with the total and seronegative pwNID control group (54.8% vs. 30.2% vs. 27.3%, p = 0.02 and p = 0.005, respectively). After a 6-month follow-up, significantly lower numbers of pwNID treated with tixagevimab and cilgavimab had breakthrough COVID-19 when compared with the control pwNID group (6.5% vs. 34.1%, p = 0.002) and seronegative control pwNID group (6.5% vs. 38.6%, p < 0.001). All COVID-19 infections in Evusheld-treated pwNID were mild, whereas 9/43 COVID-19 infections in the control group were moderate/severe. No side effects to tixagevimab and cilgavimab were recorded. CONCLUSION: In pwNID treated with immunosuppressive therapies, tixagevimab and cilgavimab (Evusheld™) significantly reduced the numbers and severity of breakthrough COVID-19 infections during the Omicron (BA.2-BA.5 variants) wave.
 In the developing central nervous system, oligodendrocyte precursor cells (OPCs) differentiate into oligodendrocytes, which form myelin around axons. Oligodendrocytes and myelin are essential for the function of the central nervous system, as evidenced by the severe neurological symptoms that arise in demyelinating diseases such as multiple sclerosis and leukodystrophy. Although many cell-intrinsic mechanisms that regulate oligodendrocyte development and myelination have been reported, it remains unclear whether interactions among oligodendrocyte-lineage cells (OPCs and oligodendrocytes) affect oligodendrocyte development and myelination. Here, we show that blocking vesicle-associated membrane protein (VAMP) 1/2/3-dependent exocytosis from oligodendrocyte-lineage cells impairs oligodendrocyte development, myelination, and motor behavior in mice. Adding oligodendrocyte-lineage cell-secreted molecules to secretion-deficient OPC cultures partially restores the morphological maturation of oligodendrocytes. Moreover, we identified L-type prostaglandin D synthase as an oligodendrocyte-lineage cell-secreted protein that promotes oligodendrocyte development and myelination in vivo. These findings reveal a novel autocrine/paracrine loop model for the regulation of oligodendrocyte and myelin development.
 According to the World Health Organization, both indoor and urban air pollution are responsible for the deaths of around 3.5 million people annually. During the last few decades, the interest in understanding the composition and health consequences of the complex mixture of polluted air has steadily increased. Today, after decades of detailed research, it is well-recognized that polluted air is a complex mixture containing not only gases (CO, NO(x), and SO(2)) and volatile organic compounds but also suspended particles such as particulate matter (PM). PM comprises particles with sizes in the range of 30 to 2.5 μm (PM(30), PM(10), and PM(2.5)) and ultrafine particles (UFPs) (less than 0.1 μm, including nanoparticles). All these constituents have different chemical compositions, origins and health consequences. It has been observed that the concentration of PM and UFPs is high in urban areas with moderate traffic and increases in heavy traffic areas. There is evidence that inhaling PM derived from fossil fuel combustion is associated with a wide variety of harmful effects on human health, which are not solely associated with the respiratory system. There is accumulating evidence that the brains of urban inhabitants contain high concentrations of nanoparticles derived from combustion and there is both epidemiological and experimental evidence that this is correlated with the appearance of neurodegenerative human diseases. Neurological disorders, such as Alzheimer's and Parkinson's disease, multiple sclerosis, and cerebrovascular accidents, are among the main debilitating disorders of our time and their epidemiology can be classified as a public health emergency. Therefore, it is crucial to understand the pathophysiology and molecular mechanisms related to PM exposure, specifically to UFPs, present as pollutants in air, as well as their correlation with the development of neurodegenerative diseases. Furthermore, PM can enhance the transmission of airborne diseases and trigger inflammatory and immune responses, increasing the risk of health complications and mortality. Therefore, understanding the different levels of this issue is important to create and promote preventive actions by both the government and civilians to construct a strategic plan to treat and cope with the current and future epidemic of these types of disorders on a global scale.
 Estrogen is a disease-modifying factor in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) via estrogen receptor alpha (ERα). However, the mechanisms by which ERα signaling contributes to changes in disease pathogenesis have not been completely elucidated. Here, we demonstrate that ERα deletion in dendritic cells (DCs) of mice induces severe neurodegeneration in the central nervous system in a mouse EAE model and resistance to interferon beta (IFNβ), a first-line MS treatment. Estrogen synthesized by extragonadal sources is crucial for controlling disease phenotypes. Mechanistically, activated ERα directly interacts with TRAF3, a TLR4 downstream signaling molecule, to degrade TRAF3 via ubiquitination, resulting in reduced IRF3 nuclear translocation and transcription of membrane lymphotoxin (mLT) and IFNβ components. Diminished ERα signaling in DCs generates neurotoxic effector CD4(+) T cells via mLT-lymphotoxin beta receptor (LTβR) signaling. Lymphotoxin beta receptor antagonist abolished EAE disease symptoms in the DC-specific ERα-deficient mice. These findings indicate that estrogen derived from extragonadal sources, such as lymph nodes, controls TRAF3-mediated cytokine production in DCs to modulate the EAE disease phenotype.
 Psoriasis is a systemic immune-mediated disease associated with an increased risk of comorbidities, such as psoriatic arthritis, cardiovascular disease, metabolic syndrome, inflammatory bowel disease, psychiatric disorders, and malignancy. In recent years, with the advent of biological agents, the efficacy and safety of psoriasis treatments have dramatically improved. Presently, tumor necrosis factor-α inhibitors, interleukin-17 inhibitors, interleukin-12/23 inhibitors, and interleukin-23 inhibitors are approved to treat moderate-to-severe psoriasis. Small-molecule inhibitors, such as apremilast and deucravacitinib, are also approved for the treatment of psoriasis. Although it is still unclear, systemic agents used to treat psoriasis also have a significant impact on its comorbidities by altering the systemic inflammatory state. Data from clinical trials and studies on the safety and efficacy of biologics and small-molecule inhibitors provide important information for the personalized care and treatment for patients with psoriasis. Notably, treatment with interleukin-17 inhibitors is associated with new-onset or exacerbations of inflammatory bowel disease. In addition, great caution needs to be taken when using tumor necrosis factor-α inhibitors in patients with psoriasis with concomitant congestive heart failure, multiple sclerosis, and malignancy. Apremilast may induce weight loss as an adverse effect, presenting also with some beneficial metabolic actions. A better understanding of the characteristics of biologics and small-molecule inhibitors in the treatment of psoriasis comorbidities can provide more definitive guidance for patients with distinct comorbidities.
 INTRODUCTION: Alopecia areata (AA) is the most common form of immune-mediated hair loss. Studies have begun to establish the most frequent comorbid diseases of AA; however, results have been inconsistent with few prospective studies. METHODS: A total of 63,692 women in the Nurses' Health Study, 53-80 years, were prospectively followed from 2002 to 2014 to determine whether history of immune-mediated disease was associated with AA risk. Hazard ratios (HRs) and 95% confidence intervals (CIs) for AA in relation to immune-mediated conditions were computed using Cox proportional hazard models, adjusted for AA risk factors. RESULTS: 133 AA cases were identified during follow-up. Personal history of any immune-mediated disease was associated with increased AA risk (HR 1.72, 95% CI 1.24-2.37). History of systemic lupus erythematosus (HR 5.43, 95% CI 2.11-13.97), multiple sclerosis (HR 4.10, 95% CI 1.40-11.96), vitiligo (HR 3.13, 95% CI 1.08-9.10), psoriasis (HR 2.01, 95% CI 1.00-4.03), hypothyroidism (HR 1.88, 95% CI 1.30-2.71), and rheumatoid arthritis (HR 1.66, 95% CI 1.09-2.52) were associated with increased AA risk. History of inflammatory bowel disease or Graves' disease/hyperthyroidism was not significantly associated with AA risk. CONCLUSIONS: In this prospective study, personal history of immune-mediated diseases either individually or overall was associated with increased AA risk.
 BACKGROUND: Familial associations can be indicators of shared genetic susceptibility between two diseases. Previous data on familial autoimmunity in patients with idiopathic inflammatory myopathies (IIM) are scarce and inconsistent. OBJECTIVES: To investigate which autoimmune diseases (ADs) may share genetic susceptibility with IIM, we examined the familial associations between IIM and different ADs. METHODS: In this Swedish population-based family study, we assembled 7615 first-degree relatives (FDRs) of 1620 patients with IIM and 37,309 relatives of 7797 matched individuals without IIM. Via register linkages, we ascertained rheumatoid arthritis, other rheumatic inflammatory diseases (RIDs), multiple sclerosis, inflammatory bowel diseases (IBD), type 1 diabetes mellitus, autoimmune thyroid diseases (AITD), coeliac disease (CeD) and myasthenia gravis among the FDRs. We estimated the familial association between IIM and each AD using conditional logistic regression and performed subgroup analyses by kinship. RESULTS: Patients with IIM had significantly higher odds of having ≥1 FDR affected by other RIDs (adjusted odds ratio [aOR] = 1.40, 95% confidence interval [CI] 1.11-1.78) and greater odds of having ≥2 FDRs affected by CeD (aOR = 3.57, 95% CI 1.28-9.92) compared to the individuals without IIM. In the analyses of any FDR pairs, we observed familial associations for other RIDs (aOR = 1.34, 95% CI 1.14-1.56), IBD (aOR = 1.20, 95% CI 1.02-1.41), AITD (aOR = 1.10, 95% CI 1.02-1.19) and CeD (aOR = 1.37, 95% CI 1.08-1.74) while associations for other ADs were not statistically significant. CONCLUSION: The observed familial associations may suggest that IIM shares genetic susceptibility with various ADs, information that may be useful for clinical counselling and guiding future genetic studies of IIM.
 AIM: To analyze the global incidence trends for four autoimmune diseases (ADs) including rheumatoid arthritis (RA), inflammatory bowel disease (IBD), multiple sclerosis (MS) and psoriasis from 1990 to 2019, and further predict their changes to 2040 at global, regional, and national levels. METHODS: The estimates and 95% uncertainty intervals (UIs) for case number and agestandardized incidence rate (ASIR) of RA, IBD, MS and psoriasis were derived from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. Estimated annual percentage change (EAPC) was utilized to quantify the global incidence trends for RA, IBD, MS and psoriasis from 1990 to 2019. Furthermore, a log-linear age-period-cohort model was adopted to predict the new case number and incidence rates for these four ADs through 2040. RESULTS: From 1990 to 2019, the global ASIR rose significantly for RA (EAPC = 0.30%, 95% CI: 0.26 to 0.34) whereas declined significantly for IBD (EAPC = -0.60%, 95% CI: -0.72 to - 0.48), MS (EAPC = -0.19%, 95% CI: -0.24 to -0.13) and psoriasis (EAPC = -0.77%, 95% CI: -0.78 to -0.76). From 2020 to 2040, the global ASIR of RA, IBD, and psoriasis was predicted to decrease whereas the global ASIR of MS was predicted to increase, with continuous increasing case number of all these diseases. Furthermore, the predicted incidence trends of these four ADs varied significantly across 195 countries and territories, with a prominent higher burden in high-income North America and Western Europe. CONCLUSIONS: There are strong heterogeneities in the global incidence trends (1990-2019) and predicted changes (2020-2040) of ADs across the world, highlighting prominent challenges in the control of ADs, including both growing case number and distributive disparities of these diseases worldwide, which may be instructive for better public health policy establishment and healthcare resource allocation.
 Despite global vaccination efforts, immunocompromized patients remain at high risk for COVID-19-associated morbidity. In particular, patients with impaired humoral immunity have shown a high risk of persistent infection. We report a case series of adult patients with B cell malignancies and/or undergoing B cell targeting therapies with persisting SARS-CoV-2 infection and treated with a combination antiviral therapy of remdesivir and nirmatrelvir/ritonavir, in three Italian tertiary academic hospitals. A total of 14 patients with impaired adaptive humoral immunity and prolonged SARS-CoV-2 infection were treated with the dual antiviral therapy. The median age was 60 (IQR 56-68) years, and 11 were male. Twelve patients had B cell lymphoma, one patient had chronic lymphocytic leukemia and one patient had multiple sclerosis. Thirteen out of 14 patients had received prior B cell-targeting therapies, consisting of anti-CD20 monoclonal antibodies in 11 patients, and chimeric antigen receptor T therapy in 2 patients. The median time between diagnosis and therapy start was 42.0 (IQR 35-46) days. Seven patients had mild, 6 moderate and one severe disease. Nine patients had signs of interstitial pneumonitis on chest computed tomography scans before treatment. The median duration of nirmatrelvir/ritonavir and remdesivir combination therapy was 10 days. All patients showed resolution of COVID-19-related symptoms after a median of 6 (IQR 4-11) days and viral clearance after 9 (IQR 5-11) days. Combination therapy with remdesivir and nirmatrelvir/ritonavir is a promising treatment option for persistent COVID-19 in immunocompromized patients with humoral immunity impairment, worthy of prospective comparative trials.
 BACKGROUND: Cardiovascular health optimization during middle age benefits brain health. The American Heart Association's Life's Simple 7 recently added sleep duration as a key determinant of cardiovascular health becoming the Life's Essential 8. We tested the hypothesis that suboptimal sleep duration is associated with poorer neuroimaging brain health profiles in asymptomatic middle-aged adults. METHODS: We conducted a prospective MRI neuroimaging study in middle-aged persons without stroke, dementia, or multiple sclerosis enrolled in the UK Biobank. Self-reported sleep duration was categorized as short (<7 hours), optimal (7-<9 hours), or long (≥9 hours). Evaluated neuroimaging markers of brain health included white matter hyperintensities (presence and volume) and diffusion tensor imaging metrics (fractional anisotropy and mean diffusivity) evaluated in 48 distinct neuroanatomical regions. We used multivariable logistic and linear regression models, as appropriate, to test for association between sleep duration and neuroimaging markers of brain health. RESULTS: We evaluated 39,502 middle-aged persons (mean age 55, 53% female). Of these, 28,712 (72.7%) had optimal, 8,422 (21.3%) short, and 2,368 (6%) long sleep. Compared to optimal sleep, short sleep was associated with higher risk (OR 1.11; 95% CI 1.05-1.17; P<0.001) and larger volume (beta=0.06, SE=0.01; P<0.001) of white matter hyperintensities, while long sleep was associated with higher volume (beta=0.04, SE=0.02; P=0.01) but not higher risk (P>0.05) of white matter hyperintensities. Short (beta=0.03, SE=0.01; P=0.004) and long sleep (beta=0.07, SE=0.02; P<0.001) were associated with worse fractional anisotropy, while only long sleep associated with worse mean diffusivity (beta=0.05, SE=0.02; P=0.005). CONCLUSIONS: Among middle-aged adults without clinically observed neurological disease, suboptimal sleep duration is associated with poorer neuroimaging brain health profiles. Because the evaluated neuroimaging markers precede stroke and dementia by several years, our findings support early interventions aimed at correcting this modifiable risk factor.
 Ferroptosis is a programmed cell death pathway that is recently linked to Parkinson's disease (PD), where the key genes and molecules involved are still yet to be defined. Acyl-CoA synthetase long-chain family member 4 (ACSL4) esterifies polyunsaturated fatty acids (PUFAs) which is essential to trigger ferroptosis, and is suggested as a key gene in the pathogenesis of several neurological diseases including ischemic stroke and multiple sclerosis. Here, we report that ACSL4 expression in the substantia nigra (SN) was increased in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated model of PD and in dopaminergic neurons in PD patients. Knockdown of ACSL4 in the SN protected against dopaminergic neuronal death and motor deficits in the MPTP mice, while inhibition of ACSL4 activity with Triacsin C similarly ameliorated the parkinsonism phenotypes. Similar effects of ACSL4 reduction were observed in cells treated with 1-methyl-4-phenylpyridinium (MPP(+)) and it specifically prevented the lipid ROS elevation without affecting the mitochondrial ROS changes. These data support ACSL4 as a therapeutic target associated with lipid peroxidation in PD.
 Multiple sclerosis (MS) is an autoimmune, inflammatory demyelinating disorder of the central nervous system. Accumulating evidence has underscored the therapeutic potential of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSC-Exos) containing bioactive compounds in MS. Herein, the current study sought to characterize the mechanism of BMSC-Exos harboring miR-367-3p both in BV2 microglia by Erastin-induced ferroptosis and in experimental autoimmune encephalomyelitis (EAE), a typical animal model of MS. Exosomes were firstly isolated from BMSCs and identified for further use. BV2 microglia were co-cultured with miR-367-3p-containing BMSC-Exos, followed by an assessment of cell ferroptosis. Mechanistic exploration was furthered by the interaction of miR-367-3p and its downstream regulators. Lastly, BMSC-Exos harboring miR-367-3p were injected into EAE mice for in vivo validation. BMSC-Exos carrying miR-367-3p restrained microglial ferroptosis in vitro. Mechanistically, miR-367-3p could bind to Enhancer of zeste homolog 2 (EZH2) and restrain EZH2 expression, leading to the over-expression of solute carrier family 7 member 11 (SLC7A11). Meanwhile, over-expression of SLC7A11 resulted in Glutathione Peroxidase 4 (GPX4) activation and ferroptosis suppression. Ectopic expression of EZH2 in vitro negated the protective effects of BMSC-Exos. Furthermore, BMSC-Exos containing miR-367-3p relieved the severity of EAE by suppressing ferroptosis and restraining EZH2 expression in vivo. Collectively, our findings suggest that BMSC-Exos carrying miR-367-3p brings about a significant decline in microglia ferroptosis by repressing EZH2 and alleviating the severity of EAE in vivo, suggesting a possible role of miR-367-3p overexpression in the treatment strategy of EAE. AVAILABILITY OF DATA AND MATERIALS: The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.
 Protein aggregation, mitochondrial dysfunction, iron dyshomeostasis, increased oxidative damage and inflammation are pathognomonic features of Parkinson's disease (PD) and other neurodegenerative disorders characterized by abnormal iron accumulation. Moreover, the existence of positive feed-back loops between these pathological components, which accelerate, and sometimes make irreversible, the neurodegenerative process, is apparent. At present, the available treatments for PD aim to relieve the symptoms, thus improving quality of life, but no treatments to stop the progression of the disease are available. Recently, the use of multifunctional compounds with the capacity to attack several of the key components of neurodegenerative processes has been proposed as a strategy to slow down the progression of neurodegenerative processes. For the treatment of PD specifically, the necessary properties of new-generation drugs should include mitochondrial destination, the center of iron-reactive oxygen species interaction, iron chelation capacity to decrease iron-mediated oxidative damage, the capacity to quench free radicals to decrease the risk of ferroptotic neuronal death, the capacity to disrupt α-synuclein aggregates and the capacity to decrease inflammatory conditions. Desirable additional characteristics are dopaminergic neurons to lessen unwanted secondary effects during long-term treatment, and the inhibition of the MAO-B and COMPT activities to increase intraneuronal dopamine content. On the basis of the published evidence, in this work, we review the molecular basis underlying the pathological events associated with PD and the clinical trials that have used single-target drugs to stop the progress of the disease. We also review the current information on multifunctional compounds that may be used for the treatment of PD and discuss the chemical characteristics that underlie their functionality. As a projection, some of these compounds or modifications could be used to treat diseases that share common pathology features with PD, such as Friedreich's ataxia, Multiple sclerosis, Huntington disease and Alzheimer's disease.
 CONTEXT: Worldwide, large numbers of people have Alzheimer's disease and other forms of dementia, Parkinson's disease, and multiple sclerosis. Unfortunately, approved medications are highly ineffective and have costly, untoward side effects. One alternative for neurodegenerative disorders may be use of plasmalogens, a type of phospholipid. OBJECTIVE: The objective of the study was to assess the effectiveness of a unique extract of plasmalogen from scallops for older adults with concerns either about memory and cognition or some form of actual memory loss or cognitive dysfunction. DESIGN: This pilot study was a 90-day intervention. SETTING: The study took place in the homes of participants. PARTICIPANTS: Participants were nine older adults from South Florida. INTERVENTION: Participants were randomly assigned to one of two groups taking different amounts of Hokkaido Scallop Oil Plasmalogen (HSOP) per day: (1) one 0.5-mg capsule-five participants or (2) two 0.5-mg capsules-four participants. OUTCOME MEASURES: The participants completed the assessments at baseline and postintervention. To determine if HSOP would have an effect on cognitive function, participants completed the Mini-Mental State Examination (MMSE). To evaluate issues with activities and depressive symptoms or disorders, participants completed assessments with the Activities of Daily Living (ADL) and Independent Activities of Daily Living (IADL) and the Center for Epidemiological Survey-Depression (CESD). The outcome measures were compared from baseline to postintervention, and the differences were assessed for statistical significance with paired-samples t tests. Correlation coefficients were assessed at baseline and postintervention between age and the outcome measures as well. RESULTS: The average score of the MMSE at baseline was 19.1 (SD = 9.7), the average score at postintervention improved to 21.9 (SD = 10.2), and the difference from baseline to postintervention was statistically significant (t(6) = -2.7, P = .04). All other changes on the outcome measures were insignificant. For the MMSE, five subjects improved, one subject remained the same, and one subject worsened. For the CESD, one subject worsened, and five subjects improved. For the IADL and ADL, five subjects remained the same, and one subject improved. At baseline and as expected, age was inversely correlated with the MMSE (r = -0.88, P = .002), and the MMSE was inversely correlated with the ADL (r = -0.93, P = .002). No other correlations were significant. The correlations at postintervention showed a similar pattern to those at baseline. CONCLUSIONS: The pilot study showed that HSOP is safe to take and may provide some benefits for cognitive function and depressive symptoms, based on the clinically relevant changes in the MMSE and CESD over the 90-day period. Given the lack of efficacy of treatments for people with age-associated memory and cognitive dysfunction, HSOP may provide a natural and safe alternative for those faced with such challenges.
 OBJECTIVES: Studies have suggested that fingolimod, a sphingosine-1-phosphate receptor modulator, exerts neuroprotective and anti-inflammatory effects. Although fingolimod is approved for the treatment of relapsing-remitting multiple sclerosis, limited studies have investigated its effects in patients with schizophrenia. This study investigated the efficacy and safety of fingolimod adjuvant to risperidone in schizophrenia treatment. METHODS: This eight-week, randomized, double-blinded, placebo-controlled trial included 80 (clinical trials registry code: IRCT20090117001556N137) patients with chronic schizophrenia. Participants were assigned to two equal arms and received risperidone plus either fingolimod (0.5 mg/day) or a matched placebo. The positive and negative symptom scale (PANSS) was used to measure and compare the effectiveness of treatment strategies at baseline and weeks 2, 4, 6, and 8. Treatment side effects were also compared. RESULTS: Seventy participants completed the trial (35 in each arm). The baseline characteristics of the groups were comparable (P-value > 0.05). There were significant time-treatment interaction effects on negative symptoms (P-value = 0.003), general symptoms (P-value = 0.037), and the PANSS total score (P-value = 0.035), suggesting greater improvement in symptoms following the fingolimod adjuvant therapy. In contrast, the longitudinal changes in positive and depressive symptoms were similar between the groups (P-values > 0.05). Regarding the safety of treatments, there were no differences in extrapyramidal symptoms [assessed by the extrapyramidal symptom rating scale (ESRS)] or frequency of other complications between the fingolimod and the placebo groups (P-values > 0.05). CONCLUSIONS: This study indicated that fingolimod is a safe and effective adjuvant agent for schizophrenia treatment. However, further clinical trials are required to suggest extensive clinical application.
 BACKGROUND: Epstein Barr virus (EBV) infects ~ 95% of the population worldwide and is known to cause adverse health outcomes such as Hodgkin's, non-Hodgkin's lymphomas, and multiple sclerosis. There is substantial interest and investment in developing infection-preventing vaccines for EBV. To effectively deploy such vaccines, it is vital that we understand the risk factors for infection. Why particular individuals do not become infected is currently unknown. The current literature, describes complex, often conflicting webs of intersecting factors-sociodemographic, clinical, genetic, environmental-, rendering causality difficult to decipher. We aimed to use Mendelian randomization (MR) to overcome the issues posed by confounding and reverse causality to determine the causal risk factors for the acquisition of EBV. METHODS: We mapped the complex evidence from the literature prior to this study factors associated with EBV serostatus (as a proxy for infection) into a causal diagram to determine putative risk factors for our study. Using data from the UK Biobank of 8422 individuals genomically deemed to be of white British ancestry between the ages of 40 and 69 at recruitment between the years 2006 and 2010, we performed a genome wide association study (GWAS) of EBV serostatus, followed by a Two Sample MR to determine which putative risk factors were causal. RESULTS: Our GWAS identified two novel loci associated with EBV serostatus. In MR analyses, we confirmed shorter time in education, an increase in number of sexual partners, and a lower age of smoking commencement, to be causal risk factors for EBV serostatus. CONCLUSIONS: Given the current interest and likelihood of a future EBV vaccine, these factors can inform vaccine development and deployment strategies by completing the puzzle of causality. Knowing these risk factors allows identification of those most likely to acquire EBV, giving insight into what age to vaccinate and who to prioritise when a vaccine is introduced.
 INTRODUCTION: Multiple sclerosis (MS) is the most common chronic inflammatory, demyelinating disease of the central nervous system. Dimethyl fumarate (DMF) and monomethyl fumarate (MMF) belong to the disease-modifying drugs in treatment of MS. There is evidence that astrocytes and microglia are involved in MS pathology, but few studies are available about MMF and DMF effects on astrocytes and microglia. The aim of this study was to investigate the effects of MMF and DMF on microglial activation and morphology as well as potential effects on glial viability, Cx43, and AQP4 expressions in different set-ups of an in vitro astrocyte-microglia co-culture model of inflammation. METHODS: Primary rat glial co-cultures of astrocytes containing 5% (M5, mimicking "physiological" conditions) or 30% (M30, mimicking "pathological, inflammatory" conditions) of microglia were treated with different concentrations of MMF (0.1, 0.5, and 2 μg/mL) or DMF (1.5, 5, and 15 μM) for 24 h. Viability, proliferation, and cytotoxicity of glial cells were examined using MTT assay. Immunocytochemistry was performed to analyze the microglial phenotypes. Connexin 43 (Cx43) and aquaporin 4 (AQP4) expressions were quantified by immunoblot analysis. RESULTS: Treatment with different concentrations of MMF or DMF for 24 h did not change the glial cell viability in M5 and M30 co-cultures. Microglial phenotypes were not altered by DMF under physiological M5 conditions, but treatment with higher concentration of DMF (15 μM) induced microglial activation under inflammatory M30 conditions. Incubation with different concentrations of MMF had no effects on microglial phenotypes. The Cx43 expression in M5 and M30 co-cultures was not changed significantly by immunoblot analysis after incubation with different concentrations of DMF or MMF for 24 h. The AQP4 expression was significantly increased in M5 co-cultures after incubation with 5 μm DMF. Under the other conditions, AQP4 expression was not affected by DMF or MMF. DISCUSSION: In different set-ups of the astrocyte-microglia co-culture model of inflammation, MMF has not shown significant effects. DMF had only limited effects on microglia phenotypes and AQP4 expression. In summary, mechanisms of action of fumarates probably do not involve direct effects on microglia phenotypes as well as Cx43 and AQP4 expression.
 BACKGROUND AND OBJECTIVE: Diffusion MRI (dMRI) has been considered one of the most popular non-invasive techniques for studying the human brain's white matter (WM). dMRI is used to delineate the brain's microstructure by approximating the WM region's fiber tracts. The achieved fiber tracts can be utilized to assess mental diseases like Multiple sclerosis, ADHD, Seizures, Intellectual disability, and others. New techniques such as high angular resolution diffusion-weighted imaging (HARDI) have been developed, providing precise fiber directions, and overcoming the limitation of traditional DTI. Unlike Single-shell, Multi-shell HARDI provides tissue fractions for white matter, gray matter, and cerebrospinal fluid, resulting in a Multi-shell Multi-tissue fiber orientation distribution function (MSMT fODF). This MSMT fODF comes up with more precise fiber directions than a Single-shell, which helps to get correct fiber tracts. In addition, various multi-compartment diffusion models, including as CHARMED and NODDI, have been developed to describe the brain tissue microstructural information. This type of model requires multi-shell data to obtain more specific tissue microstructural information. However, a major concern with multi-shell is that it takes a longer scanning time restricting its use in clinical applications. In addition, most of the existing dMRI scanners with low gradient strengths commonly acquire a single b-value (shell) upto b=1000s/mm(2) due to SNR (Signal-to-noise ratio) reasons and severe imaging artifacts. METHODS: To address this issue, we propose a CNN-based ordinary differential equations solver for the reconstruction of MSMT fODF from under-sampled and fully sampled Single-shell (b=1000s/mm(2)) dMRI. The proposed architecture consists of CNN-based Adams-Bash-forth and Runge-Kutta modules along with two loss functions, including L(1) and total variation. RESULTS: We have shown quantitative results and visualization of fODF, fiber tracts, and structural connectivity for several brain regions on the publicly available HCP dataset. In addition, the obtained angular correlation coefficients for white matter and full brain are high, showing the proposed network's utility.Finally, we have also demonstrated the effect of noise by adjusting SNR from 5 to 50 and observed the network robustness. CONCLUSION: We can conclude that our model can accurately predict MSMT fODF from under-sampled or fully sampled Single-shell dMRI volumes.
 Autism spectrum disorder (ASD) affects 1 in 44 children. Chromatin regulatory proteins are overrepresented among genes that contain high risk variants in ASD. Disruption of the chromatin environment leads to widespread dysregulation of gene expression, which is traditionally thought of as a mechanism of disease pathogenesis associated with ASD. Alternatively, alterations in chromatin dynamics could also lead to dysregulation of alternative splicing, which is understudied as a mechanism of ASD pathogenesis. The anticonvulsant valproic acid (VPA) is a well-known environmental risk factor for ASD that acts as a class I histone deacetylase inhibitor. However, the precise molecular mechanisms underlying defects in human neuronal development associated with exposure to VPA are understudied. To dissect how VPA exposure and subsequent chromatin hyperacetylation influence molecular signatures involved in ASD pathogenesis, we conducted RNA sequencing (RNA-seq) in human cortical neurons that were treated with VPA. We observed that differentially expressed genes (DEGs) were enriched for mRNA splicing, mRNA processing, histone modification and metabolism related gene sets. Furthermore, we observed widespread increases in the number and the type of alternative splicing events. Analysis of differential transcript usage (DTU) showed that exposure to VPA induces extensive alterations in transcript isoform usage across neurodevelopmentally important genes. Finally, we find that DEGs and genes that display DTU overlap with known ASD-risk genes. Altogether, these findings suggest that, in addition to differential gene expression, changes in alternative splicing correlated with alterations in the chromatin environment could act as an additional mechanism of disease in ASD.
 Myasthenia gravis (MG) is an autoantibody-mediated autoimmune disease characterized by skeletal muscle weakness exacerbated with exercise. There is a need for novel drugs effective in refractory MG. We aimed to test the potential of teriflunomide, an immunomodulatory drug currently used in rheumatoid arthritis and multiple sclerosis treatment, in a murine experimental autoimmune myasthenia gravis (EAMG) model. EAMG was induced by immunizations with recombinant acetylcholine receptor (AChR). Teriflunomide treatment (10 mg/kg/day, intraperitoneal) was initiated to one group of mice (n = 21) following the third immunization and continued for 5 weeks. The disease control group (n = 19) did not receive medication. Naïve mice (n = 10) received only mock immunization. In addition to the clinical scorings, the numbers of B cells and T cells, and cytokine profiles of T cells were examined by flow cytometry. Anti-AChR-specific antibodies in the peripheral blood serum were quantified by ELISA. Teriflunomide significantly reduced clinical disease scores and the absolute numbers of CD4+ T cells and some of their cytokine-producing subgroups (IFN-γ, IL 2, IL22, IL-17A, GM-CSF) in the spleen and the lymph nodes. The thymic CD4+ T cells were also significantly reduced. Teriflunomide mostly spared CD8+ T cells' numbers and cytokine production, while reducing CD138+CD19+lambda+ plasma B cells' absolute numbers and CD138 mean fluorescent intensities, probably decreasing the number of IgG secreting more mature plasma cells. It also led to some selective changes in the measurements of anti-AChR-specific antibodies in the serum. Our results showed that teriflunomide may be beneficial in the treatment of MG in humans.
 BACKGROUND: Dynamic contrast-enhanced MRI (DCE-MRI) has seen increasing use for quantification of low level of blood-brain barrier (BBB) leakage in various pathological disease states and correlations with clinical outcomes. However, currently there exists limited studies on reproducibility in healthy controls, which is important for the establishment of a normality threshold for future research. PURPOSE: To investigate the reproducibility of DCE-MRI and to evaluate the effect of arterial input function (AIF) selection and manual region of interests (ROI) delineation vs. automated global segmentation. STUDY TYPE: Prospective. POPULATION: A total of 16 healthy controls; 11 females; mean age 28.7 years (SD 10.1). FIELD STRENGTH/SEQUENCE: A 3T; GE DCE; 3D TFE T1WI. 2D TSE T2. ASSESSMENT: The influx constant K(i) , a measure of BBB permeability, and V(p) , the blood plasma volume, was calculated using the Patlak model. Cerebral blood flow (CBF) was calculated using Tikhonov model free deconvolution. Manual tissue ROIs, drawn by H.J.S. (30+ years of experience), were compared to automatic tissue segmentation. STATISTICAL TESTS: Intraclass correlation coefficient (ICC) and repeatability coefficient (RC) was used to assess reproducibility. Bland-Altman plots were used to evaluate agreement between measurements day 1 vs. day 2, and manual vs. segmentation method. RESULTS: K(i) showed excellent reproducibility in both white and gray matter with an ICC between 0.79 and 0.82 and excellent agreement between manual ROI and automatic segmentation, with an ICC of 0.89 for K(i) in WM. Furthermore, K(i) values in gray and white matter conforms with histological tissue characteristics, where gray matter generally has a 2-fold higher vessel density. The highest reproducibility measures of K(i) (ICC = 0.83), CBF (ICC = 0.77) and V(d) (ICC = 0.83) was obtained with the AIF sampled in the internal carotid artery (ICA). DATA CONCLUSION: DCE-MRI shows excellent reproducibility of pharmacokinetic variables derived from healthy controls. EVIDENCE LEVEL: 2 TECHNICAL EFFICACY: Stage 2.
 BACKGROUND AND OBJECTIVES: Although the international community collectively seeks to reduce global temperature rise to less than 1.5°C before 2100, irreversible environmental changes have already occurred, and as the planet warms, these changes will continue to occur. As we witness the effects of a warming planet on human health, it is imperative that neurologists anticipate how the epidemiology and incidence of neurologic disease may change. In this review, we organized our analysis around 3 key themes related to climate change and neurologic health: extreme weather events and temperature fluctuations, emerging neuroinfectious diseases, and pollutant impacts. Across each of these themes, we appraised and reviewed recent literature relevant to neurologic disease and practice. METHODS: Studies were identified using search terms relating to climate change, pollutants, and neurologic disease in PubMed, OVID MEDLINE, EMBASE, PsycInfo, and gray literature. Studies published between 1990 and 2022 were included if they pertained to human incidence or prevalence of disease, were in English, and were relevant to neurologic disease. RESULTS: We identified a total of 364 articles, grouped into the 3 key themes of our study: extreme weather events and temperature fluctuations (38 studies), emerging neuroinfectious diseases (37 studies), and pollutant impacts (289 studies). The included studies highlighted the relationships between neurologic symptom exacerbation and temperature variability, tick-borne infections and warming climates, and airborne pollutants and cerebrovascular disease incidence and severity. DISCUSSION: Temperature extremes and variability both associated with stroke incidence and severity, migraine headaches, hospitalization in patients with dementia, and multiple sclerosis exacerbations. Exposure to airborne pollutants, especially PM2.5 and nitrates, associated with stroke incidence and severity, headaches, dementia risk, Parkinson disease, and MS exacerbation. Climate change has demonstrably expanded favorable conditions for zoonotic diseases beyond traditional borders and poses the risk of disease in new, susceptible populations. Articles were biased toward resource-rich regions, suggesting a discordance between where research occurs and where changes are most acute. As such, 3 key priorities emerged for further study: neuroinfectious disease risk mitigation, understanding the pathophysiology of airborne pollutants on the nervous system, and methods to improve delivery of neurologic care in the face of climate-related disruptions.
 Amyotrophic lateral sclerosis (ALS), also known as “Lou Gehrig disease,” is a neurodegenerative disease of the motor neurons. No single etiology has been proven; rather, multiple pathways (both heritable and sporadic) have been shown to result in unmistakably similar disease entities. ALS necessarily affects both upper and lower motor neurons with variable patterns of onset, most commonly beginning with signs of lower motor neuron degeneration within proximal limbs. As it is a progressive disease, it will eventually lead to paralysis and, inevitably, death. There is no cure for ALS; however, multiple medications and interventions can reduce symptoms and prolong life, sometimes up to 10 or more years.

 Pachydermodactyly (PDD) is a rare benign condition characterized by painless soft tissue swelling of small joints of hands. The most common presentation is bilateral Symmetrical swelling of proximal interphalangeal and metacarpophalangeal joint similar to Rheumatoid arthritis. The etiology of this disease is unknown, and it sometimes can coexist with other diseases. We present here a case of PDD coexisting with Tuberous Sclerosis, an autosomal dominant genetic disorder characterized by of formation of multiple benign multisystem tumors.
 Tuberous sclerosis complex is a rare autosomal dominant genetic disorder that affects multiple organ systems, primarily affecting the central nervous system. It develops with a pathogenic mutation in tumour suppressor genes i.e. Tuberous Sclerosis Complex 1 or Tuberous Sclerosis Complex 2 which codes for protein hamartin and tuberin leading to unopposed hyperactivation of the mammalian target of the rapamycin signalling pathway. It presents with a triad of facial angiofibroma, intellectual disability, and epilepsy. We present a case of a 17-month female toddler with abnormal body movement with loss of consciousness and later developing into generalised jerky movements. On magnetic resonance imaging, a diagnosis of tuberous sclerosis was made. The patient underwent symptomatic management with anti-epileptic. As seizures in these cases are subtle, they remain undiagnosed for a long time leading to delays in management and developing refractory seizures. KEYWORDS: angiofibroma; case reports; seizures; tuberous sclerosis; tumor suppressor gene.
 CLINICAL DESCRIPTION: Individuals with biotinidase deficiency who are diagnosed before they have developed symptoms (e.g., by newborn screening) and who are treated with biotin have normal development. Symptoms including seizures, developmental delay, cutaneous manifestations (skin rash, alopecia), optic atrophy, hearing loss, and respiratory problems occur only in those individuals with biotinidase deficiency prior to biotin treatment. Symptoms of untreated profound biotinidase deficiency (<10% mean normal serum biotinidase activity) usually appear between ages one week and ten years, typically with optic atrophy, hypotonia, seizures, hair loss, and skin rash. Affected children often have ataxia and developmental delay. Individuals with partial biotinidase deficiency (10%-30% of mean normal serum biotinidase activity) may develop symptoms only when stressed, such as during infection. Some symptoms, such as feeding issues, cutaneous manifestations, and respiratory issues, usually resolve with biotin therapy, whereas other manifestations presenting prior to biotin treatment, such as optic atrophy, hearing loss, and developmental delay, may improve but are usually not completely reversible with the initiation of biotin therapy. Untreated adolescents and adults usually exhibit myelopathy and optic neuropathy and are often initially diagnosed with multiple sclerosis. Most of these individuals experience improvement in their symptoms with biotin supplementation. DIAGNOSIS/TESTING: The diagnosis of biotinidase deficiency is established in a proband whose newborn screening or biochemical findings indicate multiple carboxylase deficiency based on EITHER of the following: Detection of deficient biotinidase enzyme activity in serum/plasma. Identification of biallelic pathogenic variants in BTD on molecular genetic testing when the results of enzymatic testing are ambiguous. MANAGEMENT: Treatment of manifestations: All individuals with profound biotinidase deficiency (<10% mean normal serum enzyme activity) and those with partial biotinidase deficiency (10%-30% of mean normal serum enzyme activity) should be treated with oral biotin in the free form as opposed to the protein-bound form; biotin therapy is lifelong. Targeted therapy: Oral biotin of 5-10 mg/day for those who have <10% mean normal serum enzyme activity and 2.5-10 mg/day in those who have 10%-30% of mean normal serum enzyme activity. Supportive care in symptomatic individuals: Hydration and bicarbonate in those with metabolic decompensation and acidosis, although biotin therapy can rapidly resolve the metabolic derangements within hours to days; supportive developmental therapies and educational resources for those with developmental delay; subspecialist ophthalmologic care for those with optic atrophy; hearing aids and, if severe, consideration of cochlear implants for those with hearing loss. Prevention of primary manifestations: Compliance with biotin therapy can prevent symptom development, and also improves symptoms in symptomatic individuals. Surveillance: Evaluation by a clinical geneticist or metabolic specialist annually for those with profound biotinidase deficiency and every two years for those with partial biotinidase deficiency. If symptoms return with biotin therapy, consider obtaining urine organic acids analysis to evaluate for non-compliance with biotin therapy. Measurement of growth parameters, assessment for new manifestations (seizures, changes in tone, movement disorders), monitoring of developmental progress and educational needs, and assessment for cutaneous manifestations (eczematous rash, alopecia, thrush, and/or candidiasis) at each visit. Ophthalmology and audiology evaluations annually for those with profound biotinidase deficiency and every two years for those with partial biotinidase deficiency. Agents/circumstances to avoid: Raw eggs should be avoided because they contain avidin, an egg white protein that binds biotin, thus decreasing its bioavailability. However, thoroughly cooked eggs present no problem because heating inactivates avidin, rendering it incapable of binding biotin. Evaluation of relatives at risk: If prenatal testing has not been performed, a newborn with an older sib with biotinidase deficiency should be treated at birth with biotin pending results of the definitive biotinidase enzyme activity assay and/or molecular genetic testing (if the BTD pathogenic variants in the family are known). The genetic status of older sibs (even if asymptomatic) of a child with biotinidase deficiency should be clarified by assay of biotinidase enzyme activity or molecular genetic testing (if the BTD pathogenic variants in the family are known) so that biotin therapy can be instituted in a timely manner. Pregnancy management: There have been females with profound biotinidase deficiency who are taking biotin therapy who have had normal pregnancies and offspring. GENETIC COUNSELING: Biotinidase deficiency is inherited in an autosomal recessive manner. If both parents are known to be heterozygous for a BTD pathogenic variant, each sib of an affected individual has at conception a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Molecular genetic carrier testing for at-risk relatives and prenatal and preimplantation genetic testing are possible if the pathogenic variants in the family are known.
 PURPOSE OF REVIEW: Amyotrophic lateral sclerosis (ALS) is a severe disease characterized by the degeneration of motor neurons. Large-scale genetic studies have now identified over 60 genes that are associated with ALS, which in large part have also been functionally characterized. The purpose of this review is to outline how these advances are being translated into novel therapeutic strategies. RECENT FINDINGS: The emergence of techniques that allow the specific therapeutic targeting of a (mutant) gene, in particular antisense oligonucleotide therapy (ASOs), have led to the first successful gene therapy for SOD1-ALS and multiple other gene-targeted trials are underway. This includes genetic variants that modify the disease phenotype as well as causal mutations. SUMMARY: Technological and methodological advances are enabling researchers to unravel the genetics of ALS. Both causal mutations and genetic modifiers are viable therapeutic targets. By performing natural history studies, the phenotype-genotype correlations can be characterized. In conjunction with biomarkers for target engagement and international collaboration, this makes performing gene-targeted trials ALS feasible. The first effective treatment has now been developed for SOD1-ALS and, with multiple studies underway, it seems realistic that more therapies will follow.
 BACKGROUND AND OBJECTIVES: The primary objective is to examine potential racial and ethnic (R/E) disparities in ambulatory neurology quality measures within the American Academy of Neurology Axon Registry. R/E disparities in neurologic US morbidity and mortality have been clearly documented. Despite these findings, there have been no nationwide examinations of how ambulatory neurologic care affects these negative health outcomes. METHODS: This was a retrospective nonrandomized cohort study of patients in the AAN Axon Registry. The Axon Registry is a neurology-specific outpatient quality registry that collects, reports, and analyzes real-world deidentified electronic health record (EHR) data. Patients were included in the study if they contributed toward one of the selected quality measures for multiple sclerosis, epilepsy, Parkinson disease, or headache during the study period of January 1, 2019-December 31, 2019. Descriptive analyses of patient demographics were performed and then stratified by race and ethnicity. RESULTS: There were a total of 633,672 patients included in these analyses. Separate analyses were performed for race (64% White, 8% Black, 1% Asian, and 27% unknown) and ethnicity (52% not Hispanic, 5% Hispanic, and 43% unknown). The mean age ranged from 18 to 55 years, with 61% female and 39% male. Quality measures were chosen based on completeness of R/E data and were either process or outcomes focused. Statistically significant differences were noted after controlling for multiple comparisons. DISCUSSION: The large proportion of missing or unknown R/E data and low overall rate of performance on these quality measures made the relevance of small differences difficult to determine. This analysis demonstrates the feasibility of using the Axon Registry to assess neurologic disparities in outpatient care. More education and training are required on the accurate capture of R/E data in the EHR.
 Coronavirus disease 2019 (COVID-19) is caused by a new member of the Coronaviridae family known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). There are structural and non-structural proteins (NSPs) in the genome of this virus. S, M, H, and E proteins are structural proteins, and NSPs include accessory and replicase proteins. The structural and NSP components of SARS-CoV-2 play an important role in its infectivity, and some of them may be important in the pathogenesis of chronic diseases, including cancer, coagulation disorders, neurodegenerative disorders, and cardiovascular diseases. The SARS-CoV-2 proteins interact with targets such as angiotensin-converting enzyme 2 (ACE2) receptor. In addition, SARS-CoV-2 can stimulate pathological intracellular signaling pathways by triggering transcription factor hypoxia-inducible factor-1 (HIF-1), neuropilin-1 (NRP-1), CD147, and Eph receptors, which play important roles in the progression of neurodegenerative diseases like Alzheimer's disease, epilepsy, and multiple sclerosis, and multiple cancers such as glioblastoma, lung malignancies, and leukemias. Several compounds such as polyphenols, doxazosin, baricitinib, and ruxolitinib could inhibit these interactions. It has been demonstrated that the SARS-CoV-2 spike protein has a stronger affinity for human ACE2 than the spike protein of SARS-CoV, leading the current study to hypothesize that the newly produced variant Omicron receptor-binding domain (RBD) binds to human ACE2 more strongly than the primary strain. SARS and Middle East respiratory syndrome (MERS) viruses against structural and NSPs have become resistant to previous vaccines. Therefore, the review of recent studies and the performance of current vaccines and their effects on COVID-19 and related diseases has become a vital need to deal with the current conditions. This review examines the potential role of these SARS-CoV-2 proteins in the initiation of chronic diseases, and it is anticipated that these proteins could serve as components of an effective vaccine or treatment for COVID-19 and related diseases. Video Abstract.
 IMPORTANCE: Recent studies have highlighted an association between epilepsy and Parkinson disease (PD). The role of antiepileptic drugs (AEDs) has not been explored. OBJECTIVE: To investigate the association between AEDs and incident PD. DESIGN, SETTING, AND PARTICIPANTS: This nested case-control study started collecting data from the UK Biobank (UKB) in 2006, and data were extracted on June 30, 2021. Individuals with linked primary care prescription data were included. Cases were defined as individuals with a Hospital Episode Statistics (HES)-coded diagnosis of PD. Controls were matched 6:1 for age, sex, race and ethnicity, and socioeconomic status. Prescription records were searched for AEDs prescribed prior to diagnosis of PD. The UKB is a longitudinal cohort study with more than 500 000 participants; 45% of individuals in the UKB have linked primary care prescription data. Participants living in the UK aged between 40 and 69 years were recruited to the UKB between 2006 and 2010. All participants with UKB-linked primary care prescription data (n = 222 106) were eligible for enrollment in the study. Individuals with only a self-reported PD diagnosis or missing data for the matching variables were excluded. In total, 1477 individuals were excluded; 49 were excluded due to having only self-reported PD, and 1428 were excluded due to missing data. EXPOSURES: Exposure to AEDs (carbamazepine, lamotrigine, levetiracetam, and sodium valproate) was defined using routinely collected prescription data derived from primary care. MAIN OUTCOMES AND MEASURES: Odds ratios and 95% CIs were calculated using adjusted logistic regression models for individuals prescribed AEDs before the first date of HES-coded diagnosis of PD. RESULTS: In this case-control study, there were 1433 individuals with an HES-coded PD diagnosis (cases) and 8598 controls in the analysis. Of the 1433 individuals, 873 (60.9%) were male, 1397 (97.5%) had their race and ethnicity recorded as White, and their median age was 71 years (IQR, 65-75 years). An association was found between AED prescriptions and incident PD (odds ratio, 1.80; 95% CI, 1.35-2.40). There was a trend for a greater number of prescription issues and multiple AEDs being associated with a greater risk of PD. CONCLUSIONS AND RELEVANCE: This study, the first to systematically look at PD risk in individuals prescribed the most common AEDs, to our knowledge, found evidence of an association between AEDs and incident PD. With the recent literature demonstrating an association between epilepsy and PD, this study provides further insights.
 Experimental autoimmune encephalomyelitis (EAE) is a classical animal model of human multiple sclerosis (MS) that is most commonly used to study the neuropathology and therapeutic effects of the disease. Telocytes (TCs) are a specialized type of interstitial or mesenchymal cell first identified by Popescu in various tissues and organs. However, the existence, distribution and role of CD34(+) stromal cells (SCs)/TCs in the EAE-induced mouse spleen remain to be elucidated. We conducted immunohistochemistry, immunofluorescence (double staining for CD34 and c-kit, vimentin, F4/80, CD163, Nanog, Sca-1, CD31 or tryptase) and transmission electron microscopy experiments to investigate the existence, distribution and role of CD34(+) SCs/TCs in the EAE-induced mouse spleen. Interestingly, immunohistochemistry, double-immunofluorescence, and transmission electron microscopy results revealed that CD34(+) SCs/TCs were significantly upregulated in the EAE mouse spleen. Immunohistochemical or double-immunofluorescence staining of CD34(+) SCs/TCs showed positive expression for CD34, c-kit, vimentin, CD34/vimentin, c-kit/vimentin and CD34/c-kit, and negative expression for CD31 and tryptase. Transmission electron microscopy (TEM) results demonstrated that CD34(+) SCs/TCs established close connections with lymphocytes, reticular cells, macrophages, endothelial cells and erythrocytes. Furthermore, we also found that M1 (F4/80) or M2 (CD163) macrophages, and haematopoietic, pluripotent stem cells were markedly increased in EAE mice. Our results suggest that CD34(+) SCs/TCs are abundant and may play a contributing role in modulating the immune response, recruiting macrophages and proliferation of haematopoietic and pluripotent stem cells following injury to promote tissue repair and regeneration in EAE mouse spleens. This suggests that their transplantation combined with stem cells might represent a promising therapeutic target for the treatment and prevention of multiple autoimmune and chronic inflammatory disorders.
 TSC2/PKD1 contiguous gene deletion syndrome is a disease caused by the deletions of the TSC2 and PKD1 genes. This is a rare contiguous genomic disease with clinical manifestations of tuberous sclerosis and polycystic kidney disease. To our knowledge, this case report is the first known case of TSC2/PKD1 contiguous gene deletions in a pregnant woman. The patient had multiple renal cysts, angiomyolipoma, hypomelanotic macules, shagreen patch, subependymal giant cell astrocytoma, multiple cortical tubers, and subependymal nodules. The patient underwent genetic testing. To exclude genetic defects in the fetus, prenatal fetal genetic testing was performed after obtaining the patient's consent. We found an increasing trend in the size of renal cysts and renal angiomyolipomas in patients with polycystic kidney with tuberous sclerosis during pregnancy. Through enhanced clinical monitoring of patients and prenatal genetic testing of the fetus, timely and effective clinical intervention for the mother may be achieved, thus obtaining the best possible outcome for both mother and fetus.
 Encapsulating peritoneal sclerosis (EPS) is a clinical syndrome where a thickened fibro-collagenous peritoneal membrane can encase parts of the small intestine, leading to recurrent small bowel obstructions and malnutrition. This rare disorder is most strongly associated with long-term peritoneal dialysis, as dialysis can cause chronic inflammation and subsequent sclerosis.  Multiple episodes of severe peritoneal infections or systemic inflammatory disorders can predispose a patient to EPS. EPS is also a potential late-onset complication of kidney transplantation in the absence of systemic inflammation. Despite this, many cases of EPS remain idiopathic. Due to the rarity of this debilitating condition, diagnosis is often delayed.
 Fused in sarcoma (FUS), coded by FUS, is a heterogeneous nuclear ribonucleoprotein (hnRNP). FUS mutations are among the major mutations in familial amyotrophic lateral sclerosis (ALS-FUS: ALS6). The pathological hallmarks of ALS-FUS are FUS-positive neuronal cytoplasmic inclusions (NCI). We examined various hnRNPs in FUS NCIs in the hippocampus in ALS-FUS cases with different FUS mutations (Case 1, H517P; Case 2, R521C). We also examined TDP43-positive NCIs in sporadic ALS hippocampi. Immunohistochemistry was performed using primary antibodies against FUS, p-TDP43, TDP43, hnRNPA1, hnRNPD, PCBP1, PCBP2, and p62. Numerous FUS inclusions were found in the hippocampal granule and pyramidal cell layers. Double immunofluorescence revealed colocalization of FUS and p-TDP43, and FUS and PCBP2 (p-TDP43/FUS: 64.3%, PCBP2/FUS: 23.9%). Colocalization of FUS and PCBP1, however, was rare (PCBP1/FUS: 7.6%). In the hippocampi of patients with sporadic ALS, no colocalization was observed between TDP43-positive inclusions and other hnRNPs. This is the first study to show that FUS inclusions colocalize with other hnRNPs, such as TDP43, PCBP2, and PCBP1. These findings suggest that in ALS-FUS, FUS inclusions are the initiators, followed by alterations of multiple other hnRNPs, resulting in impaired RNA metabolism.
 Tuberous sclerosis (TS) is a rare autosomal-dominant neurocutaneous disorder that is characterized by hamartomas affecting a variety of organs, including the brain, heart, kidneys, skin, lungs, and liver. TS can emerge in a wide variety of clinical and phenotypic forms at any age, all with varying degrees of severity, and is brought on by mutations in the tumor suppressor genes TSC1 or TSC2. This case report is about a 40-year-old female with facial angiofibromas and abdominal symptoms who was referred to the radiology department of our hospital for ultrasonography of the abdomen, which revealed echogenic mass lesions/angiomyolipomas in bilateral kidneys. Subsequent contrast-enhanced computed tomography of the abdomen revealed large fat-attenuating mass lesions which were confirmed to be angiomyolipomas. Similarly, noncontrast computed tomography of the head showed multiple calcified nodules/tubers in subependymal, subcortical, and cortical locations of the brain. High-resolution computed tomography of the chest showed multiple cystic lesions in bilateral lungs suggestive of lymphangioleiomyomatosis. The aim of this case report is to highlight the late presentation of tuberous sclerosis complex.
 Although anterior temporal lobectomy (ATL) is an established surgery for medically intractable mesial temporal lobe epilepsy (MTLE), it can harm memory function, especially in dominant-side MTLE patients without hippocampal sclerosis (HS). To avoid this complication, multiple hippocampal transection (MHT) was developed, but its efficacy has not been fully elucidated. We report the detailed treatment results of MHT compared with that of ATL. We retrospectively analysed the records of 30 patients who underwent surgery for dominant-side MTLE. ATL was completed for 23 patients with HS, and MHT was completed for 7 patients without HS. The seizure control status, number of anti-seizure medicines, neurocognitive function, and psychiatric disorders of each patient were reviewed. The mean follow-up period was 70 months. Seizure control of Engel class I was achieved in 16 patients (70%) in the ALT group versus 5 patients (71%) in the MHT group. The mean number of anti-seizure medicines administered in the ATL group changed significantly from 2.4 to 1.9 (p = 0.01), while that in the MHT group was unchanged (from 2.1 to 2.0, p = 0.77). Eleven patients (48%) in the ATL group developed psychiatric disorders during the postoperative follow-up period, whereas no psychological complications were observed in the MHT group. Neither group showed neurocognitive decline after the surgery in any of the WAIS-III or WMS-R subtests. In conclusion, MHT may achieve reasonable postoperative seizure reduction, preserve neurocognitive function, and reduce postoperative psychiatric complications. Therefore, it can be considered as a therapeutic option for dominant-side MTLE without HS.
 • Cardiac rhabdomyomas are commonly associated with TSC. • They are often the first presentation of TSC, diagnosed prenatally or in neonates. • Fetal or neonatal echocardiography is useful for their early detection. • Familial TSC may be seen even in cases with phenotypically normal parents. • Rhabdomyomas in both dizygotic twins, suggesting familial TSC, is very rare.
 Parkinson disease (PD) is an age-related neurodegenerative disease, which is associated with the loss of dopaminergic neurons (DA neurons) in the substantia nigra pars compacta (SNpc), and neuroinflammation may lead to the occurrence of PD. Wuzi Yanzong Pill (WYP) has demonstrated neuroprotective and anti-inflammatory properties, but its molecular mechanism of action is still unclear. In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice and LPS-mediated BV2 microglia to explore WYP intervention, anti-inflammatory effect and molecular mechanism in vivo and in vitro. The results showed that oral administration of WYP in MPTP-induced PD mice for 2 weeks ameliorated abnormal motor dysfunction, attenuated the loss of TH + neurons in SNpc, protected dopaminergic neurons, and inhibited the activation of microglia in MPTP-induced PD mice and LPS-stimulated BV2 cell. Meanwhile, WYP intervention inhibited the expression of IL-6, TNF-α, Pro-IL-1β, IL-1β, Pro-IL-18, IL-18 and enhanced the expression of IL-10 in the SNpc of PD mice. Simultaneously, WYP intervention inhibited the expression of NLRP3 inflammasome, accompanied by the decrease of the TLR4/MyD88/NF-κB pathway. However, the exact target and interaction of WYP on NLRP3 inflammasome and TLR4/MyD88/NF-κB pathway still needs to be further investigated.
 PURPOSE: To examine the refractive errors, retinal manifestations, and genotype in tuberous sclerosis complex (TSC) patients in a Korean population. MATERIALS AND METHODS: A total of 98 patients with TSC were enrolled in Severance Hospital for a retrospective cohort study. The number of retinal astrocytic hamartoma and retinal achromic patch within a patient, as well as the size, bilaterality, and morphological type were studied. In addition, the refractive status of patients and the comorbidity of intellectual disability and epilepsy were also examined. RESULTS: Retinal astrocytic hamartoma was found in 37 patients, and bilateral invasion was observed in 20 patients (54%). TSC1 mutation was associated with myopia (p=0.01), while TSC2 mutation was associated with emmetropia (p=0.01). Retinal astrocytic hamartoma was categorized into three morphological types and examined as follows: type I (87%), type II (35%), and type III (14%). Single invasion of retinal astrocytic hamartoma was identified in 32% of the patients, and multiple invasions in 68%. The TSC1/TSC2 detection rate was 91% (41/45). Among them, TSC1 variant was detected in 23 patients (54%), whereas TSC2 variant was detected in 18 patients (40%). The results showed that TSC2 mutations are correlated with a higher rate of retinal astrocytic hamartoma involvement (all p<0.05), and multiple and bilateral involvement of retinal hamartomas (all p<0.05). However, the size of retinal astrocytic hamartomas, comorbidity of epilepsy, or intellectual disability did not show correlation with the genetic variant. CONCLUSION: TSC1 variant patients were more myopic, while TSC2 variant patients showed association with more extensive involvement of retinal astrocytic hamartoma.
 OBJECTIVE: To describe a child meeting diagnostic criteria for tuberous sclerosis complex (TSC) carrying a pathogenic somatic variant in RHEB, but no pathogenic variants in the 2 known TSC genes, TSC1 or TSC2. METHODS: We present the clinical and imaging findings in a child presenting with drug-resistant focal seizures and multiple cortical tubers, a subependymal giant cell astrocytoma and multiple subependymal nodules in 1 cerebral hemisphere. Targeted panel sequencing and exome sequencing were performed on genomic DNA derived from blood and resected tuber tissue. RESULTS: The child satisfied clinical diagnostic criteria for TSC, having 3 major features, only 2 of which are required for diagnosis. Genetic testing did not identify pathogenic variants or copy number variations in TSC1 or TSC2 but identified a pathogenic somatic RHEB variant (NM_005614.4:c.104_105delACinsTA [p.Tyr35Leu]) in the cortical tuber. DISCUSSION: RHEB is a partner of the TSC1/2 complex in the mechanistic target of rapamycin pathway. Somatic variants in RHEB are associated with focal cortical dysplasia and hemimegalencephaly. We propose that variants in RHEB may explain some of the genetically undiagnosed TSC cases and may be the third gene for TSC, or TSC3.
 Thoracoabdominal aortic aneurysms in toddlers are extremely rare. However, we experienced an extent III thoracoabdominal aortic aneurysm in a boy with tuberous sclerosis who underwent 3 open repairs and 1 endovascular aortic repair between the ages of 4 years and 18 years. This case highlights the potential for severe recurrent vascular aneurysms in the thoracic and abdominal aorta as a complication of tuberous sclerosis in children. Although aortic aneurysms in children are rare, it is vital to recognize these cases to prevent death due to rupture.
 Overlap syndrome is a clinical entity of myositis concomitant with one or more collagen diseases such as systemic lupus erythematosus, systemic sclerosis, and/or rheumatoid arthritis. It is not evident whether the myopathology of overlap syndrome is disease-specific or categorizes one of the four major subsets: inclusion body myositis, immune-mediated necrotizing myopathy, dermatomyositis, and antisynthetase syndrome. We report a patient with overlap syndrome who exhibited autoantibodies against multiple transfer-RNA components by RNA immunoprecipitation, suggesting antisynthetase syndrome. A 64-year-old woman developed systemic lupus erythematosus, systemic sclerosis, and myositis. Muscle biopsy showed perifascicular necrosis and perimysial alkaline phosphatase positivity, suggesting antisynthetase syndrome. Enzyme-linked immunosorbent assay was negative for autoantibodies to aminoacyl transfer-RNA synthetase, whereas RNA immunoprecipitation revealed a novel antibody to multiple transfer-RNA components. Although the myopathology of overlap syndrome may be diagnosed as any one of various subsets, this case suggests that the myopathological features of overlap syndrome may include antisynthetase syndrome.
 Tuberous sclerosis complex (TSC) is a rare genetic multisystem disorder that was first described by Von Recklinghausen. We describe a case of a female, who initially presented with hematuria and was later found to have multiple manifestations of the disease. The report emphasizes the value of investigations on suspected cases.
 Adult camel leukosis is an emerging hematological and neoplastic disease in dromedaries. It has been hypothesized that bovine leukemia virus (BLV) or its genetic variants may be associated with adult camel leukosis. In this study, we used next-generation sequencing (NGS) to detect all possible viruses in five lung samples from five dromedaries with histopathological evidence of adult camel leukosis and four tissue samples from two control dromedaries. A total throughput of 114.7 Gb was achieved, with an average of 12.7 Gb/sample. For each sample, all the pair-end 151-bp reads were filtered to remove rRNA sequences, bacterial genomes and redundant sequences, resulting in 1-7 Gb clean reads, of which <3% matched to viruses. The largest portion of these viral sequences was composed of bacterial phages. About 100-300 reads in each sample matched "multiple sclerosis-associated retrovirus", but manual analysis showed that they were only repetitive sequences commonly present in mammalian genomes. All viral reads were also extracted for analysis, confirming that no BLV or its genetic variants or any other virus was detected in the nine tissue samples. NGS is not only useful for detecting microorganisms associated with infectious diseases, but also important for excluding an infective cause in scenarios where such a possibility is suspected.
 OBJECTIVE: This study was undertaken to investigate factors associated with aquaporin-4 (AQP4)-IgG serostatus change using a large serological database. METHODS: This retrospective study utilizes Mayo Clinic Neuroimmunology Laboratory data from 2007 to 2021. We included all patients with ≥2 AQP4-IgG tests (by cell-based assay). The frequency and clinical factors associated with serostatus change were evaluated. Multivariable logistic regression analysis examined whether age, sex, or initial titer was associated with serostatus change. RESULTS: There were 933 patients who had ≥2 AQP4-IgG tests with an initial positive result. Of those, 830 (89%) remained seropositive and 103 (11%) seroreverted to negative. Median interval to seroreversion was 1.2 years (interquartile range [IQR] = 0.4-3.5). Of those with sustained seropositivity, titers were stable in 92%. Seroreversion was associated with age ≤ 20 years (odds ratio [OR] = 2.25; 95% confidence interval [CI] = 1.09-4.63; p = 0.028) and low initial titer of ≤1:100 (OR = 11.44, 95% CI = 3.17-41.26, p < 0.001), and 5 had clinical attacks despite seroreversion. Among 62 retested after seroreversion, 50% returned to seropositive (median = 224 days, IQR = 160-371). An initial negative AQP4-IgG test occurred in 9,308 patients. Of those, 99% remained seronegative and 53 (0.3%) seroconverted at a median interval of 0.76 years (IQR = 0.37-1.68). INTERPRETATION: AQP4-IgG seropositivity usually persists over time with little change in titer. Seroreversion to negative is uncommon (11%) and associated with lower titers and younger age. Seroreversion was often transient, and attacks occasionally occurred despite prior seroreversion, suggesting it may not reliably reflect disease activity. Seroconversion to positive is rare (<1%), limiting the utility of repeat testing in seronegative patients unless clinical suspicion is high. ANN NEUROL 2023.
 Epstein-Barr virus (EBV) causes infectious mononucleosis, triggers multiple sclerosis, and is associated with 200,000 cancers/year. EBV colonizes the human B cell compartment and periodically reactivates, inducing expression of 80 viral proteins. However, much remains unknown about how EBV remodels host cells and dismantles key antiviral responses. We therefore created a map of EBV-host and EBV-EBV interactions in B cells undergoing EBV replication, uncovering conserved herpesvirus versus EBV-specific host cell targets. The EBV-encoded G-protein-coupled receptor BILF1 associated with MAVS and the UFM1 E3 ligase UFL1. Although UFMylation of 14-3-3 proteins drives RIG-I/MAVS signaling, BILF1-directed MAVS UFMylation instead triggered MAVS packaging into mitochondrial-derived vesicles and lysosomal proteolysis. In the absence of BILF1, EBV replication activated the NLRP3 inflammasome, which impaired viral replication and triggered pyroptosis. Our results provide a viral protein interaction network resource, reveal a UFM1-dependent pathway for selective degradation of mitochondrial cargo, and highlight BILF1 as a novel therapeutic target.
 BACKGROUND: Pregabalin is a first-line therapy of pain with additional positive effects on the states of depression and anxiety that often occur in patients with chronic pain, thus improving their quality of life. OBJECTIVE: The aim of this study was to demonstrate the efficacy of pregabalin in reducing neuropathic pain and improving quality of life in patients with peripheral and central chronic neuropathic pain in Bosnia and Herzegovina. Also, the aim was to monitor the safety of therapy with pregabalin. METHODS: The study included patients with neuropathic pain lasting more than 3 months. Based on the underlying disease, patients were divided into 5 groups: DM-patients with diabetes mellitus, M-patients after stroke, D-patients with lower back pain, MS-patients with multiple sclerosis, and P group-patients with spinal cord injury. During the baseline visit, the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) was used to assess neuropathic pain. During two follow-up visits (1.5 and 3 months after baseline), the 36-Item Short-Form Health Survey (SF 36) was used to assess the effectiveness of therapy on quality of life. The safety of the treatment was evaluated by monitoring the incidence of adverse drug reactions. RESULTS: The study included 125 patients. During treatment with pregabalin, there was a statistically significant reduction in pain intensity in the DM, M, D and MS groups. In group P, the decrease in pain intensity was not statistically significant (p = 0.070). There was a significant improvement in different parameters of the quality of life in all analyzed groups, with the most prominent effects in the DM group. The effectiveness of treatment was rated as "good" and "very good" in more than 70% of subjects in each group. The expected side effects of treatment were recorded in 27.1% of patients in the DM group, in 20.0% in the M group and in 22.2% in the MS group. Unexpected side effects of treatment were observed in one patient (2.1%) in the DM group. Assessment of tolerability of the applied treatment showed "good" and "very good" response in 68.7% of patients in DM group, 73.3% in M group, 74.5% in D group, 88.9% in MS group and 85.8% in P group. CONCLUSION: Pregabalin is a safe and effective drug in treatment of neuropathic pain of different etiology.
 The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis (MS). However, the impact of endothelial-derived factors on CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream of Cholesterol-25-hydroxylase (Ch25h), promote neuroinflammation but their functions in the CNS are not well-understood. Using floxed-reporter Ch25h knock-in mice, we trace Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrate that Ch25h ablation specifically from ECs attenuates experimental autoimmune encephalomyelitis (EAE). Mechanistically, inflamed Ch25h-deficient CNS ECs display altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) expansion, which suppresses encephalitogenic T lymphocyte proliferation. Additionally, endothelial Ch25h-deficiency combined with immature neutrophil mobilization into the blood circulation nearly completely protects mice from EAE. Our findings reveal a central role for CNS endothelial Ch25h in promoting neuroinflammation by inhibiting the expansion of immunosuppressive myeloid cell populations.
 BACKGROUND: Anti-Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Associated Disease (MOGAD) is an emerging disorder recognized as a clinical entity distinct from Multiple Sclerosis and Aquaporin-4-positive Neuromyelitis Optica Spectrum Disorders (NMOSD-AQP4+), and its phenotypic spectrum continues to expand. Most information about its clinical course has emerged from retrospective studies, and treatment response both in acute and chronic-relapsing disease is still limited. We aimed to describe the clinical and paraclinical characteristics of monophasic and relapsing, paediatric and adult patients with MOGAD under regular clinical care in Chile, highlighting some challenging cases that are far from being considered benign. METHODS: Observational, retrospective, and prospective longitudinal multicentre study including patients with positive serum MOG-IgG assessed by cell-based assay. RESULTS: We include 35 patients, 71% women, median age at onset 30 years (range 1-68), 23% had paediatric onset, with a median disease-duration 24 months (range 12-348). In the whole cohort, the most frequent symptoms at onset were isolated optic neuritis (ON) (34%) and myelitis (22%). Encephalitis with seizures or encephalomyelitis was the most common presentation in paediatric-onset patients 75% (n = 6), compared to 11% (n = 3) of the adult-onset patients (p < 0.001). A relapsing course was observed in 34%, these patients were younger (25 vs. 34 years, p = 0.004) and with a longer disease duration (64 vs. 6 months, p = 0.004) compared to monophasic patients. Two patients developed encephalitis with seizures/status epilepticus, with concomitant positive CSF anti-NMDAR-IgG. Chronic immunotherapy was ever prescribed in 77%, the most frequent was rituximab (35%). Relapses under chronic immunotherapy occurred in 5/27 patients (18.5%), two of them under rituximab, one paediatric patient who started combined therapy with monthly IVIG and one adult patient that switched to satralizumab plus mycophenolate. The median EDSS at the last follow-up was 1.5 (range 0-6.0). CONCLUSION: In Chile, patients with MOGAD exhibit a wide spectrum of clinical presentations at disease onset and during relapses. Close monitoring is needed, particularly in younger patients with short follow-up periods.
 BACKGROUND: In Germany about one million patients suffer from neurogenic lower urinary tract dysfunction (NLUTD). If left untreated, various forms of NLUTD can lead to secondary damage of the lower and upper urinary tract. Thus, the guideline was developed for the drug therapy of patients with NLUTD, who frequently require lifelong care and aftercare. METHODS: The guideline was developed in a consensus process with several meetings and online reviews, and final recommendations were decided on in online consensus meetings. Ballots were sent to elected officials of the contributing professional societies. Level of consensus was given for each coordinated recommendation ( https://www.awmf.org/leitlinien/detail/ll/043-053.html ). RESULTS/MOST IMPORTANT RECOMMENDATIONS: (Video)urodynamic classification of the NLUTD should be conducted before the use of antimuscarinic drugs (84.2%). Approved oral antimuscarinics should be used as first choice. Contraindications must be respected (100%). If oral treatment is ineffective or in the case of adverse drug reaction (ADRs) alternatively instillation of oxybutynin solution intravesically (83%) or onabotulinumneurotoxine (OBoNT) injection should be offered (89.5%). In case of failure or ADRs of antimuscarinics, β3 sympathomimetic mirabegron can be used to treat neurogenic detrusor overactivity (NDO) (off-label use) (100%). In case of paraplegia below C8 or multiple sclerosis with an expanded disability status scale (EDSS) of ≤ 6.5, OBoNT injection can be offered as an alternative (89.5%). Drug therapy for NDO should be started early in newborns/young children (84.2%). Conservative, nondrug therapy should be considered in frail elderly (94.7%). No parasympathomimetic therapy should be used to treat neurogenic detrusor underactivity (94.7%). CONCLUSION: Precise knowledge of the neurological underlying disease/sequence of trauma and the exact classification of the NLUTD are required for development of individualized therapy.
 Introduction: Aluminium (Al) is accumulated in the brain causing neurotoxicity and neurodegenerative disease like Alzheimer's disease (AD), multiple sclerosis, autism and epilepsy. Hence, attenuation of Al-induced neurotoxicity has become a "hot topic" in looking for an intervention that slow down the progression of neurodegenerative diseases. Objective: Our study aims to introduce a new strategy for hampering aluminum chloride (AlCl3)-induced neurotoxicity using a combination of sesamol with the probiotic bacteria; Lactobacillus rhamnosus (L. rhamnosus) and also to test their possible ameliorative effects on AlCl(3)-induced hepatotoxicity. Methods: Sprague-Dawley male rats were randomly divided into five groups (n = 10/group) which are control, AlCl(3), AlCl(3) + Sesamol, AlCl(3) + L. rhamnosus and AlCl(3) + Sesamol + L. rhamnosus. We surveilled the behavioral, biochemical, and histopathological alterations centrally in the brain and peripherally in liver. Results: This work revealed that the combined therapy of sesamol and L. rhamnosus produced marked reduction in brain amyloid-β, p-tau, GSK-3β, inflammatory and apoptotic biomarkers, along with marked elevation in brain free β-catenin and Wnt3a, compared to AlCl(3)-intoxicated rats. Also, the combined therapy exerted pronounced reduction in hepatic expressions of JAK-2/STAT-3, inflammatory (TNF-α, IL-6, NF-κB), fibrotic (MMP-2, TIMP-1, α-SMA) and apoptotic markers, (caspase-3), together with marked elevation in hepatic PPAR-γ expression, compared to AlCl(3) -intoxicated rats. Behavioral and histopathological assessments substantiated the efficiency of this combined regimen in halting the effect of neurotoxicity. Discussion: Probiotics can be used as an add-on therapy with sesamol ameliorate AlCl(3) -mediated neurotoxicity and hepatotoxicity.
 Cannabinoids are naturally occurring bioactive compounds with the potential to help treat chronic illnesses including epilepsy, Parkinson's disease, dementia and multiple sclerosis. Their general structures and efficient syntheses are well documented in the literature, yet their quantitative structure-activity relationships (QSARs), particularly 3-dimensional (3-D) conformation-specific bioactivities, are not fully resolved. Cannabigerol (CBG), an antibacterial precursor molecule for the most abundant phytocannabinoids, was characterised herein using density functional theory (DFT), together with selected analogues, to ascertain the influence of the 3D structure on their activity and stability. Results showed that the CBG family's geranyl chains tend to coil around the central phenol ring while its alkyl side-chains form H-bonds with the para-substituted hydroxyl groups as well as CH⋯π interactions with the aromatic density of the ring itself, among other interactions. Although weakly polar, these interactions are structurally and dynamically influential, effectively 'stapling' the ends of the chains to the central ring structure. Molecular docking of the differing 3-D poses of CBG to cytochrome P450 3A4 resulted in lowered inhibitory action by the coiled conformers, relative to their fully-extended counterparts, helping explain the trends in the inhibition of the metabolic activity of the CYP450 3A4. The approach detailed herein represents an effective method for the characterisation of other bioactive molecules, towards improved understanding of their QSARs and in guiding the rational design and synthesis of related compounds.
 It is well established that neurological and non-neurological autoimmune disorders can be triggered by viral infections. It remains unclear whether SARS-CoV-2 infection induces similar conditions and whether they show a distinctive phenotype. We retrospectively identified patients with acute inflammatory CNS conditions referred to our laboratory for antibody testing during the pandemic (March 1 to August 31, 2020). We screened SARS-COV-2 IgA/IgG in all sera by ELISA and confirmed the positivity with additional assays. Clinical and paraclinical data of SARS-COV-2-IgG seropositive patients were compared to those of seronegative cases matched for clinical phenotype, geographical zone, and timeframe. SARS-CoV-2-IgG positivity was detected in 16/339 (4%) sera, with paired CSF positivity in 3/16. 5 of these patients had atypical demyelinating disorders and 11 autoimmune encephalitis syndromes. 9/16 patients had a previous history of SARS-CoV-2 infection and 6 of them were symptomatic. In comparison with 32 consecutive seronegative controls, SARS-CoV-2-IgG-positive patients were older, frequently presented with encephalopathy, had lower rates of CSF pleocytosis and other neurological autoantibodies, and were less likely to receive immunotherapy. When SARS-CoV-2 seropositive versus seronegative cases with demyelinating disorders were compared no differences were seen. Whereas seropositive encephalitis patients less commonly showed increased CSF cells and protein, our data suggest that an antecedent symptomatic or asymptomatic SARS-CoV-2 infection can be detected in patients with autoimmune neurological conditions. These cases are rare, usually do not have specific neuroglial antibodies.
 BACKGROUND: Coronaviruses such as Severe Acute Respiratory Syndrome coronavirus (SARS), Middle Eastern Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) are associated with critical illnesses, including severe respiratory disorders. SARS-CoV-2 is the causative agent of the deadly COVID-19 illness, which has spread globally as a pandemic. SARS-CoV-2 may enter the human body through olfactory lobes and interact with the angiotensin-converting enzyme2 (ACE2) receptor, further facilitating cell binding and entry into the cells. Reports have shown that the virus can pass through the blood-brain barrier (BBB) and enter the central nervous system (CNS), resulting in various disorders. Cell entry by SARS-CoV-2 largely relies on TMPRSS2 and cathepsin L, which activate S protein. TMPRSS2 is found on the cell surface of respiratory, gastrointestinal and urogenital epithelium, while cathepsin-L is a part of endosomes. AIM: The current review aims to provide information on how SARS-CoV-2 infection affects brain function.. Furthermore, CNS disorders associated with SARS-CoV-2 infection, including ischemic stroke, cerebral venous thrombosis, Guillain-Barré syndrome, multiple sclerosis, meningitis, and encephalitis, are discussed. The many probable mechanisms and paths involved in developing cerebrovascular problems in COVID patients are thoroughly detailed. MAIN BODY: There have been reports that the SARS-CoV-2 virus can cross the blood-brain barrier (BBB) and enter the central nervous system (CNS), where it could cause a various illnesses. Patients suffering from COVID-19 experience a range of neurological complications, including sleep disorders, viral encephalitis, headaches, dysgeusia, and cognitive impairment. The presence of SARS-CoV-2 in the cerebrospinal fluid (CSF) of COVID-19 patients has been reported. Health experts also reported its presence in cortical neurons and human brain organoids. The possible mechanism of virus infiltration into the brain can be neurotropic, direct infiltration and cytokine storm-based pathways. The olfactory lobes could also be the primary pathway for the entrance of SARS-CoV-2 into the brain. CONCLUSIONS: SARS-CoV-2 can lead to neurological complications, such as cerebrovascular manifestations, motor movement complications, and cognitive decline. COVID-19 infection can result in cerebrovascular symptoms and diseases, such as strokes and thrombosis. The virus can affect the neural system, disrupt cognitive function and cause neurological disorders. To combat the epidemic, it is crucial to repurpose drugs currently in use quickly and develop novel therapeutics.
 OBJECTIVE: Improving synergy among regulation, health technology assessment (HTA) and clinical guideline development is relevant as these independent processes are building on shared evidence-based grounds. The two objectives were first to assess how convergence of evidentiary needs among stakeholders may be achieved, and second, to determine to what extent convergence can be achieved. DESIGN: Qualitative study using eight online dual-moderator focus groups. SETTING: Discussions had a European focus and were contextualised in four case studies on head and neck cancer, diabetes mellitus, multiple sclerosis and myelodysplastic syndromes. PARTICIPANTS: Forty-two experienced (over 10 years) European regulators, HTA representatives and clinicians participated in the discussion. INTERVENTIONS: Participants received information on the case study and research topic in advance. An introductory background presentation and interview guide for the moderators were used to steer the discussion. RESULTS: Convergence may be achieved through improved communication institutionalised in multistakeholder early dialogues, shared definitions and shared methods. Required data sets should be inclusive rather than aligned. Deliberation and decision-making should remain independent. Alignment could be sought for pragmatic clinical trial designs and patient registries. Smaller and lower-income countries should be included in these efforts. CONCLUSION: Actors in the field expressed that improving synergy among stakeholders always involves trade-offs. A balance needs to be found between the convergence of processes and the institutional remits or geographical independence. A similar tension exists between the involvement of more actors, for example, patients or additional countries, and the level of collaboration that may be achieved. Communication is key to establishing this balance.
 OBJECTIVES: To determine the timing and predictors of T2-lesion resolution in myelin-oligodendrocyte-glycoprotein-antibody-associated disease (MOGAD). METHODS: This retrospective observational study using standard of care data had inclusion criteria of: MOGAD diagnosis, >2 MRI's 12 months apart, and >1 brain/spinal cord T2-lesion. The median (interquartile-range[IQR]) number of MRI's (82% at disease onset) per-patient were: brain, 5(2-8); spine, 4(2-8). Predictors of T2-lesion resolution were assessed with age- and sex-adjusted generalized estimating equations and stratified by T2-lesion size (small <1 cm; large ≥1 cm). RESULTS: We studied 583 T2-lesions (brain, 512[88%]; spinal cord, 71[12%]) from 55 patients. At last MRI (median follow-up 54 months[IQR, 7-74]), 455 T2-lesions (78%) resolved. The median (IQR) time to resolution was 3 months (1.4-7.0). Small T2-lesions resolved more frequently and faster than large T2-lesions. Acute T1-hypointesity decreased the likelihood (odds ratio[95% confidence interval]) of T2-lesion resolution independent of size (small: 0.23[0.09, 0.60], p=0.002; large: 0.30[0.16, 0.55], p<0.001) while acute steroids favored resolution of large T2-lesions (1.75[1.01, 3.03], p=0.046). Notably, 32/55 (58%) T2-lesions resolved without treatment. DISCUSSION: The high frequency of spontaneous T2-lesion resolution suggests this represents MOGAD's natural history. The speed of T2-lesion resolution and influence of size, corticosteroids and T1-hypointensity on this phenomenon gives insight into MOGAD pathogenesis.
 Background: One in five individuals live with chronic pain globally, which often co-occurs with sleep problems, anxiety, depression, and substance use disorders. Although these conditions are commonly managed with cannabinoid-based medicines (CBM), health care providers report lack of information on the risks, benefits, and appropriate use of CBM for therapeutic purposes. Aims: We present these clinical practice guidelines to help clinicians and patients navigate appropriate CBM use in the management of chronic pain and co-occurring conditions. Materials and Methods: We conducted a systematic review of studies investigating the use of CBM for the treatment of chronic pain. Articles were dually reviewed in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Clinical recommendations were developed based on available evidence from the review. Values and preferences and practical tips have also been provided to support clinical application. The GRADE system was used to rate the strength of recommendations and quality of evidence. Results: From our literature search, 70 articles met inclusion criteria and were utilized in guideline development, including 19 systematic reviews and 51 original research studies. Research typically demonstrates moderate benefit of CBM in chronic pain management. There is also evidence for efficacy of CBM in the management of comorbidities, including sleep problems, anxiety, appetite suppression, and for managing symptoms in some chronic conditions associated with pain including HIV, multiple sclerosis, fibromyalgia, and arthritis. Conclusions: All patients considering CBM should be educated on risks and adverse events. Patients and clinicians should work collaboratively to identify appropriate dosing, titration, and administration routes for each individual. Systematic Review Registration: PROSPERO no. 135886.
 One-third of boys with X-linked adrenoleukodystrophy (ALD) develop inflammatory demyelinating lesions, typically at the splenium. These lesions share similarities with multiple sclerosis, including cerebral hypoperfusion and links to vitamin D insufficiency. We hypothesized that increasing vitamin D levels would increase cerebral blood flow (CBF) in ALD boys. We conducted an exploratory analysis of vitamin D supplementation and CBF using all available data from participants enrolled in a recent single-arm interventional study of vitamin D supplementation in boys with ALD. We measured whole brain and splenium CBF using arterial spin labeling (ASL) from three study time points (baseline, 6 months, and 12 months). We used linear generalized estimating equations to evaluate CBF changes between time points and to test for an association between CBF and vitamin D. ASL data were available for 16 participants, aged 2-22 years. Mean vitamin D levels increased by 72.7% (p < .001) after 6 months and 88.6% (p < .01) after 12 months. Relative to baseline measures, mean CBF of the whole brain (6 months: +2.5%, p = .57; 12 months: +6.1%, p = .18) and splenium (6 months: +1.2%, p = .80; 12 months: +7.4%, p = .058) were not significantly changed. Vitamin D levels were positively correlated with CBF in the splenium (slope = .59, p < .001). In this exploratory analysis, we observed a correlation between vitamin D levels and splenial CBF in ALD boys. We confirm the feasibility of measuring CBF in this brain region and population, but further work is needed to establish a causal role for vitamin D in modulating CBF.
 Programmed death-1 (PD-1), an immune checkpoint receptor, is expressed on activated lymphocytes, macrophages, and some types of tumor cells. While PD-1(+) cells have been implicated in outcomes of cancer immunity, autoimmunity, and chronic infections, the exact roles of these cells in various physiological and pathological processes remain elusive. Molecules that target and deplete PD-1(+) cells would be instrumental in defining the roles unambiguously. Previously, an immunotoxin has been generated for the depletion of PD-1(+) cells though its usage is impeded by its low production yield. Thus, a more practical molecular tool is desired to deplete PD-1(+) cells and to examine functions of these cells. We designed and generated a novel anti-PD1 diphtheria immunotoxin, termed PD-1 DIT, targeting PD-1(+) cells. PD-1 DIT is comprised of two single chain variable fragments (scFv) derived from an anti-PD-1 antibody, coupled with the catalytic and translocation domains of the diphtheria toxin. PD-1 DIT was produced using a yeast expression system that has been engineered to efficiently produce protein toxins. The yield of PD-1 DIT reached 1-2 mg/L culture, which is 10 times higher than the previously reported immunotoxin. Flow cytometry and confocal microscopy analyses confirmed that PD-1 DIT specifically binds to and enters PD-1(+) cells. The binding avidities between PD-1 DIT and two PD-1(+) cell lines are approximately 25 nM. Moreover, PD-1 DIT demonstrated potent cytotoxicity toward PD-1(+) cells, with a half maximal effective concentration (EC(50) ) value of 1 nM. In vivo experiments further showed that PD-1 DIT effectively depleted PD-1(+) cells and enabled mice inoculated with PD-1(+) tumor cells to survive throughout the study. Our findings using PD-1 DIT revealed the critical role of pancreatic PD-1(+) T cells in the development of type-1 diabetes (T1D). Additionally, we observed that PD-1 DIT treatment ameliorated relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), a mouse model of relapsing-remitting multiple sclerosis (RR-MS). Lastly, we did not observe significant hepatotoxicity in mice treated with PD-1 DIT, which had been reported for other immunotoxins derived from the diphtheria toxin. With its remarkable selective and potent cytotoxicity toward PD-1(+) cells, coupled with its high production yield, PD-1 DIT emerges as a powerful biotechnological tool for elucidating the physiological roles of PD-1(+) cells. Furthermore, the potential of PD-1 DIT to be developed into a novel therapeutic agent becomes evident.
 BACKGROUND: In idiopathic intracranial hypertension (IIH), certain MRI features are promising diagnostic markers, but whether these have prognostic value is currently unknown. METHODS: We included patients from the Vienna-Idiopathic-Intracranial-Hypertension (VIIH) database with IIH according to Friedman criteria and cranial MRI performed at diagnosis. Presence of empty sella (ES), perioptic subarachnoid space distension (POSD) with or without optic nerve tortuosity (ONT), posterior globe flattening (PGF) and transverse sinus stenosis (TSS) was assessed and multivariable regression models regarding visual outcome (persistent visual impairment/visual worsening) and headache outcome (headache improvement/freedom of headache) were fitted. RESULTS: We included 84 IIH patients (88.1% female, mean age 33.5 years, median body mass index 33.7). At baseline, visual impairment was present in 70.2% and headache in 84.5% (54.8% chronic). Persistent visual impairment occurred in 58.3%, visual worsening in 13.1%, headache improvement was achieved in 83.8%, freedom of headache in 26.2%. At least one MRI feature was found in 78.6% and 60.0% had ≥3 features with POSD most frequent (64.3%) followed by TSS (60.0%), ONT (46.4%), ES (44.0%) and PGF (23.8%). In multivariable models, there was no association of any single MRI feature or their number with visual impairment, visual worsening, headache improvement or freedom. Visual impairment at baseline predicted persistent visual impairment (odds ratio 6.3, p<0.001), but not visual worsening. Chronic headache at baseline was significantly associated with lower likelihood of headache freedom (odds ratio 0.48, p=0.013), but not with headache improvement. CONCLUSIONS: MRI features of IIH are neither prognostic of visual nor headache outcome.
 BACKGROUND: Observational studies have suggested that immune-mediated inflammatory diseases (IMIDs) are associated with a higher risk of valvular heart disease (VHD). But the potential causal association is not clear. Therefore, we used Mendelian randomization (MR) analysis to assess the causal association of IMIDs with VHD risk. METHODS: A two-sample MR analysis was performed to confirm the causal association of several common IMIDs (systemic lupus erythematosus, SLE; rheumatoid arthritis, RA; multiple sclerosis, MS; ankylosing spondylitis, AS; psoriasis, PSO; inflammatory bowel disease, IBD) with the risk of VHD. The exposure data is derived from published genome-wide association studies (GWASs) and outcome data come from the FinnGen database (47,003 cases and 182,971 controls). Inverse-variance weighted (IVW), MR-Egger, and weighted median methods were performed to assess the causal association. The study design applied univariable MR and multivariable MR. RESULTS: The MR analysis indicated that several genetically predicted IMIDs increased the risk of VHD, including SLE (odds ratio (OR) = 1.014; 95% confidence interval (CI) =  < 1.001,1.028 > ; p = 0.036), RA (OR = 1.017; 95% CI =  < 1.002,1.031 > ; p = 0.025), and IBD (OR = 1.018; 95% CI =  < 1.002,1.033 > ; p = 0.023). Multivariable MR indicated that the adverse effect of these IMIDs on VHD was dampened to varying degrees after adjusting for smoking, obesity, coronary artery disease, and hypertension. CONCLUSION: Our findings support the first genetic evidence of the causality of genetically predicted IMIDs with the risk of developing into VHD. Our results deliver a viewpoint that further active intervention needs to be explored to mitigate VHD risk in patients with SLE, RA, and IBD. Key Points • Genetically predicted systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD) are causally associated with valvular heart disease (VHD). • To reduce the risk of VHD in patients with SLE, RA, and IBD, active interventions should be further explored.
 Myelin basic protein (MBP) is an intrinsically disordered protein and in the central nervous system (CNS) mainly responsible for connecting the cytoplasmic surfaces of the multilamellar, compact myelin. Increased posttranslational modification of MBP is linked to both, the natural development (from adolescent to adult brains) of myelin, and features of multiple sclerosis. Here, we study how a combination of this intrinsically disordered myelin protein with varying the natural cholesterol content may alter the characteristics of myelin-like membranes and interactions between these membranes. Large unilamellar vesicles (LUVs) with a composition mimicking the cytoplasmic leaflet of myelin were chosen as the model system, in which different parameters contributing to the interactions between the lipid membrane and MBP were investigated. While we use cryo-transmission electron microscopy (TEM) for imaging, dynamic light scattering (DLS) and electrophoretic measurements through continuously-monitored phase-analysis light scattering (cmPALS) were used for a more global overview of particle size and charge, and electron paramagnetic resonance (EPR) spectroscopy was utilized for local behavior of lipids in the vesicles' membranes in aqueous solution. The cholesterol content was varied from 060 % in these LUVs and measurements were performed in the presence and absence of MBP. We find that the composition of the lipid layers is relevant to the interaction with MBP. Not only the size, the shape and the aggregation behavior of the vesicles depend on the cholesterol content, but also within each membrane, cholesterol's freedom of movement, its environmental polarity and its distribution were found to depend on the content using the EPR-active spin-labeled cholesterol (CSOSL). In addition, DLS and EPR measurements probing the transition temperatures of the lipid phases allow a correlation of specific behavior with the human body temperature of 37 °C. Overall, our results aid in understanding the importance of the native cholesterol content in the healthy myelin membrane, which serves as the basis for stable and optimum protein-bilayer interactions. Although studied in this specific myelin-like system, from a more general and materials science-oriented point of view, we could establish how membrane and vesicle properties depend on cholesterol and/or MBP content, which might be useful generally when specific membrane and vesicle characteristics are sought for.
 INTRODUCTION: Coronavirus disease 2019 (COVID-19), a global pandemic, has infected approximately 10% of the world's population. This comprehensive review aimed to determine the prevalence of various neurological disorders in COVID-19 without overlapping meta-analysis errors. METHODS: We searched for meta-analyses on neurological disorders following COVID-19 published up to March 14, 2023. We obtained 1,184 studies, of which 44 meta-analyses involving 9,228,588 COVID-19 patients were finally included. After confirming the forest plot of each study and removing overlapping individual studies, a re-meta-analysis was performed using the random-effects model. RESULTS: The summarized combined prevalence of each neurological disorder is as follows: stroke 3.39% (95% confidence interval, 1.50-5.27), dementia 6.41% (1.36-11.46), multiple sclerosis 4.00% (2.50-5.00), epilepsy 5.36% (-0.60-11.32), Parkinson's disease 0.67% (-1.11-2.45), encephalitis 0.66% (-0.44-1.77), and Guillain-Barré syndrome 3.83% (-0.13-7.80). In addition, the mortality risk of patients with comorbidities of COVID-19 is as follows: stroke OR 1.63 (1.23-2.03), epilepsy OR 1.71 (1.00-2.42), dementia OR 1.90 (1.31-2.48), Parkinson's disease OR 3.94 (-2.12-10.01). CONCLUSION: Our results show that the prevalence and mortality risk may increase in some neurological diseases during the COVID-19 pandemic. Future studies should elucidate the precise mechanisms for the link between COVID-19 and neurological diseases, determine which patient characteristics predispose them to neurological diseases, and consider potential global patient management.
 BACKGROUND: Primary cardiac tumors are extremely rare. Cardiac rhabdomyoma is the most common primary cardiac tumor. 50-80% of solitary rhabdomyomas and all multiple rhabdomyomas are associated with tuberous sclerosis complex. Due to spontaneous regression, surgery is necessary only in severe hemodynamic compromise and persistent arrhythmias. Everolimus, a mechanistic target of rapamycin (mTOR) inhibitor, can be used in the treatment of rhabdomyomas seen in tuberous sclerosis complex. We aimed to evaluate the clinical progression of rhabdomyomas followed-up in our center between the years 2014-2019 and evaluate the efficacy and safety of everolimus treatment on tumor regression. METHODS: Clinical features, prenatal diagnosis, clinical findings, tuberous sclerosis complex presence, treatment and follow-up results were evaluated retrospectively. RESULTS: Among 56 children with primary cardiac tumors, 47 were diagnosed as rhabdomyomas, 28/47 patients (59.6%) had prenatal diagnosis, 85.1% were diagnosed before one year of age and 42/47 patients (89.3%) were asymptomatic. Multiple rhabdomyomas were present in 51% and median diameter of tumors was 16mm (4.5 - 52 mm). In 29/47 patients (61.7%) no medical or surgical treatment were necessary while 34% of these had spontaneous regression. Surgery was necessary in 6/47 patients (12.7%). Everolimus was used in 14/47 patients (29.8%). Indications were seizures (2 patients) and cardiac dysfunction (12 patients). Regression in size of rhabdomyomas was achieved in 10/12 patients (83%). Although, in the long-term, the amount of tumor mass shrinkage was not significantly different between patients who received everolimus and untreated patients (p=0.139), the rate of mass reduction was 12.4 times higher in patients who received everolimus. Leukopenia was not detected in any of the patients, but, hyperlipidemia was noted in 3/14 patients (21.4%). CONCLUSIONS: According to our results, everolimus accelerates tumor mass reduction, but not amount of mass regression in the long term. Everolimus may be considered for treatment of rhabdomyomas which cause hemodynamic compromise or life-threatening arrhythmias before surgical intervention.
 Systemic sclerosis, an autoimmune disease characterized by fibrosis and vasculopathy of the skin and other multiple organs has been associated with an increased risk of malignancy. We present the case of a 74-year-old woman who had diffused cutaneous systemic sclerosis and uterine cervical cancer. The patient was initially diagnosed with stage IIB squamous cell carcinoma and concurrent chemoradiotherapy was planned. However, cisplatin could not be administered due to acute renal failure, so the patient was treated solely with radiotherapy. However, complications of systemic sclerosis progressed rapidly, and the patient died 63 days later from pulmonary edema. An autopsy later revealed that uterine cervix had primary signet ring cell carcinoma. We suspected that this patient had a combination of signet ring cell carcinoma and squamous cell carcinoma, with squamous cell carcinoma disappearing after radiotherapy. This case highlighted the importance of systemic management for cancers associated with systemic sclerosis.
 Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by neuropsychiatric symptoms and multiple dysplastic organ lesions, caused by loss of function mutations in either TSC1 or TSC2. The peripheral blood mononuclear cells (PBMCs) from a patient carrying mosaic nonsense mutation of TSC2 gene were reprogrammed using the CytoTune-iPS2.0 Sendai Reprogramming Kit. The human induced pluripotent cell (hiPSC) lines with the mutation and without the mutation were established. The heterozygous nonsense mutation in TSC2 will cause the truncated protein, which is known to associated with TSC. The established hiPSC lines will enable proper in vitro disease modelling of TSC.
 Tuberous sclerosis complex (TSC) is an autosomal dominant disease characterised by abnormal cell proliferation and differentiation that affects multiple organs and can lead to the growth of hamartomas. Tuberous sclerosis complex is caused by the disinhibition of the protein mTOR (mammalian target of rapamycin). In the past, various therapeutic approaches, even if only symptomatic, have been attempted to improve the clinical effects of this disease. While all of these therapeutic strategies are useful and are still used and indicated, they are symptomatic therapies based on the individual symptoms of the disease and therefore not fully effective in modifying long-term outcomes. A new therapeutic approach is the introduction of allosteric inhibitors of mTORC1, which allow restoration of metabolic homeostasis in mutant cells, potentially eliminating most of the clinical manifestations associated with Tuberous sclerosis complex. Everolimus, a mammalian target of the rapamycin inhibitor, is able to reduce hamartomas, correcting the specific molecular defect that causes Tuberous sclerosis complex. In this review, we report the findings from the literature on the use of everolimus as an effective and safe drug in the treatment of TSC manifestations affecting various organs, from the central nervous system to the heart.
 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective degeneration of upper and lower motor neurons. Currently, there are no effective biomarkers and fundamental therapies for this disease. Dysregulation in RNA metabolism plays a critical role in the pathogenesis of ALS. With the contribution of Next Generation Sequencing, the functions of non-coding RNAs (ncRNAs) have gained increasing interests. Especially, micro RNAs (miRNAs), which are tissue-specific small ncRNAs of about 18-25 nucleotides, have emerged as key regulators of gene expression to target multiple molecules and pathways in the central nervous system (CNS). Despite intensive recent research in this field, the crucial links between ALS pathogenesis and miRNAs remain unclear. Many studies have revealed that ALS-related RNA binding proteins (RBPs), such as TAR DNA-binding protein 43 (TDP-43) and fused in sarcoma/translocated in liposarcoma (FUS), regulate miRNAs processing in both the nucleus and cytoplasm. Of interest, Cu(2+)/Zn(2+) superoxide dismutase (SOD1), a non-RBP associated with familial ALS, shows partially similar properties to these RBPs via the dysregulation of miRNAs in the cellular pathway related to ALS. The identification and validation of miRNAs are important to understand the physiological gene regulation in the CNS, and the pathological implications in ALS, leading to a new avenue for early diagnosis and gene therapies. Here, we offer a recent overview regarding the mechanism underlying the functions of multiple miRNAs across TDP-43, FUS, and SOD1 with the context of cell biology, and challenging for clinical applications in ALS.
 Extrarenal retroperitoneal angiomyolipomas are rare benign tumors that may mimic other benign or malignant retroperitoneal tumors. We describe 68 Ga-FAPI-04 PET/MRI findings in a case of tuberous sclerosis complex with an extrarenal retroperitoneal angiomyolipoma and multiple angiomyolipomas involving bilateral kidneys. The extrarenal retroperitoneal angiomyolipoma and most of the renal angiomyolipomas were 68 Ga-FAPI-04-avid. One left renal angiomyolipoma with extensive hemorrhage and fibrosis had no significant 68 Ga-FAPI-04 uptake. Angiomyolipoma should be included in the differential diagnosis of FAPI-avid renal or extrarenal retroperitoneal lesions.
 Tuberous sclerosis complex (TSC) is a neurogenetic disorder due to loss-of-function TSC1 or TSC2 variants, characterized by tumors affecting multiple organs, including skin, brain, heart, lung, and kidney. Mosaicism for TSC1 or TSC2 variants occurs in 10%-15% of individuals diagnosed with TSC. Here, we report comprehensive characterization of TSC mosaicism by using massively parallel sequencing (MPS) of 330 TSC samples from a variety of tissues and fluids from a cohort of 95 individuals with mosaic TSC. TSC1 variants in individuals with mosaic TSC are much less common (9%) than in germline TSC overall (26%) (p < 0.0001). The mosaic variant allele frequency (VAF) is significantly higher in TSC1 than in TSC2, in both blood and saliva (median VAF: TSC1, 4.91%; TSC2, 1.93%; p = 0.036) and facial angiofibromas (median VAF: TSC1, 7.7%; TSC2 3.7%; p = 0.004), while the number of TSC clinical features in individuals with TSC1 and TSC2 mosaicism was similar. The distribution of mosaic variants across TSC1 and TSC2 is similar to that for pathogenic germline variants in general TSC. The systemic mosaic variant was not present in blood in 14 of 76 (18%) individuals with TSC, highlighting the value of analysis of multiple samples from each individual. A detailed comparison revealed that nearly all TSC clinical features are less common in individuals with mosaic versus germline TSC. A large number of previously unreported TSC1 and TSC2 variants, including intronic and large rearrangements (n = 11), were also identified.
 PURPOSE: To report a case with branch retinal vein occlusion secondary to a retinal astrocytic hamartoma in a patient with tuberous sclerosis complex. OBSERVATIONS: A fourteen-year-old boy, a known case of tuberous sclerosis complex, with multiple bilateral retinal astrocytic hamartomas was followed by 6 months intervals. In his last follow-up, 6 months after initial presentation, the patient developed angiographic signs of branch retinal vein occlusion (BRVO) in the superotemporal arcade of the right eye distal to one of the retinal astrocytic hamartomas. He underwent targeted retinal laser photocoagulation. No secondary complication related to BRVO was observed during the next six-month follow-up. CONCLUSION: And Importance: Although the co-occurrence of branch retinal vein occlusion and astrocytic hamartoma may represent an incidental finding, awareness of BRVO as a possible complication associated with retinal astrocytic hamartoma helps timely diagnosis and prompt treatment of this complication, improving the visual prognosis of these patients.
 Systemic sclerosis (scleroderma, SSc) is an autoimmune disease that causes significant dysfunction to multiple organ systems, including the musculoskeletal system. It poses significant challenges to the hand surgeon, including calcinosis, ischemic changes, Raynaud phenomenon, tendinopathies, synovitis, and joint contractures. Patients with SSc also suffer from multiorgan dysfunction, which makes them high-risk surgical patients. The hand surgeon must understand the pathophysiology, treatment strategies, and special operative considerations required in this population to avoid complications and help maintain or improve hand function.
 The symptoms of amyotrophic lateral sclerosis (ALS) can mimic those of compressive neuropathies, such as carpal and cubital tunnel syndromes, especially early in a patient's clinical course. We surveyed members of the American Society for Surgery of the Hand and found that 11% of active and retired members have performed nerve decompression surgeries on patients later diagnosed with ALS. Hand surgeons are commonly the first providers to evaluate patients with undiagnosed ALS. As such, it is important to be aware of the history, signs, and symptoms of ALS to provide an accurate diagnosis and prevent unnecessary morbidities, such as nerve decompression surgery, which invariably results in poor outcomes. The major "red flag" symptoms warranting further work-up include weakness without sensory symptoms, profound weakness and atrophy in multiple nerve distributions, progressively bilateral and global symptoms, presence of bulbar symptoms (such as tongue fasciculations and speech/swallowing difficulties), and, if surgery is performed, failure to improve. If any of these red flags are present, we recommend neurodiagnostic testing and prompt referral to a neurologist for further work-up and treatment.
 BACKGROUND: Subependymal giant cell astrocytoma (SEGA) is a benign intraventricular tumor classically arising near the Foramen of Monro. SEGAs almost always present as a component of tuberous sclerosis complex (TSC), an autosomal dominant disorder characterized by lesions in multiple organs. OBSERVATIONS: A 22-year-old female with no past medical history presented with new-onset right-eye pressure, floaters in the right visual field, and pulsatile tinnitus. Imaging revealed an avidly enhancing mass abutting the right Foramen of Monro, causing obstructive hydrocephalus. Following resection, histopathological analysis identified the lesion as a SEGA. However, on further workup, the patient was found to have no genetic or clinical findings of TSC, which exemplifies a rare case of SEGA in the absence of a TSC diagnosis. LESSONS: It is essential for physicians to be aware of the possibility of SEGA in the absence of other characteristics of TSC, which has many implications for a patient's clinical course. The authors present the seventh case of SEGA without genetic or clinical features of TSC described in the literature.
 For patients with immune-mediated inflammatory diseases (IMIDs), concerns exist about increased disease activity after vaccination. We aimed to assess changes in disease activity after SARS-CoV-2 vaccination in patients with IMIDs, and determine risk factors for increased disease activity. In this substudy of a prospective observational cohort study (Target-to-B!), we included patients with IMIDs who received a SARS-CoV-2 vaccine. Patients reported changes in disease activity on a five-point Likert scale every 60 days for up to twelve months after first vaccination. In case of self-reported increased activity, hospital records were screened whether the treating physician reported increased activity, and for potential intensification of immunosuppressive (ISP) treatment. Mixed models were used to study determinants for self-reported increased disease activity. In total, 2111 patients were included for analysis after primary immunization (mean age 49.7 years [SD 13.7], 1329/2111 (63.0%) female), from which 1266 patients for analysis after first additional vaccination. Increased disease activity at 60 days after start of primary immunization was reported by 223/2111 (10.6%). In 96/223 (43.0%) the increase was confirmed by the treating physician and in 36/223 (16.1%) ISP treatment was intensified. Increased disease activity at seven to 60 days after additional vaccination, was reported by 139/1266 (11.0%). Vaccinations were not temporally associated with self-reported increased disease activity. Conversely, increased disease activity before first vaccination, neuromuscular disease, and multiple sclerosis were associated. Altogether, self-reported increased disease activity after vaccination against SARS-CoV-2 was recorded in a minority of patients and was generally mild. Moreover, multivariate analyses suggest that disease related factors, but not vaccinations are the major determinants for self-reported increased disease activity.
 Systemic sclerosis (SSc) is an intricate systemic autoimmune disease with pathological features such as vascular injury, immune dysregulation, and extensive fibrosis of the skin and multiple organs. Treatment options are limited; however, recently, mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have been acknowledged in preclinical and clinical trials as being useful in treating autoimmune diseases and are likely superior to MSCs alone. Recent research has also shown that MSC-EVs can ameliorate SSc and the pathological changes in vasculopathy, immune dysfunction, and fibrosis. This review summarizes the therapeutic effects of MSC-EVs on SSc and the mechanisms that have been discovered to provide a theoretical basis for future studies on the role of MSC-EVs in treating SSc.
 BACKGROUND: Observational studies have indicated associations between inflammatory bowel disease (IBD) and neurodegenerative diseases, including Parkinson's disease (PD). OBJECTIVE: To evaluate the causal associations of IBD with PD and other selected neurodegenerative disorders using updated data. METHODS: Bidirectional two-sample Mendelian randomization studies using genome-wide association studies summary statistics of IBD and PD. RESULTS: We found a lack of evidence for the causal association of IBD on PD (odds ratio [OR], 1.014; 95% confidence interval [CI], 0.967-1.063; P = 0.573). Reverse analysis also indicated no evidence of a causal effect for PD on IBD (OR, 0.978; 95% CI, 0.910-1.052; P = 0.549). The causality between IBD and Alzheimer's disease, amyotrophic lateral sclerosis, and multiple sclerosis was unfounded (all P > 0.05). CONCLUSIONS: The updated analyses provide no clear evidence for causal associations of IBD with PD or the other three neurodegenerative diseases. Potential confounders might contribute to the previously observed associations, and further investigations are warranted. © 2023 International Parkinson and Movement Disorder Society.
 OBJECTIVE: The study objective was to prioritize topics for future patient-centered research to increase uptake of common vaccines, such as for pneumococcal pneumonia, influenza, herpes zoster, human papillomavirus, and severe acute respiratory syndrome coronavirus 2, among adults living with autoimmune conditions. METHODS: A steering committee (SC) was formed that included clinicians, patients, patient advocates, and researchers associated with rheumatic diseases (psoriatic arthritis, rheumatoid arthritis, vasculitis), inflammatory bowel disease, and multiple sclerosis. Through a scoping review and discussions, SC members identified research topics regarding vaccine uptake and/or hesitancy for prioritization. A larger multistakeholder alliance that included patients and patient advocates, clinicians, researchers, policy makers, regulators, and vaccine manufacturers conducted a modified Delphi exercise online with three rating rounds and one ranking round. Frequency analysis and comparisons across stakeholder groups were conducted. A weighted ranking score was generated for each item in the ranking round for final prioritization. RESULTS: Through the Delphi process, 33 research topics were identified, of which 13 topics were rated as critical by more than 70% of all stakeholders (n = 31). The two highest ranked critical topics per the full stakeholder group were "How well a vaccine works for adults with autoimmune conditions" and "How beliefs about vaccine safety affect vaccine uptake." CONCLUSION: A multistakeholder group identified key topics as critically important priorities for future research to decrease vaccine hesitancy and improve uptake of vaccines for adults with autoimmune conditions.
 Reports of cognitive impairment in inflammatory bowel disease (IBD) have been mixed. IBD and cardiovascular disease are often co-morbid, yet it remains unknown whether vascular comorbidity confers a risk for decreased cognitive functioning, as observed in other populations. Participants with IBD were recruited from a longitudinal study of immune-mediated disease. Participants were administered a standardized neuropsychological test protocol, evaluating information processing speed, verbal learning and memory, visual learning and memory, and verbal fluency/executive function. Cognitive test scores were standardized using local regression-based norms, adjusting for age, sex, and education. Vascular risk was calculated using a modified Framingham Risk Score (FRS). We tested the association between FRS and cognitive test scores using a quantile regression model, adjusting for IBD type. Of 84 IBD participants, 54 had ulcerative colitis and 30 had Crohn's disease; mean (SD) age was 53.36 (13.95) years, and a high proportion were females (n = 58). As the risk score (FRS) increased, participants demonstrated lower performance in information processing speed (β = - 0.12; 95% CI - 0.24, - 0.006) and verbal learning (β = - 0.14; 95% CI - 0.28, - 0.01) at the 50(th) percentile. After adjusting for IBD type and disease activity, higher FRS remained associated with lower information processing speed (β = - 0.14; 95% CI - 0.27, - 0.065). Vascular comorbidity is associated with lower cognitive functioning in persons with IBD, particularly in the area of information processing speed. These findings suggest that prevention, identification, and treatment of vascular comorbidity in IBD may play a critical role for improving functional outcomes in IBD.
 Background In recent years, there has been an increase in the use of the internet and information technology for accessing health information. This study aimed to determine the factors that affect patients with neurological disabilities and their willingness to search for information via the internet. In addition, we aimed to assess how patients manage this information, considering the increasing availability of online information and websites that discuss health and diseases, as well as the spread of communication technology and its accessibility to the public. Methodology A cross-sectional, online, self-administered, questionnaire study was conducted in Saudi Arabia. The study targeted patients with neurological diseases who had disabilities. The questionnaire was designed to measure the demographic data, physical disability using the 10-item physical function component of the 36-Item Short Form Health survey, the perceived usefulness of online health information, the perceived ease of use, and the perceived risk of online health information. Lastly, the questionnaire measured online health information-seeking intentions and information use. Data analysis was performed using RStudio (R version 4.1.1, Posit, Boston, USA). Results We received 1,179 responses, of which 399 were excluded due to using another way to get information rather than the internet, 31 did not have neurological disabilities, and 136 did not complete the questionnaire. The remaining 613 responses were included in the final analysis. The participants were mostly male (54.6%), not married (54.6%), and had a bachelor's degree (49.99%). The average age of participants was 18-25 years (24.5%) and 26-35 years (23.2%), Additionally, most participants resided in the western (26.9%) and eastern (25.9%) regions. Most participants (39.5%) had a monthly income of 5,000 to 10,000 SAR. Further, the most common neurological diseases were multiple sclerosis and epilepsy (26.9% and 23.2%, respectively). Based on the analysis of the data, the most important factor affecting online health information-seeking intention was that people with higher monthly incomes were more likely to seek online health information; these included people with an income of 10,000-20,000 SAR and >20,000 SAR. The most common factor affecting information use was the region of residence. The southern and western regions were less likely to adopt information use. Conclusions The monthly income and the area of residence had the greatest impact on people with neurological disabilities who sought online health information in the Kingdom of Saudi Arabia. Educational campaigns and workshops should be arranged to increase the population's awareness of this topic, as well as to reveal the extent and prevalence of online health information seeking among disabled patients.
 The activation of the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome triggers pyroptosis proinflammatory cell death in experimental autoimmune encephalomyelitis (EAE). However, the underlying mechanisms of the inflammatory processes of microglia in EAE remain unclear. Our previous studies suggested that interleukin-1 receptor-associated kinase (IRAK)-M down-regulates the toll-like receptor 4/interleukin-1 receptor signaling pathway. Here, we used IRAK-M knockout (IRAK-M(-/-)) mice and their microglia to dissect the role of IRAK-M in EAE. We found that deletion of IRAK-M increased the incidence rate and exacerbated the clinical symptoms in EAE mice. We then found that IRAK-M deficiency promoted the activation of microglia, activated NLRP3 inflammasomes, and enhanced GSDMD-mediated pyroptosis in the microglia of EAE. In contrast, over-expression of IRAK-M exerted inhibitory effects on neuroinflammation, NLRP3 activation, and pyroptosis. Moreover, IRAK-M deficiency enhanced the phosphorylation of IRAK1, while IRAK-M over-expression downregulated the level of phosphorylated IRAK1. Finally, we found upregulated binding of IRAK1 and TNF receptor-associated factor 6 (TRAF6) in IRAK-M(-/-) EAE mice compared to WT mice, which was blocked in AAV(IRAK-M) EAE mice. Our study reveals a complex signaling network of IRAK-M, which negatively regulates microglial NLRP3 inflammasomes and pyroptosis by inhibiting IRAK1 phosphorylation during EAE. These findings suggest a potential target for the novel therapeutic approaches of multiple sclerosis (MS)/EAE and NLRP3-related inflammatory diseases.
 PURPOSE: Acute optic neuritis (ON) is variably treated with glucocorticoids. We aimed to describe factors associated with glucocorticoid use. METHODS: In this retrospective, longitudinal cohort study of insured patients in the United States (2005-2019), adults 18-50 years old with one inpatient or ≥2 outpatient diagnoses of ON within 90 days were included. Glucocorticoid use was classified as none, any dose, and high-dose (>100 mg prednisone equivalent ≥1 days). The primary outcome was glucocorticoid receipt within 90 days of the first ON diagnosis. Multivariable logistic regression models assessed the relationship between glucocorticoid use and sociodemographics, comorbidities, clinician specialty, visit number, and year. RESULTS: Of 3026 people with ON, 65.8% were women (n = 1991), median age (interquartile range) was 38 years (31,44), and 68.6% were white (n = 2075). Glucocorticoids were received by 46% (n = 1385); 54.6% (n = 760/1385) of whom received high-dose. The odds of receiving glucocorticoids were higher among patients with multiple sclerosis (OR 1.61 [95%CI 1.28-2.04]; P < .001), MRI (OR 1.75 [95%CI 1.09-2.80]; P = .02), 3 (OR 1.80 [95%CI 1.46-2.22]; P < .001) or more (OR 4.08 [95%CI 3.37-4.95]; P < .001) outpatient ON visits, and in certain regions. Compared to ophthalmologists, patients diagnosed by neurologists (OR 1.36 [95%CI: 1.10-1.69], p = .005), emergency medicine (OR 3.97 [95%CI: 2.66-5.94]; P < .001) or inpatient clinicians (OR 2.94 [95%CI: 2.22-3.90]; P < .001) had higher odds of receiving glucocorticoids. Use increased 1.1% annually (P < .001). CONCLUSIONS: Demyelinating disease, care intensity, setting, region, and clinician type were associated with glucocorticoid use for ON. To optimize care, future studies should explore reasons for ON care variation, and patient/clinician preferences.
 Synthetic cannabidiol (CBD) derivative VCE-004.8 is a peroxisome proliferator-activated receptor gamma (PPARγ) and cannabinoid receptor type 2 (CB(2)) dual agonist with hypoxia mimetic activity. The oral formulation of VCE-004.8, termed EHP-101, possesses anti-inflammatory properties and is currently in phase 2 clinical trials for relapsing forms of multiple sclerosis. The activation of PPARγ or CB(2) receptors exerts neuroprotective effects by dampening neuroinflammation in ischemic stroke models. However, the effect of a dual PPARγ/CB(2) agonist in ischemic stroke models is not known. Here, we demonstrate that treatment with VCE-004.8 confers neuroprotection in young mice subjected to cerebral ischemia. Male C57BL/6J mice, aged 3-4 months, were subjected to 30-min transient middle cerebral artery occlusion (MCAO). We evaluated the effect of intraperitoneal VCE-004.8 treatment (10 or 20 mg/kg) either at the onset of reperfusion or 4h or 6h after the reperfusion. Seventy-two hours after ischemia, animals were subjected to behavioral tests. Immediately after the tests, animals were perfused, and brains were collected for histology and PCR analysis. Treatment with VCE-004.8 either at the onset or 4h after reperfusion significantly reduced infarct volume and improved behavioral outcomes. A trend toward reduction in stroke injury was observed in animals receiving the drug starting 6h after recirculation. VCE-004.8 significantly reduced the expression of pro-inflammatory cytokines and chemokines involved in BBB breakdown. Mice receiving VCE-004.8 had significantly lower levels of extravasated IgG in the brain parenchyma, indicating protection against stroke-induced BBB disruption. Lower levels of active matrix metalloproteinase-9 were found in the brain of drug-treated animals. Our data show that VCE-004.8 is a promising drug candidate for treating ischemic brain injury. Since VCE-004.8 has been shown to be safe in the clinical setting, the possibility of repurposing its use as a delayed treatment option for ischemic stroke adds substantial translational value to our findings.
 In inflammatory neuropathies, oxidative stress results in neuronal and Schwann cell (SC) death promoting early neurodegeneration and clinical disability. Treatment with the short-chain fatty acid propionate showed a significant immunoregulatory and neuroprotective effect in multiple sclerosis patients. Similar effects have been described for patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Therefore, Schwann cell's survival and dorsal root ganglia (DRG) outgrowth were evaluated in vitro after propionate treatment and application of H2O2 or S-nitroso-N-acetyl-D-L-penicillamine (SNAP) to evaluate neuroprotection. In addition, DRG resistance was evaluated by the application of oxidative stress by SNAP ex vivo after in vivo propionate treatment. Propionate treatment secondary to SNAP application on DRG served as a neuroregeneration model. Histone acetylation as well as expression of the free fatty acid receptor (FFAR) 2 and 3, histone deacetylases, neuroregeneration markers, and antioxidative mediators were investigated. β-hydroxybutyrate was used as a second FFAR3 ligand, and pertussis toxin was used as an FFAR3 antagonist. FFAR3, but not FFAR2, expression was evident on SC and DRG. Propionate-mediated activation of FFAR3 and histone 3 hyperacetylation resulted in increased catalase expression and increased resistance to oxidative stress. In addition, propionate treatment resulted in enhanced neuroregeneration with concomitant growth-associated protein 43 expression. We were able to demonstrate an antioxidative and neuroregenerative effect of propionate on SC and DRG mediated by FFAR3-induced histone acetylases expression. Our results describe a pathway to achieve neuroprotection/neuroregeneration relevant for patients with immune-mediated neuropathies.
 BACKGROUND: Cognitive behavioural therapy (CBT) is effective in reducing fatigue across long-term conditions (LTCs). This study evaluated whether cognitive and behavioural responses to symptoms: 1) differ between LTCs and 2) moderate and/or mediate the effect of CBT on fatigue. METHOD: Data were used from four Randomized Controlled Trials testing the efficacy of CBT for fatigue in Chronic Fatigue Syndrome/ME (N = 240), Multiple Sclerosis (N = 90), Type 1 Diabetes Mellitus (N = 120) and Q-fever fatigue syndrome (N = 155). Fatigue severity, assessed with the Checklist Individual Strength, was the primary outcome. Differences in fatigue perpetuating factors, assessed with the Cognitive Behavioural Responses to Symptoms Questionnaire (CBRQ), between diagnostic groups were tested using ANCOVAs. Linear regression and mediation analyses were used to investigate moderation and mediation by CBRQ scores of the treatment effect. RESULTS: There were small to moderate differences in CBRQ scores between LTCs. Patients with higher scores on the subscales damage beliefs and avoidance/resting behaviour at baseline showed less improvement following CBT, irrespective of diagnosis. Reduction in fear avoidance, catastrophising and avoidance/resting behaviour mediated the positive effect of CBT on fatigue across diagnostic groups. DISCUSSION: The same cognitive-behavioural responses to fatigue moderate and mediate treatment outcome across conditions, supporting a transdiagnostic approach to fatigue.
 OBJECTIVE: Postpartum, patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) have increased risk for disease activity. Anti-CD20 IgG1 monoclonal antibodies (mAb) are increasingly used as disease-modifying therapies (DMTs). Patients may wish to both breastfeed and resume DMT postpartum. This study aimed to determine the transfer of anti-CD20 IgG1 mAbs, ocrelizumab, and rituximab (OCR/RTX), into mature breastmilk and describe maternal and infant outcomes. METHODS: Fifty-seven cis-women receiving OCR/RTX after 59 pregnancies and their infants were enrolled and followed up to 12M postpartum or 90 days post-infusion. Breastmilk was collected pre-infusion and serially up to 90 days and assayed for mAb concentration. Medical records and patients' questionnaire responses were obtained to assess neurologic, breastfeeding, and infant development outcomes. RESULTS: The median average concentration of mAb in breastmilk was low (OCR: 0.08 μg/mL, range 0.05-0.4; RTX: 0.03 μg/mL, range 0.005-0.3). Concentration peaked 1-7 days post-infusion in most (77%) and was nearly undetectable after 90 days. Median average relative infant dose was <1% (OCR: 0.1%, range 0.07-0.7; RTX: 0.04%, range 0.005-0.3). Forty-three participants continued to breastfeed post-infusion. At 8-12 months, the proportion of infants' growth between the 3rd and 97th World Health Organization percentiles did not differ for breastfed (36/40) and non-breastfed (14/16, p > 0.05) infants; neither did the proportion with normal development (breastfed: 37/41, non-breastfed: 11/13; p > 0.05). After postpartum infusion, two mothers experienced a clinical relapse. INTERPRETATION: These confirm minimal transfer of mAb into breastmilk. Anti-CD20 mAb therapy stabilizes MS activity before conception to the postpartum period, and postpartum treatments appears to be safe and well-tolerated for both mother and infant.
 INTRODUCTION: Spasticity and cervical dystonia (CD) are movement disorders with considerable direct and indirect healthcare cost implications. Although several studies have discussed their clinical impact, few have calculated the economic burden of these disorders. This study aimed to understand treatment/injection patterns of botulinum toxins type A (BoNT-As) and the characteristics, healthcare resource utilization (HCRU), and costs among patients with spasticity or CD. METHODS: Retrospective analyses were conducted using administrative healthcare claims from the IQVIA PharMetrics(®) Plus database, from October 1, 2015 to December 31, 2019. Eligible patients were selected based on Healthcare Common Procedure Coding System codes for BoNT-A (index date) and ICD-10 diagnosis codes for spasticity or CD with 6 months of continuous enrollment pre-index and 12 months post-index. Patients were stratified into adult spasticity, pediatric spasticity, and CD cohorts, and were evaluated for injection patterns, HCRU, and costs in the post-index period. RESULTS: Overall, 2452 adults with spasticity, 1364 pediatric patients with spasticity, and 1529 adults with CD were included. Total mean all-cause healthcare costs were US$42,562 (adult spasticity), $54,167 (pediatric spasticity), and $25,318 (CD). Differences were observed in the cost of BoNT-A injection visits between toxins, with abobotulinumtoxinA (aboBoNT-A) having the lowest injection cost across all indications. CONCLUSIONS: AboBoNT-A had the lowest injection visit costs across indications. These results are suggestive of real-world resource utilization patterns and costs, and, while helpful in informing insurers' BoNT-A management strategies, further research into cost differences is warranted.
 INTRODUCTION: Myeloid cells play a critical role in the pathogenesis of Inflammatory Bowel Diseases (IBDs), including Ulcerative Colitis (UC) and Crohn's Disease (CD). Dysregulation of the JAK/STAT pathway is associated with many pathological conditions, including IBD. Suppressors Of Cytokine Signaling (SOCS) are a family of proteins that negatively regulate the JAK/STAT pathway. Our previous studies identified that mice lacking Socs3 in myeloid cells developed a hyper-activated phenotype of macrophages and neutrophils in a pre-clinical model of Multiple Sclerosis. METHODS: To better understand the function of myeloid cell Socs3 in the pathogenesis of colitis, mice with Socs3 deletion in myeloid cells (Socs3 (ΔLysM)) were utilized in a DSS-induced colitis model. RESULTS: Our results indicate that Socs3 deficiency in myeloid cells leads to more severe colitis induced by DSS, which correlates with increased infiltration of monocytes and neutrophils in the colon and increased numbers of monocytes and neutrophils in the spleen. Furthermore, our results demonstrate that the expression of genes related to the pathogenesis and diagnosis of colitis such as Il1β, Lcn2, S100a8 and S100a9 were specifically enhanced in Socs3-deficient neutrophils localized to the colon and spleen. Conversely, there were no observable differences in gene expression in Ly6C(+) monocytes. Depletion of neutrophils using a neutralizing antibody to Ly6G significantly improved the disease severity of DSS-induced colitis in Socs3-deficient mice. DISCUSSION: Thus, our results suggest that deficiency of Socs3 in myeloid cells exacerbates DSS-induced colitis and that Socs3 prevents overt activation of the immune system in IBD. This study may provide novel therapeutic strategies to IBD patients with hyperactivated neutrophils.
 Fingolimod (Fin), an FDA-approved drug, is used to control relapsing-remitting multiple sclerosis (MS). This therapeutic agent faces crucial drawbacks like poor bioavailability rate, risk of cardiotoxicity, potent immunosuppressive effects, and high cost. Here, we aimed to assess the therapeutic efficacy of nano-formulated Fin in a mouse model of experimental autoimmune encephalomyelitis (EAE). Results showed the suitability of the present protocol in the synthesis of Fin-loaded CDX-modified chitosan (CS) nanoparticles (NPs) (Fin@CSCDX) with suitable physicochemical features. Confocal microscopy confirmed the appropriate accumulation of synthesized NPs within the brain parenchyma. Compared to the control EAE mice, INF-γ levels were significantly reduced in the group that received Fin@CSCDX (p < 0.05). Along with these data, Fin@CSCDX reduced the expression of TBX21, GATA3, FOXP3, and Rorc associated with the auto-reactivation of T cells (p < 0.05). Histological examination indicated a low-rate lymphocyte infiltration into the spinal cord parenchyma after the administration of Fin@CSCDX. Of note, HPLC data revealed that the concentration of nano-formulated Fin was about 15-fold less than Fin therapeutic doses (TD) with similar reparative effects. Neurological scores were similar in both groups that received nano-formulated fingolimod 1/15th of free Fin therapeutic amounts. Fluorescence imaging indicated that macrophages and especially microglia can efficiently uptake Fin@CSCDX NPs, leading to the regulation of pro-inflammatory responses. Taken together, current results indicated that CDX-modified CS NPs provide a suitable platform not only for the efficient reduction of Fin TD but also these NPs can target the brain immune cells during neurodegenerative disorders.
 BACKGROUND: In addition to decreasing the level of cholesterol, proprotein convertase subtilis kexin 9 (PCSK9) inhibitor has pleiotropic effects, including immune regulation. However, the impact of PCSK9 on autoimmune diseases is controversial. Therefore, we used drug target Mendelian randomization (MR) analysis to investigate the effect of PCSK9 inhibitor on different autoimmune diseases. METHODS: We collected single nucleotide polymorphisms (SNPs) of PCSK9 from published genome-wide association studies statistics and conducted drug target MR analysis to detect the causal relationship between PCSK9 inhibitor and the risk of autoimmune diseases. 3-Hydroxy-3-methylglutaryl-assisted enzyme A reductase (HMGCR) inhibitor, the drug target of statin, was used to compare the effect with that of PCSK9 inhibitor. With the risk of coronary heart disease as a positive control, primary outcomes included the risk of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), myasthenia gravis (MG), multiple sclerosis (MS), asthma, Crohn's disease (CD), ulcerative colitis (UC), and type 1 diabetes (T1D). RESULTS: PCSK9 inhibitor significantly reduced the risk of SLE (OR [95%CI] = 0.47 [0.30 to 0.76], p = 1.74 × 10(-3)) but increased the risk of asthma (OR [95%CI] = 1.15 [1.03 to 1.29], p = 1.68 × 10(-2)) and CD (OR [95%CI] = 1.38 [1.05 to 1.83], p = 2.28 × 10(-2)). In contrast, HMGCR inhibitor increased the risk of RA (OR [95%CI] = 1.58 [1.19 to 2.11], p = 1.67 × 10(-3)), asthma (OR [95%CI] = 1.21 [1.04 to 1.40], p = 1.17 × 10(-2)), and CD (OR [95%CI] = 1.60 [1.08 to 2.39], p = 2.04 × 10(-2)). CONCLUSIONS: PCSK9 inhibitor significantly reduced the risk of SLE but increased the risk of asthma and CD. In contrast, HMGCR inhibitor may be a risk factor for RA, asthma, and CD.
 PURPOSE: The main purpose of this study is to explore characteristics of patients with chronic kidney disease in tuberous sclerosis (TSC) and to underline differences in clinical characteristics between end-stage renal disease (ESRD) patients and patients in earlier stages of chronic kidney disease. METHODS: This multicentric, retrospective study included data for 48 patients from seven South-Eastern European countries (Albania, Bosnia and Herzegovina, Croatia, Greece, Montenegro, Serbia, Slovenia) in the period from February to August 2020. Researchers collected data from local and national nephrological and neurological registries and offered clinical and laboratory results from medical histories in follow-up periods. RESULTS: This study enrolled 48 patients with a median age of 32.3 years (range, 18-46 years), and predominant female gender (60.45%). The percentage of patients with chronic kidney disease (CKD) diagnosis of the total number of patients was 66.90%, with end-stage renal disease development in 39.6%. The most prevalent renal lesions leading to chronic kidney disease were angiomyolipomas (AMLs) in 76.6%, while multiple renal cysts were present in 42.6% of patients. Nephrectomy was performed in 43% of patients, while the mTOR inhibitors were used in 18 patients (37.5%). The majority of patients had cutaneous manifestations of tuberous sclerosis-83.30% had hypomelanotic cutaneous lesions, and 68.80% had angiofibromas. Multiple retinal nodular hamartomas and "confetti" skin lesions were more frequent in end-stage renal disease (ESRD) than in patients with earlier stages of chronic kidney disease (p-0.033 and 0.03, respectively). CONCLUSION: Our study has also shown that retinal hamartomas and "confetti" skin lesions are more frequent in end-stage renal diseases (ESRD) patients than in other chronic kidney disease (CKD) patients. Usage of mTOR inhibitors can also reduce the number of complications and associated with tuberous sclerosis, such as dermatological manifestations and retinal hamartoma, which are more common in the terminal stage of chronic kidney disease.
 OBJECTIVE: To explore the relationship between Tuberous sclerosis complex (TSC) and cardiac tumors at our institution over the past five years and to evaluate the value of imaging technologies and genetic testing in the prenatal diagnosis of TSC. METHODS: Fetal echocardiography (FE) was performed in the whole population between 2016 and 2020. Fetuses detected with cardiac tumor(s) were included. Fetal cranial magnetic resonance imaging (MRI) and gene mutation tests were further examined. Those who declined genetic testing were excluded in the final analysis. RESULTS: A total of 40 fetuses were included in our study. There were 27 cases performed cranial magnetic resonance imaging (MRI) and the rest of 13 cases refused. Among 10 fetuses with cranial lesions detected by MRI, all of them were eventually diagnosed with TSC. And for 17 fetuses without cranial lesions, none of them were identified with a pathogenic variation in gene TSC1/2. The prevalence of TSC was significantly higher in the multiple tumors group than in the solitary group (9/20 vs. 2/20, P = 0.034). 11 fetuses had TSC1 (n = 3) or TSC2 (n = 8) causative or suspected causative mutations, of which 9 were sporadic mutations and 2 were familial mutations. CONCLUSION: Fetal cranial MRI should be recommended to evaluate brain lesions, and genetic mutation should be examined, if possible, especially for those with multiple heart tumors. When typical cardiac tumors and cranial lesions are detected, the diagnosis of TSC can almost be made even without genetic mutation results.
 Identification of therapeutic targets from genome-wide association studies (GWAS) requires insights into downstream functional consequences. We harmonized 8,613 RNA-sequencing samples from 14 brain datasets to create the MetaBrain resource and performed cis- and trans-expression quantitative trait locus (eQTL) meta-analyses in multiple brain region- and ancestry-specific datasets (n ≤ 2,759). Many of the 16,169 cortex cis-eQTLs were tissue-dependent when compared with blood cis-eQTLs. We inferred brain cell types for 3,549 cis-eQTLs by interaction analysis. We prioritized 186 cis-eQTLs for 31 brain-related traits using Mendelian randomization and co-localization including 40 cis-eQTLs with an inferred cell type, such as a neuron-specific cis-eQTL (CYP24A1) for multiple sclerosis. We further describe 737 trans-eQTLs for 526 unique variants and 108 unique genes. We used brain-specific gene-co-regulation networks to link GWAS loci and prioritize additional genes for five central nervous system diseases. This study represents a valuable resource for post-GWAS research on central nervous system diseases.
 Systemic sclerosis (SSc) is typically characterized by positive antinuclear antibodies (ANA) and Raynaud's phenomenon (RP). We present the case of a male patient with progressive diffuse skin tightening, interstitial lung disease (ILD), pericardial tamponade, renal failure, and gastrointestinal dysmotility who was diagnosed with severe, rapidly progressive SSc despite negative ANA, absent RP, and a negative malignancy workup. The patient's clinical course was complicated by scleroderma renal crisis (SRC) requiring dialysis and eventual kidney transplantation. He also had severe gastrointestinal dysmotility requiring gastrostomy tube placement and total parenteral nutrition. Multiple agents were required for treatment, including mycophenolate mofetil (MMF) and rituximab. The patient eventually had improvement in his skin fibrosis and has been doing well in follow-up after kidney transplantation. Treatment of SSc can be challenging given the heterogeneity of the disease, and recognition of this subset of SSc patients is needed to help prevent early mortality among them.
 Sphingosine-1-phosphate (S1P) receptors control endothelial cell proliferation, migration, and survival. Evidence of the ability of S1P receptor modulators to influence multiple endothelial cell functions suggests their potential use for antiangiogenic effect. The main purpose of our study was to investigate the potential of siponimod for the inhibition of ocular angiogenesis in vitro and in vivo. We investigated the effects of siponimod on the metabolic activity (thiazolyl blue tetrazolium bromide assay), cell toxicity (lactate dehydrogenase release), basal proliferation and growth factor-induced proliferation (bromodeoxyuridine assay), and migration (transwell migration assay) of human umbilical vein endothelial cells (HUVEC) and retinal microvascular endothelial cells (HRMEC). The effects of siponimod on HRMEC monolayer integrity, barrier function under basal conditions, and tumor necrosis factor alpha (TNF-α)-induced disruption were assessed using the transendothelial electrical resistance and fluorescein isothiocyanate-dextran permeability assays. Siponimod's effect on TNF-α-induced distribution of barrier proteins in HRMEC was investigated using immunofluorescence. Finally, the effect of siponimod on ocular neovascularization in vivo was assessed using suture-induced corneal neovascularization in albino rabbits. Our results show that siponimod did not affect endothelial cell proliferation or metabolic activity but significantly inhibited endothelial cell migration, increased HRMEC barrier integrity, and reduced TNF-α-induced barrier disruption. Siponimod also protected against TNF-α-induced disruption of claudin-5, zonula occludens-1, and vascular endothelial-cadherin in HRMEC. These actions are mainly mediated by sphingosine-1-phosphate receptor 1 modulation. Finally, siponimod prevented the progression of suture-induced corneal neovascularization in albino rabbits. In conclusion, the effects of siponimod on various processes known to be involved in angiogenesis support its therapeutic potential in disorders associated with ocular neovascularization. SIGNIFICANCE STATEMENT: Siponimod is an extensively characterized sphingosine-1-phosphate receptor modulator already approved for the treatment of multiple sclerosis. It inhibited retinal endothelial cell migration, potentiated endothelial barrier function, protected against tumor necrosis factor alpha-induced barrier disruption, and also inhibited suture-induced corneal neovascularization in rabbits. These results support its use for a novel therapeutic indication in the management of ocular neovascular diseases.
 OBJECTIVES: Motor neuron disease (MND) is an incurable progressive neurodegenerative disease with limited treatment options. There is a pressing need for innovation in identifying therapies to take to clinical trial. Here, we detail a systematic and structured evidence-based approach to inform consensus decision making to select the first two drugs for evaluation in Motor Neuron Disease-Systematic Multi-arm Adaptive Randomised Trial (MND-SMART: NCT04302870), an adaptive platform trial. We aim to identify and prioritise candidate drugs which have the best available evidence for efficacy, acceptable safety profiles and are feasible for evaluation within the trial protocol. METHODS: We conducted a two-stage systematic review to identify potential neuroprotective interventions. First, we reviewed clinical studies in MND, Alzheimer's disease, Huntington's disease, Parkinson's disease and multiple sclerosis, identifying drugs described in at least one MND publication or publications in two or more other diseases. We scored and ranked drugs using a metric evaluating safety, efficacy, study size and study quality. In stage two, we reviewed efficacy of drugs in MND animal models, multicellular eukaryotic models and human induced pluripotent stem cell (iPSC) studies. An expert panel reviewed candidate drugs over two shortlisting rounds and a final selection round, considering the systematic review findings, late breaking evidence, mechanistic plausibility, safety, tolerability and feasibility of evaluation in MND-SMART. RESULTS: From the clinical review, we identified 595 interventions. 66 drugs met our drug/disease logic. Of these, 22 drugs with supportive clinical and preclinical evidence were shortlisted at round 1. Seven drugs proceeded to round 2. The panel reached a consensus to evaluate memantine and trazodone as the first two arms of MND-SMART. DISCUSSION: For future drug selection, we will incorporate automation tools, text-mining and machine learning techniques to the systematic reviews and consider data generated from other domains, including high-throughput phenotypic screening of human iPSCs.
 In recent years, there has been an emphasis on the role of phase-separated biomolecular condensates, especially stress granules, in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). This is largely due to several ALS-associated mutations occurring in genes involved in stress granule assembly and observations that pathological inclusions detected in ALS patient neurons contain stress granule proteins, including the ALS-linked proteins TDP-43 and FUS. However, protein components of stress granules are also found in numerous other phase-separated biomolecular condensates under physiological conditions which are inadequately discussed in the context of ALS. In this review, we look beyond stress granules and describe the roles of TDP-43 and FUS in physiological condensates occurring in the nucleus and neurites, such as the nucleolus, Cajal bodies, paraspeckles and neuronal RNA transport granules. We also discuss the consequences of ALS-linked mutations in TDP-43 and FUS on their ability to phase separate into these stress-independent biomolecular condensates and perform their respective functions. Importantly, biomolecular condensates sequester multiple overlapping protein and RNA components, and their dysregulation could contribute to the observed pleiotropic effects of both sporadic and familial ALS on RNA metabolism.
 Anti-RuvBL1/2 autoantibodies have recently been detected in patients with systemic sclerosis (SSc) and scleromyositis overlap syndromes. These autoantibodies exhibit a distinct speckled pattern in an indirect immunofluorescent assay on Hep-2 cells. We report the case of a 48 year old man with facial changes, Raynaud's phenomenon, puffy fingers, and muscle pain. A speckled pattern on Hep-2 cells was identified, but the conventional antibody testing was negative. Based on the clinical suspicion and the ANA pattern, further testing was sought demonstrating anti-RuvBL1/2 autoantibodies. Hence, a review of the English literature was performed to define this newly emerging clinical-serological syndrome. With the one here reported, a total of 52 cases have been described to date (December 2022). Anti-RuvBL1/2 autoantibodies are highly specific for SSc and are associated with SSc/PM overlaps. Apart from myopathy, gastrointestinal and pulmonary involvement are frequently observed in these patients (94% and 88%, respectively).
 Tuberous sclerosis complex (TSC) is a disease of varying presentations characterised by the presence of multiple hamartomas in various organ systems in the body. This is an Autosomal dominant disease with damages in two suppressor genes namely TSC1 and TSC2 located on chromosome 9 (9q34-hamartin) and chromosome 16 (16p13.3-tuberin). It is a lifelong disease with neurological manifestations, for example, epilepsy, mental retardation and autism and major dermatological features like facial fibromas (adenoma sebaceum), periungual fibromas, shagreen patches and hypopigmented macules. Some conditions, for example, autosomal dominant polycystic kidney disease can co-exist with TSC as a result of concurrent deletion of both polycystic kidney disease 1 and TSC2 genes present on chromosome 16p13.3. We present a cluster of three families with TSC having varied presentations.
 BACKGROUND: Full-cohort and sibling-comparison designs have yielded inconsistent results about the impacts of caesarean delivery on offspring health outcomes, with the effect estimates from the latter being more likely directed towards the null value. We hypothesized that the seemingly conservative results obtained from the sibling-comparison design might be attributed to inadequate adjustment for non-shared confounders between siblings, particularly maternal age at delivery. METHODS: A systematic review and meta-analysis was first conducted. PubMed, Embase, and the Web of Science were searched from database inception to April 6, 2022. Included studies (1) examined the association of caesarean delivery, whether elective or emergency, with offspring health outcomes; (2) simultaneously conducted full-cohort and sibling-comparison analyses; and (3) reported adjusted effect estimates with 95% confidence intervals (95% CIs). No language restrictions were applied. Data were extracted by 2 reviewers independently. Three-level meta-analytic models were used to calculate the pooled odds ratios (ORs) and 95% CIs for caesarean versus vaginal delivery on multiple offspring health outcomes separately for full-cohort and sibling-comparison designs. Subgroup analyses were performed based on the method of adjustment for maternal age at delivery. A simulation study was then conducted. The simulated datasets were generated with some key parameters derived from the meta-analysis. RESULTS: Eighteen studies involving 21,854,828 individuals were included. The outcomes assessed included mental and behavioral disorders; endocrine, nutritional and metabolic diseases; asthma; cardiorespiratory fitness; and multiple sclerosis. The overall pooled OR for estimates from the full-cohort design was 1.14 (95% CI: 1.11 to 1.17), higher than that for estimates from the sibling-comparison design (OR = 1.08; 95% CI: 1.02 to 1.14). Stratified analyses showed that estimates from the sibling-comparison design varied considerably across studies using different methods to adjust for maternal age at delivery in multivariate analyses, while those from the full-cohort design were rather stable: in studies that did not adjust maternal age at delivery, the pooled OR of full-cohort vs. sibling-comparison design was 1.10 (95% CI: 0.99 to 1.22) vs. 1.06 (95% CI: 0.85 to 1.31), in studies adjusting it as a categorical variable, 1.15 (95% CI: 1.11 to 1.19) vs. 1.07 (95% CI: 1.00 to 1.15), and in studies adjusting it as a continuous variable, 1.12 (95% CI: 1.05 to 1.19) vs. 1.12 (95% CI: 0.98 to 1.29). The severe underestimation bias related to the inadequate adjustment of maternal age at delivery in sibling-comparison analyses was fully replicated in the simulation study. CONCLUSIONS: Sibling-comparison analyses may underestimate the association of caesarean delivery with multiple offspring health outcomes due to inadequate adjustment of non-shared confounders, such as maternal age at delivery. Thus, we should be cautious when interpreting the seemingly conservative results of sibling-comparison analyses in delivery-related studies.
 The real-world evidence data from multiple sources which includes information on patient health status and medical behavior in routine clinical setup can give deeper insights into drugs 'safety and efficacy. The RWE-based analysis in this study revealed a statistically significant link between biologics usage and hepatotoxicity in patients. To the best of our knowledge, this study is the first to conduct a large-scale multi-cohort analysis on the hepatotoxic profiles of biologics. Biologics are among the most prescribed medicines for several chronic inflammatory diseases. These agents target critical pathogenic pathways, but they may also have serious side effects. It is important to analyze whether biologics agents are an added concern or therapeutic opportunity. Real-world evidence (RWE) data were extracted for patients using biologics to monitor the safety and effectiveness of the biologics. All six biologics included in this analysis-are mostly highly prescribed biologics. The aim of the study was to assess the hepatotoxic profiles of subjects using different biologics. We evaluated the safety of current treatment regimens for patients in a large real-world cohort from multiple health care centers. Total number of eligible patients retrieved from the database is 38,112,285. Of these 38 million patients, 2.3 million take biologics. The primary objective was to assess the potential adverse hepatotoxic effects of the six biologics; adalimumab, trastuzumab, prevnar13, pegfilgrastim, interferon-beta1a and insulin glargine across different indications like diabetes mellitus, encounter for immunization, malignant neoplasm of breast, multiple sclerosis, malignant neoplasm of kidney, aplastic anaemias, radiation sickness, Crohn's disease, psoriasis, rheumatoid arthritis, spondylopathies. Data from patients using the six most-used biologics-adalimumab, trastuzumab, prevnar13, pegfilgrastim, interferon-beta1a and insulin glargine were retrieved from a global research network covering 250 million patients' data from 19 countries, and assigned to the cohorts 1 and 2, respectively. The cohorts were propensity score matched for age and sex. After defining the primary outcome as "hepatotoxicity" (endpoint defined as ICD-10 code: K71 (hepatotoxic liver disease), a Kaplan-Meier survival analysis was performed, and risk ratios (RR), odds ratios (OR), and hazard ratios (HR) were determined. A total number of 2,312,655 subjects were eligible who take biologics, and after matching total cohorts accounted for 2,303,445. We have considered the clinical data as a 1:1 matched-study design, using propensity score-matched sub-cohorts to better control for confounding associations that might stem from different distributions of age and gender between the whole dataset and the subset of patients. We discovered evidence supporting the hepatotoxic-causing effect of biologic drugs: (i) all biologics considered together had an OR of 1.9 (95% CI, 1.67-2.35), with (ii) Adalimumab 1.9 (95% CI, 1.72-2.20), Trastuzumab 1.7 (95% CI, 1.2-2.3), Prevnar13 2.3 (95% CI, 2.16-2.60), Pegfilgrastim 2.3 (95% CI, 2.0-2.50), Interferon-Beta1a 1.7 (95% CI, 1.18-2.51), and Insulin glargine 1.9 (95% CI, 1.8-1.99). Our findings indicate that clinicians should consider evaluating hepatic profiles of patients undergoing treatment with biologic drugs and counsel them regarding the risk of developing hepatic injury. Strengths of the study includes a large sample size and robust statistical techniques. Limitations of this study include lack of detailed information regarding clinical severity. Major biologics are associated with hepatotoxicity. We discovered evidence supporting the hepatotoxicity-causing effects of biologics: all biologics considered together had an OR of 1.9 (95% CI, 1.67-2.35).
 NOD-Like Receptor Family Pyrin Domain Containing 3 (NLRP3) inflammasome modulation has emerged as a potential therapeutic approach targeting inflammation amplified by pyroptotic innate immune cell death. In diseases characterized by non-cell autonomous neurodegeneration including amyotrophic lateral sclerosis (ALS), the activation of several inflammasomes has been reported. Since functional redundancy can exist among inflammasome pathways, here we investigate the effects of NLRP3 inhibition on NLRP3, NLR family CARD Domain Containing 4 (NLRC4) and non-canonical pathways to understand whether NLRP3 blockade alone can mitigate pro-inflammatory cytokine release and pyroptotic cell death in contexts where single or multiple inflammasome pathways independent of NLRP3 are activated. In this study we do not limit our insights into inflammasome biology by solely relying on the THP-1 monocytic line under the LPS/nigericin-mediated NLRP3 pathway activation paradigm. We assess therapeutic potential and limitations of NLRP3 inhibition in multi-inflammasome activation contexts utilizing various human cellular systems including cell lines expressing gain of function (GoF) mutations for several inflammasomes, primary human monocytes, macrophages, healthy and Amyotrophic Lateral Sclerosis (ALS) patient induced pluripotent stem cells (iPSC)-derived microglia (iMGL) stimulated for canonical and non-canonical inflammasome pathways. We demonstrate that NLRP3 inhibition can modulate the NLRC4 and non-canonical inflammasome pathways; however, these effects differ between immortalized, human primary innate immune cells, and iMGL. We extend our investigation in more complex systems characterized by activation of multiple inflammasomes such as the SOD1(G93A) mouse model. Through deep immune phenotyping by single-cell mass cytometry we demonstrate that acute NLRP3 inhibition does not ameliorate spinal cord inflammation in this model. Taken together, our data suggests that NLRP3 inhibition alone may not be sufficient to address dynamic and complex neuroinflammatory pathobiological mechanisms including dysregulation of multiple inflammasome pathways in neurodegenerative disease such as ALS.
 COVID-19 has been associated with a variety of multi-organs complications, with an increasing proportion of patients presenting with neurologic manifestations. There is still an uncertainty in the relationship between stroke and COVID-19. Therefore, in this study, the authors report 18 cases of acute stroke occurring in the setting of COVID-19 infection, including 11 ischaemic strokes and 7 haemorrhagic strokes and identified in a Lebanese tertiary hospital. In this case series, patients with ischaemic and haemorrhagic stroke had elevated markers of inflammation and coagulation. Ischaemic stroke patients were treated with different regimens of anti-platelets, anticoagulants, and thrombolytic therapies. Death was the most common outcome observed and was associated with the severity of COVID-19 infection.
 We report two children with molecularly confirmed mitochondrial disease mimicking Neuromyelitis Optica Spectrum Disorder (NMOSD). The first patient presented at the age of 15 months with acute deterioration following a pyrexial illness with clinical features localising to the brainstem and spinal cord. The second patient presented at 5 years with acute bilateral visual loss. In both cases, MOG and AQP4 antibodies were negative. Both patients died within a year of symptoms onset from respiratory failure. Arriving at an early genetic diagnosis is important for redirection of care and avoiding potentially harmful immunosuppressant therapies.
 INTRODUCTION: Autosomal dominant mutations in the C-terminal part of TREX1 (pVAL235Glyfs(*)6) result in fatal retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCLS) without any treatment options. Here, we report on a treatment of a RVCLS patient with anti-retroviral drugs and the janus kinase (JAK) inhibitor ruxolitinib. METHODS: We collected clinical data of an extended family with RVCLS (TREX1 pVAL235Glyfs(*)6). Within this family we identified a 45-year-old woman as index patient that we treated experimentally for 5 years and prospectively collected clinical, laboratory and imaging data. RESULTS: We report clinical details from 29 family members with 17 of them showing RVCLS symptoms. Treatment of the index patient with ruxolitinib for >4 years was well-tolerated and clinically stabilized RVCLS activity. Moreover, we noticed normalization of initially elevated CXCL10 mRNA in peripheral blood monocular cells (PBMCs) and a reduction of antinuclear autoantibodies. DISCUSSION: We provide evidence that JAK inhibition as RVCLS treatment appears safe and could slow clinical worsening in symptomatic adults. These results encourage further use of JAK inhibitors in affected individuals together with monitoring of CXCL10 transcripts in PBMCs as useful biomarker of disease activity.
 INTRODUCTION: Systemic sclerosis (SSc) is associated with esophageal dysmotility. Autologous hematopoietic cell transplantation (HCT) results in improvement of skin tightness and lung function. Whether esophageal motility improves after HCT is unknown. METHODS: Esophageal motility was studied using high-resolution esophageal manometry in 21 SSc patients before and at multiple time points after autologous HCT. Median posttransplant follow-up was 2 years (range, 6 months to 5 years). RESULTS: Prior to HCT, all 21 patients had abnormal motility-10 (48%) had unmeasurable and 11 (52%) had measurable peristalsis. Manometric diagnosis in the former 10 patients was "absent contractility" and in the latter 11 patients "ineffective esophageal motility (IEM)." After HCT, among the 10 patients with absent contractility, 9 continued to have absent contractility and one demonstrated weak measurable peristalsis. Of the 11 patients with IEM, 5 experienced SSc relapse, and 2 out of these 5 patients developed absent contractility. Among the 6 non-relapsed patients, 4 continued to have IEM, and 2 developed normal motility. CONCLUSIONS: HCT appears to have no beneficial effect on motility in patients with unmeasurable peristalsis. In patients with measurable peristalsis, HCT appears to stabilize and in some normalize motility, unless relapse occurs. Key Points • In patients with systemic sclerosis, esophageal dysmotility is a significant contributor to morbidity and so far, there has been no data describing the effects of hematopoietic cell transplantation on esophageal motility. • Our work demonstrated that in patients with systemic sclerosis and unmeasurable esophageal peristalsis prehematopoietic cell transplantation, there was no measurable beneficial effect of transplantation on esophageal motility. • In patients with systemic sclerosis and measurable peristalsis prehematopoietic cell transplantation, esophageal motility stabilized, except in relapsed patients.
 The aim of the study was to report a case of orbital perivascular epithelioid cell tumor (PEComa) in a known diagnosed patient of tuberous sclerosis and retinal astrocytic hamartoma. 43-year-old female presented with rapid progressive painful proptosis in the left eye, also reported new mass growing in her upper back. The patient past medical history is significant for left renal angiomyolipoma and multiple bilateral lung cysts of which she underwent right nephrectomy and lung biopsy, respectively. The lung biopsy turned diagnostic for lymphangiomyomatosis. On external examination, the left eye was grossly proptotic with hypoglobus. A typical butterfly distribution of sebaceous adenoma was noted across the patient cheeks and nose. Visual acuity in the right eye was 20/20 and the left eye, 20/25. Funduscopic examination identified type 1, 2, and 3 retinal astrocytic hamartomas. MRI brain and orbit was significant for a lesion arising from the lateral orbital wall with extensive bone destruction, displacing the left optic nerve medially. CT chest showed left extrathoracic mass had same radiological features as the orbital lesion; thus, an incisional biopsy performed on the former was diagnostic for PEComa with atypical features. This is the first observed case of PEComa in a known diagnosed patent with TS and retinal astrocytic hamartoma. The association of tuberous sclerosis complex and orbital PEComa is rarely and poorly reported in the literature compared to extraocular PEComa.
 Multiple sources of evidence suggest that changes in metabolism may precede the onset of motor symptoms in amyotrophic lateral sclerosis. This study aimed to seek evidence for alterations in the levels of blood indices collected routinely in the primary care setting prior to the onset of motor symptoms in amyotrophic lateral sclerosis. Premorbid data, measured as part of routine health screening, for total cholesterol, high-density and low-density lipoprotein cholesterol, triglyceride, glycated haemoglobin A1c and creatinine were collected retrospectively from (i) a cohort of amyotrophic lateral sclerosis patients attending a specialist clinic (n = 143) and (ii) from primary care-linked data within UK Biobank. Data were fitted using linear mixed effects models with linear b-splines to identify inflection points, controlling for age and sex. In specialist amyotrophic lateral sclerosis clinic cases, models indicated decreasing levels of total and low-density lipoprotein cholesterol prior to an inflection point in the years before symptom onset (total cholesterol 3.25 years, low-density lipoprotein cholesterol 1.25 years), after which they stabilized or rose. A similar pattern was observed in amyotrophic lateral sclerosis cases within UK Biobank, occurring several years prior to diagnosis (total cholesterol 7 years, low-density lipoprotein cholesterol 7.25 years), differing significantly from matched controls. High-density lipoprotein cholesterol followed a similar pattern but was less robust to sensitivity analyses. Levels of triglyceride remained stable throughout. Glycated haemoglobin temporal profiles were not consistent between the clinic and biobank cohorts. Creatinine level trajectories prior to amyotrophic lateral sclerosis did not differ significantly from controls but decreased significantly in the symptomatic period after an inflection point of 0.25 years after symptom onset (clinic cohort) or 0.5 years before diagnosis (UK Biobank). These data provide further evidence for a pre-symptomatic period of dynamic metabolic change in amyotrophic lateral sclerosis, consistently associated with alterations in blood cholesterols. Such changes may ultimately contribute to biomarkers applicable to population screening and for pathways guiding the targeting of preventative therapy.
 INTRODUCTION AND IMPORTANCE: Penile sclerosis lipogranuloma, a disease that occurs as a result of the body's reaction to lipid-based foreign substances, is a rare case with manifestations that can occur years after injection. Reactions that emerge can be disturbing to the point of causing functional impairment, so proper therapy needs to be done to restore and maintain penis function and prevent complications. Here, we present a case of penile sclerosis lipogranuloma that was treated surgically with a scrotal flap and VY plasty, including circumcision. CASE PRESENTATION: We report here the case of a 19-year-old Asian male who came in with multiple, irregular, nodular masses in his penis after a candlenut oil injection that had been performed a year before presentation. An extensive excision and extraction of the penile lipogranuloma, including all areas invaded by oil injection, were performed. Then a scrotal flap and VY plasty were used to reconstruct the exposed penile shaft. The operative procedure was successful, and the patient experienced positive functional and aesthetic outcomes. CLINICAL DISCUSSION: Determining therapy for penile sclerosis granuloma becomes important to improve or restore normal penile function and for performance function. Therapy includes the complete removal of the substance and the affected part. The recommended reconstruction for the penile shaft is a scrotal flap with penile scrotal invagination and VY plasty. CONCLUSION: Proper treatment of the penis and its surroundings in cases of penile lipogranuloma is important to prevent further complications and maintain penile function.
 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons (MNs) with large unmet medical needs. Multiple pathological mechanisms are considered to contribute to the progression of ALS, including neuronal oxidative stress and mitochondrial dysfunction. Honokiol (HNK) has been reported to exert therapeutic effects in several neurologic disease models including ischemia stroke, Alzheimer's disease and Parkinson's disease. Here we found that honokiol also exhibited protective effects in ALS disease models both in vitro and in vivo. Honokiol improved the viability of NSC-34 motor neuron-like cells that expressed the mutant G93A SOD1 proteins (SOD1-G93A cells for short). Mechanistical studies revealed that honokiol alleviated cellular oxidative stress by enhancing glutathione (GSH) synthesis and activating the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response element (ARE) pathway. Also, honokiol improved both mitochondrial function and morphology via fine-tuning mitochondrial dynamics in SOD1-G93A cells. Importantly, honokiol extended the lifespan of the SOD1-G93A transgenic mice and improved the motor function. The improvement of antioxidant capacity and mitochondrial function was further confirmed in the spinal cord and gastrocnemius muscle in mice. Overall, honokiol showed promising preclinical potential as a multiple target drug for ALS treatment.
 BACKGROUND: Although shear wave elastography (SWE) has been found to have the potential to evaluate skin lesions in systemic sclerosis (SSc), current research fails to answer the following questions: (I) can high-frequency ultrasound (HFUS) and SWE at multiple sites throughout the body distinguish SSc subtypes; (II) is HFUS and SWE at every site equally affected by clinical characteristics; and (III) is SWE a supplement or a choice to HFUS. This prospective study aimed to compare the value of SWE-based skin stiffness and HFUS-based skin thickness in distinguishing different SSc subtypes, verify the influence of clinical features on SWE and HFUS, and provide a basis for the screening of the optimal evaluation sites and indicators in the future. METHODS: Forty-nine limited and 51 diffuse SSc patients were included in this study. Their skin was assessed at 17 sites by palpation using the modified Rodnan skin score (mRSS), skin thickness measured by HFUS, and skin stiffness by SWE. Clinical features, including age, sex, body mass index, and disease duration, were collected. RESULTS: The diffuse SSc patients had higher skin stiffness at most sites (P<0.05), except for the finger, foot, and forehead, and a thicker skin layer at most sites (P<0.05), except for the finger. The area under the curve (AUC) of HFUS, SWE, and the combination of the two in distinguishing diffused and limited SSc were 0.866, 0.921, and 0.973, respectively. The differences were statistically significant (combination vs. SWE, P=0.002, combination vs. HFUS, P=0.021). Longer disease duration was associated with a thinner skin layer at the forearm, arm, chest wall, abdominal wall, and thigh in limited SSc, including the leg in diffused SSc. SWE was less affected by clinical features than HFUS. SWE could achieve greater discrimination between different mRSSs at multiple sites, such as fingers and arms, than HFUS. CONCLUSION: For the assessment of SSc skin, SWE has several advantages over HFUS, including less influence by clinical features and greater sensitivity to discriminate different mRSSs. SWE has the potential to become a primary imaging assessment tool as well as HFUS.
 PURPOSE: Despite the usefulness of blood oxygenation level-dependent (BOLD) MRI in assessing glomerulonephritis activity, its relationship with histological findings remains unclear. Because glomerulonephritis presents multiple complex injury patterns, analysis of each pattern is essential. We aimed to elucidate the relationship between the histological findings of the kidney and BOLD MRI findings in mesangial proliferative glomerulonephritis. METHODS: Children under 16 years of age diagnosed with mesangial proliferative glomerulonephritis by kidney biopsy at our university hospital between January 2013 and September 2022 were included in this study. Cortical and medullary spin relaxation rate (R2*) values were measured using BOLD MRI at 3T within two weeks before and after the kidney biopsy. The R2* values, including the fluctuations with low-dose oxygen administration, were retrospectively examined in relation to the cortical (mesangial proliferation, endothelial cell proliferation, crescent, sclerosis, and fibrosis) and medullary findings (fibrosis). RESULTS: Sixteen times kidney biopsies were performed for glomerulonephritis during the study period, and one patient was excluded because of comorbidities; the remaining 14 patients included six boys with a mean age of 11.9 ± 3.5 years at the BOLD examination. None of the patients had medullary fibrosis. Among the kidney tissue parameters, only sclerosis showed a significant correlation with R2* values: medulla with R2* values under atmospheric pressure (r = 0.53, P < 0.05) and cortex with the rate of change in R2* values with low-dose oxygen administration (r = -0.57, P < 0.03). In the multiple regression analysis, only sclerosis was an independent contributor to the change in R2* values with oxygen administration in the cortex (regression coefficient -0.109, P < 0.05). CONCLUSION: Since the R2* values reflect histological changes in the kidney, BOLD MRI may facilitate the evaluation of mesangial proliferative glomerulonephritis, potentially reducing the patient burden.
 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that leads to death by progressive paralysis and respiratory failure within 2-4 years of onset. About 90-95% of ALS cases are sporadic (sALS), and 5-10% are inherited through family (fALS). Though the mechanisms of the disease are still poorly understood, so far, approximately 40 genes have been reported as ALS causative genes. The mutations in some crucial genes, like SOD1, C9ORF72, FUS, and TDP-43, are majorly associated with ALS, resulting in ROS-associated oxidative stress, excitotoxicity, protein aggregation, altered RNA processing, axonal and vesicular trafficking dysregulation, and mitochondrial dysfunction. Recent studies show that dysfunctional cellular pathways get restored as a result of the repair of a single pathway in ALS. In this review article, our aim is to identify putative targets for therapeutic development and the importance of a single suppressor to reduce multiple symptoms by focusing on important mutations and the phenotypic suppressors of dysfunctional cellular pathways in crucial genes as reported by other studies.
 Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative condition, triggered by various factors causing the degeneration of upper and lower motor neurons, resulting in progressive muscle wasting, paralysis, and death. Multiple in vivo and in vitro models have been established to unravel the molecular events leading to the deterioration of motor neurons in ALS. The canonical and non-canonical Wnt signaling pathway has been implicated to play a crucial role in the progression of neurodegenerative disorders. This review discusses the role of Wnt signaling in the reported causes of ALS such as oxidative stress, mitochondrial dysfunction, autophagy, and apoptosis. Mutations in ALS-associated genes such as SOD1, C9orf72, TDP43, FUS, and OPTN cause an imbalance in neuronal integrity and homeostasis leading to motor neuron demise. Wnt signaling is also observed to play a crucial role in the muscle sparing of oculomotor neurons. The non-canonical Wnt/Ca(2+) pathway which regulates intrinsic electrophysiological properties and mobilizes calcium ions to maintain neuronal integrity has been found to be altered in the stem cell-derived ALS model. Thus, the interplay of dysregulated canonical and non-canonical Wnt pathways in multiple motor neuron disease models has shown that Wnt contributes to disease progression indicating it to be utilized as a potential target for ALS.
 OBJECTIVE: The objective of this study is to explore the role of adjunctive percutaneous revascularization of the hand in the management of patients with systemic sclerosis-associated refractory digital ischemia. METHODS: We present our initial experience of using percutaneous upper extremity interventions to treat patients with systemic sclerosis and symptomatic Raynaud's phenomenon who presented with either refractory digital ischemia or non-healing ulcers. We discuss patient characteristics, procedural findings, and short-term clinical outcomes of these interventions. RESULTS: We performed 14 interventions in 6 patients with non-healing digital ulcers or refractory ischemia secondary to systemic sclerosis. Angioplasty was performed at or below the wrist in conjunction with intravenous prostaglandin therapy, started prior to or immediately after the revascularization procedure. All patients experienced symptomatic relief and demonstrated accelerated wound healing. Two patients required an additional procedure to treat recurrent ischemia (without new ulceration) in the treated digit. Three of the patients underwent multiple procedures during the study period to treat new ischemic lesions or Raynaud's phenomenon symptoms, highlighting the progressive nature of the vascular occlusions in systemic sclerosis. There were no adverse events related to the interventions. CONCLUSIONS: Our retrospective analysis suggests that percutaneous revascularization in combination with vasodilator therapy in systemic sclerosis-associated digital ischemia is safe and can facilitate the healing of long-standing ulcers. Its role in the management of refractory digital ischemia in patients with systemic sclerosis should be explored further.
 The multiple functions of mitochondria, including adenosine triphosphate synthesis, are controlled by the coordination of both the mitochondrial DNA (mtDNA) and the nuclear DNA (nDNA) genomes. Mitochondrial disorders manifest because of impairment of energy metabolism. This article focuses on mutations in two nuclear genes and their effect on mitochondrial function. Mutations in the polymerase gamma, or POLG, gene are associated with multisystemic disease processes, including Alpers Syndrome, a severe childhood-onset syndrome. Mutations in the OPA1 gene are associated with autosomal dominant optic atrophy and other neurologic, musculoskeletal, and ophthalmologic symptoms. When assessing for disorders affecting energy metabolism, sequencing of both the mtDNA genome and the nDNA whole exome sequencing is necessary.
 Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder characterized by the presence of hamartomas in multiple organs. At the molecular level, the disease is caused by pathogenic variants in the TSC1 and TSC2 genes, and only 10% to 25% of clinically diagnosed patients remain negative after multiplex ligation-dependent probe amplification and exon sequencing of both genes. Here, to improve the molecular diagnosis of TSC, we developed an integral approach that includes multiplex ligation-dependent probe amplification and deep-coverage next-generation sequencing of the entire TSC1 and TSC2 genes, along with an adapted bioinformatic pipeline to detect variants at low allele frequencies (>1%). Using this workflow, the molecular cause was identified in 29 of 42 patients with TSC, describing here, for the first time, 12 novel pathogenic variants in TSC genes. These variants included seven splicing variants, five of which were studied at the cDNA level, determining their effect on splicing. In addition, 8 of the 29 pathogenic variants were detected in mosaicism, including four patients with previous negative study results who presented extremely low mosaic variants (allele frequency, <16%). We demonstrate that this integral approach allows the molecular diagnosis of patients with TSC and improves the conventional one by adapting the technology to the detection of low-frequency mosaics.
 Amyotrophic lateral sclerosis (ALS) is an adult-onset disease which causes the progressive degeneration of cortical and spinal motoneurons, leading to death a few years after the first symptom onset. ALS is mainly a sporadic disorder, and its causative mechanisms are mostly unclear. About 5-10% of cases have a genetic inheritance, and the study of ALS-associated genes has been fundamental in defining the pathological pathways likely also involved in the sporadic forms of the disease. Mutations affecting the DJ-1 gene appear to explain a subset of familial ALS forms. DJ-1 is involved in multiple molecular mechanisms, acting primarily as a protective agent against oxidative stress. Here, we focus on the involvement of DJ-1 in interconnected cellular functions related to mitochondrial homeostasis, reactive oxygen species (ROS) levels, energy metabolism, and hypoxia response, in both physiological and pathological conditions. We discuss the possibility that impairments in one of these pathways may affect the others, contributing to a pathological background in which additional environmental or genetic factors may act in favor of the onset and/or progression of ALS. These pathways may represent potential therapeutic targets to reduce the likelihood of developing ALS and/or slow disease progression.
 BACKGROUND: we aimed to estimate the prevalence of Amino acyl-transfer ribonucleic acid synthetase antibodies (Anti-ARS); myositis specific antibodies, among patients with systemic sclerosis (SSc), to evaluate the clinical associations of anti-ARS antibodies in SSc patients and to identify risk factors for development of interstitial lung disease (ILD) in SSc. METHODS: A prospective study of 71 systemic sclerosis patients in our rheumatology clinic in Israel. Sera were tested for myositis antibodies. Data on patients clinical and serological manifestations and treatment were collected and compared according to anti-ARS antibodies and ILD. RESULTS: Prevalence of anti-ARS antibodies was 6% (4/71) with anti PL-7, anti- OJ and Jo-1 positivity. Anti Ro-52 was found in 27%, anti-PM/Scl 75, anti-PM/Scl 100 and anti-SRP in 6%, anti-Ku in 3%, anti-Mi-2 beta and anti-Mi-2 alfa in 4%, anti- NXP2 and anti-TIF1gamma in 1%. ILD complication was observed in 42% of patients and was associated with anti RNAP-III, anti Scl-70 and Anti-ARS antibodies. In multiple logistic regression, anti Scl-70 was associated with 6-fold higher risk for ILD. CONCLUSION: Anti-ARS antibodies were observed in 6% of SSc patients. All of them had ILD. Due to the low prevalence of anti-ARS, this study could not describe clinical associations of anti-ARS antibodies in SSc patients.
 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder in which patients lose motor functions due to progressive loss of motor neurons in the cortex, brainstem, and spinal cord. Whilst the loss of neurons is central to the disease, it is becoming clear that glia, specifically astrocytes, contribute to the onset and progression of neurodegeneration. Astrocytes play an important role in maintaining ion homeostasis in the extracellular milieu and regulate multiple brain functions by altering their extracellular concentrations. In this study, we have investigated the ability of astrocytes to maintain K(+) homeostasis in the brain via direct measurement of the astrocytic K(+) clearance rate in the motor and somatosensory cortices of an ALS mouse model (SOD1(G93A) ). Using electrophysiological recordings from acute brain slices, we show region-specific alterations in the K(+) clearance rate, which was significantly reduced in the primary motor cortex but not the somatosensory cortex. This decrease was accompanied by significant changes in astrocytic morphology, impaired conductivity via Kir4.1 channels and low coupling ratio in astrocytic networks in the motor cortex, which affected their ability to form the K(+) gradient needed to disperse K(+) through the astrocytic syncytium. These findings indicate that the supportive function astrocytes typically provide to motoneurons is diminished during disease progression and provides a potential explanation for the increased vulnerability of motoneurons in ALS.
 Scleroderma, or systemic sclerosis, is a multisystem autoimmune disorder characterized by hardening and fibrosis of the skin. To date, only a small number of case reports have established a relationship between scleroderma and external cervical resorption (ECR). The aim of this case report is to document the case of a patient with multiple external cervical resorption lesions, who was referred to our unit. A 54-year-old female patient, with a 10-year history of systemic sclerosis diagnosed by her rheumatologist, was referred to our unit regarding extensive ECR. A total of 14 maxillary and mandibular teeth with ECR were detected by clinical examination and cone-beam computed tomography. The characteristic vascularity of resorptive defects with profuse bleeding upon probing was not evident. The patient declined any active treatment owing to the desire to avoid lengthy and unpredictable treatment, which may hasten the loss of her teeth. General practitioners should be aware of the relationship between connective tissue disorders and ECR. Although not well established in the literature, the vascular changes implicated in scleroderma may stimulate the odontoclastic processes involved in ECR.
 We report the case of a massive fetal cardiac rhabdomyoma recently occurred at our clinic. A woman at 23 weeks of gestational age was referred to our center for a fetal cardiac echogenic mass of 26 mm detected at the second-trimester screening ultrasound. During pregnancy, though, the mass progressively increased its dimensions until reaching 48 mm in diameter at 37 weeks of gestation. Fetal echoencephalography and brain magnetic resonance did not show any further fetal anomalies, but molecular genetic testing at amniocentesis revealed a heterozygotic missense variant of gene TSC2 associated with Tuberous Sclerosis. The mass was therefore most likely preferable to a single large rhabdomyoma of gradually increasing dimensions. The baby was delivered at term with a cesarean section. Because of the rhabdomyoma remarkable size and newborn ECG electrical alterations, postnatal therapies with Flecainide and Everolimus were started. Everolimus treatment led to a significant and progressive reduction in the cardiac mass volume. This case, therefore, shows the efficacy of what seems to be a promising treatment in pediatric patients with large rhabdomyomas.Learning points:Rhabdomyomas may present with different features: most often they appear as multiple masses along the interventricular sept, but they may also appear as a single large thoracic mass.When a rhabdomyoma is suspected, genetic counseling is recommended.Both before and after birth, a multidisciplinary approach is useful to choose the appropriate therapy for the newborn.mTOR inhibitors therapies look like promising therapeutic approaches to stimulate the involution of rhabdomyomas.
 Amyotrophic Lateral Sclerosis (ALS) is the most common, adult-onset, progressive motor neurodegenerative disorder that results in death within 3 years of the clinical diagnosis. Due to the clinicopathological heterogeneity, any reliable biomarkers for diagnosis or prognosis of ALS have not been identified till date. Moreover, the only three clinically approved treatments are not uniformly effective in slowing the disease progression. Over the last 15 years, there has been a rapid advancement in research on the complex pathomechanistic landscape of ALS that has opened up new avenues for successful clinical translation of targeted therapeutics. Multiple studies suggest that the age-dependent interaction of risk-associated genes with environmental factors and endogenous modifiers is critical to the multi-step process of ALS pathogenesis. In this review, we provide an updated discussion on the dysregulated cross-talk between intracellular homeostasis processes, the unique molecular networks across selectively vulnerable cell types, and the multisystemic nature of ALS pathomechanisms. Importantly, this work highlights the alteration in epigenetic and epitranscriptomic landscape due to gene-environment interactions, which have been largely overlooked in the context of ALS pathology. Finally, we suggest that precision medicine research in ALS will be largely benefitted from the stratification of patient groups based on the clinical phenotype, onset and progression, genome, exposome, and metabolic identities.
 BACKGROUND: In a chronic and progressive disease such as multiple sclerosis (MS), the improvement on Expanded Disability Status Scale (EDSS) can be a transient event. Therefore, estimating the prevalence of disability improvement over time, accounting both for improvement incidence and duration, is of interest. The aim of this study was to show the application of a simple estimator for the proportion of patients with sustained improvement over time using data from the long-term extension of the PRISMS trial. METHODS: A total of 534 relapsing-remitting MS (RRMS) patients from the PRISMS trial were included. Patients with a baseline EDSS of 0 were excluded. Patients were randomized to placebo (n = 178), subcutaneous interferon beta-1a (sc IFN β-1a) 22 µg (n = 181) or sc IFN β-1a 44 µg (n = 175). At Year 2, patients receiving placebo were re-randomized to sc IFN β-1a 22 µg or 44 µg (delayed sc IFN β-1a) while patients receiving sc IFN β-1a 22 µg or 44 µg continued their initial regimen. Patients were followed up for over 7 years post-randomization. Disability improvement was defined as a 1-point decrease in EDSS from baseline confirmed at 6 months. Prevalence of improvement was estimated as difference of Kaplan-Meier (KM) estimators while the cumulative incidence of improvement was calculated using the standard KM curves. RESULTS: No significant differences in cumulative incidence of EDSS improvement at 3 years between delayed sc IFN β-1a (20.3%) and sc IFN β-1a 22 µg (20.8%; p = 0.49) or 44 µg (21.3%; p = 0.33). When taking duration of improvement into account, the proportion of patients showing an improved condition after 3 years was 10.1% with delayed sc IFN β-1a, 11.3% with sc IFN β-1a 22 µg (p = 0.17) and 15.4% with sc IFN β-1a 44 µg (p = 0.037) that was substantially maintained over the long term. CONCLUSIONS: With the use of this new statistical methodology, it is possible to estimate the time to improvement as well as the duration of improvement, information that is better suited to describing a non-final outcome like disability improvement. In this case, early sc IFN β-1a 44 µg initiation had a greater proportion of patients with a sustained disability improvement over a long period of follow-up as compared to patients who had initially been randomized to placebo. In contrast, no significant differences on the cumulative incidence of improvement were observed.
 BACKGROUND: Rheumatoid arthritis (RA) shares genetic variants with other autoimmune conditions, but existing studies test the association between RA variants with a pre-defined set of phenotypes. The objective of this study was to perform a large-scale, systemic screen to determine phenotypes that share genetic architecture with RA to inform our understanding of shared pathways. METHODS: In the UK Biobank (UKB), we constructed RA genetic risk scores (GRS) incorporating human leukocyte antigen (HLA) and non-HLA risk alleles. Phenotypes were defined using groupings of International Classification of Diseases (ICD) codes. Patients with an RA code were excluded to mitigate the possibility of associations being driven by the diagnosis or management of RA. We performed a phenome-wide association study, testing the association between the RA GRS with phenotypes using multivariate generalized estimating equations that adjusted for age, sex, and first five principal components. Statistical significance was defined using Bonferroni correction. Results were replicated in an independent cohort and replicated phenotypes were validated using medical record review of patients. FINDINGS: We studied n = 316,166 subjects from UKB without evidence of RA and screened for association between the RA GRS and n = 1317 phenotypes. In the UKB, 20 phenotypes were significantly associated with the RA GRS, of which 13 (65%) were immune mediated conditions including polymyalgia rheumatica, granulomatosis with polyangiitis (GPA), type 1 diabetes, and multiple sclerosis. We further identified a novel association in Celiac disease where the HLA and non-HLA alleles had strong associations in opposite directions. Strikingly, we observed that the non-HLA GRS was exclusively associated with greater risk of the validated conditions, suggesting shared underlying pathways outside the HLA region. INTERPRETATION: This study replicated and identified novel autoimmune phenotypes verified by medical record review that share immune pathways with RA and may inform opportunities for shared treatment targets, as well as risk assessment for conditions with a paucity of genomic data, such as GPA. FUNDING: This research was funded by the US National Institutes of Health (P30AR072577, R21AR078339, R35GM142879, T32AR007530) and the Harold and DuVal Bowen Fund.
 Cannabidiol (CBD) is a non-psychoactive cannabinoid purported to reduce symptoms of discomfort. Individuals are now using CBD to treat symptoms of multiple sclerosis, seizures, and chronic pain. Animal models indicate that CBD may be effective at reducing inflammation post fatiguing exercise. However, little evidence is available to evaluate these findings in humans. Therefore, the purpose of this investigation was to evaluate the impact of two doses of CBD oil on inflammation (IL-6), performance, and pain after an eccentric loading protocol. Participants (n = 4) participated in three conditions (placebo, low dose, and high dose), in this randomized, counterbalanced design. Each condition took 72 hours to complete, with a 1-week washout period between conditions. At the beginning of each week, participants were subjected to a loading protocol of six sets of ten eccentric only repetitions in the single-arm bicep curl. Participants consumed capsules of either a placebo, low dose (2mg/kg) or high dose (10mg/kg) of CBD oil immediately following the session and continued every twelve hours for 48 hours. Venipunctures were taken before exercise and repeated at 24, 48, and 72 hours post exercise. Blood samples were centrifuged for 15 minutes in gel and lithium heparin vacutainers. Plasma was separated from cells and stored at -80° until analysis. Samples were analyzed using an immunometric assay for IL-6 (ELISA). Data were analyzed using a three (condition) by four (time) repeated measure ANOVA. There were no differences in inflammation between conditions (F(2,6) = 0.726, p = 0.522, n(p) (2) = 0.195) or across time (F(3,9) = 0.752, p = 0.548, n(p) (2) = 0.200), handgrip strength between conditions (F(2,6) = 0.542, p = 0.607, n(p) (2) = .153) or across time (F(3,9) = 2.235, p = .153, n(p) (2) = .427), or bicep curl strength between conditions (F(2,6) = 0.675, p = 0.554, n(p) (2) = .184) or across time (F(3,9) = 3.513, p = .150, n(p) (2) = .539). There were no differences in pain between conditions (F(2,6) = 0.495, p = 0.633, n(p) (2) = .142), but there was a difference across time (F(3,9) = 7.028, p = .010, n(p) (2) = .701). There were no significant interactions to note. Although there was no statistical significance between conditions (likely due to the low sample size), there was a visible increase in IL-6 48 (4.88 ± 6.53) and 72 hours (3.12 ± 4.26) post exercise in the placebo condition which was not observed in the low (48: 0.35 ± 2.22; 72: 1.34 ± 5.6) and high dose condition (48: 1.34 ± 1.34; 72: -0.79 ± 5.34). Future investigations should consider implementing eccentric resistance training across a larger portion of the body to improve ecological validity of the exercise. A larger sample would reduce risk of researchers committing a type II statistical error and give strength to detecting differences between conditions.
 Molecular docking is a key method used in virtual screening (VS) campaigns to identify small-molecule ligands for drug discovery targets. While docking provides a tangible way to understand and predict the protein-ligand complex formation, the docking algorithms are often unable to separate active ligands from inactive molecules in practical VS usage. Here, a novel docking and shape-focused pharmacophore VS protocol is demonstrated for facilitating effective hit discovery using retinoic acid receptor-related orphan receptor gamma t (RORγt) as a case study. RORγt is a prospective target for treating inflammatory diseases such as psoriasis and multiple sclerosis. First, a commercial molecular database was flexibly docked. Second, the alternative docking poses were rescored against the shape/electrostatic potential of negative image-based (NIB) models that mirror the target's binding cavity. The compositions of the NIB models were optimized via iterative trimming and benchmarking using a greedy search-driven algorithm or brute force NIB optimization. Third, a pharmacophore point-based filtering was performed to focus the hit identification on the known RORγt activity hotspots. Fourth, free energy binding affinity evaluation was performed on the remaining molecules. Finally, twenty-eight compounds were selected for in vitro testing and eight compounds were determined to be low μM range RORγt inhibitors, thereby showing that the introduced VS protocol generated an effective hit rate of ~29%.
 OBJECTIVES: This study aims to evaluate the utility of simultaneous multislice (SMS) acceleration for routine magnetic resonance neurography (MRN) at 3 T. MATERIALS AND METHODS: Patients with multiple sclerosis underwent MRN of the sciatic nerve consisting of a standard fat-saturated T2-weighted turbo spin echo (TSE) sequence using integrated parallel acquisition technique (PAT2) acceleration and 2 T2 TSE sequences using a combination of PAT-SMS acceleration (1) to reduce scan time (PAT2-SMS2; SMS-TSE FAST ) and (2) for time neutral increase of in-plane resolution (PAT1-SMS2; SMS-TSE HR ). Acquisition times were 5:29 minutes for the standard T2 TSE, 3:12 minutes for the SMS-TSE FAST , and 5:24 minutes for the SMS-TSE HR . Six qualitative imaging parameters were analyzed by 2 blinded readers using a 5-point Likert scale and T2 nerve lesions were quantified, respectively. Qualitative and quantitative image parameters were compared, and both interrater and intrarater reproducibility were statistically assessed. In addition, signal-to-noise ratio/contrast-to-noise ratio (CNR) was obtained in healthy controls using the exact same imaging protocol. RESULTS: A total of 15 patients with MS (mean age ± standard deviation, 38.1 ± 11 years) and 10 healthy controls (mean age, 29.1 ± 7 years) were enrolled in this study. CNR analysis was highly reliable (intraclass correlation coefficient, 0.755-0.948) and revealed a significant CNR decrease for the sciatic nerve for both SMS protocols compared with standard T2 TSE (SMS-TSE FAST /SMS-TSE HR , -39%/-55%; P ≤ 0.01). Intrarater and interrater reliability of qualitative image review was good to excellent (κ: 0.672-0.971/0.617-0.883). Compared with the standard T2 TSE sequence, both SMS methods were shown to be superior in reducing pulsatile flow artifacts ( P < 0.01). Ratings for muscle border sharpness, detailed muscle structures, nerve border sharpness, and nerve fascicular structure did not differ significantly between the standard T2 TSE and the SMS-TSE FAST ( P > 0.05) and were significantly better for the SMS-TSE HR than for standard T2 TSE ( P < 0.001). Muscle signal homogeneity was mildly inferior for both SMS-TSE FAST ( P > 0.05) and SMS-TSE HR ( P < 0.001). A significantly higher number of T2 nerve lesions were detected by SMS-TSE HR ( P ≤ 0.01) compared with the standard T2 TSE and SMS-TSE FAST , whereas no significant difference was observed between the standard T2 TSE and SMS-TSE FAST . CONCLUSIONS: Implementation of SMS offers either to substantially reduce acquisition time by over 40% without significantly impeding image quality compared with the standard T2 TSE or to increase in-plane resolution for a high-resolution approach and improved depiction of T2 nerve lesions while keeping acquisition times constant. This addresses the specific needs of MRN by providing different imaging approaches for 2D clinical MRN.
 Abnormal myelination underlies the pathology of white matter diseases such as preterm white matter injury and multiple sclerosis. Osteopontin (OPN) has been suggested to play a role in myelination. Murine OPN mRNA is translated into a secreted isoform (sOPN) or an intracellular isoform (iOPN). Whether there is an isoform-specific involvement of OPN in myelination is unknown. Here we generated mouse models that either lacked both OPN isoforms in all cells (OPN-KO) or lacked sOPN systemically but expressed iOPN specifically in oligodendrocytes (OLs-iOPN-KI). Transcriptome analysis of isolated oligodendrocytes from the neonatal brain showed that genes and pathways related to increase of myelination and altered cell cycle control were enriched in the absence of the two OPN isoforms in OPN-KO mice compared to control mice. Accordingly, adult OPN-KO mice showed an increased axonal myelination, as revealed by transmission electron microscopy imaging, and increased expression of myelin-related proteins. In contrast, neonatal oligodendrocytes from OLs-iOPN-KI mice compared to control mice showed differential regulation of genes and pathways related to the increase of cell adhesion, motility, and vasculature development, and the decrease of axonal/neuronal development. OLs-iOPN-KI mice showed abnormal myelin formation in the early phase of myelination in young mice and signs of axonal degeneration in adulthood. These results suggest an OPN isoform-specific involvement, and a possible interplay between the isoforms, in myelination, and axonal integrity. Thus, the two isoforms of OPN need to be separately considered in therapeutic strategies targeting OPN in white matter injury and diseases.
 Myelinating oligodendrocytes are essential for neuronal communication and homeostasis of the central nervous system (CNS). One of the most abundant molecules in the mammalian CNS is N-acetylaspartate (NAA), which is catabolized into L-aspartate and acetate by the enzyme aspartoacylase (ASPA) in oligodendrocytes. The resulting acetate moiety is thought to contribute to myelin lipid synthesis. In addition, affected NAA metabolism has been implicated in several neurological disorders, including leukodystrophies and demyelinating diseases such as multiple sclerosis. Genetic disruption of ASPA function causes Canavan disease, which is hallmarked by increased NAA levels, myelin and neuronal loss, large vacuole formation in the CNS, and early death in childhood. Although NAA's direct role in the CNS is inconclusive, in peripheral adipose tissue, NAA-derived acetate has been found to modify histones, a mechanism known to be involved in epigenetic regulation of cell differentiation. We hypothesize that a lack of cellular differentiation in the brain contributes to the disruption of myelination and neurodegeneration in diseases with altered NAA metabolism, such as Canavan disease. Our study demonstrates that loss of functional Aspa in mice disrupts myelination and shifts the transcriptional expression of neuronal and oligodendrocyte markers towards less differentiated stages in a spatiotemporal manner. Upon re-expression of ASPA, these oligodendrocyte and neuronal lineage markers are either improved or normalized, suggesting that NAA breakdown by Aspa plays an essential role in the maturation of neurons and oligodendrocytes. Also, this effect of ASPA re-expression is blunted in old mice, potentially due to limited ability of neuronal, rather than oligodendrocyte, recovery.
 Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder that can involve multiple organ systems. Diagnosis is based on independent clinical diagnostic criteria and genetic diagnostic criteria (pathogenic variants on TSC1 and TSC2 genes). To make a definitive diagnosis can be especially difficult in oligosymptomatic or asymptomatic patients and in those patients with genetic variants of uncertain significance (VUS). Early diagnosis and lifelong surveillance are paramount to avoid morbidity and potentially life-threatening complications. To increase diagnostic sensibility, less known manifestations of TSC can be helpful. Herein we show a case in which SBLs were used as a diagnostic clue to help diagnose three generations of oligosymptomatic TSC carrying a VUS in TSC1. SBLs are commonly detected in imaging studies of patients with TSC and have been recently included as a minor clinical diagnostic criterion. Clinicians and radiologists should be aware of their significance as they can be mistaken with osteoblastic metastases.
 Neurodegenerative diseases are characterized by the progressive decline of neuronal function in several brain areas, and are always associated with cognitive, psychiatric, or motor deficits due to the atrophy of certain neuronal populations. Most neurodegenerative diseases share common pathological mechanisms, such as neurotoxic protein misfolding, oxidative stress, and impairment of autophagy machinery. Amyotrophic lateral sclerosis (ALS) is one of the most common adult-onset motor neuron disorders worldwide. It is clinically characterized by the selective and progressive loss of motor neurons in the motor cortex, brain stem, and spinal cord, ultimately leading to muscle atrophy and rapidly progressive paralysis. Multiple recent studies have indicated that the amyloid precursor protein (APP) and its proteolytic fragments are not only drivers of Alzheimer's disease (AD) but also one of the earliest signatures in ALS, preceding or anticipating neuromuscular junction instability and denervation. Indeed, altered levels of APP peptides have been found in the brain, muscles, skin, and cerebrospinal fluid of ALS patients. In this short review, we discuss the nature and extent of research evidence on the role of APP peptides in ALS, focusing on the intracellular C-terminal peptide and its regulatory motif (682)YENPTY(687), with the overall aim of providing new frameworks and perspectives for intervention and identifying key questions for future investigations.
 BACKGROUND AND OBJECTIVES: CTLA4 deficiency (CTLA4d) is a disease with multisystem auto-immune features, including neurological manifestations. We aimed to describe neurological involvement in these patients. METHODS: We performed a cross-sectional observational study using the French Reference Centre for Primary Immunodeficiencies (CEREDIH) registry, plus a surveillance in national society networks. Participants with confirmed CTLA4d and neurological involvement were included. Clinical, laboratory and radiological features were collected, as well as treatments. Available MRI were double-reviewed. RESULTS: Among 70 patients with CTLA4d, 13 patients (21%) had neurological involvement. Neurological symptoms began at a median age of 18 [15-45] years, mostly occurring after systemic manifestations (median delay: 8.5 [4.5-10.5] years). Main symptoms included headaches, focal deficit (54% each) and seizures (38%). MRI detected at least one large contrast-enhancing lesion in eight patients. Lesions reminiscent of multiple sclerosis lesions were found in six patients. Cerebellar (6 patients) and large spinal cord lesions (3 patients) were common. Ten patients were treated with Abatacept, of whom nine (90%) showed good clinical and radiological response. DISCUSSION: Neurologic involvement is common among patients with CTLA4d. Despite its rarity, and considering the suspected efficacy of Abatacept, neurologists should be aware of the characteristics of CTLA4d neurological involvement.
 Blood protein extravasation through a disrupted blood-brain barrier and innate immune activation are hallmarks of neurological diseases and emerging therapeutic targets. However, how blood proteins polarize innate immune cells remains largely unknown. Here, we established an unbiased blood-innate immunity multiomic and genetic loss-of-function pipeline to define the transcriptome and global phosphoproteome of blood-induced innate immune polarization and its role in microglia neurotoxicity. Blood induced widespread microglial transcriptional changes, including changes involving oxidative stress and neurodegenerative genes. Comparative functional multiomics showed that blood proteins induce distinct receptor-mediated transcriptional programs in microglia and macrophages, such as redox, type I interferon and lymphocyte recruitment. Deletion of the blood coagulation factor fibrinogen largely reversed blood-induced microglia neurodegenerative signatures. Genetic elimination of the fibrinogen-binding motif to CD11b in Alzheimer's disease mice reduced microglial lipid metabolism and neurodegenerative signatures that were shared with autoimmune-driven neuroinflammation in multiple sclerosis mice. Our data provide an interactive resource for investigation of the immunology of blood proteins that could support therapeutic targeting of microglia activation by immune and vascular signals.
 BACKGROUND: Neuromyelitis optica spectrum disorders (NMOSD) most commonly cause severe disability which is related to disease attacks. However, some patients retain good neurological function for a long time after disease onset. OBJECTIVES: To determine the frequency, demographic and the clinical features of good outcome NMOSD, and analyze their predictive factors. METHODS: We selected patients who met the 2015 International Panel for NMOSD diagnostic criteria from seven MS Centers. Assessed data included age at disease onset, sex, race, number of attacks within the first and three years from onset, annualized relapsing rate (ARR), total number of attacks, aquaporin-IgG serum status, presence of cerebrospinal fluid (CSF)-specific oligoclonal bands (OCB) and the Expanded Disability Status Scale (EDSS) score at the last follow-up visit. NMOSD was classified as non-benign if patients developed sustained EDSS score >3.0 during the disease course, or benign if patients had EDSS score ≤3.0 after ≥15 years from disease onset. Patients with EDSS <3.0 and disease duration shorter than 15 years were not qualified for classification. We compared the demographic and clinical characteristics of benign and non-benign NMOSD. Logistic regression analysis identified predictive factors of outcome. RESULTS: There were 16 patients with benign NMOSD (3% of the entire cohort; 4.2% of those qualified for classification; and 4.1% of those who tested positive for aquaporin 4-IgG), and 362 (67.7%) with non-benign NMOSD, whereas 157 (29.3%) did not qualify for classification. All patients with benign NMOSD were female, 75% were Caucasian, 75% tested positive for AQP4-IgG, and 28.6% had CSF-specific OCB. Regression analysis showed that female sex, pediatric onset, and optic neuritis, area postrema syndrome, and brainstem symptoms at disease onset, as well as fewer relapses in the first year and three years from onset, and CSF-specific OCB were more commonly found in benign NMOSD, but the difference did not reach statistical significance. Conversely, non-Caucasian race (OR: 0.29, 95% CI: 0.07-0.99; p = 0.038), myelitis at disease presentation (OR: 0.07, 95% CI: 0.01-0.52; p <0.001), and high ARR (OR: 0.07, 95% CI: 0.01-0.67; p = 0.011) were negative risk factors for benign NMOSD. CONCLUSION: Benign NMOSD is very rare and occurs more frequently in Caucasians, patients with low ARR, and those who do not have myelitis at disease onset.
 Necroptosis has been implicated in various inflammatory diseases including tumor-necrosis factor-α (TNF-α)-induced systemic inflammatory response syndrome (SIRS). Dimethyl fumarate (DMF), a first-line drug for treating relapsing-remitting multiple sclerosis (RRMS), has been shown to be effective against various inflammatory diseases. However, it is still unclear whether DMF can inhibit necroptosis and confer protection against SIRS. In this study, we found that DMF significantly inhibited necroptotic cell death in macrophages induced by different necroptotic stimulations. Both the autophosphorylation of receptor-interacting serine/threonine kinase 1 (RIPK1) and RIPK3 and the downstream phosphorylation and oligomerization of MLKL were robustly suppressed by DMF. Accompanying the suppression of necroptotic signaling, DMF blocked the mitochondrial reverse electron transport (RET) induced by necroptotic stimulation, which was associated with its electrophilic property. Several well-known anti-RET reagents also markedly inhibited the activation of the RIPK1-RIPK3-MLKL axis accompanied by decreased necrotic cell death, indicating a critical role of RET in necroptotic signaling. DMF and other anti-RET reagents suppressed the ubiquitination of RIPK1 and RIPK3, and they attenuated the formation of necrosome. Moreover, oral administration of DMF significantly alleviated the severity of TNF-α-induced SIRS in mice. Consistent with this, DMF mitigated TNF-α-induced cecal, uterine, and lung damage accompanied by diminished RIPK3-MLKL signaling. Collectively, DMF represents a new necroptosis inhibitor that suppresses the RIPK1-RIPK3-MLKL axis through blocking mitochondrial RET. Our study highlights DMF's potential therapeutic applications for treating SIRS-associated diseases.
 Parkinson's disease (PD) is a neurodegenerative disorder that frequently occurs in the older population. Previous epidemiological studies have suggested an association between PD and autoimmune diseases (AIDs). However, some studies have shown conflicting results. This study aimed to summarize existing epidemiological studies on the association between PD with AIDs and to conduct a meta-analysis of combinable results. Four electronic databases (PubMed, Embase, Web of Science Core Collection, and MEDLINE) were searched from each database's inception date until December 12, 2022. All studies that explored the relationship between PD and AIDs were included for quantitative analysis and qualitative review. The pooled relative risk with 95% confidence intervals (CIs) was calculated using a random or fixed effects model. A total of 46 observational studies involving 873,643 patients and 13,402,821 controls were included; ultimately, 38 studies were included in the meta-analysis. The risk of PD combined with AIDs was significantly higher (odds ratio [OR]=1.55, 95% CI: 1.33-1.81), and subgroup analysis found no significant differences in risk by study type, gender, age, and race. Regarding the AID types, the results showed an increased risk of PD combined with bullous pemphigoid (OR=2.67, 95% CI: 2.15-3.31), inflammatory bowel disease (OR=1.30, 95% CI: 1.18-1.45), Crohn's disease (OR=1.30, 95% CI: 1.20-1.42), ulcerative colitis (OR=1.31, 95% CI: 1.14-1.50), Sjögren's syndrome (OR=1.61, 95% CI: 1.24-2.09), and Graves' disease (OR=1.45, 95% CI: 1.24-1.70) than controls. However, there appeared to be no significant association between PD and systemic lupus erythematosus (OR=0.82, 95% CI: 0.66-1.03), multiple sclerosis (OR=2.02, 95% CI: 0.87-4.70), rheumatoid arthritis (OR=0.79, 95% CI: 0.61-1.03), or celiac disease (OR=1.16, 95% CI: 0.79-1.69). This study supports the existence of a strong link between AIDs and PD. When PD and AIDs are identified, clinicians need to be aware of the possibility of coexistence. However, there are some limitations of this study, such as the apparent heterogeneity of some of the results and the fact that most of the included study types were retrospective. Therefore, future larger prospective cohort studies are needed to further explore the interaction between PD and AIDs. SYSTEMATIC REVIEW REGISTRATION: INPLASY, identifier INPLASY202280088.
 The research aimed to evaluate the efficacy of the NeuroAssist, a parallel robotic system comprised of three robotic modules equipped with human-robot interaction capabilities, an internal sensor system for torque monitoring, and an external sensor system for real-time patient monitoring for the motor rehabilitation of the shoulder, elbow, and wrist. The study enrolled 10 consecutive patients with right upper limb paresis caused by stroke, traumatic spinal cord disease, or multiple sclerosis admitted to the Neurology I Department of Cluj-Napoca Emergency County Hospital. The patients were evaluated clinically and electrophysiologically before (T1) and after the intervention (T2). The intervention consisted of five consecutive daily sessions of 30-45 min each of 30 passive repetitive movements performed with the robot. There were significant differences (Wilcoxon signed-rank test) between baseline and end-point clinical parameters, specifically for the Barthel Index (53.00 ± 37.72 vs. 60.50 ± 36.39, p = 0.016) and Activities of Daily Living Index (4.70 ± 3.43 vs. 5.50 ± 3.80, p = 0.038). The goniometric parameters improved: shoulder flexion (70.00 ± 56.61 vs. 80.00 ± 63.59, p = 0.026); wrist flexion/extension (34.00 ± 28.75 vs. 42.50 ± 33.7, p = 0.042)/(30.00 ± 22.97 vs. 41.00 ± 30.62, p = 0.042); ulnar deviation (23.50 ± 19.44 vs. 33.50 ± 24.15, p = 0.027); and radial deviation (17.50 ± 18.14 vs. 27.00 ± 24.85, p = 0.027). There was a difference in muscle activation of the extensor digitorum communis muscle (1.00 ± 0.94 vs. 1.40 ± 1.17, p = 0.046). The optimized and dependable NeuroAssist Robotic System improved shoulder and wrist range of motion and functional scores, regardless of the cause of the motor deficit. However, further investigations are necessary to establish its definite role in motor recovery.
 BACKGROUND: Bafiertam® (monomethyl fumarate [MMF]) and Vumerity® (diroximel fumarate [DRF]) are two FDA approved drug products for the treatment of relapsing forms of multiple sclerosis (MS) to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in adults. Vumerity® is a prodrug of MMF which requires enzymatic conversion of DRF to the active drug MMF, the moiety responsible for the therapeutic efficacy; whereas Bafiertam® contains MMF, providing the active drug directly without any need for enzymatic conversion. OBJECTIVE: The objective of this study was to evaluate the pharmacokinetics and relative bioavailability of MMF from oral administration of two Bafiertam® capsules each containing 95 mg of MMF in comparison to two Vumerity® capsules each containing 231 mg of DRF, the therapeutic doses of each product. METHODS: This was a single-dose, open-label, randomized, 2-way crossover study evaluating two treatments over two periods with a washout interval between treatments. Forty-four healthy male or female subjects were planned to receive each of the two treatments to assure 40 completed dosing: a single dose of 2  ×  95 mg Bafiertam® capsules and a single dose of 2  ×  231 mg Vumerity® capsules under fasting conditions in a randomized crossover fashion. Blood samples were obtained prior to dosing and at prespecified time points through 24 h post-dose to determine plasma concentrations of MMF. MMF pharmacokinetic [PK] parameters were calculated and included maximum observed concentration (C(max)), time to reach C(max) (t(max)), apparent half-life of MMF in plasma (t(1/2)), AUC(0-t) which is the area under the plasma concentration vs. time curve (AUC) from time zero (dosing time) to the last time point, t, with quantifiable MMF concentration, and AUC(0-inf) which is AUC(0-t) plus the extrapolated AUC from time t to infinity. RESULTS: Forty-one subjects completed the study as planned. MMF in Bafiertam® capsules was well and readily absorbed with a median t(max) occurring at 4 h post dose, approximately 1 h later than that of Vumerity® capsules. However, the mean MMF C(max) from Bafiertam® (1969 ng/mL) was higher than that from Vumerity® (1121 ng/mL). The mean MMF AUC(0-t) and AUC(0-inf) from Bafiertam® (3503 and 3531 h*ng/mL) were also higher than those from Vumerity® (3123 and 3227 h*ng/mL), respectively. The geometric least-squares mean (GLSM) ratios (90% confidence interval), Bafiertam® vs. Vumerity®, for MMF C(max,) AUC(0-t) and AUC(0-inf) were 181.8 (158.2 - 208.8)%, 116.8 (107.9-126.5)% and 113.8 (105.3 - 123.0)%, respectively.  Both products were safe and well tolerated, as expected, with flushing being the most common adverse event for both products. CONCLUSIONS: The mean MMF AUC(0-t) and AUC(0-inf) were 14-17% higher after administration of Bafiertam® as compared to Vumerity® at their respective therapeutic doses under fasting conditions, however, this difference was not statistically or clinically significant. Although more clinical studies would be needed before making strong recommendations, results of this study may help with selecting appropriate fumarate products, especially when administering the product with food is clinically recommended.
 BACKGROUND AND PURPOSE: Improvement of cognitive deficits in schizophrenia remains an unmet need owing to the lack of new therapies and drugs. Recent studies have reported that fingolimod, an immunomodulatory drug for treating multiple sclerosis, demonstrates anti-inflammatory and neuroprotective effects in several neurological disease models. This suggests its usefulness for ameliorating cognitive dysfunction in schizophrenia. Herein, we assessed the efficacy profile and mechanism of fingolimod in a rat model of phencyclidine (PCP)-induced schizophrenia. EXPERIMENTAL APPROACH: Male Sprague-Dawley rats were treated with PCP for 14 days. The therapeutic effect of fingolimod on cognitive function was assessed using the Morris water maze and fear conditioning tests. Hippocampal neurogenesis and the expression of astrocytes and microglia were evaluated using immunostaining. Cytokine expression was quantified using multiplexed flow cytometry. Brain-derived neurotrophic factor expression and phosphorylation of extracellular signal-regulated kinase were determined using western blot analysis. KEY RESULTS: Fingolimod attenuated cognitive deficits and restored hippocampal neurogenesis in a dose-dependent manner in PCP-treated rats. Fingolimod treatment exerted anti-inflammatory effects by inhibiting microglial activation and IL-6 and IL-1β pro-inflammatory cytokine expression. The underlying mechanism involves the upregulation of brain-derived neurotrophic factor protein expression and activation of the ERK signalling pathway. CONCLUSION AND IMPLICATIONS: This is the first preclinical assessment of the effects of fingolimod on cognitive function in a model for schizophrenia. Our results suggest the immune system plays an crucial role in cognitive alterations in schizophrenia and highlight the potential of immunomodulatory strategies to improve cognitive deficits in schizophrenia.
 BACKGROUND: Magnetic Resonance Spin TomogrAphy in Time-domain (MR-STAT) can reconstruct whole-brain multi-parametric quantitative maps (eg, T(1) , T(2) ) from a 5-minute MR acquisition. These quantitative maps can be leveraged for synthetization of clinical image contrasts. PURPOSE: The objective was to assess image quality and overall diagnostic accuracy of synthetic MR-STAT contrasts compared to conventional contrast-weighted images. STUDY TYPE: Prospective cross-sectional clinical trial. POPULATION: Fifty participants with a median age of 45 years (range: 21-79 years) consisting of 10 healthy participants and 40 patients with neurological diseases (brain tumor, epilepsy, multiple sclerosis or stroke). FIELD STRENGTH/SEQUENCE: 3T/Conventional contrast-weighted imaging (T(1) /T(2) weighted, proton density [PD] weighted, and fluid-attenuated inversion recovery [FLAIR]) and a MR-STAT acquisition (2D Cartesian spoiled gradient echo with varying flip angle preceded by a non-selective inversion pulse). ASSESSMENT: Quantitative T(1) , T(2) , and PD maps were computed from the MR-STAT acquisition, from which synthetic contrasts were generated. Three neuroradiologists blinded for image type and disease randomly and independently evaluated synthetic and conventional datasets for image quality and diagnostic accuracy, which was assessed by comparison with the clinically confirmed diagnosis. STATISTICAL TESTS: Image quality and consequent acceptability for diagnostic use was assessed with a McNemar's test (one-sided α = 0.025). Wilcoxon signed rank test with a one-sided α = 0.025 and a margin of Δ = 0.5 on the 5-level Likert scale was used to assess non-inferiority. RESULTS: All data sets were similar in acceptability for diagnostic use (≥3 Likert-scale) between techniques (T(1) w:P = 0.105, PDw:P = 1.000, FLAIR:P = 0.564). However, only the synthetic MR-STAT T(2) weighted images were significantly non-inferior to their conventional counterpart; all other synthetic datasets were inferior (T(1) w:P = 0.260, PDw:P = 1.000, FLAIR:P = 1.000). Moreover, true positive/negative rates were similar between techniques (conventional: 88%, MR-STAT: 84%). DATA CONCLUSION: MR-STAT is a quantitative technique that may provide radiologists with clinically useful synthetic contrast images within substantially reduced scan time. EVIDENCE LEVEL: 1 Technical Efficacy: Stage 2.
 BACKGROUND: The clinical and radiological characteristics of neuromyelitis optica spectrum disorder (NMOSD) from Pakistan is unknown. Our study aimed to describe the clinical and radiological features of NMOSD patients presenting to a Pakistani tertiary care center. MATERIALS AND METHODS: This retrospective, observational study was conducted at the Neurology Department, Pakistan Institute of Medical Sciences between January 2017 and September 2021 (56 months). The study included patients diagnosed with neuromyelitis optica spectrum disorder (NMOSD) according to the 2015 International Panel for NMO Diagnosis (IPND) criteria, with the exclusion of patients under 12 years of age and those who tested positive for Myelin oligodendrocyte glycoprotein (MOG) IgG antibody. The patients were divided into two groups based on clinical presentation and the presence of NMO-IgG antibodies: NMO-IgG positive NMO (Seropositive NMO) and NMO-IgG negative (Seronegative NMO). The clinical features of NMOSD were recorded, and data was analyzed using SPSS version 26.0. RESULTS: Among 204 patients with suspected demyelination, multiple sclerosis was diagnosed in 100 individuals (49.02%), while acute disseminated encephalomyelitis (ADEM), clinically isolated syndrome (CIS), and neuromyelitis optica (NMO) were found in 5 patients each (2.45%, 2.45%, and 17.65%, respectively). Out of 36 patients with NMO, 32 (88.89%) tested positive for NMO-Ab, while the remaining 4 (11.11%) were seronegative for both NMO and anti-MOG Abs. The mean age of NMO-positive patients who tested positive for NMO antibodies was 31.03±10.12 years, compared to 27.95±2.5 years for NMO-negative patients, though this difference was not statistically significant (p>0.05). Females were more commonly affected by NMO, accounting for 72.2% of the NMO-positive group, and there was a significant difference in clinical phenotypes between the two groups (p<0.05). The NMO-positive group predominantly had relapsing NMO presentation (75%), and 72.8% of these patients showed longitudinally extensive transverse myelitis on the MRI spine. Azathioprine was the most frequently administered treatment for positive NMO patients (69.44%), followed by rituximab and MMF. The follow-up period for the study participants lasted 24 months. CONCLUSION: This is the first study on NMOSD cases in Pakistan. According to the present study, NMOSD is most prevalent among women in their forties. Relapsing NMO was the most common form of presentation. 89% of patients had antibodies against AQP4. 72.8% of patients suffered from LETM during the course of their disease. There are some features of our NMOSD cases that appear comparable with those around the world, despite some limitations in testing and access to care. It is clear that the clinical and radiological spectrums of patients with NMO and NMOSD in this cohort are similar. It is reasonable to suspect NMO if demyelinating episodes are not characteristic of MS.
 INTRODUCTION: Identifying responsive outcome measures for assessing functional change related to cognition, communication, and quality of life for individuals with neurodegenerative disease is important for intervention design and clinical care. Goal Attainment Scaling (GAS) has been used as an outcome measure to formally develop and systematically measure incremental progress toward functional, patient-centered goals in clinical settings. Evidence suggests that GAS is reliable and feasible for use in older adult populations and in adult populations with cognitive impairment, but no review has assessed the suitability of GAS in older adults with neurodegenerative disease experiencing dementia or cognitive impairment, based on responsiveness. This study conducted a systematic review to evaluate the suitability of GAS as an outcome measure for older adult populations with neurodegenerative disease experiencing dementia or cognitive impairment, based on responsiveness. METHODS: The review was registered with PROSPERO and performed by searching ten electronic scientific databases (PubMed, Medline OVID, CINAHL, Cochrane, Embase, Web of Science, PsycINFO, Scopus, OTSeeker, REHABDATA) and four registries (<ext-link ext-link-type="uri" xlink:href="http://Clinicaltrials.gov" xmlns:xlink="http://www.w3.org/1999/xlink">Clinicaltrials.gov</ext-link>, Grey Literature Report, Mednar, OpenGrey). A summary measure of responsiveness (post-intervention minus pre-intervention mean GAS T-score) was compared across eligible studies using a random-effects meta-analysis. Risk of bias in included studies was assessed using the NIH Quality Assessment Tool for Before-After (Pre-Post) Studies with No Control Group. RESULTS: 882 eligible articles were identified and screened by two independent reviewers. Ten studies met inclusion criteria for the final analysis. Of the ten included reports, 3 focus on all-cause dementia, 3 on multiple sclerosis, 1 on Parkinson's disease, 1 on mild cognitive impairment, 1 on Alzheimer's disease, and 1 on primary progressive aphasia. Responsiveness analyses showed pre- and post-intervention GAS goals were significantly different from zero (Z = 7.48, p &lt; 0.001), with post-intervention GAS scores being higher than pre-intervention GAS scores. Three included studies showed a high risk of bias, 3 showed a moderate risk of bias, and 4 showed a low risk of bias. Overall risk of bias of included studies was rated as moderate. CONCLUSION: GAS showed an improvement in goal attainment across different dementia patient populations and intervention types. The overall moderate risk of bias suggests that while bias is present across included studies (e.g., small sample size, unblinded assessors), the observed effect likely represents the true effect. This suggests that GAS is responsive to functional change and may be suitable for use in older adult populations with neurodegenerative disease experiencing dementia or cognitive impairment.
 Background: Idiopathic pulmonary fibrosis (IPF) is a serious lung disease characterized by lung scarring, which results in breathing difficulty. Currently, patients with IPF exhibit a poor survival rate and have access to very limited therapeutic options. Interferon beta (IFN-β) has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of relapsing forms of multiple sclerosis, and it has also been shown to exhibit therapeutic potential in IPF. However, clinical use of IFN-β did not lead to improved overall survival in IPF patients in existing studies. One possibility is the limited efficiency of IFN-β delivery through intravenous or subcutaneous injection. Materials and Methods: The aerosol particle size distribution was determined with a laser diffraction particle size analyzer to characterize the droplet size and fine particle fraction generated by three types of nebulizers: jet, ultrasonic, and mesh. A breathing simulator was used to assess the delivery efficiency of IFN-β, and the temperature in the medication reservoirs was monitored with a thermocouple during nebulization. To further evaluate the antifibrotic activity of IFN-β pre- and postnebulization, bleomycin (BLM)- or transforming growth factor-beta (TGF-β)-treated human lung fibroblast (HLF) cells were used. Cell viability was measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Transwell migration assay and Q-PCR analysis were used to evaluate cell migration and the myofibroblast differentiation ability, respectively. IFN-β protein samples were prepared using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) sample loading buffer, and the expression of IFN-β was assessed by western blotting. Results: Among the current drug delivery systems, aerosolized medication has shown increased efficacy of drug delivery for treating respiratory diseases when compared with parenteral drugs. It was found that neither the structural integrity nor the biological function of nebulized IFN-β was compromised by the nebulization process of the mesh nebulizer. In addition, in BLM dose-response or TGF-β-induced lung fibroblast proliferation assays, these effects could be reversed by both parenteral and inhaled IFN-β nebulized with the mesh nebulizer. Nebulized IFN-β with the mesh nebulizer also significantly inhibited the migration and myofibroblast differentiation ability of TGF-β-treated HLF cells. Conclusions: The investigations revealed the potential efficacy of IFN-β in the treatment of IPF with the mesh nebulizer, demonstrating the higher efficiency of IFN-β delivered through the mesh nebulizer.
 Mitoxantrone (MTX) is an antineoplastic agent used to treat advanced breast cancer, prostate cancer, acute leukemia, lymphoma and multiple sclerosis. Although it is known to cause cumulative dose-related cardiotoxicity, the underlying mechanisms are still poorly understood. This study aims to compare the cardiotoxicity of MTX and its' pharmacologically active metabolite naphthoquinoxaline (NAPHT) in an in vitro cardiac model, human-differentiated AC16 cells, and determine the role of metabolism in the cardiotoxic effects. Concentration-dependent cytotoxicity was observed after MTX exposure, affecting mitochondrial function and lysosome uptake. On the other hand, the metabolite NAPHT only caused concentration-dependent cytotoxicity in the MTT reduction assay. When assessing the effect of different inhibitors/inducers of metabolism, it was observed that metyrapone (a cytochrome P450 inhibitor) and phenobarbital (a cytochrome P450 inducer) slightly increased MTX cytotoxicity, while 1-aminobenzotriazole (a suicide cytochrome P450 inhibitor) decreased fairly the MTX-triggered cytotoxicity in differentiated AC16 cells. When focusing in autophagy, the mTOR inhibitor rapamycin and the autophagy inhibitor 3-methyladenine exacerbated the cytotoxicity caused by MTX and NAPHT, while the autophagy blocker, chloroquine, partially reduced the cytotoxicity of MTX. In addition, we observed a decrease in p62, beclin-1, and ATG5 levels and an increase in LC3-II levels in MTX-incubated cells. In conclusion, in our in vitro model, neither metabolism nor exogenously given NAPHT are major contributors to MTX toxicity as seen by the residual influence of metabolism modulators used on the observed cytotoxicity and by NAPHT's low cytotoxicity profile. Conversely, autophagy is involved in MTX-induced cytotoxicity and MTX seems to act as an autophagy inducer, possibly through p62/LC3-II involvement.
 Systemic sclerosis (SSc) is a chronic immune-mediated disease characterized by microangiopathy, immune dysregulation, and progressive fibrosis of the skin and internal organs. Though not fully understood, the pathogenesis of SSc is dominated by microvascular injury, endothelial dysregulation, and immune response that are thought to be associated with fibroblast activation and related fibrogenesis. Among the main clinical subsets, diffuse SSc (dSSc) is a progressive form with rapid and disseminated skin thickening accompanied by internal organ fibrosis and dysfunction. Despite recent advances and multiple randomized clinical trials in early dSSc patients, an effective disease-modifying treatment for progressive skin fibrosis is still missing, and there is a crucial need to identify new targets for therapeutic intervention. Eotaxin-2 (CCL24) is a chemokine secreted by immune cells and epithelial cells, which promotes trafficking of immune cells and activation of pro-fibrotic cells through CCR3 receptor binding. Higher levels of CCL24 and CCR3 were found in the skin and sera of patients with SSc compared with healthy controls; elevated levels of CCL24 and CCR3 were associated with fibrosis and predictive of greater lung function deterioration. Growing evidence supports the potency of a CCL24-blocking antibody as an anti-inflammatory and anti-fibrotic modulating agent in multiple preclinical models that involve liver, skin, and lung inflammation and fibrosis. This review highlights the role of CCL24 in orchestrating immune, vascular, and fibrotic pathways, and the potential of CCL24 inhibition as a novel treatment for SSc.
 BACKGROUND Anti-PL-12 syndrome is a rare form of myositis. Amyotrophic lateral sclerosis (ALS) is the commonest of the motor neuron disorders. However, the 2 conditions have not been reported to occur together in a single individual. This case report describes a patient who was diagnosed with anti-PL-12 anti-synthetase syndrome and then subsequently was diagnosed with ALS. CASE REPORT A 55-year-old male patient had anti-PL-12 syndrome and ALS occurring together. The patient initially presented with musculoskeletal complaints and was diagnosed with anti-PL-12 syndrome. He later went on to develop shortness of breath. Neurophysiological testing subsequently confirmed ALS as the patient experienced worsening muscle weakness over a 2-year period. A muscle biopsy performed showed neurogenic and myopathic process. The patient eventually lost the ability to ambulate without mobility assistance and suffered cardiac arrest due to complications from ALS, specifically diaphragmatic dysfunction. CONCLUSIONS This case report represents the first documented case of a patient having both anit-PL-12 syndrome and ALS together. It has been suggested that having an autoimmune disease (AID) may increase the subsequent risk of developing ALS. Previous studies did not conduct evaluation to ascertain serological markers for AS antibodies. Lab tests were rechecked and revalidated multiple times in separate facilities for confirmation of results in case of initial lab error. This may suggest a common etiology for both anti-PL-12 syndrome and ALS.
 After experiencing a fall, an 82-year-old woman developed progressive loss of lower limb strength and was diagnosed with inclusion body myositis. Although falls and muscle weakness are often regarded as consequences of aging, inclusion body myositis should be considered in a patient with a history of multiple falls.
 Systemic sclerosis, also known as scleroderma, is a rare and complex autoimmune connective-tissue disease. Once considered an untreatable and unpredictable condition, research advancements have improved our understanding of its disease pathogenesis and clinical phenotypes and expanded our treatment armamentarium. Early and accurate diagnosis is essential, while ongoing efforts to risk stratify patients have a central role in predicting both organ involvement and disease progression. A holistic approach is required when choosing the optimal therapeutic strategy, balancing the side-effect profile with efficacy and tailoring the treatment according to the goals of care of the patient. This Seminar reviews the multiple clinical dimensions of systemic sclerosis, beginning at a precursor very early stage of disease, with a focus on timely early detection of organ involvement. This Seminar also summarises management considerations according to the pathological hallmarks of systemic sclerosis (eg, inflammation, fibrosis, and vasculopathy) and highlights unmet needs and opportunities for future research and discovery.
 OBJECTIVE: C9orf72 mutation carriers with different neurological phenotypes show cortical and subcortical atrophy in multiple different brain regions, even in pre-symptomatic phases. Despite there is a substantial amount of knowledge, small sample sizes, clinical heterogeneity, as well as different choices of image analysis may hide anatomical abnormalities that are unique to amyotrophic lateral sclerosis (ALS) patients with this genotype or that are indicative of the C9orf72-specific trait overlain in fronto-temporal dementia patients. METHODS: Brain structural and resting state functional magnetic imaging was obtained in 24 C9orf72 positive (ALSC9+) ALS patients paired for burden disease with 24 C9orf72 negative (ALSC9-) ALS patients. A comprehensive structural evaluation of cortical thickness and subcortical volumes between ALSC9+ and ALSC9- patients was performed while a region of interest (ROI)-ROI analysis of functional connectivity was implemented to assess functional alterations among abnormal cortical and subcortical regions. Results were corrected for multiple comparisons. RESULTS: Compared to ALSC9- patients, ALSC9+ patients exhibited extensive disease-specific patterns of thalamo-cortico-striatal atrophy, supported by functional alterations of the identified abnormal regions. Cortical thinning was most pronounced in posterior areas and extended to frontal regions. Bilateral atrophy of the mediodorsal and pulvinar nuclei was observed, emphasizing a focal rather than global thalamus atrophy. Volume loss in a large portion of bilateral caudate and left putamen was reported. The marked reduction of functional connectivity observed between the left posterior thalamus and almost all the atrophic cortical regions support the central role of the thalamus in the pathogenic mechanism of C9orf72-mediated disease. CONCLUSIONS: These findings constitute a coherent and robust picture of ALS patients with C9orf72-mediated disease, unveiling a specific structural and functional characterization of thalamo-cortico-striatal circuit alteration. Our study introduces new evidence in the characterization of the pathogenic mechanisms of C9orf72 mutation.
 Systemic sclerosis (SSc) is a rare autoimmune connective tissue disorder that causes fibrosis due to an accelerated inflammatory response. One of the most frequent co-morbidities with SSc is interstitial lung disease (ILD), which is also one of the biggest killers among SSc patients. CASE PRESENTATION: The authors present a rare case of diffuse SSc with ILD and myocardial infarction having a history of Raynaud phenomenon, skin thickening, and shortness of breath. Antinuclear antibody and antitopoisomerase antibody tests were positive. The patient was managed medically and the condition of patient is improving. CLINICAL DISCUSSION: SSC can affect the skin as well as other organs, with the lungs being the most frequently involved and seriously impacted. SSc patients can have multiple organ involvement like the skin, lungs, heart, kidneys, and gastrointestinal tract. Because ILD is the leading cause of death among people with SSC, early diagnosis and high suspicion of lung involvement can reduce mortality. CONCLUSION: The mortality rate for SSC associated with ILD is extremely high. Even though ILD is common in SSc, it might be difficult to identify and detect early for which a high-resolution CT scan can be used. In SSc patients, heart involvement can coexist with ILD.
 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by the loss of upper and lower motor neurons, which eventually may lead to death. Critical to the mission of developing effective therapies for ALS is the discovery of biomarkers that can illuminate mechanisms of neurodegeneration and have diagnostic, prognostic, or pharmacodynamic value. Here, we merged unbiased discovery-based approaches and targeted quantitative comparative analyses to identify proteins that are altered in cerebrospinal fluid (CSF) from patients with ALS. Mass spectrometry (MS)-based proteomic approaches employing tandem mass tag (TMT) quantification methods from 40 CSF samples comprising 20 patients with ALS and 20 healthy control (HC) individuals identified 53 proteins that are differential between the two groups after CSF fractionation. Notably, these proteins included both previously identified ones, validating our approach, and novel ones that have the potential for expanding biomarker repertoire. The identified proteins were subsequently examined using parallel reaction monitoring (PRM) MS methods on 61 unfractionated CSF samples comprising 30 patients with ALS and 31 HC individuals. Fifteen proteins (APOB, APP, CAMK2A, CHI3L1, CHIT1, CLSTN3, ERAP2, FSTL4, GPNMB, JCHAIN, L1CAM, NPTX2, SERPINA1, SERPINA3, and UCHL1) showed significant differences between ALS and the control. Taken together, this study identified multiple novel proteins that are altered in ALS, providing the foundation for developing new biomarkers for ALS.
 Autoimmune movement disorders are increasingly recognized, but isolated tremor is extremely rare. We describe a 70-year-old male with rapidly progressive, severe postural and intention tremor and weight loss. His cerebrospinal fluid was inflammatory and harbored a neural tissue-restricted antibody. The autoantigen was identified by immunoprecipitation and mass spectrometry and confirmed by antigen-specific assays to be specific for tenascin-R. He was investigated for cancer and diagnosed with follicular lymphoma that expressed tenascin-R suggesting a paraneoplastic origin; cancer treatment and immunotherapy led to complete recovery. With this individualized patient approach and antibody discovery, we expand the spectrum of antibodies accompanying autoimmune hyperkinetic movement disorders. ANN NEUROL 2023;94:502-507.
 Central nervous system vasculitis (CNSV) is a group of disorders leading to inflammatory vasculopathy within the brain, spinal cord, and leptomeninges. CNSV is divided into primary angiitis of the central nervous system (PACNS) and secondary CNSV based on the underlying etiology. PACNS is a rare inflammatory disorder with poorly understood pathophysiology and heterogeneous and highly variable clinical features. The diagnosis depends on a combination of clinical and laboratory variables, multimodal imaging, and histopathological examination as well as exclusion of mimics. Several systemic vasculitides, infectious etiologies and connective tissue disorders have been shown to cause secondary CNSV and require prompt recognition.
 Tuberous sclerosis complex (TSC) is a genetic disorder that affects multiple systems. It is inherited in an autosomal dominant fashion and is characterized by an increased predisposition to hamartoma formation. It results from mutations in the genes TSC1 and TSC2 and is known for causing neurological disorders including epilepsy and intellectual disability. TSC is usually diagnosed in childhood or infancy, and the affected individuals may present with developmental delay, skin manifestations, or seizures. However, it may also be diagnosed earlier or later, based on a wide array of clinical manifestations. Some manifestations may be present prenatally, such as cardiac rhabdomyomas or cortical tubers. While other signs, including osseous, renal, or pulmonary lesions are commonly diagnosed in adulthood. The presentation of the disease will vary depending on the developmental stage of the individual. While skin lesions are detected in 90% of patients of all ages, hypopigmented macules are usually found in early childhood. Ungual fibromas appear near puberty, and facial angiofibromas are more common in adolescence. This disease has a highly variable clinical course. Prognosis may be uncertain, and follow-up requires a comprehensive evaluation, often in specialized institutions. This disorder may be overwhelming for some patients and family members; thus, orientation and counseling play a vital role.
 Systemic sclerosis (SSc) is a rare multisystem autoimmune disease characterized by fibrosis, vasculopathy, and autoimmunity. There are multiple complications inherent to SSc and its management. One of these complications is increased infection risk, which can lead to decreased quality of life and increased morbidity and mortality. Patients with SSc have lower vaccination rates and decreased vaccine seroconversion secondary to immunosuppressive medications compared with the general population. The purpose of this review is to provide clinicians with an approach to vaccinations in SSc.
 Despite the devastating clinical outcome of the neurodegenerative disease, amyotrophic lateral sclerosis (ALS), its etiology remains mysterious. Approximately 90% of ALS is characterized as sporadic, signifying that the patient has no family history of the disease. The development of an impactful disease modifying therapy across the ALS spectrum has remained out of grasp, largely due to the poorly understood mechanisms of disease onset and progression. Currently, ALS is invariably fatal and rapidly progressive. It is hypothesized that multiple factors can lead to the development of ALS, however, treatments are often focused on targeting specific familial forms of the disease (10% of total cases). There is a strong need to develop disease modifying treatments for ALS that can be effective across the full ALS spectrum of familial and sporadic cases. Although the onset of disease varies significantly between patients, there are general disease mechanisms and progressions that can be seen broadly across ALS patients. Therefore, this review explores the targeting of these widespread disease mechanisms as possible areas for therapeutic intervention to treat ALS broadly. In particular, this review will focus on targeting mechanisms of defective protein homeostasis and RNA processing, which are both increasingly recognized as design principles of ALS pathogenesis. Additionally, this review will explore the benefits of gene therapy as an approach to treating ALS, specifically focusing on the use of adeno-associated virus (AAV) as a vector for gene delivery to the CNS and recent advances in the field.
 Tuberous sclerosis complex (TSC) is a neurogenetic disorder that affects multiple organ systems, including the heart, kidneys, eyes, skin, and central nervous system. The neurologic manifestations have the highest morbidity and mortality, in particular in children. Clinically, patients with TSC often present with new-onset seizures within the first year of life. TSC-associated epilepsy is often difficult to treat and refractory to multiple antiseizure medications. Refractory TSC-associated epilepsy is associated with increased risk of neurodevelopmental comorbidities, including developmental delay, intellectual disability, autism spectrum disorder, and attention hyperactivity disorder. An increasing body of research suggests that early, effective treatment of TSC-associated epilepsy during critical neurodevelopmental periods can potentially improve cognitive outcomes. Therefore, it is important to treat TSC-associated epilepsy aggressively, whether it be with pharmacological therapy, surgical intervention, and/or neuromodulation. This review discusses current and future pharmacological treatments for TSC-associated epilepsy, as well as the importance of early surgical evaluation for refractory epilepsy in children with TSC and consideration of neuromodulatory interventions in young adults.
 The fragile X protein (FXP) family comprises the multifunctional RNA-binding proteins FMR1, FXR1, and FXR2 that play an important role in RNA metabolism and regulation of translation, but also in DNA damage and cellular stress responses, mitochondrial organization, and more. FMR1 is well known for its implication in neurodevelopmental diseases. Recent evidence suggests substantial contribution of this protein family to amyotrophic lateral sclerosis (ALS) pathogenesis. ALS is a highly heterogeneous neurodegenerative disease with multiple genetic and unclear environmental causes and very limited treatment options. The loss of motoneurons in ALS is still poorly understood, especially because pathogenic mechanisms are often restricted to patients with mutations in specific causative genes. Identification of converging disease mechanisms evident in most patients and suitable for therapeutic intervention is therefore of high importance. Recently, deregulation of the FXPs has been linked to pathogenic processes in different types of ALS. Strikingly, in many cases, available data points towards loss of expression and/or function of the FXPs early in the disease, or even at the presymptomatic state. In this review, we briefly introduce the FXPs and summarize available data about these proteins in ALS. This includes their relation to TDP-43, FUS, and ALS-related miRNAs, as well as their possible contribution to pathogenic protein aggregation and defective RNA editing. Furthermore, open questions that need to be addressed before definitively judging suitability of these proteins as novel therapeutic targets are discussed.
 Amyotrophic lateral sclerosis (ALS) is a lethal progressive neurodegenerative disease, characterized by a loss of function of upper and lower motor neurons. This study aimed to explore probable pathological alterations occurring in individuals with ALS compared to neurologically healthy controls through the analysis of cerebrospinal fluid (CSF), a medium, which directly interacts with brain parenchyma. A total of 7 ALS patients with disease-associated mutations (ATXN2, C9ORF72, FUS, SOD1, and TARDBP) and 13 controls were included in the study. Multiple analytical approaches were employed, including metabolomic and metallomics profiling, as well as genetic screening, using CSF samples obtained from the brain compartment. Data analysis involved the application of multivariate statistical methods. Advanced hyphenated selenium and redox metal (iron, copper, and manganese) speciation techniques and nontargeted Fourier transform ion cyclotron resonance mass spectrometry-based metabolomics were used for data acquisition. Nontargeted metabolomics showed reduced steroids, including sex hormones; additionally, copper and manganese species were found to be the most relevant features for ALS patients. This indicates a potential alteration of sex hormone pathways in the ALS-affected brain, as reflected in the CSF.
 PURPOSE: Episodic nocturnal hypercapnia (eNH) in transcutaneous carbon dioxide pressure (PtcCO(2)) corresponding to rapid eye movement sleep hypoventilation is a useful biomarker for detecting nocturnal hypoventilation. However, the relationship between eNH and neurodegenerative diseases with sleep-related breathing disorders (SRBDs) is unknown. The aim of this study was to evaluate the relationship between eNH and nocturnal hypoventilation in neurodegenerative diseases. METHODS: Patients with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), Parkinson's disease, progressive supranuclear palsy, corticobasal syndrome, and idiopathic normal pressure hydrocephalus, were enrolled and received overnight PtcCO(2) monitoring. The patients were divided into groups for eNH and sleep-associated hypoventilation (SH) prevalence analysis: A (ALS), B (MSA), and C (others). RESULTS: Among 110 patients, twenty-three (21%) and 10 (9%) of the patients met eNH and SH criteria, respectively. eNH and SH were significantly more frequent in groups A and B than in C. The prevalence of SH in the patients with eNH was 39% whereas most of patients with SH (90%) presented with eNH. Among patients with daytime carbon dioxide pressure in arterial blood ≤ 45 mmHg, eNH frequency was 13%, whereas none of the patients met SH criteria. The frequency of noninvasive positive pressure ventilation after PtcCO(2) monitoring was significantly higher in those with than without eNH. CONCLUSIONS: eNH is common in patients with MSA and ALS who present with SRBD. eNH with overnight PtcCO(2) monitoring is a useful biomarker to detect hypoventilation among neurodegenerative diseases with different SRBD mechanisms.
 The four Janus kinase (JAK) proteins and the seven Signal Transducers of Activated Transcription (STAT) mediate intracellular signal transduction downstream of cytokine receptors, which are involved in the pathology of allergic, autoimmune, and inflammatory diseases. The development of targeted small-molecule treatments with diverse selective inhibitory profiles, such as JAK inhibitors (JAKi), has supported an important change in the treatment of multiple disorders. Indeed, JAKi inhibit intracellular signalling controlled by numerous cytokines implicated in the disease process of rheumatoid arthritis and several other inflammatory and immune diseases. Therefore, JAKi have the capacity to target multiple pathways of those diseases. Other autoimmune diseases treated with JAKi include systemic sclerosis, systemic lupus erythematosus, dermatomyositis, primary Sjogren's syndrome, and vasculitis. In all of these cases, innate immunity stimulation activates adaptive immunity, resulting in the production of autoreactive T cells as well as the stimulation and differentiation of B cells. Mechanism-based treatments that target JAK-STAT pathways have the possibility of improving outcomes by reducing the consumption of glucocorticoids and/or non-specific immunosuppressive drugs in the management of systemic immune-mediated inflammatory diseases.
 A 26-year-old woman with tuberous sclerosis complex (TSC) received outpatient treatment for the complication of systemic lupus erythematosus (SLE) at our hospital. She visited our hospital with a chief complaint of pitting oedema in bilateral lower legs for 3 days. The urinalysis showed massive proteinuria with a lot of white blood cell casts. The blood tests revealed hypoalbuminaemia, hypercholesterolaemia, hypocomplementaemia, and elevated anti-double-stranded DNA antibody titre. Renal biopsy was not performed because of multiple renal angiomyolipomas, which was one of the features of TSC. She was diagnosed with a nephrotic state due to lupus nephritis. Although she had a standard therapy with high-dose corticosteroid and mycophenolate mofetil and tacrolimus, complete remission had not been achieved leading to a steroid-dependent nephrotic syndrome. During the follow-up, the angiomyolipomas became larger and had a risk of rupture at the age of 29 years. Everolimus, a mechanistic target of rapamycin (mTOR) inhibitor, was started for the treatment of angiomyolipomas, and mycophenolate mofetil and tacrolimus were terminated instead. The activity of lupus nephritis was surprisingly ameliorated, and the amount of corticosteroid successfully tapered. Everolimus has been continued for 6 years without severe side effects. Accumulating evidence suggests that the activated mTOR pathway plays a key role in the pathogenesis of SLE. We reported the long-term efficacy and safety of everolimus for refractory SLE in a patient with TSC for the first time. This case suggests that everolimus can be a promising option for the treatment of lupus nephritis.
 First- and second-degree relatives of people with amyotrophic lateral sclerosis report higher rates of neuropsychiatric disorders, indicating that risk genes may be pleiotropic, causing multiple phenotypes within kindreds. Such phenotypes may constitute a disease endophenotype that associates with disease liability. We have directly investigated cognitive functioning and neuropsychiatric traits among relatives of people with amyotrophic lateral sclerosis to identify potential endophenotypes of the disease. In a family-based, cross-sectional study design, first- and second-degree relatives of people with amyotrophic lateral sclerosis (n = 149) were compared to controls (n = 60) using an in-depth neuropsychological and neuropsychiatric assessment. Subgroup analyses examined the effect of family history and C9orf72 repeat expansion status (n = 16 positive carriers). Relatives of people with amyotrophic lateral sclerosis had lower scores on executive functioning, language and memory tasks compared to controls, with large effect sizes observed on object naming (d = 0.91, P = 0.00001) and phonemic verbal fluency (d = 0.81, P = 0.0003). Relatives also had higher autism quotient attention to detail traits (d = -0.52, P = 0.005), lower conscientiousness (d = 0.57, P = 0.003) and lower openness to experience personality traits (d = 0.54, P = 0.01) than controls. These effects were typically larger in relatives of people with familial, rather than sporadic, amyotrophic lateral sclerosis and were present in both gene carrier and non-carrier relatives of probands with a C9orf72 repeat expansion. Poorer phonemic fluency and object naming, along with autism and personality traits, are more frequent in relatives of people with amyotrophic lateral sclerosis. Among kindreds carrying the C9orf72 repeat expansion, these traits were identified in relatives regardless of their carrier status, suggesting the presence of a disease-associated endophenotype that is not exclusively mediated by the C9orf72 expansion.
 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons in the spinal cord, cerebral cortex, and medulla oblongata. Most patients present a clinical phenotype of classic ALS-with predominant atrophy, muscle weakness, and fasciculations-and survival of 3 to 5 years following diagnosis. In the present review, we performed a literature search to provide an update on the etiology and pathophysiological mechanisms involved in ALS. There are two types of ALS: the familial form with genetic involvement, and the sporadic form with a multifactorial origin. ALS pathophysiology is characterized by involvement of multiple processes, including oxidative stress, glutamate excitotoxicity, and neuroinflammation. Moreover, it is proposed that conditioning risk factors affect ALS development, such as susceptibility to neurodegeneration in motor neurons, the intensity of performed physical activity, and intestinal dysbiosis with involvement of the enteric nervous system, which supports the existing theories of disease generation. To improve patients' prognosis and survival, it is necessary to further deepen our understanding of the etiopathogenesis of ALS.
 OBJECTIVE: Paresis of muscle groups in patients with amyotrophic lateral sclerosis (ALS) tends to present split phenomena. We explored the split phenomenon of fasciculation in multiple antagonistic muscle groups in ALS patients. METHODS: One hundred and forty ALS patients and 66 non-ALS patients were included from a single ALS center. Muscle ultrasonography (MUS) was performed to detect fasciculation in elbow flexor-extensor, wrist flexor-extensor, knee flexor-extensor, and ankle flexor-extensor. Split phenomena of fasciculation between different antagonistic muscle groups were summarized, and the possible influence factors were analyzed through stratified analysis. RESULTS: The frequency of split phenomenon of fasciculation intensity was significantly higher than those of muscle strength (26.1% vs. 7.1% for elbow flexor-extensor, 38.3% vs. 5.7% for wrist flexor-extensor, 37.9% vs. 3.0% for knee extensor-flexor, and 33.6% vs. 14.4% for ankle flexor-extensor) (P < 0.01). For muscles with 0-1 level of muscle strength (the Medical Research Council, MRC, score), significance difference in mean fasciculation intensity was observed only in ankle flexor-extensor. For muscles with 2-5 level of muscle strength, significant dissociation of fasciculation grade was common, especially among patients with slow rapid progression rate and both upper and lower motor neuron (UMN and LMN) involvement. As for non-ALS patients, no significant difference was observed in fasciculation intensity between antagonistic muscles. CONCLUSION: Split phenomenon of fasciculation between antagonistic muscles was common and relatively specific in ALS patients. Muscle strength, progression rate, and UMN involvement were influence factors of the split phenomenon of fasciculation intensity.
 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive degeneration of upper and lower motor neurons. To study its underlying mechanisms, a variety of models are currently used at the cellular level and in animals with mutations in multiple ALS associated genes, including SOD1, C9ORF72, TDP-43, and FUS. Key mechanisms involved in the disease include excitotoxicity, oxidative stress, mitochondrial dysfunction, neuroinflammatory, and immune reactions. In addition, significant metabolism alterations of various lipids classes, including phospholipids, fatty acids, sphingolipids, and others have been increasingly recognized. Recently, the mechanisms of programmed cell death (apoptosis), which may be responsible for the degeneration of motor neurons observed in the disease, have been intensively studied. In this context, sphingolipids, which are the most important sources of secondary messengers transmitting signals for cell proliferation, differentiation, and apoptosis, are gaining increasing attention in the context of ALS pathogenesis given their role in the development of neuroinflammatory and immune responses. This review describes changes in lipids content and activity of enzymes involved in their metabolism in ALS, both summarizing current evidence from animal models and clinical studies and discussing the potential of new drugs among modulators of lipid metabolism enzymes.
 OBJECTIVE: There are limited studies exploring the support and education needs of individuals at-risk for or diagnosed with hereditary frontotemporal degeneration (FTD) and/or amyotrophic lateral sclerosis (ALS). This study evaluated a novel conference for this population to assess conference efficacy, probe how participants assessed relevant resources, and identify outstanding needs of persons at-risk/diagnosed. METHODS: We implemented a post-conference electronic survey that probed participants' satisfaction, prior experience with resources, and unmet needs. Along with multiple-choice, free-text items were included to gather qualitative context. RESULTS: Survey completion rate was 31% (115/376 attendees who were emailed the survey). There was positive interest in pursuing genetic counseling among eligible responders: 61% indicated they planned to seek genetic counseling because of the conference, which was significantly more than those who were undecided (21%) or did not plan to seek genetic counseling (18%). Qualitative data demonstrated need for additional education, support, and research opportunities. CONCLUSION: Conference reactions indicate this is a valued resource. Results indicated the importance of raising awareness about existing resources, and the need for further resource development, especially for at-risk communities. INNOVATION: While most resources are developed for caregivers' needs, this unique program targets at-risk individuals and unites ALS and FTD communities.
 OBJECTIVE: To systematically assess credibility and certainty of associations between cannabis, cannabinoids, and cannabis based medicines and human health, from observational studies and randomised controlled trials (RCTs). DESIGN: Umbrella review. DATA SOURCES: PubMed, PsychInfo, Embase, up to 9 February 2022. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Systematic reviews with meta-analyses of observational studies and RCTs that have reported on the efficacy and safety of cannabis, cannabinoids, or cannabis based medicines were included. Credibility was graded according to convincing, highly suggestive, suggestive, weak, or not significant (observational evidence), and by GRADE (Grading of Recommendations, Assessment, Development and Evaluations) (RCTs). Quality was assessed with AMSTAR 2 (A Measurement Tool to Assess Systematic Reviews 2). Sensitivity analyses were conducted. RESULTS: 101 meta-analyses were included (observational=50, RCTs=51) (AMSTAR 2 high 33, moderate 31, low 32, or critically low 5). From RCTs supported by high to moderate certainty, cannabis based medicines increased adverse events related to the central nervous system (equivalent odds ratio 2.84 (95% confidence interval 2.16 to 3.73)), psychological effects (3.07 (1.79 to 5.26)), and vision (3.00 (1.79 to 5.03)) in people with mixed conditions (GRADE=high), improved nausea/vomit, pain, spasticity, but increased psychiatric, gastrointestinal adverse events, and somnolence among others (GRADE=moderate). Cannabidiol improved 50% reduction of seizures (0.59 (0.38 to 0.92)) and seizure events (0.59 (0.36 to 0.96)) (GRADE=high), but increased pneumonia, gastrointestinal adverse events, and somnolence (GRADE=moderate). For chronic pain, cannabis based medicines or cannabinoids reduced pain by 30% (0.59 (0.37 to 0.93), GRADE=high), across different conditions (n=7), but increased psychological distress. For epilepsy, cannabidiol increased risk of diarrhoea (2.25 (1.33 to 3.81)), had no effect on sleep disruption (GRADE=high), reduced seizures across different populations and measures (n=7), improved global impression (n=2), quality of life, and increased risk of somnolence (GRADE=moderate). In the general population, cannabis worsened positive psychotic symptoms (5.21 (3.36 to 8.01)) and total psychiatric symptoms (7.49 (5.31 to 10.42)) (GRADE=high), negative psychotic symptoms, and cognition (n=11) (GRADE=moderate). In healthy people, cannabinoids improved pain threshold (0.74 (0.59 to 0.91)), unpleasantness (0.60 (0.41 to 0.88)) (GRADE=high). For inflammatory bowel disease, cannabinoids improved quality of life (0.34 (0.22 to 0.53) (GRADE=high). For multiple sclerosis, cannabinoids improved spasticity, pain, but increased risk of dizziness, dry mouth, nausea, somnolence (GRADE=moderate). For cancer, cannabinoids improved sleep disruption, but had gastrointestinal adverse events (n=2) (GRADE=moderate). Cannabis based medicines, cannabis, and cannabinoids resulted in poor tolerability across various conditions (GRADE=moderate). Evidence was convincing from observational studies (main and sensitivity analyses) in pregnant women, small for gestational age (1.61 (1.41 to 1.83)), low birth weight (1.43 (1.27 to 1.62)); in drivers, car crash (1.27 (1.21 to 1.34)); and in the general population, psychosis (1.71 (1.47 to 2.00)). Harmful effects were noted for additional neonatal outcomes, outcomes related to car crash, outcomes in the general population including psychotic symptoms, suicide attempt, depression, and mania, and impaired cognition in healthy cannabis users (all suggestive to highly suggestive). CONCLUSIONS: Convincing or converging evidence supports avoidance of cannabis during adolescence and early adulthood, in people prone to or with mental health disorders, in pregnancy and before and while driving. Cannabidiol is effective in people with epilepsy. Cannabis based medicines are effective in people with multiple sclerosis, chronic pain, inflammatory bowel disease, and in palliative medicine but not without adverse events. STUDY REGISTRATION: PROSPERO CRD42018093045. FUNDING: None.
 Skeletal fluorosis is a metabolic bone disease caused by excessive consumption of fluoride from fluoride-contaminated water or foods. Such a condition often takes place in developing countries without proper handling of drinking water or food. However, in recent years, multiple cases of skeletal fluorosis have been observed in the United States due to the increasing frequency of recreational substance abuse. In this case report, a 26-year-old male with a history of polysubstance use disorder presented to the emergency department after being assaulted by store employees when attempting to steal computer cleaner inhalants. On evaluation for acute traumatic injury, he was incidentally found to have diffuse sclerosis of all visualized bones on knee, femur, and hip X-rays. Labs were significant for elevated serum alkaline phosphatase levels, secondary hyperparathyroidism, and hypovitaminosis D. Given the patient's history of computer cleaner inhalant misuse and imaging findings, serum and urine fluoride levels were obtained and supported the diagnosis of skeletal fluorosis. Skeletal pain and diffuse sclerosis on imaging should prompt clinicians to include skeletal fluorosis in the differential diagnosis. Cessation of substance use is the primary treatment of fluorosis in the setting of computer cleaner inhalant abuse. However, clinical symptoms and laboratory and imaging abnormalities may take decades to resolve due to the prolonged half-life of fluoride in bone. Proper hydration is crucial, as nephrolithiasis and hypercalciuria have been described during the skeletal unloading of fluoride.
 BACKGROUND: Juvenile systemic sclerosis (jSSc) is a systemic inflammatory and fibrotic autoimmune disease. Adult guidelines recommend obtaining a screening high-resolution computed tomography scan (CT) at diagnosis. As these recommendations are adopted as standard of care for jSSc, increased screening with CT may lead to increased detection of nodules. The implications of nodules identified in jSSc are unclear and unreported. METHODS: A retrospective chart review was performed on the prospectively enrolled National Registry for Childhood-Onset Scleroderma (NRCOS) cohort over an enrollment period of 20 years. Clinical associations with presence of nodules and nodule characteristics were investigated. RESULTS: In this jSSc cohort, the prevalence of pulmonary nodules was 31% (n = 17 of 54). Nodule characteristics were heterogeneous, and most displayed stability over time. More participants with nodules had structural esophageal abnormalities, restriction, and reduced diffusing capacity on lung function tests, and follow-up imaging. Most participants had multiple nodules, and although most nodules were <5 mm, most participants had at least one nodule >5 mm. CONCLUSIONS: Pulmonary nodules are seen in children with jSSc and may be related to more severe disease and/or esophageal dysfunction. More work is needed to provide guidance on radiologic follow-up and clinical management of pulmonary nodules in jSSc.
 Tuberous sclerosis complex (TSC) is a multiple system neurocutaneous syndrome with a genetic disorder caused by different mutations in TSC1 or TSC2. Usually, TSC causes tumors in the heart, brain, kidneys, eyes, and lungs. However, tumors can also develop in any other organs. The prenatal diagnosis of TCS is based on the identification of fetal cardiac tumors by ultrasound and brain subependymal nodules, usually identified by fetal magnetic resonance imaging (MRI). We present two case reports of the prenatal diagnosis of TCS using both ultrasound and MRI, which were confirmed by clinical and radiological methods in the postnatal period accordingly.
 OBJECTIVES: Using diffusion basis spectrum imaging (DBSI) to examine the microstructural changes in the substantia nigra (SN) and global white matter (WM) tracts of patients with early-stage PD. METHODS: Thirty-seven age- and sex-matched patients with early-stage PD and 22 healthy controls (HCs) were enrolled in this study. All participants underwent clinical assessments and diffusion-weighted MRI scans, analyzed by diffusion tensor imaging (DTI) and DBSI to assess the pathologies of PD in SN and global WM tracts. RESULTS: The lower DTI fraction anisotropy (FA) was seen in SN of PD patients (PD: 0.316 ± 0.034 vs HCs: 0.331 ± 0.019, p = 0.015). The putative cells marker-DBSI-restricted fraction (PD: 0.132 ± 0.051 vs HCs: 0.105 ± 0.039, p = 0.031) and the edema/extracellular space marker-DBSI non-restricted-fraction (PD: 0.150 ± 0.052 vs HCs: 0.122 ± 0.052, p = 0.020) were both significantly higher and the density of axons/dendrites marker-DBSI fiber-fraction (PD: 0.718 ± 0.073 vs HCs: 0.773 ± 0.071, p = 0.003) was significantly lower in SN of PD patients. DBSI-restricted fraction in SN was negatively correlated with HAMA scores (r = - 0.501, p = 0.005), whereas DTI-FA was not correlated with any clinical scales. In WM tracts, only higher DTI axial diffusivity (AD) among DTI metrics was found in multiple WM regions in PD, while lower DBSI fiber-fraction and higher DBSI non-restricted-fraction were detected in multiple WM regions. DBSI non-restricted-fraction in both left fornix (cres)/stria terminalis (r = -0.472, p = 0.004) and right posterior thalamic radiation (r = - 0.467, p = 0.005) was negatively correlated with MMSE scores. CONCLUSION: DBSI could potentially detect and quantify the extent of inflammatory cell infiltration, fiber/dendrite loss, and edema in both SN and WM tracts in patients with early-stage PD, a finding remains to be further investigated through more extensive longitudinal DBSI analysis. CLINICAL RELEVANCE STATEMENT: Our study shows that DBSI indexes can potentially detect early-stage PD's pathological changes, with a notable ability to distinguish between inflammation and edema. This implies that DBSI has the potential to be an imaging biomarker for early PD diagnosis. KEY POINTS: • Diffusion basis spectrum imaging detected higher restricted-fraction in Parkinson's disease, potentially reflecting inflammatory cell infiltration. • Diffusion basis spectrum imaging detected higher non-restricted-fraction and lower fiber-fraction in Parkinson's disease, indicating the presence of edema and/or dopaminergic neuronal/dendritic loss. • Diffusion basis spectrum imaging metrics correlated with non-motor symptoms, suggesting its potential diagnostic role to detect early-stage PD dysfunctions.
 Tuberous sclerosis complex (TSC) is a rare, multisystem genetic disorder that leads to the development of benign tumors in multiple organs and neurological symptoms. TSC clinical manifestations show a great heterogenicity, with most patients presenting severe neuropsychiatric and neurological disorders. TSC is caused by loss-of-function mutations in either TSC1 or TSC2 genes, leading to overexpression of the mechanistic target of rapamycin (mTOR) and, consequently, abnormal cellular growth, proliferation and differentiation as well as to cell migration defects. Beside the growing interest, TSC remains a disorder poorly understood, with limited perspectives in the field of therapeutic strategies. Here we used murine postnatal subventricular zone (SVZ) neural stem progenitor cells (NSPCs) deficient of Tsc1 gene as a TSC model to unravel novel molecular aspects of the pathophysiology of this disease. 2D-DIGE-based proteomic analysis detected 55 differently represented spots in Tsc1-deficient cells, compared to wild-type counterparts, which were associated with 36 protein entries after corresponding trypsinolysis and nanoLC-ESI-Q-Orbitrap-MS/MS analysis. Proteomic results were validated using various experimental approaches. Bioinformatics associated differently represented proteins with oxidative stress and redox pathways, methylglyoxal biosynthesis, myelin sheath, protein S-nitrosylation and carbohydrate metabolism. Because most of these cellular pathways have already been linked to TSC features, these results were useful to clarify some molecular aspects of TSC etiopathogenesis and suggested novel promising therapeutic protein targets. SIGNIFICANCE: Tuberous Sclerosis Complex (TSC) is a multisystemic disorder caused by inactivating mutations of TSC1 or TSC2 genes, which induce overactivation of the mTOR component. The molecular mechanisms underlying the pathogenesis of TSC remain unclear, probably due to complexity of mTOR signaling network. To have a picture of protein abundance changes occurring in TSC disorder, murine postnatal subventricular zone (SVZ) neural stem progenitor cells (NSPCs) deficient of Tsc1 gene were used as a model of disease. Thus, Tsc1-deficient SVZ NSPCs and wild-type cells were comparatively evaluated by proteomics. This analysis evidenced changes in the abundance of proteins involved in oxidative/nitrosative stress, cytoskeleton remodelling, neurotransmission, neurogenesis and carbohydrate metabolism. These proteins might clarify novel molecular aspects of TSC etiopathogenesis and constitute putative molecular targets for novel therapeutic management of TSC-related disorders.
 The common γ chain (γc; IL-2RG) is a subunit of the interleukin (IL) receptors for the γc cytokines IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. The lack of appropriate neutralizing antibodies recognizing IL-2RG has made it difficult to thoroughly interrogate the role of γc cytokines in inflammatory and autoimmune disease settings. Here, we generated a γc cytokine receptor antibody, REGN7257, to determine whether γc cytokines might be targeted for T cell-mediated disease prevention and treatment. Biochemical, structural, and in vitro analysis showed that REGN7257 binds with high affinity to IL-2RG and potently blocks signaling of all γc cytokines. In nonhuman primates, REGN7257 efficiently suppressed T cells without affecting granulocytes, platelets, or red blood cells. Using REGN7257, we showed that γc cytokines drive T cell-mediated disease in mouse models of graft-versus-host disease (GVHD) and multiple sclerosis by affecting multiple aspects of the pathogenic response. We found that our xenogeneic GVHD mouse model recapitulates hallmarks of acute and chronic GVHD, with T cell expansion/infiltration into tissues and liver fibrosis, as well as hallmarks of immune aplastic anemia, with bone marrow aplasia and peripheral cytopenia. Our findings indicate that γc cytokines contribute to GVHD and aplastic anemia pathology by promoting these characteristic features. By demonstrating that broad inhibition of γc cytokine signaling with REGN7257 protects from immune-mediated disorders, our data provide evidence of γc cytokines as key drivers of pathogenic T cell responses, offering a potential strategy for the management of T cell-mediated diseases.
 INTRODUCTION: Early treatment is associated with better long-term outcomes in patients with a first demyelinating event and early multiple sclerosis (MS). However, magnetic resonance (MR) findings are not usually integrated to construct propensity scores (PS) when evaluating outcomes. We assessed the association of receiving very early treatment with the risk of long-term disability including an MR Score (MRS) in patients with a first demyelinating event. METHODS: We included 580 patients with a first demyelinating event prospectively collected between 1994 and 2021, who received at least one disease modifying drug (DMD). Patients were classified into tertiles according to the cohort's distribution of the time from the first demyelinating event to the first DMD: First tertile (FT) or very early treatment (6 months; N=194); second (ST) (6.1-16 months, N=192), and third tertile (TT) (16.1 months, N=194). A 5-point MRS was built according to the sum of the following indicators: ≥9 brain lesions (1pt); ≥1 infratentorial lesion (1pt); ≥1 spinal cord (SC) lesion (1pt); ≥1 contrast-enhancing (CE) brain lesion (1pt); ≥1 CE SC lesion (1pt). PS based on covariates and the MRS was computed for each of the outcomes. Inverse PS-weighted Cox and linear regression models assessed the risk of different outcomes between tertile groups. Finally, to confirm the role of MR in treatment decision, we studied the time elapsed from the first demyelinating event to treatment initiation according to the MRS in all patients with radiological available information, re-named as raw-MRS. RESULTS: Very early treatment decreased the risk of reaching EDSS 3.0 (HR 0.55 [95% CI 0.32; 0.97]), secondary progressive MS (HR 0.40 [95% CI 0.19; 0.85]), sustained disease progression at 12 months after treatment initiation (HR 0.50 [95% CI 0.29; 0.84]), when compared to patients from the TT group. Patients from the FT had a lower disability progression rate (β estimate, -0.009 [95% CI -0.016; -0.002]) and a lower severe disability measured by the PDDS (β estimate, -0.52 [95% CI -0.91; -0.13]) than the TT groups. Finally, there was a 62.4% reduction in the median time between the first demyelinating event and the first-ever treatment initiation from patients displaying a raw-MRS 1 to patients with a raw-MRS 5. CONCLUSION: Using PS models with and without MRS, we showed that treatment initiation at very early stages is associated with a reduction in the risk of long-term disability accrual in patients with a first demyelinating event. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that earlier treatment of MS patients presenting with a first demyelinating event is associated with improved clinical outcomes.
 Multiple myeloma (MM) frequently induces persisting osteolytic manifestations despite hematologic treatment response. This study aimed to establish a biometrically valid study endpoint for bone remineralization through quantitative and qualitative analyses in sequential CT scans. Twenty patients (seven women, 58 ± 8 years) with newly diagnosed MM received standardized induction therapy comprising the anti-SLAMF7 antibody elotuzumab, carfilzomib, lenalidomide, and dexamethasone (E-KRd). All patients underwent whole-body low-dose CT scans before and after six cycles of E-KRd. Two radiologists independently recorded osteolytic lesion sizes, as well as the presence of cortical destruction, pathologic fractures, rim and trabecular sclerosis. Bland-Altman analyses and Krippendorff's α were employed to assess inter-reader reliability, which was high for lesion size measurement (standard error 1.2 mm) and all qualitative criteria assessed (α ≥ 0.74). After six cycles of E-KRd induction, osteolytic lesion size decreased by 22% (p < 0.001). While lesion size response did not correlate with the initial lesion size at baseline imaging (Pearson's r = 0.144), logistic regression analysis revealed that the majority of responding osteolyses exhibited trabecular sclerosis (p < 0.001). The sum of osteolytic lesion sizes on sequential CT scans defines a reliable study endpoint to characterize bone remineralization. Patient level response is strongly associated with the presence of trabecular sclerosis.
 CLINICAL CHARACTERISTICS: Most females with osteopathia striata with cranial sclerosis (OS-CS) present with macrocephaly and characteristic facial features (frontal bossing, hypertelorism, epicanthal folds, depressed nasal bridge, and prominent jaw). Approximately half have associated features including orofacial clefting and hearing loss, and a minority have some degree of developmental delay (usually mild). Radiographic findings of cranial sclerosis, sclerosis of long bones, and metaphyseal striations (in combination with macrocephaly) can be considered pathognomonic. Males can present with a mild or severe phenotype. Mildly affected males have clinical features similar to affected females, including macrocephaly, characteristic facial features, orofacial clefting, hearing loss, and mild-to-moderate learning delays. Mildly affected males are more likely than females to have congenital or musculoskeletal anomalies. Radiographic findings include cranial sclerosis and sclerosis of the long bones; Metaphyseal striations are more common in males who are mosaic for an AMER1 pathogenic variant. The severe phenotype manifests in males as a multiple-malformation syndrome, lethal in mid-to-late gestation, or in the neonatal period. Congenital malformations include skeletal defects (e.g., polysyndactyly, absent or hypoplastic fibulae), congenital heart disease, and brain, genitourinary, and gastrointestinal anomalies. Macrocephaly is not always present and longitudinal metaphyseal striations have not been observed in severely affected males, except for those who are mosaic for the AMER1 pathogenic variant. DIAGNOSIS/TESTING: The diagnosis of OS-CS is established in a female proband with characteristic features and a heterozygous pathogenic variant in AMER1 identified by molecular genetic testing. The diagnosis of OS-CS is established in a male proband with characteristic features and a hemizygous pathogenic variant in AMER1 identified by molecular genetic testing. MANAGEMENT: Treatment: Scoliosis management per orthopedic surgeon; physiotherapy may be helpful for joint contractures; management of oral facial clefts per otolaryngologist; hearing loss is managed by audiology, speech and language therapy, and otolaryngology; vision loss management per ophthalmologist and neurosurgery for nerve compression as indicated; early intervention services and special education as indicated; standard treatments for cardiac, genitourinary, and gastrointestinal anomalies and Wilms tumor or other malignancy. Surveillance: Annual clinical assessment for skeletal manifestations such as scoliosis, joint contractures, stress fractures, and persistent bone pain. Annual audiology and ophthalmology evaluations for evidence of cranial nerve compression due to sclerotic bone disorder. Consider abdominal ultrasound every three months until age seven years to screen for Wilms tumor. GENETIC COUNSELING: OS-CS is inherited in an X-linked manner. The risk to sibs of a male proband depends on the genetic status of the mother. The risk to sibs of a female proband depends on the genetic status of the mother and the father. If the mother of the proband has an AMER1 pathogenic variant, the chance of transmitting it in each pregnancy is 50%. If the father of the proband has an AMER1 pathogenic variant, it should be presumed he will transmit the AMER1 pathogenic variant to all his daughters and none of his sons (to date, paternal transmission has only been reported in mosaic fathers). Females who inherit an AMER1 pathogenic variant will be heterozygotes and will have variable manifestations of OS-CS. Males who inherit a pathogenic variant will be hemizygotes and will have variable manifestations ranging from mid-late gestation and neonatal lethality to the mild phenotype. Once the AMER1 pathogenic variant is identified in an affected family member, prenatal and preimplantation genetic testing are possible.
 Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal neurodegenerative disorder. The only established epidemiological risk factors for ALS are male sex and increasing age. The role of physical activity has been debated as an environmental risk factor. Over the last decade multiple studies have attempted to delineate the architecture of ALS. These have not yet established definite risk factors, often due to low-powered studies, lack of focus on at-risk genotypes and sub-optimal methodology. We have conducted a review of all the studies published between 2009 and December 2021. The free text search terms were [(motor neuron disease) OR (MND) OR (Amyotrophic Lateral Sclerosis) OR (ALS)] AND [(Exercise) or (Physical Activity) or (PA) or (sport)]. We identified common themes, for example soccer, head injury and the physiological mechanisms that differ in ALS patients. We have analysed the relevant, available studies (n = 93), highlighting the underlying reasons for any reported discrepancies. Overall, we have found that the more highly powered studies using validated exposure methodologies, linked strenuous, anaerobic physical activity as a risk factor for ALS. Future large-scale studies focusing on specific at-risk genotypes and physical activity should be conducted to confirm this finding. This will strengthen the evidence already surrounding strenuous physical activity as an environmental risk factor for ALS and allow advice to be given to at-risk family members. Increasing our understanding of the genetic-environmental interactions in the pathophysiology of ALS will allow for the possibility of developing preventative therapeutic approaches.
 The aim of this study was to determine whether there are any differences in morphology between temporomandibular joint ankylosis (TMJA) of traumatic and infective origin. Cone beam computed tomography (CBCT) scans of 25 patients (28 joints) with TMJA of traumatic origin (trauma group) and 15 patients (15 joints) with TMJA of infectious origin (infection group) were included. The following morphological parameters were evaluated on multiple sections of the CBCT scans: lateral juxta-articular bone growth, residual condyle, residual glenoid fossa, ramus thickening, ankylotic mass fusion line, sclerosis of the ankylosed condyle and spongiosa of the glenoid fossa, and mastoid and glenoid fossa air cell obliteration. Lateral juxta-articular bone growth, juxta-articular extension of fusion, and the presence of normal medial residual condyle and residual glenoid fossa were exclusively found in post-traumatic TMJA. There were differences in ramus thickening (82.1% in trauma vs 53.3% in infection), sclerosis of the ankylosed condyle (100% in trauma vs 60% in infection), and sclerosis of the spongiosa of the glenoid fossa (100% in trauma vs 46.7% in infection) between the trauma and infection groups. Mastoid and glenoid fossa air cell obliteration was found more frequently in the infection group (mastoid obliteration: 23.1% in infection vs 4% in trauma; glenoid obliteration: 66.7% in infection vs 55.6% in trauma ). CBCT imaging can be helpful in differentiating between TMJA of traumatic and infectious origin.
 This study aimed to explore the characteristics of sleep disorders and their relationship with abnormal white-matter integrity in patients with sporadic amyotrophic lateral sclerosis. One hundred and thirty-six patients and 80 healthy controls were screened consecutively, and 56 patients and 43 healthy controls were ultimately analyzed. Sleep disorders were confirmed using the Pittsburgh sleep quality index, the Epworth sleepiness scale, and polysomnography; patients were classified into those with poor and good sleep quality. White-matter integrity was assessed using diffusion tensor imaging and compared between groups to identify the white-matter tracts associated with sleep disorders. The relationship between scores on the Pittsburgh sleep quality index and impaired white-matter tracts was analyzed using multiple regression. Poor sleep quality was more common in patients (adjusted odds ratio, 4.26; p = 0.005). Compared to patients with good sleep quality (n = 30), patients with poor sleep quality (n = 26; 46.4%) showed decreased fractional anisotropy, increased mean diffusivity, and increased radial diffusivity of projection and commissural fibers, and increased radial diffusivity of the right thalamus. The Pittsburgh score showed the best fit with the mean fractional anisotropy of the right anterior limb of the internal capsule (r = - 0.355, p = 0.011) and the mean radial diffusivity of the right thalamus (r = 0.309, p = 0.028). We conclude that sleep disorders are common in patients with sporadic amyotrophic lateral sclerosis and are associated with reduced white-matter integrity. The pathophysiology of amyotrophic lateral sclerosis may contribute directly to sleep disorders.
 BACKGROUND: Tuberous sclerosis complex (TSC) is a multisystem genetic disorder associated with a wide spectrum of cognitive impairments that can often result in impaired academic, social and adaptive functioning. However, studies investigating TSC have found it difficult to determine whether TSC is associated with a distinct cognitive phenotype and more specifically which aspects of functioning are impaired. Furthermore, children with TSC living in low-income and middle-income countries, like South Africa, experience additional burdens due to low socio-economic status, high mortality rates and poor access to health care and education. Hence, the clinical population of South Africa may vary considerably from those populations from high-income countries discussed in the literature. METHODS: A comprehensive neuropsychological battery composed of internationally recognised measures examining attention, working memory, language comprehension, learning and memory, areas of executive function and general intellectual functioning was administered to 17 children clinically diagnosed with TSC. RESULTS: The exploration of descriptive data indicated generalised cognitive difficulties in most cognitive domains, aside from memory. With only two participants performing in the average to above-average ranges, the rest of the sample showed poor verbal comprehension, perceptual reasoning, working memory, processing speed, disinhibition, and problems with spatial planning, problem solving, frustration tolerance, set shifting and maintaining a set of rules. Furthermore, correlational findings indicated several associations between socio-demographic and cognitive variables. CONCLUSIONS: Importantly, this is the first study to comprehensively examine multiple domains of neurocognitive functioning in a low-resource setting sample of children with TSC. Current study findings showed that children with TSC have generalised impairments across several cognitive domains, rather than domain-specific impairments. Therefore, although examining individual aspects of cognition, such as those found in previous literature, is important, this approach is limiting. With a comprehensive assessment, including understanding the associations between domains, appropriate and directed support can be provided to ensure all aspects of development are addressed and considered.
 OBJECTIVE: Depressive and anxiety disorders are prevalent among employees in general. Still, knowledge regarding the contribution of these disorders to the dynamics of the labor market in terms of working time, sickness absence, and unemployment is scarce. We aim to quantify the linkage of depressive and anxiety disorders with labor market participation using the expected labor market affiliation method (ELMA), in a large sample of Danish employees. METHODS: We combined three survey waves on occupational health with six high-quality national registers in N = 43,148 Danish employees, of which the 2012 survey contributed 29,665 person years, the 2014 survey 33,043 person years, and the 2016 survey 35,375 person years. We used the new ELMA method to estimate the multi-state transition probabilities and 2-year expected time in work, sickness absence, and unemployment. Depressive and anxiety disorders were assessed by the Major Depression Inventory and the SCL-ANX4 scales, respectively. We adjusted for multiple variables by applying inverse probability weighting in groups of gender and age. RESULTS: Depressive and anxiety disorders among employees link to reduced labor market affiliation by significantly changed transitions probabilities between the labor markets states, viewed as reduced working time by 4-51 days (in two years), increased time in sickness absence by 6-44 days (in two years), and unemployment by 6-12 days (in two years) when compared to employees without depression or anxiety disorders. The results were most pronounced for women employees and for employees with both depression and anxiety disorders. CONCLUSIONS: The study reveals detailed insight into what extent depression and anxiety disorders influence the labor market affiliation, in terms of the complex interrelation between working time, sickness absence, and unemployment. The study emphasizes the importance of preventing and handling depressive and anxiety disorders among employees for strengthening work participation.
 Background: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease associated with loss of upper and lower motor neurones. It leads to death by respiratory failure and has a typical prognosis of 2-3 years. The immune system has been shown to play a role in the pathophysiology of ALS. Some of the most important immune genes are within the human leukocyte antigen (HLA) region, and a recent genome-wide association study (GWAS) has identified a risk allele for ALS within the HLA region. Older studies have also suggested an HLA association with ALS, with certain HLA alleles showing differing expression between patients and controls. This systematic review and meta-analysis examines the previous studies performed in this field.Methods: We used established publication search engines. Findings were excluded if they did not meet the selection criteria. We then undertook statistical meta-analysis on the eligible papers, using a fixed effects model.Results: There were eight eligible papers. There were three statistically significant meta-analysis findings, although these would not be significant after correction for multiple comparisons. The frequencies of HLA-A9 and HLA-DR4 genotypes were lower in ALS subjects than controls, and HLA-B35 was higher in ALS subjects.Discussion: This systematic review and meta-analysis do not confirm all the previously reported associations of HLA with ALS, but shows three alleles of interest. However, there are limitations to the studies, which include the use of older serotyping methodology and the small numbers of subjects. Given the recent GWAS association with HLA, further modern HLA studies are warranted.
 When highly purified cannabidiol (CBD; Epidiolex) and the mammalian target of rapamycin inhibitor everolimus are used concomitantly in the treatment of tuberous sclerosis complex, there is evidence of a pharmacokinetic (PK) interaction, leading to increased everolimus systemic exposure. We evaluated the effect of steady-state CBD exposure following multiple clinically relevant CBD doses on everolimus PK in healthy adult participants in a single-center, fixed-sequence, open-label, phase 1 study. All participants received oral everolimus 5 mg on day 1, followed by a 7-day washout. On days 9-17, participants received CBD (100 mg/mL oral solution) at 12.5 mg/kg in the morning and evening. On the morning of day 13, participants also received a single dose of oral everolimus 5 mg. Medications were taken 30 or 45 minutes (morning or evening dose) after starting a standardized meal. Maximum concentration and area under the concentration-time curve (AUC) from time of dosing to the last measurable concentration and extrapolated to infinity, of everolimus in whole blood were estimated using noncompartmental analysis, with geometric mean ratios and 90% confidence intervals for the ratios of everolimus dosed with CBD to everolimus dosed alone. A single dose of everolimus 5 mg was well tolerated when administered with multiple doses of CBD. Log-transformed everolimus maximum concentration, AUC from time of dosing to the last measurable concentration, and AUC extrapolated to infinity values increased by ≈2.5-fold, and everolimus half-life remained largely unchanged in the presence of steady-state CBD relative to everolimus dosed alone. Everolimus blood concentration monitoring should be strongly advised with appropriate dose reduction when coadministered with CBD.
 Which population factors have predisposed people to disregard government safety guidelines during the COVID-19 pandemic and what justifications do they give for this non-compliance? To address these questions, we analyse fixed-choice and free-text responses to survey questions about compliance and government handling of the pandemic, collected from tens of thousands of members of the UK public at three 6-monthly timepoints. We report that sceptical opinions about the government and mainstream-media narrative, especially as pertaining to justification for guidelines, significantly predict non-compliance. However, free text topic modelling shows that such opinions are diverse, spanning from scepticism about government competence and self-interest to full-blown conspiracy theories, and covary in prevalence with sociodemographic variables. These results indicate that attempts to counter non-compliance through argument should account for this diversity in peoples' underlying opinions, and inform conversations aimed at bridging the gap between the general public and bodies of authority accordingly.
 BACKGROUND: Many neurologic complications have been described after severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) including atypical cases of optic neuritis (ON), positive to myelin oligodendrocyte glycoprotein (MOG) IgG. OBJECTIVE: To report a case of MOG-IgG-associated ON and discuss why SARS-CoV-2 infection could be a potential trigger. METHODS: Retrospective single case report. RESULTS: We report a case of ON with positive MOG-IgG developed 15 days after presentation of SARS-CoV-2 infection. CONCLUSION: This report suggests that SARS-CoV-2 infection may have triggered autoantibodies production against MOG leading to ON.
 We report here a retrospective case series of 3 MG patients suffering from difficulty opening eyes that appeared together with a diagnosis of MG. All are male patients with late-onset MG who are seropositive for anti-acetylcholine receptor antibodies. The phenomenon was characterized by difficulty opening the eyes after forced closure or reflex eye closure, improving with the ice pack test and with repeated forced eye closure but worsening with pyridostigmine treatment. We provide a detailed clinical, serological, imaging and electrophysiological examination of these patients. Electromyography evaluation did not show spontaneous muscle activity or myotonia at rest in the orbital part of the orbicularis oculi muscle. However, there was sustained muscle activity lasting several seconds in the pre-tarsal and pre-septal parts of this muscle. Videos of those reported symptoms were produced and provided. We discuss the possible neurological pathophysiology of this disorder and suggest to name this rare ocular disorder "myotonia-like disorder of the pre-tarsal and pre-septal parts of the orbicularis oculi". This study expands our knowledge of this rare clinical feature of MG and highlights the need for increased awareness of it and further investigation of this ocular manifestation.
 Autoantibodies against contactin-associated protein 2 (CASPR2) are usually associated with autoimmune encephalitis and neuromyotonia. Their association with inflammatory neuropathies has been described in case reports albeit all with distal symmetric manifestation. Here, we report a patient who developed distal arm paresis, dominantly of the right arm, over the course of 1 year. Electroneurography showed a conduction block of motor nerve conduction, nerve ultrasonography a swelling of the right median and ulnar nerve and flow cytometry an increase in natural killer (NK cells) in the blood and natural killer T (NKT) cells in the cerebrospinal fluid (CSF), therefore indicating a multifocal motor neuropathy-like (MMN-like) phenotype. CASPR2 autoantibodies were detected in serum and CSF. Through immunotherapy with intravenous immunoglobulins the patient showed clinical and neurographic improvement. We therefore describe the first association of CASPR2 autoantibodies with a MMN-like clinical manifestation, extending the spectrum of CASPR2-associated diseases.
 Comprehensive autoantibody evaluation is essential for the management of autoimmune disorders. However, conventional methods suffer from poor sensitivity, low throughput, or limited availability. Here, using a proteome-wide human cDNA library, we developed a novel multiplex protein assay (autoantibody array assay; A-Cube) covering 65 antigens of 43 autoantibodies that are associated with systemic sclerosis (SSc) and polymyositis/dermatomyositis (PM/DM). The performance of A-Cube was validated against immunoprecipitation and established enzyme-linked immunosorbent assay. Further, through an evaluation of serum samples from 357 SSc and 172 PM/DM patients, A-Cube meticulously illustrated a diverse autoantibody landscape in these diseases. The wide coverage and high sensitivity of A-Cube also allowed the overlap and correlation analysis between multiple autoantibodies. Lastly, reviewing the cases with distinct autoantibody profiles by A-Cube underscored the importance of thorough autoantibody detection. Together, these data highlighted the utility of A-Cube as well as the clinical relevance of autoantibody profiles in SSc and PM/DM.
 Due to the limitations of the present risk genes in understanding the etiology of amyotrophic lateral sclerosis (ALS), it is necessary to find additional causative genes utilizing novel approaches. In this study, we conducted a two-stage proteome-wide association study (PWAS) using ALS genome-wide association study (GWAS) data (N = 152,268) and two distinct human brain protein quantitative trait loci (pQTL) datasets (ROSMAP N = 376 and Banner N = 152) to identify ALS risk genes and prioritized candidate genes with Mendelian randomization (MR) and Bayesian colocalization analysis. Next, we verified the aberrant expression of risk genes in multiple tissues, including lower motor neurons, skeletal muscle, and whole blood. Six ALS risk genes (SCFD1, SARM1, TMEM175, BCS1L, WIPI2, and DHRS11) were found during the PWAS discovery phase, and SARM1 and BCS1L were confirmed during the validation phase. The following MR (p = 2.10 × 10(-7)) and Bayesian colocalization analysis (ROSMAP PP4 = 0.999, Banner PP4 = 0.999) confirmed the causal association between SARM1 and ALS. Further differential expression analysis revealed that SARM1 was markedly downregulated in lower motor neurons (p = 7.64 × 10(-3)), skeletal muscle (p = 9.34 × 10(-3)), and whole blood (p = 1.94 × 10(-3)). Our findings identified some promising protein candidates for future investigation as therapeutic targets. The dysregulation of SARM1 in multiple tissues provides a new way to explain ALS pathology.
 AIM: To examine the association of the numerical density of the tubulointerstitium infiltrate with pathohistological changes in the glomeruli and the estimated glomerular filtration rate (eGFR) at kidney biopsy and after 18 months. METHODS: This retrospective study enrolled 44 patients (43.2% male) with antineutrophil cytoplasmic antibodies-associated glomerulonephritis treated at the University Clinical Center of Vojvodina between 2017 and 2020. The numerical density of infiltrates in the tubulointerstitium was determined with the Weibel (M-2) system. Data on biochemical, clinical, and pathohistological parameters were obtained. RESULTS: The mean age was 57.7±10.23 years. Global sclerosis in more than 50% of glomeruli and crescents in more than 50% of glomeruli were significantly associated with a mean lower eGFR (17.6±11.78; 32.0±26.13, respectively) at kidney biopsy (P=0.002; P<0.001, respectively), but not after 18 months. The average numerical density of infiltrates was significantly higher in patients with more than 50% of globally sclerotic glomeruli (P<0.001) and with crescents in more than 50% of glomeruli (P<0.001). The average numerical density of infiltrates significantly correlated with eGFR at biopsy (r=-0.614), but not after 18 months. Our results were confirmed by using multiple linear regression. CONCLUSION: Numerical density of infiltrates, and global glomerular sclerosis and crescents in more than 50% of glomeruli significantly affect eGFR at biopsy, but not after 18 months.
 Pathologies that are causative for neurodegenerative disease (ND) are also frequently present in unimpaired, older individuals. In this retrospective study of 1647 autopsied individuals, we report the incidence of 10 pathologies across ND and normal ageing in attempt to clarify which pathological combinations are disease-associated and which are ageing-related. Eight clinically defined groups were examined including unimpaired individuals and those with clinical Alzheimer's disease, mixed dementia, amyotrophic lateral sclerosis, frontotemporal degeneration, multiple system atrophy, probable Lewy body disease or probable tauopathies. Up to seven pathologies were observed concurrently resulting in a heterogeneous mix of 161 pathological combinations. The presence of multiple additive pathologies associated with older age, increasing disease duration, APOE e4 allele and presence of dementia across the clinical groups. Fifteen to 67 combinations occurred in each group, with the unimpaired group defined by 35 combinations. Most combinations occurred at a <5% prevalence including 86 that were present in only one or two individuals. To better understand this heterogeneity, we organized the pathological combinations into five broad categories based on their age-related frequency: (i) 'Ageing only' for the unimpaired group combinations; (ii) 'ND only' if only the expected pathology for that individual's clinical phenotype was present; (iii) 'Other ND' if the expected pathology was not present; (iv) 'ND + ageing' if the expected pathology was present together with ageing-related pathologies at a similar prevalence as the unimpaired group; and (v) 'ND + associated' if the expected pathology was present together with other pathologies either not observed in the unimpaired group or observed at a greater frequency. ND only cases comprised a minority of cases (19-45%) except in the amyotrophic lateral sclerosis (56%) and multiple system atrophy (65%) groups. The ND + ageing category represented 9-28% of each group, but was rare in Alzheimer's disease (1%). ND + associated combinations were common in Alzheimer's disease (58%) and Lewy body disease (37%) and were observed in all groups. The Ageing only and Other ND categories accounted for a minority of individuals in each group. This observed heterogeneity indicates that the total pathological burden in ND is frequently more than a primary expected clinicopathological correlation with a high frequency of additional disease- or age-associated pathologies.
 INTRODUCTION: TP73 was recently identified as a novel causative gene for amyotrophic lateral sclerosis (ALS). We aimed to determine the contribution of variations in TP73 in the Chinese ALS population and to further explore the genotype-phenotype correlations. METHODS: We screened rare, putative pathogenic TP73 mutations in a large Chinese ALS cohort and performed association analysis of both rare and common TP73 variations between cases and controls. RESULTS: Of the 985 ALS patients studied, six rare, heterozygous putative pathogenic variants in TP73 were identified among six unrelated sALS patients. Exon 14 of TP73 might be a mutant hotspot in our cohort. Patients with ALS with only rare, putative pathogenic TP73 mutations exhibited a characteristic clinical profile. Patients harboring multiple mutations in TP73 and other ALS-related genes displayed a significantly earlier onset of ALS. Association analysis revealed that rare TP73 variants in the untranslated regions (UTRs) were enriched among ALS patients; meanwhile, two common variants in the exon-intron boundary were discovered to be associated with ALS. DISCUSSION: We demonstrate that TP73 variations also have contributed to ALS in the Asian population and broaden the genotypic and phenotypic spectrum of TP73 variants in the ALS-frontotemporal dementia (FTD) spectrum. Furthermore, our findings first suggest that TP73 is not only a causative gene, but also exerts a disease-modifying effect. These results may contribute to a better understanding of the molecular mechanism of ALS.
 Systemic sclerosis (SSc) is a debilitating autoimmune disease that affects multiple systems. It is characterized by immunological deregulation, functional and structural abnormalities of small blood vessels, and fibrosis of the skin, and, in some cases, internal organs. Fibrosis has a devastating impact on a patient's life and lung fibrosis is associated with high morbimortality. Several immune populations contribute to the progression of SSc, and plasmacytoid dendritic cells (pDCs) have been identified as crucial mediators of fibrosis. Research on murine models of lung and skin fibrosis has shown that pDCs are essential in the development of fibrosis, and that removing pDCs improves fibrosis. pDCs are a subset of dendritic cells (DCs) that are specialized in anti-viral responses and are also involved in autoimmune diseases, such as SSc, systemic lupus erythematosus (SLE) and psoriasis, mostly due to their capacity to produce type I interferon (IFN). A type I IFN signature and high levels of CXCL4, both derived from pDCs, have been associated with poor prognosis in patients with SSc and are correlated with fibrosis. This review will examine the recent research on the molecular mechanisms through which pDCs impact SSc.
 Amyotrophic lateral sclerosis (ALS) is a rare deadly progressive neurological disease that primarily affects the upper and lower motor neurons with an annual incidence rate of 0.6 to 3.8 per 100,000 people. Weakening and gradual atrophy of the voluntary muscles are the first signs of the disease onset affecting all aspects of patients' lives, including eating, speaking, moving, and even breathing. Only 5-10% of patients have a familial type of the disease and show an autosomal dominant pattern, but the cause of the disease is unknown in the remaining 90% of patients (Sporadic ALS). However, in both types of disease, the patient's survival is 2 to 5 years from the disease onset. Some clinical and molecular biomarkers, magnetic resonance imaging (MRI), blood or urine test, muscle biopsy, and genetic testing are complementary methods for disease diagnosis. Unfortunately, with the exception of Riluzole, the only medically approved drug for the management of this disease, there is still no definitive cure for it. In this regard, the use of mesenchymal stem cells (MSCs) for the treatment or management of the disease has been common in preclinical and clinical studies for many years. MSCs are multipotent cells having immunoregulatory, anti-inflammatory, and differentiation ability that makes them a good candidate for this purpose. This review article aims to discuss multiple aspects of ALS disease and focus on MSCs' role in disease management based on performed clinical trials.
 Baicalein (5,6,7-trihydroxyflavone) is a traditional Chinese medicine with multiple pharmacological and biological activities including anti-inflammatory and anti-fibrotic effects. However, whether baicalein has a therapeutic impact on peritoneal fibrosis has not been reported yet. In the present study, network pharmacology and molecular docking approaches were performed to evaluate the role and the potential mechanisms of baicalein in attenuating peritoneal dialysis-associated peritoneal fibrosis. The results were validated in both animal models and the cultured human mesothelial cell line. Nine intersection genes among baicalein targets and the human peritoneum RNA-seq dataset including four encapsulating peritoneal sclerosis samples and four controls were predicted by network analysis. Among them, MMP2, BAX, ADORA3, HIF1A, PIM1, CA12, and ALOX5 exhibited higher expression in the peritoneum with encapsulating peritoneal sclerosis compared with those in the control, which might be crucial targets of baicalein against peritoneal fibrosis. Furthermore, KEGG and GO enrichment analyses suggested that baicalein played an anti-peritoneal fibrosis role through the regulating cell proliferation, inflammatory response, and AGE-RAGE signaling pathway. Moreover, molecular docking analysis revealed a strong potential binding between baicalein and MMP2, which was consistent with the predictive results. Importantly, using a mouse model of peritoneal fibrosis by intraperitoneally injecting 4.25% glucose dialysate, we found that baicalein treatment significantly attenuated peritoneal fibrosis, as evident by decreased collagen deposition, protein expression of α-SMA and fibronectin, and peritoneal thickness, at least, by reducing the expression of MMP2, suggesting that baicalein may have therapeutic potential in suppressing peritoneal dialysis-related fibrosis.
 Micro RNAs (miRNAs) are short, non-coding RNAs with significant potential as diagnostic and prognostic biomarkers. However, a lack of reproducibility across studies has hindered their introduction into clinical settings. Inconsistencies between studies include a lack of consensus on the miRNAs associated with a specific disease and the direction of regulation. These differences may reflect the heterogenous nature of pathologies with multiple phenotypes, such as amyotrophic lateral sclerosis (ALS). It is also possible that discrepancies are due to different sampling, processing, and analysis protocols across labs. Using miRNA extracted from L1CAM immunoaffinity purified extracellular vesicles (neural-enriched extracellular vesicles or NEE), we thrice replicated an 8-miRNA fingerprint diagnostic of ALS, which includes the miRNA species and direction of regulation. We aimed to determine if the extra purification steps required to generate NEE created a unique extracellular vesicle (EV) fraction that might contribute to the robustness and replicability of our assay. We compared three fractions from control human plasma: 1) total heterogenous EVs (T), 2) L1CAM/neural enriched EVs (NEE), and 3) the remaining total-minus-NEE fraction (T-N). Each fraction was characterized for size, total protein content, and protein markers, then total RNA was extracted, and qPCR was run on 20 miRNAs. We report that the miRNA expression within NEE was different enough compared to T and T-N to justify the extra steps required to generate this fraction. We conclude that L1CAM immunocapture generates a unique fraction of EVs that consistently and robustly replicates a miRNA fingerprint which differentiates ALS patients from controls.
 Systemic sclerosis (SSc) is an intractable autoimmune disease with unmet medical needs. Conventional immunosuppressive therapies have modest efficacy and obvious side effects. Targeted therapies with small molecules and antibodies remain under investigation in small pilot studies. The major breakthrough was the development of autologous haematopoietic stem cell transplantation (AHSCT) to treat refractory SSc with rapidly progressive internal organ involvement. However, AHSCT is contraindicated in patients with advanced visceral involvement. Mesenchymal stem cells (MSCs) which are characterized by immunosuppressive, antifibrotic and proangiogenic capabilities may be a promising alternative option for the treatment of SSc. Multiple preclinical and clinical studies on the use of MSCs to treat SSc are underway. However, there are several unresolved limitations and safety concerns of MSC transplantation, such as immune rejections and risks of tumour formation, respectively. Since the major therapeutic potential of MSCs has been ascribed to their paracrine signalling, the use of MSC-derived extracellular vesicles (EVs)/secretomes/exosomes as a "cell-free" therapy might be an alternative option to circumvent the limitations of MSC-based therapies. In the present review, we overview the current knowledge regarding the therapeutic efficacy of MSCs in SSc, focusing on progresses reported in preclinical and clinical studies using MSCs, as well as challenges and future directions of MSC transplantation as a treatment option for patients with SSc.
 INTRODUCTION: Systemic sclerosis (SSc) is a severe, and often life-threatening, autoimmune disease, which causes inflammation and fibrosis of the skin and internal organs. There are currently limited effective therapeutic options for patients with SSc. There are recently completed and ongoing phase 2 and 3 studies looking at biologic therapies for SSc that target the underlying pathogenesis of the disease. AREAS COVERED: The purpose of this review is to describe completed and ongoing trials of different biologic therapies for the treatment of SSc. This review discusses biologic therapy directed at multiple pathways that are believed to contribute to inflammation and fibrosis in SSc including T cell, B cell, direct cytokines, and JAK signaling. Data presented is based on authors' expertise of completed and ongoing trials. EXPERT OPINION: Tocilizumab and rituximab have supporting data to advocate for use in early SSc. Data from tocilizumab showed preservation of forced vital capacity (FVC) and beneficial effects on global composite measure. Recent data from different trials with rituximab in SSc (with and without interstitial lung disease) show beneficial effects on skin and FVC with good tolerability. We highlight the molecular heterogeneity in early SSc phenotype and the need to account for this in future trials.
 Neurodegenerative diseases are a large class of neurological disorders characterized by progressive dysfunction and death of neurones. Examples include Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. Aging is the primary risk factor for neurodegeneration; individuals over 65 are more likely to suffer from a neurodegenerative disease, with prevalence increasing with age. As the population ages, the social and economic burden caused by these diseases will increase. Therefore, new therapies that address both aging and neurodegeneration are imperative. Ketogenic diets (KDs) are low carbohydrate, high-fat diets developed initially as an alternative treatment for epilepsy. The classic ketogenic diet provides energy via long-chain fatty acids (LCFAs); naturally occurring medium chain fatty acids (MCFAs), on the other hand, are the main components of the medium-chain triglyceride (MCT) ketogenic diet. MCT-based diets are more efficient at generating the ketone bodies that are used as a secondary energy source for neurones and astrocytes. However, ketone levels alone do not closely correlate with improved clinical symptoms. Recent findings suggest an alternative mode of action for the MCFAs, e.g., via improving mitochondrial biogenesis and glutamate receptor inhibition. MCFAs have been linked to the treatment of both aging and neurodegenerative disease via their effects on metabolism. Through action on multiple disease-related pathways, MCFAs are emerging as compounds with notable potential to promote healthy aging and ameliorate neurodegeneration. MCFAs have been shown to stimulate autophagy and restore mitochondrial function, which are found to be disrupted in aging and neurodegeneration. This review aims to provide insight into the metabolic benefits of MCFAs in neurodegenerative disease and healthy aging. We will discuss the use of MCFAs to combat dysregulation of autophagy and mitochondrial function in the context of "normal" aging, Parkinson's disease, amyotrophic lateral sclerosis and Alzheimer's disease.
 PURPOSE: Neuroendocrine neoplasms can occur as part of inherited disorders, usually in the form of well-differentiated, slow-growing tumors (NET). The main predisposing syndromes include: multiple endocrine neoplasias type 1 (MEN1), associated with a large spectrum of gastroenteropancreatic and thoracic NETs, and type 4 (MEN4), associated with a wide tumour spectrum similar to that of MEN1; von Hippel-Lindau syndrome (VHL), tuberous sclerosis (TSC), and neurofibromatosis 1 (NF-1), associated with pancreatic NETs. In the present review, we propose a reappraisal of the genetic basis and clinical features of gastroenteropancreatic and thoracic NETs in the setting of inherited syndromes with a special focus on molecularly targeted therapies for these lesions. METHODS: Literature search was systematically performed through online databases, including MEDLINE (via PubMed), and Scopus using multiple keywords' combinations up to June 2022. RESULTS: Somatostatin analogues (SSAs) remain the mainstay of systemic treatment for NETs, and radiolabelled SSAs can be used for peptide-receptor radionuclide therapy for somatostatin receptor (SSTR)-positive NETs. Apart of these SSTR-targeted therapies, other targeted agents have been approved for NETs: the mTOR inhibitor everolimus for lung, gastroenteropatic and unknown origin NET, and sunitinib, an antiangiogenic tyrosine kinase inhibitor, for pancreatic NET. Novel targeted therapies with other antiangiogenic agents and immunotherapies have been also under evaluation. CONCLUSIONS: Major advances in the understanding of genetic and epigenetic mechanisms of NET development in the context of inherited endocrine disorders have led to the recognition of molecular targetable alterations, providing a rationale for the implementation of treatments and development of novel targeted therapies.
 Astrocytic hamartoma is a benign glial tumor. It may be associated with tuberous sclerosis and can also be found incidentally on retinal examination as an isolated presentation. Here, we describe multimodal imaging characteristics of astrocytic hamartoma in a patient with retinitis pigmentosa. Spectral domain optical coherence tomography of both eyes showed moth-eaten optically empty spaces and hyperreflective dots along with foveal thinning. Multicolor image highlighted mulberry appearance of the lesion with green shift signifying elevated lesion. In infrared reflectance, lesion was hyporeflective with its margins well delineated. Green reflectance and blue reflectance highlighted calcification as multiple hyperreflective dots. Autofluorescence showed typical hyperautofluorescence.
 Tuberous sclerosis complex (TSC) is an autosomal dominant neurocutaneous syndrome causing hamartomatous growths in multiple organs. Facial angiofibromas occur in up to 80% of patients and can be highly disfiguring. Treatment for these lesions is challenging. Recently, topical rapamycin has been proposed as an effective option to treat angiofibromas but a commercially available compound has not yet been developed in Europe. We conducted a retrospective review with the aim to update the current data on the use of topical rapamycin in the treatment of angiofibromas in TSC, focusing on the optimal concentration and trying to establish which vehicle should be preferred. Thirty-nine reports describing the use of topical rapamycin in the treatment of angiofibromas in TSC were considered, involving a total of 483 patients. An improvement of the lesions has been shown in over 90% of subjects, particularly if the treatment was started at early stages. Several different formulations (ointment, gel, solution and cream) with a wide range of concentrations (0.003%-1%) were proposed, of which a pharmacological analysis has also been performed. Topical rapamycin can be considered an effective and safe option for the treatment and the prevention of facial angiofibromas in younger patients, but the best formulation has yet to be established. Our review demonstrates that ointment and gel should be preferred, but it is not clear which concentration is optimal. However, according to this study, the 0.1% concentration represents the first choice. Long-term and comparative studies between topical rapamycin formulations are required in order to establish which treatment has a better outcome and lower recurrence rate.
 BACKGROUND AND PURPOSE: This study aimed at estimating the prevalence of language impairment (LI) in a large, clinic-based cohort of non-demented amyotrophic lateral sclerosis (ALS) patients and assessing its underpinnings at motor and non-motor levels. METHODS: Non-demented ALS patients (N = 348) underwent the Edinburgh Cognitive and Behavioural ALS Screen (ECAS), as well as an assessment of behavioural/psychiatric and motor-functional features. The prevalence of LI was estimated based on the proportion of patients showing a performance below the age- and education-adjusted cut-off on the ECAS-Language. Multiple regression models were run to assess the determinants of language functioning and impairment. RESULTS: The prevalence of LI was 22.7%. 46.6% of the variance of ECAS-Language scores remained unexplained, with only the ECAS-Executive positively predicting them (p < 0.001; η(2)  = 0.07). Similarly, only a lower score on the ECAS-Executive predicted a higher probability of a below cut-off ECAS-Language performance (p < 0.001). Spelling and Naming tasks were the major drivers of ECAS-Language performance. CONCLUSIONS: This study suggests that, in non-demented ALS patients, LI occurs in ≈23% of cases, is significantly driven by executive dysfunction but, at the same time, partially independent of it and is not associated with other motor or non-motor features.
 BACKGROUND: The novel optic neuritis (ON) diagnostic criteria include intereye differences (IED) of optical coherence tomography (OCT) parameters. IED has proven valuable for ON diagnosis in multiple sclerosis but has not been evaluated in aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4+NMOSD). We evaluated the diagnostic accuracy of intereye absolute (IEAD) and percentage difference (IEPD) in AQP4+NMOSD after unilateral ON >6 months before OCT as compared with healthy controls (HC). METHODS: Twenty-eight AQP4+NMOSD after unilateral ON (NMOSD-ON), 62 HC and 45 AQP4+NMOSD without ON history (NMOSD-NON) were recruited by 13 centres as part of the international Collaborative Retrospective Study on retinal OCT in Neuromyelitis Optica study. Mean thickness of peripapillary retinal nerve fibre layer (pRNFL) and macular ganglion cell and inner plexiform layer (GCIPL) were quantified by Spectralis spectral domain OCT. Threshold values of the ON diagnostic criteria (pRNFL: IEAD 5 µm, IEPD 5%; GCIPL: IEAD: 4 µm, IEPD: 4%) were evaluated using receiver operating characteristics and area under the curve (AUC) metrics. RESULTS: The discriminative power was high for NMOSD-ON versus HC for IEAD (pRNFL: AUC 0.95, specificity 82%, sensitivity 86%; GCIPL: AUC 0.93, specificity 98%, sensitivity 75%) and IEPD (pRNFL: AUC 0.96, specificity 87%, sensitivity 89%; GCIPL: AUC 0.94, specificity 96%, sensitivity 82%). The discriminative power was high/moderate for NMOSD-ON versus NMOSD-NON for IEAD (pRNFL: AUC 0.92, specificity 77%, sensitivity 86%; GCIP: AUC 0.87, specificity 85%, sensitivity 75%) and for IEPD (pRNFL: AUC 0.94, specificity 82%, sensitivity 89%; GCIP: AUC 0.88, specificity 82%, sensitivity 82%). CONCLUSIONS: Results support the validation of the IED metrics as OCT parameters of the novel diagnostic ON criteria in AQP4+NMOSD.
 Dysregulation of the interleukin-1 (IL-1) pathway leads to immune diseases that can result in chronic tissue and organ inflammation. Although IL-1 blockade has shown promise in ameliorating these symptoms and improving patients' quality of life, there is an urgent need for more effective, long-lasting treatments. We developed a lentivirus (LV)-mediated gene transfer strategy using transplanted autologous hematopoietic stem/progenitor cells (HSPCs) as a source of IL-1 receptor antagonist (IL-1RA) for systemic delivery to tissues and organs. Transplantation of mouse and human HSPCs transduced with an IL-1RA-encoding LV ensured stable IL-1RA production while maintaining the clonogenic and differentiation capacities of HSPCs in vivo. We examined the efficacy of cell-mediated IL-1RA delivery in three models of IL-1-dependent inflammation, for which treatment hindered neutrophil recruitment in an inducible model of gout, prevented systemic and multi-tissue inflammation in a genetic model of cryopyrin-associated periodic syndromes, and reduced disease severity in an experimental autoimmune encephalomyelitis model of multiple sclerosis. Our findings demonstrate HSPC-mediated IL-1RA delivery as a potential therapeutic modality that can be exploited to suppress tissue and organ inflammation in diverse immune-related diseases involving IL-1-driven inflammation.
 The prevalence of nonalcoholic fatty liver disease (NAFLD) is much higher in patients with type II diabetes (T2D). Inflammasomes are multimolecular complexes reported to involve inflammatory conditions. The nuclear factor (erythroid-derived 2)-like factor 2/antioxidant responsive element (Nrf2/ARE) pathway is an important regulator of antioxidant status in cells. Antidiabetic drug glibenclamide (GLB) is reported as  NACHT, leucine-rich repeat, and pyrin domain domains-containing protein 3 (NLRP3) inflammasome inhibitor, whereas anti-multiple sclerosis drug dimethyl fumarate (DMF) is reported as an Nrf2/ARE pathway activator. Both GLB and DMF possess anti-inflammatory and antioxidant properties, therefore, the hypothesis was made to look into the alone as well as the combination potential of GLB, DMF, and GLB + DMF, against NAFLD in diabetic rats. This study was aimed to investigate (1) the involvement of NLRP3 inflammasome and Nrf2/ARE signaling in diabetes-associated NAFLD (2) the effect of GLB, DMF, GLB + DMF, and metformin (MET) interventions on NLRP3 inflammasome and Nrf2/ARE signaling in diabetes-associated NAFLD. The rats were injected with streptozotocin (STZ) 35 mg/kg and fed a high-fat diet (HFD) for 17 consecutive weeks to induce diabetic NAFLD. The oral treatment of GLB 0.5 mg/kg/day, DMF 25 mg/kg/day, their combination and MET 200 mg/kg/day, were provided from the 6th to the 17th week. Treatment with GLB, DMF, GLB + DMF, and MET significantly alleviated HFD + STZ-induced plasma glucose, triglycerides, cholesterol, %HbA1c, hepatic steatosis, NLRP3, apoptosis-associated speck-like protein containing a caspase activation and recruitment domain, CARD, caspase-1, interleukin-1β (IL-1β), nuclear factor-κB (NF-κB), Nrf2, superoxide dismutase 1, catalase, IGF 1, heme oxygenase 1, receptor for the advanced glycation end product (RAGE), and collagen-1 in diabetic rats. Further, a mechanistic molecular study employing other specific NLRP3 inhibitors and Nrf2 activators will significantly contribute to the development of novel therapy for fatty liver diseases.
 The aim of this consensus paper is to discuss the roles of the cerebellum in human gait, as well as its assessment and therapy. Cerebellar vermis is critical for postural control. The cerebellum ensures the mapping of sensory information into temporally relevant motor commands. Mental imagery of gait involves intrinsically connected fronto-parietal networks comprising the cerebellum. Muscular activities in cerebellar patients show impaired timing of discharges, affecting the patterning of the synergies subserving locomotion. Ataxia of stance/gait is amongst the first cerebellar deficits in cerebellar disorders such as degenerative ataxias and is a disabling symptom with a high risk of falls. Prolonged discharges and increased muscle coactivation may be related to compensatory mechanisms and enhanced body sway, respectively. Essential tremor is frequently associated with mild gait ataxia. There is growing evidence for an important role of the cerebellar cortex in the pathogenesis of essential tremor. In multiple sclerosis, balance and gait are affected due to cerebellar and spinal cord involvement, as a result of disseminated demyelination and neurodegeneration impairing proprioception. In orthostatic tremor, patients often show mild-to-moderate limb and gait ataxia. The tremor generator is likely located in the posterior fossa. Tandem gait is impaired in the early stages of cerebellar disorders and may be particularly useful in the evaluation of pre-ataxic stages of progressive ataxias. Impaired inter-joint coordination and enhanced variability of gait temporal and kinetic parameters can be grasped by wearable devices such as accelerometers. Kinect is a promising low cost technology to obtain reliable measurements and remote assessments of gait. Deep learning methods are being developed in order to help clinicians in the diagnosis and decision-making process. Locomotor adaptation is impaired in cerebellar patients. Coordinative training aims to improve the coordinative strategy and foot placements across strides, cerebellar patients benefiting from intense rehabilitation therapies. Robotic training is a promising approach to complement conventional rehabilitation and neuromodulation of the cerebellum. Wearable dynamic orthoses represent a potential aid to assist gait. The panel of experts agree that the understanding of the cerebellar contribution to gait control will lead to a better management of cerebellar ataxias in general and will likely contribute to use gait parameters as robust biomarkers of future clinical trials.
 BACKGROUND: In idiopathic intracranial hypertension (IIH), sustained weight loss is the main pillar in modifying disease course, whereby glucagon-like peptide-1 receptor agonists (GLP-1-RAs) could present an attractive treatment option. METHODS: In this open-label, single-center, case-control pilot study, patients with IIH (pwIIH) and a body mass index (BMI) of ≥ 30 kg/m(2) were offered to receive a GLP-1-RA (semaglutide, liraglutide) in addition to the usual care weight management (UCWM). Patients electing for UCWM only served as a control group matched for age-, sex- and BMI (1:2 ratio). The primary endpoint was the percentage weight loss at six months (M6) compared to baseline. Secondary endpoints included the rate of patients with a weight loss of ≥ 10%, monthly headache days (MHD), the rate of patients with a ≥ 30% and ≥ 50% reduction in MHD, visual outcome parameters, and adverse events (AEs). RESULTS: We included 39 pwIIH (mean age 33.6 years [SD 8.0], 92.3% female, median BMI 36.3 kg/m(2) [IQR 31.4-38.3]), with 13 patients being treated with GLP-1-RAs. At M6, mean weight loss was significantly higher in the GLP-1-RA group (-12.0% [3.3] vs. -2.8% [4.7]; p < 0.001). Accordingly, weight loss of ≥ 10% was more common in this group (69.2% vs. 4.0%; p < 0.001). Median reduction in MHD was significantly higher in the GLP-1-RA group (-4 [-10.5, 0.5] vs. 0 [-3, 1]; p = 0.02), and the 50% responder rate was 76.9% vs. 40.0% (p = 0.04). Visual outcome parameters did not change significantly from baseline to M6. Median reduction in acetazolamide dosage was significantly higher in the GLP-1-RA group (-16.5% [-50, 0] vs. 0% [-25, 50]; p = 0.04). AEs were mild or moderate and attributed to gastrointestinal symptoms in 9/13 patients. None of the AEs led to premature treatment discontinuation. CONCLUSIONS: This open-label, single-center pilot study suggests that GLP-1-RAs are an effective and safe treatment option for achieving significant weight loss with a favorable effect on headache, leading to reduced acetazolamide dosage in pwIIH.
 OBJECTIVE: To investigate the protective effects and its possible mechanism of Wuzi Yanzong Pill (WYP) on Parkinson's disease (PD) model mice. METHODS: Thirty-six C57BL/6 male mice were randomly assigned to 3 groups including normal, PD, and PD+WYP groups, 12 mice in each group. One week of intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to establish the classical PD model in mice. Meanwhile, mice in the PD+WYP group were administrated with 16 g/kg WYP, twice daily by gavage. After 14 days of administration, gait test, open field test and pole test were measured to evaluate the movement function. Tyrosine hydroxylase (TH) neurons in substantia nigra of midbrain and binding immunoglobulin heavy chain protein (GRP78) in striatum and cortex were observed by immunohistochemistry. The levels of TH, GRP78, p-PERK, p-eIF2α, ATF4, p-IRE1α, XBP1, ATF6, CHOP, ASK1, p-JNK, Caspase-12, -9 and -3 in brain were detected by Western blot. RESULTS: Compared with the PD group, WYP treatment ameliorated gait balance ability in PD mice (P<0.05). Similarly, WYP increased the total distance and average speed (P<0.05 or P<0.01), reduced rest time and pole time (P<0.05). Moreover, WYP significantly increased TH positive cells (P<0.01). Immunofluorescence showed WYP attenuated the levels of GRP78 in striatum and cortex. Meanwhile, WYP treatment significantly decreased the protein expressions of GRP78, p-PERK, p-eIF2α, ATF4, p-IRE1 α, XBP1, CHOP, Caspase-12 and Caspase-9 (P<0.05 or P<0.01). CONCLUSIONS: WYP ameliorated motor symptoms and pathological lesion of PD mice, which may be related to the regulation of unfolded protein response-mediated signaling pathway and inhibiting the endoplasmic reticulum stress-mediated neuronal apoptosis pathway.
 Metabolic fluxes involving fatty acid biosynthesis play essential roles in controlling the differentiation of T helper 17 (T(H)17) cells. However, the exact enzymes and lipid metabolites involved, as well as their link to promoting the core gene transcriptional signature required for the differentiation of T(H)17 cells, remain largely unknown. From a pooled CRISPR-based screen and unbiased lipidomics analyses, we identified that 1-oleoyl-lysophosphatidylethanolamine could act as a lipid modulator of retinoid-related orphan receptor gamma t (RORγt) activity in T(H)17 cells. In addition, we specified five enzymes, including Gpam, Gpat3, Lplat1, Pla2g12a, and Scd2, suggestive of the requirement of glycerophospholipids with monounsaturated fatty acids being required for the transcription of Il17a. 1-Oleoyl-lysophosphatidylethanolamine was reduced in Pla2g12a-deficient T(H)17 cells, leading to the abolition of interleukin-17 (IL-17) production and disruption to the core transcriptional program required for the differentiation of T(H)17 cells. Furthermore, mice with T cell-specific deficiency of Pla2g12a failed to develop disease in an experimental autoimmune encephalomyelitis model of multiple sclerosis. Thus, our data indicate that 1-oleoyl-lysophosphatidylethanolamine is a lipid metabolite that promotes RORγt-induced T(H)17 cell differentiation and the pathogenicity of T(H)17 cells.
 SIGNIFICANCE STATEMENT: The optimal choice of vascular access for patients undergoing hemodialysis-arteriovenous fistula (AVF) or arteriovenous graft (AVG)-remains controversial. In a pragmatic observational study of 692 patients, the authors found that among patients who initiated hemodialysis with a central vein catheter (CVC), a strategy that maximized AVF placement resulted in a higher frequency of access procedures and greater access management costs for patients who initially received an AVF than an AVG. A more selective policy that avoided AVF placement if an AVF was predicted to be at high risk of failure resulted in a lower frequency of access procedures and access costs in patients receiving an AVF versus an AVG. These findings suggest that clinicians should be more selective in placing AVFs because this approach improves vascular access outcomes. BACKGROUND: The optimal choice of initial vascular access-arteriovenous fistula (AVF) or graft (AVG)-remains controversial, particularly in patients initiating hemodialysis with a central venous catheter (CVC). METHODS: In a pragmatic observational study of patients who initiated hemodialysis with a CVC and subsequently received an AVF or AVG, we compared a less selective vascular access strategy of maximizing AVF creation (period 1; 408 patients in 2004 through 2012) with a more selective policy of avoiding AVF creation if failure was likely (period 2; 284 patients in 2013 through 2019). Prespecified end points included frequency of vascular access procedures, access management costs, and duration of catheter dependence. We also compared access outcomes in all patients with an initial AVF or AVG in the two periods. RESULTS: An initial AVG placement was significantly more common in period 2 (41%) versus period 1 (28%). Frequency of all access procedures per 100 patient-years was significantly higher in patients with an initial AVF than an AVG in period 1 and lower in period 2. Median annual access management costs were significantly higher among patients with AVF ($10,642) versus patients with AVG ($6810) in period 1 but significantly lower in period 2 ($5481 versus $8253, respectively). Years of catheter dependence per 100 patient-years was three-fold higher in patients with AVF versus patients with AVG in period 1 (23.3 versus 8.1, respectively), but only 30% higher in period 2 (20.8 versus 16.0, respectively). When all patients were aggregated, the median annual access management cost was significantly lower in period 2 ($6757) than in period 1 ($9781). CONCLUSIONS: A more selective approach to AVF placement reduces frequency of vascular access procedures and cost of access management.
 We conducted a single-centre retrospective cohort study in a French University Hospital between 2010 and 2018 to describe the risk of severe infectious event (SIE) within 2 years after the date of first rituximab infusion (T0) prescribed after the evidence of acquired hypogammaglobulinemia (gamma globulins [GG] ≤ 6 g/L) in the setting of autoimmune diseases (AID) other than rheumatoid arthritis. SIE occurred in 26 out of 121 included patients. Two years cumulative incidence rates were 12.7 % (95 % CI 5.1-23.9) in the multiple sclerosis/neuromyelitis optica spectrum disorder group (n = 48), 27.6 % (95 % CI 15.7-40.9) in the ANCA-associated vasculitis group (n = 48) and 30.6 % (95 % CI 13.1-50.3) in the 'other AID' group (n = 25). Median GG level at T0 was 5.3 g/l (IQR 4.1-5.6) in the 'SIE' group and 5.6 g/l (IQR 4.7-5.8) in the 'no SIE' group (p = 0.04). In regression analysis, risk of SIE increased with Charlson comorbidity index ≥ 3 (OR 2.77; 95 % CI 1.01-7.57), lung disease (OR 3.20; 95 % CI 1.27-7.99), GG < 4 g/L (OR 3.39; 95 % CI 1.02-11.19), concomitant corticosteroid therapy (OR 4.13; 95 % CI 1.63-10.44), previous cyclophosphamide exposure (OR 2.69; 95 % CI 1.10-6.61), a lymphocyte count < 1000 cells/µL (OR 2.86; 95 % CI 1.12-7.21) and absence of pneumococcal vaccination (OR 3.50; 95 % CI 1.41-8.70). These results may help to inform clinical decision when considering a treatment by rituximab in immunosuppressed AID patients with hypogammaglobulinemia.
 Due to commonalities in pathophysiology, age-related macular degeneration (AMD) represents a uniquely accessible model to investigate therapies for neurodegenerative diseases, leading us to examine whether pathways of disease progression are shared across neurodegenerative conditions. Here we use single-nucleus RNA sequencing to profile lesions from 11 postmortem human retinas with age-related macular degeneration and 6 control retinas with no history of retinal disease. We create a machine-learning pipeline based on recent advances in data geometry and topology and identify activated glial populations enriched in the early phase of disease. Examining single-cell data from Alzheimer's disease and progressive multiple sclerosis with our pipeline, we find a similar glial activation profile enriched in the early phase of these neurodegenerative diseases. In late-stage age-related macular degeneration, we identify a microglia-to-astrocyte signaling axis mediated by interleukin-1β which drives angiogenesis characteristic of disease pathogenesis. We validated this mechanism using in vitro and in vivo assays in mouse, identifying a possible new therapeutic target for AMD and possibly other neurodegenerative conditions. Thus, due to shared glial states, the retina provides a potential system for investigating therapeutic approaches in neurodegenerative diseases.
 OBJECTIVE: Multiple sclerosis (MS) is an immune regulatory disease that affects the central nervous system (CNS). The main pathological features include demyelination and neurodegeneration, and the pathogenesis is associated with astrocytic neuroinflammation. Taurochenodeoxycholic acid (TCDCA) is one of the conjugated bile acids in animal bile, and it is not clear whether TCDCA could improve MS by inhibiting the activation of astrocytes. This study was aimed to evaluate the effects of TCDCA on experimental autoimmune encephalomyelitis (EAE)-a classical animal model of MS, and to probe its mechanism from the aspect of suppressing astrocytic neuroinflammation. It is expected to prompt the potential application of TCDCA for the treatment of MS. RESULTS: TCDCA effectively alleviated the progression of EAE and improved the impaired neurobehavior in mice. It mitigated the hyperactivation of astrocytes and down-regulated the mRNA expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the brain cortex. In the C6 astrocytic cell line induced by lipopolysaccharide (LPS), TCDCA treatment dose-dependently decreased the production of NO and the protein expression of iNOS and glial fibrillary acidic protein (GFAP). TCDCA consistently inhibited the mRNA expressions of COX2, iNOS and other inflammatory mediators. Furthermore, TCDCA decreased the protein expression of phosphorylated serine/threonine kinase (AKT), inhibitor of NFκB α (IκBα) and nuclear factor κB (NFκB). And TCDCA also inhibited the nuclear translocation of NFκB. Conversely, as an inhibitor of the G-protein coupled bile acid receptor Gpbar1 (TGR5), triamterene eliminated the effects of TCDCA in LPS-stimulated C6 cells. CONCLUSION: TCDCA improves the progress of EAE by inhibiting the astrocytic neuroinflammation, which might be exerted by the regulation of TGR5 mediated AKT/NFκB signaling pathway. These findings may prompt the potential application of TCDCA for MS therapy by suppressing astrocyte inflammation.
 IMPORTANCE: Internal tremors and vibrations symptoms have been described as part of neurologic disorders but not fully described as a part of long COVID. OBJECTIVE: To compare demographics, socioeconomic characteristics, pre-pandemic comorbidities, new-onset conditions, and long COVID symptoms between people with internal tremors and vibrations as part of their long COVID symptoms and people with long COVID but without these symptoms. DESIGN: A cross-sectional study, Listen to Immune, Symptom and Treatment Experiences Now (LISTEN), of adults with and without long COVID and post-vaccination syndrome, defined by self-report. SETTING: Hugo Health Kindred, a decentralized digital research platform hosting a network of English-speaking adults interested in contributing to COVID-related research. No geographic limitation applied. PARTICIPANTS: The study population included 423 participants who enrolled in LISTEN between May 2022 and June 2023, completed the initial and the conditions and symptoms surveys, reported long COVID, and did not report post-vaccination syndrome. EXPOSURE: Long COVID symptoms of internal tremors and vibrations. MAIN OUTCOMES AND MEASURES: Demographics, pre-pandemic comorbidities, and current conditions, other symptoms, and quality of life at the time of surveys. RESULTS: Of the 423 participants (median age, 46 years [IQR, 38-56]), 74% were female, 87% were Non-Hispanic White, 92% lived in the United States, 46% were infected before the Delta wave, and 158 (37%) reported "internal tremors, or buzzing/vibration" as a long COVID symptom. Before long COVID, the groups had similar comorbidities. Participants with internal tremors were different from others in having worse health as measured by the Euro-QoL visual analogue scale (median: 40 points [IQR, 30-60] vs. 50 points [IQR, 35-62], P = 0.007), having financial difficulties caused by the pandemic (very much financial difficulties, 22% [95% CI, 16-30] vs. 11% [7.3-15], P < 0.001), often feeling socially isolated (43% [95% CI, 35-52] vs. 37% [31-43], P = 0.039), and having higher rates of self-reported new-onset mast cell disorders (11% [95% CI, 7.1-18] vs. 2.6% [1.2-5.6], Bonferroni-adjusted P = 0.008) and neurologic conditions (including but not limited to seizures, dementia, multiple sclerosis, Parkinson's disease, neuropathy, etc.; 22% [95% CI, 16-29] vs. 8.3% [5.4-12], Bonferroni-adjusted P = 0.004). CONCLUSIONS AND RELEVANCE: Among people with long COVID, those with internal tremors and vibrations have several other associated symptoms and worse health status, despite having similar pre-pandemic comorbidities, suggesting it may reflect a severe phenotype of long COVID. KEY POINTS: Question: Do people with long COVID symptoms of internal tremors and vibrations differ from others with long COVID but without these symptoms?Findings: In this cross-sectional study that included 423 adults with long COVID, 158 (37%) reported having "internal tremors, or buzzing/vibration," had worse quality of life, more financial difficulties, and higher rates of new-onset mast cell disorders and neurologic conditions, compared with others with long COVID but without internal tremors and vibrations.Meaning: Internal tremors and vibrations may reflect a severe phenotype of long COVID.
 BACKGROUND AND OBJECTIVES: The objective of this study was to determine the external validity of the Axon Registry by comparing the 2019 calendar year data with 2 nationally representative, publicly available data sources, specifically the National Ambulatory Medical Care Survey (NAMCS) and the Medical Expenditure Panel Survey (MEPS). The Axon Registry is the American Academy of Neurology's neurology-focused qualified clinical data registry that reports and analyzes electronic health record data from participating US neurology providers. Its key function is to support quality improvement within ambulatory neurology practices while also promoting high-quality evidence-based care in clinical neurology. We compared demographics of patients who had an outpatient or office visit with a neurologist along with prevalence of selected neurologic conditions and neurologic procedures across the 3 data sets. METHODS: We performed a cross-sectional, retrospective comparison of 3 data sets: NAMCS (2012-2016), MEPS (2013-2017, 2019), and Axon Registry (2019). We obtained patient demographics (age, birth sex, race, ethnicity), patient neurologic conditions (headache, epilepsy, cerebrovascular disease, multiple sclerosis, parkinsonism, dementia, spinal pain, and polyneuropathy), provider location, and neurologic procedures (neurology visits, MR/CT neuroimaging studies and EEG/EMG neurophysiologic studies). Parameter estimates from the pooled 5-year samples of the 2 public data sets, calculated at the visit level, were compared descriptively with those of the Axon Registry. We calculated Cohen h and performed Wald tests (α = 0.05) to conduct person-level statistical comparisons between MEPS 2019 and Axon Registry 2019 data. RESULTS: The Axon Registry recorded 1.3 M annual neurology visits (NAMCS, 11 M; MEPS, 22 M) and 645 K people with neurologic conditions (MEPS, 10 M). Compared with the pooled national surveys, the Axon Registry has similar patient demographics, neurologic condition prevalence, neuroimaging and neurophysiologic utilization, and provider location. In direct comparison with MEPS 2019, the Axon Registry 2019 had fewer children (2% vs 7%), more elderly persons (21% vs 16%), fewer non-Black and non-White race persons (5% vs 8%), less number of patients with epilepsy (10% vs 13%), more patients with dementia (8% vs 6%), more patients with cerebrovascular disease (11% vs 8%), and a greater predominance of neurology providers in the Midwest (25% vs 20%). The only difference with a non-negligible effect size was the proportion of people younger than 15 years (Cohen h = 0.25). DISCUSSION: The Axon Registry demonstrates high concordance with 2 nationally representative surveys. Recruiting more and diverse neurology providers will further improve the volume, representativeness, and value of the Axon Registry.
 Siponimod (Sp) is a Sphingosine 1-phosphate (S1P) receptor modulator, and it suppresses S1P- mediated autoimmune lymphocyte transport and inflammation. Theiler's murine encephalomyelitis virus (TMEV) infection mouse model of multiple sclerosis (MS) exhibits inflammation-driven acute and chronic phases, spinal cord lesions, brain and spinal cord atrophy, and white matter injury. The objective of the study was to investigate whether Sp treatment could attenuate inflammation-induced pathology in the TMEV model by inhibiting microglial activation and preventing the atrophy of central nervous tissue associated with neurodegeneration. Clinical disability score (CDS), body weight (BW), and rotarod retention time measures were used to assess Sp's impact on neurodegeneration and disease progression in 4 study groups of 102 animals, including 44 Sp-treated (SpT), 44 vehicle-treated, 6 saline-injected, and 8 age-matched healthy controls (HC). Next, 58 (22 SpT, 22 vehicle, 6 saline injected, and 8 HC) out of the 102 animals were further evaluated to assess the effect of Sp on brain region-specific and spinal cord volume changes, as well as microglial activation. Sp increased CDS and decreased BW and rotarod retention time in TMEV mice, but did not significantly affect most brain region volumes, except for lateral ventricle volume. Sp suppressed ventricular enlargement, suggesting reduced TMEV-induced inflammation in LV. No significant differences in spine volume changes were observed between Sp- and vehicle-treated animals, but there were differences between HC and TMEV groups, indicating TMEV-induced inflammation contributed to increased spine volume. Spine histology revealed no significant microglial density differences between groups in gray matter, but HC animals had higher type 1 morphology and lower type 2 morphology percentages in gray and white matter regions. This suggests that Sp did not significantly affect microglial density but may have modulated neuroinflammation in the spinal cord. Sp may have some effects on neuroinflammation and ventricular enlargement. However, it did not demonstrate a significant impact on neurodegeneration, spinal volume, or lesion volume in the TMEV mouse model. Further investigation is required to fully understand Sp's effect on microglial activation and its relevance to the pathophysiology of MS. The differences between the current study and previous research using other MS models, such as EAE, highlight the differences in pathological processes in these two disease models.
 Valid, responsive blood biomarkers specific to peripheral nerve damage would improve management of peripheral nervous system (PNS) diseases. Neurofilament light chain (NfL) is sensitive for detecting axonal pathology but is not specific to PNS damage, as it is expressed throughout the PNS and central nervous system (CNS). Peripherin, another intermediate filament protein, is almost exclusively expressed in peripheral nerve axons. We postulated that peripherin would be a promising blood biomarker of PNS axonal damage. We demonstrated that peripherin is distributed in sciatic nerve, and to a lesser extent spinal cord tissue lysates, but not in brain or extra-neural tissues. In the spinal cord, anti-peripherin antibody bound only to the primary cells of the periphery (anterior horn cells, motor axons and primary afferent sensory axons). In vitro models of antibody-mediated axonal and demyelinating nerve injury showed marked elevation of peripherin levels only in axonal damage and only a minimal rise in demyelination. We developed an immunoassay using single molecule array (Simoa) technology for the detection of serum peripherin as a biomarker for PNS axonal damage. We examined longitudinal serum peripherin and NfL concentrations in individuals with Guillain-Barré syndrome (GBS, n = 45, 179 timepoints), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP, n = 35, 70 timepoints), multiple sclerosis (MS, n = 30), dementia (as non-inflammatory CNS controls, n = 30) and healthy individuals (n = 24). Peak peripherin levels were higher in GBS than all other groups (median 18.75 pg/mL vs. < 6.98 pg/mL, p < 0.0001). Peak NfL was highest in GBS (median 220.8 pg/mL) and lowest in healthy controls (median 5.6 pg/mL), but NfL did not distinguish between CIDP (17.3 pg/mL), MS (21.5 pg/mL) and dementia (29.9 pg/mL). While peak NfL levels were higher with older age (rho=+0.39, p < 0.0001), peak peripherin levels did not vary with age. In GBS, local regression analysis of serial peripherin in the majority of individuals with 3 or more timepoints of data (16/25) displayed a rise-and-fall pattern with the highest value within the first week of initial assessment. Similar analysis of serial NfL concentrations showed a later peak at 16 days. Group analysis of serum peripherin and NfL levels in GBS and CIDP patients were not significantly associated with clinical data, but in some individuals with GBS, peripherin levels appeared to better reflect clinical outcome measure improvement. Serum peripherin is a promising new, dynamic, and specific biomarker of acute PNS axonal damage.
 Introduction: Accurately assessing people's gait, especially in real-world conditions and in case of impaired mobility, is still a challenge due to intrinsic and extrinsic factors resulting in gait complexity. To improve the estimation of gait-related digital mobility outcomes (DMOs) in real-world scenarios, this study presents a wearable multi-sensor system (INDIP), integrating complementary sensing approaches (two plantar pressure insoles, three inertial units and two distance sensors). Methods: The INDIP technical validity was assessed against stereophotogrammetry during a laboratory experimental protocol comprising structured tests (including continuous curvilinear and rectilinear walking and steps) and a simulation of daily-life activities (including intermittent gait and short walking bouts). To evaluate its performance on various gait patterns, data were collected on 128 participants from seven cohorts: healthy young and older adults, patients with Parkinson's disease, multiple sclerosis, chronic obstructive pulmonary disease, congestive heart failure, and proximal femur fracture. Moreover, INDIP usability was evaluated by recording 2.5-h of real-world unsupervised activity. Results and discussion: Excellent absolute agreement (ICC >0.95) and very limited mean absolute errors were observed for all cohorts and digital mobility outcomes (cadence ≤0.61 steps/min, stride length ≤0.02 m, walking speed ≤0.02 m/s) in the structured tests. Larger, but limited, errors were observed during the daily-life simulation (cadence 2.72-4.87 steps/min, stride length 0.04-0.06 m, walking speed 0.03-0.05 m/s). Neither major technical nor usability issues were declared during the 2.5-h acquisitions. Therefore, the INDIP system can be considered a valid and feasible solution to collect reference data for analyzing gait in real-world conditions.
 BACKGROUND: More than 200 years after James Parkinsondescribed a clinical syndrome based on his astute observations, Parkinson's disease (PD) has evolved into a complex entity, akin to the heterogeneity of other complex human syndromes of the central nervous system such as dementia, motor neuron disease, multiple sclerosis, and epilepsy. Clinicians, pathologists, and basic science researchers evolved arrange of concepts andcriteria for the clinical, genetic, mechanistic, and neuropathological characterization of what, in their best judgment, constitutes PD. However, these specialists have generated and used criteria that are not necessarily aligned between their different operational definitions, which may hinder progress in solving the riddle of the distinct forms of PD and ultimately how to treat them. OBJECTIVE: This task force has identified current in consistencies between the definitions of PD and its diverse variants in different domains: clinical criteria, neuropathological classification, genetic subtyping, biomarker signatures, and mechanisms of disease. This initial effort for "defining the riddle" will lay the foundation for future attempts to better define the range of PD and its variants, as has been done and implemented for other heterogeneous neurological syndromes, such as stroke and peripheral neuropathy. We strongly advocate for a more systematic and evidence-based integration of our diverse disciplines by looking at well-defined variants of the syndrome of PD. CONCLUSION: Accuracy in defining endophenotypes of "typical PD" across these different but interrelated disciplines will enable better definition of variants and their stratification in therapeutic trials, a prerequisite for breakthroughs in the era of precision medicine. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
 BACKGROUND AND OBJECTIVES: Based on the Global Burden of Diseases, Injuries, and Risk Factors (GBD) study, neurologic disorders are a major cause of morbidity and mortality worldwide. However, there has been no comprehensive assessment of neurologic disorders in Asia. Data from the GBD 1990-2019 study were investigated to provide new details for neurologic disorders in Asia. METHODS: The burden of common neurologic disorders in Asia was calculated for 1990 and 2019 as incidence, prevalence, deaths, and disability-adjusted life-years (DALYs). Thirteen common neurologic disorders were analyzed. Data are presented as totals and by sex, age, year, location, risk factors, and sociodemographic index (SDI) and shown as counts and rates. RESULTS: In 2019, the most burdensome neurologic disorders in Asia for the absolute number of DALYs were stroke (98.8 million, 95% uncertainty interval [UI] 91.0-107.0), migraine (24.6 million, 95% UI 3.4-56.4), and Alzheimer disease (AD) and other dementias (13.5 million, 95% UI 5.9-29.8). From 1990 to 2019, the absolute number of DALYs and deaths caused by combined neurologic disorders (deaths by 60.7% and DALYs by 17.6%) increased, but the age-standardized rates (deaths by 34.1% and DALYs by 36.3%) decreased. The burden of neurologic disorders peaked among individuals aged 65-74 years and was higher among male than among female individuals; moreover, this burden varied considerably across Asian subregions and countries. Risk-attributable DALYs accounted for 86.9%, 28.5%, and 11.1% of DALYs for stroke, AD and other dementias, and multiple sclerosis, respectively. SDI was associated with both stroke and communicable neurological disorders. In terms of crude rate, the higher the SDI value, the higher the prevalence of stroke, and the lower all metrics of communicable neurological disorders. DISCUSSION: Neurologic disorders were the leading cause of DALYs and the second leading cause of deaths in Asia in 2019, and the burden may likely increase with the growth and aging of the Asian population. Urgent measures are needed for prevention, treatment, rehabilitation, and support services for common neurologic disorders regionally and nationally.
 Damage-associated molecular patterns (DAMPs) are intracellular molecules released under cellular stress or recurring tissue injury, which serve as endogenous ligands for toll-like receptors (TLRs). Such DAMPs are either actively secreted by immune cells or passively released into the extracellular environment from damaged cells or generated as alternatively spliced mRNA variants of extracellular matrix (ECM) glycoproteins. When recognized by pattern recognition receptors (PRRs) such as TLRs, DAMPs trigger innate immune responses. Currently, the best-characterized PRRs include, in addition to TLRs, nucleotide-binding oligomerization domain-like receptors, RIG-I-like RNA helicases, C-type lectin receptors, and many more. Systemic sclerosis (SSc) is a chronic autoimmune condition characterized by inflammation and progressive fibrosis in multiple organs. Using an unbiased survey for SSc-associated DAMPs, we have identified the ECM glycoproteins fibronectin-containing extra domain A and tenascin C as the most highly upregulated in SSc skin and lung biopsies. These DAMPs activate TLR4 on resident stromal cells to elicit profibrotic responses and sustained myofibroblasts activation resulting in progressive fibrosis. This review summarizes the current understanding of the complex functional roles of DAMPs in the progression and failure of resolution of fibrosis in general, with a particular focus on SSc, and considers viable therapeutic approaches targeting DAMPs.
 Traditional Chinese medicine, such as Tripterygium wilfordii and Paeonia lactiflora, has potential values in treating systemic sclerosis (SSc) and other autoimmune diseases, while their toxic side effect elimination and precise tropical drug delivery are still challenges. Here, we present multiple traditional Chinese medicine integrated photoresponsive black phosphorus (BP) microneedles (MNs) with the desired features for the SSc treatment. By employing a template-assisted layer-by-layer curing method, such MNs with triptolide (TP)/paeoniflorin (Pae) needle tips and BP-hydrogel needle bottoms could be well generated. The combined administration of TP and Pae can not only provide anti-inflammatory, detoxification, and immunomodulatory effects to treat skin lesions in the early stage of SSc but also remarkably reduce the toxicity of single drug delivery. Besides, the additive BPs possess good biocompatibility and near-infrared (NIR) responsiveness, imparting the MN photothermal-controlled drug release capability. Based on these features, we have demonstrated that the traditional Chinese medicine integrated responsive MNs could effectively improve skin fibrosis and telangiectasia, reduce collagen deposition, and reduce epidermal thickness in the SSc mouse models. These results indicated that the proposed Chinese medicine integrated responsive MNs had enormous potential in clinical therapy of SSc and other diseases.
 Tuberous sclerosis complex (TSC) is an autosomal dominant disorder with different initial symptoms and complex clinical manifestations. A 14-year-old female patient presented with persistent fever and severe headache. Medical imaging examinations revealed multiple abnormal intracranial lesions. The patient had previously been misdiagnosed with "encephalitis and acute disseminated encephalomyelitis" after visiting numerous hospitals. Eventually, by combing the characteristics of the case and genetic testing results, the patient was diagnosed with TSC accompanied by Mycoplasma pneumoniae infection. The purpose of this case report and literature review is to improve understanding of the clinical diagnosis and treatment of TSC so as to avoid misdiagnosis, missed diagnosis, and overtreatment.
 OBJECTIVE: Nintedanib (NIN) is an antifibrotic drug approved to slow the progression of idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-related interstitial lung disease (SSc-ILD). NIN can frequently cause gastrointestinal adverse effects. We aimed to investigate the NIN safety profile in a real life setting, comparing IPF and SSc-ILD patients and evaluating the strategies adopted to manage NIN adverse effects. METHODS: Patients taking NIN for IPF or SSc-ILD were enrolled. Alongside epidemiological and disease-specific data, the period of NIN use and the need for dosage reduction and/or interruption were investigated. Particular attention was paid to possible adverse effects and strategies adopted to manage them. RESULTS: Twenty-seven SSc-ILD and 82 IPF patients were enrolled. No significant differences emerged between the two cohorts regarding the frequency of any possible adverse effect. Although the rates of NIN dosage reduction or interruption were similar between the two subgroups, SSc-ILD presented a mean period before NIN dosage reduction and NIN interruption significantly shorter than IPF (3 ± 2.6 vs 10.5 ± 8.9 months-p < 0.001 and 2.3 ± 0.5 vs 10.3 ± 9.9 months-p = 0.008, respectively). Several different strategies were tried to manage NIN adverse effects: especially in SSc-ILD, the variable combination of diet adjustment set by a nutritionist, probiotics and diosmectite was ultimately successful in maintaining patients on an adequate dose of NIN. CONCLUSION: We presented data on the NIN safety profile in a real life setting, which was similar between SSc-ILD and IPF. A combination of multiple managing strategies and dose adjustment appears essential to cope optimally with NIN adverse effects.
 OBJECTIVE: Multiple observations indicate a role for lymphocytes in driving autoimmunity in systemic sclerosis (SSc). While T and NK cells have been studied in SSc whole blood and bronchoalveolar lavage fluid, their role remains unclear, partly because no studies have analyzed these cell types in SSc-ILD lung tissue. This research aimed to identify and analyze the lymphoid subpopulations in SSc-ILD lung explants. METHODS: Lymphoid populations from 13 SSc-ILD and 6 healthy control (HC) lung explants were analyzed using Seurat following single cell RNA sequencing. Lymphoid clusters were identified by their differential gene expression. Absolute cell numbers and cell proportions in each cluster were compared between cohorts. Additional analyses were performed using pathway analysis, pseudotime, and cell ligand-receptor interactions. RESULTS: Activated CD16+ NK cells, CD8+ tissue resident memory T cells, and regulatory T cells (Tregs) were proportionately higher in SSc-ILD compared with HC lungs. Activated CD16+ NK in SSc-ILD showed upregulated granzyme B, interferon-gamma, and CD226. Amphiregulin, highly upregulated by NK cells, was predicted to interact with epidermal growth factor receptor on several bronchial epithelial cell populations. Shifts in CD8+ T cell populations indicated a transition from resting to effector to tissue resident phenotypes in SSc-ILD. CONCLUSIONS: SSc-ILD lungs show activated lymphoid populations. Activated cytotoxic NK cells suggest they may kill alveolar epithelial cells, while their expression of amphiregulin suggests they may also induce bronchial epithelial cell hyperplasia. CD8+ T cells in SSc-ILD appear to transition from resting to tissue resident memory phenotype.
 OBJECTIVE: The pharyngeal phase of swallowing involves a coordinated sequence of events. Event durations may be prolonged in people with Parkinson disease (PwPD), and amyotrophic lateral sclerosis (PwALS); however, the cumulative effect of these changes is unexplored. We compared event latencies relative to hyoid burst (HYB) (time zero) to understand differences in deglutatory event timing. We hypothesized PwPD and PwALS would display similarly prolonged cumulative pharyngeal phase durations compared to healthy controls, with greater prolongations with increasing bolus viscosity. METHOD: We retrospectively evaluated videofluoroscopic data of healthy adults (n = 78), PwPD (n = 17), and PwALS (n = 20). Participants swallowed 15 boluses of 20% (w/v) barium across five liquid consistencies. Paired raters evaluated nine deglutitive events using the ASPEKT method. Latencies were plotted by consistency relative to HYB and compared across cohorts using Mann-Whitney U tests (p ≤ .05). Cohen's d was calculated for all statistically significant results to determine effect size. RESULTS: In PwPD, significantly prolonged latencies were observed on thin liquid boluses compared to healthy controls. Latencies to all post-HYB events were significantly prolonged except for maximum upper esophageal sphincter distension. In PwALS, significantly prolonged latencies for events preceding and following HYB were noted on all consistencies compared to healthy controls and PwPD. CONCLUSION: In PwPD, event latencies for multiple components of the swallowing sequence were prolonged culminating in overall prolongation of the pharyngeal phase on thin liquid. A similar pattern, but with significantly greater prolongation, was seen in the PwALS, and extended to swallows of all liquid consistencies.
 The article describes a clinical case of cardiac rhabdomyoma first diagnosed in an 18-year-old girl. At the age of 12 months, the patient first developed generalized, prolonged convulsive seizure with the eyeballs rolling upward, tonic arm tension, and profuse salivation. From 1.5 to 2 years, according to her mother, the girl had frequent "freezing" with fixed stare. Anticonvulsant therapy was not administered. From the age of 2 years 8 months, the child began to experience episodes of drowsiness, lethargy, blurred speech, and repeated vomiting lasting up to 2 weeks. The patient was regularly treated at the neurological department. According to CT at the age of four, the patient showed characteristic alterations in the brain and was diagnosed with tuberous sclerosis, symptomatic generalized epilepsy, and psychoorganic syndrome. Only at the age of 18, cardiac ultrasound detected a 7x6 mm hyperechoic formation with endogenous growth buried in the myocardium of the left ventricular (LV) anterior-lateral wall and another one in the area of the LV lateral wall with endogenous growth of 2×4 mm. Magnetic resonance imaging (MRI) revealed multiple focal formations with clear, even contours in the area of the middle anterior septal segment (closely adjacent to papillary muscles) in the region of the apex, buried in the myocardium. The formation sizes were 9×7 mm, 8×13 mm, and 7.5×6 mm, respectively, and they moderately accumulated the contrast agent. Lesions with identical characteristics and a diameter up to 4.5 mm were visualized on the anterior wall in the region of the apex, in the depth of the myocardium. Due to the absence of arrhythmias and hemodynamic disorders, immunosuppressive therapy was not administered. Follow-up and dynamic MRI control of the heart were recommended. If signs of tumor growth are detected, consider immunosuppressive therapy with everolimus. The case is of interest for a long asymptomatic growth of rhabdomyoma. Generally, cardiac rhabdomyomas are diagnosed in the postnatal period and may be the earliest manifestation of tuberous sclerosis.
 Respiratory failure is the most common cause of death in patients with amyotrophic lateral sclerosis (ALS) and occurs with great variability among patients according to different phenotypic features. Early predictors of respiratory failure in ALS are important to start non-invasive ventilation (NIV). Venous serum chloride values correlate with carbonate (HCO3-) blood levels and reflect metabolic compensation of respiratory acidosis. Despite its wide availability and low cost, few data on serum chloride as a prognostic marker exist in ALS literature. In the present study, we evaluated serum chloride values at diagnosis as prognostic biomarkers for overall survival and NIV adaptation in a retrospective center-based cohort of ALS patients. We collected all ALS patients with serum chloride assessment at diagnosis, identified through the Piemonte and Valle d'Aosta Register for ALS, evaluating the correlations among serum chloride, clinical features, and other serum biomarkers. Thereafter, time-to-event analysis was modeled to predict overall survival and NIV start. We found a significant correlation between serum chloride and inflammatory status markers, serum sodium, forced vital capacity (FVC), ALS functional rating scale-revised (ALSFRS-R) item 10 and 11, age at diagnosis, and weight loss. Time-to-event analysis confirmed both in univariate analysis and after multiple confounders' adjustment that serum chloride value at diagnosis significantly influenced survival and time to NIV start. According to our analysis, based on a large ALS cohort, we found that serum chloride analyzed at diagnosis is a low-cost marker of impending respiratory decompensation. In our opinion, it should be added among the serum prognostic biomarkers that are able to stratify patients into different prognostic categories even when performed in the early phases of the disease.
 Tuberous sclerosis complex (TSC) is a neurocutaneous disease caused by a mutation in the TSC1 or TSC2 gene. There are several neuropsychiatric manifestations associated with TSC known as TSC-associated neuropsychiatric disorder (TAND). This article concerns neuropsychiatric manifestations in children with the TSC2 gene mutation, with genetic analysis findings using whole-exome sequencing. CASE: A 17-year-old girl presented with TSC, absence and focal epilepsy, borderline intellectual functioning, organic psychosis, and renal angiomyolipoma. She was emotionally unstable and preoccupied with irrelevant fears. In the physical examination, we found multiple hypomelanotic maculae, angiofibroma, and a shagreen patch. The intellectual assessment result with the Wechsler Adult Intelligence Scale at 17 was borderline intellectual functioning. Brain MRI showed cortical and subcortical tubers in the parietal and occipital lobes. Whole-exome sequencing was conducted, and the result was a missense mutation in exon 39 of the TSC2 gene [NM_000548.5:c.5024C>T (NP_000539.2:p.Pro1675Leu)]. The Sanger sequencing of the patient's parents revealed no mutations in the TSC2 gene, confirming the patient's de novo mutation. The patient was given several antiepileptic and antipsychotic drugs. CLINICAL DISCUSSION: Neuropsychiatric manifestation is a common phenotype in the TSC variant, and psychosis is one of the rare TAND symptoms in children. CONCLUSIONS: The neuropsychiatric phenotype and genotype in TSC patients are rarely reported and evaluated. We reported a female child with epilepsy, borderline intellectual functioning, and organic psychosis associated with a de novo mutation of the TSC2 gene. Organic psychosis is a rare symptom of TAND which also manifested in our patient.
 Aminaphtone is a chemical drug that has been used for more than thirty years to treat a variety of vascular disorders, with good clinical results and a satisfying safety profile. In the last two decades, multiple clinical studies have reported the efficacy of the drug in different clinical scenarios of altered microvascular reactivity, describing the downregulation of adhesion molecules (i.e., VCAM, ICAM, Selectins), vasoconstrictor peptides (i.e., Endothelin-1), and pro-inflammatory cytokine expression (i.e., IL-6, IL-10, VEGF, TGF-beta) by Aminaphtone. In this review, we summarize the current knowledge concerning Aminaphtone, with particular attention to rheumatological conditions in which microvascular disfunction plays a pivotal role, such as Raynaud's phenomenon and systemic sclerosis. These latter conditions may represent a promising field of application for Aminaphtone, due to the growing pre-clinical, clinical, and instrumental reports of efficacy. However, randomized, double-blind, placebo-controlled clinical trials are lacking and are desirable.
 Objective: This pilot study explores the influence of acute alcohol exposure on cell mechanical properties of steady-state and activated leukocytes conducted with real-time deformability cytometry. Methods: Nineteen healthy male volunteers were enrolled to investigate the effect of binge drinking on biophysical properties and cell counts of peripheral blood leukocytes. Each participant consumed an individualized amount of alcohol to achieve a blood alcohol concentration of 1.2 ‰ as a mean peak. In addition, we also incubated whole blood samples from healthy donors with various ethanol concentrations and performed stimulation experiments using lipopolysaccharide and CytoStim™ in the presence of ethanol. Results: Our findings indicate that the biophysical properties of steady-state leukocytes are not significantly affected by a single episode of binge drinking within the first two hours. However, we observed significant alterations in relative cell counts and a shift toward a memory T cell phenotype. Moreover, exposure to ethanol during stimulation appears to inhibit the cytoskeleton reorganization of monocytes, as evidenced by a hindered increase in cell deformability. Conclusion: Our observations indicate the promising potential of cell mechanical analysis in understanding the influence of ethanol on immune cell functions. Nevertheless, additional investigations in this field are warranted to validate biophysical properties as biomarkers or prognostic indicators for alcohol-related changes in the immune system.
 The phenotypic spectrum of myelin oligodendrocyte glycoprotein (MOG)-IgG associated disorders (MOGAD) has broadened in the past few years, and atypical phenotypes are increasingly recognized. Febrile meningoencephalitis has rarely been reported as a feature of MOGAD and represents a diagnostic challenge. We report the case of 24-year-old women with high-grade fever, meningoencephalomyelitis, and persistently positive MOG-IgG, for whom an extensive infectious work-up was negative and who responded to high-dose intravenous methylprednisolone. The full clinical spectrum of MOGAD is yet to be completely elucidated. In patients presenting with febrile meningoencephalitis, MOG-IgG testing should be considered particularly if infectious work-up is negative.
 The RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (A1) regulates RNA metabolism, which is crucial to maintaining cellular homeostasis. A1 dysfunction mechanistically contributes to reduced cell viability and loss, but molecular mechanisms of how A1 dysfunction affects cell viability and loss, and methodologies to attenuate its dysfunction, are lacking. Utilizing in silico molecular modeling and an in vitro optogenetic system, this study examined the consequences of RNA oligonucleotide (RNAO) treatment on attenuating A1 dysfunction and its downstream cellular effects. In silico and thermal shift experiments revealed that binding of RNAOs to the RNA Recognition Motif 1 of A1 is stabilized by sequence- and structure-specific RNAO-A1 interactions. Using optogenetics to model A1 cellular dysfunction, we show that sequence- and structure-specific RNAOs significantly attenuated abnormal cytoplasmic A1 self-association kinetics and A1 cytoplasmic clustering. Downstream of A1 dysfunction, we demonstrate that A1 clustering affects the formation of stress granules, activates cell stress, and inhibits protein translation. With RNAO treatment, we show that stress granule formation is attenuated, cell stress is inhibited, and protein translation is restored. This study provides evidence that sequence- and structure-specific RNAO treatment attenuates A1 dysfunction and its downstream effects, thus allowing for the development of A1-specific therapies that attenuate A1 dysfunction and restore cellular homeostasis.
 Time-of-day is rarely considered during experimental protocols investigating motor behavior and neural activity. The goal of this work was to investigate differences in functional cortical connectivity at rest linked to the time of the day using functional Near-Infrared Spectroscopy (fNIRS). Since resting-state brain is shown to be a succession of cognitive, emotional, perceptual, and motor processes that can be both conscious and nonconscious, we studied self-generated thought with the goal to help in understanding brain dynamics. We used the New-York Cognition Questionnaire (NYC-Q) for retrospective introspection to explore a possible relationship between the ongoing experience and the brain at resting-state to gather information about the overall ongoing experience of subjects. We found differences in resting-state functional connectivity in the inter-hemispheric parietal cortices, which was significantly greater in the morning than in the afternoon, whilst the intra-hemispheric fronto-parietal functional connectivity was significantly greater in the afternoon than in the morning. When we administered the NYC-Q we found that the score of the question 27 ("during RS acquisition my thoughts were like a television program or film") was significantly greater in the afternoon with respect to the morning. High scores in question 27 point to a form of thought based on imagery. It is conceivable to think that the unique relationship found between NYC-Q question 27 and the fronto-parietal functional connectivity might be related to a mental imagery process during resting-state in the afternoon.
 BACKGROUND AND OBJECTIVES: Creutzfeldt-Jakob disease (CJD) is a rapidly progressive and universally fatal neurodegenerative disorder with highly variable survival times, ranging from weeks to years. However, there are currently no tools for prognosticating a patient's survival time. This study aims to fill this gap by examining the relationship between CSF total tau (t-tau) levels and time to death in patients with CJD. METHODS: We use cases with CJD recorded in the electronic health record of a tertiary academic medical center from 2010 to 2022. RESULTS: We identified 29 cases with diagnosis of CJD. Using a Cox proportional hazards model, we find that elevated t-tau levels (>4,000 pg/mL) are associated with 9.62 (95% confidence interval: 1.93-47.92) times the hazard of death compared with CJD patients with t-tau less than 4,000 pg/mL. DISCUSSION: This finding supports the use of CSF t-tau as a prognostic biomarker for CJD.
 Systemic sclerosis (SSc) is an autoimmune disease characterized by progressive skin fibrosis. It has 2 main clinical subtypes-diffuse cutaneous scleroderma and limited cutaneous scleroderma. Non-cirrhotic portal hypertension (NCPH) is defined as presence of elevated portal vein pressures without cirrhosis. It is often a manifestation of an underlying systemic disease. On histopathology, NCPH may be found to be secondary to multiple abnormalities such as nodular regenerative hyperplasia (NRH) and obliterative portal venopathy. There have been reports of NCPH in patients with both subtypes of SSc secondary to NRH. However, simultaneous presence of obliterative portal venopathy has not been reported. We present a case of NCPH due to NRH and obliterative portal venopathy as a presenting sign of limited cutaneous scleroderma. The patient was initially found to have pancytopenia and splenomegaly and was erroneously labeled as cirrhosis. She underwent workup to rule out leukemia, which was negative. She was referred to our clinic and diagnosed with NCPH. Due to pancytopenia, she could not be started on immunosuppressive therapy for her SSc. Our case describes the presence of these unique pathological findings in the liver and highlights the importance of an aggressive search for an underlying condition in all patients diagnosed with NCPH.
 Spinocerebellar ataxia 38 (SCA 38) is a rare autosomal neurological disease whose clinical features include, among others, severe gait disturbances that have not yet been fully characterized. In this study, we employed a computerized 3D gait analysis to obtain spatio-temporal parameters of gait and the kinematics in the sagittal plane in the hip, knee, and ankle joints of seven individuals with SCA 38, which were then compared with those of twenty unaffected individuals matched for age, sex, and anthropometric features. The results show that, in comparison with unaffected individuals, those with SCA 38 are characterized by a significantly reduced speed, stride length, and duration of the swing phase, as well as an increased step width and stance and double support phase durations. The point-by-point comparison of the angular trends at the hip, knee, and ankle joints revealed significant alterations during most part of the stance phase for hip joint and at pre-swing/swing phases for knee and ankle joints. For these latter joints, a significantly reduced dynamic range of motion was also found. Such findings provide some new insights into hip and knee kinematics for this specific form of ataxia and may be useful for monitoring the disease's progression and designing specific, tailored rehabilitative interventions.
 Traumatic brain injuries (TBIs) are among the most important clinical and research areas in neurosurgery, owing to their devastating effects and high prevalence. Over the last few decades, there has been increasing research on the complex pathophysiology of TBI and secondary injuries following TBI. A growing body of evidence has shown that the renin-angiotensin system (RAS), a well-known cardiovascular regulatory pathway, plays a role in TBI pathophysiology. Acknowledging these complex and poorly understood pathways and their role in TBI could help design new clinical trials involving drugs that alter the RAS network, most notably angiotensin receptor blockers and angiotensin-converting enzyme inhibitors. This study aimed to briefly review the molecular, animal, and human studies on these drugs in TBI and provide a clear vision for researchers to fill knowledge gaps in the future.
 Tele-neuropsychology, i.e., the application of remote audio-visual technologies to neuropsychological evaluation or rehabilitation, has become increasingly popular and widespread during and after the COVID-19 pandemic. New tools with updated normative data and appropriate methodological developments are necessary. We present Tele-GEMS, a telephone-based cognitive screening developed on N = 601 Italian participants. It yields a global score tapping on orientation, memory, spatial representation, language, and pragmatic abilities. Its administration lasts about 10 min. Clinical cut-offs are provided, accounting for demographic variables (age, education, and sex) and also for a comprehensive index taking into account cognitively stimulating life experiences that can build up a cognitive reserve. Tele-GEMS shows good internal consistency and a good inter-rater agreement. The test includes the thresholds for estimating a significant change after repeated measurements. Tele-GEMS has a good construct validity as assessed with MoCA and a suitable criterion validity assessed with its in-person version (GEMS). All the materials and the instructions, including scripts and an online Application for the automatic calculation of cut-offs, are accessible on OSF at https://osf.io/t3bma/ under a Creative Commons license.
 Prolactin (PRL) is an endocrine hormone secreted by the anterior pituitary gland that has a variety of physiological effects, including milk production, immune system regulation, and anti-inflammatory effects. Elevated levels of PRL have been found in several viral infections, including 2019 coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), a viral pathogen that has recently spread worldwide. PRL production is increased in SARS-CoV2 infection. While PRL can trigger the production of proinflammatory cytokines, it also has several anti-inflammatory effects that can reduce hyperinflammation. The exact mechanism of PRL's contribution to the severity of COVID-19 is unknown. The purpose of this review is to discuss the interaction between PRL and SARS-CoV2 infection and its possible association with the severity of COVID-19.
 Lichen sclerosus (LS) is a chronic inflammatory disease. It was first described by Hallopeau in 1881. Since then, multiple names have been used to describe this condition such as leukoplakia, kraurosis vulvae, balanitis xerotica obliterans, and lichen sclerosis et atrophicus. In 1976, the International Society for the Study of Vulvovaginal Disease adopted the term of lichen sclerosus. LS is a mucocutaneous autoimmune disorder characterized by hypopigmentation and skin atrophy. It involves most commonly the genital skin, less often the extragenital sites. LS is more common in women than in men. It may cause phimosis or scarring of the vaginal introitus. The diagnosis is based on the clinical features, but it is often confirmed by biopsy. The lesions can evolve towards the destruction of anatomic structures, functional impairment and a potential risk for malignant evolution. Thus, treatment and long term follow-up are mandatory.
 Hard-to-heal or recurrent leg ulcers can have multiple aetiologies. One of these is incompetent veins. The main focus of this article is to discuss the common treatment for venous leg ulcers with the use of sclerotherapy. This simple surgical procedure obliterates smaller veins and telangiectasia. Veins with larger diameters (varicosities) can be treated with ablation therapy. The intent of sclerosis or ablation therapy is to destroy the incompetent veins and allow the collateral circulation to improve venous return, decreasing venous hypertension, which then enhances skin closure, wound healing and the resolution of the ulcer.
 BACKGROUND: Genome-wide association studies (GWAS) have indicated moderate genetic overlap between Alzheimer's disease (AD) and related dementias (ADRD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), neurodegenerative disorders traditionally considered etiologically distinct. However, the specific genetic variants and loci underlying this overlap remain almost entirely unknown. METHODS: We leveraged state-of-the-art GWAS for ADRD, PD, and ALS. For each pair of disorders, we examined each of the GWAS hits for one disorder and tested whether they were also significant for the other disorder, applying Bonferroni correction for the number of variants tested. This approach rigorously controls the family-wise error rate for both disorders, analogously to genome-wide significance. RESULTS: Eleven loci with GWAS hits for one disorder were also associated with one or both of the other disorders: one with all three disorders (the MAPT/KANSL1 locus), five with ADRD and PD (near LCORL, CLU, SETD1A/KAT8, WWOX, and GRN), three with ADRD and ALS (near GPX3, HS3ST5/HDAC2/MARCKS, and TSPOAP1), and two with PD and ALS (near GAK/TMEM175 and NEK1). Two of these loci (LCORL and NEK1) were associated with an increased risk of one disorder but decreased risk of another. Colocalization analysis supported a shared causal variant between ADRD and PD at the CLU, WWOX, and LCORL loci, between ADRD and ALS at the TSPOAP1 locus, and between PD and ALS at the NEK1 and GAK/TMEM175 loci. To address the concern that ADRD is an imperfect proxy for AD and that the ADRD and PD GWAS have overlapping participants (nearly all of which are from the UK Biobank), we confirmed that all our ADRD associations had nearly identical odds ratios in an AD GWAS that excluded the UK Biobank, and all but one remained nominally significant (p < 0.05) for AD. CONCLUSIONS: In one of the most comprehensive investigations to date of pleiotropy between neurodegenerative disorders, we identify eleven genetic risk loci shared among ADRD, PD, and ALS. These loci support lysosomal/autophagic dysfunction (GAK/TMEM175, GRN, KANSL1), neuroinflammation/immunity (TSPOAP1), oxidative stress (GPX3, KANSL1), and the DNA damage response (NEK1) as transdiagnostic processes underlying multiple neurodegenerative disorders.
 Cardiac rhabdomyoma is a rare and benign mesenchymal tumor of striated muscle origin. It most commonly involves the head and neck. It classifies under cardiac and extracardiac types. Extracardiac are further classified into adult, fetal, and germ cell tumors. Cardiac rhabdomyoma (CR) is the most common pediatric heart tumor, mostly occurring before the age of 1 year. Anatomically, they are considered hamartomas. Most cardiac rhabdomyomas are associated with tuberous sclerosis (TS) and appear in the ventricular myocardium, the atria, the cavoatrial junction, or the epicardial surface. Most cardiac rhabdomyomas are multiple and pursue a course of spontaneous regression; surgical resection is not advisable unless the patient is symptomatic. The symptoms develop as a result of the obstruction of blood inflow or outflow, resulting in congestive heart failure. Arrhythmias can also occur ranging from bradycardia secondary to sinus or atrioventricular node (AVN) dysfunction to atrial/ventricular tachycardia, AVN reentrant tachycardia, or ventricular pre-excitation.
 OBJECTIVE: Cognitive impairment is one of the most common symptoms of anti-leucine rich glioma inactivated 1 (anti-LGI-1) encephalitis, but little is known about the cognitive profile of these patients. This study characterized the cognitive profile of patients with anti-LGI-1 encephalitis and compared patterns of impairment to healthy controls and other patient groups with known temporal lobe/limbic involvement. METHODS: A retrospective analysis of adult patients with anti-LGI-1 encephalitis who underwent neuropsychological assessment was conducted. Performance patterns of anti-LGI-1 patients were compared to patients deemed cognitively healthy (HC), as well as patients with amnestic mild cognitive impairment (aMCI) and temporal lobe epilepsy (TLE). RESULTS: Among 10 anti-LGI encephalitis patients (60% male, median age 67.5 years) who underwent neuropsychological testing (median = 38.5 months from symptom onset), cognitive deficits were common, with 100% of patients showing impairment (≤1.5 SD below mean) on 1+ measures and 80% on 2+ measures. Patients with anti-LGI-1 encephalitis performed worse than controls on measures of basic attention, vigilance, psychomotor speed, complex figure copy, and aspects of learning/memory. Of measures which differed from controls, there were no differences between the anti-LGI-1 and TLE patients, while the anti-LGI-1 patients exhibited higher rates of impairment in basic attention and lower rates of delayed verbal memory impairment compared to the aMCI patients. CONCLUSIONS: Long-term cognitive deficits are common in patients with anti-LGI-1 encephalitis and involve multiple domains. Future research in larger samples is needed to confirm these findings.
 Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by the loss of motor neurons and neuromuscular impairment leading to complete paralysis, respiratory failure and premature death. The pathogenesis of the disease is multifactorial and noncell-autonomous involving the central and peripheral compartments of the neuromuscular axis and the skeletal muscle. Advanced clinical trials on specific ALS-related pathways have failed to significantly slow the disease. Therapy with stem cells from different sources has provided a promising strategy to protect the motor units exerting their effect through multiple mechanisms including neurotrophic support and excitotoxicity and neuroinflammation modulation, as evidenced from preclinical studies. Several phase I and II clinical trial of ALS patients have been developed showing positive effects in terms of safety and tolerability. However, the modest results on functional improvement in ALS patients suggest that only a coordinated effort between basic and clinical researchers could solve many problems, such as selecting the ideal stem cell source, identifying their mechanism of action and expected clinical outcomes. A promising approach may be stem cells selected or engineered to deliver optimal growth factor support at multiple sites along the neuromuscular pathway. This review covers recent advances in stem cell therapies in animal models of ALS, as well as detailing the human clinical trials that have been done and are currently undergoing development.
 BACKGROUND AND OBJECTIVES: We sought to identify early factors associated with relapse and outcome in paediatric-onset myelin oligodendrocyte glycoprotein antibody-associated disorders (MOGAD). METHODS: In a multicenter retrospective cohort of pediatric MOGAD (≤18 years), onset features and treatment were compared in patients with monophasic vs relapsing disease (including cases with follow-up ≥12 months after onset or relapse at any time) and in patients with final Expanded Disability Status Scale (EDSS) 0 vs ≥1 at last follow-up (including cases with follow-up >3 months after last event or EDSS0 at any time). Multivariable logistic regression models were used to evaluate factors associated with relapsing disease course and EDSS ≥ 1 at final follow-up. RESULTS: Seventy-five children were included (median onset age 7 years; median 30 months of follow-up). Presentation with acute disseminated encephalomyelitis was more frequent in children aged 8 years or younger (66.7%, 28/42) than in older patients (30.3%, 10/33) (p = 0.002), whereas presentation with optic neuritis was more common in children older than 8 years (57.6%, 19/33) than in younger patients (21.4%, 9/42) (p = 0.001). 40.0% (26/65) of patients relapsed. Time to first relapse was longer in children aged 8 years or younger than in older patients (median 18 vs 4 months) (p = 0.013). Factors at first event independently associated with lower risk of relapsing disease course were immunotherapy <7 days from onset (6.7-fold reduced odds of relapsing course, OR 0.15, 95% CI 0.03-0.61, p = 0.009), corticosteroid treatment for ≥5 weeks (6.7-fold reduced odds of relapse, OR 0.15, 95% CI 0.03-0.80, p = 0.026), and abnormal optic nerves on onset MRI (12.5-fold reduced odds of relapse, OR 0.08, 95% CI 0.01-0.50, p = 0.007). 21.1% (15/71) had EDSS ≥ 1 at final follow-up. Patients with a relapsing course had a higher proportion of final EDSS ≥ 1 (37.5%, 9/24) than children with monophasic disease (12.8%, 5/39) (p = 0.022, univariate analysis). Each 1-point increment in worst EDSS at onset was independently associated with 6.7-fold increased odds of final EDSS ≥ 1 (OR 6.65, 95% CI 1.33-33.26, p = 0.021). DISCUSSION: At first attack of pediatric MOGAD, early immunotherapy, longer duration of corticosteroid treatment, and abnormal optic nerves on MRI seem associated with lower risk of relapse, whereas higher disease severity is associated with greater risk of final disability (EDSS ≥ 1).
 Pancreatic neuroendocrine tumors (PanNETs) in familial tuberous sclerosis (TSC1 and TSC2 mutations) have been known and studied. However, little is known about PanNET patients harboring the very rare (less than 2%) sporadic TSC mutations. Some renal tumors have been shown to harbor sporadic TSC mutations, with a distinctive morphological correlate. We hereby describe this rather unusual molecular alteration in well-differentiated pancreatic neuroendocrine tumors (WD PanNETs) with a focus on their morphology and treatment outcomes. Six cases of WD PanNETs harboring sporadic TSC mutations were identified retrospectively. H&E slides and corresponding immunostains were reviewed for all cases. Clinical, molecular, and radiological information was obtained using the electronic medical records. Cohort consisted of 4 males and 2 females. Median age at diagnosis was 50 years (range 33-74 years). Origin of neoplasm was the pancreas and, in all but one, patient had liver metastasis by the time of presentation. Six out of six cases demonstrated a unique tumor morphology, with ample eosinophilic cytoplasm. Tumors were arranged in sheets and nests; prominent cystic change was noted in one case. Two cases were additionally biopsied post-treatment with capecitabine and temozolomide, and showed even more abundant oncocytic cytoplasm, eccentric nuclei, and a prominent cherry red nucleolus, and were arranged in a cluster of 3-4 cells, separated by stromal cells. Every patient had a different TSC2 variant with no cases of TSC1 mutations. Other common variants included MEN1 (4/6), DAXX (2/6), and TP53 (2/6). Per the WH0 2019 classification, tumors were graded as NET-G3 (n = 3) and NET-G2 (n = 3). Ki-67 s ranged from 7.2 to 60. All cases had retained MMR protein expression. The majority of patients (4/6) have expired. Although they received multiple treatments, a consistent pattern observed in patients was marked radiologic response to chemotherapy with capecitabine and temozolomide (offered in 5/6 patients) with duration of responses reaching 11 months in the majority of cases, with one patient showing near complete pathologic response of localized disease. TSC2 mutations may confer distinctive appearance in WD PanNETs, reminiscent of their effects in renal tumors. Although not entirely specific, this distinct morphological pattern with abundant eosinophilic cytoplasm in WD PanNETs could be reflective of an associated TSC mutation, with suggestions of significant therapeutic response to a specific cytotoxic chemotherapy.
 BACKGROUND: Motor capacity is crucial in amyotrophic lateral sclerosis (ALS) clinical trial design and patient care. However, few studies have explored the potential of multimodal MRI to predict motor capacity in ALS. This study aims to evaluate the predictive value of cervical spinal cord MRI parameters for motor capacity in ALS compared to clinical prognostic factors. METHODS: Spinal multimodal MRI was performed shortly after diagnosis in 41 ALS patients and 12 healthy participants as part of a prospective multicenter cohort study, the PULSE study (NCT00002013-A00969-36). Motor capacity was assessed using ALSFRS-R scores. Multiple stepwise linear regression models were constructed to predict motor capacity at 3 and 6 months from diagnosis, based on clinical variables, structural MRI measurements, including spinal cord cross-sectional area (CSA), anterior-posterior, and left-to-right cross-section diameters at vertebral levels from C1 to T4, and diffusion parameters in the lateral corticospinal tracts (LCSTs) and dorsal columns. RESULTS: Structural MRI measurements were significantly correlated with the ALSFRS-R score and its sub-scores. And as early as 3 months from diagnosis, structural MRI measurements fit the best multiple linear regression model to predict the total ALSFRS-R (R(2) = 0.70, p value = 0.0001) and arm sub-score (R(2) = 0.69, p value = 0.0002), and combined with DTI metric in the LCST and clinical factors fit the best multiple linear regression model to predict leg sub-score (R(2) = 0.73, p value = 0.0002). CONCLUSIONS: Spinal multimodal MRI could be promising as a tool to enhance prognostic accuracy and serve as a motor function proxy in ALS.
 Although parathyroid bone disease is rarely seen nowadays, skeletal manifestation can be the first sign of hyperparathyroidism (HPT) in some clinical practice. Nevertheless, the diagnosis of HPT is often overlooked. We describe three cases of multiple brown tumors (BT) in which bone pain and destruction were the first symptoms that masqueraded as a malignancy. However, according to the results of bone scan and targeted single-photon emission computed tomography/computed tomography (SPECT/CT), we considered BTs as the diagnosis in all of three cases. The final diagnoses were confirmed by laboratory tests and post-parathyroidectomy pathology. Parathyroid hormone (PTH) is significantly elevated in primary hyperparathyroidism (PHPT) as we know. However, such elevation is virtually never seen in malignancies. Diffuse or multiple foci of tracer uptakes in the bone scan were always seen in bone metastasis, multiple myeloma, and other bone neoplasm. When patients visited nuclear medicine for first consultation without biochemical results, radiological evidence from planar bone scan and targeted SPECT/CT can help in distinguishing the skeletal diseases. Lytic bone lesions with sclerosis, intra-focal or ectopic ossification and calcification, fluid-fluid level, and distribution of the lesions may be helpful in the differential diagnosis in these reported cases. In conclusion, when patients present with multiple foci of uptake on bone scan, targeted SPECT/CT is acquired for suspicious lesions, which can increase the diagnostic sensitivity and reduce unnecessary interventions and treatment. Moreover, BTs should be always kept in differential diagnosis of multiple lesions without a conclusive primary tumor.
 OBJECTIVES: Mutations in TSC1 or TSC2 genes have been proposed as the main causative factors responsible for developing Tuberous Sclerosis Complex (TSC). Given the effect of these two genes on the mTOR pathway, rapamycin has emerged as a novel therapeutic agent. The present study evaluated the effectiveness and safety of rapamycin on the multiple manifestations of TSC. MATERIALS & METHODS: Twenty-three eligible children were enrolled in the present cross-sectional study. They were prescribed rapamycin 1mg tablet twice daily for the first two weeks of treatment and then once daily for at least one year. Periodic evaluations through follow-up visits were performed. Besides, growth and developmental statuses were evaluated. All data, including the number and size of brain tuberomas, size of renal angiomyolipomas, and skin lesions, were gathered and recorded, and then analyzed. RESULTS: During the study period, the mean number of epileptic episodes significantly reduced (p<0.0001), and nine cases were seizure-free at the final visit. The mean number of brain tuberomas decreased from 19.3±11.0 at the initial visit to 11.1±5.6 and 8.2±3.2 in the subsequent visits (p<0.001). The mean size of brain tuberomas similarly decreased from 17.9±18.5 cm at enrollment to 13.7±5.1 cm and 6.9±5.1 cm in the second and third visits, respectively (p=0.029). The mean size of renal angiomyolipomas significantly decreased (p<0.001). A significant trend toward a decrease in the number of skin lesions was observed (p<0.0001). No relationship was observed between the effects of rapamycin and the patient's age or sex (p>0.05). Changes in patients' growth and developmental features were not statistically significant through subsequent visits (p=0.507). CONCLUSION: This study revealed the effectiveness and safety of rapamycin on TSC among our patients.
 INTRODUCTION/AIMS: Reliable neurophysiological markers in amyotrophic lateral sclerosis (ALS) are of great interest. The compound muscle action potential (CMAP) amplitude has been a conventional marker, although it is greatly influenced by the electrode position. We propose the far-field potential of the CMAP (FFP-CMAP) as a new neurophysiological marker in ALS. METHODS: Patients with ALS and age-matched healthy controls were enrolled. We used a proximal reference (pref) in addition to the conventional distal reference (dref). Routine CMAP was recorded from the belly-dref lead and FFP-CMAP from the dref-pref lead for the ulnar and tibial nerves. Multiple point stimulation motor unit number estimation (MUNE) was also examined in the ulnar nerve. Inter-rater reproducibility was evaluated by two examiners, and some patients were followed up every 3 mo for 1 y. RESULTS: We tested 17 patients with ALS and 10 controls. The amplitudes of routine CMAP and FFP-CMAP in the ulnar and tibial nerves, and hypothenar MUNE value in the ulnar nerve were significantly decreased in ALS compared to controls. Ulnar FFP-CMAP achieved the highest inter-rater intraclass correlation coefficient (ICC) value (0.942) when compared with routine CMAP (0.880) and MUNE (0.839). The tibial FFP-CMAP had a higher ICC value (0.986) than the routine CMAP (0.697). In this way, the FFP-CMAP showed high inter-rater reproducibility because its shape was not much influenced by the electrode position. During 1-y follow-up, decline of CMAP, FFP, and MUNE showed significant correlations with the Amyotrophic Lateral Sclerosis Functional Rating Scale - Revised (ALSFRS-R). DISCUSSION: The FFP-CMAP shows promise as a reliable marker for ALS.
 Introduction: The aim of the present study was to establish a simple method for the determination of riluzole in human plasma by ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) and apply it for the determination of riluzole in amyotrophic lateral sclerosis (ALS) patients. Methods: Samples were prepared by protein precipitation and were then gradient-eluted on a column of ACQUITY UPLC(®) HSS T3 by using 0.1% formic acid acetonitrile and 0.1% formic acid water as the mobile phase. Detection was performed on a Xevo TQ-S tandem mass spectrometer in the multiple-reaction monitoring mode using positive electrospray ionization. Validation was performed in the range of 5-800 ng/mL. Results and discussion: Three batches of precision accuracy, selectivity, matrix effects, extraction recovery, and stability were also verified and met the requirements. The results showed that the method was reliable and successfully applied to the pharmacokinetics study of riluzole in Chinese amyotrophic lateral sclerosis patients. Meanwhile, in comparison with other prior published methods, our method has the advantages of simple sample preparation, relatively short running time, and small plasma sample consumption, which represented a high-throughput sample determination potential.
 AIMS: Amyotrophic lateral sclerosis (ALS) is characterised by a progressive loss of upper and lower motor neurons leading to muscle weakness and eventually death. Frontotemporal dementia (FTD) presents clinically with significant behavioural decline. Approximately 10% of cases have a known family history, and disease-linked mutations in multiple genes have been identified in FTD and ALS. More recently, ALS and FTD-linked variants have been identified in the CCNF gene, which accounts for an estimated 0.6% to over 3% of familial ALS cases. METHODS: In this study, we developed the first mouse models expressing either wild-type (WT) human CCNF or its mutant pathogenic variant S621G to recapitulate key clinical and neuropathological features of ALS and FTD linked to CCNF disease variants. We expressed human CCNF WT or CCNF(S621G) throughout the murine brain by intracranial delivery of adeno-associated virus (AAV) to achieve widespread delivery via somatic brain transgenesis. RESULTS: These mice developed behavioural abnormalities, similar to the clinical symptoms of FTD patients, as early as 3 months of age, including hyperactivity and disinhibition, which progressively deteriorated to include memory deficits by 8 months of age. Brains of mutant CCNF_S621G mice displayed an accumulation of ubiquitinated proteins with elevated levels of phosphorylated TDP-43 present in both CCNF_WT and mutant CCNF_S621G mice. We also investigated the effects of CCNF expression on interaction targets of CCNF and found elevated levels of insoluble splicing factor proline and glutamine-rich (SFPQ). Furthermore, cytoplasmic TDP-43 inclusions were found in both CCNF_WT and mutant CCNF_S621G mice, recapitulating the key hallmark of FTD/ALS pathology. CONCLUSIONS: In summary, CCNF expression in mice reproduces clinical presentations of ALS, including functional deficits and TDP-43 neuropathology with altered CCNF-mediated pathways contributing to the pathology observed.
 Systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis, and Sjögren's syndrome are four major autoimmune rheumatic diseases characterized by the presence of autoantibodies, caused by a dysregulation of the immune system that leads to a wide variety of clinical manifestations. These conditions present complex etiologies strongly influenced by multiple environmental and genetic factors. The human leukocyte antigen (HLA) region was the first locus identified to be associated and still represents the strongest susceptibility factor for each of these conditions, particularly the HLA class II genes, including DQA1, DQB1, and DRB1, but class I genes have also been associated. Over the last two decades, the genetic component of these disorders has been extensively investigated and hundreds of non-HLA risk genetic variants have been uncovered. Furthermore, it is widely accepted that autoimmune rheumatic diseases share molecular disease pathways, such as the interferon (IFN) type I pathways, which are reflected in a common genetic background. Some examples of well-known pleiotropic loci for autoimmune rheumatic diseases are the HLA region, DNASEL13, TNIP1, and IRF5, among others. The identification of the causal molecular mechanisms behind the genetic associations is still a challenge. However, recent advances have been achieved through mouse models and functional studies of the loci. Here, we provide an updated overview of the genetic architecture underlying these four autoimmune rheumatic diseases, with a special focus on the HLA region.
 OBJECTIVE: We conducted a systematic review and meta-analysis to evaluate postoperative seizure and memory outcomes of temporal lobe epilepsy with different hippocampal sclerosis (HS) subtypes classified by ILAE Consensus Guidelines in 2013. METHOD: Following the PRISMA and MOOSE guidelines, we searched PubMed, Embase, Web of Science, and Cochrane Library from January 1, 2013 to August 6, 2023. Observational studies reporting seizure and memory outcomes among different HS subtypes were included. We used the Newcastle-Ottawa scale to assess the risk of bias and the GRADE approach to grade the quality of evidence. Seizure freedom and improved outcome (Engel 1 or ILAE class 1-2) ≥1 year after surgery were defined as the primary and secondary seizure outcome. A random-effects meta-analysis with DerSimonian and Laird method was performed to obtain pooled risk ratio (RR) with 95% confidence interval (CI). The memory impairment was narratively reviewed because of various evaluation tools. RESULTS: Fifteen cohort studies with 2,485 patients were eligible for the meta-analysis of seizure outcome. Six cohorts with detailed information of postoperative memory outcome were included. The pooled RR of seizure freedom, with moderate to substantial heterogeneity, were 0.98 (95% CI 0.84 to 1.15) between HS Type 2 and Type 1, 1.11 (95% CI 0.82 to 1.52) between Type 3 and Type 1, and 0.80 (95% CI 0.62 to 1.03) between no-HS and HS group. No significant difference of improved outcome was found between different subtypes (P >0.05). The quality of evidence was deemed as low to very low according to GRADE. The long-term seizure outcome (≥5 years after surgery) and memory impairment remained controversial. SIGNIFICANCE: Similar postoperative seizure outcome and inconsistent postsurgical memory changes were found among different HS pathological subtypes. Multiple factors including but not limited to pathological changes, may influence the postsurgical seizure and cognitive outcomes.
 A significant number of individuals with tuberous sclerosis complex (TSC) exhibit language difficulties. Here, we examined the language-related brain morphometry in 59 participants (7 participants with TSC and comorbid autism spectrum disorder (ASD) (TSC + ASD), 13 with TSC but no ASD (TSC-ASD), 10 with ASD-only (ASD), and 29 typically developing (TD) controls). A hemispheric asymmetry was noted in surface area and gray matter volume of several cortical language areas in TD, ASD, and TSC-ASD groups, but not in TSC + ASD group. TSC + ASD group demonstrated increased cortical thickness and curvature values in multiple language regions for both hemispheres, compared to other groups. After controlling for tuber load in the TSC groups, within-group differences stayed the same but the differences between TSC-ASD and TSC + ASD were no longer statistically significant. These preliminary findings suggest that comorbid ASD in TSC as well as tuber load in TSC is associated with changes in the morphometry of language regions. Future studies with larger sample sizes will be needed to confirm these findings.
 INTRODUCTION: Systemic sclerosis (SSc) is a chronic rheumatic disease that affects multiple organ systems, including the peripheral nervous system. However, studies into the involvement of polyneuropathies (PNP) have shown inconsistent results. The aim of this study was to determine the prevalence of small (SFN) and large (LFN) fibre neuropathy among SSc patients and the impact on health-related quality of life (HRQoL). MATERIAL AND METHODS: The study enrolled 67 patients with diagnosed SSc. The severity of neuropathic symptoms was evaluated using shortened and revised total neuropathy scoring criteria. Nerve conduction studies were used for LFN, and quantitative sensory testing was used to evaluate SFN. Neuropathic pain was evaluated using a Douleur Neuropathique en 4 questionnaire, and the severity of anxiety symptoms was assessed using a Generalised Anxiety Disorder-7 scale. The Health Assessment Questionnaire-Disability Index was used to assess HRQoL. Previous data on antinuclear autoantibodies (ANA) test results was obtained. Statistical analysis was performed using SPSS software. RESULTS: LFN was diagnosed in 47.8% (n = 32/67) and SFN in 40.3% (n = 27/67) of the subjects. ANA positivity was not associated with the presence of LFN/SFN. The severity of neuropathic pain had a significant correlation with anxiety symptoms (r = 0.61, p < 0.001), the severity of neuropathy symptoms (r = 0.51, p < 0.001) and HRQoL (r = 0.45, p < 0.001). The severity of neuropathy symptoms correlated with HRQoL (r = 0.39, p = 0.001). CONCLUSIONS: We demonstrated that PNP are found in almost all SSc patients. Also, SFN is as common as LFN. Additionally, we found that the severity of neuropathy symptoms and neuropathic pain are both associated with a worse HRQoL.
 Scleroderma renal crisis (SRC) is a life-threatening complication of systemic sclerosis (SSc) with a mortality of 20% at 6 months. Once the leading cause of mortality in scleroderma (SSc), it remains a serious complication, often necessitating level three care for patients affected. Whilst renal outcomes have significantly improved following the advent of angiotensin-converting enzyme inhibitor (ACEi) therapy, SRC remains a precarious challenge for clinicians, due to lack of preventative measures and the fact that patients can rapidly decline despite best medical management. Large cohort studies spanning decades have allowed clear identification of phenotypes particularly at risk of developing SRC thus allowing enhanced monitoring and early identification in those individuals. Novel urinary biomarkers for renal disease in SSc may offer a new window for early identification of SRC patients and response to treatment. Multiple studies have demonstrated increased activity of complement pathways in SRC with some anecdotal cases exhibiting serological response to treatment with eculizumab where ACEi and therapeutic plasma exchange (TPE) were not successful. Endothelin-1 blockade, a therapeutic strategy in other SSc vasculopathies, has shown potential as a target but clinical trials are yet to show a clear treatment benefit. Clear guidelines for the management of SRC are in place to standardise care and facilitate early collaboration between rheumatology and renal physicians. Outcomes following renal transplant have improved but the mortality of SRC remains high, indicating the need for continued exploration of the mechanisms precipitating and exacerbating SRC in order to develop novel therapies.
 OBJECTIVE: This study aimed to investigate whether the physical activity scale for the elderly (PASE) is a valid tool in measuring physical activity (PA) in people with motor neuron disease (MND) and to identify the demographic and clinical factors that predict PA participation in this population. DESIGN: A prospective, observational study involving 100 ambulant participants with MND. SETTING: This study was conducted at a multidisciplinary specialist MND clinic. The clinic is fully funded by the local public health system and patients receiving care here are not expected to pay for their consultation. PARTICIPANTS: 190 patients with MND who had a physiotherapy appointment at the specialist clinic between July and October 2018 were screened. Of these, 100 participants (mean age 67 years [SD=12], 64% [n=64] men) who were ambulant (with or without assistance) were recruited (N=100). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: PASE questionnaire, amyotrophic lateral sclerosis functional rating scale-Revised (ALSFRS-r), forced vital capacity (FVC). RESULTS: The results showed that engagement in PA is generally low, with median PASE score of 57. The PASE had fair-moderate correlation with ALSFRS-R total scores (rho=0.607; P<.000) and FVC (rho=0.250; P=.030). Standard multiple regression analyses showed that disease severity (ALSFRS-R total score) was the strongest predictor of PA levels (β= 0.54; 95% confidence interval 0.02,0.06). The most frequently selected physical activities of choice for people with MND were activities around their homes and the biggest barrier to participation is fatigue. CONCLUSION: Present findings suggest that the PASE can be used to measure PA participation in people with MND. Details about activity of choice and barriers to participation present important considerations in designing exercise programs in this population to maximize compliance and therefore effectiveness.
 Introduction/Aims. Primary lateral sclerosis (PLS) is exceedingly rare and has been an enigmatic disease. Recent progress has drastically changed this perception, with early biomarkers being investigated and potential medications for PLS emerging at the preclinical stage. The aim of this paper is to describe a study of PLS natural history and discuss the limitations and proposed solutions to the study of a rare and slowly progressive disease. Methods. The PLS Natural History Study is a 30-site, 24-month, prospective study that is supported by multiple funding sources. The study aims to enroll 50 early PLS (disease duration ≤4 years) and 50 definite PLS (disease duration 4 to 15 years) participants using modified PLS Diagnostic Criteria. Smartphone-based assessments including semi-quantitative and quantitative measures and patient-reported outcomes are utilized. In-person quantitative measures are also completed during site visits. The change in the PLS Functional Rating Scale score is the primary outcome. The study utilizes the NeuroBANK(®) patient-centric data capture and management platform. The biostatistical analysis plan has been developed. Results. In one year, 28 participants have been recruited. Enrollment has been much slower than anticipated due to the COVID-19 pandemic, the rarity of PLS, and potential study competition for internal resources from ALS clinical trials. Discussion. We discuss the need for more innovative methods to enroll and study individuals with such rare diseases and propose a number of mechanisms by which more efficient enrollment could be facilitated.
 Dystussia is prevalent in individuals with amyotrophic lateral sclerosis (ALS), leading to a diminished physiologic capacity to effectively defend the airway. We aimed to identify predictors of peak expiratory cough flow rate in individuals with ALS. One hundred and thirty-four individuals with a confirmed diagnosis of ALS (El-Escorial criteria revised) completed the ALS Functional Rating Scale-Revised (ALSFRS-R) and underwent pulmonary function and cough spirometry testing. Pearson's correlation coefficients and hierarchical multiple regression modeling were conducted to determine predictors of voluntary cough peak expiratory flow rate (p < 0.05). The full model including age, bulbar disease, cough spirometry metrics, and respiratory parameters had a marginal R(2) = 0.635, F (7, 126) = 30.241, p < 0.0005, adjusted R(2) = 0.61. Maximum expiratory pressure, compression phase, and vital capacity did not contribute and were therefore removed (p < 0.05). The most parsimonious predictive model included age, bulbar disease, peak inspiratory flow rate and duration, peak expiratory rise time, and inspiratory pressure generation with a marginal R(2) = 0.543. Although expiratory pressure generation has historically served as the therapeutic target to improve dystussia in ALS, the current dataset highlighted that the inability to quickly and forcefully inspire during the inspiratory phase of voluntary cough places patients at a mechanical disadvantage to generate subsequent high-velocity expiratory airflow to clear the airway. Thus, therapeutic training programs that include both inspiratory and expiratory strength targets may optimize airway clearance capacity in this challenging patient population.
 Systemic sclerosis (SSc) is a rare and chronic autoimmune disease characterized by a pathogenic triad of immune dysregulation, vasculopathy, and progressive fibrosis. Clinical tools commonly used to assess patients, including the modified Rodnan skin score, difference between limited or diffuse forms of skin involvement, presence of lung, heart or kidney involvement, or of various autoantibodies, are important prognostic factors, but still fail to reflect the large heterogeneity of the disease. SSc treatment options are diverse, ranging from conventional drugs to autologous hematopoietic stem cell transplantation, and predicting response is challenging. Genome-wide technologies, such as high throughput microarray analyses and RNA sequencing, allow accurate, unbiased, and broad assessment of alterations in expression levels of multiple genes. In recent years, many studies have shown robust changes in the gene expression profiles of SSc patients compared to healthy controls, mainly in skin tissues and peripheral blood cells. The objective analysis of molecular patterns in SSc is a powerful tool that can further classify SSc patients with similar clinical phenotypes and help predict response to therapy. In this review, we describe the journey from the first discovery of differentially expressed genes to the identification of enriched pathways and intrinsic subsets identified in SSc, using machine learning algorithms. Finally, we discuss the use of these new tools to predict the efficacy of various treatments, including stem cell transplantation. We suggest that the use of RNA gene expression-based classifications according to molecular subsets may bring us one step closer to precision medicine in Systemic Sclerosis.
 BACKGROUND: Physical activity in Amyotrophic Lateral Sclerosis (ALS) plays a controversial role. In some epidemiological studies, both recreational or professional sport exercise has been associated to an increased risk for ALS but the mechanisms underlying the effects of exercise have not been fully elucidated in either patients or animal models. OBJECTIVE AND METHODS: To better reproduce the influence of this environmental factor in the pathogenesis of ALS, we exposed SOD1G93A low-copy male mice to multiple exercise sessions at asymptomatic and pre-symptomatic disease stages in an automated home-cage running-wheel system for about 3 months. RESULTS: Repeated voluntary running negatively influenced disease progression by anticipating disease onset, impairing neuromuscular transmission, worsening neuromuscular decline, and exacerbating muscle atrophy. Muscle fibers and neuromuscular junctions (NMJ) as well as key molecular players of the nerve-muscle circuit were similarly affected. CONCLUSION: It thus appears that excessive physical activity can be detrimental in predisposed individuals and these findings could model the increased risk of developing ALS in predisposed and specific professional athletes.
 In patients with amyotrophic lateral sclerosis (ALS), disease symptoms and pathology typically spread in a predictable spatiotemporal pattern beginning at a focal site of onset and progressing along defined neuroanatomical tracts. Like other neurodegenerative diseases, ALS is characterized by the presence of protein aggregates in postmortem patient tissue. Cytoplasmic, ubiquitin-positive aggregates of TDP-43 are observed in approximately 97% of sporadic and familial ALS patients, while SOD1 inclusions are likely specific to cases of SOD1-ALS. Additionally, the most common subtype of familial ALS, caused by a hexanucleotide repeat expansion in the first intron of the C9orf72 gene (C9-ALS), is further characterized by the presence of aggregated dipeptide repeat proteins (DPRs). As we will describe, cell-to-cell propagation of these pathological proteins tightly correlates with the contiguous spread of disease. While TDP-43 and SOD1 are capable of seeding protein misfolding and aggregation in a prion-like manner, C9orf72 DPRs appear to induce (and transmit) a 'disease state' more generally. Multiple mechanisms of intercellular transport have been described for all of these proteins, including anterograde and retrograde axonal transport, extracellular vesicle secretion, and macropinocytosis. In addition to neuron-to-neuron transmission, transmission of pathological proteins occurs between neurons and glia. Given that the spread of ALS disease pathology corresponds with the spread of symptoms in patients, the various mechanisms by which ALS-associated protein aggregates propagate through the central nervous system should be closely examined.
 Early generalized morphea can clinically mimic mycosis fungoides. The microscopic features of early inflammatory morphea may show variable degrees of infiltration and do not have the characteristic dermal collagen sclerosis. We report the case of a 63-year-old female patient who presented with a 2-month history of an asymptomatic skin rash. Physical examination revealed multiple erythematous to dusky patches on the trunk and thighs, resembling the patch stage of mycosis fungoides. Two skin biopsies were performed, both of which showed prominent interstitial lymphoid infiltration in the reticular dermis without dermal sclerosis. Small lymphocyte exocytosis and lining along the dermal-epidermal junction were observed focally in the epidermis. Small clusters of plasma cells and eosinophils were observed in perivascular areas. Although no predominant clonality was found for CD4 and CD8 stains, 50% loss of CD5 antigen and 90% loss of CD7 antigen expression were apparent in immunohistochemical studies. Subsequent blood tests showed a normal blood cell count and positive human T-lymphotropic virus Type 1 antibodies. The overall findings suggested interstitial mycosis fungoides or early adult T-cell lymphoma-leukemia. The patient refused aggressive treatment, and 3 months later, she presented with indurated plaques from the previous rash. A repeat biopsy revealed the typical features of morphea. This report discussed the pitfalls in the clinical and histopathological diagnosis of early generalized inflammatory morphea that both clinicians and pathologists should consider.
 The C9ORF72-linked diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are characterized by the nuclear depletion and cytoplasmic accumulation of TAR DNA-binding protein 43 (TDP-43). Recent studies have shown that the loss of TDP-43 function leads to the inclusion of cryptic exons (CE) in several RNA transcript targets of TDP-43. Here, we show for the first time the detection of CEs in a single-nuclei RNA sequencing (snRNA-seq) dataset obtained from frontal and occipital cortices of C9ORF72 patients that phenotypically span the ALS-FTD disease spectrum. We assessed each cellular cluster for detection of recently described TDP-43-induced CEs. Transcripts containing CEs in the genes STMN2 and KALRN were detected in the frontal cortex of all C9ORF72 disease groups with the highest frequency in excitatory neurons in the C9ORF72-FTD group. Within the excitatory neurons, the cluster with the highest proportion of cells containing a CE had transcriptomic similarities to von Economo neurons, which are known to be vulnerable to TDP-43 pathology and selectively lost in C9ORF72-FTD. Differential gene expression and pathway analysis of CE-containing neurons revealed multiple dysregulated metabolic processes. Our findings reveal novel insights into the transcriptomic changes of neurons vulnerable to TDP-43 pathology.
 PURPOSE: To evaluate the effectiveness of plasma exchange (PLEX) for optic neuritis (ON). METHODS: We conducted an international multicenter retrospective study evaluating the outcomes of ON following PLEX. Outcomes were compared to raw data from the Optic Neuritis Treatment Trial (ONTT) using a matched subset. RESULTS: A total of 395 ON attack treated with PLEX from 317 patients were evaluated. The median age was 37 years (range 9-75), and 71% were female. Causes of ON included multiple sclerosis (108), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) (92), aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) (75), seronegative-NMOSD (34), idiopathic (83), and other (3). Median time from onset of vision loss to PLEX was 2.6 weeks (interquartile range [IQR], 1.4-4.0). Median visual acuity (VA) at the time of PLEX was count fingers (IQR, 20/200-hand motion), and median final VA was 20/25 (IQR, 20/20-20/60) with no differences among etiologies except MOGAD-ON, which had better outcomes. In 81 (20.5%) ON attacks, the final VA was 20/200 or worse. Patients with poor outcomes were older (P = .002), had worse VA at the time of PLEX (P < .001), and longer delay to PLEX (P < .001). In comparison with the ONTT subset with severe corticosteroid-unresponsive ON, a final VA of worse than 20/40 occurred in 6 of 50 (12%) PLEX-treated ON vs 7 of 19 (37%) from the ONTT treated with intravenous methylprednisolone without PLEX (P = .04). CONCLUSION: Most ON attacks improved with PLEX, and outcomes were better than attacks with similar severity in the ONTT. The presence of severe vision loss at nadir, older age, and longer delay to PLEX predicted a worse outcome whereas MOGAD-ON had a more favorable prognosis. NOTE: Publication of this article is sponsored by the American Ophthalmological Society.
 Systemic rheumatic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis, are chronic autoimmune diseases affecting multiple organs and tissues. Despite recent advances in treatment, patients still experience significant morbidity and disability. Mesenchymal stem/stromal cell (MSC)-based therapy is promising for treating systemic rheumatic diseases due to the regenerative and immunomodulatory properties of MSCs. However, several challenges need to be overcome to use MSCs in clinical practice effectively. These challenges include MSC sourcing, characterization, standardization, safety, and efficacy issues. In this review, we provide an overview of the current state of MSC-based therapies in systemic rheumatic diseases, highlighting the challenges and limitations associated with their use. We also discuss emerging strategies and novel approaches that can help overcome the limitations. Finally, we provide insights into the future directions of MSC-based therapies for systemic rheumatic diseases and their potential clinical applications.
 Aim: To profile the plasma proteomics and metabolomics of patients with renal cysts, sporadic angiomyolipoma (S-AML) and tuberous sclerosis complex related angiomyolipoma (TSC-RAML) before and after everolimus treatment, and to find potential diagnostic and prognostic biomarkers as well as reveal the underlying mechanism of TSC tumorigenesis. Materials and Methods: We retrospectively measured the plasma proteins and metabolites from November 2016 to November 2017 in a cohort of pre-treatment and post-treatment TSC-RAML patients and compared them with renal cyst and S-AML patients by ultra-performance liquid chromatography-mass spectrometer (UPLC-MS). The tumor reduction rates of TSC-RAML were assessed and correlated with the plasma protein and metabolite levels. In addition, functional analysis based on differentially expressed molecules was performed to reveal the underlying mechanisms. Results: Eighty-five patients with one hundred and ten plasma samples were enrolled in our study. Multiple proteins and metabolites, such as pre-melanosome protein (PMEL) and S-adenosylmethionine (SAM), demonstrated both diagnostic and prognostic effects. Functional analysis revealed many dysregulated pathways, including angiogenesis synthesis, smooth muscle proliferation and migration, amino acid metabolism and glycerophospholipid metabolism. Conclusion: The plasma proteomics and metabolomics pattern of TSC-RAML was clearly different from that of other renal tumors, and the differentially expressed plasma molecules could be used as prognostic and diagnostic biomarkers. The dysregulated pathways, such as angiogenesis and amino acid metabolism, may shed new light on the treatment of TSC-RAML.
 Nitric oxide, a ubiquitous molecule found throughout the natural world, is a key molecule implicated in many central and benefic molecular pathways and has a well-established role in the function of the central nervous system, as numerous studies have previously shown. Dysregulation of its metabolism, mainly the upregulation of nitric oxide production, has been proposed as a trigger and/or aggravator for many neurological affections. Increasing evidence supports the implication of this molecule in prevalent neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, or amyotrophic lateral sclerosis. The mechanisms proposed for its neurotoxicity mainly center around the increased quantities of nitric oxide that are produced in the brain, their cause, and, most importantly, the pathological metabolic cascades created. These cascades lead to the formation of neuronal toxic substances that impair the neurons' function and structure on multiple levels. The purpose of this review is to present the main causes of increased pathological production, as well as the most important pathophysiological mechanisms triggered by nitric oxide, mechanisms that could help explain a part of the complex picture of neurodegenerative diseases and help develop targeted therapies.
 Scleroderma-like cutaneous lesions have been found in many pathological conditions and they have the clinical appearance of sclerotic or scleroatrophic lesions. Affected skin biopsies described histopathological changes similar to those of scleroderma located strictly on the skin or those of systemic sclerosis. These skin lesions can be found in inflammatory diseases with autoimmune substrate (generalized morphea, chronic graft versus host disease, eosinophilic fasciitis), tissue storage diseases (scleredema, scleromyxedema, nephrogenyc systemic fibrosis, systemic amyloidosis), metabolic diseases (porphyrya cutanea tarda, phenylketonuria, hypothyroidism, scleredema diabeticorum), progeroid syndromes. Given the multiple etiologies of sclerodermal lesions, a correct differential diagnosis is necessary to establish the appropriate treatment.
 Cutaneous angiofibroma is a term used to define a group of lesions with different clinical presentations but with the same histologic findings. They are benign fibrous neoplasms comprised of a proliferation of stellate and spindled cells, thin-walled blood vessels with dilated lumina in the dermis, and concentric collagen bundles. Cutaneous angiofibromas can be located on different areas of the body including the face where they are commonly called fibrous papules or adenoma sebaceum on the penis where they are called pearly penile papules, underneath the nail where they are called periungual angiofibromas or Koenen tumors, and in the mouth where they are called oral fibromas.  Facial angiofibromas are considered one of the most obvious clinical presentations of tuberous sclerosis (TS), an autosomal dominant hamartomatous disorder that affects the skin, kidneys, heart, brain, and lungs. With TS, angiofibromas typically arise on the face in childhood and early adulthood. Both facial angiofibromas (greater than or equal to 3 needed) and periungual angiofibroma (greater than or equal to 2 needed) are 2 of the major criteria for TS. Multiple facial angiofibromas are also found in multiple endocrine neoplasia type 1 (MEN-1) and Birt-Hogg-Dube syndrome. Pearly penile papules are chronic, asymptomatic, papules found on the coronal margin and sulcus of the penis. They are more common in uncircumcised men.
 Gastro-entero-pancreatic (GEP-NET) and thoracic neuroendocrine tumours (NETs) are one of the most heritable groups of neoplasms in the body, being multiple endocrine neoplasia syndrome type 1 (MEN1), the genetic syndrome most frequently associated with this type of tumours. Moreover, Von Hippel Lindau syndrome, tuberous sclerosis, type 4 multiple neoplasia syndrome, and type 1 neurofibromatosis are associated with an increased risk of developing GEP-NETs. Another important aspect in GEP-NETs and thoracic NETs is the knowledge of the molecular background since the molecular profile of these tumours may have implications in the prognosis and in the response to specific treatments. This review summarizes the main indications for performing a genetic study in patients with GEP-NETs and thoracic NETs, and the methods used to carry it out. Moreover, it offers a description of the main hereditary syndromes associated with these NETs and their molecular background, as well as the clinical implications of the molecular profile.
 Amyotrophic lateral sclerosis is one of several chronic neurodegenerative conditions in which mitochondrial abnormalities are posited to contribute to disease progression. Therapeutic options targeting mitochondria include enhancing metabolism, suppressing reactive oxygen production and disrupting mitochondria-mediated programmed cell death pathways. Herein is reviewed mechanistic evidence supporting a meaningful pathophysiological role for the constellation of abnormal mitochondrial fusion, fission and transport, collectively designated mitochondrial dysdynamism, in ALS. Following this is a discussion on preclinical studies in ALS mice that seemingly validate the idea that normalizing mitochondrial dynamism can delay ALS by interrupting a vicious cycle of mitochondrial degeneration, leading to neuronal die-back and death. Finally, the relative benefits of suppressing mitochondrial fusion vs. enhancing mitochondrial fusion in ALS are speculated upon, and the paper concludes with the prediction that the two approaches could be additive or synergistic, although a side-by-side comparative trial may be challenging to perform.
 Interstitial lung disease (ILD) has a high prevalence among patients with systemic sclerosis (SSc), carrying high mortality and morbidity. During the last decade, the emergence of new pharmacological therapies for SSc-associated ILD (SSc-ILD) and improved tools for its diagnosis and monitoring have changed the prevailing clinical approach, highlighting the need for early recognition and prompt treatment for SSc-ILD. Furthermore, the recent approval of multiple therapies for SSc-ILD poses challenges for the rheumatologist and pulmonologist in choosing the appropriate therapy for individual clinical scenarios. We review the pathophysiology of SSc-ILD, and the mechanisms of action and rationale behind current therapies. We also review the evidence of the efficacy and safety of immunosuppressive drugs, antifibrotic agents, and immunomodulators from cyclophosphamide and mycophenolate to novel agents such as nintedanib and tocilizumab. We also emphasise the importance of early diagnosis and monitoring and describe our approach to pharmacological therapy for SSc-ILD patients.
 BACKGROUND: Although amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease and unfortunately incurable yet, incremental attention has been drawn to targeting the health of corticospinal motor neurons. Focused ultrasound combined with systemically circulating microbubbles (FUS/MB) is an emerging modality capable of site-specific molecular delivery temporarily and noninvasively within a range of appropriate parameters. OBJECTIVE: To investigate the effect of FUS/MB-enhanced delivery of therapeutics to the motor cortex on the disease progression by using a transgenic mouse model of ALS. METHODS: Multiple FUS/MB-enhanced deliveries of Edaravone (Eda) to the motor cortex were performed on the SOD1(G93A) mouse model of ALS. The motor function of the animals was evaluated by gait analysis, grip strength and wire hanging tests. Corticospinal and spinal motor neuronal health, misfolded SOD1 protein and neuroinflammation after treatments were evaluated by histological examination. RESULTS: Ultrasound-enhanced delivery of Eda in the targeted motor cortex was achieved by a two-fold increase without gross tissue damage. Compared with the ALS mice administered Eda treatments only, the animals given additionally FUS/MB-enhanced brain delivery of Eda (FUS/MB + Eda) exhibited further improvements in neuromuscular functions characterized by gait patterns, muscular strength, and motor coordination along with rescued muscle atrophy. FUS/MB + Eda treatments conferred remarkable neuroprotection to both upper and lower motor neurons revealed by normalized neuronal morphology with increasing cell body size and profoundly alleviated neuroinflammation and misfolded SOD1 protein in the brains and lumbar spinal cords. CONCLUSION: We report a pilot study that non-invasive ultrasound-enhanced brain delivery of Eda provides additive amelioration on disease progression of ALS and suggest that broadening the target from spinal to cortical network functions using the FUS/MB-enhanced delivery can be a rational therapeutic strategy of this debilitating disorder.
 Amyotrophic lateral sclerosis is a heterogeneous, fatal neurodegenerative disease, characterized by motor neuron loss and in 50% of cases also by cognitive and/or behavioral changes. Mendelian forms of ALS comprise approximately 10-15% of cases. The majority is however considered sporadic, but also with a high contribution of genetic risk factors. To explore the contribution of somatic mutations and/or epigenetic changes to disease risk, we performed whole genome sequencing and methylation analyses using samples from multiple tissues on a cohort of 26 monozygotic twins discordant for ALS, followed by in-depth validation and replication experiments. The results of these analyses implicate several mechanisms in ALS pathophysiology, which include a role for de novo mutations, defects in DNA damage repair and accelerated aging.
 BACKGROUND: Tuberous sclerosis complex (TSC) is a genetic disorder associated with multiple neurological manifestations. Cortical tubers (CT) are recognized as the hallmark brain lesions of TSC and contribute to neurological and psychiatric symptoms. To understand the molecular mechanism of neuropsychiatric features of TSC, the differentially expressed genes (DEGs) in CT from patients with TSC and those in normal cortex (NC) from participants acting as healthy controls were investigated. METHODS: The dataset of GSE16969, which had already been published and described (https://onlinelibrary.wiley.com/doi/10.1111/j.1750-3639.2009.00341.x), was downloaded from the Gene Expression Omnibus (GEO), including samples of 4 CT and 4 NC. The R package "limma" was used to screen DEGs in CT and NC. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analyses of the DEGs were conducted using the R package "clusterProfiler". The online software Ingenuity Pathway Analysis (IPA) was used to explore activation/inaction of canonical pathways. The hub gene was selected based on the protein-protein interaction (PPI) network constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database and Cytoscape software. Subsequently, the hub genes at messenger (mRNA) and transcriptional levels were tested. We also explored immune cell-type enrichment using the online database xCell, and assessed the correlation between cell types and C3 expression. Then, we verified the source of C3 by constructing TSC2 knockout cells in the U87 astrocyte cell line. The human neuronal cell line SH-SY5Y was used to examine the effects of excessive complement C3 levels. RESULTS: A total of 455 DEGs were identified. A large number of pathways were involved in the immune response process based on the results of GO, KEGG, and IPA. C3 was identified as a hub gene. Complement C3 was also upregulated in the human CT and peripheral blood. Furthermore, based on the enrichment of functions and signaling pathways, complement C3 played a critical role in immune injury in CT of TSC. In the in vitro experiments, we found that excessive complement C3 was derived from TSC2 knockout U87 cells, and there was an increased intracellular reactive oxygen species (ROS) level in SH-SY5Y cells. CONCLUSIONS: Complement C3 is activated in patients with TSC and can mediate immune injury.
 Transactive response DNA binding-protein 43 (TDP-43) is a conserved RNA/DNA-binding protein with a role in RNA metabolism and homeostasis. Aberrant TDP-43 functioning has been considered a major culprit in amyotrophic lateral sclerosis (ALS). Caenorhabditis elegans can be used to phenocopy ALS in vivo . Since disrupted locomotion is a strong readout of toxicity, we examined multiple motor phenotypes of a C. elegans model expressing human wild-type TDP-43 ( hTDP-43 ) pan-neuronally. Our data reveal that impaired locomotion includes more than the common deficits in crawling capacity and the presence of early-onset paralysis. We show that reduced thrashing, abnormal coiling, and decreased pharyngeal pumping are also observed, in a temperature-dependent fashion.
 Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular endothelial dysfunction and skin fibrosis. Recently, the presence and pathogenic role of immune complexes (ICs) of SSc patients were reported. However, the identities of antigens in these ICs are unknown. Therefore, we examined ICs in the serum of SSc patients to elucidate SSc pathogenesis. In this study, IC concentrations in serum samples from SSc and systemic lupus erythematosus (SLE) patients were measured by C1q enzyme-linked immunosorbent assays; immune complex analysis was used for comprehensive identification and comparison of antigens incorporated into ICs (IC-antigens). The expression patterns of SSc-specific IC-antigens in skin sections were investigated by immunohistochemistry. Compared with SLE patients who developed disease because of IC deposition, SSc patients had a greater number of IC-antigens and a smaller difference in IC concentrations, suggesting that SSc pathogenesis is affected by the proteins present in ICs. In contrast, the IC concentration and number of IC-antigens did not significantly differ according to the clinical phenotype of SSc. We identified 478 IC-antigens in SSc patients, including multiple RNAP II-associated proteins that were targeted by antibodies previously associated with SSc pathogenesis. The most frequently detected RNAP II-associated protein, RNA polymerase II transcription subunit 30 (MED30), was strongly expressed at lesion sites and reportedly regulates endothelial differentiation. Therefore, increased expression of MED30 in lesions may have an antigenic effect, and MED30 function may be impaired or inhibited by IC formation. RNAP II-associated proteins may SSc pathogenesis through mechanisms such as the MED30 pathway.
 OBJECTIVE: To explore the feasibility of superb microvascular imaging (SMI) in evaluating microcirculation damage of the finger of systemic sclerosis (SSc), and determining the optimal scanning method by assessing the effect of scanning position (finger pulp or nail bed), plane (transverse or sagittal) and Doppler gain on the results. METHODS: In the study, 32 SSc patients and 32 non-SSc volunteers admitted to Peking University Third Hospital from February to October 2022 were included. The SMI image under different gain set (40 dB or 35 dB) of the third fingertip (sagittal scans or transverse scan of nail bed or pulp) of both hands were collected while vascular index (VI) was measured. RESULTS: Non-SSc volunteer presented abundant SMI signal distributed in the third fingertip. Arteriole of nail bed was observed on the dorsal side of the distal phalanx under SMI and gave off multiple vertical branches towards the nail. The arteriole of finger pulp ran parallel to the skin and gave off vertical branches towards the skin distributing subcutaneously as a network. In SSc group, the SMI signal in nail bed and finger pulp was reduced. The arteriole of nail bed and finger pulp was discontinuous and presented as sporadic dots and short rod-like color signal under SMI. The vascular index of the SSc patients was significantly lower than that of the non-SSc controls (P < 0.001). Among different positions and sections, the area under the receiver operating characteristic curve (AUC) of the sagittal plane of nail bed was the highest. Under low gain, the AUC of sagittal plane of nail bed was 0.871, the cut-off value was 5.4%, the sensitivity was 90.6%, and the specificity was 74.2%. Under high gain, the AUC was 0.893, the cut-off value was 14.0%, the sensitivity was 75.0%, and the specificity was 93.6%. Multivariate analysis showed that there was statistical significance on the diagnostic impact of the sagittal plane of nail bed (P < 0.005 for high gain condition; P < 0.05 for low gain condition). CONCLUSION: SMI can be used to evaluate the abnormal changes of vascular in patients with SSc. Using the sagittal scan of nail bed with high gain can evaluate the vascular loss of the fingertip in SSc patient accurately and specifically.
 INTRODUCTION: Amyotrophic Lateral Sclerosis (ALS) is a paralyzing, multifactorial neurodegenerative disease with limited therapeutics and no known cure. The study goal was to determine which pathophysiological treatment targets appear most beneficial. METHODS: A big data approach was used to analyze high copy SOD1 G93A experimental data. The secondary data set comprised 227 published studies and 4,296 data points. Treatments were classified by pathophysiological target: apoptosis, axonal transport, cellular chemistry, energetics, neuron excitability, inflammation, oxidative stress, proteomics, or systemic function. Outcome assessment modalities included onset delay, health status (rotarod performance, body weight, grip strength), and survival duration. Pairwise statistical analysis (two-tailed t-test with Bonferroni correction) of normalized fold change (treatment/control) assessed significant differences in treatment efficacy. Cohen's d quantified pathophysiological treatment category effect size compared to "all" (e.g., all pathophysiological treatment categories combined). RESULTS: Inflammation treatments were best at delaying onset (d = 0.42, p > 0.05). Oxidative stress treatments were significantly better for prolonging survival duration (d = 0.18, p < 0.05). Excitability treatments were significantly better for prolonging overall health status (d = 0.22, p < 0.05). However, the absolute best pathophysiological treatment category for prolonging health status varied with disease progression: oxidative stress was best for pre-onset health (d = 0.18, p > 0.05); excitability was best for prolonging function near onset (d = 0.34, p < 0.05); inflammation was best for prolonging post-onset function (d = 0.24, p > 0.05); and apoptosis was best for prolonging end-stage function (d = 0.49, p > 0.05). Finally, combination treatments simultaneously targeting multiple pathophysiological categories (e.g., polytherapy) performed significantly (p < 0.05) better than monotherapies at end-stage. DISCUSSION: In summary, the most effective pathophysiological treatments change as function of assessment modality and disease progression. Shifting pathophysiological treatment category efficacy with disease progression supports the homeostatic instability theory of ALS disease progression.
 BACKGROUND: Recent initiatives, such as earlier diagnosis and treatment, have enhanced the survival of patients with systemic sclerosis (SSc). Despite these initiatives, there is extreme variability in rehabilitation strategies for these patients. In 2006, the Glittre-ADL test (TGlittre) was developed to evaluate functional capacity using multiple tasks similar to the activities of daily living (ADLs). OBJECTIVES: To evaluate the impact of therapist-oriented home rehabilitation (TOHR) on functional capacity using TGlittre and to examine the effects of TOHR on physical function, hand function, and quality of life (QoL) among women with SSc. METHODS: This quasi-experimental and longitudinal study included 12 women with SSc who underwent TOHR 3 times per week for 12 weeks. Before and after TOHR, functional capacity was assessed using TGlittre, physical function was examined by the Health Assessment Questionnaire Disability Index (HAQ-DI), hand function was evaluated using the Cochin Hand Functional Scale (CHFS) and handgrip strength (HGS), and QoL was evaluated using the Short Form-36 Health Survey Questionnaire (SF-36). RESULTS: When comparing the pre- and post-TOHR values of TGlittre, a significant reduction was found in total time (p= 0.002) and manual time (p= 0.010). There was a nonsignificant decrease in HAQ-DI scores between pre- and post-TOHR (p= 0.07). Regarding hand function, there was a significant reduction in the CHFS between pre- and post-TOHR (p= 0.036), although no significant difference was observed in HGS between pre- and post-TOHR (p= 0.08). Regarding QoL, there was an increase in all SF-36 categories, although physical function was the only category that was significantly increased (p= 0.008). CONCLUSION: After TOHR, patients with SSc are able to more quickly perform TGlittre tasks when considering both total and manual times. TOHR also positively affects manual skills and QoL.
 BACKGROUND AND OBJECTIVES: Amyotrophic lateral sclerosis (ALS) is a rare neurodegenerative disorder affecting upper and lower motor neurons. Due to its rarity and rapidly progressive nature, studying the epidemiology of ALS is challenging, and a comprehensive picture of the global burden of this disease is lacking. The objective of this systematic review was to describe the global incidence and prevalence of ALS. METHODS: We searched MEDLINE, Embase, Global Health, PsycInfo, Cochrane Library, and CINAHL to identify articles published between January 1, 2010, and May 6, 2021. Studies that were population based and reported estimates of prevalence, incidence, and/or mortality of ALS were eligible for inclusion. This study focuses on the incidence and prevalence. Quality assessment was performed using a tool developed to evaluate methodology relevant to prevalence and incidence studies. This review was registered with PROSPERO, CRD42021250559. RESULTS: This search generated 6,238 articles, of which 140 were selected for data extraction and quality assessment. Of these, 85 articles reported on the incidence and 61 on the prevalence of ALS. Incidence ranged from 0.26 per 100,000 person-years in Ecuador to 23.46 per 100,000 person-years in Japan. Point prevalence ranged from 1.57 per 100,000 in Iran to 11.80 per 100,000 in the United States. Many articles identified cases with ALS from multiple data sources. DISCUSSION: There is variation in reported incidence and prevalence estimates of ALS across the world. While registries are an important and powerful tool to quantify disease burden, such resources are not available everywhere. This results in gaps in reporting of the global epidemiology of ALS, as highlighted by the degree of variation (and quality) in estimates of incidence and prevalence reported in this review.
 Amyotrophic lateral sclerosis (ALS) is a devastating disease caused by degeneration of motor neurons. As with all major neurodegenerative disorders, development of disease-modifying therapies has proven challenging for multiple reasons. Nevertheless, ALS is one of the few neurodegenerative diseases for which disease-modifying therapies are approved. Significant discoveries and advances have been made in ALS preclinical models, genetics, pathology, biomarkers, imaging and clinical readouts over the last 10-15 years. At the same time, novel therapeutic paradigms are being applied in areas of high unmet medical need, including neurodegenerative disorders. These developments have evolved our knowledge base, allowing identification of targeted candidate therapies for ALS with diverse mechanisms of action. In this Review, we discuss how this advanced knowledge, aligned with new approaches, can enable effective translation of therapeutic agents from preclinical studies through to clinical benefit for patients with ALS. We anticipate that this approach in ALS will also positively impact the field of drug discovery for neurodegenerative disorders more broadly.
 BACKGROUND: The terminal complement C5 inhibitor eculizumab is approved in Japan for relapse prevention in aquaporin-4 antibody-positive (AQP4+) neuromyelitis optica spectrum disorder (NMOSD) and is undergoing mandatory post-marketing surveillance (PMS) of clinical use. OBJECTIVES: The objective of the study is to assess the real-world, long-term safety and effectiveness of eculizumab in Japanese patients with AQP4+ NMOSD. DESIGN: Regulatory-mandated PMS analysis implemented as an all-case surveillance of all patients with AQP4+ NMOSD who have been treated with eculizumab in Japan since its approval in November 2019. METHODS: This PMS interim analysis assessed the safety and effectiveness of eculizumab in Japanese patients with AQP4+ NMOSD from November 2019 to April 2022. RESULTS: Of 147 patients treated with eculizumab who consented to publication, 71 had at least one case report form collected and locked at the interim analysis data cut-off, constituting the safety analysis set; three patients from PREVENT (NCT01892345) were excluded from the effectiveness analysis set. Twelve and 10 patients in the safety and effectiveness analysis sets discontinued, respectively. In the safety analysis set, 67/71 patients (94.4%) were female, mean illness duration was 6.8 [standard deviation (SD): 6.2] years, mean age at eculizumab initiation was 50.7 (SD: 13.3) years, and mean eculizumab treatment duration was 44.6 (SD: 23.7) weeks. At diagnosis of NMOSD, 34/71 patients (47.9%) and 35/71 patients (49.3%) in the safety analysis set had symptoms of optic neuritis and transverse myelitis, respectively. In the safety analysis set, 19/71 patients (26.8%) reported adverse events, 10/71 (14.1%) reported adverse drug reactions (ADRs), and 7/71 (9.9%) reported serious ADRs; no meningococcal infections were observed. In the effectiveness analysis set, 64/68 patients (94.1%) were female, mean disease duration was 6.9 (SD: 6.3) years, mean age at eculizumab initiation was 50.6 (SD: 13.2) years, and 27/68 (39.7%) were tested for C5 genetic polymorphism (all negative). In the 2 years before eculizumab, 51/68 patients (75.0%) experienced relapse. Relapse rate was 0.02/patient-year after eculizumab initiation versus 0.74/patient-year in the 2 years before eculizumab. Overall, 37/68 patients (54.4%) were prescribed immunosuppressants in the 6 months before and 19/40 (47.5%) in the 6-12 months after starting eculizumab treatment. The proportion of patients taking >10 mg/day of prednisolone decreased from 45.6% at 24-20 weeks before to 23.1% and 0% at 48-52 and 100-104 weeks after eculizumab, respectively. CONCLUSION: This article reports interim PMS data for Japanese patients and provides updated real-world evidence for the safety of eculizumab and its effectiveness at preventing relapses in patients with AQP4+ NMOSD. Safety and effectiveness results are consistent with those from PREVENT.
 Gulf War Illness (GWI) is an unrelenting multi-symptom illness with chronic central nervous system and peripheral pathology affecting veterans from the 1991 Gulf War and for which effective treatment is lacking. An increasing number of studies indicate that persistent neuroinflammation is likely the underlying cause of cognitive and mood dysfunction that affects veterans with GWI. We have previously reported that fingolimod, a drug approved for the treatment of relapsing-remitting multiple sclerosis, decreases neuroinflammation and improves cognition in a mouse model of Alzheimer's disease. In this study, we investigated the effect of fingolimod treatment on cognition and neuroinflammation in a mouse model of GWI. We exposed C57BL/6 J male mice to GWI-related chemicals pyridostigmine bromide, DEET, and permethrin, and to mild restraint stress for 28 days (GWI mice). Control mice were exposed to the chemicals' vehicle only. Starting 3 months post-exposure, half of the GWI mice and control mice were orally treated with fingolimod (1 mg/kg/day) for 1 month, and the other half were left untreated. Decreased memory on the Morris water maze test was detected in GWI mice compared to control mice and was reversed by fingolimod treatment. Immunohistochemical analysis of brain sections with antibodies to Iba1 and GFAP revealed that GWI mice had increased microglia activation in the hippocampal dentate gyrus, but no difference in reactive astrocytes was detected. The increased activation of microglia in GWI mice was decreased to the level in control mice by treatment with fingolimod. No effect of fingolimod treatment on gliosis in control mice was detected. To explore the signaling pathways by which decreased memory and increased neuroinflammation in GWI may be protected by fingolimod, we investigated the involvement of the inflammatory signaling pathways of protein kinase R (PKR) in the cerebral cortex of these mice. We found increased phosphorylation of PKR in the brain of GWI mice compared to controls, as well as increased phosphorylation of its most recognized downstream effectors: the α subunit of eukaryotic initiation factor 2 (eIF2α), IκB kinase (IKK), and the p65 subunit of nuclear factor-κB (NFκB-p65). Furthermore, we found that the increased phosphorylation level of these three proteins were suppressed in GWI mice treated with fingolimod. These results suggest that activation of PKR and NFκB signaling may be important for the regulation of cognition and neuroinflammation in the GWI condition and that fingolimod, a drug already approved for human use, may be a potential candidate for the treatment of GWI.
 BACKGROUND: Medical cannabinoids are controversial. Their use is comparatively rare, but it is rising. Since 2017, cannabinoids can be prescribed in Germany for a broader range of indications. Patient surveys on these drugs are hampered by the stigmatization of cannabinoids and their (still) low prevalence in medical contexts. Against this background, patients' willingness to provide information is limited. Moreover, it is logistically challenging to reach them with a survey. A thorough knowledge of currently ongoing therapies and their effects and side effects, however, is important for a more appropriate and effective use of cannabinoids in the future. OBJECTIVE: This study is an exploratory data collection using a representative sample. The main goal is to provide a detailed picture of the current use of medical cannabinoids in Germany. It is intended to identify subgroups that may benefit particularly well or poorly. METHODS: We are conducting a representative, anonymous, cross-sectional, one-time, web-based survey based on mixed methods in 3 German federal states. Health conditions under cannabinoid therapy and before are documented with validated, symptom-specific questionnaires. This allows an estimation of the effect sizes of these therapies. The selection of parameters and questionnaires was based on the results of independent qualitative interviews in advance. Representative samples of the hard-to-reach study population are obtained by cluster sampling via contracted physicians of the statutory health insurance companies. RESULTS: Recruitment was ongoing until the end of June 2022, with 256 enrolled participants. Validated questionnaires on pain, spasticity, anorexia or wasting, multiple sclerosis, nausea or vomiting, depression, and attention deficit hyperactivity disorder (ADHD) were selected. Symptom scores are being assessed for both current conditions under cannabinoid therapy and conditions prior to this therapy (in retrospect). Validated questionnaires are also used for treatment satisfaction and general quality of life. These are supplemented by existing diagnoses, a detailed medication history, any previous experiences with cannabis or illegal substances, experiences with the prescription process, and sociodemographic data. Based on the results of the previous qualitative interviews, questions were added regarding prior experience with relaxation methods and psychotherapy, personal opinions about cannabinoids, pre-existing or symptom-related psychological trauma, and different experiences with different cannabis-based therapies. CONCLUSIONS: The exploratory mixed methods approach of this project is expected to provide valid and relevant data as a basis for future clinical research. The study design may be representative for a large proportion of outpatients treated with cannabinoids in the German federal states studied. It may have less bias toward social desirability and may provide valuable information in addition to existing studies. Due to the observational and cross-sectional nature of this study, various limitations apply. Causal relations cannot be drawn. TRIAL REGISTRATION: German Clinical Trials Register DRKS00023344; https://drks.de/search/en/trial/DRKS00023344. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/38814.
 OBJECTIVE: To compare incidences of neuroinflammatory events, including demyelinating disease (DML), inflammatory polyneuropathies (IPN) and multiple sclerosis (MS), in patients with rheumatoid arthritis (RA) or spondyloarthritis (SpA; including psoriatic arthritis) starting a tumour necrosis factor inhibitor (TNFi), investigating whether monoclonal TNFi antibodies (other TNFis (oTNFis)) confer higher risk than etanercept. METHODS: This is an observational cohort study including patients from the five Nordic countries starting a TNFi in 2001-2020. Time to first neuroinflammatory event was identified through register linkages. We calculated crude incidence rates (cIR) per 1000 person-years and used multivariable-adjusted Cox regression to compare incidences of neuroinflammatory events overall and for DML, IPN and MS with oTNFi versus etanercept. We further examined individual TNFis and indications. RESULTS: 33 883 patients with RA and 28 772 patients with SpA were included, initiating 52 704 and 46 572 treatment courses, respectively. In RA, we observed 135 neuroinflammatory events (65% DML) with cIR of 0.38 with oTNFi and 0.34 with etanercept. The HR of oTNFi versus etanercept was 1.07 (95% CI 0.74 to 1.54) for any neuroinflammatory event, 0.79 (95% CI 0.51 to 1.22) for DML, 2.20 (95% CI 1.05 to 4.63) for IPN and 0.73 (95% CI 0.34 to 1.56) for MS. In SpA, we observed 179 events (78% DML) with cIR of 0.68 with oTNFi and 0.65 with etanercept. The HR for any neuroinflammatory event, DML, IPN and MS was 1.06 (95% CI 0.75 to 1.50), 1.01 (95% CI 0.68 to 1.50), 1.28 (95% CI 0.61 to 2.69) and 0.94 (95% CI0.53 to 1.69), respectively. CONCLUSION: The cIRs of neuroinflammatory events are higher in SpA than in RA, but the choice of specific TNFi does not seem to play an important role in the risk of neuroinflammatory events.
 BACKGROUND: Oligodendrocytes have robust regenerative ability and are key players in remyelination during physiological and pathophysiological states. However, the mechanisms of brain microenvironmental cue in regulation of the differentiation of oligodendrocytes still needs to be further investigated. RESULTS: We demonstrated that myelin-associated glycoprotein (MAG) was a novel receptor for angiopoietin-like protein 2 (ANGPTL2). The binding of ANGPTL2 to MAG efficiently promoted the differentiation of oligodendrocytes in vitro, as evaluated in an HCN cell line. Angptl2-null mice had a markedly impaired myelination capacity in the early stage of oligodendrocyte development. These mice had notably decreased remyelination capacities and enhanced motor disability in a cuprizone-induced demyelinating mouse model, which was similar to the Mag-null mice. The loss of remyelination ability in Angptl2-null/Mag-null mice was similar to the Angptl2-WT/Mag-null mice, which indicated that the ANGPTL2-mediated oligodendrocyte differentiation effect depended on the MAG receptor. ANGPTL2 bound MAG to enhance its phosphorylation level and recruit Fyn kinase, which increased Fyn phosphorylation levels, followed by the transactivation of myelin regulatory factor (MYRF). CONCLUSION: Our study demonstrated an unexpected cross-talk between the environmental protein (ANGPTL2) and its surface receptor (MAG) in the regulation of oligodendrocyte differentiation, which may benefit the treatment of many demyelination disorders, including multiple sclerosis.
 BACKGROUND: A 36-year-old man presented with a palpable mass in the right axillary tail for four months. He was referred to breast imaging for diagnostic work-up. He does not have a family history of breast cancer. AIM: Breast imaging work-up for diagnosis of lymphoma is unusual and even more so in a male patient. CASE PRESENTATION: After Breast Mammography and targeted Ultrasound of the axillary tail and axilla, Magnetic Resonance Imaging (MRI) was performed and suggested lymphoproliferative disorder. Excisional biopsy was performed after the breast MRI with removal of right axillary tissue measuring 15.0 × 5.5 × 2.0 cm and containing multiple lymph nodes. Excisional biopsy revealed Classic Hodgkin lymphoma of nodular sclerosis type. Staging [18F]-FDG PET/CT revealed early stage of disease. CONCLUSION: The presentation and diagnostic elements of Hodgkin Lymphoma are described in this case report emphasizing the significance of breast imaging in multiple populations.
 Aging population is at higher risk of developing severe COVID-19, including hospitalization and death. In this work, to further understand the relationship between host age-related factors, immunosenescence/exhaustion of the immune system and the response to the virus, we characterized immune cell and cytokine responses in 58 COVID-19 patients admitted to the hospital and 40 healthy controls of different age ranges. Lymphocyte populations and inflammatory profiles were studied in blood samples, using different panels of multicolor flow cytometry. As expected, our analysis reveals differences at both the cellular and cytokine level in COVID-19 patients. Interestingly, when the age range analysis was carried out, the immunological response to the infection was found to differ with age, being especially affected in the group of 30-39 years. In this age range, an increased exhausted T cell response and a decrease of naïve T helper lymphocytes was found in patients, as well as a reduced concentration of the proinflammatory TNF, IL-1β and IL-8 cytokines. Besides, the correlation between age and the study variables was evaluated, and multiple cell types and interleukins were found to correlate with donor age. Notably, the correlations of T helper naïve and effector memory cells, T helper 1-17 cells, TNF, IL-10, IL-1β, IL-8, among others, showed differences between healthy controls and COVID-19 patients. Our findings, in the context of other previous studies, suggest that aging affects the behavior of the immune system in COVID-19 patients. They suggest that young individuals are able to mount an initial response to SARS-CoV-2, but some of them present an accelerated exhaustion of the cell response and an insufficient inflammatory response, resulting in a moderate to severe COVID-19. On the other hand, in older patients there is a smaller immune cell response to the virus, reflected in fewer differences in immune populations between COVID-19 patients and controls. Nevertheless, old patients show more evidence of an inflammatory phenotype, suggesting that the underlying inflammation associated with their age is exacerbated by the SARS-CoV-2 infection.
 IMPORTANCE: Every third to sixth patient with medical diseases receives antidepressants, but regulatory trials typically exclude comorbid medical diseases. Meta-analyses of antidepressants have shown small to medium effect sizes, but generalizability to clinical settings is unclear, where medical comorbidity is highly prevalent. OBJECTIVE: To perform an umbrella systematic review of the meta-analytic evidence and meta-analysis of the efficacy and safety of antidepressant use in populations with medical diseases and comorbid depression. DATA SOURCES: PubMed and EMBASE were searched from inception until March 31, 2023, for systematic reviews with or without meta-analyses of randomized clinical trials (RCTs) examining the efficacy and safety of antidepressants for treatment or prevention of comorbid depression in any medical disease. STUDY SELECTION: Meta-analyses of placebo- or active-controlled RCTs studying antidepressants for depression in individuals with medical diseases. DATA EXTRACTION AND SYNTHESIS: Data extraction and quality assessment using A Measurement Tool for the Assessment of Multiple Systematic Reviews (AMSTAR-2 and AMSTAR-Content) were performed by pairs of independent reviewers following PRISMA guidelines. When several meta-analyses studied the same medical disease, the largest meta-analysis was included. Random-effects meta-analyses pooled data on the primary outcome (efficacy), key secondary outcomes (acceptability and tolerability), and additional secondary outcomes (response and remission). MAIN OUTCOMES AND MEASURES: Antidepressant efficacy presented as standardized mean differences (SMDs) and tolerability (discontinuation for adverse effects) and acceptability (all-cause discontinuation) presented as risk ratios (RRs). RESULTS: Of 6587 references, 176 systematic reviews were identified in 43 medical diseases. Altogether, 52 meta-analyses in 27 medical diseases were included in the evidence synthesis (mean [SD] AMSTAR-2 quality score, 9.3 [3.1], with a maximum possible of 16; mean [SD] AMSTAR-Content score, 2.4 [1.9], with a maximum possible of 9). Across medical diseases (23 meta-analyses), antidepressants improved depression vs placebo (SMD, 0.42 [95% CI, 0.30-0.54]; I2 = 76.5%), with the largest SMDs for myocardial infarction (SMD, 1.38 [95% CI, 0.82-1.93]), functional chest pain (SMD, 0.87 [95% CI, 0.08-1.67]), and coronary artery disease (SMD, 0.83 [95% CI, 0.32-1.33]) and the smallest for low back pain (SMD, 0.06 [95% CI, 0.17-0.39]) and traumatic brain injury (SMD, 0.08 [95% CI, -0.28 to 0.45]). Antidepressants showed worse acceptability (24 meta-analyses; RR, 1.17 [95% CI, 1.02-1.32]) and tolerability (18 meta-analyses; RR, 1.39 [95% CI, 1.13-1.64]) compared with placebo. Antidepressants led to higher rates of response (8 meta-analyses; RR, 1.54 [95% CI, 1.14-1.94]) and remission (6 meta-analyses; RR, 1.43 [95% CI, 1.25-1.61]) than placebo. Antidepressants more likely prevented depression than placebo (7 meta-analyses; RR, 0.43 [95% CI, 0.33-0.53]). CONCLUSIONS AND RELEVANCE: The results of this umbrella systematic review of meta-analyses found that antidepressants are effective and safe in treating and preventing depression in patients with comorbid medical disease. However, few large, high-quality RCTs exist in most medical diseases.
 BACKGROUND: MND-SMART is a platform, multi-arm, multi-stage, multi-centre, randomised controlled trial recruiting people with motor neuron disease. Initially, the treatments memantine and trazodone will each be compared against placebo, but other investigational treatments will be introduced into the trial later. The co-primary outcomes are the Amyotrophic Lateral Sclerosis Functional Rating Scale Revised (ALS-FRS-R) functional outcome, which is assessed longitudinally, and overall survival. METHODS: Initially in MND-SMART, participants are randomised 1:1:1 via a minimisation algorithm to receive placebo or one of the two investigational treatments with up to 531 to be randomised in total. The comparisons between each research arm and placebo will be conducted in four stages, with the opportunity to cease further randomisations to poorly performing research arms at the end of stages 1 or 2. The final ALS-FRS-R analysis will be at the end of stage 3 and final survival analysis at the end of stage 4. The estimands for the co-primary outcomes are described in detail. The primary analysis of ALS-FRS-R at the end of stages 1 to 3 will involve fitting a normal linear mixed model to the data to calculate a mean difference in rate of ALS-FRS-R change between each research treatment and placebo. The pairwise type 1 error rate will be controlled, because each treatment comparison will generate its own distinct and separate interpretation. This publication is based on a formal statistical analysis plan document that was finalised and signed on 18 May 2022. DISCUSSION: In developing the statistical analysis plan, we had to carefully consider several issues such as multiple testing, estimand specification, interim analyses, and statistical analysis of the repeated measurements of ALS-FRS-R. This analysis plan attempts to balance multiple factors, including minimisation of bias, maximising power and precision, and deriving clinically interpretable summaries of treatment effects. TRIAL REGISTRATION: EudraCT Number, 2019-000099-41. Registered 2 October 2019, https://www.clinicaltrialsregister.eu/ctr-search/search?query=mnd-smart ClinicalTrials.gov, NCT04302870 . Registered 10 March 2020.
 Observational studies consistently disclose brain imaging-derived phenotypes (IDPs) as critical markers for early diagnosis of both brain disorders and cardiovascular diseases. However, it remains unclear about the shared genetic landscape between brain IDPs and the risk of brain disorders and cardiovascular diseases, restricting the applications of potential diagnostic techniques through brain IDPs. Here, we reported genetic correlations and putative causal relationships between 921 brain IDPs, 20 brain disorders and six cardiovascular diseases by leveraging their large-scale genome-wide association study (GWAS) summary statistics. Applications of Mendelian randomization (MR) identified significant putative causal effects of multiple region-specific brain IDPs in relation to the increased risks for amyotrophic lateral sclerosis (ALS), major depressive disorder (MDD), autism spectrum disorder (ASD) and schizophrenia (SCZ). We also found brain IDPs specifically from temporal lobe as a putatively causal consequence of hypertension. The genome-wide colocalization analysis identified three genomic regions in which MDD, ASD and SCZ colocalized with the brain IDPs, and two novel SNPs to be associated with ASD, SCZ, and multiple brain IDPs. Furthermore, we identified a list of candidate genes involved in the shared genetics underlying pairs of brain IDPs and MDD, ASD, SCZ, ALS and hypertension. Our results provide novel insights into the genetic relationships between brain disorders and cardiovascular diseases and brain IDP, which may server as clues for using brain IDPs to predict risks of diseases.
 Postinfectious neurological syndromes (PINS), among which acute disseminated encephalomyelitis (ADEM), are inflammatory and mostly monophasic disorders. We previously reported that PINS patients can show relapses, or even disease progression. Here we describe a cohort of patients with progressive-PINS and >5 years of follow-up, that developed a progressive worsening without radiological/cerebrospinal fluid analysis evidence of inflammation. At onset 5 patients fulfilled diagnostic criteria for ADEM and none for MS. Progression occurred after a median of 22 months from onset (in 4/7 after 1/more relapses), manifesting as ascending tetraparesis with bulbar functions involvement in 5/7. Five/7 patients received high dose steroids and/or IvIG and 6/7 Rituximab(n = 4) and/or cyclophosphamide(n = 2), with no impact on disease progression in 6/7. NfL levels were higher in patients with progressive-PINS compared to monophasic-ADEM (p = 0.023) and healthy controls (p = 0.004). Progression is rare, but possible, in PINS. Immunotherapy seems to be ineffective in these patients, and elevated serum NfL in serum suggest persistent axonal damage.
 Background Cluster headache exists diagnostically in a chronic and episodic variant between which patients can convert. We aimed to describe how many patients change phenotype, elucidate possible factors associated with this transition and identify differences in clinical features between primary and secondary phenotypes.Methods 540 well-defined cluster headache patients according to current ICHD-criteria completed a cross-sectional semi-structured interview.Results Total transition-incidence for the cohort was 20.7%. Conversion from chronic to episodic was reported by 6.3% and transition from episodic to chronic by 14.4% with attack side shift as a possible predictor (p = 0.007). Compared to primary chronic patients, secondary chronic patients had more frequent (60 vs 34 per month, p = 0.0487), but shorter (60 vs 90 minutes, p = 0.041) attacks. Secondary episodic patients experienced shorter remission periods than primary episodic patients (6 vs 11 months, p = 0.010). Treatment response was poor in all groups and only one third had effective prevention.Conclusion Cluster headache is a fluctuating disorder with a fifth of our cohort having experienced at least one phenotype change during course of disease. Apart from attack side shifts, no predictors for transition were identified. Severity differed between primary and secondary subtypes. Overall, there is an urgent need for better understanding of cluster headache.
 BACKGROUND: Copay cards are intended to mitigate patient out-of-pocket (OOP) expenses. This qualitative, exploratory focus group study aimed to capture patient perceptions of copay cards and copay adjustment programs (CAPs; insurers' accumulator and maximizer policies), which redirect the copay card utilization benefits intended for patients' OOP expenses. METHODS: Patients with chronic conditions were recruited through Janssen's Patient Engagement Research Council program. They completed a survey and attended a live virtual session to provide feedback on copay cards. RESULTS: Among 33 participants (median age, 49 years [range, 24-78]), the most frequent conditions were cardiovascular-metabolic disease and inflammatory bowel disease. Patients associated copay cards with lessening financial burden, improving general and mental health, and enabling medication adherence. An impact on medication adherence was identified by 10 (63%) White and nine (100%) Black respondents. Some patients were unaware of CAPs despite having encountered them; they recommended greater copay card education and transparency about CAPs. CONCLUSION: Patients relied on copay cards to help afford their prescribed medication OOP expenses and maintain medication adherence. Use of CAPs may increase patient OOP expenses. Patients would benefit from awareness programs and industry - healthcare provider partnerships that facilitate and ensure access to copay cards.
 Mean-field (MF) models are computational formalism used to summarize in a few statistical parameters the salient biophysical properties of an inter-wired neuronal network. Their formalism normally incorporates different types of neurons and synapses along with their topological organization. MFs are crucial to efficiently implement the computational modules of large-scale models of brain function, maintaining the specificity of local cortical microcircuits. While MFs have been generated for the isocortex, they are still missing for other parts of the brain. Here we have designed and simulated a multi-layer MF of the cerebellar microcircuit (including Granule Cells, Golgi Cells, Molecular Layer Interneurons, and Purkinje Cells) and validated it against experimental data and the corresponding spiking neural network (SNN) microcircuit model. The cerebellar MF was built using a system of equations, where properties of neuronal populations and topological parameters are embedded in inter-dependent transfer functions. The model time constant was optimised using local field potentials recorded experimentally from acute mouse cerebellar slices as a template. The MF reproduced the average dynamics of different neuronal populations in response to various input patterns and predicted the modulation of the Purkinje Cells firing depending on cortical plasticity, which drives learning in associative tasks, and the level of feedforward inhibition. The cerebellar MF provides a computationally efficient tool for future investigations of the causal relationship between microscopic neuronal properties and ensemble brain activity in virtual brain models addressing both physiological and pathological conditions.

 We report the singular case of a 31-year-old woman who developed very serious Fluphenazine-induced parkinsonism over a few days due to a doubly incongruent drug prescription by indication and dosage having been applied to a healthy subject over one week instead of seven months. Unlike gradual drug-induced parkinsonism, our patient experienced acute extrapyramidal syndrome (EPS), reaching significant motor and sphincter disability in just a few days, followed by a gradual incomplete recovery over more than six months. In fact, after drug discontinuation, hypomimia and slight left hemi-somatic rigidity with bradykinesia remained, as well as stable non-progressive memory disturbances. Despite bio-humoral and instrumental investigations and DaTScan were negative, MRI post-analysis evidenced a 6.5% loss in brain volume. Specifically, irreversible cortical and sub-cortical grey matter reduction and cerebrospinal fluid space enlargement with spared white matter were found. Our observations suggest that the sudden availability of Fluphenazine results in a kind of plateau effect of parkinsonism presentation, partially reversible due to the neurotoxic drug effect on the cortical and sub-cortical grey matter, resulting in asymmetric EPS and stable memory loss, respectively. Our report confirms the debated neurotoxicity of first-generation neuroleptics and the postulated theory of differential susceptibility to the cytotoxic stressors on the central nervous system.
 PURPOSE OF REVIEW: Tumor-like brain lesions are rare and commonly suggest a neoplastic etiology. Failure to rapidly identify non-neoplastic causes can lead to increased morbidity and mortality. In this review, we describe 10 patients who presented with atypical, non-neoplastic tumor-like brain lesions in which brain biopsy was essential for a correct diagnosis and treatment. RECENT FINDINGS: There has been increasing recognition of autoimmune conditions affecting the nervous system, and many of those diseases can cause tumor-like brain lesions. Currently available reports of non-neoplastic tumor-like brain lesions are scarce. Most case series focus on tumefactive demyelinating lesions, and a comprehensive review including other neuroimmunological conditions such as CNS vasculitis, neurosarcoidosis, histiocytic and infectious etiologies is lacking. SUMMARY: We review the literature on tumor-like brain lesions intending to increase the awareness and differential diagnosis of non-neoplastic brain tumor mimics. We advocate for earlier brain biopsies, which, in our case series, significantly changed diagnosis, management, and outcomes.
 INTRODUCTION: Neural circuit alterations lay at the core of brain physiopathology, and yet are hard to unveil in living subjects. The Virtual Brain (TVB) modeling, by exploiting structural and functional magnetic resonance imaging (MRI), yields mesoscopic parameters of connectivity and synaptic transmission. METHODS: We used TVB to simulate brain networks, which are key for human brain function, in Alzheimer's disease (AD) and frontotemporal dementia (FTD) patients, whose connectivity and synaptic parameters remain largely unknown; we then compared them to healthy controls, to reveal novel in vivo pathological hallmarks. RESULTS: The pattern of simulated parameter differed between AD and FTD, shedding light on disease-specific alterations in brain networks. Individual subjects displayed subtle differences in network parameter patterns that significantly correlated with their individual neuropsychological, clinical, and pharmacological profiles. DISCUSSION: These TVB simulations, by informing about a new personalized set of networks parameters, open new perspectives for understanding dementias mechanisms and design personalized therapeutic approaches.
 A characteristic feature of human cognition is our ability to 'multi-task'-performing two or more tasks in parallel-particularly when one task is well learned. How the brain supports this capacity remains poorly understood. Most past studies have focussed on identifying the areas of the brain-typically the dorsolateral prefrontal cortex-that are required to navigate information-processing bottlenecks. In contrast, we take a systems neuroscience approach to test the hypothesis that the capacity to conduct effective parallel processing relies on a distributed architecture that interconnects the cerebral cortex with the cerebellum. The latter structure contains over half of the neurons in the adult human brain and is well suited to support the fast, effective, dynamic sequences required to perform tasks relatively automatically. By delegating stereotyped within-task computations to the cerebellum, the cerebral cortex can be freed up to focus on the more challenging aspects of performing the tasks in parallel. To test this hypothesis, we analysed task-based fMRI data from 50 participants who performed a task in which they either balanced an avatar on a screen (balance), performed serial-7 subtractions (calculation) or performed both in parallel (dual task). Using a set of approaches that include dimensionality reduction, structure-function coupling, and time-varying functional connectivity, we provide robust evidence in support of our hypothesis. We conclude that distributed interactions between the cerebral cortex and cerebellum are crucially involved in parallel processing in the human brain.
 BACKGROUND: Patients with inflammatory bowel disease (IBD) suffer from a wide range of comorbidities such as migraine. In studies, the prevalence of migraine in cases with IBD was reported differently. The goal of this systematic review and meta-analysis was to estimate the pooled prevalence of migraine in IBD cases. METHODS: Two researchers independently and systematically searched PubMed, Scopus, EMBASE, Web of Science, and google scholar. They also searched the gray literature including references of the included studies and conference abstracts which were published up to May 2021. Cross-sectional studies were included. RESULTS: The literature search revealed 840 articles, and after deleting duplicates, 650 remained. For the meta-analysis, 10 studies were included. Totally, 62,554 patients were evaluated. The pooled prevalence of migraine in patients with IBD was 19% (95% CI: 15-22%). The pooled prevalence of migraine in ulcerative colitis (UC) was 10% (95% CI: 4-15%) (I(2) = 99.8%, P < 0.001). The pooled prevalence of migraine in the Crohn's disease (CD) group was 24% (95% CI: 17-30%) (I(2) = 98.8%, P < 0.001). The pooled odds of developing migraine in IBD cases was 1.51 (95% CI: 1-2.27) (I(2) = 90.8%, P < 0.001). CONCLUSIONS: The result of this systematic review and meta-analysis showed that the pooled prevalence of migraine in patients with IBD was 19% (95% CI: 15-22%).
 Manual dexterity is referred to as the skill to perform fine motor movements and it has been assumed to be associated to the cognitive domain, as well as the sensorimotor one. In this work, we investigated with functional near-infrared spectroscopy the cortical activations elicited by the execution of the 9-HPT, i.e., a standard test evaluating manual dexterity in which nine pegs were taken, placed into and then removed from nine holes on a board as quickly as possible. For comparison, we proposed a new active control task mainly involving the sensorimotor domain, in which the pegs must be placed and removed using the same single hole (1-HPT). Behaviorally, we found two distinct groups based on the difference between the execution time of the 9-HPT and the 1-HPT (ΔHPT). Cortical areas belonging to the network controlling reaching and grasping movements were active in both groups; however, participants showing a large ΔHPT presented significantly higher activation in prefrontal cortical areas (right BA10 and BA11) during 9-HPT and 1-HPT performance with respect to the participants with a small ΔHPT, who showed a deactivation in BA10. Unexpectedly, we observed a significant linear relationship between ΔHPT and right BA10 activity. This suggested that participants performing the 9-HPT more slowly than the 1-HPT recruited prefrontal areas implicitly exploiting the cognitive skills of planning, perhaps in search of a motor strategy to solve the test activating attentional and cognitive control processes, but this resulted not efficient and instead increased the time to accomplish a manual dexterity task.
 Migraine is one of the most common neurological diseases and it has a huge social and personal impact. Although head pain is the core symptom, individuals with migraine can have a plethora of non-headache symptoms that precede, accompany, or follow the pain. Neuroimaging studies have shown that the involvement of specific brain areas can explain many of the symptoms reported during the different phases of migraine. Recruitment of the hypothalamus, pons, spinal trigeminal nucleus, thalamus, and visual and pain-processing cortical areas starts during the premonitory phase and persists through the headache phase, contributing to the onset of pain and associated symptoms. Once the pain stops, the involvement of most brain areas ends, although the pons, hypothalamus, and visual cortex remain active after acute treatment intake and resolution of migraine symptoms. A better understanding of the correlations between imaging findings and migraine symptomatology can provide new insight into migraine pathophysiology and the mechanisms of novel migraine-specific treatments.
 Previous studies found conflicting results about associations of vitiligo with different autoimmune diseases. To evaluate associations of vitiligo with multiple autoimmune diseases. A cross-sectional study representative of 612,084,148 US patients from the Nationwide Emergency Department Sample (NEDS) 2015-2019 was performed. Vitiligo and autoimmune diseases were identified using International Classification of Diseases-10 codes. The most frequent autoimmune disorders in patients with vitiligo were type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus (SLE), autoimmune thyroiditis, Addison's disease, and systemic sclerosis (SSc). Vitiligo was associated with any autoimmune disorder (adjusted odds ratio [95% confidence interval] 1.45 [1.32-1.58]). Cutaneous disorders with largest effect-sizes were alopecia areata (186.22 [115.31-300.72]) and SSc (32.13 [25.28-40.82]). Non-cutaneous comorbidities with largest effect-sizes were primary sclerosing cholangitis (43.12 [18.98-97.99]), pernicious anemia (41.26 [31.66-53.78]), Addison's disease (33.85 [26.68-42.9]), and autoimmune thyroiditis (31.65 [26.34-38.02]). Vitiligo is associated with multiple cutaneous and non-cutaneous autoimmune diseases, especially in females and older age.
 Amyotrophic lateral sclerosis (ALS) is a major life-threatening disease caused by motor neuron degeneration. More effective treatments through drug discovery are urgently needed. Here, we established an effective high-throughput screening system using induced pluripotent stem cells (iPSCs). Using a Tet-On-dependent transcription factor expression system carried on the PiggyBac vector, motor neurons were efficiently and rapidly generated from iPSCs by a single-step induction method. Induced iPSC transcripts displayed characteristics similar to those of spinal cord neurons. iPSC-generated motor neurons carried a mutation in fused in sarcoma (FUS) and superoxide dismutase 1 (SOD1) genes and had abnormal protein accumulation corresponding to each mutation. Calcium imaging and multiple electrode array (MEA) recordings demonstrated that ALS neurons were abnormally hyperexcitable. Noticeably, protein accumulation and hyperexcitability were ameliorated by treatment with rapamycin (mTOR inhibitor) and retigabine (Kv7 channel activator), respectively. Furthermore, rapamycin suppressed ALS neuronal death and hyperexcitability, suggesting that protein aggregate clearance through the activation of autophagy effectively normalized activity and improved neuronal survival. Our culture system reproduced several ALS phenotypes, including protein accumulation, hyperexcitability, and neuronal death. This rapid and robust phenotypic screening system will likely facilitate the discovery of novel ALS therapeutics and stratified and personalized medicine for sporadic motor neuron diseases.
 Mitochondrial involvement in neurodegenerative diseases is widespread and multifactorial. Targeting mitochondrial pathology is therefore of interest. The recent development of bioactive molecules that modulate mitochondrial dynamics (fusion, fission and motility) offers a new therapeutic approach for neurodegenerative diseases with either indirect or direct mitochondrial involvement. Here, we asked: (1) Can enhanced mitochondrial fusion and motility improve secondary mitochondrial pathology in superoxide dismutase1 (SOD1) mutant amyotrophic lateral sclerosis (ALS)? And: (2) What is the impact of enhancing mitochondria fitness on in vivo manifestations of SOD1 mutant ALS? We observed that small molecule mitofusin activators corrected mitochondrial fragmentation, depolarization and dysmotility in genetically diverse ALS patient reprogrammed motor neurons and fibroblasts, and in motor neurons, sensory neurons and fibroblasts from SOD1 G93A mice. Continuous, but not intermittent, pharmacologic mitofusin activation delayed phenotype progression and lethality in SOD1 G93A mice, reducing neuron loss and improving neuromuscular connectivity. Mechanistically, mitofusin activation increased mitochondrial motility, fitness and residency within neuromuscular synapses; reduced mitochondrial reactive oxygen species production; and diminished apoptosis in SOD1 mutant neurons. These benefits were accompanied by improved mitochondrial respiratory coupling, despite characteristic SOD1 mutant ALS-associated downregulation of mitochondrial respiratory complexes. Targeting mitochondrial dysdynamism is a promising approach to alleviate pathology caused by secondary mitochondrial dysfunction in some neurodegenerative diseases.
 Chiari 1 Malformation (CM1) is classically defined as a caudal displacement of the cerebellar tonsils through the foramen magnum into the spinal cord. Modern imaging techniques and experimental studies disclose a different etiology for the development of CM1, but the main etiology factor is a structural defect in the skull as a deformity or partial reduction, which push down the lower part of the brain and cause the cerebellum to compress into the spinal canal. CM1 is classified as a rare disease. CM1 can present with a wide variety of symptoms, also non-specific, with consequent controversies on diagnosis and surgical decision-making, particularly in asymptomatic or minimally symptomatic. Other disorders, such as syringomyelia (Syr), hydrocephalus, and craniocervical instability can be associated at the time of the diagnosis or appear secondarily. Therefore, CM1-related Syr is defined as a single or multiple fluid-filled cavities within the spinal cord and/or the bulb. A rare CM1-related disorder is syndrome of lateral amyotrophic sclerosis (ALS mimic syndrome). We present a unique clinical case of ALS mimic syndrome in a young man with CM1 and a huge singular syringomyelic cyst with a length from segment C2 to Th12. At the same time, the clinical picture showed upper hypotonic-atrophic paraparesis in the absence of motor disorders in the lower extremities. Interestingly, this patient did not have a disorder of superficial and deep types of sensitivity. This made it difficult to diagnose CM1. For a long time, the patient's symptoms were regarded as a manifestation of ALS, as an independent neurological disease, and not as a related disorder of CM1. Surgical treatment for CM1 was not effective, but it allowed to stabilize the course of CM1-related ALS mimic syndrome over the next two years.
 Amyotrophic lateral sclerosis, a fatal neurodegeneration disease affecting motor neurons in the brain and spinal cord, is difficult to diagnose and treat. The objective of this study is to identify novel candidate genes related to ALS. Transcriptome-wide association study of ALS was conducted by integrating the genome-wide association study summary data (including 1234 ALS patients and 2850 controls) and pre-computed gene expression weights of different tissues. The ALS-associated genes identified by TWAS were further compared with the differentially expressed genes detected by the mRNA expression profiles of the sporadic ALS. Functional enrichment and annotation analysis of identified genes were performed by an R package and the functional mapping and annotation software. TWAS identified 761 significant genes (P(TWAS) < 0.05), 627 Gene ontology terms, and 8 Kyoto Encyclopedia of Genes and Genomes pathways for ALS, such as C9orf72, with three expression quantitative trait loci were found significantly: rs2453554 (P(TWAS CBRS) = 4.68 × 10(-10), P(TWAS CBRS) = 2.54 × 10(-9)), rs10967976 (P(TWAS CBRS) = 7.85 × 10(-10), P(TWAS CBRS) = 8.91 × 10(-9), P(TWAS CBRS) = 1.49 × 10(-7), P(TWAS CBRS) = 5.59 × 10(-7)), rs3849946 (P(TWAS CBRS) = 7.69 × 10(-4), P(TWAS YBL) = 4.02 × 10(-2)), Mitochondrion (P(adj) = 4.22 × 10(-16)), and Cell cycle (P(adj) = 2.04 × 10(-3)). Moreover, 107 common genes, 4 KEGG pathways and 41 GO terms were detected by integrating mRNA expression profiles of sALS, such as CPVL (FC = 2.06, P(mRNA) = 6.99 × 10(-6), P(TWAS CBR) = 2.88 × 10(-2), P(TWAS CBR) = 4.37 × 10(-2)), Pyrimidine Metabolism (P(adj) = 2.43 × 10(-2)), and Cell Activation (P(adj) = 5.54 × 10(-3)). Multiple candidate genes and pathways were detected for ALS. Our findings may provide novel clues for understanding the genetic mechanism of ALS.
 Mitochondria play a key role in both health and disease. Their function is not limited to energy production but serves multiple mechanisms varying from iron and calcium homeostasis to the production of hormones and neurotransmitters, such as melatonin. They enable and influence communication at all physical levels through interaction with other organelles, the nucleus, and the outside environment. The literature suggests crosstalk mechanisms between mitochondria and circadian clocks, the gut microbiota, and the immune system. They might even be the hub supporting and integrating activity across all these domains. Hence, they might be the (missing) link in both health and disease. Mitochondrial dysfunction is related to metabolic syndrome, neuronal diseases, cancer, cardiovascular and infectious diseases, and inflammatory disorders. In this regard, diseases such as cancer, Alzheimer's, Parkinson's, amyotrophic lateral sclerosis (ALS), chronic fatigue syndrome (CFS), and chronic pain are discussed. This review focuses on understanding the mitochondrial mechanisms of action that allow for the maintenance of mitochondrial health and the pathways toward dysregulated mechanisms. Although mitochondria have allowed us to adapt to changes over the course of evolution, in turn, evolution has shaped mitochondria. Each evolution-based intervention influences mitochondria in its own way. The use of physiological stress triggers tolerance to the stressor, achieving adaptability and resistance. This review describes strategies that could recover mitochondrial functioning in multiple diseases, providing a comprehensive, root-cause-focused, integrative approach to recovering health and treating people suffering from chronic diseases.
 OBJECTIVE: Age at onset (AAO) is an essential clinical feature associated with disease progression and mortality in amyotrophic lateral sclerosis (ALS). Identification of genetic variants and environmental risk factors influencing AAO of ALS could help better understand the disease's biological mechanism and provide clinical guidance. However, most genetic studies focused on the risk of ALS, while the genetic background of AAO is less explored. This study aimed to identify genetic and environmental determinants for AAO of ALS. METHODS: We performed a genome-wide association analysis using a Cox proportional hazards model on AAO of ALS in 10,068 patients. We further conducted colocalization analysis and in-vitro functional exploration for the target variants, as well as Mendelian randomization analysis to identify risk factors influencing AAO of ALS. RESULTS: The total heritability of AAO of ALS was ~0.16 (standard error [SE] = 0.03). One novel locus rs2046243 (CTIF) was significantly associated with earlier AAO by ~1.29 years (p = 1.68E-08, beta = 0.10, SE = 0.02). Functional exploration suggested this variant was associated with increased expression of CTIF in multiple tissues including the brain. Colocalization analysis detected a colocalization signal at the locus between AAO of ALS and expression of CTIF. Causal inference indicated higher education level was associated with later AAO. INTERPRETATION: These findings improve the current knowledge of the genetic and environmental etiology of AAO of ALS, and provide a novel target CTIF for further research on ALS pathogenesis and potential therapeutic options to delay the disease onset. ANN NEUROL 2023.
 Systemic sclerosis (SSc) is a complex autoimmune inflammatory disorder with multiple organ involvement. Skin changes present the hallmark of SSc and coincide with poor prognosis. Interstitial lung diseases (ILD) are the most widely reported complications in SSc patients and the primary cause of death. It has been proposed that the processes of autophagy and apoptosis could play a significant role in the pathogenesis and clinical course of different autoimmune diseases, and accordingly in SSc. In this manuscript, we review the current knowledge of autophagy and apoptosis processes in the skin and lungs of patients with SSc. Profiling of markers involved in these processes in skin cells can be useful to recognize the stage of fibrosis and can be used in the clinical stratification of patients. Furthermore, the knowledge of the molecular mechanisms underlying these processes enables the repurposing of already known drugs and the development of new biological therapeutics that aim to reverse fibrosis by promoting apoptosis and regulate autophagy in personalized treatment approach. In SSc-ILD patients, the molecular signature of the lung tissues of each patient could be a distinctive criterion in order to establish the correct lung pattern, which directly impacts the course and prognosis of the disease. In this case, resolving the role of tissue-specific markers, which could be detected in the circulation using sensitive molecular methods, would be an important step toward development of non-invasive diagnostic procedures that enable early and precise diagnosis and preventing the high mortality of this rare disease.
 Trichoscopy is a diagnostic tool for hair and scalp diseases. It was recently shown that it also allows the identification of features associated with disorders that typically do not affect the scalp. The aim of this article was to analyse and outline the usefulness of trichoscopy in suspecting such diseases. Connective tissue diseases were the most investigated systemic disorders in regard to trichoscopy. The most common features of systemic lupus erythematosus, systemic sclerosis and dermatomyositis are thick arborizing and tortuous vessels. Avascular areas are present in systemic sclerosis. Spermatozoa-like vessels may be observed in cutaneous T-cell lymphomas, while salmon-coloured areas with arborizing and linear vessels may be seen in patients with cutaneous B-cell lymphomas. In patients with advanced multiple myeloma, follicular spicules may be observed. Trichoscopic features of angiosarcomas include pink areas, red, polymorphic areas and dark red to purple areas. Polymorphous vessels and whitish areas on a pink background are the predominating trichoscopic features of metastases of malignant tumours to the scalp. Cutaneous sarcoidosis is characterized by orange-coloured areas and telangiectasias. Systemic amyloidosis may manifest with salmon-coloured perifollicular halos, while the most common trichoscopic features of syphilitic alopecia are as follows: decreased number of hairs per follicular unit, vellus hairs, background erythema, focal atrichia and yellow dots. In conclusion, dermatologists may suspect some systemic diseases on the basis of trichoscopic findings.
 Protein aggregation is a hallmark of many neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS). Although mutations in TARDBP, encoding transactive response DNA-binding protein 43 kDa (TDP-43), account for less than 1% of all ALS cases, TDP-43-positive aggregates are present in nearly all ALS patients, including patients with sporadic ALS (sALS) or carrying other familial ALS-causing (fALS-causing) mutations. Interestingly, TDP-43 inclusions are also present in subsets of patients with frontotemporal dementia, Alzheimer's disease, and Parkinson's disease; therefore, methods of activating intracellular protein quality control machinery capable of clearing toxic cytoplasmic TDP-43 species may alleviate disease-related phenotypes. Here, we identify a function of nemo-like kinase (Nlk) as a negative regulator of lysosome biogenesis. Genetic or pharmacological reduction of Nlk increased lysosome formation and improved clearance of aggregated TDP-43. Furthermore, Nlk reduction ameliorated pathological, behavioral, and life span deficits in 2 distinct mouse models of TDP-43 proteinopathy. Because many toxic proteins can be cleared through the autophagy/lysosome pathway, targeted reduction of Nlk represents a potential approach to therapy development for multiple neurodegenerative disorders.
 Amyotrophic lateral sclerosis (ALS), the major adult-onset motor neuron disease, has been viewed almost exclusively as a disease of upper and lower motor neurons, with muscle changes interpreted as a consequence of the progressive loss of motor neurons and neuromuscular junctions. This has led to the prevailing view that the involvement of muscle in ALS is only secondary to motor neuron loss. Skeletal muscle and motor neurons reciprocally influence their respective development and constitute a single functional unit. In ALS, multiple studies indicate that skeletal muscle dysfunction might contribute to progressive muscle weakness, as well as to the final demise of neuromuscular junctions and motor neurons. Furthermore, skeletal muscle has been shown to participate in disease pathogenesis of several monogenic diseases closely related to ALS. Here, we move the narrative towards a better appreciation of muscle as a contributor of disease in ALS. We review the various potential roles of skeletal muscle cells in ALS, from passive bystanders to active players in ALS pathophysiology. We also compare ALS to other MN diseases and draw perspectives for future research and treatment.
 The purpose of this study was to examine how neurodegeneration secondary to amyotrophic lateral sclerosis (ALS) impacts speech sound accuracy over time and how speech sound accuracy, in turn, is related to speech intelligibility. Twenty-one participants with ALS read the Bamboo Passage over multiple data collection sessions across several months. Phonemic and orthographic transcriptions were completed for all speech samples. The percentage of phonemes accurately produced was calculated across each phoneme, sound class (i.e. consonants versus vowels), and distinctive feature (i.e. features involved in Manner of Articulation, Place of Articulation, Laryngeal Voicing, Tongue Height, and Tongue Advancement). Intelligibility was determined by calculating the percentage of words correctly transcribed orthographically by naive listeners. Linear mixed effects models were conducted to assess the decline of each distinctive feature over time and its impact on intelligibility. The results demonstrated that overall phonemic production accuracy had a nonlinear relationship with speech intelligibility and that a subset of features (i.e. those dependent on precise lingual and labial constriction and/or extensive lingual and labial movement) were more important for intelligibility and were more impacted over time than other features. Furthermore, findings revealed that consonants were more strongly associated with intelligibility than vowels, but consonants did not significantly differ from vowels in their decline over time. These findings have the potential to (1) strengthen mechanistic understanding of the physiological constraints imposed by neuronal degeneration on speech production and (2) inform the timing and selection of treatment and assessment targets for individuals with ALS.
 BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with no cure. Although the etiology of sporadic ALS is largely unknown, environmental exposures may affect ALS risk. OBJECTIVE: We investigated relationships between exposure to long-term ambient particulate matter (PM) and gaseous air pollution (AP) and ALS mortality. METHODS: Within the Women's Health Initiative (WHI) cohort of 161,808 postmenopausal women aged 50-79 years at baseline (1993-1998), we performed a nested case-control study of 256 ALS deaths and 2486 matched controls with emphasis on PM constituents (PM(2.5), PM(10), and coarse PM [PM(10)-(2.5)]) and gaseous pollutants (NO(x), NO(2), SO(2), and ozone). Time-varying AP exposures estimates were averaged 5, 7.5, and 10 years prior to ALS death using both a GIS-based spatiotemporal generalized additive mixed model and ordinary kriging (empirical and multiple imputation, MI). Conditional logistic regression was used to estimate the relative risk of ALS death. RESULTS: In general, PM(2.5) and PM(10)-related risks were not significantly elevated using either method. However, for PM(10-2.5), odds ratios (ORs) were >1.0 for both methods at all time periods using MI and empirical data for PM(10-2.5) (coarse) except for 5 and 7.5 years using the kriging method with covariate adjustment. CONCLUSION: This investigation adds to the body of information on long-term ambient AP exposure and ALS mortality. Specifically, the 2019 US Environmental Protection Agency (EPA) Integrated Science Assessment summarized the neurotoxic effects of PM(2.5), PM(10,) and PM(10)-(2.5.) The conclusion was that evidence of an effect of coarse PM is suggestive but the data is presently not sufficient to infer a causal relationship. Further research on AP and ALS is warranted. As time from symptom onset to death in ALS is ∼2-4 years, earlier AP measures may also be of interest to ALS development. This is the first study of ALS and AP in postmenopausal women controlling for individual-level confounders.
 BACKGROUND: People with motor neuron disease (pwMND) are routinely offered gastrostomy feeding tube placement and (non-invasive and invasive) ventilation to manage the functional decline associated with the disease. This study aimed to synthesise the findings from the qualitative literature to understand how individual, clinical team and organisational factors influence pwMND decisions about these interventions. METHODS: The study design was guided by the enhancing transparency in reporting the synthesis of qualitative research (ENTREC) statement. The search of five bibliography databases and an extensive supplementary search strategy identified 27 papers that included qualitative accounts of pwMND, caregivers and healthcare professionals' (HCPs) experiences of making decisions about gastrostomy and ventilation. The findings from each study were included in a thematic synthesis. FINDINGS: Making decisions about interventions is an emotional rather than simply a functional issue for pwMND. The interventions can signal an end to normality, and increasing dependence, where pwMND consider the balance between quality of life and extending survival. Interactions with multiple HCPs and caregivers can influence the process of decision-making and the decisions made. These interactions contribute to the autonomy pwMND are able to exert during decision-making. HCPs can both promote and threaten pwMND perceived agency over decisions through how they approach discussions about these interventions. Though there is uncertainty over the timing of interventions, pwMND who agree to interventions report reaching a tipping point where they accept the need for change. CONCLUSION: Discussion of gastrostomy and ventilation options generate an emotional response in pwMND. Decisions are the consequence of interactions with multiple external agents, including HCPs treading a complex ethical path when trying to improve health outcomes while respecting pwMND right to autonomy. Future decision support interventions that address the emotional response and seek to support autonomy have the potential to enable pwMND to make informed and timely decisions about gastrostomy placement and ventilation. PATIENT OR PUBLIC CONTRIBUTION: The lead author collaborated with several patient and participant involvement (PPI) groups with regards to the conceptualisation and design of this project. Decisions that have been influenced by discussions with multiple PPI panels include widening the scope of decisions about ventilation in addition to gastrostomy placement and the perceptions of all stakeholders involved (i.e., pwMND, caregivers and HCPs).
 Myalgia, myopathy and myositis are the most important types of muscle impairment in immune-mediated inflammatory arthropathies and connective tissue diseases. Multiple pathogenetic and histological changes occur in the striated muscles of these patients. Clinically, the most important muscle involvement is the one that causes complaints to the patients. In everyday practice, insidious symptoms present a serious problem for the clinician; in many cases, it is difficult to decide when and how to treat the muscle symptoms that are often present only subclinically. In this work, authors review the international literature on the types of muscle problems in autoimmune diseases. In scleroderma histopathological picture of muscle shows a very heterogeneous picture, necrosis and atrophy are common. In rheumatoid arthritis and systemic lupus erythematosus, myopathy is a much less defined concept, further studies are needed to describe it. According to our view, overlap myositis should be recognized as a separate entity, preferably with distinct histological and serological characteristics. More studies are needed to describe muscle impairment in autoimmune diseases which may help to explore this topic more in depth and be of clinical use.
 Mitochondria are critical to multiple cellular processes, from the production of adenosine triphosphate (ATP), maintenance of calcium homeostasis, synthesis of key metabolites, and production of reactive oxygen species (ROS) to maintain necrosis, apoptosis, and autophagy. Therefore, proper clearance and regulation are essential to maintain various physiological processes carried out by the cellular mechanism, including mitophagy and autophagy, by breaking down the damaged intracellular connections under the influence of various genes and proteins and protecting against various neurodegenerative diseases such as Parkinson disease (PD), amyotrophic lateral sclerosis (ALS), Alzheimer disease (AD), and Huntington disease (HD). In this review, we will discuss the role of autophagy, selective macroautophagy, or mitophagy, and its role in neurodegenerative diseases along with normal physiology. In addition, this review will provide a better understanding of the pathways involved in neuron autophagy and mitophagy and how mutations affect these pathways in the various genes involved in neurodegenerative diseases. Various new findings indicate that the pathways that remove dysfunctional mitochondria are impaired in these diseases, leading to the deposition of damaged mitochondria. Apart from that, we have also discussed the therapeutic strategies targeting autophagy and mitophagy in neurodegenerative diseases. The mitophagy cycle results in the degradation of damaged mitochondria and the biogenesis of new healthy mitochondria, also highlighting different stages at which a particular neurodegenerative disease could occur.
 Systemic sclerosis is a rare connective tissue disease; and interstitial lung disease (SSc-ILD) is associated with significant morbidity and mortality. There are no clinical, radiologic features, nor biomarkers that identify the specific time when patients are at risk for progression at which the benefits from treatment outweigh the risks. Our study aimed to identify blood protein biomarkers associated with progression of interstitial lung disease in patients with SSc-ILD using an unbiased, high-throughput approach. We classified SSc-ILD as progressive or stable based on change in forced vital capacity over 12 months or less. We profiled serum proteins by quantitative mass spectrometry and analyzed the association between protein levels and progression of SSc-ILD via logistic regression. The proteins associated with at a p value of < 0.1 were queried in the ingenuity pathway analysis (IPA) software to identify interaction networks, signaling, and metabolic pathways. Through principal component analysis, the relationship between the top 10 principal components and progression was evaluated. Unsupervised hierarchical clustering with heatmapping was done to define unique groups. The cohort consisted of 72 patients, 32 with progressive SSc-ILD and 40 with stable disease with similar baseline characteristics. Of a total of 794 proteins, 29 were associated with disease progression. After adjusting for multiple testing, these associations did not remain significant. IPA identified five upstream regulators that targeted proteins associated with progression, as well as a canonical pathway with a higher signal in the progression group. Principal component analysis showed that the ten components with the highest Eigenvalues represented 41% of the variability of the sample. Unsupervised clustering analysis revealed no significant heterogeneity between the subjects. We identified 29 proteins associated with progressive SSc-ILD. While these associations did not remain significant after accounting for multiple testing, some of these proteins are part of pathways relevant to autoimmunity and fibrogenesis. Limitations included a small sample size and a proportion of immunosuppressant use in the cohort, which could have altered the expression of inflammatory and immunologic proteins. Future directions include a targeted evaluation of these proteins in another SSc-ILD cohort or application of this study design to a treatment naïve population.
 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder with phenotypic and genetic heterogeneity. Recent studies have suggested an oligogenic basis of ALS, in which the co-occurrence of two or more genetic variants has additive or synergistic deleterious effects. To assess the contribution of possible oligogenic inheritance, we profiled a panel of 43 relevant genes in 57 sporadic ALS (sALS) patients and eight familial ALS (fALS) patients from five pedigrees in east China. We filtered rare variants using the combination of the Exome Aggregation Consortium, the 1000 Genomes and the HuaBiao Project. We analyzed patients with multiple rare variants in 43 known ALS causative genes and the genotype-phenotype correlation. Overall, we detected 30 rare variants in 16 different genes and found that 16 of the sALS patients and all the fALS patients examined harbored at least one variant in the investigated genes, among which two sALS and four fALS patients harbored two or more variants. Of note, the sALS patients with one or more variants in ALS genes had worse survival than the patients with no variants. Typically, in one fALS pedigree with three variants, the family member with three variants (Superoxide dismutase 1 (SOD1) p.V48A,  Optineurin (OPTN) p.A433V and TANK binding kinase 1 (TBK1) p.R573H) exhibited much more severe disease phenotype than the member carrying one variant (TBK1 p.R573H). Our findings suggest that rare variants could exert a negative prognostic effect, thereby supporting the oligogenic inheritance of ALS.
 The RNA/DNA helicase senataxin (SETX) has been involved in multiple crucial processes related to genome expression and integrity such us transcription termination, the regulation of transcription-replication conflicts and the resolution of R-loops. SETX has been the focus of numerous studies since the discovery that mutations in its coding gene are the root cause of two different neurodegenerative diseases: Ataxia with Oculomotor Apraxia type 2 (AOA2) and a juvenile form of Amyotrophic Lateral Sclerosis (ALS4). A plethora of cellular phenotypes have been described as the result of SETX deficiency, yet the precise molecular function of SETX as well as the molecular pathways leading from SETX mutations to AOA2 and ALS4 pathologies have remained unclear. However, recent data have shed light onto the biochemical activities and biological roles of SETX, thus providing new clues to understand the molecular consequences of SETX mutation. In this review we summarize near two decades of scientific effort to elucidate SETX function, we discuss strengths and limitations of the approaches and models used thus far to investigate SETX-associated diseases and suggest new possible research avenues for the study of AOA2 and ALS4 pathogenesis.
 Genetic frontotemporal lobar degeneration caused by autosomal dominant gene mutations provides an opportunity for targeted drug development in a highly complex and clinically heterogeneous dementia. These neurodegenerative disorders can affect adults in their middle years, progress quickly relative to other dementias, are uniformly fatal and have no approved disease-modifying treatments. Frontotemporal dementia, caused by mutations in the GRN gene which encodes the protein progranulin, is an active area of interventional drug trials that are testing multiple strategies to restore progranulin protein deficiency. These and other trials are also examining neurofilament light as a potential biomarker of disease activity and disease progression and as a therapeutic endpoint based on the assumption that cerebrospinal fluid and blood neurofilament light levels are a surrogate for neuroaxonal damage. Reports from genetic frontotemporal dementia longitudinal studies indicate that elevated concentrations of blood neurofilament light reflect disease severity and are associated with faster brain atrophy. To better inform patient stratification and treatment response in current and upcoming clinical trials, a more nuanced interpretation of neurofilament light as a biomarker of neurodegeneration is now required, one that takes into account its relationship to other pathophysiological and topographic biomarkers of disease progression from early presymptomatic to later clinically symptomatic stages.
 Leveraging genome-wide association statistics generated from a large study of amyotrophic lateral sclerosis (ALS; 29,612 cases and 122,656 controls) and UK Biobank (UKB; 4,024 phenotypes, up to 361,194 participants), we conducted a phenome-wide analysis of ALS genetic liability and identified 46 genetically correlated traits, such as fluid intelligence score (r(g) = - 0.21, p = 1.74 × 10(-6)), "spending time in pub or social club" (r(g) = 0.24, p = 2.77 × 10(-6)), non-work related walking (r(g) = - 0.25, p = 1.95 × 10(-6)), college education (r(g) = - 0.15, p = 7.08 × 10(-5)), "ever diagnosed with panic attacks (r(g) = 0.39, p = 4.24 × 10(-5)), and "self-reported other gastritis including duodenitis" (r(g) = 0.28, p = 1.4 × 10(-3)). To assess the putative directionality of these genetic correlations, we conducted a latent causal variable analysis, identifying significant genetic causality proportions (gĉp) linking ALS genetic liability to seven traits. While the genetic component of "self-reported other gastritis including duodenitis" showed a causal effect on ALS (gĉp = 0.50, p = 1.26 × 10(-29)), the genetic liability to ALS is potentially causal for multiple traits, also including an effect on "ever being diagnosed with panic attacks" (gĉp = 0.79, p = 5.011 × 10(-15)) and inverse effects on "other leisure/social group activities" (gĉp = 0.66, p = 1 × 10(-4)) and prospective memory result (gĉp = 0.35, p = 0.005). Our subsequent Mendelian randomization analysis indicated that some of these associations may be due to bidirectional effects. In conclusion, this phenome-wide investigation of ALS polygenic architecture highlights the widespread pleiotropy linking this disorder with several health domains.
 Neurodegenerative diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS) are traditionally considered strictly neurological disorders. However, clinical presentation is not restricted to neurological systems, and non-central nervous system (CNS) manifestations, particularly gastrointestinal (GI) symptoms, are common. Our objective was to understand the systemic distribution of pathology in archived non-CNS tissues, taken as part of routine clinical practice during life from people with ALS. We examined tissue from 13 people who went on to develop ALS; including sporadic ALS (n = 12) and C9orf72 hexanucleotide repeat expansion (n = 1). The tissue cohort consisted of 68 formalin-fixed paraffin embedded samples from 21 surgical cases (some patients having more than one case over their lifetimes), from 8 organ systems, which we examined for evidence of phosphorylated TDP-43 (pTDP-43) pathology. We identified pTDP-43 aggregates in multiple cell types of the GI tract, including macrophages and dendritic cells within the lamina propria; as well as ganglion/neuronal and glial cells of the myenteric plexus. Aggregates were also noted within lymph node parenchyma, blood vessel endothelial cells, and chondrocytes. We note that in all cases with non-CNS pTDP-43 pathology, aggregates were present prior to ALS diagnosis and in some instances preceded neurological symptom onset by more than 10 years. These data imply that patients with microscopically unexplained non-CNS symptoms could have occult protein aggregation that could be detected many years prior to neurological involvement.
 INTRODUCTION: The apolipoprotein E (APOE) genotype is a driver of cognitive decline and dementia. We used causal mediation methods to characterize pathways linking the APOE genotype to late-life cognition through Alzheimer's disease (AD) and non-AD neuropathologies. METHODS: We analyzed autopsy data from 1671 individuals from the Religious Orders Study, Memory and Aging Project, and Minority Aging Research Study (ROS/MAP/MARS) studies with cognitive assessment within 5 years of death and autopsy measures of AD (amyloid beta (Aβ), neurofibrillary tangles), vascular (athero/arteriolo-sclerosis, micro-infarcts/macro-infarcts), and non-AD neurodegenerative neuropathologies (TAR DNA protein 43 [TDP-43], Lewy bodies, amyloid angiopathy, hippocampal sclerosis). RESULTS: The detrimental effect of APOE ε4 on cognition was mediated by summary measures of AD and non-AD neurodegenerative neuropathologies but not vascular neuropathologies; effects were strongest in individuals with dementia. The protective effect of APOE ε2 was partly mediated by AD neuropathology and stronger in women than in men. DISCUSSION: The APOE genotype influences cognition and dementia through multiple neuropathological pathways, with implications for different therapeutic strategies targeting people at increased risk for dementia. HIGHLIGHTS: Both apolipoprotein E (APOE) ε2 and APOE ε4 effects on late-life cognition are mediated by AD neuropathology. The estimated mediated effects of most measures of AD neuropathology were similar. Non-Alzheimer's disease (AD) neurodegenerative pathologies mediate the effect of ε4 independently from AD. Non-AD vascular pathologies did not mediate the effect of the APOE genotype on cognition. The protective effect of APOE ε2 on cognition was stronger in women.
 The spectrum of neuropsychiatric phenomena observed in amyotrophic lateral sclerosis (ALS) is wide and not fully understood. Disorders of laughter and crying stand among the most common manifestations. The aim of this study is to report the results of an educational consensus organized by the Brazilian Academy of Neurology to evaluate the definitions, phenomenology, diagnosis, and management of the disorders of laughter and crying in ALS patients. Twelve members of the Brazilian Academy of Neurology - considered to be experts in the field - were recruited to answer 12 questions about the subject. After exchanging revisions, a first draft was prepared. A face-to-face meeting was held in Fortaleza, Brazil on 9.23.22 to discuss it. The revised version was subsequently emailed to all members of the ALS Scientific Department from the Brazilian Academy of Neurology and the final revised version submitted for publication. The prevalence of pseudobulbar affect/pathological laughter and crying (PBA/PLC) in ALS patients from 15 combined studies and 3906 patients was 27.4% (N = 1070), ranging from 11.4% to 71%. Bulbar onset is a risk factor but there are limited studies evaluating the differences in prevalence among the different motor neuron diseases subtypes, including patients with and without frontotemporal dementia. Antidepressants and a combination of dextromethorphan and quinidine (not available in Brazil) are possible therapeutic options. This group of panelists acknowledge the multiple gaps in the current literature and reinforces the need for further studies.
 BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder. An increasing number of researchers have found extra motor features in ALS, which are also called ALS-plus syndromes. Besides, a great majority of ALS patients also have cognitive impairment. However, clinical surveys of the frequency and genetic background of ALS-plus syndromes are rare, especially in China. METHODS: We investigated a large cohort of 1015 patients with ALS, classifying them into six groups according to different extramotor symptoms and documenting their clinical manifestations. Meanwhile, based on their cognitive function, we divided these patients into two groups and compared demographic characteristics. Genetic screening for rare damage variants (RDVs) was also performed on 847 patients. RESULTS: As a result, 16.75% of patients were identified with ALS-plus syndrome, and 49.5% of patients suffered cognitive impairment. ALS-plus group had lower ALSFRS-R scores, longer diagnostic delay time, and longer survival times, compared to ALS pure group. RDVs occurred less frequently in ALS-plus patients than in ALS-pure patients (P = 0.042) but showed no difference between ALS-cognitive impairment patients and ALS-cognitive normal patients. Besides, ALS-cognitive impairment group tends to harbour more ALS-plus symptoms than ALS-cognitive normal group (P = 0.001). CONCLUSION: In summary, ALS-plus patients in China are not rare and show multiple differences from ALS-pure patients in clinical and genetic features. Besides, ALS-cognitive impairment group tends to harbour more ALS-plus syndrome than ALS-cognitive normal group. Our observations correspond with the theory that ALS involves several diseases with different mechanisms and provide clinical validation.
 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that results from many diverse genetic causes. Although therapeutics specifically targeting known causal mutations may rescue individual types of ALS, these approaches cannot treat most cases since they have unknown genetic etiology. Thus, there is a pressing need for therapeutic strategies that rescue multiple forms of ALS. Here, we show that pharmacological inhibition of PIKFYVE kinase activates an unconventional protein clearance mechanism involving exocytosis of aggregation-prone proteins. Reducing PIKFYVE activity ameliorates ALS pathology and extends survival of animal models and patient-derived motor neurons representing diverse forms of ALS including C9ORF72, TARDBP, FUS, and sporadic. These findings highlight a potential approach for mitigating ALS pathogenesis that does not require stimulating macroautophagy or the ubiquitin-proteosome system.
 Systemic rheumatoid diseases (SRDs) are autoimmune and inflammatory disorders that affect multiple organ systems, impacting patients' quality of life, and survival rates. Standard treatment requires continuous drug therapy and immunosuppression. Chimeric antigen receptor (CAR) T cell therapy has the potential to target and eliminate pathologically activated immune cells and re-establish tolerance in organs affected by dysregulated immunity, making them a promising treatment option for autoimmune diseases. In autoimmune diseases, CAR T cells have the advantage of being able to kill B cells effectively without the need for an accessory cell type. Additionally, CAR T cells targeting CD19 have shown promise in comprehensive B cell aplasia, preserving pre-existing humoral immunity, and specifically eliminating pathogenic B cells. CAR T cell therapy's limited use in SRDs is due to its inability to effectively target the various autoreactive lymphocytes present. Researchers are developing a universal CAR T cell therapy that detects and targets autoreactive lymphocytes using major epitope peptides, though further studies are required. Moreover, adoptive transfer of CAR-Tregs has shown promise for effectively reducing inflammation and treating autoimmunity. Through this exploration, the authors hope to provide a comprehensive understanding of the current state of research on this topic, identify areas for further study, and promote the advancement of CAR T cell therapy as a treatment option for SRDs.
 BACKGROUND: Dysfunctional processes in Alzheimer's disease and other neurodegenerative diseases lead to neural degeneration in the central and peripheral nervous system. Research demonstrates that neurodegeneration of any kind is a systemic disease that may even begin outside of the region vulnerable to the disease. Neurodegenerative diseases are defined by the vulnerabilities and pathology occurring in the regions affected. METHOD: A random forest machine learning analysis on whole blood transcriptomes from six neurodegenerative diseases generated unbiased disease-classifying RNA transcripts subsequently subjected to pathway analysis. RESULTS: We report that transcripts of the blood transcriptome selected for each of the neurodegenerative diseases represent fundamental biological cell processes including transcription regulation, degranulation, immune response, protein synthesis, apoptosis, cytoskeletal components, ubiquitylation/proteasome, and mitochondrial complexes that are also affected in the brain and reveal common themes across six neurodegenerative diseases. CONCLUSION: Neurodegenerative diseases share common dysfunctions in fundamental cellular processes. Identifying regional vulnerabilities will reveal unique disease mechanisms. HIGHLIGHTS: Transcriptomics offer information about dysfunctional processes. Comparing multiple diseases will expose unique malfunctions within diseases. Blood RNA can be used ante mortem to track expression changes in neurodegenerative diseases. Protocol standardization will make public datasets compatible.
 OBJECTIVE: To report multiple cause of death (MCOD) occurrence among patients in the United States with amyotrophic lateral sclerosis (ALS). METHODS: Using death certificate data for all ALS deaths from 50 U.S. states and the District of Columbia, 2011-2014, we tabulated MCOD, used association rules mining (ARM) to determine if MCOD occurred together, and calculated standardized mortality odds ratios (SMOR) for select causes, comparing ALS with other U.S. decedents. RESULTS: Among 24,328 death certificates, there were 25,704 MCOD, excluding ALS. ALS was listed as the sole cause of death in n = 11,263 (46%). The most frequent causes of death co-occurring with ALS were respiratory failure (n = 6503; 25.3%), cardiovascular disease (n = 6077; 12.6%), pneumonia (n = 1345; 5.2%), and pneumonitis (n = 856; 3.3%). The SMORs among ALS decedents compared with non-ALS decedents for falls and accidents were 3.4 (95% CI 2.6, 4.3) and 3.0 (95% CI 2.2, 4.2), respectively. From ARM analysis, falls and accidents were both associated with injuries. The most common causes identified were weakly to very strongly associated with being an ALS decedent compared with other U.S. deaths, with SMOR point estimates ranging from 1.3 to 51.1. INTERPRETATION: This study provides information about the natural history of ALS. With knowledge that some causes of death may be preventable, healthcare providers may be able to optimize patient care and possibly postpone mortality and reduce morbidity. Moreover, this study located gaps in data; medical certifiers completing death certificates for ALS decedents should ensure all MCOD data are recorded.
 RNA translation is tightly controlled in eukaryotic cells to regulate gene expression and maintain proteome homeostasis. RNA binding proteins, translation factors, and cell signaling pathways all modulate the translation process. Defective translation is involved in multiple neurological diseases including amyotrophic lateral sclerosis (ALS). ALS is a progressive neurodegenerative disorder and poses a major public health challenge worldwide. Over the past few years, tremendous advances have been made in the understanding of the genetics and pathogenesis of ALS. Dysfunction of RNA metabolisms, including RNA translation, has been closely associated with ALS. Here, we first introduce the general mechanisms of translational regulation under physiological and stress conditions and review well-known examples of translation defects in neurodegenerative diseases. We then focus on ALS-linked genes and discuss the recent progress on how translation is affected by various mutant genes and the repeat expansion-mediated non-canonical translation in ALS.
 The vitamin D binding protein (DBP), encoded by the group-specific component (GC) gene, is a component of the vitamin D system. In a genome-wide association study of DBP concentration in 65,589 neonates we identify 26 independent loci, 17 of which are in or close to the GC gene, with fine-mapping identifying 2 missense variants on chromosomes 12 and 17 (within SH2B3 and GSDMA, respectively). When adjusted for GC haplotypes, we find 15 independent loci distributed over 10 chromosomes. Mendelian randomization analyses identify a unidirectional effect of higher DBP concentration and (a) higher 25-hydroxyvitamin D concentration, and (b) a reduced risk of multiple sclerosis and rheumatoid arthritis. A phenome-wide association study confirms that higher DBP concentration is associated with a reduced risk of vitamin D deficiency. Our findings provide valuable insights into the influence of DBP on vitamin D status and a range of health outcomes.
 Interleukin-17 family (IL-17s) comprises six structurally related members (IL-17A to IL-17F); sequence homology is highest between IL-17A and IL-17F, displaying certain overlapping functions. In general, IL-17A and IL-17F play important roles in chronic inflammation and autoimmunity, controlling bacterial and fungal infections, and signaling mainly through activation of the nuclear factor-kappa B (NF-κB) pathway. The role of IL-17A and IL-17F has been established in chronic immune-mediated inflammatory diseases (IMIDs), such as psoriasis (PsO), psoriatic arthritis (PsA), axial spondylarthritis (axSpA), hidradenitis suppurativa (HS), inflammatory bowel disease (IBD), multiple sclerosis (MS), and asthma. CD4(+) helper T cells (Th17) activated by IL-23 are well-studied sources of IL-17A and IL-17F. However, other cellular subtypes can also produce IL-17A and IL-17F, including gamma delta (γδ) T cells, alpha beta (αβ) T cells, type 3 innate lymphoid cells (ILC3), natural killer T cells (NKT), or mucosal associated invariant T cells (MAIT). Interestingly, the production of IL-17A and IL-17F by innate and innate-like lymphocytes can take place in an IL-23 independent manner in addition to IL-23 classical pathway. This would explain the limitations of the inhibition of IL-23 in the treatment of patients with certain rheumatic immune-mediated conditions such as axSpA. Despite their coincident functions, IL-17A and IL-17F contribute independently to chronic tissue inflammation having somehow non-redundant roles. Although IL-17A has been more widely studied, both IL-17A and IL-17F are overexpressed in PsO, PsA, axSpA and HS. Therefore, dual inhibition of IL-17A and IL-17F could provide better outcomes than IL-23 or IL-17A blockade.
 INTRODUCTION: Neuropathological substrates associated with neurodegeneration occur in brains of the oldest old. How does this affect cognitive performance? METHODS: The 100-plus Study is an ongoing longitudinal cohort study of centenarians who self-report to be cognitively healthy; post mortem brain donation is optional. In 85 centenarian brains, we explored the correlations between the levels of 11 neuropathological substrates with ante mortem performance on 12 neuropsychological tests. RESULTS: Levels of neuropathological substrates varied: we observed levels up to Thal-amyloid beta phase 5, Braak-neurofibrillary tangle (NFT) stage V, Consortium to Establish a Registry for Alzheimer's Disease (CERAD)-neuritic plaque score 3, Thal-cerebral amyloid angiopathy stage 3, Tar-DNA binding protein 43 (TDP-43) stage 3, hippocampal sclerosis stage 1, Braak-Lewy bodies stage 6, atherosclerosis stage 3, cerebral infarcts stage 1, and cerebral atrophy stage 2. Granulovacuolar degeneration occurred in all centenarians. Some high performers had the highest neuropathology scores. DISCUSSION: Only Braak-NFT stage and limbic-predominant age-related TDP-43 encephalopathy (LATE) pathology associated significantly with performance across multiple cognitive domains. Of all cognitive tests, the clock-drawing test was particularly sensitive to levels of multiple neuropathologies.
 Systemic sclerosis (SSc) is a rare autoimmune disease of the connective tissue that can affect multiple organs. The esophagus is the most affected gastrointestinal tract, while interstitial lung disease (ILD) is a main feature associated with SSc. The aim of the present study was to evaluate the association and prognostic implication between motor esophageal disorders and pulmonary involvement in SSc patients. We retrospectively assessed patients with SSc who underwent both the HRM with the new Chicago Classification 4.0 and pulmonary evaluation comprehensive of function tests and high-resolution computer tomography (HrCT) with the use of Warrick score. A total score ≥ 7 was considered predictive of ILD, while a score ≥ 10 in a HrCT acquired prospectively from baseline evaluation was considered to establish significant interstitial involvement. Forty-two patients were included. We found a score ≥ 7 in 11 patients with aperistalsis, in 6 subjects with IEM and in 6 patients with a normal manometry. Otherwise, a score < 7 was observed in 3 patients with aperistalsis, and in 2 and 14 patients with IEM and with a normal contractility, respectively. Higher scores were observed in subjects with absent contractility or ineffective esophageal motility than subjects with normal motility, indeed DCI and HrCT score were inversely correlated in linear and logarithmic regression analysis. Prospectively, lower baseline LESP and greater HrCT scores at follow-up evaluation were significantly correlated. This study shows an association between motor esophageal disorder and pulmonary involvement in SSc patients: more severe is the esophageal involvement, more critical is the pulmonary disease.
 BACKGROUND: Interstitial lung disease (ILD) is the leading cause of mortality in systemic sclerosis (SSc). OBJECTIVE: We performed an overview of the diagnostic approaches, follow-up and treatment strategies used in France for the management of SSc-associated ILD (SSc-ILD). DESIGN STRUCTURED NATIONWIDE ONLINE SURVEYMETHODS: A structured nationwide online survey was submitted to participants via the French Medical Societies for Internal Medicine and Pneumology, and research groups on SSc-ILD from May 2018 to June 2020. The 79 multiple-choice and 9 open-ended questions covered the screening of ILD at baseline, monitoring of patients with established SSc-ILD and its management. Fourteen optional vignettes exploring different clinical phenotypes of SSc-ILD were submitted to evaluate therapeutic decisions. RESULTS: All of the 93 participants screened SSc patients for ILD at baseline with 83 (89%) participants relying on a systematic chest computed tomography (CT) scan. Pulmonary function tests (PFT) were prescribed by 87 (94%) participants at baseline and during follow-up. Treatment was started based on abnormal PFT (95%), chest CT scan characteristics (89%), worsening dyspnoea (72%) and drop in SpO(2) during 6-min walk tests (66%). First-line therapy was cyclophosphamide (CYC) (89%), mycophenolate mofetil (MMF) (83%) and prednisone (73%). Rituximab as second-line immunosuppressive therapy (41%) was preferred to antifibrotic agents (18%), and a median daily prednisone dose of 10 mg (interquartile range, 10-15) was prescribed by 73% participants. Extensive SSc-ILD with worsening PFT (95%), regardless of diffusing capacity for carbon monoxide values and skin extension, were more likely to be treated, and CYC was favoured over MMF (p < 0.01). Extensive SSc-ILD with disease duration of less than 5 years was also a criterium for treatment initiation. CONCLUSION: This overview of practices in diagnosis, follow-up and treatment of SSc-ILD in France describes real-life management of patients. It highlights heterogeneity in this management and gaps in current strategies that should be addressed to improve and harmonize clinical practices in SSc-ILD.
 BACKGROUND: The present article is an English-language version of the French National Diagnostic and Care Protocol, a pragmatic tool to optimize and harmonize the diagnosis, care pathway, management and follow-up of lymphangioleiomyomatosis in France. METHODS: Practical recommendations were developed in accordance with the method for developing a National Diagnosis and Care Protocol for rare diseases of the Haute Autorité de Santé and following international guidelines and literature on lymphangioleiomyomatosis. It was developed by a multidisciplinary group, with the help of patient representatives and of RespiFIL, the rare disease network on respiratory diseases. RESULTS: Lymphangioleiomyomatosis is a rare lung disease characterised by a proliferation of smooth muscle cells that leads to the formation of multiple lung cysts. It occurs sporadically or as part of a genetic disease called tuberous sclerosis complex (TSC). The document addresses multiple aspects of the disease, to guide the clinicians regarding when to suspect a diagnosis of lymphangioleiomyomatosis, what to do in case of recurrent pneumothorax or angiomyolipomas, what investigations are needed to make the diagnosis of lymphangioleiomyomatosis, what the diagnostic criteria are for lymphangioleiomyomatosis, what the principles of management are, and how follow-up can be organised. Recommendations are made regarding the use of pharmaceutical specialties and treatment other than medications. CONCLUSION: These recommendations are intended to guide the diagnosis and practical management of pulmonary lymphangioleiomyomatosis.
 OBJECTIVES: Systemic sclerosis (SSc) represents extremely rare disease with majority of data coming from adults. Studies comparing juvenile- (jSSc) and adult-onset (aSSc) patients are limited. We aimed to compare clinical features, treatment modalities and survival rates of jSSc and aSSc patients. METHODS: A retrospective study among pediatric and adult Scl patients has been performed. Demographic characteristics, clinical features, autoantibody profiles, and treatment data were retrieved from the databases. Survival analysis was done using Kaplan-Meier plot and factors associated with mortality were identified with multiple regression analysis. RESULTS: A total of 158 adults and 58 juvenile Scl patients were identified. The mean age at the disease onset was 37±14.7 vs. 8.8 ± 4.1 years, mean age at diagnosis 42±15.2 vs. 10.4 ± 3.8 years and mean follow-up duration was 6.3 ± 4.9 years vs. 6.6 ± 4.9 years for aSSc and jSSc patients, respectively. The frequency of interstitial lung disease (ILD) (50.9% vs 30%, p<0.001) and systemic hypertension (17.9% vs 0, p = 0.009) was significantly higher among aSSc. While aSSc patients had presented mostly with limited cutaneous subset (74.1%), diffuse cutaneous subset was the dominant subset among jSSc (76.7%), (p<0.001). The mortality rate was significantly higher among adults (p = 0.005). The ILD (p = 0.03) and cardiac insufficiency (p = 0.05) were independent risk factors of mortality in both aSSc and jSSc patients. CONCLUSION: Juvenile and adult-onset Scl represent rarely seen conditions with different clinical phenotypes. Pediatric patients with LS are more commonly seen by pediatric rheumatologists, in contrary to adults. Diffuse disease subset is the dominant form among juvenile patients, whereas limited form is the main disease subset among adults. On the other hand, juvenile-onset patients have a better survival than those with adult-onset.
 OBJECTIVE: Neuronata-R® (lenzumestrocel) is an autologous bone marrow-derived mesenchymal stem cell (BM-MSC) product, which was conditionally approved by the Korean Ministry of Food and Drug Safety (KMFDS, Republic of Korea) in 2013 for the treatment of amyotrophic lateral sclerosis (ALS). In the present study, we aimed to investigate the long-term survival benefits of treatment with intrathecal lenzumestrocel. METHODS: A total of 157 participants who received lenzumestrocel and whose symptom duration was less than 2 years were included in the analysis (BM-MSC group). The survival data of placebo participants from the Pooled-Resource Open-Access ALS Clinical Trials (PROACT) database were used as the external control, and propensity score matching (PSM) was used to reduce confounding biases in baseline characteristics. Adverse events were recorded during the entire follow-up period after the first treatment. RESULTS: Survival probability was significantly higher in the BM-MSC group compared to the external control group from the PROACT database (log-rank, p < 0.001). Multivariate Cox proportional hazard analysis showed a significantly lower hazard ratio for death in the BM-MSC group and indicated that multiple injections were more effective. Additionally, there were no serious adverse drug reactions found during the safety assessment, lasting a year after the first administration. CONCLUSION: The results of the present study showed that lenzumestrocel treatment had a long-term survival benefit in real-world ALS patients.
 Autism spectrum disorder (ASD) is a neurodevelopmental condition causing a range of social and communication impairments. Although the role of multiple genes and environmental factors has been reported, the effects of the interplay between genes and environment on the onset and progression of the disease remains elusive. We housed wild-type (Tsc2+/+) and tuberous sclerosis 2 deficient (Tsc2+/-) Eker rats (ASD model) in individually ventilated cages or enriched conditions and conducted a series of behavioural tests followed by the histochemical analysis of dendritic spines and plasticity in three age groups (days 45, 90 and 365). The elevated plus-maze test revealed a reduction of anxiety by enrichment, whereas the mobility of young and adult Eker rats in the open field was lower compared to the wild type. In the social interaction test, an enriched environment reduced social contact in the youngest group and increased anogenital exploration in 90- and 365-day-old rats. Self-grooming was increased by environmental enrichment in young and adult rats and decreased in aged Eker rats. Dendritic spine counts revealed an increased spine density in the cingulate gyrus in adult Ekers irrespective of housing conditions, whereas spine density in hippocampal pyramidal neurons was comparable across all genotypes and groups. Morphometric analysis of dendritic spines revealed age-related changes in spine morphology and density, which were responsive to animal genotype and environment. Taken together, our findings suggest that under TSC2 haploinsufficiency and mTORC1 hyperactivity, the expression of behavioural signs and neuroplasticity in Eker rats can be differentially influenced by the developmental stage and environment.
 BACKGROUND: Deregulation of transcription in the pathogenesis of sporadic Amyotrophic Lateral Sclerosis (sALS) is taking central stage with RNA-sequencing analyses from sALS patients tissues highlighting numerous deregulated long non-coding RNAs (lncRNAs). The oncogenic lncRNA ZEB1-AS1 is strongly downregulated in peripheral blood mononuclear cells of sALS patients. In addition, in cancer-derived cell lines, ZEB1-AS1 belongs to a negative feedback loop regulation with hsa-miR-200c, acting as a molecular sponge for this miRNA. The role of the lncRNA ZEB1-AS1 in sALS pathogenesis has not been characterized yet, and its study could help identifying a possible disease-modifying target. METHODS: the implication of the ZEB1-AS1/ZEB1/hsa-miR-200c/BMI1 pathway was investigated in multiple patients-derived cellular models (patients-derived peripheral blood mononuclear cells and induced pluripotent stem cells-derived neural stem cells) and in the neuroblastoma cell line SH-SY5Y, where its function was inhibited via RNA interference. Molecular techniques such as Real Time PCR, Western Blot and Immunofluorescence were used to assess the pathway dysregulation. RESULTS: Our results show a dysregulation of a signaling pathway involving ZEB1-AS1/hsa-miR-200c/β-Catenin in peripheral blood mononuclear cells and in induced pluripotent stem cells-derived neural stem cells from sALS patients. These results were validated in vitro on the cell line SH-SY5Y with silenced expression of ZEB1-AS1. Moreover, we found an increase for ZEB1-AS1 during neural differentiation with an aberrant expression of β-Catenin, highlighting also its aggregation and possible impact on neurite length. CONCLUSIONS: Our results support and describe the role of ZEB1-AS1 pathway in sALS and specifically in neuronal differentiation, suggesting that an impairment of β-Catenin signaling and an alteration of the neuronal phenotype are taking place.
 Effective therapies are urgently needed to safely target TDP-43 pathology as it is closely associated with the onset and development of devastating diseases such as frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) and amyotrophic lateral sclerosis (ALS). In addition, TDP-43 pathology is present as a co-pathology in other neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Our approach is to develop a TDP-43-specific immunotherapy that exploits Fc gamma-mediated removal mechanisms to limit neuronal damage while maintaining physiological TDP-43 function. Thus, using both in vitro mechanistic studies in conjunction with the rNLS8 and CamKIIa inoculation mouse models of TDP-43 proteinopathy, we identified the key targeting domain in TDP-43 to accomplish these therapeutic objectives. Targeting the C-terminal domain of TDP-43 but not the RNA recognition motifs (RRM) reduces TDP-43 pathology and avoids neuronal loss in vivo. We demonstrate that this rescue is dependent on Fc receptor-mediated immune complex uptake by microglia. Furthermore, monoclonal antibody (mAb) treatment enhances phagocytic capacity of ALS patient-derived microglia, providing a mechanism to restore the compromised phagocytic function in ALS and FTD patients. Importantly, these beneficial effects are achieved while preserving physiological TDP-43 activity. Our findings demonstrate that a mAb targeting the C-terminal domain of TDP-43 limits pathology and neurotoxicity, enabling clearance of misfolded TDP-43 through microglia engagement, and supporting the clinical strategy to target TDP-43 by immunotherapy. SIGNIFICANCE STATEMENT: TDP-43 pathology is associated with various devastating neurodegenerative disorders with high unmet medical needs such as frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and Alzheimer's disease. Thus, safely and effectively targeting pathological TDP-43 represents a key paradigm for biotechnical research as currently there is little in clinical development. After years of research, we have determined that targeting the C-terminal domain of TDP-43 rescues multiple patho-mechanisms involved in disease progression in two animal models of FTD/ALS. In parallel, importantly, our studies establish that this approach does not alter the physiological functions of this ubiquitously expressed and indispensable protein. Together, our findings substantially contribute to the understanding of TDP-43 pathobiology and support the prioritization for clinical testing of immunotherapy approaches targeting TDP-43.
 BACKGROUND: A rise in the incidence of some autoimmune disorders has been described. However, contemporary estimates of the overall incidence of autoimmune diseases and trends over time are scarce and inconsistent. We aimed to investigate the incidence and prevalence of 19 of the most common autoimmune diseases in the UK, assess trends over time, and by sex, age, socioeconomic status, season, and region, and we examine rates of co-occurrence among autoimmune diseases. METHODS: In this UK population-based study, we used linked primary and secondary electronic health records from the Clinical Practice Research Datalink (CPRD), a cohort that is representative of the UK population in terms of age and sex and ethnicity. Eligible participants were men and women (no age restriction) with acceptable records, approved for Hospital Episodes Statistics and Office of National Statistics linkage, and registered with their general practice for at least 12 months during the study period. We calculated age and sex standardised incidence and prevalence of 19 autoimmune disorders from 2000 to 2019 and used negative binomial regression models to investigate temporal trends and variation by age, sex, socioeconomic status, season of onset, and geographical region in England. To characterise co-occurrence of autoimmune diseases, we calculated incidence rate ratios (IRRs), comparing incidence rates of comorbid autoimmune disease among individuals with a first (index) autoimmune disease with incidence rates in the general population, using negative binomial regression models, adjusted for age and sex. FINDINGS: Among the 22 009 375 individuals included in the study, 978 872 had a new diagnosis of at least one autoimmune disease between Jan 1, 2000, and June 30, 2019 (mean age 54·0 years [SD 21·4]). 625 879 (63·9%) of these diagnosed individuals were female and 352 993 (36·1%) were male. Over the study period, age and sex standardised incidence rates of any autoimmune diseases increased (IRR 2017-19 vs 2000-02 1·04 [95% CI 1·00-1·09]). The largest increases were seen in coeliac disease (2·19 [2·05-2·35]), Sjogren's syndrome (2·09 [1·84-2·37]), and Graves' disease (2·07 [1·92-2·22]); pernicious anaemia (0·79 [0·72-0·86]) and Hashimoto's thyroiditis (0·81 [0·75-0·86]) significantly decreased in incidence. Together, the 19 autoimmune disorders examined affected 10·2% of the population over the study period (1 912 200 [13·1%] women and 668 264 [7·4%] men). A socioeconomic gradient was evident across several diseases, including pernicious anaemia (most vs least deprived area IRR 1·72 [1·64-1·81]), rheumatoid arthritis (1·52 [1·45-1·59]), Graves' disease (1·36 [1·30-1·43]), and systemic lupus erythematosus (1·35 [1·25-1·46]). Seasonal variations were observed for childhood-onset type 1 diabetes (more commonly diagnosed in winter) and vitiligo (more commonly diagnosed in summer), and regional variations were observed for a range of conditions. Autoimmune disorders were commonly associated with each other, particularly Sjögren's syndrome, systemic lupus erythematosus, and systemic sclerosis. Individuals with childhood-onset type 1 diabetes also had significantly higher rates of Addison's disease (IRR 26·5 [95% CI 17·3-40·7]), coeliac disease (28·4 [25·2-32·0]), and thyroid disease (Hashimoto's thyroiditis 13·3 [11·8-14·9] and Graves' disease 6·7 [5·1-8·5]), and multiple sclerosis had a particularly low rate of co-occurrence with other autoimmune diseases. INTERPRETATION: Autoimmune diseases affect approximately one in ten individuals, and their burden continues to increase over time at varying rates across individual diseases. The socioeconomic, seasonal, and regional disparities observed among several autoimmune disorders in our study suggest environmental factors in disease pathogenesis. The inter-relations between autoimmune diseases are commensurate with shared pathogenetic mechanisms or predisposing factors, particularly among connective tissue diseases and among endocrine diseases. FUNDING: Research Foundation Flanders.
 Spinocerebellar ataxia 38 (SCA 38) is a very rare autosomal dominant inherited disorder caused by a mutation in ELOV5 gene, specifically expressed in cerebellar Purkinje cells, encoding an enzyme involved in the synthesis of fatty acids. Seven symptomatic SCA 38 patients of a Sardinian family were administered 15 sessions of cerebellar anodal transcranial direct current stimulation (tDCS) in a cross-over study, employing deltoid cerebellar-only (C-tDCS) and cerebello-spinal (CS-tDCS) cathodal montage. Clinical evaluation was performed at baseline (T0), after 15 sessions of tDCS (T1) and after 1 month of follow-up (T2). Modified International Cooperative Ataxia Rating Scale (MICARS) and the Robertson dysarthria profile were used to rate ataxic and dysarthric symptoms, respectively. Alertness and split attention tests from Zimmermann test battery for attentional performance were employed to rate attentive functions. Moreover, 3D computerized gait analysis was employed to obtain a quantitative measure of efficacy of tDCS on motor symptoms. While clinical data showed that both CS and C-tDCS improved motor, dysarthric, and cognitive scores, the quantitative analysis of gait revealed significant improvement in spatio-temporal parameters only for C-tDCS treatment. Present findings, yet preliminary and limited by the small size of the tested sample, confirm the therapeutic potential of cerebellar tDCS in improving motor and cognitive symptoms in spinocerebellar ataxias and underline the need to obtain quantitative and objective measures to monitor the efficacy of a therapeutic treatment and to design tailored rehabilitative interventions. ClinicalTrials.gov identifier: NCT05951010.
 OBJECTIVE: To estimate the pooled incidence of Bell's palsy after COVID-19 vaccination. METHODS: PubMed, Scopus, EMBASE, Web of Science, and Google Scholar were searched by 2 independent researchers. We also searched the grey literature including references of the references and conference abstracts. We extracted data regarding the total number of participants, first author, publication year, the country of origin, sex, type of vaccines, and the number of patients who developed Bell's palsy after COVID-19 vaccination. RESULTS: The literature search revealed 370 articles, subsequently deleting duplicates 227 remained. After careful evaluation of the full texts, 20 articles remained for meta-analysis. The most commonly administered vaccines were Pfizer followed by Moderna. In total, 4.54e+07 individuals received vaccines against COVID-19, and 1739 cases developed Bell's palsy. In nine studies, controls (individuals without vaccination) were enrolled. The total number of controls was 1 809 069, of whom 203 developed Bell's palsy. The incidence of Bell's palsy after COVID-19 vaccines was ignorable. The odds of developing Bell's palsy after COVID-19 vaccines was 1.02 (95% CI: 0.79-1.32) (I2 = 74.8%, P < .001). CONCLUSION: The results of this systematic review and meta-analysis show that the incidence of peripheral facial palsy after COVID-19 vaccination is ignorable and vaccination does not increase the risk of developing Bell's palsy. Maybe, Bell's palsy is a presenting symptom of a more severe form of COVID-19, so clinicians must be aware of this.
 OBJECTIVE: Automated brain volumetric analysis based on high-resolution T1-weighted MRI datasets is a frequently used tool in neuroimaging for early detection, diagnosis, and monitoring of various neurological diseases. However, image distortions can corrupt and bias the analysis. The aim of this study was to explore the variability of brain volumetric analysis due to gradient distortions and to investigate the effect of distortion correction methods implemented on commercial scanners. MATERIAL AND METHODS: 36 healthy volunteers underwent brain imaging using a 3T magnetic resonance imaging (MRI) scanner, including a high-resolution 3D T1-weighted sequence. For all participants, each T1-weighted image was reconstructed directly on the vendor workstation with (DC) and without (nDC) distortion correction. For each participant's set of DC and nDC images, FreeSurfer was used for the determination of regional cortical thickness and volume. RESULTS: Overall, significant differences were found in 12 cortical ROIs comparing the volumes of the DC and nDC data and in 19 cortical ROIs comparing the thickness of the DC and nDC data. The most pronounced differences for cortical thickness were found in the precentral gyrus, the lateral occipital and postcentral ROI (2.69, -2.91% and -2.79%, respectively) while cortical volumes differed most prominently in the paracentral, the pericalcarine and lateral occipital ROI (5.52%, -5.40% and -5.11%, respectively). CONCLUSION: Correcting for gradient non-linearities can have significant influence on volumetric analysis of cortical thickness and volume. Since the distortion correction is an automatic feature of the MR scanner, it should be stated by each study that applies volumetric analysis which images were used.
 During human pregnancy, placenta-derived extravillous trophoblasts (EVTs) invade the decidua and communicate with maternal immune cells. The decidua distinguishes into basalis (decB) and parietalis (decP). The latter remains unaffected by EVT invasion. By defining a specific gating strategy, we report the accumulation of macrophages in decB. We describe a decidua basalis-associated macrophage (decBAM) population with a differential transcriptome and secretome compared with decidua parietalis-associated macrophages (decPAMs). decBAMs are CD11c(hi) and efficient inducers of Tregs, proliferate in situ, and secrete high levels of CXCL1, CXCL5, M-CSF, and IL-10. In contrast, decPAMs exert a dendritic cell-like, motile phenotype characterized by induced expression of HLA class II molecules, enhanced phagocytosis, and the ability to activate T cells. Strikingly, EVT-conditioned media convert decPAMs into a decBAM phenotype. These findings assign distinct macrophage phenotypes to decidual areas depending on placentation and further highlight a critical role for EVTs in the induction of decB-associated macrophage polarization.
 Altered RNA metabolism is a common pathogenic mechanism linked to familial and sporadic Amyotrophic lateral sclerosis (ALS). ALS is characterized by mislocalization and aggregation of TDP-43, an RNA-binding protein (RBP) with multiple roles in post-transcriptional RNA processing. Recent studies have identified genetic interactions between TDP-43 and Ataxin-2, a polyglutamine (polyQ) RBP in which intermediate length polyQ expansions confer increased ALS risk. Here, we used live-cell confocal imaging, photobleaching and translation reporter assays to study the localization, transport dynamics and mRNA regulatory functions of TDP-43/Ataxin-2 in rodent primary cortical neurons. We show that Ataxin-2 polyQ expansions aberrantly sequester TDP-43 within ribonucleoprotein (RNP) condensates, and disrupt both its motility along the axon and liquid-like properties. Our data suggest that Ataxin-2 governs motility and translation of neuronal RNP condensates and that Ataxin-2 polyQ expansions fundamentally perturb spatial localization of mRNA and suppress local translation. Overall, these results indicate Ataxin-2 polyQ expansions have detrimental effects on stability, localization, and translation of transcripts critical for axonal and cytoskeletal integrity, particularly important for motor neurons.
 Single-cell transcriptomics allows characterization of cerebrospinal fluid (CSF) cells at an unprecedented level. Here, we report a robust cryopreservation protocol adapted for the characterization of fragile CSF cells by single-cell RNA sequencing (RNA-seq) in moderate- to large-scale studies. Fresh CSF was collected from twenty-one participants at two independent sites. Each CSF sample was split into two fractions: one was processed fresh, while the second was cryopreserved for months and profiled after thawing. B and T cell receptor sequencing was also performed. Our comparison of fresh and cryopreserved data from the same individuals demonstrates highly efficient recovery of all known CSF cell types. We find no significant difference in cell type proportions and cellular transcriptomes between fresh and cryopreserved cells. Results were comparable at both sites and with different single-cell sequencing chemistries. Cryopreservation did not affect recovery of T and B cell clonotype diversity. Our CSF cell cryopreservation protocol provides an important alternative to fresh processing of fragile CSF cells.
 BACKGROUND: Neoehrlichia mikurensis (N. mikurensis) is a newly discovered tick-borne pathogen that can inflict life-threatening illness in immunocompromised patients. N. mikurensis infection is only detectable by polymerase chain reaction (PCR)-based methodologies. We describe three distinct clinical manifestations of N. mikurensis infection (neoehrlichiosis) in Danish patients receiving B-lymphocyte-depleting therapy, rituximab, for underlying hematological, rheumatological, or neurological disorders. All three patients went through a protracted pre-diagnostic period. METHODS: N. mikurensis DNA was detected and confirmed using two methods. Blood was tested by specific real-time PCR targeting the groEL gene and by 16S and 18S profiling followed by sequencing. Bone marrow was analyzed by 16S and 18S profiling. RESULTS: N. mikurensis was detected in blood samples in all three cases and in bone marrow from one of the three. The severity of the symptoms ranged from prolonged fever lasting more than 6 months to life-threatening hyperinflammation in the form of hemophagocytic lymphohistiocytosis (HLH). Interestingly, all patients presented with splenomegaly and two with hepatomegaly. After starting doxycycline therapy, symptoms were relieved within a few days, and biochemistry and organomegaly quickly normalized. CONCLUSION: We present three Danish patients recognized by the same clinician over a period of 6 months, strongly suggesting that many cases are going unrecognized. Second, we describe the first case of N. mikurensis-induced HLH and emphasize the potential severity of undetected neoehrlichiosis.
 Fibrosis is the excessive deposition of extracellular matrix that results from chronic inflammation and injury, leading to the loss of tissue integrity and function. Cadherins are important adhesion molecules that classically mediate calcium-dependent cell-to-cell adhesion and play important roles in tissue development and cellular migration but likely have functions beyond these important roles. Cadherin-11 (CDH11), a member of the cadherin family, has been implicated in several pathological processes including cancer. More recent evidence suggests that CDH11 is a central mediator of tissue fibrosis. CDH11 expression is increased in patients with fibrotic diseases such as idiopathic pulmonary fibrosis and systemic sclerosis. CDH11 expression is increased in mouse models of lung, skin, liver, cardiac, renal, and intestinal fibrosis. Targeting CDH11 in murine models of fibrosis clearly demonstrates that CDH11 is a common mediator of fibrosis across multiple tissues. Insight into potential mechanisms at the cellular and molecular level is emerging. In this review, we present the evolving evidence for the involvement of CDH11 in tissue fibrosis. We also discuss some of the proposed mechanisms and highlight the potential of CDH11 as a common therapeutic target and biomarker in different fibrotic pathologies.
 INTRODUCTION: In 2015/2016, annual national expenditure on neurological conditions exceeded $A3 billion. However, a comprehensive study of the Australian neurological workforce and supply/demand dynamics has not previously been undertaken. METHODS: Current neurological workforce was defined using neurologist survey and other sources. Workforce supply modelling used ordinary differential equations to simulate neurologist influx and attrition. Demand for neurology care was estimated by reference to literature regarding incidence and prevalence of selected conditions. Differences in supply versus demand for neurological workforce were calculated. Potential interventions to increase workforce were simulated and effects on supply versus demand estimated. RESULTS: Modelling of the workforce from 2020 to 2034 predicted an increase in neurologist number from 620 to 89. We estimated a 2034 capacity of 638 024 Initial and 1 269 112 Review encounters annually, and deficits against demand estimated as 197 137 and 881 755, respectively. These deficits were proportionately greater in regional Australia, which has 31% of Australia's population (Australian Bureau of Statistics) but is served by only 4.1% of its neurologists as determined by our 2020 survey of Australia and New Zealand Association of Neurologists members. Nationally, simulated additions to the neurology workforce had some effect on the review encounter supply deficit (37.4%), but in Regional Australia, this impact was only 17.2%. INTERPRETATION: Modelling of the neurologist workforce in Australia for 2020-2034 demonstrates a significant shortfall of supply relative to current and projected demand. Interventions to increase neurologist workforce may attenuate this shortfall but will not eliminate it. Thus, additional interventions are needed, including improved efficiency and additional use of support staff.
 Many cases of aseptic meningitis or meningoencephalitis, unresponsive to antimicrobial treatments, have been reported recently in patients with established/new-onset central nervous system (CNS) inflammatory demyelinating diseases (CNSIDDs). Given the higher probability of infectious etiologies, CNSIDDs are rarely considered among the differentials in meningitis or meningoencephalitis cases. We gathered and tabulated cases of non-infectious, steroid-responsive meningitis or meningoencephalitis associated with neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein-associated disease (MOGAD). This conceptual review highlights the need to bolster routine infectious workups with immunological workups in cases of meningoencephalitis or meningitis where potential autoimmune etiologies can be suspected. Although differentiating CNSIDDs with meningeal involvement from infectious meningitis may not substantially affect acute treatment strategies, long-term management and follow-up of the two are entirely different. We also discuss future research directions and hypotheses on how CNSIDDs may be associated with meningitis-like presentations, e.g. overlapping glial fibrillary acidic protein astrocytopathy or autoimmune encephalitis, alterations in regulatory T-helper cells function, and undetected viral agents.
 BACKGROUND: Parenteral nutrition is commonly used to ensure nutrition support and prevent the harmful effects of malnutrition, which frequently occurs after allogeneic hematopoietic stem cell transplantation (aHSCT). Nevertheless, enteral nutrition supports the restoration of the gut barrier and microbiome as well as protects against infectious complications and acute graft-vs-host disease. Percutaneous endoscopic gastrostomy (PEG) may also be beneficial for gastric decompression and drug administration. METHODS: We performed a retrospective cohort study to evaluate the impact of PEG on treatment outcomes in 75 children who underwent aHSCT with (n = 34) or without (n = 41) PEG from 2005 to 2016. RESULTS: In 34 patients, PEG was used to ensure enteral nutrition support (n = 30), oral drug intake (n = 28), and abdominal decompression (n = 2). During the study period, we observed a beneficial association between PEG placement and transplant-related mortality as well as 5-year overall survival compared with the non-PEG group (12.9% vs 59.0%, P = 0.000; 85.3% vs 35.1%, P = 0.000, respectively). The beneficial impact of PEG was most prominent on 5-year overall survival in older children (12-17 years) with grafts from matched unrelated donors. CONCLUSIONS: PEG placement had a positive association with transplant outcomes in pediatric patients undergoing aHSCT. To confirm these results, larger prospective studies are needed.
 The V57E pathological variant of the mitochondrial coiled-coil-helix-coiled-coil-helix domain-containing protein 10 (CHCHD10) plays a role in frontotemporal dementia. The wild-type and V57E mutant CHCHD10 proteins contain intrinsically disordered regions, and therefore, these regions hampered structural characterization of these proteins using conventional experimental tools. For the first time in the literature, we represent that the V57E mutation is pathogenic to mitochondria as it increases mitochondrial superoxide and impairs mitochondrial respiration. In addition, we represent here the structural ensemble properties of the V57E mutant CHCHD10 and describe the impacts of V57E mutation on the structural ensembles of wild-type CHCHD10 in aqueous solution. We conducted experimental and computational studies for this research. Namely, MitoSOX Red staining and Seahorse Mito Stress experiments, atomic force microscopy measurements, bioinformatics, homology modeling, and multiple-run molecular dynamics simulation computational studies were conducted. Our experiments show that the V57E mutation results in mitochondrial dysfunction, and our computational studies present that the structural ensemble properties of wild-type CHCHD10 are impacted by the frontotemporal dementia-associated V57E genetic mutation.
 Neurofilament light polypeptide (NfL) is a component of the neuronal cytoskeleton and particularly abundant in large-caliber axons. When axonal injury occurs, NfL is released and reaches the cerebrospinal fluid and the blood. Associations between NfL and white matter alterations have previously been observed in studies based on patients with neurological diseases. The current study aimed to explore the relationship between serum NfL (sNfL) and white matter characteristics in a population-based sample. The cross-sectional associations between sNfL as dependent variable, fractional anisotropy (FA), and white matter lesion (WML) volume were analyzed with linear regression models in 307 community-dwelling adults aged between 35 and 65 years. These analyses were repeated with additional adjustment for the potential confounders age, sex, and body mass index (BMI). Longitudinal associations over a mean follow-up of 5.39 years were analyzed with linear mixed models. The unadjusted cross-sectional models yielded significant associations between sNfL, WML volume, and FA, respectively. However, after the adjustment for confounders, these associations did not reach significance. In the longitudinal analyses, the findings corroborated the baseline findings showing no significant associations between sNfL and white matter macrostructure and microstructure beyond the effects of age. In synopsis with previous studies in patients with acute neurological diseases showing a significant association of sNfL with white matter changes beyond the effects of age, the present results based on a sample from the general population suggest the perspective that changes in sNfL reflect age-related effects that also manifest in altered white matter macrostructure and microstructure.
 COVID-19 pandemic has put the protocols and the capacity of our Hospitals to the test. The management of severe patients admitted to the Intensive Care Units has been a challenge for all health systems. To assist in this challenge, various models have been proposed to predict mortality and severity, however, there is no clear consensus for their use. In this work, we took advantage of data obtained from routine blood tests performed on all individuals on the first day of hospitalization. These data has been obtained by standardized cost-effective technique available in all the hospitals. We have analyzed the results of 1082 patients with COVID19 and using artificial intelligence we have generated a predictive model based on data from the first days of admission that predicts the risk of developing severe disease with an AUC = 0.78 and an F1-score = 0.69. Our results show the importance of immature granulocytes and their ratio with Lymphocytes in the disease and present an algorithm based on 5 parameters to identify a severe course. This work highlights the importance of studying routine analytical variables in the early stages of hospital admission and the benefits of applying AI to identify patients who may develop severe disease.
 The vascular niche of malignant gliomas is a key compartment that shapes the immunosuppressive brain tumor microenvironment (TME). The blood-brain-barrier (BBB) consisting of specialized endothelial cells (ECs) and perivascular cells forms a tight anatomical and functional barrier critically controlling transmigration and effector function of immune cells. During neuroinflammation and tumor progression, the metabolism of the essential amino acid tryptophan (Trp) to metabolites such as kynurenine has long been identified as an important metabolic pathway suppressing immune responses. Previous studies have demonstrated that indoleamine-2,3-dioxygenase-1 (IDO1), a key rate-limiting enzyme in tryptophan catabolism, is expressed within the TME of high-grade gliomas. Here, we investigate the role of endothelial IDO1 (eIDO1) expression for brain tumor immunity. Single-cell RNA sequencing data revealed that in human glioma tissue, IDO1 is predominantly expressed by activated ECs showing a JAK/STAT signaling pathway-related CXCL11(+) gene expression signature. In a syngeneic experimental glioma model, eIDO1 is induced by low-dose tumor irradiation. However, cell type-specific ablation of eIDO1 in experimental gliomas did not alter frequency and phenotype of tumor-infiltrating T cells nor tumor growth. Taken together these data argue against a dominant role of eIDO1 for brain tumor immunity.
 Tryptophan (Trp) metabolism has been implicated in neuroinflammatory and neurodegenerative disorders, but its relationship with neuromyelitis optica spectrum disorder (NMOSD) is unclear. In this pilot study, cerebrospinal fluid (CSF) was prospectively collected from 26 NMOSD patients in relapse and 16 controls with noninflammatory diseases and 6 neurometabolites in the tryptophan metabolic pathway, including 5-hydroxytryptamine (5-HT), kynurenine (KYN), melatonin (MLT), 5-hydroxyindoleacetic acid (5HIAA), 3-hydroxy-o-aminobenzoic acid (3-HAA), and kynurenic acid (KYA), were measured by ultrahigh-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). The association of Trp metabolites with NMOSD and its clinical parameters was evaluated. The role of KYN, which is a Trp metabolite involved in the binding of NMOSD-IgG antibody to aquaporin 4 (AQP4), was also evaluated in vitro. CSF KYN was significantly decreased in patients with relapsing NMOSD compared to controls, and CSF KYN was associated with CSF white blood cells in NMOSD. In vitro experiments showed that NMOSD-IgG specifically recognized KYN, which reversed the NMOSD-IgG-induced downregulation of AQP4 expression. Our results show that abnormal Trp metabolism occurs in NMOSD and that KYN might be a potential target for the treatment of AQP4-IgG-positive NMOSD patients.
 Injuries to peripheral nerves are frequent, yet no drug therapies are available for effective nerve repair. The slow growth rate of axons and inadequate access to growth factors challenge natural repair of nerves. A better understanding of the molecules that can promote the rate of axon growth may reveal therapeutic opportunities. Molecular profiling of injured neurons at early intervals of injury, when regeneration is at the maximum, has been the gold standard for exploring growth promoters. A complementary in vitro regenerative priming model was recently shown to induce enhanced outgrowth in adult sensory neurons. In this work, we exploited the in vitro priming model to reveal novel candidates for adult nerve regeneration. We performed a whole-tissue proteomics analysis of the in vitro primed dorsal root ganglia (DRGs) from adult SD rats and compared their molecular profile with that of the in vivo primed, and control DRGs. The proteomics data generated are available via ProteomeXchange with identifier PXD031927. From the follow-up analysis, Bioinformatics interventions, and literature curation, we identified several molecules that were differentially expressed in the primed DRGs with a potential to modulate adult nerve regrowth. We then validated the growth promoting roles of mesencephalic astrocyte-derived neurotrophic factor (MANF), one of the hits we identified, in adult rat sensory neurons. Overall, in this study, we explored two growth priming paradigm and shortlisted several candidates, and validated MANF, as potential targets for adult nerve regeneration. We also demonstrate that the in vitro priming model is a valid tool for adult nerve regeneration studies.
 Osteoarthritis (OA) is a chronic degenerative joint disease characterized by progressive cartilage degradation, synovial membrane inflammation, osteophyte formation, and subchondral bone sclerosis. Pathological changes in cartilage and subchondral bone are the main processes in OA. In recent decades, many studies have demonstrated that activin-like kinase 3 (ALK3), a bone morphogenetic protein receptor, is essential for cartilage formation, osteogenesis, and postnatal skeletal development. Although the role of bone morphogenetic protein (BMP) signalling in articular cartilage and bone has been extensively studied, many new discoveries have been made in recent years around ALK3 targets in articular cartilage, subchondral bone, and the interaction between the two, broadening the original knowledge of the relationship between ALK3 and OA. In this review, we focus on the roles of ALK3 in OA, including cartilage and subchondral bone and related cells. It may be helpful to seek more efficient drugs or treatments for OA based on ALK3 signalling in future.
 PURPOSE: Identifying efficacious measures to characterize dysphonia in complex neurodegenerative diseases is key to optimal assessment and intervention. This study evaluates the validity and sensitivity of acoustic features of phonatory disruption in amyotrophic lateral sclerosis (ALS). METHOD: Forty-nine individuals with ALS (40-79 years old) were audio-recorded while producing a sustained vowel and continuous speech. Perturbation/noise-based (jitter, shimmer, and harmonics-to-noise ratio) and cepstral/spectral (cepstral peak prominence, low-high spectral ratio, and related features) acoustic measures were extracted. The criterion validity of each measure was assessed using correlations with perceptual voice ratings provided by three speech-language pathologists. Diagnostic accuracy of the acoustic features was evaluated using area-under-the-curve analysis. RESULTS: Perturbation/noise-based and cepstral/spectral features extracted from /a/ were significantly correlated with listener ratings of roughness, breathiness, strain, and overall dysphonia. Fewer and smaller correlations between cepstral/spectral measures and perceptual ratings were observed for the continuous speech task, although post hoc analyses revealed stronger correlations in speakers with less perceptually impaired speech. Area-under-the-curve analyses revealed that multiple acoustic features, particularly from the sustained vowel task, adequately differentiated between individuals with ALS with and without perceptually dysphonic voices. CONCLUSIONS: Our findings support using both perturbation/noise-based and cepstral/spectral measures of sustained /a/ to assess phonatory quality in ALS. Results from the continuous speech task suggest that multisubsystem involvement impacts cepstral/spectral analyses in complex motor speech disorders such as ALS. Further investigation of the validity and sensitivity of cepstral/spectral measures during continuous speech in ALS is warranted.
 BACKGROUND: Some oldest-old individuals can maintain superior cognition despite advanced age. Little is known about the neuropathological changes in the brains of oldest-old superior cognitive performers. OBJECTIVE: Our objective was to examine the associations between Alzheimer's disease (AD) and non-AD neuropathologic features in relation to superior cognitive performance in oldest-old individuals. METHODS: We analyzed brain autopsy data from 102 participants with normal cognition from The 90+ Study. Superior global cognitive performers (SGCP) were defined as having Mini-Mental State Examination (MMSE) score ≥28 in the last visit 12 to 2 months before death. To examine the associations between individual and multiple comorbid neuropathologic features with SGCP status we used multiple logistic regression models adjusting for age, sex, and education. RESULTS: Alzheimer's disease neuropathological change (ADNC) and low levels of vascular pathologic change were not associated with superior cognition. In contrast, participants with limbic (OR = 8.37; 95% CI: 1.48-47.44) and neocortical (OR = 10.80;95% CI: 1.03-113.82) Lewy body disease (LBD), or with hippocampal sclerosis (HS) (OR = 5.28; 95% CI: 1.10-25.47) were more likely to be non-SGCP. High total burden of multiple comorbid neuropathologic features was associated with a lower likelihood of being SGCP. CONCLUSION: Oldest-old superior cognitive performers were resilient to ADNC and low levels of vascular pathologic change and were resistant to non-AD neurodegenerative changes and multiple comorbid neuropathologic features. Understanding the factors underlying the ability of superior cognitive performers to resist these changes might provide useful insights on maintenance of superior cognition despite advanced age.
 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by many diverse genetic etiologies. Although therapeutics that specifically target causal mutations may rescue individual types of ALS, such approaches cannot treat most patients since they have unknown genetic etiology. Thus, there is a critical need for therapeutic strategies that rescue multiple forms of ALS. Here, we combine phenotypic chemical screening on a diverse cohort of ALS patient-derived neurons with bioinformatic analysis of large chemical and genetic perturbational datasets to identify broadly effective genetic targets for ALS. We show that suppressing the gene-encoding, spliceosome-associated factor SYF2 alleviates TDP-43 aggregation and mislocalization, improves TDP-43 activity, and rescues C9ORF72 and causes sporadic ALS neuron survival. Moreover, Syf2 suppression ameliorates neurodegeneration, neuromuscular junction loss, and motor dysfunction in TDP-43 mice. Thus, suppression of spliceosome-associated factors such as SYF2 may be a broadly effective therapeutic approach for ALS.
 OBJECTIVES: This study aims to investigate the genome-wide DNA methylation and transcriptome expression profiles of peripheral blood mononuclear cells (PBMCs) in patients with systemic sclerosis (SSc) with interstitial lung disease (ILD), and to analyze the effects of DNA methylation on Wnt/β-catenin and chemokine signaling pathways. METHODS: PBMCs were collected from 19 patients with SSc (SSc group) and 18 healthy persons (control group). Among SSc patients, there were 10 patients with ILD (SSc with ILD subgroup) and 9 patients without ILD (SSc without ILD subgroup). The genome-wide DNA methylation and gene expression level were analyzed by using Illumina 450K methylation chip and Illumina HT-12 v4.0 gene expression profiling chip. The effect of DNA methylation on Wnt/β-catenin and chemokine signal pathways was investigated. RESULTS: Genome-wide DNA methylation analysis identified 71 hypermethylated CpG sites and 98 hypomethylated CpG sites in the SSc with ILD subgroup compared with the SSc without ILD subgroup. Transcriptome analysis distinguished 164 upregulated genes and 191 downregulated genes in the SSc with ILD subgroup as compared with the SSc without ILD subgroup. In PBMCs of the SSc group, 35 genes in Wnt/β-catenin signaling pathway were hypomethylated, while frizzled-1 (FZD1), mitogen-activated protein kinase 9 (MAPK9), mothers against DPP homolog 2 (SMAD2), transcription factor 7-like 2 (TCF7L2), and wingless-type MMTV integration site family, member 5B (WNT5B) mRNA expressions were upregulated as compared with the control group (all P<0.05). Compared with the SSc without ILD subgroup, the mRNA expressions of dickkopf homolog 2 (DKK2), FZD1, MAPK9 were upregulated in the SSc with ILD subgroup, but the differences were not statistically significant (all P>0.05). In PBMCs of the SSc group, 38 genes in chemokine signaling pathway were hypomethylated, while β-arrestin 1 (ARRB1), C-X-C motif chemokine ligand 10 (CXCL10), C-X-C motif chemokine ligand 16 (CXCL16), FGR, and neutrophil cytosolic factor 1C (NCF1C) mRNA expressions were upregulated as compared with the control group (all P<0.05). Compared with the SSc without ILD subgroup, the mRNA expressions of ARRB1, CXCL10, CXCL16 were upregulated in the SSc with ILD subgroup, but the differences were not statistically significant (all P>0.05). CONCLUSIONS: There are differences in DNA methylation and transcriptome profiles between SSc with ILD and SSc without ILD. The expression levels of multiple genes in Wnt/β- catenin and chemokine signaling pathways are upregulated, which might be associatea with the pathogenesis of SSc.
 Aggregation of the RNA-binding protein, TDP-43, is the unifying hallmark of amyotrophic lateral sclerosis and frontotemporal dementia. TDP-43-related neurodegeneration involves multiple changes to normal physiological TDP-43, which undergoes nuclear depletion, cytoplasmic mislocalisation, post-translational modification, and aberrant liquid-liquid phase separation, preceding inclusion formation. Along with toxic cytoplasmic aggregation, concurrent depletion and dysfunction of normal nuclear TDP-43 in cells with TDP-43 pathology is likely a key potentiator of neurodegeneration, but is not well understood. To define processes driving TDP-43 dysfunction, we used CRISPR/Cas9-mediated fluorescent tagging to investigate how disease-associated stressors and pathological TDP-43 alter abundance, localisation, self-assembly, aggregation, solubility, and mobility dynamics of normal nuclear TDP-43 over time in live cells. Oxidative stress stimulated liquid-liquid phase separation of endogenous TDP-43 into droplet-like puncta, or spherical shell-like anisosomes. Further, nuclear RNA-binding-ablated or acetylation-mimicking TDP-43 readily sequestered and depleted free normal nuclear TDP-43 into dynamic anisosomes, in which recruited endogenous TDP-43 proteins remained soluble and highly mobile. Large, phosphorylated inclusions formed by nuclear or cytoplasmic aggregation-prone TDP-43 mutants also caused sequestration, but rendered endogenous TDP-43 immobile and insoluble, indicating pathological transition. These findings suggest that RNA-binding deficiency and post-translational modifications including acetylation exacerbate TDP-43 aggregation and dysfunction by driving sequestration, mislocalisation, and depletion of normal nuclear TDP-43 in neurodegenerative diseases.
 The occurrence of anti-Ku antibody-positive idiopathic inflammatory myopathy (IIM) in pediatric patients is rare, and therefore, the clinical phenotypes of this disease in such patients remain obscure. We herein report two cases of Japanese female pediatric patients with anti-Ku antibody-positive IIM. One case was unique in that it was complicated by pericardial effusion. Another patient had severe and refractory myositis with immune-mediated necrotizing myopathy. In addition, we reviewed literatures involving a total of 11 pediatric patients with anti-Ku antibody-positive IIM. The median age of the patients was 11 years, and most of them were girls. Skin rash, including erythematous nodules, malar rash, multiple brownish plaques, butterfly rash, heliotrope rash, periorbital edema, and Gottron's papules, was observed in 54.5% of the patients, scleroderma in 81.8%, and skin ulcer in 18.2%. Their serum creatine kinase level ranged from 504 to 10,840 IU/L. Furthermore, joint involvement was observed in 91% of the patients, interstitial lung disease in 18.2%, and esophageal involvement in 9.1%. All patients were treated with corticosteroids in combination with immunosuppressants. Pediatric patients with anti-Ku antibody-positive IIM had unique characteristics compared to adult patients. Skin manifestations, joint involvement and elevation of serum CK levels were more common in children than in adults. In contrast, ILD and esophageal involvement were less common in children than in adults. Although pediatric cases of anti-Ku antibody-positive IIM are rare, patients with IIM need to be tested for the presence of anti-Ku antibodies.
 INTRODUCTION: Obesity has been linked to vascular dysfunction, cognitive impairment and neurodegenerative diseases. However, experimental models that recapitulate brain pathology in relation to obesity and vascular dysfunction are still lacking. METHODS: In this study we performed the histological and histochemical characterization of brains from Ldlr-/-.Leiden mice, an established model for obesity and associated vascular disease. First, HFD-fed 18 week-old and 50 week-old Ldlr-/-.Leiden male mice were compared with age-matched C57BL/6J mice. We then assessed the effect of high-fat diet (HFD)-induced obesity on brain pathology in Ldlr-/-.Leiden mice and tested whether a treatment with an anti-complement component 5 antibody, a terminal complement pathway inhibitor recently shown to reduce vascular disease, can attenuate neurodegeneration and neuroinflammation. Histological analyses were complemented with Next Generation Sequencing (NGS) analyses of the hippocampus to unravel molecular pathways underlying brain histopathology. RESULTS: We show that chow-fed Ldlr-/-.Leiden mice have more severe neurodegeneration and show an age-dependent astrogliosis that is not observed in age-matched C57BL/6J controls. This was substantiated by pathway enrichment analysis using the NGS data which showed that oxidative phosphorylation, EIF2 signaling and mitochondrial dysfunction pathways, all associated with neurodegeneration, were significantly altered in the hippocampus of Ldlr-/-.Leiden mice compared with C57BL/6J controls. Obesity-inducing HFD-feeding did not aggravate neurodegeneration and astrogliosis in Ldlr-/-.Leiden mice. However, brains from HFD-fed Ldlr-/-.Leiden mice showed reduced IBA-1 immunoreactivity and increased CD68 immunoreactivity compared with chow-fed Ldlr-/-.Leiden mice, indicating alteration of microglial immunophenotype by HFD feeding. The systemic administration of an anti-C5 treatment partially restored the HFD effect on microglial immunophenotype. In addition, NGS data of hippocampi from Ldlr-/-.Leiden mice showed that HFD feeding affected multiple molecular pathways relative to chow-fed controls: HFD notably inactivated synaptogenesis and activated neuroinflammation pathways. The anti-C5 treatment restored the HFD-induced effect on molecular pathways to a large extent. CONCLUSION: This study shows that the Ldlr-/-.Leiden mouse model is suitable to study brain histopathology and associated biological processes in a context of obesity and provides evidence of the potential therapeutic value of anti-complement therapy against obesity-induced neuroinflammation.
 Cat eye syndrome (CES), also known as Schmid-Fraccaro syndrome, is a complex genetic syndrome with a highly variable phenotype that includes ocular coloboma, anal atresia, preauricular skin tags and pits, heart defects, kidney malformations, dysmorphic facial features, and mild to moderate intellectual disability. We describe a case of a 23-year-old male with a past medical history of CES with short stature, mild learning disability, and some dysmorphic facial features who presented with recurrent pruritus and rashes and had mild liver dysfunction. Furthermore, the patient did not have the classic presentation of CES but a clinically milder expression of the phenotypes. Abnormalities in the abdominal ultrasound prompted an ultrasound-guided liver biopsy, which showed bile ductular proliferation with mild portal inflammation composed of lymphocytes and plasma cells, and bridging fibrosis. The patient's labs showed elevated immunoglobulins with the highest increase observed in IgG, along with negative antinuclear antibodies (ANA), negative anti-mitochondrial antibody, and negative hepatitis A/B/C but a weak positive anti-smooth muscle antibody (ASMA). These findings indicated that the patient most likely had autoimmune hepatitis (AIH) or an overlap syndrome with primary sclerosing cholangitis (PSC). The patient was initially treated with steroids and antihistamines for pruritus, which led to some clinical improvement. After dermatological evaluation, the patient was diagnosed with atopic dermatitis and was recently started on a dupilumab 600 mg loading dose and would continue with biweekly dupilumab 300 mg injections. This dermatological finding may require additional examination and can be a unique presentation in patients with CES. This case illustrates that even patients with milder CES expression can experience intense dermatological complications if not effectively managed. CES is a multifactorial disease that requires intervention from multiple specialists. Therefore, primary care physicians must be aware of the potential complications of CES and make adequate referrals to closely monitor patients' symptoms.
 Unstable DNA repeat expansions and insertions have been found to cause more than 50 neurodevelopmental, neurodegenerative, and neuromuscular disorders. One of the main hallmarks of repeat expansion diseases is the formation of abnormal RNA or protein aggregates in the neuronal cells of affected individuals. Recent evidence indicates that alterations of the dynamic or material properties of biomolecular condensates assembled by liquid/liquid phase separation are critical for the formation of these aggregates. This is a thermodynamically-driven and reversible local phenomenon that condenses macromolecules into liquid-like compartments responsible for compartmentalizing molecules required for vital cellular processes. Disease-associated repeat expansions modulate the phase separation properties of RNAs and proteins, interfering with the composition and/or the material properties of biomolecular condensates and resulting in the formation of abnormal aggregates. Since several repeat expansions have arisen in genes encoding crucial players in transcription, this raises the hypothesis that wide gene expression dysregulation is common to multiple repeat expansion diseases. This review will cover the impact of these mutations in the formation of aberrant aggregates and how they modify gene transcription.
 BACKGROUND: Neuromuscular disease (NMD) research is experiencing tremendous growth as a result of progress in diagnostics and therapeutics yet there continues to be a significant clinical data shortage for these rare diseases. To maximize the development and impact of new therapies, the Muscular Dystrophy Association (MDA) created the neuroMuscular ObserVational Research Data Hub (MOVR) as an observational research study that collects disease-specific measures from individuals living with NMDs in the United States. OBJECTIVE: This manuscript provides a description of MOVR, participants enrolled in MOVR, and longitudinal data availability. METHODS: MOVR collects longitudinal data from individuals diagnosed with ALS, BMD, DMD, FSHD, LGMD, Pompe disease, or SMA, and who are seen for care at a participating MDA Care Center. Data are entered from medical records into standardized electronic case report forms (eCRFs). These eCRFs capture participants' demographics, diagnostic journeys, clinical visits, and discontinuation from the study. RESULTS: From January 2019 to May 2022, MOVR collected data from 50 participating care centers and 1,957 participants. Data from 1,923 participants who participated in MDA's pilot registry were migrated into MOVR, creating a total of 3,880 participants in MOVR. Initial analysis of aggregated data demonstrated that 91% of eCRFs were complete. Forty-three percent of participants had 3 or more encounters and 50% of all encounters were 5 months or less from the previous encounter. DISCUSSION: As a centralized data hub for multiple NMDs, MOVR serves as a platform that can be used to inform disease understanding, guide clinical trial design, and accelerate drug development for NMDs.
 As a novel way for incumbent firms to discover and utilize entrepreneurial opportunities in the digital era, corporate digital entrepreneurship (CDE) is significant for realizing digital transformation through dealing with organizational sclerosis and bureaucratization. Previous studies have identified the variables having positive effects on CDE and put forward practical solutions to promoting CDE. However, the majority of them have ignored the variables having negative effects on CDE and how to mitigate the inhibitory effects. In order to fill the research gap, this study investigates the causal relationship between organizational inertia (OI) and CDE and examines the moderating roles of internal factors such as digital capability (DC) and entrepreneurial culture (EC) as well as external factors such as institutional support (IS) and strategic alliance (SA). Based on multiple linear regression (symmetric) and fuzzy-set qualitative comparative analysis (asymmetric) using survey data from 349 Chinese firms, the results demonstrate that OI has a significant negative effect on CDE. In addition, DC, EC, and SA play negative moderating roles in the relationship between OI and CDE, which means that they could reduce the inhibitory effect derived from OI when incumbent firms implement CDE. Moreover, dividing OI into three dimensions discovers that the moderating roles of DC, EC, and SA present different features. This study enriches the literature on corporate entrepreneurship and provides valuable practical implications for incumbent firms to achieve successful CDE by revealing how to overcome the inertia deeply embedded in organizations.
 p62/Sequestosome-1 (SQSTM1) is a stress-inducible scaffold protein involved in multiple cellular processes, including apoptosis, inflammation, cell survival, and selective autophagy. SQSTM1 mutations are associated with a spectrum of multisystem proteinopathy, including Paget disease of the bone, amyotrophic lateral sclerosis, frontotemporal dementia, and distal myopathy with rimmed vacuoles (MRV). Herein, we report a new phenotype of SQSTM1-associated proteinopathy, a novel frameshift mutation in SQSTM1 causing proximal MRV. A 44-year-old Chinese patient presented with progressive limb-girdle weakness. She had asymmetric proximal limb weakness and myopathic features on electromyography. The magnetic resonance images showed fatty infiltration into muscles, predominantly in the thighs and medial gastrocnemius, sparing the tibialis anterior. Muscle histopathology revealed abnormal protein deposition, p62/SQSTM1-positive inclusions, and rimmed vacuoles. Next-generation sequencing showed a novel pathogenic SQSTM1 frameshift mutation, c.542_549delACAGCCGC (p. H181Lfs(*)66). We expanded the pathogenic genotype of SQSTM1 to include a new, related phenotype: proximal MRV. We suggest that SQSTM1 variations should be screened in cases of proximal MRV.
 Although anion channel activities have been demonstrated in sarcoplasmic reticulum/endoplasmic reticulum (SR/ER), their molecular identities and functions remain unclear. Here, we link rare variants of Chloride Channel CLIC Like 1 (CLCC1) to amyotrophic lateral sclerosis (ALS)-like pathologies. We demonstrate that CLCC1 is a pore-forming component of an ER anion channel and that ALS-associated mutations impair channel conductance. CLCC1 forms homomultimers and its channel activity is inhibited by luminal Ca(2+) but facilitated by phosphatidylinositol 4,5-bisphosphate (PIP2). We identified conserved residues D25 and D181 in CLCC1 N-terminus responsible for Ca(2+) binding and luminal Ca(2+)-mediated inhibition on channel open probability and K298 in CLCC1 intraluminal loop as the critical PIP2-sensing residue. CLCC1 maintains steady-state [Cl(-)](ER) and [K(+)](ER) and ER morphology and regulates ER Ca(2+) homeostasis, including internal Ca(2+) release and steady-state [Ca(2+)](ER). ALS-associated mutant forms of CLCC1 increase steady-state [Cl(-)](ER) and impair ER Ca(2+) homeostasis, and animals with the ALS-associated mutations are sensitized to stress challenge-induced protein misfolding. Phenotypic comparisons of multiple Clcc1 loss-of-function alleles, including ALS-associated mutations, reveal a CLCC1 dosage dependence in the severity of disease phenotypes in vivo. Similar to CLCC1 rare variations dominant in ALS, 10% of K298A heterozygous mice developed ALS-like symptoms, pointing to a mechanism of channelopathy dominant-negatively induced by a loss-of-function mutation. Conditional knockout of Clcc1 cell-autonomously causes motor neuron loss and ER stress, misfolded protein accumulation, and characteristic ALS pathologies in the spinal cord. Thus, our findings support that disruption of ER ion homeostasis maintained by CLCC1 contributes to ALS-like pathologies.
 Telomere length (TL) attrition, epigenetic age acceleration, and mitochondrial DNA copy number (mtDNAcn) decline are established hallmarks of aging. Each has been individually associated with Alzheimer's dementia, cognitive function, and pathologic Alzheimer's disease (AD). Epigenetic age and mtDNAcn have been studied in brain tissue directly but prior work on TL in brain is limited to small sample sizes and most studies have examined leukocyte TL. Importantly, TL, epigenetic age clocks, and mtDNAcn have not been studied jointly in brain tissue from an AD cohort. We examined dorsolateral prefrontal cortex (DLPFC) tissue from N = 367 participants of the Religious Orders Study (ROS) or the Rush Memory and Aging Project (MAP). TL and mtDNAcn were estimated from whole genome sequencing (WGS) data and cortical clock age was computed on 347 CpG sites. We examined dementia, MCI, and level of and change in cognition, pathologic AD, and three quantitative AD traits, as well as measures of other neurodegenerative diseases and cerebrovascular diseases (CVD). We previously showed that mtDNAcn from DLPFC brain tissue was associated with clinical and pathologic features of AD. Here, we show that those associations are independent of TL. We found TL to be associated with β-amyloid levels (beta = - 0.15, p = 0.023), hippocampal sclerosis (OR = 0.56, p = 0.0015) and cerebral atherosclerosis (OR = 1.44, p = 0.0007). We found strong associations between mtDNAcn and clinical measures of AD. The strongest associations with pathologic measures of AD were with cortical clock and there were associations of mtDNAcn with global AD pathology and tau tangles. Of the other pathologic traits, mtDNAcn was associated with hippocampal sclerosis, macroscopic infarctions and CAA and cortical clock was associated with Lewy bodies. Multi-modal age acceleration, accelerated aging on both mtDNAcn and cortical clock, had greater effect size than a single measure alone. These findings highlight for the first time that age acceleration determined on multiple genomic measures, mtDNAcn and cortical clock may have a larger effect on AD/AD related disorders (ADRD) pathogenesis than single measures.
 OBJECTIVE: The Cochin Hand Function Scale (CHFS) is commonly used among people with systemic sclerosis (SSc), including study participants who speak different languages, are of different sexes, or have different disease subtypes. It is not known, however, whether CHFS displays differential item functioning (DIF) and if scores from participants in different groups can be treated equivalently. We evaluated the degree that the CHFS generates scores that are comparable across language, sex, and disease subtype. METHODS: We included participants enrolled in the Scleroderma Patient-centered Intervention Network (SPIN) Cohort who completed the CHFS at their baseline assessment between April 2014 and September 2020. Confirmatory factor analysis (CFA) was used to test unidimensionality, and Multiple Indicator Multiple Cause (MIMIC) models were used for DIF analysis based on language, sex, and disease subtype. Both intraclass correlation coefficient (ICC) and Pearson's correlation were calculated using factor scores obtained from unadjusted and DIF-adjusted MIMIC models to evaluate agreement and correlation between scores. RESULTS: 2155 participants were included. CFA with covarying error terms supported a good fit of the model (χ2[127] =1754.671, P < 0.001, TLI = 0.985, CFI = 0.987, RMSEA = 0.077). Nine items displayed statistically significant DIF for language of administration, 10 items for sex, and 10 items for disease subtype. However, the overall impact of DIF was negligible when comparing factor scores that did and did not account for DIF (ICC= 0.999, r = 0.999). CONCLUSION: The CHFS has score comparability in SSc regardless of participants' language, sex, and disease subtype. This article is protected by copyright. All rights reserved.
 Fibrosis is regulated by interactions between immune and mesenchymal cells. However, the capacity of cell types to modulate human fibrosis pathology is poorly understood due to lack of a fully humanized model system. MISTRG6 mice were engineered by homologous mouse/human gene replacement to develop an immune system like humans when engrafted with human hematopoietic stem cells (HSCs). We utilized MISTRG6 mice to model scleroderma by transplantation of healthy or scleroderma skin from a patient with pansclerotic morphea to humanized mice engrafted with unmatched allogeneic HSC. We identified that scleroderma skin grafts contained both skin and bone marrow-derived human CD4 and CD8 T cells along with human endothelial cells and pericytes. Unlike healthy skin, fibroblasts in scleroderma skin were depleted and replaced by mouse fibroblasts. Furthermore, HSC engraftment alleviated multiple signatures of fibrosis, including expression of collagen and interferon genes, and proliferation and activation of human T cells. Fibrosis improvement correlated with reduced markers of T cell activation and expression of human IL-6 by mesenchymal cells. Mechanistic studies supported a model whereby IL-6 trans-signaling driven by CD4 T cell-derived soluble IL-6 receptor complexed with fibroblast-derived IL-6 promoted excess extracellular matrix gene expression. Thus, MISTRG6 mice transplanted with scleroderma skin demonstrated multiple fibrotic responses centered around human IL-6 signaling, which was improved by the presence of healthy bone marrow-derived immune cells. Our results highlight the importance of IL-6 trans-signaling in pathogenesis of scleroderma and the ability of healthy bone marrow-derived immune cells to mitigate disease.
 BACKGROUND: Case reports suggest that SARS-CoV-2 infection could lead to immune dysregulation and trigger autoimmunity while COVID-19 vaccination is effective against severe COVID-19 outcomes. We aim to examine the association between COVID-19 and development of autoimmune diseases (ADs), and the potential protective effect of COVID-19 vaccination on such an association. METHODS: A retrospective cohort study was conducted in Hong Kong between 1 April 2020 and 15 November 2022. COVID-19 was confirmed by positive polymerase chain reaction or rapid antigen test. Cox proportional hazard regression with inverse probability of treatment weighting was applied to estimate the risk of incident ADs following COVID-19. COVID-19 vaccinated population was compared against COVID-19 unvaccinated population to examine the protective effect of COVID-19 vaccination on new ADs. FINDINGS: The study included 1,028,721 COVID-19 and 3,168,467 non-COVID individuals. Compared with non-COVID controls, patients with COVID-19 presented an increased risk of developing pernicious anaemia [adjusted Hazard Ratio (aHR): 1.72; 95% Confidence Interval (CI): 1.12-2.64]; spondyloarthritis [aHR: 1.32 (95% CI: 1.03-1.69)]; rheumatoid arthritis [aHR: 1.29 (95% CI: 1.09-1.54)]; other autoimmune arthritis [aHR: 1.43 (95% CI: 1.33-1.54)]; psoriasis [aHR: 1.42 (95% CI: 1.13-1.78)]; pemphigoid [aHR: 2.39 (95% CI: 1.83-3.11)]; Graves' disease [aHR: 1.30 (95% CI: 1.10-1.54)]; anti-phospholipid antibody syndrome [aHR: 2.12 (95% CI: 1.47-3.05)]; immune mediated thrombocytopenia [aHR: 2.1 (95% CI: 1.82-2.43)]; multiple sclerosis [aHR: 2.66 (95% CI: 1.17-6.05)]; vasculitis [aHR: 1.46 (95% CI: 1.04-2.04)]. Among COVID-19 patients, completion of two doses of COVID-19 vaccine shows a decreased risk of pemphigoid, Graves' disease, anti-phospholipid antibody syndrome, immune-mediated thrombocytopenia, systemic lupus erythematosus and other autoimmune arthritis. INTERPRETATION: Our findings suggested that COVID-19 is associated with an increased risk of developing various ADs and the risk could be attenuated by COVID-19 vaccination. Future studies investigating pathology and mechanisms would be valuable to interpreting our findings. FUNDING: Supported by RGC Collaborative Research Fund (C7154-20GF).
 BACKGROUND: Although digital mobility outcomes (DMOs) can be readily calculated from real-world data collected with wearable devices and ad-hoc algorithms, technical validation is still required. The aim of this paper is to comparatively assess and validate DMOs estimated using real-world gait data from six different cohorts, focusing on gait sequence detection, foot initial contact detection (ICD), cadence (CAD) and stride length (SL) estimates. METHODS: Twenty healthy older adults, 20 people with Parkinson's disease, 20 with multiple sclerosis, 19 with proximal femoral fracture, 17 with chronic obstructive pulmonary disease and 12 with congestive heart failure were monitored for 2.5 h in the real-world, using a single wearable device worn on the lower back. A reference system combining inertial modules with distance sensors and pressure insoles was used for comparison of DMOs from the single wearable device. We assessed and validated three algorithms for gait sequence detection, four for ICD, three for CAD and four for SL by concurrently comparing their performances (e.g., accuracy, specificity, sensitivity, absolute and relative errors). Additionally, the effects of walking bout (WB) speed and duration on algorithm performance were investigated. RESULTS: We identified two cohort-specific top performing algorithms for gait sequence detection and CAD, and a single best for ICD and SL. Best gait sequence detection algorithms showed good performances (sensitivity > 0.73, positive predictive values > 0.75, specificity > 0.95, accuracy > 0.94). ICD and CAD algorithms presented excellent results, with sensitivity > 0.79, positive predictive values > 0.89 and relative errors < 11% for ICD and < 8.5% for CAD. The best identified SL algorithm showed lower performances than other DMOs (absolute error < 0.21 m). Lower performances across all DMOs were found for the cohort with most severe gait impairments (proximal femoral fracture). Algorithms' performances were lower for short walking bouts; slower gait speeds (< 0.5 m/s) resulted in reduced performance of the CAD and SL algorithms. CONCLUSIONS: Overall, the identified algorithms enabled a robust estimation of key DMOs. Our findings showed that the choice of algorithm for estimation of gait sequence detection and CAD should be cohort-specific (e.g., slow walkers and with gait impairments). Short walking bout length and slow walking speed worsened algorithms' performances. Trial registration ISRCTN - 12246987.
 BACKGROUND AND OBJECTIVES: Acute inflammatory CNS diseases include neuromyelitis optica spectrum disorders (NMOSDs) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Both MOGAD and acute disseminated encephalomyelitis (ADEM) have been reported after vaccination. Consequently, the mass SARS-CoV-2 vaccination program could result in increased rates of these conditions. We described the features of patients presenting with new acute CNS demyelination resembling NMOSDs or MOGAD within 8 weeks of SARS-CoV-2 vaccination. METHODS: The study included a prospective case series of patients referred to highly specialized NMOSD services in the UK from the introduction of SARS-CoV-2 vaccination program up to May 2022. Twenty-five patients presented with new optic neuritis (ON) and/or transverse myelitis (TM) ± other CNS inflammation within 8 weeks of vaccination with either AstraZeneca (ChAdOx1S) or Pfizer (BNT162b2) vaccines. Their clinical records and paraclinical investigations including MRI scans were reviewed. Serologic testing for antibodies to myelin oligodendrocyte glycoprotein (MOG) and aquaporin 4 (AQP4) was performed using live cell-based assays. Patients' outcomes were graded good, moderate, or poor based on the last clinical assessment. RESULTS: Of 25 patients identified (median age 38 years, 14 female), 12 (48%) had MOG antibodies (MOGIgG+), 2 (8%) had aquaporin 4 antibodies (AQP4IgG+), and 11 (44%) had neither. Twelve of 14 (86%) antibody-positive patients received the ChAdOx1S vaccine. MOGIgG+ patients presented most commonly with TM (10/12, 83%), frequently in combination with ADEM-like brain/brainstem lesions (6/12, 50%). Transverse myelitis was longitudinally extensive in 7 of the 10 patients. A peak in new MOGAD cases in Spring 2021 was attributable to postvaccine cases. Both AQP4IgG+ patients presented with brain lesions and TM. Four of 6 (67%) seronegative ChAdOx1S recipients experienced longitudinally extensive TM (LETM) compared with 1 of 5 (20%) of the BNT162b2 group, and facial nerve inflammation was reported only in ChAdOx1S recipients (2/5, 40%). Guillain-Barre syndrome was confirmed in 1 seronegative ChAdOx1S recipient and suspected in another. DISCUSSION: ChAdOx1S was associated with 12/14 antibody-positive cases, the majority MOGAD. MOGAD patients presented atypically, only 2 with isolated ON (1 after BNT162b2 vaccine) but with frequent ADEM-like brain lesions and LETM. Within the seronegative group, phenotypic differences were observed between ChAdOx1S and BNT162b2 recipients. These observations might support a causative role of the ChAdOx1S vaccine in inflammatory CNS disease and particularly MOGAD. Further study of this cohort could provide insights into vaccine-associated immunopathology.
 Myelin is required for the function of neuronal axons in the central nervous system, but the mechanisms that support myelin health are unclear. Although macrophages in the central nervous system have been implicated in myelin health(1), it is unknown which macrophage populations are involved and which aspects they influence. Here we show that resident microglia are crucial for the maintenance of myelin health in adulthood in both mice and humans. We demonstrate that microglia are dispensable for developmental myelin ensheathment. However, they are required for subsequent regulation of myelin growth and associated cognitive function, and for preservation of myelin integrity by preventing its degeneration. We show that loss of myelin health due to the absence of microglia is associated with the appearance of a myelinating oligodendrocyte state with altered lipid metabolism. Moreover, this mechanism is regulated through disruption of the TGFβ1-TGFβR1 axis. Our findings highlight microglia as promising therapeutic targets for conditions in which myelin growth and integrity are dysregulated, such as in ageing and neurodegenerative disease(2,3).
 Cell-cell interactions in the central nervous system play important roles in neurologic diseases. However, little is known about the specific molecular pathways involved, and methods for their systematic identification are limited. Here, we developed a forward genetic screening platform that combines CRISPR-Cas9 perturbations, cell coculture in picoliter droplets, and microfluidic-based fluorescence-activated droplet sorting to identify mechanisms of cell-cell communication. We used SPEAC-seq (systematic perturbation of encapsulated associated cells followed by sequencing), in combination with in vivo genetic perturbations, to identify microglia-produced amphiregulin as a suppressor of disease-promoting astrocyte responses in multiple sclerosis preclinical models and clinical samples. Thus, SPEAC-seq enables the high-throughput systematic identification of cell-cell communication mechanisms.
 Clinical variants of TARDBP are associated with frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and other degenerative diseases. The predicted C. elegans ortholog of TARDBP is encoded by tdp-1 , but functional orthology has not been demonstrated in vivo. We undertook CRISPR/Cas9-based genome editing of the tdp-1 locus to create a complete loss of function allele; all tdp-1 exons and introns were deleted, creating tdp-1(tgx58) , which resulted in neurodegeneration after oxidative stress. Next, we undertook CRISPR-based genome editing to replace tdp-1 exons with human TARDBP coding sequences, creating humanized ( hTARDBP ) C. elegans expressing TDP-43 . Based on the efficiency of this genome editing, we suggest that iterative genome editing of the tdp-1 target locus using linked coCRISPR markers, like dpy-10 , would be a more efficient strategy for sequential assembly of the large engineered transgenes. hTARDBP decreased the neurodegeneration defect of tdp-1(tgx58) , demonstrating functional cross-species orthology. To develop C. elegans models of FTD and ALS, we inserted five different patient TARDBP variants in the C. elegans hTARDBP locus. Only one clinical variant increased stress-induced neurodegeneration; other variants caused inconsistent or negligible defects under these conditions. Combined, this work yielded an unambiguous null allele for tdp-1 , a validated, humanized hTARDBP, and multiple ALS/FTD patient-associated variant models that can be used for future studies.
 The disturbance in mitochondrial functions and homeostasis are the major features of neuron degenerative conditions, like Parkinson's disease, Amyotrophic Lateral Sclerosis, and Alzheimer's disease, along with protein misfolding. The aberrantly folded proteins are known to link with impaired mitochondrial pathways, further contributing to disease pathogenesis. Despite their central significance, the implications of mitochondrial homeostasis disruption on other organelles and cellular processes remain insufficiently explored. Here, we have reviewed the dysfunction in mitochondrial physiology, under neuron degenerating conditions. The disease misfolded proteins impact quality control mechanisms of mitochondria, such as fission, fusion, mitophagy, and proteasomal clearance, to the detriment of neuron. The adversely affected mitochondrial functional roles, like oxidative phosphorylation, calcium homeostasis, and biomolecule synthesis as well as its axes and contacts with endoplasmic reticulum and lysosomes are also discussed. Mitochondria sense and respond to multiple cytotoxic stress to make cell adapt and survive, though chronic dysfunction leads to cell death. Mitochondria and their proteins can be candidates for biomarkers and therapeutic targets. Investigation of internetworking between mitochondria and neurodegeneration proteins can enhance our holistic understanding of such conditions and help in designing more targeted therapies.
 PURPOSE: The purpose of this study was to assess CBCT scans of patients with medication related osteonecrosis of the jaws (MRONJ), osteoradionecrosis (ORN), osteomyelitis (OM) and jaw metastatic disease (JM), evaluate the presence and extent of radiologic findings, identify radiologic parameters that may distinguish the four entities and last, introduce a new modified radiographic index (CRIm), in order to contribute to the diagnosis of these conditions. METHODS: Τwo major databases were retrospectively searched for fully documented and diagnosed CBCT scans of MRONJ, ORN, OM and JM from 2006 to 2019. 335 CBCT scans met the inclusion criteria and were assessed under standardized viewing conditions blindly by 2 observers. The CRIm index proposed in this study evaluates: lytic changes, sclerosis, periosteal bone formation, sequestration, non-healing extraction sockets and other findings which included: sinus implication, inferior alveolar canal implication and jaw fracture. Lytic changes, sclerosis, periosteal bone formation, sequestration and non-healing extraction sockets were scored as: absent (0), localized/single (1) and extensive/multiple (2). Each one of other findings were scored individually as: absent (0) and present (1). For statistical analysis t-test, Pearson's r correlation coefficient, one-way ANOVA and Bonferonni were performed. RESULTS: Extensive lytic changes were the most common finding, especially for ORN, where it occurred in all CBCT scans (100%). The mean value of the CRIm index differs significantly between CBCT scans with MRONJ and JM, as well as between those with OM and JM (Bonferroni p < 0.001). CONCLUSIONS: The new modified Composite Radiographic Index introduced in this study, appears to have improved an objective approach to the previously used Composite Radiographic Index by means of cumulative radiologic features. Τhe predominance of certain radiologic features in one or more of these entities may lead the diagnostician towards the correct diagnosis.
 Background  Articular cartilage (AC) loss and deterioration, as well as bone remodeling, are all symptoms of osteoarthritis (OA). As a result, an ideal imaging technique for researching OA is required, which must be sensitive to both soft tissue and bone health. Objective  The aim of this study was to assess the potential of simultaneous 18F sodium fluoride (18F-NaF) positron emission tomography/magnetic resonance imaging (PET/MRI) to identify as well as classify osseous metabolic abnormalities in knee OA and to see if degenerative changes in the cartilage and bone on MRI might be correlated with subchondral 18F-NaF uptake on PET. Methods  Sixteen (32 knees) volunteers with no past history of knee injury, with or without pain, were enrolled for the research from January to July 2021. The images of both knees were taken utilizing an molecular magnetic resonance (mMR) body matrix coil on a simultaneous PET/MRI biograph mMR. The acquisition was conducted after 45 minutes of intravenous infusion of 18F-NaF 185-370 MBq (5-10 mCi) over one PET bed for 40 minutes, while MRI sequences were performed simultaneously. Results  All pathologies showed significantly higher maximum standardized uptake value (SUV (max) ) than the background. Thirty-four subchondral magic spots were identified on 18F-NaF PET without any structural alteration on MRI. Bone marrow lesions (BMLs) and osteophytes with higher MRI osteoarthritis knee score (MOAKS) score showed higher 18F-NaF uptake (grade1˂grade2˂grade3). BMLs had corresponding AC degeneration. There was discordance between grade 1 osteophytes (86.6%), sclerosis (53.7%) and grade 1 BML in cruciate ligament insertion site (91.66%); they did not have high uptake of 18F-NaF. In case of cartilage, there was significant difference between AC grades and average subchondral SUV (max) and T2* relaxometry (grade0˂grade1˂grade2˂grade3˂grade4). BMLs are much more metabolically active than other pathologies, while sclerosis is the least. We also found that the subchondral uptake was statistically increased in the areas of pathology: Conclusion  18F-NaF PET/MRI was able to detect knee abnormalities unseen on MRI alone and simultaneously assessed metabolic and structural markers of knee OA across multiple tissues in the joint. Thus, it is a promising tool for detection of early metabolic changes in OA.
 Dysosteosclerosis (DSS) refers to skeletal dysplasias that radiographically feature focal appendicular osteosclerosis with variable platyspondyly. Genetic heterogeneity is increasingly reported for the DSS phenotype and now involves mutations of SLC29A3, TNFRSF11A, TCIRG1, LRRK1, and CSF1R. Typical radiological findings are widened radiolucent long bones with thin cortices yet dense irregular metaphyses, flattened vertebral bodies, dense ribs, and multiple fractures. However, the radiographic features of DSS evolve, and the metaphyseal and/or appendicular osteosclerosis variably fades with increasing patient age, likely due to some residual osteoclast function. Fractures are the principal presentation of DSS, and may even occur in infancy with SLC29A3-associated DSS. Cranial base sclerosis can lead to cranial nerve palsies such as optic atrophy, and may be the initial presentation, though not observed with SLC29A3-associated DSS. Gene-specific extra-skeletal features can be the main complication in some forms of DSS such as CSF1R- associated DSS. Further genetic heterogeneity is likely, especially for X-linked recessive DSS and cases currently with an unknown genetic defect. Distinguishing DSS can be challenging due to variable clinical and radiological features and an evolving phenotype. However, defining the DSS phenotype is important for predicting complications, prognosis, and instituting appropriate health surveillance and treatment.
 Single cell RNA sequencing has opened a window into clarifying the complex underpinnings of disease, particularly in quantifying the relevance of tissue- and cell-type-specific gene expression. To identify the cell types and genes important to therapeutic target development across the neurodegenerative disease spectrum, we leveraged genome-wide association studies, recent single cell sequencing data, and bulk expression studies in a diverse series of brain region tissues. We were able to identify significant immune-related cell types in the brain across three major neurodegenerative diseases: Alzheimer's Disease, Amyotrophic Lateral Sclerosis, and Parkinson's Diseases. Subsequently, we identified the major role of 30 fine-mapped loci implicating seven genes in multiple neurodegenerative diseases and their pathogenesis.
 Stress granules are the RNA/protein condensates assembled in the cells under stress. They play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). However, how stress granule assembly is regulated and related to ALS/FTD pathomechanism is incompletely understood. Mutation in the C9orf72 gene is the most common cause of familial ALS and FTD. C9orf72 mutation causes the formation of toxic dipeptide repeats. Here we show that the two most toxic dipeptide repeats [i.e., poly(GR) and poly(PR)] activate c-Jun N-terminal kinase (JNK) via the ER-stress response protein IRE1 using fly and cellular models. Further, we show that activated JNK promotes stress granule assembly in cells by promoting the transcription of one of the key stress granule proteins (i.e., G3BP1) by inducing histone 3 phosphorylation. Consistent with these findings, JNK or IRE1 inhibition reduced stress granule formation, histone 3 phosphorylation, G3BP1 mRNA and protein levels, and neurotoxicity in cells overexpressing poly(GR) and poly(PR) or neurons derived from male and female C9ALS/FTD patient-induced pluripotent stem cells. Our findings connect ER stress, JNK activation, and stress granule assembly in a unified pathway contributing to C9ALS/FTD neurodegeneration.SIGNIFICANCE STATEMENT c-Jun N-terminal kinase (JNK) is a part of the mitogen-activated protein kinase pathway, which is the central node for the integration of multiple stress signals. Cells are under constant stress in neurodegenerative diseases, and how these cells respond to stress signals is a critical factor in determining their survival or death. Previous studies have shown JNK as a major contributor to cellular apoptosis. Here, we show the role of JNK in stress granule assembly. We identify that toxic dipeptide repeats produced in ALS/FTD conditions activate JNK. The activated JNK in the nucleus can induce histone modifications which increase G3BP1 expression, thus promoting stress granule assembly and neurodegeneration.
 RNA-binding proteins (RBPs) have emerged as important players in multiple biological processes including transcription regulation, splicing, R-loop homeostasis, DNA rearrangement, miRNA function, biogenesis, and ribosome biogenesis. A large number of RBPs had already been identified by different approaches in various organisms and exhibited regulatory functions on RNAs' fate. RBPs can either directly or indirectly interact with their target RNAs or mRNAs to assume a key biological function whose outcome may trigger disease or normal biological events. They also exert distinct functions related to their canonical and non-canonical forms. This review summarizes the current understanding of a wide range of RBPs' functions and highlights their emerging roles in the regulation of diverse pathways, different physiological processes, and their molecular links with diseases. Various types of diseases, encompassing colorectal carcinoma, non-small cell lung carcinoma, amyotrophic lateral sclerosis, and Severe acute respiratory syndrome coronavirus 2, aberrantly express RBPs. We also highlight some recent advances in the field that could prompt the development of RBPs-based therapeutic interventions.
 Platform trials allow efficient evaluation of multiple interventions for a specific disease. The HEALEY ALS Platform Trial is testing multiple investigational products in parallel and sequentially in persons with amyotrophic lateral sclerosis (ALS) with the goal of rapidly identifying novel treatments to slow disease progression. Platform trials have considerable operational and statistical efficiencies compared with typical randomized controlled trials due to their use of shared infrastructure and shared control data. We describe the statistical approaches required to achieve the objectives of a platform trial in the context of ALS. This includes following regulatory guidance for the disease area of interest and accounting for potential differences in outcomes of participants within the shared control (potentially due to differences in time of randomization, mode of administration, and eligibility criteria). Within the HEALEY ALS Platform Trial, the complex statistical objectives are met using a Bayesian shared parameter analysis of function and survival. This analysis serves to provide a common integrated estimate of treatment benefit, overall slowing in disease progression, as measured by function and survival while accounting for potential differences in the shared control group using Bayesian hierarchical modeling. Clinical trial simulation is used to provide a better understanding of this novel analysis method and complex design. ANN NEUROL 2023;94:547-560.
 OBJECTIVE: To provide interim advice and considerations to the CF Community around CF nutrition in the current era. METHODS: The Cystic Fibrosis (CF) Foundation organized a multidisciplinary committee to develop a Nutrition Position Paper based on the rapidly changing nutrition landscape in CF, due in part to widespread use of cystic fibrosis transmembrane regulator highly effective modulator therapy (HEMT). Four workgroups were formed: Weight Management, Eating Behavior/Food Insecurity, Salt Homeostasis and Pancreatic Enzyme use. Each workgroup conducted their own focused review of the literature. RESULTS: The committee summarized current understanding of issues pertaining to the four workgroup topics and provided 6 key take-aways around CF Nutrition in the new era. CONCLUSION: People with CF (pwCF) are living longer, particularly with the advent of HEMT. The traditional high fat, high calorie CF diet may have negative nutritional and cardiovascular consequences as pwCF age. Individuals with CF may have poor diet quality, food insecurity, distorted body image, and an higher incidence of eating disorders. An increase in overweight and obesity may lead to new considerations for nutritional management, given potential effects of overnutrition on pulmonary and cardiometabolic parameters.
 BACKGROUND: Regulatory agencies have been responsive to public demand for inclusion of the patient experience in evaluating and approving therapies. Over the years, patient-reported outcome measures (PROMs) have become increasingly prevalent in clinical trial protocols; however, their influence on regulators, payers, clinicians, and patients' decision-making is not always clear. We recently conducted a cross-sectional study aimed at investigating the use of PROMs in new regulatory approvals of drugs for neurological conditions between 2017 and 2022 in Europe. METHODS: We reviewed European Public Assessment Reports (EPARs) and recorded on a predefined data extraction form whether they considered PROMs, their characteristics (e.g., primary/secondary endpoint, generic/specific instrument) and other relevant information (e.g., therapeutic area, generic/biosimilar, orphan status). Results were tabulated and summarized by means of descriptive statistics. RESULTS: Of the 500 EPARs related to authorized medicines between January 2017 and December 2022, 42 (8%) concerned neurological indications. Among the EPARs of these products, 24 (57%) reported any use of PROMs, typically considered as secondary (38%) endpoints. In total, 100 PROMs were identified, of which the most common were the EQ-5D (9%), the SF-36 (6%), or its shorter adaptation SF-12, the PedsQL (4%). CONCLUSIONS: Compared to other disease areas, neurology is one where the use of patient-reported outcomes evidence is inherently part of the clinical evaluation and for which core outcome sets exist. Better harmonization of the instruments recommended for use would facilitate the consideration of PROMs at all stages in the drug development process.
 The mammalian adult brain contains two neural stem and precursor (NPC) niches: the subventricular zone [SVZ] lining the lateral ventricles and the subgranular zone [SGZ] in the hippocampus. From these, SVZ NPCs represent the largest NPC pool. While SGZ NPCs typically only produce neurons and astrocytes, SVZ NPCs produce neurons, astrocytes and oligodendrocytes throughout life. Of particular importance is the generation and replacement of oligodendrocytes, the only myelinating cells of the central nervous system (CNS). SVZ NPCs contribute to myelination by regenerating the parenchymal oligodendrocyte precursor cell (OPC) pool and by differentiating into oligodendrocytes in the developing and demyelinated brain. The neurosphere assay has been widely adopted by the scientific community to facilitate the study of NPCs in vitro. Here, we present a streamlined protocol for culturing postnatal and adult SVZ NPCs and OPCs from primary neurosphere cells. We characterize the purity and differentiation potential as well as provide RNA-sequencing profiles of postnatal SVZ NPCs, postnatal SVZ OPCs and adult SVZ NPCs. We show that primary neurospheres cells generated from postnatal and adult SVZ differentiate into neurons, astrocytes and oligodendrocytes concurrently and at comparable levels. SVZ OPCs are generated by subjecting primary neurosphere cells to OPC growth factors fibroblast growth factor (FGF) and platelet-derived growth factor-AA (PDGF-AA). We further show SVZ OPCs can differentiate into oligodendrocytes in the absence and presence of thyroid hormone T3. Transcriptomic analysis confirmed the identities of each cell population and revealed novel immune and signalling pathways expressed in an age and cell type specific manner.
 PURPOSE: Neuromuscular immune-related adverse events (irAEs) associated with immune checkpoint inhibitors (ICIs) have been increasingly recognized as a consequence of expanding use of ICIs in advanced cancers. We aimed to evaluate the frequency, phenotypes, rescue treatment, and clinical outcomes of severe neuromuscular irAEs of ICIs at National Cancer Center (NCC), Korea. MATERIALS AND METHODS: Consecutive patients with newly developed severe neuromuscular irAEs (common terminology criteria for adverse events grade 3 or greater) after ICI treatment at NCC in Korea between December 2018 and April 2022 were included by searching neuromuscular diagnostic codes in electronic medical records and/or reviewing neurological consultation documentations. RESULTS: Of the 1,503 ICI-treated patients, nine (0.6%) experienced severe neuromuscular irAEs; five with pembrolizumab and four with atezolizumab. The patients included five women and four men; their median age at onset was 59 years. The irAEs included Guillain-Barre syndrome (n = 5) and myasthenia gravis (MG) crisis with myositis (n = 4), and developed after a median of one (range 1-5) ICI cycle. The median modified Rankin score (mRS) was 4 (range 3-5) at the nadir. ICIs were discontinued in all patients, and rescue immunotherapy included corticosteroids (n = 9), intravenous immunoglobulin (n = 7), and plasmapheresis (n = 2). Eight patients showed improvements, with a median mRS of 3 (range 1-4); however, one patient (who had MG crisis with myocarditis) died. CONCLUSIONS: In this real-world monocentric study, ICI-induced neuromuscular irAEs were rare but potentially devastating; thus, physicians should remain vigilant to enable prompt recognition and management of irAEs.
 The olfactory bulb (OB) is one of two regions of the mammalian brain which undergo continuous neuronal replacement during adulthood. A significant fraction of the cells added in adulthood to the bulbar circuitry is constituted by dopaminergic (DA) neurons. We took advantage of a peculiar property of dopaminergic neurons in transgenic mice expressing eGFP under the tyrosine hydroxylase (TH) promoter: while DA neurons located in the glomerular layer (GL) display full electrophysiological maturation, eGFP+ cells in the mitral layer (ML) show characteristics of immature cells. In addition, they also display a lower fluorescence intensity, possibly reflecting different degrees of maturation. To investigate whether this difference in maturation might be confirmed at the gene expression level, we used a fluorescence-activated cell sorting technique on enzymatically dissociated cells of the OB. The cells were divided into two groups based on their level of fluorescence, possibly corresponding to immature ML cells and fully mature DA neurons from the GL. Semiquantitative real-time PCR was performed to detect the level of expression of genes linked to the degree of maturation of DA neurons. We showed that indeed the cells expressing low eGFP fluorescence are immature neurons. Our method can be further used to explore the differences between these two groups of DA neurons.
 Genome-wide studies related to neurological disorders and neurodegenerative diseases have pointed to the role of epigenetic changes such as DNA methylation, histone modification, and noncoding RNAs. DNA methylation machinery controls the dynamic regulation of methylation patterns in discrete brain regions. OBJECTIVE: This review aims to describe the role of DNA methylation in inhibiting and progressing neurological and neurodegenerative disorders and therapeutic approaches. METHODS: A Systematic search of PubMed, Web of Science, and Cochrane Library was conducted for all qualified studies from 2000 to 2022. RESULTS: For the current need of time, we have focused on the DNA methylation role in neurological and neurodegenerative diseases and the expression of genes involved in neurodegeneration such as Alzheimer's, Depression, and Rett Syndrome. Finally, it appears that the various epigenetic changes do not occur separately and that DNA methylation and histone modification changes occur side by side and affect each other. We focused on the role of modification of DNA methylation in several genes associated with depression (NR3C1, NR3C2, CRHR1, SLC6A4, BDNF, and FKBP5), Rett syndrome (MECP2), Alzheimer's, depression (APP, BACE1, BIN1 or ANK1) and Parkinson's disease (SNCA), as well as the co-occurring modifications to histones and expression of non-coding RNAs. Understanding these epigenetic changes and their interactions will lead to better treatment strategies. CONCLUSION: This review captures the state of understanding of the epigenetics of neurological and neurodegenerative diseases. With new epigenetic mechanisms and targets undoubtedly on the horizon, pharmacological modulation and regulation of epigenetic processes in the brain holds great promise for therapy.
 Hereditary transthyretin-related (hATTR) amyloidosis is a rare disease, causing a disabling and life-threatening axonal length-dependent polyneuropathy. Monitoring of disease progression and treatment response is difficult. We aimed to determine if serum neurofilament light chain (sNfL) is a reliable and early biomarker of peripheral neuropathy in hATTR amyloidosis. We prospectively included 20 hATTR patients, 14 symptomatic and 6 asymptomatic. Patients were assessed at baseline and 1 year, including a full clinical examination with disease severity and functional scores, electrochemical skin conductance measurement with Sudoscan and nerve conduction studies, and sNfL level. hATTR patient sNfL were also compared with sNfL of 4532 healthy controls of a reference database by calculating age and BMI-adjusted Z scores. At baseline, median sNfL concentration was 3.6-fold higher in symptomatic than asymptomatic hATTR patients (P = .003), and this difference was also found in our under 60-years-old patients (P = .003). There was no significant difference of sNfL concentration between asymptomatic patients and healthy controls (Z-score of -0.29), but a significant difference between symptomatic patients and healthy controls (Z-score of 2.52). We found a significant correlation between sNfL levels and most clinical and electrophysiological disease severity scores, the strongest correlation being with the NIS score. sNfL seems to be a reliable biomarker of peripheral neuropathy severity in hATTR amyloidosis and can distinguish between asymptomatic and symptomatic patients. sNfL could also become a reliable biomarker to establish disease onset and treatment response.
 Synapse loss correlates with cognitive decline in Alzheimer's disease (AD). Data from mouse models suggests microglia are important for synapse degeneration, but direct human evidence for any glial involvement in synapse removal in human AD remains to be established. Here we observe astrocytes and microglia from human brains contain greater amounts of synaptic protein in AD compared with non-disease controls, and that proximity to amyloid-β plaques and the APOE4 risk gene exacerbate this effect. In culture, mouse and human astrocytes and primary mouse and human microglia phagocytose AD patient-derived synapses more than synapses from controls. Inhibiting interactions of MFG-E8 rescues the elevated engulfment of AD synapses by astrocytes and microglia without affecting control synapse uptake. Thus, AD promotes increased synapse ingestion by human glial cells at least in part via an MFG-E8 opsonophagocytic mechanism with potential for targeted therapeutic manipulation.
 Inflammation and metabolic dysregulations are likely to underlie atypical, energy-related depressive symptoms such as appetite and sleep alterations. Indeed, increased appetite was previously identified as a core symptom of an immunometabolic subtype of depression. The aim of this study was 1) to replicate the associations between individual depressive symptoms and immunometabolic markers, 2) to extend previous findings with additional markers, and 3) to evaluate the relative contribution of these markers to depressive symptoms. We analyzed data from 266 persons with major depressive disorder (MDD) in the last 12 months from the German Health Interview and Examination Survey for Adults and its mental health module. Diagnosis of MDD and individual depressive symptoms were determined by the Composite International Diagnostic Interview. Associations were analyzed using multivariable regression models, adjusting for depression severity, sociodemographic/behavioral variables, and medication use. Increased appetite was associated with higher body mass index (BMI), waist circumference (WC), insulin, and lower high-density lipoprotein. In contrast, decreased appetite was associated with lower BMI, WC, and fewer metabolic syndrome (MetS) components. Insomnia was associated with higher BMI, WC, number of MetS components, triglycerides, insulin, and lower albumin, while hypersomnia was associated with higher insulin. Suicidal ideation was associated with higher number of MetS components, glucose, and insulin. None of the symptoms were associated with C-reactive protein after adjustment. Appetite alterations and insomnia were most important symptoms associated with metabolic markers. Longitudinal studies should investigate whether the candidate symptoms identified here are predicted by or predict the development of metabolic pathology in MDD.
 In this study, we addressed the functional significance of co-operative DNA binding of the cytokine-driven transcription factor STAT1 (signal transducer and activator of transcription 1) in an experimental murine model of acute myocardial infarction (MI). STAT1 knock-in mice expressing a phenylalanine-to-alanine substitution at position 77 in the STAT1 amino-terminal domain were examined for the early clinical effects produced by ligation of the left anterior descending coronary artery (LAD), an established model for MI. The F77A mutation has been previously reported to disrupt amino-terminal interactions between adjacent STAT1 dimers resulting in impaired tetramerization and defective co-operative binding on DNA, while leaving other protein functions unaffected. Our results demonstrate that a loss of STAT1 tetramer stabilization improves survival of adult male mice and ameliorates left ventricular dysfunction in female mice, as determined echocardiographically by an increased ejection fraction and a reduced left intra-ventricular diameter. We found that the ratio of STAT3 to STAT1 protein level was higher in the infarcted tissue in knock-in mice as compared to wild-type (WT) mice, which was accompanied by an enhanced infiltration of immune cells in the infarcted area, as determined by histology. Additionally, RNA sequencing of the infarcted tissue 24 h after LAD ligation revealed an upregulation of inflammatory genes in the knock-in mice, as compared to their WT littermates. Concomitantly, genes involved in oxidative phosphorylation and other metabolic pathways showed a significantly more pronounced downregulation in the infarcted tissue from STAT1(F77A/F77A) mice than in WT animals. Based on these results, we propose that dysfunctional STAT1 signalling owing to a lack of oligomerisation results in a compensatory increase in STAT3 expression and promotes early infiltration of immune cells in the infarcted area, which has beneficial effects on left ventricular remodelling in early MI following LAD ligation.
 BACKGROUND: Genetic variants are considered to have a crucial impact on the occurrence of ischemic stroke. In clinical routine, the diagnostic value of next-generation sequencing (NGS) in the medical clarification of acute juvenile stroke has not been investigated so far. MATERIAL AND METHODS: We analyzed an exome-based gene panel of 349 genes in 172 clinically well-characterized patients with magnetic resonance imaging (MRI)-proven, juvenile (age ≤ 55 years), ischemic stroke admitted to a single comprehensive stroke center. RESULTS: Monogenetic diseases causing ischemic stroke were observed in five patients (2.9%): In three patients with lacunar stroke (1.7%), we identified pathogenic variants in NOTCH3 causing cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Hence, CADASIL was identified at a frequency of 12.5% in the lacunar stroke subgroup. Further, in two male patients (1.2%) suffering from lacunar and cardioembolic stroke, pathogenic variants in GLA causing Fabry's disease were present. Additionally, genetic variants in monogenetic diseases lacking impact on stroke occurrence, variants of unclear significance (VUS) in monogenetic diseases, and (cardiovascular-) risk genes in ischemic stroke were observed in a total of 15 patients (15.7%). CONCLUSION: Genetic screening for Fabry's disease in cardioembolic and lacunar stroke as well as CADASIL in lacunar stroke might be beneficial in routine medical work-up of acute juvenile ischemic stroke.
 Foraging theory prescribes when optimal foragers should leave the current option for more rewarding alternatives. Actual foragers often exploit options longer than prescribed by the theory, but it is unclear how this foraging suboptimality arises. We investigated whether the upregulation of cholinergic, noradrenergic, and dopaminergic systems increases foraging optimality. In a double-blind, between-subject design, participants (N = 160) received placebo, the nicotinic acetylcholine receptor agonist nicotine, a noradrenaline reuptake inhibitor reboxetine, or a preferential dopamine reuptake inhibitor methylphenidate, and played the role of a farmer who collected milk from patches with different yield. Across all groups, participants on average overharvested. While methylphenidate had no effects on this bias, nicotine, and to some extent also reboxetine, significantly reduced deviation from foraging optimality, which resulted in better performance compared to placebo. Concurring with amplified goal-directedness and excluding heuristic explanations, nicotine independently also improved trial initiation and time perception. Our findings elucidate the neurochemical basis of behavioral flexibility and decision optimality and open unique perspectives on psychiatric disorders affecting these functions.
 BACKGROUND AND OBJECTIVES: First-line treatment for trigeminal neuralgia (TN) is limited to carbamazepine and oxcarbazepine, and in refractory cases, alternatives are scarce. Lacosamide has been suggested as a valid option. In this study, we describe a series of patients who received oral lacosamide as treatment for TN after first-line drug failure. METHODS: In this retrospective descriptive cohort study, we included patients with refractory TN who attended a tertiary center between 2015 and 2021 and were prescribed oral lacosamide after first-line treatment failure. The primary endpoints were pain relief and adverse effects. We secondarily analyzed clinical outcomes and compared responders versus nonresponders in the search for potential predictors of response. RESULTS: Eighty-six patients were included (mean age: 62 [SD 15.6] years; 54/86 [63%] female). The TN etiology was secondary in 16/86 (19%) patients. Concomitant continuous pain was present in 29/86 (34%) patients. The mean number of previous treatments was 2.7 [SD 1.5]. Pain relief was achieved in 57/86 (66%) cases, with 28/86 (33%) patients presenting adverse effects, all of which were mild. No statistically significant differences were observed between responders and nonresponders, but subtle clinical differences suggested potential predictors of response. CONCLUSION: Lacosamide may be an effective and relatively safe treatment for refractory pain in TN patients after first-line treatment failure.
 Microbial secondary infections can contribute to an increase in the risk of mortality in COVID-19 patients, particularly in case of severe diseases. In this study, we collected and evaluated the clinical, laboratory and microbiological data of COVID-19 critical ill patients requiring intensive care (ICU) to evaluate the significance and the prognostic value of these parameters. One hundred seventy-eight ICU patients with severe COVID-19, hospitalized at the S. Francesco Hospital of Nuoro (Italy) in the period from March 2020 to May 2021, were enrolled in this study. Clinical data and microbiological results were collected. Blood chemistry parameters, relative to three different time points, were analyzed through multivariate and univariate statistical approaches. Seventy-four percent of the ICU COVID-19 patients had a negative outcome, while 26% had a favorable prognosis. A correlation between the laboratory parameters and days of hospitalization of the patients was observed with significant differences between the two groups. Moreover, Staphylococcus aureus, Enterococcus faecalis, Candida spp, Pseudomonas aeruginosa and Klebsiella pneumoniae were the most frequently isolated microorganisms from all clinical specimens. Secondary infections play an important role in the clinical outcome. The analysis of the blood chemistry tests was found useful in monitoring the progression of COVID-19.
 In preclinical studies rapamycin was found to target neuroinflammation, by expanding regulatory T cells, and affecting autophagy, two pillars of amyotrophic lateral sclerosis (ALS) pathogenesis. Herein we report a multicenter, randomized, double-blind trial, in 63 ALS patients who were randomly assigned in a 1:1:1 ratio to receive rapamycin 2 mg/m(2)/day,1 mg/m(2)/day or placebo (EUDRACT 2016-002399-28; NCT03359538). The primary outcome, the number of patients exhibiting an increase >30% in regulatory T cells from baseline to treatment end, was not attained. Secondary outcomes were changes from baseline of T, B, NK cell subpopulations, inflammasome mRNA expression and activation status, S6-ribosomal protein phosphorylation, neurofilaments; clinical outcome measures of disease progression; survival; safety and quality of life. Of the secondary outcomes, rapamycin decreased mRNA relative expression of the pro-inflammatory cytokine IL-18, reduced plasmatic IL-18 protein, and increased the percentage of classical monocytes and memory switched B cells, although no corrections were applied for multiple tests. In conclusion, we show that rapamycin treatment is well tolerated and provides reassuring safety findings in ALS patients, but further trials are necessary to understand the biological and clinical effects of this drug in ALS.
 OBJECTIVES: Sleep disturbances are increasingly recognized as adversely affecting brain health in aging. Our aim was to investigate interrelations between subjective sleep-related symptoms, obesity, cardiometabolic disorders, brain structure and cognitive decline in a population-based aging sample. METHODS: Data were extracted from the UK Biobank for anthropometric and demographic information, self-reported sleep behaviours, cardiometabolic measures, structural brain magnetic resonance imaging and cognitive test scores. "Sleep-related symptoms" (SRS) were measured using four questionnaire items: loud snoring, daytime sleepiness, likelihood to nap and difficulty getting up in the morning. Associations were tested using a structural equation model (SEM), adjusted for confounders. Further, multiple regression analysis was used to test for direct relationships between SRS and specific cognitive domains. RESULTS: Among 36,468 participants with an average age of 63.6 (SD 7.5) years and 46.7% male, we found that SRS were associated with obesity and several pre-existing cardiometabolic disturbances. In turn, cardiometabolic disorders were associated with increased white matter hyperintensities and cortical thinning, which were related to cognitive dysfunction. SRS were also directly related to several structural brain changes and to cognitive dysfunction. Regression analyses showed that SRS were directly associated with slower reaction times, and lower scores in fluid intelligence, working memory and executive function. CONCLUSIONS: Self-reported sleep-related symptoms were associated with cognitive dysfunction directly and through pre-existing cardiometabolic disorders and brain structural alterations. These findings provide evidence that symptoms of sleep disturbances, here defined primarily by hypersomnolence and snoring, are important risk factors or markers for cognitive dysfunction in an aging population.
 Polyphenols, also known as phenolic compounds, are chemical substances containing aromatic rings as well as at least two hydroxyl groups. Natural phenolic compounds exist widely in plants, which protect plants from ultraviolet radiation and other insults. Phenolic compounds have superior pharmacological and nutritional properties (antimicrobial, antibacterial, antiviral, anti-sclerosis, antioxidant, and anti-inflammatory activities), which have been paid more and more attention by the scientific community. Phenols can protect key cellular components from reactive free radical damage, which is mainly due to their property to activate antioxidant enzymes and alleviate oxidative stress and inflammation. It can also inhibit or isolate reactive oxygen species and transfer electrons to free radicals, thereby avoiding cell damage. It has a regulatory role in glucose metabolism, which has a promising prospect in the prevention and intervention of diabetes. It also prevents cardiovascular disease by regulating blood pressure and blood lipids. Polyphenols can inhibit cell proliferation by affecting Erk1/2, CDK, and PI3K/Akt signaling pathways. Polyphenols can function as enhancers of intrinsic defense systems, including superoxide dismutase (SOD) and glutathione peroxidase (GPX). Simultaneously, they can modulate multiple proteins and transcription factors, making them promising candidates in the investigation of anti-cancer medications. This review focuses on multiple aspects of phenolic substances, including their natural origins, production process, disinfection activity, oxidative and anti-inflammatory functions, and the effects of different phenolic substances on tumors.
 BACKGROUND: Amyotrophic Lateral Sclerosis (ALS) is a heterogeneous neurodegenerative condition featuring variable degrees of motor decline and cognitive impairment. We test the hypothesis that cognitive reserve (CR), defined by occupational histories involving more complex cognitive demands, may protect against cognitive decline, while motor reserve (MR), defined by working jobs requiring complex motor skills, may protect against motor dysfunction. METHODS: Individuals with ALS (n=150) were recruited from the University of Pennsylvania's Comprehensive ALS Clinic. Cognitive performance was evaluated using the Edinburgh Cognitive and Behavioral ALS Screen (ECAS), and motor functioning was measured using Penn Upper Motor Neuron (PUMNS) scale and ALS Functional Rating Scales (ALSFRS-R). The Occupational Information Network (O*NET) Database was used to derive 17 factors representing distinct worker characteristics, occupational requirements, and worker requirements, which were related to ECAS, PUMNS, and ALSFRS-R scores using multiple linear regression. RESULTS: A history of working jobs involving greater reasoning ability (β=2.12, p<.05), social ability (β=1.73, p<.05), analytic skills, (β=3.12, p<.01) and humanities knowledge (β=1.83, p<.01) was associated with better performance on the ECAS, while jobs involving more exposure to environmental hazards (β=-2.57, p<.01) and technical skills (β=-2.16, p<.01) were associated with lower ECAS Total Scores. Jobs involving greater precision skills (β=1.91, p<.05) were associated with greater disease severity on the PUMNS. Findings for the ALSFRS-R did not survive correction for multiple comparisons. DISCUSSION: Jobs requiring greater reasoning abilities, social skills, and humanities knowledge were related to preserved cognitive functioning consistent with CR, while jobs with greater exposure to environmental hazards and technical demands were linked to poorer cognitive functioning. We did not find evidence of MR as no protective effects of occupational skills and requirements were found for motor symptoms, and jobs involving greater precision skills and reasoning abilities were associated with worse motor functioning. Occupational history provides insight into protective and risk factors for variable degrees of cognitive and motor dysfunction in ALS.
 Optineurin is a ubiquitin-binding adaptor protein involved in multiple cellular processes, including innate inflammatory signalling. Mutations in optineurin were found in amyotrophic lateral sclerosis, an adult-onset fatal neurodegenerative disease that targets motor neurons. Neurodegeneration results in generation of neuronal debris, which is primarily cleared by myeloid cells. To assess the role of optineurin in phagocytosis, we performed a flow cytometry-based phagocytic assay of apoptotic neuronal debris and E. coli bioparticles in bone marrow-derived macrophages (BMDMs), and primary neonatal microglia from wild-type (WT) and optineurin-insufficient (Optn(470T)) mice. We found no difference in phagocytosis efficiency and the accompanying cytokine secretion in WT and Optn(470T) BMDMs and microglia. This was true at both steady state and upon proinflammatory polarization with lipopolysaccharide. When we analysed the effect of ageing as a major risk factor for neurodegeneration, we found a substantial decrease in the percentage of phagocytic cells and proinflammatory cytokine secretion in BMDMs from 2-year-old mice. However, this ageing-induced phagocytic decline was unaffected by optineurin insufficiency. All together, these results indicate that ageing is the factor that perturbs normal phagocytosis and proinflammatory cytokine secretion, but that optineurin is dispensable for these processes.
 Evidence showing that the immature brain is vulnerable to seizure-induced damage has been accumulating for decades. Clinical data have always suggested that some early-life seizures are associated with negative sequelae, but clinical observations are frequently obscured by multiple uncontrolled contributing factors and can rarely establish causality. Determining with certainty that seizures, per se, can cause neuronal death and can irreversibly disrupt critical developmental processes, required the development of suitable model systems. Several experimental seizure models clearly show that the immature brain can sustain neuronal injury as a result of uncontrolled seizure activity and that even in the absence of observable neuronal death, the developing brain is selectively vulnerable to interruptions of required growth programs. Severe early-life seizures inhibit DNA, RNA, and protein synthesis, and they can reduce the accumulation of myelin and synaptic markers in the developing nervous system, leading to functional delays in development. Depending on the seizure pathway involved, and the developmental period under study, classic neurodegeneration, excitotoxicity, and apoptosis can result in permanent damage to critical neural networks in the temporal lobe and in many other brain regions. This conclusion is further supported by recent clinical studies showing that prolonged febrile status epilepticus can lead to hippocampal injury, which evolves into hippocampal atrophy and hippocampal sclerosis. A growing body of experimental data demonstrates that the metabolic compromise and cellular loss produced by seizures during critical phases of brain development negatively affect later hippocampal physiology including learning and memory functions in maturity.
 Systemic autoimmune rheumatic diseases (SARDs) are defined by the potential to affect multiple organ systems, and cardiac involvement is a prevalent but often overlooked sequela. Myocardial involvement in SARDs is medicated by macrovascular disease, microvascular dysfunction, and myocarditis. Systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, eosinophilic granulomatosis with polyangiitis, and sarcoidosis are associated with the greatest risk of myocardial damage and heart failure, though myocardial involvement is also seen in other SARDs or their treatments. Management of myocardial involvement should be disease-specific. Further research is required to elucidate targetable mechanisms of myocardial involvement in SARDs.
 Febrile seizures (FSs) are convulsions caused by a sudden increase in body temperature during a fever. FSs are one of the commonest presentations in young children, occurring in up to 4% of children between the ages of about 6 months and 5 years old. FSs not only endanger children's health, cause panic and anxiety to families, but also have many adverse consequences. Both clinical and animal studies show that FSs have detrimental effects on neurodevelopment, that cause attention deficit hyperactivity disorder (ADHD), increased susceptibility to epilepsy, hippocampal sclerosis and cognitive decline during adulthood. However, the mechanisms of FSs in developmental abnormalities and disease occurrence during adulthood have not been determined. This article provides an overview of the association of FSs with neurodevelopmental outcomes, outlining both the underlying mechanisms and the possible appropriate clinical biomarkers, from histological changes to cellular molecular mechanisms. The hippocampus is the brain region most significantly altered after FSs, but the motor cortex and subcortical white matter may also be involved in the development disorders induced by FSs. The occurrence of multiple diseases after FSs may share common mechanisms, and the long-term role of inflammation and γ-aminobutyric acid (GABA) system are currently well studied.
 Protein misfolding diseases (PMDs) in humans are characterized by the deposition of protein aggregates in tissues, including Alzheimer's disease, Parkinson's disease, type 2 diabetes, and amyotrophic lateral sclerosis. Misfolding and aggregation of amyloidogenic proteins play a central role in the onset and progression of PMDs, and these processes are regulated by multiple factors, especially the interaction between proteins and bio-membranes. Bio-membranes induce conformational changes in amyloidogenic proteins and affect their aggregation; on the other hand, the aggregates of amyloidogenic proteins may cause membrane damage or dysfunction leading to cytotoxicity. In this review, we summarize the factors that affect the binding of amyloidogenic proteins and membranes, the effects of bio-membranes on the aggregation of amyloidogenic proteins, mechanisms of membrane disruption by amyloidogenic aggregates, technical approaches for detecting these interactions, and finally therapeutic strategies targeting membrane damage caused by amyloidogenic proteins.
 BACKGROUND Tarlov cysts are rare, with a prevalence of 3.3% in the Asian population, and symptomatic cases are even rarer. Here, we report a case of a young woman with multiple Tarlov cysts presenting in primary care with severe low back pain. CASE REPORT A 23-year-old Malay woman presented to a primary care clinic with sudden-onset, severe, and persistent low back pain for 1 week, affecting her activities of daily living (ADL), especially as a medical student, as she could not stand for more than 10 minutes. There were no other associated symptoms or recent trauma prior to the onset of back pain. Examinations revealed para-vertebrae muscle tenderness and restricted movements at the L4/L5 lumbosacral spine. A plain radiograph of the lumbosacral spine showed sclerosis and erosion of the right pedicle at the L4/L5 levels. Tuberculosis and haematological tests were normal. A lumbosacral MRI of the spine was ordered and the patient was urgently referred to the orthopaedic spine team. The MRI confirmed the diagnosis of multiple Tarlov cysts, with the dominant cyst located at the S2 level. Her symptoms and ADL improved with conservative management. She is being monitored closely by the orthopaedic team and primary care physician. CONCLUSIONS This case highlights red flag symptoms, ie, sudden-onset, severe, and persistent low back pain, that warrant further investigation. Tarlov cysts should be considered as a differential diagnosis. Close monitoring is vital and early surgical intervention is indicated if symptoms worsen, to prevent potential irreversible nerve damage.
 PURPOSE: Identifying relationships between clinical features and quantitative characteristics of the amygdala-hippocampal and thalamic subregions in mesial temporal lobe epilepsy (mTLE) may offer insights into pathophysiology and the basis for imaging prognostic markers of treatment outcome. Our aim was to ascertain different patterns of atrophy or hypertrophy in mesial temporal sclerosis (MTS) patients and their associations with post-surgical seizure outcomes. To assess this aim, this study is designed in 2 folds: (1) hemispheric changes within MTS group and (2) association with postsurgical seizure outcomes. METHODS AND MATERIALS: 27 mTLE subjects with mesial temporal sclerosis (MTS) were scanned for conventional 3D T1w MPRAGE images and T2w scans. With respect to 12 months post-surgical seizure outcomes, 15 subjects reported being seizure free (SF) and 12 reported continued seizures. Quantitative automated segmentation and cortical parcellation were performed using Freesurfer. Automatic labeling and volume estimation of hippocampal subfields, amygdala, and thalamic subnuclei were also performed. The volume ratio (VR) for each label was computed and compared between (1) between contralateral and ipsilateral MTS using Wilcoxon rank-sum test and (2) SF and not seizure free (NSF) groups using linear regression analysis. False Discovery rate (FDR) with significant level of 0.05 were used in both analyses to correct for multiple comparisons. RESULTS: Amygdala: The medial nucleus of the amygdala was the most significantly reduced in patients with continued seizures when compared to patients who remained seizure free. Hippocampus: Comparison of ipsilateral and contralateral volumes with seizure outcomes showed volume loss was most evident in the mesial hippocampal regions such as CA4 and hippocampal fissure. Volume loss was also most explicit in the presubiculum body in patients with continued seizures at the time of their follow-up. Ipsilateral MTS compared to contralateral MTS analysis showed the heads of the ipsilateral subiculum, presubiculum, parasubiculum, dentate gyrus, CA4, and CA3 were more significantly affected than their respective bodies. Volume loss was most noted in mesial hippocampal regions. Thalamus: VPL and PuL were the most significantly reduced thalamic nuclei in NSF patients. In all statistically significant areas, volume reduction was observed in the NSF group. No significant volume reductions were noted in the thalamus and amygdala when comparing ipsilateral to contralateral sides in mTLE subjects. CONCLUSIONS: Varying degrees of volume loss were demonstrated in the hippocampus, thalamus, and amygdala subregions of MTS, especially between patients who remained seizure-free and those who did not. The results obtained can be used to further understand mTLE pathophysiology. CLINICAL RELEVANCE/APPLICATION: In the future, we hope these results can be used to deepen the understanding of mTLE pathophysiology, leading to improved patient outcomes and treatments.
 Cyanobacteria produce a wide range of structurally diverse cyanotoxins and bioactive cyanopeptides in freshwater, marine, and terrestrial ecosystems. The health significance of these metabolites, which include genotoxic- and neurotoxic agents, is confirmed by continued associations between the occurrence of animal and human acute toxic events and, in the long term, by associations between cyanobacteria and neurodegenerative diseases. Major mechanisms related to the neurotoxicity of cyanobacteria compounds include (1) blocking of key proteins and channels; (2) inhibition of essential enzymes in mammalian cells such as protein phosphatases and phosphoprotein phosphatases as well as new molecular targets such as toll-like receptors 4 and 8. One of the widely discussed implicated mechanisms includes a misincorporation of cyanobacterial non-proteogenic amino acids. Recent research provides evidence that non-proteinogenic amino acid BMAA produced by cyanobacteria have multiple effects on translation process and bypasses the proof-reading ability of the aminoacyl-tRNA-synthetase. Aberrant proteins generated by non-canonical translation may be a factor in neuronal death and neurodegeneration. We hypothesize that the production of cyanopeptides and non-canonical amino acids is a more general mechanism, leading to mistranslation, affecting protein homeostasis, and targeting mitochondria in eukaryotic cells. It can be evolutionarily ancient and initially developed to control phytoplankton communities during algal blooms. Outcompeting gut symbiotic microorganisms may lead to dysbiosis, increased gut permeability, a shift in blood-brain-barrier functionality, and eventually, mitochondrial dysfunction in high-energy demanding neurons. A better understanding of the interaction between cyanopeptides metabolism and the nervous system will be crucial to target or to prevent neurodegenerative diseases.
 Biologic therapies targeting B-cells are emerging as an effective strategy to treat a variety of immune-mediated diseases. One of the most studied B-cell-targeted therapies is rituximab, an anti-CD20 monoclonal antibody that exemplifies B-cell depletion therapy and has served as the prototype for other anti-CD20 monoclonal antibodies and the development of biosimilars. While there are multiple studies on the use of rituximab in dermatology, a comprehensive review of rituximab therapy in autoimmune skin conditions is lacking. In this literature review, we summarize indications, treatment efficacy, and safety of rituximab among common autoimmune diseases of the skin: pemphigus vulgaris, cutaneous lupus erythematous, dermatomyositis, systemic sclerosis, thyroid dermopathy, autoimmune pemphigoid diseases, and cutaneous vasculitis diseases. Existing data on rituximab support the approach of rituximab, biosimilars, and newer B-cell-targeting therapies in immune-mediated cutaneous diseases. Overall, rituximab, which targets CD20, provides an effective alternative or concomitant option to traditional immunosuppressants in the management of various autoimmune diseases of the skin. Further studies are necessary to expand the understanding and possible utility of B-cell-targeted therapies among autoimmune skin diseases.
 Objective: Previously, we demonstrated that Amyloid Precursor Protein (APP) contributes to pathology in the SOD1(G93A) mouse model of ALS and that genetic ablation of APP in SOD1(G93A) mice significantly improved multiple disease parameters, including muscle innervation and motor neuron survival. We also observed elevated levels of potentially neurotoxic Aß peptides that have been implicated in Alzheimer's Disease (AD) pathogenesis, within motor neurons and astrocytes in SOD1(G93A) mice. More recently, it has been shown that blocking Aß production improves outcome measures in SOD1(G93A) mice. The cyclodextrin, (2-Hydroxypropyl)-ß-cyclodextrin (HP-β-CD), has previously been shown to deplete intraneuronal unesterified cholesterol, resulting in effective reduction of Aß production and amelioration of disease progression in mouse models of AD and Niemann Pick Type C (NPC) disease. Here, we tested whether HP-β-CD could also improve phenotypic progression in SOD1(G93A) mice. Methods: Pre-symptomatic male SOD1(G93A) mice were randomly assigned to the following treatment groups: HP-β-CD (4000mg/kg, n = 9) or vehicle (saline; n = 10), delivered by weekly subcutaneous injection, commencing at 67 days of age. Longitudinal grip-strength and body mass analysis was performed until late-stage disease (120 days of age), followed by in vivo bilateral isometric muscle tension analysis of tibialis anterior (TA) and extensor digitorum longus (EDL) muscles. Results: HP-β-CD administration had no effect on body mass or grip-strength compared to vehicle treated SOD1(G93A) mice. Similarly, HP-β-CD treatment had no effect on muscle force, contractile properties or motor unit number estimates (MUNE) at late-stage disease in SOD1(G93A) mice. Conclusion: This study shows that HP-β-CD does not confer any therapeutic benefit in SOD1(G93A) mice. However, the absence of detrimental effects is informative, given the common use of cyclodextrins as complexing agents for other pharmaceutical products, their standalone therapeutic potential and the emerging association between dyslipidaemia and ALS progression.
 Neuronal cells are highly functioning but also extremely stress-sensitive cells. By defending the neuronal cells against pathogenic insults, microglial cells, a unique cell type, act as the frontline cavalry in the central nervous system (CNS). Their remarkable and unique ability to self-renew independently after their creation is crucial for maintaining normal brain function and neuroprotection. They have a wide range of molecular sensors that help maintain CNS homeostasis during development and adulthood. Despite being the protector of the CNS, studies have revealed that persistent microglial activation may be the root cause of innumerable neurodegenerative illnesses, including Alzheimer's disease (AD), Parkinson's disease (PD), and Amyotrophic Lateral Sclerosis (ALS). From our vigorous review, we state that there is a possible interlinking between pathways of Endoplasmic reticulum (ER) stress response, inflammation, and oxidative stress resulting in dysregulation of the microglial population, directly influencing the accumulation of pro-inflammatory cytokines, complement factors, free radicals, and nitric oxides leading to cell death via apoptosis. Recent research uses the suppression of these three pathways as a therapeutic approach to prevent neuronal death. Hence, in this review, we have spotlighted the advancement in microglial studies, which focus on their molecular defenses against multiple stresses, and current therapeutic strategies indirectly targeting glial cells for neurodevelopmental diseases.
 In autosomal dominant skin disorders, pronounced mosaic involvement may sometimes occur in the neonate, originating in a heterozygous embryo from early loss of heterozygosity, probably during the first week after fertilization. In biallelic phenotypes, such overlaying mosaic involvement may coexist with disseminated mosaicism, for example, in neurofibromatosis or tuberous sclerosis. In other phenotypes, however, classical nonsegmental involvement tends to appear much later, which is why the superimposed mosaic is a heralding feature. In Brooke-Spiegler syndrome (eccrine cylindromatosis), a large pedigree documented a 5-year-old boy with multiple, congenital small eccrine cylindromas along the lines of Blaschko. Disseminated cylindromas were absent because they usually appear in adulthood. ̶ In Hornstein-Knickenberg syndrome, an affected woman had an 8-year-old son with a nevus comedonicus-like lesion exemplifying a forerunner of the syndrome. ("Birt-Hogg-Dubé syndrome" represents a nonsyndromic type of hereditary perifollicular fibromas.) In glomangiomatosis, neonatal superimposed mosaicism is a heralding feature because disseminated lesions appear during puberty or adulthood. Linear porokeratosis is a harbinger of disseminated porokeratosis that develops 30 or 40 years later. ̶ Cases of superimposed linear Darier disease were forerunners of nonsegmental manifestation. ̶ In a case of Hailey-Hailey disease, neonatal mosaic lesions heralded nonsegmental involvement that began 22 years later.
 Transarterial embolization (TAE) of renal angiomyolipoma (AML) is effective in treating and preventing hemorrhage. We report our experience using EVOH with a single-center retrospective study of all AML embolized with EVOH between June 2013 and March 2022 at the Montpellier University Hospital. A total of 29 embolizations were carried out in 24 consecutive patients (mean age: 53.86 years; 21 women and 3 men) with 25 AMLs for severe bleeding, symptomatic AML, tumor size > 4 cm, or presence of aneurysm(s) > 5 mm. Data collected included imaging and clinical outcomes, tuberous sclerosis complex status, change in AML volume, rebleeding, renal function, volume and concentration of EVOH used, and complications. Out of 29 embolizations performed for 25 AMLs, four were performed in an emergency. Technical success was achieved for 24/25 AMLs. Mean AML volume reduction was 53.59% after a mean follow-up time of 446 days using MRI or CT scan. Aneurysms on angiogram and the symptomatological nature of AML, as well as secondary TAE and multiple arterial pedicles, were statistically associated (p < 0.05). Two patients (8%) underwent nephrectomy after TAE. Four patients had a second embolization. Minor and major complication rates were 12% and 8%, respectively. Neither rebleeding nor renal function impairment was noticed. TAE of AML using EVOH is, thus, highly effective and safe.
 Intrinsically Disordered Proteins (IDPs) play crucial roles in numerous diseases like Alzheimer's and ALS by forming irreversible amyloid fibrils. The effectiveness of force fields (FFs) developed for globular proteins and their modified versions for IDPs varies depending on the specific protein. This study assesses 13 FFs, including AMBER and CHARMM, by simulating the R2 region of the FUS-LC domain (R2-FUS-LC region), an IDP implicated in ALS. Due to the flexibility of the region, we show that utilizing multiple measures, which evaluate the local and global conformations, and combining them together into a final score are important for a comprehensive evaluation of force fields. The results suggest c36m2021s3p with mTIP3p water model is the most balanced FF, capable of generating various conformations compatible with known ones. In addition, the mTIP3P water model is computationally more efficient than those of top-ranked AMBER FFs with four-site water models. The evaluation also reveals that AMBER FFs tend to generate more compact conformations compared to CHARMM FFs but also more non-native contacts. The top-ranking AMBER and CHARMM FFs can reproduce intra-peptide contacts but underperform for inter-peptide contacts, indicating there is room for improvement.
 Accumulation of cytoplasmic inclusions of TAR-DNA binding protein 43 (TDP-43) is seen in both neurons and glia in a range of neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer's disease (AD). Disease progression involves non-cell autonomous interactions among multiple cell types, including neurons, microglia and astrocytes. We investigated the effects in Drosophila of inducible, glial cell type-specific TDP-43 overexpression, a model that causes TDP-43 protein pathology including loss of nuclear TDP-43 and accumulation of cytoplasmic inclusions. We report that TDP-43 pathology in Drosophila is sufficient to cause progressive loss of each of the 5 glial sub-types. But the effects on organismal survival were most pronounced when TDP-43 pathology was induced in the perineural glia (PNG) or astrocytes. In the case of PNG, this effect is not attributable to loss of the glial population, because ablation of these glia by expression of pro-apoptotic reaper expression has relatively little impact on survival. To uncover underlying mechanisms, we used cell-type-specific nuclear RNA sequencing to characterize the transcriptional changes induced by pathological TDP-43 expression. We identified numerous glial cell-type specific transcriptional changes. Notably, SF2/SRSF1 levels were found to be decreased in both PNG and in astrocytes. We found that further knockdown of SF2/SRSF1 in either PNG or astrocytes lessens the detrimental effects of TDP-43 pathology on lifespan, but extends survival of the glial cells. Thus TDP-43 pathology in astrocytes or PNG causes systemic effects that shorten lifespan and SF2/SRSF1 knockdown rescues the loss of these glia, and also reduces their systemic toxicity to the organism.
 Chlamydia is a zoonotic pathogen that mainly infects poultry and pet birds. This Gram-negative obligate intracellular parasite also causes human psittacosis, the severity of which varies from mild flu-like symptoms to life-threatening severe pneumonia, including sepsis, acute respiratory distress syndrome, and multiple organ failure. Inhalation of aerosols from contaminated bird excreta through the respiratory tract is the main route of transmission to humans. Here, we present a case of Chlamydia psittaci pneumonia accompanied by lower extremity atherosclerotic occlusive disease. A 48-year-old man was admitted to the emergency department with a four-day history of cough and dyspnea. A detailed history revealed his contact with domestic pigeons. The results of metagenomic next-generation sequencing of bronchoalveolar lavage fluid suggested C. psittaci infection. Antibacterial agents were switched to targeted doxycycline, but in the next week, skin examination revealed acrocyanosis of both lower extremities, and the remarkable palpable purpura progressively worsened. Re-examination of the lower extremity vascular ultrasound suggested left dorsalis pedis artery occlusion and right peroneal vein thrombosis, which resulted in the amputation of both legs. This case is the first report of C. psittaci pneumonia combined with arterioocclusive sclerosis of both lower extremities.
 Osteoarthritis (OA) is the most common degenerative joint disease affecting the older populations globally. Phosphatidylinositol-4-phosphate 5-kinase type-1 gamma (Pip5k1c), a lipid kinase catalyzing the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2), is involved in various cellular processes, such as focal adhesion (FA) formation, cell migration, and cellular signal transduction. However, whether Pip5k1c plays a role in the pathogenesis of OA remains unclear. Here we show that inducible deletion of Pip5k1c in aggrecan-expressing chondrocytes (cKO) causes multiple spontaneous OA-like lesions, including cartilage degradation, surface fissures, subchondral sclerosis, meniscus deformation, synovial hyperplasia, and osteophyte formation in aged (15-month-old) mice, but not in adult (7-month-old) mice. Pip5k1c loss promotes extracellular matrix (ECM) degradation, chondrocyte hypertrophy and apoptosis, and inhibits chondrocyte proliferation in the articular cartilage of aged mice. Pip5k1c loss dramatically downregulates the expressions of several key FA proteins, including activated integrin β1, talin, and vinculin, and thus impairs the chondrocyte adhesion and spreading on ECM. Collectively, these findings suggest that Pip5k1c expression in chondrocytes plays a critical role in maintaining articular cartilage homeostasis and protecting against age-related OA.
 Neurodegenerative diseases are a serious problem throughout the world. There are several causes of neurodegenerative diseases; these include genetic predisposition, accumulation of misfolded proteins, oxidative stress, neuroinflammation, and excitotoxicity. Oxidative stress increases the production of reactive oxygen species (ROS) that advance lipid peroxidation, DNA damage, and neuroinflammation. The cellular antioxidant system (superoxide dismutase, catalase, peroxidase, and reduced glutathione) plays a crucial role in scavenging free radicals. An imbalance in the defensive actions of antioxidants and overproduction of ROS intensify neurodegeneration. The formation of misfolded proteins, glutamate toxicity, oxidative stress, and cytokine imbalance promote the pathogenesis of Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Antioxidants are now attractive molecules to fight against neurodegeneration. Certain vitamins (A, E, C) and polyphenolic compounds (flavonoids) show excellent antioxidant properties. Diet is the major source of antioxidants. However, diet medicinal herbs are also rich sources of numerous flavonoids. Antioxidants prevent ROS-mediated neuronal degeneration in post-oxidative stress conditions. The present review is focused on the pathogenesis of neurodegenerative diseases and the protective role of antioxidants. KEY TEACHING POINTSThis review shows that multiple factors are directly or indirectly associated with the pathogenesis of neurodegenerative diseases.Failure to cellular antioxidant capacity increases oxidative stress that intensifies neuroinflammation and disease progression.Different vitamins, carotenoids, and flavonoids, having antioxidant capacity, can be considered protective agents.
 Skin carcinomas are the most common form of cancer, and every year thousands of people die from skin cancer-related malignancies. Chronic inflammation is linked to the development and progression of cancer in multiple organ systems - about 20% of all human cancers are a result of chronic inflammation - skin included. While acute inflammation under normal circumstances is a mechanism for host defence and tissue regeneration following insult by trauma or infection by pathogens, over the long term it can drive oncogenic transformation of epithelial cells and promote cancer development, growth and metastasis. Therefore, inflammatory conditions may put individuals at a higher risk to developing skin malignancies. Many skin conditions are characterized by chronic inflammatory processes. These conditions may be particularly susceptible to malignant transformation and predispose patients to develop skin malignancies. As more pathophysiology of chronic inflammatory skin conditions is unveiled, we find that many of these conditions are characterized by immune dysregulation and signalling that result in chronic activation and upregulation of pro-inflammatory chemokines and cytokines, leading to downstream processes that further exacerbate inflammatory processes and cause abnormal cell growth and apoptosis. Here, we review the major chronic cutaneous inflammatory diseases that may have an increased risk of skin malignancies, including atopic dermatitis, psoriasis, discoid lupus erythematosus, lichen planus, hidradenitis suppurativa, prurigo nodularis, lichen sclerosus, systemic sclerosis and morphea, chronic leg ulcers, seborrheic keratoses and basal cell carcinoma. We evaluate the evidence for increased incidence and prevalence, the risk factors associated, the populations at heightened risk and the best management practices.
 Parkinson disease (PD) is closely linked to the misfolding and accumulation of α-synuclein (α-syn) into Lewy bodies. HtrA1 is a PDZ serine protease that degrades fibrillar tau, which is associated with Alzheimer disease (AD). Further, inactivating mutations to mitochondrial HtrA2 have been implicated in PD. Here, we establish that HtrA1 inhibits the aggregation of α-syn as well as FUS and TDP-43, which are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). We demonstrate that the protease domain of HtrA1 is necessary and sufficient for inhibition of aggregation, yet this activity is independent of HtrA1 proteolytic activity. Further, we find that HtrA1 also disaggregates preformed α-syn fibrils, which may promote their clearance. Treatment of α-syn fibrils with HtrA1 renders α-syn incapable of seeding the aggregation of endogenous α-syn in mammalian biosensor cells. We find that HtrA1 remodels α-syn by specifically targeting the NAC domain, which is the key domain that catalyzes α-syn oligomerization and fibrillization. Finally, in a primary neuron model of α-syn aggregation, we show that HtrA1 and its proteolytically inactive form both detoxify α-syn and prevent the formation of hyperphosphorylated α-syn accumulations. Our findings suggest that HtrA1 prevents aggregation and promotes disaggregation of multiple disease-associated proteins, and may be a therapeutic target for treating a range of neurodegenerative disorders.
 Background: Data from published studies about the effect of HFE polymorphisms on ALS risk, phenotype, and survival are still inconclusive. We aimed at evaluating whether the p.H63D polymorphism is a modifier of phenotype and survival in SOD1-mutated patients. Methods: We included 183 SOD1-mutated ALS patients. Mutations were classified as severe or mild according to the median survival of the study population. Patients were screened for the HFE p.H63D polymorphism. Survival was calculated using the Kaplan-Meier modeling, and differences were measured by the log-rank test. Multivariable analysis was performed with the Cox proportional hazards model (stepwise backward). Results: SOD1 severe mutation carriers show more frequent familial history for ALS and shorter survival compared to mild mutation carriers. Carriers and non-carriers of the p.H63D polymorphism did not differ in terms of sex ratio, frequency of positive familial history, age at onset, and bulbar/spinal ratio. In univariate and in Cox multivariable analysis using sex, age at onset, site of onset, family history, country of origin, and mutation severity as covariates, p.H63D carriers had a longer survival (p = 0.034 and p = 0.004). Conclusions: We found that SOD1-mutated ALS patients carrying the p.H63D HFE polymorphism have a longer survival compared to non-carriers, independently of sex, age and site of onset, family history, nation of origin, and severity of mutations, suggesting a possible role as disease progression modifier for the p.H63D HFE polymorphism in SOD1-ALS.
 The etiologies of Parkinson's disease (PD) remain unclear. Some, such as certain genetic mutations and head trauma, are widely known or easily identified. However, these causes or risk factors do not account for the majority of cases. Other, less visible factors must be at play. Among these is a widely used industrial solvent and common environmental contaminant little recognized for its likely role in PD: trichloroethylene (TCE). TCE is a simple, six-atom molecule that can decaffeinate coffee, degrease metal parts, and dry clean clothes. The colorless chemical was first linked to parkinsonism in 1969. Since then, four case studies involving eight individuals have linked occupational exposure to TCE to PD. In addition, a small epidemiological study found that occupational or hobby exposure to the solvent was associated with a 500% increased risk of developing PD. In multiple animal studies, the chemical reproduces the pathological features of PD.Exposure is not confined to those who work with the chemical. TCE pollutes outdoor air, taints groundwater, and contaminates indoor air. The molecule, like radon, evaporates from underlying soil and groundwater and enters homes, workplaces, or schools, often undetected. Despite widespread contamination and increasing industrial, commercial, and military use, clinical investigations of TCE and PD have been limited. Here, through a literature review and seven illustrative cases, we postulate that this ubiquitous chemical is contributing to the global rise of PD and that TCE is one of its invisible and highly preventable causes. Further research is now necessary to examine this hypothesis.
 OBJECTIVES: This Grading of Recommendations Assessment, Development and Evaluation (GRADE) concept article offers systematic reviewers, guideline authors, and other users of evidence assistance in addressing randomized trial situations in which interventions or comparators differ from those in the target people, interventions, comparators, and outcomes. To clarify what GRADE considers under indirectness of interventions and comparators, we focus on a particular example: when comparator arm participants receive some or all aspects of the intervention management strategy (treatment switching). STUDY DESIGN AND SETTING: An interdisciplinary panel of the GRADE working group members developed this concept article through an iterative review of examples in multiple teleconferences, small group sessions, and e-mail correspondence. After presentation at a GRADE working group meeting in November 2022, attendees approved the final concept paper, which we support with examples from systematic reviews and individual trials. RESULTS: In the presence of safeguards against risk of bias, trials provide unbiased estimates of the effect of an intervention on the people as enrolled, the interventions as implemented, the comparators as implemented, and the outcomes as measured. Within the GRADE framework, differences in the people, interventions, comparators, and outcomes elements between the review or guideline recommendation targets and the trials as implemented constitute issues of indirectness. The intervention or comparator group management strategy as implemented, when it differs from the target comparator, constitutes one potential source of indirectness: Indirectness of interventions and comparators-comparator group receipt of the intervention constitutes a specific subcategory of said indirectness. The proportion of comparator arm participants that received the intervention and the apparent magnitude of effect bear on whether one should rate down, and if one does, to what extent. CONCLUSION: Treatment switching and other differences between review or guideline recommendation target interventions and comparators vs. interventions and comparators as implemented in otherwise relevant trials are best considered issues of indirectness.
 Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is rare, poorly understood, with heterogeneous characteristics resulting in difficult diagnosis. We aimed to systematically review evidence of soluble markers in peripheral blood or bronchoalveolar lavage fluid (BALF) as biomarkers in SSc-ILD. METHOD: Five databases were screened for observational or interventional, peer-reviewed studies in adults published between January 2000 and September 2021 that assessed levels of biomarkers in peripheral blood or BALF of SSc-ILD patients compared with healthy controls. Qualitative assessment was performed using Critical Appraisal Skills Programme (CASP) checklists. Standardised mean difference (SMD) in biomarkers were combined in random-effects meta-analyses where multiple independent studies reported quantitative data. RESULTS: 768 published studies were identified; 38 articles were included in the qualitative synthesis. Thirteen studies were included in the meta-analyses representing three biomarkers: KL6, SP-D and IL-8. Greater IL-8 levels were associated with SSc-ILD in both peripheral blood and BALF, overall SMD 0.88 (95% CI 0.61 to 1.15; I(2)=1%). Greater levels of SP-D and KL-6 were both estimated in SSc-ILD peripheral blood compared with healthy controls, at an SMD of 1.78 (95% CI 1.50 to 2.17; I(2)=8%) and 1.66 (95% CI 1.17 to 2.14; I(2)=76%), respectively. CONCLUSION: We provide robust evidence that KL-6, SP-D and IL-8 have the potential to serve as reliable biomarkers in blood/BALF for supporting the diagnosis of SSc-ILD. However, while several other biomarkers have been proposed, the evidence of their independent value in diagnosis and prognosis is currently lacking and needs further investigation. PROSPERO REGISTRATION NUMBER: CRD42021282452.
 The Rho kinase inhibitor fasudil exerts neuroprotective effects. We previously showed that fasudil can regulate M1/M2 microglia polarization and inhibit neuroinflammation. Here, the therapeutic effect of fasudil on cerebral ischemia‑reperfusion (I/R) injury was investigated using the middle cerebral artery occlusion and reperfusion (MCAO/R) model in Sprague‑Dawley rats. The effect of fasudil on the phenotype of microglia and neurotrophic factors in the I/R brain and its potential molecular mechanism was also explored. It was found that fasudil ameliorated neurological deficits, neuronal apoptosis, and inflammatory response in rats with cerebral I/R injury. Fasudil also promoted the polarization of microglia into the M2 phenotype, in turn promoting the secretion of neurotrophic factors. Furthermore, fasudil significantly inhibited the expression of TLR4 and NF‑κB. These findings suggest that fasudil could inhibit the neuroinflammatory response and reduce brain injury after I/R injury by regulating the shift of microglia from an inflammatory M1 phenotype to an anti‑inflammatory M2 phenotype, which may be related to the regulation of the TLR4/ NF‑κB signal pathway.
 INTRODUCTION: The association of myelin oligodendrocyte glycoprotein (MOG) antibody associated disease (MOGAD) and tumors has seldom been reported. We aim to investigate the occurrence of tumors in a cohort of patients with MOGAD and to describe their clinical features, in addition to previously reported cases. METHODS: We retrospectively identified patients with MOGAD (i.e., compatible clinical phenotype and positive MOG antibodies analysed with a live cell-based assay) from 1/1/2015 to 1/1/2023 who had a neoplasm diagnosed within 2  years from MOGAD onset. Furthermore, we performed systematic review of literature to identify previously reported cases. Clinical, paraclinical and oncological findings were collected and reported as median (range) or number (percentage). RESULTS: Two of 150 MOGAD patients (1%) had a concomitant neoplasm in our cohort. Fifteen additional cases were retrieved from literature. Median age was 39 (16-73) years-old, 12 patients were female. ADEM (n = 4;23.5%), encephalomyelitis (n = 3;17.6%), and monolateral optic neuritis (n = 2;11.8%) were the most frequent phenotypes. Median number of treatments was 1 (range 1-4), improvement was reported in 14/17 cases (82.4%). Oncological accompaniments were teratoma (n = 4), CNS (n = 3), melanoma (n = 2), lung (n = 2), hematological (n = 2), ovary (n = 1), breast (n = 1), gastrointestinal (n = 1), and thymic (n = 1) neoplasms. Median time from tumor diagnosis to MOGAD onset was 0 (range - 60 to 20) months. MOG expression in neoplastic tissue was reported in 2/4 patients. Median PNS-CARE score was 3 (range 0-7): 11 patients were classified as "non-PNS," 5 as "possible PNS," and 1 as "probable PNS." DISCUSSION: Our study confirms that MOG is a low-risk antibody for paraneoplastic neurological syndromes and that the clinical presentation and oncological accompaniments are extremely variable. Most of these patients were classified as non-PNS, whereas only a minority was diagnosed with possible/probable PNS, frequently in association with ovarian teratoma. These findings support the notion that MOGAD is not a paraneoplastic disease.
 IMPORTANCE: Systemic inflammation has been suggested to explain reported associations between infections and dementia. Associations between autoimmune diseases and dementia also suggest a role for peripheral systemic inflammation. OBJECTIVE: To investigate the associations of infections and autoimmune diseases with subsequent dementia incidence and to explore potential shared signals presented by the immune system in the 2 conditions. DESIGN, SETTING, AND PARTICIPANTS: This nationwide, population-based, registry-based cohort study was conducted between 1978 and 2018 (40-year study period). All Danish residents born 1928 to 1953, alive and in Denmark on January 1, 1978, and at age 65 years were included. Persons with prior registered dementia and those with HIV infections were excluded. Data were analyzed between May 2022 and January 2023. EXPOSURES: Hospital-diagnosed infections and autoimmune diseases. MAIN OUTCOMES AND MEASURES: All-cause dementia, defined as the date of a first registered dementia diagnosis after age 65 years in the registries. Poisson regression with person-years at risk as an offset variable was used to analyze time to first dementia diagnosis. RESULTS: A total of 1 493 896 individuals (763 987 women [51%]) were followed for 14 093 303 person-years (677 147 [45%] with infections, 127 721 [9%] with autoimmune diseases, and 75 543 [5%] with dementia). Among individuals with infections, 343 504 (51%) were men, whereas among those with autoimmune diseases, 77 466 (61%) were women. The dementia incidence rate ratio (IRR) following any infection was 1.49 (95% CI, 1.47-1.52) and increased along with increasing numbers of infections in a dose-dependent manner. Dementia rates were increased for all infection sites in the short term, but not always in the long term. The dementia IRR following any autoimmune disease was 1.04 (95% CI, 1.01-1.06), but no dose-dependent increase was observed, and only a few autoimmune conditions showed increased IRRs for dementia. CONCLUSIONS AND RELEVANCE: These findings may point toward a role for infection-specific processes in the development of dementia, rather than general systemic inflammation, as previously hypothesized. Assessing these 2 conditions in a single setting may allow for additional insights into their roles in dementia and for hypotheses on possible underlying mechanisms.
 BACKGROUND: High emotional demands at work require sustained emotional effort and are associated with adverse health outcomes. We tested whether individuals in occupations with high emotional demands, compared with low demands, had a higher future risk of all-cause long-term sickness absence (LTSA). We further explored whether the risk of LTSA associated with high emotional demands differed by LTSA diagnoses. METHODS: We conducted a prospective, nationwide cohort study on the association between emotional demands and LTSA (>30 days) in the workforce in Sweden (n = 3 905 685) during a 7-year follow-up. Using Cox regression, we analyzed sex-stratified risks of all-cause and diagnosis-specific LTSA due to common mental disorders (CMD), musculoskeletal disorders (MSD) and all other diagnoses. Multivariable adjusted models included age, birth country, education, living area, family situation and physical work demands. RESULTS: Working in emotionally demanding occupations was associated with a higher risk of all-cause LTSA in women [hazard ratio (HR) = 1.92, 95% confidence interval (CI): 1.88-1.96] and men (HR = 1.23, 95% CI: 1.21-1.25). In women, the higher risk was similar for LTSA due to CMD, MSD and all other diagnoses (HR of 1.82, 1.92 and 1.93, respectively). In men, risk of LTSA due to CMD was pronounced (HR = 2.01, 95% CI: 1.92-2.11), whereas risk of LTSA due to MSD and all other diagnoses was only slightly elevated (HR of 1.13, both outcomes). CONCLUSIONS: Workers in occupations with high emotional demands had a higher risk of all-cause LTSA. In women, risk of all-cause and diagnosis-specific LTSA were similar. In men, the risk was more pronounced for LTSA due to CMD.
 Neuromyelitis optica spectrum disorder (NMOSD) is a rare and severe inflammatory disorder of the central nervous system (CNS). It is strongly associated with anti-aquaporin 4 antibodies (AQP4-IgG), and it mainly affects young women from non-white ethnicities. However, ∼ 5 to 10% of all cases have onset during childhood. Children and adolescents share the same clinical, radiologic, and laboratory presentation as adults. Thus, the same NMOSD diagnostic criteria are also applied to pediatric-onset patients, but data on NMOSD in this population is still scarce. In seronegative pediatric patients, there is a high frequency of the antibody against myelin oligodendrocyte glycoprotein (MOG-IgG) indicating another disease group, but the clinical distinction between these two diseases may be challenging. Three drugs (eculizumab, satralizumab, and inebilizumab) have been recently approved for the treatment of adult patients with AQP4-IgG-positive NMOSD. Only satralizumab has recruited adolescents in one of the two pivotal clinical trials. Additional clinical trials in pediatric NMOSD are urgently required to evaluate the safety and efficacy of these drugs in this population.
 OBJECTIVE: Some individuals with systemic sclerosis (SSc) report positive mental health, despite severe disease manifestations, which may be associated with resilience, but no resilience measure has been validated in SSc. This study was undertaken to assess the validity, reliability, and differential item functioning (DIF) between English- and French-language versions of the 10-item Connor-Davidson Resilience Scale (CD-RISC-10) in SSc. METHODS: Eligible participants were enrolled in the Scleroderma Patient-centered Intervention Network Cohort and completed the CD-RISC-10 between August 2022 and January 2023. We used confirmatory factor analysis (CFA) to evaluate the CD-RISC-10 factor structure and conducted DIF analysis across languages with Multiple Indicators Multiple Causes models. We tested convergent validity with another measure of resilience and measures of self-esteem and depression and anxiety symptoms. We assessed internal consistency and test-retest reliability using Cronbach's alpha and intraclass correlation coefficient (ICC). RESULTS: A total of 962 participants were included in this analysis. CFA supported a single-factor structure (Tucker-Lewis index = 0.99, comparative fit index = 0.99, root mean square error of approximation = 0.08 [90% confidence interval (90% CI) 0.07, 0.09]). We found no meaningful DIF. Internal consistency was high (α = 0.93 [95% CI 0.92, 0.94]), and we found that correlations with other measures of psychological functioning were moderate to large (|r| = 0.57-0.78) and confirmed study hypotheses. The scale showed good 1-2-week test-retest reliability (ICC 0.80 [95% CI 0.75, 0.85]) in a subsample of 230 participants. CONCLUSION: The CD-RISC-10 is a valid and reliable measure of resilience in SSc, with score comparability across English and French versions.
 INTRODUCTION: Hepatic fibrosis is an inevitable process of hepatic sclerosis, malignancy, and insufficiency, and hydronidone is an innovative antifibrosis drug. This study focus on the pharmacokinetic interaction of hydronidone and entecavir in healthy Chinese male subjects. METHODS: An open-label, three-period, multiple-dosage, self-controlled clinical trial was executed in 12 healthy male subjects. In period 1, the subjects took hydronidone 60 mg, q8h, for 7 days. In period 2, they were given entecavir 0.5 mg once daily for 9 days. Then, hydronidone and entecavir were given in combination for 6 days (days 20-26). Blood samples were taken up to 24 h post-dosing, while pre-dose blood samples were drawn on days 7, 19, and 26. RESULTS: The area under the curve (AUC)(0-t_ss) of entecavir slightly increased from 15.56 ± 2.67 to 16.17 ± 2.77 ng h/ml with coadministration with hydronidone, while the other pharmacokinetic parameters of hydronidone and entecavir were comparable between monotherapy and combination therapy. The geometric mean ratios (GMRs) [90% confidence intervals (CIs)] of C(max_ss), AUC(0-t_ss), and AUC(0-∞_ss) of entecavir after coadministration compared with entecavir alone were 107.21% (97.04-118.45%), 103.85% (100.94-106.83%), and 110.81% (97.19-126.33%), respectively. And the GMRs and 90% CIs of C(max,ss), AUC(0-t_ss), and AUC(0-∞_ss) for combination therapy compared with the hydronidone monotherapy group were 102.72% (84.21-125.29%), 106.52% (97.06-116.90%), and 108.86% (96.42-122.89%), respectively. CONCLUSIONS: There was no drug-drug interaction between hydronidone and entecavir in healthy male volunteers. However, multiple doses of hydronidone have a risk with increasing exposure to entecavir in vivo, which needs to be further clarified. REGISTRATION NUMBER: ChiCTR2200059683 (retrospectively registered).
 BACKGROUND: Amyotrophic lateral sclerosis (ALS) is currently an incurable and fatal disease, which often comes with a high symptom burden at the end-of-life stage. Little is known about nurses' experiences in this context. OBJECTIVE: To explore the experience of nurses caring for people with ALS at end-of-life. DESIGN: A qualitative multiple-case study design. METHOD: Individual semi-structured interviews were conducted between February and August 2022 with nurses from Quebec, Canada, who had provided care to at least one person living with ALS at the end-of-life in the past 12 months. The content analysis method was used for data analysis and within-case and cross-case analyses were conducted, as well as comparative analyses according to the type of position held by the participants that determined the cases: (1) home care, (2) hospital and (3) palliative care home. RESULTS: Participating in the study were 24 nurses: 9 were from home care, 8 from hospitals and 7 from palliative care homes. Five main themes were identified: (1) identifying the end-of-life period, (2) communication issues, (3) supporting the need for control, (4) accompanying in the fight culture and (5) the extent of the need for care. A sixth theme was also added in order to report the need expressed by nurses to improve their care of patients living with ALS at end-of-life. CONCLUSIONS: Although nurses' experiences varied among the different settings, the study identifies the pressing need for better education and, above all, more resources when caring for a person living with ALS at end-of-life. Future research should explore the experiences of other members of the healthcare team and test interventions designed to improve the quality of life and end-of-life of people living with ALS.
 Systemic sclerosis (SSc) is a clinically heterogeneous fibrotic disease with no effective treatment. Myofibroblasts are responsible for unresolving synchronous skin and internal organ fibrosis in SSc, but the drivers of sustained myofibroblast activation remain poorly understood. Using unbiased transcriptome analysis of skin biopsies, we identified the downregulation of SPAG17 in multiple independent cohorts of patients with SSc, and by orthogonal approaches, we observed a significant negative correlation between SPAG17 and fibrotic gene expression. Fibroblasts and endothelial cells explanted from SSc skin biopsies showed reduced chromatin accessibility at the SPAG17 locus. Remarkably, mice lacking Spag17 showed spontaneous skin fibrosis with increased dermal thickness, collagen deposition and stiffness, and altered collagen fiber alignment. Knockdown of SPAG17 in human and mouse fibroblasts and microvascular endothelial cells was accompanied by spontaneous myofibroblast transformation and markedly heightened sensitivity to profibrotic stimuli. These responses were accompanied by constitutive TGF-β pathway activation. Thus, we discovered impaired expression of SPAG17 in SSc and identified, to our knowledge, a previously unreported cell-intrinsic role for SPAG17 in the negative regulation of fibrotic responses. These findings shed fresh light on the pathogenesis of SSc and may inform the search for innovative therapies for SSc and other fibrotic conditions through SPAG17 signaling.
 OBJECTIVE: Obesity and nutrient oversupply increase mammalian target of rapamycin (mTOR) signaling in multiple cell types and organs, contributing to the onset of insulin resistance and complications of metabolic disease. However, it remains unclear when and where mTOR activation mediates these effects, limiting options for therapeutic intervention. The objective of this study was to isolate the role of constitutive mTOR activation in Nav1.8-expressing peripheral neurons in the onset of diet-induced obesity, bone loss, and metabolic disease. METHODS: In humans, loss of function mutations in tuberous sclerosis complex 2 (TSC2) lead to maximal constitutive activation of mTOR. To mirror this in mice, we bred Nav1.8-Cre with TSC2(fl/fl) animals to conditionally delete TSC2 in Nav1.8-expressing neurons. Male and female mice were studied from 4- to 34-weeks of age and a subset of animals were fed a high-fat diet (HFD) for 24-weeks. Assays of metabolism, body composition, bone morphology, and behavior were performed. RESULTS: By lineage tracing, Nav1.8-Cre targeted peripheral sensory neurons, a subpopulation of postganglionic sympathetics, and several regions of the brain. Conditional knockout of TSC2 in Nav1.8-expressing neurons (Nav1.8-TSC2(KO)) selectively upregulated neuronal mTORC1 signaling. Male, but not female, Nav1.8-TSC2(KO) mice had a 4-10% decrease in body size at baseline. When challenged with HFD, both male and female Nav1.8-TSC2(KO) mice resisted diet-induced gains in body mass. However, this did not protect against HFD-induced metabolic dysfunction and bone loss. In addition, despite not gaining weight, Nav1.8-TSC2(KO) mice fed HFD still developed high body fat, a unique phenotype previously referred to as 'normal weight obesity'. Nav1.8-TSC2(KO) mice also had signs of chronic itch, mild increases in anxiety-like behavior, and sex-specific alterations in HFD-induced fat distribution that led to enhanced visceral obesity in males and preferential deposition of subcutaneous fat in females. CONCLUSIONS: Knockout of TSC2 in Nav1.8+ neurons increases itch- and anxiety-like behaviors and substantially modifies fat storage and metabolic responses to HFD. Though this prevents HFD-induced weight gain, it masks depot-specific fat expansion and persistent detrimental effects on metabolic health and peripheral organs such as bone, mimicking the 'normal weight obesity' phenotype that is of growing concern. This supports a mechanism by which increased neuronal mTOR signaling can predispose to altered adipose tissue distribution, adipose tissue expansion, impaired peripheral metabolism, and detrimental changes to skeletal health with HFD - despite resistance to weight gain.
 BACKGROUND AND PURPOSE: Spatial registration is crucial in establishing correspondence between anatomic brain regions for research and clinical purposes. The insular cortex (IC) and gyri (IG) are implicated in various functions and pathologies including epilepsy. Optimizing registration of the insula to a common atlas can improve the accuracy of group-level analyses. Here, we compared six nonlinear, one linear, and one semiautomated registration algorithms (RAs) for registering the IC and IG to the Montreal Neurologic Institute standard space (MNI152). METHODS: 3T images acquired from 20 controls and 20 temporal lobe epilepsy patients with mesial temporal sclerosis underwent automated segmentation of the insula. This was followed by manual segmentation of the entire IC and six individual IGs. Consensus segmentations were created at 75% agreement for IC and IG before undergoing registration to MNI152 space with eight RAs. Dice similarity coefficients (DSCs) were calculated between segmentations after registration and the IC and IG in MNI152 space. Statistical analysis involved the Kruskal-Wallace test with Dunn's test for IC and two-way analysis of variance with Tukey's honest significant difference test for IG. RESULTS: DSCs were significantly different between RAs. Based on multiple pairwise comparisons, we report that certain RAs performed better than others across population groups. Additionally, registration performance differed according to specific IG. CONCLUSION: We compared different methods for registering the IC and IG to MNI152 space. We found differences in performance between RAs, which suggests that algorithm choice is important factor in analyses involving the insula.
 OBJECTIVES: SSc is an autoimmune disease characterized by excessive fibrosis in multiple organs, including the gastrointestinal (GI) tract. GI symptoms of SSc such as intestinal pseudo-obstruction (IPO) are often refractory to conventional intervention and can result in longer in-hospital stay or even increased mortality. We aimed to summarize the insights to date regarding the efficacy of IVIG against GI symptoms of SSc to unveil what we should focus on in future studies. METHODS: Herein we report the response of GI symptoms in three cases with SSc-myositis overlap who received IVIG administration. We also conducted a systematic literature review to summarize previous reports regarding the efficacy of IVIG upon the GI manifestations of SSc, according to the PRISMA 2020 guideline. RESULTS: The case series demonstrated remarkable and rapid improvement of GI symptoms, including IPO, after IVIG administration. The literature review revealed that previous reports also support the efficacy and safety of IVIG against GI manifestations of SSc. However, they were all retrospective studies and lacking description of the short-term outcome after IVIG administration with objective and quantitative metrics. CONCLUSION: IVIG seems to be a promising therapeutic option for the management of GI symptoms in SSc, including IPO. Investigators should focus more on short-term outcomes to properly assess the therapeutic benefit of IVIG, ideally using reliable quantitative measures in a multicentre randomized placebo-controlled setting.
 OBJECTIVE: Tuberous sclerosis complex (TSC) is a neurodevelopmental disorder caused by autosomal-dominant pathogenic variants in either the TSC1 or TSC2 gene, and it is characterized by hamartomas in multiple organs, such as skin, kidney, lung, and brain. These changes can result in epilepsy, learning disabilities, and behavioral complications, among others. The mechanistic link between TSC and the mechanistic target of the rapamycin (mTOR) pathway is well established, thus mTOR inhibitors can potentially be used to treat the clinical manifestations of the disorder, including epilepsy. METHODS: In this study, we tested the efficacy of a novel mTOR catalytic inhibitor (here named Tool Compound 1 or TC1) previously reported to be more brain-penetrant compared with other mTOR inhibitors. Using a well-characterized hypomorphic Tsc2 mouse model, which displays a translationally relevant seizure phenotype, we tested the efficacy of TC1. RESULTS: Our results show that chronic treatment with this novel mTOR catalytic inhibitor (TC1), which affects both the mTORC1 and mTORC2 signaling complexes, reduces seizure burden, and extends the survival of Tsc2 hypomorphic mice, restoring species typical weight gain over development. INTERPRETATION: Novel mTOR catalytic inhibitor TC1 exhibits a promising therapeutic option in the treatment of TSC.
 Localized scleroderma is a complex autoimmune disease characterized by dermal fibrosis and loss of cutaneous fat. While cytotherapy offers a promising treatment option, stem cell transplantation results in low survival rates and fails in target cell differentiation. In this study, we aimed to prefabricate syngeneic adipose organoids (ad-organoids) using microvascular fragments (MVFs) via three-dimensional (3D) culturing and transplant them beneath the fibrotic skin to restore subcutaneous fat and reverse the pathological manifestation of localized scleroderma. We employed 3D culturing of syngeneic MVFs with stepwise angiogenic and adipogenic induction to produce ad-organoids and evaluated their microstructure and paracrine function in vitro. C57/BL6 mice with induced skin scleroderma were treated with adipose-derived stem cells (ASCs), adipocytes, ad-organoids, and Matrigel, and the therapeutic effect was assessed histologically. Our results showed that ad-organoids derived from MVF contained mature adipocytes and a well-established vessel network, secreted multiple adipokines, promoted adipogenic differentiation of ASCs, and suppressed proliferation and migration of scleroderma fibroblasts. Subcutaneous transplantation of ad-organoids reconstructed the subcutaneous fat layer and stimulated dermal adipocyte regeneration in bleomycin-induced scleroderma skin. It reduced collagen deposition and dermal thickness, attenuating dermal fibrosis. Moreover, ad-organoids suppressed macrophage infiltration and promoted angiogenesis in the skin lesion. In conclusion, 3D culturing of MVFs with stepwise angiogenic and adipogenic induction is an effective strategy for the fabrication of ad-organoids, and the transplantation of prefabricated ad-organoids can improve skin sclerosis by restoring cutaneous fat and attenuating skin fibrosis. These findings offer a promising therapeutic approach for the treatment of localized scleroderma.
 Rosmarinic acid (RA) is a natural phenolic compound present in culinary herbs of the Boraginaceae, Lamiaceae/Labiatae, and Nepetoideae families. While the medicinal applications of these plants have been known for ages, RA has only been relatively recently established as an effective ameliorative agent against various disorders including cardiac diseases, cancer, and neuropathologies. In particular, several studies have confirmed the neuroprotective potential of RA in multiple cellular and animal models, as well as in clinical studies. The neuroprotective effects mediated by RA stem from its multimodal actions on a plethora of cellular and molecular pathways; including oxidative, bioenergetic, neuroinflammatory, and synaptic signaling. In recent years, RA has garnered tremendous interest as an ideal therapeutic candidate for treating neurodegenerative diseases. This review first briefly discusses the pharmacokinetics of RA and then proceeds to detail the neuroprotective mechanisms of RA at the molecular levels. Finally, the authors focus on the ameliorative potential of RA against several central nervous system (CNS) disorders, ranging from neuropsychological stress and epilepsy to neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, Parkinson's disease, Lewy body dementia, and amyotrophic lateral sclerosis.
 This study assessed the relationship between clinical symptoms and magnetic resonance imaging (MRI) findings in temporomandibular disorders (TMD). A total of 324 temporomandibular joints (TMJs) from 162 patients were included. The TMJs were divided into three groups based on disc positions on MRI: normal disc position, anterior disc displacement with reduction (ADDwR), and anterior disc displacement without reduction (ADDwoR). Clinical findings included TMJ pain, TMJ noise, and maximum mouth opening (MMO). The disc configuration, disc positions, condylar morphology, and joint effusion were evaluated in proton density-weighted and T2-weighted open and closed-mouth sagittal sections. Patients comprised 135 females and 27 males, with a mean age of 37.63 ± 13.86 years. The VAS score was significantly higher in ADDwoR than in ADDwR (p = 0.007). Condylar sclerosis (β coefficient: 1.449, 95% confidence interval (CI): 0.505-2.393, p = 0.003) and condylar flattening (β coefficient: 1.024, 95% CI: 0.209-1.840, p = 0.014) had higher VAS scores than the other MRI findings in multiple regression analyses. Limited mouth opening (MO) was independently associated with ADDwoR. ADDwoR had a higher risk of having limited MO than normal disc position (odds ratio: 5.268), while there were no associations between limited MO and other MRI findings. None of the MRI findings showed significant performance in predicting TMJ noise. The convex and folded disc configuration percentages, the frequencies of osteophyte formation, and grade 3 effusion were significantly higher in the ADDwoR group. More severe clinical symptoms and a higher degree of disc deformity, osteophyte formation, and high-grade effusion were shown to be associated with ADDwoR.
 Osteoarthritis is a disorder affecting the joints and is characterized by cellular stress and degradation of the extracellular matrix cartilage. It begins with the presence of micro- and macro-lesions that fail to repair properly, which can be initiated by multiple factors: genetic, developmental, metabolic, and traumatic. In the case of the knee, osteoarthritis affects the tissues of the diarthrodial joint, manifested by morphological, biochemical, and biomechanical modifications of the cells and the extracellular matrix. All this leads to remodeling, fissuring, ulceration, and loss of articular cartilage, as well as sclerosis of the subchondral bone with the production of osteophytes and subchondral cysts. The symptomatology appears at different time points and is accompanied by pain, deformation, disability, and varying degrees of local inflammation. Repetitive concentric movements, such as while cycling, can produce the microtrauma that leads to osteoarthritis. Aggravation of the gradual lesion in the cartilage matrix can evolve to an irreversible injury. The objective of the present review is to explain the evolution of knee osteoarthritis in cyclists, to show the scarce research performed in this particular field and extract recommendations to propose future therapeutic strategies.
 Newly diagnosed malignancy during pregnancy is rare affecting approximately 1 in 1,000 pregnancies. Breast followed by hematologic malignancies are most common. Hodgkin's lymphoma (HL) is a lymphoid neoplasm which can present with lymphadenopathy or mediastinal mass and represents 6% of all malignancies diagnosed during pregnancy. Treatment involves a combination of chemotherapy with or without adjuvant radiation which poses significant challenges when diagnosed antepartum. We highlight a 28-year-old primigravida at 26 weeks gestation who presented to the emergency department in Japan with cough, dyspnea, and sore throat for 3-5 days. Initial chest radiography demonstrated a large perihilar mass with mediastinal shift. Follow-up CT chest revealed an anterior mediastinal mass measuring 8 cm × 19 cm × 16 cm with features concerning for aggressive lymphoma. The patient was subsequently transferred to a stateside tertiary care center for expedited workup. She underwent two core needle biopsies, both of which were non-diagnostic. Cardiothoracic surgery performed a cervical mediastinoscopy with excision of the enlarged right supraclavicular lymph node. Pathologic analysis revealed classical HL, nodular sclerosis subtype. Treatment was initiated with adriamycin, bleomycin, vinblastine, and dacarbazine with two cycles planned antepartum followed by additional cycles postpartum. The patient had an uncomplicated vaginal delivery at 38 weeks gestation. Diagnosis of HL in pregnancy is rare, and expedited diagnosis can be challenging as multiple diagnostic and treatment modalities may impact pregnancy. Management in pregnancy requires a multidisciplinary approach, and decisions regarding treatment and delivery timing should be weighed against risk to the fetus.
 Significance: Cells depend on well-functioning mitochondria for essential processes such as energy production, redox signaling, coordination of metabolic pathways, and cofactor biosynthesis. Mitochondrial dysfunction, metabolic decline, and protein stress have been implicated in the etiology of multiple late-onset diseases, including various ataxias, diabetes, sarcopenia, neuromuscular disorders, and neurodegenerative diseases such as parkinsonism, amyotrophic lateral sclerosis, and glaucoma. Recent Advances: New evidence supports that increased energy metabolism protects neuron function during aging. Key energy metabolic enzymes, however, are susceptible to oxidative damage making it imperative that the mitochondrial proteome is protected. More than 40 different enzymes have been identified as important factors for guarding mitochondrial health and maintaining a dynamic pool of mitochondria. Critical Issues: Understanding shared mechanisms of age-related disorders of neurodegenerative diseases such as glaucoma, Alzheimer's disease, and Parkinson's disease is important for developing new therapies. Functional mitochondrial shape and dynamics rely on complex interactions between mitochondrial proteases and membrane proteins. Identifying the sequence of molecular events that lead to mitochondrial dysfunction and metabolic stress is a major challenge. Future Directions: A critical need exists for new strategies that reduce mitochondrial protein stress and promote mitochondrial dynamics in age-related neurological disorders. Discovering how mitochondria-associated degradation is related to proteostatic mechanisms in mitochondrial compartments may reveal new opportunities for therapeutic interventions. Also, little is known about how protein and membrane contacts in the inner and outer mitochondrial membrane are regulated, even though they are pivotal for mitochondrial architecture. Future work will need to delineate the molecular details of these processes.
 Although the "multiple hits" theory is a widely accepted pathogenesis in IgA nephropathy (IgAN), increasing evidence suggests that the mononuclear/macrophage system plays important roles in the progression of IgAN; however, the exact mechanism is unclear. In the present study, we explored 1,067 patients in 15 studies and found that the number of macrophages per glomerulus was positively related with the degree of hematuria, and the macrophages in the glomeruli were mainly related to mesangial proliferation (M) in renal biopsy. In the tubulointerstitium, macrophages were significantly paralleled to tubulointerstitial α-SMA and NF-kB expression, tubulointerstitial lesion, tubule atrophy/interstitial fibrosis (T), and segmental glomerulosclerosis (S). In the glomeruli and tubulointerstitium, M1 accounted for 85.41% in the M classification according to the Oxford MEST-C, while in the blood, M1 accounted for 100%, and the patients with low CD89(+) monocyte mean fluorescence intensity displayed more severe pathological characteristics (S1 and T1-2) and clinical symptoms. M1 (CD80(+)) macrophages were associated with proinflammation in the acute phase; however, M2 (CD163(+)) macrophages participated in tissue repair and remodeling, which correlated with chronic inflammation. In the glomeruli, M2 macrophages activated glomerular matrix expansion by secreting cytokines such as IL-10 and tumor necrosis factor-β (TGF-β), and M0 (CD68(+)) macrophages stimulated glomerular hypercellularity. In the tubulointerstitium, M2 macrophages played pivotal roles in renal fibrosis and sclerosis. It is assumed that macrophages acted as antigen-presenting cells to activate T cells and released diverse cytokines to stimulate an inflammatory response. Macrophages infiltrating glomeruli destroy the integrity of podocytes through the mesangio-podocytic-tubular crosstalk as well as the injury of the tubule.
 Amyotrophic lateral sclerosis (ALS) is an adult devastating neurodegenerative disease characterized by the loss of upper and lower motor neurons (MNs), resulting in progressive paralysis and death. Genetic animal models of ALS have highlighted dysregulation of synaptic structure and function as a pathogenic feature of ALS-onset and progression. Alternative pre-mRNA splicing (AS), which allows expansion of the coding power of genomes by generating multiple transcript isoforms from each gene, is widely associated with synapse formation and functional specification. Deciphering the link between aberrant splicing regulation and pathogenic features of ALS could pave the ground for novel therapeutic opportunities. Herein, we found that neural progenitor cells (NPCs) derived from the hSOD1(G93A) mouse model of ALS displayed increased proliferation and propensity to differentiate into neurons. In parallel, hSOD1(G93A) NPCs showed impaired splicing patterns in synaptic genes, which could contribute to the observed phenotype. Remarkably, master splicing regulators of the switch from stemness to neural differentiation are de-regulated in hSOD1(G93A) NPCs, thus impacting the differentiation program. Our data indicate that hSOD1(G93A) mutation impacts on neurogenesis by increasing the NPC pool in the developing mouse cortex and affecting their intrinsic properties, through the establishment of a specific splicing program.
 Radiologists routinely analyze hippocampal asymmetries in magnetic resonance (MR) images as a biomarker for neurodegenerative conditions like epilepsy and Alzheimer's Disease. However, current clinical tools rely on either subjective evaluations, basic volume measurements, or disease-specific models that fail to capture more complex differences in normal shape. In this paper, we overcome these limitations by introducing NORHA, a novel NORmal Hippocampal Asymmetry deviation index that uses machine learning novelty detection to objectively quantify it from MR scans. NORHA is based on a One-Class Support Vector Machine model learned from a set of morphological features extracted from automatically segmented hippocampi of healthy subjects. Hence, in test time, the model automatically measures how far a new unseen sample falls with respect to the feature space of normal individuals. This avoids biases produced by standard classification models, which require being trained using diseased cases and therefore learning to characterize changes produced only by the ones. We evaluated our new index in multiple clinical use cases using public and private MRI datasets comprising control individuals and subjects with different levels of dementia or epilepsy. The index reported high values for subjects with unilateral atrophies and remained low for controls or individuals with mild or severe symmetric bilateral changes. It also showed high AUC values for discriminating individuals with hippocampal sclerosis, further emphasizing its ability to characterize unilateral abnormalities. Finally, a positive correlation between NORHA and the functional cognitive test CDR-SB was observed, highlighting its promising application as a biomarker for dementia.
 BACKGROUND: UVA1 phototherapy is a treatment used for multiple dermatological conditions. The optimal therapeutic regimens and dosing of UVA1 are a matter of debate. The dosages used vary widely between published studies and there are no evidence-based protocols that provide data on dosage, duration, or the role of maintenance therapy. The purpose of this study is to evaluate the experience in our medical center regarding treatment with UVA1, as well as the degree of patient satisfaction with the treatment according to their pathology. METHODS: We present a retrospective evaluation of outcomes, treatment tolerability, and satisfaction in adult patients using a low dose of UVA1 phototherapy, administered in our dermatologic service between 2019 and 2022. RESULTS: A total of 78 patients were treated with UVA1, of whom 46 patients (59%) were over 18 years old, completed treatment, and gave their consent. The overall objective clinical response rate was 91.30% (42/46), achieving a complete response in 17 (36.96%) patients, partial response in 25 (54.34%), and no response in 4 (8.70%). The complete response rates recorded were high in morphea, scleredema, or chronic hand eczema. In terms of the level of satisfaction objectively measured by TSQM-9 version 1.4, highlighting high scores obtained in mastocytosis, systemic sclerosis, morphea, scleredema, chronic hand eczema, or prurigo nodularis (over 65 points). CONCLUSIONS: We present a review of treatment with UVA1 phototherapy at low doses with good response in a wide variety of dermatological pathologies.
 INTRODUCTION: Bifurcation analysis allows the examination of steady-state, non-linear dynamics of neurons and their effects on cell firing, yet its usage in neuroscience is limited to single-compartment models of highly reduced states. This is primarily due to the difficulty in developing high-fidelity neuronal models with 3D anatomy and multiple ion channels in XPPAUT, the primary bifurcation analysis software in neuroscience. METHODS: To facilitate bifurcation analysis of high-fidelity neuronal models under normal and disease conditions, we developed a multi-compartment model of a spinal motoneuron (MN) in XPPAUT and verified its firing accuracy against its original experimental data and against an anatomically detailed cell model that incorporates known MN non-linear firing mechanisms. We used the new model in XPPAUT to study the effects of somatic and dendritic ion channels on the MN bifurcation diagram under normal conditions and after amyotrophic lateral sclerosis (ALS) cellular changes. RESULTS: Our results show that somatic small-conductance Ca(2+)-activated K (SK) channels and dendritic L-type Ca(2+) channels have the strongest effects on the bifurcation diagram of MNs under normal conditions. Specifically, somatic SK channels extend the limit cycles and generate a subcritical Hopf bifurcation node in the V-I bifurcation diagram of the MN to replace a supercritical node Hopf node, whereas L-type Ca(2+) channels shift the limit cycles to negative currents. In ALS, our results show that dendritic enlargement has opposing effects on MN excitability, has a greater overall impact than somatic enlargement, and dendritic overbranching offsets the dendritic enlargement hyperexcitability effects. DISCUSSION: Together, the new multi-compartment model developed in XPPAUT facilitates studying neuronal excitability in health and disease using bifurcation analysis.
 Background: Functionally relevant coronary artery disease (fCAD), causing symptoms of myocardial ischemia, can currently only be reliably detected with advanced cardiac imaging. Serum neurofilament light chain (sNfL) is a biomarker for neuro-axonal injury known to be elevated by cardiovascular (CV) risk factors and cerebrovascular small-vessel diseases. Due to their pathophysiological similarities with fCAD and the link to CV risk factors, we hypothesised that sNfL may have diagnostic and prognostic value for fCAD and adverse cardiovascular outcomes.Methods: Of the large prospective Basel VIII study (NCT01838148), 4'016 consecutive patients undergoing cardiac work-up for suspected fCAD were included (median age 68 years, 32.5% women, 46.9% with history of CAD). The presence of fCAD was adjudicated using myocardial perfusion imaging single-photon emission tomography (MPI-SPECT) and coronary angiography. sNfL was measured using a high-sensitive single-molecule array assay. All-cause and cardiovascular death, myocardial infarction (MI), and stroke/transient ischaemic attack (TIA) during 5-year follow-up were the prognostic endpoints.Results: The diagnostic accuracy of sNfL for fCAD as quantified by the area under the curve (AUC) was low (0.58, 95%CI 0.56-0.60). sNfL was strongly associated with age, renal dysfunction, and body mass index and was a strong and independent predictor of all-cause death, cardiovascular death, and stroke/TIA but not MI. Time-dependent AUC for cardiovascular-death at 1-year was 0.85, 95%CI 0.80-0.89, and 0.81, 95%CI 0.77-0.86 at 2-years.Conclusion: While sNfL concentrations did not show a diagnostic role for fCAD, in contrast, sNfL was a strong and independent predictor of cardiovascular outcomes, including all-cause death, cardiovascular death and stroke/TIA.
 In vitro data suggest the monoclonal antibody sotrovimab may have lost inhibitory capability against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant. We aimed to provide real-life data on clinical outcomes in hospitalized patients. We retrospectively analyzed patients who were treated at the University Medical Center Hamburg-Eppendorf, Germany, between December 2021 and June 2022. Out of all 1,254 patients, 185 were treated with sotrovimab: 147 patients received sotrovimab monotherapy, and 38 received combination treatment with sotrovimab and remdesivir. We compared in-hospital mortality for the different treatment regimens for patients treated on regular wards and the intensive care unit separately and performed propensity score matching by age, sex, comorbidities, immunosuppression, and additional dexamethasone treatment to select patients who did not receive antiviral treatment for comparison. No difference in in-hospital mortality was observed between any of the treatment groups and the respective control groups. These findings underline that sotrovimab adds no clinical benefit for hospitalized patients with SARS-CoV-2 Omicron variant infections. IMPORTANCE This study shows that among hospitalized patients with SARS-CoV-2 Omicron variant infection at risk of disease progression, treatment with sotrovimab alone or in combination with remdesivir did not decrease in-hospital mortality. These real-world clinical findings in combination with previous in vitro data about lacking neutralizing activity of sotrovimab against SARS-CoV-2 Omicron variant do not support sotrovimab as a treatment option in these patients.
 Salt sensitivity concerns blood pressure alterations after a change in salt intake (sodium chloride). The heart is a pump, and vessels are tubes; sodium can affect both. A high salt intake increases cardiac output, promotes vascular dysfunction and capillary rarefaction, and chronically leads to increased systemic vascular resistance. More recent findings suggest that sodium also acts as an important second messenger regulating energy metabolism and cellular functions. Besides endothelial cells and fibroblasts, sodium also affects innate and adaptive immunometabolism, immune cell function, and influences certain microbes and microbiota-derived metabolites. We propose the idea that the definition of salt sensitivity should be expanded beyond high blood pressure to cellular and molecular salt sensitivity.
 BACKGROUND AND PURPOSE: Previous studies investigating cardiovascular disorders in patients with Parkinson's disease (PD) showed heterogeneous results regarding whether there is a higher or lower risk of myocardial infarction (MI) in these patients compared to the general population. Because of the inconsistency in findings, herein the aim was to perform a systematic review and meta-analysis to investigate the risk of MI in patients with PD. METHODS: A comprehensive literature search was performed using four databases, PubMed, Web of Science, Scopus and Embase, in June 2022. Peer-reviewed observational studies comprising case-controls, cohort, cross-sectional and longitudinal studies that reported MI in the PD population were included. RESULTS: After the screening, 20 studies with a total of 80,441 patients with PD and 802,857 controls were included in our qualitative and quantitative synthesis. The pooled estimated odds ratio for MI in PD patients compared to controls was 0.80 (95% confidence interval [CI] 0.56-1.05) which indicates that there is no association. The pooled prevalence of MI was 5% (95% CI 3%-7%) with a range of 1%-20% amongst patients with PD. The men (6%, 95% CI 1%-13%) and women (6%, 95% CI 1%-14%, Q = 29.27, I(2) = 98.50%, p < 0.001) had similar MI prevalence. CONCLUSION: This comprehensive systematic review and meta-analysis provide compelling evidence that PD is associated with a reduced risk of MI. Whilst the exact mechanism underlying this association remains to be fully elucidated, it is clear that certain risk factors for cardiac events appear to be less present in PD patients, which may serve as a protective factor. However, given the reports of increased risk for cerebrovascular events in PD patients, it is possible that the major risk factors for MI and cardiovascular accidents in this population differ. These findings have important implications for clinical management and further research in this area is warranted.
 C9ORF72 hexanucleotide repeat expansion is the most common genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). One pathogenic mechanism is the accumulation of toxic dipeptide repeat (DPR) proteins like poly-GA, GP and GR, produced by the noncanonical translation of the expanded RNA repeats. However, how different DPRs are synthesized remains elusive. Here, we use single-molecule imaging techniques to directly measure the translation dynamics of different DPRs. Besides initiation, translation elongation rates vary drastically between different frames, with GP slower than GA and GR the slowest. We directly visualize frameshift events using a two-color single-molecule translation assay. The repeat expansion enhances frameshifting, but the overall frequency is low. There is a higher chance of GR-to-GA shift than in the reversed direction. Finally, the ribosome-associated protein quality control (RQC) factors ZNF598 and Pelota modulate the translation dynamics, and the repeat RNA sequence is important for invoking the RQC pathway. This study reveals that multiple translation steps modulate the final DPR production. Understanding repeat RNA translation is critically important to decipher the DPR-mediated pathogenesis and identify potential therapeutic targets in C9ORF72-ALS/FTD.
 BACKGROUND AND PURPOSE: Currently there is an unmet need for a highly standardized blood biomarker test to monitor treatment response in Lyme neuroborreliosis (LNB). Differentiating between active or past infection is challenged by the relatively high frequency of persistent symptoms after the end of antibiotic treatment (estimated 15%-20%), the variable clinical course and the long-lasting Borrelia burgdorferi antibodies. The aim was therefore to evaluate plasma neurofilament light chain (pNfL) as a marker for disease activity in LNB. METHODS: This was a prospective cohort of definite LNB (N = 36) with blood samples and clinical evaluation including Glasgow Outcome Score at treatment initiation and 3 and 6 months' follow-up. Consecutive plasma was retrospectively analysed for the content of neurofilament light chain by Quanterix® kits (Simoa® NF-light Kit). RESULTS: Plasma neurofilament light chain significantly decreased between treatment initiation and the 3-month follow-up (median 83 pg/ml vs. median 14 pg/ml (25 pairs), p < 0.0001). No significant change was observed between 3 and 6 months' follow-up (median 14 pg/ml vs. median 12 pg/ml (21 pairs), p = 0.33). At treatment initiation 90% had pNfL above the age-defined reference compared to only 23% and 7% respectively at 3 and 6 months' follow-up. Decreases in pNfL were mirrored by increasing Glasgow Outcome Score. Reporting persistent symptoms at the 6-month follow-up was not associated with pNfL (relative change from reference or actual values) at baseline or at 6 months' follow-up. CONCLUSION: Plasma neurofilament light chain decreases following antibiotic treatment in LNB and is not associated with reporting persistent symptoms. It was therefore speculated that it may prove useful as a treatment response biomarker in LNB.
 Freezing of gait (FOG) is an episodic gait pattern that is common in advanced Parkinson's disease (PD) and other atypical parkinsonism syndromes. Recently, disturbances in the pedunculopontine nucleus (PPN) and its connections have been suggested to play a critical role in the development of FOG. In this study, we aimed to demonstrate possible disturbances in PPN and its connections by performing the diffusion tensor imaging (DTI) technique. We included 18 patients of PD with FOG [PD-FOG], 13 patients of PD without FOG [PD-nFOG] and 12 healthy subjects as well as a group of patients with progressive supranuclear palsy (PSP), an atypical parkinsonism syndrome which is very often complicated with FOG [6 PSP-FOG, 5 PSP-nFOG]. To determine the specific cognitive parameters that can be related to FOG, deliberate neurophysiological evaluations of all the individuals were performed. The comparative analyses and correlation analyses were performed to reveal the neurophysiological and DTI correlates of FOG in either group. We have found disturbances in values reflecting microstructural integrity of the bilateral superior frontal gyrus (SFG), bilateral fastigial nucleus (FN), left pre-supplementary motor area (SMA) in the PD-FOG group relative to the PD-nFOG group. The analysis of the PSP group also demonstrated disturbance in left pre-SMA values in the PSP-FOG group likewise, while negative correlations were determined between right STN, left PPN values and FOG scores. In neurophysiological assessments, lower performances for visuospatial functions were demonstrated in FOG ( +) individuals for either patient group. The disturbances in the visuospatial abilities may be a critical step for the occurrence of FOG. Together with the results of DTI analyses, it might be suggested that impairment in the connectivity of disturbed frontal areas with disordered basal ganglia, maybe the key factor for the occurrence of FOG in the PD group, whereas left PPN which is a nondopaminergic nucleus may play a more prominent role in the process of FOG in PSP. Moreover, our results support the relationship between right STN, and FOG as mentioned before, as well as introduce the importance of FN as a new structure that may be involved in FOG pathogenesis.
 This umbrella review aimed to systematically identify the peri-operative risk factors associated with post-operative cognitive dysfunction (POCD) using meta-analyses of observational studies. To date, no review has synthesised nor assessed the strength of the available evidence examining risk factors for POCD. Database searches from journal inception to December 2022 consisted of systematic reviews with meta-analyses that included observational studies examining pre-, intra- and post-operative risk factors for POCD. A total of 330 papers were initially screened. Eleven meta-analyses were included in this umbrella review, which consisted of 73 risk factors in a total population of 67,622 participants. Most pertained to pre-operative risk factors (74%) that were predominantly examined using prospective designs and in cardiac-related surgeries (71%). Overall, 31 of the 73 factors (42%) were associated with a higher risk of POCD. However, there was no convincing (class I) or highly suggestive (class II) evidence for associations between risk factors and POCD, and suggestive evidence (class III) was limited to two risk factors (pre-operative age and pre-operative diabetes). Given that the overall strength of the evidence is limited, further large-scale studies that examine risk factors across various surgery types are recommended.
 BACKGROUND AND AIMS: Mitofusin 1 (MFN1) and MFN2 are outer mitochondrial membrane fusogenic proteins regulating mitochondrial network morphology. MFN2 mutations cause Charcot-Marie-Tooth type 2A (CMT2A), an axonal neuropathy characterized by mitochondrial fusion defects, which in the case of a GTPase domain mutant, were rescued following wild-type MFN1/2 (MFN1/2(WT) ) overexpression. In this study, we compared the therapeutic efficiency between MFN1(WT) and MFN2(WT) overexpression in correcting mitochondrial defects induced by the novel MFN2(K357T) mutation located in the highly conserved R3 region. METHODS: Constructs expressing either MFN2(K357T) , MFN2(WT) , or MFN1(WT) under the ubiquitous chicken β-actin hybrid (CBh) promoter were generated. Flag or myc tag was used for their detection. Differentiated SH-SY5Y cells were single transfected with MFN1(WT) , MFN2(WT) , or MFN2(K357T) , as well as double transfected with MFN2(K357T) /MFN2(WT) or MFN2(K357T) /MFN1(WT) . RESULTS: SH-SY5Y cells transfected with MFN2(K357T) exhibited severe perinuclear mitochondrial clustering with axon-like processes devoid of mitochondria. Single transfection with MFN1(WT) resulted in a more interconnected mitochondrial network than transfection with MFN2(WT) , accompanied by mitochondrial clusters. Double transfection of MFN2(K357T) with either MFN1(WT) or MFN2(WT) resolved the mutant-induced mitochondrial clusters and led to detectable mitochondria throughout the axon-like processes. MFN1(WT) showed higher efficacy than MFN2(WT) in rescuing these defects. INTERPRETATION: These results further demonstrate the higher potential of MFN1(WT) over MFN2(WT) overexpression to rescue CMT2A-induced mitochondrial network abnormalities due to mutations outside the GTPase domain. This higher phenotypic rescue conferred by MFN1(WT) , possibly due to its higher mitochondrial fusogenic ability, may be applied to different CMT2A cases regardless of the MFN2 mutation type.
 Maternal viral infection and immune response are known to increase the risk of altered development of the foetal brain. Given the ongoing global pandemic of coronavirus disease 2019 (COVID-19), investigating the impact of SARS-CoV-2 on foetal brain health is of critical importance. Here, we report the presence of SARS-CoV-2 in first and second trimester foetal brain tissue in association with cortical haemorrhages. SARS-CoV-2 spike protein was sparsely detected within progenitors and neurons of the cortex itself, but was abundant in the choroid plexus of haemorrhagic samples. SARS-CoV-2 was also sparsely detected in placenta, amnion and umbilical cord tissues. Cortical haemorrhages were linked to a reduction in blood vessel integrity and an increase in immune cell infiltration into the foetal brain. Our findings indicate that SARS-CoV-2 infection may affect the foetal brain during early gestation and highlight the need for further study of its impact on subsequent neurological development.
 Cerebral cortical encephalitis (CCE) is a recently described myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) phenotype. In this observational retrospective study, we characterized 19 CCE patients (6.7% of our MOGAD cohort). Headache (n = 15, 79%), seizures (n = 13, 68%), and encephalopathy (n = 12, 63%) were frequent. Magnetic resonance imaging revealed unilateral (n = 12, 63%) or bilateral (n = 7, 37%) cortical T2 hyperintensity and leptomeningeal enhancement (n = 17, 89%). N-Methyl-D-aspartate receptor autoantibodies coexisted in 2 of 15 tested (13%). CCE pathology (n = 2) showed extensive subpial cortical demyelination (n = 2), microglial reactivity (n = 2), and inflammatory infiltrates (perivascular, n = 1; meningeal, n = 1). Most received high-dose steroids (n = 17, 89%), and all improved, but 3 had CCE relapses. This study highlights the CCE spectrum and provides insight into its pathogenesis. ANN NEUROL 2023;93:297-302.
 BACKGROUND: Given that the pathogenetic process of ALS begins many years prior to its clinical onset, examining patients' residential histories may offer insights on the disease risk factors. Here, we analyzed the spatial distribution of a large ALS cohort in the 50 years preceding the disease onset. METHODS: Data from the PARALS register were used. A spatial cluster analysis was performed at the time of disease onset and at 1-year intervals up to 50 years prior to that. RESULTS: A total of 1124 patients were included. The analysis revealed a higher-incidence cluster in a large area (435,000 inhabitants) west of Turin. From 9 to 2 years before their onset, 105 cases were expected and 150 were observed, resulting in a relative risk of 1.49 (P = 0.04). We also found a surprising high number of patients pairs (51) and trios (3) who lived in the same dwelling while not being related. Noticeably, these occurrences were not observed in large dwellings as we would have expected. The probability of this occurring in smaller buildings only by chance was very low (P = 0.01 and P = 0.04 for pairs and trios, respectively). CONCLUSIONS: We identified a higher-incidence ALS cluster in the years preceding the disease onset. The cluster area being densely populated, many exposures could have contributed to the high incidence ALS cluster, while we could not find a shared exposure among the dwellings where multiple patients had lived. However, these findings support that exogenous factors are likely involved in the ALS pathogenesis.
 Mechanistic target of rapamycin complex 1 (mTORC1) is a serine-threonine kinase that is activated by extracellular signals, such as nutrients and growth factors. It plays a key role in the control of various biological processes, such as protein synthesis and energy metabolism by mediating or regulating the phosphorylation of multiple target molecules, some of which remain to be identified. We have here reanalysed a large-scale phosphoproteomics data set for mTORC1 target molecules and identified pre-B cell leukemia transcription factor 2 (PBX2) as such a novel target that is dephosphorylated downstream of mTORC1. We confirmed that PBX2, but not other members of the PBX family, is dephosphorylated in an mTORC1 activity-dependent manner. Furthermore, pharmacological and gene knockdown experiments revealed that glycogen synthase kinase 3 (GSK3) and protein phosphatase 1 (PP1) are responsible for the phosphorylation and dephosphorylation of PBX2, respectively. Our results thus suggest that the balance between the antagonistic actions of GSK3 and PP1 determines the phosphorylation status of PBX2 and its regulation by mTORC1.
 Autoreactive B cell subsets have been described in a variety of settings, using multiple classification schemes and cell surface markers also found on healthy cells. CD19(+) CD21(lo) B cells have been identified as an autoreactive-prone subset of B cells, although the downregulation of CD21 has been observed on a variety of B cell subsets in health and disease. This variation has led to confusion regarding the meaning and applicability of the loss or reduction of CD21 in peripheral B cells. To better understand the relationships between commonly used B cell markers and their associated characteristics, we analyzed human B cells from healthy participants using multiparameter flow cytometry and the visualization algorithm, tSNE. This approach revealed significant phenotypic overlap amongst five previously described autoimmune-prone B cell subsets, including CD19(+) CD10(-) CD27(-) CD21(lo) B cells. Interestingly, 12 different subpopulations of CD19(+) CD21(lo) B cells were identified, some of which mapped to previously described autoreactive populations, while others were consistent with healthy B cells. This suggests that CD21 is downregulated in a variety of circumstances involving B cell activation, all of which are present in low numbers even in healthy individuals. These findings describe the utility of unbiased multiparameter analysis using a relatively limited panel of flow cytometry markers to analyze autoreactive-prone and normal activated B cells.
 Ethical challenges in medical decision making are commonly encountered by clinicians caring for patients afflicted by neurological injury or disease at the end of life (EOL). In many of these cases, there are conflicting opinions as to what is right and wrong originating from multiple sources. There is a particularly high prevalence of impaired patient judgment and decision-making capacity in this population that may result in a misrepresentation of their premorbid values and goals. Conflict may originate from a discordance between what is legal or from stakeholders who view and value life and existence differently from the patient, at times due to religious or cultural influences. Promotion of life, rather than preservation of existence, is the goal of many patients and the foundation on which palliative care is built. Those who provide EOL care, while being respectful of potential cultural, religious, and legal stakeholder perspectives, must at the same time recognize that these perspectives may conflict with the optimal ethical course to follow. In this chapter, we will attempt to review some of the more notable ethical challenges that may arise in the neurologically afflicted at the EOL. We will identify what we believe to be the most compelling ethical arguments both in support of and opposition to specific EOL issues. At the same time, we will consider how ethical analysis may be influenced by these legal, cultural, and religious considerations that commonly arise.

 BACKGROUND AND AIMS: To investigate the prognostic value of blood neurofilament light chain protein (NfL) levels in the acute phase of coronavirus disease 2019 (COVID-19). METHODS: We conducted an individual participant data (IPD) meta-analysis after screening on MEDLINE and Scopus to May 23rd 2022. We included studies with hospitalized adult COVID-19 patients without major COVID-19-associated central nervous system (CNS) manifestations and with a measurement of blood NfL in the acute phase as well as data regarding at least one clinical outcome including intensive care unit (ICU) admission, need of mechanical ventilation (MV) and death. We derived the age-adjusted measures NfL Z scores and conducted mixed-effects modelling to test associations between NfL Z scores and other variables, encompassing clinical outcomes. Summary receiver operating characteristic curves (SROCs) were used to calculate the area under the curve (AUC) for blood NfL. RESULTS: We identified 382 records, of which 7 studies were included with a total of 669 hospitalized COVID-19 cases (mean age 66.2 ± 15.0 years, 68.1% males). Median NfL Z score at admission was elevated compared to the age-corrected reference population (2.37, IQR: 1.13-3.06, referring to 99th percentile in healthy controls). NfL Z scores were significantly associated with disease duration and severity. Higher NfL Z scores were associated with a higher likelihood of ICU admission, need of MV, and death. SROCs revealed AUCs of 0.74, 0.80 and 0.71 for mortality, need of MV and ICU admission, respectively. CONCLUSIONS: Blood NfL levels were elevated in the acute phase of COVID-19 patients without major CNS manifestations and associated with clinical severity and poor outcome. The marker might ameliorate the performance of prognostic multivariable algorithms in COVID-19.
 Heart failure with preserved ejection fraction (HFpEF) is characterized by obesity, hypertension, diabetes mellitus, and chronic kidney disease. Obese ZSF1 rats, a model of HFpEF, exhibit multiple such comorbidities that can disturb cardiac function. Little attention has been paid to how these comorbidities affect renal disease in ZSF1 rats. HFpEF is found predominantly in women in whom obesity and hypertension are particularly prevalent. Therefore, we characterized the renal phenotype in female and male lean and obese ZSF1 rats and investigated additional effects of worsened hypertension on disease severity. Systolic blood pressure and renal function were assessed biweekly from 12 to 26 wk. From 19 wk, rats were implanted with either a deoxycorticosterone acetate pellet and fed a high-salt diet (DS) or a placebo pellet and fed a normal-salt diet. At 26 wk of age, terminal glomerular filtration rate was assessed via inulin clearance under isoflurane. Renal sections were processed for histological analysis. Lean and obese ZSF1 rats, both female and male, were mildly hypertensive (systolic blood pressure: 140-150 mmHg). All obese ZSF1 rats showed HFpEF. In female normoglycemic ZSF1 rats, obesity associated with mild proteinuria, decreased glomerular filtration rate, and glomerular hypertrophy. DS-worsened hypertension enhanced proteinuria and triggered glomerulosclerosis. Male obese ZSF1 rats were hyperglycemic and showed proteinuria, glomerular hypertrophy and sclerosis, and tubulointerstitial damage. DS-worsened hypertension aggravated this phenotype in male ZSF1 rats. In conclusion, female obese ZSF1 rats develop mild renal dysfunction and DS-worsened hypertension compromises renal function and structure in normoglycemic female obese ZSF1 rats as in hyperglycemic male obese ZSF1 rats.NEW & NOTEWORTHY Chronic kidney disease coexists with heart failure with a preserved ejection fraction (HFpEF), which is associated with multiple comorbidities and the female sex. We showed that obese, mildly hypertensive female ZSF1 rats, an animal model for HFpEF, simultaneously develop renal disease with diastolic dysfunction. Exacerbation of their hypertension, a comorbidity highly prevalent in HFpEF, compromised renal function and structure similarly in normoglycemic obese female ZSF1 rats and hyperglycemic obese male ZSF1 rats.
 This scientific commentary refers to ‘Data-driven neuropathological staging and subtyping of TDP-43 proteinopathies’ by Young et al. (https://doi.org/10.1093/brain/awad145).
 BACKGROUND: Oxycodone is increasingly prescribed for postpartum analgesia in lieu of codeine owing to concerns regarding the neonatal safety of codeine during lactation. We examined whether initiation of oxycodone after delivery was associated with an increased risk of persistent opioid use relative to initiation of codeine. METHODS: We conducted a population-based cohort study of people who filled a prescription for either codeine or oxycodone within 7 days of discharge from hospital after delivery between Sept. 1, 2012, and June 30, 2020. The primary outcome was persistent opioid use, defined as 1 or more additional prescriptions for an opioid within 90 days of the first postpartum prescription and 1 or more additional prescriptions in the 91 to 365 days thereafter. We used inverse probability of treatment weighting to assess the risk of persistent postpartum opioid use, comparing people who initiated oxycodone with those who initiated codeine. RESULTS: Over the 8-year study period, we identified 70 607 people who filled an opioid prescription within 7 days of discharge from hospital: 21 308 (30.2%) received codeine and 49 299 (69.8%) oxycodone. Compared with people who filled a prescription for codeine, receipt of oxycodone was not associated with persistent opioid use (relative risk [RR] 1.04, 95% confidence interval [CI] 0.91-1.20). We found an association between a prescription for oxycodone and persistent use after vaginal delivery (RR 1.63, 95% CI 1.31-2.03), but not after cesarean delivery (RR 0.85, 95% CI 0.73-1.00). INTERPRETATION: Initiation of oxycodone (v. codeine) was not associated with an increased risk of persistent opioid use, except after vaginal delivery.
 Gastric antral vascular ectasia (GAVE), also known as "Watermelon stomach", is a rare cause of upper gastrointestinal bleeding (UGIB). It is characterized by an endoscopic appearance of flat red blood vessels traveling from the pylorus to the antrum. Patients often present with chronic blood loss resulting in iron deficiency anemia, or, less commonly, with acute gastropathy resulting in massive hemorrhage. The etiology of GAVE is unknown but the disorder has been more commonly observed in patients with cirrhosis, especially with portal hypertension, as well as in those with systemic sclerosis and other connective tissue disease. There is no definitive cure for GAVE, but the condition can be managed with a variety of endoscopic techniques, including heater probes, bipolar probes, plasma coagulators, laser therapy, and radiofrequency ablation. In rare cases, patients also require blood transfusions. Here we present an interesting case of upper GI bleeding resulting in symptomatic anemia in a 69-year-old female patient with GAVE following cocaine use. The patient was initially admitted for fatigue and shortness of breath and required multiple units of pRBCs. She was also found to have a urine drug screen positive for cocaine. Following stabilization, she underwent endoscopy which revealed the characteristic "watermelon stomach" appearance consistent with GAVE syndrome. The patient was discharged on an oral proton-pump inhibitor with instructions to follow-up outpatient with Gastroenterology. This case is presented as an example of a risk factor for acute exacerbation of a rare cause of UGIB. This patient presentation also represents an example of the importance of strict follow-up for those with risk factors for exacerbation of chronic GI conditions.
 Lymphangioleiomyomatosis (LAM) is a tuberous sclerosis complex (TSC)-associated tumor, characterized by the expression of neural crest lineages including neuronal markers. Neural crest cells can differentiate into multiple cell types that contribute to tissues associated with TSC-related tumors, and TSC-related tumors could be specifically associated with distinct neural crest subtypes. This study aimed to clarify the clinicopathological effects of expression of neuronal markers in LAM. Lung tissues from 40 patients with LAM (of whom 13, 1, and 26 had undergone lung transplantation, lobectomy, and partial lung resection, respectively) were immunohistochemically analyzed. All patients were women, and their median age was 36 years (range: 24-62 y). All patients who underwent lung transplantation or lobectomy were classified as LAM histologic score (LHS)-3, whereas those who underwent partial lung resection were classified as LHS-1. LAM cells expressed peripherin (65%), and neuron-specific βIII-tubulin (43%). A comparison of the early (LHS-1) and advanced (LHS-3) stages of LAM revealed that neuron-specific βIII-tubulin was significantly expressed in the early stage of LAM (P = 0.0009). Neuron-specific βIII-tubulin-positive LAM was associated with younger age (P < 0.0001), the coexistence of renal angiomyolipoma (P = 0.027), and the absence of retroperitoneal LAM (P = 0.045). Furthermore, based on the expression levels of immunohistochemical markers in LAM, 2 distinct clusters with different expression levels of neuronal markers were observed. Approximately 40% to 60% of patients with LAM expressed neuron-specific βIII-tubulin and peripherin. Neuronal expression may be associated with disease severity.
 Altered autophagy is a hallmark of neurodegeneration but how autophagy is regulated in the brain and dysfunctional autophagy leads to neuronal death has remained cryptic. Being a key cellular waste-recycling and housekeeping system, autophagy is implicated in a range of brain disorders and altering autophagy flux could be an effective therapeutic strategy and has the potential for clinical applications down the road. Tight regulation of proteins and organelles in order to meet the needs of complex neuronal physiology suggests that there is distinct regulatory pattern of neuronal autophagy as compared to non-neuronal cells and nervous system might have its own separate regulator of autophagy. Evidence has shown that circRNAs participates in the biological processes of autophagosome assembly. The regulatory networks between circRNAs, autophagy, and neurodegeneration remains unknown and warrants further investigation. Understanding the interplay between autophagy, circRNAs and neurodegeneration requires a knowledge of the multiple steps and regulatory interactions involved in the autophagy pathway which might provide a valuable resource for the diagnosis and therapy of neurodegenerative diseases. In this review, we aimed to summarize the latest studies on the role of brain-protective mechanisms of autophagy associated circRNAs in neurodegenerative diseases (including Alzheimer's disease, Parkinson's disease, Huntington's disease, Spinal Muscular Atrophy, Amyotrophic Lateral Sclerosis, and Friedreich's ataxia) and how this knowledge can be leveraged for the development of novel therapeutics against them. Autophagy stimulation might be potential one-size-fits-all therapy for neurodegenerative disease as per considerable body of evidence, therefore future research on brain-protective mechanisms of autophagy associated circRNAs will illuminate an important feature of nervous system biology and will open the door to new approaches for treating neurodegenerative diseases.
 Background The risk for dementia increases exponentially from the seventh decade of life. Identifying and understanding the biochemical changes that sensitize the ageing brain to neurodegeneration will provide new opportunities for dementia prevention and treatment. This study aimed to determine how ageing and major genetic risk factors for dementia affect the hippocampal proteome and lipidome of neurologically-normal humans over the age of 65. The hippocampus was chosen as it is highly susceptible to atrophy with ageing and in several neurodegenerative diseases. Methods Mass spectrometry-based proteomic and lipidomic analysis of CA1 hippocampus samples from 74 neurologically normal human donors, aged 66-104, was used in combination with multiple regression models and gene set enrichment analysis to identify age-dependent changes in the proteome and lipidome. ANOVA was used to test the effect of major dementia risk alleles in the TMEM106B and APOE genes on the hippocampal proteome and lipidome, adjusting for age, gender, and post-mortem interval. Results Forty proteins were associated with age at false discovery rate-corrected P < 0.05, including proteins that regulate cell adhesion, the cytoskeleton, amino acid and lipid metabolism, and ribosomal subunits. Transmembrane protein 106B (TMEM106B), a regulator of lysosomal and oligodendrocyte function, was regulated with greatest effect size. The increase in TMEM106B levels with age was specific to carriers of the rs1990622-A allele in the TMEM106B gene that is associated with increased risk for frontotemporal dementia, Alzheimer's disease, Parkinson's disease, and hippocampal sclerosis with ageing. Hippocampal lipids were not significantly affected by APOE genotype, however levels of myelin-enriched sulfatides and hexosylceramides were significantly lower, and polyunsaturated phospholipids were higher, in rs1990622-A carriers after controlling for APOE genotype. Conclusions Our study provides the first evidence that TMEM106B protein abundance is increased with brain ageing in humans, and the first evidence that the major TMEM106B dementia risk allele affects brain lipid homeostasis, with a clear effect on myelin lipid content. Our data implies that TMEM106B is one of a growing list of major dementia risk genes that affect glial lipid metabolism.
 Glutamine is an essential cerebral metabolite. Several critical brain processes are directly linked to glutamine, including ammonia homeostasis, energy metabolism and neurotransmitter recycling. Astrocytes synthesize and release large quantities of glutamine, which is taken up by neurons to replenish the glutamate and GABA neurotransmitter pools. Astrocyte glutamine hereby sustains the glutamate/GABA-glutamine cycle, synaptic transmission and general brain function. Cerebral glutamine homeostasis is linked to the metabolic coupling of neurons and astrocytes, and relies on multiple cellular processes, including TCA cycle function, synaptic transmission and neurotransmitter uptake. Dysregulations of processes related to glutamine homeostasis are associated with several neurological diseases and may mediate excitotoxicity and neurodegeneration. In particular, diminished astrocyte glutamine synthesis is a common neuropathological component, depriving neurons of an essential metabolic substrate and precursor for neurotransmitter synthesis, hereby leading to synaptic dysfunction. While astrocyte glutamine synthesis is quantitatively dominant in the brain, oligodendrocyte-derived glutamine may serve important functions in white matter structures. In this review, the crucial roles of glial glutamine homeostasis in the healthy and diseased brain are discussed. First, we provide an overview of cellular recycling, transport, synthesis and metabolism of glutamine in the brain. These cellular aspects are subsequently discussed in relation to pathological glutamine homeostasis of hepatic encephalopathy, epilepsy, Alzheimer's disease, Huntington's disease and amyotrophic lateral sclerosis. Further studies on the multifaceted roles of cerebral glutamine will not only increase our understanding of the metabolic collaboration between brain cells, but may also aid to reveal much needed therapeutic targets of several neurological pathologies.
 Arteriolar hyalinosis in kidneys is an independent predictor of cardiovascular disease, the main cause of mortality in chronic kidney disease (CKD). The underlying molecular mechanisms of protein accumulation in the subendothelial space are not well understood. Using single cell transcriptomic data and whole slide images from kidney biopsies of patients with CKD and acute kidney injury in the Kidney Precision Medicine Project, the molecular signals associated with arteriolar hyalinosis were evaluated. Co-expression network analysis of the endothelial genes yielded three gene set modules as significantly associated with arteriolar hyalinosis. Pathway analysis of these modules showed enrichment of transforming growth factor beta / bone morphogenetic protein (TGFβ / BMP) and vascular endothelial growth factor (VEGF) signaling pathways in the endothelial cell signatures. Ligand-receptor analysis identified multiple integrins and cell adhesion receptors as over-expressed in arteriolar hyalinosis, suggesting a potential role of integrin-mediated TGFβ signaling. Further analysis of arteriolar hyalinosis associated endothelial module genes identified focal segmental glomerular sclerosis as an enriched term. On validation in gene expression profiles from the Nephrotic Syndrome Study Network cohort, one of the three modules was significantly associated with the composite endpoint (> 40% reduction in estimated glomerular filtration rate (eGFR) or kidney failure) independent of age, sex, race, and baseline eGFR, suggesting poor prognosis with elevated expression of genes in this module. Thus, integration of structural and single cell molecular features yielded biologically relevant gene sets, signaling pathways and ligand-receptor interactions, underlying arteriolar hyalinosis and putative targets for therapeutic intervention.
 Traumatic brain injury (TBI) is a major health problem that affects millions of persons worldwide every year among all age groups, mainly young children, and elderly persons. It is the leading cause of death for children under the age of 16 and is highly correlated with a variety of neuronal disorders, such as epilepsy, and neurodegenerative disease, such as Alzheimer's disease or amyotrophic lateral sclerosis. Over the past few decades, our comprehension of the molecular pathway of TBI has improved, yet despite being a major public health issue, there is currently no U.S. Food and Drug Administration-approved treatment for TBI, and a gap remains between these advances and their application to the clinical treatment of TBI. One of the major hurdles for pushing TBI research forward is the accessibility of TBI models and tools. Most of the TBI models require costume-made, complex, and expensive equipment, which often requires special knowledge to operate. In this study, we present a modular, three-dimensional printed TBI induction device, which induces, by the pulse of a pressure shock, a TBI-like injury on any standard cell-culture tool. Moreover, we demonstrate that our device can be used on multiple systems and cell types and can induce repetitive TBIs, which is very common in clinical TBI. Further, we demonstrate that our platform can recapitulate the hallmarks of TBI, which include cell death, decrease in neuronal functionality, axonal swelling (for neurons), and increase permeability (for endothelium). In addition, in view of the continued discussion on the need, benefits, and ethics of the use of animals in scientific research, this in vitro, high-throughput platform will make TBI research more accessible to other labs that prefer to avoid the use of animals yet are interested in this field. We believe that this will enable us to push the field forward and facilitate/accelerate the availability of novel treatments.
 INTRODUCTION: A hexanucleotide repeat expansion (HRE) intronic to chromosome 9 open reading frame 72 ( C9orf72 ) is recognized as the most common genetic cause of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and ALS-FTD. Identifying genes that show similar regional co-expression patterns to C9orf72 may help identify novel gene targets and biological mechanisms that mediate selective vulnerability to ALS and FTD pathogenesis. METHODS: We leveraged mRNA expression data in healthy brain from the Allen Human Brain Atlas to evaluate C9orf72 co-expression patterns. To do this, we correlated average C9orf72 expression values in 51 regions across different anatomical divisions (cortex, subcortex, cerebellum) with average gene expression values for 15,633 protein-coding genes, including 50 genes known to be associated with ALS, FTD, or ALS-FTD. We then evaluated whether the identified C9orf72 co-expressed genes correlated with patterns of cortical thickness in symptomatic C9orf72 pathogenic HRE carriers (n=19). Lastly, we explored whether genes with significant C9orf72 radiogenomic correlations (i.e., ' C9orf72 gene network') were enriched in specific cell populations in the brain and enriched for specific biological and molecular pathways. RESULTS: A total of 1,748 genes showed an anatomical distribution of gene expression in the brain similar to C9orf72 and significantly correlated with patterns of cortical thickness in C9orf72 HRE carriers. This C9orf72 gene network was differentially expressed in cell populations previously implicated in ALS and FTD, including layer 5b cells, cholinergic motor neurons in the spinal cord, and medium spiny neurons of the striatum, and was enriched for biological and molecular pathways associated with multiple neurotransmitter systems, protein ubiquitination, autophagy, and MAPK signaling, among others. CONCLUSIONS: Considered together, we identified a network of C9orf72 -associated genes that may influence selective regional and cell-type-specific vulnerabilities in ALS/FTD.
 OBJECTIVE: This review aimed to systematically analyse the influence of clinical variables, diagnostic parameters and the overall image acquisition process on automation and deep learning in TMJ disorders. METHODS: Articles were screened in late 2022 according to a predefined eligibility criteria adhering to the PRISMA protocol. Eligible studies were extracted from databases hosted by MEDLINE, EBSCOHost, Scopus, PubMed and Web of Science. Critical appraisals were performed on individual studies following Nature Medicine's MI-CLAIM checklist while a combined appraisal of the image acquisition procedures was conducted using Cochrane's GRADE approach. RESULTS: Twenty articles were included for full review following eligibility screening. The average experience possessed by the clinical operators within the eligible studies was 13.7 years. Bone volume, trabecular number and separation, and bone surface-to-volume ratio were clinical radiographic parameters while disc shape, signal intensity, fluid collection, joint space narrowing and arthritic changes were successful parameters used in MRI-based deep machine learning. Entropy was correlated to sclerosis in CBCT and was the most stable radiomic parameter in MRI while contrast was the least stable across thermography and MRI. Adjunct serum and salivary biomarkers, or clinical questionnaires only marginally improved diagnostic outcomes through deep learning. Substantial data was classified as unusable and subsequently discarded owing to a combination of suboptimal image acquisition and data augmentation procedures. Inadequate identification of the participant characteristics and multiple studies utilising the same dataset and data acquisition procedures accounted for serious risks of bias. CONCLUSION: Deep-learned models diagnosed osteoarthritis as accurately as clinicians from 2D and 3D radiographs but, in comparison, performed poorly when detecting disc disorders from MRI datasets. Complexities in clinical classification criteria; non-standardised diagnostic parameters; errors in image acquisition; cognitive, contextual or implicit biases were influential variables that generally affected analyses of inflammatory joint changes and disc disorders.
 Developmental and epileptic encephalopathies (DEEs) are rare neurodevelopmental disorders characterised by early-onset and often intractable seizures and developmental delay/regression, and include Dravet syndrome and Lennox-Gastaut syndrome (LGS). Rufinamide, fenfluramine, stiripentol, cannabidiol and ganaxolone are antiseizure medications (ASMs) with diverse mechanisms of action that have been approved for treating specific DEEs. Rufinamide is thought to suppress neuronal hyperexcitability by preventing the functional recycling of voltage-gated sodium channels from the inactivated to resting state. It is licensed for adjunctive treatment of seizures associated with LGS. Fenfluramine increases extracellular serotonin levels and may reduce seizures via activation of specific serotonin receptors and positive modulation of the sigma-1 receptor. Fenfluramine is licensed for adjunctive treatment of seizures associated with Dravet syndrome and LGS. Stiripentol is a positive allosteric modulator of type-A gamma-aminobutyric acid (GABA(A)) receptors. As a broad-spectrum inhibitor of cytochrome P450 enzymes, its antiseizure effects may additionally arise through pharmacokinetic interactions with co-administered ASMs. Stiripentol is licensed for treating seizures associated with Dravet syndrome in patients taking clobazam and/or valproate. The mechanism(s) of action of cannabidiol remains largely unclear although multiple targets have been proposed, including transient receptor potential vanilloid 1, G protein-coupled receptor 55 and equilibrative nucleoside transporter 1. Cannabidiol is licensed as adjunctive treatment in conjunction with clobazam for seizures associated with Dravet syndrome and LGS, and as adjunctive treatment of seizures associated with tuberous sclerosis complex. Like stiripentol, ganaxolone is a positive allosteric modulator at GABA(A) receptors. It has recently been licensed in the USA for the treatment of seizures associated with cyclin-dependent kinase-like 5 deficiency disorder. Greater understanding of the causes of DEEs has driven research into the potential use of other novel and repurposed agents. Putative ASMs currently in clinical development for use in DEEs include soticlestat, carisbamate, verapamil, radiprodil, clemizole and lorcaserin.
 Treatments for neurodegenerative disorders remain rare, although recent FDA approvals, such as Lecanemab and Aducanumab for Alzheimer's Disease, highlight the importance of the underlying biological mechanisms in driving discovery and creating disease modifying therapies. The global population is aging, driving an urgent need for therapeutics that stop disease progression and eliminate symptoms. In this study, we create an open framework and resource for evidence-based identification of therapeutic targets for neurodegenerative disease. We use Summary-data-based Mendelian Randomization to identify genetic targets for drug discovery and repurposing. In parallel, we provide mechanistic insights into disease processes and potential network-level consequences of gene-based therapeutics. We identify 116 Alzheimer's disease, 3 amyotrophic lateral sclerosis, 5 Lewy body dementia, 46 Parkinson's disease, and 9 Progressive supranuclear palsy target genes passing multiple test corrections (pSMR_multi < 2.95x10-6 and pHEIDI > 0.01). We created a therapeutic scheme to classify our identified target genes into strata based on druggability and approved therapeutics - classifying 41 novel targets, 3 known targets, and 115 difficult targets (of these 69.8% are expressed in the disease relevant cell type from single nucleus experiments). Our novel class of genes provides a springboard for new opportunities in drug discovery, development and repurposing in the pre-competitive space. In addition, looking at drug-gene interaction networks, we identify previous trials that may require further follow-up such as Riluzole in AD. We also provide a user-friendly web platform to help users explore potential therapeutic targets for neurodegenerative diseases, decreasing activation energy for the community [https://nih-card-ndd-smr-home-syboky.streamlit.app/].
 The geroscience hypothesis states that a therapy that prevents the underlying aging process should prevent multiple aging related diseases. The mTOR (mechanistic target of rapamycin)/insulin and NAD+ (nicotinamide adenine dinucleotide) pathways are two of the most validated aging pathways. Yet, it’s largely unclear how they might talk to each other in aging. In genome-wide CRISPRa screening with a novel class of N-O-Methyl-propanamide-containing compounds we named BIOIO-1001, we identified lipid metabolism centering on SIRT3 as a point of intersection of the mTOR/insulin and NAD+ pathways. In vivo testing indicated that BIOIO-1001 reduced high fat, high sugar diet-induced metabolic derangements, inflammation, and fibrosis, each being characteristic of non-alcoholic steatohepatitis (NASH). An unbiased screen of patient datasets suggested a potential link between the anti-inflammatory and anti-fibrotic effects of BIOIO-1001 in NASH models to those in amyotrophic lateral sclerosis (ALS). Directed experiments subsequently determined that BIOIO-1001 was protective in both sporadic and familial ALS models. Both NASH and ALS have no treatments and suffer from a lack of convenient biomarkers to monitor therapeutic efficacy. A potential strength in considering BIOIO-1001 as a therapy is that the blood biomarker that it modulates, namely plasma triglycerides, can be conveniently used to screen patients for responders. More conceptually, to our knowledge BIOIO-1001 is a first therapy that fits the geroscience hypothesis by acting on multiple core aging pathways and that can alleviate multiple conditions after they have set in. BRIEF SUMMARY: These studies characterize a novel gerotherapy, BIOIO-1001, that identifies lipid metabolism as an intersection of the mTOR and NAD+ pathways.
 BACKGROUND: Migraine is a historically unilateral head pain condition, the cause of which is not currently known. A growing body of literature suggests individuals who experience migraine with left-sided headache ("left-sided migraine") may be distinguished from those who experience migraine with right-sided headache ("right-sided migraine"). OBJECTIVE: In this scoping review, we explore migraine unilaterality by summarizing what is currently known about left- and right-sided migraine. METHODS: Two senior medical librarians worked with the lead authors to construct and refine a set of search terms to identify studies of subjects with left- or right-sided migraine published between 1988, which is the year of publication of the first edition of the International Classification of Headache Disorders (ICHD), and December 8, 2021 (the date the searches were conducted). The following databases were searched: Medline, Embase, PsycINFO, PubMed, Cochrane Library, and Web of Science. Abstracts were loaded into Covidence review software, deduplicated, then screened by two authors to determine study eligibility. Eligible studies were those involving subjects diagnosed with migraine (according to ICHD criteria) in which the authors either: a) compared left- to right-sided migraine; or b) described (with analysis) a characteristic that differentiated the two. Data were extracted by the lead author, including ICHD version, the definition of unilateral migraine used by the authors, sample size, whether the findings were collected during or between attacks, and their key findings. The key findings were grouped into the following themes: handedness, symptoms, psychiatric assessments, cognitive testing, autonomic function, and imaging. RESULTS: After deduplication, the search yielded 5428 abstracts for screening. Of these, 179 met eligibility criteria and underwent full text review. 26 articles were included in the final analysis. All of the studies were observational. One study was performed during attack, nineteen between attacks, and six both during and between attacks. Left- and right-sided migraine were found to differ across multiple domains. In several cases, reciprocal findings were reported in left- and right-migraine. For example, both left- and right-sided migraine were associated with ipsilateral handedness, tinnitus, onset of first Parkinson's symptoms, changes in blood flow across the face, white matter hyperintensities on MRI, activation of the dorsal pons, hippocampal sclerosis, and thalamic NAA/Cho and NAA/Cr concentrations. In other cases, however, the findings were specific to one migraine laterality. For example, left-sided migraine was associated with worse quality of life, anxiety, bipolar disorder, PTSD, lower sympathetic activity, and higher parasympathetic activity. Whereas right-sided migraine was associated with poorer performance on multiple cognitive tests, a greater degree of anisocoria, changes in skin temperature, higher diastolic blood pressure, changes in blood flow through the middle cerebral and basilar arteries, and changes on EEG. CONCLUSION: Left- and right-sided migraine differed across a wide range of domains, raising the possibility that the pathophysiology of left- and right-migraine may not be identical.
 OBJECTIVES: In this study, we aimed to evaluate the factors associated with disability and quality of life (QoL) in Turkish patients with systemic sclerosis (SSc). PATIENTS AND METHODS: Between January 2018 and January 2019, a total of 256 SSc patients (20 males, 236 females; mean age: 50.9±12.4 years; range, 19 to 87 years) who were diagnosed with SSc were included in the study. Disability and health-related QoL (HRQoL) were evaluated by the Health Assessment Questionnaire (HAQ), scleroderma HAQ (SHAQ), Duruöz Hand Index (DHI), and Short Form-36 (SF-36). Linear regression analysis methods were used to describe factors associated with disability and QoL of the patients. RESULTS: All disability scores were higher and HRQoL scores were lower in diffuse cutaneous SSc patients compared limited cutaneous SSc, and differentiations were significant (p=0.001 and p=0.007). In multiple regression, pain (VAS) was the strongest predictor for high disability and low QoL scores (p<0.001) as HAQ (β=0.397, 0.386, 0.452), SHAQ (β=0.397, 0.448, 0.372), DHI (β=0.446, 0.536, 0.389), PCS (β=-0.417,-0.499, -0.408) and MCS (β=-0.478, -0.441, -0.370) in combined, lcSSc and dcSSc patients respectively. The factors associated with high disability and low QoL scores were forced vital capacity for HAQ (β=-0.172, p=0.002) and SF-36 PCS (β=0.187, p=0.001); disease duration for HAQ (β=0.208, p<0.001), DHI (β=0.147, p=0.006), and SF-36 PCS (β=-0.134, p=0.014); 6-minute walk test for HAQ (β=-0.161, p=0.005) and SF-36 PCS (β=0.153, p=0.009); and modified Rodnan skin score for SHAQ (β=0.250, p<0.001) and DHI (β=0.233, p<0.001) in SSc patients. Diffusing capacity of the lungs for carbon monoxide for HAQ (β=-0.189, p=0.010) and SHAQ (β=-0.247, p=0.002); erythrocyte sedimentation rate for DHI (β=0.322, p<0.001); age for SF-36 PCS (β=-0.221, p=0.003) and body mass index for SF-36 PCS (β=-0.200, p=0.008) and MCS (β=-0.175, p=0.034) were the other variables associated with high disability or low QoL scores in SSc subsets. CONCLUSION: Clinicians should consider the management of the pain and its sources as a key to improve better functional state and quality of daily life in SSc.
 BACKGROUND AND PURPOSE: As in the brain reserve concept, a larger cervical canal area may also protect against disability. In this context, a semiautomated pipeline has been developed to obtain quantitative estimations of the cervical canal area. The aim of the study was to validate the pipeline, to evaluate the consistency of the cervical canal area measurements during a 1-year period, and to compare cervical canal area estimations obtained from brain and cervical MRI acquisitions. MATERIALS AND METHODS: Eight healthy controls and 18 patients with MS underwent baseline and follow-up 3T brain and cervical spine sagittal 3D MPRAGE. The cervical canal area was measured in all acquisitions, and estimations obtained with the proposed pipeline were compared with manual segmentations performed by 1 evaluator using the Dice similarity coefficient. The cervical canal area estimations obtained on baseline and follow-up T1WI were compared; brain and cervical cord acquisitions were also compared using the individual and average intraclass correlation coefficients. RESULTS: The agreement between the manual cervical canal area masks and the masks provided by the proposed pipeline was excellent, with a mean Dice similarity coefficient mean of 0.90 (range, 0.73-0.97). The cervical canal area estimations obtained from baseline and follow-up scans showed a good level of concordance (intraclass correlation coefficient = 0.76; 95% CI, 0.44-0.88); estimations obtained from brain and cervical MRIs also had good agreement (intraclass correlation coefficient = 0.77; 95% CI, 0.45-0.90). CONCLUSIONS: The proposed pipeline is a reliable tool to estimate the cervical canal area. The cervical canal area is a stable measure across time; moreover, when cervical sequences are not available, the cervical canal area could be estimated using brain T1WI.
 Anti-aquaporin-4 antibody (AQP4-IgG)-positive neuromyelitis optica spectrum disorder (NMOSD) and Sjögren syndrome (SS) are likely comorbidities. However, the exact effects of age and disease duration on the positivity rates of serum anti-Ro/SSA and anti-La/SSB (anti-SSA/SSB) antibodies and the presence of sicca symptoms in patients with AQP4-IgG remain unknown. In the present study, we evaluated the data from patients with suspected NMOSD who had neurological episodes and tested for serum AQP4-IgG. Associations between the presence of serum AQP4-IgG and SS-related findings were evaluated. The presence of anti-SSA/SSB antibodies [odds ratio (OR), 7.34; 95% confidence interval (CI), 5.71-9.43; p < 0.0001] and that of sicca symptoms (OR, 2.08; 95% CI, 1.67-2.58; p < 0.0001) were both higher in patients with AQP4-IgG (n = 1,651) than in those without AQP4-IgG (n = 2,796). Meanwhile, neither age nor the elapsed time from neurological onset was linked to the prevalence of anti-SSA/SSB antibodies or sicca symptoms, and the prevalence rates of the SS-related factors were elevated since the onset of neurological episodes in those with AQP4-IgG. The frequency of sicca symptoms among those with anti-SSA/SSB antibodies was irrespective of AQP4-IgG (OR, 1.11; 95% CI, 0.67-1.85; p = 0.6892). The measured AQP4-IgG titers did not differ significantly according to the presence of anti-SSA/SSB antibodies (p = 0.2386; Mann-Whitney U test). In summary, age and duration of NMOSD were not the factors producing an elevated prevalence of anti-SSA/SSB antibodies and sicca symptoms in patients with AQP4-IgG, implying that the occurrence of comorbid SS is likely to temporarily precede or synchronize with the onset of AQP4-IgG-positive NMOSD.
 BACKGROUND: Circulating autoantibodies (AB) against brain-antigens, often deemed pathological, receive increasing attention. We assessed predispositions and seroprevalence/characteristics of 49 AB in > 7000 individuals. METHODS: Exploratory cross-sectional cohort study, investigating deeply phenotyped neuropsychiatric patients and healthy individuals of GRAS Data Collection for presence/characteristics of 49 brain-directed serum-AB. Predispositions were evaluated through GWAS of NMDAR1-AB carriers, analyses of immune check-point genotypes, APOE4 status, neurotrauma. Chi-square, Fisher's exact tests and logistic regression analyses were used. RESULTS: Study of N = 7025 subjects (55.8 % male; 41 ± 16 years) revealed N = 1133 (16.13 %) carriers of any AB against 49 defined brain-antigens. Overall, age dependence of seroprevalence (OR = 1.018/year; 95 % CI [1.015-1.022]) emerged, but no disease association, neither general nor with neuropsychiatric subgroups. Males had higher AB seroprevalence (OR = 1.303; 95 % CI [1.144-1.486]). Immunoglobulin class (N for IgM:462; IgA:487; IgG:477) and titers were similar. Abundant were NMDAR1-AB (7.7 %). Low seroprevalence (1.25 %-0.02 %) was seen for most AB (e.g., amphiphysin, KCNA2, ARHGAP26, GFAP, CASPR2, MOG, Homer-3, KCNA1, GLRA1b, GAD65). Non-detectable were others. GWAS of NMDAR1-AB carriers revealed three genome-wide significant SNPs, two intergenic, one in TENM3, previously autoimmune disease-associated. Targeted analysis of immune check-point genotypes (CTLA4, PD1, PD-L1) uncovered effects on humoral anti-brain autoimmunity (OR = 1.55; 95 % CI [1.058-2.271]) and disease likelihood (OR = 1.43; 95 % CI [1.032-1.985]). APOE4 carriers (∼19 %) had lower seropositivity (OR = 0.766; 95 % CI [0.625-0.933]). Neurotrauma predisposed to NMDAR1-AB seroprevalence (IgM: OR = 1.599; 95 % CI [1.022-2.468]). CONCLUSIONS: Humoral autoimmunity against brain-antigens, frequent across health and disease, is predicted by age, gender, genetic predisposition, and brain injury. Seroprevalence, immunoglobulin class, or titers do not predict disease.
 OBJECTIVE: Childhood trauma has been implicated as a risk factor for the etiology of psychogenic nonepileptic seizures (PNES). Relatively little attention has been paid to whether profiles of specific trauma types differ between patients with epilepsy and PNES. Investigating childhood trauma profiles in these patient groups may identify psychological vulnerabilities that predispose to developing PNES, and aid early diagnoses, prevention, and treatment. METHODS: Data were collected from two cohorts (n(Retrospective)  = 203; n(Prospective)  = 209) admitted to video-electroencephalography (EEG) monitoring units in Melbourne Australia. The differences in Childhood Trauma Questionnaire domain score between patient groups were investigated using standardized effect sizes and general linear mixed-effects models (GLMMs). Receiver-operating characteristic curves were used to investigate classification accuracy. RESULTS: In the retrospective cohort, patients diagnosed with PNES reported greater childhood emotional abuse, emotional neglect, physical abuse, sexual abuse, and physical neglect relative to patients with epilepsy. These differences were replicated in the prospective cohort, except for physical abuse. GLMMs revealed significant main effects for group in both cohorts, but no evidence for any group by domain interactions. Reported sexual abuse showed the best screening performance of PNES, although no psychometric scores were adequate as isolated measures. SIGNIFICANCE: Patients with PNES report a greater frequency of childhood trauma than patients with epilepsy. This effect appears to hold across all trauma types, with no strong evidence emerging for a particular trauma type that is more prevalent in PNES. From a practical perspective, inquiry regarding a history of sexual abuse shows the most promise as a screening measure.
 BACKGROUND AND PURPOSE: This study aimed to investigate if pre-existing neurological conditions, such as dementia and a history of cerebrovascular disease, increase the risk of severe outcomes including death, intensive care unit (ICU) admission and vascular events in patients hospitalized with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in 2022, when Omicron was the predominant variant. METHODS: A retrospective analysis was conducted of all patients with SARS-CoV-2 infection, confirmed by polymerase chain reaction test, admitted to the University Medical Center Hamburg-Eppendorf from 20 December 2021 until 15 August 2022. In all, 1249 patients were included in the study. In-hospital mortality was 3.8% and the ICU admission rate was 9.9%. Ninety-three patients with chronic cerebrovascular disease and 36 patients with pre-existing all-cause dementia were identified and propensity score matching by age, sex, comorbidities, vaccination status and dexamethasone treatment was performed in a 1:4 ratio with patients without the respective precondition using nearest neighbor matching. RESULTS: Analysis revealed that neither pre-existing cerebrovascular disease nor all-cause dementia increased mortality or the risk for ICU admission. All-cause dementia in the medical history also had no effect on vascular complications under investigation. In contrast, an increased odds ratio for both pulmonary artery embolism and secondary cerebrovascular events was observed in patients with pre-existing chronic cerebrovascular disease and myocardial infarction in the medical history. CONCLUSION: These findings suggest that patients with pre-existing cerebrovascular disease and myocardial infarction in their medical history may be particularly susceptible to vascular complications following SARS-CoV-2 infection with presumed Omicron variant.
 BACKGROUND: Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular transitory condition characterized by severe headache, possible concomitant acute neurological symptoms, evidence of diffuse multifocal segmental constriction of cerebral arteries, and usually spontaneously resolving within 3 months. Putative causes and/or precipitating factors are vasoactive drugs-e.g., antidepressants, α-sympathomimetics, triptans-post-partum, and immunosuppressants. CASE PRESENTATION: We report the case of a middle-aged woman referred to the emergency room (ER) with a 7-day long intense headache and vomit. Cerebral non-contrast computed tomography (CT) was negative for acute ischemic lesions or intracranial bleedings. She was again referred to ER 7 days later with additional fluctuating episodes of weakness in left arm and both lower limbs. A new brain CT was negative. Due to worsening headache, a transcranial color-coded Doppler (TCCD) was performed, which showed diffuse multifocal blood flow acceleration in all principal intracranial vessels, and particularly on the right hemisphere. These findings were subsequently confirmed at MR angiogram and digital subtraction angiography. CONCLUSION: TCCD imaging is a non-invasive and relatively inexpensive tool which provides real-time information on cerebrovascular function, blood flow velocities, and hemodynamic changes. TCCD may be a powerful tool in the early detection of acute infrequent cerebrovascular conditions, as well as in monitoring their course and the therapeutic response.
 BACKGROUND: The self-administered iPad-based Cleveland Clinic Cognitive Battery (C3B) was designed specifically for the efficient screening of cognitive functioning of older adults in a primary care setting. OBJECTIVE: 1) Generate regression-based norms from healthy participants to enable demographic corrections to facilitate clinical interpretation; 2) estimate test-retest reliability and practice effects; 3) examine ability to discriminate mild cognitive impairment (MCI) from healthy aging; 4) d etermine validity of screening in a distracting clinical environment; and 5) determine completion rates and patient satisfaction in a primary care setting. METHODS: Study 1 (S1) recruited a stratified sample of 428 healthy adults, ages 18-89, to generate regression-based equations. S2 assessed 2-week test-retest reliability and practice effects in 30 healthy elders. S3 recruited 30 MCI patients and 30 demographically-matched healthy controls. In S4, 30 healthy elders self-administered the C3B in a distracting environment and in a quiet private room in counterbalanced order. In a demonstration project, 470 consecutive primary care patients were administered the C3B as part of routine clinical care (S5). RESULTS: C3B performance was primarily influenced by age, education, and race (S1), had acceptably high test-retest reliability and minimal practice effects (S2), discriminated MCI from healthy controls (S3), was not negatively impacted by a distracting clinical environment (S4), had high completion rates (>92%) and positive ratings from primary care patients (S5). CONCLUSION: The C3B is a computerized cognitive screening tool that is reliable, validated, self-administered, and is conducive to integration into a busy primary care clinical workflow for detecting MCI, early Alzheimer's disease, and other related dementias.
 BACKGROUND AND PURPOSE: The response to cluster headache treatments has a high interindividual variation. To date, treatment response has only been assessed by a candidate gene approach and no investigations into metabolic pathways have been performed. Our aim was to investigate the association between the polygenetic risk of cluster headache and treatment response to first-line cluster headache treatments as well as known functional variants of CYP3A4 and the response to verapamil. Further, it was aimed to replicate previous single nucleotide polymorphisms found to be associated with treatment response in cluster headache and/or migraine. METHODS: In, 508 cluster headache patients diagnosed according to the International Classification of Headache Disorders were genotyped and participated in a semi-structured interview to evaluate treatment response. Polygenetic risk scores were calculated by the effect retrieved from a meta-analysis of the latest two genome-wide association studies on cluster headache. RESULTS: Inferior treatment response to oxygen, triptans and verapamil is associated with chronicity of cluster headache were confirmed but no evidence was found that a response could be predicted by a high genetic risk of cluster headache. Likewise, verapamil response was not associated with functional variants of CYP3A4. No support of the genetic variants previously reported to be associated with treatment response to triptans or verapamil was found. CONCLUSION: The clinically relevant variation in treatment response for cluster headache was not influenced by genetic factors in the present study.
 OBJECTIVE: This study explored the impact of time-restricted eating (TRE) versus standard dietary advice (SDA) on bone health. METHODS: Adults with ≥1 component of metabolic syndrome were randomized to TRE (ad libitum eating within 12 hours) or SDA (food pyramid brochure). Bone turnover markers and bone mineral content/density by dual energy x-ray absorptiometry were assessed at baseline and 6-month follow-up. Statistical analyses were performed in the total population and by weight loss response. RESULTS: In the total population (n = 42, 76% women, median age 47 years [IQR: 31-52]), there were no between-group differences (TRE vs. SDA) in any bone parameter. Among weight loss responders (≥0.6 kg weight loss), the bone resorption marker β-carboxyterminal telopeptide of type I collagen tended to decrease after TRE but increase after SDA (between-group differences p = 0.041), whereas changes in the bone formation marker procollagen type I N-propeptide did not differ between groups. Total body bone mineral content decreased after SDA (p = 0.028) but remained unchanged after TRE (p = 0.31) in weight loss responders (between-group differences p = 0.028). Among nonresponders (<0.6 kg weight loss), there were no between-group differences in bone outcomes. CONCLUSIONS: TRE had no detrimental impact on bone health, whereas, when weight loss occurred, it was associated with some bone-sparing effects compared with SDA.
 BACKGROUND AND PURPOSE: Outcome and rechallenge data on central nervous system (CNS) autoimmunity triggered by immune checkpoint inhibitors (ICIs) are limited. We aim to describe a large series of patients with ICI-triggered CNS autoimmunity, and to compare these patients with spontaneous paraneoplastic syndromes (PNS). METHODS: We retrospectively reviewed Mayo Clinic patients with ICI-triggered CNS autoimmunity (February 2015-June 2021). Clinical characteristics were compared to spontaneous PNS patients (with antineuronal nuclear antibody [ANNA]-1 or anti-Hu neurological autoimmunity, and/or neuroendocrine tumors [NET]) evaluated within the same period. RESULTS: Thirty-one patients were included (55% female, median age = 63 years, range = 39-76). Median time from ICI initiation was 3.65 months (range = 0.8-44.5). The most common associated malignancies were melanoma and small cell lung cancer. CNS manifestations included encephalitis (n = 16), meningoencephalitis (n = 8), cerebellar ataxia (n = 4), demyelinating syndrome (n = 2), and myelopathy (n = 1). Magnetic resonance imaging was abnormal in 62%. Cerebrospinal fluid was inflammatory in 70%. Neural autoantibodies were identified in 47%, more frequently in patients with NET (p = 0.046). ICI was discontinued in 97%; 90% received immunosuppressive treatment. After median 6.8 months follow-up (range = 0.7-46), 39% had unfavorable outcomes (grade ≥ 3). This was associated with higher severity degree at onset, shorter period from ICI to neurological symptom onset, and encephalitis. Four patients were rechallenged with ICI, and one relapsed. Patients with NET and with ANNA-1 ICI-triggered CNS autoimmunity had associated peripheral nervous system manifestations more frequently than their spontaneous counterparts (p = 0.007 and p = 0.028, respectively). CONCLUSIONS: One third of ICI-related CNS autoimmunity patients have unfavorable outcomes. Relapses may occur after ICI rechallenge. Neural autoantibodies are often present, more commonly in patients with NET.
 BACKGROUND AND OBJECTIVES: Autoimmune encephalitis (AE) is an inflammatory disease of the central nervous system which can result in long-term seizures and cognitive dysfunction despite treatment with immunotherapy. The role of the innate immune system in AE is not well established. To investigate the contribution of innate immunity to AE and its long-term outcomes we evaluated peripheral monocytes and serum cytokines in the periphery of patients with AE. METHODS AND RESULTS: We recruited 40 patients with previously diagnosed AE and 28 healthy volunteers to our cross-sectional observation study and evaluated their peripheral blood monocytes via flow cytometry and serum cytokines (CCL-2, CCL-17, G-CSF, GM-CSF, IFNγ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-17, TNFα) via ELISA.Compared with controls the AE cohort had expansion of the 'pro-inflammatory' CD14(+)CD16(+) monocyte sub-population (7.13% vs 5.46%, p < 0.01) with higher levels of serum IL-6 (2.34 pg/mL vs 0.54 pg/mL, p < 0.001). These changes were most significant in anti-LGI-1 antibody mediated AE, an AE subtype with poor long-term cognitive outcomes. CONCLUSION: Expansion of the peripheral CD14(+)CD16(+) monocyte population and increased serum IL-6 in AE is reflective of changes seen in other systemic inflammatory and neurodegenerative conditions. These changes may indicate a persistent pro-inflammatory state in AE and may contribute to poor long-term outcomes.
 INTRODUCTION: Pulmonary arterial hypertension (PAH) and interstitial lung disease (ILD) are the leading causes of death in systemic sclerosis (SSc). Until now, no prospective biomarker to predict new onset of SSc-ILD or SSc-PAH in patients with SSc has reached clinical application. In homeostasis, the receptor for advanced glycation end products (RAGE) is expressed in lung tissue and involved in cell-matrix adhesion, proliferation and migration of alveolar epithelial cells, and remodeling of the pulmonary vasculature. Several studies have shown that sRAGE levels in serum and pulmonary tissue vary according to the type of lung-related complication. Therefore, we investigated levels of soluble RAGE (sRAGE) and its ligand high mobility group box 1 (HMGB1) in SSc and their abilities to predict SSc-related pulmonary complications. METHODS: One hundred eighty-eight SSc patients were followed retrospectively for the development of ILD, PAH, and mortality for 8 years. Levels of sRAGE and HMGB1 were measured in serum by ELISA. Kaplan-Meier survival curves were performed to predict lung events and mortality and event rates were compared with a log-rank test. Multiple linear regression analysis was performed to examine the association between sRAGE and important clinical determinants. RESULTS: At baseline, levels of sRAGE were significantly higher in SSc-PAH-patients (median 4099.0 pg/ml [936.3-6365.3], p = 0.011) and lower in SSc-ILD-patients (735.0 pg/ml [IQR 525.5-1988.5], p = 0.001) compared to SSc patients without pulmonary involvement (1444.5 pg/ml [966.8-2276.0]). Levels of HMGB1 were not different between groups. After adjusting for age, gender, ILD, chronic obstructive pulmonary disease, anti-centromere antibodies, the presence of puffy fingers or sclerodactyly, use of immunosuppression, antifibrotic therapy, or glucocorticoids, and use of vasodilators, higher sRAGE levels remained independently associated with PAH. After a median follow-up of 50 months (25-81) of patients without pulmonary involvement, baseline sRAGE levels in the highest quartile were predictive of development of PAH (log-rank p = 0.01) and of PAH-related mortality (p = 0.001). CONCLUSIONS: High systemic sRAGE at baseline might be used as a prospective biomarker for patients with SSc at high risk to develop new onset of PAH. Moreover, high sRAGE levels could predict lower survival rates due to PAH in patients with SSc.
 OBJECTIVE: Juvenile systemic sclerosis (SSc) is an orphan disease, associated with high morbidity and mortality. New treatment strategies are much needed, but clearly defining appropriate outcomes is necessary if successful therapies are to be developed. Our objective here was to propose such outcomes. METHODS: This proposal is the result of 4 face-to-face consensus meetings with a 27-member multidisciplinary team of pediatric rheumatologists, adult rheumatologists, dermatologists, pediatric cardiologists, pulmonologists, gastroenterologists, a statistician, and patients. Throughout the process, we reviewed the existing adult data in this field, the more limited pediatric literature for juvenile SSc outcomes, and data from 2 juvenile SSc patient cohorts to assist in making informed, data-driven decisions. The use of items for each domain as an outcome measure in an open label 12-month clinical trial of juvenile SSc was voted and agreed upon using a nominal group technique. RESULTS: After voting, the domains agreed on were global disease activity, skin, Raynaud's phenomenon, digital ulcers, musculoskeletal, cardiac, pulmonary, renal, and gastrointestinal involvement, and quality of life. Fourteen outcome measures had 100% agreement, 1 item had 91% agreement, and 1 item had 86% agreement. The domains of biomarkers and growth/development were moved to the research agenda. CONCLUSION: We reached consensus on multiple domains and items that should be assessed in an open label, 12-month clinical juvenile SSc trial as well as a research agenda for future development.
 OBJECTIVE: To investigate the relationship between glucose metabolism and functional activity in the epileptogenic network of patients with mesial temporal lobe epilepsy (MTLE) and to determine whether this relationship is associated with surgical outcomes. METHODS: (18)F-FDG PET and resting-state functional MRI (rs-fMRI) scans were performed on a hybrid PET/MR scanner in 38 MTLE patients with hippocampal sclerosis (MR-HS), 35 MR-negative patients and 34 healthy controls (HC). Glucose metabolism was measured using (18)F-FDG PET standardized uptake value ratio (SUVR) relative to cerebellum; Functional activity was obtained by fractional amplitude of low-frequency fluctuation (fALFF). The betweenness centrality (BC) of metabolic covariance network and functional network were calculated using graph theoretical analysis. Differences in SUVR, fALFF, BC and the spatial voxel-wise SUVR-fALFF couplings of the epileptogenic network, consisting of default mode network (DMN) and thalamus, were evaluated by Mann-Whitney U test (using the false discovery rate [FDR] for multiple comparison correction). The top ten SUVR-fALFF couplings were selected by Fisher score to predict surgical outcomes using logistic regression model. RESULTS: The results showed decreased SUVR-fALFF coupling in the bilateral middle frontal gyrus (P(FDR) = 0.0230, P(FDR) = 0.0296) in MR-HS patients compared to healthy controls. Coupling in the ipsilateral hippocampus was marginally increased (P(FDR) = 0.0802) in MR-HS patients along with decreased BC of metabolic covariance network and functional network (P(FDR) = 0.0152; P(FDR) = 0.0429). With Fisher score ranking, the top ten SUVR-fALFF couplings in regions from DMN and thalamic subnuclei could predict surgical outcomes with the best performance being a combination of ten SUVR-fALFF couplings with an AUC of 0.914. CONCLUSION: These findings suggest that the altered neuroenergetic coupling in the epileptogenic network is associated with surgical outcomes of MTLE patients, which may provide insight into their pathogenesis and help with preoperative evaluation.
 BACKGROUND AND OBJECTIVES: Intratumoral hemorrhage (ITH) in vestibular schwannoma (VS) after stereotactic radiosurgery (SRS) is exceedingly rare. The aim of this study was to define its incidence and describe its management and outcomes in this subset of patients. METHODS: A retrospective multi-institutional study was conducted, screening 9565 patients with VS managed with SRS at 10 centers affiliated with the International Radiosurgery Research Foundation. RESULTS: A total of 25 patients developed ITH (cumulative incidence of 0.26%) after SRS management, with a median ITH size of 1.2 cm3. Most of the patients had Koos grade II-IV VS, and the median age was 62 years. After ITH development, 21 patients were observed, 2 had urgent surgical intervention, and 2 were initially observed and had late resection because of delayed hemorrhagic expansion and/or clinical deterioration. The histopathology of the resected tumors showed typical, benign VS histology without sclerosis, along with chronic inflammatory cells and multiple fragments of hemorrhage. At the last follow-up, 17 patients improved and 8 remained clinically stable. CONCLUSION: ITH after SRS for VS is extremely rare but has various clinical manifestations and severity. The management paradigm should be individualized based on patient-specific factors, rapidity of clinical and/or radiographic progression, ITH expansion, and overall patient condition.
 Nuclear to cytoplasmic mislocalization and aggregation of multiple RNA-binding proteins (RBPs), including Fused in sarcoma (FUS), are the main neuropathological features of the majority of cases of amyotrophic lateral sclerosis (ALS) and frontotemporal lobular degeneration (FTLD). In ALS-FUS these aggregates arise from disease-associated mutations in FUS, whereas in FTLD-FUS the cytoplasmic inclusions do not contain mutant FUS, suggesting different molecular mechanisms of FUS pathogenesis in FTLD that remain to be investigated. We have previously shown that phosphorylation of the C-terminal Tyr526 of FUS results in increased cytoplasmic retention of FUS due to impaired binding to the nuclear import receptor Transportin 1 (TNPO1). Inspired by the above notions, in the current study we developed a novel antibody against the C-terminally phosphorylated Tyr526 FUS (FUSp-Y526) that is specifically capable of recognizing phosphorylated cytoplasmic FUS, which is poorly recognized by other commercially available FUS antibodies. Using this FUSp-Y526 antibody, we demonstrated a FUS phosphorylation-specific effect on the cytoplasmic distribution of soluble and insoluble FUSp-Y526 in various cells and confirmed the involvement of the Src kinase family in Tyr526 FUS phosphorylation. In addition, we found that FUSp-Y526 expression pattern corelates with active pSrc/pAbl kinases in specific brain regions of mice, indicating preferential involvement of cAbl in the cytoplasmic mislocalization of FUSp-Y526 in cortical neurons. Finally, the pattern of immunoreactivity of active cAbl kinase and FUSp-Y526 revealed altered cytoplasmic distribution of FUSp-Y526 in cortical neurons of post-mortem frontal cortex tissue from FTLD patients compared with controls. The overlap of FUSp-Y526 and FUS signals was found preferentially in small diffuse inclusions and was absent in mature aggregates, suggesting possible involvement of FUSp-Y526 in the formation of early toxic FUS aggregates in the cytoplasm that are largely undetected by commercially available FUS antibodies. Given the overlapping patterns of cAbl activity and FUSp-Y526 distribution in cortical neurons, and cAbl induced sequestration of FUSp-Y526 into G3BP1 positive granules in stressed cells, we propose that cAbl kinase is actively involved in mediating cytoplasmic mislocalization and promoting toxic aggregation of wild-type FUS in the brains of FTLD patients, as a novel putative underlying mechanism of FTLD-FUS pathophysiology and progression.
 The use of cannabidiol (CBD) for therapeutic purposes is receiving considerable attention, with speculation that CBD can be useful in a wide range of conditions. Only one product, a purified form of plant-derived CBD in solution (Epidiolex), is approved for the treatment of seizures in patients with Lennox-Gastaut syndrome, Dravet syndrome, or tuberous sclerosis complex. Appraisal of the therapeutic evidence base for CBD is complicated by the fact that CBD products sometimes have additional phytochemicals (like tetrahydrocannabinol (THC)) present, which can make the identification of the active pharmaceutical ingredient (API) in positive studies difficult. The aim of the present review is to critically review clinical studies using purified CBD products only, in order to establish the upcoming indications for which purified CBD might be beneficial. The areas in which there is the most clinical evidence to support the use of CBD are in the treatment of anxiety (positive data in 7 uncontrolled studies and 17 randomised controlled trials (RCTs)), psychosis and schizophrenia (positive data in 1 uncontrolled study and 8 RCTs), PTSD (positive data in 2 uncontrolled studies and 4 RCTs) and substance abuse (positive data in 2 uncontrolled studies and 3 RCTs). Seven uncontrolled studies support the use of CBD to improve sleep quality, but this has only been verified in one small RCT. Limited evidence supports the use of CBD for the treatment of Parkinson's (3 positive uncontrolled studies and 2 positive RCTs), autism (3 positive RCTs), smoking cessation (2 positive RCTs), graft-versus-host disease and intestinal permeability (1 positive RCT each). Current RCT evidence does not support the use of purified oral CBD in pain (at least as an acute analgesic) or for the treatment of COVID symptoms, cancer, Huntington's or type 2 diabetes. In conclusion, published clinical evidence does support the use of purified CBD in multiple indications beyond epilepsy. However, the evidence base is limited by the number of trials only investigating the acute effects of CBD, testing CBD in healthy volunteers, or in very small patient numbers. Large confirmatory phase 3 trials are required in all indications.
 OBJECTIVES: To use multimodal imaging techniques to characterise features of retinal astrocytomas (RA) which would aid practitioners distinguish them from other causes of non-pigmented fundal lesions. METHODS: Retrospective analysis of notes and imaging of 17 patients diagnosed with RA at a single centre between January 2012 and June 2021 was conducted. Demographics, examination findings and imaging including colour fundus photography, optical coherence tomography (OCT), infra-red (IR) and ultrasound (US) were analysed. These were compared to differential diagnoses, including retinoblastomas, amelanotic choroidal melanomas, choroidal metastases and idiopathic scleromas. RESULTS: Fourteen patients (82%; 14/17) had idiopathic RA and three (18%; 3/17) were associated with tuberous sclerosis. Mean age at presentation was 43 years. Twelve patients (71%; 12/17) were asymptomatic. Thirteen (76%; 13/17) had better than 6/12 vision, with 41% (7/17) better than 6/6. All lesions were creamy-white. There were two distinct appearances, seven (39%; 7/18) were poorly-defined translucent retinal elevations and eleven (61%; 11/18) were well-defined solid opaque retinal masses. Six (33%; 6/18) displayed clustered, calcified spherules giving them the pathognomonic 'mulberry-like' appearance. On OCT, all appeared as dome-shaped retinal thickening with disruption of the inner retinal layers and nine (60%; 9/15) had intra-retinal cystic spaces giving a 'moth-eaten' appearance. Mean basal diameter and thickness on OCT was 2.93 mm and 0.86 mm, respectively. High internal reflectivity on US was noted in 92% (11/12). CONCLUSIONS: RAs display characteristic clinical, demographic and imaging features which can aid differentiating them from other non-pigmented fundal lesions. We advise using multiple imaging modalities when diagnosing these lesions.
 Glaucoma, a leading cause of irreversible blindness, is a highly heritable human disease. Previous genome-wide association studies have identified over 100 loci for the most common form, primary open-angle glaucoma. Two key glaucoma-associated traits also show high heritability: intraocular pressure and optic nerve head excavation damage quantified as the vertical cup-to-disc ratio. Here, since much of glaucoma heritability remains unexplained, we conducted a large-scale multitrait genome-wide association study in participants of European ancestry combining primary open-angle glaucoma and its two associated traits (total sample size over 600,000) to substantially improve genetic discovery power (263 loci). We further increased our power by then employing a multiancestry approach, which increased the number of independent risk loci to 312, with the vast majority replicating in a large independent cohort from 23andMe, Inc. (total sample size over 2.8 million; 296 loci replicated at P < 0.05, 240 after Bonferroni correction). Leveraging multiomics datasets, we identified many potential druggable genes, including neuro-protection targets likely to act via the optic nerve, a key advance for glaucoma because all existing drugs only target intraocular pressure. We further used Mendelian randomization and genetic correlation-based approaches to identify novel links to other complex traits, including immune-related diseases such as multiple sclerosis and systemic lupus erythematosus.
 The SPIN-CHAT Program was designed to support mental health among individuals with systemic sclerosis (SSc; commonly known as scleroderma) and at least mild anxiety symptoms at the onset of COVID-19. The program was formally evaluated in the SPIN-CHAT Trial. Little is known about program and trial acceptability, and factors impacting implementation from the perspectives of research team members and trial participants. Thus, the propose of this follow-up study was to explore research team members' and trial participants' experiences with the program and trial to identify factors impacting acceptability and successful implementation. Data were collected cross-sectionally through one-on-one, videoconference-based, semi-structured interviews with 22 research team members and 30 purposefully recruited trial participants (Mage = 54.9, SD = 13.0 years). A social constructivist paradigm was adopted, and data were analyzed thematically. Data were organized into seven themes: (i) getting started: the importance of prolonged engagement and exceeding expectations; (ii) designing the program and trial: including multiple features; (iii) training: research team members are critical to positive program and trial experiences; (iv) offering the program and trial: it needs to be flexible and patient-oriented; (v) maximizing engagement: navigating and managing group dynamics; (vi) delivering a videoconference-based supportive care intervention: necessary, appreciated, and associated with some barriers; and (vii) refining the program and trial: considering modification when offered beyond the period of COVID-19 restrictions. Trial participants were satisfied with and found the SPIN-CHAT Program and Trial to be acceptable. Results offer implementation data that can guide the design, development, and refinement of other supportive care programs seeking to promote psychological health during and beyond COVID-19.
 PURPOSE: To explore the impact of different user interfaces (UIs) for artificial intelligence (AI) outputs on radiologist performance and user preference in detecting lung nodules and masses on chest radiographs. MATERIALS AND METHODS: A retrospective paired-reader study with a 4-week washout period was used to evaluate three different AI UIs compared with no AI output. Ten radiologists (eight radiology attending physicians and two trainees) evaluated 140 chest radiographs (81 with histologically confirmed nodules and 59 confirmed as normal with CT), with either no AI or one of three UI outputs: (a) text-only, (b) combined AI confidence score and text, or (c) combined text, AI confidence score, and image overlay. Areas under the receiver operating characteristic curve were calculated to compare radiologist diagnostic performance with each UI with their diagnostic performance without AI. Radiologists reported their UI preference. RESULTS: The area under the receiver operating characteristic curve improved when radiologists used the text-only output compared with no AI (0.87 vs 0.82; P < .001). There was no difference in performance for the combined text and AI confidence score output compared with no AI (0.77 vs 0.82; P = .46) and for the combined text, AI confidence score, and image overlay output compared with no AI (0.80 vs 0.82; P = .66). Eight of the 10 radiologists (80%) preferred the combined text, AI confidence score, and image overlay output over the other two interfaces. CONCLUSION: Text-only UI output significantly improved radiologist performance compared with no AI in the detection of lung nodules and masses on chest radiographs, but user preference did not correspond with user performance.Keywords: Artificial Intelligence, Chest Radiograph, Conventional Radiography, Lung Nodule, Mass Detection© RSNA, 2023.
 The mammalian holobiont harbors a complex and interdependent mutualistic gut bacterial community. Shifts in the composition of this bacterial consortium are known to be a key element in host health, immunity and disease. Among many others, dietary habits are impactful drivers for a potential disruption of the bacteria-host mutualistic interaction. In this context, we previously demonstrated that a high-salt diet (HSD) leads to a dysbiotic condition of murine gut microbiota, characterized by a decrease or depletion of well-known health-promoting gut bacteria. However, due to a controlled and sanitized environment, conventional laboratory mice (CLM) possess a less diverse gut microbiota compared to wild mice, leading to poor translational outcome for gut microbiome studies, since a reduced gut microbiota diversity could fail to depict the complex interdependent networks of the microbiome. Here, we evaluated the HSD effect on gut microbiota in CLM in comparison to wildling mice, which harbor a natural gut ecosystem more closely mimicking the situation in humans. Mice were treated with either control food or HSD and gut microbiota were profiled using amplicon-based methods targeting the 16S ribosomal gene. In line with previous findings, our results revealed that HSD induced significant loss of alpha diversity and extensive modulation of gut microbiota composition in CLM, characterized by the decrease in potentially beneficial bacteria from Firmicutes phylum such as the genera Lactobacillus, Roseburia, Tuzzerella, Anaerovorax and increase in Akkermansia and Parasutterella. However, HSD-treated wildling mice did not show the same changes in terms of alpha diversity and loss of Firmicutes bacteria as CLM, and more generally, wildlings exhibited only minor shifts in the gut microbiota composition upon HSD. In line with this, 16S-based functional analysis suggested only major shifts of gut microbiota ecological functions in CLM compared to wildling mice upon HSD. Our findings indicate that richer and wild-derived gut microbiota is more resistant to dietary interventions such as HSD, compared to gut microbiota of CLM, which may have important implications for future translational microbiome research.
 Psoriasis is a chronic inflammatory skin disease with an autoimmune component and associated with joint inflammation in up to 30% of cases. To investigate autoreactive T cells, we developed an imiquimod-induced psoriasis-like inflammation model in K5-mOVA.tg C57BL/6 mice expressing ovalbumin (OVA) on the keratinocyte membrane, adoptively transferred with OT-I OVA-specific CD8(+) T cells. We evaluated the expansion of OT-I CD8(+) T cells and their localization in skin, blood, and spleen. scRNA-seq and TCR sequencing data from patients with psoriatic arthritis were also analyzed. In the imiquimod-treated K5-mOVA.tg mouse model, OT-I T cells were markedly expanded in the skin and blood at early time points. OT-I T cells in the skin showed mainly CXCR3(+) effector memory phenotype, whereas in peripheral blood there was an expansion of CCR4(+) CXCR3(+) OT-I cells. At a later time point, expanded OVA-specific T-cell population was found in the spleen. In patients with psoriatic arthritis, scRNA-seq and TCR sequencing data showed clonal expansion of CCR4(+) T(CM) cells in the circulation and further expansion in the synovial fluid. Importantly, there was a clonotype overlap between CCR4(+) T(CM) in the peripheral blood and CD8(+) T-cell effectors in the synovial fluid. This mechanism could play a role in the generation and spreading of autoreactive T cells to the synovioentheseal tissues in psoriasis patients at risk of developing psoriatic arthritis.
 BACKGROUND: Hospitalized older adults spend as much as 95% of their time in bed, which can result in adverse events and delay recovery while increasing costs. Observational studies have shown that general mobility interventions (e.g., ambulation) can mitigate adverse events and improve patients' functional status. Mobility technicians (MTs) may address the need for patients to engage in mobility interventions without overburdening nurses. There is no data, however, on the effect of MT-assisted ambulation on adverse events or functional status, or on the cost tradeoffs if a MT were employed. The AMBULATE study aims to determine whether MT-assisted ambulation improves mobility status and decreases adverse events for older medical inpatients. It will also include analyses to identify the patients that benefit most from MT-assisted mobility and assess the cost-effectiveness of employing a MT. METHODS: The AMBULATE study is a multicenter, single-blind, parallel control design, individual-level randomized trial. It will include patients admitted to a medical service in five hospitals in two regions of the USA. Patients over age 65 with mild functional deficits will be randomized using a block randomization scheme. Those in the intervention group will ambulate with the MT up to three times daily, guided by the Johns Hopkins Mobility Goal Calculator. The intervention will conclude at hospital discharge, or after 10 days if the hospitalization is prolonged. The primary outcome is the Short Physical Performance Battery score at discharge. Secondary outcomes are discharge disposition, length of stay, hospital-acquired complications (falls, venous thromboembolism, pressure ulcers, and hospital-acquired pneumonia), and post-hospital functional status. DISCUSSION: While functional decline in the hospital is multifactorial, ambulation is a modifiable factor for many patients. The AMBULATE study will be the largest randomized controlled trial to test the clinical effects of dedicating a single care team member to facilitating mobility for older hospitalized patients. It will also provide a useful estimation of cost implications to help hospital administrators assess the feasibility and utility of employing MTs. TRIAL REGISTRATION: Registered in the United States National Library of Medicine clinicaltrials.gov (# NCT05725928). February 13, 2023.
 BACKGROUND AND OBJECTIVES: To assess the clinical practice applicability of autoimmune encephalitis (AE) criteria (2016). METHODS: Medical records of 538 adults diagnosed with AE or related autoimmune encephalopathy at Mayo Clinic (not including pure movement disorders) were reviewed and AE guideline criteria applied. RESULTS: Of 538 patients, 288 were male (52%). The median symptom onset age was 55 years (range, 11-97 years; 16 had onset as children). All had other non-AE diagnoses reasonably excluded. Of 538 patients, 361 (67%) met at least possible criteria, having all 3 of subacute onset; memory deficits, altered mental status or psychiatric symptoms, and ≥1 supportive feature (new focal objective CNS finding, N = 285; new-onset seizures, N = 283; supportive MRI findings, N = 251; or CSF pleocytosis, N = 160). Of 361 patients, AE subgroups were as follows: definite AE (N = 221, 61%, [87% AE-specific IgG positive]), probable seronegative AE (N = 18, 5%), Hashimoto encephalopathy (N = 20, 6%), or possible AE not otherwise categorizable (N = 102, 28%). The 221 patients with definite AE had limbic encephalitis (N = 127, 57%), anti-NMDA-R encephalitis (N = 32, 15%), ADEM (N = 8, 4%), or other AE-specific IgG defined (N = 54, 24%). The 3 most common definite AE-IgGs detected were as follows: LGI1 (76, 34%), NMDA-R (32, 16%), and high-titer GAD65 (23, 12%). The remaining 177 patients (33%) not meeting possible AE criteria had the following: seizures only (65, 12% of all 538 patients), brainstem encephalitis without supratentorial findings (55, 10%; none had Bickerstaff encephalitis), or other (57, 11%). Those 57 "others" lacked sufficient supportive clinical, radiologic, or CSF findings (N = 26), had insidious or initially episodic onset of otherwise typical disorders (N = 21), or had atypical syndromes without clearcut memory deficits, altered mental status, or psychiatric symptoms (N = 10). Fifteen of 57 were AE-specific IgG positive (26%). Among the remaining 42, evidence of other organ-specific autoimmunity (mostly thyroid) was encountered in 31 (74%, ≥1 coexisting autoimmune disease [21, 50%] or ≥1 non-AE-specific antibodies detected [23, 53%]), and all but 1 had an objective immunotherapy response (97%). DISCUSSION: The 2016 AE guidelines permit autoimmune causation assessment in subacute encephalopathy and are highly specific. Inclusion could be improved by incorporating AE-IgG-positive patients with isolated seizures or brainstem disorders. Some patients with atypical presentations but with findings supportive of autoimmunity may be immune therapy responsive.
 OBJECTIVE: CHAMPION-NMOSD (NCT04201262) is a phase 3, open-label, externally controlled interventional study evaluating the efficacy and safety of the terminal complement inhibitor ravulizumab in adult patients with anti-aquaporin-4 antibody-positive (AQP4+) neuromyelitis optica spectrum disorder (NMOSD). Ravulizumab binds the same complement component 5 epitope as the approved therapeutic eculizumab but has a longer half-life, enabling an extended dosing interval (8 vs 2 weeks). METHODS: The availability of eculizumab precluded the use of a concurrent placebo control in CHAMPION-NMOSD; consequently, the placebo group of the eculizumab phase 3 trial PREVENT (n = 47) was used as an external comparator. Patients received weight-based intravenous ravulizumab on day 1 and maintenance doses on day 15, then once every 8 weeks. The primary endpoint was time to first adjudicated on-trial relapse. RESULTS: The primary endpoint was met; no patients taking ravulizumab (n = 58) had an adjudicated relapse (during 84.0 patient-years of treatment) versus 20 patients with adjudicated relapses in the placebo group of PREVENT (during 46.9 patient-years; relapse risk reduction = 98.6%, 95% confidence interval = 89.7%-100.0%, p < 0.0001). Median (range) study period follow-up time was 73.5 (11.0-117.7) weeks for ravulizumab. Most treatment-emergent adverse events were mild/moderate; no deaths were reported. Two patients taking ravulizumab experienced meningococcal infections. Both recovered with no sequelae; one continued ravulizumab treatment. INTERPRETATION: Ravulizumab significantly reduced relapse risk in patients with AQP4+ NMOSD, with a safety profile consistent with those of eculizumab and ravulizumab across all approved indications. ANN NEUROL 2023;93:1053-1068.
 BACKGROUND: The functional deterioration and loss of motor neurons are tightly associated with degenerative motor neuron diseases and aging-related muscle wasting. Motor neuron diseases or aging-related muscle wasting in turn contribute to increased risk of adverse health outcomes in the elderly. Cdon (cell adhesion molecule-downregulated oncogene) belongs to the immunoglobulin superfamily of cell adhesion molecule and plays essential roles in multiple signalling pathways, including sonic hedgehog (Shh), netrin, and cadherin-mediated signalling. Cdon as a Shh coreceptor plays a critical role in motor neuron specification during embryonic development. However, its role in adult motor neuron function is unknown. METHODS: Hb9-Cre recombinase-driven motor neuron-specific Cdon deficient mice (mnKO) and a compound mutant mice (mnKO::SOD1(G93A) ) were generated to investigate the role of Cdon in motor neuron degeneration. Motor neuron regeneration was examined by using a sciatic nerve crush injury model. To investigate the phenotype, physical activity, compound muscle action potential, immunostaining, and transmission electron microscopy were carried out. In the mechanism study, RNA sequencing and RNA/protein analyses were employed. RESULTS: Mice lacking Cdon in motor neurons exhibited middle age onset lethality and aging-related decline in motor function. In the sciatic nerve crush injury model, mnKO mice exhibited an impairment in motor function recovery evident by prolonged compound muscle action potential duration (4.63 ± 0.35 vs. 3.93 ± 0.22 s for f/f, P < 0.01) and physical activity. Consistently, neuromuscular junctions of mnKO muscles were incompletely occupied (49.79 ± 5.74 vs. 79.39 ± 3.77% fully occupied neuromuscular junctions for f/f, P < 0.0001), suggesting an impaired reinnervation. The transmission electron microscopy analysis revealed that mnKO sciatic nerves had smaller axon diameter (0.88 ± 0.13 vs. 1.43 ± 0.48 μm for f/f, P < 0.0001) and myelination defects. RNA sequencing of mnKO lumbar spinal cords showed alteration in genes related to neurogenesis, inflammation and cell death. Among the altered genes, ErbB4 and FgfR expressions were significantly altered in mnKO as well as in Cdon-depleted NSC34 motor neuron cells. Consistently, Cdon-depleted NSC34 cells exhibited elevated levels of cleaved Caspase3 and γH2AX proteins, as well as Bax transcription. Cdon-depleted NSC34 cells also exhibited impaired activation of Akt in response to neuregulin-1 (NRG1) treatment. CONCLUSIONS: Our current data demonstrate the functional importance of Cdon in motor neuron function and nerve repair. Cdon ablation causes alterations in neurotrophin signalling that leads to motor neuron degeneration.
 Neuroinvasive infection is the most common cause of meningoencephalitis in people living with human immunodeficiency virus (HIV), but autoimmune etiologies have been reported. We present the case of a 51-year-old man living with HIV infection with steroid-responsive meningoencephalitis whose comprehensive pathogen testing was non-diagnostic. Subsequent tissue-based immunofluorescence with acute-phase cerebrospinal fluid revealed anti-neural antibodies localizing to the axon initial segment (AIS), the node of Ranvier (NoR), and the subpial space. Phage display immunoprecipitation sequencing identified ankyrinG (AnkG) as the leading candidate autoantigen. A synthetic blocking peptide encoding the PhIP-Seq-identified AnkG epitope neutralized CSF IgG binding to the AIS and NoR, thereby confirming a monoepitopic AnkG antibody response. However, subpial immunostaining persisted, indicating the presence of additional autoantibodies. Review of archival tissue-based staining identified candidate AnkG autoantibodies in a 60-year-old woman with metastatic ovarian cancer and seizures that were subsequently validated by cell-based assay. AnkG antibodies were not detected by tissue-based assay and/or PhIP-Seq in control CSF (N = 39), HIV CSF (N = 79), or other suspected and confirmed neuroinflammatory CSF cases (N = 1,236). Therefore, AnkG autoantibodies in CSF are rare but extend the catalog of AIS and NoR autoantibodies associated with neurological autoimmunity.
 OBJECTIVE: We explored the potential of neurofilament light chain (NfL) in serum and cerebrospinal fluid as a biomarker for neurodestruction in status epilepticus. METHODS: In a retrospective analysis, we measured NfL in serum and cerebrospinal fluid samples of patients with status epilepticus using a highly sensitive single-molecule array technique (Simoa). Status epilepticus was diagnosed according to ILAE criteria. Additionally, we employed an alternative classification with more emphasis on the course of status epilepticus. We used data from three large control groups to compare NfL in status epilepticus versus neurologically healthy controls. RESULTS: We included 28 patients (mean age: 69.4 years, SD: 15 years) with a median status duration of 44 h (IQR: 80 h). Twenty-one patients (75%) suffered from convulsive status epilepticus and seven (25%) from non-convulsive status epilepticus. Six patients died (21%). Cerebrospinal fluid and serum NfL concentrations showed a high correlation (r = 0.73, p < 0.001, Pearson). The main determinant of NfL concentration was the status duration. NfL concentrations did not differ between convulsive status epilepticus and convulsive status epilepticus classified according to the ILAE or to the alternative classification without and with adjusting for status duration and time between status onset and sampling. We found no association of NfL concentration with death, treatment refractoriness, or prognostic scores. CONCLUSION: The results suggest that neurodestruction in status epilepticus measured by NfL is mainly determined by status duration, not status type nor therapy refractoriness. Therefore, our results suggest that regarding neurodestruction convulsive and non-convulsive status epilepticus are both neurological emergencies of comparable urgency.
 BACKGROUND: Optic neuropathy is a near ubiquitous feature of Friedreich's ataxia (FRDA). Previous studies have examined varying aspects of the anterior and posterior visual pathways but none so far have comprehensively evaluated the heterogeneity of degeneration across different areas of the retina, changes to the macula layers and combined these with volumetric MRI studies of the visual cortex and frataxin level. METHODS: We investigated 62 genetically confirmed FRDA patients using an integrated approach as part of an observational cohort study. We included measurement of frataxin protein levels, clinical evaluation of visual and neurological function, optical coherence tomography to determine retinal nerve fibre layer thickness and macular layer volume and volumetric brain MRI. RESULTS: We demonstrate that frataxin level correlates with peripapillary retinal nerve fibre layer thickness and that retinal sectors differ in their degree of degeneration. We also shown that retinal nerve fibre layer is thinner in FRDA patients than controls and that this thinning is influenced by the AAO and GAA1. Furthermore we show that the ganglion cell and inner plexiform layers are affected in FRDA. Our MRI data indicate that there are borderline correlations between retinal layers and areas of the cortex involved in visual processing. CONCLUSION: Our study demonstrates the uneven distribution of the axonopathy in the retinal nerve fibre layer and highlight the relative sparing of the papillomacular bundle and temporal sectors. We show that thinning of the retinal nerve fibre layer is associated with frataxin levels, supporting the use the two biomarkers in future clinical trials design. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
 During an immune response, T cells migrate from blood vessel walls into inflamed tissues by migrating across the endothelium and through extracellular matrix (ECM). Integrins facilitate T cell binding to endothelial cells and ECM proteins. Here, we report that Ca(2+) microdomains observed in the absence of T cell receptor (TCR)/CD3 stimulation are initial signaling events triggered by adhesion to ECM proteins that increase the sensitivity of primary murine T cells to activation. Adhesion to the ECM proteins collagen IV and laminin-1 increased the number of Ca(2+) microdomains in a manner dependent on the kinase FAK, phospholipase C (PLC), and all three inositol 1,4,5-trisphosphate receptor (IP(3)R) subtypes and promoted the nuclear translocation of the transcription factor NFAT-1. Mathematical modeling predicted that the formation of adhesion-dependent Ca(2+) microdomains required the concerted activity of two to six IP(3)Rs and ORAI1 channels to achieve the increase in the Ca(2+) concentration in the ER-plasma membrane junction that was observed experimentally and that required SOCE. Further, adhesion-dependent Ca(2+) microdomains were important for the magnitude of the TCR-induced activation of T cells on collagen IV as assessed by the global Ca(2+) response and NFAT-1 nuclear translocation. Thus, adhesion to collagen IV and laminin-1 sensitizes T cells through a mechanism involving the formation of Ca(2+) microdomains, and blocking this low-level sensitization decreases T cell activation upon TCR engagement.
 BACKGROUND: Unpredictable vegetative deteriorations made the treatment of patients with acute COVID-19 on intensive care unit particularly challenging during the first waves of the pandemic. Clinical correlates of dysautonomia and their impact on the disease course in critically ill COVID-19 patients are unknown. METHODS: We retrospectively analyzed data collected during a single-center observational study (March 2020-November 2021) which was performed at the University Medical Center Hamburg-Eppendorf, a large tertiary medical center in Germany. All patients admitted to ICU due to acute COVID-19 disease during the study period were included (n = 361). Heart rate variability (HRV) and blood pressure variability (BPV) per day were used as clinical surrogates of dysautonomia and compared between survivors and non-survivors at different time points after admission. Intraindividual correlation of vital signs with laboratory parameters were calculated and corrected for age, sex and disease severity. RESULTS: Patients who deceased in ICU had a longer stay (median days ± IQR, survivors 11.0 ± 27.3, non-survivors 14.1 ± 18.7, P = 0.85), in contrast time spent under invasive ventilation was not significantly different (median hours ± IQR, survivors 322 ± 782, non-survivors 286 ± 434, P = 0.29). Reduced HRV and BPV predicted lethal outcome in patients staying on ICU longer than 10 days after adjustment for age, sex, and disease severity. Accordingly, HRV was significantly less correlated with inflammatory markers (e.g. CRP and Procalcitonin) and blood carbon dioxide in non-survivors in comparison to survivors indicating uncoupling between autonomic function and inflammation in non-survivors. CONCLUSIONS: Our study suggests autonomic dysfunction as a contributor to mortality in critically ill COVID-19 patients during the first waves of the pandemic. Serving as a surrogate for disease progression, these findings could contribute to the clinical management of COVID-19 patients admitted to the ICU. Furthermore, the suggested measure of dysautonomia and correlation with other laboratory parameters is non-invasive, simple, and cost-effective and should be evaluated as an additional outcome parameter in septic patients treated in the ICU in the future.
 OBJECTIVE: This study was undertaken to characterize somatic symptoms and related disorders (SSD) in epilepsy. METHODS: Adults with epilepsy under active follow-up at a tertiary epilepsy center were consecutively enrolled. The diagnosis of SSD was performed by an experienced psychologist based on the structured clinical interview for Statistical Manual of Mental Disorders, 5th edition. Detailed social/demographic data, epilepsy features, psychiatric features, life quality, disability, and economic burden were collected and compared between people with SSD and those without. Bodily distress syndrome checklist, Somatic Symptom Disorder-B Criteria Scale, Patient Health Questionnaire-9, and Generalized Anxiety Disorder seven-item scale (GAD-7) were used to evaluate SSD individuals' somatic symptoms, symptom-related psychological distress, and depressive and anxious symptoms. Quality of life and disability were assessed by Quality of Life in Epilepsy Inventory 31 (QOLIE-31) and World Health Organization Disability Assessment Schedule V.2.0 (WHO DAS 2.0). A risk prediction nomogram was generated using least absolute shrinkage and selection operator (LASSO) analysis and validated. RESULTS: One hundred fifty of 631 participants (24%) were diagnosed with SSD. In people with SSD, the top three most common somatic symptoms were memory impairment, headache, and dizziness (85%, 80%, and 78%, respectively), and multiple systems were involved in most (82%) people with SSD. Compared with people without SSD, those with SSD had lower QOLIE-31 total scores, and higher WHO DAS 2.0 scores and disease economic burdens. LASSO analysis suggested that a history of severe traumatic brain injury, hippocampal sclerosis, low seizure worry and medication effects scores on QOLIE-31, multiple systems affected by somatic symptoms, and a high GAD-7 score were risk factors of SSD. The nomogram was validated for good accuracy in the training and testing cohorts. SIGNIFICANCE: SSD are likely to be a common comorbidity in epilepsy and harm epilepsy prognosis. Our risk prediction nomogram was successfully developed but needs further validation in larger cohorts.
 BACKGROUND: Positive antineutrophil cytoplasmic antibody (ANCA) serology in adult-onset lupus nephritis (LN) is associated with more active disease and distinct renal pathology, but data with respect to childhood-onset LN remain scarce. Here, we aimed to determine the impact of positive ANCA serology on clinical and histopathologic features and renal outcomes in children with LN from multiple centers. METHODS: Clinical and histopathologic data of 61 ANCA-positive and 330 ANCA-negative LN children (1<age≤18 years) retrospectively enrolled from three pediatric nephrology centers were analyzed. Among them, 217 children were followed and survival analysis was performed. RESULTS: Among 61 ANCA-positive LN children, 86.9% of them had antimyeloperoxidase antibodies. Both ANCA-positive and ANCA-negative children had high disease activities with median SLEDAI-2K of 16 (13, 20). Hematuria was more prominent (urinary RBC +++ ∼ ++++: 45.9% vs 26.7%, p = 0.011), while fever (42.6% vs. 58.2%, p = 0.035), alopecia (3.3% vs. 14.5%, p = 0.019), photosensitivity (0% vs. 8.2%, p = 0.013), and pleurisy (4.9% vs. 15.8%, p = 0.026) were less common in ANCA-positive children. Higher proportions of segmental sclerosis (23.7% vs. 9.8%, p = 0.025), crescentic formation (36.4% vs. 16.3%, p = 0.009), and capillary wall thickening (24.5% vs. 11.0%, p = 0.01) were observed in biopsies of ANCA-positive children. Long-term renal survival did not differ significantly between two groups (p = 0.300). CONCLUSIONS: Positive ANCA serology in LN children was associated with different clinical and histopathologic features compared to those with negative ANCA serology. Further studies are needed to clarify the pathogenic role of ANCAs in childhood-onset LN and confirm their association with prognosis.
 Novel and effective antiseizure medications are needed to treat refractory and rare forms of epilepsy. Cannabinoids, which are obtained from the cannabis plant, have a long history of medical use, including for neurologic conditions. In 2018, the US Food and Drug Administration approved the first phytocannabinoid, cannabidiol (CBD, Epidiolex), which is now indicated for severe seizures associated with three rare forms of developmental and epileptic encephalopathy: Dravet syndrome, Lennox-Gastaut syndrome, and tuberous sclerosis complex. Compelling evidence supports the efficacy of CBD in experimental models and patients with epilepsy. In randomized clinical trials, highly-purified CBD has demonstrated efficacy with an acceptable safety profile in children and adults with difficult-to-treat seizures. Although the underlying antiseizure mechanisms of CBD in humans have not yet been elucidated, the identification of novel antiseizure targets of CBD preclinically indicates multimodal mechanisms that include non-cannabinoid pathways. In addition to antiseizure effects, CBD possesses strong anti-inflammatory and neuroprotective activities, which might contribute to protective effects in epilepsy and other conditions. This article provides a succinct overview of therapeutic approaches and clinical foundations of CBD, emphasizing the clinical utility of CBD for the treatment of seizures associated with refractory and rare epilepsies. CBD has shown to be a safe and effective antiseizure medicine, demonstrating a broad spectrum of efficacy across multiple seizure types, including those associated with severe epilepsies with childhood onset. Despite such promise, there are many perils with CBD that hampers its widespread use, including limited understanding of pharmacodynamics, limited exposure-response relationship, limited information for seizure freedom with continued use, complex pharmacokinetics with drug interactions, risk of adverse effects, and lack of expert therapeutic guidelines. These scientific issues need to be resolved by further investigations, which would decide the unique role of CBD in the management of refractory epilepsy.
 OBJECTIVE: The mechanistic target of rapamycin (mTOR) kinase is one of the master coordinators of cellular stress responses, regulating metabolism, autophagy, and apoptosis. We recently reported that staufen1 (STAU1), a stress granule (SG) protein, was overabundant in fibroblast cell lines from patients with spinocerebellar ataxia type 2 (SCA2), amyotrophic lateral sclerosis, frontotemporal degeneration, Huntington's, Alzheimer's, and Parkinson's diseases as well as animal models, and patient tissues. STAU1 overabundance is associated with mTOR hyperactivation and links SG formation with autophagy. Our objective was to determine the mechanism of mTOR regulation by STAU1. METHODS: We determined STAU1 abundance with disease- and chemical-induced cellular stressors in patient cells and animal models. We also used RNA-binding assays to contextualize STAU1 interaction with MTOR mRNA. RESULTS: STAU1 and mTOR were overabundant in bacterial artificial chromosome (BAC)-C9ORF72, ATXN2(Q127) , and Thy1-TDP-43 transgenic mouse models. Reducing STAU1 levels in these mice normalized mTOR levels and activity and autophagy-related marker proteins. We also saw increased STAU1 levels in HEK293 cells transfected to express C9ORF72-relevant dipeptide repeats (DPRs). Conversely, DPR accumulations were not observed in cells treated by STAU1 RNA interference (RNAi). Overexpression of STAU1 in HEK293 cells increased mTOR levels through direct MTOR mRNA interaction, activating downstream targets and impairing autophagic flux. Targeting mTOR by rapamycin or RNAi normalized STAU1 abundance in an SCA2 cellular model. INTERPRETATION: STAU1 interaction with mTOR drives its hyperactivation and inhibits autophagic flux in multiple models of neurodegeneration. Staufen, therefore, constitutes a novel target to modulate mTOR activity and autophagy, and for the treatment of neurodegenerative diseases. ANN NEUROL 2023;93:398-416.
 N-acetyltransferase 10 (NAT10), a nuclear acetyltransferase and a member of the GNAT family, plays critical roles in RNA stability and translation processes as well as cell proliferation. Little is known about regulatory effects of NAT10 in lung epithelial cell proliferation. We firstly investigated NTA10 mRNA expression in alveolar epithelial types I and II, basal, ciliated, club, and goblet/mucous epithelia from heathy and patients with chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, lung adenocarcinoma, para-tumor tissue, and systemic sclerosis, respectively. We selected A549 cells for representative of alveolar epithelia or H1299 and H460 cells as airway epithelia with different genetic backgrounds and studied dynamic responses of NAT10-down-regulated epithelia to high temperature, lipopolysaccharide, cigarette smoking extract (CSE), drugs, radiation, and phosphoinositide 3-kinase (PI3K) inhibitors at various doses. We also compared transcriptomic profiles between alveolar and airway epithelia, between cells with or without NAT10 down-regulation, between early and late stages, and between challenges. The present study demonstrated that NAT10 expression increased in human lung epithelia and varied among epithelial types, challenges, and diseases. Knockdown of NAT10 altered epithelial mitochondrial functions, dynamic responses to LPS, CSE, or PI3K inhibitors, and transcriptomic phenomes. NAT10 regulates biological phenomes, and behaviors are more complex and are dependent upon multiple signal pathways. Thus, NAT10-associated signal pathways can be a new alternative for understanding the disease and developing new biomarkers and targets.
 Advanced glycation end products (AGEs) are compounds formed after the non-enzymatic addition of reducing sugars to lipids, proteins, and nucleic acids. They are associated with the development of various clinical complications observed in diabetes and cardiovascular diseases, such as retinopathy, nephropathy, diabetic neuropathy, and others. In addition, compelling evidence indicates that these molecules participate in the progression of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Multiple cellular and molecular alterations triggered by AGEs that could alter homeostasis have been identified. One of the main targets for AGE signaling is the receptor for advanced glycation end-products (RAGE). Importantly, this receptor is the target of not only AGEs, but also amyloid β peptides, HMGB1 (high-mobility group box-1), members of the S100 protein family, and glycosaminoglycans. The activation of this receptor induces intracellular signaling cascades that are involved in pathological processes and cell death. Therefore, RAGE represents a key target for pharmacological interventions in neurodegenerative diseases. This review will discuss the various effects of AGEs and RAGE activation in the pathophysiology of neurodegenerative diseases, as well as the currently available pharmacological tools and promising drug candidates.
 Progressive pulmonary fibrosis results from a dysfunctional tissue repair response and is characterized by fibroblast proliferation, activation, and invasion and extracellular matrix accumulation. Lung fibroblast heterogeneity is well recognized. With single-cell RNA sequencing, fibroblast subtypes have been reported by recent studies. However, the roles of fibroblast subtypes in effector functions in lung fibrosis are not well understood. In this study, we incorporated the recently published single-cell RNA-sequencing datasets on murine lung samples of fibrosis models and human lung samples of fibrotic diseases and analyzed fibroblast gene signatures. We identified and confirmed the novel fibroblast subtypes we reported recently across all samples of both mouse models and human lung fibrotic diseases, including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease, and coronavirus disease (COVID-19). Furthermore, we identified specific cell surface proteins for each fibroblast subtype through differential gene expression analysis, which enabled us to isolate primary cells representing distinct fibroblast subtypes by flow cytometry sorting. We compared matrix production, including fibronectin, collagen, and hyaluronan, after profibrotic factor stimulation and assessed the invasive capacity of each fibroblast subtype. Our results suggest that in addition to myofibroblasts, lipofibroblasts and Ebf1(+) (Ebf transcription factor 1(+)) fibroblasts are two important fibroblast subtypes that contribute to matrix deposition and also have enhanced invasive, proliferative, and contraction phenotypes. The histological locations of fibroblast subtypes are identified in healthy and fibrotic lungs by these cell surface proteins. This study provides new insights to inform approaches to targeting lung fibroblast subtypes to promote the development of therapeutics for lung fibrosis.
 INTRODUCTION: Differentiating the soft tissue abscess from other types of skin and soft tissue infections (SSTIs) poses a particular challenge because they have similar physical evaluation findings, but each disease has a different course, outcome, and treatment. This meta-analysis aimed to investigate the diagnostic accuracy of point-of-care ultrasonography for diagnosis of soft tissue abscess in the emergency departments. METHODS: A comprehensive literature search of MEDLINE, Scopus, Web of Science, Embase, and Google Scholar, from inception to January 2023, was conducted to identify relevant studies investigating the diagnostic performance of point-of-care ultrasonography for identification of abscess. Methodological quality of the included studies was assessed using a revised tool for the quality assessment of diagnostic accuracy studies (QUADAS-2). RESULTS: The pooled estimates of diagnostic parameters of ultrasonography for diagnosis of abscess were as follows: sensitivity, 0.93 (95% CI: 0.92-0.94); specificity, 0.87 (95% CI: 0.85-0.89), and the area under the summary receiver-operating characteristic (SROC), 0.95. The pooled sensitivity, specificity, and area under the SROC of studies in adult patients were 0.98 (95% CI: 0.92-1), 0.92 (95% CI: 0.86-0.95), and 0.99, respectively. The pooled sensitivity, specificity, and area under the SROC of studies in pediatric patients were 0.9 (95% CI: 0.87-0.92), 0.78 (95% CI: 0.73-0.82), and 0.91, respectively. CONCLUSION: Our meta-analysis demonstrated that the point-of-care ultrasonography has excellent diagnostic value for the abscess in the emergency department. Furthermore, we found that the diagnostic performance of point-of-care ultrasonography for diagnosis of abscess was higher for adult cases than for pediatric patients.
 BACKGROUND: The potential therapeutic benefit of intravenous immunoglobulins (IVIGs) for acute attacks of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is unknown. OBJECTIVE: The objective was to describe the outcomes of IVIG treatment for acute MOGAD attacks. METHODS: A retrospective observational study involving seven tertiary neuroimmunology centers. Data collection included patients' demographics, Expanded Disability Status Scale (EDSS), and visual acuity (VA) before the attack, at the nadir of the attack before IVIG treatment, and at follow-up visits ⩾3 months after treatment. RESULTS: Thirty-nine patients were included, of which 21 (53.8%) were female. The median age was 23 years (range 5-74 years), and the median disease duration was 4 months (range 0-93 months). The most common type of attack treated with IVIG was isolated optic neuritis (ON) (unilateral n = 14, bilateral n = 5, associated with transverse myelitis (TM), n = 1), followed by acute disseminated encephalomyelitis (ADEM) (n = 8), multifocal (n = 7), TM (n = 3), brainstem (n = 1), and other encephalitis (n = 1). A significant improvement in both the EDSS and VA measures was observed at follow-up compared to the time of IVIG treatment initiation (p < 0.0001 for both outcome measures). CONCLUSION: IVIG may be an effective treatment option for acute MOGAD attacks. Further prospective studies are warranted to validate our results.
 BACKGROUND: Neurological symptoms are common manifestation in acute COVID-19. This includes hyper- and hypokinetic movement disorders. Data on their outcome, however, is limited. METHODS: Cases with new-onset COVID-19-associated movement disorders were identified by searching the literature. Authors were contacted for outcome data which were reviewed and analyzed. RESULTS: Movement disorders began 12.6 days on average after the initial onset of COVID-19. 92% of patients required hospital admission (mean duration 23 days). In a fraction of patients (6 of 27; 22%; 4 males/2 females, mean age 66.8 years) the movement disorder (ataxia, myoclonus, tremor, parkinsonism) was still present after a follow-up period of 7.5 ± 3 weeks. Severe COVID-19 in general and development of encephalopathy were risk factors, albeit not strong predictors, for the persistence. CONCLUSIONS: The prognosis of new-onset COVID-19-associated movement disorder appears to be generally good. The majority recovered without residual symptoms within several weeks or months. Permanent cases may be due to unmasking of a previous subclinical movement disorder or due to vascular/demyelinating damage. Given the relatively low response rate of one third only and the heterogeneity of mechanisms firm conclusions on the (long-term) outome cannot, however, be drawn.
 The intestinal immune system interacts with commensal microbiota to maintain gut homeostasis. Furthermore, stress alters the microbiome composition, leading to impaired brain function; yet how the intestinal immune system mediates these effects remains elusive. Here we report that colonic γδ T cells modulate behavioral vulnerability to chronic social stress via dectin-1 signaling. We show that reduction in specific Lactobacillus species, which are involved in T cell differentiation to protect the host immune system, contributes to stress-induced social-avoidance behavior, consistent with our observations in patients with depression. Stress-susceptible behaviors derive from increased differentiation in colonic interleukin (IL)-17-producing γδ T cells (γδ17 T cells) and their meningeal accumulation. These stress-susceptible cellular and behavioral phenotypes are causally mediated by dectin-1, an innate immune receptor expressed in γδ T cells. Our results highlight the previously unrecognized role of intestinal γδ17 T cells in the modulation of psychological stress responses and the importance of dectin-1 as a potential therapeutic target for the treatment of stress-induced behaviors.
 INTRODUCTION: Small vessel disease (SVD) causes most spontaneous intracerebral haemorrhage (ICH) and is associated with widespread microstructural brain tissue disruption, which can be quantified via diffusion tensor imaging (DTI) metrics: mean diffusivity (MD) and fractional anisotropy (FA). Little is known about the impact of whole-brain microstructural alterations after SVD-related ICH. We aimed to investigate: (1) association between whole-brain DTI metrics and functional outcome after ICH; and (2) predictive ability of these metrics compared to the pre-existing ICH score. METHODS: Sixty-eight patients (38.2% lobar) were retrospectively included. We assessed whole-brain DTI metrics (obtained within 5 days after ICH) in cortical and deep grey matter and white matter. We used univariable logistic regression to assess the associations between DTI and clinical-radiological variables and poor outcome (modified Rankin Scale > 2). We determined the optimal predictive variables (via LASSO estimation) in: model 1 (DTI variables only), model 2 (DTI plus non-DTI variables), model 3 (DTI plus ICH score). Optimism-adjusted C-statistics were calculated for each model and compared (likelihood ratio test) against the ICH score. RESULTS: Deep grey matter MD (OR 1.04 [95% CI 1.01-1.07], p = 0.010) and white matter MD (OR 1.11 [95% CI 1.01-1.23], p = 0.044) were associated (univariate analysis) with poor outcome. Discrimination values for model 1 (0.67 [95% CI 0.52-0.83]), model 2 (0.71 [95% CI 0.57-0.85) and model 3 (0.66 [95% CI 0.52-0.82]) were all significantly higher than the ICH score (0.62 [95% CI 0.49-0.75]). CONCLUSION: Our exploratory study suggests that whole-brain microstructural disruption measured by DTI is associated with poor 6-month functional outcome after SVD-related ICH. Whole-brain DTI metrics performed better at predicting recovery than the existing ICH score.
 Gastrointestinal infections are a major cause for serious clinical complications in infants. The induction of antibody responses by B cells is critical for protective immunity against infections and requires CXCR5(+)PD-1(++) CD4(+) T cells (T(FH) cells). We investigated the ontogeny of CXCR5(+)PD-1(++) CD4(+) T cells in human intestines. While CXCR5(+)PD-1(++) CD4(+) T cells were absent in fetal intestines, CXCR5(+)PD-1(++) CD4(+) T cells increased after birth and were abundant in infant intestines, resulting in significant higher numbers compared to adults. These findings were supported by scRNAseq analyses, showing increased frequencies of CD4(+) T cells with a T(FH) gene signature in infant intestines compared to blood. Co-cultures of autologous infant intestinal CXCR5(+)PD-1(+/-)CD4(+) T cells with B cells further demonstrated that infant intestinal T(FH) cells were able to effectively promote class switching and antibody production by B cells. Taken together, we demonstrate that functional T(FH) cells are numerous in infant intestines, making them a promising target for oral pediatric vaccine strategies.
 Synaptic dysfunction caused by soluble β-amyloid peptide (Aβ) is a hallmark of early-stage Alzheimer's disease (AD), and is tightly linked to cognitive decline. By yet unknown mechanisms, Aβ suppresses the transcriptional activity of cAMP-responsive element-binding protein (CREB), a master regulator of cell survival and plasticity-related gene expression. Here, we report that Aβ elicits nucleocytoplasmic trafficking of Jacob, a protein that connects a NMDA-receptor-derived signalosome to CREB, in AD patient brains and mouse hippocampal neurons. Aβ-regulated trafficking of Jacob induces transcriptional inactivation of CREB leading to impairment and loss of synapses in mouse models of AD. The small chemical compound Nitarsone selectively hinders the assembly of a Jacob/LIM-only 4 (LMO4)/ Protein phosphatase 1 (PP1) signalosome and thereby restores CREB transcriptional activity. Nitarsone prevents impairment of synaptic plasticity as well as cognitive decline in mouse models of AD. Collectively, the data suggest targeting Jacob protein-induced CREB shutoff as a therapeutic avenue against early synaptic dysfunction in AD.
 BACKGROUND AND OBJECTIVE: Several novel methods have been suggested to extend a conventional value assessment to capture a more comprehensive perspective of value from a patient perspective. The objective of this research was to demonstrate a framework for implementing a combined qualitative and quantitative method to elicit and prioritize patient experience value elements in rare diseases. Neuromyelitis optica spectrum disorder was used as a case study. METHODS: The method for eliciting and prioritizing patient experience value elements involved a three-step process: (1) collecting potential patient experience value elements from existing literature sources followed by deliberation by a multi-stakeholder research team; (2) a pre-workshop webinar and survey to identify additional patient-reported value elements; and (3) a workshop to discuss, prioritize the value elements using a swing weighting method. Outcomes were prioritized value elements with normalized weights for patients considering a treatment for neuromyelitis optica spectrum disorder. RESULTS: A literature review and deliberation resulted in the following initial value elements: ability to reach important personal milestones, patient's financial burden, value of hope/balance or timing of risks and benefits, Uncertainty about long-term benefits and safety of the treatment, Patient empowerment through therapeutic advancement and technology, Caregiver/family's financial burden, patient experience related to treatment regimen, Therapeutic options, and Caregiver/family's quality of life. Eight patients with neuromyelitis optica spectrum disorder participated in the case study. In the online survey, participants found the nine proposed patient experience value elements both understandable and important with no additions. During the workshop, 'Uncertainty about long-term benefits and safety,' 'Patient experience related to treatment regimen,' and 'Patient's financial burden' were found to be the most important patient experience value elements, with a respective weight of 25%, 19.2%, and 14.4% (out of total 100%). CONCLUSIONS: This case study provides a framework for eliciting and prioritizing patient experience value elements using direct patient input. Although elements/weights may differ by disease, and even in neuromyelitis optica spectrum disorder, additional research is needed, value frameworks, researchers, and manufacturers can use this practical method to generate patient experience value elements and evaluate their impact on treatment selection.
 STUDY OBJECTIVES: Obstructive sleep apnea (OSA) is common in Parkinson disease (PD). Questionnaires can be used as screening tools and have been used as a surrogate definition of OSA in large-scale research. This study aimed to validate the performance of STOP, STOP-BANG, STOP-BAG, STOP-B28, and GOAL and OSA predictors as tools to identify OSA in PD. METHODS: Data were analyzed from a PD cohort study in which OSA was diagnosed using laboratory polysomnography. We calculated sensitivity and specificity of each questionnaire for OSA using different definitions and performed receiver operating characteristics curve analysis. Linear regression was used to assess adjusted associations between questionnaires and outcomes: Montreal Cognitive Assessment, Epworth Sleepiness Scale, and Movement Disorder Society revision of the Unified Parkinson Disease Rating Scale. RESULTS: Questionnaire data were available for 68 PD patients (61.8% male, mean age 64.5 [standard deviation 9.9] years, and Hoehn and Yahr score 2.1 [0.8]). OSA (apnea-hypopnea index ≥ 15 events/h) occurred in 69.4% of participants. STOP-B28 ≥ 2 presented a higher sensitivity for OSA than STOP ≥ 2 (0.76 vs 0.65, respectively) and slightly lower specificity (0.65 vs 0.70, respectively). GOAL ≥ 2 had the highest sensitivity but poor specificity. Loud snoring had sensitivity 0.63 and specificity 0.65. STOP and snoring were significantly associated with Montreal Cognitive Assessment, Epworth Sleepiness Scale, and Movement Disorder Society revision of the Unified Parkinson Disease Rating Scale (total, motor, and nonmotor); STOP-BANG, STOP-BAG, and STOP-B28 showed associations with most outcomes, but the GOAL showed none. CONCLUSIONS: The STOP-B28 followed by STOP and presence of loud snoring alone seem to have the best overall properties to identify PD patients with OSA, whose clinical characteristics differ from the general population with OSA. CITATION: Gomes T, Benedetti A, Lafontaine A-L, Kimoff RJ Robinson A, Kaminska M. Validation of STOP, STOP-BANG, STOP-BAG, STOP-B28, and GOAL screening tools for identification of obstructive sleep apnea in patients with Parkinson disease. J Clin Sleep Med. 2023;19(1):45-54.
 ETHNOPHARMACOLOGICAL RELEVANCE: Type I interferon (IFN) is believed to play a pathogenic role in systemic sclerosis (SSc, also called scleroderma), which is an autoimmune rheumatic disease. Our previous studies have found that Chinese medicine formula Si-Ni-San (SNS, composed of Glycyrrhiza uralensis Fisch., Bupleurum chinense DC., Paeonia lactiflora Pall., and Citrus aurantium L.) had inhibitory effects on type I IFN responses. Among these herbal products, Paeonia lactiflora Pall. has been traditionally used to treat inflammation-related diseases, yet its therapeutic effects against type I IFN-related diseases and potential bioactive ingredients are not characterized. AIM OF THE STUDY: We aim to identify bioactive ingredient with anti-type I IFN activity from herbal products in SNS and further elucidate its therapeutic effect against scleroderma and underlying mechanisms. MATERIALS AND METHODS: We constructed a Gaussia-luciferase (Gluc) reporter assay system to identify ingredients with anti-type I IFN activities from SNS. In RAW264.7 cells, real-time PCR (RT-PCR) and western blotting were used to investigate the induction of type I IFN pathway. Additionally, in a bleomycin (BLM)-induced experimental scleroderma model, the expression of fibrotic genes, type I IFN-related genes, inflammatory cytokines, and cytotoxic granules were measured by RT-PCR, and the histopathological changes were determined by H&E staining, Masson's staining and immunohistochemistry analysis. RESULTS: Our data demonstrated that total glucosides of paeony (TGP) was the bioactive component of SNS that selectively inhibited TLR3-mediated type I IFN responses and blocked type I IFN-induced downstream JAK-STAT signaling pathways. In the BLM-induced scleroderma mouse model, TGP ameliorated skin fibrosis by inhibiting multiple targets in the upstream and downstream of type I IFN signaling. Further research found that TGP hindered polarization of M2 macrophages and their profibrotic effects and reduced cytotoxic T lymphocytes and their cytotoxic granules by suppressing Cxcl9 and Cxcl10 in the skin tissue of scleroderma mice. CONCLUSIONS: Our study not only sheds novel lights into the immunoregulative effects of TGP but also provides convincing evidence to develop TGP-based therapies in the treatment of scleroderma and other autoimmune diseases associated with type I IFN signatures. CLASSIFICATION: Skin.
 Neuroinflammation plays a pivotal role in neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis and stroke, and is accompanied by excessive release of inflammatory cytokines and mediators by activated microglia. Microglial inflammatory response inhibition may be an effective strategy for preventing inflammatory disorders. However, the reciprocal connections between the central nervous system (CNS) and immune system have not been elucidated. Thus far, these links have been proven to mainly involve immuno- and neuropeptides. The pentapeptide thymopentin (TP-5) exerts a significant immunomodulatory effect; however, its antineuroinflammatory effects and underlying mechanism are still unclear. In this study, lipopolysaccharide (LPS) was used to establish an inflammation model, and the therapeutic effect of TP-5 was evaluated. Behavioral tests showed that TP-5 treatment could improve the performance of LPS-treated mice in the open field and pole test, but not hanging wire test. TP-5 also attenuated neuronal lesions in the brains of LPS-treated mice. TP-5 reduced cytotoxicity and morphological changes in activated microglia. Label-free quantitative analysis indicated that the expression of multiple proteins and the activation of associated signaling pathways were altered by TP-5. Moreover, TP-5 could inhibit LPS-induced neuroinflammation in the brain and BV2 microglia and the expression of major genes in the NF-κB/NLRP3 signaling pathway. Additionally, tyrosine hydroxylase (TH) expression downregulation was rescued in the LPS + TP-5 group compared with the LPS group. We conclude that TP-5 exerts neuroprotection by alleviating LPS-induced inflammatory damage and dopaminergic neurodegeneration. The protective effect of TP-5 may involve the NF-κB/NLRP3 signaling pathway.
 BACKGROUND: Dementia is a common and devastating symptom of Parkinson's disease (PD). Visual function and retinal structure are both emerging as potentially predictive for dementia in Parkinson's but lack longitudinal evidence. METHODS: We prospectively examined higher order vision (skew tolerance and biological motion) and retinal thickness (spectral domain optical coherence tomography) in 100 people with PD and 29 controls, with longitudinal cognitive assessments at baseline, 18 months and 36 months. We examined whether visual and retinal baseline measures predicted longitudinal cognitive scores using linear mixed effects models and whether they predicted onset of dementia, death and frailty using time-to-outcome methods. RESULTS: Patients with PD with poorer baseline visual performance scored lower on a composite cognitive score (β=0.178, SE=0.05, p=0.0005) and showed greater decreases in cognition over time (β=0.024, SE=0.001, p=0.013). Poorer visual performance also predicted greater probability of dementia (χ² (1)=5.2, p=0.022) and poor outcomes (χ² (1) =10.0, p=0.002). Baseline retinal thickness of the ganglion cell-inner plexiform layer did not predict cognitive scores or change in cognition with time in PD (β=-0.013, SE=0.080, p=0.87; β=0.024, SE=0.001, p=0.12). CONCLUSIONS: In our deeply phenotyped longitudinal cohort, visual dysfunction predicted dementia and poor outcomes in PD. Conversely, retinal thickness had less power to predict dementia. This supports mechanistic models for Parkinson's dementia progression with onset in cortical structures and shows potential for visual tests to enable stratification for clinical trials.
 New onset refractory status epilepticus (NORSE), including its subtype with a preceding febrile illness known as febrile infection-related epilepsy syndrome (FIRES), is one of the most severe forms of status epilepticus. The exact causes of NORSE are currently unknown, and there is so far no disease-specific therapy. Identifying the underlying pathophysiology and discovering specific biomarkers, whether immunologic, infectious, genetic, or other, may help physicians in the management of patients with NORSE. A broad spectrum of biomarkers has been proposed for status epilepticus patients, some of which were evaluated for patients with NORSE. Nonetheless, none has been validated, due to significant variabilities in study cohorts, collected biospecimens, applied analytical methods, and defined outcome endpoints, and to small sample sizes. The NORSE Institute established an open NORSE/FIRES biorepository for health-related data and biological samples allowing the collection of biospecimens worldwide, promoting multicenter research and sharing of data and specimens. Here, we suggest standard operating procedures for biospecimen collection and biobanking in this rare condition. We also propose criteria for the appropriate use of previously collected biospecimens. We predict that the widespread use of standardized procedures will reduce heterogeneity, facilitate the future identification of validated biomarkers for NORSE, and provide a better understanding of the pathophysiology and best clinical management for these patients.
 BACKGROUND: To evaluate the association of age with long-term outcome after thrombectomy. METHODS: In a retrospective cohort study based on routine healthcare data from Germany between 2010 and 2018, we included 18 506 patients with acute ischaemic stroke treated with mechanical thrombectomy. Association between age and mortality, disability, and level of care at 1 year was assessed. RESULTS: The median age was 76 years, 36.3% were aged ≥80 years and 55.8% were women. Patients aged ≥80 compared with those <80 years had a higher mortality (55.4% vs 28.5%; adjusted HR 1.13; 95% CI 1.05 to 1.31), more often had moderate/severe disability (35.5% vs 33.2%, adjusted HR 1.14; 95% CI 1.06 to 1.23) and less frequently had no/slight disability (17.4% vs 41.0%) at 1 year. Older age was associated with a higher likelihood of living in a nursing home (13.4% vs 9.2%, adjusted HR 1.09; 95% CI 0.97 to 1.22) and a lower likelihood of living at home (33.8% vs 62.8%) at 1 year. These associations were also robust when analysed in patients with no disability prior to stroke. Factors most strongly associated with worse 1-year outcomes in elderly patients were chronic limb-threatening ischaemia (67.9% vs 56.4%; HR 1.59, 95% CI 1.38 to 1.82), dementia at baseline (65.2% vs 47.3%; HR 1.29, 95% CI 1.17 to 1.44) and ventilation >48 hours (79.3% vs 52.2%; HR 2.91, 95% CI 2.66 to 3.18). CONCLUSIONS: In this large 'real-world' cohort, outcomes after mechanical thrombectomy were strongly associated with age. Of patients aged ≥80 years more than half were dead and less than one-fifth were functionally independent at 1 year. Certain comorbidities and ventilation >48 hours were associated with even worse outcomes.
 IMPORTANCE: Immunoglobulin G autoantibodies for aquaporin 4 (AQP4-IgG) serve as diagnostic biomarkers for neuromyelitis optica spectrum disorder (NMOSD), and the most sensitive and specific laboratory tests for their detection are cell-based assays (CBAs). Nevertheless, the limited availability of special instruments limits the widespread use of CBAs in routine laboratories. OBJECTIVE: To validate an enzyme immunodot assay for simple and rapid detection of AQP4-IgG. DESIGN, SETTING, AND PARTICIPANTS: This multicenter case-control study, conducted from May 2020 to February 2023, involved 4 medical centers (3 in China and 1 in Korea). The study included patients with AQP4-IgG-positive NMOSD, patients with other immune-related diseases, and healthy control individuals. Participants were excluded if they did not agree to participate or if their serum sample had turbidity. EXPOSURES: Serum AQP4 antibodies measured with immunodot assay. MAIN OUTCOMES AND MEASURES: The main outcome was performance of the immunodot assay compared with the gold standard CBA for detecting AQP4-IgG. To examine generalizability, cross-validation in Korea and at a second site in China, validation of patients with other immune-related diseases, and follow-up validation of the original cohort were performed. RESULTS: A total of 836 serum samples were collected; 400 were included in the diagnostic study and 436 in the validation sets. In a head-to-head diagnostic study involving 200 patients with NMOSD with AQP4-IgG (mean [SD] age, 43.1 [13.5] years; 188 [94%] female) and 200 healthy controls, use of an immunodot assay demonstrated antibody detection performance comparable to that of the gold standard (κ = 98.0%). The validation sets included 47 patients with NMOSD and 26 patients with other autoimmune diseases from Korea, 31 patients with NMOSD at a second site in China, 275 patients with other diseases, and 57 patients with NMOSD at follow-up. In the validation study, of 436 cases, 2 (<1%) were false positive and none were false negative. The CBA identified 332 AQP4-IgG-positive samples and 504 negative samples (200 [40%] in controls and 304 [60%] in patients with other diseases); 2 of the positive cases (<1%) were false negative and 4 of the negative cases (<1%) were false positive. The overall sensitivity of the immunodot assay was 99.4% (95% CI, 97.8%-99.9%), and the specificity was 99.2% (95% CI, 98.0%-99.8%). CONCLUSIONS AND RELEVANCE: This case-control study found that the immunodot assay was comparable to CBA for detecting AQP4-IgG. With its time- and cost-efficient characteristics, the immunodot assay may be a practical option for AQP4-IgG detection.
 BACKGROUND: Stiff person syndrome spectrum disorders (SPSD) are a rare group of disabling neuroimmunological disorders. SPSD often requires immune therapies, especially in the setting of inadequate response to symptomatic treatments. The safety and efficacy of therapeutic plasma exchange (TPE) in SPSD remains uncertain. OBJECTIVES: To describe the safety, tolerability, and efficacy of TPE in patients with SPSD. DESIGN: A retrospective observational study. METHODS: A retrospective review of SPSD patients seen at Johns Hopkins Hospital (JHH) from 1997 to 2021 was performed. Patient demographics/history, examination/diagnostic findings, treatment response, and TPE-related complications were recorded. Assessment for any associations between clinical characteristics, including age, sex, clinical phenotype, and time on immunotherapy, and response to TPE 3 months after treatment was performed. A subgroup of 18 patients treated with TPE at JHH and 6 patients treated with TPE at outside institutions were evaluated for any change in usage of symptomatic medications 3 months after the TPE treatment. Literature review of SPSD and TPE was also conducted. RESULTS: Thirty-nine SPSD patients were treated with TPE (21 at JHH and 18 at outside institutions); median age 48 years, 77% female, median modified Rankin Scale 3; mean initial anti-GAD65 antibody titer was 23,508 U/mL. Twenty-four patients (62%) had classic SPS, 10 (26%) had SPS-plus, 2 (5%) had progressive encephalomyelitis with rigidity and myoclonus, and 3 (8%) had pure cerebellar ataxia. All patients were on symptomatic treatments, 30 (77%) previously received IVIg, and 3 (8%) previously received rituximab. Four patients (10%) had a TPE-related adverse event. One developed asymptomatic hypotension, another had both line thrombosis and infection, and two had non-life-threatening bleeding events. Twenty-three (59%) patients reported improvement in symptoms after TPE. Of the subgroup of 24 patients evaluated for any change in usage of symptomatic medications 3 months after the TPE treatment, 14 (58%) required fewer GABAergic symptomatic medications. Literature review identified 57 additional patients with SPSD; 43 (75%) reported temporary improvement after TPE. CONCLUSION: The majority of patients treated with TPE had improvement. Moreover, most patients evaluated for any change in usage of symptomatic medications after the TPE treatment no longer required as much symptomatic medications months after TPE. TPE appears safe and well-tolerated in SPSD. Further studies are needed to assess the long-term efficacy of TPE in SPSD and identify which patients may benefit the most from TPE.
 BACKGROUND: Following spinal cord injury (SCI), disease processes spread gradually along the spinal cord forming a spatial gradient with most pronounced changes located at the lesion site. However, the dynamics of this gradient in SCI patients is not established. OBJECTIVE: This study tracks the spatiotemporal dynamics of remote anterograde and retrograde spinal tract degeneration in the upper cervical cord following SCI over two years utilizing quantitative MRI. METHODS: Twenty-three acute SCI patients (11 paraplegics, 12 tetraplegics) and 21 healthy controls were scanned with a T1-weighted sequence for volumetry and a FLASH sequence for myelin-sensitive magnetization transfer saturation (MTsat) of the upper cervical cord. We estimated myelin content from MTsat maps within the corticospinal tracts (CST) and dorsal columns (DC) and measured spinal cord atrophy by means of left-right width (LRW) and anterior-posterior width (APW) on the T1-weighted images across cervical levels C1-C3. MTsat in the CST and LRW were considered proxies for retrograde degeneration, while MTsat in the DC and APW provided evidence for anterograde degeneration, respectively. Using regression models, we compared the temporal and spatial trajectories of these MRI readouts between tetraplegics, paraplegics, and controls over a 2-year period and assessed their associations with clinical improvement. RESULTS: Linear rates and absolute differences in myelin-sensitive MTsat indicated retrograde and anterograde neurodegeneration in the CST and DC, respectively. Changes in MTsat within the CST and in LRW progressively developed over time forming a gradient towards lower cervical levels by 2 years after injury, especially in tetraplegics (change per cervical level in MTsat: -0.247 p.u./level, p = 0.034; in LRW: -0.323 mm/level, p = 0.024). MTsat within the DC was already decreased at cervical levels C1-C3 at baseline (1.5 months after injury) in both tetra- and paraplegics, while linear decreases in APW over time were similar across C1-C3, preserving the spatial gradient. The relative improvement in light touch score was associated with MTsat within the DC at baseline (r(s) = 0.575, p = 0.014). CONCLUSION: Rostral and remote to the injury, the CST and DC show ongoing structural changes, indicative of myelin reductions and atrophy within 2 years after SCI. While anterograde degeneration in the DC was already detectable uniformly at C1-C3 early following SCI, retrograde degeneration in the CST developed over time revealing specific spatial and temporal neurodegenerative gradients. Disentangling and quantifying such dynamic pathological processes may provide biomarkers for regenerative and remyelinating therapies along entire spinal pathways.
 Subunit-selective inhibition of N-methyl-d-aspartate receptors (NMDARs) is a promising therapeutic strategy for several neurological disorders, including epilepsy, Alzheimer's and Parkinson's disease, depression, and acute brain injury. We previously described the dihydroquinoline-pyrazoline (DQP) analogue 2a (DQP-26) as a potent NMDAR negative allosteric modulator with selectivity for GluN2C/D over GluN2A/B. However, moderate (<100-fold) subunit selectivity, inadequate cell-membrane permeability, and poor brain penetration complicated the use of 2a as an in vivo probe. In an effort to improve selectivity and the pharmacokinetic profile of the series, we performed additional structure-activity relationship studies of the succinate side chain and investigated the use of prodrugs to mask the pendant carboxylic acid. These efforts led to discovery of the analogue (S)-(-)-2i, also referred to as (S)-(-)-DQP-997-74, which exhibits >100- and >300-fold selectivity for GluN2C- and GluN2D-containing NMDARs (IC(50) 0.069 and 0.035 μM, respectively) compared to GluN2A- and GluN2B-containing receptors (IC(50) 5.2 and 16 μM, respectively) and has no effects on AMPA, kainate, or GluN1/GluN3 receptors. Compound (S)-(-)-2i is 5-fold more potent than (S)-2a. In addition, compound 2i shows a time-dependent enhancement of inhibitory actions at GluN2C- and GluN2D-containing NMDARs in the presence of the agonist glutamate, which could attenuate hypersynchronous activity driven by high-frequency excitatory synaptic transmission. Consistent with this finding, compound 2i significantly reduced the number of epileptic events in a murine model of tuberous sclerosis complex (TSC)-induced epilepsy that is associated with upregulation of the GluN2C subunit. Thus, 2i represents a robust tool for the GluN2C/D target validation. Esterification of the succinate carboxylate improved brain penetration, suggesting a strategy for therapeutic development of this series for NMDAR-associated neurological conditions.
 Hexanucleotide repeat expansion (HRE) within C9orf72 is the most common genetic cause of frontotemporal dementia (FTD). Thalamic atrophy occurs in both sporadic and familial FTD but is thought to distinctly affect HRE carriers. Separately, emerging evidence suggests widespread derepression of transposable elements (TEs) in the brain in several neurodegenerative diseases, including C9orf72 HRE-mediated FTD (C9-FTD). Whether TE activation can be measured in peripheral blood and how the reduction in peripheral C9orf72 expression observed in HRE carriers relates to atrophy and clinical impairment remain unknown. We used FreeSurfer software to assess the effects of C9orf72 HRE and clinical diagnosis (n = 78 individuals, male and female) on atrophy of thalamic nuclei. We also generated a novel, human, whole-blood RNA-sequencing dataset to determine the relationships among peripheral C9orf72 expression, TE activation, thalamic atrophy, and clinical severity (n = 114 individuals, male and female). We confirmed global thalamic atrophy and reduced C9orf72 expression in HRE carriers. Moreover, we identified disproportionate atrophy of the right mediodorsal lateral nucleus in HRE carriers and showed that C9orf72 expression associated with clinical severity, independent of thalamic atrophy. Strikingly, we found global peripheral activation of TEs, including the human endogenous LINE-1 element L1HS L1HS levels were associated with atrophy of multiple pulvinar nuclei, a thalamic region implicated in C9-FTD. Integration of peripheral transcriptomic and neuroimaging data from human HRE carriers revealed atrophy of specific thalamic nuclei, demonstrated that C9orf72 levels relate to clinical severity, and identified marked derepression of TEs, including L1HS, which predicted atrophy of FTD-relevant thalamic nuclei.SIGNIFICANCE STATEMENT Pathogenic repeat expansion in C9orf72 is the most frequent genetic cause of FTD and amyotrophic lateral sclerosis (ALS; C9-FTD/ALS). The clinical, neuroimaging, and pathologic features of C9-FTD/ALS are well characterized, whereas the intersections of transcriptomic dysregulation and brain structure remain largely unexplored. Herein, we used a novel radiogenomic approach to examine the relationship between peripheral blood transcriptomics and thalamic atrophy, a neuroimaging feature disproportionately impacted in C9-FTD/ALS. We confirmed reduction of C9orf72 in blood and found broad dysregulation of transposable elements-genetic elements typically repressed in the human genome-in symptomatic C9orf72 expansion carriers, which associated with atrophy of thalamic nuclei relevant to FTD. C9orf72 expression was also associated with clinical severity, suggesting that peripheral C9orf72 levels capture disease-relevant information.
 Blood cells contain functionally important intracellular structures, such as granules, critical to immunity and thrombosis. Quantitative variation in these structures has not been subjected previously to large-scale genetic analysis. We perform genome-wide association studies of 63 flow-cytometry derived cellular phenotypes-including cell-type specific measures of granularity, nucleic acid content and reactivity-in 41,515 participants in the INTERVAL study. We identify 2172 distinct variant-trait associations, including associations near genes coding for proteins in organelles implicated in inflammatory and thrombotic diseases. By integrating with epigenetic data we show that many intracellular structures are likely to be determined in immature precursor cells. By integrating with proteomic data we identify the transcription factor FOG2 as an early regulator of platelet formation and α-granularity. Finally, we show that colocalisation of our associations with disease risk signals can suggest aetiological cell-types-variants in IL2RA and ITGA4 respectively mirror the known effects of daclizumab in multiple sclerosis and vedolizumab in inflammatory bowel disease.
 INTRODUCTION AND AIMS: Digital biomarkers can provide a cost-effective, objective and robust measure for neurological disease progression, changes in care needs and the effect of interventions. Motor function, physiology and behaviour can provide informative measures of neurological conditions and neurodegenerative decline. New digital technologies present an opportunity to provide remote, high-frequency monitoring of patients from within their homes. The purpose of the living lab study is to develop novel digital biomarkers of functional impairment in those living with neurodegenerative disease (NDD) and neurological conditions. METHODS AND ANALYSIS: The Living Lab study is a cross-sectional observational study of cognition and behaviour in people living with NDDs and other, non-degenerative neurological conditions. Patients (n≥25 for each patient group) with dementia, Parkinson's disease, amyotrophic lateral sclerosis, mild cognitive impairment, traumatic brain injury and stroke along with controls (n≥60) will be pragmatically recruited. Patients will carry out activities of daily living and functional assessments within the Living Lab. The Living Lab is an apartment-laboratory containing a functional kitchen, bathroom, bed and living area to provide a controlled environment to develop novel digital biomarkers. The Living Lab provides an important intermediary stage between the conventional laboratory and the home. Multiple passive environmental sensors, internet-enabled medical devices, wearables and electroencephalography (EEG) will be used to characterise functional impairments of NDDs and non-NDD conditions. We will also relate these digital technology measures to clinical and cognitive outcomes. ETHICS AND DISSEMINATION: Ethical approvals have been granted by the Imperial College Research Ethics Committee (reference number: 21IC6992). Results from the study will be disseminated at conferences and within peer-reviewed journals.
 OBJECTIVE: Loneliness has been associated with poorer health-related quality of life but has not been studied in patients with systemic sclerosis (SSc). The current study was undertaken to examine and compare the psychometric properties of the English and French versions of the University of California, Los Angeles, Loneliness Scale-6 (ULS-6) in patients with SSc during the COVID-19 pandemic. METHODS: This study used baseline cross-sectional data from 775 adults enrolled in the Scleroderma Patient-Centered Intervention Network (SPIN) COVID-19 Cohort. Reliability and validity of ULS-6 scores overall and between languages were evaluated using confirmatory factor analysis (CFA), differential item functioning (DIF) through the multiple-indicator multiple-cause (MIMIC) model, omega/alpha calculation, and correlations of hypothesized convergent relationships. RESULTS: CFA for the total sample supported the single-factor structure (comparative fit index [CFI] 0.96, standardized root mean residual [SRMR] 0.03), and all standardized factor loadings for items were large (0.60-0.86). The overall MIMIC model with language as a covariate fit well (CFI 0.94, SRMR 0.04, root mean square error of approximation 0.11). Statistically significant DIF was found for 3 items across language (β(item2)  = 0.14, P < 0.001; β(item4)  = -0.07, P = 0.01; β(item6)  = 0.13, P < 0.001), but these small differences were without practical measurement implications. Analyses demonstrated high internal consistency with no language-based convergent validity differences. CONCLUSION: Analyses demonstrated evidence of acceptable reliability and validity of ULS-6 scores in English- and French-speaking adults with SSc. DIF analysis supported use of the ULS-6 to examine comparative experiences of loneliness without adjusting for language.
 BACKGROUND: Among different forms of de novo focal segmental glomerulosclerosis (FSGS), which can develop after kidney transplantation (KTx), collapsing glomerulopathy (CG) is the least frequent variant, but it is associated with the most severe form of nephrotic syndrome, histological findings of important vascular damage, and a 50% risk of graft loss. Here, we report two cases of de novo post-transplant CG. CLINICAL PRESENTATION: A 64-year-old White man developed proteinuria and worsening of renal function 5 years after KTx. Before the KTx, the patient was affected by an uncontrolled resistant hypertension, despite multiple antihypertensive therapies. Blood levels of calcineurin inhibitors (CNIs) were stable, with intermittent peaks. Kidney biopsy showed the presence of CG. After introduction of angiotensin receptor blockers (ARBs), urinary protein excretion progressively decreased in 6 months, but subsequent follow-up confirmed a progressive renal function decline. A 61-year-old White man developed CG 22 years after KTx. In his medical history, he was hospitalized twice to manage uncontrolled hypertensive crises. In the past, basal serum cyclosporin A levels were often detected above the therapeutic range. Low doses of intravenous methylprednisolone were administered due to the histological inflammatory signs shown on renal biopsy, followed by a rituximab infusion as a rescue therapy, but no clinical improvement was seen. DISCUSSION AND CONCLUSION: These two cases of de novo post-transplant CG were supposed to be mainly caused by the synergic effect of metabolic factors and CNI nephrotoxicity. Identifying the etiological factors potentially responsible for de novo CG development is essential for an early therapeutic intervention and the hope of better graft and overall survival.
 In the past, methods to subtype or biotype patients using brain imaging data have been developed. However, it is unclear whether and how these trained machine learning models can be successfully applied to population cohorts to study the genetic and lifestyle factors underpinning these subtypes. This work, using the Subtype and Stage Inference (SuStaIn) algorithm, examines the generalisability of data-driven Alzheimer's disease (AD) progression models. We first compared SuStaIn models trained separately on Alzheimer's disease neuroimaging initiative (ADNI) data and an AD-at-risk population constructed from the UK Biobank dataset. We further applied data harmonization techniques to remove cohort effects. Next, we built SuStaIn models on the harmonized datasets, which were then used to subtype and stage subjects in the other harmonized dataset. The first key finding is that three consistent atrophy subtypes were found in both datasets, which match the previously identified subtype progression patterns in AD: 'typical', 'cortical' and 'subcortical'. Next, the subtype agreement was further supported by high consistency in individuals' subtypes and stage assignment based on the different models: more than 92% of the subjects, with reliable subtype assignment in both ADNI and UK Biobank dataset, were assigned to an identical subtype under the model built on the different datasets. The successful transferability of AD atrophy progression subtypes across cohorts capturing different phases of disease development enabled further investigations of associations between AD atrophy subtypes and risk factors. Our study showed that (1) the average age is highest in the typical subtype and lowest in the subcortical subtype; (2) the typical subtype is associated with statistically more-AD-like cerebrospinal fluid biomarkers values in comparison to the other two subtypes; and (3) in comparison to the subcortical subtype, the cortical subtype subjects are more likely to associate with prescription of cholesterol and high blood pressure medications. In summary, we presented cross-cohort consistent recovery of AD atrophy subtypes, showing how the same subtypes arise even in cohorts capturing substantially different disease phases. Our study opened opportunities for future detailed investigations of atrophy subtypes with a broad range of early risk factors, which will potentially lead to a better understanding of the disease aetiology and the role of lifestyle and behaviour on AD.
 The aim was to determine school performance and psychiatric comorbidity in children with childhood absence epilepsy (CAE). We reviewed the medical records in children with ICD-10 codes for idiopathic generalized epilepsy before 18 years of age, and pediatric neurologists confirmed the International League Against Epilepsy criteria for CAE were met. Control groups were the general pediatric population or children with non-neurological chronic disease. Outcomes were from nationwide and population-based registers on school performance and psychiatric comorbidity. We compared the mean grade point average using linear regression and estimated hazard ratios (HR) using Cox regression for the other outcomes. Analyses were adjusted for the child's sex, and year of birth, and parental highest education, receipt of cash benefits or early disability pension. We included 114 children with CAE with a median age at onset of 5.9 years (interquartile range = 4.5-7.3 years). Compared with both population controls and non-neurological chronically ill children, children with CAE had increased hazard of special needs education (HR = 2.7, 95% confidence interval (CI) = 1.8-4.1, p < 0.0001), lower grade point average at 9th grade by 1.7 grade points (95% CI = -2.5 to -1.0, p < 0.001), increased ADHD medicine use (HR = 4.4, 95% CI = 2.7-7.2, p < 0.001), increased sleep medicine use (HR = 2.7, 95% CI = 1.7-4.3, p < 0.001), and increased psychiatry visits (HR = 2.1, 95% CI = 1.1-4.0, p = 0.03). In conclusion, children with CAE have increased psychiatric comorbidity and a considerable proportion of these children receive special needs education in primary/secondary school, albeit insufficient to normalize their considerably lower grade point average in the 9th grade.
 PURPOSE: The role of cerebral blood flow (CBF) in the early stages of Alzheimer's disease is complex and largely unknown. We investigated cross-sectional and longitudinal associations between CBF, amyloid burden, and cognition, in cognitively normal individuals with subjective cognitive decline (SCD). METHODS: We included 187 cognitively normal individuals with SCD from the SCIENCe project (65 ± 8 years, 39% F, MMSE 29 ± 1). Each underwent a dynamic (0-70 min) [(18)F]florbetapir PET and T1-weighted MRI scan, enabling calculation of mean binding potential (BP(ND); specific amyloid binding) and R(1) (measure of relative (r)CBF). Eighty-three individuals underwent a second [(18)F]florbetapir PET (2.6 ± 0.7 years). Participants annually underwent neuropsychological assessment (follow-up time 3.8 ± 3.1 years; number of observations n = 774). RESULTS: A low baseline R(1) was associated with steeper decline on tests addressing memory, attention, and global cognition (range betas 0.01 to 0.27, p < 0.05). High BP(ND) was associated with steeper decline on tests covering all domains (range betas - 0.004 to - 0.70, p < 0.05). When both predictors were simultaneously added to the model, associations remained essentially unchanged. Additionally, we found longitudinal associations between R(1) and BP(ND). High baseline BP(ND) predicted decline over time in R(1) (all regions, range betas(BP×time) - 0.09 to - 0.14, p < 0.05). Vice versa, low baseline R(1) predicted increase in BP(ND) in frontal, temporal, and composite ROIs over time (range betas(R1×time) - 0.03 to - 0.08, p < 0.05). CONCLUSION: Our results suggest that amyloid accumulation and decrease in rCBF are two parallel disease processes without a fixed order, both providing unique predictive information for cognitive decline and each process enhancing the other longitudinally.
 Obesity is associated with cognitive decline. Recent observations in mice propose an adipose tissue (AT)-brain axis. We identified 188 genes from RNA sequencing of AT in three cohorts that were associated with performance in different cognitive domains. These genes were mostly involved in synaptic function, phosphatidylinositol metabolism, the complement cascade, anti-inflammatory signaling, and vitamin metabolism. These findings were translated into the plasma metabolome. The circulating blood expression levels of most of these genes were also associated with several cognitive domains in a cohort of 816 participants. Targeted misexpression of candidate gene ortholog in the Drosophila fat body significantly altered flies memory and learning. Among them, down-regulation of the neurotransmitter release cycle-associated gene SLC18A2 improved cognitive abilities in Drosophila and in mice. Up-regulation of RIMS1 in Drosophila fat body enhanced cognitive abilities. Current results show previously unidentified connections between AT transcriptome and brain function in humans, providing unprecedented diagnostic/therapeutic targets in AT.
 OBJECTIVE: To assign clinical meanings to the Family Reported Outcome Measure (FROM-16) scores through the development of score bands using the anchor-based approach. DESIGN AND SETTING: A cross-sectional online study recruited participants through UK-based patient support groups, research support platforms (HealthWise Wales, Autism Research Centre-Cambridge University database, Join Dementia Research) and through social service departments in Wales. PARTICIPANTS: Family members/partners (aged ≥18 years) of patients with different health conditions. INTERVENTION: Family members/partners of patients completed the FROM-16 questionnaire and a Global Question (GQ). MAIN OUTCOME MEASURE: Various FROM-16 band sets were devised as a result of mapping of mean, median and mode of the GQ scores to FROM-16 total score, and receiver operating characteristic-area under the curve cut-off values. The band set with the best agreement with GQ based on weighted kappa was selected. RESULTS: A total of 4413 family members/partners (male=1533, 34.7%; female=2858, 64.8%; Prefer not to say=16, 0.4%; other=6, 0.14%) of people with a health condition (male=1994, 45.2%; female=2400, 54.4%; Prefer not to say=12, 0.3%; other=7, 0.16%) completed the online survey: mean FROM-16 score=15.02 (range 0-32, SD=8.08), mean GQ score=2.32 (range 0-4, SD=1.08). The proposed FROM-16 score bandings are: 0-1=no effect on the quality of life of family member; 2-8=small effect on family member; 9-16=moderate effect on family member; 17-25=very large effect on family member; 26-32=extremely large effect on family member (weighted kappa=0.60). CONCLUSION: The FROM-16 score descriptor bands provide new information to clinicians about interpreting scores and score changes, allowing better-informed treatment decisions for patients and their families. The score banding of FROM-16, along with a short administration time, demonstrates its potential to support holistic clinical practice.
 A major evolution from purely clinical diagnoses to biomarker supported clinical diagnosing has been occurring over the past years in neurology. High-throughput methods, such as next-generation sequencing and mass spectrometry-based proteomics along with improved neuroimaging methods, are accelerating this development. This calls for a consensus framework that is broadly applicable and provides a spot-on overview of the clinical validity of novel biomarkers. We propose a harmonized terminology and a uniform concept that stratifies biomarkers according to clinical context of use and evidence levels, adapted from existing frameworks in oncology with a strong focus on (epi)genetic markers and treatment context. We demonstrate that this framework allows for a consistent assessment of clinical validity across disease entities and that sufficient evidence for many clinical applications of protein biomarkers is lacking. Our framework may help to identify promising biomarker candidates and classify their applications by clinical context, aiming for routine clinical use of (protein) biomarkers in neurology.
 PURPOSE: The retina provides biomarkers of neuronal and vascular health that offer promising insights into cognitive ageing, mild cognitive impairment and dementia. This article described the rationale and methodology of eye and vision assessments with the aim of supporting the study of dementia in the UK Biobank Repeat Imaging study. PARTICIPANTS: UK Biobank is a large-scale, multicentre, prospective cohort containing in-depth genetic, lifestyle, environmental and health information from half a million participants aged 40-69 enrolled in 2006-2010 across the UK. A subset (up to 60 000 participants) of the cohort will be invited to the UK Biobank Repeat Imaging Study to collect repeated brain, cardiac and abdominal MRI scans, whole-body dual-energy X-ray absorptiometry, carotid ultrasound, as well as retinal optical coherence tomography (OCT) and colour fundus photographs. FINDINGS TO DATE: UK Biobank has helped make significant advances in understanding risk factors for many common diseases, including for dementia and cognitive decline. Ophthalmic genetic and epidemiology studies have also benefited from the unparalleled combination of very large numbers of participants, deep phenotyping and longitudinal follow-up of the cohort, with comprehensive health data linkage to disease outcomes. In addition, we have used UK Biobank data to describe the relationship between retinal structures, cognitive function and brain MRI-derived phenotypes. FUTURE PLANS: The collection of eye-related data (eg, OCT), as part of the UK Biobank Repeat Imaging study, will take place in 2022-2028. The depth and breadth and longitudinal nature of this dataset, coupled with its open-access policy, will create a major new resource for dementia diagnostic discovery and to better understand its association with comorbid diseases. In addition, the broad and diverse data available in this study will support research into ophthalmic diseases and various other health outcomes beyond dementia.
 Minocycline has anti-inflammatory, antioxidant, and anti-apoptotic properties that explain the renewed interest in its use as an adjunctive treatment for psychiatric and neurological conditions. Following the completion of several new clinical trials using minocycline, we proposed an up-to-date systematic review and meta-analysis of the data available. The PICO (patient/population, intervention, comparison and outcomes) framework was used to search 5 databases aiming to identify randomized controlled trials that used minocycline as an adjunctive treatment for psychiatric and neurological conditions. Search results, data extraction, and risk of bias were performed by two independent authors for each publication. Quantitative meta-analysis was performed using RevMan software. Literature search and review resulted in 32 studies being included in this review: 10 in schizophrenia, 3 studies in depression, and 7 in stroke, with the benefit of minocycline being used in some of the core symptoms evaluated; 2 in bipolar disorder and 2 in substance use, without demonstrating a benefit for using minocycline; 1 in obsessive-compulsive disorder, 2 in brain and spinal injuries, 2 in amyotrophic lateral sclerosis, 1 in Alzheimer's disease, 1 in multiple systems atrophy, and 1 in pain, with mixes results. For most of the conditions included in this review the data is still limited and difficult to interpret, warranting more well-designed and powered studies. On the other hand, the studies available for schizophrenia seem to suggest an overall benefit favoring the use of minocycline as an adjunctive treatment.
 Moderate acute intermittent hypoxia (mAIH) elicits a form of phrenic motor plasticity known as phrenic long-term facilitation (pLTF), which requires spinal 5-HT(2) receptor activation, ERK/MAP kinase signaling, and new brain-derived neurotrophic factor (BDNF) synthesis. New BDNF protein activates TrkB receptors that normally signal through PKCθ to elicit pLTF. Phrenic motor plasticity elicited by spinal drug administration (e.g., BDNF) is referred to by a more general term: phrenic motor facilitation (pMF). Although mild systemic inflammation elicited by a low lipopolysaccharide (LPS) dose (100 µg/kg; 24 h prior) undermines mAIH-induced pLTF upstream from BDNF protein synthesis, it augments pMF induced by spinal BDNF administration through unknown mechanisms. Here, we tested the hypothesis that mild inflammation shifts BDNF/TrkB signaling from PKCθ to alternative pathways that enhance pMF. We examined the role of three known signaling pathways associated with TrkB (MEK/ERK MAP kinase, PI3 kinase/Akt, and PKCθ) in BDNF-induced pMF in anesthetized, paralyzed, and ventilated Sprague Dawley rats 24 h post-LPS. Spinal PKCθ inhibitor (TIP) attenuated early BDNF-induced pMF (≤30 min), with minimal effect 60-90 min post-BDNF injection. In contrast, MEK inhibition (U0126) abolished BDNF-induced pMF at 60 and 90 min. PI3K/Akt inhibition (PI-828) had no effect on BDNF-induced pMF at any time. Thus, whereas BDNF-induced pMF is exclusively PKCθ-dependent in normal rats, MEK/ERK is recruited by neuroinflammation to sustain, and even augment downstream plasticity. Because AIH is being developed as a therapeutic modality to restore breathing in people living with multiple neurological disorders, it is important to understand how inflammation, a common comorbidity in many traumatic or degenerative central nervous system disorders, impacts phrenic motor plasticity.NEW & NOTEWORTHY We demonstrate that even mild systemic inflammation shifts signaling mechanisms giving rise to BDNF-induced phrenic motor plasticity. This finding has important experimental, biological, and translational implications, particularly since BDNF-dependent spinal plasticity is being translated to restore breathing and nonrespiratory movements in diverse clinical disorders, such as spinal cord injury (SCI) and amyotrophic lateral sclerosis (ALS).
 PURPOSE: To explore the localization value of drug-resistant temporal lobe epilepsy (TLE) aura for preoperative evaluation, based on stereoelectroencephalography (SEEG), and its prognostic value on the surgical outcome. METHODS: The data of patients with drug-resistant TLE who had SEEG electrodes implanted during preoperative evaluation at the First Affiliated Hospital of the University of Science and Technology of China (Hefei, China) were retrospectively analyzed. The patients were divided into aura-positive and aura-negative groups according to the presence of aura in seizures. To explore the clinical features of aura, we evaluated the localizing and prognostic values of aura for the outcome of anterior temporal lobectomy based on SEEG. RESULTS: Among forty patients, twenty-seven patients were in the aura-positive group and ten (25.0%) patients had multiple auras. The most common TLE aura was abdominal aura [thirteen (34.2%) patients]. The postoperative seizure frequency was significantly reduced in the preoperative aura-positive patients compared to the preoperative aura-negative patients (P = 0.011). Patients with abdominal (P = 0.029) and single (P = 0.036) auras had better surgical prognoses than aura-negative patients. In the preoperative evaluation, aura-positive patients had a better surgical outcome if the laterality of positron emission tomography-computed tomography (PET-CT) hypometabolism was concordant with the epileptogenic focus identified with SEEG (P = 0.031). A good postoperative epileptic outcome in aura-positive patients was observed among those with hippocampal sclerotic medial temporal lobe epilepsy (P = 0.025). CONCLUSION: Epileptic aura is valuable for the localization of the epileptogenic focus. Abdominal aura and single aura were good predictors of better surgical outcomes. Among patients with a preoperative diagnosis of hippocampal sclerosis or with laterality of PET-CT hypometabolism concordant with the epileptogenic focus identified using SEEG, those with aura are likely to benefit from surgery.
 BACKGROUND: Livedoid vasculopathy (LV) is a rare, disabling disease characterized by painful ulcers, livedo reticularis and atrophy blanche. Hypercoagulation, endothelial, and microcirculatory dysfunction are believed to be responsible for the pathogenesis of this difficult-to-treat disease. OBJECTIVES: This study sought to investigate the frequency of endothelial dysfunction, hypercoagulability, and nailfold capillaroscopic features in LV patients to shed light on its etiology. METHODS: This case-control study included 16 patients with LV, 24 with systemic sclerosis (SSc), and 23 control subjects. Serum markers of endothelial dysfunction soluble endoglin, endocan, endothelin-1, lipoprotein a, plasminogen activator inhibitor-1 (PAI-1), soluble thrombomodulin, and von Willebrand factor were measured using enzyme-linked immunosorbent assays. Flow-mediated dilation and carotid intima-media thickness were examined as markers of endothelial dysfunction, and microcirculation was assessed with nailfold capillaroscopy. Thrombophilia-related parameters, including gene polymorphisms of factor V Leiden, prothrombin, PAI-1 genes, methylenetetrahydrofolate reductase (MTHFR) and factor XIII mutation and serum levels of protein C, protein S, antithrombin, homocysteine, D-dimer and antiphospholipid antibodies were investigated in LV patients. RESULTS: Plasminogen activator inhibitor-1 and soluble thrombomodulin levels were significantly higher in LV patients compared to control subjects (2.3 [2.05-2.79] ng/ml vs. 1.89 [1.43-2.33] ng/ml, p = 0.007; 1.15 [0.88-1.4] ng/ml vs. 0.76 [0.56-0.9] ng/ml, p = 0.004, respectively). Flow-mediated dilation was 25.4 % lower in the LV patients compared to the control group (14.77 % [11.26-18.26] vs. 19.80 % [16.47-24.88], p = 0.034). Capillaroscopic features, including ramifications (75 % vs. 8.7 %, p < 0.001), avascular areas (25 % vs. 0 %, p = 0.011) and dilatations (33.2 % vs. 0 %, p = 0.016), were significantly higher in LV patients than in controls. LV patients had multiple biochemical or genetic abnormalities related to thrombophilia, including heterozygous factor V Leiden mutations (6.3 %), MTHFR (C677T) mutations (heterozygous 43.8 %, homozygous 18.8 %), MTHFR (A1298C) mutations (heterozygous 37.5 %, homozygous 12.5 %), factor XIII heterozygous mutation (12.5 %), antithrombin deficiency (31.3 %), protein S deficiency (12.5 %), hyperhomocysteinemia (31.3 %), D-dimer elevation (25 %), anti-β2-glycoprotein I (12.5 %), lupus anticoagulant antibodies (6.3 %), and anticardiolipin antibodies (6.3 %). CONCLUSIONS: In conclusion, LV patients were characterized by an increased presence of thrombophilia-related parameters, and also exhibited vascular endothelial and microcirculatory dysfunction, resembling SSc. These findings support the complex interaction of thrombophilia, endothelial dysfunction, and microcirculation dysregulation in the pathogenesis of LV. Thus, the treatment of LV patients should be individualized, based on the identification of the predominant pathological pathways.
 BACKGROUND AND OBJECTIVES: Whether chronic autoimmune inflammatory diseases causally affect the risk of Alzheimer disease (AD) is controversial. We characterized the relationship between inflammatory diseases and risk of AD and explored the role of circulating inflammatory biomarkers in the relationships between inflammatory diseases and AD. METHODS: We performed observational analyses for chronic autoimmune inflammatory diseases and risk of AD using data from 2,047,513 participants identified in the UK Clinical Practice Research Datalink (CPRD). Using data of a total of more than 1,100,000 individuals from 15 large-scale genome-wide association study data sets, we performed 2-sample Mendelian randomizations (MRs) to investigate the relationships between chronic autoimmune inflammatory diseases, circulating inflammatory biomarker levels, and risk of AD. RESULTS: Cox regression models using CPRD data showed that the overall incidence of AD was higher among patients with inflammatory bowel disease (hazard ratio [HR] 1.17; 95% CI 1.15-1.19; p = 2.1 × 10(-4)), other inflammatory polyarthropathies and systematic connective tissue disorders (HR 1.13; 95% CI 1.12-1.14; p = 8.6 × 10(-5)), psoriasis (HR 1.13; 95% CI 1.10-1.16; p = 2.6 × 10(-4)), rheumatoid arthritis (HR 1.08; 95% CI 1.06-1.11; p = 4.0 × 10(-4)), and multiple sclerosis (HR 1.06; 95% CI 1.04-1.07; p = 2.8 × 10(-4)) compared with the age (±5 years) and sex-matched comparison groups free from all inflammatory diseases under investigation. Bidirectional MR analysis identified relationships between chronic autoimmune inflammatory diseases and circulating inflammatory biomarkers. Particularly, circulating monokine induced by gamma interferon (MIG) level was suggestively associated with a higher risk of AD (odds ratio from inverse variance weighted [OR(IVW)] 1.23; 95% CI 1.06-1.42; p (IVW) = 0.007) and lower risk of Crohn disease (OR(IVW) 0.73; 95% CI -0.62 to 0.86; p (IVW) = 1.3 × 10(-4)). Colocalization supported a common causal single nucleotide polymorphism for MIG and Crohn disease (posterior probability = 0.74), but not AD (posterior probability = 0.03). Using a 2-sample MR approach, genetically predicted risks of inflammatory diseases were not associated with higher AD risk. DISCUSSION: Our data suggest that the association between inflammatory diseases and risk of AD is unlikely to be causal and may be a result of confounding. In support, although inflammatory biomarkers showed evidence for causal associations with inflammatory diseases, evidence was weak that they affected both inflammatory disease and AD.
 Since COVID-19 was declared a pandemic, Brazil has become one of the countries most affected by this disease. A year into the pandemic, a second wave of COVID-19 emerged, with a rapid spread of a new SARS-CoV-2 lineage of concern. Several vaccines have been granted emergency-use authorization, leading to a decrease in mortality and severe cases in many countries. However, the emergence of SARS-CoV-2 variants raises the alert for potential new waves of transmission and an increase in pathogenicity. We compared the demographic and clinical data of critically ill patients infected with COVID-19 hospitalized in Rio de Janeiro during the first and second waves between July 2020 and October 2021. In total, 106 participants were included in this study; among them, 88% had at least one comorbidity, and 37% developed severe disease. Disease severity was associated with older age, pre-existing neurological comorbidities, higher viral load, and dyspnea. Laboratory biomarkers related to white blood cells, coagulation, cellular injury, inflammation, renal, and liver injuries were significantly associated with severe COVID-19. During the second wave of the pandemic, the necessity of invasive respiratory support was higher, and more individuals with COVID-19 developed acute hepatitis, suggesting that the progression of the second wave resulted in an increase in severe cases. These results can contribute to understanding the behavior of the COVID-19 pandemic in Brazil and may be helpful in predicting disease severity, which is a pivotal for guiding clinical care, improving patient outcomes, and defining public policies.
 OBJECTIVE: Neuromyelitis optica spectrum disorders (NMOSD) represent rare autoimmune diseases of the central nervous system largely targeting optic nerve(s) and spinal cord. The present analysis used real-world data to identify clinical and epidemiological correlates of treatment change in patients with NMOSD. METHODS: CIRCLES is a longitudinal, observational study of NMOSD conducted at 15 centers across North America. Patients with ≥ 60 days of follow-up and receiving on-study maintenance treatment were evaluated. The mean annual relapse rate (ARR) was estimated using negative binomial models; the likelihood of treatment change was estimated using Cox proportional hazards models. Relapses were included as time-varying covariates to estimate the relationship to treatment change. RESULTS: Of 542 patients included, 171 (31.5%) experienced ≥ 1 relapse on the study and 133 patients (24.5%) had ≥ 1 change in the treatment regimen. Two categories of variables significantly correlated with the likelihood of treatment change: (1) relapse: any on-study relapse (hazard ratio [HR] = 2.91; p < 0.001), relapse phenotypes (HR range = 2.15-5.49; p < 0.001), and pre-study ARR > 0.75 (HR 2.28; p < 0.001); 2) disease phenotype: brain syndrome only vs transverse myelitis involvement at onset (HR 2.44; p = 0.008), disease duration < 1 vs > 5 years (HR 1.66; p = 0.028), or autoimmune comorbidity (HR 1.55; p = 0.015). A subset of these factors significantly correlated with shorter time to first rituximab discontinuation. CONCLUSIONS: In CIRCLES, relapse patterns and disease phenotype significantly correlated with changes in the maintenance treatment regimen. Such findings may facilitate the identification of patients with NMOSD who are likely to benefit from treatment change to reduce relapse risk or disease burden and enhance the quality of life.
 Persistent somatic and neuropsychiatric symptoms have been frequently described in patients after infection with severe acute respiratory syndrome coronavirus 2 even after a benign clinical course of the acute infection during the early phases of the coronavirus severe acute respiratory syndrome coronavirus 2 pandemic and are part of Long COVID. The Omicron variant emerged in November 2021 and has rapidly become predominant due to its high infectivity and suboptimal vaccine cross-protection. The frequency of neuropsychiatric post-acute sequelae after infection with the severe acute respiratory syndrome coronavirus 2 Omicron and adequate vaccination status is not known. Here, we aimed to characterize post-acute symptoms in individuals with asymptomatic or mildly symptomatic breakthrough infection with severe acute respiratory syndrome coronavirus 2. These individuals had either proven infection with the Omicron variant (n = 157) or their infection occurred in 2022 where Omicron was the predominant variant of severe acute respiratory syndrome coronavirus 2 in Germany (n = 107). This monocentric cross-sectional study was conducted at the University Medical Center Hamburg-Eppendorf between 11 February 2022 and 11 April 2022. We employed questionnaires addressing self-reported somatic symptom burden (Somatic Symptom Scale 8) and neuropsychiatric symptoms including mood (Patient Health Questionnaire 2), anxiety (Generalized Anxiety Disorder 7), attention (Mindful Attention Awareness Scale) and fatigue (Fatigue Assessment Scale) in a cohort of hospital workers. Scores were compared between 175 individuals less than 4 weeks after positive testing for severe acute respiratory syndrome coronavirus 2, 88 individuals more than 4 weeks after positive testing and 87 severe acute respiratory syndrome coronavirus 2 uninfected controls. The majority (n = 313; 89.5%) of included individuals were vaccinated at least three times. After recovery from infection, no significant differences in scores assessing neuropsychiatric and somatic symptoms were detected between the three groups (severe acute respiratory syndrome coronavirus 2 uninfected controls, individuals less and more than 4 weeks after positive testing) independent of age, sex, preconditions and vaccination status. In addition, self-reported symptom burden did not significantly correlate with the number of vaccinations against severe acute respiratory syndrome coronavirus 2, time from recovery or the number of infections. Notably, in all three groups, the mean scores for each item of our questionnaire lay below the pathological threshold. Our data show that persistent neuropsychiatric and somatic symptoms after recovery from severe acute respiratory syndrome coronavirus 2 infection in fully vaccinated hospital workers do not occur more frequently than that in uninfected individuals. This will guide healthcare professionals in the clinical management of patients after recovery from breakthrough infections with severe acute respiratory syndrome coronavirus 2.
 BACKGROUND AND OBJECTIVE: Myelin-oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) frequently initiates during childbearing years. This study investigated the impact of pregnancy and post-partum on MOGAD activity. METHODS: Retrospective analysis of clinical and demographic data from a multicenter French cohort of adult patients with MOGAD. All adult female patients who had a pregnancy after disease onset or in the year before disease onset were included. The annualized relapse rate was evaluated in patients who had a pregnancy after disease onset, to evaluate the impact of pregnancy and post-partum on MOGAD course. RESULTS: Twenty-five informative pregnancies after disease onset were identified. No relapse was recorded during these pregnancies and only three relapses occurred during the first 3 months post-partum. The annualized relapse rate decreased from 0.67 (95% confidence interval: 0.40-1.10) during the pre-pregnancy period to 0 (95% confidence interval: 0-0.21) during pregnancy and to 0.22 (95% confidence interval: 0.09-0.53) during the first year post-partum. Among 144 female patients in their childbearing age recorded in the database, 18 (12.5%) reported their first symptoms during pregnancy or in the 12 months post-partum. DISCUSSION: Our study suggests a marked reduction of MOGAD relapse rate during pregnancy and the post-partum period. Prospective studies on the role of pregnancy and delivery in MOGAD course are needed.
 Huntington's disease (HD) is an incurable inherited brain disorder characterised by massive degeneration of striatal neurons, which correlates with abnormal accumulation of misfolded mutant huntingtin (mHTT) protein. Research on HD has been hampered by the inability to study early dysfunction and progressive degeneration of human striatal neurons in vivo. To investigate human pathogenesis in a physiologically relevant context, we transplanted human pluripotent stem cell-derived neural progenitor cells (hNPCs) from control and HD patients into the striatum of new-born mice. Most hNPCs differentiated into striatal neurons that projected to their target areas and established synaptic connexions within the host basal ganglia circuitry. Remarkably, HD human striatal neurons first developed soluble forms of mHTT, which primarily targeted endoplasmic reticulum, mitochondria and nuclear membrane to cause structural alterations. Furthermore, HD human cells secreted extracellular vesicles containing mHTT monomers and oligomers, which were internalised by non-mutated mouse striatal neurons triggering cell death. We conclude that interaction of mHTT soluble forms with key cellular organelles initially drives disease progression in HD patients and their transmission through exosomes contributes to spread the disease in a non-cell autonomous manner.
 OBJECTIVE: To generate comparative efficacy evidence of belimumab versus anifrolumab in SLE that can inform treatment practices. METHODS: The SLE Responder Index (SRI)-4 response at 52 weeks of belimumab versus anifrolumab was evaluated with an indirect treatment comparison. The evidence base consisted of randomised trials that were compiled through a systemic literature review.A feasibility assessment was performed to comprehensively compare the eligible trials and to determine the most appropriate indirect treatment comparison analysis method. A multilevel network meta-regression (ML-NMR) was implemented that adjusted for differences across trials in four baseline characteristics: SLE Disease Activity Index-2K, anti-double-stranded DNA antibody positive, low complement (C)3 and low C4. Additional analyses were conducted to explore if the results were robust to different sets of baseline characteristics included for adjustment, alternative adjustment methods and changes to the trials included in the evidence base. RESULTS: The ML-NMR included eight trials: five belimumab trials (BLISS-52, BLISS-76, NEA, BLISS-SC, EMBRACE) and three anifrolumab trials (MUSE, TULIP-1, TULIP-2). Belimumab and anifrolumab were comparable in terms of SRI-4 response (OR (95% credible interval), 1.04 (0.74-1.45)), with the direction of the point estimate slightly favouring belimumab. Belimumab had a 0.58 probability of being the more effective treatment. The results were highly consistent across all analysis scenarios. CONCLUSIONS: Our results suggest that the SRI-4 response of belimumab and anifrolumab are similar at 52 weeks in the general SLE population, but the level of uncertainty around the point estimate means we cannot rule out the possibility of a clinically meaningful benefit for either treatment. It remains to be seen if specific groups of patients could derive a greater benefit from anifrolumab or from belimumab, and there is certainly an unmet need to identify robust predictors towards more personalised selection of available biological agents in SLE.
 BACKGROUND: Primary open-angle glaucoma (POAG) is an optic neuropathy characterized by progressive degeneration of the optic nerve that leads to irreversible visual impairment. Multiple epidemiological studies suggest an association between POAG and major neurodegenerative disorders (Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal dementia, and Parkinson's disease). However, the nature of the overlap between neurodegenerative disorders, brain morphology and glaucoma remains inconclusive. METHOD: In this study, we performed a comprehensive assessment of the genetic and causal relationship between POAG and neurodegenerative disorders, leveraging genome-wide association data from studies of magnetic resonance imaging of the brain, POAG, and four major neurodegenerative disorders. FINDINGS: This study found a genetic overlap and causal relationship between POAG and its related phenotypes (i.e., intraocular pressure and optic nerve morphology traits) and brain morphology in 19 regions. We also identified 11 loci with a significant local genetic correlation and a high probability of sharing the same causal variant between neurodegenerative disorders and POAG or its related phenotypes. Of interest, a region on chromosome 17 corresponding to MAPT, a well-known risk locus for Alzheimer's and Parkinson's disease, was shared between POAG, optic nerve degeneration traits, and Alzheimer's and Parkinson's diseases. Despite these local genetic overlaps, we did not identify strong evidence of a causal association between these neurodegenerative disorders and glaucoma. INTERPRETATION: Our findings indicate a distinctive and likely independent neurodegenerative process for POAG involving several brain regions although several POAG or optic nerve degeneration risk loci are shared with neurodegenerative disorders, consistent with a pleiotropic effect rather than a causal relationship between these traits. FUNDING: PG was supported by an NHMRC Investigator Grant (#1173390), SM by an NHMRC Senior Research Fellowship and an NHMRC Program Grant (APP1150144), DM by an NHMRC Fellowship, LP is funded by the NEIEY015473 and EY032559 grants, SS is supported by an NIH-Oxford Cambridge Fellowship and NIH T32 grant (GM136577), APK is supported by a UK Research and Innovation Future Leaders Fellowship, an Alcon Research Institute Young Investigator Award and a Lister Institute for Preventive Medicine Award.
 OBJECTIVES: To estimate the prevalence of long-term exposure to glucocorticoids (GCs) and to identify factors associated with, and variations in prescribing practices over time and across recruiting countries. METHODS: We included patients with SSc having a visit recorded in the EUSTAR database from January 2013 onward. We analysed the prevalence and the main features of GCs users, their exposure to GCs over time, and their GCs dosages. Multivariable linear regression was used to analyse the factors identified as associated with GCs intake duration. Time trends, and variations in GCs utilization across recruiting countries were explored. Missing data were imputed using multiple imputation with chained equations. RESULTS: The 9819 patients included were mostly females (85%), the majority had lcSSc (73%), and the median age was 58 years. At baseline, 34% of patients (n = 2769/8109) (48% dcSSc vs 29% lcSSc) were on GCs, and the median dose was 7.5 mg/day. GCs users were more frequently males and anti-Scl70 positive, and more commonly had dcSSc and more severe disease. On average, GCs users spent 25% of their follow-up time (median 33.2 months) on GCs, with no significant between-subsets difference. Notably, 33% (n = 971/2959) and 22% (n = 647/2959) of patients followed up for >1 year had received GCs for >6 and >12 months, respectively. Multivariable analysis showed that patient and disease characteristics poorly explained the variability in GCs exposure (adjusted-R2 = 0.06, P < 0.001). GCs utilization varied within and across countries, and gradually decreased over time (36% in 2013 vs 23% in 2018). CONCLUSIONS: GCs are widely and long-term prescribed in SSc, with significant between-countries and within-country differences. A gradual decrease in their utilization has been observed.
 BACKGROUND AND OBJECTIVES: Neural antibodies are detected by tissue-based indirect immunofluorescence assay (IFA) in Mayo Clinic's Neuroimmunology Laboratory practice, but the process of characterizing and validating novel antibodies is lengthy. We report our assessment of human protein arrays. METHODS: Assessment of arrays (81% human proteome coverage) was undertaken using diverse known positive samples (17 serum and 14 CSF). Samples from patients with novel neural antibodies were reflexed from IFA to arrays. Confirmatory assays were cell-based (CBA) or line blot. Epitope mapping was undertaken using phage display immunoprecipitation sequencing (PhiPSeq). RESULTS: Control positive samples known to be reactive with linear epitopes of intracellular antigens (e.g., ANNA-1 [anti-Hu]) were readily identified by arrays in 20 of 21 samples. By contrast, 10 positive controls known to be enriched with antibodies against cell surface protein conformational epitopes (e.g., GluN1 subunit of NMDA-R) were indistinguishable from background signal. Three antibodies, previously characterized by other investigators (but unclassified in our laboratory), were unmasked in 4 patients using arrays (July-December 2022): Neurexin-3α, 1 patient; regulator of gene protein signaling (RGS)8, 1 patient; and seizure-related homolog like 2 (SEZ6L2), 2 patients. All were accompanied by previously reported phenotypes (encephalitis, 1; cerebellar ataxia, 3). Patient 1 had subacute onset of seizures and encephalopathy. Neurexin-3α ranked high in CSF (second ranked neural protein) but low in serum (660th overall). Neurexin-3α CBA was positive in both samples. Patient 2 presented with rapidly progressive cerebellar ataxia. RGS8 ranked the highest neural protein in available CSF sample by array (third overall). RGS8-specific line blot was positive. Patients 3 and 4 had rapidly progressive cerebellar ataxia. SEZ6L2 was the highest ranked neural antigen by arrays in all samples (CSF, 1, serum, 2; Patient 3, ranked 9th overall in CSF, 11th in serum; Patient 4, 6th overall in serum]). By PhIPSeq, diverse neurexin-3α epitopes (including cell surface) were detected in CSF from patient 1, but no SEZ6L2 peptides were detected for serum or CSF samples from Patient 3. DISCUSSION: Individualized autoimmune neurologic diagnoses may be accelerated using protein arrays. They are optimal for detection of intracellular antigen-reactive antibodies, though certain cell surface-directed antibodies (neurexin-3α and SEZ6L2) may also be detected.
 OBJECTIVE: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can be monophasic or relapsing, with early relapse being a feature. However, the relevance of early relapse on longer-term relapse risk is unknown. Here, we investigate whether early relapses increase longer-term relapse risk in patients with MOGAD. METHODS: A retrospective analysis of 289 adult- and pediatric-onset patients with MOGAD followed for at least 2 years in 6 specialized referral centers. "Early relapses" were defined as attacks within the first 12 months from onset, with "very early relapses" defined within 30 to 90 days from onset and "delayed early relapses" defined within 90 to 365 days. "Long-term relapses" were defined as relapses beyond 12 months. Cox regression modeling and Kaplan-Meier survival analysis were used to estimate the long-term relapse risk and rate. RESULTS: Sixty-seven patients (23.2%) had early relapses with a median number of 1 event. Univariate analysis revealed an elevated risk for long-term relapses if any "early relapses" were present (hazard ratio [HR] = 2.11, p < 0.001), whether occurring during the first 3 months (HR = 2.70, p < 0.001) or the remaining 9 months (HR = 1.88, p = 0.001), with similar results yielded in the multivariate analysis. In children with onset below aged 12 years, only delayed early relapses were associated with an increased risk of long-term relapses (HR = 2.64, p = 0.026). INTERPRETATION: The presence of very early relapses and delayed early relapses within 12 months of onset in patients with MOGAD increases the risk of long-term relapsing disease, whereas a relapse within 90 days appears not to indicate a chronic inflammatory process in young pediatric-onset disease. ANN NEUROL 2023;94:508-517.
 Neural tube defects (NTDs) are severe congenital malformations that can lead to lifelong disability. Wuzi Yanzong Pill (WYP) is an herbal formula of traditional Chinese medicine (TCM) that has been shown to have a protective effect against NTDs in a rodent model induced by all-trans retinoic acid (atRA), but the mechanism remains unclear. In this study, the neuroprotective effect and mechanism of WYP on NTDs were investigated in vivo using an atRA-induced mouse model and in vitro using cell injury model induced by atRA in Chinese hamster ovary (CHO) cells and Chinese hamster dihydrofolate reductase-deficient (CHO/dhFr) cells. Our findings suggest that WYP has an excellent preventive effect on atRA-induced NTDs in mouse embryos, which may be related to the activation of the PI3K/Akt signaling pathway, improved embryonic antioxidant capacity, and anti-apoptotic effects, and this effect is not dependent on folic acid (FA). Our results demonstrated that WYP significantly reduced the incidence of NTDs induced by atRA; increased the activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and content of glutathione (GSH); decreased the apoptosis of neural tube cells; up-regulated the expression of phosphatidylinositol 3 kinase (PI3K), phospho protein kinase B (p-Akt), nuclear factor erythroid-2 related factor (Nrf2), and b-cell lymphoma-2 (Bcl-2); and down-regulated the expression of bcl-2-associated X protein (Bax). Our in vitro studies suggested that the preventive effect of WYP on atRA-treated NTDs was independent of FA, which might be attributed to the herbal ingredients of WYP. The results suggest that WYP had an excellent prevention effect on atRA-induced NTDs mouse embryos, which may be independent of FA but related to the activation of the PI3K/Akt signaling pathway and improvement of embryonic antioxidant capacity and anti-apoptosis.
 BACKGROUND: Patients with myasthenia gravis (MG) are potentially prone for a severe COVID-19 course, but there are limited real-world data available on the risk associated with COVID-19 for patients with MG. Here, we investigate whether current immunosuppressive therapy (IST) influences the risk of SARS-CoV-2 infection and COVID-19 severity. METHODS: Data from the German myasthenia gravis registry were analyzed from May 2020 until June 2021 and included patient demographics, MG disease duration, comorbidities, current IST use, COVID-19 characteristics, and outcomes. Propensity score matching was employed to match MG patients with IST to those without, and multivariable binary logistic regression models were used to determine associations between IST with (1) symptomatic SARS-CoV-2 infection and (2) severe COVID-19 course, as measured by hospitalization or death. RESULTS: Of 1379 patients with MG, 95 (7%) patients (mean age 58 (standard deviation [SD] 18) presented with COVID-19, of which 76 (80%) received IST at time of infection. 32 patients (34%) were hospitalized due to COVID-19; a total of 11 patients (12%) died. IST was a risk factor for hospitalization or death in the group of COVID-19-affected MG patients (odds ratio [OR] 3.04, 95% confidence interval [CI] = 1.02-9.06, p = 0.046), but current IST was not associated with a higher risk for SARS-CoV-2 infection itself. DISCUSSION: In this national MG cohort study, current IST use was a risk factor for a severe disease course of COVID-19 but not for SARS-CoV-2 infection itself. These data support the consequent implementation of effective strategies to prevent COVID-19 in this high-risk group. TRIAL REGISTRATION INFORMATION: German clinical trial registry ( https://www.drks.de ), DRKS00024099, first patient enrolled: February 4th, 2019.
 BACKGROUND: Few studies have tested longitudinal associations between ultra-processed food consumption and depressive outcomes. As such, further investigation and replication are necessary. The aim of this study is to examine associations of ultra-processed food intake with elevated psychological distress as an indicator of depression after 15 years. METHOD: Data from the Melbourne Collaborative Cohort Study (MCCS) were analysed (n = 23,299). We applied the NOVA food classification system to a food frequency questionnaire (FFQ) to determine ultra-processed food intake at baseline. We categorised energy-adjusted ultra-processed food consumption into quartiles by using the distribution of the dataset. Psychological distress was measured by the ten-item Kessler Psychological Distress Scale (K10). We fitted unadjusted and adjusted logistic regression models to assess the association of ultra-processed food consumption (exposure) with elevated psychological distress (outcome and defined as K10 ≥ 20). We fitted additional logistic regression models to determine whether these associations were modified by sex, age and body mass index. RESULTS: After adjusting for sociodemographic characteristics and lifestyle and health-related behaviours, participants with the highest relative intake of ultra-processed food were at increased odds of elevated psychological distress compared to participants with the lowest intake (aOR: 1.23; 95%CI: 1.10, 1.38, p for trend = 0.001). We found no evidence for an interaction of sex, age and body mass index with ultra-processed food intake. CONCLUSION: Higher ultra-processed food intake at baseline was associated with subsequent elevated psychological distress as an indicator of depression at follow-up. Further prospective and intervention studies are necessary to identify possible underlying pathways, specify the precise attributes of ultra-processed food that confer harm, and optimise nutrition-related and public health strategies for common mental disorders.
 OBJECTIVE: Our aim was to assess the real-world effectiveness of immune checkpoint inhibitors for treatment of patients with progressive multifocal leukoencephalopathy (PML). METHODS: We conducted a multicenter survey compiling retrospective data from 79 PML patients, including 38 published cases and 41 unpublished cases, who received immune checkpoint inhibitors as add-on to standard of care. One-year follow-up data were analyzed to determine clinical outcomes and safety profile. Logistic regression was used to identify variables associated with 1-year survival. RESULTS: Predisposing conditions included hematological malignancy (n = 38, 48.1%), primary immunodeficiency (n = 14, 17.7%), human immunodeficiency virus/acquired immunodeficiency syndrome (n = 12, 15.2%), inflammatory disease (n = 8, 10.1%), neoplasm (n = 5, 6.3%), and transplantation (n = 2, 2.5%). Pembrolizumab was most commonly used (n = 53, 67.1%). One-year survival was 51.9% (41/79). PML-immune reconstitution inflammatory syndrome (IRIS) was reported in 15 of 79 patients (19%). Pretreatment expression of programmed cell death-1 on circulating T cells did not differ between survivors and nonsurvivors. Development of contrast enhancement on follow-up magnetic resonance imaging at least once during follow-up (OR = 3.16, 95% confidence interval = 1.20-8.72, p = 0.02) was associated with 1-year survival. Cerebrospinal fluid JC polyomavirus DNA load decreased significantly by 1-month follow-up in survivors compared to nonsurvivors (p < 0.0001). Thirty-two adverse events occurred among 24 of 79 patients (30.4%), and led to treatment discontinuation in 7 of 24 patients (29.1%). INTERPRETATION: In this noncontrolled retrospective study of patients with PML who were treated with immune checkpoint inhibitors, mortality remains high. Development of inflammatory features or overt PML-IRIS was commonly observed. This study highlights that use of immune checkpoint inhibitors should be strictly personalized toward characteristics of the individual PML patient. ANN NEUROL 2023;93:257-270.
 Oculomotor tasks generate a potential wealth of behavioural biomarkers for neurodegenerative diseases. Overlap between oculomotor and disease-impaired circuitry reveals the location and severity of disease processes via saccade parameters measured from eye movement tasks such as prosaccade and antisaccade. Existing studies typically examine few saccade parameters in single diseases, using multiple separate neuropsychological test scores to relate oculomotor behaviour to cognition; however, this approach produces inconsistent, ungeneralizable results and fails to consider the cognitive heterogeneity of these diseases. Comprehensive cognitive assessment and direct inter-disease comparison are crucial to accurately reveal potential saccade biomarkers. We remediate these issues by characterizing 12 behavioural parameters, selected to robustly describe saccade behaviour, derived from an interleaved prosaccade and antisaccade task in a large cross-sectional data set comprising five disease cohorts (Alzheimer's disease/mild cognitive impairment, amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease, and cerebrovascular disease; n = 391, age 40-87) and healthy controls (n = 149, age 42-87). These participants additionally completed an extensive neuropsychological test battery. We further subdivided each cohort by diagnostic subgroup (for Alzheimer's disease/mild cognitive impairment and frontotemporal dementia) or degree of cognitive impairment based on neuropsychological testing (all other cohorts). We sought to understand links between oculomotor parameters, their relationships to robust cognitive measures, and their alterations in disease. We performed a factor analysis evaluating interrelationships among the 12 oculomotor parameters and examined correlations of the four resultant factors to five neuropsychology-based cognitive domain scores. We then compared behaviour between the abovementioned disease subgroups and controls at the individual parameter level. We theorized that each underlying factor measured the integrity of a distinct task-relevant brain process. Notably, Factor 3 (voluntary saccade generation) and Factor 1 (task disengagements) significantly correlated with attention/working memory and executive function scores. Factor 3 also correlated with memory and visuospatial function scores. Factor 2 (pre-emptive global inhibition) correlated only with attention/working memory scores, and Factor 4 (saccade metrics) correlated with no cognitive domain scores. Impairment on several mostly antisaccade-related individual parameters scaled with cognitive impairment across disease cohorts, while few subgroups differed from controls on prosaccade parameters. The interleaved prosaccade and antisaccade task detects cognitive impairment, and subsets of parameters likely index disparate underlying processes related to different cognitive domains. This suggests that the task represents a sensitive paradigm that can simultaneously evaluate a variety of clinically relevant cognitive constructs in neurodegenerative and cerebrovascular diseases and could be developed into a screening tool applicable to multiple diagnoses.
 Age is a major common risk factor underlying neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Previous studies reported that chronological age correlates with differential gene expression across different brain regions. However, prior datasets have not disambiguated whether expression associations with age are due to changes in cell numbers and/or gene expression per cell. In this study, we leveraged single nucleus RNA-sequencing (snRNAseq) to examine changes in cell proportions and transcriptomes in four different brain regions, each from 12 donors aged 20-30 years (young) or 60-85 years (old). We sampled 155,192 nuclei from two cortical regions (entorhinal cortex and middle temporal gyrus) and two subcortical regions (putamen and subventricular zone) relevant to neurodegenerative diseases or the proliferative niche. We found no changes in cellular composition of different brain regions with healthy aging. Surprisingly, we did find that each brain region has a distinct aging signature, with only minor overlap in differentially associated genes across regions. Moreover, each cell type shows distinct age-associated expression changes, including loss of protein synthesis genes in cortical inhibitory neurons, axonogenesis genes in excitatory neurons and oligodendrocyte precursor cells, enhanced gliosis markers in astrocytes and disease-associated markers in microglia, and genes critical for neuron-glia communication. Importantly, we find cell type-specific enrichments of age associations with genes nominated by Alzheimer's disease and Parkinson's disease genome-wide association studies (GWAS), such as apolipoprotein E ( APOE ), and leucine-rich repeat kinase 2 ( LRRK2 ) in microglia that are independent of overall expression levels across cell types. We present this data as a new resource which highlights, first, region- and cell type-specific transcriptomic changes in healthy aging that may contribute to selective vulnerability and, second, provide context for testing GWAS-nominated disease risk genes in relevant subtypes and developing more targeted therapeutic strategies. The data is readily accessible without requirement for extensive computational support in a public website, https://brainexp-hykyffa56a-uc.a.run.app/. HIGHLIGHTS: Establishment of a single nuclei atlas of human aging in four brain regionsEach region and cell type exhibits a unique aging-associated transcriptome signatureGene expression changes occur in absence of overt cell loss and are categorically unique across cell typesNeurological disease-associated genes have age-associated expression patterns in specific cell types in the context of healthy aging.
 The scaffold protein IRS-1 is an essential node in insulin/IGF signaling. It has long been recognized that the stability of IRS-1 is dependent on its endomembrane targeting. However, how IRS-1 targets the intracellular membrane, and what type of intracellular membrane is actually targeted, remains poorly understood. Here, we found that the phase separation-mediated IRS-1 puncta attached to endoplasmic reticulum (ER). VAPB, an ER-anchored protein that mediates tethers between ER and membranes of other organelles, was identified as a direct interacting partner of IRS-1. VAPB mainly binds active IRS-1 because IGF-1 enhanced the VAPB-IRS-1 association and replacing of the nine tyrosine residues of YXXM motifs disrupted the VAPB-IRS-1 association. We further delineated that the Y745 and Y746 residues in the FFAT-like motif of IRS-1 mediated the association with VAPB. Notably, VAPB targeted IRS-1 to the ER and subsequently maintained its stability. Consistently, ablation of VAPB in mice led to downregulation of IRS-1, suppression of insulin signaling, and glucose intolerance. The amyotrophic lateral sclerosis (ALS)-derived VAPB P56S mutant also impaired IRS-1 stability by interfering with the ER-tethering of IRS-1. Our findings thus revealed a previously unappreciated condensate-membrane contact (CMC), by which VAPB stabilizes the membraneless IRS-1 signalosome through targeting it to ER membrane.
 G protein-coupled receptors (GPCR) are involved in various physiological and pathophysiological processes. Functional autoantibodies targeting GPCRs have been associated with multiple disease manifestations in this context. Here we summarize and discuss the relevant findings and concepts presented in the biennial International Meeting on autoantibodies targeting GPCRs (the 4th Symposium), held in Lübeck, Germany, 15-16 September 2022. The symposium focused on the current knowledge of these autoantibodies' role in various diseases, such as cardiovascular, renal, infectious (COVID-19), and autoimmune diseases (e.g., systemic sclerosis and systemic lupus erythematosus). Beyond their association with disease phenotypes, intense research related to the mechanistic action of these autoantibodies on immune regulation and pathogenesis has been developed, underscoring the role of autoantibodies targeting GPCRs on disease outcomes and etiopathogenesis. The observation repeatedly highlighted that autoantibodies targeting GPCRs could also be present in healthy individuals, suggesting that anti-GPCR autoantibodies play a physiologic role in modeling the course of diseases. Since numerous therapies targeting GPCRs have been developed, including small molecules and monoclonal antibodies designed for treating cancer, infections, metabolic disorders, or inflammatory conditions, anti-GPCR autoantibodies themselves can serve as therapeutic targets to reduce patients' morbidity and mortality, representing a new area for the development of novel therapeutic interventions.
 Human herpesviruses (HHVs) can establish latency and be reactivated, also are neurotropic viruses that can trigger neurological disorders. HHV-6 is a herpesvirus that is associated with neurological disorders. Studies have reported the detection of HHV-6 in patients with COVID-19 and neurological manifestations. However, specific diagnoses of the neurological disorders caused by these viruses tend to be invasive or difficult to interpret. This study aimed to establish a relationship between miRNA and neurological manifestations in patients co-infected with COVID-19 and HHV-6 and evaluate miRNAs as potential biomarkers. Serum samples from COVID-19 patients in the three cohorts were analyzed. miRNA analysis by real-time polymerase chain reaction (qPCR) revealed miRNAs associated with neuroinflammation were highly expressed in patients with neurological disorders and HHV-6 detection. When compared with the group of patients without detection of HHVs DNA and without neurological alterations, the group with detection of HHV-6 DNA and neurological alteration, displayed significant differences in the expression of mir-21, mir-146a, miR-155 and miR-let-7b (p < 0.01). Our results reinforce the involvement of miRNAs in neurological disorders and provide insights into their use as biomarkers for neurological disorders triggered by HHV-6. Furthermore, understanding the expression of miRNAs may contribute to therapeutic strategies.
 BACKGROUND: There is mounting interest in the potential efficacy of low carbohydrate and very low carbohydrate ketogenic diets in various neurological and psychiatric disorders. AIMS: To conduct a systematic review and narrative synthesis of low carbohydrate and ketogenic diets (LC/KD) in adults with mood and anxiety disorders. METHOD: MEDLINE, Embase, PsycINFO and Cochrane databases were systematically searched for articles from inception to 6 September 2022. Studies that included adults with any mood or anxiety disorder treated with a low carbohydrate or ketogenic intervention, reporting effects on mood or anxiety symptoms were eligible for inclusion. PROSPERO registration CRD42019116367. RESULTS: The search yielded 1377 articles, of which 48 were assessed for full-text eligibility. Twelve heterogeneous studies (stated as ketogenic interventions, albeit with incomplete carbohydrate reporting and measurements of ketosis; diet duration: 2 weeks to 3 years; n = 389; age range 19 to 75 years) were included in the final analysis. This included nine case reports, two cohort studies and one observational study. Data quality was variable, with no high-quality evidence identified. Efficacy, adverse effects and discontinuation rates were not systematically reported. There was some evidence for efficacy of ketogenic diets in those with bipolar disorder, schizoaffective disorder and possibly unipolar depression/anxiety. Relapse after discontinuation of the diet was reported in some individuals. CONCLUSIONS: Although there is no high-quality evidence of LC/KD efficacy in mood or anxiety disorders, several uncontrolled studies suggest possible beneficial effects. Robust studies are now needed to demonstrate efficacy, to identify clinical groups who may benefit and whether a ketogenic diet (beyond low carbohydrate) is required and to characterise adverse effects and the risk of relapse after diet discontinuation.
 We characterized the role of structural variants, a largely unexplored type of genetic variation, in two non-Alzheimer's dementias, namely Lewy body dementia (LBD) and frontotemporal dementia (FTD)/amyotrophic lateral sclerosis (ALS). To do this, we applied an advanced structural variant calling pipeline (GATK-SV) to short-read whole-genome sequence data from 5,213 European-ancestry cases and 4,132 controls. We discovered, replicated, and validated a deletion in TPCN1 as a novel risk locus for LBD and detected the known structural variants at the C9orf72 and MAPT loci as associated with FTD/ALS. We also identified rare pathogenic structural variants in both LBD and FTD/ALS. Finally, we assembled a catalog of structural variants that can be mined for new insights into the pathogenesis of these understudied forms of dementia.
 Nucleus basalis of Meynert (NbM), one of the earliest targets of Alzheimer's disease (AD), may act as a seed for pathological spreading to its connected regions. However, the underlying basis of regional vulnerability to NbM dysconnectivity remains unclear. NbM functional dysconnectivity was assessed using resting-state fMRI data of health controls and mild cognitive impairment (MCI) patients from the Alzheimer's disease Neuroimaging Initiative (ADNI2/GO phase). Transcriptional correlates of NbM dysconnectivity was explored by leveraging public intrinsic and differential post-mortem brain-wide gene expression datasets from Allen Human Brain Atlas (AHBA) and Mount Sinai Brain Bank (MSBB). By constructing an individual-level tissue-specific gene set risk score (TGRS), we evaluated the contribution of NbM dysconnectivity-correlated gene sets to change rate of cerebral spinal fluid (CSF) biomarkers during preclinical stage of AD, as well as to MCI onset age. An independent cohort of health controls and MCI patients from ADNI3 was used to validate our main findings. Between-group comparison revealed significant connectivity reduction between the right NbM and right middle temporal gyrus in MCI. This regional vulnerability to NbM dysconnectivity correlated with intrinsic expression of genes enriched in protein and immune functions, as well as with differential expression of genes enriched in cholinergic receptors, immune, vascular and energy metabolism functions. TGRS of these NbM dysconnectivity-correlated gene sets are associated with longitudinal amyloid-beta change at preclinical stages of AD, and contributed to MCI onset age independent of traditional AD risks. Our findings revealed the transcriptional vulnerability to NbM dysconnectivity and their crucial role in explaining preclinical amyloid-beta change and MCI onset age, which offer new insights into the early AD pathology and encourage more investigation and clinical trials targeting NbM.
 The aim of this study was to determine the role of endothelin-1 (ET-1), a molecule involved in multiple vascular and fibrosing abnormalities, as a biomarker of interstitial lung disease (ILD), as well as its use for the differential diagnosis between idiopathic pulmonary fibrosis (IPF) and ILD associated with autoimmune diseases (AD-ILD), using a large and well-defined cohort of patients with ILD. A total of 112 patients with IPF, 91 patients with AD-ILD (28 rheumatoid arthritis (RA), 26 systemic sclerosis, 20 idiopathic inflammatory myositis and 17 interstitial pneumonia with autoimmune features) and 44 healthy controls were included. ET-1 serum levels were determined by enzyme-linked immunosorbent assay. A significant increase in ET-1 levels was found in patients with IPF compared to controls. Likewise, AD-ILD patients also showed higher ET-1 levels than controls when the whole cohort was stratified by the type of AD. Similar ET-1 levels were found in IPF and AD-ILD patients, regardless of the underlying AD. Interestingly, increased ET-1 levels were correlated with worse lung function in IPF and RA-ILD patients. Our study supports that serum ET-1 may be useful as a biomarker of ILD, although it could not help in the differential diagnosis between IPF and AD-ILD. Moreover, ET-1 levels may be associated with ILD severity.
 BACKGROUND: Individuals with lung cancer (LC) face a variety of symptoms that significantly impact their lives. We use extensive patient input to determine the relative importance and prevalence of these symptoms and identify which demographic features are associated with a higher level of disease burden. METHODS: We performed semi-structured qualitative interviews with participants with LC to identify potentially important symptoms. We then conducted a cross-sectional study, in which participants rated the relative importance of 162 individual symptoms covering 14 symptomatic themes. Participant responses were analyzed by age, sex, disability status, disease duration, LC stage, type of treatment received, and smoking history, among other categories. RESULTS: Our cross-sectional study had 139 participants with LC. The most prevalent symptomatic themes reported by this population were fatigue (85.5%), impaired sleep and daytime sleepiness (73.5%), and emotional issues (73.0%). The symptomatic themes that had the greatest average impact (on a scale of 0 to 4, with 4 being the most impactful) were social role dissatisfaction (1.67), inability to do activities (1.64), and fatigue (1.60). Disability status had the strongest association with symptomatic theme prevalence. LC stage (stage IV), receipt of therapy, and smoking experience were also associated with higher frequency of symptomatic themes. CONCLUSIONS: Individuals with LC face diverse and disease-specific symptoms that affect their daily lives. Patient insight on the prevalence and relative importance of these symptoms is invaluable to advance meaningful therapeutic interventions.
 BACKGROUND AND OBJECTIVES: A variety of neurologic disorders have been reported as presentations or complications of coronavirus disease 2019 (COVID-19) infection. The objective of this study was to determine their incidence dynamics and long-term functional outcome. METHODS: The Neuro-COVID Italy study was a multicenter, observational, cohort study with ambispective recruitment and prospective follow-up. Consecutive hospitalized patients presenting new neurologic disorders associated with COVID-19 infection (neuro-COVID), independently from respiratory severity, were systematically screened and actively recruited by neurology specialists in 38 centers in Italy and the Republic of San Marino. The primary outcomes were incidence of neuro-COVID cases during the first 70 weeks of the pandemic (March 2020-June 2021) and long-term functional outcome at 6 months, categorized as full recovery, mild symptoms, disabling symptoms, or death. RESULTS: Among 52,759 hospitalized patients with COVID-19, 1,865 patients presenting 2,881 new neurologic disorders associated with COVID-19 infection (neuro-COVID) were recruited. The incidence of neuro-COVID cases significantly declined over time, comparing the first 3 pandemic waves (8.4%, 95% CI 7.9-8.9; 5.0%, 95% CI 4.7-5.3; 3.3%, 95% CI 3.0-3.6, respectively; p = 0.027). The most frequent neurologic disorders were acute encephalopathy (25.2%), hyposmia-hypogeusia (20.2%), acute ischemic stroke (18.4%), and cognitive impairment (13.7%). The onset of neurologic disorders was more common in the prodromic phase (44.3%) or during the acute respiratory illness (40.9%), except for cognitive impairment whose onset prevailed during recovery (48.4%). A good functional outcome was achieved by most patients with neuro-COVID (64.6%) during follow-up (median 6.7 months), and the proportion of good outcome increased throughout the study period (r = 0.29, 95% CI 0.05-0.50; p = 0.019). Mild residual symptoms were frequently reported (28.1%) while disabling symptoms were common only in stroke survivors (47.6%). DISCUSSION: Incidence of COVID-associated neurologic disorders decreased during the prevaccination phase of the pandemic. Long-term functional outcome was favorable in most neuro-COVID disorders, although mild symptoms commonly lasted more than 6 months after infection.
 BACKGROUND AND PURPOSE: The aim of this study was to assess the neurological complications of SARS-CoV-2 infection and compare phenotypes and outcomes in infected patients with and without selected neurological manifestations. METHODS: The data source was a registry established by the European Academy of Neurology during the first wave of the COVID-19 pandemic. Neurologists collected data on patients with COVID-19 seen as in- and outpatients and in emergency rooms in 23 European and seven non-European countries. Prospective and retrospective data included patient demographics, lifestyle habits, comorbidities, main COVID-19 complications, hospital and intensive care unit admissions, diagnostic tests, and outcome. Acute/subacute selected neurological manifestations in patients with COVID-19 were analysed, comparing individuals with and without each condition for several risk factors. RESULTS: By July 31, 2021, 1523 patients (758 men, 756 women, and nine intersex/unknown, aged 16-101 years) were registered. Neurological manifestations were diagnosed in 1213 infected patients (79.6%). At study entry, 978 patients (64.2%) had one or more chronic general or neurological comorbidities. Predominant acute/subacute neurological manifestations were cognitive dysfunction (N = 449, 29.5%), stroke (N = 392, 25.7%), sleep-wake disturbances (N = 250, 16.4%), dysautonomia (N = 224, 14.7%), peripheral neuropathy (N = 145, 9.5%), movement disorders (N = 142, 9.3%), ataxia (N = 134, 8.8%), and seizures (N = 126, 8.3%). These manifestations tended to differ with regard to age, general and neurological comorbidities, infection severity and non-neurological manifestations, extent of association with other acute/subacute neurological manifestations, and outcome. CONCLUSIONS: Patients with COVID-19 and neurological manifestations present with distinct phenotypes. Differences in age, general and neurological comorbidities, and infection severity characterize the various neurological manifestations of COVID-19.
 Autopsy studies have demonstrated that comorbid neurodegenerative and cerebrovascular disease occur in the great majority of subjects with Alzheimer disease dementia (ADD), and are likely to additively alter the rate of decline or severity of cognitive impairment. The most important of these are Lewy body disease (LBD), TDP-43 proteinopathy and cerebrovascular disease, including white matter rarefaction (WMR) and cerebral infarcts. Comorbidities may interfere with ADD therapeutic trials evaluation of ADD clinical trials as they may not respond to AD-specific molecular therapeutics. It is possible, however, that at least some comorbidities may be, to some degree, secondary consequences of AD pathology, and if this were true then effective AD-specific therapeutics might also reduce the extent or severity of comorbid pathology. Comorbidities in ADD caused by autosomal dominant mutations such as those in the presenilin-1 ( PSEN1 ) gene may provide an advantageous perspective on their pathogenesis, and deserve attention because these subjects are increasingly being entered into clinical trials. As ADD associated with PSEN1 mutations has a presumed single-cause etiology, and the average age at death is under 60, any comorbidities in this setting may be considered as at least partially secondary to the causative AD mechanisms rather than aging, and thus indicate whether effective ADD therapeutics may also be effective for comorbidities. In this study, we sought to compare the rates and types of ADD comorbidities between subjects with early-onset sporadic ADD (EOSADD; subjects dying under age 60) versus ADD associated with different types of PSEN1 mutations, the most common cause of early-onset autosomal dominant ADD. In particular, we were able to ascertain, for the first time, the prevalences of a fairly complete set of ADD comorbidities in United States (US) PSEN1 cases as well as the Colombian E280A PSEN1 kindred. Data for EOSADD and US PSEN1 subjects (with multiple different mutation types) was obtained from the National Alzheimer Coordinating Center (NACC). Colombian cases all had the E280A mutation and had a set of neuropathological observations classified, like the US cases according to the NACC NP10 definitions. Confirmatory of earlier reports, NACC-defined Alzheimer Disease Neuropathological Changes (ADNC) were consistently very severe in early-onset cases, whether sporadic or in PSEN1 cases, but were slightly less severe in EOSADD. Amyloid angiopathy was the only AD-associated pathology type with widely-differing severity scores between the 3 groups, with median scores of 3, 2 and 1 in the PSEN1 Colombia, PSEN1 US and EOSADD cases, respectively. Apoliprotein E genotype did not show significant proportional group differences for the possession of an E-4 or E-2 allele. Of ADD comorbidities, LBD was most common, being present in more than half of all cases in all 3 groups. For TDP-43 co-pathology, the Colombian PSEN1 group was the most affected, at about 27%, vs 16% and 11% for the US PSEN1 and sporadic US cases, respectively. Notably, hippocampal sclerosis and non-AD tau pathological conditions were not present in any of the US or Colombian PSEN1 cases, and was seen in only 3% of the EOSADD cases. Significant large-vessel atherosclerosis was present in a much larger percentage of Colombian PSEN1 cases, at almost 20% as compared to 0% and 3% of the US PSEN1 and EOSADD cases, respectively. Small-vessel disease, or arteriolosclerosis, was much more common than large vessel disease, being present in all groups between 18% and 37%. Gross and microscopic infarcts, however, as well as gross or microscopic hemorrhages, were generally absent or present at very low percentages in all groups. White matter rarefaction (WMR) was remarkably common, at almost 60%, in the US PSEN1 group, as compared to about 18% in the EOSADD cases, a significant difference. White matter rarefaction was not assessed in the Colombian PSEN1 cases. The results presented here, as well as other evidence, indicates that LBD, TDP-43 pathology and WMR, as common comorbidities with autosomal dominant and early-onset sporadic ADD, should be considered when planning clinical trials with such subjects as they may increase variability in response rates. However, they may be at least partially dependent on ADNC and thus potentially addressable by anti-amyloid or and/anti-tau therapies.
 BACKGROUND AND OBJECTIVES: To develop a valid, disease-specific, patient-reported outcome (PRO) measure for adolescents and adults with Friedreich ataxia (FA) for use in therapeutic trials. METHODS: We conducted semistructured qualitative interviews and a national cross-sectional study of individuals with FA to determine the most prevalent and burdensome symptoms and symptomatic themes to this population. These symptoms and symptomatic themes were included as questions in the first version of the Friedreich's Ataxia-Health Index (FA-HI). We subsequently used factor analysis, beta interviews with 17 individuals with FA, and test-retest reliability assessments with 20 individuals with FA to evaluate, refine, and optimize the FA-HI. Finally, we determined the capability of the FA-HI to differentiate between subgroups of FA participants with varying levels of disease severity. RESULTS: Participants with FA identified 18 symptomatic themes of importance to be included as subscales in the FA-HI. The FA-HI demonstrates high internal consistency and test-retest reliability, and it was identified by participants as highly relevant, comprehensive, and easy to complete. FA-HI total and subscale scores statistically differentiated between subgroups of participants with varying levels of disease burden. DISCUSSION: Initial evaluation of the FA-HI supports its validity and reliability as a PRO for assessing how individuals with FA feel and function.
 IMPORTANCE: Autoimmune encephalitis misdiagnosis can lead to harm. OBJECTIVE: To determine the diseases misdiagnosed as autoimmune encephalitis and potential reasons for misdiagnosis. DESIGN, SETTING, AND PARTICIPANTS: This retrospective multicenter study took place from January 1, 2014, to December 31, 2020, at autoimmune encephalitis subspecialty outpatient clinics including Mayo Clinic (n = 44), University of Oxford (n = 18), University of Texas Southwestern (n = 18), University of California, San Francisco (n = 17), University of Washington in St Louis (n = 6), and University of Utah (n = 4). Inclusion criteria were adults (age ≥18 years) with a prior autoimmune encephalitis diagnosis at a participating center or other medical facility and a subsequent alternative diagnosis at a participating center. A total of 393 patients were referred with an autoimmune encephalitis diagnosis, and of those, 286 patients with true autoimmune encephalitis were excluded. MAIN OUTCOMES AND MEASURES: Data were collected on clinical features, investigations, fulfillment of autoimmune encephalitis criteria, alternative diagnoses, potential contributors to misdiagnosis, and immunotherapy adverse reactions. RESULTS: A total of 107 patients were misdiagnosed with autoimmune encephalitis, and 77 (72%) did not fulfill diagnostic criteria for autoimmune encephalitis. The median (IQR) age was 48 (35.5-60.5) years and 65 (61%) were female. Correct diagnoses included functional neurologic disorder (27 [25%]), neurodegenerative disease (22 [20.5%]), primary psychiatric disease (19 [18%]), cognitive deficits from comorbidities (11 [10%]), cerebral neoplasm (10 [9.5%]), and other (18 [17%]). Onset was acute/subacute in 56 (52%) or insidious (>3 months) in 51 (48%). Magnetic resonance imaging of the brain was suggestive of encephalitis in 19 of 104 patients (18%) and cerebrospinal fluid (CSF) pleocytosis occurred in 16 of 84 patients (19%). Thyroid peroxidase antibodies were elevated in 24 of 62 patients (39%). Positive neural autoantibodies were more frequent in serum than CSF (48 of 105 [46%] vs 7 of 91 [8%]) and included 1 or more of GAD65 (n = 14), voltage-gated potassium channel complex (LGI1 and CASPR2 negative) (n = 10), N-methyl-d-aspartate receptor by cell-based assay only (n = 10; 6 negative in CSF), and other (n = 18). Adverse reactions from immunotherapies occurred in 17 of 84 patients (20%). Potential contributors to misdiagnosis included overinterpretation of positive serum antibodies (53 [50%]), misinterpretation of functional/psychiatric, or nonspecific cognitive dysfunction as encephalopathy (41 [38%]). CONCLUSIONS AND RELEVANCE: When evaluating for autoimmune encephalitis, a broad differential diagnosis should be considered and misdiagnosis occurs in many settings including at specialized centers. In this study, red flags suggesting alternative diagnoses included an insidious onset, positive nonspecific serum antibody, and failure to fulfill autoimmune encephalitis diagnostic criteria. Autoimmune encephalitis misdiagnosis leads to morbidity from unnecessary immunotherapies and delayed treatment of the correct diagnosis.
 INTRODUCTION: The credibility of model-based economic evaluations of Alzheimer's disease (AD) interventions is central to appropriate decision-making in a policy context. We report on the International PharmacoEconomic Collaboration on Alzheimer's Disease (IPECAD) Modeling Workshop Challenge. METHODS: Two common benchmark scenarios, for the hypothetical treatment of AD mild cognitive impairment (MCI) and mild dementia, were developed jointly by 29 participants. Model outcomes were summarized, and cross-comparisons were discussed during a structured workshop. RESULTS: A broad concordance was established among participants. Mean 10-year restricted survival and time in MCI in the control group ranged across 10 MCI models from 6.7 to 9.5 years and 3.4 to 5.6 years, respectively; and across 4 mild dementia models from 5.4 to 7.9 years (survival) and 1.5 to 4.2 years (mild dementia). DISCUSSION: The model comparison increased our understanding of methods, data used, and disease progression. We established a collaboration framework to assess cost-effectiveness outcomes, an important step toward transparent and credible AD models.
 Mitochondria are a culprit in the onset of Parkinson's disease, but their role during disease progression is unclear. Here we used Cox proportional hazards models to exam the effect of variation in the mitochondrial genome on longitudinal cognitive and motor progression over time in 4064 patients with Parkinson's disease. Mitochondrial macro-haplogroup was associated with reduced risk of cognitive disease progression in the discovery and replication population. In the combined analysis, patients with the super macro-haplogroup J, T, U# had a 41% lower risk of cognitive progression with P = 2.42 × 10-6 compared to those with macro-haplogroup H. Exploratory analysis indicated that the common mitochondrial DNA variant, m.2706A>G, was associated with slower cognitive decline with a hazard ratio of 0.68 (95% confidence interval 0.56-0.81) and P = 2.46 × 10-5. Mitochondrial haplogroups were not appreciably linked to motor progression. This initial genetic survival study of the mitochondrial genome suggests that mitochondrial haplogroups may be associated with the pace of cognitive progression in Parkinson's disease over time.
 The IMPACC cohort, composed of >1,000 hospitalized COVID-19 participants, contains five illness trajectory groups (TGs) during acute infection (first 28 days), ranging from milder (TG1-3) to more severe disease course (TG4) and death (TG5). Here, we report deep immunophenotyping, profiling of >15,000 longitudinal blood and nasal samples from 540 participants of the IMPACC cohort, using 14 distinct assays. These unbiased analyses identify cellular and molecular signatures present within 72 h of hospital admission that distinguish moderate from severe and fatal COVID-19 disease. Importantly, cellular and molecular states also distinguish participants with more severe disease that recover or stabilize within 28 days from those that progress to fatal outcomes (TG4 vs. TG5). Furthermore, our longitudinal design reveals that these biologic states display distinct temporal patterns associated with clinical outcomes. Characterizing host immune responses in relation to heterogeneity in disease course may inform clinical prognosis and opportunities for intervention.
 The global burden of neurological disorders is substantial and increasing, especially in low-resource settings. The current increased global interest in brain health and its impact on population wellbeing and economic growth, highlighted in the World Health Organization's new Intersectoral Global Action Plan on Epilepsy and other Neurological Disorders 2022-2031, presents an opportunity to rethink the delivery of neurological services. In this Perspective, we highlight the global burden of neurological disorders and propose pragmatic solutions to enhance neurological health, with an emphasis on building global synergies and fostering a 'neurological revolution' across four key pillars - surveillance, prevention, acute care and rehabilitation - termed the neurological quadrangle. Innovative strategies for achieving this transformation include the recognition and promotion of holistic, spiritual and planetary health. These strategies can be deployed through co-design and co-implementation to create equitable and inclusive access to services for the promotion, protection and recovery of neurological health in all human populations across the life course.
 Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disabling long-term condition of unknown cause. The National Institute for Health and Care Excellence (NICE) published a guideline in 2021 that highlighted the seriousness of the condition, but also recommended that graded exercise therapy (GET) should not be used and cognitive-behavioural therapy should only be used to manage symptoms and reduce distress, not to aid recovery. This U-turn in recommendations from the previous 2007 guideline is controversial.We suggest that the controversy stems from anomalies in both processing and interpretation of the evidence by the NICE committee. The committee: (1) created a new definition of CFS/ME, which 'downgraded' the certainty of trial evidence; (2) omitted data from standard trial end points used to assess efficacy; (3) discounted trial data when assessing treatment harm in favour of lower quality surveys and qualitative studies; (4) minimised the importance of fatigue as an outcome; (5) did not use accepted practices to synthesise trial evidence adequately using GRADE (Grading of Recommendations, Assessment, Development and Evaluations trial evidence); (6) interpreted GET as mandating fixed increments of change when trials defined it as collaborative, negotiated and symptom dependent; (7) deviated from NICE recommendations of rehabilitation for related conditions, such as chronic primary pain and (8) recommended an energy management approach in the absence of supportive research evidence.We conclude that the dissonance between this and the previous guideline was the result of deviating from usual scientific standards of the NICE process. The consequences of this are that patients may be denied helpful treatments and therefore risk persistent ill health and disability.
 BACKGROUND: Myotonic dystrophy type 1 results from an RNA gain-of-function mutation, in which DM1 protein kinase (DMPK) transcripts carrying expanded trinucleotide repeats exert deleterious effects. Antisense oligonucleotides (ASOs) provide a promising approach to treatment of myotonic dystrophy type 1 because they reduce toxic RNA levels. We aimed to investigate the safety of baliforsen (ISIS 598769), an ASO targeting DMPK mRNA. METHODS: In this dose-escalation phase 1/2a trial, adults aged 20-55 years with myotonic dystrophy type 1 were enrolled at seven tertiary referral centres in the USA and randomly assigned via an interactive web or phone response system to subcutaneous injections of baliforsen 100 mg, 200 mg, or 300 mg, or placebo (6:2 randomisation at each dose level), or to baliforsen 400 mg or 600 mg, or placebo (10:2 randomisation at each dose level), on days 1, 3, 5, 8, 15, 22, 29, and 36. Sponsor personnel directly involved with the trial, participants, and all study personnel were masked to treatment assignments. The primary outcome measure was safety in all participants who received at least one dose of study drug up to day 134. This trial is registered with ClinicalTrials.gov (NCT02312011), and is complete. FINDINGS: Between Dec 12, 2014, and Feb 22, 2016, 49 participants were enrolled and randomly assigned to baliforsen 100 mg (n=7, one patient not dosed), 200 mg (n=6), 300 mg (n=6), 400 mg (n=10), 600 mg (n=10), or placebo (n=10). The safety population comprised 48 participants who received at least one dose of study drug. Treatment-emergent adverse events were reported for 36 (95%) of 38 participants assigned to baliforsen and nine (90%) of ten participants assigned to placebo. Aside from injection-site reactions, common treatment-emergent adverse events were headache (baliforsen: ten [26%] of 38 participants; placebo: four [40%] of ten participants), contusion (baliforsen: seven [18%] of 38; placebo: one [10%] of ten), and nausea (baliforsen: six [16%] of 38; placebo: two [20%] of ten). Most adverse events (baliforsen: 425 [86%] of 494; placebo: 62 [85%] of 73) were mild in severity. One participant (baliforsen 600 mg) developed transient thrombocytopenia considered potentially treatment related. Baliforsen concentrations in skeletal muscle increased with dose. INTERPRETATION: Baliforsen was generally well tolerated. However, skeletal muscle drug concentrations were below levels predicted to achieve substantial target reduction. These results support the further investigation of ASOs as a therapeutic approach for myotonic dystrophy type 1, but suggest improved drug delivery to muscle is needed. FUNDING: Ionis Pharmaceuticals, Biogen.
 Institute of Neuropathology, University Hospital Münster, Münster, Germany; Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, QC, Canada. Electronic address: tanja.kuhlmann@ukmuenster.de. Multiple Sclerosis Clinical Care and Research Centre, Department of Neurosciences, Federico II University of Naples, Naples, Italy. National Multiple Sclerosis Society (USA), New York, NY, USA. Department of Neurology, Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Fleni, Department of Neurology, Buenos Aires, Argentina; Institute of Biological Chemistry and Biophysics (IQUIFIB), CONICET/UBA, Buenos Aires, Argentina. Department of Neurosciences, University of California, San Diego, CA, USA. Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Multiple Sclerosis Centre of Catalonia and Department of Neurology-Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada; Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, NIHR University College London Hospitals Biomedical Research Centre, Faculty of Brain Sciences, University College London, London, UK. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Electronic address: daniel.reich@nih.gov.
 Department of Neurosciences, University of California, San Diego, CA, USA; Pediatric Multiple Sclerosis Center, Rady Children's Hospital, San Diego, CA, USA; Department of Neurology, San Diego VA Hospital, San Diego, CA, USA. Electronic address: jgraves@health.ucsd.edu. Division of Neurology, Department of Medicine, Li Ka Shing Knowledge Institute, St Michael's Hospital, University of Toronto, Toronto, ON, Canada. Department of Neurology, Cleveland Clinic, Lou Ruvo Center for Brain Health, Las Vegas, NV, USA. Department of Neurology, Johns Hopkins University, Baltimore, MD, USA; Division of Neuroscience, IRCCS San Raffaele Scientific Institute and Vita-Salute San Raffaele University, Milan, Italy. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK. Department of Neurology and the Neuroscience Research Institute, The Ohio State University, Columbus, OH, USA.
 Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, PR China. Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, PR China. Center of Multiple Sclerosis and Related Disorders, Peking Union Medical College Hospital, Beijing, 100730, PR China. Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, PR China.
 Cleveland Clinic, Department of Neurology, Cleveland, OH 44195, USA. Cleveland Clinic, Lou Ruvo Center for Brain Health, Las Vegas, NV 89106, USA.
 Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China.
 Children's National Hospital, Washington, DC; George Washington School of Medicine and Health Sciences, Washington, DC. Children's National Hospital, Washington, DC; George Washington School of Medicine and Health Sciences, Washington, DC. Electronic address: ilkahn@childrensnational.org.
 Department of Neuroscience, Istituto Superiore di Sanità, Rome, Italy. Electronic address: francesca.aloisi@iss.it. Preventive Neurology Unit, Wolfson Institute of Preventive Medicine and Blizard Institute, Queen Mary University, London, UK. Department of Neurosciences, Mental Health and Sensory Organs, Sapienza University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli, Italy.
 Division of Neurology, Department of Medicine, St Michael's Hospital, University of Toronto, Toronto, ON, Canada; Li Ka Shing Knowledge Institute, Toronto, ON, Canada. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University London, London, UK; Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London, UK. Department of Medicine, Division of Neurology, Amiri Hospital, Sharq, Kuwait. Department NEUROFARBA, Section of Neurosciences, University of Florence, Florence, Italy; IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. UCSF Weill Institute for Neuroscience, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, Katholisches Klinikum, Ruhr University Bochum, Bochum, Germany. Multiple Sclerosis and Headache Research Institute, Santos, Brazil; Departamento de Neurologia, Universidade Metropolitana de Santos, Santos, Brazil. Department of Neurology, Partners MS Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neuroscience, Monash University, Melbourne, VIC, Australia; Department of Neurology, Alfred Health, Melbourne, VIC, Australia. Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Neurology, Neurosciences Center, AIIMS, New Delhi, India. Department of Neurology, Katholisches Klinikum, Ruhr University Bochum, Bochum, Germany. Department of Neurology-Neuroimmunology, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain. Hospices Civils de Lyon, Hôpital Neurologique Pierre Wertheimer, Service de Neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, Bron, France; Centre de Recherche en Neurosciences de Lyon, Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR 5292, Lyon, France; Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France; Eugène Devic EDMUS Foundation against multiple sclerosis, state-approved foundation, Bron, France. Department of Neurology, Katholisches Klinikum, Ruhr University Bochum, Bochum, Germany. Electronic address: kerstin.hellwig@rub.de.
 Multiple Sclerosis Center, Sant'Andrea Hospital, Rome, Italy. Department of Human Neuroscience, University Sapienza, Rome, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy. Interdepartmental Center of Research for Multiple Sclerosis and Neuro-inflammatory and Degenerative Diseases, University of Ferrara, Ferrara, Italy. Inserm U1172 LilNCog, CHU Lille, FHU Precise, University of Lille, Lille, France. Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Section of Neurology, Neurosciences Center, King Faisal Specialist Hospital and Research Center, College of Medicine, Al Faisal University, Riyadh, Kingdom of Saudi Arabia. Division of Clinical Neurosciences, University of Turku, Turku, Finland. Neurocenter of Turku University Hospital, Turku, Finland. Department of Neurology, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. Departamento de Medicina, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Madrid, Spain.
 Department of Neurology, Maxine Mesinger Multiple Sclerosis Comprehensive Care Center, 7200 Cambridge Street, Suite 9A, Houston, TX, USA. Electronic address: Carlos.Perez@bcm.edu. Department of Neurology, Maxine Mesinger Multiple Sclerosis Comprehensive Care Center, 7200 Cambridge Street, Suite 9A, Houston, TX, USA. Department of Neurology, Maxine Mesinger Multiple Sclerosis Comprehensive Care Center, 7200 Cambridge Street, Suite 9A, Houston, TX, USA.
 Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland. Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD, USA. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. aascheri@hsph.harvard.edu. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. aascheri@hsph.harvard.edu. Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA. aascheri@hsph.harvard.edu.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. NeuroRx Research, Montreal, QC, Canada. McGill University, Montreal, QC, Canada. Department of Radiology and Nuclear Medicine, Amsterdam UMC, Vrije Universiteit, Amsterdam, Netherlands. Queen Square Institute of Neurology and Centre for Medical Image Computing, University College London, London, UK. Department of Neurology, University of Maryland School of Medicine, Baltimore, MD, USA. Department of Neurology, Baltimore VA Medical Center, Baltimore, MD, USA. Department of Neurology, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium. Department of Neurology, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA. Department of Neurology, Cemcat, Hospital Vall d'Hebron, Autonomous University of Barcelona, Barcelona, Spain. Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Department of Neurology, University of Virginia, Charlottesville, VA, USA. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy.
 Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. fitzgerald@jhmi.edu. Department of Epidemiology, Johns Hopkins University, Baltimore, MD, USA. fitzgerald@jhmi.edu.
 Department of Neurology, Centre d'Esclerosi Mútiple de Catalunya (Cemcat), Barcelona, Spain. Department of Brain Sciences, UK Dementia Research Institute Centre at Imperial College London, London, UK. F. Hoffmann-La Roche, Global Access, Basel, Switzerland. PHMR Ltd, Berkley Grove, London, UK. PHMR Ltd, Berkley Grove, London, UK. F. Hoffmann-La Roche, Global Access, Basel, Switzerland. Ente Ospedaliero Cantonale (EOC), Lugano, Ticino, Switzerland. Department of Neurology, University Hospital, University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital, University of Basel, Basel, Switzerland.
 Rehabilitation Division, Centro Neurolesi "Bonino Pulejo", IRCSS, Messina, Italy. Department G.F. Ingrassia, Section of Neuroscience, University of Catania, Catania, Italy. Department G.F. Ingrassia, Section of Neuroscience, University of Catania, Catania, Italy. Department G.F. Ingrassia, Section of Neuroscience, University of Catania, Catania, Italy. Electronic address: patti@unict.it.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, 1919 W. Taylor Street, AHSB 545, Chicago, IL 60612, United States. Electronic address: psilic2@uic.edu. Department of Kinesiology and Nutrition, University of Illinois Chicago, 1919 W. Taylor Street, AHSB 545, Chicago, IL 60612, United States. Department of Psychiatry, University of Illinois Chicago, 912 S. Wood Street, MC 913, Chicago, IL 60612, United States.
 Department of Neurology, Oregon Health & Science University, Portland, OR, USA. wdanielchapman@gmail.com. College of Pharmacy, Oregon Health & Science University/Oregon State University, Portland, OR, USA. Department of Neurology, Oregon Health & Science University and VA Portland Health Care System, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA.

 Service de neurologie, Centre hospitalier universitaire François-Mitterrand Dijon Bourgogne, 2B boulevard Maréchal-de-Lattre-de-Tassigny, 21000 Dijon, France; Centre de ressources et de compétences sclérose en plaques Bourgogne-Franche-Comté, Centre hospitalier universitaire François-Mitterrand Dijon Bourgogne, 2B boulevard Maréchal-de-Lattre-de-Tassigny, 21000 Dijon, France. Electronic address: thibault.moreau@chu-dijon.fr.
 A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital. Harvard Medical School, Boston, Massachusetts, USA. A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital. Harvard Medical School, Boston, Massachusetts, USA. A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital. Ospedale Sant'Andrea, University "La Sapienza", Rome, Italy.
 Third Rock Ventures, Boston, MA, USA; Abata Therapeutics, 100 Forge Road, Suite 200, Boston, MA 02472, USA. Electronic address: rransohoff@abatatx.com.
 Department of Neurology, The Walton Centre NHS Foundation Trust, Liverpool, UK shuda@nhs.net. Clinical Neurology, John Radcliffe Hospital, Oxford, UK.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Institute of Biostatistics and Clinical Research, University of Münster, Münster, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, JGU, Mainz, Germany. Competence Network Parkinson's Disease, Central Information Office, Philipps-University Marburg, Marburg, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, München, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, JGU, Mainz, Germany. Department of Neurology, St Josef-Hospital, Ruhr-Universitat Bochum, Bochum, Germany. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Department of Neurology, St Josef-Hospital, Ruhr-Universitat Bochum, Bochum, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, München, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, JGU, Mainz, Germany. Clinic and Polyclinic for Neurology, University Hospital Leipzig, University Leipzig, UL, Leipzig, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany. Department of Neurology, Faculty of Medicine, University of Augsburg, 86156, Augsburg, Germany. Department of Neurology, University of Ulm, Ulm, Germany. Department of Neurology, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Division of Neuroimmunology, Department of Neurology, University Medicine Rostock Center of Neurology, Rostock, Germany. NeuroCure Clinical Research Center and Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, CHA, Berlin, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, UKE, Hamburg, Germany. Institute for Clinical Neuroimmunology, University Hospital und Centre for Biomedicine, Ludwig-Maximilians-University Munich, Munchen, Germany. Department of Neurology, St Josef-Hospital, Ruhr-Universitat Bochum, Bochum, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, München, Germany. Department of Neurology, Technische Universitat Munchen and Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, JGU, Mainz, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster and University of Münster, Faculty of Medicine, Munster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster and University of Münster, Faculty of Medicine, Munster, Germany jan.luenemann@ukmuenster.de.
 Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. Royal Victoria Hospital, Belfast, United Kingdom. Belfast City Hospital, Belfast, United Kingdom. Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. KTU Medical Faculty Farabi Hospital, Trabzon, Turkey. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. Dokuz Eylul University, Konak/Izmir, Turkey. Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Department of Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia. Department of Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia. Department of Neurology, The Alfred Hospital, Melbourne, Victoria, Australia. Department of Neurology, The Alfred Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, The Alfred Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. School of Medicine and Public Health, University Newcastle, Newcastle, New South Wales, Australia. Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, New South Wales, Australia. Departments of Medicine, Biomedicine, and Clinical Research, Neurologic Clinic and Policlinic, University Hospital and University of Basel, Basel, Switzerland. Medical Faculty, 19 Mayis University, Samsun, Turkey. Department of Neurology, Ghent University Hospital, Ghent, Belgium. Department of Neurology, Ghent University Hospital, Ghent, Belgium. Department of Neurology, Monash Health, Melbourne, Victoria, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Melbourne, Victoria, Australia. CISSS Chaudière-Appalache, Levis, Canada. Neuro Rive-Sud, Longueuil, Québec, Canada. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Danish Multiple Sclerosis Center, Rigshospitalet Glostrup, Copenhagen University Hospital, Denmark. Department of Neurology, Aarhus University Hospital, Aarhus, Denmark. Department of Neurology, Aarhus University Hospital, Aarhus, Denmark. Aalborg University Hospital, Denmark. The Multiple Sclerosis Clinic, Department of Neurology, Odense University Hospital, Odense C, Denmark. Department of Neurology, Esbjerg Hospital, University Hospital of Southern Denmark, Esbjerg, Denmark. Department of Regional Health Research, University of Southern Denmark, Esbjerg, Denmark. Neurological Department, Viborg Hospital, Denmark. Department of Neurology and Physiotherapy, Gødstrup Hospital, Herning, Denmark. Neurology Department Herlev Hospital, Denmark. Faculty of Health and Medical Sciences, Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, North Zealand Hospital, Hillerod, Denmark. Hospital of Southern Jutland, University of Southern Denmark, Aabenraa, Denmark. Danish Multiple Sclerosis Center, Rigshospitalet Glostrup, Copenhagen University Hospital, Denmark. South Eastern HSC Trust, Belfast, United Kingdom. Danish Multiple Sclerosis Center, Rigshospitalet Glostrup, Copenhagen University Hospital, Denmark. Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia.
 First Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. efrosink@gmail.com. Aristotle University of Thessaloniki, Thessaloniki, Greece. Aristotle University of Thessaloniki, Thessaloniki, Greece. Aristotle University of Thessaloniki, Thessaloniki, Greece. Aristotle University of Thessaloniki, Thessaloniki, Greece. Nursing School, International University of Greece, Sindos, Thessaloniki, Greece. Aristotle University of Thessaloniki, Thessaloniki, Greece.
 Laboratory of Neuromuscular & Cardiovascular Study of Motion (LANECASM), University of West Attica, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. Second Dept of Neurology, Attikon University Hospital, National & Kapodistrian University of Athens, Rimini 1, 12462, Athens, Greece. sgiannop@uoi.gr. Laboratory of Neuromuscular & Cardiovascular Study of Motion (LANECASM), University of West Attica, Athens, Greece. Department of Physiotherapy, University of West Attica, Athens, Greece.
 Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Electronic address: chrishawkes@msn.com. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Dept of Neurology, John Hunter Hospital, University Newcastle, Australia. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Department of Paediatrics (Neurology), Hospital for Sick Children, University of Toronto, Ontario, Canada.
 "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania. Department of Pediatric Neurology, "Dr. Victor Gomoiu" Children's Hospital, 022102 Bucharest, Romania. Research Institute of the University of Bucharest-ICUB, University of Bucharest, 050657 Bucharest, Romania. Department of Science and Engineering of Oxide Materials and Nanomaterials, Politehnica University of Bucharest, 011061 Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania. Department of Pediatric Neurology, "Dr. Victor Gomoiu" Children's Hospital, 022102 Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania. Department of Pediatric Neurology, "Dr. Victor Gomoiu" Children's Hospital, 022102 Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania. Department of Pediatric Neurology, "Dr. Victor Gomoiu" Children's Hospital, 022102 Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania. Department of Neurosurgery, Emergency University Hospital, 050098 Bucharest, Romania.
 Department of Epidemiology, School of Public Health, Shahroud University of Medical Sciences, Shahroud, Iran. Department of Community Medicine, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran. Department of Epidemiology and Biostatistics, Iranshahr University of Medical Sciences, Iranshahr, Iran. Ophthalmic Epidemiology Research Center, Shahroud University of Medical Sciences, Shahroud, Iran. Electronic address: aliyari@shmu.ac.ir.
 Department of Neurology, John L Trotter MS Center, Washington University in St. Louis, St. Louis, USA. brierm@wustl.edu. Department of Neurology, Medical University of South Carolina, Charleston, USA.
 Department of Health Sciences, University of Genoa, Genoa, Italy/IRCCS Ospedale Policlinico San Martino, Genova, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/National Institute for Health Research, University College London Hospitals, Biomedical Research Centre, London, UK/Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Predictive Analytics and Comparative Effectiveness (PACE) Center, Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, MA, USA. Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
 Department of Neurology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: konen.felix@mh-hannover.de. Department of Neurology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: moehn.nora@mh-hannover.de. Department of Rheumatology and Clinical Immunology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: witte.torsten@mh-hannover.de. Department of Dermatology, Allergology and Venerology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: schefzyk.matthias@mh-hannover.de. Department of Internal Medicine, Division of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, 30625 Hannover, Germany. Electronic address: wiestler.miriam@mh-hannover.de. Department of Nephrology and Hypertension, Hannover Medical School, 30625 Hannover, Germany. Electronic address: lovric.svjetlana@mh-hannover.de. University Eye Hospital, Hannover Medical School, 30625 Hannover, Germany. Electronic address: hufendiek.karsten@mh-hannover.de. Department of Neurology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: schwenkenbecher.philipp@mh-hannover.de. Department of Neurology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: suehs.kurt-wolfram@mh-hannover.de. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg 20251, Germany. Electronic address: manuel.friese@zmnh.uni-hamburg.de. Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany. Electronic address: luisa.klotz@ukmuenster.de. Department of Neurology, University Medicine Essen, Essen, Germany; Center for Translational Neuro- and Behavioral Sciences, University Hospital Essen, Essen 45147, Germany. Electronic address: refik.pul@uk-essen.de. Department of Neurology, Medical Faculty, Heinrich Heine University Dusseldorf, 40225 Dusseldorf, Germany. Electronic address: marcguenter.pawlitzki@med.uni-duesseldorf.de. Allergy and Clinical Immunology Unit, Department of Medicine, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, University of Tel Aviv, 6 Weizmann St., Tel-Aviv 6423906, Israel. Electronic address: Davidha@tlvmc.gov.il. Department of Neurology, University Medicine Essen, Essen, Germany; Center for Translational Neuro- and Behavioral Sciences, University Hospital Essen, Essen 45147, Germany. Electronic address: christoph.kleinschnitz@uk-essen.de. Department of Neurology, Medical Faculty, Heinrich Heine University Dusseldorf, 40225 Dusseldorf, Germany. Electronic address: meuth@uni-duesseldorf.de. Department of Neurology, Hannover Medical School, 30625 Hannover, Germany.. Electronic address: skripuletz.thomas@mh-hannover.de.
 Neuroscience Laboratory, Centre Hospitalier Universitaire de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, Québec City, QC G1V 4G2, Canada. Platform for Research and Analysis in Environmental Science (PRASE) and Biology Department, Faculty of Sciences - I, Lebanese University, Beirut 1003, Lebanon. Neuroscience Laboratory, Centre Hospitalier Universitaire de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, Québec City, QC G1V 4G2, Canada.
 Rouen University Hospital, Rouen, France. Electronic address: bertrand.bourre@chu-rouen.fr. Pathologies Inflammatoires du Système Nerveux, Neurologie, Department of Neurology, CRC-SEP, CHU of Grenoble-Alpes and T-RAIG (Translational Research in Autoimmunity and Inflammation Group), University of Grenoble-Alpes, Rouen, France. Toulouse University Hospital, Toulouse, France. Department of Neurology, Rothschild Foundation, Paris, France. Department of Neurology, Lille Catholic University, Lille Catholic Hospitals, Lille, France. Inserm, NEURODOL, CHU of Clermont-Ferrand, University of Clermont Auvergne, Clermont-Ferrand, France. Department of Neurology, CHU of Limoges, Limoges, France. Inserm, INM, Department of Neurology, MS Center and National Reference Center of Adult Leukodystrophies, University of Montpellier, Montpellier University Hospital, Montpellier, France.
 Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON M5B 1W8, Canada; BARLO MS Centre, St. Michael's Hospital, Toronto, ON M5B 1W8, Canada. Electronic address: kristen.krysko@mail.utoronto.ca.
 Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada; Department of Immunology, University of Toronto, Toronto, ON, Canada. Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada; Department of Immunology, University of Toronto, Toronto, ON, Canada. Department of Psychiatry, Sunnybrook Health Sciences Centre and University of Toronto, Toronto, ON, Canada. Electronic address: ant.feinstein@utoronto.ca.
 Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Health Sciences, University of Genoa, Genoa, Italy/IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department of Health Sciences, University of Genoa, Genoa, Italy. Department of Oncology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. REVAL Rehabilitation Research Center, REVAL, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium/Universitair MS Centrum, UMSC, Hasselt, Belgium. Departments of Clinical Neurosciences, Community Health Sciences, Medicine, and Radiology, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Departments of Clinical Neurosciences, Community Health Sciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Neurology, Section on Statistical Planning and Analysis, UT Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Health Research Methods, Evidence and Impact, McMaster University, Hamilton, ON, Canada. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Section on Statistical Planning and Analysis, UT Southwestern Medical Center, Dallas, TX, USA. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/National Institute for Health Research, University College London Hospitals, Biomedical Research Centre, London, UK/Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK.
 Department of Neurosciences, Istituto Superiore di Sanità, Rome, Italy. Department of Neurosciences, Istituto Superiore di Sanità, Rome, Italy. Department of Neurosciences, Istituto Superiore di Sanità, Rome, Italy. Electronic address: paola.margutti@iss.it.
 School of Mathematical Sciences, Queensland University of Technology, Brisbane, Australia. School of Mathematical Sciences, Queensland University of Technology, Brisbane, Australia. School of Biomedical Sciences, Centre for Immunology and Infection Control, Faculty of Health, Queensland University of Technology, Brisbane, Australia. School of Mathematical Sciences, Queensland University of Technology, Brisbane, Australia. adrianne.jenner@qut.edu.au.
 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; Paramedical School, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Epidemiology and Biostatistics, School of Public Health, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; Paramedical School, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran. Electronic address: Mehdi.sanayei@gmail.com. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: i_adibi@med.mui.ac.ir.
 Center of Clinical Neuroscience, Department of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany. Electronic address: tjalf.ziemssen@uniklinikum-dresden.de.
 Brenda BanwellChildren's Hospital of Philadelphia, Grace E. Loeb Chair in Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
 Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
 Department of Biochemistry, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania. Department of Internal Medicine, University of Medicine and Pharmacy of Craiova, 200638 Craiova, Romania. Laboratory of Human Genomics, University of Medicine and Pharmacy of Craiova, 200638 Craiova, Romania. Regional Center for Medical Genetics Dolj, Emergency County Hospital Craiova, 200638 Craiova, Romania. Department of Biochemistry, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania. Department of Neurology, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania. Department of Biochemistry, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
 Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Pediatrics, Division of Child Neurology, Istanbul, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Pediatrics, Division of Child Neurology, Istanbul, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Neurology, Istanbul, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Neurology, Istanbul, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Neurology, Istanbul, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Neurology, Istanbul, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Neurology, Istanbul, Turkey. Electronic address: uguruygunoglu@gmail.com.

 Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BR, Av. Dr. Arnaldo, 455 - Cerqueira César, São Paulo, SP 01246-903, Brazil. Electronic address: leonardo.pipek@fm.usp.br. Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, BR, Av. Dr. Arnaldo, 455 - Cerqueira César, São Paulo, SP 01246-903, Brazil. Faculty of Medicine of ABC, São Paulo, Brazil. Department of Neurology Hospital of Clinics, University of São Paulo, São Paulo, Brazil. Department of Neurology Hospital of Clinics, University of São Paulo, São Paulo, Brazil. Department of Neurology Hospital of Clinics, University of São Paulo, São Paulo, Brazil.
 Department of Mathematics and Computer Science, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy. Electronic address: alessia.rondinella@unicampus.it. Department of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 97, Catania, 95125, Italy. Department of Mathematics and Computer Science, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy. Department of Mathematics and Computer Science, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy. Department of Mathematics and Computer Science, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy. UOC Radiologia, ARNAS Garibaldi, P.zza S. Maria di Gesù, Catania, 95124, Italy. Centro Sclerosi Multipla, UOC Neurologia, ARNAS Garibaldi, P.zza S. Maria di Gesù, Catania, 95124, Italy. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy. Department of Mathematics and Computer Science, University of Catania, Viale Andrea Doria 6, Catania, 95125, Italy.
 Department of Urology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, PR China. Electronic address: liuqiangzhao2022@163.com. Department of Urology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, PR China. Department of Urology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, PR China. Department of Neurology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, PR China. Department of Radiology, Lanzhou University Second Hospital, Lanzhou, Gansu 730000, PR China. Department of Urology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, PR China.
 Klinik für Diagnostische und Interventionelle, Neuroradiologie, Universitätsklinikum des Saarlandes, Kirrberger Straße, 66424, Homburg-Saar, Deutschland. Armin.Bachhuber@uks.eu.
 University of Missouri - Kansas City, Kansas City, MO, USA. Children's Mercy, Kansas City, MO, USA.
 Department of Neurology, Bladin-Berkovic Comprehensive Epilepsy Program, Austin Health, Melbourne, VIC, Australia/Department of Medicine, Austin Health, The University of Melbourne, Melbourne, VIC, Australia/Melbourne Brain Centre, Melbourne, VIC, Australia. Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia/Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand/Department of Neurology, Auckland City Hospital, Auckland, New Zealand. CORe, Department of Medicine, The University of Melbourne, Melbourne, VIC, Australia. Department of Neurology, Bladin-Berkovic Comprehensive Epilepsy Program, Austin Health, Melbourne, VIC, Australia/Department of Medicine, Austin Health, The University of Melbourne, Melbourne, VIC, Australia/Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia/Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia/Department of Neurology, Alfred Health, Melbourne, VIC, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia/CORe, Department of Medicine, The University of Melbourne, Melbourne, VIC, Australia.


 Department of Research, MS Society UK, London, UK. Department of Research, MS Society UK, London, UK. Department of Research, MS Society UK, London, UK. Research Network, MS Society UK, London, UK. Research Network, MS Society UK, London, UK. Research Network, MS Society UK, London, UK/ Faculty of Medicine and Health Sciences, University of East Anglia, Norwich, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Biostatistics Unit, Department of Health Sciences, University of Genoa, Genoa, Italy/IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK/Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK.
 MS Unit, Department of Neurology, St James's Hospital, Ireland. Electronic address: SQuigley@stjames.ie. MS Unit, Department of Neurology, St James's Hospital, Ireland. Department of Neurology, St James's Hospital, Ireland. Radiology Department, St James's Hospital, Ireland. Clinical Neuroscience, School of Medicine, University College Cork, Ireland; Department of Neurology, Cork University Hospital, Ireland. MS Unit, Department of Neurology, St James's Hospital, Ireland.
 Heliodor Swiecicki University Hospital in Poznan, Poznan, Poland. Department of Neurology, Division of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, Poznan, Poland. alicjakal@yahoo.com.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. katherine.kenyon@monash.edu. Centre for Neuroscience of Speech, University of Melbourne, Melbourne, VIC, Australia. katherine.kenyon@monash.edu. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Centre for Neuroscience of Speech, University of Melbourne, Melbourne, VIC, Australia. Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia. Redenlab Inc, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Centre for Neuroscience of Speech, University of Melbourne, Melbourne, VIC, Australia. Redenlab Inc, Melbourne, VIC, Australia. Division of Translational Genomics of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research, University of Tübingen, Germany & Center for Neurology, University Hospital Tübingen, Tübingen, Germany. The Bionics Institute, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Medicine and Radiology, University of Melbourne, Parkville, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia. The Bionics Institute, Melbourne, VIC, Australia.
 Department of Neurology, Yale School of Medicine, New Haven, CT. Department of Neurology, Yale School of Medicine, New Haven, CT; Department of Pediatrics, Yale School of Medicine, New Haven, CT. Electronic address: Naila.makhani@yale.edu.
 Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Nova Scotia Health and the Departments of Psychiatry, Psychology & Neuroscience, and Medicine, Dalhousie University, Halifax, NS, Canada. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States. College of Pharmacy, University of Manitoba, Winnipeg, MB, Canada. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden. Schools of Pharmacy and Public Health & Health Systems, University of Waterloo, Waterloo, ON, Canada. Department of Medicine, University of Toronto, Toronto, ON, Canada. St. Michael's Hospital, Toronto, ON, Canada. Department of Neurology, UT Southwestern, Dallas, TX, United States. Department of Medicine (Neurology) and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC, Canada.
 Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department NEUROFARBA, University of Florence, Florence, Italy.
 Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Institute of Medical Sciences, Medical College of Rzeszow University, Rzeszow, Poland. Department of Neurology, University Hospital Sestre Milosrdnice, Zagreb, Croatia. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, School of Medicine, Technical University Munich, Munich, Germany. Clinic of Neurology, University Clinical Centre of Serbia, Belgrade, Serbia. Department of Neurology, School of Medicine, Technical University Munich, Munich, Germany; Munich Cluster for System Neurology (SyNergy), Munich, Germany. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology, University Clinical Centre Ljubljana, Ljubljana, Slovenia. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Danish Multiple Sclerosis Center, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Medical University of Lublin, Lublin, Poland. Department of Neurology, University Hospital Bucharest, Bucharest, Romania. 1st Department of Neurology, Faculty of Medicine, Comenius University and University Hospital Bratislava, Bratislava, Slovakia. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary; Department of Radiology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary; MTA-SZTE Neuroscience Research Group, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary. Electronic address: bencsik.krisztina@med.u-szeged.hu.
 Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Warren Alpert Medical School of Brown University, Women and Infants Hospital, Providence, Rhode Island. Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Warren Alpert Medical School of Brown University, Women and Infants Hospital, Providence, Rhode Island.
 Center for Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, Department of Pharmacology, University of São Paulo, Ribeirão Preto, SP, Brazil. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Ribeirão Preto, SP, Brazil. Department of Neurology, Medical Faculty, University Hospital Düsseldorf, Düsseldorf, Germany. Laboratory of Ultrastructure, Aggeu Magalhães Institute (IAM), Recife, PE, Brazil. National Institute of Science and Technology on Neuroimmunomodulation (INCT-NIM), Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.
 Peoples' Friendship University of Russia, Moscow, Russia. Peoples' Friendship University of Russia, Moscow, Russia. Peoples' Friendship University of Russia, Moscow, Russia. Moscow City Clinical Hospital 24, Moscow, Russia. Sechenov First Moscow State Medical University, Moscow, Russia. Peoples' Friendship University of Russia, Moscow, Russia. Consultative and Diagnostic Center No. 6 of the Moscow Health Department, Moscow, Russia.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: sarabagherieh20@gmail.com.
 College of Social Science, School of Psychology, University of Lincoln, Lincoln, UK. Institute of Mental Health, Nottinghamshire Healthcare NHS Foundation Trust, Nottingham, UK. Mental Health & Clinical Neurosciences, University of Nottingham, Nottingham, UK. College of Social Science, School of Psychology, University of Lincoln, Lincoln, UK. College of Social Science, School of Psychology, University of Lincoln, Lincoln, UK. Mental Health & Clinical Neurosciences, University of Nottingham, Nottingham, UK. Health Services Research, SINTEF, Trondheim, Norway.
 Liver and Transplantation Unit, Montpellier School of Medicine, 34080 Montpellier, France. Liver and Transplantation Unit, Montpellier School of Medicine, 34080 Montpellier, France.
 Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN 55905, USA. Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN 55905, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA. Department of Immunology, Mayo Clinic, Rochester, MN 55905, USA.
 Neurobiological Foundations of Cognitive Development - Neuropsy Lab, HSE University, 101000, Myasnitskaya st.-20, Moscow, Russian Federation. I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991, Trubetskaya st.-8/2, Moscow, Russian Federation. bogdanova_m_d@staff.sechenov.ru. Scientific Research and Practical Center of Pediatric Psychoneurology, Michurinskiy pr.-74, 119602, Moscow, Russian Federation. bogdanova_m_d@staff.sechenov.ru. Neurobiological Foundations of Cognitive Development - Neuropsy Lab, HSE University, 101000, Myasnitskaya st.-20, Moscow, Russian Federation. York University, 4700 Keele St, Toronto, ON, M3J 1P3, Canada.
 Department of Sport, Exercise & Rehabilitation, Northumbria University, Newcastle upon Tyne, United Kingdom. Department of Nursing, Midwifery and Health, Northumbria University, Newcastle upon Tyne, United Kingdom. Department of Sport, Exercise & Rehabilitation, Northumbria University, Newcastle upon Tyne, United Kingdom. Department of Sport, Exercise & Rehabilitation, Northumbria University, Newcastle upon Tyne, United Kingdom. School of Health and Social Care, Teesside University, Middlesbrough, United Kingdom. Department of Sport, Exercise & Rehabilitation, Northumbria University, Newcastle upon Tyne, United Kingdom.
 Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China. Department of Neurology, China-Japan Union hospital of Jilin University, Changchun city, Jilin, P.R. China.
 Monash University, Melbourne, Victoria, Australia; Alfred Health, Melbourne, Victoria, Australia; Eastern Health, Melbourne, Victoria, Australia. Electronic address: yi.foong@monash.edu. Monash University, Melbourne, Victoria, Australia; Alfred Health, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia; Eastern Health, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia. Eastern Health, Melbourne, Victoria, Australia; Melbourne Health, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia; Alfred Health, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia; Alfred Health, Melbourne, Victoria, Australia.
 Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), 6431 Fannin Street MSB 7.221 Houston, TX 77030, USA. Electronic address: hossein.mousavi@uth.tmc.edu. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), 6431 Fannin Street MSB 7.221 Houston, TX 77030, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), 6431 Fannin Street MSB 7.221 Houston, TX 77030, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), 6431 Fannin Street MSB 7.221 Houston, TX 77030, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), 6431 Fannin Street MSB 7.221 Houston, TX 77030, USA.
 Department of Brain Sciences, Imperial College London, London, UK. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Brain Sciences, Imperial College London, London, UK. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Department of Brain Sciences, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. p.muraro@imperial.ac.uk.
 Department of Neuroscience, City of Health and Science University Hospital of Turin, Turin, Italy. Department of Neuroscience, City of Health and Science University Hospital of Turin, Turin, Italy.
 Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology, Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology, Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology, Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland.
 Multiple Sclerosis Research Flagship, Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Multiple Sclerosis Research Flagship, Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Multiple Sclerosis Research Flagship, Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, Tasmania, Australia. Neurology Department, Royal Hobart Hospital, Hobart, Tasmania, Australia. School of Psychological Sciences, University of Tasmania, Launceston, Tasmania, Australia. Multiple Sclerosis Research Flagship, Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia.
 Department of Neurology, Erasmus Medical Center, Sophia Children's Hospital, Rotterdam, the Netherlands. Electronic address: r.neuteboom@erasmusmc.nl.
 From the Comprehensive Clinical Trials Unit at UCL (E.B.), Institute of Clinical Trials and Methodology, University College London, United Kingdom; Department of Applied Health Research (R.M.H.), Institute of Epidemiology and Health Care, University College London, United Kingdom. From the Comprehensive Clinical Trials Unit at UCL (E.B.), Institute of Clinical Trials and Methodology, University College London, United Kingdom; Department of Applied Health Research (R.M.H.), Institute of Epidemiology and Health Care, University College London, United Kingdom. r.hunter@ucl.ac.uk.
 Department of Pediatrics, Division of Neurology, Nationwide Children's Hospital, Columbus, OH, USA. Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. William G. Lowrie Department of Chemical and Biomolecular Engineering, The Ohio State University, Columbus, OH, USA. Department of Pediatrics, Division of Neurology, Nationwide Children's Hospital, Columbus, OH, USA. Electronic address: Setty.Magana@nationwidechildrens.org.
 School of Medicine, Isfahan University of Medical Sciences, Hezar Jerib St., Isfahan 8174673461, Iran. Students' Scientific Research Center, Exceptional Talents Development Center, Tehran University of Medical Sciences, Keshavarz Blvrd, Vesal Shirazi St., Tehran 1417613151, Iran. School of Medicine, Hormozgan University of Medical Sciences Chamran Blvrd., Hormozgan 7919693116, Bandar Abbass, Iran. School of Medicine, Shiraz University of Medical Sciences, Fars, Zand St., Shiraz 7134814336, Iran. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Hezar Jerib St., Isfahan 8174673461, Iran. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Hezar Jerib St., Isfahan 8174673461, Iran. Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fars, Ibn Sina Sq., Fasa 7461686688, Iran. Department of Immunology, School of Medicine, Kashan University of Medical Sciences, Ravandi Blvrd, Isfahan, Kashan 8715988141, Iran. Student's Research Committee, Pharmaceutical Sciences Branch, Islamic Azad University, Yakhchal St., Tehran 193951498, Iran. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Hezar Jerib St., Isfahan 8174673461, Iran. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Hezar Jerib St., Isfahan 8174673461, Iran.
 Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, University College London, London, UK. z.mendelsohn@ucl.ac.uk. Department of Medical Physics and Bioengineering, Centre for Medical Image Computing (CMIC), University College London, London, UK. z.mendelsohn@ucl.ac.uk. Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, University College London, London, UK. z.mendelsohn@ucl.ac.uk. Department of Neuroradiology, Charité School of Medicine and University Hospital Berlin, Berlin, Germany. z.mendelsohn@ucl.ac.uk. Department of Radiology, Charité School of Medicine and University Hospital Berlin, Berlin, Germany. z.mendelsohn@ucl.ac.uk. Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Medical Physics and Bioengineering, Centre for Medical Image Computing (CMIC), University College London, London, UK. GE Healthcare, Amersham, UK. Stepping Hill Hospital, NHS Foundation Trust, Stockport, UK. Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Medical Physics and Bioengineering, Centre for Medical Image Computing (CMIC), University College London, London, UK. Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, University College London, London, UK. Department of Medical Physics and Bioengineering, Centre for Medical Image Computing (CMIC), University College London, London, UK. Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, University College London, London, UK. E-Health Centre, Universitat Oberta de Catalunya, Barcelona, Spain. Department of Neuroradiology, Charité School of Medicine and University Hospital Berlin, Berlin, Germany. Department of Radiology, Charité School of Medicine and University Hospital Berlin, Berlin, Germany. Berlin Institute of Health at Charité - Universitätsmedizin Berlin, BIH Biomedical Innovation Academy, BIH Charité Digital Clinician Scientist Program, Berlin, Germany. Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Medical Physics and Bioengineering, Centre for Medical Image Computing (CMIC), University College London, London, UK. Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, University College London, London, UK. Radiology & Nuclear Medicine, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam, The Netherlands.
 Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran. Department of Biology, University College of Nabi Akram, Tabriz, Iran. Department of Medical Genetics, School of Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran. Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
 Department of Neurology, Pyhrn-Eisenwurzen Hospital Steyr, Steyr, Austria; Medical Faculty, Johannes Kepler University Linz, Linz, Austria. Electronic address: michael.guger@ooeg.at. Medical Faculty, Johannes Kepler University Linz, Linz, Austria; Clinic for Neurology 2, Med Campus III, Kepler University Hospital, Linz, Austria. Medical Faculty, Johannes Kepler University Linz, Linz, Austria; Department of Neuroradiology, Neuromed Campus, Kepler University Hospital GmbH, Linz, Austria. Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria. Medical Faculty, Johannes Kepler University Linz, Linz, Austria; Department of Neuropathology, Neuromed Campus, Kepler University Hospital, Linz, Austria. Department of Neurology and Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Graz, Graz, Austria.
 McGovern Medical School, University of Texas, Houston, TX. Blanton Eye Institute, Houston Methodist Hospital, Houston, TX. Blanton Eye Institute, Houston Methodist Hospital, Houston, TX. Blanton Eye Institute, Houston Methodist Hospital, Houston, TX. Blanton Eye Institute, Houston Methodist Hospital, Houston, TX; Weill Cornell Medicine, New York, NY; University of Texas Medical Branch, Galveston, TX; University of Texas MD Anderson Cancer Center, Houston, TX; Texas A&M College of Medicine, Bryan, TX; University of Iowa Hospitals and Clinics, Iowa City, IA. Electronic address: aglee@houstonmethodist.org.
 Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
 Sleep Disorders Center, Division of Neuroscience, San Raffaele Scientific Institute, Via Stamira d'Ancona 20, 20127, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Clinical Neurophysiology Research Unit, Oasi Research Institute-IRCCS, Troina, Italy. Department of Surgery and Medical-Surgical Specialties, University of Catania, Catania, Italy. Department of Developmental and Social Psychology, Sapienza University, Rome, Italy. University of California San Francisco, Fresno, CA, USA. Sleep Research Centre, Department of Neurology IC, Oasi Research Institute - IRCCS, Troina, Italy. Sleep Disorders Center, Division of Neuroscience, San Raffaele Scientific Institute, Via Stamira d'Ancona 20, 20127, Milan, Italy. ferinistrambi.luigi@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. ferinistrambi.luigi@hsr.it.
 Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540136 Targu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540136 Targu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540136 Targu Mures, Romania. Doctoral School, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, Romania. Center for Advanced Medical and Pharmaceutical Research, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540136 Targu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540136 Targu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540136 Targu Mures, Romania. Doctoral School, 'George Emil Palade' University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, Romania.
 Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Department of Neurology, University Hospital of Wales, Cardiff, UK. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
 Department of Experimental Psychology, Heinrich Heine University, Düsseldorf, Germany. COGITO Centre for Applied Neurocognition and Neuropsychological Research, Life Science Centre, Düsseldorf, Germany. Department of Experimental Psychology, Heinrich Heine University, Düsseldorf, Germany. Department of Neurology, University of Cologne, Cologne, Germany. Institute of Neuroscience and Medicine (INM-3), Research Centre, Cognitive Neuroscience, Jülich, Germany. Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin (CBF), Charité Universitätsmedizin Berlin, Berlin, Germany. Medical Department, Section Psychosomatics, Charité Universitätsmedizin Berlin, Berlin, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology, University Medical Center, Hamburg-Eppendorf, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany. iris-katharina.penner@insel.ch. COGITO Centre for Applied Neurocognition and Neuropsychological Research, Life Science Centre, Düsseldorf, Germany. iris-katharina.penner@insel.ch. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. iris-katharina.penner@insel.ch.
 Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada. Department of Neurology, The Ohio State University, Columbus. Mellen Center for Multiple Sclerosis, Department of Neurology, Cleveland Clinic, Cleveland, Ohio.
 Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Radiology, New York University Langone Medical Center, 660 First Ave, New York, NY, 10016, USA. Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. katharina.eikermann-haerter@nyulangone.org. Department of Radiology, New York University Langone Medical Center, 660 First Ave, New York, NY, 10016, USA. katharina.eikermann-haerter@nyulangone.org.
 Department of Neurology, The Central Hospital of Shaoyang, Shaoyang, Hunan, China. Department of Clinical Medicine, Xiangnan University, Chenzhou, Hunan, China. Department of Neurology, The Central Hospital of Shaoyang, Shaoyang, Hunan, China. Department of Neurology, The Central Hospital of Shaoyang, Shaoyang, Hunan, China. Department of Neurology, The Central Hospital of Shaoyang, Shaoyang, Hunan, China.
 NEUROFARBA Department, University of Florence, Florence, Italy. NEUROFARBA Department, University of Florence, Florence, Italy. NEUROFARBA Department, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy.
 Department of Neurology, Wollongong Hospital, Wollongong, New South Wales, Australia. Research Central, Wollongong Hospital, Wollongong, New South Wales, Australia. Department of Neurology, Wollongong Hospital, Wollongong, New South Wales, Australia.
 Multiple Sclerosis Unit. Neurology Department, Hospital Universitario 12 de Octubre, Madrid, Spain. Electronic address: anagmlp@gmail.com. Multiple Sclerosis Unit. Neurology Department, Hospital Universitario 12 de Octubre, Madrid, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain; Department of Medicine, Universidad Complutense, Madrid, Spain. Multiple Sclerosis Unit. Neurology Department, Hospital Universitario 12 de Octubre, Madrid, Spain. Multiple Sclerosis Unit. Neurology Department, Hospital Universitario 12 de Octubre, Madrid, Spain. Multiple Sclerosis Unit. Neurology Department, Hospital Universitario 12 de Octubre, Madrid, Spain.
 From the Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark. koch-henriksen@stofanet.dk.
 German Academy for Transplantation Medicine, Munich, Germany. land.w.damps@gmail.com. Laboratoire d'ImmunoRhumatologie Moléculaire, INSERM U1109, FHU OMICARE, ITI TRANSPLANTEX NG, Faculté de Médecine, Université de Strasbourg, Strasbourg, France. land.w.damps@gmail.com.
 Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Address: via Is Guadazzonis 2, Cagliari 09126, Italy. Electronic address: lorena.lorefice@hotmail.it. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Address: via Is Guadazzonis 2, Cagliari 09126, Italy. Department of Neurosciences, ARNAS Brotzu, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Address: via Is Guadazzonis 2, Cagliari 09126, Italy.
 Faculty of Health Sciences, University of Burgundy, F-21000 Dijon, France. Faculty of Health Sciences, University of Burgundy, F-21000 Dijon, France. Department of Biochemistry, University Hospital of Dijon, F-21000 Dijon, France. INSERM U1231, 3 Bd Lattre de Tassigny, F-21000 Dijon, France.
 Department of Biostatistics, School of Health, Kermanshah University of Medical Sciences, Kermanshah, Iran. Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. Student Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Anatomical Sciences, Medical School, Baqiyatallah University of Medical Sciences, Tehran, Iran. Department of Computer Engineering, Sharif University of Technology, Tehran, Iran. Department of Neurology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Biology, Faculty of Science, University Putra Malaysia, Serdang, Selangor, Malaysia. Cellular and Molecular Research Center, Gerash University of Medical Sciences, Gerash, Iran. Masoud.mohammadi1989@yahoo.com.
 Pakistan Institute of Medical sciences, Islamabad. Aga Khan University, Karachi, Pakistan.
 Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal,. Electronic address: moura.neuro@chporto.min-saude.pt. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal,; Unit of Multidisciplinary Research in Biomedicine, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal; Laboratory for Integrative and Translational Research in Population Health) (ITR), Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal,; Unit of Multidisciplinary Research in Biomedicine, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal; Laboratory for Integrative and Translational Research in Population Health) (ITR), Porto, Portugal. Department of Neurology, Hospital de Santo António, Centro Hospitalar Universitário do Porto, Porto, Portugal,; Unit of Multidisciplinary Research in Biomedicine, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal; Laboratory for Integrative and Translational Research in Population Health) (ITR), Porto, Portugal.
 Academic Clinical Neurology, School of Medicine, University of Nottingham, Nottingham, UK. Department of Neurology, Nottingham University Hospitals National Health Service Trust, Queen's Medical Centre, Nottingham, UK. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
 Minimally Invasive Surgery Research Center, Iran University of Medical Sciences, Tehran, Iran. Taunton and Somerset Foundation Trust, Taunton, UK. Bariatric and Metabolic Surgery Unit, Ospedale Evangelico Betania, Naples, Italy. Division of Minimally Invasive and Bariatric Surgery, Department of Surgery, Minimally Invasive Surgery Research Center, Rasool-E Akram Hospital, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. mkermansaravi@yahoo.com. Center of Excellence of European Branch of International Federation for Surgery of Obesity, Hazrat-e Rasool Hospital, Tehran, Iran. mkermansaravi@yahoo.com.
 Department of Maternal Infantile and Urological Sciences, Sapienza University of Rome, 00161 Rome, Italy. Department of Maternal Infantile and Urological Sciences, Sapienza University of Rome, 00161 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Neurology Unit, Medicine Department, San Filippo Neri Hospital, 00135 Rome, Italy. Gynecologic Oncology Unit, Department of Experimental Clinical Oncology, IRCCS "Regina Elena" National Cancer Institute, 00144 Rome, Italy. Obstetrics and Gynecology, Saint Camillus International University of Health and Medical Sciences, 00131 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Anesthesiology, Critical Care Medicine and Pain Therapy, Sapienza University of Rome, 00185 Rome, Italy. Department of Experimental Clinical Oncology, Anesthesia, Resuscitation, and Intensive Care Unit IRCCS "Regina Elena" National Cancer Institute, 00144 Rome, Italy. Department of Maternal Infantile and Urological Sciences, Sapienza University of Rome, 00161 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy.
 Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada. robert.simpson@uhn.ca. University of Glasgow, Glasgow, UK. robert.simpson@uhn.ca. Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada. Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada. Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada. University of Glasgow, Glasgow, UK. Glasgow Caledonian University, Glasgow, UK. Glasgow Caledonian University, Glasgow, UK. University of Edinburgh, Edinburgh, UK. Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada. Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada.
 Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. michela.ponzio@aism.it. Department of Public Health, Experimental and Forensic Medicine, Unit of Biostatistics and Clinical Epidemiology, University of Pavia, Pavia, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Public Health, Experimental and Forensic Medicine, Unit of Biostatistics and Clinical Epidemiology, University of Pavia, Pavia, Italy. Department of Medical, Oral and Biotechnological Sciences, Laboratory of Biostatistics, University ''G. d'Annunzio'' Chieti-Pescara, Chieti, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society, Genoa, Italy. Legal Medicine Unit, IRCCS Mondino Foundation, Pavia, Italy. Department of Public Health, Experimental and Forensic Medicine, Forensic Science Unit, University of Pavia, Pavia, Italy. Department of Public Health, Experimental and Forensic Medicine, Unit of Biostatistics and Clinical Epidemiology, University of Pavia, Pavia, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy.
 Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. djakimovski@bnac.net. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. djakimovski@bnac.net.
 Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China.
 Department of Neurology, Aneurin Bevan University Health Board, Newport, UK katharineharding@doctors.org.uk. Neurology Department, Swansea Bay University Health Board, Swansea, UK. Helen Durham Centre for Neuroinflammatory Disease, Cardiff and Vale University Health Board, Cardiff, UK. Institute of Psychological Medicine and Neurology, Cardiff University, Cardiff, UK. Department of Neurology, Aneurin Bevan University Health Board, Newport, UK. Helen Durham Centre for Neuroinflammatory Disease, Cardiff and Vale University Health Board, Cardiff, UK. Helen Durham Centre for Neuroinflammatory Disease, Cardiff and Vale University Health Board, Cardiff, UK. Helen Durham Centre for Neuroinflammatory Disease, Cardiff and Vale University Health Board, Cardiff, UK. Institute of Psychological Medicine and Neurology, Cardiff University, Cardiff, UK. Institute of Advanced Biomedical Technologies (ITAB), Department of Neuroscience and Imaging and Clinical Sciences, Multiple Sclerosis Center, Neurological Clinic, SS Annunziata Hospital, Università degli Studi Gabriele d'Annunzio Chieti Pescara, Chieti, Italy. Neurology Department, Swansea Bay University Health Board, Swansea, UK. Helen Durham Centre for Neuroinflammatory Disease, Cardiff and Vale University Health Board, Cardiff, UK. Institute of Psychological Medicine and Neurology, Cardiff University, Cardiff, UK.
 Neuropsychiatric Department, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt. Neuropsychiatric Department, Faculty of Medicine, Aswan University Hospital, Aswan, Egypt. Neuropsychiatric Department, Faculty of Medicine, South Valley University, Qena University Hospital, Qena, Egypt. Neuropsychiatric Department, Faculty of Medicine, South Valley University, Qena University Hospital, Qena, Egypt. Neuropsychiatric Department, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt. Doaa_Mokhtar@med.aun.edu.eg. Neuropsychiatric Department, Faculty of Medicine, South Valley University, Qena University Hospital, Qena, Egypt.
 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Department of Neurology, Sheba Medical Center, Ramat Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Arrow Project for Medical Research Education, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Radiology Department, Sheba Medical Center, Ramat-Gan, Israel. School of Public Health, University of Haifa, Haifa, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Arrow Project for Medical Research Education, Sheba Medical Center, Ramat-Gan, Israel.
 From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. kaarina.kowalec@gmail.com. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston. From the College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology & Biostatistics (K.K., A.H., S.H., Y.L.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (K.C.F.), Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology (A.S.), UT Southwestern, Dallas, TX; Department of Internal Medicine (C.D., C.N.B., R.A.M.), Department of Psychiatry (J.B.), and Department of Community Health Sciences (J.B., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Biostatistics (G.R.C., A.P., H.K.T.), University of Alabama at Birmingham; Department of Clinical Health Psychology (L.A.G.), and Department of Rheumatology (C.A.H.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Icahn School of Medicine at Mount Sinai (F.L.), New York, NY; Department of Clinical Neuroscience (K.A.M.), Karolinska Institutet, Stockholm, Sweden; Department of Community Health Sciences (S.B.P.), Cumming School of Medicine, University of Calgary, Alberta, Canada; and Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston.
 Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg Eppendorf, Hamburg 20246, Germany. Electronic address: heesen@uke.de. Nursing Research Unit, Institute of Social Medicine and Epidemiology, University of Lübeck, Lübeck, Germany.
 Dow University of Health Sciences, Baba-E-Urdu Road, Karachi 74200, Pakistan. Electronic address: anusha.ashkar17@dmc.duhs.edu.pk. Dow University of Health Sciences, Baba-E-Urdu Road, Karachi 74200, Pakistan. Dow University of Health Sciences, Baba-E-Urdu Road, Karachi 74200, Pakistan. Dow University of Health Sciences, Baba-E-Urdu Road, Karachi 74200, Pakistan. Dow University of Health Sciences, Baba-E-Urdu Road, Karachi 74200, Pakistan. Jinnah Sindh Medical University, Pakistan.
 University of Waterloo, Waterloo, ON, Canada. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital, University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital, University of Basel, Basel, Switzerland. Ulm University, Ulm, Germany.
 Clinical and Experimental Neuropsychology Laboratory, Faculty of Psychology, University of Geneva, Switzerland. Faculty of Medicine, University of Geneva, Switzerland. Clinical and Experimental Neuropsychology Laboratory, Faculty of Psychology, University of Geneva, Switzerland. Neurology Department, Geneva University Hospitals, Switzerland. Faculty of Medicine, University of Geneva, Switzerland. Leenaards Memory Center, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Clinical and Experimental Neuropsychology Laboratory, Faculty of Psychology, University of Geneva, Switzerland. Clinical and Experimental Neuropsychology Laboratory, Faculty of Psychology, University of Geneva, Switzerland. Neurology Department, Geneva University Hospitals, Switzerland. Faculty of Medicine, University of Geneva, Switzerland. Clinical and Experimental Neuropsychology Laboratory, Faculty of Psychology, University of Geneva, Switzerland. Neurology Department, Geneva University Hospitals, Switzerland.
 Key Laboratory of Physical Fitness and Exercise, Ministry of Education, Beijing Sport University, Beijing, China. School of Physical Education & Sports Science, South China Normal University, Guangzhou, China. Key Laboratory of Physical Fitness and Exercise, Ministry of Education, Beijing Sport University, Beijing, China. School of Sport Sciences, Beijing Sport University, Beijing, China. Department of Sports Performance, Beijing Sport University, Beijing, China. Department of Sports Performance, Beijing Sport University, Beijing, China. Key Laboratory of Physical Fitness and Exercise, Ministry of Education, Beijing Sport University, Beijing, China. sunflowerlyy@bsu.edu.cn. China Institute of Sport and Health Science, Beijing Sport University, Beijing, China. sunflowerlyy@bsu.edu.cn. Key Laboratory of Physical Fitness and Exercise, Ministry of Education, Beijing Sport University, Beijing, China. yulaikang@126.com. Department of Sports Performance, Beijing Sport University, Beijing, China. yulaikang@126.com.

 Nur Neyal Department of Radiology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Medical Genetics, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Women's Health Research Center, Mayo Clinic, Rochester, MN, USA.
 Department of Advanced Medical and Surgical Sciences, II Division of Neurology, Multiple Sclerosis Center, University of Campania "L. Vanvitelli", Naples, Italy. Novartis Farma S.P.A, Origgio, VA, Italy. Department of Neurosciences Reproductive Sciences and Odontostomatology, Multiple Sclerosis Center, Federico II University, Naples, Italy. Department of Advanced Medical and Surgical Sciences, Università Della Campania Luigi Vanvitelli, Naples, Italy. Department of Advanced Medical and Surgical Sciences, Università Della Campania Luigi Vanvitelli, Naples, Italy. Unità Operativa Complessa Neurology, Multiple Sclerosis Center, ARNAS Garibaldi, Catania, Italy. Novartis Farma S.P.A, Origgio, VA, Italy. laura.malerba@novartis.com. Multiple Sclerosis Center, "A. Cardarelli" Hospital, Naples, Italy. Department of Neurosciences Reproductive Sciences and Odontostomatology, Multiple Sclerosis Center, Federico II University, Naples, Italy. UOC of Neurology and Multiple Sclerosis Center, DAI of Diagnostic and Interventistic Radiology and Stroke, AOIP "P. Giaccone", Palermo, Italy. Novartis Farma S.P.A, Origgio, VA, Italy. Neurology and Stroke Unit, Multiple Sclerosis Center, ARNAS CIVICO, Palermo, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", Messina, Italy. Neurology and Neuromuscular Unit, Multiple Sclerosis Centre, "G. Martino" University Hospital, Messina, Italy. Neurology and Multiple Sclerosis Center, Unità Operativa Complessa (UOC), Foundation Institute "G. Giglio", Cefalù, PA, Italy.
 Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy. v.pozzilli@unicampus.it. Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy. Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy. Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy. Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy. Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy. Unit of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy. Unit of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy. Unit of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, University Campus Bio-Medico, Rome, Italy.
 Physical Education and Sports School, Soochow University, Suzhou, 215021, PR China. School of Public Health, Suzhou Medical College of Soochow University, Suzhou, 215021, PR. China. Physical Education and Sports School, Soochow University, Suzhou, 215021, PR China. Physical Education and Sports School, Soochow University, Suzhou, 215021, PR China. Physical Education and Sports School, Soochow University, Suzhou, 215021, PR China. Physical Education and Sports School, Soochow University, Suzhou, 215021, PR China. Physical Education and Sports School, Soochow University, Suzhou, 215021, PR China. Electronic address: qxzhang@suda.edu.cn. Rehabilitation Diagnosis and Treatment Center, Shanghai Yongci Rehabilitation Hospital, Shanghai, 201107, PR. China. Electronic address: shenjianzhong@shyongci.com.
 Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey; Neuromuscular Diseases Research Laboratory, Hacettepe University School of Medicine, Ankara, Turkey. Electronic address: canebru@yahoo.co.uk. Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey. Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey. Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey; Neuromuscular Diseases Research Laboratory, Hacettepe University School of Medicine, Ankara, Turkey. Department of Hematology, University of Health Sciences Diskapi Yildirim Beyazit Research and Training Hospital, Ankara, Turkey. Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey; Neuromuscular Diseases Research Laboratory, Hacettepe University School of Medicine, Ankara, Turkey. Department of Neurology, Hacettepe University School of Medicine, Ankara, Turkey; Neuromuscular Diseases Research Laboratory, Hacettepe University School of Medicine, Ankara, Turkey.
 Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois, 1011 Lausanne. Service de neuropsychologie et de neuro-réhabilitation, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois, 1011 Lausanne.
 The New York Stem Cell Foundation Research Institute, New York, NY, USA. vfossati@nyscf.org. Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, UK. Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, UK.
 Functional Neurosurgery Research Center, Shohada Tajrish Neurosurgical Comprehensive Center of Excellence, Shohada-E-Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Qods Sq., Building no 1, 4th floor, Tajrish, Tehran, Iran. Functional Neurosurgery Research Center, Shohada Tajrish Neurosurgical Comprehensive Center of Excellence, Shohada-E-Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Qods Sq., Building no 1, 4th floor, Tajrish, Tehran, Iran. Functional Neurosurgery Research Center, Shohada Tajrish Neurosurgical Comprehensive Center of Excellence, Shohada-E-Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Qods Sq., Building no 1, 4th floor, Tajrish, Tehran, Iran. drsafari.s@gmail.com. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. Functional Neurosurgery Research Center, Shohada Tajrish Neurosurgical Comprehensive Center of Excellence, Shohada-E-Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Qods Sq., Building no 1, 4th floor, Tajrish, Tehran, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.

 Clinical Neurosciences, University of Turku, Turku, Finland; Department of Neurology, Siun Sote North Karelia Central Hospital, Joensuu, Finland. Electronic address: jussi.sipila@utu.fi.
 Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada. Department of Medicine, University of Toronto, Toronto, ON, Canada. Faculty of Science, Queen's University, Kingston, ON, Canada. Faculty of Science, University of Western Ontario, London, ON, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada; Division of Neurology, St. Michael's Hospital-Unity Health Toronto, Toronto, ON, Canada. Electronic address: manav.vyas@mail.utoronto.ca.
 Barts and The London School of Medicine and Dentistry, QMUL, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Charterhouse Square, London, EC1M 6BW, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Charterhouse Square, London, EC1M 6BW, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Charterhouse Square, London, EC1M 6BW, UK. Department of Neurology, Massachusetts General Hospital and Brigham and Women's Hospital, Boston, MA, USA. Preventive Neurology Unit, Wolfson Institute of Population Health, Charterhouse Square, London, EC1M 6BW, UK. Department of Neurology, Royal London Hospital, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Charterhouse Square, London, EC1M 6BW, UK. Ruth.dobson@qmul.ac.uk. Department of Neurology, Royal London Hospital, London, UK. Ruth.dobson@qmul.ac.uk.
 School of Physics, University of Melbourne, Melbourne, VIC 3010, Australia. Department of Ophthalmology, Miguel Servet University Hospital, Zaragoza, Spain; Aragon Institute for Health Research (IIS Aragon). Miguel Servet Ophthalmology Innovation and Research Group (GIMSO), University of Zaragoza, Spain. Biomedical Engineering Group, Department of Electronics, University of Alcalá, Alcalá de Henares, Spain. Faculty of Medicine, Complutense University of Madrid, Madrid 28040, Spain. Department of Ophthalmology, Miguel Servet University Hospital, Zaragoza, Spain; Aragon Institute for Health Research (IIS Aragon). Miguel Servet Ophthalmology Innovation and Research Group (GIMSO), University of Zaragoza, Spain. Department of Ophthalmology, Miguel Servet University Hospital, Zaragoza, Spain; Aragon Institute for Health Research (IIS Aragon). Miguel Servet Ophthalmology Innovation and Research Group (GIMSO), University of Zaragoza, Spain. Biomedical Engineering Group, Department of Electronics, University of Alcalá, Alcalá de Henares, Spain. Biomedical Engineering Group, Department of Electronics, University of Alcalá, Alcalá de Henares, Spain. Department of Ophthalmology, Miguel Servet University Hospital, Zaragoza, Spain; Aragon Institute for Health Research (IIS Aragon). Miguel Servet Ophthalmology Innovation and Research Group (GIMSO), University of Zaragoza, Spain. Electronic address: egmvivax@yahoo.com.
 Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada/Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
 Amsterdam UMC, Department of Neurology, Vrije Universiteit Amsterdam, MS Centre and Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Ophthalmology, Vrije Universiteit Amsterdam, Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Neurology, Vrije Universiteit Amsterdam, MS Centre and Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Anatomy and Neurosciences, Vrije Universiteit Amsterdam, MS Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Anatomy and Neurosciences, Vrije Universiteit Amsterdam, MS Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Neurology, Vrije Universiteit Amsterdam, MS Centre and Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Ophthalmology, Vrije Universiteit Amsterdam, Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Department of Ophthalmology, Onze Lieve Vrouwe Gasthuis, 1091 AC Amsterdam, The Netherlands. Amsterdam UMC, Department of Neurology, Vrije Universiteit Amsterdam, MS Centre and Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Amsterdam UMC, Department of Ophthalmology, Vrije Universiteit Amsterdam, Neuro-ophthalmology Expertise Centre Amsterdam, Amsterdam Neuroscience, 1081 HZ Amsterdam, The Netherlands. Moorfields Eye Hospital, The National Hospital for Neurology and Neurosurgery and the Queen Square Institute of Neurology, UCL, London EC1V 2PD, UK.
 Eccles Institute of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia. ted.maddess@anu.edu.au. Eccles Institute of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia. Eccles Institute of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia. Eccles Institute of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia. Royal North Shore Hospital, Saint Leonards, New South Wales, Australia. Eccles Institute of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia. Department of Immunology and Infectious Disease, John Curtin School of Medical Research, Australian National University, Acton, ACT, Australia. National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT, Australia. Department of Neurology, The Canberra Hospital, Canberra, ACT, Australia. Australian National University Medical School, Acton, ACT, Australia.
 Departamento de Psicobiologia, Universidade Federal de São Paulo, Napoleão de Barros, 925, Vila Clementino, São Paulo, 04024-002, Brazil. Departamento de Psicobiologia, Universidade Federal de São Paulo, Napoleão de Barros, 925, Vila Clementino, São Paulo, 04024-002, Brazil. Departamento de Psicobiologia, Universidade Federal de São Paulo, Napoleão de Barros, 925, Vila Clementino, São Paulo, 04024-002, Brazil. Departamento de Psicobiologia, Universidade Federal de São Paulo, Napoleão de Barros, 925, Vila Clementino, São Paulo, 04024-002, Brazil. ml.andersen12@gmail.com.
 Department of NEUROFARBA, University of Florence, Florence, Italy. mariapia.amato@unifi.it. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. mariapia.amato@unifi.it. Department of NEUROFARBA, University of Florence, Florence, Italy.
 Gryphon Scientific, Takoma Park, Maryland, USA. Accelerated Cure Project, Waltham, Massachusetts, USA. Gryphon Scientific, Takoma Park, Maryland, USA. Gryphon Scientific, Takoma Park, Maryland, USA. Gryphon Scientific, Takoma Park, Maryland, USA. Accelerated Cure Project, Waltham, Massachusetts, USA. Accelerated Cure Project, Waltham, Massachusetts, USA. Department of Veterans Affairs Multiple Sclerosis Center of Excellence, University of Maryland School of Medicine, Baltimore, Maryland, USA.
 NMR Research Unit, Queen Square Multiple Sclerosis Centre, University College London Institute of Neurology, United Kingdom; Department of Biomedical Imaging and Image Guided Therapy, Medical University of Vienna, Austria. NMR Research Unit, Queen Square Multiple Sclerosis Centre, University College London Institute of Neurology, United Kingdom. Electronic address: karen.chung@nhs.net. Department of Neuroradiology, Medical University of Innsbruck, Austria; Neuroimaging Core Facility, Medical University of Innsbruck, Austria. NMR Research Unit, Queen Square Multiple Sclerosis Centre, University College London Institute of Neurology, United Kingdom. NMR Research Unit, Queen Square Multiple Sclerosis Centre, University College London Institute of Neurology, United Kingdom; National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, United Kingdom. NMR Research Unit, Queen Square Multiple Sclerosis Centre, University College London Institute of Neurology, United Kingdom; National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, United Kingdom. NMR Research Unit, Queen Square Multiple Sclerosis Centre, University College London Institute of Neurology, United Kingdom; National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, United Kingdom; Centre for Medical Image Computing (CMIC), Department of Medical Physics and Biomedical Engineering, University College London, United Kingdom; Department of Radiology and Nuclear Medicine, VU University Medical Centre, Amsterdam, NL, USA.
 Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy. Department of Rehabilitation, C.R.R.F. "Mons. L. Novarese", Loc. Trompone, Moncrivello, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy. Electronic address: alice.laroni@unige.it.
 Department of Neurosurgery, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China. Electronic address: 13822660137@163.com. Department of Neurosurgery, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China. Department of Neurosurgery, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Regenerative Medicine, Royan Institute for Stem Cell Technology and Biology, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Booalicina Hospital, Mazandaran University of Medical Sciences, Sari, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Iranian Center of Neurological Research, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran. Department of Neurology, School of Medicine, Neuroscience Research Center, Shahid Beheshti Hospital, Qom University of Medical Sciences, Qom, Iran. Department of Internal Medicine, School of Medicine, Shohadaye Ashayer Hospital, Lorestan, University of Medical Sciences, Khorramabad, Iran. Department of Neurology, Shahrekord University of Medical Sciences and Health Services, Shahrekord, Iran. Department of Neurology, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Qazvin University of Medical Sciences, Qazvin, Iran. Clinical Development and Research Unit of Ghaem Hospital, Gilan University of Medical Sciences, Rasht. Iran. Department of Neurology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: sh_eskandarieh@yahoo.com. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: abdorrezamoghadasi@gmail.com.
 General Hospital Zabok, Zabok, Croatia. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. ivan.adamec@yahoo.com. School of Medicine, University of Zagreb, Zagreb, Croatia. ivan.adamec@yahoo.com. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. School of Medicine, University of Zagreb, Zagreb, Croatia.
 Neurology Department, Faculty of Medicine, Cairo University, Giza, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Giza, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Giza, Egypt. Neurology Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Giza, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Giza, Egypt. amro.fouad@kasralainy.edu.eg.
 From the Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado School of Medicine, Aurora. jeffrey.bennett@cuanschutz.edu.
 From the Cognitive Neuroscience Division, Department of Neurology (V.M.L.), Columbia University Irving Medical Center. VL2337@cumc.columbia.edu.
 Institute of Bioengineering, Research Center of Biotechnology, Russian Academy of Science, 117312 Moscow, Russia. École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. I.M. Sechenov First Moscow State Medical University, 119991 Moscow, Russia. Department of Biomedical Physics, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia. The National Medical Research Center for Endocrinology, 117036 Moscow, Russia. Institute of Bioengineering, Research Center of Biotechnology, Russian Academy of Science, 117312 Moscow, Russia. Department of Biomedical Physics, Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Russia. The National Medical Research Center for Endocrinology, 117036 Moscow, Russia.
 Mellen Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio. Department of Neurology, Washington University, St Louis, Missouri.
 MS Clinic, Baghdad Teaching Hospital, Medical City Complex, Baghdad, Iraq. Department of Neurology, Nehme and Therese Multiple Sclerosis Center, American University of Beirut, Beirut, Lebanon. Department of Medicine, Neurology Section, King Hussein Medical Centre, Amman, Jordan. Al-Quds University-School of Medicine, Abu-Dis, East Jerusalem, West Bank, Palestine; Internal Medicine Department, Palestine Medical Complex, Ramallah, West Bank, Palestine. Merck Serono Middle East FZ-Ltd, Dubai, United Arab Emirates. Merck Serono Middle East FZ-Ltd, Dubai, United Arab Emirates. Merck Serono Middle East FZ-Ltd, Dubai, United Arab Emirates. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: sahraian1350@yahoo.com.
 Neurology Department, Cluj Emergency County Hospital, 400012 Cluj-Napoca, Romania; Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Neurology Department, Cluj Emergency County Hospital, 400012 Cluj-Napoca, Romania; Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Department of Pharmacology, Toxicology and Clinical Pharmacology, Faculty of Medicine, Iuliu Haţieganu University of Medicine and Pharmacy, 400349 Cluj-Napoca, Romania. Neurology Department, Cluj Emergency County Hospital, 400012 Cluj-Napoca, Romania; Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Electronic address: cristinapinzaru@yahoo.com. Department of Pharmacology, Toxicology and Clinical Pharmacology, Faculty of Medicine, Iuliu Haţieganu University of Medicine and Pharmacy, 400349 Cluj-Napoca, Romania. Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Department of Internal Medicine, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. University of the Aegean, Mytilene, Greece.
 Institute for Neuroradiology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany. Institute for Neuroradiology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany. Institute for Neuroradiology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Focus Program Translational Neuroscience and Immunotherapy, Rhine-Main Neuroscience Network, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience and Immunotherapy, Rhine-Main Neuroscience Network, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience and Immunotherapy, Rhine-Main Neuroscience Network, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, Institute of Translational Neurology, University of Münster, Münster, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Max Planck Institute of Psychiatry, Munich, Germany. Neurological Clinic, Sana Clinic Cham, Cham, Germany. Department of Neurology, University of Regensburg, Regensburg, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig Maximilian University of Munich, Munich, Germany. Department of Neurology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany. Institute for Neuroradiology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. abdorrezamoghadasi@gmail.com.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Electronic address: robmotl@uic.edu. School of Kinesiology, University of Michigan, Ann Arbor, MI, USA. Department of Health Behavior, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Department of Health Behavior, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA.
 Discipline of Physiology, School of Biomedicine, The University of Adelaide, S433, Helen Mayo South, Frome Rd, 5005, South Australia, Australia. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Via Montelungo 7, 37131 Verona, Italy. Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute (SAHMRI), PO Box 11060, Adelaide 5001, South Australia, Australia. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Via Montelungo 7, 37131 Verona, Italy. Discipline of Physiology, School of Biomedicine, The University of Adelaide, S433, Helen Mayo South, Frome Rd, 5005, South Australia, Australia. Electronic address: simran.sidhu@adelaide.edu.au.
 Department of Neurology, Bouali Hospital, Qazvin University of Medical Scineces, Qazvin, Iran. Department of Otorhinolaryngology, Qhods Hospital, Qazvin University of Medical Scineces, Qazvin, Iran. Department of Neurology, Bouali Hospital, Qazvin University of Medical Scineces, Qazvin, Iran.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. School of Electrical and Computer Engineering, University of Tehran, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: sh_eskandarieh@yahoo.com.
 Department of Advanced Biomedical Sciences, University of Naples "Federico II", Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University of Naples "Federico II", Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences and Electrical Engineering and Information Technology, University of Naples "Federico II", Naples, Italy; Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom; Department of Radiology and Nuclear Medicine, VU Medical Centre, Amsterdam, the Netherlands. Department of Molecular Medicine and Medical Biotechnology, University of Naples "Federico II", Naples, Italy; Multiple Sclerosis Unit, AOU "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University of Naples "Federico II", Naples, Italy. Electronic address: sirio.cocozza@unina.it. Department of Advanced Biomedical Sciences, University of Naples "Federico II", Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University of Naples "Federico II", Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples "Federico II", Naples, Italy. Department of Human Neurosciences, University of Rome Sapienza, Rome, Italy.
 A' Neurology Clinic, AHEPA Hospital, Aristotle University, Thessaloniki, Greece. Electronic address: ekoutsou@auth.gr.
 Department of Neurology, Hospital of Lithuanian University of Health Sciences Kauno Klinikos, 50161 Kaunas, Lithuania. Department of Neurology, Faculty of Medicine, Lithuanian University of Health Sciences, 50161 Kaunas, Lithuania. Department of Maxillofacial Surgery, Faculty of Medicine, Lithuanian University of Health Sciences, 50161 Kaunas, Lithuania. Department of Neurology, Hospital of Lithuanian University of Health Sciences Kauno Klinikos, 50161 Kaunas, Lithuania. Department of Neurology, Faculty of Medicine, Lithuanian University of Health Sciences, 50161 Kaunas, Lithuania. Department of Neurology, Hospital of Lithuanian University of Health Sciences Kauno Klinikos, 50161 Kaunas, Lithuania. Department of Neurology, Faculty of Medicine, Lithuanian University of Health Sciences, 50161 Kaunas, Lithuania.
 Division of Facial Plastic and Reconstructive Surgery, Department of Otolaryngology-Head and Neck Surgery, New York University Grossman School of Medicine, New York. Department of Neurology, New York University Grossman School of Medicine, New York. Division of Facial Plastic and Reconstructive Surgery, Department of Otolaryngology-Head and Neck Surgery, New York University Grossman School of Medicine, New York.
 Department of Neurology, University Hospital12 de Octubre, Avenida de Córdoba 41, Community of Madrid 28026, Spain. Electronic address: labiano@salud.madrid.org. Department of Neurology, University Hospital Ramón y Cajal, Universidad de Alcalá, Ramón y Cajal Institute for Health Research (IRYCIS), Spanish Network of Multiple Sclerosis (REEM), Colmenar Viejo, km 9,100, Community of Madrid 28034, Spain. Department of Neurology, University Hospital Ramón y Cajal, Universidad de Alcalá, Ramón y Cajal Institute for Health Research (IRYCIS), Spanish Network of Multiple Sclerosis (REEM), Colmenar Viejo, km 9,100, Community of Madrid 28034, Spain. Department of Neurology, University Hospital Ramón y Cajal, Universidad de Alcalá, Ramón y Cajal Institute for Health Research (IRYCIS), Spanish Network of Multiple Sclerosis (REEM), Colmenar Viejo, km 9,100, Community of Madrid 28034, Spain. Department of Neurology, University Hospital Ramón y Cajal, Universidad de Alcalá, Ramón y Cajal Institute for Health Research (IRYCIS), Spanish Network of Multiple Sclerosis (REEM), Colmenar Viejo, km 9,100, Community of Madrid 28034, Spain. Department of Neurology, University Hospital Infanta Elena, Avda. de los Reyes Católicos 21Valdemoro, Community of Madrid 28342, Spain. Department of Neurology, University Hospital Ramón y Cajal, Universidad de Alcalá, Ramón y Cajal Institute for Health Research (IRYCIS), Spanish Network of Multiple Sclerosis (REEM), Colmenar Viejo, km 9,100, Community of Madrid 28034, Spain.
 Faculty of Medicine, Masaryk University, Brno, Czech Republic; Department of Neurology, University Hospital Brno, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic; Department of Neurology, University Hospital Brno, Czech Republic. Electronic address: vlckova.eva@fnbrno.cz.
 Department of Neurology, St. Vincent's University Hospital, Dublin 4, Ireland. School of Medicine, University College Dublin, Dublin, Ireland. Neuropsychology Service, Department of Psychology, St. Vincent's University Hospital, Dublin 4, Ireland. Neuropsychology Service, Department of Psychology, St. Vincent's University Hospital, Dublin 4, Ireland. School of Psychology, University College Dublin, Dublin, Ireland. Neuropsychology Service, Department of Psychology, St. Vincent's University Hospital, Dublin 4, Ireland. Trinity Centre for Biomedical Engineering, Trinity College, The University of Dublin, Dublin 2, Ireland. Department of Neurology, St. Vincent's University Hospital, Dublin 4, Ireland. School of Medicine, University College Dublin, Dublin, Ireland. Department of Neurology, St. Vincent's University Hospital, Dublin 4, Ireland. Department of Neurology, St. Vincent's University Hospital, Dublin 4, Ireland. School of Medicine, University College Dublin, Dublin, Ireland. Trinity Centre for Biomedical Engineering, Trinity College, The University of Dublin, Dublin 2, Ireland. Neuropsychology Service, Department of Psychology, St. Vincent's University Hospital, Dublin 4, Ireland. School of Psychology, University College Dublin, Dublin, Ireland. Trinity Centre for Biomedical Engineering, Trinity College, The University of Dublin, Dublin 2, Ireland. School of Medicine, Trinity College, The University of Dublin, Dublin 2, Ireland. School of Engineering, Trinity College, The University of Dublin, Dublin 2, Ireland. Department of Neurology, St. Vincent's University Hospital, Dublin 4, Ireland. School of Medicine, University College Dublin, Dublin, Ireland.
 Department of Neurology. Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus. Department of Neurology. Department of Neurology. Department of Neurology. Department of Pathology, Italian Hospital of Buenos Aires, Buenos Aires, Argentina. Department of Neurology. Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus. Section of Neuroradiology and Magnetic Resonance Unit, Department of Radiology (IDI), Vall d'Hebron Institut de Recerca, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus. Section of Neuroradiology and Magnetic Resonance Unit, Department of Radiology (IDI), Vall d'Hebron Institut de Recerca, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 Department of Psychology, Université du Québec à Montréal, Montreal, Canada. Department of Psychology, Université du Québec à Montréal, Montreal, Canada. Department of Psychology, Université du Québec à Montréal, Montreal, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, Canada. Department of Psychology, Université du Québec à Montréal, Montreal, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, Canada.
 Department of Neurology, National Institute of Mental Health & Neurosciences, Bengaluru, India. Department of Neurology, National Institute of Mental Health & Neurosciences, Bengaluru, India. Department of Neurology, National Institute of Mental Health & Neurosciences, Bengaluru, India. Electronic address: sundernetra@yahoo.co.in.
 Advanced Technologies for Medicine and Signals Laboratory 'ATMS', National Engineering School of Sfax, Sfax University, Sfax, Tunisia. mnassribesma2@gmail.com. Advanced Technologies for Medicine and Signals Laboratory 'ATMS', National Engineering School of Sfax, Sfax University, Sfax, Tunisia. Advanced Technologies for Medicine and Signals Laboratory 'ATMS', National Engineering School of Sfax, Sfax University, Sfax, Tunisia. National School of Electronics and Communications, Sfax University, Sfax, Tunisia. Department IS, College of Computer Science, King Khalid University 'KKU', Abha, Saudi Arabia. Department of Neurology, CHU Habib Bourguiba, Sfax, Tunisia. Department of Neurology, CHU Habib Bourguiba, Sfax, Tunisia. Department of Radiology, CHU Habib Bourguiba, Sfax, Tunisia.
 Department of Gastroenterology, Sheba Medical Center, Tel HaShomer, Israel. Department of Gastroenterology, Sheba Medical Center, Tel HaShomer, Israel. Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel.
 Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Department of Biological Sciences, Kent State University, Kent, OH 44242, USA. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Department of Biological Sciences, Kent State University, Kent, OH 44242, USA. Health Sciences Library System, University of Pittsburgh, Pittsburgh, PA 15250, USA. Department of Biological Sciences, Kent State University, Kent, OH 44242, USA. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA. Electronic address: sbasu@kent.edu.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. IRCCS, Fondazione Don Carlo Gnocchi, Milan, Italy. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. djakimovski@bnac.net.
 Université de Reims Champagne-Ardenne, Laboratoire Cognition, Santé et Société (C2S), Reims, France. Department of Psychiatry, Reims University Hospital, EPSMM, Reims, France. Université de Reims Champagne-Ardenne, Laboratoire Cognition, Santé et Société (C2S), Reims, France. Université de Reims Champagne-Ardenne, Laboratoire Cognition, Santé et Société (C2S), Reims, France. Faculté des Sciences Humaines et Sociales (Institut Catholique de Lille), Groupement des hôpitaux de l'Institut Catholique de Lille - Service de Neurologie - Hôpital St Vincent de Paul, Lille, France. Faculté des Sciences Humaines et Sociales (Institut Catholique de Lille), Groupement des hôpitaux de l'Institut Catholique de Lille - Service de Neurologie - Hôpital St Vincent de Paul, Lille, France. Faculté des Sciences Humaines et Sociales (Institut Catholique de Lille), Groupement des hôpitaux de l'Institut Catholique de Lille - Service de Neurologie - Hôpital St Vincent de Paul, Lille, France.
 Department of Biomedical Molecular Biology, Ghent university, Ghent, Belgium. VIB-UGent Center for Inflammation Research, Ghent, Belgium. Department of Human Structure and Repair, Ghent University, Ghent, Belgium. Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium. Department of Environmental Health and Occupational Health, University of Pittsburgh, Pittsburgh, PA, USA. Department of Environmental Health and Occupational Health, University of Pittsburgh, Pittsburgh, PA, USA. Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan. Department of Biomedical Molecular Biology, Ghent university, Ghent, Belgium. VIB-UGent Center for Inflammation Research, Ghent, Belgium. Department of Pharmaceutical Sciences, University of Antwerp, Antwerp, Belgium. Department of Biomedical Molecular Biology, Ghent university, Ghent, Belgium. VIB-UGent Center for Inflammation Research, Ghent, Belgium. Research Unit Analytical BioGeoChemistry, Helmholtz Zentrum München, Munich, Germany. Department of Pathology, University Medical Center, Goettingen, Germany. Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan. Center for Low-temperature Plasma Sciences, Nagoya University, Furo-cho, Chikusa, Nagoya, Japan. Department of Environmental Health and Occupational Health, University of Pittsburgh, Pittsburgh, PA, USA. Children's Neuroscience Institute, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. Department of Biomedical Molecular Biology, Ghent university, Ghent, Belgium. VIB-UGent Center for Inflammation Research, Ghent, Belgium. Methusalem program, Ghent University, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent university, Ghent, Belgium. VIB-UGent Center for Inflammation Research, Ghent, Belgium. Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium. Department of Biomedical Molecular Biology, Ghent university, Ghent, Belgium. Tom.VandenBerghe@uantwerp.be. VIB-UGent Center for Inflammation Research, Ghent, Belgium. Tom.VandenBerghe@uantwerp.be. Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium. Tom.VandenBerghe@uantwerp.be.
 Department of Neurology, University of Health Sciences, Trabzon Kanuni Training and Research Hospital, Trabzon, Turkey. Electronic address: dr.nuraycan@hotmail.com. Karadeniz Technical University, School of Medicine, Trabzon, Turkey. Department of Neurology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
 Neurology Department, Hospital Universitario de Fuenlabrada, Madrid, Spain. Electronic address: rodriguezdeantonio@yahoo.es. Universidad Rey Juan Carlos, Facultad de Ciencias de la Salud, Madrid, Spain. Neurology Department, Hospital Universitario de Fuenlabrada, Madrid, Spain. Neurology Department, Hospital Clínico San Carlos, Madrid, Spain.
 Multiple Sclerosis Center, Second Department of Neurology, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Psychology, Royal Holloway, University of London, Egham, UK. Multiple Sclerosis Center, Second Department of Neurology, Aristotle University of Thessaloniki, Thessaloniki, Greece.

 Department of Internal Medicine, College of Medicine, Qassim University, KSA. rufaidhebrahim@gmail.com.
 Psychosomatic Medicine Unit, Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
 Northern General Hospital, Sheffield, UK laura.chapman38@nhs.net.
 Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. SIENA Imaging SRL, Siena, Italy. Welcome Centre for Integrative Neuroimaging (WIN), FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Australian Institute of Machine Learning (AIML), School of Computer and Mathematical Sciences, University of Adelaide, Adelaide, South Australia, Australia. South Australian Health and Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia. Welcome Centre for Integrative Neuroimaging (WIN), FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Welcome Centre for Integrative Neuroimaging (WIN), OHBA, Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. SIENA Imaging SRL, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. SIENA Imaging SRL, Siena, Italy. Anna Meyer Children's University Hospital, Florence, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. SIENA Imaging SRL, Siena, Italy.
 Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden/Centre for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden/Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Department of Neurology, CHU UCL Namur Site Godinne, Université Catholique de Louvain (UCLouvain), 1 Avenue G. Thérasse, Yvoir B-5530, Belgium. Electronic address: londonfrederic@gmail.com. Department of Neurology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Radiology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain (UCLouvain), Brussels, Belgium.
 Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
 Faculty of Medicine of the University of Porto, Al. Prof. Hernâni Monteiro, Porto 4200-319, Portugal. Electronic address: up201606005@edu.med.up.pt. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal; Department of Clinical Neurosciences and Mental Health, Faculty of Medicine of the University of Porto, Portugal; Center for Drug Discovery and Innovative Medicines (MedInUP), University of Porto, Portugal. Neuropsychological Unit, Department of Psychology, Centro Hospitalar Universitário São João, Porto, Portugal. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal; Department of Clinical Neurosciences and Mental Health, Faculty of Medicine of the University of Porto, Portugal; i3S, University of Porto, Portugal. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal; Department of Clinical Neurosciences and Mental Health, Faculty of Medicine of the University of Porto, Portugal. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal. Neurology Department, Centro Hospitalar Universitário São João, Porto, Portugal; Faculty of Health Sciences, University Fernando Pessoa, Porto, Portugal.
 Department of Public Health, Federico II University, Naples, Italy. Department of Public Health, Federico II University, Naples, Italy; Department of Primary Care and Public Health, Imperial College, London, United Kingdom; Interdepartmental Research Center on Management and Innovation in Healthcare (CIRMIS), Naples, Italy. Electronic address: raffaele.palladino@unina.it. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy; Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Regional Healthcare Society (So.Re.Sa), Naples, Italy. Regional Healthcare Society (So.Re.Sa), Naples, Italy. Innovation and Data Analitycs (So.Re.Sa), Naples, Italy. Department of Public Health, Federico II University, Naples, Italy. UOC of Forensic Medicine (ASL Toscana sud est), Arezzo, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy; Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Public Health, Federico II University, Naples, Italy; Interdepartmental Research Center on Management and Innovation in Healthcare (CIRMIS), Naples, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy; Department of Molecular Medicine and Medical Biotechnology, Federico II University, Naples, Italy.
 Department of Radiology, The Second Affiliated Hospital, Shantou University Medical College, Shantou, China. Department of Radiology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
 Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Yamanote 5-Jo 7-Chome, Nishi-Ku, Sapporo, 063-0005, Japan. niino.masaaki.tc@mail.hosp.go.jp. Department of Neurology, Graduate School of Medical Sciences, Neurological Institute, Kyushu University, Fukuoka, Japan. Department of Neurology, Osaka University Graduate School of Medicine, Suita, Japan. Department of Neurology and Neurological Science, Tokyo Medical and Dental University, Tokyo, Japan. Department of Neurology, Saitama Medical Center, Saitama Medical University, Saitama, Japan. Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan. Department of Neurology, Tokyo Women's Medical University Yachiyo Medical Center, Chiba, Japan. Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan. Department of Neurology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan. Department of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Department of Neurology, Brain Research Institute, Niigata University Medical Education Center, Niigata University School of Medicine, Niigata, Japan. Department of Neurology, Graduate School of Medical Sciences, Neurological Institute, Kyushu University, Fukuoka, Japan. Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Yamanote 5-Jo 7-Chome, Nishi-Ku, Sapporo, 063-0005, Japan. Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Yamanote 5-Jo 7-Chome, Nishi-Ku, Sapporo, 063-0005, Japan. School of Economics and Management, Kochi University of Technology, Kochi, Japan.
 Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, United States; Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, United States. Electronic address: vinicius.schoeps@ucsf.edu. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, United States. Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, United States; Department of Clinical Neurosciences, Calgary Stroke Program, University of Calgary, AB, Canada.
 Department of Ophthalmology, East Tallinn Central Hospital, Tallinn, Estonia. Department of Ophthalmology, East Tallinn Central Hospital, Tallinn, Estonia. Department of Ophthalmology, Tartu University Hospital, Tartu, Estonia. Department of Ophthalmology, East Tallinn Central Hospital, Tallinn, Estonia. Department of Ophthalmology, University Hospital Zurich, Zurich, Switzerland. Department of Neurology, Tartu University Hospital, Tartu, Estonia.
 Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Electronic address: mathias.buron@regionh.dk. Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. MS clinic Southern Denmark, Department of Neurology, University of Southern Denmark, Hospital of Southern Jutland, Denmark. Department of Neurology, Aarhus University Hospital, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Viborg Regional Hospital, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
 Neurosciences Department, Hospital Regional de Alta Especialidad Bajío. Department of Internal Medicine, Hospital Regional de Alta Especialidad Bajío. Department of Medicine and Nutrition, Universidad de Guanajuato. León, Guanajuato, Mexico.
 Section of Psychiatry, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Electronic address: giulia.menculini@unipg.it. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Psychiatry, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia Italy.
 Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Parkville, VIC, Australia. Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Parkville, VIC, Australia. Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Parkville, VIC, Australia/MS Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia. Isfahan University of Medical Sciences, Isfahan, Iran. Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey. KTU Faculty of Medicine, Farabi Hospital, Trabzon, Turkey. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Department of Neurology, Kasr Al-Ainy MS Research Unit (KAMSU), Cairo University, Cairo, Egypt. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Department of Neurology, School of Medicine, Koç University, Istanbul, Turkey. Rashid Hospital, Dubai, United Arab Emirates. Department of Neurology, King Fahad Specialist Hospital, Dammam, Saudi Arabia. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Parkville, VIC, Australia/MS Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia.
 Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States. Electronic address: christopher.cagna@rutgers.edu. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, New York, NY 10029, United States. Electronic address: ahmet.ceceli@mssm.edu. Department of Psychology, Montclair State University, 1 Normal Avenue, Montclair, NJ 07043, United States. Electronic address: sandryj@mail.montclair.edu. Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States. Electronic address: bhanji@psychology.rutgers.edu. Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States. Electronic address: etricomi@psychology.rutgers.edu. Center for Traumatic Brain Injury Research, Kessler Foundation, 120 Eagle Rock Avenue, East Hanover, NJ 07936, United States. Electronic address: edobryakova@kesslerfoundation.org.
 Serviço de Neurologia. Centro Hospitalar e Universitário de São João. Porto. Portugal. Serviço de Neurologia. Centro Hospitalar Universitário do Algarve. Faro. Portugal. Serviço de Neurologia. Centro Hospitalar Universitário de Lisboa Central. Lisboa. Portugal. Serviço de Neurologia. Hospital de Braga. Braga. Portugal. Serviço de Neurologia. Hospital Garcia de Orta. Almada. Portugal. Serviço de Neurologia. Hospital Dr. Nélio Mendonça. Funchal. Portugal. Serviço de Neurologia. Hospital de Santa Maria. Centro Hospitalar Universitário de Lisboa Norte. Lisboa. Portugal. Serviço de Neurologia. Hospital Professor Doutor Fernando Fonseca. Amadora. Portugal. Serviço de Neurologia. Centro Hospitalar Universitário do Porto. Porto. Portugal. Serviço de Neurologia. Hospital Beatriz Ângelo. Loures. Portugal. Serviço de Neurologia. Centro Hospitalar e Universitário de Coimbra. Coimbra. Portugal.
 Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy.
 Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. ltychy@sina.com. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. lymzhang70@aliyun.com.

 Sports Medicine Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Physiotherapy, School of Rehabilitation, Tehran University of Medical Sciences, Tehran, Iran. Department of Physiotherapy, School of Rehabilitation, Tehran University of Medical Sciences, Tehran, Iran. nakhostin@sina.tums.ac.ir. Research Center for War-affected People, Tehran University of Medical Sciences, #594, First floor, Taleghani Ave, Tehran, 14178, Iran. nakhostin@sina.tums.ac.ir. Sports Medicine Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Sports Medicine Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Physiotherapy, School of Rehabilitation, Tehran University of Medical Sciences, Tehran, Iran. Research Center for War-affected People, Tehran University of Medical Sciences, #594, First floor, Taleghani Ave, Tehran, 14178, Iran. Drug Design and Development Research Center, Tehran University of Medical Sciences, Tehran, Iran. Physiotherapy Clinic, Iran MS Society, Tehran, Iran. Department of Physical Therapy, Augusta University, Augusta, GA, USA.
 Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA.
 Unit of Child Neuropsychiatry, Department of Medicine, Surgery and Pharmacy, University Hospital of Sassari, University of Sassari, Viale San Pietro 42, 07100, Sassari, Italy. stefanos@uniss.it. Unit of Child Neuropsychiatry, Department of Medicine, Surgery and Pharmacy, University Hospital of Sassari, University of Sassari, Viale San Pietro 42, 07100, Sassari, Italy. Pediatric Neurology and Epileptology Unit, Pediatric Department, ARNAS Brotzu, Cagliari, Italy. Unit of Child Neuropsychiatry, Department of Medicine, Surgery and Pharmacy, University Hospital of Sassari, University of Sassari, Viale San Pietro 42, 07100, Sassari, Italy. Multiple Sclerosis Centre, Department of Medicine, Surgery and Pharmacy, University Hospital of Sassari, Sassari, Italy. Unit of Child Neuropsychiatry, Department of Medicine, Surgery and Pharmacy, University Hospital of Sassari, University of Sassari, Viale San Pietro 42, 07100, Sassari, Italy.

 Département de neurologie,; Centre de ressources et de compétences sclérose en plaques Paris-GH Pitié-Salpêtrière, Hôpital Pitié-Salpêtrière, AP-HP, 47-83 boulevard de l'Hôpital, 75013 Paris, France. Electronic address: elisabeth.maillart@aphp.fr.
 Department of Nursing, Yusuf Şerefoğlu Faculty of Health Sciences, Kilis 7 Aralık University, Kilis, Turkey (Ms Sungur); Faculty of Health Sciences, Sanko University, Gaziantep, Turkey (Dr Ovayolu); and Faculty of Medicine, Department of Internal Medicine, Department of Neurology, Gaziantep University, Gaziantep, Turkey (Dr Akçalı).
 Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Swiss Paraplegic Research, Guido A. Zäch Institute, Nottwil, Switzerland; Department of Health Sciences and Medicine, University of Lucerne, Lucerne, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, Ospedale Regionale di Lugano, EOC, Lugano, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Neuropsychology and Behavioral Neurology Unit, Division of Cognitive and Molecular Neuroscience, University of Basel, Switzerland. Swiss Multiple Sclerosis Society, Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Electronic address: viktor.vonwyl@uzh.ch.
 Department of Psychology, Ariel University, Ariel, Israel; Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, Ramat Gan, Israel. Electronic address: roya@ariel.ac.il. Department of Psychology, Ben-Gurion University of the Negev, Beer Sheva, Israel. Department of Psychology, Ariel University, Ariel, Israel. Department of Psychology, Ariel University, Ariel, Israel. Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, Ramat Gan, Israel; Incumbent of the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
 Division of Neuroimmunology, Department of Neurology, University of Campinas, Campinas, Brazil. gabrieldedeusvieira@gmail.com. Division of Neuroimmunology, Department of Neurology, University of Campinas, Campinas, Brazil. Division of Neuroimmunology, Department of Neurology, University of Campinas, Campinas, Brazil. Division of Neuroimmunology, Department of Neurology, University of Campinas, Campinas, Brazil. Division of Neuroimmunology, Department of Neurology, University of Campinas, Campinas, Brazil.
 Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Piazzale L.A. Scuro 10, Verona, 37134, Italy. alberto.gajofatto@univr.it. Unit of Neurology, Regional Multiple Sclerosis Center, Borgo Roma Hospital, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. alberto.gajofatto@univr.it. Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Piazzale L.A. Scuro 10, Verona, 37134, Italy. Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Piazzale L.A. Scuro 10, Verona, 37134, Italy. Unit of Neurology, Regional Multiple Sclerosis Center, Borgo Roma Hospital, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Piazzale L.A. Scuro 10, Verona, 37134, Italy. Unit of Neurology, Regional Multiple Sclerosis Center, Borgo Roma Hospital, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Unit of Neurology, Regional Multiple Sclerosis Center, Borgo Roma Hospital, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Unit of Neurology, Regional Multiple Sclerosis Center, Borgo Roma Hospital, Azienda Ospedaliera Universitaria Integrata, Verona, Italy.
 Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Via Pansini 5, 80131, Naples, Italy. giuseppinamiele20@gmail.com. Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Via Pansini 5, 80131, Naples, Italy. Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Via Pansini 5, 80131, Naples, Italy. Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Via Pansini 5, 80131, Naples, Italy.
 Hospital Clínico Universitario de Valladolid, Valladolid, España. Hospital Clínico Universitario de Valladolid, Valladolid, España. Hospital Clínico Universitario de Valladolid, Valladolid, España.
 Servicio de Neurología Hospital Universitario La Paz, Spain. Electronic address: eldamaselda@gmail.com. Servicio de Neurología Hospital Universitario La Paz, Spain. Servicio de Neurología Hospital Universitario La Paz, Spain. Servicio de Neurología Hospital Universitario La Paz, Spain. Servicio de Medicina Interna Hospital Universitario La Paz, Spain.
 Carolyn Ann Wilder, BSN, RN , is registered nurse, Neurosciences Division, University of California San Diego; and PhD student, Loma Linda University School of Nursing, CA.
 Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy. Divisione di Neurologia, Presidio Ospedaliero S. Francesco, ASL Numero 3 Nuoro, 08100 Nuoro, Italy. Divisione di Neurologia, Presidio Ospedaliero S. Francesco, ASL Numero 3 Nuoro, 08100 Nuoro, Italy. Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy.
 Ophthalmology Unit, Department of Medicine and Surgery, University Hospital of Parma, Italy. Ophthalmology Unit, Department of Medicine and Surgery, University Hospital of Parma, Italy. Ophthalmology Unit, Department of Medicine and Surgery, University Hospital of Parma, Italy. Child Neuropsychiatric Unit, Maternal and Child Health Department, University Hospital of Parma, Italy. Eye Clinic, University of Cagliari, Italy. RINGGOLD: 3111 Radiology Unit, University Hospital of Parma, Italy. RINGGOLD: 9370 Radiology Unit, University Hospital of Parma, Italy. RINGGOLD: 9370 Ophthalmology Unit, Department of Medicine and Surgery, University Hospital of Parma, Italy.
 Unité de Recherche Clinique - Centre Mémoire, Centre de Gérontologie Clinique RAINIER III, Centre Hospitalier Princesse Grace, Monaco 98000, Monaco. Electronic address: kevin.polet@chpg.mc. Unité de Recherche Clinique - Centre Mémoire, Centre de Gérontologie Clinique RAINIER III, Centre Hospitalier Princesse Grace, Monaco 98000, Monaco. Centre de Ressources et de Compétences SEP, CHU Nice Pasteur 2, UR2CA URRIS, Université Nice Côte d'Azur, Nice 06000, France. Centre de Ressources et de Compétences SEP, CHU Nice Pasteur 2, UR2CA URRIS, Université Nice Côte d'Azur, Nice 06000, France. Unité de Recherche Clinique - Centre Mémoire, Centre de Gérontologie Clinique RAINIER III, Centre Hospitalier Princesse Grace, Monaco 98000, Monaco; Département de Santé Publique, CHU de Nice, Université Nice Côte d'Azur, Nice 06100, France. Unité de Recherche Clinique - Centre Mémoire, Centre de Gérontologie Clinique RAINIER III, Centre Hospitalier Princesse Grace, Monaco 98000, Monaco; Association de Recherche Bibliographique pour les Neurosciences (AREBISN), 4 Boulevard de Cimiez, Nice 06100, France. Centre de Ressources et de Compétences SEP, CHU Nice Pasteur 2, UR2CA URRIS, Université Nice Côte d'Azur, Nice 06000, France. Unité de Recherche Clinique - Centre Mémoire, Centre de Gérontologie Clinique RAINIER III, Centre Hospitalier Princesse Grace, Monaco 98000, Monaco. Association de Recherche Bibliographique pour les Neurosciences (AREBISN), 4 Boulevard de Cimiez, Nice 06100, France. Centre de Ressources et de Compétences SEP, CHU Nice Pasteur 2, UR2CA URRIS, Université Nice Côte d'Azur, Nice 06000, France.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA/Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences University at Buffalo, The State University of New York, Buffalo, NY, USA. National Multiple Sclerosis Society, New York, NY, USA. NYU Langone Ambulatory Care, East Meadow. East Meadow, NY, USA. State University of New York at Stony Brook, Stony Brook, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA/Center for Biomedical Imaging at Clinical Translational Science Institute, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences University at Buffalo, The State University of New York, Buffalo, NY, USA.
 Physical and Rehabilitation Medicine Center of Bobigny, 359, avenue Paul-Vaillant-Couturier, Bobigny 93000, France. Physical and Rehabilitation Medicine Unit, University Hospital of Martinique, Fort De France 97200, Martinique. CHU de Nice Pasteur 2, Université Nice Côte d'Azur, UR2CA URRIS, Nice, France. Neurology Service, Hôpital Pierre Zobda-Quitman, Fort de France, Martinique, France. Department of Clinical Research and Innovation, University Hospital of Martinique, Fort-de-France, Martinique, France. PCCEI, Univ Montpellier, Univ Antilles, INSERM, EFS, Montpellier, France. Electronic address: jose-luis.barnay@chu-martinique.fr.
 Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH), Bethesda, MD, United States of America. Electronic address: charidimos.tsagkas@usb.ch. Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland; Medical Image Analysis Center AG, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Medical Image Analysis Center AG, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland; Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, DKD HELIOS Klinik Wiesbaden, Wiesbaden, Germany. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland; Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Reha Rheinfelden, Rheinfelden, Switzerland.
 Department of Pharmaceutical Sciences, State University of New York, Buffalo, NY 14214-8033, USA. Biotechnical and Clinical Laboratory Sciences, State University of New York, Buffalo, NY, USA. Neurology, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, State University of New York, Buffalo, NY, USA. Neurology, State University of New York, Buffalo, NY, USA; Buffalo Neuroimaging Analysis Center, State University of New York, Buffalo, NY, USA. Department of Pharmaceutical Sciences, State University of New York, Buffalo, NY 14214-8033, USA; Neurology, State University of New York, Buffalo, NY, USA. Electronic address: murali@buffalo.edu.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne 3004, Australia; Department of Neurology, Alfred Hospital, 55 Commercial Road, Melbourne 3004, Australia. Electronic address: Lucy.vivash@monash.edu.
 Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany.
 From the Departments of Neurology (L.M.-J., P.H., V.S.), and Infectious Diseases and Respiratory Medicine (H.K.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin; Berlin Institute of Health (P.H., L.M.J.), Charité-Universitätsmedizin Berlin; and private practice (K.A.), Berlin, Germany. leonie.mueller-jensen@charite.de. From the Departments of Neurology (L.M.-J., P.H., V.S.), and Infectious Diseases and Respiratory Medicine (H.K.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin; Berlin Institute of Health (P.H., L.M.J.), Charité-Universitätsmedizin Berlin; and private practice (K.A.), Berlin, Germany. From the Departments of Neurology (L.M.-J., P.H., V.S.), and Infectious Diseases and Respiratory Medicine (H.K.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin; Berlin Institute of Health (P.H., L.M.J.), Charité-Universitätsmedizin Berlin; and private practice (K.A.), Berlin, Germany. From the Departments of Neurology (L.M.-J., P.H., V.S.), and Infectious Diseases and Respiratory Medicine (H.K.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin; Berlin Institute of Health (P.H., L.M.J.), Charité-Universitätsmedizin Berlin; and private practice (K.A.), Berlin, Germany. From the Departments of Neurology (L.M.-J., P.H., V.S.), and Infectious Diseases and Respiratory Medicine (H.K.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin; Berlin Institute of Health (P.H., L.M.J.), Charité-Universitätsmedizin Berlin; and private practice (K.A.), Berlin, Germany.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurorehabilitation Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Neurophysiology Service, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy rocca.mara@hsr.it. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy.
 Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE e.a.statsenko@gmail.com daryasm@uaeu.ac.ae taleb.almansoor@uaeu.ac.ae. Medical Imaging Platform, ASPIRE Precision Medicine Research Institute Abu Dhabi, Al Ain, Abu Dhabi Emirate, UAE. Big Data Analytics Center, United Arab Emirates University, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE e.a.statsenko@gmail.com daryasm@uaeu.ac.ae taleb.almansoor@uaeu.ac.ae. Medical Imaging Platform, ASPIRE Precision Medicine Research Institute Abu Dhabi, Al Ain, Abu Dhabi Emirate, UAE. Psychology Department, College of Natural and Health Sciences, Zayed University, Abu Dhabi, Abu Dhabi Emirate, UAE. National Medical Library, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi Emirate, UAE. Library, Örebro University, Örebro, Sweden. Big Data Analytics Center, United Arab Emirates University, Al Ain, Abu Dhabi Emirate, UAE. Department of Computer Science, College of Information Technology, United Arab Emirates University, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Medical Imaging Platform, ASPIRE Precision Medicine Research Institute Abu Dhabi, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Medical Imaging Platform, ASPIRE Precision Medicine Research Institute Abu Dhabi, Al Ain, Abu Dhabi Emirate, UAE. Internal Medicine Department, Maimonides Medical Center, New York, New York, USA. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Department of Oncohematology, Minsk Scientific and Practical Center for Surgery, Transplantology and Hematology, Minsk, Belarus. Physiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Neuroscience Platform, ASPIRE Precision Medicine Research Institute Abu Dhabi, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Biomedical Engineering Department, Wayne State University, College of Engineering, Detroit, Michigan, USA. Radiology Department, Siriraj Hospital, Faculty of Medicine, Mahidol University, Bangkok, Thailand. Provost Office, United Arab Emirates University, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE e.a.statsenko@gmail.com daryasm@uaeu.ac.ae taleb.almansoor@uaeu.ac.ae. Neurology Department, Mediclinic Parkview Hospital, Dubai, Dubai Emirate, UAE. Neurology Department, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, Dubai Emirate, UAE. Internal Medicine Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Division of Neurology, Department of Medicine, Tawam Hospital, Al Ain, Abu Dhabi Emirate, UAE. Pediatrics Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi, UAE. Physiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, Abu Dhabi Emirate, UAE. Neuroscience Platform, ASPIRE Precision Medicine Research Institute Abu Dhabi, Al Ain, Abu Dhabi Emirate, UAE.
 Department of Physical Medicine and Rehabilitation, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. m.ghajarzadeh@gmail.com.
 Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden Anna.He@ki.se. Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Neuroinflammation, UCL Institute of Neurology, London, UK. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
 MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Electronic address: e.coerver@amsterdamumc.nl. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Radiology & Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Rijnstate Hospital, Department of Radiology, Arnhem, The Netherlands. MS Center Amsterdam, Radiology & Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands; Queen Square Institute of Neurology and Centre for Medical Image Computing, University College London, United Kingdom. Rijnstate Hospital, Department of Neurology, Arnhem, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands.
 Department of neurology, Strasbourg university hospital, Strasbourg, France. Electronic address: lucas.gauer@chru-strasbourg.fr. Department of neurology, Strasbourg university hospital, Strasbourg, France; Clinical investigation center 1434, Strasbourg university hospital, Strasbourg, France; Inserm 1119 biopathologie de la myéline, Strasbourg, France. Department of neurology, Besançon university hospital, Besançon, France. Department of neurology, Nancy university hospital, Nancy, France. Department of neurology, Dijon university hospital, Dijon, France. Department of neurology, Strasbourg university hospital, Strasbourg, France; Clinical investigation center 1434, Strasbourg university hospital, Strasbourg, France; Inserm 1119 biopathologie de la myéline, Strasbourg, France.
 Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. F. Hoffmann-La Roche Ltd., Basel, Switzerland. NeuroRx Research, Montreal, QC, Canada. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. NeuroRx Research, Montreal, QC, Canada. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. NeuroRx Research, Montreal, QC, Canada/Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada.
 Clinic of Neurology, University Clinical Centre Maribor, 2000 Maribor, Slovenia. Clinic of Neurology, University Clinical Centre Maribor, 2000 Maribor, Slovenia. Department of Neurology, Faculty of Medicine, University of Maribor, 2000 Maribor, Slovenia. Center for Human Molecular Genetics and Pharmacogenomics, Faculty of Medicine, University of Maribor, 2000 Maribor, Slovenia. Center for Human Molecular Genetics and Pharmacogenomics, Faculty of Medicine, University of Maribor, 2000 Maribor, Slovenia. Laboratory of Biochemistry, Molecular Biology and Genomics, Faculty of Chemistry and Chemical Engineering, University of Maribor, 2000 Maribor, Slovenia. Department for Science and Research, University Clinical Centre Maribor, 2000 Maribor, Slovenia. Center for Human Molecular Genetics and Pharmacogenomics, Faculty of Medicine, University of Maribor, 2000 Maribor, Slovenia.
 Department of Neurology, Goztepe Prof. Dr. Suleyman Yalcin Hospital, Istanbul, Turkey. Department of Audiology, Istanbul Medipol University, Istanbul, Turkey, bernamutlu094@gmail.com. Department of Audiology, Istanbul Medipol University, Istanbul, Turkey. Department of ENT, Istanbul Medipol University, Istanbul, Turkey.
 University of Alberta, Edmonton, Canada. University of Alberta, Edmonton, Canada. Women and Children's Health Research Institute, Edmonton, Canada.
 Second Department of Neurology, Faculty of Medicine, Comenius University in Bratislava, University Hospital Bratislava, Slovakia. Second Department of Neurology, Faculty of Medicine, Comenius University in Bratislava, University Hospital Bratislava, Slovakia. Department of Magnetic Resonance Imaging, Dr. Magnet Ltd., Bratislava, Slovakia. Second Department of Neurology, Faculty of Medicine, Comenius University in Bratislava, University Hospital Bratislava, Slovakia. Second Department of Neurology, Faculty of Medicine, Comenius University in Bratislava, University Hospital Bratislava, Slovakia. Centre of Experimental Medicine, Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovakia. Second Department of Neurology, Faculty of Medicine, Comenius University in Bratislava, University Hospital Bratislava, Slovakia. mmminar@gmail.com.
 From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. andrew.solomon@uvm.edu. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom. From the Department of Neurological Sciences (A.J.S.), Larner College of Medicine at the University of Vermont, Burlington; Departments of Internal Medicine and Community Health Science (R.A.M.), Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada; Department of Neurology (S.V.), Kuala Lumpur Hospital, Malaysia; Departamento de Neurologia (J.C.), Fleni, Buenos Aires; Institute of Biological Chemistry and Physical Chemistry (IQUIFIB) (J.C.), National Council for Scientific and Technical Research/University of Buenos Aires, Argentina; Department of Neurology (M.M.), Rigshospitalet, Copenhagen University Hospital, Denmark; Division of Psychological Medicine and Clinical Neuroscience (N.P.R.), Department of Neurology, Cardiff University, University Hospital of Wales, United Kingdom; Department of Neurology (D.R.S.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (D.R.S.), University Teaching Hospital, Lusaka, Zambia; McKing Consulting Corporation (W.K., L.R.), Atlanta, GA; Department of Biostatistics, Epidemiology, and Informatics (E.B., R.S.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Multiple Sclerosis International Federation (R.K., J.L.-D., A.H.), London, United Kingdom.
 Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden kelsi.smith@ki.se. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre of Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Academic Specialist Centre, Centre of Neurology, SLSO, Stockholm, Sweden. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre of Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Academic Specialist Centre, Centre of Neurology, SLSO, Stockholm, Sweden. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre of Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Centre of Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre of Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden. Clinical Epidemiology and Biostatistics, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Orebro, Sweden. Department of Epidemiology and Public Health, University College London, London, UK.
 Departamento de Neurología, Fleni, Buenos Aires, Argentina. Departamento de Neurología, Fleni, Buenos Aires, Argentina. Departamento de Neurología, Fleni, Buenos Aires, Argentina. Departamento de Neurología, Fleni, Buenos Aires, Argentina. Departamento de Neurología, Fleni, Buenos Aires, Argentina. Unidad de Neuroinmunología, Departamento de Neurociencias, Hospital Alemán, Buenos Aires, Argentina. Unidad de Neuroinmunología, Departamento de Neurociencias, Hospital Alemán, Buenos Aires, Argentina. Departamento de Neurología, Fleni, Buenos Aires, Argentina. Departamento de Neurología, Fleni, Buenos Aires, Argentina/Instituto de Química y Fisicoquímica Biológicas (IQUIFIB), CONICET/Universidad de Buenos Aires, Buenos Aires, Argentina.
 The Webb Waring Center and Department of Medicine, The University of Colorado Anschutz Medical Campus, 12850 East Montview Blvd, Aurora, CO 80045, United States of America. The Webb Waring Center and Department of Medicine, The University of Colorado Anschutz Medical Campus, 12850 East Montview Blvd, Aurora, CO 80045, United States of America. The Webb Waring Center and Department of Medicine, The University of Colorado Anschutz Medical Campus, 12850 East Montview Blvd, Aurora, CO 80045, United States of America. The Department of Neurology, The University of Colorado Anschutz Medical Campus, 12850 East Montview Blvd, Aurora, CO 80045, United States of America. The Department of Neurology, The University of Colorado Anschutz Medical Campus, 12850 East Montview Blvd, Aurora, CO 80045, United States of America. The Webb Waring Center and Department of Medicine, The University of Colorado Anschutz Medical Campus, 12850 East Montview Blvd, Aurora, CO 80045, United States of America. Electronic address: David.Wagner@CUAnschutz.edu.
 Department of Medicine, CORe, University of Melbourne, Melbourne, Victoria, Australia. Department of Medicine, CORe, University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Department of Medicine, CORe, University of Melbourne, Melbourne, Victoria, Australia. Department of Medicine, CORe, University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Medical and Surgical Sciences and Advanced Technologies, GF Ingrassia, Catania, Italy. Isfahan University of Medical Sciences, Isfahan, Iran. Dokuz Eylul University, Konak/Izmir, Turkey. Hospital Universitario Virgen Macarena, Seville, Spain. Hospital Universitario Virgen Macarena, Seville, Spain. Department of Neuroscience, Imaging, and Clinical Sciences, D'Annunzio University, Chieti, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. CHUM Mississippi Center and University of Montreal, Montreal, Quebec, Canada. CHUM Mississippi Center and University of Montreal, Montreal, Quebec, Canada. CHUM Mississippi Center and University of Montreal, Montreal, Quebec, Canada. School of Medicine, Ondokuz Mayis University, Samsun, Turkey. KTU Medical Faculty, Farabi Hospital, Trabzon, Turkey. Neuro Rive-Sud, Quebec City, Quebec, Canada. Neurology, Kasr Al Ainy MS Research Unit, Cairo, Egypt. Department of Neuroscience, Azienda Ospedaliera Universitaria, Modena, Italy. Department of Neuroscience, Azienda Ospedaliera Universitaria, Modena, Italy. CISSS Chaudière-Appalache, Levis, Sainte-Marie, Quebec, Canada. Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Central Clinical School, Monash University, Melbourne, Victoria, Australia. Central Clinical School, Monash University, Melbourne, Victoria, Australia. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Department of Neurology, School of Medicine, Koc University, Istanbul, Turkey. Koc University Research Center for Translational Medicine, Istanbul, Turkey. Zuyderland Medical Center, Sittard-Geleen, the Netherlands. Cliniques Universitaires Saint-Luc, Louvain, Brussels, Belgium. Center of Neuroimmunology, Service of Neurology, Hospital Clinic of Barcelona, Barcelona, Spain. Garibaldi Hospital, Catania, Italy. School of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia. IRCCS Mondino Foundation, Pavia, Italy. Hacettepe University, Ankara, Turkey. Ospedali Riuniti di Salerno, Salerno, Italy. St Vincent's University Hospital, Dublin, Ireland. UOC Neurologia, Azienda Sanitaria Unica Regionale Marche-AV3, Macerata, Italy. Brain and Mind Centre, Sydney, New South Wales, Australia. Royal Victoria Hospital, Belfast, UK. Department of Neurology, Centro Hospitalar Universitário de São João, Porto, Portugal. Department of Neurology, ASL3 Genovese, Genoa, Italy. Department of Rehabilitation, ML Novarese Hospital Moncrivello, Genoa, Italy. Departments of Medicine and Clinical Research, Neurologic Clinic and Policlinic, University Hospital and University of Basel, Basel, Switzerland. Trias and Pujol Brothers University Hospital, Badalona, Spain. Hospital Italiano, Buenos Aires, Argentina. Liverpool Hospital, Sydney, New South Wales, Australia. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino, Italy. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Aarhus University Hospital, Aarhus, Denmark. Flinders University, Adelaide, South Australia, Australia. Monash Medical Centre, Melbourne, Victoria, Australia. Department of Medicine and Surgery, University of Parma, Parma, Italy. Groene Hart Ziekenhuis, Gouda, the Netherlands. University of Queensland, Brisbane, Queensland, Australia. Nemocnice Jihlava, Jihlava, Czech Republic. Rehabilitation and MS Center Overpelt and Hasselt University, Hasselt, Belgium. Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia. Austin Health, Melbourne, Victoria, Australia. CSSS Saint-Jerome, Saint-Jerome, Quebec, Canada. Medical Center Leeuwarden, Leeuwarden, the Netherlands. Hospital de Galdakao-Usansolo, Galdakao, Spain. Westmead Hospital, Sydney, New South Wales, Australia. University Hospital Ghent, Ghent, Belgium. University Hospital Ghent, Ghent, Belgium. Postgraduate Institute of Medical Education and Research, Chandigarh, India. Austin Health, Melbourne, Victoria, Australia. Department of Neurology, Razi Hospital, Manouba, Tunisia. Instituto de Investigacion Sanitaria Biodonostia, Hospital Universitario Donostia, San Sebastian, Spain. South East Trust, Belfast, UK. University Hospital Reina Sofia, Cordoba, Spain. Department of Medicine, Sultan Qaboos University Hospital, Seeb, Oman. University Hospital Geelong, Geelong, Victoria, Australia. Hospital Fernandez, Buenos Aires, Argentina. Neurology Department, King Fahad Specialist Hospital-Dammam, Dammam, Saudi Arabia. Universidade Metropolitana de Santos, Santos, Brazil. Department of Neurology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Hospital General Universitario de Alicante, Alicante, Spain. Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Mexico City, Mexico. Waikato Hospital, Hamilton, New Zealand. Jewish General Hospital, Montreal, Quebec, Canada. Department of Medicine, CORe, University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia.
 Department of Neurology, Mannheim Center of Translational Neurosciences (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Department of Neurology, Mannheim Center of Translational Neurosciences (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Institute for Clinical Chemistry, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Department of Neurology, Mannheim Center of Translational Neurosciences (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany/German. Consortium of Translational Cancer Research (DKTK), Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Department of Neurology, Mannheim Center of Translational Neurosciences (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany/Mannheim Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Department of Neurology, Ulm University, Ulm, Germany. Department of Neurology, Mannheim Center of Translational Neurosciences (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Department of Neurology, Mannheim Center of Translational Neurosciences (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
 Division of Neurology, Amiri Hospital, Arabian Gulf Street, Sharq 13041, Kuwait; MS Clinic, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait; Department of Neurology, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait; Department of Neurology and Psychiatry, Minia University, P.O. Box 61519, Minia 61111, Egypt. Electronic address: samerelshayb@hotmail.com.
 Division Neurological Rehabilitation, Department of NEUROFARBA, University of Florence, Florence, Italy. Division Neurological Rehabilitation, Department of NEUROFARBA, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy.
 Mellen Center for Multiple Sclerosis, Department of Neurology, Cleveland Clinic, Cleveland, Ohio. Mellen Center for Multiple Sclerosis, Department of Neurology, Cleveland Clinic, Cleveland, Ohio. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California.
 Department of Neurology, Virginia Commonwealth University, Richmond, VA. Division of Child Neurology, Department of Neurology, University of Virginia, Charlottesville, VA. Electronic address: jnb8h@virginia.edu.
 Department of Biomedical Engineering, College of Medical Science and Technologies, Tehran Science and Research Branch, Islamic Azad University, Tehran, Iran. Electronic address: Hamed.abdi.bme@gmail.com. Department of Biomedical Engineering, College of Medical Science and Technologies, Tehran Science and Research Branch, Islamic Azad University, Tehran, Iran. Electronic address: K.hasani@srbiau.ac.ir. Department of Biomedical Engineering, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
 Department of Social Work, Faculty of Law, University of Zagreb, Zagreb, Croatia. Department of Social Work, Faculty of Law, University of Zagreb, Zagreb, Croatia.
 Student Research Committee, Babol University of Medical Sciences, Babol, Iran; Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Mobility Impairment Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Medical Genetics, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Mobility Impairment Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Student Research Committee, Babol University of Medical Sciences, Babol, Iran; Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Electronic address: mousamohammadnia@yahoo.com.
 Pharmacology, Toxicology and Biochemistry Department, Faculty of Pharmacy, Future University in Egypt, 90 street, 5(th) Settlement, Cairo, Egypt. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Electronic address: nancy.shahin@pharma.cu.edu.eg. Pharmacology, Toxicology and Biochemistry Department, Faculty of Pharmacy, Future University in Egypt, 90 street, 5(th) Settlement, Cairo, Egypt. Pharmacology, Toxicology and Biochemistry Department, Faculty of Pharmacy, Future University in Egypt, 90 street, 5(th) Settlement, Cairo, Egypt. Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
 Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Dept. of Neuroscience and Mental Health, City of Health and Science University Hospital of Torino, Turin, Italy. Dept. of Neuroscience and Mental Health, City of Health and Science University Hospital of Torino, Turin, Italy. Multiple Sclerosis Study Center, ASST Valle Olona, Gallarate, VA, Italy. Multiple Sclerosis Study Center, ASST Valle Olona, Gallarate, VA, Italy. Dept. of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Dept. of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Multiple Sclerosis Center, G.F. Ingrassia, University of Catania, Catania, Italy. Multiple Sclerosis Center, G.F. Ingrassia, University of Catania, Catania, Italy. Dept. of Neuroscience, Mental Health and Sensory Organs, Sapienza University, S. Andrea Hospital-site, Rome, Italy. Multiple Sclerosis Clinical Care and Research Centre, Dept. of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Center, Policlinico SS. Annunziata, Chieti, Italy. Multiple Sclerosis Center, Dept. of Neuroscience, Biomedicine and Movement Sciences, University Hospital of Verona, Verona, Italy. Multiple Sclerosis Center, Dept. of Medical Sciences and Public Health, Binaghi Hospital, ASL Cagliari, University of Cagliari, Cagliari, Italy. Section of Neurology, Dept. of Medicine and Surgery, University of Perugia, Perugia, Italy. Institute of Neurology, University of Catanzaro "Magna Graecia", Catanzaro, Italy. Multiple Sclerosis Center, Dept. of Neuroscience, Biomedicine and Movement Sciences, University Hospital of Verona, Verona, Italy. Dysimmune Neuropathies Unit, Dept. of Systems Medicine, Tor Vergata University of Rome, Rome, Italy. Dept. of Neuroscience, Riuniti Hospital of Foggia, Foggia, Italy. Institute of Neurology, Fondazione Policlinico Universitario "A. Gemelli", IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy. Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, Dept. of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Electronic address: antonio.gallo@unicampania.it.
 Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Department of Experimental Psychology, Heinrich Heine University, Düsseldorf, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Department of Experimental Psychology, Heinrich Heine University, Düsseldorf, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. iris-katharina.penner@insel.ch. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. iris-katharina.penner@insel.ch. Department of Neurology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany. iris-katharina.penner@insel.ch.
 Department of Neurology, Division of Neuroimmunology, Northwestern University, 710 North Lake Shore Drive #1411, Chicago, IL 60611, USA. Electronic address: edith.graham@northwestern.edu.
 Department of Neurology, Clinic of Optic Neuritis, The Danish Multiple Sclerosis Center (DMSC), Rigshospitalet and University of Copenhagen, Valdemar Hansens Vej 13, 2600, Glostrup, Denmark. Electronic address: mathias.falck.schmidt@regionh.dk. Department of Neurology, Clinic of Optic Neuritis, The Danish Multiple Sclerosis Center (DMSC), Rigshospitalet and University of Copenhagen, Valdemar Hansens Vej 13, 2600, Glostrup, Denmark. Department of Ophthalmology, Rigshospitalet and University of Copenhagen, Valdemar Hansens Vej 13, 2600, Glostrup, Denmark. Department of Neurology, Clinic of Optic Neuritis, The Danish Multiple Sclerosis Center (DMSC), Rigshospitalet and University of Copenhagen, Valdemar Hansens Vej 13, 2600, Glostrup, Denmark. Professor of Clinical Ophthalmology, Department of Ophthalmology, Rigshospitalet and University of Copenhagen, Valdemar Hansens Vej 13, 2600, Glostrup, Denmark. Professor of Clinical Neurology, Department of Neurology, Clinic of Optic Neuritis, The Danish Multiple Sclerosis Center (DMSC), Rigshospitalet and University of Copenhagen, Valdemar Hansens Vej 13, 2600 Glostrup, Denmark.
 School of Medicine, Neurology Department, Sivas Cumhuriyet University, Sivas, Turkey. figulgokce@gmail.com. School of Medicine, Neurology Department, Sivas Cumhuriyet University, Sivas, Turkey. School of Medicine, Neurology Department, Sivas Cumhuriyet University, Sivas, Turkey. School of Medicine, Radiology Department, Sivas Cumhuriyet University, Sivas, Turkey.
 Department of Medical and Surgical Sciences, Institute of Neurology, Magna Graecia University, Catanzaro, Italy. Department of Medical and Surgical Sciences, Institute of Neurology, Magna Graecia University, Catanzaro, Italy. Department of Medical and Surgical Sciences, Institute of Neuroradiology, Magna Graecia University, Catanzaro, Italy. Department of Medical and Surgical Sciences, Institute of Neurology, Magna Graecia University, Catanzaro, Italy. Department of Medical and Surgical Sciences, Institute of Neurology, Magna Graecia University, Catanzaro, Italy. p.vale@unicz.it.
 Research Centre for Linguistics, Eötvös Loránd Research Network, Budapest, Hungary. Eötvös Lorand Research Network - University of Szeged, Research Group on Artificial Intelligence, Szeged, Hungary. Research Centre for Linguistics, Eötvös Loránd Research Network, Budapest, Hungary.
 Internal Medicine Program, Oman Medical Specialty Board (OMSB), Muscat, Oman. Neurology Unit, Department of Medicine, College of Medicine & Health Sciences and Sultan Qaboos University Hospital, Sultan Qaboos University, Muscat, Oman. Electronic address: alasm@squ.edu.om. Research Department, Oman Medical Specialty Board (OMSB), Muscat, Oman. Neurology Unit, Department of Medicine, College of Medicine & Health Sciences and Sultan Qaboos University Hospital, Sultan Qaboos University, Muscat, Oman.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
 Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, Viale Europa, Catanzaro 88100, Italy. Electronic address: simona.raimo@unicz.it. Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, Viale Europa, Catanzaro 88100, Italy. Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, Viale Europa, Catanzaro 88100, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", Caserta, Italy. Neurology Unit "San Giuseppe Moscati", Hospital Avellino, Avellino, Italy. Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, Viale Europa, Catanzaro 88100, Italy. Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, Viale Europa, Catanzaro 88100, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", Caserta, Italy.
 Department of Medical Imaging, John Hunter Hospital, Newcastle, NSW, Australia; Newcastle University Faculty of Health, Callaghan Campus, Newcastle, NSW, Australia. Electronic address: grant.bateman@health.nsw.gov.au. School of Mechanical Engineering, University of New South Wales, Sydney, NSW, Australia. Newcastle University Faculty of Health, Callaghan Campus, Newcastle, NSW, Australia; Department of Neurology, John Hunter Hospital, Newcastle, NSW, Australia; Hunter Medical Research Institute, Newcastle, NSW, Australia.
 Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. Department of Immunology, Multiple Sclerosis Unit, Hospital Ramon y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain. Department of Neurology, Multiple Sclerosis Unit, Hospital Ramon y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain. Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain. Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain. Genetics, Microbiology and Statistics Department, Universitat de Barcelona, Barcelona, Spain. Proteomics Unit, Centre de Regulació Genòmica (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. Proteomics Unit, Universitat Pompeu Fabra, Barcelona, Spain. Proteomics Unit, Centre de Regulació Genòmica (CRG), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. Proteomics Unit, Universitat Pompeu Fabra, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 Twin Valley Behavioral Healthcare, Columbus, OH, USA.
 U.N.E.D. Instituto de Salud Carlos III. Hospital San Pedro.
 Department of Information Science and Media Studies, University of Bergen, Bergen, Norway. Department of Information Science and Media Studies, University of Bergen, Bergen, Norway. Department of Biomedical Engineering, Linköping University, Linköping, Sweden.
 Department of Neurology, Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology & Neurological Sciences, Stanford University School of Medicine, Palo Alto, CA, USA. Department of Neurology, University of Southern California, Los Angeles, CA, USA. Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Department of Statistics, Tigermed, Somerset, NJ, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA. Department of Medical Affairs, Eonian Stanzas LLC, Potomac, MD, USA. Department of Research & Development, Brainstorm Cell Therapeutics, New York, NY, USA.
 Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran. Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran. Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
 The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet, Copenhagen University Hospital, Glostrup, Denmark. Electronic address: tine@iskov.dk. The Fertility Clinic, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; Institute of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Urology, Zealand University Hospital, Roskilde, Denmark. The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet, Copenhagen University Hospital, Glostrup, Denmark; Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, Copenhagen University Hospital, Glostrup, Denmark.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden/The Karolinska Neuroimmunology & Multiple Sclerosis Centre, Department of Clinical Neurosciences, Karolinska Institutet, Centre for Molecular Medicine, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. School of Population and Public Health, The University of British Columbia, Vancouver, BC, Canada/Centre for Health Evaluation and Outcome Sciences, University of British Columbia, Vancouver, BC, Canada. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden/Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
 Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece; Department of Physical Therapy, University of West Attica, Greece; Laboratory of Neuromuscular and Cardiovascular Study of Motion-LANECASM, University of West Attica, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Physical Therapy, University of West Attica, Greece; Laboratory of Neuromuscular and Cardiovascular Study of Motion-LANECASM, University of West Attica, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Department of Neurology, Attikon University Hospital Greece, School of Medicine, National and Kapodistrian University of Athens, Greece. Electronic address: sgiannop@uoi.gr.
 Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland. Electronic address: mkiczmer@szpital.zabrze.pl. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland. Department of Biochemistry, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland.
 University of Health Sciences, Bursa Sehir Training & Research Hospital, Department of Internal Medicine, Bursa, Turkey. University of Health Sciences, Bursa Yuksek Ihtisas Training and Research Hospital, Department of Neurology, Bursa, Turkey.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland; Center for Reproducible Science, University of Zurich, Zurich, Switzerland; Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden; Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Health (NIH), Bethesda, MA, USA. Electronic address: Benjaminvictor.ineichen@uzh.ch. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Center of Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. National Centre for Pathology (NCP), Laboratoire National de Santé, Dudelange, Luxembourg; Luxembourg Centre for Neuropathology (LCNP), Laboratoire National de Santé, Dudelange, Luxembourg. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Health (NIH), Bethesda, MA, USA. Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Center of Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Health (NIH), Bethesda, MA, USA. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden.
 epartment of Neurology and Clinical Neuroimmunology of the Specialist Hospital in Grudziadz, Grudziądz, Poland. Department of Clinical Nutrition, Medical University of Gdansk, Gdańsk, Poland.
 Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Spitalstrasse 2, 4031, Basel, Switzerland. Neuropsychology and Behavioral Neurology Unit, Department of Psychology and Interdisciplinary Platform Psychiatry and Psychology, Division of Molecular and Cognitive Neuroscience, University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Spitalstrasse 2, 4031, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Spitalstrasse 2, 4031, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Spitalstrasse 2, 4031, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Clinical Trial Unit, University Hospital Basel, Basel, Switzerland. Healios AG, Basel, Switzerland. Neuropsychology and Behavioral Neurology Unit, Department of Psychology and Interdisciplinary Platform Psychiatry and Psychology, Division of Molecular and Cognitive Neuroscience, University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Spitalstrasse 2, 4031, Basel, Switzerland. Ludwig.kappos@usb.ch. Department of Neurology, University Hospital Basel, Basel, Switzerland. Ludwig.kappos@usb.ch.
 Temedica GmbH, Munich, Germany; Neuromuscular Diagnostics, Technical University of Munich, Germany. Temedica GmbH, Munich, Germany. Temedica GmbH, Munich, Germany. Noventi Health SE, Munich, Germany. Roche Pharma AG, Grenzach-Wyhlen, Germany. Temedica GmbH, Munich, Germany. Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Temedica GmbH, Munich, Germany. Electronic address: benjamin.friedrich@temedica.com. Center of Clinical Neurosciences, University Hospital Carl Gustav Carus, Dresden, Germany.
 Institute of X-ray Physics, University of Göttingen, Germany. Institute of Computer Science, University of Göttingen, Germany. Institute of X-ray Physics, University of Göttingen, Germany. Institute of X-ray Physics, University of Göttingen, Germany. Institute of Neuropathology, Universical Medical Center Göttingen, Germany. Institute of Neuropathology, Universical Medical Center Göttingen, Germany; Cluster of Excellence 'Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells' (MBExC), University of Göttingen, Germany. Institute of X-ray Physics, University of Göttingen, Germany; Cluster of Excellence 'Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells' (MBExC), University of Göttingen, Germany. Electronic address: tsaldit@gwdg.de.
 Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran. Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran. s.hassanpour@srbiau.ac.ir. Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
 Department of Neuroimmunology, University of California System, San Francisco, California, USA sonam.dilwali@ucsf.edu. Department of Neuroradiology, University of California San Francisco, San Francisco, California, USA. Department of Neuroimmunology, University of California System, San Francisco, California, USA.
 University of Reading, United Kingdom of Great Britain and Northern Ireland, UK. Electronic address: H.Morris-Bankole@pgr.reading.ac.uk. University of Reading, United Kingdom of Great Britain and Northern Ireland, UK.
 Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark. Electronic address: Helene.hoejsgaard.chow@regionh.dk. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Amager and Hvidovre, Copenhagen Denmark, Kettegård Alle 30, 2650 Hvidovre, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Amager and Hvidovre, Copenhagen Denmark, Kettegård Alle 30, 2650 Hvidovre, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Copenhagen, Denmark. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Amager and Hvidovre, Copenhagen Denmark, Kettegård Alle 30, 2650 Hvidovre, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Copenhagen, Denmark; Department of Neurology, Copenhagen University Hospital Bispebjerg and Frederiksberg, Bispebjerg Bakke 23, 2400 Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Nordre Ringvej 57, 2600 Glostrup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Copenhagen, Denmark.
 Department of physical and rehabilitation medicine, Groupement des Hôpitaux de l'Institut Catholique de Lille, Faculté de médecine et de maïeutique de Lille, Lille, France. Electronic address: donze.cecile@ghicl.net. Department of physical and rehabilitation medicine, Groupement des Hôpitaux de l'Institut Catholique de Lille, Faculté de médecine et de maïeutique de Lille, Lille, France. Department of neurology, MS expert center, Caen university hospital, Caen, France. University Lille, Inserm UMR-S1172 LilNCog, CHU Lille, FHU precise, Lille, France. Department of neurology, Arras hospital, Arras, France. Department of neurology, Calais Hospital, Calais, France. Department of neurology, Amiens university hospital, Amiens, France. Department of neurology, Sambre-Avesnoy hospital, Maubeuge, France. Department of neurology, Boulogne hospital, Boulogne, France. Department of neurology, Groupement des Hôpitaux de l'Institut Catholique de Lille, Lille, France. Department of physical and rehabilitation medicine, Groupement des Hôpitaux de l'Institut Catholique de Lille, Faculté de médecine et de maïeutique de Lille, Lille, France. Department of clinical research, Groupement des Hôpitaux de l'Institut Catholique de Lille, Lille, France. Department of neurology, Groupement des Hôpitaux de l'Institut Catholique de Lille, Faculté de médecine et de maïeutique de Lille, Lille, France.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Department of Neurology, Royal London Hospital, London, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. Population Data Science, Swansea University Medical School, Swansea, UK. Population Data Science, Swansea University Medical School, Swansea, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Department of Neurology, Royal London Hospital, London, UK. Population Data Science, Swansea University Medical School, Swansea, UK. Population Data Science, Swansea University Medical School, Swansea, UK. r.m.middleton@swansea.ac.uk.
 Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy; Department of Biomedical and Biotechnological Sciences (BIOMETEC), University of Catania, Catania, Italy. Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy. Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy. Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy. Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy. Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy. Department "GF Ingrassia", Section of Neurosciences, Neurology Clinic, University of Catania, 9126 Catania, Italy. Electronic address: patti@unict.it.
 Department of Clinical Pharmacy, College of Pharmacy, King Saud University, P.O. Box: 2457, Riyadh, 11451, Saudi Arabia. halomar@ksu.edu.sa. Health Technology Assessment Unit (HTAU), College of Pharmacy, King Saud University, P.O. Box: 2457, Riyadh, 11451, Saudi Arabia. halomar@ksu.edu.sa. Department of Pharmacy Services, King Saud University Medical City, P.O. Box: 2457, Riyadh, 11472, Saudi Arabia. nadalsowaida@gmail.com. Department of Pharmacy, Maternity and Children Hospital, Ministry of Health, Al Kharj, 16278, Saudi Arabia. Department of Clinical Pharmacy, College of Pharmacy, King Saud University, P.O. Box: 2457, Riyadh, 11451, Saudi Arabia. Department of Neurology, Neurosciences Center, King Fahd Specialist Hospital, Dammam, 32253, Saudi Arabia. Department of Neurology, King Fahad Medical City, Ministry of Health, Riyadh, 11525, Saudi Arabia. jumahm@gmail.com.
 Penn Statistics in Imaging and Visualization Center, Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Penn Statistics in Imaging and Visualization Center, Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Penn Statistics in Imaging and Visualization Center, Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Center for Biomedical Image Computing and Analytics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurological Sciences, Larner College of Medicine at The University of Vermont, Burlington, Vermont, USA.
 Sorbonne university, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Department of neuro-urology, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Clinical investigation center,1429 Inserm, Raymond-Poincarré hospital, 104, boulevard Raymond-Poincaré, 92380 Garches, Hospital-University Group, AP-HP, Paris-Saclay University, Paris, France. Electronic address: eliane.tan@aphp.fr. Sorbonne university, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Department of neuro-urology, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Department of physical and rehabilitation, Casanova hospital, 11, rue Danielle-Casanova, 93205 Saint-Denis, France. Department of physical and rehabilitation, Mutualiste center, Kerpape, BP 78, 56275 Ploemeur, France. Department of physical and rehabilitation, Henry-Gabrielle HCL hospital, 20, routes de Vourles, 69230 St-Genis-Laval, France. Department of physical and rehabilitation, Calvé center, fondation Hopale, 62600 Berck-sur-Mer, France. Department of physical and rehabilitation, INSERM/UPS, ToNIC (Toulouse NeuroImaging Center), Purpan university hospital center, pavillon Baudot, place du Docteur-Baylac, 31024 Toulouse, France. Neurourology and andrology unit, department of physical medicine and rehabilitation, UMR 1179 Inserm, Raymond-Poincarré hospital, 104, boulevard Raymond-Poincaré, 92380 Garches, France. Sorbonne university, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Department of neuro-urology, Tenon hospital, 4, rue de la Chine, 75020 Paris, France. Sorbonne university, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Department of neuro-urology, Tenon hospital, 4, rue de la Chine, 75020 Paris, France. Sorbonne university, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Tenon hospital, 4, rue de la Chine, 75020 Paris, France; Department of neuro-urology, Tenon hospital, 4, rue de la Chine, 75020 Paris, France.
 Department of Primary Care and Public Health, School of Public Health, Imperial College of London, London, UK/Department of Public Health, Federico II University, Naples, Italy. Departments of Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Primary Care and Public Health, School of Public Health, Imperial College of London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/National Institute for Health Research, University College London Hospitals, Biomedical Research Centre, London, UK.
 Department of Microbiology & Immunology, Virginia Commonwealth University School of Medicine, Massey Cancer Center, Richmond, Virginia, USA.
 Department of Social Work, University of Gothenburg, Gothenburg, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Ankara Private Bayindir Hospital, Ankara, Turkey. Department of Radiology, Vocational School of Health Services, Atilim University, Ankara, Turkey. Department of Radiology, Medical Faculty, Ataturk University, Erzurum, Turkey. Department of Radiology, Medical Faculty, Duzce University, Arapçiftliği Mahallesi, 2901. Sokak, Numara 10, Duzce, Turkey. drhogul@gmail.com.
 School of Biomedical Science and Pharmacy, University of Newcastle, Newcastle, NSW, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Hunter Medical Research Institute, Immune Health research program, Newcastle, NSW, Australia. Department of Neurology, John Hunter Hospital, Newcastle, NSW, Australia. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia. Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Neuro-Immunology Registry, MSBase Foundation, Melbourne, VIC, Australia. Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia. School of Biomedical Science and Pharmacy, University of Newcastle, Newcastle, NSW, Australia. New South Wales (NSW) Health Pathology, John Hunter Hospital, Newcastle, NSW, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. School of Biomedical Science and Pharmacy, University of Newcastle, Newcastle, NSW, Australia. Centre of Genomics and Personalised Health, School of Biomedical Sciences, Queensland University of Technology, Kelvin Grove, QLD, Australia. Hunter Medical Research Institute, Immune Health research program, Newcastle, NSW, Australia. Department of Neurology, John Hunter Hospital, Newcastle, NSW, Australia. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia.
 Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences (UIPS), Utrecht University, Utrecht, The Netherlands. National Health Care Institute (ZIN), Diemen, The Netherlands. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences (UIPS), Utrecht University, Utrecht, The Netherlands. National Health Care Institute (ZIN), Diemen, The Netherlands. Department of Pharmacoeconomics, Medical University of Warsaw, Warsaw, Poland. Department of Pharmacoeconomics, Medical University of Warsaw, Warsaw, Poland. National Institute for Health and Care Excellence (NICE), London, UK. Faculty of Pharmacy, Clinical Pharmacy Department, Cairo University, Cairo, Egypt. Department of Neurology, Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, MS Center Amsterdam, Amsterdam, The Netherlands. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences (UIPS), Utrecht University, Utrecht, The Netherlands. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences (UIPS), Utrecht University, Utrecht, The Netherlands. National Health Care Institute (ZIN), Diemen, The Netherlands.
 Sanofi, Cambridge, MA 02141, USA. Axtria Inc., Berkeley Heights, NJ 07922, USA. Sanofi, Cambridge, MA 02141, USA. Sanofi, Cambridge, MA 02141, USA. Sanofi, Cambridge, MA 02141, USA.
 From the Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD. From the Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD. From the Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD. dgold7@jhmi.edu.

 Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Turku PET Centre, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Åbo Akademi University, Turku, Finland. Turku PET Centre, Turku, Finland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. IRCCS NEUROMED, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Advanced Medical and Surgical Sciences, and 3T MRI-Center, University of Campania 'Luigi Vanvitelli', Naples, Italy. Department of Advanced Medical and Surgical Sciences, and 3T MRI-Center, University of Campania 'Luigi Vanvitelli', Naples, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Biologisch-Medizinisches Forschungszentrum (BMFZ), Genomics and Transcriptomics Labor, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Electronic address: gerd.mzh@uni-muenster.de.
 Servicio de Neurología, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain. Electronic address: sllufriu@clinic.cat. Servicio de Neurología, Hospital Universitario Reina Sofía, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Córdoba, Spain. Servicio de Neurología, Hospital Universitario Ramón y Cajal, Madrid, Spain. Servicio de Neurología, Hospital Virgen de la Salud, Toledo, Spain. Servicio de Neurología, Hospital Universitario Dr. Peset, Valencia, Spain. Sección de Neurorradiología, Servicio de Radiología, Hospital Universitario Ramón y Cajal, Madrid, Spain. CSUR Esclerosis Múltiple y Unidad de Neuroinmunología Clínica, Servicio de Neurología, Hospital Clínico Universitario Virgen de la Arrixaca, IMIB-Arrixaca, Murcia, Spain. Servicio de Neurología, Hospital Moisès Broggi, Sant Joan Despí, Barcelona, Spain. Sección de Neurorradiología, Servicio de Radiología, Hospital Universitario Reina Sofía, Córdoba, Spain. Sección de Neurorradiología, Servicio de Radiología, Hospital Universitario 12 de Octubre, Madrid, Spain. Servicio de Neurología, Hospital Virgen de la Salud, Toledo, Spain. Sección de Neurorradiología, Servicio de Radiología, Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, Spain. Sección de Neurorradiología, Servicio de Radiología, Hospital Universitario 12 de Octubre, Madrid, Spain. Sección de Neurorradiología, Servicio de Radiodiagnóstico, Hospital Universitario Dr. Peset, Valencia, Spain. Sección de Neurorradiología, Servicio de Radiodiagnóstico, Hospital Universitario Dr. Peset, Valencia, Spain. Servicio de Neurología, Hospital Moisès Broggi, Sant Joan Despí, Barcelona, Spain. Sección de Neurorradiología, Servicio de Radiología, Hospital Universitario Vall d'Hebron, Barcelona, Spain.
 Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. European Medical Affairs, Teva Pharmaceuticals Europe B.V., Amsterdam, The Netherlands.
 Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Genentech, Inc, South San Francisco, California, USA. Amerita Specialty Infusion Services, Denver, Colorado, USA. Amerita Specialty Infusion Services, Denver, Colorado, USA. University of Colorado Hospital, Aurora, Colorado, USA. University of Colorado Hospital, Aurora, Colorado, USA. University of Colorado Hospital, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Genentech, Inc, South San Francisco, California, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology, Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
 Neurology Department, Cairo University, Giza, Egypt. Clinical Pathology Department, Cairo University, Giza, Egypt. Neurology Department, Cairo University, Giza, Egypt. Neurology Department, Cairo University, Giza, Egypt. drdahshanneuro@kasralainy.edu.eg.
 Nationaal Multiple Sclerose Centrum, Melsbroek, Belgium. Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Brussels, Belgium. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium. Neurology Department, Universitair Ziekenhuis Brussel, Brussels, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium. Nationaal Multiple Sclerose Centrum, Melsbroek, Belgium. Neurology Department, Universitair Ziekenhuis Brussel, Brussels, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. Nationaal Multiple Sclerose Centrum, Melsbroek, Belgium. Neurology Department, Universitair Ziekenhuis Brussel, Brussels, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Brussels, Belgium. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium. Neurology Department, Universitair Ziekenhuis Brussel, Brussels, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. St Edmund Hall, University of Oxford, Oxford, UK. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium. Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Brussels, Belgium.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Molecular and Clinical Medicine/Wallenberg Lab, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden. Department of Molecular and Clinical Medicine/Wallenberg Lab, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Molecular and Clinical Medicine/Wallenberg Lab, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Laboratory Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden; Department of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg 413 85, Sweden. Electronic address: maria.k.blomqvist@vgregion.se.
 Department of Medicine, Kuwait and Head Neurology Unit, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait. Neurology Unit, Mubarak al Kabeer Hospital, Ministry of Health, Jabriya, Kuwait. Neurology Unit, Mubarak al Kabeer Hospital, Ministry of Health, Jabriya, Kuwait. Department of Medicine, Kuwait and Head Neurology Unit, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait. Department of Population Medicine, Qatar University, Doha, Qatar.
 Doctoral School, Catholic University of Valencia San Vicente Mártir, 46001 Valencia, Spain. Psicoforma Integral Psychology Center, 46001 Valencia, Spain. Department of Psychology, European University of Valencia, 46010 Valencia, Spain. Department of Psychology and Sociology, University of Zaragoza, Campus Teruel, 44003 Teruel, Spain. Department of Basic Medical Sciences, Catholic University of Valencia, 46001 Valencia, Spain. Department of Basic Medical Sciences, Catholic University of Valencia, 46001 Valencia, Spain. Department of Medicine and Animal Surgery, Catholic University of Valencia, 46001 Valencia, Spain. Department of Basic Medical Sciences, Catholic University of Valencia, 46001 Valencia, Spain. Department of Basic Medical Sciences, Catholic University of Valencia, 46001 Valencia, Spain.
 Tunisian Research Laboratory "Sport Performance Optimisation", (LR09SEP01) National Center of Medicine and Science in Sport, Tunis, Tunisia. Department of Neurology, (LR 18SP03), Clinical Investigation Centre Neurosciences and Mental Health, Razi University Hospital-1, Tunis, LR, Tunisia. University of Tunis El Manar, Faculty of Medicine of Tunis, Tunis, Tunisia. Farhat HACHED Hospital, Heart Failure (LR12SP09) Research Laboratory, University of Sousse, Sousse, Tunisia. ASPETAR, Orthopaedic and Sports Medicine Hospital, FIFA Medical Centre of Excellence, Doha, Qatar.
 Multiple Sclerosis Center, II Division of Neurology, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, II Division of Neurology, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Neurosciences, Reproductive and Odontostomatological Sciences, University Federico II, Naples, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", Caserta, Italy. Multiple Sclerosis Center "A. Cardarelli" Hospital, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center "A. Cardarelli" Hospital, Naples, Italy. Multiple Sclerosis Center, II Division of Neurology, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Neurosciences, Reproductive and Odontostomatological Sciences, University Federico II, Naples, Italy. Multiple Sclerosis Center, II Division of Neurology, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Neurosciences, Reproductive and Odontostomatological Sciences, University Federico II, Naples, Italy. Electronic address: francesco.sacca@unina.it. Department of Neurosciences, Reproductive and Odontostomatological Sciences, University Federico II, Naples, Italy.
 Uveitis Service, LV Prasad Eye Institute, Hyderabad, India. Immunology Laboratory, Brien Holden Eye Research Centre, LV Prasad Eye Institute, Hyderabad, India. Research Unit, Nizam's Institute of Medical Sciences Multi-disciplinary, Hyderabad, India. Ophthalmic Pathology Laboratory, LV Prasad Eye Institute, Hyderabad, India. Uveitis Service, LV Prasad Eye Institute, Hyderabad, India. Immunology Laboratory, Brien Holden Eye Research Centre, LV Prasad Eye Institute, Hyderabad, India.
 University of Health Sciences Türkiye, Sultan 2. Abdulhamid Han Training and Research Hospital, Clinic of Ophthalmology, İstanbul, Türkiye. University of Health Sciences Türkiye, Sultan 2. Abdulhamid Han Training and Research Hospital, Clinic of Ophthalmology, İstanbul, Türkiye. University of Health Sciences Türkiye, Sultan 2. Abdulhamid Han Training and Research Hospital, Clinic of Ophthalmology, İstanbul, Türkiye. University of Health Sciences Türkiye, Sancaktepe Şehit Prof. Dr. İlhan Varank Training and Research Hospital, Clinic of Neurology, İstanbul, Türkiye. University of Health Sciences Türkiye, Sultan 2. Abdulhamid Han Training and Research Hospital, Clinic of Ophthalmology, İstanbul, Türkiye.
 Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Parkville, Victoria, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Victoria, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Victoria, Australia. School of Medical, Indigenous and Health Sciences, University of Wollongong, Wollongong, New South Wales, Australia. Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Victoria, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Victoria, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Victoria, Australia.
 University of Ljubljana, Faculty of Pharmacy, Aškerčeva cesta 7, Ljubljana 1000, Slovenia; University Medical Centre Ljubljana, Division of Neurology, Multiple Sclerosis Centre, Zaloška cesta 2, Ljubljana 1000, Slovenia. University of Ljubljana, Faculty of Pharmacy, Aškerčeva cesta 7, Ljubljana 1000, Slovenia. University Medical Centre Ljubljana, Division of Neurology, Multiple Sclerosis Centre, Zaloška cesta 2, Ljubljana 1000, Slovenia. University Medical Centre Ljubljana, Division of Neurology, Multiple Sclerosis Centre, Zaloška cesta 2, Ljubljana 1000, Slovenia; University of Ljubljana, Faculty of Medicine, Vrazov trg 2, Ljubljana 1000, Slovenia. University of Ljubljana, Faculty of Pharmacy, Aškerčeva cesta 7, Ljubljana 1000, Slovenia. Electronic address: kosm@ffa.uni-lj.si.
 Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility, Berlin, Germany. Hasso Plattner Institute for Digital Engineering, University of Potsdam, Germany. Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility, Berlin, Germany. Experimental and Clinical Research Center, a joint cooperation between the Charité Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility, Berlin, Germany. SRH Fernhochschule - The Mobile University, Riedlingen, Germany. Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility, Berlin, Germany. MRI.TOOLS GmbH, Berlin, Germany. Hasso Plattner Institute for Digital Engineering, University of Potsdam, Germany. Medicinal Chemistry, Leibniz-Institut fϋr Molekulare Pharmakologie (FMP), Berlin, Germany. Experimental and Clinical Research Center, a joint cooperation between the Charité Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Berlin, Germany. Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility, Berlin, Germany. Experimental and Clinical Research Center, a joint cooperation between the Charité Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility, Berlin, Germany. Experimental and Clinical Research Center, a joint cooperation between the Charité Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
 Department of Neurology, University Hospital, Rennes, France. maelle.chappuis@chu-rennes.fr. Research Management Department, University Hospital, Rennes, France. Department of Epidemiology and Public Health, University Hospital, Rennes, France. Department of Neurology, University Hospital, Nantes, France. Department of Neurology, University Hospital, Nantes, France. Department of Neurology, University Hospital, Rennes, France. CIC-P 1414 Inserm, University Hospital, Rennes, France. Department of Neurology, University Hospital, Rennes, France. CIC-P 1414 Inserm, University Hospital, Rennes, France. Department of Neurology, University Hospital, Rennes, France. CIC-P 1414 Inserm, University Hospital, Rennes, France. Department of Neurology, University Hospital, Rennes, France. CIC-P 1414 Inserm, University Hospital, Rennes, France.
 Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Department of Basic Oncology, Health Institute of Ege University, Izmir, Turkey. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Research Center for Integrative Medicine in Aging, Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. shaafis@tbzmed.ac.ir.
 School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. School of Persian Medicine, Tehran University of Medical Sciences, Tehran, Iran. Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
 Undergraduate of the Physiotherapy Course, Escola de Educação Fìsica, terapia e Dança, Universidade Federal do Rio Grande do Sul, Rua Felizardo, 750. Bairro Jardim Botânco. Porto Alegre, RS CEP 90690-200, Brasil. Professor of the Physiotherapy Course, Escola de Educação Fìsica, Fisioterapia e Dança, Universidade Federal do Rio Grande do Sul. Rua Felizardo, 750. Bairro Jardim Botânco. Porto Alegre, RS CEP 90690-200, Brasil. Professor of the Physiotherapy Course, Escola de Educação Fìsica, Fisioterapia e Dança, Universidade Federal do Rio Grande do Sul. Rua Felizardo, 750. Bairro Jardim Botânco. Porto Alegre, RS CEP 90690-200, Brasil. Electronic address: lucianopalmeiro@gmail.com.
 Department of Neurology, Mount Auburn Hospital, Harvard Medical School, USA. Electronic address: mabdelrazek@mah.harvard.edu. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Departments of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Departments of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
 Faculty of Residency, Riga Stradins University, LV-1007 Riga, Latvia. Department of Neurology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Radiology, Riga Stradins University, LV-1002 Riga, Latvia. Institute of Diagnostic Radiology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Faculty of Residency, Riga Stradins University, LV-1007 Riga, Latvia. Department of Neurology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Radiology, Riga Stradins University, LV-1002 Riga, Latvia. Institute of Diagnostic Radiology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Radiology, Riga Stradins University, LV-1002 Riga, Latvia. Institute of Diagnostic Radiology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Faculty of Medicine, Riga Stradins University, LV-1007 Riga, Latvia. Faculty of Medicine, Riga Stradins University, LV-1007 Riga, Latvia. Department of Neurology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Neurology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Neurology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Neurology and Neurosurgery, Riga Stradins University, LV-1007 Riga, Latvia. Department of Neurology, Pauls Stradins Clinical University Hospital, LV-1002 Riga, Latvia. Department of Neurology and Neurosurgery, Riga Stradins University, LV-1007 Riga, Latvia. Statistics Unit, Riga Stradins University, LV-1007 Riga, Latvia. Institute of Life Sciences and Technology, Daugavpils University, LV-5401 Daugavpils, Latvia.
 Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain, pablo.arroyo@bellvitgehospital.cat. Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Headache Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Departament de Ciències Clíniques, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain. Multiple Sclerosis Unit, Neurology Department, Hospital Universitari de Bellvitge-IDIBELL, Hospitalet de Llobregat, Spain. Departament de Ciències Clíniques, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain.
 From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy. From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy. Department of Neurology. Department of Neurology. From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy. From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy. From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy. Department of Neurology. Biomedical Center Martin. Clinic of Neurology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia. Department of Neurology. Clinic of Neurology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia. From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy. From the High Field MR Centre, Department of Biomedical Imaging and Image-Guided Therapy.
 Roche Products Ltd. Electronic address: jordanne.florio-smith@roche.com. University Hospital of Southampton NHS Foundation Trust, UKMSSNA Co chair. Electronic address: mavis.ayer@uhs.nhs.uk. Lead Clinical Nurse Specialist in MS, Queen Elizabeth Hospital, Birmingham. Electronic address: samantha.colhoun@uhb.nhs.uk. Multiple Sclerosis Nurse Specialist, Nottingham City Care, Nottingham. Electronic address: nicola.daykin@nhs.net. Multiple Sclerosis Nursing Service, Northern Health & Social Care Trust, Northern Ireland United Kingdom. Electronic address: Brenda.Hamill@northerntrust.hscni.net. Ipsos MORI UK Ltd. Electronic address: Xierong.Liu@ipsos.com. Ipsos MORI UK Ltd. Electronic address: Emma.Rogers@ipsos.com. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London. Electronic address: a.thomson@qmul.ac.uk. Roche Products Ltd. Electronic address: roberta.pace_balzan@roche.com.
 Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. University Centre for Statistics in the Biomedical Sciences (CUSSB), Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. University Centre for Statistics in the Biomedical Sciences (CUSSB), Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Centre for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Centre for Neurology, Academic Specialist Center, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. Centre for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Centre for Neurology, Academic Specialist Center, Karolinska University Hospital, Stockholm, Sweden. Centre for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Centre for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Basel, Switzerland. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Centre for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Centre for Neurology, Academic Specialist Center, Karolinska University Hospital, Stockholm, Sweden.
 Molecular Biophysics Laboratory, Department of Physics, University of Calabria, 87036, Rende, Italy. STAR Research Infrastructure, University of Calabria, 87036, Rende, CS, Italy. Molecular Biophysics Laboratory, Department of Physics, University of Calabria, 87036, Rende, Italy. CNR-Nanotec Rende, Via P. Bucci, 87036, Rende, Italy. Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036, Rende, CS, Italy. Neurological and Stroke Unit, Multiple Sclerosis Clinic, Annunziata Hospital, 87100, Cosenza, Italy. SOC Neurologia-Azienda Ospedaliera Pugliese-Ciaccio, 88100, Catanzaro, Italy. Neurological and Stroke Unit, Multiple Sclerosis Clinic, Annunziata Hospital, 87100, Cosenza, Italy. SOC Neurologia-Ospedale Jazzolino, Azienda Ospedaliera Provinciale, 89900, Vibo Valentia, Italy. Neurological and Stroke Unit, Multiple Sclerosis Clinic, Annunziata Hospital, 87100, Cosenza, Italy. Department of Economics, Statistics and Finance "Giovanni Anania", University of Calabria, Arcavacata di Rende, CS, Italy. Molecular Biophysics Laboratory, Department of Physics, University of Calabria, 87036, Rende, Italy. rita.guzzi@fis.unical.it. CNR-Nanotec Rende, Via P. Bucci, 87036, Rende, Italy. rita.guzzi@fis.unical.it.
 Nottingham Centre for Multiple Sclerosis and Neuroinflammation, Department of Neurology, Queen's Medical Centre, Nottingham University Hospitals NHS Trust, Nottingham, UK. Nottingham Centre for Multiple Sclerosis and Neuroinflammation, Department of Neurology, Queen's Medical Centre, Nottingham University Hospitals NHS Trust, Nottingham, UK. aimee.hibbert@nuh.nhs.uk. Helen Durham Centre for Neuroinflammatory Disease, University Hospital of Wales, Cardiff, UK. Division of Psychological Medicine and Clinical Neuroscience, Cardiff University, Cardiff, UK. Department of Neurology, Aneurin Bevan University Health Board, Newport, UK. Nottingham Centre for Multiple Sclerosis and Neuroinflammation, Department of Neurology, Queen's Medical Centre, Nottingham University Hospitals NHS Trust, Nottingham, UK. Division of Psychological Medicine and Clinical Neuroscience, Cardiff University, Cardiff, UK. Department of Neurology, Aneurin Bevan University Health Board, Newport, UK. Department of Neurology, Morriston Hospital, Swansea, UK. Department of Neurosciences, University Hospitals Coventry and Warwickshire, Coventry, UK. Department of Neurology, Morriston Hospital, Swansea, UK. School of Health and Social Care, University of Lincoln, Lincoln, UK. Mental Health and Clinical Neurosciences Academic Unit, University of Nottingham, Nottingham, UK.
 Neurology Section, Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers, New Jersey Medical School, Newark, NJ, USA. Department of Neurology, Rutgers, New Jersey Medical School, Newark, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers, New Jersey Medical School, Newark, NJ, USA. Neuropsychology and Neuroscience Lab, Kessler Foundation, East Hanover, NJ, USA. Neurology Section, Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå stråket 7, 413 45, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå stråket 7, 413 45, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå stråket 7, 413 45, Gothenburg, Sweden. anna.nordin@neuro.gu.se.
 Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Mater Salutis Hospital, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Section, Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy.
 Frances Payne Bolton School of Nursing, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH, USA. map208@case.edu. Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, OH, USA. Frances Payne Bolton School of Nursing, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH, USA.
 Institute of Graduate Studies, Istanbul University-Cerrahpasa, Istanbul, Turkey. Goztepe Training and Research Hospital Neurology Clinic, Istanbul Medeniyet University, Istanbul, Turkey. Florence Nightingale Faculty of Nursing, Istanbul University-Cerrahpasa, Abidei Hurriyet Cd. 34381 Sisli, Istanbul, Turkey. ztulek@iuc.edu.tr.
 Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada; Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada. Electronic address: rmarrie@hsc.mb.ca. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada. Department of Psychiatry, Max Rady College of Medicine Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada. Nova Scotia Health Authority, Departments of Psychiatry, Psychology & Neuroscience, and Medicine, Dalhousie University, Halifax, CAN, Canada. Department of Neurology and Epidemiology, Johns Hopkins University, Baltimore, MD, USA. Department of Clinical Health Psychology, Max Rady College of Medicine Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada. College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada; Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, SWE, Sweden. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada. Departments of Community Health Sciences & Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, CAN, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada; Department of Neurology, Section on Statistical Planning and Analysis, UT Southwestern Medical Center, Dallas, TX, USA. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, CAN, Canada.
 Demyelinating Diseases Unit, 1st Department of Neurology, School of Medicine, Aeginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Department of Neuropathology, University of Göttingen Medical Center, Göttingen, Germany. Mass Cytometry-CyTOF Laboratory, Center for Clinical Research, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece. Center for Clinical Research, Experimental Surgery and Translational Research Biomedical Research Foundation of the Academy of Athens, Athens, Greece. Division of Basic Sciences, University of Crete Medical School, Heraklion, Greece. Center for Clinical Research, Experimental Surgery and Translational Research Biomedical Research Foundation of the Academy of Athens, Athens, Greece. Demyelinating Diseases Unit, 1st Department of Neurology, School of Medicine, Aeginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Demyelinating Diseases Unit, 1st Department of Neurology, School of Medicine, Aeginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Research Unit of Radiology, 2nd Department of Radiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece. Department of Neuropathology, University of Göttingen Medical Center, Göttingen, Germany. Demyelinating Diseases Unit, 1st Department of Neurology, School of Medicine, Aeginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Demyelinating Diseases Unit, 1st Department of Neurology, School of Medicine, Aeginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Demyelinating Diseases Unit, 1st Department of Neurology, School of Medicine, Aeginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Department of Neurology, Henry Dunant Hospital Center, Athens, Greece.
 Baylor College of Medicine/Texas Children's Hospital, Neurology and Developmental Neuroscience, Houston, Texas. Electronic address: malani@bcm.edu. Department of Pediatrics, University of Utah, Salt Lake City, Utah. Center for Pediatric-Onset Demyelinating Disease, Children's Hospital of Alabama, Birmingham, Alabama. Center for Pediatric-Onset Demyelinating Disease, Children's Hospital of Alabama, Birmingham, Alabama. Mass General Brigham Pediatric MS Center, Massachusetts General Hospital for Children, Yawkey Center for Outpatient Care, Boston, Massachusetts. Baylor College of Medicine/Texas Children's Hospital, Neurology and Developmental Neuroscience, Houston, Texas. Pediatric Multiple Sclerosis and Related Disorders Program, Boston Children's Hospital, Department of Neurology, Boston, Massachusetts. Pediatric Multiple Sclerosis and Related Disorders Program, Boston Children's Hospital, Department of Neurology, Boston, Massachusetts. Pediatric MS Center of the Jacobs Neurological Institute, Buffalo, New York. Pediatric Multiple Sclerosis Center at Loma Linda University Children's Hospital, San Bernardino, California. Pediatric MS Center, Mayo Clinic, Rochester, Minnesota. Pediatric MS Center, Mayo Clinic, Rochester, Minnesota. New York University Langone Medical Center, Pediatric Multiple Sclerosis Center, New York, New York. Rocky Mountain MS Center, University of Colorado, Aurora, Colorado. Pediatric MS and other Demyelinating Disease Center, Washington University, St. Louis, Missouri. Pediatric MS and other Demyelinating Disease Center, Washington University, St. Louis, Missouri. Cleveland Clinic, Mellen Center for Multiple Sclerosis, Cleveland, Ohio. Cleveland Clinic, Mellen Center for Multiple Sclerosis, Cleveland, Ohio. Department of Neurology, University of Utah, Salt Lake City, Utah. Department of Pediatrics, University of Utah, Salt Lake City, Utah. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. UCSF, Weill Institute for Neurosciences, San Francisco, California.
 Department of Neurology, Mayo Clinic, Rochester, MN, USA; Division of Neurology, Department of Medicine, Dalhousie University, Halifax, NS, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Division of Neurology, Department of Medicine, Dalhousie University, Halifax, NS, USA; Dell Medical School at the University of Texas at Austin, Austin, TX, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Rochester, MN, USA; Department of Neurology, Bon Secours Mercy Health St. Vincent Medical Center, Toledo, OH, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Rochester, MN, USA. Electronic address: tobin.oliver@mayo.edu.
 Psychological Sciences, Kent State University, Kent, OH, USA. Cleveland Clinic, Neurological Institute, Section of Neuropsychology, Cleveland, OH, USA. Psychological Sciences, Kent State University, Kent, OH, USA. Brain Health Research Institute, Kent State University, Kent, OH, USA. Cleveland Clinic, Neurological Institute, Section of Neuropsychology, Cleveland, OH, USA. Cleveland Clinic, Mellen Center for Multiple Sclerosis, Cleveland, OH, USA.
 Neurological Institute, Section of Neuropsychology, Cleveland Clinic, Cleveland, OH USA. Neurological Institute, Section of Neuropsychology, Cleveland Clinic, Cleveland, OH USA. Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, OH, USA. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH USA. Neurological Institute, Section of Neuropsychology, Cleveland Clinic, Cleveland, OH USA; Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH USA. Electronic address: GALIOTR@ccf.org.
 Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Electronic address: freja.johanne.krogsgaard.jespersen@regionh.dk. Department of Hematology Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Blood bank, Department of Clinical Immunology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
 Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Biomedical Sciences and Human Oncology, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy. paolo.taurisano@uniba.it. Department of Translational Biomedicine and Neuroscience, University of Bari "Aldo Moro", Piazza G. Cesare, 11, Bari, 70121, Italy.
 Center for Drug of Clinical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Center for Drug of Clinical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Center for Drug of Clinical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Center for Drug of Clinical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Center for Drug of Clinical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: lilujin666@163.com. Center for Drug of Clinical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: qingshan.zheng@drugchina.net.
 Providence Brain and Spine Institute, Portland, OR, USA. Providence Brain and Spine Institute, Portland, OR, USA. Providence Brain and Spine Institute, Portland, OR, USA. Providence Brain and Spine Institute, Portland, OR, USA. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, WA, USA. Providence Brain and Spine Institute, Portland, OR, USA.
 Department of Neurology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Department of Neurology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Department of Neurology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Department of Clinical Pharmacy, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran. Pharmaceutical Sciences Research Center, Department of Clinical Pharmacy, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran. Electronic address: ghazaeianm@gmail.com.
 Centre médical Germaine-Revel, 707 route de la Condamine, Saint-Maurice-sur-Dargoire, 69440  Chabanière, France. Centre médical Germaine-Revel, 707 route de la Condamine, Saint-Maurice-sur-Dargoire, 69440  Chabanière, France. Electronic address: alexandra.viadere@cmgr.fr.
 Psychology Department, Montclair State University, Montclair, NJ, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
 Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Karl-Franzens University, Graz, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Laboratory Medicine, Paracelsus Medical University and Salzburger Landeskliniken, Salzburg, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. fritz.leutmezer@meduniwien.ac.at. Clinic for Neurology 2, Kepler University Clinic, Linz, Austria.
 Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Inselspital, Bern University Hospital, Bern, Switzerland. Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Inselspital, Bern University Hospital, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Inselspital, Bern University Hospital, Bern, Switzerland. Swiss Institute for Translational and Entrepreneurial Medicine, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. ARTORG Center for Biomedical Research, University of Bern, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Inselspital, Bern University Hospital, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Inselspital, Bern University Hospital, Bern, Switzerland. Swiss Institute for Translational and Entrepreneurial Medicine, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Inselspital, Bern University Hospital, Bern, Switzerland.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it.
 Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, 5 East 98th Street, Box 1138, New York, NY 10029, United States. Electronic address: sarah.levy@mssm.edu. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, 5 East 98th Street, Box 1138, New York, NY 10029, United States. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, 5 East 98th Street, Box 1138, New York, NY 10029, United States. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, 5 East 98th Street, Box 1138, New York, NY 10029, United States. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, 5 East 98th Street, Box 1138, New York, NY 10029, United States.
 Joi Life Wellness MS Center, 767 Concord Rd SE, Smyrna, GA, 30082, USA. Electronic address: mitzijwilliamsmd@gmail.com. North Texas Institute of Neurology and Headache, 6201 Dallas Pkwy, Plano, TX, 75024, USA. Washington University in St. Louis School of Medicine, 660 S Euclid Ave, St Louis, MO, 63110, USA. University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390, USA. Weill Cornell Medical College, 1305 York Ave, New York, NY, 10021, USA. Andrew C. Carlos MS Institute, Shepherd Center, 2020 Peachtree Road, NW, Atlanta, GA, 30309, USA. University of Chicago Medicine, 5841 S Maryland Ave, Chicago, IL, 60637, USA. Atlanta Neuroscience Institute/Multiple Sclerosis Center of Atlanta, 3200 Downwood Cir NW, Atlanta, GA, 30327, USA. Washington University in St. Louis School of Medicine, 660 S Euclid Ave, St Louis, MO, 63110, USA. Wayne State University School of Medicine, 540 E Canfield St, Detroit, MI, 48201, USA. Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. Johns Hopkins Hospital, 600 N Wolfe St, Pathology 627, Baltimore, MD, 21287, USA. Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. Keck School of Medicine, University of Southern California, 1975 Zonal Ave, Los Angeles, CA, 90033, USA.
 Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Department of Biomedical Engineering, University of Basel, Basel, Switzerland; Medical Image Analysis Center AG, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Medical Image Analysis Center AG, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Department of Biomedical Engineering, University of Basel, Basel, Switzerland/Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Department of Neurology, DKD HELIOS Klinik Wiesbaden, Wiesbaden, Germany. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Basel, Switzerland/Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland/Translational Imaging in Neurology (ThINk) Basel, Departments of Head, Spine and Neuromedicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland; Reha Rheinfelden, Rheinfelden, Switzerland.
 Department of Cell Biology and Genetics, Institute of Molecular Medicine and Oncology, Chongqing Medical University, Medical School Road 1#, Yuzhong District, Chongqing 400016, China. Department of Cell Biology and Genetics, Institute of Molecular Medicine and Oncology, Chongqing Medical University, Medical School Road 1#, Yuzhong District, Chongqing 400016, China. Department of Cell Biology and Genetics, Institute of Molecular Medicine and Oncology, Chongqing Medical University, Medical School Road 1#, Yuzhong District, Chongqing 400016, China. Department of Cell Biology and Genetics, Institute of Molecular Medicine and Oncology, Chongqing Medical University, Medical School Road 1#, Yuzhong District, Chongqing 400016, China. Department of Cell Biology and Genetics, Institute of Molecular Medicine and Oncology, Chongqing Medical University, Medical School Road 1#, Yuzhong District, Chongqing 400016, China. Department of Cell Biology and Genetics, Institute of Molecular Medicine and Oncology, Chongqing Medical University, Medical School Road 1#, Yuzhong District, Chongqing 400016, China.
 Neuropsychological Therapy Centre (NTC), Faculty of Psychology, Ruhr University Bochum, Bochum, Germany. Neuropsychological Therapy Centre (NTC), Faculty of Psychology, Ruhr University Bochum, Bochum, Germany. Practice for Neuropsychology and Psychotherapy, Bochum, Germany. Department of Cognitive Psychology, Institute of Cognitive Neuroscience, Faculty of Psychology, Ruhr University Bochum, Bochum, Germany. Neuropsychological Therapy Centre (NTC), Faculty of Psychology, Ruhr University Bochum, Bochum, Germany.
 Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA. Electronic address: john.corboy@cuanschutz.edu. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. NYU MS Comprehensive Care Center, Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA. Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA. TGH Consulting, New York, NY, USA. The Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
 Service de Neurologie, CRCSEP, Unité de Recherche Clinique Cote d'Azur (UR2CA-URRIS), Centre Hospitalier Universitaire Pasteur 2, 30 Voie Romaine Cedex, Nice 06002, France. Electronic address: cohen.m@chu-nice.fr. Service de Radiologie, CRCSEP, Unité de Recherche Clinique Cote d'Azur (UR2CA-URRIS), Centre Hospitalier Universitaire Pasteur 2, 30 Voie Romaine Cedex, Nice 06002, France. Service de Neurologie, CRCSEP, Unité de Recherche Clinique Cote d'Azur (UR2CA-URRIS), Centre Hospitalier Universitaire Pasteur 2, 30 Voie Romaine Cedex, Nice 06002, France. Service de Neurologie, CRCSEP, Unité de Recherche Clinique Cote d'Azur (UR2CA-URRIS), Centre Hospitalier Universitaire Pasteur 2, 30 Voie Romaine Cedex, Nice 06002, France.
 Biogen Digital Health, Biogen, Cambridge, MA, USA. Electronic address: bastien.caba@biogen.com. TheraPanacea, Paris, France. TheraPanacea, Paris, France. Montreal Neurological Institute, McGill University, Montreal, QC, Canada; NeuroRx Research, Montreal, QC, Canada. NeuroRx Research, Montreal, QC, Canada. Biogen Digital Health, Biogen, Cambridge, MA, USA. Biogen Digital Health, Biogen, Cambridge, MA, USA. Biogen Digital Health, Biogen, Cambridge, MA, USA. Biogen Digital Health, Biogen, Cambridge, MA, USA. Biogen Digital Health, Biogen, Cambridge, MA, USA. CentraleSupélec, University of Paris-Saclay, Gif-sur-Yvette, France; TheraPanacea, Paris, France.
 Department of Neurology, Tamil Nadu Government Multi Super Speciality Hospital, Chennai, India. Department of Neurology, Tamil Nadu Government Multi Super Speciality Hospital, Chennai, India. Department of Audiology, All India Institute of Speech and Hearing, Mysuru, India. Department of Audiology, All India Institute of Speech and Hearing, Mysuru, India.
 Department of Neurology, Ibn Sina Hospital, Safat, Kuwait. dr.ismail.ibrahim2012@gmail.com. Department of Radiology, Ibn Sina Hospital, Safat, Kuwait. Diagnostic Radiology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
 Department of Medical Sciences, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Section Neurosciences, Department NEUROFARBA, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society, Via Operai 30, 16149, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. Faculty of Brain Sciences, Queen Square MS Centre, UCL Queen Square Institute of Neurology, UCL, London, UK. Biomedical Research Centre, National Institute for Health Research, University College London Hospitals, London, UK. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine & Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. Exercise Biology, Department of Public Health, Aarhus University, Dalgas Avenue 4, 8000, Aarhus, Denmark. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine & Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Faculty of Brain Sciences, Queen Square MS Centre, UCL Queen Square Institute of Neurology, UCL, London, UK. Faculty of Rehabilitation Sciences, REVAL, Hasselt University, Diepenbeek, Belgium. UMSC Hasselt, Pelt, Belgium. Faculty of Health, School of Health Professions, University of Plymouth, Devon, UK. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Psychiatry, University of Toronto and Sunnybrook Health Sciences Centre, Toronto, ON, M5R 3B6, Canada. Section on Statistical Planning and Analysis, Department of Neurology, UT Southwestern Medical Center, Dallas, TX, USA. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine & Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Department of Psychiatry, University of Toronto and Sunnybrook Health Sciences Centre, Toronto, ON, M5R 3B6, Canada. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Analysis Group, Inc., 111 Huntington Ave., 14th floor, Boston, MA 02199, United States of America. Electronic address: elyse.swallow@analysisgroup.com. Bristol Myers Squibb, 3401 Princeton Pike, Lawrence Township, NJ 08648, United States of America. Analysis Group, Inc., 111 Huntington Ave., 14th floor, Boston, MA 02199, United States of America. Analysis Group, Inc., 333 S. Hope St., #27, Los Angeles, CA 90071, United States of America. Analysis Group, Inc., 111 Huntington Ave., 14th floor, Boston, MA 02199, United States of America. Analysis Group, Inc., 111 Huntington Ave., 14th floor, Boston, MA 02199, United States of America. Bristol Myers Squibb, 3401 Princeton Pike, Lawrence Township, NJ 08648, United States of America. Bristol Myers Squibb, 3401 Princeton Pike, Lawrence Township, NJ 08648, United States of America.
 Brain Research Imaging Centre, Cardiff University, Cardiff, UK. Student Counselling and Wellbeing, University of Limerick, Limerick, Ireland. School of Social Science, Technological University of the Shannon IE, Athlone, Ireland. Health Research Board Clinical Research Facility, National University of Ireland Galway, Galway, Ireland. Discipline of Occupational Therapy, School of Health Sciences, National University of Ireland Galway, Galway, Ireland. Discipline of Occupational Therapy, School of Health Sciences, National University of Ireland Galway, Galway, Ireland.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department NEUROFARBA, Section Neurosciences, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. Exercise Biology, Department of Public Health, Aarhus University, Aarhus, Denmark. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. REVAL, Faculty of Rehabilitation Sciences, Hasselt University, Diepenbeek, Belgium. Faculty of Health, School of Health Professions, University of Plymouth, Plymouth, UK. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Psychiatry, University of Toronto and Sunnybrook Health Sciences Centre, Toronto, ON, Canada. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Department of Neurology, Section on Statistical Planning and Analysis, UT Southwestern Medical Center, Dallas, TX, USA. Kessler Foundation, West Orange, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Department of Psychiatry, University of Toronto and Sunnybrook Health Sciences Centre, Toronto, ON, Canada. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it.
 Department of Neurology, St. Josef-Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr University Bochum, Bochum, Germany.
 Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle WA, USA. Electronic address: linkk2@uw.edu. Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle WA, USA. Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle WA, USA; Department of Neurology, University of Washington School of Medicine, Seattle, WA, USA. Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle WA, USA.
 Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9. CLSC des Faubourgs, CIUSSS du Centre-Sud-de-l'Ile-de-Montréal, Montreal, QC, Canada. Department of Microbiology, Infectious Diseases, and Immunology and Department of Pediatrics, Université de Montréal, Centre de Recherche du Centre Hospitalier Universitaire Sainte-Justine (CHU Sainte-Justine), Montreal, Quebec, Canada. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9; MS-CHUM Clinic 900 St-Denis Street, Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9; MS-CHUM Clinic 900 St-Denis Street, Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9; MS-CHUM Clinic 900 St-Denis Street, Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9; MS-CHUM Clinic 900 St-Denis Street, Montreal, QC, Canada, H2X0A9. Department of Neurosciences, Université de Montréal and Centre de Recherche du CHUM (CRCHUM) 900 St-Denis Street Montreal, QC, Canada, H2X0A9. Electronic address: nathalie.arbour@umontreal.ca.
 Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Centre for Translational Research in Cancer, Sichuan Cancer Hospital and Institute, No.55 South Renmin Road, Chengdu, 610000, China. School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, China. Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, 610041, China. Centre for Translational Research in Cancer, Sichuan Cancer Hospital and Institute, No.55 South Renmin Road, Chengdu, 610000, China. Centre for Translational Research in Cancer, Sichuan Cancer Hospital and Institute, No.55 South Renmin Road, Chengdu, 610000, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, China. School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, 610000, China. Department of Neurology, West China Hospital, Sichuan University, No.28 Dianxin Nan Street, Chengdu, 610041, China. zhouhy@scu.edu.cn. Centre for Translational Research in Cancer, Sichuan Cancer Hospital and Institute, No.55 South Renmin Road, Chengdu, 610000, China. mu.yang@uestc.edu.cn. School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, China. mu.yang@uestc.edu.cn.
 Department of Occupational Therapy Education, School of Health Professions, University of Kansas Medical Center, Kansas City, KS, USA; Mobility Core, University of Kansas Center for Community Access, Rehabilitation Research, Education and Service, Kansas City, KS, USA. Electronic address: tzanotto@kumc.edu. Mobility Core, University of Kansas Center for Community Access, Rehabilitation Research, Education and Service, Kansas City, KS, USA; Department of Physical Therapy, Rehabilitation Science, and Athletic Training, School of Health Professions, University of Kansas Medical Center, Kansas City, KS, USA; MS Research Collaborative, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Crawford Research Institute, Shepherd Center, Atlanta, GA, USA. Department of Kinesiology and Community Health, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Occupational Therapy Education, School of Health Professions, University of Kansas Medical Center, Kansas City, KS, USA. Department of Physical Medicine and Rehabilitation, Michigan Medicine, University of Michigan, Ann Arbor, MI, USA. Department of Occupational Therapy, University of Illinois at Chicago, Chicago, IL, USA. MS Research Collaborative, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Department of Kinesiology and Community Health, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Center on Health, Aging and Disability, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
 Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland; Division of Radiological Physics, Department of Radiology, University Hospital Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Advanced Clinical Imaging Technology, Siemens Healthineers International AG, Lausanne, Switzerland. Advanced Clinical Imaging Technology, Siemens Healthineers International AG, Lausanne, Switzerland. Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Electronic address: cristina.granziera@usb.ch.
 Pirogov Russian National Research Medical University, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies» of the Federal Medical Biological Agency, Moscow, Russia.
 Department of Kinesiology, Health Promotion, and Recreation, University of North Texas, Denton, USA. Electronic address: stephanie.silveira@unt.edu. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Department of Neurology, Section on Statistical Planning and Analysis, University of Texas Southwestern, Dallas, TX, USA. Department of Neurology, Section on Statistical Planning and Analysis, University of Texas Southwestern, Dallas, TX, USA.
 School of Social Sciences, College of Health, Science and Society, University of the West of England, Bristol, United Kingdom. School of Health and Social Wellbeing, College of Health, Science and Society, University of the West of England, Bristol, United Kingdom. Faculty of Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom. School of Science, Department of Psychological Sciences, Birkbeck University of London, London, United Kingdom. School of Science, Department of Psychological Sciences, Birkbeck University of London, London, United Kingdom.
 Neuroimmunology Unit, Department of Neurology, Neurological Institute of Thailand, 312 Ratchathewi, Bangkok 10400, Thailand. Electronic address: Saharatau@hotmail.com. Neuroimmunology Unit, Department of Neurology, Neurological Institute of Thailand, 312 Ratchathewi, Bangkok 10400, Thailand.
 Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States. Electronic address: ccagna@kesslerfoundation.org. Center for Traumatic Brain Injury Research, Kessler Foundation, 120 Eagle Rock Avenue, Suite 100, East Hanover, NJ 07936, United States. Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States. Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States. Department of Psychology, Rutgers University - Newark, 101 Warren Street, Newark, NJ 07102, United States.
 Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Fırat University, Elazığ, Turkey. Electronic address: fzt.furkanbilek@gmail.com. Department of Nursing, Faculty of Health Sciences, Fırat University, Elazığ, Turkey. Department of Nursing, Faculty of Health Sciences, Istanbul Sabahattin Zaim University, Istanbul, Turkey.
 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. ricardoalonsohrm@gmail.com. Servicio de Neurología, Hospital Universitario Sanatorio Guemes, Buenos Aires, Argentina. ricardoalonsohrm@gmail.com. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. Servicio de Neurología, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, Hospital Universitario CEMIC, CABA, Argentina. Centro de Esclerosis Múltiple, Buenos Aires, Argentina. Instituto de Neurociencias de Fundación Favaloro E INECO, Buenos Aires, Argentina. Neurology Department, Neuroimmunology Unit, Hospital de Clinicas "José de San Martín", Buenos Aires, Argentina. Centro de Esclerosis Múltiple, Buenos Aires, Argentina. MS Unit Hospital Británico Buenos Aires, Buenos Aires, Argentina. IIPBA, FFyHUCCuyo, San Juan, Argentina. Instituto de Neurociencias de Fundación Favaloro E INECO, Buenos Aires, Argentina. Hospital Austral, Buenos Aires, Argentina. Servicio de Neurología, Hospital Universitario Sanatorio Guemes, Buenos Aires, Argentina. Hospital Enrique Tornú, CABA, Argentina. INECO Neurociencias Oroño, Santa Fe, Argentina. Sanatorio Anchorena, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. Instituto de Neurociencias Cognitivas y Traslacional (INCyT), Fundación INECO, Universidad Favaloro, CONICET, Buenos Aires, Argentina. Hospital Español de Rosario, Santa Fe, Argentina. Hospital Central de Mendoza, Mendoza, Argentina. Instituto de Neurociencias Rosario, Santa Fe, Argentina. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Ecarnerocontentti@hospitalaleman.com.
 Department of Neurology, Peking Union Medical College Hospital, 1 Shui Fu Yuan, Dongcheng District, Beijing 100730, China. Department of Neurology, Peking Union Medical College Hospital, 1 Shui Fu Yuan, Dongcheng District, Beijing 100730, China. Toronto Health Economics and Technology Assessment Collaborative, University of Toronto, Toronto, Canada. Department of Neurology, Peking Union Medical College Hospital, 1 Shui Fu Yuan, Dongcheng District, Beijing 100730, China. Electronic address: xuyanpumch@hotmail.com.
 Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Ostrava, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic. Department of Laboratory Medicine, University Hospital Brno, Brno, Czech Republic. Department of Imaging Methods, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. Department of Clinical Biochemistry, Institute of Laboratory Medicine, University Hospital Ostrava, Ostrava, Czech Republic. Institute of Laboratory Medicine, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic.
 Department of Neurology, Neurology A-205, MC-2030, University of Chicago Medicine, Chicago, Illinois, USA. Department of Neurology, Neurology A-205, MC-2030, University of Chicago Medicine, Chicago, Illinois, USA. Department of Neurology, Neurology A-205, MC-2030, University of Chicago Medicine, Chicago, Illinois, USA. Department of Neurology, Neurology A-205, MC-2030, University of Chicago Medicine, Chicago, Illinois, USA. Department of Neurology, Neurology A-205, MC-2030, University of Chicago Medicine, Chicago, Illinois, USA.
 Biogen, Cambridge, MA, USA. tammy.jiang@biogen.com. Center of Clinical Neuroscience, Carl Gustav Carus University Hospital, Dresden, Germany. Hope Neurology MS Center, Knoxville, TN, USA. Biogen, Cambridge, MA, USA. Biogen, Upplands-Väsby, Sweden. Biogen, Cambridge, MA, USA. Biogen, Baar, Switzerland. University of Ottawa, Ottawa, ON, Canada.
 Department of Internal Medicine, St. Vincent Charity Medical Center, Cleveland, OH.
 Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands a.toorop@amsterdamumc.nl. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Biologics Laboratory, Department of Immunopathology, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Department of Neurology, Ommelander Hospital Groningen, Scheemda, The Netherlands. Department of Neurology, Medical Centre Leeuwarden, Leeuwarden, The Netherlands. Department of Neurology, Canisius Wilhelmina Hospital, Nijmegen, The Netherlands. Department of Neurology, Slingeland Hospital, Doetinchem, The Netherlands. Department of Neurology, Elisabeth-TweeSteden Hospital, Tilburg, The Netherlands. Department of Neurology, Alrijne Hospital, Leiden, The Netherlands. Department of Epidemiology and Data Science, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Biologics Laboratory, Department of Immunopathology, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Landsteiner Laboratory, Amsterdam UMC Location AMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands.
 Pathology and Laboratory Medicine, The Aga Khan University, Karachi, Pakistan. Pathology and Laboratory Medicine, The Aga Khan University, Karachi, Pakistan sibtain.ahmed@aku.edu. Pathology and Laboratory Medicine, The Aga Khan University, Karachi, Pakistan. Pathology and Laboratory Medicine, The Aga Khan University, Karachi, Pakistan. Biostatistics Master's Program, State University of Maringá, Maringa, Brazil. Pathology and Laboratory Medicine, The Aga Khan University, Karachi, Pakistan. Pathology and Laboratory Medicine, The Aga Khan University, Karachi, Pakistan.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Electronic address: suzi.claflin@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia.
 Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Clinical Immunology and Allergology, University Hospital Hradec Králové, Hradec Králové, Czech Republic. Department of Clinical Immunology and Allergology, University Hospital Hradec Králové, Hradec Králové, Czech Republic. Department of Clinical Immunology and Allergology, University Hospital Hradec Králové, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Neurology, University Hospital and Masaryk University, Brno, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Plzen, Charles University in Prague, Plzeň, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic.
 Neurology Department, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran. Iranian Center of Neurological Research, Neuroscience Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran. Iranian Center of Neurological Research, Neuroscience Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran. Iranian Center of Neurological Research, Neuroscience Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences, Tehran, Iran. Iranian Center of Neurological Research, Neuroscience Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Leeds Centre for Neurosciences, Leeds teaching Hospitals NHS Trust, Leeds, UK. Centre of Neuroscience, Department of Medicine, Imperial College London, London, UK. Hillingdon and Imperial NHS Trust, London, UK. Department of Neurology, Nottingham University Hospitals NHS Trust, Mental Health and Clinical Neuroscience Academic Unit, University of Nottingham School of Medicine, Nottingham, UK. Barts and the London Genome Centre, Queen Mary University of London, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Bradford Teaching Hospital Foundation Trust, Bradford, UK. Manchester Centre for Clinical Neurosciences, Northern Care Alliance NHS Trust, Manchester, UK. Research and Innovation, Queen's Hospital, BHRUT, London, UK. Kings College Hospital and Lewisham and Greenwich NHS Trusts, London, UK. Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK. Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK. Department of Clinical Neurology, University Hospital of Wales, Cardiff, UK. Barts and the London Genome Centre, Queen Mary University of London, London, UK. Leeds Centre for Neurosciences, Leeds teaching Hospitals NHS Trust, Leeds, UK. University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK. Leeds Centre for Neurosciences, Leeds teaching Hospitals NHS Trust, Leeds, UK. Northern Care Alliance NHS Trust, Manchester, UK. Hillingdon and Imperial NHS Trust, Uxbridge, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Northern Care Alliance NHS Trust, Manchester, UK. Department of Neurology, University Hospital of Wales, Cardiff, UK. Population Data Science, Swansea University Medical School, Swansea, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Mid and South Essex NHS Foundation Trust, Southend-on-Sea, UK. Leeds Centre for Neurosciences, Leeds teaching Hospitals NHS Trust, Leeds, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Department of neuroscience, Queen's Hospital, BHRUT NHS Trust, Romford, UK. Queen Elizabeth Hospital (Lewisham and Greenwich NHS Trust), London, UK. Department of Neurology, Nottingham University Hospitals NHS Trust; Mental Health and Clinical Neuroscience Academic Unit, University of Nottingham School of Medicine, Nottingham, UK. Northern Care Alliance NHS Trust, Manchester, UK. Bradford Teaching Hospital Foundation Trust, Bradford, UK. Research and Innovation, Queen's Hospital, BHRUT, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Department of Neurology, Nottingham University Hospitals NHS Trust; Mental Health and Clinical Neuroscience Academic Unit, University of Nottingham School of Medicine, Nottingham, UK. Lancashire Teaching Hospital NHS Foundation Trust, Preston, UK. Population Data Science, Swansea University Medical School, Swansea, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Bradford Teaching Hospital Foundation Trust, Bradford, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Lancashire Teaching Hospital NHS Foundation Trust, Preston, UK. Lancashire Teaching Hospital NHS Foundation Trust, Preston, UK. Mid and South Essex NHS Foundation Trust, Southend-on-Sea, UK. Northern Care Alliance NHS Trust, Manchester, UK. University of Cambridge, Department of Clinical Neuroscience, Addenbrookes Hospital, Hills Road, Cambridge, UK. University Hospitals of Coventry and Warwickshire, Coventry, UK. Research and Innovation, Queen's Hospital, BHRUT, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Northern Care Alliance NHS Trust, Manchester, UK. St George's University Hospitals NHS Foundation Trust, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Kings College Hospital and Lewisham and Greenwich NHS Trusts, London, UK. Department of Clinical and Movement Neuroscience, UCL Queen Square Institute of Neurology, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK ruth.dobson@qmul.ac.uk.
 Discipline of Occupational Therapy, School of Health Sciences, National University of Ireland Galway, Galway, Ireland. Health Research Board Clinical Research Facility, National University of Ireland Galway, Galway, Ireland. Discipline of Occupational Therapy, School of Health Sciences, National University of Ireland Galway, Galway, Ireland. Department of Neurology, University Hospital Galway, Galway, Ireland. Qualitative Research Trials Centre (QUESTS), School of Nursing & Midwifery, National University of Ireland Galway, Galway, Ireland. Discipline of Occupational Therapy, School of Health Sciences, National University of Ireland Galway, Galway, Ireland. sinead.hynes@nuigalway.ie.
 Instituto Superior Miguel Torga, Coimbra, Portugal. Center for Research in Neuropsychology and Cognitive and Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Instituto Superior Miguel Torga, Coimbra, Portugal. Instituto Superior Miguel Torga, Coimbra, Portugal. Center for Research in Neuropsychology and Cognitive and Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Lusófona University, HEI-Lab: Digital Human-Environment Interaction Lab, Lisbon, Portugal.
 Department of Clinical Pharmacy, College of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan. Department of Clinical Pharmacy, College of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan.
 Tisch Multiple Sclerosis Research Center of New York, New York, New York, United States of America. Tisch Multiple Sclerosis Research Center of New York, New York, New York, United States of America. Tisch Multiple Sclerosis Research Center of New York, New York, New York, United States of America. Tisch Multiple Sclerosis Research Center of New York, New York, New York, United States of America. Tisch Multiple Sclerosis Research Center of New York, New York, New York, United States of America.
 From the Division of Neurogenetics (A.J., C.S., N.J.A.), Department of Neurology, NYU Grossman School of Medicine; Lincoln Memorial University DeBusk College of Osteopathic Medicine (A.J.), Harrogate, TN; Multiple Sclerosis Comprehensive Care Center (V.P.A., I.K.), Department of Neurology; and Division of Neuroradiology (M.J.B.), Department of Radiology, NYU Grossman School of Medicine, New York,. From the Division of Neurogenetics (A.J., C.S., N.J.A.), Department of Neurology, NYU Grossman School of Medicine; Lincoln Memorial University DeBusk College of Osteopathic Medicine (A.J.), Harrogate, TN; Multiple Sclerosis Comprehensive Care Center (V.P.A., I.K.), Department of Neurology; and Division of Neuroradiology (M.J.B.), Department of Radiology, NYU Grossman School of Medicine, New York,. From the Division of Neurogenetics (A.J., C.S., N.J.A.), Department of Neurology, NYU Grossman School of Medicine; Lincoln Memorial University DeBusk College of Osteopathic Medicine (A.J.), Harrogate, TN; Multiple Sclerosis Comprehensive Care Center (V.P.A., I.K.), Department of Neurology; and Division of Neuroradiology (M.J.B.), Department of Radiology, NYU Grossman School of Medicine, New York,. From the Division of Neurogenetics (A.J., C.S., N.J.A.), Department of Neurology, NYU Grossman School of Medicine; Lincoln Memorial University DeBusk College of Osteopathic Medicine (A.J.), Harrogate, TN; Multiple Sclerosis Comprehensive Care Center (V.P.A., I.K.), Department of Neurology; and Division of Neuroradiology (M.J.B.), Department of Radiology, NYU Grossman School of Medicine, New York,. From the Division of Neurogenetics (A.J., C.S., N.J.A.), Department of Neurology, NYU Grossman School of Medicine; Lincoln Memorial University DeBusk College of Osteopathic Medicine (A.J.), Harrogate, TN; Multiple Sclerosis Comprehensive Care Center (V.P.A., I.K.), Department of Neurology; and Division of Neuroradiology (M.J.B.), Department of Radiology, NYU Grossman School of Medicine, New York,. From the Division of Neurogenetics (A.J., C.S., N.J.A.), Department of Neurology, NYU Grossman School of Medicine; Lincoln Memorial University DeBusk College of Osteopathic Medicine (A.J.), Harrogate, TN; Multiple Sclerosis Comprehensive Care Center (V.P.A., I.K.), Department of Neurology; and Division of Neuroradiology (M.J.B.), Department of Radiology, NYU Grossman School of Medicine, New York,. nicolas.abreu@nyulangone.org.
 Translational Immunology Research Program, University of Helsinki, Helsinki, Finland. Department of Neurology, HUS Brain Center, Hyvinkää Hospital, Hyvinkää, Finland. Medical Imaging Center, Helsinki University Hospital, Helsinki, Finland. Department of Neurology, HUS Brain Center, Helsinki University Hospital, Helsinki, Finland. Department of Clinical Neurosciences, University of Helsinki, Helsinki, Finland. Translational Immunology Research Program, University of Helsinki, Helsinki, Finland. Department of Neurology, HUS Brain Center, Helsinki University Hospital, Helsinki, Finland. Translational Immunology Research Program, University of Helsinki, Helsinki, Finland. Department of Neurology, HUS Brain Center, Helsinki University Hospital, Helsinki, Finland.
 Neuroscience Program, University of Illinois Urbana-Champaign, Urbana, IL. Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, Urbana, IL. Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, Urbana, IL. Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, Urbana, IL. Department of Food Science and Human Nutrition, Division of Nutritional Sciences, University of Illinois Urbana-Champaign, Urbana, IL; Division of Nutritional Sciences, University of Illinois Urbana-Champaign, Urbana, IL. Department of Health Sciences, University of Colorado Colorado Springs, Colorado Springs, CO. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL. Neuroscience Program, University of Illinois Urbana-Champaign, Urbana, IL; Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, Urbana, IL; Division of Nutritional Sciences, University of Illinois Urbana-Champaign, Urbana, IL; Beckman Institute for Advanced Science and Technology, University of Illinois Urbana-Champaign, Urbana, IL. Electronic address: nakhan2@illinois.edu.
 Sanofi, 450 Water Street, Cambridge, MA, USA. Nupur.Greene@sanofi.com. Modus Outcomes, A Division of THREAD, Lyon, France. Sanofi, 450 Water Street, Cambridge, MA, USA. Modus Outcomes, A Division of THREAD, Lyon, France. Modus Outcomes, A Division of THREAD, Lyon, France. Modus Outcomes, A Division of THREAD, Lyon, France. Modus Outcomes, A Division of THREAD, Lyon, France. Sanofi, 450 Water Street, Cambridge, MA, USA.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Mater Research Institute, Translational Research Institute, Woolloongabba, Queensland, Australia. Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, USA. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Neuroepidemiology Unit, The University of Melbourne School of Population and Global Health, Melbourne, Victoria, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. School of Medicine, Griffith University, Gold Coast, Queensland, Australia. Murdoch Children's Research Institute, Royal Children's Hospital, University of Melbourne, Parkville, Victoria, Australia. Neuroepidemiology Group, The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia Yuan.Zhou@utas.edu.au.
 NeuroRx Research, Montreal, QC, Canada. Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada/McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, Montreal, QC, Canada/Department of Biomedical Engineering, McGill University, Montreal, QC, Canada. NeuroRx Research, Montreal, QC, Canada/Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. NeuroRx Research, Montreal, QC, Canada/Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada/McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, Montreal, QC, Canada/Department of Biomedical Engineering, McGill University, Montreal, QC, Canada. NeuroRx Research, Montreal, QC, Canada/Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA.
 Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. Department of Radiology and Imaging Sciences, Emory University School of Medicine, 1364 Clifton Road NE, Suite BG20, Atlanta, GA, 30322, USA. ranliang.hu@emory.edu.
 Mellen Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
 Novartis Pharma AG, Basel, Switzerland. Electronic address: gustavo.seifer@gmail.com. Department of Neurosciences, University Hospitals of Coventry and Warwickshire, Level 4, Central Wing, Coventry CV2 2DX, UK. Department of Neurology, Central Lisbon University Hospital Centre, Lisbon, Portugal. Department of Neurology, University Hospital Ghent, Ghent, Belgium. Adelphi Real World, Manchester, UK. Novartis Global Service Center, Dublin, Ireland. Medical Affairs, Astellas Gene Therapies, San Francisco, US. Novartis Pharma AG, Basel, Switzerland. Department of Translational Biomedicine and Neuroscience, University of Bari Aldo Moro, Bari, Italy.
 Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Cell Therapy and Transfusion Medicine Unit, Careggi University Hospital, Florence, Italy. Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Cell Therapy and Transfusion Medicine Unit, Careggi University Hospital, Florence, Italy. Cell Therapy and Transfusion Medicine Unit, Careggi University Hospital, Florence, Italy. Neuroradiology Unit, Careggi University Hospital, Florence, Italy. Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy. Cell Therapy and Transfusion Medicine Unit, Careggi University Hospital, Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy.
 Department of Neurology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil. Department of Neurology, Pontifícia Universidade Católica de São Paulo, São Paulo, Brazil. Department of Neurosurgery, Hospital Saúde, Caxias do Sul, Rio Grande do Sul, Brazil. Department of Internal Medicine, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil. Faculty of Medicine, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos 2400, Bairro Santa Cecília, Porto Alegre, RS, CEP 90035-002, Brazil. cpiccini.md@gmail.com. Department of Neurology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.
 Department of Medicine, The University of Melbourne, Parkville, VIC 3050, Australia; School of Allied Health, Human Services and Sport, La Trobe University, Bundoora, VIC 3086, Australia. Electronic address: e.cofrelizama@latrobe.edu.au. Department of Medicine, The University of Melbourne, Parkville, VIC 3050, Australia. School of Mathematics and Statistics, The University of Melbourne, Parkville, VIC 3050, Australia. Department of Mechanical Engineering, The University of Melbourne, Parkville, VIC 3010, Australia. CORe, Department of Medicine, The University of Melbourne, Parkville, VIC 3050, Australia; Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Australia. Department of Medicine, The University of Melbourne, Parkville, VIC 3050, Australia; Australian Rehabilitation Research Centre, Royal Park Campus, Parkville, VIC 3052, Australia.
 Goethe University Frankfurt, University Hospital, Institute of Neuroradiology, Germany. Electronic address: katharina.wenger@kgu.de. Goethe University Frankfurt, University Hospital, Institute of Neuroradiology, Germany. Goethe University Frankfurt, University Hospital, Department of Neurology, Germany. Goethe University Frankfurt, University Hospital, Department of Neurology, Germany. Goethe University Frankfurt, University Hospital, Institute of Neuroradiology, Germany. Department of Neurology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. Department of Neurology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. Goethe University Frankfurt, University Hospital, Institute of Neuroradiology, Germany. Goethe University Frankfurt, University Hospital, Department of Neurology, Germany. Goethe University Frankfurt, University Hospital, Department of Neurology, Germany; Department of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
 School of Dentistry, The University of Queensland, Brisbane, Queensland, Australia. School of Dentistry, The University of Queensland, Brisbane, Queensland, Australia. Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia. Mater Centre for Neuroscience, Mater Hospital, Brisbane, Queensland, Australia. Surgical, Treatment and Rehabilitation Service (STARS), Metro North Hospital and Health Service, Queensland Health, Brisbane, Australia. Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia. Mater Centre for Neuroscience, Mater Hospital, Brisbane, Queensland, Australia. School of Psychology, The University of Queensland, Brisbane, Queensland, Australia.
 Departamento de Neurologia. Hospital Cesar Milstein, Buenos Aires, Argentina. Departamento de Neurologia. Hospital Cesar Milstein, Buenos Aires, Argentina. Departamento de Neurologia. Hospital Cesar Milstein, Buenos Aires, Argentina. Departamento de Neurologia. Hospital Cesar Milstein, Buenos Aires, Argentina. Departamento de Neurologia. Hospital Cesar Milstein, Buenos Aires, Argentina. Servicio de Neurología, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Centro de esclerosis múltiple de Buenos Aires, CABA, Buenos Aires, Argentina. Centro de Investigaciones Diabaid, CABA. Sección de Neuroinmunología y Enfermedades Desmielinizantes, Servicio de Neurología, Hospital de Clínicas José de San Martín, CABA. Departamento de Enfermedades desmielinizantes - Sanatorio Allende, Córdoba. Centro Universitario de Esclerosis Múltiple. Hospital Ramos Mejía, CABA. Centro Universitario de Esclerosis Múltiple. Hospital Ramos Mejía, CABA. Centro Universitario de Esclerosis Múltiple. Hospital Ramos Mejía, CABA. Centro Universitario de Esclerosis Múltiple. Hospital Ramos Mejía, CABA. Departamento de Neurología - FLENI, CABA. Departamento de Neurología - FLENI, CABA. Departamento de Neurología - FLENI, CABA. Departamento de Neurología - FLENI, CABA. Servicio de Neurología - Hospital San Bernardo, Salta. Sanatorio Güemes, CABA. Sección de Enfermedades Desmielinizantes - Hospital Británico, CABA. Predigma/Posadas/Argentina, Posadas, Argentina. Hospital de Agudos, Dr. Teodoro Álvarez, CABA. Sección de Enfermedades Desmielinizantes - Hospital Británico, CABA. INECO Neurociencias Oroño, Rosario, Santa Fe. Servicio de Neurología, Hospital Carlos G Durand, Buenos Aires, Argentina. Hospital de Clínicas Nuestra Señora del Carmen, Tucuman, Argentina. Hospital de Agudos, Dr. Teodoro Álvarez, CABA. Neuroimmunology Unit, Department of Neurosciences, Hospital Alemán, Buenos Aires, Argentina. Clínica Universitaria Reina Fabiola, Córdoba. Servicio de Neurología - Hospital Córdoba, Córdoba. Hospital Presidente Perón de Avellaneda, Avellaneda, Argentina. Neurocomp, Buenos Aires, Argentina. Clínica Universitaria Reina Fabiola, Córdoba. Instituto Lennox, Córdoba. Sección de Enfermedades Desmielinizantes - Hospital Británico, CABA. Sección de Enfermedades Desmielinizantes - Hospital Británico, CABA. Servicio de Neurología, Hospital Posadas, Buenos Aires, Argentina. Sección de Neuroinmunología y Enfermedades Desmielinizantes, Servicio de Neurología, Hospital de Clínicas José de San Martín, CABA. Neuroimmunology Unit, Department of Neurosciences, Hospital Alemán, Buenos Aires, Argentina. Hospital San Martín, Paraná, Entre Ríos. Hospital Español, Rosario, Santa Fe. Hospital Ramón Santamarina, Tandil, Argentina. Hospital Central de Mendoza, Mendoza. Fundación Sinapsis, Santa Rosa, Argentina. Fundación Sinapsis, Santa Rosa, Argentina. Sección de Enfermedades Desmielinizantes - Hospital Británico, CABA. Sanatorio Británico, Rosario, Santa Fe. Hospital Español de la Plata, Buenos Aires, Argentina. Hospital Militar Campo de Mayo, Buenos Aires, Argentina. Hospital Universitario Fundación Favaloro, Buenos Aires, Argentina. Hospital Central de Mendoza, Mendoza. Instituto de Neurociencias de Rosario, Santa Fe. Servicio de clínica médica, Hospital Italiano de Buenos Aires, CABA. Centro de esclerosis múltiple de Buenos Aires, CABA, Buenos Aires, Argentina. Servicio de Neurología, Hospital Universitario de CEMIC, CABA. Departamento de Neurologia. Hospital Cesar Milstein, Buenos Aires, Argentina.
 Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia; Faculty of Medicine and Health, University of New South Wales, Sydney, Australia. Electronic address: y.okubo@neura.edu.au. Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia; Faculty of Medicine and Health, University of New South Wales, Sydney, Australia. Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia. Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia. Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia. Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia; Faculty of Medicine and Health, University of New South Wales, Sydney, Australia. Falls, Balance, and Injury Research Centre, Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker Street Randwick, Sydney, NSW, 2031 Australia; Faculty of Medicine and Health, University of New South Wales, Sydney, Australia.
 Neurology department, University Hospital of Rennes, CIC1414 INSERM, CRC-SEP, Rennes, France. Electronic address: Simon.LAMY@chu-rennes.fr. Epidemiology and Public Health Department, University Hospital of Rennes, Rennes, France. Healthcare-at-home service, HAD35, Rennes, France. Neurology department, University Hospital of Rennes, CIC1414 INSERM, CRC-SEP, EMPENN research unit (U 1228, université de Rennes 1, INSERM, CNRS, INRIA), Rennes, France. Neurology department, University Hospital of Rennes, CIC1414 INSERM, CRC-SEP, Rennes, France. Epidemiology and Public Health Department, University Hospital of Rennes, Rennes, France. Epidemiology and Public Health Department, University Hospital of Rennes, Rennes, France. Neurology department, University Hospital of Rennes, CIC1414 INSERM, CRC-SEP, Rennes, France. Neurology department, University Hospital of Rennes, CIC1414 INSERM, CRC-SEP, Rennes, France.
 Department of Neurology, The University of Wisconsin, 600 Highland Ave, Madison, WI, USA. Electronic address: abuaf@neurology.wisc.edu. Department of Neurology, The University of Chicago, Chicago, IL, USA. Department of Psychiatry and Behavioral Neuroscience, The University of Chicago, Chicago, IL, USA. Department of Radiology, The University of Chicago, Chicago, IL, USA. Department of Neurology, The University of Chicago, Chicago, IL, USA. Department of Neurology, The University of Chicago, Chicago, IL, USA.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it.
 Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Theodor-Kutzer-Ufer 1 - 3, 68167 Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Theodor-Kutzer-Ufer 1 - 3, 68167 Mannheim, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1; Gebäude A1, Westturm, Ebene 5, 48149 Münster, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Theodor-Kutzer-Ufer 1 - 3, 68167 Mannheim, Germany; German Consortium of Translational Cancer Research (DKTK), Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Theodor-Kutzer-Ufer 1 - 3, 68167 Mannheim, Germany; Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Theodor-Kutzer-Ufer 1 - 3, 68167 Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Theodor-Kutzer-Ufer 1 - 3, 68167 Mannheim, Germany. Electronic address: philipp.eisele@medma.uni-heidelberg.de.
 Department of Neurology, Faculty of Medicine, Tekirdag Namık Kemal University, Kampus street,.Süleymanpasa, Tekirdag 59100, Turkey. Department of Neurology, Faculty of Medicine, Tekirdag Namık Kemal University, Kampus street,.Süleymanpasa, Tekirdag 59100, Turkey. Electronic address: aysuneu@yahoo.com. Department of Neurology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey. Bakırköy Research and Training Hospital, Istanbul, Turkey. Department of Neurology, Ondokuz Mayıs University, Samsun, Turkey. Department of Neurology, Faculty of Medicine, Sakarya University, Sakarya, Turkey. Department of Neurology, Faculty of Medicine, Dicle University, Diyarbakir, Turkey. Department of Neurology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey. Department of Neurology, Faculty of Medicine, Trakya University, Edirne, Turkey. Department of Neurology, Faculty of Medicine, Bursa Uludag University, Bursa, Turkey. Bilim University, Florence Nightingale Hospital, Istanbul, Turkey. Haseki Research and Training Hospital, Istanbul, Turkey. Department of Neurology, Faculty of Medicine, Tekirdag Namık Kemal University, Kampus street,.Süleymanpasa, Tekirdag 59100, Turkey. Department of Neurology, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey. Department of Neurology, Faculty of Medicine, Marmara University, Istanbul, Turkey. Department of Neurology, Faculty of Medicine, Marmara University, Istanbul, Turkey. Department of Neurology, Faculty of Medicine, Marmara University, Istanbul, Turkey. Davranis Degisim Akademisi, Istanbul, Turkey.
 Clinical Pharmacology and Pharmacogenomics Research Group, Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt. Clinical Pharmacology and Pharmacogenomics Research Group, Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt. Department of Neurology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt. Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Clinical Pharmacology and Pharmacogenomics Research Group, Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo, Egypt.
 Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Center for Biomedical Imaging at Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. IRCCS, Fondazione Don Carlo Gnocchi ONLUS, Milan, Italy. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Wayne State University, Detroit, MI, USA. University of Nebraska Medical Center, Omaha, NE, USA. Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. Negroski Neurology, LLP, Sarasota, Sarasota, FL, USA. Michigan Institute for Neurological Disorders (MIND), Farmington Hills, MI, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. rzivadinov@bnac.net. Center for Biomedical Imaging at Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. rzivadinov@bnac.net.
 Department of Clinical Neuroscience, Division of Insurance Medicine, Karolinska Institutet, Stockholm 171 77, Sweden. Electronic address: fitsum.teni@ki.se. Department of Clinical Neuroscience, Division of Insurance Medicine, Karolinska Institutet, Stockholm 171 77, Sweden. Department of Clinical Neuroscience, Division of Insurance Medicine, Karolinska Institutet, Stockholm 171 77, Sweden. Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm 171 77, Sweden. Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm 171 77, Sweden. Institute of Health and Care Sciences, Sahlgrenska Academy, University of Gothenburg, Box 457, Gothenburg 405 30, Sweden. Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm 171 77, Sweden. Department of Clinical Neuroscience, Division of Insurance Medicine, Karolinska Institutet, Stockholm 171 77, Sweden. Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Stockholm 171 77, Sweden. Department of Clinical Neuroscience, Division of Insurance Medicine, Karolinska Institutet, Stockholm 171 77, Sweden.
 Interdisciplinary College of Engineering Medicine, Texas A&M, Bryan, Texas, USA. Interdisciplinary College of Engineering Medicine, Texas A&M, Bryan, Texas, USA. Interdisciplinary College of Engineering Medicine, Texas A&M, Bryan, Texas, USA. College of Medicine, Texas A&M, Bryan, Texas, USA. Department of Radiology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA. Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA. Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, USA. Translational Imaging Core, Houston Methodist Research Institute, Houston, Texas, USA. Department of Urology, Houston Methodist Hospital, Houston, Texas, USA. Department of Urology, Houston Methodist Hospital, Houston, Texas, USA.
 MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. Queen Square Institute of Neurology and Centre for Medical Image Computing, University College London, London, UK. Departments of Clinical Neurosciences and Community Health Sciences, University of Calgary, Calgary, Alberta, Canada. Department of Neurology, Rijnstate Hospital, Arnhem, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, Amsterdam, the Netherlands.
 Department of Ophthalmology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 24, 8091, Zurich, Switzerland. Department of Ophthalmology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 24, 8091, Zurich, Switzerland. Department of Neurology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland. Department of Otorhinolaryngology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 24, 8091, Zurich, Switzerland. Department of Neuroradiology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 24, 8091, Zurich, Switzerland. Department of Neuroradiology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 24, 8091, Zurich, Switzerland. Radiologie und Neuroradiologie am Glattzentrum, Industriestrasse 63, 8304, Wallisellen, Switzerland. Department of Ophthalmology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 24, 8091, Zurich, Switzerland. konrad.weber@usz.ch. Department of Neurology, University Hospital Zurich, University of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland. konrad.weber@usz.ch.
 Kahramanmaraş Sutçu Imam University, Faculty of Health Science, Department of Physiotherapy and Rehabilitation, Kahramanmaras, Turkey. Electronic address: ipekkatirci@hotmail.com. Kahramanmaraş Sutçu Imam University, Faculty of Health Science, Department of Physiotherapy and Rehabilitation, Kahramanmaras, Turkey. Kahramanmaraş Sutçu Imam University, Faculty of Health Science, Department of Physiotherapy and Rehabilitation, Kahramanmaras, Turkey. Kahramanmaraş Sutçu Imam University, Faculty of Health Science, Department of Physiotherapy and Rehabilitation, Kahramanmaras, Turkey. Kahramanmaras Sutcu Imam University, Faculty of Medicine, Kahramanmaras, Turkey. Kahramanmaras Sutcu Imam University, Faculty of Medicine, Kahramanmaras, Turkey.
 School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: i.adibi@gmail.com. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: mehdi.sanayei@gmail.com.
 Department of Neurology and Neurological Science, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan. Department of Neurology and Neurological Science, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan. Radiology Center, Division of Integrated Facilities, Tokyo Medical and Dental University Hospital, Tokyo, Japan. Department of Neurology and Neurological Science, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan. Department of Neurology and Neurological Science, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan. Department of Neurology and Neurological Science, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan.
 Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. anna.pietroboni@policlinico.mi.it. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. University of Milan, Milan, Italy. Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. University of Milan, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. University of Milan, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Politecnico di Milano, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. University of Milan, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122, Milan, Italy. University of Milan, Milan, Italy.
 Centro Universitario de Esclerosis Múltiple (CUEM), Hospital JM Ramos Mejía, Buenos Aires, Argentina; Sección Enfermedades Desmielinizantes, Hospital Italiano de Buenos Aires, Argentina. Electronic address: berenice.silva@gmail.com. Unidad de Neuroinmunología, Departamento de Neurociencias, Hospital Alemán de Buenos Aires, Argentina. Hospital São Lucas - Pontifícia Universidade Católica do Rio Grande do Sul, Brazil. Sección Zoopatología y Parasitología Médica, Hospital Muñiz, Buenos Aires, Argentina. Hospital Militar Escuela Managua, Nicaragua. Clínica Alemana y Universidad del Desarrollo, Santiago, Chile. Centro Universitario de Esclerosis Múltiple (CUEM), Hospital JM Ramos Mejía, Buenos Aires, Argentina. Hospital Santo Tomas, Panama. Departamento de Neurología, Hospital IMT, Paraguay; Departamento de Neurología de Diagnostico, Codas Thompson, Paraguay. Departamento De Neurociencias, CUCS, Universidad De Guadalajara, México. Clínica Enfermedad Desmielinizantes, Clinica Universitaria Colombia, Colombia. Servicio de Infectología, Sanatorio Güemes, Buenos Aires, Argentina. Service of Neurology, Hospital Universitario CEMIC, Buenos Aires, Argentina; Centro de Esclerosis Múltiple de Buenos Aires (CEMBA), Buenos Aires, Argentina. CIEN, FLENI, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple (CUEM), Hospital JM Ramos Mejía, Buenos Aires, Argentina; Servicio de Neurología, Sanatorio Güemes, Buenos Aires, Argentina. Unidad de Neuroinmunología, Departamento de Neurociencias, Hospital Alemán de Buenos Aires, Argentina.
 Department of Ophthalmology, Queen Elizabeth Hospital, Adelaide, Australia. Department of Ophthalmology, Queen Elizabeth Hospital, Adelaide, Australia.
 Hospital Queen Elizabeth, Kota Kinabalu, Sabah, Malaysia. Hospital Queen Elizabeth, Kota Kinabalu, Sabah, Malaysia. Hospital Queen Elizabeth, Kota Kinabalu, Sabah, Malaysia. Universiti Malaysia Sarawak (UNIMAS), Kota Samarahan, Sarawak, Malaysia. ltlim@unimas.my.
 Altai State Medical University, Barnaul, Russia. Altai State Medical University, Barnaul, Russia. Altai State Medical University, Barnaul, Russia. Altai State Medical University, Barnaul, Russia.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. American Sports Medicine Institute, Birmingham, AL, USA. Kessler Foundation, West Orange, NJ, USA. Interdisciplinary School of Health Sciences, University of Ottawa, Ottawa, ON, Canada. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. Center for Innovation and Applied Research, Urbana, IL, USA. Program in Exercise Science, Department of Physical Therapy, Marquette University, Milwaukee, WI, USA.
 Department of Primary Care and Public Health, Imperial College London, London, United Kingdom; Department of Public Health, Federico II University of Naples, Naples, Italy. Department of Public Health, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, via Sergio Pansini 5, Naples 80131, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, via Sergio Pansini 5, Naples 80131, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, via Sergio Pansini 5, Naples 80131, Italy. Department of Public Health, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, via Sergio Pansini 5, Naples 80131, Italy. Department of Primary Care and Public Health, Imperial College London, London, United Kingdom; Department of Public Health, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, via Sergio Pansini 5, Naples 80131, Italy. Electronic address: marcello.moccia@unina.it.
 Biogen, 225 Binney Street, Cambridge, MA 02142, USA. Electronic address: phoebe.jiang@biogen.com. Biogen, 225 Binney Street, Cambridge, MA 02142, USA. Biogen, 225 Binney Street, Cambridge, MA 02142, USA. NeuroRx Research, Montreal, Quebec, Canada; McGill University, Montreal, Quebec, Canada. NeuroRx Research, Montreal, Quebec, Canada. Biogen, 225 Binney Street, Cambridge, MA 02142, USA. Biogen, 225 Binney Street, Cambridge, MA 02142, USA. Biogen, 225 Binney Street, Cambridge, MA 02142, USA. Biogen, 225 Binney Street, Cambridge, MA 02142, USA.
 Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy. Electronic address: silvia.miante@gmail.com. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy; Padova Neuroscience Centre (PNC), University of Padua, Padua, Italy. Padova Neuroscience Centre (PNC), University of Padua, Padua, Italy; Department of Information Engineering, University of Padua, Padua, Italy. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy. DISSAL, Department of Health Science, University of Genoa, Genoa, Italy. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy. Padova Neuroscience Centre (PNC), University of Padua, Padua, Italy; Department of Information Engineering, University of Padua, Padua, Italy. Institute for Next Generation Healthcare, Icahn School of Medicine at Mount Sinai, NY. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy. Padova Neuroscience Centre (PNC), University of Padua, Padua, Italy; Department of Information Engineering, University of Padua, Padua, Italy. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy. Multiple Sclerosis Centre, Neurology Clinic, Department of Neuroscience, University of Padua, Padua, Italy.
 Department of Medicine, Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; Siena Imaging SRL, 53100 Siena, Italy. Electronic address: gentile@sienaimaging.it. MS Center Amsterdam, Radiology and Nuclear Medicine, Amsterdam Neuroscience, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Amsterdam Neuroscience, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Amsterdam Neuroscience, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands. Epidemiology and Data Science, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands. Research Center for Clinical Neuroimmunology, and Neuroscience Basel (RC2NB), University Hospital Basel, CH-4031 Basel, Switzerland; Neurology Departments of Head, Spine and Neuromedicine, Biomedical Engineering and Clinical Research, University of Basel, Basel, Switzerland. Department of Medicine, University of Ottawa, Ottawa ON, K1N 6N5, Ontario, Canada; Ottawa Hospital Research Institute, Ottawa ON, K1H 8L6, Ontario, Canada. Università Vita Salute San Raffaele, Casa di Cura del Policlinico, 20132 Milan, Italy. Merck Serono Ltd, Feltham, TW14 8HD, UK, an affiliate of Merck KGaA. MS Center Amsterdam, Radiology and Nuclear Medicine, Amsterdam Neuroscience, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands; UCL Institutes of Neurology and Healthcare Engineering, London, WC1E 6BT, UK. Department of Medicine, Surgery and Neuroscience, University of Siena, 53100 Siena, Italy. MS Center Amsterdam, Radiology and Nuclear Medicine, Amsterdam Neuroscience, Amsterdam UMC location VUmc, De Boelelaan 1118, 1081 HZ Amsterdam, the Netherlands. Department of Medicine, Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; Siena Imaging SRL, 53100 Siena, Italy.
 Department of Health and Exercise Science, Rowan University, Glassboro, NJ 08028, USA. Electronic address: uygurm@rowan.edu. Neurological Institute, Cooper University Health Care, Cherry Hill, NJ 08002, USA.
 Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Computer Science, The University of Texas at Dallas, Richardson, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Computer Science, The University of Texas at Dallas, Richardson, TX, USA. Department of Radiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Radiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA. icometrix, Leuven, Belgium. icometrix, Leuven, Belgium. icometrix, Leuven, Belgium. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Computer Science, The University of Texas at Dallas, Richardson, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
 Department of Psychiatry, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. Computational Bio-Medicine Laboratory, Institute of Computer Science, Foundation for Research and Technology, Hellas, Heraklion, Crete, Greece. Department of Psychiatry, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. Department of Psychiatry, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. Department of Psychiatry, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. Institute of Applied Mathematics, Foundation for Research and Technology, Hellas, Heraklion, Crete, Greece. Department of Radiology, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. Department of Neurology, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. Computational Bio-Medicine Laboratory, Institute of Computer Science, Foundation for Research and Technology, Hellas, Heraklion, Crete, Greece. fpapada@otenet.gr. Department of Radiology, School of Medicine, University of Crete, University Hospital of Heraklion, Crete, Greece. fpapada@otenet.gr.
 Post graduate school in cardiovascular diseases "Sapienza" University, Roma, Italy. Istituto Superiore di Sanità, Roma, Italy. Digital Medicine Department, Technoscience Science and Technology Park, Latina, Italy. Medicine undergraduate Modena University Italy. Life Balance Chiropractic and Wellness Center Toronto, Canada. Ars chirurgica, private office, Roma, Italy.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy rocca.mara@hsr.it. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Clinic, MS Center/Headache Center, Neurocenter of Southern Switzerland EOC, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Neurology Clinic, MS Center/Headache Center, Neurocenter of Southern Switzerland EOC, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC - Locatie VUMC, Amsterdam, Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC - Locatie VUMC, Amsterdam, Netherlands. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Locatie VUmc, Amsterdam, Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC - Locatie VUMC, Amsterdam, Netherlands. Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC - Locatie VUMC, Amsterdam, Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC - Locatie VUMC, Amsterdam, Netherlands. Department of Advanced Medical and Surgical Sciences, and 3T MRI-Center, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Advanced Medical and Surgical Sciences, and 3T MRI-Center, University of Campania Luigi Vanvitelli, Naples, Italy. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Neurology/Neuroimmunology, Multiple Sclerosis Centre of Catalonia, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Department of Neurology, and Mannheim Center of Translational Neurosciences (MCTN), Ruprecht Karls University Heidelberg Faculty of Medicine Mannheim, Mannheim, Germany. Department of Neurology, and Mannheim Center of Translational Neurosciences (MCTN), Ruprecht Karls University Heidelberg Faculty of Medicine Mannheim, Mannheim, Germany. Institute of Neuroradiology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Radiology and Nuclear Medicine, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Institute of Neuroradiology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neurorehabilitation Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neurophysiology Service, IRCCS Ospedale San Raffaele, Milano, Italy.
 Department of Pharmacy, University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Pharmacy, University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Pharmacy, University of Texas Southwestern Medical Center, Dallas, TX, USA.
 Department of Neurology, Mayo Clinic, Rochester, MN, USA. Desert Neurology & Sleep, La Quinta, CA, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA; Departments of Clinical and Translational Science, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Poznan University of Medical Sciences, Poland. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Electronic address: tobin.oliver@mayo.edu.
 Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. caglaozkul@hotmail.com. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Department of Neurology, Lokman Hekim Hospital, Ankara, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey.
 Kessler Foundation, Center for Neuropsychology and Neuroscience Research, West Orange, NJ, United States; Department of Physical Medicine & Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Electronic address: bsandroff@kesslerfoundation.org. Kessler Foundation, Center for Neuropsychology and Neuroscience Research, West Orange, NJ, United States; Department of Physical Medicine & Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Kessler Foundation, Center for Neuropsychology and Neuroscience Research, West Orange, NJ, United States; Department of Physical Medicine & Rehabilitation, Rutgers NJ Medical School, Newark, NJ, USA. Kessler Foundation, Center for Neuropsychology and Neuroscience Research, West Orange, NJ, United States. University of Illinois Chicago, Department of Kinesiology and Nutrition, Chicago, IL, United States.
 Department of Neurosciences, Institute of Ophthalmology, University of Bari, Bari, Italy. Department of Neurosciences, Institute of Ophthalmology, University of Bari, Bari, Italy. Department of Neurosciences, Institute of Neurology, University of Bari, Bari, Italy. Department of Neurosciences, Institute of Ophthalmology, University of Bari, Bari, Italy. Department of Neurosciences, Institute of Neurology, University of Bari, Bari, Italy. 27287Local Health Authority Brindisi, Social Health District, Brindisi, Italy. Department of Neurosciences, Institute of Ophthalmology, University of Bari, Bari, Italy. Department of Neurosciences, Institute of Neurology, University of Bari, Bari, Italy. Department of Neurosciences, Institute of Ophthalmology, University of Bari, Bari, Italy.
 Department of Biomedical Imaging and Radiological Sciences, National Yang Ming Chiao Tung University, No. 155, Sec. 2, Li-Nong St., Taipei 11221, Taiwan. Department of Biomedical Imaging and Radiological Sciences, National Yang Ming Chiao Tung University, No. 155, Sec. 2, Li-Nong St., Taipei 11221, Taiwan. Department of Psychiatry, Far Eastern Memorial Hospital, No. 21, Sec. 2, Nanya S. Rd., Banciao Dist., New Taipei City 220, Taiwan. Institute of Public Health, National Yang Ming Chiao Tung University School of Medicine, No. 155, Sec. 2, Li-Nong St., Taipei 11221, Taiwan. Department of Biomedical Imaging and Radiological Sciences, National Yang Ming Chiao Tung University, No. 155, Sec. 2, Li-Nong St., Taipei 11221, Taiwan.
 Center for Neuroinflammation and Experimental Therapeutics, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: amitbar@pennmedicine.upenn.edu. F. Hoffmann-La Roche Ltd., Basel, Switzerland. Genentech, Inc., South San Francisco, CA, USA. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. Washington University School of Medicine, St Louis, MO, USA. Genentech, Inc., South San Francisco, CA, USA. F. Hoffmann-La Roche Ltd., Basel, Switzerland. University of California, San Francisco, San Francisco, CA, USA. Genentech, Inc., South San Francisco, CA, USA. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. F. Hoffmann-La Roche Ltd., Basel, Switzerland. Genentech, Inc., South San Francisco, CA, USA. Genentech, Inc., South San Francisco, CA, USA.
 Washington Neuropsychology Research Group, LLC, 3020 Hamaker Ct., Ste. 103, Fairfax, VA 22031, USA; Department of Neurology, Georgetown University Medical Center, Georgetown University, 3800 Reservoir Road, N.W., Washington, DC 20007, USA. Electronic address: jwilken@neuropsychologyfairfax.com. Division of Neurology, Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC V6T 2B5, Canada. Department of Neurology, University of Miami, Miami, 1150 NW 14th St #609, FL 33136, USA. Department of Neurology, University of Massachusetts Chan Medical School, 55N Lake Ave, Worcester, MA 01655, USA. Division of Neurology, Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC V6T 2B5, Canada. Washington Neuropsychology Research Group, LLC, 3020 Hamaker Ct., Ste. 103, Fairfax, VA 22031, USA. Washington Neuropsychology Research Group, LLC, 3020 Hamaker Ct., Ste. 103, Fairfax, VA 22031, USA. Sanofi, 50 Binney Street, Cambridge, MA 02142, USA. Sanofi, 50 Binney Street, Cambridge, MA 02142, USA. Sanofi, 50 Binney Street, Cambridge, MA 02142, USA. Sanofi, 50 Binney Street, Cambridge, MA 02142, USA. Center for Multiple Sclerosis Research, Kessler Foundation, 1199 Pleasant Valley Way, West Orange, NJ 07052-1424, USA; Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Rutgers Division of Biomedical and Health Sciences, Rutgers University, Medical Science Building, 185 South Orange Avenue, Newark, NJ 07103, USA.
 From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. From the Department of Neurology (H.E., J.L., H.M., E.S.V., G.K., O.C.M., A.G.F., N.P., M.D., S.D., N.N., A.Q., C.H., A.Z.L., A.D., K.C.F., P.A.C., E.S.S., S.S.), Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD; and Mellen Center for Multiple Sclerosis (R.B.), Cleveland Clinic, OH. ssaidha2@jhmi.edu.
 Data Analytics and Imaging, Pharma Personalized Healthcare, Genentech Inc., 600 E Grand Ave., South San Francisco, CA, 94080, USA. krishnan.anithapriya@gene.com. Data Analytics and Imaging, Pharma Personalized Healthcare, Genentech Inc., 600 E Grand Ave., South San Francisco, CA, 94080, USA. Clinical Imaging Group, gRED, Genentech Inc., South San Francisco, CA, USA. Translational Medicine OMNI - Biomarker Development, Genentech Inc., South San Francisco, CA, USA. Clinical Imaging Group, gRED, Genentech Inc., South San Francisco, CA, USA. Data Analytics and Imaging, Pharma Personalized Healthcare, Genentech Inc., 600 E Grand Ave., South San Francisco, CA, 94080, USA.
 Department of Neuroradiology, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. Department of Internal Medicine, Spital Walenstadt, Walenstadt, Switzerland. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neurology, University of Michigan, Ann Arbor, USA. Department of Neuroradiology, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. Department of Neuroradiology, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. Division of Experimental Radiology, Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany. Department of Neuroradiology, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. Department of Neuroradiology, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. jennifer.hayes@med.uni-heidelberg.de.
 From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. From the MS Center Amsterdam (J.Y.B., W.H.F., H.E.d.V., G.K.), Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc; Leiden University Medical Centre (LUMC) (J.Y.B., M.H., M.A.G.), Center of Proteomics and Metabolomics; MS Center Amsterdam (F.C.L., L.R.J.d.R., W.H.F., E.M.M.S., J.K., B.M.J.U.), Neurology, Vrije Universiteit Amsterdam, MS Center Amsterdam (M.M.T.E.E.G., C.T.), Neurochemistry Laboratory, Department of Clinical Chemistry, and MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, the Netherlands. g.kooij@amsterdamumc.nl.
 Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk. Corresponding Author: David R. Spiegel, MD, Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, 825 Fairfax Avenue, Norfolk, Virginia 23507 (spiegedr@evms.edu). Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk. Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk. Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk.
 Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK; Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Department of Neurology, NHS Greater Glasgow and Clyde, UK. Tayside Centre for Clinical Neurosciences, University of Dundee, UK. Department of Neurology, Aberdeen Royal Infirmary, NHS Grampian, UK. Department of Neurology, Raigmore Hospital, NHS Highlands, Inverness, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Electronic address: Siddharthan.Chandran@ed.ac.uk. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Electronic address: Peter.Foley@nhslothian.scot.nhs.uk.
 GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Psychology and Cognitive Neuroscience Research Unit, University of Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Clinical Neuroimmunology Unit, Neurology Department, CHU Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Psychology and Cognitive Neuroscience Research Unit, University of Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Psychology and Cognitive Neuroscience Research Unit, University of Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Psychology and Cognitive Neuroscience Research Unit, University of Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Clinical Neuroimmunology Unit, Neurology Department, CHU Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. Clinical Neuroimmunology Unit, Neurology Department, CHU Liège, Liège, Belgium. GIGA CRC In Vivo Imaging, University of Liège, Liège, Belgium. GIGA In Silico Medicine, University of Liège, Liège, Belgium.
 From the Institute of Radiology. Institute of Neuroradiology. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen. From the Institute of Radiology. Institute of Neuroradiology. Institute of Neuroradiology.
 Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Hematology, The Third People's Hospital of Chengdu, Qingyang District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China. Department of Neurology, The First People's Hospital of Longquanyi District Chengdu, Longquanyi District, Chengdu, China.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine, and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA. Bristol Myers Squibb, Summit, NJ, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine, and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine, and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA; Center for Biomedical Imaging at Clinical and Translational Science Institute, University of Buffalo, State University of New York, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine, and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA; Center for Biomedical Imaging at Clinical and Translational Science Institute, University of Buffalo, State University of New York, NY, USA. Electronic address: rzivadinov@bnac.net.
 From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York. npbergsland@bnac.net. From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York. From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York. From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York. From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York. From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York. From the Buffalo Neuroimaging Analysis Center (N.B., M.G.D., D.J., R.Z.), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York; IRCCS (N.B.), Fondazione Don Carlo Gnocchi ONLUS, Milan; Multiple Sclerosis Centre (E.T.), IRCCS Mondino Foundation, Pavia, Italy; Department of Neurology (R.H.B.B., B.W.-G.), University at Buffalo, University Neurology, NY; and Center for Biomedical Imaging at Clinical Translational Research Center (R.Z.), Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York.
 Patient Access Services, Novartis Ireland Ltd, Dublin, Ireland. Patient Access Services, Novartis Healthcare Pvt. Ltd, Hyderabad, India. Patient Access Services, Novartis Healthcare Pvt. Ltd, Hyderabad, India. Novartis de Colombia SA, Bogotá, Colombia. Health Economics and Outcomes Research, Novartis Pharma AG, Basel, Switzerland.
 Department of Neurology and German Center for Vertigo and Balance Disorders, Ludwig Maximilians University, Munich, Germany. olympia.kremmyda@helios-gesundheit.de. Department of Neurology, Helios Klinikum München West, Steinerweg 5, 81241, Munich, Germany. olympia.kremmyda@helios-gesundheit.de. Department of Neurology and Stroke, University Hospital Tübingen, Tübingen, Germany. Department of Neurology and German Center for Vertigo and Balance Disorders, Ludwig Maximilians University, Munich, Germany. Department of Neurology and German Center for Vertigo and Balance Disorders, Ludwig Maximilians University, Munich, Germany.
 Neuroscience Nurse Consultant, Oak Brook, IL, USA. aperrinros@aol.com. Novartis Pharma AG, Basel, Switzerland. Novartis Healthcare Pvt. Ltd, Hyderabad, India. Novartis Pharma AG, Basel, Switzerland. Adelphi Research, Bollington, UK. University College London Hospitals, London, UK.
 Department of Neurology, CHU UCL Namur Site Godinne, Université catholique de Louvain (UCLouvain), 1 avenue G. Thérasse, B-5530, Yvoir, Belgium. londonfrederic@gmail.com. Department of Neurology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Radiology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium. Department of Neurology, Cliniques Universitaires Saint-Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
 Moscow Regional Research and Clinical Institute («MONIKI»), Moscow, Russia. Moscow Regional Research and Clinical Institute («MONIKI»), Moscow, Russia. Moscow Regional Research and Clinical Institute («MONIKI»), Moscow, Russia. Moscow Regional Research and Clinical Institute («MONIKI»), Moscow, Russia. Moscow Regional Research and Clinical Institute («MONIKI»), Moscow, Russia.
 Medical University of Plovdiv, Plovdiv, Bulgaria.
 Department of Neurology, Dokkyo Medical University Saitama Medical Center. Department of Neurology, Dokkyo Medical University Saitama Medical Center. Department of Neurology, Showa University. Department of Neurology, Dokkyo Medical University Saitama Medical Center. Department of Neurology, Dokkyo Medical University Saitama Medical Center. Department of Neurology, Dokkyo Medical University Saitama Medical Center. Department of Neurology, Dokkyo Medical University Saitama Medical Center.
 Department of Neurology and Radiology, Mayo Clinic, Rochester, MN, USA. Electronic address: zeydan.burcu@mayo.edu.
 Peter O'Donnell Jr Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA; VA North Texas Health Care System, Dallas, TX, USA. Munich, Germany. Electronic address: tugemann@mailbox.org.
 Nature Reviews Neurology, . lisa.kiani@nature.com.

 Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neuroradiology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Neurology department, Hopital Fondation Adolphe de Rothschild, 25-29 rue Manin, Paris, France. Electronic address: cbensa@for.paris.
 Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA. roee.holtzer@yu.edu. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. roee.holtzer@yu.edu. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois, Chicago, IL, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Multiple Sclerosis Center, Holy Name Medical Center, Teaneck, NJ, USA. Multiple Sclerosis Center, Holy Name Medical Center, Teaneck, NJ, USA. Department of Radiology, Gruss Magnetic Resonance Research Center, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA. Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA. Villanova University, Electrical and Computer Engineering, Villanova, PA, USA. Department of Kinesiology and Community Health, College of Applied Health Sciences, University of Illinois, Urbana-Champaign, Urbana, IL, USA. Department of Radiology, Gruss Magnetic Resonance Research Center, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA.
 AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium; Department of Pharmaceutical and Pharmacological Sciences, Research Group Experimental Pharmacology (EFAR), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium. Electronic address: thomas.jonathan.scheinok@vub.be. Nationaal Multiple Sclerose Centrum, Vanheylenstraat 16, 1820 Melsbroek, Belgium. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium; St Edmund Hall, University of Oxford, Queen's Lane, Oxford, UK. Department of Pharmaceutical and Pharmacological Sciences, Research Group Experimental Pharmacology (EFAR), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium. AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium; Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium.
 Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA, USA/Division of Brain, Imaging and Behaviour-Systems Neuroscience, Krembil Brain Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada/Institute of Medical Science, Faculty of Medicine, University of Toronto, Toronto, ON, Canada. Division of Neurology, Department of Medicine, St. Michael's Hospital, Toronto, ON, Canada. Division of Brain, Imaging and Behaviour-Systems Neuroscience, Krembil Brain Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Division of Brain, Imaging and Behaviour-Systems Neuroscience, Krembil Brain Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada/Division of Neuroradiology, Joint Department of Medical Imaging, Toronto Western Hospital, University Health Network, Toronto, ON, Canada. Division of Brain, Imaging and Behaviour-Systems Neuroscience, Krembil Brain Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada/Division of Neuroradiology, Joint Department of Medical Imaging, Toronto Western Hospital, University Health Network, Toronto, ON, Canada. Department of Neurological Sciences, Larner College of Medicine at the University of Vermont, Burlington, VT, USA. Division of Brain, Imaging and Behaviour-Systems Neuroscience, Krembil Brain Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada/Institute of Medical Science, Faculty of Medicine, University of Toronto, Toronto, ON, Canada/Department of Surgery, Faculty of Medicine, University of Toronto, Toronto, ON, Canada/Division of Neurosurgery, Krembil Neuroscience Centre, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
 Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia.
 Serviço de Neurologia, Centro Hospitalar de Entre o Douro e Vouga, Rua Dr. Cândido Pinho, No. 5, 4520-220, Santa Maria da Feira, Portugal. daniela.s.oliveira29@gmail.com. Serviço de Neurologia, Centro Hospitalar de Entre o Douro e Vouga, Rua Dr. Cândido Pinho, No. 5, 4520-220, Santa Maria da Feira, Portugal. Serviço de Neurologia, Centro Hospitalar de Entre o Douro e Vouga, Rua Dr. Cândido Pinho, No. 5, 4520-220, Santa Maria da Feira, Portugal. Instituto de Saúde Pública, Universidade do Porto, Rua das Taipas, No. 135, 4050-600, Porto, Portugal. Laboratório para a Investigação Integrativa e Translacional em Saúde Populacional (ITR), Rua das Taipas, No. 135, 4050-600, Porto, Portugal. Faculdade de Medicina da Universidade do Porto, Alameda Prof. Hernâni Monteiro, 4200-319, Porto, Portugal.
 MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. Electronic address: m.schoonheim@amsterdamumc.nl. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands.
 Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, Bispebjerg Bakke 23, Copenhagen 2400, Denmark; Danish Multiple Sclerosis Registry, Department of Neurology, University Hospital-Rigshospitalet, Glostrup, Copenhagen, Denmark. Electronic address: josefine.windfeld-mathiasen@regionh.dk. Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, Bispebjerg Bakke 23, Copenhagen 2400, Denmark; Department of Clinical Medicine, University of Copenhagen, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, University Hospital-Rigshospitalet, Glostrup, Copenhagen, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, University Hospital-Rigshospitalet, Glostrup, Copenhagen, Denmark. Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, Bispebjerg Bakke 23, Copenhagen 2400, Denmark; Department of Clinical Medicine, University of Copenhagen, Denmark. Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, Bispebjerg Bakke 23, Copenhagen 2400, Denmark; Department of Clinical Medicine, University of Copenhagen, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, University Hospital-Rigshospitalet, Glostrup, Copenhagen, Denmark; Department of Clinical Medicine, University of Copenhagen, Denmark.
 The Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Valdemar Hansens Vej 2, 2600 Glostrup, Denmark. Electronic address: rolf.pringler.holm@regionh.dk. The Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Valdemar Hansens Vej 2, 2600 Glostrup, Denmark. The Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Valdemar Hansens Vej 2, 2600 Glostrup, Denmark. The Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Valdemar Hansens Vej 2, 2600 Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 13, 2600 Glostrup, Denmark. The Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Valdemar Hansens Vej 2, 2600 Glostrup, Denmark; Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 13, 2600 Glostrup, Denmark.
 Department of Neurology, Faculty of Medicine, Adiyaman University, Adiyaman, Turkey. Electronic address: ealtunisik@adiyaman.edu.tr. Department of Neurology, Dr. Ersin Arslan Education and Research Hospital, Gaziantep, Turkey. Department of Neurology, Mersin City Hospital, Mersin, Turkey.
 Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, Magdeburg 39120, Germany. Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, Magdeburg 39120, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg 39106, Germany; German Center for Neurodegenerative Diseases (DZNE), Magdeburg 39120, Germany. Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, Magdeburg 39120, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg 39106, Germany. Electronic address: tino.zaehle@ovgu.de.
 Faculty of Medicine, Ostrava University, Czech Republic; Department of Neurology, University Hospital Ostrava, Czech Republic. Electronic address: pavel.hradilek@seznam.cz. Faculty of Medicine, Ostrava University, Czech Republic; Department of Neurology, University Hospital Ostrava, Czech Republic. Faculty of Medicine in Pilsen, The Institute for the Care of Mother and Child, Prague, Czech Republic. Department of Neurology, and Center of Clinical Neuroscience, 1st Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. IMPULS Endowment Fund, ReMuS Registry, Czech Republic; Department of Economic Statistics, Prague University of Economics and Business, Prague, Czech Republic. Department of Neurology, and Center of Clinical Neuroscience, 1st Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic; IMPULS Endowment Fund, ReMuS Registry, Czech Republic. IMPULS Endowment Fund, ReMuS Registry, Czech Republic; Prague University of Economics and Business, Czech Republic. Department of Neurology, 3rd Faculty of Medicine, Charles University in Prague and Hospital Kralovske Vinohrady, Prague, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Kralove, Charles University in Prague, Czech Republic. Department of Neurology, Second Faculty of Medicine and Motol University Hospital, Charles University, Prague, Czech Republic. Department of Neurology, University Hospital and Masaryk University Brno, Czech Republic. Department of Neurology, Hospital Ceske Budejovice, Czech Republic. Department of Neurology, Hospital of Jihlava, Czech Republic. Department of Neurology, and Center of Clinical Neuroscience, 1st Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic; Department of Neurology, KZ a.s., Hospital Teplice, Czech Republic. 1st Department of Neurology, University Hospital U Svate Anny, Brno, Czech Republic. Department of Neurology, Hospital Pardubice, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital in Pilsen, Charles University. Department of Neurology, Tomas Bata Hospital, Zlin, Czech Republic. Department of Neurology, Faculty of Medicine, Palacky University and University Hospital Olomouc, Czech Republic. Department of Neurology, and Center of Clinical Neuroscience, 1st Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic.
 U1195 Inserm, Paris-Saclay University, Kremlin-Bicêtre, France. U1195 Inserm, Paris-Saclay University, Kremlin-Bicêtre, France. UMR996 Inserm, Paris-Saclay University, Clamart, France. UMR996 Inserm, Paris-Saclay University, Clamart, France. Paris Brain Institute, Sorbonne University, Paris, France. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh BioQuarter, Edinburgh, UK. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh BioQuarter, Edinburgh, UK. M et P Pharma AG, Emmetten, Switzerland. UMR996 Inserm, Paris-Saclay University, Clamart, France. U1195 Inserm, Paris-Saclay University, Kremlin-Bicêtre, France. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh BioQuarter, Edinburgh, UK. Paris Brain Institute, Sorbonne University, Paris, France. U1195 Inserm, Paris-Saclay University, Kremlin-Bicêtre, France. elisabeth.traiffort@inserm.fr.
 Academic Unit of Mental Health and Clinical Neuroscience, Section of Clinical Neurology, University of Nottingham, Nottingham Centre for MS and Neuroinflammation, Nottingham University Hospitals QMC, Nottingham, NG7 2UH, UK. University Hospitals of North Midlands NHS Trust, Royal Stoke MS Centre of Excellence, Stoke On Trent, UK. Academic Unit of Mental Health and Clinical Neuroscience, Section of Clinical Neurology, University of Nottingham, Nottingham Centre for MS and Neuroinflammation, Nottingham University Hospitals QMC, Nottingham, NG7 2UH, UK. Academic Unit of Mental Health and Clinical Neuroscience, Section of Clinical Neurology, University of Nottingham, Nottingham Centre for MS and Neuroinflammation, Nottingham University Hospitals QMC, Nottingham, NG7 2UH, UK. cris.constantinescu@nottingham.ac.uk. Cooper University Hospital, Cooper Neurological Institute, Cooper Medical School at Rowan University, Camden, NJ, 08103, USA. cris.constantinescu@nottingham.ac.uk.
 Department of Neurology, Odense University Hospital, J.B. Winsloewsvej 4, 5000 Odense C, Denmark; OPEN, Odense Patient Data Explorative Network, Odense University Hospital, Odense, J.B. Winsloewsvej 4, 5000 Odense C, Denmark. Electronic address: asta.theodorsdottir@rsyd.dk. Department of Neurology, Odense University Hospital, J.B. Winsloewsvej 4, 5000 Odense C, Denmark; Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winsloewsvej 21, st., 5000 Odense C, Denmark; BRIDGE - Brain Research - Inter Disciplinary Guided Excellence, Department of Clinical Research, J.B. Winsloewsvej 19, 3., 5000 Odense C, Denmark. Filadelfia Epilepsy Hospital, Kolonivej 1, 4293 Dianalund, Denmark. Department of Neurology, Odense University Hospital, J.B. Winsloewsvej 4, 5000 Odense C, Denmark; Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winsloewsvej 21, st., 5000 Odense C, Denmark; BRIDGE - Brain Research - Inter Disciplinary Guided Excellence, Department of Clinical Research, J.B. Winsloewsvej 19, 3., 5000 Odense C, Denmark.
 Robert Wood Johnson Medical - Rutgers, Pediatrics & Neurology, 89 French Street, Suite 2300, New Brunswick, NJ 08901, USA. Electronic address: bhisevi@rwjms.rutgers.edu. University of Utah, Pediatrics, USA. University of Utah, Pediatrics, USA. Loma Linda University, Neurology, USA. Massachusetts General Hospital, Partners Pediatric Multiple Sclerosis Center, Neurology, USA. Brigham and Women's Hospital, Neurology, USA. Massachusetts General Hospital, Partners Pediatric Multiple Sclerosis Center, USA. Washington University in Saint Louis, Neurology, USA. The University of Alabama at Birmingham School of Medicine Tuscaloosa, Neurology, USA. Texas Childrens Hospital, Child Neurology, USA. Washington University St. Louis, Neurology, USA. Cleveland Clinic, Neurology, USA. Cleveland Clinic Neurological Institute, Pediatric Neurology, USA. Mayo Clinic, Neurology, USA. University of Utah, Neurology, USA. University of Colorado School of Medicine, Neurology, USA. Texas Children's Hospital, Child Neurology, USA. University of California San Francisco, Regional Pediatric Multiple Sclerosis Center, USA. University at Buffalo - The State University of New York, Pharmaceutical Sciences, USA. University of Alabama at Birmingham, Pediatrics, USA. New York University Medical Center, Neurology, USA. Mayo Clinic, Neurology, USA.
 Department of Neurology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey. Electronic address: zeynepecekaya@hotmail.com. Department of Neurology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa Medical School, Istanbul University-Cerrahpasa, Istanbul, Turkey.
 Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. Institute of Neurology, University Magna Graecia of Catanzaro, Viale Europa, Germaneto, 88100, Catanzaro, CZ, Italy. p.vale@unicz.it.
 Rocky Mountain Multiple Sclerosis Clinic, Salt Lake City, UT 84103, USA. Electronic address: jfoley@rmmsc.com. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA.
 Save Sight Institute, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, AustraliaScott Kolbe Monash University, Melbourne, VIC, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia/Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Monash University, Melbourne, VIC, Australia. Royal North Shore Hospital, Sydney, NSW, Australia. Royal North Shore Hospital, Sydney, NSW, Australia. Save Sight Institute, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia.
 Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Biostatistics, The University of Alabama at Birmingham, Birmingham, AL, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Biostatistics, The University of Alabama at Birmingham, Birmingham, AL, USA. Department of Diagnostic and Interventional Imaging and Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
 Research Unit of Clinical Medicine, Neurology, University of Oulu, P.O. Box 5000, FI-90014 University of Oulu, Finland. Neuro Center, Neurology Outpatient Clinic, Kuopio University Hospital, P.O. Box 100, FI-70029 Kuopio, Finland; Institute of Clinical Medicine-Neurology, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland. Southern Savo Hospital District, Department of Neurology, Porrassalmenkatu 35-37, FI-50100 Mikkeli, Finland. Masku Neurological Rehabilitation Centre, Vaihemäentie 10, FI-21250 Masku, Finland; Department of Psychology, FI-20014 University of Turku, Finland. Faculty of Medicine, University of Oulu, P.O. Box 8000, FI-90014 University of Oulu, Finland; Biobank Borealis of Northern Finland, Northern Ostrobothnia Hospital District, P.O. Box 10, FI-90029 Oulu University Hospital, Finland. Research Unit of Clinical Medicine, Neurology, University of Oulu, P.O. Box 5000, FI-90014 University of Oulu, Finland; Medical Research Center, Oulu University Hospital, P.O. Box 10, FI-90029 OYS, Oulu, Finland; Clinical Neurosciences, P.O. Box 4, Yliopistonkatu 3, FI-00014 University of Helsinki, Finland. Research Unit of Clinical Medicine, Neurology, University of Oulu, P.O. Box 5000, FI-90014 University of Oulu, Finland; Medical Research Center, Oulu University Hospital, P.O. Box 10, FI-90029 OYS, Oulu, Finland; Neurocenter, Neurology, Oulu University Hospital, P.O. Box 10, FI-90029 OYS, Oulu, Finland. Research Unit of Clinical Medicine, Neurology, University of Oulu, P.O. Box 5000, FI-90014 University of Oulu, Finland; Medical Research Center, Oulu University Hospital, P.O. Box 10, FI-90029 OYS, Oulu, Finland; Neurocenter, Neurology, Oulu University Hospital, P.O. Box 10, FI-90029 OYS, Oulu, Finland. Electronic address: johanna.kruger@oulu.fi.
 Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.
 Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine, University of Bergen, Bergen, Norway. Electronic address: ellen.skorve@helse-bergen.no. Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine, University of Bergen, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Mohn Medical Imaging and Visualization Centre (MMIV), Department of Radiology, Haukeland University Hospital, Bergen, Norway. Mohn Medical Imaging and Visualization Centre (MMIV), Department of Radiology, Haukeland University Hospital, Bergen, Norway; Department of Physics and Technology, University of Bergen, N-5007 Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine, University of Bergen, Bergen, Norway.
 School of Health Sciences, University of Newcastle College of Health, Medicine and Wellbeing, Callaghan, NSW, Australia. RINGGOLD: 64834 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 Department of Radiology, Imam Abdulrahman Bin Faisal University King Fahd University Hospital, Dammam, Saudi Arabia. RINGGOLD: 48102 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 School of Biomedical Sciences and Pharmacy, University of Newcastle College of Health, Medicine and Wellbeing, Callaghan, NSW, Australia. RINGGOLD: 64834 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 School of Psychological Sciences, University of Newcastle College of Health, Medicine and Wellbeing, Callaghan, NSW, Australia. RINGGOLD: 64834 School of Health Sciences, University of Newcastle College of Health, Medicine and Wellbeing, Callaghan, NSW, Australia. RINGGOLD: 64834 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 College of Applied Medical Sciences, University of Jeddah, Jeddah, Saudi Arabia. RINGGOLD: 441424 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW, Australia. RINGGOLD: 439651 School of Medicine and Public Health, University of Newcastle College of Health, Medicine and Wellbeing, Callaghan, NSW, Australia. RINGGOLD: 64834 School of Health Sciences, University of Newcastle College of Health, Medicine and Wellbeing, Callaghan, NSW, Australia. RINGGOLD: 64834 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568
 Department of Occupational Therapy, New York University, New York, NY, USA/Kessler Foundation, West Orange, NJ, USA. Kessler Foundation, West Orange, NJ, USA/Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Rutgers University, Newark, NJ, USA.
 Department of Neuroradiology, Univ. Lille, INSERM, CHU Lille, U1172, Degenerative and Vascular Cognitive Disorders, 59000, Lille, France. Department of Neurology, Multiple Sclerosis Center of Lille, Univ. Lille, 59000, Lille, France. Department of Neuroradiology, Univ. Lille, INSERM, CHU Lille, U1172, Degenerative and Vascular Cognitive Disorders, 59000, Lille, France. Department of Neuroradiology, Univ. Lille, INSERM, CHU Lille, U1172, Degenerative and Vascular Cognitive Disorders, 59000, Lille, France. Department of Neuroradiology, Univ. Lille, INSERM, CHU Lille, U1172, Degenerative and Vascular Cognitive Disorders, 59000, Lille, France. olivier.outteryck@chru-lille.fr.
 CRCSEP Neurologie Pasteur 2, CHU de Nice, Université Cote d'Azur, UMR2CA (URRIS), Nice, France. University of Texas Southwestern Medical Center, Dallas, TX, USA.
 Department of Neurology, MS Center Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands. Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada. Department of Neurology, MS Center Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.
 Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy. Department of Surgery, Dentistry, Paediatrics and Gynaecology, University of Verona, 37134 Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy. Roche Pharma Research & Early Development (pRED), Biomarkers & Translational Technologies (BTT), F. Hoffmann-La Roche Ltd., CH-4070 Basel, Switzerland. Roche Pharma Research & Early Development (pRED), Biomarkers & Translational Technologies (BTT), F. Hoffmann-La Roche Ltd., CH-4070 Basel, Switzerland. Roche Pharma Research & Early Development (pRED), Biomarkers & Translational Technologies (BTT), F. Hoffmann-La Roche Ltd., CH-4070 Basel, Switzerland. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.
 Neurology Department, Hospital Egas Moniz, Centro Hospitalar Lisboa Ocidental, Portugal. Electronic address: mtteixeira@chlo.min-saude.pt. Neurology Department, Hospital Egas Moniz, Centro Hospitalar Lisboa Ocidental, Portugal. Neurology Department, Hospital dos Capuchos, Centro Hospitalar Universitário Lisboa Central, Portugal. Neurology Department, Hospital Egas Moniz, Centro Hospitalar Lisboa Ocidental, Portugal; CEDOC - Chronic Diseases Research Centre, NOVA Medical School, Universidade Nova de Lisboa, Portugal.
 Department of Neurology, University of Campinas (UNICAMP), Campinas, Brazil; Laboratory of Neuroimaging, University of Campinas (UNICAMP), Campinas, Brazil. Electronic address: alfredodamasceno@hotmail.com. Laboratory of Neuroimaging, University of Campinas (UNICAMP), Campinas, Brazil. Department of Neurology, University of Campinas (UNICAMP), Campinas, Brazil. Department of Neurology, University of Campinas (UNICAMP), Campinas, Brazil; Laboratory of Neuroimaging, University of Campinas (UNICAMP), Campinas, Brazil.
 Department of Forensic Medicine, University of Peradeniya, Peradeniya, Sri Lanka. chathula_wick@yahoo.com. Department of Forensic Medicine, University of Peradeniya, Peradeniya, Sri Lanka. Department of Pathology, University of Peradeniya, Peradeniya, Sri Lanka. Department of Pathology, University of Peradeniya, Peradeniya, Sri Lanka.
 DynaLIFE Medical Labs, Edmonton, AB, Canada; Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada. Electronic address: victoria.higgins@dynalife.ca. Department of Laboratory Medicine, St. Michael's Hospital, Toronto, ON, Canada; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON, Canada; Department of Laboratory Medicine & Pathobiology, University of Toronto, Toronto, ON, Canada. Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada. DynaLIFE Medical Labs, Edmonton, AB, Canada; Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada. DynaLIFE Medical Labs, Edmonton, AB, Canada; Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada; Current Affiliation: LifeLabs, Toronto, ON, Canada. DynaLIFE Medical Labs, Edmonton, AB, Canada; Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada. DynaLIFE Medical Labs, Edmonton, AB, Canada; Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada. Electronic address: michelle.parker@dynalife.ca.
 Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
 The Corinne Goldsmith Dickinson Center for Multiple Sclerosis and Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. The Corinne Goldsmith Dickinson Center for Multiple Sclerosis and Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
 Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. kania.karolina@spsk2.pl. Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. Poznan University of Medical Sciences, Poznan, Poland. Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. Division of Neurochemistry and Neuropathology, Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland.
 Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, Washington, USA. Department of Neurology, Rijnstate Hospital, Arnhem, The Netherlands. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, Washington, USA. Department of Medicine, Neurology service, Hôpital Maisonneuve-Rosemont, Montreal, Quebec, Canada. Département de neurosciences, Faculté de médecine, Université de Montréal, Montreal, Quebec, Canada. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
 Laboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, NSW 2007, Australia. Laboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, NSW 2007, Australia.
 Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, CNRS, Inria, Inserm, AP-HP, Hôpital de la Pitié Salpêtrière, F-75013 Paris, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, CNRS, Inria, Inserm, AP-HP, Hôpital de la Pitié Salpêtrière, F-75013 Paris, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, CNRS, Inserm, AP-HP, Hôpital de la Pitié Salpêtrière, F-75013 Paris, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, CNRS, Inserm, AP-HP, Hôpital de la Pitié Salpêtrière, F-75013 Paris, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, CNRS, Inserm, AP-HP, Hôpital Saint-Antoine, F-75012 Paris, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, CNRS, Inria, Inserm, AP-HP, Hôpital de la Pitié Salpêtrière, F-75013 Paris, France. Electronic address: olivier.colliot@cnrs.fr.
 Department of Internal Medicine, University of Iowa, Iowa City, IA, USA; Department of Epidemiology, University of Iowa, Iowa City, IA, USA. Electronic address: Tyler-Titcomb@uiowa.edu. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Institute for Clinical and Translational Science, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Electronic address: Terry-Wahls@uiowa.edu. Department of Epidemiology, University of Iowa, Iowa City, IA, USA.
 Complejo Hospitalario Universitario de A Coruña, Spain. Electronic address: ana.maria.lopez.real@sergas.es. Complejo Hospitalario Universitario de Vigo, Spain. Hospital Universitario Cabueñes, Spain. Hospital Universitario Marqués de Valdecilla, Spain. Complejo Hospitalario Universitario de Santiago de Compostela, Spain. Hospital Rivera Povisa. Vigo, Spain. Complejo Hospitalario Universitario de Ferrol, Spain. Complejo Hospitalario Universitario de Ourense, Spain. Complejo Hospitalario Universitario de Pontevedra, Spain. Hospital Universitario Lucus Augusti. Lugo, Spain. Hospital Universitario San Agustín. Avilés, Spain.
 Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China. Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China. jiayanjie1971@zzu.edu.cn.
 Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Department of Neuroradiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Department of Neuroradiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Institute of Radiology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Division of Medical Physics in Radiology, German Cancer Research Centre (DKFZ), Heidelberg, Germany.
 Department of Cardiology, Bursa Uludag University Faculty of Medicine, Bursa, Turkey. Electronic address: seydagunay@uludag.edu.tr. Department of Neurology, Bursa Uludag University Faculty of Medicine, Bursa, Turkey. Department of Biostatistics, Bursa Uludag University Faculty of Medicine, Bursa, Turkey. Department of Neurology, Bursa Uludag University Faculty of Medicine, Bursa, Turkey. Department of Cardiology, Bursa Uludag University Faculty of Medicine, Bursa, Turkey. Department of Neurology, Bursa Uludag University Faculty of Medicine, Bursa, Turkey.
 Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic; Department of Epidemiology and Biostatistics, Third Faculty of Medicine, Charles University in Prague, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic; IMPULS Endowment Fund, Prague, Czech Republic. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Bata Regional Hospital, Zlín, Czech Republic. Department of Neurology, Hospital České Budějovice, České Budějovice, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, Faculty of Medicine and Dentistry, Palacký University and University Hospital Olomouc, Olomouc, Czech Republic. Department of Neurology, Second Faculty of Medicine and Motol University Hospital, Charles University in Prague, Prague, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Hradec Králové, Czech Republic. Department of Clinical Neuroscience, Medical Faculty, Ostrava University and Department of Neurology, University Hospital, Ostrava, Czech Republic. Department of Neurology, Hospital Jihlava, Jihlava, Czech Republic. Department of Neurology, Third Faculty of Medicine, Charles University in Prague and University Hospital Kralovske Vinohrady, Prague, Czech Republic. Department of Neurology, Faculty of Medicine in Pilsen and University Hospital Pilsen, Charles University in Prague, Pilsen, Czech Republic. Department of Neurology, Hospital Pardubice, Pardubice, Czech Republic. Department of Neurology, University Hospital Brno, Brno, Czech Republic. Department of Neurology, Thomayer Hospital, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic; Department of Neurology, KZ a.s., Hospital Teplice, Teplice, Czech Republic. First Department of Neurology, Masaryk University, St. Anne's University Hospital, Brno, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Electronic address: dana.horakova@vfn.cz.
 Exercise Biology, Department of Public Health, Aarhus University, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Denmark; The Danish MS Hospitals, Ry and Haslev, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Denmark; The Danish MS Hospitals, Ry and Haslev, Denmark. Electronic address: lhvid@ph.au.dk.
 Department of Adult Neurology, Faculty of Medicine, Medical University of Gdańsk, Dębinki 7, 80-211, Gdańsk, Poland. magdalena.chylinska@gumed.edu.pl. Department of Adult Neurology, Faculty of Medicine, Medical University of Gdańsk, Dębinki 7, 80-211, Gdańsk, Poland. bartosz@karaszewski.org. Department of Adult Neurology, Faculty of Medicine, Medical University of Gdańsk, Dębinki 7, 80-211, Gdańsk, Poland. Department of Adult Neurology, Faculty of Medicine, Medical University of Gdańsk, Dębinki 7, 80-211, Gdańsk, Poland. Department of Adult Neurology, Faculty of Medicine, Medical University of Gdańsk, Dębinki 7, 80-211, Gdańsk, Poland. Second Department of Radiology, Faculty of Medicine, Medical University of Gdańsk, Gdańsk, Poland. Second Department of Radiology, Faculty of Medicine, Medical University of Gdańsk, Gdańsk, Poland.
 Department of Neurological Sciences, Larner College of Medicine at the University of Vermont, University Health Center, Burlington, VT, USA. Electronic address: andrew.solomon@uvm.edu. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. National Hospital for Neurology and Neurosurgery, Queen Square, London, UK. Departments of Neurology and Laboratory Medicine and Pathology and the Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department NEUROFARBA, University of Florence, Florence, Italy; IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Department of Neurology, University of Southern California, Keck School of Medicine, Los Angeles, CA, USA. Department of Neurology, University of Pennsylvania, Division of Child Neurology, Philadelphia, PA, USA; Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, USA. Department of Radiology and Nuclear Medicine, Amsterdam UMC, Vrije Universiteit, Amsterdam, Netherlands; Queen Square Institute of Neurology and Centre for Medical Image Computing, University College London, London, UK. Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA. Department of Neurology, Fleni Institute of Biological Chemistry and Physical Chemistry (IQUIFIB), Buenos Aires, Argentina; National Council for Scientific and Technical Research/University of Buenos Aires, Buenos Aires, Argentina. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University School of Medicine, Koriyama, Japan; Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan. Department of Neurosciences, University of California, San Diego, CA, USA. Cleveland Clinic Libraries, Cleveland Clinic, Cleveland, OH, USA. Department of Neurology, Klinikum rechts der Isar, Medical Faculty, Technische Universität München, Munich, Germany; Munich Cluster for Systems Neurology, Munich, Germany. Department of Neurology, John Hunter Hospital, Newcastle, NSW Australia; Hunter Medical Research Institute Neurology, University of Newcastle, Newcastle, NSW, Australia. Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Neuroimaging Research Unit, Division of Neuroscience, Neurology Unit, IRCCS San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. Department of Neurobiology and Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA, USA. Weill Institute for Neuroscience, University of California, San Francisco, San Francisco, CA, USA. Neurology Institute, Harley Street Medical Center, Abu Dhabi, United Arab Emirates. Mellen Center for MS Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
 Department of Internal Medicine, University of Missouri-Kansas City, Kansas City, MO. Department of Hematopathology, National Institutes of Health, Bethesda, MD. Department of Medical Oncology, UT Health San Antonio, San Antonio, TX. Department of Hematologic Oncology and Blood Disorders, Atrium Health Levine Cancer Institute, Charlotte, NC. Hematology & Oncology Fellowship Program, National Cancer Institute, National Institutes of Health, Bethesda, MD.
 Bashkir State Medical University, Ufa, Russia. Institute of Biochemistry and Genetics, Ufa, Russia. Institute of Biochemistry and Genetics, Ufa, Russia. Bashkir State Medical University, Ufa, Russia. Bashkir State Medical University, Ufa, Russia. Bashkir State Medical University, Ufa, Russia. Republican Clinical Psychiatric Hospital, Ufa, Russia.
 Laboratory for Neuroimmunology, Department of Neurosciences, KU Leuven Brain Institute, Leuven, Belgium. Department of Neurology, University Hospitals Leuven, Herestraat 49, 3000, Leuven, Belgium. Laboratory for Neuroimmunology, Department of Neurosciences, KU Leuven Brain Institute, Leuven, Belgium. Department of Neurology, University Hospitals Leuven, Herestraat 49, 3000, Leuven, Belgium. Department of Ophthalmology, University Hospitals Leuven, Leuven, Belgium. Department of Ophthalmology, University Hospitals Leuven, Leuven, Belgium. Laboratory for Neuroimmunology, Department of Neurosciences, KU Leuven Brain Institute, Leuven, Belgium. benedicte.dubois@uzleuven.be. Department of Neurology, University Hospitals Leuven, Herestraat 49, 3000, Leuven, Belgium. benedicte.dubois@uzleuven.be.
 Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain; Servei de Medicina Física i Rehabilitació, Departament de logopèdia, Hospital Universitari de la Santa Creu i Sant Pau, Barcelona, Spain. Electronic address: mrenom@santpau.cat. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Departament de Farmacologia Clínica. Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Centre Neurorehabilitador Miquel Martí i Pol, Fundació Esclerosi Múltiple, Lleida, Spain. Centre Neurorehabilitador Mas Sabater, Reus, Tarragona, Spain. Hospital Clínico Universidad Católica de Chile, Santiago de Chile, Chile. Asociación de Esclerosis Múltiple de Bizkaya (ADEMBI), Bilbao, Spain. Asociación de Esclerosis Múltiple de Bizkaya (ADEMBI), Bilbao, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Medicina Física i Rehabilitació, Departament de logopèdia, Hospital Universitari de la Santa Creu i Sant Pau, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Medicina Física i Rehabilitació, Departament de logopèdia, Hospital Universitari de la Santa Creu i Sant Pau, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Rehabilitació, Hospital Universitari de Vic, Barcelona, Spain; Institut Guttmann Hospital de Neurorehabilitació, Badalona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 Neurology Clinic, University Clinical Center of Serbia, Dr Subotica 6, 11000, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Dr Subotica 6, 11000, Belgrade, Serbia. Faculty of Medicine, University of Belgrade, Dr Subotica 8, 11000, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Dr Subotica 6, 11000, Belgrade, Serbia. Institute of Epidemiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Dr Subotica 6, 11000, Belgrade, Serbia. drulovicjelena@gmail.com. Faculty of Medicine, University of Belgrade, Dr Subotica 8, 11000, Belgrade, Serbia. drulovicjelena@gmail.com.
 Nature Reviews Neurology, . nrneuro@nature.com.
 Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States. Department of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, United States. Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States; Brain and Mind Centre, School of Medical Sciences, University of Sydney, Camperdown, NSW, Australia. Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States. Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States. Electronic address: chahins@wustl.edu.
 Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, St. Anna University Hospital, 44124 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Interdepartmental Research Center for the Study of Multiple Sclerosis and Inflammatory and Degenerative Diseases of the Nervous System, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, 40139 Bologna, Italy. Department of Neuroscience and Rehabilitation, St. Anna University Hospital, 44124 Ferrara, Italy. Department of Medicine and Surgery, University of Parma, 43124 Parma, Italy. Microbiome Research Hub, University of Parma, 43124 Parma, Italy. Microbiome Research Hub, University of Parma, 43124 Parma, Italy. Laboratory of Probiogenomics, Department Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, St. Anna University Hospital, 44124 Ferrara, Italy. Interdepartmental Research Center for the Study of Multiple Sclerosis and Inflammatory and Degenerative Diseases of the Nervous System, University of Ferrara, 44121 Ferrara, Italy.
 Department of Neurosciences and Mental Health, AOU Città della Salute e della Scienza di Torino via Cherasco 15, 10126 Torino, Italy. Electronic address: marco.vercellino@unito.it. Department of Neurosciences and Mental Health, AOU Città della Salute e della Scienza di Torino via Cherasco 15, 10126 Torino, Italy; Department of Neurosciences, University of Turin, via Cherasco 15, 10126 Torino, Italy. Department of Neurosciences and Mental Health, AOU Città della Salute e della Scienza di Torino via Cherasco 15, 10126 Torino, Italy. Department of Neurosciences, University of Turin, via Cherasco 15, 10126 Torino, Italy. Department of Neurosciences, University of Turin, via Cherasco 15, 10126 Torino, Italy. Department of Neurosciences and Mental Health, AOU Città della Salute e della Scienza di Torino via Cherasco 15, 10126 Torino, Italy. Department of Neurosciences and Mental Health, AOU Città della Salute e della Scienza di Torino via Cherasco 15, 10126 Torino, Italy.
 Dipartimento di Scienze della Salute, Università degli Studi del Piemonte Orientale "Amedeo Avogadro," Novara, Italy. Department of Neurology, Eras MS Center, Erasmus University Medical Center, Rotterdam, The Netherlands.
 From the Department of Anesthesiology, Critical Care & Pain Management, Hospital for Special Surgery, New York, New York. From the Department of Anesthesiology, Critical Care & Pain Management, Hospital for Special Surgery, New York, New York. From the Department of Anesthesiology, Critical Care & Pain Management, Hospital for Special Surgery, New York, New York. Department of Anesthesiology, Weill Cornell Medicine, New York, New York. Department of Anesthesiology, Perioperative Medicine and Intensive Care Medicine, Paracelsus Medical University, Salzburg, Austria. Department of Population Health Science & Policy/Department of Orthopedics, Institute for Healthcare Delivery Science, Icahn School of Medicine at Mount Sinai, New York, New York. From the Department of Anesthesiology, Critical Care & Pain Management, Hospital for Special Surgery, New York, New York. Department of Anesthesiology, Weill Cornell Medicine, New York, New York. Department of Health Policy and Research, Weill Cornell Medical College, New York, New York.
 MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands; MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, location VUmc, Amsterdam, the Netherlands. Electronic address: bmj.uitdehaag@amsterdamumc.nl.
 Universitair MS Centrum (UMSC) Hasselt-Pelt, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Biomedical Research Institute (BIOMED), Agoralaan, Diepenbeek 3590, Belgium; Noorderhart, Revalidatie en MS, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Rehabilitation Research Center, Agoralaan, Diepenbeek 3590, Belgium. Electronic address: sofie.aerts@uhasselt.be. Universitair MS Centrum (UMSC) Hasselt-Pelt, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Biomedical Research Institute (BIOMED), Agoralaan, Diepenbeek 3590, Belgium; UHasselt, Data Science Institute, Agoralaan, Diepenbeek 3590, Belgium; The D-Lab, Department of Precision Medicine, GROW - School for Oncology, Maastricht University, Universiteitssingel 40, Maastricht 6229 ER, the Netherlands. Universitair MS Centrum (UMSC) Hasselt-Pelt, Boemerangstraat 2, Pelt 3900, Belgium; Noorderhart, Revalidatie en MS, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Rehabilitation Research Center, Agoralaan, Diepenbeek 3590, Belgium. Universitair MS Centrum (UMSC) Hasselt-Pelt, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Biomedical Research Institute (BIOMED), Agoralaan, Diepenbeek 3590, Belgium; Noorderhart, Revalidatie en MS, Boemerangstraat 2, Pelt 3900, Belgium. Universitair MS Centrum (UMSC) Hasselt-Pelt, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Biomedical Research Institute (BIOMED), Agoralaan, Diepenbeek 3590, Belgium; UHasselt, Data Science Institute, Agoralaan, Diepenbeek 3590, Belgium. Universitair MS Centrum (UMSC) Hasselt-Pelt, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Biomedical Research Institute (BIOMED), Agoralaan, Diepenbeek 3590, Belgium; Noorderhart, Revalidatie en MS, Boemerangstraat 2, Pelt 3900, Belgium; UHasselt, Rehabilitation Research Center, Agoralaan, Diepenbeek 3590, Belgium.
 From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). llramio@idibgi.org equintana@idibgi.org. From the Neuroinflammation and Neurodegeneration Group (M.M.-S.M., I.G., A.Q.-V., M.G.R., R.R.C., G.Á., A.M., E.Q., L.R.-T.), Girona Biomedical Research Institute (IDIBGI), Salt, Spain; CERCA Programme/Generalitat de Catalunya; Neurology Department (R.R.C., G.Á., L.R.-T.), Girona Neuroimmunology and Multiple Sclerosis Unit, Dr. Josep Trueta University Hospital and Santa Caterina Hospital; Red Española de Esclerosis Múltiple (REEM) (R.R.C., E.Q., L.R.-T.) Medical Sciences Department (R.R.C., E.Q., L.R.-T.), University of Girona (UdG), Spain; Girona Biomedical Research Institute (IDIBGI) (M.B.), Spain; Immunology Department (L.M.V.), Hospital Ramón y Cajal, Madrid, Spain; IRYCIS; and Unitat de Neuroimmunologia, Hospital Universitari i Politècnic La Fe.València (J.C.-V., B.C.). llramio@idibgi.org equintana@idibgi.org.
 Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
 Independent, Albany, CA, United States.
 Departments of Clinical Neurosciences and the Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada; Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada. Departments of Clinical Neurosciences and the Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada; Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada. Departments of Clinical Neurosciences and the Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada. Departments of Clinical Neurosciences and the Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada; Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada. Electronic address: Carlos.Camara-Lemarroy@albertahealthservices.ca.
 Institute of Higher Nervous Activity and Neurophysiology, Butlerova street 5a, Moscow 117485, Russia. Electronic address: hydrohinon@mail.ru. Bujanov Moscow City Clinical Hospital, Moscow, Russia. Institute of Higher Nervous Activity and Neurophysiology, Butlerova street 5a, Moscow 117485, Russia; Federal State Budget Educational Institution of Higher Education M.V.Lomonosov Moscow State University, Moscow, Russia. City Clinical Hospital № 24, Moscow, Russia. Research Center of Neurology, Moscow, Russia. Research Center of Neurology, Moscow, Russia; Pavlov First Saint Petersburg Medical University, Saint Petersburg, Russia. Pavlov First Saint Petersburg Medical University, Saint Petersburg, Russia. Bujanov Moscow City Clinical Hospital, Moscow, Russia. Bujanov Moscow City Clinical Hospital, Moscow, Russia. Bujanov Moscow City Clinical Hospital, Moscow, Russia. Bujanov Moscow City Clinical Hospital, Moscow, Russia. Pavlov First Saint Petersburg Medical University, Saint Petersburg, Russia. Institute of Higher Nervous Activity and Neurophysiology, Butlerova street 5a, Moscow 117485, Russia; Bujanov Moscow City Clinical Hospital, Moscow, Russia; Moscow Research and Clinical Center for Neuropsychiatry, Moscow Healthcare Department, Russia. Moscow Research and Clinical Center for Neuropsychiatry, Moscow Healthcare Department, Russia; Pirogov Russian National Research Medical University, Moscow, Russia.
 Département de neurologie, Hôpital Pitié-Salpêtrière, AP-HP, 47-83 boulevard de l'Hôpital, 75013 Paris, France. Electronic address: marie-helene.colpaert@aphp.fr. Département de neurologie, Hôpital Pitié-Salpêtrière, AP-HP, 47-83 boulevard de l'Hôpital, 75013 Paris, France; Centre de ressources et de compétences sclérose en plaques Paris-GH Pitié-Salpêtrière, Hôpital Pitié-Salpêtrière, AP-HP, 47-83 boulevard de l'Hôpital, 75013 Paris, France.
 Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada. Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada. Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Alberta, Canada. Department of Medicine (Dermatology), University of Alberta, Edmonton, Alberta, Canada. Department of Pathology, University of Alberta, Alberta, Canada. Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada. Electronic address: jmccombe@ualberta.ca.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. abdorrezamoghadasi@gmail.com.
 Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology (IDI), Vall d'Hebron University Hospital, Spain, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology (IDI), Vall d'Hebron University Hospital, Spain, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology (IDI), Vall d'Hebron University Hospital, Spain, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology (IDI), Vall d'Hebron University Hospital, Spain, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Research institute of Computer Vision and Robotics, University of Girona, Girona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology (IDI), Vall d'Hebron University Hospital, Spain, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Research institute of Computer Vision and Robotics, University of Girona, Girona, Spain. Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: ctur@cem-cat.org.
 Department of Neurology, Oregon Health & Science University, Portland, OR, USA. College of Pharmacy, Oregon Health & Science University/Oregon State University, Portland, OR, USA.
 From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. From the Department of Clinical Neurosciences (N.C., M.W.K.), University of Calgary, Canada; Department of Neurology (J.M.), Rijnstate Hospital, Arnhem, The Netherlands; Multiple Sclerosis Center (P.R., J.D.B.), Swedish Neuroscience Institute, Seattle, WA; Department of Neurology (B.M.J.U., E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands; Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. mwkoch@ucalgary.ca.
 MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. m.vandam2@amsterdamumc.nl. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Neurochemistry Lab, Department of Clinical Chemistry, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, De Boelelaan 1117, Amsterdam, The Netherlands. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Department of Medical Psychology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, De Boelelaan 1117, Amsterdam, The Netherlands. Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, De Boelelaan 1117, Amsterdam, The Netherlands. Department of Medical Psychology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, De Boelelaan 1117, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Neurochemistry Lab, Department of Clinical Chemistry, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, De Boelelaan 1117, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Institute of Psychology, Health, Medical and Neuropsychology Unit, Leiden University, Wassenaarseweg 52, Leiden, The Netherlands.
 Neuropsychiatric Department, Faculty of Medicine, South Valley University, Qena University, Qena, Egypt. Department of Neuropsychiatry, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt. Department of Neuropsychiatry, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt. Radiology Department, Faculty of Medicine, Assiut University, Assiut, Egypt. Neuropsychiatric Department, Faculty of Medicine, South Valley University, Qena University, Qena, Egypt. Department of Neuropsychiatry, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt. emankhedr99@aun.edu.eg. Neuropsychiatric Department, Faculty of Medicine, Aswan University, Aswan, Egypt. emankhedr99@aun.edu.eg.
 IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy/Department of Biomolecular Sciences, University of Urbino "Carlo Bo," Urbino, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. Department of Medicine and Health Sciences "Vincenzo Tiberio," Unimol, Campobasso, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Hospital, Milan, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Hospital, Milan, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Roma, Italy/Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Roma, Italy/Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Rome, Italy. IRCSS Neuromed, Pozzilli, Italy/Department of Systems Medicine, Tor Vergata University, Rome, Italy. IRCSS Neuromed, Pozzilli, Italy.
 Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Faculty of Psychology, Universidad Autónoma de Madrid, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Faculty of Psychology, Universidad Autónoma de Madrid, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, San Carlos Institute for Health Research (IdiSSC), Universidad Complutense, Madrid, Spain.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurorehabilitation Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Neurophysiology Service, IRCCS Osepdale San raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy rocca.mara@hsr.it. Neurology Unit, IRCCS Ospedale San Raffaele, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy.
 Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. William S. Middleton VA Medical Center, Madison, WI, USA. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Neurology, Instituto de Investigacion Sanitaria San Carlos (IdISSC), Hospital Clinico San Carlos, Madrid, Spain.
 Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. Centro Sclerosi Multipla, Az. Osp. S. Camillo Forlanini, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Multiple Sclerosis Center, Gallarate Hospital, ASST della Valle Olona, Gallarate, Italy. Ospedale San Pietro fatebenefratelli, Rome, Italy. Centro Per Lo Studio E La Cura Della Sclerosi Multipla E Malattie Demielinizzanti, Dipartimento Di Neuroscienze, Riabilitazione, Oftalmologia, Genetica E Scienze Materno-Infantili, Clinica Neurologica-Ospedale Policlinico San Martino (DiNOGMI), Genoa, Italy. Neurology Unit, NESMOS Department, S. Andrea Hospital, Sapienza University of Rome, Rome, Italy. Multiple Sclerosis Center, Policlinico Umberto I, Sapienza, University of Rome, Rome, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, Catania, Italy. Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari "Aldo Moro", Bari, Italy. Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.
 Pre-Clinical Research Unit, King Fahad Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia; Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Electronic address: mohdzubairalam@yahoo.com.
 Department of Neurology, Rigshospitalet Glostrup, Valdemar Hansens vej 13, 2600 Glostrup, Denmark; Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. Department of Neurology, Rigshospitalet Glostrup, Valdemar Hansens vej 13, 2600 Glostrup, Denmark. Department of Neurology, Rigshospitalet Glostrup, Valdemar Hansens vej 13, 2600 Glostrup, Denmark; Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. Department of Autoimmunology, Statens Serum Institut, Ørestads boulevard 5, 2300 Copenhagen S, Denmark. Institute of Biotechnology, University of Vilnius, Saulėtekio al. 7, 10257 Vilnius, Lithuania. Institute of Biotechnology, University of Vilnius, Saulėtekio al. 7, 10257 Vilnius, Lithuania. Department of Neurology, Rigshospitalet Glostrup, Valdemar Hansens vej 13, 2600 Glostrup, Denmark. Department of Neurology, Rigshospitalet Glostrup, Valdemar Hansens vej 13, 2600 Glostrup, Denmark; Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark; Department of Autoimmunology, Statens Serum Institut, Ørestads boulevard 5, 2300 Copenhagen S, Denmark. Electronic address: gunnar.houen@regionh.dk.
 Brigham Multiple Sclerosis Center & Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, United States; Harvard Medical School, Boston, MA, United States. Electronic address: tbkaplan@bwh.harvard.edu. Brigham Multiple Sclerosis Center & Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, United States; University of Massachusetts Chan Medical School, Worcester, MA, United States. Brigham Multiple Sclerosis Center & Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, United States; Harvard Medical School, Boston, MA, United States. Harvard Medical School, Boston, MA, United States. Brigham Multiple Sclerosis Center & Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, United States; Harvard Medical School, Boston, MA, United States. Brigham Multiple Sclerosis Center & Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, United States; Harvard Medical School, Boston, MA, United States.
 Health Economic Evaluation program. School of Economic Sciences and School of Medicine, Universidad de Antioquia, Medellín, Colombia. Electronic address: cenavarroc@unal.edu.co. Health Economic Evaluation program. School of Economic Sciences and School of Medicine, Universidad de Antioquia, Medellín, Colombia.
 Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. Medical Genetics Division, Department of Pediatrics, CHU Sainte-Justine, University of Montreal, Montreal, Quebec, Canada. Medical Genetics Division, Department of Pediatrics, CHU Sainte-Justine, University of Montreal, Montreal, Quebec, Canada. Department of Clinical Laboratory Medicine, OPTILAB Montreal CHU Sainte-Justine, Montreal, Quebec, Canada. Medical Genetics Division, Department of Pediatrics, CHU Sainte-Justine, University of Montreal, Montreal, Quebec, Canada. Molecular Diagnostic Laboratory, CHU Sainte-Justine, Montreal, Quebec, Canada. Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. Department of Diagnostic Radiology, McGill University, Montreal, Quebec, Canada.
 Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ssaidha2@jhmi.edu. RTI Health Solutions, Manchester, UK. RTI Health Solutions, Manchester, UK. RTI Health Solutions, Manchester, UK. RTI Health Solutions, Manchester, UK. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
 Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Department of Ophthalmology and Vision Science, Eye and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Department of Ophthalmology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Department of Ophthalmology and Vision Science, Eye and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Novartis Pharmaceuticals, Shanghai, China. Novartis Pharmaceuticals, Shanghai, China. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Novartis Corporation (Malaysia) Sdn. Bhd., Petaling Jaya, Malaysia. Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China. National Center for Neurological Disorders, Shanghai, China. Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
 Dept of Neurology, Virginia Commonwealth University, Richmond, VA, USA. Medical University of South Carolina, Charleston SC, USA. Dept of Neurology, University of Virginia, Charlottesville VA, USA; Division of Child Neurology, Dept. of Neurology, University of Virginia, Charlottesville, VA, USA. Dept of Neurology, University of Virginia, Charlottesville VA, USA. Dept of Public Health Sciences, University of Virginia, Charlottesville VA, USA. Dept of Neurology, Virginia Commonwealth University, Richmond, VA, USA. Medical University of South Carolina, Charleston SC, USA; Dept of Neurology, University of Virginia, Charlottesville VA, USA. Electronic address: jnb8h@virginia.edu.
 Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Universitat de Barcelona, Barcelona, Spain. Office of Therapies for Neurological and Psychiatric Disorders, Human Medicines Division, European Medicines Agency, Amsterdam, The Netherlands. Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany. phil.albrecht@gmail.com. Department of Neurology, Maria Hilf Clinic, Mönchengladbach, Germany. phil.albrecht@gmail.com. Department of Neurology, LVR-Klinikum Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
 Department of Counselling, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Counselling, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Counseling, Faculty of Education and Psychology, University of Mohaghegh Ardabili, Ardabil, Iran. Department of Psychology, Buinzahra Branch, Islamic Azad University, Qazvin, Iran. Department of Clinical Psychology, Medical Science Branch, Islamic Azad University, Tehran, Iran. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Electronic address: ecarnerocontentti@hospitalaleman.com.
 The National Hospital for Neurology and Neurosurgery, London, UK. School of Health Sciences, City, University of London, London, UK. School of Health Sciences, City, University of London, London, UK. The National Hospital for Neurology and Neurosurgery, London, UK. Department of Organization Science, Faculty of Social Sciences, VU Amsterdam, Amsterdam, The Netherlands.
 Research Immunogenetics Laboratory, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. Research Immunogenetics Laboratory, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. Research Immunogenetics Laboratory, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, NKUA, Aeginition University Hospital, Vassilisis Sofias Ave 72-74, 11528, Athens, Greece. Research Immunogenetics Laboratory, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. Research Immunogenetics Laboratory, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. Aghia Sophia Children's Hospital, University Research Institute of Maternal and Child Health and Precision Medicine and UNESCO Chair On Adolescent Health Care, National and Kapodistrian University of Athens, 11527, Athens, Greece. Neuroimmunology Unit, Department of Pathophysiology, National and Kapodistrian University of Athens, Athens, Greece. Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA. 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, NKUA, Aeginition University Hospital, Vassilisis Sofias Ave 72-74, 11528, Athens, Greece. Research Immunogenetics Laboratory, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. managnost@med.uoa.gr. 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, NKUA, Aeginition University Hospital, Vassilisis Sofias Ave 72-74, 11528, Athens, Greece. managnost@med.uoa.gr. Multiple Sclerosis and Demyelinating Diseases Unit, 1st, Department of Neurology, Medical School, National and Kapodistrian University of Athens, Aeginition University Hospital, Athens, Greece. managnost@med.uoa.gr.
 Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, New Jersey. Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, New Jersey. Department of Pediatrics, Rutgers Robert Wood Johnson Medical School, Rutgers University, New Brunswick, New Jersey. Department of Biostatistics and Epidemiology, Rutgers School of Public Health, Rutgers University, Piscataway, New Jersey. Department of Pediatrics, Rutgers Robert Wood Johnson Medical School, Rutgers University, New Brunswick, New Jersey. Department of Neurology, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey. Department of Neurology, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey. Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, New Jersey. Department of Biostatistics and Epidemiology, Rutgers School of Public Health, Rutgers University, Piscataway, New Jersey. Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, New Jersey. Department of Pharmacy Practice and Administration, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey.
 Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy.
 Springer Nature, Private Bag 65901, Mairangi Bay, Auckland, 0754, New Zealand. dru@adis.com.
 From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. tjalf.ziemssen@uniklinikum-dresden.de. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland. From the Center of Clinical Neuroscience (T.Z.), Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Germany; Division of Neurology (Medicine) (V.B.), University of British Columbia, Vancouver, Canada; Queen Square Multiple Sclerosis Centre (J.C.), UCL Queen Square Institute of Neurology, London, United Kingdom; Partners Pediatric Multiple Sclerosis Centre (T.C.), Massachusetts General Hospital, Boston; Department of Neurology (B.A.C.C.), Weill Institute for Neurosciences, UCSF, San Francisco, CA; Department of Neurology and Center of Clinical Neuroscience (E.K.H.), First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic; Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Switzerland; Multiple Sclerosis Clinic (P.L.), Department of Neurology, Montpellier University Hospital, France; Department of Neurology (A.M.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.N.), Keio University School of Medicine, Tokyo, Japan; Department of Neurology (C.O.-G.), Hospital Clinico San Carlos, IdISSC, Departametno de medicina, Universidad Complutense de Madrid, Spain; Nuffield Department of Clinical Neurosciences (J.P.), John Radcliffe Hospital, University of Oxford, United Kingdom; The MS Center for Innovations in Care (B.S.), Missouri Baptist Medical Center, St Louis, MO; Department of Basic Medical Sciences (M.T.), Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy; Novartis Healthcare Pvt. Ltd. (A.P.), Hyderabad, India; Novartis Pharma GmbH (B.R.), Nuremberg, Germany; and Novartis Pharma AG (T.H.), Basel, Switzerland.
 College of Medical Informatics, Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. College of Medical Informatics, Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: lymzhang70@163.com.

 UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. Genetic Epidemiology and Genomics Laboratory, Divisions of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, California, USA. University of Utah Health, Salt Lake City, Utah, USA. University of Utah Health, Salt Lake City, Utah, USA. University of Utah Health, Salt Lake City, Utah, USA. Mayo Clinic, Rochester, Minnesota, USA. Mayo Clinic, Rochester, Minnesota, USA. Brigham and Women's Hospital, Harvard Medical school, Boston, Massachusetts, USA. University of California San Diego, San Diego, California, USA. Childrens Hospital Boston, Boston, Massachusetts, USA. Cleveland Clinic, Cleveland, Ohio, USA. New York University Medical Center, New York City, New York, USA. Division of Child Neurology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Jacobs School of Medicine and Biomedical Sciences University of Buffalo, Buffalo, New York, USA. Texas Children's Hospital, Houston, Texas, USA. University of Texas Southwestern Medical Center, Dallas, Texas, USA. Loma Linda University Children's Hospital, Loma Linda, California, USA. Washington University in St. Louis, St Louis, Missouri, USA. Denver Children's Hospital, Denver, Colorado, USA. UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. Neuroepidemiology Unit, The University of Melbourne School of Population and Global Health, Melbourne, Carlton, Australia. Clinical Outcomes Research Unit (CORe), Royal Melbourne Hospital, The University of Melbourne, Melbourne, Parkville, Australia. Multiple Sclerosis Flagship, Menzies Institute for Medical Research, University of Tasmania, Tasmania, Hobart, Australia. Department of Systems Pharmacology and Translational Therapeutics (SPATT), University of Pennsylvania, Philadelphia, Pennsylvania, USA. Genetic Epidemiology and Genomics Laboratory, Divisions of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, California, USA. Department of Integrative Biology, University of California Berkeley, Berkeley, California, USA. UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA emmanuelle.waubant@ucsf.edu.
 Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Piazza d'Armi, 09123, Cagliari, Italy. massimiliano.pau@unica.it. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Piazza d'Armi, 09123, Cagliari, Italy. Multiple Sclerosis Centre, Binaghi Hospital, ATS Sardegna, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Centre, Binaghi Hospital, ATS Sardegna, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Centre, Binaghi Hospital, ATS Sardegna, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Centre, Binaghi Hospital, ATS Sardegna, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Centre, Binaghi Hospital, ATS Sardegna, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
 The University of British Columbia, Vancouver, British Columbia, Canada.
 DRK Kliniken Berlin Köpenick, Neurology Department, S.-Allende-Str. 2-8, 12555, Berlin, Germany. Clinical Trials Unit, Special Unit for Biomedical Research and Education & Department of Clinical Pharmacology School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece.
 Division of Neuroimmunology and Neurological Infections, Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA/Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
 Department of Pharmaceutical Sciences, Bill Gatton College of Pharmacy, East Tennessee State University, Johnson City, TN 37614, United States. Department of Pharmaceutical Sciences, Bill Gatton College of Pharmacy, East Tennessee State University, Johnson City, TN 37614, United States. Department of Pharmaceutical Sciences, Bill Gatton College of Pharmacy, East Tennessee State University, Johnson City, TN 37614, United States. Electronic address: puria1@etsu.edu.
 Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Multiple Sclerosis Patient and Public Involvement Group, Nottingham, UK. School of Health Sciences, University of Nottingham, Nottingham, UK. Swansea Centre for Health Economics, College of Human and Health Sciences, Swansea University, Swansea, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Department of Neurology, Nottingham University Hospitals NHS Trust, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Institute of Mental Health, Nottinghamshire Healthcare NHS Trust, Nottingham, UK.
 Cytel Inc., Potsdamer Straße 58, 10785, Berlin, Germany. Electronic address: rachel.knapp@cytel.com. Cytel Inc., Potsdamer Straße 58, 10785, Berlin, Germany. IPAM e.V., Alter Holzhafen 19, 23966, Wismar, Germany. Electronic address: thomas.wilke@ipam-wismar.de. AOK PLUS, Sternplatz 7, 01067, Dresden, Germany. F. Hoffmann-La Roche Ltd, Grenzacherstrasse 124, 4070, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Grenzacherstrasse 124, 4070, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Grenzacherstrasse 124, 4070, Basel, Switzerland.
 Associate Professor of Neurology, Neurology Department of Vali-e-Asr Hospital, Zanjan University of Medical Sciences, Zanjan, Iran. Department of Neurology, Zanjan University of Medical Sciences, Zanjan, Iran. Resident of Neurology, Neurology Department of Vali-e-Asr Hospital, Zanjan University of Medical Sciences, Zanjan, Iran.
 MSBase Foundation, Melbourne, Australia. Dokuz Eylul University, Izmir, Turkey. Amiri Hospital, Sharq, Kuwait. Department of Neurology 19 Mayis University, Samsun, Turkey. Liverpool Hospital, Sydney, Australia. University Hospital Ghent, Ghent, Belgium. MS Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia. Neurology Institute, Harley Street Medical Center, Abu Dhabi, United Arab Emirates. American University of Beirut Medical Center, Beirut, Lebanon. School of Medicine & Public Health, University of Newcastle, Newcastle, Australia. Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, Australia. Bakirkoy Education & Research Hospital for Psychiatric & Neurological Diseases, Istanbul, Turkey. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine & Neuromedicine, Biomedicine & Clinical Research, University Hospital Basel & University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology & Neuroscience (RC2NB), University Hospital & University of Basel, Switzerland. Department of Neurology, Galdakao-Usansolo University Hospital, Osakidetza-Basque Health Service, Biocruces-Bizkaia Health Research Institute, Galdakao, Spain. Center of Neuroimmunology, Service of Neurology, Hospital Clinic de Barcelona, Barcelona, Spain. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino, Italy. Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. Department of Neurology & Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague & General University Hospital, Prague, Czech Republic. Nemocnice Jihlava, Jihlava, Czech Republic. Department of Medical & Surgical Sciences & Advanced Technologies, GF Ingrassia, Catania, Italy. Department of Neurology, Austin Health, Melbourne, Australia. Neurology Unit, Department of Medicine, College of Medicine & Health Sciences & Sultan Qaboos University Hospital, SQU, Al Khodh, Oman. Academic MS Center Zuyderland, Department of Neurology, Zuyderland Medical Center, Sittard-Geleen, The Netherlands. School for Mental Health & Neuroscience, Maastricht University, Maastricht, The Netherlands. Division of Neurology, St Michael's Hospital, University of Toronto, Toronto, Canada. Koc University School of Medicine & Koc University Research Center for Translational Medicine (KUTTAM) Istanbul, Turkey. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. MSBase Foundation, Melbourne, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
 Servicio de Medicina Física y Rehabilitación, Complexo Hospitalario Universitario de A Coruña, A Coruña, España. Electronic address: jacobofor@gmail.com. Servicio de Neurología, Complexo Hospitalario Universitario de A Coruña, A Coruña, España.
 Hospital General Universitario Rafael Méndez, 30800 Lorca, España. Hospital General Universitario Morales Meseguer, Murcia, España. Hospital General Universitario Rafael Méndez, 30800 Lorca, España. Hospital General Universitario Rafael Méndez, 30800 Lorca, España. Hospital Universitario Virgen de la Arrixaca, Murcia, España. Servicio de Urgencias y Atención Primaria, Aguilas, España.
 Department of Neurology, Soonchunhyang University Hospital Cheonan, Soonchunhyang University College of Medicine, Cheonan, South Korea. Department of Artificial Intelligence, Korea University, Seoul, South Korea. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. Department of Neurology, Neuroscience Center, Samsung Medical Center, Seoul, South Korea. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. Department of Neurology, Neuroscience Center, Samsung Medical Center, Seoul, South Korea. Department of Radiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. Department of Artificial Intelligence, Korea University, Seoul, South Korea. jkseong@korea.ac.kr. School of Biomedical Engineering, Korea University, Seoul, South Korea. jkseong@korea.ac.kr. Interdisciplinary Program in Precision Public Health, Korea University, Seoul, South Korea. jkseong@korea.ac.kr. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. juhongm@skku.edu. Department of Neurology, Neuroscience Center, Samsung Medical Center, Seoul, South Korea. juhongm@skku.edu. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology (SAIHST), Sungkyunkwan University, 50 Irwon-dong, Gangnam-gu, Seoul, 135-710, South Korea. juhongm@skku.edu.
 Faculty of Pharmacy, Department of Analytical Chemistry, Ege University, 35100, Izmir, Bornova, Turkey; Graduate School of Natural and Applied Sciences, Department of Biomedical Technologies, Ege University, 35100, Izmir, Bornova, Turkey. Faculty of Pharmacy, Department of Analytical Chemistry, Ege University, 35100, Izmir, Bornova, Turkey. Electronic address: pinar.kara@ege.edu.tr.
 Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, California. UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, David Geffen School of Medicine at the University of California, Los Angeles, California; UCLA Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine at the University of California, Los Angeles, California. Electronic address: amg@ucla.edu.
 City Clinical Hospital No. 7, Kazan, Russia. City Clinical Hospital No. 7, Kazan, Russia. Kazan State Medical Academy - Branch of the Russian Medical Academy of Continuing Professional Education, Kazan, Russia. City Clinical Hospital No. 7, Kazan, Russia. Kazan State Medical Academy - Branch of the Russian Medical Academy of Continuing Professional Education, Kazan, Russia.
 School of Nursing, Duke University, Durham, North Carolina, USA. School of Nursing, University of Michigan, Ann Arbor, Michigan, USA. Applied Biostatistics Laboratory, University of Michigan, Ann Arbor, Michigan, USA. Division of Multiple Sclerosis & Neuroimmunology, Department of Neurology, Michigan Medicine, Ann Arbor, Michigan, USA. School of Public Health, University of Michigan, Ann Arbor, Michigan, USA. School of Nursing, University of Michigan, Ann Arbor, Michigan, USA.
 Department of Neurology, Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland david.leppert@unibas.ch. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Division of Neuroscience, Institute of Experimental Neurology, San Raffaele Hospital, Milan, Italy. Laboratory of Neuroimmunology, National Neurological Institute C. Mondino, Pavia, Italy. Quanterix Corp, Lexington, Massachusetts, USA. Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neurology, Brain and Nerve Center, Fukuoka Central Hospital, International University of Health and Welfare, Fukuoka, Japan. Translational Neuroscience Center, Graduate School of Medicine, and School of Pharmacy at Fukuoka, International University of Health and Welfare, Okawa, Japan. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland.
 Neuro-ophthalmology Division, Department of Ophthalmology, Massachusetts Eye and Ear/Harvard Medical School, Boston, MA, USA. Neuro-ophthalmology Division, Department of Ophthalmology, Massachusetts Eye and Ear/Harvard Medical School, Boston, MA, USA. Neuro-immunology Division, Department of Neurology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA.
 Servicio de Neurología, Complejo Hospitalario de Navarra- IdiSNA (Navarra Institute for Health Research), Navarra, Spain. Electronic address: aioraostolaza@gmail.com. Servicio de Neurología, Complejo Hospitalario de Navarra- IdiSNA (Navarra Institute for Health Research), Navarra, Spain. Servicio de Neurología, Complejo Hospitalario de Navarra- IdiSNA (Navarra Institute for Health Research), Navarra, Spain.
 Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Bochum, Germany. European Medical Affairs, Teva Pharmaceuticals Europe B.V., Amsterdam, the Netherlands. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St Josef Hospital, Katholisches Klinikum Bochum gGmbH, Ruhr University Bochum, Bochum, Germany. Electronic address: kerstin.hellwig@rub.de.
 Department of Neurology, San Francisco & the San Francisco VA Medical Center, University of California, San Francisco, San Francisco, California, United States of Ameirca. Kaiser Permanente, Walnut Creek Medical Center, Dublin, California, United States of Ameirca. Center for Neuro-Engineering and Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, United States of Ameirca. INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, Nantes Université, Nantes, France.
 School of Health Sciences, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; College of Applied Medical Sciences, University of Jeddah, Jeddah, Saudi Arabia. Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; School of Biomedical Sciences and Pharmacy, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia. Olea Medical, La Ciotat, France. Olea Medical, La Ciotat, France. School of Health Sciences, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; Department of Radiology, King Fahd Hospital of the University, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia. Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. Siemens Healthcare GmbH, Erlangen, Germany. School of Health Sciences, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. Electronic address: saadallah.ramadan@newcastle.edu.au. Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW, Australia; School of Medicine and Public Health, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia.
 Department of Medicine, Division of Neurology, University of Alberta, 7-132B Clinical Sciences Building, 8440 112 Street NW, Edmonton, AB, T6G 2B7, Canada. EPICORE (Epidemiology Coordinating and Research) Centre, Department of Medicine, University of Alberta, Edmonton, AB, Canada. EPICORE (Epidemiology Coordinating and Research) Centre, Department of Medicine, University of Alberta, Edmonton, AB, Canada. Department of Pharmacology, University of Alberta, Edmonton, AB, Canada. EPICORE (Epidemiology Coordinating and Research) Centre, Department of Medicine, University of Alberta, Edmonton, AB, Canada. EPICORE (Epidemiology Coordinating and Research) Centre, Department of Medicine, University of Alberta, Edmonton, AB, Canada. Department of Pharmacology, University of Alberta, Edmonton, AB, Canada. Department of Medicine, University of Alberta, Edmonton, AB, Canada. Department of Medicine, Division of Neurology, University of Alberta, 7-132B Clinical Sciences Building, 8440 112 Street NW, Edmonton, AB, T6G 2B7, Canada. smyth@ualberta.ca.
 Neuroradiology Group, Vall d'Hebron Research Institute (VHIR), Barcelona 08035, Spain. Department of Neurology, Multiple Sclerosis center of Catalonia (Cemcat), Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain. Center of Neuroimmunology and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona 08036, Spain. Department of Neurology, Multiple Sclerosis center of Catalonia (Cemcat), Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona (UAB), Barcelona 08035, Spain. Center of Neuroimmunology and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona 08036, Spain. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Rhine Main Neuroscience Network (rmn2), Mainz 55131, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Rhine Main Neuroscience Network (rmn2), Mainz 55131, Germany. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy. Vita-Salute, San Raffaele University, Milan 20132, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy. Vita-Salute, San Raffaele University, Milan 20132, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy. Department of Neurology, Oslo University Hospital, Oslo 0450 , Norway. Department of Psychology, University of Olso, Oslo 0315, Norway. Department of Neurology, Oslo University Hospital, Oslo 0450 , Norway. Institute of Clinical Medicine, University of Oslo, Oslo 0315, Norway. Queen Square MS Centre, Dept of Neuroinflammation, Institute of Neurology, University College London, London WC1N 3BG, United Kingdom. Queen Square MS Centre, Dept of Neuroinflammation, Institute of Neurology, University College London, London WC1N 3BG, United Kingdom. Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam 1081 HZ, The Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam 1081 HZ, The Netherlands. Queen Square MS Centre, Dept of Neuroinflammation, Institute of Neurology, University College London, London WC1N 3BG, United Kingdom. Departments of Advanced Biomedical Sciences and Electrical Engineering and Information Technology, University of Naples "Federico II", Naples 80138, Italy. Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam 1081 HZ, The Netherlands. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples "Federico II", Naples 80138, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Neuroradiology Group, Vall d'Hebron Research Institute (VHIR), Barcelona 08035, Spain. Radiology (IDI), Vall d'Hebron University Hospital, Barcelona 08036, Spain. Center for Brain and Cognition, Computational Neuroscience Group, Department of Information and Communication Technologies, Universitat Pompeu Fabra, Barcelona 08018, Spain. Institució Catalana de la Recerca i Estudis Avançats, Universitat Pompeu Fabra, Barcelona 08010, Spain. Neuroradiology Group, Vall d'Hebron Research Institute (VHIR), Barcelona 08035, Spain. Radiology (IDI), Vall d'Hebron University Hospital, Barcelona 08036, Spain.
 Faculty of Medicine (Neurology), University of British Columbia and The Djavad Mowafaghian Centre for Brain Health, UBC Hospital, Vancouver, BC, Canada. Faculty of Medicine (Neurology), University of British Columbia and The Djavad Mowafaghian Centre for Brain Health, UBC Hospital, Vancouver, BC, Canada/College of Medicine and Public Health, Flinders University, Bedford Park, SA, Australia. Faculty of Medicine (Neurology), University of British Columbia and The Djavad Mowafaghian Centre for Brain Health, UBC Hospital, Vancouver, BC, Canada. Faculty of Medicine (Neurology), University of British Columbia and The Djavad Mowafaghian Centre for Brain Health, UBC Hospital, Vancouver, BC, Canada. Faculty of Medicine (Neurology), University of British Columbia and The Djavad Mowafaghian Centre for Brain Health, UBC Hospital, Vancouver, BC, Canada.
 From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering charidimos.tsagkas@usb.ch. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland charidimos.tsagkas@usb.ch. Department of Medicine and Biomedical Engineering; Division of Radiological Physics (T.H., M.W., O.B.). From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. Medical Image Analysis Center AG (M.A., A.A.), Basel, Switzerland. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Department of Radiology; Department of Neuroradiology (A.T.), Clinic for Radiology & Nuclear Medicine; and Research Center for Clinical Neuroimmunology. Medical Image Analysis Center AG (M.A., A.A.), Basel, Switzerland. From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. Medical Faculty (M.L., P.C.), University of Basel, Basel, Switzerland. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Department of Medicine and Biomedical Engineering; Division of Radiological Physics (T.H., M.W., O.B.). Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Department of Neurology (T.S.), DKD Helios Klinik Wiesbaden, Wiesbaden, Germany. From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Neuroscience Basel (RC2NB) (L.K.), Departments of Medicine, Clinical Research, and Biomedical Imaging, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Medicine and Biomedical Engineering; Division of Radiological Physics (T.H., M.W., O.B.). Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. Department of Biomedical Engineering (A.H.-H., M.A., A.C., M.B., M.W., S.P., O.B., C.G., P.C.), University of Basel, Allschwil, Switzerland. Medical Faculty (M.L., P.C.), University of Basel, Basel, Switzerland. From the Neurologic Clinic and Policlinic, Departments of Medicine (C.T., M.A., J.M., M.W., T.S., L.K., C.G., K.P.), Clinical Research and Biomedical Engineering. Translational Imaging in Neurology Basel (C.T., A.T., J.M., A.C., M.B., M.W., C.G., K.P.). Reha Rheinfelden (K.P.), Rheinfelden, Switzerland.
 Turku PET Centre, Turku University Hospital, Po Box 52, 20521, Turku, Finland. jussi.lehto@tyks.fi. Neurocenter, Turku University Hospital, Turku, Finland. jussi.lehto@tyks.fi. Turku PET Centre, Turku University Hospital, Po Box 52, 20521, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Turku PET Centre, Turku University Hospital, Po Box 52, 20521, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku University Hospital, Po Box 52, 20521, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku University Hospital, Po Box 52, 20521, Turku, Finland. Faculty of Science and Engineering, Åbo Akademi University, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland.
 Biochemistry Department, Faculty of Science, Suez University, PO Box 43518, Suez 43533, Egypt. Electronic address: Ahmed.Kamal@sci.suezuni.edu.eg. Biochemistry Department, Biotechnology Research Institute, High Throughput Molecular and Genetic Laboratory, Central Laboratories Network and the Centers of Excellence, National Research Centre, Dokki, Giza, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Egypt. Biochemistry Department, Faculty of Science, Suez University, PO Box 43518, Suez 43533, Egypt. Biochemistry Department, Faculty of Science, Suez University, PO Box 43518, Suez 43533, Egypt.
 Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain and Neurotechnologies, Moscow, Russia. Siberian State Medical University, Tomsk, Russia. Orden of the Red Banner of Labor City Clinical Hospital No. 1, Chelyabinsk, Russia. Rostov State Medical University, Rostov-on-Don, Russia. Ulyanovsk Regional Clinical Hospital, Ulyanovsk, Russia. Leningrad Regional Clinical Hospital, St. Petersburg, Russia. Vladimirsky Moscow Regional Research Clinical Institute, Moscow, Russia. State Novosibirsk Regional Clinical Hospital, Novosibirsk, Russia. Pyatigorsk City Clinical Hospital No. 2, Pyatigorsk, Russia. Semashko Nizhny Novgorod Regional Clinical Hospital, Nizhny Novgorod, Russia. Seredavin Samara Regional Clinical Hospital, Samara, Russia. N. Bechtereva Institute of the Human Brain, St. Petersburg, Russia. Medical and Sanitary unit «Neftyanik», Tyumen, Russia. Regional Clinical Hospital, Barnaul, Russia. Academician I.P. Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russia. Rostov Regional Clinical Hospital, Rostov-on-Don, Russia. Wagner Perm State Medical University, Perm, Russia. Republican Clinical Nerological Center, Kazan, Russia. Municipal Filatov Clinical Hospital No. 15, Moscow, Russia. AO BIOCAD, St. Petersburg, Russia. AO BIOCAD, St. Petersburg, Russia. AO BIOCAD, St. Petersburg, Russia. AO BIOCAD, St. Petersburg, Russia.
 From the Departments of Neuroradiology. Neurology, Heidelberg University Hospital, Heidelberg, Germany. From the Departments of Neuroradiology. From the Departments of Neuroradiology. Neurology, Heidelberg University Hospital, Heidelberg, Germany. Neurology, Heidelberg University Hospital, Heidelberg, Germany. Neurology, Heidelberg University Hospital, Heidelberg, Germany. From the Departments of Neuroradiology. From the Departments of Neuroradiology.
 Krasnov Research Institute of Eye Diseases, Moscow, Russia. Research Center of Neurology, Moscow, Russia. Research Center of Neurology, Moscow, Russia. Sechenov First Moscow State Medical University, Moscow, Russia. Krasnov Research Institute of Eye Diseases, Moscow, Russia. Krasnov Research Institute of Eye Diseases, Moscow, Russia. Sechenov First Moscow State Medical University, Moscow, Russia. Bochkov Research Centre for Medical Genetics, Moscow, Russia. Bochkov Research Centre for Medical Genetics, Moscow, Russia. Research Center of Neurology, Moscow, Russia.
 Department of Neuroradiology, Fondation Adolphe de Rothschild Hospital, 75019 Paris, France; University Paris Cité, 75006 Paris, France. Electronic address: alecler@for.paris.
 Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China husttjouyang110@163.com.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: bnourba1@jhmi.edu.
 Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Electronic address: sammi@ohsu.edu. Department of Neurology, Oregon Health & Science University, Portland, OR, USA; Department of Veterans Affairs MS Center of Excellence-West, Portland, OR, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA; Department of Veterans Affairs MS Center of Excellence-West, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA; Department of Veterans Affairs MS Center of Excellence-West, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA; Department of Veterans Affairs MS Center of Excellence-West, Portland, OR, USA. Electronic address: yadavv@ohsu.edu.
 Department of Biotechnology, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India. Computational and Molecular Biophysics Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India. Department of Biotechnology, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India. Computational and Molecular Biophysics Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India. Computational and Molecular Biophysics Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India.
 Department of Neurology, Obihiro Kosei General Hospital, Obihiro, Japan. Department of Neurology, Obihiro Kosei General Hospital, Obihiro, Japan. Department of Neurology, Hokuto Hospital, Obihiro, Japan. Department of Neurology, Tohoku University, Sendai Japan. Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Yamanote 5-jo 7-chome, Nishi-ku, Sapporo 063-0005, Japan. Electronic address: niino.masaaki.tc@mail.hosp.go.jp.
 Faculty of Physiotherapy and Nursing, University of Castilla La Mancha, 45071 Toledo, Spain. Research Group in Pediatric and Neurologic Physiotherapy, ImproveLab, University of Castilla La Mancha, 45071 Toledo, Spain. Faculty of Physiotherapy and Nursing, University of Castilla La Mancha, 45071 Toledo, Spain. Health and Social Research Center, University of Castilla-La Mancha, 16071 Cuenca, Spain. Health and Social Research Center, University of Castilla-La Mancha, 16071 Cuenca, Spain. Faculty of Physiotherapy and Nursing, University of Castilla La Mancha, 45071 Toledo, Spain. Health and Social Research Center, University of Castilla-La Mancha, 16071 Cuenca, Spain. Faculty of Physiotherapy and Nursing, University of Castilla La Mancha, 45071 Toledo, Spain. Research Group in Pediatric and Neurologic Physiotherapy, ImproveLab, University of Castilla La Mancha, 45071 Toledo, Spain. Health and Social Research Center, University of Castilla-La Mancha, 16071 Cuenca, Spain.
 Faculty of Law and Social Sciences, University of Castilla la Mancha, Toledo, Spain. Juan.OlivaMoreno@uclm.es.
 Institute of Radiology, Military Medical Academy, Belgrade, Serbia. Faculty of Medicine of the Military Medical Academy, University of Defence, Belgrade, Serbia. Faculty of Medicine of the Military Medical Academy, University of Defence, Belgrade, Serbia. Clinic for Neurology, Military Medical Academy, Belgrade, Serbia. Institute of Radiology, Military Medical Academy, Belgrade, Serbia. Faculty of Medicine of the Military Medical Academy, University of Defence, Belgrade, Serbia. Clinic for Neurology, Military Medical Academy, Belgrade, Serbia. Institute of Radiology, Military Medical Academy, Belgrade, Serbia. nece84@hotmail.com. Faculty of Medicine of the Military Medical Academy, University of Defence, Belgrade, Serbia. nece84@hotmail.com. Special Hospital for Cerebrovascular Diseases "Sveti Sava", Belgrade, Serbia. Institute of Radiology, Military Medical Academy, Belgrade, Serbia. Faculty of Medicine of the Military Medical Academy, University of Defence, Belgrade, Serbia. MRI Unit, Institute for Children and Adolescents Health Care of Vojvodina, Medical Faculty, University of Novi Sad, Novi Sad, Serbia.
 Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: pss@rh.dk. The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet, Glostrup, Denmark. The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Aarhus University Hospital, Aarhus, Denmark. Department of Neurology, Aalborg University Hospital, Aalborg, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark; The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
 Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Health Sciences, University of Genoa and Ospedale Policlinico San Martino IRCCS, Genoa, Italy. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Merck Group, Neurology and Immunology Darmstadt, Hessen, Delaware, USA. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy.
 Riverside Methodist Hospital, Columbus, OH, USA. Riverside Methodist Hospital, Columbus, OH, USA. Ohio University Heritage College of Osteopathic Medicine, Athens, Ohio, USA. Riverside Methodist Hospital, Columbus, OH, USA.
 Multiple Sclerosis Research Center, Neuroscience Institute. Department of Neurology, Sina Hospital. Department of Social Medicine. Multiple Sclerosis Research Center, Neuroscience Institute. Neuroscience Research Center, Qom University of Medical Sciences, Qom. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran. Department of Neurology, Valiasr Hospital, Zanjan University of Medical Sciences, Zanjan. Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran. Multiple Sclerosis Research Center, Neuroscience Institute.
 From the Department of Rehabilitation and Australian Rehabilitation Research Centre, Royal Melbourne Hospital, Parkville, Australia; and Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Parkville, Australia.
 Klinik für Neurologie mit Klinischer Neurophysiologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland. Klinik für Neurologie mit Klinischer Neurophysiologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland. Institut für Diagnostische und Interventionelle Neuroradiologie, Medizinische Hochschule Hannover, Hannover, Deutschland. Klinik für Neurologie mit Klinischer Neurophysiologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland. skripuletz.thomas@mh-hannover.de.
 Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Electronic address: chrishawkes@msn.com. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Department of Neurology, John Hunter Hospital, University Newcastle, Australia. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States. Department of Paediatrics (Neurology), Hospital for Sick Children, University of Toronto, Ontario, Canada.
 Federal Center of Brain and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Federal Center of Brain and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia.
 Department of Neurology, Pyhrn-Eisenwurzen Klinikum Steyr, Steyr, Austria. Department of Neurology, Klinikum Bad Hall and Bad Schallerbach, Bad Schallerbach, Austria. Department of Neurology, Medical University Vienna, Vienna, Austria.
 Dental Sector, 424 General Military Training Hospital, Thessaloniki, Greece. Electronic address: atsimpir@gmail.com. Dental School, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Dental Sector, 424 General Military Training Hospital, Thessaloniki, Greece; Department of Preventive Dentistry, Periodontology and Implant Biology, Dental School, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Hygiene, Social-Preventive Medicine and Medical Statistics, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Unit of Reproductive Endocrinology, 1st Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece. 2nd Department of Neurology, AHEPA Hospital, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece.
 The Fertility Department, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark. The Laboratory of Reproductive Biology, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark. The Fertility Department, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark. The Fertility Department, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark. Electronic address: kirsten.louise.tryde.macklon@regionh.dk.
 Department of Audiometry, Vocational School of Health Services, Yuksek Ihtisas University, Ankara 06291, Turkey. Electronic address: denizbarc@yiu.edu.tr. Department of Anatomy, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir 26480, Turkey. Department of Neurology, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir 26480, Turkey.
 Department of Neurology, Karadeniz Technical University Medical Faculty, 61080, Trabzon, Turkey. cavitb@yahoo.com. Department of Neurology, Dokuz Eylul University, Izmir, Turkey. Department of Neurology, Ondokuz Mayis University, Samsun, Turkey. Department of Neurology, Hacettepe University, Ankara, Turkey. Department of Neurology, Mersin University, Mersin, Turkey. Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Department of Neurology, Haseki Educational and Research Center, Istanbul, Turkey. Department of Neurology, Kocaeli University, Izmit, Turkey. Department of Neurology, Uludag University, Bursa, Turkey. Department of Neurology, Ege University, Izmir, Turkey. Department of Neurology, Erciyes University, Kayseri, Turkey. Department of Neurology, Karadeniz Technical University Medical Faculty, 61080, Trabzon, Turkey. Department of Neurology, Cukurova University, Adana, Turkey. Department of Neurology, Trakya University, Edirne, Turkey. Department of Neurology, Marmara University, Istanbul, Turkey. Department of Neurology, Aydın Adnan Menderes University, Aydin, Turkey. Department of Neurology, Dokuz Eylul University, Izmir, Turkey. Department of Neurology, Hacettepe University, Ankara, Turkey. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey.
 Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Neurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Program Neuroinflammation, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands/Department of Neurology, Amsterdam Neuroscience, Program Neuroinflammation, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands. MS Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, MöIndal, Sweden/Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, MöIndal, Sweden/Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK/UK Dementia Research Institute at UCL, London, UK/Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. NeuroRx, Montreal, QC, Canada. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA.
 Faculty of Health Sciences, Department of Rehabilitation Sciences, Cyprus University of Technology, Limassol, Cyprus. Physiotherapy Unit, Neurology Clinics, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Basic and Clinical Sciences, Medical School, University of Nicosia, Nicosia, Cyprus. Centre for Neuroscience and Integrative Brain Research (CENIBRE), University of Nicosia Medical School, Nicosia, Cyprus. Neuroepidemiology Department, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Biostatistics Unit, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Faculty of Health Sciences, Department of Rehabilitation Sciences, Cyprus University of Technology, Limassol, Cyprus.
 From the Neurology Service (R.I.S.), VA Portland Health Care System, OR; Department of Neurology (R.I.S.), Oregon Health and Science University, Portland; Department of Pathology and Immunology (L.P.), Washington University in St. Louis, MO; Brain and Mind Centre (L.P.), School of Medical Sciences, University of Sydney, NSW, Australia; and Neurology Department (A.M.L.-G.), Southern California Permanente Medical Group/Kaiser Permanente, Los Angeles Medical Center, CA. spainr@ohsu.edu. From the Neurology Service (R.I.S.), VA Portland Health Care System, OR; Department of Neurology (R.I.S.), Oregon Health and Science University, Portland; Department of Pathology and Immunology (L.P.), Washington University in St. Louis, MO; Brain and Mind Centre (L.P.), School of Medical Sciences, University of Sydney, NSW, Australia; and Neurology Department (A.M.L.-G.), Southern California Permanente Medical Group/Kaiser Permanente, Los Angeles Medical Center, CA. From the Neurology Service (R.I.S.), VA Portland Health Care System, OR; Department of Neurology (R.I.S.), Oregon Health and Science University, Portland; Department of Pathology and Immunology (L.P.), Washington University in St. Louis, MO; Brain and Mind Centre (L.P.), School of Medical Sciences, University of Sydney, NSW, Australia; and Neurology Department (A.M.L.-G.), Southern California Permanente Medical Group/Kaiser Permanente, Los Angeles Medical Center, CA.
 Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia. Laboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Stilponos Kiriakides Str. 1, 54636 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Stilponos Kiriakides Str. 1, 54636 Thessaloniki, Greece. Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia.
 OhioHealth Multiple Sclerosis Center, Riverside Methodist Hospital, 3535 Olentangy River Rd., Suite 1501, Columbus, OH 43214, USA. Electronic address: Jacqueline.Nicholas@ohiohealth.com. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Jazz Pharmaceuticals, Inc., Carlsbad, CA, USA. Jazz Pharmaceuticals, Inc., Carlsbad, CA, USA. Jazz Pharmaceuticals, Inc., Cambridge, UK. Bridgend Clinic, Wales, UK. Jazz Pharmaceuticals, Inc., Carlsbad, CA, USA.
 Saidu Medical College, KPK, Pakistan. Electronic address: bakhtmuhammad47@gmail.com. Medical college: Gomal Medical College, KPK, Dera Ismail khan, Pakistan.
 Institute for Advanced Biomedical Technologies (ITAB) and Department of Neurosciences, Imaging and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy; MS Centre, SS. Annunziata University Hospital, Chieti, Italy. Institute for Advanced Biomedical Technologies (ITAB) and Department of Neurosciences, Imaging and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy; MS Centre, SS. Annunziata University Hospital, Chieti, Italy. Institute for Advanced Biomedical Technologies (ITAB) and Department of Neurosciences, Imaging and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy; MS Centre, SS. Annunziata University Hospital, Chieti, Italy. Institute for Advanced Biomedical Technologies (ITAB) and Department of Neurosciences, Imaging and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy; MS Centre, SS. Annunziata University Hospital, Chieti, Italy. Electronic address: valentina.tomassini@unich.it.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. d.vannederpelt@amsterdamumc.nl. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Department of Epidemiology and Data Science, Amsterdam Public Health Research Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, 1007MB, Amsterdam, The Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. Institutes of Neurology and Healthcare Engineering, UCL London, London, UK. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands.
 Department of Neurology, Washington University in St. Louis, St Louis, Missouri, USA. Department of Neurology, Washington University in St. Louis, St Louis, Missouri, USA. Mallinckrodt Institute of Radiology, Washington University in St. Louis, St Louis, Missouri, USA. Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Department of Mathematics and Statistics, Washington University in St. Louis, St Louis, Missouri, USA. Department of Mathematics and Statistics, Washington University in St. Louis, St Louis, Missouri, USA. Department of Mathematics and Statistics, Washington University in St. Louis, St Louis, Missouri, USA. Department of Neurology, Washington University in St. Louis, St Louis, Missouri, USA. Mallinckrodt Institute of Radiology, Washington University in St. Louis, St Louis, Missouri, USA. Department of Neurology, Washington University in St. Louis, St Louis, Missouri, USA. Department of Neurology, Washington University in St. Louis, St Louis, Missouri, USA.
 From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. elliot.frohman@austin.utexas.edu. From the Department of Neurology (D.A.P.M., S.N.), Johns Hopkins Hospital, Baltimore, MD; Department of Neurology (R.L.), Wayne State University, Detroit, MI; Departments of Neurology (S.G., L.B.), Population Health, and Ophthalmology, NYU Grossman School of Medicine; Department of Neurology (T.V.), Dell Medical School, The University of Texas at Austin; Department of Neurology (A.G.), University of Rochester, NY; Department of Neurosciences (J.G.), University of California at San Diego; Quest Diagnostics (M.R.), Secaucus, NJ; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA.
 Department of Neurology, Jüdisches Krankenhaus Berlin, Heinz-Galinski-Strasse 1, Berlin-Mitte 13347, Federal Republic of Germany. Electronic address: juliane.klehmet@charite.de. Audimedes GmbH, Waageplatz 8, Göttingen 37073, Federal Republic of Germany. Biogen GmbH, Riedenburger Straße 7, München 81677, Federal Republic of Germany. Biogen GmbH, Riedenburger Straße 7, München 81677, Federal Republic of Germany. Biogen GmbH, Riedenburger Straße 7, München 81677, Federal Republic of Germany.
 Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Anáhuac Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Anáhuac Puebla. Puebla, México. Universidad Popular Autónoma del Estado de Puebla. Puebla, México; Laboratorios Ruiz. Laboratorios SYNLAB Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México; Universidad Popular Autónoma del Estado de Puebla. Puebla, México. Electronic address: gruiz1@clinicaruiz.com.
 Leeds Institute of Health Sciences, University of Leeds, Leeds, UK. e.j.d.webb@leeds.ac.uk. Leeds Institute of Health Sciences, University of Leeds, Leeds, UK. School of Law, University of Leeds, Leeds, UK. Leeds Teaching Hospitals NHS Trust, Leeds, UK. Leeds Institute of Health Sciences, University of Leeds, Leeds, UK. The Research Centre for Patient Involvement, Central Denmark Region, Aarhus, Denmark. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London, London, UK. Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Shift.ms, Leeds, UK. Centre for Primary Care and Public Health (Unisanté), University of Lausanne, Lausanne, Switzerland. Centre for Decision Research, Leeds University Business School, University of Leeds, Leeds, UK. Department of Communication, Pompeu Fabra University, Barcelona, Spain. Dental Translational and Clinical Research Unit, School of Dentistry, University of Leeds, Leeds, UK. Blizard Institute (Neuroscience) Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Clinical Board Medicine (Neuroscience), The Royal London Hospital, Barts Health NHS Trust, London, UK. School of Sociology and Social Policy, University of Leeds, Leeds, UK.
 Department of Orthopedic Surgery, NYU Langone Orthopedic Hospital, New York, USA. Department of Orthopedic Surgery, NYU Langone Orthopedic Hospital, New York, USA. Department of Neurology, NYU Langone Health, New York, USA. Department of Orthopedic Surgery, NYU Langone Orthopedic Hospital, New York, USA.
 Section of Dermatology - Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy. Section of Dermatology - Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy. Section of Dermatology - Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy. Section of Dermatology - Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy.
 Department of Neurology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Tehran Heart Center, Cardiovascular Research Center, Tehran University of Medical Science, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Tehran University of Medical Science, Tehran, Iran. Tehran University of Medical Science, Tehran, Iran. Tehran University of Medical Science, Tehran, Iran. Department of Neurology, School of Medicine, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Infectious Diseases, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Infectious and Tropical Diseases, Be'sat Hospital, AJA University of Medical Sciences, Tehran, Iran. Department of Neurology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran. Electronic address: ranjbar1382@yahoo.com.
 Section of Psychiatry, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Psychiatry, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy massimiliano.difilippo@unipg.it.

 Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA; Graduate Program in Immunology, Program in Biomedical Sciences, University of Michigan Medical School, Ann Arbor, MI, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA.
 Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada. UANL School of Medicine, Monterrey, Mexico. Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada. Section of Ophthalmology, Department of Surgery, University of Calgary, Calgary, Alberta, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada. Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada.
 Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Internal and Subintensive Medicine, Ospedali Riuniti, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy. Neurological Clinic, Marche Polytechnic University, Via Conca 71, Ancona 60020, Italy.
 Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
 School of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen 518055, Guangdong, China. School of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen 518055, Guangdong, China. School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen 518055, Guangdong, China. School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen 518055, Guangdong, China. School of Psychology, Shenzhen University, Shenzhen 518060, Guangdong, China. Electronic address: mushuhua@szu.edu.cn. School of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen 518055, Guangdong, China. Electronic address: jzhanghappy@163.com.
 Selcuk University, Faculty of Medicine, Department of Neurology, Konya, Turkey. Electronic address: dreren42@hotmail.com. University of Health Sciences Turkey, Konya City Hospital, Neurology Clinic, Konya, Turkey. Selcuk University, Faculty of Medicine, Department of Neurology, Konya, Turkey. Selcuk University, Faculty of Medicine, Department of Neurology, Konya, Turkey.
 Department of Neurology & Rocky Mountain MS Center, University of Colorado School of Medicine, Academic Office 1, B-185, 12631 East 17th Avenue, Aurora, CO 80045, USA. Electronic address: Anna.2.Shah@cuanschutz.edu. Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI, USA. Saint Alphonsus Medical Group, Boise, ID, USA. Saint Alphonsus Medical Group, Boise, ID, USA. Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI, USA. Department of Neurological Sciences, Lartner College of Medicine at the University of Vermont School, Burlington, VT, USA.
 Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States. Electronic address: tjcovey@buffalo.edu. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, United States.
 Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Department of Biostatistics and Epidemiology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Department of Internal Medicine, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Psychiatry and Behavioral Sciences, Northwestern Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Cell and Molecular Medicine, Rush University Medical Center, Chicago, IL 60607, USA. School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Department of Neurology, University of Visayas, Gullas College of Medicine, Cebu city, 600 Cebu, Philippines. Department of Psychiatry and Behavioral Sciences, Northwestern Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Psychiatry and Behavioral Sciences, Northwestern Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, University of Visayas, Gullas College of Medicine, Cebu city, 600 Cebu, Philippines. Department of Biological Sciences, University of Calgary, Calgary, AB T2N 1N4, Canada. Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Electronic address: alirostami1984@gmail.com.
 Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Kielo Research, Zug, Switzerland Evidera, London, UK. Innovus Consulting Ltd, London, UK. Actelion Pharmaceuticals, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Actelion Pharmaceuticals, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Evidera, Bethesda, MD, USA. Actelion Pharmaceuticals, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Janssen Research & Development, LLC, Titusville, NJ, USA. Janssen Research & Development, LLC, Titusville, NJ, USA.
 Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Medicine, University of California, San Francisco, CA 94143. Department of Epidemiology & Biostatistics, University of California, San Francisco, CA 94143. Multimodal Imaging Physics Group, Department of Mathematics and Technology, Koblenz University of Applied Sciences, 53424 Koblenz, Germany. Institute for Medical Engineering and Information Processing, University of Koblenz and Landau, 56070 Koblenz, Germany. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA 94143. Department of Ophthalmology, University of California, San Francisco, CA 94143.
 Pirogov Russian National Research Medical University, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia.
 Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/Department of Neurology, Great Ormond Street Hospital NHS Trust, London, UK. Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/NIHR University College London Hospitals Biomedical Research Centre, London, UK.
 Mental Health Center and Psychiatric Laboratory, the State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, Sichuan, China. Mental Health Center and Psychiatric Laboratory, the State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, Sichuan, China. Department of Neurology, the 3rd Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China. Department of Emergency Medicine, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, China. Mental Health Center and Psychiatric Laboratory, the State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
 Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA William S. Middleton VA Medical Center, Madison, WI, USA. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA Cleveland Clinic Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Neurology, Instituto de Investigacion Sanitaria San Carlos (IdISSC), Hospital Clinico San Carlos, Madrid, Spain.
 The Chicago School of Professional Psychology, Washington, D.C., USA. Electronic address: djackson4@ego.thechicagoschool.edu. Immaculata University, Immaculata, PA, USA. Washington Neuropsychology Research Group, Fairfax, VA, USA. Washington Neuropsychology Research Group, Fairfax, VA, USA. South Shore Neurologic Associates, Patchogue, NY, USA. South Shore Neurologic Associates, Patchogue, NY, USA. South Shore Neurologic Associates, Patchogue, NY, USA. South Shore Neurologic Associates, Patchogue, NY, USA. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. University of Wisconsin School of Medicine, Madison, WI, USA; William S. Middleton VA Medical Center, Madison, WI, USA. Multiple Sclerosis and Neuroimmunology Center, Clalit Health Services, Nazareth, Israel; Department of Neurology, Lady Davis Carmel Medical Center, Haifa, Israel; Ruth and Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel. NeuroTrax Corporation, Modiin, Israel. School of Allied Health Science and Practice, University of Adelaide, Adelaide, Australia. Katz School of Science & Health, Yeshiva University, New York, NY, USA. Department of Neurology, Division of Cognitive and Behavioral Neurosciences, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA. South Shore Neurologic Associates, Patchogue, NY, USA.
 Departments of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: sachi.patil@nyulangone.org. Neurology, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: binu.joseph@nyulangone.org. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Electronic address: ptagliani@cem-cat.org. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Electronic address: jsastre-garriga@cem-cat.org. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Electronic address: cem-cat@cem-cat.org. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Electronic address: avidal@cem-cat.org. Departments of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA; Neurology, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: steven.galetta@nyulangone.org. Departments of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA; Neurology, New York University Grossman School of Medicine, New York, NY, USA; Population Health, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: laura.balcer@nyulangone.org. Neurology, New York University Grossman School of Medicine, New York, NY, USA; Population Health, New York University Grossman School of Medicine, New York, NY, USA; Departments of Radiology and Radiological Sciences, Vanderbilt University School of Medicine, Nashville, TN, USA; Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA. Electronic address: rachel.kenney@vumc.org.
 Departments of Diagnostic and Interventional Imaging, University of Texas Health Science Center at Houston (UTHealth Houston), Houston, Texas. Departments of Neurology, University of Texas Health Science Center at Houston (UTHealth Houston), Houston, Texas. Departments of Diagnostic and Interventional Imaging, University of Texas Health Science Center at Houston (UTHealth Houston), Houston, Texas. Departments of Diagnostic and Interventional Imaging, University of Texas Health Science Center at Houston (UTHealth Houston), Houston, Texas.
 Department of Clinical Neuroscience, Karolinska Institutet, Department of Neurology, Karolinska University Hospital, Stockholm, Sweden Centre for Neurology, Academic Specialist Centre, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Department of Neurology, Karolinska University Hospital, Stockholm, Sweden Department of Medicine, Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden Centre for Neurology, Academic Specialist Centre, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. Center for Obstetrics and Pediatrics, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Southern California Permanente Medical Group, Kaiser Permanente, Los Angeles, CA, USA. Department of Clinical Neuroscience, Karolinska Institutet, Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. Department of Medicine, Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden. Department of Medicine, Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden.
 Collaboration for Outcomes Research and Evaluation (CORE), Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada. School of Population and Public Health, The University of British Columbia, Vancouver, BC, Canada Centre for Health Evaluation and Outcome Sciences (CHÉOS), St. Paul's Hospital, Vancouver, BC, Canada. Collaboration for Outcomes Research and Evaluation (CORE), Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada. Collaboration for Outcomes Research and Evaluation (CORE), Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada. Department of Psychiatry, University of Calgary, Calgary, AB, Canada. Division of Neurology, Department of Medicine, The University of British Columbia, Vancouver, BC, Canada. Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Division of Neurology, Department of Medicine, The University of British Columbia, Vancouver, BC, Canada. Department of Neurology, Faculty of Medicine, Université de Montreal, Montreal, QC, Canada. School of Biomedical Engineering, The University of British Columbia, Vancouver, BC, Canada. Collaboration for Outcomes Research and Evaluation (CORE), Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada Centre for Health Evaluation and Outcome Sciences (CHÉOS), St. Paul's Hospital, Vancouver, BC, Canada.
 Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: fquintana@rics.bwh.harvard.edu.
 Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Industrial Development Center of Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Electronic address: liumeiy@aliyun.com. School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PR China. Electronic address: kaili-hu@163.com.
 Department of Physical Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, P.O. Box 80200, Jeddah 21589, Saudi Arabia; Department of Physical Therapy, King Fahad Hospital, Jeddah, Saudi Arabia. Department of Physical Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, P.O. Box 80200, Jeddah 21589, Saudi Arabia. Department of Physical Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, P.O. Box 80200, Jeddah 21589, Saudi Arabia. Department of Physical Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, P.O. Box 80200, Jeddah 21589, Saudi Arabia. Department of Physical Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, P.O. Box 80200, Jeddah 21589, Saudi Arabia. Electronic address: fayazrkhan@gmail.com.
 Servicio de Oftalmología, Hospital Clínico San Carlos, Calle Profesor Martin Lagos s/n, 28040 Madrid, Spain. Electronic address: antoniopascualsantiago18@gmail.com. Servicio de Oftalmología, Hospital Clínico San Carlos, Calle Profesor Martin Lagos s/n, 28040 Madrid, Spain. Servicio de Oftalmología, Hospital Clínico San Carlos, Calle Profesor Martin Lagos s/n, 28040 Madrid, Spain. Servicio de Oftalmología, Hospital Clínico San Carlos, Calle Profesor Martin Lagos s/n, 28040 Madrid, Spain.
 Montreal Neurological Institute, McGill University, Québec, Canada. Montreal Neurological Institute, McGill University, Québec, Canada. Institute of Neuropathology, University Hospital Münster, Münster, Germany.
 From the Department of Ophthalmology (S.A.P., L.J.B, S.G.), New York University Grossman School of Medicine, NY; Department of Neurology (S.G., L.J.B., S. Galetta), New York University Grossman School of Medicine, NY; Department of Radiology and Radiological Sciences (R.K.), Vanderbilt University School of Medicine, Nashville, TN; Department of Population Health (L.J.B.), New York University Grossman School of Medicine, NY. sachi.patil@nyulangone.org. From the Department of Ophthalmology (S.A.P., L.J.B, S.G.), New York University Grossman School of Medicine, NY; Department of Neurology (S.G., L.J.B., S. Galetta), New York University Grossman School of Medicine, NY; Department of Radiology and Radiological Sciences (R.K.), Vanderbilt University School of Medicine, Nashville, TN; Department of Population Health (L.J.B.), New York University Grossman School of Medicine, NY. From the Department of Ophthalmology (S.A.P., L.J.B, S.G.), New York University Grossman School of Medicine, NY; Department of Neurology (S.G., L.J.B., S. Galetta), New York University Grossman School of Medicine, NY; Department of Radiology and Radiological Sciences (R.K.), Vanderbilt University School of Medicine, Nashville, TN; Department of Population Health (L.J.B.), New York University Grossman School of Medicine, NY. From the Department of Ophthalmology (S.A.P., L.J.B, S.G.), New York University Grossman School of Medicine, NY; Department of Neurology (S.G., L.J.B., S. Galetta), New York University Grossman School of Medicine, NY; Department of Radiology and Radiological Sciences (R.K.), Vanderbilt University School of Medicine, Nashville, TN; Department of Population Health (L.J.B.), New York University Grossman School of Medicine, NY. From the Department of Ophthalmology (S.A.P., L.J.B, S.G.), New York University Grossman School of Medicine, NY; Department of Neurology (S.G., L.J.B., S. Galetta), New York University Grossman School of Medicine, NY; Department of Radiology and Radiological Sciences (R.K.), Vanderbilt University School of Medicine, Nashville, TN; Department of Population Health (L.J.B.), New York University Grossman School of Medicine, NY.
 School of Rehabilitation Therapy, Queen's University, Kingston ON, Canada. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium; UMSC Hasselt, Pelt, Belgium. Exercise Biology, Department of Public Health, Aarhus University, Aarhus, Denmark. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; National Multiple Sclerosis Center Melsbroek, Steenokkerzeel, Belgium.
 Biogen, Cambridge, MA, USA. stephanie.loomis@biogen.com. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Genentech, South San Francisco, CA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Genentech, South San Francisco, CA, USA. Genentech, South San Francisco, CA, USA. Biogen, Cambridge, MA, USA.
 Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Division of Neuroimmunology and Neurological Infections, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA. Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD,USA.
 From the Department of Neurology, King Fahad Specialist Hospital, Dammam, Kingdom of Saudi Arabia. From the Department of Neurology, King Fahad Specialist Hospital, Dammam, Kingdom of Saudi Arabia.
 Department of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Psychiatry, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Institute of Diagnostic and Interventional Radiology and Neuroradiology, University Hospital Essen, Essen, Germany. Department of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden. Department of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. Department of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. kincses.zsigmond.tamas@med.u-szeged.hu. Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, Hungary. kincses.zsigmond.tamas@med.u-szeged.hu.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroradiology Unit and CERMAC, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it.
 Department of Physical Medicine and Rehabilitation, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; VA Research Service, Rocky Mountain Regional VA Medical Center, Aurora, CO, USA. Electronic address: mark.manago@cuanschutz.edu. Department of Rehabilitation Sciences, Medical University of South Carolina, Charleston, SC, USA; Muscle Morphology, Mechanics and Performance Lab, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Research Service, Washington DC VA Medical Center, Washington, DC, USA. Muscle Morphology, Mechanics and Performance Lab, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. VA Multiple Sclerosis Center of Excellence and Neurology Service, Washington DC VA Medical Center, Washington, DC, USA. VA Multiple Sclerosis Center of Excellence and Neurology Service, Washington DC VA Medical Center, Washington, DC, USA. Muscle Morphology, Mechanics and Performance Lab, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Research Service, Washington DC VA Medical Center, Washington, DC, USA. Research Service, Washington DC VA Medical Center, Washington, DC, USA; Departments of Medicine and Rehabilitation Medicine, Georgetown University, Washington, DC, USA; Department of Medicine, George Washington University, Washington, DC, USA. Department of Physical Medicine and Rehabilitation, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; VA Research Service, Rocky Mountain Regional VA Medical Center, Aurora, CO, USA; Muscle Morphology, Mechanics and Performance Lab, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Research Service, Washington DC VA Medical Center, Washington, DC, USA; Geriatric Service, Washington DC VA Medical Center, Washington, DC, USA.
 Weill Cornell Medicine, Department of Neurology, Judith Jaffe Multiple Sclerosis Center, New York 10021, USA.
 Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom. Department of Psychology, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. UK Dementia Research Institute, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, United Kingdom. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom. Edinburgh Imaging, University of Edinburgh, Edinburgh, United Kingdom.
 Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China. Cell Therapy Center, Beijing Institute of Geriatrics, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, Beijing, China. Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, China. Stomatology College of Inner Mongolia Medical University, Hohhot, China. Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China. Department of Neurobiology, Care Sciences & Society, Karolinska Institute, Karolinska University Hospital Solna, Stockholm, Sweden. Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
 Syracuse DVAMC, Syracuse, USA. Department of Physical Medicine and Rehabilitation, SUNY Upstate Medical University, Syracuse, USA. Syracuse DVAMC, Syracuse, USA. Department of Neurology, SUNY Upstate Medical University, Syracuse, USA. Syracuse DVAMC, Syracuse, USA. Department of Neurology, SUNY Upstate Medical University, Syracuse, USA. Syracuse DVAMC, Syracuse, USA. Department of Physical Medicine and Rehabilitation, SUNY Upstate Medical University, Syracuse, USA.
 Department of Psychology, Maynooth University, Maynooth, Ireland; Assisting Living and Learning Institute, Maynooth University, Maynooth, Ireland. Electronic address: rebecca.maguire@mu.ie. Department of Psychology, Maynooth University, Maynooth, Ireland. Department of Psychology, Maynooth University, Maynooth, Ireland. The Multiple Sclerosis Society of Ireland, Dublin, Ireland. The Multiple Sclerosis Society of Ireland, Dublin, Ireland; School of Allied Health, Physical Activity for Health Research Cluster, University of Limerick, Limerick. Ireland.
 Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark; Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark. Electronic address: klp@ssi.dk. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark; Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark; Department of Hematology, Copenhagen University Hospital, Copenhagen, Denmark; Department of Clinical Medicine, Copenhagen University, Copenhagen, Denmark.
 Department of Neurology, University Hospital Münster, Germany. Electronic address: t.rademacher@uni-muenster.de. Department of Neurology, University Hospital Düsseldorf, Germany. Department of Neurology, University Hospital Münster, Germany. Department of Neurology, University Hospital Münster, Germany. Department of Neurology, University Hospital Münster, Germany. Electronic address: nils.c.landmeyer@uni-muenster.de.
 University of Catania, Department of Biomedical and Biotechnological Science, Via S. Sofia, 64, 95125 Catania (CT), Italy. Studio di Psicoterapia Relazionale e Riabilitazione Cognitiva, viale Europa, 107, 98121, Messina (ME), Italy. I.O.M.I. "Franco Scalabrino", Via Consolare Pompea, 360, 98165 Ganzirri, Messina (ME), Italy. Studio di Riabilitazione Nutrizionale e Cognitiva, Via Sant'Agostino, 14, 98122, Messina (ME), Italy. Azienda Ospedaliera Universitaria di Messina "G. Martino", Via Consolare Valeria, 98125, Messina (ME), Italy. Azienda Ospedaliera Universitaria di Messina "G. Martino", Via Consolare Valeria, 98125, Messina (ME), Italy. Azienda Ospedaliera Universitaria di Messina "G. Martino", Via Consolare Valeria, 98125, Messina (ME), Italy. IRCCS Centro Neurolesi "Bonino Pulejo", S.S. 113, Contrada Casazza 98124, Messina, Italy. Electronic address: salbro77@tiscali.it.
 Université de Nantes, Université de Tours, Inserm, UMR1246 Sphere, Nantes, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France/Hospices Civils de Lyon, Service de Neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, Lyon, France/Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, Lyon, France/EUGENE DEVIC EDMUS Foundation against Multiple Sclerosis, State-Approved Foundation, Lyon, France. Hospices Civils de Lyon, Service de Neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, Lyon, France/Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, Lyon, France/Faculté de médecine Lyon Est, Université Claude Bernard Lyon 1, Lyon, France. EHESP, Université de Rennes, Rennes, France. Department of Neurology, Nancy University Hospital, Hôpital Central, Service de Neurologie, Nancy, France/Université de Lorraine, Nancy, France. Department of Neurology and Clinical Investigation Center, CHU de Strasbourg, Strasbourg, France. Department of Neurology, Hôpital Pierre-Paul Riquet, CHU de Toulouse, Toulouse, France. Université de Nantes, Nantes, France/Service de Neurologie, Centre de Ressources et de Compétences Sclérose en Plaques, Centre Hospitalier Universitaire de Nantes, Nantes, France. University of Bordeaux, Bordeaux, France/Department of Neurology, CHU de Bordeaux, Bordeaux, France. Aix Marseille University, APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie, Marseille, France. University of Lille, Lille, France. Clinical Neuroscience Centre, Rennes University Hospital, Rennes, France/Microenvironment, Cell Differentiation, Immunology and Cancer Unit, Rennes, France/Neurology Department, Rennes University Hospital, Rennes, France. Service de neurologie, CRCSEP, CHU de Nice, UR2CA-URRIS, Nice, France. Université Clermont Auvergne, CHU de Clermont-Ferrand, Inserm, Neuro-Dol, Clermont-Ferrand, France. Department of Neurology, Nimes University Hospital, Nimes, France/Institut de Génomique Fonctionnelle, Université de Montpellier, Montpellier, France. Department of Neurology, Hôpital Nord, CHU de Saint-Étienne, Saint-Étienne, France. CHU de Reims, Reims, France. Sorbonne Universités, Brain and Spine Institute, ICM, Hôpital de la Pitié Salpêtrière, Paris, France/Department of Neurology, AP-HP, Saint-Antoine Hospital, Paris, France. Department of Neurology, CHU d'Amiens, Amiens, France. Department of Neurology, CHU de la Martinique, Fort-de-France, France. Département de Neurologie, AP-HP, Hôpital Pitié-Salpêtrière, Paris, France/Centre de Ressources et de Compétences SEP, Paris, France. Service de Neurologie Besançon, CHU de Besançon, Besançon, France. Department of Neurology, Hôpital de Poissy, Poissy, France. Department of Neurology, Centre Hospitalier de Saint-Denis, Hôpital Pierre Delafontaine, Saint-Denis, France. Department of Neurology, CHU de Dijon, Dijon, France. Department of Neurology, Fondation Rothschild, Paris, France. Rouen University Hospital, Rouen, France. Department of Neurology, AP-HP, Hôpital Henri Mondor, Créteil, France. CRC SEP, Montpellier University Hospital, INSERM, Université de Montpellier, Montpellier, France. Department of Neurology, Hôpital Dupuytren, CHU de Limoges, Limoges, France. CHU de Caen, MS Expert Centre, Department of Neurology, Normandy University, Caen, France. CRC SEP and Department of Neurology, Hôpital Bretonneau, CHU de Tours, Tours, France. Department of Neurology, Hôpital Jean Bernard, CHU La Milétrie, Poitiers, France. Department of Neurology, CHU Bicêtre, Le Kremlin-Bicêtre, France. Department of Neurology, Hôpital Sud Francilien, Corbeil-Essonnes, France. Department of Neurology, Hopital Andre Mignot, Le Chesnay, France. Department of Neurology, CHU Grenoble Alpes, Grenoble, France. Université de Nantes, Nantes, France/Service de Neurologie, Centre de Ressources et de Compétences Sclérose en Plaques, Centre Hospitalier Universitaire de Nantes, Nantes, France. Yohann Foucher CIC 1402, CHU de Poitiers, Université de Poitiers, Poitiers, France.
 Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. Harvard Medical School, Boston, MA, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. Harvard Medical School, Boston, MA, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. Harvard Medical School, Boston, MA, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. Harvard Medical School, Boston, MA, USA. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Harvard Medical School, Boston, MA, USA. Department of Neurology, Massachusetts General Hospital, Boston, USA. UMass Memorial Medical Center, University Campus, Worcester, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, 149 Thirteenth Street, Charlestown, Boston, MA, 02129, USA. cmainero@mgh.harvard.edu. Harvard Medical School, Boston, MA, USA. cmainero@mgh.harvard.edu.
 Department of Pharmacy, Peking University Third Hospital, Beijing, China. Department of Bioengineering and Therapeutic Sciences, Schools of Pharmacy and Medicine, University of California San Francisco, San Francisco, California, USA. Department of Pharmacy, Peking University Third Hospital, Beijing, China. Department of Bioengineering and Therapeutic Sciences, Schools of Pharmacy and Medicine, University of California San Francisco, San Francisco, California, USA. Department of Pharmacy, Peking University Third Hospital, Beijing, China. School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China. Weill Institute for Neurosciences and San Francisco Multiple Sclerosis Center, University of California San Francisco, San Francisco, California, USA. Department of Pharmacy, Peking University Third Hospital, Beijing, China. Department of Pharmacy, Peking University Third Hospital, Beijing, China. Department of Bioengineering and Therapeutic Sciences, Schools of Pharmacy and Medicine, University of California San Francisco, San Francisco, California, USA.
 Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Bandirma Onyedi Eylul University, Bandirma, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Faculty of Medicine, Department of Neurology, Hacettepe University, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey.
 From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.). From the MS Center Amsterdam, Anatomy & Neurosciences, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, the Netherlands (P.M.B., S.N., F.A.N.S., M.M.S., J.J.G.G., M.D.S.); Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (E.S.B., D.S.R.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY (E.S.B.); Bio-imaging Institute, University of Bordeaux, Bordeaux, France (G.B.); Neurology Section, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy (M. Castellaro, M. Calabrese); Department of Information Engineering, University of Padova, Padova, Italy (M. Castellaro); NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (D.T.C.); National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK (D.T.C.); Departments of Neuroradiology (P.E., B.W.) and Neurology (M.M.), School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Neuroimaging Research Unit, Division of Neuroscience Neurology Unit, IRCCS San Raffaele Scientific Institute Vita-Salute San Raffaele University, Milan, Italy (M.F., P.P., M.A.R.); Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genoa, Italy (M.I., C.L.); IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genoa, Italy (M.I., C.L.); Center for Neurologic Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (A.M., A.M.P., C.R.G.G.); Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (B.M.); Department of Epidemiology and Data Science, Amsterdam University Medical Center, Amsterdam, the Netherlands (J.W.R.T.); Anatomy & Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (L.E.J.); and Amsterdam Neuroscience, Brain Imaging and Neurodegeneration, Amsterdam, the Netherlands (L.E.J.).
 Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy/HNSR, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. UO Neuroradiologia, IRCCS Istituto Giannina Gaslini, Genoa, Italy/Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. UO Neuropsichiatria Infantile, IRCCS Istituto Giannina Gaslini, Genoa, Italy. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy/IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
 Institut für Neuroimmunologie und Multiple Sklerose, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Department of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Klinik und Poliklinik für Neurologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Department of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Klinik und Poliklinik für Neurologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health (BIH), Klinik für Psychiatrie & Psychotherapie und Medizinische Klinik m.S. Psychosomatik, Campus Benjamin Franklin (CBF), Berlin, Germany. Institut für Neuroimmunologie und Multiple Sklerose, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Department of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. APHM, Hopital de la Timone, CEMEREM, Marseille, France. Aix-Marseille Université, CNRS, CRMBM, UMR 7339, Marseille, France.
 Department of Neuroscience, Monash University, Melbourne, VIC, Australia. maria.campagna@monash.edu. School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia. Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia. Department of Neuroscience, Monash University, Melbourne, VIC, Australia. Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia. Neurology Department, John Hunter Hospital, Hunter New England, Newcastle, NSW, Australia. College of Medicine and Public Health, Flinders University, Adelaide, Australia. Department of Neuroscience, Monash University, Melbourne, VIC, Australia. Neurology Department, Alfred Health, Melbourne, VIC, Australia. Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia. School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia. Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia. Department of Neuroscience, Monash University, Melbourne, VIC, Australia. Neurology Department, Alfred Health, Melbourne, VIC, Australia. Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia. Neurology Department, John Hunter Hospital, Hunter New England, Newcastle, NSW, Australia. Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia. Queensland University of Technology, Brisbane, QLD, Australia. Department of Neuroscience, Monash University, Melbourne, VIC, Australia. Neurology Department, Alfred Health, Melbourne, VIC, Australia. Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia.
 Department of Immunology, University of Toronto, Toronto, ON, Canada. Department of Immunology, University of Toronto, Toronto, ON, Canada. Department of Immunology, University of Toronto, Toronto, ON, Canada.
 From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. From the Department of Clinical Neuroscience (C.S.C., E.L., N.R., B.E., I.K., M.J., F.A.N., F.P.), Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine (C.S.C., N.R., I.K., M.J., F.A.N., F.P.), Karolinska University Hospital, Stockholm, Sweden; Department of Neurology (B.E., F.P.), Karolinska University Hospital, Stockholm, Sweden; Center for Neurology (C.S.C., I.K., M.J., F.A.N., F.P.), Academic Specialist Center, Stockholm, Sweden; and Clinical Epidemiology Division (T.F.), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. fredrik.piehl@ki.se.
 From the Queen Square Multiple Sclerosis Centre (A.T.T.), Department of Neuroinflammation, Queen Square UCL Institute of Neurology, University College London, United Kingdom; and Servicio de Neurología (A.V.-J.), Centro de Esclerosis Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain. a.toosy@ucl.ac.uk. From the Queen Square Multiple Sclerosis Centre (A.T.T.), Department of Neuroinflammation, Queen Square UCL Institute of Neurology, University College London, United Kingdom; and Servicio de Neurología (A.V.-J.), Centro de Esclerosis Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden. United Kingdom (UK) Dementia Research Institute at University College London (UCL), London, United Kingdom. Department of Neurodegenerative Disease, University College London (UCL) Queen Square Institute of Neurology, London, United Kingdom. Hong Kong Centre for Neurodegenerative Diseases, Hong Kong SAR, China. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, United States. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
 From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark. marina.rode.von.essen@regionh.dk. From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark. From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark. From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark. From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark. From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark. From the Danish Multiple Sclerosis Center (M.R.E., J.T., R.H.H.H., H.H.C., F.S.), Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup; Danish Research Centre for Magnetic Resonance (H.L., H.R.S.), Copenhagen University Hospital - Amager and Hvidovre; Department of Clinical Medicine (H.R.S.), University of Copenhagen; and Department of Neurology (H.R.S.), Copenhagen University Hospital - Bispebjerg and Frederiksberg, Denmark.
 IRCCS Fondazione Don Carlo Gnocchi ONLUS, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, Italy. Electronic address: frossetto@dongnocchi.it. Brain and Behavioral Science Department, University of Pavia, Sezione di Psicologia Piazza Botta, Pavia, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, Italy.
 MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands.
 Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Immunology-Immunopathology-Immunotherapy (i3)-UMRS_959, Sorbonne Université- INSERM, Paris, France. Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Clinical Investigation Center for Biotherapies (CIC-BTi) and Immunology-Inflammation-Infectiology and Dermatology Department (3iD), Paris, France. Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Immunology-Immunopathology-Immunotherapy (i3)-UMRS_959, Sorbonne Université- INSERM, Paris, France. Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Clinical Investigation Center for Biotherapies (CIC-BTi) and Immunology-Inflammation-Infectiology and Dermatology Department (3iD), Paris, France. Immunology-Immunopathology-Immunotherapy (i3)-UMRS_959, Sorbonne Université- INSERM, Paris, France. Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Clinical Investigation Center for Biotherapies (CIC-BTi) and Immunology-Inflammation-Infectiology and Dermatology Department (3iD), Paris, France. Immunology-Immunopathology-Immunotherapy (i3)-UMRS_959, Sorbonne Université- INSERM, Paris, France. Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Clinical Investigation Center for Biotherapies (CIC-BTi) and Immunology-Inflammation-Infectiology and Dermatology Department (3iD), Paris, France. Immunology-Immunopathology-Immunotherapy (i3)-UMRS_959, Sorbonne Université- INSERM, Paris, France. Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Pharmacie à Usage Intérieur, Reqpharm Unit, Paris, France. Neuroradiology Department, Sorbonne University, Assistance Publique Hôpitaux de Paris, Paris, France. Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Assistance Publique Hôpitaux de Paris, Lariboisière Hospital, Clinical Trial Unit, Paris, France. Sorbonne University, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, Department of Neurology, CIC neurosciences, Paris, France. Immunology-Immunopathology-Immunotherapy (i3)-UMRS_959, Sorbonne Université- INSERM, Paris, France. david.klatzmann@sorbonne-universite.fr. Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Clinical Investigation Center for Biotherapies (CIC-BTi) and Immunology-Inflammation-Infectiology and Dermatology Department (3iD), Paris, France. david.klatzmann@sorbonne-universite.fr.
 Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Electronic address: azzolinveronica@hotmail.com. Clinical Research Center of São Lucas Hospital, Pontifical Catholic University of Rio Grande do Sul, 6690 Ipiranga Av., 4th floor, Porto Alegre, RS, 90619-900, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Clinical Research Center of São Lucas Hospital, Pontifical Catholic University of Rio Grande do Sul, 6690 Ipiranga Av., 4th floor, Porto Alegre, RS, 90619-900, Brazil. Clinical Research Center of São Lucas Hospital, Pontifical Catholic University of Rio Grande do Sul, 6690 Ipiranga Av., 4th floor, Porto Alegre, RS, 90619-900, Brazil. Clinical Research Center of São Lucas Hospital, Pontifical Catholic University of Rio Grande do Sul, 6690 Ipiranga Av., 4th floor, Porto Alegre, RS, 90619-900, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Open University Foundation for the Third Age, 11430 Brazil Av., Santo Antônio, Manaus, AM, 69029-040, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Lutheran University of Brazil, BR-287, S/N - Boca do Monte, Santa Maria, RS, 97030-080, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil. Clinical Research Center of São Lucas Hospital, Pontifical Catholic University of Rio Grande do Sul, 6690 Ipiranga Av., 4th floor, Porto Alegre, RS, 90619-900, Brazil. Laboratory of Biogenomics, Department of Morphology, Health Sciences Center, Federal University of Santa Maria, 1000 Roraima Av., Building 19, Camobi, Santa Maria, RS, 97105-900, Brazil.
 Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK; United Kingdom of Great Britain and Northern Ireland, UK. Electronic address: g.giovannoni@qmul.ac.uk. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK; United Kingdom of Great Britain and Northern Ireland, UK. Department of Neurology, John Hunter Hospital, University Newcastle, Australia. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, United States. Department of Pediatrics (Neurology), SickKids Research Institute, Division of Neurosciences and Mental Health, Hospital for Sick Children, University of Toronto, Canada.
 Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Gabrichevsky Research Institute for Epidemiology and Microbiology, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Gabrichevsky Research Institute for Epidemiology and Microbiology, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia.
 Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX. Department of Neurology, Mayo Clinic, Rochester, MN. Department of Neurology, Universitaire de Nice, Nice, France. Department of Health Sciences, University of Genoa, Genoa, Italy. Department of Health Sciences, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neurology, University of Southern California, Los Angeles, CA. Department of Health Sciences, University of Genoa, Genoa, Italy. Department of Neurology, Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, NV. Department of Neurology, University of Southern California, Los Angeles, CA. Department of Neurology-Neuroimmunology and Neurological Infections, Johns Hopkins University, Baltimore, MD. Alexion, Astra Zeneca Rare Disease, Boston, MA. Biogen Inc., Cambridge, MA. Thirteen Consulting Group, Inc., Berlin, MA. Takeda Pharmaceutical Company, Tokyo, Japan. Department of Neurology, Columbia University Medical Center, New York, NY. Department of Neuroimmunology, Multicare Auburn Medical Center, Tacoma, WA. Department of Neurology, Washington University, St. Louis, MO. Department of Neurology, Baylor University Medical Center, Dallas, TX. Oklahoma Medical Research Foundation, Oklahoma City, OK. Department of Neurology, Swedish Medical Center, Seattle, WA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX. Neurology Section, Dallas Veterans Affairs Medical Center, Dallas, TX. Department of Neurology, Cerrahpasa School of Medicine, Istanbul, Turkey. Department of Neurology, University of Southern California, Los Angeles, CA.
 Paediatric Neurology Unit, Children's Medicine Department, Children's Hospital, University Hospital of Nancy, France. Electronic address: a.saponaro@chru-nancy.fr. Sorbonne Université, CNRS, IRD, INRA, Institute of Ecology and Environmental Sciences, iEES Paris, UMR7618, France. Electronic address: thomas.tully@sorbonne-universite.fr. Department of Neurology, National Reference Center for Rare Inflammatory and auto-immune Brain and Spinal Diseases, Pitie Salpetriere Hospital, APHP, Paris, France. Department of Pediatric Neurology, National Reference Center for Rare Inflammatory and auto-immune Brain and Spinal Diseases, Hopitaux Universitaires Paris-Saclay, Hôpital Bicêtre, Le Kremlin-Bicetre, 94276, France. Department of Pediatric Neurology, National Reference Center for Rare Inflammatory and auto-immune Brain and Spinal Diseases, Hopitaux Universitaires Paris-Saclay, Hôpital Bicêtre, Le Kremlin-Bicetre, 94276, France; UMR 1184, Immunology of Viral Infections and Autoimmune Diseases, Universite Paris Saclay, Le Kremlin-Bicetre, France. Electronic address: kumaran.deiva@aphp.fr.
 IRCCS Fondazione Don Carlo Gnocchi ONLUS, Milan, Italy. Electronic address: jjonsdottir@dongnocchi.it. Neurology-Neuroimmunology Department & Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia (Cemcat), Barcelona, Spain; Department of Physiotherapy, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, C/ Josep Trueta sn, 08195 Sant Cugat del Vallès, Barcelona, Spain. Electronic address: csantoyo@cem-cat.org. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Izmir Katip Celebi University, Izmir, Turkey. Electronic address: turhan.kahraman@ikcu.edu.tr. Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, and Sagol School of Neuroscience, Tel-Aviv University, Israel; Multiple Sclerosis Center, Sheba Medical Center, Tel Hashomer, Israel. Department of Rehabilitation, Third Faculty of Medicine, Charles University, Prague, Czech Republic. UMSC Hasselt, Pelt, Belgium; REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium; IPEM Institute of Psychoacoustics and Electronic Music, Faculty of Arts and Philosophy, Ghent University, Ghent, Belgium. Electronic address: lousin.moumdjian@uhasselt.be. Centre of Physical Activity for Health, Health Research Institute, University of Limerick, Limerick, Ireland; Multiple Sclerosis Society of Ireland and Physical Activity for Health Research Centre, Ireland. Electronic address: susanc@ms-society.ie. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genova, Italy. Electronic address: andrea.tacchino@aism.it. CRRF "Mons. L. Novarese", Moncrivello (VC), Italy. Department of Physiotherapy, Haukeland University Hospital, Helse Bergen, Bergen, Norway,; Department of Neurology, Multiple Sclerosis Competence Centre, Haukeland University Hospital, Helse Bergen, Bergen, Norway. Electronic address: tori.smedal@helse-bergen.no. Nord University, Faculty of nursing and health sciences, Bodø, Norway. Electronic address: ellenarntzen@me.com. Discipline of Exercise Science, Murdoch University, Murdoch, Australia; Centre for Molecular Medicine and Innovative Therapeutics, Centre for Healthy Ageing, Health Futures Institute, Murdoch University, Murdoch, Australia; Perron Institute for Neurological and Translational Science, Nedlands, Australia. Electronic address: yvonne.learmonth@murdoch.edu.au. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. Electronic address: ludovico.pedulla@aism.it. Physiotherapy Department, St. James's Hospital, Dublin, Ireland. Department of Rehabilitation Sciences, KU Leuven, Leuven 1501-3001, Belgium; National MS Center, Melsbroek, Belgium. Electronic address: daphne.kos@kuleuven.be.
 Department of Medicine, The University of British Columbia, Vancouver, BC, V6T 2B5, Canada. Department of Neurology, Memorial University of Newfoundland, St. John's, NL, A1B 3V6, Canada. Department of Medicine, Division of Neurology, Queen's University, Kingston, ON, K7L 3N6, Canada. EVERSANA, Burlington, ON, L7N 3H8, Canada. EVERSANA, Burlington, ON, L7N 3H8, Canada. Novartis Canada Inc., Dorval, QC, H9S 1A9, Canada. Novartis Pharma AG, Basel,4056, Switzerland. Novartis Ireland Limited, Dublin, D04 NN12, Ireland. Novartis Healthcare Pvt. Ltd., Hyderabad, 500081, India. EVERSANA, Burlington, ON, L7N 3H8, Canada. EVERSANA, Burlington, ON, L7N 3H8, Canada. Novartis Canada Inc., Dorval, QC, H9S 1A9, Canada. Novartis Canada Inc., Dorval, QC, H9S 1A9, Canada.
 Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy. Electronic address: valentina.torri@istituto-besta.it. Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy. Urology Unit - ASST NORD Milano - E. Bassini Hospital, Cinisello Balsamo, Milan, Italy. Urology Unit - ASST NORD Milano - E. Bassini Hospital, Cinisello Balsamo, Milan, Italy. Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy. Neurology Unit - ASST Santi Paolo e Carlo, Milan, Italy. Neurology Unit-ASST Garbagnate Milanese, Milan, Italy. Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy. Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy. Department of Research and Clinical Development, Scientific Directorate, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy. Department of Neuroimmunology and Neuromuscular Diseases, Neurological Institute C. Besta IRCCS Foundation, Via Celoria n° 11, Milan 20133, Italy.
 Department of Medical Physics, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Department of Electrical Engineering, School of Electrical Engineering, Islamic Azad University Najafabad Branch, Najafabad, Iran. RINGGOLD: 201564 Department of Medical Physics, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Department of Radiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455
 Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Department of Neurology, University Hospital Complex of Pontevedra, Pontevedra, Spain. Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain monica.perez.rios@usc.es. Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. Department of Neurology, Rio Hortega University Hospital, Valladolid, Spain. Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA. Department of Health Policy and Management, Yale University School of Public Health, New Haven, Connecticut, USA. Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
 Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada. Department of Medicine, Univeristy of Ottawa, The Ottawa Hospital Research Institute, Ottawa, ON, Canada. Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. Meso Scale Diagnostics, LLC. (MSD), Rockville, MD, USA. Meso Scale Diagnostics, LLC. (MSD), Rockville, MD, USA. Meso Scale Diagnostics, LLC. (MSD), Rockville, MD, USA. Meso Scale Diagnostics, LLC. (MSD), Rockville, MD, USA. Department of Medicine, Univeristy of Ottawa, The Ottawa Hospital Research Institute, Ottawa, ON, Canada. Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA. Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, ON, Canada. Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada. Department of Clinical Biochemistry, University Health Network, Toronto, ON, Canada.
 Tasmanian School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania 7000, Australia. Tasmanian School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia. Electronic address: brad.sutherland@utas.edu.au.
 Eastern Switzerland University of Applied Sciences, School of Health Sciences, Institute of Applied Nursing Science, St. Gallen, Switzerland. Eastern Switzerland University of Applied Sciences, School of Health Sciences, Institute of Applied Nursing Science, St. Gallen, Switzerland; Rehabilitation Centre Valens, Valens, Switzerland. Eastern Switzerland University of Applied Sciences, School of Health Sciences, Institute of Applied Nursing Science, St. Gallen, Switzerland. Eastern Switzerland University of Applied Sciences, School of Health Sciences, Institute of Applied Nursing Science, St. Gallen, Switzerland. Rehabilitation Centre Valens, Valens, Switzerland. Karl Landsteiner University of Health Sciences, Department of General Health Studies, Division Nursing Science with focus on Person-Centred Care Research, Krems, Austria. Eastern Switzerland University of Applied Sciences, School of Health Sciences, Institute of Applied Nursing Science, St. Gallen, Switzerland; Rehabilitation Centre Valens, Valens, Switzerland. Electronic address: myrta.kohler@ost.ch.
 Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran. Drug Research Program Division of Pharmaceutical Chemistry and Technology Faculty of Pharmacy, University of Helsinki, Helsinki, 00014, Finland. Zanjan Pharmaceutical Nanotechnology Research Center (ZPNRC), Zanjan University of Medical Sciences, Zanjan, 45139-56184, Iran. Department of Micro and Nanotechnology, Technical University of Denmark, Kgs, Lyngby, DK-2800, Denmark. Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran. Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran. hashrafi@sums.ac.ir.
 Department of Physical Therapy, University of Alabama at Birmingham, CH19 Room 301, 933 19th Street South, Birmingham, AL 35205, USA. Electronic address: trinhhlt@uab.edu. Department of Kinesiology, Health Promotion, and Recreation, University of North Texas, Denton, TX, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA.
 Department of Biostatistics, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Biotechnical and Laboratory Sciences, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Pharmaceutical Sciences, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Neurology, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Neurology, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Neurology, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Pharmaceutical Sciences, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Neurology, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Institute for Artificial Intelligence and Data Science, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. Department of Biostatistics, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. hageman@buffalo.edu. Institute for Artificial Intelligence and Data Science, University at Buffalo, The State University of New York at Buffalo, Buffalo, NY, USA. hageman@buffalo.edu.
 Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Department of Diagnostic Imaging, Sheba Medical Center, Ramat-Gan, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Department of Diagnostic Imaging, Sheba Medical Center, Ramat-Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Department of Diagnostic Imaging, Sheba Medical Center, Ramat-Gan, Israel. Brain Imaging Research Center (BIRC), Ben-Gurion University, Beer-Sheva, Israel. Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel. Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Center for Advanced Imaging Innovation and Research (CAI2R), New York University, New York, New York, USA. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.
 Department of Molecular Biology and Genetics, Faculty of Science and Letters, Istanbul Technical University, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Biostatistics and Bioinformatics, Institute of Health Sciences, Acibadem University, Istanbul, Turkey. Department of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Acibadem University, Istanbul, Turkey. Department of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Acibadem University, Istanbul, Turkey. Department of Medical Biology, Faculty of Medicine, Basic Medical Sciences, Bahcesehir University, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Biostatistics and Medical Informatics, Faculty of Medicine, Akdeniz University, Antalya, Turkey. Department of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Acibadem University, Istanbul, Turkey. Graduate School of Natural and Applied Sciences, Molecular and Translational Biomedicine Program, Acibadem University, Istanbul, Turkey. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
 School of Kinesiology, Auburn University, Auburn, AL. College of Health Solutions, Arizona State University, Phoenix, AZ. School of Biological and Health Systems Engineering, Arizona State University, Tempe, AZ. Department of Health and Exercise Science, Colorado State University, Fort Collins, CO. Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, KS. College of Health Solutions, Arizona State University, Phoenix, AZ; Phoenix VA Health Care Center, Phoenix, AZ. Electronic address: Daniel.peterson1@asu.edu.
 Department of Medical Science, Clinical Chemistry, Uppsala University, Uppsala, Swede, Sweden. Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. Department of Biochemistry and Biophysics, Science for Life Laboratory, National Bioinformatics Infrastructure Sweden, Stockholm University, Solna, Sweden. Department of Medical Science, Clinical Chemistry, Uppsala University, Uppsala, Swede, Sweden. Department of Medical Science, Clinical Chemistry, Uppsala University, Uppsala, Swede, Sweden. Department of Medical Science, Clinical Chemistry, Uppsala University, Uppsala, Swede, Sweden. Department of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden. Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. Division of Hematology, Uppsala University Hospital, Uppsala, Sweden. Department of Medical Science, Neuroscience, Uppsala University, Uppsala, Sweden. Department of Medical Science, Clinical Chemistry, Uppsala University, Uppsala, Swede, Sweden.
 Department of Neurology, Collegium Medicum, Jan Kochanowski University, Kielce, Poland. wbrola@wp.pl.
 Center for Brain Imaging Science and Technology, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, Zhejiang, China. Key Laboratory for Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou, Zhejiang, China. Center for Brain Imaging Science and Technology, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, Zhejiang, China. MR Collaborations, Siemens Healthineers Ltd, Shanghai, China. Department of Radiology, Stanford University, Stanford, California, USA. Department of Electrical Engineering, Stanford University, Stanford, California, USA. Department of Radiology, Stanford University, Stanford, California, USA. Department of Electrical Engineering, Stanford University, Stanford, California, USA. Department of Neurology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Radiology, Stanford University, Stanford, California, USA. Department of Electrical Engineering, Stanford University, Stanford, California, USA. Neusoft Medical Systems, Shanghai, China. State Key Laboratory of Modern Optical Instrumentation, College of Optical Science and Engineering, Zhejiang University, Hangzhou, Zhejiang, China. Research Center for Healthcare Data Science, Zhejiang Lab, Hangzhou, Zhejiang, China. Center for Brain Imaging Science and Technology, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, Zhejiang, China. Key Laboratory for Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou, Zhejiang, China. School of Physics, Zhejiang University, Hangzhou, Zhejiang, China. Center for Brain Imaging Science and Technology, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, Zhejiang, China. Department of Imaging Sciences, University of Rochester, Rochester, New York, USA.
 Akdeniz University, Antalya, Turkey. Istanbul University, İstanbul, Turkey. Sancaktepe Şehit Prof. Dr. İlhan Varank Training and Research Hospital, Istanbul, Turkey.
 Department of Physical Education, Birjand Branch, Islamic Azad University, Birjand, Iran. Department of Physical Education, Birjand Branch, Islamic Azad University, Birjand, Iran. Department of Physical Education, Birjand Branch, Islamic Azad University, Birjand, Iran. Department of Sport Sciences, Faculty of Literature and Humanities, University of Zabol, Zabol, Iran.
 Department of Radiology, Samsun Education and Research Hospital, İlkadım, Samsun, 55060, Turkey. barisgenc12@gmail.com. Department of Neurology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey. Department of Neurology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey. Department of Radiology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey. Department of Radiology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey.
 IRCCS Centro Neurolesi "Bonino-Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Cardiff University Brain Research Imaging Centre, School of Psychology, Cardiff University, Cardiff, UK. School of Computer Science and Informatics, Cardiff University, Cardiff, UK. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. rocca.mara@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. rocca.mara@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. rocca.mara@hsr.it.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Center for Neuroinflammation and Neurotherapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Sanofi, Cambridge, MA, USA. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. wiendl@uni-muenster.de.
 Pediatric Department, General Hospital of Kastoria, Kastoria, Greece. Department of Paediatrics, University of Crete, Heraklion, Greece. Department of Radiology, Medical School, University Hospital of Heraklion, University of Crete, Heraklion, Greece. Pediatric Intensive Care Unit, School of Medicine, University of Crete, Heraklion, Greece. Pediatric Department, Venizelion General Hospital Heraklion, Heraklion, Crete, Greece. Agri-Food and Life Sciences Institute, University Research Center, Hellenic Mediterranean University, 105 Isavron street, 71303, Heraklion, Crete, Greece. vorgia.pedia@gmail.com.
 Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain Research and Neurotechnology of the Federal Medical Biological Agency, Moscow, Russia. Scientific Center of Neurology, Moscow, Russia.
 Jönköping Academy for Improvement of Health and Welfare, School of Health and Welfare, Jönköping University, Jönköping, Sweden. Futurum Academy for Health and Care, Jönköping, Sweden. Jönköping Academy for Improvement of Health and Welfare, School of Health and Welfare, Jönköping University, Jönköping, Sweden. Department of Care Science, Malmö University, Malmö, Sweden. Jönköping Academy for Improvement of Health and Welfare, School of Health and Welfare, Jönköping University, Jönköping, Sweden. Futurum Academy for Health and Care, Jönköping, Sweden. Jönköping Academy for Improvement of Health and Welfare, School of Health and Welfare, Jönköping University, Jönköping, Sweden. Section of Neurology, Department of Internal Medicine, County Hospital Ryhov, Jönköping, Sweden. Division of Neurobiology, Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
 Costello Medical Consulting Ltd, Cambridge, UK. Costello Medical Consulting Ltd, Cambridge, UK. Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK. Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK. Department of Brain Sciences, Imperial College Healthcare NHS Trust, London, UK. Novartis Pharmaceuticals UK Ltd, London, UK.
 UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. Department of Occupational Therapy, Steinhardt School of Culture, Education, and Human Development, New York University, New York, NY, USA; Kessler Foundation, East Hanover, NJ, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. Electronic address: Riley.bove@ucsf.edu.
 Elytis Hospital Hope, Iasi, Romania. catalina_nastac@yahoo.com. "Prof. Dr. N. Oblu" Neurosurgery Clinical Emergency Hospital, Neurology Department, Iasi, Romania. "Prof. Dr. N. Oblu" Neurosurgery Clinical Emergency Hospital, Neurology Department, Iasi, Romania. University of Medicine and Pharmacy "Gr. T. Popa", Iasi, Romania.
 Department of Radiology, Albert Einstein College of Medicine, Gruss Magnetic Resonance Research Center, Bronx, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Department of Neuropsychology and Psychosocial Research, Holy Name Medical Center, Multiple Sclerosis Center, Teaneck, NJ, USA. Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Radiology, Albert Einstein College of Medicine, Gruss Magnetic Resonance Research Center, Bronx, NY, USA. Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA. Department of Electrical and Computer Engineering, Villanova University, Villanova, PA, USA. Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Neurology, Holy Name Hospital, Teaneck, NJ, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA.
 Klinik für Urologie und Kinderurologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland. Fabian.Queissert@ukmuenster.de. Klinik für Urologie und Kinderurologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.
 School of Nursing, Abadan University of Medical Sciences, Abadan, Iran. Department of Nursing, School of Nursing and Midwifery, Shahroud University of Medical Sciences, Shahroud, Iran. School of Nursing and Midwifery, Research Institute for Prevention of Non - Communicable Diseases, Qazvin University of Medical Sciences, Qazvin, Iran. Department of Psychiatric Nursing, Health Sciences Faculty, Ordu University, Ordu, Turkey. Department of Community Health of Nursing, School of Nursing and Midwifery, Mashhad University of Medical Sciences, Mashhad, Iran.
 Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. Health Education and Health Promotion, Social Determinants in Health Promotion Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. hosseinishirin@ymail.com.
 Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Experimental Imaging Center, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Institute of Experimental Neurology (INSpe), Division of Neuroscience, IRCCS Scientific Institute San Raffaele, Milan, Italy. Electronic address: farina.cinthia@hsr.it.
 Neurology Outpatient Clinic, Amsterdam UMC location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands Department of Immunopathology, Sanquin Research, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Central Diagnostic Laboratory, Amsterdam UMC location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Neurology Outpatient Clinic, Amsterdam UMC location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands Department of Immunopathology, Sanquin Research, Amsterdam, The Netherlands Landsteiner Laboratory, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. Neurology Outpatient Clinic, Amsterdam UMC location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
 Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstraße 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstraße 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstraße 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstraße 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstraße 56, 44791 Bochum, Germany.
 Ophthalmology Clinic, Gebze Fatih State Hospital, 41400, Kocaeli, Turkey. mgtoprak@hotmail.com. Department of Ophthalmology, Acibadem Mehmet Ali Aydınlar University, 34398, Istanbul, Turkey. Neurology Clinic, Pasaalani Private Sevgi Hospital, 10100, Balıkesir, Turkey. Department of Neurology, Kocaeli University, 41100, Kocaeli, Turkey. Department of Ophthalmology, Kocaeli University, 41100, Kocaeli, Turkey. Department of Ophthalmology, Kocaeli University, 41100, Kocaeli, Turkey.
 Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, 20072 Pieve Emanuele, Milan, Italy. Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, 20072 Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. Electronic address: elvezia_maria.paraboschi@hunimed.eu. Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, 20072 Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, 20072 Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. Department of Translational Medicine, University of Ferrara, Italy. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA. IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. Department of Translational Medicine, University of Ferrara, Italy; Center Haemostasis & Thrombosis, University of Ferrara, Italy. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA; Brain and Mind Centre, University of Sydney, Sydney, NSW 2050, Australia. Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, 20072 Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy. IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy; Department of Medical Biotechnology and Translational Medicine, Milan University, Milan, Italy. Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, 20072 Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Milan, Italy.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. abdorrezamoghadasi@gmail.com.
 Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Institute for Clinical and Translational Science, University of Iowa, Iowa City, IA, USA. Department of Epidemiology, University of Iowa, Iowa City, IA, USA. Department of Psychiatry and the Iowa Neuroscience Institute, University of Iowa, Iowa City, IA, USA. Department of Epidemiology, University of Iowa, Iowa City, IA, USA. Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. Electronic address: terry-wahls@uiowa.edu.
 Medical Direction, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Rome, Italy. Department of Clinical Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Istituti Fisioterapici Ospitalieri (IFO), Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Clinical Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Istituti Fisioterapici Ospitalieri (IFO), Rome, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Clinical Pathology and Cancer Biobank, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Clinical Pathology and Microbiology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Gallicano Dermatological Institute, Rome, Italy. Clinical Pathology and Cancer Biobank, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Rome, Italy. Clinical Pathology and Cancer Biobank, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Rome, Italy. Department of Clinical Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Istituti Fisioterapici Ospitalieri (IFO), Rome, Italy. Neuroscience and Imaging, Fatebenefratelli Hospital, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Unità Operativa Complessa (UOC) Neurology, San Giovanni-Addolorata Hospital, Rome, Italy. Department of Clinical Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Istituti Fisioterapici Ospitalieri (IFO), Rome, Italy. Department of Clinical Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Istituti Fisioterapici Ospitalieri (IFO), Rome, Italy. Department of Clinical Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Regina Elena National Cancer Institute, Istituti Fisioterapici Ospitalieri (IFO), Rome, Italy. Department of Neuroscience Mental Health and Sensory Organs (NEMOS), Sapienza University, Rome, Italy. Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Neurologico Mediterraneo Neuromed, Pozzilli, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neurology, Mount Sinai Hospital, New York, NY, United States.
 The National Hospital for Neurology and Neurosurgery & Moorfields Eye Hospital, London, UK; Neuro-ophthalmology Expert Centre, Amsterdam University Medical Centre, Amsterdam, Netherlands. Electronic address: a.petzold@ucl.ac.uk. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
 Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon. Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon. Nehme and Therese Tohme Multiple Sclerosis Center, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon. Medical Imaging Sciences Program, Division of Health Professions, Faculty of Health Sciences, American University of Beirut, Beirut, Lebanon.
 Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Healthand Disorders, Ministry of Education Key Laboratory of Child Development and Disorders. Chongqing Key Laboratory of Pediatrics, Chongqing, 400014, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: zhuqiyuan1997@163.com. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: lymzhang70@163.com.
 Department of Neurology, University Hospital of Basel and University of Basel, Basel, Switzerland; Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland; Department of Biomedical Engineering, University Hospital of Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital of Basel and University of Basel, Basel, Switzerland; Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland. Electronic address: anne-katrin.proebstel@usb.ch.
 Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States. Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, United States. Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States; Department of Neurology, University of South Florida, Tampa, FL, United States. Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States. Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States. Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States. Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, MO, United States. Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States. Electronic address: crossa@wustl.edu.
 Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Immunology Department, La Paz University Hospital, IdiPAZ Health Research Institute, Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area La Paz Hospital Institute for Health Research-IdiPAZ (La Paz University Hospital-Universidad Autónoma de Madrid), Madrid, Spain.
 Neuroimmunology Unit-Department of Genetics, Microbiology and Immunology-Institute of Biology, University of Campinas, Campinas 13083-970, Brazil. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Neuroimmunology Unit-Department of Genetics, Microbiology and Immunology-Institute of Biology, University of Campinas, Campinas 13083-970, Brazil. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Neuroimmunology Unit-Department of Genetics, Microbiology and Immunology-Institute of Biology, University of Campinas, Campinas 13083-970, Brazil. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Partners Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MS 02115, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
 Department of Ophthalmology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China. Electronic address: duyi@gxmu.edu.cn. Department of Geriatric Neurology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
 Department of Clinical Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. r_amani@nutr.mui.ac.ir. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Biostatistics and Epidemiology, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Clinical Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. r_amani@nutr.mui.ac.ir.
 School of Rehabilitation Therapy, Faculty of Health Sciences, Queen's University, Kingston, ON, Canada. Health Sciences Program, Faculty of Health Sciences, Queen's University, Kingston, ON, Canada. Aging and Health Program, School of Rehabilitation Therapy, Faculty of Health Sciences, Queen's University, Kingston, ON, Canada.
 Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Siberian State Medical University, Tomsk, Russia. City Clinical Hospital No. 1, Chelyabinsk, Russia. Rostov State Medical University, Rostov-on-Don, Russia. Ulyanovsk Regional Clinical Hospital, Ulyanovsk, Russia. Leningrad Regional Clinical Hospital, St. Petersburg, Russia. Vladimirsky Moscow Regional Research Clinical Institute, Moscow, Russia. State Novosibirsk Regional Clinical Hospital, Novosibirsk, Russia. Pyatigorsk City Clinical Hospital No. 2, Pyatigorsk, Russia. Semashko Nizhny Novgorod Regional Clinical Hospital, Nizhny Novgorod, Russia. Seredavin Samara Regional Clinical Hospital, Samara, Russia. N. Bechtereva Institute of the Human Brain, St. Petersburg, Russia. Medical and Sanitary unit «Neftyanik», Tyumen, Russia. Regional Clinical Hospital, Barnaul, Russia. Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russia. Rostov Regional Clinical Hospital, Rostov-on-Don, Russia. Wagner Perm State Medical University, Perm, Russia. Republican Clinical Nerological Center, Kazan, Russia. Belgorod Regional Clinical Hospital of St. Joasaph, Belgogrod, Russia. Municipal Filatov Clinical Hospital No. 15, Moscow, Russia. Center for Cardiology and Neurology», Kirov, Russia. Federal Siberian Scientific and Clinical Center, Krasnoyarsk, Russia. JSC BIOCAD, St. Petersburg, Russia. JSC BIOCAD, St. Petersburg, Russia. JSC BIOCAD, St. Petersburg, Russia. JSC BIOCAD, St. Petersburg, Russia.
 Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina (IBIMA Plataforma BIONAND), Universidad de Málaga, C/Severo Ochoa, 35, 29590 Málaga, Spain. Unidad de Neurología, Hospital Universitario Virgen de la Macarena, Av. Dr. Fedriani, 3, 41009 Sevilla, Spain. Biosfer Teslab, 43201 Reus, Spain. Department of Basic Medical Sciences, University Rovira I Virgili, IISPV, CIBERDEM, 43201 Reus, Spain. Statistics Department, Computing Center (SGAI-CSIC), Pinar 19, Madrid 28006, Spain. Instituto de Parasitologia y Biomedicina ″Lopez-Neyra″, Avda. del Conocimiento 17. P. T. Ciencias de la Salud, 18016 Granada, Spain. Unidad de Neurología, Hospital Universitario Virgen de la Macarena, Av. Dr. Fedriani, 3, 41009 Sevilla, Spain. Unidad de Neurología, Hospital Universitario Virgen de la Macarena, Av. Dr. Fedriani, 3, 41009 Sevilla, Spain. Unidad de Neurología, Hospital Universitario Virgen de la Macarena, Av. Dr. Fedriani, 3, 41009 Sevilla, Spain. Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina (IBIMA Plataforma BIONAND), Universidad de Málaga, C/Severo Ochoa, 35, 29590 Málaga, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials & Nanomedicine (CIBER-BBN), 29590 Málaga, Spain.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neurology, Alfred Health, Melbourne, VIC 3004, Australia. Department of Medicine, University of Melbourne, Melbourne, VIC 3050, Australia. Department of Neurology, Melbourne Health, Melbourne, VIC 3050, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, 500 05 Prague, Czech Republic. Department of Cell Biology and Immunology, Instituto de Parasitología y Biomedicina López Neyra, CSIC, 18016 Granada, Spain. Department of Neurology and Division of Genetics, Department of Medicine Brigham and Women's Hospital, Harvard Medical School, Brookline, MA 02115, USA. Department of Neurology, Hospital Universitario Virgen Macarena, 41009 Sevilla, Spain. College of Medicine and Public Health, Flinders University, Adelaide, SA 5042, Australia. Department of Neurology, John Hunter Hospital, Newcastle, NSW 2305, Australia. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia. Genomics Research Centre, Centre of Genomics and Personalised Health, Queensland University of Technology, Brisbane, QLD 4000, Australia. Department of Neurology, Melbourne Health, Melbourne, VIC 3050, Australia. Melbourne Neuroscience Institute, University of Melbourne, Parkville, VIC 3010, Australia. Department of Neurology, Melbourne Health, Melbourne, VIC 3050, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, VIC 3050, Australia. Multiple Sclerosis Center and the Center for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University, New York, NY 10027, USA. John. P. Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL 33136, USA. John. P. Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL 33136, USA. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS 7000, Australia. Westmead Institute, University of Sydney, Sydney, NSW 2145, Australia. Department of Medicine, University of Melbourne, Melbourne, VIC 3050, Australia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, 500 05 Prague, Czech Republic. UGC Neurología. Hospital Universitario Virgen Macarena, Nodo Biobanco del Sistema Sanitario Público de Andalucía, 41009 Sevilla, Spain. Department of Cell Biology and Immunology, Instituto de Parasitología y Biomedicina López Neyra, CSIC, 18016 Granada, Spain. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neurology, Alfred Health, Melbourne, VIC 3004, Australia. Department of Medicine, University of Melbourne, Melbourne, VIC 3050, Australia. Department of Neurology, Melbourne Health, Melbourne, VIC 3050, Australia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, 500 05 Prague, Czech Republic. Department of Neurology, Hospital Universitario Virgen Macarena, 41009 Sevilla, Spain. Department of Neurology, Fundación DINAC, 41009 Sevilla, Spain. Department of Neurology and Division of Genetics, Department of Medicine Brigham and Women's Hospital, Harvard Medical School, Brookline, MA 02115, USA. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, 500 05 Prague, Czech Republic. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neurology, Alfred Health, Melbourne, VIC 3004, Australia. Department of Medicine, University of Melbourne, Melbourne, VIC 3050, Australia. Department of Neurology, Melbourne Health, Melbourne, VIC 3050, Australia.
 Merck Research Labs Information Technology, Merck Sharp, & Dohme, Kenilworth, NJ, USA; Epidemiology Biostatistics and Prevention Institute, University of Zürich, Zürich, Switzerland. Electronic address: ashley.polhemus1@msd.com. Institute of Psychiatry, King's College London, London, UK. Institute of Psychiatry, King's College London, London, UK. Institute of Psychiatry, King's College London, London, UK. Institute of Psychiatry, King's College London, London, UK. Institute of Psychiatry, King's College London, London, UK. RADAR-CNS Patient Advisory Board, King's College London, London, UK. RADAR-CNS Patient Advisory Board, King's College London, London, UK. Merck Research Labs Information Technology, Merck Sharp, & Dohme, Kenilworth, NJ, USA. Merck Research Labs Information Technology, Merck Sharp, & Dohme, Kenilworth, NJ, USA. Merck Research Labs Information Technology, Merck Sharp, & Dohme, Kenilworth, NJ, USA. Institute of Psychiatry, King's College London, London, UK; South London and Maudsley NHS Foundation Trust, London, UK. The RADAR-CNS Consortium (www.radar-cns.org).
 School of Psychological Sciences, University of Tasmania, Launceston, Australia. School of Psychological Sciences, University of Tasmania, Hobart, Australia. School of Applied Psychology & The Hopkins Centre, Griffith University, Mount Gravatt, Australia. School of Psychological Sciences, University of Tasmania, Launceston, Australia.
 Department of Neurosciences, University of California San Diego, San Diego, California, USA. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland.
 Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Department of Neurobiology, University of Pittsburgh, Pittsburgh, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Section on Neural Function, National Institute of Mental Health, National Institutes of Health, Bethesda, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Switzerland, Switzerland. Viral Immunology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Cerebral Microcirculation Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences, Bethesda, United States. Department of Neurobiology, University of Pittsburgh, Pittsburgh, United States. Cerebral Microcirculation Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Vertex Pharmaceuticals Incorporated, Boston, United States. Viral Immunology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States. Neuroimaging Program, Department of Neurology, Cedars Sinai, Los Angeles, United States. Translational Neuroradiology Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, United States.
 Department of Neurosurgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: Sepideh.paybast@yahoo.com. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: abdorrezamoghadasi@gmail.com.
 Adelaide Medical School, University of Adelaide, Adelaide, Australia; South Australian Health and Medical Research Institute, Adelaide, Australia. Electronic address: anna.fragkoudi@adelaide.edu.au. Adelaide Medical School, University of Adelaide, Adelaide, Australia; South Australian Health and Medical Research Institute, Adelaide, Australia. Adelaide Medical School, University of Adelaide, Adelaide, Australia; South Australian Health and Medical Research Institute, Adelaide, Australia; College of Medicine and Public Health, Flinders University, Adelaide, Australia.
 Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. National Health Commission Key Laboratory of Diagnosis and Treatment On Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China. Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. National Health Commission Key Laboratory of Diagnosis and Treatment On Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. qinxinyuecqchina@hotmail.com. Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. fengjinzhou@hotmail.com.
 Medical Imaging and Therapeutic Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa. Electronic address: KempMe@cput.ac.za. Internal Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa. Chemical Pathology, Department of Pathology, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa. Data Analysis, Centre for Statistical Consultation, Department of Statistics and Actuarial Sciences, Stellenbosch University, Stellenbosch, South Africa. Medical Imaging and Therapeutic Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa. Chemical Pathology, Department of Pathology, Faculty of Medicine and Health Sciences, Stellenbosch University and National Health Laboratory Service, Cape Town, South Africa. Medical Imaging and Therapeutic Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa.
 From the Department of Neurology (E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, The Netherlands; Department of Clinical Neurosciences (M.W.K.), University of Calgary, Canada; and Department of Community Health Sciences (M.W.K.), University of Calgary, Canada. e.strijbis@amsterdamumc.nl. From the Department of Neurology (E.M.M.S.), MS Center Amsterdam, Amsterdam University Medical Centers, The Netherlands; Department of Clinical Neurosciences (M.W.K.), University of Calgary, Canada; and Department of Community Health Sciences (M.W.K.), University of Calgary, Canada.
 F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. TranScrip Partners LLP, Wokingham, UK. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Electronic address: erwan.muros@roche.com.
 School of Indigenous, Medical and Health Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia. School of Computing and Information Technology, Faculty of Engineering and Information Sciences, University of Wollongong, Wollongong, New South Wales, Australia. School of Indigenous, Medical and Health Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia; Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia. Electronic address: vguan@uow.edu.au.
 Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Clinical Outcomes Research Unit, Royal Melbourne Hospital, Melbourne, VIC, Australia. Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia.
 From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. From the Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (G.B., E.S., G.L.M., M.I.), University of Genoa; Biostatistics Unit (A.S., M.P.S.), Department of Health Sciences, University of Genoa; Department of Neurosciences Drugs and Child Health (L. Massacesi, A.M.), University of Florence; and Department of Neurology 2 (L. Massacesi, A.M., A.M.R.), Careggi University Hospital, Florence; Department of Neurology (S.C.), A.R.N.A.S. CIVICO, Palermo; Department NEUROFARBA (M.P.A.), Section Neurological Sciences University of Florence; IRCCS Fondazione Don Carlo Gnocchi, (M.P.A) Florence; Department of Neurology (C.G.), Ospedale San Camillo-Forlanini, Rome; Neurology Unit (L. Moiola, M.F.), Neurorehabilitation Unit (F.M.), Neurophysiology Service (F.M.), Neuroimaging Research Unit, Division of Neuroscience (F.M.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (F.M.), Milan; Department Biomedical Metabolic and Neural Sciences (S.M.), University of Modena and Reggio Emilia, Modena, Italy; Department of Neuroscience, Neurology Unit (S.M., P.S.), Azienda Ospedaliera Universitaria, Modena; Neurosciences and Reproductive and Odontostomatological Sciences (V.B.M.), University "Federico II," Naples; Department of Biomedicine, Neurosciences and Advanced Diagnostics (G.S.), University of Palermo; Department of Medical and Surgical Sciences and Advanced Technologies (F.P.), AOU Policlinico-San Marco, University of Catania; MS Centre, Neurology Unit (G.D.L.), SS. Annunziata University Hospital, Chieti; Department of Advanced Medical and Surgical Sciences (G.L.), 2nd Division of Neurology, University of Campania "Luigi Vanvitelli," Naples; Centro Sclerosi Multipla (M.Z.), ASST della Valle Olona, Ospedale di Gallarate, Italy; IRCCS Neuromed (A.C.), Pozzilli (IS); Department of Human Neuroscience (A.C., R.N.) and Dipartimento di Neuroscienze, Salute Mentale e Organi di Senso (NESMOS) (S.R.) Sapienza University, Rome; S.Andrea Multiple Sclerosis Center (R.N.), Sapienza University, Rome; S.Andrea Hospital (S.R.), Rome; Department of Medical and Surgical Sciences (U.A.), Magna Greacia University of Catanzaro; Unit of Neurosciences, Department of Medicine and Surgery (F.G.), University of Parma; Department of Neurosciences (S.G.), San Camillo-Forlanini Hospital, Rome; Department of Neuroscience and Rehabilitation (L.M.C.), Azienda Ospedaliero-Universitaria di Ferrara; IRCCS Istituto delle Scienze Neurologiche di Bologna (A.L.); Dipartimento di Scienze Biomediche e Neuromotorie (A.L.), Università di Bologna; Department of Basic Medical Sciences, Neurosciences and Sense Organs (P.I., M.T.), University of Bari Aldo Moro; Department of Medical Science and Public Health (E.C), University of Cagliari, Cagliari; Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari; Department of Cellular Therapies and Transfusion Medicine (R.S.), Careggi University Hospital, Florence; Ematologia e Terapie Cellulari (E.A.), Ospedale Policlinico IRCCS San Martino (M.P.S.), Genoa; Istituti Clinici Scientifici Maugeri (G.L.M.), Pavia; Ospedale Policlinico IRCCS San Martino (M.I.), Genoa, Italy. m.inglese@unige.it.
 National University of Ireland, Ireland. National University of Ireland, Ireland. National University of Ireland, Ireland. National University of Ireland, Ireland. National University of Ireland, Ireland. National University of Ireland, Ireland.
 Rocky Mountain MS Clinic, Salt Lake City, UT 80031, USA. Neurology Program, Los Angeles County, & USC Medical Center, Los Angeles, CA 90033, USA. South Shore Neurologic Associates, Patchogue, NY 11772, USA. MyHealthTeam, San Francisco, CA 94104, USA. MyHealthTeam, San Francisco, CA 94104, USA. Biogen, Cambridge, MA 02142, USA. Biogen, Cambridge, MA 02142, USA. Biogen, Cambridge, MA 02142, USA. Biogen, Cambridge, MA 02142, USA. Biogen, Cambridge, MA 02142, USA.
 Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. Region Västra Götaland, Sahlgrenska University Hospital, Gothenburg, Sweden. Department of Anesthesiology and Intensive Care, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Region Västra Götaland, Sahlgrenska University Hospital, Gothenburg, Sweden. Department of Anesthesiology and Intensive Care, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. Wallenberg Center of Molecular and Translational Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.
 The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. The University of Texas Medical Branch at Galveston, 301 University Blvd. # 3.908, Galveston, TX 77555-1142, United States. Electronic address: abarmste@utmb.edu.
 From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. From the CHU Nantes (A.G., E.D., S.S., J.M., A.N., S.W., P.-A.G., L.B., D.L.), Nantes Université, INSERM UMR1064, Center for Research in Transplantation and Translational Immunology (CR2TI); CRCSEP (C.L.-F.), CHU de Nice Pasteur 2, Université Nice Côte d'Azur UR2CA URRIS; Service de Neurologie (E.T.), CHU de Nîmes, Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM; Service de Neurologie et Centre d'Investigation Clinique (J.D.S.), CHU de Strasbourg; Service de Neurologie (E.L.P.), CHU Pontchaillou, Rennes; Université de Lyon (S.V.), Université Claude Bernard Lyon 1; Service de Neurologie (S.V.), sclérose en plaques, pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron; Observatoire Français de la Sclérose en Plaques (S.V.), Centre de Recherche en Neurosciences de Lyon; EUGENE DEVIC EDMUS Foundation Against Multiple sclerosis (S.V.), state-approved Foundation, Bron; Service de Neurologie (A.M.), CHU Bretonneau, Tours; Service de Neurologie (E.B.), CHU de Besançon; Service de Neurologie (O.C.), CHU de Grenoble; Service de Neurologie (P.L.), CHU de Montpellier, Montpellier; Service de Neurologie (A.R.), CHU de Bordeaux; Université de Bordeaux (A.R.), INSERM, Neurocentre Magendie; F. Hoffmann-La Roche Ltd (C.R., F.B., R.B.) CIC INSERM 1413 (F.L.F., S.W., D.L.), Nantes; CHU Nantes (S.W., D.L.), Nantes Université, Service de Neurologie; and CHU Nantes (P.-A.G.), Nantes Université, Clinique des données, France. david.laplaud@univ-nantes.fr.
 Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Electronic address: isobe.noriko.342@m.kyushu-u.ac.jp.
 Department of Neurology, Pyhrn-Eisenwurzen Hospital Steyr, Sierninger Straße 170, 4400, Steyr, Austria. Michael.Guger@ooeg.at. Medical Faculty, Johannes Kepler University Linz, Linz, Austria. Michael.Guger@ooeg.at. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Laboratory Medicine, Paracelsus Medical University and Salzburger Landeskliniken, Salzburg, Austria. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. Hermesoft, Data Management, Graz, Austria. Hermesoft, Statistics, Graz, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Institute of Human Genetics, Genetic Epidemiology, University of Münster, Münster, 48149, Germany. Institute for Neuropathology, University of Münster, Münster, 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Institute for Neuropathology, University of Münster, Münster, 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Institute of Neuropathology, University Medical Center, Georg August University, Göttingen, 37073, Germany. Department of Neurology, University Hospital Düsseldorf, Düsseldorf, 40225, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Institute for Neuropathology, University of Münster, Münster, 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany. Institute of Human Genetics, Genetic Epidemiology, University of Münster, Münster, 48149, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster 48149, Germany.
 Child and Adolescent Neuropsychiatry Unit, University of Torino, Regina Margherita Hospital, Torino, Italy. Child and Adolescent Neuropsychiatry Unit, University of Torino, Regina Margherita Hospital, Torino, Italy. Child and Adolescent Neuropsychiatry Unit, University of Torino, Regina Margherita Hospital, Torino, Italy. Child Neuropsychiatry Unit, SS. Antonio e Biagio e Cesare Arrigo Hospital, Alessandria, Italy. Infantile Neuropsychiatric Unit, University Hospital Maggiore della Carità, Novara, Italy. Child Neurology and Psychiatry Unit, S. Croce and Carle Hospital, Cuneo, Italy. Child Neurology and Psychiatry Unit, S. Croce and Carle Hospital, Cuneo, Italy. Infantile Neuropsychiatric Unit, University Hospital Maggiore della Carità, Novara, Italy. Child Neuropsychiatry Unit, SS. Antonio e Biagio e Cesare Arrigo Hospital, Alessandria, Italy. Child and Adolescent Neuropsychiatry Unit, University of Torino, Regina Margherita Hospital, Torino, Italy. Child and Adolescent Neuropsychiatry Unit, University of Torino, Regina Margherita Hospital, Torino, Italy. Child and Adolescent Neuropsychiatry Unit, University of Torino, Regina Margherita Hospital, Torino, Italy.
 School of Public Health, University of Haifa, Haifa, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat Gan, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel.
 Raabe College of Pharmacy, Ohio Northern University, Ada, OH, USA. Raabe College of Pharmacy, Ohio Northern University, Ada, OH, USA. Raabe College of Pharmacy, Ohio Northern University, Ada, OH, USA. Department of Pharmaceutical & Biomedical Sciences, Raabe College of Pharmacy, Ohio Northern University, Ada, OH, USA.
 Julius Centrum voor Gezondheidswetenschappen en Eerstelijns Geneeskunde, Utrecht, Netherlands. RINGGOLD: 168086 Smart Data Analysis and Statistics B.V., Utrecht, Netherlands. Biogen, Toronto, Canada. Fondazione IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. Department of Epidemiology, Bioastatistics and Occupational Health, McGill University, Quebec, Canada. Biogen Inc, Cambridge, USA. RINGGOLD: 2191 Biogen Spain SL, Madrid, Spain. RINGGOLD: 38783 Biogen Inc, Cambridge, USA. RINGGOLD: 2191
 Centre for Social Issues, Department of Psychology, University of Limerick, Limerick, Ireland. Centre for Social Issues, Department of Psychology, University of Limerick, Limerick, Ireland. Health Research Institute, University of Limerick, Limerick, Ireland. Centre for Social Issues, Department of Psychology, University of Limerick, Limerick, Ireland. Health Research Institute, University of Limerick, Limerick, Ireland. Health Research Institute, University of Limerick, Limerick, Ireland. Department of Clinical Therapies, University of Limerick, Ireland. Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, Urbana, IL, USA. Health Research Institute, University of Limerick, Limerick, Ireland. Department of Clinical Therapies, University of Limerick, Ireland.
 CORe, Department of Medicine, The University of Melbourne, Parkville, Australia; Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Australia; Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Department of Neurology, Townsville University Hospital, Douglas, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, Australia. Department of Neurology, John Hunter Hospital, New Lambton, Australia; Hunter Medical Research Institute, New Lambton, Australia; School of Health Sciences, Faculty of Health and Medicine, University of Newcastle, Callaghan, Australia. Geelong Clinical School, School of Medicine, Deakin University, Geelong, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. CORe, Department of Medicine, The University of Melbourne, Parkville, Australia; Neuroimmunology Centre, The Royal Melbourne Hospital, Melbourne, Australia. Department of Neuroscience, Monash University, Melbourne, Australia. Department of Neurology, Townsville University Hospital, Douglas, Australia. Electronic address: mike.boggild@health.qld.gov.au.
 Avenier, Centres of Vaccination and Travel Medicine, Brno and Ostrava, Czechia. Department of Public Health, Faculty of Medicine, Masaryk University, Brno, Czechia. Department of Epidemiology and Public Health, Faculty of Medicine, University of Ostrava, Ostrava, Czechia, petra.macounova@osu.cz. Department of Public Health, Faculty of Medicine, Masaryk University, Brno, Czechia. Avenier, Centres of Vaccination and Travel Medicine, Brno and Ostrava, Czechia. Department of Epidemiology and Public Health, Faculty of Medicine, University of Ostrava, Ostrava, Czechia.
 From the Departments of Neuroradiology. From the Departments of Neuroradiology. From the Departments of Neuroradiology. Siemens Healthcare SAS, Saint-Denis, France.
 Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, University of California, Irvine, Irvine, California, USA. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Institute for Experimental Neuroimmunology, Technical University of Munich, Munich, Germany. Munich Cluster of Systems Neurology (SyNergy), Munich, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany. Munich Cluster of Systems Neurology (SyNergy), Munich, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine and the Helmholtz Association, Charité - University Medicine Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Klinikum rechts der Isar, TUM School of Medicine, Technical University of Munich, Munich, Germany.
 Multiple Sclerosis Center, ASL Cagliari, Department of Medical Sciences and Public Health, Binaghi Hospital, University of Cagliari, via Is Guadazzonis 2, Cagliari 09126, Italy. Institute for Genetic and Biomedical Research, National Research Council, Monserrato, Italy. Department of Neurosciences, ARNAS Brotzu, Cagliari. Multiple Sclerosis Center, ASL Cagliari, Department of Medical Sciences and Public Health, Binaghi Hospital, University of Cagliari, via Is Guadazzonis 2, Cagliari 09126, Italy. Multiple Sclerosis Center, ASL Cagliari, Department of Medical Sciences and Public Health, Binaghi Hospital, University of Cagliari, via Is Guadazzonis 2, Cagliari 09126, Italy. Electronic address: lorena.lorefice@aslcagliari.it.
 Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Electronic address: nataliamorawiec007@gmail.com. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland. Department of Microbiology and Immunology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. Jordana 19, 41-808 Zabrze, Poland. Department of Microbiology and Immunology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. Jordana 19, 41-808 Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, ul. 3 Maja 13-15, 41-800 Zabrze, Poland.
 Department of Neurology, Dartmouth Hitchcock Medical Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA. Department of Neurology, EpiCURA Centre Hospitalier, Ath, Belgium. Hearthrhythmanagement, UZB, Brussels, Belgium.
 Department of Psychology, Université du Québec à Montréal, CP 8888, succ. Centre-ville, QC, Montreal H3C 3P8, Canada. Department of Psychology, Université du Québec à Montréal, CP 8888, succ. Centre-ville, QC, Montreal H3C 3P8, Canada. Department of Psychology, Université du Québec à Montréal, CP 8888, succ. Centre-ville, QC, Montreal H3C 3P8, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal, 900 Rue Saint-Denis, QC H2 X 3H8, Montréal, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal, 900 Rue Saint-Denis, QC H2 X 3H8, Montréal, Canada. Department of Psychology, Université du Québec à Montréal, CP 8888, succ. Centre-ville, QC, Montreal H3C 3P8, Canada; Centre de Recherche du Centre Hospitalier de l'Université de Montréal, 900 Rue Saint-Denis, QC H2 X 3H8, Montréal, Canada. Electronic address: rouleau.isabelle@uqam.ca.
 Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Napoli, Italy. Electronic address: rosaiodice81@gmail.com. Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Napoli, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Napoli, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Napoli, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Napoli, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Napoli, Italy.
 From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild. From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild. From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild. From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild. From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild. From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild. From the Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild.
 Tisch Multiple Sclerosis Research Center of New York, 521 W. 57th St., 4th floor, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, 521 W. 57th St., 4th floor, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, 521 W. 57th St., 4th floor, New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, 521 W. 57th St., 4th floor, New York, NY 10019, USA.
 Department of Persian Medicine, School of Persian Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Shahid Beheshti University of Medical Science, Tehran, Iran. Center for Neuroscience and Cognition, Royan Institute, Tehran, Iran. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, Imam Khomeini Hospital, Iranian Center of Neurological Research, Tehran University of Medical Sciences, Tehran, Iran. Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran; Persian Medicine Network (PMN), Universal Scientific Education and Research Network (USERN), Tehran, Iran. Ingham Institute for Applied Medical Research, 1 Campbell St, Liverpool, NSW, Australia; Department of Neurophysiology, Liverpool Hospital, NSW, Australia. Traditional Medicine Clinical Trial Research Center, Shahed University, Tehran, Iran. Electronic address: naseri@shahed.ac.ir.
 Neuroscience Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran. Neuroscience Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran. Neuroscience Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Applied Virology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
 Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, Clinical Pharmacology and Pharmacogenomics Research Group, Head of Clinical Pharmacology and Pharmacogenomics Research Group, German University in Cairo, Cairo 11835, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, Clinical Pharmacology and Pharmacogenomics Research Group, Head of Clinical Pharmacology and Pharmacogenomics Research Group, German University in Cairo, Cairo 11835, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, Clinical Pharmacology and Pharmacogenomics Research Group, Head of Clinical Pharmacology and Pharmacogenomics Research Group, German University in Cairo, Cairo 11835, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, Clinical Pharmacology and Pharmacogenomics Research Group, Head of Clinical Pharmacology and Pharmacogenomics Research Group, German University in Cairo, Cairo 11835, Egypt. Electronic address: hend.saber@guc.edu.eg.
 Neurology Department, Cluj Emergency County Hospital, Cluj-Napoca 400012, Romania; Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca 400012, Romania. Neurology Department, Cluj Emergency County Hospital, Cluj-Napoca 400012, Romania; Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca 400012, Romania. Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca 400349, Romania. Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca 400349, Romania. Electronic address: cvacaras@yahoo.ro. Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca 400349, Romania. Neurology Department, Cluj Emergency County Hospital, Cluj-Napoca 400012, Romania; Department of Neurosciences, Faculty of Medicine, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca 400012, Romania.
 Institute of Nuclear Physics, Polish Academy of Sciences, Radzikowskiego 152, 31-342 Krakow, Poland. Electronic address: karolina.chrabaszcz@ifj.edu.pl. Institute of Medical Sciences, Medical College of Rzeszow University, Kopisto 2a, 35-315 Rzeszow, Poland. Institute of Nuclear Physics, Polish Academy of Sciences, Radzikowskiego 152, 31-342 Krakow, Poland; SOLARIS, National Synchrotron Radiation Centre, Jagiellonian University, Czerwone Maki 98, 30-392, Krakow, Poland. Institute of Nuclear Physics, Polish Academy of Sciences, Radzikowskiego 152, 31-342 Krakow, Poland. Institute of Nuclear Physics, Polish Academy of Sciences, Radzikowskiego 152, 31-342 Krakow, Poland. Department of Neurology, Institute of Medical Sciences, Medical College of Rzeszow University, Warzywna 1a, 35-310 Rzeszow, Poland. Department of Neurology, Institute of Medical Sciences, Medical College of Rzeszow University, Warzywna 1a, 35-310 Rzeszow, Poland. Institute of Nuclear Physics, Polish Academy of Sciences, Radzikowskiego 152, 31-342 Krakow, Poland. Institute of Physics, College of Natural Sciences, University of Rzeszow, Pigonia Street 1, 35-959 Rzeszow, Poland. Institute of Nuclear Physics, Polish Academy of Sciences, Radzikowskiego 152, 31-342 Krakow, Poland.
 Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Nutrition, School of Allied Medical Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Nutrition, School of Allied Medical Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Neurology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Statistics and Epidemiology, School of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
 Department of Nursing/Faculty of Health Science, University of Alicante, San Vicente del Raspeig, Alicante, Spain. Department of Nursing/Faculty of Health Science, University of Alicante, San Vicente del Raspeig, Alicante, Spain. Department of Nursing/Faculty of Health Science, University of Alicante, San Vicente del Raspeig, Alicante, Spain. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, United States of America. Department of Nursing/Faculty of Health Science, University of Alicante, San Vicente del Raspeig, Alicante, Spain.
 Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Ontario, Canada. Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Ontario, Canada. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada. Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Ontario, Canada; Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada. Electronic address: edward.margolin@uhn.ca.
 From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. nicolas.fissolo@vhir.org. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain. From the Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron (N.F., A.P., J.R., L.G., X.M., M.C.); Departments of Immunology and Neurology (L.M.V.), Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid; Statistics and Bioinformatics Unit, Vall d'Hebron Institut de Recerca (VHIR) (S.P.-H., A.S.); and Genetics, Microbiology and Statistics Department (A.S.), Universitat de Barcelona, Spain.
 SRM Modinagar College of Pharmacy, SRM Institute of Science and Technology (Deemed to be University), Delhi-NCR Campus, Modinagar, Ghaziabad, Uttar Pradesh 201204, India. Electronic address: nitishkumarpharma@gmail.com. SRM Modinagar College of Pharmacy, SRM Institute of Science and Technology (Deemed to be University), Delhi-NCR Campus, Modinagar, Ghaziabad, Uttar Pradesh 201204, India. Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, (An Autonomous College), Moga, Punjab 142001, India. SRM Modinagar College of Pharmacy, SRM Institute of Science and Technology (Deemed to be University), Delhi-NCR Campus, Modinagar, Ghaziabad, Uttar Pradesh 201204, India.
 Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. San Luigi Gonzaga University Hospital, Orbassano, Italy. San Luigi Gonzaga University Hospital, Orbassano, Italy. Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. San Luigi Gonzaga University Hospital, Orbassano, Italy.
 Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Neurology, Air Force Medical Center of PLA, Beijing 100142, China. Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Radiology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Cardiology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Electronic address: llihongzeng@163.com. Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an 710038, China. Electronic address: guojun_81@163.com.
 Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA/Biostatistics Center, Massachusetts General Hospital, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA/Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA/Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Center for Neurological Imaging, Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA/Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA/Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Harvard Medical School, Boston, MA, USA/Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA/Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA.
 Department of Child Neurology, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Catholic University of Uruguay, Montevideo, Uruguay. Department of Child Neurology, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Department of Child Neurology, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Department of Child Neurology, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina.
 From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. f.loonstra@amsterdamumc.nl. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom. From the MS Center Amsterdam (F.C.L., L.R.J.R., E.M.M.S., B.M.J.U., J.K.), Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; Neurochemistry Laboratory (M.J.A.K.-S., C.T.), Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; MS Center Amsterdam (B.M., F.B.), Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, The Netherlands; andQueen Square Institute of Neurology and Centre for Medical Image Computing (F.B.), University College London, United Kingdom.
 Department of Neurology with Institute of Translational Neurology, University of Münster, 48149 Münster, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149 Münster, Germany.
 Department of Laboratory Medicine, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Electronic address: lmichetti@asst-pg23.it. Department of Laboratory Medicine, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Department of Laboratory Medicine, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Department of Neurology and Multiple Sclerosis Center, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Department of Neurology and Multiple Sclerosis Center, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Department of Neurology and Multiple Sclerosis Center, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy. Department of Laboratory Medicine, Papa Giovanni XXIII Hospital, Piazza OMS, 1, 24127 Bergamo, Italy.
 Neuroscience Research Group (NRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. fardinnabizade1378@gmail.com. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. fardinnabizade1378@gmail.com. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Imam Khomeini Hospital Complex (IKHC), Tehran University of Medical Science, Tehran, Iran. Student's Scientific Research Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Student's Scientific Research Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
 Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Haematology Research Centre, Department of Immunology and Inflammation, Imperial College London, London, UK. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Laboratorios Ruiz, Clínica Ruiz, Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Laboratorios Ruiz, Clínica Ruiz, Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México.
 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Department of Electrophysiology, Heart Center Leipzig at University of Leipzig, Leipzig, Germany. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. omid.mirmosayyeb@gmail.com. Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. omid.mirmosayyeb@gmail.com. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. omid.mirmosayyeb@gmail.com.
 Laboratory of Clinical Functional Exploration of Movement, University Hospital of Besançon, 25000 Besançon, France. Clinical Investigation Center, INSERM 1431, University Hospital of Besançon, 25000 Besançon, France. Department of Physical Medicine and Rehabilitation, Dijon-Bourgogne University Hospital, 21000 Dijon, France. Clinical Investigation Center, INSERM 1431, University Hospital of Besançon, 25000 Besançon, France. EA4266 Agents Pathogènes et Inflammation, University of Bourgogne-Franche-Comte, 25000 Besançon, France. Laboratory Performance, Santé, Métrologie, Société (PSMS), UFR STAPS, 51000 Reims, France. Laboratory of Clinical Functional Exploration of Movement, University Hospital of Besançon, 25000 Besançon, France. Clinical Investigation Center, INSERM 1431, University Hospital of Besançon, 25000 Besançon, France. Integrative and Clinical Neurosciences EA481, Bourgogne Franche-Comte University, 25000 Besançon, France. Laboratory of Clinical Functional Exploration of Movement, University Hospital of Besançon, 25000 Besançon, France. Integrative and Clinical Neurosciences EA481, Bourgogne Franche-Comte University, 25000 Besançon, France. Rehabilitation Department, HFR, 1700 Fribourg, Switzerland.
 Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Technology Platform Pluripotent Stem Cells, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Institute of Biochemistry and. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Institute of Biometry and Clinical Epidemiology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Genomics Technology Platform, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
 Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hospices Civils de Lyon, Hôpital Neurologique Pierre Wertheimer, Bron, France/INSERM 1028 et CNRS UMR 5292, Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, Lyon, France/Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France/Eugène Devic EDMUS Foundation against Multiple Sclerosis, State-Approved Foundation, Bron, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France/Hospices Civils de Lyon, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron, France/FORGETTING Team, INSERM 1028 et CNRS UMR5292, Centre des Neurosciences de Lyon, Lyon, France. Centre Ressources et Compétences Sclérose en Plaques (CRC-SEP) et Service de Neurologie B4, Hôpital Pierre-Paul Riquet, CHU Toulouse Purpan, Toulouse, France/INSERM UMR1291 - CNRS UMR5051, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse III, Toulouse, France. Department of Neurology, CHU Rouen, Rouen, France. CRCSEP Côte d'Azur, CHU de Nice Pasteur 2, Nice, France/UR2CA-URRIS, Université Nice Côte d'Azur, Nice, France. CRC-SEP, Neurology Department, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, CHU Rouen, Rouen, France. CRC-SEP, Service de Neurologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France. Hospices Civils de Lyon, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron, France. CRC-SEP, Neurology Department, Hôpital Gui de Chauliac, CHU de Montpellier, Montpellier, France. CIC_P1414 INSERM, Neurology Department, Rennes University Hospital, Rennes, France. EHESP, CNRS, Inserm, Arènes - UMR 6051, RSMS (Recherche sur les Services et Management en Santé), Université de Rennes, Rennes, France. CRC SEP Service de Neurologie, CHU Tours, Tours, France. INSERM, Center for Research in Transplantation and Translational Immunology, Nantes Université, Nantes, France/CIC INSERM 1413, CRC-SEP Pays de la Loire, CHU Nantes, Nantes, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hospices Civils de Lyon, Hôpital Neurologique Pierre Wertheimer, Bron, France/Ramsay Santé, Clinique de la Sauvegarde, Lyon, France. CRC-SEP, Neurology Department, Hôpital Fondation Adolphe de Rothschild, Paris, France. CRC-SEP, Service de Neurologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France. Centre Ressources et Compétences Sclérose en Plaques (CRC-SEP) et Service de Neurologie B4, Hôpital Pierre-Paul Riquet, CHU Toulouse Purpan, Toulouse, France/INSERM UMR1291 - CNRS UMR5051, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse III, Toulouse, France. Service de Neurologie, CHU de Caen Normandie, Caen, France. Neurologie, Pathologies Inflammatoires du Système Nerveux, CHU Grenoble Alpes, Grenoble, France/TIMC-IMAG, T-RAIG (Translational Research in Autoimmunity and Inflammation Group), Université de Grenoble Alpes, Grenoble, France. Service de Neurologie, CHU de Besançon, Besançon, France. Faculté de Médecine et de Maïeutique de Lille, Groupement des Hôpitaux de l'Institut Catholique de Lille, Hôpital Saint Philibert, Lille, France. APHP-6, Department of Neurology, Saint-Antoine Hospital, Paris, France/Sorbonne University, Paris, France. CRC-SEP, Hôpital Pellegrin, CHU de Bordeaux, Bordeaux, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hospices Civils de Lyon, Hôpital Neurologique Pierre Wertheimer, Bron, France. Department of Neurology, CHU Rouen, Rouen, France. Department of Neurology, Lille Catholic Hospitals, Lille Catholic University, Lille, France. Service de Neurologie, Centre Hospitalier de Lens, Lens, France. CNRS, CRMBM, UMR 7339, Aix-Marseille Université, Marseille, France/APHM, Hôpital de la Timone, Marseille, France. Department of Neurology, Gonesse Hospital, Gonesse, France. Service de Neurologie, Hôpital Central, Centre Hospitalier Régional Universitaire de Nancy, Nancy, France. Inserm, Neuro-Dol, Université Clermont Auvergne, Clermont-Ferrand, France/Department of Neurology et CRC-SEP, CHU Clermont-Ferrand, Clermont-Ferrand, France. CRC-SEP, Hôpital Pellegrin, CHU de Bordeaux, Bordeaux, France. CRC-SEP, Neurology Department, Pitié-Salpêtrière Hospital, Paris, France. CRC-SEP, Neurology Department, Pitié-Salpêtrière Hospital, Paris, France. CRCSEP Côte d'Azur, CHU de Nice Pasteur 2, Nice, France/UR2CA-URRIS, Université Nice Côte d'Azur, Nice, France.
 Department of Neuroscience, School of Medicine, Laboratory for Human and Experimental Neurophysiology (LAHEN), University of Split, Split, Croatia. Department of Psychology, University of Zadar, Zadar, Croatia. Department of Psychology, University of Zadar, Zadar, Croatia. Institute of Physical Medicine and Rehabilitation with Rheumatology, University Hospital of Split, Split, Croatia. Department of Health Studies, University of Split, Split, Croatia. Department of Neuroscience, School of Medicine, Laboratory for Human and Experimental Neurophysiology (LAHEN), University of Split, Split, Croatia. Sleep Medical Centre, University Hospital of Split, Split, Croatia. Department of Neuroscience, School of Medicine, Laboratory for Human and Experimental Neurophysiology (LAHEN), University of Split, Split, Croatia.
 Dept. of Microbiology Immunology and Biochemistry, UTHSC, Memphis, TN, United States. Dept. of Microbiology Immunology and Biochemistry, UTHSC, Memphis, TN, United States. College of Graduate Health Sciences, UTHSC, Memphis, TN, United States. Gliknik, Inc., Baltimore, MD, United States. Gliknik, Inc., Baltimore, MD, United States. College of Medicine, UTHSC, Memphis, TN, United States. Dept. of Pathology, UTHSC, Memphis, TN, United States. Div. of Biostatistics, Dept. of Preventive Medicine, UTHSC, Memphis, TN, United States. Gliknik, Inc., Baltimore, MD, United States. Gliknik, Inc., Baltimore, MD, United States. Dept. of Microbiology Immunology and Biochemistry, UTHSC, Memphis, TN, United States. Dept. of Microbiology Immunology and Biochemistry, UTHSC, Memphis, TN, United States.
 School of Health Sciences, University of Canterbury, Christchurch, New Zealand. School of Physiotherapy, Centre for Health, Activity, and Rehabilitation Research (CHARR), University of Otago, Christchurch, New Zealand. School of Health Sciences, University of Canterbury, Christchurch, New Zealand. School of Product Design, University of Canterbury, Christchurch, New Zealand. School of Health Sciences, University of Canterbury, Christchurch, New Zealand.
 Department of Neurology and Department of Pediatrics, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA. Electronic address: Benjamin.Greenberg@UTSouthwestern.edu. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Mile End Rd, Bethnal Green, London E1 4NS, United Kingdom.
 John Walsh Centre for Rehabilitation Research, The Kolling Institute of Medical Research, Northern Sydney Medical School, University of Sydney, Sydney, Australia. John Walsh Centre for Rehabilitation Research, The Kolling Institute of Medical Research, Northern Sydney Medical School, University of Sydney, Sydney, Australia. Research School of Psychology, Australian National University, Canberra, Australia.
 Physical Therapy for Neurology, Faculty of Physical Therapy, Cairo University, Egypt. Physical Therapy for Pediatrics, Faculty of Physical Therapy, Cairo University, Egypt. Physical Therapy for Cardiovascular/respiratory disorders and Geriatrics, Faculty of Physical Therapy, Cairo University, Egypt. Electronic address: hady612@cu.edu.eg. Physiotherapy in Motion, Multispeciality Research Group (PTinMOTION), University of Valencia, 46010 Valencia, Spain. Physical Therapy for Neurology, Faculty of Physical Therapy, Cairo University, Egypt.
 Signal Processing, Analysis, and Advanced Diagnostics Research and Education Laboratory (SPAADREL), Faculty of Maritime Studies, University of Split, 21000 Split, Croatia. Department of Neurology, University Hospital of Split, 21000 Split, Croatia. Signal Processing, Analysis, and Advanced Diagnostics Research and Education Laboratory (SPAADREL), Faculty of Maritime Studies, University of Split, 21000 Split, Croatia. Laboratory for Human and Experimental Neurophysiology, Department of Neuroscience, School of Medicine, University of Split, 21000 Split, Croatia.
 Department of Physical Medicine and Rehabilitation, University of Colorado, Aurora, CO, United States. VA Eastern Colorado Geriatric Research, Education, and Clinical Center, Rocky Mountain Regional VA Medical Center, Aurora, CO, United States. Department of Physical Therapy, High Point University, One University Parkway, High Point, NC United States. Department of Physical Medicine and Rehabilitation, University of Colorado, Aurora, CO, United States. VA Eastern Colorado Geriatric Research, Education, and Clinical Center, Rocky Mountain Regional VA Medical Center, Aurora, CO, United States. Department of Physical Medicine and Rehabilitation, University of Colorado, Aurora, CO, United States. Department of Physical Medicine and Rehabilitation, University of Colorado, Aurora, CO, United States. VA Eastern Colorado Geriatric Research, Education, and Clinical Center, Rocky Mountain Regional VA Medical Center, Aurora, CO, United States. Department of Neurology, University of Colorado Anschutz Medical Campus Aurora, CO, United States.
 Discipline of Exercise Science, Murdoch University, Perth, WA, Australia; Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Ageing, Murdoch University, WA, Australia; Perron Institute for Neurological and Translational Science, Perth, WA, Australia. Electronic address: learmonth@murdoch.edu.au. Disability and Health Unit, Melbourne School of Population and Global Health, University of Melbourne, VIC, Australia. Discipline of Psychology, Murdoch University, Perth, WA, Australia. University of Western Australia, Crawley, WA, Australia. Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Ageing, Murdoch University, WA, Australia; Centre for Neuromuscular and Neurological Disorders, Perron Institute for Neurological and Translational Science, University of Western Australia, Perth, WA, Australia. Disability and Health Unit, Melbourne School of Population and Global Health, University of Melbourne, VIC, Australia.
 Rehabilitation of Health Sciences Department, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia. pt.hanadi@gmail.com. Rehabilitation of Health Sciences Department, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.
 NYU Langone Multiple Sclerosis Comprehensive Care Center, 240 E. 38th St., 13th Floor, New York, NY 10016, USA. NYU Langone Multiple Sclerosis Comprehensive Care Center, 240 E. 38th St., 13th Floor, New York, NY 10016, USA. NYU Langone Multiple Sclerosis Comprehensive Care Center, 240 E. 38th St., 13th Floor, New York, NY 10016, USA. NYU Langone Multiple Sclerosis Comprehensive Care Center, 240 E. 38th St., 13th Floor, New York, NY 10016, USA. NYU Langone Multiple Sclerosis Comprehensive Care Center, 240 E. 38th St., 13th Floor, New York, NY 10016, USA. Electronic address: Lauren.krupp@nyulangone.org.
 Ares Trading SA, An Affiliate of Merck KGaA, Eysins, Switzerland. Ares Trading SA, An Affiliate of Merck KGaA, Eysins, Switzerland. Biostatistics, Evi-Science, Geneva, Switzerland. Ares Trading SA, An Affiliate of Merck KGaA, Eysins, Switzerland. Global Biostatistics, Merck Healthcare KGaA, Darmstadt, Germany. Merck Serono Ltd, An Affiliate of Merck KGaA, Feltham, UK. Connected Health and Devices unit, Merck Santé S.A.S. an Affiliate of Merck KGaA, Lyon, France.
 Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, NV, USA. Electronic address: hual@ccf.org. Department of Neurology and the Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Providence Multiple Sclerosis Center, Providence Brain and Spine Institute, Portland, OR, USA. Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Stony Brook University, Stony Brook, NY, USA. UCSF, Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Mellen Center for Multiple Sclerosis Treatment and Research Neurological Institute Cleveland Clinic, Cleveland, OH, USA.
 Institute of Health and Wellbeing, University of Glasgow, Glasgow, UK. robert.simpson@uhn.ca. Division of Physical Medicine and Rehabilitation, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada. robert.simpson@uhn.ca. University Health Network, Toronto Rehabilitation Institute, 347 Rumsey Rd, East York, Toronto, ON, M4G 2V6, Canada. robert.simpson@uhn.ca. St. John's Rehab Research Program, Sunnybrook Research Institute, Toronto, Canada. Division of Physical Medicine and Rehabilitation, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada. Institute of Health and Wellbeing, University of Glasgow, Glasgow, UK. St. John's Rehab Research Program, Sunnybrook Research Institute, Toronto, Canada. Rehabilitation Sciences Institute, University of Toronto, Toronto, Canada. St. John's Rehab Research Program, Sunnybrook Research Institute, Toronto, Canada. Division of Physical Medicine and Rehabilitation, Department of Medicine, Sunnybrook Health Sciences Centre, Toronto, Canada. Rehabilitation Sciences Institute, University of Toronto, Toronto, Canada. KITE Research Institute, University Health Network, Toronto, Canada. Division of Physical Medicine and Rehabilitation, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada. KITE Research Institute, University Health Network, Toronto, Canada. University Health Network, Toronto Rehabilitation Institute, 347 Rumsey Rd, East York, Toronto, ON, M4G 2V6, Canada. Department of Psychiatry, Sunnybrook Health Sciences Centre, Toronto, Canada. Consultation/Liaison Psychiatry, University of Toronto, Toronto, Canada.
 Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France; Faculty of Medicine and Health Sciences, Department of Human Structure and Repair, Ghent University, Ghent, Belgium. Electronic address: rebecca.haddad@aphp.fr. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France. Sorbonne Universté, GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, AP-HP, Hôpital Tenon, F-75020 Paris, France.
 School of Rehabilitation Therapy, Queen's University, Louise D. Acton Building, 31 George Street, Kingston K7L 3N6, Canada. Electronic address: a.fakolade@queensu.ca. School of Rehabilitation Therapy, Queen's University, Louise D. Acton Building, 31 George Street, Kingston K7L 3N6, Canada; Research Department, Humber River Hospital, Toronto, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Canada. Faculty of Health Sciences, Queen's University, Kingston, Canada. Department of Psychology, Queen's University, Kingston, Canada; Department of Biology, Queen's University, Kingston, Canada. Faculty of Health Sciences, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Louise D. Acton Building, 31 George Street, Kingston K7L 3N6, Canada; Department of Physical Therapy, College of Medical Rehabilitation, Qassim University, Buraydah 52645, Saudi Arabia. Bracken Health Sciences Library, Queen's University, Kingston, Canada. Centre for Trials Research, Cardiff University, Cardiff, United Kingdom.
 Neurocentre, Lucerne Cantonal Hospital, Lucerne, Switzerland. Neurocentre, Lucerne Cantonal Hospital, Lucerne, Switzerland; Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. Electronic address: christian.kamm@luks.ch. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Department of Neurology, Schulthess Clinic Zurich, Switzerland; Department of Health Sciences and Technology, ETH Zurich, Switzerland. Multiple Sclerosis Center, Department of Neurology, Neurocenter of Southern Switzerland, Ospedale Civico, Via Tesserete 46, Lugano 6903, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera Italiana, Via Buffi 13, Lugano 6900, Switzerland. Division of Molecular and Cognitive Neuroscience, Neuropsychology and Behavioral Neurology Unit, University of Basel, Basel, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Neurocentre, Lucerne Cantonal Hospital, Lucerne, Switzerland.

 Department of Health Sciences, University of Colorado Colorado Springs, 1420 Austin Bluffs Pkwy, Colorado Springs, CO 80907, USA. Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, 506 S. Wright St., Urbana, IL 61801, USA. Department of Recreation, Sport, and Tourism, University of Illinois at Urbana-Champaign, 506 S. Wright St., Urbana, IL 61801, USA. Department of Health Sciences, University of Colorado Colorado Springs, 1420 Austin Bluffs Pkwy, Colorado Springs, CO 80907, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, 1200 West Harrison St., Chicago, IL 60607, USA.
 Department of Neurology, Amsterdam University Medical Centers, Universiteit Amsterdam, Amsterdam, The Netherlands/MS Center Amsterdam, Amsterdam, The Netherlands/Amsterdam Neuroscience, Amsterdam, The Netherlands. Institute for Computing and Information Sciences, Radboud University, Nijmegen, The Netherlands. MS Sherpa BV, Nijmegen, The Netherlands. Orikami Digital Health Products, Nijmegen, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Universiteit Amsterdam, Amsterdam, The Netherlands/MS Center Amsterdam, Amsterdam, The Netherlands/Amsterdam Neuroscience, Amsterdam, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Universiteit Amsterdam, Amsterdam, The Netherlands/MS Center Amsterdam, Amsterdam, The Netherlands/Amsterdam Neuroscience, Amsterdam, The Netherlands. Institute for Computing and Information Sciences, Radboud University, Nijmegen, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Universiteit Amsterdam, Amsterdam, The Netherlands/MS Center Amsterdam, Amsterdam, The Netherlands/Amsterdam Neuroscience, Amsterdam, The Netherlands. MS Center Amsterdam, Amsterdam, The Netherlands/Amsterdam Neuroscience, Amsterdam, The Netherlands/Department of Rehabilitation Medicine, Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
 Neuroscience Research Group (NRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. fardinnabizade1378@gmail.com. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. fardinnabizade1378@gmail.com. Neuroscience Research Group (NRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
 General Hospital Celje, Department of Neurology, Oblakova Ulica 5, 3000 Celje, Slovenia. General Hospital Celje, Department of Neurology, Oblakova Ulica 5, 3000 Celje, Slovenia. Electronic address: breclova.eva@gmail.com. University Medical Centre Ljubljana, Department of Haematology, Zaloška Cesta 2, 1000 Ljubljana, Slovenia; University of Ljubljana, Faculty of Medicine, Vrazov Trg 2, 1000 Ljubljana, Slovenia. General Hospital Celje, Department of Neurology, Oblakova Ulica 5, 3000 Celje, Slovenia; University of Ljubljana, Faculty of Medicine, Vrazov Trg 2, 1000 Ljubljana, Slovenia.
 Institute of Hospitalization and Care of a Scientific Character "Santa Lucia" Foundation, Behavioral Neuropsychology, Rome, Italy. Institute of Hospitalization and Care of a Scientific Character "Santa Lucia" Foundation, Behavioral Neuropsychology, Rome, Italy. Institute of Hospitalization and Care of a Scientific Character "Santa Lucia" Foundation, Behavioral Neuropsychology, Rome, Italy. University of Rome "Tor Vergata", Department of Clinical Sciences and Translational Medicine, Rome, Italy.
 Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic. Electronic address: v.pesakova@fno.cz. Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic. Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Children Neurology, Department of Neurology, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic. Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic. Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic.
 Center for Precision Health, School of Biomedical Informatics, The University of Texas Health Science Center, Houston, TX 77030, USA. Center for Precision Health, School of Biomedical Informatics, The University of Texas Health Science Center, Houston, TX 77030, USA. Center for Precision Health, School of Biomedical Informatics, The University of Texas Health Science Center, Houston, TX 77030, USA. Department of Neurology, Dell Medical School, The University of Texas, Austin, TX 78712, USA. Center for Precision Health, School of Biomedical Informatics, The University of Texas Health Science Center, Houston, TX 77030, USA. Human Genetics Center, School of Public Health, The University of Texas Health Science Center, Houston, TX 77030, USA.
 School of Nursing, Istanbul University, Istanbul 34116, Turkey. Kumluca Faculty of Health Sciences, Akdeniz University, Antalya 07350, Turkey. Department of Neurology, Sancaktepe Şehit Prof. Dr. İlhan Varank Training and Research Hospital, Istanbul 34785, Turkey.
 Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, 39120, Magdeburg, Germany. Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, 39120, Magdeburg, Germany. Center for Behavioral Brain Sciences (CBBS), 39106, Magdeburg, Germany. German Center for Neurodegenerative Diseases (DZNE), 39120, Magdeburg, Germany. Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, 39120, Magdeburg, Germany. tino.zaehle@ovgu.de. Center for Behavioral Brain Sciences (CBBS), 39106, Magdeburg, Germany. tino.zaehle@ovgu.de.
 From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. edith.graham@northwestern.edu. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA. From the Department of Neurology (E.L.G., G.P.G., C.J.B.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (J.B.B., E.S.J.), Division of Reproductive Endocrinology and Infertility, Northwestern University, Chicago, IL; UCSF Weill Institute for the Neurosciences (A.A., B.O., R.B.), Department of Neurology, University of California, San Francisco (UCSF); Division of Biostatistics (N.L.), Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; Feinberg School of Medicine (A.D.), Northwestern University, Chicago, IL; Department of Obstetrics and Gynecology (A.C.V.), Division of Reproductive Endocrinology and Infertility, Brigham and Women's Hospital, Boston, MA; UCSF Center for Reproductive Health (E.M.-L., D.H.), Mission Bay Campus, San Francisco, CA; Department of Neurology (D.J.), University of Pennsylvania, Philadelphia; and Department of Neurology (T.B.K., M.K.H.), Brigham and Women's Hospital, Boston, MA.
 Institute of Biochemistry and Genetics of Ufa Federal Research Centre, Ufa, Russia. Bashkir State Medical University, Ufa, Russia. Institute of Biochemistry and Genetics of Ufa Federal Research Centre, Ufa, Russia. Institute of Biochemistry and Genetics of Ufa Federal Research Centre, Ufa, Russia. Institute of Biochemistry and Genetics of Ufa Federal Research Centre, Ufa, Russia. Bashkir State Medical University, Ufa, Russia. Bashkir State Medical University, Ufa, Russia. Bashkir State Medical University, Ufa, Russia.
 Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Military of Education, Naval Medical University, Shanghai, 200433, China. Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Military of Education, Naval Medical University, Shanghai, 200433, China. Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Military of Education, Naval Medical University, Shanghai, 200433, China. Department of Naval Medicine, Naval Medical University, Shanghai, 200433, China. Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Military of Education, Naval Medical University, Shanghai, 200433, China. Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Military of Education, Naval Medical University, Shanghai, 200433, China. Department of Naval Medicine, Naval Medical University, Shanghai, 200433, China. Center of Hydrogen Science, Shanghai Jiao Tong University, Shanghai, 200030, China. Department of Neurosurgery, Third Affiliated Hospital, Naval Medical University, Shanghai, 200438, China. hehua1624@smmu.edu.cn. Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Military of Education, Naval Medical University, Shanghai, 200433, China. caoli@smmu.edu.cn.
 II Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Health Sciences - Section of Biostatistics University of Genoa, Italy. II Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. II Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Health Sciences - Section of Biostatistics University of Genoa, Italy. Ospedale del Mare, (ASL napoli 1), Naples, Italy. II Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. MS Centre, II Division of Neurology, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Neurology and Stroke Unit "A. Cardarelli Hospital", Naples, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University of Naples, Naples, Italy. MS Centre, II Division of Neurology, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Health Sciences - Section of Biostatistics University of Genoa, Italy. I Division of Neurology, University of Campania Luigi Vanvitelli, Naples, Italy. II Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Electronic address: simona.bonavita@unicampania.it.
 Division of Neurology, Department of Pediatrics, University of Toronto, Toronto, ON, Canada/Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada. Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada. Division of Neurology, Department of Pediatrics, University of Toronto, Toronto, ON, Canada. ShadowLab Research Inc., Toronto, ON, Canada. Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada. McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada. Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada. Division of Neurology, Department of Pediatrics, University of Toronto, Toronto, ON, Canada. Departments of Clinical Neurosciences and Surgery, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Ophthalmology and Visual Sciences, The University of Toronto, Toronto, ON, Canada. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada/Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada. McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada. Department of Diagnostic Imaging, University of Toronto, Toronto, ON, Canada. Division of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada. Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada. Division of Neurology, Department of Pediatrics, University of Toronto, Toronto, ON, Canada/Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Electronic address: suzi.claflin@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia.
 Department of Health Education, Faculty of Health, Research Committee, Arak University of Medical Sciences, StudentArak, Iran. Department of Health Education and Health Promotion, Faculty of Health, Arak University of Medical Sciences, Arak, Iran. mohsen_shamsi1360@yahoo.com. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University Of Medical Sciences, Tehran, Iran. Department of Health Education and Health Promotion, Faculty of Health, Arak University of Medical Sciences, Arak, Iran. Department of Epidemiology, Faculty of Health, Arak University of Medical Sciences, Arak, Iran.
 Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA. Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA. Mellen Center for MS Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA. Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA.
 Department of Psychology, The Pennsylvania State University, University Park, PA 16802, United States. Department of Psychology, The Pennsylvania State University, University Park, PA 16802, United States. Department of Psychology, The Pennsylvania State University, University Park, PA 16802, United States. Department of Psychiatry, Tufts University School of Medicine, Boston, MA 02111, United States. Department of Psychology, The Pennsylvania State University, University Park, PA 16802, United States.
 Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Neurology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Neurology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Radiology, Third Faculty of Medicine, Charles University, 100 34 Prague, Czech Republic. Department of Neurology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Neurology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, 121 08 Prague, Czech Republic.
 Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Department of Bioengineering, Interdisciplinary Health Science Institute, Urbana, Illinois, USA. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India. Carle Illinois Advanced Imaging Center, Carle Foundation Hospital, Urbana, Illinois, USA.
 Department of Radiology, Beijing Tiantan Hospital, Beijing, China. Department of Radiology, Beijing Tiantan Hospital, Beijing, China. Department of Radiology, Beijing Tiantan Hospital, Beijing, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, China. Department of Radiology, Huashan Hospital Fudan University, Shanghai, China. Department of Radiology, Huashan Hospital Fudan University, Shanghai, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China. Department of Radiology, The First Affiliated Hospital of Nanchang University, Nanchang, China. Department of Radiology, The First Affiliated Hospital of Nanchang University, Nanchang, China. Department of Neurology, Beijing Tiantan Hospital, Beijing, China. Department of Radiology, Beijing Tiantan Hospital, Beijing, China. Department of Radiology and Nuclear Medicine, Neuroscience Campus Amsterdam, VU University Medical Centre Amsterdam, Amsterdam, The Netherlands. Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK. Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK. Dementia Research Centre, Queen Square Institute of Neurology, University College London, London, UK. Department of Radiology, Beijing Tiantan Hospital, Beijing, China yaouliu80@163.com.
 Annie Taylor Dee School of Nursing, Weber State University, Ogden, Utah (Drs Robert, Hales Reynolds, and Rocha); and Yoga Moves MS, Franklin, Michigan (Ms Eisenberg).
 Section of Gastroenterology, Portland VA Medical Center, Portland, Oregon, USA. Division of Gastroenterology and Hepatology, Oregon Health & Science University, Portland, Oregon, USA.
 Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON, Canada. Department of Immunology, 1 King's College Circle, Toronto, ON, Canada. Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON, Canada. Department of Immunology, 1 King's College Circle, Toronto, ON, Canada. Women's College Research Institute, Women's College Hospital, Toronto, ON, Canada.
 Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Institute of Neuropathology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Department of Neurosurgery, Department of Neurology and Neurosurgery, McGill University Health Centre, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Department of Pediatric Neurosurgery, Montreal Children's Hospital, 1001 Decarie Blvd, Montreal, QC, H4A 3J1, Canada. Division of Pediatric Neurology, Montreal Children's Hospital, 1001 Decarie Blvd, Montreal, QC, H4A 3J1, Canada. Department of Neuroscience, Faculty of Medicine, Université de Montréal, Pavillon Roger- Gaudry, 2900 Edouard Montpetit Blvd, Montreal, QC, H3T 1J4, Canada. Department of Neuroscience, Faculty of Medicine, Université de Montréal, Pavillon Roger- Gaudry, 2900 Edouard Montpetit Blvd, Montreal, QC, H3T 1J4, Canada. Department of Neuroscience, Faculty of Medicine, Université de Montréal, Pavillon Roger- Gaudry, 2900 Edouard Montpetit Blvd, Montreal, QC, H3T 1J4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Department of Neurology, Mayo Clinic Foundation, 1216 2nd St SW, Rochester, MN, 55902, USA. Institute of Neuropathology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 Rue University, Montreal, QC, H3A 2B4, Canada. jack.antel@mcgill.ca.
 Berlin Ultrahigh Field Facility (B.U.F.F.), Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany. Department of Physics, Humboldt Universität zu Berlin, 12489 Berlin, Germany. Berlin Ultrahigh Field Facility (B.U.F.F.), Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany. Digital Health-Machine Learning Research Group, Digital Health Center, Hasso Plattner Institute, University of Potsdam, 14482 Potsdam, Germany. Berlin Ultrahigh Field Facility (B.U.F.F.), Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany. Experimental and Clinical Research Center, A Joint Cooperation between the Charité Medical Faculty and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Campus Berlin-Buch, 13125 Berlin, Germany. Experimental and Clinical Research Center, A Joint Cooperation between the Charité Medical Faculty and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Campus Berlin-Buch, 13125 Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin, 10117 Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin, 10117 Berlin, Germany. Experimental and Clinical Research Center, A Joint Cooperation between the Charité Medical Faculty and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Campus Berlin-Buch, 13125 Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin, 10117 Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin, 10117 Berlin, Germany. Berlin Ultrahigh Field Facility (B.U.F.F.), Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany. Experimental and Clinical Research Center, A Joint Cooperation between the Charité Medical Faculty and the Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Campus Berlin-Buch, 13125 Berlin, Germany.
 Department of Family Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea. Department of Digital Healthcare, Seoul National University Bundang Hospital, Seongnam, South Korea. Department of Neurology, College of Medicine, Gyeongsang Institute of Health Science, Gyeongsang National University, Jinju, South Korea. Department of Statistics and Actuarial Science, Soongsil University, Seoul, Korea. Department of Biostatics, The Catholic University of Korea, Seoul, South Korea. Department of Family Medicine & Supportive Care Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea. Department of Family Medicine & Supportive Care Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. dwshin.md@gmail.com. Department of Clinical Research Design and Evaluation/Department of Digital Health, Samsung Advanced Institute of Health Science and Technology (SAIHST), Sungkyunkwan University, 50 Irwon-Dong, Gangnam-Gu, Seoul, 135-710, South Korea. dwshin.md@gmail.com. Center for Wireless and Population Health Systems, University of California, San Diego, La Jolla, CA, USA. dwshin.md@gmail.com. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-Dong, Gangnam-Gu, Seoul, 135-710, South Korea. juhongm@skku.edu. Neuroscience Center, Samsung Medical Center, Seoul, South Korea. juhongm@skku.edu. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology (SAIHST), Sungkyunkwan University, Seoul, South Korea. juhongm@skku.edu.
 Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Brigham Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
 Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Department of Gastroenterology, University of Manitoba, Winnipeg, Manitoba, Canada. Clinical Health Psychology, University of Manitoba, Winnipeg, Manitoba, Canada. Community Health Sciences & Psychiatry, University of Calgary Cumming School of Medicine, Calgary, Alberta, Canada. Department of Psychiatry, University of Manitoba, Winnipeg, Manitoba, Canada. Nova Scotia Health Authority, Halifax, Nova Scotia, Canada. Departments of Psychiatry, Psychology & Neuroscience, and Medicine, Dalhousie University, Halifax, Nova Scotia, Canada. Internal Medicine, University of Manitoba College of Medicine, Winnipeg, Manitoba, Canada. Internal Medicine, University of Manitoba College of Medicine, Winnipeg, Manitoba, Canada. Internal Medicine, University of Manitoba College of Medicine, Winnipeg, Manitoba, Canada rmarrie@hsc.mb.ca.
 Department of Internal Medicine, Faculty of Medicine & Health Sciences, Stellenbosch University, Cape Town, 7500, South Africa. Division of Chemical Pathology, Department of Pathology, Faculty of Medicine & Health Sciences, Stellenbosch University, & National Health Laboratory Service (NHLS), Cape Town, 7500, South Africa. Department of Medical Imaging & Therapeutic Sciences, Faculty of Health & Wellness Sciences, Cape Peninsula University of Technology, Bellville campus, Cape Town, 7530, South Africa. Gknowmix (Pty) Ltd, Bellville, 7530, South Africa. Faculty of Health & Wellness Sciences, Cape Peninsula University of Technology, Cape Town, 7530, South Africa. Department of Statistics & Actuarial Sciences, Stellenbosch University, Private Bag X1, Matieland, 7602, South Africa. Department of Pediatrics & Child Health, Faculty of Medicine & Health Sciences, Stellenbosch University, Cape Town, 7500, South Africa. Department of Medical Imaging & Therapeutic Sciences, Faculty of Health & Wellness Sciences, Cape Peninsula University of Technology, Bellville, 7530, South Africa. Cape University Body Imaging Centre, Faculty of Human Biology, University of Cape Town, Cape Town, 7925 South Africa. Division of Chemical Pathology, Department of Pathology, Faculty of Medicine & Health Sciences, Stellenbosch University, Cape Town, 7500, South Africa. Division of Chemical Pathology, Department of Pathology, Faculty of Medicine & Health Sciences, Stellenbosch University, & National Health Laboratory Service (NHLS), Cape Town, 7500, South Africa.
 Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Hasso Plattner Institute, University of Potsdam, Potsdam, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Regional Health Research and Molecular Medicine, University of Southern Denmark, Odense, Denmark. Department of Neurology, Slagelse Hospital, Slagelse, Denmark. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Phil.Albrecht@gmail.com. Department of Neurology, Maria Hilf Clinics, Moenchengladbach, Germany. Phil.Albrecht@gmail.com.
 Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Radiology, Weill Medical College of Cornell University, New York, NY 10065, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Psychological and Brain Science Department, Johns Hopkins University, Baltimore, MD 21218, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. IRCCS Fondazione Don Carlo Gnocchi ONLUS, Milan 20148, Italy. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY 14203, United States.
 Santa Casa de São Paulo, Faculdade de Ciências Médicas, São Paulo SP, Brazil. Santa Casa de São Paulo, Faculdade de Ciências Médicas, São Paulo SP, Brazil. Universidade de São Paulo, Faculdade de Medicina, Departamento de Ginecologia, São Paulo SP, Brazil. Santa Casa de São Paulo, Faculdade de Ciências Médicas, São Paulo SP, Brazil. Santa Casa de São Paulo, Faculdade de Ciências Médicas, São Paulo SP, Brazil.
 Central Clinical School, Monash University, Melbourne, VIC, Australia/Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia. Central Clinical School, Monash University, Melbourne, VIC, Australia/Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia. Central Clinical School, Monash University, Melbourne, VIC, Australia/Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia/MS Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia. Liverpool Hospital, Sydney, NSW, Australia. Hospital Universitario Virgen Macarena, Sevilla, Spain. MS Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia/CORe, Department of Medicine, The University of Melbourne, Melbourne, VIC, Australia. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia/Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, NSW, Australia. MS Centre, Department of Neurology, The Royal Melbourne Hospital, Melbourne, VIC, Australia/Department of Neurosciences, Eastern Health Clinical School, Monash University, Box Hill Hospital, Melbourne, VIC, Australia. Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia/Department of Neurosciences, Eastern Health Clinical School, Monash University, Box Hill Hospital, Melbourne, VIC, Australia. Cliniques Universitaires Saint-Luc, UCLouvain, Brussels, Belgium. Monash Medical Centre, Melbourne, VIC, Australia. CSSS Saint-Jérôme, Saint-Jérôme, QC, Canada. CHUM and Universite de Montreal, Montreal, QC, Canada. Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Central Clinical School, Monash University, Melbourne, VIC, Australia/Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia. Central Clinical School, Monash University, Melbourne, VIC, Australia/Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia.
 Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Multiple Sclerosis Comprehensive Care Center, Holy Name Medical Center, Teaneck, NJ, USA.
 Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Orthopedics, Ahvaz Jundishapour University of Medical Sciences, Ahvaz, Iran. Medical School, Sabzevar University of Medical Sciences, Sabzevar, Iran. School of Paramedical, Gerash University of Medical Sciences, Gerash, Iran. Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. School of Paramedical, Gerash University of Medical Sciences, Gerash, Iran. Applied Biotechnology Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran. Applied Biotechnology Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran.
 Department of Pharmacy, King Saud Medical City, Riyadh, 12746, Saudi Arabia. Department of Pharmacy, King Saud Medical City, Riyadh, 12746, Saudi Arabia. Department of Neurology, King Saud Medical City, Riyadh, 12746, Saudi Arabia. Department of Clinical Pharmacy, College of Pharmacy, Umm Al-Qura University, Makkah, 24382, Saudi Arabia. Department of Medicine, Neurology Division, College of Medicine, King Saud University, P.O. Box 3145, Riyadh, 12372, Saudi Arabia. Department of Medicine, Neurology Division, College of Medicine, King Saud University, P.O. Box 3145, Riyadh, 12372, Saudi Arabia. Department of Pharmacy, King Khalid University Hospital, P.O. Box 3145, Riyadh, 12372, Saudi Arabia. Department of Clinical Pharmacy, College of Pharmacy, King Saud University, P.O. Box 2454, Riyadh, 11451, Saudi Arabia. Yazeed@ksu.edu.sa. Pharmacoeconomics Research Unit, Department of Clinical Pharmacy, College of Pharmacy, King Saud University, P.O. Box 2454, Riyadh, 11451, Saudi Arabia. Yazeed@ksu.edu.sa.
 Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/National Institute for Health Research, University College London Hospitals, Biomedical Research Centre, London, UK/Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. The Multi-Regional Clinical Trials Center of Brigham and Women's Hospital and Harvard, Cambridge, MA, USA/Harvard Medical School, Boston, MA, USA. School of Rehabilitation Therapy, Faculty of Health Sciences, Queen's University, Kingston, ON, Canada. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain/Office of Therapies for Neurological and Psychiatric Disorders, Human Medicines Division, European Medicines Agency, Amsterdam, The Netherlands. Foundation for Angelman Syndrome Therapeutics, Austin, TX, USA. Department of Health Sciences, University of Genoa, Genoa, Italy. Joi Life Wellness Group MS Center, Atlanta, GA, USA. Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
 Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands a.toorop@amsterdamumc.nl. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Department of Epidemiology and Data Science, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, The Netherlands. Landsteiner Laboratory, Amsterdam UMC Location AMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam UMC Location VUMC, Amsterdam, The Netherlands.
 Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA. Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA. Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Neurology, University of California, San Francisco, San Francisco, CA, USA. Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA. Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA.
 Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Department of Neurology, Brigham MS Center, Brigham and Women's Hospital, Boston, MA, 02115, USA. Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Department of Neurology, Brigham MS Center, Brigham and Women's Hospital, Boston, MA, 02115, USA. Department of Neurology, Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. tchitnis@rics.bwh.harvard.edu. Harvard Medical School, Boston, MA, 02115, USA. tchitnis@rics.bwh.harvard.edu. Department of Neurology, Brigham MS Center, Brigham and Women's Hospital, Boston, MA, 02115, USA. tchitnis@rics.bwh.harvard.edu.
 Department of Occupational Therapy Education, School of Health Professions, University of Kansas Medical Center, Kansas City, Kansas, USA. Mobility Core, University of Kansas Center for Community Access, Rehabilitation Research, Education and Service, Kansas City, Kansas, USA. Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, School of Health Professions, University of Kansas Medical Center, Kansas City, Kansas, USA. Neuroimmunology and Multiple Sclerosis Unit of the Neurology Division, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. Neuroimmunology and Multiple Sclerosis Unit of the Neurology Division, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. NeuroCure, Charité - Universitaetsmedizin Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitaetsmedizin Berlin, Berlin, Germany. NeuroCure, Charité - Universitaetsmedizin Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitaetsmedizin Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, School of Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA. Mobility Core, University of Kansas Center for Community Access, Rehabilitation Research, Education and Service, Kansas City, Kansas, USA. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, School of Health Professions, University of Kansas Medical Center, Kansas City, Kansas, USA. Mobility Core, University of Kansas Center for Community Access, Rehabilitation Research, Education and Service, Kansas City, Kansas, USA. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, School of Health Professions, University of Kansas Medical Center, Kansas City, Kansas, USA. Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. Department of Physical Therapy, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Rush Alzheimer's Disease Center and Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois, USA. Mobility Core, University of Kansas Center for Community Access, Rehabilitation Research, Education and Service, Kansas City, Kansas, USA. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, School of Health Professions, University of Kansas Medical Center, Kansas City, Kansas, USA.
 Department of Preventive Medicine and Public Health, Faculty of Medicine, University of Seville, Seville, Spain. Department of Preventive Medicine and Public Health, Faculty of Medicine, University of Seville, Seville, Spain. Department of Preventive Medicine and Public Health, Faculty of Medicine, University of Seville, Seville, Spain.
 Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Electronic address: viola.biberacher@tum.de. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Paul Schmidt, Statistical Consulting, Große Seestraße 8, Berlin 13086, Germany. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neuroradiology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany; Munich Cluster for Systems Neurology (SyNergy), Feodor-Lynen-Str. 17, Munich 81377, Germany. Neurology, Technische Universität München, Ismaninger Str. 22, Munich 81541, Germany.
 Department of Medical Safety, Tokyo Women's Medical University School of Medicine.
 Department of Health Sciences, University of Genoa, Genoa, Italy alessio.signori@medicina.unige.it. Neurologic Clinic and Policlinic, Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Service de Neurologie A, Hopital Neurologique, Hospices Civils de Lyon, Lyon Bron, France. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari Aldo Moro, Bari, Italy. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Biogen International, Zurich, Switzerland. Biogen International, Zurich, Switzerland. Department of Neurology, Danish Multiple Sclerosis Center, Rigshospitalet, Copenhagen, Denmark. Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Rigshospitalet, Copenhagen, Denmark. Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Monash University Central Clinical School, Melbourne, Victoria, Australia. Department of Neurology and Center of Clinical Neuroscience, Charles University in Prague, 1st Faculty of Medicine and General University Hospital in Prague, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, Charles University in Prague, 1st Faculty of Medicine and General University Hospital in Prague, Prague, Czech Republic. CHUM and Universite de Montreal, Montreal, Quebec, Canada. Neurology, Hospital Universitario Virgen Macarena, Sevilla, Spain. Neuro Rive-Sud, Quebec, Quebec, Canada. Department of Neurology, Zuyderland Medical Center, Sittard-Geleen, The Netherlands. School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Ondokuz Mayis Üniversitesi, Samsun, Turkey. Dokuz Eylul University, İzmir, Turkey. Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Monash University Central Clinical School, Melbourne, Victoria, Australia. Neurology, Cliniques Universitaires Saint-Luc, Brussels, Belgium. Neurology, Centro Hospitalar de São João, Porto, Portugal. Faculty of Health Sciences, University Fernando Pessoa, Porto, Portugal. Centre integre de sante et de services sociaux des Laurentides point de service de Saint-Jerome, Saint-Jerome, Quebec, Canada. Amiri Hospital, Kuwait City, Kuwait. UQCCR, The University of Queensland, Brisbane, Queensland, Australia. Department of Neurology, Razi Hospital, Manouba, Tunisia. Department of Neurology, Razi University Hospital, Manouba, Tunisia. Faculty of Medicine of Tunis, University of Tunis El Manar, Tunis, Tunisia. Neurology, Donostia University Hospital, San Sebastian, Spain. Neuroscience, Centre Clinical School, Monash University, Victoria, Australia. Groene Hart Ziekenhuis, Gouda, The Netherlands. Neurology, Galdakao Hospital, Vizcaya, Spain. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Department of Health Sciences, University of Genoa, Genoa, Italy. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Neuroscience, Centre Clinical School, Monash University, Victoria, Australia. Managing Director, MSBase Foundation, Melbourne, Victoria, Australia.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia; Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Illawarra Health and Medical Research Institute, Wollongong, Australia; School of Medicine, University of Wollongong, Wollongong, Australia. Curtin School of Population Health, Curtin University, Perth, Australia. Murdoch Children's Research Institute, Royal Children's Hospital, University of Melbourne, VIC, Australia; The Florey Institute of Neuroscience & Mental Health, Parkville, VIC, Australia. School of Medicine, Griffith University, Gold Coast, Australia. Department of Neurology, John Hunter Hospital, Newcastle, New South Wales, Australia; Faculty of Medicine and Public Health, Hunter Medical Research Institute, University of Newcastle, New South Wales, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Electronic address: ingrid.vanderMei@utas.edu.au.
 School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia. School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia. Centre for Health Sciences Research, The University of Queensland, Brisbane, Australia. School of Clinical Sciences, Queensland University of Technology, Brisbane, Australia. School of Allied Health Sciences, Griffith University, Gold Coast, Australia. School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia. Laboratory Movement, Interactions, Performance EA 4334, University of Nantes, Nantes, France. School of Health & Social Care, Teesside University, Middlesbrough, UK. School of Clinical Sciences, Auckland University of Technology, Auckland, New Zealand. Institute of Health Biomedical Innovation, Queensland University of Technology, Brisbane, Australia. School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia.
 Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden/Centre for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
 From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. From the Collaboration for Outcomes Research and Evaluation (A.K., E.R.L., K.D.M., L.D.L.), Faculty of Pharmaceutical Sciences, and Division of Neurology (A.T.), Department of Medicine, University of British Columbia, Vancouver; Department of Community Health Sciences (S.B.P.), University of Calgary, AB; Division of Neurology (J.O.), St. Michael's Hospital, University of Toronto; and Centre for Health Evaluation and Outcome Sciences (CHÉOS) (L.D.L.), St. Paul's Hospital, Vancouver, BC, Canada. larry.lynd@ubc.ca.
 Weill Institute for Neurosciences, University of California San Francisco (UCSF), San Francisco, CA, USA. Weill Institute for Neurosciences, University of California San Francisco (UCSF), San Francisco, CA, USA. Weill Institute for Neurosciences, University of California San Francisco (UCSF), San Francisco, CA, USA. Weill Institute for Neurosciences, University of California San Francisco (UCSF), San Francisco, CA, USA. Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Helen Diller Family Comprehensive Cancer Center, University of California San Francisco (UCSF), San Francisco, CA, USA. Weill Institute for Neurosciences, University of California San Francisco (UCSF), San Francisco, CA, USA.
 MS Center, Neurology and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University Basel, Basel, Switzerland. Massachusetts General Hospital for Children, Boston, MA, USA. Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA, USA. Hôpitaux Universitaires Paris-Sud, Paris, France. McGill University, Montréal, QC, Canada NeuroRx Research, Montréal, QC, Canada. Sanofi, Cambridge, MA, USA. Sanofi, Cambridge, MA, USA. Sanofi, Cambridge, MA, USA. Sanofi, Cambridge, MA, USA. Sanofi, Cambridge, MA, USA. MS Center, Neurology and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University Basel, Basel, Switzerland.
 Department of Neurology, Geisel School of Medicine at Dartmouth and Dartmouth Hitchcock Medical Center, Lebanon, NH 03756, USA. Integrative Neuroscience at Dartmouth, Guarini School of Graduate and Advanced Studies, Hanover, NH 03755, USA. Department of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. Department of Neurology, Geisel School of Medicine at Dartmouth and Dartmouth Hitchcock Medical Center, Lebanon, NH 03756, USA. Integrative Neuroscience at Dartmouth, Guarini School of Graduate and Advanced Studies, Hanover, NH 03755, USA. Department of Neurology, Geisel School of Medicine at Dartmouth and Dartmouth Hitchcock Medical Center, Lebanon, NH 03756, USA.
 The Blizard Institute, Centre for Neuroscience, Surgery & Trauma, Barts & The London School of Medicine & Dentistry, Queen Mary University of London, London, UK. Clinical Board Medicine (Neuroscience), The Royal London Hospital, Barts Health NHS Trust, London, UK. Department of Neurology, Institute of Translational Neurology, University of Münster, Münster, Germany. Department of Neurology, IdISSC, Hospital Universitario Clinico San Carlos, Madrid, Spain. Departamento de Medicina, Universidad Complutense de Madrid, Madrid, Spain. Laboratory of Synaptic Immunopathology, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology & Neurorehabilitation, IRCCS Neuromed, Pozzilli, Italy. Clinical Research Services, Cytel Inc., Geneva, Switzerland. Global Medical Affairs, Ares Trading S.A., Eysins, Switzerland (an affiliate of Merck KGaA). Neurology & Immunology, Ares Trading S.A., Eysins, Switzerland (an affiliate of Merck KGaA).
 Amrita School of Nanosciences and Molecular Medicine, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Amrita School of Nanosciences and Molecular Medicine, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Amrita School of Nanosciences and Molecular Medicine, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Amrita School of Nanosciences and Molecular Medicine, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Department of Neurology, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Department of Neurology, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Central Animal Laboratory, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041Kerala, India. Central Animal Laboratory, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041Kerala, India. Central Animal Laboratory, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041Kerala, India. Amrita School of Nanosciences and Molecular Medicine, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India. Amrita School of Nanosciences and Molecular Medicine, Amrita Vishwa Vidyapeetham, Ponekkara, Kochi682 041, Kerala, India.
 Department of Physical Medicine and Rehabilitation, Tehran University of Medical Sciences, Tehran, Iran. Department of Physical Medicine and Rehabilitation, Tehran University of Medical Sciences, Tehran, Iran. Department of Physical Medicine and Rehabilitation, Tehran University of Medical Sciences, Tehran, Iran. Student's Scientific Research Center, Tehran University of Medical Sciences, Tehran, Mahsa Ghajarzadeh, Iran. Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. mghajar2@jhmi.edu. Multiple Sclerosis Research Group (MSRG), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. mghajar2@jhmi.edu.
 Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
 Department of Neurology, Lithuanian University of Health Sciences Medical Academy, A. Mickevičiaus g.9, LT-44307 Kaunas, Lithuania. Department of Neurology, Lithuanian University of Health Sciences Medical Academy, A. Mickevičiaus g.9, LT-44307 Kaunas, Lithuania. Department of Neurology, Lithuanian University of Health Sciences Medical Academy, A. Mickevičiaus g.9, LT-44307 Kaunas, Lithuania. Department of Neurology, Lithuanian University of Health Sciences Medical Academy, A. Mickevičiaus g.9, LT-44307 Kaunas, Lithuania. Department of Otorhinolaringology, Lithuanian University of Health Sciences Medical Academy, A. Mickevičiaus g.9, LT-44307 Kaunas, Lithuania.
 Department of Neurology, Medical University of Graz, 8036 Graz, Austria. Department of Neurosurgery, Medical University of Graz, 8036 Graz, Austria. Otto Loewi Research Center, Department of Physiological Medicine, Medical University of Graz, 8010 Graz, Austria. Department of Neurology, Medical University of Graz, 8036 Graz, Austria. Faculty of Health, University of Applied Sciences Wiener Neustadt, Campus 1, 2700 Wiener Neustadt, Austria. Department of Neurosurgery, Medical University of Graz, 8036 Graz, Austria. Department of Clinical Neuroscience, Karolinska Institutet, 171 64 Stockholm, Sweden. Department of Neurology, Medical University of Graz, 8036 Graz, Austria. Department of Neurology, Medical University of Graz, 8036 Graz, Austria. Department of Neurology, Medical University of Graz, 8036 Graz, Austria.
 Nature Reviews Neurology, . lisa.kiani@nature.com.
 Department of Neurology, Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, United States. Multiple Sclerosis Comprehensive Care Center, University of Southern California, Los Angeles, CA, United States. Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States. Department of Neurology, University of Texas Southwestern Medical Center (UT), Dallas, TX, United States. Department of Neurology, University of Texas Southwestern Medical Center (UT), Dallas, TX, United States. Multiple Sclerosis Comprehensive Care Center, University of Southern California, Los Angeles, CA, United States. Department of Neurology, University of Chicago, Chicago, IL, United States. Department of Neurology, Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, United States. Department of Neurology, University of Texas Southwestern Medical Center (UT), Dallas, TX, United States.
 From the Department of Medical Sciences, Neurology, Uppsala University, Sweden. From the Department of Medical Sciences, Neurology, Uppsala University, Sweden. From the Department of Medical Sciences, Neurology, Uppsala University, Sweden. From the Department of Medical Sciences, Neurology, Uppsala University, Sweden. From the Department of Medical Sciences, Neurology, Uppsala University, Sweden. From the Department of Medical Sciences, Neurology, Uppsala University, Sweden. joachim.burman@neuro.uu.se.
 University of Muenster, Institute of Epidemiology and Social Medicine, Muenster, Germany. Electronic address: kris.jalusic@uni-muenster.de. MS Forschungs- und Projektentwicklungs-gGmbH, German MS Register, Hannover, Germany. MS Forschungs- und Projektentwicklungs-gGmbH, German MS Register, Hannover, Germany. University of Muenster, Institute of Epidemiology and Social Medicine, Muenster, Germany.
 Novartis Pharma AG, Lichtstrasse 35, CH-4056, Basel, Switzerland. Novartis Pharma AG, Lichtstrasse 35, CH-4056, Basel, Switzerland. Novartis Pharma AG, Lichtstrasse 35, CH-4056, Basel, Switzerland.
 Multiple Sclerosis Comprehensive Care Center, Department of Neurology, NYU Langone Health, New York, NY, USA. Pediatric Multiple Sclerosis Center, University of California San Francisco, San Francisco, CA, USA. Data Coordinating and Analysis Center, The University of Utah, Salt Lake City, UT, USA. Data Coordinating and Analysis Center, The University of Utah, Salt Lake City, UT, USA. Multiple Sclerosis Comprehensive Care Center, Department of Neurology, NYU Langone Health, New York, NY, USA. Center for Pediatric-Onset Demyelinating Disease, The University of Alabama at Birmingham, Birmingham, AL, USA. Center for Pediatric-Onset Demyelinating Disease, The University of Alabama at Birmingham, Birmingham, AL, USA. Pediatric Multiple Sclerosis Center, University of California San Diego, San Diego, CA, USA. Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital, Boston, MA, USA. Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital, Boston, MA, USA. Washington University in St. Louis, St. Louis, MO, USA. Washington University in St. Louis, St. Louis, MO, USA. Rocky Mountain Multiple Sclerosis Center, Children's Hospital Colorado, University of Colorado Denver, Aurora, CO, USA. Jacobs Pediatric Multiple Sclerosis Center, State University of New York at Buffalo, Buffalo, NY, USA. Mayo Clinic Pediatric Multiple Sclerosis Center, Mayo Clinic, Rochester, MN, USA. Mayo Clinic Pediatric Multiple Sclerosis Center, Mayo Clinic, Rochester, MN, USA. The Blue Bird Circle Clinic for Multiple Sclerosis, Texas Children's Hospital, Baylor College of Medicine, Houston, TX, USA. Pediatric Multiple Sclerosis Center, Loma Linda University Children's Hospital, Loma Linda, CA, USA. Cleveland Clinic Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. Data Coordinating and Analysis Center, The University of Utah, Salt Lake City, UT, USA. Partners Pediatric Multiple Sclerosis Center, Massachusetts General Hospital, Boston, MA, USA. Multiple Sclerosis Comprehensive Care Center, Department of Neurology, NYU Langone Health, New York, NY, USA. Multiple Sclerosis Comprehensive Care Center, Department of Neurology, NYU Langone Health, New York, NY, USA.
 Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Italy. Division of Gynecology and Obstetrics, Department of Surgical Sciences, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Italy. Clinical Metabolomics Unit, Department of Biomedical Sciences, University of Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Italy. Department of Neurosciences, ARNAS Brotzu, Cagliari, Italy. Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Clinical Metabolomics Unit, Department of Biomedical Sciences, University of Cagliari, Italy. Division of Gynecology and Obstetrics, Department of Surgical Sciences, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Italy. Electronic address: lorena.lorefice@hotmail.it.
 Recovery & Performance Laboratory, Faculty of Medicine, Leonard A Miller Centre, Memorial University of Newfoundland, Rm. 400, 100 Forest Road, St. John's, Newfoundland and Labrador A1A 1E5, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Leonard A Miller Centre, Memorial University of Newfoundland, Rm. 400, 100 Forest Road, St. John's, Newfoundland and Labrador A1A 1E5, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Leonard A Miller Centre, Memorial University of Newfoundland, Rm. 400, 100 Forest Road, St. John's, Newfoundland and Labrador A1A 1E5, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Leonard A Miller Centre, Memorial University of Newfoundland, Rm. 400, 100 Forest Road, St. John's, Newfoundland and Labrador A1A 1E5, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Leonard A Miller Centre, Memorial University of Newfoundland, Rm. 400, 100 Forest Road, St. John's, Newfoundland and Labrador A1A 1E5, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Leonard A Miller Centre, Memorial University of Newfoundland, Rm. 400, 100 Forest Road, St. John's, Newfoundland and Labrador A1A 1E5, Canada. Electronic address: Michelle.ploughman@med.mun.ca.
 Department of Health Psychology, School of Behavioral Sciences and Mental Health (Tehran Institute of Psychiatry), Iran University of Medical Sciences, Tehran, Iran. Electronic address: mojtaba66dehqan@gmail.com. Urmia University, Iran. Kharazmi University, Iran. Electronic address: hasanimehr57@yahoo.com. University of Liverpool, Liverpool, UK. Royal Holloway University of London, UK.
 Department of Physical Medicine and Rehabilitation, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA; Dean's Office, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: yumikim@uab.edu. Department of Family and Community Medicine, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Birmingham, AL, USA; Dean's Office, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Tanner Foundation for Neurological Disease, Birmingham, AL, USA. Dean's Office, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Health Behavior, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA. Dean's Office, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Health Services Administration, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA.
 Research Center for Evidence-Based Medicine, Iranian EBM Centre: A Joanna Briggs Institute (JBI) Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Talebi511@yahoo.com.
 From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. amyli8282@gmail.com. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA. From the Georgetown Multiple Sclerosis and Neuroimmunology Center (A.L.S., B.O., R.K.S.), Department of Neurology, MedStar Georgetown University Hospital, Washington, DC; Brigham Multiple Sclerosis Center (T.C.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Department of Neurosciences (J.S.G.), University of California San Diego School of Medicine, La Jolla; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Department of Pathology (I.H.S.), Brigham and Women's Hospital, Boston, MA.
 Department of Neuroradiology, Clinic of Radiology and Nuclear Medicine, University Hospital of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Division of Radiological Physics, Department of Radiology, University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Medical Image Analysis Center (MIAC) and qbig, Department of Biomedical Engineering, University Basel, Basel, Switzerland. Department of Neurology, Cantonal Hospital St. Gallen, St. Gallen, Switzerland. Department of Neurology, Cantonal Hospital Aarau, Switzerland. Department of Neurology, Cantonal Hospital St. Gallen, St. Gallen, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, EOC, Lugano, Switzerland. Department of Neurology, Cantonal Hospital Aarau, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland. Department of Clinical Neurosciences, Geneva University Hospital and Faculty of Medicine, Geneva, Switzerland. Department of Clinical Neurosciences, Geneva University Hospital and Faculty of Medicine, Geneva, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, EOC, Lugano, Switzerland. Faculty of Biomedical Sciences, University of Italian Switzerland, Lugano, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Radiology, Cantonal Hospital Aarau, Switzerland. Department of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Radiology, Geneva University Hospital and Faculty of Medicine, Geneva, Switzerland. Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland. Faculty of Biomedical Sciences, University of Italian Switzerland, Lugano, Switzerland. Department of Neuroradiology, Neurocenter of Southern Switzerland, Lugano, Switzerland. Department of Radiology, Cantonal Hospital St. Gallen, St. Gallen, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, EOC, Lugano, Switzerland. Faculty of Biomedical Sciences, University of Italian Switzerland, Lugano, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Medical Image Analysis Center (MIAC) and qbig, Department of Biomedical Engineering, University Basel, Basel, Switzerland. Advanced Clinical Imaging Technology, Siemens Healthineers International, Lausanne, Switzerland. Department of Radiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. LTS5, École Polytechnique FÉdÉrale de Lausanne (EPFL), Lausanne, Switzerland. Advanced Clinical Imaging Technology, Siemens Healthineers International, Lausanne, Switzerland. Department of Radiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. LTS5, École Polytechnique FÉdÉrale de Lausanne (EPFL), Lausanne, Switzerland. Advanced Clinical Imaging Technology, Siemens Healthineers International, Lausanne, Switzerland. Department of Radiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. LTS5, École Polytechnique FÉdÉrale de Lausanne (EPFL), Lausanne, Switzerland. Department of Neuroradiology, Clinic of Radiology and Nuclear Medicine, University Hospital of Basel, Basel, Switzerland. Department of Neuroradiology, Clinic of Radiology and Nuclear Medicine, University Hospital of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. CIBM Center for Biomedical Imaging, Radiology Department, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Switzerland, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland.
 School of Occupational Therapy, Dalhousie University, Halifax, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada.
 Institute of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy. Centro Sclerosi Multipla, Università Cattolica del Sacro Cuore, 00168 Rome, Italy. Institute of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
 Epidemiological Department, Azienda Zero, Veneto Region, Italy. Epidemiological Department, Azienda Zero, Veneto Region, Italy. Epidemiological Department, Azienda Zero, Veneto Region, Italy. Epidemiological Department, Azienda Zero, Veneto Region, Italy. Research Department of Primary Care and Population Health, University College London, London, UK.
 Department of basic health sciences, Innovation in Mental Health and Social Wellbeing Research Group (ISaMBeS), Centre for Health and Social Care Research (CESS), Universitat de Vic - Universitat Central de Catalunya, C/ Sagrada Familia, 7, Vic 08500 - Spain; Department of Health Sciences, Universitat de Vic-Universitat Central de Catalunya, Vic, Catalonia, Spain. Electronic address: Laia.briones@uvic.cat. Department of basic health sciences, Innovation in Mental Health and Social Wellbeing Research Group (ISaMBeS), Centre for Health and Social Care Research (CESS), Universitat de Vic - Universitat Central de Catalunya, C/ Sagrada Familia, 7, Vic 08500 - Spain. Global Research on Wellbeing (GRoW), Blanquerna School of Health Sciences-Ramon Llull University, Barcelona, Spain. Hospital Universitari Institut Pere Mata, Reus, Spain. Neurology Department, Consorci Hospitalari de Vic, Vic, Catalonia, Spain. Psychology Department, Health Psychology Section, Institute for Psychiatry, Psychology and Neuroscience, King's College London, London, UK. Sport and Physical Activity Research Group, Centre for Health and Social Care Research, Universitat de Vic - Universitat Central de Catalunya, Vic, Catalonia, Spain. Psychology Department, Health Psychology Section, Institute for Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
 Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan. Electronic address: yamamura@ncnp.go.jp.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, 1919 W. Taylor St, Chicago, IL, 60612, USA. robmotl@uic.edu. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, USA. Kessler Foundation, West Orange, NJ, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, 1919 W. Taylor St, Chicago, IL, 60612, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, 1919 W. Taylor St, Chicago, IL, 60612, USA.
 Department of Neurology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Generation R Study Group, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Immunology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Neurology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Generation R Study Group, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Pediatrics, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Immunology and Pathology, Central Clinical School, Monash University and Alfred Hospital, Melbourne, Victoria, Australia. Department of Child and Adolescent Psychiatry, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Radiology and Nuclear Medicine, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Generation R Study Group, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Immunology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Neurology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Immunology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Neurology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands.
 Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W. Taylor St., Chicago, IL 60612, USA. Electronic address: pxzheng@uic.edu. Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W. Taylor St., Chicago, IL 60612, USA; Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W. Taylor St., Chicago, IL 60612, USA; Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA.
 Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Laboratório de Biologia Celular e Tecidual, Universidade Estadual do Norte Fluminense Darcy Ribeiro, Campos dos Goytacazes, Brazil. Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Instituto Biomédico, Universidade Federal do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
 Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. School of Medicine, Islamic Azad Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. School of Medicine, Neyshabur University of Medical Sciences, Neyshabur, Iran.
 Department of Neurology, Barrow Neurological Institute, Phoenix, AZ, United States of America. Electronic address: michael.robers@dignityhealth.org. Department of Neurology, Keck School of Medicine of University of Southern California, Los Angeles, CA, United States of America. College of Pharmacy, University of New Mexico, Albuquerque, New Mexico. Department of First Nations Studies, University of Northern British Columbia, Prince George, British Columbia, Canada. Accelerated Cure Project, Waltham, MA, United States of America. Department of Neurology, Keck School of Medicine of University of Southern California, Los Angeles, CA, United States of America.
 CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Department of Physical Therapy and Human Movement Sciences, Northwestern University, Chicago, IL, USA. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Institute for Advanced Biomedical Technologies, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging and Clinical Sciences, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Wales Institute of Social and Economic Research and Data, Cardiff University, Cardiff, UK. Cardiff University School of Medicine, Cardiff, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Department of Psychology, University of Bath, Bath, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Department of Anaesthetics, Intensive Care and Pain Medicine, Cwm Taf Morgannwg University Health Board, Abercynon, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Cardiff University School of Medicine, Cardiff, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Institute for Advanced Biomedical Technologies, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging and Clinical Sciences, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy. MS Centre, Neurology Unit, "SS. Annunziata" University Hospital, Chieti, Italy. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Helen Durham Centre for Neuroinflammation, University Hospital of Wales, Cardiff, UK. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. Institute for Advanced Biomedical Technologies, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging and Clinical Sciences, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy.
 Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Piazza d'Armi, Cagliari 09123, Italy. Electronic address: massimiliano.pau@unica.it. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Piazza d'Armi, Cagliari 09123, Italy. IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy. Department of Pathophysiology and Transplantation, University of Milano, Milano, Italy. Multiple Sclerosis Centre, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy; Department of Pathophysiology and Transplantation, University of Milano, Milano, Italy.
 University of Health Sciences, Kartal Dr. Lutfi Kirdar City Hospital, Department of Neurology - Istanbul, Turkey. University of Health Sciences, Kartal Dr. Lutfi Kirdar City Hospital, Department of Neurology - Istanbul, Turkey. University of Health Sciences, Kartal Dr. Lutfi Kirdar City Hospital, Department of Neurology - Istanbul, Turkey. University of Health Sciences, Kartal Dr. Lutfi Kirdar City Hospital, Department of Neurology - Istanbul, Turkey.
 Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Department of Radiology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Harvard Medical School, 60 Fenwood Road, 9002 K, Boston, MA 02115, USA; Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Electronic address: tchitnis@rics.bwh.harvard.edu.
 J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, 32611, USA. Department of Anatomy and Cell Biology, College of Medicine, University of Florida, Gainesville, FL, 32610, USA. J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, 32611, USA. J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, 32611, USA. Department of Anatomy and Cell Biology, College of Medicine, University of Florida, Gainesville, FL, 32610, USA. Department of Immunology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL, 33612, USA. Electronic address: dorina.avram@moffitt.org. J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, 32611, USA; Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville FL, 32610, USA. Electronic address: bkeselowsky@bme.ufl.edu.
 Hospital Británico de Buenos Aires, Argentina. E-mail: acarra@hbritanico.com.ar. Sanatorio Allende, Córdoba, Argentina. MS-Synthon-Bagó, Buenos Aires, Argentina. MS-Synthon-Bagó, Buenos Aires, Argentina. IC-PROJECTS, Buenos Aires, Argentina. IC-PROJECTS, Buenos Aires, Argentina.
 Department of Bacteriology, Faculty of Medical Science, Tarbiat Modares University, Tehran, Iran. Department of Bacteriology, Faculty of Medical Science, Tarbiat Modares University, Tehran, Iran. Department of Clinical Biochemistry and Applied Cell Sciences, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Ahmadi.m@tbzmed.ac.ir.
 The Czech Technical University in Prague, Karlovo namesti 13, 121 35, Prague, Czech Republic. Institute of Computer Science of the Czech Academy of Sciences, Pod Vodarenskou vezi 2/271, 182 00, Prague, Czech Republic. National Institute of Mental Health, Topolova 748, 250 67, Klecany, Czech Republic. National Institute of Mental Health, Topolova 748, 250 67, Klecany, Czech Republic. Institute for Clinical and Experimental Medicine, Videnska 1958, 140 21, Prague, Czech Republic. National Institute of Mental Health, Topolova 748, 250 67, Klecany, Czech Republic. Institute for Clinical and Experimental Medicine, Videnska 1958, 140 21, Prague, Czech Republic. Institute of Computer Science of the Czech Academy of Sciences, Pod Vodarenskou vezi 2/271, 182 00, Prague, Czech Republic. National Institute of Mental Health, Topolova 748, 250 67, Klecany, Czech Republic. Institute for Clinical and Experimental Medicine, Videnska 1958, 140 21, Prague, Czech Republic. University of Nottingham, Queen's Medical Centre, NG7 2UH, Nottingham, UK. National Institute for Health Research, Nottingham Biomedical Research Centre, NG1 5DU, Nottingham, UK. Charles University, Ruska 87, 100 00, Prague, Czech Republic. Institute of Computer Science of the Czech Academy of Sciences, Pod Vodarenskou vezi 2/271, 182 00, Prague, Czech Republic. hlinka@cs.cas.cz. National Institute of Mental Health, Topolova 748, 250 67, Klecany, Czech Republic. hlinka@cs.cas.cz.
 Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China; Key Laboratory of Ocular Fundus Diseases, Chinese Academy of Medical Sciences, Beijing, 100730, China; Department of Ophthalmology, Beijing Jishuitan Hospital, Beijing, 100035, China. Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China; Key Laboratory of Ocular Fundus Diseases, Chinese Academy of Medical Sciences, Beijing, 100730, China. Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China; Key Laboratory of Ocular Fundus Diseases, Chinese Academy of Medical Sciences, Beijing, 100730, China. Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China; Key Laboratory of Ocular Fundus Diseases, Chinese Academy of Medical Sciences, Beijing, 100730, China. Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China; Key Laboratory of Ocular Fundus Diseases, Chinese Academy of Medical Sciences, Beijing, 100730, China. Electronic address: zhongy@pumch.cn.
 Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Medical Physics, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Obstetrics and Gynecology, Imam Hossein Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. smojaver@sina.tums.ac.ir. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. smojaver@sina.tums.ac.ir.
 Department of Chemistry, University of Patras, Rion Patras, Greece. Vianex S.A., Nea Erythrea, Greece. Department of Chemistry, University of Patras, Rion Patras, Greece. Department of Chemistry, University of Patras, Rion Patras, Greece.
 MS Center ErasMS, Department of Neurology, Erasmus Medical Center, Rotterdam, The Netherlands.
 Hospital Regional Universitario de Málaga, Málaga, España. Hospital Universitari Vall d'Hebron-CEMCAT, Barcelona, España. Hospital Universitario Reina Sofía, Madrid, España. Hospital Universitario de Getafe, 28905 Getafe, España. Hospital Regional Universitario de Málaga, Málaga, España. Hospital Universitario Quirónsalud, Madrid, España. Hospital Universitari Arnau de Vilanova-Universitat de Lleida, Lleida, España. Hospital Universitari Son Espases, Palma de Mallorca, España. Hospital Universitario Ramón y Cajal, Madrid, España. Hospital Universitario Virgen Macarena, 41003 Sevilla, España. Hospital Universitario Gregorio Marañón, Madrid, España. Hospital Nuestra Señora de Candelaria, Santa Cruz de Tenerife, España. Hospital Universitario Doctor Peset, Valencia, España. Complejo Hospitalario Universitario de Ferrol, Ferrol, España. Hospital Clínic de Barcelona-IDIBAPS, Barcelona, España. Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, España. Hospital Universitario de La Princesa, 28006 Madrid, España. Hospital Universitari Vall d'Hebron-CEMCAT, Barcelona, España. Hospital Sant Joan Despí Moisés Broggi, Sant Joan Despí, España. Hospital Clínico San Carlos-IDISSC-UCM, Madrid, España. Universitat de Girona, Girona, España. Hospital Universitari de Girona Dr. Josep Trueta-IDIBGI, Girona, España. Hospital de Santa Caterina, Girona, España. Hospital Clínico Universitario de Valladolid, Valladolid, España. Hospital Universitari de Bellvitge-IDIBELL, L´Hospitalet de Ll., España. Hospital Universitario Cruces, Bilbao, España.

 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA/Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA/Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA/IRCCS, Fondazione Don Carlo Gnocchi, Milan, Italy. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA/Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
 Department of Pharmacy, School of Health Sciences, Frederick University, 1036, Nicosia, Cyprus. hsc.np@frederick.ac.cy. Department of Pharmaceutical Chemistry, School of Pharmacy, Aristotle University of Thessaloniki, 54124, Thessaloniki, Greece.
 Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 040 11 Košice, Slovakia. Department of Medical and Clinical Biophysics, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 040 11 Košice, Slovakia. Department of Medical and Clinical Biophysics, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 040 11 Košice, Slovakia. Department of Biophysics, Institute of Physics, Faculty of Science, Pavol Jozef Šafárik University in Košice, Jesenná 5, 041 54 Košice, Slovakia. Department of Biophysics, Institute of Physics, Faculty of Science, Pavol Jozef Šafárik University in Košice, Jesenná 5, 041 54 Košice, Slovakia. Department of Condensed Matter Physics, Institute of Physics, Faculty of Science, Pavol Jozef Šafárik University in Košice, Park Angelinum 9, 041 54 Košice, Slovakia. Department of Magnetism, Institute of Experimental Physics, Slovak Academy of Sciences, Watsonova 47, 040 01 Košice, Slovakia. Department of Opthalmology, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 040 11 Košice, Slovakia. Department of Condensed Matter Physics, Institute of Physics, Faculty of Science, Pavol Jozef Šafárik University in Košice, Park Angelinum 9, 041 54 Košice, Slovakia. Department of Magnetism, Institute of Experimental Physics, Slovak Academy of Sciences, Watsonova 47, 040 01 Košice, Slovakia.
 Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT 06112, USA; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT 06473, USA; Department of Medical Sciences, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT 06473, USA; Department of Neurology, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA. Electronic address: elizabeth.gromisch@trinityhealthofne.org. Department of Rehabilitation Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT 06112, USA; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT 06473, USA. Department of Rehabilitation Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA; Multiple Sclerosis Center of Excellence West, Veterans Affairs, 1660 South Columbian Way, Seattle, WA 98108, USA; Rehabilitation Care Service, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA; Department of Epidemiology, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA. Department of Family Medicine, University of Connecticut Health Center, 99 Woodland Street, Hartford, CT 06105, USA; Center for Quantitative Medicine, University of Connecticut Health Center, 195 Farmington Avenue, Farmington, CT 06032, USA. Department of Computer Science and Engineering, University of Connecticut, Storrs, CT, 06269, USA. Department of Rehabilitation Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA; Multiple Sclerosis Center of Excellence West, Veterans Affairs, 1660 South Columbian Way, Seattle, WA 98108, USA; Rehabilitation Care Service, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA.
 Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Neurology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. Miguel Servet Ophthalmology Research and Innovation Group (GIMSO), Aragon Institute for Health Research (IIS Aragón), University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain.
 Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Forensic Medicine, Section of Forensic Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Forensic Medicine, Section of Forensic Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Forensic Medicine, Section of Forensic Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Forensic Medicine, Section of Forensic Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Radiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark.
 From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.). From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.). From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.) giuseppe.pontillo@unina.it. Electrical Engineering and Information Technology (G.P.). Neurosciences and Reproductive and Odontostomatological Sciences (F.F., C.C., M.M., R.L., V.B.M., M.P.), University of Naples "Federico II," Naples, Italy. Neurosciences and Reproductive and Odontostomatological Sciences (F.F., C.C., M.M., R.L., V.B.M., M.P.), University of Naples "Federico II," Naples, Italy. Neurosciences and Reproductive and Odontostomatological Sciences (F.F., C.C., M.M., R.L., V.B.M., M.P.), University of Naples "Federico II," Naples, Italy. Institute of Biostructure and Bioimaging (S.M.), National Research Council, Naples, Italy. Neurosciences and Reproductive and Odontostomatological Sciences (F.F., C.C., M.M., R.L., V.B.M., M.P.), University of Naples "Federico II," Naples, Italy. Neurosciences and Reproductive and Odontostomatological Sciences (F.F., C.C., M.M., R.L., V.B.M., M.P.), University of Naples "Federico II," Naples, Italy. Institute of Nanotechnology (G.P.), National Research Council, Lecce, Italy. Neurosciences and Reproductive and Odontostomatological Sciences (F.F., C.C., M.M., R.L., V.B.M., M.P.), University of Naples "Federico II," Naples, Italy. Department of Human Neurosciences (M.P.), Sapienza University of Rome, Rome, Italy. From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.). From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.). From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.). From the Departments of Advanced Biomedical Sciences (A.S., M.T., G.P., E.T., A.E., A.B., S.C.).
 Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. Grupo de Neuroimagen y Psicofisiología, Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Castelló, Spain. Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. Department of Psychology, The Pennsylvania State University, University Park, PA, USA. Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain.
 Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Department of Hematology, School of Medicine, Tarbiat Modares University (TMU), Tehran, Iran. Department of Internal Medicine, Imam Hossein Hospital, School of Medicine Shahid Beheshti University of Medical Science, Tehran, Iran. Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Islamic Azad University, Tehran Medical Branch, Tehran, Iran. Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: s.parkhideh@sbmu.ac.ir. Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: elham.roshandel@gmail.com.
 CRC-SEP, Department of Neurology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France. CRC-SEP, Department of Neurology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France; Infinity, INSERM UMR1291 - CNRS UMR5051, University Toulouse III, Toulouse Cedex 3, F-31024, France. CRC-SEP, Department of Neurology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France. CRC-SEP, Department of Neurology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France. CRC-SEP, Department of Neurology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France. Laboratory of Immunology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France; Infinity, INSERM UMR1251, University Toulouse III, Toulouse Cedex 3, F-31024, France. CRC-SEP, Department of Neurology, University Hospital of Toulouse, Toulouse Cedex 9, F-31059, France; Infinity, INSERM UMR1291 - CNRS UMR5051, University Toulouse III, Toulouse Cedex 3, F-31024, France. Electronic address: ciron.j@chu-toulouse.fr.
 Division of Medical Physics in Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Faculty of Medicine, Heidelberg University, Heidelberg, Germany. Division Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Division of Medical Physics in Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Division Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Division of Medical Physics in Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Faculty of Medicine, Heidelberg University, Heidelberg, Germany. Faculty of Physics and Astronomy, Heidelberg University, Heidelberg, Germany. Division Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
 Value & Evidence, EVERSANA™, Burlington, Ontario, Canada. Value & Evidence, EVERSANA™, Burlington, Ontario, Canada. Value & Evidence, EVERSANA™, Burlington, Ontario, Canada. Novartis Healthcare Private Limited, Hyderabad, India. Novartis Corporate Center Dublin, Dublin, Ireland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Department of Neurology, University Hospital Münster, Westfälische-Wilhelms-University Münster, Münster, Germany. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland.
 Department of Physical Therapy, University of Alabama at Birmingham, 3810 Ridgeway Drive, Birmingham, AL 35209, USA; University of North Texas, Department of Kinesiology, Health Promotion, and Recreation, 35209, United States. Electronic address: stephanie.silveira@unt.edu. Craig Neurorehabilitation and Research Hospital, 3425 S. Clarkson St., Englewood, CO, 80113, USA. Electronic address: KFroehlich-Grobe@Craighospital.org. Department of Physical Therapy, University of Alabama at Birmingham, 3810 Ridgeway Drive, Birmingham, AL 35209, USA. Electronic address: robmotl@uic.edu.
 Hôpital La Pitié- Salpêtrière, service de neurologie, Paris, France. CRC-SEP Paris. Centre des maladies inflammatoires rares du cerveau et de la moelle de l'enfant et de l'adulte (Mircem). Hôpital La Pitié- Salpêtrière, service de neurologie, Paris, France. CRC-SEP Paris. Centre des maladies inflammatoires rares du cerveau et de la moelle de l'enfant et de l'adulte (Mircem). Hôpital La Pitié- Salpêtrière, service de neurologie, Paris, France. CRC-SEP Paris. Centre des maladies inflammatoires rares du cerveau et de la moelle de l'enfant et de l'adulte (Mircem).
 Janssen-Cilag Spain, Part of Janssen Pharmaceutical Companies, Madrid, Spain. Janssen-Cilag Italy, Part of Janssen Pharmaceutical Companies, Cologno Monzese, Italy. SGS Exprimo NV, Mechelen, Belgium. Actelion Pharmaceuticals Ltd, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Janssen-Cilag Spain, Part of Janssen Pharmaceutical Companies, Madrid, Spain.
 Clinica Neurologica, Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy/Department of NEUROFARBA, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy.
 Department of Psychological and Brain Sciences, Drexel University, Philadelphia, Pennsylvania, USA. Department of Psychological and Brain Sciences, Drexel University, Philadelphia, Pennsylvania, USA. Department of Psychological and Brain Sciences, Drexel University, Philadelphia, Pennsylvania, USA. Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Psychological and Brain Sciences, Drexel University, Philadelphia, Pennsylvania, USA. Department of Psychological and Brain Sciences, Drexel University, Philadelphia, Pennsylvania, USA. Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
 Department of Neurology, Kokura Memorial Hospital. Shiraishi Internal Medicine Clinic. Department of Neurosurgery, Kokura Memorial Hospital. Department of Neurology, Kokura Memorial Hospital. Department of Pathology, Kokura Memorial Hospital. Department of Neurosurgery, Kokura Memorial Hospital. Department of Neurology, Kokura Memorial Hospital.
 Department of Neurology, Hannover Medical School, Hannover 30625, Germany. Department of Neurology, Hannover Medical School, Hannover 30625, Germany. Department of Ophthalmology, Hannover Medical School, Hannover 30625, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Hannover Medical School, Hannover 30625, Germany. Electronic address: skripuletz.thomas@mh-hannover.de.
 Life and Health Sciences Research Institute, School of Medicine, University of Minho, 4710-057 Braga, Portugal. ICVS/3B's, PT Government Associate Laboratory, 4710-057 Braga, Portugal. Life and Health Sciences Research Institute, School of Medicine, University of Minho, 4710-057 Braga, Portugal. ICVS/3B's, PT Government Associate Laboratory, 4710-057 Braga, Portugal. Life and Health Sciences Research Institute, School of Medicine, University of Minho, 4710-057 Braga, Portugal. ICVS/3B's, PT Government Associate Laboratory, 4710-057 Braga, Portugal. Division of Infectious Diseases, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institutet, 17176 Stockholm, Sweden. Porto University Hospital Center, 4099-001 Porto, Portugal. Porto University Hospital Center, 4099-001 Porto, Portugal. Multidisciplinary Unit for Biomedical Research (UMIB)-ICBAS, University of Porto, 4050-346 Porto, Portugal. University Hospital Complex of Vigo, 36312 Vigo, Spain. Álvaro Cunqueiro Hospital, 36312 Vigo, Spain. Life and Health Sciences Research Institute, School of Medicine, University of Minho, 4710-057 Braga, Portugal. ICVS/3B's, PT Government Associate Laboratory, 4710-057 Braga, Portugal. Hospital of Braga, 4710-243 Braga, Portugal. Clinical Academic Centre, Hospital of Braga, 4710-243 Braga, Portugal. Life and Health Sciences Research Institute, School of Medicine, University of Minho, 4710-057 Braga, Portugal. ICVS/3B's, PT Government Associate Laboratory, 4710-057 Braga, Portugal. Division of Infectious Diseases, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institutet, 17176 Stockholm, Sweden. Life and Health Sciences Research Institute, School of Medicine, University of Minho, 4710-057 Braga, Portugal. ICVS/3B's, PT Government Associate Laboratory, 4710-057 Braga, Portugal.
 Neurología, Fundación Cardio Infantil Instituto de Cardiología, Universidad del Rosario, Bogotá, Colombia. Electronic address: marigaviria8@hotmail.com. Neurología y Epidemiología, Fundación Cardio Infantil Instituto de Cardiología, Bogotá, Colombia. Neurología, Universidad del Rosario, Bogotá, Colombia. Neurología, Universidad del Rosario, Bogotá, Colombia. Grupo de investigación en Neurociencias (NEUROS), Universidad del Rosario, Bogotá, Colombia. Epidemiología, Fundación Cardio Infantil Instituto de Cardiología, Bogotá, Colombia.
 University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Department of Neurology, Izmir, Turkey. Izmir Katip Celebi University, Ataturk Education and Research Hospital, Department of Radiology, Izmir, Turkey. University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Department of Neurology, Izmir, Turkey. University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Department of Radiology, Izmir, Turkey. Izmir Katip Celebi University, Department of Biostatistics, Izmir, Turkey.
 Department of Neurology, Heinrich-Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Department of Neurology, Heinrich-Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Department of Neurology, Heinrich-Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Department of Neurology, Maria Hilf Clinic, Moenchengladbach, Germany. Department of Neurology, Heinrich-Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Department of Neurology, Heinrich-Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Department of Neurology, Palacky University in Olomouc, Olomouc, Czechia. Department of Neurology, Barzilai Medical Center, Ashkelon, Israel. Department of Neurology, Heinrich-Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany. Department of Neurology, Palacky University in Olomouc, Olomouc, Czechia. Brain and Mind Center, Medical Faculty, The University of Sydney, Sydney, NSW, Australia.
 Diagnostic Services Laboratory, Hellenic Pasteur Institute, Athens, Greece. Diagnostic Services Laboratory, Hellenic Pasteur Institute, Athens, Greece. Diagnostic Services Laboratory, Hellenic Pasteur Institute, Athens, Greece mentisaf@gmail.com. University Research Institute of Maternal and Child Health and Precision Medicine, National and Kapodistrian University of Athens, Athens, Greece. University Research Institute of Maternal and Child Health and Precision Medicine, National and Kapodistrian University of Athens, Athens, Greece.
 Pirogov National Medical Research University, Moscow, Russia. Federal Center for Brain Research and Neurotechnologies, Moscow, Russia. Kuvatov Republican Clinical Hospital, Ufa, Russia. Federal Center for Brain Research and Neurotechnologies, Moscow, Russia. Center for Cardiology and Neurology, Kirov, Russia. Leningrad Regional Clinical Hospital, St. Petersburg, Russia. Regional Clinical Hospital, Novosibirsk, Russia. Semashko Regional Clinical Hospital, Nizhny Novgorod, Russia. Seredavin Regional Clinical Hospital, Samara, Russia. Medical and Sanitary Unit «Neftyanik», Tyumen, Russia. Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russia. Filatov Moscow City Clinical Hospital No. 15, Moscow, Russia. Republican Clinical Neurological Center, Kazan, Russia. Rostov State Medical University, Rostov-on-Don, Russia. Research Center of Neurology, Moscow, Russia. JSC «BIOCAD», St. Petersburg, Russia. JSC «BIOCAD», St. Petersburg, Russia. JSC «BIOCAD», St. Petersburg, Russia. JSC «BIOCAD», St. Petersburg, Russia. JSC «BIOCAD», St. Petersburg, Russia.
 LaRiCE lab: Gait and Balance Disorders Laboratory, Department of Neurorehabilitation, IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy. LaRiCE lab: Gait and Balance Disorders Laboratory, Department of Neurorehabilitation, IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy. Electronic address: egervasoni@dongnocchi.it. LaRiCE lab: Gait and Balance Disorders Laboratory, Department of Neurorehabilitation, IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy. Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics and Maternal Child Health, University f Genova, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics and Maternal Child Health, University f Genova, Genova, Italy. LaRiCE lab: Gait and Balance Disorders Laboratory, Department of Neurorehabilitation, IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy. Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics and Maternal Child Health, University f Genova, Genova, Italy. Multiple Sclerosis Center, Neurology Unit S. Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152 Rome, Italy. LaRiCE lab: Gait and Balance Disorders Laboratory, Department of Neurorehabilitation, IRCSS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, Milano 20148, Italy; Department of Physiopathology and Transplants, University of Milan, Milan 20100, Italy.
 American International School Hong Kong, Kowloon Tong, Hong Kong, SAR PR China. Department of Infectious Diseases and Public Health, City University of Hong Kong, Kowloon Tong, Hong Kong, SAR PR China.
 Department of Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. Electronic address: barbara.serafini@iss.it. Department of Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. Electronic address: barbara.rosicarelli@iss.it. Department of Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. Electronic address: caterina.veroni@iss.it. Department of Neuroscience, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. Electronic address: francesca.aloisi@iss.it.
 Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany. Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany. NeuroPoint Patientenakademie, Ulm, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany. Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany. Department of Neurology, Medical Faculty, University of Augsburg, Augsburg, Germany.
 Center for Neuropsychology and Neuroscience Research, Kessler Foundation, 1199 Pleasant Valley Way, West Orange, NJ 07052, USA. Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ 07103, USA. Center for Neuropsychology and Neuroscience Research, Kessler Foundation, 1199 Pleasant Valley Way, West Orange, NJ 07052, USA. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL 60607, USA.
 Postgraduate School, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Neuroimmunology Department, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Postgraduate School, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. B' Neurology Department, School of Medicine, National and Kapodistrian University of Athens, "Attikon" Univeristy Hospital, 10676 Athens, Greece. Tzartos NeuroDiagnostics, 3, Eslin Street, 11523 Athens, Greece. Tzartos NeuroDiagnostics, 3, Eslin Street, 11523 Athens, Greece. Tzartos NeuroDiagnostics, 3, Eslin Street, 11523 Athens, Greece. Clinical Sciences, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Clinical Sciences, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Postgraduate School, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Postgraduate School, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Neuroimmunology Department, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Postgraduate School, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus. Neuroimmunology Department, The Cyprus Institute of Neurology and Genetics, Nicosia 2371, Cyprus.
 Department of Neurology, Neuroimmunology Laboratory, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Neuroimmunology Laboratory, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Neuroimmunology Laboratory, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Neuroimmunology Laboratory, Medical University of Innsbruck, Innsbruck, Austria. Department of Statistics, Faculty of Economics and Statistics, University of Innsbruck, Innsbruck, Austria. Department of Neurology, Neuroimmunology Laboratory, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Neuroimmunology Laboratory, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: harald.hegen@i-med.ac.at.
 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; St. George's Hospital Medical School, University of London, London, United Kingdom; Arrow project for medical research education, Sheba Medical Center, Ramat-Gan, Israel. Electronic address: EitanGershon.Shavit@sheba.health.gov.il. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Electronic address: Shay.Menascu@sheba.health.gov.il. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Electronic address: Anat.Achiron@sheba.health.gov.il. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Electronic address: Michael.Gurevich@sheba.health.gov.il.
 Institute of Physiology I, Westfälische Wilhelms-Universität, Robert-Koch-Str. 27a, D-48149 Münster, Germany. Department of Neurology with Institute of Translational Neurology, D-48149 Münster, Germany. Institute of Physiology I, Westfälische Wilhelms-Universität, Robert-Koch-Str. 27a, D-48149 Münster, Germany.
 From the Neurologic Clinic and Polyclinic (J.M., C.G.), Translational Imaging in Neurology (ThINk) and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital and University of Basel, Switzerland; and MS Center Amsterdam (S.N., M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Location VUmc, the Netherlands. From the Neurologic Clinic and Polyclinic (J.M., C.G.), Translational Imaging in Neurology (ThINk) and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital and University of Basel, Switzerland; and MS Center Amsterdam (S.N., M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Location VUmc, the Netherlands. From the Neurologic Clinic and Polyclinic (J.M., C.G.), Translational Imaging in Neurology (ThINk) and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital and University of Basel, Switzerland; and MS Center Amsterdam (S.N., M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Location VUmc, the Netherlands. From the Neurologic Clinic and Polyclinic (J.M., C.G.), Translational Imaging in Neurology (ThINk) and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital and University of Basel, Switzerland; and MS Center Amsterdam (S.N., M.M.S.), Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Location VUmc, the Netherlands. m.schoonheim@amsterdamumc.nl.
 Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, UK. Universitat Oberta de Catalunya, Barcelona, Spain. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Comprehensive Clinical Trials Unit, Institute of Clinical Trials and Methodology, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK. Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, UK. Department of Radiology & Nuclear Medicine, VU University Medical Centre, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. National Institute for Health Research, Biomedical Research Centre, University College London Hospitals, London, UK.
 From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA. elliot.frohman@austin.utexas.edu. From the Mellen Center for Multiple Sclerosis Treatment and Research (C.G.), Cleveland Clinic, OH; Departments of Neurology (S.L.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.L.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Quest Diagnostics (A.H., M.K.R.), Secaucus, NJ; Department of Microbial Infection and Immunity (A.E.L.-R.), Department of Neuroscience Ohio State University Wexner Medical Center, Columbus; Department of Neurology (R.C.), Doctors Hospital at Renaissance; Department of Neurology (R.C.), University of Texas Rio Grande Valley; Division of Microbiology and Immunology (M.S.P.), Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA; Department of Neurology (N.S., L.S.), Stanford University School of Medicine, Palo Alto, CA; Department of Neurology and Program in Immunology (S.S.Z.), University of California San Francisco; and Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA.
 Hospital de Santa Maria. Centro hospitalario Lisboa Norte, Lisboa, Portugal. Hospital de Santa Maria. Centro hospitalario Lisboa Norte, Lisboa, Portugal. Universidade do Algarve, Algarve, Portugal.

 Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Cedars-Sinai Medical Center, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. Division of Immunology & Rheumatology, Stanford University, Palo Alto, CA, USA. Global Clinical Development, Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA. Global Clinical Development, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. ECD-Early Clinical Development, Pfizer, Cambridge, Massachusetts, USA. Biostatistics, Merck Healthcare KGaA, Darmstadt, Germany. EMD Serono Inc., Billerica, MA, USA, a healthcare business of Merck KGaA. Global Patient Safety, Merck Healthcare KGaA, Darmstadt, Germany.
 Department of Nephrology, National Hospital Organization Higashihiroshima Medical Center, Higashi-Hiroshima, Japan. t.irifuku@gmail.com. Department of Nephrology, National Hospital Organization Higashihiroshima Medical Center, Higashi-Hiroshima, Japan. Department of Diagnostic Pathology, Otsu City Hospital, Otsu, Japan. Department of Nephrology, Hiroshima University Hospital, Hiroshima, Japan.
 London School of Hygiene and Tropical Medicine, London, UK. victorgitman@yahoo.com. Department of Medicine, McMaster University, Hamilton, Canada. Centre for Mathematical Modelling of Infectious Diseases, London School of Hygiene and Tropical Medicine, London, UK.
 Neurology Clinic, University Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Neurology Clinic, University Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. drulovicjelena@gmail.com.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London (QMUL), London, UK. Department of Women's Health, The Royal London Hospital, Barts Health NHS Trust, London, UK. Department of Neurology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield Institute for Translational Neuroscience (SITraN), Sheffield, UK. Evelina Women's and Children's Team, King's College London, London, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, UK / Department of Neurology, Forth Valley Royal Hospital, Larbert, UK. Department of Neurology, Belfast Health and Social Care Trust, Belfast, UK. Department of Neurology, Leeds Teaching Hospitals NHS Trust, Leeds, UK / School of Medicine, University of Leeds, Leeds, UK. Department of Neurology, Morriston Hospital, Swansea, UK. Department of Neurology, St. George's Hospital NHS Foundation Trust, London, UK. Department of Neurology, Forth Valley Royal Hospital, Larbert, UK. Department of Neurology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield Institute for Translational Neuroscience (SITraN), Sheffield, UK. UK MS Register, Swansea University, Swansea, UK. UK MS Register, Swansea University, Swansea, UK. Department of Neurology, King's College Hospital NHS Foundation Trust, London, UK. Manchester Centre for Clinical Neurosciences, Salford Royal NHS Foundation Trust, Salford, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London (QMUL), London, UK / Department of Neurology, The Royal London Hospital, Barts Health NHS Trust, London, UK.
 Department of Electrical Engineering and Automation, Aalto University, Espoo, Finland. Department of Neuroscience and Biomedical Engineering, Aalto University, Espoo, Finland. Pattern Analysis and Computer Vision, Istituto Italiano di Tecnologia, Genova, Italy. Center for Autism Research, Kessler Foundation, East Hanover, New Jersey, USA. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Pattern Analysis and Computer Vision, Istituto Italiano di Tecnologia, Genova, Italy. Dipartimento di Informatica, University of Verona, Verona, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita Salute San Raffaele University, Milan, Italy. Pattern Analysis and Computer Vision, Istituto Italiano di Tecnologia, Genova, Italy. Dipartimento di Informatica, University of Verona, Verona, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita Salute San Raffaele University, Milan, Italy. Pattern Analysis and Computer Vision, Istituto Italiano di Tecnologia, Genova, Italy. Data Science for Health, Center for Digital Health and Wellbeing, Fondazione Bruno Kessler, Trento, Italy.
 Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China. Department of Endocrinology, Jilin Province People's Hospital, Changchun, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China.
 Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis 1007, Tunisia; Research laboratory LR12SP01, Charles Nicolle Hospital, Tunis 1006, Tunisia. Electronic address: jamoussihela@gmail.com. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis 1007, Tunisia; Research laboratory LR12SP01, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis 1007, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis 1007, Tunisia; Research laboratory LR12SP01, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis 1007, Tunisia; Research laboratory LR12SP01, Charles Nicolle Hospital, Tunis 1006, Tunisia. Department of neurology, Charles Nicolle Hospital, Tunis 1006, Tunisia; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis 1007, Tunisia; Research laboratory LR12SP01, Charles Nicolle Hospital, Tunis 1006, Tunisia.
 Hospital Clínico San Carlos, Neurology Department, C/ Prof Martín Lagos, 28040 Madrid, Spain. HEALTH VALUE, HE Department, C/ Virgen de Aránzazu, 21, 28034 Madrid, Spain. Merck, SLU, C/ María de Molina, 40, 28006 Madrid, Spain, an affiliate of Merck KGaA. HEALTH VALUE, HE Department, C/ Virgen de Aránzazu, 21, 28034 Madrid, Spain. Merck, SLU, C/ María de Molina, 40, 28006 Madrid, Spain, an affiliate of Merck KGaA. Merck, SLU, C/ María de Molina, 40, 28006 Madrid, Spain, an affiliate of Merck KGaA. Merck, SLU, C/ María de Molina, 40, 28006 Madrid, Spain, an affiliate of Merck KGaA.
 Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden korinna.karampampa@ki.se. Institute of Health and Care Sciences, University of Gothenburg, Goteborg, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
 Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, QLD, 4072, Australia. d.craik@imb.uq.edu.au.
 Department of Neurology, University Medical Center, Göttingen, Germany. Department of Translational Neuroinflammation and Automated Microscopy, Fraunhofer Institute for Translational Medicine and Pharmacology, Göttingen, Germany. Department of Translational Neuroinflammation and Automated Microscopy, Fraunhofer Institute for Translational Medicine and Pharmacology, Göttingen, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Department of Neurology, University Medical Center, Göttingen, Germany. Department of Translational Neuroinflammation and Automated Microscopy, Fraunhofer Institute for Translational Medicine and Pharmacology, Göttingen, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany.
 From the Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St, Buffalo, NY 14203; and Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY. From the Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St, Buffalo, NY 14203; and Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY.
 From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. From the Department of Neuroinflammation (R.C., F.P.C., C.T., A.B., W.B., F.D.A., I.D.L.P., F.G., L.H., L.M., A.T., M.Y., A.T.T., Y.H.R.C.P.C.H., F.B., O.C.), Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London; Department of Medicine (R.C.), Surgery and Neuroscience, University of Siena, Italy; Department of Medical Physics and Biomedical Engineering (F.P.C., B.K., F.B.), Centre for Medical Imaging Computing, University College of London; Universitat Oberta de Catalunya (F.P.C.), Barcelona, Spain; MS Centre of Catalonia (Cemcat) (C.T.), Vall d'Hebron Institute of Research, Spain; Radiomics Group (F.G.), Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Barcelona, Spain; Department of Biomedical Imaging and Image Guided Therapy (L.H.), Medical University of Vienna, Austria; NMO Clinical Service at the Walton Centre (A.J.), Liverpool, United Kingdom; Division of Multiple Sclerosis and Autoimmune Neurology (A.J.), Neurological Institute, Cleveland Clinic Abu Dhabi, United Arab Emirates; Division of Brain Sciences (R.S.N.), Department of Medicine, Imperial College London; National Institute for Health Research (NIHR) (A.T., F.B., O.C.), University College London Hospitals (UCLH), Biomedical Research Centre; and Department of Radiology and Nuclear Medicine (F.B.), Amsterdam University Medical Centre, the Netherlands. o.ciccarelli@ucl.ac.uk.
 Neurocast B.V., Amsterdam, The Netherlands. Neurocast B.V., Amsterdam, The Netherlands. giovanni@neurocast.nl. Neurocast B.V., Amsterdam, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, 635 Barnhill Dr, Indianapolis, IN, 46202, USA. Department of Microbiology and Immunology, Indiana University School of Medicine, 635 Barnhill Dr, MS420, Indianapolis, IN, 46202, USA.
 From the Unit of Diagnostic Imaging and Interventional Radiology, Fondazione Policlinico Campus Bio-Medico di Roma. From the Unit of Diagnostic Imaging and Interventional Radiology, Fondazione Policlinico Campus Bio-Medico di Roma. From the Unit of Diagnostic Imaging and Interventional Radiology, Fondazione Policlinico Campus Bio-Medico di Roma. Unit of Neurology, Policlinico Tor Vergata. Unit of Neurology, Policlinico Tor Vergata. Units of Dermatology. Pathology, Fondazione Policlinico Universitario Campus Bio-Medico di Roma, Rome, Italy. Unit of Neurology, Policlinico Tor Vergata. From the Unit of Diagnostic Imaging and Interventional Radiology, Fondazione Policlinico Campus Bio-Medico di Roma.
 From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. steffen.pfeuffer@neuro.med.uni-giessen.de. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. From the Department of Neurology (S.P.), University Hospital Giessen and Marburg, Justus-Liebig-University Giessen; Department of Neurology (L.R., J.I., M.K., S.R., T.R., S.S., A.G.W., O.A., H.-P.H., S.G.M.), University Hospital Duesseldorf, Germany; Brain and Mind Center (H.-P.H.), University of Sydney, NSW, Australia; Department of Neurology (H.-P.H.), Palacky University, Olomouc, Czech Republic; Department of Neurology (H.-P.H.), Medical University of Vienna, Austria; Department of Neurology and Centre for Translational Neuro- and Behavioural Sciences (C-TNBS) (R.P., K.K., C.K.), University Hospital Essen, Germany; and Neurologic Clinic and Policlinic (L.K.), Departments of Medicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland.
 Multiple Sclerosis Unit, Department of Neurosciences, Hospital Universitari Germans Trias i Pujol-IGTP, 08916 Badalona, Spain. Department of Immunology, Hospital Universitari Germans Trias i Pujol-IGTP, Universitat Autònoma de Barcelona, 08916 Badalona, Spain. Multiple Sclerosis Unit, Department of Neurosciences, Hospital Universitari Germans Trias i Pujol-IGTP, 08916 Badalona, Spain. Multiple Sclerosis Unit, Department of Neurosciences, Hospital Universitari Germans Trias i Pujol-IGTP, 08916 Badalona, Spain.
 IRCCS Neuromed, Pozzilli (IS), Pozzilli 86077, Italy; Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy; Multiple Sclerosis Center, S. Andrea Hospital, Department of Neurology and Psychiatry, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. IRCCS Neuromed, Pozzilli (IS), Pozzilli 86077, Italy; Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy; Multiple Sclerosis Center, S. Andrea Hospital, Department of Neurology and Psychiatry, Sapienza University of Rome, Rome 00185, Italy. IRCCS Neuromed, Pozzilli (IS), Pozzilli 86077, Italy; Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. IRCCS Neuromed, Pozzilli (IS), Pozzilli 86077, Italy; Department of Human Neurosciences, Sapienza University of Rome, Rome 00185, Italy. Electronic address: antonella.conte@uniroma1.it.
 Department of Nutrition and Dietetics, Faculty of Health Sciences, Ondokuz Mayıs University, Samsun, Turkey. Department of Neurology, Faculty of Medicine, Ondokuz Mayıs University, Samsun, Turkey. Department of Nutrition and Dietetics, Faculty of Health Sciences, Ondokuz Mayıs University, Samsun, Turkey. Department of Neurology, Faculty of Medicine, Ondokuz Mayıs University, Samsun, Turkey.
 Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Electronic address: kharr133@jhmi.edu. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Biostatistics, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri; Department of Radiology, Washington University in St. Louis School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University in St. Louis School of Medicine, St. Louis, Missouri.
 Department of Psychiatry, Wroclaw Medical University, Wroclaw, Poland. Department of Psychiatry, Pomeranian Medical University, Szczecin, Poland. Department of Psychiatry, Wroclaw Medical University, Wroclaw, Poland. Department of Psychiatry and Psychotherapy, LVR-Klinikum Düsseldorf, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. WHO Collaborating Centre on Quality Assurance and Empowerment in Mental Health, DEU-131, Düsseldorf, Germany. Department of Neurology, Inselspital, Bern University Hospital, University Bern, Switzerland. Interdisciplinary Sleep-Wake-Epilepsy-Center, Inselspital, Bern University Hospital, University Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University Bern, Switzerland. Université Paris Cité, INSERM, U1266 (Institute of Psychiatry and Neuroscience of Paris), Paris, France. CMME, GHU Paris Psychiatrie et Neurosciences, Hôpital Sainte-Anne, Paris, France. Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Madrid, Spain. Department of Psychiatry, Institute of Psychiatric Phenomics and Genomics, University Hospital, Ludwig Maximilian University, Munich, Germany. Collaborative Antwerp Psychiatric Research Institute, University of Antwerp, B-2610Antwerp, Belgium. Multiversum Psychiatric Hospital, B-2530Boechout, Belgium. Unit of Clinical Psychiatry, Department of Clinical Neurosciences/DIMSC, Polytechnic University of Marche, 60126Ancona, Italy. Department of Psychiatry, Medical University of Warsaw, Warsaw, Poland. Department of Psychiatry, St. Janos Hospital, Budapest, Hungary. President of GAMIAN-Europe, Ixelles, Belgium. European Federation of Associations of Families of People with Mental Illness (EUFAMI), Leuven, Belgium. Century House, Wargrave Road, Henley-on-Thames, OxfordshireRG9 2LT, UK. Department of Psychiatry, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Nussbaumstraße 7, 80336Munich, Germany.
 Institute of Computer Vision and Robotics, University of Girona, Spain. Electronic address: albert.clerigues@udg.edu. Tensor Medical, Girona, Spain. Institute of Computer Vision and Robotics, University of Girona, Spain. Institute of Computer Vision and Robotics, University of Girona, Spain. Institute of Computer Vision and Robotics, University of Girona, Spain.
 Laboratorio de Biomédica-Mecatrónica, Subdirección de Investigación y Extensión, Centro de Enseñanza Técnica Industrial Plantel Colomos, Guadalajara 44638, Mexico. Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara 44340, Mexico. Laboratorio C. de Neuronutrición y Memoria, Departamento de Promoción, Preservación y Desarrollo de la Salud, Centro Universitario del Sur, Universidad de Guadalajara, Ciudad Guzmán 49000, Mexico. Departamento de Neurociencias, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara 44340, Mexico. Departamento de Fisiología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara 44340, Mexico. Departamento de Clínicas de la Reproducción Humana, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara 44340, Mexico. Programa de Bacteriología, Facultad de Ciencias de la Salud, Universidad Católica de Manizales, Manizales 170002, Colombia. Departamento de Clínicas Médicas, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara 44340, Mexico. Coordinación de Investigación, Instituto Jalisciense de Cancerología, Guadalajara 44280, Mexico.
 Laboratorio de Neuroinmunobiología Molecular, Instituto de Investigación en Ciencias Biomédicas (IICB), Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara, Guadalajara 44340, Mexico. Unidad Médica de Alta Especialidad (UMAE), Hospital de Especialidades (HE), Centro Médico Nacional de Occidente (CMNO), IMSS, Guadalajara 44340, Mexico. Pharmacology Section, Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institute of Neuroscience, Universitat de Barcelona, 08028 Barcelona, Spain. CiberNed, Network Center for Neurodegenerative Diseases, National Spanish Health Institute Carlos III, 28220 Madrid, Spain. Pharmacology Section, Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institute of Neuroscience, Universitat de Barcelona, 08028 Barcelona, Spain. CiberNed, Network Center for Neurodegenerative Diseases, National Spanish Health Institute Carlos III, 28220 Madrid, Spain. Laboratorio de Psicoinmunología, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Mexico City 14370, Mexico. Banco de Sangre Central, Unidad Médica de Alta Especialidad (UMAE), Hospital de Especialidades (HE), Centro Médico Nacional de Occidente (CMNO), IMSS, Guadalajara 44340, Mexico. Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingenierías (CUCEI), Universidad de Guadalajara, Guadalajara 44340, Mexico. Laboratorio de Neuroinmunobiología Molecular, Instituto de Investigación en Ciencias Biomédicas (IICB), Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara, Guadalajara 44340, Mexico.
 Kahramanmaras Sutcu Imam University, Faculty of Health Science, Department of Physiotherapy and Rehabilitation, Kahramanmaraş, Turkey. Electronic address: ikirmaci@sanko.edu.tr. Kahramanmaras Sutcu Imam University, Faculty of Health Science, Department of Physiotherapy and Rehabilitation, Kahramanmaraş, Turkey. Pamukkale University, Faculty of Physiotherapy and Rehabilitation, Denizli, Turkey. Kahramanmaras Sutcu Imam University, Faculty of Medicine, Kahramanmaras, Turkey. Kahramanmaras Sutcu Imam University, Faculty of Medicine, Kahramanmaras, Turkey.
 Sleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. Sleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. Sleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. Sleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. Sleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington. Sleep Research Laboratory, Center for Integrative Neuroscience and Inflammatory Diseases, Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, Virginia. Sleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
 Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA. Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine, Quinnipiac University, North Haven, CT, USA. Department of Medical Sciences, Frank H. Netter MD School of Medicine, Quinnipiac University, North Haven, CT, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, CT, USA. Multiple Sclerosis Center of Excellence West, Seattle, WA, USA. Rehabilitation Care Service, VA Puget Sound Health Care System, Seattle, WA, USA. Department of Rehabilitation Medicine, University of Washington, Seattle, WA, USA. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA. Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine, Quinnipiac University, North Haven, CT, USA. Multiple Sclerosis Center of Excellence West, Seattle, WA, USA. Rehabilitation Care Service, VA Puget Sound Health Care System, Seattle, WA, USA. Department of Rehabilitation Medicine, University of Washington, Seattle, WA, USA. Department of Epidemiology, University of Washington, Seattle, WA, USA. Neuroscience Program, Trinity College, Hartford, CT, USA. Department of Psychology, Trinity College, Hartford, CT, USA.
 Istanbul Technical University, Graduate School, Department of Applied Informatics, Istanbul, 34469, Turkey. Electronic address: saricab@itu.edu.tr. Istanbul Technical University, Civil Engineering Faculty, Department of Geomatics Engineering, Istanbul, 34469, Turkey. Electronic address: seker@itu.edu.tr. Yildiz Technical University, Civil Engineering Faculty, Department of Geomatics Engineering, Istanbul, 34220, Turkey. Electronic address: bayram@yildiz.edu.tr.
 Physical Therapy Department, Hunter College, City University of New York, New York, NY, USA. Rusk Rehabilitation Department, New York University Langone Health, New York, NY, USA. Physical Therapy Department, Hunter College, City University of New York, New York, NY, USA. Rusk Rehabilitation Department, New York University Langone Health, New York, NY, USA. Rusk Rehabilitation Department, New York University Langone Health, New York, NY, USA.
 Institute for Clinical and Economic Review, Boston, MA. Department of Medicine and Philip R Lee Institute for Health Policy Studies, University of California, San Francisco. Institute for Clinical and Economic Review, Boston, MA. Institute for Clinical and Economic Review, Boston, MA. Institute for Clinical and Economic Review, Boston, MA. Institute for Clinical and Economic Review, Boston, MA. Institute for Clinical and Economic Review, Boston, MA. Institute for Clinical and Economic Review, Boston, MA.
 Unidad de Esclerosis Múltiple. Servicio de Neurología. Hospital Vithas-Nisa, Sevilla, España; Instituto de Biomedicina de Sevilla, IBiS (Universidad de Sevilla, HUVR, Junta de Andalucía, CSIC) y Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Universidad de Sevilla, Sevilla, España. Instituto de Biomedicina de Sevilla, IBiS (Universidad de Sevilla, HUVR, Junta de Andalucía, CSIC) y Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Universidad de Sevilla, Sevilla, España. Facultad de Medicina, Universidad de Sevilla, Sevilla, España. Facultad de Medicina, Universidad de Sevilla, Sevilla, España. Unidad de Esclerosis Múltiple. Servicio de Neurología. Hospital Vithas-Nisa, Sevilla, España. Electronic address: g.i.ayuso@gmail.com.
 From the Department of Ophthalmology (V.D., S.A.T., H.E.E., M.O.S.), Marmara University School of Medicine, Istanbul, Turkey. Electronic address: volkandr@gmail.com. From the Department of Ophthalmology (V.D., S.A.T., H.E.E., M.O.S.), Marmara University School of Medicine, Istanbul, Turkey. From the Department of Ophthalmology (V.D., S.A.T., H.E.E., M.O.S.), Marmara University School of Medicine, Istanbul, Turkey. From the Department of Ophthalmology (V.D., S.A.T., H.E.E., M.O.S.), Marmara University School of Medicine, Istanbul, Turkey. and the Department of Neurology (E.E., G.S., K.A.), Marmara University School of Medicine, Istanbul, Turkey. and the Department of Neurology (E.E., G.S., K.A.), Marmara University School of Medicine, Istanbul, Turkey. and the Department of Neurology (E.E., G.S., K.A.), Marmara University School of Medicine, Istanbul, Turkey. and the Department of Ophthalmology and Visual Sciences (E.T.), West Virginia University, Morgantown, West Virginia, USA.
 Institute for Brain Sciences Research, School of Life Sciences, Henan University, Kaifeng, Henan, China. Pacific Center for Neurological Disease (PCND) Neuroscience Research Institute, Poway, CA, USA. Division of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.
 School of Life Sciences, Forman Christian College (A Chartered University) Lahore, Lahore, Pakistan. Rashid Latif Medical College, Lahore, Pakistan. Rashid Latif Medical College, Lahore, Pakistan. Punjab Institute of Neurosciences, Lahore, Punjab, Pakistan. Punjab Institute of Neurosciences, Lahore, Punjab, Pakistan. College of Applied Medical Sciences, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia. Neuroscience Center, King Fahad Specialist Hospital, Dammam, Saudi Arabia. School of Life Sciences, Forman Christian College (A Chartered University) Lahore, Lahore, Pakistan.
 Department of Biostatistics and Epidemiology, Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Regenerative Biomedicine, Royan Institute for Stem Cell Biology and Technology, ACCR, Tehran, Iran. Department of Brain and Cognition, Royan Institute for Stem Cell Biology and Technology, ACCR, Tehran, Iran. Department of Neurology, Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Nutritional Sciences, School of Allied Medical Sciences, Nutrition, and Metabolic Disease Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Biostatistics and Epidemiology, School of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Biostatistics and Epidemiology, School of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. tabib.m@ajums.ac.ir.
 Central Clinical School, Monash University, Melbourne, VIC, Australia, and Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Electronic address: tim@burnet.edu.au. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Dokuz Eylul University, Konak, Izmir, Turkey. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. Department of Neuroscience, Imaging, and Clinical Sciences, University G. d'Annunzio, Chieti, Italy. CORe, Department of Medicine, University of Melbourne, and Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia. Hôpital Notre Dame, Montreal, QC, Canada, and CHUM and Université de Montréal, Montreal, QC, Canada. Medical Faculty, 19 Mayis University, Samsun, Turkey. CISSS de Chaudière-Appalaches, Lévis, QC, Canada. Department of Medical and Surgical Sciences and Advanced Technologies, GF Ingrassia, AOU Policlinico Vittorio Emanuele, and Policlinico G. Rodolico, Catania, Italy. Department of Neurology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. KTU Medical Faculty Farabi Hospital, Trabzon, Turkey. School of Medicine and Public Health, University Newcastle, and Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, NSW, Australia. Neurosciences Unit, Department of Medicine and Surgery, University of Parma, Parma, Italy. Neuro Rive-Sud, QC, Canada. Department of Neurology, Monash University, Melbourne, VIC, Australia. Department of Neurology, Monash University, Melbourne, VIC, Australia. Central Clinical School and Department of Neurology, Monash University, and Department of Neurology, Alfred Hospital, Melbourne, VIC, Australia.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University, London, UK ruth.dobson@qmul.ac.uk. Department of Neurology, The Royal London Hospital, London, UK. Manchester Centre for Clinical Neurosciences, Salford Royal NHS Foundation Trust, Salford, UK. Department of Women and Children's Health, King's College London, London, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Department of Neurology, Forth Valley Royal Hospital, Larbert, UK. Department of Neurology, Belfast Health and Social Care Trust, Belfast, UK. Department of Neurology, Leeds Teaching Hospitals NHS Trust, Leeds, UK. Department of Neurosciences, University of Leeds Faculty of Medicine and Health, Leeds, UK. Department of Neurology, Morriston Hospital, Swansea, UK. Department of Neurology, St George's Hospitals NHS Trust, London, UK. Department of Neurology, Forth Valley Royal Hospital, Larbert, UK. Department of Neurology, The Royal London Hospital, London, UK. Department of Obstetrics, Guy's and St Thomas' Hospitals NHS Trust, London, UK. Department of Obstetrics, King's College Hospital NHS Foundation Trust, London, UK. Department of Neurology, King's College Hospital NHS Foundation Trust, London, UK.
 Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran 19816-19573, Iran. Department of Human Nutrition, Foods, and Exercise, College of Agriculture and Life Science, Virginia Tech, Blacksburg, VA 24060, USA. Department of Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran 14496-14535, Iran. Cardiovascular Diseases Research Center, Department of Cardiology, Heshmat Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht 41937-1311, Iran. Department of Clinical Nutrition, School of Medicine, Guilan University of Medical Sciences, Rasht 41937-1311, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran 14167-53955, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran 19816-19573, Iran. Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19839-69411, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran 19816-19573, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran 19816-19573, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran 14167-53955, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran 19816-19573, Iran. Department of Virology, Pasteur Institute of Iran, Tehran 13169-43551, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran 19816-19573, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran 14167-53955, Iran.
 Department of Neurology, Keio University School of Medicine.
 Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Service de Neurologie, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron, France/INSERM 1028 et CNRS UMR 5292, Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, Bron, France/Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France/Eugène Devic EDMUS Foundation against Multiple Sclerosis, State-approved Foundation, Bron, France. Neurology Department, Hôpital Gui de Chauliac, CHU de Montpellier, Montpellier, France. Centre Ressources et Compétences sclérose en plaques (CRC-SEP) et Service de Neurologie B4, Hôpital Pierre-Paul Riquet, CHU Toulouse Purpan, Toulouse, France INSERM UMR1291 - CNRS UMR5051, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse 3, Toulouse, France. Neurology Department, Pitié-Salpêtrière Hospital, CRC-SEP, Paris, France. Neurology Department, CIC_P1414 INSERM, Rennes University Hospital, Rennes, France. EHESP, CNRS, Inserm, Arènes - UMR 6051, RSMS (Recherche sur les Services et Management en Santé) - U 1309, Université de Rennes, Rennes, France. CRC SEP et Service de Neurologie, CHU Tours, Tours, France. Department of Neurology, CHU Rouen, Rouen, France. Center for Research in Transplantation and Translational Immunology, UMR 1064, Nantes Université and INSERM, Nantes, France/CIC INSERM 1413, CRC-SEP Pays de la Loire, CHU Nantes, Nantes, France. Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Service de Neurologie, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron, France/Clinique de la Sauvegarde, Ramsay Santé, Lyon, France. CRC-SEP, Neurology Department, Hôpital Fondation Adolphe de Rothschild, Paris, France. CRC-SEP, Service de Neurologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France. Centre Ressources et Compétences sclérose en plaques (CRC-SEP) et Service de Neurologie B4, Hôpital Pierre-Paul Riquet, CHU Toulouse Purpan, Toulouse, France INSERM UMR1291 - CNRS UMR5051, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse 3, Toulouse, France. Service de Neurologie, CHU de Caen Normandie, Caen, France. Pathologies Inflammatoires du Système Nerveux, Neurologie, CHU Grenoble Alpes, Grenoble, France/Translational Research in Autoimmunity and Inflammation Group (T-RAIG), TIMC-IMAG, Université de Grenoble Alpes, Grenoble, France. CRCSEP Côte d'Azur, CHU de Nice Pasteur 2, Nice, France/Université Nice Côte d'Azur UR2CA-URRIS, Nice, France. Service de Neurologie, CHU de Besançon, Besançon, France. CRC-SEP, Neurology Department, Hôpital Fondation Adolphe de Rothschild, Paris, France. Hôpital saint Philibert, Groupement des Hôpitaux de l'Institut Catholique de Lille, Faculté de médecine et de maïeutique de Lille, Lomme, France. Department of Neurology, Saint-Antoine Hospital, APHP-6, Paris, France/Sorbonne University, Paris, France. CRC-SEP, Hôpital Pellegrin, CHU de Bordeaux, Bordeaux, France. Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Service de Neurologie, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Department of Neurology, CHU Rouen, Rouen, France. Department of Neurology, CHU Rouen, Rouen, France. CRC-SEP, Service de Neurologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France. Department of Neurology, Lille Catholic Hospitals, Lille Catholic University, Lille, France. Service de Neurologie, Centre Hospitalier de Lens, Lens, France. CRMBM, UMR 7339, CNRS, Aix-Marseille Université, Marseille, France/APHM Hôpital de la Timone, Marseille, France. Department of Neurology, Gonesse Hospital, Gonesse, France. Service de neurologie, Centre Hospitalier Régional Universitaire de Nancy - Hôpital Central, Nancy, France. Neuro-Dol, Inserm, Université Clermont Auvergne, Clermont-Ferrand, France/Department of neurology et CRC-SEP, CHU Clermont-Ferrand, Clermont-Ferrand, France. CRC-SEP, Hôpital Pellegrin, CHU de Bordeaux, Bordeaux, France. Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Service de Neurologie, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron, France/INSERM 1028 et CNRS UMR 5292, Centre de Recherche en Neurosciences de Lyon, Bron, France/Université Claude Bernard Lyon 1, Lyon, France. Neurology Department, Pitié-Salpêtrière Hospital, CRC-SEP, Paris, France. Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Service de Neurologie, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron, France/INSERM 1028 et CNRS UMR 5292, Centre de Recherche en Neurosciences de Lyon, Lyon, France/Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France. Service de Neurologie, CHU de Besançon, Besançon, France/Université Nice Côte d'Azur UR2CA-URRIS, Nice, France.
 Department "GF Ingrassia" Section of Neurosciences, University of Catania, via S. Sofia 78, Catania 95129, Italy. Electronic address: patti@unict.it. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, via S. Sofia 78, Catania 95129, Italy. Multiple Sclerosis Center, Hospital of Gallarate - ASST della Valle Olona, Gallarate, Italy. Operative Unit of Neurology and Stroke Unit, Varese, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy. Operative Unit of Neurology - Valduce Hospital, Como, Italy. Department of Neurology, ASST Papa Giovanni XXIII, Bergamo, Italy. Department of Human Neurosciences, Sapienza, University of Rome, Italy. Unit of Neurology - IRCCS Neuromed, Pozzilli, Isernia, Italy. Department of Neuroscience, UO of Neurology, AOU Policlinico OB, Modena, Italy. Unit of Neurology - IRCCS Neuromed, Pozzilli, Isernia, Italy. Neurology Department, San Gerardo Hospital, Monza, Italy. Department of Neurology, General Regional Hospital "Miulli", Acquaviva delle Fonti, Bari, Italy. Emergency Department, Neurology Unit, G. da Saliceto Hospital, Piacenza, Italy. Unit of Clinical Neurology - AOU Sassari, Italy. SCDO Neurologia-CRESM, University Hospital San Luigi Gonzaga, Orbassano, Turin, Italy. Multiple Sclerosis Center, Cardarelli Hospital, Naples, Italy. Department of Systems Medicine, Multiple Sclerosis Clinical & Research Center, "Tor Vergata" University, Rome, Italy. Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari "Aldo Moro", Bari, Italy. Multiple Sclerosis Center, Neurological Clinic, University Hospital of Padua, Italy. Operative Unit of Neurology and Stroke Unit, IRCCS Hospital San Martino, Genoa, Italy. Department of Neurology, Demyelinating Disease Center, San Salvatore Hospital, L'Aquila, Italy. Department of Neurology, Mondovì General Hospital, Local Health Authority CN1, Mondovì, Cuneo, Italy. Neurology, University Magna Graecia, Catanzaro, Italy. Multiple Sclerosis Center, Hospital of Gallarate - ASST della Valle Olona, Gallarate, Italy. Operative Unit of Neurology, Mirano, Venice, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy; Unit of Neurology - IRCCS Neuromed, Pozzilli, Isernia, Italy. Electronic address: centonze@uniroma2.it.
 Preventive Medicine and Epidemiology Department, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. CRCSEP Nice, CHU de Nice Pasteur2, Universite ́ Nice Cote d'Azur UR2CA-URRIS, Nice, France. Fundación Santa Fe de Bogotá, Bogotá, Colombia. School of Medicine, Universidad de los Andes, Bogotá, Colombia. Barts and The London School of Medicine and Dentistry, Blizard Institute, Queen Mary University of London, London, UK. Department NEUROFARBA, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Preventive Medicine and Epidemiology Department, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Centro para la Investigación de Enfermedades Neuroinmunológicas (CIEN), FLENI, Buenos Aires, Argentina. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, Neurorehabilitation Unit, and Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Department of Paediatric Neurology, Great Ormond Street Hospital for Children, London, UK. Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, London, UK. Department of Neurology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Patient representative, Multiple Sclerosis International Federation, London, UK. Department of Neurology, Danish Multiple Sclerosis Center and the Danish Multiple Sclerosis Registry, Rigshospitalet and University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Departamento de Medicina, Hospital Clínico San Carlos, IdISSC, Universidad Complutense, Madrid, Spain. Department of Neurology, Istanbul University Cerrahpasa School of Medicine, Cerrahpasa, 34098, Istanbul, Turkey. Service de neurologie, Sclérose en plaques, Pathologies de la myéline et neuro-inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon/Bron, France. Centre des Neurosciences de Lyon, Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR5292, Lyon, France. Faculté de médecine Lyon Est, Université Claude Bernard Lyon 1, Lyon, France. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 College of Healthcare Sciences, James Cook University, Townsville, Queensland, Australia. Discipline of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Australia. College of Public Health, Medical and Vet Sciences, James Cook University, Townsville, Queensland, Australia. College of Public Health, Medical and Vet Sciences, James Cook University, Townsville, Queensland, Australia. College of Healthcare Sciences, James Cook University, Townsville, Queensland, Australia.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, USA. Electronic address: robmotl@uic.edu. Kessler Foundation, USA. Interdisciplinary School of Health Sciences, University of Ottawa, Canada. Department of Biostatistics, University of Alabama at Birmingham, USA. Center for Innovation and Applied Research, Canada. American Sports Medicine Institute, USA. Program in Exercise Science, Department of Physical Therapy, Marquette University, USA.
 Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Electronic address: cecilie.ammitzboell@regionh.dk. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark; Department of Applied Mathematics and Computer Science, Technical University of Denmark, Lyngby, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark. Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark; Department of Neurology, Copenhagen University Hospital - Bispebjerg and Frederiksberg, Copenhagen, Denmark; Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Valdemar Hansens Vej 17, Glostrup 2600, Denmark; Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
 Brigham and Women's Hospital and Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. Electronic address: tchitnis@rics.bwh.harvard.edu.
 Regina Berkovich MD PhD Inc MS Neurology, West Hollywood, CA, United States; USC-LAC Neurology, Los Angeles, CA, United States. Negroski Neurology, Sarasota, FL, United States. Consultants in Neurology MS Center, Northbrook, IL, United States. Negroski Neurology, Sarasota, FL, United States. Sanofi, Cambridge, MA, United States; Worldwide Clinical Trials, Research Triangle Park, NC, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Sanofi, Cambridge, MA, United States. Lou Ruvo Center for Brain Health, Las Vegas, NV, United States. International Neurorehabilitation Institute, Baltimore, MD, USA; Johns Hopkins Hospital, Baltimore, MD, United States. Electronic address: db@inirehab.com.
 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Electronic address: attiasm@ksu.edu.sa. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia. Department of Pharmaceutics, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia.
 Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Electronic address: yavor.yalachkov@kgu.de. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Neurology, University Medical Center Mainz, Mainz, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Psychiatry and Psychotherapy, University Medical Center Mainz, Mainz, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Medical Center Mainz, Mainz, Germany. Department of Neurology, University Medical Center Mainz, Mainz, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Neurology, RKH Klinikum Ludwigsburg, Ludwigsburg, Germany.
 Department of Neurology, Medical University of Warsaw, 02-097 Warsaw, Poland. Department of Neurology, Hochzirl Hospital, 6170 Hochzirl, Austria. Department of Clinical Neurosciences, University of Calgary, Calgary, AB T2N 1N4, Canada. Department of Bioethics, Medical University of Warsaw, 02-091 Warsaw, Poland.
 College of Health Solutions, Arizona State University, Phoenix, USA. South Shore Neurologic Associates, Patchogue, NY11772, USA. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, University at Buffalo, Buffalo, USA. Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, USA. Washington Neuropsychology Research Group, Fairfax, VA, USA. Department of Neurology, Georgetown University, Washington, DC, USA. Department of Neurology, Lady Davis Carmel Medical Center, Haifa, Israel. The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. South Shore Neurologic Associates, Patchogue, NY11772, USA. South Shore Neurologic Associates, Patchogue, NY11772, USA. South Shore Neurologic Associates, Patchogue, NY11772, USA. Stony Brook University, Stony Brook, NY, USA. College of Health Solutions, Arizona State University, Phoenix, USA. College of Health Solutions, Arizona State University, Phoenix, USA. Phoenix Veterans Affairs Medical Center, Phoenix, AZ, USA.
 Department of Biomedical Engineering, TOBB University of Economics and Technology, Ankara, Turkey. Department of Biomedical Engineering, TOBB University of Economics and Technology, Ankara, Turkey. Department of Biomedical Engineering, TOBB University of Economics and Technology, Ankara, Turkey. Neurology Clinic, Ankara City Hospital, Ankara, Turkey. Department of Biochemistry, Faculty of Medicine, Yildirim Beyazit University, Ankara, Turkey. Department of Biochemistry, Faculty of Medicine, Yildirim Beyazit University, Ankara, Turkey.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Gynecological Endocrinology and Reproductive Medicine, Medical University of Innsbruck, Innsbruck, Austria. Department of Statistics, Faculty of Economics and Statistics, University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Central Institute of Medical and Chemical Laboratory Diagnostics (ZIMCL), University Hospital of Innsbruck, Innsbruck, Austria. Central Institute of Medical and Chemical Laboratory Diagnostics (ZIMCL), University Hospital of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
 Department of Economics, The University of the West Indies, St Augustine Campus, Trinidad and Tobago; HEU, Centre for Health Economics, The University of the West Indies, St Augustine Campus, Trinidad and Tobago. Electronic address: hhbailey@gmail.com. Department of Clinical Medical Sciences, Faculty of Medical Sciences, The University of the West Indies, St. Augustine Campus, Trinidad and Tobago. HEU, Centre for Health Economics, The University of the West Indies, St Augustine Campus, Trinidad and Tobago. Department of Internal Medicine, Eric Williams Medical Sciences Complex, Mt. Hope, Trinidad and Tobago.
 Bank of Tissues and Cells, Hospices Civils de Lyon, Hôpital Edouard Herriot, Place d'Arsonval, F-69003 Lyon, France. Stem-Cell and Brain Research Institute, 18 Avenue de Doyen Lépine, F-69500 Bron, France. Lyon-Est School of Medicine, University Claude Bernard Lyon 1, 43 Bd du 11 Novembre 1918, F-69100 Villeurbanne, France.
 IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. Ospedale San Paolo, ASST Santi Paolo e Carlo, Clinical Neurology Unit, Department of Health Sciences, University of Milan, 20142 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148 Milan, Italy. Pathophysiology and Transplantation Department, University of Milan, 20122 Milan, Italy.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Electronic address: simon.englund@ki.se. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden. Department of Neuroscience, Uppsala University, Uppsala, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Clinical and Translational Neuroscience, Southern California Permanente Medical Group, Kaiser Permanente, Pasadena, United States. Department of Clinical Neuroscience, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Sciences, Division of Neurology, Lund University, Lund, Sweden. Department of Pharmacology and Clinical Neuroscience, Umea University, Umeå, Sweden. Clinical Sciences, Danderyd Hospital Stockholm, Stockholm, Sweden. Department of Biomedical and Clinical Sciences, Division of Neurobiology, Linköping University, Linköping, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Department of Animal Biology, Faculty of Natural Science, University of Tabriz, Tabriz, Iran. Safaralizadeh@tabrizu.ac.ir.
 Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. DKTK CCU Neuroimmunology and Brain Tumor Immunology, DKFZ, Heidelberg, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany.
 Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. MS Center Noord Nederland, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. MS Center Noord Nederland, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. MS Center Noord Nederland, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. MS Center Noord Nederland, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. w.baron@umcg.nl. MS Center Noord Nederland, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. w.baron@umcg.nl.
 From the Department of Neurosciences, University of California, San Diego. jgraves@ucsd.edu.
 Hackensack Meridian Medical Group - Neurology, Jersey Shore University Medical Center, Neptune City, NJ, United States of America. Electronic address: lana.zhovtisryerson@hmhn.org. Rocky Mountain MS Clinic, Salt Lake City, UT, United States of America. Department of Neurology, Centre Hospitalier Universitaire de Caen, Caen, France. Mellen MS Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, United States of America. Montréal Neurological Institute, McGill University, Montréal, QC, Canada; NeuroRx Research, Montréal, QC, Canada. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. University of Alabama at Birmingham, School of Public Health, Birmingham, AL, United States of America. Blizard Institute, Barts and The London School of Medicine and Dentistry, London, UK; Queen Mary University of London, London, UK. Department of Neurology, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam, Netherlands. Department of Neurology with Institute of Translational Neurology, University of Münster, Münster, Germany. Biogen, Cambridge, MA, United States of America. Biogen, Baar, Switzerland. Biogen, Cambridge, MA, United States of America. Biogen, Cambridge, MA, United States of America.
 Student Research Committee, School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran. Community Based Psychiatric Care Research Center, School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Neurology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. Department of Nursing, School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran. zahrakhademian@yahoo.com.
 Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. Electronic address: davide.angeletti@gu.se. Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
 Department of Neuroradiology, AP-HP, Henri Mondor University Hospital, 92010 Créteil, France. Siemens Healthcare SAS, 93210 Saint-Denis, France. Department of Neuroradiology, AP-HP, Henri Mondor University Hospital, 92010 Créteil, France. MOX, Department of Mathematics, Politecnico di Milano, 20133 Milano, Italy; Research Center, INRIA, 75012 Paris, France. Department of Neuroradiology, AP-HP, Henri Mondor University Hospital, 92010 Créteil, France. Department of Neurology, AP-HP, Henri Mondor University Hospital, 92010 Créteil, France; Faculty of Medicine, Université Paris Est Créteil, 92010 Créteil, France. Siemens Healthcare, 91052 Erlangen, Germany. Department of Neuroradiology, AP-HP, Henri Mondor University Hospital, 92010 Créteil, France; Faculty of Medicine, Université Paris Est Créteil, 92010 Créteil, France. Electronic address: blanche.bapst@aphp.fr.
 Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 59 boulevard Pinel, 69677, Bron, France. philippe.nicolas@chu-lyon.fr. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM) Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 69677, Bron, France. philippe.nicolas@chu-lyon.fr. Université Claude Bernard-Lyon 1, Lyon, France. philippe.nicolas@chu-lyon.fr. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 59 boulevard Pinel, 69677, Bron, France. Université Claude Bernard-Lyon 1, Lyon, France. Laboratoire d'immunologie-Hôpital E. Herriot-Hospices Civils de Lyon, 69437, Lyon, France. Centre International de Recherche en Infectiologie (CIRI), Inserm U1111, CNRS, UMR5308, Ecole Normale Supérieure de Lyon, Lyon, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 59 boulevard Pinel, 69677, Bron, France. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM) Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 69677, Bron, France. Université Claude Bernard-Lyon 1, Lyon, France. Université Claude Bernard-Lyon 1, Lyon, France. Laboratoire d'immunologie-Hôpital E. Herriot-Hospices Civils de Lyon, 69437, Lyon, France. EA 7426 Pathophysiology of Injury-Induced Immunosuppression (Université Claude Bernard Lyon 1-Hospices Civils de Lyon-bioMérieux), Joint Research Unit HCL-bioMérieux, Edouard Herriot Hospital, 69437, Lyon, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 59 boulevard Pinel, 69677, Bron, France. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM) Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, 69677, Bron, France. Université Claude Bernard-Lyon 1, Lyon, France. Université Claude Bernard-Lyon 1, Lyon, France. Laboratoire d'immunologie-Hôpital E. Herriot-Hospices Civils de Lyon, 69437, Lyon, France. Centre International de Recherche en Infectiologie (CIRI), Inserm U1111, CNRS, UMR5308, Ecole Normale Supérieure de Lyon, Lyon, France.
 Multiple Sclerosis Treatment Center, Griffin Hospital, 350 Seymour Ave., Suite 1C, Derby, Connecticut, 06418, USA. cthealthcarealliance@gmail.com. Yale-Griffin Prevention Research Center, Griffin Hospital, 130 Division St., Derby, Connecticut, 06418, USA. Department of Psychiatry, Yale Stress Center, Yale University, New Haven, Connecticut, 06510, USA. Yale-Griffin Prevention Research Center, Griffin Hospital, 130 Division St., Derby, Connecticut, 06418, USA. Yale-Griffin Prevention Research Center, Griffin Hospital, 130 Division St., Derby, Connecticut, 06418, USA. Yale-Griffin Prevention Research Center, Griffin Hospital, 130 Division St., Derby, Connecticut, 06418, USA. Department of Psychiatry, Yale Stress Center, Yale University, New Haven, Connecticut, 06510, USA.
 Department of Psychiatry, Sunnybrook Health Sciences Centre, and Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto (Freedman, Feinstein); Division of Neurology, Department of Medicine, St. Michael's Hospital, and Division of Neurology, Temerty Faculty of Medicine, University of Toronto, Toronto (Oh). Department of Psychiatry, Sunnybrook Health Sciences Centre, and Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto (Freedman, Feinstein); Division of Neurology, Department of Medicine, St. Michael's Hospital, and Division of Neurology, Temerty Faculty of Medicine, University of Toronto, Toronto (Oh). Department of Psychiatry, Sunnybrook Health Sciences Centre, and Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto (Freedman, Feinstein); Division of Neurology, Department of Medicine, St. Michael's Hospital, and Division of Neurology, Temerty Faculty of Medicine, University of Toronto, Toronto (Oh).
 Neurology, University of Health Sciences Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. Radiology, University of Health Sciences Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. Neurology, University of Health Sciences Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. Neurology, University of Health Sciences Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. Biostatistics, Izmir Katip Celebi University Faculty of Medicine, Izmir, Turkey.
 Machine Learning and Data Analytics Lab, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Bavaria, Germany; Computer Science Department, Faculty of Computers and Information, Assiut University, Egypt. Electronic address: Alzhraa.ahmed@fau.de. Department of Medical Informatics, Biometry and Epidemiology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Bavaria, Germany. Department of Molecular Neurology, University Hospital Erlangen, Erlangen, Bavaria, Germany; Fraunhofer Institut for Integrated Circuits, Erlangen, Bavaria, Germany. Department of Neurology, University Hospital Erlangen, Erlangen, Bavaria, Germany. Machine Learning and Data Analytics Lab, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Bavaria, Germany. Machine Learning and Data Analytics Lab, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Bavaria, Germany.
 Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Carenity, Paris, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Electronic address: pmcarrieri@aol.com. Carenity, Paris, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France.
 Mental Health and Neuroscience, QIMR Berghofer Medical Research Institute, Herston, Qld, 4006, Australia. Tony.White@qimrberghofer.edu.au.
 Norwegian Multiple Sclerosis Competence Centre, sDept. of Neurology, Haukeland University Hospital; Dept. of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Dept. of Neurology, Haukeland University Hospital, Bergen, Norway. Electronic address: nina.grytten@helse-bergen.no. Dept. of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Dept. of Neurology, Haukeland University Hospital, Bergen, Norway. Dept of Neurology, Oslo University Hospital Ullevål, Oslo, Norway; Institute of clinical medicine, University of Oslo, Oslo, Norway. Dept. of Neurology, Nordland Hospital, Bodø, Norway. Dept. of Neurology, Molde Hospital, Molde, Norway; Norwegian University of Science and Technology. Dept. of Rehabilitation, Southern Norway Hospital. The Norwegian Multiple Sclerosis Registry and Biobank, Dept. of Neurology, Haukeland University Hospital, Bergen, Norway. The Norwegian Multiple Sclerosis Registry and Biobank, Dept. of Neurology, Haukeland University Hospital, Bergen, Norway; Dept. of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. Dept. of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Dept. of Neurology, Haukeland University Hospital, Bergen, Norway.
 Department of Neurology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran. Electronic address: amoghtaderi@gmail.com. Department of Neurology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran. Department of Epidemiology and Biostatistics, School of Public Health, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran. Department of Neurology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran.
 Department of Neurology and Stroke, Center for Neurology, Eberhard Karls University of Tübingen, Tübingen, Germany. Hertie-Institute for Clinical Brain Research, Eberhard Karls University of Tübingen, Tübingen, Germany. Quantitative Biology Center (QBiC), Eberhard Karls University of Tübingen, Tübingen, Germany. Hertie-Institute for Clinical Brain Research, Eberhard Karls University of Tübingen, Tübingen, Germany. Core Facility for Medical Bioanalytics (CFMB), Eberhard Karls University of Tübingen, Tübingen, Germany. Core Facility for Medical Bioanalytics (CFMB), Eberhard Karls University of Tübingen, Tübingen, Germany. Department of Neurology and Stroke, Center for Neurology, Eberhard Karls University of Tübingen, Tübingen, Germany. Hertie-Institute for Clinical Brain Research, Eberhard Karls University of Tübingen, Tübingen, Germany. Department of Neurology and Stroke, Center for Neurology, Eberhard Karls University of Tübingen, Tübingen, Germany. Hertie-Institute for Clinical Brain Research, Eberhard Karls University of Tübingen, Tübingen, Germany. Quantitative Biology Center (QBiC), Eberhard Karls University of Tübingen, Tübingen, Germany. Biomedical Data Science, Department of Computer Science, Eberhard Karls University of Tübingen, Tübingen, Germany. Department of Neurology and Stroke, Center for Neurology, Eberhard Karls University of Tübingen, Tübingen, Germany. Hertie-Institute for Clinical Brain Research, Eberhard Karls University of Tübingen, Tübingen, Germany.
 Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Human Neurosciences, Sapienza University, Rome, Italy. Department of Public Health, University of Naples "Federico II", Naples, Italy. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Columbia University Medical Center, New York, NY, USA. Department of Neurology, New York University School of Medicine, New York, NY, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; DINOGMI, University of Genoa, Genoa, Italy; Ospedale Policlinico San Martino-IRCSS, Genoa, Italy. Electronic address: m.inglese@unige.it.
 Department of Biosciences, University of Exeter, Exeter, UK. Downing LLP, London, UK. Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Electronic address: suzi.claflin@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia.
 Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt. Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt. yarasayed89@gmail.com. Department of Cytology and Histology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt. Department of Pathology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt. Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt. Department of Biomedical Research, Armed Forces College of Medicine, Cairo, 12211, Egypt. Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt. Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
 Vulvar Disorders and Dermatology Unit, Royal Women's Hospital Melbourne, Parkville, Australia. Department of Dermatology, St Vincent's Hospital Melbourne, 41 Victoria Parade, Fitzroy, Australia. Vulvar Disorders and Dermatology Unit, Royal Women's Hospital Melbourne, Parkville, Australia. Department of Dermatology, St Vincent's Hospital Melbourne, 41 Victoria Parade, Fitzroy, Australia.
 Department of Neurology, Athens Naval Hospital, Athens, Greece. A' Department of Neurology, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, AHEPA University Hospital, Thessaloniki, Greece. Department of Neurology, Faculty of Medicine, University of Thessaly, Larissa, Greece. Neurology Department, General Military Hospital of Athens, 401, Athens, Greece. Ntoskas K. Triantafillos Private Practice, K. Papakonstantinou 4, Paiania, 19002, Athens, Greece. The Neurological Institute of Athens, 51, Leof. Vasilissis Sofias Ave, 10676, Athens, Greece. Department of Neurology, General Oncology Hospital of Kifissia "Agioi Anargiroi", Athens, Greece. Department of Neurology, University Hospital of Alexandroupolis, Alexandroupolis, Greece. Novartis Hellas SACI, Athens, Greece. B' Department of Neurology, School of Medicine, Faculty of Health Sciences, Multiple Sclerosis Center, Aristotle University of Thessaloniki, AHEPA University Hospital, Kiriakidi 1, 54621, Thessaloniki, Greece. ngrigoriadis@auth.gr.
 Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Hannover Medical School, Hannover, Germany. Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran. Clinical Research Development Unit, Amiralmomenin Hospital, Arak University of Medical Sciences, Arak, Iran. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Medical Laboratory Sciences, Khomein University of Medical Sciences, Khomein, Iran. maryam.azimzade@khomeinums.ac.ir. Molecular and Medicine Research Center, Khomein University of Medical Sciences, Khomein, Iran. maryam.azimzade@khomeinums.ac.ir.
 Department of Kinesiology, 110 Totman Building, School of Public Health and Health Sciences, University of Massachusetts Amherst, 30 Eastman Lane, Amherst, MA 01003-9258, USA; Department of Exercise and Sport Studies, 410 Scott Gym, Smith College, 102 Lower College Lane, Northampton, MA 01063, USA. Electronic address: sjones00@smith.edu. Department of Kinesiology, 110 Totman Building, School of Public Health and Health Sciences, University of Massachusetts Amherst, 30 Eastman Lane, Amherst, MA 01003-9258, USA.
 Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Microbiology of Golestan University of Medical Sciences, Golesatn, Iran. Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Virology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Department of Biochemistry, Faculty of Basic Sciences, Sanandaj Branch, Islamic Azad University, Sanandaj, Iran. Department of Biochemistry, Faculty of Basic Sciences, Sanandaj Branch, Islamic Azad University, Sanandaj, Iran. Department of Microbiology, Faculty of Veterinary Medical, Urmia University, Urmia, West Azarbaijan, Iran. Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Urology Research Center, Tehran University of Medical Sciences, Tehran, Iran. Faculty of Medicine, Islamic Azad University, Shiraz University of Medical Science, Shiraz, Iran. Department of Virology, Faculty of Medicine, Tarbiat Modares University, Tehran, Iran. Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Epidemiology and Biostatistics, School of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Department of Microbiology of Golestan University of Medical Sciences, Golesatn, Iran. Faculty of Paramedicine, Tabriz University of Medical Science, Tabriz, Iran. Medical Virology Student, Department of Virology, Lorestan University of Medical Science, Khorramabad, Iran. Department of Microbiology, Faculty of Sciences, Karaj Branch, Islamic Azad University, Karaj, Iran. Department of Medical Sciences, Faculty of Paramedicl, Qom Branch, Islamic Azad University, Qom, Iran. Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Virology, Faculty of Medicine, Hamadan University of Medical Science, Hamadan, Iran. Department of Clinical Biochemistry, Shahid Beheshti University of Medical Science, Tehran, Iran. Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: kiani.j@iums.ac.ir. Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Vet.s.ghorbani@gmail.com.
 Neuroimmunology Fellow, Mellen Center, Cleveland Clinic, Cleveland, OH. Mellen Center, Cleveland Clinic, Cleveland, OH; Associate Professor of Neurology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH. Mellen Center, Cleveland Clinic, Cleveland, OH; Assistant Professor of Neurology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH. Mellen Center, Cleveland Clinic, Cleveland, OH; Professor of Neurology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH. Mellen Center, Cleveland Clinic, Clevland, OH; Clinical Assistant Professor of Neurology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH kunchoa@ccf.org.
 Department of Pathology, Stanford University School of Medicine, Stanford, CA. Department of Dermatology, Stanford University School of Medicine, Stanford, CA. Department of Dermatology, Stanford University School of Medicine, Stanford, CA. Department of Pathology, Stanford University School of Medicine, Stanford, CA. Division of Neuroimmunology, Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA. Department of Dermatology, Stanford University School of Medicine, Stanford, CA. Department of Pathology, Stanford University School of Medicine, Stanford, CA. Department of Dermatology, Stanford University School of Medicine, Stanford, CA.
 From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. Dina.Jacobs2@pennmedicine.upenn.edu. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco. From the Division of Multiple Sclerosis (S.T., S.G., C.L., E.J.K., C.P., L.Z., L.D.Y., M.K.S., J.R.B., C.M., A.B.-O., R.F., R.B., A.A.P., D.A.J.), Hospital of the University of Pennsylvania and Perelman School of Medicine; Division of Infectious Diseases (C.C.), Department of Medicine; and Weill Institute for Neurosciences (M.R.W.), Department of Neurology, University of California, San Francisco.
 School of Advanced Technologies in Medicine, Medical Image and Signal Processing Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. School of Advanced Technologies in Medicine, Medical Image and Signal Processing Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité- Universitätsmedizin Berlin, Berlin, Germany; NeuroCure Clinical Research Center- Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité- Universitätsmedizin Berlin, Berlin, Germany; NeuroCure Clinical Research Center- Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité- Universitätsmedizin Berlin, Berlin, Germany; NeuroCure Clinical Research Center- Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; Department of Neurology, University of California, Irvine, CA, USA. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité- Universitätsmedizin Berlin, Berlin, Germany; NeuroCure Clinical Research Center- Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. School of Advanced Technologies in Medicine, Medical Image and Signal Processing Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; NeuroCure Clinical Research Center- Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; Department of Engineering, Durham University, Durham, UK. Electronic address: Raheleh.kafieh@durham.ac.uk.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK. Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK/Centre for Oral Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Clinical Neurology, Academic Unit of Mental Health and Clinical Neurosciences, University of Nottingham, Nottingham, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK/Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK/Department of Neurology, Barts Health NHS Trust, London, UK. Department of Neurology, Royal Gwent Hospital, Newport, UK. Clinical Neurology, Academic Unit of Mental Health and Clinical Neurosciences, University of Nottingham, Nottingham, UK. Department of Neurology, Morriston Hospital, Swansea, UK. Immunodeficiency Centre for Wales, University Hospital of Wales, Cardiff, UK/School of Medicine, Cardiff University, Cardiff, UK. Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK/Centre for Oral Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Wales Newborn Screening Laboratory, Department of Medical Biochemistry, Immunology and Toxicology, University Hospital of Wales, Cardiff, UK/School of Medicine, Cardiff University, Cardiff, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK/Department of Neurology, University Hospital of Wales, Cardiff, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK. Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK/Department of Neurology, Barts Health NHS Trust, London, UK. Department of Neurology, University Hospital of Wales, Cardiff, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London, UK/Department of Neurology, Barts Health NHS Trust, London, UK. Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK/Department of Neurology, University Hospital of Wales, Cardiff, UK.
 Department of Neurobiology, Care Sciences and Society, 27106Karolinska Institutet, Huddinge, Sweden. Department of Neurobiology, Care Sciences and Society, 27106Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Karolinska University Hospital, Stockholm, Sweden. Department of Occupational Therapy, University of Illinois, Chicago, IL, USA. Department of Neurobiology, Care Sciences and Society, 27106Karolinska Institutet, Huddinge, Sweden. School of Education and Learning, Dalarna University, Falun, Sweden. Department of Neurobiology, Care Sciences and Society, 27106Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Karolinska University Hospital, Stockholm, Sweden. Department of Neurobiology, Care Sciences and Society, 27106Karolinska Institutet, Huddinge, Sweden. Academic Specialist Center, Center of Neurology, Stockholm Health Services, Stockholm, Sweden. Department of Neurobiology, Care Sciences and Society, 27106Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Karolinska University Hospital, Stockholm, Sweden.
 Michigan State University, East Lansing, MI, USA. University of Illinois-Urbana Champaign, Champaign, IL, USA. Elon University, Elon, NC, USA. University of North Texas, Denton, TX, USA.
 Department of Neurology, Medical Campus Upper Frankonia, Klinikum Bayreuth GmbH, Bayreuth, Germany. roy.mueller@klinikum-bayreuth.de. Department of Sports Science, Friedrich Schiller University Jena, Jena, Germany. Department of Neurology, Medical Campus Upper Frankonia, Klinikum Bayreuth GmbH, Bayreuth, Germany. Department of Cognition, Emotion and Neuropsychology, Otto-Friedrich-University, Bamberg, Germany. Department of Neurology, Medical Campus Upper Frankonia, Klinikum Bayreuth GmbH, Bayreuth, Germany.
 Melbourne School of Psychological Sciences, Mood and Anxiety Disorders Lab, Faculty of Medicine, Dentistry, and Health Sciences, The University of Melbourne, Melbourne, VIC, 3010, Australia. Melbourne School of Psychological Sciences, Mood and Anxiety Disorders Lab, Faculty of Medicine, Dentistry, and Health Sciences, The University of Melbourne, Melbourne, VIC, 3010, Australia. litzak@unimelb.edu.au.
 Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Department of Neurology, Neurosurgery and Medical Genetics, Federal Center of Brain Research and Neurotechnologies, Pirogov Russian National Research Medical University, Moscow, Russia. Department of Neurology, FLENI Institute, Buenos Aires, Argentina. Department of Neurology, University Hospital of Rennes, Rennes, France. Department of Medicine and the Ottawa Hospital Research Institute, University of Ottawa, Ottawa, ON, Canada. Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitario Vall d'Hebron, Barcelona, Spain. MS Research Center, School of Medicine, University of Miami, Miami, FL, USA. Department of Neurological Sciences, Rush Medical College, Chicago, IL, USA. Neurology Institute, Harley Street Medical Center, Abu Dhabi, UAE/American University of Beirut Medical Center, Beirut, Lebanon. Division of Clinical Neuroimmunology, Comprehensive MS Center, Jefferson University, Philadelphia, PA, USA. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. Merck Healthcare KGaA, Darmstadt, Germany. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA.
 Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. michael.hecker@rocketmail.com. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Clinic III (Hematology, Oncology and Palliative Medicine), Special Hematology Laboratory, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany. Core Facility for Cell Sorting and Cell Analysis, Rostock University Medical Center, Schillingallee 70, 18057, Rostock, Germany. Core Facility for Cell Sorting and Cell Analysis, Rostock University Medical Center, Schillingallee 70, 18057, Rostock, Germany. Miltenyi Biotec B.V. & Co. KG, Robert-Koch-Str. 1, 17166, Teterow, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany. Institute of Immunology, Rostock University Medical Center, Schillingallee 70, 18057, Rostock, Germany. Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147, Rostock, Germany.
 Department of Psychology, The Pennsylvania State University, State College, USA. Department of Psychology, The Pennsylvania State University, State College, USA. Department of Psychology, The Pennsylvania State University, State College, USA. Department of Psychiatry, Tufts University, School of Medicine, Boston, USA. Department of Psychology, The Pennsylvania State University, State College, USA.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia/Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, VIC, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Cancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Department of Nutrition, Connecting Health Innovations LLC, Columbia, SC, USA/Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. Cancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Department of Nutrition, Connecting Health Innovations LLC, Columbia, SC, USA/Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. Curtin School of Population Health, Curtin University, Perth, WA, Australia. Murdoch Children's Research Institute, Royal Children's Hospital, The University of Melbourne, Melbourne, VIC, Australia/The Florey Institute of Neuroscience & Mental Health, Parkville, VIC, Australia. School of Medicine, Griffith University, Gold Coast, QLD, Australia. Department of Neurology, John Hunter Hospital, Newcastle, NSW, Australia/Faculty of Medicine and Public Health, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia.
 Girona Neuroimmunology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Salt, Spain. Girona Neuroimmunology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Salt, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Instituto de Salud Carlos III, Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Madrid, Spain. Girona Neuroimmunology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Salt, Spain. Instituto de Salud Carlos III, Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Madrid, Spain. Medical Sciences Department, University of Girona, Girona, Spain. Neurology Department, Dr. Josep Trueta University Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Instituto de Salud Carlos III, Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Madrid, Spain. Radiology Department, Dr. Josep Trueta University Hospital, Girona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology, University of California, San Francisco, California, USA. Girona Neuroimmunology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Salt, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Instituto de Salud Carlos III, Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Madrid, Spain. Medical Sciences Department, University of Girona, Girona, Spain. Neurology Department, Dr. Josep Trueta University Hospital, Girona, Spain.
 Department of Biophysics, International School of Medicine, University of Health Sciences, Istanbul, Turkey, 34668. Hamidiye School of Medicine, University of Health Sciences, Istanbul, Turkey, 34668. Hamidiye International School of Medicine, University of Health Sciences, Istanbul, Turkey, 34668. School of Medicine, Bezmialem Vakif University, Istanbul, Turkey, 34093. Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece, 115 27.
 Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China. Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China. Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China. Electronic address: shamay.ng@polyu.edu.hk.
 Department of Value-Based Healthcare, St. Antonius Hospital, Utrecht/Nieuwegein, the Netherlands; Radboud university medical center, Radboud Institute for Health Sciences, Scientific Center for Quality of Healthcare (IQ healthcare), the Netherlands. Electronic address: k.daniels@antoniusziekenhuis.nl. Department of Neurology, St. Antonius Hospital, Utrecht/Nieuwegein, the Netherlands. Department of Clinical Pharmacy, St. Antonius Hospital, Utrecht/Nieuwegein, the Netherlands; Division of Pharmacoepidemiology and Clinical Pharmacology, Faculty of Science, Utrecht University, Utrecht, the Netherlands. Department of Internal Medicine, Leiden University Medical Center, Leiden, the Netherlands; Department of Internal Medicine, University Medical Centre Utrecht, Utrecht, the Netherlands. Radboud university medical center, Radboud Institute for Health Sciences, Scientific Center for Quality of Healthcare (IQ healthcare), the Netherlands. Department of Value-Based Healthcare, St. Antonius Hospital, Utrecht/Nieuwegein, the Netherlands; Radboud university medical center, Radboud Institute for Health Sciences, Scientific Center for Quality of Healthcare (IQ healthcare), the Netherlands.
 Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy.
 National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry (Shaanxi Normal University), The Ministry of Education, College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi, 710119, China. National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry (Shaanxi Normal University), The Ministry of Education, College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi, 710119, China. Electronic address: xingli_xian@126.com.
 Departamento de Medicina, Universidad de Oviedo, Oviedo, Spain. Department of Neurology, Hospital Universitario Central de Asturias, Oviedo, Spain. Grupo de Investigación Clínica-Básica en Neurología, Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
 Department of Physiotherapy and Rehabilitation, Institute of Graduate Studies, Istanbul University-Cerrahpasa, Istanbul, Turkey; Department of Medical Services and Techniques, Vocational School of Health Services, Physiotherapy Program, Istanbul Aydin University, Istanbul, Turkey. Electronic address: pelin.vural@medipol.edu.tr. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Pediatric Neurology, Faculty of Medicine, Biruni University, Istanbul, Turkey. Department of Pediatric Neurology, Cerrahpasa Medicine Faculty, Istanbul University-Cerrahpasa, Istanbul, Turkey.
 EMD Serono Research & Development Institute, Inc. (an affiliate of Merck KGaA), 45 Middlesex Turnpike, Billerica, MA, 01821, USA. irina.kalatskaya@emdserono.com. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Division of Clinical Neuroimmunology, Jefferson University, Comprehensive MS Center, Philadelphia, PA, USA. EMD Serono Research & Development Institute, Inc. (an affiliate of Merck KGaA), 45 Middlesex Turnpike, Billerica, MA, 01821, USA. BISC Global, Boston, MA, USA. Ares Trading S.A. (an affiliate of Merck KGaA), Eysins, Switzerland. EMD Serono Research & Development Institute, Inc. (an affiliate of Merck KGaA), 45 Middlesex Turnpike, Billerica, MA, 01821, USA.
 School of Biomedical Sciences and Pharmacy, Hunter Medical Research Institute, University of Newcastle, New Lambton Heights, NSW 2305, Australia. School of Medicine and Public Health, Hunter Medical Research Institute, University of Newcastle, New Lambton Heights, NSW 2305, Australia. Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 17176 Stockholm, Sweden. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. School of Biomedical Sciences and Pharmacy, Hunter Medical Research Institute, University of Newcastle, New Lambton Heights, NSW 2305, Australia. Biological and Environmental Science and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia. Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia. Unit of Computational Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, L8:05, 17176 Stockholm, Sweden. Science for Life Laboratory, Tomtebodavagen 23A, 17165 Solna, Sweden. College of Medicine and Public Health, Flinders University, Bedford Park, SA 5042, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. MSBase Foundation, Melbourne, VIC 3004, Australia. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 17176 Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 17176 Stockholm, Sweden. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC 3052, Australia. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 17176 Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 17176 Stockholm, Sweden. Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC 3052, Australia. National Centre for Epidemiology and Public Health, Australian National University, Canberra, ACT 2601, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS 7000, Australia. School of Biomedical Sciences and Pharmacy, Hunter Medical Research Institute, University of Newcastle, New Lambton Heights, NSW 2305, Australia. Department of Molecular Genetics, Pathology North, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia. School of Medicine and Public Health, Hunter Medical Research Institute, University of Newcastle, New Lambton Heights, NSW 2305, Australia. Centre for Genomics and Personalised Health, School of Biomedical Science, Queensland University of Technology, Kelvin Grove, QLD 4059, Australia. School of Medicine and Public Health, Hunter Medical Research Institute, University of Newcastle, New Lambton Heights, NSW 2305, Australia. Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
 Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, San Martino Hospital, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Neurology Department, St. Antoine Hospital, APHP, Paris, France. Institute of Experimental Neurology, Division of Neuroscience, Vita-Salute San Raffaele University and Hospital, Milan, Italy. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Neurology Department, St. Antoine Hospital, APHP, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Université Paris-Saclay, CEA, CNRS, Inserm, BioMaps, Service Hospitalier Frédéric Joliot, Orsay, France. Université Paris-Saclay, CEA, CNRS, Inserm, BioMaps, Service Hospitalier Frédéric Joliot, Orsay, France. Unité de Recherche Clinique, Pitié-Salpêtrière Hospital, APHP, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Neurology Department, Pitié-Salpêtrière Hospital, APHP, Paris, France. Université Paris-Saclay, CEA, CNRS, Inserm, BioMaps, Service Hospitalier Frédéric Joliot, Orsay, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Neurology Department, St. Antoine Hospital, APHP, Paris, France. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm, Paris, France. Neurology Department, St. Antoine Hospital, APHP, Paris, France.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Electronic address: maria.campagna@monash.edu. School of Medicine and Public Health, University of Newcastle, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; Department of Neurology, John Hunter Hospital, New Lambton Heights, New South Wales, Australia. School of Medicine and Public Health, University of Newcastle, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; Department of Neurology, John Hunter Hospital, New Lambton Heights, New South Wales, Australia. School of Medicine and Public Health, University of Newcastle, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; Centre for Genomics and Personalised Health, School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Queensland, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia; Department of Neurology, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia; Department of Neurology, Alfred Health, Melbourne, Victoria, Australia.
 Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Neuroimmunology, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Neuroimmunology, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Department of Pathology, VUMC, Amsterdam, The Netherlands. Department of Neuroimmunology, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Cellular and Molecular Medicine, Center for Healthy Ageing, University of Copenhagen, Copenhagen, Denmark. Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
 School of Physiotherapy, University of Otago, Dunedin, New Zealand. School of Physiotherapy, University of Otago, Christchurch, New Zealand. School of Physiotherapy, Centre for Health, Activity, and Rehabilitation Research (CHARR), University of Otago, Wellington, New Zealand.
 Queen Square MS Centre, Department of Neuroinflammation, Institute of Neurology, Faculty of Brain Sciences, University College London (UCL), London, UK. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Queen Square MS Centre, Department of Neuroinflammation, Institute of Neurology, Faculty of Brain Sciences, University College London (UCL), London UK/Centre for Medical Image Computing (CMIC), Department of Medical Physics and Biomedical Engineering, University College London, London, UK/e-Health Centre, Universitat Oberta de Catalunya, Barcelona, Spain. Queen Square MS Centre, Department of Neuroinflammation, Institute of Neurology, Faculty of Brain Sciences, University College London (UCL), London, UK/Biomedical Research Centre, National Institute for Health Research (NIHR) and University College London Hospitals (UCLH), London, UK. Queen Square MS Centre, Department of Neuroinflammation, Institute of Neurology, Faculty of Brain Sciences, University College London (UCL), London, UK/Biomedical Research Centre, National Institute for Health Research (NIHR) and University College London Hospitals (UCLH), London, UK. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia (CEMCAT), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia (CEMCAT), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Queen Square MS Centre, Department of Neuroinflammation, Institute of Neurology, Faculty of Brain Sciences, University College London (UCL), London, UK/Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia (CEMCAT), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Queen Square MS Centre, Department of Neuroinflammation, Institute of Neurology, Faculty of Brain Sciences, University College London (UCL), London, UK/Centre for Medical Image Computing (CMIC), Department of Medical Physics and Biomedical Engineering, University College London, London, UK Biomedical Research Centre, National Institute for Health Research (NIHR) and University College London Hospitals (UCLH), London, UK/Radiology & Nuclear medicine, VU University Medical Centre, Amsterdam, The Netherlands.
 Division of Child Neurology, Children's Hospital of Philadelphia, Department of Neurology and Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, PA, USA. Electronic address: banwellb@chop.edu. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, USA. Service de neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France; Centre de Recherche en Neurosciences de Lyon, Lyon, France; Université Claude Bernard Lyon, Lyon, France. Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, South Korea. Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, Sydney, Australia; School of Medical Sciences, Faculty of Medicine and Health and Brain and Mind Centre, University of Sydney, Sydney, Australia. Departments of Neurology, Laboratory Medicine and Pathology and Center MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Concord Hospital, Translational Neuroimmunology Group, Kids Neuroscience Centre, Children's Hospital at Westmead, Sydney, Australia; Brain and Mind Centre and Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Paediatric Neuroimmunology Clinic, Department of Neurology, National Paediatric Hospital Dr J P Garrahan, Ciudad de Buenos Aires, Argentina. Department of Neurosciences, University of California, San Diego, CA, USA. Department of Pediatric Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, University of California, Irvine, CA, USA. Department of Paediatric Neurology, Great Ormond Street Hospital, London, UK; Institute of Neurology, UCL, London, UK. Department of Neurology, MS Center ErasMS, Sophia Children's Hospital, Erasmus MC University Medical Center Rotterdam, Rotterdam, Netherlands. Center for Advanced Neurological Research, Nitte University Mangalore, Mangalore, India. Clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Neuroimmunology and Multiple Sclerosis Unit, Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain; Facultat de Medicina i Ciencies de la Salut, Universitat de Barcelona, Barcelona, Spain. School of Medicine and Institute for Geriatrics and Gerontology, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil. Department of Paediatric Neurology, Children'sHospital Datteln, University Witten and Herdecke, Datteln, Germany. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Departments of Neurology, Laboratory Medicine, and Pathology and Center MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University School of Medicine, Fukushima, Japan; Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan. Department of Neurology John Radcliffe Hospital Oxford and Nuffield Department of Clinical Neurosciences Oxford University, Oxford, UK.
 Medical Unit Occupational Therapy and Physiotherapy, Function Allied Health Professionals, Karolinska University Hospital, Stockholm, Sweden. Gillisdotter Caregivers Consulting AB, Upplaends Vaesby, Sweden. Department of Neurobiology, Care Sciences and Society, Division of Occupational Therapy, Karolinska Institutet, Stockholm, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden. Department of Health Sciences, Lund University, Lund, Sweden. Department of Neurology and Rehabilitation Medicine, Skåne University Hospital, Lund-Malmö, Sweden.
 Computer Science Department, University of Zaragoza, Zaragoza, Spain. Aragon Institute on Engineering Research, Zaragoza, Spain. Computer Science Department, University of Zaragoza, Zaragoza, Spain. Aragon Institute on Engineering Research, Zaragoza, Spain. Ophtalmology Department, Miguel Servet Hospital, Zaragoza, Spain. Ophtalmology Department, Miguel Servet Hospital, Zaragoza, Spain. Computer Science Department, University of Zaragoza, Zaragoza, Spain. Aragon Institute on Engineering Research, Zaragoza, Spain. Ophtalmology Department, Miguel Servet Hospital, Zaragoza, Spain.
 Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Center for Neurological Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Center for Neurological Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Partners Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Partners Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Center for Neurological Imaging, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
 Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, China. Department of Neurology, Huai'an Hospital of Huai'an City, Huai'an, Jiangsu 223001, China. Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, China. Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, China. Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, China. Electronic address: lujieyx@126.com.
 Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. assuntatrinchillo94@gmail.com. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Advanced Biomedical Sciences, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Infectious Diseases Unit, "Federico II" University, Naples, Italy. Infectious Diseases Unit, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Québec, Canada. Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Québec, Canada. tanja.kuhlmann@ukmuenster.de. Institute of Neuropathology, University Hospital Münster, Münster, Germany. tanja.kuhlmann@ukmuenster.de.

 Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Dep. of Physiology, School of Medicine, Aja University of Medical Sciences, Tehran, Iran. emirzaii@alumnus.tums.ac.ir. Department of Neurology, School of Medicine, Skull Base Research Center, Five Senses Health Research Institute, Hazrat-E Rasool General Hospital, Iran University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
 Department of Personality, Assessment, and Psychological Treatment, University of Seville, Seville, Spain. Department of Personality, Assessment, and Psychological Treatment, University of Seville, Seville, Spain. Department of Psychosomatic Medicine and Psychotherapy, University Hospital Bonn, Bonn, Germany. Department of Psychosomatic Medicine and Psychotherapy, University Hospital Muenster, Muenster, Germany. Department of Personality, Assessment, and Psychological Treatment, University of Seville, Seville, Spain.
 Osmaneli Vocational School, Department of Patient Care at Home, Bilecik Seyh Edebali University, Bilecik, Turkey. keseburak@gmail.com. Faculty of Physiotherapy and Rehabilitation, Department of Neurologic Physiotherapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Faculty of Physiotherapy and Rehabilitation, Department of Neurologic Physiotherapy and Rehabilitation, Hacettepe University, Ankara, Turkey.
 Neurology, Oregon Health & Science University, Portland, Oregon, USA wooliscr@ohsu.edu. Neurology, Portland VA Medical Center, Portland, Oregon, USA. Neurology, Oregon Health & Science University, Portland, Oregon, USA. Biostatistics and Design Program Core, Oregon Health & Science University, Portland, Oregon, USA. Advanced Imaging Research Center, Oregon Health & Science University, Portland, Oregon, USA. Neurology, Oregon Health & Science University, Portland, Oregon, USA. Neurology, Oregon Health & Science University, Portland, Oregon, USA. Neurology, Portland VA Medical Center, Portland, Oregon, USA. School of Medicine, Oregon Health & Science University, Portland, Oregon, USA. Neurology, Oregon Health & Science University, Portland, Oregon, USA. Neurology, Oregon Health & Science University, Portland, Oregon, USA. Neurology, Portland VA Medical Center, Portland, Oregon, USA.
 Institute of Virology, Vaccines and Sera "Torlak", Belgrade, Serbia. University of Belgrade-Faculty of Pharmacy, Department of Microbiology and Immunology, Belgrade, Serbia. University of Belgrade-Faculty of Pharmacy, Department of Pathobiology, Belgrade, Serbia. Electronic address: gordana.leposavic@pharmacy.bg.ac.rs.
 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Psychiatry & Behavioral Medicine, Lahey Hospital & Medical Center (LHMC), Harvard Medical School, Burlington, MA, USA. Department of Social Work, Brigham and Women's Health Care Center, Westwood, MA, USA. Department of Neuroscience, Georgia State University, Atlanta, GA, USA. Emory University, Atlanta, GA, USA. Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
 Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany cha.schubert@uke.de. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Social Medicine and Epidemiology, University of Lübeck, Lübeck, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, Ruhr University Bochum, Bochum, Germany. Faculty of Medicine and University Hospital Cologne, University Hospital Cologne, Köln, Germany. Unit of Neuroepidemiology, Foundation IRCCS Carlo Besta Neurological Institute, Milano, Italy. Unit of Neuroepidemiology, Foundation IRCCS Carlo Besta Neurological Institute, Milano, Italy. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Psychiatry and Neurosciences, Charite Universitatsmedizin Berlin, Berlin, Germany. Medical Statistics, University Medical Center Göttingen, Göttingen, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Social Medicine and Epidemiology, University of Lübeck, Lübeck, Germany.
 Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. sven.jarius@med.uni-heidelberg.de. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, a Cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, and Berlin Institute of Health, and Max Delbrück Center for Molecular Medicine, Berlin, Germany. Department of Neurology, School of Medicine, Technical University Munich, Klinikum rechts der Isar, Munich, Germany. Department of Neurology, School of Medicine, Technical University Munich, Klinikum rechts der Isar, Munich, Germany. Department of Neurology and Institute of Neuroimmunology and MS (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Ludwig-Maximilians-Universität München, Munich, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, Münster, Germany. Department of Neurology and Pain Treatment, Immanuel Klinik Rüdersdorf, University Hospital of the Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany. Faculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany. Department of Neurology and Stroke, University Hospital of Tübingen, Tübingen, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, a Cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, and Berlin Institute of Health, and Max Delbrück Center for Molecular Medicine, Berlin, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Center for Neurology and Neuropsychiatry, LVR-Klinikum, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, University of Ulm, Ulm, Germany. Department of Neurology and Institute of Neuroimmunology and MS (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. APHM, Hopital de la Timone, CEMEREM, Marseille, France. Aix Marseille Univ, CNRS, CRMBM, Marseille, France. Department of Neurology, University of Leipzig, Leipzig, Germany. Department of Neurology, University of Ulm, Ulm, Germany. Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. trebst.corinna@mh-hannover.de.
 Hospital Universitario La Paz, Madrid, España. Centre d'esclerosi múltiple de Catalunya, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Hospital Universitari Vall d'Hebron, 08035 Barcelona, España. Centre d'esclerosi múltiple de Catalunya, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Centre d'esclerosi múltiple de Catalunya, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España. Centre d'esclerosi múltiple de Catalunya, Barcelona, España. Hospital Universitari Vall d'Hebron-UAB, Barcelona, España.
 Student Research Committee, School of Pharmacy, Ardabil University of Medical Sciences, Ardabil, Iran. Department of Medicinal Chemistry, School of Pharmacy, Medicinal Plants and Natural Products Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Medicinal Chemistry School of Pharmacy, Ardabil University of Medical Sciences, Ardabil PO code: 5618953141, Iran. Electronic address: n.razzaghi@arums.ac.ir.
 Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, Razi University, Kermanshah, Iran. Research Center for Sport and Physical Activity, Faculty of Sport Sciences and Physical Education, University of Coimbra, Coimbra, Portugal. Department of Exercise Physiology, Faculty of Physical Education and Sports Sciences, Allameh Tabataba'i University, Tehran, Iran. Department of Biology, Faculty of Science, Payame-Noor University, Tehran, Iran. Institute of Primary Care, University of Zurich, Zurich, Switzerland. beat.knechtle@hispeed.ch. Medbase St. Gallen Am Vadianplatz, Vadianstrasse 26, 9001, St. Gallen, Switzerland. beat.knechtle@hispeed.ch.
 Department of Neurology, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands. Department of Neurology, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands. Department of Neurology, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, location AMC, University of Amsterdam, Amsterdam, The Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, location AMC, University of Amsterdam, Amsterdam, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, location AMC, University of Amsterdam, Amsterdam, The Netherlands. Sanquin Diagnostic Services, Sanquin Laboratory, Amsterdam, The Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, The Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, The Netherlands. Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands. Department of Pediatric Immunology, Rheumatology and Infectious Disease, Amsterdam UMC, location AMC, University of Amsterdam, Amsterdam, The Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, The Netherlands. Department of Rheumatology, Amsterdam Rheumatology and Immunology Center, Amsterdam, The Netherlands. Sanquin Diagnostic Services, Sanquin Laboratory, Amsterdam, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, location AMC, University of Amsterdam, Amsterdam, The Netherlands. Department of Clinical Neurophysiology, St. Antonius Hospital, Nieuwegein, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, location AMC, University of Amsterdam, Amsterdam, The Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, The Netherlands. Department of Neurology, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands. Department of Neurology, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands.
 Zhejiang Bioinformatics International Science and Technology Cooperation Center, Wenzhou-Kean University, Wenzhou, Zhejiang Province, China. Wenzhou Municipal Key Lab of Applied Biomedical and Biopharmaceutical Informatics, Wenzhou-Kean University, Wenzhou, Zhejiang Province, China. Department of Neurology, Wenzhou Central Hospital Medical Group, Wenzhou 325000, China. Department of Applied Data Science, Noroff University College, Kristiansand, Norway. Artificial Intelligence Research Center (AIRC), Ajman University, Ajman 346, UAE. Department of Electrical and Computer Engineering, Lebanese American University, Byblos, Lebanon. Department of Computer Science, HITEC University, Taxila, Pakistan. Computer Sciences Department, College of Computer and Information Sciences, Princess Nourah Bint Abdulrahman University, Riyadh 11671, Saudi Arabia. Wenzhou-Kean University, School of Science and Technology, Wenzhou, Zhejiang Province, China. Wenzhou-Kean University, School of Science and Technology, Wenzhou, Zhejiang Province, China. College of Computer Engineering and Sciences, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia.
 Bioinformatics and Biostatistics Unit, Principe Felipe Research Center (CIPF), 46012 Valencia, Spain. Foundation Valencian Institute of Oncology (FIVO), 46009 Valencia, Spain. Bioinformatics and Biostatistics Unit, Principe Felipe Research Center (CIPF), 46012 Valencia, Spain. Bioinformatics and Biostatistics Unit, Principe Felipe Research Center (CIPF), 46012 Valencia, Spain. Bioinformatics and Biostatistics Unit, Principe Felipe Research Center (CIPF), 46012 Valencia, Spain; Faculty of Health Sciences, San Jorge University, 50830 Zaragoza, Spain. Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana (IDIPHISA), Grupo de Investigación en Linfomas, C/Joaquín Rodrigo 2, Majadahonda, 28222 Madrid, Spain. Bioinformatics and Biostatistics Unit, Principe Felipe Research Center (CIPF), 46012 Valencia, Spain. Biomedical Imaging Unit FISABIO-CIPF, Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana, 46012 Valencia, Spain. Biomedical Imaging Unit FISABIO-CIPF, Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana, 46012 Valencia, Spain. Department of Pharmacology, Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Bioinformatics and Biostatistics Unit, Principe Felipe Research Center (CIPF), 46012 Valencia, Spain. Electronic address: fgarcia@cipf.es.
 Department of Physical Therapy, School of Health Professions, University of Texas Medical Branch at Galveston, 301 University Boulevard, SHP 3.808, Galveston, TX 77555-1144, USA. Electronic address: gabrusol@utmb.edu. Department of Occupational Therapy, School of Health Professions, University of Texas Medical Branch at Galveston, Galveston, TX, USA. Department of Nutrition, Metabolism, and Rehabilitation Sciences, School of Health Professions, University of Texas Medical Branch at Galveston, Galveston, TX, USA.
 Division of Neuroimmunology and Glial Biology, Weill Neurosciences Center, University of California San Francisco, San Francisco. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, New York.
 Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113 Street, 90-549 Lodz, Poland. Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113 Street, 90-549 Lodz, Poland. Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113 Street, 90-549 Lodz, Poland. Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113 Street, 90-549 Lodz, Poland. Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113 Street, 90-549 Lodz, Poland. Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113 Street, 90-549 Lodz, Poland.
 Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States. Tisch Multiple Sclerosis Research Center of New York, New York, NY, United States.
 Department of Internal Medicine, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada rmarrie@hsc.mb.ca. Department of Community Health Sciences, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Psychiatry, Medicine, Psychology, and Neuroscience, Dalhousie University, Halifax, Nova Scotia, Canada. Manitoba Centre for Health Policy, CAN, Winnipeg, Manitoba, Canada. Department of Psychiatry, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Psychiatry, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Community Health Sciences, University of Calgary, Calgary, Alberta, Canada. Department of Family Medicine, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Community Health Sciences, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Internal Medicine, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Clinical Health Psychology, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Anesthesiology, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Community Health Sciences, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Manitoba Centre for Health Policy, CAN, Winnipeg, Manitoba, Canada. Department of Family Medicine, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Internal Medicine, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada. Department of Internal Medicine, University of Manitoba Max Rady College of Medicine, Winnipeg, Manitoba, Canada.
 Department of Neurology, Université de Sherbrooke, Qc, Canada. Department of Neurosurgery, Université de Sherbrooke, Qc, Canada. Department of Neurosurgery, Université de Sherbrooke, Qc, Canada. Department of Neurosurgery, Université de Sherbrooke, Qc, Canada. Department of Neurosurgery, Université de Sherbrooke, Qc, Canada.
 Section of Gastroenterology, Portland VA Medical Center, P3-GI, Portland, OR, 97239, USA. sonnenbe@ohsu.edu. Division of Gastroenterology and Hepatology, Oregon Health & Science University, Portland, OR, USA. sonnenbe@ohsu.edu.
 Department of Biology and Environmental Science, Linnaeus University, Kalmar, Sweden. Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden; Department of Clinical Physiology, St.Göran Hospital, 112 81 Stockholm, Sweden. Electronic address: per.roos@ki.se.
 Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 40-055 Katowice, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 40-055 Katowice, Poland. Department of Otorhinolaryngology and Oncological Laryngology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 40-055 Katowice, Poland.
 Division of Automatic Control, Department of Electrical Engineering, Linköping University, Linköping, Sweden. Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden. sandra.hellberg@liu.se. Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Obstetrics and Gynecology, Region Kalmar County, Kalmar, Sweden. Department of Neurology, Linköping University, Linköping, Sweden. Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Clinical Immunology and Transfusion Medicine, Linköping University, Linköping, Sweden. Department of Neurology, Linköping University, Linköping, Sweden. Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden. Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Obstetrics and Gynecology, Linköping University, Linköping, Sweden. Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Division of Automatic Control, Department of Electrical Engineering, Linköping University, Linköping, Sweden. Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden. mika.gustafsson@liu.se. Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Clinical Immunology and Transfusion Medicine, Linköping University, Linköping, Sweden.
 Center for the Study of Movement, Cognition and Mobility, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Miriam and Sheldon G. Adelson School of Graduate Studies, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Center for the Study of Movement, Cognition and Mobility, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. NeuroCure Clinical Research Center and Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin and Max Delbrueck Center for Molecular Medicine, Berlin, Germany. Humboldt-Universität Zu Berlin, Berlin, Germany. Berlin Institute of Health, NeuroCure Clinical Research Center, Berlin, Germany. Department of Physical Therapy, Georgia State University Atlanta, Atlanta, GA, USA. Neuroimmunology and Multiple Sclerosis Unit of the Neurology Division, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. Neuroimmunology and Multiple Sclerosis Unit of the Neurology Division, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Center for the Study of Movement, Cognition and Mobility, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Center for the Study of Movement, Cognition and Mobility, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, University of Kansas Medical Center, Kansas City, KS, USA. NeuroCure Clinical Research Center and Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin and Max Delbrueck Center for Molecular Medicine, Berlin, Germany. Humboldt-Universität Zu Berlin, Berlin, Germany. Berlin Institute of Health, NeuroCure Clinical Research Center, Berlin, Germany. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, University of Kansas Medical Center, Kansas City, KS, USA. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, University of Kansas Medical Center, Kansas City, KS, USA. Center for the Study of Movement, Cognition and Mobility, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. jhausdor@tlvmc.gov.il. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. jhausdor@tlvmc.gov.il. Department of Physical Therapy, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. jhausdor@tlvmc.gov.il. Rush Alzheimer's Disease Center and Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA. jhausdor@tlvmc.gov.il.
 Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Medicine, Dow University of Health Sciences, Karachi, Pakistan. Department of Neurology, King Edward Medical University, Lahore, Pakistan. Faculty of Medicine, Aleppo University, Aleppo, Syria. Adjunct Clinical Professor of Medicine, Texas A&M University, College Station, Texas, USA.
 Huaxi MR Research Center (HMRRC), Department of Radiology, West China Hospital of Sichuan University, Chengdu, China. Department of Radiology, West China Hospital of Sichuan University, Chengdu, China. Department of Radiology, West China Hospital of Sichuan University, Chengdu, China. IT Center, West China Hospital of Sichuan University, Chengdu, China. Department of Neurology, West China Hospital of Sichuan University, Chengdu, China. Electronic address: leilei_25@126.com. Huaxi MR Research Center (HMRRC), Department of Radiology, West China Hospital of Sichuan University, Chengdu, China. Electronic address: sunhuaiqiang@scu.edu.cn.
 Neurological Private Practice, Stołeczna 7/109, 15-879, Białystok, Poland. Department of Biophysics, Medical University of Białystok, Mickiewicza 2a, 15-089, Białystok, Poland. marzena.tylicka@umb.edu.pl. Department of Pediatric Surgery, Medical University of Białystok, Waszyngtona 17, 15-274, Białystok, Poland. Department of Pediatric Surgery, Medical University of Białystok, Waszyngtona 17, 15-274, Białystok, Poland. Bioanalysis Laboratory, Faculty of Chemistry, University of Białystok, Ciolkowskiego 1K, 15-245, Białystok, Poland. Bioanalysis Laboratory, Faculty of Chemistry, University of Białystok, Ciolkowskiego 1K, 15-245, Białystok, Poland. Department of Clinical Pharmacy, Medical University of Białystok, Mickiewicza 2C, 15-222, Białystok, Poland. Department of Bromatology, Medical University of Białystok, Mickiewicza 2 d, 15-222, Białystok, Poland. Department of Bromatology, Medical University of Białystok, Mickiewicza 2 d, 15-222, Białystok, Poland. Department of Neurology, Medical University of Białystok, M. Skłodowskiej - Curie 24A, 15-276, Białystok, Poland. Department of Invasive Neurology, Medical University of Białystok, M. Skłodowskiej-Curie 24a, 15-276, Białystok, Poland. Department of Clinical Laboratory Diagnostics, Medical University of Białystok, Waszyngtona 15A, 15-269, Białystok, Poland. Department for Laboratory Diagnostics, University Clinical Centre Maribor SI, Ljubljanska Ulica 5, 2000, Maribor, Slovenia. Department for Clinical Biochemistry, Medical Faculty, University of Maribor, Maribor, Slovenia. Department of Clinical Laboratory Diagnostics, Medical University of Białystok, Waszyngtona 15A, 15-269, Białystok, Poland. o.koper@wp.pl.
 The Danish Multiple Sclerosis Society, Valby, Denmark; Center for Healthy Aging, Section for Health Services Research, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. Electronic address: sob@scleroseforeningen.dk. The Research Unit for General Practice and Section of General Practice, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. Center for Healthy Aging, Section for Health Services Research, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. The Danish Multiple Sclerosis Society, Valby, Denmark.
 Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia. Mater Research Institute, Translational Research Institute, South Brisbane 4101, Australia. Institute for Molecular Bioscience, The University of Queensland, Brisbane 4072, Australia. Department of Medicine, University of Melbourne, Melbourne 3010, Australia. Melbourne Brain Centre, Royal Melbourne Hospital, University of Melbourne, Melbourne 3052, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne 3800, Australia. The University of Queensland Diamantina Institute, The University of Queensland, Brisbane, QLD 4072, Australia. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. Department of Neuroscience, Central Clinical School, Monash University, Melbourne 3800, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia. Clinical Outcomes Research Unit, Royal Melbourne Hospital, The University of Melbourne, Melbourne 3050, Australia. Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne 3053, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne 3800, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart 7000, Australia.
 CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia/Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Medical and Surgical Sciences and Advanced Technologies, G.F. Ingrassia, Catania, Italy/Multiple Sclerosis Center, University of Catania, Catania, Italy. Isfahan University of Medical Sciences, Isfahan, Iran. Dokuz Eylul University, İzmir, Turkey. Hospital Universitario Virgen Macarena, Sevilla, Spain. Hospital Universitario Virgen Macarena, Sevilla, Spain. University G. d'Annunzio, Chieti, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy/IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. CHUM MS Center and Universite de Montreal, Montreal, QC, Canada. CHUM MS Center and Universite de Montreal, Montreal, QC, Canada. CHUM MS Center and Universite de Montreal, Montreal, QC, Canada. 19 Mayis University, Samsun, Turkey. KTU Medical Faculty Farabi Hospital, Trabzon, Turkey. Neuro Rive-Sud, Greenfield Park, QC, Canada. Department of Neuroscience, Azienda Ospedaliera Universitaria, Modena, Italy. Department of Neuroscience, Azienda Ospedaliera Universitaria, Modena, Italy. CISSS Chaudière-Appalache, Levis, QC, Canada. Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Department of Neurology, Box Hill Hospital, Melbourne, VIC, Australia/Monash University, Melbourne, VIC, Australia/Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, VIC, Australia. Department of Neurology, Box Hill Hospital, Melbourne, VIC, Australia/The Alfred Hospital, Melbourne, VIC, Australia. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Department of Neurology, School of Medicine and Koc University Research Center for Translational Medicine (KUTTAM), Koc University, Istanbul, Turkey. Zuyderland Medical Center, Sittard-Geleen, The Netherlands/School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Cliniques Universitaires Saint-Luc, Brussels, Belgium/Université Catholique de Louvain, Ottignies-Louvain-la-Neuve, Belgium. Center of Neuroimmunology, Service of Neurology, Hospital Clinic de Barcelona, Barcelona, Spain. Centro Sclerosi Multipla, UOC Neurologia, ARNAS Garibaldi, Catania, Italy. School of Medicine and Public Health, University Newcastle, Newcastle, NSW, Australia/Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, NSW, Australia. IRCCS Mondino Foundation, Pavia, Italy. Hacettepe University, Ankara, Turkey. St. Vincent's University Hospital, Dublin, Ireland. UOC Neurologia, Azienda Sanitaria Unica Regionale Marche-AV3, Macerata, Italy. Brain and Mind Centre, Sydney, NSW, Australia. Royal Victoria Hospital, Belfast, UK. Department of Neurology, Centro Hospitalar Universitario de Sao Joao, Porto, Portugal. Department of Neurology, ASL3 Genovese, Genova, Italy/Department of Rehabilitation, M.L. Novarese Hospital Moncrivello, Moncrivello, Italy. Hospital Germans Trias i Pujol, Badalona, Spain. Immune Tolerance Laboratory, Ingham Institute and Department of Medicine, University of New South Wales, Sydney, NSW, Australia. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino, Italy. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Aarhus University Hospital, Aarhus, Denmark. Department of Medicine and Surgery, University of Parma, Parma, Italy/Department of Emergency and General Medicine, Parma University Hospital, Parma, Italy. Groene Hart Ziekenhuis, Gouda, The Netherlands. The University of Queensland, Brisbane, QLD, Australia/Royal Brisbane and Women's Hospital, Herston, QLD, Australia. Nemocnice Jihlava, Jihlava, Czech Republic. Rehabilitation & MS Centre, University MS Centre, Noorderhart Hospital, Pelt, Belgium/Pelt and Hasselt University, Hasselt, Belgium. Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia/Central Clinical School, Monash University, Clayton, VIC, Australia. Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia/Central Clinical School, Monash University, Clayton, VIC, Australia. CSSS Saint-Jérôme, Saint-Jerome, QC, Canada. Hospital de Galdakao-Usansolo, Galdakao, Spain. Department of Neurology, University Hospital Ghent, Ghent, Belgium. Department of Neurology, Razi Hospital, Manouba, Tunisia. Hospital Universitario Donostia and IIS Biodonostia, San Sebastián, Spain. South Eastern HSC Trust, Belfast, UK. University Hospital Reina Sofia, Cordoba, Spain. Department of Medicine, Sultan Qaboos University Hospital, Al-Khodh, Oman. Geelong Hospital, Geelong, VIC, Australia. Hospital Fernandez, Capital Federal, Buenos Aires, Argentina. Neurology Department, King Fahad Specialist Hospital-Dammam, Khobar, Saudi Arabia. Universidade Metropolitana de Santos, Santos, Brazil. Department of Neurology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Hospital General Universitario de Alicante, Alicante, Spain. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico. Waikato Hospital, Hamilton, New Zealand. Jewish General Hospital, Montreal, QC, Canada. CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia/Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia/Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia.
 Department of Psychology, Mount Saint Vincent University, 166 Bedford Hwy, Halifax, NS, B3M 2J6, Canada. Department of Psychiatry, Dalhousie University, Halifax, NS, Canada. Department of Psychology, Mount Saint Vincent University, 166 Bedford Hwy, Halifax, NS, B3M 2J6, Canada. Department of Psychiatry, Dalhousie University, Halifax, NS, Canada. Department of Psychology, St. Francis Xavier University, Antigonish, NS, Canada. Department of Psychology, Mount Saint Vincent University, 166 Bedford Hwy, Halifax, NS, B3M 2J6, Canada. Department of Psychology, Mount Saint Vincent University, 166 Bedford Hwy, Halifax, NS, B3M 2J6, Canada. Department of Psychology, St. Francis Xavier University, Antigonish, NS, Canada. Department of Psychiatry, Dalhousie University, Halifax, NS, Canada. Department of Psychology, St. Francis Xavier University, Antigonish, NS, Canada. Department of Psychology, Mount Saint Vincent University, 166 Bedford Hwy, Halifax, NS, B3M 2J6, Canada. derek.fisher@msvu.ca. Department of Psychiatry, Dalhousie University, Halifax, NS, Canada. derek.fisher@msvu.ca. Nova Scotia Health Authority, Halifax, NS, Canada. derek.fisher@msvu.ca.
 Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. doriana.landi@gmail.com. Department of Health Sciences, Section of Biostatistics, University of Genoa, Genoa, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
 Department of Dermatology, Kumagaya General Hospital, Saitama, Japan. Division of Cutaneous Science, Department of Dermatology, Nihon University School of Medicine, Tokyo, Japan. Division of Cutaneous Science, Department of Dermatology, Nihon University School of Medicine, Tokyo, Japan.
 Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Immunology, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Medicine, Division of Rheumatology, Helsinki University Central Hospital, Helsinki, Finland. Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
 Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
 Department of Medical Physics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Medical Physics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Medical Physics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Medical Physics and Biomedical Engineering, Tehran University of Medical Sciences, Tehran, Iran. Research Center for Molecular and Cellular Imaging (RCMCI), Advanced Medical Technologies and Equipment Institute (AMTEI), Tehran University of Medical Sciences (TUMS), Tehran, Iran. Department of Radiation Oncology, University of Pittsburgh School of Medicine and UPMC Hillman Cancer Center, Pittsburgh, PA, United States of America.
 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. Isfahan University of Medical Sciences, Isfahan, Iran. Dokuz Eylul University, Izmir, Turkey. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. KTU Medical Faculty Farabi Hospital, Trabzon, Turkey. Department of Medical and Surgical Sciences and Advanced Technologies, GF Ingrassia, Catania, Italy Multiple Sclerosis Center, University of Catania, Catania, Italy. Department of Neuroscience, Imaging and Clinical Sciences, University G. D'Annunzio, Chieti, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Hospital Universitario Virgen Macarena, Sevilla, Spain. CHUM and Universite de Montreal, Montreal, QC, Canada. CHUM and Universite de Montreal, Montreal, QC, Canada. CHUM and Universite de Montreal, Montreal, QC, Canada. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Department of Neurology, Neuroscience Research Center, Golestan University of Medical Sciences, Gorgan, Iran. Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Department of Neurology, School of Medicine and Koc University Research Center for Translational Medicine (KUTTAM), Koc University, Istanbul, Turkey. Department of Neurology, Box Hill Hospital, Melbourne, VIC, Australia Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia. Department of Neurology, Box Hill Hospital, Melbourne, VIC, Australia Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia MS Centre, Royal Melbourne Hospital, Melbourne, VIC, Australia. CISSS Chaudière-Appalache, Levis, QC, Canada. Hacettepe University, Ankara, Turkey. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia Department of Neurology, The Alfred Hospital, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Centro Sclerosi Multipla, UOC Neurologia, ARNAS Garibaldi, Catania, Italy. School of Medicine and Public Health, University Newcastle, Newcastle, NSW, Australia Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, NSW, Australia. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Monash Medical Centre, Melbourne, VIC, Australia Department of Medicine, School of Clinical Sciences, Monash University, Melbourne, VIC, Australia. CSSS Saint-Jérôme, Saint-Jerome, QC, Canada. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino, Italy. Hospital Germans Trias i Pujol, Badalona, Spain. Academic MS Center Zuyderland, Department of Neurology, Zuyderland Medical Center, Sittard-Geleen, The Netherlands School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Ospedali Riuniti di Salerno, Salerno, Italy. Department of Neuroscience, Neurology Unit, S. Maria delle Croci Hospital of Ravenna, AUSL Romagna, Ravenna, Italy. Nemocnice Jihlava, Jihlava, Czech Republic. Cliniques Universitaires Saint-Luc, Brussels, Belgium Université Catholique de Louvain, Ottignies-Louvain-la-Neuve, Belgium. Brain and Mind Centre, Sydney, NSW, Australia. Neurology, Kasr Al Ainy MS Research Unit (KAMSU), Cairo, Egypt. Department of Neurology, National MS Center, Melsbroek, Belgium. Neurology, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Centro Hospitalar Universitario de Sao Joao, Porto, Portugal Faculty of Health Sciences, University Fernando Pessoa, Porto, Portugal. Perron Institute for Neurological and Translational Science, University of Western Australia, Nedlands, WA, Australia Centre for Molecular Medicine and Innovative Therapeutics, Murdoch University, Perth, WA, Australia. Perron Institute for Neurological and Translational Science, University of Western Australia, Nedlands, WA, Australia Institute of Immunology and Infectious Diseases, Murdoch University, Perth, WA, Australia Sir Charles Gairdner Hospital, Nedlands, WA, Australia. Department of Neurology, University Hospital Razi - Manouba, Tunis, Tunisia Faculty of Medicine of Tunis, University of Tunis El Manar, Tunis, Tunisia. Department of Neurology, University Hospital Razi - Manouba, Tunis, Tunisia. Immune Tolerance Laboratory, Ingham Institute and Department of Medicine, University of New South Wales (UNSW), Sydney, NSW, Australia. Department of Neurology, University Hospital Ghent, Ghent, Belgium. Department of Neurology, University Hospital Ghent, Ghent, Belgium. Austin Health, Melbourne, VIC, Australia. Department of Neurology, Hospital Clinico San Carlos, Madrid, Spain. Centro de Esclerosis Múltiple de Buenos Aires (CEMBA), Buenos Aires, Argentina. The University of Queensland, Brisbane, QLD, Australia Royal Brisbane and Women's Hospital, Herston, QLD, Australia. Hospital de Galdakao-Usansolo, Galdakao, Spain. Bombay Hospital Institute of Medical Sciences, Mumbai, India. Center of Neuroimmunology, Service of Neurology, Hospital Clinic de Barcelona, Barcelona, Spain. Royal Victoria Hospital, Belfast, UK. Westmead Hospital, Sydney, NSW, Australia. Department of Neurology, ASL3 Genovese, Genova, Italy Department of Rehabilitation, M.L. Novarese Hospital, Moncrivello, Italy. St. Vincent's University Hospital, Dublin, Ireland. Royal Hobart Hospital, Hobart, TAS, Australia. Groene Hart Ziekenhuis, Gouda, The Netherlands. Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia University of Zagreb, School of Medicine, Zagreb, Croatia. College of Medicine & Health Sciences and Sultan Qaboos University Hospital, Sultan Qaboos University, Seeb, Oman. Department of Neurology, Victor Babes University of Medicine and Pharmacy, Timișoara, Romania. Hospital Universitario Donostia and IIS Biodonostia, San Sebastián, Spain. Neurology Department, King Fahad Specialist Hospital-Dammam, Khobar, Saudi Arabia. Hospital Universitario de CEMIC, Buenos Aires, Argentina. South Eastern HSC Trust, Belfast, UK. Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. University MS Centre, Hasselt-Pelt, Belgium Noorderhart Rehabilitation & MS Center, Pelt and Hasselt University, Hasselt, Belgium. AHEPA University Hospital, Thessaloniki, Greece. Rashid Hospital, Dubai, United Arab Emirates. St. Michael's Hospital, Toronto, ON, Canada. University Hospital Reina Sofia, Cordoba, Spain. Universidade Metropolitana de Santos, Santos, Brazil. Jewish General Hospital, Montreal, QC, Canada. Geelong Hospital, Geelong, VIC, Australia. Booali Sina Hospital, Neurology Department, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. St. Vincent's Hospital, Fitzroy, Melbourne, VIC, Australia. Department of Neurology, Antwerp University Hospital, Edegem, Belgium Translational Neurosciences Research Group, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium. Concord Repatriation General Hospital, Sydney, NSW, Australia. AZ Alma Ziekenhuis, Damme, Belgium. Hospital General Universitario de Alicante, Alicante, Spain. Lyell McEwin Hospital, Elizabeth Vale, SA, Australia. Division of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK Helen Durham Centre for Neuroinflammation, University Hospital of Wales, Cardiff, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. MS Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. MS Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia Melbourne School of Psychological Sciences, University of Melbourne, Melbourne, VIC, Australia. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. MS Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
 Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Demyelinating Diseases Clinic, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico. Electronic address: benpio76@hotmail.com.
 University Hospital Center Zagreb, Department of Neurology, Referral Center for Autonomic Nervous System Disorders, Zagreb, Croatia. University Hospital Center Zagreb, Department of Neurology, Referral Center for Autonomic Nervous System Disorders, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. University Hospital Center Zagreb, Department of Neurology, Referral Center for Autonomic Nervous System Disorders, Zagreb, Croatia; Faculty of Electrical Engineering, University of Zagreb, Zagreb, Croatia. University Hospital Center Zagreb, Department of Neurology, Referral Center for Autonomic Nervous System Disorders, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. Electronic address: mhabek@mef.hr.

 Pirogov Russian National Research Medical University, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Institute of Chemical Biology and Fundamental Medicine - Genomics Core Facility, Novosibirsk, Russia. Institute of Chemical Biology and Fundamental Medicine - Genomics Core Facility, Novosibirsk, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia.
 From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.). From the Departments of Neurology (W.K.) and Radiology (H.L., D.P., J.J.), Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Banpo-daero 222, Seocho-gu, Seoul 06591, Republic of Korea; Department of Electrical and Computer Engineering, Seoul National University, Seoul, Republic of Korea (H.G.S., J.L.); Department of Radiology, School of Medicine, Johns Hopkins University, Baltimore, Md (H.G.S.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, Md (H.G.S.); and Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Republic of Korea (J.K., Y.N.).
 Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. Department of Anatomy and Cell Biology, Brody School of Medicine, East Carolina University, Greenville, NC, 27834, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, 94158, USA. jorge.oksenberg@ucsf.edu.
 Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Department of Chemistry, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, 50, Yonsei-ro, Seodaemun-gu, Seoul 03722, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Division of Bio-Medical Science & Technology, KIST School, University of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Division of Bio-Medical Science & Technology, KIST School, University of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, 50, Yonsei-ro, Seodaemun-gu, Seoul 03722, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. New Drug Development Center, Daegu Gyeongbuk Medical Innovation Foundation, 80 Cheombok-ro, Dong-gu, Daegu 41061, Republic of Korea. New Drug Development Center, Daegu Gyeongbuk Medical Innovation Foundation, 80 Cheombok-ro, Dong-gu, Daegu 41061, Republic of Korea. Doping Control Center, Research Resources Division, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Doping Control Center, Research Resources Division, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. New Drug Development Center, Daegu Gyeongbuk Medical Innovation Foundation, 80 Cheombok-ro, Dong-gu, Daegu 41061, Republic of Korea. Department of Chemistry, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Division of Bio-Medical Science & Technology, KIST School, University of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Division of Bio-Medical Science & Technology, KIST School, University of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Division of Bio-Medical Science & Technology, KIST School, University of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea. Division of Bio-Medical Science & Technology, KIST School, University of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul 02792, Republic of Korea.
 Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital at Solna, Stockholm, Sweden. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital at Solna, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital at Solna, Stockholm, Sweden. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of General Surgery, Jiading Hospital of Traditional Chinese Medicine, Shanghai, 201800, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital at Solna, Stockholm, Sweden. robert.harris@ki.se. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, 200032, China. jwangf@shmu.edu.cn.
 Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Data Tecnica International LLC, Washington DC, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Data Tecnica International LLC, Washington DC, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA; University of Tuebingen, Tuebingen, Germany. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Data Tecnica International LLC, Washington DC, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Data Tecnica International LLC, Washington DC, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Longitudinal Studies Section, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Data Tecnica International LLC, Washington DC, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Data Tecnica International LLC, Washington DC, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Electronic address: nallsm@nih.gov.
 Department of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Electronic address: ingrid.lie@uib.no. Department of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Immunology and Transfusion Medicine, Haukeland University Hospital, Bergen, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Neurology, Akershus University Hospital, Lørenskog, Norway. Department of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Clinical Medicine, University of Bergen, Bergen, Norway; Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Norwegian MS Registry and Biobank, Haukeland University Hospital, Bergen, Norway.
 Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany. Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany. Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany. Institute of Developmental Immunology, Medical University of Innsbruck, 6020 Innsbruck, Austria. Department of Transfusion Medicine, University Medical Center Göttingen, 37075 Göttingen, Germany. Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, 37075 Göttingen, Germany. Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, 37075 Göttingen, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany. Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany.
 Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Octave Bioscience, Inc., Menlo Park, California, USA. Rocky Mountain Multiple Sclerosis Clinic, Salt Lake City, Utah, USA. Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, 60612, United States. Electronic address: Vflores1@uic.edu. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, 60612, United States. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, 60612, United States. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, 60612, United States. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, 60612, United States. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, 60612, United States.
 Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Siberian State Medical University, Tomsk, Russia. Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk, Russia. Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk, Russia. Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk, Russia.
 Queen Elizabeth University Hospital, Glasgow, UK. Electronic address: fraser@tonnard.co.uk. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Chancellor's Building, Edinburgh, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's Building, Edinburgh, UK; Department of Neurology, RWTH Aachen University, Aachen, Germany. University of Edinburgh, Edinburgh, UK. University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Chancellor's Building, Edinburgh, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's Building, Edinburgh, UK; Euan MacDonald Centre for Motor Neurone Disease Research, University of Edinburgh, Chancellor's Building, Edinburgh, UK; UK Dementia Research Institute at University of Edinburgh, Chancellor's Building, Edinburgh, UK. Department of Clinical Neurosciences, NHS Lothian, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Chancellor's Building, Edinburgh, UK; Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's Building, Edinburgh, UK.
 Department of Neurology, University Hospital Frankfurt, Goethe-University, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Goethe-University, Frankfurt am Main, Germany. Department of Psychiatry and Psychotherapy, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. Institute of Neuroradiology, University Hospital Frankfurt, Goethe-University, Frankfurt am Main, Germany. Neurologische Gemeinschaftspraxis am Kaiserplatz, Frankfurt am Main, Germany. Kopfschmerzzentrum Frankfurt, Frankfurt am Main, Germany. Department of Neurology, Sana Klinikum Offenbach, Offenbach, Germany. Department of Neurology, University Medical Center of Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, University Medical Center of Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, University Hospital Frankfurt, Goethe-University, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Goethe-University, Frankfurt am Main, Germany. Department of Neurology, Klinikum Ludwigsburg, Ludwigsburg, Germany.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Air Quality Research Unit, Swedish Meteorological and Hydrological Institute, Norrköping, Sweden. Department of Environmental Science, Stockholm University, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Center for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Center for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden.
 School of Systems Biology, George Mason University, Manassas, USA. Research Centre for Medical Genetics, Moscow, Russia. School of Systems Biology, George Mason University, Manassas, USA. Department of Biology, Howard University, Washington, USA. Mind-Body Interface Laboratory (MBI-Lab), Department of Psychiatry, China Medical University Hospital, Taichung, Taiwan. College of Medicine, China Medical University Hospital, Taichung, Taiwan. An-Nan Hospital, China Medical University Hospital, Tainan, Taiwan. Institute of Neuropsychiatry, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China. Department of Psychiatry, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China.
 Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
 Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Department of Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Department of Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Department of Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Department of Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Department of Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, 02115, USA. Harvard Medical School, Boston, MA, 02115, USA. Translational Neuroimmunology Research Center (TNRC), Ann Romney Center for Neurologic Diseases (ARCND), Department of Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9002K, Boston, MA, 02115, USA. tchitnis@rics.bwh.harvard.edu. Brigham MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, MA, 02115, USA. tchitnis@rics.bwh.harvard.edu. Harvard Medical School, Boston, MA, 02115, USA. tchitnis@rics.bwh.harvard.edu.
 Department of Clinical Medicine and Neuroscience, CUNY School of Medicine, New York, NY, United States; Department of Medicine, Section of Internal Medicine and Neurology, White Plains Hospital, White Plains, NY, United States. Electronic address: youngd01@nyu.edu.
 Institute of Social Medicine and Epidemiology, Nursing Research Unit, University of Lübeck, Allee 160, Ratzeburger D-23538 Lübeck. Electronic address: julia.peper@uksh.de. Institute of Nursing Science, University of Cologne, Medical Faculty & University Hospital Cologne, Gleueler Str. 176-78, D-50935 Cologne. Unit of Neuroepidemiology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Via Celoria 11, IT-20133 Milano. Unit of Neuroepidemiology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Via Celoria 11, IT-20133 Milano. Institute for Neuroimmunology and Multiple Sclerosis, University Medical Centre Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg; Department of Psychiatry Campus Benjamin Franklin (CBF), Charité University Medicine Berlin, Hindenburgdamm 30, D-12203 Berlin; Charité Universitätsmedizin Berlin, Department of Psychiatry, Campus Benjamin Franklin (CBF), Hindenburgdamm 30, D-12203 Berlin. Department of Neurology, St. Josef Hospital Bochum, Ruhr University Bochum, Gudrunstrasse 56, D-44791 Bochum. Institute for Neuroimmunology and Multiple Sclerosis, University Medical Centre Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg. Martin Luther University Halle-Wittenberg, Institute for Health and Nursing Science, Magdeburger Str. 8, D-06112 Halle (Saale). Institute for Neuroimmunology and Multiple Sclerosis, University Medical Centre Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg; Department of Neurology, University Medical Centre Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg. Institute of Social Medicine and Epidemiology, Nursing Research Unit, University of Lübeck, Allee 160, Ratzeburger D-23538 Lübeck.
 Kansai Multiple Sclerosis Centre, Irino Clinic Inc, TCA Building 4F, 2-3-19 Motomachi, Naniwa-ku, Osaka-shi, Osaka, Japan. msnet@bg.wakwak.com. Kansai Multiple Sclerosis Centre, Kyoto Neurology Clinic, Ukyo-ku, Uzumasa-Yurigamoto-cho 8-32, Kyoto, 616-8144, Japan. msnet@bg.wakwak.com. Kansai Multiple Sclerosis Centre, Irino Clinic Inc, TCA Building 4F, 2-3-19 Motomachi, Naniwa-ku, Osaka-shi, Osaka, Japan. Biogen Japan Ltd, Nihonbashi 1-chome Mitsui Building 14F 1-4-1, Nihonbashi, Chuo-ku, Tokyo, Japan. Biogen Japan Ltd, Nihonbashi 1-chome Mitsui Building 14F 1-4-1, Nihonbashi, Chuo-ku, Tokyo, Japan.
 Student Research Committee, Jiroft University of Medical Sciences, Jiroft, Iran. Department of Parasitology and Mycology, School of Medicine, Jiroft University of Medical Science, Jiroft, Kerman, Iran. Research Center for Hydatid Disease in Iran, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran. Student Research Committee, Jiroft University of Medical Sciences, Jiroft, Iran. Student Research Committee, Yasuj University of Medical sciences, Yasuj, Iran. Research Center for Hydatid Disease in Iran, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran. Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. Department of Anesthesiology, Friedrich-Alexander-University Erlangen-Nuremberg, University Hospital Erlangen, Krankenhausstraße, Germany. Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran.
 MS Center Amsterdam, Neurology Department, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers (Amsterdam UMC), Location VUmc, De boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. f.loonstra@amsterdamumc.nl. MS Center Amsterdam, Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology Department, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers (Amsterdam UMC), Location VUmc, De boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology Department, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers (Amsterdam UMC), Location VUmc, De boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology Department, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers (Amsterdam UMC), Location VUmc, De boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. MS Center Amsterdam, Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, Location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology Department, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers (Amsterdam UMC), Location VUmc, De boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. MS Center Amsterdam, Molecular Cell Biology and Immunology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam University Medical Centers, Location VUmc, Amsterdam, The Netherlands.
 School of Medicine, Tehran University of Medical Sciences, Pour Sina St, Keshavarz Blvd, Tehran, 1417613151, Iran. School of Medicine, Tehran University of Medical Sciences, Pour Sina St, Keshavarz Blvd, Tehran, 1417613151, Iran. School of Medicine, Tehran University of Medical Sciences, Pour Sina St, Keshavarz Blvd, Tehran, 1417613151, Iran. mohamsa@gmail.com. Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, USA. Department of Neurology, New York University Langone Medical Center, New York, NY, USA. School of Medicine, Tehran University of Medical Sciences, Pour Sina St, Keshavarz Blvd, Tehran, 1417613151, Iran. Laboratory of Neuroimmunology, Stanford University School of Medicine, Stanford, CA, USA. Laboratory of Neuroimmunology, Stanford University School of Medicine, Stanford, CA, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, Stanford Multiple Sclerosis Center, Stanford University, Stanford, USA. Department of Neurology, Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, NeuroCure Clinical Research Center, Charité Universitätsmedizin Berlin, Berlin, Germany.
 Department of Communicative Disorders and Sciences, University at Buffalo, The State University of New York. Department of Biostatistics, University at Buffalo, The State University of New York. Department of Communicative Disorders and Sciences, University at Buffalo, The State University of New York.
 From the Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum Rechts der Isar. From the Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum Rechts der Isar. From the Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum Rechts der Isar. Deepc GmbH. Deepc GmbH. Department of Neurology, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. From the Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum Rechts der Isar. From the Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum Rechts der Isar.
 School of Medicine, College of Medicine, Taipei Medical University, Taipei. Department of Medical Education, China Medical University Hospital, Taichung. Department of Physical Medicine and Rehabilitation, China Medical University Hospital, Taichung. Department of Physical Medicine and Rehabilitation, Shuang Ho Hospital, Taipei Medical University, New Taipei City. Department of General Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung. School of Biomedical Engineering, College of Biomedical Engineering, Taipei Medical University, Taipei. Department of Physical Medicine and Rehabilitation, Shuang Ho Hospital, Taipei Medical University, New Taipei City. Department of Physical Medicine and Rehabilitation, School of Medicine, College of Medicine, Taipei Medical University, Taipei. Center for Evidence-Based Health Care, Shuang Ho Hospital, Taipei Medical University, New Taipei City.
 Institute of Clinical Neuroimmunology, Ludwig-Maximilians-Universität München, 81377 Munich, Germany. Institute of Clinical Neuroimmunology, Ludwig-Maximilians-Universität München, 81377 Munich, Germany. Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke gGmbH, 82335 Berg, Germany. Institute of Medical Information Processing, Biometry, and Epidemiology, Faculty of Medicine, Ludwig-Maximilians-Universität München, 81377 Munich, Germany. Institute of Clinical Neuroimmunology, Ludwig-Maximilians-Universität München, 81377 Munich, Germany. Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke gGmbH, 82335 Berg, Germany. Department of Neurology, Ruhr-University Bochum, 44791 Bochum, Germany. Institute of Clinical Neuroimmunology, Ludwig-Maximilians-Universität München, 81377 Munich, Germany. Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
 Institute of Biomedical Engineering, University of New Brunswick, Fredericton, Canada. Faculty of Kinesiology, University of New Brunswick, Fredericton, Canada. Institute of Biomedical Engineering, University of New Brunswick, Fredericton, Canada. Assistive Technology Clinic, Toronto, Canada. Toronto Rehabilitation Institute, Toronto, Canada. Shirley Ryan AbilityLab/Rehabilitation Institute of Chicago, Chicago, IL, USA. Shirley Ryan AbilityLab/Rehabilitation Institute of Chicago, Chicago, IL, USA. Assistive Technology Clinic, Toronto, Canada. Department of Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, Charlestown, MA, USA. Department of Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, Charlestown, MA, USA. Department of Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, Charlestown, MA, USA.
 Nature Reviews Neurology, . nrneuro@nature.com.
 Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. emartind@recerca.clinic.cat. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. elisabeth.solana@recerca.clinic.cat. Imaging of Mood- and Anxiety-Related Disorders Group, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, and CIBERSAM, Barcelona, Spain. Imaging of Mood- and Anxiety-Related Disorders Group, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, and CIBERSAM, Barcelona, Spain. Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Early Psychosis Interventions and Clinical-Detection (EPIC) Lab, Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. E-Health Center, Universitat Oberta de Catalunya, Barcelona, Spain. Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, UK. Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Department of Neurology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile, Chile. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Calle Villarroel 170, 08036, Barcelona, Spain.
 From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. ant.gavoille@gmail.com. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France. From the Service de Neurologie (A.G., F.R., R.C., S.V.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Université de Lyon (A.G., M.R., F.S.), Université Claude Bernard Lyon 1, CNRS, Laboratoire de Biométrie et Biologie Évolutive UMR 5558, Villeurbanne; Service de Biostatistique-Bioinformatique (A.G., M.R., F.S.), Hospices Civils de Lyon; Université de Lyon (F.R., R.C., S.V.), Université Claude Bernard Lyon 1; Observatoire Français de La Sclérose en Plaques (F.R., R.C., S.V.), Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR; EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis (F.R., R.C., S.V.), State-approved Foundation, Bron; Nancy University Hospital (M.D.), Department of Neurology, Université de Lorraine, APEMAC; CHU Pontchaillou (E.L.P.), CIC1414 INSERM, Rennes; CHU de Toulouse (J.C.), Hôpital Pierre-Paul Riquet, Department of Neurology, CRC-SEP, Toulouse; Infinity (J.C.), INSERM UMR1291-CNRS UMR5051, Université Toulouse III; CHU de Strasbourg (J.D.S.), Department of Neurology and Clinical Investigation Center, CIC 1434, INSERM 1434; Univ. Bordeaux (A.R.), F-33000 Bordeaux INSERM U1215, Neurocentre Magendie, F-33000 Bordeaux CHU de Bordeaux, Department of Neurology, CIC Bordeaux CIC1401; Département de Neurologie (E.M.), Hôpital Pitié-Salpêtrière, APHP, Paris; Centre de Ressources et de Compétences SEP Paris (E.M.); CHU de Montpellier (P.L.), MS Unit; University of Montpellier (MUSE) (P.L.); CHU Lille (H.Z.), CRCSEP Lille, Univ Lille, U1172; Fondation Rotschild (C. Papeix), Department of Neurology, Paris; CHU de Caen (G.D.), MS Expert Centre, Department of Neurology, Avenue de La Côte-de-Nacre, Normandy University, Caen; Neurology (C.L.-F.), UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice; CHU de Dijon (T.M.), Department of Neurology, EA4184; CHU de Nantes (D.A.L.), Service de Neurologie & CIC015 INSERM; CRTI-Inserm U1064 (D.A.L.), Nantes; CHU de Besançon (E.B.), Service de Neurologie; Sorbonne Universités (B.S.), UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de La Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital; CHU Clermont-Ferrand (Pierre Clavelou), Department of Neurology, F-63000 Clermont-Ferrand Université Clermont Auvergne, Inserm, Neuro-Dol, F-63000 Clermont-Ferrand; Department of Neurology (E.T.), Nimes University Hospital; Institut de Génomique Fonctionnelle (E.T.), UMR5203, INSERM 1191, Univ. Montpellier; Hôpital de Poissy (O.H.), Department of Neurology; Aix Marseille Univ (J.P.), APHM, Hôpital de La Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; CHU d'Amiens (A.A.K.), Department of Neurology; CHU Grenoble Alpes (O.C.), Department of Neurology, La Tronche/Grenoble; CHU de Rouen (B.B.), Department of Neurology; CHU de La Martinique (Philippe Cabre), Department of Neurology, Fort-de-France; APHP (A.W.), Hôpital Henri Mondor, Department of Neurology, Créteil; CHU de Limoges (L.M.), Hôpital Dupuytren, Department of Neurology; CHU de Saint-Étienne (J.-P.C.), Hôpital Nord, Department of Neurology; CHU de Tours (A.M.), Hôpital Bretonneau, CRC SEP and Department of Neurology; CHU de Reims (S.M.), CRC-SEP, Department of Neurology; Hôpital Sud Francilien (N.H.B.), Department of Neurology, Corbeil Essonnes; CHU Bicêtre (D.D.B.), Department of Neurology, Le Kremlin Bicêtre; Department of Neurology (K.H.), Hôpital Pierre Delafontaine, Centre Hospitalier de Saint-Denis; CHU La Milétrie (J.-P.N.), Hôpital Jean Bernard, Department of Neurology, Poitiers; CH de Pontoise (C. Pottier), Hôpital René Dubos, Department of Neurology; and Centre Hospitalier de Versailles (C.N.), Department of Neurology, F-78150 Le Chesnay, France.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Swedish National Transport Research Institute, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Occupational Therapy and Physical Therapy, Sahlgrenska University Hospital, Gothenburg, Sweden.
 Johns Hopkins Home Care Group, Baltimore, MD, USA. Northwestern Medicine, Chicago, IL, USA. Johns Hopkins Home Care Group, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Johns Hopkins Home Care Group, Baltimore, MD, USA. Johns Hopkins Home Care Group, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: snewsom2@jhmi.edu.

 From the Universitair Ziekenhuis Brussel (UZ Brussel) (G.P., G.N., M.D.), Department of Neurology, Belgium; Nationaal Multiple Sclerose Centrum (NMSC) (G.P., A.V.R., M.D.), Melsbroek, Belgium; Vrije Universiteit Brussel (VUB) (G.N., J.V.S., M.D.), Center for Neurosciences (C4N), NEUR and AIMS, Brussels, Belgium; Icometrix (G.N.), Leuven, Belgium; and Vrije Universiteit Brussel (VUB) (J.V.S.), Department of Electronics and Informatics (ETRO), Belgium. From the Universitair Ziekenhuis Brussel (UZ Brussel) (G.P., G.N., M.D.), Department of Neurology, Belgium; Nationaal Multiple Sclerose Centrum (NMSC) (G.P., A.V.R., M.D.), Melsbroek, Belgium; Vrije Universiteit Brussel (VUB) (G.N., J.V.S., M.D.), Center for Neurosciences (C4N), NEUR and AIMS, Brussels, Belgium; Icometrix (G.N.), Leuven, Belgium; and Vrije Universiteit Brussel (VUB) (J.V.S.), Department of Electronics and Informatics (ETRO), Belgium. From the Universitair Ziekenhuis Brussel (UZ Brussel) (G.P., G.N., M.D.), Department of Neurology, Belgium; Nationaal Multiple Sclerose Centrum (NMSC) (G.P., A.V.R., M.D.), Melsbroek, Belgium; Vrije Universiteit Brussel (VUB) (G.N., J.V.S., M.D.), Center for Neurosciences (C4N), NEUR and AIMS, Brussels, Belgium; Icometrix (G.N.), Leuven, Belgium; and Vrije Universiteit Brussel (VUB) (J.V.S.), Department of Electronics and Informatics (ETRO), Belgium. From the Universitair Ziekenhuis Brussel (UZ Brussel) (G.P., G.N., M.D.), Department of Neurology, Belgium; Nationaal Multiple Sclerose Centrum (NMSC) (G.P., A.V.R., M.D.), Melsbroek, Belgium; Vrije Universiteit Brussel (VUB) (G.N., J.V.S., M.D.), Center for Neurosciences (C4N), NEUR and AIMS, Brussels, Belgium; Icometrix (G.N.), Leuven, Belgium; and Vrije Universiteit Brussel (VUB) (J.V.S.), Department of Electronics and Informatics (ETRO), Belgium. From the Universitair Ziekenhuis Brussel (UZ Brussel) (G.P., G.N., M.D.), Department of Neurology, Belgium; Nationaal Multiple Sclerose Centrum (NMSC) (G.P., A.V.R., M.D.), Melsbroek, Belgium; Vrije Universiteit Brussel (VUB) (G.N., J.V.S., M.D.), Center for Neurosciences (C4N), NEUR and AIMS, Brussels, Belgium; Icometrix (G.N.), Leuven, Belgium; and Vrije Universiteit Brussel (VUB) (J.V.S.), Department of Electronics and Informatics (ETRO), Belgium. miguel.dhaeseleer@uzbrussel.be.
 Serviço de Neurologia, Departamento de Neurociências e Saúde Mental, Hospital Santa Maria/CHULN. Serviço de Neurologia, Centro Hospitalar Universitário de Lisboa Central, E.P.E., Lisboa. Serviço de Neurologia, Centro Hospitalar de Setúbal E.P.E., Setúbal. Serviço de Neurologia, Hospital Prof. Doutor Fernando Fonseca, Amadora, Portugal, Universidade do Porto. Serviço de Neurologia, Centro Hospitalar Universitário de Lisboa Central, E.P.E., Lisboa. Serviço de Neurologia, Centro Hospitalar Universitário de Lisboa Central, E.P.E., Lisboa. Serviço de Neurologia, Hospital Prof. Doutor Fernando Fonseca, Amadora, Portugal, Universidade do Porto. Serviço de Neurologia, Hospital Prof. Doutor Fernando Fonseca, Amadora, Portugal, Universidade do Porto. Serviço de Neurologia, Centro Hospitalar Universitário de Lisboa Central, E.P.E., Lisboa. Serviço de Neurologia, Departamento de Neurociências e Saúde Mental, Hospital Santa Maria/CHULN.
 Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Proteomic Unit, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. Immuno-rheumatology Research Laboratory, Rheumatology Department, Research - IdiPAZ (La Paz University Hospital - Universidad Autónoma de Madrid), Madrid, Spain. Chronic Disease Programme, UFIEC, Instituto de Salud Carlos III, Madrid, Spain. Chronic Disease Programme, UFIEC, Instituto de Salud Carlos III, Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Electronic address: mgutierrezfernandez@salud.madrid.org. Neurological Sciences and Cerebrovascular Research Laboratory, Department of Neurology, Neurology and Cerebrovascular Disease Group, Neuroscience Area of Hospital La Paz Institute for Health Research - IdiPAZ (La Paz University Hospital- Universidad Autónoma de Madrid), Madrid, Spain. Electronic address: laura.otero@salud.madrid.org.
 Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran. Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran. Thalassemia Research Center (TRC), Hemoglobinopathy Institute, Department of Research, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Neurology Department, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
 Department of Rehabilitation and Movement Science, University of Vermont, Burlington, USA. Department of Rehabilitation and Movement Science, University of Vermont, Burlington, USA. Electronic address: Susan.Kasser@med.uvm.edu.
 Institut du Cerveau et de la Moelle Épinière (ICM), Centre National de la Recherche Scientifique (CNRS), Hôpital Pitié Salpêtrière, Paris, France. Département d'Études Cognitives, École Normale Supérieure, Université Paris Sciences et Lettres (PSL University), Paris, France. Translational Neuromodeling Unit (TNU), Institute for Biomedical Engineering, University of Zurich and ETH, Zurich, Switzerland. Translational Neuromodeling Unit (TNU), Institute for Biomedical Engineering, University of Zurich and ETH, Zurich, Switzerland. Wellcome Centre for Human Neuroimaging, University College London, London, UK. Department of Experimental Psychology, University College London, London, UK. Max Planck UCL Centre for Computational Psychiatry and Ageing Research, University College London, London, UK. Translational Neuromodeling Unit (TNU), Institute for Biomedical Engineering, University of Zurich and ETH, Zurich, Switzerland. Max Planck Institute for Metabolism Research, Cologne, Germany. Department of Neurology, Schulthess Clinic, Zurich, Switzerland. Department of Health Sciences and Technology, ETH, Zurich, Switzerland.
 School of Biomedical Engineering, Shanghai Jiao Tong University, China; Department of Nuclear Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. School of Biomedical Engineering, Shanghai Jiao Tong University, China; College of Medical Imaging, Shanghai University of Medicine and Health Sciences, China. Department of Neurology and Institute of Neurology, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. Department of Nuclear Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. Department of Nuclear Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. School of Biomedical Engineering, Shanghai Jiao Tong University, China. School of Biomedical Engineering, Shanghai Jiao Tong University, China; Department of Nuclear Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. School of Biomedical Engineering, Shanghai Jiao Tong University, China. School of Biomedical Engineering, Shanghai Jiao Tong University, China. School of Biomedical Engineering, Shanghai Jiao Tong University, China. Department of Nuclear Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. Electronic address: lb10363@rjh.com.cn. Department of Neurology and Institute of Neurology, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China; Co-innovation Center of Neuroregeneration, Nantong University, China. Electronic address: mztcs@163.com. Department of Nuclear Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, China. Electronic address: zm11518@rjh.com.cn.
 Student Research Committee, School of Public Health, Shahroud University of Medical Sciences, Shahroud, Iran; Department of Epidemiology, School of Public Health, Shahroud University of Medical Sciences, Shahroud, Iran. Department of Epidemiology, School of Public Health, Shahroud University of Medical Sciences, Shahroud, Iran. Deputy of Curative Affairs, Shahroud university of medical science, Shahroud, Iran. Department of Epidemiology, School of Public Health, Shahroud University of Medical Sciences, Shahroud, Iran. Electronic address: hoseinzade@shmu.ac.ir.
 Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. novotna.klara.k@gmail.com. MS Rehab Z.S., Prague, Czech Republic. novotna.klara.k@gmail.com. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. 2nd Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital in Prague, Katerinska 30, 120 00, Prague, Czech Republic.
 Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Stockholm, Sweden jing.wu@ki.se. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Centre for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Universidade Federal do Rio de Janeiro, Departamento de Radiologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Radiologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Radiologia, Rio de Janeiro RJ, Brazil. Universidade Estadual do Rio de Janeiro, Departamento de Farmacologia e Psicobiologia, Rio de Janeiro RJ, Brazil. Rede Dor, São Luiz, Rio de Janeiro RJ, Brazil. Universidade Federal Fluminense, Departamento de Radiologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Neurologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Neurologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Neurologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Radiologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Departamento de Neurologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Laboratório de Neurociências Translacional. Soniza Vieira Alves-Leon, Rio de Janeiro RJ, Brazil.
 Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Department of Internal Medicine, Hospital Alemán, Buenos Aires, Argentina. Neurology Department, Hospital J.M. Ramos Mejía, University of Buenos Aires, Buenos Aires, Argentina. Neurology Department, Hospital J.M. Ramos Mejía, University of Buenos Aires, Buenos Aires, Argentina/Sección Enfermedades Desmielinizantes, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Instituto de Neurociencias de Rosario, Santa Fe, Argentina. Neurology Department, Hospital Carlos Andrade Marin, Universidad Central del Ecuador, Quito, Ecuador. Clínica Alemana de Santiago, Santiago, Chile; Universidad del Desarrollo, Santiago, Chile. Clínica Enfermedad Desmielinizante, Clinica Universitaria Colombia, Bogotá, Colombia. Neurology Department, Hospital Universitario de Maracaibo, Maracaibo, Venezuela. Centro Nacional de Esclerosis Multiple, Asuncion, Paraguay. Hospital Santo Tomas, Universidad Interamericana de Panamá, Panama City, Panamá. Neuroimmunology Section, Department of Neurology, Hospital de Clínicas "José de San Martín," Buenos Aires, Argentina. Department of Neurology, University of Virginia, Charlottesville, VA, USA. Centro de Esclerosis Múltiple de Buenos Aires (CEMBA), Buenos Aires, Argentina.
 Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain. Department of Physical Therapy, University of Murcia, Murcia, Spain. Facultad de Fisioterapia y Enfermería, Universidad de Castilla-La Mancha, Toledo, Spain. Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain. Facultad de Enfermería de Cuenca, Universidad de Castilla-La Mancha, Cuenca, Spain. Universidad Politécnica y Artística del Paraguay, Asunción, Paraguay. Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain. Facultad de Enfermería de Cuenca, Universidad de Castilla-La Mancha, Cuenca, Spain. Rehabilitation in Health Research Center (CIRES), Universidad de las Americas, Santiago, Chile. Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain. Facultad de Fisioterapia y Enfermería, Universidad de Castilla-La Mancha, Toledo, Spain. Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain. School of Education, Universidad de Castilla-La Mancha, Ciudad Real, Spain. Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain. Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Talca, Chile.
 MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Vrije Universiteit Amsterdam, PO Box 7057, Amsterdam, 1007 MB, the Netherlands. Electronic address: i.nauta1@amsterdamumc.nl. Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands; Klimmendaal Rehabilitation Center, Arnhem, the Netherlands. Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands; Klimmendaal Rehabilitation Center, Arnhem, the Netherlands. Alzheimer Center Amsterdam, Neurology, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Vrije Universiteit Amsterdam, PO Box 7057, Amsterdam, 1007 MB, the Netherlands. Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands; Klimmendaal Rehabilitation Center, Arnhem, the Netherlands; Department of Medical Psychology, Radboud University Medical Center, Nijmegen, the Netherlands; Vincent van Gogh Institute for Psychiatry, Venray, the Netherlands. Department of Psychiatry, Radboud University Medical Center, Nijmegen, the Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Vrije Universiteit Amsterdam, PO Box 7057, Amsterdam, 1007 MB, the Netherlands.
 Service neurologie, centre hospitalier universitaire de Rennes, 2 rue Henri-le-Guilloux, 35000 Rennes, France; Association Neuro-Bretagne, centre hospitalier universitaire de Rennes, 2 rue Henri-le-Guilloux, 35000 Rennes, France. Electronic address: marie.guillet@chu-rennes.fr.
 Neuroimaging Laboratory, Department of Neurology, University of Campinas, Campinas, São Paulo, Brazil; Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), University of Campinas, Campinas, São Paulo, Brazil. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany; Biomedical Center (BMC), Medical Faculty, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany; Biomedical Center (BMC), Medical Faculty, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany; Biomedical Center (BMC), Medical Faculty, Ludwig-Maximilians-Universität München, Martinsried, Germany. Electronic address: edgar.meinl@med.uni-muenchen.de.
 Lower Merion High School, Ardmore, PA, USA; Department of Genetics, Franklin College of Arts and Sciences, University of Georgia, Athens, GA, USA. Department of Genetics, Franklin College of Arts and Sciences, University of Georgia, Athens, GA, USA. Department of Genetics, Franklin College of Arts and Sciences, University of Georgia, Athens, GA, USA; Sunny Hills High School, Fullerton, CA, USA. Department of Medicine, University of Connecticut Health Center, Farmington, CT, USA. Department of Genetics, Franklin College of Arts and Sciences, University of Georgia, Athens, GA, USA; Institute of Bioinformatics, University of Georgia, Athens, GA, USA. Electronic address: Kaixiong.Ye@uga.edu.
 Research Department, Abreos Biosciences, LA Jolla, California.
 Department of Medical Parasitology and Mycology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Medical Parasitology and Mycology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Anatomy Department, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Medical Parasitology and Mycology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Medical Parasitology and Mycology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Electronic address: a.h.maghsood@umsha.ac.ir.
 Department of Neurology, Military Institute of Medicine, Warsaw, Poland. astepien@wim.mil.pl. Department of Neurology, Military Institute of Medicine, Warsaw, Poland. Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. Department of Neurology, Jagiellonian University Medical College, Krakow, Poland. Department of Neurology, Upper-Silesian Medical Center of the Silesian Medical University, Katowice, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Zabrze, Poland. Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland. Department of Neurology, SPZOZ MSWiA, Poznan, Poland. Department of Neurology, Medical University of Lublin, Lublin, Poland. Department of Neurology, University of Rzeszow, Rzeszow, Poland. Department of Neurology, Medical University of Lublin, Lublin, Poland.
 Brain Rehabilitation Research Center, Malcom Randall VA Medical Center, Gainesville, FL 32608, USA. Department of Neurology, University of Florida, Gainesville, FL 32608, USA. Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80521, USA. Molecular, Cellular, and Integrative Neuroscience Program, Colorado State University, Fort Collins, CO 80521, USA.
 Institute of Biochemistry and Molecular Biology, Faculty of Medicine, University of Bonn, Bonn, Germany. Institute of Biochemistry and Molecular Biology, Faculty of Medicine, University of Bonn, Bonn, Germany. Institute of Biochemistry and Molecular Biology, Faculty of Medicine, University of Bonn, Bonn, Germany. thbecker@uni-bonn.de.
 Department of Health Sciences, University of Genoa, Building 3, L.Go R. Benzi, 10-16132, Genoa, Italy. bruno.kusznir.vitturi@edu.unige.it. Department of Health Sciences, University of Genoa, Building 3, L.Go R. Benzi, 10-16132, Genoa, Italy. Department of Health Sciences, University of Genoa, Building 3, L.Go R. Benzi, 10-16132, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Occupational Medicine Unit, Genoa, Italy. Department of Health Sciences, University of Genoa, Building 3, L.Go R. Benzi, 10-16132, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Occupational Medicine Unit, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Occupational Medicine Unit, Genoa, Italy. Italian Multiple Sclerosis Association (AISM), Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. Department of Life Sciences, University of Siena, Siena, Italy. Italian Multiple Sclerosis Association (AISM), Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DiNOGMI) and Center of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Neurology Unit, Genoa, Italy. Italian Workers' Compensation Authority (INAIL), Rome, Italy. Department of Health Sciences, University of Genoa, Building 3, L.Go R. Benzi, 10-16132, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Occupational Medicine Unit, Genoa, Italy.
 From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. Edgar.Meinl@med.uni-muenchen.de Simone.Mader@med.uni-muenchen.de. From the Institute of Clinical Neuroimmunology (S.H., E.O., H.K.W., A.V., I.M., F.T., T.K., E.M., S.M.), Biomedical Center and University Hospitals, Ludwig-Maximilians-Universität München; Graduate School of Systemic Neurosciences (S.H.), Ludwig-Maximilians-Universität München, Germany; Department of Neurology (A.V.), Koc University School of Medicine; Department of Neuroscience (V.Y., E.T.), Aziz Sancar Institute of Experimental Medicine, Istanbul University; Department of Neurology (R.T.), Haydarpasa Numune Education and Research Hospital, Istanbul, Türkiye; Core Facility Bioinformatics (T.S.), Biomedical Center, Ludwig-Maximilians-Universität München, Germany; Munich Cluster for Systems Neurology (SyNergy) (F.T.), Germany. Edgar.Meinl@med.uni-muenchen.de Simone.Mader@med.uni-muenchen.de.
 Hospital Regional Universitario de Málaga, Málaga, España. Hospital Universitari Vall d'Hebron-CEMCAT, Barcelona, España. Hospital Universitario Reina Sofía, Madrid, España. Hospital Universitario de Getafe, 28905 Getafe, España. Hospital Regional Universitario de Málaga, Málaga, España. Hospital Universitario Quirónsalud, Madrid, España. Hospital Universitari Arnau de Vilanova-Universitat de Lleida, Lleida, España. Hospital Universitari Son Espases, Palma de Mallorca, España. Hospital Universitario Ramón y Cajal, Madrid, España. Hospital Universitario Virgen Macarena, 41003 Sevilla, España. Hospital Universitario Gregorio Marañón, Madrid, España. Hospital Nuestra Señora de Candelaria, Santa Cruz de Tenerife, España. Hospital Universitario Doctor Peset, Valencia, España. Complejo Hospitalario Universitario de Ferrol, Ferrol, España. Hospital Clínic de Barcelona-IDIBAPS, Barcelona, España. Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, España. Hospital Universitario de La Princesa, 28006 Madrid, España. Hospital Universitari Vall d'Hebron-CEMCAT, Barcelona, España. Hospital Sant Joan Despí Moisés Broggi, Sant Joan Despí, España. Hospital Clínico San Carlos-IDISSC-UCM, Madrid, España. Universitat de Girona, Girona, España. Hospital Universitari de Girona Dr. Josep Trueta-IDIBGI, Girona, España. Hospital de Santa Caterina, Girona, España. Hospital Clínico Universitario de Valladolid, Valladolid, España. Hospital Universitari de Bellvitge-IDIBELL, L´Hospitalet de Ll., España. Hospital Universitario Cruces, Bilbao, España.
 Service pathologies professionnelles et environnementales-Maintien dans l'emploi, Centre hospitalier universitaire de Lille, 1 avenue Oscar-Lambret, 59000 Lille, France; Centre de recherche droits et perspectives du droit, EA 4487, Université de Lille, 1 place Déliot, 59000 Lille, France. Electronic address: fanquin@wanadoo.fr.
 Department of Rehabilitation and Australian Rehabilitation Research Centre, Royal Melbourne Hospital, Parkville, VIC, Australia. Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Parkville, VIC, Australia. Department of Clinical Haematology, The Royal Melbourne Hospital and Peter MacCallum Cancer Centre, Parkville, VIC, Australia. Department of Rehabilitation and Australian Rehabilitation Research Centre, Royal Melbourne Hospital, Parkville, VIC, Australia. Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Parkville, VIC, Australia. Department of Clinical Haematology, The Royal Melbourne Hospital and Peter MacCallum Cancer Centre, Parkville, VIC, Australia.
 Department of Neurology, Obihiro Kosei General Hospital, Obihiro, Japan. Department of Neurology, Obihiro Kosei General Hospital, Obihiro, Japan. Departmentof Neurology, Hokuto Hospital, Obihiro, Hokkaido, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan. Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Sapporo, Japan niino.masaaki.tc@mail.hosp.go.jp.
 c/o Soins, 65 avenue Camille-Desmoulins, 92442 Issy-les-Moulineaux cedex, France. Electronic address: soins@elsevier.com.
 Department of NEUROFARBA, University of Florence, Florence, Italy. Department of Health Sciences, Section of Biostatistics, University of Genova, Genova, Italy. Department of NEUROFARBA, University of Florence, Florence, Italy. Department of NEUROFARBA, University of Florence, Florence, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genova, Italy/Department of Life Sciences, University of Siena, Siena, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy. Italian Multiple Sclerosis Society Foundation, Genova, Italy. Kocaeli University School of Medicine, Kocaeli, Kocaeli, Turkey. The Multiple Sclerosis Centre, Department of Neurosciences, Biomedicine and Movement, University Hospital of Verona, Verona, Italy. Department of Neurology, Santa Croce and Carle Hospital, Cuneo, Italy. MS Center, Department of Neuroscience, City of Health and Science, University Hospital of Turin, Turin, Italy. Servizio Malattie Demielinizzanti, SC di Neurofisiopatologia, AO di Perugia, Perugia, UK. Clinical and Biological Sciences Department, University of Turin, Turin, Italy. Centro Sclerosi Multipla Ospedale Binaghi, Cagliari, Italy. Università Vita-Salute San Raffaele, Milan, Italy. Multiple Sclerosis Centre, IRCCS Foundation "Carlo Besta" Neurological Institute, Milan, Italy. Department of Human Neurosciences, Sapienza, University of Rome, Rome, Italy/IRCCS Neuromed, Pozzilli (IS), Department of Human Neuroscience, Sapienza University, Rome, Italy. Centro Sclerosi Multipla ASST Spedali Civili di Brescia, Montichiari, Italy/MS Centre, Neurology Unit, SS. Annunziata University Hospital, Chieti, Italy. MS Centre, Neurology Unit, SS. Annunziata University Hospital, Chieti, Italy. Centro Sclerosi Multipla ASST Spedali Civili di Brescia, Montichiari, Italy/MS Centre, Neurology Unit, SS. Annunziata University Hospital, Chieti, Italy. Neurology Unit and MS Center, Neurorehabilitation Unit and Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. Selcuk University School of Medicine, Konya, Turkey. Emergency Department, Neurology Unit, G. da Saliceto Hospital, Piacenza, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Genova, Italy/IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Hacettepe University School of Medicine, Ankara, Turkey. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy/Neurology Unit, Michele e Pietro Ferrero Hospital, Verduno, Italy. Neurology Unit, Michele e Pietro Ferrero Hospital, Verduno, Italy. Centro Sclerosi Multipla Ospedale Binaghi, Cagliari, Italy. UOC Neurologia-Stroke Unit, Presidio "A. Manzoni," ASST Lecco, Italy/Department of Neurology, Ospedale Santa Chiara, Trento, Italy. Department of Systems Medicine, Multiple Sclerosis Clinical & Research Center, "Tor Vergata" University, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Department of NEUROFARBA, University of Florence, Florence, Italy. SC Neurologia 1, Ospedale Maria Vittoria, Torino, Italy. Department of Neurology and Multiple Sclerosis Center, ASST Papa Giovanni XXIII, Bergamo, Italy. Neurology Unit, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Centro Regionale Sclerosi Multipla, Dipartimento di Neuroscienze, Azienda Ospedale Università di Padova, Padova, Italy. Multiple Sclerosis Center, UO Neurology, Fidenza, Fidenza, Italy. UOC Neurologia, ASUR Marche, Fermo, Italy. Centro Regionale Sclerosi Multipla, Dipartimento di Neuroscienze, Azienda Ospedale Università di Padova, Padova, Italy. Centro Sclerosi Multipla Ospedale Binaghi, Cagliari, Italy. IRCCS Neuromed, Pozzilli (IS), Department of Human Neuroscience, Sapienza University, Rome, Italy/Neurology Unit, Department of Neurosciences, Mental Health and Sensory Organs (NESMOS), Sapienza University of Rome, Rome, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital, ASUGI, University of Trieste, Trieste, Italy. IRCCS Institute of Neurological Sciences, UOSI Multiple Sclerosis Rehabilitation, Bologna, Italy. Ondokuz Mayis University School of Medicine, Samsun, Turkey. Cerrahpasa School of Medicine, Istanbul University, Istanbul, Istanbul, Turkey. UOC di Neurologia, Ospedale Morgagni-Pierantoni, Forlì, Italy. Multiple Sclerosis Outpatient Clinic, Clinical Neurology and Stroke Unit, Central Country Hospital, Bolzano, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli," Naples, Italy. Department of Basic Medical Sciences, Neurosciences, and Sense Organs, University of Bari, Bari, Italy. Cerrahpasa School of Medicine, Istanbul University, Istanbul, Istanbul, Turkey. Department of Neuroscience, Città della Salute e della Scienza University Hospital, Turin, Italy. Department of Health Sciences, Section of Biostatistics, University of Genova, Genova, Italy/IRCCS Ospedale Policlinico San Martino, Genova, Italy. Department of NEUROFARBA, University of Florence, Florence, Italy/IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy.
 Department of Performance and Health (Sports Medicine), Institute of Sport and Sport Science, TU Dortmund University, Otto-Hahn-Straße 3, 44227, Dortmund, Germany. Department of Performance and Health (Sports Medicine), Institute of Sport and Sport Science, TU Dortmund University, Otto-Hahn-Straße 3, 44227, Dortmund, Germany. Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke gGmbH, Milchberg 21, 82335, Berg, Germany. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317, Valens, Switzerland. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317, Valens, Switzerland. Department of Health, OST - Eastern Switzerland University of Applied Sciences, Rosenbergstrasse 59, 9001, Sankt Gallen, Switzerland. Department of Performance and Health (Sports Medicine), Institute of Sport and Sport Science, TU Dortmund University, Otto-Hahn-Straße 3, 44227, Dortmund, Germany. philipp.zimmer@tu-dortmund.de.
 Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Dept. of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Dept. of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. Dept. of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Dept. of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Dept. of Neuroradiology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. mark.muehlau@tum.de. TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Munich, Germany. mark.muehlau@tum.de.
 Department of Preventive Medicine and Epidemiology, Vall d'Hebron Barcelona Hospital, Barcelona, Spain Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital, Barcelona, Spain. CRC-SEP Nice, CHU de Nice, Universite Nice Cote d'Azur UR2CA-URRIS, Nice, France. Fundación Santa Fe de Bogotá, Bogotá, Colombia School of Medicine, Universidad de los Andes, Bogotá, Colombia Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Department NEUROFARBA, University of Florence, Florence, Italy IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Department of Preventive Medicine and Epidemiology, Vall d'Hebron Barcelona Hospital, Barcelona, Spain. Centro para la Investigación de Enfermedades Neuroinmunológicas (CIEN), FLENI, Buenos Aires, Argentina. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy Neurology Unit, Neurorehabilitation Unit, and Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy Vita-Salute San Raffaele University, Milan, Italy. Department of Paediatric Neurology, Great Ormond Street Hospital for Children, London, UK Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, London, UK. Department of Neurology, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Multiple Sclerosis International Federation, London, UK. Department of Neurology, Danish Multiple Sclerosis Center and the Danish Multiple Sclerosis Registry, Rigshospitalet and University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Hospital Clínico San Carlos, IdISSC, Departamento de Medicina, Universidad Complutense, Madrid, Spain. Department of Neurology, School of Medicine, Istanbul University Cerrahpasa, Cerrahpasa, Istanbul, Turkey. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Centre des Neurosciences de Lyon, Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR5292, Lyon, France Université Claude Bernard Lyon 1, Faculté de Médecine Lyon Est, Lyon, France. Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital, Barcelona, Spain.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Statistics, Faculty of Economics and Statistics, University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Centre d'Esclerosi Múltiple de Catalunya, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autónoma de Barcelona, Barcelona, Spain. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Laboratory of Hematology, Sheba Medical Center, Ramat Gan, Israel. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Laboratory Medicine and Pathology and Department of Neurology, Mayo Clinic, Rochester, MN, USA. Neurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Vrije Universiteit, Amsterdam UMC, Amsterdam, The Netherlands. CSF Laboratory, Department of Neurology, University of Ulm, Ulm, Germany. Immunology Department, Hospital Universitario Ramón y Cajal, Madrid, Spain. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden/Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden/Department of Neurodegenerative Disease, Queen Square Institute of Neurology, University College London, London, UK/UK Dementia Research Institute, University College London, London, UK/Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
 Specialty Pharmacy Services, Vanderbilt University Medical Center, 726 Melrose Ave, Nashville, TN 37211, United States. Electronic address: Autumn.zuckerman@vumc.org. Department of Biostatistics, Vanderbilt University Medical Center, United States. Fairview Specialty Pharmacy, 711 Kasota Ave SE, Minneapolis, MN 55414, United States. Fairview Pharmacy Services, 711 Kasota Ave SE, Minneapolis, MN 55414, United States. WVU Medicine Specialty Pharmacy Services, Allied Health Solutions, 3040 University Ave Suite 1400, Morgantown, WV 26505, United States. Specialty Pharmacy Services, Vanderbilt University Medical Center, 726 Melrose Ave, Nashville, TN 37211, United States. University of Rochester Specialty Pharmacy, UR Medicine, 601 Elmwood Ave, Rochester NY 14642, United States. University of Rochester Specialty Pharmacy, UR Medicine, 601 Elmwood Ave, Rochester NY 14642, United States. WVU Medicine Specialty Pharmacy Services, Allied Health Solutions, 3040 University Ave Suite 1400, Morgantown, WV 26505, United States. Department of Biostatistics, Vanderbilt University Medical Center, United States.
 Department of Histology, Jagiellonian University Medical College, Krakow, Poland. Department of Histology, Jagiellonian University Medical College, Krakow, Poland. Department of Histology, Jagiellonian University Medical College, Krakow, Poland.
 Department of Neurology, Massachusetts General Hospital, Boston, USA; Department of Neurology, Brigham and Women's Hospital, Boston, USA; Harvard Medical School, Boston, MA, USA. Department of Neurology, Massachusetts General Hospital, Boston, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA; Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA; Harvard Medical School, Boston, MA, USA. Department of Neurology, Massachusetts General Hospital, Boston, USA; Harvard Medical School, Boston, MA, USA. Electronic address: fmateen@mgh.harvard.edu.
 First Department of Neurology, School of Medicine, National Kapodistrian University of Athens, Athens, Greece. Eginiteion Hospital, Athens, Greece. First Department of Neurology, School of Medicine, National Kapodistrian University of Athens, Athens, Greece. First Department of Neurology, School of Medicine, National Kapodistrian University of Athens, Athens, Greece. Eginiteion Hospital, Athens, Greece. First Department of Neurology, School of Medicine, National Kapodistrian University of Athens, Athens, Greece. Eginiteion Hospital, Athens, Greece.
 Unit of Neuroepidemiology, Fondazione IRRCS Istituto Neurologico Carlo Besta, Via Celoria 11, Milan, 20133, Italy. Department of Psychology, University of Turin, Turin, Italy. Department of Human and Social Sciences, University of Aosta Valley, Aosta, Italy. Department of Biomedical and Clinical Sciences, Università di Milano, Milan, Italy. Department of Territorial Activities, Azienda Sanitaria Provinciale, Health District, Catania, Italy. Neurology Unit & Regional Referral Multiple Sclerosis Centre (CReSM), University Hospital San Luigi Gonzaga, Orbassano, Italy. Department of Neuroscience, San Camillo-Forlanini Hospital, Rome, Italy. Department of Neurosciences, Imaging and Clinical Sciences, University G. d'Annunzio, Chieti, Italy. Psychological Service - Neurological and Neurological Rehabilitation Units, IRCCS San Raffaele, Milan, Italy. Laboratory of Clinical Neuropsychology, Psychology Unit, ASST Lariana, Como, Italy. IRCCS Don Gnocchi Foundation, Florence, Italy. Multiple Sclerosis Center, Neurology Unit, Hospital of Vaio, Fidenza, Italy. Azienda Sanitaria Locale, ASL-BA, Bari, Italy. Multiple Sclerosis Center, Unit of Neuroimmunology and Neuromuscular Diseases, Fondazione IRRCS Istituto Neurologico Carlo Besta, Milan, Italy. Unit of Neuroepidemiology, Fondazione IRRCS Istituto Neurologico Carlo Besta, Via Celoria 11, Milan, 20133, Italy. Multiple Sclerosis Center, Unit of Neuroimmunology and Neuromuscular Diseases, Fondazione IRRCS Istituto Neurologico Carlo Besta, Milan, Italy. Department of Medical Science and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Center, ASL Cagliari, ATS Sardegna, Cagliari, Italy. Multiple Sclerosis Unit, IRCCS S. Lucia Foundation, Rome, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. UOC Psicologia Ospedaliera, AUSL di Bologna, Bologna, Italy. Department of Clinical Sciences and Translational Medicine, University of Rome "Tor Vergata", Rome, Italy. Behavioral Neuropsychology Laboratory, IRCCS S. Lucia Foundation, Rome, Italy. Neurologia ad indirizzo Neuroimmunologico - Centro Sclerosi Multipla, Ospedale di Gallarate - ASST della Valle Olona, Gallarate, Italy. Mathematics and Statistics, La Trobe University, Melbourne, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. Unit of Neuroepidemiology, Fondazione IRRCS Istituto Neurologico Carlo Besta, Via Celoria 11, Milan, 20133, Italy. alessandra.solari@istituto-besta.it. Department of Psychology, University of Turin, Turin, Italy.
 Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA. Division of Clinical and Translational Sciences, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, USA; Biostatistics/Epidemiology/Research Design (BERD) component, Center for Clinical and Translational Sciences (CCTS), The University of Texas Health Science Center at Houston, Houston, Texas, USA. Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA. Electronic address: john.w.lindsey@uth.tmc.edu.
 Department of Radiology and Nuclear Medicine, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. H.Vrenken@amsterdamumc.nl. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Radiology and Nuclear Medicine, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. Department of Radiology and Nuclear Medicine, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. Department of Radiology, Federal University of Paraná, Curitiba, Paraná, Brazil. Neuroradiology Department, Neurological Institute of Curitiba (INC/CETAC), Curitiba, Paraná, Brazil. Global Biostatistics, Merck Healthcare KGaA, Darmstadt, Germany. Global Medical Affairs, Merck Serono Ltd, (an affiliate of Merck KGaA), Feltham, UK. Department of Health Sciences, University of Genoa and Ospedale Policlinico San Martino IRCCS, Genoa, Italy. Department of Neurology, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. Department of Radiology and Nuclear Medicine, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. Department of Radiology and Nuclear Medicine, Biomedical Imaging Group Rotterdam, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands. Università Vita-Salute San Raffaele, Casa di Cura Privata del Policlinico, Milan, Italy. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB) and Neurology Departments of Head, Spine and Neuromedicine, Biomedical Engineering and Clinical Research, University Hospital, University of Basel, Basel, Switzerland. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Radiology and Nuclear Medicine, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. UCL Institutes of Neurology and Healthcare Engineering, London, UK.
 Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Electronic address: g.giovannoni@qmul.ac.uk. Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. The University of Newcastle, Australia. Massachusetts General Hospital and Harvard Medical School, MA, United States. Department of Paediatrics (Neurology), Hospital for Sick Children, Division of Neuroscience and Mental Health, The Hospital for Sick Children Research Institute University of Toronto, Canada.
 CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. Multiple Sclerosis Unit, Hospital Universitario Virgen Macarena, Sevilla, Andalucía, Spain. Multiple Sclerosis Unit, Hospital Universitario Virgen Macarena, Sevilla, Andalucía, Spain. Neuroscience, Department of Surgical and Medical Sciences and Advanced Technologies 'G.F. Ingrassia', University of Catania, Catania, Italy. Department of Neurology and Centre of Clinical Neuroscience, Charles University First Faculty of Medicine, Praha, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, Charles University First Faculty of Medicine, Praha, Czech Republic. Centre Hospitalier, Université de Montréal, Montreal, Québec, Canada. Department of Neuroscience, Université de Montréal, Montreal, Québec, Canada. Centre Hospitalier, Université de Montréal, Montreal, Québec, Canada. Faculté de Médecine, Université de Montréal, Montreal, Québec, Canada. Centre Hospitalier, Université de Montréal, Montreal, Québec, Canada. Faculté de Médecine, Université de Montréal, Montreal, Québec, Canada. Neuro Rive-Sud, Longueuil, Quebec, Canada. Department of Neurosciences, Imaging and Clinical Sciences, Gabriele d'Annunzio University of Chieti-Pescara, Chieti, Italy. UOSI Riabilitazione Sclerosi Multipla, IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. Centre intégré de santé et de services sociaux de Chaudière-Appalaches du Québec Centre de Recherche, Levis, Québec, Canada. Department of Neurology, Dokuz Eylul University, İzmir, Turkey. Department of Neurological Siences, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Department of Neurology, Zuyderland Medical Centre, Sittard-Geleen, The Netherlands. Neurology Unit, Azienda Ospedaliero-Universitaria of Modena, Modena, Italy. Department of Neuroscience, Azienda Ospedaliero-Universitaria di Modena, Modena, Emilia-Romagna, Italy. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy. Department of Neurology, Box Hill Hospital, Box Hill, Victoria, Australia. Department of Neurology, Box Hill Hospital, Box Hill, Victoria, Australia. School of Medicine and Public Health, The University of Newcastle, Callaghan, New South Wales, Australia. Department of Neurology, John Hunter Hospital, Newcastle, New South Wales, Australia. Department of Medicine, Al-Amiri Hospital, Kuwait City, Kuwait. Department of Neurology, Karadeniz Technical University, Trabzon, Turkey. Department of Neurology, Cliniques Universitaires Saint-Luc, Brussels, Belgium. UOC Neurologia, Azienda Sanitaria Unica Regionale Marche-AV3, Macerata, Italy. Ondokuz Mayis Üniversitesi, Samsun, Turkey. UO Neurologia, Ospedale Garibaldi, Catania, Italy. Department of Neurosciences, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Department of Neurology, American University of Beirut, Beirut, Lebanon. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. American University of Beirut, Beirut, Lebanon. UOC Neurologia e Stroke, AORN San Giuseppe Moscati, Avellino, Italy. Department of Neurology, Centro Hospitalar de São João, Porto, Portugal. Health Sciences Faculty, Fernando Pessoa University, Porto, Portugal. Hospital Clinic de Barcelona, Barcelona, Catalunya, Spain. Multiple Sclerosis Centre, Neurosciences, University of Parma, Parma, Italy. Department of Neurology, Flinders Medical Centre, Adelaide, South Australia, Australia. Department of Neurology, Monash Medical Centre Clayton, Clayton, Victoria, Australia. Department of Neurology, Hopital Razi, La Manouba, Tunisia. Department of Neurology, Razi Hospital, Rasht, Gilan, Iran. Multiple Sclerosis Centre, Neurological Institute C.Mondino, Pavia, Italy. Department of Neurology, Hacettepe University Faculty of Medicine, Ankara, Turkey. Department of Neurology, Nemocnice Jihlava, Jihlava, Czech Republic. Department of Neurology, Hospital Galdakao-Usansolo, Galdacano, País Vasco, Spain. Centre integre de sante et de services sociaux des Laurentides point de service de Saint-Jerome, Saint-Jerome, Quebec, Canada. Department of Neurology, Donostia University Hospital, San Sebastian, Spain. UQCCR, The University of Queensland, Saint Lucia, Queensland, Australia. Department of Neurology, Austin Health, Heidelberg, Victoria, Australia. Department of Neurology, University Hospital Ghent, Gent, Oost-Vlaanderen, Belgium. Department of Neurology, University Hospital Ghent, Gent, Oost-Vlaanderen, Belgium. Division of Neurology, Department of Medicine, St Michael's Hospital, Toronto, Ontario, Canada. Department of Neurology, Koc Universitesi, Istanbul, Turkey. Koç University Research Center for Translational Medicine (KUTTAM), Koç University, Istanbul, Turkey. Department of Neurology, Groene Hart Ziekenhuis, Gouda, Zuid-Holland, The Netherlands. Department of Neurology, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Multiple Sclerosis and Neuroimmunology Unit, Monash University Central Clinical School, Melbourne, Victoria, Australia. Department of Neuroscience, Monash University Central Clinical School, Melbourne, Victoria, Australia. Department of Neurology, The Alfred, Melbourne, Victoria, Australia. Department of Neurology, Westmead Hospital, Westmead, New South Wales, Australia. Brain and Mind Centre, The University of Sydney, Sydney, New South Wales, Australia. Centro de Esclerosis Múltiple de Buenos Aires, Hospital Italiano de Buenos Aires, Buenos Aires, Federal District, Argentina. Department of Neurology, Liverpool Hospital, Liverpool, New South Wales, Australia. Ospedali Riuniti di Salerno, Salerno, Italy. Neurologic Clinic and Policlinic, Departments of Medicine, Biomedicine, and Clinical Research, University Hospital Basel, Basel, Switzerland. Research Centre for Clinical Neuroimmunology and Neuroscience, University Hospital Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, Departments of Medicine, Biomedicine, and Clinical Research, University Hospital Basel, Basel, Switzerland. Research Centre for Clinical Neuroimmunology and Neuroscience, University Hospital Basel, Basel, Switzerland. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, Istanbul, Turkey. Department of Neurology, University at Buffalo Jacobs School of Medicine and Biomedical Sciences, Buffalo, New York, USA. Universitair MS Centrum, Hasselt University, Hasselt-Pelt, Belgium. Rehabilitation & MS Centre, Pelt, Belgium. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia tomas.kalincik@unimelb.edu.au. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia.
 Queen Square Institute of Neurology, University College London, London, UK.
 Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Director and Chief Executive Officer, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Department of Neurology, Neurosciences Institute, Medanta - The Medicity, Gurugram, Haryana, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India. Department of Neurology, Neurosciences Centre, AIIMS, New Delhi, India.
 Institute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075, Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075, Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075, Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075, Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075, Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075, Göttingen, Germany. imetz@gwdg.de.
 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Electronic address: Mostafa.mohammed@pharma.cu.edu.eg.
 Department of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. n_ghasemi@med.mui.ac.ir.
 MS Center and 3T-MRI Research Unit, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Napoli, Italy. Department of Electrical, Electronic, and Information Engineering "Guglielmo Marconi" - DEI, Alma Mater Studiorum - University of Bologna, Bologna, Italy. MS Center and 3T-MRI Research Unit, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Napoli, Italy. Department of Electrical, Electronic, and Information Engineering "Guglielmo Marconi" - DEI, Alma Mater Studiorum - University of Bologna, Bologna, Italy. Alma Mater Research Institute for Human-Centered Artificial Intelligence, University of Bologna, Bologna, Italy. MS Center and 3T-MRI Research Unit, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Napoli, Italy. MS Center and 3T-MRI Research Unit, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Napoli, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", Napoli, Italy. Neuroimaging Research Unit, Division of Neuroscience, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology and Neurophysiology Unit, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology and Neurophysiology Unit, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, Vita-Salute San Raffaele University, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. IRCCS Neuromed, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. MS Center and 3T-MRI Research Unit, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Napoli, Italy. MS Center and 3T-MRI Research Unit, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Napoli, Italy.
 Department of Pediatrics, Centro Hospitalar do Médio Ave, V. N. Famalicão, Portugal. Department of Pediatric Neurology, Centro Materno Infantil do Norte/Centro Hospitalar Universitário do Porto, Porto, Portugal. Department of Neurology, Hospital Santo António/Centro Hospitalar Universitário do Porto, Porto, Portugal. Multidisciplinary Unit for Biomedical Research, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal. Department of Neurology, Hospital Santo António/Centro Hospitalar Universitário do Porto, Porto, Portugal. Multidisciplinary Unit for Biomedical Research, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal. Department of Neurology, Hospital Santo António/Centro Hospitalar Universitário do Porto, Porto, Portugal. Multidisciplinary Unit for Biomedical Research, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal. Department of Pediatric Neurology, Centro Materno Infantil do Norte/Centro Hospitalar Universitário do Porto, Porto, Portugal.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Laboratory of Hematology, Sheba Medical Center, Ramat Gan, Israel. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA/Department of Neurology, Mayo Clinic, Rochester, MN, USA. Neurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Program Neuroinflammation, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. CSF Laboratory, Department of Neurology, University of Ulm, Ulm, Germany. Biostatistics Unit, Department of Immunology, Hospital Universitario Ramón y Cajal, Madrid, Spain. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden/Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden/Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK/UK Dementia Research Institute at UCL, London, UK/Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
 Department of Neuroradiology, Radiology and Neurology, 13704Southern Tohoku Research Institute for Neuroscience, Southern Tohoku General Hospital, Koriyama, Fukushima, Japan. Department of Neuroradiology, Radiology and Neurology, 13704Southern Tohoku Research Institute for Neuroscience, Southern Tohoku General Hospital, Koriyama, Fukushima, Japan. Department of Neuroradiology, Radiology and Neurology, 13704Southern Tohoku Research Institute for Neuroscience, Southern Tohoku General Hospital, Koriyama, Fukushima, Japan. Department of Neuroradiology, Radiology and Neurology, 13704Southern Tohoku Research Institute for Neuroscience, Southern Tohoku General Hospital, Koriyama, Fukushima, Japan. Department of Neuroradiology, Radiology and Neurology, 13704Southern Tohoku Research Institute for Neuroscience, Southern Tohoku General Hospital, Koriyama, Fukushima, Japan.
 John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA 02139. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA 02139. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115. John A. Paulson School of Engineering & Applied Sciences, Harvard University, Allston, MA 02134. Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115.
 Professor in Department of Clinical Pharmacology and Therapeutic Medicine, College of Medicine, ALmustansiriyiah University, M. B. Ch. B, FRCP, Box 14132, Baghdad, Iraq. Professor in Department of Clinical Pharmacology and Therapeutic Medicine, College of Medicine, ALmustansiriyiah University, M. B. Ch. B, FRCP, Box 14132, Baghdad, Iraq. Department of Pathology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matrouh, 51744, Egypt. heba.magdy@mau.edu.eg. Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, AlBeheira, Egypt. gaberbatiha@gmail.com.
 Department of Basic Sciences, Faculty of Physical Therapy, Suez University, Suez Governorate, Egypt. Electronic address: s.essa@the.suezuni.edu.eg. Department of Cardiopulmonary Rehabilitation, Faculty of Physical Therapy, Cairo University, Giza, Egypt. Electronic address: aelokda@fgcu.edu. Department of Basic Sciences, Faculty of Physical Therapy, Cairo University, Giza, Egypt. Electronic address: drdaliamosaad@gmail.com. Department of Neurological Disorders and Its Surgery, Faculty of Physical Therapy, Cairo University, Giza, Egypt. Electronic address: dr_shendy@hotmail.com. Department of Neurology, Faculty of Medicine, Cairo University, Giza, Egypt. Electronic address: Magednaseer@hotmail.com. Department of Neurology, Faculty of Medicine, Cairo University, Giza, Egypt. Electronic address: Asmaa.ebraheim@kasralainy.edu.eg. Department of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Giza, Egypt. Electronic address: Hadeel.mohammad@gmail.com. Department of Neurology, Faculty of Medicine, Cairo University, Giza, Egypt. Electronic address: Alaa_elmazny@kasralainy.edu.eg. Department of Neurology, Police Forces Hospital, Giza, Egypt. Electronic address: Dr_eman_magdy@yahoo.com.
 F. Hoffmann-La Roche Ltd, Basel, Switzerland. Department of Neurosciences, University of California San Diego, San Diego, CA, USA. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. florian.lipsmeier@roche.com. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain. Department of Neurology, University of California San Francisco, San Francisco, CA, USA. F. Hoffmann-La Roche Ltd, Basel, Switzerland.
 Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands Z.vankempen@amsterdamumc.nl. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, location VUMC, Amsterdam, The Netherlands. Biologics Laboratory, Sanquin Diagnostic Services, Amsterdam, the Netherlands. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, location VUMC, Amsterdam, The Netherlands. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, location VUMC, Amsterdam, The Netherlands. Amsterdam Institute for Infection and Immunity, Amsterdam, the Netherlands. Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, location VUMC, Amsterdam, The Netherlands. Swammerdam Insitute for Life Sciences, Amsterdam UMC, Amsterdam, The Netherlands. Pediatric Immunology, Rheumatology and Infectious Diseases, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, location VUMC, Amsterdam, The Netherlands. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands. Clinical Neurophysiology, St. Antonius Hospital, Nieuwegein, the Netherlands. Neurology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands.
 Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Nodo Biobanco Hospital Virgen Macarena (Biobanco del Sistema Sanitario Público de Andalucía), Hospital Universitario Virgen Macarena, Sevilla, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and Universitat de Barcelona, Barcelona, Spain. Grupo Investigación de Factores Ambientales en Enfermedades Degenerativas, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos, Madrid, Spain. Multiple Sclerosis and Neuroimmunology Research Group, Fundación para la Investigación La Fe, Valencia, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit, Department of Neurology, Doctor Josep Trueta University Hospital, Girona, Spain. Neuroimmunology and Multiple Sclerosis Research Group, Girona Biomedical Research Institute, Doctor Josep Trueta University Hospital, Catalonia, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Neurology Department, Hospital del Mar Medical Research Institute, Barcelona, Spain. Hospital Arnau de Vilanova de Lleida, Universitat de Lleida Medicine Department, Institut de Recerca Biomèdica de Lleida, Lleida, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and Universitat de Barcelona, Barcelona, Spain. Multiple Sclerosis Unit, Hospital Virgen Macarena, Sevilla, Spain. Center of Neuroimmunology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clinic Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and Universitat de Barcelona, Barcelona, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Multiple Sclerosis and Neuroimmunology Research Group, Fundación para la Investigación La Fe, Valencia, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya, Institut de Recerca Vall d'Hebron, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit, Department of Neurology, Doctor Josep Trueta University Hospital, Girona, Spain. Neuroimmunology and Multiple Sclerosis Research Group, Girona Biomedical Research Institute, Doctor Josep Trueta University Hospital, Catalonia, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Grupo Investigación de Factores Ambientales en Enfermedades Degenerativas, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos, Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Radiology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, La Red Española de Esclerosis Múltiple, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain.
 c/o Soins, 65 rue Camille-Desmoulins, 92442 Issy-les-Moulineaux cedex, France. Electronic address: herissonbrigitte@yahoo.fr.
 Department of Neurosciences, University of California, San Diego, United States. Electronic address: aeminer@bu.edu. Department of Neurosciences, University of California, San Diego, United States. Department of Neurosciences, University of California, San Diego, United States. Department of Neurosciences, University of California, San Diego, United States.
 Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece. Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece. Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece. Department of Psychology, University of Western Macedonia, 53100 Florina, Greece. Catalink, 1040 Nicosia, Cyprus. Catalink, 1040 Nicosia, Cyprus. Wellics, London N1 7GU, UK. Wellics, London N1 7GU, UK. Eginition Hospital, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, 15772 Athens, Greece. Eginition Hospital, 1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, 15772 Athens, Greece. Department of Computer Science, School of Sciences and Engineering, University of Nicosia, 2417 Nicosia, Cyprus. Department of Computer Science, School of Sciences and Engineering, University of Nicosia, 2417 Nicosia, Cyprus. Department of Computer Science, University Politechnica of Bucharest, 060042 Bucharest, Romania. Department of Computer Science, University Politechnica of Bucharest, 060042 Bucharest, Romania. Wise Angle, 08330 Barcelona, Spain. Wise Angle, 08330 Barcelona, Spain. Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece. Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece. Fondazione Italiana Sclerosi Multipla, 16149 Genoa, Italy. Fondazione Italiana Sclerosi Multipla, 16149 Genoa, Italy. Institute of Communication and Computer Systems, National Technical University of Athens, 10682 Athens, Greece. Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece. Information Technologies Institute, Centre for Research and Technology Hellas, 57001 Thermi, Greece.
 Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands/Department of Clinical Neurophysiology and MEG center, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Clinical Neurophysiology and MEG center, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Medical Psychology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands/Department of Clinical Neurophysiology and MEG center, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands/Department of Clinical Neurophysiology and MEG center, Amsterdam Neuroscience, Amsterdam UMC and Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
 Cleveland Clinic Mellen Center for Multiple Sclerosis, 9500 Euclid Ave/ U10, Cleveland, OH 44195, USA. Electronic address: tworekg@ccf.org. Department of Quantitative Health Sciences, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195, USA; Center for Outcomes Research & Evaluation, Neurological Institute, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195, USA. Cleveland Clinic Mellen Center for Multiple Sclerosis, 9500 Euclid Ave/ U10, Cleveland, OH 44195, USA. Cleveland Clinic Mellen Center for Multiple Sclerosis, 9500 Euclid Ave/ U10, Cleveland, OH 44195, USA.
 Department of Neurology, Wellington Regional Hospital, Wellington, New Zealand rleadbetter20@gmail.com. New Zealand Brain Research Institute, Christchurch, New Zealand. New Zealand Brain Research Institute, Christchurch, New Zealand. Department of Medicine, University of Otago, Christchurch, New Zealand. New Zealand Brain Research Institute, Christchurch, New Zealand. Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia. Department of Neurology, Wellington Regional Hospital, Wellington, New Zealand. New Zealand Brain Research Institute, Christchurch, New Zealand. Department of Medicine, University of Otago, Christchurch, New Zealand. Department of Neurology, Christchurch Hospital, Christchurch, New Zealand.
 Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. bittner@uni-mainz.de. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. zipp@uni-mainz.de.
 Department of Bioinformatics, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India. Electronic address: lramya174@gmail.com. Department of Bioinformatics, School of Chemical and Biotechnology, SASTRA Deemed University, Thirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India.
 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples 80131, Italy. Electronic address: gianmarco.abbadessa@unicampania.it. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples 80131, Italy. Department of Neuroscience and Mental Health, City of Health and Science University Hospital of Turin, Turin 10147, Italy. Institute of Neurology, University "Magna Graecia", Catanzaro 88100, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome 00133, Italy. Department of Neuroscience and Mental Health, City of Health and Science University Hospital of Turin, Turin 10147, Italy. Institute of Neurology, University "Magna Graecia", Catanzaro 88100, Italy. Section of Medical Statistics, Department of Mental Health and Public Medicine, University of Campania Luigi Vanvitelli, Naples 80138, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples 80131, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples 80131, Italy.
 Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Center for Occupational and Environmental Medicine, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Laboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium. Center for Microbiology, VIB Center for Microbiology, VIB, Leuven, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Jette, Belgium. Laboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium. Center for Microbiology, VIB Center for Microbiology, VIB, Leuven, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Jette, Belgium. Department of Neurology, Universitair Ziekenhuis Brussel, Jette, Belgium. National Multiple Sclerosis Center, Melsbroek, Belgium. National Multiple Sclerosis Center, Melsbroek, Belgium. Laboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium. Center for Microbiology, VIB Center for Microbiology, VIB, Leuven, Belgium. Institute of Medical Microbiology and Hygiene, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany. Laboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium. Center for Microbiology, VIB Center for Microbiology, VIB, Leuven, Belgium. Institute of Medical Microbiology and Hygiene, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany. Center for Neurosciences, Vrije Universiteit Brussel, Jette, Belgium. Department of Neurology, Universitair Ziekenhuis Brussel, Jette, Belgium. St. Edmund Hall, University of Oxford, Oxford, UK. Center for Neurosciences, Vrije Universiteit Brussel, Jette, Belgium. Department of Neurology, Universitair Ziekenhuis Brussel, Jette, Belgium. Laboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium. Center for Microbiology, VIB Center for Microbiology, VIB, Leuven, Belgium. Center for Neurosciences, Vrije Universiteit Brussel, Jette, Belgium. Department of Neurology, Universitair Ziekenhuis Brussel, Jette, Belgium. National Multiple Sclerosis Center, Melsbroek, Belgium.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. snewsom2@jhmi.edu. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA. snewsom2@jhmi.edu. Department of Mathematics, Tufts University, Medford, USA. Department of Neurology, Rush University, Chicago, IL, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA. National Multiple Sclerosis Society, New York, NY, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA. Department of Medicine, Division of Endocrinology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Medicine, Division of Endocrinology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Baltimore, MD, USA.
 Department of Physical Therapy and Athletic Training, University of Utah, 520 Wakara Way, Salt Lake City, UT 84108, USA; Army-Baylor University Doctoral Program in Physical Therapy, Fort Sam Houston, TX, 78234 USA. Electronic address: angela.weston@utah.edu. Department of Physical Therapy and Athletic Training, University of Utah, 520 Wakara Way, Salt Lake City, UT 84108, USA. Electronic address: Lee.Dibble@hsc.utah.edu. Army-Baylor University Doctoral Program in Physical Therapy, Fort Sam Houston, TX, 78234 USA. Electronic address: carrie.w.hoppes.mil@army.mil. School of Physical Therapy and Rehabilitation Sciences, University of Montana, 32 Campus Dr., Missoula, MT 59812, USA. Electronic address: brian.loyd@mso.umt.edu.
 Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden. Division of Neurology, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden. Institute of Health and Care Sciences, Sahlgrenska Academy, University of Gothenburg, SE-405 30, Gothenburg, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden. Division of Neurology, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 77, Stockholm, Sweden.
 Department of Neurology, MS center ErasMS, Erasmus Medical Center, Rotterdam, Netherlands. Department of Immunology, MS center ErasMS, Erasmus Medical Center, Rotterdam, Netherlands. Neuroimmunology Research group, Netherlands Institute for Neuroscience, Amsterdam, Netherlands. Department of Animal Sciences, College of Agricultural, Consumer, and Environmental Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, United States. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, United States. Division of Nutritional Sciences, University of Illinois Urbana-Champaign Urbana, Urbana, IL, United States. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, United States. Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Champaign, IL, United States. Beckman Institute for Advanced Science and Technology, Urbana, IL, United States.
 Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Motion Study Laboratory 151A, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Department of Neurology, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio, USA. Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio, USA. Assistant Professor, Department of Neurology, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
 Department of Endocrinology and Nutrition, Hospital Clinico Universitario de Valencia, Valencia, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Clinico Universitario de Valencia, Valencia, Spain. Department of Endocrinology and Nutrition, Hospital Clinico Universitario de Valencia, Valencia, Spain. Department of Endocrinology and Nutrition, Hospital Clinico Universitario de Valencia, Valencia, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Clinico Universitario de Valencia, Valencia, Spain. Department of Endocrinology and Nutrition, Hospital Clinico Universitario de Valencia, Valencia, Spain. Department of Endocrinology and Nutrition, Hospital Clinico Universitario de Valencia, Valencia, Spain. INCLIVA (Instituto de Investigacion Sanitaria), Valencia, Spain. CIBERDEM (Centro de investigación biomedica en red de diabetes y enfermedades metabólicas asociadas), Madrid, Spain.
 Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm. Neurology Department, Pitié-Salpêtrière Hospital. Sorbonne Université, Paris Brain Institute, ICM, CNRS, Inserm. Neurology Department, St Antoine Hospital, APHP-Sorbonne, Paris, France.
 Department of Pharmacology and Toxicology, Molecular Pharmacology Research Group, Faculty of Pharmacy and Biotechnology, Head of Molecular Genetics and Pharmacology Research Group, German University in Cairo, Cairo 11835, Egypt. Department of Pharmacology and Toxicology, Molecular Pharmacology Research Group, Faculty of Pharmacy and Biotechnology, Head of Molecular Genetics and Pharmacology Research Group, German University in Cairo, Cairo 11835, Egypt. Electronic address: hend.saber@guc.edu.eg.
 Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. ProMeFa, Proteomics and Metabolomics Facility, Center for Omics Sciences (COSR), IRCCS San Raffaele Scientific Institute, Milan, Italy. ProMeFa, Proteomics and Metabolomics Facility, Center for Omics Sciences (COSR), IRCCS San Raffaele Scientific Institute, Milan, Italy. ProMeFa, Proteomics and Metabolomics Facility, Center for Omics Sciences (COSR), IRCCS San Raffaele Scientific Institute, Milan, Italy. Center for Omics Sciences (COSR), IRCCS San Raffaele Scientific Institute, Milan, Italy. Haematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neuroradiology and CERMAC, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Clinical Trial Center, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. M. Tettamanti Research Center, Pediatric Clinic University of Milano-Bicocca, San Gerardo Hospital, Monza, Italy. Laboratorio di Terapia Cellulare e Genica Stefano Verri, ASST-Monza, Ospedale San Gerardo, Monza, Italy. M. Tettamanti Research Center, Pediatric Clinic University of Milano-Bicocca, San Gerardo Hospital, Monza, Italy. Laboratorio di Terapia Cellulare e Genica Stefano Verri, ASST-Monza, Ospedale San Gerardo, Monza, Italy. M. Tettamanti Research Center, Pediatric Clinic University of Milano-Bicocca, San Gerardo Hospital, Monza, Italy. Laboratorio di Terapia Cellulare e Genica Stefano Verri, ASST-Monza, Ospedale San Gerardo, Monza, Italy. M. Tettamanti Research Center, Pediatric Clinic University of Milano-Bicocca, San Gerardo Hospital, Monza, Italy. Laboratorio di Terapia Cellulare e Genica Stefano Verri, ASST-Monza, Ospedale San Gerardo, Monza, Italy. University Vita-Salute San Raffaele, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Haematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. Department of Neuroradiology and CERMAC, IRCCS San Raffaele Scientific Institute, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. Haematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Gynaecology, IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy. Biostatistics Unit, Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. University Vita-Salute San Raffaele, Milan, Italy. Italian Multiple Sclerosis Foundation, Genoa, Italy. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. University Vita-Salute San Raffaele, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. M. Tettamanti Research Center, Pediatric Clinic University of Milano-Bicocca, San Gerardo Hospital, Monza, Italy. Laboratorio di Terapia Cellulare e Genica Stefano Verri, ASST-Monza, Ospedale San Gerardo, Monza, Italy. Neuroimmunology Unit, Institute of Experimental Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. martino.gianvito@hsr.it. Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy. martino.gianvito@hsr.it. University Vita-Salute San Raffaele, Milan, Italy. martino.gianvito@hsr.it.
 Melbourne Brain Centre Imaging Unit, Department of Radiology, University of Melbourne, Melbourne, VIC, Australia/MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. Department of Neurosciences, Central Clinical School, Monash University, Melbourne, VIC, Australia. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, the Netherlands.
 Centro de Esclerosis Múltiple (CEMHUN), Deparatmento de Neurología, Hospital Universitario Nacional de Colombia, Bogotá, Colombia; Unidad de Neurología, Departamento de Medicina Interna, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá, Colombia. Instituto de Investigaciones Clínicas, Universidad Nacional de Colombia, Bogotá, Colombia/Hospital Universitario Nacional de Colombia, Bogotá, Colombia. Hospital Universitario Nacional de Colombia, Bogotá, Colombia. Centro de Esclerosis Múltiple (CEMHUN), Deparatmento de Neurología, Hospital Universitario Nacional de Colombia, Bogotá, Colombia. Centro de Esclerosis Múltiple (CEMHUN), Deparatmento de Neurología, Hospital Universitario Nacional de Colombia, Bogotá, Colombia.
 Instituto de Investigaciones en Medicina Traslacional (IIMT), CONICET-Universidad Austral, Derqui, Pilar, Buenos Aires, Argentina. Instituto de Investigaciones en Medicina Traslacional (IIMT), CONICET-Universidad Austral, Derqui, Pilar, Buenos Aires, Argentina. CONICET, Comisión Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Medicina Traslacional (IIMT), CONICET-Universidad Austral, Derqui, Pilar, Buenos Aires, Argentina. CONICET, Comisión Nacional de Investigaciones Científicas y Técnicas.
 Department of Neurology, Teikyo University School of Medicine, Kaga 2-11-1, Tokyo 1738605, Japan. Electronic address: ta_kanba@med.teikyo-u.ac.jp. Department of Neurology, Teikyo University School of Medicine, Kaga 2-11-1, Tokyo 1738605, Japan. Electronic address: ogawago@med.teikyo-u.ac.jp. Department of Neurology, Teikyo University School of Medicine, Kaga 2-11-1, Tokyo 1738605, Japan. Electronic address: footballer0704@yahoo.co.jp. Department of Neurology, Teikyo University School of Medicine, Kaga 2-11-1, Tokyo 1738605, Japan. Electronic address: k1-hokkoku@hotmail.co.jp. Department of Neurology, Faculty of Medicine, Kyorin University, Tokyo, Japan. Electronic address: chizuko-o@mte.biglobe.ne.jp. Department of Neurology, Teikyo University School of Medicine, Kaga 2-11-1, Tokyo 1738605, Japan. Electronic address: y-hata@med.teikyo-u.ac.jp. Department of Neurology, Teikyo University School of Medicine, Kaga 2-11-1, Tokyo 1738605, Japan. Electronic address: sonoom@med.teikyo-u.ac.jp.
 Food Microbiology Research Center, Tehran University of Medical Sciences, Tehran, Iran. minoo_chakamian@yahoo.com. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. behruz.robatjazi@yahoo.com. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. abdorrezamoghadasi@gmail.com. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. harir.mansoori@yahoo.com. Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. nodehimasoume008@gmail.com. Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. e_motevaseli@tums.ac.ir. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran AND Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. izadm@sina.tums.ac.ir. Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. yekaninejad@yahoo.com. Department of Microbial Biotechnology, School of Biology and Center of Excellence in Phylogeny of Living Organisms, College of Science, University of Tehran, Tehran, Iran. mahdiehshirzad@gmail.com. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. kianabidad@gmail.com. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. mona.oraei@yahoo.com. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. b.ansaripour@yahoo.com. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. asaboor@tums.ac.ir.
 Department of Medicine, University of Toronto, Toronto, ON, Canada/MS Clinic, St. Michael's Hospital, Toronto, ON, Canada. Departments of Epidemiology, Biostatistics and Occupational Health and Medicine, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, Canada/Research Institute of the McGill University Health Centre, Montreal, QC, Canada. Division of Neurology, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. Department of Medicine, University of Ottawa, Ottawa, ON, Canada/Ottawa Hospital Research Institute, Ottawa, ON, Canada. Western University, London, ON, Canada/London Health Sciences Centre, London, ON, Canada. Department of Medicine, University of Toronto, Toronto, ON, Canada/Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada. Departments of Clinical Neurosciences and Community Health Sciences, University of Calgary, Calgary, AB, Canada. St. Michael's Hospital, Toronto, ON, Canada/Applied Health Research Centre and MAP Centre for Urban Health Solutions, Li Ka Shing Knowledge Institute, St Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada/Division of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. St. Michael's Hospital, Toronto, ON, Canada. Department of Sociology, University of New Brunswick, Fredericton, NB, Canada. Departments of Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
 Department of Neurology, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. Cleveland Clinic Lerner College of Medicine, Cleveland, OH. Department of Biostatistics, Epidemiology, and Informatics, Penn Statistics in Imaging and Visualization Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. Department of Biostatistics, Epidemiology, and Informatics, Penn Statistics in Imaging and Visualization Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. Neurological Institute, Cleveland Clinic, Cleveland, OH. QMENTA, Inc., Boston, MA. Functional MRI Facility, NIMH, NIH, Bethesda, MD. Department of Neurology, University of Southern California, Los Angeles, CA. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. Department of Neurology, University of California at San Francisco, San Francisco, CA. Department of Neurology, Johns Hopkins University, Baltimore, MD. Department of Neurology, University of California at San Francisco, San Francisco, CA. Department of Neurology, Dell Medical School, The University of Texas at Austin, Austin, TX. Department of Neurology, University of California at San Francisco, San Francisco, CA. Department of Neurology, Yale University, New Haven, CT. Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH. Division of Neurology, St. Michael's Hospital, University of Toronto, ON, Canada. Department of Neurology, University of California at San Francisco, San Francisco, CA. Department of Neurology, University of Southern California, Los Angeles, CA. Department of Neurology, The University of Texas Health Science Center at Houston, Houston, TX. Department of Medical Imaging, St. Michael's Hospital, University of Toronto, ON, Canada. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. Department of Neurology, Johns Hopkins University, Baltimore, MD. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA. Department of Neurological Sciences, Larner College of Medicine, The University of Vermont, Burlington, VT. Department of Biostatistics, Epidemiology, and Informatics, Penn Statistics in Imaging and Visualization Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA.
 Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, 100 Forest Rd., St. John's, NL A1A 1E5, Canada. Electronic address: Michelle.ploughman@med.mun.ca. Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, 100 Forest Rd., St. John's, NL A1A 1E5, Canada. Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, 100 Forest Rd., St. John's, NL A1A 1E5, Canada. Program in Physical Therapy, Department of Neurology, Washington University School of Medicine in St. Louis, St. Louis, MO, USA. Department of Neurology, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. Department of Neurology, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. Department of Neurology and Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. School of Rehabilitation Science, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
 DEPARTMENT OF NEUROLOGY FACULTY OF MEDICAL SCIENCES IN ZABRZE, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND. DEPARTMENT OF NEUROLOGY FACULTY OF MEDICAL SCIENCES IN ZABRZE, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND. DEPARTMENT OF NEUROLOGY FACULTY OF MEDICAL SCIENCES IN ZABRZE, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND. DEPARTMENT OF NEUROLOGY FACULTY OF MEDICAL SCIENCES IN ZABRZE, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND. DEPARTMENT OF NEUROLOGY FACULTY OF MEDICAL SCIENCES IN ZABRZE, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND. DEPARTMENT OF INFECTIOUS DISEASES AND HEPATOLOGY, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND. DEPARTMENT OF NEUROLOGY FACULTY OF MEDICAL SCIENCES IN ZABRZE, MEDICAL UNIVERSITY OF SILESIA, ZABRZE, POLAND.
 Faculty of Science and Technology, Mount Royal University, Calgary, AB T3E 6K6, Canada. Faculty of Science and Technology, Mount Royal University, Calgary, AB T3E 6K6, Canada. Hotchkiss Brain Institute, Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada. Alberta Child Health Research Institute, Department of Medical Genetics, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada. Faculty of Science and Technology, Mount Royal University, Calgary, AB T3E 6K6, Canada.
 Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, 66421, Homburg, Germany. Institut des Neurosciences de la Timone (INT), Aix-Marseille Université, CNRS UMR7289, 13005, Marseille, France. Centre Européen de Recherche en Imagerie Médicale (CERIMED), Aix-Marseille Université, Marseille, France. Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, 66421, Homburg, Germany. Institut des Neurosciences de la Timone (INT), Aix-Marseille Université, CNRS UMR7289, 13005, Marseille, France. Centre Européen de Recherche en Imagerie Médicale (CERIMED), Aix-Marseille Université, Marseille, France. Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, 66421, Homburg, Germany. Institut des Neurosciences de la Timone (INT), Aix-Marseille Université, CNRS UMR7289, 13005, Marseille, France. franck.debarbieux@univ-amu.fr. Centre Européen de Recherche en Imagerie Médicale (CERIMED), Aix-Marseille Université, Marseille, France. franck.debarbieux@univ-amu.fr. Institut Universitaire de France (IUF), Paris, France. franck.debarbieux@univ-amu.fr.
 Ege University Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Izmir, Turkey. Electronic address: yesim.akkoc@ege.edu.tr. Health Sciences University, Istanbul Physical Medicine and Rehabilitation Training and Research Hospital, Istanbul, Turkey. Pamukkale University Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Denizli, Turkey. Kutahya Health Sciences University, Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Kutahya, Turkey. Istanbul Medeniyet University Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Istanbul, Turkey. Health Sciences University, Istanbul Physical Medicine and Rehabilitation Training and Research Hospital, Istanbul, Turkey. Pamukkale University Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Denizli, Turkey. Ege University Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Izmir, Turkey. Health Sciences University, Istanbul Physical Medicine and Rehabilitation Training and Research Hospital, Istanbul, Turkey. Istanbul Medeniyet University Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Istanbul, Turkey. Kutahya Health Sciences University, Faculty of Medicine, Department of Neurology, Kutahya, Turkey. Ege University Faculty of Medicine, Department of Neurology, Izmir, Turkey. Ege University Faculty of Medicine, Department of Psychiatry, Izmir, Turkey. Ege University Faculty of Medicine, Department of Neurology, Izmir, Turkey.
 Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA. Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA. Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA.
 Department of Rehabilitation, CRRF "Mons. Luigi Novarese", Moncrivello, Italy. Department of Rehabilitation, CRRF "Mons. Luigi Novarese", Moncrivello, Italy. Department of Rehabilitation, CRRF "Mons. Luigi Novarese", Moncrivello, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genoa, Italy. LaRice Lab, Don Carlo Gnocchi Foundation, Institute of Hospitalization and Scientific Care, Milan, Italy. Multiple Sclerosis Center, Institute of Neurological Sciences, University of Catania, Catania, Italy. Multiple Sclerosis Center, Institute of Neurological Sciences, University of Catania, Catania, Italy. Department of Neurosciences, S. Camillo-Forlanini Hospital, Rome, Italy. Department of Neurosciences, S. Camillo-Forlanini Hospital, Rome, Italy. Department of Psychology, University of Turin, Turin, Italy. LaRice Lab, Don Carlo Gnocchi Foundation, Institute of Hospitalization and Scientific Care, Milan, Italy. Department of Physiopathology and Transplants, University of Milan, Milan, Italy. Department of Psychology, University of Turin, Turin, Italy.
 Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, USA. Electronic address: bopelt1@jhmi.edu. Department of Psychology, University of Maryland, Baltimore County, Baltimore, USA. Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, USA.
 Department of Neurology, Keck School of Medicine, University of Southern California, USA. Electronic address: lamezcua@usc.edu. One Technology Place, EMD Serono, Inc., Rockland, MA, USA. One Technology Place, EMD Serono, Inc., Rockland, MA, USA. One Technology Place, EMD Serono, Inc., Rockland, MA, USA. Joi Life Wellness Group MS Center, GA, USA.
 Department of Functional Diagnostics and Physical Medicine, Faculty of Health Sciences, Pomeranian Medical University, Szczecin, Poland. Department of Humanities and Occupational Therapy, Pomeranian Medical University, Szczecin, Poland. Department of Functional Diagnostics and Physical Medicine, Faculty of Health Sciences, Pomeranian Medical University, Szczecin, Poland - anna.lubkowska@pum.edu.pl.
 Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Hospital Vithas Nisa, Unidad de Investigación y Tratamiento de la Esclerosis Múltiple, Sevilla, Spain. Neurociencias, Novartis Farmacéutica, S.A., Barcelona, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Hospital Vithas Nisa, Unidad de Investigación y Tratamiento de la Esclerosis Múltiple, Sevilla, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Hospital Vithas Nisa, Unidad de Investigación y Tratamiento de la Esclerosis Múltiple, Sevilla, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Hospital Vithas Nisa, Unidad de Investigación y Tratamiento de la Esclerosis Múltiple, Sevilla, Spain. Neurociencias, Novartis Farmacéutica, S.A., Barcelona, Spain. Departamento de Neurología, Fundación para el Desarrollo de la Investigación y Asistencia de Enfermedades Neurológicas y Afines Crónicas (DINAC), Castilleja de la Cuesta, Sevilla, Spain. Departamento de Neurología, Hospital Vithas Nisa, Unidad de Investigación y Tratamiento de la Esclerosis Múltiple, Sevilla, Spain.
 Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Laboratory of immunology Charles Nicolle Hospital, El Manar University, Tunis, Tunisia. Department of Nephrology, Dialysis, and Transplantation La Marsa Hospital, El Manar University, Tunis, Tunisia. Department of Pathology, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia. Department of Pathology, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia.
 Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy. Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy. Department of Chronic Diseases and Metabolism (CHROMETA), Katholieke Universiteit Leuven, 3000 Leuven, Belgium. Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy. Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy. Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy. Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy. Department of Drug Sciences, University of Pavia, 27100 Pavia, Italy.
 Department of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmacy, Yarmouk University, Irbid, Jordan. omar.gammoh@yu.edu.jo.
 1st Department of Neurology, Faculty of Medicine, Comenius University, 813 69 Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, 813 69 Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, 813 69 Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, 813 69 Bratislava, Slovakia. Institute of Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, 845 05 Bratislava, Slovakia. Institute of Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, 845 05 Bratislava, Slovakia. Institute of Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, 845 05 Bratislava, Slovakia. Institute of Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, 845 05 Bratislava, Slovakia. Institute of Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, 845 05 Bratislava, Slovakia. Institute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Faculty of Medicine, Comenius University, 811 08 Bratislava, Slovakia. Department of Neurology, Faculty Hospital, 917 75 Trnava, Slovakia. Department of Neurology, Faculty Hospital, 911 01 Trencin, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, 813 69 Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, 813 69 Bratislava, Slovakia.
 REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium. Renee.Veldkamp@uhasselt.be. UMSC, Hasselt-Pelt, Belgium. Renee.Veldkamp@uhasselt.be. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium. UMSC, Hasselt-Pelt, Belgium. National MS Center Melsbroek, Steenokkerzeel, Belgium. Kessler Foundation, East Hanover, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, USA. Kessler Foundation, East Hanover, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, USA. National MS Center Melsbroek, Steenokkerzeel, Belgium. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Department of Neurology, Section on Statistical Planning and Analysis, UT Southwestern Medical Center, Dallas, TX, USA. Department of Psychiatry, University of Toronto and Sunnybrook Health Sciences Centre, Toronto, ON, M5R 3B6, Canada. Department NEUROFARBA, Section Neurosciences, University of Florence, Largo Brambilla 3, 50134, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society (AISM), Via Operai 30, 16149, Genoa, Italy. Queen Square MS Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Queen Square MS Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Kessler Foundation, East Hanover, NJ, USA. Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, USA. Exercise Biology, Department of Public Health, Aarhus University, Dalgas Avenue 4, 8000, Aarhus, Denmark. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, and Neurology Unit, IRCCS, San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. School of Health Professions, Faculty of Health, University of Plymouth, Devon, UK. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. Department of Psychiatry, University of Toronto and Sunnybrook Health Sciences Centre, Toronto, ON, M5R 3B6, Canada. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, and Neurology Unit, IRCCS, San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, USA. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium. UMSC, Hasselt-Pelt, Belgium.
 MS Center Amsterdam, Rehabilitation Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam. Electronic address: a.gravesteijn@amsterdamumc.nl. MS Center Amsterdam, Rehabilitation Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam. Electronic address: h.beckerman@amsterdamumc.nl. MS Center Amsterdam, Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam; Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel, University of Basel, Spitalstrasse 2, CH-4031 Basel, Switzerland. Electronic address: Eline.Willemse@usb.ch. MS Center Amsterdam, Anatomy and Neuroscience, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam; Leiden University, Faculty of Social Sciences, Institute of Psychology, Health, Medical and Neuropsychology unit, Leiden, PO Box 9500, 2300 RA Leiden, The Netherlands. Electronic address: h.e.hulst@fsw.leidenuniv.nl. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam. Electronic address: b.dejong@amsterdamumc.nl. MS Center Amsterdam, Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam. Electronic address: c.teunissen@amsterdamumc.nl. MS Center Amsterdam, Rehabilitation Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands, PO Box 7057, 1007 MB Amsterdam. Electronic address: v.degroot@amsterdamumc.nl.
 Department of Neurology and MS Center, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, Basel, Switzerland. Department of Neurology and MS Center, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, Basel, Switzerland. Healios AG, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital, University of Basel, Basel, Switzerland. Department of Psychiatry, Sunnybrook Health Sciences Centre, Toronto, Canada. Department of Neurology and MS Center, University Hospital and University of Basel, Basel, Switzerland. Neuropsychology and Behavioral Neurology Unit, Division of Molecular and Cognitive Neuroscience, University of Basel, Basel, Switzerland. Ophthalmology, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, Basel, Switzerland. Department of Neurology and MS Center, University Hospital and University of Basel, Basel, Switzerland. johannes.lorscheider@usb.ch. Research Center for Clinical Neuroimmunology and Neuroscience Basel, Basel, Switzerland. johannes.lorscheider@usb.ch. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. johannes.lorscheider@usb.ch. Department of Neurology and MS Center, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, Basel, Switzerland.
 jung diagnostics GmbH, Hamburg, Germany. jung diagnostics GmbH, Hamburg, Germany. jung diagnostics GmbH, Hamburg, Germany. jung diagnostics GmbH, Hamburg, Germany. Institute of Diagnostic and Interventional Neuroradiology, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany. Multimodal Imaging in Neuroimmunological Diseases (MINDS), Center for Neuroscience Zurich (ZNZ), Federal Institute of Technology (ETH), University of Zurich, Zürich, Switzerland. Department of Diagnostic and Interventional Radiology and Nuclear Medicine, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246, Hamburg, Germany. r.buchert@uke.de.
 Vascular Immunology Unit, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia. Vascular Immunology Unit, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia. Vascular Immunology Unit, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia. Central West Neurology and Neurosurgery, Orange, NSW 2800, Australia. Vascular Immunology Unit, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia. Liver Injury and Cancer Program, Centenary Institute, Sydney, NSW 2006, Australia. Human Cancer and Viral Immunology Laboratory, The University of Sydney, Sydney, NSW 2006, Australia. Vascular Immunology Unit, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia.
 NeuroTransData, Neuburg an der Donau, Germany. sbraune@neurotransdata.com. Roche Pharma AG, Grenzach-Wyhlen, Germany. Roche Pharma AG, Grenzach-Wyhlen, Germany. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Roche Pharma AG, Grenzach-Wyhlen, Germany. PricewaterhouseCoopers (PwC), Zurich, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. NeuroTransData, Neuburg an der Donau, Germany.
 Department of Community Medicine and Behavioural Sciences, College of Medicine, Kuwait University, PO Box 24923, Safat, 13110, Kuwait. saeed.akhtar@ku.edu.kw. Department of Medicine, College of Medicine, Kuwait University, PO Box 24923, Safat, 13110, Kuwait. Department of Neurology, Ibn Sina Hospital, Kuwait City, Kuwait. Division of Neurology, Department of Medicine, Amiri Hospital, Arabian Gulf Street, Sharq, 13041, Kuwait.
 Gustave Roussy, Université Paris-Saclay, Département des Innovations Thérapeutiques et Essais Précoces, Villejuif, France. Gustave Roussy, Université Paris-Saclay, Département d'Oncologie Médicale et des Soins de Support, Villejuif, France. Gustave Roussy Institute, Department of oncology, Villejuif, France. Assistance Publique - Hôpitaux de Paris, Hôpital Bicêtre, Service de Neurologie Adulte, Le Kremlin Bicêtre, France. Gustave Roussy, Université Paris-Saclay, Département des Innovations Thérapeutiques et Essais Précoces, Villejuif, France; Université Paris-Saclay, Gustave Roussy, Unité Mixte de Recherche 1170, Villejuif, France. Electronic address: jean-marie.michot@gustaveroussy.fr.
 Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Department of Neurophysics, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany. Cardiff University Brain Research Imaging Centre, School of Psychology, Cardiff University, Cardiff, UK. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. MS Centre, Department of Clinical Neurology, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. MS Centre, Department of Clinical Neurology, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. MS Centre, Department of Clinical Neurology, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. MS Centre, Department of Clinical Neurology, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. MS Centre, Department of Clinical Neurology, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Department of Paediatrics, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Behavioral Neurology and Molecular Neurology Units, Centre for Advanced Studies and Technology, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Cardiff University Brain Research Imaging Centre, School of Physics and Astronomy, Cardiff University, Cardiff, UK. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Cardiff University Brain Research Imaging Centre, School of Psychology, Cardiff University, Cardiff, UK. MS Centre, Department of Clinical Neurology, SS. Annunziata University Hospital, Chieti, Italy. Department of Neurosciences, Imaging, and Clinical Sciences, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Institute for Advanced Biomedical Technologies, G. d'Annunzio University of Chieti-Pescara, Chieti, Italy. Cardiff University Brain Research Imaging Centre, School of Psychology, Cardiff University, Cardiff, UK.
 Department of Health Education and Health Promotion, Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Health Education and Health Promotion, School of Health, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Health Education and Health Promotion, School of Health, Mashhad University of Medical Sciences, Mashhad, Iran. Social Determinants of Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Medical Surgical Nursing, School of Nursing and Midwifery, Mashhad University of Medical Sciences, Mashhad, Iran. Social Determinants of Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Biostatistics, School of Health, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Health Education and Health Promotion, School of Health, Mashhad University of Medical Sciences, Mashhad, Iran. Tehranih@mums.ac.ir. Social Determinants of Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Tehranih@mums.ac.ir.
 INERE Instituto de Neurociencias Restaurativas, CABA Buenos Aires, Argentina. Electronic address: mlsaladino@inere.com.ar. INEBA, Instituto de neurociencias Buenos aires CABA Buenos Aires, Argentina. INEBA, Instituto de neurociencias Buenos aires CABA Buenos Aires, Argentina. Fundación Sinapsis Santa Rosa La Pampa, Argentina. Fundación Sinapsis Santa Rosa La Pampa, Argentina. Neurocomp Trelew Chubut, Argentina. Neurocomp Trelew Chubut, Argentina. Instituto Lennox Córdoba, Argentina. Instituto Lennox Córdoba, Argentina. Instituto Lennox Córdoba, Argentina. Instituto Lennox Córdoba, Argentina. Hospital José Néstor Lencinas Mendoza, Argentina. Hospital José Néstor Lencinas Mendoza, Argentina. INERE Instituto de Neurociencias Restaurativas, CABA Buenos Aires, Argentina.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: f_ashtari@med.mui.ac.ir. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran. Paramedical School, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran; Cognetivity Ltd, London, United Kingdom. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran; School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran.
 MSBase Foundation, Melbourne, VIC, Australia. Dokuz Eylul University, Izmir, Turkey. Al-Amiri Hospital, Kuwait City, Kuwait. Department of Neurology, 19 Mayis University, Samsun, Turkey. Liverpool Hospital, Sydney, NSW, Australia. University Hospital Ghent, Ghent, Belgium. MS Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia/CORe, Department of Medicine, University of Melbourne, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Neurology Institute, Harley Street Medical Center, Abu Dhabi, United Arab Emirates/American University of Beirut Medical Center, Beirut, Lebanon. School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia/Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, NSW, Australia. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland/Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, Galdakao-Usansolo University Hospital, Osakidetza-Basque Health Service, Biocruces-Bizkaia Health Research Institute, Galdakao, Spain. Center of Neuroimmunology, Service of Neurology, Hospital Clinic de Barcelona, Barcelona, Spain. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino, Ital. Cliniques Universitaires Saint-Luc (UCLouvain), Brussels, Belgium. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Nemocnice Jihlava, Jihlava, Czech Republic. Department of Medical and Surgical Sciences and Advanced Technologies, GF Ingrassia, Catania, Italy. Department of Neurology, Austin Health, Melbourne, VIC, Australia. Neurology Unit, Department of Medicine, College of Medicine & Health Sciences and Sultan Qaboos University Hospital, Sultan Qaboos University (SQU), Al Khodh, Oman. Academic MS Center Zuyderland, Department of Neurology, Zuyderland Medical Center, Sittard-Geleen, The Netherlands/School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Koc University School of Medicine and Koc University Research Center for Translational Medicine (KUTTAM), Istanbul, Turkey. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. MSBase Foundation, Melbourne, VIC, Australia/Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia.
 From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. mary.horton@berkeley.edu. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco. From the Division of Epidemiology (M.K.H., S.C.R., X.S., H.Q., D.Q., L.F.B.), School of Public Health, University of California, Berkeley; Computational Biology Graduate Group (M.K.H., L.F.B.), University of California, Berkeley; Kaiser Permanente Division of Research (V.C., K.H.B., P.D., J.M., T.C., T.J.M., C.A.S., L.F.B.), Oakland, CA; The Permanente Medical Group (N.B.), Walnut Creek, CA; The Permanente Medical Group (J.F.M.), San Francisco, CA; and Departments of Pediatrics and Neurology (E.W.), University of California, San Francisco.
 Cochrane Brazil Rio de Janeiro, Petrópolis Medical School, Petrópolis, Brazil. Center of Health Technology Assessment, Hospital Sírio-Libanês, São Paulo, Brazil. Núcleo de Ensino e Pesquisa em Saúde Baseada em Evidências e Avaliação de Tecnologias em Saúde (Nepsbeats), Universidade Federal de São Paulo, São Paulo, Brazil. Cochrane Brazil, Centro de Estudos de Saúde Baseada em Evidências e Avaliação Tecnológica em Saúde, São Paulo, Brazil. Cochrane Brazil Rio de Janeiro, Petrópolis Medical School, Petrópolis, Brazil. Center of Health Technology Assessment, Hospital Sírio-Libanês, São Paulo, Brazil. Núcleo de Ensino e Pesquisa em Saúde Baseada em Evidências e Avaliação de Tecnologias em Saúde (Nepsbeats), Universidade Federal de São Paulo, São Paulo, Brazil. Postgraduate Program in Health and Environment, Universidade Metropolitana de Santos (UNIMES), Santos, Brazil. Cochrane Brazil Rio de Janeiro, Petrópolis Medical School, Petrópolis, Brazil. Center of Health Technology Assessment, Hospital Sírio-Libanês, São Paulo, Brazil. Núcleo de Ensino e Pesquisa em Saúde Baseada em Evidências e Avaliação de Tecnologias em Saúde (Nepsbeats), Universidade Federal de São Paulo, São Paulo, Brazil. Centro Universitário São Camilo, São Paulo, Brazil.
 Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway. Center for Fertility and Health, Norwegian Institute of Public Health, Oslo, Norway. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Hematology, Copenhagen University Hospital, Copenhagen, Denmark.
 Department of Kinesiology and Health, Georgia State University, Atlanta, GA, 30303, USA. Department of Kinesiology and Health, Georgia State University, Atlanta, GA, 30303, USA. Electronic address: fyang@gsu.edu.
 THERMOSENSELAB, School of Design and Creative Arts, Loughborough University, Loughborough, LE11 3TU, United Kingdom. School of Design and Creative Arts, Loughborough University, Loughborough, LE11 3TU, United Kingdom. THERMOSENSELAB, School of Design and Creative Arts, Loughborough University, Loughborough, LE11 3TU, United Kingdom; THERMOSENSELAB, Skin Sensing Research Group, School of Health Sciences, University of Southampton, Southampton, SO17 1BJ, United Kingdom. Electronic address: d.filingeri@soton.ac.uk.
 Comprehensive MS Center, UConn Health, Farmington, Connecticut, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, Connecticut, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, Connecticut, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, Connecticut, USA. Comprehensive MS Center, UConn Health, Farmington, Connecticut, USA. Department of Diagnostic Imaging & Therapeutics, University of Connecticut School of Medicine, Farmington, Connecticut, USA. Department of Diagnostic Imaging & Therapeutics, University of Connecticut School of Medicine, Farmington, Connecticut, USA. Comprehensive MS Center, UConn Health, Farmington, Connecticut, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, Connecticut, USA. Department of Diagnostic Imaging & Therapeutics, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
 Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Laboratory of Anesthesia and Critical Care Medicine, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Laboratory of Anesthesia and Critical Care Medicine, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Department of Surgery, Xuanwei Hospital of traditional Chinese Medicine, Xuanwei, China. Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Laboratory of Anesthesia and Critical Care Medicine, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China. Laboratory of Anesthesia and Critical Care Medicine, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China.
 University of Virginia School of Medicine, Charlottesville, VA, USA. Department of Neurology, Division of Pediatric Neurology, University of Virginia Medical Center, Charlottesville, VA USA.
 Department of Dermatology, Brigham and Women's Hospital, Boston, Massachusetts. Electronic address: jbarbieri@bwh.harvard.edu.
 USF Health Department of Radiology, 2 Tampa General Circle, STC 6103, 33612, Tampa, FL, USA. jdmayfield@usf.edu. Department of Radiology, James A. Haley VA Medical Center, Tampa, FL, USA. Artificial Intelligence Service, AI Center Lead, USF Morsani College of Medicine, National Artificial Intelligence Institute, James A. Haley Veterans' Hospital, Tampa, FL, USA. Department of Radiology, James A. Haley VA Medical Center, Tampa, FL, USA.

 Vision Center of Excellence, Defense Health Agency, Silver Spring, MD 20910, USA. Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. Vision Center of Excellence, Defense Health Agency, Silver Spring, MD 20910, USA. Vision Center of Excellence, Defense Health Agency, Silver Spring, MD 20910, USA. Vision Center of Excellence, Defense Health Agency, Silver Spring, MD 20910, USA. Vision Center of Excellence, Defense Health Agency, Silver Spring, MD 20910, USA.
 Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands. Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands. Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Abu-Haidar Neuroscience Institute, American University of Beirut Medical Center, Beirut, Lebanon. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Hariri School of Nursing, American University of Beirut, Beirut, Lebanon. University of Michigan, Ann Arbor, Michigan, United States of America. Service de Neurologie, Hôpital Henri Mondor, Créteil, France. Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands. Centre for Economic Evaluations and Machine Learning, Trimbos Institute, Utrecht, The Netherlands. Department of Natural Sciences, Lebanese American University, School of Arts and Sciences, Byblos, Lebanon. Institut National de Santé Publique, d'Épidémiologie Clinique et de Toxicologie (INSPECT-Lb), Beirut, Lebanon.
 Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel; Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel; Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel; Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Department of Neurology, Barzilai University Medical Center, Ashkelon, Israel; Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Electronic address: ronm@bmc.gov.il.

 Jacobs Comprehensive MS Treatment & Research Center, Department of Neurology, Jacobs School of Medicine & Biomedical Sciences University at Buffalo, Buffalo, NY 14202, USA. Jacobs Comprehensive MS Treatment & Research Center, Department of Neurology, Jacobs School of Medicine & Biomedical Sciences University at Buffalo, Buffalo, NY 14202, USA. Jacobs Comprehensive MS Treatment & Research Center, Department of Neurology, Jacobs School of Medicine & Biomedical Sciences University at Buffalo, Buffalo, NY 14202, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine & Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Jacobs Comprehensive MS Treatment & Research Center, Department of Neurology, Jacobs School of Medicine & Biomedical Sciences University at Buffalo, Buffalo, NY 14202, USA. Biogen, 133 Boston Post Rd, Weston, MA 20493, USA. Biogen, 133 Boston Post Rd, Weston, MA 20493, USA. Jacobs Comprehensive MS Treatment & Research Center, Department of Neurology, Jacobs School of Medicine & Biomedical Sciences University at Buffalo, Buffalo, NY 14202, USA.
 From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. From the Department of Neurology (S.D., A.M., A.R., C.B., F.H., J.P., B.A.), CRMBM, APHM, Aix Marseille University; and Centre Hospitalier d'Ajaccio (P.D.), France. bertrand.audoin@ap-hm.fr.
 Department of Neurology, Cerrahpaşa Medical Faculty, Istanbul University-Cerrahpaşa, Istanbul, Turkey.
 Institute for Brain Research and Rehabilitation, South China Normal University, Zhongshan Avenue West 55, Tianhe District, Guangzhou, 510631, China. School of Health Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Oxford Road, Manchester, M13 9PT, UK. Institute for Brain Research and Rehabilitation, South China Normal University, Zhongshan Avenue West 55, Tianhe District, Guangzhou, 510631, China. Institute for Brain Research and Rehabilitation, South China Normal University, Zhongshan Avenue West 55, Tianhe District, Guangzhou, 510631, China. Institute for Brain Research and Rehabilitation, South China Normal University, Zhongshan Avenue West 55, Tianhe District, Guangzhou, 510631, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, No.119, The West Southern 4th Ring Road, Fengtai District, Beijing, 100070, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, 130031, Jilin, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, No.119, The West Southern 4th Ring Road, Fengtai District, Beijing, 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, No.119, The West Southern 4th Ring Road, Fengtai District, Beijing, 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, No.119, The West Southern 4th Ring Road, Fengtai District, Beijing, 100070, China. Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China. China National Clinical Research Center for Neurological Diseases, Beijing, 100070, China. Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China. Department of Radiology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. Department of Radiology, The First Affiliated Hospital, Nanchang University, Nanchang, 330006, Jiangxi, China. Neuroimaging Lab, Jiangxi Province Medical Imaging Research Institute, Nanchang, 330006, Jiangxi, China. Department of Radiology, The First Affiliated Hospital, Nanchang University, Nanchang, 330006, Jiangxi, China. Neuroimaging Lab, Jiangxi Province Medical Imaging Research Institute, Nanchang, 330006, Jiangxi, China. Department of Radiology, Huashan Hospital, Fudan University, Shanghai, 200040, China. Department of Radiology, Huashan Hospital, Fudan University, Shanghai, 200040, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, 300052, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, 300052, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, 300052, China. Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China. China National Clinical Research Center for Neurological Diseases, Beijing, 100070, China. Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. School of Mechanical and Manufacturing Engineering (SMME), National University of Sciences and Technology (NUST), Islamabad, Pakistan. School of Health Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Oxford Road, Manchester, M13 9PT, UK. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, No.119, The West Southern 4th Ring Road, Fengtai District, Beijing, 100070, China. liuyaou@bjtth.org. Institute for Brain Research and Rehabilitation, South China Normal University, Zhongshan Avenue West 55, Tianhe District, Guangzhou, 510631, China. jinhui.wang.1982@m.scnu.edu.cn. Key Laboratory of Brain, Cognition and Education Sciences, Ministry of Education, Guangzhou, 510631, China. jinhui.wang.1982@m.scnu.edu.cn. Guangdong Key Laboratory of Mental Health and Cognitive Science, South China Normal University, Guangzhou, 510631, China. jinhui.wang.1982@m.scnu.edu.cn. Center for Studies of Psychological Application, South China Normal University, Guangzhou, 510631, China. jinhui.wang.1982@m.scnu.edu.cn.
 Department of Neurology, University of Rostock, Gehlsheimer Strasse 20, 18147, Rostock, Germany. Neuroimmunological Section, Department of Neurology, University of Rostock, Gehlsheimer Strasse 20, 18147, Rostock, Germany. Kliniken im Theodor-Wenzel-WerkKlinik für Psychiatrie, Potsdamer Chaussee 69, 14129, Berlin, Germany. Department of Neurology, University of Rostock, Gehlsheimer Strasse 20, 18147, Rostock, Germany. Neuroimmunological Section, Department of Neurology, University of Rostock, Gehlsheimer Strasse 20, 18147, Rostock, Germany. Department of Tropical Medicine and Infectious Diseases, University of Rostock, Ernst Heydemann Strasse 6, 18059, Rostock, Germany. micha.loebermann@uni-rostock.de.
 Department of Neurology, St James's Hospital, Dublin, Ireland. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom. Department of Neurology, St James's Hospital, Dublin, Ireland; Computational Neuroimaging Group (CNG), TBSI, Trinity College Dublin, Ireland. Centre for Advanced Medical Imaging, St James's Hospital and Trinity College Dublin, Dublin, Ireland. Department of Neurology, St James's Hospital, Dublin, Ireland; Academic Unit of Neurology, Trinity College Dublin, Ireland. Electronic address: KEARNEYH@tcd.ie.
 Department of Neurology, Yale School of Medicine, Yale University, New Haven, CT, USA. Electronic address: sharon.stoll@yale.edu. Yale University and Yale New Haven Hospital, New Haven, CT, USA. Yale University and Yale New Haven Hospital, New Haven, CT, USA.
 Department of Clinical Neurosciences, University of Medicine and Pharmacy Carol Davila, Bucharest, Romania. Department of Neurology, Colentina Clinical Hospital, Bucharest, Romania. Department of Neurology, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK. Department of Multiple Sclerosis and Neuroimmunology, CHU Grenoble, Grenoble, France. Academic Clinical Neurology, Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK. Department of Neurology, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK. Academic Clinical Neurology, Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK. Academic Clinical Neurology, Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK. Department of Neurology, Cooper Neurological Institute, Camden, NJ, USA. Department of Clinical Neurosciences, University of Medicine and Pharmacy Carol Davila, Bucharest, Romania. Department of Neurology, Colentina Clinical Hospital, Bucharest, Romania. Department of Neurology, Queen's Medical Centre, Nottingham University Hospitals, Nottingham, UK. Academic Clinical Neurology, Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK.
 Department of Nutrition and Movement Sciences, School of Nutrition and Translational Research in Metabolism, Maastricht University, The Netherlands; Department of Internal Medicine, Division of Rheumatology, Maastricht Universitair Medisch Centrum, and Care and Public Health Research Institute, The Netherlands; REVAL Rehabilitation Research Center, REVAL, Faculty of Rehabilitation Sciences, Hasselt University, Belgium. Electronic address: kyra.theunissen@maastrichtuniversity.nl. Department of Nutrition and Movement Sciences, School of Nutrition and Translational Research in Metabolism, Maastricht University, The Netherlands. Department of Internal Medicine, Division of Rheumatology, Maastricht Universitair Medisch Centrum, and Care and Public Health Research Institute, The Netherlands. REVAL Rehabilitation Research Center, REVAL, Faculty of Rehabilitation Sciences, Hasselt University, Belgium. REVAL Rehabilitation Research Center, REVAL, Faculty of Rehabilitation Sciences, Hasselt University, Belgium; Universitair MS Centrum Hasselt-Pelt, UMSC, Belgium. REVAL Rehabilitation Research Center, REVAL, Faculty of Rehabilitation Sciences, Hasselt University, Belgium; Universitair MS Centrum Hasselt-Pelt, UMSC, Belgium. Department of Nutrition and Movement Sciences, School of Nutrition and Translational Research in Metabolism, Maastricht University, The Netherlands.
 Department of Bio-Organic Synthesis, Leiden Institute of Chemistry, Leiden, the Netherlands. Department of Bio-Organic Synthesis, Leiden Institute of Chemistry, Leiden, the Netherlands. Section Molecular Neurobiology, Department Biomedical Sciences of Cells & Systems, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Department of Bio-Organic Synthesis, Leiden Institute of Chemistry, Leiden, the Netherlands. Department of Immunobiology, Biomedical Primate Research Center, Rijswijk, the Netherlands. Section Molecular Neurobiology, Department Biomedical Sciences of Cells & Systems, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Department of Immunobiology, Biomedical Primate Research Center, Rijswijk, the Netherlands. Department of Bio-Organic Synthesis, Leiden Institute of Chemistry, Leiden, the Netherlands. Section Molecular Neurobiology, Department Biomedical Sciences of Cells & Systems, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Electronic address: w.baron@umcg.nl. Department of Bio-Organic Synthesis, Leiden Institute of Chemistry, Leiden, the Netherlands. Electronic address: s.i.van.kasteren@chem.leidenuniv.nl.
 Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Ali.amini.harandi@gmail.com. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 Medical Resident, Department of Neurology and Neurosurgery, Sao Paulo Federal University, SP, Brazil. Department of Anesthesiology, Oncology and Radiology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. Rheumatology Division, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Sao Paulo University, SP, Brazil. Department of Anesthesiology, Oncology and Radiology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. University of Mississippi Medical Center, Jackson, MS. Department of Radiology and Diagnostic Imaging, HCPA, Porto Alegre, Rio Grande do Sul, Brazil. Department of Anesthesiology, Oncology and Radiology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. Department of Orthopedics, Rheumatology and Traumatology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. Department of Neurology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. Department of Anesthesiology, Oncology and Radiology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. Electronic address: fabianoreis2@gmail.com.
 Department of Neurology, St Vincent's Hospital, Darlinghurst, NSW 2010, Australia; Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia. Electronic address: jennifer.massey@svha.org.au. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia. Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia; Department of Haematology, St Vincent's Hospital; Darlinghurst, NSW 2010, Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia; Department of Haematology, St Vincent's Hospital; Darlinghurst, NSW 2010, Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia; School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia; Department of Haematology, St Vincent's Hospital; Darlinghurst, NSW 2010, Australia. School of Clinical Medicine, St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, UNSW, Sydney, Australia; Department of Neurology, St Vincent's Clinic; Darlinghurst, NSW 2010, Australia.
 Imaging Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: bhattap@ccf.org. Neurological Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: foxr@ccf.org. Imaging Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: sakaiek@ccf.org. Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: benaj@ccf.org. Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: harveyt16@ccf.org. Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: pxo11@case.edu. Imaging Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: linj2@ccf.org. Imaging Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: lowem1@ccf.org.
 Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Division of Clinical Neurosciences, University of Turku, Turku, Finland; Neurocenter Turku, University Hospital, Turku, Finland. Electronic address: sjkorp@utu.fi. Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Division of Clinical Neurosciences, University of Turku, Turku, Finland; Neurocenter Turku, University Hospital, Turku, Finland. Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Division of Clinical Neurosciences, University of Turku, Turku, Finland; Neurocenter Turku, University Hospital, Turku, Finland. Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Division of Clinical Neurosciences, University of Turku, Turku, Finland; Neurocenter Turku, University Hospital, Turku, Finland. Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Division of Clinical Neurosciences, University of Turku, Turku, Finland; Neurocenter Turku, University Hospital, Turku, Finland. Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Faculty of Science and Engineering, Åbo Akademi University, Turku, Finland. Department of Radiology, University of Turku and Turku University Hospital, Turku, Finland. Turku PET Centre, Turku University Hospital and University of Turku, Turku, Finland; Division of Clinical Neurosciences, University of Turku, Turku, Finland; Neurocenter Turku, University Hospital, Turku, Finland.
 Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco. Department of Neurology, University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, Basel, Switzerland. Weill Institute for Neurosciences, Department of Neurology, University of California at San Francisco.
 Unidad de Investigación en Salud (UIS), Chihuahua, Mexico. Electronic address: merced.velazquez@uis.com.mx. UIS Southern Mexico, Mexico City, Mexico. Faculty of Medicine, Universidad Autónoma de Chihuahua, Chihuahua, Mexico. Hospital General de Zona #2, IMSS, Hermosillo, Sonora, Mexico. Hospital General del ISSSTE, San Luis Potosí, Mexico. Clínica de Enfermedades Desmielinizantes, Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", Mexico City, Mexico. Hospital General de Zona #46, IMSS, Tabasco, Mexico.
 Government Medical College, Kerala University of Health Sciences (KUHS), Thiruvananthapuram, India. archajames@gmail.com. Government Medical College, Kerala University of Health Sciences (KUHS), Thiruvananthapuram, India. Department of Endocrinology, Diabetes and Metabolism, UnityPoint Clinic, UnityPoint Health-Methodist Hospital, Peoria, IL, USA.
 Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, Bordeaux, France. University of Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux, France. Department of Medical Imaging, The University of Arizona, Tucson, AZ, USA. University of Bordeaux, CNRS, Bordeaux INP, LABRI, UMR5800, Talence, France. Service de neurologie, CHU de Bordeaux, Bordeaux, France. Service de neurologie, CHU de Bordeaux, Bordeaux, France. Service de neurologie, CHU de Bordeaux, Bordeaux, France. Canon Medical Systems Europe, Zoetermeer, The Netherlands. Department of Radiology, Stanford University, Stanford, CA, USA. Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, Bordeaux, France/University of Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux, France. University of Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux, France. University of Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux, France/Service de neurologie, CHU de Bordeaux, Bordeaux, France. Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, Bordeaux, France/University of Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux, France.
 College of Engineering, University of South Florida, Tampa, FL, USA.
 Zabol university of medical sciences, Zabol, Iran. Student's Scientific research center, Tehran University of Medical Sciences, Tehran, Iran. Faculty of Medicine, Tabriz University of Medical Science, Tabriz, Iran. Multiple Sclerosis Research Group (MSRG), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Group (MSRG), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Group (MSRG), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. mghajar2@jhmi.edu. Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. mghajar2@jhmi.edu.
 Division of Infection Control, Section for Immunology, Norwegian Institute of Public Health, Oslo, Norway. Division of Infection Control, Section for Immunology, Norwegian Institute of Public Health, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Division of Infection Control, Section for Immunology, Norwegian Institute of Public Health, Oslo, Norway. Division of Infection Control, Section for Immunology, Norwegian Institute of Public Health, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Neurology, Akershus University Hospital, Lørenskog, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Center for Treatment of Rheumatic and Musculoskeletal Diseases, Diakonhjemmet Hospital, Oslo, Norway. Department of Gastroenterology, Akershus University Hospital, Lørenskog, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Department of Psychology and. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. KG Jebsen Centre for B Cell Malignancy, University of Oslo, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Division of Infection Control, Section for Immunology, Norwegian Institute of Public Health, Oslo, Norway.
 Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium; Neuroinflammation Imaging Lab (NIL), Université Catholique de Louvain, Brussels, Belgium; Centre Hospitalier Universitaire Vaudois, Université de Lausanne, Lausanne, Switzerland. Electronic address: pietro.maggi@uclouvain.be. Neuroinflammation Imaging Lab (NIL), Université Catholique de Louvain, Brussels, Belgium. Institute of Experimental Neurology, Division of Neuroscience, Vita-Salute San Raffaele University and IRCCS San Raffaele Hospital, Milan, Italy. Plateforme Technologique de Support en Méthodologie et Calcul Statistique, Université Catholique de Louvain, Brussels, Belgium. Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium. Neuroinflammation Imaging Lab (NIL), Université Catholique de Louvain, Brussels, Belgium. Neuroinflammation Imaging Lab (NIL), Université Catholique de Louvain, Brussels, Belgium. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Hôpital Erasme, Université Libre de Bruxelles, Bruxelles, Belgium. Hôpital Erasme, Université Libre de Bruxelles, Bruxelles, Belgium. Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium. Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD, USA. Institute of Experimental Neurology, Division of Neuroscience, Vita-Salute San Raffaele University and IRCCS San Raffaele Hospital, Milan, Italy; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: absinta.martina@hsr.it.
 McGill University, Montreal Neurological Institute, Montreal, Quebec, Canada. McGill University, Montreal Neurological Institute, Montreal, Quebec, Canada. McGill University, Montreal Neurological Institute, Montreal, Quebec, Canada. McGill University, Montreal Neurological Institute, Montreal, Quebec, Canada.
 Department of Molecular Biology, Faculty of Medicine, Islamic Azad University, Shiraz, Iran. Regenerative Medicine, Organ Procurement and Transplantation Multi Disciplinary Center, Razi Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran. Department of Medical Genetics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Medical Genetics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Immunology and Autoimmune Diseases Research Center, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Molecular Biology, Faculty of Medicine, Islamic Azad University, Shiraz, Iran.
 Nature Immunology, . stephanie.houston@us.nature.com.
 Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster (UKM), Münster, Germany. Department of Neurology, University of Düsseldorf, Dusseldorf, Germany. Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Weill Institute for Neurosciences, Department of Neurology, UCSF, San Francisco, California, USA. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany. Chica and Heinz Schaller Research Group, Institute of Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany. Optical Microscopy Facility, Max Planck Institute for Medical Research, Heidelberg, Germany. Electron Microscopy Core Unit, Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany. Cluster of Excellence, "Multiscale Bioimaging: from Molecular Machines to Network of Excitable Cells" (MBExC), University of Göttingen, Göttingen, Germany. Weill Institute for Neurosciences, Department of Neurology, UCSF, San Francisco, California, USA. Weill Institute for Neurosciences, Department of Neurology, UCSF, San Francisco, California, USA. Neurologic Clinic and Policlinic and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Medicine, Biomedicine, and Clinical Research, University Hospital of Basel, University of Basel, Basel, Switzerland. Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster (UKM), Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster (UKM), Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster (UKM), Münster, Germany. Department of Neurology, University of Düsseldorf, Dusseldorf, Germany. Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Chica and Heinz Schaller Research Group, Institute of Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany. Weill Institute for Neurosciences, Department of Neurology, UCSF, San Francisco, California, USA. Institute for Genetics of Heart Diseases (IfGH), Cellular Electrophysiology and Molecular Biology, UKM, Münster, Germany. University of Münster, Chembion, Münster, Germany. University of Münster, Chembion, Münster, Germany. Institute of Physiology I, University of Münster, Münster, Germany. Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research and. Department of Pediatrics, UCSF, San Francisco, California, USA. Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research and. Department of Pediatrics, UCSF, San Francisco, California, USA. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) and Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany. Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Institute for Genetics of Heart Diseases (IfGH), Cellular Electrophysiology and Molecular Biology, UKM, Münster, Germany. Electron Microscopy Core Unit, Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology, Munich, Germany. Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), INF 280, Heidelberg, Germany. Interdisciplinary Center for Neurosciences (IZN) and. Mannheim Center for Translational Neuroscience and Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) and Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, Germany. Neurocure Cluster of Excellence, Charité University Medicine Berlin, Berlin, Germany. Mannheim Center for Translational Neuroscience and Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Institute of Neuroanatomy, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Institute of Anatomy and Cell Biology, Johannes Kepler University Linz, Linz, Austria. Institute of Physiology I, University of Münster, Münster, Germany. Electron Microscopy Core Unit, Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany. Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany. Weill Institute for Neurosciences, Department of Neurology, UCSF, San Francisco, California, USA. Department of Ophthalmology, UCSF, San Francisco, California, USA. Chica and Heinz Schaller Research Group, Institute of Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany. Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research and. Department of Pediatrics, UCSF, San Francisco, California, USA. Wellcome Trust-Medical Research Council Stem Cell Institute and. Department of Paediatrics, University of Cambridge, Cambridge, United Kingdom. Department of Neurosurgery, UCSF, San Francisco, California, USA. Department of Neurology with Institute of Translational Neurology, University Hospital Münster (UKM), Münster, Germany. Department of Neurology, University of Düsseldorf, Dusseldorf, Germany. Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Interdisciplinary Center for Neurosciences (IZN) and. Mannheim Center for Translational Neuroscience and Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
 Neurology MS Clinic Nice, Pasteur 2 University Hospital, UR2CA-URRIS, Côte d'Azur University, Nice 06002, France. Neuroinnovation Program, Multiple Sclerosis, and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Department of Neurology, Istanbul University Cerrahpasa School of Medicine, 34098 Istanbul, Turkey. Neurology MS Clinic Nice, Pasteur 2 University Hospital, UR2CA-URRIS, Côte d'Azur University, Nice 06002, France. Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Neurology MS Clinic Nice, Pasteur 2 University Hospital, UR2CA-URRIS, Côte d'Azur University, Nice 06002, France. Neurology MS Clinic, Montpellier University Hospital, 34295 Montpellier, France. University of Montpellier (MUSE), 34295 Montpellier, France. Inserm UMR-S 1172 LilNcog, Lille University, Lille University Hospital Precise, 59000 Lille, France. Department of Neurology, Sorbonne University, AP-HP, Pitié-Salpêtrière Hospital, 75013 Paris, France. Neurology MS Clinic, Neurological Hospital Pierre Wertheimer, Lyon University Hospital, 69500 Lyon/Bron, France. Neurology MS Clinic Rennes, Clinical Investigation Centre CIC-P 1414, Rennes University Hospital, 35000 Rennes, France. Neurology, Rothschild Foundation, 75019 Paris, France. Neurology MS Clinic Bordeaux, University Hospital, 33000 Bordeaux, France. Neurocentre Magendie, Bordeaux University, INSERM, U1215, 33000 Bordeaux, France. Neurology MS Clinic, Toulouse University Hospital, 31300 Toulouse, France. Infinity, INSERM UMR1291, CNRS UMR5051, Toulouse III University, 31300 Toulouse, France. Neurology, Nantes University Hospital, CIC1314 INSERM, 44000 Nantes, France. CR2TI INSERM U1064, Nantes University, 44000 Nantes, France. Neurology MS Clinic Grenoble, Grenoble Alpes University Hospital, 38700 Grenoble, France. T-RAIG, TIMC-IMAG, Grenoble Alpes University, 38700 Grenoble, France. Neurology, Nancy University Hospital, 54000 Nancy, France. Vandoeuvre-Lès-Nancy, Lorraine University, EA 4360 APEMAC, 54000 Nancy, France. Clinical Investigation Center, Neurology, Strasbourg University Hospital, INSERM 1434, 67200 Strasbourg, France. Neurology and Radiology, Mayo Clinic, Rochester, MN 55905, USA. Pediatrics and Neurology, Yale School of Medicine, New Haven, CT 06510, USA. Department of Neurology, Istanbul University Cerrahpasa School of Medicine, 34098 Istanbul, Turkey. Neurology MS Clinic Nice, Pasteur 2 University Hospital, UR2CA-URRIS, Côte d'Azur University, Nice 06002, France. Neurology MS Clinic Nice, Pasteur 2 University Hospital, UR2CA-URRIS, Côte d'Azur University, Nice 06002, France. Neurology, Nîmes University Hospital, 30900 Nîmes, France. IGF, Montpellier University, CNRS, INSERM, 34295 Montpellier, France. Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Neurology, Mayo Clinic, Rochester, MN 55905, USA.
 Adis, Auckland, New Zealand. sue.pochon@springer.com.
 Department of Applied Economics, Public Economics and Political Economy, University Complutense of Madrid, Pl. Menéndez Pelayo 4, 28040, Madrid, Spain. Graduate School of Health Economics and Management (Alta Scuola Di Economia E Management Dei Sistemi Sanitari), Universitá Cattolica del Sacro Cuore, Rome, Italy. Economic Analysis and Finance Department, Faculty of Law and Social Sciences, University of Castilla-La Mancha, 45071, Toledo, Spain. Economic Analysis and Finance Department, Faculty of Law and Social Sciences, University of Castilla-La Mancha, 45071, Toledo, Spain. Economic Analysis and Finance Department, Faculty of Social Sciences, University of Castilla-La Mancha, Avda. Real Fábrica de Seda s/n, 45600, Talavera de la Reina, Toledo, Spain. isaac.aranda@uclm.es. Graduate School of Health Economics and Management (Alta Scuola Di Economia E Management Dei Sistemi Sanitari), Universitá Cattolica del Sacro Cuore, Rome, Italy. Faculty of Health Sciences, Universidad Castilla-La Mancha, 45600, Talavera de la Reina, Toledo, Spain.
 Ferkauf Graduate School of Psychology. Ferkauf Graduate School of Psychology. Ferkauf Graduate School of Psychology. Ferkauf Graduate School of Psychology. Multiple Sclerosis Comprehensive Care Center. Ferkauf Graduate School of Psychology.
 Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Psychology, Stockholm University, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Division of Neurology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China. State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Screening, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, China Pharmaceutical University, Nanjing, China. Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China. Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China. State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Screening, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, China Pharmaceutical University, Nanjing, China. Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China. Department of Neurology, Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University of Chinese Medicine, Nanjing University, Nanjing, Jiangsu, China. Institute of Brain Sciences, Institute of Brain Disorder Translational Medicine, Nanjing University, Nanjing, Jiangsu, China. Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu, China. Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu, China.
 Laboratory of Neuroimmunology, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Laboratory of Molecular Virology and Antiviral Research, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Laboratory of Molecular Virology and Antiviral Research, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Laboratory of Neuroimmunology, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. San Luigi Gonzaga University Hospital, Orbassano, Italy. Laboratory of Neuroimmunology, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Laboratory of Molecular Virology and Antiviral Research, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. Laboratory of Neuroimmunology, Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. San Luigi Gonzaga University Hospital, Orbassano, Italy.
 Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
 Immuno-oncology Branch, Research Institute, National Cancer Center, Goyang, Korea; Yonsei University College of Medicine, Seoul, Korea; Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Immuno-oncology Branch, Research Institute, National Cancer Center, Goyang, Korea; Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Immuno-oncology Branch, Research Institute, National Cancer Center, Goyang, Korea; Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Immuno-oncology Branch, Research Institute, National Cancer Center, Goyang, Korea; Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Immuno-oncology Branch, Research Institute, National Cancer Center, Goyang, Korea. Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Yonsei University College of Medicine, Seoul, Korea. Immuno-oncology Branch, Research Institute, National Cancer Center, Goyang, Korea; Department of Neurology, Hospital of National Cancer Center, Goyang, Korea. Electronic address: hojinkim@ncc.re.kr.
 Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic; Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic. Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic; Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic. Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic; Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic. Electronic address: pavel.sistik@fno.cz. Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic; Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic. Clinic of Neurology, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic; Clinic of Neurology, University Hospital Ostrava, Ostrava, Czech Republic. Department of Clinical Pharmacology, Institute of Laboratory Medicine, University Hospital Ostrava, 17. listopadu 1790, 708 52 Ostrava, Czech Republic; Department of Clinical Pharmacology, Faculty of Medicine, University of Ostrava, Syllabova 19, 703 00 Ostrava, Czech Republic.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. Department of Physiology and Neurology, Shanxi Medical University, 030001, Taiyuan, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. Department of Physiology and Neurology, Shanxi Medical University, 030001, Taiyuan, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. Department of Neuroscience, City University of Hong Kong, Tat Chee Avenue, Hong Kong. gkumar@cityu.edu.hk. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. 779734216@qq.com. Institute of Brain Science, Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases, Medical School of Shanxi Datong University, 037009, Datong, China. 779734216@qq.com. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China. macungen@sxtcm.edu.cn. Institute of Brain Science, Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases, Medical School of Shanxi Datong University, 037009, Datong, China. macungen@sxtcm.edu.cn.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 School of Chemistry and Biochemistry, Georgia Institute of Technology, Atlanta, Georgia, USA; Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Neuroscience Program, Beckman Institute, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Neuroscience Program, Beckman Institute, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Department of Bioengineering, Cancer Center at Illinois, Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Electronic address: asteelma@illinois.edu. School of Chemistry and Biochemistry, Georgia Institute of Technology, Atlanta, Georgia, USA; Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA; Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. Electronic address: aditi.das@chemistry.gatech.edu.
 Institute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes-Gutenberg University, Hanns-Dieter-Hüsch-Weg 15, 55128 Mainz, Germany. Institute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes-Gutenberg University, Hanns-Dieter-Hüsch-Weg 15, 55128 Mainz, Germany.
 Department of Immunology, School of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran. Department of Immunology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Cardiovascular Diseases, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Mashhad University of Medical Sciences, Mashhad, Iran. Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
 Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON, Canada. Department of Immunology, University of Toronto, Toronto, ON, Canada. Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON, Canada. Shannon.Dunn@unityhealth.to. Department of Immunology, University of Toronto, Toronto, ON, Canada. Shannon.Dunn@unityhealth.to. Women's College Research Institute, Toronto, ON, Canada. Shannon.Dunn@unityhealth.to.
 Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia. National Research Center Institute of Immunology of the Federal Medical Biological Agency, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. National Research Center Institute of Immunology of the Federal Medical Biological Agency, Moscow, Russia. Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia. Pirogov Russian National Research Medical University, Moscow, Russia.
 Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Denmark. Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Denmark. Department of Radiology, Rigshospitalet Glostrup, Denmark. Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Denmark. Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Denmark. Department of Neurosurgery, Rigshospitalet Blegdamsvej, Denmark. Department of Neurosurgery, Rigshospitalet Blegdamsvej, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet Glostrup, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Science, University of Copenhagen, Denmark. Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Denmark. Danish Headache Center, Department of Neurology, Rigshospitalet Glostrup, Denmark.
 Sanford Burnham Prebys Medical Discovery Institute, United States of America. Electronic address: ykihara@sbpdiscovery.org. Sanford Burnham Prebys Medical Discovery Institute, United States of America.
 MS Clinic, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
 Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University, Daegu, Republic of Korea. Department of Physical Medicine and Rehabilitation, Daegu Fatima Hospital, Ayang-Ro 99 Gil, Dong-Gu, Daegu, 41199, Republic of Korea. Department of Physical Medicine and Rehabilitation, Ulsan University Hospital, Ulsan University College of Medicine, Ulsan, Korea. Department of Physical Medicine and Rehabilitation, Ulsan University Hospital, Ulsan University College of Medicine, Ulsan, Korea. Department of Physical Medicine and Rehabilitation, Daegu Fatima Hospital, Ayang-Ro 99 Gil, Dong-Gu, Daegu, 41199, Republic of Korea. bdome@hanmail.net. Department of Neurology, Ulsan University Hospital, Ulsan University College of Medicine, 877 Bangeojin sunhwando-ro, Dong-gu, 44033, Ulsan, Korea. sykim@uuh.ulsan.kr.
 Research Center of Neurology, Moscow, Russia. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia. Research Center of Neurology, Moscow, Russia. Research Institute of Eye Diseases, Moscow, Russia. Research Institute of Eye Diseases, Moscow, Russia. Research Institute of Eye Diseases, Moscow, Russia. Research Centre for Medical Genetics, Moscow, Russia. Research Centre for Medical Genetics, Moscow, Russia. Research Center of Neurology, Moscow, Russia. Research Institute of Eye Diseases, Moscow, Russia.
 Department of Biomedical Sciences, Division of Neuroscience and Clinical Pharmacology, University of Cagliari, Italy. Electronic address: dedoni@unica.it. Department of Biomedical Sciences, Division of Neuroscience and Clinical Pharmacology, University of Cagliari, Italy. Electronic address: mscherma@unica.it. Department of Biomedical Sciences, Division of Neuroscience and Clinical Pharmacology, University of Cagliari, Italy. Electronic address: chiara.camoglio@unica.it. Department of Biomedical Sciences, Division of Neuroscience and Clinical Pharmacology, University of Cagliari, Italy. Department of Life and Environmental Sciences, Section of Neuroscience and Anthropology, University of Cagliari, Monserrato (Cagliari), Italy. Electronic address: dazzi@unica.it. Department of Life and Environmental Sciences, Section of Neuroscience and Anthropology, University of Cagliari, Monserrato (Cagliari), Italy. Electronic address: roberta.puliga@unica.it. Regional Multiple Sclerosis Center, ASSL Cagliari, ATS Sardegna, Italy. Regional Multiple Sclerosis Center, ASSL Cagliari, ATS Sardegna, Italy; Department Medical Science and Public Health, University of Cagliari, Italy. Electronic address: ecocco@unica.it. Department of Biomedical Sciences, Division of Neuroscience and Clinical Pharmacology, University of Cagliari, Italy; Neuroscience Institute, Section of Cagliari, National Research Council of Italy (CNR), Cagliari, Italy. Electronic address: p.fadda@unica.it.
 Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. Department of Public Health, Federico II University of Naples, Naples, Italy. Centre for Advanced Biotechnology (CEINGE), Naples, Italy. Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Department of Translational Medical Sciences, Federico II University of Naples, Naples, Italy. Centre for Advanced Biotechnology (CEINGE), Naples, Italy. Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. Department of Human Neuroscience, Sapienza University of Rome, Rome, Italy. Department of Translational Medical Sciences, Federico II University of Naples, Naples, Italy. Centre for Advanced Biotechnology (CEINGE), Naples, Italy. Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. Multiple Sclerosis Unit, Federico II University Hospital, Via Sergio Pansini 5, 80131, Naples, Italy. moccia.marcello@gmail.com. Department of Molecular Medicine and Medical Biotechnology, Federico II University of Naples, Via Sergio Pansini 5, 80131, Naples, Italy. moccia.marcello@gmail.com.
 Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, 66421 Homburg, Germany. Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, 66421 Homburg, Germany.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA. Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Cancer Prevention Research Center, Omid Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Biostatistics and Epidemiology, Faculty of Health, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. University of Cincinnati, Cincinnati, OH, USA. Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: shaghayegh.haghjoo@gmail.com. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: shaygannejad@med.mui.ac.ir.
 Department of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, United States. Electronic address: claudia.cantoni@barrowneuro.org. Department of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States; Department of Biomedical, Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy; Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, 20122 Milan, Italy. Department of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States. Department of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States. Department of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States; Charles Perkins Centre, School of Medical Sciences, The University of Sydney, Sydney, NSW, Australia.
 Department of Neuroimmunology, Netherlands Institute for Neuroscience, Royal Netherlands Academy for Arts and Sciences, Amsterdam, the Netherlands. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Department of Neuroimmunology, Netherlands Institute for Neuroscience, Royal Netherlands Academy for Arts and Sciences, Amsterdam, the Netherlands. Department of Experimental Immunology, Amsterdam Institute for Infection and Immunity, Amsterdam University Medical Centers, Amsterdam, the Netherlands. Department of Neuroimmunology, Netherlands Institute for Neuroscience, Royal Netherlands Academy for Arts and Sciences, Amsterdam, the Netherlands. Department of Neurology and Immunology, Multiple Sclerosis Center ErasMS, Erasmus Medical Center, Rotterdam, the Netherlands. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Department of Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Department of Axonal Signaling, Netherlands Institute for Neuroscience, Royal Netherlands Academy for Arts and Sciences, Amsterdam, the Netherlands. Cell Biology, Neurobiology, and Biophysics, Department of Biology, Faculty of Science, University of Utrecht, Utrecht, the Netherlands. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Department of Neuroimmunology, Netherlands Institute for Neuroscience, Royal Netherlands Academy for Arts and Sciences, Amsterdam, the Netherlands. Center for Neuroscience, Swammerdam Institute for Life Sciences, Faculty of Science, University of Amsterdam, Amsterdam, the Netherlands.
 Clinical Department of Neurology, Medical University of Innsbruck, Austria; Department of Rehabilitation Research, Rehab Centre Münster, Austria. Electronic address: barbara.seebacher@i-med.ac.at. Clinical Department of Neurology, Medical University of Innsbruck, Austria. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Izmir Katip Celebi University, Turkey.
 IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. IRCSS Neuromed, Pozzilli, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Laboratorio di Immunologia, Istituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), 80131 Napoli, Italy; Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, 00179 Rome, Italy. IRCSS Neuromed, Pozzilli, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Italy; Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Italy. Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Italy; Department of Systems Medicine, Tor Vergata University, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Italy; Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Italy. Laboratorio di Immunologia, Istituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), 80131 Napoli, Italy; Treg Cell Lab, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II," 80131 Napoli, Italy. IRCSS Neuromed, Pozzilli, Italy; Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Italy. Electronic address: centonze@uniroma2.it. IRCSS Neuromed, Pozzilli, Italy.
 Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Laboratory of Neuro-Oncology, Clinical and Cancer Proteomics, Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Laboratory of Neuro-Oncology, Clinical and Cancer Proteomics, Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Laboratory of Neuro-Oncology, Clinical and Cancer Proteomics, Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Division of Child Neurology, Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Center for Neuroinflammation and Experimental Therapeutics and Division of Multiple Sclerosis and Related Disorders, Department of Neurology, Perelman Center for Advanced Medicine (PCAM), University of Pennsylvania. Laboratory of Neuro-Oncology, Clinical and Cancer Proteomics, Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands.
 Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Joannaakulikowska@gmail.com. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Bialystok, Poland. Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Independent statistic consultant. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Bialystok, Poland. Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland.
 Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria. Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria. Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria. Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria. Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria. Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria. Department of Neurology, Medical University of Vienna, 1090 Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria.
 Springer Medizin, Neu-Isenburg, Germany.
 Department of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, Florence, Italy. Electronic address: daniela.buonvicino@unifi.it. Department of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, Florence, Italy. Imaging Platform, Department of Experimental & Clinical Medicine, University of Florence, Florence, Italy. Department of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, Florence, Italy. Department of Neuroscience, Psychology, Drug Sciences, and Child Health (NEUROFARBA),University of Florence, Florence, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy. Department of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, Florence, Italy.
 Department of Biology, College of Science, University of Baghdad, Baghdad, Iraq. Department of Biology, College of Science, University of Baghdad, Baghdad, Iraq. Tropical-Biological Research Unit, College of Science, University of Baghdad, Al-Jadriya, Baghdad, Iraq. dr.ahadhiah@sc.uobaghdad.edu.iq.
 The Corinne Goldsmith Dickinson Center for MS at Icahn School of Medicine at Mount Sinai Hospital, New York, NY, USA. Multiple Sclerosis Clinical and Research Center, Columbia University Irving Medical Center, New York Presbyterian, New York, NY, USA. Neurological Associates of Long Island, New Hyde Park, NY, USA. Biostatistics Unit, Feinstein Institutes for Medical Research, Northwell Health, Great Neck, NY, USA. NYU Multiple Sclerosis Comprehensive Care Center, NYU Langone Health, New York, NY, USA. Neurological Associates of Long Island, New Hyde Park, NY, USA. NYU Multiple Sclerosis Comprehensive Care Center, NYU Langone Health, New York, NY, USA. Northwell Comprehensive Multiple Sclerosis Center, Lenox Hill Hospital and North Shore University Hospital, New York, NY, USA.
 Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, South Carolina, USA.
 Colorado State University, Fort Collins, CO, USA. Colorado State University, Fort Collins, CO, USA. Colorado State University, Fort Collins, CO, USA. Colorado State University, Fort Collins, CO, USA. Colorado State University, Fort Collins, CO, USA. Clemson University, Clemson, SC, USA. Clemson University, Clemson, SC, USA. Colorado State University, Fort Collins, CO, USA.
 IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, 20147 Milan, Italy. Pathophysiology and Transplantation Department, University of Milan, 20122 Milan, Italy.
 Student Research Committee, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Department of Microbiology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. hamidrezamozhgani@gmail.com. Non-communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran. hamidrezamozhgani@gmail.com.
 University of Southern California, Los Angeles, California. Electronic address: ilan@usc.edu. University of Florida, Gainesville, Florida.
 Hospital do Servidor Público Estadual de São Paulo, Serviço de Neurologia, São Paulo SP, Brazil. Hospital do Servidor Público Estadual de São Paulo, Serviço de Neurologia, São Paulo SP, Brazil. Hospital do Servidor Público Estadual de São Paulo, Serviço de Neurologia, São Paulo SP, Brazil. Hospital do Servidor Público Estadual de São Paulo, Serviço de Neurologia, São Paulo SP, Brazil.
 Department of Neurology, University of Chicago Medicine, Chicago, IL, USA. Peter O'Donnell Jr. Brain Institute, UT Southwestern Medical Center, Dallas, TX, USA; VA North Texas Health Care System, Dallas VA Medical Center, Dallas, TX, USA. Mount Sinai Health System, New York, NY, USA. Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
 Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, International Campus, Tehran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology and MS Research Center, Neuroscience Institute, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, International Campus, Tehran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
 Department of Neurosciences, King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia; Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Department of Quantitative Health Sciences, Cleveland Clinic Foundation, Cleveland, OH, USA. Population Health Research Institute, The MetroHealth System, Cleveland, OH, USA; Department of Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Department of Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
 Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT, 06112, United States; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT, 06473, United States. Electronic address: heather.delmastro@TrinityHealthOfNE.org. Department of Physical Therapy, School of Health Sciences at Quinnipiac University, 370 Bassett Road, North Haven, CT, 06473, United States. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT, 06112, United States; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT, 06473, United States; Department of Medical Sciences, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT, 06473, United States; Department of Neurology, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT, 06030, United States. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT, 06112, United States; Rehabilitation Medicine, Department of Veterans Affairs, 555 Willard Avenue, Newington, CT, 06111 United States. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT, 06112, United States; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT, 06473, United States; Department of Medical Sciences, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT, 06473, United States.
 Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA. Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA/ Department of Neurology, Mercy Health, Toledo, OH, USA. Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA. Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA. Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA/ Department of Neurology, UVA Health, Charlottesville, VA, USA. Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA.
 Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Sveti Duh, Zagreb, Croatia. jbartolo@kbsd.hr. Department of Speech and Language Pathology (Z.K.), University of Rijeka, Rijeka, Croatia. Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Sveti Duh, Zagreb, Croatia. Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Sveti Duh, Zagreb, Croatia.
 Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA/Center for Computational Biology, College of Engineering, University of California, Berkeley, CA, USA. Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA. Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA/Department of Human Genetics, University of Utah, Salt Lake City, UT, USA. Department of Neurosciences, School of Medicine, University of California, San Diego, CA, USA/Department of Neurology, University of California, San Francisco, CA, USA. Pediatric MS Center, Loma Linda University Children's Hospital, San Bernardino, CA, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Pediatric-Onset Demyelinating Diseases and Autoimmune Encephalitis Center, St. Louis Children's Hospital, Washington University School of Medicine, St. Louis, MO, USA. Alabama Center for Pediatric-Onset Demyelinating Disease, Children's Hospital of Alabama, Birmingham, AL, USA. Pediatric Multiple Sclerosis Center, Jacobs Neurological Institute, SUNY Buffalo, NY, USA. Division of Neurology, Children's Hospital of Philadelphia, Philadelphia, PA, USA. Children's Hospital Colorado, University of Colorado, Denver, CO, USA. Mayo Clinic's Pediatric Multiple Sclerosis Center, Rochester, MN, USA. Mayo Clinic's Pediatric Multiple Sclerosis Center, Rochester, MN, USA. Partners Pediatric Multiple Sclerosis Center, Massachusetts General Hospital for Children, Boston, MA, USA. Lourie Center for Pediatric Multiple Sclerosis, Stony Brook Children's Hospital, Stony Brook, NY, USA. Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, UT, USA. Mellen Center, Cleveland Clinic, Cleveland, OH, USA. Regional Pediatric MS Center, Neurology, University of California, San Francisco, CA, USA. Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA/Center for Computational Biology, College of Engineering, University of California, Berkeley, CA, USA. Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA/Center for Computational Biology, College of Engineering, University of California, Berkeley, CA, USA. Kaiser Permanente Division of Research, Oakland, CA, USA. Department of Neurology, University of California, San Francisco, CA, USA. Division of Epidemiology, School of Public Health, University of California, Berkeley, CA, USA/Center for Computational Biology, College of Engineering, University of California, Berkeley, CA, USA/Kaiser Permanente Division of Research, Oakland, CA, USA.
 Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. DHQ Teaching Hospital Timergara, Lower Dir, Timergara, Pakistan. Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmaceutical Sciences, Pak-Austria Fachhochschule Institute of Applied Sciences and Technology, Haripur, Pakistan. Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Faculty of Pharmaceutical Sciences, Abasyn University, Peshawar, Pakistan. Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Division of Physical Sciences, Department of Chemistry and Biochemistry, University of California, Santa Cruz, California, USA. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan. Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan.
 Department of Pharmaceutics, Novel Drug Delivery Systems Research Centre, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: sharifian@pharm.mui.ac.ir. Department of Pharmaceutics, Novel Drug Delivery Systems Research Centre, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: varshosaz@pharm.mui.ac.ir. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: maliomrani@pharm.mui.ac.ir. Department of Genetics, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: kazemigenetics@gmail.com.
 Translational Neuroscience Program, Wayne State University, Detroit, Michigan, USA. Neuroimaging and Neurorehabilitation Laboratory, Wayne State University, Detroit, Michigan, USA. Translational Neuroscience Program, Wayne State University, Detroit, Michigan, USA. Department of Psychiatry and Behavioral Neurosciences, Wayne State University, Detroit, Michigan, USA. Department of Psychology, Wayne State University, Detroit, Michigan, USA. Institute of Gerontology, Wayne State University, Detroit, Michigan, USA. Department of Psychiatry and Behavioral Neurosciences, Wayne State University, Detroit, Michigan, USA. Division of Physical Therapy, Department of Rehabilitation Medicine, Emory University School of Medicine, Atlanta, Georgia, USA. Translational Neuroscience Program, Wayne State University, Detroit, Michigan, USA. Neuroimaging and Neurorehabilitation Laboratory, Wayne State University, Detroit, Michigan, USA. Department of Health Care Sciences, Wayne State University, Detroit, Michigan, USA. Department of Neurology, Wayne State University, Detroit, Michigan, USA.
 Rocky Mountain Multiple Sclerosis Center, University of Colorado, Aurora, CO, USA. Rocky Mountain Multiple Sclerosis Center, University of Colorado, Aurora, CO, USA. HealthCore, Inc, Wilmington, DE, USA. HealthCore, Inc, Wilmington, DE, USA. HealthCore, Inc, Wilmington, DE, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
 Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Service Hospitalier Frédéric Joliot, Université Paris-Saclay, CEA, CNRS, Inserm, BioMaps, Orsay, France. Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Neurology Department, St Antoine Hospital, APHP, Paris, France. Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Neurology Department, St Antoine Hospital, APHP, Paris, France. Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Neurology Department, Pitié-Salpêtrière Hospital, APHP, Paris, France. Service Hospitalier Frédéric Joliot, Université Paris-Saclay, CEA, CNRS, Inserm, BioMaps, Orsay, France. Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Neurology Department, St Antoine Hospital, APHP, Paris, France. Paris Brain Institute, Sorbonne Université, ICM, CNRS, Inserm, Paris, France. Neurology Department, St Antoine Hospital, APHP, Paris, France.

 Health Economist and Research Director, Studio di Economia Sanitaria, Via Stefanardo da Vimercate, 19, 20128, Milan, Italy. carlo.lazzaro@tiscalinet.it. School of Pharmacology, Biology and Biotechnologies Department "Lazzaro Spallanzani", University of Pavia, 27100, Pavia, Italy. carlo.lazzaro@tiscalinet.it.
 Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Parmaceutical Analysis Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Research Center for Integrative Medicine in Aging, Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran. Emergency and Trauma Care Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran. Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran; Faculty of Pharmacy, Near East University, POBOX:99138, Nicosia, North Cyprus, Mersin 10, Turkey. Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: alizadehaa@tbzmed.ac.ir.
 Unidad de Neuroinmunología- Esclerosis múltiple, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), |Universitat de Barcelona, Barcelona, Spain. Unidad de Neuroinmunología- Esclerosis múltiple, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), |Universitat de Barcelona, Barcelona, Spain. Hospital Universitari Mútua de Terrassa, Terrassa, Barcelona, Spain. Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. Hospital Residencia Sant Camil, Sant Pere de Ribes, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Hospital Universitari Arnau de Vilanova, Lleida, Spain. Hospital Universitari Arnau de Vilanova, Lleida, Spain. Hospital de Figueres, Fundació Salut Empordà, Figueres, Girona, Spain. Hospital de Figueres, Fundació Salut Empordà, Figueres, Girona, Spain. Hospital de Sant Joan Despí-Moisès Broggi, Sant Joan Despí, Barcelona, Spain. Centre Neurorehabilitador Mas Sabaté, Fundació Esclerosi Multiple, Reus, Tarragona, Spain. Hospital Sant Joan de Déu Althaia de Manresa, Manresa, Barcelona, Spain. Hospital Universitari de Bellvitge, Barcelona, Spain. Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain. Hospital Verge de la Cinta de Tortosa, Tortosa, Tarragona, Spain. Hospital del Vendrell, Vendrell, Tarragona, Spain. Hospital del Mar, Barcelona, Spain. Consorci Hospitalari de Vic, Vic, Barcelona, Spain. Unidad de Neuroinmunología- Esclerosis múltiple, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), |Universitat de Barcelona, Barcelona, Spain. Unidad de Neuroinmunología- Esclerosis múltiple, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), |Universitat de Barcelona, Barcelona, Spain. Secció de Neurologia, Hospital Universitari Sant Joan de Reus, Institut d'Investigació Sanitària Pere Virgili (IISPV), Reus, Tarragona, Spain.
 School of Psychology, Queen's University Belfast, Belfast, UK. Parkinson Vereniging, Bunnik, The Netherlands. Independent Researcher, The Netherlands. Leyden Academy on Vitality and Ageing, Leiden, The Netherlands. LAPS, Research Institute for Art and Public Space, Gerrit Rietveld Academy, Amsterdam, The Netherlands. Independent Researcher, The Netherlands. Leyden Academy on Vitality and Ageing, Leiden, The Netherlands. Department of Ethics, Law & Medical Humanities, Amsterdam UMC, Amsterdam, The Netherlands. Department of Public Health and Primary Care, Leiden University Medical Centre, Leiden, The Netherlands.
 Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: tchitnis@rics.bwh.harvard.edu. Rocky Mountain Multiple Sclerosis Clinic, Salt Lake City, UT, USA. Electronic address: ldjfoley@gmail.com. University of Massachusetts Medical School, Worcester, MA, USA. Electronic address: carolina.ionete@umassmemorial.org. Nehme and Thgerese Tohme Multiple Sclerosis Center, American University of Beirut, Beirut, Lebanon. Electronic address: ne42@aub.edu.lb. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: ssaxena3@bwh.harvard.edu. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: pgaitanwalsh@bwh.harvard.edu. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: hlokhande@bwh.harvard.edu. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: apaul12@bwh.harvard.edu. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: fermisk.x@gmail.com. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: hweiner@rics.bwh.harvard.edu. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: fqureshi@octavebio.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: mjbecich@gmail.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: fatima.rubio@gmail.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: vmgehman@gmail.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: fujun2@yahoo.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: akeshavan@octavebio.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: kianj@octavebio.com. Octave Bioscience, Inc., Menlo Park, CA, USA. Electronic address: aghoreyshi@octavebio.com. Nehme and Thgerese Tohme Multiple Sclerosis Center, American University of Beirut, Beirut, Lebanon. Electronic address: sk88@aub.edu.lb.
 Hotchkiss Brain Institute and the Department of Clinical Neuroscience, University of Calgary, Calgary, Alberta T2N 4N1, Canada. Hotchkiss Brain Institute and the Department of Clinical Neuroscience, University of Calgary, Calgary, Alberta T2N 4N1, Canada. Hotchkiss Brain Institute and the Department of Clinical Neuroscience, University of Calgary, Calgary, Alberta T2N 4N1, Canada. Department of Biochemistry, Microbiology, and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada. Hotchkiss Brain Institute and the Department of Clinical Neuroscience, University of Calgary, Calgary, Alberta T2N 4N1, Canada. Hotchkiss Brain Institute and the Department of Clinical Neuroscience, University of Calgary, Calgary, Alberta T2N 4N1, Canada jeff.dong@usask.ca vyong@ucalgary.ca. Department of Biochemistry, Microbiology, and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada jeff.dong@usask.ca vyong@ucalgary.ca.
 Klinikum rechts der Isar, Technische Universität München, Abteilung für Diagnostische und Interventionelle Neuroradiologie, München, Deutschland. Klinikum rechts der Isar, Technische Universität München, Neurologische Klinik und Poliklinik, München, Deutschland. Klinikum rechts der Isar, Technische Universität München, Abteilung für Diagnostische und Interventionelle Neuroradiologie, München, Deutschland. Radiologische Universitätsklinik Tübingen, Abteilung Diagnostische und Interventionelle Neuroradiologie, Tübingen, Deutschland. Radiologische Universitätsklinik Tübingen, Abteilung Diagnostische und Interventionelle Neuroradiologie, Tübingen, Deutschland. Radiologische Universitätsklinik Tübingen, Abteilung Diagnostische und Interventionelle Neuroradiologie, Tübingen, Deutschland. Universitätsmedizin Mannheim, Klinik für Radiologie und Nuklearmedizin, Mannheim, Deutschland. Klinikum rechts der Isar, Technische Universität München, Abteilung für Diagnostische und Interventionelle Neuroradiologie, München, Deutschland. Klinikum rechts der Isar, Technische Universität München, Abteilung für Diagnostische und Interventionelle Neuroradiologie, München, Deutschland. Klinikum der Universität München, LMU, Institut für diagnostische und interventionelle Neuroradiologie, München, Deutschland. Klinikum der Universität München, LMU, Institut für diagnostische und interventionelle Neuroradiologie, München, Deutschland. LMU Klinikum, Institut für Klinische Neuroimmunologie, Ludwig-Maximilians-Universität, München, Deutschland. Universitätsklinikum Augsburg, Klinik für Diagnostische und Interventionelle Neuroradiologie, Augsburg, Deutschland. Universitätsklinikum Augsburg, Klinik für Diagnostische und Interventionelle Neuroradiologie, Augsburg, Deutschland. Klinik für Diagnostische und Interventionelle Radiologie, Universitätsklinikum Ulm, Ulm, Deutschland. Klinik für Diagnostische und Interventionelle Radiologie, Universitätsklinikum Ulm, Ulm, Deutschland. Klinikum rechts der Isar, Technische Universität München, Abteilung für Diagnostische und Interventionelle Neuroradiologie, München, Deutschland. Klinik für Diagnostische und Interventionelle Radiologie, Universitätsklinikum Ulm, Ulm, Deutschland. Klinikum rechts der Isar, Technische Universität München, Abteilung für Diagnostische und Interventionelle Neuroradiologie, München, Deutschland.
 Department of Neurology, Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Department of Neurology, Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
 Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. brigitta.bonaldo@unito.it. Department of Neuroscience "Rita Levi-Montalcini", University of Turin, Via Cherasco 15, Turin, 10126, Italy. brigitta.bonaldo@unito.it. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. Department of Neuroscience "Rita Levi-Montalcini", University of Turin, Via Cherasco 15, Turin, 10126, Italy. School of Pharmacy, Pharmacology Unit, University of Camerino, Via Madonna delle Carceri, 9, Camerino, 62032, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. Neurobiology Unit, Neurology, CReSM (Regional Referring Center of Multiple Sclerosis), San Luigi Gonzaga University Hospital, Orbassano, Italy. Department of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. Department of Oncology, University of Turin, San Luigi Hospital, Orbassano, Turin, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. Department of Neuroscience "Rita Levi-Montalcini", University of Turin, Via Cherasco 15, Turin, 10126, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. Department of Neuroscience "Rita Levi-Montalcini", University of Turin, Via Cherasco 15, Turin, 10126, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole, 10-10043, Orbassano, Turin, Italy. Department of Neuroscience "Rita Levi-Montalcini", University of Turin, Via Cherasco 15, Turin, 10126, Italy.
 Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Neurology, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. Neurology, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Switzerland. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Electronic address: Emmanuelle.Waubant@ucsf.edu.
 Department of Neurology, School of Medicine, Marmara University, İstanbul, Turkey. Department of Neurology, School of Medicine, Marmara University, İstanbul, Turkey. Department of Neurology, School of Medicine, Marmara University, İstanbul, Turkey. Department of Neurology, School of Medicine, Marmara University, İstanbul, Turkey. Department of Neurology, School of Medicine, Marmara University, İstanbul, Turkey.
 Department of Neurology, Neuroimmunological Section, University of Rostock, Rostock, Germany. Department of Neurology, Medical University of Vienna, Vienna, Austria. paulus.rommer@meduniwien.ac.at.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: harald.hegen@i-med.ac.at. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria. FH Campus Wien, University of Applied Sciences, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria. FH Campus Wien, University of Applied Sciences, Vienna, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Statistics, Faculty of Economics and Statistics, University of Innsbruck, Innsbruck, Austria. Electronic address: janette.walde@uibk.ac.at. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
 Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA 94720, USA. Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA 94720, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Department of Neurology, Graduate School of medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan. Kaiser Permanente Division of Research, Oakland, CA 94612, USA. John P. Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL, USA. Dr. John T. Macdonald Department of Human Genetics, Miller School of Medicine, University of Miami, Miami, FL, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Systems Biology and Computer Science Program, Ann Romney Center for Neurological Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, 02115 MA, USA. Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Harvard Medical School, Boston, MA 02115, USA. Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Division of Epidemiology and Biostatistics, School of Public Health, University of California Berkeley, Berkeley, CA 94720, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA 94158, USA.
 Institute for Biomedical Engineering, ETH Zurich and University of Zurich, Zurich, Switzerland. Institute for Biomedical Engineering, ETH Zurich and University of Zurich, Zurich, Switzerland. Institute for Biomedical Engineering, ETH Zurich and University of Zurich, Zurich, Switzerland. Neuroimmunology and MS Research Section, Neurology Clinic, University of Zurich, University Hospital Zurich, Zurich, Switzerland. Institut Curie, Immunity and Cancer Unit 932, Paris, France. Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland. Center for Reproducible Science, University of Zurich, Zurich, Switzerland. Institute for Biomedical Engineering, ETH Zurich and University of Zurich, Zurich, Switzerland.
 Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain manuel.comabella@vhir.org. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain. Servei de Neuroradiología, Vall d'Hebron University Hospital, Barcelona, Spain. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain. Neurology, Faculty of Medicine, University of Münster, Munster, Germany. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Barcelona, Spain.
 Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA. Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA. Department of Biological Chemistry, University of California, Irvine, Irvine, CA. Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA. Department of Biological Chemistry, University of California, Irvine, Irvine, CA. Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA. Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA.
 Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK. Wellcome Trust-MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK. Institute of Anatomy, Rostock University Medical Center, Rostock, Germany. Department of Neuroinflammation, The UCL Queen Square Institute of Neurology, University College London, London, UK. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Faculty of Medicine, Department of Medicine, Hammersmith Campus, London, UK. Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK. Department of Immunobiology, Biomedical Primate Research Centre, Rijswijk, The Netherlands. Department of Immunobiology, Biomedical Primate Research Centre, Rijswijk, The Netherlands. Department Pathology and Medical Biology and MS Center Noord Nederland (MSCNN), University Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department of Immunobiology, Biomedical Primate Research Centre, Rijswijk, The Netherlands. Department Pathology and Medical Biology and MS Center Noord Nederland (MSCNN), University Groningen, University Medical Center Groningen, Groningen, The Netherlands. Department Anatomy and Neuroscience, Amsterdam University Medical Center (VUMC), Amsterdam, Netherlands. Department of Neurology and Immunology, Mayo College of Medicine and Science, Rochester, Minnesota, USA. Wellcome Trust-MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Department of Neuroimmunology, Center for Brain Research, Medical University Vienna, Vienna, Austria. Department of Neuroscience, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia; Department of Neurology, Alfred Health, Melbourne, Victoria, Australia. Electronic address: Francesca.bridge@monash.edu. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia; Department of Neurology, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia; Department of Neurology, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia; Department of Neurology, Alfred Health, Melbourne, Victoria, Australia.
 Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil; Laboratory of Cytochemistry and Immunocytochemistry, Department of Biochemistry and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil. Autoimmune Research Laboratory, Department of Genetics, Microbiology, and Immunology, Institute of Biology, State University of Campinas, Campinas, Brazil. Autoimmune Research Laboratory, Department of Genetics, Microbiology, and Immunology, Institute of Biology, State University of Campinas, Campinas, Brazil. Autoimmune Research Laboratory, Department of Genetics, Microbiology, and Immunology, Institute of Biology, State University of Campinas, Campinas, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil. Laboratory of Cytochemistry and Immunocytochemistry, Department of Biochemistry and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, Brazil. Laboratory of Cytochemistry and Immunocytochemistry, Department of Biochemistry and Tissue Biology, Institute of Biology, State University of Campinas, Campinas, Brazil. Autoimmune Research Laboratory, Department of Genetics, Microbiology, and Immunology, Institute of Biology, State University of Campinas, Campinas, Brazil; Experimental Medicine Research Cluster, University of Campinas, Campinas, Brazil; Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil. Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, State University of Campinas, SP, Brazil; Experimental Medicine Research Cluster, University of Campinas, Campinas, Brazil; Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil. Electronic address: pmvieira@unicamp.br.
 Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain xavier.montalban@cem-cat.org. Cedars-Sinai Medical Center, David Geffen School of Medicine, University of California, Los Angeles, California, USA. Division of Immunology and Rheumatology, Stanford University, Palo Alto, California, USA. Global Clinical Development, Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA. Global Clinical Development, EMD Serono Research & Development Institute, Inc, Billerica, Massachusetts, USA, an affiliate of Merck KGaA (affiliation at the time the research was conducted). ECD-Early Clinical Development, Pfizer, Cambridge, Massachusetts, USA. Biostatistics, Merck Healthcare KGaA, Darmstadt, Germany. Translational Innovation Platform in Immunology & Neuroscience, EMD Serono Research & Development Institute, Inc, Billerica, Massachusetts, USA, an affiliate of Merck KGaA. Global Patient Safety, Merck Healthcare KGaA, Darmstadt, Germany.
 Physical Medicine and Rehabilitation Clinic, Goztepe Prof Dr Suleyman Yalcin City Hospital, Istanbul Medeniyet University, Kadıköy, 34730, Istanbul, Turkey. bilincdogruoz@hotmail.com. Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Istanbul Medeniyet University, Istanbul, Turkey. Department of Biostatistics, Faculty of Medicine, Bezmialem Foundation University, Istanbul, Turkey.
 Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Medical Image Analysis Center and Department of Biomedical Engineering, University Basel, Basel, Switzerland. Experimental and Clinical Research Center Max Delbrueck Center for Molecular Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany. University of Irvine, Irvine, CA, USA. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, DKD Helios Klinik Wiesbaden, Wiesbaden, Germany. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. athina.papadopoulou@usb.ch. Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. athina.papadopoulou@usb.ch. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. athina.papadopoulou@usb.ch. Department of Clinical Research, University Hospital and University of Basel, Basel, Switzerland. athina.papadopoulou@usb.ch.
 Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. PRASE and Biology Department, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon. Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. serge.rivest@crchudequebec.ulaval.ca.
 Feil Family Brain and Mind Research Institute. Feil Family Brain and Mind Research Institute. Feil Family Brain and Mind Research Institute. Feil Family Brain and Mind Research Institute. Feil Family Brain and Mind Research Institute. Jill Roberts Institute for Research in Inflammatory Bowel Disease. Joan and Sanford I. Weill Department of Medicine, and. Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Immunology and Microbial Pathogenesis Program and. Applied Bioinformatics Core, Division of Hematology/Oncology, Department of Medicine, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, New York, USA. Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, Cornell University, New York, New York, USA. Applied Bioinformatics Core, Division of Hematology/Oncology, Department of Medicine, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, New York, USA. Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, Cornell University, New York, New York, USA. Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, Cornell University, New York, New York, USA. Departments of Pharmacology and Neurosciences, UCSD, San Diego, California, USA. Feil Family Brain and Mind Research Institute. Harold and Margaret Milliken Hatch Laboratory of Neuro-endocrinology and. Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, New York, USA. Department of Neurology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, New York, USA. Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. California Animal Health and Food Safety Laboratory, School of Veterinary Medicine, UCD, Davis, California, USA. Department of Neurology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Feil Family Brain and Mind Research Institute. Astoria Biologica Inc., Norwalk, Connecticut, USA. Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, Cornell University, New York, New York, USA. Feil Family Brain and Mind Research Institute. Department of Neurology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Department of Neurology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Department of Neurology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Meinig School of Biomedical Engineering, Cornell University, Ithaca, USA. Division of Biostatistics, Department of Population Health Sciences, and. Genomics Resources Core Facility, Core Laboratories Center, Weill Cornell Medicine, New York, New York, USA. Applied Bioinformatics Core, Division of Hematology/Oncology, Department of Medicine, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, New York, USA. Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, Cornell University, New York, New York, USA. Departments of Pharmacology and Neurosciences, UCSD, San Diego, California, USA. Jill Roberts Institute for Research in Inflammatory Bowel Disease. Joan and Sanford I. Weill Department of Medicine, and. Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, New York, USA. Immunology and Microbial Pathogenesis Program and. Feil Family Brain and Mind Research Institute. Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, Cornell University, New York, New York, USA. Feil Family Brain and Mind Research Institute. Immunology and Microbial Pathogenesis Program and. Department of Neurology, Weill Cornell Medical College, Cornell University, New York, New York, USA.
 Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy. Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Naples, Italy.
 Nature Reviews Neurology, . nrneuro@nature.com.
 Kumluca Faculty of Health Sciences, Akdeniz University, Antalya, Turkey. School of Nursing, Istanbul University, Turkey.
 From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.). From the Neuroimaging Research Unit, Division of Neuroscience (M.A.R., M.M., E.P., P.P., L.S., P.V., M.F.), Neurology Unit (M.A.R., M.M., P.P., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy (M.A.R., P.P., M.F.); Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy (M.B.); Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK (A.E.); Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK (A.E.); VISN20 NW Mental Illness Research, Education, and Clinical Center, VA Puget Sound Healthcare System, Seattle, Wash (J.I.); Department of Psychiatry and Behavioral Sciences and Department of Neurology, University of Washington School of Medicine, Seattle, Wash (J.I.); and Department of Innovative Biomedical Visualization (iBMV), Department of Radiology, Nagoya University Graduate School of Medicine, Aichi, Japan (T.T.).
 Department of Neurology, Medical University of Vienna, Vienna, Austria/Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria/Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria. Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria/Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria. Center for Brain Research, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria/Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.
 Clinical Epidemiology and Biostatistics, Faculty of Medicine and Health, School of Medical Sciences, Örebro University, Campus USÖ, Södra Grev Rosengatan 30, Örebro 703 62, Sweden; Department of Public Health Sciences, Stockholm University, Stockholm SE-106 91, Sweden; Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 7HB, United Kingdom. Neuroimmunology Unit, Blizard Institute, Queen Mary, University of London, UK. Department of Ophthalmology, King's College Hospital, London SE5 9RS, UK. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm 171 77, Sweden. Neuroimmunology Unit, Blizard Institute, Queen Mary, University of London, UK. Clinical Epidemiology and Biostatistics, Faculty of Medicine and Health, School of Medical Sciences, Örebro University, Campus USÖ, Södra Grev Rosengatan 30, Örebro 703 62, Sweden; Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 7HB, United Kingdom; Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm 171 77, Sweden. Electronic address: Scott.Montgomery@oru.se.
 Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Radiology, University of British Columbia, Vancouver, British Columbia, Canada. International Collaboration on Repair and Discoveries, University of British Columbia, Vancouver, British Columbia, Canada. Department of Statistics, University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Radiology, University of British Columbia, Vancouver, British Columbia, Canada. Department of Physics and Astronomy, University of British Columbia, Vancouver, British Columbia, Canada. International Collaboration on Repair and Discoveries, University of British Columbia, Vancouver, British Columbia, Canada. Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada. School of Biomedical Engineering, University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Radiology, University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Department of Radiology, University of British Columbia, Vancouver, British Columbia, Canada. Department of Physics and Astronomy, University of British Columbia, Vancouver, British Columbia, Canada. International Collaboration on Repair and Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
 Université de Lille, CHU Lille, FHU PRECISE, Service de Rhumatologie, Lille, France. Université de Lille, CHU Lille, INSERM UMR1172 LilNCog, FHU PRECISE, Service de Neurologie, Lille, France. Université de Lille, CHU Lille, FHU PRECISE, Service de Rhumatologie, Lille, France.
 Department of Histology, Jagiellonian University Medical College, Kopernika 7, 31-034 Krakow, Poland. Electronic address: grazyna.pyka-fosciak@uj.edu.pl. Medical Department, Novartis Poland Sp. z o.o., Marynarska 15, 02-674 Warszawa, Poland. Department of Biophysical Microstructures, Institute of Nuclear Physics, Polish Academy of Sciences, PL-31342 Krakow, Poland. Department of Histology, Jagiellonian University Medical College, Kopernika 7, 31-034 Krakow, Poland. Department of Histology, Jagiellonian University Medical College, Kopernika 7, 31-034 Krakow, Poland. Department of Biophysical Microstructures, Institute of Nuclear Physics, Polish Academy of Sciences, PL-31342 Krakow, Poland.
 Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Izmir Katip Celebi University, Izmir, Turkey. Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Izmir Katip Celebi University, Izmir, Turkey. Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey. Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey. Multiple Sclerosis Research Association, Izmir, Turkey. Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey. Multiple Sclerosis Research Association, Izmir, Turkey. Faculty of Physical Therapy and Rehabilitation, Department of Neurological Physiotherapy-Rehabilitation, Dokuz Eylül University, Izmir, Turkey. Faculty of Medicine, Department of Neurology, Dokuz Eylül University, Izmir, Turkey.
 Department of Neurology, Hôpital de Hautepierre, Clinical Investigation Center, Institut National de la Santé et de la Recherche Médicale (INSERM), Strasbourg, France. Fédération de Médecine Translationelle, Institut National de la Santé et de la Recherche Médicale (INSERM), Strasbourg, France. Department of Neurology, Pitié Salpêtrière Hospital, Paris, France. Centre de Ressources et de Compétences Sclérose en Plaques, Paris, France. Department of Neurology, Rothschild Ophthalmologic Foundation, Paris, France. Department of Neurology, Centre Hospitalier Universitaire (CHU) Nantes, Nantes Université, Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Investigation Clinique (CIC), Center for Research in Transplantation and Translational Immunology, UMR, UMR1064, Nantes, France. Clinical Neuroscience Centre, CIC_P1414 Institut National de la Santé et de la Recherche Médicale (INSERM), Rennes University Hospital, Rennes University, Rennes, France. Microenvironment, Cell Differentiation, Immunology and Cancer Unit, Institut National de la Santé et de la Recherche Médicale (INSERM), Rennes I University, French Blood Agency, Rennes, France. Neurology Department, Rennes University Hospital, Rennes, France. Department of Neurology, Centre Hospitalier Universitaire (CHU) Nîmes, University of Montpellier, Nîmes, France. Institut de Génomique Fonctionnelle, UMR, Institut National de la Santé et de la Recherche Médicale (INSERM), University of Montpellier, Montpellier, France. University of Lille, Institut National de la Santé et de la Recherche Médicale (INSERM) U1172, Centre Hospitalier Universitaire (CHU), Lille, France. Université Claude Bernard Lyon 1, Hospices Civils de Lyon, Institut National de la Santé et de la Recherche Médicale (INSERM), CNRS, Lyon Neuroscience Research Center, Lyon, France. Centre Ressources et Compétences Sclérose En Plaques (CRC-SEP) and Department of Neurology, Centre Hospitalier Universitaire (CHU) Toulouse Purpan - Hôpital Pierre-Paul Riquet, Toulouse, France. Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), University of Toulouse, CNRS, Institut National de la Santé et de la Recherche Médicale (INSERM), UPS, Toulouse, France. Department of Immunology, Toulouse University Hospital, Toulouse, France.
 Department of Brain Sciences and UK Dementia Research Institute at Imperial College London, Burlington Danes Building, Hammersmith Hospital, DuCane Road, London, UK. Electronic address: p.matthews@imperial.ac.uk. Bridge Medical Consulting Limited, 2 Marsault Court, 11 Kew Foot Road, Richmond, London, TW9 2SS, UK. Bridge Medical Consulting Limited, 2 Marsault Court, 11 Kew Foot Road, Richmond, London, TW9 2SS, UK. Department of Brain Sciences and UK Dementia Research Institute at Imperial College London, Burlington Danes Building, Hammersmith Hospital, DuCane Road, London, UK; Department of Computing, Imperial College London, William Penny Building, South Kensington Campus, London, UK. Imperial College Healthcare Trust, Centre of Neuroscience, Department of Medicine, Charing Cross Hospital, Fulham Palace Rd, London W6 8RF, UK. Bristol-Myers Squibb, Uxbridge Business Park, Sanderson Road, Uxbridge, UB8 1DH, UK. Bristol-Myers Squibb, Uxbridge Business Park, Sanderson Road, Uxbridge, UB8 1DH, UK. Bristol-Myers Squibb, Uxbridge Business Park, Sanderson Road, Uxbridge, UB8 1DH, UK.
 From the Department of Neuropathology (E.S.F., D.H., M.S.W.), University Medical Center; Department of Neurology (E.S.F., M.S.W.), University Medical Center; and Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP (D.H., M.S.W.), Göttingen, Germany. From the Department of Neuropathology (E.S.F., D.H., M.S.W.), University Medical Center; Department of Neurology (E.S.F., M.S.W.), University Medical Center; and Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP (D.H., M.S.W.), Göttingen, Germany. From the Department of Neuropathology (E.S.F., D.H., M.S.W.), University Medical Center; Department of Neurology (E.S.F., M.S.W.), University Medical Center; and Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP (D.H., M.S.W.), Göttingen, Germany. martin.weber@med.uni-goettingen.de.
 Stanford University School of Medicine, Stanford, California. Department of Veterans Affairs Multiple Sclerosis Center of Excellence, Baltimore, Maryland. University of Maryland School of Medicine, Baltimore. Southern California Permanente Medical Group, Pasadena. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. University of Alabama at Birmingham. McKing Consulting Corporation, Atlanta, Georgia. McKing Consulting Corporation, Atlanta, Georgia. Stanford University School of Medicine, Stanford, California. National Multiple Sclerosis Society, New York, New York. Stanford University School of Medicine, Stanford, California. Department of Veterans Affairs Multiple Sclerosis Center of Excellence, Baltimore, Maryland. University of Maryland School of Medicine, Baltimore.
 NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/UK e-Health Center, Universitat Oberta de Catalunya, Barcelona, Spain. Salk Institute for Biological Studies, San Diego, CA, USA. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, UK. Lysholm Department of Neuroradiology, National Hospital for Neurology and Neurosurgery, London, UK. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/Brain Connectivity Center, C. Mondino National Neurological Institute, Pavia, Italy Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK/NIHR University College London Hospitals Biomedical Research Centre, London, UK. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/NIHR University College London Hospitals Biomedical Research Centre, London.
 Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston, Houston, Texas, USA. Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston, Houston, Texas, USA. Baylor College of Medicine, Houston, Texas, USA. Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston, Houston, Texas, USA. Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston, Houston, Texas, USA.
 Clinical Pharmacology and Pharmacometrics, AbbVie, North Chicago, IL. Clinical Pharmacology and Pharmacometrics, AbbVie, North Chicago, IL. Neuroscience, AbbVie, North Chicago, IL. Neuroscience, AbbVie, North Chicago, IL. Clinical Pharmacology and Pharmacometrics, AbbVie, North Chicago, IL. Weill Institute of Neurosciences, Department of Neurology, University of California, San Francisco, San Francisco, CA.
 FLENI, Buenos Aires, Argentina. RINGGOLD: 58782 FLENI, Buenos Aires, Argentina. RINGGOLD: 58782 FLENI, Buenos Aires, Argentina. RINGGOLD: 58782 FLENI, Buenos Aires, Argentina. RINGGOLD: 58782
 Medical Faculty, Lithuanian University of Health Sciences, Medical Academy, Eiveniu Str. 2, 50161, Kaunas, Lithuania. Laboratory of Ophthalmology, Neuroscience Institute, Lithuanian University of Health Sciences, Medical Academy, Eiveniu Str. 2, 50161, Kaunas, Lithuania. greta.gedvilaite@lsmuni.lt. Laboratory of Ophthalmology, Neuroscience Institute, Lithuanian University of Health Sciences, Medical Academy, Eiveniu Str. 2, 50161, Kaunas, Lithuania. Laboratory of Ophthalmology, Neuroscience Institute, Lithuanian University of Health Sciences, Medical Academy, Eiveniu Str. 2, 50161, Kaunas, Lithuania. Laboratory of Ophthalmology, Neuroscience Institute, Lithuanian University of Health Sciences, Medical Academy, Eiveniu Str. 2, 50161, Kaunas, Lithuania. Department of Ophthalmology, Lithuanian University of Health Sciences, Medical Academy, Eiveniu 2 Str, 50161, Kaunas, Lithuania. Laboratory of Ophthalmology, Neuroscience Institute, Lithuanian University of Health Sciences, Medical Academy, Eiveniu Str. 2, 50161, Kaunas, Lithuania. Department of Ophthalmology, Lithuanian University of Health Sciences, Medical Academy, Eiveniu 2 Str, 50161, Kaunas, Lithuania.
 Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Injury, Inflammation and Recovery Sciences, School of Medicine, University of Nottingham, Nottingham, UK. Nottingham Multiple Sclerosis Patient and Public Involvement Group, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Department of Neurology, Nottingham University Hospitals NHS Trust, Nottingham, UK. Rehabilitation Research Group, School of Health Sciences, University of Nottingham, Nottingham, UK. Mental Health and Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Institute of Mental Health, Nottinghamshire Healthcare NHS Trust, Nottingham, UK. Health Division, SINTEF, Trondheim, Norway.
 Department of Neurology, Faculty of Medical Sciences in Katowice, Medical University of Silesia, 40-752 Katowice, Poland. Department of Neurology, Faculty of Medical Sciences in Katowice, Medical University of Silesia, 40-752 Katowice, Poland. Department of Neurology, Faculty of Medical Sciences in Katowice, Medical University of Silesia, 40-752 Katowice, Poland. Department of Neurology, Faculty of Health Sciences in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.
 Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Laboratory Medicine, University Hospital "P. Giaccone", 90127 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Laboratory Medicine, University Hospital "P. Giaccone", 90127 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Laboratory Medicine, University Hospital "P. Giaccone", 90127 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Laboratory Medicine, University Hospital "P. Giaccone", 90127 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Laboratory Medicine, University Hospital "P. Giaccone", 90127 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University of Palermo, 90127 Palermo, Italy. Department of Laboratory Medicine, University Hospital "P. Giaccone", 90127 Palermo, Italy.
 Institute of Medical Immunology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, China. Department of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China. Department of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China. Department of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China. Department of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China. Department of Laboratory Medicine, Jiangsu Key Laboratory of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, China. Department of Obstetrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China. Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China. Institute of Medical Immunology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, China. ruike@ujs.edu.cn. Department of Laboratory Medicine, Affiliated Hospital of Jiangsu University, Zhenjiang, China. ruike@ujs.edu.cn.
 Center for Traumatic Brain Injury Research, Kessler Foundation, 120 Eagle Rock Ave., East Hanover, NJ, USA. New Jersey Institute of Technology, Newark, NJ, USA. Center for Traumatic Brain Injury Research, Kessler Foundation, 120 Eagle Rock Ave., East Hanover, NJ, USA. Electronic address: oiosipchuk@kesslerfoundation.org. Psychology Department, Montclair State University, 1 Normal Ave., Montclair, NJ, USA. New Jersey Institute of Technology, Newark, NJ, USA.
 Institut d'Investigacions Biomediques August Pi Sunyer, Rosello 149, 08036, Barcelona, Spain. pvillosl@recerca.clinic.cat. Bionure Farma/Accure Therapeutics SL, Barcelona, Spain. Bionure Farma/Accure Therapeutics SL, Barcelona, Spain. Simbec-Orion, Merthyr Tydfil, UK. Simbec-Orion, Merthyr Tydfil, UK.
 Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Service of Internal Medicine, Hospital Sierrallana-IDIVAL, Torrelavega, Spain. Service of Internal Medicine, Hospital Sierrallana-IDIVAL, Torrelavega, Spain. Service of Radiology, Hospital Sierrallana, Torrelavega, Spain. Service of Radiology, Hospital Sierrallana, Torrelavega, Spain. Service of Pharmacy, Hospital Sierrallana, Torrelavega, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Centro de Investigación en Red de Enfermedades Neurodegenerativas, CIBERNED, Instituto Carlos III, Madrid, Spain. Service of Neurology, Hospital Sierrallana-Institute of Research Valdecilla (IDIVAL), Torrelavega, Spain. Centro de Investigación en Red de Enfermedades Neurodegenerativas, CIBERNED, Instituto Carlos III, Madrid, Spain. Department of Medicine and Psychiatry, University of Cantabria, Santander, Spain. Red Española de Esclerosis Múltiple, Madrid, Spain.
 Department of Radiology and Precision Health Program, Michigan State University, East Lansing, MI, USA. Division of Physiological Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-17 177, Stockholm, Sweden. Department of Neurology, University of Massachusetts, Worcester, MA, USA. Department of Neurology, University of Massachusetts, Worcester, MA, USA. Department of Neurology, University of Massachusetts, Worcester, MA, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA. Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA, USA. Department of Neurology, University of Massachusetts, Worcester, MA, USA. Electronic address: Carolina.Ionete@umassmemorial.org. Division of Physiological Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-17 177, Stockholm, Sweden. Electronic address: Amirata.saei.dibavar@ki.se. Department of Radiology and Precision Health Program, Michigan State University, East Lansing, MI, USA. Electronic address: mahmou22@msu.edu.
 Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy. jessica.podda@aism.it. Movendo Technology S.R.L, Genoa, Italy. Movendo Technology S.R.L, Genoa, Italy. Movendo Technology S.R.L, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society, Genoa, Italy. Department of Physiopathology, Experimental Medicine and Public Health, University of Siena, Siena, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Via Operai 40, 16149, Genoa, Italy.
 Clinic of Chest Diseases, İstanbul Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, İstanbul, Türkiye. Clinic of Chest Diseases, İstanbul Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, İstanbul, Türkiye. Clinic of Chest Diseases, İstanbul Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, İstanbul, Türkiye. Clinic of Chest Diseases, Başakşehir Çam and Sakura City Hospital, İstanbul, Türkiye. Department of Chest Diseases, İstanbul Medeniyet University Faculty of Medicine, İstanbul, Türkiye. Clinic of Chest Diseases, İstanbul Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, İstanbul, Türkiye.
 Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias de La Vida, Universidad Andres Bello, Santiago, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias de La Vida, Universidad Andres Bello, Santiago, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias de La Vida, Universidad Andres Bello, Santiago, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Chile; Departamento de Endocrinología, Escuela de Medicina, Facultad de Medicina, Pontificia Universidad Católica, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias de La Vida, Universidad Andres Bello, Santiago, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Chile. Electronic address: pagonzalez@bio.puc.cl.
 Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. Department of Pharmaceutical Sciences, Faculty of Pharmacy, King Faisal University, Al-Ahsa 31982, Saudi Arabia. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Sinai University, Ismailia 45511, Egypt. Department of Pathology, Faculty of Veterinary Medicine, Cairo University, Cairo 12211, Egypt. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.
 Stress Research, Stockholm University, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Center for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden anna.hedstrom@ki.se. Karolinska University Hospital, Stockholm, Sweden.
 University of Paris Cité, ECEVE UMR 1123, Inserm, Paris, France. AP-HP, Sorbonne University, GHU Pitié-Salpêtrière, Paris, France. AP-HP, Sorbonne University, GHU Pitié-Salpêtrière, Paris, France. APHP, Sorbonne University, GHU Pitié Salpêtrière, Department 2-Mazarin, Paris, France. APHP, Sorbonne University, GHU Pitié Salpêtrière, Department 2-Mazarin, Paris, France. AP-HP, Sorbonne University, GHU Pitié-Salpêtrière, Paris, France. APHP, Sorbonne University, GHU Pitié Salpêtrière, Department of neurology, Paris, France. University of Paris, Paris, France. APHP, Sorbonne University, GHU Pitié Salpêtrière, Department of neurology, Paris, France. EHESP, Paris, France. APHP, Sorbonne University, GHU Pitié Salpêtrière, Department 2-Mazarin, Paris, France. University of Paris Cité, ECEVE UMR 1123, Inserm, Paris, France. ARS Ile-de-France, Paris, France.
 School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China. School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China. The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China. School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China. School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China. School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China.
 Miami Itch Center, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA. Multiple Sclerosis Center of Excellence, Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida, USA. Multiple Sclerosis Center of Excellence, Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida, USA. Multiple Sclerosis Center of Excellence, Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida, USA. Multiple Sclerosis Center of Excellence, Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida, USA. Department of Biostatistics, Yong Loo Lin School of Medicine, Singapore, Singapore. Miami Itch Center, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.
 Department of Neurology, Shandong Provincial Hospital affiliated to Cheeloo College of Medicine, Shandong University, Jinan, China. Department of Neurology, Shandong Provincial Hospital affiliated to Cheeloo College of Medicine, Shandong University, Jinan, China. Department of Neurology, Shandong Provincial Hospital affiliated to Cheeloo College of Medicine, Shandong University, Jinan, China. Department of Neurology, Shandong Provincial Hospital affiliated to Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan, China. Department of Neurology, Shandong Provincial Hospital affiliated to Cheeloo College of Medicine, Shandong University, Jinan, China. Department of Neurology, Shandong Provincial Hospital affiliated to Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan, China.
 Department of Histology and Embryology, Medical College, Nanchang University, Nanchang 330006, China. Queen Mary School, Medical College, Nanchang University, Nanchang 330006, China. Department of Histology and Embryology, Medical College, Nanchang University, Nanchang 330006, China. Queen Mary School, Medical College, Nanchang University, Nanchang 330006, China. Department of Histology and Embryology, Medical College, Nanchang University, Nanchang 330006, China.

 Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Melbourne School of Psychological Sciences, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. Centre for Digital Transformation of Health, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St Carlton, Melbourne, VIC, 3053, Australia. sandra.neate@unimelb.edu.au.
 Department of Physical Therapy, Marquette University, Milwaukee, WI,USA. Rehabilitation Science, The University of Alabama at Birmingham, Birmingham, AL,USA. Rehabilitation Science, The University of Alabama at Birmingham, Birmingham, AL,USA. Department of Physical Therapy, The University of Alabama at Birmingham, Birmingham, AL,USA.
 Department of Biology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran. Department of Biology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran. Department of Genetic, School of Medicine, Kazerun Branch, Islamic Azad University, Kazerun, Iran.
 Centro Universitario de Esclerosis Múltiple, Hospital Dr. J.M. Ramos Mejía, CABA, Argentina. Electronic address: ricardoalonsohrm@gmail.com. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, CABA, Argentina. Hospital Santa Isabel de Hungría, Guaymallén, Mendoza, Argentina. Axis Neurociencias, Bahía Blanca, Buenos Aires, Argentina. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, CABA, Argentina; Swiss Medical Center, CABA, Argentina. Hospital Español, Rosario, Santa Fe, Argentina. Department of Neurology, Fleni, CABA, Argentina. Hospital Italiano, CABA, Argentina. Hospital Universitario Austral, CABA, Argentina; Instituto de Neurociencias, Fundación Favaloro, CABA, Argentina. INECO Neurociencias Oroño, Rosario, Santa Fe, Argentina. Biogen S.R.L., Buenos Aires, Argentina.
 Department of Neurology, Stanford University, Palo Alto, CA, USA. Center for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA, USA.
 State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. Electronic address: zhuhaomiao10090@qiluhospital.com. State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. Electronic address: fanyu@nankai.edu.cn. State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, College of Life Sciences, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tongyan Road, Haihe Education Park, Tianjin 300350, China. Electronic address: wzhao@nankai.edu.cn.
 Department of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. Department of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. Department of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. guanyangtai@renji.com.
 Department of Neurology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Pathology 627, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Pathology 627, Baltimore, MD, 21287, USA. pbharga2@jhmi.edu.
 Section of Pharmacology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Pharmacology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. claudia.volpi@unipg.it.
 Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Recludix Pharma, San Diego, USA. Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. Novartis Institutes for Biomedical Research, Basel, Switzerland. bruno.cenni@novartis.com.
 Neuromuscular Rehabilitation Research Center, Semnan University of Medical Sciences, Semnan, 3513138111, Iran. Neuromuscular Rehabilitation Research Center, Semnan University of Medical Sciences, Semnan, 3513138111, Iran. f.ehsani@semums.ac.ir. Neuromuscular Rehabilitation Research Center, Semnan University of Medical Sciences, Semnan, 3513138111, Iran. Neurology Ward, Department of Internal Medicine, Kowsar Hospital, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Non-invasive Brain Stimulation & Neuroplasticity Laboratory, Department of Physiotherapy, Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne, Australia.
 Evidera Inc., Waltham, MA 02451, USA. Evidera Inc., Waltham, MA 02451, USA. Evidera Inc., Saint-Laurent, QC H4S 1V3, Canada. Evidera Inc., Saint-Laurent, QC H4S 1V3, Canada. University of Genoa, Department of Health Sciences, Genoa, Italy. University of Alabama at Birmingham, School of Public Health, Birmingham, AL, USA. Unversity Medical Center Utrecht, Utrecht, The Netherlands. Smart Data Analysis & Statistics B.V., Utrecht, The Netherlands. Formerly Biogen, Cambridge, MA 02142, USA.
 Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA. Imaging Institute, Cleveland Clinic, Cleveland, Ohio, USA. Imaging Institute, Cleveland Clinic, Cleveland, Ohio, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA. Imaging Institute, Cleveland Clinic, Cleveland, Ohio, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA.
 From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. gabriel.bsteh@meduniwien.ac.at. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria. From the Department of Neurology (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Comprehensive Center for Clinical Neurosciences and Mental Health (G.B., P.A., B.K., N.K., F.L., S.M., P.S.R., K.Z., G.Z., T.Z., T.B.), Medical University of Vienna; Department of Neurology (H.H., M.A., K.B., F.D.P., F.D.), Medical University of Innsbruck; and Department of Ophthalmology (B.P.), Medical University of Vienna, Austria.
 Department of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institute of Virology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany/German Centre for Infection Research (DZIF), Berlin, Germany. Institute of Virology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany/German Centre for Infection Research (DZIF), Berlin, Germany. Institute of Virology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany/German Centre for Infection Research (DZIF), Berlin, Germany. Institute of Virology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany/German Centre for Infection Research (DZIF), Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institute for Infection Medicine, Christian-Albrechts-Universität zu Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany/Labor Dr. Krause und Kollegen MVZ GmbH, Kiel, Germany. Institute for Infection Medicine, Christian-Albrechts-Universität zu Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany. Institute of Virology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany/German Centre for Infection Research (DZIF), Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institute of Virology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany/German Centre for Infection Research (DZIF), Berlin, Germany/Labor Berlin-Charité Vivantes GmbH, Berlin, Germany.
 Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, Medical University of Graz, Graz, Austria. Division of Neuroradiology, Vascular and Interventional Radiology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria.
 Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Laboratory of Primary Health Care, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Laboratory of Primary Health Care, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Neurology, Medical School, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. angelospapadopoulos@gmail.com. Laboratory of Primary Health Care, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. Department of Speech and Language Therapy, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. nicktrimmis@upatras.gr. Laboratory of Primary Health Care, School of Health Rehabilitation Sciences, University of Patras, Patras, Greece. nicktrimmis@upatras.gr.
 Neuroscience Program, University of Illinois Urbana-Champaign, United States of America. Vida Health, United States of America. Neuroscience Program, University of Illinois Urbana-Champaign, United States of America. School of Medicine, The City University of New York, United States of America. Department of Psychology, Eastern Illinois University, United States of America. Illinois College of Optometry, United States of America. Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, United States of America; Department of Health Sciences, University of Colorado Colorado Springs, United States of America; Multiple Sclerosis Research Collaborative, University of Illinois, Urbana, IL, United States of America. Department of Health Sciences, Central Michigan University, United States of America. Surgery, University of Illinois College of Medicine, United States of America. Department of Kinesiology and Nutrition, University of Illinois Chicago, United States of America; Multiple Sclerosis Research Collaborative, University of Illinois, Urbana, IL, United States of America. Neuroscience Program, University of Illinois Urbana-Champaign, United States of America; Department of Kinesiology and Community Health, University of Illinois Urbana-Champaign, United States of America; Division of Nutritional Sciences, University of Illinois Urbana-Champaign, United States of America; Multiple Sclerosis Research Collaborative, University of Illinois, Urbana, IL, United States of America. Electronic address: nakhan2@illinois.edu.
 Division of Multiple Sclerosis and Clinical Neuroimmunology, Department of Neurology, University of Michigan, Ann Arbor, MI, USA/Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, MI, USA. Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, MI, USA. Department of Psychology, University of Michigan, Ann Arbor, MI, USA. Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, MI, USA.
 Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, Mainz, 55131, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, Mainz, 55131, Germany. Department of Transfusion Medicine, University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, Mainz, 55131, Germany. Department of Transfusion Medicine, University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, Mainz, 55131, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, Mainz, 55131, Germany. Electronic address: bittner@uni-mainz.de. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Centre of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, Mainz, 55131, Germany. Electronic address: zipp@uni-mainz.de.
 Medical Faculty, Institute of Neuroanatomy, University of Bonn, 53115, Bonn, Germany. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054, Erlangen, Germany. Medical Faculty, Institute of Neuroanatomy, University of Bonn, 53115, Bonn, Germany. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054, Erlangen, Germany. Department of Cardiology and Angiology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen University Hospital, 91054, Erlangen, Germany. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054, Erlangen, Germany. Medical Faculty, Institute of Neuroanatomy, University of Bonn, 53115, Bonn, Germany. stefanie.kuerten@uni-bonn.de. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054, Erlangen, Germany. stefanie.kuerten@uni-bonn.de.
 Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Electronic address: chengxia2003@163.com. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Electronic address: zhuwenzhen8612@163.com.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States. Department of Neurology, The Ohio State University College of Medicine, Columbus, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States. The Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States.
 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy/Neurology Unit, Department of Medical Sciences, San Giovanni di Dio and Ruggi d'Aragona, Salerno, Italy. S. Camillo-Forlanini Hospital, Rome, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. IRCCS Neuromed, Pozzilli, Italy. Department of Neuroscience and Mental Health, City of Health and Science University Hospital of Torino, Turin, Italy. MS Center, ASST Valle Olona, Gallarate Hospital, Gallarate, Italy. Department of Neurology, ASST Papa Giovanni XXIII Hospital, Bergamo, Italy. Montichiari Hospital, ASST Spedali Civili di Brescia, Brescia, Italy. Centro Sclerosi Multipla, Fondazione Policlinico Universitario "A. Gemelli," IRCCS, University Cattolica del Sacro Cuore, Rome, Italy. Tor Vergata Hospital, Rome, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, University of Palermo, Palermo, Italy. Neurology Unit, Department of Medical Sciences, San Giovanni di Dio and Ruggi d'Aragona, Salerno, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, UOSI Riabilitazione Sclerosi Multipla, Bologna, Italy. Neuroimmunology and Neuromuscular Diseases Unit, Fondazione I.R.C.C.S. Istituto Neurologico Carlo Besta, Milan, Italy. Department of Neurosciences, Imaging and Clinical Sciences, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro," Bari, Italy. S. Camillo-Forlanini Hospital, Rome, Italy. S. Camillo-Forlanini Hospital, Rome, Italy. CRRF Mons. Luigi Novarese, Vercelli, Italy. Binaghi Hospital, Azienda Tutela della Salute (ATS) Sardegna, Cagliari, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy.
 CRRF "Mons. Luigi Novarese", Moncrivello, VC, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. CRRF "Mons. Luigi Novarese", Moncrivello, VC, Italy. Neurology Unit, Galliera Hospital, Genoa, Italy. CRRF "Mons. Luigi Novarese", Moncrivello, VC, Italy. Department of Psychology, University of Turin, Turin, Italy. davide.marengo@unito.it.
 From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. From the Department of Epidemiology (L.G.S.), College of Public Health, University of Iowa, Iowa City; Department of Kinesiology (J.J.C., S.S.F.), Central College, Pella, IA; Hardin Library for the Health Sciences (H.S.H.), University of Iowa, Iowa City; William S. Middleton Memorial Veterans Hospital (M.L.S.), Madison, WI; Division of Life Sciences and Medicine (W.B.), University of Science and Technology of China, Hefei, Anhui; Departments of Neurology (J.K.), and Internal Medicine (T.J.T.), Carver College of Medicine, University of Iowa, Iowa City. tyler-titcomb@uiowa.edu.
 Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland. Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland. Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
 The Virgen de la Arrixaca Hospital, 30120 Murcia, Spain. Faculty of Health Sciences, Department of Nursing, Physiotherapy and Medicine, University of Almeria, 04120 Almeria, Spain. Health Research Center, University of Almería, 04120 Almeria, Spain. Faculty of Health Sciences, Department of Nursing, Physiotherapy and Medicine, University of Almeria, 04120 Almeria, Spain. Laboratory of Neuroscience, CINBIO, University of Vigo, 36310 Vigo, Spain. Laboratory of Neuroscience, Galicia Sur Health Research Institute (IISGS), 15706 Vigo, Spain. Faculty of Health Sciences, Department of Nursing, Physiotherapy and Medicine, University of Almeria, 04120 Almeria, Spain. Health Research Center, University of Almería, 04120 Almeria, Spain.
 Exercise Biology, Department of Public Health, Aarhus University, Aarhus, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Aarhus, Denmark. The Danish MS Hospitals, Ry and Haslev, Denmark. The Multiple Sclerosis Clinic, Department of Neurology, Aarhus University Hospital, Aarhus, Denmark. Department of Regional Health Research, University of Southern Denmark, Odense, Denmark. MS-Clinic of Southern Jutland (Sønderborg, Esbjerg, Kolding), Department of Neurology, Sønderborg, Denmark. Exercise Biology, Department of Public Health, Aarhus University, Aarhus, Denmark.
 Servei de Neurologia / Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Secció de Neuroradiologia, Servei de Radiologia, Hospital Universitari Vall d'Hebron, Barcelona, Spain alex.rovira.idi@gencat.cat. Secció de Neuroradiologia, Servei de Radiologia, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Servei de Neurologia / Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Secció de Neuroradiologia, Servei de Radiologia, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Servei de Neurologia / Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Secció de Neuroradiologia, Servei de Radiologia, Hospital Universitari Vall d'Hebron, Barcelona, Spain. Servei de Neurologia / Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Servei de Neurologia / Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Secció de Neuroradiologia, Servei de Radiologia, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
 International Chair of Sports Medicine, Catholic University of Murcia, Murcia, Spain. Faculty of Sport, Catholic University of Murcia, Murcia, Spain. LFE Research Group, Department of Health and Human Performance, Faculty of Physical Activity and Sport Science-INEF, Madrid, Spain. Faculty of Sport, Catholic University of Murcia, Murcia, Spain. LFE Research Group, Department of Health and Human Performance, Faculty of Physical Activity and Sport Science-INEF, Madrid, Spain. UCAM Research Center for High Performance Sport, Catholic University of Murcia, Murcia, Spain. Department of Analytical Chemistry, Nutrition and Food Sciences Faculty of Sciences, University of Alicante, Alicante, Spain. Health Research Centre, Department of Education, Faculty of Educational Sciences, University of Almería, Almería, Spain.
 Turku PET Centre, Turku, Finland maija.saraste@utu.fi. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Faculty of Science and Engineering, Åbo Akademi University, Abo, Finland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Turku PET Centre, Turku, Finland. Neurocenter, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku, Turku, Finland.
 Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne, Victoria, Australia. CORe, Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. University of Ottawa, Department of Medicine, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada. Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada. Department of Medical Sciences, Neurology, Uppsala University, Uppsala, Sweden. Department of Neurology, St Vincent's Hospital Sydney, Sydney, New South Wales, Australia. St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia. Department of Neurology, St Vincent's Hospital Sydney, Sydney, New South Wales, Australia. University of Sydney, Sydney, New South Wales, Australia. St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia. Department of Haematology, St Vincent's Hospital Sydney, Sydney, New South Wales, Australia. Department of Neurology, Austin Health, Melbourne, Victoria, Australia. University of Melbourne, Melbourne, Victoria, Australia. University of Melbourne, Melbourne, Victoria, Australia. Department of Haematology, Austin Health, Melbourne, Victoria, Australia. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Haematology, Haukeland University Hospital, Bergen, Norway. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Haematology, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Haematology, 3rd Faculty of Medicine, Charles University in Prague, and University Hospital Kralovske Vinohrady, Prague, Czech Republic. Department of Neurology, The Alfred Hospital, Melbourne, Victoria, Australia. Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, The Alfred Hospital, Melbourne, Victoria, Australia. Central Clinical School, Monash University, Melbourne, Victoria, Australia. University of Queensland, Brisbane, Queensland, Australia. Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia. Department of Neurology, The Alfred Hospital, Melbourne, Victoria, Australia. Department of Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Monash University, Melbourne, Victoria, Australia. School of Medicine and Public Health, University Newcastle, Newcastle, New South Wales, Australia. Department of Neurology, John Hunter Hospital, Hunter New England Health, Newcastle, New South Wales, Australia. Department of Neurology, Antwerp University Hospital, Edegem, Belgium. Translational Neurosciences Research Group, Faculty of Medicine and Health Sciences, University of Antwerp, Wilrijk, Belgium. UOC Neurologia, Azienda Sanitaria Unica Regionale Marche-AV3, Macerata, Italy. Dokuz Eylul University, Konak, Izmir, Turkey. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq, Kuwait. Neurologic Clinic and Policlinic, Departments of Medicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Medical and Surgical Sciences and Advanced Technologies, GF Ingrassia, Catania, Italy. Multiple Sclerosis Center, University of Catania, Catania, Italy. CHUM MS Center and Universite de Montreal, Montreal, Quebec, Canada. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Flinders University, Adelaide, South Australia, Australia. Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Liverpool Hospital, Sydney, New South Wales, Australia. Monash Medical Centre, Melbourne, Victoria, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Melbourne, Victoria, Australia. Garibaldi Hospital, Catania, Italy. Department of Neurology, Centro Hospitalar Universitario de Sao Joao, Porto, Portugal. Cliniques Universitaires Saint-Luc, Brussels, Belgium. Université Catholique de Louvain, Ottignies-Louvain-la-Neuve, Belgium. Academic MS Center Zuyderland, Department of Neurology, Zuyderland Medical Center, Sittard-Geleen, the Netherlands. School for Mental Health and Neuroscience, Maastricht University, Maastricht, the Netherlands. Department of Neurology, University Hospital Ghent, Ghent, Belgium. Department of Neurology, University Hospital Ghent, Ghent, Belgium. Department of Neurology, Hacettepe University Hospitals, Ankara, Turkey. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino, Italy. Department of Neurology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Department of Neurology, Razi University Hospital, Manouba, Tunis, Tunisia. Faculty of Medicine of Tunis, University of Tunis El Manar, Tunis, Tunisia. Hospital Universitario Donostia, San Sebastián, Spain. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Royal Hobart Hospital, Hobart, Tasmania, Australia. Department of Neurology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Department of Haematology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Department of Neurology, Razi University Hospital, Manouba, Tunis, Tunisia. Faculty of Medicine of Tunis, University of Tunis El Manar, Tunis, Tunisia. Westmead Hospital, Sydney, New South Wales, Australia. Hospital de Galdakao-Usansolo, Galdakao, Spain. University Hospital Reina Sofia, Cordoba, Spain. Center of Neuroimmunology, Service of Neurology, Hospital Clinic de Barcelona, Barcelona, Spain. Department of Medicine, Sultan Qaboos University Hospital, Al-Khodh, Oman. Department of Neurology, Buffalo General Medical Center, Buffalo, New York. Universidade Metropolitana de Santos, Santos, Brazil. Groene Hart Ziekenhuis, Gouda, the Netherlands. Perron Institute, University of Western Australia, Nedlands, Western Australia, Australia. Institute of Immunology and Infectious Diseases, Sir Charles Gairdner Hospital, Murdoch University, Perth, Western Australia, Australia.
 Discipline of Exercise Science, Murdoch University, Perth, Australia. Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Ageing, Murdoch University, Perth, Australia. Perron Institute for Neurological and Translational Science, Perth, Australia. Centre for Health Equity, Melbourne School of Population & Global Health, Melbourne, Australia. Child and Community Wellbeing Unit, Centre for Health Equity, Melbourne School of Population & Global Health, Melbourne, Australia. School of Plant Biology, University of Western Australia, Crawley, Australia. Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Ageing, Murdoch University, Perth, Australia. Centre for Neuromuscular and Neurological Disorders, Perron Institute for Neurological and Translational Science, University of Western Australia, Perth, Australia. Centre for Health Equity, Melbourne School of Population & Global Health, Melbourne, Australia.
 Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. valeryfuh.ngwa@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. Menzies Health Institute Queensland and School of Medicine, Griffith University, Gold Coast, QLD, 4222, Australia. Florey Institute for Neuroscience and Mental Health, Parkville, VIC, 3052, Australia. Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. Neuroepidemiology Unit, Center for Epidemiology and Biostatistics, The University of Melbourne School of Population & Global Health, Melbourne, VIC, 3053, Australia. School of Medicine and Public Health New Lambton, Hunter New England Health, New Lambton Heights, NSW, Australia. Department of Neurology, The University of Newcastle Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia. bruce.taylor@utas.edu.au.
 Mallinckrodt Institute of Radiology, Division of Neuroradiology, Washington University in St. Louis, St. Louis, MO, USA. Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA. Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA. Mallinckrodt Institute of Radiology, Division of Neuroradiology, Washington University in St. Louis, St. Louis, MO, USA. Department of Surgery, Division of Public Health Sciences, Washington University in St. Louis, St. Louis, MO, USA. Department of Physics, Washington University in St. Louis, St. Louis, MO, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO, USA. Department of Physics, Washington University in St. Louis, St. Louis, MO, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO, USA. Mallinckrodt Institute of Radiology, Division of Neuroradiology, Washington University in St. Louis, St. Louis, MO, USA. Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA. Mallinckrodt Institute of Radiology, Division of Neuroradiology, Washington University in St. Louis, St. Louis, MO, USA. Charles F. and Joanne Knight Alzheimer Disease Research Center, Washington University in St Louis, St. Louis, MO, USA. Department of Medicine, Division of Geriatrics and Nutritional Science, Washington University in St. Louis, St. Louis, MO, USA. Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA. Hope Center for Neurological Disorders, Washington University in St. Louis, St. Louis, MO, USA. Brain and Mind Centre, School of Medical Sciences, The University of Sydney, NSW, Australia. Charles Perkin Centre, The University of Sydney NSW, Australia. Mallinckrodt Institute of Radiology, Division of Neuroradiology, Washington University in St. Louis, St. Louis, MO, USA. Charles F. and Joanne Knight Alzheimer Disease Research Center, Washington University in St Louis, St. Louis, MO, USA.
 Faculty of Medical Science, Jinan University, Guangzhou, 510632, China. Faculty of Medical Science, Jinan University, Guangzhou, 510632, China. Department of Pediatrics, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangdong, Guangzhou, 510655, China. Zhuhai Hospital Affiliated with Jinan University (Zhuhai People's Hospital), Jinan University, Zhuhai, 519000, China. Zhuhai Hospital Affiliated with Jinan University (Zhuhai People's Hospital), Jinan University, Zhuhai, 519000, China. Electronic address: huangfang67@sohu.com. Faculty of Medical Science, Jinan University, Guangzhou, 510632, China. Electronic address: liuzonghua@jnu.edu.cn.
 College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea. Faculty of Pharmacy, Ton Duc Thang University, Ho Chi Minh City, Vietnam. College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea. College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea. College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea.
 Department of Medical Biophysics, Faculty of Medicine in Hradec Kralove, Charles University, Simkova 870, Hradec Kralove, Czech Republic. Department of Medical Biophysics, Faculty of Medicine in Hradec Kralove, Charles University, Simkova 870, Hradec Kralove, Czech Republic. kremlacek@lfhk.cuni.cz.
 Department of Neuroscience, Section for Physiotherapy, Uppsala, Sweden. Department of Neuroscience, Section for Physiotherapy, Uppsala, Sweden. Department of Neuroscience, Section for Physiotherapy, Uppsala, Sweden. Department of Neuroscience, Section for Physiotherapy, Uppsala, Sweden. Department of Health Care Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden. Region Örebro County, University Research Health Care Centre, Sweden. Department of Neuroscience, Section for Physiotherapy, Uppsala, Sweden.
 Service de Médecine Physique et de Réadaptation, Hôpital Saint Philibert, Lomme, France; Faculté de Médecine et de Maïeutique, ICL, France; Université Lille Nord de France, Lille, France; UPHF, LAMIH, Valenciennes, France; CNRS, UMR 8201, Valenciennes, France. Electronic address: Massot.Caroline@ghicl.net. Faculté de Médecine et de Maïeutique, ICL, France. Université Lille Nord de France, Lille, France; UPHF, LAMIH, Valenciennes, France; CNRS, UMR 8201, Valenciennes, France. Université Lille Nord de France, Lille, France; UPHF, LAMIH, Valenciennes, France; CNRS, UMR 8201, Valenciennes, France. Service de Médecine Physique et de Réadaptation, Hôpital Saint Philibert, Lomme, France; Faculté de Médecine et de Maïeutique, ICL, France. Université Lille Nord de France, Lille, France; UPHF, LAMIH, Valenciennes, France; CNRS, UMR 8201, Valenciennes, France. Université Lille Nord de France, Lille, France; UPHF, LAMIH, Valenciennes, France; CNRS, UMR 8201, Valenciennes, France.
 Department of Rehabilitation Medicine, First Hospital of jilin University, Changchun, China. Department of Rehabilitation Medicine, First Hospital of jilin University, Changchun, China. Department of Rehabilitation Medicine, First Hospital of jilin University, Changchun, China. Department of Rehabilitation Medicine, First Hospital of jilin University, Changchun, China. Department of Rehabilitation Medicine, First Hospital of jilin University, Changchun, China. Department of Rehabilitation Medicine, First Hospital of jilin University, Changchun, China.
 Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. College of Medicine, Neurology Division, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Biomedical Sciences, WCVM, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. College of Medicine, Neurology Division, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
 Amrita School of Pharmacy, AIMS Health Science Campus, Amrita Vishwa Vidyapeetham, Kochi, Kerala, 682041, India. Department of Pharmaceutical Chemistry and Analysis, Amrita School of Pharmacy, AIMS Health Science Campus, Amrita Vishwa Vidyapeetham, Kochi, Kerala, India. saiprabhavn@gmail.com. Department of Pharmacology, Amrita School of Pharmacy, AIMS Health Science Campus, Amrita Vishwa Vidyapeetham, Kochi, Kerala, India. krishnadas.madhu77@gmail.com.
 Department of Pharmacology and Clinical Pharmacology, Centre for Brain Research, School of Medical Science, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. Department of Pharmacology and Clinical Pharmacology, Centre for Brain Research, School of Medical Science, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
 Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Phystech School of Biological and Medical Physics, Moscow Institute of Physics and Technology (National Research University), 141701 Dolgoprudny, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. School of Biopharmacy, China Pharmaceutical University, Nanjing 211198, China. National Research Center, "Kurchatov Institute", 123182 Moscow, Russia. National Research Center, "Kurchatov Institute", 123182 Moscow, Russia. Institute of Biomedical Systems and Biotechnologies, Peter the Great St. Petersburg Polytechnic University, 195251 St. Petersburg, Russia. Petersburg Nuclear Physics Institute Named by B.P. Konstantinov of National Research Centre, Kurchatov Institute, 188300 Gatchina, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Department of Biological Chemistry, Ministry of Health of Russian Federation, Evdokimov Moscow State University of Medicine and Dentistry, 127473 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
 Department of Neurology, Northwestern Memorial Hospital, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
 Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Preventive Medicine, Shantou University Medical College, Shantou, Guangdong, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China. Department of Ophthalmology, Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou University Medical College, Shantou, China.
 Department of Neurology, Division of Multiple Sclerosis, Rush University Medical Center, 1625 W. Harrison St, Chicago, IL 60612, United States of America. Department of Neurology, Division of Multiple Sclerosis, Rush University Medical Center, 1625 W. Harrison St, Chicago, IL 60612, United States of America. Department of Neurology, Division of Multiple Sclerosis, Rush University Medical Center, 1625 W. Harrison St, Chicago, IL 60612, United States of America. Department of Neurology, Division of Multiple Sclerosis, Rush University Medical Center, 1625 W. Harrison St, Chicago, IL 60612, United States of America. Department of Neurology, Division of Multiple Sclerosis, Rush University Medical Center, 1625 W. Harrison St, Chicago, IL 60612, United States of America. Electronic address: Fabian_SierraMorales@rush.edu.
 Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Swiss Institute for Translational and Entrepreneurial Medicine, sitem-insel, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Swiss Institute for Translational and Entrepreneurial Medicine, sitem-insel, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Support Center for Advanced Neuroimaging (SCAN), University Institute of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.
 Department of Medicine, The University of Sydney, Camperdown, NSW, Australia. Department of Medicine, The University of Sydney, Camperdown, NSW, Australia.
 Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Republican Clinical Neurological Center, Republic of Tatarstan, 420021 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Department of Medical Biology and Genetic, Kazan State Medical University, 420088 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Department of Immunology, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang 471003, China. Department of Biotechnology, Thapar Institute of Engineering and Technology, Patiala 147004, India. Department of Biotechnology, Thapar Institute of Engineering and Technology, Patiala 147004, India. Department of Biotechnology, Thapar Institute of Engineering and Technology, Patiala 147004, India. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia.
 Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
 School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. Institute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany. Center for Biomedicine and Innovations, Faculty of Medicine, Macau University of Science and Technology, Taipa, Macau 999078, China. Institute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany. Institute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany. School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. Department of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China. School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. Department of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China. Department of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China. School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. Institute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany. Institute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany. Department of Neurology, University Medical Center Rostock, University of Rostock, 18057 Rostock, Germany.
 University of Colorado School of Medicine, Aurora, CO david.rubinstein@cuanschutz.edu.
 Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. First Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Department of Neurology, University Hospital of Larissa, School of Health Sciences, Faculty of Medicine, University of Thessaly, Larissa, Greece. First Department of Psychiatry, Aiginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Allergy Department, "Sotiria" General Hospital, Athens, Greece. Department of Hygiene, Epidemiology and Medical Statistics, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Fourth Department of Internal Medicine, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; Department of Neurology, University of Tennessee Health Science Center, Memphis, TN, USA. Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
 Research Group Molecular Nutritional Medicine, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany. Experimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Einstein Center Digital Future, Berlin, Germany. Experimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
 Department of Neurology, CRC-SEP, CHU de Nice, Pasteur 2 Hospital, Nice, France UR2CA-URRIS, Côte d'Azur University, Nice, France. Department of Neurology, CRC-SEP, CHU de Nice, Pasteur 2 Hospital, Nice, France. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey. The University of Texas Southwestern Medical Center, Dallas, TX, USA. School of Medicine, Hacettepe University, Ankara, Turkey. School of Medicine, Kocaeli University, Kocaeli, Turkey. School of Medicine, Ondokuz Mayis University, Samsun, Turkey. Department of Neurology, CRC-SEP, CHU de Montpellier, Gui de Chauliac Hospital, Montpellier, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Institut de Génomique Fonctionnelle, Université de Montpellier, Centre National de Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, Montpellier, France. Department of Neurology, Centre de Ressource et Competence Sclérose En Plaques, Centre Hospitalier Universitaire de Toulouse, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Institut National de la Santé et de la Recherche Médicale Unité Mixte de Recherche1291, Centre National de Recherche Scientifique Unité Mixte de Recherche 5051, Université Toulouse III, Toulouse, France. Université de Lille, Inserm Unité Mixte de Recherche-S 1172 LilNcog, Centre Hospitalier Universitaire Lille, Fédération Hospitalo-Universitaire Precise, Lille, France. Department of Neurology, CHU Rouen, Rouen, France. Pathologies Inflammatoires du Système Nerveux, Neurologie, CHU Grenoble Alpes, T-RAIG (Translational Research in Autoimmunity and Inflammation Group) TIMC-IMAG, Université de Grenoble-Alpes, CHU Grenoble-Alpes, Grenoble, France. Department Clinical Investigation Center, Department of Neurology, Centre Hospitalier Universitaire de Strasbourg, Institut National de la Santé et de la Recherche Médicale, Strasbourg, France. Department of Neurology, Centre Hospitalier Universitaire de Dijon, Dijon, France. Department of Neurology, Centre Hospitalier Universitaire de Poitiers, Poitiers, France. University of Southern California, Los Angeles, CA, USA. Mayo Clinic, Rochester, MN, USA. Department of Neurology, Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey. Department of Neurology, Centre Hospitalier Universitaire de Caen Normandie, Caen, France. Neurology Department, CRC-SEP, Hopital Fondation Adolphe de Rothschild, Paris, France. CIC Neurosciences, Department of Neurology, Sorbonne University, Assistance Publique des Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris, France. Department of Neurology, CRC-SEP, CHU de Nice, Pasteur 2 Hospital, Nice, France UR2CA-URRIS, Côte d'Azur University, Nice, France. Department of Neurology, CRC-SEP, CHU de Nice, Pasteur 2 Hospital, Nice, France UR2CA-URRIS, Côte d'Azur University, Nice, France. Department of Neurology, CRC-SEP, CHU de Nice, Pasteur 2 Hospital, Nice, France UR2CA-URRIS, Côte d'Azur University, Nice, France.
 Hospital Universitario de Burgos, Burgos, España. Hospital Universitario de Burgos, Burgos, España.
 Department of Neurology, Division of Neuroimmunology and Neuroinfectious Disease, Massachusetts General Hospital and Harvard Medical School, Boston, USA; Multiple Sclerosis Comprehensive Care Center, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: lotan.itay1@gmail.com. ICometrix, Leuven, Belgium. ICometrix, Leuven, Belgium. ICometrix, Leuven, Belgium. Department of Radiology, New York University Langone Medical Center, New York, NY, USA. Multiple Sclerosis Comprehensive Care Center, New York University Grossman School of Medicine, New York, NY, USA. Department of Radiology, New York University Langone Medical Center, New York, NY, USA.
 Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Radiology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA; Department of Ophthalmology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA; Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA; Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA; Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, 200 1(st) St. SW, Rochester, MN, USA. Electronic address: flanagan.eoin@mayo.edu.
 Department of Applied Behavioral Science, University of Kansas, Lawrence, KS, USA. Cofrin-Logan Center for Addiction Research and Treatment, University of Kansas, Lawrence, KS, USA. Healthcare Institute for Innovations in Quality, University of Missouri-Kansas City, Kansas City, MO, USA. Department of Applied Behavioral Science, University of Kansas, Lawrence, KS, USA. Cofrin-Logan Center for Addiction Research and Treatment, University of Kansas, Lawrence, KS, USA. Behavioral Pharmacology Research Unit, Johns Hopkins School of Medicine, Baltimore, MD, USA. Center for Children's Healthy Lifestyles and Nutrition, Children's Mercy Hospital, Kansas City, MO, USA. Department of Pediatrics, University of Kansas Medical Center, Kansas City, KS, USA. Department of Applied Behavioral Science, University of Kansas, Lawrence, KS, USA. Cofrin-Logan Center for Addiction Research and Treatment, University of Kansas, Lawrence, KS, USA. Department(s) of Biomedical and Health Informatics, University of Missouri-Kansas City School of Medicine, Kansas City, MO, USA.
 Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole 10, 10043 Orbassano, Italy; CRESM Biobank, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy. Electronic address: paolaval81@hotmail.com. Department of Neurology and CRESM, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole 10, 10043 Orbassano, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole 10, 10043 Orbassano, Italy; Department of Neuroscience "Rita Levi Montalcini", University of Turin, Italy, Via Cherasco 15, 10100 Turin, Italy. Department of Neurology, S. Croce e Carle Hospital, Via Michele Coppino, 26, 12100 Cuneo, Italy. Department of Neurology and CRESM, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy. Department of Neurology and CRESM, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy. Department of Neurology and CRESM, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy. CRESM Biobank, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy; Department of Neurology and CRESM, University Hospital San Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano, Italy. Neuroscience Institute Cavalieri Ottolenghi (NICO), Regione Gonzole 10, 10043 Orbassano, Italy; Koelliker Hospital, C.so Galileo Ferraris, 247/255, 10134 Turin, Italy.
 Department of Clinical Neurology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK gavin.brittain@sheffield.ac.uk. Sheffield Institute for Translational Neuroscience, The University of Sheffield, Sheffield, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. Neuroscience and Trauma, Blizard Institute of Cell and Molecular Science, London, UK. Department of Brain Sciences, Imperial College London, London, UK. Department of Clinical Neurology, University of Oxford, Oxford, UK. Clinical Trials Research Unit, The University of Sheffield, Sheffield, UK. Department of Haematology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. Institute of Clinical Neurosciences, University of Bristol, Bristol, UK. Department of Neurology, Gloucestershire Royal Hospital, Gloucester, UK. Department of Haematology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. Department of Oncology and Metabolism, The University of Sheffield, Sheffield, UK. Department of Clinical Neurology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. Sheffield Institute for Translational Neuroscience, The University of Sheffield, Sheffield, UK.
 Department of Integrative Physiology, University of Colorado, Boulder, Colorado, United States. Department of Mechanical Engineering, University of Colorado, Colorado, Boulder, United States. Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States. Department of Integrative Physiology, University of Colorado, Boulder, Colorado, United States. Department of Mechanical Engineering, University of Colorado, Colorado, Boulder, United States.
 Université Paris-Saclay, INRAE, MGP, 78350, Jouy-en-Josas, France. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, 2600, Glostrup, Denmark. Department of Clinical Medicine, University of Copenhagen, 2200, Copenhagen, Denmark. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Université Paris-Saclay, INRAE, MGP, 78350, Jouy-en-Josas, France. Université Paris-Saclay, INRAE, MGP, 78350, Jouy-en-Josas, France. Université Paris-Saclay, INRAE, MGP, 78350, Jouy-en-Josas, France. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, 2600, Glostrup, Denmark. Center for Clinical Research and Prevention, Bispebjerg and Frederiksberg University Hospital, 2400, Frederiksberg, Denmark. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Experimental and Clinical Research Center, A Cooperation of Charité-Universitätsmedizin and the Max-Delbrück Center, 10117, Berlin, Germany. Max Delbrück Center for Molecular Medicine (MDC), 13125, Berlin, Germany. Charité-Universitätsmedizin Berlin, 10117, Berlin, Germany. DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, 10785, Berlin, Germany. Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117, Heidelberg, Germany. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Department of Medicine, Rønne Hospital, 3700, Bornholm, Denmark. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. Department of Biotechnology and Biomedicine, Technical University of Denmark, 2800, Kongens Lyngby, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, 2600, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, 2600, Glostrup, Denmark. Université Paris-Saclay, INRAE, MGP, 78350, Jouy-en-Josas, France. Department of Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, WC1N 3RX, UK. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, 2200, Copenhagen, Denmark. oluf@sund.ku.dk. Center for Clinical Metabolic Research, Herlev-Gentofte University Hospital, Hellerup, 2900, Copenhagen, Denmark. oluf@sund.ku.dk.
 From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France. bertrand.audoin@ap-hm.fr. From the Department of Neurology (B.A., M.P., A.R., C.B., S.D., F.H., J.P., A.M.), CRMBM, University Hospital of Marseille, Aix-Marseille University; Service d'immunologie (D.C., F.V.), Marseille Immunopôle, APHM, Aix Marseille University, CNRS, INSERM, CIML; Faculté de Pharmacie (R.C.), Aix-Marseille University; and Centre hospitalier d'Ajaccio (P.D.), Service de Neurologie, France.
 Molecular Medicine Research Centre, Universitätsklinikum Jena, Jena, Germany; Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran. Student Research Committee, Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of New Scientist, Faculty of Medical Sciences, Tehran Branch, Islamic Azad University, Tehran, Iran. Student Research Committee, Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Zhino-Gene Research Services Co., Tehran, Iran. Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Regenerative Medicine Group (REMED), Universal Scientific Education & Research Network (USERN), Tehran, Iran. Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: h.zali@sbmu.ac.ir.
 Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Department of Medical Biology and Genetics, Kazan State Medical University, 420012 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Department of Medical Biology and Genetics, Kazan State Medical University, 420012 Kazan, Russia. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. Department of Medical Biology and Genetics, Kazan State Medical University, 420012 Kazan, Russia.
 Radiodiagnosis (Neuroradiology and Nuclear Medicine), University of Rochester Medical Center, Rochester, NY 14618, USA. Electronic address: drneetusoni98@gmail.com. Department of Nuclear Medicine, SGPGIMS, Lucknow, Uttar Pradesh, India. Upstate University Hospital, Syracuse, NY, USA. Division of Hematology-Oncology at the University of Vermont Medical Center, Burlington, VT, USA. Radiodiagnosis (Neuroradiology and Nuclear Medicine), University of Rochester Medical Center, Rochester, NY 14618, USA. Radiology, Mayo Clinic in Florida, San Pablo Dr, Jacksonville, FL 32224-1865, USA. Radiodiagnosis (Neuroradiology and Nuclear Medicine), University of Rochester Medical Center, Rochester, NY 14618, USA. Department of Radiology, Mayo Clinic, USA.
 Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Therapeutic Biologics Protein Team, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Information Management Services, Inc., Rockville, Maryland, USA. Spaulding Clinical Research, West Bend, Wisconsin, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Office of Therapeutic Biologics and Biosimilars, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Therapeutic Biologics Protein Team, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. Division of Applied Regulatory Science, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA.
 Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Department of Human Neurosciences, University of Rome La Sapienza, Rome, Italy. Neuroimmunology Unit, Santa Lucia Foundation Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Unità Operativa Semplice (UOS) Professioni Sanitarie Tecniche, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Clinical Division of Infectious Diseases, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Cellular Immunology Laboratory, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Department of Pediatric Hematology and Oncology, Bambino Gesu Pediatric Hospital, Rome, Italy. UOC Emerging Infections and Centro di Riferimento AIDS (CRAIDS), National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, Rome, Italy. Clinical Division of Infectious Diseases, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani Institute for Hospitalization and Care Scientific, Rome, Italy delia.goletti@inmi.it.
 Neuropsychology Department, Morriston Hospital, Swansea, UK. Brain Injury Research Group, Swansea University, Swansea, UK. Neuropsychology Department, Morriston Hospital, Swansea, UK.
 Department of Pediatrics and Neurology, Children's Hospital of Colorado, University of Colorado, Aurora, CO, USA. Boston Children's Pediatric MS Center, Boston, MA, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. University of Utah, Salt Lake City, UT, USA. George E. Wahlen Department of Veterans Affairs Medical Center, University of Utah, Salt Lake City, UT, USA. Boston Children's Pediatric MS Center, Boston, MA, USA. Boston Children's Pediatric MS Center, Boston, MA, USA. Washington University, St. Louis, MO, USA. NYU Langone, New York, NY, USA. Baylor College of Medicine, Houston, TX, USA. Washington University, St. Louis, MO, USA. University of Alabama at Birmingham, Birmingham, AL, USA. Cleveland Clinic, Cleveland, OH, USA. University of Utah, Salt Lake City, UT, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. George E. Wahlen Department of Veterans Affairs Medical Center, University of Utah, Salt Lake City, UT, USA. Baylor College of Medicine, Houston, TX, USA. UCSF, San Francisco, CA, USA. University of Alabama at Birmingham, Birmingham, AL, USA. University of Utah, Salt Lake City, UT, USA. Brigham and Women's Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
 From the Internal Medicine Department (Alshammari A), College of Medicine, College of Medicine (Alshammari K, Alshammari S, Aldhaifi S), From Ear, Nose, and Throat (ENT) Department (Alqahtani), College of Medicine, University of Hail, Hail, Kingdom of Saudi Arabia. From the Internal Medicine Department (Alshammari A), College of Medicine, College of Medicine (Alshammari K, Alshammari S, Aldhaifi S), From Ear, Nose, and Throat (ENT) Department (Alqahtani), College of Medicine, University of Hail, Hail, Kingdom of Saudi Arabia. From the Internal Medicine Department (Alshammari A), College of Medicine, College of Medicine (Alshammari K, Alshammari S, Aldhaifi S), From Ear, Nose, and Throat (ENT) Department (Alqahtani), College of Medicine, University of Hail, Hail, Kingdom of Saudi Arabia. From the Internal Medicine Department (Alshammari A), College of Medicine, College of Medicine (Alshammari K, Alshammari S, Aldhaifi S), From Ear, Nose, and Throat (ENT) Department (Alqahtani), College of Medicine, University of Hail, Hail, Kingdom of Saudi Arabia. From the Internal Medicine Department (Alshammari A), College of Medicine, College of Medicine (Alshammari K, Alshammari S, Aldhaifi S), From Ear, Nose, and Throat (ENT) Department (Alqahtani), College of Medicine, University of Hail, Hail, Kingdom of Saudi Arabia.
 Department of Neurology, Esztergomi Vaszary Kolos Hospital, 2500 Esztergom, Hungary. Department of Neurology, Faculty of Medicine, University of Szeged, Semmelweis u. 6., H-6725 Szeged, Hungary. Danube Neuroscience Research Laboratory, ELKH-SZTE Neuroscience Research Group, Eötvös Loránd Research Network, University of Szeged (ELKH-SZTE), Tisza Lajos krt. 113, H-6725 Szeged, Hungary.
 Department of Philosophical and Methodological Disciplines and Service of Molecular Biology in Medicine Hospital, Civil University Health Sciences Center, University of Guadalajara, Guadalajara 44340, Jalisco, Mexico. Department of Neurology, High Specialty Medical Unit, Western National Medical Center of the Mexican Institute of Social Security, Guadalajara 44329, Jalisco, Mexico. Department of Philosophical and Methodological Disciplines and Service of Molecular Biology in Medicine Hospital, Civil University Health Sciences Center, University of Guadalajara, Guadalajara 44340, Jalisco, Mexico. Neurosciences Division, Western Biomedical Research Center, Mexican Social Security Institute (Instituto Mexicano del Seguro Social, IMSS), Guadalajara 44340, Jalisco, Mexico. Neurosciences Division, Western Biomedical Research Center, Mexican Social Security Institute (Instituto Mexicano del Seguro Social, IMSS), Guadalajara 44340, Jalisco, Mexico. Neurosciences Division, Western Biomedical Research Center, Mexican Social Security Institute (Instituto Mexicano del Seguro Social, IMSS), Guadalajara 44340, Jalisco, Mexico. Coordination of Academic Activities, Western Biomedical Research Center, Mexican Social Security Institute (Instituto Mexicano del Seguro Social, IMSS), Guadalajara 44340, Jalisco, Mexico. Department of Neurology, High Specialty Medical Unit, Western National Medical Center of the Mexican Institute of Social Security, Guadalajara 44329, Jalisco, Mexico. Department of Neurology, High Specialty Medical Unit, Western National Medical Center of the Mexican Institute of Social Security, Guadalajara 44329, Jalisco, Mexico. Department of Medical and Life Sciences, University Center of la Cienega, University of Guadalajara, Ocotlan 47820, Jalisco, Mexico.
 Clinical Neuropsychology Laboratory, National Institute of Neurology and Neurosurgery, Mexico. Faculty of Medicine, National Autonomous University of Mexico, Mexico. Clinical Neuropsychology Laboratory, National Institute of Neurology and Neurosurgery, Mexico. Clinical Neurodegenerative Diseases Laboratory, National Institute of Neurology and Neurosurgery. Clinical Neurodegenerative Diseases Laboratory, National Institute of Neurology and Neurosurgery. Faculty of Medicine, National Autonomous University of Mexico, Mexico; Clinical Neurodegenerative Diseases Laboratory, National Institute of Neurology and Neurosurgery. Electronic address: coronav@unam.mx.
 Section of General Pathology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: maria.tredicine@unicatt.it. Section of General Pathology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy; Fondazione Policlinico Universitario A. Gemelli IRCCS, Department Laboratory and Infectious diseases Sciences, Largo Agostino Gemelli 1-8, 00168, Rome, Italy. Electronic address: francesco.ria@unicatt.it. Department of Biology, University of Rome "TorVergata", Via della Ricerca Scientifica 1, 00173, Rome, Italy. Electronic address: noemi.poerio@uniroma2.it. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC of Neurology, Largo Agostino Gemelli 8, 00168, Rome, Italy; Department of Neurosciences, Centro di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: matteo.lucchini@policlinicogemelli.it. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC of Neurology, Largo Agostino Gemelli 8, 00168, Rome, Italy; Department of Neurosciences, Centro di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: assunta.bianco@policlinicogemelli.it. Department of Biology, University of Rome "TorVergata", Via della Ricerca Scientifica 1, 00173, Rome, Italy. Electronic address: federica.desa92@gmail.com. Section of Pathology, Department of Woman, Child and Public Health Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli 1-8, 00168, Rome, Italy. Electronic address: mariagrazia.valentini@guest.policlinicogemelli.it. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC of Neurology, Largo Agostino Gemelli 8, 00168, Rome, Italy; Department of Neurosciences, Centro di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: valeria.dearcangelis@guest.policlinicogemelli.it. Department of Surgery and Medicine, Institute of Human, Clinical and Forensic Anatomy, Piazza L. Severi 1, 06125, Perugia, Italy. Electronic address: mario.rende@unipg.it. Department of Surgery and Medicine, Institute of Human, Clinical and Forensic Anatomy, Piazza L. Severi 1, 06125, Perugia, Italy. Electronic address: anna.stabile@unipg.it. Department of Surgery and Medicine, Institute of Human, Clinical and Forensic Anatomy, Piazza L. Severi 1, 06125, Perugia, Italy. Electronic address: alessandra.pistilli@unipg.it. Section of General Pathology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy; Institute of Chemical Sciences and Technologies ''Giulio Natta'' (SCITEC)-CNR, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: chiara.camponeschi94@gmail.com. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC of Neurology, Largo Agostino Gemelli 8, 00168, Rome, Italy; Department of Neurosciences, Centro di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: viviana.nociti@policlinicogemelli.it. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC of Neurology, Largo Agostino Gemelli 8, 00168, Rome, Italy; Department of Neurosciences, Centro di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. Electronic address: massimiliano.mirabella@policlinicogemelli.it. Department of Biology, University of Rome "TorVergata", Via della Ricerca Scientifica 1, 00173, Rome, Italy. Electronic address: fraziano@bio.uniroma2.it. Section of General Pathology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy; Department of Surgery and Medicine, Institute of Human, Clinical and Forensic Anatomy, Piazza L. Severi 1, 06125, Perugia, Italy. Electronic address: gabriele.disante@unipg.it.
 Immunology Laboratory, CHU Timone AP-HM, Marseille, France. Immunology Laboratory, CHU Timone AP-HM, Marseille, France. Immunology Laboratory, CHU Timone AP-HM, Marseille, France. Immunology Laboratory, CHU Timone AP-HM, Marseille, France. Immunology Laboratory, CHU Timone AP-HM, Marseille, France. Referral Centre for Neuromuscular Diseases and ALS, CHU Timone, Marseille, France. Referral Centre for Neuromuscular Diseases and ALS, CHU Timone, Marseille, France. Department of Neurology and Neuropsychology, CHU Timone, AP-HM and UMR 7249, CNRS, Centrale Marseille, Institut Fresnel, AMU, Marseille, France. Department of Neurology, CHU Timone, APHM, Marseille, and CRMBM/UMR CNRS 7339, AMU, Marseille, France. Immunology Laboratory, CHU Timone AP-HM, Marseille, France. Immunology Laboratory, CHU Timone AP-HM, Marseille, France. AMU, Institut de Neurosciences des Systèmes (INS, UMR1106), Marseille, France.
 Department of Biomedical Sciences (L.V., G.M., L.C., F.D., A.M.), University of Sassari, Sassari, Italy; Department of Sport Sciences (P.M.N., D.B., F.J.V.G.), Sports Research Centre, Miguel Hernández University of Elche, Elche (Alicante), Spain; Department of Physical Therapy (A.K., Z.D.), Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; and Unit of Endocrinology (F.D.), Nutritional and Metabolic Disorders, AOU Sassari, Sassari, Italy.
 Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China; National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Electronic address: duchangsheng@tongji.edu.cn.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. rocca.mara@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. rocca.mara@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. rocca.mara@hsr.it.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, University of Texas Southwestern Medical Center at Dallas, TX, USA. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Psychosomatic Research Center, Department of Psychiatry, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: barzegar_mahdi73@yahoo.com.
 UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA/Department of Physical Therapy and Rehabilitation Science, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA/Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA/Department of Medicine, University of California San Francisco, San Francisco, CA, USA. Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA. Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA/Department of Radiology, University of California San Francisco, San Francisco, CA, USA.
 Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, The First College of Clinical Medical Science, China Three Gorges University and Yichang Central People's Hospital, Yichang 443000, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Electronic address: lzwcy@xwhosp.org.
 Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN), and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Electronic address: katrin.pape@unimedizin-mainz.de.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. VASCage Research Centre on Vascular Ageing and Stroke, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. VASCage Research Centre on Vascular Ageing and Stroke, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
 NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. Department of Radiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. Shandong University of Traditional Chinese Medicine, Jinan, Shandong Province, 250355, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. Department of Radiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, 107 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China. NMPA Key Laboratory for Technology Research and Evaluation of Drug Products and Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 Cultural West Road, Jinan, Shandong Province, 250012, P. R. China.
 Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. lucchinimatteo87@gmail.com. Centro Di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168, Rome, Italy. lucchinimatteo87@gmail.com. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Oncologia Medica, Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. Centro Di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168, Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. Centro Di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168, Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. Dipartimento Di Medicina e Chirurgia, Sezione Di Anatomia Umana, Clinica e Forense, Università Degli Studi Di Perugia, Perugia, Italy. Dipartimento Di Medicina E Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Rome, Italy. Dipartimento Di Scienze Di Laboratorio Ed Infettivologiche, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. Centro Di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168, Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, Rome, Italy. Centro Di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168, Rome, Italy.
 Department of Neurology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 11 Košice, Slovakia. Department of Social and Behavioural Medicine, Faculty of Medicine, Pavol Jozef Šafárik University, 040 11 Košice, Slovakia. Department of Neurology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 11 Košice, Slovakia. Department of Neurology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 11 Košice, Slovakia. Institute of Neuroimmunology, Slovak Academy of Science, 845 10 Bratislava, Slovakia. Institute of Neuroimmunology, Slovak Academy of Science, 845 10 Bratislava, Slovakia. Magnetic Resonance Imaging, ProMagnet, 041 91 Košice, Slovakia. Department of Neurology, Faculty of Medicine, Pavol Jozef Šafárik University, 040 11 Košice, Slovakia.
 Department of Chemical and Biological Sciences, Institute of Biosciences, São Paulo State University (UNESP), Botucatu 18618-689, Brazil. Laboratory of Mucosal Immunology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo 05508-000, Brazil. Department of Chemical and Biological Sciences, Institute of Biosciences, São Paulo State University (UNESP), Botucatu 18618-689, Brazil.
 Department of Community Health Nursing, School of Nursing, Jahrom University of Medical Sciences, Jahrom, Iran. Electronic address: ali.dehghani2000@gmail.com. Department of Nursing, School of Nursing, Jahrom University of Medical Sciences, Jahrom, Iran. Department of Nursing, School of Nursing, Jahrom University of Medical Sciences, Jahrom, Iran.
 Institute of Ophthalmology, University College London, London, UK. Jules-Gonin Eye Hospital, Lausanne University, Lausanne, Switzerland. Departments of Ophthalmology and Neurology, Scheie Eye Institute, University of Pennsylvania, 51 N 39th Street, Philadelphia, PA, 19104, USA. Institute of Ophthalmology, University College London, London, UK. Departments of Ophthalmology and Neurology, Scheie Eye Institute, University of Pennsylvania, 51 N 39th Street, Philadelphia, PA, 19104, USA. Institute of Ophthalmology, University College London, London, UK. School of Pharmacy, University College London, London, UK. Institute of Ophthalmology, University College London, London, UK. Imperial College London Ophthalmology Research Group, London, UK. Western Eye Hospital, London, UK. Departments of Ophthalmology and Neurology, Scheie Eye Institute, University of Pennsylvania, 51 N 39th Street, Philadelphia, PA, 19104, USA. kenneth.shindler@pennmedicine.upenn.edu.
 Department of Urology, University of Lille, Claude Huriez Hospital, Lille University Hospital, Lille, France. Department of Urology, University of Lille, Claude Huriez Hospital, Lille University Hospital, Lille, France. GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, Sorbonne Université, Assistance Publique-Hôpitaux de Paris (AP-HP), Tenon Academic Hospital, Paris, France. Department of Urology, Hotel Dieu Hospital, University of Nantes, Nantes, France. Department of Urology, Assistance-Publique-Hôpitaux de Marseille (AP-HM), La Conception Academic Hospital, Marseille, France. Department of Urology, University of Rennes, Rennes Academic Hospital, Rennes, France. Department of Urology, University of Rennes, Rennes Academic Hospital, Rennes, France. Department of Urology, Hotel Dieu Hospital, University of Nantes, Nantes, France. Department of Biostatistics, CHU Lille, Lille, France. Department of Urology, Sorbonne Université, Assistance Publique-Hôpitaux de Paris (AP-HP), La Pitié-Salpêtrière Academic Hospital, Paris, France. Department of Urology, University of Bordeaux, Bordeaux Academic Hospital, Bordeaux, France. Department of Urology, University of Rouen Normandy, Rouen Academic Hospital, Rouen, France. Department of Rehabilitation and Physical Medicine, Université of Toulouse, Rangueil Academic Hospital, Toulouse, France. Department of Urology, University of Toulouse, Rangueil Academic Hospital, Toulouse, France. Department of Urology, Assistance-Publique-Hôpitaux de Marseille (AP-HM), La Conception Academic Hospital, Marseille, France. Department of Urology, Hospices Civils de Lyon, Lyon Sud Hospital, Pierre-Bénite, France. Department of Rehabilitation and Physical Medicine, Université Paris-Saclay, Assistance Publique-Hôpitaux de Paris (AP-HP), Raymond Poincaré Academic Hospital, Garches, France/Inserm UMR 1179, END-ICAP, Laboratoire Handicap Neuromusculaire: Physiopathologie, Biothérapie et Pharmacologie Appliquées, UFR Simone Veil, Université Paris-Saclay, Paris, France. Department of Rehabilitation and Physical Medicine, Université Paris-Saclay, Assistance Publique-Hôpitaux de Paris (AP-HP), Raymond Poincaré Academic Hospital, Garches, France. Department of Rehabilitation and Physical Medicine, Université Paris-Saclay, Assistance Publique-Hôpitaux de Paris (AP-HP), Raymond Poincaré Academic Hospital, Garches, France. GRC 001, GREEN Groupe de Recherche Clinique en Neuro-Urologie, Sorbonne Université, Assistance Publique-Hôpitaux de Paris (AP-HP), Tenon Academic Hospital, Paris, France. Department of Urology, Sorbonne Université, Assistance Publique-Hôpitaux de Paris (AP-HP), Tenon Academic Hospital, Paris, France. Department of Urology, University of Lille, Claude Huriez Hospital, Lille University Hospital, Lille, France/Inserm UMR-S1172 LilNCog, Lille Neuroscience and Cognition, University of Lille, CHU Lille, Lille, France.
 Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Aging, Health Futures Institute, Murdoch University, Murdoch, Australia. Discipline of Exercise Science, Murdoch University, Murdoch, Australia. Perron Institute for Neurological and Translational Science, Nedlands, Australia. Discipline of Psychology, Murdoch University, Murdoch, Australia. Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
 Institute of Neuroanatomy, Medical Faculty, University of Bonn, Bonn, Germany. Clinic for Neurology, Klinikum St. Marien Amberg, Amberg, Germany. Institute of Neuroanatomy, Medical Faculty, University of Bonn, Bonn, Germany.
 Hurstwood Park Neurological Centre, Haywards Heath, UK/Clinical Imaging Sciences Centre, Brighton and Sussex Medical School, Brighton, UK. Hurstwood Park Neurological Centre, Haywards Heath, UK. Sussex Community NHS Foundation Trust, Brighton, UK. Hurstwood Park Neurological Centre, Haywards Heath, UK. Hurstwood Park Neurological Centre, Haywards Heath, UK. Hurstwood Park Neurological Centre, Haywards Heath, UK/Department of Global Health and Infection, Brighton and Sussex Medical School, Brighton, UK. Hurstwood Park Neurological Centre, Haywards Heath, UK. Clinical Imaging Sciences Centre, Brighton and Sussex Medical School, Brighton, UK/Department of Nuclear Medicine, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK. Department of Brain Sciences, Imperial College London, London, UK. Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Hurstwood Park Neurological Centre, Haywards Heath, UK/Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
 Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neuroradiology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria.
 Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China. Electronic address: wqlu@bio.ecnu.edu.cn. Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China. Electronic address: huangjin@ecust.edu.cn.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT 06112, USA; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT 06473, USA; Department of Medical Sciences, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT 06473, USA; Department of Neurology, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA. Electronic address: elizabeth.gromisch@trinityhealthofne.org. Neuroscience Program, Trinity College, 300 Summit Street, Hartford, CT 06106, USA; Department of Psychology, Trinity College, 300 Summit Street, Hartford, CT 06106, USA. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, 490 Blue Hills Avenue, Hartford, CT 06112, USA; Department of Rehabilitative Medicine, Frank H. Netter MD School of Medicine at Quinnipiac University, 370 Bassett Road, North Haven, CT 06473, USA. Multiple Sclerosis Center of Excellence West, Veterans Affairs, 1660 South Columbian Way, Seattle, WA 98108, USA; Rehabilitation Care Service, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA; Department of Rehabilitation Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA; Department of Epidemiology, University of Washington, 325 Ninth Avenue, Seattle, WA, 98104, USA. Multiple Sclerosis Center of Excellence West, Veterans Affairs, 1660 South Columbian Way, Seattle, WA 98108, USA; Rehabilitation Care Service, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA; Department of Rehabilitation Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA.
 Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA, Amsterdam, The Netherlands. Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands; Department of Neurology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Department of Viroscience, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA, Amsterdam, The Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA, Amsterdam, The Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA, Amsterdam, The Netherlands; Department of Experimental Immunology, Amsterdam Institute for Infection and Immunity, Amsterdam University Medical Centers, 1007 MB, Amsterdam, The Netherlands. Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands; Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA, Amsterdam, The Netherlands; Department of Neurology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Department of Immunology, MS Center ErasMS, Erasmus MC, University Medical Center Rotterdam, 3015 CN, Rotterdam, The Netherlands. Electronic address: m.vanluijn@erasmusmc.nl.
 Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany. Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany. Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany. Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany. Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany. Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany. Department of Neurology, Maria Hilf Clinics, Mönchengladbach, Germany. Department of Neurology, Medical Faculty of the Heinrich-Heine University, Düsseldorf, Germany.
 Department of Computer Engineering, Bilkent University, Ankara, Turkey. Research Institute for Health Sciences and Technologies (SABITA), Istanbul Medipol University, Istanbul, Turkey. Graduate School of Health Sciences, Department of Neuroscience, Istanbul Medipol University, Istanbul, Turkey. Goztepe Prof. Dr. Suleyman Yalcin City Hospital, Istanbul, Turkey. Research Institute for Health Sciences and Technologies (SABITA), Istanbul Medipol University, Istanbul, Turkey. Department of Medical Biology, School of Medicine, Nisantasi University, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Istanbul Medipol University, Istanbul, Turkey. Wellcome Sanger Institute, Hinxton, United Kingdom. Research Institute for Health Sciences and Technologies (SABITA), Istanbul Medipol University, Istanbul, Turkey. Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States. Department of Computer Engineering, Bilkent University, Ankara, Turkey.
 Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. University of Wisconsin-Madison, School of Medicine and Public Health, Electron Microscope Facility, USA. Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA; Present address: Department of Biomedical Sciences, College of Veterinary Medicine, University of Georgia, 501 DW Brooks Drive, Athens, GA 30602, USA.. Electronic address: jayshree.samanta@uga.edu.
 Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Biomedical Imaging, Genentech Inc., South San Francisco, California, USA. Department of Pathology, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Pathology, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA. Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA. Department of Neuroscience, Genentech Inc., South San Francisco, California, USA.
 Biochemistry Department, Clínica Universidad de Navarra, Spain; Department of Biochemistry and Molecular Biology. Faculty of Medicine. University of Malaga, Spain. Electronic address: jmarotogarc@unav.es. Department of Biochemistry and Molecular Biology. Faculty of Medicine. University of Malaga, Spain; Laboratory Medicine, Hospital Clínico Universitario Virgen de la Arrixaca, IMIB-ARRIXACA, Murcia, Spain. Neurology Department, Hospital Universitario Virgen de la Victoria, Malaga, Spain. Neurology Department, Hospital Universitario Virgen de la Victoria, Malaga, Spain. Biochemistry Department, Clínica Universidad de Navarra, Spain. Biochemistry Department, Clínica Universidad de Navarra, Spain. Clinical Analysis Service, Hospital Universitario Virgen de la Victoria, Malaga, Spain; The Biomedical Research Institute of Malaga (IBIMA), Malaga, Spain. Department of Biochemistry and Molecular Biology. Faculty of Medicine. University of Malaga, Spain; Clinical Analysis Service, Hospital Universitario Virgen de la Victoria, Malaga, Spain; The Biomedical Research Institute of Malaga (IBIMA), Malaga, Spain.
 Department of Physiology and Pharmacology, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran. Department of Physiology and Pharmacology, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran. Department of Physiology and Pharmacology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. The Health of Plant and Livestock Products Research Center, Mazandaran University of Medical Sciences, Sari, Iran. Department of Physiology and Pharmacology, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran. Department of Pharmacology and Toxicology, University of Toronto, 27 King's College Circle, Toronto, ON, M5S 3H7, Canada. Institute for Mental Health Policy Research, Centre for Addiction and Mental Health, Toronto, ON, M6J 1H4, Canada. Campbell Family Mental Health Research Institute, Toronto, ON, M5T 1R8, Canada. Research Center of Physiology, Department of Pharmacology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. hoomanbozorgi100@gmail.com.
 Department of Soil Science, Islamic Azad University, Isfahan (Khorasgan) Branch, Jei Street , Isfahan, 81551-39998, Iran. Department of Soil Science, Islamic Azad University, Isfahan (Khorasgan) Branch, Jei Street , Isfahan, 81551-39998, Iran. nhonarjoo@khuisf.ac.ir. inter 3 - Institute Fur Resource Management, Berlin, Germany. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, 81744, Iran.
 Infectious Disease Clinic, Policlinico San Martino IRCCS, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Infectious Disease Clinic, Policlinico San Martino IRCCS, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neurology, Ospedale Policlinico San Martino IRCCS, Genoa, Italy. Infectious Disease Clinic, Policlinico San Martino IRCCS, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neurology, Ospedale Policlinico San Martino IRCCS, Genoa, Italy. Department of Health Science (DISSAL), Infectious Diseases Unit, University of Genoa, Italy. Infectious Disease Clinic, Policlinico San Martino IRCCS, Genoa, Italy. Department of Health Science (DISSAL), Infectious Diseases Unit, University of Genoa, Italy.
 Department of Physical Medicine and Rehabilitation, University of Saskatchewan, Saskatoon, Canada. Department of Physical Medicine and Rehabilitation, University of Saskatchewan, Saskatoon, Canada. School of Rehabilitation Science, University of Saskatchewan, Saskatoon, Canada. School of Health and Life Sciences, Glasgow Caledonian University, Glasgow, UK.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
 ETHICS (EA7446), Lille Catholic University, FLSH, Lille, France. UMR 9193-SCALab-Sciences Cognitives et Sciences Affectives, CNRS, University of Lille, Lille, France. ETHICS (EA7446), Lille Catholic University, FLSH, Lille, France. ETHICS (EA7446), Lille Catholic University, FLSH, Lille, France; Neurology Department, Groupement des hôpitaux de l'institut catholique de Lille (GHICL), Lille, France.
 Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria; Center for Biomarker Research in Medicine, Stiftingtalstrasse 5, 8010 Graz, Austria. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria; Center for Biomarker Research in Medicine, Stiftingtalstrasse 5, 8010 Graz, Austria. Department of Neurology, Medical University of Graz, Auenbruggerplatz 22, 8036 Graz, Austria. Department of Neurology, Medical University of Graz, Auenbruggerplatz 22, 8036 Graz, Austria. Department of Neurology, Medical University of Graz, Auenbruggerplatz 22, 8036 Graz, Austria. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria; Center for Biomarker Research in Medicine, Stiftingtalstrasse 5, 8010 Graz, Austria. Department of Neurology, Medical University of Graz, Auenbruggerplatz 22, 8036 Graz, Austria; Department of Neurology, Hospital Murtal, Gaaler Strasse 10, 8720 Knittelfeld, Austria. Electronic address: thomas.seifert-held@kages.at.
 Department of Neurological Sciences, Rush University Medical Center, Chicago, IL. Department of Neurological Sciences, Rush University Medical Center, Chicago, IL. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL. Department of Neurological Sciences, Rush University Medical Center, Chicago, IL. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL. Department of Neurological Sciences, Rush University Medical Center, Chicago, IL. Department of Neurological Sciences, Rush University Medical Center, Chicago, IL. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL.
 College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. College of Computer Science and Information Technology, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, Dammam 31441, Saudi Arabia. Department of Computer Science, Kettering University, Flint, MI 48504, USA.
 Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Biology and Genetics, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Neurology, Klinik fur Neurologie, DRK Kliniken Berlin Kopenick, Berlin 12559, Germany. Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Psychiatry and Psychotherapy, School of Medicine, Technical University of Munich, Munich, Germany. School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Biology and Genetics, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Clinical Trials Unit, Special Unit for Biomedical Research and Education, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
 Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Division of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, Poznan, Poland. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Center for Brain Research, Medical University of Vienna, Wien, Austria. Department of Neurosurgery, Medical College of Wisconsin, Milwaukee, Wisconsin, USA. Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA.
 Department of Clinical Neurosciences, University of Calgary, Canada; Department of Community Health Sciences, University of Calgary, Canada. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, USA. Department of Neurology, Rijnstate Hospital, Arnhem, The Netherlands. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, USA. Department of Medicine, Neurology service, Hôpital Maisonneuve-Rosemont, Montreal, Canada; Département de neurosciences, Faculté de médecine, Université de Montréal, Montreal, Canada. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, USA.
 Department of Rehabilitation Medicine, University of Washington School of Medicine. Department of Physical Medicine and Rehabilitation, University of Michigan. Department of Physical Medicine and Rehabilitation, University of Michigan. Department of Clinical Psychology, Seattle Pacific University. Department of Rehabilitation Medicine, University of Washington School of Medicine. Department of Rehabilitation Medicine, University of Washington School of Medicine.
 Laboratory of Biomedical Signal Interpretation and Computational Simulation (BSICoS), University of Zaragoza, 50018 Zaragoza, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28006 Barcelona, Spain. Laboratory of Biomedical Signal Interpretation and Computational Simulation (BSICoS), University of Zaragoza, 50018 Zaragoza, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28006 Barcelona, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28006 Barcelona, Spain. Department of Microelectronics and Electronic Systems, Autonomous University of Barcelona, 08193 Bellaterra, Spain. Department of Medicine and Surgery, University Vita-Salute and Hospital San Raffaele, 20132 Milan, Italy. Department of Medicine and Surgery, University Vita-Salute and Hospital San Raffaele, 20132 Milan, Italy. Department of Medicine and Surgery, University Vita-Salute and Hospital San Raffaele, 20132 Milan, Italy. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital Rigshospitalet, 2100 Copenhagen, Denmark. Multiple Sclerosis Center of Catalonia (CEMCAT), Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, 08035 Barcelona, Spain. Multiple Sclerosis Center of Catalonia (CEMCAT), Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, 08035 Barcelona, Spain. Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 8AF, UK. Janssen Research and Development, LLC, Titusville, NJ 08560, USA. Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 8AF, UK. Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 8AF, UK. Institute of Health Informatics, University College London, London NW1 2DA, UK. Davos Alzheimer's Collaborative, Wayne, PA 19087, USA. Department of Medicine and Surgery, University Vita-Salute and Hospital San Raffaele, 20132 Milan, Italy. Department of Medicine and Surgery, University Vita-Salute and Hospital San Raffaele, 20132 Milan, Italy. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital Rigshospitalet, 2100 Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital Rigshospitalet, 2100 Copenhagen, Denmark. Multiple Sclerosis Center of Catalonia (CEMCAT), Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, 08035 Barcelona, Spain. Laboratory of Biomedical Signal Interpretation and Computational Simulation (BSICoS), University of Zaragoza, 50018 Zaragoza, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28006 Barcelona, Spain. Department of Medicine and Surgery, University Vita-Salute and Hospital San Raffaele, 20132 Milan, Italy. Casa di Cura del Policlinico, 20144 Milan, Italy.
 National Center for Applied Mathematics in Hunan, Xiangtan University, Hunan, China. Key Laboratory of Intelligent Computing and Information Processing of Ministry of Education, Xiangtan University, Hunan, China. National Center for Applied Mathematics in Hunan, Xiangtan University, Hunan, China. Key Laboratory of Intelligent Computing and Information Processing of Ministry of Education, Xiangtan University, Hunan, China.
 Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Department of Pathology and Biomedical Science, University of Otago Christchurch, Christchurch, New Zealand. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Histology Core, The Centre for Phenogenomics, Toronto, ON, Canada. Histology Core, The Centre for Phenogenomics, Toronto, ON, Canada. UHN Bioinformatics and HPC Core, Toronto, ON, Canada. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Department of Immunobiology, School of Medicine, Yale University, New Haven, CT, 06520, USA. Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, 06520, USA. Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. tmak@uhnres.utoronto.ca. Departments of Immunology and Medical Biophysics, University of Toronto, Toronto, ON, Canada. tmak@uhnres.utoronto.ca. Department of Pathology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. tmak@uhnres.utoronto.ca. Centre for Oncology and Immunology, Hong Kong Science Park, Hong Kong SAR, China. tmak@uhnres.utoronto.ca.
 Department of Ophthalmology, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping District, Shenyang, 110001, People's Republic of China. Department of Neurology, People's Hospital, China Medical University, 33 Wenyi Road, Shenhe District, Shenyang, 110016, People's Republic of China. Department of Ophthalmology, The First Hospital of China Medical University, 155 Nanjingbei Street, Heping District, Shenyang, 110001, People's Republic of China. zhangruijun196502@163.com.
 Department of Medicine, Division of Neurology and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, UBC Hospital, Vancouver, BC, Canada. Department of Medicine, Division of Neurology and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, UBC Hospital, Vancouver, BC, Canada. Department of Medicine, Division of Neurology and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, UBC Hospital, Vancouver, BC, Canada. Department of Medicine, Division of Neurology and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, UBC Hospital, Vancouver, BC, Canada. UNICAEN, CHU de Caen, INSERM U1086 ANTICIPE, Pôle de Recherche, Normandie University, Caen, France. EHESP Rennes, Sorbonne Paris Cité, Rennes, France; CIC-P 1414, CHU Rennes, West Neuroscience Network of Excellence (WENNE), Rennes, France. UNICAEN, CHU de Caen Normandie Department of Neurology, MS Expert Center, Normandie University, Caen, France; Réseau Bas-Normand Pour la Prise en Charge de la SEP, Caen, France. College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK, Canada. Nova Scotia Health Authority and the Departments of Psychiatry, Psychology and Neuroscience, and Medicine, Dalhousie University, Halifax, NS, Canada. Departments of Internal Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Medicine, Division of Neurology and the Djavad Mowafaghian Centre for Brain Health, University of British Columbia, UBC Hospital, Vancouver, BC, Canada.
 Department of Neurology, Centro Hospitalar Universitário de São João, Porto, Portugal. Electronic address: franciscaibarrosferreira@gmail.com. Department of Neurology, Centro Hospitalar Universitário de São João, Porto, Portugal; Department of Clinical Neurosciences and Mental Health, Faculdade de Medicina da Universidade do Porto, Porto, Portugal. Department of Neurology, Centro Hospitalar Universitário de São João, Porto, Portugal; Department of Clinical Neurosciences and Mental Health, Faculdade de Medicina da Universidade do Porto, Porto, Portugal. Department of Neurology, Centro Hospitalar Universitário de São João, Porto, Portugal; Department of Clinical Neurosciences and Mental Health, Faculdade de Medicina da Universidade do Porto, Porto, Portugal.
 From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. From the Department of Neurology (E.S.V., C.H., E.S.S., S.S., E.M.M., P.A.C., K.C.F.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Internal Medicine (C.N.B.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Neurology (F.L.), Icahn School of Medicine at Mount Sinai, New York, NY; Department of Neurology (J.S.W.), McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth); Department of Biostatistics (G.R.C.), University of Alabama at Birmingham; College of Pharmacy (K.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Medical Epidemiology and Biostatistics (K.K.), Karolinska Institute, Solna, Sweden; Department of Neurology (A.S.), University of Texas Southwestern, Dallas; and Department of Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. fitzgerald@jhmi.edu.
 Department of Clinical Microbiology, Umeå University, Umeå, Sweden. Department of Clinical Microbiology, Umeå University, Umeå, Sweden. Department of Clinical Microbiology, Umeå University, Umeå, Sweden. Department of Clinical Microbiology, Umeå University, Umeå, Sweden. Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå, Sweden. Wallenberg Centre for Molecular Medicine (WCMM), Umeå University, Umeå, Sweden. Department of Clinical Microbiology, Umeå University, Umeå, Sweden. Department of Clinical Sciences, Neurosciences, Umeå University, Umeå, Sweden. Department of Clinical Microbiology, Umeå University, Umeå, Sweden.
 School of Medicine, Western Sydney University, Penrith, NSW, Australia. Peter Duncan Neuroscience Research Unit, St Vincent's Centre for Applied Medical Research, Darlinghurst, Sydney, 2010, Australia. Charles Perkins Centre, School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW, 2006, Australia. School of Biomedical Sciences, UNSW Sydney, Sydney, NSW, 2052, Australia. School of Medicine, Western Sydney University, Penrith, NSW, Australia. Peter Duncan Neuroscience Research Unit, St Vincent's Centre for Applied Medical Research, Darlinghurst, Sydney, 2010, Australia. bruce.brew@svha.org.au. School of Biomedical Sciences, UNSW Sydney, Sydney, NSW, 2052, Australia. bruce.brew@svha.org.au. Department of Neurology, St Vincent's Hospital, Darlinghurst, 2010, Australia. bruce.brew@svha.org.au.
 Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Systems Biology and Computer Science Program, Department of Neurology, Ann Romney Center for Neurological Diseases, Brigham and Women's Hospital, Boston, Massachusetts, USA. Harvard Medical School, Boston, Massachusetts, USA. Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. Departamento de Bioquímica, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Departamento de Bioquímica, Hospital Universitari Vall D'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Genomic Systems, Valencia, Spain. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 Department of Oncology, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, China. Department of Pathophysiology, College of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, China. Department of Nuclear Medicine, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China. Medical Research Institute, Southwest University, Chongqing, China. Department of Dermatology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China. Department of Pathophysiology, College of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, China. Department of Oncology, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, China. Department of Pathophysiology, College of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, China.
 Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Suzi.Claflin@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Julie.Campbell@utas.edu.au. Curtin University, Perth, Australia. New Zealand Brain Research Institute, Christchurch, New Zealand. CORe The University of Melbourne, Melbourne, Australia. Department of Neurology, The Royal Melbourne Hospital, Melbourne, Australia. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Neuroepidemiology Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. Department of Neuroscience, Monash University, Melbourne, Australia. Perron Institute, Nedlands, Australia. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Centre for Health Policy, School of Population and Global Health, The University of Melbourne, Melbourne, Australia. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Menzies Institute for Medical Research, University of Tasmania, Medical Science Precinct, 17 Liverpool Street, Hobart, TAS, 7000, Australia. Bruce.Taylor@utas.edu.au.
 Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China; School of Medicine, South China University of Technology, Guangzhou 510006, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; School of Medicine, South China University of Technology, Guangzhou 510006, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China. Department of Paediatrics, Zhujiang Hospital of Southern Medical University, Guangzhou, China. Faculty of Synthetic Biology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China; Cord Blood Bank, Guangzhou Institute of Eugenics and Perinatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China; State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong SAR, China. David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; Sepulveda Ambulatory Care Center, Veterans Affairs Greater Los Angeles Healthcare System, North Hills, CA, USA. Electronic address: Felix.Leung@va.gov. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China; School of Medicine, South China University of Technology, Guangzhou 510006, China; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China. Electronic address: shaweihong@gdph.org.cn. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China; The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China; School of Medicine, South China University of Technology, Guangzhou 510006, China; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou 510080, China. Electronic address: chenhao@gdph.org.cn.
 Centre for Research in Neuroscience and BRaIN Program, Research Institute of the McGill University Health Centre (RI-MUHC), Livingston Hall, Room L7-210, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, QC, H2X 0A9, Canada. Department of Neuroscience, Faculty of Medicine, Université de Montréal, Montreal, Canada. Centre for Research in Neuroscience and BRaIN Program, Research Institute of the McGill University Health Centre (RI-MUHC), Livingston Hall, Room L7-210, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada. Centre for Research in Neuroscience and BRaIN Program, Research Institute of the McGill University Health Centre (RI-MUHC), Livingston Hall, Room L7-210, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada. Research Unit Analytical BioGeoChemistry, Helmholz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. Comprehensive Cancer Center Mainfranken, University Hospital Würzburg, 97080, Würzburg, Germany. Centre for Research in Neuroscience and BRaIN Program, Research Institute of the McGill University Health Centre (RI-MUHC), Livingston Hall, Room L7-210, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, QC, H2X 0A9, Canada. Department of Neuroscience, Faculty of Medicine, Université de Montréal, Montreal, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, QC, H2X 0A9, Canada. Department of Neuroscience, Faculty of Medicine, Université de Montréal, Montreal, Canada. Centre for Research in Neuroscience and BRaIN Program, Research Institute of the McGill University Health Centre (RI-MUHC), Livingston Hall, Room L7-210, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada. sam.david@mcgill.ca.
 Adelphi Values, Adelphi Mill, Grimshaw Lane, Bollington, SK10 5JB, Cheshire, UK. sophi.tatlock@adelphivalues.com. Adelphi Values, Adelphi Mill, Grimshaw Lane, Bollington, SK10 5JB, Cheshire, UK. Adelphi Values, Adelphi Mill, Grimshaw Lane, Bollington, SK10 5JB, Cheshire, UK. Adelphi Values, Adelphi Mill, Grimshaw Lane, Bollington, SK10 5JB, Cheshire, UK. Adelphi Values, Adelphi Mill, Grimshaw Lane, Bollington, SK10 5JB, Cheshire, UK. Novartis Pharma AG, 4002, Basel, Switzerland. Novartis Pharma AG, 4002, Basel, Switzerland. Novartis Pharma AG, 4002, Basel, Switzerland. University of East Anglia, Norwich Research Park, Norwich, NR4 7TJ, Norfolk, UK.
 Federal State Budgetary Educational Institution of Higher Education "South-Ural State Medical University" of the Ministry of Healthcare of the Russian Federation, Petersburg, Russian Federation. Federal State Budgetary Educational Institution of Higher Education "South-Ural State Medical University" of the Ministry of Healthcare of the Russian Federation, Petersburg, Russian Federation. Federal State Budgetary Educational Institution of Higher Education "South-Ural State Medical University" of the Ministry of Healthcare of the Russian Federation, Petersburg, Russian Federation. Multiple Sclerosis and Demyelinating Diseases Center, FSBIS N P Bechtereva Institute of the Human Brain of the Russian Academy of Sciences: FGBUN Institut Mozga Celoveka Im N P Behterevoj Rossijskoj Akademii Nauk, Petersburg, Russian Federation. eldementyeva@gmail.com. Federal State Budgetary Educational Institution of Higher Education "South-Ural State Medical University" of the Ministry of Healthcare of the Russian Federation, Petersburg, Russian Federation.
 Section of Pathology, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, 95123 Catania, Italy. Laboratory of Neuro-Biomechanics, Section of Physiology, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, 95123 Catania, Italy. Laboratory of Neuro-Biomechanics, Section of Physiology, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, 95123 Catania, Italy. Section of Pathology, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, 95123 Catania, Italy.
 Division of Pediatric Neurology, Department of Neurology, University of Virginia, Charlottesville, VA, USA. Department of Pathology and Immunology, Washington University in St Louis, St Louis, MO, USA; Brain and Mind Centre, School of Medical Sciences, University of Sydney, Camperdown, NSW, Australia.
 Department of Neurology, Albert Szent-Györgyi Health Centre, University of Szeged, Semmelweis u.6, Szeged, 6725, Hungary. rajda.cecilia@med.u-szeged.hu. Department of Neurology, Jahn Ferenc Teaching Hospital, Köves u. 1, Budapest, 1204, Hungary. Department of Neurology, Szent Borbála Hospital, Dózsa György u. 77, Tatabánya, 2800, Hungary. Department of Neurology, Jahn Ferenc Teaching Hospital, Köves u. 1, Budapest, 1204, Hungary. Department of Neurology, Faculty of Medicine, Semmelweis University, Balassa u. 6, Budapest, 1083, Hungary. Department of Neurology, Uzsoki Hospital, Uzsoki u. 29-41, Budapest, 1145, Hungary. Department of Neurology, Medical School, University of Pécs, Rét u. 2, Pécs, 7623, Hungary. Petz Aladár Department of Neurology, County Teaching Hospital, Vasvári Pál u. 2-4, Győr, 9024, Hungary. Department of Neurology, Faculty of Medicine, Semmelweis University, Balassa u. 6, Budapest, 1083, Hungary. Department of Neurology, Bács-Kiskun County Teaching Hospital, Kecskemét, Nyíri u. 38, Kecskemét, 6000, Hungary. Department of Neurology, Flór Ferenc Hospital, Semmelweis tér 1, Kistarcsa, 2143, Hungary. Department of Neurology, Medical School, University of Pécs, Rét u. 2, Pécs, 7623, Hungary. Department of Neurology, Csolnoky Ferenc Hospital, Kórház u. 1, Veszprém, 8200, Hungary. Department of Neurology, Markhot Ferenc Teaching Hospital, Knézich K. u. 1, Eger, 3300, Hungary. Department of Neurology, Kaposi Mór Teaching Hospital, Tallián Gyula u 20-32, Kaposvár, 7400, Hungary. Department of Neurology, Odense University Hospital, Institute of Clinical Research, University of Southern Denmark, Winslows vej 4, Odense, 5000, Denmark. Department of Neurology, Faculty of Medicine, University of Debrecen, Móricz Zs. Krt. 22, Debrecen, 4032, Hungary.
 Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, UK. Center for Medical Imaging Computing, Medical Physics and Biomedical Engineering, UCL, London, UK. Universitat Oberta de Catalunya, Barcelona, Spain. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, UK. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, UK. NMO Clinical Service at the Walton Centre, Liverpool, UK. Department of Neurology, Cleveland Clinic, AbuDhabi, UAE. Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK. Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitaetsmedizin Berlin, Berlin, Germany. Hoffmann LaRoche, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Departamento de Radiologia e Oncologia, Universidade de São Paulo, Faculdade de Medicina, São Paulo SP, Brazil. Departamento de Neurologia, Universidade de São Paulo, Faculdade de Medicina, São Paulo SP, Brazil. Faculdade de Medicina, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre RS, Brazil. Division of Neuroscience, Neuroimaging Research Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Division of Neuroscience, Neuroimaging Research Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Division of Neuroscience, Neuroimaging Research Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Department of Neurosciences, S. Camillo-Forlanini Hospital, Rome, Italy. Department of Neurosciences, S. Camillo-Forlanini Hospital, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Neuroimmunology Unit, IRCSS Fondazione Santa Lucia, Rome, Italy. Department NEUROFARBA, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Neurology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, University Medicine of Greifswald, Greifswald, Germany. Center of Neuroimmunology, Service of Neurology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Barcelona, Spain. Center of Neuroimmunology, Service of Neurology, Laboratory of Advanced Imaging in Neuroimmunological Diseases, Hospital Clínic of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Barcelona, Spain. St. Josef Hospital, Institute of Neuroradiology, Ruhr University Bochum, Bochum, Germany. St. Josef Hospital, Institute of Neuroradiology, Ruhr University Bochum, Bochum, Germany. St. Josef Hospital, Institute of Neuroradiology, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital and Faculty of Medicine, University of Oslo, Oslo, Norway. Department of Neurology, University Hospital, Kantonsspital, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital, Kantonsspital, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. ICM, Pitié Salpêtrière Hospital, Sorbonne University, Paris Brain Institute, Paris, France. ICM, Pitié Salpêtrière Hospital, Sorbonne University, Paris Brain Institute, Paris, France. Epidemiology and Biostatistics, University of Genoa, Genoa, Italy. Epidemiology and Biostatistics, University of Genoa, Genoa, Italy. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, UK. Center for Medical Imaging Computing, Medical Physics and Biomedical Engineering, UCL, London, UK. Radiology and Nuclear Medicine, VU University Medical Centre, Amsterdam, The Netherlands. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, UK. National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, London, UK.
 Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Institute of Veterinary Pharmacology and Toxicology, University of Zürich-Vetsuisse, CH-8057 Zürich, Switzerland. GeNeuro Innovation, 69008 Lyon, France. Institute of Veterinary Pharmacology and Toxicology, University of Zürich-Vetsuisse, CH-8057 Zürich, Switzerland. Neuroscience Center Zurich, University of Zürich and ETH Zürich, CH-8057 Zürich, Switzerland. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Brain and Mind Center, University of Sydney, NSW 2050 Sydney, Australia. Department of Neurology, Palacky University Olomouc, 77146 Olomouc, Czech Republic. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. GeNeuro Innovation, 69008 Lyon, France. Institute of Veterinary Pharmacology and Toxicology, University of Zürich-Vetsuisse, CH-8057 Zürich, Switzerland. Neuroscience Center Zurich, University of Zürich and ETH Zürich, CH-8057 Zürich, Switzerland. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, University of Bern, CH-3010 Bern, Switzerland.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Nursing and Midwifery Department, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: shaygannejad@med.mui.ac.ir.
 From the Rehabilitation Research Center, Department of Physiotherapy, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran. From the Rehabilitation Research Center, Department of Physiotherapy, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran. Electronic address: noorizadeh.sh@iums.ac.ir. Rehabilitation Research Center, Department of Basic Sciences in Rehabilitation, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran. From the Rehabilitation Research Center, Department of Physiotherapy, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran.
 College of Science, Health, Engineering and Education, Murdoch University, Murdoch, Western Australia, Australia. Psychological Sciences, Australian College of Applied Professions, Perth, Western Australia, Australia. College of Science, Health, Engineering and Education, Murdoch University, Murdoch, Western Australia, Australia. School of Rehabilitation Therapy, Queen's University, Kingston, Ontario, Canada. Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Aging, Health Futures Institute, Murdoch University, Murdoch, Western Australia, Australia. Discipline of Exercise Science, Murdoch University, Murdoch, Western Australia, Australia. Perron Institute for Neurological and Translational Science, Nedlands, Western Australia, Australia.
 Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, Israel. Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel - alonkalr@tauex.tau.ac.il. Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, Israel. Sagol School of Neurosciences, Tel-Aviv University, Tel-Aviv, Israel.
 Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Health Sciences, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Cameco MS Neuroscience Research Centre, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. Department of Anatomy, Physiology and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
 Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, Magdeburg 39120, Germany. Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, Magdeburg 39120, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg 39106, Germany; German Center for Neurodegenerative Diseases (DZNE), Magdeburg 39120, Germany. Department of Neurology, Otto-von-Guericke-University Magdeburg, Leipziger Street 44, Magdeburg 39120, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg 39106, Germany. Electronic address: tino.zaehle@ovgu.de.
 Department of Occupational Therapy, New York University, New York, NY, USA/Kessler Foundation, West Orange, NJ, USA. The University of Texas Southwestern Medical Center, Dallas, TX, USA. Kessler Foundation, West Orange, NJ, USA/Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Rutgers University, Newark, NJ, USA.
 Laboratório de Neurociências Translacional, Instituto Biomédico, Universidade Federal do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Programa de pós-graduação em Medicina (Neurologia/Neurociências), Universidade Federal Fluminense, Rio de Janeiro, Brazil. Laboratório de Neurociências Translacional, Instituto Biomédico, Universidade Federal do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Departamento de Farmacologia e Psicobiologia, Instituto de Biologia Roberto Alcântara Gomes, Universidade Estadual do Rio de Janeiro, Rio de Janeiro, Brazil. Programa de Engenharia de Sistemas e Computação-COPPE, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Laboratório de Neurociências Translacional, Instituto Biomédico, Universidade Federal do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Programa de pós-graduação em Medicina (Neurologia/Neurociências), Universidade Federal Fluminense, Rio de Janeiro, Brazil. Laboratório de Neurociências Translacional, Instituto Biomédico, Universidade Federal do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. sonizavieiraalvesleon@gmail.com. Hospital Universitário Clementino Fraga Filho, Centro de Referência em Doenças Inflamatórias Desmielinizantes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. sonizavieiraalvesleon@gmail.com.
 Department of Neurosciences, Mental Health and Sensory Organs, Centre for Experimental Neurological Therapies (CENTERS), Sapienza University of Rome, Rome, Italy. Merck Serono S.p.A., An Affiliate of Merck KGaA, Rome, Italy. Department of Health Sciences, University of Genoa, Genoa, Italy. Merck Serono S.p.A., An Affiliate of Merck KGaA, Rome, Italy. Department of Neurosciences, Mental Health and Sensory Organs, Centre for Experimental Neurological Therapies (CENTERS), Sapienza University of Rome, Rome, Italy. Department of Neurosciences, Mental Health and Sensory Organs, Centre for Experimental Neurological Therapies (CENTERS), Sapienza University of Rome, Rome, Italy. Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Neurologico Mediterraneo Neuromed, Pozzilli, Italy. Department of Neurosciences, Mental Health and Sensory Organs, Centre for Experimental Neurological Therapies (CENTERS), Sapienza University of Rome, Rome, Italy. Neuroimmunology Unit, Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy.
 Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Vall d'Hebron University Hospital, Spain. Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Vall d'Hebron University Hospital, Spain. Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Vall d'Hebron University Hospital, Spain. Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Vall d'Hebron University Hospital, Spain. Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia, Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 The Wistar Institute, Philadelphia, PA, USA. The Wistar Institute, Philadelphia, PA, USA. lieberman@wistar.org.
 Lyon University, University Claude Bernard Lyon 1, F-69000, Lyon, France; Hospices Civils de Lyon, Neurology Department, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, F-69677, Bron, France; Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, INSERM 1028 and CNRS UMR 5292, F-69003, Lyon, France; EUGENE DEVIC EDMUS Foundation against Multiple Sclerosis, State-Approved Foundation, F-69677, Bron, France. Lyon University, University Claude Bernard Lyon 1, F-69000, Lyon, France; Hospices Civils de Lyon, Neurology Department, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, F-69677, Bron, France; Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, INSERM 1028 and CNRS UMR 5292, F-69003, Lyon, France; EUGENE DEVIC EDMUS Foundation against Multiple Sclerosis, State-Approved Foundation, F-69677, Bron, France. Hospices Civils de Lyon, Biological Ressource Center (BRIF N BB-0033-00046), F-69677, Bron, France. Lyon University, University Claude Bernard Lyon 1, Research on Healthcare Performance (RESHAPE), INSERM U1290, F-69000, Lyon, France; Hospices Civils de Lyon, Neurology Department, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), F-69677, Bron, France. Neurology Department, Rennes University Hospital, Rennes, France; Clinical Neuroscience Centre, CIC_P1414 INSERM, Rennes University Hospital, Rennes University, Rennes, France. Lille University Hospital, Inserm, Lille University, Biological Resource Center of CIC 1403 (BRIF N BB-0033-00030), F-59000, Lille, France. University of Montpellier, INM, INSERM, Department of Neurology, Montpellier University Hospital, Montpellier, France. Montpellier University, INM INSERM, Montpellier University Hospital IRMB (BRIF N BB-0033-00059), Montpellier, France. Department of Neurology, Nimes University Hospital, F-30029, Nimes, France; Institut de Génomique Fonctionnelle, UMR5203, INSERM 1191, Montpellier University, F-34094, Montpellier, France. Nantes University, Nantes University Hospital, Biological Resource Center (BRIF N BB-0033-00040), F-44000, Nantes, France. Department of Neurology, University Hospital of Strasbourg, Strasbourg, France; Center for Clinical Investigation, INSERM U1434, Strasbourg, France; Biopathology of Myelin, Neuroprotection and Therapeutic Strategy, INSERM U1119, Strasbourg, France; University Department of Pharmacology, Addictology, Toxicology and Therapeutic, Strasbourg University, Strasbourg, France. Amiens Picardie University Hospital, Research Department, Biobanque de Picardie (BRIF N BB-0033-00017), F-80000, Amiens, France. Nice Côte d'Azur University UR2CA-URRIS, Pasteur2 University Hospital, Neurology MS Clinic, Nice, France. MRI Center Lyon Sud Hospital, Hospices Civils de Lyon, Lyon, France; CREATIS - CNRS UMR 5220 & INSERM U1044, University Claude Bernard Lyon 1, Lyon, France. Strasbourg University Hospital, Hautepierre Hospital, Service des Maladies Inflammatoires du Système Nerveux - Neurology, Strasbourg, France. CIC 1433 Epidémiologie Clinique, Nancy University Hospital, Inserm and Lorraine University, Nancy, France. Department of Neurology, Dijon Bourgogne University Hospital, EA4184, F-21000, Dijon, France. Aix Marseille University, APHM, Timone Hospital, Pôle de Neurosciences Cliniques, Neurologie Department, F-13005, Marseille, France. Sorbonne University, UPMC Paris 06, Brain and Spine Institute, ICM, Hôpital de la Pitié Salpêtrière, Inserm UMR S 1127, CNRS UMR 7225, and Department of Neurology, AP-HP, Saint-Antoine Hospital, F-75000, Paris, France. Lyon University, University Claude Bernard Lyon 1, F-69000, Lyon, France; Hospices Civils de Lyon, Neurology Department, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, F-69677, Bron, France; Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, INSERM 1028 and CNRS UMR 5292, F-69003, Lyon, France; EUGENE DEVIC EDMUS Foundation against Multiple Sclerosis, State-Approved Foundation, F-69677, Bron, France. Lille University, Inserm U1172, Lille University Hospital, Lille, France. Nantes University Hospital, Neurology Department, CRC-SEP, Nantes University, INSERM, CIC 1413, Center for Research in Transplantation and Translational Immunology, UMR 1064, F-44000, Nantes, France. Electronic address: David.Laplaud@univ-nantes.fr.
 Faculty of Medicine, Division of Biomedical Sciences, Memorial University of Newfoundland, St. John's, NL A1B 3V6, Canada. Faculty of Medicine, Division of Biomedical Sciences, Memorial University of Newfoundland, St. John's, NL A1B 3V6, Canada. Faculty of Medicine, Division of Biomedical Sciences, Memorial University of Newfoundland, St. John's, NL A1B 3V6, Canada. Health Sciences Centre, Room HSC4364, 300 Prince Philip Drive, St. John's, NL A1B 3V6, Canada.
 Endocrinology Research Centre. Endocrinology Research Centre. Endocrinology Research Centre. I.M. Sechenov First Moscow State Medical University. Endocrinology Research Centre. Endocrinology Research Centre. Endocrinology Research Centre.
 Institute for Physiology, Medical Faculty, Otto-Von-Guericke-University, Leipziger Str. 44, 39120, Magdeburg, Germany. lessmann@med.ovgu.de. Center for Behavioral Brain Sciences, Magdeburg, Germany. lessmann@med.ovgu.de. Institute for Physiology, Medical Faculty, Otto-Von-Guericke-University, Leipziger Str. 44, 39120, Magdeburg, Germany. Institute of Neuro- and Sensory Physiology, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany. Institute for Physiology, Medical Faculty, Otto-Von-Guericke-University, Leipziger Str. 44, 39120, Magdeburg, Germany. Institute of Neuro- and Sensory Physiology, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany. Department of Neurology, Medical Faculty and University Hospital Düsseldorf, Duesseldorf, Germany. Institute of Neuro- and Sensory Physiology, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany. Kurt.Gottmann@uni-duesseldorf.de.
 Achucarro Basque Center for Neuroscience, 48940 Leioa, Spain. Department of Neurosciences, University of the Basque Country UPV/EHU, 48940 Leioa, Spain. Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), 28031 Madrid, Spain. Achucarro Basque Center for Neuroscience, 48940 Leioa, Spain. Department of Neurosciences, University of the Basque Country UPV/EHU, 48940 Leioa, Spain. Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), 28031 Madrid, Spain.
 From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. michael.levraut@gmail.com. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France. From the URRIS (M.L., C.L.-C., M.C., L.M., C.L.-F.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Service de Médecine Interne (M.L.), Hôpital l'Archet 1, Centre Hospitalier Universitaire de Nice; Service de Biostatistique-Bioinformatique (A.G.), Hospices Civils de Lyon; Service de Neurologie (A.G.), Sclérose en Plaques, Pathologies de La Myéline et Neuro-inflammation, Hôpital Neurologique Pierre-Wertheimer, Hospices Civils de Lyon, Bron; Service de Neurologie (M.C., S.B., C.L.-F.), Centre de Ressource et Compétence - Sclérose En Plaques, Hôpital Pasteur 2; ImmunoPredict (B.S.-P.), Unité Mixte de Recherche Clinique Côte d'Azur (UMR2CA); Laboratoire d'Immunologie (B.S.-P.), Hôpital l'Archet 1; and Service de Radiologie (L.M.), Hôpital Pasteur 2, Centre Hospitalier Universitaire de Nice, France.
 Department of Pharmacoeconomics and Pharmaceutical Management, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Non-Communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran; Department of Toxicology and Pharmacology, Faculty of Pharmacy, Kerman University of Medical Sciences, Kerman, Iran. Department of Health Management, Policy & Economics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran; Head of the National Institute of Health Research (NIHR), Tehran University of Medical Sciences, Tehran, Iran. MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Sina Hospital, Tehran University Medical Sciences, Tehran, Iran. Non-Communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran; Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Pharmacoeconomics and Pharmaceutical Management, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: fsoleymani@tums.ac.ir.
 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.. Electronic address: Anat.achiron@sheba.health.gov.il. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. School of Public Health, University of Haifa, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel. Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gan, Israel; Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
 Department of Neurology, HeinrichHeine University Düsseldorf, 40225 Duesseldorf, Germany. Department of Neurology, University Hospital Giessen and Marburg, Justus-Liebig-University Giessen, 35392 Giessen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology, HeinrichHeine University Düsseldorf, 40225 Duesseldorf, Germany. Department of Neurology, HeinrichHeine University Düsseldorf, 40225 Duesseldorf, Germany. Department of Neurology, HeinrichHeine University Düsseldorf, 40225 Duesseldorf, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany. Department of Neurology, HeinrichHeine University Düsseldorf, 40225 Duesseldorf, Germany. Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany. Center for Translational Neuro and Behavioral Sciences (C-TNBS), University Medicine Essen, 45127 Essen, Germany.
 Department of Bio-Sciences, Faculty of Sports Sciences, Razi University, Kermanshah, Iran. Department of Bio-Sciences, Faculty of Sports Sciences, Razi University, Kermanshah, Iran. Electronic address: a.parnw@razi.ac.ir. Medical Biology Research Center, Department of Anatomical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran.
 From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. jeannette.lechner-scott@health.nsw.gov.au. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. From the School of Medicine and Public Health (V.M., R.L., J.L.-S.), University of Newcastle, University Drive, Callaghan; Immune Health Program (V.M., A.X., J.L.-S.), Hunter Medical Research Institute; Department of Neurology (V.M., J.L.-S.), John Hunter Hospital, New Lambton Heights; School of Biomedical Sciences and Pharmacy (A.X.), University of Newcastle, University Drive, Callaghan, Australia; Department of Clinical Neuroscience (E.E., L.K., M.J.), Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Neuroscience (M.-P.C., S.S., H.B., V.J.), Central Clinical School, Monash University, Victoria; Division of Molecular Genetics (R.J.S.), Pathology North, John Hunter Hospital, New Lambton Heights; MSBase Foundation (H.B.), Melbourne, Australia; Institute of Clinical Medicine (S.B.), University of Oslo,; Department of Neurology (S.B.), Oslo University Hospital, Norway; Flinders University (M.S.), Adelaide; Menzies Institute for Medical Research (I.A.M., B.V.T.), University of Tasmania, Hobart; Florey Institute of Neuroscience and Mental Health (A.-L.P.), The University of Melbourne; Centre of Epidemiology and Biostatistics (A.-L.P.), School of Population and Global Health, University of Melbourne; Murdoch Children's Research Institute (A.-L.P.), Royal Children's Hospital, Melbourne; and Centre for Genomics and Personalized Health (R.L.), School of Biomedical Science, Queensland University of Technology, Kelvin Grove, Australia. jeannette.lechner-scott@health.nsw.gov.au.
 Department of Pathology, The Affiliated Hospital of Weifang Medical University, Weifang, 261053, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, 100069, China. State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China. Chinese Institute for Brain Research, Beijing, China. Department of Anesthesiology, The Affiliated Hospital of Weifang Medical University, Weifang, 261053, China. Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, 100069, China. liuguiyou1981@163.com. Chinese Institute for Brain Research, Beijing, China. liuguiyou1981@163.com. Key Laboratory of Cerebral Microcirculation in Universities of Shandong; Department of Neurology, Second Affiliated Hospital; Shandong First Medical University & Shandong Academy of Medical Sciences, Taian, 271000, Shandong, China. liuguiyou1981@163.com. Beijing Key Laboratory of Hypoxia Translational Medicine, National Engineering Laboratory of Internet Medical Diagnosis and Treatment Technology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. liuguiyou1981@163.com.
 Department of Biology, Faculty of Sciences, University of Zabol, Zabol, Iran. Department of Medical Biotechnology and Molecular Science, North Khorasan University of Medical Science, Bojnurd, Iran. Department of Biology, Faculty of Sciences, University of Zabol, Zabol, Iran. Institute of Neuroanatomy, RWTH University Hospital Aachen, 52074 Aachen, Germany. Department of Biology, Faculty of Sciences, University of Zabol, Zabol, Iran; Institute of Neuroanatomy, RWTH University Hospital Aachen, 52074 Aachen, Germany. Electronic address: nsanadgol@ukaachen.de. Institute of Anatomy, Department of Biomedicine, University of Basel, 4001 Basel, Switzerland.
 School of Health and Exercise Sciences, University of British Columbia, Kelowna, BC, Canada. International Collaboration on Repair Discoveries (ICORD), University of British Columbia, Vancouver, BC, Canada. Centre for Human Movement Sciences, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands. Centre for Human Movement Sciences, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands. Department of Community Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. George and Fay Yee Centre for Healthcare Innovation, University of Manitoba, Winnipeg, MB, Canada. School of Epidemiology and Public Health, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada. School of Health and Exercise Sciences, University of British Columbia, Kelowna, BC, Canada. Department of Community Health Sciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Strategic Clinical Networks™, Provincial Clinical Excellence, Alberta Health Services, Calgary, AB, Canada. School of Epidemiology and Public Health, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada. CanChild Centre for Childhood Disability Research, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. UBC Okanagan Library, University of British Columbia, Kelowna, BC, Canada. School of Health and Exercise Sciences, University of British Columbia, Kelowna, BC, Canada. International Collaboration on Repair Discoveries (ICORD), University of British Columbia, Vancouver, BC, Canada.
 From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. stephen.hauser@ucsf.edu. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland. From the UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (S.L.H.); Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics (A.B.-O.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; Institute of Neuropathology and Department of Neurology (M.S.W.), Universitätsmedizin Göttingen Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany; F. Hoffmann-La Roche Ltd (H. Kletzl, A.G., M.M., F. Model, F. Mercier, C.P., Q.W., H. Koendgen), Basel, Switzerland; NeuMatRx Ltd (T.S.), Bath, UK; and University Hospital Basel (L.K.), University of Basel, Switzerland.
 Institut für Biochemie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Institut für Biochemie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Institut für Biochemie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Institut für Biochemie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Institut für funktionelle und klinische Anatomie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Molecular Physiology, Center for Integrative Physiology and Molecular Medicine, University of Saarland, Homburg, Germany. Molecular Physiology, Center for Integrative Physiology and Molecular Medicine, University of Saarland, Homburg, Germany. Institut für Biochemie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
 Student Scientific Group, Department of Forensic Medicine, Medical University of Lublin, ul. Jaczewskiego 8b, 20-090 Lublin, Poland. Student Scientific Group, Department of Forensic Medicine, Medical University of Lublin, ul. Jaczewskiego 8b, 20-090 Lublin, Poland. Student Scientific Group, Department of Anatomy, Medical University of Lublin, ul. Jaczewskiego 4, 20-090 Lublin, Poland. Student Scientific Group, Department of Forensic Medicine, Medical University of Lublin, ul. Jaczewskiego 8b, 20-090 Lublin, Poland. Student Scientific Group, Department of Forensic Medicine, Medical University of Lublin, ul. Jaczewskiego 8b, 20-090 Lublin, Poland. Student Scientific Group, Department of Forensic Medicine, Medical University of Lublin, ul. Jaczewskiego 8b, 20-090 Lublin, Poland. Department of Analytical Chemistry, Medical University of Lublin, Chodźki 4A, 20-093 Lublin, Poland. Department of Forensic Medicine, Medical University of Lublin, Jaczewskiego 8b, 20-090, Lublin, Poland. Department of Forensic Medicine, Medical University of Lublin, Jaczewskiego 8b, 20-090, Lublin, Poland. I Department of Psychiatry, Psychotherapy and Early Intervention, Medical University of Lublin, 20-059 Lublin, Poland. Department of Anatomy, Medical University of Lublin, ul. Jaczewskiego 4, 20-090 Lublin, Poland.
 Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiotherapy, School of Rehabilitation Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiotherapy, School of Rehabilitation Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Rehabilitation Management, Rehabilitation Research Center, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran. Department of Physical Therapy, School of Paramedical Sciences, Mashhad University of Medical Sciences, Mashhad, Iran. Orthopedic Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiotherapy, School of Rehabilitation Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
 Scientific Research Area, Italian Multiple Sclerosis Foundation, Genova, Italy jessica.podda@aism.it. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genova, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genova, Italy. Department of Physiopathology, Experimental Medicine and Public Health, University of Siena, Siena, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genova, Italy. AISM Rehabilitation Service, Italian Multiple Sclerosis Society, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genova, Italy.
 Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. giuseppe.pontillo@unina.it. Department of Electrical Engineering and Information Technology, University "Federico II", Naples, Italy. giuseppe.pontillo@unina.it. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Institute of Biostructure and Bioimaging, National Research Council, Naples, Italy. Institute of Biostructure and Bioimaging, National Research Council, Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Multiple Sclerosis Centre, II Division of Neurology, Department of Clinical and Experimental Medicine, "Luigi Vanvitelli" University, Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. Institute of Nanotechnology, National Research Council, Lecce, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy.
 Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA/Vita-Salute San Raffaele University, Milan, Italy/Neuroimaging Research Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA/Division of Neurology, Department of Medicine, University of Alberta, Edmonton, AB, Canada. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA/Department of Ophthalmology, Mayo Clinic College of Medicine, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, Jacksonville, FL, USA. University of Sassari, Sassari, Italy. Department of Neuroinflammation, Queen Square Multiple Sclerosis Centre, University College London, Institute of Neurology, London, UK. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA/Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN, USA. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA/Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN, USA.
 From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. From the Neuroimmunology Research Laboratory (A.P.F., O.T., M.C., C.H., L.B., W.K., S.L., F.T., C.L., N.A., S.Z., A.P.), Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM); Department of Neurosciences (A.P.F., C.L., N.A., S.Z., A.P.), Faculty of Medicine, Université de Montréal; Multiple Sclerosis Clinic (C.L., A.P.), Division of Neurology, Centre Hospitalier de l'Université de Montréal (CHUM); Department of Human Genetics (J.R.), McGill University, Montréal; and McGill Genome Centre (Y.C.W., J.R.), Montréal, Québec, Canada. a.prat@umontreal.ca.
 The First Clinical Medical School, Henan University of Chinese Medicine, Zhengzhou, China. The First Clinical Medical School, Henan University of Chinese Medicine, Zhengzhou, China. Department of Neuroscience, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Department of Neuroscience, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Department of Neuroscience, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
 Department of Neuro-Urology and Andrology, Raymond-Poincaré Hospital, Assistance Publique-Hôpitaux de Paris, Garches, France. Functional Urology, CES University Clinic, Medellín, Colombia. Specialized Center in Urology, Oswaldo Cruz German Hospital, São Paulo, Brazil. Chief Urology Section, Atlantic Urology Medical Group, Long Beach, California, USA. Division of Urology, University of São Paulo, São Paulo, Brazil. Department of Urology, Pirogov Russian National Research Medical University, Moscow, Russia. Urology Division, Department of Surgery, Faculty of Medicine, Sherbrooke University Hospital Center, Sherbrooke, Quebec, Canada. Department of Neurourology, Careggi University Hospital, Florence, Italy. June Pharma Consulting, London, UK. R&D, Clinical Development Operations Department, Biostatistics and Sataistical Programing Group, Ipsen Innovation, Les Ulis, France. R&D, Clinical Development Operations Department, Biostatistics and Sataistical Programing Group, Ipsen Innovation, Les Ulis, France. Department of Urology, Atrium Health, Carolinas Medical Center, Charlotte, North Carolina, USA.
 Department of Biophysics, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey. arzuay78@yahoo.com. Department of Biophysics, Faculty of Medicine, Haliç University, Istanbul, 34060, Turkey. Department of Medical Genetics, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey. Department of Medical Genetics, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey. Department of Biophysics, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey. Department of Neurology, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey. Department of Biophysics, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey. Department of Biostatistics and Medical Informatics, Faculty of Medicine, Trakya University, Edirne, 22030, Turkey.
 Office of Data Science and Emerging Technologies, National Institute of Allergy and Infectious Diseases, Rockville, MD, USA. lakecm@nih.gov. Division of Allergy, Immunology and Transplantation, National Institute of Allergy and Infectious Diseases, Rockville, MD, USA.
 Department of Allied Health Professions, College of Health, Wellbeing and Life Sciences, Sheffield Hallam University, Sheffield, UK. Department of Allied Health Professions, College of Health, Wellbeing and Life Sciences, Sheffield Hallam University, Sheffield, UK. Department of Nursing and Midwifery, College of Health, Wellbeing and Life Sciences, Sheffield Hallam University, Sheffield, UK. Graduate School of Biomedical Engineering, University of New South Wales, Sydney, Australia. Academy of Sport and Physical Activity, College of Health, Wellbeing and Life Sciences, Sheffield Hallam University, Sheffield, UK.
 Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Network of Immunity in Infection, Malignancy, and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Isfahan, Iran. Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Research Committee of Multiple Sclerosis (IRCOMS), Isfahan Multiple Sclerosis Center, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Functional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran.
 From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. k.hellwig@klinikum-bochum.de. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group. From the Department of Neurology (K.H., S.T., S.H., A.I.C., R.G.), St. Josef-Hospital-Katholisches Klinikum Bochum, Ruhr University Bochum; Department of Medical Informatics (M.T., N.T.), Biometry and Epidemiology, Ruhr University Bochum, Germany; Department of Neurology (A.M.L.-G.), Los Angeles Medical Center, Southern California Permanente Medical Group.
 Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Department of Health Sciences and Technology, ETH Zurich, Zürich, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Department of Health Sciences and Technology, ETH Zurich, Zürich, Switzerland.
 Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, c/Monforte de Lemos, 3-5, 28029, Madrid, Spain. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, c/Monforte de Lemos, 3-5, 28029, Madrid, Spain. Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Rd, Belfast, BT9 7BL, Northern Ireland, UK. Departamento de Neurología, Hospital Universitario de Toledo, Av. del Río Guadiana, 45007, Toledo, Spain. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Departamento de Neurología, Hospital General Universitario Gregorio Marañón, Calle del Dr. Esquerdo 46, 28007, Madrid, Spain. Departamento de Neurología, Hospital General Universitario Gregorio Marañón, Calle del Dr. Esquerdo 46, 28007, Madrid, Spain. Servicio de Citometría de Flujo, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Departamento de Neurología, Hospital Universitario de Toledo, Av. del Río Guadiana, 45007, Toledo, Spain. Departamento de Neurología, Hospital Universitario de Toledo, Av. del Río Guadiana, 45007, Toledo, Spain. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, c/Monforte de Lemos, 3-5, 28029, Madrid, Spain. Departamento de Neurología, Hospital General Universitario Gregorio Marañón, Calle del Dr. Esquerdo 46, 28007, Madrid, Spain. Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Rd, Belfast, BT9 7BL, Northern Ireland, UK. Grupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, SESCAM, Finca "La Peraleda" s/n, 45071, Toledo, Spain. dclemente@sescam.jccm.es. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Carlos III Health Institute, c/Monforte de Lemos, 3-5, 28029, Madrid, Spain. dclemente@sescam.jccm.es.
 Department of Neurology, Medical University of Bialystok, M. Skłodowskiej-Curie 24A St., 15-276 Bialystok, Poland. Department of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland. Department of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland. Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland. Department of Neurology, Medical University of Bialystok, M. Skłodowskiej-Curie 24A St., 15-276 Bialystok, Poland. Department of Neurology, Medical University of Bialystok, M. Skłodowskiej-Curie 24A St., 15-276 Bialystok, Poland.
 Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran; Network of Immunity in Infection Malignancy and Autoimmunity (NIIMA), Universal Scientific, Education, and Research Network (USERN), Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran; Network of Immunity in Infection Malignancy and Autoimmunity (NIIMA), Universal Scientific, Education, and Research Network (USERN), Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Functional Neurosurgery Research Center, Shohada Tajrish Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran; Network of Immunity in Infection Malignancy and Autoimmunity (NIIMA), Universal Scientific, Education, and Research Network (USERN), Isfahan, Iran. Electronic address: nahad.sedaghat@gmail.com.
 Department of Biological Sciences, Boise State University, Boise, ID, 83725, USA. Department of Biological Sciences, Arizona State University, Tempe, AZ, 85281, USA. Department of Biological Sciences, Boise State University, Boise, ID, 83725, USA. Department of Biological Sciences, Boise State University, Boise, ID, 83725, USA. Electronic address: jochoareparaz@boisestate.edu.
 Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan Province, 412000, China. 1779342446@qq.com. Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan Province, 412000, China. Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan Province, 412000, China. Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan Province, 412000, China. Department of Neurology, Affiliated First Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan Province, 412000, China.
 Bristol Myers Squibb, Princeton, NJ, USA. Bristol Myers Squibb, Princeton, NJ, USA. Bristol Myers Squibb, Princeton, NJ, USA. Bristol Myers Squibb, Princeton, NJ, USA. Bristol Myers Squibb, Princeton, NJ, USA. Electronic address: Richard.Hargreaves@BMS.com.
 Laboratoire de Mathématiques Jean Leray, Université de Nantes, Nantes, France. UmanIT, Nantes, France. Laboratoire de Mathématiques Jean Leray, Université de Nantes, Nantes, France. UmanIT, Nantes, France. UmanIT, Nantes, France. CRTI-Inserm U1064, CIC, Service de Neurologie, CHU et Université de Nantes, Nantes, France. Centre de Recherche en Transplantation et Immunologie, UMR 1064, ATIP-Avenir, Université de Nantes, CHU de Nantes, INSERM, Nantes, France. CRTI-Inserm U1064, CIC, Service de Neurologie, CHU et Université de Nantes, Nantes, France. Laboratoire de Mathématiques Jean Leray, Université de Nantes, Nantes, France.
 Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan. Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. s-miyake@juntendo.ac.jp.
 Department of Clinical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava and University Hospital Martin, Martin, Slovak Republic. Department of Clinical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava and University Hospital Martin, Martin, Slovak Republic. Clinic of Neurology, Jessenius Faculty of Medicine, Comenius University in Bratislava and University Hospital Martin, Martin, Slovak Republic. Department of Clinical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava and University Hospital Martin, Martin, Slovak Republic. Biomedical Center Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovak Republic. Department of Immunology, Faculty of Medicine, Comenius University in Bratislava, Bratislava, Slovak Republic. Clinic of Neurology, Jessenius Faculty of Medicine, Comenius University in Bratislava and University Hospital Martin, Martin, Slovak Republic. Department of Medical Biochemistry and BioMed, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovak Republic.
 Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510000, China. CAS Key Laboratory for Biomedical Effects of Nanomaterials & Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing, 100190, China. CAS Key Laboratory for Biomedical Effects of Nanomaterials & Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing, 100190, China. School of Nanoscience and Engineering, University of Chinese Academy of Sciences, 100049, Beijing, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510000, China. CAS Key Laboratory for Biomedical Effects of Nanomaterials & Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing, 100190, China. School of Nanoscience and Engineering, University of Chinese Academy of Sciences, 100049, Beijing, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510000, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510000, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510000, China. CAS Key Laboratory for Biomedical Effects of Nanomaterials & Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing, 100190, China. School of Nanoscience and Engineering, University of Chinese Academy of Sciences, 100049, Beijing, China. CAS Key Laboratory for Biomedical Effects of Nanomaterials & Nanosafety, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing, 100190, China. School of Nanoscience and Engineering, University of Chinese Academy of Sciences, 100049, Beijing, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510000, China.
 Laboratoire des Biomolécules, Venins et Applications Théranostiques (LR20IPT01), Institut Pasteur de Tunis, Université de Tunis El Manar, Tunis, 1002, Tunisia. Electronic address: ines.bini@pasteur.tn. Laboratoire des Biomolécules, Venins et Applications Théranostiques (LR20IPT01), Institut Pasteur de Tunis, Université de Tunis El Manar, Tunis, 1002, Tunisia. Electronic address: neilinourelhouda1@gmail.com.
 Department of Pediatrics, Division of Pediatric Neurology, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA. Electronic address: ggombol@emory.edu. Department of Pediatrics, Division of Pediatric Neurology, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA.
 Department of Neurology, University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. yaprakunsal@gmail.com. Department of Neurology, University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. Department of Neurology, Private Emotplus Hospital, Izmir, Turkey.
 Faculty of Health Science, Research Centre for Health and Welfare Technology, Programme for Rehabilitation, VIA University College, Hedeager 2, Aarhus N 8200, Denmark. Electronic address: jobr@via.dk. Department of Public Health - Exercise Biology, Aarhus University, Dalgas Avenue 4, Aarhus 8000, Denmark. Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet, Stockholm, Sweden; Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden. Faculty of Health Science, Research Centre for Health and Welfare Technology, Programme for Rehabilitation, VIA University College, Hedeager 2, Aarhus N 8200, Denmark. Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet, Stockholm, Sweden; Rehab Station Stockholm, Research and Development Unit, Solna, Sweden. Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet, Stockholm, Sweden; Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden.
 Faculty of Sport Sciences, Department of Physical Education and Sport, University of Granada, Granada,Spain. Department of Physical Education and Sport, University of Granada, Granada,Spain. Department of Physical Education and Sport, University of Granada, Granada,Spain. Department of Physical Education and Sport, University of Granada, Granada,Spain.
 Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. AP-HP, Saint-Antoine Hospital, F-75012 Paris, France. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France. AP-HP, GH Pitié-Salpêtrière, F-75013 Paris, France. Bard College, 30 Campus Rd, Annandale-on-Hudson, NY 12504, USA. Sorbonne Université, Inserm, CNRS, ICM-GH Pitié-Salpêtrière, F-75013 Paris, France.
 Division of Physiotherapy, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden. Aleris Rehab Station Stockholm, Research and Development Unit, Stockholm, Sweden. Division of Physiotherapy, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden. Stockholm Sjukhem Foundation, Research and Development Unit, Stockholm, Sweden. Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Medical Psychology, Karolinska University Hospital, Stockholm, Sweden. Division of Physiotherapy, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden.
 Department of Agriculture, Food, Natural Resources and Engineering (DAFNE), University of Foggia, 71122 Foggia, Italy. Department of Agriculture, Food, Natural Resources and Engineering (DAFNE), University of Foggia, 71122 Foggia, Italy. Department of Agriculture, Food, Natural Resources and Engineering (DAFNE), University of Foggia, 71122 Foggia, Italy. Department of Agriculture, Food, Natural Resources and Engineering (DAFNE), University of Foggia, 71122 Foggia, Italy. Department of Agriculture, Food, Natural Resources and Engineering (DAFNE), University of Foggia, 71122 Foggia, Italy.
 Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
 Faculty of Health Sciences, International PhD School, Rey Juan Carlos University, 28008, Madrid, Spain. selena.marcos@urjc.es. Department of Physical Therapy, Occupational Therapy, Physical Medicine and Rehabilitation, Faculty of Health Sciences, Rey Juan Carlos University, 28922, Alcorcón, Madrid, Spain. selena.marcos@urjc.es. Asociación de Leganés de Esclerosis Múltiple (ALEM), 28915, Leganés, Madrid, Spain. selena.marcos@urjc.es. Robotics Lab, Department of Systems Engineering and Automation, University Carlos III of Madrid, 28911, Leganés, Madrid, Spain. Robotics Lab, Department of Systems Engineering and Automation, University Carlos III of Madrid, 28911, Leganés, Madrid, Spain. Asociación de Leganés de Esclerosis Múltiple (ALEM), 28915, Leganés, Madrid, Spain. Rey Juan Carlos University Hospital of Móstoles, 28933, Madrid, Spain. Department of Physical Therapy, Occupational Therapy, Physical Medicine and Rehabilitation, Faculty of Health Sciences, Rey Juan Carlos University, 28922, Alcorcón, Madrid, Spain.
 Discipline of Pathology, Sydney Medical School, Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. roger.pamphlett@sydney.edu.au. Department of Neuropathology, Royal Prince Alfred Hospital, Sydney, NSW, Australia. roger.pamphlett@sydney.edu.au. Hyphenated Mass Spectrometry Laboratory, School of Mathematical and Physical Sciences, University of Technology Sydney, Sydney, NSW, Australia. roger.pamphlett@sydney.edu.au. Discipline of Pathology, Sydney Medical School, Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Department of Neuropathology, Royal Prince Alfred Hospital, Sydney, NSW, Australia. Hyphenated Mass Spectrometry Laboratory, School of Mathematical and Physical Sciences, University of Technology Sydney, Sydney, NSW, Australia.
 CEMAD Digestive Disease Center, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Catholic University of Rome, Rome, Italy. UOSD DH Medicina Interna e Gastroenterologia, Fondazione Policlinico A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy. UOSD DH Medicina Interna e Gastroenterologia, Fondazione Policlinico A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy. Electronic address: carusocristiano1@gmail.com. UOC Neurologia, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy. CEMAD Digestive Disease Center, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Catholic University of Rome, Rome, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Medical and Surgical Sciences, UOC Dermatologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. Department of Medical and Surgical Sciences, UOC Dermatologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. Oasi Research Institute-IRCCS, Troina, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy.
 Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. Institute of Infection, Immunity, and Inflammation, College of Medical, Veterinary, and Life Sciences, Glasgow Biomedical Research Centre, Glasgow, UK. Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. Institute of Infection, Immunity, and Inflammation, College of Medical, Veterinary, and Life Sciences, Glasgow Biomedical Research Centre, Glasgow, UK. Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK.
 Metabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. Neuroimmunology Group, Department of Medicine, University of Lleida (UdL)-IRBLleida, 25198, Lleida, Spain. luis.brieva@udl.cat. Department of Neurology, Hospital Universitari Arnau de Vilanova, 25198, Lleida, Spain. luis.brieva@udl.cat.
 Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing Engineering Research Center for Nervous System Drugs, Beijing 100053, China. Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing Engineering Research Center for Nervous System Drugs, Beijing 100053, China. Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing Engineering Research Center for Nervous System Drugs, Beijing 100053, China. Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing Engineering Research Center for Nervous System Drugs, Beijing 100053, China. Electronic address: ycctmg@126.com. Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing Engineering Research Center for Nervous System Drugs, Beijing 100053, China; Phase I Clinical Trial Unit, Beijing Ditan Hospital Capital Medical University, Beijing 100015, China. Electronic address: hucarol@126.com.
 From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. areder@neurology.bsd.uchicago.edu xfeng@neurology.bsd.uchicago.edu. From the Department of Neurology A-205 (T.W.H., Q.H.-P., C.R., X.F., A.T.R.), MC-2030 University of Chicago Medicine, IL; and Department of Neurology (F.D.T.), University of Illinois Chicago, IL. areder@neurology.bsd.uchicago.edu xfeng@neurology.bsd.uchicago.edu.
 NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address: vera.fominykh@medisin.uio.no. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway; Department of Medical Genetics, Oslo University Hospital, Oslo, Norway. Department of Complex Trait Genetics, Centre for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. Department of Complex Trait Genetics, Centre for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. Department of Complex Trait Genetics, Centre for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands; Department of Child and Adolescent Psychiatry and Pediatric Psychology, Section Complex Trait Genetics, Amsterdam Neuroscience, Vrije Universiteit Medical Center, Amsterdam, the Netherlands. Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway; Norwegian National Centre for Ageing and Health, Vestfold Hospital Trust, Tonsberg, Vestfold, Norway. Department of Radiology, University of California San Diego, La Jolla, California, USA; Multimodal Imaging Laboratory, University of California San Diego, La Jolla, California, USA; Department of Psychiatry, University of California San Diego, La Jolla, California, USA; Department of Neurosciences, University of California San Diego, La Jolla, California, USA. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Medical Genetics, Oslo University Hospital, Oslo, Norway; K.G. Jebsen Centre for Neurodevelopmental disorders, University of Oslo and Oslo University Hospital, Oslo, Norway. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Informatics, Centre for Bioinformatics, University of Oslo, Norway. NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway; K.G. Jebsen Centre for Neurodevelopmental disorders, University of Oslo and Oslo University Hospital, Oslo, Norway.
 Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada/Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada. Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of Alberta, Edmonton, AB, Canada.
 Achucarro Basque Center for Neuroscience and Department of Neuroscience, University of the Basque Country UPV/EHU, E-48940, Leioa, Spain. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Leioa, Spain. Achucarro Basque Center for Neuroscience and Department of Neuroscience, University of the Basque Country UPV/EHU, E-48940, Leioa, Spain. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Leioa, Spain. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany, 20251, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany, 20251, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany, 20251, Hamburg, Germany. Achucarro Basque Center for Neuroscience and Department of Neuroscience, University of the Basque Country UPV/EHU, E-48940, Leioa, Spain. Achucarro Basque Center for Neuroscience and Department of Neuroscience, University of the Basque Country UPV/EHU, E-48940, Leioa, Spain. Ikerbasque Foundation, E-48009, Bilbao, Spain. Achucarro Basque Center for Neuroscience and Department of Neuroscience, University of the Basque Country UPV/EHU, E-48940, Leioa, Spain. carlos.matute@ehu.eus. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Leioa, Spain. carlos.matute@ehu.eus. Achucarro Basque Center for Neuroscience and Department of Neuroscience, University of the Basque Country UPV/EHU, E-48940, Leioa, Spain. maria.domercq@ehu.eus. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Leioa, Spain. maria.domercq@ehu.eus.
 Department of Neurology, Faculty of Medicine, Zonguldak Bulent Ecevit University, Zonguldak, Turkey. Electronic address: mustafaacikgoz01@gmail.com. Department of Neurology, Faculty of Medicine, Zonguldak Bulent Ecevit University, Zonguldak, Turkey. Department of Neurology, Faculty of Medicine, Zonguldak Bulent Ecevit University, Zonguldak, Turkey. Department of Neurology, Faculty of Medicine, Zonguldak Bulent Ecevit University, Zonguldak, Turkey. Department of Neurology, Bursa Dr. Ayten Bozkaya Spastic Children's Hospital and Rehabilitation Center, Bursa, Turkey. Department of Otorhinolaryngology, Kocaeli Health and Technology University, Kocaeli, Turkey. Department of Neurology, Faculty of Medicine, Zonguldak Bulent Ecevit University, Zonguldak, Turkey.
 Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St, Carlton, Melbourne, VIC 3053, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St, Carlton, Melbourne, VIC 3053, Australia; Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St, Carlton, Melbourne, VIC 3053, Australia. Melbourne School of Psychological Sciences, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St, Carlton, Melbourne, VIC 3053, Australia. Faculty of Medicine and Health Sciences, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Level 3, 207 Bouverie St, Carlton, Melbourne, VIC 3053, Australia. Electronic address: jreece@unimelb.edu.au.
 Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. pablo.arroyo@bellvitgehospital.cat. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain. Neurology Department, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Carrer de la Feixa Llarga S/N, 08907, Barcelona, Spain.
 Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, United States. Electronic address: bjeng@uic.edu. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, United States. Electronic address: psilic2@uic.edu. Program in Exercise Science, Department of Physical Therapy, Marquette University, Milwaukee, WI, United States. Electronic address: rachel.bollaert@marquette.edu. Center for Neuropsychology and Neuroscience Research, Kessler Foundation, West Orange, NJ, United States; Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, United States. Electronic address: bsandroff@kesslerfoundation.org. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, United States. Electronic address: robmotl@uic.edu.
 Department of Health Sciences, University of Jaén, Campus Las Lagunillas, s/n, Jaén, Spain. Department of Health Sciences, University of Jaén, Campus Las Lagunillas, s/n, Jaén, Spain. FREMAP, Mutual Collaborator With Social Security Nº 61, Santo Reino, 7, Jaén, Spain. Department of Health Sciences, University of Jaén, Campus Las Lagunillas, s/n, Jaén, Spain. Department of Health Sciences, University of Jaén, Campus Las Lagunillas, s/n, Jaén, Spain. eobrero@ujaen.es. Center for Neuropsychological Assessment and Neurorehabilitation (CERNEP), University of Almería, Almería, Spain. Department of Psychology, University of Almería, Ctra. Sacramento, s/n, La Cañada, Almería, Spain.
 Department of Immunology, Zanjan University of Medical Sciences, Zanjan, Iran. A46reza@zums.ac.ir. Cancer Gene Therapy Research Center (CGRC), Zanjan University of Medical Sciences, Zanjan, Iran. A46reza@zums.ac.ir. School of Medicine, Zanjan University of medical sciences, Zanjan, Iran. School of Medicine, Zanjan University of medical sciences, Zanjan, Iran.
 Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France. Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Université Paris-Saclay, Orsay 91401, France.
 Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China; National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China. Electronic address: ducs2015@163.com.
 School of Nursing and Midwifery, Hamadan University of Medical Science, Hamadan, Iran. Department of Ethics Education in Medical Sciences, Department of Medical-Surgical Nursing, School of Nursing and Midwifery, Hamadan University of Medical Science, Hamadan, Iran. Modeling of Noncommunicable Diseases Research Center, Hamadan University of Medical Science, Hamadan, Iran. Department of Neurology, Medical School, Hamadan University of Medical Science, Hamadan, Iran. Department of Medical-Surgical Nursing, School of Nursing and Midwifery, Hamadan University of Medical Science, Hamadan, Iran. sr.borzu@umsha.ac.ir.
 Section of Biostatistics, Department of Health Sciences, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. Centro Sclerosi Multipla Binaghi, ASL Cagliari, Cagliari, Italy. Centro Sclerosi Multipla, II Clinica Neurologica, Università della Campania Luigi Vanvitelli, Naples, Italy. Department of Neurology, MS Center, F. Tappeiner Hospital, Merano, Italy. Clinica Neurologica e Malattie Neurometaboliche, Università degli Studi di Siena, Siena, Italy. Neuroimmunology, Neurological Unit, Cerobrovascular Department, Center for Multiple Sclerosis, ASST Crema, Crema, Italy. Department of Neurology, Imperia Hospital, Imperia, Italy. Neurology Unit, Galliera Hospital, Genoa, Italy. Centro Sclerosi Multipla S.C. Neurologia Asl 3 Genovese, Genoa, Italy. AISM Rehabilitation Center, Genoa, Italy. Neurology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. UOC Neurologia e Centro SM Fondazione Istituto G. Giglio, Cefalù, Italy. Department of Medical Sciences, Surgery, and Neurosciences, University of Siena, Siena, Italy. Multiple Sclerosis Center, Fabrizio Spaziani Hospital, Frosinone, Italy. Department of Neurology, Ospedale Regionale, Aosta, Italy. Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, Turin, Italy. Department of Human Neuroscience, Sapienza University of Rome, Rome, Italy. IRCCS Istituto Neurologico Mediterraneo Neuromed, Pozzilli, Italy. IRCCS Istituto Neurologico Mediterraneo Neuromed, Pozzilli, Italy. Department of Neurosciences, Mental Health, and Sensory Organs, Center for Experimental Neurological Therapies, Sapienza University of Rome, Rome, Italy. Research Department, Italian Multiple Sclerosis Foundation, Genoa, Italy. Department of Life Sciences, University of Siena, Siena, Italy. IRCCS Mondino Foundation, Pavia, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy. Section of Biostatistics, Department of Health Sciences, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
 Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven Cancer Institute, University of Leuven, Leuven 3000, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Cardiology and Organ Systems, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan. Department of Cardiology and Organ Systems, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Oncology, Laboratory of Lipid Metabolism and Cancer, Leuven Cancer Institute, University of Leuven, Leuven 3000, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek 3590, Belgium.
 Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Multiple Sclerosis Center, Sheba Medical Center, Tel Hashomer, Israel. Department of Health Science, Faculty of Psychology and Human Movement, Institute of Human Movement Science, University Hamburg, Hamburg, Germany. Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel - alonkalr@tuaex.tau.ac.il. Multiple Sclerosis Center, Sheba Medical Center, Tel Hashomer, Israel. Sagol School of Neurosciences, Tel-Aviv University, Tel-Aviv, Israel.
 Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Clinical Epidemiology Unit, National Institute for Infectious Disease Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. UOS Professioni Sanitarie Tecniche, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Laboratory of Virology, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Clinical Division of Infectious Diseases, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Cellular Immunology Laboratory, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Cellular Immunology Laboratory, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Department of Pediatric Hematology and Oncology, IRCCS Bambino Gesù Children's Hospital, 00146 Rome, Italy. UOC Emerging Infections and Centro di Riferimento AIDS (CRAIDS), National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Clinical Division of Infectious Diseases, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy. Department of Neurosciences, San Camillo Forlanini Hospital, 00152 Rome, Italy. Translational Research Unit, National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, 00149 Rome, Italy.
 Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Bioinformatics Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Bioinformatics Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Neuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
 Department of Neuroscience and Regenerative Medicine, Augusta University, Medical College of Georgia, 1120 15th Street, Augusta, GA 30912-2620, USA; Laboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, R. Weigla 12, 53-114 Wroclaw, Poland. Electronic address: maria.podbielska@hirszfeld.pl. Laboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, R. Weigla 12, 53-114 Wroclaw, Poland. Department of Lipids and Liposomes, University of Wroclaw, F. Joliot-Curie 14a, 50-383 Wroclaw, Poland. Department of Biochemistry & Molecular Biology, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC 29425-2503, USA. Department of Neurosurgery, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland; Bacteriophage Laboratory, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, R. Weigla 12, 53-114 Wroclaw, Poland. Department of Neurology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland. Laboratory of Glycobiology, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, R. Weigla 12, 53-114 Wroclaw, Poland. Department of Neurology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland. Department of Neuroscience and Regenerative Medicine, Augusta University, Medical College of Georgia, 1120 15th Street, Augusta, GA 30912-2620, USA; Department of Neurology, Medical University of South Carolina, 96 Jonathan Lucas Street, Charleston, SC 29425-8900, USA. Department of Neurology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland.
 Department of clinical medicine, University of Bergen, Norway. Department of clinical medicine, University of Bergen, Norway. Norwegian MS-registry and biobank, Dept of Neurology, Haukeland University Hospital, Bergen, Norway. Department of clinical medicine, University of Bergen, Norway; Neuro-SysMed, Haukeland University Hospital, Bergen, Norway. Department of clinical medicine, University of Bergen, Norway; Neuro-SysMed, Haukeland University Hospital, Bergen, Norway. Department of clinical medicine, University of Bergen, Norway; Neuro-SysMed, Haukeland University Hospital, Bergen, Norway. Department of clinical medicine, University of Bergen, Norway; Neuro-SysMed, Haukeland University Hospital, Bergen, Norway. Department of clinical medicine, University of Bergen, Norway; Norwegian MS-registry and biobank, Dept of Neurology, Haukeland University Hospital, Bergen, Norway; Neuro-SysMed, Haukeland University Hospital, Bergen, Norway. Electronic address: stig.wergeland@helse-bergen.no.
 Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. School of Medical, Indigenous and Health Sciences, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Baker Heart and Diabetes Research Institute, Melbourne, Australia. Mathematics and Statistics, School of Computing, Engineering and Mathematical Sciences, La Trobe University, Melbourne, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. steve.simpsonyap@unimelb.edu.au. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. steve.simpsonyap@unimelb.edu.au.
 Sverdlovsk Regional Clinical Hospital No. 1, Yekaterinburg, Russia.
 Shepherd Center, Virginia C. Crawford Research Institute, Atlanta, GA. Electronic address: Brad.Willingham@shepherd.org. Department of Kinesiology, University of Georgia, Athens, GA. Shepherd Center, Virginia C. Crawford Research Institute, Atlanta, GA.
 Department of Computer Science and Engineering, University of Bologna, Bologna, Italy. Faculty of Computer Science, Free University of Bozen-Bolzano, Bolzano, Italy. Department of Computer Science and Engineering, University of Bologna, Bologna, Italy.
 T.C. Saglik Bakanligi Başakşehir Cam ve Sakura Sehir Hastanesi, Communication, T.C. Saglik Bakanligi Başakşehir Cam ve Sakura Sehir Hastanesi, Istanbul, Turkey. Pamukkale Universitesi Tip Fakultesi Hastanesi, Communication, Pamukkale Universitesi Tip Fakultesi Hastanesi, Denizli, Turkey. Pamukkale Universitesi Tip Fakultesi Hastanesi, Communication, Pamukkale Universitesi Tip Fakultesi Hastanesi, Denizli, Turkey. Pamukkale Universitesi Tip Fakultesi Hastanesi, Communication, Pamukkale Universitesi Tip Fakultesi Hastanesi, Denizli, Turkey. Pamukkale Universitesi Tip Fakultesi Hastanesi, Communication, Pamukkale Universitesi Tip Fakultesi Hastanesi, Denizli, Turkey. Pamukkale Universitesi Tip Fakultesi Hastanesi, Communication, Pamukkale Universitesi Tip Fakultesi Hastanesi, Denizli, Turkey.
 Research, Health and Podiatry Group, Department of Health Sciences, Faculty of Nursing and Podiatry, Industrial Campus of Ferrol, Universidade da Coruña, Ferrol, Spain. UICISA: E, Instituto Politécnico de Viana do Castelo, Escola Superior de Saúde, Viana do Castelo, Portugal. Faculty of Health Sciences, Universidad Rey Juan Carlos, Madrid, Spain. Faculty of Nursing, Physiotherapy and Podiatry, Universidad Complutense de Madrid, Madrid, Spain. Department of Sociology, Social Work and Public Health, Universidad de Huelva, Huelva, Spain. Safety and Health Postgraduate Programme, Universidad Espíritu Santo, Guayaquil, Ecuador. Faculty of Sport Sciences, Universidad Europea de Madrid, Madrid, Spain. Nursing and Podiatry Department, University of Málaga, Málaga, Spain. Instituto de Investigación Biomédica de Málaga (IBIMA), Málaga, Spain. Research, Health and Podiatry Group, Department of Health Sciences, Faculty of Nursing and Podiatry, Industrial Campus of Ferrol, Universidade da Coruña, Ferrol, Spain.
 Physical Therapy Program, Department of Physical Medicine and Rehabilitation, University of Colorado, Aurora (M.M.M., C.L.C., M.B.); Department of Neurology, School of Medicine, University of Colorado, Aurora (M.M.M.); Geriatric Research Education and Clinical Center, VA Eastern Colorado Healthcare System, Denver, Colorado (M.M.M., C.L.C., M.B.); Department of Physical Therapy, Arcadia University, Glenside, Pennsylvania (E.T.C.); and Department of Neurology, School of Medicine, Oregon Health & Science University, Portland, and VA Portland Health Care System, Portland, Oregon (M.H.C.).
 Department of Neurology, School of Medicine, West Virginia University, Morgantown, WV, USA. Division of Multiple Sclerosis and Neuroimmunology Department of Neurology, McGovern Medical School (UT Health), University of Texas Health Science Center at Houston, Houston, TX, USA. Mahatma Gandhi Memorial Medical College, Indore, India. Division of Multiple Sclerosis and Neuroimmunology Department of Neurology, McGovern Medical School (UT Health), University of Texas Health Science Center at Houston, Houston, TX, USA; West Virginia Clinical Transitional Science, Morgantown, WV, USA. Electronic address: shitiz.k.sriwastava@uth.tmc.edu.
 Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Psychiatry, University of Münster, 48149, Münster, Germany; Department of Psychiatry, Maria Brunn Hospital, 48163, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology, Erasmus MC University Medical Center, 3015 GD, Rotterdam, the Netherlands. Institute of Clinical Chemistry, University Hospital Schleswig-Holstein, 24105, Kiel, Lübeck, Germany. Institute of Biochemistry II, Goethe University Frankfurt, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt am Main, Germany; Frankfurt Cancer Institute, Frankfurt am Main, Germany; Cardio-Pulmonary Institute, Frankfurt am Main, Germany. Epilepsy Center Frankfurt Rhine-Main, Center of Neurology and Neurosurgery, University Hospital Frankfurt, Goethe University Frankfurt, 60528 Frankfurt am Main, Germany; LOEWE Center for Personalized Translational Epilepsy Research (CePTER), Goethe University Frankfurt, Frankfurt am Main, Germany. Department of Neurology, Erasmus MC University Medical Center, 3015 GD, Rotterdam, the Netherlands. Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Immunology, Weizmann Institute of Science, 7610001, Rehovot, Israel. Institute of Clinical Chemistry, University Hospital Schleswig-Holstein, 24105, Kiel, Lübeck, Germany; Department of Neurology, Faculty of Medicine, Kiel University, 24105, Kiel, Germany. Department of Neurology, Erasmus MC University Medical Center, 3015 GD, Rotterdam, the Netherlands. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, 48149, Münster, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Düsseldorf, Germany. Electronic address: Nico.Melzer@med.uni-duesseldorf.de.
 Neurocenter, Lucerne Cantonal Hospital, 6000 Lucerne, Switzerland; Department of Neurology, Inselspital, Bern University Hospital and University of Bern, 3010 Bern, Switzerland. Electronic address: christian.kamm@luks.ch. 12 Parsec, Oberfeld 3, 6037 Root, Switzerland. Holonautic AG, Tannegg 4, 6005 St., Niklausen LU, Switzerland. Neurocenter, Lucerne Cantonal Hospital, 6000 Lucerne, Switzerland; Gerontechnology and Rehabilitation Group, University of Bern, 3010 Bern, Switzerland.
 Vrije Universiteit Brussel, Center for Neurosciences (C4N), Jette, Brussels, Belgium. Universiteit Antwerpen, Department of Biomedical Sciences and Institute Born-Bunge, Reference Center for Biological Markers of Dementia (BIODEM), Wilrijk, Antwerp, Belgium. Universitair Ziekenhuis Brussel, Department of Neurology, Jette, Brussels, Belgium. Vrije Universiteit Brussel, Center for Neurosciences (C4N), Jette, Brussels, Belgium. Universiteit Antwerpen, Department of Biomedical Sciences and Institute Born-Bunge, Reference Center for Biological Markers of Dementia (BIODEM), Wilrijk, Antwerp, Belgium. Universitair Ziekenhuis Brussel, Department of Neurology, Jette, Brussels, Belgium. Vrije Universiteit Brussel, Center for Neurosciences (C4N), Jette, Brussels, Belgium. Universiteit Antwerpen, Department of Biomedical Sciences and Institute Born-Bunge, Reference Center for Biological Markers of Dementia (BIODEM), Wilrijk, Antwerp, Belgium. Universitair Ziekenhuis Brussel, Department of Neurology, Jette, Brussels, Belgium. Universitair Ziekenhuis Brussel, Department of Clinical Biology, Laboratory of Clinical Neurochemistry, Jette, Brussels, Belgium. Vrije Universiteit Brussel, Center for Neurosciences (C4N), Jette, Brussels, Belgium. Universitair Ziekenhuis Brussel, Department of Neurology, Jette, Brussels, Belgium. National MS Center (NMSC), Neurology, Melsbroek, Steenokkerzeel, Belgium.
 Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, UK. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Institute of Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Institute of Anatomy, Leipzig University, Leipzig, Germany. Institute of Anatomy, Leipzig University, Leipzig, Germany. Cellular Neuroanatomy, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Department of Neurophysics, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany. Institute of Anatomy, Leipzig University, Leipzig, Germany. Paul Flechsig Institute of Brain Research, Leipzig University, Leipzig, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Paul Flechsig Institute of Brain Research, Leipzig University, Leipzig, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Institute of Functional and Applied Anatomy, Research Core Unit Electron Microscopy, Hannover Medical School, Hannover, Germany. Institute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany. Institute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany. Centre for NeuroModulation (NeuroModBasics), University of Freiburg, Freiburg, Germany. Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Institute of Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Robert.Fledrich@medizin.uni-leipzig.de. Institute of Anatomy, Leipzig University, Leipzig, Germany. Robert.Fledrich@medizin.uni-leipzig.de. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. nave@mpinat.mpg.de. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Ruth.Stassart@medizin.uni-leipzig.de. Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Ruth.Stassart@medizin.uni-leipzig.de.
 Department of Neurological Rehabilitation, Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Electronic address: mertdogan@hacettepe.edu.tr. Department of Neurological Rehabilitation, Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Department of Neurological Rehabilitation, Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey.
 Universitätsklinik für Neurologie, Medizinische Universität Innsbruck, Österreich. Karl Landsteiner Institut für Interdisziplinäre Rehabilitationsforschung, Reha Zentrum Münster, Österreich. Psychometric Laboratory for Health Sciences, Faculty of Medicine and Health, University of Leeds, UK. Universitätsklinik für Neurologie, Medizinische Universität Innsbruck, Österreich. Karl Landsteiner Institut für Interdisziplinäre Rehabilitationsforschung, Reha Zentrum Münster, Österreich. Department für Neurologie, Reha Zentrum Münster, Österreich. Karl Landsteiner Institut für Interdisziplinäre Rehabilitationsforschung, Reha Zentrum Münster, Österreich. Department für Neurologie, Reha Zentrum Münster, Österreich. Universitätsklinik für Neurologie, Medizinische Universität Innsbruck, Österreich. Department of Neurology, Walton Centre NHS Foundation Trust, Liverpool, UK.
 Department of Biomedical and Clinical Sciences, Universita degli Studi di Milano. Department of Biomedical and Clinical Sciences, Universita degli Studi di Milano. Health District of Catania, Azienda Sanitaria Provinciale di Catania. Neurology and Neurological Rehabilitation Unit, San Raffaele Hospital. Laboratory of Neuropsychology, Psychology Unit, ASST Lariana. IRCCS Fondazione Don Carlo Gnocchi. Multiple Sclerosis Centre, Neurology Unit, Hospital of Vaio-Fidenza. Department of Neurosciences, Imaging and Clinical Sciences, Universita G. d'Annunzio Chieti-Pescara. Department of Neuroscience, San Camillo-Forlanini Hospital. Department of Basic Medical Sciences, Neurosciences and Sense Organs, Universita di Bari. Multiple Sclerosis Centre, Neurology Unit, Hospital of Vaio-Fidenza. IRCCS Fondazione Don Carlo Gnocchi. Neurology and Neurological Rehabilitation Unit, San Raffaele Hospital. Multiple Sclerosis Centre, SS. Annunziata University Hospital. Department of Neuroscience, San Camillo-Forlanini Hospital. Neurology and Neurological Rehabilitation Unit, San Raffaele Hospital. Multiple Sclerosis Centre, University Polyclinic Hospital G. Rodolico. Department of Basic Medical Sciences, Neurosciences and Sense Organs, Universita di Bari. Department of Pathophysiology and Transplantation, Universita degli Studi di Milano.
 Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. University MS Center (UMSC) Hasselt, Pelt, Belgium. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. University MS Center (UMSC) Hasselt, Pelt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. University MS Center (UMSC) Hasselt, Pelt, Belgium. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. University MS Center (UMSC) Hasselt, Pelt, Belgium. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. University MS Center (UMSC) Hasselt, Pelt, Belgium. Institute of Biomedical and Clinical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK. Stem Cell Institute, Department of Development and Regeneration, KU Leuven, Leuven, Belgium. Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg. Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg. Institute of Neurogenetics, University of Lübeck, Lübeck, Germany. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Institute of Biomedical and Clinical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK. University MS Center (UMSC) Hasselt, Pelt, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wuerzburg, Würzburg, Germany. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium. tim.vanmierlo@uhasselt.be. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. tim.vanmierlo@uhasselt.be. University MS Center (UMSC) Hasselt, Pelt, Belgium. tim.vanmierlo@uhasselt.be.
 Multiple Sclerosis Research Center, Neuroscience Institute, Sina MS Research Center, Sina Hospital, Tehran University of Medical Sciences, Hasan Abad Sq, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Sina MS Research Center, Sina Hospital, Tehran University of Medical Sciences, Hasan Abad Sq, Tehran, Iran. Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashahd, Iran. Iranian Tissue Bank and Research Center, Gene, Cell and Tissue Institute, Tehran University of Medical Sciences and Health Services, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Sina MS Research Center, Sina Hospital, Tehran University of Medical Sciences, Hasan Abad Sq, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Sina MS Research Center, Sina Hospital, Tehran University of Medical Sciences, Hasan Abad Sq, Tehran, Iran. Electronic address: drnavardi@gmail.com.

 Department of Neurosurgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Department of Neurosurgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Department of Neurosurgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Department of Neurosurgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Jiangnan University, Wuxi, China. Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Department of Neurosurgery, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
 Doctoral Degree School, Catholic University of Valencia San Vicente Mártir, C/Quevedo, 2, 46001 Valencia, Spain. m.cuerda@mail.ucv.es. Department of Nursing, Catholic University of Valencia San Vicente Mártir, C/Espartero, 7, 46007 Valencia, Spain. beprool@mail.ucv.es. Department of Physiotherapy, Catholic University of Valencia San Vicente Mártir, C/Quevedo, 2, 46001 Valencia, Spain. jorge.alarcon@ucv.es. Department of Physiotherapy, Catholic University of Valencia San Vicente Mártir, C/Quevedo, 2, 46001 Valencia, Spain. jorge.alarcon@ucv.es. Department of Physiotherapy, European University of Valencia, Avda/Alameda, 7, 46010, Valencia, Spain. carlosalberto.villaron@universidadeuropea.es. Department of Law, Economical and Social Sciences, Multimedia Area, Catholic University of Valencia San Vicente Mártir, C/Guillem de Castro, 94, 46001 Valencia, Spain. jlajara@ucv.es. Department of Nursing, Catholic University of Valencia San Vicente Mártir, C/Espartero, 7, 46007 Valencia, Spain. beprool@mail.ucv.es.
 Neurological Rehabilitation Center Godeshoehe GmbH, Department of Therapeutic Science, Bonn, Germany. Department of Epidemiology, CAPHRI Care and Public Health Research Institute, Maastricht University, Maastricht, The Netherlands. Department of Nutrition and Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands. Neuromotor Rehabilitation Research Group, Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Department of Health Sciences & Technology, Institute of Human Movement Sciences and Sport, ETH Zurich, Zurich, Switzerland. Division of Sports and Exercise Medicine, Department of Sport, Exercise, and Health, University of Basel, Basel, Switzerland.
 Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Microbiology, Infectious Diseases and Immunology, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Division of Neurosurgery, Centre Hospitalier de l'Université de Montréal (CHUM), Montreal, Quebec H2X 0C1, Canada. Department of Surgery, Université de Montréal, Montreal, Quebec H3C 3J7, Canada. Division of Neurosurgery, Centre Hospitalier de l'Université de Montréal (CHUM), Montreal, Quebec H2X 0C1, Canada. Department of Surgery, Université de Montréal, Montreal, Quebec H3C 3J7, Canada. Clinical Department of Laboratory Medicine, CHUM, Montreal, Quebec H2X 0C1, Canada. Department of Pathology and Cell Biology, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Multiple Sclerosis Clinic, Division of Neurology, CHUM, Montreal, Quebec H2L 4M1, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. Multiple Sclerosis Clinic, Division of Neurology, CHUM, Montreal, Quebec H2L 4M1, Canada.
 Department of Neurology, Odense University Hospital, J.B. Winsloews Vej 4, 5000 Odense C, Denmark; Orthopaedic Research Unit, Department of Clinical Research, University of Southern Denmark, J.B. Winsloews Vej 19, 3., 5000 Odense C, Denmark; Department of Neurobiology Research, Department of Molecular Medicine, University of Southern Denmark, J.B. Winsloews Vej 21, st., 5000 Odense C, Denmark; BRIDGE - Brain Research - Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, J.B. Winsloews Vej 19, 3., 5000 Odense C, Denmark. Electronic address: maria.thorning.christensen@rsyd.dk. Department of Neurology, Odense University Hospital, J.B. Winsloews Vej 4, 5000 Odense C, Denmark; Department of Neurobiology Research, Department of Molecular Medicine, University of Southern Denmark, J.B. Winsloews Vej 21, st., 5000 Odense C, Denmark; BRIDGE - Brain Research - Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, J.B. Winsloews Vej 19, 3., 5000 Odense C, Denmark. Department of Neurology, Odense University Hospital, J.B. Winsloews Vej 4, 5000 Odense C, Denmark; Orthopaedic Research Unit, Department of Clinical Research, University of Southern Denmark, J.B. Winsloews Vej 19, 3., 5000 Odense C, Denmark. Department of Neurobiology Research, Department of Molecular Medicine, University of Southern Denmark, J.B. Winsloews Vej 21, st., 5000 Odense C, Denmark; Department of Orthopaedics, Hospital Soenderjylland, Kresten Philipsens Vej 15, 6200 Aabenraa, Denmark; Department of Regional Health Research, University of Southern Denmark, J.B Winsloews Vej 19. 3,. 5000 Odense C, Denmark. Department of Brain and Nerve Diseases, Sygehus Lillebaelt, Sygehusvej 24, 6000, Kolding, Denmark; Department of Regional Health Research, University of Southern Denmark, J.B Winsloews Vej 19. 3,. 5000 Odense C, Denmark. Department of Orthopaedics and Traumatology, Odense University Hospital, J.B. Winsloews Vej 4, 5000 Odense C, Denmark; Orthopaedic Research Unit, Department of Clinical Research, University of Southern Denmark, J.B. Winsloews Vej 19, 3., 5000 Odense C, Denmark. Department of Neurology, Odense University Hospital, J.B. Winsloews Vej 4, 5000 Odense C, Denmark; Department of Neurobiology Research, Department of Molecular Medicine, University of Southern Denmark, J.B. Winsloews Vej 21, st., 5000 Odense C, Denmark; BRIDGE - Brain Research - Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, J.B. Winsloews Vej 19, 3., 5000 Odense C, Denmark.
 From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. wolf.lagreze@uniklinik-freiburg.de. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. From the Eye Center (S.K., S.P.H., W.A.L.); Clinical Trials Unit (G.I., B.G.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg; Department of Ophthalmology (F.B.), University Hospital, University of Heidelberg; Department of Neurology (P.A.), Medical Faculty, Heinrich Heine-Universität Düsseldorf; Aalen University of Applied Sciences (J.U., M.W.), Competence Center Vision Research; Pharmacy (M.J.H.), Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany; Department of Ophthalmology (S.W.), Inselspital, University Hospital, University of Bern, Switzerland; and Department of Neurology and National Center for Tumor Diseases (R.D.), Faculty of Medicine, University Hospital Heidelberg, Germany. wolf.lagreze@uniklinik-freiburg.de.
 Department of Neurology and Neurological Sciences and Pediatrics, Stanford University , Stanford, CA, USA. Access Health International , Ridgefield, CT, USA. Access Health International , Ridgefield, CT, USA.
 From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. ratuszny.dominica@mh-hannover.de. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany. From the Department of Neurology (D.R., T. Skripuletz, E.V., K.-W.S.); Clinic for Anesthesiology and Intensive Care (T. Stüber), Hannover Medical School; Outpatient Clinic of Neurology (K.G.), Neurozentrum, Itzehoe; Departments of Neurosurgery (P.E.), Nuclear Medicine (J.A.M.), Diagnostic and Interventional Neuroradiology (M.P.W.), and Neuropathology (F.F.), Institute of Pathology, Hannover Medical School, Germany.
 Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts pbrugarolas@mgh.harvard.edu.
 Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Bioengineering and Therapeutic Sciences, School of Pharmacy, University of California San Francisco, San Francisco, CA, USA. Department of Bioengineering, College of Engineering, California Institute for Quantitative Biosciences, QB3, University of California Berkeley, Berkeley, CA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Broad Institute of MIT and Harvard, Cambridge, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Broad Institute of MIT and Harvard, Cambridge, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Bioengineering, College of Engineering, California Institute for Quantitative Biosciences, QB3, University of California Berkeley, Berkeley, CA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Neuroimmunology Research Lab, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada. Neuroimmunology Research Lab, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada. Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. fquintana@rics.bwh.harvard.edu. Broad Institute of MIT and Harvard, Cambridge, MA, USA. fquintana@rics.bwh.harvard.edu. Department of Bioengineering and Therapeutic Sciences, School of Pharmacy, University of California San Francisco, San Francisco, CA, USA. adam@abatelab.org.
 Department of Pathophysiology and Transplantation, Università Degli Studi di Milano, 20100, Milan, Italy. Department of Pathophysiology and Transplantation, Università Degli Studi di Milano, 20100, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148, Milan, Italy. egervasoni@dongnocchi.it. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148, Milan, Italy. Department of Pathophysiology and Transplantation, Università Degli Studi di Milano, 20100, Milan, Italy. Department of Pathophysiology and Transplantation, Università Degli Studi di Milano, 20100, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148, Milan, Italy. Department of Pathophysiology and Transplantation, Università Degli Studi di Milano, 20100, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Via Capecelatro 66, 20148, Milan, Italy.
 Department of Neurochemistry, Institute of Psychiatry and Neurology, Warsaw, Poland. nchmielewska@ipin.edu.pl. Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland.
 Department of General Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Department of General Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. CAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China. Department of General Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China. Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, China.
 Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Indore 453552, Madhya Pradesh, India. Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Indore 453552, Madhya Pradesh, India. Department of Atomic Energy, Optical Coatings Laboratory, High Energy Lasers & Optics Section, Laser Technology Division, Laser Group, Raja Ramanna Centre for Advanced Technology, Indore 452013, Madhya Pradesh, India. Department of Atomic Energy, Optical Coatings Laboratory, High Energy Lasers & Optics Section, Laser Technology Division, Laser Group, Raja Ramanna Centre for Advanced Technology, Indore 452013, Madhya Pradesh, India. Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Indore 453552, Madhya Pradesh, India.
 Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Department of Neurology, İstanbul Faculty of Medicine (ÇAPA), İstanbul University, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, Samsun Ondokuz Mayıs University, Samsun, Turkey. Department of Neurology, Faculty of Medicine, İstanbul University Cerrahpaşa, İstanbul, Turkey. Department of Clinical Pharmacy, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey. Department of Neurology, Faculty of Medicine, Ege University, İzmir, Turkey. Department of Neurology, Faculty of Medicine, Ege University, İzmir, Turkey. İstanbul Haydarpasa Numune Training and Research Hospital, University of Health Sciences, İstanbul, Turkey. Bakırköy Psychiatric and Neurological Diseases Hospital, İstanbul, Turkey. Bakırköy Psychiatric and Neurological Diseases Hospital, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey. Department of Neurology, Faculty of Medicine, İzmir Kâtip Çelebi University, İzmir, Turkey. Department of Neurology, Faculty of Medicine, Uludağ University, Bursa, Turkey. Department of Neurology, Faculty of Medicine, Çukurova University, Adana, Turkey. Florence Nightingale Hospital, Science University, İstanbul, Turkey. Florence Nightingale Hospital, Science University, İstanbul, Turkey. Göztepe Professor Doctor Süleyman Yalçın City Hospital, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, Medipol University, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, İnönü University, Malatya, Turkey. Department of Neurology, Faculty of Medicine, İnönü University, Malatya, Turkey. Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Bakırköy Psychiatric and Neurological Diseases Hospital, İstanbul, Turkey. Haseki Training and Research Hospital, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey. Department of Neurology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey. Department of Neurology, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey. Başkent University Hospital, Ankara, Turkey. Department of Neurology, Faculty of Medicine, Kütahya Health Sciences University, Kütahya, Turkey. Department of Neurology, Faculty of Medicine, Akdeniz University, Antalya, Turkey. Department of Neurology, Faculty of Medicine, Mersin University, Mersin, Turkey. Department of Neurology, Faculty of Medicine, Mersin University, Mersin, Turkey. Department of Neurology, Faculty of Medicine, Fırat University, Elazığ, Turkey. Department of Neurology, Faculty of Medicine, Fırat University, Elazığ, Turkey. Department of Neurology, Faculty of Medicine, Adnan Menderes University, Aydın, Turkey. Bakırköy Psychiatric and Neurological Diseases Hospital, İstanbul, Turkey. Novartis Health Food and Agriculture Products Industry and Trade Inc., İstanbul, Turkey. Novartis Health Food and Agriculture Products Industry and Trade Inc., İstanbul, Turkey. Novartis Health Food and Agriculture Products Industry and Trade Inc., İstanbul, Turkey. Okan University Hospital, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, İstanbul University Cerrahpaşa, İstanbul, Turkey. Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Department of Neurology, Faculty of Medicine, İstanbul University Cerrahpaşa, İstanbul, Turkey. Department of Neurology, İstanbul Faculty of Medicine (ÇAPA), İstanbul University, İstanbul, Turkey.
 Department of Internal Medicine, University of Manitoba, Winnipeg, MB, Canada. Division of Child Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, ON, Canada/Canadian Centre for Health Economics, Toronto, ON, Canada. Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, ON, Canada/Canadian Centre for Health Economics, Toronto, ON, Canada. Center for Neuroinflammation and Experimental Therapeutics and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Pediatrics, University of Toronto, Toronto, ON, Canada/Division of Neurology, The Hospital for Sick Children, Neurosciences and Mental Health, SickKids Research Institute, Toronto, ON, Canada. Departments of Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
 Department of Surgery, Section of Ophthalmology. Department of Surgery, Section of Ophthalmology. Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada.
 From the Center of Innovation for Complex Chronic Healthcare, Edward Hines, Jr VA Hospital, Hines, Illinois (MW, FMW, RK, CTE, MAF); Center for Health Equity Research and Promotion, VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvania (KJS); University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania (KJS); VA Puget Sound Healthcare System, Seattle, Washington (SPB); University of Washington School of Medicine, Seattle, Washington (SPB); Loyola University Chicago Parkinson School of Health Sciences and Public Health, Maywood, Illinois (FMW); University of Illinois at Chicago College of Nursing, Chicago, Illinois (EC); University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin (NS); William S. Middleton VA Hospital, Madison, Wisconsin (NS); Northwestern University Feinberg School of Medicine, Chicago, Illinois (CTE); and Loyola University Chicago Stritch School of Medicine, Maywood, Illinois (MAF).
 Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, USA. bjeng@uic.edu. Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Physical Therapy, School of Health Professions, University of Alabama at Birmingham, Birmingham, AL, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, USA.
 Department of Biology, Loyola University Chicago, Chicago, Illinois, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Department of Biology, Loyola University Chicago, Chicago, Illinois, USA. Department of Biology, Loyola University Chicago, Chicago, Illinois, USA. Weill Institute for Neuroscience, Department of Neurology, University of California, San Francisco, California, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA.
 From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. heinz.wiendl@ukmuenster.de. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. From the Department of Neurology with Institute of Translational Neurology (H.W.), University of Münster, Germany and Brain and Mind Center, University of Sydney, Australia; The Blizard Institute (K.S.), Centre for Neuroscience, Surgery & Trauma, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK; Clinical Board Medicine (Neuroscience) (K.S.), The Royal London Hospital, Barts Health NHS Trust, UK; Ingham Institute for Applied Medical Research (S.H.), University of New South Wales Medicine, Sydney, Australia; Department of Neurology (T.D.), University Hospital Basel, Switzerland; Department of Neurology (Andrew Chan), Inselspital, Bern University Hospital, University of Bern, Switzerland; Danish MS Center (F.S.), Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine (F.S.), University of Copenhagen, Denmark; Multiple Sclerosis Center (A.A.), Sheba Academic Medical Center, Ramat Gan, Israel; Sackler School of Medicine (A.A.), Tel-Aviv University, Israel; Department of Neurology-Neuroimmunology (X.M.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Spain; Department of Neurosciences and CRCHUM (A.P.), Université de Montréal, QC, Canada; Department of Neurological and Behavioural Sciences (N.D.S.), University of Siena, Italy; Department of Radiology (F.B.), VU University Medical Center, Amsterdam, The Netherlands; UCL Institute of Neurology (F.B.), London, UK; Experimental Neurophysiology Unit (L.L.), Vita-Salute San Raffaele University, Milan, Italy; Univ. Lille (P.V.), Inserm U1172 LilNCog, CHU Lille, FHU Precise, France; Cytel Inc (Anita Chudecka), Geneva, Switzerland; InScience Communications (C.M.), Springer Healthcare Ltd, Chester, UK; EMD Serono (K.H.H.), Billerica, MA; and Ares Trading SA (U.B., S.R.), Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany.
 National Center for Global Health, Istituto Superiore di Sanità, 00161 Rome, Italy. National Center for Global Health, Istituto Superiore di Sanità, 00161 Rome, Italy. National Center for Global Health, Istituto Superiore di Sanità, 00161 Rome, Italy. Multiple Sclerosis Center, Sapienza University of Rome, 00161 Rome, Italy. Multiple Sclerosis Center, Sapienza University of Rome, 00161 Rome, Italy. National Center for Global Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
 From the Spinoza Centre for Neuroimaging, Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 75, 1105 BK Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Computational Cognitive Neuroscience and Neuroimaging, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Philips Healthcare, Copenhagen, Denmark (M.A.); Lund University Bioimaging Centre, Lund University, Lund, Sweden (M.A.); Department of Experimental and Applied Psychology, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (S.O.D.); Department of Experimental Psychology, Utrecht University, Utrecht, the Netherlands (S.O.D.); and Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark (V.O.B.). From the Spinoza Centre for Neuroimaging, Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 75, 1105 BK Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Computational Cognitive Neuroscience and Neuroimaging, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Philips Healthcare, Copenhagen, Denmark (M.A.); Lund University Bioimaging Centre, Lund University, Lund, Sweden (M.A.); Department of Experimental and Applied Psychology, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (S.O.D.); Department of Experimental Psychology, Utrecht University, Utrecht, the Netherlands (S.O.D.); and Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark (V.O.B.). From the Spinoza Centre for Neuroimaging, Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 75, 1105 BK Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Computational Cognitive Neuroscience and Neuroimaging, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Philips Healthcare, Copenhagen, Denmark (M.A.); Lund University Bioimaging Centre, Lund University, Lund, Sweden (M.A.); Department of Experimental and Applied Psychology, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (S.O.D.); Department of Experimental Psychology, Utrecht University, Utrecht, the Netherlands (S.O.D.); and Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark (V.O.B.). From the Spinoza Centre for Neuroimaging, Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 75, 1105 BK Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Computational Cognitive Neuroscience and Neuroimaging, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Philips Healthcare, Copenhagen, Denmark (M.A.); Lund University Bioimaging Centre, Lund University, Lund, Sweden (M.A.); Department of Experimental and Applied Psychology, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (S.O.D.); Department of Experimental Psychology, Utrecht University, Utrecht, the Netherlands (S.O.D.); and Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark (V.O.B.). From the Spinoza Centre for Neuroimaging, Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 75, 1105 BK Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Computational Cognitive Neuroscience and Neuroimaging, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands (N.P., S.O.D., W.v.d.Z.); Philips Healthcare, Copenhagen, Denmark (M.A.); Lund University Bioimaging Centre, Lund University, Lund, Sweden (M.A.); Department of Experimental and Applied Psychology, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands (S.O.D.); Department of Experimental Psychology, Utrecht University, Utrecht, the Netherlands (S.O.D.); and Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark (V.O.B.).
 Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK/Academic Neurology, Nottingham University Hospitals NHS Trust, Nottingham, UK. School of Psychology, University of Nottingham, Nottingham, UK. Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK/Academic Neurology, Nottingham University Hospitals NHS Trust, Nottingham, UK. The MetroHealth System and Case Western Reserve University, Cleveland, OH, USA. Centre for Statistics in Medicine, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK/Institute of Mental Health, Nottinghamshire Healthcare NHS Foundation Trust, Nottingham, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/National Institute for Health Research, University College London Hospitals Biomedical Research Centre, London, UK/MRC CTU at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Helen Durham Neuro-Inflammatory Unit, University Hospital of Wales, Cardiff, UK/Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK/Academic Neurology, Nottingham University Hospitals NHS Trust, Nottingham, UK.
 AUSL di Bologna, Bologna, Italia. AUSL di Bologna, Bologna, Italia. AUSL di Bologna, Bologna, Italia. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italia. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italia.
 Service de Neurologie, CHRU-Nancy, Université de Lorraine, 54000 Nancy, France. Service de Neurologie, CHRU-Nancy, Université de Lorraine, 54000 Nancy, France; Inserm, CIC-1433 Épidemiologie Clinique, CHRU-Nancy, Université de Lorraine, 54000 Nancy, France; EA 4360 APEMAC, Université de Lorraine, 54000 Nancy, France. Service de Neurologie, CHRU-Nancy, Université de Lorraine, 54000 Nancy, France. Service de Neurologie, CHRU-Nancy, Université de Lorraine, 54000 Nancy, France; Inserm, CIC-1433 Épidemiologie Clinique, CHRU-Nancy, Université de Lorraine, 54000 Nancy, France; EA 4360 APEMAC, Université de Lorraine, 54000 Nancy, France. Electronic address: m.debouverie@chru-nancy.fr.
 Rehabilitation Engineering Laboratory, Institute of Robotics and Intelligent Systems, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland. Electronic address: relab.publications@hest.ethz.ch. Rehabilitation Engineering Laboratory, Institute of Robotics and Intelligent Systems, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland; Future Health Technologies, Singapore-ETH Centre, Campus for Research Excellence And Technological Enterprise (CREATE), Singapore. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium; Universitair MS Centrum UMSC Hasselt, Pelt, Belgium. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium; Universitair MS Centrum UMSC Hasselt, Pelt, Belgium. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium; Universitair MS Centrum UMSC Hasselt, Pelt, Belgium. Rehabilitation Engineering Laboratory, Institute of Robotics and Intelligent Systems, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland; Future Health Technologies, Singapore-ETH Centre, Campus for Research Excellence And Technological Enterprise (CREATE), Singapore. Rehabilitation Engineering Laboratory, Institute of Robotics and Intelligent Systems, Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland; Future Health Technologies, Singapore-ETH Centre, Campus for Research Excellence And Technological Enterprise (CREATE), Singapore. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Hasselt, Belgium; Universitair MS Centrum UMSC Hasselt, Pelt, Belgium; Noorderhart Rehabilitation and MS Centre, Pelt, Belgium.
 Department of Pharmacology and Experimental Neuroscience, Center for Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA. Department of Pharmacology and Experimental Neuroscience, Center for Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA. Department of Pharmacology and Experimental Neuroscience, Center for Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.
 From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. riley.bove@ucsf.edu. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA. From the UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, CA.
 Department of Biochemistry, Faculty of Pharmacy, Cairo University, Kasr El Ainy st., 11562 Cairo, Egypt. Electronic address: tarek.motawi@pharma.cu.edu.eg. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Kasr El Ainy st., 11562 Cairo, Egypt. Electronic address: shohda.elmaraghy@pharma.cu.edu.eg. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Kasr El Ainy st., 11562 Cairo, Egypt. Electronic address: ahmed.seifeldin@pharma.cu.edu.eg. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Kasr El Ainy st., 11562 Cairo, Egypt. Electronic address: salma.essam@pharma.cu.edu.eg. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Kasr El Ainy st., 11562 Cairo, Egypt. Electronic address: mona.kortam@pharma.cu.edu.eg.
 From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., W.O.T., J.J.C., S.A.B., V.R., J.-M.T., Y.G., S.J.P., C.F.L., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., F.M., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Radiology (P.M.), Department of Ophthalmology (J.J.C.), Mayo Clinic, Rochester, MN; Department of Neurology (P.E.), San Antonio Military Medical Center, Fort Sam Houston, TX; Neurology Unit (F.M., M.A.R., M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Department of Neurology (N.Z.), Mayo Clinic, Scottsdale, AZ; Neurorehabilitation Unit (M.F.), IRCCS San Raffaele Scientific Institute; Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN. flanagan.eoin@mayo.edu.
 From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. From the Department of Medicine (G.F), University of Ottawa, Ottawa Hospital Research Institute; Montreal Neurological Institute (A.C.P., S.N., D.L.A., D.L.C.), McGill University, Quebec; Department of Community Health Sciences (J.O.M., R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Nuffield Department of Clinical Neurosciences (P.W.), John Radcliffe Hospital, University of Oxford, United Kingdom; Department of Pediatrics (E.A.Y.), University of Toronto, Ontario, Canada; Center for Neuroinflammation and Neurotherapeutics (A.B.-O.), and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia; Department of Internal Medicine (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; and Division of Child Neurology (B.B.), Department of Neurology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania. banwellb@email.chop.edu.
 Axe Neuroscience, Centre de Recherche du CHU de Québec - Université Laval, Québec, Québec, Canada. Département de Médecine Moléculaire de la Faculté de Médecine, Université Laval, Québec, Québec, Canada. Axe Neuroscience, Centre de Recherche du CHU de Québec - Université Laval, Québec, Québec, Canada. Département de Médecine Moléculaire de la Faculté de Médecine, Université Laval, Québec, Québec, Canada. Axe Neuroscience, Centre de Recherche du CHU de Québec - Université Laval, Québec, Québec, Canada. Département de Médecine Moléculaire de la Faculté de Médecine, Université Laval, Québec, Québec, Canada. Axe Neuroscience, Centre de Recherche du CHU de Québec - Université Laval, Québec, Québec, Canada. david.gosselin@crchudequebec.ulaval.ca. Département de Médecine Moléculaire de la Faculté de Médecine, Université Laval, Québec, Québec, Canada. david.gosselin@crchudequebec.ulaval.ca.
 Predictive Medicine Group, Boston Children's Hospital Informatics Program, Boston, MA, United States of America. Technion, Israeli Institute of Technology, Haifa, Israel. Partners Research Information Systems and Computing, Boston, MA, United States of America. Predictive Medicine Group, Boston Children's Hospital Informatics Program, Boston, MA, United States of America. Department of Psychiatry, Massachusetts General Hospital, Boston, MA, United States of America. Department of Psychology, Harvard University, Boston, MA, United States of America. Department of Psychiatry, Massachusetts General Hospital, Boston, MA, United States of America. Psychiatric and Neurodevelopmental Genetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, United States of America. Harvard Medical School, Boston, MA, United States of America. Predictive Medicine Group, Boston Children's Hospital Informatics Program, Boston, MA, United States of America. Harvard Medical School, Boston, MA, United States of America.
 Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Department of Neurology, University Hospital Zurich, Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland. Neurocentre, Lucerne Cantonal Hospital, Lucerne, Switzerland; Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. Neurocentre, Lucerne Cantonal Hospital, Lucerne, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Department of Psychiatry, Psychotherapy and Psychosomatics, Psychiatric University Hospital Zurich (PUK), Zurich, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, Ospedale Regionale di Lugano, EOC, Lugano, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, Ospedale Regionale di Lugano, EOC, Lugano, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich (UZH), Zurich, Switzerland; Institute for Implementation Science in Health Care, University of Zurich (UZH), Zurich, Switzerland. Electronic address: viktor.vonwyl@uzh.ch.
 Emory University School of Medicine, Atlanta, Georgia. Division of Pediatric Neurology, Emory University, Children's Healthcare of Atlanta, Atlanta, Georgia. Electronic address: ggombol@emory.edu.
 Department of Anatomical Sciences, Medical School, Baqiyatallah University of Medical Sciences, Tehran, Iran. Department of Anatomical Sciences, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran. Baqiyatallah Research Center for Gastroenterology and Liver Diseases (BRCGL), Baqiyatallah University of Medical Sciences, Tehran, Iran. Health Research Center, Life Style Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran. Applied Virology Research Center, Medical School, Baqiyatallah University of Medical Sciences, Tehran, Iran.
 Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan. Department of Infectious Disease Control, Faculty of Medicine, Japan; Research Center for GLOBAL and LOCAL Infectious Diseases, Oita University, Oita, Japan. Electronic address: takashik@oita-u.ac.jp.
 Neuroimmunology Unit, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. PhD Program in Molecular Biosciences, Doctoral School, Universidad Autónoma de Madrid, Madrid, Spain. Bioinformatics Unit, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. Department of Neurology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain. Demyelinating Diseases Unit, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain. School of Mathematics, University of Edinburgh, Edinburgh, United Kingdom. Bioinformatics Unit, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. Flow Cytometry Core Facility, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. Sequencing Core Facility, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. Department of Neurology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain. Radiodiagnostic Division, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain. Neuroimmunology Unit, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. Neuroimmunology Unit, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. Department of Neurology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain. Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain. Red Española de Esclerosis Múltiple (REEM), Barcelona, Spain. Neuroimmunology Unit, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain. Red Española de Esclerosis Múltiple (REEM), Barcelona, Spain. Biobank, Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Madrid, Spain.
 Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Novartis Institutes for BioMedical Research (NIBR), Basel, Switzerland. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Department of Cell Biology and Physiology, Washington University in St Louis, St. Louis, MO, USA. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Neuroproteomics, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Department of Pathology and Immunology, Division of Clinical Pathology, University & University Hospitals of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, Division of Clinical Pathology, University & University Hospitals of Geneva, Geneva, Switzerland. Institute for Diabetes and Obesity, Helmholtz Zentrum München, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. Department of Neuroradiology, University Hospital Heidelberg, Heidelberg, Germany. Transgenic Core Facility, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. Institute for Diabetes and Obesity, Helmholtz Zentrum München, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Department of Pathology and Immunology, Division of Clinical Pathology, University & University Hospitals of Geneva, Geneva, Switzerland. German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Neuroproteomics, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität (LMU) München, Munich, Germany. martin.kerschensteiner@med.uni-muenchen.de. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. martin.kerschensteiner@med.uni-muenchen.de. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. martin.kerschensteiner@med.uni-muenchen.de. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. thomas.misgeld@tum.de. German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. thomas.misgeld@tum.de. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. thomas.misgeld@tum.de.
 Rocky Mountain Multiple Sclerosis Clinic, Salt Lake City, UT, USA. Biogen, Cambridge, MA, USA. Rocky Mountain Multiple Sclerosis Clinic, Salt Lake City, UT, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA.
 Department of Radiology, Stanford University. Department of Radiology, Stanford University. Department of Radiology, Stanford University. Department of Radiology, Stanford University. Department of Radiology, Stanford University. Department of Radiology, Stanford University. Department of Radiology, Stanford University; Department of Neurology and Neurological Sciences, Stanford University; mljames@stanford.edu.
 Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
 Department of Forensic Medicine, Defense Institute of Forensic Science, Criminal Investigation Command, Ministry of National Defense, Seoul, Korea. Department of Forensic Medicine, Defense Institute of Forensic Science, Criminal Investigation Command, Ministry of National Defense, Seoul, Korea. Department of Forensic Medicine, Defense Institute of Forensic Science, Criminal Investigation Command, Ministry of National Defense, Seoul, Korea. Department of Forensic Medicine, Defense Institute of Forensic Science, Criminal Investigation Command, Ministry of National Defense, Seoul, Korea. Department of Forensic Medicine, Defense Institute of Forensic Science, Criminal Investigation Command, Ministry of National Defense, Seoul, Korea. Department of Forensic Medicine, Defense Institute of Forensic Science, Criminal Investigation Command, Ministry of National Defense, Seoul, Korea. sanghan111@gmail.com. Department of Pathology and Translational Genomics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. ylsuh76@skku.edu.
 IRCCS, Fondazione Santa Lucia, 00179 Rome, Italy. PhD Program in Evolutionary Biology and Ecology, Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy; Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Laboratory of Resolution of Neuroinflammation, IRCCS Santa Lucia Foundation, 00179 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. The State Key Laboratory of Pharmaceutical Biotechnology; Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong SAR, China. The State Key Laboratory of Pharmaceutical Biotechnology; Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong SAR, China; Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. The State Key Laboratory of Pharmaceutical Biotechnology; Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong SAR, China. The State Key Laboratory of Pharmaceutical Biotechnology; Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Resolution of Neuroinflammation, IRCCS Santa Lucia Foundation, 00179 Rome, Italy; PhD program in Immunology, Molecular Medicine and Applied biotechnologies, University of Rome Tor Vergata, 00133 Rome, Italy. Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea. Pathology Unit, University Hospital Campus Bio-Medico of Rome, 00128 Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Pisana, 00163 Rome, Italy. Department of Systems Medicine, Tor Vergata University, 00133 Rome, Italy; Unit of Neurology, IRCCS Neuromed, 86077 Pozzilli, Italy. PhD Program in Evolutionary Biology and Ecology, Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy; Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Neurology Unit, Fondazione PTV Policlinico Tor Vergata, Viale Oxford 81, 00133 Rome, Italy. Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; Brain Science and Engineering Institute, Kyungpook National University, Daegu 41944, Republic of Korea. Department of Systems Medicine, Tor Vergata University, 00133 Rome, Italy; Unit of Neurology, IRCCS Neuromed, 86077 Pozzilli, Italy. The State Key Laboratory of Pharmaceutical Biotechnology; Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Resolution of Neuroinflammation, IRCCS Santa Lucia Foundation, 00179 Rome, Italy; Institute of Translational Pharmacology, National Research Council, 00133 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. IRCCS, Fondazione Santa Lucia, 00179 Rome, Italy; Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Electronic address: daniele.lettieri.barbato@uniroma2.it.
 From the Turku PET Centre (E.P., M.M., M.N., M.S., L.M.A.); Clinical Neurosciences (E.P., M.N., M.S., L.M.A.), University of Turku; Faculty of Science and Engineering (M.M.), Åbo Akademi University; and Neurocenter (M.S., L.M.A.), Turku University Hospital, Finland. From the Turku PET Centre (E.P., M.M., M.N., M.S., L.M.A.); Clinical Neurosciences (E.P., M.N., M.S., L.M.A.), University of Turku; Faculty of Science and Engineering (M.M.), Åbo Akademi University; and Neurocenter (M.S., L.M.A.), Turku University Hospital, Finland. From the Turku PET Centre (E.P., M.M., M.N., M.S., L.M.A.); Clinical Neurosciences (E.P., M.N., M.S., L.M.A.), University of Turku; Faculty of Science and Engineering (M.M.), Åbo Akademi University; and Neurocenter (M.S., L.M.A.), Turku University Hospital, Finland. From the Turku PET Centre (E.P., M.M., M.N., M.S., L.M.A.); Clinical Neurosciences (E.P., M.N., M.S., L.M.A.), University of Turku; Faculty of Science and Engineering (M.M.), Åbo Akademi University; and Neurocenter (M.S., L.M.A.), Turku University Hospital, Finland. From the Turku PET Centre (E.P., M.M., M.N., M.S., L.M.A.); Clinical Neurosciences (E.P., M.N., M.S., L.M.A.), University of Turku; Faculty of Science and Engineering (M.M.), Åbo Akademi University; and Neurocenter (M.S., L.M.A.), Turku University Hospital, Finland. laura.airas@utu.fi.
 Department of Physical and Rehabilitation Medicine, Raymond-Poincaré Teaching Hospital, APHP, Université Paris-Saclay, 92380 Garches, France. Unité INSERM 1179, University of Versailles Saint-Quentin-en-Yvelines, 78180 Montigny-Le-Bretonneux, France. PKCS, 69130 Ecully, France. Ipsen, 92100 Boulogne-Billancourt, France. Ipsen, 92100 Boulogne-Billancourt, France. Department of Physical and Rehabilitation Medicine, Raymond-Poincaré Teaching Hospital, APHP, Université Paris-Saclay, 92380 Garches, France. Unité INSERM 1179, University of Versailles Saint-Quentin-en-Yvelines, 78180 Montigny-Le-Bretonneux, France.
 DNA Laboratory, Analytical Laboratories, Hamilton, New Zealand. National Standard Organization of Iran, Tehran, Iran. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran. Department of Immunology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran; Department of Physiology and Pharmacology, Faculty of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Electronic address: m.godarzvand@abzums.ac.ir.

 Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy (L.P., A.T.); Rehabilitation in Multiple Sclerosis (RIMS), Leuven, Belgium (L.P., C.S.-M., K.N., L.M., T.S., E.C.A., M.L.L., Y.L., A.K., F.G., U.N., D.K., J.J., S.C., A.T.); Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Neurology-Neuroimmunology Department & Neurorehabilitation Unit, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain (C.S.-M.); Department of Physiotherapy, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain (C.S.-M.); Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic (K.N.); Department of Rehabilitation Medicine, First Faculty of Medicine and General University Hospital in Prague, Prague, Czech Republic (K.N.); UMSC Hasselt, Pelt, Belgium (L.M.); REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, Diepenbeek, Belgium (L.M.); IPEM Institute of Psychoacoustics and Electronic Music, Faculty of Arts and Philosophy, Ghent University, Gent, Belgium (L.M.); The Norwegian Multiple Sclerosis Competence Centre, Department of Neurology, Haukeland University Hospital, Bergen, Norway (T.S.); The Norwegian Multiple Sclerosis Registry and Biobank, Department of Neurology, Haukeland University Hospital, Bergen, Norway (T.S.); Department of Physiotherapy, Haukeland University Hospital, Bergen, Norway (T.S.); Faculty of Nursing and Health Science, Nord University, Bodø, Norway (E.C.A.); Department of Health and Work, Nordland Hospital Trust, Bodø, Norway (E.C.A.); Centre for Health, Activity and Rehabilitation Research, Queen Margaret University, Edinburgh, Musselburgh, United Kingdom (M.L.L.); Discipline of Exercise Science, Murdoch University, Perth, Australia (Y.L.); Centre for Molecular Medicine and Innovative Therapeutics, and Centre for Healthy Ageing, Murdoch University, Perth, Australia (Y.L.); Perron Institute for Neurological and Translational Science, Perth, Australia (Y.L.); Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel (A.K.); Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, Israel (A.K.); Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Istanbul University-Cerrahpasa, Istanbul, Turkey (F.G.); Centre for Physical Medicine and Rehabilitation, University Clinical Centre of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia (U.N.); Research Group for Neurorehabilitation, Department of Rehabilitation Sciences, KU Leuven, Belgium (D.K.); National Multiple Sclerosis Center Melsbroek, Melsbroek, Belgium (D.K.); IRCCS Fondazione Don Carlo Gnocchi ONLUS, Milan, Italy (J.J.); Multiple Sclerosis Society of Ireland and Physical Activity for Health Research Centre, Dublin, Ireland (S.C.); and University of Limerick, Limerick, Ireland (S.C.).
 Department of Neurology, Oslo University Hospital, Oslo, Norway makoni@ous-hf.no. Department of Neurology, Sørlandet Sykehus HF, Kristiansand, Norway. The Norwegian National Advisory Unit on Tick-borne Diseases, Arendal, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Institute of Clinical Medicine, University of Bergen, Bergen, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Department of Neurology, Sørlandet Sykehus HF, Kristiansand, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Department of Neurology, Sørlandet Sykehus HF, Kristiansand, Norway. Institute of Clinical Medicine, University of Bergen, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Norwegian MS Registry and Biobank, Haukeland University Hospital, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Norwegian MS Registry and Biobank, Haukeland University Hospital, Bergen, Norway. Department of Infectious Disease Immunology, Norwegian Institute of Public Health, Oslo, Norway. Institute of Clinical Medicine, University of Bergen, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Neurology, Akershus University Hospital, Lorenskog, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Mechanical, Electronic and Chemical Engineering, Oslo Metropolitan University, Oslo, Norway. Department of Research, Innovation and Education, Division of Clinical Neuroscience, Oslo University Hospital, Oslo, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Institute of Clinical Medicine, University of Bergen, Bergen, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Pharmacology, Oslo University Hospital, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. K.G. Jebsen Centre for B cell malignancies, University of Oslo, Oslo, Norway. Department of Microbiology, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Department of Immunology, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway.
 Department of Neurology, Washington University School of Medicine, St. Louis, Missouri. Electronic address: lghezzi@wustl.edu. Department of Neurology, Washington University School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University School of Medicine, St. Louis, Missouri; Brain and Mind Centre and Charles Perkins Centre, School of Medical Sciences, Neuroscience, University of Sydney, Sydney, New South Wales, Australia. Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri. Department of Neurology, Washington University School of Medicine, St. Louis, Missouri.
 Fischell Department of Bioengineering, University of Maryland, College Park, MD, United States. Fischell Department of Bioengineering, University of Maryland, College Park, MD, United States. US Department of Veterans Affairs, Veterans Affairs Maryland Health Care System, Baltimore, MD, United States. Robert E. Fischell Institute for Biomedical Devices, College Park, MD, United States. Department of Microbiology and Immunology, University of Maryland Medical School, Baltimore, MD, United States. Marlene and Stewart Greenebaum Cancer Center, Baltimore, MD, United States.
 Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, 75123 Uppsala, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. Institute of Environmental Medicine, Karolinska Institute, 171 77 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Institute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. mgharag1@jh.edu. Division of Neuroimmunology and Neurological Infections, Johns Hopkins Hospital, Pathology Building 509, 600 N. Wolfe St, Baltimore, MD, 21287, USA. mgharag1@jh.edu. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Neuraly Inc, Gaithersburg, MD, USA. Neuraly Inc, Gaithersburg, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. Calabresi@jhmi.edu. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, MD, 21205, USA. Calabresi@jhmi.edu. Division of Neuroimmunology and Neurological Infections, Johns Hopkins Hospital, Pathology Building 509, 600 N. Wolfe St, Baltimore, MD, 21287, USA. Calabresi@jhmi.edu.
 Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran; Institute for Brain and Cognition, Tarbiat Modares University, Tehran, Iran. Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran; Institute for Brain and Cognition, Tarbiat Modares University, Tehran, Iran; Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Electronic address: mjavan@modares.ac.ir.
 Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. Harold and Margaret Milliken Hatch Laboratory of Neuro-Endocrinology Rockefeller University, New York, NY 10065, USA. Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, NY 10065, USA. Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, NY 10065, USA. Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA.
 Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran. Institute for Futures Studies in Health, Modeling in Health Research Center, Kerman University of Medical Sciences, Kerman, Iran. Faculty of Public Health, Department of Biostatistics and Epidemiology, Kerman University of Medical Sciences, Kerman, Iran. Tehran University of Medical Sciences, Tehran, Iran. Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran. Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran. Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Biostatistics and Epidemiology, Faculty of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology and Rehabilitation Medicine, University of Cincinnati, Cincinnati, OH, USA. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. omid.mirmosayyeb@gmail.com. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. omid.mirmosayyeb@gmail.com.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, United States. Electronic address: pxzheng@uic.edu. Interdisciplinary School of Health Science, University of Ottawa, Ottawa, Ontario, Canada; Brain and Mind Research Institute, University of Ottawa, Ottawa, Ontario, Canada. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, United States. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, United States.
 Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Carenity, Paris, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France. Carenity, Paris, France. Aix Marseille Univ, Inserm, IRD, SESSTIM, Sciences Economiques & Sociales de la Santé & Traitement de l'Information Médicale, ISSPAM, Marseille, France.
 Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Electronic address: mauro_afg@hotmail.com. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil; Instituto Federal do Paraná, Palmas, PR, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil; Centro Universitário UNA, Pouso Alegre, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil; Centro de Ciências Biológicas e da Saúde, Universidade Federal do Oeste Baiano, Barreiras, BA, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Genética, Evolução e Ecologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Genética, Evolução e Ecologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Electronic address: afaria@icb.ufmg.br.
 pRED, Neuroscience, Discovery and Translational Area (NRD), F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070, Basel, Switzerland. sybille.seiler@roche.com. Biozentrum, University of Basel, Spitalstrasse 41, 4056, Basel, Switzerland. sybille.seiler@roche.com. pRED, Neuroscience, Discovery and Translational Area (NRD), F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070, Basel, Switzerland. pRED, Neuroscience, Discovery and Translational Area (NRD), F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070, Basel, Switzerland. Quantified Biology, Cornell Tech, New York, NY, 10044, USA. pRED, Neuroscience, Discovery and Translational Area (NRD), F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070, Basel, Switzerland. lynette.foo@roche.com.
 Department of Neurology, San Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy. luca.prosperini@gmail.com. Department of Neurology, San Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy. Department of Human Neurosciences, Sapienza University, Viale dell'Università 30, 00185, Rome, Italy. Neuroimmunology Unit, Santa Lucia Foundation, Via del Fosso Di Fiorano 64/65, 00143, Rome, Italy. Department of Neurology, San Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy. Department of Neurology, San Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy.
 Center for Laser Microscopy, Institute of Physiology and Biochemistry "Jean Giaja", Faculty of Biology, University of Belgrade, 11000 Belgrade, Serbia. Center for Laser Microscopy, Institute of Physiology and Biochemistry "Jean Giaja", Faculty of Biology, University of Belgrade, 11000 Belgrade, Serbia. Department of Life Sciences, Institute for Multidisciplinary Research, University of Belgrade, 11000 Belgrade, Serbia. Center for Laser Microscopy, Institute of Physiology and Biochemistry "Jean Giaja", Faculty of Biology, University of Belgrade, 11000 Belgrade, Serbia. Department of Neurophysiology, Institute for Biological Research "Siniša Stanković", National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.
 Department of Emergency Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. Department of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China. Department of Emergency Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China. The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China. The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China. The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China. The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China. Department of Internal Medicine, Medical Intensive Care Unit and Division of Respiratory Diseases, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Experimental Center of Teaching and Scientific Research, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China. The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China. Department of Rheumatology and Clinical Immunology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
 Neurology Division, University of São Paulo, Dr Enéas de Carvalho Aguiar, 255, São Paulo, Brazil. Electronic address: guilherme.diogo@hc.fm.usp.br. Neurology Division, University of São Paulo, Dr Enéas de Carvalho Aguiar, 255, São Paulo, Brazil. Neurology Division, University of São Paulo, Dr Enéas de Carvalho Aguiar, 255, São Paulo, Brazil.
 Complejo Asistencial Universitario de León, 24001 León, España. FIBAO-Hospital de Jaén, Jaén, España. Hospital Universitario Virgen Macarena, 41003 Sevilla, España. Hospital Universitario Virgen de las Nieves, 18013 Granada, España. Hospital Universitario Virgen de Valme, 41014 Sevilla, España. Hospital Regional Universitario de Málaga, Málaga, España. Hospital Universitario Virgen de la Victoria, 29010 Málaga, España. Hospital Universitario Reina Sofía, 14004 Córdoba, España. Hospital Universitario Virgen del Rocío, Sevilla, España. Hospital Universitario San Cecilio, Granada, España. Hospital Universitario Torrecárdenas, Almería, España. Hospital Universitario Juan Ramón Jiménez, Huelva, España. Hospital Universitario Virgen del Rocío, Sevilla, España. Hospital Universitario Virgen de las Nieves, 18013 Granada, España. Hospital Universitario Cruces, Baracaldo, España. Hospital Universitario Basurto, Bilbao, España.

 Vladimirsky Moscow Regional Research Clinical Institute, Moscow, Russia. Vladimirsky Moscow Regional Research Clinical Institute, Moscow, Russia. Vladimirsky Moscow Regional Research Clinical Institute, Moscow, Russia.
 Neuropsychopharmacology and Psychobiology Research Group, Department of Neuroscience, University of Cádiz, 11003, Cádiz, Spain. Ciber de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, 28029, Madrid, Spain. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. Neuropsychopharmacology and Psychobiology Research Group, Department of Neuroscience, University of Cádiz, 11003, Cádiz, Spain. Ciber de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, 28029, Madrid, Spain. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. Neuropsychopharmacology and Psychobiology Research Group, Department of Neuroscience, University of Cádiz, 11003, Cádiz, Spain. Ciber de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, 28029, Madrid, Spain. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. Ciber de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, 28029, Madrid, Spain. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. Neuropsychopharmacology and Psychobiology Research Group, Department of Cell Biology and Histology, University of Cádiz, 11003, Cádiz, Spain. Neuropsychopharmacology and Psychobiology Research Group, Department of Neuroscience, University of Cádiz, 11003, Cádiz, Spain. Ciber de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, 28029, Madrid, Spain. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. Department of Biomedicine, Biotechnology and Public Health (Immunology Area), University of Cádiz, 11003, Cádiz, Spain. Neuropsychopharmacology and Psychobiology Research Group, Department of Neuroscience, University of Cádiz, 11003, Cádiz, Spain. esther.berrocoso@uca.es. Ciber de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, 28029, Madrid, Spain. esther.berrocoso@uca.es. Instituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Hospital Universitario Puerta del Mar, 11009, Cádiz, Spain. esther.berrocoso@uca.es.
 Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria. Research Management (RM): Biostatistics and Publication of Clinical Studies Team, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Ophthalmology and Optometry, Paracelsus Medical University, 5020 Salzburg, Austria. Research Program Experimental Ophthalmology and Glaucoma Research, Paracelsus Medical University, 5020 Salzburg, Austria. Division of Neuroradiology, Christian Doppler Medical Center, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Medical University of Graz, 8036 Graz, Austria. Department of Neurology, Medical University of Graz, 8036 Graz, Austria. Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria. Neuroscience Institute, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria. Department of Dermatology and Allergology, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University and Center for Cognitive Neuroscience, European Reference Network EpiCARE, 5020 Salzburg, Austria.
 Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Departments of Neurology and Ophthalmology, Mayo Clinic, Rochester, MN, USA. Departments of Neurology and Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Departments of Neurology and Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
 Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany. Department of Neurology, Kliniken Valens, Rehabilitation Centre Valens, Valens, Switzerland. Department of Health, OST-Eastern Swiss University of Applied Sciences, St. Gallen, Switzerland. Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany. Sportmed-Cardiomed, Linz, Austria. University Clinic for Hematology and Internal Oncology, Kepler University Hospital Linz, Johannes Kepler University Linz, Linz, Austria. Department of Neurology, Kliniken Valens, Rehabilitation Centre Valens, Valens, Switzerland. Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany.
 Dipartimento di Scienze della Vita e Sanità Pubblica, Università Cattolica del Sacro Cuore, 00168 Rome, Italy. Dipartimento di Scienze della Vita e Sanità Pubblica, Università Cattolica del Sacro Cuore, 00168 Rome, Italy. Dipartimento di Scienze della Vita e Sanità Pubblica, Università Cattolica del Sacro Cuore, 00168 Rome, Italy. Fondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy. Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Rome, Italy. Dipartimento di Medicina, Università di LUM, 70010 Casamassima, Italy. Istituto di Scienze e Tecnologie Chimiche "Giulio Natta" SCITEC, Centro Nazionale delle Ricerche, 20133 Rome, Italy. Dipartimento di Medicina e Chirurgia, Università di Perugia, 06123 Perugia, Italy.
 Department of Sport Science, Sports Research Centre, Miguel Hernández University of Elche, Elche, Alicante, Spain. Department of Sport Science, Sports Research Centre, Miguel Hernández University of Elche, Elche, Alicante, Spain. Department of Sport Science, Sports Research Centre, Miguel Hernández University of Elche, Elche, Alicante, Spain. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Department of Sport Science, Sports Research Centre, Miguel Hernández University of Elche, Elche, Alicante, Spain; Institute for Health and Biomedical Research (ISABIAL Foundation), Miguel Hernández University of Elche, Alicante, Spain. Electronic address: dbarbado@umh.es. Department of Sport Science, Sports Research Centre, Miguel Hernández University of Elche, Elche, Alicante, Spain; Institute for Health and Biomedical Research (ISABIAL Foundation), Miguel Hernández University of Elche, Alicante, Spain.
 Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neuroradiology, Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires La Pitié Salpêtrière - Sorbonne Université, Paris, France. Department of Neuroradiology, Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts, Paris, France. Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Department of Neurology, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Lyon, France. Department of Radiology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neuro-Ophthalmolology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Immunology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Pitié-Salpêtrière, Paris, France. Department of Immunology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Pitié-Salpêtrière, Paris, France. Department of Neurology, Centre de référence des maladies inflammatoires rares du cerveau et de la moelle (MIRCEM). Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires La Pitié Salpêtrière- Sorbonne Université, Paris, France. Department of Immunology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Pitié-Salpêtrière, Paris, France. Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Sorbonne Université, Inserm, Paris, France.
 Institute of Neuropathology, University Medical Center, Göttingen, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin, Berlin, Germany. Max-Delbrück-Center for Molecular Medicine, Berlin, Germany. Institute of Neuropathology, University Medical Center, Göttingen, Germany. Department of Neurology, University Medical Center, Göttingen, Germany. Fraunhofer Institute for Translational Medicine and Pharmacology, Göttingen, Germany.
 Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. National Research Center for the Control and Prevention of Infectious Disease, Nagasaki University, Nagasaki, Japan. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Autoimmunity Biological Solutions, Galveston, United States. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Human Pathophysiology and Translational Medicine Program, Institute for Translational Sciences, University of Texas Medical Branch, Galveston, United States. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Department of Molecular Genetics and Microbiology, Duke University, Durham, United States. Department of Molecular Genetics and Microbiology, Duke University, Durham, United States. Duke Molecular Physiology Institute, Duke University, Durham, United States. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Department of Preventive Medicine and Population Health, University of Texas Medical Branch, Galveston, United States. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Department of Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, United States. Department of Molecular Genetics and Microbiology, Duke University, Durham, United States. Duke Molecular Physiology Institute, Duke University, Durham, United States. Department of Neurology, Duke University School of Medicine, Durham, United States. Department of Molecular Genetics and Microbiology, Duke University, Durham, United States. Division of Infectious Diseases, Department of Medicine, Duke University, Durham, United States. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Transplant Division, Department of Surgery, University of Texas Medical Branch, Galveston, United States. Institute of Human Infections and Immunity, University of Texas Medical Branch, Galveston, United States. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, United States. Department of Internal Medicine, University of Texas Medical Branch, Galveston, United States. Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, United States.
 Faculty of Medicine and Life Sciences, Sports Medicine Research Center, SMRC, BIOMED, Biomedical Research Institute, Hasselt University, Hasselt, Belgium. Department of Nutrition and Movement Sciences, Faculty of Health, Medicine and Life Sciences, NUTRIM, School for Nutrition and Translation Research Maastricht, Maastricht University, Maastricht, Netherlands. University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. Faculty of Medicine and Life Sciences, Sports Medicine Research Center, SMRC, BIOMED, Biomedical Research Institute, Hasselt University, Hasselt, Belgium. Department of Nutrition and Movement Sciences, Faculty of Health, Medicine and Life Sciences, NUTRIM, School for Nutrition and Translation Research Maastricht, Maastricht University, Maastricht, Netherlands. Faculty of Rehabilitation Sciences, REVAL-Rehabilitation Research Center, Hasselt University, Hasselt, Belgium. Department of Public Health and Primary Care, KU Leuven, Leuven, Belgium. Faculty of Medicine and Life Sciences, Sports Medicine Research Center, SMRC, BIOMED, Biomedical Research Institute, Hasselt University, Hasselt, Belgium. University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. Department of Movement and Sports Sciences, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium. Department of Nutrition and Movement Sciences, Faculty of Health, Medicine and Life Sciences, NUTRIM, School for Nutrition and Translation Research Maastricht, Maastricht University, Maastricht, Netherlands. Faculty of Medicine and Life Sciences, Sports Medicine Research Center, SMRC, BIOMED, Biomedical Research Institute, Hasselt University, Hasselt, Belgium. University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium.
 School of Pharmacy and Biomolecular Sciences, Royal College of Surgeons in Ireland, Dublin, Ireland. SFI Centre for Research Training in Genomics Data Sciences, University of Galway, H91 TK33, Galway, Ireland. FutureNeuro SFI Research Centre, Royal College of Surgeons in Ireland, Dublin, Ireland. School of Pharmacy and Biomolecular Sciences, Royal College of Surgeons in Ireland, Dublin, Ireland. Genomic Oncology Research Group, Department of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland. simonfurney@rcsi.ie.
 Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Research Centre, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran. Clinical Research Development Unit, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Research Centre, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Research Centre, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Research Centre, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Biostatistics and Epidemiology, School of Health, Management and Social, Determinants of Health Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: boostanir@mums.ac.ir. Rheumatic Diseases Research Centre, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: Rafatpanahh@mums.ac.ir.
 College of Medicine and Health, University of Exeter, Exeter, UK geraldine.goldsmith@nhs.net. College of Medicine and Health, University of Exeter, Exeter, UK. College of Medicine and Health, University of Exeter, Exeter, UK. Faculty of Health, School of Health Professions, University of Plymouth, Plymouth, UK. College of Medicine and Health, University of Exeter, Exeter, UK.
 School of Communication Sciences and Disorders, The University of Memphis, TN.
 Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL; Department of Kinesiology, Health Promotion, and Recreation, University of North Texas, Denton, TX. Electronic address: stephanie.silveira@unt.edu. Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL; Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL. Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL; Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL.
 Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Venom and Biotherapeutics Molecules Lab, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran. Electronic address: rasul.micro92@gmail.com.
 Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China; Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei, Anhui, China. Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China. Electronic address: jiangzhengxuan@ahmu.edu.cn. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Electronic address: panhaifeng@ahmu.edu.cn.
 Department of Radiodiagnosis, Radio-Diagnosis, Pacific Institute of Medical Sciences, Udaipur, Rajasthan, India. Department of Radiodiagnosis, Radio-Diagnosis, Pacific Institute of Medical Sciences, Udaipur, Rajasthan, India. Department of Radiodiagnosis, Radio-Diagnosis, Pacific Institute of Medical Sciences, Udaipur, Rajasthan, India. Department of Radiodiagnosis, Radio-Diagnosis, Pacific Institute of Medical Sciences, Udaipur, Rajasthan, India.
 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli, Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow, 226002, Uttar Pradesh, India. Department of Regulatory Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli, Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow, 226002, Uttar Pradesh, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli, Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow, 226002, Uttar Pradesh, India. rakesh.singh@niperraebareli.edu.in.
 School of Physical Therapy and Rehabilitation, Kırşehir Ahi Evran University, Kırşehir, Turkey. School of Physical Therapy and Rehabilitation, Kırşehir Ahi Evran University, Kırşehir, Turkey. School of Physical Therapy and Rehabilitation, Kırşehir Ahi Evran University, Kırşehir, Turkey. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Muş Alparslan University, Muş, Turkey. Department of Neurology, Faculty of Medicine, Kırşehir Ahi Evran University, Kırşehir, Turkey.
 Department of Rheumatology and Immunology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH 44106, USA. Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA. Sinopharm Dongfeng General Hospital (Hubei Clinical Research Center of Hypertension), Hubei University of Medicine, Shiyan, Hubei 442000, China. Sinopharm Dongfeng General Hospital (Hubei Clinical Research Center of Hypertension), Hubei University of Medicine, Shiyan, Hubei 442000, China. Sinopharm Dongfeng General Hospital (Hubei Clinical Research Center of Hypertension), Hubei University of Medicine, Shiyan, Hubei 442000, China. Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Rheumatology, Jiangxi Provincial People's Hospital, Nanchang, Jiangxi 330006, China. Electronic address: lh-duan@163.com. Department of Rheumatology and Immunology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China. Electronic address: tjhdongll@163.com. Department of Rheumatology and Immunology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH 44106, USA; Institute of Allergy and Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China; Key Laboratory of Vascular Aging (HUST), Ministry of Education, Wuhan, Hubei 430030, China. Electronic address: jxzhong@tjh.tjmu.edu.cn.
 Pediatric Immunology, Hematology and Rheumatology Unit, Necker-Enfants Malades Hospital, Assistance Publique-Hopitaux de Paris, Université de Paris, Paris, France. Electronic address: pierre.quartier@aphp.fr. Department of Internal Medicine and Clinical Immunology, RHU IMAP, Sorbonne University, AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Paris, France. Electronic address: david.saadoun@aphp.fr. Department of Pediatric Nephrology, Rheumatology, Dermatology, Mère-Enfant Hospital, Hospices Civils de Lyon, Université Claude Bernard-Lyon 1, 69500 Bron, France. Department of Ophthalmology, Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts, Paris, France. Department of Internal Medicine and Clinical Immunology, CHU La Conception, Assistance Publique-Hôpitaux de Marseille (AP-HM), Marseille, France. Department of Ophthalmology, Hôpital universitaire de la Croix-Rousse, Hospices Civils de Lyon, Lyon, France. Department of Pediatric Rheumatology, CHU de Bicêtre, APHP, University of Paris Saclay, Le Kremlin Biĉetre, France. Departement of rhumatology, Hôpital Cochin, Université de Paris, Paris, France. Department of Ophthalmology, Université de Paris, Hôpital Cochin, Paris, France. Departement of rhumatology, Toulouse University Hospital (CHU de Toulouse), 330 Avenue de Grande-Bretagne, 31300 Toulouse, France. Department of Internal Medicine, Croix-Rousse University Hospital, Hospices Civils de Lyon, Université Claude Bernard-Lyon 1, 69004 Lyon, France. Paediatric Rheumatology Unit, Centre Hospitalier Universitaire de Clocheville, Tours, France. Department of Ophthalmology, Centre Hospitalier Universitaire de Nantes, 44000 Nantes, France. Departement of Ophthalmology, IHU FOReSIGHT, Sorbonne University, APHP, Paris, France. Electronic address: bahram.bodaghi@aphp.fr.
 Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Washington University in St. Louis, St. Louis, MO 63130, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94305, USA. Division of Hematology, Department of Oncology, Geneva University Hospitals, Geneva 1205, Switzerland. Translational Research Centre in Onco-Haematology, Faculty of Medicine, University of Geneva, Geneva 1205, Switzerland. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94305, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Pathology, Stanford University, Stanford, CA 94305, USA. Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94305, USA. Chan Zuckerberg Biohub, San Francisco, CA 94158, USA. Department of Radiology, Stanford University, Stanford, CA 94305, USA. Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94305, USA.
 Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians University Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians University Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians University Munich, Munich, Germany. joachim.havla@med.uni-muenchen.de. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. joachim.havla@med.uni-muenchen.de.
 Department of Medicine, Viborg Regional Hospital, Viborg, Denmark. as.greve.munch@midt.rm.dk. Department of Neurology, Viborg Regional Hospital, Viborg, Denmark. Department of Pathology, Aarhus University Hospital, Aarhus, Denmark. Department of Medicine, Viborg Regional Hospital, Viborg, Denmark. Research Unit of Multimorbidity, Viborg Regional Hospital, Viborg, Denmark.
 From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. From the Experimental Medicine Program (L.L., J.A.A.-Z., M.E.), Division of Rheumatology (J.A.A.-Z.), Department of Medicine, Division of Neurology (H.T.), Faculty of Medicine, and Departments of Ophthalmology and Visual Sciences (M.E.), Medicine and Pharmacology, University of British Columbia, Vancouver; Arthritis Research Canada (L.L., J.A.A.-Z., H.X.), Vancouver, British Columbia; Departments of Internal Medicine (C.N.B., R.A.M.) and Community Health Sciences (R.A.M.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; Departments of Medicine and Community Health Sciences (G.G.K.), University of Calgary, Alberta; The Djavad Mowafaghian Centre for Brain Health (H.T.), Vancouver, British Columbia; Faculty of Health Sciences (H.X.), Simon Fraser University, Burnaby, British Columbia; and Department of Community Health and Epidemiology (J.-N.P.-S.), College of Medicine, University of Saskatchewan, Saskatoon, Canada. etminanm@mail.ubc.ca.
 Institute of Human Genetics, Universitätsklinikum Schleswig-Holstein, University of Lübeck and University of Kiel, 23562, Lübeck, Germany. Institute of Human Genetics, Universitätsklinikum Schleswig-Holstein, University of Lübeck and University of Kiel, 23562, Lübeck, Germany. malte.spielmann@uksh.de. Human Molecular Genomics Group, Max Planck Institute for Molecular Genetics, 14195, Berlin, Germany. malte.spielmann@uksh.de. German Centre for Cardiovascular Research (DZHK), Partner Site Hamburg/Lübeck/Kiel, 23562, Lübeck, Germany. malte.spielmann@uksh.de.
 Department of Pharmaceutical Sciences, State University of New York, Buffalo, New York, USA. Department of Biotechnical and Clinical Laboratory Sciences, State University of New York, Buffalo, New York, USA. Department of Biotechnical and Clinical Laboratory Sciences, State University of New York, Buffalo, New York, USA. Department of Pharmaceutical Sciences, State University of New York, Buffalo, New York, USA. Buffalo Neuroimaging Analysis Center, State University of New York, Buffalo, New York, USA. Department of Neurology, State University of New York, Buffalo, New York, USA. Buffalo Neuroimaging Analysis Center, State University of New York, Buffalo, New York, USA. Department of Neurology, State University of New York, Buffalo, New York, USA. Department of Pharmaceutical Sciences, State University of New York, Buffalo, New York, USA. Department of Neurology, State University of New York, Buffalo, New York, USA.
 Department of Physiology, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, Australia. Electronic address: pippaiva21@gmail.com. Department of Physiology, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, Australia. Department of Neurosciences, Central Clinical School, Alfred Hospital, Monash University, Melbourne, VIC, Australia. Department of Neurosciences, Central Clinical School, Alfred Hospital, Monash University, Melbourne, VIC, Australia. Department of Neurosciences, Central Clinical School, Alfred Hospital, Monash University, Melbourne, VIC, Australia. Department of Physiology, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, Australia. Department of Neurosciences, Central Clinical School, Alfred Hospital, Monash University, Melbourne, VIC, Australia. Department of Physiology, Biomedicine Discovery Institute, Monash University, Melbourne, VIC, Australia.
 Department of Neuroscience, Monash University, Melbourne, VIC, Australia.
 Department of Prevention & Healthcare, Southwest Hospital, Third Military Medical University, 400038 Chongqing, China. Department of Hepatobiliary & Pancreatic Surgery, The Fifth People's Hospital of Chongqing, 400062 Chongqing, China. Department of Neurology, Southwest Hospital, Third Military Medical University, 400038 Chongqing, China.
 Department of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. Department of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran. Department of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. Traditional and Complementary Medicine Research Center (TCMRC), Arak University of Medical Sciences, Arak, Iran. Department of Immunology, School of Medicine, Arak University of Medical Sciences, Arak, Iran. Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Iran.
 Cerrahpaşa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Electronic address: tutuncumelih@iuc.edu.tr. Neurology Department, Sancaktepe Şehit Prof. Dr. Ilhan Varank Research and Training Hospital, Istanbul, Turkey. Faculty of Medicine, Department of Physiology, Ondokuz Mayıs University, Samsun, Turkey. Faculty Of Pharmacy, Department Of Pharmaceutical Microbiology, Bezmialem Vakıf University, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Ondokuz Mayıs University, Samsun, Turkey. Istanbul Faculty of Medicine, Department of Neurology, Istanbul University, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Katip Celebi University, Izmir, Turkey. Faculty of Medicine, Department of Neurology, Selçuk University, Konya, Turkey. Department of Neurology, Istanbul Bakırköy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Education and Research Hospital, Istanbul, Turkey. Cerrahpaşa Faculty of Medicine, Department of Medical Microbiology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Dokuz Eylül University, Izmir, Turkey. Department of Neurology, Istanbul Bakırköy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Education and Research Hospital, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Kocaeli University, İzmit/Kocaeli, Turkey. Cerrahpaşa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Neurology Department, Sancaktepe Şehit Prof. Dr. Ilhan Varank Research and Training Hospital, Istanbul, Turkey. Department of Neurosciences, Dokuz Eylül University, Institute of Health Sciences, Izmir, Turkey. Faculty of Medicine, Department of Neurology, Haccettepe University, Ankara, Turkey. Faculty of Medicine, Department of Neurology, Uludag University, Bursa, Turkey. Cerrahpaşa Faculty of Medicine, Department of Hematology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Cerrahpaşa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Istanbul Faculty of Medicine, Department of Neurology, Istanbul University, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Katip Celebi University, Izmir, Turkey. Neurology Department, Sancaktepe Şehit Prof. Dr. Ilhan Varank Research and Training Hospital, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Uludag University, Bursa, Turkey. Faculty of Medicine, Department of Neurology, Karadeniz Technical University, Trabzon, Turkey. Faculty of Medicine, Department of Neurology, Ondokuz Mayıs University, Samsun, Turkey. Faculty of Medicine, Department of Neurology, Haccettepe University, Ankara, Turkey. Cerrahpaşa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Haccettepe University, Ankara, Turkey. Cerrahpaşa Faculty of Medicine, Department of Microbiology, Istanbul University-Cerrahpaşa, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Kocaeli University, İzmit/Kocaeli, Turkey. Faculty of Medicine, Department of Biostatistics and Medical Informatics, Akdeniz University, Antalya, Turkey. Cerrahpaşa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpaşa, Istanbul, Turkey; Faculty of Medicine, Department of Neurology, Uludag University, Bursa, Turkey.
 Institute of Clinical Exercise & Health Sciences, School of Science and Sport, University of the West of Scotland, Stephenson Place, Hamilton International Technology Park, South Lanarkshire, Scotland G72 0HL, United Kingdom. Electronic address: eilidh.macdonald@uws.ac.uk. Institute of Clinical Exercise & Health Sciences, School of Science and Sport, University of the West of Scotland, Stephenson Place, Hamilton International Technology Park, South Lanarkshire, Scotland G72 0HL, United Kingdom. Institute of Clinical Exercise & Health Sciences, School of Science and Sport, University of the West of Scotland, Stephenson Place, Hamilton International Technology Park, South Lanarkshire, Scotland G72 0HL, United Kingdom. Douglas Grant Rehabilitation Unit, Ayrshire Central Hospital, Kilwinning Road, Irvine, Ayrshire, Scotland KA12 8SS, United Kingdom. Institute of Clinical Exercise & Health Sciences, School of Science and Sport, University of the West of Scotland, Stephenson Place, Hamilton International Technology Park, South Lanarkshire, Scotland G72 0HL, United Kingdom.
 Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA. Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA. Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, MI, USA. Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, MI, USA. Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, MI, USA/Division of Multiple Sclerosis and Clinical Neuroimmunology, Department of Neurology, University of Michigan, Ann Arbor, MI, USA.
 Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy; Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli, IS, Italy. Department of Neurosciences, Mental Health, and Sensory Organs (NESMOS), Sapienza, University of Rome, Rome, Italy. Department of Neurosciences, Mental Health, and Sensory Organs (NESMOS), Sapienza, University of Rome, Rome, Italy. IRCCS Neuromed, Pozzilli, IS, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. S. Filippo Neri Hospital, Rome, Italy. S. Filippo Neri Hospital, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. IRCCS Neuromed, Pozzilli, IS, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli, IS, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. S. Filippo Neri Hospital, Rome, Italy. IRCCS Neuromed, Pozzilli, IS, Italy; Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. IRCCS Neuromed, Pozzilli, IS, Italy; Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. IRCCS Neuromed, Pozzilli, IS, Italy; Department of Neurosciences, Mental Health, and Sensory Organs (NESMOS), Sapienza, University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli, IS, Italy. Electronic address: antonella.conte@uniroma1.it.
 Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Adnan Saygun Caddesi, 06100-Samanpazari, Ankara, Turkey. Electronic address: ecemkaranfil@windowslive.com. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Adnan Saygun Caddesi, 06100-Samanpazari, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Adnan Saygun Caddesi, 06100-Samanpazari, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Adnan Saygun Caddesi, 06100-Samanpazari, Ankara, Turkey. Faculty of Medicine, Department of Neurology, Hacettepe University, Adnan Saygun Caddesi, 06100-Samanpazari, Ankara, Turkey.
 Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Interdisciplinary Division of Neuro-Oncology, Center for Neuro-Oncology, Comprehensive Cancer Center Tübingen Stuttgart, University Hospital Tübingen, Eberhard-Karls University Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Department of Neurology & Stroke, and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany.
 Department of Neurosciences, Biomedicine and Movement Sciences, Neuromotor and Cognitive Rehabilitation Research Centre (CRRNC), University of Verona, 37134 Verona, Italy. Department of Electrical and Information Engineering, Politecnico di Bari, Italy. The BioRobotics Institute, Scuola Superiore Sant'Anna, Pisa, Italy. Department of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy. San Raffaele Institute of Sulmona, Sulmona (AQ), Italy. Department of Psychology, University Sapienza of Rome, Italy. Smart Lab, IRCCS Santa Lucia Foundation, Rome, Italy. Master in Riabilitazione Neurologica, University of Verona, Italy. Fondazione IRCCS San Gerardo dei Tintori, Riabilitazione Specialistica, 20900, Monza, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, Neuromotor and Cognitive Rehabilitation Research Centre (CRRNC), University of Verona, 37134 Verona, Italy.
 Department of Neurology, Dongsan Hospital, Keimyung University School of Medicine, 1035 Dalgubeol-daero, Dalseo-gu, Daegu, 42601, Republic of Korea. Department of Neurology, Dongsan Hospital, Keimyung University School of Medicine, 1035 Dalgubeol-daero, Dalseo-gu, Daegu, 42601, Republic of Korea. shy2354@gmail.com. Department of Neurology, Korea University College of Medicine, Seoul, Republic of Korea. shy2354@gmail.com.
 Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA. Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. Molecular, Cellular and Integrative Neurosciences Program, Colorado State University, Fort Collins, CO 80523, USA.
 KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006. KOKOS-MS trial group: Anne Müller, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Beatrix Münzberg, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Clemens Warnke, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Dirk Müller, is from the Faculty of Medicine and University Hospital, Institute for Health Economics and Clinical Epidemiology (IGKE), University of Cologne, Cologne, Germany. Dorthe Hobus, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Gundula Palmbach, is from the Faculty of Medicine and University Hospital, Clinical Trials Centre Cologne (CTCC), University of Cologne, Cologne, Germany. Heidrun Golla, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Isabel Franke, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Kim Dillen, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Martin Hellmich, is from the Faculty of Medicine and University Hospital, Institute of Medical Statistics and Computational Biology (IMSB), University of Cologne, Cologne, Germany. Monika Höveler, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Solveig Ungeheuer, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Sophia Kochs, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Veronika Dunkl, is from the Department of Palliative Medicine, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Yasemin Göreci, is from the Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Anne Müller, MA , studied social work (BA) and rehabilitation sciences (MA). She is currently working as a researcher and case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne and perusing her PhD studies in health sciences at the University of Cologne. Kim Dillen, PhD, is a postdoctoral researcher at the Department of Palliative Medicine of the University Hospital Cologne. She has published research carried out in various patient populations and has many years of research as well as clinical experience as neuropsychologist in both Canada and Germany. Thomas Dojan, MSc, studied psychology (MSc) and philosophy (BA). He is a licensed psycho-oncologist (Deutsche Krebsgesellschaft), currently working as a researcher at the Department of Palliative Medicine of the University Hospital Cologne as well as perusing PhD studies in philosophy at the University of Cologne and The Polish Academy of Sciences. Solveig Ungeheuer, BA, worked as a palliative care nurse and studied social work (BA). She is currently working as a certified case manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Yasemin Göreci, MD, is a neurology resident working in the department of neurology at the University Hospital of Cologne. She is a clinical scientist and study physician at the COCOS-MS research project. Her main research focus is neuroimmunology and clinical studies regarding patients with multiple sclerosis. Veronika Dunkl, MD, studied medicine and is a specialist for neurology and palliative care medicine. She did her doctorate in medicine in 2015. She is currently working as a physician and project manager in the COCOS-MS study at the Department of Palliative Medicine of the University Hospital Cologne. Raymond Voltz, MD, is professor and since 2004, he is chair for palliative medicine at the University Hospital Cologne, and currently, he is the chair of its research ethics committee. One of his research focuses is the improvement of care of severely affected patients in the palliative context. Peter Loecherbach, PhD , is professor of social work at the Catholic University of Applied Sciences in Mainz, where he served as rector for 7 years. He studied social work and pedagogy. He is case management instructor and chairman of the German Society for Care and Case Management (DGCC). Warnke, MD, is professor, consultant of neurology at the University Hospital Cologne since 2017. At his current affiliation, he is cohead of the MS center including an outpatient MS clinic. Focus of his research is clinical neuroimmunology, including clinical MS research and neurovirology with focus on progressive multifocal leukoencephalopathy (PML). Heidrun Golla, MD, professor, is neurologist, psychotherapist, pychoanalyst (DGIP), and palliative care physician. After her training as a neurologist at the University Clinic of Tübingen, she has been working at the Department of Palliative Medicine of the University Hospital Cologne since 2006.
 Department of Infectious Diseases and Clinical Microbiology, Dışkapı Yıldırım Beyazıt Training and Research Hospital, University of Health Sciences, Ankara, Turkey. Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Sakarya University, Sakarya, Turkey. Department of Infectious Diseases and Clinical Microbiology Faculty of Medicine, Lokman Hekim University, Ankara, Turkey. Department of Microbiology Reference Laboratory and Biological Products, General Directorate of Public Health, Republic of Turkey Ministry of Health , Ankara, Turkey. Department of Microbiology Reference Laboratory and Biological Products, General Directorate of Public Health, Republic of Turkey Ministry of Health , Ankara, Turkey. Department of Communicable Diseases, Ankara Sincan Provincial Health Directorate, Republic of Turkey Ministry of Health, Ankara, Turkey. Department of Infectious Diseases and Clinical Microbiology, Ünye State Hospital, Republic of Turkey Ministry of Health, Ordu, Turkey. Department of Infectious Diseases and Clinical Microbiology, Fethi Sekin City Hospital, University of Health Sciences, Elazığ, Turkey. Department of Infectious Diseases and Clinical Microbiology, Gazi Yaşargil Research and Training Hospital, University of Health Sciences, Diyarbakır, Turkey. Department of Infectious Diseases and Clinical Microbiology, Kırıkhan State Hospital, Republic of Turkey Ministry of Health, Hatay, Turkey. Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Gaziosmanpaşa University, Tokat, Turkey. Department of Infectious Diseases and Clinical Microbiology, Çorlu State Hospital, Republic of Turkey Ministry of Health, Tekirdağ, Turkey. Department of Infectious Diseases and Clinical Microbiology, Kahramankazan State Hospital, Republic of Turkey Ministry of Health, Ankara, Turkey. Department of Infectious Diseases and Clinical Microbiology, Sungurlu State Hospital, Republic of Turkey Ministry of Health, Çorum, Turkey. Department of Infectious Diseases and Clinical Microbiology, Van Research and Training Hospital, Republic of Turkey Ministry of Health, Van, Turkey. Department of Infectious Diseases and Clinical Microbiology, Dışkapı Yıldırım Beyazıt Training and Research Hospital, University of Health Sciences, Ankara, Turkey. Department of Infectious Diseases and Clinical Microbiology, Batman Research and Training Hospital, Republic of Turkey Ministry of Health, Batman, Turkey. Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, İstanbul Medeniyet University, İstanbul, Turkey Fenerbahçe University, İstanbul, Turkey. Department of Infectious Diseases, Fenerbahçe University, İstanbul, Turkey. Department of Infectious Diseases and Clinical Microbiology, Kayseri Medicine Faculty, University of Health Sciences, Kayseri, Turkey. Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Ege University, İzmir, Turkey. Department of Microbiology and Clinical Microbiology, Faculty of Medicine, Ege University, İzmir, Turkey. Department of Infectious Diseases and Clinical Microbiology, Antalya Education and Research Hospital, University of Health Sciences, Antalya, Turkey. Department of Infectious Diseases and Microbiology, İstanbul Training and Research Hospital, University of Health Sciences, İstanbul, Turkey. Department of Medical Microbiology, Faculty of Medicine, İstanbul Medeniyet University, İstanbul, Turkey. Department of Infectious Diseases and Clinical Microbiology, Dışkapı Yıldırım Beyazıt Training and Research Hospital, University of Health Sciences, Ankara, Turkey. Department of Infectious Diseases and Clinical Microbiology, Viranşehir State Hospital, Republic of Turkey Ministry of Health, Şanlıurfa, Turkey. Department of Infectious Diseases and Clinical Microbiology, Sancaktepe İlhan Varank Training and Research Hospital, Republic of Turkey Ministry of Health, İstanbul, Turkey. Department of Infectious Diseases and Clinical Microbiology, Sancaktepe İlhan Varank Training and Research Hospital, Republic of Turkey Ministry of Health, İstanbul, Turkey. Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Ege University, İzmir, Turkey. Department of Infectious Diseases and Clinical Microbiology, Haseki Training and Research Hospital, Republic of Turkey Ministry of Health, İstanbul, Turkey ; Department of Medical Microbiology, Institute of Graduate Studies, İstanbul University-Cerrahpasa, İstanbul, Turkey.
 Department of Agricultural Sciences, University of Naples "Federico II", Portici, Italy. CEINGE Biotecnologie Avanzate "Franco Salvatore", Naples, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Faculty of Psychology, Uninettuno Telematic International University, Rome, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. CEINGE Biotecnologie Avanzate "Franco Salvatore", Naples, Italy. Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "Luigi Vanvitelli", Caserta, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. CEINGE Biotecnologie Avanzate "Franco Salvatore", Naples, Italy. Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "Luigi Vanvitelli", Caserta, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. CEINGE Biotecnologie Avanzate "Franco Salvatore", Naples, Italy. Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "Luigi Vanvitelli", Caserta, Italy.
 Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland. Graduate School for Health Sciences, University of Bern, Switzerland. Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. BDH, Biogen Spain, Madrid, Spain. Centre for Health Economics, University of York, York, UK. Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland.
 CIC Neurosciences, Hôpital de la Pitié Salpêtrière, INSERM, CNRS, Assistance Publique Hôpitaux de Paris, Sorbonne Université, Paris Brain Institute-ICM, Paris, France. Département de Santé Publique, Groupe Hospitalier Universitaire APHP-Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Site Pitié-Salpêtrière, Sorbonne Université, Paris, France. Laboratoire de Virologie, Assistance Publique Hôpitaux de Paris, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Sorbonne Université, Paris, France. CIC Neurosciences, Hôpital de la Pitié Salpêtrière, INSERM, CNRS, Assistance Publique Hôpitaux de Paris, Sorbonne Université, Paris Brain Institute-ICM, Paris, France. CIC Neurosciences, Hôpital de la Pitié Salpêtrière, INSERM, CNRS, Assistance Publique Hôpitaux de Paris, Sorbonne Université, Paris Brain Institute-ICM, Paris, France. Département de Santé Publique, Groupe Hospitalier Universitaire APHP-Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Site Pitié-Salpêtrière, Sorbonne Université, Paris, France. CIC Neurosciences, Hôpital de la Pitié Salpêtrière, INSERM, CNRS, Assistance Publique Hôpitaux de Paris, Sorbonne Université, Paris Brain Institute-ICM, Paris, France. CIC Neurosciences, Hôpital de la Pitié Salpêtrière, INSERM, CNRS, Assistance Publique Hôpitaux de Paris, Sorbonne Université, Paris Brain Institute-ICM, Paris, France. Laboratoire de Virologie, Assistance Publique Hôpitaux de Paris, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Sorbonne Université, Paris, France. Laboratoire de Virologie, Assistance Publique Hôpitaux de Paris, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Sorbonne Université, Paris, France. Reqpharm Unit, Pharmacie à Usage Intérieur, Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, France. INSERM Inflammation-Immunopathology-Immunotherapy Department (i3) and AP-HP, Hôpital Pitié-Salpêtrière, Clinical Investigation Center for Biotherapies (CIC-BTi), Sorbonne Université, Paris, France. Laboratoire de Virologie, Assistance Publique Hôpitaux de Paris, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Sorbonne Université, Paris, France. Laboratoire de Virologie, Assistance Publique Hôpitaux de Paris, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Sorbonne Université, Paris, France. Service de Maladies infectieuses et Tropicales, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, AP-HP, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Sorbonne Université, Paris, France.
 Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Institute of Biophysics and Informatics of the First Faculty of Medicine, Charles University in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. 2nd Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. Laboratory of Clinical Immunology and Allergology, Institute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Laboratory of Clinical Immunology and Allergology, Institute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Laboratory of Clinical Immunology and Allergology, Institute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Institute of Immunology and Microbiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Laboratory of Clinical Immunology and Allergology, Institute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Medical Radiation Physics and Nuclear Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Radiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Center of Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Center of Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden.
 From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco. zamvil@ucsf.neuroimmunol.org. From the Department of Neurology (B.H., L.A.), University of Southern California (USC), Keck School of Medicine; Distinguished Senior Fellows (Sabbatical) Neuroimmunology Laboratory of Professor Lawrence Steinman (E.M.F., T.C.F.), Stanford University School of Medicine, Palo Alto, CA; Departments of Neurology (S.G., L.J.B.), Population Health (L.J.B.) and Ophthalmology (L.J.B., S.G.), New York University Grossman School of Medicine; Department of Neurology (R.P.L.), Wayne State University, Detroit MI; Department of Neurology (S.D.N.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Neurosciences (J.S.G.), University of California, San Diego; and Department of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco.
 Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVa), 47003 Valladolid, Spain. Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVa), 47003 Valladolid, Spain. Laboratory of Pharmacognosy and Natural Products Chemistry, Department of Pharmacy, National and Kapodistrian University of Athens, Panepistimiopolis Zografou, 15771 Athens, Greece. Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVa), 47003 Valladolid, Spain. Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVa), 47003 Valladolid, Spain. Laboratorio de Biología Molecular y Microbiología, Instituto Tecnológico Agrario de Castilla y León (ITACyL), 47071 Valladolid, Spain. Laboratory of Pharmacognosy and Natural Products Chemistry, Department of Pharmacy, National and Kapodistrian University of Athens, Panepistimiopolis Zografou, 15771 Athens, Greece. Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVa), 47003 Valladolid, Spain. Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVa), 47003 Valladolid, Spain.
 Rehabilitation Medicine Center, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. Integrative & Optimized Medicine Research center, China-USA Institute for Acupuncture and Rehabilitation, Wenzhou Medical University, Wenzhou, China. State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, China. The Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, School of Ophthalmology & Optometry and Eye Hospital, Wenzhou Medical University, Wenzhou, China. State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, China. The Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, School of Ophthalmology & Optometry and Eye Hospital, Wenzhou Medical University, Wenzhou, China. State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, China. The Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, School of Ophthalmology & Optometry and Eye Hospital, Wenzhou Medical University, Wenzhou, China. Rehabilitation Medicine Center, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. Integrative & Optimized Medicine Research center, China-USA Institute for Acupuncture and Rehabilitation, Wenzhou Medical University, Wenzhou, China. Rehabilitation Medicine Center, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. Integrative & Optimized Medicine Research center, China-USA Institute for Acupuncture and Rehabilitation, Wenzhou Medical University, Wenzhou, China. Alberta Institute, Wenzhou Medical University, Wenzhou, China. Alberta Institute, Wenzhou Medical University, Wenzhou, China. Rehabilitation Medicine Center, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. Integrative & Optimized Medicine Research center, China-USA Institute for Acupuncture and Rehabilitation, Wenzhou Medical University, Wenzhou, China. State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, China. The Molecular Neuropharmacology Laboratory and the Eye-Brain Research Center, School of Ophthalmology & Optometry and Eye Hospital, Wenzhou Medical University, Wenzhou, China.
 Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China; Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei, Anhui, China; Department of clinical medicine, The First School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China; Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Preventive Medicine, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China; Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China. Electronic address: jiangzhengxuan@ahmu.edu.cn. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Electronic address: nijing@ahmu.edu.cn. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Electronic address: panhaifeng@ahmu.edu.cn.
 Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. fabrizio.esposito@unicampania.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Via Olgettina 58, 20132, Milan, Italy. Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università, 30, 00185, Rome, Italy. Institute of Applied Physics "Nello Cararra" (IFAC), National Research Council (CNR), Via Madonna del Piano, 10, Sesto Fiorentino, 50019, Florence, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università, 30, 00185, Rome, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Via Olgettina 58, 20132, Milan, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy.
 Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of Medical Sciences, PO Box 91779-48564, Mashhad, Iran. Applied Biomedical Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of Medical Sciences, PO Box 91779-48564, Mashhad, Iran. Applied Biomedical Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Medical Biotechnology Research Center, School of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran. Laboratory of Experimental Biochemistry & Molecular Biology, IRCCS Istituto Ortopedico Galeazzi, Via Riccardo Galeazzi, 4, 20161, Milan, Italy. amalvandi@gmail.com. Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of Medical Sciences, PO Box 91779-48564, Mashhad, Iran. Mohammadipa@mums.ac.ir.
 Epidemiology, Biostatistics and Prevention Institute, University of Zürich, Zurich, Switzerland. Institute for Medical Information Processing, Biometry and Epidemiology, Ludwig-Maximilians-Universität München, Munich, Germany. lnstitute of Clinical Neuroimmunology, Ludwig-Maximilians-Universität München, Munich, Germany. Institute for Medical Information Processing, Biometry and Epidemiology, Ludwig-Maximilians-Universität München, Munich, Germany. Pettenkofer School of Public Health, Munich, Germany. University Library, University of Zurich, Zurich, Switzerland. Institute for Medical Information Processing, Biometry and Epidemiology, Ludwig-Maximilians-Universität München, Munich, Germany. Institute for Medical Information Processing, Biometry and Epidemiology, Ludwig-Maximilians-Universität München, Munich, Germany. Institute of Health Services Research in Dentistry, University of Münster, Muenster, Germany. Epidemiology, Biostatistics and Prevention Institute, University of Zürich, Zurich, Switzerland. IGDORE, Munich, Germany. Institute for Medical Information Processing, Biometry and Epidemiology, Ludwig-Maximilians-Universität München, Munich, Germany. Pettenkofer School of Public Health, Munich, Germany. Epidemiology, Biostatistics and Prevention Institute, University of Zürich, Zurich, Switzerland.
 Department of Neurology and Neuroimaging Laboratory, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil. Department of Neurology and Neuroimaging Laboratory, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil. Department of Anesthesiology, Oncology and Radiology, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil. Department of Neurology and Neuroimaging Laboratory, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil. Electronic address: mcfjr@unicamp.br.
 Department of Pathology, Albert Einstein College of Medicine, New York, NY 10461, USA. Department of Biochemistry, Albert Einstein College of Medicine, New York, NY 10461, USA. Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA. Department of Pathology, Albert Einstein College of Medicine, New York, NY 10461, USA. Rocky Mountain MS Brain Bank, Department of Neurology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Departments of Neurology and Neuroscience, Yale School of Medicine, Boyer Center for Molecular Medicine, New Haven, CT 06510, USA. Analytic Imaging Facility, Albert Einstein College of Medicine, New York, NY 10461, USA. Department of Anatomic and Clinical Pathology, Montefiore Medical Center, Bronx, NY 10467, USA. Department of Anatomic and Clinical Pathology, Montefiore Medical Center, Bronx, NY 10467, USA. Department of Pathology, Albert Einstein College of Medicine, New York, NY 10461, USA. Department of Biochemistry, Albert Einstein College of Medicine, New York, NY 10461, USA. UCLA Brain Bank, VA Healthcare System, Los Angeles, CA 90073, USA. Department of Biochemistry, Albert Einstein College of Medicine, New York, NY 10461, USA.
 Division of Physiology, Department of Basic Science, School of Veterinary Medicine, Shiraz University, Shiraz, Iran. Division of Physiology, Department of Basic Science, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
 Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel. Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel. Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel. Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel. Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel. Department of Physiology and Cell Biology, Ben-Gurion University of the Negev, Beer-Sheva 84710501, Israel. Department of Physiology and Cell Biology, Ben-Gurion University of the Negev, Beer-Sheva 84710501, Israel. ARO Volcani Center, Bet Dagan 50250, Israel. Eastern Regional Research and Development Center, Judea Center, Kiryat Arba 90100, Israel. Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel.
 Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany. Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. Department of Neurology, University Medical Centre Göttingen, Göttingen, Germany. Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. Department of Neurosurgery, Charité-Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany. Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. martin.weber@med.uni-goettingen.de. Fraunhofer-Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany. martin.weber@med.uni-goettingen.de. Department of Neurology, University Medical Centre Göttingen, Göttingen, Germany. martin.weber@med.uni-goettingen.de.
 IRCCS Mondino Foundation, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, 27100 Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, 27100 Pavia, Italy. IRCCS Mondino Foundation, 27100 Pavia, Italy.
 Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA. olamideadebiyi24@gmail.com. Department of Veterinary Physiology and Biochemistry, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria. olamideadebiyi24@gmail.com. Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA. msb76@cornell.edu.
 Department of Neurology, University of California San Francisco, San Francisco, CA, USA. Division of Neuroimmunology, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Department of Neurology, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, University of California San Francisco, San Francisco, CA, USA. West Coast Metabolomics Center, University of California Davis, Davis, CA, USA. West Coast Metabolomics Center, University of California Davis, Davis, CA, USA United States Department of Agriculture, Agricultural Research Service, Western Human Nutrition Research Center, Davis, CA, USA Department of Nutrition, University of California Davis, Davis, CA, USA. Department of Neurology, University of California San Francisco, San Francisco, CA, USA.
 From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. From the Laboratory of Neurological Complex Disorders (M.S., S.S., L.F., E.M., F.C., A.G., M.C., F.E.), Division of Neuroscience, Institute of Experimental Neurology (INSPE), IRCCS San Raffaele Scientific Institute; Neurology and Neurorehabilitation Unit (L.F., A.G., M.C., M.L., V.M., M.F., F.E.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.F.); Neurophysiology Unit (M.F.), IRCCS San Raffaele Scientific Institute; and Neuroimaging Research Unit, Division of Neuroscience, Institute of Experimental Neurology (INSPE) (P.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy. esposito.federica@hsr.it.
 IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. Department of Physiopathology and Transplants, University of Milan, Milan, Italy.
 Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan; Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China. Department of Sustainable Health Science, Chiba University Center for Preventive Medical Sciences, Chiba 263-8522, Japan. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Department of Sustainable Health Science, Chiba University Center for Preventive Medical Sciences, Chiba 263-8522, Japan; Department of Bioenvironmental Medicine, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan. Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba 260-8670, Japan. Electronic address: hashimoto@faculty.chiba-u.jp.
 Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
 Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa 078-8510, Japan. Department of Neurosurgery, Asahikawa Medical University, Asahikawa 078-8510, Japan. Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa 078-8510, Japan. Department of Neurosurgery, Asahikawa Medical University, Asahikawa 078-8510, Japan. Institute for Social Innovation and Cooperation, Niigata University, Niigata 951-8510, Japan. Daiichi Sankyo Co., Ltd., Tokyo 140-8710, Japan. Daiichi Sankyo Co., Ltd., Tokyo 140-8710, Japan. Department of Cell Physiology, The Jikei University School of Medicine, Tokyo 105-8461, Japan. Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa 078-8510, Japan. Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa 078-8510, Japan. Department of Anatomy, Akita University Graduate School of Medicine, Hondo 1-1-1, Akita 010-8543, Japan.
 Division of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Ubon Ratchathani University, Ubon Ratchathani, Thailand. Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand; Siriraj Neuroimmunology Center, Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand; Bumrungrad International Hospital, Bangkok, Thailand. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Division of Clinical Pharmacy, Department of Pharmacy, Faculty of Pharmacy, Mahidol University, 447 Sri Ayutthaya Road, Ratchathewi, Bangkok 10400, Thailand. Electronic address: thanarat.sua@mahidol.ac.th.
 Department of Biology and Center for Cell Reprogramming, Georgetown University, Washington, DC, 20057, USA; Department of Anatomy, Division of Histology and Cell Biology, School of Medicine, Jichi Medical University, Shimotsuke, Japan. Electronic address: ryamazaki@jichi.ac.jp. Department of Anatomy, Division of Histology and Cell Biology, School of Medicine, Jichi Medical University, Shimotsuke, Japan. Department of Anatomy, Division of Histology and Cell Biology, School of Medicine, Jichi Medical University, Shimotsuke, Japan. Department of Biology and Center for Cell Reprogramming, Georgetown University, Washington, DC, 20057, USA. Department of Anatomy, Division of Histology and Cell Biology, School of Medicine, Jichi Medical University, Shimotsuke, Japan; Division of Ultrastructural Research, National Institute for Physiological Sciences, Okazaki, Japan.
 Department of Neurology, Konya Numune State Hospital, Selcuklu, Konya 42060, Turkiye. Electronic address: drrmelike@gmail.com. Department of Biochemistry, Selcuk University Faculty of Medicine, Konya, Turkiye. Department of Neurology, Selcuk University Faculty of Medicine, Konya, Turkiye. Department of Neurology, Selcuk University Faculty of Medicine, Konya, Turkiye. Department of Biochemistry, Selcuk University Faculty of Medicine, Konya, Turkiye. Department of Biochemistry, Selcuk University Faculty of Medicine, Konya, Turkiye.
 Department of Neurology and Department of Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, USA. Electronic address: jeffrey.bennett@cuanschutz.edu. Departments of Clinical Neurosciences and Surgery, University of Calgary, Calgary, AB, Canada. Department of Ophthalmology and Department of Neurology, Mayo Clinic, Rochester, MN, USA. National Hospital for Neurology and Neurosurgery, University College London Hospital, London, UK; Moorfields Eye Hospital, London, UK; Neuro-ophthalmology Expert Centre, Amsterdam, Netherlands. Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA, USA; Department of Neurology, Emory University School of Medicine, Atlanta, GA, USA. Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA, USA; Department of Neurology, Emory University School of Medicine, Atlanta, GA, USA; Department of Neurological Surgery, Emory University School of Medicine, Atlanta, GA, USA. Department of Neurology and Department of Opthalmology, NYU Langone Medical Center, New York, NY, USA.
 Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
 Department of Neurology, Brigham and Women's Hospital, Boston, Massachusetts. Department of Neurology, Brigham and Women's Hospital, Boston, Massachusetts.
 Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Disease Neurogenomics and the Icahn Institute for Data Science and Genomic Technology and the Departments of Psychiatry and Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Disease Neurogenomics and the Icahn Institute for Data Science and Genomic Technology and the Departments of Psychiatry and Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Center for Genomic Medicine, Department of Pathology, Massachusetts General Hospital, Boston, MA, USA; Department of Pathology, Harvard Medical School, Boston, MA, USA. Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Human Immune Monitoring Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland. Departments of Medicine, Clinical Research and Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland. Human Immune Monitoring Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Center for Genomic Medicine, Department of Pathology, Massachusetts General Hospital, Boston, MA, USA; Department of Pathology, Harvard Medical School, Boston, MA, USA. Department of Pharmacology and Department Chemistry, University of Oxford, Oxford, UK. Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Disease Neurogenomics and the Icahn Institute for Data Science and Genomic Technology and the Departments of Psychiatry and Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Mental Illness Research Education and Clinical Center, James J. Peters VA Medical Center, New York, NY, USA; Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Biomedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Friedman Brain Institute and the Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Systems Biology and the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: cameron.mcalpine@mssm.edu.
 Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 1201 Welch Rd, MSLS BLG P212, Stanford, CA, 94305, USA. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 1201 Welch Rd, MSLS BLG P212, Stanford, CA, 94305, USA. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 1201 Welch Rd, MSLS BLG P212, Stanford, CA, 94305, USA. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 1201 Welch Rd, MSLS BLG P212, Stanford, CA, 94305, USA. Chan Zuckerberg Biohub, San Francisco, CA, USA. Chan Zuckerberg Biohub, San Francisco, CA, USA. Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 1201 Welch Rd, MSLS BLG P212, Stanford, CA, 94305, USA. mayhan@stanford.edu.
 UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. University Children's Hospital Regensburg, Hospital St Hedwig of the Order of St John, University of Regensburg, Regensburg, Germany. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. University Children's Hospital Regensburg, Hospital St Hedwig of the Order of St John, University of Regensburg, Regensburg, Germany. University Children's Hospital Regensburg, Hospital St Hedwig of the Order of St John, University of Regensburg, Regensburg, Germany. Paediatric Office Laub, Rosenheim, Germany. Paediatric Office Dr Leipold, Regensburg, Germany. Multiple Sclerosis Center, Department of Neurology, Neurocenter of Southern Switzerland, Lugano, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Multiple Sclerosis Center, Department of Neurology, Neurocenter of Southern Switzerland, Lugano, Switzerland; Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, University of Ulm, Ulm, Germany; German Center for Neurodegenerative Diseases, Ulm, Germany. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland; Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA. University Children's Hospital Regensburg, Hospital St Hedwig of the Order of St John, University of Regensburg, Regensburg, Germany. Electronic address: sven.wellmann@barmherzige-regensburg.de. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland; Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Electronic address: jens.kuhle@usb.ch.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
 Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Finetech in Medicine Research Center, Iran University of Medical Sciences, Tehran, Iran. Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. shnoori@sbmu.ac.ir. Department of Traditional Medicine, School of Persian Medicine, Tehran University of Medical Sciences, Tehran, Iran. School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 Patient Engagement, Novartis Pharma AG, Basel, Switzerland. Department of Clinical Pharmacology; Novartis Institutes for Biomedical Research, Basel, Switzerland. Department of Autoimmunity, Transplantation & Inflammation; Novartis Institutes for Biomedical Research, Basel, Switzerland. Patient Engagement, Novartis Pharma AG, Basel, Switzerland. Novartis Farma S.p.A., Origgio, Italy. Department of Neuroscience; Novartis Institutes for Biomedical Research, Basel, Switzerland. Patient Engagement, Novartis Pharma AG, Basel, Switzerland. Patient Engagement, Novartis Pharma AG, Basel, Switzerland. Department of Autoimmunity, Transplantation & Inflammation; Novartis Institutes for Biomedical Research, Basel, Switzerland. Independent Consultant, Freiburg, Germany. Department of Physiology and Pharmacology, University Sapienza of Rome, Rome, Italy. Department of Molecular Neuropharmacology, IRCCS Neuromed, Pozzilli, Italy.
 University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. Julie.Campbell@utas.edu.au. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. Centre for Health Economics, Monash University, VIC, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. School of Population and Global Health, Neuroepidemioloy Unit, The University of Melbourne, Melbourne VIC, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. University of Tasmania, Menzies Institute for Medical Research, Hobart, TAS, Australia. School of Population and Global Health, Health Economics Unit, The University of Melbourne, Melbourne VIC, Australia.
 Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research (IMSF), University Medical Center Goettingen, Goettingen, Germany. Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research (IMSF), University Medical Center Goettingen, Goettingen, Germany. Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.
 National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei 430070, China; MAO Laboratory for Risk Assessment of Quality and Safety of Livestock and Poultry Products, Huazhong Agricultural University, Wuhan, Hubei 430070, China. National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei 430070, China. National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei 430070, China. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12). 28040, Madrid, Spain. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12). 28040, Madrid, Spain. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12). 28040, Madrid, Spain. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12). 28040, Madrid, Spain. National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei 430070, China; The State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei 430070, China. Electronic address: wangxu@mail.hzau.edu.cn. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12). 28040, Madrid, Spain. Electronic address: aanadon@ucm.es. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12). 28040, Madrid, Spain.
 Department of Neurology, University Clinic Heidelberg, 69120 Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, 69120 Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, 69120 Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, 69120 Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, 69120 Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
 Division of Infectious Diseases, Department of Pediatrics, University of Florida, Gainesville, FL 32610, USA. Division of Infectious Diseases, Department of Pediatrics, University of Florida, Gainesville, FL 32610, USA. Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA.
 Interdepartmental Research Unit of Peptide and Protein Chemistry and Biology, Department of Chemistry "Ugo Schiff", University of Florence, Sesto Fiorentino, Italy. Interdepartmental Research Unit of Peptide and Protein Chemistry and Biology, Department of Chemistry "Ugo Schiff", University of Florence, Sesto Fiorentino, Italy. Institute of Chemistry of Organometallic Compounds (ICCOM), National Research Council of Italy (CNR), Sesto Fiorentino, Italy. Interdepartmental Research Unit of Peptide and Protein Chemistry and Biology, Department of Chemistry "Ugo Schiff", University of Florence, Sesto Fiorentino, Italy. University of Burgos, Burgos, Spain. Department of Pharmacy, University of Naples "Federico II", Naples, Italy. Department of Pharmacy, University of Naples "Federico II", Naples, Italy. Interdepartmental Research Unit of Peptide and Protein Chemistry and Biology, Department of Chemistry "Ugo Schiff", University of Florence, Sesto Fiorentino, Italy. Interdepartmental Research Unit of Peptide and Protein Chemistry and Biology, Department of NeuroFarBa, University of Florence, Sesto Fiorentino, Italy.
 Department of Clinical Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China. Department of Clinical Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China. Department of Clinical Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China. Department of Clinical Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China.
 Institute of Neuropathology, University Hospital Münster, Münster, Germany. Institute of Neuropathology, University Hospital Münster, Münster, Germany. Institute of Neuropathology, University Hospital Münster, Münster, Germany. Institute of Neuropathology, University Hospital Münster, Münster, Germany. Institute of Neuropathology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Institute of Neuropathology, University Hospital Münster, Münster, Germany.
 Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. School of Pharmacy, Second Military Medical University, No.325, Guo He Road, Shanghai 30025, China. Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, No. 358, Datong road, Pudong New Area, Shanghai 200137, China. School of Pharmacy, Second Military Medical University, No.325, Guo He Road, Shanghai 30025, China. School of Pharmacy, Second Military Medical University, No.325, Guo He Road, Shanghai 30025, China. Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. Medical College, Dalian University, Dalian 116622, China. Electronic address: wangqianqian@dlu.edu.cn. Department of Pharmaceutical Analysis, School of Pharmacy, Key Laboratory of Hui Ethnic Medicine Modernization, Ministry of Education, Ningxia Medical University, 1160 Shenli Street, Yinchuan 750004, China. Electronic address: maxueqin217@126.com. Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China. Electronic address: hmq1115@126.com.
 Department of Neurology, National Institute of Mental Health & Neuro Sciences (NIMHANS), Hosur Road, Bangalore 560029, Karnataka, India. Department of Neurology, National Institute of Mental Health & Neuro Sciences (NIMHANS), Hosur Road, Bangalore 560029, Karnataka, India. Department of Neurology, National Institute of Mental Health & Neuro Sciences (NIMHANS), Hosur Road, Bangalore 560029, Karnataka, India.
 Technical University of Denmark, Center for Nanomedicine and Theranostics, Department of Chemistry, Kemitorvet 207, 2800 Kgs. Lyngby, Denmark. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark. Technical University of Denmark, Department of Chemistry, Kemitorvet 207, 2800 Kgs. Lyngby, Denmark. The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA; Department of Neurobiology Research, Institute of Molecular Medicine, and BRIDGE - Brain Research Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, Odense 5230, Denmark. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark. Electronic address: anders.bach@sund.ku.dk. Technical University of Denmark, Center for Nanomedicine and Theranostics, Department of Chemistry, Kemitorvet 207, 2800 Kgs. Lyngby, Denmark. Electronic address: mhc@kemi.dtu.dk.
 IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy. Department of Physiopathology and Transplants, University of Milan, Milan, Italy.
 Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humbolt-Universität Zu Berlin, and Berlin Institute of Health, 10117, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humbolt-Universität Zu Berlin, and Berlin Institute of Health, 10117, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humbolt-Universität Zu Berlin, and Berlin Institute of Health, 10117, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany. volker.siffrin@charite.de. Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humbolt-Universität Zu Berlin, and Berlin Institute of Health, 10117, Berlin, Germany. volker.siffrin@charite.de. Experimental and Clinical Research Center (ECRC), Charité - Universitätsmedizin Berlin und Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, Lindenberger Weg 80, 13125, Berlin, Germany.
 Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. Immudex, Copenhagen, Denmark. Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark. Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. LEO Foundation Skin Immunology Research Center, Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; Section for Periodontology, Department of Odontology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: claus.henrik.nielsen@regionh.dk.
 Division of Clinical Neurology, Vetsuisse Faculty, University of Bern, Bern, Switzerland. Division of Clinical Neurology, Vetsuisse Faculty, University of Bern, Bern, Switzerland. Division of Neurological Sciences, Vetsuisse Faculty, University of Bern, Bern, Switzerland. Department of Neurology, University of Zurich, Zurich, Switzerland. Department of Neurology, University of Zurich, Zurich, Switzerland. Department of Clinical Research and Public Health, Vetsuisse Faculty, University of Bern, Bern, Switzerland. Institute of Laboratory Animal Science, University of Zurich, Zurich, Switzerland. Division of Clinical Neurology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
 Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Institute of Neuropathology, University of Freiburg, Freiburg, Germany. Institute of Neuropathology, University of Freiburg, Freiburg, Germany. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Institute of Laboratory Animal Science, University of Zurich, Zurich, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Institute of Laboratory Animal Science, University of Zurich, Zurich, Switzerland. Institute of Neuropathology, University of Freiburg, Freiburg, Germany. Center for Basics in NeuroModulation (NeuroModulBasics), Faculty of Medicine, University of Freiburg, Freiburg, Germany. Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012, Bern, Switzerland. giuseppe.locatelli@novartis.com.
 Dipartimento di Elettronica, Informazione e Bioingegneria, Politecnico di Milano, Milano, Italy. Electronic address: alessandra.angelucci@polimi.it. Neurorehabilitation Unit, Istituto Clinico Quarenghi, San Pellegrino Terme, Bergamo, Italy. Dipartimento di Elettronica, Informazione e Bioingegneria, Politecnico di Milano, Milano, Italy. Department of Rehabilitation, Istituto Clinico Quarenghi, San Pellegrino Terme, Bergamo, Italy.
 Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey. Electronic address: tubaozdogar@yyu.edu.tr. Faculty of Physical Therapy and Rehabilitation, Dokuz Eylül University, Izmir, Turkey. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Izmir Katip Celebi University, Izmir, Turkey. Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey. Department of Neurology, Faculty of Medicine, Dokuz Eylül University, Izmir, Turkey.
 International Neurorehabilitation Institute, Lutherville, MD, United States. International Neurorehabilitation Institute, Lutherville, MD, United States. International Neurorehabilitation Institute, Lutherville, MD, United States. International Neurorehabilitation Institute, Lutherville, MD, United States. International Neurorehabilitation Institute, Lutherville, MD, United States. International Neurorehabilitation Institute, Lutherville, MD, United States; John Hopkins University School of Medicine, Department of Neurology, Baltimore, MD, United States. Electronic address: db@inirehab.com.
 Department of Pharmaceutical Biotechnology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Pharmaceutical Biotechnology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Tumor Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Department of Pharmacology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Pharmaceutical Biotechnology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Pharmaceutical Biotechnology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
 Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; Hertie Institute for Clinical Brain Research, Tübingen, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; Hertie Institute for Clinical Brain Research, Tübingen, Germany. Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Electronic address: thomas.misgeld@tum.de. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Electronic address: martin.kerschensteiner@med.uni-muenchen.de.
 School of Allied Health Science and Practice, University of Adelaide, Adelaide, Australia. Electronic address: hans.bogaardt@adelaide.edu.au. Multiple Sclerosis and Neuroimmunology Center, Clalit Health Services, Nazareth, Israel; Department of Neurology, Lady Davis Carmel Medical Center, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. Katz School of Science and Health, Yeshiva University, New York, United States. School of Allied Health Science and Practice, University of Adelaide, Adelaide, Australia. South Shore Neurologic Associates, New York, United States. South Shore Neurologic Associates, New York, United States. South Shore Neurologic Associates, New York, United States. South Shore Neurologic Associates, New York, United States; Department of Nursing, State University of Stony Brook, Stony Brook, NY, United States. Georgetown University Dept of Neurology, Washington D.C. United States; Washington Neuropsychology Research Group, LLC., Fairfax, VA, United States. Department of Clinical Research, NeuroTrax Corporation, Modiin, Israel. Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. Consortium of Multiple Sclerosis Centers, Hackensack, NJ, United States. London Health Sciences Centre, University Hospital, University of Western Ontario (Western), Canada. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States. Katz School of Science and Health, Yeshiva University, New York, United States.
 Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea. Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea. Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea. Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea. Dementia Research Group, Korea Brain Research Institute, Daegu 41068, Republic of Korea. Korean Medicine-based Drug Repositioning Cancer Research Center, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea. Department of Medical Science, Catholic Kwandong University College of Medicine, Gangneung, Gangwon-do 25601, Republic of Korea. Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea; Institute of Convergence Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea. Electronic address: ihcho@khu.ac.kr.
 Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul, Republic of Korea. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Biological Sciences, College of Science, Sungkyunkwan University, Suwon, Republic of Korea. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul, Republic of Korea.
 Immunology Graduate Program, University of Iowa, Iowa City, IA. Carver College of Medicine, University of Iowa, Iowa City, IA. Informatics Graduate Program, University of Iowa, Iowa City, IA. Immunology Graduate Program, University of Iowa, Iowa City, IA. Informatics Graduate Program, University of Iowa, Iowa City, IA. Department of Pathology, University of Iowa Hospitals and Clinics, Iowa City. Iowa City VA Health System, Iowa City, IA.
 From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. yavor.yalachkov@kgu.de. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany. From the Department of Neurology (Y.Y., J.H.S., L.F., C.F., M.A.S.-P.), University Hospital Frankfurt; and Department of Neurology (J.J., F.S., S.B.), Universitätsmedizin Mainz, Germany.
 Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. Department of Neurology, University Hospital Düsseldorf, Düsseldorf, Germany. Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. Institute of Medical Informatics, University of Münster, Münster, Germany. Institute of Medical Informatics, University of Münster, Münster, Germany. Department of Neurology, University Hospital Düsseldorf, Düsseldorf, Germany. Division of General Internal Medicine, Nephrology and Rheumatology, Department of Medicine D, University Hospital of Münster, Münster, Germany. Department of Translational Rheumatology and Immunology, Institute of Musculoskeletal Medicine, University of Münster, Münster, Germany. Section of Rheumatology and Clinical Immunology, Department of Medicine, University Hospital Münster, Münster, Germany. Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. gerd.mzh@uni-muenster.de.
 Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. Department of Pharmacology, Vanderbilt University, Nashville, TN, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. vivian.k.kawai@vumc.org. Division of Clinical Pharmacology, 536 RRB, Vanderbilt University School of Medicine, Nashville, TN, 37232, USA. vivian.k.kawai@vumc.org.
 Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Lab Animal Facilities, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Translational Medicine Research Group, Aston Medical School, Aston University, Birmingham, UK. Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA.
 Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Santa Maria 97105-900, RS, Brazil. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Clinical Pharmacology Unit, Department of Health Sciences, University of Florence, 50139 Florence, Italy. Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Santa Maria 97105-900, RS, Brazil.
 Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Department of Rhinology and Allergy, Renmin Hospital of Wuhan University, Wuhan, China. Research Institute of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China. Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University, Wuhan, China.
 From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. amandine.mathias@chuv.ch. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland. From the Laboratories of Neuroimmunology (A.M., V.P., S.P., M.C., S.J., L.O., C.P., R.A.D), Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Service of Neurology (V.P., R.B.-V., M.T., C.P., R.A.D.), Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Paris Brain Institute (V.P.), Lubetzki-Stankoff group of Myelination, France; Service of Immunology and Allergy (M.M., C.F.), Department of Medicine, Lausanne University Hospital and University of Lausanne, Switzerland.
 Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa, Hokkaido, 078-8510, Japan. efurube@asahikawa-med.ac.jp. Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa, Hokkaido, 078-8510, Japan. Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa, Hokkaido, 078-8510, Japan.
 Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Interdepartmental Research Center for the Study of Multiple Sclerosis and Inflammatory and Degenerative Diseases of the Nervous System, University of Ferrara, 44121 Ferrara, Italy. Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Neurology Unit, "S. Anna" University Hospital, 44124 Ferrara, Italy. Department of Neurosciences and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Interdepartmental Research Center for the Study of Multiple Sclerosis and Inflammatory and Degenerative Diseases of the Nervous System, University of Ferrara, 44121 Ferrara, Italy.
 From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. From the Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. bittner@uni-mainz.de.
 Department of Neurology, Washington University Pediatric MS and Other Demyelinating Disease Center, St. Louis, MO, USA. Department of Neurology, Washington University Pediatric MS and Other Demyelinating Disease Center, St. Louis, MO, USA. Department of Pediatrics, University of Utah, Salt Lake City, UT, USA. Department of Pediatrics, University of Utah, Salt Lake City, UT, USA. Department of Neurology and Laboratory Medicine and Pathology and the Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Pediatrics, Pediatric Multiple Sclerosis Center at Loma Linda University Children's Hospital, Loma Linda University, Loma Linda, CA, USA. Department of Neurology, Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Partners Pediatric MS Center, Massachusetts General Hospital, Boston, MA, USA. Department of Neurology, UCSF Regional Pediatric MS Center, San Francisco, CA, USA. Department of Neurology, Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, Washington University Pediatric MS and Other Demyelinating Disease Center, St. Louis, MO, USA. Department of Neurology, University of California San Diego Health, Rady Children's Hospital San Diego, San Diego, CA, USA. Department of Neurology, University of Texas Southwestern and Children's Health, Dallas, TX, USA. Department of Neurology, UCSF Regional Pediatric MS Center, San Francisco, CA, USA. Department of Neurology, New York University, Pediatric MS Center, Neurology, New York, NY, USA. Texas Children's Hospital, Baylor College of Medicine, Houston, TX, USA. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, USA. Department of Neurology and Laboratory Medicine and Pathology and the Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. Mayo Clinic Pediatric MS Center, Mayo Clinic, Rochester, MN, USA. Department of Neurology, University of Utah, Salt Lake City, UT, USA. Rocky Mountain MS Center, Children's Hospital Colorado, University of Colorado, Aurora, CO, USA. Mayo Clinic Pediatric MS Center, Mayo Clinic, Rochester, MN, USA. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, USA. Department of Neurology, The Pediatric MS Center at the Jacobs Neurological Institute, State University of New York at Buffalo, Buffalo, NY, USA. Center for Pediatric-Onset Demyelinating Disease at the Children's of Alabama, University of Alabama, Birmingham, AL, USA. Department of Neurology, UCSF Regional Pediatric MS Center, San Francisco, CA, USA. Department of Neurology and Laboratory Medicine and Pathology and the Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA.
 British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK. Australian Centre for Precision Health, Unit of Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia. South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia. Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. Centre for Global Health Research, Usher Institute, University of Edinburgh, Edinburgh, UK. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Development and Medical, Pfizer Worldwide Research, Stockholm, Sweden. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Estonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia. Department of Immunology, Genetics, and Pathology, Biomedical Center, SciLifeLab Uppsala, Uppsala University, Uppsala, Sweden. Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, Imperial College London, London, UK. School of Immunology and Microbial Sciences, King's College London, London, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Nucleus Genomics ltd, New York, NY, USA. Institute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany. Department of Endocrinology and Diabetology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. German Center for Diabetes Research, Munich-Neuherberg, Germany. Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. Research Unit of Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. British Heart Foundation Centre of Research Excellence, School of Clinical Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK. Health Data Research UK, Wellcome Genome Campus and University of Cambridge, Hinxton, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK. British Heart Foundation Centre of Research Excellence, School of Clinical Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK. Centre for Genomics Research, Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK. Medical School, University of Split, Split, Croatia. German Center for Diabetes Research, Munich-Neuherberg, Germany. Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. German Center for Diabetes Research, Munich-Neuherberg, Germany. Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. Research Unit of Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. Institute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany. Department of Endocrinology and Diabetology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. German Center for Diabetes Research, Munich-Neuherberg, Germany. Estonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia. Estonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia. MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Western General Hospital, Edinburgh, UK. Department of Immunology, Genetics, and Pathology, Biomedical Center, SciLifeLab Uppsala, Uppsala University, Uppsala, Sweden. Department of Immunology, Genetics, and Pathology, Biomedical Center, SciLifeLab Uppsala, Uppsala University, Uppsala, Sweden. Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, Imperial College London, London, UK. Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden. Skåne University Hospital, Malmö, Sweden. Wallenberg Centre for Molecular Medicine, Lund University, Lund, Sweden. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden. Department of Neurology, Skåne University Hospital, Lund University, Lund, Sweden. Centre for Global Health Research, Usher Institute, University of Edinburgh, Edinburgh, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK. British Heart Foundation Centre of Research Excellence, School of Clinical Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK. Health Data Research UK, Wellcome Genome Campus and University of Cambridge, Hinxton, UK. NIHR Blood and Transplant Research Unit in Donor Health and Behaviour, University of Cambridge, Cambridge, UK. Department of Human Genetics, Wellcome Sanger Institute, Hinxton, UK. Division of Rheumatology, Department of Medicine (Solna), Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Division of Rheumatology, Department of Medicine (Solna), Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden. Centre for Global Health Research, Usher Institute, University of Edinburgh, Edinburgh, UK. MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Western General Hospital, Edinburgh, UK. Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Development and Medical, Pfizer Worldwide Research, Stockholm, Sweden. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. asb38@medschl.cam.ac.uk. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK. asb38@medschl.cam.ac.uk. British Heart Foundation Centre of Research Excellence, School of Clinical Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK. asb38@medschl.cam.ac.uk. Health Data Research UK, Wellcome Genome Campus and University of Cambridge, Hinxton, UK. asb38@medschl.cam.ac.uk. NIHR Blood and Transplant Research Unit in Donor Health and Behaviour, University of Cambridge, Cambridge, UK. asb38@medschl.cam.ac.uk. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. j.peters@imperial.ac.uk. Health Data Research UK, Wellcome Genome Campus and University of Cambridge, Hinxton, UK. j.peters@imperial.ac.uk. Department of Immunology and Inflammation, Imperial College London, London, UK. j.peters@imperial.ac.uk.
 Host-Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland. Department of Neurology and the Neuroscience Research Institute, The Ohio State University Wexner Medical Center, Columbus, USA; Department of Neurology, University of Michigan, Ann Arbor, USA. Host-Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland. University College Dublin School of Medicine, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland. Electronic address: stephen.lalor@ucd.ie.
 Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Department of Vascular Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Department of Neurology, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, China. Department of Rheumatology and Clinical Immunology, The Affiliated Hospital of Qingdao University, Qingdao, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Electronic address: 93046792@qq.com.
 University of Toronto, Toronto, Ontario, Canada. ICES, Toronto, Ontario, Canada. University of Toronto, Toronto, Ontario, Canada. McGill University, Montreal, Quebec, Canada. Sinai Health System, University of Toronto, Toronto, Ontario, Canada. Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada. Toronto Western Hospital, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada. University of Waterloo, Waterloo, Ontario, Canada. McGill University, Montreal, Quebec, Canada. Schroeder Arthritis Institute, Krembil Research Institute, University Health Network, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada. Sunnybrook Research Institute, ICES, University of Toronto, Toronto, Ontario, Canada.
 Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Graduate School of Systemic Neuroscience, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Chair of Genetics, Department of Biology, Friedrich Alexander University of Erlangen-Nürnberg, 91058 Erlangen, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany. Chair of Genetics, Department of Biology, Friedrich Alexander University of Erlangen-Nürnberg, 91058 Erlangen, Germany. Chair of Genetics, Department of Biology, Friedrich Alexander University of Erlangen-Nürnberg, 91058 Erlangen, Germany. Medical Immunology Campus Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen 91058, Germany. Department of Neuroimmunology, Center for Brain Research, Medical University of Vienna, 1090 Vienna, Austria. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany. Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
 Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology, University of Florence, Viale G. Pieraccini 6, I-50139, Florence, Italy. Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology, University of Florence, Viale G. Pieraccini 6, I-50139, Florence, Italy. nicoletta.galeotti@unifi.it.
 Institute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, PR China. Institute of Human Anatomy, Histology and Embryology, Basic Medical College, Zhejiang Chinese Medical University, Hangzhou, PR China. Institute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, PR China. Department of Neurology, Sir Run Run Shaw Hospital, Medical College, Zhejiang University, Hangzhou, PR China. Department of Neurology, Sir Run Run Shaw Hospital, Medical College, Zhejiang University, Hangzhou, PR China. Department of Electrophysiology, Sir Run Run Shaw Hospital, Medical College, Zhejiang University, Hangzhou, PR China. Medical Molecular Biology Laboratory, School of Medicine, Jinhua Polytechnic, Jinhua, PR China. Institute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, PR China.
 Department of Health Sciences, Section of Biostatistics, University of Genova, Genova 16132, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Largo Daneo 3, Genova, Italy. IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Largo Daneo 3, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Largo Daneo 3, Genova, Italy. IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Largo Daneo 3, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Department of Health Sciences, Section of Biostatistics, University of Genova, Genova 16132, Italy; IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Largo Daneo 3, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child University of Genova, Largo Daneo 3, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi, Genova, Italy. Electronic address: alice.laroni@unige.it.
 Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Environmental, Agricultural and Occupational Health, University of Nebraska Medical Center, Omaha, NE, 68198, USA. Zalgen Labs, LLC, 12635 E. Montview Blvd., Suite 131, Aurora, Colorado, 80045, USA. Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA. Xiaoli.yu@cuanschutz.edu.
 Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL. Department of Neuroscience, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; and. Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL. Department of Neuroscience, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH. Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL. Department of Neuroscience, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; and. Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL.
 Neurology Section of Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. roberta.magliozzi@univr.it. Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK. roberta.magliozzi@univr.it. Neurology Section of Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Institute of Life Sciences, Swansea University, Swansea, UK. Neurology Section of Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK. Centre for Molecular Neuropathology, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.
 Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. t-akaishi@med.tohoku.ac.jp. Department of Education and Support for Regional Medicine, Tohoku University Hospital, Sendai, Japan. t-akaishi@med.tohoku.ac.jp. Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University, Fukushima, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. Department of Neurology, National Hospital Organization Yonezawa National Hospital, Yonezawa, Japan. Department of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. Department of Education and Support for Regional Medicine, Tohoku University Hospital, Sendai, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Seiryo-Machi 1-1, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan. Department of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan.
 Department of Physical Therapy, Physical Therapy Department for Neuromuscular and Neurosurgical Disorder and Its Surgery, Cairo University, Egypt. Department of Rehabilitation, Faculty of Medicine, Al Baath University, Homs, Syria. Department of Physical Therapy, Albaath University, Homs, Syria. Department of Physical Education, Neijiang Normal University, Neijiang, Sichuan, China. Department of Rehabilitation, Faculty of Medicine, Al Baath University, Homs, Syria. Department of Physical Therapy, Albaath University, Homs, Syria. Department of Rehabilitation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
 From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. From the Neurology Unit (S.C., A.G., S.F., S.M.), Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Italy; Servei de Neurologia-Neuroimmunologia (A.C.C., G.A., M.T.), Centre d'Esclerosi Múltiple de Catalunya, (CEMCAT), Vall d'Hebron Institut de Recerca, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Spain; Pediatric Neuroimmunology Unit (T.A.), Sant Joan de Déu Children's Hospital, University of Barcelona, Spain; Neuroimmunology and Multiple Sclerosis Unit (T.A., A.S., M.S., E.M-H., G.O-C.), Service of Neurology, Hospital Clinic de Barcelona, Neuroimmunology Program, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and, University of Barcelona, Spain; Division of Pediatric Neurology (C.L., M.B.), Department of Pediatric and Adolescent Medicine, Medical University of Innsbruck, Austria; Division of Pediatric Neurology (K.R.), University of Witten/Herdecke Childrens' Hospital, Datteln, Germany; Division of Pediatric Pulmonology (M.B.), Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Austria; Division of Neuropathology and Neurochemistry (R.H.), Department of Neurology, Medical University of Vienna, Austria; Department of Neurology (I.A., C.S.), St. Josef-Hospital, Ruhr-University Bochum, Germany; Department of Clinical Neurosciences (R.B-V., R.d.P.), Service of Neurology, Lausanne University Hospital and University of Lausanne, Switzerland; Faculty of Medicine and Health and Brain and Mind Centre (F.B.), Brain Autoimmunity Group, Kids Neuroscience Centre, Kids Research at the Children's Hospital at Westmead, School of Medical Sciences, The University of Sydney, Australia; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, Children's Hospital at Westmead; Sydney Medical School and Brain and Mind Centre, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Sydney, Australia; Clinical Department of Neurology (K.S., M.R.), Medical University of Innsbruck, Austria; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology, Department of Laboratory Medicine and Pathology (E.P.F., S.J.P., V.R.), Mayo Clinic College of Medicine and Science, Rochester; Service de Neurologie (R.M.), Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, France. sara.mariotto@gmail.com.
 Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Neurology Unit, Fondazione Policlinico Universitario 'A.Gemelli' IRCCS, Rome, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Neurology Department, Fleni, Buenos Aires, Argentina. Clinical Neurosciences, Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. Translational Immunology Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland. Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Uppsala University Hospital, Uppsala, Sweden. Department of Medical Sciences, Section of Neurology, Uppsala University, Uppsala, Sweden. Department of Ophthalmology, CHU St Pierre and Brugmann, Brussels, Belgium. Neurology Unit, Fondazione Policlinico Universitario 'A.Gemelli' IRCCS, Rome, Italy. Neurology Department, Fleni, Buenos Aires, Argentina. Neurology Department, Fleni, Buenos Aires, Argentina. Institute of Biological Chemistry and Biophysics (IQUIFIB) CONICET, University of Buenos Aires, Buenos Aires, Argentina. Department of Neurology, Neurocenter, Helsinki University Hospital, Helsinki, Finland. Research Program of Translational Immunology, Faculty of Medicine, University of Helsinki, Helsinki, Finland. Neurology Unit, Fondazione Policlinico Universitario 'A.Gemelli' IRCCS, Rome, Italy. Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Neurology Unit, Fondazione Policlinico Universitario 'A.Gemelli' IRCCS, Rome, Italy. Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy.
 Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Electronic address: rdeschamps@for.paris. Department of Radiology, Hôpital Fondation Adolphe de Rothschild, Paris, France; Department of Neuro-Radiology, Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires La Pitié Salpêtrière - Sorbonne Université, Paris, France. Department of Neuro-Ophthalmology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Clinical Research Department, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Radiology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hospices civils de Lyon, Hôpital neurologique Pierre Wertheimer, Lyon/Bron, France. Clinical Research Department, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, Hôpital Fondation Adolphe de Rothschild, Paris, France. Department of Neuro-Ophthalmology, Hôpital Fondation Adolphe de Rothschild, Paris, France.
 Faculty of Dentistry, Department of Basic Medical Sciences, Marmara University, Istanbul, Turkey. eiemekli@marmara.edu.tr. Faculty of Medicine, Department of Biochemistry, Istanbul University-Cerrahpaşa, Istanbul, Turkey.
 Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata , Mohanpur, West Bengal, India. Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata , Mohanpur, West Bengal, India. Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata , Mohanpur, West Bengal, India. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA. Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University , Philadelphia, Pennsylvania, USA. Department of Neurosciences, Cleveland Clinic , Cleveland, Ohio, USA. Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA. Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata , Mohanpur, West Bengal, India.
 State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou, China. Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Guangzhou, China.
 The Foundation for Orthopaedics and Regenerative Medicine, Glenview, Illinois 60025, USA. The Foundation for Orthopaedics and Regenerative Medicine, Glenview, Illinois 60025, USA. The Foundation for Orthopaedics and Regenerative Medicine, Glenview, Illinois 60025, USA. The Foundation for Orthopaedics and Regenerative Medicine, Glenview, Illinois 60025, USA.
 Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts; Medically Engineered Solutions in Healthcare Incubator, Innovation in Operations Research Center (MESH IO), Massachusetts General Hospital, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts; Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts; Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts. Siemens Medical Solutions, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts; Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts; Medically Engineered Solutions in Healthcare Incubator, Innovation in Operations Research Center (MESH IO), Massachusetts General Hospital, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street Boston, Boston, Massachusetts; Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts. Electronic address: susie.huang@mgh.harvard.edu.
 Division of Food Science and Biotechnology, Department of Science and Technology Agriculture, Graduate School of Medicine, Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Department of Agricultural and Life Science, Faculty of Agriculture, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Science and Technology Agriculture, Graduate School of Medicine, Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan; Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan; Department of Agricultural and Life Science, Faculty of Agriculture, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan; Division of Innovative Biomolecular Science, Interdisciplinary Cluster for Cutting Edge, Institute for Biomedical Sciences, Shinshu University, 8304 Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Division of Food Science and Biotechnology, Department of Science and Technology Agriculture, Graduate School of Medicine, Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan; Division of Food Science and Biotechnology, Department of Agriculture, Graduate School of Science and Technology, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan; Department of Agricultural and Life Science, Faculty of Agriculture, Shinshu University, Minami-minowa, Kami-ina, Nagano, 399-4598, Japan. Electronic address: tanakasa@shinshu-u.ac.jp.
 i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal; ICBAS - Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal; IUCS - Instituto Universitário de Ciências da Saúde, CESPU, Rua Central de Gandra 1317, 4585-116 Gandra, Portugal. i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal; FEUP - Faculdade de Engenharia da Universidade do Porto, Universidade do Porto, Dr. Roberto Frias, 4200-465 Porto, Portugal. i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal; ICBAS - Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal. Advanced Drug Delivery and Biomaterials, Louvain Drug Research Institute, University of Louvain, 1200 Brussels, Belgium. i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal; FEUP - Faculdade de Engenharia da Universidade do Porto, Universidade do Porto, Dr. Roberto Frias, 4200-465 Porto, Portugal. i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal; ICBAS - Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal; IUCS - Instituto Universitário de Ciências da Saúde, CESPU, Rua Central de Gandra 1317, 4585-116 Gandra, Portugal. Electronic address: bruno.sarmento@i3s.up.pt.
 From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). From the Weill Institute for Neurosciences (F.C.C.O., A.K., S.C.-M., C.C., A.A., A.J.G.), Department of Neurology, University of California San Francisco (UCSF); Experimental and Clinical Research Center (F.C.C.O., S.M., H.G.Z., C.B., J.B.-S., F.P., A.U.B.), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Department of Neurology with Institute of Translational Neurology (J.K., H.W.), University Hospital Münster, Germany; University of California Berkeley (A.K.); Department of Neurology (N.G.D., O.A., S.G.M., P.A.), Medical Faculty, Heinrich-Heine University and University Hospital Düsseldorf, Germany; Department of Neurology (P.A.), Maria Hilf Clinic Moenchengladbach, Germany; Queen Square MS Centre (A.T., A.P.), University College London, UK; Department of Neurology (K.R., F.P.),-Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany; Moorfield's Eye Hospital & The National Hospital for Neurology and Neurosurgery (A.P.); Queen Square Institute of Neurology, University College London, UK; Dutch Neuro-ophthalmology Expertise Centre, Amsterdam, NL; Department of Neurology (A.U.B.), University of California Irvine (UCI); and Department of Ophthalmology (A.J.G.), University of California San Francisco (UCSF). agreen@ucsf.edu.
 Department of Biomedical Sciences, Sassari University, Sassari, Italy. Department of Neurology, Juntendo University, Tokyo, Japan. Juntendo University, Biomedical Research Core Facilities, Tokyo, Japan. Department of Neurology, Juntendo University, Tokyo, Japan. Juntendo University, Division of Cell Biology, Tokyo, Japan. Department of Biomedical Sciences, Sassari University, Sassari, Italy. SC Microbiologia AOU Sassari, Sassari, Italy. Department of Neurology, Juntendo University, Tokyo, Japan.
 Iowa City Veterans Affairs Medical Center, Iowa City, IA. Department of Pathology Graduate Program, University of Iowa, Iowa City, IA. Iowa City Veterans Affairs Medical Center, Iowa City, IA. Department of Pathology Graduate Program, University of Iowa, Iowa City, IA. Department of Pathology, University of Iowa Carver College of Medicine, Iowa City, IA. Iowa City Veterans Affairs Medical Center, Iowa City, IA. Department of Pathology Graduate Program, University of Iowa, Iowa City, IA. Department of Pathology, University of Iowa Carver College of Medicine, Iowa City, IA. Iowa City Veterans Affairs Medical Center, Iowa City, IA. Department of Pathology, University of Iowa Carver College of Medicine, Iowa City, IA.
 Neurology, Hospital Clínico San Carlos, IdISSC, Madrid, Spain; Department of Medicine, Faculty of Medicine, Universidad Complutense de Madrid, Spain. Queen Square MS Centre, National Hospital for Neurology and Neurosurgery, London, United Kingdom. Department of Neurology, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Systems Medicine, Tor Vergata University, Rome, Italy; Unit of Neurology, IRCCS Neuromed, Pozzilli (IS), Italy. Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Department of Neurology, Liverpool Hospital, and UNSW Sydney, New South Wales, Australia. Department of Neurology and Center for Translational and Behavioural Neurosciences (C-TNBS), University Hospital Essen, Essen, Germany. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital, Rigshospitalet, Denmark. Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada. Univ. Lille, Inserm U1172, CHU Lille, FHU Precise, Lille, France. Department of Neurology, Institute of Translational Neurology, University of Münster, Münster, Germany. University MS Centre, Hasselt-Pelt, Hasselt University, Belgium. Ares Trading SA, Eysins, Switzerland (An Affiliate of Merck KGaA). Neurology Institute, Harley Street Medical Center, Abu Dhabi, UAE; American University of Beirut, Lebanon. Electronic address: yamoutba@gmail.com.
 From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. From the Department of Neurology (S.G., S.A.S., C.S., R.D., S.L.H., M.R.W., S.S.Z.), Weill Institute for Neurosciences, University of California San Francisco, CA; Department of Cellular Molecular Pharmacology (M.S., J.D., W.L.), University of California San Francisco Cell Design Institute, CA; Veterans Affairs Health Care System (R.A.S.), Department of Pathology, Stanford University School of Medicine, CA; Departments of Neurology and Pathology and Immunology (G.F.W.), Washington University in St. Louis, MO; and Chan Zuckerberg Biohub (W.W., J.E.P.), San Francisco, CA. zamvil@ucsf.neuroimmunol.org.
 Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Arthritis & Clinical Immunology, Oklahoma Medical Research Foundation, OK, USA. Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA; Oklahoma City VA Medical Center, Oklahoma City, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Advanced Magnetic Resonance Center, Oklahoma Medical Research Foundation, OK, USA. Advanced Magnetic Resonance Center, Oklahoma Medical Research Foundation, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA; Oklahoma City VA Medical Center, Oklahoma City, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA. Advanced Magnetic Resonance Center, Oklahoma Medical Research Foundation, OK, USA. Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, OK, USA; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, OK, USA; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma City VA Medical Center, Oklahoma City, OK, USA. Arthritis & Clinical Immunology, Oklahoma Medical Research Foundation, OK, USA. Electronic address: bob-axtell@omrf.org. Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, OK, USA; Oklahoma City VA Medical Center, Oklahoma City, OK, USA. Electronic address: Holly-VanRemmen@omrf.org.
 Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado School of Medicine, Aurora, CO 80045. F. Hoffmann-La Roche, 4070 Basel, Switzerland. Department of Medicine, University of British Columbia, Vancouver, BC V6T 2B5, Canada. Multiple Sclerosis Center of Northeastern New York, Comprehensive MS Care Center Affiliated with the National MS Society, Latham, NY 12110. Department of Neurology, Ohio State University Medical Center, Columbus, OH 43210. Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, QC H3A 2B4, Canada. Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Departments of Neurology and Immunobiology, Yale School of Medicine, New Haven, CT 06510. Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01655. Judith Jaffe Multiple Sclerosis Center, Weill Cornell Medicine, New York, NY 10021. Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA 94304. Department of Neurology, Yale University, New Haven, CT 06510. Oklahoma Medical Research Foundation, Multiple Sclerosis Center of Excellence, Oklahoma City, OK 73104. Department of Clinical Neuroscience, Karolinska Institute, SE-171 76 Stockholm, Sweden. Department of Neurology, Karolinska University Hospital, SE-171 77 Stockholm, Sweden. Neuroimmunology Unit, Center for Molecular Medicine, Karolinska University Hospital, Karolinska Institute, SE-171 77 Stockholm, Sweden. Institute of Neuropathology, University Medical Center, 37075 Göttingen, Germany. Department of Neurology, University Medical Center, 37075 Göttingen, Germany. Fraunhofer-Institute for Translational Medicine and Pharmackology ITMP, 37075 Göttingen, Germany. Department of Neurology, Center of Clinical Neuroscience, University Hospital Carl Gustav Carus, Technical University of Dresden, 01307 Dresden, Germany. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Weill Institute for Neurosciences, University of California, San Francisco, CA 94158. Department of Neurology, University of California, San Francisco, CA 94158. Department of Neurology, Washington University School of Medicine, Saint Louis, MO 63110. Genentech, Inc., South San Francisco, CA 94080. Genentech, Inc., South San Francisco, CA 94080. Genentech, Inc., South San Francisco, CA 94080. Genentech, Inc., South San Francisco, CA 94080. Genentech, Inc., South San Francisco, CA 94080. Genentech, Inc., South San Francisco, CA 94080. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104. Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA 19104.
 Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Neuroscience Graduate Program, University of Virginia, Charlottesville Virginia, United States of America. Center for Brain Immunology and Glia, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Neuroscience Graduate Program, University of Virginia, Charlottesville Virginia, United States of America. Center for Brain Immunology and Glia, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Neuroscience Graduate Program, University of Virginia, Charlottesville Virginia, United States of America. Center for Brain Immunology and Glia, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Neuroscience Graduate Program, University of Virginia, Charlottesville Virginia, United States of America. Center for Brain Immunology and Glia, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Department of Neuroscience, University of Virginia, Charlottesville, Virginia, United States of America. Center for Brain Immunology and Glia, University of Virginia, Charlottesville, Virginia, United States of America.
 Department of Molecular Neurobiology, Groningen Institute of Evolutionary Life Science (GELIFES), University of Groningen, 9747 AG, Groningen, The Netherlands. Institute of Cell Biology and Immunology, University of Stuttgart, 70569, Stuttgart, Germany. Stuttgart Research Centre Systems Biology, University of Stuttgart, 70569, Stuttgart, Germany. Division of Neuroimmunology, Center for Brain Research, Medical University of Vienna, 1090, Vienna, Austria. Institute of Cell Biology and Immunology, University of Stuttgart, 70569, Stuttgart, Germany. Stuttgart Research Centre Systems Biology, University of Stuttgart, 70569, Stuttgart, Germany. Department of Molecular Neurobiology, Groningen Institute of Evolutionary Life Science (GELIFES), University of Groningen, 9747 AG, Groningen, The Netherlands. Department of Molecular Neurobiology, Groningen Institute of Evolutionary Life Science (GELIFES), University of Groningen, 9747 AG, Groningen, The Netherlands. Institute of Cell Biology and Immunology, University of Stuttgart, 70569, Stuttgart, Germany. Stuttgart Research Centre Systems Biology, University of Stuttgart, 70569, Stuttgart, Germany. Institute of Cell Biology and Immunology, University of Stuttgart, 70569, Stuttgart, Germany. Stuttgart Research Centre Systems Biology, University of Stuttgart, 70569, Stuttgart, Germany. Neuroimmune Connections and Repair (NIC&R) Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, 3590, Hasselt, Belgium. University MS Centre, 3590, Hasselt/Pelt, Belgium. Neuroimmune Connections and Repair (NIC&R) Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, 3590, Hasselt, Belgium. University MS Centre, 3590, Hasselt/Pelt, Belgium. Neuroimmune Connections and Repair (NIC&R) Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, 3590, Hasselt, Belgium. University MS Centre, 3590, Hasselt/Pelt, Belgium. Department Biomedical Sciences of Cells and Systems (BSCS), Section Molecular Neurobiology, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands. Department Pathology and Medical Biology, University Medical Centre Groningen (UMCG), University of Groningen, 9713 GZ, Groningen, The Netherlands. Department of Molecular Neurobiology, Groningen Institute of Evolutionary Life Science (GELIFES), University of Groningen, 9747 AG, Groningen, The Netherlands. u.l.m.eisel@rug.nl.
 Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (Rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. luessi@uni-mainz.de.
 Department of Neurology, School of Medicine, University of Maryland, College Park, USA. sandhava@umd.edu. Research Service, Institute of Human Virology, VA Maryland Health Care System, 725 W Lombard St, Baltimore, MD, 21201, USA. sandhava@umd.edu. Department of Neurology, School of Medicine, University of Maryland, College Park, USA. Department of Neurology, School of Medicine, University of Maryland, College Park, USA. Department of Neurology, School of Medicine, University of Maryland, College Park, USA. Department of Neurosurgery, School of Medicine, University of Maryland, College Park, USA. Department of Neurosurgery, School of Medicine, University of Maryland, College Park, USA. Department of Neurosurgery, School of Medicine, University of Maryland, College Park, USA. Department of Neurology, School of Medicine, University of Maryland, College Park, USA. Department of Neurology, School of Medicine, University of Maryland, College Park, USA. Research Service, Institute of Human Virology, VA Maryland Health Care System, 725 W Lombard St, Baltimore, MD, 21201, USA. Department of Veterans Affairs, Office of Research and Development, Washington, USA.
 From the Neuroradiology Group (D.P., J.F.C., A.G.-V., C.A., À.R.), Vall d'Hebron Research Institute, Barcelona, Spain deborah.pareto.idi@gencat.cat. Section of Neuroradiology (D.P., J.F.C., M.A., À.R.), Radiology Department, Vall d'Hebron University Hospital, Barcelona, Spain. From the Neuroradiology Group (D.P., J.F.C., A.G.-V., C.A., À.R.), Vall d'Hebron Research Institute, Barcelona, Spain. Section of Neuroradiology (D.P., J.F.C., M.A., À.R.), Radiology Department, Vall d'Hebron University Hospital, Barcelona, Spain. From the Neuroradiology Group (D.P., J.F.C., A.G.-V., C.A., À.R.), Vall d'Hebron Research Institute, Barcelona, Spain. Section of Neuroradiology (D.P., J.F.C., M.A., À.R.), Radiology Department, Vall d'Hebron University Hospital, Barcelona, Spain. From the Neuroradiology Group (D.P., J.F.C., A.G.-V., C.A., À.R.), Vall d'Hebron Research Institute, Barcelona, Spain. Department of Neurology and Neuroimmunology (J.R., N.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology and Neuroimmunology (J.R., N.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology and Neuroimmunology (J.R., N.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain. From the Neuroradiology Group (D.P., J.F.C., A.G.-V., C.A., À.R.), Vall d'Hebron Research Institute, Barcelona, Spain. Section of Neuroradiology (D.P., J.F.C., M.A., À.R.), Radiology Department, Vall d'Hebron University Hospital, Barcelona, Spain.
 Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Hospital, Sendai 980-8574, Japan. Department of Neurology, National Hospital Organization Yonezawa National Hospital, Yonezawa 992-1202, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Hospital, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Hospital, Sendai 980-8574, Japan. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University, Fukushima 960-1295, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. Department of Neurology, Tohoku University Hospital, Sendai 980-8574, Japan.
 Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Assistance Publique Hôpitaux de Paris, Hôpital Pitié Salpêtrière, Département de Santé Publique, Centre de Pharmacoépidémiologie (Cephepi), Unité de Recherche Clinique PSL-CFX, Paris, France. Sorbonne Université, Assistance Publique des Hôpitaux de Paris, Hôpital de la Pitié Salpêtrière, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Neuroscience Clinical Investigation Center, Paris Brain Institute, Paris, France. Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Assistance Publique Hôpitaux de Paris, Hôpital Pitié Salpêtrière, Département de Santé Publique, Centre de Pharmacoépidémiologie (Cephepi), Unité de Recherche Clinique PSL-CFX, Paris, France. Department of Neurology, CRC-SEP, Montpellier University Hospital, Montpellier, France/Institute for Neurosciences of Montpellier, INSERM and University of Montpellier, Montpellier, France. Sorbonne Université, Assistance Publique des Hôpitaux de Paris, Hôpital de la Pitié Salpêtrière, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Neuroscience Clinical Investigation Center, Paris Brain Institute, Paris, France. Department of Neurology and Clinical Investigation Center, CHU de Strasbourg, CIC 1434, INSERM 1434, Strasbourg, France. Department of Neurology, CHU Lille, INSERM U1172, University of Lille, Lille, France. Aix Marseille University, Assistance Publique Hopitaux de Marseille, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie, Marseille, France. Association des Neurologues Libéraux de Langue Française, Bergerac, France. Département de Neurologie, Hôpital Fondation Adolphe de Rothschild, Paris, France. Département de Neurologie, CRC-SEP, Centre Hospitalier de Poissy-St Germain-en-Laye, France. Neurologie, Pathologies Inflammatoires du Système Nerveux, CHU Grenoble Alpes, Grenoble, France / Techniques de l'Ingénierie Médicale et de la Complexité-Informatique, Mathématiques et Applications, Grenoble, Translational Research in Autoimmunity and Inflammation Group, Université de Grenoble Alpes, Grenoble, France. Centre Ressources et Compétences Sclérose en Plaques (CRC-SEP) et Service de Neurologie B4, Hôpital Pierre-Paul Riquet, CHU Toulouse Purpan, Toulouse, France INSERM UMR1291-CNRS UMR5051, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse 3, Toulouse, France. Department of Neurology, CHU Rouen, Rouen, France. Hospices Civils de Lyon, Hôpital Neurologique, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Bron, France. CRC-SEP and Department of Neurology, CHU de Tours, Hôpital Bretonneau, Tours, France. CHU de Besançon, Service de Neurologie, Besançon, France. CHU de Nantes, Service de Neurologie & CIC015 INSERM, Nantes, France. CRC-SEP CHU Nice, UR2CA-URRIS, Université Nice Cote d'Azur, Hôpital Pasteur 2, Nice, France. Assistance Publique Hôpitaux de Paris, Sorbonne Université, Department of Neurology, Saint-Antoine Hospital, CRC-SEP Paris, Paris, France. Service de Neurologie, CHU de Caen Normandie, Caen, France. Department of Neurology, Nimes University Hospital, Nimes, France. Institut de Génomique Fonctionnelle, UMR5203, INSERM 1191, Université de Montpellier, Montpellier, France. Department of Neurology, CHU Clermont-Ferrand, Clermont-Ferrand, France. Département de Neurologie, Hôpitaux Civils de Colmar, Unité INSERM U-1118, Faculté de Médecine, Université de Strasbourg, Strasbourg, France. Department of Neurology, Gonesse Hospital, Gonesse, France. Department of Neurology, CHU de Dijon, Dijon, France. Département de Neurologie, Hôpital Fondation Adolphe de Rothschild, Paris, France. Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Assistance Publique Hôpitaux de Paris, Hôpital Pitié Salpêtrière, Département de Santé Publique, Centre de Pharmacoépidémiologie (Cephepi), Unité de Recherche Clinique PSL-CFX, Paris, France. Sorbonne Université, Assistance Publique des Hôpitaux de Paris, Hôpital de la Pitié Salpêtrière, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Neuroscience Clinical Investigation Center, Paris Brain Institute, Paris, France.
 From the Duke University School of Medicine (J.B.L., B.G.H.); Duke University Fuqua School of Business (J.B.L.); Duke University Department of Population Health Sciences (M.N.H., A.G.C., B.G.H.); Duke University Health System (J.B.); Duke University Department of Medicine (J.B.); and Duke University Department of Neurology (M.W.L.), Durham, NC. From the Duke University School of Medicine (J.B.L., B.G.H.); Duke University Fuqua School of Business (J.B.L.); Duke University Department of Population Health Sciences (M.N.H., A.G.C., B.G.H.); Duke University Health System (J.B.); Duke University Department of Medicine (J.B.); and Duke University Department of Neurology (M.W.L.), Durham, NC. From the Duke University School of Medicine (J.B.L., B.G.H.); Duke University Fuqua School of Business (J.B.L.); Duke University Department of Population Health Sciences (M.N.H., A.G.C., B.G.H.); Duke University Health System (J.B.); Duke University Department of Medicine (J.B.); and Duke University Department of Neurology (M.W.L.), Durham, NC. From the Duke University School of Medicine (J.B.L., B.G.H.); Duke University Fuqua School of Business (J.B.L.); Duke University Department of Population Health Sciences (M.N.H., A.G.C., B.G.H.); Duke University Health System (J.B.); Duke University Department of Medicine (J.B.); and Duke University Department of Neurology (M.W.L.), Durham, NC. From the Duke University School of Medicine (J.B.L., B.G.H.); Duke University Fuqua School of Business (J.B.L.); Duke University Department of Population Health Sciences (M.N.H., A.G.C., B.G.H.); Duke University Health System (J.B.); Duke University Department of Medicine (J.B.); and Duke University Department of Neurology (M.W.L.), Durham, NC. From the Duke University School of Medicine (J.B.L., B.G.H.); Duke University Fuqua School of Business (J.B.L.); Duke University Department of Population Health Sciences (M.N.H., A.G.C., B.G.H.); Duke University Health System (J.B.); Duke University Department of Medicine (J.B.); and Duke University Department of Neurology (M.W.L.), Durham, NC. brad.hammill@duke.edu.
 Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Internal Medicine, Japan Self Defense Forces Hanshin Hospital, Kawanishi City 666-0024, Hyogo, Japan. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashiosaka City 577-8502, Osaka, Japan. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Arts and Science, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Neurology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Immunology, School of Medicine, Duke University, Durham, NC 27710, USA. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Department of Neurology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan. Japan Community Health care Organization (JCHO) Headquarters, Minato City 108-8583, Tokyo, Japan. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama City 589-8511, Osaka, Japan.
 Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Crump Institute for Molecular Imaging, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Crump Institute for Molecular Imaging, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Crump Institute for Molecular Imaging, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Crump Institute for Molecular Imaging, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Department of Medicine, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Ahmanson Translational Imaging Division, University of California, Los Angeles, Los Angeles, California, USA. Department of Medicine, University of California, Los Angeles, Los Angeles, California, USA. Enosi Life Sciences, Eugene, Oregon, USA. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Ahmanson Translational Imaging Division, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Ahmanson Translational Imaging Division, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, California, USA. Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Ahmanson Translational Imaging Division, University of California, Los Angeles, Los Angeles, California, USA. Trethera Corporation, Los Angeles, California, USA. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California, USA. Crump Institute for Molecular Imaging, University of California, Los Angeles, Los Angeles, California, USA. Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, California, USA.
 Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China; Department of Neurology, Baoding First Central Hospital, Baoding, China. Department of Pharmacy, Shijiazhuang People's Hospital, Shijiazhuang, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, China; Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, China; Key Laboratory of Neurology of Hebei Province, Shijiazhuang, China. Electronic address: jack511@163.com.
 Centro de Esclerosis Múltiple de Buenos Aires, Buenos Aires, Argentina. E-mail: rojasjuanignacio@gmail.com. Servicio de Neurología, Unidad de Esclerosis Múltiple y Enfermedades Desmielinizantes, Hospital Universitario de CEMIC, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple - Hospital Dr. J. M. Ramos Mejía, Facultad de Medicina - UBA, Buenos Aires, Argentina. Sanatorio Güemes, Buenos Aires, Argentina. Hospital Militar Campo de Mayo, Buenos Aires, Argentina. Unidad de Neuroimnunología, Departamento de Neurociencias, Hospital Alemán, Buenos Aires, Argentina. Centro de Esclerosis Múltiple de Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, Hospital Fernández, Buenos Aires, Argentina. Servicio de Neurología, Hospital Carlos G. Durand, Buenos Aires, Argentina. Unidad de Neuroimnunología, Departamento de Neurociencias, Hospital Alemán, Buenos Aires, Argentina. Instituto de Neurociencias de Rosario, Rosario, Santa Fe, Argentina. Centro de Esclerosis Múltiple de Buenos Aires, Buenos Aires, Argentina. Sección de Neuroinmunología y Enfermedades Desmielinizantes, Servicio de Neurología, Hospital de Clínicas José de San Martín, Buenos Aires, Argentina. FLENI, Buenos Aires, Argentina. Departamento de Neurología, Hospital César Milstein, Buenos Aires, Argentina. Universidad de Buenos Aires, Facultad de Medicina, Buenos Aires, Argentina. CONICET - Universidad de Buenos Aires, Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Buenos Aires, Argentina. CONICET - Universidad de Buenos Aires, Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Buenos Aires, Argentina. Universidad de Buenos Aires, Facultad de Medicina, Departamento de Microbiología, Parasitología e Inmunología, Buenos Aires, Argentina. Universidad de Buenos Aires, Facultad de Medicina, Buenos Aires, Argentina. CONICET - Universidad de Buenos Aires, Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Buenos Aires, Argentina. CONICET - Universidad de Buenos Aires, Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Buenos Aires, Argentina. Universidad de Buenos Aires, Facultad de Medicina, Departamento de Microbiología, Parasitología e Inmunología, Buenos Aires, Argentina. Unidad de Infectología, Sanatorio Güemes, Departamento de Investigación Epidemiológica, Fundación Sanatorio Güemes, Buenos Aires, Argentina.
 Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa 31982, Saudi Arabia. Department of Pharmacology, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh 33516, Egypt. Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, Al-Ahsa 31982, Saudi Arabia. Department of Pharmacology, Faculty of Medicine, Minia University, El-Minia 61511, Egypt. Department of Anatomy, College of Veterinary Medicine, King Faisal University, Al-Ahsa 31982, Saudi Arabia. Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa 31982, Saudi Arabia.
 Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Surgery, University of Milano Bicocca, 20126 Milan, Italy. Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Surgery, University of Milano Bicocca, 20126 Milan, Italy. Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Rehabilitation, Policlinico di Monza, 20900 Monza, Italy. Department of Medicine and Surgery, University of Milano Bicocca, 20126 Milan, Italy.
 Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran. Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran. Department of Biochemistry, Faculty of Medicine, Lorestan University of Medical Sciences, Khorramabad 68138-33946, Iran. Electronic address: hassan46ahmadvand@gmail.com. Razi Herbal Medicine Research Center and Department of physiology, Lorestan University of Medical Sciences, Khorramabad, Iran. Electronic address: mojkhaksar@yahoo.com. Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
 National Centre for Epidemiology and Population Health, Australian National University, Canberra, Australian Capital Territory, Australia. Clinical Virology Department, Centre for Infectious Diseases & Microbiology Laboratory Services, Institute of Clinical Pathology & Medical Research, Westmead Hospital, Westmead, New South Wales, Australia. ANU Medical School, Australian National University, Canberra, Australian Capital Territory, Australia. National Centre for Epidemiology and Population Health, Australian National University, Canberra, Australian Capital Territory, Australia. Clinical Virology Department, Centre for Infectious Diseases & Microbiology Laboratory Services, Institute of Clinical Pathology & Medical Research, Westmead Hospital, Westmead, New South Wales, Australia. University of Adelaide, Adelaide, South Australia, Australia. Menzies Research Institute Tasmania, Hobart, Tasmania, Australia. Clinical Virology Department, Centre for Infectious Diseases & Microbiology Laboratory Services, Institute of Clinical Pathology & Medical Research, Westmead Hospital, Westmead, New South Wales, Australia. Howard Florey Institute, Melbourne, Victoria, Australia.
 Department of Neurology, National Neuroscience Institute, Singapore, Singapore. yeo.tianrong@singhealth.com.sg. Duke-NUS Medical School, Singapore, Singapore. yeo.tianrong@singhealth.com.sg. Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore. yeo.tianrong@singhealth.com.sg. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Duke-NUS Medical School, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Duke-NUS Medical School, Singapore, Singapore. Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. Department of Neurology, National Neuroscience Institute, Singapore, Singapore. Duke-NUS Medical School, Singapore, Singapore.
 Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, MD, USA. Departments of Biochemistry and Computer Science, Purdue University, West Lafayette, IN, USA. Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, MD, USA. Departments of Biochemistry and Computer Science, Purdue University, West Lafayette, IN, USA. Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, MD, USA. Electronic address: behdad.afzali@nih.gov.
 Siriraj Neuroimmunology Center, Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Department of Medicine, Chumphon Khet Udomsak Hospital, Chumphon 86000, Thailand. Siriraj Neuroimmunology Center, Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Bumrungrad International Hospital, Bangkok 10110, Thailand. Siriraj Neuroimmunology Center, Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Department of Neurology, Neurological Institute of Thailand, Bangkok 10400, Thailand. Department of Research and Development, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Siriraj Neuroimmunology Center, Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Siriraj Neuroimmunology Center, Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Electronic address: jiraporn.jit@mahidol.ac.th.
 Institute of Chemical Biology and Fundamental Medicine, SB of the Russian Academy of Sciences, Lavrentiev Ave., 8, Novosibirsk 630090, Russia. Institute of Chemical Biology and Fundamental Medicine, SB of the Russian Academy of Sciences, Lavrentiev Ave., 8, Novosibirsk 630090, Russia. Institute of Chemical Biology and Fundamental Medicine, SB of the Russian Academy of Sciences, Lavrentiev Ave., 8, Novosibirsk 630090, Russia. Institute of Chemical Biology and Fundamental Medicine, SB of the Russian Academy of Sciences, Lavrentiev Ave., 8, Novosibirsk 630090, Russia.
 Department of Neurology, "Dr. Carol Davila" Central Military Emergency University Hospital, Bucharest, Romania. Department of Neurology, "Dr. Carol Davila" Central Military Emergency University Hospital, Bucharest, Romania. Department of Neurology, "Dr. Carol Davila" Central Military Emergency University Hospital, Bucharest, Romania. Department of Natural Sciences, University of Pitesti, Faculty of Sciences, Physical Education and Informatics, Piteşti, Romania. Department of Health Care and Physical Therapy, University of Pitesti, Faculty of Sciences, Physical Education and Informatics, Piteşti, Romania. Biochemistry Department, "Carol Davila" University of Medicine and Pharmacy, Faculty of Pharmacy, Bucharest, Romania; and. Department of Neurology, "Dr. Carol Davila" Central Military Emergency University Hospital, Bucharest, Romania. Clinical Neurosciences Department, University of Medicine and Pharmacy "Carol Davila" Bucharest, Romania.
 From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. From the Department of Neurology (S.A.L., E.L.E., H.W., B.M., S.D., A.P., M.R.W., B.A.C.C., H.-C.B.), Weill Institute for Neurosciences; Biomedical Sciences Graduate Program (N.B.S.); Bakar Computational Health Sciences Institute and Department of Pediatrics (M.S.); Department of Bioengineering and Therapeutic Sciences (R.D.H.), University of California, San Francisco, CA; Department of Human Genetics (R.D.H.), McGill University, Montreal, QC, Canada; and OMNI Biomarker Development (A.E.H.), Genentech, Inc., South San Francisco, CA. h-christian.von_buedingen@roche.com.
 Department of Neurology, Alfried Krupp Krankenhaus Essen, Alfried-Krupp-Straße 21, 45131, Essen, Germany. daniel.strunk@krupp-krankenhaus.de. Department of Neurology, Alfried Krupp Krankenhaus Essen, Alfried-Krupp-Straße 21, 45131, Essen, Germany. Department of Neurology, Alfried Krupp Krankenhaus Essen, Alfried-Krupp-Straße 21, 45131, Essen, Germany. Department of Brain Sciences, Imperial College London, London, UK. Department of Neurology, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. CENTOGENE GmbH, Rostock, Germany. CENTOGENE GmbH, Rostock, Germany. Medical Service Center of Johanna-Odebrecht-Stiftung, Greifswald, Germany. Arcenus Diagnostics, Hoboken, NJ, 07030, USA. Department of Behavioral Neuroscience, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Alfried Krupp Krankenhaus Essen, Alfried-Krupp-Straße 21, 45131, Essen, Germany. Department of Neurology, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
 Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. School of Life and Medical Sciences, University of Hertfordshire Hosted by Global Academic Foundation, New Administrative Capital, Cairo 11578, Egypt. Egyptian Drug Authority (EDA), Ministry of Health and Population, Cairo 11567, Egypt. Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University, Cairo 11562, Egypt. Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.
 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: v.shaygannejad@gmail.com. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran; Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
 Living Robotics Laboratory, Istanbul Medipol University, Biomedical Engineering, Istanbul, Türkiye. Ozyegin University, Mechanical Engineering, Istanbul, Türkiye. Living Robotics Laboratory, Istanbul Medipol University, Electrical and Electronics Engineering, Istanbul, Türkiye. Research Institute for Health Sciences and Technologies (SABITA), Istanbul Medipol University, Istanbul, Türkiye.
 Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade do Estado do Rio de Janeiro, Departamento de Farmacologia e Psicobiologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal Fluminense, Hospital Universitário Antônio Pedro, Departamento de Neurologia, Niterói RJ, Brazil. Universidade Federal Fluminense, Hospital Universitário Antônio Pedro, Departamento de Radiologia, Niterói RJ, Brazil. Universidade Federal Fluminense, Hospital Universitário Antônio Pedro, Departamento de Radiologia, Niterói RJ, Brazil. Universidade Federal Fluminense, Hospital Universitário Antônio Pedro, Departamento de Radiologia, Niterói RJ, Brazil. Universidade Federal do Rio de Janeiro, Instituto de Biologia, Departamento de Genética, Rio de Janeiro RJ, Brazil. Hospital São Francisco na Providência de Deus, Departamento de Neurologia, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Hospital Universitário Clementino Fraga Filho, Departamento de Neurocirurgia, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Departamento de Genética e Biologia Molecular, Grupo de Bioinformática e Biologia Computacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Estado do Rio de Janeiro, Programa de Pós-Graduação em Neurologia, Laboratório de Neurociências Translacional, Rio de Janeiro RJ, Brazil. Universidade Federal do Rio de Janeiro, Hospital Universitário Clementino Fraga Filho, Centro de Referência e Pesquisa em Esclerose Múltipla e Outras Doenças Desmielinizantes Inflamatórias Idiopáticas do SNC, Rio de Janeiro RJ, Brazil.
 Department of Ophthalmology and Neurology, Mayo Clinic, Rochester, MN, USA. Department of Ophthalmology and Neurology, Mayo Clinic, Rochester, MN, USA. chen.john@mayo.edu.
 From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. From the Multiple Sclerosis Center (G.D., R.S., J.J.E., C.Z., C.G.), Neurocenter of Southern Switzerland, Ente Ospedaliero Cantonale, Lugano; Institute for Research in Biomedicine (A.G., F.M., F.S.), Università Della Svizzera Italiana, Bellinzona; Institute of Laboratory Medicine (M.C., F.K.), Ente Ospedaliero Cantonale, Bellinzona; Department of Medicine (E.B.), Ente Ospedaliero Cantonale, Lugano; Faculty of Biomedical Sciences (E.B., F.S., C.Z., C.G.), Università Della Svizzera Italiana, Lugano; and Institute of Microbiology (F.S.), ETH Zurich, Switzerland. claudio.gobbi@eoc.ch.
 Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands; University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands; University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands; University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. Department of Cardio and Organ Systems, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Department of Cardio and Organ Systems, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Department of Cardio and Organ Systems, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Department of Pharmacy, Section of Medicinal Chemistry, University of Genoa, Genova, Italy. Department of Pharmacy, Section of Medicinal Chemistry, University of Genoa, Genova, Italy. Department of Pharmacy, Section of Pharmacology and Toxicology, University of Genova, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy. IRCCS Ospedale Policlinico San Martino, Genova, Italy; Department of Experimental Medicine, Section of General Pathology, University of Genova, Genova, Italy. MRC Centre for Regenerative Medicine and MS Society Edinburgh Centre, Edinburgh bioQuarter, University of Edinburgh, Edinburgh, UK. Department of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY, USA. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Department of Biomedical Sciences of Cells and Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. Rewind Therapeutics NV, Gaston Geenslaan 2, B-3001, Leuven, Belgium. Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg. Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg. Stem Cell Institute, Department of Development and Regeneration, KU Leuven, Belgium. University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium; Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium; Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. MERLN Institute for Technology-Inspired Regenerative Medicine, Complex Tissue Regeneration department, Maastricht University, Maastricht, the Netherlands. University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium; Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands. Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands; University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. Electronic address: t.vanmierlo@maastrichtuniversity.nl.
 Departments of1Radiology. 2Neurosurgery, and. 2Neurosurgery, and. 3College of Pharmacy, University of Minnesota, Minneapolis, Minnesota. 4Diagnostic and Biological Sciences, University of Minnesota; and. 2Neurosurgery, and. 2Neurosurgery, and.
 Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Pathology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea; kangbt@chungbuk.ac.kr. Laboratory of Veterinary Pathology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea skim0026@cbnu.ac.kr.
 Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy; Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Electronic address: alice.mariottini@unifi.it. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy; University "La Sapienza", Rome, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy; Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy; Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy. Department of Neurology 2 and Tuscan Region Multiple Sclerosis Referral Centre, Careggi University Hospital, Florence, Italy.
 Institute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia. Institute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia. Institute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia. Institute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia. Department of Neurology, University Medicine Essen, 45147 Essen, Germany. Center for Translational Neuro- and Behavioral Sciences, University Hospital Essen, 45147 Essen, Germany. Institute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia. Institute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.
 Department of Performance and Health (Sports Medicine), Institute of Sport and Sport Science, TU Dortmund University, Otto-Hahn-Str. 3, 44227 Dortmund, Germany. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland. Department of Performance and Health (Sports Medicine), Institute of Sport and Sport Science, TU Dortmund University, Otto-Hahn-Str. 3, 44227 Dortmund, Germany. Bevital AS, Laboratoriebygget, 9 etg, Jonas Lies vei 87, 5021 Bergen, Norway. Bevital AS, Laboratoriebygget, 9 etg, Jonas Lies vei 87, 5021 Bergen, Norway. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland; Department of Health, OST - Eastern Switzerland University of Applied Sciences, Rosenbergstrasse 59, 9000 Sankt Gallen, Switzerland. Department of Performance and Health (Sports Medicine), Institute of Sport and Sport Science, TU Dortmund University, Otto-Hahn-Str. 3, 44227 Dortmund, Germany. Electronic address: philipp.zimmer@tu-dortmund.de.
 Laboratory of Ion Channel Pathophysiology, Graduate School of Brain Science, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Center for Research in Neurodegenerative Diseases, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Department of Pharmacology, National Research Institute for Child Health and Development, Setagayaku, Tokyo, Japan. Laboratory of Ion Channel Pathophysiology, Graduate School of Brain Science, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Department of Neuropathology, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Department of Medical Neuroscience, Graduate School of Medical Sciences, Kanazawa University, Kanazawa-shi, Ishikawa, Japan. Department of Medical Neuroscience, Graduate School of Medical Sciences, Kanazawa University, Kanazawa-shi, Ishikawa, Japan. Center for Research in Neurodegenerative Diseases, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Department of Neuropathology, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Laboratory of Ion Channel Pathophysiology, Graduate School of Brain Science, Doshisha University, Kyotanabe-shi, Kyoto, Japan. Center for Research in Neurodegenerative Diseases, Doshisha University, Kyotanabe-shi, Kyoto, Japan.
 Theodor Kocher Institute, University of Bern, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Bern, Switzerland. Institute of Pathology, Experimental Pathology, University of Bern, Bern, Switzerland. Department of Pathology and Immunology, Division of Clinical Pathology, University and University Hospitals of Geneva, Geneva, Switzerland. Theodor Kocher Institute, University of Bern, Bern, Switzerland. Toulouse Institute for infectious and inflammatory diseases, University of Toulouse, CNRS, INSERM, UPS, Toulouse, France. Toulouse Institute for infectious and inflammatory diseases, University of Toulouse, CNRS, INSERM, UPS, Toulouse, France. Department of Oncology, Hematology and Bone Marrow Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute for Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany. Mayo Clinic Graduate School of Biomedical Sciences, College of Medicine, Mayo Clinic, Rochester, MN, USA. Institute of Pathology, Experimental Pathology, University of Bern, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Bern, Switzerland. Department of Pathology and Immunology, Division of Clinical Pathology, University and University Hospitals of Geneva, Geneva, Switzerland. Theodor Kocher Institute, University of Bern, Bern, Switzerland. britta.engelhardt@tki.unibe.ch.
 School of Clinical Medicine, School of Pharmacy and School of Basic Medicine, Yunnan University of Traditional Chinese Medicine, Kunming 650021, PR China. School of Clinical Medicine, School of Pharmacy and School of Basic Medicine, Yunnan University of Traditional Chinese Medicine, Kunming 650021, PR China. School of Clinical Medicine, School of Pharmacy and School of Basic Medicine, Yunnan University of Traditional Chinese Medicine, Kunming 650021, PR China. School of Clinical Medicine, School of Pharmacy and School of Basic Medicine, Yunnan University of Traditional Chinese Medicine, Kunming 650021, PR China. School of Clinical Medicine, School of Pharmacy and School of Basic Medicine, Yunnan University of Traditional Chinese Medicine, Kunming 650021, PR China. Department of Anesthesia & Critical Care, and Tang Center for Herbal Medicine Research, University of Chicago, Chicago, IL 60637, USA. School of Clinical Medicine, School of Pharmacy and School of Basic Medicine, Yunnan University of Traditional Chinese Medicine, Kunming 650021, PR China. Electronic address: wanchunping1012@163.com. Department of Anesthesia & Critical Care, and Tang Center for Herbal Medicine Research, University of Chicago, Chicago, IL 60637, USA.
 From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. From the Harvard Medical School (C.B., B.C.H., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.); Ann Romney Center for Neurologic Diseases (C.B., B.C.H., Y.L., S.S., A.P., M.P.-T., C.R.G.G., R.B., H.L.W., T.C.), Brigham and Women's Hospital; Brigham Multiple Sclerosis Center (R.B., H.L.W., T.C.), Department of Neurology, Brigham and Women's Hospital; Center for Neurological Imaging (C.R.G.G.), Department of Radiology, Brigham and Women's Hospital; Biostatistics Center (B.C.H.), Massachusetts General Hospital, Boston, MA; and Novartis Pharma AG (H.K.), Basel, Switzerland. tchitnis@rics.bwh.harvard.edu.
 Department of Therapeutic Chemistry, Pharmaceutical and Drug Industries Research Institute, National Research Centre, 33 El-Bohouth St., Dokki, Cairo 12622, Egypt. Electronic address: ghadhaibrahim@yahoo.com. Pathology Department, Faculty of Veterinary Medicine, Cairo University, Giza 12211, Egypt. Electronic address: kawkababdelaziz@cu.edu.eg.
 Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité - Universitätsmedizin Berlin, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany; Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany; Charité - Universitätsmedizin Berlin, Einstein Center for Neurosciences Berlin, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute of Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Berlin, Germany; Medical School Berlin, Department of Human Medicine, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute of Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Berlin, Germany; Institute of Chemistry, Freie Universität Berlin, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité - Universitätsmedizin Berlin, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany; Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute of Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Berlin, Germany; Institute of Biology, Freie Universität Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Radiology, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Radiology, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Department of Cardiology and Angiology, Berlin, Germany; DZHK (German Center for Cardiovascular Research), Partner Site, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute of Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Berlin, Germany; Medical School Berlin, Department of Human Medicine, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité - Universitätsmedizin Berlin, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany; Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Electronic address: carmen.infante@charite.de.
 UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. Novartis Pharmaceuticals, East Hanover, NJ, USA. Novartis Pharmaceuticals, East Hanover, NJ, USA. Novartis Pharmaceuticals, East Hanover, NJ, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. Electronic address: riley.bove@ucsf.edu.
 Department of Human Histology and Embryology, Guizhou Medical University, Guiyang, Guizhou 550025, China. Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, China. Department of Human Histology and Embryology, Guizhou Medical University, Guiyang, Guizhou 550025, China. Department of Human Histology and Embryology, Guizhou Medical University, Guiyang, Guizhou 550025, China. Department of Human Histology and Embryology, Guizhou Medical University, Guiyang, Guizhou 550025, China. Department of Allied Health Science, University of Connecticut, 1390 Storrs Road, Storrs, CT 06269, USA. School of Public Health, the Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education / Guizhou Provincial Engineering Research Center of Food Nutrition and Health Guizhou Medical University, Guiyang, Guizhou 550025, China; State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang 550014, China. Electronic address: luopeng@gmc.edu.cn. Department of Human Histology and Embryology, Guizhou Medical University, Guiyang, Guizhou 550025, China; Center for Tissue Engineering and Stem Cell Research, Key Laboratory of regenerative medicine in Guizhou Province, Guizhou Medical University, Guiyang, Guizhou 550004, China; Key Laboratory for Adult Stem Cell Translational Research, Chinese Academy of Medical Sciences, Guiyang, Guizhou 550004, China. Electronic address: sumin@gmc.edu.cn. Department of Human Histology and Embryology, Guizhou Medical University, Guiyang, Guizhou 550025, China; Characteristic Key Laboratory of Translational Medicine Research of Cardiovascular and Cerebrovascular Diseases in Guizhou Province, Guizhou Medical University, Guiyang, Guizhou 550025, China. Electronic address: hurong@gmc.edu.cn.
 Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Departamento de Neurologia, Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Medical Imaging Analysis Center (MIAC), University of Basel, Basel, Switzerland. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Departamento de Neurologia, Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Departamento de Neurologia, Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Instituto de Medicina Tropical de Sao Paulo, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Departamento de Neurologia, Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Departamento de Oftalmologia e Laboratorio de Oftalmologia (LIM/33), Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Departamento de Oftalmologia e Laboratorio de Oftalmologia (LIM/33), Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Departamento de Neurologia, Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Neurocure Cluster of Excellence, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Max Delbrueck Center for Molecular Medicine, Experimental and Clinical Research Center, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Neurosciences, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Neurocure Cluster of Excellence, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Max Delbrueck Center for Molecular Medicine, Experimental and Clinical Research Center, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institut für Integrative Neuroanatomie, Berlin, Germany. Department of Neurology, St Josef-Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St Josef-Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St Josef-Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, St Josef-Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Center for Neurology and Neuropsychiatry, LVR-Klinikum, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Neurocure Cluster of Excellence, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Max Delbrueck Center for Molecular Medicine, Experimental and Clinical Research Center, Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Neurosciences, Berlin, Germany. Departamento de Neurologia, Instituto Central, Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland.
 University of Health Sciences, International Faculty of Medicine, Department of Biophysics, Istanbul, Turkey. Electronic address: enesakyuz25@gmail.com. Yozgat Bozok University, Medical Faculty, Department of Histology and Embryology, Yozgat, Turkey. Yozgat Bozok University, Medical Faculty, Department of Histology and Embryology, Yozgat, Turkey. Yozgat Bozok University, Medical Faculty, Department of Anatomy, Yozgat, Turkey. Kayseri Erciyes University, Medical Faculty, Department of Anatomy, Kayseri, Turkey. Istinye University, Faculty of Medicine, Department of Medical Biology, Istanbul, Turkey.
 From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. michael.levraut@gmail.com. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France. From the Unité de Recherche Clinique Cote d'Azur-UR2CA URRIS (M.L., C.L.-F.), Centre Hospitalier Universitaire de Nice; Département de Biostatistiques (S.L.-C.), Epidémiologie clinique et Santé Publique, Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (X.A., P.L.), Centre Hospitalier Universitaire de Montpellier, Montpellier; Département de Neurologie (K.B., J.D.S.), Centre Hospitalier Universitaire de Strasbourg; Service de Neurologie (M.R., E.T.), Centre Hospitalier Universitaire de Nîmes; Laboratoire de Biochimie (S.S.), Centre Hospitalier Universitaire de Nîmes; Département de Neurologie (H.Z., T.A.), Centre Hospitalier Universitaire de Lille; Centre Hospitalier Universitaire de Lille (J.-D.P.), Service de Biochimie Automatisée, Protéines (UF 8833), Lille; Département de Neurologie (J.C., D.B.), Centre Hospitalier Universitaire de Toulouse, Hôpital Pierre-Paul Riquet, CRC-SEP, F-31059, Toulouse Cedex 9; Laboratoire d'Immunologie (B.P.-L.), Centre Hospitalier Universitaire de Toulouse; Département de Neurologie (J.-P.C.), Centre Hospitalier Universitaire de Saint-Etienne; Laboratoire de Biochimie (Y.T.), Centre Hospitalier Universitaire de Saint-Etienne; Département de Neurologie (O.C.), Centre Hospitalier Universitaire de Grenoble Alpes; Univ. Grenoble Alpes (B.T.), CNRS, UMR 5525, VetAgro Sup, Grenoble INP, CHU Grenoble Alpes, TIMC; Laboratoire de Biochimie (B.T., J.M.), Centre Hospitalier Universitaire de Grenoble Alpes; Département de Neurologie (T.M.), Centre Hospitalier de Dijon; Laboratoire de Biochimie (D.L., A.T.), Centre Hospitalier Universitaire de Dijon; Département de Neurologie (E.M.), Assistance-Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière; Laboratoire d'Immunologie (D.S.), Assistance Publique des Hôpitaux de Paris, Centre Hospitalier Universitaire de la Pitié-Salpêtrière, Paris; Département de Neurologie (A.M., A.R.), Centre Hospitalier Universitaire de Tours; Université de Nantes (D.A.L.), C2RTI Inserm UMR1064, service de Neurologie, CHU Nantes; Département de Biochimie (E.B.-C., P.-O.B.), Centre Hospitalier Universitaire de Nantes; Aix Marseille Univ (J.P.), APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie; Laboratoire de Biochimie (J.B.), Assistance Publique des Hôpitaux de Marseille, Centre Hospitalier Universitaire de La Conception; Laboratoire d'Immunologie (T.V.), Centre Hospitalier Universitaire de Montpellier; Laboratoire d'Immunologie (I.J.), Centre Hospitalier Universitaire Strasbourg; Laboratoire d'Immunologie (B.S.-P.), Centre Hospitalier Universitaire de Nice; Institut de Génomique Fonctionnelle (E.T.), Université de Montpellier, CNRS, INSERM, Montpellier; and Département de Neurologie (C.L.-F.), Centre Hospitalier Universitaire de Nice, France.
 Institute of Neuroanatomy, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Institute of Anatomy and Cell Biology, University of Erlangen-Nuremberg, 91054 Erlangen, Germany. Institute of Neuroanatomy, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Institute of Anatomy and Cell Biology, University of Erlangen-Nuremberg, 91054 Erlangen, Germany. Institute of Neuroanatomy, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Institute of Neuroanatomy, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Department of Biology, Animal Physiology, University of Erlangen-Nuremberg, 91058 Erlangen, Germany. Department of Biology, Animal Physiology, University of Erlangen-Nuremberg, 91058 Erlangen, Germany. Institute of Human Genetics, University Hospital Erlangen, University of Erlangen-Nuremberg, 91054 Erlangen, Germany. Institute of Human Genetics, University Hospital Erlangen, University of Erlangen-Nuremberg, 91054 Erlangen, Germany. Institute of Anatomy and Cell Biology, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Institute of Neuroanatomy, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Institute of Neuroanatomy, Medical Faculty, University of Bonn, 53115 Bonn, Germany. Institute of Anatomy and Cell Biology, University of Erlangen-Nuremberg, 91054 Erlangen, Germany.
 Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom. Electronic address: david.baker@qmul.ac.uk. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom; Centre for Oral Immunobiology and Regenerative Medicine, Dental Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom; Clinical Board Medicine (Neuroscience), The Royal London Hospital, Barts Health NHS Trust, London, United Kingdom. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom; Clinical Board Medicine (Neuroscience), The Royal London Hospital, Barts Health NHS Trust, London, United Kingdom.
 Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology and Allergy, Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Nervous System Stem Cells Research Center and Department of Tissue Engineering and Applied Cellular Sciences, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran.
 Department of Neuroscience, Imaging, and Clinical Sciences, "G. D'Annunzio" University of Chieti-Pescara, Chieti, Italy. maria.dapolito93@gmail.com. Department of Neuroscience, Imaging, and Clinical Sciences, "G. D'Annunzio" University of Chieti-Pescara, Chieti, Italy. Department of Neuroscience, Imaging, and Clinical Sciences, "G. D'Annunzio" University of Chieti-Pescara, Chieti, Italy. Department of Neuroscience, Imaging, and Clinical Sciences, "G. D'Annunzio" University of Chieti-Pescara, Chieti, Italy. Department of Neuroscience, Imaging, and Clinical Sciences, "G. D'Annunzio" University of Chieti-Pescara, Chieti, Italy. Department of Neurology, "SS. Annunziata" University Hospital, 66100, Chieti, Italy. Department of Radiology, University "G. D'Annunzio" of Chieti, Chieti, Italy. Department of Neuroscience, Imaging, and Clinical Sciences, "G. D'Annunzio" University of Chieti-Pescara, Chieti, Italy. Department of Neurology, "SS. Annunziata" University Hospital, 66100, Chieti, Italy.
 From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. jacobsons@ninds.nih.gov lieberman@Wistar.org. From the Neuroimmunology Branch (M.C.G.M., A.C., R.J.H., S.J.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; The Wistar Institute (S.S.S., C.S., J.F.C., R.J.P., F.L., T.E.M., P.M.L.), Philadelphia, PA; and Neuroimmunology Clinic (F.C.A., J.O.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. jacobsons@ninds.nih.gov lieberman@Wistar.org.
 Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL, USA. Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL, USA. Metaorganism Immunity Section, Laboratory of Host Immunity and Microbiome, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. NIH Center for Human Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA. Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. CCR Collaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Advanced Biomedical Computational Sciences, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, USA. Metaorganism Immunity Section, Laboratory of Host Immunity and Microbiome, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Molecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Nuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Philadelphia, PA, USA. Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA. Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. Metaorganism Immunity Section, Laboratory of Host Immunity and Microbiome, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. vanja.lazarevic@nih.gov.
 Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Izmir Institute of Technology, The Department of Molecular Biology and Genetics Gulbahce, Urla, Izmir. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Hunstman Cancer Institute, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Department of Pathology, Division of Microbiology and Immunology, University of Utah, Salt Lake City, UT. Hunstman Cancer Institute, University of Utah, Salt Lake City, UT.
 Division of Pediatric Pulmonology, Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria. Electronic address: markus.breu@meduniwien.ac.at. Division of Pediatric Neurology, Department of Pediatrics I, Medical University of Innsbruck, Innsbruck, Austria. Division of Infectious Diseases, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria. Division of Infectious Diseases, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria. Division of Infectious Diseases, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria. Division of Pediatric Pulmonology, Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria. Division of Pediatric Neurology, Department of Pediatrics I, Medical University of Innsbruck, Innsbruck, Austria. Division of Pediatric Pulmonology, Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria.
 Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Plastic and Reconstructive Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Plastic and Reconstructive Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21231, USA. Institute for NanoBioTechnology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Oncology, Sidney Kimmel Comprehensive Cancer Center and the Bloomberg~Kimmel Institute for Cancer Immunotherapy, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Public Health, Baltimore, MD 21231, USA. Department of Plastic and Reconstructive Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Translational Tissue Engineering Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21231, USA. Institute for NanoBioTechnology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Oncology, Sidney Kimmel Comprehensive Cancer Center and the Bloomberg~Kimmel Institute for Cancer Immunotherapy, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. Department of Materials Science and Engineering, Johns Hopkins University, Baltimore, MD 21231, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
 Department of Immunology and Molecular Microbiology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Republic of Korea. Department of Immunology and Molecular Microbiology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Republic of Korea.
 Neurology Department(,)Isfahan Neuroscience Research Center(,)Isfahan University of Medical Science(,) Iran. Isfahan Neuroscience Research Center(,) Isfahan University of Medical Science(,)Iran. Electronic address: roshym13@gmail.com. Isfahan Neuroscience Research Center(,) Isfahan University of Medical Science(,)Iran. Isfahan University of Medical Sciences(,) Isfahan(,) Iran.
 University Children's Hospital Regensburg (KUNO) at the Hospital St. Hedwig of the Order of St. John, University of Regensburg, Regensburg, Germany. Electronic address: tobias.geis@barmherzige-regensburg.de. University Children's Hospital Regensburg (KUNO) at the Hospital St. Hedwig of the Order of St. John, University of Regensburg, Regensburg, Germany. Department of Pediatrics, University Hospital of Patras, Patras, Greece. Institute of Laboratory Medicine, Microbiology and Hygiene, Hospital of the Order of St. John, Regensburg, Germany. Neurologic Clinic and Policlinic, MS Centre and Research Centre for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Centre and Research Centre for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel, University of Basel, Basel, Switzerland. Research and Development Campus Regensburg (WECARE), at the Hospital St. Hedwig of the Order of St. John, University of Regensburg, Regensburg, Germany; Department of Neonatology, University Children's Hospital Regensburg (KUNO) at the Hospital St. Hedwig of the Order of St. John, University of Regensburg, Regensburg, Germany.
 Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA. Department of Anatomy and Cell Biology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
 Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA. Nantes Université, INSERM, CNRS, Center for Research in Transplantation et Translational Immunology, UMR 1064, Nantes, France. Institute of Molecular Oncology and Functional Genomics, Center for Translational Cancer Research (TranslaTUM), Technical University of Munich, Munich, Germany. Department of Medicine II, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Institute of Molecular Oncology and Functional Genomics, Center for Translational Cancer Research (TranslaTUM), Technical University of Munich, Munich, Germany. Department of Medicine II, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA. Institute of Molecular Oncology and Functional Genomics, Center for Translational Cancer Research (TranslaTUM), Technical University of Munich, Munich, Germany. Department of Medicine II, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. The Broad Institute of Harvard and MIT, Cambridge, MA, USA. Department of Neurology, University Hospital, Friedrich-Alexander University Erlangen Nuremberg, Erlangen, Germany. veit.rothhammer@fau.de. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. veit.rothhammer@fau.de.
 Institute of Cell Biology, National Academy of Sciences of Ukraine, Drahomanov st., 14/16, Lviv 79005, Ukraine. Institute of Cell Biology, National Academy of Sciences of Ukraine, Drahomanov st., 14/16, Lviv 79005, Ukraine. Institute of Cell Biology, National Academy of Sciences of Ukraine, Drahomanov st., 14/16, Lviv 79005, Ukraine. Municipal Non-commercial Enterprise of Lviv Regional Council "Lviv Regional Infection Clinical Hospital", Pekarska St., 54, 79010, Lviv, Ukraine. Municipal Non-commercial Enterprise of Lviv Regional Council "Lviv Regional Infection Clinical Hospital", Pekarska St., 54, 79010, Lviv, Ukraine. Lviv Regional Phthysio-pulmonology Clinical Medical and Diagnostic Center, Zelena st., 477, 79035, Lviv, Ukraine. Lviv Regional Phthysio-pulmonology Clinical Medical and Diagnostic Center, Zelena st., 477, 79035, Lviv, Ukraine. Interregional Academy of Personnel Management, Frometivska st., 2, Kyiv 01001, Ukraine. Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha 2713, Qatar; University of Edinburgh, Edinburgh EH4 2XU, the, UK. Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha 2713, Qatar. Institute of Cell Biology, National Academy of Sciences of Ukraine, Drahomanov st., 14/16, Lviv 79005, Ukraine. Oranta CancerDiagnostics AB, Uppsala 75263, Sweden. Institute of Cell Biology, National Academy of Sciences of Ukraine, Drahomanov st., 14/16, Lviv 79005, Ukraine. Electronic address: stoika.rostyslav@gmail.com.
 Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Electronic address: fashaikh@ksu.edu.sa. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy King Saud University, Riyadh 11451, Saudi Arabia.
 Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Department of Orthopaedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Inage, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Inage, Japan. Laboratory of Histology and Cytology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Department of Dentistry, Tsurumi University, Yokohama, Japan. Laboratory of Histology and Cytology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Neuroimmunology, National Institute for Physiological Sciences, National Institute for Natural Sciences, Okazaki, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Inage, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Neuroimmunology, National Institute for Physiological Sciences, National Institute for Natural Sciences, Okazaki, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Inage, Japan. Division of Molecular Psychoimmunology, Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Inage, Japan. Division of Molecular Neuroimmunology, National Institute for Physiological Sciences, National Institute for Natural Sciences, Okazaki, Japan. Institute for Vaccine Research and Development, Hokkaido University, Sapporo, Japan.
 From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. From the Servei de Neurologia-Neuroimmunologia (S.M., A.P., J.R., X.M., M.C.), Centre d´Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d´Hebron (VHIR), Hospital Universitari Vall d´Hebron, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute of Murcia (IMIB-Arrixaca) (L.H.-N., P.P.), University Clinical Hospital Virgen de la Arrixaca, Spain; Departments of Neurology and Immunology (L.M.M.V.), Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigacion Sanitaria, Madrid, Spain; and Department of Biochemistry and Molecular Biology B and Immunology (P.P.), Faculty of Medicine, University of Murcia, Murcia, Spain. manuel.comabella@vhir.org.
 Biological Science Department, College of Science, King Faisal University, P.O. Box 400, Al-Ahsa 31982, Saudi Arabia. Molecular Biology Division, Pondicherry Centre for Biological Sciences and Educational Trust, Kottakuppam 605104, India. Camel Research Center, King Faisal University, P.O. Box 400, Al-Ahsa 31982, Saudi Arabia. Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, Al-Ahsa 31982, Saudi Arabia. Department of Pharmacognosy, Faculty of Pharmacy, Minia University, Minia 61519, Egypt. Biological Science Department, College of Science, King Faisal University, P.O. Box 400, Al-Ahsa 31982, Saudi Arabia. Botany and Microbiology Department, Faculty of Science, Beni-Suef University, Beni-Suef 62511, Egypt.
 Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, and Max Delbrück Center for Molecular Medicine, Berlin, Germany/Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany/ Department of Neurology, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, and Max Delbrück Center for Molecular Medicine, Berlin, Germany/Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, and Max Delbrück Center for Molecular Medicine, Berlin, Germany/Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany/Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Bochum, Germany. Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. Department of Neurology, University of Ulm, Ulm, Germany. Department of Neurology, School of Medicine, Technical University Munich, Klinikum rechts der Isar, Munich, Germany. Department of Neurology, School of Medicine, Technical University Munich, Klinikum rechts der Isar, Munich, Germany. Department of Neurology, University Medical Center, Johannes Gutenberg University of Mainz, Mainz, Germany. Department of Neurology, University Medicine of Greifswald, Greifswald, Germany. Department of Neurology, University of Münster, Münster, Germany. Department of Psychiatry, Social Psychiatry and Psychotherapy, Hannover Medical School, Hannover, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, Asklepios Expert Clinic Teupitz, Teupitz, Germany. Department of Neurology, Herford Hospital, Herford, Germany. Department of Neurology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. Department of Neurology, University of Leipzig, Leipzig, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany/Department of Neurology, Center for Neurology and Neuropsychiatry, LVR-Klinikum, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology and Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany/Aix-Marseille Univ, CNRS, CRMBM, UMR 7339, Marseille, France/APHM, Hopital de la Timone, CEMEREM, Marseille, France. Department of Neurology and Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität München, Munich, Germany/Data Integration for Future Medicine Consortium, LMU Hospital, Ludwig-Maximilians Universität München, Munich, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
 Department of Biochemistry, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Department of Biochemistry, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Electronic address: sajithakrishnan@aims.amrita.edu. Department of Biochemistry, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Neuroimmunology Laboratory, Department of Neurology, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Neuroimmunology Laboratory, Department of Neurology, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Neuroimmunology Laboratory, Department of Neurology, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Department of biostatistics, Amrita Institute of Medical Sciences, Amrita Viswavidyapeetham University, Kochi, Kerala, India 682041. Department of Neurology, Government Medical College, Thiruvananthapuram, Kerala, India. 695011. Department of Neurology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India 342005.
 From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain. From the Neuroimmunology and Multiple Sclerosis Unit (Y.B., D.E., S.L., R.R.G., M.A., S.A., J.M.C.-M., M.G., A.H., E.M.-H., M.S., T.A., J.D., A.S.), Hospital Clinic de Barcelona, and Universitat de Barcelona; Neurommunology Program, Fundació de Recerca Clinic Barcelona-IDIBAPS (Y.B., S.L., R.R.G., M.A., E.A., M.A., E.C., J.M.C.-M., E.F., M.G., E.M.-H., G.O.-C., M.R., L.S., M.S., E.S., T.A., J.D., A.S.), Barcelona; Neuromuscular Diseases Unit, Neurology Department (C.L., L.M.-A., C.T.-I., N.V.-F., L.Q.), Hospital de Sant Pau, Barcelona; Centro para la Investigación en Red en Enfermedades Raras (CIBERER) (C.L., M.G., C.T.-I., J.D., L.Q.), Madrid; Department of Immunology (N.E., R.R.G.), Hospital Clinic de Barcelona; Department of Preventive Medicine and Epidemiology (M.A., A.V.), Hospital Clinic de Barcelona, Spain; Department of Neurology (E.F.), School of Medicine, Pontificia Universidad Católica de Chile, Santiago de Chile; Pediatric Neurology Unit (G.O.-C.), Hospital Parc Taulí de Sabadell, Barcelona; Infectious Diseases Unit, Department of Internal Medicine, (J.L.-C., A.R.) Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Immunology Department (L.M.-M.), Sant Pau, Institut de Recerca del Hospital de Sant Pau, Universitat Autónoma de Barcelona, Barcelona; Department of Pediatrics, and Infectious Diseases Department (C.F.), Institut de Recerca Pediàtrica Hospital de Sant Joan de Déu, Esplugues de Llobregat, Barcelona; Pediatric Neuroimmunology Unit, Department of Neurology (S.J.D.), Sant Joan de Déu Children´s Hospital (T.A), University of Barcelona, Spain; Department of Neurology, (J.D.) Perelman School of Medicine, University of Pennsylvania, Philadelphia; and Catalan Institute for Research and Advanced Studies (ICREA) (J.D.), Barcelona, Spain.
 Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA; Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: hchung2@houstonmethodist.org. Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA; Department of Pediatrics, Section of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA. Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA. Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA; Howard Hughes Medical Institute and Department of Genetics, Harvard Medical School, Boston, MA, USA. Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA; Department of Pediatrics, Section of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: hyunkyol@bcm.edu. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030, USA. Electronic address: hbellen@bcm.edu.
 Institute for Physiology and Pathophysiology, Friedrich-Alexander-University Erlangen-Nuremberg (FAU), 91054 Erlangen, Germany. Institute for Physiology and Pathophysiology, Friedrich-Alexander-University Erlangen-Nuremberg (FAU), 91054 Erlangen, Germany. Department of Neurosurgery, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg (FAU), 91054 Erlangen, Germany. Department of Public Health Neukölln, District Office Neukölln of Berlin Neukölln, 12359 Berlin, Germany. Department of Neurosurgery, Paracelsus Medical University, 90471 Nuremberg, Germany. Department of Neurosurgery, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg (FAU), 91054 Erlangen, Germany. Department of Neurosurgery, Paracelsus Medical University, 90471 Nuremberg, Germany.
 Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Department of Surgical Sciences, Obstetrics and Gynecology 1, University of Turin, 10126 Turin, Italy. Pathology Unit, Department Laboratory Medicine, AOU Città della Salute e della Scienza di Torino, 10126 Turin, Italy. Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Department of Surgical Sciences, Obstetrics and Gynecology 1, University of Turin, 10126 Turin, Italy. Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Department of Surgical Sciences, Obstetrics and Gynecology 1, University of Turin, 10126 Turin, Italy. Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy. Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Charles University in Prague and General University Hospital, Prague, Czech Republic. School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Box Hill Hospital, Melbourne, Victoria, Australia. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia. Amiri Hospital, Sharq, Kuwait. Hospital Universitario Virgen Macarena, Sevilla, Spain. Hospital Universitario Virgen Macarena, Sevilla, Spain. University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center, University of Catania, Catania, Italy. Neuro Rive-Sud, Longueuil, Québec, Canada. Liverpool Hospital, Sydney, New South Wales, Australia. CISSS Chaudière-Appalache, Levis, Québec, Canada. University Newcastle, Newcastle, New South Wales, Australia. Monash Medical Centre, Melbourne, Victoria, Australia. CHUM MS Center and Université de Montréal, Montréal, Québec, Canada. CHUM MS Center and Université de Montréal, Montréal, Québec, Canada. CHUM MS Center and Université de Montréal, Montréal, Québec, Canada. Austin Health, Melbourne, Victoria, Australia. Buffalo General Medical Center, Buffalo, New York. Dokuz Eylul University, Konak/Izmir, Turkey. Flinders University, Adelaide, South Australia, Australia. Centro Hospitalar Universitario de São João, Porto, Portugal. Cliniques Universitaires Saint-Luc, Brussels, Belgium. Brain and Mind Centre, Sydney, New South Wales, Australia. Rehabilitation and MS-Centre Overpelt and Hasselt University, Hasselt, Belgium. Zuyderland Medical Center, Sittard-Geleen, the Netherlands. CSSS Saint-Jérôme, Saint-Jerome, Québec, Canada. 19 Mayis University, Samsun, Turkey. KTU Medical Faculty Farabi Hospital, Trabzon, Turkey. Universitary Hospital Ghent, Ghent, Belgium. Universitary Hospital Ghent, Ghent, Belgium. University of Western Australia, Nedlands, Western Australia, Australia. Westmead Hospital, Sydney, New South Wales, Australia. American University of Beirut Medical Center, Beirut, Lebanon. American University of Beirut Medical Center, Beirut, Lebanon. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia.
 Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey. Department of Gastroenterology and Hepatology, School of Medicine, Koҫ University, Istanbul, Turkey. Department of Neurology, School of Medicine, Koҫ University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey; Department of Neurology, School of Medicine, Koҫ University, Istanbul, Turkey. Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Research Center for Translational Medicine (KUTTAM), Koҫ University, Istanbul, Turkey; Department of Neurology, School of Medicine, Koҫ University, Istanbul, Turkey. Electronic address: ygursoy@ku.edu.tr.
 Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China. Department of Neurology and Institute of Neurology, Huashan Hospital, National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Electronic address: jintai_yu@fudan.edu.cn.
 Department of Neuroscience, King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia. Electronic address: bashirah@kfshrc.edu.sa. Department of Medicine, Aseer Central Hospital, Abha, Saudi Arabia. Department of Medicine, Aseer Central Hospital, Abha, Saudi Arabia. Centre for Genomic Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia. Electronic address: aalfares@kfshrc.edu.sa. Department of Neuroscience, King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia. Electronic address: ahassan69@kfshrc.edu.sa.
 Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Child Neurology and Psychiatry Unit, Department of System Medicine, Tor Vergata University of Rome, Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Child Neurology and Psychiatry Unit, Department of System Medicine, Tor Vergata University of Rome, Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Clinical Immunology and Vaccinology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Chair of Pediatrics, Department of Systems Medicine, Tor Vergata University of Rome, Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy. Center for Sensory-Motor Interaction, Aalborg University, Denmark, Neurology Unit, Aalborg, Denmark.
 Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany. BioNtech SE, An der Goldgrube 12, 55131, Mainz, Germany. Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany. Immatics Biotechnologies GmbH, Paul-Ehrlich-Str. 15, 72076, Tübingen, Germany. Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany. Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany. Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. Department of Neurology, University Clinic Heidelberg, University of Heidelberg, Otto-Mayerhof-Zentrum (OMZ), Im Neuenheimer Feld 350, 69120, Heidelberg, Germany. s.williams@Dkfz-heidelberg.de. Clinical Cooperation Unit (CCU) Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. s.williams@Dkfz-heidelberg.de.
 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Electronic address: fashaikh@ksu.edu.sa.
 Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Alberta, Canada. Sina MS Research Center, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Alberta, Canada. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Immunoregulation Research Center, Shahed University, Tehran, Iran. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. f-noorbakhsh@sina.tums.ac.ir. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. asaboor@tums.ac.ir.
 Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Henan Province Engineering Research Center of Clinical Application, Evaluation and Transformation of Traditional Chinese Medicine, Henan Provincial Key Laboratory for Clinical Pharmacy of Traditional Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Henan Province Engineering Research Center of Clinical Application, Evaluation and Transformation of Traditional Chinese Medicine, Henan Provincial Key Laboratory for Clinical Pharmacy of Traditional Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Henan Province Engineering Research Center of Clinical Application, Evaluation and Transformation of Traditional Chinese Medicine, Henan Provincial Key Laboratory for Clinical Pharmacy of Traditional Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Chengdu University of Chinese Medicine, Chengdu, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China. Chengdu University of Chinese Medicine, Chengdu, China. School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China. Department of Pharmacy, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China. Henan Province Engineering Research Center of Clinical Application, Evaluation and Transformation of Traditional Chinese Medicine, Henan Provincial Key Laboratory for Clinical Pharmacy of Traditional Chinese Medicine, Zhengzhou, China. School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China.
 Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Immunology and Theranostics, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd., Duarte, CA, 91010, USA.
 Internal Medicine, NewYork Presbyterian - Brooklyn Methodist Hospital, New York, USA. Internal Medicine, NewYork Presbyterian - Brooklyn Methodist Hospital, New York, USA. Internal Medicine, NewYork Presbyterian - Brooklyn Methodist Hospital, New York, USA. Internal Medicine, NewYork Presbyterian - Brooklyn Methodist Hospital, New York, USA. Internal Medicine, NewYork Presbyterian - Brooklyn Methodist Hospital, New York, USA.
 Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Clinical Sciences, Karolinska Institutet Danderyd Hospital, Stockholm SE-171 77, Sweden. Department of Cell and Molecular Biology, Uppsala University, Uppsala SE-751 23, Sweden. Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala SE-751 85, Sweden.
 Departamento de Neurología, Fleni, Buenos Aires, Argentina. Instituto de Química y Fisicoquímica Biológicas (IQUIFIB), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina. Department of Medicine-Neurosciences, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, ON, Canada. Departamento de Neurologia, Hospital Central de Mendoza, Mendoza, Argentina.
 Samsun University, Samsun, Turkey. University of Health Sciences Turkey, Etlik City Hospital, Ankara, Turkey. Hacettepe University, Ankara, Turkey. Dokuz Eylul University, Izmir, Turkey.
 Department of Brain Sciences, Imperial College London, London W120BZ, UK. Population Data Science, Swansea University Medical School, Swansea SA2 8PP, UK. Population Data Science, Swansea University Medical School, Swansea SA2 8PP, UK. Department of Brain Sciences, Imperial College London, London W120BZ, UK. Department of Brain Sciences, Imperial College London, London W120BZ, UK. Population Data Science, Swansea University Medical School, Swansea SA2 8PP, UK.
 Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Department of Clinical Health Psychology, Max Rady College of Medicine Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Departments of Community Health Sciences & Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, Canada. Department of Psychiatry, Max Rady College of Medicine Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Nova Scotia Health Authority, Departments of Psychiatry, Psychology & Neuroscience, and Medicine, , Halifax, CanadaDalhousie University. RINGGOLD: 3688 Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 St. Michael's Hospital, Toronto, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664 Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, , Winnipeg, CanadaUniversity of Manitoba. RINGGOLD: 8664
 Liver Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. rosanna.villani@unifg.it. Liver Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. Department of Medical and Surgical Sciences, Multiple Sclerosis Center, University of Foggia, Foggia, Italy. Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. Department of Medical and Surgical Sciences, Multiple Sclerosis Center, University of Foggia, Foggia, Italy.
 Erciyes University Faculty of Medicine Pediatric Cardiology Department, Kayseri, Turkey. Erciyes University Faculty of Medicine Pediatric Cardiology Department, Kayseri, Turkey. Erciyes University Faculty of Medicine Pediatric Neurology Department, Kayseri, Turkey.
 Ningxia Key Laboratory of Craniocerebral Diseases, School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China. Ningxia Key Laboratory of Craniocerebral Diseases, School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China. Ningxia Key Laboratory of Craniocerebral Diseases, School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China. Ningxia Key Laboratory of Craniocerebral Diseases, School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China. Ningxia Key Laboratory of Craniocerebral Diseases, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China.
 MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Department of Radiology and nuclear medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Department of Radiology and nuclear medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Department of Anesthesiology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Department of Radiology and nuclear medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Department of Radiology and nuclear medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Department of Radiology and nuclear medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, 1081 HZ, The Netherlands. Health, Medical and Neuropsychology Unit, Institute of Psychology, Leiden University, Leiden, 2333 AK, The Netherlands.
 Department of Neurology, Peking University First Hospital, Beijing, China. Department of Neurology, Peking University First Hospital, Beijing, China. Department of Neurology, Peking University First Hospital, Beijing, China. Department of Neurology, Peking University First Hospital, Beijing, China.
 Faculty of Health Sciences, Department of Occupational Therapy, Fenerbahçe University, İstanbul, Turkey. Faculty of Health Sciences, Department of Occupational Therapy, Hacettepe University, Ankara, Turkey.
 Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Experimental Pharmacology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland. Department of Neurology, University Hospital Regensburg, Regensburg, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany.
 Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London, UK. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London, UK. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London, UK. Centre for Primary Care, Wolfson Institute of Population Health, Queen Mary University London, London, UK. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London, UK. Blizard Institute, Queen Mary University London, London, UK. Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University London, London, EC1M 6BQ, UK. ruth.dobson@qmul.ac.uk. Department of Neurology, Royal London Hospital, London, UK. ruth.dobson@qmul.ac.uk.
 Radiology, Fundación Santa Fe de Bogotá, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Radiology, Fundación Santa Fe de Bogotá, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Fundación Universitaria de Ciencias de la Salud (FUCS), Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Radiology, Fundación Santa Fe de Bogotá, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia. Radiology, Fundación Santa Fe de Bogotá, Bogotá, Colombia. Universidad El Bosque, Bogotá, Colombia.
 Department of Biological Sciences, Boise State University, Boise, ID, United States. Department of Biological Sciences, Boise State University, Boise, ID, United States. Department of Biological Sciences, Boise State University, Boise, ID, United States. Department of Biological Sciences, Boise State University, Boise, ID, United States.
 Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden. Department of Pharmacy, Science for Life Laboratory, Uppsala University, Uppsala SE-751 23, Sweden. Department of Medical Sciences, Neurology, Uppsala University, Uppsala SE-751 85, Sweden.
 Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK.
 Maxine Mesinger Multiple Sclerosis Center, Baylor College of Medicine, Houston, TX 77030, USA. Maxine Mesinger Multiple Sclerosis Center, Baylor College of Medicine, Houston, TX 77030, USA. Maxine Mesinger Multiple Sclerosis Center, Baylor College of Medicine, Houston, TX 77030, USA. Maxine Mesinger Multiple Sclerosis Center, Baylor College of Medicine, Houston, TX 77030, USA. Maxine Mesinger Multiple Sclerosis Center, Baylor College of Medicine, Houston, TX 77030, USA.
 Department of Medicine, Division of Gastroenterology, Schulich School of Medicine, Western University, London, Ontario, Canada. Department of Clinical Neurological Sciences, Schulich School of Medicine, Western University, London, Ontario, Canada. Department of Medicine, Division of Gastroenterology, Schulich School of Medicine, Western University, London, Ontario, Canada.
 Royal Sussex County Hospital, Brighton, UK (MC, ML); Plant Based Health Online, Bordon, UK(LF, SK); Conor Devine, Belfast, UK (CD); The Sensitive Foodie, Brighton, UK (KL); King's College London, London, UK (SK); and University of Winchester, Hampshire, UK (SK). RINGGOLD: 156800. RINGGOLD: 4616 Royal Sussex County Hospital, Brighton, UK (MC, ML); Plant Based Health Online, Bordon, UK(LF, SK); Conor Devine, Belfast, UK (CD); The Sensitive Foodie, Brighton, UK (KL); King's College London, London, UK (SK); and University of Winchester, Hampshire, UK (SK). RINGGOLD: 156800. RINGGOLD: 4616 Royal Sussex County Hospital, Brighton, UK (MC, ML); Plant Based Health Online, Bordon, UK(LF, SK); Conor Devine, Belfast, UK (CD); The Sensitive Foodie, Brighton, UK (KL); King's College London, London, UK (SK); and University of Winchester, Hampshire, UK (SK). RINGGOLD: 156800. RINGGOLD: 4616 Royal Sussex County Hospital, Brighton, UK (MC, ML); Plant Based Health Online, Bordon, UK(LF, SK); Conor Devine, Belfast, UK (CD); The Sensitive Foodie, Brighton, UK (KL); King's College London, London, UK (SK); and University of Winchester, Hampshire, UK (SK). RINGGOLD: 156800. RINGGOLD: 4616 Royal Sussex County Hospital, Brighton, UK (MC, ML); Plant Based Health Online, Bordon, UK(LF, SK); Conor Devine, Belfast, UK (CD); The Sensitive Foodie, Brighton, UK (KL); King's College London, London, UK (SK); and University of Winchester, Hampshire, UK (SK). RINGGOLD: 156800. RINGGOLD: 4616 Royal Sussex County Hospital, Brighton, UK (MC, ML); Plant Based Health Online, Bordon, UK(LF, SK); Conor Devine, Belfast, UK (CD); The Sensitive Foodie, Brighton, UK (KL); King's College London, London, UK (SK); and University of Winchester, Hampshire, UK (SK). RINGGOLD: 156800. RINGGOLD: 4616
 Neurology Section, Department of Medicine, Aseer Central Hospital, Abha, Saudi Arabia. Department of Neuroscience, King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia. Department of Radiological Science, King Khalid University, Abha, Saudi Arabia. College of Medicine, King Khalid University, Abha, Saudi Arabia.
 Department of Biomedical Engineering. Department of Biomedical Engineering. Department of Biomedical Engineering. Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, Oregon, USA. Department of Biomedical Engineering. Department of Biomedical Engineering. Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, Oregon, USA.
 Department of Veterinary Anatomy and Animal Behavior, College of Veterinary Medicine and BK21 FOUR program, Chonnam National University, Gwangju, Republic of Korea. Department of Veterinary Anatomy and Animal Behavior, College of Veterinary Medicine and BK21 FOUR program, Chonnam National University, Gwangju, Republic of Korea. Department of Veterinary Anatomy, College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju, Republic of Korea. Department of Veterinary Anatomy and Animal Behavior, College of Veterinary Medicine and BK21 FOUR program, Chonnam National University, Gwangju, Republic of Korea.
 UT Southwestern Medical Center, Neurology, Section on Statistical Planning and Analysis, Dallas, TX, USA. Janssen Scientific Affairs, Real World Value & Evidence, Titusville, NJ, USA. RINGGOLD: 155246 Janssen Scientific Affairs, Real World Value & Evidence, Titusville, NJ, USA. RINGGOLD: 155246 Janssen Global Commercial Strategy Organization, Global Market Access, Titusville, NJ, USA. Janssen Global Commercial Strategy Organization, Global Medical Affairs, Titusville, NJ, USA. UT Southwestern Medical Center, Neurology, Section on Statistical Planning and Analysis, Dallas, TX, USA. Department of Biostatistics, University of Alabama Birmingham, Birmingham, AL, USA. Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada.
 Dermatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Dermatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Department of Neurology, Multiple Sclerosis Center, San Salvatore Hospital, L'Aquila, Italy. Dermatology, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
 Department of Ophthalmology, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Neurology & Rocky Mountain MS Center, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Ophthalmology, University of Colorado School of Medicine, Aurora, Colorado, USA. Department of Ophthalmology, University of Colorado School of Medicine, Aurora, Colorado, USA.
 Neurology, Neurophysiology and Neurobiology Unit, Department of Medicine, Campus Bio-Medico of Rome University, Rome, Italy. Neurology, Neurophysiology and Neurobiology Unit, Department of Medicine, Campus Bio-Medico of Rome University, Rome, Italy. Neurology, Neurophysiology and Neurobiology Unit, Department of Medicine, Campus Bio-Medico of Rome University, Rome, Italy. Neurology, Neurophysiology and Neurobiology Unit, Department of Medicine, Campus Bio-Medico of Rome University, Rome, Italy. Neurology, Neurophysiology and Neurobiology Unit, Department of Medicine, Campus Bio-Medico of Rome University, Rome, Italy. Neurology, Neurophysiology and Neurobiology Unit, Department of Medicine, Campus Bio-Medico of Rome University, Rome, Italy.
 Department of Neurology, University of Regensburg, Regensburg, Germany.
 Department of Neurology, The Ohio State University College of Medicine, Columbus, OH, United States. Department of Neurology, The Ohio State University College of Medicine, Columbus, OH, United States. Department of Neurology, The Ohio State University College of Medicine, Columbus, OH, United States.
 Weill Cornell Medicine, Brain and Mind Research Institute, New York, NY 10065, USA. University of Texas Southwestern Medical Center, O'Donnell Brain Institute, Dallas, TX 75390, USA. University of Texas Southwestern Medical Center, Department of Cell Biology, Dallas, TX 75390, USA. Morehouse School of Medicine, Department of Community Health and Preventative Medicine, Atlanta, GA 30310, USA. University of Texas Southwestern Medical Center, Peter O-Donnell Jr. School of Public Health, Dallas, TX 75390, USA. Morehouse School of Medicine, Institute of Genomic Medicine, Atlanta, GA 30310, USA. Weill Cornell Medicine, Brain and Mind Research Institute, New York, NY 10065, USA. University of Texas Southwestern Medical Center, O'Donnell Brain Institute, Dallas, TX 75390, USA.
 Second Department of Pediatrics, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania. niculae.alexandru.stefan@elearn.umfcluj.ro. Department of Neonatology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania. Faculty of Medicine, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania. Second Department of Neurology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
 Discipline of Clinical Psychology, Graduate School of Health, University of Technology Sydney, Australia. School of Psychology, University of Adelaide, Australia. School of Psychology, University of Adelaide, Australia. Discipline of Clinical Psychology, Graduate School of Health, University of Technology Sydney, Australia. Electronic address: Ian.Kneebone@uts.edu.au.
 Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, IL, United States. Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, IL, United States. Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, IL, United States. Department of Electrical and Computer Engineering, Missouri University of Science and Technology, Rolla, MO, United States. Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, IL, United States. Department of Electrical and Computer Engineering, Missouri University of Science and Technology, Rolla, MO, United States.
 Department of Medicine, Mater Dei Hospital, Msida, Malta jessica-marie.barbara@gov.mt. Department of Neurology, Gozo General Hospital, Victoria, Malta.
 Frontiers Media SA, Lausanne, Switzerland.
 Department of Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Department of Neurology, Hospital Sotero Del Rio, Santiago, Chile. Department of Neurology, EpiCURA Centre Hospitalier, Ath, Belgium. Heart Rhythm Management Centre, Universitair Ziekenhuis Brussel - Vrije Universiteit Brussel, Brussel, Belgium. Multiple Sclerosis Center Medicarte, Medellin, Colombia.
 Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. MS Center Amsterdam, Anatomy and Neurosciences, Amsterdam Neuroscience, Amsterdam UMC location VUmc, 1081 HV Amsterdam, The Netherlands. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA. MS Center Amsterdam, Anatomy and Neurosciences, Amsterdam Neuroscience, Amsterdam UMC location VUmc, 1081 HV Amsterdam, The Netherlands. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.

 Department of Neurology and Stroke, Medical University of Lodz, ul. Zeromskiego 113, 90-549 Lodz, Poland. Department of Neurology and Stroke, Medical University of Lodz, ul. Zeromskiego 113, 90-549 Lodz, Poland.
 Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases, Centro para la Investigación Biomédica en Red en Enfermedades Raras (CIBERER), 28029 Madrid, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Immunology Department, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, 08025 Barcelona, Spain. Immunology Department, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, 08025 Barcelona, Spain. Immunology Department, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, 08025 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases, Centro para la Investigación Biomédica en Red en Enfermedades Raras (CIBERER), 28029 Madrid, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases, Centro para la Investigación Biomédica en Red en Enfermedades Raras (CIBERER), 28029 Madrid, Spain. Department of Radiology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, 08025 Barcelona, Spain. Department of Neurology, Hospital Arnau de Vilanova, 25198 Lleida, Spain. Department of Neurology, Hospital Arnau de Vilanova, 25198 Lleida, Spain. Department of Neurology, Hospital Arnau de Vilanova, 25198 Lleida, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Departament de Ciències Clíniques, Facultat de Medicina, Universitat de Barcelona, 08907 Barcelona, Spain. Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Institut d'Investigació Biomèdica Sant Pau, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Neuromuscular Diseases, Centro para la Investigación Biomédica en Red en Enfermedades Raras (CIBERER), 28029 Madrid, Spain.
 Department of Philosophy, Sociology, Education and Applied Psychology, University of Padua, 35133 Padua, Italy. Multiple Sclerosis Centre, Department of Neuroscience, University-Hospital of Padua, 35128 Padua, Italy. Department of Philosophy, Sociology, Education and Applied Psychology, University of Padua, 35133 Padua, Italy. Department of Philosophy, Sociology, Education and Applied Psychology, University of Padua, 35133 Padua, Italy. Human Inspired Technology Centre (HIT), University of Padua, 35121 Padua, Italy. Department of Philosophy, Sociology, Education and Applied Psychology, University of Padua, 35133 Padua, Italy. Department of Philosophy, Sociology, Education and Applied Psychology, University of Padua, 35133 Padua, Italy. Multiple Sclerosis Centre, University-Hospital of Padua, 35128 Padua, Italy. Multiple Sclerosis Centre, University-Hospital of Padua, 35128 Padua, Italy. Multiple Sclerosis Centre, Department of Neuroscience, University-Hospital of Padua, 35128 Padua, Italy. Multiple Sclerosis Centre, Department of Neuroscience, University-Hospital of Padua, 35128 Padua, Italy. Department of Philosophy, Sociology, Education and Applied Psychology, University of Padua, 35133 Padua, Italy. Human Inspired Technology Centre (HIT), University of Padua, 35121 Padua, Italy.
 Neuroscience Research Center, Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon. Neuroscience Research Center, Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon. Neuroscience Research Center, Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon. Faculty of Pedagogy, Lebanese University, Furn-El-Chebbak, Lebanon. Neuroscience Research Center, Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon. LBN, University Montpellier, Montpellier, France. Faculty of Arts and Sciences, Holy Spirit University of Kaslik, Jounieh, Lebanon. School of Engineering, Holy Spirit University of Kaslik, Jounieh, Lebanon. Neuroscience Research Center, Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon. LBN, University Montpellier, Montpellier, France. Faculty of Arts and Sciences, Holy Spirit University of Kaslik, Jounieh, Lebanon.

 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University London, Charterhouse Square, London, EC1M 6BQ, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University London, Charterhouse Square, London, EC1M 6BQ, UK. ruth.dobson@qmul.ac.uk. Department of Neurology, Royal London Hospital, London, UK. ruth.dobson@qmul.ac.uk.
 Special Education, Rehabilitation, and Counseling, Auburn University, Auburn, United States. Electronic address: eac0006@auburn.edu. Special Education, Rehabilitation, and Counseling, Auburn University, Auburn, United States. Special Education, Rehabilitation, and Counseling, Auburn University, Auburn, United States. Special Education, Rehabilitation, and Counseling, Auburn University, Auburn, United States.
 Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. University of Colorado School of Medicine, Aurora, CO, USA. Shift.ms, Chelmsford, UK. Department of Neurology, Alexianer St Josefs Hospital, Potsdam, Germany. , Neuruppin, GermanyBrandenburg Medical School Theodor Fontane. RINGGOLD: 477107 Multiple Sclerosis Center, Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, People's Republic of China. University of Lille, Inserm UMR U1172 LilNCog, CHU Lille, FHU Precise, Lille, France. Multiple Sclerosis Center, University Hospital San Carlos, Madrid, Spain. Department of Basic Medical Science, Neurosciences and Sense Organs, University of Bari, Bari, Italy. Department of Neurology, St Josef-Hospital/Ruhr-University Bochum, Bochum, Germany. Neuroimmunology and Multiple Sclerosis Unit, Girona, Spain. , Basel, SwitzerlandNovartis Pharma AG. RINGGOLD: 111826 , Basel, SwitzerlandNovartis Pharma AG. RINGGOLD: 111826 , Basel, SwitzerlandNovartis Pharma AG. RINGGOLD: 111826 Center of Clinical Neuroscience, Department of Neurology, Carl Gustav Carus University Clinic, Technische Universität Dresden, Dresden, Germany.
 Department of Urology, Shahid Labbafinejad Medical Center, Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Urology, Zahedan University of Medical Sciences, Zahedan, Iran. Department of Urology, Shahid Labbafinejad Medical Center, Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Faculty of land and food systems, University of British Colombia Vancouver, Vancouver, Canada. Clinical Research Development Unit of Labbafinejad Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Physical Medicine and Rehabilitation, Urology Research Center, Sina & Imam Khomeini Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Urology, Shahid Labbafinejad Medical Center, Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Urology, Shahid Labbafinejad Medical Center, Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Urology, Shahid Labbafinejad Medical Center, Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Urology, Shahid Labbafinejad Medical Center, Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 Rehabilitation Sciences Department, College of Applied Medical Sciences, King Saud University, Riyadh, Kingdom of Saudi Arabia. Rehabilitation Sciences Department, College of Applied Medical Sciences, King Saud University, Riyadh, Kingdom of Saudi Arabia. Physical Therapy Department, Ministry of Health, Riyadh, Kingdom of Saudi Arabia.
 Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Department of Neurology, School of Medicine Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Department of Neurology, School of Medicine Isfahan University of Medical Sciences Isfahan Iran.
 Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy. Neurology Unit, Department of Medicine, Surgery and Health Sciences, Cattinara University Hospital ASUGI, University of Trieste, 34149 Trieste, Italy.
 Department of Neurology, Veterans Affairs Medical Center, Portland, OR, United States. Department of Neurology, Oregon Health and Sciences University, Portland, OR, United States. Department of Neurology, Veterans Affairs Medical Center, Portland, OR, United States. Department of Neurology, Oregon Health and Sciences University, Portland, OR, United States. Department of Radiology, Neuroradiology Section, Oregon Health & Sciences University, Portland, OR, United States. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, United States. Knight Cancer Institute, Oregon Health & Science University, Portland, OR, United States. Department of Human Physiology, University of Oregon, Eugene, OR, United States. Department of Neurology, Veterans Affairs Medical Center, Portland, OR, United States. Department of Neurology, Oregon Health and Sciences University, Portland, OR, United States.
 Department and Clinic of Neurology, Wroclaw Medical University, Wroclaw, Poland. Department of Neurology and Neurorehabilitation, Inselspital, University Hospital Bern, Bern, Switzerland. MS Centre Casa di Cura Igea, Vita Salute San Raffaele University, Milan, Italy.
 Atara Biotherapeutics, Thousand Oaks, CA, USA. cwatson@atarabio.com. Atara Biotherapeutics, Thousand Oaks, CA, USA. Atara Biotherapeutics, Thousand Oaks, CA, USA. Adelphi Real World, Bollington, Cheshire, UK. Atara Biotherapeutics, Thousand Oaks, CA, USA. Atara Biotherapeutics, Thousand Oaks, CA, USA.
 Department of Brain Sciences, Imperial College London, London, United Kingdom; Department of Neurosciences, Drug and Child Health, University of Florence, Florence, Italy. Department of Brain Sciences, Imperial College London, London, United Kingdom. Cell Therapy and Transfusion Medicine Unit, Careggi University Hospital, Largo Brambilla 3, 50134, Florence, Italy. Electronic address: riccardo.saccardi@unifi.it.
 Department of Neurology, Hacettepe University, Ankara, TUR. Department of Dermatology, Hacettepe University, Ankara, TUR. Department of Pathology, Hacettepe University, Ankara, TUR. Department of Neurology, Hacettepe University, Ankara, TUR. Department of Neurology, Hacettepe University, Ankara, TUR.
 Department of Neurology, University Hospital Reina Sofía, Menéndez Pidal, S/N Av., 14004, Córdoba, Spain. aldocosva_01@hotmail.com. Department of Neurology, University Hospital Reina Sofía, Menéndez Pidal, S/N Av., 14004, Córdoba, Spain.
 Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States.
 Department of Neurology Bharati Vidyapeeth University Medical College Pune Pune India. Internal Medicine Al-Kindy College of Medicine University of Baghdad Baghdad Iraq. Internal Medicine, Travancore Medical College Kollam India. Internal Medicine, Government Medical College Chennai India. Internal Medicine, Mayo Clinic Rochester New York USA. Internal Medicine, Maharajgunj Medical Campus Tribhuvan University Kathmandu Nepal. Internal Medicine, B.J. Medical College Ahmedabad India. Department of Neurology Virginia Tech Carilion School of Medicine Roanoke Virginia USA. Internal Medicine Al-Kindy College of Medicine University of Baghdad Baghdad Iraq. Internal Medicine, Al Manhal Academy Khartoum Sudan.
 California Northstate University California Northstate University College of Medicine
 Faculty of Medicine & Dentistry, The Blizard Institute, Centre for Neuroscience, Surgery & Trauma, Queen Mary University of London, London, UK. Clinical Board Medicine (Neuroscience), The Royal London Hospital, Barts Health NHS Trust, London, UK.
 Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece. Hacettepe University Medical School, Ankara, Turkey. School of Medicine, Koç University, Istanbul, Turkey. Laboratory of Experimental Neurology and Neuroimmunology and Multiple Sclerosis Center, 2nd Neurological University Department, AHEPA General Hospital of Thessaloniki, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece.
 Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT,USA. Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT,USA. Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT,USA. Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT,USA. Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT,USA.
 Department of Internal Medicine, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Family Medicine, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Biostatistics, University of Alabama in Birmingham, Birmingham, AL, United States. Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, United States. Department of Neurology, UT Southwestern, Dallas, TX, United States.
 Neurology, Kocaeli University, Kocaeli, TUR.
 Department of Psychology, Royal Holloway, University of London, Egham, Surrey TW20 0EX, UK. Department of Psychology, Royal Holloway, University of London, Egham, Surrey TW20 0EX, UK.
 IRCCS San Camillo Hospital, Venice, Italy. Department of Neuroscience, Padova Neuroscience Centre, University of Padova, Padua, Italy. IRCCS San Camillo Hospital, Venice, Italy. Department of Neurology, ULSS2 Marca Trevigiana, Conegliano, Italy. IRCCS San Camillo Hospital, Venice, Italy. Department of General Psychology, University of Padova, Padua, Italy. Department of Humanities and Life Sciences, University School for Advanced Studies IUSS, Pavia, Italy. IRCCS San Camillo Hospital, Venice, Italy.
 Hamad Medical Corporation, Ophthalmology department, Ambulatory Care Centre, Doha, Qatar. rehab_hilal@hotmail.com. Hamad Medical Corporation, Ophthalmology department, Ambulatory Care Centre, Doha, Qatar. Hamad Medical Corporation, Ophthalmology department, Ambulatory Care Centre, Doha, Qatar. Hamad Medical Corporation, Ophthalmology department, Ambulatory Care Centre, Doha, Qatar.
 Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA, USA. Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
 Department of Neurological Sciences, , Omaha, NE, USAUniversity of Nebraska Medical Center. RINGGOLD: 12284 Department of Neurological Sciences, , Omaha, NE, USAUniversity of Nebraska Medical Center. RINGGOLD: 12284 Department of Neurological Sciences, , Omaha, NE, USAUniversity of Nebraska Medical Center. RINGGOLD: 12284
 Department of Neurosciences, Cleveland Clinic, Cleveland, OH, United States. Department of Neurology, University of Texas Southwestern Medical Center, Peter O'Donnell Brain Institute, Neurology Section, VA North Texas Health Care System, Dallas, TX, United States.
 Department of Otolaryngology, Head and Neck Surgery, 38084Keio University School of Medicine, Tokyo, Japan. Department of Otolaryngology, Head and Neck Surgery, 38084Keio University School of Medicine, Tokyo, Japan. Department of Otolaryngology, Head and Neck Surgery, 38084Keio University School of Medicine, Tokyo, Japan.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran.
 Ross University, Kern Medical Center California Northstate University Ohio University Heritage College of OM
 Dipartimento di Scienze della Salute, Università Piemonte Orientale A. Avogadro, Via Solaroli 17, 28100, Novara, Italy. ghezzangelo@gmail.com. Department of Neurology, ErasMS Center, Erasmus MC, PO Box 2040, 3000, Rotterdam, The Netherlands.
 Department of Neurology, Poznan University of Medical Sciences, Poznań, Poland. Department of Neurology, Poznan University of Medical Sciences, Poznań, Poland. Department of Neurology, Poznan University of Medical Sciences, Poznań, Poland. Department of Neurology, Division of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, Poznań, Poland.
 CORe, Department of Medicine, The University of Melbourne, Melbourne 3050, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne 3050, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne 3050, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne 3050, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne 3050, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, University of Melbourne, Melbourne 3050, Australia. Menzies Institute for Medical Research, University of Tasmania, Tasmania 7000, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne 3050, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne 3050, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne 3050, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne 3050, Australia. Hospital Germans Trias i Pujol, Badalona 08916, Spain. Dokuz Eylul University, Konak/Izmir 35220, Turkey. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague 12808, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague 12808, Czech Republic. Department of Medical and Surgical Sciences and Advanced Technologies, GF Ingrassia, Catania 95123, Italy. Division of Neurology, Department of Medicine, Amiri Hospital, Sharq 73767, Kuwait. Hospital Universitario Virgen Macarena, Sevilla 41009, Spain. Hospital Universitario Virgen Macarena, Sevilla 41009, Spain. KTU Medical Faculty Farabi Hospital, Trabzon 61080, Turkey. Ain Shams University, Cairo 11566, Egypt. Department of Neuroscience, Imaging, and Clinical Sciences, University G. d'Annunzio, Chieti 66013, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna 40139, Italy. Department of Neurology, Buffalo General Medical Center, Buffalo 14202, United States. CHUM MS Center and Universite de Montreal, Montreal H2L 4M1, Canada. CHUM MS Center and Universite de Montreal, Montreal H2L 4M1, Canada. CHUM MS Center and Universite de Montreal, Montreal H2L 4M1, Canada. Medical Faculty, 19 Mayis University, Samsun 55160, Turkey. Department NEUROFARBA, University of Florence, Florence 50134, Italy. Hacettepe University, Ankara 6100, Turkey. Neuro Rive-Sud, Quebec J4V 2J2, Canada. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut 1107 2020, Lebanon. CISSS Chaudière-Appalache, Levis G6X 0A1, Canada. School of Medicine and Public Health, University Newcastle, Newcastle 2305, Australia. Department of Neurology, Box Hill Hospital, Melbourne 3128, Australia. Department of Neurology, Box Hill Hospital, Melbourne 3128, Australia. Department of Neurology, The Alfred Hospital, Melbourne 3000, Australia. Department of Neurology, The Alfred Hospital, Melbourne 3000, Australia. Haydarpasa Numune Training and Research Hospital, Istanbul 34668, Turkey. Department of Neurology, School of Medicine, Koc University, Koc University Research Center for Translational Medicine (KUTTAM), Istanbul 34450, Turkey. Garibaldi Hospital, Catania 95124, Italy. Perron Institute, University of Western Australia, Nedlands 6009, Australia. Neurology, Kasr Al Ainy MS Research Unit (KAMSU), Cairo 11562, Egypt. Cliniques Universitaires Saint-Luc, Brussels 1200 BXL, Belgium. Monash Medical Centre, Melbourne 3168, Australia. Department of Neurology, Razi Hospital, Manouba 2010, Tunisia. Department of Neurology, Razi Hospital, Manouba 2010, Tunisia. Department of Neurology, Razi Hospital, Manouba 2010, Tunisia. Clinical Investigation Center Neurosciences and Mental Health, Faculty of Medicine, University Tunis El Manar, Tunis 1068, Tunisia. Academic MS Center Zuyderland, Department of Neurology, Zuyderland Medical Center, Sittard-Geleen 5500, Netherlands. School for Mental Health and Neuroscience, Department of Neurology, Maastricht University Medical Center, Maastricht 6131 BK, Netherlands. Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul 34147, Turkey. Brain and Mind Centre, Sydney 2050, Australia. Neurologic Clinic and Policlinic, Departments of Medicine and Clinical Research, University Hospital and University of Basel, Basel 4000, Switzerland. Royal Victoria Hospital, Belfast BT12 6BA, United Kingdom. Department of Neurology, Centro Hospitalar Universitario de Sao Joao, Porto 4200-319, Portugal. Liverpool Hospital, Sydney 2170, Australia. Department of Neurology, Hospital Clinico San Carlos, Madrid 28050, Spain. Nemocnice Jihlava, Jihlava 58633, Czech Republic. Aarhus University Hospital, Arhus C 8000, Denmark. Hospital Germans Trias i Pujol, Badalona 08916, Spain. Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati Avellino, Avellino 83100, Italy. Royal Brisbane and Women's Hospital, University of Queensland, Brisbane 4000, Australia. Royal Hobart Hospital, Hobart 7000, Australia. CSSS Saint-Jérôme, Saint-Jerome J7Z 5T3, Canada. Department of Neuroscience, Neurology Unit, S. Maria delle Croci Hospital of Ravenna, Ravenna 48121, Italy. Flinders University, Adelaide 5042, Australia. St Vincent's University Hospital, Dublin D04 T6F4, Ireland. Department of Neurology, Universitary Hospital Ghent, Ghent 9000, Belgium. Department of Neurology, Universitary Hospital Ghent, Ghent 9000, Belgium. Groene Hart Ziekenhuis, Gouda 2800 BB, Netherlands. Department of Rehabilitation, CRRF 'Mons. Luigi Novarese', Moncrivello (VC) 16153, Italy. St. Michael's Hospital, Toronto M5B1W8, Canada. Austin Health, Melbourne 3084, Australia. University Hospital Reina Sofia, Cordoba 14004, Spain. Bombay Hospital Institute of Medical Sciences, Mumbai 400020, India. South Eastern HSC Trust, Belfast BT16, UK. Westmead Hospital, Sydney 2145, Australia. Rehabilitation and MS-Centre Overpelt and Hasselt University, Hasselt 3900, Belgium. Clinic of Neurology II, Emergency Clinical County Hospital 'Pius Brinzeu', Timisoara 300723, Romania. Romania University of Medicine and Pharmacy 'Victor Babes Timisoara', 300041, Romania. Hospital Universitario Donostia, San Sebastián 20014, Spain. Hospital de Galdakao-Usansolo, Galdakao 48660, Spain. PGIMER, Chandigarh 160012, India. Department of Medicine, Sultan Qaboos University Hospital, Al-Khodh 123, Oman. Neurology Department, King Fahad Specialist Hospital-Dammam, Khobar 31952, Saudi Arabia. Hospital Fernandez, Capital Federal, 1425, Argentina. Universidade Metropolitana de Santos, Santos 11045-002, Brazil. Department of Clinical Neurosciences, Division of Neurology, Faculty of Medicine, Geneva University Hospital, Geneva 1211, Switzerland. Medical Center Leeuwarden, Leeuwarden 8934 ad, Netherlands. Geelong Hospital, Geelong 3220, Australia. St Vincents Hospital, Fitzroy, Melbourne 3065, Australia. Department of Neurology, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary. Hospital General Universitario de Alicante, Alicante 3010, Spain. Jewish General Hospital, Montreal H3T 1E2, Canada. AZ Alma Ziekenhuis, Sijsele-Damme 8340, Belgium. Department of Neurology, Antwerp University Hospital, Edegem, Belgium. Translational Neurosciences Research Group, Faculty of Medicine and Health Sciences, University of Antwerp, Wilrijk 2650, Belgium. Ospedale Civico Lugano, Lugano 6900, Switzerland. St Vincent's Hospital Sydney, Sydney 2010, Australia. Concord Repatriation General Hospital, Sydney 2139, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne 3050, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Melbourne 3050, Australia.
 Department of Occupational Therapy, Faculty of Rehabilitation Sciences, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Occupational Therapy, Faculty of Rehabilitation Sciences, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Occupational Therapy, Faculty of Rehabilitation Sciences, Social Determinants of Health Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Occupational Therapy, Faculty of Rehabilitation Sciences, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Biostatistics and Epidemiology, Faculty of Rehabilitation Sciences, Iranian Research of Aging, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Occupational Therapy, Faculty of Rehabilitation Sciences, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran.
 Graduate Medical Education University of Central Florida College of Medicine Orlando Florida USA. HCA Florida North Florida Hospital Internal Medicine Residency Program Gainesville Florida USA. Graduate Medical Education University of Central Florida College of Medicine Orlando Florida USA. HCA Florida North Florida Hospital Internal Medicine Residency Program Gainesville Florida USA. Graduate Medical Education University of Central Florida College of Medicine Orlando Florida USA. HCA Florida North Florida Hospital Internal Medicine Residency Program Gainesville Florida USA. Graduate Medical Education University of Central Florida College of Medicine Orlando Florida USA. HCA Florida North Florida Hospital Gainesville Florida USA.
 Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Neurophysiology, IRCCS Neuromed, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Neurophysiology, IRCCS Neuromed, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Neurophysiology, IRCCS Neuromed, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Neurophysiology, IRCCS Neuromed, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Neurophysiology, IRCCS Neuromed, Pozzilli, Italy.
 Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Institute for Genetic and Biomedical Research, National Research Council, Cagliari, Italy. Dpt of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Department of Neurosciences, ARNAS Brotzu, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
 Department of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway. K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway. Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. Department of Neurology, Akershus University Hospital, Lørenskog, Norway. Department of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway. K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway. Department of Neurology, Akershus University Hospital, Lørenskog, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway. K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway. Department of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway. K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway. Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. Department of Neurology, Akershus University Hospital, Lørenskog, Norway.
 Unit of Neurology and Stroke Unit, IRCCS Policlinico San Donato, Milan, Italy. Department of Neurology, Azienda Ospedaliera di Melegnano e Della Martesana, Melegnano, Italy. Department of Arrhythmology, IRCCS Policlinico San Donato, Milan, Italy. Medical Genetics, Department of Health Sciences, Università Degli Studi di Milano, Milan, Italy. Medical Genetics, Department of Health Sciences, Università Degli Studi di Milano, Milan, Italy. Department of Biomedical Sciences for Health, University of Milan, Milan, Italy. Unit of Radiology, IRCCS Policlinico, San Donato, Milan, Italy. Department of Arrhythmology, IRCCS Policlinico San Donato, Milan, Italy. Medical Genetics, Department of Health Sciences, Università Degli Studi di Milano, Milan, Italy. Medical Genetics Unit, ASST Santi Paolo e Carlo, Milan, Italy. Medical Genetics, Department of Health Sciences, Università Degli Studi di Milano, Milan, Italy. Medical Genetics Unit, ASST Santi Paolo e Carlo, Milan, Italy. Unit of Neurology and Stroke Unit, IRCCS Policlinico San Donato, Milan, Italy.
 Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. ymahjoub@ucalgary.ca. Department of Pathology and Laboratory Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
 AcariaHealth, FL, Orlando, USA. AcariaHealth, FL, Orlando, USA. Biogen Inc., Cambridge, MA, USA. Biogen Inc., Cambridge, MA, USA. Biogen Inc., Cambridge, MA, USA. Biogen Inc., Cambridge, MA, USA. Biogen Inc., Cambridge, MA, USA. jim.lewin@biogen.com.
 Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China. Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China. Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China. Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China. Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
 Cleveland Clinic Foundation, OH, USA. Prevea Health, Green Bay, WI, USA. Kent State University, OH, USA. VA Boston Healthcare System, Boston, MA, USA. Cleveland Clinic Foundation, Mellen Center for Multiple Sclerosis, OH, USA.
 St. Katharinen-Hospital Frechen, Department of Neurology, Kapellenstraße 1-6, 50226 Frechen, Germany. St. Katharinen-Hospital Frechen, Department of Neurology, Kapellenstraße 1-6, 50226 Frechen, Germany. St. Katharinen-Hospital Frechen, Department of Neurology, Kapellenstraße 1-6, 50226 Frechen, Germany.
 Neuromuscular Rehabilitation Research Center, Semnan University of Medical Sciences, Semnan, Iran. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. Rehabilitation Research Center, Occupational Therapy Department, School of Rehablitation Sciences, Iran University of Medical Sciences, Tehran, Iran. Rehabilitation Research Center, Occupational Therapy Department, School of Rehablitation Sciences, Iran University of Medical Sciences, Tehran, Iran. Department of Occupational Therapy, School of Rehabilitation, Semnan University of Medical Sciences, Semnan, Iran.
 Department of Mathematics and Computer Science, University of Catania, Viale Andrea Doria 6, Catania 95125, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 97, Catania 95125, Italy. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania 95125, Italy. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania 95125, Italy. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania 95125, Italy. InSilicoTrials Technologies BV, 's Hertogenbosch, the Netherlands. InSilicoTrials Technologies BV, 's Hertogenbosch, the Netherlands. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania 95125, Italy. Mimesis SRL, Catania, Italy. Centro Sclerosi Multipla, UOC Neurologia, ARNAS Garibaldi, P.zza S. Maria di Gesù, Catania 95124, Italy. Department of Drug and Health Sciences, University of Catania, Viale Andrea Doria 6, Catania 95125, Italy.
 Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Department of Neurology, Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady in Prague, Czech Republic. Department of Neurology, Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady in Prague, Czech Republic. Department of Neurology, Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady in Prague, Czech Republic. Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Department of Neurology, Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady in Prague, Czech Republic. Department of Neurology, Third Faculty of Medicine, Charles University and University Hospital Kralovske Vinohrady in Prague, Czech Republic. Department of Internal Medicine, Second Faculty of Medicine, Charles University and University Hospital Motol in Prague, Czech Republic.
 Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Química Biológica, Cátedra de Química Biológica Patológica; Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas Prof. Dr. Alejandro C. Paladini, Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina. Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Química Biológica, Cátedra de Química Biológica Patológica; Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas Prof. Dr. Alejandro C. Paladini, Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina. Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Química Biológica, Cátedra de Química Biológica Patológica; Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química y Fisicoquímica Biológicas Prof. Dr. Alejandro C. Paladini, Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina.
 MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
 From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). Department of Physiotherapy, School of Medicine and Health Sciences, Universitat Internacional de Catalunya, Barcelona, Spain (CS-M). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM). From the Neurology-Neuroimmunology Department and Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia, Vall d'Hebron University Hospital Barcelona, Barcelona, Spain (CS-M, MJC, DFX, GLS, SSP, IGC, ERMM, JS-G, XM).
 Cardiff University School of Medicine, Cardiff, UK. RINGGOLD: 2111 La Paz University Hospital, Universidad Autónoma de Madrid, Madrid, Spain. RINGGOLD: 16268 Cardiff University School of Medicine, Cardiff, UK Fondazione IRCCS Ca' Granda Ospedale Policlinico Maggiore, Milan, Italy University of Milan, Milan, Italy. RINGGOLD: 2111 Cardiff University School of Medicine, Cardiff, UK. RINGGOLD: 2111 Advanced Neurosciences Institute, Franklin, TN, USA. Department of Neurology, University of Warmia and Mazury, Olsztyn, Poland. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany Brain and Mind Centre, University of Sydney, Sydney, Australia Department of Neurology, Medical University of Vienna, Vienna, Austria Department of Neurology, Palacky University Olomouc, Olomouc, Czech Republic. First Medical Faculty, Department of Neurology, Charles University, Prague, Czech Republic. North Central Neurology Associates, Cullman, AL, USA. Center of Clinical Neuroscience, Carl Gustav Carus University Hospital, Dresden, Germany. Universitair MS Centrum, Hasselt-Pelt, Belgium. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Sanofi, Cambridge, MA, USA. Sanofi, Cambridge, MA, USA. Sanofi, Cambridge, MA, USA. University of Alberta, Edmonton, Alberta, Canada. RINGGOLD: 3158
 Montreal Neurological Institute and Hospital, Montreal, Québec, Canada. St. Michael's Hospital, Toronto, Ontario, Canada. London Health Sciences Centre, London, Ontario, Canada. CHU de Québec, Québec City, Québec, Canada. Memorial University, St. John's, Newfoundland-Labrador, Canada. University of British Columbia, Vancouver, British Columbia, Canada. University of Alberta, Edmonton, Alberta, Canada.
 Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Institute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China.
 Institute of Neuropathology, University Hospital Münster, 48149 Münster, Germany. Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Québec, Canada. Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Québec, Canada.
 Department of Medical Microbiology/Infectious Diseases, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Department of Medical Microbiology/Infectious Diseases, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Department of Medical Microbiology/Infectious Diseases, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Department of Medical Microbiology/Infectious Diseases, Max Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
 From the Danish MS Society, Valby, Denmark (CSK, LS, ML, JLS). From the Danish MS Society, Valby, Denmark (CSK, LS, ML, JLS). From the Danish MS Society, Valby, Denmark (CSK, LS, ML, JLS). From the Danish MS Society, Valby, Denmark (CSK, LS, ML, JLS).
 Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany. Department for Molecular and Cellular Sports Medicine, Institute for Cardiovascular Research and Sports Medicine, German Sport University Cologne, Cologne, Germany. Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany. Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany. Department for Molecular and Cellular Sports Medicine, Institute for Cardiovascular Research and Sports Medicine, German Sport University Cologne, Cologne, Germany. Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke gGmbH, Berg, Germany. Department for Molecular and Cellular Sports Medicine, Institute for Cardiovascular Research and Sports Medicine, German Sport University Cologne, Cologne, Germany. Neurological Rehabilitation Centre Godeshöhe, Bonn, Germany. Department of Research and Development, Kliniken Valens, Valens, Switzerland. Department of Health, OST - Eastern Swiss University of Applied Sciences, St. Gallen, Switzerland. Department of Neurology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. Division of Performance and Health, Institute for Sport and Sport Science, Technical University Dortmund, Dortmund, Germany.
 Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Electronic address: sahla.el.mahdaoui.01@regionh.dk. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark.
 Dept. of Hepatology, University of Leipzig, Leipzig, Germany. Dept. of Gastroenterology, University of Leipzig, Leipzig, Germany. Dept. of Hepatology, University of Leipzig, Leipzig, Germany. Helios Klinik Leisnig, Leisnig, Germany. Dept. of Gastroenterology, University of Leipzig, Leipzig, Germany. Institute of Pathology, University of Leipzig, Leipzig, Germany. Dept. of Hepatology, University of Leipzig, Leipzig, Germany.
 University of Massachusetts Charleston Area Medical Center University of Miami/Jackson Memorial Hospital
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. sh_eskandarieh@yahoo.com.
 Laboratory of Neuromuscular and Cardiovascular Study of Motion (LANECASM) Physiotherapy Department, Faculty of Health and Care Sciences, University of West Attica, Athens, GRC. Physical Therapy, University of West Attica, Athens, GRC. 2nd Neurological Department, Attikon University Hospital, Athens, GRC. 2nd Neurological Department, Attikon University Hospital, Athens, GRC.
 Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom.
 Department of Electrical and Electronic Engineering, University of Cagliari, Cagliari, Italy. Department of Electrical and Electronic Engineering, University of Cagliari, Cagliari, Italy. Department of Electrical and Electronic Engineering, University of Cagliari, Cagliari, Italy. Department of Electrical and Electronic Engineering, University of Cagliari, Cagliari, Italy. Department of Medical Science and Public Health, Centro Sclerosi Multipla, University of Cagliari, Cagliari, Italy. Department of Medical Science and Public Health, Centro Sclerosi Multipla, University of Cagliari, Cagliari, Italy. Unit of Oncology and Molecular Pathology, Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Medical Genetics, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Centre for Research University Services, University of Cagliari, Monserrato, Italy. AART-ODV (Association for the Advancement of Research on Transplantation), Cagliari, Italy. Medical Genetics, R. Binaghi Hospital, ASSL Cagliari, ATS Sardegna, Cagliari, Italy. Medical Genetics, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Centre for Research University Services, University of Cagliari, Monserrato, Italy. AART-ODV (Association for the Advancement of Research on Transplantation), Cagliari, Italy. Medical Genetics, R. Binaghi Hospital, ASSL Cagliari, ATS Sardegna, Cagliari, Italy.
 Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, University of Medicine, Pharmacy, Science and Technology Târgu Mures, 540136 Târgu Mures, Romania. Department of Laboratory Medicine, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, Romania. Laboratory Medicine, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, University of Medicine, Pharmacy, Science and Technology Târgu Mures, 540136 Târgu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, University of Medicine, Pharmacy, Science and Technology Târgu Mures, 540136 Târgu Mures, Romania. Ist Neurology Clinic, Emergency Clinical County Hospital Targu Mures, 540136 Targu Mures, Romania. Department of Neurology, University of Medicine, Pharmacy, Science and Technology Târgu Mures, 540136 Târgu Mures, Romania.
 Division of Internal Medicine Nursing, Wroclaw Medical University, Wroclaw, Poland. Division of Internal Medicine Nursing, Wroclaw Medical University, Wroclaw, Poland. Cardinal Stefan Wyszynski Institute of Cardiology, Warsaw, Poland. Department of Nursing and Obstetrics Collegium Mazovia, Siedlce, Poland. Department of Neurology, Wroclaw Medical University, Wroclaw, Poland.
 Neurology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America. Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, United States of America. Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, United States of America. Neurology, University of Colorado School of Medicine, Aurora, United States of America.
 Pharmacy Unit, Hospital Santa Bárbara, Street Malagón S/N, 13500, Puertollano, Spain. pnietog90@gmail.com. Pharmacy Unit, Hospital Santa Bárbara, Street Malagón S/N, 13500, Puertollano, Spain.
 Department of Laboratory Medicine, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, People's Republic of China. Gene Engineering Drug and Biotechnology Beijing Key Laboratory, College of Life Sciences, Beijing Normal University, Beijing 100875, People's Republic of China. Department of Pathology, Henan Provincial People's Hospital; People's Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China. Medical Research Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China. Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences/School of Basic Medicine, Peking Union Medical College, Beijing, People's Republic of China. Gene Engineering Drug and Biotechnology Beijing Key Laboratory, College of Life Sciences, Beijing Normal University, Beijing 100875, People's Republic of China.
 Neurology, Bharati Vidyapeeth University Medical College Pune. University of Baghdad, Al-Kindy College of Medicine, Baghdad, Iraq. St. George's University School of Medicine, University Centre Grenada, West Indies. Internal Medicine, Government Medical College, Omandurar, Chennai. Internal Medicine, Postdoctoral Research Fellow, Mayo Clinic, USA. Odessa National Medical University, Odessa, Ukraine. Somervell Memorial CSI Medical College and Hospital, Karakonam, Trivandrum. Asfendiyarov Kazakh National Medical University, Almaty, Kazakhstan. Internal Medicine, BJ Medical College, Ahmedabad, India. University of Baghdad, Al-Kindy College of Medicine, Baghdad, Iraq. Internal Medicine, Al-Manhal Academy, Khartoum, Sudan.
 Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Neuroscape, University of California, San Francisco, San Francisco, CA, United States. Department of Psychiatry, University of California, San Francisco, San Francisco, CA, United States. Institute for Creative Studies, University of Southern California, Los Angeles, CA, United States. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Neuroscape, University of California, San Francisco, San Francisco, CA, United States. Kessler Foundation, East Hanover, NJ, United States. Department of Physical Medicine & Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, United States. Kessler Foundation, East Hanover, NJ, United States. Department of Physical Medicine & Rehabilitation, Rutgers New Jersey Medical School, Newark, NJ, United States. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Neuroscape, University of California, San Francisco, San Francisco, CA, United States. Department of Psychiatry, University of California, San Francisco, San Francisco, CA, United States. Department of Physiology, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States.
 Institute of Neuroimmunology and Multiple Sclerosis, University Clinic Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Clinic Hamburg-Eppendorf, Hamburg, Germany. Department of Research and Clinical Development, Unit of Neuroepidemiology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
 Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Institute of Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Institute for Anatomy and Cell Biology, University of Giessen, Giessen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany. Institute of Clinical Chemistry and Laboratory Medicine, University Hospital of Regensburg, Regensburg, Germany. Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany. Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany. Experimental Neurology Group, Department of Neurology, University of Giessen, Giessen, Germany.
 Department of Medical Physics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Department of Medical Physics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Iranian Center of Neurological Research, Imam Khomeini Hospital, Faculty of Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. Department of Radiology, Imam Khomeini Hospital, Faculty of Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. Department of Radiology, Imam Khomeini Hospital, Faculty of Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. Department of Radiology, Imam Khomeini Hospital, Faculty of Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.
 Multiple Sclerosis Comprehensive Care Center, RWJ Barnabas Health, Livingston, NJ, USA. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Hospices Civils de Lyon, Hôpital Neurologique Pierre Wertheimer, Bron, France. Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, Lyon, France. RINGGOLD: 57484 Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France. RINGGOLD: 27098 Eugène Devic EDMUS Foundation Against Multiple Sclerosis, Bron, France. Formerly: Biogen, Cambridge, MA, USA. Biogen, Baar, Switzerland. Biogen, Cambridge, MA, USA. Formerly: Biogen, Cambridge, MA, USA. Christian Doppler Medical Center, Paracelsus Medical University, Salzburg, Austria.
 IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy. IRCCS Centro Neurolesi "Bonino-Pulejo", S.S. 113 Via Palermo, C/da Casazza, 98124 Messina, Italy.
 Department of Neurology, Mayo Clinic, Rochester, United States of America. Department of Neurology, Mayo Clinic, Rochester, United States of America. Department of Neurology, Mayo Clinic, Rochester, United States of America. Department of Neurology, Mayo Clinic, Rochester, United States of America. Department of Neurology, Mayo Clinic, Rochester, United States of America. Department of Neurology, Mayo Clinic, Rochester, United States of America. Guggenheim 1542C, Mayo Clinic, Rochester, United States of America.
 Neurology Research Center, Department of Neurology, Kerman University of Medical Sciences, Kerman, Iran. Neurology Research Center, Department of Neurology, Kerman University of Medical Sciences, Kerman, Iran. Department of Radiology, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran. Department of Immunology, Medical School, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Department of Immunology, Medical School, Kerman University of Medical Sciences, Kerman, Iran.

 Mental Health and Clinical Neurosciences Unit, School of Medicine, Institute of Mental Health, University of Nottingham, Nottingham, UK. College of Social Science, University of Lincoln, Lincoln, UK. Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, UK. Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, UK; SINTEF Digital, Trondheim, Norway.
 "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. Ophthalmology Emergency Hospital, Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. Department of Ophthalmology, University Emergency Hospital, Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. Department of Neurology, University Emergency Hospital, Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. Department of Ophthalmology, University Emergency Hospital, Bucharest, Romania.
 Ambulatory Department, Centura Health at Home, Denver, Colorado, USA. RINGGOLD: 129455 Department of Surgery, University of Arizona School of Medicine, Phoenix, Arizona, USA. Multiple Sclerosis, Overseeing Neurologist, Littleton, Colorado, USA.
 School of Medicine and Public Health, University of Newcastle, Callaghan, Australia; Department of Neurology, John Hunter Hospital, New Lambton Heights, Australia; Hunter Medical Research Institute, New Lambton, NSW, Australia. Electronic address: jeannette.lechnerscott@health.nsw.gov.au. MSSN John Hunter Hospital, Hunter New England Health, Australia. Multiple Sclerosis Nurse Consultant, Monash Health, Australia. Department of Neurology, Alfred Hospital, Melbourne, Australia; Department of Neurology, Royal Melbourne Hospital, Parkville, Australia; Florey Institute of Neuroscience and Mental Health, Melbourne, Australia. Clinical Research Unit, Brain & Mind Research Institute, University of Sydney, Sydney, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia; Department of Neurology, MSNI Service, Alfred Health, Melbourne, Australia.
 Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Electronic address: lunin@pbcras.ru. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia. Institute of Cell Biophysics RAS, Pushchino, Moscow region, Russia.
 Psychology department The University of Jordan. Psychology department The University of Jordan.
 Neurology Department, Sheikh Shakhbout Medical City, Abu Dhabi, ARE. College of Medicine and Health Sciences, Khalifa University, Abu Dhabi, ARE. Neurology Department, Sheikh Shakhbout Medical City, Abu Dhabi, ARE. Neurology Department, Sheikh Shakhbout Medical City, Abu Dhabi, ARE.
 Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, NIHR University College London Hospitals Biomedical Research Centre, Faculty of Brain Sciences, University College London, London, UK. Department of Molecular Biology and Molecular Biotechnology, Federico II University of Naples, Naples, Italy Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department NEUROFARBA, Section of Neurosciences, University of Florence, Florence, Italy IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Department of Neurology and The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. School of Rehabilitation Therapy, Queens University, Kingston, ON, Canada. University of Exeter Medical School, University of Exeter, Exeter, UK. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Departments of Medicine & Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Multiple Sclerosis Centre of Catalonia and Department of Neurology-Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Neurvati Neurosciences, New York, NY, USA. Department of Health Sciences, University of Genoa, Genoa, Italy IRCCS Ospedale Policlinico San Martino, Genoa, Italy. RealTalk MS, Long Beach, CA, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. National Multiple Sclerosis Society, 733 Third Avenue, New York, NY 10017, USA. National Multiple Sclerosis Society, New York, NY, USA.
 Neurology, State University of New York Upstate Medical University, Syracuse, USA. Neurology, State University of New York Upstate Medical University, Syracuse, USA. Neurology, State University of New York Upstate Medical University, Syracuse, USA.
 Department of Clinical Neurological Sciences, Western University, London, ON, Canada. Sarah.Morrow@lhsc.on.ca. Department of Clinical Neurological Sciences, London Health Sciences Centre, University Hospital, 339 Windermere Road, London, ON, N6A 5A5, Canada. Sarah.Morrow@lhsc.on.ca. Patient Advocate, Rome, Italy. Professor of Neuropsychology, Royal Holloway, University of London, London, UK. Global Medical Affairs, Neurology and Immunology, The Healthcare Business of Merck KGaA, Darmstadt, Germany.
 Department of Internal Medicine, University of Iowa, Iowa City, IA, United States. Independent Researcher, Greensboro, NC, United States. Department of Neurology, Medical College of Wisconsin, Milwaukee, WI, United States.
 Boston Children's Hospital, Department of Neurology 300 Longwood Avenue, Boston, MA 02115, United States; Massachusetts General Brigham Hospital, Department of Neurology 55 Fruit Street, Boston, MA 02114, United States. Electronic address: liz.v.wilson@gmail.com. Massachusetts General Brigham Hospital, Department of Neurology 55 Fruit Street, Boston, MA 02114, United States. Boston Children's Hospital, Critical care medicine 300 Longwood Avenue, Boston, MA 02115, United States. Boston Children's Hospital, Office of Ethics 300 Longwood Avenue, Boston, MA 02115, United States. Boston Children's Hospital, Department of Neurology 300 Longwood Avenue, Boston, MA 02115, United States. Boston Children's Hospital, Department of Neurology 300 Longwood Avenue, Boston, MA 02115, United States.
 Department of Neurology, Hospital of Merano (SABES-ASDAA), Via Rossini, 5, 39012, Merano-Meran, Italy. dr.francescobrigo@gmail.com. UOC Neurology and Stroke Unit, ASST Lecco, Merate, Italy. Private Practice, Brou, France.
 Biotechnology Program, School of Science and Engineering, American University in Cairo, New Cairo 11835, Egypt. Biotechnology Program, School of Science and Engineering, American University in Cairo, New Cairo 11835, Egypt. Biology Department, School of Science and Engineering, American University in Cairo, New Cairo 11835, Egypt. Biotechnology Program, School of Science and Engineering, American University in Cairo, New Cairo 11835, Egypt. Biology Department, School of Science and Engineering, American University in Cairo, New Cairo 11835, Egypt. Department of Chemical and Biomolecular Engineering, University of Notre Dame, Notre Dame, IN 46556, USA.
 Unit of Integrative Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Unit of Integrative Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China. Med-X Center for Informatics, Sichuan University, Chengdu, China. Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Unit of Integrative Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
 Department of Medical-Surgical Nursing, School of Nursing & Midwifery Tehran University of Medical Sciences Tehran Iran. Islamic Azad University, Kashan Branch Kashan Iran. Department of Medical-Surgical Nursing, School of Nursing & Midwifery Tehran University of Medical Sciences Tehran Iran. School of Nursing and Midwifery Tehran University of Medical Sciences Tehran Iran. Social Determinants of Health Research Center Alborz University of Medical Sciences Karaj Iran. Neuroscience Research Center Tabriz University of Medical Sciences Tabriz Iran.
 Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich 81377, Germany. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Eli and Edythe L Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich 81675, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen 91054, Germany.
 Laboratory of Stress, Immunity, Pathogens (EA7300), Medical School, University of Lorraine, 54500, Vandœuvre-les-Nancy, France. Laboratory of Stress, Immunity, Pathogens (EA7300), Medical School, University of Lorraine, 54500, Vandœuvre-les-Nancy, France. CHRU Nancy, Vandœuvre-les-Nancy, France.
 Department of Medicine, Aseer Central Hospital, Abha, Saudi Arabia. halgahtani@hotmail.com. Neurology Section, Department of Medicine, King Abdulaziz Medical City, P.O. Box: 12723, Jeddah, 21483, Saudi Arabia. halgahtani@hotmail.com. Department of Neuroscience, King Faisal Specialist Hospital & Research Centre, Jeddah, Saudi Arabia. College of Medicine, King Khalid University, Abha, Saudi Arabia. Department of Medicine, Aseer Central Hospital, Abha, Saudi Arabia. Neurology Department, Kasr Al Ainy Hospital, Faculty of Medicine, Cairo University, Cairo, Egypt. College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London EC1M 6BQ, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London E1 1FR, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London E1 1FR, UK. Blizard Institute, Queen Mary University of London, London E1 2AT, UK. Blizard Institute, Queen Mary University of London, London E1 2AT, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London E1 1FR, UK. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University of London, London EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, London E1 1FR, UK.
 Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China. Department of Thyroid Breast Surgery, Xi'an No.3 Hospital, The Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China. Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China. Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China. Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
 Department of Ophthalmology and Visual Sciences, School of Medical Science, Health Campus, Universiti Sains Malaysia, Kubang Kerian, MYS. Ophthalmology, Raja Perempuan Zainab II Hospital, Kubang Kerian, MYS. Ophthalmology Clinic, Hospital Universiti Sains Malaysia, Kubang Kerian, MYS. Ophthalmology, Raja Perempuan Zainab II Hospital, Kubang Kerian, MYS. Department of Ophthalmology and Visual Sciences, School of Medical Science, Health Campus, Universiti Sains Malaysia, Kubang Kerian, MYS. Ophthalmology Clinic, Hospital Universiti Sains Malaysia, Kubang Kerian, MYS.
 Unità Operativa Complessa di Medicina Riabilitativa, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. LaRiCE lab (Gait and Balance Disorders Laboratory), Don Gnocchi Foundation IRCCS, Milan, Italy. LaRiCE lab (Gait and Balance Disorders Laboratory), Don Gnocchi Foundation IRCCS, Milan, Italy. AISM Rehabilitation Center, Italian MS Society, Genoa, Italy. DATER Riabilitazione Ospedaliera, Azienda USL di Bologna, Bologna, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
 Students Research Office, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Midwifery and Reproductive Health, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran. h.riazi@sbmu.ac.ir. Department of Midwifery and Reproductive Health, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Biostatistics, School of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Population Health Research Group, Health Metrics Research Center, Iranian Institute for Health Sciences Research, ACECR, Tehran, Iran. montazeri@acecr.ac.ir. Faculty of Humanity Sciences, University of Science and Culture, Tehran, Iran. montazeri@acecr.ac.ir.
 Department of Neurology, Jena University Hospital, Jena, Germany. Department of Neurology, Jena University Hospital, Jena, Germany. Department of Internal Medicine IV (Gastroenterology, Hepatology, and Infectious Diseases), Jena University Hospital, Jena, Germany. Institute of Pathology, Ruhr University Bochum, Bochum, Germany. Department of Neurology, Jena University Hospital, Jena, Germany.
 Università Vita Salute San Raffaele, Centro Sclerosi Multipla Ospedale Gallarate, Milan, Italy. Experimental Neurophysiology Unit, INSPE IRCCS Ospedale San Raffaele, Università Vita Salute San Raffaele, Milan, Italy. Department of Clinical Neurosciences, San Raffaele Scientific Institute, Sleep Disorders Center, Università Vita Salute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, INSPE IRCCS Ospedale San Raffaele, Università Vita Salute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, INSPE IRCCS Ospedale San Raffaele, Università Vita Salute San Raffaele, Milan, Italy. Neurosciences, Reproductive and Odontostomatological Sciences Department, Federico II, University of Naples, Italy. Multiple Sclerosis Center, II Division of Neurology, University of Campania 'L. Vanvitelli' Napoli, Italy. UOC Neurologia, Azienda Ospedaliera Sant'Andrea, Roma, Italy. UO Neurologia Ospedale Antonio Segni di Ozieri, Ozieri, Italy. Università Campus Bio-Medico, Roma, Italy. RINGGOLD: 9317 Centro Sclerosi Multipla Fondazione Istituto 'G. Giglio', Cefalù (PA), Italy. UOC Neurologia e Neurofisiopatologia Policlinico 'Paolo Giaccone', Palermo, Italy. Biogen, Milano, Italy. Biogen, Milano, Italy.
 Department of Neurology, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Faculty of Philosophy, Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin, Germany. A cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin, Experimental and Clinical Research Center, Berlin, Germany. Neuroscience Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Experimental and Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. A cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin, Experimental and Clinical Research Center, Berlin, Germany. Neuroscience Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Department of Psychiatry and Neurosciences, , Charitéplatz, Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Department of Neurology, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 A cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin, Experimental and Clinical Research Center, Berlin, Germany. Neuroscience Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Berlin Institute of Health, Berlin, Germany. A cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin, Experimental and Clinical Research Center, Berlin, Germany. Neuroscience Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Experimental and Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. A cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin, Experimental and Clinical Research Center, Berlin, Germany. Experimental and Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Department of Neurology, University of California, Irvine, CA, USA. Faculty of Philosophy, Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin, Germany. Berlin Center for Advanced Neuroimaging, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Bernstein Center for Computational Neuroscience, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Department of Neurology, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 A cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin, Experimental and Clinical Research Center, Berlin, Germany. Neuroscience Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Experimental and Clinical Research Center, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Berlin Institute of Health, Berlin, Germany. Department of Neurology, , Berlin, GermanyCharité-Universitätsmedizin Berlin. RINGGOLD: 14903 Faculty of Philosophy, Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin, Germany.
 UNICAEN, CHU de Caen, INSERM U1086 ANTICIPE, Pôle de Recherche, Normandy University, Caen 14000, France. Department of Neurology, UNICAEN, Normandy University, MS Expert Center, CHU de Caen Normandy, Caen 14000, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon 69000, France. Hospices Civils de Lyon, Hôpital Neurologique, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Bron 69500, France. Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR 5292, Lyon 69000, France. EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis, State-Approved Foundation, Bron, France. Service de Biostatistique-Bioinformatique, Pôle Santé Publique, Hospices Civils de Lyon, Lyon 69000, France. Université Lyon 1, CNRS, UMR 5558, Laboratoire de Biométrie et Biologie Evolutive, Lyon 69000, France. Service de Biostatistique-Bioinformatique, Pôle Santé Publique, Hospices Civils de Lyon, Lyon 69000, France. Université Lyon 1, CNRS, UMR 5558, Laboratoire de Biométrie et Biologie Evolutive, Lyon 69000, France. UNICAEN, CHU de Caen, INSERM U1086 ANTICIPE, Pôle de Recherche, Normandy University, Caen 14000, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon 69000, France. Hospices Civils de Lyon, Hôpital Neurologique, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation, Bron 69500, France. Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, INSERM 1028 et CNRS UMR 5292, Lyon 69000, France. EUGENE DEVIC EDMUS Foundation Against Multiple Sclerosis, State-Approved Foundation, Bron, France. CHU Pontchaillou, CIC1414 INSERM, Rennes F-35000, France. Department of Neurology, Nancy University Hospital, Nancy, France. Université de Lorraine, APEMAC, Nancy F-54000, France. Department of Neurology, CHU de Toulouse, CRC-SEP, Toulouse Cedex 9 F-31059, France. Université Toulouse III, Infinity, INSERM UMR1291 - CNRS UMR5051, Toulouse Cedex 3 F-31024, France. Univ. Bordeaux, Bordeaux F-33000, France. INSERM U1215, Neurocentre Magendie, Bordeaux F-33000, France. Department of Neurology, CHU de Bordeaux, CIC Bordeaux CIC1401, Bordeaux F-33000, France. Department of Neurology and Clinical Investigation Center, CHU de Strasbourg, CIC 1434, INSERM 1434, Strasbourg F-67000, France. CHU Lille, CRCSEP Lille, Univ Lille, U1172, Lille F-59000, France. Department of Neurology, CHU de Dijon, EA4184, Dijon F-21000, France. Neurology, UR2CA, Centre Hospitalier Universitaire Pasteur2, Université Nice Côte d'Azur, Nice, France. Nantes Université, CHU Nantes, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, CIC INSERM 1413, Service de Neurologie, Nantes F-44000, France. Department of Neurology, CHU Clermont-Ferrand, Clermont-Ferrand F-63000, France. Université Clermont Auvergne, Inserm, Neuro-Dol, Clermont-Ferrand F-63000, France. MS Unit, CHU de Montpellier, Montpellier Cedex 5 F-34295, France. University of Montpellier (MUSE), Montpellier F-34000, France. CHU de Besançon, Service de Neurologie 25 030, Besançon, France. Aix Marseille Univ, APHM, Hôpital de la Timone, Pôle de Neurosciences Cliniques, Service de Neurologie, Marseille 13005, France. Departement of Neurology, Hôpital de Poissy, Poissy F-78300, France. Department of Neurology, Nimes University Hospital, Nimes Cedex 9 F-30029, France. Institut de Génomique Fonctionnelle, UMR5203, INSERM 1191, Univ. Montpellier, Montpellier Cedex 5 F-34094, France. Department of Neurology, CHU de Saint-Étienne, Hôpital Nord, Saint-Étienne F-42000, France. Univ Rennes, EHESP, CNRS, Inserm, Arènes - UMR 6051, RSMS (Recherche sur les Services et Management en Santé) - U 1309, Rennes F-35000, France. UNICAEN, CHU de Caen, INSERM U1086 ANTICIPE, Pôle de Recherche, Normandy University, Caen 14000, France. Department of Neurology, UNICAEN, Normandy University, MS Expert Center, CHU de Caen Normandy, Caen 14000, France.
 Division of Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic, Rochester, MN, United States. Division of Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic, Rochester, MN, United States. Department of Radiology, Mayo Clinic, Rochester, MN, United States. Division of Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic, Rochester, MN, United States. Department of Radiology, Mayo Clinic, Rochester, MN, United States. Mayo Clinic College of Medicine and Science, Library-Public Services, Mayo Clinic, Rochester, MN, United States. Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, TX, United States. Division of Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic, Rochester, MN, United States.
 Inserm U1094, IRD U270, University Limoges, CHU Limoges, EpiMaCT - Epidemiology of Chronic Diseases in Tropical Zone, Institute of Epidemiology and Tropical Neurology, Omega Health, Limoges, France; Neurology Institute, Harley Street Medical Center, Abu Dhabi, United Arab Emirates. Electronic address: mzeineddine39@gmail.com. Faculty of Pharmacy, Lebanese University, Beirut, Lebanon; National Institute of Public Health, Clinical Epidemiology and Toxicology (INSPECT-LB), Beirut, Lebanon. Faculty of Pharmacy, Lebanese University, Beirut, Lebanon; National Institute of Public Health, Clinical Epidemiology and Toxicology (INSPECT-LB), Beirut, Lebanon; School of Medicine, Lebanese American University, Byblos, Lebanon; Department of Primary Care and Population Health, University of Nicosia Medical School, Nicosia 2417, Cyprus. Multiple Sclerosis International Federation, London, United Kingdom. Multiple Sclerosis International Federation, London, United Kingdom. Inserm U1094, IRD U270, University Limoges, CHU Limoges, EpiMaCT - Epidemiology of Chronic Diseases in Tropical Zone, Institute of Epidemiology and Tropical Neurology, Omega Health, Limoges, France. Neurology Institute, Harley Street Medical Center, Abu Dhabi, United Arab Emirates.
 Department of Medical and Surgical Sciences, "Magna Graecia" University of Catanzaro, Catanzaro, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli," Caserta, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli," Caserta, Italy. Department of Precision Medicine, University of Campania "Luigi Vanvitelli," Napoli, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli," Caserta, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli," Caserta, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli," Caserta, Italy. Multiple Sclerosis Center, II Neurological Clinic, University of Campania "Luigi Vanvitelli," Napoli, Italy. Department of Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli," Napoli, Italy. Multiple Sclerosis Center, II Neurological Clinic, University of Campania "Luigi Vanvitelli," Napoli, Italy. Department of Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli," Napoli, Italy.
 Department of Speech and Language Therapy, School of Health Sciences, University of Ioannina, Ioannina, Greece. B' Department of Neurology, Multiple Sclerosis Center, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. B' Department of Neurology, Multiple Sclerosis Center, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Speech and Language Therapy, School of Health Sciences, University of Ioannina, Ioannina, Greece. Department of Neurology, University Hospital of Larissa, School of Health Sciences, University of Thessaly, Larissa, Greece. Department of Mechanical Engineering and Aeronautics, University of Patras, Patras, Greece. Lab of Cognitive Neuroscience, School of Psychology, Aristotle University of Thessaloniki, Greece. Communication Sciences and Disorders, School of Health Sciences, The University of Sydney, Australia, and. Department of Speech and Language Therapy, School of Health Sciences, University of Ioannina, Ioannina, Greece. Department of German Language and Literature, Aristotle University of Thessaloniki. Department of Neurology, University Hospital of Larissa, School of Health Sciences, University of Thessaly, Larissa, Greece. Department of Speech and Language Therapy, School of Health Sciences, University of Ioannina, Ioannina, Greece.
 Division of Ophthalmology, Department of Biomedical and Clinical Sciences, Faculty of Medicine, Linköping University, 581 83 Linköping, Sweden. Division of Ophthalmology, Department of Biomedical and Clinical Sciences, Faculty of Medicine, Linköping University, 581 83 Linköping, Sweden. Division of Ophthalmology, Department of Biomedical and Clinical Sciences, Faculty of Medicine, Linköping University, 581 83 Linköping, Sweden. Division of Neurology, Department of Biomedical and Clinical Sciences, Linköping University, 581 85 Linköping, Sweden.
 Department of Nutrition and Dietetics, Baskent University, Ankara, Turkey. Department of Nutrition and Dietetics, Baskent University, Ankara, Turkey. Department of Neurology, Baskent University, Ankara, Turkey.
 Department of Medicine and Surgery, Ladoke Akintola University of Technology, Ogbomoso, Nigeria. Department of Medicine and Surgery, Ladoke Akintola University of Technology, Ogbomoso, Nigeria. Department of Medicine and Surgery, Ladoke Akintola University of Technology, Ogbomoso, Nigeria.
 Gazi University School of Medicine, Department of Neurology, Ankara, Turkey. Gazi University School of Medicine, Department of Neurology, Ankara, Turkey. Ondokuz Mayıs University School of Medicine, Department of Neurology, Samsun, Turkey. İstanbul Hamidiye Faculty of Medicine, University of Health Sciences, Department of Neurology, İstanbul, Turkey. Ondokuz Mayıs University School of Medicine, Department of Neurology, Samsun, Turkey.
 Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Electronic address: m.maestri@ao-pisa.toscana.it. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Section of Statistics, University Hospital of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy. Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa, via Roma 67, Pisa 56126, Italy.
 Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. Maxine Mesinger Multiple Sclerosis Comprehensive Care Center, Department of Neurology, Baylor College of Medicine, Houston, TX, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. Inova, Fairfax, VA, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA.
 Department of Cardiology, Kanazawa Medical University, Japan. Department of Cardiology, Kanazawa Medical University, Japan. Department of Cardiology, Kanazawa Medical University, Japan. Department of Cardiology, Kanazawa Medical University, Japan. Department of Cardiology, Kanazawa Medical University, Japan. Department of Cardiology, Kanazawa Medical University, Japan.
 Department of Neuroscience, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkiye. Department of Neuroscience, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkiye. Department of Neuroscience, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkiye. Department of Neuroscience, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkiye. Department of Neurology, Istanbul University Istanbul Faculty of Medicine, Istanbul, Turkiye. Department of Neurology, Istanbul University Istanbul Faculty of Medicine, Istanbul, Turkiye. Department of Neurology, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkiye. Department of Neuroscience, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkiye.
 Morsani College of Medicine, University of South Florida, Tampa, FL, USA. Morsani College of Medicine, University of South Florida, Tampa, FL, USA. Morsani College of Medicine, University of South Florida, Tampa, FL, USA. Center of Excellence for Aging & Brain Repair, Department of Neurosurgery & Brain Repair, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
 Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Università Cattolica del Sacro Cuore, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Università Cattolica del Sacro Cuore, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Università Cattolica del Sacro Cuore, Roma, Italy. Department of Urology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy. Università Cattolica del Sacro Cuore, Roma, Italy.
 Charité - Universitätsmedizin Berlin, Klinik für Psychiatrie und Psychotherapie, Berlin, Germany. Charité - Universitätsmedizin Berlin, Medizinische Klinik m.S. Psychosomatik, Berlin, Germany. Charité - Universitätsmedizin Berlin, Klinik für Psychiatrie und Psychotherapie, Berlin, Germany. Charité - Universitätsmedizin Berlin, Medizinische Klinik m.S. Psychosomatik, Berlin, Germany. Charité - Universitätsmedizin Berlin, Experimental and Clinical Research Center, Berlin, Germany. Charité - Universitätsmedizin Berlin, Neuroscience Clinical Research Center, Berlin, Germany.
 Rocky Mountain MS Clinic, 370 East 9th Avenue, Suite 106, 111, 208, Salt Lake City, UT, 84103, USA. croman.np@gmail.com. Department of Neurology, James Q. Miller MS Center of Excellence, University of Virginia, Charlottesville, VA, USA.
 From the Department of Clinical Neuropsychology, Free University, Amsterdam, the Netherlands (RJS, CvK, IC). Tante Louise, Bergen op Zoom, the Netherlands (MJvD). Atlant, Kuiltjesweg, Beekbergen, the Netherlands (AJP). From the Department of Clinical Neuropsychology, Free University, Amsterdam, the Netherlands (RJS, CvK, IC). From the Department of Clinical Neuropsychology, Free University, Amsterdam, the Netherlands (RJS, CvK, IC). Department of Neurology, Amsterdam University Medical Centers, Amsterdam, the Netherlands (JK). Department of Neurology, Onze Lieve Vrouwe Gasthuis, Amsterdam, the Netherlands (HW).
 College of Medicine, King Saud University, Riyadh, Saudi Arabia. Department of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. Department of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. College of Medicine, King Saud University, Riyadh, Saudi Arabia. The University Sleep Disorders Center, College of Medicine, King Saud University, Riyadh, Saudi Arabia. National Plan for Science and Technology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neurology, Alfred Health, Melbourne, VIC, Australia. Australian Centre for the Prevention of Cervical Cancer (Formerly Victorian Cytology Service), Carlton South, VIC, Australia. Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neurology, Alfred Health, Melbourne, VIC, Australia. Department of Neurosciences, Eastern Health, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neurology, Alfred Health, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neurology, Alfred Health, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neurology, Alfred Health, Melbourne, VIC, Australia.
 Faculty of Medicine, Aja University of Medical Science, Tehran, Iran. Department of Radiology, Faculty of Medicine, Aja University of Medical Science, Tehran, Iran. Department of Radiology, Faculty of Medicine, Aja University of Medical Science, Tehran, Iran. MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Radiology, Faculty of Medicine, Aja University of Medical Science, Tehran, Iran. Radiation Sciences Research Center, Aja University of Medical Science, Tehran, Iran.
 Department of Medical and Surgical Sciences and Advanced Technologies "G.F. Ingrassia, " University of Catania, Via S. Sofia 78, 95100, Catania, Italy. Multiple Sclerosis Center, Fondazione Policlinico Universitario "Agostino Gemelli" IRCCS, Rome, Italy. Multiple Sclerosis Clinical Care, Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Neurology Section of Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Unit of Neurology, Department of Medicine, Neurophysiology, and Neurobiology, University Campus Bio-Medico of Rome, Rome, Italy. Multiple Sclerosis Center, Department of Neuroscience, City of Health and Science University Hospital, Turin, Italy. Multiple Sclerosis Center, Neurology Unit, Ospedale Civile Di Ciriè, Turin, Italy. Department of Translational Medicine, Neurology Unit, University of Piemonte Orientale, Novara, Italy. Neurological Clinic, Marche Polytechnic University, Ancona, Italy. Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, Milan, Italy. Vita-Salute San Raffaele University, 20132, Milan, Italy. Neuroimaging Research Unit, IRCCS San Raffaele Hospital, 20132, Milan, Italy. Neurophysiology Unit, IRCCS San Raffaele Hospital, 20132, Milan, Italy. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro, Bari, Italy. Multiple Sclerosis Clinical Care, Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Department of Medical and Surgical Sciences and Advanced Technologies "G.F. Ingrassia, " University of Catania, Via S. Sofia 78, 95100, Catania, Italy. Multiple Sclerosis Center, Neurology Unit and Stroke Unit, "Pugliese-Ciaccio" Hospital, Catanzaro, Italy. IRCCS Institute of Neurological Science of Bologna, Bologna, Italy. Department of Biomedical Science and Neuromotricity, University of Bologna, Bologna, Italy. Second Division of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Multiple Sclerosis Center, Fabrizio Spaziani Hospital, Frosinone, Italy. Multiple Sclerosis Center, Fondazione Policlinico Universitario "Agostino Gemelli" IRCCS, Rome, Italy. Department of Neurosciences, Centro di Ricerca per la Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Rome, Italy. Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, Milan, Italy. Neurology Unit - Specialistic Department - ULSS5 , Polesana, Rovigo, Italy. Multiple Sclerosis Centre, Neurology Unit and Stroke Unit, AOOR "Villa Sofia-Cervello, " Palermo, Italy. Department of Medical and Surgical Sciences and Advanced Technologies "G.F. Ingrassia, " University of Catania, Via S. Sofia 78, 95100, Catania, Italy. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro, Bari, Italy. Department of Translational Medicine, Neurology Unit, University of Piemonte Orientale, Novara, Italy. Department of Medical and Surgical Sciences and Advanced Technologies "G.F. Ingrassia, " University of Catania, Via S. Sofia 78, 95100, Catania, Italy. patti@unict.it.
 QIMR Berghofer Centre for Immunotherapy and Vaccine Development, Infection and Inflammation Program QIMR Berghofer Medical Research Institute Herston QLD Australia. QIMR Berghofer Centre for Immunotherapy and Vaccine Development, Infection and Inflammation Program QIMR Berghofer Medical Research Institute Herston QLD Australia.
 Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
 Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. AISM Rehabilitation Center Liguria, Italian Multiple Sclerosis Society (AISM), Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation (FISM), Genoa, Italy. AISM Rehabilitation Center Liguria, Italian Multiple Sclerosis Society (AISM), Genoa, Italy.
 MS Clinic, Department of Neurology, University Hospital Center of São João, Oporto, Portugal. Neuropsychological Unit, Department of Psychology, University Hospital Center of São João, Oporto, Portugal. Faculty of Psychology and Educational Sciences, University of Porto, Porto, Portugal. MS Clinic, Department of Neurology, University Hospital Center of São João, Oporto, Portugal. Neuropsychological Unit, Department of Psychology, University Hospital Center of São João, Oporto, Portugal. Faculty of Psychology and Educational Sciences, University of Porto, Porto, Portugal. MS Clinic, Department of Neurology, University Hospital Center of São João, Oporto, Portugal. Neuropsychological Unit, Department of Psychology, University Hospital Center of São João, Oporto, Portugal. Faculty of Psychology and Educational Sciences, University of Porto, Porto, Portugal. MS Clinic, Department of Neurology, University Hospital Center of São João, Oporto, Portugal. Faculty of Medicine, University of Porto, Porto, Portugal. Faculty of Psychology and Educational Sciences, University of Porto, Porto, Portugal. MS Clinic, Department of Neurology, University Hospital Center of São João, Oporto, Portugal. Faculty of Health Sciences, University Fernando Pessoa, Porto, Portugal.
 Ross University, Kern Medical Center University of Chicago
 Center of Clinical Neuroscience, Neurological Clinic, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany. Center of Clinical Neuroscience, Neurological Clinic, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany. Center of Clinical Neuroscience, Neurological Clinic, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany. Center of Clinical Neuroscience, Neurological Clinic, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany. Center of Clinical Neuroscience, Neurological Clinic, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany.
 Neurology Service, Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain. Biomedicine Department, Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain. IIS Aragon, Universidad de Zaragoza, Departamento de Fisiatría y Enfermería, Facultad de Ciencias de la Salud, Zaragoza, Spain. Neurology Service, Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain. Biomedicine Department, Universidad de Las Palmas de Gran Canaria, Las Palmas, Spain.
 Department of Neurology, Oslo University Hospital, Oslo, Norway. MS Center Hakadal, Hakadal, Norway. MS Center Hakadal, Hakadal, Norway. SINTEF Digital, Smart Sensor and Micro Systems, Oslo, Norway. SINTEF Digital, Smart Sensor and Micro Systems, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Informatics, University of Oslo, Oslo, Norway. Department of Informatics, University of Oslo, Oslo, Norway.
 Department of Pharmacy, The Eighth Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China. Electronic address: liwenting1111@126.com. School of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Electronic address: wumeilingcrow@hotmail.com. Department of Pharmacy, The Eighth Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China. Electronic address: Yuzhen628@126.com. School of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Electronic address: shenjg@hku.hk.
 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Napoli, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Napoli, Italy.
 Neuroimmunology Unit, Neurology Department, Hospital Clinico Universitario, Valencia, Spain. Neuroimmunology Unit, La Fe University and Polytechnic Hospital, Valencia, Spain. Neurology Department, Dr. Josep Trueta University Hospital, Girona, Spain. Department of Neurology, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. Department of Neurology, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. Neuroimmunology Unit, La Fe University and Polytechnic Hospital, Valencia, Spain. Neurology Department, Clinical Hospital of Barcelona, Barcelona, Spain. Neurology Department, General University Hospital of Valencia, Valencia, Spain. Neuroimmunology Unit, La Fe University and Polytechnic Hospital, Valencia, Spain. Neurology Department, Ramón y Cajal University Hospital, Madrid, Spain. Neurology Department, Ramón y Cajal University Hospital, Madrid, Spain. Neurology Department, Del Mar Hospital, Barcelona, Spain. Neuroimmunology Unit, Neurology Department, Hospital Clinico Universitario, Valencia, Spain. Neurology Department, Son Espases University Hospital, Palma de Mallorca, Spain. Neurology Department, Álvaro Cunqueiro Hospital, Vigo, Spain. Neurology Department, Mutua de Terrasssa University Hospital, Barcelona, Spain. Neurology Department, Marqués de Valdecilla University Hospital, Santander, Spain. Systems and Applications Engineer Department, Subdirectorate of Information Systems Hospital La Fe, Valencia, Spain. Neuroimmunology Unit, La Fe University and Polytechnic Hospital, Valencia, Spain. Neuroimmunology Unit, La Fe University and Polytechnic Hospital, Valencia, Spain.
 Department of Pathology, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, United Kingdom. Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany. Department of Pathology, Amsterdam UMC, Location VUmc, Amsterdam, The Netherlands. Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, United Kingdom. Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany.
 Students' Scientific Research Program, Tehran University of Medical Sciences, Tehran, Iran. Interdisciplinary Neuroscience Research Program, Tehran University of Medical Sciences, Tehran, Iran. Students' Scientific Research Program, Tehran University of Medical Sciences, Tehran, Iran. Interdisciplinary Neuroscience Research Program, Tehran University of Medical Sciences, Tehran, Iran. Students' Scientific Research Program, Tehran University of Medical Sciences, Tehran, Iran. Interdisciplinary Neuroscience Research Program, Tehran University of Medical Sciences, Tehran, Iran. Department of Neuroscience, Padova Neuroscience Center, University of Padova, Padova, Italy.
 Department of Medicine, University of Toronto, Toronto, Ontario, Canada. Department of Neurology, University of Toronto, Toronto, Ontario, Canada. Department of Internal Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California, USA. Department of Neurology, Rush University Medical Center, Chicago, Illinois, USA. Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA. Division of Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, New York, USA. Department of Neurological Sciences, Larner College of Medicine at the University of Vermont, Burlington, Vermont, USA. Department of Medicine, Duke University School of Medicine, Durham, North Carolina, USA. Department of Internal Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
 School of Health and Sports Sciences, University of Brighton, Brighton, UK. School of Health and Sports Sciences, University of Brighton, Brighton, UK.
 Saint Antoine Hospital, Assistance publique des Hôpitaux de Paris (AP-HP), Paris, France. Electronic address: Annelaure.dubessy@aphp.fr. Sleep Disorder Unit, Pitié-Salpêtrière Hospital and Sorbonne University, Paris, France; National Reference Network for Orphan Diseases: Narcolepsy and Rare Hypersomnias, Paris, France.
 Vita-Salute San Raffaele University, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Casa di Cura Igea, Milan, Italy.
 Department of Neurology, Medical University of Białystok, Białystok, Poland. Department of Neurology, Medical University of Białystok, Białystok, Poland. Department of Radiology, Medical University of Białystok, Białystok, Poland. Department of Neurology, Medical University of Białystok, Białystok, Poland. Department of Neurology, Medical University of Białystok, Białystok, Poland. Department of Neurology, Medical University of Białystok, Białystok, Poland. Department of Neurology, Medical University of Białystok, Białystok, Poland.
 Centro Hospitalar e Universitário de Coimbra (CHUC), Coimbra, Portugal. Departamento de Neurociências Clínicas e Saúde Mental, Faculdade de Medicina, Universidade do Porto, Porto, Portugal. Centro Hospitalar Universitário de São João (CHUSJ), Porto, Portugal. Unidade Local de Saúde de Matosinhos (ULSM) - Hospital Pedro Hispano, Matosinhos, Portugal. Hospital Garcia de Orta, Almada, Portugal. Centro Hospitalar Universitário de Santo António (CHUdSA), Porto, Portugal.
 Neurocenter, Lucerne Cantonal Hospital, Lucerne, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Holonautic AG, Horw, Switzerland. 12 Parsec, Root, Switzerland.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia. Laboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Thessaloniki, Greece. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia.
 Department of Neurology, University of Kragujevac, Faculty of Medical Sciences, Kragujevac 34000, Sumadija, Serbia. stojanovick@yahoo.com. Department of Neurology, University of Kragujevac, Faculty of Medical Sciences, Kragujevac 34000, Sumadija, Serbia. Department of Pharmacy, University of Kragujevac, Faculty of Medical Sciences, Kragujevac 34000, Sumadija, Serbia. Department of Psychiatry, University of Kragujevac, Faculty of Medical Sciences, Kragujevac 34000, Sumadija, Serbia.
 Departments of Neurology and Pathology & Immunology, Washington University School of Medicine, St. Louis, MO, United States. Neurology Service, VA St. Louis Health Care System, St. Louis, MO, United States.
 Marshall B. Ketchum University, Fullerton, CA, USA. cmadiraju@ketchum.edu. Noorda College of Osteopathic Medicine, Provo, UT, USA. Marshall B. Ketchum University, Fullerton, CA, USA. Marshall B. Ketchum University, Fullerton, CA, USA. Cellestan Immunoquant (CIQ), Inc, Oceanside, CA, USA. Cellestan Immunoquant (CIQ), Inc, Oceanside, CA, USA. Department of Neurology, Jagiellonian University Medical College, Krakow, Poland. Department of Neurology, Jagiellonian University Medical College, Krakow, Poland. QuantiScientifics, LLC, Orange, CA, USA.
 Departamento de Fisiología y Farmacología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico. Departamento de Fisiología y Farmacología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico. Departamento de Fisiología y Farmacología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico. Departamento de Fisiología y Farmacología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico. Departamento de Fisiología y Farmacología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico.
 Department of Neurology, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Department of Psychiatry, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Department of Psychiatry, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Faculty of Medicine, University of Sarajevo. Primary Healthcare Centre Gracanica. Department of Neurology, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Department of Psychiatry, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Faculty of Medicine, University of Sarajevo. Primary Healthcare Centre Gracanica. Department of Neurology, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Department of Psychiatry, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina. Faculty of Medicine, University of Sarajevo. Primary Healthcare Centre Gracanica.
 Department of Neurology, Faculty of Medicine, University of Augsburg, Augsburg, Germany. Department of Neurology, Faculty of Medicine, University of Augsburg, Augsburg, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, Jüdisches Krankenhaus Berlin, Berlin, Germany. Department of Neurology and Center for Translational and Behavioral Neurosciences (C-TNBS), University Medicine Essen, Essen, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Moorenstr. 5, Düsseldorf 40225, Nordrhein-Westfalen, Germany.
 Department of Physical Therapy, the University of Alabama at Birmingham, Birmingham, AL. Electronic address: trinhhlt@uab.edu. Department of Kinesiology, Health Promotion, and Recreation, University of North Texas, Denton, TX. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL.
 Department of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmacy, Yarmouk University, Irbid, Jordan. RINGGOLD: 59179 Department of Neurology, Al-Bashir Hospital, Amman, Jordan. RINGGOLD: 275537
 Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China. Department of Neurology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Zhejiang, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China. Department of Neurology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Zhejiang, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu 610041, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China.
 The University of Texas Southwestern Medical Center, Dallas, TX 75390-8806, USA. Florida Atlantic University, Boca Raton, FL 33431, USA. Nova Southeastern University, Fort Lauderdale, FL 33314, USA. Summit Analytical, Denver, CO 80238, USA. RVL Pharmaceuticals, Inc., Bridgewater, NJ 08807, USA. Advanced Neuroscience Institute, Franklin, TN 37064, USA.

 Department of Gastroenterology, Adiyaman Training and Research Hospital, Adiyaman, Turkiye. Department of Gastroenterology, Inonu University School of Medicine, Malatya, Turkiye. Department of Pathology, Inonu University School of Medicine, Malatya, Turkiye. Department of Internal Medicine, Malatya Training and Research Hospital, Malatya, Turkiye. Department of General Surgery, Liver Transplantation Institute, Inonu University School of Medicine, Malatya, Turkiye.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical sciences, Tehran, Iran. Physical Medicine and Rehabilitation Department, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical sciences, Tehran, Iran. Department of Neurology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical sciences, Tehran, Iran.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran.
 Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia. Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel 40700, Israel. Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Faculty of Medicine, University of Cyprus, Nicosia 2029, Cyprus. Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, Second Department of Neurology, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece.
 Servicio de Farmacia, Hospital Infanta Leonor, Madrid, España. Electronic address: asantiagop@salud.madrid.org. Servicio de Farmacia, Hospital Infanta Leonor, Madrid, España. Servicio de Farmacia, Hospital Alvaro Cunqueiro (EOXI Vigo), Vigo, España. Servicio de Farmacia, Hospital Miguel Servet, Zaragoza, España. Servicio de Farmacia, Hospital Vall d'Hebron, Barcelona, España. Servicio de Farmacia, Hospital de Bellvitge, L'Hospitalet de Llobregat, España. Servicio de Farmacia, Hospital Universitario Nuestra Sra. de Candelaria, Santa Cruz de Tenerife, España. Servicio de Farmacia, Complejo Asistencial Universitario de Salamanca, Salamanca, España.
 Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran.
 Department of Radiology, Weill Cornell Medicine, New York, NY, USA. Horace Greeley High School, Chappaqua, NY, USA. Department of Radiology, Weill Cornell Medicine, New York, NY, USA. Department of Radiology, Weill Cornell Medicine, New York, NY, USA. Judith Jaffe Multiple Sclerosis Center, Weill Cornell Medicine, New York, NY, USA. Department of Neurology, Weill Cornell Medical College, New York, NY, USA. Department of Radiology, Weill Cornell Medicine, New York, NY, USA. Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA.
 School of Allied Health, University of Limerick, Limerick, Ireland. Ageing Research Centre, Health Research Institute, University of Limerick, Limerick, Ireland. School of Allied Health, University of Limerick, Limerick, Ireland. Centre of Physical Activity for Health, Health Research Institute, University of Limerick, Limerick, Ireland. Multiple Sclerosis Society of Ireland, Limerick, Ireland. School of Allied Health, University of Limerick, Limerick, Ireland. Ageing Research Centre, Health Research Institute, University of Limerick, Limerick, Ireland.
 Departments of Internal Medicine and Community Health Sciences, Rady Faculty of Health Sciences, Max-Rady College of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Electronic address: rmarrie@hsc.mb.ca. Schools of Pharmacy and Public Health Sciences, University of Waterloo, Waterloo, Ontario, Canada; ICES, Toronto, Ontario, Canada. Department of Medicine, University of Toronto, 6, Queen's Park Crescent West, 3rd floor, M5S 3H2 Toronto, Ontario, Canada; Saint-Michael's Hospital, 30, Bond Street, M5B 1W8 Toronto, Ontario, Canada. Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. Faculty of Medicine (Neurology), University of British Columbia, Vancouver, BC, Canada.
 Servicio de Farmacia, Hospital Infanta Leonor, Madrid, Spain. Electronic address: asantiagop@salud.madrid.org. Servicio de Farmacia, Hospital Infanta Leonor, Madrid, Spain. Servicio de Farmacia, Hospital Alvaro Cunqueiro (EOXI Vigo), Vigo, Spain. Servicio de Farmacia, Hospital Miguel Servet, Zaragoza, Spain. Servicio de Farmacia, Hospital Vall d'Hebron, Barcelona, Spain. Servicio de Farmacia, Hospital de Bellvitge, L'Hospitalet de Llobregat, Spain. Servicio de Farmacia, Hospital Universitario Ntra, Sra. de Candelaria, Santa Cruz de Tenerife, Spain. Servicio de Farmacia, Complejo Asistencial Universitario de Salamanca, Salamanca, Spain.
 Division of Radiological Physics, Department of Radiology, University Hospital Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic. Department of Neurology, University Hospital Basel, Basel, Switzerland. Medical Image Analysis Center (MIAC) AG, Basel, Switzerland. Novartis Institutes for BioMedical Research Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Department of Clinical Research, Faculty of Medicine, University Hospital Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Department of Clinical Research, Faculty of Medicine, University Hospital Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. University Hospital Zürich, Zurich, Switzerland. Medical Image Analysis Center (MIAC) AG, Basel, Switzerland. Department of Neurology, University Hospital Basel, Basel, Switzerland. Department of Clinical Research, Faculty of Medicine, University Hospital Basel, Basel, Switzerland. Division of Radiological Physics, Department of Radiology, University Hospital Basel, Basel, Switzerland. Department of Biomedical Engineering, University of Basel, Allschwil, Switzerland. Division of Neuroradiology, Department of Radiology, University Hospital Basel, Basel, Switzerland. meritxell.garciaalzamora@usz.ch. Department of Neuroradiology, University Hospital Zürich, Frauenklinikstrasse 10, 8091, Zurich, Switzerland. meritxell.garciaalzamora@usz.ch.
 Washington Neuropsychology Research Group, Fairfax, Virginia. Electronic address: cbergmann@neuropsychologyfairfax.com. Department of Veteran Affairs, Cedar Park, Texas, United States; Senseye, Inc., Austin, Texas, United States. Washington Neuropsychology Research Group, Fairfax, Virginia. Washington Neuropsychology Research Group, Fairfax, Virginia; Department of Neurology, Georgetown University, Washington, D.C, United States. Washington Neuropsychology Research Group, Fairfax, Virginia; Department of Neurology, Georgetown University, Washington, D.C, United States. Multiple Sclerosis and Neuroimmunology Center, Clalit Health Services, Nazareth, Israel; Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. NYU Langone South Shore Neurologic Associates, New York University, Patchogue, New York, USA. NYU Langone South Shore Neurologic Associates, New York University, Patchogue, New York, USA. NYU Langone South Shore Neurologic Associates, New York University, Patchogue, New York, USA; Department of Nursing, State University of Stony Brook, Stony Brook, New York, USA. NYU Langone South Shore Neurologic Associates, New York University, Patchogue, New York, USA. Division of Cognitive and Behavioral Neurosciences, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Sherman Hall Annex Room 114, Buffalo, NY 14214, USA; Neuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA. Department of Clinical Research, NeuroTrax Corporation, Modiin, Israel. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, United States. School of Allied Health Science and Practice, University of Adelaide, Adelaide, Australia. Katz School of Science & Health, Yeshiva University, New York, NY, USA. London Health Sciences Centre, University of Western Ontario, Canada. NYU Langone South Shore Neurologic Associates, New York University, Patchogue, New York, USA.
 Department of Physical Medicine and Rehabilitation, University School of Medicine, Baltimore, MD, USAJohns Hopkins. RINGGOLD: 1466 Department of Physical Medicine and Rehabilitation, University School of Medicine, Baltimore, MD, USAJohns Hopkins. RINGGOLD: 1466 Department of Psychology, The Chicago School of Professional Psychology, Washington, DC, USA. Department of Physical Medicine and Rehabilitation, University School of Medicine, Baltimore, MD, USAJohns Hopkins. RINGGOLD: 1466 Department of Psychology, , Baltimore, MD, USAUniversity of Loyola Maryland. RINGGOLD: 28521 Department of Physical Medicine and Rehabilitation, University School of Medicine, Baltimore, MD, USAJohns Hopkins. RINGGOLD: 1466 Department of Psychology, The Chicago School of Professional Psychology, Washington, DC, USA. Department of Physical Medicine and Rehabilitation, University School of Medicine, Baltimore, MD, USAJohns Hopkins. RINGGOLD: 1466 Department of Physical Medicine and Rehabilitation, University School of Medicine, Baltimore, MD, USAJohns Hopkins. RINGGOLD: 1466
 Department of Psychiatry and Mental Health, Alborz University of Medical Sciences, Karaj, Iran; Student Research Committee, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Electronic address: armanshafieemd@gmail.com. Student Research Committee, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Student Research Committee, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran.
 Institut für Pharmakoökonomie und Arzneimittellogistik e.V. (IPAM e.V.), 23966 Wismar, Germany. Cytel Inc., 10785 Berlin, Germany. ZKN, Zentrum für Klinische Neurowissenschaften, Neurologische Klinik und Poliklinik für Neurologie, Universitätsklinikum Carl Gustav Carus, 01307 Dresden, Germany. AOK PLUS, 01067 Dresden, Germany. AOK PLUS, 01067 Dresden, Germany. Institut für Pharmakoökonomie und Arzneimittellogistik e.V. (IPAM e.V.), 23966 Wismar, Germany. ZKN, Zentrum für Klinische Neurowissenschaften, Neurologische Klinik und Poliklinik für Neurologie, Universitätsklinikum Carl Gustav Carus, 01307 Dresden, Germany.
 Military Medical Academy, Institute of Medical Biochemistry, Belgrade. University of Belgrade, Faculty of Pharmacy, Department of Medical Biochemistry, Belgrade. University of Belgrade, Faculty of Pharmacy, Pharmaceutical Chemistry, Belgrade. University of Belgrade, Faculty of Pharmacy, Department of Medical Biochemistry, Belgrade. Military Medical Academy, Neurology Clinic, Belgrade.
 BartsMS, The Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. BartsMS, The Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. BartsMS, The Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. Wolfson Institute for Biomedical Research, University College London, London WC1E 6BT, UK. BartsMS, The Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
 Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, IK Gujral Punjab Technical University, Jalandhar 144603, India. Department of Pharmaceutics, ISF College of Pharmacy, IK Gujral Punjab Technical University, Jalandhar 144603, India. Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, IK Gujral Punjab Technical University, Jalandhar 144603, India.
 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Neuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, H3A 2B4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Microbiology, Immunology and Infectiology, Université de Montréal, Montreal, H2X 3E4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Neuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, H3A 2B4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Microbiology, Immunology and Infectiology, Université de Montréal, Montreal, H2X 3E4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada. Neuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, H3A 2B4, Canada. Neuroimmunology Unit, Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, H3A 2B4, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, H2X 0A9, Canada. Department of Neurosciences, Université de Montréal, Montreal, H3T 1J4, Canada.
 Center for Community Research, DePaul University, Chicago, IL, USA. Department of Psychology, Chicago State University, Chicago, IL, USA. Center for Community Research, DePaul University, Chicago, IL, USA. Center for Community Research, DePaul University, Chicago, IL, USA.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Octave Bioscience, Menlo Park, CA 94025, USA. Department of Pharmaceutical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14214, USA. Octave Bioscience, Menlo Park, CA 94025, USA. Octave Bioscience, Menlo Park, CA 94025, USA. Octave Bioscience, Menlo Park, CA 94025, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. IRCCS, Fondazione Don Carlo Gnocchi, Milan 20113, Italy. Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY 14203, USA.
 Cellular and Molecular Signaling, New York, NY 10022, USA.
 ProHealth Research Team, Health Sciences Faculty, Valencian International University. Calle Pintor Sorolla 21, Valencia, Spain. ProHealth Research Team, Health Sciences Faculty, Valencian International University. Calle Pintor Sorolla 21, Valencia, Spain. ProHealth Research Team, Health Sciences Faculty, Valencian International University. Calle Pintor Sorolla 21, Valencia, Spain. ProHealth Research Team, Health Sciences Faculty, Valencian International University. Calle Pintor Sorolla 21, Valencia, Spain. Suportias. Av, Juan Carlos I, Alcalá de Henares, Spain.
 Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran. RINGGOLD: 154203 Nursing Care Research Center, Semnan University of Medical Sciences, Semnan, Iran. RINGGOLD: 154203 Department of Nursing, Faculty of Nursing and Midwifery, Semnan University of Medical Sciences, Semnan, Iran. RINGGOLD: 154203 Department of Nursing, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. RINGGOLD: 41616 Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. RINGGOLD: 108887 Nursing Care Research Center, Semnan University of Medical Sciences, Semnan, Iran. RINGGOLD: 154203 Department of Nursing, Faculty of Nursing and Midwifery, Semnan University of Medical Sciences, Semnan, Iran. RINGGOLD: 154203
 Department of Psychology, The Pennsylvania State University, University Park, PA, USA. Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Brigham and Women's Hospital, Boston, MA, USA. Department of Psychology, The Pennsylvania State University, University Park, PA, USA. Psychology Service, VA Connecticut Healthcare System, West Haven, CT, USA. Department of Psychology, The Pennsylvania State University, University Park, PA, USA. Geisel School of Medicine, Dartmouth College, Hanover, NH, USA. Department of Psychology, The Pennsylvania State University, University Park, PA, USA.
 Oncology Centre, King Faisal Specialist Hospital and Research Centre, Section of Adult Hematology/HSCT, PO Box 3354, Riyadh, 11471, Saudi Arabia. halfadil@kfshrc.edu.sa. Oncology Centre, King Faisal Specialist Hospital and Research Centre, Section of Adult Hematology/HSCT, PO Box 3354, Riyadh, 11471, Saudi Arabia. Oncology Centre, King Faisal Specialist Hospital and Research Centre, Section of Adult Hematology/HSCT, PO Box 3354, Riyadh, 11471, Saudi Arabia. Alneelin University, National Centre for Neurological Science, Khartoum, Sudan. Oncology Centre, King Faisal Specialist Hospital and Research Centre, Section of Adult Hematology/HSCT, PO Box 3354, Riyadh, 11471, Saudi Arabia.
 Dept. of Neurology, University Medicine Greifswald, Germany. Dept. of Neurology, University Medicine Greifswald, Germany. Dept. of Neurology, University Medicine Greifswald, Germany. Dept. of Neurology, University Medicine Greifswald, Germany. Dept. of Neurology, University Medicine Greifswald, Germany. Dept. of Internal Medicine B, University Medicine Greifswald, Greifswald, Germany. Dept. of Neurology, Carl-Thiem-Klinikum, Cottbus, Germany. Department of Microbial Natural Products, Helmholtz-Institute for Pharmaceutical Research Saarland (HIPS), Helmholtz Centre for Infection Research (HZI) and Department of Pharmacy, Saarland University, Campus E8 1, 66123 Saarbrücken, Germany. Dept. of Neurology, University Medicine Greifswald, Germany. Electronic address: johanna.ruhnau@uni-greifswald.de. Dept. of Neurology, University Medicine Greifswald, Germany. Electronic address: antje.vogelgesang@uni-greifswald.de.
 Department of Applied Linguistics and Phonetics, ELTE Eötvös Loránd University, Budapest, Hungary.
 Department of General Biochemistry, Institute of Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland. Department of General Biochemistry, Institute of Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland. Department of General Biochemistry, Institute of Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
 Department of Neurology, Aeginition University Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece. Preventive Neurology Unit, Wolfson Institute of Population Health, QMUL, London EC1M 6BQ, UK. Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London E1 1FR, UK.
 Radiological Sciences Department, College of Applied Medical Sciences, Taif University, Taif 21944, Saudi Arabia.
 Department of Physiotherapy and Rehabilitation, Hatay Mustafa Kemal University Health Science Faculty, Hatay, Turkiye. Department of Neurology, Hatay Mustafa Kemal University Faculty of Medicine, Hatay, Turkiye.
 Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 40000, P.R. China. Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 40000, P.R. China. Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 40000, P.R. China. Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 40000, P.R. China. Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 40000, P.R. China.
 11 rue Sainte-Anastase, 75003 Paris, France. 11 rue Sainte-Anastase, 75003 Paris, France. Electronic address: nathanael.altmann@gmail.com.
 The University of Queensland, UQ Centre for Clinical Research, Royal Brisbane & Women's Hospita, Brisbane, QLD, Australia. The University of Queensland, UQ Centre for Clinical Research, Royal Brisbane & Women's Hospita, Brisbane, QLD, Australia. The University of Queensland, UQ Centre for Clinical Research, Royal Brisbane & Women's Hospita, Brisbane, QLD, Australia.
 Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy. Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy. Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy. The Center for Biomedical Computing (CBMC), University of Verona, Verona, Italy. Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
 NMR Research Unit, Department of Neuroinflammation, Queen Square MS Centre, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom. NMR Research Unit, Department of Neuroinflammation, Queen Square MS Centre, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom. NMR Research Unit, Department of Neuroinflammation, Queen Square MS Centre, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom.
 From the Multiple Sclerosis University Center, Ramos Mejia Hospital, Buenos Aires, Argentina (MBE, CY, NC, RA, BS, OG). The Research Institute in Psychology, School of Psychology, Buenos Aires University, Buenos Aires, Argentina (MBE, NC, MSR, SV). From the Multiple Sclerosis University Center, Ramos Mejia Hospital, Buenos Aires, Argentina (MBE, CY, NC, RA, BS, OG). From the Multiple Sclerosis University Center, Ramos Mejia Hospital, Buenos Aires, Argentina (MBE, CY, NC, RA, BS, OG). The Research Institute in Psychology, School of Psychology, Buenos Aires University, Buenos Aires, Argentina (MBE, NC, MSR, SV). The Research Institute in Psychology, School of Psychology, Buenos Aires University, Buenos Aires, Argentina (MBE, NC, MSR, SV). The Institute of Restorative Neurosciences, Buenos Aires, Argentina (MSR, FC, SV). From the Multiple Sclerosis University Center, Ramos Mejia Hospital, Buenos Aires, Argentina (MBE, CY, NC, RA, BS, OG). From the Multiple Sclerosis University Center, Ramos Mejia Hospital, Buenos Aires, Argentina (MBE, CY, NC, RA, BS, OG). From the Multiple Sclerosis University Center, Ramos Mejia Hospital, Buenos Aires, Argentina (MBE, CY, NC, RA, BS, OG). The Institute of Restorative Neurosciences, Buenos Aires, Argentina (MSR, FC, SV). The Research Institute in Psychology, School of Psychology, Buenos Aires University, Buenos Aires, Argentina (MBE, NC, MSR, SV). The Institute of Restorative Neurosciences, Buenos Aires, Argentina (MSR, FC, SV).
 Fundación Neumológica Colombiana, Bogotá, Colombia. Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, Sweden.
 Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, 09124 Cagliari, Italy. Department of Medical Science and Public Health, University of Cagliari, 09124 Cagliari, Italy. Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, 09124 Cagliari, Italy. Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, 09124 Cagliari, Italy. Department of Medical Science and Public Health, University of Cagliari, 09124 Cagliari, Italy. Department of Medical Science and Public Health, University of Cagliari, 09124 Cagliari, Italy. Department of Medical Science and Public Health, University of Cagliari, 09124 Cagliari, Italy. Department of Health Science, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy. Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, 09124 Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASSL Cagliari, 09126 Cagliari, Italy.
 Institute of Neuroimmunology and Multiple Sclerosis (MH, JP, CH, ACR), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (MH, JP, CH, ACR), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (MH, JP, CH, ACR), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. private practice, Hamburg, Germany (MH). Institute of Neuroimmunology and Multiple Sclerosis (MH, JP, CH, ACR), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology (CH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (MH, JP, CH, ACR), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Nursing Research Unit, Institute of Social Medicine and Epidemiology, University of Lübeck, Lübeck, Germany (ACR).
 Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Iranian Multiple Sclerosis and Neuroimmunology Research Center, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Iranian Multiple Sclerosis and Neuroimmunology Research Center, Isfahan, Iran.
 Neurological Institute, Section of Neuropsychology, Cleveland Clinic, Cleveland, OH USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH USA. Neurological Institute, Section of Neuropsychology, Cleveland Clinic, Cleveland, OH USA. Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Prevea Health, Green Bay, WI USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH USA. Neurological Institute, Section of Neuropsychology, Cleveland Clinic, Cleveland, OH USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH USA.
 Department of Neurology, Laboratory of Neuroimmunology, Faculty of Medicine, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland.
 Department of Pharmacoeconomic and Pharmaceutical Management, School of Pharmacy and Pharmaceutical Sciences, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Health Management and Economics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Pharmacoeconomic and Pharmaceutical Management, School of Pharmacy and Pharmaceutical Sciences, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Department of Pharmaceutics, Faculty of Pharmacy and Pharmaceutical Sciences, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
 Department of Neurobiology, School of Basic Medical Sciences of Tongji Medical College of Huazhong University of Science and Technology, 430030, Wuhan, China. Department of Neurobiology, School of Basic Medical Sciences of Tongji Medical College of Huazhong University of Science and Technology, 430030, Wuhan, China. Department of Neurobiology, School of Basic Medical Sciences of Tongji Medical College of Huazhong University of Science and Technology, 430030, Wuhan, China.
 Department of Biomedical Engineering, Faculty of Engineering, University of Isfahan, Isfahan, Iran. Department of Biomedical Engineering, Faculty of Engineering, University of Isfahan, Isfahan, Iran. Electronic address: rasti@eng.ui.ac.ir. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: etemadifar.m@med.mui.ac.ir.
 Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Cogito Center for Applied Neurocognition and Neuropsychological Research, Düsseldorf, Germany. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
 Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. kilian.froehlich@uk-erlangen.de. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neuroradiology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neuroradiology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany.
 Department of Psychology, College of Human Science, Saveh Branch, Islamic Azad University, Saveh, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
 Mohn Medical Imaging and Visualization Centre (MMIV), Department of Radiology, Haukeland University Hospital, 5021, Bergen, Norway. f.riemer@web.de. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway. f.riemer@web.de. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway. Department of Clinical Medicine, University of Bergen, 5020, Bergen, Norway. Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02215, USA. Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02215, USA. Department of Imaging, Cambridge University Hospitals NHS Foundation Trust, Cambridge Biomedical Campus, CB2 0QQ, Cambridge, United Kingdom. Department of Radiology, University of Cambridge, CB2 0QQ, Cambridge, United Kingdom. Investigative Medicine Division, Radcliffe Department of Medicine, University of Oxford, OX3 9DU, Oxford, United Kingdom. Department of Biological and Medical Psychology, University of Bergen, 5020, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway. Department of Clinical Medicine, University of Bergen, 5020, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway. Department of Clinical Medicine, University of Bergen, 5020, Bergen, Norway. Mohn Medical Imaging and Visualization Centre (MMIV), Department of Radiology, Haukeland University Hospital, 5021, Bergen, Norway. Department of Physics and Technology, University of Bergen, 5007, Bergen, Norway.
 Theagenio Oncological Hospital of Thessaloniki, Greece. 3rd Departement of Psychiatry, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece. Multiple Sclerosis Center, 2nd Department of Neurology, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece. Multiple Sclerosis Center, 2nd Department of Neurology, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece. Multiple Sclerosis Center, 2nd Department of Neurology, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece. Multiple Sclerosis Center, 2nd Department of Neurology, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece. 3rd Departement of Psychiatry, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece.
 Laboratory of Biomedical Signal Interpretation and Computational Simulation (BSICoS), University of Zaragoza, Zaragoza, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Barcelona, Spain. Laboratory of Biomedical Signal Interpretation and Computational Simulation (BSICoS), University of Zaragoza, Zaragoza, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Barcelona, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Barcelona, Spain. Department of Microelectronics and Electronic Systems, Autonomous University of Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (CEMCAT), Department of Neurology/Neuroimmunology, Hospital Universitari Vall D'Hebron, Universitat Autónoma de Barcelona, Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (CEMCAT), Department of Neurology/Neuroimmunology, Hospital Universitari Vall D'Hebron, Universitat Autónoma de Barcelona, Barcelona, Spain. Faculty of Medicine and Surgery, Vita Salute San Raffaele University, Milan, Italy. Faculty of Medicine and Surgery, Vita Salute San Raffaele University, Milan, Italy. Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. RADAR-CNS Patient Advisory Board, London, United Kingdom. Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. Research and Development Information Technology, London, United Kingdom. Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. Institute of Health Informatics, University College London, London, United Kingdom. Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. Institute of Health Informatics, University College London, London, United Kingdom. Danish Multiple Sclerosis Centre, Department of Neurology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark. Faculty of Medicine and Surgery, Vita Salute San Raffaele University, Milan, Italy. Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. Research and Development Information Technology, London, United Kingdom. Faculty of Medicine and Surgery, Vita Salute San Raffaele University, Milan, Italy. Danish Multiple Sclerosis Centre, Department of Neurology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark. Danish Multiple Sclerosis Centre, Department of Neurology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark. Multiple Sclerosis Centre of Catalonia (CEMCAT), Department of Neurology/Neuroimmunology, Hospital Universitari Vall D'Hebron, Universitat Autónoma de Barcelona, Barcelona, Spain. Laboratory of Biomedical Signal Interpretation and Computational Simulation (BSICoS), University of Zaragoza, Zaragoza, Spain. Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Barcelona, Spain. Faculty of Medicine and Surgery, Vita Salute San Raffaele University, Milan, Italy. Casa di Cura del Policlinico, Milan, Italy. The RADAR-CNS Consortium, London, United Kingdom.
 Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Rehabilitation, King Khalid University Hospital, King Saud University, Riyadh 11461, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia. Department of Health Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh 11433, Saudi Arabia.
 Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Clinical Research Outcomes Unit, The Royal Melbourne Hospital, Melbourne, VIC, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia. Neuroepidemiology Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia.
 Department of Physics and Astronomy, University of British Columbia, Vancouver, British Columbia, Canada. Department of Pediatrics, University of British Columbia, Vancouver, British Columbia, Canada. Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital Amager & Hvidovre, Copenhagen, Denmark. Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria. Centre for Brain Research, Medical University of Vienna, Vienna, Austria. Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital Amager & Hvidovre, Copenhagen, Denmark. Faculty of Medicine (Division Neurology), University of British Columbia, Vancouver, British Columbia, Canada. Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria. Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria. Centre for Brain Research, Medical University of Vienna, Vienna, Austria. Department of Physics and Astronomy, University of British Columbia, Vancouver, British Columbia, Canada. Department of Pediatrics, University of British Columbia, Vancouver, British Columbia, Canada. Department of Radiology, University of British Columbia, Vancouver, British Columbia, Canada. BC Children's Hospital Research Institute, University of British Columbia, Vancouver, British Columbia, Canada.
 Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Multiple Sclerosis Center- PO Muscatello di Augusta, ASP Siracusa, Siracusa, Italy. Institute Foundation &G. Giglio&, Multiple Sclerosis Centre, Cefalù-Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics (BiND), University of Palermo, Palermo, Italy. Multiple Sclerosis Centre, Neurology Unit and Stroke Unit, AOOR &Villa Sofia-Cervello&, Palermo, Italy. Azienda Ospedaliera di Rilievo Nazionale e di Alta Specializzazione "Civico Di Cristina e Benfratelli&, Palermo, Italy. Centro Sclerosi Multipla, UOC Neurologia, ARNAS Garibaldi, Catania, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy. Department "GF Ingrassia" Section of Neurosciences, University of Catania, Catania, Italy.
 Bharati Vidyapeeth University Medical College, Pune. Government Medical College Omandurar, Chennai, Tamil Nadu. St. George's University School of Medicine, University Centre Grenada, West Indies, Grenada. Postdoctoral Research Fellow, Mayo Clinic, USA. University of Baghdad, Al-Kindy College of Medicine. Multan Medical and Dental College, Pakistan. Government Medical College, Patiala, Punjab. BJ Medical College, Ahmedabad, India. University of Baghdad, College of Medicine, Baghdad, Iraq. University of Baghdad, Al-Kindy College of Medicine. Al-Manhal Academy, Khartoum, Sudan.
 From the Reno School of Medicine, University of Nevada, Reno, NV, USA (ET, KS). From the Reno School of Medicine, University of Nevada, Reno, NV, USA (ET, KS). Nevada Surgical Associates, Reno, NV, USA (KS).
 Hadassah Medical Center, Jerusalem, Israel. petroupanayiota@gmail.com. Sheba Medical Center, Ramat Gan, Israel. Schneider Children's Hospital, Tel Aviv University, Tel Aviv, Israel. Bnei Zion Medical Center, Haifa, Israel. Sheba Medical Center, Ramat Gan, Israel. Meir Medical Center, Kfar Saba, Israel. Barzilai Medical Center, Ashkelon, Israel. Tel Aviv Medical Center, Tel Aviv, Israel. Hadassah Medical Center, Jerusalem, Israel. Rabin Medical Center, Petah Tikva, Israel. Hadassah Medical Center, Jerusalem, Israel.
 UK DRI Care Research and Technology Centre, Department of Brain Sciences, Imperial College London, 926, Sir Michael Uren Hub, 86 Wood Lane, London W12 0BZ, UK.
 Department of Neurology, Cantonal Hospital Aarau, Aarau, Switzerland. Department of Neurology, Multiple Sclerosis Center (MSC), Neurocenter of Southern Switzerland, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana (USI), Lugano, Switzerland. Department of Neurology, Cantonal Hospital Aarau, Aarau, Switzerland. Neurocenter, Cantonal Hospital Lucerne, Luzern, Switzerland. Department of Neurology, Inselspital, University Hospital Bern and University of Bern, Bern, Switzerland. Department of Neurology, Cantonal Hospital St. Gallen, St. Gallen, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic, University Hospital Zurich & University of Zurich, Zurich, Switzerland. Department of Neurology, Multiple Sclerosis Center (MSC), Neurocenter of Southern Switzerland, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana (USI), Lugano, Switzerland. Biogen Switzerland AG, Zug, Switzerland. Biogen Switzerland AG, Zug, Switzerland. Department of Neurology, Cantonal Hospital Aarau, Aarau, Switzerland.
 Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, PR China. Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, PR China. Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, PR China; Department of Cell Biology, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, PR China. Electronic address: weijiangzhao@jiangnan.edu.cn.
 Department of Neurology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Tehran Heart Center, Cardiovascular Research Center, Tehran University of Medical Science, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Tehran University of Medical Science, Tehran, Iran. Tehran University of Medical Science, Tehran, Iran. Tehran University of Medical Science, Tehran, Iran. Department of Neurology, School of Medicine, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Infectious Diseases, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Infectious and Tropical Diseases, Be'sat Hospital, AJA University of Medical Sciences, Tehran, Iran. Department of Neurology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran.
 Department of Anatomy, School of Medicine, Ilam University of Medical Sciences, Ilam, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: borhanihm@gmail.com.

 Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Biomedical Scientist Training Program (Department of Neurosciences), Case Western Reserve University, Cleveland, OH, USA. Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44106, USA; Kent State University, Neurosciences, School of Biomedical Sciences, Cleveland, OH, USA. Electronic address: PANICKN@ccf.org.
 Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. College of Pharmacy, University of Kentucky, Lexington, KY, USA. Department of Cognitive Neuroscience, Institute for Cognitive Sciences Studies, Tehran, Iran. School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Cognitive Sciences Lab, Allameh Tabataba'i University, Tehran, Iran. School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.

 INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. Service de Neurologie, CHU Nantes, Nantes 44000, France. CIC Inserm 1413, CHU Nantes, Nantes 44000, France. Service de Neurologie, CHU Nantes, Nantes 44000, France. CIC Inserm 1413, CHU Nantes, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. Service de Neurologie, CHU Nantes, Nantes 44000, France. CIC Inserm 1413, CHU Nantes, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. Neurologie, Institute of Neuroscience, Université Catholique de Louvain, Bruxelles 1200, Belgium. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. INSERM, Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology (CR2TI), UMR 1064, Nantes 44000, France. Service de Neurologie, CHU Nantes, Nantes 44000, France. CIC Inserm 1413, CHU Nantes, Nantes 44000, France.
 Department of Neurology, Yale University School of Medicine, New Haven, CT, United States; Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, United States; Department of Biomedical Engineering, Columbia University Fu Foundation, School of Engineering and Applied Science, New York, NY, United States; Department of Radiology, Columbia University College of Physicians and Surgeons, New York, NY, United States. Electronic address: cwj2112@columbia.edu. Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, United States; Department of Biomedical Engineering, Columbia University Fu Foundation, School of Engineering and Applied Science, New York, NY, United States. Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, United States. Department of Neurology, Yale University School of Medicine, New Haven, CT, United States; Department of Neurology, University of Southern California Keck School of Medicine, Los Angeles, CA, United States.
 Department of Pathology, Brain and Mind Centre, School of Medical Sciences, The University of Sydney, Sydney, NSW, Australia. Department of Neuropathology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia. Hyphenated Mass Spectrometry Laboratory, School of Mathematical and Physical Sciences, University of Technology Sydney, Sydney, NSW, Australia. Hyphenated Mass Spectrometry Laboratory, School of Mathematical and Physical Sciences, University of Technology Sydney, Sydney, NSW, Australia.
 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. RINGGOLD: 541318 Servicio de Neurología, Sanatorio Güemes, Buenos Aires, Argentina. RINGGOLD: 62948 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. RINGGOLD: 541318 Servicio de Neurología, Sanatorio Güemes, Buenos Aires, Argentina. RINGGOLD: 62948 Servicio de Neurología, Hospital Tornú, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. RINGGOLD: 541318 Centro de esclerosis Múltiple Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, CEMIC, Buenos Aires, Argentina. Centro de esclerosis Múltiple Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, Hospital San Bernardo, Salta, Argentina. Servicio de Neurología, Sanatorio Allende, Córdoba, Spain. Servicio de Neurología, Clínica Universitaria Reina Fabiola, Córdoba, Spain. Sección de nueroinmunología, Hospital Alemán, Buenos Aires, Argentina. DIABAI, Buenos Aires, Argentina. Instituto Neurociencias, Rosario, Argentina. Servicio de neurología, Hospital Italiano, Buenos Aires, Argentina. Servicio de neurología, Hospital Militar, Campo de Mayo, Buenos Aires, Argentina. Servicio de neurología, Hospital Posadas, Buenos Aires, Argentina. Servicio de neurología, Hospital Cesar Milstein, Buenos Aires, Argentina. Servicio de neurología, Hospital de Clínica José de San Martín, Buenos Aires, Argentina. RINGGOLD: 126635 Servicio de neurología, Hospital Español, La Plata, Argentina. RINGGOLD: 62997 Sección de nueroinmunología, Hospital Alemán, Buenos Aires, Argentina. Servicio de neurología, Hospital Álvarez, Buenos Aires, Argentina. Servicio de neurología, Hospital Español, Rosario, Argentina. RINGGOLD: 62997 Servicio de neurología, Hospital Nuestra Señora del Carmen, Tucumán, Argentina. Servicio de neurología, Hospital Córdoba, Córdoba, Spain. Servicio de neurología, Hospital Durand, Buenos Aires, Argentina. Instituto Neurociencias, Rosario, Argentina. Servicio de neurología, Hospital de San Luis, San Luis, Argentina. Hospital Italiano, Buenos Aires, Argentina. RINGGOLD: 37533 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. RINGGOLD: 541318 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. RINGGOLD: 541318 Servicio de neurología, Hospital Italiano, Buenos Aires, Argentina.
 Department of Physical Therapy, University of AL at Birmingham, Birmingham, AL, USA. American Sports Medicine Institute, Birmingham, AL, USA. Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA. Division of Occupational Therapy, Shenandoah University, Winchesterm, VA, USA. Department of Kinesiology and Nutrition, University of IL Chicago, Chicago, IL, USA.
 Department of Neuroanaesthesia, Institute of Neurosciences Kolkata, West Bengal, India. Department of Anaesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, Guwahati, Assam, India. Department of Anaesthesiology, Medica Superspeciality Hospital, Kolkata, West Bengal, India. Department of Neurosurgery, Medica Superspecialty Hospital, Kolkata, West Bengal, India.
 2nd Department of Radiology, Medical University of Gdańsk, Smoluchowskiego 17, 80-214 Gdańsk, Poland. Department of Anesthesiology and Intensive Care, Medical University of Gdańsk, Debinki 7, 80-210 Gdańsk, Poland. Neuroinformatics and Artificial Intelligence Lab, Department of Neurophysiology, Neuropsychology and Neuroinformatics, Medical University of Gdańsk, Debinki 7, 80-210 Gdańsk, Poland. Department of Medical Immunology, Medical University of Gdańsk, Debinki 7, 80-210 Gdańsk, Poland. 2nd Department of Radiology, Medical University of Gdańsk, Smoluchowskiego 17, 80-214 Gdańsk, Poland.
 Programa de Doctorado Neurociencias, University of Salamanca, Salamanca, Spain. Department of Biochemistry and Molecular Biology, Institute of Neurosciences of Castilla and Leon (INCYL), Institute of Biomedical Research of Salamanca (IBSAL), University of Salamanca, Salamanca, Spain. Motion Analysis, Ergonomics, Biomechanics and Motor Control Laboratory (LAMBECOM), Department of Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine, Faculty of Health Sciences, Rey Juan Carlos University, Madrid, Spain. Department of Nursing and Physiotherapy, University of Salamanca, Salamanca, Spain.
 Servei de Neurologia/Neuroimmunologia, Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Secció de Neurologia Pediàtrica, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Radiología, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia/Neuroimmunologia, Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia/Neuroimmunologia, Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. MSc of Clinical Psychology, Department of Clinical Psychology, Faculty of Medical Sciences, Hamedan Branch, Islamic Azad University, Hamedan, Iran. Department of Nursing, Faculty of Medical Sciences, Hamedan Branch, Islamic Azad University, Hamedan, Iran. Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. yazdiravandi@umsha.ac.ir.
 Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran. Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran. Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Department of Neurology, Medical School, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Health Education and Health Promotion, School of Health, Occupational Environment Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
 Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland. Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland. Department of Neurology, Medical University of Graz, Graz, Austria. Neuroimmunological Lab, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technical University Dresden, Dresden, Germany. Neuroimmunological Lab, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technical University Dresden, Dresden, Germany. Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, Medical University of Graz, Graz, Austria. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biomedicine, University of Basel and University Hospital Basel, Neurologic Clinic and Policlinic, MS Center Petersgraben 4, 4031 Basel, Switzerland.
 Department of Neurology, Hospital Álvaro Cunqueiro, Vigo, Spain. Electronic address: clara.helena.lopez.caneda@sergas.es. Biostatech, Advice, Training and Innovation in Biostatistics, Santiago de Compostela, SL, Spain. Department of Neurology, Hospital Álvaro Cunqueiro, Vigo, Spain. Department of Neurology, Hospital Álvaro Cunqueiro, Vigo, Spain. Department of Neurology, Hospital Álvaro Cunqueiro, Vigo, Spain. Department of Neurology, Hospital Álvaro Cunqueiro, Vigo, Spain. Department of Neurology, Hospital Álvaro Cunqueiro, Vigo, Spain.
 Department of Neurology, OR Health & Science University, Portland, OR, USA. Department of Physical Medicine and Rehabilitation, Cleveland Clinic, Cleveland, OH, USA. Crawford Research Institute, Shepherd Center, Atlanta, GA, USA. Department of Rehabilitation Medicine, Emory University School of Medicine, Atlanta, GA, USA. Evidera, Waltham, MA, USA. Evidera, London, UK. Evidera, Waltham, MA, USA. Former employee of Greenwich Biosciences, Inc., now part of Jazz Pharmaceuticals, Carlsbad, CA, USA. Former employee of Greenwich Biosciences, Inc., now part of Jazz Pharmaceuticals, Carlsbad, CA, USA. Jazz Pharmaceuticals, Inc, Philadelphia, PA, USA.
 Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research Darlinghurst NSW Australia. St. Vincent's Clinical School, Faculty of Medicine University of New South Wales (UNSW) Darlinghurst NSW Australia. John Curtin School of Medical Research Australian National University Canberra ACT Australia. St. Vincent's Clinical School, Faculty of Medicine University of New South Wales (UNSW) Darlinghurst NSW Australia. Department of Neurology St Vincent's Clinic Darlinghurst NSW Australia. Blood Stem Cell and Cancer Research Group, St Vincent's Centre for Applied Medical Research Darlinghurst NSW Australia. St. Vincent's Clinical School, Faculty of Medicine University of New South Wales (UNSW) Darlinghurst NSW Australia. Department of Neurology St Vincent's Clinic Darlinghurst NSW Australia. Department of Neurology St Vincent's Hospital Darlinghurst NSW Australia.
 Faculty of Sports and Exercise Science, Universiti Malaya, Kuala Lumpur 50603, Malaysia. Faculty of Sports and Exercise Science, Universiti Malaya, Kuala Lumpur 50603, Malaysia. Faculty of Sports and Exercise Science, Universiti Malaya, Kuala Lumpur 50603, Malaysia. Department of Biomedical Engineering, Faculty of Engineering, Universiti Malaya, Kuala Lumpur 50603, Malaysia. Department of Medicine, Faculty of Medicine, Universiti Malaya, Kuala Lumpur 50603, Malaysia. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz 7193635899, Iran.
 Consultant Neurologist, Kettering General Hospital, Kettering, UK tharukaherath11@gmail.com. Neurology Fellow, Kettering General Hospital, Kettering, UK. Consultant Neurologist, Kettering General Hospital, Kettering, UK. Consultant Radiologist, Kettering General Hospital, Kettering, UK. Consultant Radiologist, Kettering General Hospital, Kettering, UK. Consultant Neurologist, Kettering General Hospital, Kettering, UK.


 Department of Medical Biology, Faculty of Medicine, EGE University, Izmir, Turkey. Department of Biology, Islamic Azad University, Tehran Medicine Branch, Tehran, Iran. Department of Biology, Faculty of Sciences, University of Guilan, Rasht, Iran. Department of Medical Biology, Faculty of Medicine, EGE University, Izmir, Turkey. Department of Medical Biology, Faculty of Medicine, EGE University, Izmir, Turkey. Department of Medical Biology, Faculty of Medicine, EGE University, Izmir, Turkey. Social Determinants of Health Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran; Department of Basic Medical Sciences, Khoy University of Medical Sciences, Khoy, Iran. Electronic address: noorazarian_a@khoyums.ac.ir.
 University of California, Riverside University of Miami/Jackson Memorial Hospital LECOM/ St. Vincent's Southside Riverside Comm Hosp, UC Riverside
 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece.

 Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. xiaoya_c@163.com. Department of Radiology, the First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. lymzhang70@aliyun.com.
 Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL; Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL. Electronic address: bjeng@uic.edu. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL. Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL; Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL.
 Institute of Health Sciences, College of Medical Sciences, University of Rzeszow, Poland. Institute of Health Sciences, College of Medical Sciences, University of Rzeszow, Poland.
 Radboud University Nijmegen, The Netherlands. Radboud University Nijmegen, The Netherlands.
 Department of Biomedicine and Prevention, University of Rome 'Tor Vergata', Via Montpellier 1, 00133 Rome, Italy. Massachusetts General Hospital, Boston, MA 02114, USA. A. A. Martinos Center for Biomedical Imaging, Boston, MA 02129, USA. Massachusetts General Hospital, Boston, MA 02114, USA. A. A. Martinos Center for Biomedical Imaging, Boston, MA 02129, USA. Massachusetts General Hospital, Boston, MA 02114, USA. A. A. Martinos Center for Biomedical Imaging, Boston, MA 02129, USA. Massachusetts General Hospital, Boston, MA 02114, USA. A. A. Martinos Center for Biomedical Imaging, Boston, MA 02129, USA. Department of Biomedicine and Prevention, University of Rome 'Tor Vergata', Via Montpellier 1, 00133 Rome, Italy. Massachusetts General Hospital, Boston, MA 02114, USA. A. A. Martinos Center for Biomedical Imaging, Boston, MA 02129, USA.
 School of Medicine, University of Split, 21000 Split, Croatia. Department of Neurology, University Hospital of Split, 21000 Split, Croatia. Signal Processing, Analysis, and Advanced Diagnostics Research and Education Laboratory (SPAADREL), Faculty of Maritime Studies, University of Split, 21000 Split, Croatia. Signal Processing, Analysis, and Advanced Diagnostics Research and Education Laboratory (SPAADREL), Faculty of Maritime Studies, University of Split, 21000 Split, Croatia. Laboratory for Human and Experimental Neurophysiology (LAHEN), Department of Neuroscience, School of Medicine, University of Split, 21000 Split, Croatia.
 Department of Neurology, Seoul National University Bundang Hospital, Seongnam, Korea. Department of Neurology, Seoul National University College of Medicine, Seoul, Korea.
 Athens, Greece Department of Psychology, Panteion University of Social and Political Sciences. GRID: grid.14906.3a. ISNI: 0000 0004 0622 3029 Athens, Greece Department of Psychology, Panteion University of Social and Political Sciences. GRID: grid.14906.3a. ISNI: 0000 0004 0622 3029 Athens, Greece Department of Psychology, Panteion University of Social and Political Sciences. GRID: grid.14906.3a. ISNI: 0000 0004 0622 3029
 Department of Neurology, University of Chicago, Chicago, IL, USA. Division of Neuroimmunology, Division of Neuroinfectious Diseases, Northwestern University, Chicago, IL, USA. Division of Neuroimmunology, Rush University, Chicago, IL, USA. Division of Neuroimmunology, Division of Neuroinfectious Diseases, Northwestern University, Chicago, IL, USA. edith.graham@northwestern.edu.
 Department of Immunology and Histocompatibility, Hospital Dr Carlos G. Durand, Buenos Aires, Argentina. Department of Allergy and Immunology, Hospital Británico, Buenos Aires, Argentina. Department of Immunology and Histocompatibility, Hospital Dr Carlos G. Durand, Buenos Aires, Argentina. Department of Allergy and Immunology, Hospital Británico, Buenos Aires, Argentina.
 Department of Neurology, North Karelia Central Hospital, Siun Sote, 80210 Joensuu, Finland. Clinical Neurosciences, University of Turku, 50520 Turku, Finland.
 Department of Neurology, Ruhr University Bochum, Bochum 44791, Germany. Brain and Mind Centre, University of Sydney and Royal Prince Alfred Hospital, Sydney, NSW, Australia. Department of Neurology, Inselspital (Bern University Hospital), University of Bern, Bern, Switzerland. Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Neurology, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Neurology Department, Multiple Sclerosis Center of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Department of Neurology, Institute of Neuroimmunology, Tianjin Medical University General Hospital, Tianjin, China. Neurology Department, Multiple Sclerosis Center of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou, China. Department of Neurology, Tianjin Medical University General Hospital, Tianjin, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, China.
 Department of NEUROFARBA, Section of Neurosciences, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. IRCCS Mondino Foundation, Pavia, Italy. Unit of Neurology and Neurorehabilitation, IRCCS Neuromed, Pozzilli, Italy. Fondazione Policlinico Universitario 'Agostino Gemelli' IRCCS, Neurology Unit, Rome, Italy. Centro di Ricerca Sclerosi Multipla (CERSM), Università Cattolica del Sacro Cuore, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Demyelinating Disease Center, San Salvatore Hospital, L'Aquila, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy. Department of Neuroscience, Reproductive Science and Odontostomatology, University Federico II, Multiple Sclerosis Clinical Care and Research Centre, Naples, Italy. Department of Medical and Surgical Sciences, "Magna Graecia" University, Catanzaro, Italy. Regional Epilepsy Centre, Great Metropolitan Hospital, Reggio Calabria, Italy. Department of Translational Medicine and Interdisciplinary Research Center of Autoimmune Diseases, University of Piemonte Orientale, Novara, Italy. Department of Neuroscience and Mental Health, City of Health and Science University Hospital of Turin, Multiple Sclerosis Center, Turin, Italy. ASST della Valle Olona, Hospital of Gallarate, Neuroimmunology Unit, Gallarate, Italy. IRCCS Fondazione Don Carlo Gnocchi Onlus, Multiple Sclerosis Center, Milan, Italy. Foundation Institute "G. Giglio", MS Center, Cefalù-Palermo, Italy. Unit of Clinical Neurology, AOU Sassari, Sassari, Italy. University Hospital San Luigi Gonzaga, SCDO Neurologia-CRESM, Orbassano, Turin, Italy. Department of Neuroscience and Rehabilitation, S. Anna Hospital, Multiple Sclerosis Center, Ferrara, Italy. Neurology and Stroke Unit, Villa Sofia Cervello Hospital, Palermo, Italy. Santo Stefano Hospital, Neurology Unit, Prato, Italy. University Hospital of Padua, Multiple Sclerosis Centre of the Veneto Region (CeSMuV), Padua, Italy. Department of Neurology, 'G. Mazzini' Hospital, Teramo, Italy. Department of NEUROFARBA, Section of Neurosciences, University of Florence, Florence, Italy. Medical Department, Sanofi, Milan, Italy. Medical Department, Sanofi, Milan, Italy. Medical Department, Sanofi, Milan, Italy. Medical Department, Sanofi, Milan, Italy. Medical Department, Sanofi, Milan, Italy. Medical Department, Sanofi, Milan, Italy. Medical Department, Sanofi, Milan, Italy. IRCCS San Raffaele Scientific Institute, Neurology Unit, Milan, Italy. IRCCS San Raffaele Scientific Institute, Neurorehabilitation Unit, Milan, Italy. IRCCS San Raffaele Scientific Institute, Neurophysiology Service, Milan, Italy. Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Neuroimaging Research Unit, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. School of Medicine, University "Aldo Moro" of Bari, Bari, Italy. maria.troiano@uniba.it.
 Department of Chemistry, School of Basic & Applied Sciences, Harcourt Butler Technical University, Kanpur, India. Research Institute for Medicines (IMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Pharmaceutical and Pharmacological Sciences Department, University of Padova, Padova, Italy.
 From the School of Health and Life Sciences, Glasgow Caledonian University, Glasgow, UK (ED, AW, LP). Directorate of Research and Knowledge Exchange, Royal Conservatoire of Scotland, Glasgow, UK (ED, BW). From the School of Health and Life Sciences, Glasgow Caledonian University, Glasgow, UK (ED, AW, LP). Directorate of Research and Knowledge Exchange, Royal Conservatoire of Scotland, Glasgow, UK (ED, BW). From the School of Health and Life Sciences, Glasgow Caledonian University, Glasgow, UK (ED, AW, LP).
 Clinical Pharmacology Unit, Regional Pharmacovigilance Centre, University Hospital of Catania, Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. Clinical Pharmacology Unit, Regional Pharmacovigilance Centre, University Hospital of Catania, Catania, Italy. Clinical Pharmacology Unit, Regional Pharmacovigilance Centre, University Hospital of Catania, Catania, Italy. Clinical Pharmacology Unit, Regional Pharmacovigilance Centre, University Hospital of Catania, Catania, Italy. Clinical Pharmacology Unit, Regional Pharmacovigilance Centre, University Hospital of Catania, Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. Centre for Research and Consultancy in HTA and Drug Regulatory Affairs (CERD), University of Catania, Catania, Italy.
 Tehran University of Medical Sciences, Tehran, Iran. Iran University of Medical Sciences, Tehran, Iran. Padova Neuroscience Center (PNC), University of Padova, Padova, Italy. Padova Neuroscience Center (PNC), University of Padova, Padova, Italy.
 Department of Neurology, Shandong Key Laboratory of Rheumatic Disease and Translational Medicine, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Institute of Neuroimmunology, Jinan, Shandong, China. Institute of Surface Analysis and Chemical Biology, The University of Jinan, Jinan, Shangdong, China. Institute of Surface Analysis and Chemical Biology, The University of Jinan, Jinan, Shangdong, China. Institute of Surface Analysis and Chemical Biology, The University of Jinan, Jinan, Shangdong, China. Institute of Surface Analysis and Chemical Biology, The University of Jinan, Jinan, Shangdong, China.
 University of Calgary, Canada. University of Calgary, Canada. University of Calgary, Canada. University of Calgary, Canada. Tehran University of Medical Sciences, Iran, Islamic Republic of. University of Calgary, Canada mhollenb@ucalgary.ca. Physiology & Pharmacology and Medicine, University of Calgary, Canada mhollenb@ucalgary.ca.
 Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland and Labrador, St. John's, Newfoundland and Labrador, Canada. Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland and Labrador, St. John's, Newfoundland and Labrador, Canada. Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland and Labrador, St. John's, Newfoundland and Labrador, Canada. Recovery and Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland and Labrador, St. John's, Newfoundland and Labrador, Canada.
 Laboratoire de Virologie ULR3610, Université de Lille, CHU Lille, 59000 Lille, France. Laboratoire de Virologie ULR3610, Université de Lille, CHU Lille, 59000 Lille, France. Laboratoire de Virologie ULR3610, Université de Lille, CHU Lille, 59000 Lille, France.
 Clinical and Developmental Neuropsychology, University of Groningen, Groningen, Netherlands. Centre of Expertise for blind and partially sighted people, Royal Dutch Visio, Huizen, Netherlands. Clinical and Developmental Neuropsychology, University of Groningen, Groningen, Netherlands. Centre of Expertise for blind and partially sighted people, Royal Dutch Visio, Huizen, Netherlands. Clinical and Developmental Neuropsychology, University of Groningen, Groningen, Netherlands. Centre of Expertise for blind and partially sighted people, Royal Dutch Visio, Huizen, Netherlands. Centre of Expertise for blind and partially sighted people, Royal Dutch Visio, Huizen, Netherlands. Centre of Expertise for blind and partially sighted people, Royal Dutch Visio, Huizen, Netherlands. Department of Neurology, University of Groningen, University Medical Centre Groningen, Groningen, Netherlands. MS Centrum Noord Nederland, Groningen, Netherlands. Department of Neurology, Martini Hospital Groningen, Groningen, Netherlands. MS Centrum Noord Nederland, Groningen, Netherlands. Clinical and Developmental Neuropsychology, University of Groningen, Groningen, Netherlands. Centre of Expertise for blind and partially sighted people, Royal Dutch Visio, Huizen, Netherlands.
 Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Faculté de Médecine, Université Saint-Joseph de Beyrouth, Beirut, Lebanon. Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada.
 From the Multiple Sclerosis Center, 2nd Department of Neurology (CB, IN, M-KB, EG, EK, NG), Aristotle University of Thessaloniki, Thessaloniki, Greece. From the Multiple Sclerosis Center, 2nd Department of Neurology (CB, IN, M-KB, EG, EK, NG), Aristotle University of Thessaloniki, Thessaloniki, Greece. From the Multiple Sclerosis Center, 2nd Department of Neurology (CB, IN, M-KB, EG, EK, NG), Aristotle University of Thessaloniki, Thessaloniki, Greece. From the Multiple Sclerosis Center, 2nd Department of Neurology (CB, IN, M-KB, EG, EK, NG), Aristotle University of Thessaloniki, Thessaloniki, Greece. C' Department of Psychiatry (M-VK), Aristotle University of Thessaloniki, Thessaloniki, Greece. The Department of Computer Science, School of Sciences and Engineering, University of Nicosia, Nicosia, Cyprus (TM). From the Multiple Sclerosis Center, 2nd Department of Neurology (CB, IN, M-KB, EG, EK, NG), Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Clinical Pharmacology (GP), Aristotle University of Thessaloniki, Thessaloniki, Greece. From the Multiple Sclerosis Center, 2nd Department of Neurology (CB, IN, M-KB, EG, EK, NG), Aristotle University of Thessaloniki, Thessaloniki, Greece.
 Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, Naples, Italy. Department of Mental Health and Public Medicine, Unit of Medical Statistics, Università degli Studi della Campania Luigi Vanvitelli, Naples, Italy. Multiple Sclerosis Clinical and Research Unit, University Hospital of Rome Tor Vergata, Rome, Italy. Multiple Sclerosis Clinical and Research Unit, University Hospital of Rome Tor Vergata, Rome, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, Naples, Italy.
 School of Medical, Indigenous and Health Sciences, University of Wollongong, Northfields Avenue, Wollongong, NSW 2522, Australia. School of Medical, Indigenous and Health Sciences, University of Wollongong, Northfields Avenue, Wollongong, NSW 2522, Australia. Electronic address: yasmine@uow.edu.au.
 Peninsula Schools of Medicine and Dentistry, University of Plymouth, Plymouth, UK. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Peninsula Schools of Medicine and Dentistry, University of Plymouth, Plymouth, UK. jeremy.hobart@plymouth.ac.uk.
 Institut of Biomedical Research (IRB) of Lleida, Neuroimmunology Group, Lleida, Spain. Institut of Biomedical Research (IRB) of Lleida, Neuroimmunology Group, Lleida, Spain. Institut of Biomedical Research (IRB) of Lleida, Neuroimmunology Group, Lleida, Spain. Institut of Biomedical Research (IRB) of Lleida, Neuroimmunology Group, Lleida, Spain. Institut of Biomedical Research (IRB) of Lleida, Neuroimmunology Group, Lleida, Spain. Arnau de Vilanova University Hospital of Lleida, Neurology department, Lleida, Spain. Arnau de Vilanova University Hospital of Lleida, Neurology department, Lleida, Spain. Multiple Sclerosis Foundation (FEM) of Lleida, Lleida, España. Arnau de Vilanova University Hospital of Lleida, Neurology department, Lleida, Spain. Institut of Biomedical Research (IRB) of Lleida, Neuroimmunology Group, Lleida, Spain. Arnau de Vilanova University Hospital of Lleida, Neurology department, Lleida, Spain.
 Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University, Fukushima, Japan. Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
 Department of Public Health, Experimental and Forensic Medicine, Human Nutrition and Eating Disorder Research Center, University of Pavia, Pavia, Italy. Laboratory of Food Education and Sport Nutrition, Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. Center for Human Nutrition and Mediterranean Foods (NUTREA), University of Catania, Catania, Italy. Department of Public Health, Experimental and Forensic Medicine, Human Nutrition and Eating Disorder Research Center, University of Pavia, Pavia, Italy. Laboratory of Food Education and Sport Nutrition, Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy. Neurological Institute-Foundation IRCCS Casimiro Mondino, Pavia, Italy. Neurological Institute-Foundation IRCCS Casimiro Mondino, Pavia, Italy. Neurological Institute-Foundation IRCCS Casimiro Mondino, Pavia, Italy. Department of Food Sciences and Nutrition, College of Food and Agriculture Sciences, King Saud University, Riyadh, Saudi Arabia. Department of Public Health, Experimental and Forensic Medicine, Human Nutrition and Eating Disorder Research Center, University of Pavia, Pavia, Italy.
 Departments of Neurology, Mayo Clinic College of Medicine & Science, Rochester, MN, USA. Electronic address: mustafa.rafid@mayo.edu. Departments of Neurology, Mayo Clinic College of Medicine & Science, Rochester, MN, USA; Laboratory Medicine and Pathology, Mayo Clinic College of Medicine & Science, Rochester, MN, USA. Biostatistics, Mayo Clinic College of Medicine & Science, Rochester, MN, USA. Department of Neurology, University of Virginia Health, Charlottesville, VA, USA. Department of Neurology, University of Utah Health, Salt Lake City, UT, USA. Department of Neurology, Mellen Center for Multiple Sclerosis, Cleveland Clinic and Cleveland Clinic Lerner College of Medicine, Cleveland, OH, USA. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Department of Neurological Sciences, Larner College of Medicine at The University of Vermont Medical Center, Burlington, VT, USA.
 Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre for Molecular Medicine (CMM), Department of Clinical Neurosciences, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Centre for Molecular Medicine (CMM), Department of Clinical Neurosciences, Karolinska Institute, Stockholm, Sweden. The Karolinska Neuroimmunology & Multiple Sclerosis Centre, Department of Clinical Neurosciences, Karolinska Institutet, Stockholm, Sweden. Centre for Molecular Medicine (CMM), Department of Clinical Neurosciences, Karolinska Institute, Stockholm, Sweden.
 Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Department of Computer Science, School of Sciences and Engineering, University of Nicosia, 2417 Nicosia, Cyprus. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece. Primary Health Center of Vari, National Health System of Greece, 16672 Athens, Greece. Independent Department of Therapeutic Protocols and Patient Registers, Hellenic Ministry of Health, 10433 Athens, Greece. Multiple Sclerosis Center, Second Department of Neurology, School of Medicine, Aristotle University of Thessaloniki, 54621 Thessaloniki, Greece.
 Department of Preventive Medicine, Saudi Board of Preventive Medicine, Ministry of Health, Madinah, SAU. Department of Family and Community Medicine, Taibah University, Madinah, SAU. Department of Neurology, King Salman Bin Abdulaziz Medical City, Madinah, SAU. Department of Preventive Medicine, Saudi Board of Preventive Medicine, Ministry of Health, Madinah, SAU. Department of Preventive Medicine, Saudi Board of Preventive Medicine, Ministry of Health, Madinah, SAU. Department of Preventive Medicine, Saudi Board of Preventive Medicine, Ministry of Health, Madinah, SAU.
 Department of Chemical Technology and Pharmaceuticals, Faculty of Pharmacy, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, 85-089, Poland. Hospital Pharmacy, Municipal Hospital in Bydgoszcz, Bydgoszcz, 85-826, Poland. Faculty of Pharmacy, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, 85-067, Poland. Department of Chemical Technology and Pharmaceuticals, Faculty of Pharmacy, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, 85-089, Poland.
 Blizard Institute, Barts & The London School of Medicine & Dentistry, Queen Mary University of London, London, UK. Pirogov Russian National Research Medical University, Department of Neurology, Neurosurgery & Medical Genetics, Federal Center of Brain Research & Neurotechnologies, Moscow, Russia. Department of Neurology, FLENI Institute, Buenos Aires, Argentina. Department of Neurology, University Hospital of Rennes, Rennes, France. University of Ottawa, Department of Medicine & the Ottawa Hospital Research Institute, Ottawa, ON, Canada. Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitario Vall d'Hebron, Barcelona, Spain. University of Miami School of Medicine, MS Research Center, Miami, FL, USA. Department of Neurological Sciences, Rush Medical College, Chicago, IL, USA. Neurology Institute, Harley Street Medical Center, Abu Dhabi, UAE. American University of Beirut Medical Center, Beirut, Lebanon. Division of Clinical Neuroimmunology, Jefferson University, Comprehensive MS Center, Philadelphia, PA, USA. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA (an affiliate of Merck KGaA). Merck Healthcare KGaA, Darmstadt, Germany. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA (an affiliate of Merck KGaA).
 Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. pablo.naval.idi@gencat.cat. Institut de Diagnòstic Per La Imatge (IDI), L'Hospitalet de Llobregat, Centre Bellvige, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. pablo.naval.idi@gencat.cat. Bellvitge Biomedical Research Institute (IDIBELL), Universitat de Barcelona (UB), L'Hospitalet de Llobregat, 08907, Barcelona, Spain. pablo.naval.idi@gencat.cat. Departament de Ciències Clíniques, Facultat de Medicina I Ciències de La Salut, Universitat de Barcelona (UB), Carrer de Casanova 143, 08036, Barcelona, Spain. pablo.naval.idi@gencat.cat. Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Institut de Diagnòstic Per La Imatge (IDI), L'Hospitalet de Llobregat, Centre Bellvige, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Bellvitge Biomedical Research Institute (IDIBELL), Universitat de Barcelona (UB), L'Hospitalet de Llobregat, 08907, Barcelona, Spain. Departament de Ciències Clíniques, Facultat de Medicina I Ciències de La Salut, Universitat de Barcelona (UB), Carrer de Casanova 143, 08036, Barcelona, Spain. Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Institut de Diagnòstic Per La Imatge (IDI), L'Hospitalet de Llobregat, Centre Bellvige, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Bellvitge Biomedical Research Institute (IDIBELL), Universitat de Barcelona (UB), L'Hospitalet de Llobregat, 08907, Barcelona, Spain. Departament de Ciències Clíniques, Facultat de Medicina I Ciències de La Salut, Universitat de Barcelona (UB), Carrer de Casanova 143, 08036, Barcelona, Spain. Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Institut de Diagnòstic Per La Imatge (IDI), L'Hospitalet de Llobregat, Centre Bellvige, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Institut de Diagnòstic Per La Imatge (IDI), L'Hospitalet de Llobregat, Centre Bellvige, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Bellvitge Biomedical Research Institute (IDIBELL), Universitat de Barcelona (UB), L'Hospitalet de Llobregat, 08907, Barcelona, Spain. Departament de Ciències Clíniques, Facultat de Medicina I Ciències de La Salut, Universitat de Barcelona (UB), Carrer de Casanova 143, 08036, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Bellvitge Biomedical Research Institute (IDIBELL), Universitat de Barcelona (UB), L'Hospitalet de Llobregat, 08907, Barcelona, Spain. Departament de Ciències Clíniques, Facultat de Medicina I Ciències de La Salut, Universitat de Barcelona (UB), Carrer de Casanova 143, 08036, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Neuroradiology Section, Department of Radiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Institut de Diagnòstic Per La Imatge (IDI), L'Hospitalet de Llobregat, Centre Bellvige, Carrer de Feixa Llarga SN, 08907, Barcelona, Spain. Bellvitge Biomedical Research Institute (IDIBELL), Universitat de Barcelona (UB), L'Hospitalet de Llobregat, 08907, Barcelona, Spain.
 Neurology & Neurophysiology Center, Postfach 20, Vienna, 1180, Austria. fifigs1@yahoo.de.
 Department of Neurology, Hospital de Egas Moniz, Lisboa, Portugal marta.icn.magrico@gmail.com. Department of Neuroradiology, Hospital de Egas Moniz, Lisboa, Portugal. Department of Neurology, Hospital de Egas Moniz, Lisboa, Portugal. Department of Neurology, Hospital de Egas Moniz, Lisboa, Portugal.
 Department of Neurology, Perelman School of Medicine, The University of Pennsylvania, Philadelphia, PA, United States. Department of Neurology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany. Brain and Mind Center, University of Sydney, Sydney, NSW, Australia. Department of Neurology, Palacky University, Olomouc, Czechia.
 Neuroimmunology Unit, Santa Lucia Foundation IRCCS, Rome, Italy. Institut de Génétique Moléculaire de Montpellier, Université de Montpellier, Centre National de la Recherche Scientifique (CNRS), Montpellier, France. Institute of Microbiology, ETH Zurich, Zurich, Switzerland.
 School of Chemistry, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland. School of Biochemistry & Immunology, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland. School of Chemistry, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland. School of Biochemistry & Immunology, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland. School of Biochemistry & Immunology, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland. School of Chemistry, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland. School of Chemistry, Trinity Biomedical Sciences Institute, 152-160 Pearse Street, Trinity College, Dublin, Ireland.
 Schneider Children's Medical Center, Israel. Electronic address: Laronz@clalit.org.il. Central Virology Laboratory, Public Health Services MOH, Israel. University of Washington, Seattle, WA, USA. Israel Center for Disease Control, Ministry of Health, Israel.
 GRC 01, Service de Neuro-Urologie, Green Group of Clinical Research in Neuro-Urology AP-HP, Sorbonne Université, AP-HP, Hôpital Tenon, 4, rue de la Chine, Paris F-75020, France. Electronic address: maximilien.brouchet@aphp.fr. GRC 01, Service de Neuro-Urologie, Green Group of Clinical Research in Neuro-Urology AP-HP, Sorbonne Université, AP-HP, Hôpital Tenon, 4, rue de la Chine, Paris F-75020, France. GRC 01, Service de Neuro-Urologie, Green Group of Clinical Research in Neuro-Urology AP-HP, Sorbonne Université, AP-HP, Hôpital Tenon, 4, rue de la Chine, Paris F-75020, France. GRC 01, Service de Neuro-Urologie, Green Group of Clinical Research in Neuro-Urology AP-HP, Sorbonne Université, AP-HP, Hôpital Tenon, 4, rue de la Chine, Paris F-75020, France. GRC 01, Service de Neuro-Urologie, Green Group of Clinical Research in Neuro-Urology AP-HP, Sorbonne Université, AP-HP, Hôpital Tenon, 4, rue de la Chine, Paris F-75020, France. GRC 01, Service de Neuro-Urologie, Green Group of Clinical Research in Neuro-Urology AP-HP, Sorbonne Université, AP-HP, Hôpital Tenon, 4, rue de la Chine, Paris F-75020, France.
 Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Department of Physical Therapy, University of West Attica, Athens, Greece. Laboratory of Neuromuscular & Cardiovascular Study of Motion (LANECASM), Department of Physiotherapy, Faculty oh Health and Care Sciences, University of West Attica, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Department of Physical Therapy, University of West Attica, Athens, Greece. Laboratory of Neuromuscular & Cardiovascular Study of Motion (LANECASM), Department of Physiotherapy, Faculty oh Health and Care Sciences, University of West Attica, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Laboratory of Neuromuscular & Cardiovascular Study of Motion (LANECASM), Department of Physiotherapy, Faculty oh Health and Care Sciences, University of West Attica, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece. Department of Physical Therapy, University of West Attica, Athens, Greece. Laboratory of Neuromuscular & Cardiovascular Study of Motion (LANECASM), Department of Physiotherapy, Faculty oh Health and Care Sciences, University of West Attica, Athens, Greece. Second Department of Neurology, "Attikon" University Hospital, School of Medicine National & Kapodistrian University of Athens, National & Kapodistrian University of Athens, Athens, Greece.
 Experimental Medicine Program, University of British Columbia, Vancouver, British Columbia, Canada. Arthritis Research Canada, Vancouver, British Columbia, Canada. Experimental Medicine Program, University of British Columbia, Vancouver, British Columbia, Canada. Departments of Ophthalmology and Visual Sciences, Medicine and Pharmacology, University of British Columbia, Vancouver, British Columbia, Canada. Departments of Medicine and Community Health Sciences, University of Calgary, Calgary, Alberta, Canada. Division of Neurology, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. The Djavad Mowafaghian Centre for Brain Health, Vancouver, British Columbia, Canada. Arthritis Research Canada, Vancouver, British Columbia, Canada. Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada. Experimental Medicine Program, University of British Columbia, Vancouver, British Columbia, Canada. Arthritis Research Canada, Vancouver, British Columbia, Canada. Division of Rheumatology, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
 Charité - Universitaetsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH): Institute of Microbiology, Infectious Diseases and Immunology (I-MIDI), Berlin, Germany. Departamento de Medicina, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain. Charité - Universitaetsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH): Institute of Microbiology, Infectious Diseases and Immunology (I-MIDI), Berlin, Germany. Charité - Universitaetsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH): Institute of Microbiology, Infectious Diseases and Immunology (I-MIDI), Berlin, Germany. Charité - Universitaetsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH): Institute of Microbiology, Infectious Diseases and Immunology (I-MIDI), Berlin, Germany.
 Faculty of Exact and Applied Sciences, Metropolitan Technological Institute, Medellín, Colombia. Biomedical Research and Innovation Group (GI2B), Faculty of Exact and Applied Sciences, Metropolitan Technological Institute, Medellín, Colombia. Biomedical Research and Innovation Group (GI2B), Faculty of Exact and Applied Sciences, Metropolitan Technological Institute, Medellín, Colombia. Cooperative University of Colombia, Faculty of Health Sciences, Medicine, Medellín and Envigado, Colombia. Faculty of Exact and Applied Sciences, Metropolitan Technological Institute, Medellín, Colombia. National University of Colombia - Medellín Campus, Faculty of Sciences, School of Physics, Radiological Physics Research Group, Medellín, Colombia.
 Discipline of Physiotherapy, Institute of Health and Wellbeing, Federation University, Melbourne, VIC, Australia. Non-invasive Brain Stimulation & Neuroplasticity Laboratory, Department of Physiotherapy, School of Primary and Allied Health Care (SPAHC), Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne, VIC, Australia.
 Department of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Quality Control Department, Razi Vaccine and Serum Research Institute, Agricultural Research, Education and Extension Organization (AREEO), Karaj, Iran. Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Gastrointestinal and Liver Diseases Research Center, Iran University of Medical Sciences, Tehran, Iran. Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
 Riverview Psychiatric Center, 250 Arsenal Street, State House Station #11, Augusta, ME, 04333-0011, USA. Riverview Psychiatric Center, 250 Arsenal Street, State House Station #11, Augusta, ME, 04333-0011, USA. Riverview Psychiatric Center, 250 Arsenal Street, State House Station #11, Augusta, ME, 04333-0011, USA.
 Department of Clinical Neuroscience, Therapeutic Immune Design, Centre for Molecular Medicine Karolinska Institute Stockholm Sweden. Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences University of Birmingham, Edgbaston Birmingham UK. School of Medical Sciences, Faculty of Medicine and Health The University of Sydney Camperdown NSW Australia. Charles Perkins Centre The University of Sydney Camperdown NSW Australia.
 Department of Neuropsychology, National Hospital for Neurology and Neurosurgery, London, UK. Department of NEUROFARBA, Section of Psychology, University of Florence, Florence, Italy. Department of General Psychology, University of Padua, Padua, Italy. Neurology section, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Psychology Area, Salesian University Institution of Venice and Verona (IUSVE), Venice-Mestre, Italy. Neurology section, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Neurology section, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
 Department of Pharmacy, King Abdulaziz Specialist Hospital, Taif, SAU. Department of Medicine, PHC Al-Qassim Health Cluster, Buraidah, SAU. Department of Pharmacy, Maternity and Children Hospital, Dammam, SAU. Department of Pharmacy, Armed Forces Hospital, Jazan, SAU. Department of Pharmacy, Al Thaghr Hospital, Jeddah, SAU. Faculty of Pharmacy, University of Shaqra, Al-Dawadmi, SAU. Faculty of Pharmacy, Umm Al Qura University, Mecca, SAU. Faculty of Pharmacy, Northern Border University, Rafha, SAU. Faculty of Pharmacy, Buraydah College, Al-Qassim, SAU. Department of Pharmacy, Taif University, Taif, SAU. Department of Pharmacy, King Abdulaziz Specialist Hospital, Taif, SAU. Department of Pharmacy, Community Pharmacy, Riyadh, SAU.
 Department of Internal Medicine (JO'M), University of Manitoba, Winnipeg, MB, Canada. Departments of Medicine and Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences (RAM), University of Manitoba, Winnipeg, MB, Canada. Institute of Health Policy, Management, and Evaluation (AL), University of Toronto, Toronto, ON, Canada. Dalla Lana School of Public Health (AB), University of Toronto, Toronto, ON, Canada.
 Department of Nursing, Catholic University of Valencia San Vicente Mártir, Valencia, Spain. Doctoral School, Catholic University of Valencia San Vicente Mártir, Valencia, Spain. Department of Nursing, Catholic University of Valencia San Vicente Mártir, Valencia, Spain. Faculty of Legal, Economic and Social Sciences, Catholic University of Valencia San Vicente Mártir, Valencia, Spain. Department of Nursing, Catholic University of Valencia San Vicente Mártir, Valencia, Spain. Department of Psychology and Sociology, University of Zaragoza, Teruel, Spain.
 Department of Clinical and Experimental Medicine, Psychiatry Unit, University of Catania, 95123 Catania, Italy. Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. Department of Clinical and Experimental Medicine, Psychiatry Unit, University of Catania, 95123 Catania, Italy. Department of Clinical and Experimental Medicine, Psychiatry Unit, University of Catania, 95123 Catania, Italy. Department of Clinical and Experimental Medicine, Psychiatry Unit, University of Catania, 95123 Catania, Italy. Department of Clinical and Experimental Medicine, Psychiatry Unit, University of Catania, 95123 Catania, Italy. Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. Department of Medical and Surgical Specialities, University of Foggia, 71122 Foggia, Italy. Department of Medical and Surgical Specialities, University of Foggia, 71122 Foggia, Italy. Department of Medical and Surgical Specialities, University of Foggia, 71122 Foggia, Italy. Department of Clinical and Experimental Medicine, Psychiatry Unit, University of Catania, 95123 Catania, Italy.
 Gastrointestinal Microbiology Research Group, Institute of Microbiology, Infectious Diseases and Immunology, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Gastrointestinal Microbiology Research Group, Institute of Microbiology, Infectious Diseases and Immunology, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Gastrointestinal Microbiology Research Group, Institute of Microbiology, Infectious Diseases and Immunology, Charité - University Medicine Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
 Department of Anesthesiology, Westchester Medical Center, Valhalla, United States. Department of Orthopaedic Surgery and Sports Medicine, Temple University, Philadelphia, Pennsylvania, United States. Harvard Combined Orthopaedic Residency Program, Harvard Medical School/Mass General Hospital, Boston, United States. Department of Orthopaedics, Medstar Orthopaedic Institute/Georgetown University School of Medicine, Washington, United States.
 Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA, United States. Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA, United States. Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA, United States.
 Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran. Department of Biostatistics and Epidemiology, Faculty of Health, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
 SA Health, Department of Neurology, Flinders Medical Centre, Bedford Park SA 5042, Australia; College of Medicine and Public Health, Flinders University of South Australia, Bedford Park SA 5042, Australia. SA Health, Department of Neurology, Flinders Medical Centre, Bedford Park SA 5042, Australia; College of Medicine and Public Health, Flinders University of South Australia, Bedford Park SA 5042, Australia. Electronic address: chug0018@flinders.edu.au. SA Health, Department of Neurology, Flinders Medical Centre, Bedford Park SA 5042, Australia; College of Medicine and Public Health, Flinders University of South Australia, Bedford Park SA 5042, Australia. SA Health, Department of Neurology, Flinders Medical Centre, Bedford Park SA 5042, Australia; College of Medicine and Public Health, Flinders University of South Australia, Bedford Park SA 5042, Australia.
 From the MD/MPH Program (SLH), University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA. Department of Public Health Sciences (JMS), University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA. The Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA (FB). Department of Psychiatry and Behavioral Sciences and Sylvester Comprehensive Cancer Center (ZE), University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA. Department of Physical Medicine and Rehabilitation (LTS), University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.
 Department of Neurology, Bharati Vidyapeeth University Medical College, Pune. Sri Venkateswara Medical College, Tirupati. University of Baghdad, Al-Kindy College of Medicine, Baghdad, Iraq. Internal Medicine, Government Medical College, Omandurar, Chennai, India. Internal Medicine, Mayo Clinic. Internal Medicine, Lugansk State Medical University, Lugansk, Ukraine. University of Baghdad, Al-Kindy College of Medicine, Baghdad, Iraq. University of Baghdad, Al-Kindy College of Medicine, Baghdad, Iraq. Privolzhsky Research Medical University, Nizhny Novgorod, Russia. Manhal University, Khartoum, Sudan. Mayo Clinic, Rochester, Minnesota, USA.
 Department of Neurology and Neurorehabilitation, Kliniken Valens Rehazentrum, Valens, Switzerland. Juerg.Kesselring@kliniken-valens.ch. Institute of Clinical Neurology and Department of Neuroimmunology of the Federal Centre of Brain Research and Neurotechnologies FMBA, Pirogov's Russian National Research Scientific Medical University, Moscow, Russia. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Member of the MS in the 21st Century Steering Group, Buckinghamshire, UK. Member of the MS in the 21st Century Steering Group, Overijse, Belgium. Merck KGaA, Darmstadt, Germany.
 School of Computer Science, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. School of Computer Science, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. School of Electrical and Information Engineering, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. NVIDIA Corporation, Singapore, Singapore. School of Biomedical Engineering, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. School of Biomedical Engineering, The University of Sydney, Sydney, NSW, Australia. Sydney Imaging, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia. School of Electrical and Information Engineering, The University of Sydney, Sydney, NSW, Australia. School of Computer Science, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia.
 Department of Neuroscience, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China. The First Clinical Medical School, Henan University of Chinese Medicine, Zhengzhou 450046, China. School of Pharmaceutical Sciences, Henan Key Laboratory of Targeting Therapy and Diagnosis for Critical Diseases, Zhengzhou University, Zhengzhou 450001, China. School of Pharmaceutical Sciences, Henan Key Laboratory of Targeting Therapy and Diagnosis for Critical Diseases, Zhengzhou University, Zhengzhou 450001, China. Department of Neuroscience, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China. Department of Neuroscience, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China. School of Pharmaceutical Sciences, Henan Key Laboratory of Targeting Therapy and Diagnosis for Critical Diseases, Zhengzhou University, Zhengzhou 450001, China.
 Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, 88100 Catanzaro, Italy. Department of Medical and Surgical Sciences, University "Magna Graecia" of Catanzaro, 88100 Catanzaro, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", 88100 Caserta, Italy. Neurology Unit "San Giuseppe Moscati", Hospital Avellino, 83100 Avellino, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", 88100 Caserta, Italy.
 Department of Occupational Therapy, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Neurology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Occupational Therapy, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, United States.
 Department of Health Promotion, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel. Department of Health Promotion, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel.
 Department of Pharmacy, Kut University College, Al-Kut, Wasit, Iraq. Department of Pharmacy, Kut University College, Al-Kut, Wasit, Iraq. Ministry of Health and Environment, Al-Zahraa Teaching Hospital, Al-Kut, Wasit, Iraq.



 MS Center, S'Andrea Hospital, Sapienza University of Rome, Rome, Italy. MS Center, S'Andrea Hospital, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. MS Center, S'Andrea Hospital, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. MS Center, S'Andrea Hospital, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Neuroimmunology Unit, IRCSS Fondazione Santa Lucia, Rome, Italy.
 Internal Medicine, Baylor Scott & White Medical Center, Temple, USA. Infectious Diseases, Baylor Scott & White Medical Center, Temple, USA. Internal Medicine, Baylor Scott & White Medical Center, Temple, USA.
 Department of Neurology, Katholisches Klinikum Bochum, Ruhr-Universität Bochum, Bochum, Germany. Department of Neurology, Katholisches Klinikum Bochum, Ruhr-Universität Bochum, Bochum, Germany. Medical Informatics, Biometry and Epidemiology, Ruhr-Universitat Bochum, Bochum, Germany. Medical Informatics, Biometry and Epidemiology, Ruhr-Universitat Bochum, Bochum, Germany. Department of Neurology, Katholisches Klinikum Bochum, Ruhr-Universität Bochum, Bochum, Germany. Department of Neurology, Katholisches Klinikum Bochum, Ruhr-Universität Bochum, Bochum, Germany. Research & Evaluation, Kaiser Permanente Southern California, Pasadena, California, USA. Department of Neurology, Katholisches Klinikum Bochum, Ruhr-Universität Bochum, Bochum, Germany Kerstin.Hellwig@ruhr-uni-bochum.de.
 Volyn Regional Clinical Hospital, Lutsk, Ukraine. Department of Clinical Medicine, Lesia Ukrainka Volyn National University, Ukraine. Volyn Regional Clinical Hospital, Lutsk, Ukraine. Volyn Regional Clinical Hospital, Lutsk, Ukraine.
 Centre for Rehabilitation and Ageing Research, School of Medicine, University of Nottingham, Nottingham, UK. Mental Health & Clinical Neurosciences, School of Medicine, University of Nottingham, Nottingham, UK. Health Services Research, SINTEF, Trondheim, Norway. Institute of Mental Health, Nottinghamshire Healthcare Trust, Nottingham, UK. Centre for Rehabilitation and Ageing Research, School of Medicine, University of Nottingham, Nottingham, UK.
 Mahajan Imaging Private Limited, New Delhi, India. CARPL.AI, New Delhi, India. Mahajan Imaging Private Limited, New Delhi, India. CARPL.AI, New Delhi, India. Mahajan Imaging Private Limited, New Delhi, India. CARPL.AI, New Delhi, India.
 Department of Internal Medicine, School of Medicine, Colorectal Research Center, Rasoul-E-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran. Drmhxim@gmail.com. Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Drmhxim@gmail.com. Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
 Endocrine Unit and Diabetes Centre, Department of Clinical Therapeutics, Alexandra Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. vkazakou@hotmail.com. Multiple Sclerosis & Demyelinating Diseases Unit, 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. dtzanetakos@med.uoa.gr.uoa. Second Department of Neurology, School of Medicine, National and Kapodistrian University of Athens, "Attikon" University Hospital, Athens, Greece. dtzanetakos@med.uoa.gr.uoa. Multiple Sclerosis & Demyelinating Diseases Unit, 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Second Department of Neurology, School of Medicine, National and Kapodistrian University of Athens, "Attikon" University Hospital, Athens, Greece. Multiple Sclerosis & Demyelinating Diseases Unit, 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Multiple Sclerosis & Demyelinating Diseases Unit, 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Multiple Sclerosis & Demyelinating Diseases Unit, 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Department of Endocrinology, Alexandra Hospital, Athens, Greece. 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Multiple Sclerosis & Demyelinating Diseases Unit, 1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Department of Endocrinology, Alexandra Hospital, Athens, Greece.
 Department of Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA. Center for Health Care Research and Policy, School of Medicine, Case Western Reserve University, Cleveland, OH, USA. McLean Hospital, Harvard Medical School, Belmont, MA, USA. The Mellen Center for Multiple Sclerosis and Research, Department of Neurology, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA. The Mellen Center for Multiple Sclerosis and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA. Department of Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
 GF Ingrassia Department, University of Catania, Catania, Italy. IRCCS Santa Lucia, Rome, Italy. Head and Neck Department, San Giovanni-Addolorata Hospital, Rome, Italy. The UCL Queen Square Institute of Neurology, London, United Kingdom. The UCL Queen Square Institute of Neurology, London, United Kingdom. Department of Sense Organs, University Sapienza, Rome, Italy. Department of Interventional Neuroradiologie, Hannover Medical School, Hannover, Germany. Klinik für Neurologie UKD Heinrich Heine Universität Düsseldorf, Düsseldorf, Germany. Department of Neurology, University Sapienza, Rome, Italy. Department of Radiology and Pathology, University Sapienza, Rome, Italy. Department of Otolaryngology-Head and Neck Surgery, Hannover Medical School, Hannover, Germany. Distinguished Senior Fellows (Sabbatical), Laboratory of Neuroimmunology of Professor Lawrence Steinman, Stanford University School of Medicine, Palo Alto, CA, United States. Distinguished Senior Fellows (Sabbatical), Laboratory of Neuroimmunology of Professor Lawrence Steinman, Stanford University School of Medicine, Palo Alto, CA, United States.
 School of Psychological Sciences, University of Tasmania, Launceston, Australia. Electronic address: holly.emery@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. School of Psychological Sciences, University of Tasmania, Hobart, Australia. School of Applied Psychology & The Hopkins Centre, Griffith University, Mount Gravatt, Australia. School of Nursing, University of Notre Dame, Darlinghurst, Australia. Launceston General Hospital, Launceston, Tasmania, Australia. School of Psychological Sciences, University of Tasmania, Launceston, Australia; Launceston General Hospital, Launceston, Tasmania, Australia.
 Department of Psychiatry and Psychotherapy, Center of Sleep Medicine, Medbo, University of Regensburg, Universitätsstraße 84, Regensburg D-93053, Germany; Department of Experimental Psychology, University of Regensburg, Regensburg, Germany. Department of Psychiatry and Psychotherapy, Center of Sleep Medicine, Medbo, University of Regensburg, Universitätsstraße 84, Regensburg D-93053, Germany. Department of Neurology, University of Regensburg Hospital, Regensburg, Germany. Department of Psychiatry and Psychotherapy, Center of Sleep Medicine, Medbo, University of Regensburg, Universitätsstraße 84, Regensburg D-93053, Germany. Department of Neurology, University of Regensburg Hospital, Regensburg, Germany. Department of Psychiatry and Psychotherapy, Center of Sleep Medicine, Medbo, University of Regensburg, Universitätsstraße 84, Regensburg D-93053, Germany. Electronic address: roland.popp@medbo.de.
 Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy. IRCCS Neuromed, Pozzilli, Italy. IRCCS Neuromed, Pozzilli, Italy. Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.
 Ferkauf Graduate School of Psychology, Yeshiva University, 1165 Morris Park Ave, The Bronx, NY 10461, USA. Electronic address: hcohen6@mail.yu.edu. Ferkauf Graduate School of Psychology, Yeshiva University, 1165 Morris Park Ave, The Bronx, NY 10461, USA; Department of Neurology, Albert Einstein College of Medicine, 1300 Morris Park Ave, The Bronx, NY 10416, USA. Electronic address: roee.holtzer@yu.edu.
 Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany. Department of Neurology, Medical Faculty Mannheim and Mannheim Center of Translational Neurosciences (MCTN), Heidelberg University, Mannheim, Germany.
 Computational Neuroergonomics Laboratory, Department of Industrial Engineering and Management Systems, University of Central Florida, Orlando, FL, United States. Computational Neuroergonomics Laboratory, Department of Industrial Engineering and Management Systems, University of Central Florida, Orlando, FL, United States. Computational Neuroergonomics Laboratory, Department of Industrial Engineering and Management Systems, University of Central Florida, Orlando, FL, United States. Computational Neuroergonomics Laboratory, Department of Industrial Engineering and Management Systems, University of Central Florida, Orlando, FL, United States.
 Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, SK, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Department of Neuroscience, University of Alberta, Edmonton, AB, Canada. Department of Psychology, University of Victoria, Victoria, BC, Canada.
 Sigmovir Biosystems, Inc., Rockville, MD, United States. Department of Medicine, The University of British Columbia, Vancouver, BC, Canada. Sigmovir Biosystems, Inc., Rockville, MD, United States.
 Department of Neurology, 10th Military Research Hospital and Polyclinic, Bydgoszcz, Poland. swawrzyniak@wp.pl. Department of Neurology, 10th Military Research Hospital and Polyclinic, Bydgoszcz, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Institute of Medical Sciences, Medical College of Rzeszow University, Rzeszow, Poland. Department of Neurology, Pomeranian Medical University, Szczecin, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland.
 From the Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, OH, USA (SLD, MP). From the Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, OH, USA (SLD, MP).
 Department of Chemistry, School of Sciences and Engineering, The American University in Cairo, New Cairo 11835, Egypt. Biochemistry Department, Faculty of Science, Suez University, P.O. Box 43518, Suez 43533, Egypt. Institute of Global Health and Human Ecology, School of Sciences and Engineering, The American University in Cairo, P.O. Box 74, New Cairo 11835, Egypt.
 Department of Neuroimmunology, The Cyprus Institute of Neurology and Genetics, Nicosia 2410, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia 2410, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia 2410, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia 2410, Cyprus. Department of Neuroimmunology, The Cyprus Institute of Neurology and Genetics, Nicosia 2410, Cyprus. Department of Neuroimmunology, The Cyprus Institute of Neurology and Genetics, Nicosia 2410, Cyprus.
 Translational Neuroscience Program (EME, AMD, NEF), Wayne State University, Detroit, MI, USA. Department of Health Care Sciences (EME, NEF), Wayne State University, Detroit, MI, USA. Department of Psychology (AMD), Wayne State University, Detroit, MI, USA. Institute of Gerontology (AMD), Wayne State University, Detroit, MI, USA. Translational Neuroscience Program (EME, AMD, NEF), Wayne State University, Detroit, MI, USA. Department of Health Care Sciences (EME, NEF), Wayne State University, Detroit, MI, USA. Department of Neurology (NEF), Wayne State University, Detroit, MI, USA.
 Computational Neuroergonomics Laboratory, Department of Industrial Engineering and Management Systems, University of Central Florida, Orlando, FL 32816, USA. Computational Neuroergonomics Laboratory, Department of Industrial Engineering and Management Systems, University of Central Florida, Orlando, FL 32816, USA. Department of Biostatistics, Johns Hopkins University, Baltimore, MD 21218, USA. Department of Cognitive Neuroscience and Neuroergonomics, Institute of Applied Psychology, Jagiellonian University, 30-348 Kraków, Poland. Department of Psychology, University of Central Florida, Orlando, FL 32816, USA.
 Department of Toxicology, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211, 50-556 Wrocław, Poland. Department of Neurology, Faculty of Medicine, Wroclaw Medical University, Borowska 213, 50-556 Wrocław, Poland. Department of Neurology, Faculty of Medicine, Wroclaw Medical University, Borowska 213, 50-556 Wrocław, Poland. Department of Neurology, Faculty of Medicine, Wroclaw Medical University, Borowska 213, 50-556 Wrocław, Poland. Department of Toxicology, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211, 50-556 Wrocław, Poland.
 Department of Neurology, CHU Rouen, CIC-CRB 1404, Rouen F-76000, France. Department of Digestive Physiology, CHU Rouen, CIC-CRB 1404, Rouen University Normandie, INSERM, ADEN UMR 1073, F-76000, Rouen, France. Department of Digestive Physiology, CHU Rouen, CIC-CRB 1404, Rouen University Normandie, INSERM, ADEN UMR 1073, F-76000, Rouen, France. Department of Epidemiology, CHU Rouen, CIC-CRB 1404, Rouen University Normandie, INSERM, ADEN UMR 1073, F-76000, Rouen, France. Department of Pharmacology, Endothelium, Valvulopathy, and Heart Failure, CHU Rouen, CIC-CRB 1404, University Rouen Normandie, INSERM, EnVI UMR1096, F-76000, Rouen, France. Department of Digestive Physiology, CHU Rouen, CIC-CRB 1404, Rouen University Normandie, INSERM, ADEN UMR 1073, F-76000, Rouen, France. Electronic address: anne-marie.leroi@chu-rouen.fr.
 Facultad de Informática, Universidad Autónoma de Querétaro, Querétaro 76230, Mexico. Centro de Investigación en Tecnologías de Información y Sistemas, Universidad Autónoma del Estado de Hidalgo, Pachuca 42039, Mexico. Facultad de Informática, Universidad Autónoma de Querétaro, Querétaro 76230, Mexico. Facultad de Ingeniería, Universidad Autónoma de Querétaro, Querétaro 76010, Mexico. Centro de Investigaciones en Óptica, Aguascalientes 20200, Mexico. Facultad de Ingeniería, Universidad Autónoma de Querétaro, Querétaro 76010, Mexico.
 Department of Medical Services and Techniques, Burdur Vocational School of Health Services, Burdur Mehmet Akif Ersoy University, Burdur, Türkİye. Department of Neurological Rehabilitation, Faculty of Physiotherapy and Rehabilitation, Pamukkale University, Denizli, Türkİye. Department of Neurology, Faculty of Medicine, Pamukkale University, Denizli, Türkİye. Department of Neurology, Faculty of Medicine, Pamukkale University, Denizli, Türkİye. Department of Biostatistics, Faculty of Medicine, Pamukkale University, Denizli, Türkİye.
 Department of Hematooncology, University Hospital Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Hematooncology, University Hospital Ostrava, Czech Republic. Department of Hematooncology, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Hematooncology, University Hospital Ostrava, Czech Republic. Department of Hematooncology, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Hematooncology, University Hospital Ostrava, Czech Republic. Department of Hematooncology, Faculty of Medicine, University of Ostrava, Czech Republic. Department of Neurology, University Hospital Ostrava, Czech Republic. Department of Clinical Neurosciences, Faculty of Medicine, University of Ostrava, Czech Republic.
 From the School of Medicine (LLT, RS), University of Kansas Medical Center, Kansas City, KS, USA. From the School of Medicine (LLT, RS), University of Kansas Medical Center, Kansas City, KS, USA. From the Department of Neurology (SGL), University of Kansas Medical Center, Kansas City, KS, USA. From the Department of Otolaryngology (JHD, JAV), University of Kansas Medical Center, Kansas City, KS, USA. Welch Medical Library, Johns Hopkins University, Baltimore, MD, USA (JW). From the Department of Otolaryngology (JHD, JAV), University of Kansas Medical Center, Kansas City, KS, USA.
 Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran. Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran. Epidemiology, Modeling in Health Research Center, Institute for Futures Studies in Health, Kerman University of Medical Sciences, Kerman, Iran. Department of Biostatistics and Epidemiology, Faculty of Public Health, Kerman University of Medical Sciences, Kerman, Iran. Vector-Borne Diseases Research Center, North Khorasan University of Medical Sciences, Bojnurd, Iran. Neurology Research Center, Kerman University of Medical Sciences, Kerman, Iran.
 Neurology, Taibah University, Medina, SAU.
 Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran. Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran. Department of Animal Genetics, Yasouj University, Yasuj, Iran.
 Neurodegenerative Disorders Research Pty Ltd West Perth Western Australia Australia. The University of Western Australia Nedlands Western Australia Australia. Neurodegenerative Disorders Research Pty Ltd West Perth Western Australia Australia. Neurodegenerative Disorders Research Pty Ltd West Perth Western Australia Australia. Neurodegenerative Disorders Research Pty Ltd West Perth Western Australia Australia.
 Department of Public Health, University of Naples Federico II, 80131 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy. II Clinic of Neurology, Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Translational Medical Sciences, University of Naples Federico II, 80138 Naples, Italy. Department of Translational Medical Sciences, University of Naples Federico II, 80138 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, University of Naples Federico II, 80138 Naples, Italy.
 Neurology Unit, Ospedale Provinciale "Madonna del Soccorso", 63074 San Benedetto del Tronto, Italy. Neurology Unit, Ospedale Provinciale "Madonna del Soccorso", 63074 San Benedetto del Tronto, Italy. Neurology Unit, Ospedale Provinciale "Madonna del Soccorso", 63074 San Benedetto del Tronto, Italy. Section of Biochemistry, Biology and Physics, Department of Clinical Sciences, Università Politecnica delle Marche, 60100 Ancona, Italy. Neurology Unit, Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, 60100 Ancona, Italy. Neurology Unit, Ospedale Provinciale "Madonna del Soccorso", 63074 San Benedetto del Tronto, Italy. Neurology Unit, Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, 60100 Ancona, Italy. Section of Biochemistry, Biology and Physics, Department of Clinical Sciences, Università Politecnica delle Marche, 60100 Ancona, Italy.
 Center for Clinical Neuroplasticity, Medical Park Loipl, Bischofswiesen, Germany, & Department of Neurology, University of Erlangen, Erlangen, Germany. Unit of Neurology & Neurorehabilitation, IRCCS Neuromed, Pozzilli (IS), Italy. Blizard Institute, Barts & The London School of Medicine & Dentistry, Queen Mary University of London, London, UK. Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, NV, USA. Neurology, Hospital Clínico San Carlos, IdISSC, Madrid, Spain, & Departamento de Medicina, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain. Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Danish Multiple Sclerosis Center, Department of Neurology, University of Copenhagen & Rigshospitalet, Copenhagen, Denmark. Univ. Lille, INSERM-U1172, LilNCog, CHU Lille, FHU Precise, Lille, France. Department of Neurology, Institute of Translational Neurology, University of Münster, Münster, Germany. Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA. Neurology Institute, Harley Street Medical Center, Abu Dhabi, UAE, & Nehme & Therese Tohme Multiple Sclerosis Center, American University of Beirut, Beirut, Lebanon.
 Department of Neurology, University of Washington School of Medicine, Seattle, WA, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurological Sciences, Larner College of Medicine, The University of Vermont, Burlington, VT, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
 Department of Neurology, Sichuan Taikang Hospital, Chengdu, Sichuan, China. Department of Respiratory, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China. Department of Neurology, Qionglai People's Hospital, Chengdu, Sichuan, China.
 Radiologic Sciences, Faculty of Applied Medical Sciences, King Abdullah Medical Complex, Ministry of Health, Jeddah, SAU. Radiologic Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, SAU. Diagnostic Radiology, Faculty of Medicine, Cairo University, Cairo, EGY.
 Medical School, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Internal Medicine, Richmond University Medical Center Affiliated with Mount Sinai Health System and Icahn School of Medicine, New York, USA. Internal Medicine Clinical Research, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Internal Medicine, Baroda Medical College, Vadodara, IND. Radiology, Bharati Vidyapeeth University, Pune, IND. Radiology, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Medicine and Surgery, Qingdao University College of Medical Science, Qingdao, CHN. Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Internal Medicine, Government Medical College Amritsar, Amritsar, IND. General Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Psychiatry, St. Martinus University Faculty of Medicine, Willemstad, USA. Psychiatry, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA. Internal Medicine/Family Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
 Department of Clinical Psychology, School of Behavioral Sciences and Mental Health (Tehran Institute of Psychiatry), Iran University of Medical Sciences, Tehran, Iran. Department of Clinical Psychology, School of Behavioral Sciences and Mental Health (Tehran Institute of Psychiatry), Iran University of Medical Sciences, Tehran, Iran. Department of Clinical Psychology, School of Behavioral Sciences and Mental Health (Tehran Institute of Psychiatry), Iran University of Medical Sciences, Tehran, Iran. Department of Psychology, Tarbiat Modares University, Tehran, Iran.
 Department of Neurology, Vestre Viken Hospital Trust, Drammen, Norway; Department of Neurology, Oslo University Hospital, Norway; Institute of Clinical Medicine, University of Oslo, Norway. Electronic address: line.broch@vestreviken.no. Department of Neurology, Telemark Hosptial Trust, Skien, Norway. Department of Neurology, Vestre Viken Hospital Trust, Drammen, Norway. Department of Neurology, Oslo University Hospital, Norway. University of South-Eastern Norway, Norway. Oslo Centre for Biostatistics and Epidemiology, Oslo University Hospital, Norway. Department of Neurology, Oslo University Hospital, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
 University of Health Sciences, Gulhane Faculty of Physiotherapy and Rehabilitation, Department of Physiotherapy and Rehabilitation, Ankara, Turkey. Electronic address: fatih.soke@sbu.edu.tr. University of Health Sciences, Ankara Etlik City Hospital, Department of Neurology, Ankara, Turkey. Ankara Yildirim Beyazit University, Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Ankara, Turkey. Osmangazi University, Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Eskisehir, Turkey. University of Health Sciences, Gulhane Faculty of Physiotherapy and Rehabilitation, Department of Physiotherapy and Rehabilitation, Ankara, Turkey. Ankara University, Faculty of Health Sciences, Department of Nutrition and Dietetic, Ankara, Turkey. Anadolu University, Vocational School of Health Services, Elderly Care Program, Eskisehir, Turkey. Ankara University, Faculty of Medicine, Department of Neurology, Ankara, Turkey.
 Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara 06230, Turkey. Electronic address: ezgiozb@gmail.com. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara 06230, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara 06230, Turkey. School of Medicine, Neurology Department, Hacettepe University, Ankara 06230, Turkey.
 Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Pediatrics Section, University of Salerno, 84081 Baronissi, Salerno, Italy. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Pediatrics Section, University of Salerno, 84081 Baronissi, Salerno, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, University of Naples Federico II, 80138 Naples, Naples, Italy. Department of Translational Medical Science, Section of Pediatrics, University of Naples Federico II, 80138 Naples, Naples, Italy. Department of Translational Medical Science, Section of Pediatrics, University of Naples Federico II, 80138 Naples, Naples, Italy. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Nutrition Section, University of Salerno, 84081 Baronissi, Salerno, Italy. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Pediatric Psychiatry Section, University of Salerno, 84081 Baronissi, Salerno, Italy. Department of Translational Medical Science, Section of Pediatrics, University of Naples Federico II, 80138 Naples, Naples, Italy. Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, University of Naples Federico II, 80138 Naples, Naples, Italy. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Pediatrics Section, University of Salerno, 84081 Baronissi, Salerno, Italy. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Pediatrics Section, University of Salerno, 84081 Baronissi, Salerno, Italy. Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Pediatrics Section, University of Salerno, 84081 Baronissi, Salerno, Italy.
 National Research Council (CNR), Institute of Biomedical Technologies, Bari Unit, 70125 Bari, Italy. National Research Council (CNR), Institute of Biomedical Technologies, Bari Unit, 70125 Bari, Italy. National Research Council (CNR), Institute of Biomedical Technologies, Bari Unit, 70125 Bari, Italy.

 The University of Queensland, Australia. The University of Queensland, Australia.
 Dr. B.R. Ambedkar Center for Biomedical Research (ACBR), University of Delhi, New Delhi, India. Dr. B.R. Ambedkar Center for Biomedical Research (ACBR), University of Delhi, New Delhi, India. Dr. B.R. Ambedkar Center for Biomedical Research (ACBR), University of Delhi, New Delhi, India. Department of Biophysics, All India Institute of Medical Sciences (AIIMS), New Delhi, India. Department of Neurology, All India Institute of Medical Sciences (AIIMS), New Delhi, India. Department of Neurosurgery, All India Institute of Medical Sciences (AIIMS), New Delhi, India. Electronic address: saratpchandra3@gmail.com.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. School of Education, College of Arts, Law, and Education, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia.
 Clinic for Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience Hannover, Hannover, Germany. Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany. Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany. Clinic for Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience Hannover, Hannover, Germany. Translational Medicine, Novartis Institute for Biomedical Research, Novartis, Basel, Switzerland. Clinic for Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience Hannover, Hannover, Germany. Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany.
 Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (ESG, LON, JAR, ACL). Department of Rehabilitative Medicine (ESG, LON, JAR), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Medical Sciences (ESG, JAR), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, CT, USA (ESG). Multiple Sclerosis Center of Excellence West, Veterans Affairs, Seattle, WA, USA (APT). Rehabilitation Care Service, VA Puget Sound Health Care System, Seattle, WA, USA (APT). Department of Rehabilitation Medicine, University of Washington, Seattle, WA, USA (APT). Department of Family Medicine and the Center for Quantitative Medicine, University of Connecticut Health Center, Farmington, CT, USA (TA). Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (ESG, LON, JAR, ACL). Department of Rehabilitative Medicine (ESG, LON, JAR), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (ESG, LON, JAR, ACL). Department of Rehabilitative Medicine (ESG, LON, JAR), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Medical Sciences (ESG, JAR), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Mandell Center for Multiple Sclerosis, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (ESG, LON, JAR, ACL). Department of Family Medicine and the Center for Quantitative Medicine, University of Connecticut Health Center, Farmington, CT, USA (TA). Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA (FWF). Holy Name Medical Center Multiple Sclerosis Center, Teaneck, NJ, USA (FWF).
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. The Alfred Hospital, Melbourne, Victoria, Australia. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Turku University Hospital Neurocenter and Division of Clinical Neurosciences, University of Turku, Turku, Finland. Center of Clinical Neuroscience, Department of Neurology, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Norwegian MS Registry and Biobank, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Danish Multiple Sclerosis Center and the Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Bordeaux PharmacoEpi (BPE), Université de Bordeaux, Bordeaux, France. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. Global Epidemiology, IQVIA, Amsterdam, The Netherlands. Merck Healthcare KGaA, Darmstadt, Germany.
 Department of Neurology, Amiralam Hospital, Tehran University of Medical Sciences, Tehran 11457-65111, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran 19978-66837, Iran. Food Industry Engineering, Tehran Islamic Azad University of Medical Sciences, Tehran 19395-1495, Iran. Department of Medical, Orchid Pharmed Company, Tehran 19947-66411, Iran. Department of Neurology, Amiralam Hospital, Tehran University of Medical Sciences, Tehran 11457-65111, Iran. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Unverstät zu Berlin, Experimental and Clinical Research Center, 13125 Berlin, Germany. Department of Regional Health Research and Molecular Medicine, University of Southern Denmark, 5230 Odense, Denmark.
 Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy.
 Kielo Research, Zug, Switzerland and Evidera, London, UK. Mellen Center for Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Evidera, Bethesda, MD, USA. Actelion Pharmaceuticals, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Actelion Pharmaceuticals, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Janssen Research & Development, Titusville, NJ, USA. Actelion Pharmaceuticals, Part of Janssen Pharmaceutical Companies, Allschwil, Switzerland. Innovus Consulting Ltd, London, UK.
 Complex Operative Unit of Neurology, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Laboratory of Neuroproteomics, Multiple Sclerosis Centre, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Laboratory of Neuroproteomics, Multiple Sclerosis Centre, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Department of Management, Economics, Mathematics and Statistics, University of Salento, 73100 Lecce, Italy. Complex Operative Unit of Neurology, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Department of Management, Economics, Mathematics and Statistics, University of Salento, 73100 Lecce, Italy. Complex Operative Unit of Ophthalmology, "V. Fazzi" Hospital, 73100 Lecce, Italy.
 Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Instituto de Salud Carlos III, Madrid, Spain. Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Statistical Unit, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Instituto de Salud Carlos III, Madrid, Spain. Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Instituto de Salud Carlos III, Madrid, Spain. Medical Sciences Department, University of Girona, Girona, Spain. Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Redes de Investigación Cooperativa Orientada a Resultados en Salud (RICORS), Red de Enfermedades inflamatorias (RD21/0002/0063), Instituto de Salud Carlos III, Madrid, Spain. Medical Sciences Department, University of Girona, Girona, Spain. Girona Neuroimmumology and Multiple Sclerosis Unit, Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Medical Sciences Department, University of Girona, Girona, Spain.

 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada. Department of Medicine, The Ottawa Hospital, 01 Smyth Road, Box 601, Ottawa, ON, K1H 8L6, Canada. The Ottawa Hospital Research Institute, Ottawa, Canada. Biostatistics Division, Dalla Lana School of Public Health, University of Toronto, Toronto, Canada. Department of Biostatistics, The Princess Margaret Cancer Centre, University of Toronto, Toronto, Canada. Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Canada. Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, United States of America. Biostatistics Division, Dalla Lana School of Public Health, University of Toronto, Toronto, Canada. Department of Biostatistics, The Princess Margaret Cancer Centre, University of Toronto, Toronto, Canada. Department of Physical Medicine and Rehabilitation, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, 55905, USA. Department of Physical Medicine and Rehabilitation, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, 55905, USA. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada. Lunenfeld-Tanenbaum Medicine and Pathobiology, University of Toronto, Toronto, Canada. Department of Clinical Biochemistry, University Health Network, Toronto, Canada. Mount Sinai Hospital, Joseph & Wolf Lebovic Ctr, 60 Murray St [Box 32]; Flr 6 - Rm L6-201, Toronto, ON, M5T 3L9, Canada. yprassas@gmail.com. Laboratory Medicine Program, University Health Network, Toronto, Canada. yprassas@gmail.com. Department of Medicine, The Ottawa Hospital, 01 Smyth Road, Box 601, Ottawa, ON, K1H 8L6, Canada. mfreedman@toh.ca. The Ottawa Hospital Research Institute, Ottawa, Canada. mfreedman@toh.ca.
 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. RINGGOLD: 26745 Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. RINGGOLD: 26745 Fertility Unit, Department of Obstetrics and Gynecology, Sheba Medical Center, Ramat Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel. RINGGOLD: 26744 Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. RINGGOLD: 26745
 Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA.
 From First Coast Integrative Medicine, Jacksonville Beach, FL, USA (MW). MS Achievement Center, Sacramento, CA, USA (BH). Boyer College of Music and Dance, Temple University, Philadelphia, PA, USA (WLM). A Place To Be, Middleburg, VA, USA (KL, TS). A Place To Be, Middleburg, VA, USA (KL, TS). Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA (JLW, WS). Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA (JLW, WS). John F. Kennedy Center for the Performing Arts, Washington, DC, USA (RF).
 Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA; Center for Health Care Research and Policy, Case Western Reserve School of Medicine, Cleveland, OH, USA. Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Department of Public Health Sciences, University of Miami Miller School of Medicine, Miami, FL, USA. Electronic address: farren.briggs@case.edu.
 Department of Physical Education and Sports Sciences, Faculty of Humanities, Rasht Branch, Islamic Azad University, Rasht, Iran. Department of Physical Education and Sports Sciences, Faculty of Humanities, Rasht Branch, Islamic Azad University, Rasht, Iran. Department of Physical Education and Sports Sciences, Faculty of Humanities, Rasht Branch, Islamic Azad University, Rasht, Iran.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Faculty of Medicine and Surgery, Vita-Salute San Raffaele University, 20132 Milan, Italy. Faculty of Medicine and Surgery, Vita-Salute San Raffaele University, 20132 Milan, Italy. Department of Cardiac Electrophysiology and Arrhythmology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Myocarditis Disease Unit, IRCCS San Raffaele Scientific Institute, 20019 Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Faculty of Medicine and Surgery, Vita-Salute San Raffaele University, 20132 Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Faculty of Medicine and Surgery, Vita-Salute San Raffaele University, 20132 Milan, Italy. Department of Cardiac Electrophysiology and Arrhythmology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Myocarditis Disease Unit, IRCCS San Raffaele Scientific Institute, 20019 Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Faculty of Medicine and Surgery, Vita-Salute San Raffaele University, 20132 Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
 Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Immunology, Isfahan University of Medical Science, Isfahan, Iran. Multiple Sclerosis Research Group (MSRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. Medical School, Isfahan University of Medical Science, Isfahan, Iran. Student's Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. mghajar2@jhmi.edu. Multiple Sclerosis Research Group (MSRG), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. mghajar2@jhmi.edu.

 Max Rady College of Medicine (ARV), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada; Department of Ophthalmology and Vision Sciences (NBB, JM, EM), University of Toronto, Toronto, Canada; and Division of Neurology (JM, EM), Department of Medicine, University of Toronto, Toronto, Canada.
 Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America. Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America. Department of Research, Jesse Brown VA Medical Center, Chicago, IL 60612, United States of America. Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America. Department of Research, Jesse Brown VA Medical Center, Chicago, IL 60612, United States of America; Department of Anesthesiology, University of Illinois, Chicago, IL 60612, United States of America. Electronic address: dlfeins@uic.edu. Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America. Electronic address: gmorfini@uic.edu.

 Developmental and Biomedical Genetics Laboratory, Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India. School of Computational and Integrative Science, Jawaharlal Nehru University, New Delhi, India. Developmental and Biomedical Genetics Laboratory, Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India. Developmental and Biomedical Genetics Laboratory, Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India. Developmental and Biomedical Genetics Laboratory, Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India.
 Université Paris Cité, INSERM UMRS 1266, Institute of Psychiatry and Neuroscience of Paris, GHU Paris Psychiatrie et Neurosciences, Paris, France. Institute of Biology Paris Seine, Neuroscience Paris Seine, CNRS UMR 8246, INSERM U1130, Sorbonne Université, Paris, France. Université Paris Cité, INSERM UMRS 1266, Institute of Psychiatry and Neuroscience of Paris, GHU Paris Psychiatrie et Neurosciences, Paris, France. Institute of Biology Paris Seine, Neuroscience Paris Seine, CNRS UMR 8246, INSERM U1130, Sorbonne Université, Paris, France.
 Department of Public Health and Community Medicine, Faculty of Medicine, Cairo University, Cairo, Egypt. Department of Neurology, Faculty of Medicine, Cairo University, Cairo, Egypt. Department of Clinical Nutrition, National Nutrition Institute, Cairo, Egypt. Department of Public Health and Community Medicine, Faculty of Medicine, Cairo University, Cairo, Egypt. Department of Public Health and Community Medicine, Faculty of Medicine, Cairo University, Cairo, Egypt. mr80002000@kasralainy.edu.eg.
 Case Westerns Reserve University School of Medicine, Cleveland, OH, United States of America. Case Westerns Reserve University School of Medicine, Cleveland, OH, United States of America; Multiple Sclerosis and Neuroimmunology Program, University Hospitals Cleveland Medical Center, Cleveland, OH, United States of America. Case Westerns Reserve University School of Medicine, Cleveland, OH, United States of America. Duke University Medical Center, Durham, NC, United States of America. Case Westerns Reserve University School of Medicine, Cleveland, OH, United States of America; Multiple Sclerosis and Neuroimmunology Program, University Hospitals Cleveland Medical Center, Cleveland, OH, United States of America; MS Center of Excellence, Cleveland Veterans Affairs Medical Center, United States of America. Case Westerns Reserve University School of Medicine, Cleveland, OH, United States of America; Multiple Sclerosis and Neuroimmunology Program, University Hospitals Cleveland Medical Center, Cleveland, OH, United States of America; Department of Ophthalmology, University Hospitals Cleveland Medical Center, United States of America. Case Westerns Reserve University School of Medicine, Cleveland, OH, United States of America; Multiple Sclerosis and Neuroimmunology Program, University Hospitals Cleveland Medical Center, Cleveland, OH, United States of America. Electronic address: Hesham.abboud@uhhospitals.org.
 Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin 10098, Germany. Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin 10117, Germany. Department of Experimental Neurology, Center for Stroke Research Berlin, Berlin 10117, Germany. NeuroCure Cluster of Excellence and Charité Core Facility 7T Experimental MRIs, Charité - Universitätsmedizin Berlin, Berlin 10117, Germany. Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin 10098, Germany. Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin 10117, Germany. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam 1007 MB, The Netherlands. Annenberg School for Communication, University of Pennsylvania, Philadelphia 19104, PA, USA. Department of Bioengineering, University of Pennsylvania, Philadelphia 19104, PA, USA. Leonard Davis Institute of Health Economics, University of Pennsylvania, Philadelphia 19104, PA, USA. Department of Biological Engineering, School of Engineering & Applied Science, University of Pennsylvania, Philadelphia 19104, PA, USA. Department of Physics & Astronomy, College of Arts & Sciences, University of Pennsylvania, Philadelphia 19104, PA, USA. Department of Electrical & Systems Engineering, School of Engineering and Applied Science, University of Pennsylvania, Philadelphia 19104, PA, USA. Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia 19104, PA, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia 19104, PA, USA. Santa Fe Institute, Santa Fe 87501, NM, USA. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam 1007 MB, The Netherlands. Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin 10098, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Berlin 10117, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin 10017, Germany. Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin 10098, Germany. Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin 10117, Germany.
 Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Neurology Unit, Department of Translational Medicine, AOU Maggiore della Carità Novara, University of Eastern Piedmont, Novara, Italy. Department of Neurology, Santi Antonio e Biagio e Cesare Arrigo Hospital, Alessandria, Italy. Neurology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. Department of Neuroscience, MS Center, S. Maria delle Croci Hospital, AUSL Romagna, Ravenna, Italy. Department of Biotechnological and Applied Clinical Sciences (DISCAB), University of L'Aquila, L'Aquila, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, Department of Neurosciences, Mental Health and Sensory organs (NESMOS), Sapienza University of Rome, Rome, Italy. Clinical Neurology Unit, Department of Head, Neck and Neurosciences, Santa Maria della Misericordia University Hospital, Udine, Italy. UOSC Neuro-Stroke Unit, AORN Antonio Cardarelli, Naples, Italy. Section of Neurology, Department of Biomedicine, Neurosciences and Advanced Diagnostics (BiND), University of Palermo, Palermo, Italy. Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Department of Clinical and Biological Sciences, University of Turin, Turin, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy.
 Multiple Sclerosis Comprehensive Care Center, RWJ Barnabas Health, Livingston, NJ, USA. Multiple Sclerosis Comprehensive Care Center, RWJ Barnabas Health, Livingston, NJ, USA. Multiple Sclerosis Comprehensive Care Center, RWJ Barnabas Health, Livingston, NJ, USA. Multiple Sclerosis Comprehensive Care Center, RWJ Barnabas Health, Livingston, NJ, USA. Biogen, Weston, MA, USA. Biogen, Weston, MA, USA. Biogen, Weston, MA, USA. Multiple Sclerosis Comprehensive Care Center, RWJ Barnabas Health, Livingston, NJ, USA. Matthew.Tremblay@rwjbh.org.
 Department of Neurology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Neurology, Imam Hossein Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Clinical Pharmacy, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: sahraian1350@yahoo.com.
 Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. sarah.schlaeger@tum.de. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. jung diagnostics GmbH, Hamburg, Germany. jung diagnostics GmbH, Hamburg, Germany. jung diagnostics GmbH, Hamburg, Germany. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Department of Diagnostic, Interventional and Pediatric Radiology, Inselspital, University Hospital, University of Bern, Bern, Switzerland. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. DIE RADIOLOGIE, Munich, Germany. Department of Neurology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
 Social Determinants of Health Research Center, Aligoudarz School of Nursing, Lorestan University of Medical Sciences, Khorramabad, Iran. School of Nursing and Midwifery, Hamadan University of Medical Sciences, Hamadan, Iran. Chronic Diseases (Home Care) Research Center, Department of Medical-Surgical Nursing, School of Nursing and Midwifery, Hamadan University of Medical Sciences, Hamadan, Iran. Modeling of Noncommunicable Diseases Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Neurology, Medical School, Hamadan University of Medical Sciences, Hamadan, Iran. Mother and Child Care Research Center, Department of Ethics Education in Medical Sciences, Department of Medical-Surgical Nursing, School of Nursing and Midwifery, Hamadan University of Medical Sciences, Hamadan, Iran.
 CEMEREM, APHM La Timone, 264 Rue Saint-Pierre, 13385, Marseille, France. CNRS, CRMBM, UMR 7339, Aix-Marseille Univ, Marseille, France. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Neurologische Klinik, Klinikum Aschaffenburg-Alzenau, Aschaffenburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Universitäres Kompetenzzentrum für Sport- und Bewegungsmedizin (Athleticum) und Institut und Poliklinik für Medizinische Psychologie, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Universitäres Kompetenzzentrum für Sport- und Bewegungsmedizin (Athleticum) und Institut und Poliklinik für Medizinische Psychologie, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Psychiatry and Psychotherapy, Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany. Division of Psychosomatic Medicine, Medical Department, Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany. CEMEREM, APHM La Timone, 264 Rue Saint-Pierre, 13385, Marseille, France. jan-patrick.stellmann@univ-amu.fr. CNRS, CRMBM, UMR 7339, Aix-Marseille Univ, Marseille, France. jan-patrick.stellmann@univ-amu.fr. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. jan-patrick.stellmann@univ-amu.fr.
 Speech and Language Pathology Unit, Department of Health and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Speech and Language Pathology Unit, Department of Health and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Division of Speech and Language Pathology, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. Medical Unit Speech and Language Pathology, Karolinska University Hospital, Stockholm, Sweden. Speech and Language Pathology Unit, Department of Health and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Speech and Language Pathology Unit, Department of Health and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Speech and Language Pathology Unit, Department of Health and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
 Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Ordu University, Ordu, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Sivas Cumhuriyet University, Sivas, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Aydın Adnan Menderes University, Aydın, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Lokman Hekim University, Faculty of Medicine, Department of Neurology, Neuroimmunology Unit, Ankara, Turkey.
 Department of Neurology, School of Medicine, Technical University of Munich, Klinikum rechts der Isar, München, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Klinikum rechts der Isar, München, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Klinikum rechts der Isar, München, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Klinikum rechts der Isar, München, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Klinikum rechts der Isar, München, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Klinikum rechts der Isar, Ismaninger Str. 22, München, 81675, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
 Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Imaging Department, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Center for Sensory-Motor Interaction, Denmark Neurology Unit, Aalborg University, 922 Aalborg, Denmark. Developmental Neurology Unit, Bambino Gesù Children's Hospital IRCCS, 00165 Rome, Italy. Child Neurology and Psychiatry Unit, Systems Medicine Department, Tor Vergata University of Rome, 00133 Rome, Italy.
 BD Center Ltd., Rzeszow, Poland. Clinical Hospital No 2 in Rzeszow, Rzeszow, Poland. Subcarpathian Center for Neurorehabilitation, Rzeszow, Poland. BD Center Ltd., Rzeszow, Poland. Clinical Hospital No 2 in Rzeszow, Rzeszow, Poland. Department of Physiotherapy, Institute of Health Sciences, College of Medical Sciences, University of Rzeszów, Rzeszow, Poland. Department of Physiotherapy, Institute of Health Sciences, College of Medical Sciences, University of Rzeszów, Rzeszow, Poland. Clinical Hospital No 2 in Rzeszow, Rzeszow, Poland. Department of Neurology, Institute of Medical Sciences, College of Medical Sciences, University of Rzeszów, Rzeszow, Poland.
 National Center for Health Insurance Research, Tehran, Iran. Department of Health Management and Economics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Social Welfare Management Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Social Determinants of Health Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of Occupational Therapy, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran. Department of social welfare management, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Department of social welfare management, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iranan.
 Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123, Catania, Italy. Department of Clinical and Experimental Medicine, University of Messina, 98122, Messina, Italy. Department of Medical and Surgical Sciences and Advanced Technologies, University of Catania, Via S. Sofia 78, 95123, Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123, Catania, Italy. Institute for Research in Biomedical Sciences, University Center for Health Sciences, University of Guadalajara, Guadalajara, Mexico. Institute for Research in Biomedical Sciences, University Center for Health Sciences, University of Guadalajara, Guadalajara, Mexico. Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123, Catania, Italy. ferdinic@unict.it. Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123, Catania, Italy.
 Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Institute for Brain and Cognition, Tarbiat Modares University, Tehran, Iran. Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. mjavan@modares.ac.ir. Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. mjavan@modares.ac.ir. Institute for Brain and Cognition, Tarbiat Modares University, Tehran, Iran. mjavan@modares.ac.ir. International Collaboration on Repair Discoveries (ICORD), the University of British Columbia, Vancouver, BC, Canada. mjavan@modares.ac.ir.
 Department of Radiology, Samsun Education and Research Hospital, İlkadım, 55060, Samsun, Turkey. barisgenc12@gmail.com. Department of Neuroradiology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey. Department of Neurology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey. Department of Neuroradiology, Ondokuz Mayıs University School of Medicine, Samsun, Turkey.
 Department of Neurology, Hospital Clínico Universitario de Valladolid, Valladolid, Spain. pmulero@saludcastillayleon.es. Departament of Health Sciences, Universidad Europea Miguel de Cervantes, Valladolid, Spain. Department of Neurology, Hospital Clínico Universitario de Valladolid, Valladolid, Spain. Research Support Unit, Hospital Clínico Universitario de Valladolid, Valladolid, Spain. Department of Neurology, Hospital Clínico Universitario de Valladolid, Valladolid, Spain. Institute of Molecular Biology and Genetics (IBGM-CSIC/Uva), (IBGM-CSIC/Uva), Valladolid, Spain. Institute of Molecular Biology and Genetics (IBGM-CSIC/Uva), (IBGM-CSIC/Uva), Valladolid, Spain. Institute of Molecular Biology and Genetics (IBGM-CSIC/Uva), (IBGM-CSIC/Uva), Valladolid, Spain. Institute of Molecular Biology and Genetics (IBGM-CSIC/Uva), (IBGM-CSIC/Uva), Valladolid, Spain. Department of Neurology, Hospital Clínico Universitario de Valladolid, Valladolid, Spain.
 Graduate Institute of Public Health, China Medical University, Taichung 406040, Taiwan. Genetic and Rare Disease Center, China Medical University Hospital, China Medical University, Taichung 404327, Taiwan. Graduate Institute of Public Health, China Medical University, Taichung 406040, Taiwan. Department of Healthcare Administration, Asia University, Taichung 41354, Taiwan. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404327, Taiwan. Department of Health Services Administration, College of Public Health, China Medical University, Taichung 406040, Taiwan. Genetic and Rare Disease Center, China Medical University Hospital, China Medical University, Taichung 404327, Taiwan. Center for General Education, China Medical University, Taichung 406040, Taiwan. Department of Health Services Administration, College of Public Health, China Medical University, Taichung 406040, Taiwan.
 Department of Neurology, Chungnam National University Hospital, Chungnam National University College of Medicine, Daejeon 35015, Republic of Korea. Department of Neurology, Chungnam National University Sejong Hospital, Chungnam National University College of Medicine, Daejeon 35015, Republic of Korea. Department of Radiology, Chungnam National University Hospital, Chungnam National University College of Medicine, Daejeon 35015, Republic of Korea. Department of Neurology, Chungnam National University Hospital, Chungnam National University College of Medicine, Daejeon 35015, Republic of Korea.
 Department of Pharmacy (KR, ER, JW), University of Rochester Medical Center, Rochester, NY, USA. Department of Pharmacy (KR, ER, JW), University of Rochester Medical Center, Rochester, NY, USA. Department of Neurology (JSD), University of Rochester Medical Center, Rochester, NY, USA. Clinical Nursing Research Center (BWQ), University of Rochester Medical Center, Rochester, NY, USA. Department of Pharmacy (KR, ER, JW), University of Rochester Medical Center, Rochester, NY, USA.
 Department of Radiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40000, Thailand. Department of Radiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40000, Thailand.
 Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Pharmaceutical Analysis Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Medicinal Chemistry, School of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran. Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
 Department of Ophthalmology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China. Graduate School of Peking Union Medical College, Beijing, China. Department of Ophthalmology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China. Department of Ophthalmology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China. Department of Ophthalmology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China. Department of Ophthalmology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China. Graduate School of Peking Union Medical College, Beijing, China.
 Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. Electronic address: k3717663@kadai.co.jp. Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. Electronic address: nayuhiga@m.kufm.kagoshima-u.ac.jp. Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan.
 Recovery & Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada. Recovery & Performance Laboratory, Faculty of Medicine, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada.
 Department of Physical Medicine and Rehabilitation, Giresun University Faculty of Medicine, Giresun, Türkiye. Department of Physical Medicine and Rehabilitation, Necmettin Erbakan University Meram Faculty of Medicine, Konya, Türkiye.
 Department of Psychology, Carl Von Ossietzky University Oldenburg, Oldenburg, Germany. g.garis1992@gmail.com. Department of Neurology, Klinikum Bremen-Ost, 28325, Bremen, Germany. g.garis1992@gmail.com. Kliniken Schmieder, Constance, Baden-Würtemberg, Germany. Department of Psychology, Carl Von Ossietzky University Oldenburg, Oldenburg, Germany. Department of Neurology, Klinikum Bremen-Ost, 28325, Bremen, Germany. Department of Psychology, Carl Von Ossietzky University Oldenburg, Oldenburg, Germany. helmut.hildebrandt@uni-oldenburg.de. Department of Neurology, Klinikum Bremen-Ost, 28325, Bremen, Germany. helmut.hildebrandt@uni-oldenburg.de.
 Department of Neurology, Nancy University Hospital, 54035, Nancy, France. Université de Lorraine, APEMAC, 54000, Nancy, France. CHRU-Nancy, INSERM, Université de Lorraine, CIC, Epidémiologie Clinique, 54000, Nancy, France. CHRU-Nancy, INSERM, Université de Lorraine, CIC, Epidémiologie Clinique, 54000, Nancy, France. Université de Lorraine, APEMAC, 54000, Nancy, France. CHRU-Nancy, INSERM, Université de Lorraine, CIC, Epidémiologie Clinique, 54000, Nancy, France. Department of Neurology, Nancy University Hospital, 54035, Nancy, France. Department of Neurology, Nancy University Hospital, 54035, Nancy, France. Université de Lorraine, APEMAC, 54000, Nancy, France. Department of Neurology, Nancy University Hospital, 54035, Nancy, France. g.mathey@chru-nancy.fr. Université de Lorraine, APEMAC, 54000, Nancy, France. g.mathey@chru-nancy.fr.
 Department of Biomedical Engineering, Schulich School of Engineering, University of Calgary, Calgary, AB, Canada. Department of Neuroscience, Faculty of Graduate Studies, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Department of Radiology, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Department of Radiology, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
 Department of Internal Medicine, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH, USA. The Esophageal and Swallowing Center, Division of Gastroenterology and Hepatology, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH, USA. Department of Internal Medicine, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH, USA. The Esophageal and Swallowing Center, Division of Gastroenterology and Hepatology, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH, USA.
 School of Medicine, , Baylor College of MedicineHouston, Texas, USA. School of Medicine, , Baylor College of MedicineHouston, Texas, USA. School of Medicine, , Baylor College of MedicineHouston, Texas, USA. Department of Ophthalmology, Cullen Eye Institute, , Baylor College of MedicineHouston, Texas, USA. Department of Ophthalmology, Blanton Eye Institute, , Houston Methodist HospitalHouston, Texas, USA. Departments of Ophthalmology, Neurology, and Neurosurgery, , Weill Cornell MedicineNew York, New York, USA. Department of Ophthalmology, , University of Texas Medical BranchGalveston, Texas, USA. Department of Ophthalmology, , University of Texas MD Anderson Cancer CenterHouston, Texas, USA. Department of Ophthalmology, , Texas A and M College of MedicineBryan, Texas, USA. Department of Ophthalmology, , The University of Iowa Hospitals and ClinicsIowa City, Iowa, USA.
 Department of Radiology, University of Ottawa, ON, Canada. RINGGOLD: 6363 Department of Radiology, University of Ottawa, ON, Canada. RINGGOLD: 6363 Department of Radiology, University of Ottawa, ON, Canada. RINGGOLD: 6363 Radiology Department, United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, United Arab Emirates. RINGGOLD: 62776 Department of Medicine, University of Ottawa, ON, Canada. RINGGOLD: 6363 Department of Radiology, University of Ottawa, ON, Canada. RINGGOLD: 6363
 EBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research University of Sydney Sydney NSW Australia. The Graduate School of Biomedical Engineering University of New South Wales Sydney NSW Australia. Kirby Institute University of New South Wales Sydney NSW Australia. RNA Institute University of New South Wales Sydney NSW Australia. EBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research University of Sydney Sydney NSW Australia. Department of Medicine Western Sydney University Sydney NSW Australia. EBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research University of Sydney Sydney NSW Australia. Biomedical Informatics and Digital Health, School of Medical Sciences, Faculty of Medicine and Health The University of Sydney Sydney NSW Australia.
 Health Sciences University, Hamidiye Faculty of Medicine, Department of Neurology, İstanbul, Turkey. Health Sciences University Haseki Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Health Sciences University Haseki Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Health Sciences University Haseki Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Health Sciences University, Hamidiye Faculty of Medicine, Department of Neurology, İstanbul, Turkey. Health Sciences University, Hamidiye Faculty of Medicine, Department of Neurology, İstanbul, Turkey.
 Department of Clinical Biochemistry, Manchester University NHS Foundation Trust, Manchester, UK. RINGGOLD: 5293 The Neuroscience Laboratories, The Walton Centre NHS Foundation Trust, Liverpool, UK. RINGGOLD: 195157
 Department of Neuroimmunology, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Postgraduate School, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Neuroimmunology, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Molecular Virology, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.
 Medical School, Marmara University, IstanbulTurkey. Medical School, Marmara University, IstanbulTurkey. Medical School, Marmara University, IstanbulTurkey. Medical School, Marmara University, IstanbulTurkey. Medical School, Marmara University, IstanbulTurkey. Clinic of Neurology, Istanbul Okan University, Istanbul, Turkey. The Edison Biotechnology Institute, Ohio University, Athens, OH, USA. Department of Medical Genetics, Medical School, Marmara University, IstanbulTurkey.
 Department of Neurology, Faculty of Medicine, University of Augsburg, Augsburg, Germany. Novartis Pharma GmbH, Nuremberg, Germany. Department of Neurology, Faculty of Medicine, University of Augsburg, Augsburg, Germany.
 Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. mhabek@mef.hr. School of Medicine, University of Zagreb, Zagreb, Croatia. mhabek@mef.hr. Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Department of Neurology, University Medical Centre Ljubljana, Ljubljana, Slovenia. University Clinic for Neurology Skopje, Skopje, North Macedonia. Department of Neurology, Clinical Center of Montenegro, Podgorica, Montenegro. Department of Neurology, University of Szeged, Szeged, Hungary. Department of Neurology, Medical University of Lublin, Lublin, Poland. 1St Department of Neurology, Medical Faculty, Comenius University, Bratislava, Slovak Republic.
 Unità di Urologia, Ospedale San Raffaele (IRCCS), Milan, Italy. Unità di Ricerca sulla Teoria della Mente, Dipartimento di Psicologia, Università Cattolica del Sacro Cuore, Milan, Italy. Unità di Ricerca sulla Teoria della Mente, Dipartimento di Psicologia, Università Cattolica del Sacro Cuore, Milan, Italy. Unità di Ricerca sulla Teoria della Mente, Dipartimento di Psicologia, Università Cattolica del Sacro Cuore, Milan, Italy. Unità di Ricerca sulla Teoria della Mente, Dipartimento di Psicologia, Università Cattolica del Sacro Cuore, Milan, Italy. Fondazione Don Carlo Gnocchi Onlus (IRCCS), Milan, Italy. Fondazione Don Carlo Gnocchi Onlus (IRCCS), Milan, Italy. Università Cattolica del Sacro Cuore, Milan, Italy. Fondazione Don Carlo Gnocchi Onlus (IRCCS), Milan, Italy. Fondazione Don Carlo Gnocchi Onlus (IRCCS), Milan, Italy. Unità di Ricerca sulla Teoria della Mente, Dipartimento di Psicologia, Università Cattolica del Sacro Cuore, Milan, Italy.
 1st Department of Neurology, Eginition Hospital, National and Kapodistrian University of Athens, Athens, Greece. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Greece and Joint Academic Rheumatology Program, Departments of Physiology and Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
 Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Ecumenic Hainich Hospital GmbH, 99974 Mühlhausen, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Ecumenic Hainich Hospital GmbH, 99974 Mühlhausen, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Ecumenic Hainich Hospital GmbH, 99974 Mühlhausen, Germany. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany. Ecumenic Hainich Hospital GmbH, 99974 Mühlhausen, Germany. Ecumenic Hainich Hospital GmbH, 99974 Mühlhausen, Germany. Ecumenic Hainich Hospital GmbH, 99974 Mühlhausen, Germany. Faculty of Health Sciences, University of Hull, Hull HU6 7RX, UK. The Palatine Centre, Durham Law School, Durham University, Durham DH1 3LE, UK. Section of Neuroimmunology, Department of Neurology, Rostock University Medical Centre, 18147 Rostock, Germany.
 Facultad de Medicina, Instituto de Medicina Molecular Aplicada (IMMA), Universidad San Pablo-CEU, CEU Universities, Madrid, Spain. Facultad de Medicina, Instituto de Medicina Molecular Aplicada (IMMA), Universidad San Pablo-CEU, CEU Universities, Madrid, Spain. Facultad de Medicina, Instituto de Medicina Molecular Aplicada (IMMA), Universidad San Pablo-CEU, CEU Universities, Madrid, Spain. Facultad de Medicina, Instituto de Medicina Molecular Aplicada (INMA), Universidad San Pablo-CEU, CEU Universities, Crta Boadilla del Monte Km 5,3, Madrid 28668, Spain.
 Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, NY, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
 Department of Rehabilitation, Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA. Department of Rehabilitation, Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA. Department of Rehabilitation, Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA. Department of Rehabilitation, Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA. Department of Rehabilitation, Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA. Department of Rehabilitation, Rowan-Virtua School of Osteopathic Medicine, Stratford, NJ, USA. NeuroMusculoskeletal Institute, Rowan Medicine, Stratford, NJ, USA.
 Department of Motor Sciences and Wellness, University of Naples "Parthenope", Naples, Italy. Institute of Applied Sciences and Intelligent Systems, National Research Council, Italy. Department of Social and Developmental Psychology, Sapienza University of Rome, Italy. Department of Motor Sciences and Wellness, University of Naples "Parthenope", Naples, Italy. Department of Motor Sciences and Wellness, University of Naples "Parthenope", Naples, Italy. Institute for Diagnosis and Cure Hermitage Capodimonte, Italy. Department of Motor Sciences and Wellness, University of Naples "Parthenope", Naples, Italy. Department of Motor Sciences and Wellness, University of Naples "Parthenope", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "L. Vanvitelli", Naples, Italy. Institut de Neurosciences des Systèmes, Aix-Marseille Université, Marseille, France. Department of Motor Sciences and Wellness, University of Naples "Parthenope", Naples, Italy; Institute of Applied Sciences and Intelligent Systems, National Research Council, Italy; Institute for Diagnosis and Cure Hermitage Capodimonte, Italy. Electronic address: giuseppe.sorrentino@uniparthenope.it. Institute of Applied Sciences and Intelligent Systems, National Research Council, Italy; Institut de Neurosciences des Systèmes, Aix-Marseille Université, Marseille, France; Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
 Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE)-IRCCS-Scientific Institute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE)-IRCCS-Scientific Institute San Raffaele, Milan, Italy. Faculty of Medicine, Università Vita-Salute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE)-IRCCS-Scientific Institute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE)-IRCCS-Scientific Institute San Raffaele, Milan, Italy. Faculty of Medicine, Università Vita-Salute San Raffaele, Milan, Italy. Department of Neurorehabilitation Sciences, Casa di Cura Igea, Milan, Italy. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE)-IRCCS-Scientific Institute San Raffaele, Milan, Italy. Faculty of Medicine, Università Vita-Salute San Raffaele, Milan, Italy.
 From the Dent Neurologic Institute, Buffalo, NY, USA (MMR, TSA, AGM, KM, LM). The University at Buffalo School of Pharmacy and Pharmaceutical Sciences, Buffalo, NY, USA (MMR, TSA, AGM, EL, DV). From the Dent Neurologic Institute, Buffalo, NY, USA (MMR, TSA, AGM, KM, LM). The University at Buffalo School of Pharmacy and Pharmaceutical Sciences, Buffalo, NY, USA (MMR, TSA, AGM, EL, DV). From the Dent Neurologic Institute, Buffalo, NY, USA (MMR, TSA, AGM, KM, LM). The University at Buffalo School of Pharmacy and Pharmaceutical Sciences, Buffalo, NY, USA (MMR, TSA, AGM, EL, DV). The University at Buffalo School of Pharmacy and Pharmaceutical Sciences, Buffalo, NY, USA (MMR, TSA, AGM, EL, DV). The University at Buffalo School of Pharmacy and Pharmaceutical Sciences, Buffalo, NY, USA (MMR, TSA, AGM, EL, DV). From the Dent Neurologic Institute, Buffalo, NY, USA (MMR, TSA, AGM, KM, LM). From the Dent Neurologic Institute, Buffalo, NY, USA (MMR, TSA, AGM, KM, LM).
 Faculty of Health Sciences, Universidad de León, 24071 Leon, Spain. Department of Health Sciences, European University Miguel de Cervantes, 47012 Valladolid, Spain. Research Center on Physical Disability, ASPAYM Castilla y León, 47008 Valladolid, Spain. Institute of Biomedicine (BIOMED), Universidad de León, 24071 Leon, Spain. Physiology Department, University of the Basque Country, 48940 Leioa, Spain.
 Men's Health and Reproductive Health Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Phytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Medical Biotechnology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Dietary Supplements and Probiotic Research Center, Alborz University of Medical Sciences, Karaj, Iran. Department of Clinical Analysis, College of Pharmacy, Hawler Medical University, Kurdistan Region, Erbil, Iraq. Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Institute of Human Genetics, Jena University Hospital, Jena, Germany. Department of Neurosurgery, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 Faculty of Medicine at the Getulio Vargas Hospital, Federal University of Amazonas, Tomas de Villa Nova, N. 4, Praca 14, Manaus, AM, ZIP 69020-170, Brazil. School of Health Sciences, University of Amazonas, Carvalho Leal Street, N. 1777, Manaus, AM, ZIP 69065-001, Brazil. acrmauri33@gmail.com. Faculty of Medicine at the Getulio Vargas Hospital, Federal University of Amazonas, Tomas de Villa Nova, N. 4, Praca 14, Manaus, AM, ZIP 69020-170, Brazil. Faculty of Medicine at the Getulio Vargas Hospital, Federal University of Amazonas, Tomas de Villa Nova, N. 4, Praca 14, Manaus, AM, ZIP 69020-170, Brazil. Faculty of Medicine at the Getulio Vargas Hospital, Federal University of Amazonas, Tomas de Villa Nova, N. 4, Praca 14, Manaus, AM, ZIP 69020-170, Brazil.
 Department of Psychology, Wayne State University, Detroit, MI, USA. Department of Psychology, Wayne State University, Detroit, MI, USA. Department of Neurology, Wayne State University School of Medicine, Detroit, MI, USA. Department of Physical Medicine & Rehabilitation, Wayne State University School of Medicine, Detroit, MI, USA. Department of Neurology, Wayne State University School of Medicine, Detroit, MI, USA.
 MS center, Department of Neurology, ASST Lecco, Lecco, Italy. Electronic address: vittorio.mantero@hotmail.com. MS center, Department of Neurology, ASST Lecco, Lecco, Italy. MS center, Department of Neurology, ASST Lecco, Lecco, Italy. MS center, Department of Neurology, ASST Lecco, Lecco, Italy. Neuropsychology service, ASST Lecco, Lecco, Italy. MS center, Department of Neurology, ASST Lecco, Lecco, Italy; Neuropsychology service, ASST Lecco, Lecco, Italy. UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, USA.
 Department of Neurology and Institute of Neurology of The First Affiliated Hospital, Institute of Neuroscience, Fuzhou, China. Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China. Department of Neurology and Institute of Neurology of The First Affiliated Hospital, Institute of Neuroscience, Fuzhou, China. Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China. Department of Neurology and Institute of Neurology of The First Affiliated Hospital, Institute of Neuroscience, Fuzhou, China. Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China. Department of Neurology and Institute of Neurology of The First Affiliated Hospital, Institute of Neuroscience, Fuzhou, China. Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China. Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Department of Neuroimaging, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Department of Neurology and Institute of Neurology of The First Affiliated Hospital, Institute of Neuroscience, Fuzhou, China. Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China. Department of Neurology and Institute of Neurology of The First Affiliated Hospital, Institute of Neuroscience, Fuzhou, China. Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, China. Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
 Department of Neurology, Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Rehabilitation Medicine, First Faculty of Medicine and General University Hospital, Prague, Czech Republic. Department of Neurology, Second Faculty of Medicine, Charles University and University Hospital, Motol, Czech Republic. Department of Neurology, Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology, Second Faculty of Medicine, Charles University and University Hospital, Motol, Czech Republic. Department of Neurology, Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Spin-off Application Centre, The First Faculty of Medicine, Charles University, Prague Czech Republic. Czech Technical University, Prague, Czech Republic.
 Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine Department, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Movement Analysis, Biomechanics, Ergonomics, and Motor Control Laboratory, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine Department, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Movement Analysis, Biomechanics, Ergonomics, and Motor Control Laboratory, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine Department, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Movement Analysis, Biomechanics, Ergonomics, and Motor Control Laboratory, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Movement Analysis, Biomechanics, Ergonomics, and Motor Control Laboratory, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine Department, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain. Movement Analysis, Biomechanics, Ergonomics, and Motor Control Laboratory, Faculty of Health Sciences, Rey Juan Carlos University, 28922 Madrid, Spain.
 School of Biomedical Engineering, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Radiology, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Department of Radiology, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. School of Biomedical Engineering, University of British Columbia, Vancouver, BC, Canada. Department of Radiology, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada.
 From the Mental Health Policy Unit, Health Research Institute, Faculty of Health, University of Canberra, Canberra, ACT, Australia (HT-J, NB, MAF, JAS, LS-C). From the Mental Health Policy Unit, Health Research Institute, Faculty of Health, University of Canberra, Canberra, ACT, Australia (HT-J, NB, MAF, JAS, LS-C). From the Mental Health Policy Unit, Health Research Institute, Faculty of Health, University of Canberra, Canberra, ACT, Australia (HT-J, NB, MAF, JAS, LS-C). Department of Neurology, Canberra Hospital, Canberra, ACT, Australia (CL). Australian National University Medical School, Canberra, ACT, Australia (CL). From the Mental Health Policy Unit, Health Research Institute, Faculty of Health, University of Canberra, Canberra, ACT, Australia (HT-J, NB, MAF, JAS, LS-C). From the Mental Health Policy Unit, Health Research Institute, Faculty of Health, University of Canberra, Canberra, ACT, Australia (HT-J, NB, MAF, JAS, LS-C). Department of Quantitative Methods, Loyola University Andalucia, Seville, Spain (JAS-P). From the Mental Health Policy Unit, Health Research Institute, Faculty of Health, University of Canberra, Canberra, ACT, Australia (HT-J, NB, MAF, JAS, LS-C). Menzies Centre for Health Policy, School of Public Health, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia (LS-C).
 Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada. Neurology, University of Alberta, Edmonton, Alberta, Canada. Neurology, University of Alberta, Edmonton, Alberta, Canada. Radiology and Diagnostic Imaging, University of Alberta, Edmonton, Alberta, Canada. Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada. Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada.
 Graduate School, Shandong Sport University, Jinan, Shandong, China. Graduate School, Shandong Sport University, Jinan, Shandong, China. College of Art and Design, Shaanxi University of Science and Technology, Xi'an, Shaanxi, China. Graduate School, Shandong Sport University, Jinan, Shandong, China. Graduate School, Shandong Sport University, Jinan, Shandong, China. Graduate School, Shandong Sport University, Jinan, Shandong, China. Laboratory of Sports Biomechanics, Shandong Institute of Sport Science, Jinan, Shandong, China.
 Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Rafael.Klimas@rub.de. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Facharztpraxis für Neurologie, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland. Klinik für Neurologie, St. Josef-Hospital, Ruhr-Universität Bochum, Gudrunstraße 56, 44791, Bochum, Deutschland.
 Department of Neurology, Health Research Institute of the Hospital Clínico San Carlos (IdISSC), Hospital Clinico San Carlos, Madrid, Spain. orejacbn@gmail.com. Departamento de Medicina, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Madrid, Spain. orejacbn@gmail.com. Human Reproduction Unit, Obstetrics and Gynaecology Department, Biocruces Health Research Institute, Cruces University Hospital, University of the Basque Country, Bilbao, Spain. Assisted Reproduction Institute, Fundación Jiménez Díaz, Madrid, Spain. Department of Neurology, Research Institute, Hospital Universitario de Getafe, Madrid, Spain. Neuroscience Department, Biocruces Health Research Institute, Cruces University Hospital, University of the Basque Country, Bilbao, Spain. Department of Neurology, Hospital Alvaro Cunqueiro, Vigo, Spain. Wilson Fertiliy-Balearic Center for In Vitro Fertilization CEFIVBA-Wilson Fertility, Mallorca, Spain.
 Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy. Section of Human, Clinic and Forensic Anatomy, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy. Section of General Pathology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Rome, Italy. Section of General Pathology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Rome, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy. GSTEP-Organoids Core Facility, Fondazione Policlinico Agostino Gemelli IRCCS, Rome, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy.
 Sanlıurfa Training and Research Hospital, Department of Neurology, Sanlıurfa, Turkey. Harran University School of Medicine, Department of Neurology, Sanlıurfa, Turkey. Electronic address: ozlem_uzunkaya@hotmail.com.
 Weill Cornell Medical College, Cornell University, New York, NY, USA. jaisperumal@gmail.com. Northwestern University, Chicago, IL, USA. New York University Grossman School of Medicine, New York, NY, USA. New York University Grossman School of Medicine, New York, NY, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA.
 Grup de recerca Salut i Atenció Sanitaria, University of Girona, Girona, Spain. Department of Neurology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Grup d'Investigació Multidisciplinari d'Infermeria, Vall d'Hebron Institut de Recerca (VHIR), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Expert Patient Program Catalonia, General Directorate of Health Planning and Research, Department of Health, Generalitat de Catalunya, Barcelona, Spain. Grup de recerca Salut i Atenció Sanitaria, University of Girona, Girona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Girona Multiple Sclerosis and Neuroimmunology Unit. Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona-Salt, Spain. Department of Neurology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Neurology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Neurology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Neurology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Department of Neurology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Neurodegeneration and Neuroinflammation Research Group, Girona Biomedical Research Institute (IDIBGI), Salt, Spain. Girona Multiple Sclerosis and Neuroimmunology Unit. Neurology Department, Dr. Josep Trueta University Hospital and Santa Caterina Hospital, Girona-Salt, Spain. Department of Medical Sciences, University of Girona, Girona, Spain. Grup de recerca Salut i Atenció Sanitaria, University of Girona, Girona, Spain.

 University of Ottawa, Faculty of Medicine, Ottawa, ON. Department of Ophthalmology, School of Medicine, University of Jeddah, Jeddah, Saudi Arabia; Department of Ophthalmology, University of Ottawa, Ottawa, ON. University of Ottawa, Faculty of Medicine, Ottawa, ON. Department of Ophthalmology, University of Ottawa, Ottawa, ON. Division of Neurology, University of Ottawa, Ottawa, ON. Department of Ophthalmology, University of Ottawa, Ottawa, ON. Electronic address: dalbreiki@toh.ca.
 Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Division of Gynecology and Obstetrics, Department of Surgical Sciences, University of Cagliari, Cagliari, Italy. Clinical Immunology, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy. Department of Neurosciences, ARNAS Brotzu, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
 Department of Human Anatomy, Medical University of Lublin, 4 Jaczewskiego St., 20-090 Lublin, Poland. Department of Human Anatomy, Medical University of Lublin, 4 Jaczewskiego St., 20-090 Lublin, Poland. Department of Psychiatric Nursing, Medical University of Lublin, 18 Szkolna St., 20-124 Lublin, Poland. Student Scientific Group at the Department of Family Medicine, 6a (SPSK1) Langiewicza St., 20-032 Lublin, Poland. Students Scientific Association at the Department of Human Anatomy, Medical University of Lublin, 20-090 Lublin, Poland. Students Scientific Association at the Department of Human Anatomy, Medical University of Lublin, 20-090 Lublin, Poland. Institute of Health Sciences, The John Paul II Catholic University of Lublin, Konstantynów 1 H, 20-708 Lublin, Poland.
 Institute of Biomedicine, Sports and Exercise Medicine, University of Eastern Finland, Kuopio, Finland. Electronic address: markolu@student.uef.fi. Research Unit of Clinical Medicine, Neurology, University of Oulu, Oulu, Finland; MRC, Oulu University Hospital and University of Oulu, Oulu, Finland; Clinical Neurosciences, University of Helsinki, Helsinki, Finland. Institute of Biomedicine, Sports and Exercise Medicine, University of Eastern Finland, Kuopio, Finland. School of Medicine, University of Eastern Finland, Kuopio, Finland. Institute of Biomedicine, Sports and Exercise Medicine, University of Eastern Finland, Kuopio, Finland.
 Center for Clinical Epidemiology, Odense University Hospital, Odense, Denmark. Research Unit of Clinical Epidemiology, Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Department of Gynecology and Obstetrics, University Hospital of Southern Jutland, Esbjerg, Denmark. Center for Clinical Epidemiology, Odense University Hospital, Odense, Denmark. Research Unit of Clinical Epidemiology, Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Department of Regional Research, University of Southern Denmark, Odense, Denmark. Multiple Sclerosis Clinic Hospital of Southern Jutland, Aabenraa, University of Southern Denmark, Odense, Denmark. Department of Regional Research, University of Southern Denmark, Odense, Denmark. Department of Gastroenterology, University Hospital of Southern Jutland, Esbjerg, Denmark. Center for Clinical Epidemiology, Odense University Hospital, Odense, Denmark. Research Unit of Clinical Epidemiology, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
 Central Nervous System, Blood and Peripheral Inflammation Lab, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Department of Pharmaceutical Sciences and Medicines, Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Central Nervous System, Blood and Peripheral Inflammation Lab, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Central Nervous System, Blood and Peripheral Inflammation Lab, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Central Nervous System, Blood and Peripheral Inflammation Lab, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Central Nervous System, Blood and Peripheral Inflammation Lab, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Multiple Sclerosis Group, Biodonostia Health Research Institute, Donostia-San Sebastian, Spain. Central Nervous System, Blood and Peripheral Inflammation Lab, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal. Department of Pharmaceutical Sciences and Medicines, Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
 Kufa University, Kufa College of Medicine, Al-Najaf, Iraq. Medical City, Baghdad Teaching Hospital, Baghdad, Iraq. University of Sulaimani, School of Medicine, Iraq. Medical City, Baghdad Teaching Hospital, Baghdad, Iraq. University of Fallujah, College of Medicine, Iraq. Neuroscience Teaching Hospital, Baghdad, Iraq. Basra College of Medicine, Department of Medicine, Iraq. Medical City, Baghdad Teaching Hospital, Baghdad, Iraq. Neuroscience Teaching Hospital, Baghdad, Iraq. University of Baghdad, Alkindy College of Medicine, Iraq. Medical City, Baghdad Teaching Hospital, Baghdad, Iraq. Merck KGaA Middle East Ltd., Merck KGaA, Darmstadt, Germany. Bamberg Hospital and University of Erlange, Germany.
 Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA.
 Adiyaman University Faculty of Medicine, Turkey. Electronic address: ealtunisik@adiyaman.edu.tr.
 Department of Neurology, 10th Military Research Hospital and Polyclinic, Bydgoszcz, Poland. luk.rzepinski@gmail.com. Sanitas - Neurology Outpatient Clinic, Bydgoszcz, Poland. luk.rzepinski@gmail.com. Department of Toxicology and Bromatology, Faculty of Pharmacy, Collegium Medicum of Nicolaus Copernicus University, Bydgoszcz, Poland. Multiple Sclerosis Foundation, Borne Sulinowo, Poland. Department of Toxicology and Bromatology, Faculty of Pharmacy, Collegium Medicum of Nicolaus Copernicus University, Bydgoszcz, Poland. Department of Neurology, 10th Military Research Hospital and Polyclinic, Bydgoszcz, Poland. Sanitas - Neurology Outpatient Clinic, Bydgoszcz, Poland.
 CRIC Bristol, Bristol Medical School, University of Bristol, Bristol, United Kingdom. Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom. Department of Engineering Mathematics, University of Bristol, Bristol, United Kingdom. Department of Mathematics, State University of New York at Buffalo, Buffalo, NY, United States. Department of Engineering Mathematics, University of Bristol, Bristol, United Kingdom. Laboratoire CeRSM (EA-2931), UPL, Université Paris Nanterre, Nanterre, France. Bristol and Avon Multiple Sclerosis Centre, The Brain Centre, Southmead Hospital, Bristol, United Kingdom. Bristol and Avon Multiple Sclerosis Centre, The Brain Centre, Southmead Hospital, Bristol, United Kingdom. Department of Biomedical and Health Informatics, University of Missouri - Kansas City School of Medicine, Kansas City, MO, United States. CRIC Bristol, Bristol Medical School, University of Bristol, Bristol, United Kingdom. Mental Health Research for Innovation Centre, Mersey Care NHS Foundation Trust, Hollins Park House, Warrington, United Kingdom.
 The University of Queensland, Australia. University of Bologna, Italy. University of Bologna, Italy. University of Bologna, Italy.
 Stanford University Stanford CA USA. Stanford University Stanford CA USA. Stanford University Stanford CA USA. Stanford University Stanford CA USA.
 Facultad de Química, Universidad Nacional Autónoma de México, Mexico City, Mexico. Facultad de Ciencias Químicas, Universidad Veracruzana, Xalapa, Mexico. Laboratorio de Biología Molecular, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana, Mexico City, Mexico. Departamento de Neurología y Psiquiatría, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico. Departamento de Neurología y Psiquiatría, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
 National Ayurveda Research Institute for Panchakarma, Cheruthuruthy, Thrissur, Kerala, India. Electronic address: kmpvarma@gmail.com. Department Of Kayachikitsa, VPSV Ayurveda College, Kottakkal, Kerala, India. Department of Radiology, Government Medical College, Palakkad, Kerala, India.
 University of Illinois at Urbana-Champaign, USA. University of Colorado Colorado Springs, USA. University of Colorado Colorado Springs, USA.
 Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Gehlsheimer Str. 20, 18147 Rostock, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Department of Neurology, Ecumenic Hainich Hospital gGmbH, Mühlhausen, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany. Department of Neurology, Ecumenic Hainich Hospital gGmbH, Mühlhausen, Germany. Department of Neurology, Ecumenic Hainich Hospital gGmbH, Mühlhausen, Germany. Neuroimmunology Section, Department of Neurology, Rostock University Medical Center, Rostock, Germany.
 Curtin School of Population Health, Curtin University, Perth, Australia. Curtin School of Population Health, Curtin University, Perth, Australia. Curtin Health Innovation Research Institute, Curtin University, Perth, Australia. Curtin School of Population Health, Curtin University, Perth, Australia. Curtin School of Population Health, Curtin University, Perth, Australia. Curtin School of Population Health, Curtin University, Perth, Australia.
 Diagnostic Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy. Electronic address: alessandra.sottini@asst-spedalicivili.it. Diagnostic Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy. Diagnostic Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy; Laboratorio analisi, Ospedale Civile di Sondrio, ASST Valtellina e Alto Lario, Sondrio, Italy. Neurology Department-Multiple Sclerosis Center, IRCCS San Raffaele Institute, Vita-Salute San Raffaele University, Milan, Italy. Neurology and Neurorehabilitation Units, MS Center, Headache Center, Epilepsy Center, and Stroke Unit, Neurophysiology Service, and Neuroimaging Research Unit, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. SCDO Neurologia e Centro di Riferimento Regionale Sclerosi Multipla, AOU San Luigi Gonzaga, Orbassano, Italy. SCDO Neurologia e Centro di Riferimento Regionale Sclerosi Multipla, AOU San Luigi Gonzaga, Orbassano, Italy. Department of Neuroscience (DNS), School of Medicine - University of Padua, Padua, Italy. Department of Neuroscience (DNS), School of Medicine - University of Padua, Padua, Italy. Centro Sclerosi Multipla AOU Cagliari - University of Cagliari, Italy. Centro Sclerosi Multipla ASL Cagliari, Italy. Centro Sclerosi Multipla, Ospedale di Gallarate, ASST della Valle Olona, Gallarate, Italy. Centro Sclerosi Multipla, Ospedale di Gallarate, ASST della Valle Olona, Gallarate, Italy. Centro Regionale per la Sclerosi Multipla, ASST Spedali Civili di Brescia, Montichiari, Brescia, Italy. Centro Regionale per la Sclerosi Multipla, ASST Spedali Civili di Brescia, Montichiari, Brescia, Italy; U.O. Neuroimmunologia e Malattie Neuromuscolari, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. U.O. Neuroimmunologia e Malattie Neuromuscolari, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. U.O. Neuroimmunologia e Malattie Neuromuscolari, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. UO Neurologia, ULSS 2 Marca Trevigiana, Treviso, Italy. Centro Malattie Demielinizzanti, Ospedale Civile Baggiovara, AOU Modena, Italy. Centro Malattie Demielinizzanti, Ospedale Civile Baggiovara, AOU Modena, Italy. Clinica Neurologica, Azienda Ospedaliero Universitaria delle Marche, Torrette, Ancona, Italy. Clinica Neurologica, Azienda Ospedaliero Universitaria delle Marche, Torrette, Ancona, Italy. Department of Neurology, Papa Giovanni XXIII Hospital, Bergamo, Italy. Department of Neurology, Papa Giovanni XXIII Hospital, Bergamo, Italy. Centro Regionale per la Sclerosi Multipla, ASST Spedali Civili di Brescia, Montichiari, Brescia, Italy. Diagnostic Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy; Section of Microbiology, University of Brescia, P. le Spedali Civili, 1, Brescia, Italy.
 Department of Neurology, , Perth, Western Australia, AustraliaSir Charles Gairdner Hospital. RINGGOLD: 5728 Perron Institute for Neurological and Translational Sciences, QE II Medical Centre, Perth, Australia. , Sydney, New South Wales, AustraliaUniversity of New South Wales. RINGGOLD: 7800 , Osborne Park, AustraliaClinipath Pathology. RINGGOLD: 547049 Department of Neurology, , Perth, Western Australia, AustraliaRoyal Perth Hospital. RINGGOLD: 6508 Perron Institute for Neurological and Translational Sciences, QE II Medical Centre, Perth, Australia.
 Department of Neurology, centre de ressources et de compétences SEP - Paris, Pitié-Salpêtrière University Hospital, AP-HP, 47, boulevard de l'Hôpital, 75013 Paris, France. Department of Neurology, centre de ressources et de compétences SEP - Paris, Pitié-Salpêtrière University Hospital, AP-HP, 47, boulevard de l'Hôpital, 75013 Paris, France. Paris-Brain Institute (ICM), Paris Brain Institute's Data and Analysis Core, Pitié-Salpêtrière Hospital, Sorbonne université, Inserm U1127, CNRS UMR 7225, Paris, France. Department of Neurology, Fondation Adolphe-de-Rothschild Hospital, Paris, France. Department of Neurology, centre de ressources et de compétences SEP - Paris, Pitié-Salpêtrière University Hospital, AP-HP, 47, boulevard de l'Hôpital, 75013 Paris, France. Department of Neurology, centre de ressources et de compétences SEP - Paris, Pitié-Salpêtrière University Hospital, AP-HP, 47, boulevard de l'Hôpital, 75013 Paris, France. Department of Neurology, centre de ressources et de compétences SEP - Paris, Pitié-Salpêtrière University Hospital, AP-HP, 47, boulevard de l'Hôpital, 75013 Paris, France. Department of Neurology, centre de ressources et de compétences SEP - Paris, Pitié-Salpêtrière University Hospital, AP-HP, 47, boulevard de l'Hôpital, 75013 Paris, France. Electronic address: thomas.roux@aphp.fr.
 Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield, Department of Medicine, University of Oxford and Department of Statistics, University of Oxford, Oxford, OX3 7LF, UK. Novartis Pharma AG, CH-4056 Basel, Switzerland. Novartis Pharma AG, CH-4056 Basel, Switzerland. Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Population Health, University of Oxford, Oxford, OX3 7LF, UK. Wellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK. Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield, Department of Medicine, University of Oxford and Department of Statistics, University of Oxford, Oxford, OX3 7LF, UK. Department of Statistics, University of Oxford, 24-29 St Giles', Oxford, OX1 3LB, UK.
 Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Institute for Metabolic and Neuropsychiatric Disorders, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China. Department of Neurology, Binzhou Medical University Hospital, Binzhou, China.
 Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Faculty of Medicine, University of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Faculty of Medicine, University of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro. Clinic for Neurology, Clinical Centre of Montenegro, Podgorica, Montenegro.
 Department of Neurology, School of Medicine Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran. Department of Neurology, School of Medicine Isfahan University of Medical Sciences Isfahan Iran. Isfahan Neurosciences Research Center Isfahan University of Medical Sciences Isfahan Iran.
 Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Department of Pharmacology of Chinese Materia Medica, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing, Jiangxi, China. Department of Neurology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, MB, Canada. Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Department of Pharmacology of Chinese Materia Medica, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing, Jiangxi, China. Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
 Department of Radiation Oncology, University of California San Francisco, San Francisco, California. Department of Radiation Oncology, University of California San Francisco, San Francisco, California. Department of Radiation Oncology, University of California San Francisco, San Francisco, California.
 MS & Neuroimmunology Clinic, Concord Hospital, The University of Sydney, Sydney, NSW, Australia.
 Department of Neurology, The Ohio State University, Columbus, OH, USA. benjamin.segal@osumc.edu. Neuroscience Research Institute, The Ohio State University, Columbus, OH, USA. benjamin.segal@osumc.edu.
 Institute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan. Department of Neurology, Kansai Medical University Medical Center, Moriguchi, Japan.
 Walton Centre NHS Foundation Trust, Lower Lane, Fazakerley, Liverpool, L9 7LJ, UK. Carolyn.young11@nhs.net. Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK. Carolyn.young11@nhs.net. Northern Care Alliance NHS Trust, Salford, UK. Academic Department of Neurology, University of Sheffield, Sheffield, UK. University of Nottingham, Nottingham, UK. University Hospital of North Midlands NHS Trust, Stoke-on-Trent, UK. University of Exeter Medical School, Exeter, UK. Royal Holloway, University of London, Egham, Surrey, UK. Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK. Walton Centre NHS Foundation Trust, Lower Lane, Fazakerley, Liverpool, L9 7LJ, UK. Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.
 Department of Neurology, School of Medicine, Technical University, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. Institute for AI in Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. TUM-Neuroimaging Center, School of Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University, Munich, Germany. Department of Neuroradiology, School of Medicine, Technical University, Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology, School of Medicine, Technical University, Munich, Germany mark.muehlau@tum.de. TUM-Neuroimaging Center, School of Medicine, Technical University, Munich, Germany.
 Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Department of Neuroscience, Imaging and Clinical Sciences, University 'G. D'Annunzio' of Chieti-Pescara, 66100 Chieti, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Department of Mechanical and Aerospace Engineering, "Sapienza" University of Rome, 00185 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Department of Mechanical and Aerospace Engineering, "Sapienza" University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, Università Campus Bio-Medico di Roma, 00128 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Engineering Faculty, International Telematic University Uninettuno, 00186 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Department of Neuroscience, Imaging and Clinical Sciences, University 'G. D'Annunzio' of Chieti-Pescara, 66100 Chieti, Italy. Engineering Faculty, International Telematic University Uninettuno, 00186 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Engineering Faculty, International Telematic University Uninettuno, 00186 Rome, Italy. Engineering Faculty, International Telematic University Uninettuno, 00186 Rome, Italy. Istituto Nazionale di Fisica Nucleare, Sezione Roma Tor Vergata, 00133 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Department of Mechanical and Aerospace Engineering, "Sapienza" University of Rome, 00185 Rome, Italy. Department of Mechanical and Aerospace Engineering, "Sapienza" University of Rome, 00185 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy. Laboratory of Electrophysiology for Translational neuroScience (LET'S), Laboratory of Agent-Based Social Simulation (LABSS), Italian National Research Council (CNR), Via Palestro 32, 00185 Rome, Italy.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. hasnat.ahmed@utas.edu.au. Australian Government Department of Health and Aged Care, Canberra, Australia. hasnat.ahmed@utas.edu.au. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Australian Centre for Health Services Innovation and Centre for Healthcare Transformation, School of Public Health & Social Work, Queensland University of Technology, Brisbane, QLD, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia.
 Child Growth and Development Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, School of Medicine, Iran University of Medical Sciences, Shahid Hemmat Highway, P.O Box: 14665-354, Tehran, 1449614535, Iran. Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease, Isfahan University of Medical Sciences, Isfahan, Iran. Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Laboratory of Transcriptional Regulation, Institute of Medical Biology, Polish Academy of Science, Lodz, Poland. Bio-Med-Chem Doctoral School of the University of Lodz, Lodz Institutes of the Polish Academy of Sciences, Lodz, Poland. Division of Medical Education, Brighton and Sussex Medical School, Falmer, Brighton, Sussex, BN1 9PH, UK. Department of Immunology, School of Medicine, Iran University of Medical Sciences, Shahid Hemmat Highway, P.O Box: 14665-354, Tehran, 1449614535, Iran. hoohadi@yahoo.com. Immunology Research Center, Iran University of Medical Sciences, Tehran, Iran. hoohadi@yahoo.com.
 Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital, Katerinska 30, 120 00, Prague, Czech Republic. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Multiple Sclerosis Center, Charles University and General University Hospital, Katerinska 30, 120 00, Prague, Czech Republic. tomas.uher@vfn.cz. Department of Physiotherapy, Faculty of Health Care, University of Presov, Prešov, Slovak Republic. tomas.uher@vfn.cz.
 Neurology, Southwest Jutland Hospital, Esbjerg, Region of Southern Denmark, Denmark. Department of Regional Health Research, University of Southern Denmark, Odense, Denmark. Department of Regional Health Research, University of Southern Denmark, Odense, Denmark. Department of Neurology, Southwest Jutland Hospital, Esbjerg, Denmark. Department of Regional Health Research, University of Southern Denmark, Odense, Denmark. Department of Clinical Immunology, Odense University Hospital, Odense, Denmark. Department of Clinical Immunology, Odense University Hospital, Odense, Denmark. Department of Clinical Immunology, Odense University Hospital, Odense, Denmark. Department of Neurology, Nordsjællands Hospital, Hillerod, Denmark. Neurology, Hospitalsenhed Midt, Viborg, Denmark. Department of Rheumatology, Odense Universitetshospital, Odense, Denmark. Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Department of Infectious Diseases, Odense University Hospital, Odense, Denmark. Department of Neurology, University California San Francisco, San Francisco, California, USA. Department of Neurology, University California San Francisco, San Francisco, California, USA. Department of Neurology, University California San Francisco, San Francisco, California, USA. Department of Neurology, Multiple Sclerosis Center at UCSF, San Francisco, California, USA. Department of Neurology, University California San Francisco, San Francisco, California, USA. Department of Neurology, Southwest Jutland Hospital, Esbjerg, Denmark tobias.sejbaek@rsyd.dk. Department of Regional Health Research, University Hospital of Southern Denmark, Esbjerg, Denmark.
 Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden. Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden. Department of Neuroscience, Neurology, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. Department of Biochemistry and Biophysics, National Bioinformatics Infrastructure Sweden, Science for Life Laboratory, Stockholm University, Box 1031, 17121 Solna, Sweden. Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden. Department of Neuroscience, Neurology, Uppsala University, Uppsala, Sweden. Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.
 1st Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. Rehabilitation Center Harmony n.o., Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. 1st Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
 Multiple Sclerosis Centre, ASL Cagliari, 09126 Cagliari, Italy. Multiple Sclerosis Centre, ASL Cagliari, 09126 Cagliari, Italy. Multiple Sclerosis Centre, ASL Cagliari, 09126 Cagliari, Italy. Neurologia, ARNAS G. Brotzu, 09047 Selargius, Italy. Multiple Sclerosis Centre, ASL Cagliari, 09126 Cagliari, Italy. Department of Medical Sciences and Public Health, University of Cagliari, 09124 Cagliari, Italy.

 Neurology Clinic Tsudanuma & Dowakai Chiba Hospital Funabashi, Japan.
 Department of Neurosciences, Cleveland Clinic, Cleveland, OH, United States. Department of Neurosciences, Cleveland Clinic, Cleveland, OH, United States.
 School of Psychology and Public Health, La Trobe University, Bundoora, Australia. Whitley College, University of Divinity, Melbourne, Australia.
 Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliary, Italy. Multiple Sclerosis Centre, Department of Medical Sciences and Public Health, University of Cagliari, 09124 Cagliari, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliary, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliary, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliary, Italy. Multipe Sclerosis Center, Sheba Medical Center, Tel-Hashomer 52621, Israel. Multipe Sclerosis Center, Sheba Medical Center, Tel-Hashomer 52621, Israel. Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel. Sagol School of Neurocience, Tel-Aviv University, Tel-Aviv 69978, Israel. Multipe Sclerosis Center, Sheba Medical Center, Tel-Hashomer 52621, Israel. Sagol School of Neurocience, Tel-Aviv University, Tel-Aviv 69978, Israel. Department of Physical Therapy, School of Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel.
 Department of Rehabilitation Counseling, College of Health Professions, Virginia Commonwealth University. Department of Rehabilitation Psychology and Special Education, University of Wisconsin-Madison. Department of Early Childhood, Special Education, and Counselor Education, University of Kentucky. Department of Psychology, Illinois Institute of Technology.
 Molecular Pharmacology Research Group, Department of Pharmacology, Toxicology and Clinical Pharmacy, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo 11835, Egypt. Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo 11566, Egypt. Molecular Pharmacology Research Group, Department of Pharmacology, Toxicology and Clinical Pharmacy, Faculty of Pharmacy and Biotechnology, German University in Cairo, Cairo 11835, Egypt.
 Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. Institute for Better Health, Trillium Health Partners, Mississauga, Ontario L5B1B8, Canada. Rehabilitation Sciences Institute, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5G1V7, Canada. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario M2M2G1, Canada. Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario M5T3M6, Canada. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. Institute for Better Health, Trillium Health Partners, Mississauga, Ontario L5B1B8, Canada. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. Rehabilitation Sciences Institute, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5G1V7, Canada. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario M2M2G1, Canada. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. Division of Physical Medicine & Rehabilitation, Department of Medicine, University of Alberta, Edmonton, Alberta T6G2G4, Canada. Rehabilitation Sciences Institute, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5G1V7, Canada. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario M2M2G1, Canada. Department of Occupational Science and Occupational Therapy, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5G1V7, Canada. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. Institute for Better Health, Trillium Health Partners, Mississauga, Ontario L5B1B8, Canada. School of Pharmacy, University of Waterloo, Kitchener, Ontario N2G 1C5, Canada. Department of Family and Community Medicine, University of Toronto, Toronto, Ontario M5G1V7, Canada. Women's College Research Institute, Toronto, Ontario M5G1N8, Canada. School of Pharmacy, University of Waterloo, Kitchener, Ontario N2G 1C5, Canada. Schlegel-University of Waterloo Research Institute of Aging, Waterloo, Ontario N2J0E2, Canada. Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario M5S3M2, Canada. OpenLab, University Health Network, Toronto, Ontario M5G2C4, Canada. Department of Family and Community Medicine, University of Toronto, Toronto, Ontario M5G1V7, Canada. Women's College Research Institute, Toronto, Ontario M5G1N8, Canada. Schools of Occupational Therapy and Health Administration, Dalhousie University, Halifax, Nova Scotia B3H4R2, Canada. Department of Nursing, Umeå University, Umeå, Sweden.
 Department of Neurology, Yale University, New Haven, CT erin.longbrake@yale.edu. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital; CORe, Department of Medicine, University of Melbourne, Australia.

 , Samraong, Cambodia. amnuaykleebai@gmail.com. Chandigarh University, Mohali, Punjab, India. Joesph Ayobabalola University, Ikeji-Arakeji, Nigeria.
 Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK. Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK. University College London Hospitals NHS Trust, London, UK. University College London Hospitals NHS Trust, London, UK. Worcestershire Health and Care NHS Trust, Worcester, UK. Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK.
 Department of Neurology, Nihonkai General Hospital, Yamagata, Japan. Department of Neurology, Nihonkai General Hospital, Yamagata, Japan. Department of Neurology, Nihonkai General Hospital, Yamagata, Japan. Department of Neurology, Nihonkai General Hospital, Yamagata, Japan. Department of Neurosurgery, Nihonkai General Hospital, Yamagata, Japan. Department of Pathology, Nihonkai General Hospital, Yamagata, Japan. Division of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Division of Neurology and Clinical Neuroscience, Department of Internal Medicine III, Yamagata University School of Medicine, Yamagata, Japan. Division of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Division of Neurology and Clinical Neuroscience, Department of Internal Medicine III, Yamagata University School of Medicine, Yamagata, Japan. Electronic address: yasuyuki@med.id.yamagata-u.ac.jp.
 Department of Neurology, Ophthalmology UConn Health, Farmington, Connecticut.
 Department of Physiology and Pathophysiology, Spinal Cord Research Center, Rady Faculty of Health Sciences, University of Manitoba, Children Hospital Research Institute of Manitoba, Winnipeg, MB, Canada. Department of Physiology and Pathophysiology, Spinal Cord Research Center, Rady Faculty of Health Sciences, University of Manitoba, Children Hospital Research Institute of Manitoba, Winnipeg, MB, Canada.
 Institute of AI and Informatics in Medicine, School of Medicine, Technical University of Munich, Ismaninger Str. 22, Munich 81675, Germany. Institute of General Practice and Health Services Research, School of Medicine, Technical University of Munich, Orleansstr. 47, Munich 81667, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Institute for Medical Information Processing, Biometry, and Epidemiology, Ludwig-Maximilians-Universität in Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology, Klinikum rechts der Isar School of Medicine, Technical University of Munich, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar School of Medicine, Technical University of Munich, Munich, Germany. Institute for Medical Information Processing, Biometry, and Epidemiology, Ludwig-Maximilians-Universität in Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology, Klinikum rechts der Isar School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar School of Medicine, Technical University of Munich, Munich, Germany. Institute of AI and Informatics in Medicine, School of Medicine, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology, Medical Faculty, University of Augsburg, Augsburg, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität in Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Neurology & Stroke and Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, Tübingen, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Institute of AI and Informatics in Medicine, School of Medicine, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Institute of AI and Informatics in Medicine, School of Medicine, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Institute of AI and Informatics in Medicine, School of Medicine, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Diagnostic and Interventional Neuroradiology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Data Integration for Future Medicine (DIFUTURE) Consortium, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
 School of Nursing and Midwifery Tehran University of Medical Sciences Tehran Iran. School of Nursing and Midwifery Tehran University of Medical Sciences Tehran Iran. School of Nursing and Midwifery Tehran University of Medical Sciences Tehran Iran. Department of Biostatistics, School of Public Health Hamadan University of Medical Sciences Hamadan Iran. School of Nursing and Midwifery Tehran University of Medical Sciences Tehran Iran.
 Neurology Clinic and Policlinic, Department of Head, Spine and Neuromedicine, MS Center and Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Clinical Research, Clinical Trial Unit, University Hospital Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Department of Head, Spine and Neuromedicine, MS Center and Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Clinical Research, Clinical Trial Unit, University Hospital Basel, Basel, Switzerland. Swiss Federation for Common Tasks of Health Insurances (SVK), Solothurn, Switzerland. Swiss Federation for Common Tasks of Health Insurances (SVK), Solothurn, Switzerland. Neurology Clinic and Policlinic, Department of Head, Spine and Neuromedicine, MS Center and Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Department of Head, Spine and Neuromedicine, MS Center and Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Department of Head, Spine and Neuromedicine, MS Center and Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Department of Head, Spine and Neuromedicine, MS Center and Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland.
 Department of Neurology, Hospital da Luz Lisboa, Lisbon, Portugal; Neuroimmunology clinic, Hospital da Luz Lisboa, Lisbon Portugal; Comprehensive Health Research Centre, Universidade Nova de Lisboa, Lisbon, Portugal. Electronic address: renato.silva.oliveira@hospitaldaluz.pt. Department of Neurology, Hospital da Luz Lisboa, Lisbon, Portugal. Department of Neurology, Hospital da Luz Lisboa, Lisbon, Portugal. Department of Neurology, Hospital da Luz Lisboa, Lisbon, Portugal. Department of Neurology, Hospital da Luz Lisboa, Lisbon, Portugal; Neuroimmunology clinic, Hospital da Luz Lisboa, Lisbon Portugal.
 Department of Health Care Services, Köyceğiz Vocational School of Health Services, Muğla Sıtkı Koçman University, Muğla, Turkey. fatihozden@mu.edu.tr. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Ege University, İzmir, Turkey. Department of Physiotherapy and Rehabilitation, Institute of Health Sciences, Ege University, İzmir, Turkey. Department of Neurology, Faculty of Medicine, Ege University, İzmir, Turkey.
 Department of Neurology, Institute of Medical Sciences, Medical College of Rzeszow University, Rzeszow, Poland. Department of Neurology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, Katowice, Poland. Department of Neurology, Medical University of Bialystok, Bialystok, Poland. PEX PharmaSequence, Warsaw, Poland. National Institute of Public Health NIH - National Research Institute, Warsaw, Poland. Collegium Medicum, Jan Kochanowski University, Kielce, Poland.
 Department of Neurosciences, S. Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy. luca.prosperini@gmail.com. Department of Rehabilitation Sciences and Health Professions, Sapienza University, Via Cardarelli s.n.c, 01100, Viterbo, Italy. Department of Neurosciences, S. Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy. Department of Neurosciences, S. Camillo-Forlanini Hospital, C.ne Gianicolense 87, 00152, Rome, Italy. Azienda Sanitaria Locale di Rieti, Via del Terminillo 42, 02100, Rieti, Italy. Department of Human Neurosciences, Sapienza University, Viale dell'Università 30, 00185, Rome, Italy. Neuroimmunology Unit, Santa Lucia Foundation, Via del Fosso di Fiorano 64/65, 00143, Rome, Italy.
 CEINGE Biotecnologie Avanzate Franco Salvatore, 80145 Naples, Italy. Dipartimento di Scienze e Tecnologie Ambientali, Biologiche, Farmaceutiche, Università della Campania "Luigi Vanvitelli", 81100 Caserta, Italy. Centro di Sclerosi Multipla, II Clinica Neurologica, Università della Campania "Luigi Vanvitelli", Via S. Pansini 5, 80131 Naples, Italy. Centro di Sclerosi Multipla, II Clinica Neurologica, Università della Campania "Luigi Vanvitelli", Via S. Pansini 5, 80131 Naples, Italy. CEINGE Biotecnologie Avanzate Franco Salvatore, 80145 Naples, Italy. Dipartimento di Medicina Molecolare e Biotecnologie Mediche, "Federico II" Università degli Studi di Napoli, 80131 Naples, Italy. CEINGE Biotecnologie Avanzate Franco Salvatore, 80145 Naples, Italy. Dipartimento di Scienze e Tecnologie Ambientali, Biologiche, Farmaceutiche, Università della Campania "Luigi Vanvitelli", 81100 Caserta, Italy.
 St. Jadwiga Queen Clinical Hospital No. 2, Lwowska 60, 35-301 Rzeszow, Poland. Institute of Medical Sciences, Medical College, Rzeszow University, Warzywna 1a, 35-310 Rzeszow, Poland. Institute of Medical Sciences, Medical College, Rzeszow University, Warzywna 1a, 35-310 Rzeszow, Poland. St. Jadwiga Queen Clinical Hospital No. 2, Lwowska 60, 35-301 Rzeszow, Poland. Institute of Medical Sciences, Medical College, Rzeszow University, Warzywna 1a, 35-310 Rzeszow, Poland.
 Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Rome, Italy. Department of Human Sciences and Quality of Life Promotion University of Rome San Raffaele, Rome, Italy. Department of Systems Medicine, Tor Vergata University, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Department of Systems Medicine, Tor Vergata University, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Mouse Biology Unit, European Molecular Biology Laboratory, Monterotondo Scalo, Rome, Italy. Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. Unit of Neurology, IRCCS Neuromed, Pozzilli, Isernia, Italy. Department of Systems Medicine, Tor Vergata University, Rome, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Rome, Italy. Department of Human Sciences and Quality of Life Promotion University of Rome San Raffaele, Rome, Italy.
 Department of Neurology, Rostock University Medical Center, Rostock, Germany. Department of Neurology, Rostock University Medical Center, Rostock, Germany. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Merck Healthcare Germany GmbH, Weiterstadt, Germany. Merck Healthcare Germany GmbH, Weiterstadt, Germany. Department of Neurology, Bayreuth Hospital, Bayreuth, Germany. Neurological Group Practice, Ulm, Germany. Neurological Private Practice, Hamburg, Germany. Neurocenter Itzehoe, Itzehoe, Germany. Department of Neurology, Inselspital Bern, University Hospital Bern, Bern, Switzerland. Department of Neurology, Rostock University Medical Center, Rostock, Germany.
 Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic, Cleveland, OH, USA.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W Taylor St, 650 AHSB (MC517), Chicago, IL 60612, USA. Electronic address: ndubos3@uic.edu. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W Taylor St, 650 AHSB (MC517), Chicago, IL 60612, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W Taylor St, 650 AHSB (MC517), Chicago, IL 60612, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois Chicago, 1919W Taylor St, 650 AHSB (MC517), Chicago, IL 60612, USA.
 Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston, TX, USA. Department of Pharmacy Administration, College of Pharmacy, University of Mississippi, Oxford, MS, USA. Baylor College of Medicine, Houston, TX, USA. Department of Pharmaceutical Health Outcomes and Policy, College of Pharmacy, University of Houston, TX, USA.
 Department of Medicine, Faculty of Medicine, Kuwait University, Kuwait City P.O. Box 24923, Kuwait. Neurology Unit, Department of Medicine, Mubarak al Kabeer Hospital, Ministry of Health, Jabriya 13001, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, Kuwait City P.O. Box 24923, Kuwait. Neurology Unit, Department of Medicine, Mubarak al Kabeer Hospital, Ministry of Health, Jabriya 13001, Kuwait. Department of Population Medicine, Qatar University, Doha P.O. Box 2713, Qatar. Department of Medical Sciences, Frank Netter School of Medicine, Quinnipiac University, Hamden, CT 06518, USA.
 Department of Parasitology, Faculty of Medicine, Cumhuriyet University, Sivas, Turkey.. Electronic address: g.sevimligul@gmail.com. Department of Parasitology, Faculty of Medicine, Cumhuriyet University, Sivas, Turkey. Department of Neurology, Cumhuriyet University School of Medicine, Sivas, Turkey.
 Department of Neurology, Faculty of Medicine Ain Shams University Cairo Egypt. Department of Neurology, Faculty of Medicine Ain Shams University Cairo Egypt. Department of Neurology, Faculty of Medicine Ain Shams University Cairo Egypt. Department of Radiology, Faculty of Medicine Ain Shams University Cairo Egypt. Department of Neurology, Faculty of Medicine Ain Shams University Cairo Egypt. Department of Neurology, Faculty of Medicine Ain Shams University Cairo Egypt.
 Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden. RINGGOLD: 56749 Institute of Neuroscience and Clinical Physiology, University of Gothenburg, Gothenburg, Sweden. Department of Radiology, Landspítali-The National University Hospital of Iceland, Reykjavik, Iceland. Faculty of Medicine, University of Iceland, Reykjavik, Iceland. Department of Neurology, Landspítali-The National University Hospital of Iceland, Reykjavik, Iceland.
 NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Radiomics Group, Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom. eHealth Center, Universitat Oberta de Catalunya, Barcelona, Spain. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Mohn Medical Imaging and Visualization Centre, Department of Radiology, Haukeland University Hospital, Bergen, Norway. Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. NIHR UCLH Biomedical Research Centre, London, United Kingdom. Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Brain Connectivity Research Center, IRCCS Mondino Foundation, Pavia, Italy.
 Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran. Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran. Community Based Psychiatric Care Research Center, School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran. Community Based Psychiatric Care Research Center, School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran. mzrakhshan@ymail.com. Community Based Psychiatric Care Research Center, Shiraz University of Medical Sciences, Namazi Square, Shiraz, Iran. mzrakhshan@ymail.com. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
 Department of Radiology, University of California, San Diego, San Diego, CA, United States. University Hospital Heidelberg, Heidelberg, Germany. Department of Radiology, University of California, San Diego, San Diego, CA, United States. Department of Radiology, University of California, San Diego, San Diego, CA, United States. University Hospital Heidelberg, Heidelberg, Germany. Department of Neurosciences, University of California, San Diego, San Diego, CA, United States. Department of Radiology, University of California, San Diego, San Diego, CA, United States. Department of Bioengineering, University of California, San Diego, San Diego, CA, United States. Radiology Service, Veterans Affairs San Diego Healthcare System, San Diego, CA, United States.
 School of Rehabilitation Science, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Medicine (Neurology), University of British Columbia, Vancouver, BC, Canada. Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. Department of Neurology, Royal Jubilee Hospital, Victoria, BC, Canada. Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Clinical Neurological Sciences, Western University, London, ON, Canada. Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Department of Medicine (Neurology), University of Alberta, Edmonton, AB, Canada. School of Rehabilitation Science, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
 Institute for Implementation Science in Health Care, Faculty of Medicine, University of Zürich, Zürich, Switzerland. Epidemiology and Biostatistics and Prevention Institute, Faculty of Medicine, University of Zürich, Zürich, Switzerland. Institute for Implementation Science in Health Care, Faculty of Medicine, University of Zürich, Zürich, Switzerland. Epidemiology and Biostatistics and Prevention Institute, Faculty of Medicine, University of Zürich, Zürich, Switzerland. Epidemiology and Biostatistics and Prevention Institute, Faculty of Medicine, University of Zürich, Zürich, Switzerland. Research Department Physiotherapy, Rehabilitation Centre, Valens, Switzerland. Research Department Physiotherapy, Rehabilitation Centre, Valens, Switzerland. Research Department Physiotherapy, Rehabilitation Centre, Valens, Switzerland. Institute for Implementation Science in Health Care, Faculty of Medicine, University of Zürich, Zürich, Switzerland. Epidemiology and Biostatistics and Prevention Institute, Faculty of Medicine, University of Zürich, Zürich, Switzerland.
 Pediatric Neurology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Department, Mofid Children's Hospital, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Department, Mofid Children's Hospital, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Department, Mofid Children's Hospital, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Department, Mofid Children's Hospital, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Pediatric Neurology Department, Mofid Children's Hospital, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Child and Adolescent Psychiatry Department Shahid Beheshti University of Medical Sciences, Tehran, Iran. Epidemiology and Gastrointestinal Cancer Research Center, Non-communicable Diseases Institute, Mazandaran University of Medical Sciences, Sari, Iran. Epidemiology and Gastrointestinal Cancer Research Center, Non-communicable Diseases Institute, Mazandaran University of Medical Sciences, Sari, Iran.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA (RWM). Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL, USA (JFB).
 Neurology Unit, Maggiore Della Carità Hospital, Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Neurology Unit, S. Andrea Hospital, Department of Translational Medicine, University of Piemonte Orientale, 13100 Vercelli, Italy. Neurology Unit, Maggiore Della Carità Hospital, Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Neurology Unit, Maggiore Della Carità Hospital, Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Neurology Unit, Maggiore Della Carità Hospital, Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Neurology Unit, Maggiore Della Carità Hospital, Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Neurology Unit, S. Andrea Hospital, Department of Translational Medicine, University of Piemonte Orientale, 13100 Vercelli, Italy.
 Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America. Electronic address: rxu4@jhmi.edu.
 Departamento de Psicología Experimental, Facultad de Psicología, Universidad de Sevilla, Sevilla, Spain. Electronic address: esarriaspsicologia@gmail.com. Unidad Esclerosis Múltiple, Hospital Vithas-NISA, Sevilla, Spain. Departamento de Psicología Experimental, Facultad de Psicología, Universidad de Sevilla, Sevilla, Spain.
 Department of Translational Medicine and Surgery, Section of General Pathology, Università Cattolica del Sacro Cuore, Rome, Italy. Department of Biology and Biotechnology Charles Darwin, University of Rome Sapienza, Rome, Italy. Department of Translational Medicine and Surgery, Section of General Pathology, Università Cattolica del Sacro Cuore, Rome, Italy. Department of Medicine and Surgery, Section of Human Anatomy, University of Perugia, Perugia, Italy. Department of Translational Medicine and Surgery, Section of General Pathology, Università Cattolica del Sacro Cuore, Rome, Italy. Department of Pharmaceutical Sciences, University of Perugia, Perugia, Italy. Department of Medicine and Surgery, Section of Human Anatomy, University of Perugia, Perugia, Italy. Department of Medicine and Surgery, Section of Human Anatomy, University of Perugia, Perugia, Italy. Department of Translational Medicine and Surgery, Section of General Pathology, Università Cattolica del Sacro Cuore, Rome, Italy. Department of Medicine and Surgery, Section of Human Anatomy, University of Perugia, Perugia, Italy. gabriele.disante@unipg.it.
 Translational Immunology Research Program, University of Helsinki, Helsinki, Finland; Department of Neurology, Brain Center, Helsinki University Hospital, Helsinki, Finland. Electronic address: joonas.lehikoinen@helsinki.fi. Translational Immunology Research Program, University of Helsinki, Helsinki, Finland. HUS Diagnostic Center, Clinical Microbiology, University of Helsinki and Helsinki University Hospital. Translational Immunology Research Program, University of Helsinki, Helsinki, Finland; Department of Neurology, Brain Center, Helsinki University Hospital, Helsinki, Finland. Translational Immunology Research Program, University of Helsinki, Helsinki, Finland; Department of Bacteriology and Immunology, Medicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland. Translational Immunology Research Program, University of Helsinki, Helsinki, Finland; Department of Neurology, Brain Center, Helsinki University Hospital, Helsinki, Finland.
 Department of Physical Medicine & Rehabilitation, Michigan Medicine, University of Michigan, Ann Arbor, MI, USA. Departments of Health Care Sciences & Neurology, Wayne State University, Detroit, MI, USA. Department of Physical Medicine & Rehabilitation, Michigan Medicine, University of Michigan, Ann Arbor, MI, USA.
 Department of Health Behavior, University of Alabama at Birmingham, Birmingham, AL, United States of America. Electronic address: wnneal@uab.edu. Virginia C. Crawford Research Institute, Shepherd Center, Atlanta, GA, United States of America. Department of Medicine, Division of Pulmonary/Allergy/Critical Care, University of Alabama at Birmingham, Birmingham, AL, United States of America. Department of Physical Therapy, University of Alabama at Birmingham, Birmingham, AL, United States of America. Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, Memphis, TN, United States of America. School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America. Department of Physical Therapy, Marquette University, Milwaukee, WI, United States of America. Department of Physical Medicine and Rehabilitation, Cleveland Clinic, Cleveland, OH, United States of America. Department of Physical Therapy, Marquette University, Milwaukee, WI, United States of America. Virginia C. Crawford Research Institute, Shepherd Center, Atlanta, GA, United States of America. Virginia C. Crawford Research Institute, Shepherd Center, Atlanta, GA, United States of America. Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, United States of America.
 CNRS, Univ. Bordeaux, Bordeaux INP, LABRI, Talence, France. Univ. Bordeaux, CNRS, Bordeaux, France. Centre Mémoire Ressources Recherches, Pôle de Neurosciences Cliniques, CHU de Bordeaux, Bordeaux, France. CNRS, Univ. Bordeaux, Bordeaux INP, LABRI, Talence, France. CNRS, Univ. Bordeaux, Bordeaux INP, LABRI, Talence, France. Inserm U1215 - Neurocentre Magendie, Bordeaux, France. Service de Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, Bordeaux, France. Instituto de Aplicaciones de las Tecnologías de la Información y de las Comunicaciones Avanzadas (ITACA), Universitat Politècnica de València, Valencia, Spain. Inserm U1215 - Neurocentre Magendie, Bordeaux, France. Service de Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, Bordeaux, France.
 Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Psychiatry, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Clinical Health Psychology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Medicine, University of Toronto, St. Michael's Hospital, Toronto, ON, Canada. Departments of Psychiatry, Psychology & Neuroscience, and Medicine, Dalhousie University, Halifax, NS, Canada.
 Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran. Peyvand Pathobiology and Genetic Laboratory, Shiraz, Iran. Science Foundation Ireland (SFI), Center for Research in Medical Devices (CÚRAM), University of Galway, Galway, Ireland. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Neurosurgery, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Medicinal Plants Research Center, Yasuj University of Medical Sciences, Yasuj, Iran. Department of Immunology, University of Connecticut Health Center, Farmington, Connecticut, USA. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
 Department of Diagnostic Radiology and Nuclear Medicine, Center for Advanced Imaging Research, University of Maryland School of Medicine, Baltimore, Maryland, USA. Department of Diagnostic Radiology and Nuclear Medicine, Center for Advanced Imaging Research, University of Maryland School of Medicine, Baltimore, Maryland, USA. Medical Division, Department of Neurology, Laboratory of Neuroimmunology, Collegium Medicum, University of Warmia and Mazury, Olsztyn, Poland. Department of Neurosurgery, School of Medicine, Collegium Medicum, University of Warmia and Mazury, Olsztyn, Poland.
 Medical Student, The Medical School, The University of Sheffield, Beech Hill Road, Sheffield, United Kingdom. Consultant Neurologist, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Clinical Research Fellow, Department of Neuroscience, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Associate Professor, Department of Rehabilitation Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Statistical Services Unit, University of Sheffield, Sheffield, United Kingdom. Department of Mechanical Engineering & Insigneo Institute for in Silico Medicine, University of Sheffield, Sheffield, United Kingdom. Medical Student, The Medical School, The University of Sheffield, Beech Hill Road, Sheffield, United Kingdom. NIHR Sheffield Biomedical Research Centre, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Department of Mechanical Engineering & Insigneo Institute for in Silico Medicine, University of Sheffield, Sheffield, United Kingdom.
 School of Rehabilitation Therapy (AF, MF), Queen's University, Kingston, ON, Canada. Interdisciplinary School of Health Sciences (OM, RK, LAP), University of Ottawa, Ottawa, ON, Canada. Interdisciplinary School of Health Sciences (OM, RK, LAP), University of Ottawa, Ottawa, ON, Canada. Biomedical Sciences, Faculty of Science (RK), University of Ottawa, Ottawa, ON, Canada. Faculty of Medicine (MSF), University of Ottawa, Ottawa, ON, Canada. Ottawa Hospital Research Institute, Ottawa, ON, Canada (MSF). School of Rehabilitation Therapy (AF, MF), Queen's University, Kingston, ON, Canada. School of Kinesiology and Health Studies (AEL-C), Queen's University, Kingston, ON, Canada. Interdisciplinary School of Health Sciences (OM, RK, LAP), University of Ottawa, Ottawa, ON, Canada. Brain and Mind Research Institute (LAP), University of Ottawa, Ottawa, ON, Canada.
 Department of Neurology, Strasbourg University Hospital, Strasbourg, France. Jerome.deseze@chru-strasbourg.fr. Department of Neurology, Hôpital Européen, Marseille, France. Clinique des Cèdres, Toulouse/Department of Neurology, CHU Toulouse, Toulouse, France. Department of Neurology, Gonesse Hospital, Gonesse, France. Department of Neurology, Montpellier University Hospital, Montpellier, France. Department of Neurology, Tours University Hospital, Hôpital Bretonneau, Tours, France. Department of Neurology, Caen University Hospital, Caen, France. Department of Neurology, Clermont-Ferrand University Hospital, Clermont-Ferrand, France. Department of Neurology, Nîmes University Hospital, Hopital Caremeau, Nîmes, France. Department of Neurology, CHU Rouen, 7600, Rouen, France. Department of Neurology, Fondation Rothschild Hospital, Paris, France. Department of Neurology, Amiens University Hospital, Amiens, France. CEMKA, Bourg-La-Reine, France. CEMKA, Bourg-La-Reine, France. CEMKA, Bourg-La-Reine, France. Real-World Evidence, Merck Santé (an affiliate of Merck KGaA, Darmstadt, Germany), Lyon, France. University of Lille, INSERM UMR1172 LilNCog, CHU Lille, FHU Precise, Lille, France.
 Clinic for Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience Hannover, Hannover, Germany. Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany. Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany. Clinic for Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience Hannover, Hannover, Germany. Translational Medicine, Novartis Institute for Biomedical Research, Novartis, Basel, Switzerland. Clinic for Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience Hannover, Hannover, Germany. Institute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany.
 Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Department of Radiology, Gruss Magnetic Resonance Research Center, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA. Department of Radiology, Gruss Magnetic Resonance Research Center, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA/. Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Psychiatry and Behavioral Sciences, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA. Department of Psychiatry Radiology, Columbia University Irving Medical Center, New York, NY, USA. Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA/. Department of Neurology Albert Einstein College of Medicine, Bronx, NY, USA.
 School of Medicine Tehran University of Medical Sciences Tehran Iran. School of Medicine Tehran University of Medical Sciences Tehran Iran. Non-communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute Tehran University of Medical Sciences Tehran Iran. School of Medicine Tehran University of Medical Sciences Tehran Iran. Neuroscience Research Center Shahid Beheshti University of Medical Sciences Tehran Iran. Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex Tehran University of Medical Sciences Tehran Iran. Division of Gastroenterology and Hepatology, Imam Khomeini Hospital Complex Tehran University of Medical Sciences Tehran Iran. Division of Gastroenterology and Hepatology, Imam Khomeini Hospital Complex Tehran University of Medical Sciences Tehran Iran.
 Faculy of Medicine, Vita-Salute San Raffaele University, Milan, Italy. Faculy of Medicine, Vita-Salute San Raffaele University, Milan, Italy. Multiple Sclerosis center, Casa di Cura Igea, Milan, Italy.
 Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States. Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
 Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran; Institute for Brain and Cognition, Tarbiat Modares University, Tehran, Iran. Department of Nanobiotechnology, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. Department of Nanobiotechnology, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran; Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. Department of Nanobiotechnology, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran; Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran; Institute for Brain and Cognition, Tarbiat Modares University, Tehran, Iran. Electronic address: mjavan@modares.ac.ir.
 Department of Neurology, Center of the Albert Schweitzer Hospital, MS, Dordrecht, the Netherlands. Department of Neurology, MS Center ErasMS, Erasmus University Medical Center, Rotterdam, the Netherlands. Department of Neurology, MS Center ErasMS, Erasmus University Medical Center, Rotterdam, the Netherlands. Department of Immunology, MS Center ErasMS, Erasmus University Medical Center, Rotterdam, the Netherlands. Neuroimmunology Researchgroup, Netherlands Institute for Neurosicence, Amsterdam, The Netherlands. Department of Biostatistics, Erasmus University Medical Center, Rotterdam, the Netherlands. Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands. Department of Radiology, center of the Albert Schweitzer hospital, MS, Dordrecht, the Netherlands. Department of Neurology, MS Center ErasMS, Erasmus University Medical Center, Rotterdam, the Netherlands. Department of Neurology, Center of the Albert Schweitzer Hospital, MS, Dordrecht, the Netherlands.
 Department of Neurology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310000, China. Department of Clinical Laboratory, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310000, China. School of Statistics, Renmin University of China, Beijing, 100000, China. yanbingwei@126.com. Hangzhou Cred Technology Co., Ltd, Hangzhou, 310000, China.
 Biomaterials Group, Aragon Institute of Engineering Research (I3A), University of Zaragoza, Zaragoza, Spain. Mechanical Engineering Department, University of Zaragoza, Zaragoza, Spain. Biomaterials Group, Aragon Institute of Engineering Research (I3A), University of Zaragoza, Zaragoza, Spain. Mechanical Engineering Department, University of Zaragoza, Zaragoza, Spain. Ophthalmology Department, Miguel Servet University Hospital, Zaragoza, Spain. GIMSO Research and Innovation Group, Aragon Institute for Health Research (IIS Aragon), Zaragoza, Spain. Biomaterials Group, Aragon Institute of Engineering Research (I3A), University of Zaragoza, Zaragoza, Spain. Mechanical Engineering Department, University of Zaragoza, Zaragoza, Spain.
 Urology Unit, San Carlo di Nancy Hospital, GVM Care and Research, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Department of Obstetrics and Gynecology, Del Ponte Hospital, University of Insubria, Varese, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Urology Unit, San Carlo di Nancy Hospital, GVM Care and Research, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Urology Unit, San Carlo di Nancy Hospital, GVM Care and Research, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy. Neuro-Urology Unit, IRCCS Santa Lucia, Rome, Italy. Neuro-Urology Unit, IRCCS Santa Lucia, Rome, Italy. Division of Urology, Department of Surgery, Tor Vergata University Hospital, Rome, Italy.
 Epidemiology Unit, ASL TO3 Regione Piemonte, 10095 Grugliasco, Italy. Epidemiology Unit, ASL TO3 Regione Piemonte, 10095 Grugliasco, Italy. Neurology Unit, Fondazione IRCCS Casa Sollievo della Sofferenza, 71013 San Giovanni Rotondo, Italy. Department of Health Sciences, and CAAD, University of Eastern Piedmont, 28100 Novara, Italy. Epidemiology Unit, ASL TO3 Regione Piemonte, 10095 Grugliasco, Italy. Epidemiology Unit, ASL TO3 Regione Piemonte, 10095 Grugliasco, Italy. Department of Biological and Clinical Sciences, University of Turin, 10128 Torino, Italy. Neurology Unit, Fondazione IRCCS Casa Sollievo della Sofferenza, 71013 San Giovanni Rotondo, Italy.
 Pharmacology, Toxicology and Biochemistry Department, Faculty of Pharmacy, Future University in Egypt (FUE), Cairo 11835, Egypt. Pharmacology, Toxicology and Biochemistry Department, Faculty of Pharmacy, Future University in Egypt (FUE), Cairo 11835, Egypt. Neurology Department, Faculty of Medicine, Ain Shams University, Cairo 11566, Egypt. Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.
 Lurija Institute for Rehabilitation Sciences and Health Research, Allensbach, Germany. Kalaidos University of Applied Sciences, Zürich, Switzerland. Lurija Institute for Rehabilitation Sciences and Health Research, Allensbach, Germany. Kliniken Schmieder Konstanz, Konstanz, Germany. Lurija Institute for Rehabilitation Sciences and Health Research, Allensbach, Germany. Kliniken Schmieder Konstanz, Konstanz, Germany. Lurija Institute for Rehabilitation Sciences and Health Research, Allensbach, Germany. Kliniken Schmieder Allensbach, Allensbach, Germany. Lurija Institute for Rehabilitation Sciences and Health Research, Allensbach, Germany. Klinik für Psychosomatik und Konsiliarpsychiatrie, Kantonsspital, St. Gallen, Switzerland.
 Department of Radiology, Hirosaki University Graduate School of Medicine. Department of Radiology, Aomori Prefectural Central Hospital. Department of Radiology, University of Occupational and Environmental Health, School of Medicine. Department of Radiology, Aomori Prefectural Central Hospital. Department of Radiology, Aomori Prefectural Central Hospital. Department of Radiology, Hirosaki University Graduate School of Medicine. MR Application and Workflow, GE Healthcare. MR Application and Workflow, GE Healthcare. Department of Neurology, Aomori Prefectural Central Hospital. Department of Neurology, Aomori Prefectural Central Hospital. Department of Radiology, Aomori Prefectural Central Hospital. Department of Radiology, Aomori Prefectural Central Hospital. Department of Radiology, Aomori Prefectural Central Hospital. Department of Radiology, Hirosaki University Graduate School of Medicine. Department of Radiology, Aomori Prefectural Central Hospital. Department of Neurology, Hirosaki University Graduate School of Medicine. Department of Radiology, Hirosaki University Graduate School of Medicine.
 Helfgott Research Institute, National University of Natural Medicine, Portland, OR, USA. Department of Neurology, Oregon Health and Science University, Portland, OR, USA. Department of Neurology, VA Portland Health Care System, Portland, OR, USA. Helfgott Research Institute, National University of Natural Medicine, Portland, OR, USA. Helfgott Research Institute, National University of Natural Medicine, Portland, OR, USA.
 Member of Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Physiotherapy, School of Rehabilitation Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Faculty of Pharmacy, Clinical Pharmacy Department, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Neurology, Golestan Hospital, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Biostatistics and Epidemiology, School of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Neurology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
 MS Center Amsterdam, Anatomy and Neurosciences, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA. RINGGOLD: 218916 Department of Radiology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Biomedical Engineering, College of Precision Instruments and Optoelectronics Engineering, Tianjin University, Tianjin, China. Academy of Medical Engineering and Translational Medicine, Medical College, Tianjin University, Tianjin, China. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA. RINGGOLD: 218916 Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA. RINGGOLD: 218916 Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
 Centre for Advanced Imaging, The University of Queensland, Brisbane, Australia. Al Azhar Hospital, Riyadh, Saudi Arabia. Society of Artificial Intelligence in Healthcare, Riyadh, Saudi Arabia. Department of Radiological Sciences and Medical Imaging, College of Applied Medical Sciences, Majmaah University, Majmaah, Saudi Arabia. Faculty of Medicine, School of Biomedical Sciences, The University of Queensland, Brisbane, Australia. Faculty of Medicine, School of Biomedical Sciences, The University of Queensland, Brisbane, Australia. Faculty of Medicine, School of Biomedical Sciences, The University of Queensland, Brisbane, Australia. Queensland Brain Institute, The University of Queensland, Brisbane, Australia. Centre for Advanced Imaging, The University of Queensland, Brisbane, Australia. NCRIS Australian National Imaging Facility, The University of Queensland, Brisbane, Australia. Centre for Advanced Imaging, The University of Queensland, Brisbane, Australia. NCRIS Australian National Imaging Facility, The University of Queensland, Brisbane, Australia. Centre for Advanced Imaging, The University of Queensland, Brisbane, Australia.
 The George Washington University School of Medicine and Health Sciences, Department of Anatomy and Cell Biology, Ross Hall, 2300 I St NW, Washington, DC 20037, United States of America. The George Washington University School of Medicine and Health Sciences, Department of Anatomy and Cell Biology, Ross Hall, 2300 I St NW, Washington, DC 20037, United States of America. The George Washington University School of Medicine and Health Sciences, Nanofabrication and Imaging Center, Science and Engineering Hall, 800 22(nd) St NW, Washington, DC 20037, United States of America. The George Washington University School of Medicine and Health Sciences, Department of Anatomy and Cell Biology, Ross Hall, 2300 I St NW, Washington, DC 20037, United States of America. The George Washington University School of Medicine and Health Sciences, Department of Anatomy and Cell Biology, Ross Hall, 2300 I St NW, Washington, DC 20037, United States of America. Electronic address: rhm3@gwu.edu.
 Center for Neuroinflammation and Experimental Therapeutics and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. amitbar@pennmedicine.upenn.edu. Department of Neurology-Neuroimmunology and Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain. Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Department of Neurology, Medical Faculty, Heinrich-Heine University, Dusseldorf, Germany. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Central Texas Neurology Consultants and Dell Medical School, The University of Texas at Austin, Round Rock, Austin, TX, USA.
 Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Center for Research of Endemic Parasites of Iran, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Sina Hospital, Hassan Abad Square, Tehran, Iran. Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Medical Parasitology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Department of Epidemiology and Biostatistics, School of Health, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran. Department of Parasitology and Mycology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
 Department of Physiotherapy and Rehabilitation, Graduate School of Health Sciences, Izmir Katip Celebi University, Izmir, Turkey, and Department of Physiotherapy and Rehabilitation, Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey (I.Y.); Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Izmir Katip Celebi University, Izmir, Turkey (T.K.); Department of Neurosciences, Graduate School of Health Sciences, Dokuz Eylül University, Izmir, Turkey (O.S., P.Y., C.B.); Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Van Yüzüncü Yil University, Van, Turkey (A.T.O.); and Department of Neurology, Faculty of Medicine, Dokuz Eylül University, Izmir, Turkey (S.O.).
 Department of Traditional Medicine, School of Traditional Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Traditional Medicine, School of Traditional Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. School of Persian Medicine, Tehran University of Medical Sciences, Tehran, Iran. Multiple sclerosis Research Center, Neuroscience institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Traditional Pharmacy, Faculty of Pharmacy and Pharmaceutical Sciences, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Center for Research and Training in Skin Diseases and Leprosy (CRTSDL), Tehran University of Medical Sciences (TUMS), Tehran, Iran. Department of Traditional Pharmacy, Faculty of Pharmacy and Pharmaceutical Sciences, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Brain mapping research Center, Loghman Hakim educational hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 UCSF Weill Institute for Neurosciences and Department of Neurology, University of California, San Francisco (UCSF), 1651 4th Street, Box 3126, San Francisco, CA 94143, USA. Clinical Development, Novartis Pharma B.V., Amsterdam, The Netherlands. Analytics, Novartis Healthcare Pvt. Ltd., Hyderabad, India. China Novartis Institutes for Biomedical Research Co. Ltd., Novartis, Shanghai, People's Republic of China. Global Medical, Novartis Pharma AG, Basel, Switzerland. Global Medical, Novartis Pharma AG, Basel, Switzerland. Department of Neurology, Multiple Sclerosis Division, Morsani College of Medicine, University of South Florida, Tampa, FL, USA. Department of Neurology, Mellen Center for MS Treatment and Research, Cleveland Clinic, Cleveland, OH, USA. MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Department of Head, Spine and Neuromedicine, Biomedical and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland.
 Department of Biochemistry and Diet Therapy, Nutrition Research Center, School of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, IR Iran. RINGGOLD: 48432 Cancer Prevention and Control Program, University of South Carolina, Columbia, SC 29208, USA. RINGGOLD: 49112 Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran. RINGGOLD: 391934 Department of Biochemistry and Diet Therapy, Nutrition Research Center, School of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, IR Iran. RINGGOLD: 48432 Clinical Nutrition Department, School of Nutritional Science and Dietetics, Tehran University of Medical Sciences, Tehran, Iran. RINGGOLD: 48439 Department of Clinical Nutrition & Dietetics, Faculty of Nutrition & Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran. RINGGOLD: 274949 Department of Nutrition, School of Health, Qazvin University of Medical Science, Qazvin, Iran. RINGGOLD: 113106 Health Products Safety Research Center, Qazvin University of Medical Science, Qazvin, Iran. RINGGOLD: 113106 Multiple Sclerosis Research Center, Tehran University of Medical Sciences, Tehran, Iran. RINGGOLD: 48439
 Department of Neurology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan Province Clinical Medical Center and Hainan Academician Innovation Platform, Haikou, China. Department of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, China. Department of Neurology, The National Clinical Research Center for Mental Disorders and Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing, China.
 Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. Department of Neurology, Lady Davis Carmel Medical Center, 7 Mikhal St, 3436212, Haifa, Israel. Department of Community Medicine and Epidemiology, Lady Davis Carmel Medical Center, Haifa, Israel. Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. Department of Neurology, Lady Davis Carmel Medical Center, 7 Mikhal St, 3436212, Haifa, Israel. Head Office, Clalit Health Services, Tel-Aviv, Israel. Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. danielgo1@clalit.org.il. Department of Neurology, Lady Davis Carmel Medical Center, 7 Mikhal St, 3436212, Haifa, Israel. danielgo1@clalit.org.il. Multiple Sclerosis and Neuroimmunology Center, Clalit Health Services, Nazareth, Israel. danielgo1@clalit.org.il.
 From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. From the Mass General Brigham Pediatric Multiple Sclerosis Center (R.P.U., T.C.), Massachusetts General Hospital, Boston; Harvard Medical School (R.P.U., T.C.), Boston; Neurology Department (R.P.U.), University of Massachusetts Medical School, Worcester; Department of Pediatrics (M.W., C.C.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children's Hospital; CA; Pediatric Multiple Sclerosis and Related Disorders Program at Boston Children's Hospital (L.B., Mark Gorman), MA; Pediatric Multiple Sclerosis and Demyelinating Diseases Center (Manu Goyal, S.M.), Washington University, St. Louis, MO; Department of Neuroscience (J.S.G.), University of California San Diego; UAB Center for Pediatric-Onset Demyelinating Disease (Y.H.-A.C., J.N.), University of Alabama at Birmingham; Pediatric MS Center at NYU Langone Health (L.K.), New York; The Blue Bird Circle Clinic for Multiple Sclerosis (T.E.L., N.M.S.), Texas Children's Hospital, Baylor College of Medicine, Houston, TX; Mellen Center for Multiple Sclerosis (Mary Rensel), Cleveland Clinic, OH; Rocky Mountain Multiple Sclerosis Center (T.S.), Children's Hospital Colorado, University of Colorado at Denver, Aurora; Mayo Clinic (J.-M.T., Moses Rodriguez), Rochester, MN; Department of Neurology (S.R., J.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis Center (E.W.), Weil Institute of Neuroscience, University of California San Francisco; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo; and Brigham MS Center (T.C.), Brigham and Women's Hospital, Boston, MA. tchitnis@rics.bwh.harvard.edu.
 Department of Medical Sciences and Public Health, Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, University of Cagliari, Cagliari, Italy. Department of Neurosciences, ARNAS Brotzu, Cagliari, Italy. Department of Medical Sciences and Public Health, Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, University of Cagliari, Cagliari, Italy. Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Department of Medical Sciences and Public Health, Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, University of Cagliari, Cagliari, Italy. Department of Medical Sciences and Public Health, Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, University of Cagliari, Cagliari, Italy. Radiology Unit, Binaghi Hospital, ASL Cagliari, Cagliari, Italy. Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy. Division of Gynecology and Obstetrics, Department of Surgical Sciences, University of Cagliari, Cagliari, Italy. Department of Medical Sciences and Public Health, Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, University of Cagliari, Cagliari, Italy.
 Endocrine Department, 401 General Military Hospital of Athens, 115 25 Athens, Greece. Department of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Multiple Sclerosis and Demyelinating Diseases Unit, 1st Neurology Department, School of Medicine, Aeginition University Hospital, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Neurology Department, 401 General Military Hospital of Athens, 115 25 Athens, Greece. Department of Nuclear Medicine, 401 Military Hospital of Athens, 115 25 Athens, Greece. Department for Biomedical Research, 251 Air Force General Hospital, 115 25 Athens, Greece. Center for Molecular Biology-Research Unit, 401 Military Hospital of Athens, 115 25 Athens, Greece. Department of Nuclear Medicine, 401 Military Hospital of Athens, 115 25 Athens, Greece. Center for Molecular Biology-Research Unit, 401 Military Hospital of Athens, 115 25 Athens, Greece. Department of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Department of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Endocrine Oncology Unit, First Department of Propaedeutic and Internal Medicine, Laiko Hospital, National and Kapodistrian University of Athens, 115 27 Athens, Greece. Department of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, 115 28 Athens, Greece.
 Department of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland. Department of Biochemical Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland. Department of Neurodegeneration Diagnostics, Medical University of Bialystok, Waszyngtona 15A St., 15-269 Bialystok, Poland.
 Department of Internal Medicine, University of Iowa, Iowa City, IA, United States. Department of Internal Medicine, University of Iowa, Iowa City, IA, United States. Department of Internal Medicine, University of Iowa, Iowa City, IA, United States. Department of Epidemiology, University of Iowa, Iowa City, IA, United States. Department of Internal Medicine, University of Iowa, Iowa City, IA, United States. Department of Internal Medicine, University of Iowa, Iowa City, IA, United States. Institute for Clinical and Translational Science, University of Iowa, Iowa City, IA, United States. Department of Epidemiology, University of Iowa, Iowa City, IA, United States. Department of Epidemiology, University of Iowa, Iowa City, IA, United States. Department of Internal Medicine, University of Iowa, Iowa City, IA, United States.
 Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway akash.kapali@uib.no. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. Department of Health Registry Research and Development, Norwegian Institute of Public Health, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Clinical Medicine, University of Bergen, Bergen, Norway. Department of Epidemiology, Harvard T H Chan School of Public Health, Boston, Massachusetts, USA. Department of Nutrition, Harvard T H Chan School of Public Health, Boston, Massachusetts, USA. Epidemiology and Biostatistics Unit, IRCCS Istituto Delle Scienze Neurologiche di Bologna, Bologna, Emilia-Romagna, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy. Department of Medicine, McGill University, Montreal, Québec, Canada. Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Nutrition, Harvard T H Chan School of Public Health, Boston, Massachusetts, USA.
 School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China. Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong, China. School of Rehabilitation Sciences, Southern Medical University, Guangzhou, China. Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
 Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Institute of Neurosurgery of People's Liberation Army of China (PLA), PLA's Key Laboratory of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. National Translational Science Center for Molecular Medicine and Department of Cell Biology, Fourth Military Medical University, Xi'an 710032, China. Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Department of Biomedical Engineering, Fourth Military Medical University, Xi'an 710032, China. Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Department of Health Service, Fourth Military Medical University, Xi'an 710032, China. Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Institute of Neurosurgery of People's Liberation Army of China (PLA), PLA's Key Laboratory of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Institute of Neurosurgery of People's Liberation Army of China (PLA), PLA's Key Laboratory of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
 Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France. Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France. Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France; Université Paris Cité, 75006 Paris, France. Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France. Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France. Department of Neuroradiology, Hôpital Fondation Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France. Electronic address: lduron@for.paris.
 Ace Alzheimer Center Barcelona - International University of Catalunya (UIC), Barcelona, Spain. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain. Institute of Nanoscience and Nanotechnology (IN2UB), Barcelona, Spain. Department of Pharmacy, Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain. Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain. Biosensing and Bioanalysis Group, Institut de Biotecnologia i de Biomedicina (IBB-UAB), Mòdul B Parc de Recerca UAB, Campus Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain. Grup de Sensors i Biosensors, Departament de Química, Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain. Ace Alzheimer Center Barcelona - International University of Catalunya (UIC), Barcelona, Spain. Ace Alzheimer Center Barcelona - International University of Catalunya (UIC), Barcelona, Spain. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain. Institute of Nanoscience and Nanotechnology (IN2UB), Barcelona, Spain. Department of Pharmacy, Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain. Unit of Synthesis and Biomedical Applications of Peptides, IQAC-CSIC, 08034 Barcelona, Spain. Department of Pharmaceutical Technology, Faculty of Pharmacy, University of Porto, Porto, Portugal. REQUIMTE/UCIBIO, Faculty of Pharmacy, University of Porto, Porto, Portugal. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain. Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain. Biosensing and Bioanalysis Group, Institut de Biotecnologia i de Biomedicina (IBB-UAB), Mòdul B Parc de Recerca UAB, Campus Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain. Biosensing and Bioanalysis Group, Institut de Biotecnologia i de Biomedicina (IBB-UAB), Mòdul B Parc de Recerca UAB, Campus Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain. Grup de Sensors i Biosensors, Departament de Química, Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain. Ace Alzheimer Center Barcelona - International University of Catalunya (UIC), Barcelona, Spain. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain. Ace Alzheimer Center Barcelona - International University of Catalunya (UIC), Barcelona, Spain. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain.
 Postgraduate Program of Neuroscience, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. Postgraduate Program of Pharmacology, Department of Pharmacology, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. Postgraduate Program of Pharmacology, Department of Pharmacology, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. Laboratory of Aging, Resources and Rheumatology, Department of Health Sciences, Federal University of Santa Catarina, Araranguá, Santa Catarina, Brazil. Postgraduate Program of Neuroscience, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. Postgraduate Program of Pharmacology, Department of Pharmacology, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil.
 Laboratory of Molecular Virology, Oswaldo Cruz Institute/ Fiocruz, Rio de Janeiro, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute/ Fiocruz, Rio de Janeiro, Brazil. Laboratory of Molecular Virology, Oswaldo Cruz Institute/ Fiocruz, Rio de Janeiro, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro/UNIRIO, Rio de Janeiro, Brazil. Department of Pharmacology, Institute of Biology, Rio de Janeiro State University, (UERJ), Rio de Janeiro, Brazil. Department of Neurology/Reference and Research Center for Multiple Sclerosis and Other Central Nervous System Idiopathic Demyelinating Inflammatory Diseases, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. Department of Neurology/Reference and Research Center for Multiple Sclerosis and Other Central Nervous System Idiopathic Demyelinating Inflammatory Diseases, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: vdepaula@ioc.fiocruz.br. Department of Neurology/Reference and Research Center for Multiple Sclerosis and Other Central Nervous System Idiopathic Demyelinating Inflammatory Diseases, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro/UNIRIO, Rio de Janeiro, Brazil. Electronic address: sonizavieiraalvesleon@gmail.com. Laboratory of Molecular Virology, Oswaldo Cruz Institute/ Fiocruz, Rio de Janeiro, Brazil.
 Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA. Tisch Multiple Sclerosis Research Center of New York, NY 10019, USA.
 Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples Federico II, Via Pansini 5, Naples 810145, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples Federico II, Via Pansini 5, Naples 810145, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples Federico II, Via Pansini 5, Naples 810145, Italy. Department of Molecular Medicine and Medical Biotechnology, Federico II University of Naples, Italy; MS Unit, Federico II University Hospital, Naples, Italy. Department of Public Health, University of Naples Federico II, Naples, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, Catania, Italy. MS Center, S. Andrea Hospital, Sapienza University of Rome, Rome, Italy. Multiple Sclerosis Center, Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Centro Sclerosi Multipla, ASST Spedali Civili di Brescia, Ospedale di Montichiari, Brescia, Italy. San Luigi Gonzaga Academic Hospital, Orbassano, TO 10043, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DiNOGMI), University of Genoa, Genoa, Italy. Multiple Sclerosis Centre, "E. Muscatello" Hospital - ASP8, Augusta, SR, Italy. S. Filippo Neri Hospital, Rome, Italy. NCL-Istituto di Neuroscienze Gruppo Neuromed, Rome, Italy. Intradepartmental Program of Clinical Psychology, Federico II University Hospital, Naples, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DiNOGMI), University of Genoa, Genoa, Italy; IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. San Luigi Gonzaga Academic Hospital, Orbassano, TO 10043, Italy; Department of Clinical and Biological Sciences, University of Torino, Torino 10128, Italy. Centro Sclerosi Multipla, ASST Spedali Civili di Brescia, Ospedale di Montichiari, Brescia, Italy. Multiple Sclerosis Center, Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, Catania, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Multiple Sclerosis Center, Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy. MS Center, San Pietro Hospital Fatebenefratelli, Rome, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, Catania, Italy. Department of Human Neurosciences, Sapienza University, Rome, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples Federico II, Via Pansini 5, Naples 810145, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University of Naples Federico II, Via Pansini 5, Naples 810145, Italy. Electronic address: roberta.lanzillo@unina.it.
 CEMEREM, APHM La Timone, 264 Rue Saint-Pierre, 13385, Marseille, France. CNRS, CRMBM, UMR 7339, Aix-Marseille Univ, Marseille, France. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Neurologische Klinik, Klinikum Aschaffenburg-Alzenau, Aschaffenburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Universitäres Kompetenzzentrum für Sport- und Bewegungsmedizin (Athleticum) und Institut und Poliklinik für Medizinische Psychologie, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Universitäres Kompetenzzentrum für Sport- und Bewegungsmedizin (Athleticum) und Institut und Poliklinik für Medizinische Psychologie, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Psychiatry and Psychotherapy, Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany. Division of Psychosomatic Medicine, Medical Department, Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany. CEMEREM, APHM La Timone, 264 Rue Saint-Pierre, 13385, Marseille, France. jan-patrick.stellmann@univ-amu.fr. CNRS, CRMBM, UMR 7339, Aix-Marseille Univ, Marseille, France. jan-patrick.stellmann@univ-amu.fr. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. jan-patrick.stellmann@univ-amu.fr.
 Texas Tech University Health Sciences Center, Lubbock, Texas, United States. Texas Tech University Health Sciences Center, Lubbock, Texas, United States. Department of Radiology, Midland Memorial Hospital, Midland, Texas, United States.
 Department of Anesthesiology, West China Hospital, Sichuan University & The Research Units of West China (2018RU012), Chinese Academy of Medical Sciences, West China Hospital, Sichuan University, Chengdu, China. Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, China. Department of Obstetrics and Gynecology Intensive Care Unit, West China Second University Hospital, Sichuan University, Chengdu, China. Department of Neurosurgery, Ya'an People's Hospital, Ya'an, China. Department of Anesthesiology, West China Hospital, Sichuan University & The Research Units of West China (2018RU012), Chinese Academy of Medical Sciences, West China Hospital, Sichuan University, Chengdu, China.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Swedish Neuroscience Institute, Seattle, WA, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Department of Neurology, University of Southern California Keck School of Medicine, Los Angeles, CA, United States. Department of Neurology, University of Rochester, Rochester, NY, United States. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States. Department of Neurology, University of Southern California Keck School of Medicine, Los Angeles, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
 Section of Neuroradiology, Department of Radiology, University Hospital Vall d'Hebron, Autonomous University of Barcelona, Barcelona, Spain. alex.rovira.idi@gencat.cat. Neuroradiology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. Section of Neuroradiology, Department of Radiology, University Hospital Vall d'Hebron, Autonomous University of Barcelona, Barcelona, Spain. Department of Biomedical Imaging and Image Guided Therapy, Medical University of Vienna, Vienna, Austria. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Radiology, Groupe Hospitalier Paris-Saint Joseph, Paris, France. Neuroradiology Unit, IRCCS Istituto Giannina Gaslini, Genoa, Italy. Department of Diagnostic and Interventional Neuroradiology, Hannover Medical School, Hannover, Germany. Department of Radiology, Leiden University Medical Center, Leiden, Netherlands. Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam University Medical Center, Amsterdam, Netherlands. Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy. Research Unit of Radiology, Department of Medicine and Surgery, Università Campus Bio-Medico Di Roma, Rome, Italy. Lysholm Department of Neuroradiology, UCLH National Hospital for Neurology and Neurosurgery, Neuroradiological Academic Unit, UCL Institute of Neurology, London, UK. Centre for Medical Sciences CISMed, University of Trento, Trento, Italy. Radiology, Multizonal Unit of Rovereto and Arco, APSS Provincia Autonoma Di Trento, Trento, Italy.
 Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Neuroinflammation, University College London, London, United Kingdom. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Physics and Chemistry, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy. Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy.
 College of Pharmaceutical Sciences, Southwest University, Chongqing, China. College of Pharmaceutical Sciences, Southwest University, Chongqing, China. Department of Pediatrics, Tangdu Hospital of Fourth Military Medical University, Xi'an, China. Department of Infection, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Infection and Immunity, The First Batch of Key Disciplines on Public Health in Chongqing, Chongqing, China.
 Graduate Institute of Injury Prevention and Control, College of Public Health, Taipei Medical University, Taipei, Taiwan. Department of Emergency, Min-Sheng General Hospital, Taoyuan City, Taiwan. Department of Exercise and Health Promotion, College of Kinesiology and Health, Chinese Culture University, Taipei, Taiwan. Department of Medical Research and Development, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan. Graduate Institute of Natural Products, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan. School of law (Patent), Nottingham Trent University, 50 Shakespeare St, Nottingham NG14FQ, England. Pomato IP (ignite your idea), Nottingham, England.
 DM Neurology, All India Institute of Medical Sciences, Jodhpur, India. DM Neurology, Department of Neurology, All India Institute of Medical Sciences, Jodhpur, India. MS Ophthalmology, Department of Ophthalmology, All India Institute Of Medical Sciences, Jodhpur, India.
 Hospital de Niños Pedro de Elizalde. sbruzziagustina@gmail.com. Hospital de Niños Pedro de Elizalde. salomenasif@gmail.com. Hospital de Niños Pedro de Elizalde. mcoloski@gmail.com. Hospital de Niños Pedro de Elizalde. spajarino@gmail.com. Hospital de Niños Pedro de Elizalde. fabiangambarrutta@hotmail.com. Hospital de Niños Pedro de Elizalde. palomafranco90@gmail.com. Hospital de Niños Pedro de Elizalde. jardimailen@gmail.com.
 Electrical and Computer Engineering, Morgan State University, Baltimore, MD, United States. Lyda Hill Department of Bioinformatics, Southwestern Medical Center, University of Texas, Dallas, TX, United States. Department of Computer Engineering, Faculty of Engineering, Mansoura University, Mansoura, Egypt. Department of Biomedical Equipment and Technology, Applied Health Sciences, Pharos University, Alexandria, Egypt. School of Engineering and Physical Sciences, University of Guelph, Guelph, ON, Canada. Electronics and Communications Engineering, Mansoura University, Mansoura, Egypt.
 Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), National Institute of Health and Medical Research (INSERM) U1291, CNRS U5051, Université de Toulouse III, Toulouse, France. Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, Cologne, Germany.
 Department of Advanced Biomedical Sciences, University "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Naples, Italy. sirio.cocozza@unina.it.
 University Clinic for Radiology, University of Muenster, Muenster, Germany. Department of Neurology with Institute for Translational Neurology, University of Muenster, Muenster, Germany.
 Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, GA, United States. Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, GA, United States. Department of Otolaryngology, Emory University, Atlanta, GA, United States.
 St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada. Keenan Research Centre for Biomedical Science, Unity Health Toronto, Toronto, ON, Canada. St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada. Keenan Research Centre for Biomedical Science, Unity Health Toronto, Toronto, ON, Canada. St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada. St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada. St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada. Keenan Research Centre for Biomedical Science, Unity Health Toronto, Toronto, ON, Canada. Institute of Medical Science, University of Toronto, Toronto, ON, Canada. St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada. Keenan Research Centre for Biomedical Science, Unity Health Toronto, Toronto, ON, Canada. Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
 Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Department of Neurology, Mayo Clinic, Rochester, MN, United States. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
 Medical Student, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Alzahra Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Royan Institute for Biotechnology, Isfahan, Iran. Student Research Committee, Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. Department of Biochemistry, Yazd University of Payame-Noor, Yazd, Iran. Student Research Committee, Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. Multiple Sclerosis and Neuroimmunology Research Center, Isfahan, Iran. Department of Biochemistry, Yazd University of Payame-Noor, Yazd, Iran. Department of Biochemistry, Yazd University of Payame-Noor, Yazd, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Laboratory Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Radiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Student Research Committee, Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
 Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Electroneuromyography and Neuromuscular Diseases Unit, Hôpital Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Institut de Pathologie Multisite-Site Est, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Observatoire Français de la Sclérose en Plaques, Centre de Recherche en Neurosciences de Lyon, Lyon, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France. Eugène Devic EDMUS Foundation against Multiple Sclerosis, State-Approved Foundation, Bron, France. Service de Neuro-oncologie, Hôpital Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Service de Radiologie, Centre Hospitalier Lyon-Sud, Hospices Civils de Lyon, Pierre-Bénite, France. Creatis-LRMN, CNRS UMR 5220, Inserm U630, Université Claude Bernard Lyon 1, Villeurbanne, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Pierre Wertheimer, Hospices Civils de Lyon, Bron, France. Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.
 Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France. Electronic address: augustin.moreau@chru-strasbourg.fr. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France; Clinical Investigation Center INSERM CIC 1434, Strasbourg University Hospitals, Strasbourg, France; INSERM U1119, University of Strasbourg, Strasbourg, France. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France. Department of Neurology, Civilian Hospitals Colmar, Colmar, France. Department of Neurology, Civilian Hospitals Colmar, Colmar, France. Department of Neurology, Civilian Hospitals Colmar, Colmar, France. Department of Neurology, Mulhouse and South Alsace Region Hospital Group, Mulhouse, France. Department of Neurology, Mulhouse and South Alsace Region Hospital Group, Mulhouse, France. Department of Neurology, Mulhouse and South Alsace Region Hospital Group, Mulhouse, France. Department of Neurology, Hospital Centre Haguenau, Haguenau, France. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France; Clinical Investigation Center INSERM CIC 1434, Strasbourg University Hospitals, Strasbourg, France; INSERM U1119, University of Strasbourg, Strasbourg, France. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France; Clinical Investigation Center INSERM CIC 1434, Strasbourg University Hospitals, Strasbourg, France; INSERM U1119, University of Strasbourg, Strasbourg, France. Department of Neurology, Strasbourg University Hospitals, 1 avenue Molière, Strasbourg 67200, France; Clinical Investigation Center INSERM CIC 1434, Strasbourg University Hospitals, Strasbourg, France; INSERM U1119, University of Strasbourg, Strasbourg, France.
 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Alfred Health, Melbourne, Victoria, Australia. Eastern Health, Melbourne, Victoria, Australia. Royal Hobart Hospital, Hobart, Tasmania, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Eastern Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Alfred Health, Melbourne, Victoria, Australia. Melbourne Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Eastern Health, Melbourne, Victoria, Australia. Melbourne Health, Melbourne, Victoria, Australia. The University of Newcastle, Newcastle, New South Wales, Australia. Hunter New England Health, Newcastle, New South Wales, Australia. Brain and Mind Centre, The University of Sydney, Sydney, New South Wales, Australia. Sydney Neuroimaging Analysis Centre, Camperdown, New South Wales, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Department of Medicine, CORe, University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Department of Neurology, Neuroimmunology Centre, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Florey Department of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Alfred Health, Melbourne, Victoria, Australia. Eastern Health, Melbourne, Victoria, Australia. Biogen International GmbH, Zug, Switzerland. Biogen International GmbH, Zug, Switzerland. Biogen International GmbH, Zug, Switzerland. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Alfred Health, Melbourne, Victoria, Australia.
 Specialty Pharmacy Services, Vanderbilt University Medical Center, Nashville, TN, USA. Specialty Pharmacy Services, Vanderbilt University Medical Center, Nashville, TN, USA. University of Rochester Specialty Pharmacy, UR Medicine, Rochester, NY, USA. University of Rochester Specialty Pharmacy, UR Medicine, Rochester, NY, USA. Specialty Pharmacy Development, Fairview Pharmacy Services, Minneapolis, MN, USA. Fairview Pharmacy Services, Minneapolis, MN, USA. WVU Medicine Specialty Pharmacy Services, Allied Health Solutions, Morgantown, WV, USA. WVU Medicine Specialty Pharmacy Services, Allied Health Solutions, Morgantown, WV, USA. Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA. Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA.
 Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. Department of Neurology, University Medical Centre Ljubljana, Ljubljana, Slovenia; Faculty of Medicine, University of Ljubljana, Slovenia. Department of Neurology, University of Szeged, Szeged, Hungary. Faculty of Medicine, University of Belgrade, Belgrade, Serbia; Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia. Department of Neurology, Clinical Center of Montenegro, Podgorica, Montenegro. Department of Neurology, Sestre milosrdnice University Hospital Center, Zagreb, Croatia. Department of Neurology, University Hospital Dubrava, Zagreb, Croatia. Department of Neurology, National Memorial Hospital "dr. Juraj Njavro" Vukovar, Vukovar, Croatia. Department of Neurology, General Hospital Virovitica, Virovitica, Croatia. Department of Neurology, General Hospital Bjelovar, Bjelovar, Croatia. General Hospital Zabok, Zabok, Croatia. Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. Department of Neurology, University Medical Centre Ljubljana, Ljubljana, Slovenia. Faculty of Medicine, University of Belgrade, Belgrade, Serbia; Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia. Faculty of Medicine, Institute of Epidemiology, University of Belgrade, Belgrade, Serbia. Department of Neurology, University of Szeged, Szeged, Hungary. Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia; Faculty of Electrical Engineering and Computing, University of Zagreb, Zagreb, Croatia. Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. Electronic address: mhabek@mef.hr.
 Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Experimental Medicine, Division of Pharmacology, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Medical Sciences, Neurology Unit, AOU San Giovanni and Ruggi, Salerno, Italy. Department of Experimental Medicine, Division of Microbiology and Clinical Microbiology, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Experimental Medicine, Division of Microbiology and Clinical Microbiology, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Mental Health and Public Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Mental Health and Public Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy. antonio.gallo@unicampania.it.
 Neuroscience Research Group (NRG), , Tehran, IranUniversal Scientific Education and Research Network. RINGGOLD: 557765 School of Medicine, , Tehran, IranTehran University of Medical Science. RINGGOLD: 440827 School of Medicine, , Tehran, IranIran University of Medical Sciences. RINGGOLD: 440827 School of Medicine, , Tehran, IranIran University of Medical Sciences. RINGGOLD: 440827 School of Medicine, , Tehran, IranTehran University of Medical Science. RINGGOLD: 440827 Department of Neurology, School of Medicine, The , Baltimore, MD, USAJohn Hopkins University. RINGGOLD: 1466 School of Medicine, , Tehran, IranIran University of Medical Sciences. RINGGOLD: 440827 Department of Public Health, Torbat Jam Faculty of Medical Sciences, Torbat Jam, Iran. Department of Internal Medicine, School of Medicine, Hazrat-e Rasool General Hospital, , IranIran University of Medical Sciences. RINGGOLD: 440827 Department of Parasitology and Mycology, School of Medicine, , Tehran, IranIran University of Medical Sciences. RINGGOLD: 440827 Department of Internal Medicine, School of Medicine, , Tehran, IranIran University of Medical Sciences. RINGGOLD: 440827
 The Danish MS Society, Valby, Denmark. lsk@scleroseforeningen.dk. Danish Technological Institute, Aarhus, Denmark. The Danish MS Society, Valby, Denmark. The Danish MS Society, Valby, Denmark.
 Department of Sport Biological Sciences, Physical Education and Sports Sciences Faculty, Razi University, Kermanshah, Iran. Department of Exercise Physiology, General Directorate of Education Basrah, Basrah, Iraq. Department of Sports Activities, College of Adm&Eco/Qurna, University of Basrah, Basrah, Iraq. Department of Microbiology, Faculty of Medicine, Kindai University, Osaka, Japan. School of Nursing, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States. Department of Sport, Physical Education and Health, Centre for Health and Exercise Science Research, Hong Kong Baptist University, Kowloon, Hong Kong SAR, China. Department of Physical Education and Sport Sciences, Faculty of Humanities and Social Sciences, University of Kurdistan, Sanandaj, Iran. Department of Biomedical Sciences, Gulf Medical University, Ajman, United Arab Emirates. Department of Biomedical Sciences, Gulf Medical University, Ajman, United Arab Emirates. School of Medical Sciences, Bharath Institute of Higher Education and Research (BIHER), Chennai, India. Institute of Health Sciences, Medical College of Rzeszów University, Rzeszów, Poland. Department of Orthopedics and Rehabilitation, Medical University of Warsaw, Warsaw, Poland. Department of Physiotherapy, Faculty of Health Sciences, Jagiellonian University Medical College, Kraków, Poland. Department of Family Medicine and Public Health, Sultan Qaboos University Hospital, Sultan Qaboos University, Muscat, Oman. Department of Anesthesiology, Pharmacology and Therapeutics, The University of British Columbia, Vancouver, BC, Canada. University of Rennes, M2S (Laboratoire Mouvement, Sport, Santé) - EA 1274, Rennes, France. Institute International des Sciences du Sport (2I2S), Irodouër, France.
 Department of Disability and Human Development (ARMA, JK), University of Illinois Chicago, Chicago, IL, USA. Department of Occupational Therapy (ARMA, EWP), College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, USA. Department of Occupational Therapy (ARMA, EWP), College of Applied Health Sciences, University of Illinois Chicago, Chicago, IL, USA. Department of Physical Therapy, Rehabilitation Science, and Athletic Training, University of Kansas Medical Center, Kansas City, KS, USA (JS). Virginia Crawford Research Institute, Shepherd Center, Atlanta, GA, USA (DB). Department of Kinesiology and Community Health (RY, SS, AS, LR), College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, USA. Department of Physical Medicine and Rehabilitation, Michigan Medicine, University of Michigan, Ann Arbor, MI, USA (LA). Department of Disability and Human Development (ARMA, JK), University of Illinois Chicago, Chicago, IL, USA. Department of Kinesiology and Community Health (RY, SS, AS, LR), College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, USA. Department of Kinesiology and Community Health (RY, SS, AS, LR), College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, USA. Department of Kinesiology and Community Health (RY, SS, AS, LR), College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, USA. Center on Health, Aging, and Disability (LR), College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Champaign, IL, USA.
 Department of Neurology, Valdemar Hansens vej 23, Rigshospitalet, Glostrup, Denmark; Institute of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, Odense M, Denmark. Department of Neurology, Valdemar Hansens vej 23, Rigshospitalet, Glostrup, Denmark. Department of Drug Design and Pharmacology, University of Copenhagen, Universitetsparken 2, Copenhagen Ø, Denmark. Department of Drug Design and Pharmacology, University of Copenhagen, Universitetsparken 2, Copenhagen Ø, Denmark. National Center for Cancer Immune Therapy (CCIT-DK), Department of Oncology, Borgmester Ib Juuls Vej 25C, Copenhagen University Hospital, Herlev, Denmark; Department of Immunology and Microbiology, University of Copenhagen, Blegdamsvej 3B, Copenhagen, Denmark. Department of Hematology, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, Copenhagen, Denmark; Department of Clinical Medicine, University of Copenhagen, Blegdamsvej 3B, Copenhagen N, Denmark. Department of Hematology, Zealand University Hospital Roskilde, Sygehusvej 10, Roskilde, Denmark. Department of Hematology, Zealand University Hospital Roskilde, Sygehusvej 10, Roskilde, Denmark. Department of Hematology, Zealand University Hospital Roskilde, Sygehusvej 10, Roskilde, Denmark. Department of Immunology and Microbiology, University of Copenhagen, Blegdamsvej 3B, Copenhagen, Denmark. Institute of Biotechnology, University of Vilnius, Sauletékio al. 7, Vilnius, Lithuania. Institute of Biotechnology, University of Vilnius, Sauletékio al. 7, Vilnius, Lithuania. Department of Neurology, Valdemar Hansens vej 23, Rigshospitalet, Glostrup, Denmark. Institute of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, Odense M, Denmark. Department of Neurology, Valdemar Hansens vej 23, Rigshospitalet, Glostrup, Denmark; Institute of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, Odense M, Denmark. Electronic address: gunnar.houen@regionh.dk.
 ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. Ospedale San Paolo - ASST Santi Paolo e Carlo, Milano, Italia (EG). ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia. Department of Physiopathology and Transplants, University of Milano, Italia (DC). ASTeR Lab Adult Speech-therapy Team Research and Department of Neurorehabilitation (VC, CB, MB, SG, FT, MR, DC, CV), IRCSS Fondazione Don Carlo Gnocchi, Milano, Italia.
 CSUR Esclerosis Múltiple, Hospital Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain; Cátedra de Neuroinmunología Clínica y Esclerosis Múltiple, UCAM-Universidad Católica San Antonio de Murcia, Murcia, Spain. Electronic address: pmecal@gmail.com. Unidad de Esclerosis Múltiple. Instituto de Investigación Ramón y Cajal, Hospital Universitario Ramón y Cajal, Madrid, Spain. Unidad de Neuroinmunología Clínica, Hospital Universitario y Politécnico La Fe, Valencia, Spain. Unidad de Investigación y Tratamiento de la Esclerosis Múltiple, Hospital Vithas Nisa, Sevilla, Spain. Unidad de Esclerosis Múltiple, Sanofi, Madrid, Spain. Servicio de Neurología, Hospital Universitario Cruces-Osakidetza, Bizkaia, Spain. Unidad de Esclerosis Múltiple. Hospital Universitario Son Espases, Palma de Mallorca, Spain.
 Physiotherapy Program, Department of Medical Services and Techniques, Vocational School of Health Services, Istanbul Aydin University, Istanbul, Turkey; Department of Physiotherapy and Rehabilitation, Institute of Graduate Studies, Istanbul University-Cerrahpasa, Istanbul, Turkey. Electronic address: ovacikugur@gmail.com. Department of Physiotherapy and Rehabilitation, Faculty of Health Sciences, Istanbul University-Cerrahpasa, İstanbul, Turkey. Neurology Department, Bakırköy Mazhar Osman Mental Health and Neurological Diseases Education and Research Hospital, İstanbul, Turkey.
 Department of Neurology, Trabzon Kanuni Training and Research Hospital, University of Health Sciences, Inonu Mah., Maras Cad., Ortahisar, Trabzon, Turkey. dr.nuraycan@hotmail.com. Department of Ophthalmology, Trabzon Kanuni Training and Research Hospital, University of Health Sciences, Ortahisar, Trabzon, Turkey.
 Center for Infection and Immunity and Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China. The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy and Clinical Immunology, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China. Center for Infection and Immunity and Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China. Center for Infection and Immunity and Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China. Center for Infection and Immunity and Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China. Department of Laboratory Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China. Division of Nephrology, Department of Medicine, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China. Center for Infection and Immunity and Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China. huangxi6@mail.sysu.edu.cn.
 Croatian Institute of Public Health, Zagreb, Croatia. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. School of Medicine, University of Zagreb, Zagreb, Croatia. School of Medicine, University of Zagreb, Zagreb, Croatia. School of Medicine, University of Zagreb, Zagreb, Croatia. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. School of Medicine, University of Zagreb, Zagreb, Croatia. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. School of Medicine, University of Zagreb, Zagreb, Croatia. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. Faculty of Electrical Engineering and Computing, University of Zagreb, Zagreb, Croatia. Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Center Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. mhabek@mef.hr. School of Medicine, University of Zagreb, Zagreb, Croatia. mhabek@mef.hr.
 Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK. Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK. Centre for Public Health, Queen's University Belfast, Belfast, UK. Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK. Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK. Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK. Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK. UCL Global Business School for Health, University College London, London, UK. Department of Neurology, The Royal Victoria Hospital, Belfast Health and Social Care Trust, Belfast, UK. Department of Neurology, The Royal Victoria Hospital, Belfast Health and Social Care Trust, Belfast, UK. Centre for Public Health, Queen's University Belfast, Belfast, UK. Wellcome Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK.
 Service of Cardiology, Lausanne University Hospital, Lausanne, Switzerland. Service of Cardiology, Lausanne University Hospital, Lausanne, Switzerland. Service of Cardiology, Lausanne University Hospital, Lausanne, Switzerland. Service of Neurology, Lausanne University Hospital, Lausanne, Switzerland. Intensive Care Unit, Lausanne University Hospital, Lausanne, Switzerland. Service of Cardiology, Lausanne University Hospital, Lausanne, Switzerland. Intensive Care Unit, Lausanne University Hospital, Lausanne, Switzerland.
 Physical and Rehabilitation Medicine, Department of Health Sciences, Università del Piemonte Orientale, Novara, Italy. Physical and Rehabilitation Medicine, "Ospedale Maggiore della Carità" University Hospital, Novara, Italy. Physical and Rehabilitation Medicine, Department of Health Sciences, Università del Piemonte Orientale, Novara, Italy. Physical and Rehabilitation Medicine, "Ospedale Maggiore della Carità" University Hospital, Novara, Italy. Physical and Rehabilitation Medicine, A.S.L. Vercelli, Vercelli, Italy. Rehabilitation Unit, Department of Rehabilitation, "Santi Antonio e Biagio e Cesare Arrigo" National Hospital, Alessandria, Italy. Neurorehabilitation Clinic, Department Neurological Sciences, University Hospital of Ancona, Ancona, Italy. Neuroscience and Rehabilitation Department, Ferrara University Hospital, Ferrara, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Neurorehabilitation Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy. Neurorehabilitation Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy. Neurorehabilitation Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy. Spasticity and Movement Disorder Unit, Physical Medicine and Rehabilitation, Policlinico Riuniti, University of Foggia, Foggia, Italy. Spasticity and Movement Disorder Unit, Physical Medicine and Rehabilitation, Policlinico Riuniti, University of Foggia, Foggia, Italy. Department of Translational Medicine, Unit of Medical Statistics, Università del Piemonte Orientale, Novara, Italy. Physical and Rehabilitation Medicine, Department of Health Sciences, Università del Piemonte Orientale, Novara, Italy. Dipartimento Attività Integrate Ricerca e Innovazione (DAIRI), Translational Medicine, "Santi Antonio e Biagio e Cesare Arrigo" National Hospital, Alessandria, Italy. IRCCS Fondazione Santa Lucia, Rome, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Spasticity and Movement Disorder Unit, Physical Medicine and Rehabilitation, Policlinico Riuniti, University of Foggia, Foggia, Italy.
 Department of Psychology, University of Campania "Luigi Vanvitelli", Caserta, CE, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Napoli, NA, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", Caserta, CE, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Napoli, NA, Italy. Department of Psychology, University of Campania "Luigi Vanvitelli", Caserta, CE, Italy.
 Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No.600 Yishan Road, Shanghai 200233, The People's Republic of China. Electronic address: dr_tao.cheng@hotmail.com. Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No.600 Yishan Road, Shanghai 200233, The People's Republic of China. Department of Orthopaedic Surgery, The Second Affiliated Hospital of Nanchang University, No.1 Minde Road, Nanchang 330006, The People's Republic of China. Electronic address: ndefy07018@ncu.edu.cn.
 Department of Medical Sciences, Neurology, Uppsala University, SE-751 85 Uppsala, Sweden. Department of Medical Sciences, Neurology, Uppsala University, SE-751 85 Uppsala, Sweden. Department of Medical Sciences, Neurology, Uppsala University, SE-751 85 Uppsala, Sweden. Department of Surgical Sciences, Neuroradiology, Uppsala University, SE-751 85 Uppsala, Sweden. Department of Surgical Sciences, Neuroradiology, Uppsala University, SE-751 85 Uppsala, Sweden. Department of Medical Sciences, Neurology, Uppsala University, SE-751 85 Uppsala, Sweden.
 Department of Internal Medicine, College of Medicine, Jouf University, Sakaka, Saudi Arabia. Department of Pharmacology, Toxicology and Medicine, Medical Faculty, College of Medicine, Al-Mustansiriyah University, P.O. Box 14132, Baghdad, Iraq. Department of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, NSW, 2770, Australia. AFNP Med, 1030, Vienna, Austria. Department of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Heusnerstrasse 40, 42283, Wuppertal, Germany. marios_papadakis@yahoo.gr. Biology Department, College of Science, Jouf University, Sakaka, 41412, Saudi Arabia. Department of Histology and Cytology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matruh, 51744, Egypt. Department of Pathology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matruh, 51744, Egypt. heba.magdy@mau.edu.eg. Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, Egypt.
 Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Prague, Czech Republic. Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Prague, Czech Republic. Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Technická 2, 160 00 Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and ARTORG Center for Biomedical Engineering Research, Inselspital (Bern University Hospital), University of Bern, Bern, Switzerland.
 PenCHORD (The Peninsula Collaboration for Health Operational Research and Data Science), Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286 Health Economics Group, Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286 Health Economics Group, Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286 Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, , Solna, SwedenKarolinska Institutet. RINGGOLD: 27106 Biogen UK & Ireland, Berkshire, UK. Health Economics Group, Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286 NIHR Applied Research Collaboration South West Peninsula, Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286 Population Data Science, , UKSwansea University. RINGGOLD: 7759 Health Economics Group, Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286 NIHR Applied Research Collaboration South West Peninsula, Department of Health and Community Sciences, , Exeter, UKUniversity of Exeter. RINGGOLD: 3286
 Department of Cognitive Rehabilitation, Neurological Rehabilitation Center Godeshoehe GmbH, Waldstr. 2-10, 53177 Bonn, Germany. Department of Cognitive Rehabilitation, Neurological Rehabilitation Center Godeshoehe GmbH, Waldstr. 2-10, 53177 Bonn, Germany. Department of Cognitive Rehabilitation, Neurological Rehabilitation Center Godeshoehe GmbH, Waldstr. 2-10, 53177 Bonn, Germany. Department of Cognitive Rehabilitation, Neurological Rehabilitation Center Godeshoehe GmbH, Waldstr. 2-10, 53177 Bonn, Germany. Department of Medical Psychology | Neuropsychology and Gender Studies, Center for Neuropsychological Diagnostics and Intervention (CeNDI), Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne 50937, Germany. Department of Cognitive Rehabilitation, Neurological Rehabilitation Center Godeshoehe GmbH, Waldstr. 2-10, 53177 Bonn, Germany. Department of Medical Psychology | Neuropsychology and Gender Studies, Center for Neuropsychological Diagnostics and Intervention (CeNDI), Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne 50937, Germany.
 Centro de Investigación en Ciencias de la Salud (CICSA), FCS, Universidad Anáhuac México, Campus Norte, Huixquilucan, Estado de México, México. Centro de Investigación en Ciencias de la Salud (CICSA), FCS, Universidad Anáhuac México, Campus Norte, Huixquilucan, Estado de México, México. Centro de Investigación en Ciencias de la Salud (CICSA), FCS, Universidad Anáhuac México, Campus Norte, Huixquilucan, Estado de México, México. Centro de Investigación en Ciencias de la Salud (CICSA), FCS, Universidad Anáhuac México, Campus Norte, Huixquilucan, Estado de México, México. School of Sport Sciences, Universidad Anáhuac México, Campus Norte, Huixquilucan, Estado de México, México. IIS Aragon, University of Zaragoza, Department of Physiatry and Nursing, Faculty of Health Sciences, Zaragoza, CP 50009, Spain.
 Department of Radiology, 448249University of Health Sciences, Basaksehir Cam and Sakura City Hospital, Istanbul, Turkey. Department of Radiology, 221265Bezmialem Vakif University Hospital, Istanbul, Turkey. Department of Neurology, 448249University of Health Sciences, Basaksehir Cam and Sakura City Hospital, Istanbul, Turkey. Department of Radiology, 448249University of Health Sciences, Basaksehir Cam and Sakura City Hospital, Istanbul, Turkey.
 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Neurology Unit, Ospedale del Mare-A.S.L Na1-Centro, 80147 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Medical Statistics Unit, Department of Physical and Mental Health and Preventive Medicine, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia 2, 80138 Naples, Italy. Medical Statistics Unit, Department of Physical and Mental Health and Preventive Medicine, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia 2, 80138 Naples, Italy. Human Medicines Division, European Medicines Agency, Domenico Scarlattilaan 6, 1083 HS Amsterdam, The Netherlands. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80131 Naples, Italy.
 Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Clinical Neurology, Queen's Medical Centre, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Department of Radiological Sciences, School of Health and Rehabilitation Sciences, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia. RINGGOLD: 112893 Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Clinical Neurology, Queen's Medical Centre, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Department of Radiological Sciences, School of Applied Medical Sciences, King Saud Bin Abdul-Aziz University for Health Sciences, Riyadh, Saudi Arabia. RINGGOLD: 48149 Sir Peter Mansfield Imaging Centre, School of Medicine, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 NIHR Nottingham Biomedical Research Centre, Queen's Medical Centre, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Medical Physics and Clinical Engineering, Nottingham University Hospitals NHS Trust, Nottingham, UK. RINGGOLD: 9820 Clinical Neurology, Queen's Medical Centre, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Mental Health and Clinical Neurosciences Academic Unit, School of Medicine, University of Nottingham, Nottingham, UK. RINGGOLD: 6123 Clinical Neurology, Queen's Medical Centre, University of Nottingham, Nottingham, UK. RINGGOLD: 6123
 Medicana International Izmir Hospital, Ophthalmology Clinic, Izmir, Turkey. Electronic address: bernasahan@yahoo.com. HSU Izmir Bozyaka Training and Research Hospital Department of Urology, Izmir, Turkey. Electronic address: copura@gmail.com. HSU Izmir Bozyaka Training and Research Hospital Department of Urology, Izmir, Turkey. Electronic address: drokanakmaz@hotmail.com. HSU Haseki Training and Research Hospital Department of Urology, Istanbul, Turkey. Electronic address: ufukcglr@gmail.com. HSU Izmir Bozyaka Training and Research Hospital Department of Urology, Izmir, Turkey. Electronic address: muratsahan87@hotmail.com.
 Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76 Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76 Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76 Stockholm, Sweden. Department of Medicine, Solna, Karolinska Institutet, 171 76 Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76 Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76 Stockholm, Sweden. Electronic address: lara.kular@ki.se.
 School of Infection & Immunity, University of Glasgow, Glasgow, UK. Institute for Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Institute for Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Max Planck Institute for Dynamics and Self-Organization, Göttingen, Germany. Max Planck Institute for Experimental Medicine, Göttingen, Germany. Göttingen Campus Institute for Dynamics of Biological Networks, University of Göttingen, Göttingen, Germany. School of Infection & Immunity, University of Glasgow, Glasgow, UK. School of Infection & Immunity, University of Glasgow, Glasgow, UK. School of Infection & Immunity, University of Glasgow, Glasgow, UK. School of Infection & Immunity, University of Glasgow, Glasgow, UK. Institute for Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Institute for Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Department of Neuropathology, University Hospital Essen, Essen, Germany. School of Infection & Immunity, University of Glasgow, Glasgow, UK. Institute for Neurology, University Medical Center Göttingen, Göttingen, Germany. Center Nanoscale Microscopy and Physiology of the Brain (CNMPB), Göttingen, Germany. Max Planck Institute for Dynamics and Self-Organization, Göttingen, Germany. Max Planck Institute for Experimental Medicine, Göttingen, Germany. Göttingen Campus Institute for Dynamics of Biological Networks, University of Göttingen, Göttingen, Germany. Center for Biostructural Imaging of Neurodegeneration, Göttingen, Germany. Max Planck Institute for Dynamics and Self-Organization, Göttingen, Germany. Max Planck Institute for Experimental Medicine, Göttingen, Germany. Göttingen Campus Institute for Dynamics of Biological Networks, University of Göttingen, Göttingen, Germany. Center for Biostructural Imaging of Neurodegeneration, Göttingen, Germany. Institute for Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Cluster of Excellence "Multiscale Bioimaging: from Molecular Machines to Network of Excitable Cells"(MBExC), University of Goettingen, Germany. School of Infection & Immunity, University of Glasgow, Glasgow, UK.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neurorehabilitation Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neurophysiology Service, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy rocca.mara@hsr.it. Vita-Salute San Raffaele University, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy.
 MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. s.noteboom@amsterdamumc.nl. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Neurology B, Department of Neurosciences, Biomedicine and Movement Sciences, Regional Multiple Sclerosis Center, University of Verona, Verona, Italy. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Department of Biomedical Engineering and Physics, Amsterdam UMC location AMC, Amsterdam, The Netherlands. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Institutes of Healthcare Engineering and Neurology, University College London, London, United Kingdom. Neurology B, Department of Neurosciences, Biomedicine and Movement Sciences, Regional Multiple Sclerosis Center, University of Verona, Verona, Italy. MS Center Amsterdam, Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands.
 Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Neuroimmunology and Multiple Sclerosis Research Section, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Neuroimmunology and Multiple Sclerosis Research Section, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Neuroimmunology and Multiple Sclerosis Research Section, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Neuroimmunology and Multiple Sclerosis Research Section, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Neuroimmunology and Multiple Sclerosis Research Section, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
 Department of Neurology, Academic MS center Zuyd, Zuyderland MC, Sittard-Geleen, The Netherlands; Department of Neurology, School for Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, The Netherlands. Electronic address: d.kreiter@zuyderland.nl. Faculty of Health, Medicine & Life Sciences, Maastricht University, Maastricht, The Netherlands. Zuyderland Academy, Zuyderland Medical Center, Sittard-Geleen & Heerlen, The Netherlands. Department of Neurology, Academic MS center Zuyd, Zuyderland MC, Sittard-Geleen, The Netherlands; Department of Neurology, School for Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, The Netherlands. Department of Neurology, Academic MS center Zuyd, Zuyderland MC, Sittard-Geleen, The Netherlands; Department of Neurology, School for Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, The Netherlands.
 Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. Department of Bacteriology and Virology, Semnan University of Medical Sciences, Semnan, Iran. Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran. Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. yosefi_bahman@semums.ac.ir. Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran. yosefi_bahman@semums.ac.ir. Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. dhaghmorad@gmail.com. Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran. dhaghmorad@gmail.com.
 University Hospital of Nancy, Department of Neurology, 29 av Mar De Lattre de Tassigny, 54000 NANCY, France. Pitié Salpêtrière Hospital, Department of Neurosurgery, 83 Boulevard de l'Hôpital, Bâtiment Babinski, 75013, Paris, France; INSERM (National Institute of Health and Medical Research), U0955, Translational Neuro Psychiatry team, Avenue de Maréchal de Lattre de Tassigny, 94000, Créteil, France. Electronic address: mihaela.bustuchina@inserm.fr. University Hospital of Nancy, Department of Neurology, 29 av Mar De Lattre de Tassigny, 54000 NANCY, France. University Hospital of Nancy, Department of Neurosurgery, 29 av Mar De Lattre de Tassigny, 54000 NANCY, France. Department of Neurosurgery, Clinique Brétéché, Groupe Elsan, 3 Rue De La Béraudiere, 44046 Nantes, France. INSERM (National Institute of Health and Medical Research), U0955, Translational Neuro Psychiatry team, Avenue de Maréchal de Lattre de Tassigny, 94000, Créteil, France; Henri-Mondor Hospital, University Hospital APHP, Department of Neurosurgery, 51 AV Mar de Lattre de Tassigny, 94000 Créteil, France.
 Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy. Istituti Clinici Scientifici Maugeri IRCCS, Neurorehabilitation Unit of Milan Institute, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of NEUROFARBA, University of Florence, Florence, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psichiatry, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21 - 00128 Roma, Italy; Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200 - 00128, Roma, Italy. Electronic address: f.capone@policlinicocampus.it.
 Department of Kinesiology and Nutrition, University of Illinois Chicago, 506 J AHSB, Chicago, IL 60612, USA. Electronic address: robmotl@uic.edu. American Sports Medicine Institute, USA. Center for Neuropsychology and Neuroscience Research, Kessler Foundation, USA. Interdisciplinary School of Health Sciences, University of Ottawa, Canada. Department of Biostatistics, University of Alabama at Birmingham, USA. Center for Innovation and Applied Research, USA. Program in Exercise Science, Department of Physical Therapy, Marquette University, USA.
 School of Social Science, Technological University of the Shannon, Athlone, Ireland. Discipline of Occupational Therapy, School of Health Sciences, University of Galway, Galway, Ireland. Discipline of Occupational Therapy, School of Health Sciences, University of Galway, Galway, Ireland. Discipline of Occupational Therapy, School of Health Sciences, University of Galway, Galway, Ireland.
 Neuroscience Research Group (NRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. fardinnabizade1378@gmail.com. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. fardinnabizade1378@gmail.com. Neuroscience Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran. Neuroscience Research Group (NRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. School of Medicine, Tehran University of Medical Science, Tehran, Iran. Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. School of Medicine, Tehran University of Medical Science, Tehran, Iran. Interdisciplinary Neuroscience Research Program (INRP), Tehran University of Medical Sciences, Tehran, Iran. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
 Faculty of Medical Statistics, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China. Clinical Data Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Emergency Department, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Clinical Data Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Perron Institute, University of Western Australia, Nedlands, WA 6009, Australia. Neurology Department, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Faculty of Medical Statistics, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China. Clinical Research Design Division, Clinical Research Centre, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China. Emergency Department, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
 Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Department of Neurology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran. Email: neskandari@med.mui.ac.ir.
 Department of Neurology, 10th Military Research Hospital and Polyclinic, Powstańców Warszawy 5, 85-681 Bydgoszcz, Poland. Sanitas-Neurology Outpatient Clinic, Dworcowa 110, 85-010 Bydgoszcz, Poland. Department of Ophthalmology, 10th Military Research Hospital and Polyclinic, Powstańców Warszawy 5, 85-681 Bydgoszcz, Poland. Department of Surgery, 10th Military Research Hospital and Polyclinic, Powstańców Warszawy 5, 85-681 Bydgoszcz, Poland. IRCCS-Fondazione Bietti, Via Livenza 3, 00198 Rome, Italy. Department of Ophthalmology, University of Warmia and Mazury, Żołnierska 18, 10-561 Olsztyn, Poland. Institute for Research in Ophthalmology, Foundation for Ophthalmology Development, Mickiewicza 24/3B, 60-836 Poznan, Poland.
 Department of Neurology, Klinikum Bayreuth GmbH, Bayreuth, Germany. Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen, Erlangen, Germany. Fraunhofer Institute for Integrated Circuits (IIS), Digital Health Systems, Erlangen, Germany. Department of Neurology, Klinikum Bayreuth GmbH, Bayreuth, Germany. Bayreuth Center of Sport Science, University of Bayreuth, Bayreuth, Germany. Department of Neurology, Klinikum Bayreuth GmbH, Bayreuth, Germany. Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen, Erlangen, Germany. Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen, Erlangen, Germany. Fraunhofer Institute for Integrated Circuits (IIS), Digital Health Systems, Erlangen, Germany. Department of Neurology, Klinikum Bayreuth GmbH, Bayreuth, Germany. Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen, Erlangen, Germany. Bayreuth Center of Sport Science, University of Bayreuth, Bayreuth, Germany.
 Mental Health Research Center, Department of Psychiatry, School of Medicine, Iran University of Medical Science, Tehran, Iran. Mental Health Research Center, Department of Psychiatry, School of Medicine, Iran University of Medical Science, Tehran, Iran. Mental Health Research Center, Department of Psychiatry, School of Medicine, Iran University of Medical Science, Tehran, Iran. Psychiatrist, Tehran, Iran.
 Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Laboratory of Experimental Neurosciences, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Neuroradiology, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroradiology, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Neurology, IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
 Department of Neurology, Medical University of Lodz, Kościuszki Street 4, 90-419 Lodz, Poland. Department of Neurology, Medical University of Lodz, Kościuszki Street 4, 90-419 Lodz, Poland. Department of Neurology, Medical University of Lodz, Kościuszki Street 4, 90-419 Lodz, Poland. Department of Neurology, Medical University of Lodz, Kościuszki Street 4, 90-419 Lodz, Poland. Department of Neurology, Medical University of Lodz, Kościuszki Street 4, 90-419 Lodz, Poland. Department of Neurology, Medical University of Lodz, Kościuszki Street 4, 90-419 Lodz, Poland.
 Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: aila.sarkesh@gmail.com. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Research Center for Evidence-Based Medicine, Iranian EBM Center: A Joanna Briggs Institute Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran. Research Center for Evidence-Based Medicine, Iranian EBM Center: A Joanna Briggs Institute Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Talebi511@yahoo.com.
 Department of Radiology, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Women's Health Research Center, Mayo Clinic, Rochester, MN, USA. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Women's Health Research Center, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Women's Health Research Center, Mayo Clinic, Rochester, MN, USA.
 Department of Nutrition, Faculty of Pharmacy and Medical Sciences, University of Petra, Amman, Jordan. High Institute of Sport and Physical Education of Sfax, University of Sfax, Sfax, Tunisia. Consultant Neurologist, Amman, Jordan. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, United States. The Cancer Prevention and Control Program, University of South Carolina, Columbia, SC, United States. Department of Nutrition, Connecting Health Innovations LLC, Columbia, SC, United States. Laboratory for Industrial and Applied Mathematics, Department of Statistics, York University, Toronto, ON, Canada. Human Nutrition Unit, Department of Food and Drugs, University of Parma Medical School, Parma, Italy. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, United States. The Cancer Prevention and Control Program, University of South Carolina, Columbia, SC, United States. Department of Nutrition, Connecting Health Innovations LLC, Columbia, SC, United States. Department of Psychiatry, College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Bahrain. Ministry of Health, Government Hospitals, Manama, Bahrain.
 Department of Public Health, University of Naples Federico II, Via Sergio Pansini 5, 80131, Naples, Italy. Drug Policy and Devices Unit, Regione Campania Health Department, Naples, Italy. Department of Public Health, University of Naples Federico II, Via Sergio Pansini 5, 80131, Naples, Italy. Regional Healthcare Society (So.Re.Sa), Naples, Italy. Regional Healthcare Society (So.Re.Sa), Naples, Italy. Innovation and Data Analytics (So.Re.Sa), Naples, Italy. Department of Public Health, University of Naples Federico II, Via Sergio Pansini 5, 80131, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Odontostomatology, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Public Health, University of Naples Federico II, Via Sergio Pansini 5, 80131, Naples, Italy. raffaele.palladino@unina.it. Department of Primary Care and Public Health, Imperial College, London, UK. raffaele.palladino@unina.it. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Primary Care and Public Health, Imperial College, London, UK. Department of Molecular Medicine and Medical Biotechnology, Federico II University, Naples, Italy.
 Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Immunology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Japan. Multiple Sclerosis Center, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Radiology, National Center Hospital, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Radiology, National Center Hospital, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Translational Medical Center, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Translational Medical Center, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Immunology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan. Multiple Sclerosis Center, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan.
 Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Registry, Department of Neurology, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark.
 Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University, 80131 Naples, Italy. Multiple Sclerosis Center, Department of Neuroscience, Università degli Studi di Padova, 35122 Padova, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University, 80131 Naples, Italy. Department of Neuroscience, Multiple Sclerosis Center-Neurology Unit, S. Maria delle Croci Hospital of Ravenna, AUSL Romagna, 48121 Ravenna, Italy. Department of Medical and Surgical Sciences, University of Bologna, 40126 Bologna, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University, 80131 Naples, Italy. Multiple Sclerosis Center, Department of Neuroscience, Università degli Studi di Padova, 35122 Padova, Italy. Multiple Sclerosis Center, Second Division of Neurology, Department of Advanced Medical and Surgical Science, University of Campania Luigi Vanvitelli, 80131 Naples, Italy. Department of Health Sciences, University of Genova, 16132 Genova, Italy. Department of Health Sciences, University of Genova, 16132 Genova, Italy.
 Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands e.strijbis@amsterdamumc.nl. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, Rijnstate Hospital Arnhem, Arnhem, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam University Medical Centers, Amsterdam, The Netherlands. Department of Medicine, Neurology service, Maisonneuve-Rosemont Hospital, Montreal, Québec, Canada. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, Washington, USA. Multiple Sclerosis Center, Swedish Neuroscience Institute, Seattle, Washington, USA. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA. Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada.
 Multiple Sclerosis Unit, Neurology Service, Hospital Universitario Virgen Macarena, Seville, Spain. Multiple Sclerosis Unit, Neurology Service, Hospital Universitario Virgen Macarena, Seville, Spain. Multiple Sclerosis Unit, Neurology Service, Hospital Universitario Virgen Macarena, Seville, Spain. Multiple Sclerosis Unit, Neurology Service, Hospital Universitario Virgen Macarena, Seville, Spain. Multiple Sclerosis Unit, Neurology Service, Hospital Universitario Virgen Macarena, Seville, Spain. Department of Pharmacy, Hospital Universitario Virgen Macarena, Seville, Spain. Multiple Sclerosis Unit, Sanofi, Barcelona, Spain. Multiple Sclerosis Unit, Neurology Service, Hospital Universitario Virgen Macarena, Seville, Spain.
 Department of Systems Medicine, Tor Vergata University, Via Montpellier, 1, 00133 Rome, Italy. IRCCS Neuromed, Pozzilli, Italy. Department NEUROFARBA, University of Florence, Florence, Italy. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy. Multiple Sclerosis Clinical Care and Research Center and Department of Neuroscience (NSRO), Federico II University, Naples, Italy. Department of Medical Science and Public Health and Centro Sclerosi Multipla, University of Cagliari, Cagliari, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Neurosciences, S Camillo Forlanini Hospital Rome, Rome, Italy. Department of Neuroscience, University of Padova, Padua, Italy. Department of Human Neuroscience, Sapienza University, Rome, Italy. University of Bari 'Aldo Moro', Bari, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milano, Italy.
 Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Genetics Institute, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL 32610, USA. Genetics Institute, University of Florida, Gainesville, FL 32610, USA. Department of Neuroscience, College of Medicine, University of Florida, Gainesville, FL 32610, USA.
 Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India. Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India. Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India. Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India.
 Department of Neurology, University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. yaprakunsal@gmail.com. Department of Neurology, University of Health Sciences, Izmir Bozyaka Education and Research Hospital, Izmir, Turkey. Department of Neurology, Private Emotplus Hospital, Izmir, Turkey.
 Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States. Department of Neurology, University of Chicago Medicine, Chicago, IL, United States.
 VA Puget Sound Health Care System, Seattle, WA; VA MS Center of Excellence West, Seattle, WA; Center of Excellence in Substance Addiction Treatment and Education, Seattle, WA; Department of Rehabilitation Medicine, University of Washington, Seattle, WA. Electronic address: Aaron.Turner@va.gov. Department of Anesthesiology, University of Michigan, Ann Arbor, MI. VA Puget Sound Health Care System, Seattle, WA; Center of Excellence in Substance Addiction Treatment and Education, Seattle, WA; Health Services Research & Development (HSR&D), Seattle Center of Innovation for Veteran-Centered and Value-Driven Care, Seattle, WA; Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA. VA Puget Sound Health Care System, Seattle, WA; Department of Rehabilitation Medicine, University of Washington, Seattle, WA; Clinical Learning, Evidence, and Research Center (CLEAR), University of Washington, Seattle, WA. VA Puget Sound Health Care System, Seattle, WA; Department of Rehabilitation Medicine, University of Washington, Seattle, WA. VA Puget Sound Health Care System, Seattle, WA; VA MS Center of Excellence West, Seattle, WA. VA Puget Sound Health Care System, Seattle, WA; VA MS Center of Excellence West, Seattle, WA; Department of Rehabilitation Medicine, University of Washington, Seattle, WA.
 Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Interdisciplinary Platform, Psychiatry, and Psychology, Division of Molecular and Cognitive Neuroscience, Neuropsychology, and Behavioral Neurology Unit, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Computer Science, University of Verona, Verona, Italy. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Computer Science, University of Verona, Verona, Italy. Department of Computer Science, University of Verona, Verona, Italy. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Division of Radiological Physics, Department of Radiology, University Hospital Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Interdisciplinary Platform, Psychiatry, and Psychology, Division of Molecular and Cognitive Neuroscience, Neuropsychology, and Behavioral Neurology Unit, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINk) Basel, Department of Biomedical Engineering, University Hospital Basel, University of Basel, Basel, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland.
 School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD. Electronic address: Jaqueline.hamrick@usuhs.edu. Program Director National Capital Consortium Psychiatry, Walter Reed National Military Medical Center, Bethesda, MD.
 Department of Electric and Electronic Engineering, Faculty of Engineering, University of Bristol, Bristol, UK.
 From the Urology and Nephrology Research Center, Shahid Beheshti University, Tehran, Iran.
 Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address: chaohanxu@hrbmu.edu.cn. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address: fujin@hrbmu.edu.cn.
 Univ Rennes, EHESP, CNRS, Inserm, ARENES UMR 6051, RSMS U 1309, F-35000 Rennes, France. Neurology Department CRCSEP, Rennes Clinical Investigation Centre CIC-P 1414, Rennes University Hospital Rennes University INSERM, Rennes, France. Neurology Department CRCSEP, Rennes Clinical Investigation Centre CIC-P 1414, Rennes University Hospital Rennes University INSERM, Rennes, France. Univ Rennes, EHESP, CNRS, Inserm, ARENES UMR 6051, RSMS U 1309, F-35000 Rennes, France.
 Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. giuseppe.pontillo@unina.it. Department of Electrical Engineering and Information Technology, University "Federico II", Naples, Italy. giuseppe.pontillo@unina.it. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Institute of Biostructure and Bioimaging, National Research Council, Naples, Italy. Institute of Biostructure and Bioimaging, National Research Council, Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Multiple Sclerosis Centre, II Division of Neurology, Department of Clinical and Experimental Medicine, "Luigi Vanvitelli" University, Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. Department of Neurosciences and Reproductive and Odontostomatological Sciences, University "Federico II", Naples, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy. Institute of Nanotechnology, National Research Council, Lecce, Italy. Department of Advanced Biomedical Sciences, University "Federico II", Via Pansini 5, 80131, Naples, Italy.
 Buffalo Neuroimaging Analysis Center (BNAC), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA. Buffalo Neuroimaging Analysis Center (BNAC), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA. Center for Biomedical Imaging and Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center (BNAC), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA. Buffalo Neuroimaging Analysis Center (BNAC), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA. RCCS, Fondazione Don Carlo Gnocchi ONLUS, 20121 Milan, Italy. Jacobs Comprehensive MS Treatment and Research Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14202, USA. Buffalo Neuroimaging Analysis Center (BNAC), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.
 Department of Neurology, Hospital Universitario Dr. Peset, Valencia, Spain. Gastroenterology Unit, Hospital Universitario y Politécnico La Fe, Valencia, Spain. Gastroenterology Unit, Hospital Universitario y Politécnico La Fe, Valencia, Spain. Department of Neurology, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
 Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois at Chicago, Chicago, IL, USA. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois at Chicago, Chicago, IL, USA. Interdisciplinary School of Health Sciences, University of Ottawa, Ottawa, ON, Canada. Brain and Mind Research Institute, University of Ottawa, Ottawa, ON, Canada. Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois at Chicago, Chicago, IL, USA.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Microbiology, Tumor and Cell Biology, Biomedicum Q8C, Karolinska Institutet, Stockholm, 171 77, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Department of Neurology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, BRIDGE, University of Southern Denmark, Odense, Denmark; Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark. Electronic address: maria.louise.elkjaer@rsyd.dk. Department of Neurology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, BRIDGE, University of Southern Denmark, Odense, Denmark; Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark. Department of Clinical Genetics, Odense University Hospital, Odense, Denmark; Clinical Genome Center, University of Southern Denmark & Region of Southern Denmark, Odense, Denmark; Human Genetics, Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Biogen, Cambridge, MA, USA. Department of Clinical Research, BRIDGE, University of Southern Denmark, Odense, Denmark; Department of Clinical Genetics, Odense University Hospital, Odense, Denmark; Clinical Genome Center, University of Southern Denmark & Region of Southern Denmark, Odense, Denmark; Human Genetics, Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Department of Neurology, Hospital of Southwest Jutland, Esbjerg, Denmark. Department of Neurology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, BRIDGE, University of Southern Denmark, Odense, Denmark; Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark. Electronic address: zsolt.illes@rsyd.dk.
 Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences (CAS), Shenzhen, China. Institute of Biochemistry and Cell Biology (IBBC), National Research Council (CNR), Naples, Italy. Stazione Zoologica Anton Dohrn (SZN), Napoli, Italy. China-Italy Joint Laboratory of Pharmacobiotechnology for Medical Immunomodulation, Shenzhen, China. Institute of Biochemistry and Cell Biology (IBBC), National Research Council (CNR), Naples, Italy. Stazione Zoologica Anton Dohrn (SZN), Napoli, Italy. China-Italy Joint Laboratory of Pharmacobiotechnology for Medical Immunomodulation, Shenzhen, China. Clinical Immunology and Allergy Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. Laboratory of Experimental Neuro-psychobiology, Department of Clinical and Behavioral Neurology, Santa Lucia Foundation, Rome, Italy.
 Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia. Electronic address: ustiugovaalina@gmail.com. Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia. Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia. Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia. Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia. Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
 Department of Zoology, School of Biological Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, India. Department of Pharmacology, School of Health Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, India. Department of Zoology, School of Biological Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, India. Department of Zoology, School of Biological Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, India. Department of Agricultural Sciences, Institute of Applied Sciences and Humanities, GLA University, Mathura, Uttar Pradesh, India. Department of Pharmacology, School of Health Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, India. Department of Zoology, School of Biological Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, India.
 Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8549, Japan. Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Department of Molecular Pharmacology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
 VIB Center for Inflammation Research, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. VIB Center for Inflammation Research, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. VIB Center for Inflammation Research, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. VIB Center for Inflammation Research, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
 Servicio de Dermatología, Hospital Universitario Central de Asturias (HUCA), Oviedo, España. Electronic address: bvazlosada@gmail.com. Servicio de Anatomía Patológica, Hospital Universitario Central de Asturias (HUCA), Oviedo, España. Servicio de Neurología, Hospital Universitario Central de Asturias (HUCA), Oviedo, España. Servicio de Dermatología, Hospital Universitario Central de Asturias (HUCA), Oviedo, España.

 Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Pharmaceutical Chemistry Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Pharmaceutical Chemistry Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Electronic address: ksairam.phe@iitbhu.ac.in.
 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia. Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Saudi Arabia.
 Department of Neonatology, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China. Research Institute for Reproductive Health and Genetic Diseases, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China. Department of Neonatology, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China. Research Institute for Reproductive Health and Genetic Diseases, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China. Department of Neonatology, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China. Department of Neonatology, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China. Research Institute for Reproductive Health and Genetic Diseases, Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, China.
 Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, United States; Department of Internal Medicine, Mount Sinai Hospital, Chicago, IL, United States. Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, United States; Chicago Medical School-Rosalind Franklin University, North Chicago, IL, United States. Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, United States. Electronic address: jori_fleisher@rush.edu.
 Neurology Department, Faculty of Medicine, Cairo University, Cairo, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Cairo, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Cairo, Egypt. Neurology Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
 Center for Neuroinflammation and Experimental Therapeutics, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology, Center for Neuroimmunology and Neuroinfectious Diseases, Washington University School of Medicine, St. Louis, MO, USA. Centre for Virus Research, The Westmead Institute for Medical Research, The University of Sydney, Westmead, NSW, Australia. Merck Healthcare KGaA, Darmstadt, Germany. Merck Healthcare KGaA, Darmstadt, Germany. Merck Healthcare KGaA, Darmstadt, Germany. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. Merck Healthcare KGaA, Darmstadt, Germany. Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA. Department of Neurology-Neuroimmunology, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Barcelona, Spain.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Laboratory for Clinical Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden. Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Laboratory for Clinical Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
 Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. Health Education and Health Promotion, Social Determinants in Health Promotion Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. hosseinishirin@ymail.com.
 Laboratório de Biologia Celular e Tecidual, Universidade Estadual do Norte Fluminense Darcy Ribeiro, Campos dos Goytacazes, RJ, Brazil. Laboratório de Neurobiologia Celular, Universidade Federal do Rio de Janeiro, Instituto de Ciências Biomédicas, Rio de Janeiro, RJ, Brazil. Laboratório de Neurobiologia Celular, Universidade Federal do Rio de Janeiro, Instituto de Ciências Biomédicas, Rio de Janeiro, RJ, Brazil.
 The Neuro (Montreal Neurological Institute-Hospital), McGill University, Montréal, QC, Canada. Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. The Neuro (Montreal Neurological Institute-Hospital), McGill University, Montréal, QC, Canada adil.harroud@mcgill.ca. Department of Neurology and Neurosurgery, McGill University, Montréal, QC, Canada. Department of Human Genetics, McGill University, Montréal, QC, Canada.
 Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. wb255@cam.ac.uk.
 Valentine School of Nursing at Saint Louis University, Saint Louis, MO, USA. RINGGOLD: 7547 Valentine School of Nursing at Saint Louis University, Saint Louis, MO, USA. RINGGOLD: 7547 Seahorn Advisors, Boston, MA, USA. Care Experience, Value Institute, Dartmouth Health, Lebanon, NH, USA. Departments of Community and Family Medicine, Geisel School of Medicine at Dartmouth, Psychiatry and the Dartmouth Institute, Hanover and Lebanon, NH, USA. RINGGOLD: 12285 Goldfarb School of Nursing at Barnes Jewish College, Saint Louis, MO, USA. RINGGOLD: 32989 Valentine School of Nursing at Saint Louis University, Saint Louis, MO, USA. RINGGOLD: 7547
 Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroscience, University of Catania Department of Surgical and Medical Sciences and Advanced Technologies 'G.F. Ingrassia', Catania, Italy. Multiple Sclerosis Center, University of Catania, Catania, Italy. Department of Neurology, Hospital Universitario Virgen Macarena, Sevilla, Andalucía, Spain. Department of Neurology, Hospital Universitario Virgen Macarena, Sevilla, Andalucía, Spain. MS Center, CHUM, Montreal, Quebec, Canada. Faculty of Medicine, Universite de Montreal, Montreal, Quebec, Canada. MS Center, CHUM, Montreal, Quebec, Canada. Faculty of Medicine, Universite de Montreal, Montreal, Quebec, Canada. MS Center, CHUM, Montreal, Quebec, Canada. Faculty of Medicine, Universite de Montreal, Montreal, Quebec, Canada. Department of Neuroscience, Imaging, and Clinical Sciences, Gabriele d'Annunzio University of Chieti and Pescara Department of Sciences, Chieti, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. UOSI Riabilitazione Sclerosi Multipla, IRCCS Istituto Delle Scienze Neurologiche di Bologna, Bologna, Italy. Faculty of Medicine, Dokuz Eylul Universitesi, Izmir, Turkey. Department of Neurology, Zuyderland Medical Centre, Sittard-Geleen, The Netherlands. School for Mental Health and Neuroscience, Universiteit Maastricht, Maastricht, The Netherlands. Medical Faculty, Karadeniz Technical University, Trabzon, Trabzon, Turkey. Department of Neurology, CIUSSS du Centre-Ouest-de-l'Ile-de-Montreal, Montreal, Quebec, Canada. Medical Faculty, Ondokuz Mayis University, Samsun, Turkey. Department NEUROFARBA, University of Florence, Firenze, Italy. Department of Neurology, Azienda Ospedaliera di Rilievo Nazionale e di Alta Specialità San Giuseppe Moscati, Avellino, Italy. Department of Neurology, Hospital Germans Trias i Pujol, Badalona, Spain. UO Neurologia, Azienda Ospedaliera di Rilievo Nazionale e di Alta Specializzazione Garibaldi, Catania, Sicilia, Italy. UOC Neurologia, Azienda Sanitaria Unica Regionale, Ancona, Italy. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. Department of Neurology, Box Hill Hospital, Box Hill, Victoria, Australia. Department of Medicine, Monash University, Clayton, Victoria, Australia. Department of Neurology, Box Hill Hospital, Box Hill, Victoria, Australia. Department of Medicine, Monash University, Clayton, Victoria, Australia. Department of Neurology, The Alfred, Melbourne, Victoria, Australia. Department of Neurology, The Alfred, Melbourne, Victoria, Australia. Central Clinical School, Monash University, Clayton, Victoria, Australia. Department of Neurology, The Alfred, Melbourne, Victoria, Australia. Central Clinical School, Monash University, Clayton, Victoria, Australia. Department of Neurology, Azienda Ospedaliera Universitaria 'San Giovanni di Dio e Ruggi d'Aragona' Plesso 'Ruggi', Salerno, Italy. Department of Neurology, Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia tomas.kalincik@unimelb.edu.au. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia.
 Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK elisa.colato.18@ucl.ac.uk. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Centre for Medical Image Computing (CMIC), Department of Computer Science, University College London, London, UK. Centre for Medical Image Computing (CMIC), Department of Medical Physics and Biomedical Engineering, University College London, London, UK. e-Health Center, Universitat Oberta de Catalunya, Barcelona, Spain. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Québec, Canada. McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Québec, Canada. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Brain Connectivity Centre, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Centre for Medical Image Computing (CMIC), Department of Medical Physics and Biomedical Engineering, University College London, London, UK. Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, location Vrije Universiteit, Amsterdam, Netherlands. Institute for Health Research (NIHR), University College London Hospitals (UCLH) Biomedical Research Centre (BRC), London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Institute for Health Research (NIHR), University College London Hospitals (UCLH) Biomedical Research Centre (BRC), London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Institute for Health Research (NIHR), University College London Hospitals (UCLH) Biomedical Research Centre (BRC), London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Centre for Medical Image Computing (CMIC), Department of Medical Physics and Biomedical Engineering, University College London, London, UK.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia. Murdoch Children's Research Institute, Royal Children's Hospital, The University of Melbourne, Parkville, Victoria, Australia. Menzies Health Institute Queensland, Griffith University, Southport, Queensland, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Melbourne School of Population and Global Health, The University of Melbourne, Parkville, Victoria, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia.
 Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Endowment Fund IMPULS, Prague, Czech Republic. Endowment Fund IMPULS, Prague, Czech Republic. Department of Economic Statistics, Prague University of Economics and Business, Prague, Czech Republic. Endowment Fund IMPULS, Prague, Czech Republic. Department of Economic Statistics, Prague University of Economics and Business, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. 2nd Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovak Republic. Department of Neurology, Hospital Ceske Budejovice, Ceske Budejovice, Czech Republic. Department of Neurology, Hospital of Jihlava, Jihlava, Czech Republic. First Department of Neurology, Masaryk University, St. Anne's University Hospital, Brno, Czech Republic. Department of Neurology, Thomayer Hospital, Prague, Czech Republic. Department of Neurology, University Hospital Ostrava, Ostrava, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital Olomouc, Olomouc, Czech Republic. Department of Neurology, Hospitals of the Pardubice Region, Hospital of Pardubice, Pardubice, Czech Republic. Department of Neurology, Charles University in Prague, Faculty of Medicine and University Hospital Hradec Kralove, Hradec Kralove, Czech Republic. Department of Neurology, Charles University in Prague, Faculty of Medicine in Pilsen and University Hospital Pilsen, Pilsen, Czech Republic. Department of Neurology, Tomas Bata Regional Hospital, Zlin, Czech Republic. Department of Neurology, 2nd Faculty of Medicine, Charles University in Prague and Motol University Hospital, Prague, Czech Republic. Charles University in Prague, Third Faculty of Medicine, Charles University and Hospital Kralovske Vinohrady, Prague, Czech Republic. Department of Neurology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic. Department of Neurology, KZ a.s., Hospital Teplice, Teplice, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic.
 Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. School of Basic Medical Sciences, Shanxi Medical University, Taiyuan, China. Shanxi Key Laboratory of Big Data for Clinical Decision Research, Taiyuan, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi Province, China. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi Province, China. shengxiao_zhang@163.com. Shanxi Provincial Key Laboratory of Rheumatism Immune Microecology, Taiyuan, Shanxi Province, China. shengxiao_zhang@163.com. Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, Taiyuan, Shanxi Province, China. shengxiao_zhang@163.com.
 Creighton University Asram Medical College, Eluru, India
 Department of Laboratory Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. elzbieta.cecerska.heryc@pum.edu.pl. Department of Laboratory Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. Department of Laboratory Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. Department of Laboratory Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. Department of Laboratory Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. Department of Psychiatry, Pomeranian Medical University of Szczecin, Broniewskiego 26, 71-460, Szczecin, Poland. Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. Department of Medical Analytics, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland. Department of Laboratory Medicine, Pomeranian Medical University of Szczecin, PowstancowWielkopolskich 72, 70-111, Szczecin, Poland.
 Department of Veterans Affairs Portland Health Care System, Portland, OR, United States. Neurology, Oregon Health & Science University, Portland, OR, United States. Biostatistics and Design Program, Oregon Health & Science University/Portland State University School of Public Health, Portland, OR, United States. Department of Veterans Affairs Portland Health Care System, Portland, OR, United States. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, United States. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, United States. Neurology, Oregon Health & Science University, Portland, OR, United States. Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, United States. Department of Medicine, University of Ottawa and the Ottawa Hospital Research Institute, Ottawa, ON, Canada. Department of Veterans Affairs, Salt Lake City Health Care System, Salt Lake City, UT, United States. Neurology, University of Utah, Salt Lake City, UT, United States. Neurology, Swedish Medical Center, Seattle, WA, United States. Lerner College of Medicine at the University of Vermont, Burlington, VT, United States. Neurology, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Veterans Affairs Washington DC Medical Center, Washington, DC, United States. University of Maryland School of Medicine, Baltimore, MD, United States. Department of Veterans Affairs, Puget Sound Health Care System, Seattle, WA, United States. Rehabilitation Medicine & Epidemiology, University of Washington, Seattle, WA, United States. Department of Veterans Affairs North Texas Health Care System-Dallas, Dallas, TX, United States. Neurology, University of Texas Southwestern Medical Center, Dallas, TX, United States. Peter O'Donnell Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, United States. Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Department of Veterans Affairs, Puget Sound Health Care System, Seattle, WA, United States. Rehabilitation Medicine & Epidemiology, University of Washington, Seattle, WA, United States.
 Ondokuz Mayıs University Faculty of Medicine Department of Neurology, Samsun, Turkey. Ondokuz Mayıs University Graduate School of Education, Department of Neuroscience, Samsun, Turkey. Ondokuz Mayıs University Faculty of Medicine Department of Neurology, Samsun, Turkey. Karadeniz Technical University Faculty of Medicine Department of Neurology, Trabzon, Turkey. Van Yüzüncü Yıl University Faculty of Medicine Department of Neurology, Van, Turkey. Gaziantep University Faculty of Medicine Department of Neurology, Gaziantep, Turkey. İzmir Katip Çelebi University Faculty of Medicine Department of Neurology, İzmir, Turkey. İzmir Katip Çelebi University Faculty of Medicine Department of Neurology, İzmir, Turkey. Health Sciences University Haydarpaşa Numune Training and Research Hospital, Department of Neurology, İstanbul, Turkey. Ege University Faculty of Medicine Department of Neurology, İzmir, Turkey. Kocaeli University Faculty of Medicine Department of Neurology, Kocaeli, Turkey. Kocaeli University Faculty of Medicine Department of Neurology, Kocaeli, Turkey. Bursa High Specialization Training and Research Hospital Neurology Clinic, Bursa, Turkey. Sakarya University Faculty of Medicine, Sakarya Training and Research Hospital Neurology Clinic, Sakarya, Turkey. Trakya University Faculty of Medicine Department of Neurology, Edirne, Turkey. Health Sciences University Haseki Training and Research Hospital Neurology Clinic, İstanbul, turkey. Health Sciences University Ankara Gülhane Training and Research Hospital Neurology Clinic, Ankara, Turkey. Ankara City Hospital Neurology Clinic, Ankara, Turkey. Health Sciences University Bağcılar Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Health Sciences University Bağcılar Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Ankara Gaziler Physical Therapy Rehabilitation Training and Research Hospital Neurology Clinic, Ankara, Turkey. Mersin University Faculty of Medicine Department of Neurology, Mersin, Turkey. Bolu İzzet Baysal University Faculty of Medicine Department of Neurology, Bolu, Turkey. Çanakkale On Sekiz Mart University Faculty of Medicine Department of Neurology, Çanakkale, Turkey. Erciyes University Faculty of Medicine Department of Neurology, Kayseri, Turkey. Ankara Training and Research Hospital Neurology Clinic, Ankara, Turkey. Bursa High Specialization Training and Research Hospital Neurology Clinic, Bursa, Turkey. Cumhuriyet University Faculty of Medicine Department of Neurology, Sivas, Turkey. Bezmi Alem Vakıf University Faculty of Medicine Department of Neurology, İstanbul, Turkey. Namık Kemal University Faculty of Medicine Department of Neurology, Tekirdağ, Turkey. Atatürk University Faculty of Medicine Department of Neurology, Erzurum, Turkey. Marmara University Faculty of Medicine Department of Neurology, İstanbul, Turkey. Ankara Başkent University Faculty of Medicine Department of Neurology, Ankara, Turkey. Ankara Gazi University Faculty of Medicine Department of Neurology, Ankara, Turkey. Medipol University, Faculty of Pharmacy, Ankara, Turkey. Ondokuz Mayıs University, Faculty of Arts and Sciences, Department of Statistics, Samsun, Turkey.
 Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, Napoli, Italy marcello.moccia@unina.it. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Public Health, University of Naples Federico II, Naples, Italy. Regional Healthcare Society (So.Re.Sa), Naples, Italy. Campania Region Healthcare System Commissioner Office, Naples, Italy. Innovation and Data Analytics, Regional Healthcare Society (So.Re.Sa), Naples, Italy. Department of Public Health, University of Naples Federico II, Naples, Italy. Department of Neuroscience, Reproductive Science and Odontostomatology, University of Naples Federico II, Naples, Italy. Department of Neuroscience, Reproductive Science and Odontostomatology, University of Naples Federico II, Naples, Italy. Department of Human Neurosciences, Sapienza University, Rome, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Neuroscience, Reproductive Science and Odontostomatology, University of Naples Federico II, Naples, Italy. Department of Public Health, University of Naples Federico II, Naples, Italy. Multiple Sclerosis Unit, Policlinico Federico II University Hospital, Naples, Italy. Department of Neuroscience, Reproductive Science and Odontostomatology, University of Naples Federico II, Naples, Italy. Department of Public Health, University of Naples Federico II, Naples, Italy. Department of Primary Care and Public Health, Imperial College, London, UK.
 Multiple Sclerosis Comprehensive Care Center, University of Southern California, Los Angeles, CA, USA. Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. Autoimmunity Center of Excellence, Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA. Graduate Program in Immunology, Program in Biomedical Sciences, University of Michigan Medical School, Ann Arbor, MI, USA. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Multiple Sclerosis Comprehensive Care Center, UC-Health Neurology Clinic, Fort Collins, CO, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. sai.shankar@biogen.com. , 133 Boston Post Road, Weston, MA, 02493, USA. sai.shankar@biogen.com.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China. Dept. of Neurology, First Hospital of Shanxi Medical University, Taiyuan 030001, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China; Dept. of Neurology, Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan 030032, China. Dept. of Neurosurgery/The Key Laboratory of Prevention and Treatment of Neurological Disease of Shanxi Provincial Health Commission, Sinopharm Tongmei General Hospital, Datong 037003, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China; Dept. of Neurosurgery/The Key Laboratory of Prevention and Treatment of Neurological Disease of Shanxi Provincial Health Commission, Sinopharm Tongmei General Hospital, Datong 037003, China. Dept. of Neurology, First Hospital of Shanxi Medical University, Taiyuan 030001, China. Dept. of Neurosurgery/The Key Laboratory of Prevention and Treatment of Neurological Disease of Shanxi Provincial Health Commission, Sinopharm Tongmei General Hospital, Datong 037003, China. Institute of Neurology, Huashan Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200433, China. Electronic address: bgxiao@shmu.edu.cn. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China. Electronic address: macungen@sxtcm.edu.cn.
 Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden elisa.longinetti@ki.se. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Örebro University, Orebro, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Clinical and Translational Neuroscience, Kaiser Permanente Southern California, Pasadena, California, USA. Department of Clinical Neuroscience, University of Gothenburg, Goteborg, Sweden. Department of Clinical Sciences, Division of Neurology, Lund University, Lund, Sweden. Department of Clinical Sciences, Neurosciences, Umeå University, Umeå, Sweden. Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Linköping University, Linkoping, Östergötland, Sweden. Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
 Department of Clinical Neurosciences, "Iuliu Hațieganu" University of Medicine and Pharmacy, Cluj-Napoca, 400012, Romania. Department of Clinical Neurosciences, "Iuliu Hațieganu" University of Medicine and Pharmacy, Cluj-Napoca, 400012, Romania. Department of Medical Informatics and Biostatistics, "Iuliu Hațieganu" University of Medicine and Pharmacy Cluj-Napoca, Cluj-Napoca, 400012, Romania. Department of Clinical Neurosciences, "Iuliu Hațieganu" University of Medicine and Pharmacy, Cluj-Napoca, 400012, Romania. Department of Biochemistry, "Iuliu Hațieganu" University of Medicine and Pharmacy Cluj-Napoca, Cluj-Napoca, 400012, Romania.
 Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China. Department of General Surgery, Lanzhou University Second Hospital, Lanzhou, China. Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China. Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China. Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China. Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China. Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China. wmx322@aliyun.com.
 Department of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia 97, 95123, Catania, Italy. Multiple Sclerosis Unit, University-Hospital G. Rodolico-San Marco, Via Santa Sofia 78, 95123, Catania, Italy. Multiple Sclerosis Unit, University-Hospital G. Rodolico-San Marco, Via Santa Sofia 78, 95123, Catania, Italy. Department "GF Ingrassia", Section Neuroscience, University of Catania, Via Santa Sofia 87, 95123, Catania, Italy. Multiple Sclerosis Unit, University-Hospital G. Rodolico-San Marco, Via Santa Sofia 78, 95123, Catania, Italy. Department "GF Ingrassia", Section Neuroscience, University of Catania, Via Santa Sofia 87, 95123, Catania, Italy. Central Laboratory, A.O.U. Policlinico-San Marco, Via Santa Sofia 78, 95123, Catania, Italy. Department "GF Ingrassia", Section Neuroscience, University of Catania, Via Santa Sofia 87, 95123, Catania, Italy. Multiple Sclerosis Unit, University-Hospital G. Rodolico-San Marco, Via Santa Sofia 78, 95123, Catania, Italy. patti@unict.it. Department "GF Ingrassia", Section Neuroscience, University of Catania, Via Santa Sofia 87, 95123, Catania, Italy. patti@unict.it.
 Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden. Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden. Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.
 Department of Neurology, Juntendo University, Tokyo 1138431, Japan. Biomedical Research Core Facilities, Juntendo University, Tokyo 1138431, Japan. Department of Biomedical Sciences, Sassari University, 07100 Sassari, Italy. Department of Neurology, Juntendo University, Tokyo 1138431, Japan. Department of Neurology, Juntendo University, Tokyo 1138431, Japan. Tosei Center for Neurological Diseases, Shizuoka 4180026, Japan. Division of Cell Biology, Juntendo University, Tokyo 1138431, Japan. Department of Neurology, Juntendo University, Tokyo 1138431, Japan. Comparative Medical Research Institute, Tsukuba 3050856, Japan. Department of Biomedical Sciences, Sassari University, 07100 Sassari, Italy. SC Microbiology, AOU Sassari, 07100 Sassari, Italy. Department of Neurology, Juntendo University, Tokyo 1138431, Japan. Neurodegenerative Disorders Collaborative Laboratory, RIKEN Center for Brain Science, Saitama 3510918, Japan.
 Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, 00168 Rome, Italy. Department of Neuroscience, Università Cattolica del Sacro Cuore, Centro di ricerca Sclerosi Multipla (CERSM), 00168 Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, 00168 Rome, Italy. Department of Neuroscience, Università Cattolica del Sacro Cuore, Centro di ricerca Sclerosi Multipla (CERSM), 00168 Rome, Italy. Fondazione Policlinico Universitario Agostino Gemelli IRCCS, UOC Neurologia, 00168 Rome, Italy. Department of Neuroscience, Università Cattolica del Sacro Cuore, Centro di ricerca Sclerosi Multipla (CERSM), 00168 Rome, Italy.
 Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Second Department of Internal Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Second Department of Internal Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Radiology, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. dominika.stastna@vfn.cz.
 Department of Radiology, University of California, San Diego, CA, USA. Department of Diagnostic and Interventional Radiology, University Hospital Heidelberg, Heidelberg, Germany. Department of Radiology, University of California, San Diego, CA, USA. Department of Radiology, University of California, San Diego, CA, USA. Department of Radiology, University of California, San Diego, CA, USA. Department of Interventional Radiology and Neuroradiology, Klinikum Hochsauerland, Arnsberg, Germany. Department of Neurosciences, University of California, San Diego, CA, USA. Department of Radiology, University of California, San Diego, CA, USA. Department of Bioengineering, University of California, San Diego, CA, USA. Radiology Service, Veterans Affairs San Diego Healthcare System, San Diego, CA, USA.
 Neurology and Immunology, Sanofi, Cambridge, MA, USA. Axtria Inc, Berkeley Heights, NJ, USA. Neurology and Immunology, Sanofi, Cambridge, MA, USA. Neurology and Immunology, Sanofi, Cambridge, MA, USA. Neurology and Immunology, Sanofi, Cambridge, MA, USA.
 Neurology Department, Peking University Shenzhen Hospital, Shenzhen, China. Rehabilitation Department, Shenzhen Longhua District Central Hospital, Shenzhen, China. Neurology Department, Peking University Shenzhen Hospital, Shenzhen, China. Neurology Department, Peking University Shenzhen Hospital, Shenzhen, China. Neurology Department, Peking University Shenzhen Hospital, Shenzhen, China. Neurology Department, Peking University Shenzhen Hospital, Shenzhen, China. Neurology Department, Peking University Shenzhen Hospital, Shenzhen, China.
 Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Neurology, Dell Medical School, University of Texas Austin, Austin, TX, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Neurology, Dell Medical School, University of Texas Austin, Austin, TX, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Ophthalmology, University of Texas Southwestern, Dallas, TX, USA. Department of Pathology, University of Texas Southwestern, Dallas, TX, USA. Department of Neurosurgery, University of Texas Southwestern, Dallas, TX, USA. Department of Neurosurgery, University of Texas Southwestern, Dallas, TX, USA. Center for Circadian and Sleep Medicine, Northwestern University, Chicago, IL, USA. RINGGOLD: 3270 Department of Neurology, Sleep Medicine, Northwestern University, Chicago, IL, USA. RINGGOLD: 3270 Department of Neuroscience and Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA.
 Weill Cornell Medical College, Cornell University, 1305 York Ave #2F, New York, NY, 10065, USA. jaisperumal@gmail.com. Northwestern University, Chicago, IL, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. New York University Grossman School of Medicine, New York, NY, USA. New York University Grossman School of Medicine, New York, NY, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA.
 Department of Neurology & Stroke, Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany. Department of Neurology & Stroke, Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany. Department of Neuroradiology, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany. Department of Neurology & Stroke, Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany. Department of Neuroradiology, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany. Department of Neurology & Stroke, Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany. Department of Neurology & Stroke, Hertie-Institute for Clinical Brain Research, Eberhard-Karls University of Tübingen, 72076 Tübingen, Germany.
 Department of Clinical Nutrition, School of Nutrition and Food Science Isfahan University of Medical Sciences Isfahan Iran. Clinical Neurology Research Center Shiraz University of Medical Sciences Shiraz Iran. Department of Biostatistics and Epidemiology, School of Health Isfahan University of Medical Sciences Isfahan Iran. Department of Clinical Nutrition, School of Nutrition and Food Science Isfahan University of Medical Sciences Isfahan Iran.
 Institute of Graduate Studies in HealthySciences, Istanbul University, Istanbul, Turkey; Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Department of Neuroscience, Institute of Neurological Sciences, Istanbul University-Cerrahpasa, Istanbul, Turkey. Institute of Graduate Studies in HealthySciences, Istanbul University, Istanbul, Turkey; Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Institute of Graduate Studies in HealthySciences, Istanbul University, Istanbul, Turkey; Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Department of Neuroscience, Institute of Neurological Sciences, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Neuroscience, Institute of Neurological Sciences, Istanbul University-Cerrahpasa, Istanbul, Turkey. Department of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Department of Neurology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey. Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Department of Neurology, Istanbul Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey. Department of Medical Biochemistry, Faculty of Medicine, Acibadem University, Istanbul, Turkey. Department of Medical Biochemistry, Faculty of Medicine, Acibadem University, Istanbul, Turkey. Department of Neurology, School of Medicine, Koç University, Istanbul, Turkey. Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. Electronic address: cemsmile@istanbul.edu.tr.
 Department of Radiology, , Barra da Tijuca, BrazilClínica de Diagnóstico por Imagem (CDPI)/DASA. Department of Radiology, , Niterói, BrazilFederal Fluminense University. RINGGOLD: 28110 Department of Medical Psychology, , Amsterdam, The NetherlandsAmsterdam University Medical Centers, Vrije Universiteit. RINGGOLD: 522567 Post-Graduate Program in Neurology, Hospital Universitário Gaffrée e Guinle, , Rio de Janeiro, BrazilUniversidade Federal do Estado do Rio de Janeiro. RINGGOLD: 89111 Post-Graduate Program in Neurology, Hospital Universitário Gaffrée e Guinle, , Rio de Janeiro, BrazilUniversidade Federal do Estado do Rio de Janeiro. RINGGOLD: 89111 Department of Neurology, Hospital Universitário Clementino Fraga Filho, , Rio de Janeiro, BrazilFederal University of Rio de Janeiro. RINGGOLD: 28125 Department of Neurology, Hospital Universitário Clementino Fraga Filho, , Rio de Janeiro, BrazilFederal University of Rio de Janeiro. RINGGOLD: 28125 Department of Radiology, , Barra da Tijuca, BrazilClínica de Diagnóstico por Imagem (CDPI)/DASA. Post-Graduate Program in Neurology, Hospital Universitário Gaffrée e Guinle, , Rio de Janeiro, BrazilUniversidade Federal do Estado do Rio de Janeiro. RINGGOLD: 89111 Department of Neurology, Hospital Universitário Clementino Fraga Filho, , Rio de Janeiro, BrazilFederal University of Rio de Janeiro. RINGGOLD: 28125 Department of Radiology, , Barra da Tijuca, BrazilClínica de Diagnóstico por Imagem (CDPI)/DASA. Department of Radiology, , Niterói, BrazilFederal Fluminense University. RINGGOLD: 28110
 University Pharmacy Department of Pharmacy Administration, Semmelweis University, Hőgyes Endre utca 7-9., 1092 Budapest, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. University Pharmacy Department of Pharmacy Administration, Semmelweis University, Hőgyes Endre utca 7-9., 1092 Budapest, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Division of Pancreatic Diseases, Heart and Vascular Center, Semmelweis University, Baross út 22-24, 1085 Budapest, Hungary. Carol Davila University of Medicine and Pharmacy, Dionisie Lupu Street 37, 020021, Bucharest, Romania. Fundeni Clinical Institute, Fundeni Street 258, 022328, Bucharest, Romania. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Department of Pharmacognosy, Sem-melweis University, Üllői út 26., 1085 Budapest, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Bajcsy-Zsilinszky Hospital, Maglódi Road 89-91, 1106 Bu- dapest, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Budapest Department of Biostatistics, University of Veterinary Medicine, István utca 2., 1078 Buda- pest, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Division of Pancreatic Diseases, Heart and Vascular Center, Semmelweis University, Baross út 22-24, 1085 Budapest, Hungary. János Szentágothai Research Center, University of Pécs, Szigeti út 12, 7624 Pécs, Hungary. Institute for Translational Medicine, Medical School, University of Pécs, Szigeti út 12, 7624 Pécs, Hungary. Centre for Translational Medicine, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. Institute for Translational Medicine, Medical School, University of Pécs, Szigeti út 12, 7624 Pécs, Hungary. Institute of Clinical Pharmacy, University of Szeged, Szikra utca 8, 6725 Szeged, Hungary. Department of Pharmacognosy, University of Szeged, Eötvös u. 6, 6720 Szeged, Hungary.
 Praktijk Seksualiteit en welzijn, Roermond, 6045 GL, the Netherlands. Department of Public Health and Primary Care, Ghent University, Ghent, 9000, Belgium. MS4 Research Institute, Nijmegen, 6522 KJ, the Netherlands. Department of Community and Occupational Medicine, University Medical Centre Groningen, Groningen, 9713 AV, the Netherlands. Dutch National MS Foundation, Rotterdam, 3044 AT, the Netherlands. Department of Endocrinology, Center for Sexology and Gender, Ghent University Hospital, Ghent, 9000, Belgium. Department of Endocrinology, Center for Sexology and Gender, Ghent University Hospital, Ghent, 9000, Belgium. Biostatistics Unit, Department of Public Health and Primary Care, Ghent University, Ghent, 9000, Belgium. Department of Clinical Psychological Science, Faculty of Psychology and Neurosciences, Maastricht University, Maastricht, 6229 ER, the Netherlands.
 Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Department of Health Sciences, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Phd Program in Medical Sciences and Biotechnologies, Department of Translational Medicine, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Department of Health Sciences, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Neurology Unit, Department of Translational Medicine, Maggiore della Carità Hospital, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy. Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Department of Health Sciences, University of Piemonte Orientale, Corso Mazzini 18, 28100 Novara, Italy.
 Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary. Doctoral School of Clinical Medicine, University of Szeged, Korányi fasor 6, H-6720 Szeged, Hungary. Department of Pediatrics, Albert Szent-Györgyi Faculty of Medicine, University of Szeged, H-6725 Szeged, Hungary. Danube Neuroscience Research Laboratory, ELKH-SZTE Neuroscience Research Group, Eötvös Loránd Research Network, University of Szeged (ELKH-SZTE), Tisza Lajos krt. 113, H-6725 Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary. Independent Researcher, H-6726 Szeged, Hungary. Danube Neuroscience Research Laboratory, ELKH-SZTE Neuroscience Research Group, Eötvös Loránd Research Network, University of Szeged (ELKH-SZTE), Tisza Lajos krt. 113, H-6725 Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary. Doctoral School of Clinical Medicine, University of Szeged, Korányi fasor 6, H-6720 Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary. Danube Neuroscience Research Laboratory, ELKH-SZTE Neuroscience Research Group, Eötvös Loránd Research Network, University of Szeged (ELKH-SZTE), Tisza Lajos krt. 113, H-6725 Szeged, Hungary. Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary. Danube Neuroscience Research Laboratory, ELKH-SZTE Neuroscience Research Group, Eötvös Loránd Research Network, University of Szeged (ELKH-SZTE), Tisza Lajos krt. 113, H-6725 Szeged, Hungary.
 Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Neurology, Sunshine Coast Hospital and Health Service, Birtinya, QLD 4575, Australia. School of Medicine, Griffith University, Birtinya, QLD 4575, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Monash Neurology, Monash Health, Clayton, VIC 3168, Australia. Monash Neurology, Monash Health, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Clinical Research, Faculty of Medicine, University of Bern, 3012 Bern, Switzerland.
 Department of Neurology, CHU Nîmes, University of Montpellier, Montpellier, France. Unité Transversale de Nutrition Clinique, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Neurology, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Neurology, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Neurology, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Neurology, CHU Nîmes, University of Montpellier, Montpellier, France. Unité Transversale de Nutrition Clinique, CHU Nîmes, University of Montpellier, Montpellier, France. Unité Transversale de Nutrition Clinique, CHU Nîmes, University of Montpellier, Montpellier, France. Unité Transversale de Nutrition Clinique, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Biostatistics, Clinical Epidemiology, Public Health and Innovation in Methodology, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Biostatistics, Clinical Epidemiology, Public Health and Innovation in Methodology, CHU Nîmes, University of Montpellier, Montpellier, France. Laboratory of Biochemistry and Molecular Biology, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Biostatistics, Clinical Epidemiology, Public Health and Innovation in Methodology, CHU Nîmes, University of Montpellier, Montpellier, France. Department of Neurology, CHU Nîmes, University of Montpellier, Montpellier, France. The Institute of Functional Genomics, University of Montpellier, CNRS, INSERM, Montpellier, France.
 AcariaHealth, Orlando, FL, USA. AcariaHealth, Orlando, FL, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. jim.lewin@biogen.com.
 Department of Neurosciences, Reproductive Sciences and Dentistry, University of Naples Federico II, 80131 Naples, Italy. Department of Public Health, University of Naples Federico II, 80131 Naples, Italy. Department of Neurosciences, Reproductive Sciences and Dentistry, University of Naples Federico II, 80131 Naples, Italy. Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, 80131 Naples, Italy. MS Unit, Federico II University Hospital, 80131 Naples, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, 95125 Catania, Italy. MS Center, S. Andrea Hospital, Sapienza University of Rome, 00185 Rome, Italy. Neurology Unit, Multiple Sclerosis Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Centro Sclerosi Multipla, ASST Spedali Civili di Brescia, Ospedale di Montichiari, 25018 Brescia, Italy. San Luigi Gonzaga Academic Hospital, 10043 Orbassano, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 81100 Naples, Italy. S. Filippo Neri Hospital, 00135 Rome, Italy. NCL-Istituto di Neuroscienze Gruppo Neuromed, 00178 Rome, Italy. Intradepartmental Program of Clinical Psychology, Federico II University Hospital, 80131 Naples, Italy. Department of Neurosciences, Reproductive Sciences and Dentistry, University of Naples Federico II, 80131 Naples, Italy. Intradepartmental Program of Clinical Psychology, Federico II University Hospital, 80131 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 81100 Naples, Italy. San Luigi Gonzaga Academic Hospital, 10043 Orbassano, Italy. Centro Sclerosi Multipla, ASST Spedali Civili di Brescia, Ospedale di Montichiari, 25018 Brescia, Italy. Neurology Unit, Multiple Sclerosis Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, 95125 Catania, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 81100 Naples, Italy. Neurology Unit, Multiple Sclerosis Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Vita-Salute San Raffaele University, 20132 Milan, Italy. MS Center, San Pietro Hospital Fatebenefratelli, 00189 Rome, Italy. Department "G.F. Ingrassia", MS Center, University of Catania, 95125 Catania, Italy. Department of Human Neurosciences, Sapienza University, 00185 Rome, Italy. Department of Neurosciences, Reproductive Sciences and Dentistry, University of Naples Federico II, 80131 Naples, Italy. Department of Human Neurosciences, Sapienza University, 00185 Rome, Italy. Department of Neurosciences, Reproductive Sciences and Dentistry, University of Naples Federico II, 80131 Naples, Italy.
 Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. icometrix, Leuven, Belgium. National MS Center Melsbroek, Melsbroek, Belgium. National MS Center Melsbroek, Melsbroek, Belgium. Department of Neurology, UZ Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium. Department of Neurology, UZ Brussel, Brussels, Belgium. St Edmund Hall, University of Oxford, Oxford, UK. Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Brussels, Belgium. AIMS Lab, Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium.
 Nuriel Moghavem Lilyana Amezcua Multiple Sclerosis Center, Department of Neurology, Keck School of Medicine of USC, Los Angeles, CA, USA. Keck School of Medicine of USC, Los Angeles, CA, USA. Norris Medical Library, University of Southern California, Los Angeles, CA, USA. Nuriel Moghavem Lilyana Amezcua Multiple Sclerosis Center, Department of Neurology, Keck School of Medicine of USC, Los Angeles, CA, USA.
 Department of Neuro-Urology, Clinic for Urology, University Hospital Bonn, 53127 Bonn, Germany. Department of Neuro-Urology, Johanniter Neurological Rehabilitation Center Godeshoehe GmbH, 53177 Bonn, Germany. Department of Neuro-Urology, Clinic for Urology, University Hospital Bonn, 53127 Bonn, Germany. Department of Cognitive Rehabilitation, Neurological Rehabilitation Center Godeshoehe GmbH, 53177 Bonn, Germany. Department of Medical Psychology | Neuropsychology and Gender Studies, Center for Neuropsychological Diagnostics and Intervention (CeNDI), Faculty of Medicine and University Hospital Cologne, University of Cologne, 50937 Cologne, Germany. Department of Neuro-Urology, Johanniter Neurological Rehabilitation Center Godeshoehe GmbH, 53177 Bonn, Germany. Department of Neuro-Urology, Clinic for Urology, University Hospital Bonn, 53127 Bonn, Germany. Department of Neuro-Urology, Clinic for Urology, University Hospital Bonn, 53127 Bonn, Germany. Department of Neuro-Urology, Clinic for Urology, University Hospital Bonn, 53127 Bonn, Germany. Department of Neuro-Urology, Johanniter Neurological Rehabilitation Center Godeshoehe GmbH, 53177 Bonn, Germany. Department of Neuro-Urology, Clinic for Urology, University Hospital Bonn, 53127 Bonn, Germany.
 INSERM CIC-P 1401, Bordeaux PharmacoEpi, Université de Bordeaux, Bordeaux, France. Merck Healthcare KGaA, Darmstadt, Germany. INSERM CIC-P 1401, Bordeaux PharmacoEpi, Université de Bordeaux, Bordeaux, France. Merck Healthcare KGaA, Darmstadt, Germany. INSERM CIC-P 1401, Bordeaux PharmacoEpi, Université de Bordeaux, Bordeaux, France. INSERM CIC-P 1401, Bordeaux PharmacoEpi, Université de Bordeaux, Bordeaux, France. Merck Healthcare KGaA, Darmstadt, Germany. INSERM CIC-P 1401, Bordeaux PharmacoEpi, Université de Bordeaux, Bordeaux, France.
 Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia; Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Illawarra Health and Medical Research Institute, Wollongong, Australia; School of Medicine, University of Wollongong, Wollongong, Australia. Curtin School of Population Health, Curtin University, Perth, Australia. Murdoch Children's Research Institute, Royal Children's Hospital, University of Melbourne, VIC, Australia; The Florey Institute of Neuroscience & Mental Health, Parkville, VIC, Australia. School of Medicine, Griffith University, Gold Coast, Australia. Department of Neurology, John Hunter Hospital, Newcastle, New South Wales, Australia; Faculty of Medicine and Public Health, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Electronic address: Ingrid.vanderMei@utas.edu.au.
 Department of Oral Diagnostic Sciences, Faculty of Dentistry, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Periodontics, University Dental Hospital, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Periodontics, Faculty of Dentistry, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Basic and Clinical Oral Sciences, Faculty of Dentistry, Umm Al-Qura University, Makkah 24382, Saudi Arabia. Department of Oral and Maxillofacial Surgery & Diagnostic Sciences, College of Dentistry, Jouf University, Sakaka 72345, Saudi Arabia. Periodontics Division, Department of Preventive Dental Sciences, College of Dentistry, Jouf University, Sakaka 72345, Saudi Arabia. Department of Periodontics, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 602105, India. Department of Biomedical and Surgical and Biomedical Sciences, Catania University, 95123 Catania, Italy. Multidisciplinary Department of Medical-Surgical and Dental Specialties, University of Campania Luigi Vanvitelli, 80138 Naples, Italy.
 Genentech, Inc., 350 DNA Way, South San Francisco, CA, 94080, USA. geiger.caroline@gene.com. Genentech, Inc., 350 DNA Way, South San Francisco, CA, 94080, USA. Genentech, Inc., 350 DNA Way, South San Francisco, CA, 94080, USA. Genentech, Inc., 350 DNA Way, South San Francisco, CA, 94080, USA. Genentech, Inc., 350 DNA Way, South San Francisco, CA, 94080, USA.
 Post-Graduate Program in Medicine, Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Neurology Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil. Speech Language Pathology Course, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Neurology Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil. Post-Graduate Program in Medicine, Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Neurology Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil. Post-Graduate Program in Medicine, Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Neurology Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil. Speech Language Pathology Course, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Phonetics Laboratory of the Faculty of Letters, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. Post-Graduate Program in Medicine, Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Neurology Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil. Speech Language Pathology Course, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Department of Surgery and Orthopedics, Faculdade de Odontologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
 Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Department of Military Medicine and "Tzameret", Faculty of Medicine, Hebrew University of Jerusalem, and Medical Corps, Israel Defense Forces, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Department of Obstetrics and Gynecology, Hadassah-Hebrew University Medical Center, Ein-Kerem, 91120, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. Adembinsky@gmail.com. Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, P.O.B. 12000, 91120, Jerusalem, Israel. Adembinsky@gmail.com.
 Department of Psychology, College of Human and Health Sciences, Swansea University, Swansea, UK. Rehabilitation Engineering Unit, Swansea Bay University Health Board, Morriston Hospital, Swansea, UK. Rehabilitation Engineering Unit, Swansea Bay University Health Board, Morriston Hospital, Swansea, UK. Health and Wellbeing Academy, College of Human and Health Sciences, Swansea University, Swansea, UK. Regional Neuropsychology and Community Brain Injury Service, Swansea Bay University Health Board, Morriston Hospital, Swansea, UK. Rehabilitation Engineering Unit, Swansea Bay University Health Board, Morriston Hospital, Swansea, UK. Department of Psychology, College of Human and Health Sciences, Swansea University, Swansea, UK.
 Florida Atlantic University, Boca Raton, FL, USA. Nova Southeastern University, Fort Lauderdale, FL, USA. Penn Center for Global Health, University of Pennsylvania, Philadelphia, PA, USA. Bristol Myers Squibb, Princeton, NJ, USA. Analysis Group, Inc., Boston, MA, USA. Analysis Group, Inc., Boston, MA, USA. Analysis Group, Inc., Boston, MA, USA. Bristol Myers Squibb, Princeton, NJ, USA. Komal.Singh@bms.com. Bristol Myers Squibb, 3401 Princeton Pike, Lawrenceville, NJ, 08640, USA. Komal.Singh@bms.com.
 Immunology Department, CHU de Nice, Université Nice Cote d'Azur, Nice, France. ruetsch-chelli.c@chu-nice.fr. Université Côte d'Azur, INSERM, C3M, Team Microenvironment, Signalling and Cancer, Nice, France. ruetsch-chelli.c@chu-nice.fr. The University of Texas Southwestern Medical Center, Dallas, TX, USA. Pharmacology Department, CHU Cimiez, Nice, France. Université Côte d'Azur, INSERM, C3M, Team Microenvironment, Signalling and Cancer, Nice, France. Université Côte d'Azur, INSERM, C3M, Team Microenvironment, Signalling and Cancer, Nice, France. CRCSEP CHU de Nice, UR2CA-URRIS, Université Nice Cote d'Azur, Nice, France.
 Department of Laboratory Diagnostics, University Hospital Centre Zagreb, Zagreb, Croatia. Department of Biotechnology, University of Rijeka, Rijeka, Croatia. Department of Laboratory Diagnostics, University Hospital Centre Zagreb, Zagreb, Croatia; Faculty of Pharmacy and Biochemistry, University of Zagreb, Zagreb, Croatia. Department of Neurology, University of Zagreb School of Medicine, Zagreb, Croatia; Referral Center for Autonomic Nervous System Disorders, Department of Neurology, University Hospital Centre Zagreb, Zagreb, Croatia. Department of Laboratory Diagnostics, University Hospital Centre Zagreb, Zagreb, Croatia; Faculty of Pharmacy and Biochemistry, University of Zagreb, Zagreb, Croatia. Department of Neurology, University of Zagreb School of Medicine, Zagreb, Croatia; Referral Center for Autonomic Nervous System Disorders, Department of Neurology, University Hospital Centre Zagreb, Zagreb, Croatia. Department of Laboratory Diagnostics, University Hospital Centre Zagreb, Zagreb, Croatia. Faculty of Pharmacy and Biochemistry, University of Zagreb, Zagreb, Croatia; Genos Glycoscience Research Laboratory, Zagreb, Croatia. Department of Biotechnology, University of Rijeka, Rijeka, Croatia; Genos Glycoscience Research Laboratory, Zagreb, Croatia. Electronic address: ivan.gudelj@uniri.hr.
 Division of Neurology, Amiri Hospital, Arabian Gulf Street, Sharq 13041, Kuwait; MS Clinic, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait; Department of Neurology, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait; Department of Neurology and Psychiatry, Minia University, P.O. Box 61519, Minia 61111, Egypt. Electronic address: samerelshayb@hotmail.com.
 PricewaterhouseCoopers (PwC), Zurich, Switzerland. PricewaterhouseCoopers (PwC), Zurich, Switzerland. GmbH, Neuburg an der Donau, GermanyNeuroTransData (NTD). RINGGOLD: 593067 GmbH, Neuburg an der Donau, GermanyNeuroTransData (NTD). RINGGOLD: 593067 , Basel, SwitzerlandF. Hoffman-La Roche Ltd. RINGGOLD: 27170 GmbH, Neuburg an der Donau, GermanyNeuroTransData (NTD). RINGGOLD: 593067 EHE International GmbH, St Moritz, Switzerland. European Health Economics, Mulhouse, France. Faculty of Economics, , Essen, GermanyUniversity of Duisburg-Essen. RINGGOLD: 27170
 Jordan University of Science and Technology, College of Pharmacy, Department of Clinical Pharmacy, P.O. Box 3030, Irbid 22110, Jordan. Jordan University of Science and Technology, College of Pharmacy, Department of Clinical Pharmacy, P.O. Box 3030, Irbid 22110, Jordan. Jordan University of Science and Technology, College of Science and Art, Department of Biotechnology and Genetic Engineering, P.O. Box 3030, Irbid 22110, Jordan. Jordan University of Science and Technology, College of Pharmacy, Department of Clinical Pharmacy, P.O. Box 3030, Irbid 22110, Jordan. Jordan University of Science and Technology, College of Medicine, Department of Neurology, P.O. Box 3030, Irbid 22110, Jordan.
 Brigham and Women's Hospital and Massachusetts General Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA, USA. Electronic address: tchitnis@bwh.harvard.edu.
 Department of Neurology, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium. camille.dutordoir@gmail.com. Department of Radiology, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium. Department of Neurology, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium. Department of Neurology, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium.
 Private Academic Consultant, Bangkok, Thailand. Joseph Ayobabalola University, Ikeji-Arakeji, Nigeria. GRID: grid.442554.6. ISNI: 0000 0001 1143 9471 Dr. D. Y. Patil Medical College, Dr. D. Y. Patil Vidyapeeth, Pune, India.
 Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Synaptic Immunopathology Lab, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Synaptic Immunopathology Lab, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Synaptic Immunopathology Lab, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Synaptic Immunopathology Lab, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy Faculty of Psychology Uninettuno Telematic International University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Italy Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Italy Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele Roma, Italy Department of Human Sciences and Quality of Life Promotion, University of Rome San Raffaele, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy Synaptic Immunopathology Lab, Department of Systems Medicine, Tor Vergata University, Rome, Italy. Unit of Neurology, IRCCS Neuromed, Pozzilli, Italy.
 John Ray Research Field Station, Cheshire, United Kingdom. School of Natural Sciences, Bangor University, Gwynedd, United Kingdom.
 Laboratory for Neural Stem Cells and Functional Neurogenetics, Division of Multiple Sclerosis and Neuroimmunology, University of Connecticut Health Center, Farmington, CT, United States. Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Medical Scientist Training Program, University of California, Irvine, Irvine, CA, United States. Laboratory for Neural Stem Cells and Functional Neurogenetics, Division of Multiple Sclerosis and Neuroimmunology, University of Connecticut Health Center, Farmington, CT, United States. Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Department of Neurology, Columbia University Medical Center, New York City, NY, United States. Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Department of Neurology, Columbia University Medical Center, New York City, NY, United States. Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Institute for Medical Immunology, Charité-Universitätsmedizin Berlin, Berlin, Germany. Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Alzheimer's Clinical and Translational Research Center, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States. Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. Abu Haidar Neuroscience Institute, American University of Beirut Medical Center, Beirut, Lebanon.
 Comprehensive MS Center, Neuroscience Institute, Methodist Hospitals, 200 E 89Th Avenue, Merrillville, IN, 46410, USA. billy.conte@gmail.com. First Choice Neurology/South Tampa Multiple Sclerosis Center, 2919 Swann Avenue, Suite 401, Tampa, FL, 33609, USA. Mellen Center for MS Treatment and Research, Cleveland Clinic, 9500 Euclid Avenue/U10, Cleveland, OH, 44195, USA.
 axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada. Centre for Medicines Discovery and NIHR, Oxford Biomedical Research Centre, Centre for Medicines Discovery, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7FZ, UK. Centre for Medicines Discovery and NIHR, Oxford Biomedical Research Centre, Centre for Medicines Discovery, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7FZ, UK; Alzheimer's Research UK, Oxford Drug Discovery Institute, Centre for Medicines Discovery, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7FZ, UK. axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada; Département de médecine moléculaire, Faculté de médecine, Université Laval, Québec, QC, Canada. Electronic address: manu.rangachari@crchudequebec.ulaval.ca.
 Faculty of Medicine, Institute of Neuroanatomy, University of Bonn, 53115 Bonn, Germany. University Hospital Bonn, 53127 Bonn, Germany. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany. Faculty of Medicine, Institute of Neuroanatomy, University of Bonn, 53115 Bonn, Germany. University Hospital Bonn, 53127 Bonn, Germany. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany. Department of Pathology, Amsterdam University Medical Center, 1007 MB Amsterdam, The Netherlands. Department of Pathology, Amsterdam University Medical Center, 1007 MB Amsterdam, The Netherlands. Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany. Faculty of Medicine, Institute of Neuroanatomy, University of Bonn, 53115 Bonn, Germany. University Hospital Bonn, 53127 Bonn, Germany. Institute of Anatomy and Cell Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.
 Cukurova University, Faculty of Medicine, Department of Neurology, Adana, Turkey. Cukurova University, Faculty of Medicine, Department of Medical Genetic, Adana, Turkey. Cukurova University, Faculty of Medicine, Department of Neurology, Adana, Turkey.
 Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Electronic address: runsheng.li@cityu.edu.hk. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, SAR 999077, China. Electronic address: gyang25@cityu.edu.hk.
 Department of Molecular Genetics, University of Texas (UT) Southwestern Medical Center, Dallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, Dallas, TX, USA. Department of Molecular Genetics, University of Texas (UT) Southwestern Medical Center, Dallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, Dallas, TX, USA; Department of Neuroscience, UT Southwestern Medical Center, Dallas, TX, USA; Department of Neurology and Neurotherapeutics, UT Southwestern Medical Center, Dallas, TX, USA. Department of Molecular Genetics, University of Texas (UT) Southwestern Medical Center, Dallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, Dallas, TX, USA. Electronic address: calvier.laurent@gmail.com.
 Chubu Medical Center for Prolonged Traumatic Brain Dysfunction, Gifu, Japan. Department of Neurosurgery, Gifu University Graduate School of Medicine, Gifu, Japan. Chubu Medical Center for Prolonged Traumatic Brain Dysfunction, Gifu, Japan. Department of Clinical Brain Sciences, Gifu University Graduate School of Medicine, Gifu, Japan. Chubu Medical Center for Prolonged Traumatic Brain Dysfunction, Gifu, Japan. Department of Clinical Brain Sciences, Gifu University Graduate School of Medicine, Gifu, Japan. Chubu Medical Center for Prolonged Traumatic Brain Dysfunction, Gifu, Japan. Department of Clinical Brain Sciences, Gifu University Graduate School of Medicine, Gifu, Japan. Department of Neurosurgery, Gifu University Graduate School of Medicine, Gifu, Japan.
 Department of Medicine, University of Montreal, Montreal, QC, Canada.
 Department of Pharmacology, ISF College of Pharmacy, Moga, India 142001. Department of Pharmacology, ISF College of Pharmacy, Moga, India 142001. Department of Pharmaceutical Chemistry, ISF College of Pharmacy, Moga, India. Department of Pharmaceutical Chemistry, ISF College of Pharmacy, Moga, India.
 Department of Emergency Medicine, Azienda Ospedaliero-Universitaria Pisana, Italy. University of Milan, Milan, Italy; Department of Clinical and Experimental Medicine, University of Pisa, Italy. Department of Clinical and Experimental Medicine, University of Pisa, Italy. Department of Surgical, Medical and Molecular Pathology and of Critical Area, University of Pisa, Italy. Department of Surgical, Medical and Molecular Pathology and of Critical Area, University of Pisa, Italy. Department of Surgical, Medical and Molecular Pathology and of Critical Area, University of Pisa, Italy. Department of Surgical, Medical and Molecular Pathology and of Critical Area, University of Pisa, Italy. Electronic address: alessandro.antonelli@unipi.it. Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Italy.
 Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. RINGGOLD: 16748 Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. RINGGOLD: 16748 Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. RINGGOLD: 16748 Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. RINGGOLD: 16748 Departament de Psicología Bàsica, Clínica i Psicobiología, Universitat Jaume I, Castelló de la Plana, Spain. RINGGOLD: 16748
 Trinity Translational Medicine Institute, Trinity College Dublin, Trinity Centre for Health Sciences, St James's Hospital, Dublin D08 NHY1, Ireland. Trinity Translational Medicine Institute, Trinity College Dublin, Trinity Centre for Health Sciences, St James's Hospital, Dublin D08 NHY1, Ireland.
 School of Psychological Sciences, College of Health and Medicine, University of Tasmania, Hobart and Launceston, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. School of Psychological Sciences, College of Health and Medicine, University of Tasmania, Hobart and Launceston, Australia. Macquarie Medical School, Macquarie University, Sydney, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. School of Psychological Sciences, College of Health and Medicine, University of Tasmania, Hobart and Launceston, Australia; Launceston General Hospital, Launceston, Tasmania, Australia. Electronic address: Cynthia.Honan@utas.edu.au.
 Université de Lille, Lille, France; Department of neurology, CHU de Lille, Lille, France. Department of neurology, CHU de Lille, Lille, France. GIOVANNELLI Epidemiology and clinical research counselling, Lille, France. Department of neurology, CHU de Lille, Lille, France. Department of neuroradiology, CHU de Lille, Inserm U1171 Lille, Lille, France. Home care department CHU de Lille, Lille, France. Université de Lille, Lille, France; Department of neurology, CHU de Lille, Lille, France; Inserm U1172, Lille, France. Electronic address: helene.zephir@chu-lille.fr.
 Department of Molecular and Cell Biology, Leicester Institute of Structural and Chemical Biology, University of Leicester, Leicester, UK. LifeArc, Centre for Therapeutics Discovery, Stevenage, UK. LifeArc, Centre for Therapeutics Discovery, Stevenage, UK. LifeArc, Centre for Therapeutics Discovery, Stevenage, UK. LifeArc, Centre for Therapeutics Discovery, Stevenage, UK. Institute of Pharmacology, University of Marburg, Marburg, Germany; Department of Pharmacology, Max-Planck Institute for Heart and Lung Research, Bad Nauheim, Germany. Department of Pharmacology, Max-Planck Institute for Heart and Lung Research, Bad Nauheim, Germany. LifeArc, Centre for Therapeutics Discovery, Stevenage, UK. Department of Molecular and Cell Biology, Leicester Institute of Structural and Chemical Biology, University of Leicester, Leicester, UK. Department of Molecular and Cell Biology, Leicester Institute of Structural and Chemical Biology, University of Leicester, Leicester, UK. Electronic address: gh126@leicester.ac.uk.
 Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Laboratoire de Virologie, CHU Grenoble Alpes, CS 10217, CEDEX 09, 38043 Grenoble, France. Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Laboratoire de Virologie, CHU Grenoble Alpes, CS 10217, CEDEX 09, 38043 Grenoble, France. Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Laboratoire de Virologie, CHU Grenoble Alpes, CS 10217, CEDEX 09, 38043 Grenoble, France. Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Service de Maladies Infectieuses, CHU Grenoble Alpes, CS 10217, CEDEX 09, 38043 Grenoble, France. Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Laboratoire de Virologie, CHU Grenoble Alpes, CS 10217, CEDEX 09, 38043 Grenoble, France. Institut de Biologie Structurale, Université Grenoble Alpes, UMR 5075 CEA/CNRS/UGA, 71 Avenue des Martyrs, 38000 Grenoble, France. Laboratoire de Virologie, CHU Grenoble Alpes, CS 10217, CEDEX 09, 38043 Grenoble, France.
 Esophageal Institute, Department of Surgery, Allegheny Health Network, Pittsburgh, PA, United States. Esophageal Institute, Department of Surgery, Allegheny Health Network, Pittsburgh, PA, United States. Esophageal Institute, Department of Surgery, Allegheny Health Network, Pittsburgh, PA, United States. Esophageal Institute, Department of Surgery, Allegheny Health Network, Pittsburgh, PA, United States; Department of Surgery, Drexel University, Philadelphia, PA, United States. Electronic address: shahin.ayazi@ahn.org. Esophageal Institute, Department of Surgery, Allegheny Health Network, Pittsburgh, PA, United States; Department of Surgery, Drexel University, Philadelphia, PA, United States.
 Department of Neuro Ophthalmology, Aravind Eye Hospital, Madurai, Tamil Nadu, India. Department of Neuro Ophthalmology, Aravind Eye Hospital, Madurai, Tamil Nadu, India. Department of Neuro Ophthalmology, Aravind Eye Hospital, Madurai, Tamil Nadu, India. Department of Neuro Ophthalmology, Aravind Eye Hospital, Madurai, Tamil Nadu, India.
 Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands. Department of Experimental Immunology, Amsterdam Institute for Infection and Immunity, Amsterdam University Medical Centers, 1105 AZ Amsterdam, the Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands. Bioinformatics Laboratory, Department of Epidemiology and Data Science, Amsterdam University Medical Centers, 1105 AZ Amsterdam, the Netherlands. Translational Biology, Biogen, Cambridge, MA 02142, USA. Translational Biology, Biogen, Cambridge, MA 02142, USA. Multiple Sclerosis and Neurorepair Research Unit, Biogen, Cambridge, MA 02142, USA. Bioinformatics Laboratory, Department of Epidemiology and Data Science, Amsterdam University Medical Centers, 1105 AZ Amsterdam, the Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands. Swammerdam Institute for Life Sciences, Center for Neuroscience, University of Amsterdam, 1098 XH Amsterdam, the Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands. MS Center ErasMS, Departments of Neurology and Immunology, Erasmus Medical Center, 3015 GD Rotterdam, the Netherlands. Neuroimmunology Research Group, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands. Department of Experimental Immunology, Amsterdam Institute for Infection and Immunity, Amsterdam University Medical Centers, 1105 AZ Amsterdam, the Netherlands.
 Neurology, Faculty of Medicine, Ain Shams University, Cairo, EGY. Neurology, John D. Dingell VA Medical Center, Detroit, USA. Neurology, Wayne State University School of Medicine, Detroit, USA. Neurology, Henry Ford Health, Detroit, USA.
 Serviço de Neurologia, Hospital de Egas Moniz, Centro Hospitalar de Lisboa Ocidental, Morada: Rua da Junqueira, 126, 1349-019, Lisboa, Portugal. dkrupka@chlo.min-saude.pt. Serviço de Neurologia, Hospital de Egas Moniz, Centro Hospitalar de Lisboa Ocidental, Morada: Rua da Junqueira, 126, 1349-019, Lisboa, Portugal. Serviço de Neurologia, Hospital de Egas Moniz, Centro Hospitalar de Lisboa Ocidental, Morada: Rua da Junqueira, 126, 1349-019, Lisboa, Portugal.
 Department of Neurology, University of California Irvine, 208 Sprague Hall, Mail Code 4032, Irvine, CA, 92697, USA. Department of Neurology, University of California Irvine, 208 Sprague Hall, Mail Code 4032, Irvine, CA, 92697, USA. Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Ave, Toronto, ON, M5G 1X5, Canada. Department of Neurology, University of California Irvine, 208 Sprague Hall, Mail Code 4032, Irvine, CA, 92697, USA. Department of Neurology, University of California Irvine, 208 Sprague Hall, Mail Code 4032, Irvine, CA, 92697, USA. Department of Statistics, Donald Bren School of Information and Computer Sciences, University of California Irvine, Bren Hall 2019, Irvine, CA, 92697, USA. Department of Neurology, University Hospital Basel, Mittlere Strasse 83, 4056, Basel, Switzerland. Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Ave, Toronto, ON, M5G 1X5, Canada. Department of Molecular Genetics, University of Toronto, Toronto, ON, M5S 1A8, Canada. Department of Neurology, University of California Irvine, 208 Sprague Hall, Mail Code 4032, Irvine, CA, 92697, USA. Department of Neurology, University of California Irvine, 208 Sprague Hall, Mail Code 4032, Irvine, CA, 92697, USA. mdemetri@uci.edu. Department of Microbiology and Molecular Genetics, University of California Irvine, Irvine, USA. mdemetri@uci.edu.
 Department of Ophthalmology, Mayo Clinic Hospital, Rochester, MN, USA. Department of Ophthalmology, Mayo Clinic Hospital, Rochester, MN, USA. Chen.John@mayo.edu. Department of Neurology, Mayo Clinic Hospital, Rochester, MN, USA. Chen.John@mayo.edu.
 Department of Basic Science, Medical School, University of Crete, 70013 Heraklion, Greece. Institute of Molecular Biology and Biotechnology-FORTH, 70013 Heraklion, Greece. Department of Biology, University of Crete, 70013 Heraklion, Greece. Department of Basic Science, Medical School, University of Crete, 70013 Heraklion, Greece. Institute of Molecular Biology and Biotechnology-FORTH, 70013 Heraklion, Greece. Department of Basic Science, Medical School, University of Crete, 70013 Heraklion, Greece. Institute of Molecular Biology and Biotechnology-FORTH, 70013 Heraklion, Greece.
 CarMeN Laboratory, Inserm U1060, University Claude Bernard Lyon 1, INRAE U1397, 69310 Pierre Bénite, France. CarMeN Laboratory, Inserm U1060, University Claude Bernard Lyon 1, INRAE U1397, 69310 Pierre Bénite, France. CarMeN Laboratory, Inserm U1060, University Claude Bernard Lyon 1, INRAE U1397, 69310 Pierre Bénite, France. Research Department, Hospices Civils de Lyon, 69310 Pierre Bénite, France.
 Department of Occupational Therapy, New York University, New York, NY; Kessler Foundation, East Hanover, NJ. Electronic address: yg243@nyu.edu. Kessler Foundation, East Hanover, NJ; Rutgers University, Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Newark, NJ. Kessler Foundation, East Hanover, NJ; Rutgers University, Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Newark, NJ. Kessler Foundation, East Hanover, NJ; Rutgers University, Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Newark, NJ.
 Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Section of Developmental Neurobiology, University Hospital, Würzburg, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Department of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. Department of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. Brain and Mind Center, University of Sydney, Sydney, Australia. Department of Neurology, Palacky University Olomouc, Olomouc, Czech Republic. Department of Neurology, Section of Developmental Neurobiology, University Hospital, Würzburg, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Moorenstrasse 5, 40225, Düsseldorf, Germany. kuery@uni-duesseldorf.de.
 Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Integrated Traditional and Western Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Interventional Radiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Integrated Traditional and Western Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. zhulin66zhulin@163.com.
 Samira Ghasemi, Maryam Kayvani, and Behrooz Abdoli, Department of Sport Sciences and Health, Shahid Beheshti University, Tehran, Iran. Samira Ghasemi, Maryam Kayvani, and Behrooz Abdoli, Department of Sport Sciences and Health, Shahid Beheshti University, Tehran, Iran. Electronic address: Ma_kavyani@sbu.ac.ir. Samira Ghasemi, Maryam Kayvani, and Behrooz Abdoli, Department of Sport Sciences and Health, Shahid Beheshti University, Tehran, Iran.
 Beyoglu Eye Training and Research Hospital, University of Health Sciences Turkey, Bereketzade Street Number: 2, Beyoglu, 3442, Istanbul, Turkey. byargi@hotmail.com. Beyoglu Eye Training and Research Hospital, University of Health Sciences Turkey, Bereketzade Street Number: 2, Beyoglu, 3442, Istanbul, Turkey. Beyoglu Eye Training and Research Hospital, University of Health Sciences Turkey, Bereketzade Street Number: 2, Beyoglu, 3442, Istanbul, Turkey. Beyoglu Eye Training and Research Hospital, University of Health Sciences Turkey, Bereketzade Street Number: 2, Beyoglu, 3442, Istanbul, Turkey.
 Novartis Institutes for BioMedical Research, Basel, Switzerland. marc.bigaud@novartis.com. Novartis Institutes for BioMedical Research, Basel, Switzerland. Novartis Institutes for BioMedical Research, Basel, Switzerland. Novartis Institutes for BioMedical Research, Basel, Switzerland. Novartis Institutes for BioMedical Research, Basel, Switzerland. Novartis Institutes for BioMedical Research, Basel, Switzerland. Novartis Pharma AG, Forum 1, Novartis Campus, 4056, Basel, Switzerland.
 Omnion Research International, Zagreb, Croatia. Department of Histology and Embryology, University of Zagreb School of Medicine, Zagreb, Croatia. University of Zagreb School of Medicine, Zagreb, Croatia. University of Zagreb School of Dental Medicine, Zagreb, Croatia. Department of Histology and Embryology, University of Zagreb School of Medicine, Zagreb, Croatia. Laboratory for Stem Cells, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
 School of Medicine, Bozok University, Yozgat, Turkey. School of Medicine, Bozok University, Yozgat, Turkey. Celal Bayar University School of Medicine, Manisa, Turkey.
 Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany Michelle.Maiworm@kgu.de. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany. Department of Neurology, University Hospital Frankfurt, Frankfurt am Main, Germany. Brain Imaging Center, Goethe University Frankfurt, Frankfurt am Main, Germany.

 Department of Pharmacy, Faculty of Pharmacy, Hasanuddin University, Makassar, Indonesia. Department of Pharmacy, Faculty of Pharmacy, Hasanuddin University, Makassar, Indonesia. School of Medicine, Universitas Syiah Kuala, Banda Aceh, Indonesia. Department of Pharmacy, BGC Trust University Bangladesh, Chittagong, Bangladesh.
 Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Department of Neurology, Hospital Residència Sant Camil - Consorci Sanitari Alt Penedès-Garraf, Sant Pere de Ribes, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Neuro-Oncology Unit, Hospital Universitari de Bellvitge-Institut Català d'Oncologia L'Hospitalet, IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Department of Neuroradiology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Departament de Ciències Clíniques, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Departament de Ciències Clíniques, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain. Multiple Sclerosis Unit, Department of Neurology, Hospital Universitari de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. luciaromero@bellvitgehospital.cat.
 Multiple Sclerosis Research Center, Neuroscience Institut, Tehran University of Medical Sciences, Tehran, Iran. Pediatric Cell and Gene Therapy Research Center, Gene, Cell and Tissue Research Institute , Tehran University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Microbiology and Immunology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran. Iranian Tissue Bank and Research Center, Imam Khomeini Hospital, Tehran University of Medical Science, Tehran, Iran. Department of Internal Medicine, School of Medicine, Patient Safety Research Center, Clinical Research Institute, Urmia University of Medical Science, Urmia, Iran. Pediatric Cell and Gene Therapy Research Center, Gene, Cell and Tissue Research Institute , Tehran University of Medical Sciences, Tehran, Iran. Hamid.farajifard@yahoo.com. Patient Safety Research Center, Clinical Research Institute, Urmia University of Medical Sciences, Urmia, Iran. sajjadahmadpour@yahoo.com.

 Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, China. Department of Allergy and Clinical Immunology, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA. Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon, Hong Kong, China.
 Laboratory for Biomedical Sciences, Institute of Biolectronic Medicine, Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, United States. Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, United States. Elmezzi Graduate School of Molecular Medicine, Manhasset, NY, United States. Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy. Department of Angiocardioneurology and Translational Medicine, IRCCS Neuromed, Pozzilli, Italy. Laboratory for Biomedical Sciences, Institute of Biolectronic Medicine, Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, United States. Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, United States. Elmezzi Graduate School of Molecular Medicine, Manhasset, NY, United States.
 Neurology Department, Hospital Egas Moniz, Centro Hospitalar Lisboa Ocidental, Lisbon, Portugal. mteixeira1@campus.ul.pt. Neurology Department, Hospital Egas Moniz, Centro Hospitalar Lisboa Ocidental, Lisbon, Portugal. Neurology Department, Hospital Egas Moniz, Centro Hospitalar Lisboa Ocidental, Lisbon, Portugal.
 Empenn INSERM U1228, CNRS UMR6074, Inria, University of Rennes I, Rennes, France. Empenn INSERM U1228, CNRS UMR6074, Inria, University of Rennes I, Rennes, France. Univ Lyon, INSA-Lyon, Université Claude Bernard Lyon 1, UJM-Saint Etienne, CNRS, Inserm, CREATIS UMR 5220, U1206, Lyon, France. Univ Grenoble Alpes, Inserm, U1216, CHU Grenoble Alpes, Grenoble Institut Neurosciences, GIN, Grenoble, France.
 Center for Neuropsychology and Neuroscience Research, Kessler Foundation, East Hanover, NJ 07936. Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, NJ 08901. Center for Neuropsychology and Neuroscience Research, Kessler Foundation, East Hanover, NJ 07936. Center for Neuropsychology and Neuroscience Research, Kessler Foundation, East Hanover, NJ 07936. Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, NJ 08901; Department of Neurology, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ 08901. Electronic address: michelle.chen2@rutgers.edu.
 Klinik und Poliklinik für Neurologie, Klinikum rechts der Isar der Technischen Universität München, München, Deutschland. felixhans.hess@mri.tum.de. Klinik und Poliklinik für Neurologie, Klinikum rechts der Isar der Technischen Universität München, München, Deutschland. Klinik und Poliklinik für Neurologie, Klinikum rechts der Isar der Technischen Universität München, München, Deutschland. Klinik und Poliklinik für Neurologie, Klinikum rechts der Isar der Technischen Universität München, München, Deutschland.
 Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI, 48109, USA. chhkim@umich.edu. Mary H. Weiser Food Allergy Center, Center for Gastrointestinal Research, and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, MI, 48109, USA. chhkim@umich.edu.
 Department of Psychology, Wayne State University, 5057 Woodward Ave., Detroit, MI 48202, USA. Electronic address: jeremy.grant@wayne.edu. Department of Psychology, Wayne State University, 5057 Woodward Ave., Detroit, MI 48202, USA. Department of Neurology, Wayne State University School of Medicine, Detroit, MI, USA. Department of Physical Medicine & Rehabilitation, Wayne State University School of Medicine, Detroit, MI, USA. Department of Psychology, Wayne State University, 5057 Woodward Ave., Detroit, MI 48202, USA. Department of Psychology and Department of Brain Health, University of Nevada, Las Vegas, NV, USA. Department of Neurology, Wayne State University School of Medicine, Detroit, MI, USA.
 Department of Psychology, Carl von Ossietzky University of Oldenburg, Oldenburg, Germany. Department of Neurology, Klinikum Bremen-Ost, Bremen, Germany. Department of Neurology, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany. Department of Neurology, Klinikum Bremen-Ost, Bremen, Germany. Department of Psychology, Carl von Ossietzky University of Oldenburg, Oldenburg, Germany. helmut.hildebrandt@uni-oldenburg.de. Department of Neurology, Klinikum Bremen-Ost, Bremen, Germany. helmut.hildebrandt@uni-oldenburg.de.
 Department of Ophthalmology, , The First Affiliated Hospital of Guangxi Medical UniversityNanning, China. Department of Ophthalmology, , The First Affiliated Hospital of Guangxi Medical UniversityNanning, China. Department of Geriatric Neurology, , The People's Hospital of Guangxi Zhuang Autonomous RegionNanning, China.
 Mayo Clinic Mayo Clinic
 Pediatric Department, General Hospital of Kastoria, Kastoria, Greece. Department of Paediatrics, University of Crete, Heraklion, Greece. Department of Radiology, Medical School, University Hospital of Heraklion, University of Crete, Heraklion, Greece. Pediatric Intensive Care Unit, School of Medicine, University of Crete, Heraklion, Greece. Pediatric Department, Venizelion General Hospital Heraklion, Heraklion, Crete, Greece. Agri‑Food and Life Sciences Institute, University Research Center, Hellenic Mediterranean University, 105 Isavron street, 71303, Heraklion, Crete, Greece. vorgia.pedia@gmail.com.
 Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea. Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea. S&K Therapeutics, Ajou University Campus Plaza 418, 199 Worldcup-ro, Yeongtong-gu, Suwon 16502, Republic of Korea. Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea. S&K Therapeutics, Ajou University Campus Plaza 418, 199 Worldcup-ro, Yeongtong-gu, Suwon 16502, Republic of Korea. Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea. S&K Therapeutics, Ajou University Campus Plaza 418, 199 Worldcup-ro, Yeongtong-gu, Suwon 16502, Republic of Korea.
 Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Adaptive Sensory Technology, Lübeck, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. CEMEREM, APHM, Hôpital de la Timone, Marseille, France. CRMBM, Aix Marseille Univ, CNRS, Marseille, France. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, University of California Irvine, Irvine, California, USA. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf (UKE), Hamburg, Germany jan-patrick.STELLMANN@univ-amu.fr. CEMEREM, APHM, Hôpital de la Timone, Marseille, France. CRMBM, Aix Marseille Univ, CNRS, Marseille, France.
 Department of Physiology, Umm Al-Qura University, Makkah, SAU. College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, SAU. College of Medicine, Taibah University, Medina, SAU. College of Medicine, Taibah University, Medina, SAU. College of Medicine, Taibah University, Medina, SAU. College of Medicine, Umm Al-Qura University, Makkah, SAU. College of Medicine, King Khalid University, Abha, SAU. Department of Family and Community Medicine, King Abdul Aziz University, Jeddah, SAU.
 Pharmacogenetics Laboratory, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia. Pharmacogenetics Laboratory, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia. Pharmacogenetics Laboratory, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia. Pharmacogenetics Laboratory, Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
 Temerty Faculty of Medicine (CAE, JAM), University of Toronto, Toronto, Canada; Department of Ophthalmology and Vision Sciences (JAM), University of Toronto, Toronto, Canada; Kensington Vision and Research Centre (JAM), Toronto, Canada; and Department of Ophthalmology (JAM), St. Michael's Hospital and Toronto Western Hospital, Toronto, Canada.
 Department of Internal Medicine and Clinical Immunology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France. Electronic address: perrine.guillaumejugnot@gmail.com. Department of Neuroradiology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France. Department of Neuropathology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France; Inserm, CNRS, UMR S 1127, Institut du Cerveau et de la Moelle épinière (ICM), Sorbonne Université, Paris, France. Department of Neurology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France. Unit of Dermatology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France; Reference center for mastocytosis (CEREMAST), Hôpital Pitié-Salpêtrière, Paris, France. Department of Neurology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France.
 Charité - Universitätsmedizin Berlin (corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health), Department of Psychiatry and Psychotherapy, Berlin, Germany. Bernstein Center for Computational Neuroscience, Berlin, Germany. Department of Psychiatry, Psychotherapy, and Psychosomatics, Rheinisch-Westfälische Technische Hochschule (RWTH), Aachen University, Aachen, Germany. Bernstein Center for Computational Neuroscience, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin Center for Advanced Neuroimaging, Berlin, Germany. Charité - Universitätsmedizin Berlin (corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health), Department of Psychiatry and Psychotherapy, Berlin, Germany. Bernstein Center for Computational Neuroscience, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Neurology, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Regenerative Immunology and Aging, BIH Center for Regenerative Therapies, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK. Dementia Research Centre, Institute of Neurology, University College London, London, UK. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Medical Department, Section Psychosomatic Medicine, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin (corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health), Department of Psychiatry and Psychotherapy, Berlin, Germany. Bernstein Center for Computational Neuroscience, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
 Department of Psychology, Stanford University, Stanford, CA, USA; Department of Epidemiology and Population Health, Stanford University, Stanford, CA, USA. Electronic address: bahmanid@stanford.edu. College of Applied Sciences, University of Illinois Chicago Il, USA. Department of Education and Psychology, Shahid Ashrafi Esfahani University, Isfahan, Iran. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Isfahan Neuroscies Research Center (INRC), Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: shaygannejad@med.mui.ac.ir. Isfahan Neuroscies Research Center (INRC), Isfahan University of Medical Sciences, Isfahan, Iran. Department of Psychology, Stanford University, Stanford, CA, USA.
 Department of Neurology Næstved, Slagelse and Ringsted Hospitals, CNF, the Center for Neurological Research, Slagelse, Denmark. The Research Unit PROgrez, Department of Physiotherapy and Occupational Therapy Næstved, Slagelse and Ringsted Hospitals, Slagelse, Denmark. Institute for Regional Health Research, University of Southern Denmark, Odense, Denmark. The Research Unit PROgrez, Department of Physiotherapy and Occupational Therapy Næstved, Slagelse and Ringsted Hospitals, Slagelse, Denmark. Research Unit for Musculoskeletal Function and Physiotherapy, Department of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark. The Research Unit PROgrez, Department of Physiotherapy and Occupational Therapy Næstved, Slagelse and Ringsted Hospitals, Slagelse, Denmark. The Research Unit OPEN, Open Patient data Explorative Network, University of Southern Denmark, Odense, Denmark. The Research Unit PROgrez, Department of Physiotherapy and Occupational Therapy Næstved, Slagelse and Ringsted Hospitals, Slagelse, Denmark. Institute for Regional Health Research, University of Southern Denmark, Odense, Denmark. Institute for Regional Health Research, University of Southern Denmark, Odense, Denmark. The Research Unit PROgrez, Department of Physiotherapy and Occupational Therapy Næstved, Slagelse and Ringsted Hospitals, Slagelse, Denmark. Institute for Regional Health Research, University of Southern Denmark, Odense, Denmark. Department of Neurology Næstved, Slagelse and Ringsted Hospitals, CNF, the Center for Neurological Research, Slagelse, Denmark. Institute for Regional Health Research, University of Southern Denmark, Odense, Denmark. Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
 Sakarya University Training and Research Hospital, Sakarya, Turkey. Department of Neurology, Sakarya University Faculty of Medicine, Sakarya, Turkey. Sakarya University Training and Research Hospital, Sakarya, Turkey. Sakarya University Training and Research Hospital, Sakarya, Turkey. Department of Neurology, Sakarya University Faculty of Medicine, Sakarya, Turkey. Department of Neurology, Sakarya University Faculty of Medicine, Sakarya, Turkey. Department of Neurology, Sakarya University Faculty of Medicine, Sakarya, Turkey. drkadirtunc@hotmail.com.
 Department of Health and Nutrition, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Health and Nutrition, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Health and Nutrition, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Physiology and Iranian Medicine, School of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Persian Medicine, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Department of Traditional Medicine, School of Persian Medicine, Iran University of Medical Sciences, Tehran, Iran.
 Division for Student Development and Management, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia. Mongolian Naran Society for Osteoarthritis and Musculoskeletal Health, Ulaanbaatar 14210, Mongolia. Division for Student Development and Management, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia. Mongolian Naran Society for Osteoarthritis and Musculoskeletal Health, Ulaanbaatar 14210, Mongolia. Department of Preventive Medicine, School of Public Health, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia. Department of Finance, Business School, National University of Mongolia, Ulaanbaatar 14210, Mongolia. Department of Health Social Work and Social Sciences, School of Public Health, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia. Department of Natural Sciences, Goethe High School, Ulaanbaatar 14210, Mongolia. Department of Neurosurgery, The General Hospital for State Special Servants, Ulaanbaatar 14210, Mongolia. Department of Preventive Medicine, School of Public Health, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia. Department of Health Social Work and Social Sciences, School of Public Health, Mongolian National University of Medical Sciences, Ulaanbaatar 14210, Mongolia. Department of Microbiology, Faculty of Medicine, Kindai University, Osakasayama 589-8511, Japan.
 Texas Tech University Health Sciences Center, Lubbock, TX, USA. mirla.avila@ttuhsc.edu. Texas Tech University Health Sciences Center, Lubbock, TX, USA. Texas Tech University Health Sciences Center, Lubbock, TX, USA. Texas Tech University Health Sciences Center, Lubbock, TX, USA. Baylor College of Medicine, Houston, TX, USA.
 Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Oslo, Norway. Electronic address: synne.brune-ingebretsen@medisin.uio.no. Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Oslo, Norway; Department of Psychology, University of Oslo, Oslo, Norway. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy; TomaLab, Institute of Nanotechnology, National Research Council (CNR), Rome, Italy. Department of Neurology, Oslo University Hospital, Oslo, Norway. Oslo Centre for Biostatistics and Epidemiology, Oslo University Hospital, Oslo, Norway. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, United Kingdom; UK Dementia Research Institute at UCL, London, United Kingdom; Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China; Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité-Universitaetsmedizin Berlin, Berlin, Germany; NeuroCure Clinical Research Center, Charité-Universitaetsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Berlin, Germany. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy; Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy; IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Institut d'Investigacions Biomediques August Pi Sunyer, Barcelona, Spain. Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Oslo, Norway. Department of Research, Innovation and Education, Oslo University Hospital, Oslo, Norway; Department of Mechanical, Electronic and Chemical Engineering, Oslo Metropolitan University, Oslo, Norway.
 Department of Neurology, Medical University of Lodz, Lodz, Poland. Department of Neurology, Medical University of Lodz, Lodz, Poland. Department of Neurology, Medical University of Lodz, Lodz, Poland. Department of Neurology, Medical University of Lodz, Lodz, Poland. Department of Neurology, Medical University of Lodz, Lodz, Poland. Department of Neurology, Medical University of Lodz, Lodz, Poland. Department of Neurology, Medical University of Lodz, Lodz, Poland.
 International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran. Department of Cardiovascular Diseases, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran. Department of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran.
 Department of Physical Medicine & Rehabilitation, Michigan Medicine, Ann Arbor, MI, USA. Electronic address: abouliba@med.umich.edu. Departments of Health Care Sciences & Neurology, Wayne State University, Detroit, MI, USA. Department of Physical Medicine & Rehabilitation, Michigan Medicine, Ann Arbor, MI, USA.
 Department of Neurology, Ulm University, Ulm, Germany. Department of Neurology, Ulm University, Ulm, Germany. Department of Neurology, Ulm University, Ulm, Germany. Department of Neurology, Ulm University, Ulm, Germany. Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany. German Center for Neurodegenerative Diseases (DNZE), Campus Ulm, Ulm, Germany. Department of Neurology, University Medicine Greifswald, Greifswald, Germany. Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. Neuroimmunology, Institute of Clinical Chemistry, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. Department of Neurology, Ulm University, Ulm, Germany. Department of Neurology, Ulm University, Ulm, Germany.
 Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland. Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland. Students Research Association, Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland. Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland. Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland. Dialysis Unit, Department of Nephrology and Transplantology, Wroclaw Medical University, 50-556 Wroclaw, Poland. Department of Nephrology and Transplantology, Wroclaw Medical University, 50-556 Wroclaw, Poland. Department of Dermatology, Venerology and Allergology, Wroclaw Medical University, 50-367 Wroclaw, Poland. Department of Neurology, Wroclaw Medical University, 50-556 Wroclaw, Poland. Department of Neurology, Wroclaw Medical University, 50-556 Wroclaw, Poland. Dialysis Unit, Department of Nephrology and Transplantology, Wroclaw Medical University, 50-556 Wroclaw, Poland. Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland. Department of Dermatology, Venerology and Allergology, Wroclaw Medical University, 50-367 Wroclaw, Poland. Department of Psychiatry, Wroclaw Medical University, 50-367 Wroclaw, Poland.
 Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet, Huddinge, Sweden. andreas.wallin@ki.se. Rehab Station Stockholm, Research and Development Unit, Solna, Sweden. andreas.wallin@ki.se. Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden. Stockholm Sjukhem Foundation, R&D Unit, Stockholm, Sweden. Department of Neurobiology, Care Sciences and Society, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Medical Psychology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, Karolinska University Hospital and Neuroimmunology Unit, Stockholm, Sweden. Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet, Huddinge, Sweden. Women's Health and Allied Health Professionals Theme, Medical Unit Occupational Therapy and Physiotherapy, Karolinska University Hospital, Stockholm, Sweden.
 Facultad de Medicina, Universidad Nacional Autónoma de México, Cuidad de México, Mexico. Facultad de Medicina, Universidad Nacional Autónoma de México, Cuidad de México, Mexico. Facultad de Medicina, Universidad Nacional Autónoma de México, Cuidad de México, Mexico. Facultad de Medicina, Universidad Nacional Autónoma de México, Cuidad de México, Mexico. Facultad de Medicina, Universidad Nacional Autónoma de México, Cuidad de México, Mexico. División de Neurociencias Clínicas, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Ciudad de México, México. Electronic address: neuropcm@gmail.com.
 Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. assuntatrinchillo94@gmail.com. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Advanced Biomedical Sciences, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Infectious Diseases Unit, "Federico II" University, Naples, Italy. Infectious Diseases Unit, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy. Department of Neurosciences, Reproductive Sciences and Odontostomatology, "Federico II" University, Naples, Italy.
 Texas Tech University Health Sciences Center, Lubbock, TX, USA. mirla.avila@ttuhsc.edu. Texas Tech University Health Sciences Center, Lubbock, TX, USA. Texas Tech University Health Sciences Center, Lubbock, TX, USA. Texas Tech University Health Sciences Center, Lubbock, TX, USA. Baylor College of Medicine, Houston, TX, USA.
 Medicine, King Abdulaziz University, Jeddah, SAU. Medicine, King Abdulaziz University, Jeddah, SAU. Medicine, King Abdulaziz University, Jeddah, SAU. Medicine, King Abdulaziz University, Jeddah, SAU. Medicine, King Abdulaziz University, Jeddah, SAU. Neurology, King Abdulaziz University Hospital, Jeddah, SAU.
 Department of Neurourology & North West Spinal Cord Injury Unit, Southport & Ormskirk Hospital NHS Trust, Liverpool, UK. Department of Neurourology & North West Spinal Cord Injury Unit, Southport & Ormskirk Hospital NHS Trust, Liverpool, UK. Department of Neurourology & North West Spinal Cord Injury Unit, Southport & Ormskirk Hospital NHS Trust, Liverpool, UK. Department of Neurourology & North West Spinal Cord Injury Unit, Southport & Ormskirk Hospital NHS Trust, Liverpool, UK.
 Department of Chemistry, College of Science, University of Babylon, Babylon, Iraq. 60 Beded Hospital Khurrianwala, Faisalabad, Pakistan. Rawalpindi Medical University, Rawalpindi, Pakistan. Department of Physical Education, University of Jammu, Jammu, India. College of Medicine, University of Al-Ameed, Karbala, Iraq. Medical Laboratory Technology Department, College of Medical Technology, The Islamic University, Najaf, Iraq. Azogues Campus Nursing Career, Health and Behavior Research Group (HBR), Psychometry and Ethology Laboratory, Catholic University of Cuenca, Ecuador. Doctorate in Psychology, University of Palermo, Buenos Aires, Argentina. Epidemiology and Biostatistics Research Group, CES University, Colombia. Department of Pharmaceutical Chemistry, College of Pharmacy, University of Mosul, Mosul-41001, Iraq. Institute of Pharmaceutical Research, GLA University, District-Mathura, U. P., India. Department of Biomedical Engineering, Al-Mustaqbal University College, Babylon, Iraq. Department of Pharmacology and Toxicology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj 11942, Saudi Arabia. Agricultural Genetic Engineering Research Institute (AGERI), Agricultural Research Center, Giza, Egypt. Department of Medical Physics and Radiology, Faculty of Paramedical Sciences, Kashan University of Medical Sciences, Kashan, Iran.
 Universidad de Sonora University of Arizona
 Department of Clinical Nutrition, School of Nutrition & Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: moravejolahkami@gmail.com. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: chitsaz@med.mui.ac.ir. Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: hassanzadeh.aja@gmail.com. Department of Clinical Nutrition, School of Nutrition & Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: paknahad@hlth.mui.ac.ir.
 Psychology UR CLIPSYD 4430, Paris-Nanterre University, Nanterre, France. Réseau SEP IDF Ouest, Le Vesinet, France. Inserm CIC 1429, APHP, Hôpital Raymond-Poincare, Garches, France. Inserm CIC 1429, APHP, Hôpital Raymond-Poincare, Garches, France. Clinical Research Unit, Faculty of Health and Social Sciences, Bournemouth University, Poole, Dorset, UK. Neurologie, Centre Hospitalier de Gonesse, Gonesse, France. Service de Médecine Physique et de Réadaptation, Hôpital Raymond-Poincare, APHP, Garches, France. Inserm UMR 1179, Universite Versailles Saint-Quentin-en-Yvelines, Versailles, France. CRC SEP IDF Ouest, Poissy-Garches, France. CRC SEP IDF Ouest, Poissy-Garches, France. Neurologie, CHIPS Site Hospitalier de Poissy, Poissy Cedex, France. CRC SEP IDF Ouest, Poissy-Garches, France olivier.heinzlef@ght-yvelinesnord.fr. Neurologie, CHIPS Site Hospitalier de Poissy, Poissy Cedex, France.
 Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Electronic address: seyedmassoodnabavi@gmail.com. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Reproductive Epidemiology Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. International Medicine Department, Mostafa Khomeini Medical Center, Shahed University, Tehran, Iran. Nursing Care Research Center, School of Nursing and Midwifery, Iran University of Medical Science, Tehran, Iran. Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Tehran, Iran. Electronic address: masvos@Royaninstitute.org.
 Department of Neurology, Clermont-Ferrand University Hospital, 58 Rue Montalembert, 63003, Clermont-Ferrand Cedex 1, France. pclavelou@chu-clermontferrand.fr. Department of Neurology, Nîmes University Hospital, Hopital Caremeau, Nîmes, France. Department of Infectious and Tropical Diseases, Pitié-Salpêtrière Hospital, APHP, Sorbonne Université, INSERM 1136, Institut Pierre Louis d'Epidémiologie et de Santé Publique Paris, Paris, France. Department of Neurology, Strasbourg University Hospital, Strasbourg, France. Univ. Lille, Inserm U1172 LilNCog, CHU Lille, FHU Precise, Lille, France. Global Medical Affairs Neurology and Immunology, Ares Trading SA (An affiliate of Merck KGaA, Darmstadt, Germany), Eysins, Switzerland. Neurology Department, Medical Affairs (An affiliate of Merck KGaA, Darmstadt, Germany), Merck Santé, Lyon, France. Department of Neurology, Caen University Hospital, Caen, France.
 Medical Doctoral School, University of Oradea, 410087 Oradea, Romania. Department of Ophthalmology, Faculty of Medicine, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania. Department of Ophthalmology, Faculty of Medicine, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania. Department of Medical Informatics and Biostatistics, "Iuliu Hațieganu" University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Department of Medical Informatics and Biostatistics, "Iuliu Hațieganu" University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Department of Ophthalmology, Faculty of Medicine, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania.
 Department of Personality, Assessment, and Psychological Treatment, University of Seville, 41018 Seville, Spain. Department of Personality, Assessment, and Psychological Treatment, University of Seville, 41018 Seville, Spain. Department of Personality, Assessment, and Psychological Treatment, University of Seville, 41018 Seville, Spain. Department of Psychosomatic Medicine and Psychotherapy, University Hospital Muenster, 48149 Muenster, Germany. Department of Personality, Assessment, and Psychological Treatment, University of Seville, 41018 Seville, Spain.
 Department of Radiology and Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China. Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Capital Medical University, Beijing, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China. Department of Radiology and Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China. Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Capital Medical University, Beijing, China. Department of Radiology and Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China. Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Capital Medical University, Beijing, China. Department of Radiology and Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China. Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Capital Medical University, Beijing, China. Philips Healthcare, Beijing, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China. Department of Radiology and Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China. Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Capital Medical University, Beijing, China. Department of Radiology and Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China. Beijing Key Laboratory of Magnetic Resonance Imaging and Brain Informatics, Capital Medical University, Beijing, China.
 Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Laboratory of Human Genetics of Neurological Disorders, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Vita-Salute San Raffaele University, 20132 Milan, Italy. Laboratory of Human Genetics of Neurological Disorders, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Centre Hospitalier Universitaire de Toulouse, CEDEX 9, 31059 Toulouse, France. Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), INSERM UMR1291-CNRS UMR5051-Université Toulouse III, CEDEX 3, 31024 Toulouse, France. Laboratory of Human Genetics of Neurological Disorders, IRCCS San Raffaele Hospital, 20132 Milan, Italy. AnacletoLab, Dipartimento di Informatica, Università degli Studi di Milano, 20133 Milan, Italy. Data Science Research Center, Università degli Studi di Milano, 20133 Milan, Italy. Infolife National Lab, CINI, 00185 Rome, Italy. Laboratory of Human Genetics of Neurological Disorders, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Laboratory of Human Genetics of Neurological Disorders, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Centre Hospitalier Universitaire de Toulouse, CEDEX 9, 31059 Toulouse, France. Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), INSERM UMR1291-CNRS UMR5051-Université Toulouse III, CEDEX 3, 31024 Toulouse, France. Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Vita-Salute San Raffaele University, 20132 Milan, Italy. Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), INSERM UMR1291-CNRS UMR5051-Université Toulouse III, CEDEX 3, 31024 Toulouse, France. Department of Immunology, Toulouse University Hospitals, CEDEX 3, 31024 Toulouse, France. Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Vita-Salute San Raffaele University, 20132 Milan, Italy. Neuroimaging Research Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Neurophisiology Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. AnacletoLab, Dipartimento di Informatica, Università degli Studi di Milano, 20133 Milan, Italy. Data Science Research Center, Università degli Studi di Milano, 20133 Milan, Italy. Infolife National Lab, CINI, 00185 Rome, Italy. Neurology and Neurorehabilitation Unit, IRCCS San Raffaele Hospital, 20132 Milan, Italy. Laboratory of Human Genetics of Neurological Disorders, IRCCS San Raffaele Hospital, 20132 Milan, Italy.
 Sapienza University of Rome, Rome, Italy. Sapienza University of Rome, Rome, Italy. University of Catania, Catania, Italy. Sapienza University of Rome, Rome, Italy. Sapienza University of Rome, Rome, Italy. Sapienza University of Rome, Rome, Italy. Sapienza University of Rome, Rome, Italy. Sapienza University of Rome, Rome, Italy. Sapienza University of Rome, Rome, Italy.
 Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Baylor College of Medicine, Houston, TX, USA. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Baylor College of Medicine, Houston, TX, USA. Baylor College of Medicine, Houston, TX, USA. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Universidad Anáhuac Puebla, Tlaxcalancingo, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Houston Methodist Hospital, Houston, TX, USA. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Instituto Nacional de Enfermedades Respiratorias, Ciudad de México, México. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Laboratorios Ruiz SYNLAB, Puebla, México. Clínica Ruiz, Centro de Hematología y Medicina Interna, Puebla, México. gruiz1@clinicaruiz.com. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. gruiz1@clinicaruiz.com. Laboratorios Ruiz SYNLAB, Puebla, México. gruiz1@clinicaruiz.com.
 Faculty of Biomedical Sciences, Università della Svizzera Italiana, 6900 Lugano, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland (NSI), Regional Hospital of Lugano, Ente Ospedaliero Cantonale, 6900 Lugano, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland (NSI), Regional Hospital of Lugano, Ente Ospedaliero Cantonale, 6900 Lugano, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland (NSI), Regional Hospital of Lugano, Ente Ospedaliero Cantonale, 6900 Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, 6900 Lugano, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland (NSI), Regional Hospital of Lugano, Ente Ospedaliero Cantonale, 6900 Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, 6900 Lugano, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland (NSI), Regional Hospital of Lugano, Ente Ospedaliero Cantonale, 6900 Lugano, Switzerland.
 Department of Neurological Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Electronic address: mustafacan_341@hotmail.com. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Faculty of Physical Therapy and Rehabilitation, Hacettepe University, Ankara, Turkey. Department of Neurology, Hacettepe University, Ankara, Turkey. Department of Neurology, Hacettepe University, Ankara, Turkey.
 Department of Medical Genetics, Faculty of Medicine & Dentistry, Edmonton, AB, Canada. Faculty of Medicine & Dentistry, Neuroscience and Mental Health Institute, Edmonton, AB, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, Edmonton, AB, Canada. Women and Children's Health Research Institute, 5-083 Edmonton Clinic Health Academy, University of Alberta, Edmonton, AB, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, Edmonton, AB, Canada. Faculty of Medicine & Dentistry, Neuroscience and Mental Health Institute, Edmonton, AB, Canada. Women and Children's Health Research Institute, 5-083 Edmonton Clinic Health Academy, University of Alberta, Edmonton, AB, Canada. Department of Cell Biology, Faculty of Medicine & Dentistry, Edmonton, AB, Canada. Multiple Sclerosis Centre and Department of Cell Biology, Faculty of Medicine & Dentistry, Edmonton, AB, Canada.
 Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico (UNAM), CDMX, Mexico. Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico (UNAM), CDMX, Mexico.
 College of Medicine, Taibah University, Madinah, SAU. College of Medicine, Taibah University, Madinah, SAU. College of Medicine, Imam Abdulrahman Bin Faisal University, Dammam, SAU. College of Medicine, Taibah University, Madinah, SAU. Neurology, King Fahad Specialist Hospital, Dammam, SAU. Neuroscience, Neuroscience Center, King Fahad Specialist Hospital, Dammam, SAU.

 Physiotherapy and Rehabilitation Graduate Program, Ankara Yildirim Beyazit University, Institute of Health Sciences, Ankara, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Gazi University, Ankara, Turkey. Faculty of Medicine, Department of Neurology, Ankara University, Ankara, Turkey. Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Ankara Yildirim Beyazit University, Ankara, Turkey.

 Center for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY, United States. Center for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY, United States. Center for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY, United States. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY, United States.
 Univ Lyon, UJM-Saint-Etienne, Inter-university Laboratory of Human Movement Biology, EA 7424, F-42023, Saint-Etienne, FRANCE. Univ Lyon, UJM-Saint-Etienne, Inter-university Laboratory of Human Movement Biology, EA 7424, F-42023, Saint-Etienne, FRANCE. Univ Lyon, UJM-Saint-Etienne, Inter-university Laboratory of Human Movement Biology, EA 7424, F-42023, Saint-Etienne, FRANCE. Univ Lyon, UJM-Saint-Etienne, Inter-university Laboratory of Human Movement Biology, EA 7424, F-42023, Saint-Etienne, FRANCE. Department of Radiology, CHU Hospital, Jean Monnet University, Saint Etienne, FRANCE. Department of Radiology, CHU Hospital, Jean Monnet University, Saint Etienne, FRANCE. Univ Lyon, UJM-Saint-Etienne, Inter-university Laboratory of Human Movement Biology, EA 7424, F-42023, Saint-Etienne, FRANCE. Department of Neurology, University Hospital of Saint-Etienne, Saint-Etienne, FRANCE.
 Faculty of Nursing and Midwifery, Department of Nursing and Midwifery School,Kermanshah University of Medical Sciences, Student Research Committee,Kermanshah, Iran. Department of Nursing and Midwifery School,Kermanshah University of Medical Sciences, Student Research Committee,Kermanshah, Iran. Department of Nursing and Midwifery School,Kermanshah University of Medical Sciences, Student Research Committee,Kermanshah, Iran.
 Dept. of Electrical and Computer Engineering, The Johns Hopkins University, Baltimore, MD 21218, USA. Dept. of Electrical and Computer Engineering, The Johns Hopkins University, Baltimore, MD 21218, USA. Dept. of Electrical and Computer Engineering, The Johns Hopkins University, Baltimore, MD 21218, USA. Dept. of Neurology, The Johns Hopkins University School of Medicine, MD 21287, USA. Dept. of Neurology, The Johns Hopkins University School of Medicine, MD 21287, USA. Dept. of Electrical and Computer Engineering, The Johns Hopkins University, Baltimore, MD 21218, USA.
 Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin 300052, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin 300052, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin 300052, China. Department of Radiology, The First Afliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China; Neuroimaging Lab, Jiangxi Province Medical Imaging Research Institute, Nanchang 330006, Jiangxi Province, China. Department of Radiology, The First Afliated Hospital, Nanchang University, Nanchang 330006, Jiangxi Province, China; Neuroimaging Lab, Jiangxi Province Medical Imaging Research Institute, Nanchang 330006, Jiangxi Province, China. Department of Radiology, Huashan Hospital, Fudan University, Shanghai 200040, China. Department of Radiology, Huashan Hospital, Fudan University, Shanghai 200040, China. Department of Radiology, The First Afliated Hospital of Chongqing Medical University, Chongqing 400016, China. Department of Radiology, The First Afliated Hospital of Chongqing Medical University, Chongqing 400016, China. Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin Province, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, No.119, The West Southern 4th Ring Road, Fengtai District, Beijing 100070, China. Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin 300052, China. Electronic address: znnn2010@sina.com.
 Eu2P Programme, University Bordeaux, 146, rue Léo Saignat, 33076 Bordeaux, France. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy. Multiple Sclerosis Regional Center, "A. Cardarelli" Hospital, 80131 Naples, Italy. Neurological Clinic and Stroke Unit, "A. Cardarelli" Hospital, 80131 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Dipartimento Farmaceutico, UOC Farmaceutica Convenzionata e Territoriale, ASL Napoli 1 Centro, 80131 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy. Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Regional Center of Pharmacovigilance and Pharmacoepidemiology of Campania Region, 80138 Naples, Italy.
 Exigo Consultores, Lda., Lisbon, Portugal. Exigo Consultores, Lda., Lisbon, Portugal. Exigo Consultores, Lda., Lisbon, Portugal. Neurology Department, Centro Hospitalar Universitário de Lisboa Central, EPE, Lisbon, Portugal. School of Medicine, University of Minho, Braga, Portugal. Hospital Prof Doutor Fernando Fonseca, EPE, Amadora, Portugal. F. Hoffmann-La Roche AG, Basel, Switzerland. Roche Farmacêutica e Química, Lda., Amadora, Portugal. isabel.monteiro@roche.com.
 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina; Servicio de Neurología, Sanatorio Güemes, Ciudad de Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina. Servicio de Neurología, Sanatorio Güemes, Ciudad de Buenos Aires, Argentina; Servicio de Neurología, Hospital Tornú, Ciudad de Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina. Centro de esclerosis Múltiple Buenos Aires, Ciudad de Buenos Aires, Argentina; Servicio de Neurología, CEMIC, Ciudad de Buenos Aires, Argentina. Centro de esclerosis Múltiple Buenos Aires, Ciudad de Buenos Aires, Argentina. Centro de esclerosis Múltiple Buenos Aires, Ciudad de Buenos Aires, Argentina. Centro de esclerosis Múltiple Buenos Aires, Ciudad de Buenos Aires, Argentina. Servicio de Neurología, Hospital San Bernardo, Salta, Argentina. Servicio de Neurología, Sanatorio Allende, Córdoba, Spain. Servicio de Neurología, Clínica Universitaria Reina Fabiola, Córdoba, Spain. Sección de Neuroinmunología, Hospital Alemán, Ciudad de Buenos Aires, Argentina. DIABAI, Argentina. Instituto Neurociencias, Rosario, Argentina. Servicio de neurología, Hospital Italiano, Argentina. Servicio de neurología, Hospital Militar, Campo de Mayo, Argentina. Servicio de neurología, Hospital Posadas, Ciudad de Buenos Aires, Argentina. Servicio de neurología, Hospital Cesar Milstein, Ciudad de Buenos Aires, Argentina. Servicio de neurología, Hospital de Clínica José de San Martín, Ciudad de Buenos Aires, Argentina. Servicio de neurología, Hospital Español, La Plata, Argentina. Sección de Neuroinmunología, Hospital Alemán, Ciudad de Buenos Aires, Argentina. Servicio de neurología, Hospital Álvarez, Ciudad de Buenos Aires, Argentina. Servicio de neurología, Hospital Álvarez, Ciudad de Buenos Aires, Argentina. Servicio de neurología, Hospital Español, Rosario, Argentina. Servicio de neurología, Hospital Nuestra Señora del Carmen, Tucumán, Argentina. Servicio de neurología, Hospital Córdoba, Córdoba, Spain. Servicio de neurología, Hospital Durand, Ciudad de Buenos Aires, Argentina. Instituto Neurociencias, Rosario, Argentina. Servicio de neurología, Hospital de San Luis, San Luis, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Ciudad de Buenos Aires, Argentina; Servicio de neurología, Hospital Italiano, Argentina. Electronic address: bsilva@leloir.org.ar.
 Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Harvard Medical School, Boston, Massachusetts. Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, San Francisco. Department of Medicine and the Ottawa Hospital Research Institute, The University of Ottawa, Ottawa, Ontario, Canada. Department of Neurology, Cantonal Hospital Aarau, Aarau, Switzerland. Unit of Neuroimmunology, Division of Neurology, Department of Clinical Neurosciences, University Hospital of Geneva and Faculty of Medicine, Geneva, Switzerland. Department of Neurology, Cantonal Hospital St Gallen, St Gallen, Switzerland. Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland. Department of Neurology, Bern University Hospital, University of Bern, Bern, Switzerland. Multiple Sclerosis Center, Department of Neurology, Neurocenter of Southern Switzerland, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Multiple Sclerosis Center, Department of Neurology, Neurocenter of Southern Switzerland, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany. Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Center for Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Multiple Sclerosis Center, Department of Neurology, Neurocenter of Southern Switzerland, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Translational Imaging in Neurology Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland. Unit of Neuroimmunology, Division of Neurology, Department of Clinical Neurosciences, University Hospital of Geneva and Faculty of Medicine, Geneva, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital and University of Basel, Switzerland.
 Department of Biostatistics, School of Public Health, The University of Alabama at Birmingham, Birmingham, AL, USA. Department of Neurology, Biogen Inc, Cambridge, MA, USA, at the time of these analyses. RINGGOLD: 2191 Biostatistics, Biogen Inc, Cambridge, MA, USA, at the time of these analyses. RINGGOLD: 2191 Biogen Digital Health, Biogen Inc, Cambridge, MA, USA. RINGGOLD: 2191 Value Based Medicine, Biogen Inc, Cambridge, MA, USA, at the time of these analyses. RINGGOLD: 2191 Global Medical, Biogen Inc, Cambridge, MA, USA, at the time of these analyses. RINGGOLD: 2191 Department of Neurology, Corinne Goldsmith Dickinson Center for Multiple Sclerosis, New York, NY, USA and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. RINGGOLD: 5925 McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. RINGGOLD: 2511 Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. RINGGOLD: 2511 Global Medical, Biogen Inc, Cambridge, MA, USA, at the time of these analyses. RINGGOLD: 2191
 Department of Neurology, Hospital Universitario Ramón y Cajal, , Universidad de Alcalá, Madrid, SpainIRyCIS. RINGGOLD: 537482 Medical Department, Roche Farma, Madrid, Spain. Department of Neurology, , Sevilla, SpainHospital Universitario Virgen Macarena. RINGGOLD: 16582 Department of Neurology, , Zaragoza, SpainHospital Universitario Miguel Servet. RINGGOLD: 16488 Department of Neurology, , Terrassa, SpainHospital Universitari Mútua Terrassa. RINGGOLD: 58955 Department of Neurology, Hospital Regional Universitario de Málaga, Málaga, Spain. Department of Neurology, , Ávila, SpainComplejo Asistencial de Ávila. RINGGOLD: 70690 Department of Neurology, , Alcorcón, SpainHospital Universitario Fundación Alcorcón. RINGGOLD: 16432 Department of Neurology, Hospital de Galdakao-Usansolo, Galdakao, Spain. Department of Neurology, , Granada, SpainHospital Universitario Clínico San Cecilio. RINGGOLD: 16581 Department of Neurology, Hospital Universitari Son Espases, Palma de Mallorca, Spain. Department of Neurology, , Lleida, SpainHospital Universitari Arnau de Vilanova. RINGGOLD: 16296 Department of Neurology, , Madrid, SpainHospital Universitario Puerta de Hierro. RINGGOLD: 16370 Department of Neurology, , Sevilla, SpainHospital Universitario Virgen Macarena. RINGGOLD: 16582 Department of Neurology, , Pontevedra, SpainComplexo Hospitalario Universitario de Pontevedra. RINGGOLD: 16874 Department of Neurology, , Elche, SpainHospital General Universitario de Elche. RINGGOLD: 16686 Department of Neurology, Hospital Universitario Reina Sofía, Córdoba, Spain. Department of Neurology, , Zaragoza, SpainHospital Clínico Universitario Lozano Blesa. RINGGOLD: 16479 Department of Neurology, Fundació Salut Empordà, Figueres, Spain. Department of Neurology, Hospital Francesc de Borja, Gandía, Spain. Department of Neurology, Hospital Universitario Puerta del Mar, Cádiz, Spain. Department of Neurology, , Sabadell, SpainConsorci Corporació Sanitària Parc Taulí. RINGGOLD: 16382 Medical Department, Roche Farma, Madrid, Spain. Medical Department, Roche Farma, Madrid, Spain. Department of Neurology, , San Sebastián, SpainHospital Universitario Donostia. RINGGOLD: 16650
 Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA; Cancer Biology Graduate Program, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA; Biology Graduate Program, Stanford University, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Neuroscience Graduate Program, Stanford University, Palo Alto, CA 94305, USA. Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA 94305, USA; Stem Cell Biology and Regenerative Medicine Program, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Neurology & Neurological Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Institute for Molecular Medicine, HiLIFE, University of Helsinki, Helsinki 00014, Finland. Institute for Molecular Medicine, HiLIFE, University of Helsinki, Helsinki 00014, Finland; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94305, USA. Electronic address: egibson1@stanford.edu.
 National College of Pharmacy, KMCT Group of Institutions, Manassery, Kozhikode 673602, Kerala, India. National College of Pharmacy, KMCT Group of Institutions, Manassery, Kozhikode 673602, Kerala, India. National College of Pharmacy, KMCT Group of Institutions, Manassery, Kozhikode 673602, Kerala, India. Department of Pharmaceutical Analysis, Sri Sivani College of Pharmacy, Srikakulam 532 402, Andhra Pradesh, India.
 Teva Pharmaceutical Industries Ltd, Netanya, Israel. Teva Pharmaceutical Industries Ltd, Netanya, Israel. Teva Pharmaceutical Industries Ltd, Netanya, Israel. Katholisches Klinikum Bochum gGmbH, St. Josef-Hospital, Bochum, Germany.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. rocca.mara@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. rocca.mara@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. rocca.mara@hsr.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy.
 Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. The College of Basic Medicine, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Pharmacy, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China. Department of Neurology, the Second Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou 450002, China.
 Department of Pharmacology and Toxicology, Unaizah College of Pharmacy, Qassim University, Qassim, Unaizah 51911, Saudi Arabia. Department of Pharmacology and Toxicology, Unaizah College of Pharmacy, Qassim University, Qassim, Unaizah 51911, Saudi Arabia. Electronic address: sk.alenezi@qu.edu.sa. Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Qassim, Buraydah 51452, Saudi Arabia.
 EnMed Program Texas A&M School of Engineering Medicine Houston Texas USA. Department of Urology Houston Methodist Hospital Houston Texas USA. Department of Urology Houston Methodist Hospital Houston Texas USA. Department of Urology Houston Methodist Hospital Houston Texas USA. Translational Imaging Center Houston Methodist Research Institute Houston Texas USA.
 Endocrine Unit, Department of Medicine and Surgery, University of Insubria, ASST dei Sette Laghi, 21100 Varese, Italy. Immunology and General Pathology Laboratory, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy. Molecular Cardiology Laboratory, IRCCS-Policlinico San Donato, San Donato Milanese, 20097 Milan, Italy. Center for Translational Research on Autoimmune and Allergic Disease-CAAD, Università del Piemonte Orientale, 28100 Novara, Italy. Endocrine Unit, Department of Medicine and Surgery, University of Insubria, ASST dei Sette Laghi, 21100 Varese, Italy. Endocrine Unit, Department of Medicine and Surgery, University of Insubria, ASST dei Sette Laghi, 21100 Varese, Italy. Endocrine Unit, Department of Medicine and Surgery, University of Insubria, ASST dei Sette Laghi, 21100 Varese, Italy. Endocrine Unit, Department of Medicine and Surgery, University of Insubria, ASST dei Sette Laghi, 21100 Varese, Italy. Immunology and General Pathology Laboratory, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy.
 San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy. Electronic address: gregori.silvia@hsr.it.
 Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW, Australia. RINGGOLD: 439651. RINGGOLD: 37024 Department of Neurology, Royal North Shore Hospital, St Leonards Heights, NSW, Australia. Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 Centre for Genomics and Personalised Health, School of Biomedical Science, Queensland University of Technology, Kelvin Grove, QLD, Australia. Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW, Australia. RINGGOLD: 439651. RINGGOLD: 37024 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568 Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW, Australia. RINGGOLD: 439651. RINGGOLD: 37024 Department of Neurology, John Hunter Hospital, New Lambton Heights, NSW, Australia. RINGGOLD: 439651. RINGGOLD: 37024 Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. RINGGOLD: 454568
 Emory University, 100 Woodruff Circle, Atlanta, GA, 30322, USA. Emory University School of Medicine, Department of Pediatrics, Division of Neurology, Atlanta, GA, USA. Emory University School of Medicine, Department of Pediatrics, Division of Neurology, Atlanta, GA, USA; Children's Healthcare of Atlanta, Division of Neurology, Atlanta, GA, USA. Electronic address: grace.yoonheekim.gombolay@emory.edu.
 Division of Pharmacovigilance I, Office of Surveillance and Epidemiology, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Pharmacovigilance I, Office of Surveillance and Epidemiology, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Pharmacovigilance I, Office of Surveillance and Epidemiology, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Neurology II, Office of Neuroscience, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Neurology II, Office of Neuroscience, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Neurology II, Office of Neuroscience, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Neurology II, Office of Neuroscience, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Gastroenterology, Office of Neurology, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Gastroenterology, Office of Neurology, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Gastroenterology, Office of Neurology, Office of New Drugs, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA. Division of Pharmacovigilance I, Office of Surveillance and Epidemiology, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA.
 Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Sokolská 581, 500 05, Hradec Králové, Czech Republic. Multiple Sclerosis Center, Sheba Medical Center, Tel-Hashomer, Israel. Neurology Department, Sheba Medical Center, Tel-Hashomer, Israel. Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. Department of Neurology, Medical School, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Faculty of Medicine at Palacký University and University Hospital in Olomouc, I. P. Pavlova 6, Olomouc, Czech Republic. Brain and Mind Center, University of Sydney, Sydney, Australia. Department of Neurology, Faculty of Medicine at Palacký University and University Hospital in Olomouc, I. P. Pavlova 6, Olomouc, Czech Republic. First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Sokolská 581, 500 05, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Sokolská 581, 500 05, Hradec Králové, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Sokolská 581, 500 05, Hradec Králové, Czech Republic. Memory Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic. Department of Neurology, Faculty of Medicine and University Hospital Hradec Králové, Charles University in Prague, Sokolská 581, 500 05, Hradec Králové, Czech Republic. zbysekpavelek@email.cz.
 Department of Neurology, Henry Ford Health, Detroit, MI, 48202, USA. smir2@hfhs.org. Department of Neurology, Henry Ford Health, Detroit, MI, 48202, USA. Department of Neurology, Henry Ford Health, Detroit, MI, 48202, USA. Department of Neurology, Henry Ford Health, Detroit, MI, 48202, USA. Gynecologic Oncology and Developmental Therapeutics Research Program, Henry Ford Health Hospital, Detroit, MI, 48202, USA. Department of Neurology, Henry Ford Health, Detroit, MI, 48202, USA. sgiri1@hfhs.org.
 Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel. The Department of Neurology and Laboratory of Neuroimmunology, The Agnes-Ginges Center for Human Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
 Department of Neurology, , Rotterdam, The NetherlandsErasmus Medical Center. RINGGOLD: 6993 Department of Neurology, , Rotterdam, The NetherlandsErasmus Medical Center. RINGGOLD: 6993 Huygens & Versteegh, Zwijndrecht, The Netherlands. Department of Neurology, , Rotterdam, The NetherlandsErasmus Medical Center. RINGGOLD: 6993 Department of Neurology, , Rotterdam, The NetherlandsErasmus Medical Center. RINGGOLD: 6993 Department of Neurology, , Rotterdam, The NetherlandsErasmus Medical Center. RINGGOLD: 6993
 University College Dublin, Dublin, Ireland. University College Dublin, Dublin, Ireland. St. Vincent's University Hospital, Dublin, Ireland. University College Dublin, Dublin, Ireland. St. Vincent's University Hospital, Dublin, Ireland. University College Dublin, Dublin, Ireland. St. Vincent's University Hospital, Dublin, Ireland. St. Vincent's University Hospital, Dublin, Ireland. University College Dublin, Dublin, Ireland. St. Vincent's University Hospital, Dublin, Ireland. University College Dublin, Dublin, Ireland. St. Vincent's University Hospital, Dublin, Ireland.
 Texas A&M Institute for Neuroscience, Texas A&M University, College Station, TX, United States. Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States. Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States. Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States. Texas A&M Institute for Genome Sciences and Society, Texas A&M University, College Station, TX, United States. Department of Veterinary Pathobiology, Texas A&M University, College Station, TX, United States. Texas A&M Institute for Genome Sciences and Society, Texas A&M University, College Station, TX, United States. Texas A&M Institute for Neuroscience, Texas A&M University, College Station, TX, United States. Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States.
 Department of Neurology, Ulm University Hospital, Ulm, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. German Center for Neurodegenerative Diseases (DZNE e.V.), Ulm, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. Department of Neurology, Martin-Luther-University Halle-Wittenberg, Halle, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. German Center for Neurodegenerative Diseases (DZNE e.V.), Ulm, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. German Center for Neurodegenerative Diseases (DZNE e.V.), Ulm, Germany.
 Department of Medical Biotechnology and Translational Medicine, University of Milan, Via Fratelli Cervi 93, Segrate, 20090, Milan, Italy. sara.grassi@unimi.it. Department of Medical Biotechnology and Translational Medicine, University of Milan, Via Fratelli Cervi 93, Segrate, 20090, Milan, Italy. Department of Medical Biotechnology and Translational Medicine, University of Milan, Via Fratelli Cervi 93, Segrate, 20090, Milan, Italy. Department of Medical Biotechnology and Translational Medicine, University of Milan, Via Fratelli Cervi 93, Segrate, 20090, Milan, Italy. Department of Medical Biotechnology and Translational Medicine, University of Milan, Via Fratelli Cervi 93, Segrate, 20090, Milan, Italy. Institute for Environmental and Gender Specific Medicine, Graduate School of Medicine, Juntendo University, Urayasu, Chiba, Japan. Institute for Environmental and Gender Specific Medicine, Graduate School of Medicine, Juntendo University, Urayasu, Chiba, Japan. Acorda Therapeutics, Inc., Ardsley, NY, USA. Department of Medical Biotechnology and Translational Medicine, University of Milan, Via Fratelli Cervi 93, Segrate, 20090, Milan, Italy.
 Department of Neurology, University Hospital of Liège, 4000 Liège, Belgium. Department of General Internal Medicine and Infectious Diseases, University Hospital of Liège, 4000 Liège, Belgium. Department of Hematology, University Hospital of Liège, 4000 Liège, Belgium. Department of Neurology, University Hospital of Liège, 4000 Liège, Belgium. Department of General Internal Medicine and Infectious Diseases, University Hospital of Liège, 4000 Liège, Belgium.
 Mallinckrodt Pharmaceuticals, Bridgewater, NJ, USA. Mallinckrodt Pharmaceuticals, Bridgewater, NJ, USA. Mallinckrodt Pharmaceuticals, Bridgewater, NJ, USA.
 Infectious Diseases and Tropical Medicine Research Center, Health Research Institute Babol University of Medical Sciences Babol Iran. Department of Internal Medicine, Rouhani Hospital Babol University of Medical Sciences Babol Iran. Department of Radiology, Rohani Hospital Babol University of Medical Sciences Babol Iran. Student Research Committee Babol University of Medical Sciences Babol Iran. Student Research Committee Babol University of Medical Sciences Babol Iran.
 Temedica GmbH, Munich, Germany. Temedica GmbH, Munich, Germany. Temedica GmbH, Munich, Germany. Temedica GmbH, Munich, Germany. Temedica GmbH, Munich, Germany. Temedica GmbH, Munich, Germany. , Grenzach-Wyhlen, GermanyRoche Pharma AG. RINGGOLD: 123188 Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
 NeuroPoint GmbH, 89073, Ulm, Germany. rau@neurologie-ulm.de. Hospital Universitario Virgen de La Macareona of Sevilla, Seville, Spain. MS Center, Neurology Unit, Fatebenefratelli San Pietro Hospital, Rome, Italy. 2CA Centro Clínico Académico, Braga, Portugal. Novartis Pharma GmbH, Nuremberg, Germany and working on behalf of Novartis Pharma Vertriebs GmbH, Nuremberg, Germany.
 Department of Clinical Neurosciences-Department 6 (Neurology)-"Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania. Neurology Department, Elias University Emergency Hospital, 011461 Bucharest, Romania. Department of Clinical Neurosciences-Department 6 (Neurology)-"Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania. Neurology Department, Colentina Clinical Hospital, 020125 Bucharest, Romania. Department of Clinical Neurosciences-Department 6 (Neurology)-"Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania. Neurology Department, University Emergency Hospital of Bucharest, 050098 Bucharest, Romania. Department of Clinical Neurosciences-Department 6 (Neurology)-"Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania. Neurology Department, University Emergency Hospital of Bucharest, 050098 Bucharest, Romania. Department of Clinical Neurosciences-Department 6 (Neurology)-"Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania. Ophtalmology Department, University Emergency Hospital of Bucharest, 050098 Bucharest, Romania. Department of Clinical Neurosciences-Department 6 (Neurology)-"Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania. Neurology Department, Elias University Emergency Hospital, 011461 Bucharest, Romania.
 Occupational Therapy Department, School of Health Professions, New York Institute of Technology, Old Westbury, NY, USA (MS). New York University Langone Multiple Sclerosis Comprehensive Care Center, New York, NY, USA (LK). Occupational Therapy Department, University at Buffalo, Buffalo, NY, USA (SR). Department of Physical Therapy, School of Health Technology and Management, Stony Brook University, Stony Brook, NY, USA (LMM).
 University Hospital of Parma, Italy. gianfranco.cervellin@gmail.com. Valparma Hospital, Langhirano, Italy. vincenzo.brianti@valparmahospital.it. University Hospital of Parma, Italy. lviani@ao.pr.it. Valparma Hospital, Langhirano, Italy. labanalisi@valparmahospital.it. . gianni.rastelli@valparmahospital.it.
 Neurosciences, Monash University Faculty of Medicine Nursing and Health Sciences, Melbourne, Victoria, Australia francesca.mary.bridge@gmail.com. Neurology, Alfred Health, Melbourne, Victoria, Australia. Rheumatology, Box Hill Hospital, Box Hill, Victoria, Australia. Neurology, Box Hill Hospital, Box Hill, Victoria, Australia. Neurosciences, Eastern Health, Monash University, Clayton, Victoria, Australia.
 Zucker School of Medicine at Hofstra/Northwell, 173 Lawrence St., New Hyde Park, NY 11040, United States. Northwell Multiple Sclerosis Center, 611 Northern Blvd, Great Neck, NY 11021, United States. Neurological Associates of Long Island, 1991 Marcus Ave, New Hyde Park, NY 11042, United States. Northwell Multiple Sclerosis Center, 350 Community Drive, Manhasset NY 11030, United States. Northwell Multiple Sclerosis Center, 130 East 77th Street, 8 Black Hall, NY 10075, United States. Electronic address: aharel@northwell.edu.
 Smith, Gambrell & Russell LLP, 1105 W. Peachtree Street NE, Suite 1000, Atlanta, Georgia 30309, United States. Neuroscience Institute, Georgia State University, Atlanta, Georgia 30303, United States.
 Division of Hematology and Oncology, Department of Internal Medicine, American University of Beirut Medical Center, Cairo Street, Riad El Solh, Beirut, 1107 2020, Lebanon. Division of Hematology and Oncology, Department of Internal Medicine, American University of Beirut Medical Center, Cairo Street, Riad El Solh, Beirut, 1107 2020, Lebanon. Division of Hematology and Oncology, Department of Internal Medicine, American University of Beirut Medical Center, Cairo Street, Riad El Solh, Beirut, 1107 2020, Lebanon. Pharmacy Department, Tawam Hospital, United Arab Emirates University, Al Ain, United Arab Emirates. Division of Hematology and Oncology, Department of Internal Medicine, American University of Beirut Medical Center, Cairo Street, Riad El Solh, Beirut, 1107 2020, Lebanon. ataher@aub.edu.lb.
 Department of Neurology, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. Biomedical Research Institute, Seoul National University Bundang Hospital, Seongnam, Republic of Korea. Department of Neurology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
 Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. PRASE and Biology Department, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon. Neuroscience Laboratory, CHU de Québec Research Center, Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boul., Québec City, QC, G1V 4G2, Canada. serge.rivest@crchudequebec.ulaval.ca.
 From Department of Psychiatry, Tufts Medical Center, Boston, MA (Dr. Yue); Harvard Medical School (Dr. Shah); Section of Endocrinology, Diabetes, Nutrition & Weight Management, Boston Medical Center, Boston, MA (Dr. Modzelewski); Department of Endocrinology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA (Dr. Modzelewski); Department of Psychiatry, Veteran Affairs Boston Healthcare System, Boston, MA (Drs. Knobel and Kao); BrightView Health, Boston, MA (Dr. Copeli); Power of Recovery, Revere, MA (Dr. Copeli); Department of Psychiatry, Boston University Chobanian & Avedisian School of Medicine, Boston, MA (Dr. Kao).
 Precision Immunology Program Garvan Institute of Medical Research Sydney NSW Australia. St Vincent's Healthcare Clinical Campus, Faculty of Medicine and Health, School of Clinical Medicine UNSW Sydney Sydney NSW Australia.
 Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. MS Center Amsterdam, Anatomy and Neurosciences, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. MS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. Queen Square Institute of Neurology and Centre for Medical Image Computing, University College London, London, UK. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milano, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milano, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milano, Italy. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milano, Italy. Department of Neurology, Neurostimulation and Neuroimaging, Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, Mainz, Germany. Department of Neurology, Neurostimulation and Neuroimaging, Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, Mainz, Germany. Mental Health and Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham, UK; and NIHR Nottingham Biomedical Research Centre, Nottingham, UK. Institute of Neuroradiology, St. Josef Hospital, Ruhr-University Bochum, Bochum, Germany. Institute of Neuroradiology, St. Josef Hospital, Ruhr-University Bochum, Bochum, Germany. Section of Neuroradiology, Department of Radiology, Vall d'Hebron University Hospital and Research Institute (VHIR), Barcelona, Spain. Section of Neuroradiology, Department of Radiology, Vall d'Hebron University Hospital and Research Institute (VHIR), Barcelona, Spain. Neurology-Neuroimmunology Department, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, London, UK. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, London, UK. Centre for Medical Image Computing (CMIC), Department of Medical Physics and Bioengineering, University College London, London, UK. E-health Centre, Universitat Oberta de Catalunya, Barcelona, Spain. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, London, UK. Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, London, UK. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology and Multiple Sclerosis Unit and Laboratory of Advanced Imaging in Neuroimmunological Diseases (ImaginEM), Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain SLLUFRIU@clinic.cat.
 Centre de Ressources et de Compétences Sclerose En Plaques, Neurologie Pasteur 2, CHU de Nice, Université Cote d'Azur, UMR2CA-URRIS, Nice, France. Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkiye. University of Genoa, Genoa, Italy. Ospedale Policlinico San Martino Instituti di Ricovero e Cura a Carattere Scientifico, Genoa, Italy. Centre de Ressources et de Compétences Sclerose En Plaques, Neurologie Pasteur 2, CHU de Nice, Université Cote d'Azur, UMR2CA-URRIS, Nice, France. Centre de Ressources et de Compétences Sclerose En Plaques, Neurologie Pasteur 2, CHU de Nice, Université Cote d'Azur, UMR2CA-URRIS, Nice, France. University of Genoa, Genoa, Italy. Université de Lille, Inserm, Unit 1172, LilNCog, Centre Hospitalier Universitaire de Lille, Fédération Hospitalo-Universitaire Precise, Lille, France. Assistance Publique des Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris, France. Multiple Sclerosis Clinic, Nîmes University Hospital, Nîmes, France. Multiple Sclerosis Clinic, Montpellier University Hospital, Montpellier, France. Multiple Sclerosis Clinic, Hospices Civils de Lyon, Lyon, France. Neurology, Kocaeli University Faculty of Medicine, Kocaeli, Turkiye. Multiple Sclerosis Clinic, Rennes University Hospital, Inserm, CIC1414, Rennes, France. School of Medicine, Neurology, Ondokuz Mayis University, Samsun, Turkiye. Multiple Sclerosis Clinic, Caen University Hospital, Caen, France. Multiple Sclerosis Clinic, Rouen University Hospital, Rouen, France. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Hacettepe University Medical Faculty, School of Medicine, Ankara, Turkiye. Strasbourg University Hospital, Clinical Investigation Center, INBSRM 1434, Strasbourg, France. Toulouse University Hospital, Centre de Ressources et de Compétences Sclérose en Plaques, Department of Neurology, Université Toulouse III, Infinity, Inserm UMR1291, CNRS UMR5051, Toulouse, France. Multiple Sclerosis Clinic, Clermont-Ferrand University Hospital, Clermont-Ferrand, France. Centre de Ressources et de Compétences Sclérose en Plaques and Clinical Investigation Center, Inserm, Nantes University Hospital, France. Transplantation and Immunology Transplantation Center, Inserm, Nantes, France. School of Medicine, Uludag University, Bursa, Turkiye. Ege University Medical Faculty, Bornova, Izmir, Turkiye. Centre de Ressources et de Compétences Sclerose En Plaques, Neurologie Pasteur 2, CHU de Nice, Université Cote d'Azur, UMR2CA-URRIS, Nice, France. University of South California, Los Angeles. Mayo Clinic, Rochester, Minnesota. The University of Texas Southwestern Medical Center, Dallas. Ege University Medical Faculty, Bornova, Izmir, Turkiye.
 Clinical Neurosciences Group, Shaqra University, Shaqra 11961, Saudi Arabia. Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham NG7 2UH, UK. Department of Clinical Medical Laboratories, College of Applied Medical Sciences, Shaqra University, Sahqra 11961, Saudi Arabia. Department of Clinical Neuroscience, Karolinska Institute, 171 77 Solna, Sweden. Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham NG7 2UH, UK. Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham NG7 2UH, UK. College of Applied Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh 14611, Saudi Arabia. Clinical Neurosciences Group, Shaqra University, Shaqra 11961, Saudi Arabia. Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Shaqra University, Shaqra 11961, Saudi Arabia. Clinical Neurosciences Group, Shaqra University, Shaqra 11961, Saudi Arabia. Department of Pharmacy Practice, College of Pharmacy, Shaqra University, Shaqra 11961, Saudi Arabia. Centre of Medical and Bio-Allied Health Sciences Research, Ajman University, Ajman 346, United Arab Emirates. Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham NG7 2UH, UK. Department of Neurology, Nottingham University Hospitals NHS Trust, Nottingham NG7 2UH, UK. Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham NG7 2UH, UK. Department of Neurology, Nottingham University Hospitals NHS Trust, Nottingham NG7 2UH, UK. Cooper University Hospital, Cooper Neurological Institute, Camden, NJ 08103, USA.
 Department of Radiology, Groupe Hospitalier Paris-Saint Joseph, Paris, France. jhodel@ghpsj.fr. Department of Radiology and Nuclear Medicine, Erasmus MC University Medical Center, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus MC University Medical Center, Rotterdam, The Netherlands. Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway. Neuroradiology Unit, IRCCS Istituto Giannina Gaslini, Genoa, Italy. Department of Neuroradiology, Lille University Hospital, Lille, France. Department of Neurology, AP-HP, Henri Mondor University Hospital, Université Paris Est Créteil, 4391, Creteil, EA, France. Department of Neurology, AP-HP, Henri Mondor University Hospital, Université Paris Est Créteil, 4391, Creteil, EA, France. Department of Radiology, Groupe Hospitalier Paris-Saint Joseph, Paris, France. Department of Radiology, Groupe Hospitalier Paris-Saint Joseph, Paris, France. Department of Radiology, Antwerp University Hospital, Antwerp, Belgium. Neuroradiology, Department of Radiology, University Hospital, 12 de Octubre, Madrid, Spain. Neuroradiology Unit and CERMAC, IRCCS Ospedale San Raffaele and Vita-Salute San Raffaele University, 20132, Milan, Italy. Department of Neuroradiology, University Hospital of Grenoble, Grenoble, France. Lysholm Department of Neuroradiology, UCLH National Hospital for Neurology and Neurosurgery, London, UK. Neuroradiological Academic Unit, University College London Queen Square Institute of Neurology, University College London, London, UK. Section of Neuroradiology, Department of Radiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
 University of Arizona, Tucson. Better Health Worldwide, Inc, Newfoundland, New Jersey. Workpartners LLC, Cheyenne, Wyoming. Workpartners LLC, Cheyenne, Wyoming. Care Partner Advisor. EMD Serono, Rockland, Massachusetts. EMD Serono, Rockland, Massachusetts.
 College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. Division of Neurology, King Abdulaziz Medical City, Ministry of the National Guard Health Affairs, Riyadh, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. Department of Medicine, King Abdulaziz Medical City, Ministry of the National Guard Health Affairs, Jeddah, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. Division of Neurology, King Abdulaziz Medical City, Ministry of the National Guard Health Affairs, Riyadh, Saudi Arabia. King Abdullah International Medical Research Center, Riyadh, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. Division of Neurology, King Abdulaziz Medical City, Ministry of the National Guard Health Affairs, Riyadh, Saudi Arabia. King Abdullah International Medical Research Center, Riyadh, Saudi Arabia. College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. Department of Medicine, King Abdulaziz Medical City, Ministry of the National Guard Health Affairs, Jeddah, Saudi Arabia.
 Queen Square MS Centre, UCL Institute of Neurology and NIHR UCL Hospitals Biomedical Research Centre, London, UK. Electronic address: wallace.brownlee1@nhs.net. Merck Serono Ltd., Feltham, UK. Merck Serono Ltd., Feltham, UK. Merck Serono Ltd., Feltham, UK.
 Mobility Impairment Research Center, Babol University of Medical Sciences, Babol, I.R. Iran. Department of Speech Therapy, School of Rehabilitation, Babol University of Medical Sciences, Babol, I.R.Iran. School of Paramedical Sciences and Rehabilitation, Speech Therapy Department, Mashhad University of Medical Sciences, Mashhad, Iran. Faculty of Rehabilitation, Speech Therapy Department, Ahvaz University of Medical Sciences, Ahvaz, Iran. School of Paramedical Sciences and Rehabilitation, Speech Therapy Department, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Psychology, Ferdowsi University of Mashhad, Mashhad, Iran. Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran. School of Paramedical Sciences and Rehabilitation, Speech Therapy Department, Mashhad University of Medical Sciences, Mashhad, Iran.
 Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia. Institute of Epidemiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Department of Neurology, University Hospital Center of Zagreb, Zagreb, Croatia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia; Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Department of Neurology, University Hospital Center of Zagreb, Zagreb, Croatia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia; Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia; Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia. Clinic of Neurology, University Clinical Center of Montenegro, Podgorica, Montenegro. Institute of Epidemiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Institute of Epidemiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Department of Neurology, University Hospital Center of Zagreb, Zagreb, Croatia. Department of Neurology, University Hospital Center of Zagreb, Zagreb, Croatia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia; Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Clinic of Neurology, University Clinical Center of Montenegro, Podgorica, Montenegro. Department of Neurology, University Hospital Center of Zagreb, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia. Clinic of Neurology, University Clinical Center of Serbia, Belgrade, Serbia; Faculty of Medicine, University of Belgrade, Belgrade, Serbia. Electronic address: drulovicjelena@gmail.com.
 Department of Physiotherapy, Middle East University, Amman, Jordan. Applied Science Research Center, Applied Science Private University, Amman, Jordan. Department of Physiotherapy, Middle East University, Amman, Jordan. Department of Physiotherapy, Middle East University, Amman, Jordan.
 From the Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT, USA (CG, BS, LB, MB, MV, SLK). From the Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT, USA (CG, BS, LB, MB, MV, SLK). From the Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT, USA (CG, BS, LB, MB, MV, SLK). From the Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT, USA (CG, BS, LB, MB, MV, SLK). From the Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT, USA (CG, BS, LB, MB, MV, SLK). From the Department of Rehabilitation and Movement Science, University of Vermont, Burlington, VT, USA (CG, BS, LB, MB, MV, SLK).
 Department of Surgery, MedStar Georgetown University Hospital, Washington, USA. Department of Radiation Oncology and Radiology, University of Virginia School of Medicine, Charlottesville, USA. Department of Internal Medicine, Ebonyi State University, Abakaliki, NGA. Department of Neurology, Dow University of Health Sciences, Karachi, PAK. Department of Family Medicine, School of Medicine, Caribbean Medical University, Willemstad, CUW. Department of Cardiology, University of Illinois at Chicago, Chicago, USA.
 Republican Vilnius University Hospital; Vilnius University Hospital Santaros Klinikos. Electronic address: mantas.vaisvilas@santa.lt. Vilnius University, Clinic of Neurology and Neurosurgery. Vilnius University, Clinic of Neurology and Neurosurgery. Vilnius University, Clinic of Neurology and Neurosurgery. Vilnius University, Clinic of Neurology and Neurosurgery. Vilnius University, Clinic of Neurology and Neurosurgery.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Anesthesiology and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Cancer Prevention Research Center, Omid Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: shaygannejad@med.mui.ac.ir. Department of Biostatistics and Epidemiology, Faculty of Health, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: maryamnasirian17@gmail.com.
 Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Department of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Quantitative MRI Core Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Neuroimaging Program, Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Center for Neuroinflammation and Neurotherapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Center for Neuroinflammation and Neurotherapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Center for Neuroinflammation and Neurotherapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Center for Neuroinflammation and Neurotherapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
 Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland, USA. Hasbro Children's Hospital, Brown University, Providence, Rhode Island, USA. Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Baltimore Veterans Affairs Medical Center, Baltimore, Maryland, USA.
 Department of Clinical Psychology, School of Medicine, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Department of Neurology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Department of Biostatistics, School of Public Health, Modeling of Non-Communicable Diseases Research Center, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Behavioral Disorders and Substance Abuse Research Center, Hamadan University of Medical Sciences, Hamadan 6517838636, Iran. Center for Affective, Stress and Sleep Disorders (ZASS), Psychiatric University Hospital Basel, 4002 Basel, Switzerland. Division of Sport and Psychosocial Health, Department of Sport, Exercise and Health, University of Basel, 4052 Basel, Switzerland. Sleep Disorders Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6714869914, Iran. Substance Abuse Prevention Research Center, Kermanshah University of Medical Sciences, Kermanshah 6714869914, Iran. School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran 1419733141, Iran. Center for Disaster Psychiatry and Disaster Psychology, Psychiatric Clinics of the University of Basel, 4002 Basel, Switzerland.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. IRCCS, Fondazione Don Carlo Gnocchi, Milan, Italy. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA.
 Device and Connected Solution Engineering, Global Healthcare Operations, Ares Trading SA (an affiliate of Merck KGaA), Eysins, Switzerland. Human Factors Research & Design, Emergo by UL, Utrecht, the Netherlands. Human Factors Research & Design, Emergo by UL, Cambridge, UK. Human Factors Research & Design, Emergo by UL, Utrecht, the Netherlands. Medical Unit Neurology & Immunology, Global Research & Development, Merck Serono Ltd (an affiliate of Merck KGaA), Feltham, UK. Device and Connected Solution Engineering, Global Healthcare Operations, Ares Trading SA (an affiliate of Merck KGaA), Eysins, Switzerland. Device and Connected Solution Engineering, Global Healthcare Operations, EMD Serono, Inc (an affiliate of Merck KGaA), Rockland, MA, USA.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Liverpool University Hospitals Foundation Trust, Prescot Street, Liverpool, L7 8XP, UK. Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK. University of Liverpool, Liverpool, UK. Walton Centre NHS Foundation Trust, Lower Lane, Liverpool, UK. University of Liverpool, Liverpool, UK. profcyoung@gmail.com. Walton Centre NHS Foundation Trust, Lower Lane, Liverpool, UK. profcyoung@gmail.com.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. djakimovski@bnac.net. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. Center for Biomedical Imaging at the Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High St., Buffalo, NY, 14203, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
 Department of Neurology, Fortis Hospital, Kolkata, India. Department of Neurology, Vivekananda Institute of Medical Sciences, Kolkata, India. saschakra@yahoo.com.
 Department of Neurology, Kobe City Medical Center General Hospital, Kobe, Hyogo, Japan. Department of Neurology, Kobe City Medical Center General Hospital, Kobe, Hyogo, Japan. Department of Neurology, Kobe City Medical Center General Hospital, Kobe, Hyogo, Japan.
 Division of Cognitive and Behavioral Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9016H, Boston, MA, 02115, USA. ikletenik@bwh.harvard.edu. Department of Neurology, Brigham and Women's Hospital, Boston, USA. ikletenik@bwh.harvard.edu. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. ikletenik@bwh.harvard.edu. Harvard Medical School, Boston, MA, USA. ikletenik@bwh.harvard.edu. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Department of Neurology, Boston Children's Hospital, Boston, MA, USA. Computational Radiology Laboratory, Department of Radiology, Boston Children's Hospital, Boston, MA, USA. Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School Boston, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School Boston, Boston, MA, USA. Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Department of Psychiatry, Brigham and Women's Hospital, Boston, MA, USA. Division of Cognitive and Behavioral Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9016H, Boston, MA, 02115, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Center for Alzheimer Research and Treatment, Brigham and Women's Hospital, Boston, MA, USA. Department of Neurology, Massachusetts General Hospital, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School Boston, Boston, MA, USA. Harvard Medical School, Boston, MA, USA. Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA. Center for Neurological Imaging, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School Boston, Boston, MA, USA. Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA. Division of Cognitive and Behavioral Neurology, Brigham and Women's Hospital, 60 Fenwood Road, 9016H, Boston, MA, 02115, USA. Department of Neurology, Brigham and Women's Hospital, Boston, USA. Center for Brain Circuit Therapeutics, Brigham and Women's Hospital, Boston, USA. Harvard Medical School, Boston, MA, USA. Department of Radiology, Brigham and Women's Hospital, Boston, MA, USA. Department of Psychiatry, Brigham and Women's Hospital, Boston, MA, USA. Department of Neurology, Massachusetts General Hospital, Boston, MA, USA. Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA.
 Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. ragerdi@sina.tums.ac.ir. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Sciences, 16 Azar Street, Poursina Street, Tehran, Iran. Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Faculty of Medicine, Institute of Neuroanatomy, RWTH Aachen University, Aachen, Germany. Faculty of Medicine, Institute of Neuroanatomy, RWTH Aachen University, Aachen, Germany. Faculty of Medicine, Institute of Neuroanatomy, RWTH Aachen University, Aachen, Germany. Cellular and Molecular Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
 Department of Neurology, Mayo Clinic, Rochester, MN; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN. Department of Neurology, Mayo Clinic, Rochester, MN; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN. Department of Neurology, Mayo Clinic, Rochester, MN; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN. Electronic address: dubey.divyanshu@mayo.edu.
 Department of PXL Healthcare, Centre of Expertise in Innovation in Care, PXL University College of Applied Sciences and Arts, Hasselt, Belgium. Department of PXL Healthcare, Centre of Expertise in Innovation in Care, PXL University College of Applied Sciences and Arts, Hasselt, Belgium. Centre of Expertise Smart ICT, PXL University College of Applied Sciences and Arts, Hasselt, Belgium. Department of PXL Healthcare, Centre of Expertise in Innovation in Care, PXL University College of Applied Sciences and Arts, Hasselt, Belgium. Department of PXL Healthcare, Centre of Expertise in Innovation in Care, PXL University College of Applied Sciences and Arts, Hasselt, Belgium. REVAL, Hasselt University, Hasselt, Belgium.
 Departments of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA. Neurology, New York University Grossman School of Medicine, New York, NY, USA. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Neurology Department, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. Departments of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA; Neurology, New York University Grossman School of Medicine, New York, NY, USA. Departments of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA; Neurology, New York University Grossman School of Medicine, New York, NY, USA; Population Health, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: laura.balcer@nyulangone.org. Neurology, New York University Grossman School of Medicine, New York, NY, USA; Population Health, New York University Grossman School of Medicine, New York, NY, USA; Departments of Radiology and Radiological Sciences, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.

 Department of Medicine (GEM, ESL, MA, LBG), School of Clinical Sciences at Monash Health, Faculty of Medicine, Nursing and Health Sciences, Monash University; Department of Neurology (MA), Monash Medical Centre, Monash Health, Clayton; and Department of Neurology (MA), Frankston Hospital, Peninsula Health, Frankston, Australia. Department of Medicine (GEM, ESL, MA, LBG), School of Clinical Sciences at Monash Health, Faculty of Medicine, Nursing and Health Sciences, Monash University; Department of Neurology (MA), Monash Medical Centre, Monash Health, Clayton; and Department of Neurology (MA), Frankston Hospital, Peninsula Health, Frankston, Australia. Department of Medicine (GEM, ESL, MA, LBG), School of Clinical Sciences at Monash Health, Faculty of Medicine, Nursing and Health Sciences, Monash University; Department of Neurology (MA), Monash Medical Centre, Monash Health, Clayton; and Department of Neurology (MA), Frankston Hospital, Peninsula Health, Frankston, Australia. Department of Medicine (GEM, ESL, MA, LBG), School of Clinical Sciences at Monash Health, Faculty of Medicine, Nursing and Health Sciences, Monash University; Department of Neurology (MA), Monash Medical Centre, Monash Health, Clayton; and Department of Neurology (MA), Frankston Hospital, Peninsula Health, Frankston, Australia.
 Clinique Neuro-Outaouais, Gatineau, Quebec, Canada.
 Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: roohbakhsha@mums.ac.ir.
 Institute for Neuroradiology, Goethe University Frankfurt, Frankfurt am Main, Germany. Institute for Neuroradiology, Goethe University Frankfurt, Frankfurt am Main, Germany. Institute for Neuroradiology, Goethe University Frankfurt, Frankfurt am Main, Germany.
 Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel; The Neufeld Cardiac Research Institute and Department of Physiology and Pharmacology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel.
 Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA. Research Service, Central Virginia Veterans Affairs Health Care Systems, Richmond, Virginia, USA. Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA. Department of Biochemistry, Kochi University Medical School, Kochi, Japan. Department of Medicine, University of Texas Health San Antonio, San Antonio, Texas, USA. Barshop Institute for Longevity and Aging Studies, University of Texas Health San Antonio, San Antonio, Texas, USA. Department of Medicine, University of Texas Health San Antonio, San Antonio, Texas, USA. Barshop Institute for Longevity and Aging Studies, University of Texas Health San Antonio, San Antonio, Texas, USA. Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA. Research Service, Central Virginia Veterans Affairs Health Care Systems, Richmond, Virginia, USA.
 Department of Neurology, Lanzhou University Second Hospital, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730030, China. Department of Internal Neurology, Gansu Provincial Hospital, No. 204, Donggang West Road, Lanzhou 730000, China. Department of Neurology, Lanzhou University Second Hospital, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730030, China. Department of Neurology, Lanzhou University Second Hospital, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730030, China. Department of Neurology, Lanzhou University Second Hospital, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730030, China. Department of Neurology, Lanzhou University Second Hospital, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730030, China. Department of Neurology, Lanzhou University Second Hospital, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730030, China. Electronic address: wmx32@aliyun.com.
 Department of Neurology, Center of Clinical Neuroscience, Carl Gustav Carus University Clinic, University Hospital of Dresden, Technische Universität Dresden, 01062 Dresden, Germany. Zentrum für Neurologische Studien, 57076 Siegen, Germany. Novartis Pharma GmbH, 90429 Nuremberg, Germany. Novartis Pharma GmbH, 90429 Nuremberg, Germany. Institute for Immunology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany.
 Department of Psychology, Faculty of Humanities, Khayyam University, Mashhad, Iran. Department of Psychiatric Nursing and Management, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Psychology, Faculty of Humanities, Khayyam University, Mashhad, Iran. Refractive Errors Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Psychiatry and Psychology Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Management, School of Medical Education and Management, Shahid Beheshti Medical University of Medical Sciences, Tehran, Iran. Department of Basic Sciences, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 Department of Tissue Engineering, School of Advanced Medical Sciences and Technologies, University of Medical Sciences, Shiraz, Iran. Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Tissue Engineering, School of Advanced Medical Sciences and Technologies, University of Medical Sciences, Shiraz, Iran. Department of Tissue Engineering, School of Advanced Medical Sciences and Technologies, University of Medical Sciences, Shiraz, Iran. Histomorphometry and Stereology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Tissue Engineering, School of Advanced Medical Sciences and Technologies, University of Medical Sciences, Shiraz, Iran. Histomorphometry and Stereology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iranaz Iran. Department of Pharmacology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
 Division of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA. Department of Psychiatry, Taipei Veterans General Hospital, Taipei, Taiwan. Division of Psychiatry, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan. Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan. Department of Psychiatry, University of California San Francisco, San Francisco, CA, USA. Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan. Endoscopy Center for Diagnosis and Treatment, and 7Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan. Endoscopy Center for Diagnosis and Treatment, and 7Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. Division of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
 Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Advanced Drug Delivery and Biomaterials, Avenue E. Mounier 73, 1200 Brussels, Belgium; Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Bioanalysis and Pharmacology of Bioactive Lipids, Avenue E. Mounier 73, 1200 Brussels, Belgium. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Bioanalysis and Pharmacology of Bioactive Lipids, Avenue E. Mounier 73, 1200 Brussels, Belgium. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Bioanalysis and Pharmacology of Bioactive Lipids, Avenue E. Mounier 73, 1200 Brussels, Belgium. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Advanced Drug Delivery and Biomaterials, Avenue E. Mounier 73, 1200 Brussels, Belgium. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Advanced Drug Delivery and Biomaterials, Avenue E. Mounier 73, 1200 Brussels, Belgium. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Bioanalysis and Pharmacology of Bioactive Lipids, Avenue E. Mounier 73, 1200 Brussels, Belgium. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Bioanalysis and Pharmacology of Bioactive Lipids, Avenue E. Mounier 73, 1200 Brussels, Belgium. Electronic address: giulio.muccioli@uclouvain.be. Université catholique de Louvain, UCLouvain, Louvain Drug Research Institute, Advanced Drug Delivery and Biomaterials, Avenue E. Mounier 73, 1200 Brussels, Belgium. Electronic address: anne.desrieux@uclouvain.be.
 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Piazza Miraglia, 2, 80138, Naples, Italy. Department of Neuroscience, Reproductive Sciences and Dentistry, School of Medicine, Federico II University of Naples, Naples, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Department of Diagnostics and Public Health, University of Verona, Verona, Italy. Department of Public Health, School of Medicine, Federico II University of Naples, Naples, Italy. Department of Diagnostics and Public Health, University of Verona, Verona, Italy. Multiple Sclerosis Clinical and Research Unit, Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy. Department of Public Health, School of Medicine, Federico II University of Naples, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Piazza Miraglia, 2, 80138, Naples, Italy. simona.bonavita@unicampania.it.
 High-Field MR Center - 7T MR, Department of Biomedical Imaging and Image-guided Therapy, Medical University Vienna, Lazarettgasse 14, 1090, Vienna, Austria. siegfried.trattnig@meduniwien.ac.at. High-Field MR Center - 7T MR, Department of Biomedical Imaging and Image-guided Therapy, Medical University Vienna, Lazarettgasse 14, 1090, Vienna, Austria. High-Field MR Center - 7T MR, Department of Biomedical Imaging and Image-guided Therapy, Medical University Vienna, Lazarettgasse 14, 1090, Vienna, Austria. High-Field MR Center - 7T MR, Department of Biomedical Imaging and Image-guided Therapy, Medical University Vienna, Lazarettgasse 14, 1090, Vienna, Austria. High-Field MR Center - 7T MR, Department of Biomedical Imaging and Image-guided Therapy, Medical University Vienna, Lazarettgasse 14, 1090, Vienna, Austria. Department of Imaging Methods, Institute of Measurement Science, Slovak Academy of Sciences, Dubravska cesta 9, 84104, Bratislava, Slovakia. Department of Neurology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Medical University of Vienna, Comprehensive Center for Clinical Neurosciences & Mental Health, Vienna, Austria.
 Okayama University, Japan. Ochiai Hospital, Maniwa, Japan. Kawasaki Medical School, Kurashiki, Japan. Kaneda Hospital, Maniwa, Japan. Kaneda Hospital, Maniwa, Japan. Kaneda Hospital, Maniwa, Japan.
 Department of Neurology, Dell Medical School, The University of Texas at Austin, Austin, TX, USA (LF, AL). Department of Neurology, Dell Medical School, The University of Texas at Austin, Austin, TX, USA (LF, AL). EMD Serono, Rockland, MA, USA (JZ, BH, TL). EMD Serono, Rockland, MA, USA (JZ, BH, TL). Ashfield MedComms, an Ashfield Health company, Macclesfield, United Kingdom (MG). EMD Serono, Rockland, MA, USA (JZ, BH, TL).
 Department of Radiology, The First Hospital of Jilin University, Changchun, China.
 MSc in Corrective Exercises, Department of Corrective Exercises and Sport Injuries, University of Payame-Noor, Tehran, Iran. Associate Professor in Corrective exercises and Sports injuries, University of Payame-Noor, Tehran, Iran.
 HNSR, IRRCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroradiology, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. Department of Neuroradiology, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino IRCCS, Genoa, Italy.
 Department of Ophthalmology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania. Department of Ophthalmology, Ophthalmology Emergency Hospital, Bucharest, Romania. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. School of Computer Science and Engineering, Nanyang Technological University, Singapore. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Department of Ophthalmology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. SERI-NTU Advanced Ocular Engineering (STANCE), Singapore, Singapore. School of Chemistry, Chemical Engineering and Biotechnology, Nanyang Technological University, Singapore. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. SERI-NTU Advanced Ocular Engineering (STANCE), Singapore, Singapore. School of Chemistry, Chemical Engineering and Biotechnology, Nanyang Technological University, Singapore. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. SERI-NTU Advanced Ocular Engineering (STANCE), Singapore, Singapore. Department of Clinical Pharmacology, Medical University Vienna, Vienna, Austria. Department of Ophthalmology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania. Department of Neurology, Emergency University Hospital, Bucharest, Romania. Department of Ophthalmology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania. Department of Ophthalmology, Emergency University Hospital, Bucharest, Romania. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. SERI-NTU Advanced Ocular Engineering (STANCE), Singapore, Singapore. School of Chemistry, Chemical Engineering and Biotechnology, Nanyang Technological University, Singapore. Department of Clinical Pharmacology, Medical University Vienna, Vienna, Austria. Ophthalmology and Visual Sciences Academic Clinical Program, Duke-NUS Medical School, National University of Singapore, Singapore. Center for Medical Physics and Biomedical Engineering, Medical University Vienna, Vienna, Austria. Institute of Molecular and Clinical Ophthalmology, Basel, Switzerland. Department of Ophthalmology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania. Department of Ophthalmology, Emergency University Hospital, Bucharest, Romania. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Ophthalmology and Visual Sciences Academic Clinical Program, Duke-NUS Medical School, National University of Singapore, Singapore.
 Student Research Committee, Tabriz University of Medical Sciences, Golgasht Street, Tabriz, 5166/15731, East Azerbaijan, Iran. Research Center for Evidence-Based Medicine, Iranian EBM Centre: A Joanna Briggs Institute (JBI) Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran. Zanjan Branch (IAUZ), Islamic Azad University, Zanjan, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, 5166/15731, Iran. Student Research Committee, Tabriz University of Medical Sciences, Golgasht Street, Tabriz, 5166/15731, East Azerbaijan, Iran. Medical Faculty, Yeditepe University, Istanbul, Türkiye. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, 5166/15731, Iran. Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, 5166/15731, Iran. Talebi511@yahoo.com. Student Research Committee, Tabriz University of Medical Sciences, Golgasht Street, Tabriz, 5166/15731, East Azerbaijan, Iran. naseria@tbzmed.ac.ir. Research Center for Evidence-Based Medicine, Iranian EBM Centre: A Joanna Briggs Institute (JBI) Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran. naseria@tbzmed.ac.ir.
 Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. k.evonuk@hookelabs.com. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Gossamer Bio, 3013 Science Park Road, Suite 200, San Diego, CA, 92121, USA. Gossamer Bio, 3013 Science Park Road, Suite 200, San Diego, CA, 92121, USA. Gossamer Bio, 3013 Science Park Road, Suite 200, San Diego, CA, 92121, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. Gossamer Bio, 3013 Science Park Road, Suite 200, San Diego, CA, 92121, USA. Hooke Laboratories, LLC, 439 South Union Street, Lawrence, MA, 01843, USA. s.marusic@hookelabs.com.
 Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China; Department of Hematology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; Key Laboratory of Bone Marrow Stem Cell, Jiangsu Province, Xuzhou, China. Electronic address: jianlin.qiao@gmail.com.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, 48149, Germany. Department of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, 48149, Germany. Electronic address: jan.luenemann@ukmuenster.de.
 Institute of Pharmacology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Pharmacology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Pharmacology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Histology and Embryology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Microbiology, Czech Academy of Sciences, Novy Hradek, Czech Republic. Institute of Pharmacology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Pharmacology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. Institute of Pharmacology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic.
 MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. Department of Neurology, Neuroimmunological Section, University Medical Center of Rostock, 18147 Rostock, Germany. MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. Deutsche Multiple Sklerose Gesellschaft, Bundesverband e.V. (German MS Society Federal Association [DMSG]), 30171 Hannover, Germany. Department of Tropical Medicine, Infectious Diseases and Nephrology, University Medical Center of Rostock, 18057 Rostock, Germany. MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. Gesellschaft für Versorgungsforschung mbH (Society for Health Care Research [GfV]), 30171 Hannover, Germany. Deutsche Multiple Sklerose Gesellschaft, Bundesverband e.V. (German MS Society Federal Association [DMSG]), 30171 Hannover, Germany. MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. Deutsche Multiple Sklerose Gesellschaft, Bundesverband e.V. (German MS Society Federal Association [DMSG]), 30171 Hannover, Germany. MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. MS Forschungs- und Projektentwicklungs-gGmbH (MS Research and Project Development gGmbH [MSFP]), 30171 Hannover, Germany. Deutsche Multiple Sklerose Gesellschaft, Bundesverband e.V. (German MS Society Federal Association [DMSG]), 30171 Hannover, Germany. Experimental and Clinical Research Center, a Joint Cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité Medical Faculty, Campus Berlin-Buch, 13125 Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin, 10117 Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin, 10117 Berlin, Germany. Department of Neurology, Neuroimmunological Section, University Medical Center of Rostock, 18147 Rostock, Germany.
 Institute of Physiology and Pathophysiology, Department of Cardiovascular Physiology, Ruprecht-Karls-University, Im Neuenheimer Feld 326, 69120, Heidelberg, Germany. reiner.kunze@physiologie.uni-heidelberg.de. Department of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany. Institute of Physiology and Pathophysiology, Department of Cardiovascular Physiology, Ruprecht-Karls-University, Im Neuenheimer Feld 326, 69120, Heidelberg, Germany. Department of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany. Kerckhoff-Heart-Research-Institute, Department of Cardiology, Medical School, Justus-Liebig-University, Giessen, Germany.
 Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal. Electronic address: filipaladeira@msn.com. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal; Neurology Department, Centro Hospitalar Barreiro Montijo, Barreiro, Portugal. Neurology Department, Centro Hospitalar Universitario Lisboa Central, Hospital de Santo António dos Capuchos, Alameda de Santo António dos Capuchos, Santo António, Lisbon, Portugal.
 Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Physical Therapy Department, University of West Attica, 12210 Athens, Greece. Laboratory of Neuromuscular and Cardiovascular Study of Motion (Lanecasm), 12243 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Department of Physiology, Faculty of Medicine, University of Ioannina, 45110 Ioannina, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Physical Therapy Department, University of West Attica, 12210 Athens, Greece. Laboratory of Neuromuscular and Cardiovascular Study of Motion (Lanecasm), 12243 Athens, Greece. Department of Internal Medicine, Faculty of Medicine, University of Ioannina, 45110 Ioannina, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Physical Therapy Department, University of West Attica, 12210 Athens, Greece. Laboratory of Neuromuscular and Cardiovascular Study of Motion (Lanecasm), 12243 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece. Second Department of Neurology, Attikon University Hospital, School of Medicine, National & Kapodistrian University of Athens, 15784 Athens, Greece.
 Medicine and Nanotechnology Applied Physics Group (GFAMN), Department of Physics and Meteorology, School of Sciences, São Paulo University (Unesp), Bauru 17033-360, SP, Brazil. REVAL Rehabilitation Research Center, Faculty of Rehabilitation Sciences, Hasselt University, 3500 Hasselt, Belgium. Medicine and Nanotechnology Applied Physics Group (GFAMN), Department of Physics and Meteorology, School of Sciences, São Paulo University (Unesp), Bauru 17033-360, SP, Brazil. Human Movement Research Laboratory (MOVI-LAB), Department of Physical Education, School of Sciences, São Paulo State University (Unesp), Bauru 17033-360, SP, Brazil.
 Department of Neurology, College of Medicine, Gyeongsang Institute of Health Science, Gyeongsang National University, Jinju, Republic of Korea. Department of Neurology, Gyeongsang National University Changwon Hospital, Changwon, Republic of Korea. Department of Family Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea. Department of Digital Healthcare, Seoul National University Bundang Hospital, Seongnam, Republic of Korea. Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea. Department of Family Medicine, College of Medicine, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, Republic of Korea. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Neuroscience Center, Samsung Medical Center, Seoul, Republic of Korea. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology (SAIHST), Sungkyunkwan University, Seoul, Republic of Korea. Department of Statistics and Actuarial Science, Soongsil University, Seoul, Republic of Korea. Department of Family Medicine and Supportive Care Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Department of Clinical Research Design and Evaluation, Sungkyunkwan University, Seoul, Republic of Korea. Department of Digital Health, Samsung Advanced Institute of Health Science and Technology (SAIHST), Sungkyunkwan University, Seoul, Republic of Korea. Center for Wireless and Population Health Systems, University of California San Diego, La Jolla, CA, United States. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Neuroscience Center, Samsung Medical Center, Seoul, Republic of Korea. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology (SAIHST), Sungkyunkwan University, Seoul, Republic of Korea.
 Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, 37124 Verona, Italy. Department of Biomedical, Metabolic and Neurosciences, University of Modena and Reggio Emilia, 41125 Modena, Italy. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Wexham Park Hospital, Frimley Health Foundation Trust, SL2 4HL Slough, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Wellcome Centre for Integrative Neuroimaging, Oxford Centre for Functional MRI of the Brain, Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Wellcome Centre for Integrative Neuroimaging, Oxford Centre for Functional MRI of the Brain, Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Department of Psychiatry, University of Oxford, OX3 7JX Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Wexham Park Hospital, Frimley Health Foundation Trust, SL2 4HL Slough, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, 37124 Verona, Italy. Department of Biomedical, Metabolic and Neurosciences, University of Modena and Reggio Emilia, 41125 Modena, Italy. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK. Wexham Park Hospital, Frimley Health Foundation Trust, SL2 4HL Slough, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU Oxford, UK.
 REVAL Rehabilitation Research Center, Research Institute, Faculty of Rehabilitation Sciences, Hasselt University, 3590 Diepenbeek, Belgium. University MS Centre Hasselt-Pelt, 3500 Hasselt, Belgium. National MS Center Melsbroek, 1820 Steenokkerzeel, Belgium. National MS Center Melsbroek, 1820 Steenokkerzeel, Belgium. Faculty of Kinesiology and Rehabilitation Sciences FABER, Katholieke Universiteit Leuven, 3001 Leuven, Belgium. National MS Center Melsbroek, 1820 Steenokkerzeel, Belgium. REVAL Rehabilitation Research Center, Research Institute, Faculty of Rehabilitation Sciences, Hasselt University, 3590 Diepenbeek, Belgium. University MS Centre Hasselt-Pelt, 3500 Hasselt, Belgium. Rehabilitation and MS Center Noorderhart, 3900 Pelt, Belgium. Fitness and Physiotherapy Center, 2550 Kontich, Belgium. Faculty of Kinesiology and Rehabilitation Sciences FABER, Katholieke Universiteit Leuven, 3001 Leuven, Belgium. REVAL Rehabilitation Research Center, Research Institute, Faculty of Rehabilitation Sciences, Hasselt University, 3590 Diepenbeek, Belgium. University MS Centre Hasselt-Pelt, 3500 Hasselt, Belgium.
 Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, PLA Joint Service No. 903 Hospital, Hangzhou, Zhejiang, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China. Department of Dermatology, Xijing hospital, Fourth Military Medical University, Xi'an, China.
 Neuroimmunology Unit, Department of Neurosciences, Hospital Alemán, Buenos Aires, Argentina. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, Texas, USA. Centro de esclerosis múltiple de Buenos Aires, Buenos Aires, Argentina. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Berlin, Germany. Centro Universitario de Esclerosis Múltiple (CUEM), Hospital Ramos Mejía, Buenos Aires, Argentina.
 Second Department of Neurology, Faculty of Medicine, Comenius University Bratislava, University Hospital Bratislava, Slovakia; Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Second Department of Neurology, Faculty of Medicine, Comenius University Bratislava, University Hospital Bratislava, Slovakia. Second Department of Neurology, Faculty of Medicine, Comenius University Bratislava, University Hospital Bratislava, Slovakia. Department of Information and Communication Technologies in Medicine, Faculty of Biomedical Engineering, Czech Technical University in Prague, Czechia. Second Department of Neurology, Faculty of Medicine, Comenius University Bratislava, University Hospital Bratislava, Slovakia. Second Department of Neurology, Faculty of Medicine, Comenius University Bratislava, University Hospital Bratislava, Slovakia; Centre of Experimental Medicine, Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovakia. Electronic address: peter.valkovic@gmail.com.
 Nassau University Medical Center South Nassau Communities Hospital
 School of Medicine, University of California, Irvine, CA, 92617, USA. Case Western Reserve University Ophthalmology, 10900 Euclid Ave, Cleveland, OH, 44106, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. ilivnat@hs.uci.edu. School of Medicine, University of California, Irvine, CA, 92617, USA. Medical College of Wisconsin, Wauwatosa, WI, 53226, USA. Kaiser Permanente Santa Clara Internal Medicine, Santa Clara, CA, 95051, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. Western University of Health Sciences, Pomona, CA, 91766, USA. University of California, Irvine, CA, 92617, USA. Western University of Health Sciences, Pomona, CA, 91766, USA. Institute for Clinical and Translational Sciences University, Department of Physical Medicine and Rehabilitation, University of California, Irvine, CA, 92617, USA. Institute for Mathematical Behavioral Sciences, University of California, Irvine, CA, 92617, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. Center for Translational Vision Research, University of California, Irvine, CA, 92617, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. Duke Eye Center, Department of Ophthalmology, Duke University School of Medicine, Durham, NC, 27705, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, CA, 92617, USA. Center for Translational Vision Research, University of California, Irvine, CA, 92617, USA. Department of Biomedical Engineering, University of California, Irvine, CA, 92617, USA. Institute for Clinical and Translational Sciences University, Department of Physical Medicine and Rehabilitation, University of California, Irvine, CA, 92617, USA.
 Section of Immunobiology, Department of Ophthalmology University Hospital, LMU Munich, Mathildenstr, 880336, Munich, Germany. Electronic address: gerhild.wildner@med.uni-muenchen.de.
 Comprehensive Multiple Sclerosis Center, Jefferson University, 909 Walnut Street, Philadelphia, PA 19107, United States. Electronic address: thomas.leist@jefferson.edu. Janssen Research and Development, 1125 Trenton Harbourton Rd, Titusville, NJ 08560, United States. StatInMed, 5360 Legacy Dr, Plano, TX 75024, United States. Janssen Scientific Affairs, LLC, 1125 Trenton Harbourton Rd, Titusville, NJ 08560, United States. Janssen Scientific Affairs, LLC, 1125 Trenton Harbourton Rd, Titusville, NJ 08560, United States.
 Department of Clinical Nutrition and Dietetics, Faculty of Nutrition Sciences and Food Technology, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition Sciences and Food Technology, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran. Sports Medicine Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Clinical Nutrition and Dietetics, Faculty of Nutrition Sciences and Food Technology, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
 Internal Medicine, HCA Florida Orange Park Hospital, Orange Park, USA. Internal Medicine, HCA Florida Orange Park Hospital, Orange Park, USA. Internal Medicine, HCA Florida Orange Park Hospital, Orange Park, USA. Internal Medicine, HCA Florida Orange Park Hospital, Orange Park, USA. Internal Medicine, HCA Florida Orange Park Hospital, Orange Park, USA.
 Department of Neurology, Focus Program Translational Neuroscience, Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany; State University of Medicine and Pharmacy "Nicolae Testemitanu", Chisinau, Republic of Moldova; Department of Neurology, Institute of Emergency Medicine, Chisinau, Republic of Moldova. Department of Neurology, Focus Program Translational Neuroscience, Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Mainz Comprehensive Epilepsy and Sleep Medicine Center, Department of Neurology, Johannes Gutenberg University Mainz, Mainz; Department of Neurology, Philipps-University, Marburg, Germany. Department of Neurology, Focus Program Translational Neuroscience, Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Heinrich Heine University, Düsseldorf, Germany. Department of Neurology, Focus Program Translational Neuroscience, Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
 Department of Medical Education, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA. Department of Medical Education, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA. Department of Medical Education, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA. Department of Psychiatry, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA. Department of Psychiatry, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA. Division of Periodontology, UConn Health, Farmington, USA. Department of Medical Education, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA. Electronic address: jorge.cervantes@ttuhsc.edu.
 Klinik für Urologie, Kantonsspital St. Gallen, Rorschacher Str. 95, 9007, St. Gallen, Schweiz. sarah.hagmann@kssg.ch. Institut für Pathologie, Kantonsspital St. Gallen, St. Gallen, Schweiz. Klinik für Urologie, Kantonsspital St. Gallen, Rorschacher Str. 95, 9007, St. Gallen, Schweiz. Klinik für Urologie, Kantonsspital St. Gallen, Rorschacher Str. 95, 9007, St. Gallen, Schweiz.
 Department of Pharmacy Services, University Hospitals Cleveland Medical Center, United States of America. Electronic address: Veronica.mears@uhhospitals.org. Neurology/MS, Department of Specialty Pharmacy, University Hospitals Home Care Services, United States of America. Department of Specialty Pharmacy, University Hospitals Home Care Services, United States of America. Neurology and Neuroimmunology, University Hospitals Cleveland Medical Center, United States of America. Case Western Reserve School of Medicine, Multiple Sclerosis and Neuroimmunology Program, University Hospitals Cleveland Medical Center, VA Multiple Sclerosis Center of Excellence, United States of America. Neurology, Case Western Reserve University School of Medicine, Multiple Sclerosis and Neuroimmunology Program, Parkinson's and Movement Disorders Center, 11100 Euclid Avenue, Bolwell 5, Cleveland, OH 44106, United States of America. Electronic address: Hesham.abboud@uhhospitals.org.
 Department of Neurology, University of Alabama at Birmingham, AL,USA. Mahatma Gandhi Memorial Medical College, Indore, India. Department of Neurology, Wayne State University, Detroit, MI, USA; Department of Neurology, Southern Illinois University, Springfield, IL, USA; Department of Neuropsychiatry, Minia University, Egypt. JN Medical College, Belgaum, India. West Virginia Clinical Transitional Science, Morgantown, WV, USA. Division of Multiple Sclerosis and Neuroimmunology Department of Neurology, McGovern Medical School (UT Health), University of Texas Health Science Center at Houston, Houston, TX,USA. Division of Multiple Sclerosis and Neuroimmunology Department of Neurology, McGovern Medical School (UT Health), University of Texas Health Science Center at Houston, Houston, TX,USA. Electronic address: shitiz.k.sriwastava@uth.tmc.edu.
 California Northstate University California Northstate University College of Medicine
 Departamento de Medicina Clínica, Universidade Federal do Ceará, Fortaleza (UFC), CE, Brazil. Departamento de Anatomia e Morfologia, UFC, Fortaleza, CE, Brazil. Departamento de Medicina Clínica, Universidade Federal do Ceará, Fortaleza (UFC), CE, Brazil. Hospital Universitário Walter Cantídio, UFC, Fortaleza, CE, Brazil.
 Brain and Mind Center, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Center, Sydney, NSW, Australia. Brain and Mind Center, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Center, Sydney, NSW, Australia. Brain and Mind Center, The University of Sydney, Sydney, NSW, Australia. Shanghai AI Laboratory, Shanghai, China. Brain and Mind Center, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Center, Sydney, NSW, Australia. Shanghai AI Laboratory, Shanghai, China. Brain and Mind Center, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Center, Sydney, NSW, Australia. Brain and Mind Center, The University of Sydney, Sydney, NSW, Australia. Sydney Neuroimaging Analysis Center, Sydney, NSW, Australia.
 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Mathematics, Royal Institute of Technology, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Czech National Multiple Sclerosis ReMuS, IMPULS Endowment Fund, Prague, Czech Republic. First Faculty of Medicine and General University Hospital, Department of Neurology and Center of Clinical Neuroscience, Charles University in Prague, Prague, Czech Republic. First Faculty of Medicine and General University Hospital, Department of Neurology and Center of Clinical Neuroscience, Charles University in Prague, Prague, Czech Republic. The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Copenhagen, Denmark. The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Copenhagen, Denmark. The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital, Copenhagen, Denmark. MS Forschungs- und Projektentwicklungs-gGmbH, Hannover, Germany. MS Forschungs- und Projektentwicklungs-gGmbH, Hannover, Germany. Swansea University Medical School, Swansea, UK. Swansea University Medical School, Swansea, UK. Swansea University Medical School, Swansea, UK. Swansea University Medical School, Swansea, UK. Department of Cellular and Molecular Neuroscience, Imperial College London, London, UK. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Hôpital Neurologique, Service de Neurologie A, the European Database for Multiple Sclerosis (EDMUS), Coordinating Center and INSERM U 433, Lyon, France. Division of Clinical Neurosciences, University Hospital and University of Turku, Turku, Finland. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro", Bari, Italy. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro", Bari, Italy. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Faculty of Kinesiology, University of British Columbia. Department of Kinesiology, Faculty of Applied Health Sciences, Brock University.
 Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Genetic, Tabriz Branch, Islamic Azad University, Tabriz, Iran. Department of Medical Laboratory Science, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran. Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Clinical Biochemistry, Mashhad University of Medical Sciences, Mashhad, Iran. Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
 Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran. Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran. Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. i_adibi@med.mui.ac.ir. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. i_adibi@med.mui.ac.ir. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran. i_adibi@med.mui.ac.ir. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. mehdi.sanayei@gmail.com. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran. mehdi.sanayei@gmail.com.
 Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Department of Neurology, Department of Immunology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390, United States of America. Electronic address: nancy.monson@utsouthwestern.edu.
 School of Psychology, College of Health and Life Sciences, Aston University. School of Psychology, College of Health and Life Sciences, Aston University. School of Psychology, College of Health and Life Sciences, Aston University.

 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland. Center for Reproducible Science, University of Zurich, Zurich, Switzerland. Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Center of Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. National Center of Pathology & Luxembourg Center of Neuropathology, Laboratoire National de Santé, Dudelange, Luxembourg. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Health (NIH), Bethesda MA, USA. Department of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Center of Neurology, Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Health (NIH), Bethesda MA, USA. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neuroradiology, Karolinska University Hospital, Stockholm, Sweden.
 Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA. Electronic address: Hosssein.mousavi@uth.tmc.edu. Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA. Electronic address: john.w.lindsey@uth.tmc.edu. Department of Anesthesiology & Critical Care Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. Electronic address: khigh@salud.unm.edu. Department of Anesthesiology & Critical Care Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. Electronic address: SAlles@salud.unm.edu.
 Department of Kinesiology and Nutrition, College of Applied Health Sciences, University of Illinois at Chicago, 1919 W Taylor St, Chicago, IL 60612 USA.
 Laboratory for Cognition and Neural Stimulation, University of Pennsylvania. Department of Psychology, Pennsylvania State University. Center for Neuropsychology and Neuroscience Research, Kessler Foundation. Center for Neuropsychology and Neuroscience Research, Kessler Foundation. Department of Psychology, Pennsylvania State University.
 Huangpu Mental Health Center, Shanghai, China. Xuhui Mental Health Center, Shanghai, China. Huangpu Mental Health Center, Shanghai, China. Xuhui Mental Health Center, Shanghai, China. Electronic address: lichenhu249@163.com.

 CNRS, Univ. Bordeaux, Bordeaux INP, LABRI, UMR5800, F-33400 Talence, France. Univ. Bordeaux, CNRS, UMR 5293, Institut des Maladies Neurodégénératives, F-33000 Bordeaux, France. Centre Mémoire Ressources Recherches, Pôle de Neurosciences Cliniques, CHU de Bordeaux, F-33000 Bordeaux, France. CNRS, Univ. Bordeaux, Bordeaux INP, LABRI, UMR5800, F-33400 Talence, France. CNRS, Univ. Bordeaux, Bordeaux INP, LABRI, UMR5800, F-33400 Talence, France. Inserm U1215 - Neurocentre Magendie, Bordeaux F-33000, France. Service de Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, F-33000 Bordeaux, France. Instituto de Aplicaciones de las Tecnologías de la Información y de las Comunicaciones Avanzadas (ITACA), Universitat Politècnica de València, Camino de Vera s/n, 46022, Valencia, Spain. Inserm U1215 - Neurocentre Magendie, Bordeaux F-33000, France. Service de Neuroimagerie diagnostique et thérapeutique, CHU de Bordeaux, F-33000 Bordeaux, France.
 Department of Neurology, Siun Sote, North Karelia Central Hospital, Joensuu, Finland and Clinical Neurosciences, University of Turku, Turku, Finland. StellarQ Ltd., Turku, Finland. Institute of Biomedicine, University of Turku and Clinical Microbiology, Turku University Hospital, Turku, Finland. Clinical Neurosciences, University of Turku and Neurocenter, Turku University Hospital, Turku, Finland.
 Joyce D. and Andrew J. Mandell Center for Comprehensive Multiple Sclerosis Care and Neuroscience Research, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (HMDM, JAR, ESG, LON, ACL). Department of Rehabilitative Medicine (HMDM, JAR, ESG, LON), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Joyce D. and Andrew J. Mandell Center for Comprehensive Multiple Sclerosis Care and Neuroscience Research, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (HMDM, JAR, ESG, LON, ACL). Department of Rehabilitative Medicine (HMDM, JAR, ESG, LON), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Medical Sciences (JAR, ESG, EW), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Physical Therapy (LBS), School of Health Sciences at Quinnipiac University, North Haven, CT, USA. Joyce D. and Andrew J. Mandell Center for Comprehensive Multiple Sclerosis Care and Neuroscience Research, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (HMDM, JAR, ESG, LON, ACL). Department of Rehabilitative Medicine (HMDM, JAR, ESG, LON), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Medical Sciences (JAR, ESG, EW), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Department of Neurology, University of Connecticut School of Medicine, Farmington, CT, USA (ESG). Joyce D. and Andrew J. Mandell Center for Comprehensive Multiple Sclerosis Care and Neuroscience Research, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (HMDM, JAR, ESG, LON, ACL). Department of Rehabilitative Medicine (HMDM, JAR, ESG, LON), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. School of Health Professions, Rutgers, The State University of New Jersey, Blackwood, NJ, USA (ETC). Department of Medical Sciences (JAR, ESG, EW), Frank H. Netter MD School of Medicine at Quinnipiac University, North Haven, CT, USA. Mary Free Bed Rehabilitation Hospital, Grand Rapids, MI, USA (RJK). Joyce D. and Andrew J. Mandell Center for Comprehensive Multiple Sclerosis Care and Neuroscience Research, Mount Sinai Rehabilitation Hospital, Trinity Health Of New England, Hartford, CT, USA (HMDM, JAR, ESG, LON, ACL).
 Laboratory of Molecular Neuroscience and Dementia, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia. Neuroscience, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia. Laboratory of Molecular Neuroscience and Dementia, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia. Neuroscience, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia.
 Department of Neurology, Stony Brook University, Stony Brook, NY, 11794, USA. Electronic address: patricia.coyle@stonybrookmedicine.edu. IQVIA, Wayne, PA, 19087, USA. IQVIA, Wayne, PA, 19087, USA. IQVIA, Wayne, PA, 19087, USA. IQVIA, Wayne, PA, 19087, USA. Novartis Pharmaceuticals Corp., East Hanover, NJ, 07936, USA. Novartis Pharmaceuticals Corp., East Hanover, NJ, 07936, USA. Novartis Pharmaceuticals Corp., East Hanover, NJ, 07936, USA.
 Department of Physical Therapy, MGH Institute of Health Professions, Boston, MA 02129, USA. Adult Inpatient Division, Department of Physical Therapy and Occupational Therapy, Duke University Health System, Durham, NC 27710, USA. University of North Carolina Hospitals, Department of Rehabilitation Therapies, Chapel Hill, NC 27514, USA.
 Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania. Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania. Faculty of Medicine and Pharmacy, "Dunarea de Jos" University of Galati, 800008 Galati, Romania. Faculty of General Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, 700115 Iasi, Romania. Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania. Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania. Faculty of General Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, 700115 Iasi, Romania. Public Health and Management Department, "Grigore T. Popa" University of Medicine and Pharmacy, 700115 Iasi, Romania. Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania. Faculty of General Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, 700115 Iasi, Romania. "Al. I. Cuza" University, 700506 Iasi, Romania. Faculty of Medicine and Pharmacy, "Dunarea de Jos" University of Galati, 800008 Galati, Romania.
 Queen Square MS Centre, University College London Institute of Neurology and National Institute for Health and Care Research (NIHR) University College London Hospitals Biomedical Research Centre, London, UK. Ruhr-University Bochum & St. Josef-Hospital, Bochum, Germany. EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. ICON plc, 3455 North Service Rd, Burlington, Ontario L7N 3G2, Canada. ICON plc, 3455 North Service Rd, Burlington, Ontario L7N 3G2, Canada. ICON plc, 3455 North Service Rd, Burlington, Ontario L7N 3G2, Canada. ICON plc, Marlow, United Kingdom. ICON plc, Blue Bell, PA, USA. Merck Healthcare KGaA, Darmstadt, Germany. Electronic address: gerard.harty@merckgroup.com.
 Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 7, 413 45, Gothenburg, Sweden. igal.rosenstein@vgregion.se. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 7, 413 45, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 7, 413 45, Gothenburg, Sweden. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 7, 413 45, Gothenburg, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden. UK Dementia Research Institute at UCL, London, UK. Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK. Hong Kong Centre for Neurodegenerative Diseases, Hong Kong, China. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA. Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 7, 413 45, Gothenburg, Sweden.
 Division of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California; Department of Neurology, Keck School of Medicine of the University of Southern California, Los Angeles, California. Electronic address: jdsantoro@chla.usc.edu. Division of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California. Division of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California. Division of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California. Division of Neurology, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy.
 Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Pahnke Lab (Drug Development and Chemical Biology), Lübeck Institute of Experimental Dermatology (LIED), University of Lübeck (UzL) and University Medical Center Schleswig-Holstein (UKSH), Ratzeburger Allee 160, 23538 Lübeck, Germany. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia. Department of Pathology, Section of Neuropathology/Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo (UiO) and Oslo University Hospital (OUS), Sognsvannsveien 20, 0372 Oslo, Norway. Pahnke Lab (Drug Development and Chemical Biology), Lübeck Institute of Experimental Dermatology (LIED), University of Lübeck (UzL) and University Medical Center Schleswig-Holstein (UKSH), Ratzeburger Allee 160, 23538 Lübeck, Germany. Department of Pharmacology, Faculty of Medicine, University of Latvia, Jelgavas iela 3, 1004 Rīga, Latvia. Department of Neurobiology, The Georg S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 6997801, Israel.
 Second Department of Neurology, 'Attikon' University Hospital, School of Medicine, National and Kapodistrian University of Athens, 12462 Athens, Greece. First Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. Research Unit of Radiology, Second Department of Radiology, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. Medical Physics Laboratory, School of Medicine, Democritus University of Thrace, 68100 Alexandroupoli, Greece. Research Unit of Radiology, Second Department of Radiology, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. Second Department of Neurology, 'Attikon' University Hospital, School of Medicine, National and Kapodistrian University of Athens, 12462 Athens, Greece. Research Unit of Radiology, Second Department of Radiology, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. MS Center and Other Neurodegenerative diseases, Metropolitan General Hospital, 15562 Holargos, Athens, Greece. First Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. Second Department of Neurology, 'Attikon' University Hospital, School of Medicine, National and Kapodistrian University of Athens, 12462 Athens, Greece. First Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. First Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece. First Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.
 Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Medicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Medical Image Analysis Center (MIAC AG), Basel and qbig, Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Medical Image Analysis Center (MIAC AG), Basel and qbig, Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Medicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Medicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Medical Image Analysis Center (MIAC AG), Basel and qbig, Department of Biomedical Engineering, University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Medicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Neurology Clinic and Policlinic, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland.
 Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Radiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. Guangdong Provincial Key Laboratory of Artificial Intelligence in Medical Image Analysis and Application, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Radiology, Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Berlin Institute of Health, Humboldt-Universität zu Berlin, Berlin, Germany. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Radiology, University of Illinois Hospital and Health Sciences System, Chicago, IL, United States. Department of Anatomy and Cell Biology, University of Illinois at Chicago College of Medicine, Chicago, IL, United States. Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Radiology, University of Illinois Hospital and Health Sciences System, Chicago, IL, United States.
 Laboratorio di Ricerca per il Coinvolgimento dei Cittadini in Sanità, Dipartimento di Salute Pubblica, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milan, 20156, Italy. paola.mosconi@marionegri.it. Dipartimento Scienze Mediche di Base, Neuroscienze ed Organi di Senso, Università degli Studi Aldo Moro, Bari, Italy. Laboratorio di Ricerca per il Coinvolgimento dei Cittadini in Sanità, Dipartimento di Salute Pubblica, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milan, 20156, Italy. Laboratorio di Ricerca per il Coinvolgimento dei Cittadini in Sanità, Dipartimento di Salute Pubblica, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milan, 20156, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genoa, Italy. Scientific Research Area, Italian Multiple Sclerosis Foundation, Genoa, Italy. Department of Physiopathology, Experimental Medicine and Public Health, University of Siena, Siena, Italy. Centro Sclerosi Multipla AOU Careggi, Florence, Italy. Centro Interdipartimentale Sclerosi Multipla, Fondazione Istituto Neurologico C. Mondino, Pavia, Italy. Centro Sclerosi Multipla, SC Neurologia, AO Santa Croce E Carle, Cuneo, Italy. Casa di Cura del Policlinico, Università Vita Salute San Raffaele, Milan, Italy. UOC di Neurologia e Neurofisiopatologia Azienda Ospedaliera S. Camillo-Forlanini, Rome, Italy. Centro Sclerosi Multipla AOU Policlinico Vittorio Emanuele, Catania, Italy. Centro di Servizio e Ricerca sulla Sclerosi Multipla, AOU di Ferrara, Ferrara, Italy. Dipartimento di Scienze Mediche Chirurgiche e Neuroscienze, Università degli Studi di Siena, Siena, Italy. Dipartimento Scienze Mediche di Base, Neuroscienze ed Organi di Senso, Università degli Studi Aldo Moro, Bari, Italy. Laboratorio di Ricerca per il Coinvolgimento dei Cittadini in Sanità, Dipartimento di Salute Pubblica, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milan, 20156, Italy.
 St Jude Children's Research Hospital, Memphis, TN, USA (MW). Department of Kinesiology (MW, POC, KMC), College of Education, University of Georgia, Athens, GA, USA. Department of Kinesiology (MW, POC, KMC), College of Education, University of Georgia, Athens, GA, USA. Department of Educational Psychology (KB), College of Education, University of Georgia, Athens, GA, USA. Shepherd Center, Atlanta, GA (DB). Department of Kinesiology (MW, POC, KMC), College of Education, University of Georgia, Athens, GA, USA.
 Epidemiology, Biostatistics, and Prevention Institute, University of Zurich, Zurich, Switzerland. Epidemiology, Biostatistics, and Prevention Institute, University of Zurich, Zurich, Switzerland. Institute for Implementation Science in Health, University of Zurich, Zurich, Switzerland. Epidemiology, Biostatistics, and Prevention Institute, University of Zurich, Zurich, Switzerland. Institute for Implementation Science in Health, University of Zurich, Zurich, Switzerland. Research Department Physiotherapy, Rehabilitation Centre, Valens, Switzerland. Research Department Physiotherapy, Rehabilitation Centre, Valens, Switzerland. Research Department Physiotherapy, Rehabilitation Centre, Valens, Switzerland. Epidemiology, Biostatistics, and Prevention Institute, University of Zurich, Zurich, Switzerland. Institute for Implementation Science in Health, University of Zurich, Zurich, Switzerland.
 NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY. NYU Multiple Sclerosis Comprehensive Care Center (IK, TEB), Department of Neurology; Department of Population Health (CO), NYU Grossman School of Medicine, New York; The Elliot Lewis Center for Multiple Sclerosis Care (EAD, ILOS, AB, EL, JK), Wellesley, MA; and St. Peter's MS and Headache Center (EHP), Albany, NY.
 Joi Life Wellness MS Center, Atlanta, GA, USA. Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. San Juan MS Center, Guaynabo, Puerto Rico. Providence Portland Medical Center, Portland, OR, USA. North Texas Institute of Neurology and Headache, Plano, TX, USA. Neuroinnovation Program, UT Southwestern Medical Center, Dallas, TX, USA. Columbia University Medical Center, New York City, NY, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. sarah.england@biogen.com. Biogen, Cambridge, MA, USA.
 Rashid Hospital and Dubai Medical College and Dubai Health Authority (DHA), P.O. Box 4545, Dubai, UAE. jsInshasi@emirates.net.ae. Ibn Sina Hospital, Kuwait, Kuwait. Faculty of Medicine, Minia University, Minia, Egypt. Sheikh Shakhbout Medical City, Abu Dhabi, UAE. Tawam Hospital, Abu Dhabi, UAE. College of Medicine and Health Science, United Arab Emirates University, Abu Dhabi, UAE. Tawam Hospital, Abu Dhabi, UAE. College of Medicine and Health Science, United Arab Emirates University, Abu Dhabi, UAE. Al Zahra Hospital, Dubai, UAE. Mediclinic City Hospital, Dubai, UAE. Mediclinic City Hospital, Dubai, UAE. Rashid Hospital and Dubai Medical College and Dubai Health Authority (DHA), P.O. Box 4545, Dubai, UAE. American Center for Psychiatry and Neurology, Dubai, UAE. Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE. Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE. Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE. Merck Serono Middle East FZ Ltd, Dubai, UAE. Merck Serono Middle East FZ Ltd, Dubai, UAE. Amiri Hospital, Sharq, Kuwait.
 Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Department of Ophthalmology, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Medical Education, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Epidemiology, Department of Population Health Sciences, Weill Cornell Medicine, New York, NY, USA. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar of Cornell University, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Department of Neurology, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey. Department of Neurology, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar. Division of Research, Weill Cornell Medicine-Qatar, Cornell University and Qatar Foundation, Education City, PO Box 24144, Doha, Qatar. Institute of Cardiovascular Sciences, Cardiac Centre, Faculty of Medical and Human Sciences, University of Manchester and NIHR Clinical Research Facility, Manchester, M13 9NT, UK.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. IRCCS NEUROMED, Pozzilli, Italy. Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Advanced Medical and Surgical Sciences, and 3T MRI-Center, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Advanced Medical and Surgical Sciences, and 3T MRI-Center, University of Campania "Luigi Vanvitelli", Naples, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy.
 Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. Neuroimmunology Unit, Montréal Neurological Institute, McGill University, Canada. Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO, USA. Charles Perkins Centre and School of Medical Sciences, The University of Sydney, Camperdown, NSW, Australia. Department of Pathology and Molecular Medicine, Queen's University, Kingston, ON, K7L 3N6, Canada. Université de Montréal Centre de Recherche du CHUM (CRCHUM) and Department of Neuroscience, Université de Montréal, 900 Saint Denis Street, Montréal, QC, H2X 0A9, Canada. Department of Immunology, University of Toronto, Toronto, ON, M5S 1A8, Canada. Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Departments of Neurology and Biochemistry, Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI, USA. Departments of Neurology and Biochemistry, Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI, USA. Neuroimmunology Unit, Montréal Neurological Institute, McGill University, Canada. Department of Neurology and Center for Neuroinflammation and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: amitbar@pennmedicine.upenn.edu.
 Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China. Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China. Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China. Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
 Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy. Department of Translational Medicine, University of Piemonte Orientale, 28100 Novara, Italy.
 Department of Paediatrics, Liuzhou People's Hospital Affiliated to Guangxi Medical University, Liuzhou, P. R. 545006, China. Department of Radiology, Liuzhou People's Hospital Affiliated to Guangxi Medical University, Liuzhou, P. R. 545006, China. Central Laboratory, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P. R. 541199, China. Department of Paediatrics, Liuzhou People's Hospital Affiliated to Guangxi Medical University, Liuzhou, P. R. 545006, China. Department of Paediatrics, Liuzhou People's Hospital Affiliated to Guangxi Medical University, Liuzhou, P. R. 545006, China. Central Laboratory, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P. R. 541199, China. Department of Paediatrics, Liuzhou People's Hospital Affiliated to Guangxi Medical University, Liuzhou, P. R. 545006, China. Central Laboratory, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P. R. 541199, China.
 Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Neurology Section, Veterans Affairs North Texas Health Care System, Dallas, TX 75216. Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Neurology Section, Veterans Affairs North Texas Health Care System, Dallas, TX 75216. Peter O'Donnell Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390.
 NYU Grossman School of Medicine, Department of Neurology, USA. NYU Grossman School of Medicine, Department of Neurology, USA; NYU Grossman School of Medicine, Parekh Center for Interdisciplinary Neurology, USA. NYU Grossman School of Medicine, Department of Neurology, USA. NYU Grossman School of Medicine, Department of Neurology, USA. NYU Grossman School of Medicine, Department of Neurology, USA; NYU Grossman School of Medicine, Parekh Center for Interdisciplinary Neurology, USA. NYU Grossman School of Medicine, Department of Population Health and Environmental Medicine, USA. NYU Grossman School of Medicine, Department of Neurology, USA; NYU Grossman School of Medicine, Parekh Center for Interdisciplinary Neurology, USA. Electronic address: Leigh.charvet@nyulanogne.org.
 Department of Internal Medicine (RAM, CM), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences (RAM), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Department of Internal Medicine (RAM, CM), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada. Bernard Becker Medical Library, Washington University School of Medicine, St. Louis, MO, USA (LY). Section of Statistical Planning and Analysis, Department of Neurology, University of Texas Southwestern University, Dallas, USA (AS).
 Department of Electrical and Computer Engineering, The University of Iowa, Iowa City, IA, USA. Department of Electrical and Computer Engineering, The University of Iowa, Iowa City, IA, USA. Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Capital University of Medical Science, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China. Department of Electrical and Computer Engineering, The University of Iowa, Iowa City, IA, USA.
 Department of Clinical and Developmental Neuropsychology, University of Groningen, Groningen, The Netherlands. Department of Clinical and Developmental Neuropsychology, University of Groningen, Groningen, The Netherlands. Department of Neurology and Alzheimer Center Groningen, University Medical Center Groningen, Groningen, The Netherlands. Laboratory of Neurochemistry and Behaviour, University of Antwerp, Antwerp, Belgium. Department of Neurology and Memory Clinic, Middelheim General Hospital (ZNA), Antwerp, Belgium. Department of Clinical and Developmental Neuropsychology, University of Groningen, Groningen, The Netherlands. Department of Psychiatry and Psychotherapy, University Medical Center Rostock, Rostock, Germany. Department of Psychology, Maynooth University, National University of Ireland, Maynooth, Ireland. Department of Clinical and Developmental Neuropsychology, University of Groningen, Groningen, The Netherlands. janneke.koerts@rug.nl.
 IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi 10, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi 10, Genoa, Italy. Merck Serono S.P.A., Italy an Affiliate of Merck KGaA, Piazza del Pigneto 9, Rome, Italy. Merck Serono S.P.A., Italy an Affiliate of Merck KGaA, Piazza del Pigneto 9, Rome, Italy. IRCCS Ospedale Policlinico San Martino, Largo Rosanna Benzi 10, Genoa, Italy. alice.laroni@unige.it. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Largo Daneo 3, Genoa, Italy. alice.laroni@unige.it.
 Research Service, Richmond Veterans Affairs Medical Center, Central Virginia Veterans Affairs Health Care System, Richmond, VA 23249, USA. Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond VA 23298, USA. Research Service, Richmond Veterans Affairs Medical Center, Central Virginia Veterans Affairs Health Care System, Richmond, VA 23249, USA. Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond VA 23298, USA. Department of Biology, Virginia Commonwealth University, Richmond, VA 23298, USA. Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Division of Diabetes, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Division of Diabetes, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Division of Diabetes, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Research Service, Richmond Veterans Affairs Medical Center, Central Virginia Veterans Affairs Health Care System, Richmond, VA 23249, USA. Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond VA 23298, USA.
 Chair and Department of Experimental and Clinical Physiology, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland. kaja.kasarello@wum.edu.pl. Chair and Department of Experimental and Clinical Physiology, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland. Department of Experimental Pharmacology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland. Chair and Department of Experimental and Clinical Physiology, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland. Chair and Department of Experimental and Clinical Physiology, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
 Department of Integrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Integrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan. Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
 Department of Kinesiology and Community Health, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois. Electronic address: ricela@illinois.edu. Department of Kinesiology and Community Health, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois; Center for Health, Aging, and Disability, College of Applied Health Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois.
 Department of Neurology, Hannover Medical School, Hannover, Germany. Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, A Joint Venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience, University of Veterinary Medicine Hannover, Hannover, Germany. Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, A Joint Venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany. Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, A Joint Venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience, University of Veterinary Medicine Hannover, Hannover, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, A Joint Venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany. Center for Systems Neuroscience, University of Veterinary Medicine Hannover, Hannover, Germany. Cluster of Excellence RESIST (EXC 2155), Hannover Medical School, Hannover, Germany.
 Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Department of Anatomy and Legal Medicine, Neuropsychopharmacology Group, Biomedical Research Institute of Málaga-IBIMA, Faculty of Medicine, University of Malaga, Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Málaga, Spain. Department of Medicine and Dermatology, Faculty of Medicine, University of Málaga, Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Málaga, Spain. Neuroimmunology and Neuroinflammation Group, Biomedical Research Institute of Málaga-IBIMA Plataforma Bionand, Hospital Regional Universitario de Málaga, Málaga, Spain. Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Málaga, Spain. Department of Cell Biology, Genetics and Physiology, Physiology Area. Faculty of Science University of Malaga, Málaga, Spain.
 Department of Molecular and Medical Pharmacology, UCLA School of Medicine, University of California, Los Angeles, CA 90095-1735, USA. Department of Molecular and Medical Pharmacology, UCLA School of Medicine, University of California, Los Angeles, CA 90095-1735, USA.
 Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States. Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States. Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States. Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States. Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. Genes and Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States. Dean McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. Dean McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. Dean McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States. Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.
 UCSF Weill Institute for the Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, United States. Yale University School of Medicine, Department of Neurology, New Haven, CT, United States. Yale University School of Medicine, Department of Neurology, New Haven, CT, United States. UCSF Weill Institute for the Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, United States. School of Medicine, Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, United States. Yale University School of Medicine, Department of Neurology, New Haven, CT, United States. UCSF Weill Institute for the Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, CA, United States. Electronic address: Riley.bove@ucsf.edu.
 School of Nursing, Duke University, Durham, NC. Durham VA Health Care System, Durham, NC. School of Medicine, Duke University, NC. Neurology Department, Duke University School of Medicine. MS Center of Excellence, Durham VA Medical Center, Durham VA. Durham VA Health Care System, Durham, NC. Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC. VA Mid-Atlantic Mental Illness Research, Education, and Clinical Center (MIRECC), Durham, NC. Durham VA Health Care System, Durham, NC. Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC. VA Mid-Atlantic Mental Illness Research, Education, and Clinical Center (MIRECC), Durham, NC. School of Nursing, Duke University, Durham, NC.
 From the Department of Medicine (D.R., R.S.), Division of Neurology, University of Toronto; St. Michael's Hospital (D.R., R.S.), and Keenan Research Centre for Biomedical Science (R.S.), Unity Health Toronto, Ontario, Canada. dalia.rotstein@unityhealth.to. From the Department of Medicine (D.R., R.S.), Division of Neurology, University of Toronto; St. Michael's Hospital (D.R., R.S.), and Keenan Research Centre for Biomedical Science (R.S.), Unity Health Toronto, Ontario, Canada.
 VCU Health System VCU Health Virginia Commonwealth University
 University of Miami/Jackson Memorial Hospital Un of California, Riverside SOM
 Department of Ophthalmology, Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand. Department of Ophthalmology, Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand. Department of Ophthalmology, Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand. Department of Ophthalmology, Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand. Faculty of Medicine Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand. Department of Ophthalmology, Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand. Faculty of Medicine Rajavithi Hospital, Rangsit University, 2 Phaya Thai Rd., Thung Phaya Thai, Ratchathewi, Bangkok 10400, Thailand.
 Department of Ophthalmology, National Taiwan University Hospital, No 7, Chung-Shan S. Rd., Taipei, Taiwan. Department of Medical Education, National Taiwan University Hospital, Taiwan. Department of Medical Imaging, National Taiwan University Hospital, Taiwan. Department of Medical Imaging, National Taiwan University Hospital, Taiwan. Department of Ophthalmology, National Taiwan University Hospital, No 7, Chung-Shan S. Rd., Taipei, Taiwan; Center of Frontier Medicine, National Taiwan University Hospital, Taiwan. Electronic address: tachingchen1@ntu.edu.tw.
 Servicio de Neumología, Hospital General Universitario Dr. Balmis, Spain; Instituto de Investigación Sanitaria Biomédica de Alicante (ISABIAL), Alicante, Spain. Electronic address: martagoro13@gmail.com. Servicio de Neumología, Hospital General Universitario Dr. Balmis, Spain; Instituto de Investigación Sanitaria Biomédica de Alicante (ISABIAL), Alicante, Spain. Servicio de Neurología, Hospital General Universitario Dr. Balmis, Alicante, Spain; Instituto de Investigación Sanitaria Biomédica de Alicante (ISABIAL), Grupo 1: Investigación en Neurociencias, Spain. Servicio de Neumología, Hospital General Universitario Dr. Balmis, Spain; Instituto de Investigación Sanitaria Biomédica de Alicante (ISABIAL), Alicante, Spain. Servicio de Neurología, Hospital General Universitario Dr. Balmis, Alicante, Spain; Instituto de Investigación Sanitaria Biomédica de Alicante (ISABIAL), Grupo 1: Investigación en Neurociencias, Spain; Departamento de Medicina Clínica, Universidad Miguel Hernández, Spain.
 Department of Physical Therapy and Rehabilitation Science, University of California San Francisco, San Francisco, CA, USA. caroline.guglielmetti@ucsf.edu. Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA. caroline.guglielmetti@ucsf.edu. Department of Neurology, Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, USA. Department of Radiology, C.J. Gorter MRI Center, Leiden University Medical Center, Leiden, The Netherlands. Department of Neurology, Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, CA, USA. Department of Ophthalmology, University of California at San Francisco, CA, San Francisco, USA. Department of Physical Therapy and Rehabilitation Science, University of California San Francisco, San Francisco, CA, USA. myriam.chaumeil@ucsf.edu. Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA. myriam.chaumeil@ucsf.edu.
 Assistant Professor, Hunter Bellevue School of Nursing, 425 East 25 Street, New York, NY 10010, USA. Mount Sinai Hospital, New York, NY, USA. Neuroscience Clinic, Stanford Health Care, CA, USA. Department of Psychological Sciences, University of San Diego, San Diego, CA, USA. IHS International, San Diego, CA, USA. A patient living with multiple sclerosis since 2003.
 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811 Department of Neurology, Brigham Multiple Sclerosis Center, Brigham and Women's Hospital, Boston, MA, USA. RINGGOLD: 1861 Harvard Medical School, Boston, MA, USA. RINGGOLD: 1811
 Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. B', Department of Neurology, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Stilponos Kiriakides str. 1, 54636 Thessaloniki, Macedonia, Greece. ToolGen Inc., Gangseo-gu, 07789 Seoul, Korea. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, PO Box 11099, Taif 21944, Saudi Arabia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, PO Box 11099, Taif 21944, Saudi Arabia. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. STEMCELL Technologies Inc., Vancouver, British Columbia V6A 1B6, Canada. Australian Centre for Blood Diseases, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Australian Centre for Blood Diseases, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Clinical Haematology, Alfred Hospital, Prahran, Victoria 3004, Australia. B', Department of Neurology, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Stilponos Kiriakides str. 1, 54636 Thessaloniki, Macedonia, Greece. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia. Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06536, USA. Department of Neuroscience, Central Clinical School, Monash University, Prahran, Victoria 3004, Australia.
 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. RINGGOLD: 39064 Hasso Plattner Institute, University of Potsdam, Potsdam, Germany. RINGGOLD: 536033 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. RINGGOLD: 39064 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. RINGGOLD: 39064 Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, NeuroCure Clinical Research Center, Berlin, Germany. Centre for Stroke Research Berlin, Charité - Universitätsmedizin Berlin, Berlin, Germany. RINGGOLD: 449136. RINGGOLD: 14903 Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Digital Health Center, Berlin, Germany. RINGGOLD: 522475 Department of Neurology, University Hospital Carl Gustav Carus, Dresden, Germany. RINGGOLD: 39063 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. RINGGOLD: 39064 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. RINGGOLD: 39064 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. RINGGOLD: 39064
 Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: kristingaletta@gmail.com.
 Department of Neurology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), Universidad de Alcalá, 28034 Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), 28034 Madrid, Spain. Department of Microbiology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), CIBER en Epidemiología y Salud Pública (CIBERESP), 28034 Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), Universidad de Alcalá, 28034 Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), 28034 Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), Universidad de Alcalá, 28034 Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), 28034 Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), Universidad de Alcalá, 28034 Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), 28034 Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), 28034 Madrid, Spain. Department of Microbiology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), CIBER en Epidemiología y Salud Pública (CIBERESP), 28034 Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), Universidad de Alcalá, 28034 Madrid, Spain. Department of Neurology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), Universidad de Alcalá, 28034 Madrid, Spain. Department of Immunology, Hospital Universitario Ramón y Cajal, Universidad de Alcalá, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Red Española de Esclerosis Múltiple (REEM), 28034 Madrid, Spain.
 Department of Psychology and Neuroscience, University of St. Andrews, St, Andrews, United Kingdom, KY16 9JP. Department of Psychology and Neuroscience, University of St. Andrews, St, Andrews, United Kingdom, KY16 9JP. Department of Psychology and Neuroscience, University of St. Andrews, St, Andrews, United Kingdom, KY16 9JP.
 Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St Louis, MO, USA. Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St Louis, MO, USA. Electronic address: daniel.hawiger@health.slu.edu.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy. Neurorehabilitation Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Neurophysiology Service, IRCCS Ospedale San Raffaele, Milano, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milano, Italy rocca.mara@hsr.it. Neurology Unit, IRCCS Ospedale San Raffaele, Milano, Italy. Vita-Salute San Raffaele University, Milano, Italy.
 Department of Basic Sciences, California Northstate University College of Medicine, Elk Grove, CA, USA. Department of Basic Sciences, California Northstate University College of Medicine, Elk Grove, CA, USA. Department of Basic Sciences, California Northstate University College of Medicine, Elk Grove, CA, USA.
 Ross University Augusta Un., Medical College of Georgia Uniformed Services University/Brooke AMC
 Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Laboratory Medicine, Paracelsus Medical University and Salzburger Landeskliniken, Salzburg, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. fritz.leutmezer@meduniwien.ac.at. Clinic for Neurology 2, Kepler University Clinic, Linz, Austria.
 Réseau sclérose en plaques Île-de-France Ouest, Hôpital du Vésinet, 72 avenue de la Princesse, 78110 Le Vésinet, France. Electronic address: c.rebelo56@gmail.com.
 School of Pharmacy, Sathyabama Institute of Science and Technology, Jeppiaar Nagar, Rajiv Gandhi Salai, Chennai 600 119, India. School of Pharmaceutical Sciences, Vels Institute of Science, Technology and Advanced Studies (VISTAS), Chennai, India. South Shore Neurologic Associates, Patchogue, NY, USA. Department of Neurophysiotherapy, DVVPFS College of Physiotherapy, Ahmednagar, India. Manobal Neuropsychiatric Clinic, Dombivli, India; MannSparsh Neuropsychiatric Hospital, Kalyan, India. Manasa Rehabilitation & De-Addiction Center, Titwala, India. MannSparsh Neuropsychiatric Hospital, Kalyan, India; Manasa Rehabilitation & De-Addiction Center, Titwala, India. National Institute of Pharmaceutical Education and Research (NIPER), Kolkata, India.
 Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address: zipp@uni-mainz.de.
 School of Cardiovascular & Metabolic Health, University of Glasgow, G12 8QQ Glasgow, UK. School of Cardiovascular & Metabolic Health, University of Glasgow, G12 8QQ Glasgow, UK.
 Department of Neurology, Technical University of Munich, Klinikum rechts der Isar, Munich & Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, Münster, Germany. Polpharma Biologics SA, Gdansk, Poland. Polpharma Biologics SA, Gdansk, Poland. Staburo GmbH, Munich, Germany. Sandoz Biopharmaceuticals, Holzkirchen, Germany. Sandoz Biopharmaceuticals, Holzkirchen, Germany. Department of Neurology, University of Warmia & Mazury, Olsztyn, and Center of Neurology, Lodz, Poland.
 Quanterix Corp, Billerica, MA, USA. Quanterix Corp, Billerica, MA, USA. Quanterix Corp, Billerica, MA, USA. Quanterix Corp, Billerica, MA, USA. Neurochemistry Laboratory, Department of Laboratory Medicine, Amsterdam Neuroscience, Amsterdam, University Medical Centers, Amsterdam, The Netherlands. Laboratori de Neuroinmunologia Clinica Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Vall d'Hebron Institut de Recerca, Barcelona, Spain. Laboratori de Neuroinmunologia Clinica Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Vall d'Hebron Institut de Recerca, Barcelona, Spain. Laboratori de Neuroinmunologia Clinica Centre d'Esclerosi Múltiple de Catalunya (Cemcat) Vall d'Hebron Institut de Recerca, Barcelona, Spain. National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. MS Center Dresden, Center of Clinical Neuroscience, Department of Neurology, Dresden University of Technology, Dresden, Germany. MS Center Dresden, Center of Clinical Neuroscience, Department of Neurology, Dresden University of Technology, Dresden, Germany. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK. UK Dementia Research Institute at UCL, London, UK. Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China. Institute for Neuropathology at the University Medical Center, Göttingen, Germany. Department of Neurology, Barts Health NHS Trust, The Royal London Hospital, E1 1FR, London, UK. Department of Neurology, Barts Health NHS Trust, The Royal London Hospital, E1 1FR, London, UK. University Medical Center Mainz, Department of Neurology, Mainz, Germany. University Medical Center Mainz, Department of Neurology, Mainz, Germany. Institute of Experimental Neurology, Division of Neuroscience, University Vita e Salute San Raffaele and IRCCS San Raffaele Hospital, Milan, Italy. Institute of Experimental Neurology, Division of Neuroscience, University Vita e Salute San Raffaele and IRCCS San Raffaele Hospital, Milan, Italy. Hôpital St Eloi, Montpellier, France. University of Ottawa, Department of Medicine, The Ottawa Hospital Research Institute, Ottawa, Canada. University of Ottawa, Department of Medicine, The Ottawa Hospital Research Institute, Ottawa, Canada. Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Sanofi, Framingham, MA, USA. Department of Neurology, Ulm University Hospital, Ulm, Germany. Department of Neurology, Ulm University Hospital, Ulm, Germany. German Center for Neurodegenerative Diseases (DZNE e.V.), Ulm, Germany. Quanterix Corp, Billerica, MA, USA. Quanterix Corp, Billerica, MA, USA. Department of Neurology, Medical University of Graz, Graz, Austria. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. Department of Neurology, University of Münster, Münster, Germany. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel, Departments of Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Neurochemistry Laboratory, Department of Laboratory Medicine, Amsterdam Neuroscience, Amsterdam, University Medical Centers, Amsterdam, The Netherlands. Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland.

 Laboratory of Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China. NMPA Key Laboratory for Quality Control of In Vitro Diagnostics, Beijing 100070, China. Beijing Engineering Research Center of Immunological Reagents Clinical Research, Beijing 100070, China. Laboratory of Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China. NMPA Key Laboratory for Quality Control of In Vitro Diagnostics, Beijing 100070, China. Beijing Engineering Research Center of Immunological Reagents Clinical Research, Beijing 100070, China. Laboratory of Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China. NMPA Key Laboratory for Quality Control of In Vitro Diagnostics, Beijing 100070, China. Beijing Engineering Research Center of Immunological Reagents Clinical Research, Beijing 100070, China. Laboratory of Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China. NMPA Key Laboratory for Quality Control of In Vitro Diagnostics, Beijing 100070, China. Beijing Engineering Research Center of Immunological Reagents Clinical Research, Beijing 100070, China.
 Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
 Neuroimaging and Neurorehabilitation Laboratory, Wayne State University, Detroit, MI, USA. Translational Neuroscience Program, Wayne State University, Detroit, MI, USA. Department of Psychology, Wayne State University, Detroit, MI, USA. Institute of Gerontology, Wayne State University, Detroit, MI, USA. Translational Neuroscience Program, Wayne State University, Detroit, MI, USA. Department of Psychology, Wayne State University, Detroit, MI, USA. Institute of Gerontology, Wayne State University, Detroit, MI, USA. Neuroimaging and Neurorehabilitation Laboratory, Wayne State University, Detroit, MI, USA. Translational Neuroscience Program, Wayne State University, Detroit, MI, USA. Department of Health Care Sciences, Wayne State University, Detroit, MI, USA. Department of Neurology, Wayne State University, Detroit, MI, USA.
 Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Parkville, VIC 3050, Australia. Electronic address: maya.panisset@unimelb.edu.au. Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Parkville, VIC 3050, Australia; Australian Rehabilitation Research Centre, Parkville, Australia.
 Department of Psychology, Stanford University, Stanford, CA, USA. Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Clinical Psychology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Education and Psychology, Shahid Ashrafi Esfahani University, Esfahan, Iran. Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Clinical Psychology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Psychology, Stanford University, Stanford, CA, USA. Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA.
 Institute of Biopharmaceutical Research, Liaocheng University, Liaocheng, Shandong 252000, China. zhangning1111@126.com. Institute of Biopharmaceutical Research, Liaocheng University, Liaocheng, Shandong 252000, China. zhangning1111@126.com. Institute of Biopharmaceutical Research, Liaocheng University, Liaocheng, Shandong 252000, China. zhangning1111@126.com. Institute of Biopharmaceutical Research, Liaocheng University, Liaocheng, Shandong 252000, China. zhangning1111@126.com.
 Department of Neurology, UCSF Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, Kaiser Permanente, Oakland, CA, USA. Department of Neurology, UCSF Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA, USA. Piedmont Henry Hospital, Stockbridge, GA, USA. Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University, London, UK. Department of Neurology, Royal London Hospital, London, UK. Department of Neurology, UCSF Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA, USA. Department of Neurology, UCSF Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA, USA.
 Department of Radiology, Cumming School of Medicine, University of Calgary, Canada. Department of Radiology, Cumming School of Medicine, University of Calgary, Canada. Department of Radiology, Cumming School of Medicine, University of Calgary, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Canada. Department of Radiology, Cumming School of Medicine, University of Calgary, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Canada. Alberta Neurologic Centre, Calgary, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Canada. Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Canada. Department of Radiology, Cumming School of Medicine, University of Calgary, Canada. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Canada. Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Canada.
 The Research Center of the Centre Hospitalier de l'Université de Montréal (CRCHUM), Department of Neuroscience, Faculty of Medicine, Université de Montréal, Montréal H2X 0A9, Québec, Canada. Department of Psychiatry, College of Health Sciences, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta T6G 2B7, Canada. School of Rehabilitation Therapy, Faculty of Health Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada. The Hotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, 3330 Hospital Dr NW, Calgary, Alberta T2N 4N1, Canada. The Hotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, 3330 Hospital Dr NW, Calgary, Alberta T2N 4N1, Canada. Electronic address: vyong@ucalgary.ca.
 Huntington and Rare Diseases Unit, Fondazione IRCCS Casa Sollievo Della Sofferenza Hospital, 71013, San Giovanni Rotondo, Italy. sim.migliore@gmail.com. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100, L'Aquila, Italy. Italian League for Research On Huntington (LIRH) Foundation, 00185, Rome, Italy. Italian League for Research On Huntington (LIRH) Foundation, 00185, Rome, Italy. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100, L'Aquila, Italy. Huntington and Rare Diseases Unit, Fondazione IRCCS Casa Sollievo Della Sofferenza Hospital, 71013, San Giovanni Rotondo, Italy.
 Department of Pathology, University of Iowa, Iowa City, IA, USA. Department of Pathology Graduate Program, University of Iowa, Iowa City, IA, USA. Department of Pathology, University of Iowa, Iowa City, IA, USA. Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA. Nebraska Food for Health Center, University of Nebraska-Lincoln, Lincoln, NE, USA. Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA. Nebraska Food for Health Center, University of Nebraska-Lincoln, Lincoln, NE, USA. Department of Pathology, University of Iowa, Iowa City, IA, USA. Department of Pathology Graduate Program, University of Iowa, Iowa City, IA, USA. Graduate Program in Immunology, University of Iowa, Iowa City, IA, USA. Iowa City VA Healthcare System, Iowa City, IA, USA.
 Brooke Army Medical Center Allama Iqbal Medical College East Tennessee State University
 Fujian Key Laboratory of Molecular Neurology, Institute of Neuroscience, Fujian Medical University, Fuzhou, 350004, Fujian, China. Department of Neurology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China. Department of Neurology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350212, Fujian, China. Fujian Key Laboratory of Molecular Neurology, Institute of Neuroscience, Fujian Medical University, Fuzhou, 350004, Fujian, China. Department of Neurology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China. Department of Neurology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350212, Fujian, China. Department of Neurology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China. Department of Neurology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China. Fujian Key Laboratory of Molecular Neurology, Institute of Neuroscience, Fujian Medical University, Fuzhou, 350004, Fujian, China. aiyulin@fjmu.edu.cn. Department of Neurology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China. aiyulin@fjmu.edu.cn. Department of Neurology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350212, Fujian, China. aiyulin@fjmu.edu.cn.
 Translational Medical Center, Huaihe Hospital of Henan University, Kaifeng, 475000, China. College of Life Science, Henan University, Kaifeng, 475000, China. Nutritional Immunology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, 02111, USA. Translational Medical Center, Huaihe Hospital of Henan University, Kaifeng, 475000, China. Translational Medical Center, Huaihe Hospital of Henan University, Kaifeng, 475000, China. Nutritional Immunology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, 02111, USA. Nutritional Immunology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, 02111, USA.
 Senior Department of Cardiology, The Sixth Medical Center, Chinese PLA General Hospital, Beijing, China. Department of Nephrology, First Medical Center of Chinese PLA General Hospital, Beijing, China; State Key Laboratory of Kidney Diseases, Chinese PLA General Hospital, Beijing, China. Department of neurology, School of Medicine, South China University of Technology, Guangzhou, China; Department of neurology, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China. Department of neurology, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China; Navy Clinical College, the Fifth School of Clinical Medicine, Anhui Medical University, Hefei, China. Navy Clinical College, the Fifth School of Clinical Medicine, Anhui Medical University, Hefei, China. Department of Nephrology, First Medical Center of Chinese PLA General Hospital, Beijing, China; State Key Laboratory of Kidney Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Senior Department of Neurology, The First Medical Center of PLA General Hospital, Beijing, China. Electronic address: qiufengnet@hotmail.com. Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Electronic address: xushiping@301hospital.com.cn. State Key Laboratory of Kidney Diseases, Chinese PLA General Hospital, Beijing, China; Department of Gastroenterology, The Second Medical Center, Chinese PLA General Hospital, Beijing, China; National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China. Electronic address: lilylismiling@126.com.
 Department of Medicine, University of Toronto, St. Michael's Hospital, Toronto, ON, Canada. Division of Neurology, Department of Medicine, BARLO MS Centre, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Division of Neurology, Department of Medicine, BARLO MS Centre, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada Li Ka Shing Knowledge Institute, Toronto, ON, Canada. Division of Neurology, Department of Medicine, BARLO MS Centre, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada. Division of Neurology, Department of Medicine, BARLO MS Centre, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada Li Ka Shing Knowledge Institute, Toronto, ON, Canada.
 Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade de Campinas, Campinas, Brazil. Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Laboratório de Neuroquímica e Neurofarmacologia, Departamento de Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, Brazil. Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Enzimas proteolíticas e Síntese de peptídeos, Departamento de Biofísica, Universidade Federal de São Paulo, São Paulo, Brazil. Neuroimunopatologia Experimental, Departamento de Patologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Departamento de Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Núcleo de Neurociências, Programa de Pós-graduação em Ciências Biológicas:Fisiologia e Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Núcleo de Educação e Comunicação em Ciências da Vida e da Saúde (NEDUCOM), Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
 Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Division of Clinical Pathology, Geneva University Hospital, Geneva, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland. Institute of Clinical Molecular Biology, Kiel University and University Medical Center Schleswig-Holstein, Kiel, Germany. Department of Neurology, University Hospital Ulm, Ulm, Germany. Institute of Clinical Neuroimmunology, Faculty of Medicine, University Hospital and Biomedical Center (BMC), LMU Munich, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Martinsried, Germany. Munich Cluster of Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, Faculty of Medicine, University Hospital and Biomedical Center (BMC), LMU Munich, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Martinsried, Germany. Institute of Clinical Neuroimmunology, Faculty of Medicine, University Hospital and Biomedical Center (BMC), LMU Munich, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Martinsried, Germany. Munich Cluster of Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, Faculty of Medicine, University Hospital and Biomedical Center (BMC), LMU Munich, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Martinsried, Germany. Munich Cluster of Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, Faculty of Medicine, University Hospital and Biomedical Center (BMC), LMU Munich, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Martinsried, Germany. Munich Cluster of Systems Neurology (SyNergy), Munich, Germany. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Doron.Merkler@unige.ch. Division of Clinical Pathology, Geneva University Hospital, Geneva, Switzerland. Doron.Merkler@unige.ch. Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland. ayermanos@gmail.com. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. ayermanos@gmail.com. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. ayermanos@gmail.com. Center for Translational Immunology, University Medical Center Utrecht, Utrecht, Netherlands. ayermanos@gmail.com.
 Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada; Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2E1, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada; Women and Children's Health Research Institute, University of Alberta, 5-083 Edmonton Clinic Health Academy, 11405 87 Avenue NW, Edmonton, AB T6G 1C9, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada; Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2E1, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada; Women and Children's Health Research Institute, University of Alberta, 5-083 Edmonton Clinic Health Academy, 11405 87 Avenue NW, Edmonton, AB T6G 1C9, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada. Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2E1, Canada; Department of Pharmacology, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada. Department of Medicine, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada. Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON K1H 8L6, Canada. Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2E1, Canada; Department of Pharmacology, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada; Women and Children's Health Research Institute, University of Alberta, 5-083 Edmonton Clinic Health Academy, 11405 87 Avenue NW, Edmonton, AB T6G 1C9, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada. Department of Medicine, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada; Multiple Sclerosis Centre and Department of Cell Biology, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada. Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON K1H 8L6, Canada; Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada. Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2E1, Canada; Department of Pharmacology, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada. School of Infection and Immunity, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada; Women and Children's Health Research Institute, University of Alberta, 5-083 Edmonton Clinic Health Academy, 11405 87 Avenue NW, Edmonton, AB T6G 1C9, Canada; Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2E1, Canada; Department of Cell Biology, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada; Multiple Sclerosis Centre and Department of Cell Biology, Faculty of Medicine & Dentistry, Edmonton, AB T6G 2H7, Canada. Electronic address: voronova@ualberta.ca.
 Neuroimaging Innovation Center, Barrow Neurological Institute, Phoenix, Arizona, USA. Neuroimaging Innovation Center, Barrow Neurological Institute, Phoenix, Arizona, USA. Ivy Brain Tumor Center, Barrow Neurological Institute, Phoenix, Arizona, USA. Department of Neurology, Barrow Neurological Institute, Phoenix, Arizona, USA. Department of Neuroradiology, Barrow Neurological Institute, Phoenix, Arizona, USA. Neuroimaging Innovation Center, Barrow Neurological Institute, Phoenix, Arizona, USA.
 Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, NJ, United States. Department of Neurology, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, United States. Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, NJ, United States. Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, NJ, United States. Kessler Foundation, East Hanover, NJ, United States. Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Rutgers University, Newark, NJ, United States. Department of Psychiatry, University of Illinois at Chicago, Chicago, IL, United States. Department of Psychiatry, University of Illinois at Chicago, Chicago, IL, United States. Kessler Foundation, East Hanover, NJ, United States. Department of Physical Medicine and Rehabilitation, New Jersey Medical School, Rutgers University, Newark, NJ, United States.
 Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Electronic address: gaoh3535@gmail.com. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000 Odense, Denmark. Department of Orthopaedic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150001, China. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Joint and Trauma Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000 Odense, Denmark; Department of Neurology, Odense University Hospital, 5000 Odense, Denmark; BRIDGE - Brain Research - Inter-Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, 5000 Odense, Denmark. Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000 Odense, Denmark; BRIDGE - Brain Research - Inter-Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, 5000 Odense, Denmark; The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33161, USA. Electronic address: rbrambilla@med.miami.edu. Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China; Guangdong Provincial Center for Engineering and Technology Research of Minimally Invasive Spine Surgery, Guangzhou 510630, China. Electronic address: ronglm@mail.sysu.edu.cn.
 Department of Organic Chemistry, University of Chemical Technology and Metallurgy, Sofia 1756, Bulgaria. Department of Organic Chemistry, University of Chemical Technology and Metallurgy, Sofia 1756, Bulgaria. Department of Pharmacology, Pharmacotherapy and Toxicology, Faculty of Pharmacy, Medical University, Sofia 1000, Bulgaria. Department of Pharmacology, Pharmacotherapy and Toxicology, Faculty of Pharmacy, Medical University, Sofia 1000, Bulgaria. Department of Medical Chemistry and Biochemistry, Faculty of Medicine, Medical University, Sofia 1000, Bulgaria. Institute of Organic Chemistry with Centre of Phytochemistry, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria. Institute of Organic Chemistry with Centre of Phytochemistry, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria. QSAR and Molecular Modelling Department, Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria. QSAR and Molecular Modelling Department, Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria.
 Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, 901 Blockley, 423 Guardian Drive, Philadelphia, PA, 19104, USA. Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Center for Drug Safety and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA. Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. margo@pennmedicine.upenn.edu. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, 901 Blockley, 423 Guardian Drive, Philadelphia, PA, 19104, USA. margo@pennmedicine.upenn.edu.
 Infection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, Kaifeng, 475000, China. School of Medicine, Nankai University, Tianjin, 300071, China. Infection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, Kaifeng, 475000, China. Infection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, Kaifeng, 475000, China. Infection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, Kaifeng, 475000, China. Infection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, Kaifeng, 475000, China. jpwangchina@henu.edu.cn.
 Sydney School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia. Electronic address: suzanne.mate@sydney.edu.au. Sydney School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia. Sydney School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia. Sydney School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia; Sydney Medical School, The University of Sydney, Sydney, Australia; Hinda and Arthur Marcus Institute for Aging Research, Hebrew SeniorLife, Boston, MA. Sydney School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia. Sydney School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
 Department of Computer Science and Engineering, Shanghai Jiao Tong University, Shanghai, China. Department of Ophthalmology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Department of Computing, The Hong Kong Polytechnic University, Kowloon, Hong Kong SAR, China. School of Design, The Hong Kong Polytechnic University, Kowloon, Hong Kong SAR, China. School of Computing, Gachon University, Seongnam, Republic of Korea. Biomedical and Multimedia Information Technology Research Group, School of Computer Science, The University of Sydney, Sydney, NSW, Australia. Biomedical and Multimedia Information Technology Research Group, School of Computer Science, The University of Sydney, Sydney, NSW, Australia. Department of Computer Science and Engineering, Shanghai Jiao Tong University, Shanghai, China. Biomedical and Multimedia Information Technology Research Group, School of Computer Science, The University of Sydney, Sydney, NSW, Australia. MIRALab, University of Geneva, Geneva, Switzerland. Shanghai University of Sport, Shanghai, China. Department of Computer Science and Engineering, Shanghai Jiao Tong University, Shanghai, China.
 Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China; Medical Examination Center, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Guangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, Guangdong 510632, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China. Department of Neurology, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China. Electronic address: wanglq5@mail.sysu.edu.cn.
 Multiple Sclerosis Center of Catalonia, Department of Neurology-Neuroimmunology, Vall d'Hebron University Hospital, 08035 Barcelona, Spain. Multiple Sclerosis Center of Catalonia, Department of Neurology-Neuroimmunology, Vall d'Hebron University Hospital, 08035 Barcelona, Spain. Multiple Sclerosis Center of Catalonia, Department of Neurology-Neuroimmunology, Vall d'Hebron University Hospital, 08035 Barcelona, Spain. Multiple Sclerosis Center of Catalonia, Department of Neurology-Neuroimmunology, Vall d'Hebron University Hospital, 08035 Barcelona, Spain. Multiple Sclerosis Center of Catalonia, Department of Neurology-Neuroimmunology, Vall d'Hebron University Hospital, 08035 Barcelona, Spain.
 Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain. Electronic address: gsolerenrique@gmail.com. Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain. Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain. Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain. Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain. Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain.
 Faculty of Medicine, Department of Neurology, Ondokuz Mayıs University, Samsun, Turkey. Faculty of Medicine, Department of Physiology, Ondokuz Mayıs University, Samsun, Turkey. Cerrahpasa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Neurology Department, Sancaktepe Şehit Prof. Dr. Ilhan Varank Research and Training Hospital, Istanbul, Turkey. Faculty Of Pharmacy, Department Of Pharmaceutical Microbiology, Bezmialem Vakıf University, Istanbul, Turkey. Istanbul Faculty of Medicine, Department of Neurology, Istanbul University, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Katip Celebi University, Izmir, Turkey. Faculty of Medicine, Department of Neurology, Selçuk University, Konya, Turkey. Department of Neurology, Istanbul Bakırkoy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Education and Research Hospital, Istanbul, Turkey. Cerrahpasa Faculty of Medicine, Department of Medical Microbiology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Dokuz Eylül University, Izmir, Turkey. Department of Neurology, Istanbul Bakırkoy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Education and Research Hospital, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Kocaeli University, İzmit/Kocaeli, Turkey. Cerrahpasa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Neurology Department, Sancaktepe Şehit Prof. Dr. Ilhan Varank Research and Training Hospital, Istanbul, Turkey. Department of Neurosciences, Dokuz Eylül University, Institute of Health Sciences, Izmir, Turkey. Faculty of Medicine, Department of Neurology, Haccettepe University, Ankara, Turkey. Faculty of Medicine, Department of Neurology, Uludag University, Bursa, Turkey. Cerrahpasa Faculty of Medicine, Department of Hematology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Cerrahpasa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Istanbul Faculty of Medicine, Department of Neurology, Istanbul University, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Katip Celebi University, Izmir, Turkey. Neurology Department, Sancaktepe Şehit Prof. Dr. Ilhan Varank Research and Training Hospital, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Uludag University, Bursa, Turkey. Faculty of Medicine, Department of Neurology, Karadeniz Technical University, Trabzon, Turkey. Faculty of Medicine, Department of Neurology, Ondokuz Mayıs University, Samsun, Turkey. Faculty of Medicine, Department of Neurology, Haccettepe University, Ankara, Turkey. Cerrahpasa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Haccettepe University, Ankara, Turkey. Cerrahpasa Faculty of Medicine, Department of Microbiology, Istanbul University-Cerrahpasa, Istanbul, Turkey. Faculty of Medicine, Department of Neurology, Kocaeli University, İzmit/Kocaeli, Turkey. Faculty of Medicine, Department of Biostatistics and Medical Informatics, Akdeniz University, Antalya, Turkey. Cerrahpasa Faculty of Medicine, Department of Neurology, Istanbul University-Cerrahpasa, Istanbul, Turkey.
 Department of Neurology, Neurology Clinic of Kepez State Hospital, Antalya, Turkey. Electronic address: eelifuygur@gmail.com. Neuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Unidad de Investigacion para la Generacion y Sintesis de Evidencia en Salud, Universidad San Ignacio de Loyola, Vicerrectorado de Investigacion, Lima, Peru. Istanbul Bakirkoy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Training and Research Hospital, Clinic of Neurology and Neurosurgery, Istanbul, Turkey. Neuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Istanbul Bakirkoy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Training and Research Hospital, Clinic of Neurology and Neurosurgery, Istanbul, Turkey. Neuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
 Faculty of Nursing and Health Sciences, Nord University, Bodø, Norway. Department of Biostatistics, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Physiotherapy Department, Nordland Hospital Trust, Bodø, Norway. Faculty of Nursing and Health Sciences, Nord University, Bodø, Norway. Faculty of Nursing and Health Sciences, Nord University, Bodø, Norway. Faculty of Nursing and Health Sciences, Nord University, Bodø, Norway. Faculty of Nursing and Health Sciences, Nord University, Bodø, Norway. Physiotherapy Department, Nordland Hospital Trust, Bodø, Norway. Faculty of Nursing and Health Sciences, Nord University, Bodø, Norway.
 Department of Neurology, Renmin Hospital, Wuhan University, Wuhan, China. Department of Neurology, Renmin Hospital, Wuhan University, Wuhan, China.
 Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea. Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea. Department of Medical Biotechnology, Inje University, Gimhae, Republic of Korea. Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
 Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technische Univesität Dresden, Fetscherstr. 74, 01307, Dresden, Germany. Else Kröner-Fresenius Center for Digital Health, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany. Else Kröner-Fresenius Center for Digital Health, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technische Univesität Dresden, Fetscherstr. 74, 01307, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technische Univesität Dresden, Fetscherstr. 74, 01307, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technische Univesität Dresden, Fetscherstr. 74, 01307, Dresden, Germany. tjalf.ziemssen@uniklinikum-dresden.de.
 Father Muller Medical College Hospital South Carolina Dept of Mental Health
 Mayo Clinic Mayo Clinic
 Kasralainy Hospital/Cairo University Rawalpindi Medical University Mery Fitzgerald Hospital
 Jackson Memorial Hospital
 Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India. Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India. Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India. Institute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, India.
 School of Life and Environmental Sciences and the Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia. School of Life and Environmental Sciences and the Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia.
 Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: ilana.katzsand@mssm.edu. Precision Immunology Institute, Human Immune Monitoring Center, Icahn School of Medicine at Mount Sinai, USA; Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Vaccine Research and Pandemic Preparedness (C-VARPP), Icahn School of Medicine at Mount Sinai, New York, NY, USA. Precision Immunology Institute, Human Immune Monitoring Center, Icahn School of Medicine at Mount Sinai, USA. Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Vaccine Research and Pandemic Preparedness (C-VARPP), Icahn School of Medicine at Mount Sinai, New York, NY, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Center for Vaccine Research and Pandemic Preparedness (C-VARPP), Icahn School of Medicine at Mount Sinai, New York, NY, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Precision Immunology Institute, Human Immune Monitoring Center, Icahn School of Medicine at Mount Sinai, USA; Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
 Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, 55131, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, 55131, Germany. Section of Neuroradiology, Department of Radiology (IDI), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, 08035 Barcelona, Spain. Section of Neuroradiology, Department of Radiology (IDI), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, 08035 Barcelona, Spain. Department of Neurology/Neuroimmunology, Multiple Sclerosis Centre of Catalonia, Hospital Universitari Vall d'Hebron, 08035 Barcelona, Spain. Division of Radiology and Nuclear Medicine, Oslo University Hospital, 0424 Oslo, Norway. Institute of Clinical Medicine, University of Oslo, NO-0316 Oslo, Norway. Department of Neurology, Oslo University Hospital, 0424 Oslo, Norway. Institute of Clinical Medicine, University of Oslo, NO-0316 Oslo, Norway. Department of Neurology, Oslo University Hospital, 0424 Oslo, Norway. Institute of Neuroradiology, St Josef Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. Institute of Neuroradiology, St Josef Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. Department of Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Department of Neurosciences, San Camillo-Forlanini Hospital, 00152 Rome, Italy. Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, 121 08 Prague, Czech Republic. Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital, 121 08 Prague, Czech Republic. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, 55131, Germany. Department of Neuroradiology, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Department of Neuroinflammation, Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, WC1E 6BT London, UK. Department of Neuroinflammation, Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, WC1E 6BT London, UK. Department of Neurology, Medical Faculty, Heinrich-Heine-University, 40225 Düsseldorf, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, 55131, Germany. Department of Neuroinflammation, Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, WC1E 6BT London, UK. Department of Radiology and Nuclear Medicine, Amsterdam UMC, 1100 DD Amsterdam, Netherlands. Department of Neuroinflammation, Queen Square MS Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Science, University College of London, WC1E 6BT London, UK. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, 55131, Germany.
 Center for Neuroimaging, Department of Radiology, General Hospital of Northern Theater Command, Shenyang, China. College of Medicine and Biological Information Engineering, Northeastern University, Shenyang, China.
 Department of Radiology, Haeundae-Paik Hospital, Inje University, College of Medicine, Busan, Korea. Department of Neurology, Haeundae-Paik Hospital, Inje University, College of Medicine, Busan, Korea. neurof@naver.com. Department of Radiology, Haeundae-Paik Hospital, Inje University, College of Medicine, Busan, Korea. Department of Neurology, Busan-Paik Hospital, Inje University, College of Medicine, Busan, Korea.
 Department of Neurological Surgery, Weill Cornell Medicine/New York Presbyterian Hospital, New York, New York, USA. Electronic address: joseph.carnevale.md@gmail.com. Department of Neurological Surgery, Weill Cornell Medicine/New York Presbyterian Hospital, New York, New York, USA.
 GF Ingrassia Department, Otolaryngology, University of Catania, 95124 Catania, Italy. Multiple Sclerosis Center, Neurology Department, Wayne State University, Detroit, MI 48202, USA. GF Ingrassia Department, Otolaryngology, University of Catania, 95124 Catania, Italy. Otolaryngology Department, Michigan University, Ann Arbor, MI 48109, USA. Department of Sense Organs, La Sapienza University, 00185 Rome, Italy. Oro-Maxillo-Facial Department, University of Sassari, 07100 Sassari, Italy. Department of Sense Organs, La Sapienza University, 00185 Rome, Italy. Department of Sense Organs, La Sapienza University, 00185 Rome, Italy. Department of Neurology, University La Sapienza, 00185 Rome, Italy. Distinguished Senior Fellows (Sabbatical), Laboratory of Neuroimmunology of Professor Lawrence Steinman, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Sense Organs, La Sapienza University, 00185 Rome, Italy. Distinguished Senior Fellows (Sabbatical), Laboratory of Neuroimmunology of Professor Lawrence Steinman, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Neurology, University La Sapienza, 00185 Rome, Italy.
 Department of Neurology, Brooke Army Medical Center, Fort Sam Houston, Texas, USA. Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Neurology, Vita-Salute San Raffaele University, Milano, Italy. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Neurology, Mass General Brigham Inc, Boston, Massachusetts, USA. Department of Neurology, Mayo Clinic, Jacksonville, Forida, USA. Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of pediatrics, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA flanagan.eoin@mayo.edu. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
 Department of Neurology, Referral Center for Autonomic Nervous System Disorders, University Hospital Centre Zagreb, 10000 Zagreb, Croatia. Department for Functional Genomics, Center for Translational and Clinical Research, University of Zagreb School of Medicine, University Hospital Centre Zagreb, 10000 Zagreb, Croatia. Department for Anatomy and Clinical Anatomy, University of Zagreb School of Medicine, 10000 Zagreb, Croatia. Department for Functional Genomics, Center for Translational and Clinical Research, University of Zagreb School of Medicine, University Hospital Centre Zagreb, 10000 Zagreb, Croatia. Department of Neurology, University Hospital Centre Zagreb, 10000 Zagreb, Croatia. Division of Molecular Medicine, Rudjer Bošković Institute, 10002 Zagreb, Croatia. Department of Experimental Neurodegeneration, Centre for Biostructural Imaging of Neurodegeneration, University Medical Centre Göttingen, 37075 Göttingen, Germany. Max Planck Institute for Experimental Medicine, 37075 Göttingen, Germany. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Framlington Place, Newcastle upon Tyne NE1 7RU, UK. German Centre for Neurodegenerative Diseases (DZNE), 17475 Göttingen, Germany. Department for Functional Genomics, Center for Translational and Clinical Research, University of Zagreb School of Medicine, University Hospital Centre Zagreb, 10000 Zagreb, Croatia. Department of Neurology, University Hospital Centre Zagreb, 10000 Zagreb, Croatia. Department of Neurology, University Hospital Centre Zagreb, 10000 Zagreb, Croatia.
 Laboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. Laboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. Laboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. Neurotoxin Research Group, School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. Department of Biomedical and Biotechnological Sciences, Section of Anatomy, Histology and Movement Science, School of Medicine, University of Catania, Via S. Sofia n°97, 95123 Catania, Italy. School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia. Laboratory of Cellular and Molecular Neuroscience (LCMN), School of Life Sciences, Faculty of Science, University of Technology Sydney, P.O. Box 123, Broadway, Sydney, NSW 2007, Australia.
 Biological Science Department, College of Science, King Faisal University, P.O. Box 400, Al-Ahsa 31982, Saudi Arabia. Botany and Microbiology Department, Faculty of Science, Beni-Suef University, Beni-Suef 62511, Egypt. Biological Science Department, College of Science, King Faisal University, P.O. Box 400, Al-Ahsa 31982, Saudi Arabia. Molecular Biology Division, Pondicherry Centre for Biological Sciences and Educational Trust, Pondicherry 605004, India. Camel Research Center, King Faisal University, P.O. Box 400, Al-Ahsa 31982, Saudi Arabia. Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, Al-Ahsa 31982, Saudi Arabia. Department of Pharmacognosy, Faculty of Pharmacy, Minia University, Minia 61519, Egypt.
 Neurorehabilitation Research Laboratory, Department of Neurological and Rehabilitation Sciences, IRCCS San Raffaele Roma, 00163 Rome, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148 Milan, Italy. Department of Biomedical and Neuromotor Sciences (DIBINEM), Alma Mater University of Bologna, 40138 Bologna, Italy. Unit of Occupational Medicine, IRCCS Azienda Ospedaliero-Universitaria di Bologna, 40138 Bologna, Italy. Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy. Headache Science & Neurorehabilitation Center, IRCCS Mondino Foundation, 27100 Pavia, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148 Milan, Italy. Laboratory of Healthcare Innovation Technology, IRCCS San Camillo Hospital, 30126 Venice, Italy. Neurorehabilitation Research Laboratory, Department of Neurological and Rehabilitation Sciences, IRCCS San Raffaele Roma, 00163 Rome, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148 Milan, Italy. Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy. Headache Science & Neurorehabilitation Center, IRCCS Mondino Foundation, 27100 Pavia, Italy. IRCCS Istituto delle Scienze Neurologiche di Bologna, 40139 Bologna, Italy. IRCCS Bonino-Pulejo, 98124 Messina, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148 Milan, Italy. Neurorehabilitation Research Laboratory, Department of Neurological and Rehabilitation Sciences, IRCCS San Raffaele Roma, 00163 Rome, Italy. Department of Human Sciences and Promotion of the Quality of Life, San Raffaele University, 00166 Rome, Italy.
 Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Phystech School of Biological and Medical Physics, Moscow Institute of Physics and Technology (National Research University), 141701 Dolgoprudny, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Phystech School of Biological and Medical Physics, Moscow Institute of Physics and Technology (National Research University), 141701 Dolgoprudny, Russia. Federal Research and Clinical Center of Physical-Chemical Medicine of Federal Medical Biological Agency, 119435 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia. Department of Biological Chemistry, Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russian Federation, 127473 Moscow, Russia. Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
 Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China. Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China. Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China. School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China. Chinese Academy of Sciences (CAS) Key Laboratory of Quantitative Engineering Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China. Clinical Oncology Center, Shenzhen Key Laboratory for Cancer Metastasis and Personalized Therapy, The University of Hong Kong-Shenzhen Hospital, Shenzhen 518055, China. Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Sun Yat-Sen University, Guangzhou 510120, China. Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China. Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
 From the Queen Square MS Centre (Y.L.), UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, UK; Multiple Sclerosis Centre of Catalonia (C.T.), Neurology Department, Vall d'Hebron Barcelona Hospital Campus, Spain. yael@doctors.net.uk. From the Queen Square MS Centre (Y.L.), UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, UK; Multiple Sclerosis Centre of Catalonia (C.T.), Neurology Department, Vall d'Hebron Barcelona Hospital Campus, Spain.
 Department of Biostatistics, Institute of Cell Biology and Biophysics, Leibniz University Hannover, Herrenhäuser Straße 2, 30419, Hannover, Germany. fneish@cell.uni-hannover.de. German MS-Register, MS Forschungs- und Projektentwicklungs- gGmbH [MSFP], Krausenstraße 50, 30171, Hannover, Germany. fneish@cell.uni-hannover.de. German MS-Register, MS Forschungs- und Projektentwicklungs- gGmbH [MSFP], Krausenstraße 50, 30171, Hannover, Germany. German MS-Register, MS Forschungs- und Projektentwicklungs- gGmbH [MSFP], Krausenstraße 50, 30171, Hannover, Germany. German MS-Register, MS Forschungs- und Projektentwicklungs- gGmbH [MSFP], Krausenstraße 50, 30171, Hannover, Germany. Faculty III-Media, Information, and Design, Hochschule Hannover, 30539, Hannover, Germany. Department of Biostatistics, Institute of Cell Biology and Biophysics, Leibniz University Hannover, Herrenhäuser Straße 2, 30419, Hannover, Germany.
 Laboratory of Neuroimmunology, Federal Center of Brain Research and Neurotechnology of the Federal Medical-Biological Agency of Russia, Moscow, Russia. Laboratory of Neuroimmunology, Federal Center of Brain Research and Neurotechnology of the Federal Medical-Biological Agency of Russia, Moscow, Russia. Laboratory of Neuroimmunology, Federal Center of Brain Research and Neurotechnology of the Federal Medical-Biological Agency of Russia, Moscow, Russia; Laboratory of Molecular Pharmacology and Immunology, Institute of Biochemistry and Genetics - Subdivision of the Ufa Federal Research Center of the Russian Academy of Science, Ufa, Russia. Laboratory of Neuroimmunology, Federal Center of Brain Research and Neurotechnology of the Federal Medical-Biological Agency of Russia, Moscow, Russia; Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University, Moscow, Russia; Laboratory of Clinical Immunology, National Research Center Institute of Immunology of the Federal Medical-Biological Agency of Russia, Moscow, Russia. Electronic address: medikms@yandex.ru.
 Department of Pharmaceutics, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Shivarathreeshwara Nagara, Mysuru 570015, India. Department of Pharmaceutics, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Shivarathreeshwara Nagara, Mysuru 570015, India. Department of Pharmaceutics, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Shivarathreeshwara Nagara, Mysuru 570015, India. School of Pharmacy, Sri Balaji Vidyapeeth (Deemed to be University), Puducherry 607402, India.
 Institute of Pharmacy, Freie Universität Berlin, Königin-Luise-Str. 2 + 4, 14195 Berlin, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany. Department of Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany. German Center for Neurodegenerative Diseases (DZNE), 10117 Berlin, Germany. Department of Psychiatry and Psychotherapy, School of Medicine, Technical University Munich, 81675 Munich, Germany. UK Dementia Research Institute (UK DRI), University of Edinburgh, Edinburgh EH16 4SB, UK. Department of Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany. Department of Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany. Experimental and Clinical Research Center, a Cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), 13125 Berlin, Germany. Institute of Pharmacy, Freie Universität Berlin, Königin-Luise-Str. 2 + 4, 14195 Berlin, Germany.
 Departments of Ophthalmology (YG, Y Liu, Yifan Zhang, HX, YT, Y Li, KM, Yiteng Zhang, SM, QC, MZ), Ophthalmology and Research Laboratory of Ophthalmology (YG) and Neurology (Y Lang, HZ), West China Hospital, Sichuan University, Chengdu, China; and Department of Ophthalmology (YG, Y Liu, Yifan Zhang, HX, YT, Y Li, KM, Yiteng Zhang, SM, QC, MZ), West China School of Medicine, Sichuan University, Chengdu, China.
 Department of Rehabilitation Medicine, University of Washington, Seattle, Washington, DC, USA. The Sports Institute at UW Medicine, Seattle, Washington, DC, USA. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington, DC, USA. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington, DC, USA. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington, DC, USA. The Sports Institute at UW Medicine, Seattle, Washington, DC, USA.
 Department of Medical Psychology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Amsterdam Neuroscience Research Institute, Amsterdam, The Netherlands. Amsterdam Public Health Research Institute, Amsterdam, The Netherlands. Department of Rehabilitation Medicine, Amsterdam UMC Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Amsterdam Public Health Research Institute, Amsterdam, The Netherlands. Department of Epidemiology and Data Science, Amsterdam UMC Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Medical Psychology, Amsterdam UMC Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Medical Psychology, Amsterdam UMC Location University of Amsterdam, Amsterdam, The Netherlands. Amsterdam Public Health Research Institute, Amsterdam, The Netherlands. Department of Rehabilitation Medicine, Amsterdam UMC Location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. MS Center Amsterdam, Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.
 Department Institute of Speech and Hearing, Madras Medical College, Chennai, India. Department of Audiology, School of Rehabilitation and Behavioral Sciences, Vinayaka Mission's Research Foundation, Aarupadai Veedu Medical College and Hospital Campus, Puducherry, India. Department of Neurology, Tamil Nadu Government Multi Super Specialty Hospital, Chennai, India.
 Arcadia University, Glenside, Pennsylvania (E.T.C.); University of Washington, Seattle (P.N.M.); Departments of Health Care Sciences and Neurology, Wayne State University, Detroit, Michigan (N.E.F.); University of California San Francisco/San Francisco State University, San Francisco (D.D.A.); University of Michigan-Flint, Flint (A.M.Y.); Samuel Merritt University, Oakland, California (G.L.W.); Rutgers University Libraries, New Brunswick, New Jersey (S.T.J.); and Tufts University, Seattle, Washington, (K.P.).
 School of Medicine, UCD, Belfield, Dublin 4, Ireland; Department of Radiology, St Vincent's University Hospital, Dublin 4, Ireland; School of Computer Science and Insight Centre, UCD Belfield, Dublin 4, Ireland. Electronic address: brendan.kelly@ucdconnect.ie. Multiple Sclerosis Ireland National Office, 80 Northumberland Road, Dublin 4, Ireland. School of Computer Science and Insight Centre, UCD Belfield, Dublin 4, Ireland. School of Education, Trinity College Dublin, Dublin 2, Ireland. Department of Radiology, St Vincent's University Hospital, Dublin 4, Ireland. Department of Radiology, St Vincent's University Hospital, Dublin 4, Ireland. School of Medicine, UCD, Belfield, Dublin 4, Ireland.
 Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom. Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom. Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom. Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom. Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom. The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, United Kingdom. Centre for Experimental Medicine, Queen's University Belfast, Belfast, United Kingdom. Faculty of Medicine and Health, The University of Sydney, Darlington, NSW, Australia. The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, United Kingdom. School of Medicine, UK Dementia Research Institute Cardiff and Systems Immunity Research Institute, Cardiff University, Cardiff, United Kingdom. Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom. Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom.

 Biostatistics Unit, Department of Health Sciences, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Biostatistics Unit, Department of Health Sciences, University of Genoa, Genoa, Italy. Biostatistics Unit, Department of Health Sciences, University of Genoa, Genoa, Italy. Department of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, MA. Department of Anatomy and Neuroscience, VU University Medical Center, Amsterdam, The Netherlands. Department of Medicine Surgery and Neuroscience, University of Siena, Siena, Italy.
 Department of Neurology, University of Health Sciences Ankara City Hospital, Ankara, Turkey. Department of Neurology, Private Hatem Hospital, Gaziantep, Turkey. Department of Biomedical Engineering, TOBB University of Economics and Technology, Ankara, Turkey.
 Department of Pharmacy, Chia Nan University of Pharmacy and Science, Tainan City, 71710, Taiwan. Department of Nursing, Al-Maarif University College, Anbar, Iraq. Electronic address: Hussain.riyad@uoa.edu.iq. Department of Anesthesia Techniques, AlSafwa University College, Karbala, Iraq; Department of Biochemistry, Faculty of Medicine, University of Kerbala, 56001, Karbala, Iraq. Civil Engineering Department, College of Engineering, King Khalid University, Abha 61421, Saudi Arabia. Department of computer engineering technology, Al Kitab University, Altun Kopru, Kirkuk 00964, Iraq. College of Pharmacy, Al- Mustaqbal University, 51001 Hilla, Babylon, Iraq. Collage of Pharmacy, National University of Science and Technology, Dhi Qar, Iraq. Refrigeration and Air Conditioning Technical Engineering Department, College of Technical Engineering, The Islamic University, Najaf, Iraq. Department of Applied Chemistry, South Tehran Branch, Islamic Azad University, Tehran, Iran. Electronic address: naghmeh_alikahi@yahoo.com.
 Biogen, Cambridge, MA, USA. Biogen Canada, Toronto, Ontario, Canada. Rewoso AG, Zürich, Switzerland. Rewoso AG, Zürich, Switzerland. Rewoso AG, Zürich, Switzerland. Biogen International GmbH, Baar, Switzerland. Biogen, Cambridge, MA, USA. Biogen Spain, Madrid, Spain. Department of Biomedical Data Science, , Stanford, CA, USAStanford University. RINGGOLD: 6429 NeuroTransData, Neuburg an der Donau, Germany. NeuroTransData, Neuburg an der Donau, Germany.
 Department of Physical Therapy (H.G.), Rocky Mountain University of Health Professions, Provo, Utah; Easterseals Massachusetts (C.R.), Worcester; Rocky Mountain University Foundation Community Rehabilitation Clinic (J.L., B.H.), Provo, Utah; and Rocky Mountain University of Health Professions (E.G., J.D.), Provo, Utah.

 Psicología de la Salud, Suportias, Madrid, Spain. Facultad de Medicina, Universidad Francisco de Vitoria, Madrid, Spain. Facultad de Ciencias de la Salud, Universidad Internacional de Valencia, Valencia, Spain. Facultad de Medicina, Universidad Francisco de Vitoria, Madrid, Spain. Facultad de Ciencias de la Salud, Universidad Internacional de Valencia, Valencia, Spain. Facultad de Medicina, Universidad Francisco de Vitoria, Madrid, Spain.
 Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia. Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia.
 Integrative Research Center, Miami, FL, USA. Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Assam, India. Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Assam, India. Inflammation Research Center, San Diego, CA, USA.
 Department of Chemistry, Institute of Conju-Probe, San Diego, California, USA. Department of Chemistry, Bharath University, Chennai, Tamil Nadu, 600126, India.
 UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Veronique.Miron@unityhealth.to. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Veronique.Miron@unityhealth.to. Barlo Multiple Sclerosis Centre, St Michael's Hospital, Toronto, Ontario, Canada. Veronique.Miron@unityhealth.to. Keenan Research Centre for Biomedical Science, St Michael's Hospital, Toronto, Ontario, Canada. Veronique.Miron@unityhealth.to. Department of Immunology, The University of Toronto, Toronto, Ontario, Canada. Veronique.Miron@unityhealth.to.
 Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK. e.anestis@mdx.ac.uk. Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK. Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK. Division of Health Research, Faculty of Health and Medicine, Lancaster University, Lancaster, UK.
 Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35233, USA. Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
 Department of Neurology, School of Medicine, Juntendo University, Tokyo, Japan. Department of Neurology, School of Medicine, Juntendo University, Tokyo, Japan. Department of Neurology, School of Medicine, Juntendo University, Tokyo, Japan. Department of Neurology, School of Medicine, Juntendo University, Tokyo, Japan. Department of Biomedical Sciences, Sassari University, Sassari, Italy. Department of Neurology, School of Medicine, Juntendo University, Tokyo, Japan. Tousei Center for Neurological Diseases, Shizuoka, Japan. Department of Neurology, School of Medicine, Juntendo University, Tokyo, Japan.
 Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306, USA. Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306, USA. Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306, USA.
 Centre International de Recherche en Infectiologie, Équipe d'Oncogenèse Rétrovirale, INSERM U1111 - Université Claude Bernard Lyon 1, CNRS, UMR 5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France. Equipe Labellisée par la Fondation pour la Recherche Médicale, Labex Ecofect, Lyon, France. Centre International de Recherche en Infectiologie, Team Enveloped Viruses, Vectors and Immunotherapy INSERM U1111 - Université Claude Bernard Lyon 1, CNRS, UMR 5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France. The Lyon Immunotherapy for Cancer Laboratory (LICL), Centre de Recherche en Cancérologie de Lyon (CRCL, UMR INSERM 1052 - CNRS 5286) Centre Léon Bérard, Lyon, France. Centre International de Recherche en Infectiologie Équipe Neuro-Invasion, Tropism and Viral Encephalitis, INSERM U1111 - Université Claude Bernard Lyon 1, CNRS, UMR 5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France. Centre International de Recherche en Infectiologie, Équipe d'Oncogenèse Rétrovirale, INSERM U1111 - Université Claude Bernard Lyon 1, CNRS, UMR 5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France. Equipe Labellisée par la Fondation pour la Recherche Médicale, Labex Ecofect, Lyon, France.
 Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden. Electronic address: samir.el-andaloussi@ki.se.
 Department of Chinese Medicine, Gaoxin Branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Neurology, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Neurology, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Neurology, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Neurology, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Pharmacy, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Neurology, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China. Department of Neurology, Gaoxin branch of the First Affiliated Hospital of Nanchang University, Nanchang 330000, China.
 Department of Mesenchymal Stem Cells, Center for Education, Culture and Research [ACECR], Qom Branch, Qom, Iran. Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran. Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran. Department of Medical Laboratory Sciences, Khomein University of Medical Sciences, Khomein, Iran. Department of Mesenchymal Stem Cells, Center for Education, Culture and Research [ACECR], Qom Branch, Qom, Iran. Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran. Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran.
 The First Affiliated Hospital of Yangtze University, Jingzhou 434000, Hubei, China. The First Affiliated Hospital of Yangtze University, Jingzhou 434000, Hubei, China. The First Affiliated Hospital of Yangtze University, Jingzhou 434000, Hubei, China. Electronic address: chengxianglin@yangtzeu.edu.cn.
 Faculty of Medicine, University of Geneva, Geneva, Switzerland. Faculty of Medicine, University of Geneva, Geneva, Switzerland. Division of Neurology, Department of Clinical Neuroscience, Geneva University Hospitals, Geneva, Switzerland. Faculty of Medicine, University of Geneva, Geneva, Switzerland. Division of Neurology, Department of Clinical Neuroscience, Geneva University Hospitals, Geneva, Switzerland.
 Multiple Sclerosis Lead Nurse, University Hospital Southampton NHS Foundation Trust.
 UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA. Stephen.Hauser@ucsf.edu. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB) and MS Center, and Departments of Medicine, Clinical Research, Biomedicine and Biomedical Engineering, University Hospital of Basel, University of Basel, Basel, Switzerland. Center for Neuroinflammation and Experimental Therapeutics and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Sheffield Institute of Translational Neuroscience, Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, UK. Joi Life Wellness Multiple Sclerosis Neurology Center, Atlanta, GA, USA. Department of Neurology, St Josef-Hospital/Ruhr-University Bochum, Bochum, Germany. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Department of Neurology, Barzilai Medical Center, Ashkelon/Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Univ. Lille, INSERM U1172 LilNCog, CHU Lille, FHU Precise, 59000, Lille, France.
 Aventura Hospital & Medical Center Istituto Nazionale Tumori - IRCCS - Fondazione Pascale, Via Mariano Semmola 80100, Napoli. Italy

 Department of Cardiology, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang 314000, P.R. China. Department of Gastroenterology, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang 314000, P.R. China. Department of Cardiology, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang 314000, P.R. China. Department of Infectious Diseases, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang 314000, P.R. China.
 Department of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Neurosurgery, Union Hospital, Huazhong University of Science and Technology, Jiefang Avenue No. 1277, 430022, Wuhan, China. Department of Neurosurgery, Union Hospital, Huazhong University of Science and Technology, Jiefang Avenue No. 1277, 430022, Wuhan, China. Department of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Department of Neurosurgery, Union Hospital, Huazhong University of Science and Technology, Jiefang Avenue No. 1277, 430022, Wuhan, China. Department of Neurology, Union Hospital, Huazhong University of Science and Technology, Jiefang Avenue No. 1277, 430022, Wuhan, China. Biophysics Department, Biological Faculty, Moscow State University, Moscow, Russia. Department of Medical Genetics, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. liudan_echo@mail.hust.edu.cn. Department of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. zhulq@mail.hust.edu.cn.
 West Virginia University School of Medicine Henry Ford Hospital McLaren Oakland Hosp - Michigan State Un
 M& J Western Regional Institute of Ophthalmology, Civil Hospital, Ahmedabad, India. M& J Western Regional Institute of Ophthalmology, Civil Hospital, Ahmedabad, India. Department of Pediatric Ophthalmology and Strabismus, M & J Western Regional Institute of Ophthalmology, Civil Hospital, Ahmedabad, India.
 University of Miami/Jackson Memorial Hospital University of Puerto Rico, Medical Sciences Campus, Neurosurgery Section
 Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA. Electronic address: NARULAS@chop.edu.
 Department of Neurology, Shiga University of Medical Science.
 King Faisal University Kaiser Permanente Medical Center

 Department of Clinical Psychology and Psychological Therapies, Norwich Medical School, University of East Anglia, Norwich, UK. Department of Clinical Psychology and Psychological Therapies, Norwich Medical School, University of East Anglia, Norwich, UK. Department of Clinical Psychology and Psychological Therapies, Norwich Medical School, University of East Anglia, Norwich, UK. Department of Clinical Psychology and Psychological Therapies, Norwich Medical School, University of East Anglia, Norwich, UK.
 Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia. Department of Chemistry, Faculty of Science, Albaha University, Albaha, Saudi Arabia. Department of Physiology, Neuroscience Unit, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia. Pre-Clinical Research Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia. Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia. Vitamin D Pharmacogenomics Research Group, King Abdulaziz University, Jeddah, Saudi Arabia. Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia. Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia. Pre-Clinical Research Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia. Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia. Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia. Princess Dr. Najla Bint Saud Al-Saud Center for Excellence Research in Biotechnology, King Abdulaziz University, Jeddah, Saudi Arabia.
 Krembil Research Institute, University Health Network, Toronto, ON M5T 0S8, Canada. Krembil Research Institute, University Health Network, Toronto, ON M5T 0S8, Canada. Krembil Research Institute, University Health Network, Toronto, ON M5T 0S8, Canada. Departments of Chemistry and Medicine, University of Toronto, Toronto, ON M5S 3M2, Canada.
 Maharajgunj Medical Campus Penn State College of Medicine
 Department of Laboratory Medicine and Pathobiology. Department of Laboratory Medicine and Pathobiology. Department of Laboratory Medicine and Pathobiology. Department of Laboratory Medicine and Pathobiology; Department of Immunology, University of Toronto, Toronto M5S 1A8, Ontario, Canada. Electronic address: stephen.girardin@utoronto.ca.
 Cognitive and Memory Disorders Clinic, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. ALS Clinical Research Center, Laboratory of Neurochemistry, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. ALS Clinical Research Center, Laboratory of Neurochemistry, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. vincenzo.labella@unipa.it. ALS Clinical Research Center, Laboratory of Neurochemistry, Department of Biomedicine, Neurosciences and Advanced Diagnosis, University of Palermo, via Gaetano La Loggia, 1, Palermo, I-90129, Italy. vincenzo.labella@unipa.it. Central Laboratory of Advanced Diagnosis and Biomedical Research, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. Central Laboratory of Advanced Diagnosis and Biomedical Research, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. Multiple Sclerosis Clinic, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. Central Laboratory of Advanced Diagnosis and Biomedical Research, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy. ALS Clinical Research Center, Laboratory of Neurochemistry, AOUP "Paolo Giaccone" University Teaching Hospital and BiND, University of Palermo, Palermo, Italy.
 School of Medicine, European University Cyprus, 6 Diogenous Str., 2404 Nicosia, Cyprus. School of Medicine, European University Cyprus, 6 Diogenous Str., 2404 Nicosia, Cyprus. School of Medicine, European University Cyprus, 6 Diogenous Str., 2404 Nicosia, Cyprus. School of Medicine, European University Cyprus, 6 Diogenous Str., 2404 Nicosia, Cyprus.
 Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland; MedGIFT, Institute of Informatics, School of Management, HES-SO Valais-Wallis University of Applied Sciences and Arts Western Switzerland, Sierre, Switzerland. MedGIFT, Institute of Informatics, School of Management, HES-SO Valais-Wallis University of Applied Sciences and Arts Western Switzerland, Sierre, Switzerland; Nuclear Medicine and Molecular Imaging Department, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Clinical Trial Unit, Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Ankara University School of Medicine, Ankara, Turkey. MedGIFT, Institute of Informatics, School of Management, HES-SO Valais-Wallis University of Applied Sciences and Arts Western Switzerland, Sierre, Switzerland; The Sense Research and Innovation Center, Lausanne and Sion, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. CIBM Center for Biomedical Imaging, Lausanne, Switzerland; Radiology Department, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland. Translational Imaging in Neurology (ThINK) Basel, Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel, Basel, Switzerland; Department of Neurology, University Hospital Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland. Electronic address: cristina.granziera@unibas.ch.
 Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012, Bern, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012, Bern, Switzerland. Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA. Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA. Blood-Brain Barrier Laboratory, University of Artois, Lens, France. Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012, Bern, Switzerland. Department of Neurotherapeutics, Yamaguchi University, Yamaguchi, Japan. Biogen, Cambridge, MA, USA. Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012, Bern, Switzerland. britta.engelhardt@tki.unibe.ch.
 Department of Clinical Neurological Sciences, London Health Sciences Centre, Schulich Medicine and Dentistry, Western University, London, Ontario, Canada. Department of Clinical Neurological Sciences, London Health Sciences Centre, Schulich Medicine and Dentistry, Western University, London, Ontario, Canada. Department of Clinical Neurological Sciences, London Health Sciences Centre, Schulich Medicine and Dentistry, Western University, London, Ontario, Canada. Department of Clinical Neurological Sciences, London Health Sciences Centre, Schulich Medicine and Dentistry, Western University, London, Ontario, Canada; MS Epidemiology Lab, London, Ontario, Canada. Electronic address: Juan.Racosta@lhsc.on.ca.
 Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China; School of Laboratory Medicine, Weifang Medical College, Weifang, Shandong 261053, China. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China; Medical School of Chinese PLA, Beijing 100853, China. Department of Neurology, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Department of Neurology, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Electronic address: wlyingsh@163.com. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China; School of Laboratory Medicine, Weifang Medical College, Weifang, Shandong 261053, China; Medical School of Chinese PLA, Beijing 100853, China. Electronic address: wangcbin301@163.com. Department of Laboratory Medicine, the First Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. Electronic address: liruibing@plagh.org.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States; Johns Hopkins Surgery Center for Outcomes Research, Department of Surgery, Johns Hopkins School of Medicine, Baltimore, MD, United States. Electronic address: aasemot2@jhmi.edu. Johns Hopkins Surgery Center for Outcomes Research, Department of Surgery, Johns Hopkins School of Medicine, Baltimore, MD, United States; Yale University School of Medicine, New Haven, CT, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
 Clinical School Johor Bahru, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Johor Baru, Johor, Malaysia. Clinical School Johor Bahru, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Johor Baru, Johor, Malaysia. Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. School of Science, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia. School of Dentistry and Medical Sciences, Charles Sturt University, Orange, NSW, Australia. Department of Neuroscience, Central Clinical School, Monash University, The Alfred Hospital, Melbourne, VIC, Australia. School of Science, Monash University Malaysia, Bandar Sunway, Selangor, Malaysia.
 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA. Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
 Diagnostic Imaging Department, Fleni, Montañeses, 2325 (C1428AQK), Ciudad de Buenos Aires, Argentina. hchaves@fleni.org.ar. Diagnostic Imaging Department, Fleni, Montañeses, 2325 (C1428AQK), Ciudad de Buenos Aires, Argentina. Department of Physics, University of Buenos Aires (UBA), Buenos Aires, Argentina. Physics Institute of Buenos Aires (IFIBA) CONICET, Buenos Aires, Argentina. Laboratorio de Neurociencia, Universidad Torcuato Di Tella, Buenos Aires, Argentina. ENTELAI, Buenos Aires, Argentina. Radiology Department, Diagnósticos da América SA (Dasa), Rio de Janeiro, Brazil. Diagnostic Imaging Department, Fleni, Montañeses, 2325 (C1428AQK), Ciudad de Buenos Aires, Argentina. Diagnostic Imaging Department, Fleni, Montañeses, 2325 (C1428AQK), Ciudad de Buenos Aires, Argentina. Center for Research On Neuroimmunological Diseases (CIEN), Fleni, Buenos Aires, Argentina. ENTELAI, Buenos Aires, Argentina. DasaInova, Diagnósticos da América SA (Dasa), São Paulo, São Paulo, Brazil. Diagnostic Imaging Department, Fleni, Montañeses, 2325 (C1428AQK), Ciudad de Buenos Aires, Argentina. Diagnostic Imaging Department, Fleni, Montañeses, 2325 (C1428AQK), Ciudad de Buenos Aires, Argentina. Neurology Department, Fleni, Buenos Aires, Argentina. Instituto de Investigación en Señales, Sistemas e Inteligencia Computacional, sinc(i) CONICET-UNL, Santa Fe, Argentina. Center for Research On Neuroimmunological Diseases (CIEN), Fleni, Buenos Aires, Argentina. Departamento de Computación, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina. Instituto de Investigación en Ciencias de la Computación (ICC), CONICET-UBA, Buenos Aires, Argentina. Radiology Department, Diagnósticos da América SA (Dasa), Rio de Janeiro, Brazil. Center for Research On Neuroimmunological Diseases (CIEN), Fleni, Buenos Aires, Argentina. Center for Biostatistics, Epidemiology and Public Health (CEBES), Fleni, Buenos Aires, Argentina.
 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
 Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany.
 Peninsula Schools of Medicine and Dentistry, University of Plymouth, Plymouth, UK. Electronic address: jeremy.hobart@plymouth.ac.uk. Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Division of Neurology, St Michael's Hospital, University of Toronto, Toronto, ON, Canada. LORA Group LLC, Normal, IL, USA. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, Basel, Switzerland. Acaster Lloyd Consulting Ltd, London, UK.
 Department of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha, China; Clinical Immunology Research Center of Central South University, Changsha, China. Department of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China; Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, China. Department of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China; Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, China. Clinical Immunology Research Center of Central South University, Changsha, China; Department of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China; Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, China. Electronic address: guochunchen@csu.edu.cn.
 Department of Neurosciences, Imaging and Clinical Sciences, Institute of Advanced Biomedical Technologies (ITAB), University G. d'Annunzio of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging and Clinical Sciences, Institute of Advanced Biomedical Technologies (ITAB), University G. d'Annunzio of Chieti-Pescara, Chieti, Italy. Department of Neurosciences, Imaging and Clinical Sciences, Institute of Advanced Biomedical Technologies (ITAB), University G. d'Annunzio of Chieti-Pescara, Chieti, Italy. Electronic address: valentina.tomassini@unich.it.
 Department of Immunology, College of Basic Medical Science, Dalian Medical University, Dalian, Liaoning, China. Department of Rheumatology and Immunology, Dalian Municipal Central Hospital, Dalian, Liaoning, China. Department of Immunology, College of Basic Medical Science, Dalian Medical University, Dalian, Liaoning, China. Department of Immunology, College of Basic Medical Science, Dalian Medical University, Dalian, Liaoning, China. Department of Rheumatology and Immunology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
 From the PET Imaging Program in Neurologic Diseases, Ann Romney Center for Neurologic Diseases, Department of Neurology. From the PET Imaging Program in Neurologic Diseases, Ann Romney Center for Neurologic Diseases, Department of Neurology. From the PET Imaging Program in Neurologic Diseases, Ann Romney Center for Neurologic Diseases, Department of Neurology. Division of Nuclear Medicine and Molecular Imaging, Department of Radiology. Brigham Multiple Sclerosis Center, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
 Westchester MC/New York Med. College Ochsner Health System
 Department of Neurology, North Karelia Central Hospital, Siun Sote, 80210 Joensuu, Finland. Clinical Neurosciences, Faculty of Medicine, University of Turku, 20014 Turku, Finland.
 Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts, USA. Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts, USA. Division of General Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts, USA. Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts, USA. Department of Health Policy and Management, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. Division of General Internal Medicine and Primary Care, Department of Medicine Brigham and Women's Hospital, Boston, Massachusetts, USA.
 Institute of Clinical Physiology, National Research Council (IFC-CNR), Piazza Ospedale Maggiore 3, 20159 Milano, Italy. Institute of Clinical Physiology, National Research Council (IFC-CNR), Piazza Ospedale Maggiore 3, 20159 Milano, Italy. Institute of Clinical Physiology, National Research Council (IFC-CNR), Piazza Ospedale Maggiore 3, 20159 Milano, Italy. Department of Human Sciences and Promotion of the Quality of Life, San Raffaele Roma Open University, Via di val Cannuta 247, 00166 Roma, Italy. Driatec Srl, Via Leonardo da Vinci 21/E, 20060 Cassina de' Pecchi, Italy. Department of Biomedical Sciences for Health, Università degli Studi di Milano, Via Mangiagalli 31, 20133 Milano, Italy.
 Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Center for Neuroinflammation and Experimental Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Center for Biomedical Image Computing and Analytics, Department of Radiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Penn Statistics in Imaging and Visualization Endeavor, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Center for Neuroinflammation and Experimental Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
 Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. ricardoalonsohrm@gmail.com. Servicio de Neurología, Hospital Universitario Sanatorio Guemes, Buenos Aires, Argentina. ricardoalonsohrm@gmail.com. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. Servicio de Neurología, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. Servicio de Neurología, Hospital Universitario CEMIC, CABA, Argentina. Centro de Esclerosis Múltiple, Buenos Aires, Argentina. Instituto de Neurociencias de Fundación Favaloro E INECO, Buenos Aires, Argentina. Neurology Department, Neuroimmunology Unit, Hospital de Clinicas "José de San Martín", Buenos Aires, Argentina. Centro de Esclerosis Múltiple, Buenos Aires, Argentina. MS Unit Hospital Británico Buenos Aires, Buenos Aires, Argentina. IIPBA, FFyHUCCuyo, San Juan, Argentina. Instituto de Neurociencias de Fundación Favaloro E INECO, Buenos Aires, Argentina. Hospital Austral, Buenos Aires, Argentina. Servicio de Neurología, Hospital Universitario Sanatorio Guemes, Buenos Aires, Argentina. Hospital Enrique Tornú, CABA, Argentina. INECO Neurociencias Oroño, Santa Fe, Argentina. Sanatorio Anchorena, Buenos Aires, Argentina. Centro Universitario de Esclerosis Múltiple, Hospital Ramos Mejía, Buenos Aires, Argentina. Instituto de Neurociencias Cognitivas y Traslacional (INCyT), Fundación INECO, Universidad Favaloro, CONICET, Buenos Aires, Argentina. Hospital Español de Rosario, Santa Fe, Argentina. Hospital Central de Mendoza, Mendoza, Argentina. Instituto de Neurociencias Rosario, Santa Fe, Argentina. Neuroimmunology Unit, Department of Neuroscience, Hospital Alemán, Buenos Aires, Argentina. Ecarnerocontentti@hospitalaleman.com.
 Muğla Sıtkı Koçman University, Köyceğiz Vocational School of Health Services, Department of Health Care Services, Muğla, Turkey. Ege University, Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, İzmir, Turkey. Electronic address: mehmet.ozkeskin76@gmail.com. Süleyman Demirel University, Institute of Health Sciences, Department of Physiotherapy and Rehabilitation, Isparta, Turkey. Ege University, Faculty of Medicine, Department of Neurology, İzmir, Turkey.
 Institute of Translational Immunology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Department of Applied and Health Sciences, Northumbria University, Newcastle upon Tyne, Tyne and Wear, UK. Institute for Molecular Medicine, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Department of Dermatology, University of Cologne, Koln, Germany. Institute for Molecular Medicine, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Institute for Molecular Medicine, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Institute of Translational Immunology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Institute of Translational Immunology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Institute of Translational Immunology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Department of Cardiology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Department of Neurology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Institute of Translational Immunology, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Neurology Department, University Hospital Munster, Munster, Germany. Institute for Molecular Medicine, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Neurology Department, University Hospital Munster, Munster, Germany. Institute for Molecular Medicine, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Research Center for Immunotherapy, Johannes Gutenberg Universitat Mainz, Mainz, Germany. Institute of Translational Immunology, Johannes Gutenberg Universitat Mainz, Mainz, Germany Detlef.Schuppan@unimedizin-mainz.de. Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
 Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Preventive Medicine and Public Health, University Hospital Complex of Santiago de Compostela, Santiago de Compostela, Spain. Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain alejandro.riverodeaguilar@gmail.com. Department of Neurology, University Hospital Complex of Pontevedra, Pontevedra, Spain. Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (Instituto de Investigación Sanitaria de Santiago de Compostela - IDIS), Santiago de Compostela, Spain. Consortium for Biomedical Research in Epidemiology and Public Health (CIBER en Epidemiología y Salud Pública/CIBERESP), Madrid, Spain. Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (Instituto de Investigación Sanitaria de Santiago de Compostela - IDIS), Santiago de Compostela, Spain. Consortium for Biomedical Research in Epidemiology and Public Health (CIBER en Epidemiología y Salud Pública/CIBERESP), Madrid, Spain. Department of Neurology, Central University Hospital of Asturias, Oviedo, Spain. Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (Instituto de Investigación Sanitaria de Santiago de Compostela - IDIS), Santiago de Compostela, Spain. Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain. Health Research Institute of Santiago de Compostela (Instituto de Investigación Sanitaria de Santiago de Compostela - IDIS), Santiago de Compostela, Spain. Consortium for Biomedical Research in Epidemiology and Public Health (CIBER en Epidemiología y Salud Pública/CIBERESP), Madrid, Spain.
 Faculty of Health, Physical Activity, Sport and Exercise Research (PASER) Theme, Southern Cross University, Hogbin Drive, Coffs Harbour, NSW 2450, Australia. Electronic address: christopher.stevens@scu.edu.au. Faculty of Health, Physical Activity, Sport and Exercise Research (PASER) Theme, Southern Cross University, Hogbin Drive, Coffs Harbour, NSW 2450, Australia. School of Health, Medical and Applied Sciences, Central Queensland University, Rockhampton, QLD, Australia. School of Medicine and Psychology, Australian National University, Canberra ACT, Australia. Research Institute for Sport and Exercise, University of Canberra, Canberra ACT, Australia.
 Department of Ophthalmology, University Hospital Magdeburg, Magdeburg, Germany. Department of Neurology, University Hospital Magdeburg, Magdeburg, Germany. Department of Ophthalmology, University Hospital Magdeburg, Magdeburg, Germany. Department of Neurology, University Hospital Magdeburg, Magdeburg, Germany. Department of Neurology, University Hospital Magdeburg, Magdeburg, Germany. Department of Neurology, University Hospital Magdeburg, Magdeburg, Germany. Department of Ophthalmology, University Hospital Magdeburg, Magdeburg, Germany. Department of Neurology, University Hospital Magdeburg, Magdeburg, Germany. Department of Ophthalmology, University Hospital Magdeburg, Magdeburg, Germany. Center for Behavioral Brain Sciences, Magdeburg, Germany.

 Neurology, University of Illinois College of Medicine, Chicago, IL, United States. Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL, United States. High Performance Biological Computing, and Roy J Carver Biotechnology Center, University of Illinois, Champaign, IL, United States. High Performance Biological Computing, and Roy J Carver Biotechnology Center, University of Illinois, Champaign, IL, United States. Neurology, University of Illinois College of Medicine, Chicago, IL, United States. Neurology, University of Illinois College of Medicine, Chicago, IL, United States. Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL, United States. Neurology, Jesse Brown Veterans Administration Hospital, Chicago, IL, United States.
 Department of Business Administration, Business School, Al al-Bayt University, Mafraq, Jordan. Department of Nursing, Al-maarif University College, Ramadi, Al-Anbar, Iraq. Department of Pharmaceutical Chemistry, College of Pharmacy, University of Mosul, Mosul, Iraq. Department of Anatomy, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia. Master's Programme Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia. Andrology Program, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia. Dr. Soetomo General Academic Hospital, Surabaya, Indonesia. Tashkent Medical Academy, Tashkent, Uzbekistan. College of Dentistry, Al-Ayen University, Thi-Qar, Iraq. Department of Medical Laboratory Sciences, College of Applied Medical Sciences, Majmaah University, Majmaah, Saudi Arabia. Medical Technical College, Al-Farahidi University, Baghdad, Iraq. College of Pharmacy, The Islamic University, Najaf, Iraq. College of Technical Engineering, Imam Ja'afar Al-Sadiq University, Al-Muthanna, Iraq.
 Department of Chemistry, Texas A&M University, College Station, TX, USA. Department of Chemistry, Texas A&M University, College Station, TX, USA. andythomas@tamu.edu.
 Grupo de Investigación en Neurociencias (NEUROS), Escuela de Medicina Y Ciencias de La Salud, Universidad del Rosario, Bogotá, Colombia. alejadelatorre@yahoo.com. Center For Research in Genetics and Genomics-CIGGUR, GENIUROS Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Colombia. Grupo de Investigación en Neurociencias (NEUROS), Escuela de Medicina Y Ciencias de La Salud, Universidad del Rosario, Bogotá, Colombia. Escuela Superior de Oftalmología, Instituto Barraquer de América, Bogotá, Colombia. Center For Research in Genetics and Genomics-CIGGUR, GENIUROS Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Colombia. Escuela Superior de Oftalmología, Instituto Barraquer de América, Bogotá, Colombia. Grupo de Investigación en Neurociencias (NEUROS), Escuela de Medicina Y Ciencias de La Salud, Universidad del Rosario, Bogotá, Colombia. Grupo de Investigación en Neurociencias (NEUROS), Escuela de Medicina Y Ciencias de La Salud, Universidad del Rosario, Bogotá, Colombia. Escuela Superior de Oftalmología, Instituto Barraquer de América, Bogotá, Colombia. Grupo de Investigación en Neurociencias (NEUROS), Escuela de Medicina Y Ciencias de La Salud, Universidad del Rosario, Bogotá, Colombia. INPAC Research Group, Fundación Universitaria Sanitas, Bogotá, Colombia. Center For Research in Genetics and Genomics-CIGGUR, GENIUROS Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Colombia. Center For Research in Genetics and Genomics-CIGGUR, GENIUROS Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Colombia. Grupo de Investigación en Psiquiatría (GIPSI), Departamento de Psiquiatría, Instituto de Investigaciones Medicas (IIM), Facultad de Medicina, Universidad de Antioquia, Medellin, Colombia.
 UCLA-Caltech Medical Scientist Training Program; Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Electronic address: nspivak@mednet.ucla.edu. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Internal Medicine, Kirk Kerkorian SOM, UNLV, 4505 South Maryland Parkway, Las Vegas, NV 89154, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Molecular, Cell and Developmental Biology, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA. Department of Psychiatry and Biobehavioral Sciences, DGSOM, UCLA, 300 UCLA Medical Plaza, Suite 2200, Los Angeles, CA 90095, USA.
 Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, Rishikesh, Dehradun, IND. Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, Rishikesh, Dehradun, IND. Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, Rishikesh, Dehradun, IND. Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, Rishikesh, Dehradun, IND. Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, Rishikesh, Dehradun, IND.
 Center for Movement Studies, Kennedy Krieger Institute, Baltimore, MD; Physical Medicine and Rehabilitation, Johns Hopkins School of Medicine, Baltimore, MD; Department of Health Care Sciences, Wayne State University, Detroit, MI; Department of Neurology, Wayne State University, Detroit, MI; Translational Neuroscience Program, Wayne State University, Detroit, MI. Electronic address: nora.fritz@wayne.edu. Department of Health Care Sciences, Wayne State University, Detroit, MI; Translational Neuroscience Program, Wayne State University, Detroit, MI. Electronic address: eedwards@med.wayne.edu. School of Information and Electronics, Beijing Institute of Technology, Beijing, China. Electronic address: chuyang.ye@bit.edu.cn. Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD. Electronic address: prince@jhu.edu. Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD. Electronic address: zyang11@jhu.edu. School of Medicine, Tulane University, New Orleans, LA. Electronic address: tgressett@tulane.edu. Center for Movement Studies, Kennedy Krieger Institute, Baltimore, MD. Electronic address: keller@kennedykrieger.org. Department of Health Care Sciences, Wayne State University, Detroit, MI. Electronic address: em.myers27@wayne.edu. Department of Neurology, Johns Hopkins University, Baltimore, MD; Department of Neuroscience, Johns Hopkins University, Baltimore, MD. Electronic address: pcalabr1@jhmi.edu. Center for Movement Studies, Kennedy Krieger Institute, Baltimore, MD; Physical Medicine and Rehabilitation, Johns Hopkins School of Medicine, Baltimore, MD; Department of Neurology, Johns Hopkins University, Baltimore, MD. Electronic address: kathleen.zackowski@nmss.o.
 Service de pharmacologie clinique, Département des laboratoires, Centre hospitalier universitaire vaudois, 1011 Lausanne. Service de pharmacologie clinique, Département des laboratoires, Centre hospitalier universitaire vaudois, 1011 Lausanne.
 College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. College of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
 Department of Neurology, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Korea. Department of Neurology, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Korea. Department of Neurology, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Korea. Department of Neurology, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Korea.
 School of Medicine, Eastern Virginia Medical School, Norfolk, VA 23507, USA. Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA 23507, USA. Independent Researcher, Norfolk, VA 23510, USA.


 Altos Labs, Cambridge Institute of Science, Cambridge, UK. Altos Labs, Cambridge Institute of Science, Cambridge, UK. Altos Labs, Cambridge Institute of Science, Cambridge, UK.
 Deptartment of Radiology, Lahey Hospital and Medical Center, Burlington, MA. Electronic address: Mara.M.Kunst@lahey.org. Deptartment of Radiology, Lahey Hospital and Medical Center, Burlington, MA. Deptartment of Radiology, Lahey Hospital and Medical Center, Burlington, MA. Deptartment of Radiology, Lahey Hospital and Medical Center, Burlington, MA. Deptartment of Radiology, Lahey Hospital and Medical Center, Burlington, MA.
 Department of Neurology, New York University Grossman School of Medicine, New York, NY, United States. Department of Neurology, New York University Grossman School of Medicine, New York, NY, United States.
 Mercy Catholic Medical Center UNC school of Medicine, Atrium Health
 Long Island Jewish Medical Center/Northwell Health Yale University Long Island Jewish Medical Center
 Human Pathophysiology and Translational Medicine Program, Institute for Translational Sciences, University of Texas Medical Branch, Galveston, TX 77555-5302, USA. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555-5302, USA. Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA 22903-2628, USA. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555-5302, USA. Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA 22903-2628, USA. Institute of Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX 77555-5302, USA. Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555-5302, USA.
 4D4ALL Lab, Department of Rehabilitation Sciences and Physiotherapy, Center for Health and Technology (CHaT), Faculty of Medicine and Health Sciences, University of Antwerp, 2000 Antwerpen, Belgium. 4D4ALL Lab, Department of Rehabilitation Sciences and Physiotherapy, Center for Health and Technology (CHaT), Faculty of Medicine and Health Sciences, University of Antwerp, 2000 Antwerpen, Belgium. 4D4ALL Lab, Department of Rehabilitation Sciences and Physiotherapy, Center for Health and Technology (CHaT), Faculty of Medicine and Health Sciences, University of Antwerp, 2000 Antwerpen, Belgium. 4D4ALL Lab, Department of Rehabilitation Sciences and Physiotherapy, Center for Health and Technology (CHaT), Faculty of Medicine and Health Sciences, University of Antwerp, 2000 Antwerpen, Belgium. 4D4ALL Lab, Department of Rehabilitation Sciences and Physiotherapy, Center for Health and Technology (CHaT), Faculty of Medicine and Health Sciences, University of Antwerp, 2000 Antwerpen, Belgium. 4D4ALL Lab, Department of Rehabilitation Sciences and Physiotherapy, Center for Health and Technology (CHaT), Faculty of Medicine and Health Sciences, University of Antwerp, 2000 Antwerpen, Belgium.
 Institute of Pharmacology, Biochemical Pharmacological Center, University of Marburg, 35043 Marburg, Germany. Institute of Pharmacology, Biochemical Pharmacological Center, University of Marburg, 35043 Marburg, Germany. Institute of Pharmacology, Biochemical Pharmacological Center, University of Marburg, 35043 Marburg, Germany. Institute of Pharmacology, Biochemical Pharmacological Center, University of Marburg, 35043 Marburg, Germany.
 Amity Institute of Biotechnology, Amity University Uttar Pradesh, Lucknow Campus, Gomti Nagar Extension, Lucknow 226028, India. Amity Institute of Biotechnology, Amity University Uttar Pradesh, Lucknow Campus, Gomti Nagar Extension, Lucknow 226028, India. Amity Institute of Biotechnology, Amity University Uttar Pradesh, Lucknow Campus, Gomti Nagar Extension, Lucknow 226028, India. Department of Microbiology, Dr. Ram Manohar Lohia Institute of Medical Sciences, Vibhuti Khand, Lucknow 226010, India. Department of Microbiology, Dr. Ram Manohar Lohia Institute of Medical Sciences, Vibhuti Khand, Lucknow 226010, India. Department of Chemistry, Faculty of Pharmacy, Medical University, Sofia 1000, Bulgaria.
 Department of Health Sciences and Biostatistics, School of Health Sciences, Swinburne University of Technology, John Street, Hawthorn, VIC, 3022, Australia. jxiao@swin.edu.au.
 University College London, United Kingdom. Electronic address: khaled.alkhuder@hotmail.com.
 Department of Neurology, University Hospital of Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital of Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital of Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital of Basel and University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital of Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital of Basel and University of Basel, Basel, Switzerland.
 Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Germany; Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, TU Dresden, Germany. Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Germany; Cognitive Psychology, Faculty of Psychology, Shandong Normal University, Jinan, China. Electronic address: christian.beste@uniklinikum-dresden.de. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, TU Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, TU Dresden, Germany. Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Germany; Cognitive Psychology, Faculty of Psychology, Shandong Normal University, Jinan, China. Electronic address: christian.beste@uniklinikum-dresden.de.
 Department of Molecular Biology, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, 40-055 Katowice, Poland. Department of Molecular Biology, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, 40-055 Katowice, Poland. Department of Molecular Biology, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, 40-055 Katowice, Poland. Department of Molecular Biology, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, 40-055 Katowice, Poland. Department of Molecular Biology, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, 40-055 Katowice, Poland.
 Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. IRCCS San Raffaele, 00166 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy. IRCCS San Raffaele, 00166 Rome, Italy. Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy.
 Global Medical Safety, Biogen, Cambridge, MA, USA. Drug Safety, Pharmacovigilance & Systems & Data Analytics, Biogen, Cambridge, MA, USA. Global Medical Safety, Biogen, Cambridge, MA, USA. Global Medical Safety, Biogen, Cambridge, MA, USA. Global Medical, Biogen, Cambridge, MA, USA. Biostatistics, Biogen, Cambridge, MA, USA. Biostatistics, Biogen, Cambridge, MA, USA. Global Medical, Biogen, Baar, Switzerland. Development, Biogen, Cambridge, MA, USA. Safety and Benefit Risk Management, Biogen, Cambridge, MA, USA.
 BIOLONG Corporation, USA. Electronic address: info@inmunyvital.com. BIOLONG Corporation, USA. BIOLONG Corporation, USA. BIOLONG Corporation, USA.
 Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile. Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile. Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States. Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile. Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile. Molecular Neurobiology, Department of Psychiatry & Psychotherapy, Ludwig-Maximilians-University of Munich, Munich, Germany. Center for Integrative Biology, Faculty of Science, Universidad Mayor, Santiago, Chile. Center for Integrative Biology, Faculty of Science, Universidad Mayor, Santiago, Chile. Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile. Department of Clinical Immunology and Rheumatology , School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile. Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States. Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States. Molecular Neurobiology, Department of Psychiatry & Psychotherapy, Ludwig-Maximilians-University of Munich, Munich, Germany. Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile. Central Institute of Mental Health, Faculty of Medicine, University of Heidelberg, Mannheim, Germany. Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile.
 Department of Neurology, Hospital Universitario Ramón y Cajal, Madrid, Spain. Medical Department, Roche Farma, Madrid, Spain. Department of Neurology, Hospital Universitario Donostia, San Sebastián, Spain. Department of Neurology, Hospital Universitario Virgen Macarena, Sevilla, Spain. Department of Neurology, Hospital Universitario Miguel Servet, Zaragoza, Spain. Department of Neurology, Hospital Universitari Vall d´Hebrón, Barcelona, Spain. Department of Neurology, Hospital Regional Universitario de Málaga, Málaga, Spain. Department of Neurology, Complejo Asistencial de Ávila, Ávila, Spain. Department of Neurology, Hospital Universitario Fundación Alcorcón, Alcorcón, Spain. Department of Neurology, Hospital de Galdakao-Usansolo, Galdakao, Spain. Department of Neurology, Hospital Universitario Clínico San Cecilio, Granada, Spain. Department of Neurology, Hospital Universitari Son Espases, Palma de Mallorca, Spain. Department of Neurology, Hospital Universitari Arnau de Vilanova, Lleida, Spain. Department of Neurology, Hospital Universitario Puerta de Hierro, Madrid, Spain. Department of Neurology, Hospital Universitario Virgen Macarena, Sevilla, Spain. Department of Neurology, Complexo Hospitalario Universitario de Pontevedra, Pontevedra, Spain. Department of Neurology, Hospital General Universitario de Elche, Elche, Spain. Department of Neurology, Hospital Universitario Reina Sofía, Córdoba, Spain. Department of Neurology, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain. Department of Neurology, Fundació Salut Empordà, Figueres, Spain. Department of Neurology, Hospital Francesc de Borja, Gandía, Spain. Department of Neurology, Hospital Universitario Puerta del Mar, Cádiz, Spain. Department of Neurology, Consorci Corporació Sanitària Parc Taulí, Sabadell, Spain. Medical Department, Roche Farma, Madrid, Spain.
 Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland; Graduate School for Health Sciences, University of Bern, Mittelstrasse 43, 3012 Bern, Switzerland. Electronic address: Nadine.Patt@kliniken-valens.ch. Division of Performance and Health (Sports Medicine), Institute for Sport and Sport Science, TU Dortmund University, Otto-Hahn-Straße 3, 44227 Dortmund, Germany. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland. Rehabilitation Research Laboratory 2rLab, Department of Business Economics, Health and Social Care, University of Applied Sciences and Arts of Southern Switzerland, Via Violino 11, 6928 Manno, Switzerland. Institute of Medical Statistics and Computational Biology, Medical Faculty and University Hospital of Cologne, University of Cologne, Robert-Koch-Straße 10, 50931 Cologne, Germany. Division of Performance and Health (Sports Medicine), Institute for Sport and Sport Science, TU Dortmund University, Otto-Hahn-Straße 3, 44227 Dortmund, Germany. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland. Graduate School for Health Sciences, University of Bern, Mittelstrasse 43, 3012 Bern, Switzerland; Department of Health Science, Institute of Sport Science, University of Bern, Bremgartenstrasse 145, 3012 Bern, Switzerland. Division of Performance and Health (Sports Medicine), Institute for Sport and Sport Science, TU Dortmund University, Otto-Hahn-Straße 3, 44227 Dortmund, Germany. Department of Neurology, Clinics of Valens, Rehabilitation Centre Valens, Taminaplatz 1, 7317 Valens, Switzerland; Department of Health, Physiotherapy, OST - Eastern Swiss University of Applied Sciences, Rosenbergstrasse 59, 9001 St.Gallen, Switzerland.
 Department of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar. ah.haghighi@hsu.ac.ir. Department of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar. amin.ahmadi83@gmail.com. Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University, Naples. carotenuto.antonio87@gmail.com. Department of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar. r.askari@hsu.ac.ir. Department of Neurology, Mashhad University of Medical Sciences, Mashhad. nikkhahk@mums.ac.ir. Department of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar. b.bagherzadehrahmani@hsu.ac.ir. Department of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar. h.shahrabadi@gmail.com. College of Physical Education and Dance, Federal University of Goias, Goiania. daniel_souza86@hotmail.com. ) College of Physical Education and Dance, Federal University of Goias, Goiania, Brazil; Hypertension League, Federal University of Goias, Goiania. paulogentil@hotmail.com.
 Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Von-Siebold-Straße 3a, D-37075 Göttingen, Germany. The Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg, Germany. Drug Discovery & Medicinal Chemistry, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, United Kingdom. The Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Von-Siebold-Straße 3a, D-37075 Göttingen, Germany. The Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Von-Siebold-Straße 3a, D-37075 Göttingen, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Von-Siebold-Straße 3a, D-37075 Göttingen, Germany; Department of Neurology, University Medical Center Göttingen, Robert-Koch-Straße 40, D-37075 Göttingen, Germany. Drug Discovery & Medicinal Chemistry, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, United Kingdom. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Von-Siebold-Straße 3a, D-37075 Göttingen, Germany. The Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg, Germany. Electronic address: guse@uke.de. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Von-Siebold-Straße 3a, D-37075 Göttingen, Germany. Electronic address: fluegel@med.uni-goettingen.de.
 Department of Nutrition, Dietetics, and Food, School of Clinical Sciences, Monash University, Notting Hill, VIC 3168, Australia. Department of Oncology, Sunshine Coast Hospital and Health Service, Birtinya, QLD 4575, Australia. School of Medicine and Dentistry, Griffith University, Birtinya, QLD 4575, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Diabetes and Vascular Medicine, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC 3168, Australia. Department of Oncology, Monash Health, Clayton, VIC 3168, Australia. Department of Clinical Research, Faculty of Medicine, University of Bern, 3012 Bern, Switzerland.
 Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. UCIBIO-Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. UCIBIO-Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. UCIBIO-Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. iNOVA4Health, LS4Future, NOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM), Universidade Nova de Lisboa, 1150-082 Lisboa, Portugal. iNOVA4Health, LS4Future, NOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM), Universidade Nova de Lisboa, 1150-082 Lisboa, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. UCIBIO-Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. UCIBIO-Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Unit of Anatomy, Department of Biomedicine, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal. Center for Health Technology and Services Research (CINTESIS), Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal. LAQV-REQUIMTE, Laboratory of Applied Chemistry, Department of Chemical Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. UCIBIO-Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal.
 Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. University MS Center Hasselt, Pelt, Belgium. Neuro-Immune Connections and Repair Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. VIB Laboratory of Translational Immunomodulation, VIB Center for Inflammation Research, Hasselt University, Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. VIB Laboratory of Translational Immunomodulation, VIB Center for Inflammation Research, Hasselt University, Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. Department of Oncology, Laboratory of Lipid Metabolism and Cancer, LKI - Leuven Cancer Institute, KU Leuven - University of Leuven, Leuven, Belgium. Department of Molecular Cell Biology and Immunology, Amsterdam University Medical Center, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, MS Center Amsterdam, Amsterdam, The Netherlands. Center for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, The Netherlands. Department of Biochemistry, Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, USA. Institute of Molecular Biosciences, University of Graz, Graz, Austria. BioTechMed-Graz, Graz, Austria. BioTechMed-Graz, Graz, Austria. Institute of Organic Chemistry, Graz University of Technology, Graz, Austria. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. University MS Center Hasselt, Pelt, Belgium. Neuro-Immune Connections and Repair Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. Department of Molecular Cell Biology and Immunology, Amsterdam University Medical Center, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, MS Center Amsterdam, Amsterdam, The Netherlands. Center for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, The Netherlands. Department of Oncology, Laboratory of Lipid Metabolism and Cancer, LKI - Leuven Cancer Institute, KU Leuven - University of Leuven, Leuven, Belgium. University MS Center Hasselt, Pelt, Belgium. Neuro-Immune Connections and Repair Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Maastricht University, Maastricht, The Netherlands. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. VIB Laboratory of Translational Immunomodulation, VIB Center for Inflammation Research, Hasselt University, Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. University MS Center Hasselt, Pelt, Belgium. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. jeroen.bogie@uhasselt.be. University MS Center Hasselt, Pelt, Belgium. jeroen.bogie@uhasselt.be.
 Department of Biomedical Engineering, City University of Hong Kong, Hong Kong, China. Department of Biomedical Engineering, City University of Hong Kong, Hong Kong, China. Department of Biomedical Engineering, City University of Hong Kong, Hong Kong, China. Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China. Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Biomedical Engineering, City University of Hong Kong, Hong Kong, China. Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Hong Kong Centre for Cerebro-Cardiovascular Health Engineering (COCHE), Hong Kong, China. City University of Hong Kong Shenzhen Research Institute, Shenzhen, China. Tung Biomedical Science Centre, City University of Hong Kong, Hong Kong, China.
 Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Hospital Universitari Vall d'Hebron, Spain. Universitat Autònoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Hospital Universitari Vall d'Hebron, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain. Neurology-Neuroimmunology Department Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron Barcelona Hospital Campus, Vall d´Hebron Institut de Recerca. Universitat Autònoma de Barcelona, Barcelona, Spain.
 Biochemistry and Molecular Biology Laboratory, Department of Zoology, Faculty of Science, University of Delhi, Delhi, India. Biochemistry and Molecular Biology Laboratory, Department of Zoology, Faculty of Science, University of Delhi, Delhi, India. Department of Biotechnology, Delhi Technical University, Delhi, India. Department of Zoology, Ramjas College, University of Delhi, Delhi, India. Department of Zoology, Ramjas College, University of Delhi, Delhi, India. Tech Cell Innovations Private Limited, Centre for Medical Innovation and Entrepreneurship (CMIE), All India Institute of Medical Sciences, New Delhi, India. Biochemistry and Molecular Biology Laboratory, Department of Zoology, Faculty of Science, University of Delhi, Delhi, India. Electronic address: smaurya1@zoology.du.ac.in.
 Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4975, USA. Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4975, USA. Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4975, USA. Electronic address: rez@case.edu.
 Department of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, 01655, USA. Department of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, 01655, USA. Department of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, 01655, USA. Department of Pediatrics, University of Massachusetts Chan Medical School, Worcester, MA, 01655, USA. hong.zhang@umassmed.edu.


 Department of Medicine, Universitat Autònoma de Barcelona (UAB), Bellaterra, Spain. Liver Unit, Internal Medicine Department, Hospital Universitari Vall d'Hebron, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Servei de Neurologia. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Grup d'Investigació Multidisciplinari d'Infermeria, Vall d'Hebron Institut de Recerca (VHIR), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Servei de Neurologia. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Medicina Preventiva i Epidemiologia. Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Servei de Neurologia. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Medicine, Universitat Autònoma de Barcelona (UAB), Bellaterra, Spain. Liver Unit, Internal Medicine Department, Hospital Universitari Vall d'Hebron, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain. Department of Medicine, Universitat Autònoma de Barcelona (UAB), Bellaterra, Spain. mar.riveiro@gmail.com. Liver Unit, Internal Medicine Department, Hospital Universitari Vall d'Hebron, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. mar.riveiro@gmail.com. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain. mar.riveiro@gmail.com.
 Department of Traditional Pharmacy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Traditional Pharmacy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
 UCB Pharma, Slough SL1 3WE, UK. Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter EX1 2LU, UK. Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter EX1 2LU, UK. UCB Pharma, Slough SL1 3WE, UK. Bioimaging Unit, University of Exeter, Geoffrey Pope Building, Exeter EX4 4QD, UK. NeuroResource, UCL Queen Square Institute of Neurology, London WC1N 1PJ, UK. Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter EX1 2LU, UK. Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter EX1 2LU, UK. Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter EX1 2LU, UK. UCB Pharma, Slough SL1 3WE, UK. Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter EX1 2LU, UK. Revolo Biotherapeutics, New Orleans, LA 70130, USA.
 Collaborative Antwerp Psychiatric Research Institute (CAPRI), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium; Scientific Initiative of Neuropsychiatric and Psychopharmacological Studies (SINAPS), University Psychiatric Centre Campus Duffel, Duffel, Belgium. Electronic address: livia.depicker@uantwerp.be. Collaborative Antwerp Psychiatric Research Institute (CAPRI), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium; Scientific Initiative of Neuropsychiatric and Psychopharmacological Studies (SINAPS), University Psychiatric Centre Campus Duffel, Duffel, Belgium. Center for Behavioral Sciences and Mental Health, Istituto Superiore di Sanità, Roma, Italy. Department of Psychiatry, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Department of Biofunctional Imaging, Preeminent Medical Photonics Education & Research Center, Hamamatsu University School of Medicine, Hamamatsu, Japan. LC Campbell Cognitive Neurology Unit, Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada. Clinical Neurosciences, Clinical and Experimental Sciences School, Faculty of Medicine, University of Southampton, UK. Division of Medical Sciences, University of Victoria, Victoria, BC, Canada; Centre for Advanced Materials and Related Technology (CAMTEC), University of Victoria, BC, Canada; Neurology and Neurosurgery Department, McGill University, Montréal, QC, Canada; Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, BC, Canada. Université Paris-Saclay, Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Orsay, France. Université Paris-Saclay, Inserm, CNRS, CEA, Laboratoire d'Imagerie Biomédicale Multimodale Paris-Saclay (BioMaps), Orsay, France; Université Paris-Saclay, UNIACT, Neurospin, CEA, Gif-sur-Yvette, France. LC Campbell Cognitive Neurology Unit, Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada.
 Institute for Implementation Science in Health Care, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Neurocentre, Lucerne Cantonal Hospital, Lucerne, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Switzerland. Institute for Implementation Science in Health Care, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Department of Neurology, Schulthess Klinik, Zurich, Switzerland. Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland. Institute for Implementation Science in Health Care, University of Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Switzerland.
 Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Graduate School of Systemic Neurosciences, Ludwig-Maximilians-Universität München, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Division of Transfusion Medicine, Cell Therapeutics and Haemostaseology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. martin.kerschensteiner@med.uni-muenchen.de. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. martin.kerschensteiner@med.uni-muenchen.de. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. martin.kerschensteiner@med.uni-muenchen.de. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. naoto.kawakami@med.uni-muenchen.de. Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Martinsried, Germany. naoto.kawakami@med.uni-muenchen.de.
 Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. Bristol Myers Squibb, Princeton, New Jersey, USA. Department of Neurology, Center for Neuroinflammation, and Experimental Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany. Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia. Department of Neurology, Medical University of Vienna, Vienna, Austria. Palacký University Olomouc, Olomouc, Czech Republic. Bristol Myers Squibb, Princeton, New Jersey, USA. Bristol Myers Squibb, Princeton, New Jersey, USA. Bristol Myers Squibb, Princeton, New Jersey, USA. Bristol Myers Squibb, Princeton, New Jersey, USA. Bristol Myers Squibb, Princeton, New Jersey, USA. Bristol Myers Squibb, Princeton, New Jersey, USA. Bristol Myers Squibb, Princeton, New Jersey, USA.
 Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. Medical Laboratory Technology Department, College of Medical Technology, The Islamic University, Najaf 54001, Iraq. Medical Laboratory Department, Kufa Institute, Al-Furat Al-Awsat Technical University, Najaf 54001, Iraq. Iraqi Education Ministry, Najaf 54001, Iraq. Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. Cognitive Impairment and Dementia Research Unit, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. Faculty of Medicine, University of Kufa, Kufa 54002, Iraq. Department of Chemistry, College of Science, University of Kufa, Kufa 54002, Iraq. Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. Cognitive Impairment and Dementia Research Unit, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. Department of Psychiatry, Medical University of Plovdiv, 4002 Plovdiv, Bulgaria. Research Institute, Medical University of Plovdiv, 4002 Plovdiv, Bulgaria. University of Electronic Science and Technology of China, Chengdu 611731, China.
 Laboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases, Mebabolism and Ageing, KU Leuven, Leuven, Belgium. Calcium and Bone Section, Endocrine, Diabetes and Hypertension Division, Department of Medicine Brigham and Women's Hospital, Boston, MA, USA. Population Health Program, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
 Zucker School of Medicine at Hofstra/Northwell, Unit of Neurological Surgery, Manhasset, NY, USA - maxward94@gmail.com. Unit Neurological Surgery, Vanderbilt University Medical Center, Nashville, TN, USA. Rutgers New Jersey Medical School, Newark, NJ, USA. John H. Burns Medical School, University of Hawaii at Manoa, Honolulu, HI, USA. Department of Neurological Surgery, University of California, Orange, CA, USA. Keck School of Medicine of USC, Department of Neurological Surgery, Los Angeles, CA, USA. California Institute of Technology, Pasadena, CA, USA. Department of Neurological Surgery, University of California, Orange, CA, USA. Unit of Neurological Surgery, University of California San Diego, San Diego, CA, USA. Rutgers New Jersey Medical School, Unit of Otolaryngology, Head and Neck Surgery, Newark, NJ, USA. Rutgers New Jersey Medical School, Neurological Surgery, Newark, NJ, USA.
 Ege University, Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Suat Cemile Balcioğlu Campus, İzmir, Turkey. Köyceğiz Vocational School of Health Services, Department of Health Care Services, Muğla Sıtkı Koçman University, Muğla, Turkey. Ege University, Faculty of Health Sciences, Department of Physiotherapy and Rehabilitation, Suat Cemile Balcioğlu Campus, İzmir, Turkey. Faculty of Medicine, Department of Neurology, Ege University, İzmir, Turkey.
 Klinik für Neurologie, Universitätsmedizin Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. mark.stettner@uk-essen.de. Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland. mark.stettner@uk-essen.de. Institut für Diagnostische und Interventionelle Neuroradiologie, Medizinische Hochschule Hannover, Hannover, Deutschland. Diavero Diagnosezentrum, Heidbergweg 22-24, Essen, Deutschland. Klinik für Neurologie, Universitätsmedizin Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland. Klinik für Neurologie, Universitätsmedizin Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland. Diavero Diagnosezentrum, Heidbergweg 22-24, Essen, Deutschland. Praxis für Neurologie, Psychiatrie und Psychotherapie, Bochum, Deutschland. Nervenstark Praxis für Neurologie und Psychiatrie, Essen, Deutschland. Neurologische Praxis, Neukirchen-Vluyn, Deutschland. Praxis für Neurologie, Köln, Deutschland. Radiologie am Kennedyplatz, Essen, Deutschland. Evangelische Kliniken Essen-Mitte gGmbH, Henricistraße 92, Essen, Deutschland. Radiologie der Ruhrradiologie Essen, Rüttenscheider Straße 191, Essen, Deutschland. Institut für Diagnostische und Interventionelle Radiologie und Neuroradiologie, Universitätsmedizin Essen, Essen, Deutschland. Zentrum für ambulante Neurologie, Essen, Deutschland. Radiologie am Stern, Essen, Deutschland. Klinik für Neurologie, Universitätsmedizin Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland. Radiologie und Nuklearmedizin Am Kennedyplatz, Essen, Deutschland. Diavero Diagnosezentrum, Heidbergweg 22-24, Essen, Deutschland. Dr. med. Theo Plajer & Dr. med. Heike Henrich, Fachärzte für Radiologie in Essen-Borbeck, Essen, Deutschland. Praxis für Psychotherapie, Psychiatrie und Neurologie, Drosselstraße 20, Essen, Deutschland. Neuropraxis am EKO, Virchowstraße 39, Oberhausen, Deutschland. Praxis Dr. Kytzia, Altenessener Straße 208, Essen, Deutschland. Radiologie MH, Schulstraße 13, Mülheim an der Ruhr, Deutschland. Radiologie MH, Schulstraße 13, Mülheim an der Ruhr, Deutschland. MVZ Radios, Luise-Rainer-Str. 6-10, Düsseldorf, Deutschland. Praxis Dr. Merguet, Gerichtsstraße 32, Essen-Borbeck-Mitte, Deutschland. Ruhrradiologie Essen Henricistraße, Henricistraße 40, Essen, Deutschland. Klinik für Radiologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, Münster, Deutschland. Praxis Dr. Obeid - Praktischer Arzt, Kriemhildstraße 8, Gelsenkirchen, Deutschland. Radiologie der Ruhrradiologie Essen, Rüttenscheider Straße 191, Essen, Deutschland. Ruhrradiologie Gelsenkirchen, Zum Ehrenmal 21, Gelsenkirchen, Deutschland. Dr. med. Theo Plajer & Dr. med. Heike Henrich, Fachärzte für Radiologie in Essen-Borbeck, Essen, Deutschland. Radiologische Gemeinschaftspraxis Mülheim, Schulstraße 13, Mülheim an der Ruhr, Deutschland. Radiologie MH, Schulstraße 13, Mülheim an der Ruhr, Deutschland. Evangelische Kliniken Essen-Mitte gGmbH, Henricistraße 92, Essen, Deutschland. Ruhrradiologie Essen Henricistraße, Henricistraße 40, Essen, Deutschland. Radiologie Bredeneyer Tor, Am Alfredusbad 8, Essen, Deutschland. Neuroradiologie, Alfried Krupp Krankenhaus, Rüttenscheid, Alfried-Krupp-Straße 21, Essen, Deutschland. Diavero Diagnosezentrum, Heidbergweg 22-24, Essen, Deutschland. Klinik für Neurologie, Universitätsmedizin Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland. Ruhrradiologie Essen Henricistraße, Henricistraße 40, Essen, Deutschland. Klinik für Neurologie, Universitätsmedizin Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Deutschland. Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland.
 Baylor College of Medicine, Department of Molecular Virology and Microbiology, Houston, Texas, USA. Baylor College of Medicine, Department of Pediatrics, Houston, Texas, USA. Baylor College of Medicine, Department of Pediatrics, Houston, Texas, USA. Baylor College of Medicine, Department of Pediatrics, Houston, Texas, USA.
 Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Czech Republic. Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Circuit Theory, Faculty of Electrical Engineering, Czech Technical University in Prague, Czech Republic. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic. Department of Neurology and ARTORG Center, Inselspital, Bern University Hospital, University of Bern, Switzerland.
 Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy. Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy. Department of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
 Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Clinical Chemistry, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Radiology and Nuclear Medicine, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands; Queen Square Institute of Neurology, Centre for Medical Image Computing, University College London, London, UK. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Anatomy and Neurosciences, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Clinical Chemistry, MS Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, location VUmc, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
 Massachusetts General Hospital Department of Neurology, Boston, MA, USA. RINGGOLD: 168383 Brigham and Women's Hospital Division of General Neurology, Boston, MA, USA. RINGGOLD: 571359 Massachusetts General Hospital Infectious Diseases Division, Boston, MA, USA. RINGGOLD: 551672 Massachusetts General Hospital Department of Neurology, Boston, MA, USA. RINGGOLD: 168383
 Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. kohst@ohsu.edu. Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. Aronora, Inc., Portland, OR, USA. Department of Pathology and Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA. Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA. Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA. Veterans Affairs Portland Health Care System, Portland, OR, USA. Department of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA. Department of Neurology, Oregon Health & Science University, Portland, OR, USA. Department of Biomedical Engineering, Oregon Health & Science University, 3303 S. Bond Avenue, Portland, OR, 97239, USA. Aronora, Inc., Portland, OR, USA.
 Cell and Tissue Technologies Department, Institute of Genetic and Regenerative Medicine, National Scientific Center "M.D. Strazhesko Institute of Cardiology", Clinical and Regenerative Medicine of the National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine. Laboratory of Pathophysiology and Immunology, D. F. Chebotarev Institute of Gerontology of the National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine. Cell and Tissue Technologies Department, Institute of Genetic and Regenerative Medicine, National Scientific Center "M.D. Strazhesko Institute of Cardiology", Clinical and Regenerative Medicine of the National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine. Cell and Tissue Technologies Department, Institute of Genetic and Regenerative Medicine, National Scientific Center "M.D. Strazhesko Institute of Cardiology", Clinical and Regenerative Medicine of the National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine. Department of Sensory Signaling, Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine. Department of Biomedicine and Neuroscience, Kyiv Academic University, Kyiv, Ukraine.
 Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Service de Neurologie, CHU de la Côte de Nacre, 14000, Caen, France. Unité de Biostatistiques et de Recherche Clinique, CHU de Caen-Cote de Nacre, Caen, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Service de Neurologie, CHU de la Côte de Nacre, 14000, Caen, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Service de Neurologie, CHU de la Côte de Nacre, 14000, Caen, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Service de Neurologie, CHU de la Côte de Nacre, 14000, Caen, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Unité de Recherche Clinique Côte d'azur (UR2CA), Équipe URRIS, CHU Pasteur 2, Nice, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Unité de Recherche Clinique Côte d'azur (UR2CA), Équipe URRIS, CHU Pasteur 2, Nice, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Unité de Recherche Clinique Côte d'azur (UR2CA), Équipe URRIS, CHU Pasteur 2, Nice, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Département de Neurologie, CHRU de Strasbourg Hôpital de Hautepierre, Strasbourg, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Département de Neurologie, CHRU de Strasbourg Hôpital de Hautepierre, Strasbourg, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Département de Neurologie, CHRU de Strasbourg Hôpital de Hautepierre, Strasbourg, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Département de Neurologie, CHRU de Strasbourg Hôpital de Hautepierre, Strasbourg, France. Département de Neurologie, Hôpital d'Instruction des Armées Percy, Service de Santé des Armées, Clamart, France. Département de Neurologie, Hôpital d'Instruction des Armées Percy, Service de Santé des Armées, Clamart, France. Département de Radiologie, Hôpital d'Instruction des Armées Percy, Service de Santé des Armées, Clamart, France. Département de Neurologie, Hôpital d'Instruction des Armées Percy, Service de Santé des Armées, Clamart, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP)-Département des Neurosciences, CHU Toulouse-Purpan, and Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), University of Toulouse, CNRS, INSERM, UPS, Toulouse, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP)-Département des Neurosciences, CHU Toulouse-Purpan, and Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), University of Toulouse, CNRS, INSERM, UPS, Toulouse, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP)-Département des Neurosciences, CHU Toulouse-Purpan, and Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), University of Toulouse, CNRS, INSERM, UPS, Toulouse, France. Unité de Biostatistiques et de Recherche Clinique, CHU de Caen-Cote de Nacre, Caen, France. Centre de Ressources et Compétence Sclérose en Plaques (CRCSEP), Service de Neurologie, CHU de la Côte de Nacre, 14000, Caen, France. defer-gi@chu-caen.fr.
 Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Biomedical Engineering, Yale University, New Haven, Connecticut, USA. Yale Stem Cell Center and Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut, USA. Yale Center for Analytical Sciences, Yale School of Public Health, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Repertoire Immune Medicines, Cambridge, Massachusetts, USA. Quest Diagnostics, Secaucus, New Jersey, USA. Quest Diagnostics, Secaucus, New Jersey, USA. Quest Diagnostics, Secaucus, New Jersey, USA. Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, California, USA. Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, California, USA. Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, California, USA. Department of Medicine, Division of Infectious Diseases and Global Public Health, UCSD, La Jolla, California, USA. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA. Program in Computational Biology and Bioinformatics, Yale University, New Haven, Connecticut, USA. Department of Internal Medicine. Section of Infectious Diseases, Department of Internal Medicine, and. Yale Center for Analytical Sciences, Yale School of Public Health, New Haven, Connecticut, USA. Department of Biomedical Engineering, Yale University, New Haven, Connecticut, USA. Yale Stem Cell Center and Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut, USA. Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and. Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA. Department of Neurology, and.
 Department of Neurology, Pitié-Salpêtrière University Hospital, AP-HP, Paris, France. Sorbonne University, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires Pitié Salpêtrière - Charles Foix, laboratoty of virology, Paris, France. Sorbonne University, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires Pitié Salpêtrière - Charles Foix, laboratoty of virology, Paris, France. Sorbonne Université, INSERM, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Département d'Immunologie, Assistance Publique Hôpitaux de Paris (AP-HP), Hôpital Pitié-Salpêtrière, Paris, France. Department of Neurology, Pitié-Salpêtrière University Hospital, AP-HP, Paris, France. Department of Neurology, Pitié-Salpêtrière University Hospital, AP-HP, Paris, France. Sorbonne Université, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, CIC neurosciences, Paris, France. Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, AP-HP, Hôpitaux Universitaires Pitié-Salpêtrière - Charles Foix, Département de Santé Publique, Unité de Recherche Clinique Pitié-Salpêtrière-Charles Foix, Paris, France. Sorbonne University, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Assistance Publique Hôpitaux de Paris, Hôpitaux Universitaires Pitié Salpêtrière - Charles Foix, laboratoty of virology, Paris, France. Sorbonne Université, INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, AP-HP, Hôpitaux Universitaires Pitié-Salpêtrière Charles Foix, Service de Maladies infectieuses et Tropicales, Paris, France. Department of Neurology, Pitié-Salpêtrière University Hospital, AP-HP, Paris, France celine.louapre@aphp.fr. Sorbonne Université, Paris Brain Institute - ICM, Assistance Publique Hôpitaux de Paris, Inserm, CNRS, Hôpital de la Pitié Salpêtrière, CIC neurosciences, Paris, France.
 Servicio de Radiodiagnóstico, Hospital Universitario Central de Asturias, Oviedo, Spain. Electronic address: luismartinezcamblor@gmail.com. Servicio de Radiodiagnóstico, Hospital Universitario Central de Asturias, Oviedo, Spain. Servicio de Radiodiagnóstico, Hospital Universitario Central de Asturias, Oviedo, Spain. Servicio de Radiodiagnóstico, Hospital Universitario Central de Asturias, Oviedo, Spain. Servicio de Radiodiagnóstico, Hospital Universitario Central de Asturias, Oviedo, Spain. Servicio de Radiodiagnóstico, Hospital Universitario Central de Asturias, Oviedo, Spain.
 Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. Department of Chemistry and VT Center for Drug Discovery, Virginia Tech, Blacksburg, VA 24061, USA. Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: krl2z@virginia.edu.
 Internal Medicine, Interfaith Medical Center, Brooklyn, USA. Internal Medicine, East Tennessee State University, Johnson City, USA. Internal Medicine, Saint Peter's University Hospital, New Jersey, USA. Epidemiology and Biostatistics, East Tennessee State University, Johnson City, USA. Internal Medicine, University of Illinois, Chicago, USA.
 Department of Psychiatry and Health Behavior, Augusta University Medical College of Georgia, Augusta, USA. Department of Psychiatry and Health Behavior, Augusta University Medical College of Georgia, Augusta, USA. Department of Psychiatry and Health Behavior, Augusta University Medical College of Georgia, Augusta, USA. Department of Psychiatry and Health Behavior, Augusta University Medical College of Georgia, Augusta, USA.
 Institute of Anatomy, Kiel University, 24118 Kiel, Germany. Institute of Anatomy, Kiel University, 24118 Kiel, Germany. Institute of Anatomy, Kiel University, 24118 Kiel, Germany. Institute of Anatomy, Kiel University, 24118 Kiel, Germany. Electronic address: k.hattermann@anat.uni-kiel.de.
 Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Cardiology, Jing'an District Centre Hospital of Shanghai, Fudan University, Shanghai 200040, China. Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
 Michigan State University College of Medicine/McLaren Oakland Hospital Louisiana State University School of Med
 GLA University Institute of Pharmaceutical Research Mathura India. GLA University Institute of Pharmaceutical Research Mathura India. GLA University Institute of Pharmaceutical Research Mathura India. GLA University Institute of Pharmaceutical Research Mathura India.
 Department of Neurology, Neurology and Neurophysiology Center, Vienna, Austria.
 Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia.; 2nd Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia.; Endowment Fund IMPULS, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia.; Department of Neurology, KZ a.s., Hospital Teplice, Teplice, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia. Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czechia.. Electronic address: Dana.Horakova@vfn.cz.
 Hotchkiss Brain Institute, 3330 Hospital Drive NW, Calgary, AB, Canada. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute, 3330 Hospital Drive NW, Calgary, AB, Canada. Arnie Charbonneau Cancer Institute, Calgary, AB, Canada. Department of Oncology, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute, 3330 Hospital Drive NW, Calgary, AB, Canada. vyong@ucalgary.ca. Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. vyong@ucalgary.ca. Department of Oncology, University of Calgary, Calgary, AB, Canada. vyong@ucalgary.ca.
 Department of Neurology, University of Rochester, Rochester, NY, USA. Department of Neurology, University of Rochester, Rochester, NY, USA.

 From the Center for Neuroscience and Regenerative Medicine (T.J.H.), Uniformed Services University of the Health Sciences, Bethesda; Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD; Department of Neuroinflammation (A.E.), Queen Square Multiple Sclerosis Centre, Queen Square Institute of Neurology, University College London; Centre for Medical Image Computing (A.E.), Department of Computer Science, University College London, United Kingdom. thaddeus.haight.ctr@usuhs.edu. From the Center for Neuroscience and Regenerative Medicine (T.J.H.), Uniformed Services University of the Health Sciences, Bethesda; Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD; Department of Neuroinflammation (A.E.), Queen Square Multiple Sclerosis Centre, Queen Square Institute of Neurology, University College London; Centre for Medical Image Computing (A.E.), Department of Computer Science, University College London, United Kingdom.
 Department of Clinical Neurosciences, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, United Kingdom. Department of Clinical Neurosciences, Altos Labs-Cambridge Institute of Sciences, Cambridge CB21 6GP, United Kingdom. Department of Clinical Neurosciences, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, United Kingdom. Department of Clinical Neurosciences, Altos Labs-Cambridge Institute of Sciences, Cambridge CB21 6GP, United Kingdom. Department of Clinical Neurosciences, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, United Kingdom. Department of Clinical Neurosciences, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, United Kingdom. Department of Clinical Neurosciences, Altos Labs-Cambridge Institute of Sciences, Cambridge CB21 6GP, United Kingdom. Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom. Department of Clinical Neurosciences, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, United Kingdom. Department of Clinical Neurosciences, Altos Labs-Cambridge Institute of Sciences, Cambridge CB21 6GP, United Kingdom.
 Gavin Herbert Eye Institute, UC-Irvine University of Utah University of Puerto Rico, Medical Sciences Campus, Neurosurgery Section
 Department of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. Institute of Veterinary Pharmacology and Toxicology, University of Zurich, Vetsuisse, Zurich, Switzerland. Institute of Veterinary Pharmacology and Toxicology, University of Zurich, Vetsuisse, Zurich, Switzerland; Neuroscience Center Zurich, University of Zurich and ETH Zurich, Zurich, Switzerland. Institute of Veterinary Pharmacology and Toxicology, University of Zurich, Vetsuisse, Zurich, Switzerland; Neuroscience Center Zurich, University of Zurich and ETH Zurich, Zurich, Switzerland. Electronic address: urs.meyer@vetpharm.uzh.ch. Department of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. Electronic address: kuery@uni-duesseldorf.de.
 Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada carol.hitchon@umanitoba.ca. National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada. Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. Community Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada. Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Manitoba, Canada. Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario, Canada. National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada.
 University of Michigan Medical School (AJ), Ann Arbor, Michigan; Department of Surgery (EB-S, FC) and Clinical Neurosciences (FC), University of Calgary, Calgary, Canada; Department of Ophthalmology and Visual Sciences (LAG, CAA, LBDL) and Neurology (LBDL), University of Michigan, Ann Arbor, Michigan; Department of Neurology (KK), Ohio State University, Columbus, Ohio.
 Department of Psychology, University of Milano-Bicocca, Milan, Italy. Maimonides Biomedical Research Institute of Córdoba (IMIBIC), Córdoba, Spain. Department of Psychology, University of Córdoba, Córdoba, Spain. Department of Psychology, University of Milano-Bicocca, Milan, Italy. roberta.adorni1@unimib.it. Department of Psychology, University of Milano-Bicocca, Milan, Italy. Information Technology Department, Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy. Department of Psychology, University of Milano-Bicocca, Milan, Italy. Psychology Unit of Montescano Institute, Istituti Clinici Scientifici Maugeri IRCCS, Montescano, Italy.
 Royal Adelaide Hospital, Adelaide, SA 5000, Australia; University of Adelaide, Adelaide, SA 5005, Australia. Electronic address: lydia.lam@student.adelaide.edu.au. Royal Adelaide Hospital, Adelaide, SA 5000, Australia. Flinders University, Bedford Park, SA 5042, Australia. Flinders University, Bedford Park, SA 5042, Australia. University of Adelaide, Adelaide, SA 5005, Australia. University of Adelaide, Adelaide, SA 5005, Australia. Royal Adelaide Hospital, Adelaide, SA 5000, Australia; University of Adelaide, Adelaide, SA 5005, Australia. Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 0G4, Canada. Royal Adelaide Hospital, Adelaide, SA 5000, Australia; University of Adelaide, Adelaide, SA 5005, Australia; Flinders University, Bedford Park, SA 5042, Australia. Flinders University, Bedford Park, SA 5042, Australia.
 IRCCS Fondazione Don Carlo Gnocchi ONLUS, LAMMB, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, LAMMB, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, LAMMB, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, LAMMB, 20148 Milan, Italy. IRCCS Fondazione Don Carlo Gnocchi ONLUS, LAMMB, 20148 Milan, Italy. Department of Pathophysiology and Transplantation, University of Milan, 20122 Milan, Italy.
 Neurochemistry and Biological Markers Unit, 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Department of Biopathology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Department of Biopathology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. 2nd Department of Neurology, Attikon University Hospital, Medical School, National and Kapodistrian University of Athens, 12462 Athens, Greece. Department of Biopathology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece. 1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece.
 , Cleveland, OH, USASchool of Medicine, Case Western Reserve University. RINGGOLD: 12304 Department of Neurology, and Harvard Medical School, Boston, MA, USAMassachusetts General Hospital. RINGGOLD: 2348 Department of Neurology, and Harvard Medical School, Boston, MA, USAMassachusetts General Hospital. RINGGOLD: 2348 Department of Neurology, and Harvard Medical School, Boston, MA, USAMassachusetts General Hospital. RINGGOLD: 2348
 Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Department of Neurology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Department of Neurology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Laboratory of Neurobiology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain. Department of Neurology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, 28040 Madrid, Spain.
 Department of Trauma & Orthopaedics, Tallaght University Hospital, Dublin, Ireland. Department of Trauma & Orthopaedics, Galway University Hospital, Galway, Ireland. Department of Trauma & Orthopaedics, Royal College of Surgeons Ireland, Dublin, Ireland. Department of Trauma & Orthopaedics, Tallaght University Hospital, Dublin, Ireland. Department of Trauma & Orthopaedics, Royal College of Surgeons Ireland, Dublin, Ireland. Rothman Orthopedic Institute, Thomas Jefferson University Hospital, PA, USA. Department of Trauma & Orthopaedics, Galway University Hospital, Galway, Ireland. Department of Trauma & Orthopaedics, Royal College of Surgeons Ireland, Dublin, Ireland. Department of Trauma & Orthopaedics, Tallaght University Hospital, Dublin, Ireland. Department of Trauma & Orthopaedics, St James Hospital, Dublin, Ireland. School of Medicine, University College Dublin, Dublin, Ireland. Department of Trauma & Orthopaedics, Tallaght University Hospital, Dublin, Ireland. Department of Trauma & Orthopaedics, Royal College of Surgeons Ireland, Dublin, Ireland. School of Medicine, University College Dublin, Dublin, Ireland.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Fahime.vahabizad@gmail.com. Department of Neurology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Fahime.vahabizad@gmail.com. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Abdorrezamoghadasi@gmail.com. Department of Neurology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Abdorrezamoghadasi@gmail.com.
 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Lucknow, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Lucknow, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Lucknow, India. KBI Biopharma, Analytical and Formulation Sciences, Geneva, Switzerland. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Lucknow, India.
 Service de neurologie, centre hospitalier universitaire Henri-Mondor, AP-HP Paris Est, 1 rue Gustave-Eiffel, 94000 Créteil, France; Centre de ressources et de compétences Grand Paris Est, centre hospitalier universitaire Henri-Mondor, AP-HP Paris Est, 1 rue Gustave-Eiffel, 94000 Créteil, France; Réseau sclérose en plaques et maladies inflammatoires du système nerveux (SINDEFI-SEP) Île-de-France, immeuble Expansion, 9/11 rue Georges-Enesco, 94000 Créteil, France. Electronic address: sophie.redaelli@aphp.fr. Réseau sclérose en plaques et maladies inflammatoires du système nerveux (SINDEFI-SEP) Île-de-France, immeuble Expansion, 9/11 rue Georges-Enesco, 94000 Créteil, France. Réseau sclérose en plaques et maladies inflammatoires du système nerveux (SINDEFI-SEP) Île-de-France, immeuble Expansion, 9/11 rue Georges-Enesco, 94000 Créteil, France. Service de neurologie, centre hospitalier universitaire Henri-Mondor, AP-HP Paris Est, 1 rue Gustave-Eiffel, 94000 Créteil, France; Centre de ressources et de compétences Grand Paris Est, centre hospitalier universitaire Henri-Mondor, AP-HP Paris Est, 1 rue Gustave-Eiffel, 94000 Créteil, France; Réseau sclérose en plaques et maladies inflammatoires du système nerveux (SINDEFI-SEP) Île-de-France, immeuble Expansion, 9/11 rue Georges-Enesco, 94000 Créteil, France.
 Neuro-Psychiatrisches Zentrum Riem, Munich, Germany. Electronic address: npzr.studien@gmail.com. Social Work Department, Cyprus International University, 99258 Nicosia, North Cyprus, Turkey. Neuro-Psychiatrisches Zentrum Riem, Munich, Germany. Neuro-Psychiatrisches Zentrum Riem, Munich, Germany.
 Nebraska Center for Virology, School of Biological Sciences, University of Nebraska, Lincoln, Nebraska, USA.
 Shenzhen Bao'an Traditional Chinese Medicine Hospital, Shenzhen, China. School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, China. Shenzhen Bao'an Traditional Chinese Medicine Hospital, Shenzhen, China. Shenzhen Bao'an Traditional Chinese Medicine Hospital, Shenzhen, China. Shenzhen Bao'an Traditional Chinese Medicine Hospital, Shenzhen, China. Shenzhen Bao'an Traditional Chinese Medicine Hospital, Shenzhen, China. zhaobeibei@szbazyy.net. Shenzhen Bao'an Traditional Chinese Medicine Hospital, Shenzhen, China. lanjiao@szbazyy.net.
 Alberta Health Services, Edmonton, Canada. Alberta Health Services, Edmonton, Canada. Division of Neurology, Department of Medicine, University of Alberta, Edmonton, Canada. Division of Neurology, Department of Pediatrics, University of Alberta, Edmonton, Canada. Division of Neurology, Department of Medicine, University of Alberta, Edmonton, Canada. Division of Neurology, Department of Pediatrics, University of Alberta, Edmonton, Canada. Women and Children's Health Research Institute, Edmonton, Canada.
 DIPAS: DRDO-Defence Institute of Physiology and Allied Sciences, Delhi-110054, India. kpmpgi@rediffmail.com. DIPAS: DRDO-Defence Institute of Physiology and Allied Sciences, Delhi-110054, India.
 Department of Cell Biology, Physiology and Immunology, Faculty of Veterinary Medicine, University of Cordoba, Spain; Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain. Electronic address: am1esdub@uco.es. Department of Cell Biology, Physiology and Immunology, Faculty of Veterinary Medicine, University of Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain; Department of Morphological Sciences, Histology Section, Faculty of Medicine and Nursing, University of Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain; Department of Biochemistry and Molecular Biology, Faculty of Medicine and Nursing, University of Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain; Department of Biochemistry and Molecular Biology, Faculty of Medicine and Nursing, University of Cordoba, Spain; Analysis Service, Reina Sofia University Hospital, Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain; Department of Biochemistry and Molecular Biology, Faculty of Medicine and Nursing, University of Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain; Neurology Service, Reina Sofia University Hospital, Cordoba, Spain. Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Cordoba, Spain; Department of Biochemistry and Molecular Biology, Faculty of Medicine and Nursing, University of Cordoba, Spain; Cooperative Research Thematic Excellent Network on Brain Stimulation (REDESTIM), Spain. Electronic address: itunez@uco.es.
 Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università 30, 00185, Rome, Italy. serena.ruggieri@uniroma1.it. Neuroimmunology Unit, IRCSS Fondazione Santa Lucia, Rome, Rome, Italy. serena.ruggieri@uniroma1.it. Department of Neurosciences, San Camillo-Forlanini Hospital, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università 30, 00185, Rome, Italy. Department of Maternal Infantile and Urological Sciences, Sapienza University of Rome, Rome, Italy. Unit of Neuroradiology, Department of Medical and Surgical Sciences, "Magna Graecia" University, Catanzaro, Italy. Radiology, Neurological Center of Latium, Rome, Rome, Italy. Neurology Unit, San Filippo Neri Hospital, Rome, Italy. Queen Square MS Centre, Faculty of Brain Sciences, University College London Queen Square Institute of Neurology, London, UK. National Institute for Health Research Biomedical Research Centre, University College London Hospitals, London, UK. Department of Neurosciences, San Camillo-Forlanini Hospital, Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università 30, 00185, Rome, Italy.
 Department of Neurology, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait; Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait. Electronic address: dralhasel@hotmail.com. Department of Neurology, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait; Department of Neurology and Psychiatry, Minia University, P.O. Box 61519, Minia 61111, Egypt. Department of Medicine, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait. Division of Neurology, Amiri Hospital, Arabian Gulf Street, Sharq 13041, Kuwait; MS Clinic, Ibn Sina Hospital, P.O. Box 25427, Safat 13115, Kuwait.
 Division of Biostatistics, School of Public Health. Division of Biostatistics, School of Public Health. Center for Magnetic Resonance Research, University of Minnesota. Center for Magnetic Resonance Research, University of Minnesota. Center for Magnetic Resonance Research, University of Minnesota. Division of Biostatistics, School of Public Health.
 CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Health and Biosecurity Unit, Commonwealth Scientific and Industrial Research Organisation, Melbourne, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital City Campus, Parkville, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Department of Neurology, Center of Clinical Neuroscience, Charles University, Praha, Czech Republic. General University Hospital in Prague, Praha, Czech Republic. Department of Neurology, Center of Clinical Neuroscience, Charles University, Praha, Czech Republic. General University Hospital in Prague, Praha, Czech Republic. Department of Medical and Surgical Sciences and Advanced Technologies, University of Catania 'G.F. Ingrassia', Catania, Italy. Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran (the Islamic Republic of). Dokuz Eylul University, İzmir, Turkey. Neurology, Hospital Universitario Virgen Macarena, Sevilla, Spain. Deptartment of Neuroscience, Imaging, and Clinical Sciences, Gabriele d'Annunzio University of Chieti and Pescara, Chieti, Italy. UOSI Riabilitazione Sclerosi Multipla, IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. Division of Neurology, Department of Medicine, Amiri Hospital, Kuwait City, Kuwait. CHUM MS Center, Montreal, Quebec, Canada. Universite de Montreal, Montreal, Quebec, Canada. CHUM MS Center, Montreal, Quebec, Canada. Universite de Montreal, Montreal, Quebec, Canada. CHUM MS Center, Montreal, Quebec, Canada. Universite de Montreal, Montreal, Quebec, Canada. School of Medicine, Ondokuz Mayis Universitesi, Samsun, Turkey. KTU Medical Faculty Farabi Hospital, Trabzon, Turkey. Neuro Rive-Sud, Greenfield Park, Quebec, Canada. Department of Neuroscience, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. Department of Neuroscience, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. CISSS de Chaudiere-Appalaches, Levis, Quebec, Canada. Nehme and Therese Tohme Multiple Sclerosis Center, American University of Beirut Medical Center, Beirut, Lebanon. Department of Neurology, American University of Beirut, Beirut, Lebanon. Department of Neurology, Koc Universitesi, Istanbul, Turkey. Koc University Research Center for Translational Medicine, Istanbul, Turkey. Department of Neurology, Zuyderland Medical Centre Sittard-Geleen, Sittard-Geleen, The Netherlands. School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. University of Newcastle Hunter Medical Research Institute, Newcastle, New South Wales, Australia. Department of Neurology, John Hunter Hospital, Newcastle, New South Wales, Australia. Foundation National Neurological Institute C Mondino Institute for Hospitalization and Care Scientific, Pavia, Italy. Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. Ospedali Riuniti di Salerno, Salerno, Italy. Department of Neurology, St Vincent's University Hospital, Dublin, Ireland. UOC Neurologia, Azienda Sanitaria Unica Regionale Marche - AV3, Macerata, Italy. Royal Victoria Hospital, Belfast, UK. Department of Neurology, Centro Hospitalar de São João, Porto, Portugal. Department of Neurology, ASL3 Genovese, Genova, Italy. Department of Rehabilitaiton, Casa di Cura Centro di Recupero e Rieducazione Funzionale Mons Luigi Novarese, Moncrivello, Italy. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB) and MS Center, Neurologic Clinic and Policlinic, Departments of Head, Spine and Neuromedicine and Clinical Research, University Hospital Basel, Basel, Switzerland. University of Basel, Basel, Switzerland. Liverpool Hospital, Sydney, New South Wales, Australia. Flinders University, Adelaide, South Australia, Australia. Department of Medicine and Surgery, University of Parma, Parma, Italy. Groene Hart Ziekenhuis, Gouda, The Netherlands. UQCCR, The University of Queensland, Brisbane, Queensland, Australia. Nemocnice Jihlava, Jihlava, Czech Republic. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Alfred Hospital, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Neurology, Galdakao-Usansolo Hospital, Galdakao, Spain. Westmead Hospital, Westmead, New South Wales, Australia. Universitair Ziekenhuis Gent, Gent, Belgium. Department of Neurology, Razi University Hospital, Tunis, Tunisia. Department of Neurology, University of Tunis El Manar, Tunis, Tunisia. Department of Neurology, University of Tunis El Manar, Tunis, Tunisia. Instituto de Investigacion Sanitaria Biodonostia, Hospital Universitario de Donostia, San Sebastian, Spain. South and East Belfast Health and Social Services Trust, Belfast, UK. Neurology, Hospital Universitario Reina Sofia, Cordoba, Spain. Department of Medicine, Sultan Qaboos University Hospital, Seeb, Oman. Sultan Qaboos University, Muscat, Oman. University Hospital Geelong, Geelong, Victoria, Australia. Department of Neurology, King Fahad Specialist Hospital-Dammam, Khobar, Saudi Arabia. Department of Neurology, University of Debrecen, Debrecen, Hungary. Department of Neurology, Hospital General de Alicante, Alicante, Spain. Department of Neurology, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Mexico City, Mexico. Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia tomas.kalincik@unimelb.edu.au. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital City Campus, Parkville, Victoria, Australia.
 Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India. Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India. Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India. Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India. gurjeet.singh@chitkara.edu.in.
 Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, 142001, Punjab, India. Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, 142001, Punjab, India. sidh.mehan@gmail.com.
 Department of Pharmacology & Therapeutics, School of Medicine, University of Galway, H91 TK33 Galway, Ireland. School of Psychology, University of Galway, H91 TK33 Galway, Ireland. Department of Pharmacology & Therapeutics, School of Medicine, University of Galway, H91 TK33 Galway, Ireland.
 Department of Psychiatry, Otto-von-Guericke University, Leipziger Str. 44, D-39120 Magdeburg, Germany. Electronic address: Hans-Gert.Bernstein@med.ovgu.de. Leibniz Institute for Neurobiology, RG Neuroplasticity, D-39118 Magdeburg, Germany; Institute for Pharmacology and Toxicology, Otto-von-Guericke University, Magdeburg, Germany, Center for Behavioral Brain Sciences, Magdeburg, Germany. Institute of Biochemistry and Cell Biology, Otto-von-Guericke University, Magdeburg, Germany. Department of Psychiatry, Otto-von-Guericke University, Leipziger Str. 44, D-39120 Magdeburg, Germany. Leibniz Institute for Neurobiology, RG Neuroplastcity, D-39118 Magdeburg, Germany; University Medical Center Hamburg Eppendorf, Leibniz Group "Dendritic Organelles and Synaptic Function" ZMNH, Hamburg, Germany. Department of Psychiatry, Otto-von-Guericke University, Leipziger Str. 44, D-39120 Magdeburg, Germany.
 Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan. Electronic address: yoshimura@keio.jp. Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan. Division of Allergy and Immunology, Medical Institute of Bioregulation Kyushu University, Higashi-ku, Fukuoka, Japan. Electronic address: minakoito@bioreg.kyushu-u.ac.jp.
 Institute of Chronic Disease Risks Assessment, School of Nursing and Health Sciences, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. Institute of Chronic Disease Risks Assessment, School of Nursing and Health Sciences, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. School of Life Science, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. School of Life Science, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. Institute of Chronic Disease Risks Assessment, School of Nursing and Health Sciences, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. wanglai@henu.edu.cn. School of Life Science, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. wanglai@henu.edu.cn. School of Life Science, Henan University, Henan Province, Kaifeng, 475004, People's Republic of China. yanmingwang@henu.edu.cn.
 Multiple Sclerosis and Neuroimmunology Program, Parkinson's and Movement Disorders Center, University Hospitals Cleveland Medical Center, Cleveland, OH, USA/Case Western Reserve University School of Medicine, Cleveland, OH, USA.
 Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at The University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at The University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK. UK Dementia Research Institute at UCL, London, UK. Hong Kong Center for Neurodegenerative Diseases, Hong Kong, People's Republic of China. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
 Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, Brazil. Laboratory of Molecular and Translational Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil. Department of Biosciences, Universidade Federal de São Paulo, Santos, Brazil. Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, Brazil. Laboratory of Molecular and Translational Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil. Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, Brazil. Laboratory of Molecular and Translational Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.
 Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, University of Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, University of Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, University of Münster, Münster, Germany. Institute of Translational Immunology and Research Center for Immunotherapy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, University of Münster, Münster, Germany. Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Institute of Translational Immunology and Research Center for Immunotherapy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Institute of Translational Immunology and Research Center for Immunotherapy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn²), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
 Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands. Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands. Electronic address: s.kroos@lumc.nl. Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands. Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands.
 Respiratory, Cork University Hospital, Cork, Ireland domdoyle@gmail.com. Respiratory, Cork University Hospital, Cork, Ireland. Respiratory, Cork University Hospital, Cork, Ireland. Respiratory, Cork University Hospital, Cork, Ireland.
 Department of Biological Sciences, Boise State University, Boise, ID 83725, USA. Pharmacotherapy, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA 99202, USA. Pharmacotherapy, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA 99202, USA. Department of Biological Sciences, Boise State University, Boise, ID 83725, USA. Department of Biology, Eastern Washington University, Cheney, WA 99004, USA. Pharmacotherapy, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA 99202, USA. Department of Biological Sciences, Boise State University, Boise, ID 83725, USA. Electronic address: jochoareparaz@boisestate.edu.
 Sleep Disorders Centre, Guy's and St Thomas' NHS Foundation Trust, London, UK. Sleep Disorders Centre, Neurology Service, Hospital Clínic Barcelona, Universitat de Barcelona, IDIBAPS, CIBERNED: CB06/05/0018-ISCIII, Barcelona, Spain. airanzo@clinic.cat.
 Department of Pharmacy, School of Medicine, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China. Department of Pharmacy, School of Medicine, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China.
 Maharajgunj Medical Campus, Institute of Medicine, Tribhuvan University, Kathmandu, Nepal. Maharajgunj Medical Campus, Institute of Medicine, Tribhuvan University, Kathmandu, Nepal. Maharajgunj Medical Campus, Institute of Medicine, Tribhuvan University, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal. Department of Neurology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.
 Department of Neurology, UCLA David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Department of Human Genetics, UCLA David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Department of Neurology, UCLA David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Department of Neurology, UCLA David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Department of Neurology, UCLA David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Department of Human Genetics, UCLA David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Raebareli, Transit Campus, Bijnour-sisendi Road, Sarojini Nagar, Lucknow 226002, Uttar Pradesh, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Raebareli, Transit Campus, Bijnour-sisendi Road, Sarojini Nagar, Lucknow 226002, Uttar Pradesh, India. Electronic address: rakesh.singh@niperraebareli.edu.in.
 Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. Center for Biomedical Imaging at Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. IRCCS, Fondazione Don Carlo Gnocchi ONLUS, Milan, Italy. Advisory Council, Buffalo Neuroimaging Analysis Center, Buffalo, NY, USA. Department of Neurology, Wayne State University, Detroit, MI, USA. University of Nebraska Medical Center, Omaha, NE, USA. Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. Negroski Neurology, LLP, Sarasota, Sarasota, FL, USA. Michigan Institute for Neurological Disorders (MIND), Farmington Hills, MI, USA. Department of Neurology, Jacobs Comprehensive MS Treatment and Research Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. Department of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 100 High Street, Buffalo, NY, 14203, USA. rzivadinov@bnac.net. Center for Biomedical Imaging at Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY, USA. rzivadinov@bnac.net.

 Chitkara College of Pharmacy, Chitkara University, 140401 Punjab, India. Chitkara College of Pharmacy, Chitkara University, 140401 Punjab, India. Chitkara College of Pharmacy, Chitkara University, 140401 Punjab, India. Chitkara College of Pharmacy, Chitkara University, 140401 Punjab, India. Electronic address: gurjeet.singh@chitkara.edu.in.
 Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. fabrizio.esposito@unicampania.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Via Olgettina 58, 20132, Milan, Italy. Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università, 30, 00185, Rome, Italy. Institute of Applied Physics "Nello Cararra" (IFAC), National Research Council (CNR), Via Madonna del Piano, 10, Sesto Fiorentino, 50019, Florence, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy. Department of Human Neurosciences, Sapienza University of Rome, Viale Dell'Università, 30, 00185, Rome, Italy. IRCCS Neuromed, Pozzilli, IS, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Via Olgettina 58, 20132, Milan, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, 80138, Naples, Italy.
 Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Centre Leenaards de la Mémoire, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Centre Leenaards de la Mémoire, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Centre Leenaards de la Mémoire, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neuropsychologie et de neuroréhabilitation, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne. Service de neurologie, Département des neurosciences cliniques, Centre hospitalier universitaire vaudois et Université de Lausanne, 1011 Lausanne.
 Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan. World Premier International (WPI)-Immunology Frontier Research Center, Osaka University, Osaka, Japan. Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan. World Premier International (WPI)-Immunology Frontier Research Center, Osaka University, Osaka, Japan. Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan. World Premier International (WPI)-Immunology Frontier Research Center, Osaka University, Osaka, Japan. Department of Neuro-Medical Science, Graduate School of Medicine, Osaka University, Osaka, Japan. Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
 From the University Institute for Advanced Studies (IUSS) (S.F.C.), Pavia, Italy; IRCCS Mondino Foundation (S.F.C.), Pavia, Italy; Department of Neuroinflammation (A.E.), Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, United Kingdom; and Department of Computer Science (A.E.), Centre for Medical Image Computing (CMIC), University College London, United Kingdom. stefano.cappa@iusspavia.it. From the University Institute for Advanced Studies (IUSS) (S.F.C.), Pavia, Italy; IRCCS Mondino Foundation (S.F.C.), Pavia, Italy; Department of Neuroinflammation (A.E.), Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, United Kingdom; and Department of Computer Science (A.E.), Centre for Medical Image Computing (CMIC), University College London, United Kingdom.
 Department of Ophthalmology, Bascom Palmer Eye Institute, Miller School of Medicine at University of Miami, Miami, FL, USA. Miami Integrative Metabolomics Research Center, Miami, FL, USA. Department of Ophthalmology, Bascom Palmer Eye Institute, Miller School of Medicine at University of Miami, Miami, FL, USA. Miami Integrative Metabolomics Research Center, Miami, FL, USA. University of Miami, Miami, FL, USA. Department of Ophthalmology, Bascom Palmer Eye Institute, Miller School of Medicine at University of Miami, Miami, FL, USA. sbhattacharya@med.miami.edu. Miami Integrative Metabolomics Research Center, Miami, FL, USA. sbhattacharya@med.miami.edu.
 Department of Pathology, Beijing Geriatric Hospital, Beijing 100095, China. School of Pharmaceutical Sciences, Capital Medical University, Beijing, 100069, China. School of Pharmaceutical Sciences, Capital Medical University, Beijing, 100069, China. Beijing Institute of Hepatology, Beijing You An Hospital, Capital Medical University, Beijing, 100069, China.
 Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University, Shahbad Daulatpur, Bawana Road, New Delhi, Delhi, 110042, India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University, Shahbad Daulatpur, Bawana Road, New Delhi, Delhi, 110042, India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University, Shahbad Daulatpur, Bawana Road, New Delhi, Delhi, 110042, India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University, Shahbad Daulatpur, Bawana Road, New Delhi, Delhi, 110042, India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University, Shahbad Daulatpur, Bawana Road, New Delhi, Delhi, 110042, India. pravirkumar@dtu.ac.in.
 Programa de Pós-Graduação em Biotecnologia (PPGBiotec), Grupo de Pesquisa em Neurobiotecnologia - GPN, CDTec, Universidade Federal de Pelotas, UFPel, Pelotas, RS, Brazil. Department of Symptom Research, MD Anderson Cancer Center, Houston, United States of America. Lab. de Síntese Orgânica Limpa - LASOL, CCQFA, Universidade Federal de Pelotas - UFPel, P.O. box 354 - 96010-900, Pelotas, RS, Brazil. Lab. de Síntese Orgânica Limpa - LASOL, CCQFA, Universidade Federal de Pelotas - UFPel, P.O. box 354 - 96010-900, Pelotas, RS, Brazil. Escola de Química e Alimentos , Universidade Federal do Rio Grande - FURG, Campus Carreiros, Rio Grande, RS, Brazil; Current address: Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria - UFSM. Av. Roraima, CEP: 97105-340, Santa Maria-RS, Brazil. Lab. de Bioquímica e Neurofarmacologia Molecular - LABIONEM, CCQFA, Universidade Federal de Pelotas - UFPel - 96010-900, Pelotas, RS, Brazil. Programa de Pós-Graduação em Biotecnologia (PPGBiotec), Grupo de Pesquisa em Neurobiotecnologia - GPN, CDTec, Universidade Federal de Pelotas, UFPel, Pelotas, RS, Brazil. Lab. de Síntese Orgânica Limpa - LASOL, CCQFA, Universidade Federal de Pelotas - UFPel, P.O. box 354 - 96010-900, Pelotas, RS, Brazil.

 Department of Neuroscience DNS (AM, PG), School of Medicine, University of Padua, Padua, Italy; Multiple Sclerosis Centre (AM, FR, PP, PG), University Hospital of Padua, Padua, Italy; and Department of Ophthalmology (EP), University of Padova, Padova, Italy.
 Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD 21218, USA; Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: lr_zuo@jhu.edu. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD 21218, USA. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD 21218, USA. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. Department of Computer Science, Johns Hopkins University, Baltimore, MD 21218, USA; Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD 21218, USA. Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD 21218, USA. Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD 21218, USA.
 Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile; Neurology Service, Hospital Sótero del Río, Santiago, Chile. Electronic address: elciampi@uc.cl. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile; Neurology Service, Hospital Sótero del Río, Santiago, Chile. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile; Neurology Service, Hospital Sótero del Río, Santiago, Chile. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurorradiology Department, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurorradiology Department, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology Department, Pontificia Universidad Católica de Chile, Santiago, Chile.
 Healthy Aging Research Laboratory, Department of Physical Therapy, Federal University of São Carlos, Washington Luis Highway, Km 235, São Carlos, São Paulo, Brazil. marcospbraz@gmail.com. Physical Therapy Laboratory, Department of Physical Therapy, State University of Campinas, São Paulo, Campinas, Brazil. Neurofunctional Physical Therapy Research Group, Department of Physical Therapy, State University of Londrina, Londrina, Paraná, Brazil. Mechanisms of Spinal Manual Therapy Laboratory, Department of Physical Therapy, The University of Alabama at Birmingham, Birmingham, AL, USA. Department of Medicine, Division of Pulmonary, Allergy and Critical Care, The University of Alabama at Birmingham, Birmingham, AL, USA. Neurofunctional Physical Therapy Research Group, Department of Physical Therapy, State University of Londrina, Londrina, Paraná, Brazil. Neurofunctional Physical Therapy Research Group, Department of Physical Therapy, State University of Londrina, Londrina, Paraná, Brazil.
 College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430000, China. Central Laboratory, The First Affiliated Hospital of Henan Polytechnic University (Jiaozuo Second People's Hospital), Jiaozuo, China. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430000, China. Department of Endocrinology, The First Affiliated Hospital of Henan Polytechnic University (Jiaozuo Second People's Hospital), Jiaozuo, 454000, China. Department of Thoracic Surgery, The First Affiliated Hospital of Henan Polytechnic University (Jiaozuo Second People's Hospital), Jiaozuo, 454000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. Beijing Bencaoyuan Pharmaceutical Co, Ltd, Beijing, 102629, China. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430000, China. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430000, China. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430000, China. College of Medicine, Henan Polytechnic University, Jiaozuo, 454000, China. wangzhenhui1984@163.com. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430000, China. hexiaohua@whu.edu.cn.
 United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Medical Research Council Centre for Reproductive Health, University of Edinburgh, Edinburgh, EH16 4TJ, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Medical Research Council Centre for Reproductive Health, University of Edinburgh, Edinburgh, EH16 4TJ, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Wellcome Trust Translational Neuroscience PhD programme, Edinburgh, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, DD1 5EH, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Medical Research Council Centre for Reproductive Health, University of Edinburgh, Edinburgh, EH16 4TJ, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Medical Research Council Centre for Reproductive Health, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Department of Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Medizinische Hochschule Hannover, Hannover, 30625, Germany. Department of Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Medizinische Hochschule Hannover, Hannover, 30625, Germany. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Division of Pharmaceutical Sciences, University of Wisconsin, Madison, WI, 53705, USA. Molecular and Environmental Toxicology Centre, University of Wisconsin, Madison, WI, 53706, USA. Center for Neuroscience, University of Wisconsin, Madison, WI, 53705, USA. Waisman Centre, University of Wisconsin, Madison, WI, 53705, USA. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Institute of Neuropathology, University Hospital Muenster, Muenster, D-48129, Germany. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Centre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, EH16 5UU, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Department of Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Medizinische Hochschule Hannover, Hannover, 30625, Germany. Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, DD1 5EH, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. United Kingdom Dementia Research Institute at The University of Edinburgh, Edinburgh Medical School, Edinburgh, EH16 4TJ, UK. veronique.miron@unityhealth.to. United Kingdom Multiple Sclerosis Society Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, EH16 4TJ, UK. veronique.miron@unityhealth.to. Center for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. veronique.miron@unityhealth.to. Medical Research Council Centre for Reproductive Health, University of Edinburgh, Edinburgh, EH16 4TJ, UK. veronique.miron@unityhealth.to. BARLO Multiple Sclerosis Centre, St.Michael's Hospital, Toronto, ON, M5B 1W8, Canada. veronique.miron@unityhealth.to. Keenan Centre for Biomedical Research at St.Michael's Hospital, Toronto, ON, M5B 1T8, Canada. veronique.miron@unityhealth.to. Department of Immunology, University of Toronto, Toronto, ON, M5S 1A8, Canada. veronique.miron@unityhealth.to.
 Department of Pharmaceutical Sciences, University of Piemonte Orientale, 28100, Novara, Italy. Department of Pharmaceutical Sciences, University of Piemonte Orientale, 28100, Novara, Italy. Department of Pharmaceutical Sciences, University of Piemonte Orientale, 28100, Novara, Italy. IRCCS Mondino Foundation, 27100, Pavia, Italy. A.U.O, Policlinico Umberto I, Neurosurgery Division, Human Neurosciences Department, Sapienza University, 00135, Roma, Italy. Department of Neuroscience Rita Levi Montalcini, Neurosurgery Unit, University of Turin, 10126, Turin, Italy. Department of Neuroscience Rita Levi Montalcini, Neurosurgery Unit, University of Turin, 10126, Turin, Italy. Department of Pharmaceutical Sciences, University of Piemonte Orientale, 28100, Novara, Italy. PharmaExceed S.r.l, 27100, Pavia, Italy. Department of Pharmaceutical Sciences, University of Piemonte Orientale, 28100, Novara, Italy.
 Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. College of Nursing, University of Al-Ameed, Karbala, Iraq. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: roohbakhsha@mums.ac.ir.
 Unidad de Medicina Legal, Departamento de Fisiología y Farmacología, Universidad de Cantabria, Santander, Spain. Departamento de Psiquiatría, Hospital Universitario Marqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Salud Carlos III, España; Departamento de Medicina y Psiquiatría, Facultad de Medicina, Universidad de Cantabria, Santander, Spain. Departamento de Enfermería, Universidad de Cantabria, Centro Hospitalario Padre Men, Santander, Spain. Departamento de Neurología, Hospital Sierrallana, IDIVAL, CIBERNED, Departamento de Medicina y Psiquiatría, Facultad de Medicina, Universidad de Cantabria, Santander, Spain. Unidad de Medicina Legal, Departamento de Fisiología y Farmacología, Universidad de Cantabria, Santander, Spain. Electronic address: ana.santurtun@unican.es.
 Department of Neurology, Kiel University, Kiel, Germany. Department of Neuroscience, Mental Health and Sensory Organs (NESMOS), Sapienza University of Rome, Rome, Italy. Department of Neurology, Kiel University, Kiel, Germany. Division of Surgery, Saarland University, Homburg, Germany. Department of Neurology, Kiel University, Kiel, Germany. Faculty of Engineering, Kiel University, Kiel, Germany. Department of Neurology, Kiel University, Kiel, Germany. Department of Neurology, Kiel University, Kiel, Germany. Department of Neurology, Kiel University, Kiel, Germany. Institute of Medical Informatics and Statistics, University Hospital Schleswig-Holstein, Kiel University, Kiel, Germany. Department of Neuroscience, Mental Health and Sensory Organs (NESMOS), Sapienza University of Rome, Rome, Italy. Santa Lucia Foundation, Rome, Italy. Department of Neurology, Kiel University, Kiel, Germany. Department of Neurology, Kiel University, Kiel, Germany.
 Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States; Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States. Electronic address: kurt.g.schilling.1@vumc.org. Department of Intelligent Systems Engineering, Indiana University Bloomington, Bloomington, IN, United States. The Public Health Company, California, United States. Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States. Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States; Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States. Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, United States. Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States. Neuroimaging Unit, Neuroimmunology Division, Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Neurology, VA Hospital, TN Valley Healthcare System, Nashville, TN, United States. Department of Intelligent Systems Engineering, Indiana University Bloomington, Bloomington, IN, United States. Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, United States; Department of Electrical and Computer Engineering, Vanderbilt University, Nashville, TN, United States. Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States; Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, United States. Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States; Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, United States. Electronic address: kristin.p.ogrady@vumc.org.
 Carnegie School of Sport Leeds Beckett University Leeds UK. Carnegie School of Sport Leeds Beckett University Leeds UK. Institute of Life Course and Medical Sciences University of Liverpool Liverpool UK. Carnegie School of Sport Leeds Beckett University Leeds UK. Carnegie School of Sport Leeds Beckett University Leeds UK. Division of Environmental Physiology Royal Institute of Technology Stockholm Sweden. Faculty of Kinesiology and Physical Education University of Toronto Toronto Ontario Canada. Wolfson Research Institute for Health and Well-being Durham UK.
 Department of Pain Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Department of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Pain Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Program in the McKelvey School of Engineering, Washington University in St. Louis, Saint Louis, MO 63130, USA. Department of Internal Medicine, Sinai Hospital of Baltimore, Baltimore, MD 21215, USA. Department of Economics, University of Washington, WA 98125, USA. Department of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Neurology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Department of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. Department of Pain Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Department of Pain Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Department of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
 Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. Department of Urology Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, 830054 Urumqi, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. Department of Foreign Language, Guangxi University of Chinese Medicine, 530200 Nanning, China. Department of Urology Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, 830054 Urumqi, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. Department of Foreign Language, Guangxi University of Chinese Medicine, 530200 Nanning, China. Department of Foreign Language, Guangxi University of Chinese Medicine, 530200 Nanning, China. Department of Urology Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, 830054 Urumqi, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. R & D Center, Guangxi Taimei Rensheng Biotechnology Co Ltd, 530006 Nanning, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China. Center for Translational Medicine of Integrated Traditional Chinese and Western Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, 530011 Nanning, China.
 Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran; Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neurosurgery Department, Faculty of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran. School of Medicine, Islamic Azad University of Yazd, Yazd, Iran. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Pharmacology and Toxicology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: taher.s64@gmail.com.
 Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, Texas Southern University, Houston; Department of Pharmacology and Neuroscience, University of North Texas Health Sciences Center, Fort Worth, TX; Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University, Omaha, NE, USA; Singapore Eye Research Institute (SERI); Duke-NUS Medical School, Singapore, Singapore; Department of Surgery & Cancer, Imperial College of Science and Technology, St. Mary's Campus, London, UK; Global Alliances and External Research, Ophthalmology Innovation Center, Santen Inc USA, Emeryville, CA, USA.
 School of Clinical Medicine, Institute of Hepatology and Metabolic Diseases, Hangzhou Normal University, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang, China. School of Clinical Medicine, Institute of Hepatology and Metabolic Diseases, Hangzhou Normal University, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang, China. Rugao Experimental Primary School, Nantong, China. Department of Rehabilitation Medicine, Lishui Second People's Hospital, Lishui, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Jinan Microecological Biomedicine Shandong Laboratory, Jinan, China. Department of Obstetrics, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Department of Rehabilitation Medicine, Lishui Second People's Hospital, Lishui, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Jinan Microecological Biomedicine Shandong Laboratory, Jinan, China. Department of Psychiatry, Lishui Second People's Hospital, Lishui, China.
 Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Toxicogenomics, GROW School of Oncology and Development Biology, Maastricht University, Maastricht, The Netherlands. Centre for Environmental Sciences, Hasselt University, Hasselt, Belgium. Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. msaeidhejazi@yahoo.com. Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. msaeidhejazi@yahoo.com. Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran. msaeidhejazi@yahoo.com.
 Department of Engineering Science, University of Oxford, Parks Road, Oxford, OX1 3PJ, UK. Division of Biomedical Engineering, James Watt School of Engineering, University of Glasgow, Glasgow, G12 8LT, UK. Nuffield Department of Women's and Reproductive Health, University of Oxford, The Women Centre, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, UK. Faculty of Infectious Diseases, London School of Hygiene and Tropical Medicine, Keppel St, London, WC1E 7HT, UK. Nuffield Department of Women's and Reproductive Health, University of Oxford, The Women Centre, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, UK. Soft Cell Biological Research, Attwood Innovation Center, 453 S 600 E, St. George, UT, 84770, USA. Faculty of Infectious Diseases, London School of Hygiene and Tropical Medicine, Keppel St, London, WC1E 7HT, UK. Department of Exercise Physiology and Functional Anatomy, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Swietojanska 20, Bydgoszcz, 85-077, Poland. Department of Exercise Physiology and Functional Anatomy, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Swietojanska 20, Bydgoszcz, 85-077, Poland. Department of Experimental and Clinical Physiology, Warsaw Medical University, Stefana Banacha 2a, Warszawa, 02-097, Poland. Department of Engineering Science, University of Oxford, Parks Road, Oxford, OX1 3PJ, UK. Nuffield Department of Women's and Reproductive Health, University of Oxford, The Women Centre, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, UK.
 Department of Respiratory, Hebei Chest Hospital, Shijiazhuang, 050000, Hebei, China. Department of Laboratory Medicine, The Fifth Hospital of Shijiazhuang, Hebei Medical University, Shijiazhuang, 050021, Hebei, China. College of Plant Protection, Hunan Agricultural University, Changsha, 410128, Hunan, China. Intensive Care Unit, The Fifth Hospital of Shijiazhuang, Hebei Medical University, Shijiazhuang, 050021, Hebei, China. Department of Tuberculosis, The Fifth Hospital of Shijiazhuang, Hebei Medical University, Shijiazhuang, 050021, Hebei, China. The Second Internal Medicine, The Fifth Hospital of Shijiazhuang, Hebei Medical University, Shijiazhuang, 050021, Hebei, China. Graduate School of Hebei Medical University, Shijiazhuang, 050017, Hebei, China. Graduate School of Hebei Medical University, Shijiazhuang, 050017, Hebei, China. Department of Respiratory, Hebei Chest Hospital, Shijiazhuang, 050000, Hebei, China. Department of Respiratory, Hebei Chest Hospital, Shijiazhuang, 050000, Hebei, China. Department of Laboratory Medicine, The Fifth Hospital of Shijiazhuang, Hebei Medical University, Shijiazhuang, 050021, Hebei, China. daieh2008@126.com. Department of Tuberculosis, The Fifth Hospital of Shijiazhuang, Hebei Medical University, Shijiazhuang, 050021, Hebei, China. 1149497466@qq.com. Graduate School of Hebei Medical University, Shijiazhuang, 050017, Hebei, China. 1149497466@qq.com.
 Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Sapporo, Japan. Electronic address: niino.masaaki.tc@mail.hosp.go.jp. Department of Clinical Research, National Hospital Organization Hokkaido Medical Center, Sapporo, Japan. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Tokyo, Japan. Biogen, Tokyo, Japan. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Biogen, Cambridge, MA, USA. Schey Center for Cognitive Neuroimaging, Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
 From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. From the Department of Neurology (K.T., M.A.), and Mellen Center for Multiple Sclerosis Treatment and Research (A.M., M.R., D.O., A.C.K.), Neurological Institute, and Section of Neuroradiology (S.E.J.), Imaging Institute, Cleveland Clinic, OH. kunchoa@ccf.org.
 Department of Internal Medicine, College of Medicine, Prince Sattam bin Abdulaziz University, Al-Kharj, Saudi Arabia. Department of Internal Medicine, College of Medicine, Prince Sattam bin Abdulaziz University, Al-Kharj, Saudi Arabia. Neurology Department, Faculty of Medicine, Minia University, Minia, Egypt. Department of Internal Medicine, College of Medicine, Prince Sattam bin Abdulaziz University, Al-Kharj, Saudi Arabia.
 Department of Physical Education, College of Education, King Faisal University, Al-Ahsa, Saudi Arabia. Department of Physical Education, College of Education, King Faisal University, Al-Ahsa, Saudi Arabia. Higher Institute of Sport and Physical Education of Kef, University of Jandouba, Jendouba, Tunisia.
 Neuronal Cell Biology Research Group, Department of Physiology and Neurobiology, Eötvös Loránd University, Budapest, Hungary. Membrane Trafficking and Signalling Group, Institute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany. Membrane Trafficking and Signalling Group, Institute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany; Stuttgart Research Center Systems Biology, University of Stuttgart, Stuttgart, Germany. Neuronal Cell Biology Research Group, Department of Physiology and Neurobiology, Eötvös Loránd University, Budapest, Hungary. Electronic address: schlett.katalin@ttk.elte.hu.
 School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. FutureNeuro, SFI Research Centre for Chronic and Rare Neurological Diseases, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland. School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland. School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. Department of General, Visceral & Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany. Neuroinflammation and Neurodegeneration Group, Girona Biomedical Research Institute (IDIBGI), CERCA Programme/Generalitat de Catalunya, Salt, Girona, Spain. School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. FutureNeuro, SFI Research Centre for Chronic and Rare Neurological Diseases, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland. School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. School of Pharmacy and Biomolecular Science, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland. FutureNeuro, SFI Research Centre for Chronic and Rare Neurological Diseases, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland.
 Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands. Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands.
 Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. CIBER de Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. CIBER de Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain.
 Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Florence 50139, Italy. Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy. Electronic address: laura.maggi@unifi.it. Department of Experimental and Clinical Medicine, University of Florence, Florence 50139, Italy.
 Department of Neurology, Danish Dementia Research Center, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Danish Dementia Research Center, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Regional Dementia Research Centre, Zealand University Hospital, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Medicine, Regional Dementia Research Centre, Zealand University Hospital, University of Copenhagen, Copenhagen, Denmark. Department of Geriatrics, Slagelse Hospital, Slagelse, Denmark. Department of Neurology, Danish Dementia Research Center, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Danish Dementia Research Center, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Dementia Clinic, Aarhus University Hospital, Aarhus, Denmark. Dementia Clinic, Aalborg University Hospital, Aalborg, Denmark. Department of Neurology, Dementia Clinic, Slagelse Hospital, Slagelse, Denmark. Department of Regional Health Research, University of Southern Denmark, Odense, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Danish Multiple Sclerosis Center, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Department of Neurology, Danish Dementia Research Center, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Danish Dementia Research Center, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
 Behavioral Neuropsychology Unit, I.R.C.C.S. "Santa Lucia" Foundation, Via Ardeatina, 306, 00179, Rome, Italy. o.argento@hsantalucia.it. Behavioral Neuropsychology Unit, I.R.C.C.S. "Santa Lucia" Foundation, Via Ardeatina, 306, 00179, Rome, Italy. Behavioral Neuropsychology Unit, I.R.C.C.S. "Santa Lucia" Foundation, Via Ardeatina, 306, 00179, Rome, Italy. Scientific Direction, I.R.C.C.S. "Santa Lucia" Foundation, Rome, Italy. Rehabilitation Centre-Physical Medicine and Rehabilitation Section, OORR-Hospital-University of Foggia, Foggia, Italy. Scientific Direction, "Filippo Turati" Foundation, Rehabilitation Centre, Pistoia, Italy. Behavioral Neuropsychology Unit, I.R.C.C.S. "Santa Lucia" Foundation, Via Ardeatina, 306, 00179, Rome, Italy. Department of Clinical Sciences and Translational Medicine, University of Rome "Tor Vergata", Rome, Italy.
 Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Biomedical Research Institute, Department of Immunology, Hasselt University, Hasselt 3590, Belgium. Department of Pharmacology, Biostatistics, Physiology and Cancer Biology, Thomas Jefferson University, Philadelphia, PA 19107. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Linberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, PA 19104. Department of Orthopedic Surgery, Duke University, Durham, NC 27599. Divison of Laboratory and Genomic Medicine, Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110. Divison of Laboratory and Genomic Medicine, Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110. Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095. Linberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599. Biomedical Research Institute, Department of Immunology, Hasselt University, Hasselt 3590, Belgium. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107. Department of Neurology, Neuroimmunology Division, Thomas Jefferson University, Philadelphia, PA 19107.
 Internal Medicine, Dhaka Medical College and Hospital, Dhaka, BGD. Research and Academic Affairs, Larkin Community Hospital, South Miami, USA. Internal Medicine, Icahn School of Medicine at Mount Sinai, New York City Health + Hospitals/Queens, New York, USA. Internal Medicine, Pramukhswami Medical College, Anand, IND. Internal Medicine, Pramukhswami Medical College, Anand, IND. Internal Medicine, Ross University School of Medicine, Bridgetown, BRB. Internal Medicine, Liaquat University of Medical and Health Sciences, Jamshoro, PAK. Internal Medicine, The University of Jordan, Amman, JOR. Research and Academic Affairs, Larkin Community Hospital, South Miami, USA.
 Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Department of Gastroenterology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Laboratory of Digestive Diseases of the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
 Institute for Mental Health Policy Research, Centre for Addiction and Mental Health. Institute for Mental Health Policy Research, Centre for Addiction and Mental Health. Institute for Mental Health Policy Research, Centre for Addiction and Mental Health.

 Department of Neurology, Cooper Neurological Institute, Cherry Hill, NJ 08002, USA. Department of Neurology, Cooper Neurological Institute, Cherry Hill, NJ 08002, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Neurology, Cooper Neurological Institute, Cherry Hill, NJ 08002, USA. Department of Neurology, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
 Klinika Otolaryngologii CMKP, Mazowiecki Szpital Bródnowski, ul. Kondratowicza 8, Warszawa. Department of Otolaryngology, Centre of Postgraduate Medical Education, Warsaw, Poland. Department of Otolaryngology, Centre of Postgraduate Medical Education, Mazovian Hospital Brodnowski in Warsaw, Poland.
 Retired, Laupheim, Germany. Retired, Laupheim, Germany. Retired, Laupheim, Germany.
 Department of Neuroscience, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia. RINGGOLD: 195017 The Royal College of Surgeons in Ireland, Dublin, Ireland. RINGGOLD: 8863 Department of Medicine, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia. RINGGOLD: 195017 Department of Neuroscience, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia. RINGGOLD: 195017
 King Edward Medical University McLaren Greater Lansing
 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Izmir Katip Celebi University, Izmir, Turkey. Electronic address: merve.saylam@ikc.edu.tr. Department of Biochemistry, Faculty of Pharmacy, Izmir Katip Celebi University, Izmir, Turkey. Department of Biochemistry, Faculty of Pharmacy, Ege University, Izmir, Turkey. Department of Physics, Faculty of Science, Dokuz Eylul Univeristy, Izmir, Turkey. Department of Physics, Faculty of Science, Dokuz Eylul Univeristy, Izmir, Turkey. Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Ege University, Izmir, Turkey. Electronic address: varol.pabuccuoglu@ege.edu.tr.
 Center for Complexity and Biosystems, Department of Environmental Science and Policy, University of Milan, via Celoria 26, 20133 Milano, Italy. CNR - Consiglio Nazionale delle Ricerche, Istituto di Biofisica, via De Marini 6, 16149 Genova, Italy. Center for Complexity and Biosystems, Department of Physics, University of Milan, Via Celoria 16, 20133 Milano, Italy. Center for Complexity and Biosystems, Department of Physics, University of Milan, Via Celoria 16, 20133 Milano, Italy. Center for Complexity and Biosystems, Department of Physics, University of Milan, Via Celoria 16, 20133 Milano, Italy. CNR - Consiglio Nazionale delle Ricerche, Istituto di Chimica della Materia Condensata e di Tecnologie per l'Energia, Via R. Cozzi 53, 20125 Milano, Italy. Center for Complexity and Biosystems, Department of Environmental Science and Policy, University of Milan, via Celoria 26, 20133 Milano, Italy. CNR - Consiglio Nazionale delle Ricerche, Istituto di Biofisica, via De Marini 6, 16149 Genova, Italy.
 Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan. GLIA Center, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan. Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan. skoizumi@yamanashi.ac.jp. GLIA Center, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan. skoizumi@yamanashi.ac.jp.
 Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. Xiangya School of Medicine, Central South University, Changsha, China. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. Xiangya School of Medicine, Central South University, Changsha, China. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. Xiangya School of Medicine, Central South University, Changsha, China. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. Xiangya School of Medicine, Central South University, Changsha, China. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. Xiangya School of Medicine, Central South University, Changsha, China. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Road of Kaifu District, Changsha, 410008, China. luozhaohui_xy@126.com. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. luozhaohui_xy@126.com. Clinical Research Center for Epileptic Disease of Hunan Province, Central South University, Changsha, Hunan, 410008, People's Republic of China. luozhaohui_xy@126.com.
 Department of Neurology, Assuta Medical Center, Ashdod, Israel; Neuroimmunology Clinic, Assuta Medical Center, Ashdod, Israel. Electronic address: yoavpi@assuta.co.il. Department of Neurology, Sourasky Tel Aviv Medical Center, Tel Aviv, Israel; Neuroimmunology Unit, Neurological Institute Aviv Medical Center, Tel Aviv, Israel. Department of Neurology, Sourasky Tel Aviv Medical Center, Tel Aviv, Israel; Neuroimmunology Unit, Neurological Institute Aviv Medical Center, Tel Aviv, Israel. Department of Neurology, Sourasky Tel Aviv Medical Center, Tel Aviv, Israel; Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; Neuroimmunology Unit, Neurological Institute Aviv Medical Center, Tel Aviv, Israel. Department of Neurology, Sourasky Tel Aviv Medical Center, Tel Aviv, Israel; Neuroimmunology Unit, Neurological Institute Aviv Medical Center, Tel Aviv, Israel.
 Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada.
 Department of Radiology, Avicenne Military Hospital, Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakech, MAR. Department of Radiology, Avicenne Military Hospital, Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakech, MAR. Department of Radiology, Avicenne Military Hospital, Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakech, MAR. Department of Radiology, Avicenne Military Hospital, Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakech, MAR. Department of Radiology, Avicenne Military Hospital, Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakech, MAR.
 Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark. Molecular and Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.

 Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Slagelse Hospital, Slagelse, Denmark. Institutes of Regional Health Research and Molecular Medicine, University of Southern Denmark, Odense, Denmark. Programs in Neuroscience and Immunology, Departments of Neurology and Ophthalmology, Sue Anschutz-Rodgers Eye Center, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Department of Neuro-Ophthalmology, Rabin Medical Center, Petah Tikva, Israel. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Neuroimmunology and Multiple Sclerosis Unit, Neurology Service, Hospital Clinic de Barcelona, and Institut d'Investigacions August Pi i Sunyer (IDIVAPS), University of Barcelona, Barcelona, Spain. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Ophthalmology Department, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology Unit, Department of Neuroscience, Hospital Aleman, Buenos Aires, Argentina. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Department of Ophthalmology and Neurology, Mayo Clinic, Rochester, MN, United States. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Internal Medicine, University Teaching Hospital, Lusaka, Zambia. Clinical Neuroimmunology Group, Kids Neuroscience Centre, Sydney, NSW, Australia. Faculty of Medicine and Health and Brain and Mind Centre, University of Sydney, Sydney, NSW, Australia. TY Nelson Department of Paediatric Neurology, Children's Hospital Westmead, Sydney, NSW, Australia. ICREA-IDIBAPS, Service of Neurology, Hospital Clínic, University of Barcelona, Barcelona, Spain. Department of Neurology, University of Pennsylvania, Philadelphia, PA, United States. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Laboratory Medicine and Pathology, Departments of Neurology, Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, United States. Neuro-Ophthalmology Unit, Pierre Wertheimer Neurological Hospital, Hospices Civils de Lyon, Lyon 1 University, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, IMPACT Team, Lyon, France. Pontificia Universidad Javeriana and Hospital Unviersitario San Ignacio, Bogotá, Colombia. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians-Universität München, Munich, Germany. Department of Neuro-Ophthalmology, Rabin Medical Center, Petah Tikva, Israel. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Neurology, National Cancer Center, Goyang, Republic of Korea. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Neurology Unit, IRCCS Institute of Neurological Sciences, Bologna, Italy. Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy. CIEM MS Center, Federal University of Minas Gerais Medical School, Belo Horizonte, Brazil. Department of Neurology, Oxford University Hospitals, National Health Service Trust, Oxford, United Kingdom. Department of Neurology, Hadassah Medical Center, Hebrew University, Jerusalem, Israel. Neuromyelitis Optica Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States. Neuroimmunology and Multiple Sclerosis Unit, Neurology Service, Hospital Clinic de Barcelona, Barcelona, Spain. Institut d'Investigacions August Pi i Sunyer (IDIVAPS), University of Barcelona, Barcelona, Spain. Neuroimmunology Unit, Department of Neuroscience, Hospital Aleman, Buenos Aires, Argentina. Department of Neuro-Ophthalmology, Rabin Medical Center, Petah Tikva, Israel. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Neuromyelitis Optica Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States. IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy. Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy. Neuro-Ophthalmology Unit, Pierre Wertheimer Neurological Hospital, Hospices Civils de Lyon, Lyon 1 University, Lyon Neuroscience Research Center, INSERM U1028, CNRS UMR5292, IMPACT Team, Lyon, France. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Birmingham Neuro-Ophthalmology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom. Translational Brian Science, Institute of Metabolism and Systems Research, University of Birmingham, Edgbaston, United Kingdom. Faculty of Medicine, University of Botswana, Gaborone, Botswana. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Oxford University Hospitals, National Health Service Trust, Oxford, United Kingdom. Center for Advanced Neurological Research, KS Hegde Medical Academy, Nitte (Deemed to be University), Mangalore, India. Pontificia Universidad Javeriana and Hospital Unviersitario San Ignacio, Bogotá, Colombia. Neuromyelitis Optica Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States. Faculty of Medicine and Health and Brain and Mind Centre, University of Sydney, Sydney, NSW, Australia. Translational Neuroimmunology Group, Kids Neuroscience Centre, Children's Hospital Westmead, Sydney, NSW, Australia. Department of Neurology, Concord Hospital, Sydney, NSW, Australia. Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Neuroimmunology and Multiple Sclerosis Unit, Neurology Service, Hospital Clinic de Barcelona, Barcelona, Spain. Institut d'Investigacions August Pi i Sunyer (IDIVAPS), University of Barcelona, Barcelona, Spain. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Slagelse Hospital, Slagelse, Denmark. Institutes of Regional Health Research and Molecular Medicine, University of Southern Denmark, Odense, Denmark. Ophthalmology Department, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Department of Internal Medicine, University Teaching Hospital, Lusaka, Zambia. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neuroradiology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Surgery, University of Botswana, Gaborone, Botswana. Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Neuroscience Center, Bumrungrad International Hospital, Bangkok, Thailand. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. German Center for Cardiovascular Research (DZHK), Berlin, Germany. Programs in Neuroscience and Immunology, Departments of Neurology and Ophthalmology, Sue Anschutz-Rodgers Eye Center, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Department of Neuro-Ophthalmology, Rabin Medical Center, Petah Tikva, Israel. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Neurology, Hadassah Medical Center, Hebrew University, Jerusalem, Israel. Department of Ophthalmology, Fundación Universitaria Sanitas Facultad de Medicina, Bogotá, Colombia. Department of Neurology, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Pontificia Universidad Javeriana and Hospital Unviersitario San Ignacio, Bogotá, Colombia. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Einstein Center Digital Future, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Berlin, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neuro-Ophthalmology, Rabin Medical Center, Petah Tikva, Israel. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
 Department of Clinical Research, University of Southern Denmark, Denmark. Department of Clinical Research, University of Southern Denmark, Denmark. The Interdisciplinary Center on Population Dynamics, University of Southern Denmark, Denmark. Department of Clinical Research, University of Southern Denmark, Denmark. The Interdisciplinary Center on Population Dynamics, University of Southern Denmark, Denmark. Danish Institute for Advanced Study, University of Southern Denmark, Denmark.
 Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Berlin School of Mind and Brain, Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health and Max Delbrück Center for Molecular Medicine, Berlin, Germany. NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt Universität zu Berlin, Berlin Institute of Health (BIH), Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health and Max Delbrück Center for Molecular Medicine, Berlin, Germany. Department of Neurology, RWTH Aachen University, Aachen, Germany. JARA Brain Institute Molecular Neuroscience and Neuroimaging (INM-11), Research Centre Jülich and RWTH Aachen University, Aachen, Germany. Department of Neurology, RWTH Aachen University, Aachen, Germany. JARA Brain Institute Molecular Neuroscience and Neuroimaging (INM-11), Research Centre Jülich and RWTH Aachen University, Aachen, Germany. Department of Neurology, RWTH Aachen University, Aachen, Germany. JARA Brain Institute Molecular Neuroscience and Neuroimaging (INM-11), Research Centre Jülich and RWTH Aachen University, Aachen, Germany. Institute for Medical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health and Max Delbrück Center for Molecular Medicine, Berlin, Germany. Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health and Max Delbrück Center for Molecular Medicine, Berlin, Germany. NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt Universität zu Berlin, Berlin Institute of Health (BIH), Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, RWTH Aachen University, Aachen, Germany. JARA Brain Institute Molecular Neuroscience and Neuroimaging (INM-11), Research Centre Jülich and RWTH Aachen University, Aachen, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Berlin Center for Advanced Neuroimaging, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
 Natural Products for Neuroprotection and Anti-ageing Research Unit, Chulalongkorn University, Bangkok, Thailand. Siriraj Research Group in Immunobiology and Therapeutic Sciences, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Department of Clinical Microscopy, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand. Department of Clinical Microscopy, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand. Natural Products for Neuroprotection and Anti-ageing Research Unit, Chulalongkorn University, Bangkok, Thailand. Natural Products for Neuroprotection and Anti-ageing Research Unit, Chulalongkorn University, Bangkok, Thailand. jamesmichael.b@chula.ac.th. Research, Innovation and International Affairs, Faculty of Allied Health Sciences, Chulalongkorn University, Room 409, ChulaPat-1 Building, 154 Rama 1 Road, Bangkok, 10330, Thailand. jamesmichael.b@chula.ac.th.
 Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: abdorrezamoghadasi@gmail.com.
 Department of Neurosciences, DNS, School of Medicine, University of Padua, Padua, Italy. alessandro.miscioscia@phd.unipd.it. Multiple Sclerosis Centre of the Veneto Region (CeSMuV), Neurology Clinic, University Hospital of Padua, Via Giustiniani, 5, 35128, Padua, Italy. alessandro.miscioscia@phd.unipd.it. Department of Neurosciences, DNS, School of Medicine, University of Padua, Padua, Italy. Multiple Sclerosis Centre of the Veneto Region (CeSMuV), Neurology Clinic, University Hospital of Padua, Via Giustiniani, 5, 35128, Padua, Italy. Department of Neurosciences, DNS, School of Medicine, University of Padua, Padua, Italy. Neuromuscular Center, Neurology Clinic, University Hospital of Padua, Padua, Italy. Multiple Sclerosis Centre of the Veneto Region (CeSMuV), Neurology Clinic, University Hospital of Padua, Via Giustiniani, 5, 35128, Padua, Italy. Multiple Sclerosis Centre of the Veneto Region (CeSMuV), Neurology Clinic, University Hospital of Padua, Via Giustiniani, 5, 35128, Padua, Italy. Department of Neurosciences, DNS, School of Medicine, University of Padua, Padua, Italy. Neuromuscular Center, Neurology Clinic, University Hospital of Padua, Padua, Italy. Department of Neurosciences, DNS, School of Medicine, University of Padua, Padua, Italy. Multiple Sclerosis Centre of the Veneto Region (CeSMuV), Neurology Clinic, University Hospital of Padua, Via Giustiniani, 5, 35128, Padua, Italy.
 Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. Department of Pharmacy, The Hospital of 92880 Troops, PLA Navy, Zhoushan, Zhejiang, China. Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. Institute of Medical Research, Northwestern Polytechnical University, Shaanxi, Xi'an, China. Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. Institute of Medical Research, Northwestern Polytechnical University, Shaanxi, Xi'an, China.
 Department of Biological, Chemical and Pharmaceutical Sciences and Technologies (STEBICEF), University of Palermo, 90128 Palermo, Italy. Department of Biological, Chemical and Pharmaceutical Sciences and Technologies (STEBICEF), University of Palermo, 90128 Palermo, Italy. Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Laboratory Medicine, University of Palermo, 90133 Palermo, Italy.

 LIMES Institute for Membrane Biology and Lipid Biochemistry, University of Bonn, Bonn, Germany. Electronic address: g.echten.deckert@uni-bonn.de.
 School of Infection and Immunity, University of Glasgow, 120 University Place, Glasgow, G12 8TA, UK. School of Infection and Immunity, University of Glasgow, 120 University Place, Glasgow, G12 8TA, UK. Institute of Anatomy, University of Rostock, Gertrudenstrasse 9, 18057, Rostock, Germany. Institute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany. School of Infection and Immunity, University of Glasgow, 120 University Place, Glasgow, G12 8TA, UK. School of Infection and Immunity, University of Glasgow, 120 University Place, Glasgow, G12 8TA, UK. Institute of Systems, Molecules and Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, UK. Institute of Anatomy, University of Rostock, Gertrudenstrasse 9, 18057, Rostock, Germany. Institute of Systems, Molecules and Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, UK. Centre for Glycosciences, Keele University, Keele, ST5 5BG, UK. School of Infection and Immunity, University of Glasgow, 120 University Place, Glasgow, G12 8TA, UK.
 Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Multiple Sclerosis Clinic-CHUM, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Multiple Sclerosis Clinic-CHUM, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Multiple Sclerosis Clinic-CHUM, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada. Multiple Sclerosis Clinic-CHUM, Montréal, QC, Canada. Department of Neurosciences, Faculty of Medicine, Université de Montréal, QC, Canada. Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada.
 Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis & Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: darin.okuda@UTsouthwestern.edu.
 York Health Economics Consortium, York, UK. York Health Economics Consortium, York, UK. Coloplast A/S, Humlebaek, Denmark. York Health Economics Consortium, York, UK. Coloplast A/S, Humlebaek, Denmark. Department of Urology, Moinhos de Vento Hospital, Porto Alegre, Brazil. Department of Urology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Trust, Cambridge, UK.
 From the Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, MD, USA (S.V.O., E.S.B., M.I.G., M.A., D.S.R.); qMRI Core facility, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, MD, USA (H.D., G.N.); Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA (E.S.B.); Office of Biostatistics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA (G.N.); Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences, Bethesda, MD, USA (D.L.P.); Division of Neuroscience, Vita-Salute San Raffaele University and Hospital, Milan, Italy (M.A.); Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA (M.A.); Experimental Immunotherapeutics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA (I.C.M.C.); Neuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA (A.F.); and Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD20814, USA (S.J.).
 Dept of Neurology, University of Virginia, Charlottesville, VA, USA; School of Medicine, Medical University of South Carolina, Charleston, SC, USA. Dept of Neurology, University of Virginia, Charlottesville, VA, USA; Division of Child Neurology, Dept. of Neurology, University of Virginia, Charlottesville, VA, USA. School of Medicine, University of Virginia, Charlottesville, VA, USA. Division of Child Neurology, Children's Hospital of Philadelphia, Dept. of Neurology and Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Division of Child Neurology, Children's Hospital of Philadelphia, Dept. of Neurology and Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Dept of Neurology, University of Virginia, Charlottesville, VA, USA. Dept of Public Health Sciences, University of Virginia, Charlottesville, VA, USA. Dept of Neurology, Virginia Commonwealth University, Richmond, VA, USA. Dept of Neurology, University of Virginia, Charlottesville, VA, USA; Division of Child Neurology, Dept. of Neurology, University of Virginia, Charlottesville, VA, USA. Electronic address: jnb8h@uvahealth.org.
 N-terminus Research Laboratory, Yorba Linda, California, USA. Department of Nutrition and Food Studies, George Mason University, Fairfax, Virginia, USA. Think Healthy Group, Washington, District of Columbia, USA. Division of Biogerontology, Leonard Davis School of Gerontology, The University of Southern California, Los Angeles, California, USA. Division of Molecular & Computational Biology, Dornsife College of Letters, Arts, and Sciences, The University of Southern California, Los Angeles, California, USA. Department Biochemistry & Molecular Medicine, Keck School of Medicine of USC, The University of Southern California, Los Angeles, California, USA. N-terminus Research Laboratory, Yorba Linda, California, USA.
 IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, 00179 Rome, Italy. Laboratory of Immunology, Institute of Experimental Endocrinology and Oncology, National Research Council, 80131 Naples, Italy. Treg Cell Lab, Department of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80131 Naples, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. Synaptic Immunopathology Lab, IRCCS San Raffaele, 00163 Rome, Italy. Department of Human Sciences and Quality of Life Promotion, University of Roma San Raffaele, 00166 Rome, Italy. Department of Systems Medicine, Tor Vergata University, 00133 Rome, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, 20132 Milan, Italy. Clinical Neuroimmunology Unit, Institute of Experimental Neurology (INSpe), Division of Neuroscience, San Raffaele Scientific Institute, 20132 Milan, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. Department of Systems Medicine, Tor Vergata University, 00133 Rome, Italy. Laboratory of Immunology, Institute of Experimental Endocrinology and Oncology, National Research Council, 80131 Naples, Italy. Treg Cell Lab, Department of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80131 Naples, Italy.
 Department of Clinical and Movement Neurosciences, University College London Queen Square Institute of Neurology, London, United Kingdom. Department of Medical Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia. Institute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom. British Heart Foundation University College London Research Accelerator, London, United Kingdom. Department of Cardiology, Division Heart and Lungs, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Clinical and Movement Neurosciences, University College London Queen Square Institute of Neurology, London, United Kingdom. Institute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom. British Heart Foundation University College London Research Accelerator, London, United Kingdom. Department of Cardiology, Division Heart and Lungs, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Clinical and Movement Neurosciences, University College London Queen Square Institute of Neurology, London, United Kingdom. Department of Clinical and Movement Neurosciences, University College London Queen Square Institute of Neurology, London, United Kingdom. Institute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom. British Heart Foundation University College London Research Accelerator, London, United Kingdom. Institute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom. British Heart Foundation University College London Research Accelerator, London, United Kingdom. Health Data Research UK London, University College London. Department of Clinical and Movement Neurosciences, University College London Queen Square Institute of Neurology, London, United Kingdom n.wood@ucl.ac.uk.
 Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Avenida Roraima, 1000, building 21, room 5207, Santa Maria (RS), 97105-900, Brazil. Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Avenida Roraima, 1000, building 21, room 5207, Santa Maria (RS), 97105-900, Brazil. Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Avenida Roraima, 1000, building 21, room 5207, Santa Maria (RS), 97105-900, Brazil. Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Avenida Roraima, 1000, building 21, room 5207, Santa Maria (RS), 97105-900, Brazil. Graduated Program in Biological Sciences: Toxicological Biochemistry, Federal University of Santa Maria (UFSM), Santa Maria (RS), 97105-900, Brazil. Graduate Program in Health Science, University of the Extreme South of Santa Catarina (Unesc), Criciúma, 88806-000, Brazil. Graduate Program in Health Science, University of the Extreme South of Santa Catarina (Unesc), Criciúma, 88806-000, Brazil. Graduate Program in Health Science, University of the Extreme South of Santa Catarina (Unesc), Criciúma, 88806-000, Brazil. Graduate Program in Pharmacology, Federal University of Santa Catarina (UFSC), Florianopólis, 88037-000, Brazil. Graduate Program in Pharmacology, Federal University of Santa Catarina (UFSC), Florianopólis, 88037-000, Brazil. Graduate Program in Pharmacology, Federal University of Santa Catarina (UFSC), Florianopólis, 88037-000, Brazil. Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Avenida Roraima, 1000, building 21, room 5207, Santa Maria (RS), 97105-900, Brazil. gabrielatrevisansantos@gmail.com. Graduated Program in Biological Sciences: Toxicological Biochemistry, Federal University of Santa Maria (UFSM), Santa Maria (RS), 97105-900, Brazil. gabrielatrevisansantos@gmail.com.
 The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Federal State Budgetary Scientific Institution «The Federal Research Center of Fundamental and Translational Medicine», 2 Timakova str., Novosibirsk, 630060, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. Lavrentyev Institute of Hydrodynamics, 15, Akademika Lavrent'yeva pr., Novosibirsk, 630090, Russian Federation. Regional Center for Multiple Sclerosis and other autoimmune diseases of the nervous system, State Budgetary Healthcare Institution of the Novosibirsk Region "State Novosibirsk Regional Clinical Hospital" (GBUZ NSO GNOKB); 126, Nemirovich - Danchenko str., Novosibirsk, 630087, Russian Federation. Novosibirsk State Medical University; 52, Krasny prospect av., Novosibirsk, 630091, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. Lavrentyev Institute of Hydrodynamics, 15, Akademika Lavrent'yeva pr., Novosibirsk, 630090, Russian Federation.
 Multiple Sclerosis and Neuroimmunology Program, Parkinson's and Movement Disorders Center, University Hospitals Cleveland Medical Center, Case Western Reserve School of Medicine, Cleveland, OH, USA. Electronic address: Hesham.abboud@uhhospitals.org.
 Department of Neurology, Methodist Neurological Institute, Weill Cornell Medical College, Houston Methodist Hospital, Houston, TX, United States. Electronic address: gcroman@houstonmethodist.org.
 Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi221005, U.P., India. Pharmaceutical Chemistry Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Pharmaceutical Chemistry Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi 221005, U.P., India. Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi221005, U.P., India.
 Department of Ophthalmology, Schepens Eye Research Institute of Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts. Department of Ophthalmology, Schepens Eye Research Institute of Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts. Electronic address: dongfeng_chen@meei.harvard.edu. Department of Ophthalmology, Schepens Eye Research Institute of Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts.
 Aix Marseille Univ, INSERM, INRA, C2VN, Marseille, France. lourdes.mounien@univ-amu.fr. Université Oran 1, Ahmed Ben Bella, Laboratoire de Physiologie de la Nutrition et Sécurité Alimentaire, Département de Biologie, Faculté des Sciences de la Nature et de la Vie, Oran, Algeria. Université Oran 1, Ahmed Ben Bella, Laboratoire de Physiologie de la Nutrition et Sécurité Alimentaire, Département de Biologie, Faculté des Sciences de la Nature et de la Vie, Oran, Algeria. Aix Marseille Univ, INSERM, INRA, C2VN, Marseille, France. lourdes.mounien@univ-amu.fr. PhenoMARS Aix-Marseille Technology Platform, CriBiom, Marseille, France. Aix Marseille Univ, INSERM, INRA, C2VN, Marseille, France. lourdes.mounien@univ-amu.fr. Aix Marseille Univ, INSERM, INRA, C2VN, Marseille, France. lourdes.mounien@univ-amu.fr.
 Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. Hasso Plattner Institute, University of Potsdam, Potsdam, Germany. Hasso Plattner Institute, University of Potsdam, Potsdam, Germany. Division of General Internal Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USA. Mass General Brigham, Somerville, MA, USA. Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA. Department of Neurology, Medical Faculty University Hospital Düsseldorf, Düsseldorf, Germany. Hasso Plattner Institute, University of Potsdam, Potsdam, Germany. astern@hbs.edu. Harvard Business School, Boston, MA, USA. astern@hbs.edu. Harvard-MIT Center for Regulatory Science, Boston, MA, USA. astern@hbs.edu.

 Nassau University Medical Center Kathmandu University

 Nova Southeastern University University of Utah/John Moran Eye Center; Hoopes Vision/HDR Research Center; Utah Lions Eye Bank
 Research Center of Addiction and Behavioral Sciences, Diabetes Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Department of Advanced Medical Sciences and Technologies, School of Paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. Department of Laboratory Sciences, School of Paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
 Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. filippi.massimo@hsr.it. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. filippi.massimo@hsr.it. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. filippi.massimo@hsr.it.
 Maimonides Biomedical Research Institute of Cordoba, Avda. Menéndez Pidal s/n, 14004 Córdoba, Spain. Maimonides Biomedical Research Institute of Cordoba, Avda. Menéndez Pidal s/n, 14004 Córdoba, Spain. Department of Biochemistry and Molecular Biology, Faculty of Medicine and Nursing, University of Córdoba, Avda. Menéndez Pidal s/n, 14004 Córdoba, Spain.

 Department of Chemistry, Government College Women University, Faisalabad, Pakistan. Department of Chemistry, Government College University, Faisalabad, Pakistan. Department of Chemistry, Government College Women University, Faisalabad, Pakistan. sadia1asim@gmail.com. Department of Botany, Government College Women University, Faisalabad, Pakistan.
 Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
 Center for Drug Discovery and Translational Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Center for Drug Discovery and Translational Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Center for Drug Discovery and Translational Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
 Department of Rheumatology, National Health Organization Utano National Hospital, Kyoto, Japan. Department of Clinical Immunology and Rheumatology, Medical Research Institute KITANO HOSPITAL, PIIF Tazuke-Kofukai, Osaka, Japan. Department of Neurology, National Health Organization Utano National Hospital, Kyoto, Japan. Department of Rheumatology, National Health Organization Utano National Hospital, Kyoto, Japan. Department of Rheumatology, National Health Organization Utano National Hospital, Kyoto, Japan. Department of Rheumatology, National Health Organization Utano National Hospital, Kyoto, Japan.
 School of Medicine, Chongqing University, Chongqing, 400030, China. Department of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Brain and Intelligence Research Key Laboratory of Chongqing Education Commission, Third Military Medical University, Chongqing, 400038, China. Department of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Brain and Intelligence Research Key Laboratory of Chongqing Education Commission, Third Military Medical University, Chongqing, 400038, China. School of Medicine, Chongqing University, Chongqing, 400030, China. School of Medicine, Chongqing University, Chongqing, 400030, China. xiaolan35@hotmail.com. Department of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Brain and Intelligence Research Key Laboratory of Chongqing Education Commission, Third Military Medical University, Chongqing, 400038, China. xiaolan35@hotmail.com.
 Department of Neurology, Tianjin Medical University General Hospital, Tianjin, Tianjin, China. National Clinical Research Center for Neurological Diseases of China, Beijing Tiantan Hospital, Capital Medical University, Beijing, Beijing, China. Department of Neurology, Tianjin Medical University General Hospital, Tianjin, Tianjin, China. National Clinical Research Center for Neurological Diseases of China, Beijing Tiantan Hospital, Capital Medical University, Beijing, Beijing, China. National Clinical Research Center for Neurological Diseases of China, Beijing Tiantan Hospital, Capital Medical University, Beijing, Beijing, China. National Clinical Research Center for Neurological Diseases of China, Beijing Tiantan Hospital, Capital Medical University, Beijing, Beijing, China. Department of Neurology, Tianjin Medical University General Hospital, Tianjin, Tianjin, China fshi@tmu.edu.cn. National Clinical Research Center for Neurological Diseases of China, Beijing Tiantan Hospital, Capital Medical University, Beijing, Beijing, China.
 Department of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, 147004, India. Department of Biotechnology, Thapar Institute of Engineering and Technology, Patiala, Punjab, 147004, India. mvasundhara@thapar.edu.
 Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA. Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA. jderivero@med.miami.edu.
 Department of Basic Biomedical Sciences, Touro College of Osteopathic Medicine, 60 Prospect Ave, Middletown, NY 10940, USA. Department of Basic Biomedical Sciences, Touro College of Osteopathic Medicine, 60 Prospect Ave, Middletown, NY 10940, USA. Department of Basic Biomedical Sciences, Touro College of Osteopathic Medicine, 60 Prospect Ave, Middletown, NY 10940, USA. Department of Emergency Medicine, Vassar Brothers Medical Center, 45 Reade Pl, Poughkeepsie, NY 12601, USA. Department of Obstetrics, OPTUM HEALTH, 2515 South Rd, Poughkeepsie, NY 12601, USA.
 1Norton Neuroscience Institute, Norton Healthcare, Louisville, Kentucky. 2Neurodiagnostic Center of Louisville, Louisville, Kentucky; and. 1Norton Neuroscience Institute, Norton Healthcare, Louisville, Kentucky. 1Norton Neuroscience Institute, Norton Healthcare, Louisville, Kentucky. 3Department of Neurological Surgery, University of Louisville School of Medicine, Louisville, Kentucky.
 Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Anesthesia Medical Research Center, Central South University, Changsha, Hunan, China. Clinical Laboratory, The Second Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Anesthesia Medical Research Center, Central South University, Changsha, Hunan, China. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Anesthesia Medical Research Center, Central South University, Changsha, Hunan, China. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Anesthesia Medical Research Center, Central South University, Changsha, Hunan, China. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Anesthesia Medical Research Center, Central South University, Changsha, Hunan, China.

 College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, SAU. Research and Development, King Abdullah International Medical Research Center, Jeddah, SAU. College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, SAU. Research and Development, King Abdullah International Medical Research Center, Jeddah, SAU. Department of Medicine, Ministry of the National Guard-Health Affairs, Jeddah, SAU. Department of Medicine, Ministry of the National Guard-Health Affairs, Jeddah, SAU. Department of Medicine, Ministry of the National Guard-Health Affairs, Jeddah, SAU.
 Department of Physical Therapy, Boston University, Boston, MA, United States. Salisbury NHS Foundation Trust, Salisbury, United Kingdom. Department of Physiotherapy, Imperial College Healthcare NHS, London, United Kingdom. Department of Physical Therapy, Arcadia University, Glenside, PA, United States. Department of Electronics Information and Bioengineering, Politecnico di Milano, Milan, Italy. University of Southampton, Southampton, United Kingdom. Queen Margaret University, Musselburgh, United Kingdom.
 Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Immunology & Microbiology, University of Colorado Anschutz School of Medicine, United States of America. Department of Immunology & Microbiology, University of Colorado Anschutz School of Medicine, United States of America. Scientific Affairs, EUROIMMUN, United States of America. Scientific Affairs, EUROIMMUN, United States of America. Scientific Affairs, EUROIMMUN, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Immunology & Microbiology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Department of Immunology & Microbiology, University of Colorado Anschutz School of Medicine, United States of America. Department of Immunology & Microbiology, University of Colorado Anschutz School of Medicine, United States of America; Department of Pediatrics, Section of Allergy and Immunology, University of Colorado Anschutz School of Medicine, United States of America. Department of Neurology, University of Colorado Anschutz School of Medicine, United States of America. Electronic address: Amanda.Piquet@cuanschutz.edu.
 Department of Neurology, Center of Clinical Neuroscience, Carl Gustav Carus University Clinic, University Hospital of Dresden, Technische Universität Dresden, 01307 Dresden, Germany. Novartis Pharma GmbH, 90429 Nuremberg, Germany. Novartis Pharma GmbH, 90429 Nuremberg, Germany. Institute for Immunology, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.
 Department of Medicine, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Cell and Cancer Biology, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Medicine, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Bioengineering, University of Toledo College of Engineering, Toledo, OH 43606, USA. Department of Cell and Cancer Biology, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Cell and Cancer Biology, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Medicine, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Cell and Cancer Biology, University of Toledo College of Medicine, Toledo, OH 43614, USA. Department of Bioengineering, University of Toledo College of Engineering, Toledo, OH 43606, USA.
 Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Statistics, Faculty of Economics and Statistics, University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Nuclear Medicine, Medical University of Innsbruck, Innsbruck, Austria. Central Institute of Medical and Chemical Laboratory Diagnostics (ZIMCL), University Hospital of Innsbruck, Innsbruck, Austria. Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria. Central Institute of Medical and Chemical Laboratory Diagnostics (ZIMCL), University Hospital of Innsbruck, Innsbruck, Austria. Department of Nuclear Medicine, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Clinical Division of General Internal Medicine, Department of Internal Medicine, Medical University Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: franziska.dipauli@i-med.ac.at.
 Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital of Würzburg, Würzburg, Germany. Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital of Würzburg, Würzburg, Germany. harald.wajant@mail.uni-wuerzburg.de.
 Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China. Department of Hematology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. School of Medicine, South China University of Technology, Guangzhou 510006, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. Department of Ophthalmology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. School of Medicine, South China University of Technology, Guangzhou 510006, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. Sepulveda Ambulatory Care Center, Veterans Affairs Greater Los Angeles Healthcare System, North Hills, California, USA. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China. School of Medicine, South China University of Technology, Guangzhou 510006, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China. Department of Gastroenterology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China. School of Medicine, South China University of Technology, Guangzhou 510006, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China.
 Institute for Combinatorial Advanced Research and Education (KDU-CARE), General Sir John Kotelawala Defense University, Sri Lanka. Interdisciplinary Centre for Innovation in Biotechnology and Neurosciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka. Institute for Combinatorial Advanced Research and Education (KDU-CARE), General Sir John Kotelawala Defense University, Sri Lanka. Interdisciplinary Centre for Innovation in Biotechnology and Neurosciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka. Department of Cellular Neuroscience, Faculty of Health, Medicine & Life Sciences, Maastricht University, Maastricht, Netherlands. Institute for Combinatorial Advanced Research and Education (KDU-CARE), General Sir John Kotelawala Defense University, Sri Lanka. Interdisciplinary Centre for Innovation in Biotechnology and Neurosciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka. Department of Cellular Neuroscience, Faculty of Health, Medicine & Life Sciences, Maastricht University, Maastricht, Netherlands. Interdisciplinary Centre for Innovation in Biotechnology and Neurosciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka. Department of Biomedical Engineering, University of Houston, Houston, TX, USA. Institute for Combinatorial Advanced Research and Education (KDU-CARE), General Sir John Kotelawala Defense University, Sri Lanka. Interdisciplinary Centre for Innovation in Biotechnology and Neurosciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka.
 Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. Department of Orthopaedic and Traumatology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia. Department of Orthopaedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
 Department of Basic Sciences and Social Sciences, North-Eastern Hill University, Shillong 793022, Meghalaya, India. Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia. Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia. Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia. Department of Microbiology, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim University, Aligarh 202002, India. Department of Environment and Forest Resources, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 34134, Republic of Korea.
 Department of Medical Physiology, Faculty of Medicine, Alexandria University, Alexandria, Egypt. doaa.abdelhady@alexmed.edu.eg. Department of Histology and Cell Biology, Faculty of Medicine, Alexandria University, Alexandria, Egypt. Department of Medical Physiology, Faculty of Medicine, Alexandria University, Alexandria, Egypt. Medical Biochemistry Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt. Center of Excellence for Research in Regenerative Medicine and Applications (CERRMA), Faculty of Medicine, Alexandria University, Alexandria, Egypt. Department of Clinical Pharmacology, Faculty of Medicine, Alexandria University, Alexandria, Egypt. Department of Biochemistry, Faculty of Science, Alexandria University, Alexandria, Egypt. Bioscreening and Preclinical Trial Lab, Faculty of Science, Alexandria University, Alexandria, Egypt.
 Academic and Research Collaborative in Health (ARCH), La Trobe University, Melbourne, Australia. The Victorian Rehabilitation Centre, Healthscope, Melbourne, Australia. Faculty of Medicine, Dentistry and Health Sciences, Department of Physiotherapy, 2281The University of Melbourne, Melbourne, Australia. Physiotherapy Department and Health Independence Program, 3805Austin Health, Heidelberg, Australia. Faculty of Medicine, Dentistry and Health Sciences, Department of Physiotherapy, 2281The University of Melbourne, Melbourne, Australia. Faculty of Medicine, Dentistry and Health Sciences, Department of Physiotherapy, 2281The University of Melbourne, Melbourne, Australia. Faculty of Medicine, Dentistry and Health Sciences, Department of Physiotherapy, 2281The University of Melbourne, Melbourne, Australia.
 Massachusetts General Hospital, Department of Psychiatry, Boston, MA 02114 USA; Harvard Medical School, Integrative Medicine, Boston, MA 02115 USA. The Ohio State University, Department of Psychology, Columbus, OH, 43210 USA. The Ohio State University, Department of Psychology, Columbus, OH, 43210 USA. The Ohio State University, Department of Psychology, Columbus, OH, 43210 USA. The Ohio State University, Department of Psychology, Columbus, OH, 43210 USA. OhioHealth Multiple Sclerosis Center, Columbus, OH 43214 USA. The Ohio State University, Department of Biostatistics, Columbus, Ohio, USA. The Ohio State University, Department of Psychology, Columbus, OH, 43210 USA; The Ohio State University, Center for Cognitive and Behavioral Brain Imaging, Columbus, Ohio, 43210 USA. Electronic address: prakash.30@osu.edu.
 Institute of Chemical Biology, Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, Novosibirsk 630090, Russia. Institute of Chemical Biology, Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, Novosibirsk 630090, Russia. Institute of Chemical Biology, Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, Novosibirsk 630090, Russia. Institute of Chemical Biology, Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, Novosibirsk 630090, Russia.
 Department of Exercise Physiology and Functional Anatomy, Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Toruń, Świętojańska 20, Bydgoszcz 85-077, Poland. Department of Exercise Physiology and Functional Anatomy, Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Toruń, Świętojańska 20, Bydgoszcz 85-077, Poland. Department of Exercise Physiology and Functional Anatomy, Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Toruń, Świętojańska 20, Bydgoszcz 85-077, Poland. Department of Exercise Physiology and Functional Anatomy, Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Toruń, Świętojańska 20, Bydgoszcz 85-077, Poland. Department of Exercise Physiology and Functional Anatomy, Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Toruń, Świętojańska 20, Bydgoszcz 85-077, Poland. Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Warsaw Medical University, 1b Banacha Street, Warsaw 02-097, Poland.
 Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Translational Center of Excellence for Neuroepidemiology and Neurology Outcomes Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Leonard Davis Institute for Health Economics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Translational Center of Excellence for Neuroepidemiology and Neurology Outcomes Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Translational Center of Excellence for Neuroepidemiology and Neurology Outcomes Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Leonard Davis Institute for Health Economics, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
 Program On Regulation, Therapeutics, And Law (PORTAL), Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America. Program On Regulation, Therapeutics, And Law (PORTAL), Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America. The Hastings Center, Garrison, New York, United States of America. Program On Regulation, Therapeutics, And Law (PORTAL), Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America. Program On Regulation, Therapeutics, And Law (PORTAL), Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America. Program On Regulation, Therapeutics, And Law (PORTAL), Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.
 Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Indian Scientific Education and Technology Foundation, Lucknow 226002, India. Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Faculty of Nursing and Podiatry, University of Valencia, 46010 Valencia, Spain. Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Faculty of Nursing and Podiatry, University of Valencia, 46010 Valencia, Spain. Department of Physiology, School of Medicine, University of Valencia, Blasco Ibañez 15, 46010 Valencia, Spain. Faculty of Nursing and Podiatry, University of Valencia, 46010 Valencia, Spain.
 Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Department of Endocrinology, the Second People's Hospital of Hefei, the Affiliated Hefei Hospital of Anhui Medical University, Hefei 230011, Anhui, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China; Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China. Electronic address: wangpeng19910318@sina.com. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei 230032, Anhui, China; Institute of Kidney Disease, Inflammation & Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, China. Electronic address: panhaifeng@ahmu.edu.cn.
 University of Puerto Rico, Medical Sciences Campus, Neurosurgery Section
 Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinic Research Center for Mental Disorders, Changsha, Hunan, China. National Technology Institute on Mental Disorders, Changsha, Hunan, China. Hunan Key Laboratory of Psychiatry and Mental Health, Changsha, Hunan, China. Mental Health Institute, Second Xiangya Hospital, Central South University, Changsha, China. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinic Research Center for Mental Disorders, Changsha, Hunan, China. National Technology Institute on Mental Disorders, Changsha, Hunan, China. Hunan Key Laboratory of Psychiatry and Mental Health, Changsha, Hunan, China. Mental Health Institute, Second Xiangya Hospital, Central South University, Changsha, China. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinic Research Center for Mental Disorders, Changsha, Hunan, China. National Technology Institute on Mental Disorders, Changsha, Hunan, China. Hunan Key Laboratory of Psychiatry and Mental Health, Changsha, Hunan, China. Mental Health Institute, Second Xiangya Hospital, Central South University, Changsha, China. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinic Research Center for Mental Disorders, Changsha, Hunan, China. National Technology Institute on Mental Disorders, Changsha, Hunan, China. Hunan Key Laboratory of Psychiatry and Mental Health, Changsha, Hunan, China. Mental Health Institute, Second Xiangya Hospital, Central South University, Changsha, China. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinic Research Center for Mental Disorders, Changsha, Hunan, China. National Technology Institute on Mental Disorders, Changsha, Hunan, China. Hunan Key Laboratory of Psychiatry and Mental Health, Changsha, Hunan, China. Mental Health Institute, Second Xiangya Hospital, Central South University, Changsha, China. Clinical Laboratory, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinic Research Center for Mental Disorders, Changsha, Hunan, China. National Technology Institute on Mental Disorders, Changsha, Hunan, China. Hunan Key Laboratory of Psychiatry and Mental Health, Changsha, Hunan, China. Mental Health Institute, Second Xiangya Hospital, Central South University, Changsha, China.
 School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: wsy1698@foxmail.com. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: zhaohuishouyi@ccmu.edu.cn. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: chenjie9922@163.com. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: 2414319889@qq.com. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: 15510170815@163.com. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: tmwangl@ccmu.edu.cn. School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China. Electronic address: zouhy@ccmu.edu.cn.
 Department of Nursing, West China Hospital, West China School of Nursing, Sichuan University, Chengdu, China. Key Laboratory of Veterinary Pharmaceutical Development, Ministry of Agriculture, Lanzhou, China. Key Laboratory of New Animal Drug Project of Gansu Province, Lanzhou, China. Lanzhou Institute of Husbandry and Pharmaceutical Sciences, Chinese Academy of Agricultural Sciences, Lanzhou, China. Department of Nursing, West China Hospital, West China School of Nursing, Sichuan University, Chengdu, China. Department of Nursing, West China Hospital, West China School of Nursing, Sichuan University, Chengdu, China. Department of Nursing, West China Hospital, West China School of Nursing, Sichuan University, Chengdu, China. Department of Nursing, West China Hospital, West China School of Nursing, Sichuan University, Chengdu, China. State Key Laboratory of Biogeology and Environmental Geology, China University of Geosciences, Wuhan, China. Department of Microbiology, Hazara University Mansehra, Mansehra, Pakistan. Department of Nursing, West China Hospital, West China School of Nursing, Sichuan University, Chengdu, China.
 Department of Ophthalmology (HHC), Stanford University School of Medicine, Palo Alto, California; and Departments of Pathology (SF-P), Dermatology (GHB), Pathology and Dermatology (KER), Radiology (HMD), and Ophthalmology, Neurology and Neurosciences (SJB), Stanford University School of Medicine, Stanford, California.
 Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany orhan.aktas@uni-duesseldorf.de bruce.cree@ucsf.edu. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia. Department of Neurology, Medical University Vienna, Vienna, Austria. Department of Neurology, Palacky University in Olomouc, Olomouc, Czech Republic. Horizon Therapeutics plc, Gaithersburg, Maryland, USA. Horizon Therapeutics plc, Gaithersburg, Maryland, USA. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University, Koriyama, Fukushima, Japan. Multiple Sclerosis and Neuromyelitis Optica Center, Southern Tohoku Research Institute for Neuroscience, Koriyama, Japan. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité, Universitätsmedizin Berlin, Berlin, Germany. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hopital Neurologique et Neurochirurgical Pierre Wertheimer Centre de reference des syndromes neurologiques paraneoplasiques et encephalites auto-immun, Lyon, Auvergne-Rhône-Alpes, France. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, USA. Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Republic of Korea. Department of Neurology, University of Virginia, Charlottesville, Virginia, USA. Department of Neurology and Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA. Horizon Therapeutics plc, Gaithersburg, Maryland, USA. Horizon Therapeutics plc, Gaithersburg, Maryland, USA. Horizon Therapeutics plc, Gaithersburg, Maryland, USA. Horizon Therapeutics plc, Gaithersburg, Maryland, USA. Department of Neurology, UCSF, Weill Institute for Neurosciences, University California of San Francisco, San Francisco, California, USA orhan.aktas@uni-duesseldorf.de bruce.cree@ucsf.edu.
 Department of Pharmacology, Hospital Group Paris-Saclay, Assistance Publique-Hôpitaux de Paris, Paris, France. Anti-Infective Evasion and Pharmacoepidemiology, Centre for Epidemiology and Population Health, INSERM U1018, Villejuif, France. Department of Pharmacoepidemiology, Faculty of Medicine and Health Science, University Versailles Saint-Quentin/Paris-Saclay, Paris, France. Department of Neurology, Hospital Foundation Adolphe de Rothschild, Paris, France. Department of Neurology, Faculty of Medicine, Paris-Cité University, Paris, France. [RE]MEDs, Rueil Malmaison, France. [RE]MEDs, Rueil Malmaison, France. [RE]MEDs, Rueil Malmaison, France. Department of Biostatistics, Centre Hospitalier Universitaire Rouen, Rouen, France. [RE]MEDs, Rueil Malmaison, France. [RE]MEDs, Rueil Malmaison, France. Réeseau Enquêtes Santê A L, Paris, France. Now at London School of Hygiene and Tropical Medicine, London, United Kingdom.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province; Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi Province, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province; Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, China. Institute of Brain Science/Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases/Medical School, Shanxi Datong University, Datong, Shanxi Province, China. Institute of Neurology, Huashan Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong; Institute of Brain Science/Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases/Medical School, Shanxi Datong University, Datong, Shanxi Province, China.
 Department of Clinical Laboratory Sciences, School of Health Sciences, Fukushima Medical University, Fukushima, Japan. Glycobiology Research Group, RIKEN, Saitama, Japan. Central Biomedical Laboratory, Aino University, Osaka, Japan. Glycobiology Research Group, RIKEN, Saitama, Japan. Department of Advanced Biosciences, Ochanomizu University, Tokyo, Japan. Department of Infectious Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Department of Neurology, Fukushima Medical University, Fukushima, Japan. Department of Neurology, Fukushima Medical University, Fukushima, Japan. Department of Diagnostic Pathology, Fukushima Medical University, Fukushima, Japan. Department of Neurology, Fukushima Medical University, Fukushima, Japan. Department of Advanced Biosciences, Ochanomizu University, Tokyo, Japan. Center for Translational Neuromedicine, University of Copenhagen, Copenhagen, Denmark. Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan. Division of Neurobiology and Anatomy, Niigata University, Niigata, Japan. Division of Neurobiology and Anatomy, Niigata University, Niigata, Japan. Department of Infectious Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Division of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Research Center for Asian Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Department of Clinical Laboratory Sciences, School of Health Sciences, Fukushima Medical University, Fukushima, Japan. Department of Clinical Laboratory Sciences, School of Health Sciences, Fukushima Medical University, Fukushima, Japan. Glycobiology Research Group, RIKEN, Saitama, Japan.
 Departamento de Estatística e Investigação Operacional, Faculdade de Ciências, Universidade de Lisboa, Lisboa, Portugal. Faculty of Mathematics & Information Science, Warsaw University of Technology, Warsaw, Poland. Faculty of Mathematics & Information Science, Warsaw University of Technology, Warsaw, Poland. Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal. Department of Biophysics, Physiology, And Pathophysiology, Medical University of Warsaw, Warsaw, Poland. Department of Infection Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom. Department of Statistics, Mathematical Analysis and Optimization, Universidade de Santiago de Compostela, Santiago de Compostela, Spain. Faculty of Mathematics & Information Science, Warsaw University of Technology, Warsaw, Poland. Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal. Departamento de Estatística e Investigação Operacional, Faculdade de Ciências, Universidade de Lisboa, Lisboa, Portugal. Faculty of Mathematics & Information Science, Warsaw University of Technology, Warsaw, Poland. Institute of Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin and Berlin Institute of Health, Berlin, Germany. Department of Health Studies, Institute of Biomedical Science, FH Joanneum University of Applied Sciences, Graz, Austria. Centro Integrativo de Biología y Química Aplicada (CIBQA), Universidad Bernardo O'Higgins, Santiago, Chile. Department of Clinical Research, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom. BC Women's Hospital, Vancouver, BC V6H 3N1, Canada. Department of Life Sciences and Centre for Inflammation Research and Translational Medicine, Brunel University London, United Kingdom. Department of Clinical Research, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom. Faculty of Mathematics & Information Science, Warsaw University of Technology, Warsaw, Poland. Faculty of Mathematics & Information Science, Warsaw University of Technology, Warsaw, Poland.
 International School, Jinan University, Guangzhou 510080, China. School of Basic Medicine and Public Health, Jinan University, Guangzhou 510632, China. Center for Data Science, New York University, New York, NY 10011, USA. Department of Nutrition, School of Medicine, Jinan University, Guangzhou 510632, China. Department of Nutrition, School of Medicine, Jinan University, Guangzhou 510632, China. Department of Nutrition, School of Medicine, Jinan University, Guangzhou 510632, China. Department of Nutrition, School of Medicine, Jinan University, Guangzhou 510632, China. Department of Nutrition, School of Medicine, Jinan University, Guangzhou 510632, China. School of Biomedical Engineering, Southern Medical University, Guangzhou 510515, China. Department of Nutrition, School of Medicine, Jinan University, Guangzhou 510632, China. Disease Control and Prevention Institute, Jinan University, Guangzhou 510632, China.
 Department of Integrative Biology and Physiology, UCLA School of Life Sciences, University of California, Los Angeles, Los Angeles, California, USA. Pacific Neuroscience Institute, Saint John's Cancer Institute at Providence Saint John's Health Center, Santa Monica, California, USA. Department of Integrative Biology and Physiology, UCLA School of Life Sciences, University of California, Los Angeles, Los Angeles, California, USA. Department of Entomology and Nematology, UC Davis Comprehensive Cancer Center, University of California, Davis, Davis, California, USA. Department of Entomology and Nematology, UC Davis Comprehensive Cancer Center, University of California, Davis, Davis, California, USA. UCLA Institute for Quantitative and Computational Biosciences, University of California at Los Angeles, Los Angeles, California, USA. Institute of Control and Computation Engineering, Warsaw University of Technology, Warsaw, Poland. UCLA Institute for Quantitative and Computational Biosciences, University of California at Los Angeles, Los Angeles, California, USA. Institute of Control and Computation Engineering, Warsaw University of Technology, Warsaw, Poland. Semel Institute, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. Semel Institute, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. Department of Integrative Biology and Physiology, UCLA School of Life Sciences, University of California, Los Angeles, Los Angeles, California, USA.
 Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA. Institute for Healthcare Policy and Innovation, University of Michigan, Ann Arbor, MI, USA. Institute for Healthcare Policy and Innovation, University of Michigan, Ann Arbor, MI, USA. Department of Neurology, Divisions of Neuroimmunology/Multiple Sclerosis and Sleep Medicine, University of Michigan Ann Arbor, Ann Arbor, MI, USA.
 Department of Pathobiology and Medical Laboratory Sciences, North Khorasan University of Medical Sciences, Bojnurd, Iran. Department of Internal Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran. Department of Pathobiology and Medical Laboratory Sciences, North Khorasan University of Medical Sciences, Bojnurd, Iran; Vector-borne Diseases Research Center, North Khorasan University of Medical Sciences, Bojnurd, Iran. Electronic address: namdar360@gmail.com.
 Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
 A.V. Zhirmunsky National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, Vladivostok 690041, Russia. A.V. Zhirmunsky National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, Vladivostok 690041, Russia.
 Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India. Electronic address: drlokeshsaini@gmail.com. Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India. Department of Diagnostic and Interventional Radiology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India. Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India. Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India. Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India. Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India.
 Department of Psychology, University of Southern Denmark, Campusvej 55, 5230, Odense, Denmark. ahandersen@health.sdu.dk. Department of Neurology, Odense University Hospital, Odense, Denmark. Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark. Department of Psychology, University of Southern Denmark, Campusvej 55, 5230, Odense, Denmark.
 Department of Bioengineering, Swanson School of Engineering, University of Pittsburgh, 4200 Fifth Ave, Pittsburgh, PA, 15260, USA. Department of Bioengineering, Swanson School of Engineering, University of Pittsburgh, 4200 Fifth Ave, Pittsburgh, PA, 15260, USA. Department of Epidemiology, School of Public Health, University of Pittsburgh, 4200 Fifth Ave, Pittsburgh, PA, 15260, USA. The Edward S. Rogers Department of Electrical and Computer Engineering, Faculty of Applied Science and Engineering, University of Toronto, 27 King's College Cir, Toronto, ON, M5S, Canada. esejdic@ieee.org. North York General Hospital, 4001 Leslie St., Toronto, ON, M2K, Canada. esejdic@ieee.org.
 Department of Psychology, Christ University, Bangalore. vijayapriyacv@gmail.com. Department of Psychology, Christ University, Bangalore. rmhbabu@gmail.com.
 Department of Radiology, West Virginia University, Morgantown, WV, USA. RINGGOLD: 5631 Department of Radiology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915 Department of Radiology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915 Department of Radiology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915 Department of Neurology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915 Department of Radiology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915 Department of Radiology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915 Department of Radiology, Mayo Clinic, Jacksonville, FL, USA. RINGGOLD: 6915
 Medical Toxicology and Drug Abuse Research Center (MTDRC), Birjand University of Medical Sciences (BUMS), Birjand, Iran. Department of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of medical biotechnology, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran. Medical Toxicology and Drug Abuse Research Center (MTDRC), Birjand University of Medical Sciences (BUMS), Birjand, Iran. School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool, UK. Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, School of Medicine, University of Palermo, 90133 Palermo, Italy. Surgical Oncology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. School of Medicine, The University of Western Australia, Perth, Australia. Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
 Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neuroscience Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neuroscience Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neuroscience Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Center for Translational Neuroscience, Isfahan University of Medical Sciences, Isfahan, Iran. i_adibi@med.mui.ac.ir. Isfahan Neuroscience Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. i_adibi@med.mui.ac.ir. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. i_adibi@med.mui.ac.ir.
 Tehran University of Medical Sciences, Tehran, Iran. Universal Scientific Education and Research Network (USERN), Harare, Zimbabwe. Tehran University of Medical Sciences, Tehran, Iran. Universal Scientific Education and Research Network (USERN), Tehran, Iran. Tehran University of Medical Sciences, Tehran, Iran. Universal Scientific Education and Research Network (USERN), Tehran, Iran. Universal Scientific Education and Research Network (USERN), Harare, Zimbabwe. Tehran University of Medical Sciences, Tehran, Iran. Universal Scientific Education and Research Network (USERN), Tehran, Iran. Tehran University of Medical Sciences, Tehran, Iran. Universal Scientific Education and Research Network (USERN), Tehran, Iran. Tehran University of Medical Sciences, Tehran, Iran. Tehran University of Medical Sciences, Tehran, Iran. Universal Scientific Education and Research Network (USERN), Stockholm, Sweden.
 Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, 15784, Greece. Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, 15784, Greece. Department of Clinical Therapeutics, School of Medicine, Alexandra General Hospital, National and Kapodistrian University of Athens, Athens, 11528, Greece. Department of Clinical Therapeutics, School of Medicine, Alexandra General Hospital, National and Kapodistrian University of Athens, Athens, 11528, Greece. Electronic address: eterpos@med.uoa.gr.
 All India Institute of Medical Sciences Ohio University
 Institute of pharmaceutical research, GLA University, Mathura, U.P, INDIA, 281406. Institute of pharmaceutical research, GLA University, Mathura, U.P, INDIA, 281406.
 Center for Brain Immunology and Glia (BIG), Washington University in St. Louis, St. Louis, MO, 63110, USA. t.mamuladze@wustl.edu. Department of Pathology and Immunology, School of Medicine, Washington University in St. Louis, St. Louis, MO, 63110, USA. t.mamuladze@wustl.edu. Immunology Graduate Program, School of Medicine, Washington University in St. Louis, St. Louis, MO, 63110, USA. t.mamuladze@wustl.edu. Center for Brain Immunology and Glia (BIG), Washington University in St. Louis, St. Louis, MO, 63110, USA. kipnis@wustl.edu. Department of Pathology and Immunology, School of Medicine, Washington University in St. Louis, St. Louis, MO, 63110, USA. kipnis@wustl.edu. Immunology Graduate Program, School of Medicine, Washington University in St. Louis, St. Louis, MO, 63110, USA. kipnis@wustl.edu.
 Clinical Pharmacology and Pharmacometrics, Biogen, Cambridge, MA, USA. Clinical Pharmacology and Pharmacometrics, Biogen, Cambridge, MA, USA. Clinical Pharmacology and Pharmacometrics, Biogen, Cambridge, MA, USA. Clinical Pharmacology and Pharmacometrics, Biogen, Cambridge, MA, USA. Clinical Pharmacology and Pharmacometrics, Biogen, Cambridge, MA, USA. Clinical Pharmacology and Pharmacometrics, Biogen, Cambridge, MA, USA.
 State Key Laboratory of Southwest Chinese Medicine Resources, Chengdu, Sichuan 611137, P.R. China. College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China. State Key Laboratory of Southwest Chinese Medicine Resources, Chengdu, Sichuan 611137, P.R. China. College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China. Department of Pharmacy, Zigong Hospital of Traditional Chinese Medicine, Zigong, Sichuan 643000, P.R. China. State Key Laboratory of Southwest Chinese Medicine Resources, Chengdu, Sichuan 611137, P.R. China. College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China. State Key Laboratory of Southwest Chinese Medicine Resources, Chengdu, Sichuan 611137, P.R. China. College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China. State Key Laboratory of Southwest Chinese Medicine Resources, Chengdu, Sichuan 611137, P.R. China. College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China. Institute for Interdisciplinary Medicine Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China. Shanghai Frontiers Science Center of Traditional Chinese Medicine Chemical Biology, Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China. State Key Laboratory of Southwest Chinese Medicine Resources, Chengdu, Sichuan 611137, P.R. China. College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China.
 Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Physiology, Faculty of Medicine, Aristotle University of Thessaloniki, 541 24 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. First Department of Neurology, Aeginition Hospital, National and Kapodistrian University of Athens, 115 28 Athens, Greece. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 546 36 Thessaloniki, Greece. Laboratory of Physiology, Faculty of Medicine, Aristotle University of Thessaloniki, 541 24 Thessaloniki, Greece.
 European Institute for Molecular Imaging (EIMI), Münster, Germany. Institut für Physiologie I, Münster, Germany. Cellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases (IfGH), University of Münster, Münster, Germany. Cellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases (IfGH), University of Münster, Münster, Germany. Klinik für Neurologie mit Institut für Translationale Neurologie, ICB, Münster, Germany. Institut für Physiologie I, Münster, Germany. Department of Neurosciences, Psychology, Drug Research and Child Health (NeuroFarBa), University of Florence, Florence, Italy. Klinik für Neurologie mit Institut für Translationale Neurologie, ICB, Münster, Germany. Klinik für Neurologie mit Institut für Translationale Neurologie, ICB, Münster, Germany. Universitätsklinikum Düsseldorf, Medizinische Fakultät, Klinik für Neurologie, Düsseldorf, Germany. Klinik für Neurologie mit Institut für Translationale Neurologie, ICB, Münster, Germany. Cellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases (IfGH), University of Münster, Münster, Germany. Institut für Physiologie I, Münster, Germany. European Institute for Molecular Imaging (EIMI), Münster, Germany.
 F. Hoffmann-La Roche Ltd., Global Product Strategy - Product Optimization, Grenzacher Strasse 124, CH-4070 Basel, Switzerland. GRID: grid.417570.0. ISNI: 0000 0004 0374 1269
 Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn(2)), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address: tineke.vogelaar@unimedizin-mainz.de.
 InSilicoTrials Technologies S.P.A, Riva Grumula 2, 34123, Trieste, Italy. InSilicoTrials Technologies B.V., Bruistensingel 130, 5232 AC, 's Hertogenbosch, The Netherlands. InSilicoTrials Technologies S.P.A, Riva Grumula 2, 34123, Trieste, Italy. InSilicoTrials Technologies S.P.A, Riva Grumula 2, 34123, Trieste, Italy. InSilicoTrials Technologies S.P.A, Riva Grumula 2, 34123, Trieste, Italy. InSilicoTrials Technologies S.P.A, Riva Grumula 2, 34123, Trieste, Italy. InSilicoTrials Technologies B.V., Bruistensingel 130, 5232 AC, 's Hertogenbosch, The Netherlands. roberta.bursi@insilicotrials.com.
 UiT The Arctic University of Norway, Tromsø, Norway. Centre of Clinical Research and Education, University Hospital of North Norway, Tromsø, Norway. UiT The Arctic University of Norway, Tromsø, Norway. Centre of Clinical Research and Education, University Hospital of North Norway, Tromsø, Norway.
 Internal Medicine, University of California Riverside School of Medicine, Riverside, USA. Internal Medicine, University of California Riverside School of Medicine, Riverside, USA. School of Medicine, University of California Riverside, Riverside, USA. Internal Medicine, Riverside University Health System Medical Center, Riverside, USA. Internal Medicine, Riverside University Health System Medical Center, Riverside, USA. Infectious Disease, Riverside University Health System Medical Center, Riverside, USA. Infectious Disease, Riverside University Health System Medical Center, Riverside, USA.
 Unit of Gynecologic Oncology, ARNAS "Civico-Di Cristina-Benfratelli", Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy. Unit of Gynecologic Oncology, ARNAS "Civico-Di Cristina-Benfratelli", Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90127 Palermo, Italy. Department of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy. Department of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy. System Biology Group Laboratory, Sapienza University, 00161 Rome, Italy.
 Department of Translational Immunology and Experimental Intensive Care, Centre of Postgraduate Medical Education, Warsaw, Poland. Department of Radiology, Institute of Psychiatry and Neurology, Warsaw, Poland.
 Department of Neurology, University Hospital Bonn, Venusberg Campus 1, 53127, Bonn, Germany. julian.zimmermann@ukbonn.de. Department of Neurology, University Hospital Bonn, Venusberg Campus 1, 53127, Bonn, Germany. Department of Neurology, University Hospital Bonn, Venusberg Campus 1, 53127, Bonn, Germany. Department of Neurology, University Hospital Bonn, Venusberg Campus 1, 53127, Bonn, Germany.
 Oakland University William Beaumont School of Medicine, 586 Pioneer Dr, Rochester, MI 48309 USA. GRID: grid.261277.7. ISNI: 0000 0001 2219 916X Department of Internal Medicine, Beaumont Hospital, 3601 W 13 Mile Rd, Royal Oak, MI 48073 USA. GRID: grid.427918.1 Department of Internal Medicine, Beaumont Hospital, 3601 W 13 Mile Rd, Royal Oak, MI 48073 USA. GRID: grid.427918.1
 Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Rheumatology Unit, University Clinic, AOU Cagliari, Cagliari, Italy. Department of Medical Sciences and Public health, University of Cagliari, Monserrato, Italy. Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Rheumatology Unit, University Clinic, AOU Cagliari, Cagliari, Italy. Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Rheumatology Unit, University Clinic, AOU Cagliari, Cagliari, Italy. Rheumatology Unit, University Clinic, AOU Cagliari, Cagliari, Italy. Department of Medical Sciences and Public health, University of Cagliari, Monserrato, Italy. Multiple Sclerosis Center, Binaghi Hospital, ATS Sardegna, ASSL Cagliari, Cagliari, Italy. Department of Medical Sciences and Public health, University of Cagliari, Monserrato, Italy. Radiology Department, University Clinic, AOU Cagliari, Cagliari, Italy. Department of Medical Sciences and Public health, University of Cagliari, Monserrato, Italy. Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy. Rheumatology Unit, University Clinic, AOU Cagliari, Cagliari, Italy. Department of Medical Sciences and Public health, University of Cagliari, Monserrato, Italy. Rheumatology Unit, University Clinic, AOU Cagliari, Cagliari, Italy. Department of Medical Sciences and Public health, University of Cagliari, Monserrato, Italy.
 Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Center for IT and Medical Technology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Radiology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Radiology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
 Department of Veterinary and Biomedical Sciences, Center for Molecular Toxicology and Carcinogenesis, Penn State University, University Park, PA 16802, USA. IUF-Leibniz Research Institute for Environmental Medicine, Auf'm Hennekamp 50, 40225 Düsseldorf, Germany. Department of Environmental Health, Boston University School of Public Health, 72 East Concord Street, Boston, MA 02118, USA. Department of Environmental Health, Boston University School of Public Health, 72 East Concord Street, Boston, MA 02118, USA. Department of Dermatology, Radboud University Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. Ikena Oncology, Inc., 645 Summer Street Suite 101, Boston, MA 02210, USA. Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias, Universidad de Extremadura, Avenida de Elvas s/n, 06071 Badajoz, Spain. Instituto Universitario de Investigación Biosanitaria de Extremadura (INUBE), Avenida de la Investigación s/n, 06071 Badajoz, Spain. INSERM UMR-S1124, 45 rue des Saints-Peères, 75006 Paris, France. Department of Veterinary and Biomedical Sciences, Center for Molecular Toxicology and Carcinogenesis, Penn State University, University Park, PA 16802, USA.
 Department of Sport Sciences, School of Education and Psychology, Shiraz University, Iran. Department of Sport Sciences, School of Education and Psychology, Shiraz University, Iran. Electronic address: koushkie53@yahoo.com. Department of Sport Sciences, School of Education and Psychology, Shiraz University, Iran. Department of Sport Sciences, School of Education and Psychology, Shiraz University, Iran.
 Department of Animal Model Development, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Chuoku, Niigata 951-8585, Japan. Department of Multiple Sclerosis Therapeutics, School of Medicine, Fukushima Medical University, 1 Hikarigaoka, Fukushima 960-1247, Japan. Department of Ophthalmology, Tokyo Medical University, Tokyo 160-0023, Japan. Department of Orthoptics and Visual Science, School of Allied Health Sciences, Kitasato University, Kanagawa 252-0373, Japan. Kyoto MS Center, Kyoto Min-Iren Chuo Hospital, Kyoto 616-8147, Japan. Department of Animal Model Development, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Chuoku, Niigata 951-8585, Japan. Department of Animal Model Development, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Chuoku, Niigata 951-8585, Japan. Department of Animal Model Development, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Chuoku, Niigata 951-8585, Japan. Division of Instrumental Analysis, Center for Coordination of Research Facilities, Institute for Research Administration, Niigata University, Niigata 951-8585, Japan.
 University of Medicine and Pharmacy, Craiova, Romania. Department of Neurology, Emergency County Hospital, Targu-Jiu, Romania. Department of Neurology, Emergency County Hospital, Targu-Jiu, Romania. Department of Pediatric and Adult Congenital Cardiology, University of Bordeaux, Bordeaux, France. University of Medicine and Pharmacy, Craiova, Romania. Department of Cardiology, County Hospital, Craiova, Romania. University of Medicine and Pharmacy, Craiova, Romania. Department of Cardiology, County Hospital, Craiova, Romania. University of Medicine and Pharmacy, Craiova, Romania. Department of Neurology, Neuropsychiatry Hospital, Craiova, Romania. University of Medicine and Pharmacy, Craiova, Romania. Department of Radiology, Emergency County Hospital, Craiova, Romania.
 Faculty of Medicine, The Hebrew University of Jerusalem, Campus Ein Karem; Institute of Gene Therapy, The Hadassah University Hospital -Ein Karem, Jerusalem, Israel.
 School of Medicine, Ondokuz Mayıs University, Samsun, Turkey. Electronic address: sedatsen83@hotmail.com. School of Medicine, Hacettepe University, Ankara, Turkey. School of Medicine, Ondokuz Mayıs University, Samsun, Turkey. School of Medicine, Kocaeli University, Kocaeli, Turkey. School of Medicine, Hacettepe University, Ankara, Turkey. Memorial Hospital Neurology Clinic, Istanbul, Turkey. School of Medicine, Dokuz Eylül University, Izmir, Turkey. School of Medicine, Istanbul University Cerrahpaşa, Istanbul, Turkey. School of Medicine, Istanbul University Cerrahpaşa, Istanbul, Turkey. Istanbul Bezmialem University Neurology Clinic, Turkey. School of Medicine, Hacettepe University, Ankara, Turkey. School of Medicine, Kocaeli University, Kocaeli, Turkey. School of Medicine, Istanbul University Cerrahpaşa, Istanbul, Turkey. Electronic address: akselsiva@gmail.com.
 Department of Neurology, Christian Doppler University Hospital, European Reference Network EpiCARE, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, European Reference Network EpiCARE, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, European Reference Network EpiCARE, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, European Reference Network EpiCARE, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Dermatology and Allergology, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Clinical Microbiology and Hygiene, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, European Reference Network EpiCARE, Paracelsus Medical University, 5020 Salzburg, Austria. Center for Cognitive Neuroscience, Neuroscience Institute, Christian Doppler University Hospital, Paracelsus Medical University, 5020 Salzburg, Austria. Department of Neurology, Christian Doppler University Hospital, European Reference Network EpiCARE, Paracelsus Medical University, 5020 Salzburg, Austria.
 Department of Neurology, Clinic of Optic Neuritis, The Danish Multiple Sclerosis Center (DMSC), Rigshospitalet, Glostrup, Denmark. Department of Applied Mathematics and Computer Science, Technical University of Denmark, Lyngby, Denmark. Department of Applied Mathematics and Computer Science, Technical University of Denmark, Lyngby, Denmark. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, Queen Square UCL Institute of Neurology, University College London, London, UK. Moorfields Eye Hospital NHS Foundation Trust, London, UK. Neuro-ophthalmology Expertise Centre, University Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. UCL Institute of Neurology, London, UK. Department of Ophthalmology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Multimodal Imaging in Neuroimmunological Diseases (MINDS), University Hospital Zurich and University of Zurich, Zurich, Switzerland. Department of Neurology, Clinic of Optic Neuritis, The Danish Multiple Sclerosis Center (DMSC), Rigshospitalet and University of Copenhagen, Glostrup, Denmark. Department of Ophthalmology, Rigshospitalet and University of Copenhagen, Glostrup, Denmark.
 Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (Vaxinfectio), University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium. Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (Vaxinfectio), University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium. Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (Vaxinfectio), University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium. Department of Neurology, Antwerp University Hospital, B-2650 Edegem, Belgium. Neurology, Translational Neurosciences, Born Bunge Institute, Faculty of Medicine and Health Sciences, University of Antwerp, B-2610 Antwerpen, Belgium. Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (Vaxinfectio), University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium. Center for Cell Therapy and Regenerative Medicine (CCRG), Antwerp University Hospital, Drie Eikenstraat 655, B-2650 Edegem, Belgium. Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (Vaxinfectio), University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium.
 Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China; Department of Gerontology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, 110004, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China; Department of Radiology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China; Department of Epidemiology and Health Statistics, School of Public Health, China Medical University, Shenyang, 110122, Liaoning, China. Department of Gerontology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, 110004, China. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China. Electronic address: dlwen@cmu.edu.cn. Health Sciences Institute, Key Laboratory of Obesity and Glucose/Lipid Associated Metabolic Diseases, China Medical University, Shenyang 110122, Liaoning, China. Electronic address: yyu90@cmu.edu.cn.
 Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad 380009, Gujarat, India. Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad 380009, Gujarat, India. Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad 380009, Gujarat, India. Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad 380009, Gujarat, India. Electronic address: mehul.chorawala@lmcp.ac.in. Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad 380009, Gujarat, India. Department of Pharmacology, K. B. Institute of Pharmaceutical Education and Research, Gandhinagar 380023, Gujarat, India. Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad 380009, Gujarat, India. Department of Pharmaceutical Chemistry, Institute of Pharmacy, Nirma University, Ahmedabad-382481, Gujarat, India.
 Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, China. Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University, Changsha 410013, China. Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, China; Hunan Provincial Key Laboratory of Cardiovascular Research, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, China. Electronic address: Junpeng@csu.edu.cn. Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University, Changsha 410013, China. Electronic address: xjluo22@csu.edu.cn.
 KL College of Pharmacy, Koneru Lakshmaiah Education Foundation Deemed to be University (KLU), Green Fields, Vaddeswaram, Guntur 522502, India. KL College of Pharmacy, Koneru Lakshmaiah Education Foundation Deemed to be University (KLU), Green Fields, Vaddeswaram, Guntur 522502, India. KL College of Pharmacy, Koneru Lakshmaiah Education Foundation Deemed to be University (KLU), Green Fields, Vaddeswaram, Guntur 522502, India. Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology, IIT BHU, Varanasi 221005, India. KL College of Pharmacy, Koneru Lakshmaiah Education Foundation Deemed to be University (KLU), Green Fields, Vaddeswaram, Guntur 522502, India. KL College of Pharmacy, Koneru Lakshmaiah Education Foundation Deemed to be University (KLU), Green Fields, Vaddeswaram, Guntur 522502, India. KL College of Pharmacy, Koneru Lakshmaiah Education Foundation Deemed to be University (KLU), Green Fields, Vaddeswaram, Guntur 522502, India. Department of Biotechnology, Bharathi Institute of Higher Education and Research, Chennai 600073, India. Department of Zoology, Mahila Maha Vidyalaya, Banaras Hindu University, Varanasi 221005, India. Centre of Experimental Medicine and Surgery, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India. ICMR-Rajendra Memorial Research Institute of Medical Sciences, Agamkuan, Patna 800007, India. ICMR-Rajendra Memorial Research Institute of Medical Sciences, Agamkuan, Patna 800007, India. Centre of Experimental Medicine and Surgery, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
 Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, Moscow 119435, Russia. Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, Moscow 119435, Russia. The Scientific Community for Human Microbiome Research, Moscow 119435, Russia. mmmm00@yandex.ru. Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, Moscow 119435, Russia. The Scientific Community for Human Microbiome Research, Moscow 119435, Russia. Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, Moscow 119435, Russia. Department of Human Anatomy and Histology, Sechenov University, Moscow 125009, Russia. Department of Human Anatomy and Histology, Sechenov University, Moscow 125009, Russia. N.V. Sklifosovsky Institute of Clinical Medicine, Sechenov University, Moscow 119991, Russia. Department of Clinical Immunology and Allergy, Sechenov University, Moscow 119991, Russia. Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, Moscow 119435, Russia. Department of Clinical Immunology and Allergy, Sechenov University, Moscow 119991, Russia. Department of Internal Medicine, Gastroenterology and Hepatology, Sechenov University, Moscow 119435, Russia. The Scientific Community for Human Microbiome Research, Moscow 119435, Russia.

 Department of Dermatology, University of California San Francisco, San Francisco, CA, USA. University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA. Department of Dermatology, University of California San Francisco, San Francisco, CA, USA. Kaiser Permanente, Department of Physical Medicine & Rehabilitation, Oakland, CA, USA. Department of Radiology & Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA. Department of Radiology & Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA. Department of Dermatology, University of California San Francisco, San Francisco, CA, USA. Dermatology Service, Veterans Affairs Health Care System, San Francisco, CA, USA. Department of Dermatology, University of California San Francisco, San Francisco, CA, USA.
 Journal of the American Society of Nephrology, Bernard, Maine. Department of Quantitative Health Sciences, Lerner Research Institute and Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, Ohio. Department of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio.
 Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany. Experimental and Clinical Research Center and NeuroCure Clinical Research Center, MaxDelbrueck Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Institute for Neuroradiology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Institute for Neuroradiology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany. Department of Neurology, Klinikum rechtsDer Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechtsDer Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechtsDer Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum rechtsDer Isar, Technical University of Munich, Munich, Germany. Department of Neuroradiology, Klinikum rechtsDer Isar, Technical University of Munich, Munich, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, Faculty of Medicine, University of Augsburg, Augsburg, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine University Düsseldorf, Germany. Department of Neurology, University Hospital Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Molecular Neuroimmunology Group, Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany. Department of Neurology, University of Leipzig, Leipzig, Germany. Central Information Office German Competence Network of Multiple Sclerosis, Philipps University Marburg, Marburg, Germany. Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilian-University Munich, Munich, Germany. Department of Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany. Experimental and Clinical Research Center and NeuroCure Clinical Research Center, MaxDelbrueck Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Berlin, Germany. Max Planck Institute of Psychiatry, Munich, Germany. Department of Neurology, University of Ulm, Ulm, Germany. Department of Neurology, Neuroimmunological Section, University of Rostock, Rostock, Germany. Department of Neurology, Klinikum rechtsDer Isar, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology with Institute of Translational Neurology, Medical Faculty, University Hospital, Münster, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Department of Neurology, St. Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany.
 Neurologie CHU Nice, Hôpital Pasteur2, UMR2CA-URRIS, Université Côte d'Azur, 06002 Nice, France. Neurology, Mayo Clinic, Rochester, MN 55905, USA. Istanbul University Cerrahpasa School of Medicine - Department of Neurology, Istanbul, 34098, Turkey. Keck School of Medicine. University of Southern California, Los Angeles, CA 90033, USA. The University of Texas Southwestern Medical Center, Neuroinnovation Program, Multiple Sclerosis, and Neuroimmunology Imaging Program, Dallas, TX 75390, USA.
 Department of Computer and Information Sciences, College of Natural and Applied Science, University of Houston-Victoria Texas 77901 USA TomitakaA@uhv.edu. Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University Miami Florida 33199 USA nairm@fiu.ed. Institute of NeuroImmune Pharmacology, Centre for Personalized Nanomedicine, Herbert Wertheim College of Medicine, Florida International University Miami Florida 33199 USA. Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University Miami Florida 33199 USA nairm@fiu.ed. Institute of NeuroImmune Pharmacology, Centre for Personalized Nanomedicine, Herbert Wertheim College of Medicine, Florida International University Miami Florida 33199 USA. Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University Miami Florida 33199 USA nairm@fiu.ed. Institute of NeuroImmune Pharmacology, Centre for Personalized Nanomedicine, Herbert Wertheim College of Medicine, Florida International University Miami Florida 33199 USA.
 Department of Anesthesiology, Mount Sinai Medical Center, 4300 Alton Road, Miami Beach, FL, USA. Salomon.pb@gmail.com. Creighton University School of Medicine Phoenix, Phoenix, AZ, USA. Creighton University School of Medicine Phoenix, Phoenix, AZ, USA. Creighton University School of Medicine Phoenix, Phoenix, AZ, USA. Department of Anesthesiology and Pain Medicine, Valleywise Health Medical Center, Creighton University School of Medicine Phoenix, Phoenix, AZ, USA. Department of Anesthesiology, Louisiana State University Health Shreveport, Shreveport, LA, USA. Southcoast Health Physicians Group, Southcoast Health Pain Management, Wareham, MA, USA. Innovative Pain and Wellness, Scottsdale, AZ, USA. Department of Anesthesiology, Louisiana State University Health Sciences Center Shreveport, Shreveport, LA, USA. Department of Anesthesiology, Creighton University School of Medicine, Phoenix, AZ, USA.
 National Center for Adaptive Neurotechnologies, Albany Stratton VA Medical Center, Albany, NY, United States. Department of Biomedical Sciences, School of Public Health, State University of New York, Albany, NY, United States. Department of Health Sciences and Research, College of Health Professions, Medical University of South Carolina, Charleston, SC, United States.

 Immuno-Biology Laboratory, Translational Health Science and Technology Institute, Faridabad, India. Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. Regional Biocontainment Laboratory, Center for Predictive Medicine, University of Louisville, Louisville, KY, USA.
 Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine (VMCVM), Virginia Tech, Blacksburg, VA, United States. Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine (VMCVM), Virginia Tech, Blacksburg, VA, United States. Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine (VMCVM), Virginia Tech, Blacksburg, VA, United States.
 Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University in Olomouc, Olomouc, Czech Republic. Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University in Olomouc, Olomouc, Czech Republic. Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University in Olomouc, Olomouc, Czech Republic; Laboratory of Experimental Medicine, University Hospital, Olomouc 779 00, Czech Republic. Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University in Olomouc, Olomouc, Czech Republic; Laboratory of Experimental Medicine, University Hospital, Olomouc 779 00, Czech Republic. Electronic address: petr.dzubak@upol.cz.
 Physician Assistant Department, School of Pharmacy and Health Professions, University of Maryland Eastern Shore, Princess Anne, MD, USA.
 Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States. Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States. Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States. Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States. Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States. Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
 Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA. Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA. Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA. Department of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA. Department of Population Health, New York University Grossman School of Medicine, New York, NY, USA. Department of Neurology, New York University Grossman School of Medicine, New York, NY, USA. steven.galetta@nyulangone.org. Department of Ophthalmology, New York University Grossman School of Medicine, New York, NY, USA. steven.galetta@nyulangone.org.
 Physical Medicine and Rehabilitation, Pôle MPR Saint-Hélier, Rennes, France. Physical Medicine and Rehabilitation, Pôle MPR Saint-Hélier, Rennes, France. Physical Medicine and Rehabilitation, Pôle MPR Saint-Hélier, Rennes, France. Physical Medicine and Rehabilitation, Pôle MPR Saint-Hélier, Rennes, France. Physical Medicine and Rehabilitation, Pôle MPR Saint-Hélier, Rennes, France. Physical Medicine and Rehabilitation, Pôle MPR Saint-Hélier, Rennes, France.
 Normandie Univ., UNICAEN, CERMN, 14000, Caen, France. Department of Pharmacology, Medical School, University of Crete, Heraklion, Greece; Institute of Molecular Biology & Biotechnology, Foundation for Research & Technology-Hellas (IMBB-FORTH), Heraklion, Greece. Innoprot S.L, Derio, Bizkaia, Spain. Innoprot S.L, Derio, Bizkaia, Spain. Department of Pharmacology, Medical School, University of Crete, Heraklion, Greece; Institute of Molecular Biology & Biotechnology, Foundation for Research & Technology-Hellas (IMBB-FORTH), Heraklion, Greece. Innoprot S.L, Derio, Bizkaia, Spain. Neurosys, Gardanne, France. Normandie Univ., UNICAEN, CERMN, 14000, Caen, France. Normandie Univ., UNICAEN, CERMN, 14000, Caen, France. Department of Pharmacology, Medical School, University of Crete, Heraklion, Greece; Institute of Molecular Biology & Biotechnology, Foundation for Research & Technology-Hellas (IMBB-FORTH), Heraklion, Greece. Normandie Univ., UNICAEN, CERMN, 14000, Caen, France. Electronic address: christophe.rochais@unicaen.fr.
 Unit of Histology and Medical Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. Unit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. Unit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. Unit of Pharmacology and Pharmacovigilance, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. Electronic address: lucaant@gmail.com. Unit of Histology and Medical Embryology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy; Interdepartmental Research Center "Nutraceuticals and Food for Health", University of Pisa, Pisa, Italy. Department of Neurology, Nantes Université, CHU Nantes, INSERM, Nantes, France.
 Division of Neuro-ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear. Division of Neuro-ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear. Division of Ophthalmology, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
 Immunopeptide Chemistry Lab, Institute of Nuclear & Radiological Sciences & Technology, Energy & Safety, National Centre for Scientific Research ''Demokritos", P.O. Box 60037, 153 10 Agia Paraskevi, Greece. Immunopeptide Chemistry Lab, Institute of Nuclear & Radiological Sciences & Technology, Energy & Safety, National Centre for Scientific Research ''Demokritos", P.O. Box 60037, 153 10 Agia Paraskevi, Greece.
 Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Pharmacology, School of Pharmacy, Hamadan University of Medical Science, Hamadan, Iran. Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Neuroscience, School of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran. Asadabad School of Medical Sciences, Asadabad, Iran. Student Research Committee, Asadabad School of Medical Sciences, Asadabad, Iran. Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran. Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
 Department of Ophthalmology, Weill Cornell Medical College, NY Presbyterian Hospital, New York, New York. Department of Neurology, Weill Cornell Medical College, NY Presbyterian Hospital, New York, New York. Weill Cornell Medical College, New York, New York.

 Department of Pharmaceutical Chemistry, ISF College of Pharmacy, GT Road, Ghal Kalan, Moga, 142001, Punjab, India. Department of Pharmaceutical Chemistry, ISF College of Pharmacy, GT Road, Ghal Kalan, Moga, 142001, Punjab, India. Department of Pharmaceutical Chemistry, ISF College of Pharmacy, GT Road, Ghal Kalan, Moga, 142001, Punjab, India. Department of Pharmaceutical Chemistry, ISF College of Pharmacy, GT Road, Ghal Kalan, Moga, 142001, Punjab, India. Department of Pharmaceutical Sciences and Natural Products, Central University of Punjab, Bathinda, 151001, India.
 Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Japan. Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan. Department of Neurology, Saitama Medical Center, Kawagoe, Japan. Department of Neurology, Kindai University Hospital, Osakasayama, Japan. Department of Neurology, Nagasaki Kawatana Medical Center, Kawatana, Japan. Clinical Development Department, Asahi-Kasei Medical Co., Tokyo, Japan. Department of Neurology, Nagasaki Kawatana Medical Center, Kawatana, Japan. Department of Neurology, Nagasaki National Hospital, Nagasaki, Japan.
 Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK. Electronic address: gavin@giovannoni.net. Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London, UK. The University of Newcastle, Australia. Massachusetts General Hospital and Harvard Medical School, MA, USA. Department of Paediatrics, Dalla Lana School of Public Health, University of Toronto, Canada.
 Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India. Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India. Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India. Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India. Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India. Department of Clinical Pharmacology, KEM Hospital, Mumbai, Maharashtra, India.
 Division of Neurology, Department of Clinical Neurosciences, University of Calgary, Cummings School of Medicine, Calgary, AB, Canada. Division of Neurology, Department of Clinical Neurosciences, University of Calgary, Cummings School of Medicine, Calgary, AB, Canada. jodie.burton@albertahealthservices.ca. Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada. jodie.burton@albertahealthservices.ca. Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada. jodie.burton@albertahealthservices.ca.
 Madurai Kamaraj University, Madurai, Tamil Nādu, 625021, India. Electronic address: vikashraghuvanshi2017@gmail.com. Research Assistant, Department of AFAF, Amity University Noida, Uttar Pradesh, 201313, India. Electronic address: pramodyadavk3@gmail.com. Research Assistant, Kalpana Chawla Government Medical College Karnal, Haryana, 13200, India. Electronic address: samimaligazi97@gmail.com.
 Chongqing University of Posts and Telecommunications, Chongqing, China. Institute for Advanced Sciences, Chongqing University of Posts and Telecommunications, Chongqing, China. Chongqing University of Posts and Telecommunications, Chongqing, China. Chongqing University of Posts and Telecommunications, Chongqing, China. Chongqing University of Posts and Telecommunications, Chongqing, China. Chongqing University of Posts and Telecommunications, Chongqing, China. Chongqing University of Posts and Telecommunications, Chongqing, China. School of Civil Engineering, Guangdong Communication Polytechnic, Guangzhou, China.
 University of Melbourne, Parkvile, VIC, Australia. St Vincent's Hospital, Fitzroy, VIC, Australia. RINGGOLD: 60078 Alfred Health, Melbourne, VIC, Australia. RINGGOLD: 5392 Mindful Neurology, PLLC, New York, NY, USA. University Hospital Geelong, Deakin University, Geelong, VIC, Australia. RINGGOLD: 2104
 Department of Neurosciences, Drug and Child Health, University of Florence, 50139 Florence, Italy. Department of Neurology 2, Careggi University Hospital, 50134 Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, 50139 Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, 50139 Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, 50139 Florence, Italy. Department of Neurology 2, Careggi University Hospital, 50134 Florence, Italy. Cell Therapy and Transfusion Medicine Unit, Careggi University Hospital, 50134 Florence, Italy. Department of Neurosciences, Drug and Child Health, University of Florence, 50139 Florence, Italy. Department of Neurology 2, Careggi University Hospital, 50134 Florence, Italy.
 Department of Immunology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Division of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Missouri-Kansas City, Kansas City, MO, USA. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: sahebkara@mums.ac.ir.
 Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Mobeda@tbzmed.ac.ir. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Mobeda@tbzmed.ac.ir. Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran. Mobeda@tbzmed.ac.ir. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Mobeda@tbzmed.ac.ir. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Scharsouei@tbzmed.ac.ir. Tabriz Neuroscience Research Center (NRSC), Neurology Department, Tabriz University of Medical Sciences, Tabriz, Iran. Scharsouei@tbzmed.ac.ir. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Scharsouei@tbzmed.ac.ir. Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Medicine, Imam Reza Hospital, Tabriz University of Medical Sciences, Tabriz, Iran. Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Psychology, East Azarbayjan Science and Research Branch, Islamic Azad University, Tabriz, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. School of Advanced Technologies in Medicine, Iran University of Medical Science, Tehran, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Neuroscience, Iran University of Medical Sciences, Tehran, Iran. Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
 Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Department of Physiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Viral Immunopathology Laboratory, Infection, Immunity and Inflammation Research Theme, The School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Viral Immunopathology Laboratory, Infection, Immunity and Inflammation Research Theme, The School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia. Department of Physiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Brain and Mind Centre, The University of Sydney, Sydney, New South Wales, Australia. Department of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Viral Immunopathology Laboratory, Infection, Immunity and Inflammation Research Theme, The School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia. Charles Perkins Centre, The University of Sydney, The University of Sydney, New South Wales, Australia. School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Sydney Cytometry, The University of Sydney and Centenary Institute, Sydney, New South Wales, Australia.
 Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Mail Stop C238, 12850 E. Montview Blvd., Aurora, CO, USA. robert.mcqueen@cuanschutz.edu. Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Mail Stop C238, 12850 E. Montview Blvd., Aurora, CO, USA. Department of Health Policy and Management, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA. CHOICE Institute, University of Washington School of Pharmacy, Seattle, WA, USA.
 Faculty of Medicine, University of Iceland, Iceland. Faculty of Medicine, University of Iceland, Iceland. Department of Nephrology, Lund University Hospital, Sweden. Faculty of Medicine, University of Iceland, Iceland. Department of Haematology, Rigshospitalet, Denmark. Faculty of Medicine, University of Iceland, Iceland. Department of Science and Research, Landspitali University Hospital, Iceland. Faculty of Medicine, University of Iceland, Iceland. Department of Haematology, Landspítali University Hospital, Iceland.
 Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Institute of Graduate School, Xinxiang Medical College, Xinxiang, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China. Department of Neurology, Henan Provincial People's Hospital, Zhengzhou, China.
 Department of Clinical Pharmacy and Pharmaceutical Care, Medical University of Lublin, 1 Chodźki Street, 20-093 Lublin, Poland. Department of Clinical Pharmacy and Pharmaceutical Care, Medical University of Lublin, 1 Chodźki Street, 20-093 Lublin, Poland. Scientific Circle, Department of Clincal Pharmacy and Pharmaceutical Care, Medical University of Lublin, 1 Chodźki Street, 20-093 Lublin, Poland. Chair and Department of Applied and Social Pharmacy, Medical University of Lublin, 1 Chodźki Street, 20-093 Lublin, Poland. Department of Clinical Pharmacy and Pharmaceutical Care, Medical University of Lublin, 1 Chodźki Street, 20-093 Lublin, Poland.
 Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, USA. Electronic address: scerri@mgh.harvard.edu. Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, USA; Department of Radiology, Harvard Medical School, USA. Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, USA. Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital Amager and Hvidovre, Copenhagen, Denmark. Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital Amager and Hvidovre, Copenhagen, Denmark; Department of Neurology, Copenhagen University Hospital Bispebjerg and Frederiksberg, Copenhagen, Denmark; Institute for Clinical Medicine, Faculty of Medical and Health Sciences, University of Copenhagen, Denmark. Department of Neurology and TUM-Neuroimaging Center, School of Medicine, Technical University of Munich, Germany. Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, USA; Department of Health Technology, Technical University of Denmark, Denmark.
 Department of Food Development and Food Quality, Institute of Food Science and Human Nutrition, Gottfried Wilhelm Leibniz University Hannover, Hannover, Germany. Department of Food Development and Food Quality, Institute of Food Science and Human Nutrition, Gottfried Wilhelm Leibniz University Hannover, Hannover, Germany. Department of Food Engineering, Faculty of Chemical and Metallurgical Engineering, Istanbul Technical University, Istanbul, Turkey. Hafik Kamer Ornek MYO, Cumhuriyet University, Sivas, Turkey. Department of Food Engineering, Faculty of Chemical and Metallurgical Engineering, Istanbul Technical University, Istanbul, Turkey. Institute of Food Chemistry, Technische Universität Braunschweig, Braunschweig, Germany. Food and Nutritional Sciences Program, North Carolina Agricultural and Technical State University, Greensboro, North Carolina, USA. Department of Nutrition and Dietetics, Faculty of Health Sciences, Cukurova University, Adana, Turkey. Department of Seafood Processing Technology, Faculty of Fisheries, Cukurova University, Adana, Turkey. Department of Food Engineering, Faculty of Chemical and Metallurgical Engineering, Istanbul Technical University, Istanbul, Turkey.
 Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Laboratorio Clínico de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Laboratorio Clínico de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de México, Mexico. Electronic address: aureliojara@yahoo.com.mx.
 Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan; Miyarisan Pharmaceutical Co., Ltd., Research Laboratory, 1-10-3, Kaminagazato, Kita-ku, Tokyo 114-0016, Japan. Center for Diagnostic and Therapeutic Endoscopy, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Electronic address: tsujino1224@keio.jp. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Department of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan; Medical Mycology Research Center, Chiba University, 1-8-1, Inohana, Cyuo-ku, Chiba city, Chiba 260-8673, Japan. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Department of Gastroenterology and Hepatology, Tokyo Medical Dental University (TMDU), 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. Department of Gastroenterology and Hepatology, Tokyo Medical Dental University (TMDU), 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. Laboratory of Immunology, Faculty of Pharmacy, Osaka Otani University, 3-11-1 Nshikiorikita, Tondabayshi, Osaka, 584-8584, Japan. Department of Biomedicine, University of Basel, 4031 Basel, Switzerland. Department of Biomedicine, University of Basel, 4031 Basel, Switzerland; Clarunis-University Center for Gastrointestinal and Liver Diseases, University Hospital Basel, 4002 Basel, Switzerland. Department of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. Division of Brain Sciences Institute for Advanced Medical Research, Keio University School of Medicne, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Department of Gastroenterology and Hepatology, Tokyo Medical Dental University (TMDU), 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Division of Brain Sciences Institute for Advanced Medical Research, Keio University School of Medicne, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Department of Organoid Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan; AMED-CREST, Japan Agency for Medical Research and Development, 1-7-1, Otemachi, Chiyoda-ku, Tokyo 100-0004, Japan. Electronic address: takagast@z2.keio.jp.
 Department of Pediatrics, Division of Pediatric Neurology, Ankara City Hospital, Children's' Hospital, Ankara, Turkey. Electronic address: deniz.yilmaz13@saglik.gov.tr. Department of Pediatrics, Division of Pediatric Neurology, Ankara University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Ankara City Hospital, Children's' Hospital, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Ankara University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Ankara University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Kocaeli University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Kocaeli University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Kocaeli University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Hacettepe University Faculty of Medicine, Ankara, Turkey. Department of Pediatrics, Division of Pediatric Neurology, İstanbul University Cerrahpaşa Faculty of Medicine, İstanbul, Turkey. Department of Pediatrics, Division of Pediatric Neurology, İstanbul University Cerrahpaşa Faculty of Medicine, İstanbul, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Ege University Faculty of Medicine, İzmir, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Ege University Faculty of Medicine, İzmir, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Ege University Faculty of Medicine, İzmir, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Afyonkarahisar Health Science University Faculty of Medicine, Afyon, Turkey. Izmir Faculty of Medicine, Dr. Behçet Uz Children's Education and Research Hospital, Department of Pediatrics, Division of Pediatric Neurology, University of Health Sciences, Izmir, Turkey. Izmir Faculty of Medicine, Dr. Behçet Uz Children's Education and Research Hospital, Department of Pediatrics, Division of Pediatric Neurology, University of Health Sciences, Izmir, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Celal Bayar University Faculty of Medicine, Manisa, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Pamukkale University Faculty of Medicine, Denizli, Turkey. Department of Pediatrics, Division of Pediatric Neurology, Hacettepe University Faculty of Medicine, Ankara, Turkey.
 Department of Neurology, Zhengzhou University People's Hospital/Henan Provincial People's Hospital, Zhengzhou 450003, China. Department of Neurology, Zhengzhou University People's Hospital/Henan Provincial People's Hospital, Zhengzhou 450003, China. Department of Neurology, Zhengzhou University People's Hospital/Henan Provincial People's Hospital, Zhengzhou 450003, China. Department of Neurology, Zhengzhou University People's Hospital/Henan Provincial People's Hospital, Zhengzhou 450003, China. Department of Neurology, Zhengzhou University People's Hospital/Henan Provincial People's Hospital, Zhengzhou 450003, China. Department of Neurology, Zhengzhou University People's Hospital/Henan Provincial People's Hospital, Zhengzhou 450003, China. Electronic address: zhangjwdoc@163.com.
 Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Dell Medical School, University of Texas, Austin, Texas, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, Minnesota, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Minneapolis, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA.
 Sanofi, 153/211 Second Avenue, Waltham, MA, 02451, USA. Sanofi, 450 Water Street, Cambridge, MA, 02141, USA. Sanofi, 450 Water Street, Cambridge, MA, 02141, USA. Sanofi, 450 Water Street, Cambridge, MA, 02141, USA. Sanofi, 153/211 Second Avenue, Waltham, MA, 02451, USA. Sanofi, 153/211 Second Avenue, Waltham, MA, 02451, USA. Sanofi, 1 Av. Pierre Brossolette, 91380, Chilly-Mazarin, France.
 University Hospitals Birmingham, Birmingham, UK. School of Immunology and Microbiology, King's College London, London, UK. charles.odonovan@kcl.ac.uk. Centre for Patient Reported Outcomes Research (CPROR), Institute of Applied Health Research, Birmingham Health Partners for Regulatory Science and Innovation, NIHR Birmingham Biomedical Research Centre, NIHR Applied Research Collaboration West Midlands, and NIHR Birmingham-Oxford Blood and Transplant Research Unit (BTRU) in Precision Transplant and Cellular Therapeutics, University of Birmingham, Birmingham, B15 2TT, UK. Institute of Inflammation and Ageing, University of Birmingham, University Hospitals Birmingham, Health Data Research UK, London, UK. Institute of Applied Health Research, University of Birmingham, Birmingham, UK. Centre for Patient Reported Outcomes Research (CPROR), Institute of Applied Health Research, Birmingham Health Partners for Regulatory Science and Innovation, NIHR, Birmingham Biomedical Research Centre, NIHR Surgical Reconstruction and Microbiology Centre, NIHR Applied Research Collaboration West Midlands, and NIHR Birmingham-Oxford Blood and Transplant Research Unit (BTRU) in Precision Transplant and Cellular Therapeutics, University of Birmingham, Birmingham, B15 2TT, UK. University of New South Wales, New South Wales, Australia. Institute of Inflammation and Ageing, and Centre for Patient Reported Outcomes Research (CPROR), Institute of Applied Health Research, Birmingham Health Partners for Regulatory Science and Innovation, NIHR Birmingham-Oxford Blood and Transplant Research Unit (BTRU) in Precision Transplant and Cellular Therapeutics, University of Birmingham, University Hospitals Birmingham, Health Data Research UK, London, UK. Institute of Applied Health Research, University of Birmingham, Birmingham, UK. School of Immunology and Microbiology, King's College London, and The Medical Eye Unit, Guy's and St Thomas' Hospital NHS Foundation Trust, London, UK.
 Multiple Sclerosis and Neuroimmunology Clinic, Concord Repatriation General Hospital, University of Sydney, Sydney, New South Wales, Australia. Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia.
 Neuroradiology Unit, IRCCS San Raffaele Hospital, Milan, Italy. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, UK.
 Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Quantitative Health Sciences, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA.
 Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. Laboratory of Neuroscience "R. Levi-Montalcini", Department of Biotechnology and Biosciences, NeuroMI Milan Center for Neuroscience, University of Milano-Bicocca, 20126 Milano, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. Laboratory of Neuronal Networks Morphology and System Biology, Department of Mental and Physical Health and Preventive Medicine, University of Campania ''Luigi Vanvitelli", 80138 Naples, Italy. Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
 Department of Dermatology, Tufts University School of Medicine, Boston, MA 02111, USA; Center for Blistering Diseases, Boston, MA 02135, USA. Electronic address: arahmedmd@msn.com. Center for Blistering Diseases, Boston, MA 02135, USA. Center for Blistering Diseases, Boston, MA 02135, USA.
 Institute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany. Institute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany. Institute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany. Institute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany. Institute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany. Institute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany. Electronic address: daniel.seiler@uksh.de.
 College of Computer Science, Huanggang Normal University, Huanggang, 438000, China. Department of Pathology, Faculty of Veterinary and Animal Sciences, The Islamia University of Bahawalpur, Bahawalpur, Pakistan. The University of Agriculture Peshawar, Peshawar, 25130, Khyber Pakhtunkhwa, Pakistan. College of Computer Science, Huanggang Normal University, Huanggang, 438000, China. ziaurrahman@hgnu.edu.cn.
 Faculty of Humanities, Department of Clinical Psychology, Islamic Azad University of Sirjan, Sirjan, Iran. Faculty of Humanities, Department of Clinical Psychology, Anar Islamic Azad University, Kerman, Iran. Department of Psychology and Educational Sciences, University of Allameh Tabatabaei, Tehran, Iran. Department of Clinical Psychology, Bam University of Medical Sciences, Bam, Iran. Faculty of Humanities, Department of Clinical Psychology, Islamic Azad University of Sirjan, Sirjan, Iran. Faculty of Humanities, Department of Clinical Psychology, Islamic Azad University of Sirjan, Sirjan, Iran.
 Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, Braga, Portugal. ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Portugal. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, Braga, Portugal. ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Portugal. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, Braga, Portugal. ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Portugal. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, Braga, Portugal. ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Portugal.
 International Collaboration on Repair Discoveries, The University of British Columbia, Vancouver, BC, Canada. International Collaboration on Repair Discoveries, The University of British Columbia, Vancouver, BC, Canada.
 Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India. Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India. Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India.
 Roche SAS, Boulogne, Billancourt, France. Roche SAS, Boulogne, Billancourt, France. Roche SAS, Boulogne, Billancourt, France. Keyrus Life Science, Nantes, France. Roche SAS, Boulogne, Billancourt, France.
 Independent Researcher, Escondido, CA 92029, USA.
 Department of Forensic Medicine, University of Pécs Medical School, Pécs, Hungary. Department of Anatomy, ELKH-PTE PACAP Research Team, Centre for Neuroscience, University of Pécs Medical School, Pécs, Hungary. Department of Anatomy, ELKH-PTE PACAP Research Team, Centre for Neuroscience, University of Pécs Medical School, Pécs, Hungary. Department of Anatomy, ELKH-PTE PACAP Research Team, Centre for Neuroscience, University of Pécs Medical School, Pécs, Hungary.
 Department of Neurological Surgery, NYU Langone Health, Grossman School of Medicine, New York University, New York, New York, USA.
 Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Cellular and Molecular Research Centerx, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address: khodayar-mj@ajums.ac.ir.
 Tohoku University, 13101, 2-1 Seiryo-cho, Aoba-ku, Sendai, Sendai, Miyagi, Japan, 980-8577; uruno@med.tohoku.ac.jp. Tohoku University Graduate School of Medicine, Department of Medical Biochemistry, 2-1 Seiryo-machi, Aoba-ku, Sendai, Sendai, Japan, 980-8575; masiyamamoto@med.tohoku.ac.jp.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics and Maternal Child Health, University of Genoa, Genoa, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina, 60, 20132, Milan, Italy. agosta.federica@hsr.it. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. agosta.federica@hsr.it. Vita-Salute San Raffaele University, Milan, Italy. agosta.federica@hsr.it.
 Department of Medicine 1, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen-Nürnberg, Germany. sebastian.zundler@uk-erlangen.de. Deutsches Zentrum Immuntherapie, University Hospital Erlangen, Erlangen, Germany. sebastian.zundler@uk-erlangen.de. Department of Medicine 1, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen-Nürnberg, Germany. Deutsches Zentrum Immuntherapie, University Hospital Erlangen, Erlangen, Germany. Department of Gastroenterology and Hepatology, University Hospital Zürich, Zürich, Switzerland. Deutsches Zentrum Immuntherapie, University Hospital Erlangen, Erlangen, Germany. Department of Medicine 3, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen-Nürnberg, Germany. Deutsches Zentrum Immuntherapie, University Hospital Erlangen, Erlangen, Germany. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen-Nürnberg, Germany. Department of Medicine 1, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen-Nürnberg, Germany. Deutsches Zentrum Immuntherapie, University Hospital Erlangen, Erlangen, Germany.
 Department of Cardiology, North Shore University Hospital, Northwell Health, Manhasset, New York, USA. Department of Cardiology, North Shore University Hospital, Northwell Health, Manhasset, New York, USA. Department of Cardiology, North Shore University Hospital, Northwell Health, Manhasset, New York, USA.
 Bioprocess Technology Division, School of Industrial Technology, Universiti Sains Malaysia, 11800 Gelugor, Penang, Malaysia. Electronic address: ronaldchong111@gmail.com. Bioprocess Technology Division, School of Industrial Technology, Universiti Sains Malaysia, 11800 Gelugor, Penang, Malaysia. Electronic address: nikyasmin@student.usm.my. Bioprocess Technology Division, School of Industrial Technology, Universiti Sains Malaysia, 11800 Gelugor, Penang, Malaysia. Electronic address: anamasara@usm.my.
 Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. University of Chinese Academy of Sciences, Beijing, China; CAS Key Laboratory for Receptor Research, Shanghai Institute of Materia, Medica, Chinese Academy of Sciences, Shanghai, China. Putuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China. Electronic address: ducs2015@163.com.
 Institute of Neuropathology, University Medical Center Freiburg, Freiburg, Germany. Institute of Neuropathology, University Medical Center Freiburg, Freiburg, Germany. Institute of Neuropathology, University Medical Center Freiburg, Freiburg, Germany. Institute of Neuropathology, University Medical Center Freiburg, Freiburg, Germany. Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany.
 REVIV Life Science Research, REVIV Global Ltd., Manchester M15 4PS, UK. REVIV Life Science Research, REVIV Global Ltd., Manchester M15 4PS, UK. Centre for Human Psychopharmacology, Swinburne University, Melbourne, VIC 3122, Australia. Department of Nutrition, Dietetics and Food, Monash University, Notting Hill, VIC 3168, Australia.
 Department of Anatomy and Cell Biology, The George Washington University, School of Medicine and Health Sciences, Washington, D.C., USA. Department of Anatomy and Cell Biology, The George Washington University, School of Medicine and Health Sciences, Washington, D.C., USA. Department of Anatomy and Cell Biology, The George Washington University, School of Medicine and Health Sciences, Washington, D.C., USA. Electronic address: rhm3@gwu.edu.
 Department of Food Science and Technology, Faculty of Environmental Sciences, Ionian University, GR26100 Argostoli, Cephalonia, Greece. Center for Translational Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA. Center for Translational Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA. Electronic address: ejames@benaroyaresearch.org. Laboratory of Biophysics, Biochemistry, Bioprocessing and Bioproducts, Faculty of Agricultural Technology, Technological Educational Institute of Epirus, GR47100 Arta, Greece.
 Department of Radiology and Organ Imaging, United Christian Hospital, Kwun Tong, Kowloon, Hong Kong. Department of Radiology and Organ Imaging, United Christian Hospital, Kwun Tong, Kowloon, Hong Kong. Department of Radiology and Organ Imaging, United Christian Hospital, Kwun Tong, Kowloon, Hong Kong.
 Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao C1 Refinery Engineering Research Center, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, China. Department of Anesthesiology, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, China. Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao C1 Refinery Engineering Research Center, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, China. Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao C1 Refinery Engineering Research Center, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, China. Qingdao New Energy Shandong Laboratory, Qingdao, China. China Academy of Chinese Medical Sciences, Beijing, China. Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao C1 Refinery Engineering Research Center, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, China. Shandong Energy Institute, Qingdao, China. Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao C1 Refinery Engineering Research Center, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, China. Qingdao New Energy Shandong Laboratory, Qingdao, China. Shandong Energy Institute, Qingdao, China.
 Volga Regional Medical Center of the Federal Medical-Biological Agency, Nizhny Novgorod, Russia. Privolzhsky Research Medical University, Nizhny Novgorod, Russia. Kirov State Medical University, Kirov, Russia. Privolzhsky Research Medical University, Nizhny Novgorod, Russia. Privolzhsky Research Medical University, Nizhny Novgorod, Russia.
 Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
 Fischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA. Fischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA. US Department of Veterans Affairs, VA Maryland Health Care System, Baltimore, MD, 21201, USA. Robert E. Fischell Institute for Biomedical Devices, College Park, MD, 20742, USA. Department of Microbiology and Immunology, University of Maryland Medical School, Baltimore, MD, 21201, USA. Marlene and Stewart Greenebaum Cancer Center, Baltimore, MD, 21201, USA.
 Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
 Center for Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy. Center for Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy. Center for Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy. Center for Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy. Center for Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy.
 Escuela de Kinesiología, Facultad de Odontología y Ciencias de la Rehabilitación, Universidad San Sebastián, Santiago 7500922, Chile. Departamento de Ciencias Preclínicas, Facultad de Medicina, Universidad de La Frontera, Temuco 4811230, Chile. Departamento de Medicina Interna Oriente, Facultad de Medicina, Universidad de Chile, Santiago 7500922, Chile. Center of Molecular Biology and Pharmacogenetics, Department of Basic Sciences, Faculty of Medicine, Universidad de La Frontera, Temuco 4811230, Chile.
 Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY 10065, USA. Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY 10065, USA. Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY 10065, USA. Department of Medicinal Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt. Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY 10065, USA. Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY 10065, USA.
 Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Department of Medical, Surgical and Experimental Sciences, University of Sassari - Neurology Unit Azienza Ospedaliera Universitaria (AOU), Sassari, Italy. Institute for Genetic and Biomedical Research - National Research Council (IRGB-CNR), Sassari, Italy.
 Center for the Evaluation of Value and Risk in Health, Tufts Medical Center, 800 Washington Street, #063, Boston, MA, 02111, USA. psynnott@tuftsmedicalcenter.org. Center for the Evaluation of Value and Risk in Health, Tufts Medical Center, 800 Washington Street, #063, Boston, MA, 02111, USA. Center for the Evaluation of Value and Risk in Health, Tufts Medical Center, 800 Washington Street, #063, Boston, MA, 02111, USA. Genentech, Inc, 1 DNA Way, South San Francisco, CA, 94080, USA. Center for the Evaluation of Value and Risk in Health, Tufts Medical Center, 800 Washington Street, #063, Boston, MA, 02111, USA.
 Chief Resident, Postgraduate Year 3, Division of Foot and Ankle Surgery, Western Pennsylvania Hospital, Allegheny Health Network, Pittsburgh, PA. Resident, Postgraduate Year 2, Division of Foot and Ankle Surgery, Western Pennsylvania Hospital, Allegheny Health Network, Pittsburgh, PA. Resident Physician, Department of Pathology and Laboratory Medicine, Allegheny General Hospital, Allegheny Health Network, Pittsburgh, PA. Faculty, Division of Foot & Ankle Surgery, West Penn Hospital, Allegheny Health Network, Pittsburgh, PA. Electronic address: Karl.saltrick@ahn.org.
 Alameda Highland Hospital, Department of Neurology, Oakland, CA. Alameda Highland Hospital, Department of Neurology, Oakland, CA. Sutter California Pacific Medical Center, Department of Psychiatry, San Francisco, CA. Alameda Highland Hospital, Department of Neurology, Oakland, CA. Sutter California Pacific Medical Center, Department of Neurology, San Francisco, CA. Providence Medford Medical Center, Department of Neurology, Medford, OR.
 Department of Nutritional Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Nutritional Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Human Nutrition and Dietetics Mirpur University of Science and Technology Mirpur Pakistan. Department of Food Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Food Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Food Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Nutritional Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Food Sciences Government College University Faisalabad Faisalabad Pakistan. Department of Nutritional Sciences Government College University Faisalabad Faisalabad Pakistan. Agricultural Extension Directorate, MAAR Damascus Syria.
 Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Sector 67, S.A.S. Nagar, Punjab 160062, India. CCRUM-National Research Institute of Unani Medicine for Skin Disorders (NRIUMSD), Hyderabad, Central Council for Research in Unani Medicine (CCRUM), New Delhi, India. Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Sector 67, S.A.S. Nagar, Punjab 160062, India. Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Sector 67, S.A.S. Nagar, Punjab 160062, India.
 Department of Biology, Arsanjan Branch, Islamic Azad University, Arsanjan, Iran. Department of Biology, Arsanjan Branch, Islamic Azad University, Arsanjan, Iran. Department of Immunology, Tehran University of Medical Sciences, Tehran, Iran. Department of Pathology, School of Veterinary Medicine, Shahrekord University, Shahrekord, Iran. Shiraz Molecular Pathology Research Center, Dr. Daneshbod Pathol Lab, Shiraz, Iran. Epilepsy Research Center, Department of Neurosurgery, Westfälische Wilhelms-Universitat Münster, Münster, Germany. Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran. Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran. Department of Neuroscience, Kerman University of Medical Sciences, Kerman, Iran.
 Neurology, Northwell Health, Manhasset, USA. Neurology, Northwell Health, Manhasset, USA. Neurology, Northwell Health, Manhasset, USA. Neurology, Northwell Health, Manhasset, USA. Neurology, Northwell Health, Manhasset, USA.
 The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China. The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China. The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China. The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China. The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China. The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, China.
 Department of Neurosurgery, Nakamura Memorial Hospital. Department of Neurosurgery, Nakamura Memorial Hospital. Department of Neurosurgery, Nakamura Memorial Hospital. Department of Neurosurgery, Nakamura Memorial Hospital. Department of Neurosurgery, Nakamura Memorial Hospital. Department of Neurosurgery, Nakamura Memorial Hospital. Department of Neurosurgery, Nakamura Memorial Hospital.
 Student Research Committee, Department of Nutritional Sciences, School of Nutritional Sciences and Food Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Research Center for Environmental Determinants of Health, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran. Student Research Committee, Department of Nutritional Sciences, School of Nutritional Sciences and Food Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Research Center for Environmental Determinants of Health, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Nutritional Sciences, School of Nutritional Sciences and Food Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Research Center of Oils and Fats, Kermanshah University of Medical Sciences, Kermanshah, Iran. Research Center for Environmental Determinants of Health, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Nutritional Sciences, School of Nutritional Sciences and Food Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran. Surgical Oncology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Nutrition and Food Security Research Center and Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. Surgical Oncology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Nutrition and Food Security Research Center and Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran. Laboratory of Neuroproteomics, Department of Biochemistry and Tissue Biology, Institute of Biology, University of Campinas (UNICAMP), Campinas, Brazil. Department of Psychiatry, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany. Laboratory of Translational Psychiatry, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
 University of Minnesota, Department of Radiology, MMC 292, 420 Delaware St. SE Minneapolis, MN 55455, USA. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Clinical Imaging Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Clinical Imaging Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiation Oncology, Phillips-Wangensteen Bldg Floor 1, 516 Delaware Street SE, Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, Center for Magnetic Resonance Research, 2021 6th St SE Minneapolis, MN 55455. University of Minnesota, Department of Radiology, MMC 292, 420 Delaware St. SE Minneapolis, MN 55455, USA. University of Minnesota, Department of Radiology, Center for Clinical Imaging Research, 2021 6th St SE Minneapolis, MN 55455.
 Osteopathic Medical School, Des Moines University (DMU), Des Moines, IA 50312, USA. Department of Biomedical Engineering, University of Illinois at Chicago (UIC), Chicago, IL 60607, USA. Department of Biomedical Engineering, University of Illinois at Chicago (UIC), Chicago, IL 60607, USA. Lady Davis Institute for Medical Research, SMBD-Jewish General Hospital, 3755 Cote Ste-Catherine Road, Room F-602, Montreal, QC H3T 1E2, Canada. Medical Research Institute, School of Medicine, Sungkyunkwan University (SKKU), Suwon 16419, Republic of Korea. Department of Biomedical Engineering, University of Illinois at Chicago (UIC), Chicago, IL 60607, USA. Department of Biochemistry, University of Vermont (UVM), Burlington, VT 05405, USA. Department of Biomedical Engineering, University of Illinois at Chicago (UIC), Chicago, IL 60607, USA. Jesse Brown Veterans Affairs Medical Center at Chicago (JBVAMC), Chicago, IL 60612, USA.
 Department of Neurology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China. Department of Neurology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China. Department of Pharmacy, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China. Department of Neurology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China. Department of Neurology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
 Faculty of EEMCS, University of Twente, 7500 AE Enschede, The Netherlands. Institute for Artificial Intelligence in Medicine, University of Duisburg-Essen, 45131 Essen, Germany. Hospital Group Twente (ZGT), 7555 DL Hengelo, The Netherlands. Hospital Group Twente (ZGT), 7555 DL Hengelo, The Netherlands. Institute for Artificial Intelligence in Medicine, University of Duisburg-Essen, 45131 Essen, Germany.
 Department of Oncobiology and Epigenetics, Faculty of Biology and Environmental Protection, University of Lodz, ul. Pomorska 141/143, 90-236 Lodz, Poland. Department of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, ul. Pomorska 141/143, 90-236 Lodz, Poland.
 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Ribeirão Preto Medical School, University of São Paulo - Ribeirão Preto, São Paulo 14049-900, Brazil. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA. Washington University Center for Cellular Imaging, Washington University School of Medicine, St. Louis, MO 63110, USA. Washington University Center for Cellular Imaging, Washington University School of Medicine, St. Louis, MO 63110, USA. Washington University Center for Cellular Imaging, Washington University School of Medicine, St. Louis, MO 63110, USA; Departments of Cell Biology and Physiology and Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: mcolonna@wustl.edu.
 School of Engineering, University of Guelph, Guelph, ON N1G 2W1, Canada. Department of Biomedical Engineering, University of Calgary, Calgary, AB T2N 1N4, Canada. School of Engineering, University of Guelph, Guelph, ON N1G 2W1, Canada. Department of Biomedical Engineering, University of Calgary, Calgary, AB T2N 1N4, Canada.
 State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. Laboratory of Metabolomics and Drug-induced Liver Injury, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. Department of Thyroid Surgery, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China; Laboratory of Thyroid and Parathyroid Disease, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, 610041, China. Electronic address: wenshuang_wu@163.com. State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center, Sichuan University, Chengdu, 610041, China. Electronic address: yhy1984_hb@163.com.
 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, India. Department of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas, USA. Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER)-Raebareli, Lucknow, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, India. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, India.
 Department of General Practice, Melbourne Medical School, Faculty of Medicine, Dentistry and Health Sciences of the University of Melbourne, Level 2, 780 Elizabeth Street, Melbourne, Vic. 3004, Australia; and Faculty of Medicine, Dentistry and Health Sciences of the University of Melbourne, Level 2. Faculty of Medicine, Dentistry and Health Sciences of the University of Melbourne, Level 2, Alan Gilbert Building, Grattan Street, Parkville, Vic. 3010, Australia. Health and Biomedical Research Information Technology Unit (HaBIC R2), Faculty of Medicine, Dentistry and Health Sciences of the University of Melbourne, Level 2, 780 Elizabeth Street, Melbourne, Vic. 3004, Australia. Faculty of Medicine, Dentistry and Health Sciences of the University of Melbourne, Level 2, Alan Gilbert Building, Grattan Street, Parkville, Vic. 3010, Australia; and Department of Addiction Medicine, St Vincent's Hospital, Fitzroy, Vic. 3065, Australia.
 School of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, No. 1, Qianjiang Road, 230012 Hefei, Anhui, China. School of Acupuncture and Massage, Anhui University of Chinese Medicine, 230012 Hefei, Anhui, China. School of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, No. 1, Qianjiang Road, 230012 Hefei, Anhui, China. Xin'an School, Anhui University of Chinese Medicine, 230012 Hefei, Anhui, China. School of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, No. 1, Qianjiang Road, 230012 Hefei, Anhui, China. School of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, No. 1, Qianjiang Road, 230012 Hefei, Anhui, China.
 Faculty of Medicine, University of Southampton, Southampton, SO17 1BJ, UK. b.gaastra@soton.ac.uk. Department of Neurosurgery, Wessex Neurological Centre, University Hospital Southampton, Southampton, SO16 6YD, UK. b.gaastra@soton.ac.uk. Center of Neuroscience Research, Loma Linda University, Loma Linda, CA, 92350, USA. Faculty of Medicine, University of Southampton, Southampton, SO17 1BJ, UK. Department of Neurosurgery, Wessex Neurological Centre, University Hospital Southampton, Southampton, SO16 6YD, UK. Faculty of Medicine, University of Southampton, Southampton, SO17 1BJ, UK.
 Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Weill Institute for Neuroscience, Department of Neurology, University of California, San Francisco, CA 94158, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA. Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.

 Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly Delhi College of Engineering), India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly Delhi College of Engineering), India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly Delhi College of Engineering), India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly Delhi College of Engineering), India. Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly Delhi College of Engineering), India. Electronic address: pravirkumar@dtu.ac.in.
 Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad, India. Amikachoudhary411@gmail.com. Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad, India. Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad, India. Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad, India.
 Department of Experimental Immunology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands. Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, University of Amsterdam, Netherlands. Department of Experimental Immunology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands. Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, University of Amsterdam, Netherlands. Department of Experimental Immunology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands. Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, University of Amsterdam, Netherlands. Department of Experimental Immunology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands. Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, University of Amsterdam, Netherlands.
 Department of Biomedical Engineering, University of Alberta, Edmonton, Canada. Department of Biomedical Engineering, University of Alberta, Edmonton, Canada. Department of Biomedical Engineering, University of Alberta, Edmonton, Canada. Department of Biomedical Engineering, University of Alberta, Edmonton, Canada. Department of Medicine, Division of Neurology, University of Alberta, Edmonton, Canada. Department of Medicine, Division of Neurology, University of Alberta, Edmonton, Canada. Department of Biomedical Engineering, University of Alberta, Edmonton, Canada.
 Department of Neurosciences and Behavioral Sciences, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil. Department of Neurosciences and Behavioral Sciences, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil. Department of Ophthalmology, Otorhinolaryngology and Head and Neck Surgery, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.
 School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada. School of Rehabilitation Therapy, Queen's University, Kingston, Canada.

 Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan. Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan. Electronic address: yshimoji@shinshu-u.ac.jp. Department of Radiology, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan. Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan.

 Sociedad Científica de San Fernando, Universidad Nacional Mayor de San Marcos, Lima, Peru. Grupo Peruano de Investigación Epidemiológica, Unidad Para la Generación Y Síntesis de Evidencias en Salud, Universidad San Ignacio de Loyola, Lima, Peru. Sociedad Científica de San Fernando, Universidad Nacional Mayor de San Marcos, Lima, Peru. Grupo Peruano de Investigación Epidemiológica, Unidad Para la Generación Y Síntesis de Evidencias en Salud, Universidad San Ignacio de Loyola, Lima, Peru. Academic Department, Faculty of Medical Technology, Universidad Nacional Federico Villarreal, Lima, Peru. Academic Department, Universidad Nacional Mayor De San Marcos, Lima, Peru. Research Direction, Universidad Privada del Norte, Lima, Peru. Vicerrectorado de Investigación, Universidad San Ignacio de Loyola, Lima, Peru.
 Division of Immunology, LCMN, Germans Trias i Pujol University Hospital and Research Institute, Campus Can Ruti, Badalona, Spain. Department of Cellular Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, 08193 Bellaterra (Cerdanyola del Vallès), Spain. Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK. Division of Immunology, LCMN, Germans Trias i Pujol University Hospital and Research Institute, Campus Can Ruti, Badalona, Spain. Department of Cellular Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, 08193 Bellaterra (Cerdanyola del Vallès), Spain.
 McGovern Medical School at UTHealth Houston, Houston, Texas, USA. Memorial Sloan Kettering Cancer Center, New York City, New York, USA. Department of Anesthesiology, Chronic Pain, McGovern Medical School at UTHealth Houston, Houston, Texas, USA.
 San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy. Vita-Salute San Raffaele University, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy.
 Institut Jules Bordet -Brussels, Belgium Istituto Nazionale Tumori - IRCCS Istituto Nazionale Tumori - IRCCS - Fondazione Pascale, Via Mariano Semmola 80100, Napoli. Italy
 Department of Veterinary Pathobiology, School of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX. Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS. Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS. Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS.
 Department of Chemistry and Virginia Tech Center for Drug Discovery, Virginia Tech, Blacksburg, Virginia 24061, United States. Department of Chemistry and Virginia Tech Center for Drug Discovery, Virginia Tech, Blacksburg, Virginia 24061, United States. Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, United States. Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, United States. Department of Chemistry and Virginia Tech Center for Drug Discovery, Virginia Tech, Blacksburg, Virginia 24061, United States. Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, United States. Department of Chemistry and Virginia Tech Center for Drug Discovery, Virginia Tech, Blacksburg, Virginia 24061, United States.
 Department of Biotechnology, Yeungnam University, Gyeongsan 38541, Gyeongbuk, Republic of Korea. Department of Biotechnology, Yeungnam University, Gyeongsan 38541, Gyeongbuk, Republic of Korea. Gyeongbuk Institute for Bioindustry, Andong 36618, Gyeongbuk, Republic of Korea. Gyeongbuk Institute for Bioindustry, Andong 36618, Gyeongbuk, Republic of Korea. Gyeongbuk Institute for Bioindustry, Andong 36618, Gyeongbuk, Republic of Korea. Department of Biotechnology, Yeungnam University, Gyeongsan 38541, Gyeongbuk, Republic of Korea.
 Harvard Medical School, Boston, MA, United States. Department of Neurology, Brigham and Women's Hospital, Ann Romney Center for Neurologic Diseases, Boston, MA, United States. Harvard Medical School, Boston, MA, United States. Department of Neurology, Brigham and Women's Hospital, Ann Romney Center for Neurologic Diseases, Boston, MA, United States.
 Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, USA. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, USA. Department of Neurological Sciences, Rush University Medical Center, Chicago, USA. Department of Neurological Sciences, Rush University Medical Center, Chicago, USA. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, USA. Department of Neurological Sciences, Rush University Medical Center, Chicago, USA.
 Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, United States. Department of Neurological Surgery, Oregon Health & Science University, Portland, OR, United States. Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, United States.
 Department of Anesthesiology and Intensive Care, Medical University of Sofia, University Hospital "Tzaritza Yoanna-ISUL", 1527 Sofia, Bulgaria. Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Science, 1113 Sofia, Bulgaria.
 Department of Neuroscience and Physiology, Institute of Neuroscience, New York University Langone Medical Center, New York, NY, United States. Department of Neuroscience and Physiology, Institute of Neuroscience, New York University Langone Medical Center, New York, NY, United States. Department of Neuroscience and Physiology, Institute of Neuroscience, New York University Langone Medical Center, New York, NY, United States. Department of Neurology, New York University Langone Medical Center, New York, NY, United States.
 Department of Biomedical Sciences, Humanitas University, 20072, Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, 20089, Rozzano, Milan, Italy. Electronic address: daniele.piovani@humanitasresearch.it. Department of Biomedical Sciences, Humanitas University, 20072, Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, 20089, Rozzano, Milan, Italy. Department of Biomedical Sciences, Humanitas University, 20072, Pieve Emanuele, Milan, Italy; IRCCS Humanitas Research Hospital, 20089, Rozzano, Milan, Italy.
 School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia. Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States. Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States. School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia. School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia. School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia.
 Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Microbiology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran. Department of Microbiology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran. Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Infectious Diseases & Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
 Modeling Biological System's Laboratory, Department of Biomedical Engineering, Faculty of Electrical and Computer Engineering, University of Tabriz, Tabriz, Iran. Modeling Biological System's Laboratory, Department of Biomedical Engineering, Faculty of Electrical and Computer Engineering, University of Tabriz, Tabriz, Iran. yashar.sarbaz@tabrizu.ac.ir.
 Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India. Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India. Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India.
 National Institute of Biomedical Genomics, P.O.: N.S.S., Kalyani, West Bengal 741251, India. National Institute of Biomedical Genomics, P.O.: N.S.S., Kalyani, West Bengal 741251, India; Indian Statistical Institute, 203, Barrackpore Trunk Road, Kolkata, West Bengal 700108, India. Electronic address: ppm@isical.ac.in.
 Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, University of Technology, 01307 Dresden, Germany.
 National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, 430070, China. Frontiers Science Center for Animal Breeding and Sustainable Production, Wuhan, 430070, China. National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. Wuhan Keqian Biological Co., Ltd., Wuhan, 430070, China. National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. Wuhan Academy of Agricultural Sciences, Wuhan, 430070, China. National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, 430070, China. Frontiers Science Center for Animal Breeding and Sustainable Production, Wuhan, 430070, China. National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, 430070, China. Frontiers Science Center for Animal Breeding and Sustainable Production, Wuhan, 430070, China. National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. wangxr228@mail.hzau.edu.cn. Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, 430070, China. wangxr228@mail.hzau.edu.cn. Frontiers Science Center for Animal Breeding and Sustainable Production, Wuhan, 430070, China. wangxr228@mail.hzau.edu.cn.
 Division of Pulmonology, Department of Medicine, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Division of Pulmonology, Department of Medicine, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Center for Investigation and Research in Sleep, Department of Medicine, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Division of Pulmonary Diseases, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland. Division of Pulmonology, Department of Medicine, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Division of Pulmonology, Department of Medicine, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
 Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Environmental Health Engineering, School of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Air Pollution and Respiratory Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Thalassemia & Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Environment, Ahvaz Branch, Islamic Azad University, Ahvaz, Iran. Department of Environmental Health Engineering, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
 Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Simrol, 453552, Indore India. Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Simrol, 453552, Indore India. Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Simrol, 453552, Indore India. School of Biosciences and Technology, Vellore Institute of Technology, Vellore, 632014, Tamil Nadu India. Department of Medical Biochemistry and Biophysics, Karolinska Institute, 17177 Stockholm, Sweden. Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Karwar, 342030, Jodhpur India. Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Simrol, 453552, Indore India.
 Department of Urology, The People's Hospital of Longhua, The Affiliated Hospital of Southern Medical University, Shenzhen, China. The First School of Clinical Medicine, Southern Medical University, Guangzhou, China. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China. Southern Medical University Library, Guangzhou, China. Department of Urology, The People's Hospital of Longhua, The Affiliated Hospital of Southern Medical University, Shenzhen, China. 993368974@qq.com.
 Department of Neuroscience, Catholic University of the Sacred Heart, 00168 Rome, Italy. IRCCS San Raffaele Scientific Institute, Università Vita-Salute San Raffaele, 20132 Milan, Italy. Department of Medicine, LUM University, 70010 Casamassima, Italy. Genes, Via Venti Settembre 118, 00187 Roma, Italy. Istituto di Scienze e Tecnologie Chimiche "Giulio Natta" SCITEC-CNR, 00168 Rome, Italy. Department of Pharmaceutical and Pharmacological Sciences, University of Padova, 35131 Padova, Italy. Laboratory of Epidemiology and Biotechnologies, Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", 00135 Rome, Italy. Department of Translational Medicine and Surgery, Section of General Pathology, Catholic University of the Sacred Heart, 00168 Rome, Italy. Department of Medicine and Surgery, Section of Human, Clinical and Forensic Anatomy, University of Perugia, 06132 Perugia, Italy. Department of Medicine and Surgery, Section of Human, Clinical and Forensic Anatomy, University of Perugia, 06132 Perugia, Italy. Laboratory of Epidemiology and Biotechnologies, Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", 00135 Rome, Italy.
 Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. fbustamante.1990@gmail.com. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. fbustamante.1990@gmail.com. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. fbustamante.1990@gmail.com. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. Facultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. Cells for Cells, Regenero, Las Condes, Santiago, Chile. Laboratorio de Biología Celular, Departamento de Biología Celular, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile. Escuela de Ingeniería Bioquímica, Pontificia Universidad Católica de Valparaiso, Valparaiso, Chile. Laboratorio de Inmunología Celular y Molecular, Facultad de Medicina, Universidad de los Andes, Santiago, Chile. patricia.luzc@gmail.com. Centro de Investigación e Innovación Biomédica (CiiB), Universidad de los Andes, Mons. Álvaro del Portillo 12455, Las Condes, Santiago, Chile. patricia.luzc@gmail.com. IMPACT, Center of Interventional Medicine for Precision and Advanced Cellular Therapy, Santiago, Chile. patricia.luzc@gmail.com.
 Department of Gerontology and Geriatrics, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, 110004, Shenyang, Liaoning, PR China. Department of Otolaryngology Head and Neck Surgery, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, 110004, Shenyang, Liaoning, PR China. Department of Gerontology and Geriatrics, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, 110004, Shenyang, Liaoning, PR China. Electronic address: zhangm0810@163.com.
 INSERM U1016, Institut Cochin, Département 3I "Infection, Immunité Et Inflammation", Université Paris Cité, Paris, France. R&D Department, MEDSENIC SAS, Strasbourg, France. R&D Department, MEDSENIC SAS, Strasbourg, France. INSERM U1016, Institut Cochin, Département 3I "Infection, Immunité Et Inflammation", Université Paris Cité, Paris, France. R&D Department, MEDSENIC SAS, Strasbourg, France. INSERM U1016, Institut Cochin, Département 3I "Infection, Immunité Et Inflammation", Université Paris Cité, Paris, France. INSERM U1016, Institut Cochin, Département 3I "Infection, Immunité Et Inflammation", Université Paris Cité, Paris, France. Service d'immunologie Biologique, AP-HP-Centre Université Paris Cité, Hôpital Cochin, Université Paris Cité, Faculté De Médecine, Paris, France.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Biogen, Cambridge, Massachusetts, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Lou Ruvo Center for Brain Health, Cleveland Clinic, Las Vegas, Nevada, USA. Department of Neurology, University of Rochester Medical Center, Rochester, New York, USA. Department of Neurology, University of Rochester Medical Center, Rochester, New York, USA. Mellen Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA. Department of Neurology and Centre d'Esclerosi Múltiple de Catalunya, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology and Centre d'Esclerosi Múltiple de Catalunya, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology and Centre d'Esclerosi Múltiple de Catalunya, Vall d'Hebron Hospital Universitari, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Neurology, Washington University in St. Louis, St. Louis, Missouri, USA. Department of Neurology, Washington University in St. Louis, St. Louis, Missouri, USA. Department of Neurology, New York University, New York City, New York, USA. OhioHealth Multiple Sclerosis Center, Riverside Methodist Hospital, Columbus, Ohio, USA. Center of Clinical Neuroscience, Department of Neurology, University Clinic Carl-Gustav Carus, Dresden, Germany. Center of Clinical Neuroscience, Department of Neurology, University Clinic Carl-Gustav Carus, Dresden, Germany. (formerly) Biogen, Cambridge, Massachusetts, USA. Biogen, Cambridge, Massachusetts, USA. Mellen Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
 Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Olivier.Nicolas@sanofi.com. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Department of Integrated Drug Discovery/Isotope Chemistry, Sanofi, Paris, France. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. MS Neurology Development, Sanofi, Cambridge, MA, USA. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France. Department of Translational Medicine and Early Development, Sanofi, 371 Rue Professeur Blayac, 34184, Montpellier, France.
 Geschäftsbereich Sozialmedizin und Rehabilitation, Deutsche Rentenversicherung Bund, Berlin, Deutschland. Geschäftsbereich Sozialmedizin und Rehabilitation, Deutsche Rentenversicherung Bund, Berlin, Deutschland. Fakultät für Gesundheitswissenschaften, Universität Bielefeld, Deutschland. Fakultät für Gesundheitswissenschaften, Universität Bielefeld, Deutschland. Fakultät für Gesundheitswissenschaften, Universität Bielefeld, Deutschland.

 AIRLab, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 50143, Florence, Italy. Scuola Superiore Sant'Anna, Istituto di BioRobotica, 56025, Pontedera, Italy. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. icarpinella@dongnocchi.it. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. Scuola Superiore Sant'Anna, Istituto di BioRobotica, 56025, Pontedera, Italy. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università di Milano, 20122, Milan, Italy. LAMoBIR and LaRiCE, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 20148, Milan, Italy. AIRLab, IRCCS Fondazione Don Carlo Gnocchi ONLUS, 50143, Florence, Italy.
 Graduate Program in Biological Sciences: Biochemistry Toxicology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Graduate Program in Biological Sciences: Biochemistry Toxicology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Graduate Program in Biological Sciences: Biochemistry Toxicology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Graduate Program in Biological Sciences: Biochemistry Toxicology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Laboratory of Neurotoxicity and Psychopharmacology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Laboratory of Neurotoxicity and Psychopharmacology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Laboratory of Neurotoxicity and Psychopharmacology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Graduate Program in Biological Sciences: Biochemistry Toxicology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Electronic address: saramarchesan@ufsm.br.
 Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Technology Platform for Electron Microscopy, Max Delbrück Centre for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany. Department of Neuropathology, Charité-Universitätsmedizin Berlin., Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Charité Universitätsmedizin Berlin., Berlin, Germany. Neuromuscular and Cardiovascular Cell Biology Group, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Institute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden., Dresden, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Experimental and Clinical Research Center (ECRC), Charité-Universitätsmedizin Berlin und Max Delbrück Center or Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Charité Universitätsmedizin Berlin., Berlin, Germany.
 Department of Neurology, Korea University, College of Medicine, Seoul, Korea. Department of Neurology, Soonchunhyang University Hospital Cheonan, Soonchunhyang University College of Medicine, Cheonan, Korea. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; Neuroscience Center, Samsung Medical Center, Seoul, Korea. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; Neuroscience Center, Samsung Medical Center, Seoul, Korea. Department of Neurology, Korea University, College of Medicine, Seoul, Korea. Department of Neurology, Seoul National University, College of Medicine, Seoul, Korea. Department of Neurology, Chungnam National University, College of Medicine, Daejeon, Korea. Department of Neurology, Gyeongsang Institute of Health Science, Gyeongsang National University, College of Medicine, Jinju, Korea. Department of Neurology, Jeju National University, College of Medicine, Jeju, Korea. Department of Neurology, Seoul National University, College of Medicine, Seoul, Korea. Department of Neurology, Yonsei University College of Medicine, Seoul, Korea. Department of Neurology, Ilsan Paik Hospital, Inje University College of Medicine, Goyang, Korea. Department of Neurology, Konkuk University School of Medicine, Konkuk University Medical Center, Seoul, Korea. Department of Neurology, Chungbuk National University, College of Medicine, Chungbuk, Korea. Department of Neurology, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, Korea. Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Korea. Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Korea. Department of Neurology, Korea University, College of Medicine, Seoul, Korea. Electronic address: bjkim@skku.edu. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; Neuroscience Center, Samsung Medical Center, Seoul, Korea. Electronic address: nukbj@korea.ac.kr.
 Department of Veterans Affairs Multiple Sclerosis Center of Excellence (VA MSCoE), Baltimore VA Medical Center, Baltimore, MD, United States. Department of Neurology, University of Maryland Medical Center, Baltimore, MD, United States. Health Sciences and Human Services Library, University of Maryland, Baltimore, MD, United States. Department of Veterans Affairs Multiple Sclerosis Center of Excellence (VA MSCoE), Baltimore VA Medical Center, Baltimore, MD, United States. Department of Neurology, University of Maryland Medical Center, Baltimore, MD, United States.
 Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. pbrugarolas@mgh.harvard.edu. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. Department of Radiology, Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. elfakhri.georges@mgh.harvard.edu.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030619, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030619, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030619, Jinzhong, China. Department of Traditional Chinese Medicine, Shanxi Pharmaceutical Vocational College, 030031, Taiyuan, China. Department of Neurology, the First Affiliated Hospital, Shanxi Datong University, 037048, Datong, China. Department of Neurology, the First Affiliated Hospital, Shanxi Datong University, 037048, Datong, China. Huashan Hospital, Fudan University, 200025, Shanghai, China. Modern Research Center for Traditional Chinese Medicine, Shanxi University, 030006, Taiyuan, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030619, Jinzhong, China. 13603538882@139.com. Health Commission of Shanxi Province, 030001, Taiyuan, China. 13603538882@139.com. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030619, Jinzhong, China. macungen@sxtcm.edu.cn. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030619, Jinzhong, China. chaizhi@sxtcm.edu.cn.
 Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy matteo.gastaldi@mondino.it. Clinica Pediatrica, Fondazione IRCCS Policlinico San Matteo, Università degli Studi di Pavia, Pavia, Italy. Department of Neurosciences, Università degli Studi di Pavia, Pavia, Italy. Multiple Sclerosis Centre, IRCCS Mondino Foundation, Pavia, Italy. Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy. Multiple Sclerosis Centre, IRCCS Mondino Foundation, Pavia, Italy. Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy. Department of Neurosciences, Università degli Studi di Pavia, Pavia, Italy. Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. MS Center, Spedali Civili of Brescia, Brescia, Italy. Neuroimmunology and Neuromuscolar Diseases Unit, IRCCS Foundation Carlo Besta Neurological Institute, Milano, Italy. Child Neuropsychiatry Unit, Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, and Maternal and Children's Sciences, Giannina Gaslini Institute, Genova, Italy. Child Neuropsychiatry Unit, Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, and Maternal and Children's Sciences, Giannina Gaslini Institute, Genova, Italy. Department of Biomedical Metabolic and Neurosciences, University of Modena and Reggio Emilia, Modena, Italy. Department of Neurosciences, Division of Neurology, Santobono-Pausilipon Children's Hospital, Napoli, Italy. Division of Neurology, Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania "Luigi Vanvitelli", Naples, Italy. Section of Neurology, Department of Medicine, University of Perugia, Perugia, Italy. Neurology Department, Ospedale Policlinico San Martino IRCCS, Genoa, Italy. Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Biotechnology and Life Sciences, University of insubria, Varese, Italy. Neurology and Stroke Unit, ASST SetteLaghi, Ospedale di Circolo/Fondazione Macchi, Varese, Italy. Department of Neuroscience, Institute of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Child Neuropsychiatry Unit, Mother and Child Department, University Hospital of Parma, Parma, Italy. Pediatric Neurology and Neurophysiology Unit, Department of Women's and Children's Health, University of Padua, Padua, Italy. Pediatric Neurology and Neurophysiology Unit, Department of Women's and Children's Health, University of Padua, Padua, Italy. Department of Clinical and Experimental Medicine, Section of Pediatrics and Child Neuropsychiatry, University of Catania, Catania, Italy. Clinica Pediatrica, Fondazione IRCCS Policlinico San Matteo, Università degli Studi di Pavia, Pavia, Italy. Multiple Sclerosis Centre, IRCCS Mondino Foundation, Pavia, Italy. BioData Science Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Mathematics, University of Pavia, Pavia, Italy. Department of Neurology, University of Heidelberg, Heidelberg, Germany. Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy.
 Neurology Department, Hospital Universitario de Málaga, Málaga, Spain. Pharmacy Department, Hospital Universitario Vall d'Hebron, Barcelona, Spain. Specialised Nurse, Hospital Virgen Macarena, Sevilla, Spain. Specialised Nurse, Hospital Virgen Arrixaca, Murcia, Spain. Pharmacy Department, Hospital Clínico San Carlos, Madrid, Spain. Neurology Department, Hospital Universitario La Princesa, Madrid, Spain. Neurology Department, Hospital Universitario Josep Trueta, Girona, Spain. Neurology Department, Hospital Universitario Cruces, Bilbao, Spain. Biogen, Madrid, Spain. Biogen, Madrid, Spain. Pharmacoeconomics and Outcomes Research Iberia (PORIB), Madrid, Spain. Pharmacoeconomics and Outcomes Research Iberia (PORIB), Madrid, Spain. nespinoza@porib.com. Pharmacoeconomics and Outcomes Research Iberia (PORIB), Madrid, Spain.
 Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Department of Neurology, the First Affiliated Hospital, Shanxi Medical University, Taiyuan, 030001, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Institute of Brain Science, Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases, Shanxi Datong University, Datong, Shanxi Province, 037009, China. Department of Neurology, Datong Fifth People's Hospital, Datong, Shanxi Province, 037009, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Institute of Neurology, Huashan Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200000, China. Research Center of Neurobiology, the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. macungen@sxtcm.edu.cn. Institute of Brain Science, Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases, Shanxi Datong University, Datong, Shanxi Province, 037009, China. macungen@sxtcm.edu.cn.
 Department of Rehabilitation Medicine, Chengdu Second People's Hospital, Sichuan, China. Department of Kinesiology, Shanghai University of Sport, Shanghai, China. The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. The Ninth People's Hospital of Wuxi Affiliated to Soochow University, Wuxi, China. The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
 Department of Biomedical, Surgical and Dental Sciences, University of Milan, Milan, Italy. stela.vujosevic@unimi.it. Eye Clinic, IRCCS MultiMedica, Milan, Italy. stela.vujosevic@unimi.it. Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA. Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA. Department of Ophthalmology Mater Private Network, Dublin, Ireland. Eye Clinic, IRCCS MultiMedica, Milan, Italy. University of Milan, Milan, Italy. Eye Clinic, IRCCS MultiMedica, Milan, Italy. University of Milan, Milan, Italy. Eye Clinic, IRCCS MultiMedica, Milan, Italy. Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy. Department of Biomedical, Surgical and Dental Sciences, University of Milan, Milan, Italy.
 Department of Immunology, Multiple Sclerosis Center, National Center of Neurology and Psychiatry, National Institute of Neuroscience.
 Department of Food Science and Nutrition, Kyungpook National University, Daegu, 41566, Republic of Korea; Center for Food and Nutritional Genomics, Kyungpook National University, Daegu, 41566, Republic of Korea. Department of Food Science and Nutrition, Kyungpook National University, Daegu, 41566, Republic of Korea; Center for Food and Nutritional Genomics, Kyungpook National University, Daegu, 41566, Republic of Korea. Department of Food Science and Nutrition, Kyungpook National University, Daegu, 41566, Republic of Korea; Center for Food and Nutritional Genomics, Kyungpook National University, Daegu, 41566, Republic of Korea. Omixplus, LLC., Gaithersburg, MD, 20850, USA. Cancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA. Department of Food Science and Nutrition, Kyungpook National University, Daegu, 41566, Republic of Korea; Center for Food and Nutritional Genomics, Kyungpook National University, Daegu, 41566, Republic of Korea. Electronic address: eykwon@knu.ac.kr.
 Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Indigenous Health Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. NICM Health Research Institute, Western Sydney University, Westmead, NSW 2145, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. Pharmacology Unit, School of Medicine, Western Sydney University, Campbelltown, NSW 2560, Australia. NICM Health Research Institute, Western Sydney University, Westmead, NSW 2145, Australia.
 Department of Biology, Institute of Plant Science and Microbiology, University of Hamburg, Ohnhorststr. 18, 22609, Hamburg, Germany. Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Ul. Postepu 36A, Jastrzębiec, 05-552, Magdalenka, Poland. Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Ul. Postepu 36A, Jastrzębiec, 05-552, Magdalenka, Poland. Institute of Health, Siedlce University of Natural Sciences and Humanities, Ul. Konarskiego 2, 08-110, Siedlce, Poland. Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Ul. Postepu 36A, Jastrzębiec, 05-552, Magdalenka, Poland. Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Ul. Postepu 36A, Jastrzębiec, 05-552, Magdalenka, Poland. m.sacharczuk@igbzpan.pl. Department of Pharmacodynamics, Faculty of Pharmacy, Warsaw Medical University, L Banacha 1, 02-697, Warsaw, Poland. m.sacharczuk@igbzpan.pl. Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Ul. Postepu 36A, Jastrzębiec, 05-552, Magdalenka, Poland. m.mickael@igbzpan.pl.
 , BSc(Pharm), ACPR, is with Lower Mainland Pharmacy Services, BC Children's Hospital, Vancouver, British Columbia. , BSc(Pharm), ACPR, is with Lower Mainland Pharmacy Services, BC Children's Hospital, Vancouver, British Columbia. , BSc(Pharm), PharmD, ACPR, FCSHP, is with Lower Mainland Pharmacy Services, BC Children's Hospital, and the Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, British Columbia.
 Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
 Division of Periodontology, Department of Developmental and Surgical Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN 55455, USA. Department of Preventive Dentistry, Periodontology and Implant Biology, Faculty of Dentistry, School of Health Sciences, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece. Biostatistical Design and Analysis Center, Clinical and Translational Science Institute, University of Minnesota, Minneapolis, MN 55414, USA. Biostatistical Design and Analysis Center, Clinical and Translational Science Institute, University of Minnesota, Minneapolis, MN 55414, USA. Division of Periodontology, Department of Developmental and Surgical Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN 55455, USA.
 School of Biological Sciences, The University of Western Australia, Crawley, WA 6009, Australia. Perron Institute for Neurological and Translational Science, Nedlands, WA 6009, Australia. School of Biological Sciences, The University of Western Australia, Crawley, WA 6009, Australia. Perron Institute for Neurological and Translational Science, Nedlands, WA 6009, Australia. Perron Institute for Neurological and Translational Science, Nedlands, WA 6009, Australia. Centre for Neuromuscular and Neurological Disorders, The University of Western Australia, Crawley, WA 6009, Australia. Department of Neurosurgery, Sir Charles Gairdner Hospital, QEII Medical Centre, Nedlands, WA 6009, Australia. School of Biological Sciences, The University of Western Australia, Crawley, WA 6009, Australia. Perron Institute for Neurological and Translational Science, Nedlands, WA 6009, Australia.
 Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran. Department of Bacteriology and Virology, Semnan University of Medical Sciences, Semnan, Iran. Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran; Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran. Electronic address: yosefi_bahman@semums.ac.ir.
 Chair and Department of Toxicology, Faculty of Pharmacy, Medical University of Lublin, Jaczewskiego 8b Street, 20-090 Lublin, Poland. Chair and Department of Toxicology, Faculty of Pharmacy, Medical University of Lublin, Jaczewskiego 8b Street, 20-090 Lublin, Poland. Chair and Department of Toxicology, Faculty of Pharmacy, Medical University of Lublin, Jaczewskiego 8b Street, 20-090 Lublin, Poland. Chair and Department of Toxicology, Faculty of Pharmacy, Medical University of Lublin, Jaczewskiego 8b Street, 20-090 Lublin, Poland.
 Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Boston Children's Hospital, Boston, Massachusetts, USA. Department of Family Medicine, Mayo Clinic, Rochester, New York, USA.
 Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia. Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia. Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia. Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia. Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Center, Kuala Lumpur, Malaysia. School of Life Sciences, Anhui University of Chinese Medicine, Hefei, China. Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan. Medical Innovation Research Center, Shiga University of Medical Science, Otsu, Japan. Medical Innovation Research Center, Shiga University of Medical Science, Otsu, Japan. Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia. Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia.
 Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Stanford University School of Medicine, Stanford, California, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
 Universidade Federal do Rio de Janeiro (UFRJ), Faculdade de Medicina, Departamento de Pediatria, Rio de Janeiro, RJ, Brazil; Universidade Federal do Rio de Janeiro (UFRJ), Instituto de Puericultura e Pediatria Martagão Gesteira (IPPMG), Serviço de Alergia e Imunologia, Rio de Janeiro, RJ, Brazil. Electronic address: egoudouris@gmail.com. Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Pediatria, Disciplina de Alergia, Imunologia Clínica e Reumatologia, São Paulo, SP, Brazil. Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Pediatria, Disciplina de Alergia, Imunologia Clínica e Reumatologia, São Paulo, SP, Brazil.
 Department of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Department of Immunology, Faculty of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Department of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Department of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. rafiei1710@gmail.com.
 Department of Veterinary Pathology, Faculty of Veterinary Medicine, Ondokuz Mayıs University, 55200, Atakum, Samsun, Turkey. efe.karaca@omu.edu.tr. Department of Veterinary Pathology, Faculty of Veterinary Medicine, Ondokuz Mayıs University, 55200, Atakum, Samsun, Turkey.
 College of Physical Education and Health, East China Normal University, Shanghai 200241, China; Key Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, China. School of Exercise and Health, Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Shanghai University of Sport, Shanghai 200438, China. College of Physical Education and Health, East China Normal University, Shanghai 200241, China; Key Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, China. Department of Neurosurgery, Zibo Central Hospital, Zibo 255000, Shandong, China. College of Physical Education and Health Sciences, Zhejiang Normal University, Jinhua 321004, Zhejiang, China. College of Physical Education and Health, East China Normal University, Shanghai 200241, China; Key Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, China. College of Physical Education and Health, East China Normal University, Shanghai 200241, China; Key Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, China. Electronic address: lilin.xtt@163.com.
 Department of Apiculture and Sericulture, Faculty of Animal Sciences and Biotechnologies, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, 400372 Cluj-Napoca, Romania. Department of Apiculture and Sericulture, Faculty of Animal Sciences and Biotechnologies, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, 400372 Cluj-Napoca, Romania. Department of Apiculture and Sericulture, Faculty of Animal Sciences and Biotechnologies, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, 400372 Cluj-Napoca, Romania. Department of Apiculture and Sericulture, Faculty of Animal Sciences and Biotechnologies, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, 400372 Cluj-Napoca, Romania. Department of Apiculture and Sericulture, Faculty of Animal Sciences and Biotechnologies, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, 400372 Cluj-Napoca, Romania.
 ENATSE (Ecole Nationale de Santé Publique et de Surveillance Epidémiologique), Université de Parakou, Parakou, Benin. REVAL, Rehabilitation Research Centre, Hasselt University, Hasselt, Belgium. RINGGOLD: 54496 ENATSE (Ecole Nationale de Santé Publique et de Surveillance Epidémiologique), Université de Parakou, Parakou, Benin. ENATSE (Ecole Nationale de Santé Publique et de Surveillance Epidémiologique), Université de Parakou, Parakou, Benin. ENATSE (Ecole Nationale de Santé Publique et de Surveillance Epidémiologique), Université de Parakou, Parakou, Benin. Faculty of Medicine and Healthcare Sciences, Department of Rehabilitation Sciences, Research Group of Occupational Therapy, Ghent University, Ghent, Belgium. Faculty of Medicine and Healthcare Sciences, Department of Rehabilitation Sciences, Research Group of Occupational Therapy, Ghent University, Ghent, Belgium. ENATSE (Ecole Nationale de Santé Publique et de Surveillance Epidémiologique), Université de Parakou, Parakou, Benin.
 Neurology Unit, NESMOS Department, Faculty of Medicine & Psychology, Sapienza-University of Rome, Sant'Andrea University Hospital, Rome, Italy. Neurology Unit, NESMOS Department, Faculty of Medicine & Psychology, Sapienza-University of Rome, Sant'Andrea University Hospital; Department of Clinical and Behavioral Neurology, IRCCS-Fondazione Santa Lucia, Rome, Italy. Neurology Unit, NESMOS Department, Faculty of Medicine & Psychology, Sapienza-University of Rome, Sant'Andrea University Hospital, Rome, Italy. Neurology Unit, NESMOS Department, Faculty of Medicine & Psychology, Sapienza-University of Rome, Sant'Andrea University Hospital, Rome, Italy. Neurology Unit, NESMOS Department, Faculty of Medicine & Psychology, Sapienza-University of Rome, Sant'Andrea University Hospital; Department of Clinical and Behavioral Neurology, IRCCS-Fondazione Santa Lucia, Rome, Italy. Neurology Unit, NESMOS Department, Faculty of Medicine & Psychology, Sapienza-University of Rome, Sant'Andrea University Hospital; Department of Clinical and Behavioral Neurology, IRCCS-Fondazione Santa Lucia, Rome, Italy.
 Department of Neurology, Facuty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. Department of Neurology, Facuty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. Experimental Immunotherapeutics Unit, NIH, Bethesda, MD, USA. Department of Neurology, Facuty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Centre Jülich, Jülich, Germany. Institute of Virology, National Reference Center for Papilloma- and Polyomaviruses, Faculty of Medicine, University Hospital Cologne, Cologne Germany. Department of Neurology, Hannover Medical School, Hannover, Germany. Institute of Neuropathology, University Medical Center Göttingen, Göttingen, Germany. Department of Neuroradiology, Hannover Medical School, Hannover, Germany. Department of Neurology, Facuty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany clemens.warnke@uk-koeln.de.
 Centre for Health, Activity and Rehabilitation Research, Queen Margaret University Edinburgh, Musselburgh, UK. School of Health Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, UK. Association of Chartered Physiotherapists in Neurology, UK. MS Trust, UK. Centre for Health, Activity and Rehabilitation Research, Queen Margaret University Edinburgh, Musselburgh, UK. Centre for Health, Activity and Rehabilitation Research, Queen Margaret University Edinburgh, Musselburgh, UK. Clinical Sciences and Engineering, Salisbury NHS Foundation Trust and Bournemouth University, Bournemouth, UK.
 Clinical Medical College of Jining Medical University, Jining Medical University, Jining, Shandong, China. Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China. Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China. Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China. Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China. zgx_viola@126.com. Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China. zhufqin@126.com.
 School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Clinical Biochemistry, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Cellular and Molecular Research Center, Research Institute for Prevention of Non-Communicable Diseases, Qazvin University of Medical Sciences, Qazvin, Iran; Department of Molecular Medicine, School of Medicine, Qazvin University of Medical Sciences, Qazvin, Iran. Electronic address: qmohammadi@qums.ac.ir. Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: marjannassiriasl@sbmu.ac.ir.
 School of Electronic and Information Engineering, South China University of Technology, Guangzhou, China. School of Electronic and Information Engineering, South China University of Technology, Guangzhou, China. School of Electronic and Information Engineering, South China University of Technology, Guangzhou, China. School of Future Technology, South China University of Technology, Guangzhou, China. School of Electronic and Information Engineering, South China University of Technology, Guangzhou, China. School of Future Technology, South China University of Technology, Guangzhou, China. Pazhou Lab, Guangzhou, China. School of Electronic and Information Engineering, South China University of Technology, Guangzhou, China. School of Future Technology, South China University of Technology, Guangzhou, China. Zhongshan Institute of Modern Industrial Technology of South China, University of Technology, Zhongshan, China. Department of Psychiatry, Guangzhou First People's Hospital, The Second Affiliated Hospital, South China University of Technology, Guangzhou, China. School of Electronic and Information Engineering, South China University of Technology, Guangzhou, China.
 Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, FL, USA. Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahassee, FL, USA. College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahassee, FL, USA. PBS Biotech Inc., Camarillo, CA, USA. Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA. Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, FL, USA. Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University, Tallahassee, FL, USA.
 School of Nursing, Anhui Medical University, Hefei, Anhui, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, Anhui, China. Electronic address: lengruixue@ahmu.edu.cn. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, Anhui, China. Electronic address: ydq@ahmu.edu.cn.
 The First School of Clinical Medicine , Southern Medical University, Guangzhou, 501515, China. Department of Transfusion Medicine and Department of Laboratory Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, 510282, China. Southern Medical University Library, No.1023, South Shatai Road, Baiyun District, Guangzhou, 510515, Guangdong, China. 853877559@qq.com.
 Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, Guy's Campus, King's College London, London, UK. Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, Guy's Campus, King's College London, London, UK. Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, Guy's Campus, King's College London, London, UK. Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, Guy's Campus, King's College London, London, UK. Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, Guy's Campus, King's College London, London, UK. Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, Guy's Campus, King's College London, London, UK.
 Department of Pharmacology and Physiology, School of Medicine, Saint Louis University, Saint Louis, MO, USA. Institute for Translational Neuroscience, Saint Louis University, Saint Louis, MO, USA. Department of Pharmacology and Physiology, School of Medicine, Saint Louis University, Saint Louis, MO, USA. Institute for Translational Neuroscience, Saint Louis University, Saint Louis, MO, USA.
 Department of Pharmacology, Central University of Punjab, Bathinda, Punjab, India. Department of Pharmacology, Central University of Punjab, Bathinda, Punjab, India. Department of Pharmacology, Central University of Punjab, Bathinda, Punjab, India. punnubansal79@gmail.com.
 Neuroscience Research Australia, Sydney, New South Wales, Australia. University of South Australia, Adelaide, South Australia, Australia. Neuroscience Research Australia, Sydney, New South Wales, Australia. University of New South Wales, Sydney, New South Wales, Australia. Neuroscience Research Australia, Sydney, New South Wales, Australia. University of New South Wales, Sydney, New South Wales, Australia. Neuroscience Research Australia, Sydney, New South Wales, Australia. University of New South Wales, Sydney, New South Wales, Australia.
 Department of Diagnostic Radiology, The University of Hong Kong, Hong Kong, China. Department of Diagnostic Radiology, The University of Hong Kong, Hong Kong, China. Department of Diagnostic Radiology, The University of Hong Kong, Hong Kong, China.
 RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan. Institute for Molecular and Cellular Regulation, Gunma University, Haebashi, Gunma, Japan. RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan. Department of Parasitology, National Institute of Infectious Disease, Tokyo, Japan. Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg. Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg. mahesh.desai@lih.lu. Odense Research Center for Anaphylaxis, Department of Dermatology and Allergy Center, Odense University Hospital, University of Southern Denmark, Odense, Denmark. mahesh.desai@lih.lu. RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan. hiroshi.ohno@riken.jp. Immunobiology Laboratory, Graduate School of Medical Life Science, Yokohama City University, Yokohama, Kanagawa, Japan. hiroshi.ohno@riken.jp. Laboratory for Immune Regulation, Graduate School of Medicine, Chiba University, Chiba, Chiba, Japan. hiroshi.ohno@riken.jp.
 Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia. School of Medicine, Deakin University, Melbourne, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia.
 Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, Hunan, China. Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, Hunan, China. Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, Hunan, China. Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, Hunan, China. Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, Hunan, China. Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, Hunan, China. Department of Dermatology, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, Jiangsu, China.
 Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia. Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Parkville, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia. Clinical Outcomes Research Unit (CORe), Department of Medicine, University of Melbourne, Parkville, Victoria, Australia.
 Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China. Key Laboratory of Neurology of Hebei Province, Shijiazhuang, Hebei, China.
 Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China; The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Harbin, China. Department of Neurobiology, Harbin Medical University, Harbin, China. Electronic address: yumeiliu2010@163.com.
 Jinan Microecological Biomedicine Shandong Laboratory, Shandong First Medical University, Jinan, Shandong, China. Jinan Microecological Biomedicine Shandong Laboratory, Jinan, Shandong, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Jinan Microecological Biomedicine Shandong Laboratory, Jinan, Shandong, China. Department of Intensive Care Unit, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. School of Clinical Medicine, Institute of Hepatology and Metabolic Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, Zhejiang, China. School of Biological Engineering, Hangzhou Medical College, Institute of Parasitic Diseases, Hangzhou, Zhejiang, China. Department of Obstetrics, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Jinan Microecological Biomedicine Shandong Laboratory, Jinan, Shandong, China. Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Department of Psychiatry, Quzhou Third Hospital, Quzhou, Zhejiang, China.
 Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Stanford University School of Medicine, Stanford, California, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
 Division of Ophthalmology and the Laboratory of Investigation in Ophthalmology (LIM 33), , University of São Paulo Medical SchoolSão Paulo, Brazil. Division of Ophthalmology and the Laboratory of Investigation in Ophthalmology (LIM 33), , University of São Paulo Medical SchoolSão Paulo, Brazil. Division of Ophthalmology and the Laboratory of Investigation in Ophthalmology (LIM 33), , University of São Paulo Medical SchoolSão Paulo, Brazil. Division of Ophthalmology and the Laboratory of Investigation in Ophthalmology (LIM 33), , University of São Paulo Medical SchoolSão Paulo, Brazil. Department of Neurology, , University of São Paulo Medical SchoolSão Paulo, Brazil. Neuroradiology Section, , Hospital das Clínicas da Faculdade de Medicina da Universidade de São PauloSão Paulo, Brazil. Department of Neurology, , University of São Paulo Medical SchoolSão Paulo, Brazil. Department of Neurology, , University of São Paulo Medical SchoolSão Paulo, Brazil. Division of Ophthalmology and the Laboratory of Investigation in Ophthalmology (LIM 33), , University of São Paulo Medical SchoolSão Paulo, Brazil.
 Department of Rehabilitation Medicine, University of Washington, Seattle, Washington. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington; School of Psychology, University of Queensland, Brisbane, Queensland, Australia. Department of Rehabilitation Medicine, University of Washington, Seattle, Washington.
 Department of Neurology (MJ, OMA, IF, KJ, KM, NS), Rutgers New Jersey Medical School, Newark, New Jersey; Department of Mathematics and Statistics (FBM), Texas Tech University, Lubbock, Texas; Department of Marketing (SR, KJ), Columbia Business School, New York City, New York; and Department of Public Health (HK), Texas Tech University Health Sciences Center, Lubbock, Texas.
 Department of Pathological Anatomy and Forensic Medicine, Zaporizhzhia State Medical University, Mayakovsky Avenue, 26, 69035 Zaporizhzhia, Ukraine. Department of Internal Medicine, Endocrinology Diabetes and Metabolism, Diabetes and Cardiovascular Disease Center, University of Missouri School of Medicine, One Hospital Drive, Columbia, MO 65211, USA.
 Department of Pharmaceutical Chemistry, Institute of Pharmacy, Nirma University, Ahmedabad 382481, Gujrat, India. Department of Pharmaceutical Chemistry, Institute of Pharmacy, Nirma University, Ahmedabad 382481, Gujrat, India.
 Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Institute of Allergy and Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Hubei Clinical Research Center for Nasal Inflammatory Diseases, Wuhan 430030, China. Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Institute of Allergy and Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Hubei Clinical Research Center for Nasal Inflammatory Diseases, Wuhan 430030, China. Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Institute of Allergy and Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Hubei Clinical Research Center for Nasal Inflammatory Diseases, Wuhan 430030, China.
 School of Infection and Immunity, Sir Graeme Davies Building, 120 University Place, University of Glasgow, Glasgow G12 8TA, UK. School of Infection and Immunity, Sir Graeme Davies Building, 120 University Place, University of Glasgow, Glasgow G12 8TA, UK. Institute of Systems, Molecules and Integrative Biology, University of Liverpool, Liverpool L69 7ZB, UK. TEGA Therapeutics, Inc., 3550 General Atomics Court, G02-102, San Diego, CA 92121, USA. TEGA Therapeutics, Inc., 3550 General Atomics Court, G02-102, San Diego, CA 92121, USA. Institute of Systems, Molecules and Integrative Biology, University of Liverpool, Liverpool L69 7ZB, UK. Centre for Glycosciences, Keele University, Keele ST5 5BG, UK. TEGA Therapeutics, Inc., 3550 General Atomics Court, G02-102, San Diego, CA 92121, USA. School of Infection and Immunity, Sir Graeme Davies Building, 120 University Place, University of Glasgow, Glasgow G12 8TA, UK.
 Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Neurology, Radiology, Neuroscience, Physical Therapy and Occupational Therapy, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States. Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri 63110, United States.
 Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Hubei Key Laboratory of Neural Injury and Functional Reconstruction, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Hubei Key Laboratory of Neural Injury and Functional Reconstruction, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Hubei Key Laboratory of Neural Injury and Functional Reconstruction, Huazhong University of Science and Technology, Wuhan, China. Department of Neurology, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Hubei Key Laboratory of Neural Injury and Functional Reconstruction, Huazhong University of Science and Technology, Wuhan, China.
 The Florey Institute of Neuroscience and Mental Health, Parkville, VIC 3052, Australia; Department of Anatomy & Physiology, University of Melbourne, VIC 3010, Australia. The Florey Institute of Neuroscience and Mental Health, Parkville, VIC 3052, Australia; Department of Anatomy & Physiology, University of Melbourne, VIC 3010, Australia. The Florey Institute of Neuroscience and Mental Health, Parkville, VIC 3052, Australia; Department of Anatomy & Physiology, University of Melbourne, VIC 3010, Australia. The Florey Institute of Neuroscience and Mental Health, Parkville, VIC 3052, Australia; Department of Anatomy & Physiology, University of Melbourne, VIC 3010, Australia. Electronic address: terence.pang@florey.edu.au.
 Faculty of Chemistry, University of Warsaw, 02-093 Warsaw, Poland. Faculty of Chemistry, University of Warsaw, 02-093 Warsaw, Poland. Faculty of Chemistry, University of Warsaw, 02-093 Warsaw, Poland. Faculty of Chemistry, University of Warsaw, 02-093 Warsaw, Poland. Faculty of Chemistry, University of Warsaw, 02-093 Warsaw, Poland.
 Department of Chemical Engineering, North Tehran Branch, Islamic Azad University, P.O. Box 1651153311, Tehran, Iran. Department of Chemical Engineering, North Tehran Branch, Islamic Azad University, P.O. Box 1651153311, Tehran, Iran. Electronic address: a_esmaeili@iau-tnb.ac.ir. Department of Chemical Engineering, North Tehran Branch, Islamic Azad University, P.O. Box 1651153311, Tehran, Iran.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurophysiology, University of Münster, Münster, Germany. Core Unit Proteomics, Interdisciplinary Center for Clinical Research, Medical Faculty, University of Münster, Münster, Germany. Department of Neurology, Medical Faculty and University Hospital, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Electronic address: Stjepana.Kovac@ukmuenster.de.
 Clinical Neurology Unit, San Paolo University Hospital, Department of Health Sciences and "Aldo Ravelli" Research Center for Experimental Brain Theraputics, University of Milan, ASST Santi Paolo e Carlo, Milan, Italy. Clinical Neurology Unit, San Paolo University Hospital, Department of Health Sciences and "Aldo Ravelli" Research Center for Experimental Brain Theraputics, University of Milan, ASST Santi Paolo e Carlo, Milan, Italy. Clinical Neurology Unit, San Paolo University Hospital, Department of Health Sciences and "Aldo Ravelli" Research Center for Experimental Brain Theraputics, University of Milan, ASST Santi Paolo e Carlo, Milan, Italy. alberto.priori@unimi.it.
 Musculoskeletal Research Group and Tumor Biology, Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig-Maximilians-University Munich, Pettenkoferstrasse 11, 80336, Munich, Germany. Pediatric Urology and Regenerative Medicine Research Center, Gene, Cell and Tissue Research Institute, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. Pediatric Urology and Regenerative Medicine Research Center, Gene, Cell and Tissue Research Institute, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. Musculoskeletal Research Group and Tumor Biology, Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig-Maximilians-University Munich, Pettenkoferstrasse 11, 80336, Munich, Germany. Pediatric Urology and Regenerative Medicine Research Center, Gene, Cell and Tissue Research Institute, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. Musculoskeletal Research Group and Tumor Biology, Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig-Maximilians-University Munich, Pettenkoferstrasse 11, 80336, Munich, Germany. mehdi.shakibaei@med.uni-muenchen.de. Pediatric Urology and Regenerative Medicine Research Center, Gene, Cell and Tissue Research Institute, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. masoumeh.majidizolbin@gmail.com.
 Department of Biophysics, National Institute of Mental Health and Neurosciences, Bengaluru, India. Department of Biophysics, National Institute of Mental Health and Neurosciences, Bengaluru, India. Department of Biophysics, National Institute of Mental Health and Neurosciences, Bengaluru, India. Department of Clinical Psychopharmacology and Neurotoxicology, National Institute of Mental Health and Neurosciences, Bengaluru, India. Department of Biophysics, National Institute of Mental Health and Neurosciences, Bengaluru, India.
 Intelligent Medicine Institute, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Intelligent Medicine Institute, Shanghai Medical College, Fudan University, Shanghai, 200032, China. College of Computer Science and Technology, Dalian University of Technology, Dalian, 116024, China. Intelligent Medicine Institute, Shanghai Medical College, Fudan University, Shanghai, 200032, China. Electronic address: zonefan@163.com. College of Computer Science and Technology, Dalian University of Technology, Dalian, 116024, China. Electronic address: yangzh@dlut.edu.cn. Intelligent Medicine Institute, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Shanghai Institute of Stem Cell Research and Clinical Translation, Shanghai, 200120, China. Electronic address: liulei_sibs@163.com.
 Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Anatomy, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Department of Microbiology, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa, Japan. Aoikai Sendai Hospital , Sendai, Miyagi, Japan. Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan. Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
 Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. devaraj.basavarajappa@mq.edu.au. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. vivek.gupta@mq.edu.au. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. School of Medicine, Deakin University, Geelong, VIC, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, 2109, Australia. Save Sight Institute, The University of Sydney, Sydney, NSW, 2000, Australia.
 Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Electrical Engineering Division, Department of Engineering, University of Cambridge, Cambridge, CB3 0FA, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Department of Neurological Surgery, Tri-Service General Hospital, National Defence Medical Centre, Taipei, Neihu District, 11490, Taiwan. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Electrical Engineering Division, Department of Engineering, University of Cambridge, Cambridge, CB3 0FA, UK. Electrical Engineering Division, Department of Engineering, University of Cambridge, Cambridge, CB3 0FA, UK. Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Lensfield Road, Cambridge, CB2 1EW, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Electrical Engineering Division, Department of Engineering, University of Cambridge, Cambridge, CB3 0FA, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Lensfield Road, Cambridge, CB2 1EW, UK. Cavendish Laboratory, Department of Physics, University of Cambridge, J J Thomson Ave, Cambridge, CB3 0HE, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Electrical Engineering Division, Department of Engineering, University of Cambridge, Cambridge, CB3 0FA, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK.

 Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB T2N 4N1, Canada. Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB T2N 4N1, Canada. Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB T2N 4N1, Canada.
 University Paris Cité, UFR de Médecine, Paris, France. Rheumatology Department & INSERM U1132 Bioscar, Viggo Petersen Centre, Lariboisière Hospital, Paris, France. Rheumatology Department, Pierre-Paul Riquet Hospital, Toulouse, France. University Toulouse III-Paul Sabatier & INSERM, 1291 Infinity, Toulouse, France. Rheumatology Department, UF 6501, Hautepierre Hospital, CHU Strasbourg, France. Amgen, Boulogne-Billancourt, France. Rheumatology Department & INSERM U1132 Bioscar, Viggo Petersen Centre, Lariboisière Hospital, Paris, France. Rheumatology Department, National Reference Centre for Rare Systemic Auto-immune Diseases East-South-West (RESO), CHU Strasbourg, France. Molecular Immuno-Rhumatology Laboratory, GENOMAX platform, INSERM UMR-S1109, Faculty of Medicine, Interdisciplinary Thematic Institute (ITI) of Precision Medicine of Strasbourg, Transplantex NG, Federation of Translational Medicine of Strasbourg (FMTS), University of Strasbourg, France.
 Brain Barriers Research Group, Department of Biology, Edge Hill University, Ormskirk, U.K. Department of Clinical Infection, Microbiology and Immunology, University of Liverpool, Liverpool, U.K. The School of Biomedical Sciences and Pharmacy, The University of Newcastle, Newcastle, NSW, Australia. Flocel Inc., Cleveland, OH, U.S.A. Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, U.S.A.
 Fundación San Lucas para la Neurociencia, Rosario, Argentina. Hospital Jose Maria Cullen, Santa Fe, Argentina. Hospital de San Luis, Fundación San Lucas para la Neurociencia, Rosario, Argentina. Institute of Neurology, University College London, London, UK. Ear Institute, University College London, London, UK. Institute of Neurology, University College London, London, UK.
 Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Faculty of Veterinary and Agricultural Sciences, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Faculty of Veterinary and Agricultural Sciences, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC, Australia. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia. Department of Medical Biology, The University of Melbourne, Parkville, VIC, Australia. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia. Faculty of Veterinary and Agricultural Sciences, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, VIC, Australia.
 Department of Psychology, Queen's University Belfast, Belfast, UK. Psychology Department, National College of Ireland, Dublin, Ireland. Adult Acute Neuropsychology Services, Belfast Health and Social Care Trust, Belfast, UK. Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, Tasmania, Australia. Royal Hobart Hospital, Hobart, Tasmania, Australia. Neurology Department, Leeds Teaching Hospitals NHS Trust, Leeds, UK. Department of Psychology, Queen's University Belfast, Belfast, UK. Neurology Department, Leeds Teaching Hospitals NHS Trust, Leeds, UK. Department of Psychology, Queen's University Belfast, Belfast, UK.
 Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Cologne, Germany. Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA. Neuroimmunology Unit, National and Kapodistrian University of Athens Medical School, Athens, Greece. Department of Neurology, Faculty of Medicine, University of Cologne and University Hospital Cologne, Kerpener Strasse, 62, 50937 Cologne, Germany.
 Faculty of Medicine, Baskent University, Ankara, Turkey. RINGGOLD: 63994 Department of Rheumatology, Faculty of Medicine, Baskent University, Ankara, Turkey. RINGGOLD: 63994
 Jacobi Medical Center, Montefiore Medical Center, New York, NY.
 Department of Physical Therapy, 28114Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Department of Physical Therapy, 28114Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Department of Physical Therapy, 28114Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Department of Physical Therapy, 28114Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
 NIH-Oxford-Cambridge Scholars Program, Wellcome-MRC Cambridge Stem Cell Institute and Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 1TN, UK. Altos Labs, Cambridge Institute of Science, Cambridge CB21 6GP, UK. Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
 Virginia Commonwealth University School of Medicine, Medical College of Virginia Kansas City University University of Chicago (NorthShore)
 Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China. Electronic address: ylyang377@zzu.edu.cn.
 Multiple Sclerosis Center, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. assunta.bianco@unicatt.it. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy. assunta.bianco@unicatt.it. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy. Neuroradiology Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. Institute of Radiology, Catholic University of Sacred Heart, 00168, Rome, Italy. Institute of Ophtalmology, Catholic University of Sacred Heart, 00168, Rome, Italy. Departmental Unit of Molecular and Genomic Diagnostics, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. Otorhinolaryngology Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. Department of Otorhinolaryngology, Catholic University of Sacred Heart, 00168, Rome, Italy. Multiple Sclerosis Center, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy. Multiple Sclerosis Center, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy. Multiple Sclerosis Center, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168, Rome, Italy. Department of Neurosciences, Catholic University of Sacred Heart, 00168, Rome, Italy.
 Institute of Chemical Biology and Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Novosibirsk 630090, Russia. Institute of Chemical Biology and Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Novosibirsk 630090, Russia. G. B. Elyakov Pacific Institute of Bioorganic Chemistry, Far East Division, Russian Academy of Sciences, Vladivostok 690022, Russia. Institute of Chemical Biology and Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Novosibirsk 630090, Russia. Institute of Chemical Biology and Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Novosibirsk 630090, Russia.
 Bioethics Unit, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy. Fondazione FARO, Turin, Italy. Bioethics Unit, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy. PhD Program in Clinical and Experimental Medicine, University of Modena and Reggio Emilia, Modena, Italy. Hospice 'La Torre sul Colle', Azienda USL Umbria 2, Spoleto, Italy. Unit of Neuroepidemiology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. EUPATI Fellow (European Patients Academy for Therapeutic Innovation) Italy, Rome, Italy. Bioethics Unit, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy. National Research Council (CNR), Interdepartmental Center for Research Ethics and Integrity (CID Ethics), Rome, Italy. Cambia Palliative Care Center of Excellence at UW Medicine, University of Washington, Seattle, Washington, United States of America. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America. Division of Geriatrics, School of Medicine, University of California San Francisco, San Francisco, San Francisco, California, United States of America. San Francisco Veterans Affairs Health Care System, San Francisco, California, United States of America. Cambia Palliative Care Center of Excellence at UW Medicine, University of Washington, Seattle, Washington, United States of America. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America. Cambia Palliative Care Center of Excellence at UW Medicine, University of Washington, Seattle, Washington, United States of America. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America. Unit of Neuroepidemiology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. Unit of Neuroepidemiology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
 The PGRx Study Group, Paris, France. lamiae.grimaldi@aphp.fr. Pharmacology Department, Hospital Group Paris-Saclay, Assistance Publique-Hôpitaux de Paris, Garches, France. lamiae.grimaldi@aphp.fr. University of Versailles-Paris Saclay, Montigny Le Bretonneux, France. lamiae.grimaldi@aphp.fr. Inserm U 1018 CESP, Villejuif, France. lamiae.grimaldi@aphp.fr. Neurology Department of Hospital foundation A de Rothschild, Paris, France. Paris-Cité University, Paris, France. The PGRx Study Group, Paris, France. RESAL, LA-SER Group, Paris, France. Inserm U 1018 CESP, Villejuif, France. Department of Biostatistics and Clinical Research, CHU Rouen, 76000, Rouen, France. Université de Rouen-Normandie, Rouen, France. The PGRx Study Group, Paris, France. RESAL, LA-SER Group, Paris, France. Department of Epidemiology, London School of Hygiene and Tropical Medicine, London, UK. Centre for Risk Research Inc., Montreal, Canada.
 Institute of Chemical Biology and Fundamental Medicine, Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, 630090 Novosibirsk, Russia. Institute of Chemical Biology and Fundamental Medicine, Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, 630090 Novosibirsk, Russia. G. B. Elyakov Pacific Institute of Bioorganic Chemistry, Far East Division, Russian Academy of Sciences, 690022 Vladivostok, Russia. Institute of Chemical Biology and Fundamental Medicine, Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, 630090 Novosibirsk, Russia. Institute of Chemical Biology and Fundamental Medicine, Siberian Division of Russian Academy of Sciences, Lavrentiev Ave. 8, 630090 Novosibirsk, Russia.
 Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Endocrinology, Liuzhou People's Hospital, Liuzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China. Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, China.
 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
 Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: sara.terrim@fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: guilherme.diogo@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: f.falcao@hc.fm.usp.br. Neuro-ophtalmology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, 05403-000 Sao Paulo, Brazil. Neuro-ophtalmology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, 05403-000 Sao Paulo, Brazil. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: ida.fortini@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: marcia.rubia@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: luiz.castro@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: luiz.rcomerlatti@hc.fm.usp.br. Radiology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, 05403-000 Sao Paulo, Brazil. Electronic address: carolina.rimkus@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: tarso.adoni@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil. Electronic address: samira.apostolos@hc.fm.usp.br. Neuro-ophtalmology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, 05403-000 Sao Paulo, Brazil. Electronic address: mario.monteiro@hc.fm.usp.br. Neurology Division, Hospital das Clinicas of the University of Sao Paulo, Av Dr. Enéas de Carvalho Aguiar, 255, Sao Paulo 05403-000, Brazil.
 Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Center for Systems Neuroscience, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Department of Biometry, Epidemiology and Data Processing, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Institute of Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany. Center for Systems Neuroscience, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Institute of Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany. Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Center for Systems Neuroscience, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany. Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.
 Laboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, Suita, Osaka, Japan. Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka, Japan. Laboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, Suita, Osaka, Japan. ksakurai@protein.osaka-u.ac.jp. Laboratory of Protein Profiling and Functional Proteomics, Institute for Protein Research, Osaka University, Suita, Osaka, Japan. ksakurai@protein.osaka-u.ac.jp. Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Hokkaido, Japan. Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. kato.takahiro.015@m.kyushu-u.ac.jp. Laboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, Suita, Osaka, Japan. hikida@protein.osaka-u.ac.jp.
 Department of Information Systems Engineering, Mugla Sitki Kocman University, Mugla 48000, Turkey. Department of Artificial Intelligence, Mugla Sitki Kocman University, Mugla 48000, Turkey. Department of Information Systems Engineering, Mugla Sitki Kocman University, Mugla 48000, Turkey. Department of Computer Engineering, Gachon University, Seongnam-si 13120, Republic of Korea. Daeyang AI Center, Department of Data Science, College of Software & Convergence Technology, Sejong University, Seoul 05006, Republic of Korea. Department of Robotics, Hanyang University, Ansan 15588, Republic of Korea. Department of Computer Engineering, Sir Syed University of Engineering & Technology, Karachi 75300, Pakistan.
 South West Sydney Clinical Campuses, Faculty of Medicine & Health, University of New South Wales Sydney (UNSW), Sydney, NSW 2170, Australia. Sacred Heart Health Service, St Vincent's Hospital, Darlinghurst, NSW 2010, Australia. Stats Central, University of New South Wales Sydney (UNSW), Sydney, NSW 2170, Australia. South West Sydney Clinical Campuses, Faculty of Medicine & Health, University of New South Wales Sydney (UNSW), Sydney, NSW 2170, Australia. Ingham Institute for Applied Medical Research, Liverpool, NSW 2170, Australia. Improving Palliative, Aged and Chronic Care through Clinical Research and Translation (IMPACCT), Faculty of Health, University of Technology Sydney, Ultimo, NSW 2007, Australia. South West Sydney Clinical Campuses, Faculty of Medicine & Health, University of New South Wales Sydney (UNSW), Sydney, NSW 2170, Australia. Sacred Heart Health Service, St Vincent's Hospital, Darlinghurst, NSW 2010, Australia. Ingham Institute for Applied Medical Research, Liverpool, NSW 2170, Australia. Improving Palliative, Aged and Chronic Care through Clinical Research and Translation (IMPACCT), Faculty of Health, University of Technology Sydney, Ultimo, NSW 2007, Australia.
 Department of Neurology, TOYOTA Memorial Hospital, Toyota, Japan. Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan. Department of Neurology, Nishichita General Hospital, Tokai, Japan. Department of Pathology, Asama General Hospital, Saku, Japan. Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University Hospital, Nagakute, Japan. Department of Neurology, TOYOTA Memorial Hospital, Toyota, Japan.

 Research and Innovation, Summer Foundation, Melbourne, Victoria, Australia. Living with Disability Research Centre, La Trobe University, Melbourne, Victoria, Australia. Research and Innovation, Summer Foundation, Melbourne, Victoria, Australia. Living with Disability Research Centre, La Trobe University, Melbourne, Victoria, Australia. Department of Primary Care Research, Outcome Health, Melbourne, Victoria, Australia. Research and Innovation, Summer Foundation, Melbourne, Victoria, Australia stacey.oliver@summerfoundation.org.au. Living with Disability Research Centre, La Trobe University, Melbourne, Victoria, Australia. Department of Primary Care Research, Outcome Health, Melbourne, Victoria, Australia. Department of Primary Care Research, Outcome Health, Melbourne, Victoria, Australia. Department of Primary Care Research, Outcome Health, Melbourne, Victoria, Australia.
 Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Boston, MA 02129, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Boston, MA 02129, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Pfizer World Wide Research and Development, Cambridge, MA 02139, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Pfizer World Wide Research and Development, Cambridge, MA 02139, USA. Pfizer World Wide Research and Development, Cambridge, MA 02139, USA. Pfizer World Wide Research and Development, Cambridge, MA 02139, USA. Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Boston, MA 02129, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Boston, MA 02129, USA. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
 Medizinische Klinik mit Schwerpunkt Psychosomatik, Charité Universitätsmedizin Berlin, D-12203 Berlin, Germany; Klinik für Psychiatrie, Charité Universitätsmedizin Berlin, D-12203 Berlin, Germany; Institut für Neuroimmunologie und Multiple Sklerose, Universitätklinikum Hamburg-Eppendorf, Hamburg, Germany; Good Clinical Trials Collaborative, Protas, London, UK. Electronic address: stefan.gold@charite.de. Good Clinical Trials Collaborative, Protas, London, UK; Nuffield Department of Population Health, University of Oxford, Oxford, UK. Good Clinical Trials Collaborative, Protas, London, UK. Klinik für Psychiatrie, Charité Universitätsmedizin Berlin, D-12203 Berlin, Germany.
 Department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Department of Neuroradiology, All India Institute of Medical Sciences, New Delhi, India. Department of Neurology, All India Institute of Medical Sciences, New Delhi, India. Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
 Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Institute of Agro-Bioengineering and College of Life Sciences, Guizhou University, Guizhou 550025, China. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Biomedical Genetics Section, Department of Medicine, Department of Pathology and Laboratory Medicine, Genetics and Genomics Graduate Program, Cancer Center, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Children's Hospital of Eastern Ontario Research Institute, Departments of Pediatrics and Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8L1, Canada. Department of Biostatistics, School of Public Health, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Biomedical Genetics Section, Department of Medicine, Department of Pathology and Laboratory Medicine, Genetics and Genomics Graduate Program, Cancer Center, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA. Departments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA.

 LEPABE-Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. ALiCE-Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. LEPABE-Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. ALiCE-Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. LEPABE-Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. ALiCE-Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. LEPABE-Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. ALiCE-Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. LEPABE-Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. ALiCE-Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. LEPABE-Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal. ALiCE-Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal.
 Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal; UCIBIO - Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. TOXRUN - Toxicology Research Unit, Department of Sciences, University Institute of Health Sciences, CESPU, CRL, 4585-116 Gandra, Portugal; Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, 4200-135 Porto, Portugal. CIQUP-IMS - Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto, R. Campo Alegre s/n, 4169-007 Porto, Portugal. Electronic address: ester.benfeito@fc.up.pt. Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal; UCIBIO - Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal; CIQUP-IMS - Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto, R. Campo Alegre s/n, 4169-007 Porto, Portugal. CIQUP-IMS - Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto, R. Campo Alegre s/n, 4169-007 Porto, Portugal. CIQUP-IMS - Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto, R. Campo Alegre s/n, 4169-007 Porto, Portugal. Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal; UCIBIO - Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal; UCIBIO - Applied Molecular Biosciences Unit, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal. Electronic address: rsilva@ff.up.pt.
 Immunology and Allergology Laboratory Unit, S. Giovanni di Dio Hospital, Azienda USL-Toscana Centro, Florence, Italy. Department of Microbiology, Immunology and Transplantation, University of Leuven, Leuven, Belgium; Department of Laboratory Medicine, OLV Hospital, Aalst, Belgium. Rheumatology Unit, Hospital S. Giovanni di Dio, Azienda USL-Toscana Centro, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Immunology and Allergology Laboratory Unit, S. Giovanni di Dio Hospital, Azienda USL-Toscana Centro, Florence, Italy. Department of Microbiology, Immunology and Transplantation, University of Leuven, Leuven, Belgium; Department of Laboratory Medicine, University Hospital Leuven, Leuven, Belgium. Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Immunology and Allergology Laboratory Unit, S. Giovanni di Dio Hospital, Azienda USL-Toscana Centro, Florence, Italy. Electronic address: maria2.infantino@uslcentro.toscana.it.
 SITraN University of Sheffield, Sheffield, United Kingdom. Royal Hallamshire Hospital, Sheffield, United Kingdom. Princess Royal Spinal Injuries and Neurorehabilitation Centre, Northern General Hospital, Sheffield, United Kingdom.
 Department of Neurology, University of Virginia, Charlottesville, VA, USA. Department of Neurology, Mayo Clinic, Scottsdale, AZ, USA. UCSF Weill Institute for Neurosciences, Department of Neurology and Department of Ophthalmology, University of California San Francisco, San Francisco, CA, USA. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA. Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, South Korea. Department of Neurology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University and Multiple Sclerosis and Neuromyelitis Optica Center, Southern Tohoku Research Institute for Neuroscience, Koriyama, Japan. Clinical Neuroimmunology Department, Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA. Service de Neurologie Sclérose en Plaques, Pathologies de La Myéline et Neuro-Inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany/Brain and Mind Center, University of Sydney, Sydney, NSW, Australia/ Department of Neurology, Medical University Vienna, Vienna, Austria/ Department of Neurology, Palacký University Olomouc, Olomouc, Czech Republic. Horizon Therapeutics plc, Gaithersburg, MD, USA. Horizon Therapeutics plc, Gaithersburg, MD, USA. Horizon Therapeutics plc, Gaithersburg, MD, USA. Horizon Therapeutics plc, Gaithersburg, MD, USA. Horizon Therapeutics plc, Gaithersburg, MD, USA. Horizon Therapeutics plc, Gaithersburg, MD, USA. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA, USA.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. Huashan Hospital, Fudan University, Shanghai, 200025, China. Department of Anatomy and Cell Biology, Department of Neurological Surgery, Stark Neurosciences Research Institute. Indiana University School of Medicine, Indianapolis, IN, 46202, USA. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. Electronic address: macungen@sxtcm.edu.cn. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. Electronic address: chaizhi@sxtcm.edu.cn. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. Electronic address: fanhuijie@sxtcm.edu.cn.
 Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China. State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Screening, Jiangsu Key Laboratory of Drug Discovery for Metabolic Diseases, China Pharmaceutical University, Nanjing 210009, China. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, China. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, China. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, China. Electronic address: ljw323@yeah.net. Department of Neurology of Nanjing Drum Tower Hospital, Medical School and the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Translational Medicine Institute of Brain Disorders, Nanjing University, Nanjing, Jiangsu 210008, China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, China. Electronic address: zhangcunjin516@163.com.
 International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan. Neurology, Dokkyo Ika Daigaku Saitama Iryo Center, Koshigaya, Saitama, Japan. Neurology, Hakusuikai Hatsuishi Hospital, Kashiwa, Chiba, Japan. International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan. Psychiatry, Ibaraki Prefectural Medical Center of Psychiatry, Kasama, Ibaraki, Japan. Psychiatry, Minamisaitama Hospital, Koshigaya, Saitama, Japan. Neurology, University of Tsukuba, Tsukuba, Ibaraki, Japan. Neurology, National Defense Medical College, Tokorozawa, Saitama, Japan. General Medicine, Ibaraki Prefectural University of Health Sciences, Inashiki-gun, Ibaraki, Japan. Pediatrics, Akita University, Akita, Akita, Japan. Psychiatry, Akita University, Akita, Akita, Japan. Psychiatry, Tokyo Metropolitan Geriatric Hospital, Itabashi-ku, Tokyo, Japan. Geriatric Medicine, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan. Psychiatry, Akita University, Akita, Akita, Japan. Psychiatry, Kato Hospital, Akita, Akita, Japan. International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan. International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan. General Medicine, Institute of Biomedical Sciences, Nagasaki University, Nagasaki, Nagasaki, Japan. Neurology, University of Tsukuba, Tsukuba, Ibaraki, Japan. Neurology, University of Tsukuba, Tsukuba, Ibaraki, Japan. Neurology, University of Tsukuba, Tsukuba, Ibaraki, Japan. Department of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Niigata, Japan. Neurology, University of Tsukuba, Tsukuba, Ibaraki, Japan. Neurology, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan. Department of Mental Health and Welfare, Akita Mental Health and Welfare Center, Akita, Akita, Japan. Psychiatry, Sleep and Circadian Neurobiology Laboratory, Stanford University, Stanford, California, USA. Neurology, Dokkyo Ika Daigaku Saitama Iryo Center, Koshigaya, Saitama, Japan. International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan. Neurology, Dokkyo Ika Daigaku Saitama Iryo Center, Koshigaya, Saitama, Japan. Psychiatry, Ibaraki Prefectural Medical Center of Psychiatry, Kasama, Ibaraki, Japan.
 Radiology Unit, Department of Surgical Sciences, University of Turin, Azienda Ospedaliero Universitaria (A.O.U.) Città della Salute e della Scienza di Torino, Turin, Italy. Regional Referring Center for Multiple Sclerosis (CRESM), University Hospital San Luigi Gonzaga, Orbassano, Italy. Regional Referring Center for Multiple Sclerosis (CRESM), University Hospital San Luigi Gonzaga, Orbassano, Italy. Regional Referring Center for Multiple Sclerosis (CRESM), University Hospital San Luigi Gonzaga, Orbassano, Italy. Regional Referring Center for Multiple Sclerosis (CRESM), University Hospital San Luigi Gonzaga, Orbassano, Italy. Clinical Neurobiology Unit, Neuroscience Institute Cavalieri Ottolenghi (NICO), University Hospital San Luigi Gonzaga, Orbassano, Turin, Italy. Clinical Neurobiology Unit, University Hospital San Luigi Gonzaga, Orbassano, Turin, Italy. Clinical Neurobiology Unit, Neuroscience Institute Cavalieri Ottolenghi (NICO), University Hospital San Luigi Gonzaga, Orbassano, Turin, Italy. Ospedale Koelliker, Corso Galileo Ferraris 247, Turin, Italy. Laboratory of Clinical and Microbiological Analyses, University Hospital San Luigi Gonzaga, Orbassano, Turin, Italy. Department of Neurology, "S. Croce e Carle" Hospital, Cuneo, Italy. mcapobianco1972@gmail.com. , Via Coppino 26, Cuneo, Italy. mcapobianco1972@gmail.com.
 Peter O'Donnell School of Public Health, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Harold C Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Harold C Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Harold C Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Department of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Peter O'Donnell School of Public Health, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Harold C Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Peter O'Donnell School of Public Health, University of Texas Southwestern Medical Center, Dallas, Texas, USA David.Gerber@utsouthwestern.edu. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Harold C Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
 Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China. Department of Epidemiology and Biostatistics, School of Public Health and Management, Wenzhou Medical University, Wenzhou, People's Republic of China.
 Magnetic Resonance Physics of Aging and Dementia Unit, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: zhaoyuan.gong@nih.gov. Yale School of Medicine, New Haven, CT 06510, USA. Magnetic Resonance Physics of Aging and Dementia Unit, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Magnetic Resonance Physics of Aging and Dementia Unit, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Magnetic Resonance Physics of Aging and Dementia Unit, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: bouhraram@mail.nih.gov.
 Department of Medicine/Neurology, College of Medicine, Shaqra University, Saudi Arabia.
 Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. takagi@p1.coralnet.or.jp. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Orthopaedic Surgery, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Rehabilitation Medicine, Tonami General Hospital, 1-61 Shintomi-cho, Tonami City, Toyama, 939-1395, Japan. Department of Rehabilitation Medicine, Toyama Prefectural Rehabilitation Hospital and Support Center for Children with Disabilities, 36 Shimoiino-machi, Toyama, 939-1395, Japan. Department of Rehabilitation Medicine, Kanazawa University Hospital, 13-1 Takara-machi, Kanazawa City, Ishikawa, 920-8641, Japan. Department of Orthopaedic Surgery, Graduate School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa City, Ishikawa, 920-8641, Japan.
 Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Hematopoietic Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Hematology, School of Medicine, Tarbiat Modares University (TMU), Tehran, Iran. Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran. Pharmaceutical Biotechnology Department, Pharmacy Faculty, Tabriz University of Medical Science, Tabriz, Iran. Akbarzadehp@tbzmed.ac.ir. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Shamsk@tbzmed.ac.ir.
 Department of Neurology, Qilu Hospital, Shandong University, Jinan, China. Department of Neurology, Institute of Epilepsy, Shandong University, Jinan, China. Department of Neurology, Qilu Hospital, Shandong University, Jinan, China. Department of Neurology, Institute of Epilepsy, Shandong University, Jinan, China. Department of Neurology, Qilu Hospital, Shandong University, Jinan, China. Department of Neurology, Institute of Epilepsy, Shandong University, Jinan, China. Department of Neurology, Qilu Hospital, Shandong University, Jinan, China. Department of Neurology, Institute of Epilepsy, Shandong University, Jinan, China.
 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Misr International University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Misr International University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
 Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Microbiology Department, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Alexandria, Egypt. Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Division of Molecular Neuroimmunology, Department of Homeostatic Regulation, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki, Aichi, Japan. Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Chiba, Chiba, Japan. Graduate School of Environmental Science, Hokkaido University, Sapporo, Hokkaido, Japan. Faculty of Environmental Earth Science, Hokkaido University, Sapporo, Hokkaido, Japan. Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Graduate School of Medicine, Medical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan. Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Chiba, Chiba, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Chiba, Chiba, Japan. Department of System Pathology for Neurological Disorders, Brain Research Institute, Niigata University, Niigata, Niigata, Japan. Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Chiba, Chiba, Japan. Graduate School of Environmental Science, Hokkaido University, Sapporo, Hokkaido, Japan. Faculty of Environmental Earth Science, Hokkaido University, Sapporo, Hokkaido, Japan. Division of Molecular Psychoneuroimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. Division of Molecular Neuroimmunology, Department of Homeostatic Regulation, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki, Aichi, Japan. Group of Quantum Immunology, Institute for Quantum Life Science, National Institute for Quantum and Radiological Science and Technology, Chiba, Chiba, Japan. Institute for Vaccine Research and Development (HU-IVReD), Hokkaido University, Sapporo 001-0020, Hokkaido, Japan.
 School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 102488, China. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. Department of Pathology, University of California San Diego, CA92307, USA. Electronic address: jih@health.ucsd.edu. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China. Electronic address: ybtang2007@163.com.
 Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Nephrology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Otorhinolaryngology/Head and Neck Surgery, School of Medicine, Technical University of Munich, Munich, Germany. Department of Otorhinolaryngology/Head and Neck Surgery, School of Medicine, Technical University of Munich, Munich, Germany. Department of Otorhinolaryngology/Head and Neck Surgery, Medical University Center, Freiburg, Germany. Department of Neuroradiology, Technical University of Munich, Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany.
 Department of Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham NG11 8NS, United Kingdom. Electronic address: Emina.Sher@isest.org. Faculty of Pharmacy, University of Modern Sciences - CKM, Mostar 88000, Bosnia and Herzegovina. International Society of Engineering Science and Technology, Nottingham, United Kingdom; Department of Neurology, Cantonal Hospital Zenica, Zenica 72000, Bosnia and Herzegovina. International Society of Engineering Science and Technology, Nottingham, United Kingdom; Department of Food and Nutrition Research, Juraj Strossmayer University of Osijek, Faculty of Food Technology, Croatia. International Society of Engineering Science and Technology, Nottingham, United Kingdom; Department of Radiology, Beth Israel Deaconess Medical Center (BIDMC), Boston, MA, United States. Department of Engineering, School of Science and Technology, Nottingham Trent University, Nottingham NG11 8NS, United Kingdom. Electronic address: Farooq.Sher@ntu.ac.uk.
 Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Sanofi Inc., Translational Science, 350 Water Street, Cambridge, MA, 02141, USA. Sanofi Inc., Rare and Neurologic Diseases Therapeutic Area, 350 Water Street, Cambridge, MA, 02141, USA. Sanofi Inc., Rare and Neurologic Diseases Therapeutic Area, 350 Water Street, Cambridge, MA, 02141, USA. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. Wallace H. Coulter Department of Biomedical Engineering, Emory University School of Medicine & Georgia Institute of Technology, Atlanta, GA, USA. Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Sanofi Inc., Translational Science, 350 Water Street, Cambridge, MA, 02141, USA. Department of Biomedical Engineering, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. Department of Biomedical Engineering, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. Institute for NanoBioTechnology, Johns Hopkins University, Whiting School of Engineering Baltimore, MD 21218, USA. Sanofi Inc., Rare and Neurologic Diseases Therapeutic Area, 350 Water Street, Cambridge, MA, 02141, USA. Sanofi Inc., Rare and Neurologic Diseases Therapeutic Area, 350 Water Street, Cambridge, MA, 02141, USA. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. Sanofi Inc., Translational Science, 350 Water Street, Cambridge, MA, 02141, USA. Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
 Sage Therapeutics, Inc, Cambridge, Massachusetts. National Alliance on Mental Illness, Arlington, Virginia. National Alliance on Mental Illness, Arlington, Virginia. Depression and Bipolar Support Alliance, Chicago, Illinois. Mental Health America of Ohio, Columbus, Ohio. Sage Therapeutics, Inc, Cambridge, Massachusetts. Corresponding author: Ellison D. Suthoff, MBA, 215 First St, Cambridge, MA 02142 (Ellison.Suthoff@sagerx.com). Sage Therapeutics, Inc, Cambridge, Massachusetts. Tantalus Medical Communications Ltd, Victoria, British Columbia, Canada. Tantalus Medical Communications Ltd, Victoria, British Columbia, Canada.
 Department of Anatomy, Behavioural Neuroscience Unit, Neurobiology Subdivision, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria. Department of Anatomy, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria. Department of Mental Health, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria. Department of Mental Health, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria. Department of Anatomy, Behavioural Neuroscience Unit, Neurobiology Subdivision, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
 School of Kinesiology, Shanghai University of Sport, Yangpu District, No. 200 Hengren Road, Shanghai, China. School of Kinesiology, Shanghai University of Sport, Yangpu District, No. 200 Hengren Road, Shanghai, China. School of Kinesiology, Shanghai University of Sport, Yangpu District, No. 200 Hengren Road, Shanghai, China. hsyykfkzyl@163.com. Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Jing'an District, No. 12 Wulumuqi road, Shanghai, 200040, China. hsyykfkzyl@163.com.
 Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh. Division of Neurobiology and Anatomy, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan. Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh. Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh. Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh.
 Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Diagnostics and Genomics Group, Agilent Technologies Sweden AB, Sundbyberg, Sweden. Diagnostics and Genomics Group, Agilent Technologies Deutschland GmbH, Waldbronn, Germany. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
 Laboratorios Ruiz, SYNLAB, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México. Laboratorios Ruiz, SYNLAB, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Universidad Popular Autónoma del Estado de Puebla, Puebla, México. Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, México.
 Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Faculty of Medicine, University of Cyprus, Nicosia CY-2029, Cyprus. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece. Faculty of Medicine, University of Cyprus, Nicosia CY-2029, Cyprus. Second Department of Neurology, Aristotle University of Thessaloniki, GR-54124 Thessaloniki, Greece.
 Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. CUBRIC, School of Psychology, Cardiff University, Cardiff, UK. School of Computer Science and Informatics, Cardiff University, Cardiff, UK. Siemens Healthcare S.R.L., Milan, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. HNSR, IRRCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroradiology, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. Laboratory of Medical Physics and Magnetic Resonance, IRCCS Stella Maris, Pisa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
 Department of Dermatology, The First Hospital of China Medical University, 155N Nanjing Street, Heping District, Shenyang, Liaoning 110000, China; National joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China; Key Laboratory of Immunodermatology, Ministry of Education and NHC, Shenyang, China. Department of Dermatology, The First Hospital of China Medical University, 155N Nanjing Street, Heping District, Shenyang, Liaoning 110000, China; National joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China; Key Laboratory of Immunodermatology, Ministry of Education and NHC, Shenyang, China. Department of Dermatology, Shengjing Hospital of China Medical University, 155N Nanjing Street, Heping District, Shenyang, Liaoning 110000, China. Department of Dermatology, Jincheng People's Hospital, 456N Wenchang East Street, Jincheng, Shanxi 048000, China. Department of Dermatology, The First Hospital of China Medical University, 155N Nanjing Street, Heping District, Shenyang, Liaoning 110000, China; National joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China; Key Laboratory of Immunodermatology, Ministry of Education and NHC, Shenyang, China. Department of Dermatology, The First Hospital of China Medical University, 155N Nanjing Street, Heping District, Shenyang, Liaoning 110000, China; National joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China; Key Laboratory of Immunodermatology, Ministry of Education and NHC, Shenyang, China. Department of Dermatology, The First Hospital of China Medical University, 155N Nanjing Street, Heping District, Shenyang, Liaoning 110000, China; National joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China; Key Laboratory of Immunodermatology, Ministry of Education and NHC, Shenyang, China. Electronic address: genglong2023@163.com.
 From the Department of Neurosurgery (L.v.B.), University Hospital, Ludwig-Maximilians-Universität Munich, Germany; Division of Infection & Immunity (H.J.S.), UCL Institute of Immunity & Transplantation, London, UK; and Department of Neurology with Institute of Translational Neurology (J.D.L.), University Hospital Münster, Germany. From the Department of Neurosurgery (L.v.B.), University Hospital, Ludwig-Maximilians-Universität Munich, Germany; Division of Infection & Immunity (H.J.S.), UCL Institute of Immunity & Transplantation, London, UK; and Department of Neurology with Institute of Translational Neurology (J.D.L.), University Hospital Münster, Germany. From the Department of Neurosurgery (L.v.B.), University Hospital, Ludwig-Maximilians-Universität Munich, Germany; Division of Infection & Immunity (H.J.S.), UCL Institute of Immunity & Transplantation, London, UK; and Department of Neurology with Institute of Translational Neurology (J.D.L.), University Hospital Münster, Germany. jan.luenemann@ukmuenster.de.
 BrainNet, Faculty of Applied Sciences, Simon Fraser University, Vancouver, BC, Canada. Centre for Neurology Studies, HealthTech Connex, Vancouver, BC, Canada. Brain Behaviour Laboratory, Department of Physical Therapy, Faculty of Medicine, The University of British Columbia, Vancouver, BC, Canada. BrainNet, Faculty of Applied Sciences, Simon Fraser University, Vancouver, BC, Canada. Centre for Neurology Studies, HealthTech Connex, Vancouver, BC, Canada. Centre for Neurology Studies, HealthTech Connex, Vancouver, BC, Canada. Centre for Neurology Studies, HealthTech Connex, Vancouver, BC, Canada. Brain Behaviour Laboratory, Department of Physical Therapy, Faculty of Medicine, The University of British Columbia, Vancouver, BC, Canada. Centre for Neurology Studies, HealthTech Connex, Vancouver, BC, Canada. Healthcode, Vancouver, BC, Canada. KITE Research Institute-UHN, Toronto, ON, Canada. Temerty Faculty of Medicine, Institute of Medical Science, University of Toronto, Toronto, ON, Canada. KITE Research Institute-UHN, Toronto, ON, Canada. Department of Physical Therapy, Rehabilitation Sciences Institute, University of Toronto, Toronto, ON, Canada. Royal Columbian Hospital, Fraser Health, Vancouver, BC, Canada. BrainNet, Faculty of Applied Sciences, Simon Fraser University, Vancouver, BC, Canada. Centre for Neurology Studies, HealthTech Connex, Vancouver, BC, Canada. DM Centre for Brain Health, Department of Radiology, The University of British Columbia, Vancouver, BC, Canada.
 Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States. Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States. Department of Kinesiology, University of Georgia, Athens, Georgia, United States. Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States. Department of Biomedical Science, College of Osteopathic Medicine, New York Institute of Technology, New York City, New York, United States. Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States.
 Department of Urology, Houston Methodist Hospital, Houston, TX, United States of America; Department of Urology, Nancy University Hospital, Nancy, France; Université de Lorraine, Inserm, IADI U1254, 54000 Nancy, France. Department of Urology, Houston Methodist Hospital, Houston, TX, United States of America. Université de Lorraine, Inserm, IADI U1254, 54000 Nancy, France; Department of Diagnostic and Interventional Neuroradiology, Nancy University Hospital, Nancy, France. Université de Lorraine, Inserm, IADI U1254, 54000 Nancy, France. Department of Urology, Houston Methodist Hospital, Houston, TX, United States of America. Electronic address: rkhavari@houstonmethodist.org.
 The Houston Methodist Research Institute, Transplant Immunology, Houston, TX, USA; The Houston Methodist Hospital, Department of Surgery, Houston, TX, USA. The Houston Methodist Research Institute, Transplant Immunology, Houston, TX, USA; The Houston Methodist Hospital, Department of Surgery, Houston, TX, USA. The Houston Methodist Research Institute, Transplant Immunology, Houston, TX, USA. The Houston Methodist Research Institute, Transplant Immunology, Houston, TX, USA; The Houston Methodist Hospital, Department of Surgery, Houston, TX, USA. The Houston Methodist Research Institute, Transplant Immunology, Houston, TX, USA; The Houston Methodist Hospital, Department of Surgery, Houston, TX, USA. The Houston Methodist Research Institute, Transplant Immunology, Houston, TX, USA; The Houston Methodist Hospital, Department of Surgery, Houston, TX, USA; The University of Texas, MD Anderson Cancer Center, Department of Genetics, Houston, TX, USA. Electronic address: mkloc@houstonmethodist.org.
 Department of Pharmacodynamics, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland. Department of Pharmacodynamics, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland. Department of Clinical Pharmacy, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland. Department of Pharmacodynamics, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland. Department of Internal Medicine and Metabolic, Medical University of Bialystok, M. Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland. Department of Pharmacodynamics, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland.
 State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
 Centro universitário FMABC, Santo André, São Paulo, Brazil. Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, São Paulo, Brazil. Electronic address: leonardo.pipek@fm.usp.br. Department of Neurosurgery, Santa Paula Hospital, São Paulo, Brazil; Department of Research and Innovation, Laboratory of Cellular and Molecular Biology, FMABC, Santo André, São Paulo, Brazil; Department of Neurology, School of Medicine of Pontifical Catholic University of São Paulo, Sorocaba, São Paulo, Brazil; State Serviant Public Hospital, São Paulo, Brazil.
 Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, 8331150, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, 8331150, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, 8331150, Chile; Millennium Institute on Immunology and Immunotherapy, Departamento de Ciencias Biológicas, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, 8370146, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, 8331150, Chile. Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, 8331150, Chile; Departamento de Endocrinología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, 8330023, Chile. Electronic address: akalergis@bio.puc.cl.
 Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
 Department of Conservative Dentistry and Periodontology, University Hospital, LMU Munich, Munich, Germany. Department of Conservative Dentistry and Periodontology, University Hospital, LMU Munich, Munich, Germany. Department of Conservative Dentistry and Periodontology, University Hospital, LMU Munich, Munich, Germany. Department of Medicine IV, Geriatrics, University Hospital, LMU Munich, Munich, Germany. Department of Conservative Dentistry and Periodontology, University Hospital, LMU Munich, Munich, Germany. Department of Medicine IV, Geriatrics, University Hospital, LMU Munich, Munich, Germany.
 Department of Adult Neurology, Gdańsk Medical University, Gdańsk, Poland. Department of Adult Neurology, Gdańsk Medical University, Gdańsk, Poland. Department of Adult Neurology, Gdańsk Medical University, Gdańsk, Poland. Department of Adult Neurology, Gdańsk Medical University, Gdańsk, Poland.
 Department of Nursing, General Hospital of Nikaia, Nikaia, Greece. Department of Nursing, General Hospital of Nikaia, Nikaia, Greece. Business Administration Postgraduate Programme Management in Health and Social Care Services, University of West Attica, Egaleo, Greece.
 Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Pathology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea. Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea. Department of Bioscience, University of Science and Technology, Daejeon, Republic of Korea. Laboratory of Veterinary Internal Medicine, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea; kangbt@chungbuk.ac.kr.
 Student Research Committee, Babol University of Medical Sciences, Babol, Iran. Department of Clinical Biochemistry, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran. Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Department of Physiology, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran. Infectious Diseases and Tropical Medicine Research Center, Babol University of Medical Sciences, Babol, Iran. Department of Clinical Biochemistry, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran. srostami.m@gmail.com. Department of Laboratory Sciences, Faculty of Paramedical Sciences, Babol University of Medical Sciences, Babol, Iran. srostami.m@gmail.com.
 Departament de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain; Fundació Hospital Clínic Veterinari, Facultad de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. Fundació Hospital Clínic Veterinari, Facultad de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. Unitat de Patologia Murina i Comparada (UPMiC) and Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Departament de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. Unitat de Bioestadística, Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. Departament de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain; Fundació Hospital Clínic Veterinari, Facultad de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. Electronic address: sonia.anor@uab.cat.
 MS Center ErasMS, Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Wytemaweg 80, Rotterdam 3015 CN, The Netherlands. MS Center ErasMS, Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Wytemaweg 80, Rotterdam 3015 CN, The Netherlands. MS Center ErasMS, Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Wytemaweg 80, Rotterdam 3015 CN, The Netherlands; MS Center ErasMS, Department of Neurology, Erasmus MC, University Medical Center Rotterdam, Rotterdam 3015 CN, The Netherlands; Netherlands Institute for Neuroscience, Neuroimmunology research group, Amsterdam 1105 BA, The Netherlands. MS Center ErasMS, Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Wytemaweg 80, Rotterdam 3015 CN, The Netherlands. MS Center ErasMS, Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Wytemaweg 80, Rotterdam 3015 CN, The Netherlands. Electronic address: m.vanluijn@erasmusmc.nl.
 Laboratory of Basic Psychology, Behavioral Analysis and Programmatic Development (PAD-LAB), Catholic University of Cuenca, Cuenca, Ecuador. Umanand Prasad School of Medicine and Health Science, The University of Fiji, Saweni Campus, Lautoka, Fiji. COAMS King Khalid University, Abha, Saudi Arabia. School of Medicine and Health Sciences, University of Rosario, Bogotá, Colombia. Dentistry Department, Al-Turath University College, Baghdad, Iraq. Iraqi Ministry of Education, Baghdad, Iraq. Department of Social Sciences, Faculty of Social Studies, Pontifical University of Peru. Zoology Department, Faculty of Science, Mansoura University, Mansoura 35516, Egypt. College of Engineering, Southern Luzon State University, Lucban, Quezon, Philippines. Electronic address: rmaaliw@slsu.edu.ph.
 Multiple Sclerosis Unit. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. CIBERNED, MADRID, Spain. Multiple Sclerosis Unit. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. CIBERNED, MADRID, Spain. Multiple Sclerosis Unit. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. Multiple Sclerosis Unit. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. CIBERNED, MADRID, Spain. Department of Basic Psychological Processes and Their Development, Euskal Herriko Unibertsitatea (UPV/EHU), 20018, San Sebastián, Spain. Group of Research in Primary Care. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. Research Network on Chronicity, Primary Care and Health Promotion (RICAPPS), San Sebastián, Spain. Cellular oncology group. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. IKERBASQUE, Basque Foundation for Science, Bilbao, Spain. Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento (CIBERfes), Carlos III Institute, Madrid, Spain. Multiple Sclerosis Unit. Biodonostia Health Research Institute, 20014, San Sebastián, Spain. david.otaegui@biodonostia.org. CIBERNED, MADRID, Spain. david.otaegui@biodonostia.org.
 Fundación Oftalmológica de Santander (FOSCAL), Bucaramanga, Colombia; Facultad de Ciencias de la Salud, Universidad Autónoma de Bucaramanga, Bucaramanga, Colombia. biomedica@ins.gov.co. Fundación Oftalmológica de Santander (FOSCAL), Bucaramanga, Colombia; Facultad de Ciencias de la Salud, Universidad Autónoma de Bucaramanga, Bucaramanga, Colombia. biomedica@ins.gov.co. Fundación Oftalmológica de Santander (FOSCAL), Bucaramanga, Colombia; Facultad de Ciencias de la Salud, Universidad Autónoma de Bucaramanga, Bucaramanga, Colombia. cporras186@unab.edu.co. Fundación Oftalmológica de Santander (FOSCAL), Bucaramanga, Colombia. biomedica@ins.gov.co. Fundación Oftalmológica de Santander (FOSCAL), Bucaramanga, Colombia; Facultad de Ciencias de la Salud, Universidad Autónoma de Bucaramanga, Bucaramanga, Colombia. biomedica@ins.gov.co.
 Department of Psychiatry, Jining Medical University, Jianshe South Road No. 45, Jining, Shandong, China. Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Jining Medical University, Jining, Shandong, China. Department of Psychiatry, Jining Medical University, Jianshe South Road No. 45, Jining, Shandong, China. Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Jining Medical University, Jining, Shandong, China. Department of Psychiatry, Jining Medical University, Jianshe South Road No. 45, Jining, Shandong, China. Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Jining Medical University, Jining, Shandong, China. Department of Psychiatry, Jining Medical University, Jianshe South Road No. 45, Jining, Shandong, China. yuhao@mail.jnmc.edu.cn. Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Jining Medical University, Jining, Shandong, China. yuhao@mail.jnmc.edu.cn. Department of Psychiatry, Jining Medical University, Jianshe South Road No. 45, Jining, Shandong, China. wangshuaijs@mail.jnmc.edu.cn. Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Jining Medical University, Jining, Shandong, China. wangshuaijs@mail.jnmc.edu.cn.
 Department of Personalized and Preventive Medicine, Institute of Interdisciplinary Medicine, 107113 Moscow, Russia. Department for Nervous Diseases, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia. Department of Personalized and Preventive Medicine, Institute of Interdisciplinary Medicine, 107113 Moscow, Russia. Department for Nervous Diseases, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia. Department of Personalized and Preventive Medicine, Institute of Interdisciplinary Medicine, 107113 Moscow, Russia. Russian Research Clinical Center of Gerontology of the Russian National Research Medical University Named after N.I. Pirogov, 129226 Moscow, Russia. Department of Personalized and Preventive Medicine, Institute of Interdisciplinary Medicine, 107113 Moscow, Russia. Department of Personalized and Preventive Medicine, Institute of Interdisciplinary Medicine, 107113 Moscow, Russia. Department for Nervous Diseases, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia. Department for Nervous Diseases, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia.
 Division of Digestive Diseases, Emory University School of Medicine, Atlanta, Georgia, USA. Atlanta Veterans Affairs Health Care System, Decatur, Georgia, USA. Division of Digestive Diseases, Emory University School of Medicine, Atlanta, Georgia, USA. Atlanta Veterans Affairs Health Care System, Decatur, Georgia, USA.
 Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. The Bioinformatics CRO, Sanford, Florida, 32771, USA. The Bioinformatics CRO, Sanford, Florida, 32771, USA. The Bioinformatics CRO, Sanford, Florida, 32771, USA. The Bioinformatics CRO, Sanford, Florida, 32771, USA. Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0QQ, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, CB2 0AW, UK.
 Department of Orthopedic Surgery, King Edward Medical University, Mayo Hospital, Lahore. Department of Neurology, King Edward Medical University, Mayo Hospital, Lahore, Pakistan. Department of Orthopedic Surgery, King Edward Medical University, Mayo Hospital. Department of Orthopedic Surgery, King Edward Medical University, Mayo Hospital.
 Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Chemical Engineering Department, Faculty of Engineering, Ferdowsi University of Mashhad (FUM), Mashhad, Iran. Laboratory Science, Hormozgan University of Medical Science, Bandar Abbas, Iran. Student Research Committee, School of medicine, Babol University of Medical Sciences, Babol, Iran. School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran. School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Medical Informatics, Research Center, Institute for Futures Studies in Health, Kerman, Iran. Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
 Ahead Therapeutics SL, Barcelona, Spain. Ahead Therapeutics SL, Barcelona, Spain; Immunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain. Immunology Unit, Department of Experimental Medicine, Faculty of Medicine, IRBLleida, University of Lleida, Lleida, Spain. Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Deutsches Zentrum für Immuntherapie (DZI), Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany. Sorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013 Paris, France. Ahead Therapeutics SL, Barcelona, Spain. Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Deutsches Zentrum für Immuntherapie (DZI), Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany. Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Deutsches Zentrum für Immuntherapie (DZI), Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany. Orgentec Diagnostika, Mainz, Germany. Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Deutsches Zentrum für Immuntherapie (DZI), Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany. Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Deutsches Zentrum für Immuntherapie (DZI), Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany. Sorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013 Paris, France. Immunology Unit, Department of Experimental Medicine, Faculty of Medicine, IRBLleida, University of Lleida, Lleida, Spain; CIBER of Diabetes and Associated Metabolic Disease (CIBERDEM), ISCIII, Madrid, Spain. Ahead Therapeutics SL, Barcelona, Spain. Ahead Therapeutics SL, Barcelona, Spain. Ahead Therapeutics SL, Barcelona, Spain. Ahead Therapeutics SL, Barcelona, Spain; Immunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain. Electronic address: mvives@igtp.cat.
 ITC Faculty Geo-Information Science and Earth Observation, University of Twente, Enschede. Institute for Geoinformatics, University of Münster, Münster, Germany. Department of Mathematics, University Jaume I, Castellón de la Plana, Castellón, Spain. Institute for Geoinformatics, University of Münster, Münster, Germany.
 School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, UK. Department of Genetic and Behavioural Neuroscience, Gunma University, Graduate School of Medicine, Maebashi, 371-8511, Japan. School of Biology, Faculty of Biological Sciences, University of Leeds, UK. School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, UK. School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, UK. Electronic address: S.A.Deuchars@leeds.ac.uk.
 Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia. Department of Clinical Medicine, Faculty of Medicine, Health and Human Sciences, Macquarie University, North Ryde, Sydney, NSW, Australia.
 Department of Psychiatry and Psychotherapy, Otto v. Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. Institute of Biochemistry and Cell Biology, Otto v. Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. Department of Psychiatry and Psychotherapy, Otto v. Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. Department of Psychiatry and Psychotherapy, Otto v. Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.
 Physiotherapy Department, Epworth Healthcare, Richmond, VIC, Australia. Physiotherapy Department, University of Melbourne, Carlton, VIC, Australia. Physiotherapy Department, University of Sydney, Science Rd, Camperdown, NSW, Australia.
 Hunter Bellevue School of Nursing, New York, New York, USA. The Mount Sinai Medical Center, New York, New York, USA. NP Adult Health Practice PC, New York, New York, USA. Yale New Haven Hospital, New Haven, Connecticut, USA. YNHH Long Ridge Medical Center, Stamford, Connecticut, USA. Yale New Haven Hospital, New Haven, Connecticut, USA. YNHH Old Saybrook Infusion Center, Old Saybrook, Connecticut, USA. Yale New Haven Hospital, New Haven, Connecticut, USA. YNHH Old Saybrook Infusion Center, Old Saybrook, Connecticut, USA. Yale New Haven Hospital, New Haven, Connecticut, USA. YNHH/Greenwich Hospital, Greenwich, Connecticut, USA. Department of Rehabilitation Services, Cleveland Clinic Mellen Center, Cleveland, Ohio, USA. Massachusetts General Hospital, Harvard School of Medicine, Boston, Massachusetts, USA. Yale New Haven Hospital, New Haven, Connecticut, USA. YNHH MS/Interventional Immunology Center, North Haven, Connecticut, USA.
 Department of Radiology, General Hospital of Nikea, Nikaia, Greece. Department of Nursing, General Hospital of Nikea, Nikaia, Greece. Department of Radiology, General Hospital of Nikea, Nikaia, Greece. Greek DRG Institute SA, Athens, Greece. Department of Business Administration and Director of Social Policy Division, Organization and Management of Primary Healthcare Services, Athens University of West Attica, Aigaleo, Greece.
 Department of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-0042, Japan. Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Itabashi, Tokyo, Japan. Institute for Human Life Science, Ochanomizu University, Ohtsuka, Tokyo, Japan. Department of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-0042, Japan. Ochadai Academic Production, Ochanomizu University, Ohtsuka, Tokyo, Japan. Juntendo Advanced Research Institute for Health Science, Juntendo University, Hongo, Tokyo, Japan. Department of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-0042, Japan. Department of Biochemistry, National Defense Medical College, Tokorozawa, Saitama, Japan. Department of Pharmacology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-0042, Japan. tishizu@ndmc.ac.jp.
 Çukurova State Hospital, Department of Urology, Adana, Turkey.
 Ohio Valley Medical center WVSOM OTI Uniformed Services University/Madigan Army Medical Center UNC school of Medicine, Atrium Health
 Kiskunhalasi Semmelweis Kórház, Neurológiai osztály, Kiskunhalas. Szegedi Tudományegyetem, Szent-Györgyi Albert Orvostudományi Kar, Neurológiai Klinika, Szeged. Szegedi Tudományegyetem, Szent-Györgyi Albert Orvostudományi Kar, Neurológiai Klinika, Szeged. ELKH-SZTE Idegtudományi Kutatócsoport, Szeged. Szegedi Tudományegyetem, Szent-Györgyi Albert Orvostudományi Kar, Neurológiai Klinika, Szeged.
 Department of Neurology, Juntendo University; Biomedical Research Core Facilities, Juntendo University; davide@juntendo.ac.jp. Department of Neurology, Juntendo University. Department of Neurology, Juntendo University. Department of Neurology, Juntendo University. Department of Neurology, Juntendo University; Neurodegenerative Disorders Collaborative laboratory, RIKEN Center for Brain Science.
 Institute of Applied Materials Science, Vietnam Academy of Science and Technology, 1B TL29, District 12, Ho Chi Minh City, Viet Nam. Institute of Applied Materials Science, Vietnam Academy of Science and Technology, 1B TL29, District 12, Ho Chi Minh City, Viet Nam. Department of Chemistry, Ho Chi Minh City University of Education, 280 An Duong Vuong Street, District 5, Ho Chi Minh City, Viet Nam. National Key Laboratory of Polymer and Composite Materials, Department of Energy Materials, Faculty of Materials Technology, Ho Chi Minh City University of Technology (HCMUT), 268 Ly Thuong Kiet Street, District 10, Ho Chi Minh City, Viet Nam. Vietnam National University Ho Chi Minh City, Linh Trung Ward, Thu Duc District, Ho Chi Minh City, Viet Nam. National Key Laboratory of Polymer and Composite Materials, Department of Energy Materials, Faculty of Materials Technology, Ho Chi Minh City University of Technology (HCMUT), 268 Ly Thuong Kiet Street, District 10, Ho Chi Minh City, Viet Nam. Vietnam National University Ho Chi Minh City, Linh Trung Ward, Thu Duc District, Ho Chi Minh City, Viet Nam. Institute of Applied Materials Science, Vietnam Academy of Science and Technology, 1B TL29, District 12, Ho Chi Minh City, Viet Nam. dttien@iams.vast.vn.
 University of Glasgow, 535 Wolfson Link Building, G12 8QQ Glasgow, United Kingdom. Electronic address: a.zorn.1@research.gla.ac.uk. University of Glasgow, 535 Wolfson Link Building, G12 8QQ Glasgow, United Kingdom. Electronic address: george.baillie@glasgow.ac.uk.
 Arak University of Medical Sciences, Iran. Arak University of Medical Sciences, Iran. Arak University of Medical Sciences, Iran.
 Sunnybrook Health Sciences Centre. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre. West Park Healthcare Center. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre. West Park Healthcare Center. West Park Healthcare Center. St. John's Rehab Research Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre.
 Department of Psychiatry and Psychotherapy, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany. Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, 44801 Bochum, Germany. Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, 44801 Bochum, Germany. Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, 44801 Bochum, Germany. Department of Neurology, University Hospital Knappschaftskrankenhaus Bochum, Ruhr University Bochum, 44892 Bochum, Germany.
 School of Engineering and Sciences, Campus Querétaro, Tecnologico de Monterrey, Av. Epigmenio González, No. 500 Fracc. San Pablo, Querétaro 76130, Mexico. School of Engineering and Sciences, Campus Mexico City, Tecnologico de Monterrey, Calle del Puente, No. 222 Col. Ejidos de Huipulco, Tlalpan, Mexico City 14380, Mexico. School of Engineering and Sciences, Campus Querétaro, Tecnologico de Monterrey, Av. Epigmenio González, No. 500 Fracc. San Pablo, Querétaro 76130, Mexico. Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus UNAM 3001, Juriquilla, Querétaro 76230, Mexico. International Rice Research Institute, Manila 4031, Philippines. Reliance Industries Ltd., Navi Mumbai 400701, India. Department of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, P.O. Box 1046 Blindern, 0317 Oslo, Norway. School of Engineering and Sciences, Campus Querétaro, Tecnologico de Monterrey, Av. Epigmenio González, No. 500 Fracc. San Pablo, Querétaro 76130, Mexico.
 Faculty of Medicine, Semmelweis University Campus Hamburg, Lohmühlenstraße 5/Haus P, Hamburg 20099, Germany; Neurological Clinic Bad Salzhausen, Am Hasensprung 6, Nidda 63667, Germany. Electronic address: dirk.bandorski@t-online.de. School of Medicine, Cardiology Department, Witten/Herdecke University, Witten, Germany. Electronic address: Bogossian@evk-haspe.de. Medizinische Klinik und Poliklinik II, Universitätsklinikum Giessen, Klinikstraße 33, Giessen 35392, Germany. Electronic address: ardeschir.ghofrani@innere.med.uni-giessen.de. School of Medicine, Cardiology Department, Witten/Herdecke University, Witten, Germany. Neurological Clinic Bad Salzhausen, Am Hasensprung 6, Nidda 63667, Germany. Electronic address: j.allendoerfer@asklepios.com. Klinikum Westmünsterland, St. Agnes-Hospital Bocholt Rhede, Medical Clinic, Cardiology/Electrophysiology, Barloer Weg 125, Bocholt 46397, Germany.
 Biocruces-Bizkaia Health Research Institute, Barakaldo, Spain. NeuronUP Labs, Logroño, Spain. NeuronUP Labs, Logroño, Spain. Department of Personality, Evaluation and Psychological Treatment, University of Granada, Granada, Spain. NeuronUP Labs, Logroño, Spain. NeuronUP Labs, Logroño, Spain. Biocruces-Bizkaia Health Research Institute, Barakaldo, Spain. IKERBASQUE: The Basque Foundation for Science, Bilbao, Spain. Department of Cell Biology and Histology, University of the Basque Country, Leioa, Spain.
 Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, 2200, Denmark. Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, 2200, Denmark. Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, 2200, Denmark. Department of Drug Design and Pharmacology, Jagtvej 162, University of Copenhagen, Copenhagen, 2100, Denmark. Department of Drug Design and Pharmacology, Jagtvej 162, University of Copenhagen, Copenhagen, 2100, Denmark. Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, 2200, Denmark. Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, 2200, Denmark. Electronic address: davies@sund.ku.dk.
 Department of Diagnostic Radiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. Department of Diagnostic Radiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. Department of Diagnostic Radiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. Department of Rehabilitation Science, The Hong Kong Polytechnic University, Hong Kong, China. Department of Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong, China. Department of Diagnostic Radiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. Department of Diagnostic Radiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
 School of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, 122 Luoshi Road, Wuhan, 430070, China. School of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, 122 Luoshi Road, Wuhan, 430070, China. leizhixin@whut.edu.cn. School of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, 122 Luoshi Road, Wuhan, 430070, China. suntl@whut.edu.cn. State Key Laboratory of Advanced Technology for Materials Synthesis and Processing, Wuhan University of Technology, 122 Luoshi Road, Wuhan, 430070, China. suntl@whut.edu.cn.
 Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Biology, Georgetown University, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, D.C. 20007, USA. Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C. 20007, USA. tw652@georgetown.edu. Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, D.C. 20007, USA.
 Department of Epidemiology, Erasmus MC University Medical Center Rotterdam, Office Na-2714, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus MC University Medical Center Rotterdam, Office Na-2714, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus MC University Medical Center Rotterdam, Office Na-2714, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus MC University Medical Center Rotterdam, Office Na-2714, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus MC University Medical Center Rotterdam, Office Na-2714, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. Department of Hematology, Erasmus MC University Medical Center Rotterdam, Rotterdam, The Netherlands. Department of Cardiology, Erasmus MC University Medical Center Rotterdam, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus MC University Medical Center Rotterdam, Office Na-2714, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
 School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China. School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China. School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China. School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China. Chinese Institute for Brain Research, Beijing 102206, China. State Key Laboratory of Translational Medicine and Innovative Drug Development, Nanjing 210000, China. School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China.
 Department of Neuroscience, University of Calgary, AB, Canada; Hotchkiss Brain Institute, University of Calgary, AB, Canada. Department of Neuroscience, University of Calgary, AB, Canada; Hotchkiss Brain Institute, University of Calgary, AB, Canada. Department of Radiology, University of Calgary, AB, Canada; Department of Clinical Neurosciences, University of Calgary, AB, Canada. Department of Medicine (Neurology), University of British Columbia, BC, Canada. Division of Neurology, Department of Medicine, St. Michael's Hospital, University of Toronto, Canada. Hotchkiss Brain Institute, University of Calgary, AB, Canada; Department of Radiology, University of Calgary, AB, Canada; Department of Clinical Neurosciences, University of Calgary, AB, Canada. Electronic address: yunyzhan@ucalgary.ca.
 Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, 6200 MD, Maastricht, The Netherlands. j.dahham@maastrichtuniversity.nl. Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, 6200 MD, Maastricht, The Netherlands. Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, 6200 MD, Maastricht, The Netherlands. Consultation and Research Institute, Beirut, Lebanon. Faculty of Business Administration, Beirut Arab University, Beirut, Lebanon. Department of Health Services Research, Care and Public Health Research Institute (CAPHRI), Faculty of Health Medicine and Life Sciences, Maastricht University, 6200 MD, Maastricht, The Netherlands. Centre for Economic Evaluations and Machine Learning, Trimbos Institute, Utrecht, The Netherlands. Department of Natural Sciences, School of Arts and Sciences, Lebanese American University, Byblos, Lebanon. Institut National de Santé Publique, d'Épidémiologie Clinique et de Toxicologie (INSPECT-Lb), Beirut, Lebanon.
 Department of Pharmaceutical Analysis, Chaitanya (Deemed to be University), Hanamakonda 506001, Telangana, India. School of Pharmacy, KPJ Healthcare University, Persiaran Seriemas, Nilai 71800, Negeri Sembilan, Malaysia. Department of Pharmaceutical Chemistry, College of Pharmacy, University of Ha'il, Ha'il 55476, Saudi Arabia. Department of Physics, Career Point University, Hamirpur 176041, Himachal Pradesh, India. Department of Pharmaceutical Chemistry, Narayan Institute of Pharmacy, Gopal Narayan Singh University, Jamuhar, Sasaram 821305, Bihar, India. Department of Pharmaceutical Analysis, School of Pharmacy, Anurag University, Hyderabad 500088, Telangana, India. Department of Pharmacology, METs, Institute of Pharmacy Bhujbal Knowledge City, Adgaon, Nashik 422003, Maharashtra, India. Clinical Research Associate, Clinnex, Ahmedabad 380054, Gujarat, India. Department of Pharmaceutical Chemistry, N.B.S. Institute of Pharmacy, Ausa 413520, Maharashtra, India. Centre for Applied Physics and Radiation Technologies, School of Engineering and Technology, Sunway University, Bandar Sunway 47500, Selangor, Malaysia. Department of Biomedical Physics, King Faisal Specialist Hospital and Research Center, Riyadh 11564, Saudi Arabia. Department of Physics, College of Science, Princess Nourah Bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia. Radiology and Medical Imaging Department, College of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, P.O. Box 422, Alkharj 11942, Saudi Arabia. Department of Pharmaceutical Chemistry, N.B.S. Institute of Pharmacy, Ausa 413520, Maharashtra, India. Department of Pharmacy, BGC Trust University Bangladesh, Chittagong 4381, Bangladesh. Department of Pharmacy, Faculty of Allied Health Sciences, Daffodil International University, Dhaka 1207, Bangladesh.
 Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas. Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas. Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas. Nutritional Sciences Department, College of Human Sciences, Texas Tech University, Lubbock, Texas. Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas. Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, Texas. Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, Texas. Department of Speech, Language, and Hearing Sciences, Texas Tech University Health Sciences Center, Lubbock, Texas.
 Student Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran. Student Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran. Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran. Electronic address: pharmacy.sajad@yahoo.com. Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran; Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah 6734667149, Iran. Departamento de Ciencias del Ambiente, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, Chile. Electronic address: javier.echeverriam@usach.cl.
 Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Medical Imaging, Anatomy, Preclinical Imaging Center (PRIME), Radboud Alzheimer Center, Donders Institute for Brain, Cognition, and Behavior, Radboud University Medical Center, Nijmegen, Netherlands. Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Microbiology and Systems Biology, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Medical Imaging, Anatomy, Preclinical Imaging Center (PRIME), Radboud Alzheimer Center, Donders Institute for Brain, Cognition, and Behavior, Radboud University Medical Center, Nijmegen, Netherlands. Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands. Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands.
 LBPC-PPC, Université Montpellier, CHU Montpellier, INM INSERM, Montpellier, France. LBPC-PPC, Université Montpellier, CHU Montpellier, INM INSERM, Montpellier, France. Hospital de la Santa Creu i Sant Pau - Biomedical Research Institute Sant Pau - Universitat Autònoma de Barcelona, Barcelona, Spain. Explorations neurologiques et centre SLA, Université Montpellier, CHU Gui de Chauliac, INM, INSERM, Montpellier, France. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Center and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. LBPC-PPC, Université Montpellier, CHU Montpellier, INM INSERM, Montpellier, France. LBPC-PPC, Université Montpellier, CHU Montpellier, INM INSERM, Montpellier, France. LBPC-PPC, Université Montpellier, CHU Montpellier, INM INSERM, Montpellier, France. Explorations neurologiques et centre SLA, Université Montpellier, CHU Gui de Chauliac, INM, INSERM, Montpellier, France. LBPC-PPC, Université Montpellier, CHU Montpellier, INM INSERM, Montpellier, France. Explorations neurologiques et centre SLA, Université Montpellier, CHU Gui de Chauliac, INM, INSERM, Montpellier, France.
 Director, Pharmacogenomics and Molecular Genetics Laboratories, Professor, Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202 Professor, Department of Pathology Stanford University, Palo Alto, CA 94305 Director, Stanford Medicine Clinical Genomics Laboratory, Stanford, CA 94305 David Weatherall Chair of Medicine and UK National Health Service Chair of Pharmacogenetics, University of Liverpool, Liverpool, UK Director, MRC Centre for Drug Safety Science and Wolfson Centre for Personalized Medicine, University of Liverpool, Liverpool, UK Director, Health Data Research UK North, Liverpool, UK President, British Pharmacological Society, London, UK President of the Latin American Association of Personalized Medicine, Chief Medical Officer - OneOme, Minneapolis, MN Chief, Medical Genetics and Human Variation, National Center for Biotechnology Information (NCBI), National Library of Medicine, National Institutes of Health, Bethesda, MD 20894 Project Lead, Medical Genetics and Human Variation, National Center for Biotechnology Information (NCBI), National Library of Medicine, National Institutes of Health, Bethesda, MD 20894 NCBI
 Department of Neurology, Aarhus University Hospital (AUH), 8200 Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, 8200 Aarhus, Denmark. Danish Multiple Sclerosis Center (DMSC), Department of Neurology, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Department of Neurology, Naestved, Slagelse & Ringsted Hospitals, Region Zealand, 4200 Slagelse, Denmark. Department of Neurology, Hospital of Southern Jutland, 6400 Soenderborg, Denmark. Department of Neurology, Hospital South-West Jutland Esbjerg, 6700 Esbjerg, Denmark. Department of Brain and Spinal Cord Injuries, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Department of Brain and Spinal Cord Injuries, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Danish Multiple Sclerosis Center (DMSC), Department of Neurology, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Danish Multiple Sclerosis Center (DMSC), Department of Neurology, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Department of Neurology, Naestved, Slagelse & Ringsted Hospitals, Region Zealand, 4200 Slagelse, Denmark. Institute of Regional Health Research and Molecular Medicine, University of Southern Denmark, 5000 Odense, Denmark. Danish Multiple Sclerosis Center (DMSC), Department of Neurology, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Department of Neurology, Herlev Hospital, 2730 Herlev, Denmark. Department of Neurology, Odense University Hospital, 5000 Odense, Denmark. Spinal Cord Injury Centre of Western Denmark (SCIWDK), Viborg Regional Hospital, 8800 Viborg, Denmark. Department of Neurology, Hospital of Southern Jutland and Research Unit in Neurology, Department of Regional Health Research, University of Southern Denmark, 5000 Odense, Denmark. Danish Multiple Sclerosis Center (DMSC), Department of Neurology, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Danish Multiple Sclerosis Center (DMSC), Department of Neurology, Copenhagen University Hospital, Rigshospitalet, 2600 Glostrup, Denmark. Department of Clinical Pharmacology, Aarhus University Hospital, 8000 Aarhus, Denmark. Department of Neurology, Aarhus University Hospital (AUH), 8200 Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, 8200 Aarhus, Denmark. Department of Neurology, Aarhus University Hospital (AUH), 8200 Aarhus, Denmark. Department of Neurology, Aarhus University Hospital (AUH), 8200 Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, 8200 Aarhus, Denmark. Danish Pain Research Centre, Aarhus University, 8200 Aarhus, Denmark. Department of Neurology, Aarhus University Hospital (AUH), 8200 Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, 8200 Aarhus, Denmark.
 Department of Infectious Disease Istituto Superiore di Sanità Rome Italy. Department of Infectious Disease Istituto Superiore di Sanità Rome Italy. Department of Molecular Medicine University of Padova Padua Italy. Department of Infectious Disease Istituto Superiore di Sanità Rome Italy. Department of Infectious Disease Istituto Superiore di Sanità Rome Italy. Department of Systems Medicine MS center Tor Vergata University Rome Italy. Department of Systems Medicine MS center Tor Vergata University Rome Italy. Center for Experimental Neurological Therapies Sant'Andrea Hospital Rome Italy. Department of Infectious Disease Istituto Superiore di Sanità Rome Italy. Center for Experimental Neurological Therapies Sant'Andrea Hospital Rome Italy. Neuroimmunology Unit IRCCS Fondazione Santa Lucia Rome Italy. Department of Molecular Medicine University of Padova Padua Italy. Department of Infectious-Tropical Diseases and Microbiology IRCCS Sacro Cuore Don Calabria Hospital Negrar di Valpolicella Italy. Department of Surgery, Oncology and Gastroenterology, Immunology and Oncology Section University of Padova Padua Italy. Department of Surgery, Oncology and Gastroenterology, Immunology and Oncology Section University of Padova Padua Italy. Veneto Institute of Oncology IOV - IRCCS Padua Italy. Department of Infectious-Tropical Diseases and Microbiology IRCCS Sacro Cuore Don Calabria Hospital Negrar di Valpolicella Italy. Metabolic Fitness Association Rome Italy. Department of Systems Medicine MS center Tor Vergata University Rome Italy. Center for Experimental Neurological Therapies Sant'Andrea Hospital Rome Italy. IRCCS Istituto Neurologico Mediterraneo Neuromed Pozzilli Italy. Department of Molecular Medicine University of Padova Padua Italy. Department of Infectious Disease Istituto Superiore di Sanità Rome Italy.
 UZ Leuven, BE. UZ Leuven, BE.
 Department of Pulmonology, The Indus Hospital, Karachi, Pakistan. Department of Pulmonology, The Indus Hospital, Karachi, Pakistan. Department of Pulmonology, The Indus Hospital, Karachi, Pakistan.
 Symbiosis Centre for Stem Cell Research, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis School of Biological Sciences, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis Centre for Stem Cell Research, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis School of Biological Sciences, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis Centre for Stem Cell Research, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis School of Biological Sciences, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis Centre for Stem Cell Research, Symbiosis International (Deemed University), Pune, 412115, India. Symbiosis School of Biological Sciences, Symbiosis International (Deemed University), Pune, 412115, India.
 Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA; Johns Hopkins Kavli Neuroscience Discovery Institute, Baltimore, MD 21218, USA. Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA. F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD 21205, USA; Department of Radiology and Radiological Sciences, Johns Hopkins University, Baltimore, MD 21205, USA. F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD 21205, USA; Department of Radiology and Radiological Sciences, Johns Hopkins University, Baltimore, MD 21205, USA. Electronic address: xuli@mri.jhu.edu. Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA; Johns Hopkins Kavli Neuroscience Discovery Institute, Baltimore, MD 21218, USA. Electronic address: jsulam1@jhu.edu.
 QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. vijayendra.dasari@qimr.edu.au. Elicio Therapeutics, Inc, Boston, MA, USA. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. Elicio Therapeutics, Inc, Boston, MA, USA. Elicio Therapeutics, Inc, Boston, MA, USA. Elicio Therapeutics, Inc, Boston, MA, USA. Elicio Therapeutics, Inc, Boston, MA, USA. Elicio Therapeutics, Inc, Boston, MA, USA. Elicio Therapeutics, Inc, Boston, MA, USA. Elicio Therapeutics, Inc, Boston, MA, USA. QIMR Centre for Immunotherapy and Vaccine Development, Tumour Immunology Laboratory, Infection and Inflammation Program, Berghofer Medical Research Institute, Brisbane, Australia. rajiv.khanna@qimr.edu.au.
 Department of Physiology, "Grigore T. Popa" University of Medicine and Pharmacy of Iasi, Str. Universitatii nr. 16, 700051 Iasi, România; TRANSCEND Centre - Regional Institute of Oncology (IRO) Iasi, Str. General Henri Mathias Berthelot, Nr. 2-4 Iași, România. University of Cagliari, Department of Chemical and Geological Sciences, Campus Monserrato, SS 554 bivio per Sestu, 09042 Monserrato, Italy. Centre of Advanced Research in Bionanoconjugates and Biopolymers, PetruPoni Institute of Macromolecular Chemistry Aleea Grigore Ghica-Voda, 41 A, 700487 Iasi, Romania; University of Cagliari, Department of Chemical and Geological Sciences, Campus Monserrato, SS 554 bivio per Sestu, 09042 Monserrato, Italy; Department of Materials and Environmental Chemistry, Arrhenius Laboratory, Stockholm University, SE-106 91 Stockholm, Sweden; State Key Laboratory of Materials-Oriented and Chemical Engineering, Nanjing Tech University, Nanjing 210009, PR China; Department of Engineering Sciences and Mathematics, Division of Energy Science, Luleå University of Technology, SE-97187 Luleå, Sweden. Universidade de São Paulo, Departamento de Ciências Biomoleculares, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Av. café, s/no - campus da USP, BR-14040-903 Ribeirão Preto, SP, Brazil; Department of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, NC 27695, USA. Electronic address: flbarroso@usp.br.
 Neurology Unit, Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Neurology Unit, Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Department of Clinical Neurological Sciences, Western University, London, Ontario, Canada. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Neurology Unit, Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA. Neurology Unit, Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy.
 Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China. Molecular and Experimental Surgery, University Clinic for General-, Visceral-, Vascular- and Trans-Plantation Surgery, Medical Faculty University Hospital Magdeburg, Otto-von Guericke University, 39120 Magdeburg, Germany. Molecular and Experimental Surgery, University Clinic for General-, Visceral-, Vascular- and Trans-Plantation Surgery, Medical Faculty University Hospital Magdeburg, Otto-von Guericke University, 39120 Magdeburg, Germany. Department of General, Visceral, and Transplant Surgery, Ludwig-Maximilians-University Munich, 80539 Munich, Germany. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China. Department of Gastroenterological Surgery, The Affiliated Hospital of Jiaxing University, Jiaxing 314001, China. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou 570100, China.
 Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland. Department of Biology, University of Fribourg, Fribourg 1700, Switzerland. Department of Biology, University of Fribourg, Fribourg 1700, Switzerland. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland. Research Unit Gene Vectors, Helmholtz Zentrum München, German Research Center for Environmental Health and German Center for Infection Research, D-81377 Munich, Germany. Department of Biology, University of Fribourg, Fribourg 1700, Switzerland. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland. Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8057, Switzerland.
 Neuroscience Department, Catholic University of the Sacred Heart, Rome, Italy. Neuroscience Department, Catholic University of the Sacred Heart, Rome, Italy. Neuroscience Department, Catholic University of the Sacred Heart, Rome, Italy. Neurology Unit, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy. Neuroscience Department, Catholic University of the Sacred Heart, Rome, Italy. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Neuroimmunology Laboratory, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Neuroscience Department, Catholic University of the Sacred Heart, Rome, Italy. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Neurology Unit, Mater Salutis Hospital, Legnago, Italy. Neurological Clinic and Multiple Sclerosis Center, A. Cardarelli Hospital, Naples, Italy. Multiple Sclerosis Centre, Neurology Unit, SS. Annunziata Hospital, Chieti, Italy. Neuroscience Department, Catholic University of the Sacred Heart, Rome, Italy. Neurology Unit, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.
 Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China. Central Laboratory, Shuguang Hospital, Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200021, P. R. China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE), Key Laboratory for Standardization of Chinese Medicines Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P. R. China.
 Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. christian.dorfer@meduniwien.ac.at.
 College of Pharmacy, Hangzhou Normal University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. College of Pharmacy, Hangzhou Normal University, Zhejiang, China. Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China. Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Zhejiang, China. Clinical Research Center, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Zhejiang, China. College of Pharmacy, Hangzhou Normal University, Zhejiang, China. School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang, China.
 Department of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan. Department of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan. Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan. Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan. Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan. Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan. Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan. Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan. Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan. Department of Psychiatry, Tohoku University Hospital, Miyagi, Japan. Department of Psychiatry, Graduate School of Medicine, Tohoku University, Miyagi, Japan. Department of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan. kunii@med.tohoku.ac.jp. Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan. kunii@med.tohoku.ac.jp.
 Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, 5303 Harry Hines Blvd., Dallas, TX, 75390-8806, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, 5303 Harry Hines Blvd., Dallas, TX, 75390-8806, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, 5303 Harry Hines Blvd., Dallas, TX, 75390-8806, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, 5303 Harry Hines Blvd., Dallas, TX, 75390-8806, USA. Department of Neurology, Neuroinnovation Program, Multiple Sclerosis and Neuroimmunology Imaging Program, The University of Texas Southwestern Medical Center, 5303 Harry Hines Blvd., Dallas, TX, 75390-8806, USA. darin.okuda@utsouthwestern.edu.
 Epidemiology Program, Health Outcomes Military Exposures (HOME) (12POP5), Office of Patient Care Services, U.S. Department of Veterans Affairs (VA), Washington, DC, USA. National Center for PTSD, VA Boston Health Care System, Boston, MA, USA. Boston University School of Medicine, Boston, MA, USA. San Francisco VA Health Care System, San Francisco, CA, USA. University of California-San Francisco, San Francisco, CA, USA. Epidemiology Program, Health Outcomes Military Exposures (HOME) (12POP5), Office of Patient Care Services, U.S. Department of Veterans Affairs (VA), Washington, DC, USA. Epidemiology Program, Health Outcomes Military Exposures (HOME) (12POP5), Office of Patient Care Services, U.S. Department of Veterans Affairs (VA), Washington, DC, USA. Epidemiology Program, Health Outcomes Military Exposures (HOME) (12POP5), Office of Patient Care Services, U.S. Department of Veterans Affairs (VA), Washington, DC, USA. Epidemiology Program, Health Outcomes Military Exposures (HOME) (12POP5), Office of Patient Care Services, U.S. Department of Veterans Affairs (VA), Washington, DC, USA. Epidemiology Program, Health Outcomes Military Exposures (HOME) (12POP5), Office of Patient Care Services, U.S. Department of Veterans Affairs (VA), Washington, DC, USA.
 Department of Clinical Medicine, University of Bergen, Bergen, Norway. Neuro-SysMed - Centre of Excellence for Experimental Therapy in Neurology, Departments of Neurology and Clinical Medicine, Bergen, Norway. Department of Clinical Medicine, University of Bergen, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Synaptopathies and Autoantibodies (SynatAc) Team, Institut NeuroMyoGène-MeLiS, INSERM U1314/CNRS UMR 5284, Université de Lyon, Lyon, France. French Reference Center on Paraneoplastic Neurological Syndrome, Hospices Civils de Lyon, University of Lyon, Université Claude Bernard Lyon 1, Villeurbanne, France. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Neuro-SysMed - Centre of Excellence for Experimental Therapy in Neurology, Departments of Neurology and Clinical Medicine, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway. Department of Clinical Medicine, University of Bergen, Bergen, Norway. Neuro-SysMed - Centre of Excellence for Experimental Therapy in Neurology, Departments of Neurology and Clinical Medicine, Bergen, Norway. Department of Neurology, Haukeland University Hospital, Bergen, Norway.
 School of Basic and Applied Science, Galgotias University, Gautam Buddha Nagar, Noida, Uttar Pradesh 203201 India. GRID: grid.448824.6. ISNI: 0000 0004 1786 549X Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, India. GRID: grid.467228.d. ISNI: 0000 0004 1806 4045
 Non-communicable diseases and Environment Programme, ISGlobal, Barcelona, NE4 5PL, Spain. Department of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, NE4 5PL, Spain. CIBER Epidemiología y Salud Pública, Barcelona, NE4 5PL, Spain. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Zurich, Switzerland. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. Mobilise-D Patient and Public Advisory Group. Mobilise-D Patient and Public Advisory Group. Department of Neurology, University Medical Center Schleswig-Holstein, Kiel, Germany. Department of Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Department of Neuroscience and Sheffield NIHR Translational Neuroscience BRC, Sheffield Teaching Hospitals NHS Foundation Trust & University of Sheffield, Sheffield, UK. Department of Clinical Gerontology, Robert-Bosch-Hospital, Stuttgart, Germany. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Department of Respiratory Diseases, University Hospitals Leuven, Leuven, Belgium. Department of Neurology, University Medical Center Schleswig-Holstein, Kiel, Germany. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Zurich, Switzerland. Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Zurich, Switzerland. Non-communicable diseases and Environment Programme, ISGlobal, Barcelona, NE4 5PL, Spain. Department of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, NE4 5PL, Spain. CIBER Epidemiología y Salud Pública, Barcelona, NE4 5PL, Spain.
 Department of Neurology, St. Joseph Hospital Berlin-Weissensee, Gartenstr. 1, 13088, Berlin, Germany. Center of Mental Health, Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital Würzburg, Füchsleinstrasse 15, 97080, Würzburg, Germany. Department of Neurology, Leopoldina Hospital Schweinfurt, Gustav Adolf Str. 8, 97422, Schweinfurt, Germany.
 Department of Biochemistry and Pharmacology, School of Medicine, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Department of Biochemistry and Pharmacology, School of Medicine, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Department of Biochemistry and Pharmacology, School of Medicine, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Laboratory of Systems Integration Pharmacology, Clinical & Regulatory Science, Research Institute for Medicines (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal. Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal. Laboratory of Systems Integration Pharmacology, Clinical & Regulatory Science, Research Institute for Medicines (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal. Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal. Department of Biochemistry and Pharmacology, School of Medicine, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Postgraduate Program in Structural and Functional Interactions in Rehabilitation, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Postgraduate Program in Structural and Functional Interactions in Rehabilitation, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Department of Biochemistry and Pharmacology, School of Medicine, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Postgraduate Program in Structural and Functional Interactions in Rehabilitation, University of Marília (UNIMAR), Avenida Hygino Muzzy Filho, 1001, Marília, São Paulo 17525-902, Brazil. Department of Biochemistry and Nutrition, School of Food and Technology of Marília (FATEC), Avenida Castro Alves, 62, Marília, São Paulo 17500-000, Brazil.
 Department of Neurosurgery, Institute of Psychiatry and Neurology, Warsaw, Poland. Electronic address: angelika.stapinska@gmail.com. Department of Neurosurgery, Institute of Psychiatry and Neurology, Warsaw, Poland. Department of Methodology, Laboratory of Center for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
 Fondazione Ricerca e Salute (ReS), Roma. Fondazione Ricerca e Salute (ReS), Roma. Fondazione Ricerca e Salute (ReS), Roma. Fondazione Ricerca e Salute (ReS), Roma. Fondazione Ricerca e Salute (ReS), Roma. Drugs and Health Srl, Roma. Fondazione Ricerca e Salute (ReS), Roma. Drugs and Health Srl, Roma. Fondazione Ricerca e Salute (ReS), Roma. Fondazione Ricerca e Salute (ReS), Roma. Fondazione Ricerca e Salute (ReS), Roma.
 Center for Research in Neuropsychology and Cognitive Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Neurology Department, Centro Hospitalar e Universitário de Coimbra (CHUC), Coimbra, Portugal. Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Portugal. Neurology Department, Hospital Garcia de Orta, Almada, Portugal. Center for Research in Neuropsychology and Cognitive Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Neurology Department, Centro Hospitalar e Universitário de Coimbra (CHUC), Coimbra, Portugal. Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Portugal. Neurology Department, Centro Hospitalar e Universitário de Coimbra (CHUC), Coimbra, Portugal. Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Portugal. Center for Research in Neuropsychology and Cognitive Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Center for Research in Neuropsychology and Cognitive Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Center for Research in Neuropsychology and Cognitive Behavioral Intervention (CINEICC), Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Faculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal. Neurology Department, Centro Hospitalar e Universitário de Coimbra (CHUC), Coimbra, Portugal. Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Portugal. Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
 Department of Pharmacy, International Islamic University Chittagong, Chittagong-4318, Bangladesh. Department of Pharmacy, International Islamic University Chittagong, Chittagong-4318, Bangladesh. Department of Pharmacy, International Islamic University Chittagong, Chittagong-4318, Bangladesh. Department of Chemistry, University of Swabi, Swabi, Pakistan. Department of Pharmacy, Faculty of Pharmacy, University of Dhaka, Dhaka, 1000, Bangladesh. Department of Pharmacy, BGC Trust University Bangladesh, Chittagong 4381, Bangladesh. Qassim University Medical Laboratories Buraidah Saudi Arabia. University Institute of Diet and Nutritionals Sciences, Faculty of Allied Health Sciences, The University of Lahore, Pakistan. Department of Veterinary of Medicine, College of Agriculture and Veterinary Medicine, Qassim University, Buraydah, Saudi Arabia. Department of Pathology, College of Medicine Qassim University, Buraydah, Saudi Arabia. Department of Crop Science, College of Sanghuh Life Science, Konkuk University, Seoul 05029, Republic of Korea.
 Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China. College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Department of Gastroenterology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Department of Gastroenterology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. duchangsheng@tongji.edu.cn.
 Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India. Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India. Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India; Ellen and Ronald Caplan Cancer Center, The Wistar Institute, Philadelphia, PA, 19104, USA. Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India. Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, Telangana, 500 037, India. Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India. Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India. Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, Telangana, 500 037, India. Electronic address: manoj.dandekar@niperhyd.ac.in. Department of Chemical Sciences, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India. Electronic address: nandurisrini92@gmail.com.
 Raymond Purves Bone and Joint Research Laboratory, Kolling Institute, Northern Sydney Local Health District, St. Leonards, New South Wales, Australia. Graduate School of Biomedical Engineering, University of New South Wales, Sydney, New South Wales, Australia. Sydney Medical School, Northern, The University of Sydney, Camperdown, New South Wales, Australia. Faculty of Medicine and Health, The University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia.
 Fischell Department of Bioengineering, University of Maryland College Park, Baltimore, MD, United states. Fischell Department of Bioengineering, University of Maryland College Park, Baltimore, MD, United states. Fischell Department of Bioengineering, University of Maryland College Park, Baltimore, MD, United states. United States Department of Veterans Affairs, Baltimore, MD, United states. Fischell Department of Bioengineering, University of Maryland College Park, Baltimore, MD, United states. United States Department of Veterans Affairs, Baltimore, MD, United states. Robert E Fischell Institute of Biomedical Devices, University of Maryland College Park, Baltimore, MD, United states. Department of Microbiology and Immunology, University of Maryland Medical School, Baltimore, MD, United states. Marlene and Stewart Greenebaum Cancer Center, Baltimore, MD, United states.
 Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Ooty, Tamilnadu, India. Amrita Molecular Modeling and Synthesis (AMMAS) Research Lab, Amrita Vishwavidyapeetham, Amrita Nagar, Ettimadai, Coimbatore, Tamilnadu, India. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Ooty, Tamilnadu, India. Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Ooty, Tamilnadu, India. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Ooty, Tamilnadu, India. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Ooty, Tamilnadu, India. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education and Research, Ooty, Tamilnadu, India. Electronic address: jubie@jssuni.edu.in.
 Department of Biomedical Engineering, National University of Singapore, Singapore, Singapore. Department of Biomedical Engineering, National University of Singapore, Singapore, Singapore. Department of Biomedical Engineering, National University of Singapore, Singapore, Singapore. anqi.qiu.sg@gmail.com. The N.1 Institute for Health, National University of Singapore, Singapore, Singapore. anqi.qiu.sg@gmail.com. NUS (Suzhou) Research Institute, National University of Singapore, Suzhou, China. anqi.qiu.sg@gmail.com. Institute of Data Science, National University of Singapore, Singapore, Singapore. anqi.qiu.sg@gmail.com. Department of Health Technology and Informatics, the Hong Kong Polytechnic University, Hung hom, Hong Kong. anqi.qiu.sg@gmail.com. Department of Biomedical Engineering, the Johns Hopkins University, Baltimore, MD, USA. anqi.qiu.sg@gmail.com.
 Department of Anesthesiology, School of Medicine, Emory University, Atlanta, GA, USA. Department of Anesthesiology, School of Medicine, Emory University, Atlanta, GA, USA. School of Medicine, University of Central Florida, Orlando, FL, USA. Department of Anesthesiology, Vassar Brothers Medical Center, Poughkeepsie, NY, USA. Department of Anesthesiology, School of Medicine, Emory University, Atlanta, GA, USA.
 Biochemistry and Molecular Biology Laboratory Rosilene Rodrigues Kaizer, Instituto Federal de Educação, Ciência e Tecnologia do Rio Grande do Sul, Campus Sertão, Sertão, RS, Brazil. Bioexperimentation Graduate Program, Universidade de Passo Fundo, Passo Fundo, RS, Brazil. Biochemistry and Molecular Biology Laboratory Rosilene Rodrigues Kaizer, Instituto Federal de Educação, Ciência e Tecnologia do Rio Grande do Sul, Campus Sertão, Sertão, RS, Brazil. tamagnowagner.99@gmail.com. Pharmacology Graduate Program, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil. tamagnowagner.99@gmail.com. Civil and Environmental Engineering Graduate Program, Universidade de Passo Fundo, Passo Fundo, RS, Brazil. Bioexperimentation Graduate Program, Universidade de Passo Fundo, Passo Fundo, RS, Brazil. Bioexperimentation Graduate Program, Universidade de Passo Fundo, Passo Fundo, RS, Brazil. Pharmacology Graduate Program, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
 Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. Collaborative Innovation Center, Jining Medical University, Jining, 272067, Shandong, People's Republic of China. Department of Pathophysiology, Weifang Medical University, Weifang, 261053, Shandong, People's Republic of China. Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. Collaborative Innovation Center, Jining Medical University, Jining, 272067, Shandong, People's Republic of China. The Affiliated Hospital of Jining Medical University, Jining Medical University, 89 Guhuai Road, Jining, 272029, Shandong, People's Republic of China. zhaozhankuimd@mail.jnmc.edu.cn. Department of Biochemistry, Jining Medical University, 133 Hehua Road, Jining, 272067, Shandong, People's Republic of China. yuhonglian@mail.jnmc.edu.cn. Collaborative Innovation Center, Jining Medical University, Jining, 272067, Shandong, People's Republic of China. yuhonglian@mail.jnmc.edu.cn.
 Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, China. Psychiatric Laboratory and Mental Health Center, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China. Department of Burns and Plastic Surgery, West China Hospital of Sichuan University, Chengdu, China. Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, China.
 Pharmaceutical Analysis Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Faculty of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Pharmaceutical Analysis Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Pharmacy Faculty, Tabriz University of Medical Sciences, Tabriz, Iran. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Departement of Biology, Faculty of Sciences, Payame Noor University, PO.box 19395-3697, Tehran, Iran. Pharmacy Faculty, Tabriz University of Medical Sciences, Tabriz, Iran.
 Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
 Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. Department of Medicine, University of Verona, Verona, Italy. The Center for Biomedical Computing (CBMC), University of Verona, Verona, Italy.
 Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland. Charlotte.Werner@hest.ethz.ch. Rehabilitation Engineering Laboratory, ETH Zurich, Zurich, Switzerland. Charlotte.Werner@hest.ethz.ch. Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland.
 School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. Hangzhou Wuyunshan Hospital Hangzhou Health Promotion Institution, Hangzhou, China. School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. Department of Hemodialysis, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. jinkeke@wmu.edu.cn. School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. fangyan_wang@wmu.edu.cn.
 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. RINGGOLD: 48455
 Department of Neuromedicine, Bangur Institute of Neurosciences (BIN), Kolkata, West Bengal, India. Department of Neuromedicine, Bangur Institute of Neurosciences (BIN), Kolkata, West Bengal, India. Department of General Medicine, Burdwan Medical College, and Hospital, Burdwan, West Bengal, India. Department of Psychiatry, Berhampur Mental Hospital, Berhampur, West Bengal, India. Department of Neuromedicine, Bangur Institute of Neurosciences (BIN), Kolkata, West Bengal, India. Department of Biochemistry, All India Institute of Medical Sciences (AIIMS), Patna, Bihar, India. Indian Institute of Technology (IIT), Madras, Tamil Nadu, India. School of Sciences, Indira Gandhi National Open University, New Delhi, India. Department of Neuromedicine, Bangur Institute of Neurosciences (BIN), Kolkata, West Bengal, India. Department of Neuromedicine, Bangur Institute of Neurosciences (BIN), Kolkata, West Bengal, India. Department of Neuromedicine, Bangur Institute of Neurosciences (BIN), Kolkata, West Bengal, India. Department of General Medicine, Apollo Gleneagles Hospital, Kolkata, West Bengal, India. Department of Neurology, University Hospital "12 de Octubre", Madrid, Spain. Centro de Investigación Biomódica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain. Department of Medicine, Complutense University, Madrid, Spain.
 Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, Germany. Molecular Physiology, Center for Integrative Physiology Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, Germany. Department of Neurology, Saarland University, 66421 Homburg, Germany. Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, Germany. Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, 66421 Homburg, Germany.

 Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Department of Pharmacology, Shambhunath Institute of Pharmacy (Affiliated to AKTU), Prayagraj, UP-211012, India. Department of Rehabilitation Sciences, School of Nursing Sciences and Allied Health, Jamia Hamdard, New Delhi, India. Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India. Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. asifiqubal2013@gmail.com. Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. khan.ahmed1511@gmail.com.
 Departments of Medicine, Ophthalmology and Neurology, Haukeland University Hospital, 5021 Bergen  Norway. Medicine, Ophthalmology and Neurology, Haukeland University Hospital, 5021 Bergen  Norway. Department of Endocrinology and Neurology, Stavanger University Hospital, 4019 Stavanger, Norway. Endocrinology and Neurology, Stavanger University Hospital, 4019 Stavanger, Norway. Departments of Medicine, Ophthalmology and Neurology, Haukeland University Hospital, 5021 Bergen  Norway. Department of Medicine and Ophthalmology, Drammen Hospital, Vestre Viken Health trust, 3004 Drammen, Norway. Medicine and Ophthalmology, Drammen Hospital, Vestre Viken Health trust, 3004 Drammen, Norway. Department of Neurology and Medicine, Akershus University Hospital, 1478 Oslo, Norway. Institute of Clinical Medicine, University of Oslo, 0313 Oslo, Norway. Neurology and Medicine, Akershus University Hospital, 1478 Oslo, Norway. Departments of Medicine, Ophthalmology and Neurology, Haukeland University Hospital, 5021 Bergen  Norway. Department of Clinical Medicine, University of Bergen, 5009 Bergen, Norway. Departments of Medicine, Ophthalmology and Neurology, Haukeland University Hospital, 5021 Bergen  Norway. Institute of Clinical Medicine, University of Oslo, 0313 Oslo, Norway. Neuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021 Bergen, Norway. Departments of Medicine, Ophthalmology and Neurology, Haukeland University Hospital, 5021 Bergen  Norway. Department of Clinical Medicine, University of Bergen, 5009 Bergen, Norway.
 Department of Biostatistics, Johns Hopkins University, Baltimore, MD. Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, CO. School of Medicine, Johns Hopkins University, Baltimore, MD. Department of Biostatistics, Johns Hopkins University, Baltimore, MD. Department of Biostatistics, Johns Hopkins University, Baltimore, MD.
 Department of Anatomy, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; Master's Programme Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; Dr. Soetomo General Academic Hospital, Surabaya, Indonesia. Veterinary Medicine College, Al-Qasim Green University, Al-Qasim, Iraq. College of Medical Technology, Medical Lab Techniques, Al-farahidi University, Iraq. Anesthesia Techniques, Al-Nisour University College, Iraq. Department of Anesthesia Techniques, Al-Mustaqbal University College, Iraq. College of Medicine, University of Al-Ameed, Karbala, Iraq. Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Hofuf 31982, Al-Ahsa, Saudi Arabia; Department of Pharmacology, Faculty of Veterinary Medicine, Kafrelshikh University, Kafrelshikh 33516, Egypt. Department of Biophysics, College of Applied Sciences, University Of Anbar, Anbar, Iraq. Student, Bachelor of Arts in International Relations, Webster University in Tashkent, Uzbekistan. MD, Independent Researcher, "Medcloud" educational centre, Tashkent, Uzbekistan. Gastrointestinal and Liver Diseases Research Center, Iran University of Medical Sciences, Tehran, Iran. Electronic address: sajadkarampour1987@gmail.com. Venom and Biotherapeutics Molecules Lab, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran. Electronic address: rasul.micro92@gmail.com.
 Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea. Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. Department of Neurology, Seoul National University Hospital, Seoul National University of Medicine, Seoul, Republic of Korea. Department of Neurology, Seoul National University Hospital, Seoul National University of Medicine, Seoul, Republic of Korea. Department of Neurology, Seoul National University Hospital, Seoul National University of Medicine, Seoul, Republic of Korea. Department of Pathology, Seoul National University Hospital, Seoul National University of Medicine, Seoul, Republic of Korea. Department of Neurology, Seoul National University Hospital, Seoul National University of Medicine, Seoul, Republic of Korea. Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. Electronic address: jp24@kaist.ac.kr. Department of Neurology, Seoul National University Hospital, Seoul National University of Medicine, Seoul, Republic of Korea. Electronic address: sueh916@gmail.com.
 Faculty of Medical Laboratory Sciences, National University, Khartoum, Sudan. Faculty of Pharmacy, International University of Africa, Khartoum, Sudan. Faculty of Medical Laboratory Sciences, National University, Khartoum, Sudan. Faculty of Medical Laboratory Sciences, National University, Khartoum, Sudan.
 Department of Neurology, Mayo Clinic Rochester, 200 First St SW, Rochester, MN, 55905, USA. Department of Dermatology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Hematology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Hematology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Hematology-Oncology, The University of Alabama at Birmingham, Birmingham, AL, USA. Department of Radiology, Mayo Clinic in Jacksonville, Jacksonville, FL, USA. Division of Rheumatology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Pulmonary and Critical Care Medicine, Mayo Clinic Rochester, Rochester, MN, USA. Division of Hematology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Endocrinology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Laboratory Medicine-Hematopathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA. Division of Hematology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Hematology, Mayo Clinic Rochester, Rochester, MN, USA. Division of Hematopathology, Mayo Clinic Rochester, Rochester, MN, USA. Department of Neurology, Mayo Clinic Rochester, 200 First St SW, Rochester, MN, 55905, USA. tobin.oliver@mayo.edu.
 Centre for Automation and Robotics (CAR), CSIC-UPM, Ctra Campo Real km 0.2 - La Poveda- Arganda del Rey, Madrid, 28500, Spain. carlos.cumplido@marsibionics.com. International Doctoral School, Rey Juan Carlos University, Madrid, 28922, Spain. carlos.cumplido@marsibionics.com. Department of Physical Therapy, Physical Medicine and Rehabilitation, Rey Juan Carlos University, Madrid, Spain. International Doctoral School, Rey Juan Carlos University, Madrid, 28922, Spain. Marsi Bionics S.L., Madrid, Spain. Centre for Automation and Robotics (CAR), CSIC-UPM, Ctra Campo Real km 0.2 - La Poveda- Arganda del Rey, Madrid, 28500, Spain. Marsi Bionics S.L., Madrid, Spain. Polytechnic University of Madrid, Madrid, Spain. Centre for Automation and Robotics (CAR), CSIC-UPM, Ctra Campo Real km 0.2 - La Poveda- Arganda del Rey, Madrid, 28500, Spain. Marsi Bionics S.L., Madrid, Spain. Marsi Bionics S.L., Madrid, Spain. Centre for Automation and Robotics (CAR), CSIC-UPM, Ctra Campo Real km 0.2 - La Poveda- Arganda del Rey, Madrid, 28500, Spain. elena.garcia@csic.es.
 Biostatistics & Prevention Institute, Epidemiology, University of Zurich, Zurich, Switzerland. Department of Health Sciences and Technology, Health Ethics and Policy Lab, ETH Zurich, Zurich, Switzerland. Department of Neurology, Neurocenter of Southern Switzerland, EOC, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana (USI), Lugano, Switzerland. Department of Neurology, Inselspital, University Hospital Bern and University of Bern, Bern, Switzerland. Neurology and Neurorehabilitation Center, Luzerner Kantonsspital, Lucerne, Switzerland. Neurologic Clinic and Policlinic, MS Center and Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Inselspital, University Hospital Bern and University of Bern, Bern, Switzerland. Biostatistics & Prevention Institute, Epidemiology, University of Zurich, Zurich, Switzerland. Institute for Implementation Science in Health Care, University of Zurich, Zurich, Switzerland.
 Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. Department of Neurological Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA. Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. Department of Neurological Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA. Department of Neurological Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA. Department of Neurosurgery, Rosa Ella Burkhardt Brain Tumor & Neuro-Oncology Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA. Department of Neurological Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA. Department of Neurosurgery, Rosa Ella Burkhardt Brain Tumor & Neuro-Oncology Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA. Department of Neurological Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA. Department of Neurosurgery, Rosa Ella Burkhardt Brain Tumor & Neuro-Oncology Center, Neurological Institute, Cleveland Clinic, Cleveland, Ohio, USA.
 Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Electronic address: endo@kazusa.or.jp.
 Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Division of Gastroenterology and Hepatology, Medical University Department, Kantonsspital Aarau, 5001 Aarau, Switzerland. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Pancreaticobiliary Medicine Unit, University College London Hospitals (UCLH), London W1W 6DN, UK. First Laboratory of Pharmacology, School of Medicine, Aristotle University of Thessaloniki, 54124 Thessaloniki, Macedonia, Greece. First Laboratory of Pharmacology, School of Medicine, Aristotle University of Thessaloniki, 54124 Thessaloniki, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. School of Healthcare Sciences, Midwifery Department, University of West Macedonia, Koila, 50100 Kozani, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Fifth Surgical Department, Medical School, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. 2nd Neurology Department, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, AHEPA Hospital, 54124 Thessaloniki, Macedonia, Greece. Second Medical Clinic, School of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Macedonia, Greece. Department of Nutritional Sciences and Dietetics, School of Health Sciences, International Hellenic University, Alexander Campus, 57400 Thessaloniki, Macedonia, Greece.
 Department of Microbiology, Kindai University Faculty of Medicine, Osaka 589-8511, Japan. Department of Microbiology, Kindai University Faculty of Medicine, Osaka 589-8511, Japan. Department of Microbiology, Kindai University Faculty of Medicine, Osaka 589-8511, Japan. Department of Microbiology, Kindai University Faculty of Medicine, Osaka 589-8511, Japan.
 Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. School of Sports Science, Nanjing Normal University, Nanjing, 210046, China. Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China. luodanyang@m.scnu.edu.cn.
 Department of Neuroradiology, Ospedale del Mare, Naples, Italy. RINGGOLD: 508856 Department of Advanced Biomedical Sciences, University "Federico II," Naples, Italy. RINGGOLD: 9307 Department of Advanced Biomedical Sciences, University "Federico II," Naples, Italy. RINGGOLD: 9307 Department of Neurology, Ospedale del Mare, Naples, Italy. RINGGOLD: 508856 Department of Neuroradiology, Ospedale del Mare, Naples, Italy. RINGGOLD: 508856 Department of Neuroradiology, Ospedale del Mare, Naples, Italy. RINGGOLD: 508856
 Department of Psychiatry, Max Rady College of Medicine, University of Manitoba, Canada. Electronic address: menns@hsc.mb.ca. Department of Internal Medicine, Max Rady College of Medicine, University of Manitoba, Canada. Department of Clinical Health Psychology, Max Rady College of Medicine, University of Manitoba, Canada. Department of Community Health Sciences, Max Rady College of Medicine, University of Manitoba, Canada; Centre for Healthcare Innovation, Rady Faculty of Health Sciences, University of Manitoba, Canada. Department of Internal Medicine, Max Rady College of Medicine, University of Manitoba, Canada. Nova Scotia Health and the Departments of Psychiatry, Psychology & Neuroscience, and Medicine, Dalhousie University, Canada. Centre for Healthcare Innovation, Rady Faculty of Health Sciences, University of Manitoba, Canada. Department of Internal Medicine, Max Rady College of Medicine, University of Manitoba, Canada; Department of Community Health Sciences, Max Rady College of Medicine, University of Manitoba, Canada.
 From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. Division of Clinical Immunology and Allergy, Necip Fazıl City Hospital, Kahramanmaraş, Turkey. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and. From the Division of Clinical Immunology and Allergy, Department of Internal Medicine, Necmettin Erbakan University, Meram Faculty of Medicine, Konya, Turkey, and.
 Department of Biomedical Sciences, Marshall University, Huntington, WV 25755, USA; Department of Biomedical Sciences, Edward Via College of Osteopathic Medicine, Auburn, AL 36832, USA. Department of Biomedical Sciences, Marshall University, Huntington, WV 25755, USA. Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Department of Biomedical Sciences, Marshall University, Huntington, WV 25755, USA. Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Department of Biomedical Sciences, Marshall University, Huntington, WV 25755, USA. Electronic address: morganda@marshall.edu.
 NICM Health Research Institute, University of Western Sydney, Westmead, NSW 2145, Australia. NICM Health Research Institute, University of Western Sydney, Westmead, NSW 2145, Australia. Faculty of Medicine and Health, University of Sydney, Camperdown, NSW 2006, Australia. Department of Governance and Research, Sydney Adventist Hospital, Wahroonga, NSW 2076, Australia. Centre for Digestive Diseases, Five Dock, NSW 2046, Australia. Department of Governance and Research, Sydney Adventist Hospital, Wahroonga, NSW 2076, Australia. Centre for Healthy Futures, Torrens University Australia, Ultimo, NSW 2007, Australia. NICM Health Research Institute, University of Western Sydney, Westmead, NSW 2145, Australia. Centre for Healthy Futures, Torrens University Australia, Ultimo, NSW 2007, Australia. Macquarie Medical School, Macquarie University, Macquarie Park, NSW 2109, Australia. ANU College of Health and Medicine, Australian National University, Canberra, ACT 2601, Australia.
 Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Shiraz University of Applied Science and Technology (UAST), Shiraz, Iran. Behbahan Faculty of Medical Science, Behbahan, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Histomorphometry and Stereology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Hematology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

 Department of Medicine, Ministry of the National Guard-Health Affairs, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, University of Bisha, Bisha, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia. Department of Medicine, Ministry of the National Guard-Health Affairs, Jeddah, Saudi Arabia. King Abdullah International Medical Research Center, Jeddah, Saudi Arabia. College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia.
 Departmant of Neurology, Istanbul Başaksehir Cam ve Sakura City Hospital, Istanbul, Turkey. Departmant of Neurology, Artvin State Hospital, Artvin, Turkey. Departmant of Psychiatry, Istanbul Başaksehir Cam ve Sakura City Hospital, Istanbul, Turkey. Departmant of Neurology, Istanbul Surp Pirgiç Hospital, Istanbul, Turkey. Departmant Of Neurology, Taksim Training and Research Hospital, Istanbul, Turkey. Departmant of Neurology, Istanbul Başaksehir Cam ve Sakura City Hospital, Istanbul, Turkey. Departmant of Psychiatry, Istanbul Başaksehir Cam ve Sakura City Hospital, Istanbul, Turkey. Departmant of Neurology, İstanbul Bakirköy State Hospital For Neurological and Pschiatric Disorders,Istanbul, Turkey. University of Health Sciences, Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Turkey.
 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Bezmialem Vakif University, 34093 Fatih, Istanbul, Turkey. Seed Breeding & Genetics Application Research Center, Pamukkale University, 20070 Denizli, Turkey. Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Bezmialem Vakif University, 34093 Fatih, Istanbul, Turkey. Department of Basic Medical Sciences, Faculty of Medicine, Medical Biology Erciyes University, 38039 Kayseri, Turkey. Department of Molecular Biology and Genetics, Faculty of Life and Natural Sciences, University of Abdullah Gul 38080 Kayseri, Turkey. Laboratory Animals Facility, Bilkent University, 06800 Ankara, Turkey. Department of Pharmacognosy & Phytochemistry, Faculty of Pharmacy, Bezmialem Vakif University, 34093 Fatih, Istanbul, Turkey. Department of Molecular Biology and Genetics, Faculty of Life and Natural Sciences, University of Abdullah Gul 38080 Kayseri, Turkey. Department of Biology, Faculty of Arts & Sciences, Pamukkale University, 20070 Kınıklı, Denizli, Turkey.
 Univ. Lyon, CarMeN Laboratory, INSERM, INRA, INSA Lyon, Université Claude Bernard Lyon 1, 69003 Lyon, France; CNRS, Lyon, France. Electronic address: marlene.wiart@univ-lyon1.fr. Univ. Lyon, CarMeN Laboratory, INSERM, INRA, INSA Lyon, Université Claude Bernard Lyon 1, 69003 Lyon, France; Univ. Grenoble Alpes, INSERM UA7 STROBE, 38000 Grenoble, France. Univ. Lyon, CarMeN Laboratory, INSERM, INRA, INSA Lyon, Université Claude Bernard Lyon 1, 69003 Lyon, France. INMG, SYNATAC Team, UCBL, Inserm, CNRS, 69008, Lyon, France. Univ. Lyon, CarMeN Laboratory, INSERM, INRA, INSA Lyon, Université Claude Bernard Lyon 1, 69003 Lyon, France; Hospices Civils de Lyon, Lyon, France. Université de Lyon, Ecole Normale Supérieure de Lyon, CNRS UMR 5182, Université Lyon 1, Laboratoire de Chimie, 46 allée d'Italie, 69364 Lyon, France. Université de Lyon, Ecole Normale Supérieure de Lyon, CNRS UMR 5182, Université Lyon 1, Laboratoire de Chimie, 46 allée d'Italie, 69364 Lyon, France. CNRS, Lyon, France; Univ. Lyon, Lyon Neurosciences Research Center, CNRS UMR5292, INSERM U1028, Université Claude Bernard Lyon 1, 69003 Lyon, France. Univ. Lyon, CarMeN Laboratory, INSERM, INRA, INSA Lyon, Université Claude Bernard Lyon 1, 69003 Lyon, France. INMG, SYNATAC Team, UCBL, Inserm, CNRS, 69008, Lyon, France. Department of Radiology, University of Pennsylvania, Pennsylvania, United States. Univ. Grenoble Alpes, INSERM UA7 STROBE, 38000 Grenoble, France. Univ. Grenoble Alpes, INSERM UA7 STROBE, 38000 Grenoble, France.
 Azrieli Centre for Neuro-Radiochemistry, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Brain Health Imaging Centre, Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Ontario, Canada. Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. Azrieli Centre for Neuro-Radiochemistry, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Brain Health Imaging Centre, Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Ontario, Canada. Azrieli Centre for Neuro-Radiochemistry, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Brain Health Imaging Centre, Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Ontario, Canada. Brain Health Imaging Centre, Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Ontario, Canada. Brain Health Imaging Centre, Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Ontario, Canada. Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. Department of Physiology, University of Toronto, Toronto, Ontario, Canada. Azrieli Centre for Neuro-Radiochemistry, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Brain Health Imaging Centre, Centre for Addiction and Mental Health, Campbell Family Mental Health Research Institute, Toronto, Ontario, Canada. Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
 From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. friedemann.paul@charite.de. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel. From the Experimental and Clinical Research Center (F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitaetsmedizin Berlin, Germany; Hospices Civils de Lyon (R.M.), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Bron; Centre des Neurosciences de Lyon-FORGETTING Team (R.M.), INSERM 1028 et CNRS UMR5292; Université Claude Bernard Lyon 1 (R.M.), France; John Radcliff Hospital (J.P.); Clinical Neurology Oxford University (J.P.), Oxford, United Kingdom; Servei de Neurologia-Neuroimmunologia (G.A.), Centre d'Esclerosi Múltiple de Catalunya (Cemcat); Vall d'Hebron Institut de Recerca (G.A.), Vall d'Hebron Hospital Universitari; Universitat Autònoma de Barcelona (G.A.), Spain; Departments of Regional Health Research and Molecular Medicine (N.A.), University of Southern Denmark, Odense, Denmark; Department of Neurology (N.A.), Slagelse Hospital, Denmark; Programs in Neuroscience and Immunology (J.L.B.), Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora; Department of Neurology (B.A.C.C.), UCSF Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (J.D.S.), Hôpitaux Universitaires de Strasbourg; INSERM U1119 Biopathologie de la Myéline (J.D.S.), Neuroprotection et Stratégies Thérapeutique; Clinical Investigation Center (J.D.S.), Hôpitaux Universitaires de Strasbourg, France; Department of Multiple Sclerosis Therapeutics (K.F.), Fukushima Medical University School of Medicine, and Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan; Department of Neurology (H.J.K.), Research Institute and Hospital of National Cancer Center, Goyang, South Korea; Oxford PharmaGenesis Ltd (R.H., L.L.); Department of Neurology (S.H.), Walton Centre NHS Foundation Trust, Liverpool, United Kingdom; Medical Research Center (N.K.), Marrakesh Medical School, Cadi Ayyad University; Neurology Department (N.K.), University Teaching Hospital Mohammed VI, Marrakesh, Morocco; Department of Neurology (I.K.), St Josef-Hospital, Ruhr-University Bochum; Marianne-Strauß-Klinik (I.K.), Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, Berg, Germany; Department of Neurology (S.K.), Graduate School of Medicine, Chiba University, Japan; CIEM MS Research Center (M.L.-P.), Federal University of Minas Gerais, Belo Horizonte, Brazil; John Radcliffe Hospital (M.I.L.), University of Oxford, United Kingdom; KS Hegde Medical Academy Director (L.P.), Center for Advanced Neurological Research, Nitte University, Mangalore, India; Neurology (S.J.P.), Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN; Department of Neurology and Rare Disease Center (C.Q.), National Center for Neurological Disorders, Huashan Hospital, Shanghai Medical College, Fudan University, China; Translational Neuroimmunology Group (S.R.), Kids Neuroscience Centre, and Brain and Mind Centre, Sydney Medical School, Faculty of Medicine and Health, University of Sydney; Department of Neurology (S.R.), Concord Hospital, Australia; Division of Neurology (D.R.), Department of Medicine, University of Toronto, Ontario, Canada; Neuroimmunology and Multiple Sclerosis Unit (A.S.), Service of Neurology, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), and Universitat de Barcelona, Spain; School of Medicine (D.K.S.), Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil; and Department of Neurology and Laboratory of Neuroimmunology and The Agnes-Ginges Center for Neurogenetics (A.V.-D.), Hadassah-Medical Center, Ein-Kerem, Faculty of Medicine, Hebrew University of Jerusalem, Israel.
 Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, Maine. Center for Excellence in the Neurosciences, University of New England, Biddeford, Maine. Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, Maine. Center for Excellence in the Neurosciences, University of New England, Biddeford, Maine.
 From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. From the Health Services Research Program (E.L.R., G.G., C.E.H., B.C.C.), Department of Neurology, and Department of Biostatistics (M.B.), University of Michigan, Ann Arbor; The American Academy of Neurology (A.M.), Minneapolis, MN; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; and Veterans Affairs Healthcare System (B.C.C.), Ann Arbor, MI. bcallagh@med.umich.edu.
 Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.
 Institute of Brain Science, Shanxi Datong University, Datong 037009, China. Institute of Brain Science, Shanxi Datong University, Datong 037009, China. Institute of Brain Science, Shanxi Datong University, Datong 037009, China. Institute of Brain Science, Shanxi Datong University, Datong 037009, China. Institute of Brain Science, Shanxi Datong University, Datong 037009, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619; Department of Physiology, Shanxi Medical University, Taiyuan 030001, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China. Institute of Brain Science, Shanxi Datong University, Datong 037009; The Fourth People's Hospital of Datong, Datong 037008, China. *Corresponding authors, E-mail: sxdtyjz@qq.com. Institute of Brain Science, Shanxi Datong University, Datong 037009; The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619; Department of Physiology, Shanxi Medical University, Taiyuan 030001, China. *Corresponding authors, E-mail: macungen@sxtcm.edu.cn.
 Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland. Graduate School for Health Sciences, University of Bern, Bern, Switzerland. Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland. Graduate School for Health Sciences, University of Bern, Bern, Switzerland. Biogen Digital Health, Biogen Spain, Madrid, Spain. Department of Neurology, University Hospital Basel, University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Departments of Biomedicine and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel, University of Basel, Basel, Switzerland. Multiple Sclerosis Center, Neurocenter of Southern Switzerland, EOC, Lugano, Switzerland. Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland. Department of Health Sciences, University of York, York, UK. Centre for Health Economics, University of York, York, UK. Department of Health Promotion and Human Behavior, Graduate School of Medicine/School of Public Health, Kyoto University, Kyoto, Japan. Department of Clinical Epidemiology, Graduate School of Medicine/School of Public Health, Kyoto University, Kyoto, Japan. Department of Psychiatry, University of Oxford, Oxford, UK. Oxford Health NHS Foundation Trust, Warneford Hospital, Oxford, UK. Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland.
 Institute of Experimental Immunology, University of Zurich, Zurich. Theodor Kocher Institute, University Bern, Bern, Switzerland. Institute of Laboratory Animal Science, University of Zurich, Zurich. Institute of Laboratory Animal Science, University of Zurich, Zurich. Institute of Laboratory Animal Science, University of Zurich, Zurich. Institute of Anatomy, University of Leipzig, Leipzig, Germany. Institute of Pathology, Campus Mitte, Charité -Universitätsmedizin Berlin, Berlin, Germany. Theodor Kocher Institute, University Bern, Bern, Switzerland. Institute of Neuropathology, Faculty of Medicine, University of Freiburg, Freiburg, Germany. Institute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, Munich, Germany. Institute for Pharmacology and Clinical Pharmacy, Philipps-Universität Marburg, Marburg, Germany. Groningen Research Institute of Pharmacy, Department of Molecular Pharmacology, Faculty of Science and Engineering, University of Groningen, Groningen, The Netherlands. Institute for Medical Microbiology and Hospital Hygiene, Philipps University of Marburg, Marburg, Germany. Department of Neurology, Philipps University of Marburg, Marburg, Germany. Institute for Pharmacology and Clinical Pharmacy, Philipps-Universität Marburg, Marburg, Germany. Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Institute of Anatomy, University of Leipzig, Leipzig, Germany. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. Institute of Medical Statistics and Computational Biology, Faculty of Medicine, University of Cologne, Cologne, Germany. Institute of Neuropathology, Faculty of Medicine, University of Freiburg, Freiburg, Germany. Center for Basics in NeuroModulation (NeuroModulBasics), Faculty of Medicine, University of Freiburg, Freiburg, Germany. Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. Institute of Medical Statistics and Computational Biology, Faculty of Medicine, University of Cologne, Cologne, Germany. Institute of Experimental Immunology, University of Zurich, Zurich. Institute of Experimental Immunology, University of Zurich, Zurich. Institute of Laboratory Animal Science, University of Zurich, Zurich. Institute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, Munich, Germany.
 Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Neurosciences and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Neurosciences and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Immunology and Genetics, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Neurosciences and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Immunology and Genetics, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Pharmaceutical Sciences Research Center, Ardabil University of Medical Sciences, Ardabil, Iran; Department of Nursing, School of Nursing, Larestan University of Medical Sciences, Larestan, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: baradaranb@tbzmed.ac.ir.
 Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neuroradiology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Division of Rheumatology, Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, Hospital Ludwigshafen, Ludwigshafen, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neuroradiology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany. Department of Neurology, University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany.
 The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Federal State Budgetary Scientific Institution, The Federal Research Center of Fundamental and Translational Medicine, 2 Timakova str., Novosibirsk, 630060, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. Lavrentyev Institute of Hydrodynamics, 15, Akademika Lavrent'yeva pr., Novosibirsk, 630090, Russian Federation. Regional Center for Multiple Sclerosis and other autoimmune diseases of the nervous system, State Budgetary Healthcare Institution of the Novosibirsk Region "State Novosibirsk Regional Clinical Hospital" (GBUZ NSO GNOKB); 126, Nemirovich - Danchenko str., Novosibirsk, 630087, Russian Federation. Novosibirsk State Medical University; 52, Krasny prospect av., Novosibirsk, 630091, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. The Institute International Tomography Center of the Russian Academy of Sciences, Institutskaya str., Bldg. 3а, Novosibirsk, 630090, Russian Federation. Novosibirsk State University, 1, Pirogova str., Novosibirsk, 630090, Russian Federation. Lavrentyev Institute of Hydrodynamics, 15, Akademika Lavrent'yeva pr., Novosibirsk, 630090, Russian Federation.
 Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. NMN@ssi.dk. Focused Research Unit in Neurology, Department of Neurology, Hospital of Southern Jutland, University of Southern Denmark, Aabenraa, Denmark. NMN@ssi.dk. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. Section for Clinical Mass Spectrometry, Danish Center for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark. iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Copenhagen, Denmark. Test Center Denmark, Statens Serum Institut, Copenhagen, Denmark. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Focused Research Unit in Neurology, Department of Neurology, Hospital of Southern Jutland, University of Southern Denmark, Aabenraa, Denmark. Multiple Sclerosis Clinic of Southern Jutland (Sønderborg, Kolding, Esbjerg), Department of Neurology, Hospital of Southern Jutland, University of Southern Denmark, Sønderborg, Denmark. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. The Danish National Biobank, Statens Serum Institut, Copenhagen, Denmark. Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. Pharmacovigilance Research Centre, Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark.
 Department of Neuroscience, King Fahad Specialist Hospital in Dammam, Saudi Arabia (F.A.). Division of Neurology, Faculty of Medicine and Health Sciences, Stellenbosch University, South Africa (Y.G.). Malawi-Liverpool Wellcome Trust Clinical Research Program, Kamuzu University of Health Sciences (KUHeS), Malawi (Y.G.). Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD (D.S.). University Teaching Hospital, Lusaka, Zambia (D.S.).
 Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
 Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital and the Second Clinical Medical College, Southern Medical University, Guangzhou, 510280, China; Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital and the Second Clinical Medical College, Southern Medical University, Guangzhou, 510280, China; Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital and the Second Clinical Medical College, Southern Medical University, Guangzhou, 510280, China; Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital and the Second Clinical Medical College, Southern Medical University, Guangzhou, 510280, China; Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital and the Second Clinical Medical College, Southern Medical University, Guangzhou, 510280, China; Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China. Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital and the Second Clinical Medical College, Southern Medical University, Guangzhou, 510280, China; Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, China; Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Southern Medical University, Guangzhou, 510280, China. Electronic address: 2009sht@smu.edu.cn.
 Programs in Neuroscience and Immunology, Departments of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University School of Medicine, Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan. Department of Neurology, National Cancer Center, Goyang, Republic of Korea. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuroinflammation, Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France. Departments of Neurology and Immunobiology, Yale University School of Medicine, New Haven, CT, United States. Annesley EyeBrain Center, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, PA, United States. Department of Medicine (Neurology), University of British Columbia, Vancouver, BC, Canada. Department of Neurology, University of Muenster, Münster, Germany. Medical Image Analysis Centre (MIAC AG) and University of Basel, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Department of Neurology and Program in Immunology, University of California, San Francisco, San Francisco, CA, United States. Genentech, Inc., San Francisco, CA, United States. F. Hoffmann-La Roche Ltd, Basel, Switzerland. F. Hoffmann-La Roche Ltd, Basel, Switzerland. Genentech, Inc., San Francisco, CA, United States. Roche Products Ltd, Hertfordshire, United Kingdom. Department of Neurology, Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, United States.
 Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen), Shenzhen, China. taoex@mail.sysu.edu.cn.
 Centro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, Quito 170527, Ecuador. Centro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, Quito 170527, Ecuador. Centro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, Quito 170527, Ecuador. School of Medicine, Universidad Católica Santiago de Guayaquil, Guayaquil 090615, Ecuador. Centro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, Quito 170527, Ecuador. Centro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, Quito 170527, Ecuador. Centro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, Quito 170527, Ecuador. Departamento de Bioquímica, Facultad de Ciencias Médicas, Universidad de Buenos Aires, Ciudad Autónoma de Buenos Aires C1121ABE, Argentina. Hospital Británico de Buenos Aires, Equipo de Soporte Nutricional, Ciudad Autónoma de Buenos Aires C1280AEB, Argentina. School of Medicine, Universidad Espíritu Santo, Samborondón 091952, Ecuador. "San Giovanni di Dio e Ruggi D'Aragona" University Hospital, Scuola Medica Salernitana, 84131 Salerno, Italy. Centro de Investigación de Salud Pública y Epidemiología Clínica (CISPEC), Universidad UTE, Quito 170527, Ecuador. Centro de Investigación de Salud Pública y Epidemiología Clínica (CISPEC), Universidad UTE, Quito 170527, Ecuador.
 Intensive Care Unit, Xiamen University, Zhongshan Hospital, Xiamen, 361004, China. Otolaryngology Head and Neck Surgery, Xiamen University, Zhongshan Hospital, Xiamen, 361004, China. Intensive Care Unit, Xiamen University, Zhongshan Hospital, Xiamen, 361004, China. Department of Nursing, Xiamen Cardiovascular Hospital Xiamen University, No. 2999 Jinshan Road, Xiamen, 361006, China. zhangyu99681@163.com.
 Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4th Floor, Research Block B, Chandigarh 160012, India. Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4th Floor, Research Block B, Chandigarh 160012, India. Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4th Floor, Research Block B, Chandigarh 160012, India. Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4th Floor, Research Block B, Chandigarh 160012, India. Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4th Floor, Research Block B, Chandigarh 160012, India. Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4th Floor, Research Block B, Chandigarh 160012, India. Electronic address: saha.lekha@pgimer.edu.in.
 From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. matheus.alves.123@outlook.com. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil. From the Departments of Neurology (M.A.S., B.M.C., A.L.G.Q., K.D.F.L., H.S.T., M.F.S., A.M.B.) and Department of Neuroradiology (C.M.S.C.), Beneficência Portuguesa de São Paulo, Brazil.
 IBD Center, Humanitas Research Hospital-IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, 20072 Milan, Italy. IBD Center, Humanitas Research Hospital-IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. IBD Center, Humanitas Research Hospital-IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. IBD Center, Humanitas Research Hospital-IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. IBD Center, Humanitas Research Hospital-IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, 20072 Milan, Italy. Medical Oncology and Haematology Unit, Humanitas Cancer Center, Humanitas Research Hospital IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. Child Neuropsychiatry Unit, Niguarda Hospital, 20162 Milan, Italy. IBD Center, Humanitas Research Hospital-IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy. Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, 20072 Milan, Italy.
 Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Electronic address: rgw@seas.upenn.edu. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA; School of Electrical and Computer Engineering, National Technical University of Athens, Athens, Greece. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. School of Electrical and Computer Engineering, National Technical University of Athens, Athens, Greece. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA; Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA. Center for AI and Data Science for Integrated Diagnostics, University of Pennsylvania, Philadelphia, USA; Center for Biomedical Image Computing and Analytics, University of Pennsylvania, Philadelphia, USA; Department of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA. Electronic address: christos.davatzikos@pennmedicine.upenn.edu.
 Brain Tumor Stem Cell Laboratory, Department of Neurological Surgery, Mayo Clinic, Jacksonville, FL, USA. Laboratory of Neural Stem Cells and Functional Neurogenetics, Departments of Neuroscience, Neurology, Genetics and Genome Sciences, UConn Health, Farmington, CT, 06030, USA. Brain Tumor Stem Cell Laboratory, Department of Neurological Surgery, Mayo Clinic, Jacksonville, FL, USA. Laboratory of Neural Stem Cells and Functional Neurogenetics, Departments of Neuroscience, Neurology, Genetics and Genome Sciences, UConn Health, Farmington, CT, 06030, USA. Brain Tumor Stem Cell Laboratory, Department of Neurological Surgery, Mayo Clinic, Jacksonville, FL, USA. Brain Tumor Stem Cell Laboratory, Department of Neurological Surgery, Mayo Clinic, Jacksonville, FL, USA. Division of Anatomic Pathology, Mayo Clinic, Jacksonville, USA. Laboratory of Neural Stem Cells and Functional Neurogenetics, Departments of Neuroscience, Neurology, Genetics and Genome Sciences, UConn Health, Farmington, CT, 06030, USA. imitola@uchc.edu. Laboratory for Neural Stem Cells and Functional Neurogenetics, Division of Multiple Sclerosis and Neuroimmunology, Department of Neurology, UConn Health Comprehensive Multiple Sclerosis Center, UConn School of Medicine, 263 Farmington Avenue, Farmington, 06030, USA. imitola@uchc.edu. Brain Tumor Stem Cell Laboratory, Department of Neurological Surgery, Mayo Clinic, Jacksonville, FL, USA. Quinones-Hinojosa.Alfredo@mayo.edu. Neurologic Surgery, Mayo Clinic, 4500 San Pablo Rd., Jacksonville, FL, 32224, USA. Quinones-Hinojosa.Alfredo@mayo.edu.
 School of Rehabilitation, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada. CIUSSS du Centre-Sud-de-l'Île-de-Montréal, Montreal, Quebec, Canada. School of Rehabilitation, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada. Centre for Interdisciplinary Research in Rehabilitation of Greater Montreal, Montreal, Quebec, Canada. Institut universitaire sur la réadaptation en déficience physique de Montréal du CIUSSS du Centre-Sud-de-l'Île-de-Montréal, Montreal, Quebec, Canada. School of Rehabilitation, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada. Ergo 2000 Sherbrooke, Sherbrooke, Canada. Marguerite-d'Youville Library, Université de Montréal, Quebec, Canada. Urbanisation Culture Société Library, Institut national de la recherche scientifique, Montréal, Quebec, Canada. School of Rehabilitation, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada. Centre for Interdisciplinary Research in Rehabilitation of Greater Montreal, Montreal, Quebec, Canada. Institut universitaire sur la réadaptation en déficience physique de Montréal du CIUSSS du Centre-Sud-de-l'Île-de-Montréal, Montreal, Quebec, Canada.
 University of Rochester Medical Center, Rochester, NY, USA. Electronic address: benzi_kluger@urmc.rochester.edu. The University of Melbourne, Fitzroy, VIC, Australia; St Vincent's Hospital, Melbourne, Fitzroy, VIC, Australia; Vrije Universiteit Brussel, Brussel, Belgium. University of North Carolina School of Medicine, Chapel Hill, NC, USA. Department of Nursing and Midwifery, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic. University of Washington, Seattle, WA, USA. Hinduja Hospital & Medical Research Centre, Mumbai, Maharashtra, India. University of Colorado Anschutz Medical Campus, Aurora, CO, USA. University of Rochester Medical Center, Rochester, NY, USA. University of Kent, Canterbury, UK. Department of Medicine, University of California San Francisco, San Francisco, CA, USA. University of Alberta, Edmonton, AB, Canada.
 Division of Female Pelvic Medicine and Reconstructive Surgery, Departments of Urology and Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. Urovant Sciences, Inc., Irvine, CA, USA. Urology, Urogynecology, Female Pelvic Medicine and Reconstructive Surgery, Atrium Health, Charlotte, NC, USA. Urology, Beaumont Hospital, Royal Oak, MI, USA. Allergan, an AbbVie company, Irvine, CA, USA. Neurourology Unit Department of Neurosciences, Centre Hospitalier Universitaire Vaudois, Université de Lausanne, Lausanne, Switzerland.
 Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Legal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Legal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute for Infection Research and Vaccine Development (IIRVD), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Legal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. manuel.friese@zmnh.uni-hamburg.de. Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. m.glatzel@uke.de.
 Shandong University of Traditional Chinese Medicine, Jinan 250002, China. Shandong University of Traditional Chinese Medicine, Jinan 250002, China. Qingdao Traditional Chinese Medicine Hospital (Qingdao Hiser Hospital), Qingdao 266033, China. Shandong University of Traditional Chinese Medicine, Jinan 250002, China. The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250002, China. Shandong University of Traditional Chinese Medicine, Jinan 250002, China. Shandong Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Therapy of Ocular Diseases; Shandong Academy of Eye Disease Prevention and Therapy, Medical College of Optometry and Ophthalmology, Shandong University of Traditional Chinese Medicine, Jinan 250002, China. Shandong Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Therapy of Ocular Diseases; Shandong Academy of Eye Disease Prevention and Therapy, Medical College of Optometry and Ophthalmology, Shandong University of Traditional Chinese Medicine, Jinan 250002, China.
 Centre for Health, Activity and Rehabilitation Research, Queen Margaret University, Edinburgh, UK. Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. UOC Neurorehabilitation, AOUI Verona, Verona, Italy. Clinical Sciences and Engineering, Salisbury NHS Foundation Trust and Bournemouth University, Salisbury, UK. Centre for Health, Activity and Rehabilitation Research, Queen Margaret University, Edinburgh, UK. College of Health, Psychology and Social Care, University of Derby, Derby, UK. Centre for Health, Activity and Rehabilitation Research, Queen Margaret University, Edinburgh, UK. School of Health Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, UK.
 Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA. Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA. Bioinformatic Analysis Shared Resource, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA. Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA. Department of Neurobiology and Molecular Medicine Program, University of Utah School of Medicine, Salt Lake City, UT 84112, USA. Electron Microscopy Core Laboratory, University of Utah, Salt Lake City, UT 84112, USA. Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA. Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA. Harvard Center for Mass Spectrometry, Harvard University, Cambridge, MA 02138, USA. Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA.
 Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Guizhou Province and Laboratory Animal Centre, Zunyi Medical University, Zunyi, Guizhou, China. Electronic address: chengyufengzmu@163.com. Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Guizhou Province and Laboratory Animal Centre, Zunyi Medical University, Zunyi, Guizhou, China; Sino-Jan Joint Lab of Natural Health Products Research, School of Traditional Chinese Medicines, China Pharmaceutical University, Nanjing, China. Electronic address: chen_ce13145520250@163.com. Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Guizhou Province and Laboratory Animal Centre, Zunyi Medical University, Zunyi, Guizhou, China. Electronic address: zhangfengzmc@163.com.
 Shanxi Key Lab of Bone and Soft Tissue Injury Repair, Department of Orthopaedics, The Second Hospital of Shanxi Medical University, Taiyuan, China. Department of Biochemistry, Basic Medical College, Shanxi Medical University, Taiyuan, China. Shanxi Key Lab of Bone and Soft Tissue Injury Repair, Department of Orthopaedics, The Second Hospital of Shanxi Medical University, Taiyuan, China. Department of Biochemistry, Basic Medical College, Shanxi Medical University, Taiyuan, China. Department of Biochemistry, Basic Medical College, Shanxi Medical University, Taiyuan, China. Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China. Shanxi Key Lab of Bone and Soft Tissue Injury Repair, Department of Orthopaedics, The Second Hospital of Shanxi Medical University, Taiyuan, China. Department of Biochemistry, Basic Medical College, Shanxi Medical University, Taiyuan, China. Shanxi Key Lab of Bone and Soft Tissue Injury Repair, Department of Orthopaedics, The Second Hospital of Shanxi Medical University, Taiyuan, China.
 Department of Clinical Genetics, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. d.smits@erasmusmc.nl. Department of Clinical Genetics, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. j.dekker.1@erasmusmc.nl. Department of Clinical Genetics, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. Division of Pediatric Genetics, Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, 12233, Saudi Arabia. Division of Pediatric Genetics, Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, 12233, Saudi Arabia. Department of Molecular Genetics, Proteomics Center, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. Department of Molecular Genetics, Proteomics Center, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. CENTOGENE GmbH, 18055, Rostock, Germany. Department of Pathology, Clinical Bioinformatics, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. Department of Clinical Genetics, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands. CENTOGENE GmbH, 18055, Rostock, Germany. Department of Clinical Genetics, ErasmusMC University Medical Center, 3015 CN, Rotterdam, the Netherlands.
 Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Geriatric Neuroscience Center, The Affiliated Brain Hospital of Guangzhou Medical University, Guangzhou, China. Guangdong Engineering Technology Research Center for Translational Medicine of Mental Disorders, Guangzhou, China. Department of Neurology, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China. Neurodegenerative Laboratory of Ministry of Education of the Peoples Republic of China, Beijing, China.
 Departamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), 28040 Madrid, Spain. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain. Departamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), 28040 Madrid, Spain. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain. Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), 72570 Puebla, Mexico. Departamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), 28040 Madrid, Spain. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain. Departamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), 28040 Madrid, Spain. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain. Servicio de Aparato Digestivo, Hospital General Universitario Gregorio Marañón, Departamento de Medicina, Universidad Complutense, Instituto de Investigación Sanitaria Gregorio Marañón, 28007 Madrid, Spain. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III (CIBEREHD, ISCIII), 28029 Madrid, Spain. Departamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), 28040 Madrid, Spain. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain.
 Diabetes Research Institute, University of Miami Miller School of Medicine, Miami, FL, USA. cricordi@med.miami.edu.
 Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250011, PR China. Department of Pharmacy, The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250014, China. Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250011, PR China. Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China. Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China. Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China; Shandong Institute of Neuroimmunology, Jinan 250014, PR China. Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China; Shandong Institute of Neuroimmunology, Jinan 250014, PR China. Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China; Shandong Institute of Neuroimmunology, Jinan 250014, PR China. Department of Neurology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China. Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250011, PR China; Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China; Shandong Institute of Neuroimmunology, Jinan 250014, PR China. Electronic address: ruisheng_duan@163.com. Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan 250014, PR China; Shandong Institute of Neuroimmunology, Jinan 250014, PR China. Electronic address: muyilin1991@163.com.
 UT MD Anderson Cancer Center, Houston, TX. Larkin Community Hospital, South Miami, FL. Larkin Community Hospital, South Miami, FL. Larkin Community Hospital, South Miami, FL. Larkin Community Hospital, South Miami, FL. Larkin Community Hospital, South Miami, FL.
 Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Law Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Guangdong-Hong Kong-Macao Greater Bay Area International Research Platform for Aptamer-Based Translational Medicine and Drug Discovery, Hong Kong SAR, China. Law Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Guangdong-Hong Kong-Macao Greater Bay Area International Research Platform for Aptamer-Based Translational Medicine and Drug Discovery, Hong Kong SAR, China. Law Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Guangdong-Hong Kong-Macao Greater Bay Area International Research Platform for Aptamer-Based Translational Medicine and Drug Discovery, Hong Kong SAR, China. Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China. Teaching and Research Division, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
 Department of Medicine-DIMED, University Hospital of Padua, Padua, Italy. amelia.ruffatti@unipd.it. Department of Medicine-DIMED, Rheumatology Unit, University Hospital of Padua, Padua, Italy. Department of Medicine-DIMED, Rheumatology Unit, University Hospital of Padua, Padua, Italy. Department of Medicine-DIMED, Rheumatology Unit, University Hospital of Padua, Padua, Italy. Department of Medicine-DIMED, Rheumatology Unit, University Hospital of Padua, Padua, Italy. Department of Medicine-DIMED, Rheumatology Unit, University Hospital of Padua, Padua, Italy. Department of Medicine-DIMED, General Internal Medicine Unit, Thrombotic and Hemorrhagic Disease Unit, University Hospital of Padua, Padua, Italy. Department of Medicine-DIMED, Dermatology Unit, University Hospital of Padua, Padua, Italy.
 Neurology, OhioHealth, Columbus, USA. Department of Medical Education, OhioHealth, Columbus, USA. Information Analytics, OhioHealth, Columbus, USA.
 Department of Medicine, Siriraj Piyamaharajkarun Hospital, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Department of Neurology, Neurological Institute of Thailand, Bangkok 10400, Thailand. Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Bumrungrad International Hospital, Bangkok 10110, Thailand. Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. The Bangkok Christian Hospital, Bangkok 10500, Thailand. Division of Neurology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand; Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Electronic address: natthapon.rat@mahidol.edu.

 Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Epidemiology, IQVIA, Frankfurt, Germany. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf. Clinic for Gastroenterology, Hepatology and Infectious Diseases, University Hospital Düsseldorf, Medical Faculty of Heinrich Heine University Düsseldorf, Düsseldorf.
 Geoffrey Jefferson Brain Research Centre, The Manchester Academic Health Science Centre, Northern Care Alliance and University of Manchester, Manchester, UK. RINGGOLD: 5292 Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK. RINGGOLD: 5292 Geoffrey Jefferson Brain Research Centre, The Manchester Academic Health Science Centre, Northern Care Alliance and University of Manchester, Manchester, UK. RINGGOLD: 5292 Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK. RINGGOLD: 5292 Centre for Biostatistics, University of Manchester, Manchester, UK. RINGGOLD: 5292 South Tees Hospitals NHS Foundation Trust, The James Cook University Hospital, Middlesbrough, UK. RINGGOLD: 5460 Glasgow Caledonian University, Glasgow, UK. RINGGOLD: 3525 Geoffrey Jefferson Brain Research Centre, The Manchester Academic Health Science Centre, Northern Care Alliance and University of Manchester, Manchester, UK. RINGGOLD: 5292 Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK. RINGGOLD: 5292
 Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: sajadnajafi1990@yahoo.com. Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Anatomy, Faculty of Medicine, Infectious Disease Research Center, Gonabad University of Medical Sciences, Gonabad, Iran. Department of Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Immunology and Allergy, The Persian Gulf Tropical Medicine Research Center, The Persian Gulf Biomedical Research Institute, Bushehr University of Medical Sciences, Bushehr, Iran. Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Pharmaceutical Basic Science, Faculty of Pharmacy, Tishk International University, Erbil, Kurdistan Region, Iraq. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Virology, Pasteur Institute of Iran, Tehran, Iran. Behbahan Faculty of Medical Sciences, Behbahan, Iran. Electronic address: ahmad.movahed14@gmail.com. Department of Biochemistry and Biomedicine, School of Life Sciences, University of Sussex, Brighton, United Kingdom; Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden. Electronic address: nahid.arghiani@su.se.
 Experimental and Clinical Research Center, A Cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Center for Neurology and Neuropsychiatry, LVR-Klinikum, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. Experimental and Clinical Research Center, A Cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. Department of Neurology, Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
 Translational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, Ontario, Canada. Department of Pharmacology and Toxicology, Faculty of Medicine, University of Toronto Toronto, Ontario, Canada. Translational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, Ontario, Canada. Translational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, Ontario, Canada. Department of Pharmacology and Toxicology, Faculty of Medicine, University of Toronto Toronto, Ontario, Canada. Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health Toronto, Ontario, Canada. Dalla Lana School of Public Health, University of Toronto Toronto, Ontario, Canada. Department of Psychiatry, University of Toronto Toronto, Ontario, Canada. Institute of Medical Science, Faculty of Medicine, University of Toronto Toronto, Ontario, Canada. Acute Care Program, Centre for Addiction and Mental Health Toronto, Ontario, Canada. Department of Family and Community Medicine, University of Toronto Toronto, Ontario, Canada. Addictions Division, Centre for Addiction and Mental Health Toronto, Ontario, Canada. Waypoint Research Institute, Waypoint Centre for Mental Health Care Penetanguishene, Ontario, Canada.
 Centro de Investigación en Mecatrónica y Sistemas Interactivos-MIST, Universidad Indoamérica, Av. Machala y Sabanilla, Quito 170103, Ecuador. Universidad UTE, Av. Mariscal Sucre, Quito 170129, Ecuador. Department of Rehabilitation Medicine, Erasmus MC, 3000 CA Rotterdam, The Netherlands. Faculty of Mechanical, Maritime and Materials Engineering, Delft University of Technology, Mekelweg 2, 2628 CD Delft, The Netherlands. Department of Rehabilitation Medicine, Erasmus MC, 3000 CA Rotterdam, The Netherlands. Faculty of Mechanical, Maritime and Materials Engineering, Delft University of Technology, Mekelweg 2, 2628 CD Delft, The Netherlands. Centre for Automation and Robotics (CAR UPM-CSIC), Universidad Politécnica de Madrid, 28012 Madrid, Spain. Centre for Automation and Robotics (CAR UPM-CSIC), Universidad Politécnica de Madrid, 28012 Madrid, Spain. Department of Rehabilitation Medicine, Erasmus MC, 3000 CA Rotterdam, The Netherlands.
 Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Klinik für Kinder - und Jugendmedizin, Universitätsmedizin Mannheim, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany. Present address: Clinic for Pediatrics and Adolescent Medicine, Johann Wolfgang Goethe University, Frankfurt/Main, Germany. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Present address: Department of Physiology and Pharmacology, Sapienza University, Rome, 00185, Italy. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. Present address: Department of Neurotherapeutics, Yamaguchi University, Yamaguchi, 755-8505, Japan. Laboratory of Clinical Regenerative Medicine, Department of Neurosurgery, University of Tsukuba, Tsukuba, Ibaraki, 305-8575, Japan. Klinik für Kinder - und Jugendmedizin, Universitätsmedizin Mannheim, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany. Present address: Clinic for Pediatrics and Adolescent Medicine, Sana Clinic Lichtenberg, Charité, Berlin, Germany. Klinik für Kinder - und Jugendmedizin, Universitätsmedizin Mannheim, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany. Theodor Kocher Institute, University of Bern, Freiestrasse 1, Bern, CH-3012, Switzerland. britta.engelhardt@tki.unibe.ch.
 Mymee, New York, New York, USA nicole.bundy@mymee.com. Mymee, New York, New York, USA. Mymee, New York, New York, USA. Rheumatology/Immunology, Cleveland Clinic, Cleveland, Ohio, USA. Department of Psychology, University of Florida, Gainesville, Florida, USA. Mymee, New York, New York, USA.
 Pharmaceutical Sciences and Technology Program, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand. Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, Berlin 13125, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin 13125, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, Berlin 13125, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin 13125, Germany. Center of Excellence in Biocatalyst and Sustainable Biotechnology, Department of Biochemistry, Faculty of Science, Chulalongkorn University, Bangkok 10330, Thailand. Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin 12203, Germany. Clinician Scientist Program, Berlin Institute of Health, Berlin 10117, Germany. Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin 12203, Germany. Department of Biochemistry and Microbiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand. Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany. Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, Berlin 13125, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin 13125, Germany. Department of Neurology and Experimental Neurology, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany. Center of Excellence in Biocatalyst and Sustainable Biotechnology, Department of Biochemistry, Faculty of Science, Chulalongkorn University, Bangkok 10330, Thailand. Program in Bioinformatics and Computational Biology, Graduate School, Chulalongkorn University, Bangkok 10330, Thailand. Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand. Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité-Universitätsmedizin Berlin, Berlin 13125, Germany. Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin 13125, Germany. Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand. Center of Excellence in Natural Products for Ageing and Chronic Diseases, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand.
 Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. Infectious Disease Unit, Department of System Medicine, Tor Vergata University and Hospital, 00133 Rome, Italy. Infectious Diseases Unit, Santa Maria Goretti Hospital, Sapienza University of Rome, 04110 Latina, Italy. Infectious Diseases Unit, Santa Maria Goretti Hospital, Sapienza University of Rome, 04110 Latina, Italy. Department of Neurosciences Mental Health and Sensory Organs, Sapienza University of Rome, 00185 Rome, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy. Department of Human Neurosciences, Sapienza University of Rome, 00185 Rome, Italy. IRCCS Neuromed, 86077 Pozzilli, Italy. Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00185 Rome, Italy.
 Department of Pharmacology, School of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain. Bioaraba Health Research Institute, Vitoria-Gasteiz, Spain. Department of Pharmacology, School of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain. Neurodegenerative Diseases Group, BioCruces Bizkaia Health Research Institute, Barakaldo, Bizkaia, Spain. Biocruces Bizkaia Health Research Institute, Osakidetza Basque Health Service, Galdakao-Usansolo Hospital, Basque Country Pharmacovigilance Unit, Galdakao, Spain. Department of Pharmacology, School of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain. Biocruces Bizkaia Health Research Institute, Osakidetza Basque Health Service, Galdakao-Usansolo Hospital, Basque Country Pharmacovigilance Unit, Galdakao, Spain. Bioaraba Health Research Institute, Osakidetza Basque Health Service, Araba Mental Health Network, Araba Psychiatric Hospital, Pharmacy Service, c/Alava 43, 01006, Vitoria-Gasteiz, Alava, Spain. Unax.lertxundietxebarria@osakidetza.net.
 Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, Joe R. and Teresa Lozano Long School of Medicine, University of Texas Health San Antonio, San Antonio, TX 78229, USA. Electronic address: chenc7@uthscsa.edu.
 Department of Clinical genetics, Sakai City Medical Center. Department of Neurology, Sakai City Medical Center. Department of Neurology, Sakai City Medical Center. Department of Neurology, Osaka University Graduate School of Medicine. Department of Clinical Laboratory, Sakai City Medical Center. Department of Clinical Laboratory, Sakai City Medical Center. Department of Neurology, Sakai City Medical Center. Department of Neurology, Sakai City Medical Center. Department of Neurology, Sakai City Medical Center. Department of Neurology, Sakai City Medical Center.
 Curtin School of Population Health, Curtin University, Perth, Western Australia, Australia. Curtin School of Population Health, Curtin University, Perth, Western Australia, Australia. Curtin School of Population Health, Curtin University, Perth, Western Australia, Australia. Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia. Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia. Murdoch Childrens Research Institute, Royal Children's Hospital, Melbourne, Victoria, Australia. Department of Neuroepidemiology, The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Curtin School of Population Health, Curtin University, Perth, Western Australia, Australia. lucinda.black@curtin.edu.au. Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia. lucinda.black@curtin.edu.au.
 Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Physical Medicine and Rehabilitation, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Physical Medicine and Rehabilitation, CHU Nantes, Nantes Université, Nantes, France. Department of Physical Medicine and Rehabilitation, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France. Department of Physical Medicine and Rehabilitation, CHU Nantes, Nantes Université, Nantes, France. Department of Urology, CHU Nantes, Nantes Université, Nantes, France.
 Health Psychology Section, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK. Health Psychology Section, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK. Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK. Health Psychology Section, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK. St George's University Hospitals NHS Foundation Trust, London, UK. Health Psychology Section, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience King's College London, London, UK.
 Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Electronic address: fcczhangsz@zzu.edu.cn. Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Electronic address: fcczhangj3@zzu.edu.cn. Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Electronic address: zdyfyyxb@126.com. Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Electronic address: sanxing.guo@zzu.edu.cn.
 Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts Amherst, Amherst, MA, 01003, USA. Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts Amherst, Amherst, MA, 01003, USA. Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts Amherst, Amherst, MA, 01003, USA. Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts Amherst, Amherst, MA, 01003, USA. Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts Amherst, Amherst, MA, 01003, USA. Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts Amherst, Amherst, MA, 01003, USA. Electronic address: aliciat@umass.edu.
 UCIBIO - Applied Molecular Biosciences Unit, MedTech - Laboratory of Pharmaceutical Technology, Department of Drug Sciences, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal; Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal. Electronic address: miteixeira@ff.up.pt. FFP-I3ID - Instituto de Investigação, Inovação e Desenvolvimento, FP-BHS - Biomedical and Health Sciences Research Unit, Faculdade de Ciências da Saúde, Universidade Fernando Pessoa, Rua Carlos da Maia 296, 4200-150 Porto, Portugal. Electronic address: cmlopes@ufp.edu.pt. UCIBIO - Applied Molecular Biosciences Unit, MedTech - Laboratory of Pharmaceutical Technology, Department of Drug Sciences, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal; Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal. Electronic address: hamaral@ff.up.pt. UCIBIO - Applied Molecular Biosciences Unit, MedTech - Laboratory of Pharmaceutical Technology, Department of Drug Sciences, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal; Associate Laboratory i4HB - Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira 228, 4050-313 Porto, Portugal. Electronic address: pccosta@ff.up.pt.
 Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
 Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. cxyong77@163.com. Fujian Provincial Key Laboratory of Critical Care Medicine, Fuzhou, 350001, China. cxyong77@163.com. Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. Key Laboratory of Stem Cell Engineering and Regenerative Medicine, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, 350122, China. Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. Key Laboratory of Stem Cell Engineering and Regenerative Medicine, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, 350122, China. Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. zhangxufjsl@163.com. Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, China. yinzhouw@163.com. Fujian Academy of Medical Science, Fuzhou, 350001, China. yinzhouw@163.com. Fujian Key Laboratory of Medical Analysis, Fuzhou, 350001, China. yinzhouw@163.com.
 Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. dominik.mueller@mdc-berlin.de. Charité-Universitätsmedizin Berlin, Berlin, Germany. dominik.mueller@mdc-berlin.de. DZHK (German Centre for Cardiovascular Research), Berlin, Germany. dominik.mueller@mdc-berlin.de. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. VIB Laboratory of Translational Immunomodulation, VIB Center for Inflammation Research (IRC), Hasselt University, Diepenbeek, Belgium. markus.kleinewietfeld@uhasselt.vib.be. Department of Immunology, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium. markus.kleinewietfeld@uhasselt.vib.be. University Multiple Sclerosis Center (UMSC), Hasselt University, Diepenbeek, Belgium. markus.kleinewietfeld@uhasselt.vib.be. Institute of Clinical Microbiology and Hygiene, University Hospital Regensburg and University of Regensburg, Regensburg, Germany. jonathan.jantsch@uk-koeln.de. Institute for Medical Microbiology, Immunology, and Hygiene, and Center for Molecular Medicine Cologne (CMMC), University Hospital Cologne and Faculty of Medicine, University of Cologne, Cologne, Germany. jonathan.jantsch@uk-koeln.de.
 Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Barcelona, Spain. Department of Cell Biology, Physiology and Immunology, University of Barcelona, Barcelona, Spain. Network Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Institute of Health Carlos III, Ministry of Economy and Competitiveness, Madrid, Spain. Institute of Neuroscience, University of Barcelona, Barcelona, Spain. Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Barcelona, Spain. Department of Cell Biology, Physiology and Immunology, University of Barcelona, Barcelona, Spain. Network Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Institute of Health Carlos III, Ministry of Economy and Competitiveness, Madrid, Spain. Institute of Neuroscience, University of Barcelona, Barcelona, Spain. Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Barcelona, Spain. Department of Cell Biology, Physiology and Immunology, University of Barcelona, Barcelona, Spain. Network Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Institute of Health Carlos III, Ministry of Economy and Competitiveness, Madrid, Spain. Institute of Neuroscience, University of Barcelona, Barcelona, Spain. Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), Barcelona, Spain. Department of Cell Biology, Physiology and Immunology, University of Barcelona, Barcelona, Spain. Network Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Institute of Health Carlos III, Ministry of Economy and Competitiveness, Madrid, Spain. Institute of Neuroscience, University of Barcelona, Barcelona, Spain. Clinical Neuroimmunology Group, Vall Hebron Research Institute (VHIR), Barcelona, Spain. Multiple Sclerosis Centre of Catalonia (CEM-CAT), Barcelona, Spain.
 Department of Neurology with Institute of Translational Neurology, University Hospital of Münster, Westfälische Wilhelms University Münster, Münster, Germany. Biomarkers & Translational Technologies (BTT), Pharma Research & Early Development (pRED), F. Hoffmann-La Roche Ltd., CH-4070 Basel, Switzerland. Department of Neurology with Institute of Translational Neurology, University Hospital of Münster, Westfälische Wilhelms University Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital of Münster, Westfälische Wilhelms University Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital of Münster, Westfälische Wilhelms University Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital of Münster, Westfälische Wilhelms University Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital of Münster, Westfälische Wilhelms University Münster, Münster, Germany. Electronic address: catharina.gross@ukmuenster.de.
 Department of Respiratory Medicine, National Hospital Organization Nara Medical Center, Nara, JPN. Department of Respiratory Medicine, Nara Medical University, Kashihara, JPN. Department of Diagnostic Pathology, Nara Medical University, Kashihara, JPN. Department of Respiratory Medicine, National Hospital Organization Nara Medical Center, Nara, JPN. Department of Respiratory Medicine, Nara Medical University, Kashihara, JPN.
 Departments of Neurology. Departments of Neurology. Medical Genomics. Laboratory Medicine and Pathology. Division of Hematology. Division of Hematology. Department of Medicine, Neurology Unit, Mubarak Al-Kabeer Hospital, Jabriya, Kuwait. Departments of Neurology. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN.
 Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: aboseia@ccf.org. Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Pediatric Rheumatology, Pediatric Institute, Cleveland Clinic, Cleveland, OH, USA. Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Epilepsy Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Pediatric Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA; Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
 The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Medical Sciences, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Medical Sciences, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Medical Sciences, Sydney, NSW, Australia. Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney, NSW, Australia. The University of Sydney, Sydney Informatics Hub, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Psychology, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Medical Sciences, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Medical Sciences, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. Institute of Clinical Neurosciences, Royal Prince Alfred Hospital, Sydney, NSW, Australia. The University of Sydney, Brain and Mind Centre, Sydney, NSW, Australia. The University of Sydney, School of Medical Sciences, Sydney, NSW, Australia.
 Brain, Nerve Research Center, The University of Sydney, Sydney, Australia. Electronic address: steve.vucic@sydney.edu.au. Department of Neurology, National Taiwan University Hospital Hsin-Chu Branch, Hsin-Chu, Taiwan. Brain and Mind Centre, The University of Sydney; and Department of Neurology, Royal Prince Alfred Hospital, Australia. Human Motor Control Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health, Bethesda, Maryland, United States. Department of Neurology, University Hospital of Lausanne (CHUV), Switzerland. Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, University Campus Bio-Medico of Rome, Rome, Italy. Department of Neurosci & Neurorehab IRCCS San Raffaele-Rome, Italy. Centre for Neurodegenerative Disorders, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy. IRCCS Neuromed, Pozzilli; Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy. Department of Medico-Surgical Sciences and Biotechnologies, Alfredo Fiorini Hospital, Sapienza University of Rome, Terracina, LT, Italy. Department of Neurosurgery, Technical University Munich, School of Medicine, Klinikum rechts der Isar, Munich, Germany. Univ Paris Est Creteil, EA4391, ENT, Créteil, France; Clinical Neurophysiology Unit, Henri Mondor Hospital, AP-HP, Créteil, France. Department of Neurology, National Neuroscience Institute, Singapore General Hospital, Singapore, and Duke-NUS Medical School, Singapore. Department of Neurology, Austin Health, Heidelberg VIC, Australia. Dipartimento di Scienze Biomediche e Cliniche, Università degli Studi di Milano, Milan, Italy; Istituto Di Ricovero e Cura a Carattere Scientifico, Fondazione Don Carlo Gnocchi, Milan, Italy. Department of Biomedical and Clinical Sciences University of Milan, Milan, Italy. Department of Neurosurgery, Charité-Universitätsmedizin Berlin, Cluster of Excellence: "Matters of Activity. Image Space Material," Humboldt University, Berlin Simulation and Training Center (BeST), Charité-Universitätsmedizin Berlin, Germany. Department of Medicine Waipapa Taumata Rau, University of Auckland, Auckland, Aotearoa, New Zealand. Department of Neurology, Ludwig-Maximilians-Universität München, München, Germany. Department of Human Neurophysiology, School of Medicine, Fukushima Medical University, Japan. Department of Neurology and Stroke, Eberhard Karls University of Tübingen, Hoppe-Seyler-Str. 3, 72076, Tübingen, Germany; Hertie Institute for Clinical Brain Research, Eberhard Karls University of Tübingen, Otfried-Müller-Straße 27, 72076 Tübingen, Germany. Edmond J. Safra Program in Parkinson's Disease, Morton and Gloria Shulman Movement Disorders Clinic, Toronto Western Hospital-UHN, Division of Neurology-University of Toronto, Toronto Canada.
 PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA. PTC Therapeutics, Inc., South Plainfield, New Jersey, USA.
 School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR. School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR. School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR. Center for Psycho-Oncological Research and Training, Division of Behavioral Sciences, School of Public Health, The University of Hong Kong, Hong Kong SAR. School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR. Department of Medicine, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong SAR. Department of Neurology, Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Center, Nijmegen, the Netherlands. School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR. Electronic address: jojo.yykwok@gmail.com.
 From the Bracco Imaging Spa, Milan, Italy (A.F.M., S.C.S., D.B., M.A., F.T., G.V.); Università degli Studi di Torino, Turin, Italy (A.M., A.B.); Centro Diagnostico Italiano, Milan, Italy (M.A., S.P.); Department of Radiology and Nuclear Medicine, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands (M.S.); and Medical Delta, Delft, the Netherlands (M.S.).
 Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, Tennessee. Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, Tennessee. Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Mathematics, Vanderbilt University, Nashville, Tennessee. Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, Tennessee. Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee. Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, Tennessee. Vanderbilt Center for Immunobiology, Vanderbilt University Medical Center, Nashville, Tennessee. Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee. Vanderbilt Institute of Chemical Biology, Vanderbilt University Medical Center, Nashville, Tennessee.
 School of Public Health, and Helen Wills Neuroscience Institute, University of California, Berkeley, CA, USA. Electronic address: jagust@berkeley.edu. Neurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Program Neurodegeneration, Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Amsterdam, Netherlands. Department of Neurology, University of California, Davis, CA, USA.
 Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan s-meguro@fmu.ac.jp. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
 Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada. Department of Pediatrics (Neurology), The Hospital for Sick Children, Division of Neuroscience and Mental Health, SickKids Research Institute, University of Toronto, Toronto, Ontario, Canada. Department of Psychology, The Hospital for Sick Children, Division of Neuroscience and Mental Health, SickKids Research Institute, University of Toronto, Toronto, Ontario, Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada. Department of Pediatrics (Neurology), The Hospital for Sick Children, Division of Neuroscience and Mental Health, SickKids Research Institute, University of Toronto, Toronto, Ontario, Canada. Electronic address: ann.yeh@sickkids.ca.
 Department of Biomedical Engineering, Cornell University, Ithaca, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Applied Physics, Cornell University, Ithaca, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Biomedical Engineering, Cornell University, Ithaca, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Electrical and Computer Engineering, Cornell University, Ithaca, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. Department of Biomedical Engineering, Cornell University, Ithaca, New York, USA. Department of Radiology, Weill Cornell Medicine, New York, New York, USA.
 Institute for Global Health Innovations, Duy Tan University, Da Nang, Vietnam. Faculty of Nursing, Duy Tan University, Da Nang, Vietnam. Department of Neuroscience, Hanoi Medical University, Hanoi, Vietnam. Department of Trauma and Orthopaedic, Thai Binh Medical University Hospital, Thai Binh, Vietnam. College of Medicine, University of Illinois at Chicago, Chicago, IL, United States. Université Claude Bernard Lyon 1, Villeurbanne, France. Institute for Global Health Innovations, Duy Tan University, Da Nang, Vietnam. Faculty of Nursing, Duy Tan University, Da Nang, Vietnam. Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden. Institute for Preventive Medicine and Public Health, Hanoi Medical University, Hanoi, Vietnam. Institute for Preventive Medicine and Public Health, Hanoi Medical University, Hanoi, Vietnam. Institute for Preventive Medicine and Public Health, Hanoi Medical University, Hanoi, Vietnam. Vietnam Young Physician Association, Hanoi, Vietnam. Department of Surgery, Hanoi Medical University Hospital, Hanoi, Vietnam. Institute for Preventive Medicine and Public Health, Hanoi Medical University, Hanoi, Vietnam. National Hospital of Obstetrics and Gynecology, Hanoi, Vietnam. Institute of Orthopedic and Trauma Surgery, Vietnam-Germany Hospital, Hanoi, Vietnam. Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States. Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. Institute for Health Innovation and Technology (iHealthtech), National University of Singapore, Singapore, Singapore.
 Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy. Department of Drug and Health Sciences, University of Catania, 95123 Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy. Center for Research in Ocular Pharmacology (CERFO), University of Catania, 95123 Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy. Center for Research in Ocular Pharmacology (CERFO), University of Catania, 95123 Catania, Italy. Eye Clinic, Multidisciplinary Department of Medical, Surgical and Dental Sciences, University of Campania "Luigi Vanvitelli", 80131 Napoli, Italy. Department of Ophthalmology, University of Lausanne, Fondation Asile des Aveugles, Jules Gonin Eye Hospital, 1004 Lausanne, Switzerland. Department of Medical and Surgical Sciences and Advanced Technologies "G. F. Ingrassia", University of Catania, 95123 Catania, Italy. Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy. Center for Research in Ocular Pharmacology (CERFO), University of Catania, 95123 Catania, Italy.
 Department of Physiology, Basrah Health Directorate, Basrah, IRQ. Department of Internal Medicine, College of Medicine, University of Basrah, Basrah, IRQ. Department of Physiology, College of Medicine, University of Babylon, Babylon, IRQ.
 Institut d'Investigació Biomèdica Sant Pau (IIB SANT PAU), 08041 Barcelona, Spain. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain. Institute for Research in Biomedicine (IRB Barcelona), 08028 Barcelona, Spain. Departament de Bioquímica i Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, 08028 Barcelona, Spain. Institut d'Investigació Biomèdica Sant Pau (IIB SANT PAU), 08041 Barcelona, Spain. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain. Institute for Research in Biomedicine (IRB Barcelona), 08028 Barcelona, Spain. Departament de Bioquímica i Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, 08028 Barcelona, Spain. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain. Department of Clinical Biochemistry, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain. Department de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, 08041 Barcelona, Spain. Institut d'Investigació Biomèdica Sant Pau (IIB SANT PAU), 08041 Barcelona, Spain. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain. Department of Endocrinology and Nutrition, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain.
 Pharmaceutical Chemistry, Institute for Pharmaceutical Sciences, Eberhard Karls University Tübingen, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Pharmaceutical Chemistry, Institute for Pharmaceutical Sciences, Eberhard Karls University Tübingen, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. Institute of Tropical Medicine, Eberhard Karls University Tübingen, Tübingen, Germany. Synovo GmbH, Tübingen, Germany. michael.burnet@synovo.com. Pharmaceutical Chemistry, Institute for Pharmaceutical Sciences, Eberhard Karls University Tübingen, Tübingen, Germany.
 Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. Department of Convergence Medicine, Asan Medical Center, Seoul, 05505, Republic of Korea. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. Asan Institute for Life Sciences, Asan Medical Center, Seoul, 05505, Republic of Korea. Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. Asan Institute for Life Sciences, Asan Medical Center, Seoul, 05505, Republic of Korea. kimkyunggon@gmail.com. Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. kimkyunggon@gmail.com. Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. eunjae.lee@amc.seoul.kr. Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. shinyongno1@yonsei.ac.kr.
 The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China. The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China. Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, 237 Luoyu Road, Wuhan, China. The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China. zhougang@whu.edu.cn. Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, 237 Luoyu Road, Wuhan, China. zhougang@whu.edu.cn.
 School of Public Health, Weifang Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Neuroimmunology, Jinan, China. School of Public Health, Weifang Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Neuroimmunology, Jinan, China. School of Public Health, Weifang Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Neuroimmunology, Jinan, China. School of Statistics and Mathematics, Shandong University of Finance and Economics, Jinan, China. School of Public Health, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China. School of Public Health, Weifang Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Neuroimmunology, Jinan, China; Center for Big Data Research in Health and Medicine, The First Affiliated Hospital of Shandong First Medical University, Jinan, China; Shandong Provincial Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China. Electronic address: tangfangsdu@gmail.com.
 Canary Islands Health Research Institute Foundation (FIISC), Tenerife, Spain. Evaluation Unit (SESCS), Canary Islands Health Service (SCS), Tenerife, Spain. Spanish Network of Agencies for Health Technology Assessment and Services of the National Health System (RedETS), Madrid, Spain. Research Network on Health Services in Chronic Diseases (REDISSEC), Madrid, Spain. Network for Research on Chronicity, Primary Care, and Health Promotion (RICAPPS), Madrid, Spain. Canary Islands Health Research Institute Foundation (FIISC), Tenerife, Spain. Evaluation Unit (SESCS), Canary Islands Health Service (SCS), Tenerife, Spain. Spanish Network of Agencies for Health Technology Assessment and Services of the National Health System (RedETS), Madrid, Spain. Canary Islands Health Research Institute Foundation (FIISC), Tenerife, Spain. Evaluation Unit (SESCS), Canary Islands Health Service (SCS), Tenerife, Spain. Spanish Network of Agencies for Health Technology Assessment and Services of the National Health System (RedETS), Madrid, Spain. Canary Islands Health Research Institute Foundation (FIISC), Tenerife, Spain. Evaluation Unit (SESCS), Canary Islands Health Service (SCS), Tenerife, Spain. Spanish Network of Agencies for Health Technology Assessment and Services of the National Health System (RedETS), Madrid, Spain. Quality and Patient Safety Unit, Nuestra Señora de Candelaria University Hospital, Tenerife, Spain. Teaching Unit of Family and Community Medicine 'La Laguna-Tenerife Norte', Primary Care Management of Tenerife, Canary Islands Health Service (SCS), Tenerife, Spain. Research Network on Health Services in Chronic Diseases (REDISSEC), Madrid, Spain. Network for Research on Chronicity, Primary Care, and Health Promotion (RICAPPS), Madrid, Spain. Health Technology Assessment Agency, Instituto de Salud Carlos III, Madrid, Spain. Neurology Service, Gregorio Marañón University Hospital, Madrid, Spain. Neurology Service, Alcorcón Foundation University Hospital, Madrid, Spain. Canary Islands Health Research Institute Foundation (FIISC), Tenerife, Spain. Evaluation Unit (SESCS), Canary Islands Health Service (SCS), Tenerife, Spain. Spanish Network of Agencies for Health Technology Assessment and Services of the National Health System (RedETS), Madrid, Spain. Canary Islands Health Research Institute Foundation (FIISC), Tenerife, Spain. Evaluation Unit (SESCS), Canary Islands Health Service (SCS), Tenerife, Spain. Spanish Network of Agencies for Health Technology Assessment and Services of the National Health System (RedETS), Madrid, Spain. Research Network on Health Services in Chronic Diseases (REDISSEC), Madrid, Spain. Network for Research on Chronicity, Primary Care, and Health Promotion (RICAPPS), Madrid, Spain.
 From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. rossl9@ccf.org. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA. From the Mellen Center for Multiple Sclerosis Treatment and Research (L.R., M.R.), Cerebrovascular Center (C.H., M.S.H.), Center for General Neurology (P.B.), Epilepsy Center (E.S.), Neurological Institute (R.M., G.B.), Cleveland Clinic, Cleveland, OH; Division of Pediatric Critical Care Medicine (A.M.), Department of Pediatrics, Central Michigan University, Detroit; and Department of Physical Medicine and Rehabilitation (J.K.S.), Harvard Medical School, Boston, MA.
 Biomedical Scientist, Genetics Specialization. Bachelor of Science in Nutrition, Department of Nutrition, School of Social and Health Sciences, Pontifical Catholic University of Goiás, Goiânia, Brazil. Ph.D. in Health Sciences, School of Medicine, Federal University of Goiás. Professor of Nutrition, Department of Nutrition, School of Social and Health Sciences, Pontifical Catholic University of Goiás, Goiânia, Brazil.
 CMAC Future Manufacturing Research Hub, c/o Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Technology and Innovation Centre, Glasgow, UK. CMAC Future Manufacturing Research Hub, c/o Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Technology and Innovation Centre, Glasgow, UK. Consiglio Nazionale delle Ricerche (CNR), Istituto per la Tecnologia delle Membrane (ITM), Rende, Italy. Consiglio Nazionale delle Ricerche (CNR), Istituto per la Tecnologia delle Membrane (ITM), Rende, Italy. Consiglio Nazionale delle Ricerche (CNR), Istituto di Cristallografia (IC), Bari, Italy. Consiglio Nazionale delle Ricerche (CNR), Istituto di Cristallografia (IC), Bari, Italy. Department of Environmental Engineering, University of Calabria, Rende, Italy. Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Edificio Polifunzionale, Rende, Italy. FUJIFILM Diosynth Biotechnologies, Billingham, UK. Department of Chemical Engineering, Imperial College London, London, UK. Department of Chemical Engineering, Imperial College London, London, UK. Center for Process Innovation (CPI), Darlington, UK. Center for Process Innovation (CPI), Darlington, UK. Center for Process Innovation (CPI), Darlington, UK. CMAC Future Manufacturing Research Hub, c/o Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Technology and Innovation Centre, Glasgow, UK. Consiglio Nazionale delle Ricerche (CNR), Istituto per la Tecnologia delle Membrane (ITM), Rende, Italy. g.diprofio@itm.cnr.it.
 Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: lucy.cullen@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: zoe.grange@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: karen.antal3@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: lynsey.waugh@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: Marianne.simduwaalsina@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: Cheryl.gibbons@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: laura.macdonald4@phs.scot. University of Strathclyde and Public Health Scotland, Glasgow, UK. Electronic address: chris.robertson@strath.ac.uk. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: claire.cameron2@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: diane.stockton2@phs.scot. Public Health Scotland, Glasgow, Edinburgh, UK. Electronic address: Maureen.Oleary@phs.scot.
 State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University. Electronic address: yanghui9@hotmail.com.
 Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. vincent.pernet@insel.ch. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. vincent.pernet@insel.ch. Centre de recherche du CHU de Québec-Université Laval and Department of Molecular Medicine, Faculté de médecine, Université Laval, Québec, Québec, Canada. vincent.pernet@insel.ch. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. Department of Ophthalmology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. Institute of Applied Biotechnology, Biberach University of Applied Science, Hubertus-Liebrecht-Strasse 35, Biberach, Germany. Department of Biomedical Research, University of Bern, Bern, Switzerland. Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. Institute of Applied Biotechnology, Biberach University of Applied Science, Hubertus-Liebrecht-Strasse 35, Biberach, Germany. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. LENS- European Laboratory for Non-Linear Spectroscopy, University of Florence, Sesto-Fiorentino (Firenze), Italy. LENS- European Laboratory for Non-Linear Spectroscopy, University of Florence, Sesto-Fiorentino (Firenze), Italy. LENS- European Laboratory for Non-Linear Spectroscopy, University of Florence, Sesto-Fiorentino (Firenze), Italy. LENS- European Laboratory for Non-Linear Spectroscopy, University of Florence, Sesto-Fiorentino (Firenze), Italy. National Institute of Optics - National Research Council (CNR-INO), Sesto Fiorentino, Italy. Institute of Applied Biotechnology, Biberach University of Applied Science, Hubertus-Liebrecht-Strasse 35, Biberach, Germany. Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. andrew.chan@insel.ch. Center for experimental neurology (ZEN), Bern University Hospital, University of Bern, Bern, Switzerland. andrew.chan@insel.ch. Department of Biomedical Research, University of Bern, Bern, Switzerland. andrew.chan@insel.ch.
 Jiangxi Provincial Key Laboratory of Nephrology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China. Jiangxi Provincial Key Laboratory of Nephrology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China. Jiangxi Provincial Key Laboratory of Nephrology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China. Medical College of Nanchang University, Nanchang University, 330006, Nanchang City, China. Medical College of Nanchang University, Nanchang University, 330006, Nanchang City, China. Jiangxi Provincial Key Laboratory of Nephrology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China. Jiangxi Provincial Key Laboratory of Nephrology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China. aiminzhong@126.com. Medical College of Nanchang University, Nanchang University, 330006, Nanchang City, China. aiminzhong@126.com.
 Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, 741246, India. Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, 741246, India. Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, 741246, India. National Centre for Cell Science, Ganeshkhind, Pune, India. Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, 741246, India. dassarmaj@iiserkol.ac.in. Department of Ophthalmology, University of Pennsylvania Scheie Eye Institute, Philadelphia, PA, 19104, USA. dassarmaj@iiserkol.ac.in.
 Baylor University LHSON, Dallas, TX, and Paragon Healthcare, Dallas, TX. Courtney Brandt, DNP, APRN, FNP-C, is a family nurse practitioner and clinical assistant professor of nursing at Baylor University. She has been practicing in outpatient infusion centers for 4 years and currently works for Paragon Healthcare in Dallas, Texas. She earned her DNP from University of Texas at Arlington in 2021 and her MSN from Texas Tech Health Sciences Center in 2017. She also has previous experience as a family nurse practitioner in asthma/allergy medicine, as well as a nursing background in the pediatric intensive care unit and adult medical/surgical nursing. Her areas of research interest include infusion medicine and nursing education. She lives in Arlington, Texas, with her husband and 4 young children.
 Department of Psychiatry, Faculty of Medicine, Çukurova University, Adana, Turkey. Department of Chemistry, Faculty of Science, Atatürk University, Erzurum, Turkey. Department of Basic Sciences, Faculty of Dentistry, Iğdır University, Iğdır, Turkey. St. Elisabeth KrankenhausKlinik Fur Psychiatrie Und, Psychotherapie, Hattingen, Germany. Department of Psychiatry, Faculty of Medicine, Çukurova University, Adana, Turkey. Department of Psychiatry, Faculty of Medicine, Çukurova University, Adana, Turkey. Department of Psychiatry, Faculty of Medicine, Çukurova University, Adana, Turkey. Department of Chemistry, Faculty of Science, Atatürk University, Erzurum, Turkey.
 Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Developmental Psychobiology Lab, IRCCS Mondino Foundation, Pavia, Italy. Developmental Psychobiology Lab, IRCCS Mondino Foundation, Pavia, Italy. European Commission, Joint Research Centre (JRC), Ispra, Italy. Multiple Sclerosis Center, Neurocenter of South of Switzerland, EOC, Lugano, Switzerland. Multiple Sclerosis Research Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Developmental Psychobiology Lab, IRCCS Mondino Foundation, Pavia, Italy. Molecular Biology Lab, Scientific Institute IRCCS E. Medea, Bosisio Parini, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. livio.provenzi@unipv.it. Developmental Psychobiology Lab, IRCCS Mondino Foundation, Pavia, Italy. livio.provenzi@unipv.it.
 Department of Pharmacology, All India Institute of Medical Sciences, Rajkot, Gujarat, India. Department of Pharmacology, All India Institute of Medical Sciences, Rajkot, Gujarat, India. Department of Pharmacology, All India Institute of Medical Sciences, Rajkot, Gujarat, India. Department of Medical Surgical Nursing, Shri Anand Institute of Nursing, Rajkot, Gujarat, 360005, India. Department of Anaesthesiology, All India Institute of Medical Sciences, Rajkot, Gujarat, India. Department of Physiology, Khulna City Medical College and Hospital, Khulna, Bangladesh. Unit of Pharmacology, Faculty of Medicine and Defence Health, Universiti Pertahanan Nasional Malaysia (National Defence University of Malaysia), Kuala Lumpur, 57000, Malaysia.
 Department of Translational Sciences, Imaging Research, AbbVie Inc., 1 North Waukegan Rd, North Chicago, IL, 60064, USA. peerbjacobson@gmail.com. Division of Experimental and Translational Neuroscience, Krembil Brain Institute & University Health Network, Toronto, ON, M5T 0S8, Canada. Pharmaseed Ltd, 74047, Ness Ziona, Israel. Pharmaseed Ltd, 74047, Ness Ziona, Israel. Department of Translational Sciences, Imaging Research, AbbVie Inc., 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Department of Translational Sciences, Imaging Research, AbbVie Inc., 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Data and Statistical Sciences, AbbVie Deutschland GmbH & Co. KG, Neuroscience Research, 67061, KnollstrasseLudwigshafen, Germany. Data and Statistical Sciences, AbbVie Deutschland GmbH & Co. KG, Neuroscience Research, 67061, KnollstrasseLudwigshafen, Germany. Discovery Biology, AbbVie Deutschland GmbH & Co. KG, Neuroscience Research, 67061, Knollstrasse, Ludwigshafen, Germany. Discovery Biology, AbbVie Deutschland GmbH & Co. KG, Neuroscience Research, 67061, Knollstrasse, Ludwigshafen, Germany. Discovery Biology, AbbVie Deutschland GmbH & Co. KG, Neuroscience Research, 67061, Knollstrasse, Ludwigshafen, Germany. Department of Drug Metabolism, Pharmacokinetics and Bioanalysis, AbbVie Deutschland GmbH & Co. KG, 67061, Knollstrasse, Ludwigshafen, Germany. Department of Drug Metabolism, Pharmacokinetics and Bioanalysis, AbbVie Deutschland GmbH & Co. KG, 67061, Knollstrasse, Ludwigshafen, Germany. Department of Drug Metabolism, Pharmacokinetics and Bioanalysis, AbbVie Deutschland GmbH & Co. KG, 67061, Knollstrasse, Ludwigshafen, Germany. AbbVie Biologics, AbbVie Bioresearch Center, 100 Research Drive, Worcester, MA, 01605, USA. AbbVie Biologics, AbbVie Bioresearch Center, 100 Research Drive, Worcester, MA, 01605, USA. Preclinical Safety, AbbVie Inc, 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Department of Neuroscience Development, AbbVie Inc, 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Department of Neuroscience Development, AbbVie Inc, 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Department of Neuroscience Development, AbbVie Inc, 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Department of Translational Sciences, Imaging Research, AbbVie Inc., 1 North Waukegan Rd, North Chicago, IL, 60064, USA. Division of Experimental and Translational Neuroscience, Krembil Brain Institute & University Health Network, Toronto, ON, M5T 0S8, Canada. Division of Neurosurgery, Department of Surgery, University of Toronto, Toronto, ON, M5T 2S8, Canada. Department of Neuroscience Development, AbbVie Inc, 1 North Waukegan Rd, North Chicago, IL, 60064, USA.
 Ondokuz Mayıs University Faculty of Medicine Department of Neurology, Samsun, Turkey. Ondokuz Mayıs University Graduate School of Education, Department of Neuroscience, Samsun, Turkey. Ondokuz Mayıs University Faculty of Medicine Department of Neurology, Samsun, Turkey. Karadeniz Technical University Faculty of Medicine Department of Neurology, Trabzon, Turkey. Van Yüzüncü Yıl University Faculty of Medicine Department of Neurology, Van, Turkey. Gaziantep University Faculty of Medicine Department of Neurology, Gaziantep, Turkey. İzmir Katip Çelebi University Faculty of Medicine Department of Neurology, İzmir, Turkey. İzmir Katip Çelebi University Faculty of Medicine Department of Neurology, İzmir, Turkey. Health Sciences University Haydarpaşa Numune Training and Research Hospital, Department of Neurology, İstanbul, Turkey. Ege University Faculty of Medicine Department of Neurology, İzmir, Turkey. Kocaeli University Faculty of Medicine Department of Neurology, Kocaeli, Turkey. Kocaeli University Faculty of Medicine Department of Neurology, Kocaeli, Turkey. Bursa High Specialization Training and Research Hospital Neurology Clinic, Bursa, Turkey. Sakarya University Faculty of Medicine, Sakarya Training and Research Hospital Neurology Clinic, Sakarya, Turkey. Trakya University Faculty of Medicine Department of Neurology, Edirne, Turkey. Health Sciences University Haseki Training and Research Hospital Neurology Clinic, İstanbul, turkey. Health Sciences University Ankara Gülhane Training and Research Hospital Neurology Clinic, Ankara, Turkey. Ankara City Hospital Neurology Clinic, Ankara, Turkey. Health Sciences University Bağcılar Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Health Sciences University Bağcılar Training and Research Hospital Neurology Clinic, İstanbul, Turkey. Ankara Gaziler Physical Therapy Rehabilitation Training and Research Hospital Neurology Clinic, Ankara, Turkey. Mersin University Faculty of Medicine Department of Neurology, Mersin, Turkey. Bolu İzzet Baysal University Faculty of Medicine Department of Neurology, Bolu, Turkey. Çanakkale On Sekiz Mart University Faculty of Medicine Department of Neurology, Çanakkale, Turkey. Erciyes University Faculty of Medicine Department of Neurology, Kayseri, Turkey. Ankara Training and Research Hospital Neurology Clinic, Ankara, Turkey. Bursa High Specialization Training and Research Hospital Neurology Clinic, Bursa, Turkey. Cumhuriyet University Faculty of Medicine Department of Neurology, Sivas, Turkey. Bezmi Alem Vakıf University Faculty of Medicine Department of Neurology, İstanbul, Turkey. Namık Kemal University Faculty of Medicine Department of Neurology, Tekirdağ, Turkey. Atatürk University Faculty of Medicine Department of Neurology, Erzurum, Turkey. Marmara University Faculty of Medicine Department of Neurology, İstanbul, Turkey. Ankara Başkent University Faculty of Medicine Department of Neurology, Ankara, Turkey. Ankara Gazi University Faculty of Medicine Department of Neurology, Ankara, Turkey. Medipol University, Faculty of Pharmacy, Istanbul, Turkey. Ondokuz Mayıs University, Faculty of Arts and Sciences, Department of Statistics, Samsun, Turkey.
 BlueClinical, Ltd, Senhora da Hora, 4460-439, Matosinhos, Portugal. ritabsgouveia@gmail.com. Faculty of Medicine, MedInUP-Center for Drug Discovery and Innovative Medicines, University of Porto, Porto, Portugal. ritabsgouveia@gmail.com. Neurology Department, Hospital Pedro Hispano, ULS Matosinhos, Matosinhos, Portugal. EPIUnit, Institute of Public Health, University of Porto, Porto, Portugal. Department of Mathematics, University of Aveiro, Aveiro, Portugal. BlueClinical, Ltd, Senhora da Hora, 4460-439, Matosinhos, Portugal. Faculty of Medicine, MedInUP-Center for Drug Discovery and Innovative Medicines, University of Porto, Porto, Portugal.
 Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Department of Neurology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands. Department of Medical Microbiology and Infection Prevention, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Department of Neurology, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands.
 Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Clinical Neuroscience, Karolinska Institute, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. wangyanqing@shmu.edu.cn. Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Institutes of Integrative Medicine, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. jwangf@shmu.edu.cn.
 Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA. Buffalo Neuroimaging Analysis Center (BNAC), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA. Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA. Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA. Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA. Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA. Jacobs Multiple Sclerosis Center for Treatment and Research (JMSCTR), Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14202, USA.
 Department of Psychiatry and Biobehavioral Sciences, Intellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States. Division of Neuroscience, IRCCS, San Raffaele Hospital, Milan, Italy. Department of Psychiatry and Biobehavioral Sciences, Intellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States. Department of Pathobiochemistry, Osaka Medical and Pharmaceutical University, Osaka, Japan. Hirono Satellite, Isotope Science Center, The University of Tokyo, Fukushima, Japan. Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States. Division of Neuroscience, IRCCS, San Raffaele Hospital, Milan, Italy. Department of Psychiatry and Biobehavioral Sciences, Intellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States. Brain Research Institute, University of California, Los Angeles, Los Angeles, United States. Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, United States. Molecular Biology Institute, University of California, Los Angeles, Los Angeles, United States.
 Departamento de Ciencias Químico-Biológicas, Escuela de Ciencias, Universidad de las Américas Puebla, Ex-Hda. de Santa Catarina Mártir s/n, San Andrés Cholula, 72820, Puebla, Mexico. jessica.flood@udlap.mx. Departamento de Ciencias Químico Biológicas/DIFUS, Universidad de Sonora, Mexico. Departamento de Ciencias Químico-Biológicas, Escuela de Ciencias, Universidad de las Américas Puebla, Ex-Hda. de Santa Catarina Mártir s/n, San Andrés Cholula, 72820, Puebla, Mexico. jessica.flood@udlap.mx.
 Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Pathology, Faculty of Veterinary Medicine, Beni-Suef University (BSU), Beni-Suef, Egypt. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Division of Pathophysiology, Department of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Toxicology and Forensic Medicine, College of Veterinary Medicine, Benha University, Qalyubia, Egypt. Roy J. Carver Biotechnology Center, University of Illinois Urbana-Champaign, Urbana, IL, USA. Division of Pathophysiology, Department of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Beckman Institute for Advanced Science and Technology, Urbana, IL, USA.
 Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China. Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China. Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China. Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China. Department of Dermatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. yuervictory@163.com. Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China. yuervictory@163.com. Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China. shiyuling1973@tongji.edu.cn. Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China. shiyuling1973@tongji.edu.cn.
 The Warren Alpert Medical School of Brown University, Providence, RI, USA. Department of Dermatology, The Warren Alpert Medical School, Brown University, The Warren Alpert Medical School of Brown University, 339 Eddy Street, Providence, RI, 02903, USA. The Warren Alpert Medical School of Brown University, Providence, RI, USA. The Warren Alpert Medical School of Brown University, Providence, RI, USA. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Department of Dermatology, The Warren Alpert Medical School, Brown University, The Warren Alpert Medical School of Brown University, 339 Eddy Street, Providence, RI, 02903, USA. Division of Rheumatology, The Warren Alpert Medical School of Brown University, Providence, RI, USA. Department of Dermatology, The Warren Alpert Medical School, Brown University, The Warren Alpert Medical School of Brown University, 339 Eddy Street, Providence, RI, 02903, USA. Department of Epidemiology, School of Public Health, Brown University, Providence, RI, USA. Department of Dermatology, The Warren Alpert Medical School, Brown University, The Warren Alpert Medical School of Brown University, 339 Eddy Street, Providence, RI, 02903, USA. eunyoung_cho@brown.edu. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. eunyoung_cho@brown.edu. Department of Epidemiology, School of Public Health, Brown University, Providence, RI, USA. eunyoung_cho@brown.edu.
 Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Division of Rheumatology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. ME Gastro, Derm and Rheuma, Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Division of Rheumatology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. Division of Rheumatology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
 Department of Otolaryngology, Head and Neck Surgery, The Affiliated Bozhou Hospital of Anhui Medical University, China; Scientific research and experiment center, The Affiliated Bozhou Hospital of Anhui Medical University, China. Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei, Anhui, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China; Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei, Anhui, China. Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Electronic address: panhaifeng@ahmu.edu.cn. Department of Ophthalmology, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, Anhui, China; Department of clinical medicine, The Second School of Clinical Medicine, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, China. Electronic address: fantsao@outlook.com.
 Infectious Diseases Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Infectious Diseases Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Institute of Hematology "L. e A. Seràgnoli", IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. Institute of Hematology "L. e A. Seràgnoli", IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Rome, Italy. National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Rome, Italy. National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Rome, Italy. Infectious Disease Unit, IRCCS Humanitas Research Hospital, Milan, Italy. Department of Biomedical Sciences, Humanitas University, Milan, Italy. Infectious Diseases Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Infectious Diseases Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. Microbiology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Infectious Disease Unit, IRCCS Humanitas Research Hospital, Milan, Italy. Department of Biomedical Sciences, Humanitas University, Milan, Italy. National Institute for Infectious Diseases "Lazzaro Spallanzani", IRCCS, Rome, Italy. Institute of Hematology "L. e A. Seràgnoli", IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. Infectious Diseases Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. Infectious Diseases Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.

 State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. Department of Neurosurgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China. Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, 610072, China. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. huan_xiong@163.com. Department of Neurosurgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China. huan_xiong@163.com. Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, 610072, China. huan_xiong@163.com. State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, 610041, China. peng.lei@scu.edu.cn.
 Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Vascular Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Neurology, Shanxi Provincial People's Hospital, No. 29 Shuangtasi Street, Taiyuan, Hebei 030012, Shanxi, China. Department of Rheumatology and Clinical Immunology, the Affiliated Hospital of Qingdao University, Qingdao, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Department of Neurology, Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Electronic address: 13933008784@163.com.
 Facultad de Ciencias Naturales y Matemáticas, Universidad de Ibagué, Carrera 22 Calle 67, Ibagué 730002, Colombia. Centro Integrativo de Biología y Química Aplicada (CIBQA), Universidad Bernardo O'Higgins, General Gana 1702, Santiago 8370854, Chile. Faculty of Medicine and Science, Universidad San Sebastián, Lota 2465, Santiago 7510157, Chile. Faculty of Sciences, Universidad de Chile, Las Palmeras 3425, Santiago 7800024, Chile.
 Founder and President, Morris Formulations, LLC, Miami, FL, USA. Founder and President, 7 Story Media, LLC, Sunrise, FL, USA.
 Psychiatric Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran. Iranian Center of Neurological Research, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran; Neuroscience Research Center, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Psychiatric Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran. School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Islamic Azad University, Tehran Medical Branch, Tehran, Iran. Department of Psychiatry, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Psychiatric Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran; School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Psychiatry, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran. Psychiatric Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: s.akhond@neda.net.
 Old Medical School, Usher Institute, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, UK. m.muckian@sms.ed.ac.uk. Old Medical School, Usher Institute, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, UK. MRC Human Genetics Unit, Institute of Genetics and Cancer, Western General Hospital, University of Edinburgh, Crewe Road, Edinburgh, EH4 2XU, UK. Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, B15 2TT, UK. Old Medical School, Usher Institute, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, UK. Old Medical School, Usher Institute, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, UK. Human Technopole, Viale Rita Levi-Montalcini, 1, Area MIND-Cargo 6, 20157, Milan, Italy.
 Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, Bochum, Germany. Department of Psychiatry and Psychotherapy, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany. Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, Bochum, Germany. Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, Bochum, Germany. Department of Neurology, University Hospital Knappschaftskrankenhaus Bochum, Ruhr University Bochum, Bochum, Germany.
 MANAS Lab, School of Computing and Electrical Engineering (SCEE), Indian Institute of Technology (IIT) Mandi, India. Electronic address: d16044@students.iitmandi.ac.in. Department of Mathematics and Statistics, Indian Institute of Technology Kanpur, India. Learning Research and Development Center, University of Pittsburgh, USA. Learning Research and Development Center, University of Pittsburgh, USA. MANAS Lab, School of Computing and Electrical Engineering (SCEE), Indian Institute of Technology (IIT) Mandi, India. MANAS Lab, School of Computing and Electrical Engineering (SCEE), Indian Institute of Technology (IIT) Mandi, India.
 Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA. Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science (BITS), Brown University, Providence, RI 02912, USA. Center for Computational Molecular Biology, Brown University, Providence, RI 02906, USA. Department of Pathology and Laboratory Medicine, Warren Alpert Medical School of Brown University, Providence, RI 02912, USA. Department of Pathology and Laboratory Medicine, Rhode Island Hospital and Lifespan Academic Medical Center, Providence, RI 02903, USA. Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA. Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA. UCONN Health Comprehensive Multiple Sclerosis Center, Department of Neurology, University of Connecticut School of Medicine, Farmington, CT 06030, USA. Division of Multiple Sclerosis and Translational Neuroimmunology, Department of Neurology, University of Connecticut School of Medicine, Farmington, CT 06030, USA. Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA. Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science (BITS), Brown University, Providence, RI 02912, USA. Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA. Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA. Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science (BITS), Brown University, Providence, RI 02912, USA. UCONN Health Comprehensive Multiple Sclerosis Center, Department of Neurology, University of Connecticut School of Medicine, Farmington, CT 06030, USA. Division of Multiple Sclerosis and Translational Neuroimmunology, Department of Neurology, University of Connecticut School of Medicine, Farmington, CT 06030, USA. Center for Computational Molecular Biology, Brown University, Providence, RI 02906, USA. Department of Pathology and Laboratory Medicine, Warren Alpert Medical School of Brown University, Providence, RI 02912, USA. Department of Pathology and Laboratory Medicine, Rhode Island Hospital and Lifespan Academic Medical Center, Providence, RI 02903, USA. Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA. Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science (BITS), Brown University, Providence, RI 02912, USA.
 Department of Biochemistry, Erciyes University School of Medicine, Kayseri, Turkey. emelk@erciyes.edu.tr. Department of Neurology, Erciyes University School of Medicine, Kayseri, Turkey. emelk@erciyes.edu.tr. Department of Biochemistry, Erciyes University School of Medicine, Kayseri, Turkey. Department of Biochemistry, Erciyes University School of Medicine, Kayseri, Turkey. Department of Biostatistics, Erciyes University School of Medicine, Kayseri, Turkey. Drug Application and Research Center (ERFARMA), Erciyes University, Kayseri, Turkey. Department of Medical Biology, Erciyes University School of Medicine, Kayseri, Turkey. Betul Ziya Eren Genome and Stem Cell Center, Kayseri, Turkey.
 Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark. Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark. Institute of Clinical Medicine, Faculty of Health and Medical Science, Copenhagen University, Denmark. Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark. Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark. Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark. Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet, Copenhagen, Denmark.
 From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. From the Lerner College of Medicine (S.L.), Cleveland Clinic, OH; and Neurological Institute (A.K.C., A.S., J.R., M.M., D.O., A.D.), Cleveland Clinic, OH. adhawan@qmed.ca.
 West Virginia University West Virginia University West Virginia University Hospitals WVU
 College of Medicine, University of Florida, Gainesville, Florida. Department of Dermatology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania. Department of Dermatology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania. Department of Dermatology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania. Department of Pathology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania. Department of Dermatology, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania. Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, Pennsylvania.
 Dr. Halla Tariq, MBBS., 807 Eucalyptus Court Lodi California 95242, US. Dr. Aroosha Ihsan, MBBS., Anatomy Lecturer, Wah Medical College, Pakistan. Dr. Asadullah Khan, FCPS (Medicine), FCPS, MRCP, SCE (Rheumatology)., Assistant Professor and Head of Rheumatology, Bolan Medical College, Quetta, Pakistan. Dr. Roshila Shamim, FCPS (Medicine), FCPS (Rheumatology). Karachi, Pakistan.
 Kathmandu Medical College and Teaching Hospital, Sinamangal, Kathmandu, Nepal. Kathmandu Medical College and Teaching Hospital, Sinamangal, Kathmandu, Nepal. Department of Pediatrics, Kathmandu Medical College and Teaching Hospital, Sinamangal, Kathmandu, Nepal. Department of Pediatrics, Kathmandu Medical College and Teaching Hospital, Sinamangal, Kathmandu, Nepal. Kathmandu Medical College and Teaching Hospital, Sinamangal, Kathmandu, Nepal. Kathmandu Medical College and Teaching Hospital, Sinamangal, Kathmandu, Nepal.
 Emeritus Chairman, Department of Medical Genetics, Henry Ford Hospital, Detroit, Michigan Division of Genetics, Birth Defects and Metabolism, Department of Pediatrics, Ann and Robert H Lurie Children's Hospital of Chicago, Chicago, Illinois
 Department of Neurology, UMC Utrecht Brain Center Rudolf Magnus, Utrecht, The Netherlands.
 National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN. National Institute of Neurological Disorders and Stroke (RTB), NIH, Bethesda, MD; Department of Neurology (SMB), University of Minnesota, Minneapolis; Department of Neurology (GJE), Emory University, Atlanta, GA; Department of Neurology and Rehabilitation Medicine (BK), University of Cincinnati, OH; Department of Neurology (NR), University of California, San Francisco; Department of Neurology (EM-L), University of Miami, FL; Department of Neurology (OAH), University of Texas, Houston; Department of Neurology (TTAP), Kaiser Permanente Colorado, Denver; Verana Health (MR, AT, AL, SKK), San Francisco, CA; American Academy of Neurology (KBL, AM, BS), Minneapolis, MN; and Department of Neurology (LKJ), Mayo Clinic, Rochester, MN.
 Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Research and Development Department, Sina Medical Biochemistry Technologies Co. Ltd., Shiraz, 7178795844, Iran. Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Microbiology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran. Department of Radiology, Charité - Universitätsmedizin Berlin, 10117, Berlin, Germany. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran. Department of Biological Sciences and Bioengineering, Nano Bio High-Tech Materials Research Center, Inha University, Incheon, 22212, Republic of Korea. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. hamidreza.zlpr1998@gmail.com. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran. hamidreza.zlpr1998@gmail.com. Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. b.hajikhani@gmail.com.
 Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London, United Kingdom. Preventive Neurology Unit, Wolfson Institute of Population Health, Faculty of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Department of Neurology, Royal London Hospital, Barts Health NHS Trust, London, United Kingdom.
 Henan Joint International Research Laboratory of Stem Cell Medicine, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road #601, Xinxiang City, 453003, Henan Province, China. Department of Community Health, Advanced Medical and Dental Institute, Universiti Sains Malaysia, 13200, Kepala Batas, Pulau Pinang, Malaysia. College of Life Sciences and Technology, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road # 601, Xinxiang, 453003, China. College of Life Sciences and Technology, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road # 601, Xinxiang, 453003, China. College of Life Sciences and Technology, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road # 601, Xinxiang, 453003, China. College of Life Sciences and Technology, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road # 601, Xinxiang, 453003, China. Henan Joint International Research Laboratory of Stem Cell Medicine, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road #601, Xinxiang City, 453003, Henan Province, China. College of Medical Engineering, Xinxiang Medical University, Xinxiang, 453003, China. Henan Joint International Research Laboratory of Stem Cell Medicine, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road #601, Xinxiang City, 453003, Henan Province, China. liuyanli198512@163.com. College of Life Sciences and Technology, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road # 601, Xinxiang, 453003, China. liuyanli198512@163.com. Henan Joint International Research Laboratory of Stem Cell Medicine, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road #601, Xinxiang City, 453003, Henan Province, China. linjtlin@126.com. College of Life Sciences and Technology, Stem Cell and Biotherapy Engineering Research Center of Henan, Xinxiang Medical University, East of JinSui Road # 601, Xinxiang, 453003, China. linjtlin@126.com. College of Medical Engineering, Xinxiang Medical University, Xinxiang, 453003, China. linjtlin@126.com.
 Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China. Second Clinical Medical College, Nanchang University, Nanchang, China. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China. Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
 Augusta University / University of Georgia Medical Partnership National Health Service
 Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Division of Neurology, Department of Neurology, Neuro Muscular Center, National Omuta Hospital, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Division of Neurology, Department of Neurology, Neuro Muscular Center, National Omuta Hospital, Fukuoka, Japan.
 Kathmandu Medical College. Bir Hospital, Kathmandu, Nepal. Kathmandu Medical College. Bir Hospital, Kathmandu, Nepal.
 Department of Neurosurgery, Tokyo Medical and Dental University, Tokyo, Japan. Department of Neurosurgery, Tokyo Medical and Dental University, Tokyo, Japan. Electronic address: inamnsrg@tmd.ac.jp. Department of Neurosurgery, Tokyo Medical and Dental University, Tokyo, Japan. Department of Psychiatry and Behavioral Sciences, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. Department of Neurosurgery, Tokyo Medical and Dental University, Tokyo, Japan.
 Department of Cardiology, Fortis Hospital, Mohali, Punjab, India. Department of Cardiology, Fortis Hospital, Mohali, Punjab, India.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. The First Affiliated Hospital, Shanxi University of Chinese Medicine, Taiyuan, 030024, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. Department of Anatomy and Cell Biology, Department of Neurological Surgery, Spinal Cord and Brain Injury Research Group, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. Huashan Hospital, Fudan University, Shanghai, 200025, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. bozhang@sxtcm.edu.cn. Health Commission of Shanxi Province, Taiyuan, 030001, China. bozhang@sxtcm.edu.cn. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. macungen@sxtcm.edu.cn. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong, 030619, China. chaizhi@sxtcm.edu.cn.
 The Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. Division of Pediatric Neurology, Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea. Department of Ophthalmology, Konyang University Hospital, Konyang University College of Medicine, Daejeon, Korea. The Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. The Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. The Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. sklee219@yuhs.ac.
 From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. From the Bruce Lefroy Centre, Murdoch Children's Research Institute (W.S.L., S.S., P.J.L.); Department of Paediatrics (W.S.L., E.M-L., S.S., W.M., A.S.H., P.J.L., R.J.L.), The University of Melbourne; Department of Neurology (E.M-L., A.S.H., R.J.L.), The Royal Children's Hospital; Department of Anatomical Pathology (C.D.A.), The Royal Children's Hospital; Department of Neurosurgery (W.M.), The Royal Children's Hospital, Parkville, Australia. richard.leventer@rch.org.au.
 Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at UTHealth, Houston, Texas. Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at UTHealth, Houston, Texas. Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at UTHealth, Houston, Texas. Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at UTHealth, Houston, Texas. Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at UTHealth, Houston, Texas. Electronic address: anthony.l.estrera@uth.tmc.edu.
 Department of Neurology, Keio University School of Medicine, Tokyo, Japan; Department of Neurology, The Jikei University School of Medicine, Tokyo, Japan. Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, Yokohama, Japan. Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan. Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan; Department of Genome Medicine Development, Medical Genome Center, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan. Department of Neurology, Keio University School of Medicine, Tokyo, Japan. Electronic address: sgsuzuki@keio.jp.
 Department of Internal Medicine Nepalese Army Institute of Health Sciences-College of Medicine Kathmandu Nepal. Department of Radio-diagnosis and Imaging National Academy of Medical Sciences Kathmandu Nepal. Department of Radio-diagnosis and Imaging National Academy of Medical Sciences Kathmandu Nepal. Department of Radio-diagnosis and Imaging National Academy of Medical Sciences Kathmandu Nepal. Department of Internal Medicine Nepalese Army Institute of Health Sciences-College of Medicine Kathmandu Nepal.
 Central Veterinary Research Laboratory, Dubai, United Arab Emirates. Faculty of Dentistry, The University of Hong Kong, Hong Kong Special Administrative Region, China. Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. Central Veterinary Research Laboratory, Dubai, United Arab Emirates. Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. State Key Laboratory of Emerging Infectious Diseases, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. Department of Clinical Microbiology and Infection Control, The University of Hong Kong-Shenzhen Hospital, Shenzhen 518053, China. Carol Yu Centre for Infection, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. Centre for Virology, Vaccinology and Therapeutics, Hong Kong Science and Technology Park, Hong Kong Special Administrative Region, China. Central Veterinary Research Laboratory, Dubai, United Arab Emirates. Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China. Doctoral Program in Translational Medicine and Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan. The iEGG and Animal Biotechnology Research Center, National Chung Hsing University, Taichung 402, Taiwan.
 Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Scottsdale, AZ, USA. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Scottsdale, AZ, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Immunology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, University of Virginia, Charlottesville, VA, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Ophthalmology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Cleveland Clinic, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA.
 Division of Infectious Diseases, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115, USA; Harvard Graduate Program in Virology, Boston, MA 02115, USA; Center for Integrated Solutions to Infectious Diseases, Broad Institute and Harvard Medical School, Cambridge, MA 02115, USA; Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA. Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK. Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK. Electronic address: mpw1001@cam.ac.uk. Division of Infectious Diseases, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115, USA; Harvard Graduate Program in Virology, Boston, MA 02115, USA; Center for Integrated Solutions to Infectious Diseases, Broad Institute and Harvard Medical School, Cambridge, MA 02115, USA; Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: bgewurz@bwh.harvard.edu.
 Tešanj General Hospital, Tešanj, Bosnia and Herzegovina. Health Center of Tuzla, Tuzla, Bosnia and Herzegovina. University Clinical Hospital of Mostar, Mostar, Bosnia and Herzegovina. General Hospital "Prim.dr. Abdulah Nakaš", Sarajevo, Bosnia and Herzegovina. Public Health Institute Hospital Trebinje, Trebinje, Bosnia and Herzegovina. Zenica Cantonal Hospital, Zenica, Bosnia and Herzegovina. General Hospital "Prim.dr. Abdulah Nakaš", Sarajevo, Bosnia and Herzegovina. School of Medicine, University of Mostar, Mostar, Bosnia and Herzegovina. Public Institution Sarajevo Canton Health Center, Sarajevo, Bosnia and Herzegovina.
 Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute, UCLouvain, Université Catholique de Louvain, Brussels, Belgium. Department of Oncology, University of Lausanne and Ludwig Institute for Cancer Research, Lausanne, Switzerland. SIB Swiss Institute of Bioinformatics, Lausanne, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Division of Clinical Pathology, Diagnostic Department, University Hospitals of Geneva, Geneva, Switzerland. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Division of Clinical Pathology, Diagnostic Department, University Hospitals of Geneva, Geneva, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Department of Pathology and Immunology, Geneva Medical School, Geneva, Switzerland. Radio-Oncology Laboratory, Department of Oncology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Department of Epidemiology and Health Systems, Centre for Primary Care and Public Health (Unisanté), University of Lausanne, Lausanne, Switzerland. Institute for Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Luebeck, Germany. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Division of Clinical Pathology, Diagnostic Department, University Hospitals of Geneva, Geneva, Switzerland. Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute, UCLouvain, Université Catholique de Louvain, Brussels, Belgium. Department of Pathology and Immunology, Geneva Medical School, Geneva, Switzerland. Department of Oncology, University of Lausanne and Ludwig Institute for Cancer Research, Lausanne, Switzerland. Laboratories of Neuroimmunology, Service of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
 Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Clinical Laboratory, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile; Neurology, Hospital Sótero del Río, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile; Neurology, Hospital Sótero del Río, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neuropediatrics, Clínica Las Condes, Santiago, Chile. Neurology, Clínica Indisa, Santiago, Chile. Neurology, Facultad de Medicina, Universidad Católica del Norte, campus Hospital de Coquimbo, Coquimbo, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neuroradiology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neuroradiology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile. Neurology, Pontificia Universidad Católica de Chile, Santiago, Chile; Neurology, Hospital Sótero del Río, Santiago, Chile. Electronic address: ethelciampi@gmail.com.
 Departement Neuro-Urologie, Kliniken Hartenstein - UKR, Bad Wildungen, Deutschland. jfkutzenberger@aol.com. , Fontanestr. 16, 34596, Bad Zwesten, Deutschland. jfkutzenberger@aol.com. Neuro-Urologie, Schön Klinik Vogtareuth, Vogtareuth, Deutschland. Zentrum für Neuro-Urologie, Kliniken Beelitz, Beelitz-Heilstätten, Deutschland. Neuro-Urologie, REHAB Basel, Klinik für Neurorehabilitation und Paraplegiologie, Basel, Schweiz. Klinik für Urologie und Neuro-Urologie, Unfallkrankenhaus Berlin, Berlin, Deutschland. Klinik für Paraplegiologie, Department für Orthopädie, Unfallchirurgie und Paraplegiologie, Universität Heidelberg, Heidelberg, Deutschland. Universitätsklinikum Bonn, Sektion Neuro-Urologie/, Klinik für Urologie und Kinderurologie und Neuro-Urologie, Johanniter Neurologisches Rehabilitationszentrum Godeshöhe e. V., Bonn, Deutschland.
 Clinical Pharmacy Department, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, Egypt. Pharmaceutical Sciences Department, Faculty of Pharmacy, AlMaarefa University, Riyadh, Saudi Arabia. Microbiology and Immunology Department, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt. Microbiology and Immunology Department, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt. Pharmacy Practice Department, Faculty of Pharmacy, University of Tabuk, Tabuk, Saudi Arabia. Biochemistry Department, Faculty of Pharmacy, Modern University for Technology and Information (MTI), Cairo, Egypt. Forensic Medicine and Clinical Toxicology Department, Faculty of Medicine, Tanta University, Tanta, Egypt. Clinical Medical Sciences Department, College of Medicine, Dar Al Uloom University, Riyadh, Saudi Arabia. Basic Medical Science Department, College of Medicine, Dar Al Uloom University, Riyadh, Saudi Arabia. Medical Microbiology and Immunology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Pharmacology and Toxicology Department, Faculty of Pharmacy, Modern University for Technology and Information (MTI), Cairo, Egypt. Biology Department, Faculty of Science, Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Saudi Arabia. Pharmacology and Toxicology Department, Faculty of Pharmacy, Egyptian Russian University, Cairo, Egypt. Pharmacology and Toxicology Department, Faculty of Pharmacy, Modern University for Technology and Information (MTI), Cairo, Egypt. Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Sadat City (USC), Menoufia, Egypt.
 Department of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario, L8S 4M1, Canada. kun.tian@uniroma1.it. Michael G. DeGroote Institute of Infectious Disease Research, McMaster University, Hamilton, Ontario, L8N 3Z5, Canada. Department of Chemistry, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185, Rome, Italy. Hong Kong Quantum AI Lab, 17 Science Park West Avenue, Hong Kong, China. Department of Chemistry, Hong Kong University, Hong Kong, China. Faculty of Land and Food Systems, The University of British Columbia, Vancouver, British Columbia, V6T 1Z4, Canada. Department of Chemistry, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185, Rome, Italy. Department of Chemical Science and Pharmaceutical Technologies, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185, Rome, Italy. Centre for Molecular and Materials Science, TRIUMF, 4004 Wesbrook Mall, Vancouver, BC, V6T 2A3, Canada. Faculty of Land and Food Systems, The University of British Columbia, Vancouver, British Columbia, V6T 1Z4, Canada. Department of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario, L8S 4M1, Canada. kun.tian@uniroma1.it. Department of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario, L8S 4M1, Canada. kun.tian@uniroma1.it. Michael G. DeGroote Institute of Infectious Disease Research, McMaster University, Hamilton, Ontario, L8N 3Z5, Canada. Department of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario, L8S 4M1, Canada. kun.tian@uniroma1.it. Faculty of Land and Food Systems, The University of British Columbia, Vancouver, British Columbia, V6T 1Z4, Canada. Department of Chemical Science and Pharmaceutical Technologies, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185, Rome, Italy. Department of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario, L8S 4M1, Canada. kun.tian@uniroma1.it. Faculty of Land and Food Systems, The University of British Columbia, Vancouver, British Columbia, V6T 1Z4, Canada. School of Physical and Chemical Sciences, Queen Mary University of London, London E1 4NS, UK.
 Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. alessandro.dinoto@univr.it. Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Department of Neurology, John Radcliffe Hospital, Oxford University Hospitals, Oxford, UK. Oxford Epilepsy Research Group, University of Oxford, Oxford, UK. Department of Laboratory Medicine and Pathology, Rochester, MN, USA. Department of Neurology Mayo Clinic, Rochester, MN, USA. Department of Clinical and Experimental Sciences, Neurology Unit, University of Brescia, Brescia, Italy. Department of Clinical and Experimental Sciences, Neurology Unit, University of Brescia, Brescia, Italy. Department of Clinical and Experimental Sciences, Neurology Unit, University of Brescia, Brescia, Italy. Neurology Unit, Poliambulanza Hospital, Brescia, Brescia, Italy. Multiple Sclerosis Center, ASST - Spedali Civili of Brescia, Brescia, Montichiari, Italy. Multiple Sclerosis Center, ASST - Spedali Civili of Brescia, Brescia, Montichiari, Italy. Multiple Sclerosis Center "A. Cardarelli" Hospital, Naples, Italy. Neurological Clinic and Stroke Unit "A. Cardarelli" Hospital, Naples, Italy. Department of Clinical and Experimental Sciences, Neurology Unit, University of Brescia, Brescia, Italy. Encephalitis Society, 32 Castlegate, Malton, UK. Department of Clinical Infection, Microbiology and Immunology, University of Liverpool , Liverpool, England. Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. Section of Clinical Biochemistry, University of Verona, Verona, Italy. Service of Laboratory Medicine, Pederzoli Hospital, Peschiera del Garda, Verona, Italy. Section of Clinical Biochemistry, University of Verona, Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. Department of Neurosciences, Biomedicine and Movement Sciences, Neurology Unit, University of Verona, Verona, Italy. sara.mariotto@gmail.com.
 Department of Biophysics, Panjab University, Chandigarh, India. Department of Biophysics, Panjab University, Chandigarh, India. Department of Biophysics, Panjab University, Chandigarh, India. Department of Biophysics, Panjab University, Chandigarh, India. Centre for Biomedical Engineering, Indian Institute of Technology, New Delhi, India. School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, India. Department of Biochemistry and Biophysics, Texas A & M University, College Station, TX, 77843, USA. Department of Biophysics, Panjab University, Chandigarh, India. aaksgarg@gmail.com. University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India. aaksgarg@gmail.com. University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India. gurpalsingh.ips@gmail.com. Department of Biophysics, Panjab University, Chandigarh, India. barnwal@pu.ac.in.
 Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Dutch National Health Care Institute (ZIN), Diemen, The Netherlands. Copenhagen Centre for Regulatory Science (CORS), Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, Kobenhavn, Denmark. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Copenhagen Centre for Regulatory Science (CORS), Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, Kobenhavn, Denmark. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands. Division Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands w.g.goettsch@uu.nl. Dutch National Health Care Institute (ZIN), Diemen, The Netherlands.
 Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Ophthalmology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA flanagan.eoin@mayo.edu. Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
 Department of Family and Community Medicine, University of Toronto, Toronto, Canada. Faculty of Medicine, Department of Internal Medicine, University of British Columbia, Vancouver, Canada. Canadian HIV Trials Network, University of British Columbia, Vancouver, Canada. Department of Psychology, University of British Columbia, Kelowna, Canada. Canadian AIDS Society, Ottawa, Canada. Department of Internal Medicine, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada. CancerCare Manitoba, Winnipeg, Canada. Canadian HIV Trials Network, University of British Columbia, Vancouver, Canada. MJardin Group Canada, Toronto, Canada. Canadian AIDS Society, Ottawa, Canada. Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada. Centre for Addiction and Mental Health, Institute for Mental Health Policy Research, Toronto, Canada. Department of Psychology, University of British Columbia, Kelowna, Canada. Canadian AIDS Society, Ottawa, Canada. Canadian Institute for Substance Use Research, University of Victoria, Victoria, Canada. Arthritis Society, Toronto, Canada. Department of Psychology, University of British Columbia, Kelowna, Canada. Centre for Addiction and Mental Health, Institute for Mental Health Policy Research, Toronto, Canada. Medical Cannabis Canada, Toronto, Canada. Independent Consultant, Toronto, Canada. CommParm Consulting, Inc., Barrie, Ontario, Canada. Chronic Viral Illness Service/Division of Infectious Diseases, Department of Medicine, McGill University Health Centre, Montreal, Canada. McGill Cannabis Research Centre, McGill University, Montreal, Canada. Research Institute of the McGill University Health Centre, Montreal, Canada.
 Department of Radiology, Stanford University, California, Stanford, USA. Quantitative Sciences Unit, Stanford University School of Medicine, California, Stanford, USA. Stanford University School of Medicine, California, Stanford, USA. Department of Radiology, Stanford University, California, Stanford, USA. Department of Neurology and Neurological Sciences, Stanford University, California, Stanford, USA. Department of Radiology, Stanford University, California, Stanford, USA.
 Department of Molecular Pharmaceutics, University of Utah, Salt Lake City, Utah, USA. Department of Molecular Pharmaceutics, University of Utah, Salt Lake City, Utah, USA. Department of Molecular Pharmaceutics, University of Utah, Salt Lake City, Utah, USA. Department of Molecular Pharmaceutics, University of Utah, Salt Lake City, Utah, USA. Department of Pathology, University of Utah, Salt Lake City, Utah, USA. Department of Molecular Pharmaceutics, University of Utah, Salt Lake City, Utah, USA.
 Department of Neurology, Medical University of Vienna, Vienna, Austria. gabriel.bsteh@meduniwien.ac.at. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. gabriel.bsteh@meduniwien.ac.at. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neuroradiology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences & Mental Health, Medical University of Vienna, Vienna, Austria. Department of Ophthalmology, Medical University of Vienna, Vienna, Austria.
 Department of Cardiology, Ningbo Institute of Innovation for Combined Medicine and Engineering, Lihuili Hospital Affiliated to Ningbo University, Ningbo University, Ningbo, Zhejiang, China. Department of Cardiology, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China. Clinical Research Center, First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China. Department of Cardiology, Ningbo Institute of Innovation for Combined Medicine and Engineering, Lihuili Hospital Affiliated to Ningbo University, Ningbo University, Ningbo, Zhejiang, China. Department of Cardiology, Ningbo Institute of Innovation for Combined Medicine and Engineering, Lihuili Hospital Affiliated to Ningbo University, Ningbo University, Ningbo, Zhejiang, China. Department of Cardiology, Ningbo Institute of Innovation for Combined Medicine and Engineering, Lihuili Hospital Affiliated to Ningbo University, Ningbo University, Ningbo, Zhejiang, China. Department of Cardiology, Ningbo Institute of Innovation for Combined Medicine and Engineering, Lihuili Hospital Affiliated to Ningbo University, Ningbo University, Ningbo, Zhejiang, China. hjmpin@163.com.
 Institute of Chemistry, Physical Chemistry - Complex Self-organizing Systems, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Saxony-Anhalt, Germany; Interdisciplinary Research Center HALOmem at the Martin-Luther-Universität Halle-Wittenberg, Germany. Interdisciplinary Research Center HALOmem at the Martin-Luther-Universität Halle-Wittenberg, Germany; Institute of Biochemistry, Physical Biotechnology, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany. Biocenter, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany. Department of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada. Institute of Chemistry, Physical Chemistry - Complex Self-organizing Systems, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Saxony-Anhalt, Germany; Interdisciplinary Research Center HALOmem at the Martin-Luther-Universität Halle-Wittenberg, Germany. Electronic address: dariush.hinderberger@chemie.uni-halle.de.
 Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. Department of Thoracic and Cardiovascular Surgery, Gangnam Severance Hospital, Seoul, Republic of Korea. Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. Yonsei University College of Medicine, Seoul, Republic of Korea. Center for Digital Health, Medical Science Research Institute, Kyung Hee University College of Medicine, Seoul, Republic of Korea. Department of Data Science, Sejong University College of Software Convergence, Seoul, Republic of Korea. Sungkyunkwan University School of Medicine, Suwon, Republic of Korea. Centre for Health, Performance, and Wellbeing, Anglia Ruskin University, Cambridge, UK. Parc Sanitari Sant Joan de Deu/CIBERSAM, ISCIII, Universitat de Barcelona, Fundacio Sant Joan de Deu, Sant Boi de Llobregat, Barcelona, Spain. ICREA, Pg. Lluis Companys 23, Barcelona, Spain. Department of Pediatrics, Yonsei University College of Medicine, Seoul, Republic of Korea. Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.
 Department of Pediatrics, Hacettepe University İhsan Doğramacı Children's Hospital, Ankara. Department of Pediatric Cardiology, Hacettepe University İhsan Doğramacı Children's Hospital, Ankara. Department of Pediatric Oncology, Hacettepe University Oncology Institute, Ankara, Türkiye. Department of Pediatric Oncology, Hacettepe University Oncology Institute, Ankara, Türkiye. Department of Pediatric Cardiology, Hacettepe University İhsan Doğramacı Children's Hospital, Ankara. Department of Pediatric Cardiology, Hacettepe University İhsan Doğramacı Children's Hospital, Ankara. Department of Pediatric Cardiology, Hacettepe University İhsan Doğramacı Children's Hospital, Ankara. Department of Pediatric Cardiology, Hacettepe University İhsan Doğramacı Children's Hospital, Ankara.
 Department of Obstetrics and Gynecology, Chubu Rosai Hospital, Nagoya, Japan. Department of Obstetrics and Gynecology, Chubu Rosai Hospital, Nagoya, Japan. Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan. Department of Obstetrics and Gynecology, Chubu Rosai Hospital, Nagoya, Japan. Department of Obstetrics and Gynecology, Chubu Rosai Hospital, Nagoya, Japan. Department of Obstetrics and Gynecology, Chubu Rosai Hospital, Nagoya, Japan. Department of Obstetrics and Gynecology, Chubu Rosai Hospital, Nagoya, Japan.
 Center for Clinical Genomics, Kanazawa Medical University Hospital, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan; Division of Genomic Medicine, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan. Electronic address: h-ura@kanazawa-med.ac.jp. Center for Clinical Genomics, Kanazawa Medical University Hospital, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan; Division of Genomic Medicine, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan. Division of Genomic Medicine, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan. Center for Clinical Genomics, Kanazawa Medical University Hospital, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan. Center for Clinical Genomics, Kanazawa Medical University Hospital, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan; Division of Genomic Medicine, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0923, Japan.
 Pediatric Neurology Unit, Buzzi Children's Hospital, Milan, Italy; Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy. Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. Pediatric Neurology Unit, Buzzi Children's Hospital, Milan, Italy. Pediatric Cardiology Unit, Department of Pediatric, Buzzi Children's Hospital, Milan, Italy. Pediatric Neurology Unit, Buzzi Children's Hospital, Milan, Italy. Pediatric Neurology Unit, Buzzi Children's Hospital, Milan, Italy; Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy. Pediatric Cardiology Unit, Department of Pediatric, Buzzi Children's Hospital, Milan, Italy. Electronic address: savina.mannarino@asst-fbf-sacco.it.
 Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan. Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan.
 From the Departments of Nuclear Medicine. Urology, The First Affiliated Hospital of Naval Medical University (Changhai Hospital), Shanghai, China. From the Departments of Nuclear Medicine. From the Departments of Nuclear Medicine. From the Departments of Nuclear Medicine.
 Cancer Genetics Laboratory, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address: kklonowska@bwh.harvard.edu. Cancer Genetics Laboratory, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Division of Hematology/Oncology, Cancer and Blood Disease Institute, Children's Hospital Los Angeles, Los Angeles, CA 90027, USA. Boston Dermatology and Laser Center, Massachusetts General Hospital, Boston, MA 02114, USA. Cancer Genetics Laboratory, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Center for Cancer Genomics, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Molecular Biology Core Facilities, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Department of Dermatology, Uniformed Services University, Bethesda, MA 20814, USA; Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. Department of Dermatology, Uniformed Services University, Bethesda, MA 20814, USA; Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA; Department of Dermatology, University Hospitals Cleveland Medical Center, Case Western Reserve University Cleveland, Cleveland, OH 44106, USA. Cancer Genetics Laboratory, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Division of Hospital Medicine, Barnes Jewish Hospital, Washington University in St Louis, St. Louis, MO 63110, USA. Department of Neurology and Epileptology, Children's Memorial Health Institute, Warsaw 04-736, Poland. Department of Neurology and Epileptology, Children's Memorial Health Institute, Warsaw 04-736, Poland; Research Department, Children's Memorial Health Institute, Warsaw 04-736, Poland. Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. Department of Dermatology, Uniformed Services University, Bethesda, MA 20814, USA. Cancer Genetics Laboratory, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address: dk@rics.bwh.harvard.edu.
 Retina Ward, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran. Retina Ward, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran. Retina Ward, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran. Retina Ward, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran. Retina Ward, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran.
 The Ohio State University Wexner Medical Center, Columbus, USA. The Ohio State University Wexner Medical Center, Columbus, USA. The Ohio State University Wexner Medical Center, Columbus, USA.
 Department of Orthopaedic Surgery, University of Cincinnati College of Medicine, Cincinnati, OH; Department of Orthopaedic Surgery, Warren Alpert Medical School of Brown University, Providence, RI. Electronic address: cameron_thomson@brown.edu. Department of Orthopaedic Surgery, University of Cincinnati College of Medicine, Cincinnati, OH; TriHealth Hand Surgery Specialists, Inc, Cincinnati, OH. Department of Orthopaedic Surgery, University of Cincinnati College of Medicine, Cincinnati, OH.
 1Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania; and. 2Department of Neurological Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania. 2Department of Neurological Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania.
 Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands; Department of Clinical Neurophysiology, St Antonius Hospital, Nieuwegein, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands; Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Department of Neurology, Amsterdam UMC, VU University Medical Center, Amsterdam, the Netherlands. Department of Neurology, Amsterdam UMC, VU University Medical Center, Amsterdam, the Netherlands. Department of Gastroenterology and Hepatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Amsterdam Rheumatology and Immunology Center, Location Reade, Department of Rheumatology, Amsterdam, the Netherlands. Amsterdam Rheumatology and Immunology Center, Location Reade, Department of Rheumatology, Amsterdam, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Department of Gastroenterology and Hepatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Gastroenterology and Hepatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Gastroenterology and Hepatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Dermatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Dermatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Dermatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Dermatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Dermatology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Internal Medicine, Section of Nephrology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Internal Medicine, Section of Nephrology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Internal Medicine, Section of Nephrology, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, VU University Medical Center, Amsterdam, the Netherlands. Department of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, VU University Medical Center, Amsterdam, the Netherlands. Department of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, VU University Medical Center, Amsterdam, the Netherlands; Amsterdam Rheumatology and Immunology Center, Amsterdam UMC, Department of Rheumatology and Clinical Immunology, University of Amsterdam, Amsterdam, the Netherlands. Centre for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands; Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands. Centre for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, the Netherlands. Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, the Netherlands. Department of Dermatology, Center for Blistering Diseases, University Medical Center Groningen, University Groningen, Groningen, the Netherlands. Department of Neurology, Leiden University Medical Center, Leiden, the Netherlands. Department of Neurology, Leiden University Medical Center, Leiden, the Netherlands. Department of Rheumatology, Leiden University Medical Center, Leiden, the Netherlands. Department of Rheumatology, Leiden University Medical Center, Leiden, the Netherlands. Department of Rheumatology, Leiden University Medical Center, Leiden, the Netherlands. Centre of Expertise for Lupus, Vasculitis- and Complement-mediated Systemic Diseases, Department of Internal Medicine - Nephrology Section, Leiden University Medical Centre, Leiden, the Netherlands. Department of Nephrology and Clinical Immunology, Maastricht University Medical Center, Maastricht, the Netherlands. Department of Nephrology and Clinical Immunology, Maastricht University Medical Center, Maastricht, the Netherlands. Department of Nephrology and Clinical Immunology, Maastricht University Medical Center, Maastricht, the Netherlands. Department of Neurology, Erasmus MC University Medical Center, Rotterdam, the Netherlands. Department of Neurology, Erasmus MC University Medical Center, Rotterdam, the Netherlands. Department of Neurology, Erasmus MC University Medical Center, Rotterdam, the Netherlands. Department of Dermatology, Erasmus MC University Medical Center, Rotterdam, the Netherlands. Department of Dermatology, Erasmus MC University Medical Center, Rotterdam, the Netherlands. Brain Center UMC Utrecht, Department of Neurology and Neurosurgery, Utrecht, the Netherlands. Brain Center UMC Utrecht, Department of Neurology and Neurosurgery, Utrecht, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, Amsterdam, the Netherlands; Swammerdam Institute for Life Sciences, University of Amsterdam, the Netherlands. Amsterdam Rheumatology and Immunology Center, Amsterdam UMC, Department of Rheumatology and Clinical Immunology, University of Amsterdam, Amsterdam, the Netherlands. Department of Pediatric Immunology, Rheumatology and Infectious Disease, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Electronic address: f.eftimov@amsterdamumc.nl.
 Department of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun, China. Scientific Research Center, China-Japan Union Hospital, Jilin University, Changchun, China. Department of Stomatology, China-Japan Union Hospital, Jilin University, Changchun, China. Scientific Research Center, China-Japan Union Hospital, Jilin University, Changchun, China. Department of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun, China.
 Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. The Second School of Clinical Medicine, Southern Medical University, Guangzhou, China. Department of Hematology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. Shantou University Medical College, Shantou, Guangdong, China. Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. School of Medicine, South China University of Technology, Guangzhou, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. Shantou University Medical College, Shantou, Guangdong, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. School of Medicine, South China University of Technology, Guangzhou, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. Sepulveda Ambulatory Care Center, Veterans Affairs Greater Los Angeles Healthcare System, North Hills, California, USA. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. The Second School of Clinical Medicine, Southern Medical University, Guangzhou, China. School of Medicine, South China University of Technology, Guangzhou, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China. Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. The Second School of Clinical Medicine, Southern Medical University, Guangzhou, China. School of Medicine, South China University of Technology, Guangzhou, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou, China.
 Global Healthy Living Foundation, Upper Nyack, New York. Global Healthy Living Foundation, Upper Nyack, New York. University of Pennsylvania, Philadelphia. Vasculitis Foundation, Kansas City, Missouri. Accelerated Cure Project, Waltham, Massachusetts. IBD Partners, Chapel Hill, North Carolina. New York University, New York, New York. New York University, New York, New York. University of North Carolina at Chapel Hill. Global Healthy Living Foundation, Upper Nyack, New York. Global Healthy Living Foundation, Upper Nyack, New York. Global Healthy Living Foundation, Upper Nyack, New York. University of Pennsylvania, Philadelphia. Vasculitis Foundation, Kansas City, Missouri. Vasculitis Foundation, Kansas City, Missouri. University of Alabama at Birmingham. Accelerated Cure Project, Waltham, Massachusetts. University of North Carolina at Chapel Hill. University of Pennsylvania, Philadelphia. Global Healthy Living Foundation, Upper Nyack, New York.
 Department of Clinical Health Psychology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, PZ350-771 Bannatyne Ave., Winnipeg, MB, R3E 3N4, Canada. rpatel4@hsc.mb.ca. Department of Internal Medicine, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Community Health Sciences, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Internal Medicine, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Psychiatry, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Clinical Health Psychology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, PZ350-771 Bannatyne Ave., Winnipeg, MB, R3E 3N4, Canada. Department of Internal Medicine, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Radiology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Division of Diagnostic Imaging, Winnipeg Health Sciences Centre, Winnipeg, MB, Canada. Neuroscience Research Program, Kleysen Institute for Advanced Medicine, Winnipeg Health Sciences Centre, Winnipeg, MB, Canada. Department of Radiology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Division of Diagnostic Imaging, Winnipeg Health Sciences Centre, Winnipeg, MB, Canada. Neuroscience Research Program, Kleysen Institute for Advanced Medicine, Winnipeg Health Sciences Centre, Winnipeg, MB, Canada. Department of Psychology, St. Francis Xavier University, Antigonish, NS, Canada. Department of Radiology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada. Department of Neurology, University of Rochester, Rochester, NY, USA. Departments of Psychiatry, Psychology & Neuroscience, and Medicine, Dalhousie University, Halifax, NS, Canada.
 College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, SAU. College of Medicine, King Abdulaziz University, Jeddah, SAU. College of Medicine, King Abdulaziz University, Jeddah, SAU. College of Medicine, King Khalid University, Abha, SAU. Neurology, King Faisal Hospital, Makkah, SAU. College of Medicine, King Khalid University, Abha, SAU. College of Medicine, Jazan University, Jazan, SAU. Department of Internal Medicine, King Khalid University, Abha, SAU.
 Department of Neurology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, China. Department of Neurology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. Department of Neurology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, China. Department of Neurology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. Department of Neurology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. Department of Neurology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, China. Department of Internal Medicine, University of California at Davis, Davis, CA, 95616, USA. Department of Neurology, Hospital of Liuzhou Traditional Chinese Medicine, 545001, Liuzhou, China. yingdaizhi@163.com. Department of Internal Medicine, University of California at Davis, Davis, CA, 95616, USA. jmzhang@ucdavis.edu. Comprehensive Cancer Center, University of California at Davis, Davis, CA, 95616, USA. jmzhang@ucdavis.edu. Department of Neurology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, China. wang_whh@163.com. Department of Neurology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. wang_whh@163.com.
 Department of Neurology, Michigan Medicine, Ann Arbor, Michigan, USA. Institute for Healthcare Policy and Innovation, Michigan Medicine, Ann Arbor, Michigan, USA. Department of Neurology, Michigan Medicine, Ann Arbor, Michigan, USA. Institute for Healthcare Policy and Innovation, Michigan Medicine, Ann Arbor, Michigan, USA. Department of Neurology, Michigan Medicine, Ann Arbor, Michigan, USA. Institute for Healthcare Policy and Innovation, Michigan Medicine, Ann Arbor, Michigan, USA. Institute for Healthcare Policy and Innovation, Michigan Medicine, Ann Arbor, Michigan, USA. Department of Internal Medicine, Michigan Medicine, Ann Arbor, Michigan, USA. VA Center for Clinical Management Research, VA Ann Arbor Healthcare System, Ann Arbor, Michigan, USA. Department of Neurology, Michigan Medicine, Ann Arbor, Michigan, USA. Institute for Healthcare Policy and Innovation, Michigan Medicine, Ann Arbor, Michigan, USA. Department of Internal Medicine, Michigan Medicine, Ann Arbor, Michigan, USA. VA Center for Clinical Management Research, VA Ann Arbor Healthcare System, Ann Arbor, Michigan, USA. Department of Neurology, Michigan Medicine, Ann Arbor, Michigan, USA. Institute for Healthcare Policy and Innovation, Michigan Medicine, Ann Arbor, Michigan, USA.
 Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA; Neuropharmacology Laboratory, Department of Pharmacology, Universidade Federal de Minas Gerais, Brazil. Instituto Maimónides de Investigación Biomédica de Córdoba-IMIBIC, Córdoba, Spain; Departamento de Biología Celular, Fisiología e Inmunología, Universidad de Córdoba, Córdoba, Spain; Hospital Universitario Reina Sofía, Córdoba, Spain. Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Electronic address: ecandelario@ufl.edu.
 Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, Otto-von-Guericke University, 39120 Magdeburg, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany. Department of Neurology, St. Josef Hospital, Ruhr University Bochum, 44791 Bochum, Germany.
 Amsterdam UMC Location Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, MS Center Amsterdam, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands; Amsterdam UMC Location Vrije Universiteit Amsterdam, Department of Medical Psychology, Amsterdam, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands; Amsterdam Neuroscience Research Institute, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands; Amsterdam Public Health Research Institute, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands. Electronic address: m.degier1@amsterdamumc.nl. Health Psychology Section, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience, 5th Floor Bermondsey Wing, Guy's Campus, King's College London, UK. Electronic address: federica.picariello@kcl.ac.uk. Amsterdam UMC Location Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, MS Center Amsterdam, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands. Electronic address: lenaslot@hotmail.com. Department of Medical Psychology, Radboud University Medical Center, P.O. Box 9101, 6500 HB, Nijmegen, the Netherlands. Electronic address: anthoniejanse@hotmail.com. Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, P.O. Box 9101, 6500 HB, Nijmegen, the Netherlands. Electronic address: Stephan.Keijmel@radboudumc.nl. Department of Medical Psychology, Radboud University Medical Center, P.O. Box 9101, 6500 HB, Nijmegen, the Netherlands. Electronic address: j.menting@nivel.nl. Department of Medical Psychology, Radboud University Medical Center, P.O. Box 9101, 6500 HB, Nijmegen, the Netherlands. Electronic address: m.worm@dimence.nl. Amsterdam UMC Location Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, MS Center Amsterdam, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands. Electronic address: h.beckerman@amsterdamumc.nl. Amsterdam UMC Location Vrije Universiteit Amsterdam, Department of Rehabilitation Medicine, MS Center Amsterdam, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands. Electronic address: v.degroot@amsterdamumc.nl. Health Psychology Section, Department of Psychology, Institute of Psychiatry, Psychology and Neuroscience, 5th Floor Bermondsey Wing, Guy's Campus, King's College London, UK. Electronic address: rona.moss-morris@kcl.ac.uk. Amsterdam UMC Location University of Amsterdam, Department of Medical Psychology, Meibergdreef 15, 1105AZ, Amsterdam, the Netherlands; Amsterdam Public Health Research Institute, P.O. Box 7057, 1007 MB, Amsterdam, the Netherlands. Electronic address: hans.knoop@amsterdamumc.nl.
 UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA. UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA. UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA. UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA. Department of Neurology, Northwestern University, Chicago, Illinois, USA. Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, Ruhr University Bochum, Bochum, Germany. Sutter East Bay Medical Group, Lafayette, California, USA. Icahn School of Medicine at Mount Sinai, New York, New York, USA. Texas Tech University Health Sciences Center, Amarillo, Texas, USA. Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Division of Neurology, Department of Medicine, St Michael's Hospital, University of Toronto, Toronto, ON, Canada. Li Ka Shing Knowledge Institute, University of Toronto, Toronto, ON, Canada. Department of Neurology, Yale University, New Haven, Connecticut, USA. Department of Neurology, Kaiser Permanente San Francisco, San Francisco, California, USA. Department of Neurology, Swedish Medical Center, Seattle, Washington, USA. Department of Neurology, Columbia University Irving Medical Center, New York, New York, USA. Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA. Rocky Mountain MS Center, Salt Lake City, Utah, USA. Department of Neurology, Ruhr University Bochum, Bochum, Germany. UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA. Buck Institute for Research on Aging, Novato, California, USA. UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California, USA.
 IQVIA, Falls Church, VA, USA. IQVIA, Falls Church, VA, USA. IQVIA, Falls Church, VA, USA. , Plymouth Meeting, PA, USA. Health Economics and Outcomes Research-Neuroscience, Ipsen, 1 Main St, Suite 700, Cambridge, MA, 02142, USA. jonathan.bouchard@Ipsen.com.
 Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States. Gladstone Institute of Neurological Disease, San Francisco, CA, United States. Division of Gastroenterology and Hepatology, Weill Cornell College of Medicine, New York, NY, United States. Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States. Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States.
 Department of Medical Nanotechnology, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Neuroscience and Cognitive, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Neuroscience and Cognitive, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Medical Nanotechnology, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran; Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cells Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Stem Cells Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Applied Cell Sciences, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Neuroscience and Cognitive, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Medical Biotechnology, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Polymer Research Laboratory, Faculty of Chemistry, University of Tabriz, Tabriz, Iran. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Medical Biotechnology, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Medical Nanotechnology, Advanced Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran; Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: zarebkohana@tbzmed.ac.ir. Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu, 610064, PR China. Electronic address: gaohuile@scu.edu.cn.
 Department of Neurology, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, Hunan, China. xjian1216@csu.edu.cn. Clinical Research Center for Cerebrovascular Disease of Hunan Province, Central South University, Changsha, Hunan, China. xjian1216@csu.edu.cn. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China. xjian1216@csu.edu.cn.
 Department of Nephrology, Clinical Center of Montenegro, Ljubljanska bb, 81000, Podgorica, Montenegro. vladimir.scopheurope@gmail.com. Department of Nephrology, Arterial Hypertension, Dialysis and Kidney Transplantation, University Hospital Center Zagreb, Zagreb, Croatia. Department of Nephrology and Clinic for pediatrics, University Medical Center Maribor, Maribor, Slovenia. Department of Nephrology and Clinic for pediatrics, University Medical Center Maribor, Maribor, Slovenia. Department of Nephrology and Hemodialysis, University Clinical Center Tuzla, Tuzla, Bosnia and Herzegovina. Department of Nephrology and Hemodialysis, University Clinical Center Tuzla, Tuzla, Bosnia and Herzegovina. Department of Neurology, University Hospital Center Zagreb, Zagreb, Croatia. Department of Nephrology with Plasmapheresis, University Clinical Center of the Republic of Srpska, Republic of Srpska, Banja Luka, Bosnia and Herzegovina. Department of Nephrology, General Hospital Koprivnica, Koprivnica, Croatia. Department of Nephrology, University Hospital Clinical Center "Sestre Milosrdnice", Zagreb, Croatia. Department of Nephrology, Clinical Hospital Center Rijeka, Rijeka, Croatia. Department of Nephrology, Laiko University General Hospital, Athens, Greece. General Hospital "MediGroup", Belgrade, Serbia. Clinic of Nephrology, Clinical Center of Serbia, Belgrade, Serbia. Clinic of Nephrology and Clinical Immunology, Clinical Center Vojvodina, Novi Sad, Serbia. Department of Nephrology, University Hospital Center Tirana, Tirana, Albania. Department of Nephrology, University Medical Center Ljubljana, Ljubljana, Slovenia. Department of Nephrology, Clinical Center of Montenegro, Ljubljanska bb, 81000, Podgorica, Montenegro. Center for Laboratory Diagnostic, Clinical Center of Montenegro, Podgorica, Montenegro. Department of Nephrology, Arterial Hypertension, Dialysis and Kidney Transplantation, University Hospital Center Zagreb, Zagreb, Croatia.
 Department of Obstetrics and Gynecology, Zhejiang University School of Medicine Women's Hospital, Hangzhou City, Zhejiang Province, 310006, China. Department of Obstetrics and Gynecology, Zhejiang University School of Medicine Women's Hospital, Hangzhou City, Zhejiang Province, 310006, China. Women and Children's Hospital of Jiaxing, Jiaxing City, Zhejiang Province, 314000, China. Department of Obstetrics and Gynecology, Zhejiang University School of Medicine Women's Hospital, Hangzhou City, Zhejiang Province, 310006, China. Department of Obstetrics and Gynecology, Zhejiang University School of Medicine Women's Hospital, Hangzhou City, Zhejiang Province, 310006, China.
 Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Wellcome Sanger Institute, Hinxton, UK. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Institute for Life Science and Technology, Hanze University of Applied Sciences, Groningen, The Netherlands. Oncode Institute, Groningen, The Netherlands. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Ancora Health, Groningen, The Netherlands. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Oncode Institute, Groningen, The Netherlands. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Oncode Institute, Groningen, The Netherlands. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Wellcome Sanger Institute, Hinxton, UK. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Wellcome Sanger Institute, Hinxton, UK. BioInfoRx, Inc., Madison, WI, USA. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. Department of Neurology, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands. Department of Neurology, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands. Department of Neurology, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands. MRC Integrative Epidemiology Unit, Bristol Medical School, University of Bristol, Bristol, UK. Translational Biology, Research and Development, Biogen Inc., Cambridge, MA, USA. heiko.runz@gmail.com. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. l.h.franke@umcg.nl. Oncode Institute, Groningen, The Netherlands. l.h.franke@umcg.nl. Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. h.j.westra@umcg.nl. Oncode Institute, Groningen, The Netherlands. h.j.westra@umcg.nl.
 Division of Immunology, Allergy and Rheumatology, University of Cincinnati Medical Center, Cincinnati, USA. Department of Rheumatology, Christie Clinic, Champaign, USA. Division of Immunology, Allergy and Rheumatology, University of Cincinnati College of Medicine, Cincinnati, USA.
 School of Pharmacy (R.A.A., K.B.R., C.W.), SSPC The SFI Research Centre for Pharmaceuticals, School of Pharmacy (K.B.R.), and Department of Pharmacology and Therapeutics (C.W.), University College Cork, Cork, Ireland; Department of Ophthalmology (R.G.E.Z.) and Department of Anatomy and Embryology (R.A.S.E.D.), Faculty of Medicine, Ain Shams University, Cairo, Egypt; and Department of Anatomy and Embryology, Faculty of Medicine, Newgiza University (R.A.S.E.D.). School of Pharmacy (R.A.A., K.B.R., C.W.), SSPC The SFI Research Centre for Pharmaceuticals, School of Pharmacy (K.B.R.), and Department of Pharmacology and Therapeutics (C.W.), University College Cork, Cork, Ireland; Department of Ophthalmology (R.G.E.Z.) and Department of Anatomy and Embryology (R.A.S.E.D.), Faculty of Medicine, Ain Shams University, Cairo, Egypt; and Department of Anatomy and Embryology, Faculty of Medicine, Newgiza University (R.A.S.E.D.). School of Pharmacy (R.A.A., K.B.R., C.W.), SSPC The SFI Research Centre for Pharmaceuticals, School of Pharmacy (K.B.R.), and Department of Pharmacology and Therapeutics (C.W.), University College Cork, Cork, Ireland; Department of Ophthalmology (R.G.E.Z.) and Department of Anatomy and Embryology (R.A.S.E.D.), Faculty of Medicine, Ain Shams University, Cairo, Egypt; and Department of Anatomy and Embryology, Faculty of Medicine, Newgiza University (R.A.S.E.D.). School of Pharmacy (R.A.A., K.B.R., C.W.), SSPC The SFI Research Centre for Pharmaceuticals, School of Pharmacy (K.B.R.), and Department of Pharmacology and Therapeutics (C.W.), University College Cork, Cork, Ireland; Department of Ophthalmology (R.G.E.Z.) and Department of Anatomy and Embryology (R.A.S.E.D.), Faculty of Medicine, Ain Shams University, Cairo, Egypt; and Department of Anatomy and Embryology, Faculty of Medicine, Newgiza University (R.A.S.E.D.). School of Pharmacy (R.A.A., K.B.R., C.W.), SSPC The SFI Research Centre for Pharmaceuticals, School of Pharmacy (K.B.R.), and Department of Pharmacology and Therapeutics (C.W.), University College Cork, Cork, Ireland; Department of Ophthalmology (R.G.E.Z.) and Department of Anatomy and Embryology (R.A.S.E.D.), Faculty of Medicine, Ain Shams University, Cairo, Egypt; and Department of Anatomy and Embryology, Faculty of Medicine, Newgiza University (R.A.S.E.D.) c.waeber@ucc.ie.
 Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Computer and Information Science, University of Strathclyde, Glasgow, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Royal Infirmary of Edinburgh, NHS Lothian, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Borders General Hospital, NHS Borders, Melrose, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK. College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Royal Infirmary of Edinburgh, NHS Lothian, Edinburgh, UK. College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Institute of Neurological Sciences, NHS Greater Glasgow and Clyde, Glasgow, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. School of Psychology and Neuroscience, University of Glasgow, Glasgow, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Royal Infirmary of Edinburgh, NHS Lothian, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Royal Infirmary of Edinburgh, NHS Lothian, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, UK. College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, UK. Neurology Department, NHS Forth Valley, Stirling, UK. College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, UK. Edinburgh Medical School, The University of Edinburgh, Edinburgh, UK. Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK. Institute of Evolutionary Biology, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, UK. University College London Hospitals, Biomedical Research Centre, National Institute for Health Research, London, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. Anne Rowling Regenerative Neurology Clinic, The University of Edinburgh, Edinburgh, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK Malcolm.macleod@ed.ac.uk.
 Department of Neurosciences, Université de Montréal, and CHUM Research Center, Montréal, QC, Canada. Department of Neurosciences, Université de Montréal, and CHUM Research Center, Montréal, QC, Canada. Electronic address: c.vande.velde@umontreal.ca.
 Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy. Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy. Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy. Allergology and Clinical Immunology Unit, Azienda Usl Toscana Sud Est, San Donato Hospital, 52100 Arezzo, Italy. Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy. Immunoallergology Unit, Careggi University Hospital, 50134 Firenze, Italy. Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy. Immunoallergology Unit, Careggi University Hospital, 50134 Firenze, Italy. Immunoallergology Unit, Careggi University Hospital, 50134 Firenze, Italy. Research and Development, Autoimmunity, Werfen, Autoimmunity Headquarters and Technology Center, San Diego, CA 92131-1638, USA. Research and Development, Autoimmunity, Werfen, Autoimmunity Headquarters and Technology Center, San Diego, CA 92131-1638, USA. Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy. Immunology and Cell Therapy Unit, Careggi University Hospital, 50134 Firenze, Italy. Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, 50121 Firenze, Italy.
 From the Department of Pediatrics, Dr. Rajendra Prasad Government Medical College, Kangra at Tanda, Himachal Pradesh, India. From the Department of Pediatrics, Dr. Rajendra Prasad Government Medical College, Kangra at Tanda, Himachal Pradesh, India. From the Department of Pediatrics, Dr. Rajendra Prasad Government Medical College, Kangra at Tanda, Himachal Pradesh, India. From the Department of Pediatrics, Dr. Rajendra Prasad Government Medical College, Kangra at Tanda, Himachal Pradesh, India.
 Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. zhouyubo@yeah.net. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. zhouyubo@yeah.net. Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. lihongtian@pku.edu.cn. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. lihongtian@pku.edu.cn. Center for Intelligent Public Health, Institute for Artificial Intelligence, Peking University, Beijing, China. lihongtian@pku.edu.cn. Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University Health Science Center, Beijing, China. Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, China. Center for Intelligent Public Health, Institute for Artificial Intelligence, Peking University, Beijing, China.
 Institute for Physiology and Science-IT, Charite, University Medicine Berlin, 10115, Berlin, Germany. Department Oral and Maxillofacial Surgery, Berlin Institute of Health, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany. Institute for Physiology and Science-IT, Charite, University Medicine Berlin, 10115, Berlin, Germany. Robert.preissner@charite.de.
 Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Development Science, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium. Neuroinflammation Focus Area, Neuroscience Research, Early Solutions, UCB Biopharma SRL, Braine l'Alleud, Belgium.
 Faculty of Medicine, Department of Pulmonary & Critical Care. Faculty of Medicine, Department of Internal Medicine, Beirut Arab University. Middle East and North Committee for Treatment and Research in Multiple Sclerosis (MENACTRIMS), Beirut. Department of Pulmonary & Critical Care, Rafic Hariri University Hospital, Babda, Lebanon. Faculty of Medicine, Lebanese University.
 Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/Department of Neurology, Great Ormond Street Hospital for Children, London, UK. Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/Department of Neurology, Great Ormond Street Hospital for Children, London, UK. Department of Paediatric Metabolic Medicine, Great Ormond Street Hospital for Children, London, UK. Department of Paediatric Intensive Care, Great Ormond Street Hospital for Children, London, UK. Department of Neurology, Alder Hey Children's NHS Foundation Trust, Liverpool, UK. Department of Neuroradiology, Great Ormond Street Hospital for Children, London, UK. Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK/Department of Neurology, Great Ormond Street Hospital for Children, London, UK.
 Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Virus Immunology, Leibniz Institute for Virology, Hamburg, Germany. Department of Virus Immunology, Leibniz Institute for Virology, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
 Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Daniel.levin@medportal.ca. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Alberta, Edmonton, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Alberta, Edmonton, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada. Department of Medicine, University of Calgary, Calgary, AB, Canada.
 Cleveland Clinic AbuFcoi Dhabi, Eye Institute, Abu Dhabi, United Arab Emirates. Cleveland Clinic AbuFcoi Dhabi, Eye Institute, Abu Dhabi, United Arab Emirates. Cleveland Clinic AbuFcoi Dhabi, Eye Institute, Abu Dhabi, United Arab Emirates. Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA. Cleveland Clinic AbuFcoi Dhabi, Eye Institute, Abu Dhabi, United Arab Emirates. Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
 Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
 Department of Surgery, Faculty of Medicine, Universitas Padjadjaran, Perpetua J. Safanpo General Hospital, South Papua, Indonesia. Department of Surgery, Faculty of Medicine, Universitas Padjadjaran, Perpetua J. Safanpo General Hospital, South Papua, Indonesia. Department of Surgery, Faculty of Medicine, Universitas Padjadjaran, Perpetua J. Safanpo General Hospital, South Papua, Indonesia. Electronic address: prapanca18001@mail.unpad.ac.id. Department of Surgery, Faculty of Medicine, Universitas Padjadjaran, Perpetua J. Safanpo General Hospital, South Papua, Indonesia. Electronic address: kiki.lukman@unpad.ac.id.
 State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. Department of Natural Medicines, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China. Department of Neurology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing 102218, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. New Drug Safety Evaluation Center, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. NMPA Key Laboratory for Safety Research and Evaluation of Innovative Drug, Beijing 100050, China. Department of Natural Medicines, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.
 Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China. Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China. Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China. Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China. Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China. Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China. Department of Dermatology, West China Hospital of Sichuan University, Chengdu, China. Department of Medical Ultrasound, West China Hospital of Sichuan University, Chengdu, China.
 Department of Pediatrics, Teikyo University School of Medicine. Department of Pediatrics, Teikyo University School of Medicine. Department of Pediatrics, Teikyo University School of Medicine. Department of Pediatrics, Teikyo University School of Medicine.
 Department of Biotechnology, Jaypee Institute of Information Technology, Sec-62, Noida, Uttar Pradesh, India. School of Computational and Integrative Science, Jawaharlal Nehru University, New Delhi-110067, India. Department of Biotechnology, Jaypee Institute of Information Technology, Sec-62, Noida, Uttar Pradesh, India. Department of Biotechnology, Jaypee Institute of Information Technology, Sec-62, Noida, Uttar Pradesh, India. Department of Biotechnology, Jaypee Institute of Information Technology, Sec-62, Noida, Uttar Pradesh, India. School of Biotechnology, Jawaharlal Nehru University, New Delhi-110067, India. Department of Biotechnology, Jaypee Institute of Information Technology, Sec-62, Noida, Uttar Pradesh, India.
 Division of Cancer Stem Cells and Cardiovascular Regeneration, Manipal Institute of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India. Division of Cancer Stem Cells and Cardiovascular Regeneration, Manipal Institute of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India. Division of Cancer Stem Cells and Cardiovascular Regeneration, Manipal Institute of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India. Department of Human Genetics, Faculty of Biomedical Sciences and Technology, Sri Ramachandra Institute of Higher Education and Research, Chennai 600116, India. Department of Biomedical Sciences, Faculty of Biomedical Sciences and Technology, Sri Ramachandra Institute of Higher Education and Research, Chennai 600116, India; School of Human Sciences, Faculty of Life and Physical Sciences, The University of Western Australia, Perth, Australia; Curtin Medical School, Curtin University, Perth, Western Australia, Australia. Division of Cancer Stem Cells and Cardiovascular Regeneration, Manipal Institute of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India; Cuor Stem Cellutions Pvt Ltd, Manipal Institute of Regenerative Medicine, Manipal Academy of Higher Education (MAHE), Bangalore 560065, India; Department of Biotechnology, Faculty of Biomedical Sciences and Technology, Sri Ramachandra Institute of Higher Education and Research, Chennai 600116, India. Electronic address: sudha.warrier@manipal.edu.
 Division of Rheumatology, University of Texas Health Science Center at Houston, Houston, TX, USA. Department of Internal Medicine, University of Texas Health Science Center at Houston, Houston, TX, USA. Division of Cardiology, University of Texas Health Science Center at Houston, TX, USA. Division of Rheumatology, University of Texas Health Science Center at Houston, Houston, TX, USA.
 Department of Nursing, College of Public Health, Temple University, Philadelphia, Pennsylvania.
 Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain. Laboratori Clínic Institut Català de la Salut Lleida, Hospital Universitari Arnau de Vilanova, Lleida, Spain. Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain. Unit of Rare Diseases and Hereditary Metabolic Disorders, Vall d'Hebron University Hospital, Barcelona, Spain. Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain. Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Neuromuscular and Mitochondrial Disorders Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: eduardo.tizzano@vallhebron.cat. Department of Clinical and Molecular Genetics, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain; Medicine Genetics Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Neuromuscular and Mitochondrial Disorders Group, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Raras, Instituto de Salud Carlos III, Barcelona, Spain.
 Department of Biology, University of Padova, 35131 Padova, Italy. Department of Biology, University of Padova, 35131 Padova, Italy. Study Center for Neurodegeneration (CESNE), 35100 Padova, Italy.
 Department of Internal Medicine E, Meir Medical Center, Kfar Saba 4428164, Israel; Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: Wakar.Garra@hotmail.com. Department of Internal Medicine E, Meir Medical Center, Kfar Saba 4428164, Israel; Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
 School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia. The MARCS Institute, Western Sydney University, Penrith, New South Wales, Australia.
 Department of Restorative Dentistry, Liverpool University Dental Hospital, Pembroke Place, Liverpool, United Kingdom. Electronic address: Ahmed.elmatary@liverpool.ac.uk. Department of Restorative Dentistry, Liverpool University Dental Hospital, Pembroke Place, Liverpool, United Kingdom. Department of Restorative Dentistry, Liverpool University Dental Hospital, Pembroke Place, Liverpool, United Kingdom.
 Obstetric Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy. Pediatric Cardiology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy. Obstetric Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy. Pediatric Cardiology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy. Obstetric Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy. Pediatric Cardiology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy. Obstetric Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna Italy.
 CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad 500007, Telangana, India. AcSIR-Academy of Scientific and Innovative Research, Ghaziabad 201002, Uttar Pradesh, India. CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad 500007, Telangana, India. AcSIR-Academy of Scientific and Innovative Research, Ghaziabad 201002, Uttar Pradesh, India. CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB), Hyderabad 500007, Telangana, India. AcSIR-Academy of Scientific and Innovative Research, Ghaziabad 201002, Uttar Pradesh, India.
 Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. Electronic address: alessio.signori@unige.it. Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy. University of Ottawa, Department of Medicine and the Ottawa Hospital Research Institute, Ottawa, ON, Canada. Merck Gesellschaft mbH, Vienna, Austria (an affiliate of Merck KGaA). Merck Healthcare KGaA, Darmstadt, Germany. Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy; Ospedale Policlinico San Martino IRCCS, Genoa, Italy.
 Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA. Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; VA Boston Healthcare System, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA; Center for Data Science, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA. Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA. Department of Biostatistics and Bioinformatics, Duke University, Durham, NC, USA. Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA; VA Boston Healthcare System, Boston, MA, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Division of Rheumatology, Inflammation, and Immunity, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA; VA Boston Healthcare System, Boston, MA, USA. Electronic address: kliao@bwh.harvard.edu.
 School of Kinesiology, Recreation and Sport, Bowling Green, KY, USA. School of Kinesiology, Recreation and Sport, Bowling Green, KY, USA. School of Kinesiology, Recreation and Sport, Bowling Green, KY, USA. School of Kinesiology, Recreation and Sport, Bowling Green, KY, USA. Department of Biology, Western Kentucky University, Bowling Green, KY, USA.
 MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. InFLAMES Research Flagship Center, University of Turku, FI-20014 Turku, Finland. MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. InFLAMES Research Flagship Center, University of Turku, FI-20014 Turku, Finland. Structural Bioinformatics Laboratory, Biochemistry, Faculty of Science and Engineering, Åbo Akademi University, FI-20500 Turku, Finland. InFLAMES Research Flagship Center, Åbo Akademi University, FI-20500 Turku, Finland. MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. InFLAMES Research Flagship Center, University of Turku, FI-20014 Turku, Finland. MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. InFLAMES Research Flagship Center, University of Turku, FI-20014 Turku, Finland. MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. InFLAMES Research Flagship Center, University of Turku, FI-20014 Turku, Finland. MedChem.fi, Institute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland. InFLAMES Research Flagship Center, University of Turku, FI-20014 Turku, Finland.
 From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. Magnetic Resonance, Siemens Healthcare GmbH, Erlangen. Division of Biostatistics, German Cancer Research Center (DKFZ), Heidelberg, Germany. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg. From the Department of Neuroradiology, Heidelberg University Hospital, Heidelberg.
 Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Department of Physiology and Pharmacology Karolinska Institute Stockholm Sweden. Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology Stuttgart Germany. University of Tübingen Tübingen Germany. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Henan Key Laboratory of Child Brain Injury Institute of Neuroscience and Third Affiliated Hospital of Zhengzhou University Zhengzhou China. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Department of Cardiology, Ruijin Hospital/Luwan Branch, School of Medicine Shanghai Jiao Tong University Shanghai China. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Henan Key Laboratory of Child Brain Injury Institute of Neuroscience and Third Affiliated Hospital of Zhengzhou University Zhengzhou China. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Centre of Perinatal Medicine & Health, Department of Obstetrics and Gynaecology, Institute of Clinical Sciences, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Department of Neurosurgery University of Alabama at Birmingham Birmingham Alabama USA. Department of Microbiology University of Alabama at Birmingham Birmingham Alabama USA. Centre of Perinatal Medicine & Health, Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden. Henan Key Laboratory of Child Brain Injury Institute of Neuroscience and Third Affiliated Hospital of Zhengzhou University Zhengzhou China. Centre of Perinatal Medicine & Health, Department of Obstetrics and Gynaecology, Institute of Clinical Sciences, Sahlgrenska Academy University of Gothenburg Gothenburg Sweden.
 Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA; University of Science and Technology of Kunming, People's Republic of China. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA. Heinrich Heine University, Medical School, Duesseldorf, Germany. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA. Sanderson Center for Optical Experimentation, University of Massachusetts Chan Medical School, Worcester, MA, USA. ScientiaLux LLC, Tissue-Gnostics USA-East, Worcester, MA, USA. Mass Spectrometry Core, University of Massachusetts, Amherst, MA, USA. Electron Microscopy Core, University of Massachusetts Chan Medical School, MA, USA. Department of Neurology, University of Massachusetts Chan Medical School, MA, USA. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA; Department of Neurosurgery, University of Minnesota, Minneapolis, MN, USA. Electronic address: dominic.gessler@umassmed.edu. Horae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA; Li Weibo Institute for Rare Diseases Research, University of Massachusetts Chan Medical School, Worcester, MA, USA; Department of Microbiology & Physiological Systems, University of Massachusetts Chan Medical School, Worcester, MA, USA. Electronic address: guangping.gao@umassmed.edu.
 Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain. Genetics Department and Sant Pau Biomedical Research Institute, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER, U705), IICS-Madrid, Madrid, Spain. Department of Pediatrics, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: sboronat@santpau.cat. Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.
 Division of Pharmacology, Department of Neuroscience, School of Medicine, University of Naples Federico II, 80131 Naples, Italy.
 Department of Internal Medicine and Multi-Organic Diseases, Local Referral Center for Rare Auto-immune Diseases, Montpellier University Hospital, Montpellier, France. University of Montpellier, Montpellier,France. University of Montpellier, Montpellier,France. Internal Medicine Department, CHU Nîmes, Nîmes, France. University of Montpellier, Montpellier,France. Department of Neurology, Montpellier University Hospital, Montpellier, France. INM, INSERM, Montpellier, France. Department of Internal Medicine and Multi-Organic Diseases, Local Referral Center for Rare Auto-immune Diseases, Montpellier University Hospital, Montpellier, France. University of Montpellier, Montpellier,France. Institute of Regenerative Medicine and Biotherapy, INSERM U1183, Montpellier, France. Department of Neurology, Montpellier University Hospital, Montpellier, France. Sorbonne Université, Paris, France. Institut Pierre Louis d'Epidémiologie et de Santé Publique, AP-HP, Hôpital Pitié Salpêtrière, Département de Santé Publique, F75013, Paris, France. Département de Neurologie, Hôpital Pitié Salpêtrière, AP-HP, F75013, Paris, France. University of Montpellier, Montpellier,France. Pediatrics Department, Montpellier University Hospital, Montpellier, France. Department of Internal Medicine, Amiens University Medical Center, Amiens, France. Internal Medicine Department, Bordeaux University Hospital Centre, Hôpital Haut-Lévêque, Pessac, France. Clinical Immunology Department, National Reference Center for Castleman Disease, Hôpital Saint Louis, Assistance Publique Hôpitaux de Paris (APHP), Paris, France. UMR 1149 CRI INSERM, Hôpital Saint Louis, Assistance Publique Hôpitaux de Paris (APHP), Paris, France. Université Paris Diderot, Paris, France. Clinical Immunology Department, National Reference Center for Castleman Disease, Hôpital Saint Louis, Assistance Publique Hôpitaux de Paris (APHP), Paris, France. Université Paris Diderot, Paris, France. Inserm U1126, Centre Hayem, Hôpital Saint-Louis, Paris, France. Internal medicine department, Hôpital Saint Antoine, APHP, Paris, France. Pediatric Oncology Hematology Unit, Bordeaux University Hospital, Bordeaux, France. Plurithématique CIC (CICP), Centre d'Investigation Clinique (CIC) 1401, INSERM Bordeaux, France, France. Centre de Référence National des Cytopénies Auto-immunes de l'Enfant (CEREVANCE), Bordeaux, France. Department of Internal Medicine and Multi-Organic Diseases, Local Referral Center for Rare Auto-immune Diseases, Montpellier University Hospital, Montpellier, France. Department of Internal Medicine, Saint-Nazaire Hospital, Saint-Nazaire, France. Department of Internal Medicine, Purpan University Hospital, Toulouse, France. Department of Hematology, Necker-Enfants Malades University Hospital, AP-HP, Paris, France. INSERM UMR1163 and CNRS ERL 8254, Imagine Institut, Paris, France. Descartes University, Paris, France. Descartes University, Paris, France. Pediatric Hematology-Immunology and Rheumatology Department, Hôpital Necker-Enfants Malades, AP-HP, Paris, France. Laboratory of Immunogenetics of Pediatric Autoimmunity, INSERM UMR 1163, Imagine Institute, Paris, France. Pediatric Hematology-Immunology and Rheumatology Department, Hôpital Necker-Enfants Malades, AP-HP, Paris, France. French National Reference Center for Primary Immune Deficiencies (CEREDIH), Necker Enfants Malades University Hospital, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France. University of Montpellier, Montpellier,France x-ayrignac@chu-montpellier.fr. Department of Neurology, Montpellier University Hospital, Montpellier, France. INM, INSERM, Montpellier, France.
 Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA. Quantitative Biosciences Institute, University of California, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. Quantitative Biosciences Institute, University of California, San Francisco, CA, USA. Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA, USA. Gladstone Institutes, San Francisco, CA, USA. kakassoglou@gladstone.ucsf.edu. Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA, USA. kakassoglou@gladstone.ucsf.edu. Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, CA, USA. kakassoglou@gladstone.ucsf.edu.
 Federal University of Minas Gerais Medical School, Belo Horizonte, MG, Brazil. Electronic address: marco.lanapeixoto@gmail.com. Federal University of Minas Gerais Medical School, Belo Horizonte, MG, Brazil. University of São Paulo Medical School, Sao Paulo, SP, Brazil. University of São Paulo Medical School in Ribeirao Preto, Sao Paulo, SP, Brazil. Campinas State University, Campinas, SP, Brazil. Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, Brazil. Joinville University, Joinvile, SC, Brazil. Neurological Institute of Curitiba, Curitiba, PR, Brazil.
 Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Nephrology, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Department of Fetal Medicine, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China. Department of Fetal Medicine, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China; Department of Clinical Laboratory, the Fifth Affiliated Hospital of Jinan University, Heyuan 517000, China. Department of Nephrology, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China. Electronic address: 42089537@qq.com. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China; Department of Clinical Laboratory, the Fifth Affiliated Hospital of Jinan University, Heyuan 517000, China. Electronic address: thexh@jnu.edu.cn. Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Electronic address: dongyun1967@aliyun.com.
 Department of Neurology, The First Affiliated Hospital, Multi-Omics Research Center for Brain Disorders, Hengyang Medical School, University of South China, Hengyang, Hunan, China. The First Affiliated Hospital, Clinical Research Center for Immune-Related Encephalopathy of Hunan Province, Hengyang Medical School, University of South China, Hengyang, Hunan, China. Department of Neurology, The First Affiliated Hospital, Multi-Omics Research Center for Brain Disorders, Hengyang Medical School, University of South China, Hengyang, Hunan, China. The First Affiliated Hospital, Clinical Research Center for Immune-Related Encephalopathy of Hunan Province, Hengyang Medical School, University of South China, Hengyang, Hunan, China. Department of Neurology, The First Affiliated Hospital, Multi-Omics Research Center for Brain Disorders, Hengyang Medical School, University of South China, Hengyang, Hunan, China. The First Affiliated Hospital, Clinical Research Center for Immune-Related Encephalopathy of Hunan Province, Hengyang Medical School, University of South China, Hengyang, Hunan, China. Department of Neurology, The First Affiliated Hospital, Multi-Omics Research Center for Brain Disorders, Hengyang Medical School, University of South China, Hengyang, Hunan, China. The First Affiliated Hospital, Clinical Research Center for Immune-Related Encephalopathy of Hunan Province, Hengyang Medical School, University of South China, Hengyang, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
 Neurology I Department, Cluj-Napoca Emergency Clinical County Hospital, 400012 Cluj-Napoca, Romania. Neurology Department, University of Medicine and Pharmacy "Iuliu Hatieganu", 400012 Cluj-Napoca, Romania. CESTER, Research Center for Industrial Robots Simulation and Testing, Technical University of Cluj-Napoca, 400641 Cluj-Napoca, Romania. Neurology I Department, Cluj-Napoca Emergency Clinical County Hospital, 400012 Cluj-Napoca, Romania. Neurology Department, University of Medicine and Pharmacy "Iuliu Hatieganu", 400012 Cluj-Napoca, Romania. Neurology Department, University of Medicine and Pharmacy "Iuliu Hatieganu", 400012 Cluj-Napoca, Romania. Neurosurgery Department, Cluj-Napoca Emergency Clinical County Hospital, 400349 Cluj-Napoca, Romania. Department of Psychology, Babes-Bolyai University, 400029 Cluj-Napoca, Romania. CESTER, Research Center for Industrial Robots Simulation and Testing, Technical University of Cluj-Napoca, 400641 Cluj-Napoca, Romania. CESTER, Research Center for Industrial Robots Simulation and Testing, Technical University of Cluj-Napoca, 400641 Cluj-Napoca, Romania. CESTER, Research Center for Industrial Robots Simulation and Testing, Technical University of Cluj-Napoca, 400641 Cluj-Napoca, Romania. CESTER, Research Center for Industrial Robots Simulation and Testing, Technical University of Cluj-Napoca, 400641 Cluj-Napoca, Romania. Neurology I Department, Cluj-Napoca Emergency Clinical County Hospital, 400012 Cluj-Napoca, Romania. Neurology I Department, Cluj-Napoca Emergency Clinical County Hospital, 400012 Cluj-Napoca, Romania. Faculty of Mechanics, University of Craiova, 200512 Craiova, Romania. CESTER, Research Center for Industrial Robots Simulation and Testing, Technical University of Cluj-Napoca, 400641 Cluj-Napoca, Romania.
 Banner Life Sciences LLC, 3980 Premier Dr., Suite 110, High Point, NC 27265, USA. INDAPharma, LLC, Consultant to Banner Life Sciences LLC, USA. Banner Life Sciences LLC, 3980 Premier Dr., Suite 110, High Point, NC 27265, USA. Banner Life Sciences LLC, 3980 Premier Dr., Suite 110, High Point, NC 27265, USA. Electronic address: Thomas.Lategan@bannerls.com. Regina Berkovich MD, PhD Inc. MS Center and USC Neurology Teaching Faculty (LAC-USC), USA.
 Department of Neurobiology, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Science and Brain-machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China. Department of Neurobiology, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Science and Brain-machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China. The Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China. The Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China. Department of Neurobiology, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Science and Brain-machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China. Department of Neurobiology, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Science and Brain-machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China. The Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China. The Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China. The Clinical Research Center and Department of Pathology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. The Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China. Department of Neurobiology, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine, Hangzhou, China. NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Science and Brain-machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China.
 Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Neurosciences, University of Turin, Turin, Italy. Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiology, Amsterdam University Medical Center, Amsterdam, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiology and Nuclear Medicine, University Medical Center Utrecht, Utrecht, The Netherlands. Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Medical Imaging, Radboud University Medical Center, Nijmegen, The Netherlands. Computational Imaging Group for MR Therapy and Diagnostics, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Radiotherapy, University Medical Center Utrecht, Utrecht, The Netherlands.
 Department of Neurology, Shaheed Zulfiqar Ali Bhutto Medical University (SZABMU), Islamabad, Pakistan. Department of Neurology, Shaheed Zulfiqar Ali Bhutto Medical University (SZABMU), Islamabad, Pakistan. Electronic address: drhassaanshafqat2011@gmail.com. Department of Neurology, Shaheed Zulfiqar Ali Bhutto Medical University (SZABMU), Islamabad, Pakistan.
 Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. School of Communication Sciences and Disorders, Western University, London, Ontario, Canada. Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. School of Communication Sciences and Disorders, Western University, London, Ontario, Canada. Department of Computer Science, Western University, London, Ontario, Canada. Canadian Centre for Activity and Aging, Western University, London, Ontario, Canada. Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
 HCmed Innovations Co., Ltd., Taipei, Taiwan. Department and Graduate Institute of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. HCmed Innovations Co., Ltd., Taipei, Taiwan. HCmed Innovations Co., Ltd., Taipei, Taiwan. Department and Graduate Institute of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. Department and Graduate Institute of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. Department and Graduate Institute of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. Department and Graduate Institute of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. Chemical Biology and Molecular Biophysics, Taiwan International Graduate Program in Chemical Biology and Molecular Biophysics (TIGP-CBMB), Academia Sinica, Taipei, Taiwan.
 Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313, Porto, Portugal. Department of Biological Sciences, UCIBIO - Applied Molecular Biosciences Unit, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313, Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313, Porto, Portugal. Department of Biological Sciences, UCIBIO - Applied Molecular Biosciences Unit, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313, Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313, Porto, Portugal. Department of Biological Sciences, UCIBIO - Applied Molecular Biosciences Unit, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313, Porto, Portugal. Laboratory of Organic and Pharmaceutical Chemistry, Chemistry Department, Faculty of Pharmacy, University of Porto, 4050-313, Porto, Portugal. CIIMAR-Interdisciplinary Centre of Marine and Environmental Research, 4450-208, Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313, Porto, Portugal. Department of Biological Sciences, UCIBIO - Applied Molecular Biosciences Unit, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313, Porto, Portugal. Associate Laboratory i4HB, Institute for Health and Bioeconomy, Faculty of Pharmacy, University of Porto, 4050-313, Porto, Portugal. veramcosta@ff.up.pt. Department of Biological Sciences, UCIBIO - Applied Molecular Biosciences Unit, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313, Porto, Portugal. veramcosta@ff.up.pt.
 R&D, Chemomab Ltd, Tel Aviv, Israel. R&D, Chemomab Ltd, Tel Aviv, Israel. Rheumatology Institute, Rambam Health Care Campus, Haifa, Israel. Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
 Department of Neurology, Mid-Atlantic Permanente Medical Group, Rockville, MD, USA. Department of Research, Mid-Atlantic Permanente Research Institute, Rockville, MD, USA. Department of Neurology, Mid-Atlantic Permanente Medical Group, Rockville, MD, USA. Department of Rheumatology, Mid-Atlantic Permanente Medical Group, Rockville, USA. Department of Neurology, Mid-Atlantic Permanente Medical Group, Rockville, MD, USA. Department of Neurology, Howard University Hospital, Washington, DC, USA. Department of Medicine, West Virginia School of Osteopathic Medicine, Lewisburg, WV, USA.
 Department of General Medicine HITO Medical Center Ehime Japan. Department of General Medicine HITO Medical Center Ehime Japan. Department of General Medicine HITO Medical Center Ehime Japan. Department of General Medicine HITO Medical Center Ehime Japan. Department of General Medicine HITO Medical Center Ehime Japan. Department of Neurology Ehime Prefectural Central Hospital Ehime Japan.
 Department of Medicine, Division of Rheumatology, University of California, Los Angeles, CA, USA; David Geffen School of Medicine, Los Angeles, CA, USA. Electronic address: evolkmann@mednet.ucla.edu. Department of Rheumatology, Lund University, Lund, Sweden. Department of Internal Medicine and Department of Rheumatology, Ghent University (Hospital), Ghent, Belgium; Unit for Molecular Immunology and Inflammation, VIB Inflammation Research Centre, Ghent, Belgium.
 Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy; ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. Electronic address: mario.stanziano@istituto-besta.it. Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy; School of Life Science and Technology, MOE Key Laboratory for Neuroinformation, University of Electronic Science and Technology of China, Chengdu, China. Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy. Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy. Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy. Neuroradiology Unit, CTO Hospital, AOU Città della Salute e della Scienza di Torino, Italy. Neuroradiology Unit, CTO Hospital, AOU Città della Salute e della Scienza di Torino, Italy. Neuroimaging Research Unit, Division of Neuroscience, Italy; Neurology Unit, Italy; Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, Italy; Neurology Unit, Italy; Neurorehabilitation Unit, Italy; Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy. Neuroradiology Unit, CTO Hospital, AOU Città della Salute e della Scienza di Torino, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Institute of Cognitive Sciences and Technologies, National Council of Research, Rome, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Institute of Cognitive Sciences and Technologies, National Council of Research, Rome, Italy. Neuroradiology Unit, Foundation IRCCS Neurological Institute Carlo Besta, Milan, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy.
 Department of Internal Medicine, Dhulikhel Hospital, Kathmandu University School of Medical Sciences. Kathmandu University School of Medical Sciences, Dhulikhel, Nepal. Kathmandu University School of Medical Sciences, Dhulikhel, Nepal.
 Department of Neurology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA. Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70170, USA. Department of Neurology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA. Department of Neurology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA.
 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Jacksonville, FL, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA.
 Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Cerebrovascular Center, Cleveland Clinic, Cleveland, OH, USA. Cleveland Clinic Center for Vasculitis Care and Research, Cleveland Clinic, 9500 Euclid Avenue, A50, Cleveland, OH 44195, USA. Electronic address: HAJJALR@ccf.org.
 Montefiore Medical Center Deaconess HS, IN University School Med
 Department of Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada. Department of Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada; Division of Rheumatology, St. Joseph's Health Care, London, Ontario, Canada. Division of Rheumatology, Johns Hopkins University School of Medicine, Johns Hopkins Scleroderma Center, Baltimore, MD, USA. Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, 3500 Terrace Street, Pittsburgh, PA 15261, USA. Electronic address: rtd4@pitt.edu.
 Translational Vectorology Research Unit, Children's Medical Research Institute, Faculty of Medicine and Health, The University of Sydney, Westmead, New South Wales, Australia. Department of Biomedical Sciences, Centre for Motor Neuron Disease Research, Faculty of Medicine & Health Sciences, Macquarie University, Sydney, New South Wales, Australia. Department of Neuromuscular Disease, UCL Queen Square Institute of Neurology, Queen Square, London, UK. The Francis Crick Institute, London, UK. Translational Vectorology Research Unit, Children's Medical Research Institute, Faculty of Medicine and Health, The University of Sydney, Westmead, New South Wales, Australia. Laboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine, Warsaw, Poland.
 Division of Epilepsy and Neurophysiology, Department of Neurology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. Division of Epilepsy and Neurophysiology, Department of Neurology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. Division of Epilepsy and Neurophysiology, Department of Neurology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. Division of Epilepsy and Neurophysiology, Department of Neurology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. F.M. Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
 Department of Neurology, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. Department of Neurology, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. Department of Neurology, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. Department of Neurology, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. German Center For Neurodegenerative Diseases (DZNE) Ulm, Ulm, Germany. Department of Neurology, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. axel.freischmidt@uni-ulm.de.
 Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy. Department of Neurosciences, Azienda Ospedaliero Universitaria di Modena, 41126 Modena, Italy. Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. CREAGEN Research Center of Environmental, Genetic and Nutritional Epidemiology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy. Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Analytical BioGeoChemistry Research Unit, Helmholtz Center Munich─German Research Center for Environmental Health GmbH, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany.
 Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-Ku, Hiroshima, Hiroshima, 734-8551, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. sugitkm@hiroshima-u.ac.jp. Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-Ku, Hiroshima, Hiroshima, 734-8551, Japan. sugitkm@hiroshima-u.ac.jp. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Neurology, Hiroshima City Hiroshima Citizens Hospital, 7-33 Motomachi, Naka-ku, Hiroshima, Hiroshima, 730-8518, Japan. Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-Ku, Hiroshima, Hiroshima, 734-8551, Japan.
 Rheumatology Unit, Hospital S. Giovanni di Dio, Azienda USL-Toscana Centro, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy. Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Immunology and Allergology Laboratory Unit, S. Giovanni di Dio Hospital, Azienda USL-Toscana Centro, Florence, Italy. Immunology and Allergology Laboratory Unit, S. Giovanni di Dio Hospital, Azienda USL-Toscana Centro, Florence, Italy. Immunology and Allergology Laboratory Unit, S. Giovanni di Dio Hospital, Azienda USL-Toscana Centro, Florence, Italy. Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Perugia, Italy. Electronic address: carlo.perricone@unipg.it.
 Department of Rheumatology and Allergology, NHO Osaka Minami Medical Center, Kawachinagano, Japan. Department of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. Department of Rheumatology and Allergology, NHO Osaka Minami Medical Center, Kawachinagano, Japan. Department of Rheumatology and Allergology, NHO Osaka Minami Medical Center, Kawachinagano, Japan. Department of Respiratory Medicine and Rheumatology, Suita Municipal Hospital, Suita, Japan. Department of Rheumatology and Allergology, NHO Osaka Minami Medical Center, Kawachinagano, Japan. Department of Clinical Research, NHO Osaka Minami Medical Center, Kawachinagano, Japan. Department of Rheumatology and Allergology, NHO Osaka Minami Medical Center, Kawachinagano, Japan. Department of Clinical Research, NHO Osaka Minami Medical Center, Kawachinagano, Japan.
 Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Psychology Department, Beaumont Hospital, Dublin D09 V2N0, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Psychology Department, Beaumont Hospital, Dublin D09 V2N0, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Human Cognitive Neurosciences-Psychology, School of Philosophy, Psychology, Language Sciences, The University of Edinburgh, Edinburgh EH8 9AD, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh EH16 4SB, UK. Human Cognitive Neurosciences-Psychology, School of Philosophy, Psychology, Language Sciences, The University of Edinburgh, Edinburgh EH8 9AD, UK. Euan MacDonald Centre for Motor Neuron Disease Research, The University of Edinburgh, Edinburgh EH16 4SB, UK. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Academic Unit of Neurology, Trinity Biomedical Science Institute, Dublin D02 R590, Ireland. Psychology Department, Beaumont Hospital, Dublin D09 V2N0, Ireland.
 Department of Pharmacology, Physiology and Legal and Forensic Medicine, Faculty of Medicine, University of Zaragoza, 50009 Zaragoza, Spain. i3S-Instituto de Investigação e Inovação em Saúde, Porto University, 4200-135 Porto, Portugal. Department of Biomedicine, Faculty of Medicine, Porto University, 4200-319 Porto, Portugal. Department of Obstetrics and Gynecology, Hospital-CUF Porto, 4100-180 Porto, Portugal. Department of Pharmacology, Physiology and Legal and Forensic Medicine, Faculty of Medicine, University of Zaragoza, 50009 Zaragoza, Spain. Department of Pharmacology, Physiology and Legal and Forensic Medicine, Faculty of Medicine, University of Zaragoza, 50009 Zaragoza, Spain. Department of Physiology, Faculty of Medicine and Health Sciences, University of Badajoz, 06006 Badajoz, Spain. Department of Pharmacology, Physiology and Legal and Forensic Medicine, Faculty of Medicine, University of Zaragoza, 50009 Zaragoza, Spain.
 Department of Neurology, Peking Union Medical College Hospital, Beijing, China. Department of Neurology, Peking Union Medical College Hospital, Beijing, China. Department of Neurology, Peking Union Medical College Hospital, Beijing, China. Department of Neurology, Peking Union Medical College Hospital, Beijing, China. Department of Neurology, Peking Union Medical College Hospital, Beijing, China.
 Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Kosygin Str. 4, 199334 Moscow, Russia. Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Kosygin Str. 4, 199334 Moscow, Russia. Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Kosygin Str. 4, 199334 Moscow, Russia.
 Penn Frontotemporal Degeneration Center, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA. Department of Genetic Medicine, Johns Hopkins University, Baltimore, USA. Department of Medicine, University of Pennsylvania, Philadelphia, USA. School of Nursing, University of Pennsylvania, Philadelphia, USA. Penn Frontotemporal Degeneration Center, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA. School of Nursing, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA. Penn Frontotemporal Degeneration Center, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA. Penn Frontotemporal Degeneration Center, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA. Penn Frontotemporal Degeneration Center, University of Pennsylvania, Philadelphia, USA. Department of Neurology, University of Pennsylvania, Philadelphia, USA.
 Department of Psychiatry, University of Ottawa, Ontario, ON, Canada msolmi@toh.ca. On Track: The Champlain First Episode Psychosis Program, Department of Mental Health, The Ottawa Hospital, Ontario, ON, Canada. Ottawa Hospital Research Institute, Clinical Epidemiology Program, University of Ottawa, Ottawa, ON, Canada. School of Epidemiology and Public Health, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. Early Psychosis: Interventions and Clinical detection Lab, Institute of Psychiatry, Psychology and Neuroscience, Department of Psychosis Studies, King's College London, London, UK. Centre for Innovation in Mental Health-Developmental Lab, School of Psychology, University of Southampton, and NHS Trust, Southampton, UK. Department of Child and Adolescent Psychiatry, Charité Universitätsmedizin, Berlin, Germany. Psychiatry Unit, Veris Delli Ponti Scorrano Hospital, Department of Mental Health, ASL Lecce, Lecce, Italy. Yonsei University College of Medicine, Seoul, South Korea. Yonsei University College of Medicine, Seoul, South Korea. Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. Physiotherapy Department, South London and Maudsley NHS Foundation Trust, London, UK. Centre of Chronic Illness and Ageing, University of Greenwich, London, UK. Division of Psychology and Mental Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. Greater Manchester Mental Health NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK. Neurosciences Department, Padua Neuroscience Center, University of Padua, Italy. Mental Health Department, AULSS 3 Serenissima, Mestre, Venice, Italy. Mental Health Department, AULSS 3 Serenissima, Mestre, Venice, Italy. Department of Mental Health, AULSS 7 Pedemontana Veneto, Italy. Department of Mental Health, AULSS 7 Pedemontana Veneto, Italy. Pain and Rehabilitation Centre, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden. Department of Mental Health, Asl Salerno, Salerno, Italy. European Biomedical Research Institute of Salerno, Salerno, Italy. Department of Clinical, Pharmaceutical and Biological Sciences, School of Life and Medical Sciences, University of Hertfordshire, Hatfield, UK. Mental Health Department, ULSS 6 Euganea, Padova, Italy. Psychiatry Unit, Department of Health Sciences, University of Florence, Florence, Italy. Psychiatry Unit, Department of Health Sciences, University of Florence, Florence, Italy. Section of Psychiatry, Department of Neuroscience, University School of Medicine Federico II, Naples, Italy. Institute of Neuroscience, Hospital Clinic, University of Barcelona, IDIBAPS, CIBERSAM, Barcelona, Catalonia, Spain. Institute of Neuroscience, Hospital Clinic, University of Barcelona, IDIBAPS, CIBERSAM, Barcelona, Catalonia, Spain. Early Psychosis: Interventions and Clinical detection Lab, Institute of Psychiatry, Psychology and Neuroscience, Department of Psychosis Studies, King's College London, London, UK. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. WHO Collaborating Centre for Research and Training in Mental Health and Service Evaluation, Department of Neuroscience, Biomedicine and Movement Sciences, Section of Psychiatry, University of Verona, Verona, Italy. Meta-Research Innovation Center at Stanford, Stanford University, Stanford, CA, USA. Meta-Research Innovation Center Berlin, Berlin Institute of Health, Charité Universitätsmedizin, Berlin, Germany. Departments of Medicine, of Epidemiology and Population Health, of Biomedical Data Science, and of Statistics, Stanford University, Stanford, CA, USA. IMPACT - The Institute for Mental and Physical Health and Clinical Translation, School of Medicine, Barwon Health, Deakin University, Geelong, VIC, Australia. Institut d'Investigacions Biomediques August Pi i Sunyer, CIBERSAM, Instituto de Salud Carlos III, University of Barcelona, Barcelona, Spain. Department of Child and Adolescent Psychiatry, Charité Universitätsmedizin, Berlin, Germany. Department of Psychiatry, Zucker Hillside Hospital, Northwell Health, Glen Oaks, NY, USA. Department of Psychiatry and Molecular Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, USA. Centre for Innovation in Mental Health-Developmental Lab, School of Psychology, University of Southampton, and NHS Trust, Southampton, UK. Clinical and Experimental Sciences (Central Nervous System and Psychiatry), Faculty of Medicine, University of Southampton, Southampton, UK. Solent NHS Trust, Southampton, UK. Division of Psychiatry and Applied Psychology, School of Medicine, University of Nottingham, Nottingham, UK. Hassenfeld Children's Hospital at NYU Langone, New York University Child Study Center, New York City, New York, NY, USA. Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College of London, London, UK. Department of Psychiatry, University of Tasmania, Sandy Bay, TAS, Australia. Co-Director, Centre for Mental Health Service Innovation, Department of Health, Tasmania, Australia. Department of Pediatrics, Yonsei University College of Medicine, Seoul, South Korea. Severance Underwood Meta-research Center, Institute of Convergence Science, Yonsei University, Seoul, South Korea. Pain and Rehabilitation Centre, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden. Research Laboratory Psychology of Patients, Families and Health Professionals, Department of Nursing, School of Health Sciences, University of Ioannina, Ioannina, Greece.
 Internal Medicine, Los Angeles County+University of Southern California (USC) Medical Center, Los Angeles, USA. Internal Medicine, Virginia Commonwealth University (VCU) Medical Center, Richmond, USA. Endocrinology, Los Angeles County+University of Southern California (USC) Medical Center, Los Angeles, USA.
 UPMC Internal Medicine and Pediatrics Residency Program, University of Pittsburgh, Pittsburgh, PA 15224, USA. Department of Pediatrics, Division of Radiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15224, USA. Department of Pediatrics, Division of Pulmonary Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15224, USA. Department of Pediatrics, Division of Rheumatology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15224, USA.
 Department of Woman Health, Israeli Faculty of Health Sciences Albert Einstein, São Paulo, Brazil. Service of Gynecology and Obstetrics, Municipal University Hospital of São Bernardo do Campo, São Bernardo do Campo, Brazil. Service of Gynecology and Obstetrics, Municipal University Hospital of São Bernardo do Campo, São Bernardo do Campo, Brazil. Department of Fetal Medicine, Clínica de Diagnóstico por Imagem (CDPI), Rio de Janeiro, Brazil. Department of Fetal Medicine, Clínica de Diagnóstico por Imagem (CDPI), Rio de Janeiro, Brazil. Department of Obstetrics, Paulista School of Medicine - Federal University of São Paulo (EPM-UNIFESP), São Paulo, Brazil.
 Department of Radiology, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangdong, 510310, Guangzhou, China. Biomedical MR Laboratory, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Room 2313, 4525 Scott Ave, Campus Box 8227, St. Louis, MO, 63110-1093, USA. Biomedical MR Laboratory, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Room 2313, 4525 Scott Ave, Campus Box 8227, St. Louis, MO, 63110-1093, USA. Department of Radiology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, #1 Panfu Road, Yuexiu District, Guangdong, 510180, Guangzhou, China. Department of Neurology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, #1 Panfu Road, Yuexiu District, Guangdong, 510180, Guangzhou, China. Biomedical MR Laboratory, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Room 2313, 4525 Scott Ave, Campus Box 8227, St. Louis, MO, 63110-1093, USA. Biomedical MR Laboratory, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Room 2313, 4525 Scott Ave, Campus Box 8227, St. Louis, MO, 63110-1093, USA. Department of Radiology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, #1 Panfu Road, Yuexiu District, Guangdong, 510180, Guangzhou, China. Department of Radiology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, #1 Panfu Road, Yuexiu District, Guangdong, 510180, Guangzhou, China. Biomedical MR Laboratory, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Room 2313, 4525 Scott Ave, Campus Box 8227, St. Louis, MO, 63110-1093, USA. ssong@wustl.edu. Department of Radiology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, #1 Panfu Road, Yuexiu District, Guangdong, 510180, Guangzhou, China. eyruimengyang@scut.edu.cn.
 Biochemistry and Proteomics Laboratory, Department of Veterinary Medicine, University of Perugia, Perugia, Italy. Institute of Medical Biochemistry, University of Veterinary Medicine Vienna, Vienna, Austria. Electronic address: ingrid.miller@vetmeduni.ac.at. Proteomics, Metabolomics & Mass Spectrometry Laboratory, ISPAAM, National Research Council, Portici, Italy. Biochemistry and Proteomics Laboratory, Department of Veterinary Medicine, University of Perugia, Perugia, Italy. Department of Chemistry, Biology and Biotechnology, University of Perugia, Perugia, Italy. Research and Advanced Technologies Department, IRCCS Regina Elena National Cancer Institute, Rome, Italy. Department of Chemistry, Biology and Biotechnology, University of Perugia, Perugia, Italy. Electronic address: brunella.tancini@unipg.it. Proteomics, Metabolomics & Mass Spectrometry Laboratory, ISPAAM, National Research Council, Portici, Italy. Associazione Sclerosi Tuberosa, O.N.L.U.S., Rome, Italy.
 Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA. Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.
 Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain acobo@cem-cat.org. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Department of Neurology, Hospital Universitario Doce de Octubre, Madrid, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Section of Neuroradiology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain. Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Hospital Universitari Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain.
 Department of Diagnostic and Interventional Radiology, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany. Department of Diagnostic and Interventional Radiology, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany. Department I of Internal Medicine, Center for Integrated Oncology Aachen Bonn Cologne Dusseldorf, University Hospital of Cologne, Kerpener Straße 62, 50937 Cologne, Germany. Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Härtelstraße 16-18, 04107 Leipzig, Germany. Department of Radiology and Nuclear Medicine, University Hospital Schleswig-Holstein, Ratzeburger Allee 160, 23562 Lübeck, Germany. Institute of Interventional Radiology, University Hospital Schleswig-Holstein, Ratzeburger Allee 160, 23562 Lübeck, Germany. Fraunhofer Institute for Digital Medicine MEVIS, Maria-Goeppert-Straße 3, 23562 Lübeck, Germany. Department of Diagnostic and Interventional Radiology, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany. Department of Internal Medicine II, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany. Department of Internal Medicine II, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany. Department of Internal Medicine, Klinikum Nürnberg Nord, Prof.-Ernst-Nathan-Str. 1, 90419 Nürnberg, Germany. Department of Internal Medicine II, University Hospital Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany.
 Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, Victoria, Australia Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, Victoria, Australia University of Melbourne, Melbourne, Australia
 Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK. Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK. Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK.
 Unit of Oral and Maxillofacial Surgery, Oral Health Sciences Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Unit of Oral and Maxillofacial Surgery, Oral Health Sciences Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Electronic address: drvidyarattan@gmail.com. Unit of Oral and Maxillofacial Surgery, Oral Health Sciences Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
 Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Electronic address: liuyaling@hb2h.com. Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; The Key Laboratory of Neurology (Hebei Medical University), Ministry of Education, Shijiazhuang, Hebei, 050000, PR China; Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, 050000, PR China. Electronic address: dong_ii@tom.com.
 Psychology Department, University of Cape Town, Cape Town, South Africa. Department of Paediatric Neurology, University of Cape Town and Red Cross War Memorial Children's Hospital, Cape Town, South Africa. Psychology Department, University of Cape Town, Cape Town, South Africa. Department of Paediatric Neurology, University of Cape Town and Red Cross War Memorial Children's Hospital, Cape Town, South Africa. Private. Psychology Department, University of Cape Town, Cape Town, South Africa.
 National Research Centre for the Working Environment, Copenhagen, Denmark. jpe@nfa.dk. National Research Centre for the Working Environment, Copenhagen, Denmark. The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. Finnish Institute of Occupational Health, Helsinki, Finland.
 The University of Queensland Centre for Clinical Research, Brisbane, Australia. Department of Neurology, the Royal Brisbane & Women's Hospital, Brisbane, Australia. The University of Queensland Centre for Clinical Research, Brisbane, Australia. The University of Queensland Centre for Clinical Research, Brisbane, Australia. Department of Neurology, the Royal Brisbane & Women's Hospital, Brisbane, Australia. The University of Queensland Centre for Clinical Research, Brisbane, Australia. Department of Neurology, the Royal Brisbane & Women's Hospital, Brisbane, Australia.
 GW Research Ltd, Cambridge, UK. Greenwich Biosciences, Carlsbad, California, USA. GW Research Ltd, Cambridge, UK. GW Research Ltd, Cambridge, UK. Jazz Pharmaceuticals, Palo Alto, California, USA. GW Research Ltd, Cambridge, UK. GW Research Ltd, Cambridge, UK.
 Department of Brain Sciences, Imperial College London, London, United Kingdom. Neuromodulation Lab, Department of Psychology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom. Department of Brain Sciences, Imperial College London, London, United Kingdom. Department of Brain Sciences, Imperial College London, London, United Kingdom. UKRI Centre for Doctoral Training in AI for Healthcare, Department of Computing, Imperial College London, London, United Kingdom. Department of Brain Sciences, Imperial College London, London, United Kingdom. UK Dementia Research Institute: Care Research & Technology, London, United Kingdom. Department of Brain Sciences, Imperial College London, London, United Kingdom. Engineering and Physical Sciences Research Council CDT Neurotechnology, Imperial College London, London, United Kingdom. NMR Unit, Queen Square Multiple Sclerosis Centre, UCL, Queen Square Institute of Neurology, Department of Neuroinflammation, Faculty of Brain Sciences, University College London, London, United Kingdom. Department of Brain Sciences, Imperial College London, London, United Kingdom. Centre for Neuroimaging Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. Department of Brain Sciences, Imperial College London, London, United Kingdom.
 Neuro-Ophthalmology Unit, Presidio Ospedaliero Oftalmico, Rome, Italy. RINGGOLD: 220411 Multiple Sclerosis Centre, Presidio Ospedaliero San Filippo Neri, Rome, Italy. RINGGOLD: 18660 Multiple Sclerosis Centre, Presidio Ospedaliero San Filippo Neri, Rome, Italy. RINGGOLD: 18660 Neuro-Ophthalmology Unit, Presidio Ospedaliero Oftalmico, Rome, Italy. RINGGOLD: 220411 Università Cattolica del Sacro Cuore School of Medicine, Rome, Italy. RINGGOLD: 60234 Neurology Unit, Presidio Ospedaliero San Filippo Neri, Rome, Italy. RINGGOLD: 18660 Neuro-Ophthalmology Unit, Presidio Ospedaliero Oftalmico, Rome, Italy. RINGGOLD: 220411
 Neuromuscular Diseases Unit, Department of Neurology, Neurology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel-Aviv, Israel. Movement Disorders Unit, Neurological Institute, Neurology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel-Aviv, Israel. Movement Disorders Unit, Neurological Institute, Neurology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel-Aviv, Israel. Neuroimmunology and Multiple Sclerosis Unit, Neurology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel-Aviv, Israel. Electronic address: arnonk@tlvmc.gov.il.
 Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology with Institute of Translational Neurology, University of Münster, Albert-Schweitzer-Campus 1, Building A1, Münster 48149, Germany.
 Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. ProteoBridge Corporation, Tokyo, Japan. ProteoBridge Corporation, Tokyo, Japan. ProteoBridge Corporation, Tokyo, Japan. ProteoBridge Corporation, Tokyo, Japan. Molecular Profiling Research Center for Drug Discovery, National Institute of Advanced Industrial Science and Technology, Tokyo, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Clinical Cannabinoid Research, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Dermatology, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan. Department of Dermatology, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. ProteoBridge Corporation, Tokyo, Japan. Molecular Profiling Research Center for Drug Discovery, National Institute of Advanced Industrial Science and Technology, Tokyo, Japan. Department of Dermatology, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Department of Clinical Cannabinoid Research, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
 Mental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China. Mental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China. Department of Neurology, The 3Rd Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China. Clinical Trial Center, National Medical Products Administration Key Laboratory for Clinical Research and Evaluation of Innovative Drugs, West China Hospital Sichuan University, Chengdu, People's Republic of China. Department of Emergency Medicine, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, China. Mental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China. zhangcc89@foxmail.com.
 Bojana Ljubičić, Department of Emergency Internal Medicine, University Clinical Centre of Vojvodina, Hajduk Veljkova 1, 21000 Novi Sad, Serbia, bojana.ljubicic@mf.uns.ac.rs.
 Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Psychiatry, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
 Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, China. School of Basic Medical Science, Central South University, Changsha, Hunan, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China.
 Institute of Biomedicine (iBiMED) and Department of Medical Sciences, University of Aveiro, 3810-193 Aveiro, Portugal. Institute of Biomedicine (iBiMED) and Department of Medical Sciences, University of Aveiro, 3810-193 Aveiro, Portugal. Aveiro Institute of Materials (CICECO), Department of Chemistry, University of Aveiro, 3810-193 Aveiro, Portugal. Institute of Biomedicine (iBiMED) and Department of Medical Sciences, University of Aveiro, 3810-193 Aveiro, Portugal.
 Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran. Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran. Immunology Research Center, Department of Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran. Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran. Neuroscience Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Neuroscience Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran. Immunology Research Center, Department of Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Immunology Research Center, Department of Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
 Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China.
 Brain Chemistry Labs, Jackson, Wyoming, USA. Brain Chemistry Labs, Jackson, Wyoming, USA. Brain Chemistry Labs, Jackson, Wyoming, USA.
 Department of Oncology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China. Department of Oncology, Suqian First Hospital, Suqian, Jiangsu, China. Department of Immunology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. Shuwen Biotech Company Ltd, Hangzhou, Zhejiang, China. Shuwen Biotech Company Ltd, Hangzhou, Zhejiang, China. yuanxy@shuwendx.com. Department of Medical Microbiology and Immunology, School of Preclinical Medicine, Wannan Medical College, Wuhu, China. wuyanhong849@126.com.
 Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA. Division of Rheumatology, Department of Internal Medicine, Intermountain Medical Center, Salt Lake City, UT, USA. Department of Rheumatology and Immunology, Singapore General Hospital, Singapore. Duke-National University of Singapore Medical School, Singapore. Division of Rheumatology, Department of Internal Medicine, University of Pittsburgh, Pittsburgh, PA, USA. Department of Biomedical Data Science, Department of Molecular and Systems Biology, Dartmouth School of Medicine, Hanover, NH, USA. Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
 Department of Biological Sciences, Centre for Biomedical Sciences, Royal Holloway University of London, Egham, United Kingdom. Department of Biological Sciences, Centre for Biomedical Sciences, Royal Holloway University of London, Egham, United Kingdom. Department of Biological Sciences, Centre for Biomedical Sciences, Royal Holloway University of London, Egham, United Kingdom. Department of Biological Sciences, Centre for Biomedical Sciences, Royal Holloway University of London, Egham, United Kingdom.
 Unit of Endocrinology, Department of Clinical and Experimental Medicine, University of Messina, AOU Policlinico "Gaetano Martino" University Hospital, 98125, Messina, Italy. rmruggeri@unime.it. Department of Clinical Medicine and Surgery, Endocrinology Unit, University Federico II, Naples, Italy. SSD Endocrine Disease and Diabetology, ASL TO3, Pinerolo, TO, Italy. Endocrinology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea Hospital, ENETS Center of Excellence, Sapienza University of Rome, Rome, Italy. Department of Clinical Medicine and Surgery, Endocrinology Unit, University Federico II, Naples, Italy. Endocrinology Unit, IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy. Gruppo NETTARE, Policlinico Umberto I, Università Sapienza, Rome, Italy. Department of Clinical Medicine and Surgery, Endocrinology Unit, University Federico II, Naples, Italy. UNESCO Chair "Education for Health and Sustainable Development", Federico II University, Naples, Italy. Endocrinology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea Hospital, ENETS Center of Excellence, Sapienza University of Rome, Rome, Italy.
 Department of Vitreo Retina, Aditya Birla Sankara Nethralaya, Kolkata, India. Department of Vitreo Retina, Aditya Birla Sankara Nethralaya, Kolkata, India. Department of Vitreo Retina, Aditya Birla Sankara Nethralaya, Kolkata, India. Department of Vitreo Retina, Aditya Birla Sankara Nethralaya, Kolkata, India.
 Division of Dermatology, Outpatient Consultation for Rare Diseases, Trento, Italy. Division of Dermatology, Outpatient Consultation for Rare Diseases, Trento, Italy. Division of Pediatrics, Outpatient Consultation for Rare Diseases, Trento, Italy. Hospital Pharmacy Unit, Trento General Hospital, Autonomous Province of Trento, Trento, Italy. Division of Dermatology, Outpatient Consultation for Rare Diseases, Trento, Italy. Dermatology Unit, IRCSS Policlinico di S. Orsola, Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Bologna, Italy. Division of Dermatology, Outpatient Consultation for Rare Diseases, Trento, Italy. Division of Dermatology, Outpatient Consultation for Rare Diseases, Trento, Italy.
 Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. PhD Program in Neuroscience, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics, Department of Health Sciences, International Medical School, University of Milan, Milano, Italy. ASST Santi Paolo e Carlo, San Paolo University Hospital, Milan, Italy. IRCCS Ca' Granda Foundation Maggiore Policlinico Hospital, Milan, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. Department of Pathophysiology and Transplantation, 'Dino Ferrari Center', Università degli Studi di Milano, Milan, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. Department of Pathophysiology and Transplantation, 'Dino Ferrari Center', Università degli Studi di Milano, Milan, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy. Department of Pathophysiology and Transplantation, 'Dino Ferrari Center', Università degli Studi di Milano, Milan, Italy. Department of Neurorehabilitation Sciences, Casa di Cura del Policlinico, Milan, Italy. Department of Neurology and Laboratory of Neuroscience, IRCCS Istituto Auxologico Italiano, Milan, Italy.
 NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, University of California San Francisco, San Francisco, California, USA. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Einstein Center Digital Future, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Centre for Neurology and Neuropsychiatry, Landschaftsverband Rheinland-Klinikum Düsseldorf, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, KS Hegde Medical Academy, Nitte University, Mangalore, Karnataka, India. Department of Neurology, KS Hegde Medical Academy, Nitte University, Mangalore, Karnataka, India. Hospital Clinic of Barcelona-Institut d'Investigacions, Biomèdiques August Pi Sunyer, (IDIBAPS), Barcelona, Spain. Hospital Clinic of Barcelona-Institut d'Investigacions, Biomèdiques August Pi Sunyer, (IDIBAPS), Barcelona, Spain. Hospital Clinic of Barcelona-Institut d'Investigacions, Biomèdiques August Pi Sunyer, (IDIBAPS), Barcelona, Spain. Wu Tsai Neurosciences Institute, Stanford University, Palo Alto, California, USA. Department of Neurology, Oxford University Hospitals, National Health Service Trust, Oxford, UK. Department of Neurology, Oxford University Hospitals, National Health Service Trust, Oxford, UK. Department of Neurology, Oxford University Hospitals, National Health Service Trust, Oxford, UK. Department of Ophthalmology, Oxford University Hospitals, National Health Service Trust, Oxford, UK. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE) Scientific Institute San Raffaele and University Vita-Salute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE) Scientific Institute San Raffaele and University Vita-Salute San Raffaele, Milan, Italy. Experimental Neurophysiology Unit, Institute of Experimental Neurology (INSPE) Scientific Institute San Raffaele and University Vita-Salute San Raffaele, Milan, Italy. CIEM MS Research Center, University of Minas Gerais, Medical School, Belo Horizonte, Brazil. CIEM MS Research Center, University of Minas Gerais, Medical School, Belo Horizonte, Brazil. Institute of Clinical Neuroimmunology, LMU Hospital, Ludwig-Maximilians Universität München, Munich, Germany. Kashani MS Center, Isfahan University of Medical Sciences, Isfahan, Iran. School of advanced technologies in medicine and Medical Image and Signal processing Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Ophthalmology, Isfahan Eye Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Ophthalmology, Isfahan Eye Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Neurology, Multiple Sclerosis, Myelin Disorders and Neuroinflammation, Pierre Wertheimer Neurological Hospital, Hospices Civils de Lyon, Lyon, France. Neurology, Multiple Sclerosis, Myelin Disorders and Neuroinflammation, Pierre Wertheimer Neurological Hospital, Hospices Civils de Lyon, Lyon, France. Centre d'Esclerosi Múltiple de Catalunya (Cemcat). Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark. Departments of Neurology, Slagelse Hospitals Denmark, Institute of Regional Health Research, University of Southern Denmark, Odense, Denmark. Department of Neurology, The Walton Centre NHS Foundation Trust, Liverpool, UK. Department of Neurology, Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE. Department of Neurology, The Walton Centre NHS Foundation Trust, Liverpool, UK. Department of Neurology, University of Michigan Medical School, Ann Arbor, Michigan, USA. Department of Neurology, University of California San Francisco, San Francisco, California, USA. Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Department of Medicine, Divisions of Molecular Medicine & Infectious Diseases, Harbor-University of California at Los Angeles (UCLA) Medical Center, and Lundquist Institute for Biomedical Innovation, Torrance, California, USA. Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. Departments of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan Medical School, Ann Arbor, Michigan, USA. Division of Metabolism, Endocrine and Diabetes, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA. Department of Pediatrics, University of Utah, Salt Lake City, Utah, USA. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, University of California, Irvine, Irvine, California, USA. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany friedemann.paul@charite.de. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Moorfield's Eye Hospital, The National Hospital for Neurology and Neurosurgery, Queen Square Institute of Neurology, University College London, London, UK. Neuro-ophthalmology Expert Center, Amsterdam UMC, Amsterdam, Netherlands.
 San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimmunology Unit, INSpe, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Neuroimmunology Unit, INSpe, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Processing Developmental Laboratory, San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Processing Developmental Laboratory, San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. GLP Test Facility, San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Department of Pediatrics, University of California at San Diego, La Jolla, CA 92093, USA. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. GLP Test Facility, San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Pathology Unit, Department of Experimental Oncology, IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Neuroimmunology Unit, INSpe, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy. Vita-Salute San Raffaele University, Milan, Italy. Pediatric Immunohematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), IRCCS San Raffaele Scientific Institute, Milan, Italy.
 Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S. Nagar, Punjab, India. Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S. Nagar, Punjab, India.
 Unité Des Ataxies Cérébelleuses, Department of Neurology, CHU de Charleroi, Charleroi, Belgium. pcabaraux@gmail.com. Columbia University, New York, NY, USA. Department of Neurology, Neuroscience Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China. IRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy. Department of Medico-Surgical Sciences and Biotechnologies, University of Rome Sapienza, Latina, Italy. EuroMov Digital Health in Motion, Univ Montpellier, IMT Mines Ales, Montpellier, France. Department of Neurological Sciences, University of Nebraska Medical Center, Omaha, USA. Université Versailles Saint-Quentin, Versailles, France. Service de NeuroImagerie, Centre Hospitalier National des 15-20, Paris, France. Institute of Anatomy and Cell Biology I, Ludwig Maximilians-University Munich, Munich, Germany. Section Computational Sensomotorics, Hertie Institute for Clinical Brain Research, University Tübingen, Tübingen, Germany. Department of Neurology, University of Texas Southwestern, Dallas, TX, USA. Department of Medical Education, Tokyo Medical University, Tokyo, Japan. The BioRobotics Institute, Scuola Superiore Sant'Anna, Pisa, Italy. Department of Human Neurosciences, University of Rome Sapienza, Rome, Italy. Department of Occupational and Environmental Medicine, Epidemiology and Hygiene, INAIL, Monte Porzio Catone, Rome, Italy. Department of Rehabilitation & Regenerative Medicine (Programs in Physical Therapy), Gertrude H. Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA. Department of Human Neurosciences, University of Rome Sapienza, Rome, Italy. Neuroimmunology Unit, IRCSS Fondazione Santa Lucia, Rome, Italy. Department of Systems Medicine, University of Roma Tor Vergata, Rome, Italy. Department of Medico-Surgical Sciences and Biotechnologies, University of Rome Sapienza, Latina, Italy. Movement Analysis LAB, Policlinico Italia, Rome, Italy. MARlab, Neuroscience and Neurorehabilitation Department, Bambino Gesù Children's Hospital - IRCCS, Rome, Italy. Department of Neurology and German Center for Vertigo and Balance Disorders, Hospital of the Ludwig Maximilians-University Munich, Munich, Germany. Neuroscience Training Program and Waisman Center, University of Wisconsin-Madison, Madison, WI, USA. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research and Centre of Neurology, Tübingen, Germany. Dalian Key Laboratory of Smart Medical and Health, Dalian University, Dalian, 116622, China. Department of Neurology, Tokyo Medical University, Tokyo, Japan. Department of Neurological Sciences, University of Nebraska Medical Center, Omaha, USA. Department of Kinesiology and Waisman Center, University of Wisconsin-Madison, Madison, WI, USA. School of Kinesiology, Auburn University, Auburn, AL, USA. Unité Des Ataxies Cérébelleuses, Department of Neurology, CHU de Charleroi, Charleroi, Belgium. Service Des Neurosciences, University of Mons, UMons, Mons, Belgium.
 Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Comprehensive Center for Clinical Neurosciences, Medical University of Vienna, & Mental Health, Vienna, Austria. Department of Internal Medicine III, Division of Endocrinology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Comprehensive Center for Clinical Neurosciences, Medical University of Vienna, & Mental Health, Vienna, Austria. Comprehensive Center for Clinical Neurosciences, Medical University of Vienna, & Mental Health, Vienna, Austria. Department of Neuroradiology and Musculoskeletal Radiology, Medical University of Vienna, Vienna, Austria. Department of Internal Medicine III, Division of Endocrinology, Medical University of Vienna, Vienna, Austria. Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. Comprehensive Center for Clinical Neurosciences, Medical University of Vienna, & Mental Health, Vienna, Austria. Department of Neurosurgery, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. Comprehensive Center for Clinical Neurosciences, Medical University of Vienna, & Mental Health, Vienna, Austria. Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. gabriel.bsteh@meduniwien.ac.at. Comprehensive Center for Clinical Neurosciences, Medical University of Vienna, & Mental Health, Vienna, Austria. gabriel.bsteh@meduniwien.ac.at.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Institute of Brain Science Department, Neurology of First Affiliated Hospital, Shanxi Datong University, Datong, Shanxi Province, 037009, China. Department of Anatomy and Cell Biology, Department of Neurological Surgery, Spinal Cord and Brain Injury Research Group, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. Institute of Neurology, Huashan Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200025, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. Institute of Brain Science Department, Neurology of First Affiliated Hospital, Shanxi Datong University, Datong, Shanxi Province, 037009, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, Shanxi Province, 030619, China. chaizhi@sxtcm.edu.cn.
 Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Omics Medicine, Graduate School of Medicine, Chiba University, 1-8-1 Inohana. Chuo-ku, Chiba 260-8670 Japan. AMED-CREST, AMED, Tokyo, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Laboratory of Microenvironmental Metabolic Health Sciences Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655 Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Frontier Research and Development, Laboratory of Medical Omics Research, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. Department of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa Kamatari, Kisarazu, Chiba 292-0818, Japan. AMED-CREST, AMED, Tokyo, Japan. Laboratory of Microenvironmental Metabolic Health Sciences Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655 Japan. AMED-CREST, AMED, Tokyo, Japan. Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana. Chuo-ku, Chiba 260-8670 Japan.
 Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama. Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama. Division of Transplant Surgery, University of Alabama at Birmingham, Birmingham, Alabama. Department of Public Health, University of Alabama at Birmingham, Birmingham, Alabama. Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama. Veterans Affairs Medical Center, University of Alabama at Birmingham, Birmingham, Alabama.
 Service de Médecine Interne Purpan, Centre Hospitalier Universitaire de Toulouse, France; Service des Maladies Infectieuses et Tropicales, Centre Hospitalier Universitaire de Toulouse, France. Electronic address: boumaza.x@chu-toulouse.fr. Service de Pharmacologie Médicale et Clinique, Centre Hospitalier Universitaire de Toulouse, France; Centre d'Investigation Clinique 1436, Equipe PEPSS, Centre Hospitalier Universitaire de Toulouse, INSERM, Toulouse, France. Laboratoire d'Immunologie, Institut Fédératif de Biologie, Centre Hospitalier Universitaire de Toulouse, France; Centre de Physiopathologie de Toulouse-Purpan, Centre Hospitalier Universitaire de Toulouse, France. Service de Médecine Interne Purpan, Centre Hospitalier Universitaire de Toulouse, France; Centre d'Investigation Clinique 1436, Equipe PEPSS, Centre Hospitalier Universitaire de Toulouse, INSERM, Toulouse, France. Service de Médecine Interne et immunologie clinique Rangueil, Centre Hospitalier Universitaire de, Toulouse, France. Service des Maladies Infectieuses et Tropicales, Centre Hospitalier Universitaire de Toulouse, France; Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), INSERM UMR1291 - CNRS UMR5051 - Université Toulouse III, France. Service de Neurologie, Centre Hospitalier Universitaire de Toulouse, France. Service de Neurologie, Centre Hospitalier Universitaire de Toulouse, France. Service de Rhumatologie, Centre Hospitalier Universitaire de Toulouse, France. Service de Dermatologie, Centre Hospitalier Universitaire de Toulouse, France. Service de Pharmacologie, Institut Universitaire du Cancer Oncopole, France. Service de Médecine Interne Purpan, Centre Hospitalier Universitaire de Toulouse, France; Centre d'Investigation Clinique 1436, Equipe PEPSS, Centre Hospitalier Universitaire de Toulouse, INSERM, Toulouse, France. Service de Médecine Interne et immunologie clinique Rangueil, Centre Hospitalier Universitaire de, Toulouse, France. Laboratoire d'Immunologie, Institut Fédératif de Biologie, Centre Hospitalier Universitaire de Toulouse, France; Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), INSERM UMR1291 - CNRS UMR5051 - Université Toulouse III, France. Service de Néphrologie et Transplantation d'Organes, Centre de Référence Maladies Rénales Rares, Centre Hospitalier Universitaire de Toulouse, France. Service de Médecine Interne Purpan, Centre Hospitalier Universitaire de Toulouse, France; Centre d'Investigation Clinique 1436, Equipe PEPSS, Centre Hospitalier Universitaire de Toulouse, INSERM, Toulouse, France.
 Department of Neuroscience, Yale University, New Haven, CT, USA. Department of Pathology, Yale University, New Haven, CT, USA. Department of Ophthalmology and Visual Science, Yale University, New Haven, CT, USA. Department of Ophthalmology and Visual Science, Yale University, New Haven, CT, USA. Department of Neuroscience, Yale University, New Haven, CT, USA. Department of Neurology, Yale University, New Haven, CT, USA. Yale School of Medicine, New Haven, CT, USA. Yale School of Medicine, New Haven, CT, USA. Department of Ophthalmology and Visual Science, Yale University, New Haven, CT, USA. Division of Infection, Immunity and Respiratory Medicine, University of Manchester, Manchester, UK. Department of Computer Science, Yale University, New Haven, CT, USA. Department of Applied Math, Yale University, New Haven, CT, USA. Department of Ophthalmology and Visual Science, Yale University, New Haven, CT, USA. Computational Biology, Bioinformatics Program, Yale University, New Haven, CT, USA. Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA. Department of Computer Science, Yale University, New Haven, CT, USA. Mila-Quebec AI institute, Montréal, QC, Canada. Department of Mathematics and Statistics, Université de Montréal, Montréal, QC, Canada. Department of Computer Science, Rutgers University, New Brunswick, NJ, USA. Department of Genetics, Yale University, New Haven, CT, USA. Department of Ophthalmology and Visual Science, Yale University, New Haven, CT, USA. Yale School of Medicine, New Haven, CT, USA. Department of Computational Mathematics, Science and Engineering, Michigan State University, East Lansing, MI, USA. Department of Mathematics, Michigan State University, East Lansing, MI, USA. Department of Biosystems Science and Engineering, ETH Zurich, Zurich, Switzerland. Mila-Quebec AI institute, Montréal, QC, Canada. Department of Mathematics and Statistics, Université de Montréal, Montréal, QC, Canada. Department of Computer Science, Yale University, New Haven, CT, USA. smita.krishnaswamy@yale.edu. Department of Genetics, Yale University, New Haven, CT, USA. smita.krishnaswamy@yale.edu. Department of Pathology, Yale University, New Haven, CT, USA. brian.hafler@yale.edu. Department of Ophthalmology and Visual Science, Yale University, New Haven, CT, USA. brian.hafler@yale.edu. Broad Institute of MIT and Harvard, Cambridge, MA, USA. brian.hafler@yale.edu.
 Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: zgykdxwuhui@foxmail.com. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Shanghai Key Laboratory of Compound Chinese Medicines, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, The State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: xiaojunwu320@126.com.

 From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. amwilson@mednet.ucla.edu. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA. From the Department of Neurology (A.M.W.), University of California, Los Angeles; Department of Neurology (A.M.W.), Greater Los Angeles Healthcare System, Los Angeles, CA; American Academy of Neurology (K.B.L., B.S., A.M.), Minneapolis, MN; Verana Health (A.L.), San Francisco, CA; Department of Neurology (S.M.B.), University of Minnesota, Minneapolis; Department of Neurology (G.J.E.), Emory University, Atlanta, GA; Department of Neurology (K.V.N.), University of Colorado, Denver; and Department of Neurology (J.P.N.), Edith Nourse Rogers VA Medical Center, Bedford, MA.
 Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Buffalo Neuroimaging Analysis Center, Department of Neurology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY 14203, USA. Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York, Buffalo, NY 14203, USA.
 Department of Neuromuscular Diseases, Barts Health NHS Trust, London, E1 1BB, UK. Department of Neuromuscular Diseases, University College London, London, WC1N 3BG, UK. Centre for Neuromuscular Disease, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK. Department of Neuromuscular Diseases, University College London, London, WC1N 3BG, UK. Centre for Neuromuscular Disease, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK. Department of Neuromuscular Diseases, University College London, London, WC1N 3BG, UK. Centre for Neuromuscular Disease, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK. Department of Neuromuscular Diseases, University College London, London, WC1N 3BG, UK. NHS Neuroimmunology and CSF Laboratory, Queen Square Institute of Neurology, Queen Square London WC1N 3BG, UK. NHS Neuroimmunology and CSF Laboratory, Queen Square Institute of Neurology, Queen Square London WC1N 3BG, UK. Department of Neuroinflammation, University College London, London, WC1N 3BG, UK. Department of Neuromuscular Diseases, University College London, London, WC1N 3BG, UK. UK Dementia Research Institute at UCL, London, WC1E 6BT, UK. Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK. UK Dementia Research Institute at UCL, London, WC1E 6BT, UK. Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK. Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792, USA. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, 431 41, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, 431 41, Sweden. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK. NHS Neuroimmunology and CSF Laboratory, Queen Square Institute of Neurology, Queen Square London WC1N 3BG, UK. Department of Neuroinflammation, University College London, London, WC1N 3BG, UK. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands. UCL Clinical and Movement Neurosciences Department, National Hospital for Neurology and Neurosurgery, UCL Institute of Neurology, London, WC1E 6BT, UK. Department of Neuromuscular Diseases, University College London, London, WC1N 3BG, UK. Centre for Neuromuscular Disease, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK. NHS Neuroimmunology and CSF Laboratory, Queen Square Institute of Neurology, Queen Square London WC1N 3BG, UK.
 Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Interuniversity Centre of Bioengineering of the Human Neuromusculoskeletal System (IuC BoHNes), Sassari, Italy. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Interuniversity Centre of Bioengineering of the Human Neuromusculoskeletal System (IuC BoHNes), Sassari, Italy. Department of Mechanical Engineering, Insigneo Institute for In Silico Medicine, The University of Sheffield, Sheffield, United Kingdom. Interuniversity Centre of Bioengineering of the Human Neuromusculoskeletal System (IuC BoHNes), Sassari, Italy. Department of Electronics and Telecommunications, Politecnico Di Torino, Torino, Italy. Department of Mechanical Engineering, Insigneo Institute for In Silico Medicine, The University of Sheffield, Sheffield, United Kingdom. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University, Newcastle Upon Tyne, United Kingdom. Department of Mechanical Engineering, Insigneo Institute for In Silico Medicine, The University of Sheffield, Sheffield, United Kingdom. Centre for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Centre, Tel Aviv, Israel. Department of Neurology, University Medical Centre Schleswig-Holstein Campus Kiel and Kiel University, Kiel, Germany. Department for Geriatric Rehabilitation, Robert-Bosch-Hospital, Stuttgart, Germany. Laboratory of Movement Analysis and Measurement, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Department for Geriatric Rehabilitation, Robert-Bosch-Hospital, Stuttgart, Germany. Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom. Instituto de Salud Global Barcelona, Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Faculty of Health and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain. CIBER Epidemiología y Salud Pública, Madrid, Spain. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Bologna, Italy. Health Sciences and Technologies-Interdepartmental Centre for Industrial Research (CIRI-SDV), University of Bologna, Bologna, Italy. Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Bologna, Italy. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University, Newcastle Upon Tyne, United Kingdom. Machine Learning and Data Analytics Lab, Department Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Instituto de Salud Global Barcelona, Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Faculty of Health and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain. CIBER Epidemiología y Salud Pública, Madrid, Spain. Centre for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Centre, Tel Aviv, Israel. Department of Sport, Exercise and Rehabilitation, Faculty of Health and Life Sciences, Northumbria University, Northumbia, United Kingdom. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. Machine Learning and Data Analytics Lab, Department Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Novartis Institutes of Biomedical Research, Novartis Pharma AG, Basel, Switzerland. Instituto de Salud Global Barcelona, Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Faculty of Health and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain. CIBER Epidemiología y Salud Pública, Madrid, Spain. Machine Learning and Data Analytics Lab, Department Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Department of Neurology, University Medical Centre Schleswig-Holstein Campus Kiel and Kiel University, Kiel, Germany. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. Novartis Institutes of Biomedical Research, Novartis Pharma AG, Basel, Switzerland. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. Laboratory of Movement Analysis and Measurement, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Bologna, Italy. Health Sciences and Technologies-Interdepartmental Centre for Industrial Research (CIRI-SDV), University of Bologna, Bologna, Italy. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University, Newcastle Upon Tyne, United Kingdom. Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University, Newcastle Upon Tyne, United Kingdom. Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom. Department of Neuroscience and Sheffield NIHR Translational Neuroscience BRC, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway. Department of Sport, Exercise and Rehabilitation, Faculty of Health and Life Sciences, Northumbria University, Northumbia, United Kingdom. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Interuniversity Centre of Bioengineering of the Human Neuromusculoskeletal System (IuC BoHNes), Sassari, Italy. Department of Mechanical Engineering, Insigneo Institute for In Silico Medicine, The University of Sheffield, Sheffield, United Kingdom. Interuniversity Centre of Bioengineering of the Human Neuromusculoskeletal System (IuC BoHNes), Sassari, Italy. Department of Electronics and Telecommunications, Politecnico Di Torino, Torino, Italy. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Interuniversity Centre of Bioengineering of the Human Neuromusculoskeletal System (IuC BoHNes), Sassari, Italy. Department of Mechanical Engineering, Insigneo Institute for In Silico Medicine, The University of Sheffield, Sheffield, United Kingdom. Department of Electronics and Telecommunications, Politecnico Di Torino, Torino, Italy. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University, Newcastle Upon Tyne, United Kingdom. Centre for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Centre, Tel Aviv, Israel. Department of Neurology, University Medical Centre Schleswig-Holstein Campus Kiel and Kiel University, Kiel, Germany. Department for Geriatric Rehabilitation, Robert-Bosch-Hospital, Stuttgart, Germany. Laboratory of Movement Analysis and Measurement, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle Upon Tyne, United Kingdom. Instituto de Salud Global Barcelona, Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Faculty of Health and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain. CIBER Epidemiología y Salud Pública, Madrid, Spain. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Bologna, Italy. Health Sciences and Technologies-Interdepartmental Centre for Industrial Research (CIRI-SDV), University of Bologna, Bologna, Italy. Machine Learning and Data Analytics Lab, Department Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Department of Sport, Exercise and Rehabilitation, Faculty of Health and Life Sciences, Northumbria University, Northumbia, United Kingdom. Novartis Institutes of Biomedical Research, Novartis Pharma AG, Basel, Switzerland. Department of Neuroscience and Sheffield NIHR Translational Neuroscience BRC, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom. Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway.
 Department of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Goettingen, Goettingen, Germany. Max Planck Institute for Multidisciplinary Sciences, Goettingen, Germany. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, United Kingdom. Neurological Institute, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Neurology, Columbia University Irving Medical Center, New York, New York, USA. Department of Neurosciences (DNS), Padova University, Padova, Italy. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, United Kingdom. Department of Clinical Genetics, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands. Movement Disorders Unit, Neurology Service, Internal Medicine Department, The Federal University of Minas Gerais, Belo Horizonte, Brazil. Department of Neurology, University of California Los Angeles, Los Angeles, California, USA. Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, United Kingdom. UK Dementia Research Institute at UCL and Department of Neurodegenerative Disease, UCL Institute of Neurology, University College London, London, United Kingdom. Reta Lila Weston Institute, UCL Queen Square Institute of Neurology, London, United Kingdom. UCL Movement Disorders Centre, University College London, London, United Kingdom. Institute for Advanced Study, The Hong Kong University of Science and Technology, Hong Kong, China. Brain and Care Research Foundation, Rimini, Italy. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, United Kingdom. Department of Neurology, University Medical Center, Göttingen, Germany. Paracelsus-Elena-Klinik, Kassel, Germany. Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, Michigan, USA. Department of Neurosciences, Clinical Investigation Center CIC 1436, Parkinson Toulouse Expert Centre, NS-Park/FCRIN Network and Neuro Toul COEN Centre, Toulouse University Hospital, INSERM, University of Toulouse 3, Toulouse, France. Program in Neuroscience and Division of Neurology, The Ottawa Hospital, Ottawa, Ontario, Canada. University of Ottawa Brain and Mind Research Institute, Ottawa, Ontario, Canada. The Institute of Life Sciences and The Edmond and Lily Safra Center of Brain Science, The Hebrew University of Jerusalem, Jerusalem, Israel. First Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece. Biomedical Research Foundation of the Academy of Athens, Athens, Greece. Laboratory of Clinical Pharmacology and Therapeutics, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal. Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal. CNS-Campus Neurológico, Torres Vedras, Portugal.
 From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. zmxiao@whu.edu.cn ylongwang@126.com. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. zmxiao@whu.edu.cn ylongwang@126.com. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. zmxiao@whu.edu.cn ylongwang@126.com. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. zmxiao@whu.edu.cn ylongwang@126.com. From the Department of Neurology (Yue Wang, J.L., Y.F., L.Z., Y.Z., Yajuan Wang, L.H., Z.L., Z.X.), Renmin Hospital of Wuhan University; Department of Neurology (D.Y., Yilong Wang), Beijing Tiantan Hospital, Capital Medical University; Chinese Institute for Brain Research (Yilong Wang); China National Clinical Research Center for Neurological Diseases (Yilong Wang); Advanced Innovation Center for Human Brain Protection (Yilong Wang), Capital Medical University, Beijing; and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease (Yilong Wang), China. zmxiao@whu.edu.cn ylongwang@126.com.
 Michigan Scleroderma Program, Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Michigan Scleroderma Program, Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Michigan Scleroderma Program, Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Michigan Scleroderma Program, Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Electronic address: bhattasw@umich.edu.
 Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, School of Pharmacy, Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China. State Key Laboratory of Bioelectronics, School of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, China. Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, School of Pharmacy, Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China. Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, School of Pharmacy, Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China. State Key Laboratory of Bioelectronics, School of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, China.
 Department of Neurology, Shandong Institute of Neuroimmunology, Shandong Key Laboratory of Rheumatic Disease and Translational Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, 16766 Jingshi Road, Jinan, 250014, China. Department of Neurology, Shandong Institute of Neuroimmunology, Shandong Key Laboratory of Rheumatic Disease and Translational Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, 16766 Jingshi Road, Jinan, 250014, China. Department of Gerontology, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, 16766 Jingshi Road, Jinan, 250014, China. Department of Gerontology, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, 16766 Jingshi Road, Jinan, 250014, China. Department of Gerontology, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, 16766 Jingshi Road, Jinan, 250014, China. Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan, 250014, China. Department of Gerontology, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, 16766 Jingshi Road, Jinan, 250014, China. drjinzhiliu@163.com. Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, 67 Dongchang West Road, Liaocheng, Liaocheng, 252000, China. drjinzhiliu@163.com. Department of Gerontology, Cheeloo College of Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, 44 Wenhua West Road, Jinan, 250012, China. drjinzhiliu@163.com. Department of Geriatric Neurology, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, 16766 Jingshi Road, Jinan, 250014, China. drjinzhiliu@163.com. Department of Neurology, Cheeloo College of Medicine, Liaocheng People's Hospital, Shandong University, 44 Wenhua West Road, Jinan, 250012, China. drjinzhiliu@163.com. Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, 67 Dongchang West Road, Liaocheng, Liaocheng, 252000, China. xiazhangyong2013@163.com. Department of Neurology, Cheeloo College of Medicine, Liaocheng People's Hospital, Shandong University, 44 Wenhua West Road, Jinan, 250012, China. xiazhangyong2013@163.com.
 Rheumatology Unit, University of Pisa, via Roma 67, 56123, Pisa, Italy. dibattista.marco91@gmail.com. Department of Medical Biotechnologies, University of Siena, Siena, Italy. dibattista.marco91@gmail.com. Cardiovascular Thoracic Department, University of Pisa, Pisa, Italy. Cardiovascular Thoracic Department, University of Pisa, Pisa, Italy. Cardiovascular Thoracic Department, University of Pisa, Pisa, Italy. Rheumatology Unit, University of Pisa, via Roma 67, 56123, Pisa, Italy. Rheumatology Unit, University of Pisa, via Roma 67, 56123, Pisa, Italy. Clinical Immunology and Allergy Unit, University of Pisa, Pisa, Italy. Clinical Immunology and Allergy Unit, University of Pisa, Pisa, Italy. Radiology Unit, University of Pisa, Pisa, Italy. Section of Statistics, University of Pisa, Pisa, Italy. Rheumatology Unit, University of Pisa, via Roma 67, 56123, Pisa, Italy. Rheumatology Unit, University of Pisa, via Roma 67, 56123, Pisa, Italy.
 Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pennsylvania. Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pennsylvania. Division of Pulmonary, Critical Care, and Sleep Medicine, Ohio State University College of Medicine, Columbus, Ohio. Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
 Swallowing Rehabilitation Research Laboratory KITE Research Institute-University Health Network Toronto Ontario Canada. Rehabilitation Sciences Institute University of Toronto Toronto Ontario Canada. Aerodigestive Research Core-University of Florida Gainesville Florida United States. Swallowing Rehabilitation Research Laboratory KITE Research Institute-University Health Network Toronto Ontario Canada. Rehabilitation Sciences Institute University of Toronto Toronto Ontario Canada.
 Rostov Regional Clinical Hospital. Rostov State Medical University. Rostov State Medical University.
 "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. SC Neurologia 1U, AOU Città della Salute e della Scienza di Torino, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. Neurology Unit, Department of Clinical and Biological Sciences, San Luigi Gonzaga Hospital, University of Turin, Orbassano, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. SC Neurologia 1U, AOU Città della Salute e della Scienza di Torino, Turin, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. SC Neurologia 1U, AOU Città della Salute e della Scienza di Torino, Turin, Italy. Institute of Cognitive Sciences and Technologies, Rome, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. SC Neurologia 1U, AOU Città della Salute e della Scienza di Torino, Turin, Italy. Institute of Cognitive Sciences and Technologies, Rome, Italy. "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. SC Neurologia 1U, AOU Città della Salute e della Scienza di Torino, Turin, Italy.
 Department of Child Health. Department of Child Health. Genetics Working Group. Department of Child Health, Faculty of Medicine, Public Health and Nursing, Gadjah Mada University, UGM Academic Hospital, Yogyakarta, Indonesia. Genetics Working Group. Genetics Working Group. Genetics Working Group. Genetics Working Group. Pediatric Surgery Division, Department of Surgery, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Dr. Sardjito Hospital.
 Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy. Laboratory of Experimental Rheumatology, Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS San Martino Polyclinic Hospital, 16132 Genova, Italy.
 Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine of the TU Dresden, Dresden, Germany. Biopsychology, Department of Psychology, School of Science, TU Dresden, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. Multiple Sclerosis Center, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.
 Department of Internal Medicine and Clinical Immunology, Hotel Dieu de France Hospital, Saint Joseph University, Beirut, Lebanon. RINGGOLD: 36925 Department of Psychiatry, Hotel Dieu de France Hospital, Saint Joseph University, Beirut, Lebanon. RINGGOLD: 36925 Department of Internal Medicine, Hotel Dieu de France Hospital, Saint Joseph University, Beirut, Lebanon. RINGGOLD: 36925 Department of Internal Medicine, Hotel Dieu de France Hospital, Saint Joseph University, Beirut, Lebanon. RINGGOLD: 36925 Department of Internal Medicine and Clinical Immunology, Hotel Dieu de France Hospital, Saint Joseph University, Beirut, Lebanon. RINGGOLD: 36925 Department of Neurology, Hotel Dieu de France Hospital, Saint Joseph University, Beirut, Lebanon. RINGGOLD: 36925 Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
 Department of Health Sciences, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK, Canada. Department of Medicine, Neurology Division, University of Saskatchewan, Saskatoon, SK, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK, Canada. ArGan's Lab, School of Pharmacy, Faculty of Science, University of Waterloo, Waterloo, ON, Canada. Department of Medicine, Neurology Division, University of Saskatchewan, Saskatoon, SK, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK, Canada. Department of Chemistry, Faculty of Science, University of Waterloo, Waterloo, ON, Canada. ArGan's Lab, School of Pharmacy, Faculty of Science, University of Waterloo, Waterloo, ON, Canada. Department of Health Sciences, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada. Department of Medicine, Neurology Division, University of Saskatchewan, Saskatoon, SK, Canada. Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, SK, Canada. Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK, Canada.
 Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Department of Experimental Medicine, Section of Human Physiology, University of Genoa, Genoa, Italy. Department of Developmental and Social Psychology, University of Padova, Padua, Italy. Department of Developmental and Social Psychology, University of Padova, Padua, Italy. INSERM UMR1093-CAPS, Université Bourgogne Franche-Comté, UFR des Sciences du Sport, Dijon, France. Italian Multiple Sclerosis Foundation, Scientific Research Area, Genoa, Italy. Department of Experimental Medicine, Section of Human Physiology, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
 Division of Multiple Sclerosis and Related Disorders (HC, JRB), Department of Neurology, Perelman School of Medicine at University of Pennsylvania; Perelman School of Medicine (PN), University of Pennsylvania; and Department of Biostatistics (DT, RS), Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, PA. Division of Multiple Sclerosis and Related Disorders (HC, JRB), Department of Neurology, Perelman School of Medicine at University of Pennsylvania; Perelman School of Medicine (PN), University of Pennsylvania; and Department of Biostatistics (DT, RS), Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, PA. Division of Multiple Sclerosis and Related Disorders (HC, JRB), Department of Neurology, Perelman School of Medicine at University of Pennsylvania; Perelman School of Medicine (PN), University of Pennsylvania; and Department of Biostatistics (DT, RS), Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, PA. Division of Multiple Sclerosis and Related Disorders (HC, JRB), Department of Neurology, Perelman School of Medicine at University of Pennsylvania; Perelman School of Medicine (PN), University of Pennsylvania; and Department of Biostatistics (DT, RS), Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, PA. Division of Multiple Sclerosis and Related Disorders (HC, JRB), Department of Neurology, Perelman School of Medicine at University of Pennsylvania; Perelman School of Medicine (PN), University of Pennsylvania; and Department of Biostatistics (DT, RS), Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, PA.
 National Institutes of Health, Bethesda, MD, USA. National Institutes of Health, Bethesda, MD, USA. National Institutes of Health, Bethesda, MD, USA. National Institutes of Health, Bethesda, MD, USA. National Institutes of Health, Bethesda, MD, USA. National Institutes of Health, Bethesda, MD, USA.
 Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliari, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliari, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, 09124 Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, 09126 Cagliari, Italy. U.O.C. Neurology, S.S. Trinità Hospital, ASL Cagliari, 09121 Cagliari, Italy.
 Neurological Surgery Department, Imam Khomeini Hospital Complex (IKHC), Tehran University of Medical Sciences (TUMS), Tehran, Iran. Experimental Medicine Research Center, Department of Pharmacology, Tehran University of Medical Sciences (TUMS), Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences (TUMS), Tehran, Iran. Neurological Surgery Department, Imam Khomeini Hospital Complex (IKHC), Tehran University of Medical Sciences (TUMS), Tehran, Iran.
 IRCCS San Camillo Hospital, Venice, Italy. sonia.montemurro@hsancamillo.it. Department of Philosophy, Sociology, Education and Applied Psychology (FISPPA), Università di Padova, Padova, Italy. Centro di Ateneo Servizi Clinici Universitari Psicologici (SCUP), Università di Padova, Padova, Italy. Human Inspired Technology Research Centre HIT, University of Padova, Padova, Italy. Department of Philosophy, Sociology, Education and Applied Psychology (FISPPA), Università di Padova, Padova, Italy. Human Inspired Technology Research Centre HIT, University of Padova, Padova, Italy. Department of Philosophy, Sociology, Education and Applied Psychology (FISPPA), Università di Padova, Padova, Italy. Multiple Sclerosis Centre, Department of Neurosciences-DNS, Università di Padova, Padova, Italy. Multiple Sclerosis Centre, Department of Neurosciences-DNS, Università di Padova, Padova, Italy. Multiple Sclerosis Centre, Department of Neurosciences-DNS, Università di Padova, Padova, Italy. Gruppo Veneto Diagnostica e Riabilitazione, Padova, Italy. IRCCS San Camillo Hospital, Venice, Italy.
 Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Electronic address: yrasmi@gmail.com. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Electronic address: jalalyl@yahoo.com. Department of Bioinformatics and Genetics, School of Engineering and Natural Sciences, Kadir Has University 34083, Cibali Campus Fatih, Istanbul, Turkey. Department of Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran; Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, Alkharj, Riyadh, Saudi Arabia. Department of Medical Biochemistry, Health Sciences University, Ankara Diskapi Yildirim Beyazit Training and Research Hospital, Ankara, Turkey. Electronic address: dralpaslanozturk@gmail.com. Department of Pediatric, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
 Charles Nicolle Hospital Rabta Hospital
 Temple University School of Podiatric Medicine, Philadelphia, PA, US. Temple University School of Podiatric Medicine, Philadelphia, PA, US. Temple University School of Podiatric Medicine, Philadelphia, PA, US.
 Centre for Addiction and Mental Health, 250 College Street, Toronto, M5T 1R8, Canada. Department of Psychiatry & Behavioral Sciences, University of California San Francisco, San Francisco, 94143, USA. Centre for Addiction and Mental Health, 250 College Street, Toronto, M5T 1R8, Canada. shreejoy.tripathy@camh.ca. Institute of Medical Sciences, University of Toronto, Toronto, M5S 1A8, Canada. shreejoy.tripathy@camh.ca. Department of Psychiatry, University of Toronto, Toronto, M5T 1R8, Canada. shreejoy.tripathy@camh.ca. Department of Physiology, University of Toronto, Toronto, M5S 1A8, Canada. shreejoy.tripathy@camh.ca.
 New York, Presbyterian/Queens Drexel University
 Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Lou Rouvo Center for Brain Health, Cleveland Clinic, Cleveland, OH, USA. Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis, Cleveland Clinic, Cleveland, OH, USA. Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
 Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milan 20156, Italy. Department of Neurology and ALS Centre, University of Piemonte Orientale, Maggiore Della Carità Hospital, Corso Mazzini 18, Novara 28100, Italy. Department of Neurology and ALS Centre, University of Piemonte Orientale, Maggiore Della Carità Hospital, Corso Mazzini 18, Novara 28100, Italy. Electronic address: letizia.mazzini@uniupo.it. Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, Milan 20156, Italy. Electronic address: caterina.bendotti@marionegri.it.
 From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. margherita.nosadini@gmail.com. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy. From the Paediatric Neurology and Neurophysiology Unit (M.N., I.T., Stefano Sartori), Department of Women's and Children's Health, University Hospital of Padova, Italy; Neuroimmunology Group (M.N., L.Z., Stefano Sartori), Paediatric Research Institute "Città della Speranza," Padova, Italy; School of Biomedical Engineering and Imaging Sciences (M.E.), King's College London, United Kingdom; Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; Unit of Child Neuropsychiatry (Thea Giacomini, R.C., M.M.M.), Clinical and Surgical Neurosciences Department, IRCCS Giannina Gaslini Institute, Genoa, Genoa, Liguria, Italy; Neuroscience Department (M.V., L.P., M.A.N.F.), Bambino Gesù Children's Hospital IRCCS, Rome, Italy; Department of Neurosciences (M.D.C., Antonio Varone), Pediatric Neurology, Santobono-Pausilipon Children's Hospital, Naples, Italy; Unit of Rare Diseases of the Nervous System in Childhood (A.D.P.), Department of Clinical and Experimental Medicine, University of Catania, Italy; Multiple Sclerosis Center (P.A.), ASST della Valle Olona, Hospital of Gallarate, Italy; Child Neurology and Psychiatry Unit (D.M.C., A.F.), Department of Medical and Surgical Sciences (DIMEC), SOrsola Hospital, University of Bologna, Italy; Division of Pediatrics (Giovanni Crichiutti, V.D.), Department of Medicine, University Hospital of Udine, Italy; Unit of Child Neurology and Psychiatry (G.D.R.), Department of Human Pathology of the Adult and Developmental Age "Gaetano Barresi," University of Messina, Italy; Department of Pediatric Neuroscience (E.F., T.G.., N.N., F.R., A.T.), Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; GALLO Multiple Sclerosis Centre (P.G., M.M., M.P.), Neurology Clinic, Department of Neuroscience, Università degli Studi di Padova, Italy; Neuroimmunology Laboratory (M.G.), IRCCS Mondino Foundation, Pavia, Italy; Unit of Pediatrics (L.G., C.P.), ULSS 2 Marca Trevigiana, Ca' Foncello Hospital, Treviso, Italy; Institute of Neurology (R.I.), Fondazione Policlinico Universitario "AGemelli" IRCCS, Rome, Italy; Child Neurology Unit and Laboratories (M.L., F.M.), Neuroscience Department, Meyer Children's University Hospital, Florence, Italy; Neurology Unit (Sara Mariotto), Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Policlinico GB Rossi, Italy; Child Neurology and Psychiatry Unit (Sara Matricardi, Sabrina Siliquini), "GSalesi" Children's Hospital, Ospedali Riuniti Ancona, Italy; Child Neuropsychiatry Unit (A.P.), ASST Grande Ospedale Metropolitano Niguarda, Milano; Child Neuropsychiatry Unit (F.P., E.C.T.), Department of Medicine and Surgery, University of Parma, Italy; Pediatric Clinic (Salvatore Savasta, T.F.), Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy; Clinical Neurology (Alberto Vogrig), Azienda Ospedaliero Universitaria Friuli Centrale, Udine, Italy; Department of Neurology (L.Z.), Ospedale San Bortolo, Vicenza, Italy; U.O.CPediatria (S.B., S.R.), Ospedale San Bortolo, Vicenza, Italy; Pediatric Neurology (A.O.), Pediatric University Department, Azienda Ospedaliera Universitaria Pisana, University of Pisa, Italy; Child Neuropsychiatry (Gaetano Cantalupo), Department of Surgical Sciences, Dentistry, Gynaecology and Paediatrics, University of Verona, Italy; and Department of Neuroscience (Stefano Sartori), University of Padova, Italy.
 Department of Pathology and Immunology, Washington University School of Medicine, 425 S Euclid Ave., St. Louis, MO, 63110, USA. navale@wustl.edu. Department of Pathology, Division of Pathology/Lab Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USA. Department of Medicine, Division of Oncology, Washington University Medical School, St. Louis, MO, USA.
 Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. Département de Neurology, Centre Référent SLA, CHU de Lille, Centre LICEND COEN, Lille, France. Départment de Pharmacologie Médicale, Université de Lille, INSERM UMRS_1172 LilNCog, CHU de Lille, Centre LICEND COEN, Lille, France. Départment de Pharmacologie Médicale, Université de Lille, INSERM UMRS_1172 LilNCog, CHU de Lille, Centre LICEND COEN, Lille, France. Faculté Médecine de Nice, Département de Neurologie, Université Cote d'Azur, Nice, France. CATI Multicenter Neuroimaging Platform, Paris, France. Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. APHP, Service de Neuromyologie, Hôpital Pitié-Salpêtrière, Centre Référent Maladies Neuromusculaires Rares, Paris, France. Institut de Myologie, I-Motion Clinical Trials Platform, Hôpital Pitié-Salpêtrière, Paris, France. Sorbonne Université, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, Paris, France. pierre-francois.pradat@aphp.fr. APHP, Département de Neurologie, Hôpital Pitié-Salpêtrière, Centre Référent SLA, Paris, France. pierre-francois.pradat@aphp.fr. Northern Ireland Centre for Stratified Medicine, Biomedical Sciences Research Institute Ulster University, C-TRIC, Altnagelvin Hospital, Derry/Londonderry, UK. pierre-francois.pradat@aphp.fr.
 Department of Nuclear Medicine, Beijing Luhe Hospital, Capital Medical University, Xinhua Road 82, Tong Zhou District, Beijing, 101149, China. Department of Radiology, Beijing Luhe Hospital, Capital Medical University, Xinhua Road 82, Tong Zhou District, Beijing, 101149, China. pengruchen@ccmu.edu.cn.
 Department of Neonatology, Yas Complex Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Pediatric Neurology, Bahrami Children's Hospital , Tehran University of Medical Sciences, Tehran, Iran. Department of Pediatrics, Imam Hospital, Tehran University of Medical Sciences, Tehran, Iran. Department of Community Medicine, Center for Academic and Health Policy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Neonatology, Yas Complex Hospital, Tehran University of Medical Sciences, Tehran, Iran. Maternal, Fetal and Neonatal Research Center, Family Health Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
 Department of Neurology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan. Department of Neurology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan. Department of Neurology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan. Faculty of Economics, Yokohama National University, Yokohama, Japan. Department of Neurology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan. Department of Neurology, Tenri Hospital, Tenri, Japan. Department of Neurology, Kyorin University Hospital, Mitaka, Japan. Department of Neurology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan. Department of Neurology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan. Department of Neurology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan. Department of Neurology, Utano National Hospital, Kyoto, Japan. Department of Neurology, Teikyo University School of Medicine, Tokyo, Japan.
 Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
 Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Biomedical Center (BMC), Division of Metabolic Biochemistry, Faculty of Medicine, Ludwig-Maximilians-Universität München, Munich, 81377, Germany. Centre for Motor Neuron Disease Research, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia. Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.
 Institute of Parasitology and Biomedicine López-Neyra, CSIC, Parque Tecnológico de La Salud, 18016, Granada, Spain. Institute of Parasitology and Biomedicine López-Neyra, CSIC, Parque Tecnológico de La Salud, 18016, Granada, Spain. GENYO. Center for Genomics and Oncological Research, Pfizer/University of Granada/Andalusian Regional Government, Av de la Ilustración 114, Parque Tecnológico de La Salud, 18016, Granada, Spain. marta.alarcon@genyo.es. Institute for Environmental Medicine, Karolinska Institutet, 171 77, Solna, Sweden. marta.alarcon@genyo.es.
 Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
 Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. banu.ahtam@childrens.harvard.edu. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. banu.ahtam@childrens.harvard.edu. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Department of Radiology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Harvard University, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Neuroradiology, Department of Radiology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Fetal-Neonatal Neuroimaging and Developmental Science Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA.
 Riga Stradins, Riga, Latvia. Pauls Stradins Clinical University Hospital, Riga, Latvia. Riga Stradins, Riga, Latvia. daniel.zhukovs@gmail.com. Pauls Stradins Clinical University Hospital, Riga, Latvia. daniel.zhukovs@gmail.com. Riga Stradins, Riga, Latvia. Riga Stradins, Riga, Latvia. Riga Stradins, Riga, Latvia. Pauls Stradins Clinical University Hospital, Riga, Latvia. Riga Stradins, Riga, Latvia. Pauls Stradins Clinical University Hospital, Riga, Latvia.
 UCL Centre for Rheumatology and Connective Tissue Diseases, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK. UCL Centre for Rheumatology and Connective Tissue Diseases, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK. UCL Centre for Rheumatology and Connective Tissue Diseases, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK. c.denton@ucl.ac.uk.
 Department of Physiotherapy, Calvary Health Care Bethlehem, Melbourne, Australia. Electronic address: Trinh.Sia@calvarycare.org.au. Department of Physiotherapy, Calvary Health Care Bethlehem, Melbourne, Australia. School of Primary and Allied Health Care, Faculty of Medicine, Nursing and Health Science, Monash University, Melbourne, Australia.
 Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Department of Neurology, Penn State University College of Medicine, Hershey, PA, USA. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Texas Neurology, Dallas, TX, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, NY, USA. Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA. Department of Neurology, Massachusetts General Hospital, Boston, MA, USA. Department of Neurology, Northwestern University, Chicago, IL, USA. Department of Neurological Sciences, University of Nebraska Medical Center, Omaha, NE, USA. Department of Neurology, Massachusetts General Hospital, Boston, MA, USA. Department of Neurology, Virginia Commonwealth University, Richmond, VA, USA. Department of Neurology, University of California, Irvine, Orange, CA, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neurology, University of Minnesota, Minneapolis, MN, USA. Department of Neurology, Emory University, Atlanta, GA, USA. Department of Neurology, Temple University, Philadelphia, PA, USA. Department of Neurology, University of Florida College of Medicine, Gainesville, FL, USA. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Department of Neurology, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada. Department of Neurology, University of Michigan, Ann Arbor, MI, USA. Department of Neurology, Saint Louis University, Saint Louis, MO, USA. Department of Neurology, University of Kansas Medical Center, Kansas City, KS, USA. Division of Neurology, University of Alberta, Edmonton, AB, Canada. Department of Physical Medicine and Rehabilitation, University of California, Davis, Sacramento, CA, USA. Department of Neurology, University of Kentucky, Lexington, KY, USA. Department of Neurology, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Department of Neurology, University of California, San Francisco, CA, USA. Department of Neurology, University of Florida College of Medicine, Jacksonville, FL, USA. Department of Neurology, Mayo Clinic, Jacksonville, Florida. Department of Neurology, Western University, London, ON, Canada, and. Department of Neurology, Sunnybrook Health Sciences Centre, Toronto, ON, Canada.
 Center for Collaborative Research, NOVA Southeastern University, Fort Lauderdale, FL, USA. Lgray1@nova.edu. Aerodigestive Research Core, University of Florida, Gainesville, FL, USA. Lgray1@nova.edu. Aerodigestive Research Core, University of Florida, Gainesville, FL, USA. Department of Anesthesiology and Orthopedics, College of Medicine, University of Florida, Gainesville, FL, USA. Department of Neurology, University of Florida, Gainesville, FL, USA. Department of Physical Therapy and Center for Respiratory Research and Rehabilitation, University of Florida, Gainesville, FL, USA. Aerodigestive Research Core, University of Florida, Gainesville, FL, USA. Department of Neurology, University of Florida, Gainesville, FL, USA. Speech, Language and Hearing Science Department, University of Florida, Gainesville, FL, USA.
 Rheumatology unit, Bnai-Zion Medical Center, Technion-Israel Institute of Technology, Haifa, Israel. Rheumatology unit, Bnai-Zion Medical Center, Technion-Israel Institute of Technology, Haifa, Israel. Electronic address: doron.rimar@b-zion.org.il. Unité de Médecine Interne (UF04): CRMR MATHEC, Maladies Auto-immunes et Thérapie Cellulaire, Centre de Référence des Maladies auto-immunes systémiques Rares d'Ile-de-France, AP-HP, Hôpital St-Louis, F-75010 Paris, France; Université Paris Cité, IRSL, Recherche Clinique en hématologie, immunologie et transplantation, URP3518, F-75010 Paris, France. Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel. University of Rennes, CHU Rennes, Inserm, EHESP, Irset -Institut de Recherche en Sante, Environnement et Travail-UMRS_S1085, Rennes, France. Systems immunology lab, Dept. of Immunology Rapport Faculty of Medicine Technion - Israel Institute of Technology, Israel. Unité de Médecine Interne (UF04): CRMR MATHEC, Maladies Auto-immunes et Thérapie Cellulaire, Centre de Référence des Maladies auto-immunes systémiques Rares d'Ile-de-France, AP-HP, Hôpital St-Louis, F-75010 Paris, France; Université Paris Cité, IRSL, Recherche Clinique en hématologie, immunologie et transplantation, URP3518, F-75010 Paris, France; Department of Medicine, McGill University, H3A 1A1, Montreal, Canada. Electronic address: dominique.farge-bancel@aphp.fr.
 Institute of Biochemistry and Cell Biology IBBC, National Research Council CNR, Via E. Ramarini 32, Monterotondo scalo (Roma) 00015 Italy. Institute of Biochemistry and Cell Biology IBBC, National Research Council CNR, Via E. Ramarini 32, Monterotondo scalo (Roma) 00015 Italy. Department of Mechanical and Aerospace Engineering, University of Roma 'La Sapienza', Rome, Italy. Institute of Biochemistry and Cell Biology IBBC, National Research Council CNR, Via E. Ramarini 32, Monterotondo scalo (Roma) 00015 Italy. Institute of Biochemistry and Cell Biology IBBC, National Research Council CNR, Via E. Ramarini 32, Monterotondo scalo (Roma) 00015 Italy. Institute of Biochemistry and Cell Biology IBBC, National Research Council CNR, Via E. Ramarini 32, Monterotondo scalo (Roma) 00015 Italy. DAHFMO-Unit of Histology and Medical Embryology, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, University of Roma 'La Sapienza', Rome, Italy. DAHFMO-Unit of Histology and Medical Embryology, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, University of Roma 'La Sapienza', Rome, Italy. Department of Mechanical and Aerospace Engineering, University of Roma 'La Sapienza', Rome, Italy. Environment and Health Department, Istituto Superiore di Sanità (ISS), Rome, Italy. DAHFMO-Unit of Histology and Medical Embryology, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, University of Roma 'La Sapienza', Rome, Italy. DAHFMO-Unit of Histology and Medical Embryology, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, University of Roma 'La Sapienza', Rome, Italy. Institute of Biochemistry and Cell Biology IBBC, National Research Council CNR, Via E. Ramarini 32, Monterotondo scalo (Roma) 00015 Italy.
 Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, USA; Department of Neurology, Duke University School of Medicine, Durham, NC 27710, USA. Department of Neurology, Duke University School of Medicine, Durham, NC 27710, USA. Department of Neurology, Duke University School of Medicine, Durham, NC 27710, USA. Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, USA; Department of Neurology, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: craiglb@uci.edu. Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, USA; Department of Neurology, Duke University School of Medicine, Durham, NC 27710, USA; Departments of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697, USA; Department of Neurology, University of California, Irvine, Irvine, CA, USA; Department of Biological Chemistry, University of California, Irvine, Irvine, CA, USA; UCI Center for Neurotherapeutics, University of California, Irvine, Irvine, CA 92697, USA. Electronic address: alaspada@uci.edu.
 Department of Dermatology, Region 1 Medical Center, Dagupan, Philippines. Department of Dermatology, MacKay Memorial Hospital, Taipei, Taiwan. Department of Dermatology, MacKay Memorial Hospital, Taipei, Taiwan. Department of Medicine, MacKay Medical College, New Taipei City, Taiwan.
 Department of Translational Neuroscience, Barrow Neurological Institute, 350 W Thomas Road, Phoenix, AZ, 85013, USA. Neurogenomics Division, Translational Genomics Research Institute, part of City of Hope, Phoenix, AZ, USA. Neurogenomics Division, Translational Genomics Research Institute, part of City of Hope, Phoenix, AZ, USA. Department of Translational Neuroscience, Barrow Neurological Institute, 350 W Thomas Road, Phoenix, AZ, 85013, USA. Neurogenomics Division, Translational Genomics Research Institute, part of City of Hope, Phoenix, AZ, USA. Department of Translational Neuroscience, Barrow Neurological Institute, 350 W Thomas Road, Phoenix, AZ, 85013, USA. Rita.sattler@barrowneuro.org. Neurogenomics Division, Translational Genomics Research Institute, part of City of Hope, Phoenix, AZ, USA. kjensen@tgen.org.
 Departments of Ophthalmology (J.J.C., N.C.S., K.D.C., D.A.T., S.J.); Neurology (J.J.C., E.P.F., S.J.P., N.T., D.A.T., A.K.). Electronic address: Chen.john@mayo.edu. Neurology (J.J.C., E.P.F., S.J.P., N.T., D.A.T., A.K.); Laboratory Medicine and Pathology (E.P.F., S.J.P.); Center for MS and Autoimmune Neurology (E.P.F., S.J.P., A.K.), Mayo Clinic, Rochester, Minnesota, USA. Neurology (J.J.C., E.P.F., S.J.P., N.T., D.A.T., A.K.); Laboratory Medicine and Pathology (E.P.F., S.J.P.); Center for MS and Autoimmune Neurology (E.P.F., S.J.P., A.K.), Mayo Clinic, Rochester, Minnesota, USA. Departments of Ophthalmology (J.J.C., N.C.S., K.D.C., D.A.T., S.J.). Neurology (J.J.C., E.P.F., S.J.P., N.T., D.A.T., A.K.). The Permanente Medical Group (M.T.B.), Kaiser Permanente-Northern California, Roseville, California, USA. Departments of Ophthalmology (J.J.C., N.C.S., K.D.C., D.A.T., S.J.). Departments of Ophthalmology (J.J.C., N.C.S., K.D.C., D.A.T., S.J.); Neurology (J.J.C., E.P.F., S.J.P., N.T., D.A.T., A.K.). Departments of Ophthalmology (J.J.C., N.C.S., K.D.C., D.A.T., S.J.). Neurology (J.J.C., E.P.F., S.J.P., N.T., D.A.T., A.K.); Center for MS and Autoimmune Neurology (E.P.F., S.J.P., A.K.), Mayo Clinic, Rochester, Minnesota, USA; Department of Neurology, Cleveland Clinic (A.K.), Cleveland, Ohio, USA. Departments of Neurology, Neurosurgery, and Neuro-Ophthalmology, Mayo Clinic (E.R.E.), Jacksonville, Florida, USA. Departments of Ophthalmology (M.A.D.N.); Neurosurgery, Mayo Clinic (M.A.D.N.), Scottsdale, AZ. Department of Neurology, Johns Hopkins University (E.S.S., E.S.V., A.D.H.), Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University (E.S.S., E.S.V., A.D.H.), Baltimore, Maryland, USA. Department of Neurology, Johns Hopkins University (E.S.S., E.S.V., A.D.H.), Baltimore, Maryland, USA; Department of Ophthalmology, Johns Hopkins University School of Medicine (A.D.H.), Baltimore, Maryland, USA. Department of Ophthalmology, University of California Los Angeles (A.C.A., L.B.), Los Angeles, California, USA. Department of Ophthalmology, University of California Los Angeles (A.C.A., L.B.), Los Angeles, California, USA. Department of Neurology & Neurological Sciences, Stanford University (H.E.M.), Palo Alto, California, USA; Department of Ophthalmology, Stanford University (H.E.M., S.E.V.N., T.P.), Palo Alto, California, USA. Department of Ophthalmology, Stanford University (H.E.M., S.E.V.N., T.P.), Palo Alto, California, USA. Department of Ophthalmology, Stanford University (H.E.M., S.E.V.N., T.P.), Palo Alto, California, USA; Department of Ophthalmology, Faculty of Medicine, Ramathibodi Hospital (T.P.), Mahidol University, Bangkok, Thailand. Department of Ophthalmology (H.S.-K.), Neuro-Ophthalmology Division, Rabin Medical Center and Sackler School of Medicine, Tel Aviv University, Israel; Felsenstein Medical Research Center (H.S.-K.), Tel Aviv University, Israel. Department of Neurology, Rabin Medical Center, Sackler School of Medicine (I.L., A.W.-Y.), Tel Aviv University, Israel. Department of Neurology, Rabin Medical Center, Sackler School of Medicine (I.L., A.W.-Y.), Tel Aviv University, Israel. Department of Ophthalmology, University of Auckland, New Zealand, and Vision Research Foundation (H.D.-M., S.I.), Auckland, New Zealand. Department of Ophthalmology, University of Auckland, New Zealand, and Vision Research Foundation (H.D.-M., S.I.), Auckland, New Zealand. Department of Neurology, The Walton Centre NHS Foundation Trust (S.H., M.F.), Liverpool, United Kingdom. Department of Neurology, The Walton Centre NHS Foundation Trust (S.H., M.F.), Liverpool, United Kingdom. Department of Quantitative Health Sciences, Mayo Clinic (D.H.), Jacksonville, Florida. Department of Neurology, University Hospital of Marseille (P.P., J.R., B.A.), Marseille, France; Aix-Marseille University, CRMBM UMR 7339, CNRS (P.P., J.R., B.A.), Marseille, France. Department of Neurology, University Hospital of Marseille (P.P., J.R., B.A.), Marseille, France; Aix-Marseille University, CRMBM UMR 7339, CNRS (P.P., J.R., B.A.), Marseille, France. Department of Neurology, Pitie-Salpetriere Hospital, APHP (C.P., S.S., E.M.), Paris, France; Centre de référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM) (C.P., S.S., E.M.); Department of Neurology, Adolphe de Rothschild Foundation Hospital (C.P., M.B.d.l.M., R.D.), Paris, France. Department of Neurology, Pitie-Salpetriere Hospital, APHP (C.P., S.S., E.M.), Paris, France; Centre de référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM) (C.P., S.S., E.M.). Department of Neurology, Adolphe de Rothschild Foundation Hospital (C.P., M.B.d.l.M., R.D.), Paris, France. Department of Neuro-Ophthalmology, Adolphe de Rothschild Foundation Hospital (C.V.), Paris, France. Department of Neurology, Great Ormond Street Hospital for Children (Y.H.), London, United Kingdom; Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, Faculty of Brain Sciences, University College London (Y.H.), London, United Kingdom. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon (J.P., R.M.), Lyon, France. Department of Neurology, Pitie-Salpetriere Hospital, APHP (C.P., S.S., E.M.), Paris, France; Centre de référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM) (C.P., S.S., E.M.). Department of Neurology, Adolphe de Rothschild Foundation Hospital (C.P., M.B.d.l.M., R.D.), Paris, France. Department of Neurology, University Hospital of Marseille (P.P., J.R., B.A.), Marseille, France; Aix-Marseille University, CRMBM UMR 7339, CNRS (P.P., J.R., B.A.), Marseille, France. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon (J.P., R.M.), Lyon, France.
 Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea. Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
 Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. School of Basic Medical College, Core facility of instrument, Institution of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China. Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. School of Basic Medical College, Core facility of instrument, Institution of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China. School of Basic Medical College, Core facility of instrument, Institution of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China. Clinical Research Center, National Center for Children's Health, Beijing Children's Hospital, Capital Medical University, Beijing, China. Clinical Research Center, National Center for Children's Health, Beijing Children's Hospital, Capital Medical University, Beijing, China. Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. School of Basic Medical College, Core facility of instrument, Institution of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China. Clinical Research Center, National Center for Children's Health, Beijing Children's Hospital, Capital Medical University, Beijing, China. Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
 Faculty of Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 400349 Cluj-Napoca, Romania. Faculty of Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 400349 Cluj-Napoca, Romania. Faculty of Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 400349 Cluj-Napoca, Romania. Department of Neurology, Iuliu Haţieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Department of Physical Medicine and Rehabilitation, Iuliu Haţieganu University of Medicine and Pharmacy Cluj-Napoca, Viilor Street, No. 46-50, 400347 Cluj-Napoca, Romania. Department of Ophthalmology, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania. Department of Pathophysiology, Iuliu Hațieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania.
 Department of Morphological and Functional Sciences, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Department of Morphological and Functional Sciences, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Multidisciplinary Integrated Center of Dermatological Interface Research MIC-DIR (Centrul Integrat Multidisciplinar de Cercetare de Interfata Dermatologica - CIM-CID), "Dunărea de Jos" University, Galaţi, Romania. Department of Morphological and Functional Sciences, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Multidisciplinary Integrated Center of Dermatological Interface Research MIC-DIR (Centrul Integrat Multidisciplinar de Cercetare de Interfata Dermatologica - CIM-CID), "Dunărea de Jos" University, Galaţi, Romania. Clinical Medical Department, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Department of Plastic Surgery, "Sf. Ioan" Clinical Emergency Hospital for Children, Galaţi, Romania. Clinical Medical Department, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Department of Pharmaceutical Sciences, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Clinical Surgical Department, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Clinical Medical Department, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Dermatology Department "Agrippa Ionescu" Emergency Clinical Hospital, Bucharest, Romania. Department of Morphological and Functional Sciences, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Clinical Medical Department, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Research Center in the Field of Medical and Pharmaceutical Sciences, "Dunărea de Jos" University, Galaţi, Romania. Multidisciplinary Integrated Center of Dermatological Interface Research MIC-DIR (Centrul Integrat Multidisciplinar de Cercetare de Interfata Dermatologica - CIM-CID), "Dunărea de Jos" University, Galaţi, Romania. Clinical Medical Department, Faculty of Medicine and Pharmacy, "Dunărea de Jos" University, Galaţi, Romania. Dermatology Department, "Sf. Cuvioasa Parascheva" Clinical Hospital of Infectious Diseases, Galaţi, Romania.
 Sampson Regional Medical Center Uniformed Services University of the Health Sciences
 Unidad de Neuroendocrinología, Departamento de Endocrinología y Nutrición, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Invesitigación Sanitaria (IRYCIS), Madrid, Spain; Departamento de Medicina, Universidad de Alcalá, Madrid, Spain. Electronic address: marta.araujo@salud.madrid.org.
 Department of Internal Medicine (Pharmacogenomics), Washington University School of Medicine, St. Louis, MO 63110, USA.
 Rheumatology Division, Department of Medicine, and Jefferson Institute of Molecular Medicine and Scleroderma Center, Thomas Jefferson University, Philadelphia, PA, USA. fam002@jefferson.edu. Rheumatology Division, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA. Jefferson Institute of Molecular Medicine and Scleroderma Center, Thomas Jefferson University, Philadelphia, PA, USA.
 National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Medical Key Discipline of Health Toxicology (2020-2024), Shenzhen Center for Disease Control and Prevention, Shenzhen, 518055, China. Electronic address: xifeiyang@gmail.com. National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Health Science Center, Shenzhen University, Shenzhen, 518071, China. Electronic address: chenxin@szu.edu.cn.
 Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Genetics, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Genetics, University Medical Center Utrecht, Utrecht, the Netherlands. Neurology Department University Hospitals Leuven, Department of Neurosciences and Leuven Brain Institute (LBI) KU Leuven-University of Leuven, Leuven, Belgium; VIB, Center for Brain & Disease Research, Leuven, Belgium. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Neuroscience Institute of Turin (NIT), Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Neuroscience Institute of Turin (NIT), Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Neuroscience Institute of Turin (NIT), Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Neuroscience Institute of Turin (NIT), Turin, Italy. Department of Clinical Science, Neurosciences, Umeå University Umeå, Sweden. ALS Unit, Hospital San Rafael, Madrid, Spain. Department of Neurosciences, University of California at San Diego, La Jolla, CA, USA. Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute and United Kingdom Dementia Research Institute, King's College London, London, UK; Department of Neurology, King's College Hospital, London, UK. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, SC Neurologia 1U, Turin, Italy; Neuroscience Institute of Turin (NIT), Turin, Italy. Population Genetics Laboratory, Smurfit Institute of Genetics, Trinity College Dublin, Republic of Ireland. Academic Unit of Neurology, Trinity College Dublin, Trinity Biomedical Sciences Institute, Dublin, Republic of Ireland; Department of Neurology, Beaumont Hospital, Dublin, Republic of Ireland. Neurology Department University Hospitals Leuven, Department of Neurosciences and Leuven Brain Institute (LBI) KU Leuven-University of Leuven, Leuven, Belgium; VIB, Center for Brain & Disease Research, Leuven, Belgium. Department of Neurosciences, Hospital de Santa Maria-CHLN, Lisbon, Portugal; Institute of Physiology, Institute of Molecular Medicine, Faculty of Medicine, University of Lisbon, Lisbon, Portugal. Neuromuscular Diseases Unit / ALS Clinic, Kantonsspital St.Gallen, St.Gallen, Switzerland. Neuromuscular Diseases Unit / ALS Clinic, Kantonsspital St.Gallen, St.Gallen, Switzerland. Department of Clinical Science, Neurosciences, Umeå University Umeå, Sweden. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address: m.a.vanes@umcutrecht.nl.
 Department of Pediatrics, Peking University People's Hospital, Beijing, China. Department of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China. Department of Pediatrics, Peking University People's Hospital, Beijing, China. Department of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China. Department of Pediatrics, Peking University People's Hospital, Beijing, China.
 European Research Institute for the Biology of Ageing, University of Groningen, University Medical Centre Groningen, The Netherlands. European Research Institute for the Biology of Ageing, University of Groningen, University Medical Centre Groningen, The Netherlands. European Research Institute for the Biology of Ageing, University of Groningen, University Medical Centre Groningen, The Netherlands. European Research Institute for the Biology of Ageing, University of Groningen, University Medical Centre Groningen, The Netherlands.
 Department of Molecular Pathochemistry, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Immunology and Rheumatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Electronic address: naoki-iwa@nagasaki-u.ac.jp. Department of Immunology and Rheumatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Pharmacy Practice, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Pharmacy Practice, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. Department of Dermatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Dermatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Sasebo Chuo Hospital, Sasebo, Japan. Department of Pharmaceutics, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Hospital Pharmacy, Nagasaki University Hospital, Nagasaki, Japan. Department of Hospital Pharmacy, Nagasaki University Hospital, Nagasaki, Japan. Department of Pharmacy Practice, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Immunology and Rheumatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Molecular Pathochemistry, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan; Department of Hospital Pharmacy, Nagasaki University Hospital, Nagasaki, Japan. Electronic address: k-ohyama@nagasaki-u.ac.jp.
 Department of Medical Ultrasound, Peking University Third Hospital, Beijing 100191, China. Department of Rheumatology and Immunology, Peking University Third Hospital, Beijing 100191, China. Department of Medical Ultrasound, Peking University Third Hospital, Beijing 100191, China. Department of Rheumatology and Immunology, Peking University Third Hospital, Beijing 100191, China. Department of Medical Ultrasound, Peking University Third Hospital, Beijing 100191, China.
 Laboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States. Center for Machine Learning, Georgia Institute of Technology, Atlanta, GA, United States. Laboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States. Laboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States. University of Michigan Medical School, Ann Arbor, MI, United States. Laboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States. University of Texas at Dallas, Dallas, TX, United States. Laboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States. Laboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States. Center for Machine Learning, Georgia Institute of Technology, Atlanta, GA, United States.
 Post-Graduation Programme in Medical Sciences, State University of Rio de Janeiro (UERJ), Rio de Janeiro, Brazil. Faculty of Physiotherapy, Augusto Motta University Centre (UNISUAM), Rio de Janeiro, Brazil. Faculty of Physiotherapy, Augusto Motta University Centre (UNISUAM), Rio de Janeiro, Brazil. Faculty of Physiotherapy, Augusto Motta University Centre (UNISUAM), Rio de Janeiro, Brazil. Faculty of Physiotherapy, Augusto Motta University Centre (UNISUAM), Rio de Janeiro, Brazil. Post-Graduation Programme in Medical Sciences, State University of Rio de Janeiro (UERJ), Rio de Janeiro, Brazil. Post-Graduation Programme in Medical Sciences, State University of Rio de Janeiro (UERJ), Rio de Janeiro, Brazil. Post-Graduation Programme in Rehabilitation Sciences, Augusto Motta University Centre (UNISUAM), Rio de Janeiro, Brazil.
 From the Neuroepidemiology Research Unit (C.W., D.E.G.), Research Institute of the McGill University Health Centre; Department of Medicine (C.W.), Faculty of Medicine and Health Sciences, Department of Epidemiology (C.W., F.I.), Biostatistics and Occupational Health, School of Population and Global Health, and Department of Pediatrics (M.O.), Faculty of Medicine and Health Sciences, McGill University, Montreal, Quebec, Canada. christina.wolfson@mcgill.ca. From the Neuroepidemiology Research Unit (C.W., D.E.G.), Research Institute of the McGill University Health Centre; Department of Medicine (C.W.), Faculty of Medicine and Health Sciences, Department of Epidemiology (C.W., F.I.), Biostatistics and Occupational Health, School of Population and Global Health, and Department of Pediatrics (M.O.), Faculty of Medicine and Health Sciences, McGill University, Montreal, Quebec, Canada. From the Neuroepidemiology Research Unit (C.W., D.E.G.), Research Institute of the McGill University Health Centre; Department of Medicine (C.W.), Faculty of Medicine and Health Sciences, Department of Epidemiology (C.W., F.I.), Biostatistics and Occupational Health, School of Population and Global Health, and Department of Pediatrics (M.O.), Faculty of Medicine and Health Sciences, McGill University, Montreal, Quebec, Canada. From the Neuroepidemiology Research Unit (C.W., D.E.G.), Research Institute of the McGill University Health Centre; Department of Medicine (C.W.), Faculty of Medicine and Health Sciences, Department of Epidemiology (C.W., F.I.), Biostatistics and Occupational Health, School of Population and Global Health, and Department of Pediatrics (M.O.), Faculty of Medicine and Health Sciences, McGill University, Montreal, Quebec, Canada.
 Sheffield Institute for Translational Neuroscience, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, UK. Neuroscience Institute, University of Sheffield, Sheffield, UK. Keapstone Therapeutics, The Innovation Centre, Broomhall, Sheffield, UK. Aclipse Therapeutics, Radnor, PA, US. Aclipse Therapeutics, Radnor, PA, US. MSD UK Discovery Centre, Merck, Sharp and Dohme (UK) Limited, London, UK. Sheffield Institute for Translational Neuroscience, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, UK. pamela.shaw@sheffield.ac.uk. Neuroscience Institute, University of Sheffield, Sheffield, UK. pamela.shaw@sheffield.ac.uk. Keapstone Therapeutics, The Innovation Centre, Broomhall, Sheffield, UK. pamela.shaw@sheffield.ac.uk.
 Division of Neurology, Tohoku Medical and Pharmaceutical University, 1-12-1 Fukumuro, Miyagino-ku, Sendai, Miyagi 983-8512, Japan. Department of Neurology, Keio University School of Medicine, Tokyo, Japan. Department of Neurology, Nitobe Memorial Nakano General Hospital, Tokyo, Japan. Department of Neurology, National Hospital Organization Okayama Medical Center, Okayama, Japan. Alexion Pharma GK, Tokyo, Japan. Alexion Pharma GK, Tokyo, Japan. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University School of Medicine, Fukushima, Japan. Multiple Sclerosis and Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan.
 Department of Veterans Affairs, VA Boston Healthcare System,150 S Huntington Av, Boston, MA 02130, USA; Department of Neurology, Boston University School of Medicine, 72 E Concord St, Boston, MA 02118, USA; Department of Biochemistry, Boston University School of Medicine, Boston, MA, 02118, USA. Electronic address: carreras@bu.edu. Department of Veterans Affairs, VA Boston Healthcare System,150 S Huntington Av, Boston, MA 02130, USA; Department of Neurology, Boston University School of Medicine, 72 E Concord St, Boston, MA 02118, USA; The Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, 73 High St, Boston, MA 02114, USA. Department of Veterans Affairs, VA Boston Healthcare System,150 S Huntington Av, Boston, MA 02130, USA; Department of Neurology, Boston University School of Medicine, 72 E Concord St, Boston, MA 02118, USA. Department of Veterans Affairs, VA Boston Healthcare System,150 S Huntington Av, Boston, MA 02130, USA; Department of Neurology, Boston University School of Medicine, 72 E Concord St, Boston, MA 02118, USA. Department of Veterans Affairs, VA Boston Healthcare System,150 S Huntington Av, Boston, MA 02130, USA; Department of Neurology, Boston University School of Medicine, 72 E Concord St, Boston, MA 02118, USA; Department of Radiology, Massachusetts General Hospital and Harvard Medical School, 73 High St, Boston, MA 02114, USA.
 Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Anesthesiology and Intensive Care Medicine, Pain Clinic, Hannover Medical School, Hannover, Germany. Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Anesthesiology and Intensive Care Medicine, Pain Clinic, Hannover Medical School, Hannover, Germany. Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Internal and Integrative Medicine, Immanuel Hospital Berlin, Berlin, Germany. Institute of Social Medicine, Epidemiology and Health Economics, Charité - Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Department of Internal and Integrative Medicine, Immanuel Hospital Berlin, Berlin, Germany.
 Department of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden benedicte.delcoigne@ki.se. Department of Neurology, Copenhagen University Hospital, Kobenhavn, Denmark. Department of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden. Department of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden. Center for treatment of Rheumatic and Musculoskeletal Diseases (REMEDY), Diakonhjemmet Hospital, Oslo, Norway. Department of Public Health and Sport Sciences, Inland Norway University of Applied Sciences, Elverum, Norway. Department of Medicine, Division of Rheumatology, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland. ROB-FIN, Pharmaceuticals Pricing Board, Ministry of Social Affairs and Health, Helsinki, Finland. Department of Medicine, Division of Rheumatology, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland. Faculty of Medicine, University Hospital of Iceland, Reykjavik, Iceland. Department of Rheumatology, Centre for Rheumatology Research, Reykjavik, Iceland. Department of Rheumatology Research, Landspitali University Hospital, Reykjavik, Iceland. Faculty of Medicine, University of Iceland, Reykjavik, Iceland. Center for treatment of Rheumatic and Musculoskeletal Diseases (REMEDY), Diakonhjemmet Hospital, Oslo, Norway. Department of Rheumatology, Rigshospitalet, Copenhagen University, Copenhague, Denmark. Center of Rheumatic Research Aalborg (CERRA), Aalborg University, Aalborg, Denmark. Department of Rheumatology, Aalborg University Hospital, Aalborg, Denmark. Department of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Stockholm, Sweden.
 Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. Center for Brain Science, Shanghai Children's Medical Center, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Yangzhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center), Tongji Univeirsity School of Medicine, Shanghai, China. Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Collaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China. The Fifth People's Hospital of Shanghai, the Shanghai Key Laboratory of Medical Epigenetics, The International Co-Laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Shanghai Institute of Infectious Diseases and Biosecurity, Shanghai Medical College, Fudan University, Shanghai, China. zhiganglu@fudan.edu.cn. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. zhengjunke@shsmu.edu.cn. Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. yapingzhang@shsmu.edu.cn.
 Virginia Tech Carilion School of Medicine, Roanoke, VA, USA. Department of Radiology, The Hospital of the University of Pennsylvania, Philadelphia, PA, USA. Department of Radiology and Imaging Science, Emory University School of Medicine, Atlanta, Georgia, USA.
 UGC Laboratories Gipuzkoa, Immunology Section, Osakidetza Basque Health Service, San Sebastián, Spain. Multiple Sclerosis Group, Neurosciences Area, Biodonostia Health Research Institute, San Sebastián, Spain. Multiple Sclerosis Group, Neurosciences Area, Biodonostia Health Research Institute, San Sebastián, Spain. Multiple Sclerosis Group, Neurosciences Area, Biodonostia Health Research Institute, San Sebastián, Spain. Infectious diseases Department, Donostialdea Integrated Health Organization, Osakidetza Basque Health Service, San Sebastián, Spain. Microbiology Department, Donostialdea Integrated Health Organization, Osakidetza Basque Health Service, San Sebastián, Spain. UGC Laboratories Gipuzkoa, Immunology Section, Osakidetza Basque Health Service, San Sebastián, Spain. UGC Laboratories Gipuzkoa, Immunology Section, Osakidetza Basque Health Service, San Sebastián, Spain. UGC Laboratories Gipuzkoa, Immunology Section, Osakidetza Basque Health Service, San Sebastián, Spain. UGC Laboratories Gipuzkoa, Immunology Section, Osakidetza Basque Health Service, San Sebastián, Spain. UGC Laboratories Gipuzkoa, Immunology Section, Osakidetza Basque Health Service, San Sebastián, Spain. Multiple Sclerosis Group, Neurosciences Area, Biodonostia Health Research Institute, San Sebastián, Spain. Multiple Sclerosis Group, Neurosciences Area, Biodonostia Health Research Institute, San Sebastián, Spain.
 Psychosis Research Unit, Aarhus University Hospital-Psychiatry, Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, Aarhus, Denmark. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. DZPG (German Center for Mental Health), partner site Berlin, Berlin, Germany. BIH Charité Clinician Scientist Program, BIH Biomedical Innovation Academy, Berlin Institute of Health at Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. Psychosis Research Unit, Aarhus University Hospital-Psychiatry, Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, Aarhus, Denmark. DZPG (German Center for Mental Health), partner site Berlin, Berlin, Germany. Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. DZPG (German Center for Mental Health), partner site Berlin, Berlin, Germany. Department of Psychiatry and Molecular Medicine, Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York. Center for Psychiatric Neuroscience, Feinstein Institute for Medical Research, Manhasset, New York. Department of Child and Adolescent Psychiatry, Charité Universitätsmedizin, Berlin, Germany. Department of Psychiatry, Zucker Hillside Hospital, Northwell Health, Glen Oaks, New York. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. DZPG (German Center for Mental Health), partner site Berlin, Berlin, Germany. Department of Psychosomatic Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. Department of Psychiatry and Neuroscience, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany. DZPG (German Center for Mental Health), partner site Berlin, Berlin, Germany.
 Edinburgh Clinical Trials Unit, Usher Institute, University of Edinburgh, Edinburgh, UK. Richard.Parker@ed.ac.uk. Edinburgh Clinical Trials Unit, Usher Institute, University of Edinburgh, Edinburgh, UK. Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Statistics and Epidemiology, Division of Health Sciences, Warwick Medical School, University of Warwick, Coventry, UK. Medical Research Council Clinical Trials Unit at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Euan Macdonald Centre for Motor Neuron Disease Research, University of Edinburgh, Edinburgh, EH16 4SB, UK. Euan Macdonald Centre for Motor Neuron Disease Research, University of Edinburgh, Edinburgh, EH16 4SB, UK. Centre of Clinical Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, EH16 4SB, UK. Euan Macdonald Centre for Motor Neuron Disease Research, University of Edinburgh, Edinburgh, EH16 4SB, UK. Centre of Clinical Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, EH16 4SB, UK. Euan Macdonald Centre for Motor Neuron Disease Research, University of Edinburgh, Edinburgh, EH16 4SB, UK. Centre of Clinical Brain Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK. Anne Rowling Regenerative Neurology Clinic, University of Edinburgh, Edinburgh, EH16 4SB, UK. UK Dementia Research Institute Edinburgh, University of Edinburgh, Edinburgh, EH16 4SB, UK.
 Department of Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China; School of Computer Science and Engineering, Sun Yat-Sen University, Guangzhou 510006, China. School of Computer Science and Engineering, Sun Yat-Sen University, Guangzhou 510006, China. Department of Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China. Institute of Medical Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom. School of Computer Science and Engineering, Sun Yat-Sen University, Guangzhou 510006, China. Electronic address: yangyd25@mail.sysu.edu.cn. Mater Research Institute, The University of Queensland, Brisbane, QLD, Australia. Electronic address: yuanhao.yang@mater.uq.edu.au. Department of Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China. Electronic address: zhaohy8@mail.sysu.edu.cn.
 Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy. Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy. Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; Clinical Neurophysiology Unit, IRCCS Mondino Foundation, Pavia, Italy. Clinical Neurophysiology Unit, IRCCS Mondino Foundation, Pavia, Italy. Advanced Imaging and Radiomics Center, Neuroradiology Department, IRCCS Mondino Foundation, Pavia, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy. Multiple Sclerosis Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; Department of Neuromuscular Diseases, University College London, London, United Kingdom. Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy. Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy; Neuroimmunology Research Unit, IRCCS Mondino Foundation, Pavia, Italy. Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy. Electronic address: enrico.marchioni@mondino.it.
 The Danish Headache Center, Department of Neurology, Rigshospitalet-Glostrup, University of Copenhagen, Glostrup, Denmark. The Danish Headache Center, Department of Neurology, Rigshospitalet-Glostrup, University of Copenhagen, Glostrup, Denmark. The Danish Headache Center, Department of Neurology, Rigshospitalet-Glostrup, University of Copenhagen, Glostrup, Denmark. The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet-Glostrup, University of Copenhagen, Glostrup, Denmark. The Danish Headache Center, Department of Neurology, Rigshospitalet-Glostrup, University of Copenhagen, Glostrup, Denmark. Department of Clinical Physiology and Nuclear Medicine, Centre for Functional and Diagnostic Imaging and Research, Hvidovre Hospital, Hvidovre, Denmark.
 Independent contributor and patient participant in Janssen Patient Engagement Research Council, Memphis, TN, USA. Janssen Scientific Affairs, LLC, Titusville, NJ, USA. Janssen Scientific Affairs, LLC, Titusville, NJ, USA. Janssen Scientific Affairs, LLC, Titusville, NJ, USA. CorEvitas, LLC, Waltham, MA, USA. Janssen Scientific Affairs, LLC, Titusville, NJ, USA. Janssen Scientific Affairs, LLC, Titusville, NJ, USA.
 Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Institut du Cerveau-Paris Brain Institute-ICM, Inserm, CNRS, APHP, Hôpital de la Pitié Salpêtrière, Paris, France. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Paris-Saclay University, CNRS, Saclay, France. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, UCL, London, United Kingdom. Brain Connectivity Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Brain Connectivity Center, IRCCS Mondino Foundation, Pavia, Italy.
 Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; China National Clinical Research Center for Neurological Diseases, Beijing 100070, China; Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; China National Clinical Research Center for Neurological Diseases, Beijing 100070, China; Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China. NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, Faculty of Brain Sciences, University College London, London, United Kingdom; National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, London, United Kingdom. Department of Radiology and Nuclear Medicine, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam 1007 MB, the Netherlands; Queen Square Institute of Neurology and Center for Medical Image Computing, University College London, London, United Kingdom. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Electronic address: zhuozhizheng@bjtth.org. Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing 100070, China. Electronic address: liuyaou@bjtth.org.
 Complex Operative Unit of Neurology, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Laboratory of Neuroproteomics, Multiple Sclerosis Centre, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Laboratory of Neuroproteomics, Multiple Sclerosis Centre, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Complex Operative Unit of Neurology, "F. Ferrari" Hospital, Casarano, 73042 Lecce, Italy. Complex Operative Unit of Ophthalmology, "V. Fazzi" Hospital, 73100 Lecce, Italy.
 Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK. Departments of Neurology (GSPG, LS, TC, KD, CJB, EG, RB, BAC, ELG), Pathology (PJ, RC), and Radiology (MK), Northwestern University; Department of Pathology (PP), University of Chicago, IL; and Department of Neurology (NA), University of Oklahoma Health Sciences Center, OK.
 Unit of Digital Neuroscience, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Berlin Institute of Health, Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany. Bernstein Focus State Dependencies of Learning and Bernstein Center for Computational Neuroscience, Berlin, Germany. Einstein Center for Neurosciences Berlin, Berlin, Germany. Einstein Center Digital Future, Berlin, Germany. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Laboratory of Neuroinformatics, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy. IRCCS Mondino Foundation, Pavia, Italy. Advanced Imaging and Artificial Intelligence Center, IRCCS Mondino Foundation, Pavia, Italy. IRCCS Mondino Foundation, Pavia, Italy. University Institute of Advanced Studies (IUSS), Pavia, Italy. Unit of Behavioral Neurology, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Unit of Behavioral Neurology, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Advanced Imaging and Artificial Intelligence Center, IRCCS Mondino Foundation, Pavia, Italy. IRCCS Mondino Foundation, Pavia, Italy. Institut de Neurosciences des Systèmes, INSERM, INS, Aix Marseille University, Marseille, France. Berlin Institute of Health, Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany. Bernstein Focus State Dependencies of Learning and Bernstein Center for Computational Neuroscience, Berlin, Germany. Einstein Center for Neurosciences Berlin, Berlin, Germany. Einstein Center Digital Future, Berlin, Germany. Unit of Digital Neuroscience, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, London, United Kingdom. Unit of Digital Neuroscience, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy.
 Complex Systems Research Group, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Brain Connectivity Research Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Complex Systems Research Group, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. Complex Systems Research Group, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. National Imaging Facility, Sydney, NSW, Australia. School of Biomedical Engineering, The University of Sydney, Sydney, NSW, Australia. Sydney Imaging, The University of Sydney, Sydney, NSW, Australia. Brain Connectivity Research Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, UCL, London, UK. Brain Connectivity Research Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia. School of Biomedical Engineering, The University of Sydney, Sydney, NSW, Australia. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, UCL, London, UK. Complex Systems Research Group, The University of Sydney, Sydney, NSW, Australia. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia.
 Department of Endocrinology, Razi hospital, Qazvin, Iran. Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN). Tehran, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Universal Council of Epidemiology (UCE), Universal Scientific Education and Research Network (USERN). Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
 Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy; IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Experimental Medicine, Section of Human Physiology, University of Genoa, Genoa, Italy. Department of Developmental and Social Psychology, University of Padova, Via Venezia, 8, Padua 35131, Italy. Italian Multiple Sclerosis Foundation, Scientific Research Area, Genoa, Italy. IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa, Italy. Italian Multiple Sclerosis Foundation, Scientific Research Area, Genoa, Italy. Department of Developmental and Social Psychology, University of Padova, Via Venezia, 8, Padua 35131, Italy. Electronic address: simone.cutini@unipd.it. IRCCS Ospedale Policlinico San Martino, Genoa, Italy; Department of Experimental Medicine, Section of Human Physiology, University of Genoa, Genoa, Italy. Electronic address: marco.bove@unige.it.
 Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy. NIHR King's Clinical Research Facility, King's College, London, UK; Department of Neurology, University of California, Los Angeles, CA, USA. Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy; Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy; Neurophysiology Service, IRCCS San Raffaele Scientific Institute, Milan, Italy. Electronic address: filippi.massimo@hsr.it.
 Universidad de los Andes, School of Medicine, Bogotá, DC, Colombia. Department of Dermatology, Universidad El Bosque, Bogotá, DC, Colombia. Department of Dermatology, George Washington University School of Medicine and Health Sciences, Suite 2B-425, 2150 Pennsylvania Avenue NW, Washington, DC, 20037, USA. jonathanisilverberg@gmail.com.
 Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan. Research Center of Neurology, Ono Pharmaceutical Co., Ltd., Osaka 618-8585, Japan. Research Center of Neurology, Ono Pharmaceutical Co., Ltd., Osaka 618-8585, Japan. Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan. Research Center of Neurology, Ono Pharmaceutical Co., Ltd., Osaka 618-8585, Japan. Research Center of Neurology, Ono Pharmaceutical Co., Ltd., Osaka 618-8585, Japan. Research Center of Neurology, Ono Pharmaceutical Co., Ltd., Osaka 618-8585, Japan. Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan. Department of Clinical Regenerative Medicine, Fujita Health University School of Medicine, 1-98, Dengakugakubo, Kutsukake-cho, Toyoake 470-1192, Japan. Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan. International Center for Brain Science, Fujita Health University, 1-98, Dengakugakubo, Kutsukake-cho, Toyoake 470-1192, Japan.
 Department of Internal Medicine, Washington University School of Medicine, St. Louis MO USA. Department of Psychiatry, The First Affiliated Hospital of Xi'an Jiao Tong University, Xi'an, Shaanxi 710061, China. Department of Internal Medicine, Washington University School of Medicine, St. Louis MO USA. Department of Internal Medicine, Washington University School of Medicine, St. Louis MO USA. Department of Internal Medicine, Washington University School of Medicine, St. Louis MO USA.
 Department of Physiotherapy, Faculty of Continuing Medical Education, Peoples' Friendship University of Russia, 117198 Moscow, Russia. Institute of Personalized Psychiatry and Neurology, V.M. Bekhterev National Medical Research Centre for Psychiatry and Neurology, 192019 Saint Petersburg, Russia. Shared Core Facilities "Molecular and Cell Technologies", V.F. Voino-Yasenetsky Krasnoyarsk State Medical University, 660022 Krasnoyarsk, Russia. Department of Neurogenerative Disorders, Yakut Science Centre of Complex Medical Problems, 677000 Yakutsk, Russia. Institute of Personalized Psychiatry and Neurology, V.M. Bekhterev National Medical Research Centre for Psychiatry and Neurology, 192019 Saint Petersburg, Russia. Hospital for War Veterans, 193079 Saint Petersburg, Russia. Shared Core Facilities "Molecular and Cell Technologies", V.F. Voino-Yasenetsky Krasnoyarsk State Medical University, 660022 Krasnoyarsk, Russia. Shared Core Facilities "Molecular and Cell Technologies", V.F. Voino-Yasenetsky Krasnoyarsk State Medical University, 660022 Krasnoyarsk, Russia. Shared Core Facilities "Molecular and Cell Technologies", V.F. Voino-Yasenetsky Krasnoyarsk State Medical University, 660022 Krasnoyarsk, Russia. Department of Therapy and General Medical Practice with a Course of Postgraduate Professional Education, Altai State Medical University, 656038 Barnaul, Russia.
 Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, Guangdong, 510515, People's Republic of China. School of Public Health, Health Science Center, Xi'an Jiaotong University, No. 76 Yan Ta West Road, Yanta District, Xi'an, Shaanxi, 710061, People's Republic of China. School of Public Health, Health Science Center, Xi'an Jiaotong University, No. 76 Yan Ta West Road, Yanta District, Xi'an, Shaanxi, 710061, People's Republic of China. School of Public Health, Health Science Center, Xi'an Jiaotong University, No. 76 Yan Ta West Road, Yanta District, Xi'an, Shaanxi, 710061, People's Republic of China. School of Public Health, Health Science Center, Xi'an Jiaotong University, No. 76 Yan Ta West Road, Yanta District, Xi'an, Shaanxi, 710061, People's Republic of China. Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, Guangdong, 510515, People's Republic of China. Department of Orthopaedics, the Third Affiliated Hospital of Southern Medical University, No.183, West Zhongshan Avenue, Tianhe District, Guangzhou, Guangdong, 510630, People's Republic of China. Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, Guangdong, 510515, People's Republic of China. Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, Guangdong, 510515, People's Republic of China. Department of Outpatient, Air Force Hospital of Southern Theater Command, No. 801, East Dongfeng Avenue, Yuexiu District, Guangzhou, Guangdong, 510062, People's Republic of China. School of Public Health, Health Science Center, Xi'an Jiaotong University, No. 76 Yan Ta West Road, Yanta District, Xi'an, Shaanxi, 710061, People's Republic of China. fzhxjtu@mail.xjtu.edu.cn. Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, Guangdong, 510515, People's Republic of China. fzhxjtu@mail.xjtu.edu.cn.
 Department of Physiotherapy, University of Granada, Granada, Spain. Faculty of Health Sciences, Melilla, Spain. PNI Europe, The Hague, Netherlands. Chair of Clinical Psychoneuroimmunology, University of Granada and PNI Europe, Granada, Spain. Department of Physiotherapy, University of Granada, Granada, Spain. Faculty of Health Sciences, Melilla, Spain. PNI Europe, The Hague, Netherlands. Chair of Clinical Psychoneuroimmunology, University of Granada and PNI Europe, Granada, Spain. Department of Physiotherapy, University of Granada, Granada, Spain. Faculty of Health Sciences, Melilla, Spain. PNI Europe, The Hague, Netherlands. Chair of Clinical Psychoneuroimmunology, University of Granada and PNI Europe, Granada, Spain. PNI Europe, The Hague, Netherlands. Chair of Clinical Psychoneuroimmunology, University of Granada and PNI Europe, Granada, Spain.
 Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, Laboratory of Neurodegenerative Disorders, National Clinical Research Center for Geriatric, West China Hospital, Sichuan University, Chengdu, China.
 Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia. Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia. Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia. Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia. Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia. Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia. Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Vojvode Stepe 444a, 11042 Belgrade, Serbia.
 Department of Dermatology, Medical University of Warsaw, Warsaw, Poland. Department of Dermatology, Medical University of Warsaw, Warsaw, Poland. Department of Dermatology, Medical University of Warsaw, Warsaw, Poland. Department of Dermatology, Medical University of Warsaw, Warsaw, Poland. Department of Dermatology, Medical University of Warsaw, Warsaw, Poland. Department of Dermatology, Medical University of Warsaw, Warsaw, Poland. Department of Dermatology, Medical University of Warsaw, Warsaw, Poland.
 Interdepartmental Neuroscience Program. Department of Neuroscience, and. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Interdepartmental Neuroscience Program. Department of Neuroscience, and. Interdepartmental Neuroscience Program. Department of Neuroscience, and. Interdepartmental Neuroscience Program. Department of Neuroscience, and. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Interdepartmental Neuroscience Program. Department of Neuroscience, and. Ionis Pharmaceuticals, Carlsbad, California, USA. Yale College, New Haven, Connecticut, USA. Interdepartmental Neuroscience Program. Department of Neuroscience, and. Yale College, New Haven, Connecticut, USA. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Interdepartmental Neuroscience Program. Interdepartmental Neuroscience Program. Ionis Pharmaceuticals, Carlsbad, California, USA. Ionis Pharmaceuticals, Carlsbad, California, USA. Interdepartmental Neuroscience Program. Department of Neuroscience, and. Department of Genetics, Yale School of Medicine, New Haven, Connecticut, USA. Program in Cellular Neuroscience, Neurodegeneration and Repair, and. Yale Stem Cell Center, Yale School of Medicine, New Haven, Connecticut, USA.
 Barrow Neurological Institute, Phoenix AZ, University of Arizona Phoenix, AZ, Creighton University, Phoenix, USA. DAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Scuola Superiore di Studi Avanzati Sapienza (SSAS), Rome, Italy. Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Australia. Istituti Clinici Scientifici Maugeri IRCCS, Neurorehabilitation Department, Milan, Italy. Biomedical Sciences, Faculty of Medicine, The University of Queensland, St Lucia, Australia. Département de neurosciences, CIRCA, Université de Montréal, Montréal, H7G 1T7, Canada. Instituto de Fisiologia, Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal. Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA, USA. Department of Neurology, University of Ulm, Germany. Deutsches Zentrum für neurodegenerative Erkrankungen, Ulm, Germany. Université de Strasbourg, Inserm, UMR-S1118, Mécanismes centraux et périphériques de la neurodégénérescence, CRBS, Strasbourg, France.
 Department of Rehabilitation Sciences, MGH Institute of Health Professions, Boston, Massachusetts, USA. Department of Communicative Disorders and Sciences, The State University of New York, Buffalo, New York, USA. Callier Center for Communication Disorders, University of Texas, Dallas, Texas, USA. Department of Speech-Language Pathology and Rehabilitation Sciences Institute, University of Toronto, Toronto, Ontario, Canada. Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, Toronto, Ontario, Canada. KITE Research Center, Toronto Rehabilitation Institute, Toronto, Ontario, Canada. Department of Rehabilitation Sciences, MGH Institute of Health Professions, Boston, Massachusetts, USA.
 Department of Public Health Sciences, Medical University of South Carolina, Charleston, SC, 29425, USA. Department of Biostatistics, School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA. Department of Biostatistics, School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA. Department of Epidemiology, Gillings School of Global Public Health and Department of Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA. Department of Epidemiology, School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA. Department of Epidemiology, Gillings School of Global Public Health and Department of Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA. Department of Public Health Sciences, Penn State University, Hershey, PA, 17033, USA. Department of Public Health Sciences, Penn State University, Hershey, PA, 17033, USA. Department of Epidemiology, School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA. Electronic address: Eot1@pitt.edu.
 Neurosciences Department, Faculty of Medicine Dentistry and Health, The University of Sheffield, Sheffield, UK. School of Health and Related Research (ScHARR), The University of Sheffield, Sheffield, UK. School of Health and Related Research (ScHARR), The University of Sheffield, Sheffield, UK. School of Health and Related Research (ScHARR), The University of Sheffield, Sheffield, UK. Neurosciences Department, Faculty of Medicine Dentistry and Health, The University of Sheffield, Sheffield, UK.
 Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. National Institute of Rheumatology and Physiotherapy, Budapest, Hungary. Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Division of Clinical Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. Electronic address: bodoki.levente@gmail.com.
 Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmaceutics, ISF College of Pharmacy, Moga, Punjab, 142001, India. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. artiniper@gmail.com. IK Gujral Punjab Technical University, Jalandhar, Punjab, India. artiniper@gmail.com.
 Division of Pulmonary and Critical Care Medicine, Cedars Sinai Medical Center, 8700 Beverly Blvd., South Tower Room 6723, Los Angeles, CA, 90048, USA. giuliana.cerrochiang@cshs.org. Advanced Clinical Biosystems Institute Biomedical Sciences, The Smidt Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA, USA. Advanced Clinical Biosystems Institute Biomedical Sciences, The Smidt Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA, USA. Division of General Internal Medicine and Health Services Research, University of California Los Angeles, Los Angeles, CA, USA. Advanced Clinical Biosystems Institute Biomedical Sciences, The Smidt Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA, USA. Advanced Clinical Biosystems Institute Biomedical Sciences, The Smidt Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA, USA. Division of General Internal Medicine and Health Services Research, University of California Los Angeles, Los Angeles, CA, USA. Division of Pulmonary and Critical Care Medicine, Cedars Sinai Medical Center, 8700 Beverly Blvd., South Tower Room 6723, Los Angeles, CA, 90048, USA. Advanced Clinical Biosystems Institute Biomedical Sciences, The Smidt Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA, USA. Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine., University of California, San Francisco, San Francisco, CA, USA. Division of Rheumatology, Cedars Sinai Medical Center, Los Angeles, CA, USA. Division of Pulmonary and Critical Care Medicine, Cedars Sinai Medical Center, 8700 Beverly Blvd., South Tower Room 6723, Los Angeles, CA, 90048, USA.
 Shanghai, 200040 China Department of Neurology, Huashan Hospital and Institute of Neurology, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 National Center for Neurological Disorders, Shanghai, 200040 China. Shanghai, 200438 China Department of Anthropology and Human Genetics, School of Life Sciences, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200433 China Human Phenome Institute, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200438 China Department of Anthropology and Human Genetics, School of Life Sciences, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200040 China Department of Neurology, Huashan Hospital and Institute of Neurology, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 National Center for Neurological Disorders, Shanghai, 200040 China. Shanghai, 200040 China Department of Neurology, Huashan Hospital and Institute of Neurology, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 National Center for Neurological Disorders, Shanghai, 200040 China. Shanghai, 200438 China Department of Anthropology and Human Genetics, School of Life Sciences, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200433 China Human Phenome Institute, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200438 China Department of Anthropology and Human Genetics, School of Life Sciences, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200040 China Department of Neurology, Huashan Hospital and Institute of Neurology, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 National Center for Neurological Disorders, Shanghai, 200040 China. Shanghai, 200438 China Department of Anthropology and Human Genetics, School of Life Sciences, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200433 China Human Phenome Institute, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 Shanghai, 200040 China Department of Neurology, Huashan Hospital and Institute of Neurology, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443 National Center for Neurological Disorders, Shanghai, 200040 China. Shanghai, 200433 China Human Phenome Institute, Fudan University. GRID: grid.8547.e. ISNI: 0000 0001 0125 2443
 Institut de Génétique Moléculaire de Montpellier, Univ Montpellier, CNRS, Montpellier, France. Institut de Génétique Moléculaire de Montpellier, Univ Montpellier, CNRS, Montpellier, France. Electronic address: odil.porrua@igmm.cnrs.fr.
 Department of Psychiatry and Neurochemistry, University of Gothenburg, Gothenburg, Sweden. Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden. Dementia Research Institute, University College London, London, UK. DRI Fluid Biomarker Laboratory, Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China. Department of Clinical Chemistry, Amsterdam University Medical Center, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. Department of Neurology, Erasmus Medical Center, Rotterdam, the Netherlands. Department of Clinical Research, Department of Neurology, Department of Biomedicine, Multiple Sclerosis Centre, University Hospital Basel, University of Basel, Basel, Switzerland. Department of Neurology, Memory and Aging Center, University of California San Francisco, San Francisco, CA, USA. Queen Square UCL Institute of Neurology, Dementia Research Centre, UK Dementia Research Institute, University College London, London, UK. Department of Neurology, Memory and Aging Center, University of California San Francisco, San Francisco, CA, USA. The Bluefield Project to Cure FTD, San Francisco, CA, USA. The Bluefield Project to Cure FTD, San Francisco, CA, USA. Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL, USA. The Bluefield Project to Cure FTD, San Francisco, CA, USA. Medical Affairs, Alector, Inc., South San Francisco, CA, USA. Medical Affairs, Alector, Inc., South San Francisco, CA, USA.
 Institute of Bioimaging and Molecular Physiology, National Research Council, Milan, Italy. Division of Human Genetics, Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA. Division of Human Genetics, Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA. Department of Genetics, Microbiology and Statistics, University of Barcelona, Barcelona, Catalonia, Spain. Institute of Bioimaging and Molecular Physiology, National Research Council, Milan, Italy. Institute of Bioimaging and Molecular Physiology, National Research Council, Milan, Italy. claudia.cava@ibfm.cnr.it. Division of Human Genetics, Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA.
 NHS Lothian Department of Pathology, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. EaStCHEM School of Chemistry, University of Edinburgh, Edinburgh, UK. EaStCHEM School of Chemistry, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. EaStCHEM School of Chemistry, University of Edinburgh, Edinburgh, UK. Translational Neuroscience PhD Program, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Department of Pathology, NHS Grampian, Aberdeen, UK. NHS Grampian Biorepository, Aberdeen, UK. Department of Pathology, NHS Grampian, Aberdeen, UK. NHS Grampian Biorepository, Aberdeen, UK. NHS Lothian Department of Pathology, Edinburgh, UK. Edinburgh Pathology, Institute of Genetics & Cancer, University of Edinburgh, Edinburgh, UK. EaStCHEM School of Chemistry, University of Edinburgh, Edinburgh, UK. Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK. NHS Lothian Department of Pathology, Edinburgh, UK. Department of Pathology, NHS Grampian, Aberdeen, UK. Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, California, USA. Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Department of Public Health Sciences, University of California Davis School of Medicine, Davis, California, USA. Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Departments of Medicine and Epidemiology, Columbia University Irving Medical Center, New York, New York, USA. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Canada. Harquail Centre for Neuromodulation, Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, Ontario, Canada. Rehabilitation Sciences Institute, University of Toronto, Toronto, Canada. Department of Population Health Science and Biggs Institute for Alzheimer's and Neurodegenerative Diseases, UT Health San Antonio, San Antonio, Texas, USA. Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA. Rush Alzheimer's Disease Center, Chicago, Illinois, USA. Rush University Medical Center, Chicago, Illinois, USA. Department of Neuroscience, University of California San Diego, San Diego, California, USA. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, California, USA.
 Universidade Federal do Ceará, Departamento de Clínica Médica, Núcleo de Desenvolvimento e Pesquisa de Medicamentos, Fortaleza CE, Brazil. Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia/Ebserh, Setor de Investigações nas Doenças Neuromusculares, São Paulo SP, Brazil. Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia/Ebserh, Setor de Investigações nas Doenças Neuromusculares, São Paulo SP, Brazil. Universidade de Pernambuco, Recife PE, Brazil. Universidade Federal do Cariri, Barbalha CE, Brazil. Universidade Federal do Rio Grande do Norte, Departamento de Medicina Integrada, Natal RN, Brazil. Universidade Estadual de Campinas, Departamento de Neurologia, Campinas SP, Brazil. Universidade de São Paulo, Faculdade de Medicina de Ribeirão Preto, Departamento de Neurociências, Ribeirão Preto SP, Brazil. Universidade Federal de São Paulo, Departamento de Neurologia e Neurocirurgia/Ebserh, Setor de Investigações nas Doenças Neuromusculares, São Paulo SP, Brazil. Hospital Geral de Fortaleza, Divisão de Neurologia, Fortaleza CE, Brazil. Universidade Federal de Goiás, Hospital das Clínicas, Unidade de Neurologia e Neurocirurgia/Ebserh, Goiânia GO, Brazil. Comissão de Ética da Academia Brasileira de Neurologia, São Paulo SP, Brazil.
 Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Health Management Center, Xiangya Hospital, Central South University, Changsha, People's Republic of China. Department of Neurology, Qilu Hospital of Shandong University, Jinan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, 410008, People's Republic of China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, People's Republic of China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, 410008, People's Republic of China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, People's Republic of China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, 410008, People's Republic of China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, People's Republic of China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, People's Republic of China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. School of Basic Medical Science, Central South University, Changsha, Hunan, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, 410008, People's Republic of China. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, People's Republic of China. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. Health Management Center, Xiangya Hospital, Central South University, Changsha, People's Republic of China. Department of Neurology, Xiangya Hospital, Central South University, 87 Xiangya Rd, Changsha, Hunan, People's Republic of China. junling.wang@csu.edu.cn. Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, 410008, People's Republic of China. junling.wang@csu.edu.cn. Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, People's Republic of China. junling.wang@csu.edu.cn. Engineering Research Center of Hunan Province in Cognitive Impairment Disorders, Central South University, Changsha, China. junling.wang@csu.edu.cn. National Clinical Research Center for Geriatric Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, People's Republic of China. junling.wang@csu.edu.cn.
 Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Neurology, UMass Chan Medical School, Worcester, MA 01605, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, PA 17033, USA. Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, PA 17033, USA. Department of Neurobiology, University of Southern California, Los Angeles, CA 90089, USA. Centre de Recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), Département de Pathologie et Biologie Cellulaire, Université de Montréal, Montréal, QC, Canada. Centre de Recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), Département de Pathologie et Biologie Cellulaire, Université de Montréal, Montréal, QC, Canada. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA; Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA; Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Department of Neurobiology, University of Southern California, Los Angeles, CA 90089, USA. Centre de Recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), Département de Pathologie et Biologie Cellulaire, Université de Montréal, Montréal, QC, Canada. Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, PA 17033, USA. Department of Neurology, UMass Chan Medical School, Worcester, MA 01605, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Electronic address: ichida@usc.edu.
 Danbury Hospital Nuvance Health, Danbury, Connecticut, USA. Dhulikhel Hospital, Kathmandu University School of Medical Sciences, Dhulikhel, Kavre. Nepal Medical College Teaching Hospital, Kathmandu, Nepal.
 ASU-Banner Neurodegenerative Disease Research Center, Arizona State University, Tempe, Arizona, USA. ASU-Banner Neurodegenerative Disease Research Center, Arizona State University, Tempe, Arizona, USA. University of Pennsylvania, Perelman School of Medicine, Philadelphia, Pennsylvania, USA. ASU-Banner Neurodegenerative Disease Research Center, Arizona State University, Tempe, Arizona, USA.
 Office of Innovation and Analytics, Agency for Toxic Substances and Disease Registry/Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. Office of Innovation and Analytics, Agency for Toxic Substances and Disease Registry/Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Office of Community Health Hazard Assessment, Agency for Toxic Substances and Disease Registry, Atlanta, Georgia, USA. ALS Association, Washington, District of Columbia, USA. Office of Innovation and Analytics, Agency for Toxic Substances and Disease Registry/Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
 Department of Physiology and Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Physiology and Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu.
 National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. Center for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark. Center for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark. Clinical Mass Spectrometry, Statens Serum Institut, Artillerivej 5, DK-2300, Copenhagen S, Denmark. Testcenter Denmark, Statens Serum Institut, Artillerivej 5, DK-2300, Copenhagen S, Denmark. Center for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark. Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD, Australia. Queensland Brain Institute, University of Queensland, Brisbane, QLD, Australia. Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD, Australia. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. Department of Clinical Epidemiology, Aarhus University and Aarhus University Hospital, 8200, Aarhus N, Denmark. Department of Affective Disorders, Aarhus University and Aarhus University Hospital-Psychiatry, Aarhus, Denmark. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. CIRRAU - Centre for Integrated Register-based Research, Aarhus University, Aarhus, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. Center for Genomics and Personalized Medicine, Aarhus University, Aarhus, Denmark. Department of Biomedicine and the iSEQ Center, Aarhus University, Aarhus, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. Department for Congenital Disorders, Statens Serum Institut, 2300, Copenhagen S, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. Mental Health Services in the Capital Region of Denmark, Mental Health Center Copenhagen, University of Copenhagen, 2100, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, 2200, Copenhagen N, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. Institute of Biological Psychiatry, Mental Health Services, Copenhagen University Hospital, Copenhagen N, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Lundbeck Center for Geogenetics, GLOBE Institute, University of Copenhagen, Copenhagen, Denmark. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. CIRRAU - Centre for Integrated Register-based Research, Aarhus University, Aarhus, Denmark. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, 8210, Aarhus V, Denmark. Bioinformatics Research Centre, Aarhus University, 8000, Aarhus C, Denmark. National Centre for Register-Based Research, Aarhus University, 8210, Aarhus V, Denmark. j.mcgrath@uq.edu.au. Queensland Brain Institute, University of Queensland, Brisbane, QLD, Australia. j.mcgrath@uq.edu.au. Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Brisbane, QLD, 4076, Australia. j.mcgrath@uq.edu.au.
 Department of Rheumatology, Hospital Universitario La Paz, IdiPaz, Madrid, Spain. Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. Immunology-Inflammatory Diseases, Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain. Arthritis Unit, Department of Rheumatology, Hospital Clínic and Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain. Department of Dermatology, Hospital Universitario La Princesa, Madrid, Spain. Department of Rheumatology, Hospital Universitario San Juan de Alicante, Alicante, Spain. Department of Rheumatology, Hospital Universitario Fundación Alcorcón, Alcorcón, Madrid, Spain. Department of Rheumatology, Complejo Hospitalario Universitario de A Coruña, Instituto de Investigación Biomédica de A Coruña (INIBIC), A Coruña, Spain. Department of Rheumatology, Hospital Universitario de Basurto, Bilbao, Spain. Department of Rheumatology, Hospital Universitario Fundación Alcorcón, Alcorcón, Madrid, Spain. Department of Rheumatology, Hospital Universitario 12 de Octubre, Madrid, Spain. Department of Rheumatology, Medicine Department Autonomus University of Barcelona (UAB), I3PT, University Hospital Parc Taulí Sabadell, Barcelona, Spain. Department of Rheumatology, University Hospital Bellvitge, Instituto de Investigación Biomédica de Bellvitge (IDIBELL), Barcelona, Spain. Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, Instituto de Investigación Marqués de Valdecilla (IDIVAL), Santander, Spain. Department of Dermatology, Hospital Universitario Virgen de las Nieves, Granada, Spain. Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain. Department of Dermatology, Facultad de Medicina, Universidad de Granada, Spain. Department of Rheumatology, Hospital Universitario Puerta del Hierro Majadahonda, Madrid, Spain. Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo, Asturias, Spain. Arthritis Unit, Department of Rheumatology, Hospital Clínic and Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
 Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Delft Bioinformatics Lab, Delft Technical University, Van, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, Alzheimer Center Amsterdam, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Molecular and Cellular Neuroscience, Center for Neurogenomics and Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Pathology, Neuroscience, Amsterdam, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, Alzheimer Center Amsterdam, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Pathology, Neuroscience, Amsterdam, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, Alzheimer Center Amsterdam, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Pathology, Neuroscience, Amsterdam, The Netherlands. Netherlands Institute for Neuroscience, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Epidemiology & Biostatistics, Amsterdam, The Netherlands. Faculty of Behavioural and Movement Sciences, Clinical Developmental Psychology and Clinical Neuropsychology, Vrije Universiteit Amsterdam, The Netherlands. Delft Bioinformatics Lab, Delft Technical University, Van, The Netherlands. Department of Neurology, Alzheimer Center Amsterdam, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Delft Bioinformatics Lab, Delft Technical University, Van, The Netherlands. Department of Pathology, Neuroscience, Amsterdam, The Netherlands. Department of Human Genetics, Genomics of Neurodegenerative Diseases and Aging, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Department of Neurology, Alzheimer Center Amsterdam, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
 Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. andreapasta93@gmail.com. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine DiMI, University of Genoa, IRCCS San Martino Polyclinic, Genoa, Italy. Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine DiMI, University of Genoa, IRCCS San Martino Polyclinic, Genoa, Italy. Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine DiMI, University of Genoa, IRCCS San Martino Polyclinic, Genoa, Italy. Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine DiMI, University of Genoa, IRCCS San Martino Polyclinic, Genoa, Italy. Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine DiMI, University of Genoa, IRCCS San Martino Polyclinic, Genoa, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy. Department of Surgery, Oncology and Gastroenterology, University of Padua, Padua, Italy. Gastroenterology Unit, Azienda Ospedale Università di Padua, Padua, Italy. Gastroenterology Unit, Department of Internal Medicine, University of Genoa, IRCCS-Ospedale Policlinico San Martino, 16132, Genoa, Italy.
 Department of Internal Medicine and Clinical Immunology, Centre de Référence des Maladies Auto-immunes Systémiques Rares du Nord et Nord-Ouest de France (CeRAINO), University Hospital of Lille, Rue Michel Polonovski, Hôpital Huriez, CHU Lille, F-59000 Lille, France. Univ. Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, Lille, France. INSERM, Paris, France. Department of Respiratory Diseases, University Hospital of Nice, Nice, France. Côte d'Azur University, Nice, France. Reference Centre for Systemic Autoimmune Diseases, Cochin Hospital, Paris, France. Department of Respiratory Diseases, Avicenne Hospital, Bobigny, France. Department of Respiratory Diseases, Louis Pradel Hospital, Bron, France. Department of Internal Medicine and Clinical Immunology, Saint-Antoine Hospital, Paris, France. Department of Internal Medicine and Clinical Immunology, University Hospital of Nice, Nice, France. Côte d'Azur University, Nice, France. Univ. Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, Lille, France. INSERM, Paris, France. CHU Lille, Département de Médecine Interne et Immunologie Clinique, Centre de Référence des Maladies Auto-immunes. Systémiques Rares du Nord et Nord-Ouest de France (CeRAINO), Lille, France. Infectious Diseases Department, Gustave Dron Hospital, Tourcoing, France. Department of Internal Medicine and Clinical Immunology, Centre de Référence des Maladies Auto-immunes Systémiques Rares du Nord et Nord-Ouest de France (CeRAINO), University Hospital of Lille, Rue Michel Polonovski, Hôpital Huriez, CHU Lille, F-59000 Lille, France. Univ. Lille, U1286 - INFINITE - Institute for Translational Research in Inflammation, Lille, France. INSERM, Paris, France. Department of Internal Medicine and Clinical Immunology, University Hospital of Nice, Nice, France. Côte d'Azur University, Nice, France. INSERM U1065 - Mediterranean Centre for Molecular Medicine, Control of gene expression (COdEX), Paris, France.
 Centre de Référence Coordinateur des maladies pulmonaires rares (OrphaLung), Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, ERN-LUNG, 69677 Lyon, France; UMR 754, INRAE, Université Claude Bernard Lyon 1, 8 avenue Rockefeller, 69008 Lyon, France. Electronic address: vincent.cottin@chu-lyon.fr. Centre de Compétence des maladies pulmonaires rares (OrphaLung), GH Sud Haut-Lévêque, Avenue Magellan, 33600 Pessac, France. Centre de Compétence des maladies pulmonaires rares (OrphaLung), CHU Pontchailloux, 2 rue Henri le Guilloux, 35000 Rennes, France. Service de Pneumologie, Centre Hospitalier Universitaire Vaudois, BU44/07.2137, Rue du Bugnon 46, 1011 Lausanne, Suisse. Centre de Compétence des maladies pulmonaires rares (OrphaLung), Hôpital Nord, Chemin Bourrely, 13015 Marseille, France; URMITE-CNRS-IRD UMR 6236, Aix-Marseille Université, 51 boulevard Pierre Dramard, 13344 Marseille cedex 15, France. Centre de Référence Constitutif des maladies pulmonaires rares (OrphaLung), Hôpital Bichat, 46 rue Henri Huchard, 75018 Paris, France; Université Paris-Diderot, 17 rue Jean Antoine de Baïf, 75013 Paris, France. Centre de Référence constitutif des maladies pulmonaires rares (OrphaLung), Hôpital Avicenne, 125 rue Stalingrad, 93000 Bobigny, France; Université Sorbonne Paris Nord, INSERM UMR 1272 "Hypoxie et Poumon", 1 rue Chablis, 93000 Bobigny, Paris, France. Centre de Référence constitutif des maladies pulmonaires rares, CHRU, 5 rue Oscar Lambret, 59000 Lille, France. Service de pneumologie, CHU Amiens, 1 Place Victor Pauchet, 80054 Amiens, France; UFR de médecine, 3 rue Louvels, 80000 Amiens, France. Hôpital Suisse de Paris, 10 rue Minard, 92130 Issy les Moulineaux, France. Centre de Référence constitutif des maladies pulmonaires rares, CHU de Dijon, BP 77908, 21079, Dijon, France; INSERM, LNC UMR1231, LipSTIC LabEx Team, 21000 Dijon, France. Université Sorbonne Paris Nord, INSERM UMR 1272 "Hypoxie et Poumon", 1 rue Chablis, 93000 Bobigny, Paris, France; Service de radiologie, hôpital Avicenne, 125 rue Stalingrad, 93000 Bobigny, France. Département de génétique, Hospices Civils de Lyon, 28 avenue Doyen Lepine, 69677 Lyon, France; IBCP, Université Claude Bernard Lyon 1, 8 avenue Rockefeller, 69008 Lyon, France. Service de pathologie, Groupe hospitalier est, Hospices Civils de Lyon, 28 avenue Doyen Lepine, 69677 Lyon, France; Université Claude Bernard Lyon 1, 8 avenue Rockefeller, 69008 Lyon, France. Service de pneumologie, hôpital nord, 42270 Saint Priest en Jarest, France. Association ASTB, 11 rue Parmentier, 92200 Neuilly-Sur-Seine, France. Pole imagerie, CHU Grenoble Alpes, Boulevard Chantourne, 38700 La Tronche, France. Centre de Référence Coordinateur des maladies pulmonaires rares (OrphaLung), Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, ERN-LUNG, 69677 Lyon, France. Centre de Référence Coordinateur des maladies pulmonaires rares (OrphaLung), Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, ERN-LUNG, 69677 Lyon, France. Service d'anatomopatholologie, Hôpital Avicenne, 125 rue Stalingrad, 93000 Bobigny, France. Association France Lymphangioléiomyomatose, 4, Rue des Vieux-Moulins, 56 680 Plouhinec, France. Service de radiologie, CHU Pontchailloux, 2 rue Henri le Guilloux, 35000 Rennes, France. Service de génétique, CHU Angers, 4 rue Larrey, 49100 Angers, France. Association France Lymphangioléiomyomatose, 4, Rue des Vieux-Moulins, 56 680 Plouhinec, France. Centre de Compétence des maladies pulmonaires rares (OrphaLung), Hôpital Bretonneau, CHRU Tours, 2 Boulevard Tonnellé, 37000 Tours, France; Université de Tours, CEPR INSERMU1100, 10 Boulevard Tonnellé, 37000 Tours, France. Service de chirurgie thoracique, Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, 69677 Lyon, France. Service de pneumologie, Hôpital Saint Joseph, 185 rue Raymond Losserand, 75014 Paris, France. Centre de Référence Coordinateur des maladies pulmonaires rares (OrphaLung), Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, ERN-LUNG, 69677 Lyon, France. Centre de Référence constitutif des maladies pulmonaires rares (OrphaLung), Hôpital Avicenne, 125 rue Stalingrad, 93000 Bobigny, France; Université Sorbonne Paris Nord, INSERM UMR 1272 "Hypoxie et Poumon", 1 rue Chablis, 93000 Bobigny, Paris, France. Service de radiologie, Hôpital Edouard Herriot, 5 place d'Arsonval, 69008 Lyon, France. Centre de Compétence des maladies pulmonaires rares (OrphaLung), service de pneumologie, hôpital Larrey, 24 chemin de Pouvourville, 31059 Toulouse cedex 9, France. Centre Léon Bérard, 28 rue Laenne, 69008 Lyon, France. Université Claude Bernard Lyon 1, 8 avenue Rockefeller, 69008 Lyon, France; Service de radiologie, Hôpital Edouard Herriot, 5 place d'Arsonval, 69008 Lyon, France. Université Claude Bernard Lyon 1, 8 avenue Rockefeller, 69008 Lyon, France; Service d'imagerie, Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, 69677 Lyon, France. Laboratoire de Génétique Chromosomique et Moléculaire, CHU-Hôpital Nord, Laboratoire AURAGEN (Plan France Médecine Génomique 2025), 42270 Saint Priest en Jarest, France. Centre de Référence Coordinateur des maladies pulmonaires rares (OrphaLung), Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, ERN-LUNG, 69677 Lyon, France. Service d'exploration fonctionnelle respiratoire, Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, 69677 Lyon, France. Centre de Référence constitutif des maladies pulmonaires rares (OrphaLung), Hôpital Avicenne, 125 rue Stalingrad, 93000 Bobigny, France. Centre de Référence Coordinateur des maladies pulmonaires rares (OrphaLung), Hôpital Louis Pradel, Hospices Civils de Lyon, 28 avenue Doyen Lepine, ERN-LUNG, 69677 Lyon, France.
 Koc University Hospital, Department of Pediatric Rheumatology, Turkey. Istanbul Sisli Hamidiye Etfal Training and Research Hospital, Rheumatology Department, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Pediatric Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Pediatric Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Pediatric Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Pediatric Rheumatology, Turkey. Istanbul University-Cerrahpasa, Cerrahpasa Medical School, Department of Rheumatology, Turkey. Electronic address: eseyahi@yahoo.com.
 Central Research Center, CORESTEMCHEMON Inc., Seoul, Republic of Korea. Central Research Center, CORESTEMCHEMON Inc., Seoul, Republic of Korea. Department of Biology, Kyung Hee University, Seoul, Republic of Korea. Central Research Center, CORESTEMCHEMON Inc., Seoul, Republic of Korea. College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea. Central Research Center, CORESTEMCHEMON Inc., Seoul, Republic of Korea. Central Research Center, CORESTEMCHEMON Inc., Seoul, Republic of Korea. Department of Neurology, College of Medicine, Hanyang University, Seoul, Republic of Korea. Department of Neurology, College of Medicine, Hanyang University, Seoul, Republic of Korea. Department of Neurology, College of Medicine, Hanyang University, Seoul, Republic of Korea. Department of Neurology, College of Medicine, Hanyang University, Seoul, Republic of Korea. Department of Neurology, Chung-Ang University Gwangmyeong Hospital, Gwangmyeong, Republic of Korea. Department of Neurology, School of Medicine, Kyungpook National University, Kyungpook National University Chilgok Hospital, Daegu, Republic of Korea. College of Nursing, Dankook University, Cheonan, Republic of Korea. Department of Neurology, Bethesda Gospel Hospital, Yangsan, Republic of Korea. Department of Biostatistics, Korea University College of Medicine, Seoul, Republic of Korea. Cell Therapy Center, Hanyang University Hospital, Seoul, Republic of Korea. Cell Therapy Center, Hanyang University Hospital, Seoul, Republic of Korea. Department of Neurology, College of Medicine, Hanyang University, Seoul, Republic of Korea. Cell Therapy Center, Hanyang University Hospital, Seoul, Republic of Korea.
 National Institute of Mental Health, Klecany, Czech Republic. Third Faculty of Medicine, Charles University, Prague, Czech Republic. National Institute of Mental Health, Klecany, Czech Republic. Faculty of Science, Charles University, Prague, Czech Republic. National Institute of Mental Health, Klecany, Czech Republic. National Institute of Mental Health, Klecany, Czech Republic. Laboratory of Neurophysiology of Memory, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. Third Faculty of Medicine, Charles University, Prague, Czech Republic. National Institute of Mental Health, Klecany, Czech Republic. Laboratory of Neurophysiology of Memory, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. Faculty of Science and Engineering, University of Greenwich London, Chatham Maritime, UK.
 Pediatric Research Center "Romeo ed Enrica Invernizzi", Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy. Pediatric Research Center "Romeo ed Enrica Invernizzi", Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy; Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, Pavia, Italy. Center of Functional Genomics and Rare Diseases, Department of Pediatrics, Buzzi Children's Hospital, Milan, Italy; Department of Electronics, Information and Bioengineering (DEIB), Politecnico di Milano, Milan, Italy. Pediatric Research Center "Romeo ed Enrica Invernizzi", Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy. Department of Chemistry, Materials and Chemical Engineering "Giulio Natta", Politecnico di Milano, Milan, Italy. Department of Biosciences, University of Milan, Milan, Italy. Cellular Models and Neuroepigenetics Unit, IRCCS Mondino Foundation, Pavia, Italy. Molecular Biology and Transcriptomics Unit, IRCCS Mondino Foundation, Pavia, Italy. Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy. Department of Chemistry, Materials and Chemical Engineering "Giulio Natta", Politecnico di Milano, Milan, Italy. Immunotherapy, Cell Therapy and Biobank (ITCB), IRCCS Istituto Romagnolo per lo Studio dei Tumori (IRST) "Dino Amadori", Meldola, Italy. Pediatric Research Center "Romeo ed Enrica Invernizzi", Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy; Department of Pediatrics, Buzzi Children's Hospital, Milan, Italy. Pediatric Research Center "Romeo ed Enrica Invernizzi", Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy. Electronic address: stephana.carelli@unimi.it. Center of Functional Genomics and Rare Diseases, Department of Pediatrics, Buzzi Children's Hospital, Milan, Italy.
 AC Immune SA, Lausanne, Switzerland. Electronic address: tariq.afroz@acimmune.com. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. Department of Neuropathology, University of Tübingen, Tübingen, Germany; DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany. Psychogenics Inc., Paramus, NJ, USA. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. University of Kentucky, Lexington, KY, USA. Center for Neurodegenerative Disease Research (CNDR), Institute on Aging, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Center for Neurodegenerative Disease Research (CNDR), Institute on Aging, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. AC Immune SA, Lausanne, Switzerland. Electronic address: tamara.seredenina@acimmune.com.
 Department of Public Health and Primary Care, Katholieke Universiteit Leuven, Leuven, Leuven Belgium; Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK; Deep Medicine, Nuffield Department of Women's and Reproductive Health, University of Oxford, Oxford, UK. Electronic address: nathalie.conrad@kuleuven.be. Faculty of Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK. Department of Public Health and Primary Care, Katholieke Universiteit Leuven, Leuven, Leuven Belgium; Nuffield Department of Primary Care Health Sciences, University of Oxford, Oxford, UK. Interuniversity Institute for Biostatistics and Statistical Bioinformatics (I-BioStat), Hasselt University and Katholieke Universiteit Leuven, Leuven, Belgium. Interuniversity Institute for Biostatistics and Statistical Bioinformatics (I-BioStat), Hasselt University and Katholieke Universiteit Leuven, Leuven, Belgium. Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK. Faculty of Medicine, National Heart & Lung Institute, Imperial College London, London, UK. College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, UK. Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK. College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, UK. Diabetes Research Centre, University of Leicester, Leicester, UK. Department of Rheumatology, Division of Medicine, University College London, London, UK.
 Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. angelasanna72@gmail.com. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Cagliari, Italy. Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Cagliari, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Cagliari, Italy. Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. Department of Mechanical, Chemical and Materials Engineering, University of Cagliari, Cagliari, Italy. Neurology, SS Trinità Hospital, ASL Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ASL Cagliari, Cagliari, Italy.
 Radiology Department, Taleghani Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Radiology Department, Taleghani Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran; Universal council of epidemiology (UCE), Universal Scientific Education and Research Network (USERN), Tehran University of Medical Sciences, Tehran, Iran. Electronic address: m.ghajarzadeh@gmail.com.
 Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Biomedical Engineering Department, School of Biomedical Engineering & Imaging Sciences, King's College London, London, United Kingdom. Department of Radiology, University of Calgary, Calgary, Canada. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute for Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neuroradiology, APHM La Timone, CEMEREM, Marseille, France. Aix-Marseille Univ, CNRS, CRMBM, UMR 7339, Marseille, France. Institute of Medical Biometry and Epidemiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
 Department of Obstetrics and Gynecology, Reproductive Biology Unit, Maternal-fetal Immunology Group, Medical University of Vienna, Vienna, Austria. Department of Obstetrics and Gynecology, Reproductive Biology Unit, Maternal-fetal Immunology Group, Medical University of Vienna, Vienna, Austria. Department of Obstetrics and Gynecology, Reproductive Biology Unit, Maternal-fetal Immunology Group, Medical University of Vienna, Vienna, Austria. Division of Inflammation and Infection (II), Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden. Otto Loewi Research Center, Division of Pharmacology, Medical University of Graz, Graz, Austria. Institute for Vascular Biology, Center for Physiology and Pharmacology, Medical University Vienna, Vienna, Austria; Christian Doppler Laboratory for Arginine Metabolism in Rheumatoid Arthritis and Multiple Sclerosis, Vienna, Austria. Department of Obstetrics and Gynecology, Reproductive Biology Unit, Placental Development Group, Medical University of Vienna, Vienna, Austria. Department of Obstetrics and Gynecology, Reproductive Biology Unit, Placental Development Group, Medical University of Vienna, Vienna, Austria. Department of Obstetrics and Gynecology, Reproductive Biology Unit, Maternal-fetal Immunology Group, Medical University of Vienna, Vienna, Austria. Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria. Department of Obstetrics and Gynecology, Medical University of Vienna, Vienna, Austria. Center for Pathobiochemistry and Genetics, Institute of Medical Chemistry, Medical University of Vienna, Vienna, Austria. Otto Loewi Research Center, Division of Pharmacology, Medical University of Graz, Graz, Austria. Institute for Vascular Biology, Center for Physiology and Pharmacology, Medical University Vienna, Vienna, Austria. Center for Anatomy and Cell Biology, Medical University of Vienna, Vienna, Austria. Institute for Vascular Biology, Center for Physiology and Pharmacology, Medical University Vienna, Vienna, Austria; Christian Doppler Laboratory for Arginine Metabolism in Rheumatoid Arthritis and Multiple Sclerosis, Vienna, Austria. Institute for Vascular Biology, Center for Physiology and Pharmacology, Medical University Vienna, Vienna, Austria. Department of Clinical Immunology and Transfusion Medicine, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden. Department of Obstetrics and Gynecology, Reproductive Biology Unit, Maternal-fetal Immunology Group, Medical University of Vienna, Vienna, Austria. Electronic address: juergen.pollheimer@muv.ac.at.

 Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Neuroscience and Rare Diseases (NRD), F. Hoffmann-La Roche, Ltd., Grenzacherstrasse, 4070 Basel, Switzerland. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. gRED OMNI-Biomarker Development, F. Hoffmann-La Roche, Ltd., Grenzacherstrasse, Basel, Switzerland. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Program in Neuroinfectious Diseases, Division of Critical Care and Hospitalist Neurology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Product Development Medical Affairs (PDMA) Neuroscience, F. Hoffmann-La Roche, Ltd., Grenzacherstrasse, 4070 Basel, Switzerland. University Hospital Basel, Department of Neurology and Biomedicine, University of Basel, 4031 Basel, Switzerland. Neuroscience and Rare Diseases (NRD), F. Hoffmann-La Roche, Ltd., Grenzacherstrasse, 4070 Basel, Switzerland. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. University Hospital Basel, Department of Neurology and Biomedicine, University of Basel, 4031 Basel, Switzerland. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Columbia Multiple Sclerosis Center, Department of Neurology, Columbia University Irving Medical Center, New York, NY 10032, USA. Neuroscience and Rare Diseases (NRD), F. Hoffmann-La Roche, Ltd., Grenzacherstrasse, 4070 Basel, Switzerland. MS Research Unit, Biogen, Cambridge, MA 02142, USA.
 Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Laboratory of Parasitology, Department of Bacteria, Parasites, and Fungi, Statens Serum Institut, Copenhagen, Denmark. Department of Pathology, Herlev and Gentofte Hospital, Herlev, Denmark. Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark. Department of Clinical Medicine, Aarhus University, Aarhus, Denmark. Laboratory of Parasitology, Department of Bacteria, Parasites, and Fungi, Statens Serum Institut, Copenhagen, Denmark. Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Glostrup, Denmark. Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Hematology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
 Section of Immunology, Allergy and Rheumatology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA. Section of Immunology, Allergy and Rheumatology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA. Section of Immunology, Allergy and Rheumatology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
 CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroepidemiology Unit, Melbourne School of Population & Global Health, The University of Melbourne, Carlton, VIC, Australia. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Department of Mathematics Computing, and Engineering Technologies, Swinburne University of Technology, Hawthorn, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. Concord Clinical School, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. Neurology North Shore, Auckland, New Zealand. Department of Neurology, Launceston General Hospital, Launceston, Tasmania, Australia. School of Medicine and Psychology, Australian National University, Canberra, Australian Capital Territory, Australia. Centre for Neuromuscular and Neurological Disorders, Perron Institute for Neurological and Translational Science, University of Western Australia, Nedlands, Western Australia, Australia. Neurology, Sunshine Coast University Hospital, Sunshine Coast, Queensland, Australia. CORe, Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia. Neuroimmunology Centre, Department of Neurology, The Royal Melbourne Hospital, Parkville, Victoria, Australia.
 Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Neurology, Mayo Clinic Rochester, Rochester, MN, USA; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic Rochester, Rochester, MN, USA. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran; Network of Immunity in Infection, Malignancy, and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Isfahan, Iran. Department of Cardiovascular Medicine, Center for Regenerative Medicine, Mayo Clinic, Rochester, Rochester, MN, USA. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran; Network of Immunity in Infection, Malignancy, and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Functional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Alzahra Research Institute, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran; Network of Immunity in Infection, Malignancy, and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Isfahan, Iran. Electronic address: hosein.nouri.2018@gmail.com.
 Faculty of Medicine, Vilnius University, Vilnius, Lithuania. Center for Pediatric Oncology and Hematology, Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania. Faculty of Medicine, Vilnius University, Vilnius, Lithuania. Republican Vilnius University Hospital, Vilnius, Lithuania. Division of Multiple Sclerosis, Vilnius University Santaros Klinikos, Vilnius, Lithuania. Faculty of Medicine, Vilnius University, Vilnius, Lithuania. Clinic of Dental and Oral Diseases, Faculty of Odontology, Kaunas University of Medicine, Kaunas, Lithuania. Center for Pediatric Oncology and Hematology, Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania. Center for Pediatric Oncology and Hematology, Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania. Faculty of Medicine, Vilnius University, Vilnius, Lithuania. Center for Pediatric Oncology and Hematology, Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania.
 Department of Physics, Faculty of Sciences, Zonguldak Bulent Ecevit University, Zonguldak 67100, Turkey. Department of Molecular Medicine and USF Health Byrd Alzheimer's Research Institute, Morsani College of Medicine, University of South Florida, Tampa, Florida 33612, United States. Department of Pathology, School of Medicine, Case Western Reserve University, 2103 Cornell Road, 5129 WRB, Cleveland, Ohio 44106, United States. Department of Pathology, School of Medicine, Case Western Reserve University, 2103 Cornell Road, 5129 WRB, Cleveland, Ohio 44106, United States. Louis Stokes Cleveland VA Medical Center, 10701 East Boulevard, Cleveland, Ohio 44106, United States. Department of Pathology, School of Medicine, Case Western Reserve University, 2103 Cornell Road, 5129 WRB, Cleveland, Ohio 44106, United States. Molecular Biotechnology, Turkish-German University, Sahinkaya Caddesi, No. 106, Beykoz, Istanbul 34820, Turkey.
 Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany. hermesdorf@uni-muenster.de. Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Neurology With Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany.
 Biodonostia Health Research Institute, Neurosciences Area, Multiple Sclerosis Group, San Sebastian, Spain. Osakidetza Basque Health Service, UGC Laboratories Gipuzkoa, Immunology Section, San Sebastián, Spain. Biodonostia Health Research Institute, Neurosciences Area, Multiple Sclerosis Group, San Sebastian, Spain. Biodonostia Health Research Institute, Neurosciences Area, Multiple Sclerosis Group, San Sebastian, Spain. Osakidetza Basque Health Service, UGC Laboratories Gipuzkoa, Immunology Section, San Sebastián, Spain. Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas-Instituto de Salud Carlos III (CIBER-CIBERNED-ISCIII), Madrid, Spain. Biodonostia Health Research Institute, Neurosciences Area, Multiple Sclerosis Group, San Sebastian, Spain. Butler Scientifics S.L., Barcelona, Spain. Butler Scientifics S.L., Barcelona, Spain. Infectious Diseases Department, Osakidetza Basque Health Service, Donostialdea Integrated Health Organization, San Sebastián, Spain. Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas-Instituto de Salud Carlos III (CIBER-CIBERNED-ISCIII), Madrid, Spain. Butler Scientifics S.L., Barcelona, Spain. Infectious Diseases Department, Osakidetza Basque Health Service, Donostialdea Integrated Health Organization, San Sebastián, Spain. Neuroimmune-repair Group, Hospital Nacional de Parapléjicos-SESCAM, Toledo, Spain. Microbiology Department, Biodonostia Health Research Institute, Infectious Diseases Area, Respiratory Infection and Antimicrobial Resistance Group, Osakidetza Basque Health Service, Donostialdea Integrated Health Organization, San Sebastián, Spain. Osakidetza Basque Health Service, UGC Laboratories Gipuzkoa, San Sebastián, Spain. Osakidetza Basque Health Service, UGC Laboratories Gipuzkoa, San Sebastián, Spain. Biodonostia Health Research Institute, Neurosciences Area, Multiple Sclerosis Group, San Sebastian, Spain. Osakidetza Basque Health Service, UGC Laboratories Gipuzkoa, Immunology Section, San Sebastián, Spain. Biodonostia Health Research Institute, Neurosciences Area, Multiple Sclerosis Group, San Sebastian, Spain. Osakidetza Basque Health Service, UGC Laboratories Gipuzkoa, Immunology Section, San Sebastián, Spain. Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas-Instituto de Salud Carlos III (CIBER-CIBERNED-ISCIII), Madrid, Spain.
 Department of Neurology, Mannheim Medical Center, University of Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany. Department of Neurology, Mannheim Medical Center, University of Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany. Department of Neurology, Mannheim Medical Center, University of Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany. Department of Neurology, Mannheim Medical Center, University of Heidelberg, Germany. Department of Medicine, Division of Immunology and Rheumatology, Stanford University, CA, USA. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Germany. Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Germany. Department of Neurology, Heinrich Heine University Düsseldorf, Germany. Division of Metabolic Crosstalk in Cancer, German Consortium of Translational Cancer Research (DKTK) & German Cancer Research Center (DKFZ), Heidelberg, Germany. Faculty of Bioscience, Heidelberg University, Germany. Division of Metabolic Crosstalk in Cancer, German Consortium of Translational Cancer Research (DKTK) & German Cancer Research Center (DKFZ), Heidelberg, Germany. Division of Neurosurgical Research, Department of Neurosurgery, University Hospital Heidelberg, Germany. Department of Neuropathology, Heidelberg University Hospital, Germany. DKTK Clinical Cooperation Unit Neuropathology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Department of Neurology, Mannheim Medical Center, University of Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany. Department of Neurology, Mannheim Medical Center, University of Heidelberg, Germany. DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center, Heidelberg, Germany.
 Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Department of Rehabilitation Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Multiple Sclerosis Center, Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Mental and Neurological Diseases Research Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
 Department of Anatomy, Physiology, and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada. Cameco Multiple Sclerosis Neuroscience Research Centre, Saskatoon, Saskatchewan S7K 0M7, Canada. Canadian Centre for Health and Safety in Agriculture (CCHSA), Department of Medicine, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 2Z4, Canada. Department of Anatomy, Physiology, and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada. Cameco Multiple Sclerosis Neuroscience Research Centre, Saskatoon, Saskatchewan S7K 0M7, Canada. Canadian Centre for Health and Safety in Agriculture (CCHSA), Department of Medicine, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 2Z4, Canada. Department of Chemistry, University of Waterloo, Waterloo, Ontario N2L 3G1, Canada. Department of Anatomy, Physiology, and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada. Cameco Multiple Sclerosis Neuroscience Research Centre, Saskatoon, Saskatchewan S7K 0M7, Canada. Department of Anatomy, Physiology, and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada. Cameco Multiple Sclerosis Neuroscience Research Centre, Saskatoon, Saskatchewan S7K 0M7, Canada. Department of Chemistry, University of Waterloo, Waterloo, Ontario N2L 3G1, Canada. Department of Anatomy, Physiology, and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada anand.krishnan@usask.ca. Cameco Multiple Sclerosis Neuroscience Research Centre, Saskatoon, Saskatchewan S7K 0M7, Canada.
 State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
 Department of Communication Sciences and Disorders, MGH Institute of Health Professions, Boston, MA. Department of Communication Sciences and Disorders, MGH Institute of Health Professions, Boston, MA. Speech and Hearing Bioscience and Technology Program, Harvard University, Cambridge, MA. Department of Communication Sciences and Disorders, MGH Institute of Health Professions, Boston, MA. Department of Speech-Language Pathology, University of Toronto, Ontario, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, Ontario, Canada. Toronto Rehabilitation Institute, University Health Network, Ontario, Canada. Department of Communication Sciences and Disorders, MGH Institute of Health Professions, Boston, MA. Department of Speech-Language Pathology, University of Toronto, Ontario, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, Ontario, Canada. Department of Neurology, Neurological Clinical Research Institute, Massachusetts General Hospital, Boston. Department of Neurology, Neurological Clinical Research Institute, Massachusetts General Hospital, Boston. Department of Neurology, Neurological Clinical Research Institute, Massachusetts General Hospital, Boston. Department of Communication Sciences and Disorders, MGH Institute of Health Professions, Boston, MA.
 Department of Neurology, University of California, Irvine, CA, USA. Department of Neurology, University of California, Irvine, CA, USA. Department of Neurobiology and Behavior, University of California, Irvine, CA, USA. Department of Pathology, Stanford University, Palo Alto, CA, USA. Department of Pathology, Stanford University, Palo Alto, CA, USA. Department of Epidemiology and Biostatistics, University of California, Irvine, CA, USA. Department of Neurology, University of California, Irvine, CA, USA. Department of Epidemiology and Biostatistics, University of California, Irvine, CA, USA.
 Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA; Department of Urology, University of California, San Francisco, CA 94158, USA; Bakar Computational Health Sciences Institute, University of California, San Francisco, CA 94158, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. SVision LLC, Bellevue, WA 98006, USA. SVision LLC, Bellevue, WA 98006, USA. SVision LLC, Bellevue, WA 98006, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA; Department of Urology, University of California, San Francisco, CA 94158, USA; Bakar Computational Health Sciences Institute, University of California, San Francisco, CA 94158, USA. Department of Neurology, Loma Linda University, Loma Linda, CA 92350, USA. AcuraStem Incorporated, Monrovia, CA 91016, USA. Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA; Department of Urology, University of California, San Francisco, CA 94158, USA; Bakar Computational Health Sciences Institute, University of California, San Francisco, CA 94158, USA. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC, Los Angeles, CA 90033, USA; Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. Electronic address: ichida@usc.edu.
 Department of Rheumatology, Xiangya Hospital, Central South University, Changsha 410008, China. xieyanli@csu.edu.cn. Department of Rheumatology, Xiangya Hospital, Central South University, Changsha 410008, China. Department of Rheumatology, Xiangya Hospital, Central South University, Changsha 410008, China. Department of Rheumatology, Xiangya Hospital, Central South University, Changsha 410008, China. Department of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. Department of Rheumatology, Xiangya Hospital, Central South University, Changsha 410008, China. celialiu@csu.edu.cn.
 Neurodegeneration Pathobiology Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, St. Lucia, QLD, 4072, Australia. Neurodegeneration Pathobiology Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, St. Lucia, QLD, 4072, Australia. Neurodegeneration Pathobiology Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, St. Lucia, QLD, 4072, Australia. r.sangil@uq.edu.au. Neurodegeneration Pathobiology Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, St. Lucia, QLD, 4072, Australia. adam.walker@uq.edu.au.
 Department of Pediatrics, Kansai Medical University, 2-5-1 Shin-Machi, Hirakata-Shi, Osaka, 573-1010, Japan. Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. Department of Pediatrics, Kansai Medical University, 2-5-1 Shin-Machi, Hirakata-Shi, Osaka, 573-1010, Japan. Department of Pediatrics, Kansai Medical University, 2-5-1 Shin-Machi, Hirakata-Shi, Osaka, 573-1010, Japan. matsunor@hirakata.kmu.ac.jp. Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. Department of Pediatrics, Kansai Medical University, 2-5-1 Shin-Machi, Hirakata-Shi, Osaka, 573-1010, Japan. Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. mshimizu.ped@tmd.ac.jp.
 Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Medical Imaging, Anatomy, Preclinical Imaging Center (PRIME), Radboud Alzheimer Center, Donders Institute for Brain, Cognition, and Behavior, Radboud University Medical Center, Nijmegen, Netherlands. Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Department of Microbiology and Systems Biology, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands. Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Medical Imaging, Anatomy, Preclinical Imaging Center (PRIME), Radboud Alzheimer Center, Donders Institute for Brain, Cognition, and Behavior, Radboud University Medical Center, Nijmegen, Netherlands. Department of Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands. Laboratory of Experimental Neurology and Neuroimmunology and the Multiple Sclerosis Center, 2nd Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece. Department of Metabolic Health Research, Netherlands Organisation for Applied Scientific Research (TNO), Leiden, Netherlands.
 Family Medicine, Nassau University Medical Center, New York, USA. Internal Medicine, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, USA. Internal Medicine, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, USA. Family Medicine, Nassau University Medical Center, New York, USA.
 Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Universidade do Porto, 4050-313 Porto, Portugal. Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, 4200-135 Porto, Portugal. Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, 4200-135 Porto, Portugal.
 Muscular Dystrophy Association, Chicago, IL, USA. Muscular Dystrophy Association, Chicago, IL, USA. Muscular Dystrophy Association, Chicago, IL, USA. Muscular Dystrophy Association, Chicago, IL, USA. Muscular Dystrophy Association, Chicago, IL, USA. Kinevant Sciences, New York, NY, USA. Axogen, Alachua, FL, USA. Muscular Dystrophy Association, Chicago, IL, USA.
 School of Management, Chongqing University of Technology, Chongqing, China. Institute of Digital and Intelligent Management, Chongqing University of Technology, Chongqing, China. School of Management, Chongqing University of Technology, Chongqing, China. School of Management, Chongqing University of Technology, Chongqing, China. School of Economics and Business Administration, Chongqing University, Chongqing, China.
 Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. Department of Radiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. Department of Neurology, Peking University First Hospital, Beijing, China. Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
 Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China. School of Life Sciences, Tsinghua University, Beijing, China. School of Medicine, Tsinghua University, Beijing, China. IDG/McGovern Institute for Brain Research, Tsinghua University, Beijing, China. CAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia and Medica, Chinese Academy of Sciences, Shanghai, China. University of Chinese Academy of Sciences, Beijing, China. Department of Neurology, Peking University Third Hospital, Beijing, China. IDG/McGovern Institute for Brain Research, Tsinghua University, Beijing, China. School of Pharmaceutical Sciences, Tsinghua University, Beijing, China. Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China. School of Life Sciences, Tsinghua University, Beijing, China. School of Medicine, Tsinghua University, Beijing, China. IDG/McGovern Institute for Brain Research, Tsinghua University, Beijing, China. School of Medicine, Tsinghua University, Beijing, China. Tsinghua Laboratory of Brain and Intelligence, Beijing, China. CAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia and Medica, Chinese Academy of Sciences, Shanghai, China. School of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang, China. School of Medicine, Zhejiang University City College, Hangzhou, Zhejiang, China. School of Life Sciences, Tsinghua University, Beijing, China. School of Medicine, Tsinghua University, Beijing, China. Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China. IDG/McGovern Institute for Brain Research, Tsinghua University, Beijing, China. School of Pharmaceutical Sciences, Tsinghua University, Beijing, China. Department of Neurology, Peking University Third Hospital, Beijing, China. dsfan2010@aliyun.com. Beijing Municipal Key Laboratory of Biomarker and Translational Research in Neurodegenerative Diseases, Beijing, China. dsfan2010@aliyun.com. CAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia and Medica, Chinese Academy of Sciences, Shanghai, China. zbgao@simm.ac.cn. University of Chinese Academy of Sciences, Beijing, China. zbgao@simm.ac.cn. Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China. yichangjia@tsinghua.edu.cn. School of Medicine, Tsinghua University, Beijing, China. yichangjia@tsinghua.edu.cn. IDG/McGovern Institute for Brain Research, Tsinghua University, Beijing, China. yichangjia@tsinghua.edu.cn. Tsinghua Laboratory of Brain and Intelligence, Beijing, China. yichangjia@tsinghua.edu.cn.
 Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA. Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Center for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center, New York, NY, USA. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA. Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. rmathias@jhmi.edu.
 Department of Applied Statistics, Social Science, and Humanities, New York University, New York, New York, USA. Department of Applied Statistics, Social Science, and Humanities, New York University, New York, New York, USA. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada. Department of Clinical Psychology, Radboud University, Nijmegen, the Netherlands. Department of IQ Healthcare, Radboud University Medical Center, Nijmegen, the Netherlands. Department of Psychiatry, Radboud University Medical Center, Nijmegen, the Netherlands. Department of Medicine, McGill University, Montreal, Quebec, Canada. Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada. National Scleroderma Foundation, Los Angeles, California, USA. Sclérodermie Québec, Longueuil, Quebec, Canada. Johns Hopkins University School of Medicine, Division of Rheumatology, Baltimore, Maryland, USA. Department of Psychology, San Diego State University, San Diego, California, USA. San Diego State University/University of California, San Diego Joint Doctoral Program in Clinical Psychology, San Diego, California, USA. Scleroderma Atlantic, Halifax, Nova Scotia, Canada. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada. Department of Medicine, McGill University, Montreal, Quebec, Canada. Department of Psychiatry, McGill University, Montreal, Quebec, Canada. Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Quebec, Canada. Department of Psychology, McGill University, Montreal, Quebec, Canada. Biomedical Ethics Unit, McGill University, Montreal, Quebec, Canada.
 Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520. Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06511. Program in Applied Mathematics, Yale University, New Haven, CT 06511. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520. Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520. Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520. Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520. Department of Internal Medicine, Section of Rheumatology, Allergy and Immunology, Yale School of Medicine, New Haven, CT 06520. Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520. Department of Pathology, Yale University, New Haven, CT 06511. Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06511. Program in Applied Mathematics, Yale University, New Haven, CT 06511. Department of Pathology, Yale University, New Haven, CT 06511. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520. HHMI, Chevy Chase, MD 20815.
 Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Division of Rheumatology and Clinical Immunology, Department of Medicine, The University of Hong Kong, Hong Kong SAR, China. Department of Family Medicine and Primary Care, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. Department of Family Medicine and Primary Care, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. Department of Family Medicine and Primary Care, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Centre for Safe Medication Practice and Research, Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Laboratory of Data Discovery for Health (D4H), Hong Kong Science Park, Hong Kong SAR, China. Aston Pharmacy School, Aston University, Birmingham, B4 7ET, UK.
 Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. Department of Mechanical Engineering and Insigneo Institute for in Silico Medicine, The University of Sheffield, Sheffield, UK. Laboratory of Movement Analysis and Measurement, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Machine Learning and Data Analytics Lab, Department of Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. Laboratory of Movement Analysis and Measurement, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Machine Learning and Data Analytics Lab, Department of Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Department of Biomedical Sciences, University of Sassari, Sassari, Italy. Department of Electronics and Telecommunications, Politecnico di Torino, Turin, Italy. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. Laboratory of Movement Analysis and Measurement, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Robert Bosch Gesellschaft für Medizinische Forschung, Stuttgart, Germany. Department of Electronics and Telecommunications, Politecnico di Torino, Turin, Italy. The Newcastle Upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. Department of Mechanical Engineering and Insigneo Institute for in Silico Medicine, The University of Sheffield, Sheffield, UK. School of Computing, Newcastle University, Newcastle upon Tyne, UK. Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Catalonia, Spain. CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. Department of Electronics and Telecommunications, Politecnico di Torino, Turin, Italy. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland. Department of Electronics and Telecommunications, Politecnico di Torino, Turin, Italy. Department of Electrical, Electronic and Information Engineering «Guglielmo Marconi», University of Bologna, Bologna, Italy. Health Sciences and Technologies-Interdepartmental Center for Industrial Research (CIRI-SDV), University of Bologna, Bologna, Italy. Department of Electrical, Electronic and Information Engineering «Guglielmo Marconi», University of Bologna, Bologna, Italy. Machine Learning and Data Analytics Lab, Department of Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. School of Computing, Newcastle University, Newcastle upon Tyne, UK. Grünenthal GmbH, Aachen, Germany. Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Catalonia, Spain. CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. Department of Neurology, University Medical Center Schleswig-Holstein Campus Kiel, Kiel, Germany. Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Sagol School of Neuroscience and Department of Physical Therapy, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Rush Alzheimer's Disease Center and Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA. School of Computing, Newcastle University, Newcastle upon Tyne, UK. Department of Sport, Exercise and Rehabilitation, Northumbria University Newcastle, Newcastle upon Tyne, UK. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland. Machine Learning and Data Analytics Lab, Department of Artificial Intelligence in Biomedical Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Novartis Institutes of Biomedical Research, Novartis Pharma AG, Basel, Switzerland. Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Catalonia, Spain. CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. Department of Neurology, University Medical Center Schleswig-Holstein Campus Kiel, Kiel, Germany. Department of Sport, Exercise and Rehabilitation, Northumbria University Newcastle, Newcastle upon Tyne, UK. Novartis Institutes of Biomedical Research, Novartis Pharma AG, Basel, Switzerland. McRoberts BV, The Hague, Netherlands. Department of Electrical, Electronic and Information Engineering «Guglielmo Marconi», University of Bologna, Bologna, Italy. Health Sciences and Technologies-Interdepartmental Center for Industrial Research (CIRI-SDV), University of Bologna, Bologna, Italy. Robert Bosch Gesellschaft für Medizinische Forschung, Stuttgart, Germany. Department of Mechanical Engineering and Insigneo Institute for in Silico Medicine, The University of Sheffield, Sheffield, UK. Department of Neuroscience and Sheffield NIHR Translational Neuroscience BRC, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. Digital Health R&D, AstraZeneca, Stockholm, Sweden. Insight Centre for Data Analytics, University College Dublin, Dublin, Ireland. School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland. Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway. Department of Sport, Exercise and Rehabilitation, Northumbria University Newcastle, Newcastle upon Tyne, UK. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. The Newcastle Upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. The Newcastle Upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. Department of Mechanical Engineering and Insigneo Institute for in Silico Medicine, The University of Sheffield, Sheffield, UK. Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK. silvia.del-din@ncl.ac.uk. National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC), Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. silvia.del-din@ncl.ac.uk.
 From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). anna.francis11@yahoo.co.uk. From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.). From the Nuffield Department of Clinical Neurology (A.G.F., V.C., M.F.S., K.A., M.C., A.K.N.I., M.I.L., Lars Fugger, J.P.), Oxford University; The Walton Centre NHS Foundation Trust (K.E., C.R.)Neurology Unit (V.C.), Azienda Ospedaliero-Universitaria of Modena, Italy; Neurology (M.F.S.), Department of Neurosciences and Mental Health, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal; Neurological Clinic (C.R.), Marche Polytechnic University, Ancona, Italy; Department of Neurology (P.A.-S., B.A.), Royal Free London NHS Trust; Department of Neurology (A.B., L.E.), Brighton and Sussex University Hospitals NHS Foundation Trust; Royal Cornwall Hospitals NHS Trust (O.L.); Milton Keynes University Hospital (L.M.); East Kent Hospitals University Foundation Trust (I.R.); Department of Clinical Neurology (J.O.), University of Dundee; Imperial College London (A.S.); Centre of Neuroscience (A.S.), Department of Medicine, Charing Cross Hospital; Division of Clinical Neuroscience (R.T.), University of Nottingham, United Kingdom; Nottingham Centre for Multiple Sclerosis and Neuroinflammation (R.T.), Queen's Medical Centre, Nottingham University Hospitals NHS Trust; Frimley Health NHS Foundation Trust (D.W.); and University of Liverpool (S.H.).
 UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh, UK. Departments of Molecular Pharmacology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Hasselt, Belgium. University MS Centre, Hasselt University, Hasselt, Belgium. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Barlo Multiple Sclerosis Centre, St Michael's Hospital, Toronto, Ontario, Canada. Keenan Research Centre for Biomedical Science, St Michael's Hospital, Toronto, Ontario, Canada. Department of Immunology, The University of Toronto, Toronto, Ontario, Canada. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Wellcome Trust Centre for Cell Biology, King's Buildings, The University of Edinburgh, Edinburgh, UK. Biological and Veterinary Services, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Biological and Veterinary Services, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Department of Neuropathology and Neurocure Clinical Research Center, Charité-Universitätsmedizin Berlin, Berlin, Germany. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Institute of Neuropathology, Centre for Basics in NeuroModulation, Faculty of Medicine, University of Freiburg, Freiburg, Germany. Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Institute of Neuropathology, Centre for Basics in NeuroModulation, Faculty of Medicine, University of Freiburg, Freiburg, Germany. Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Department of Neuropathology and Neurocure Clinical Research Center, Charité-Universitätsmedizin Berlin, Berlin, Germany. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Hasselt, Belgium. University MS Centre, Hasselt University, Hasselt, Belgium. Centre for Inflammation Research, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Simons Initiative for the Developing Brain, Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, UK. Muir Maxwell Epilepsy Centre, University of Edinburgh, Edinburgh, UK. Departments of Molecular Pharmacology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh, UK. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Centre for Clinical Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Department of Psychiatry and Psychotherapy, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité-Universitätsmedizin Berlin and DZNE, Berlin, Germany. UK Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Veronique.Miron@unityhealth.to. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Veronique.Miron@unityhealth.to. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Veronique.Miron@unityhealth.to. Barlo Multiple Sclerosis Centre, St Michael's Hospital, Toronto, Ontario, Canada. Veronique.Miron@unityhealth.to. Keenan Research Centre for Biomedical Science, St Michael's Hospital, Toronto, Ontario, Canada. Veronique.Miron@unityhealth.to. Department of Immunology, The University of Toronto, Toronto, Ontario, Canada. Veronique.Miron@unityhealth.to.
 Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Department of Bioengineering, College of Engineering, California Institute for Quantitative Biosciences, University of California Berkeley, Berkeley, CA 94720, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Montreal, QC H3A 2B4, Canada. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Department of Neurology, Jamaica Plain Veterans Affairs Hospital, Harvard Medical School, Boston, MA 02130, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Department of Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuernberg, Erlangen, Germany. Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Neuroimmunology Research Lab, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, QC H2X 0A9, Canada. Type 1 Diabetes Immunology, Helmholtz Diabetes Center at Helmholtz Zentrum München, 80939 Munich, Germany. Deutsches Zentrum für Diabetesforschung, 85764 Munich-Neuherberg, Germany. Division of Clinical Pharmacology, Department of Medicine IV, Ludwig-Maximilians-Universität München, 80337 Munich, Germany. Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA. Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA. Institute of Neuropathology, University of Freiburg, D-79106 Freiburg, Germany. Signaling Research Centres BIOSS and CIBSS, University of Freiburg, D-79106 Freiburg, Germany. Center for Basics in NeuroModulation, Faculty of Medicine, University of Freiburg, D-79106 Freiburg, Germany. Department of Bioengineering and Therapeutic Sciences, University of California, San Francisco, California Institute for Quantitative Biosciences, San Francisco, CA 94158, USA. Chan Zuckerberg Biohub, San Francisco, CA, USA. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA. Neuroimmunology Unit, Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Montreal, QC H3A 2B4, Canada. Neuroimmunology Research Lab, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montreal, QC H2X 0A9, Canada. Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
 Department of Neuroscience, Brown University, Providence, RI 02912. InVivo Biosystems, Eugene, OR, 79402. InVivo Biosystems, Eugene, OR, 79402. Department of Neuroscience, Brown University, Providence, RI 02912.
 Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India. Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India. Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India. Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India. Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India. Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad, India. Division of Neuroscience and Ageing Biology, Division of Toxicology and Experimental Medicine, CSIR-Central Drug Research Institute, Lucknow, India. Infection Bioengineering Group, Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Indore, Simrol, India. Department of Biotechnology, Indian Institute of Technology Roorkee, Centre for Nanotechnology, Indian Institute of Technology Roorkee, Roorkee, Uttarakhand, India. Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India.
 Department of Oral Diagnosis and Radiology, School of Dentistry, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: zyfanti@dent.uoa.gr. Section of Oral Maxillofacial Radiology, UCLA School of Dentistry, Los Angeles, CA, USA. Electronic address: stetradis@dentistry.ucla.edu. Department of Oral Medicine & Pathology and Hospital Dentistry, School of Dentistry, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: nnikitakis@dent.uoa.gr. Department of Oral Diagnosis and Radiology, School of Dentistry, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: kalexiou@dent.uoa.gr. Department of Oral Diagnosis and Radiology, School of Dentistry, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: nkmakris@dent.uoa.gr. Department of Oral Diagnosis and Radiology, School of Dentistry, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: angelopoulosc@gmail.com. Department of Oral Diagnosis and Radiology, School of Dentistry, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: ktsiklak@dent.uoa.gr.
 Department of Molecular Imaging and Nuclear Medicine, Indraprastha Apollo Hospital, New Delhi, India. Department of Radiodiagnosis and Imaging, Indraprastha Apollo Hospitals, New Delhi, India. Department of Molecular Imaging and Nuclear Medicine, Indraprastha Apollo Hospital, New Delhi, India. Apollo Hospitals Education and Research Foundation, Indraprastha Apollo Hospitals, New Delhi, India. Department of Molecular Imaging and Nuclear Medicine, Indraprastha Apollo Hospital, New Delhi, India. Department of Orthopaedics and Joint Replacement Surgery, Indraprastha Apollo Hospitals, New Delhi, India. Department of Musculoskeletal Radiology, Royal Orthopedic Hospital, Birmingham, United Kingdom. Department of Orthopaedics and Joint Replacement Surgery, Indraprastha Apollo Hospitals, New Delhi, India.
 Pediatric Endocrinology and Diabetes, Marmara University School of Medicine, Istanbul, Turkey. Electronic address: serap.turan@marmara.edu.tr.

 Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224 TalanjeriGopalakrishna.Sahana@mayo.edu ke.zhang@szbl.ac.cn. Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224. Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224. Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205. Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224. Neuroscience Graduate Program, Mayo Clinic Graduate School of Biomedical Sciences, Jacksonville, Florida 32224. Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224 TalanjeriGopalakrishna.Sahana@mayo.edu ke.zhang@szbl.ac.cn. Neuroscience Graduate Program, Mayo Clinic Graduate School of Biomedical Sciences, Jacksonville, Florida 32224. Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Gaoke Innovation Centre A16, Guangqiao Rd, Shenzhen, Guangdong 518107, China, P.R.
 INRAE, AgroParisTech, Micalis Institute, Université Paris-Saclay, 78350, Jouy-en-Josas, France. sanyadaniel86@yahoo.com. Institute of Molecular Bioimaging and Physiology, National Research Council (IBFM-CNR), Segrate, 20131, Milan, Italy. INRAE, AgroParisTech, Micalis Institute, Université Paris-Saclay, 78350, Jouy-en-Josas, France.
 Berry Consultants, Austin, Texas, USA. Berry Consultants, Austin, Texas, USA. Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Berry Consultants, Austin, Texas, USA. Berry Consultants, Austin, Texas, USA. Biostatistics Center, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA. Department of Neurology, Barrow Neurological Institute, Phoenix, Arizona, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Neurological Institute of New York, Columbia University, New York, New York, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Sean M. Healey & AMG Center for ALS at Mass General, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA. Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Boston, Massachusetts, USA. Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA. Department of Neurology, Barrow Neurological Institute, Phoenix, Arizona, USA.
 The Johns Hopkins Children's Center, Baltimore, MD, United States of America. Electronic address: amleonar@jhmi.edu. The University of Alabama at Birmingham, Birmingham, Alabama, United States of America. University of Kansas Medical Center, Kansas City, Kansas United States of America. University of Michigan Medical School, Ann Arbor, Michigan, United States of America. Northwestern Medicine, Feinberg School of Medicine, Chicago, Illinois, United States of America. Children's Hospital Colorado, Aurora, Colorado, United States of America. Community Advisor to the Cystic Fibrosis Foundation, Bethesda, Maryland, United States of America. Division of Endocrinology, Metabolism and Lipid Research. Washington University School of Medicine. St. Louis, MO, United States of America. Nationwide Children's Hospital, Columbus Ohio, United States of America. Albany Medical Center, Albany, New York, United States of America. Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America. UH Rainbow Babies & Children's Hospital, Cleveland, Ohio, United States of America. Cystic Fibrosis Foundation, Bethesda, Maryland United States of America. Cystic Fibrosis Foundation, Bethesda, Maryland United States of America. Cystic Fibrosis Foundation, Bethesda, Maryland United States of America. Columbia University Irving Medical Center, New York, New York, United States of America.
 Government, Health & Not-for-Profit Division, Center for Research On Health and Social Care Management, SDA Bocconi School of Management, Health Economics & HTA, MEO Building, Room W210, II Floor, Via Sarfatti 10, 20136, Milan, Italy. oriana.ciani@unibocconi.it. Government, Health & Not-for-Profit Division, Center for Research On Health and Social Care Management, SDA Bocconi School of Management, Health Economics & HTA, MEO Building, Room W210, II Floor, Via Sarfatti 10, 20136, Milan, Italy. Italian Multiple Sclerosis (AISM) Society, Genoa, Italy. Associazione Italiana Sclerosi Multipla (AISM) Rehabilitation Center, Genoa, Italy. Department of Human Neurosciences, Sapienza, University of Rome, Rome, Italy. IRCCS Neuromed, Pozzilli, Italy. Italian Society of Neurology (SIN), Siena, Italy. Italian Society of Neurology (SIN), Siena, Italy. Department of Neurosciences, S. Camillo Forlanini Hospital, Rome, Italy. NeMO Clinical Center, Neurorehabilitation Unit, University of Milan, Milan, Italy.
 Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2H7, Canada. Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2E1, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2H7, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2H7, Canada. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2H7, Canada. voronova@ualberta.ca. Neuroscience and Mental Health Institute, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2E1, Canada. voronova@ualberta.ca. Women and Children's Health Research Institute5-083 Edmonton Clinic Health Academy, University of Alberta, 11405 87 Avenue NW, Edmonton, Alberta, T6G 1C9, Canada. voronova@ualberta.ca. Department of Cell Biology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2H7, Canada. voronova@ualberta.ca. Multiple Sclerosis Centre, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, T6G 2H7, Canada. voronova@ualberta.ca.
 Department of Neurology, Research Institute and Hospital of National Cancer Center, 323 Ilsan-Ro, Ilsandong-gu, Goyang, Korea. jacksy12@naver.com. Department of Neurology, Research Institute and Hospital of National Cancer Center, 323 Ilsan-Ro, Ilsandong-gu, Goyang, Korea. Department of Neurology, Research Institute and Hospital of National Cancer Center, 323 Ilsan-Ro, Ilsandong-gu, Goyang, Korea. Department of Neurology, Research Institute and Hospital of National Cancer Center, 323 Ilsan-Ro, Ilsandong-gu, Goyang, Korea.
 Department of Translational Medicine and LTTA Centre, University of Ferrara, 44121 Ferrara, Italy. Interdepartmental Research Center for the Study of Multiple Sclerosis and Inflammatory and Degenerative Diseases of the Nervous System, University of Ferrara, 44121 Ferrara, Italy. Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy. Department of Translational Medicine and LTTA Centre, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy. Bio@SNS Laboratory of Biology, Scuola Normale Superiore, 56126 Pisa, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, 44121 Ferrara, Italy.
 Cellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, Iran. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences (TUMS), Tehran, Iran. Research Institute for Oncology, Hematology and Cell Therapy, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran. Dipartimento di Oncologia ed Emato-Oncologia, Università Degli Studi Di Milano, Via Festa del Perdono, Milano, Italy. Laboratory of Translatonal Neurosciences, European School of Molecular Medicine, CEINGE Biotecnologie Avanzate S.c.a.rl.Via Gaetano Salvatore, Naples, Italy. Cellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, Iran. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Stem cell and Regenerative Medicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Tissue Engineering and Applied Cell Sciences Division, Department of Anatomical Sciences, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Cellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, Iran. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran.
 Nerve-Muscle Unit, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Multiple Sclerosis Centre and Research Centre for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Nerve-Muscle Unit, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Nerve-Muscle Unit, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Nerve-Muscle Unit, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Center for Primary Care and Public Health (Unisanté), University of Lausanne, Lausanne, Switzerland. Multiple Sclerosis Centre and Research Centre for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre and Research Centre for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Nerve-Muscle Unit, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
 UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. Wellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. MRC Centre for Reproductive Health, the University of Edinburgh, Edinburgh EH16 4TJ, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. MRC Centre for Reproductive Health, the University of Edinburgh, Edinburgh EH16 4TJ, UK; The Roslin Institute, the Royal (Dick) School of Veterinary Studies, the University of Edinburgh, Edinburgh EH25 9RG, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. Department of Clinical Neurosciences, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK. Department of Clinical Neurosciences, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK. Centre for Clinical Brain Sciences, the University of Edinburgh, Edinburgh EH16 4SB, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; MRC Centre for Reproductive Health, the University of Edinburgh, Edinburgh EH16 4TJ, UK; Barlo Multiple Sclerosis Centre at St. Michael's Hospital, Keenan Research Centre for Biomedical Science, Toronto, ON M5B 1T8, Canada. Wellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. Division of Systems Medicine, School of Medicine, University of Dundee, Dundee DD1 9SY, UK. Department of Clinical Neurosciences, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK; Centre for Clinical Brain Sciences, the University of Edinburgh, Edinburgh EH16 4SB, UK. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. Electronic address: barry.mccoll@ed.ac.uk. UK Dementia Research Institute, the University of Edinburgh, Edinburgh EH8 9JZ, UK; Centre for Discovery Brain Sciences, the University of Edinburgh, Edinburgh EH8 9JZ, UK. Electronic address: tara.spires-jones@ed.ac.uk.
 Charité - Universitätsmedizin Berlin, Department of Psychiatry and Neurosciences, Campus Benjamin Franklin, Berlin, Germany. Electronic address: woo-ri.chae@charite.de. Robert-Koch Institute, Department of Epidemiology and Health Monitoring, Berlin, Germany. Robert-Koch Institute, Department of Epidemiology and Health Monitoring, Berlin, Germany. Charité - Universitätsmedizin Berlin, Department of Psychiatry and Neurosciences, Campus Benjamin Franklin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Department of Psychiatry and Neurosciences, Campus Benjamin Franklin, Berlin, Germany; Charité - Universitätsmedizin Berlin, Medical Department, Section Psychosomatic Medicine, Hindenburgdamm 30, 12203 Berlin, Germany; Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Robert-Koch Institute, Department of Epidemiology and Health Monitoring, Berlin, Germany. Charité - Universitätsmedizin Berlin, Department of Psychiatry and Neurosciences, Campus Benjamin Franklin, Berlin, Germany.
 Department of Psychosomatic Medicine and Psychotherapy, University Medical Centre Göttingen, and German Centre for Cardiovascular Research (DZHK), Partner Site Göttingen, Göttingen, Germany. Department of Psychosomatic Medicine and Psychotherapy, University Medical Centre Göttingen, and German Centre for Cardiovascular Research (DZHK), Partner Site Göttingen, Göttingen, Germany. Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany. Department of Psychosomatic Medicine and Psychotherapy, University Medical Centre Göttingen, and German Centre for Cardiovascular Research (DZHK), Partner Site Göttingen, Göttingen, Germany. Department of Psychosomatic Medicine and Psychotherapy, University Medical Centre Göttingen, and German Centre for Cardiovascular Research (DZHK), Partner Site Göttingen, Göttingen, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Centre Göttingen, Göttingen, Germany. Department of Psychiatry and Psychotherapy, University Medical Centre Göttingen, Göttingen, Germany. Division of Infections, Immunity and Microbes, School of Life Sciences, University of Nottingham, Nottingham, United Kingdom. British Heart Foundation Centre, School of Cardiovascular and Metabolic Medicine and Sciences, King's College London, London, United Kingdom. Department of Psychosomatic Medicine and Psychotherapy, University Medical Centre Göttingen, and German Centre for Cardiovascular Research (DZHK), Partner Site Göttingen, Göttingen, Germany.
 School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. School of Medicine, Institute of Medical Genetics and Applied Genomics, Eberhard Karls University, Universitaetsklinikum Tuebingen, Tuebingen, Germany. School of Medicine, Klinikum rechts der Isar, Department of Cardiology, Technical University of Munich, Munich, Germany. School of Medicine, Klinikum rechts der Isar, Technical University of Munich, Institute of Human Genetics, Munich, Germany. School of Medicine, Institute of Medical Genetics and Applied Genomics, Eberhard Karls University, Universitaetsklinikum Tuebingen, Tuebingen, Germany. School of Medicine, Centre for Rare Diseases, Eberhard Karls University, Universitaetsklinikum Tuebingen, Tuebingen, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. Munich Cluster for Systems Neurology, (SyNergy), Munich, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. School of Medicine, Klinikum rechts der Isar, Department of Neurology, Technical University of Munich, Ismaningerstr. 22, 81675, Munich, Germany. marcus.deschauer@tum.de.
 Department of Economics, Laboratory for Social and Neural Systems Research, University of Zurich, Zurich 8006, Switzerland. Department of Economics, Zurich Center for Neuroeconomics, University of Zurich, Zurich 8006, Switzerland. Department of Economics, Laboratory for Social and Neural Systems Research, University of Zurich, Zurich 8006, Switzerland. Department of Economics, Zurich Center for Neuroeconomics, University of Zurich, Zurich 8006, Switzerland. Department of Economics, Laboratory for Social and Neural Systems Research, University of Zurich, Zurich 8006, Switzerland. Department of Economics, Zurich Center for Neuroeconomics, University of Zurich, Zurich 8006, Switzerland. Experimental and Clinical Pharmacopsychology, Department of Psychiatry, Psychotherapy and Psychosomatics, Psychiatric University Hospital Zurich, University of Zurich, Zurich 8008, Switzerland. Neuroscience Center Zurich, ETH Zurich and University of Zurich, Zurich 8057, Switzerland. Department of Neurology, Section of Neuroimmunology and Multiple Sclerosis Research, University Hospital Zurich, Zurich 8091, Switzerland. National Poisons Information Centre, Tox Info Suisse, Associated Institute of the University of Zurich, Zurich 8032, Switzerland. Department of Economics, Laboratory for Social and Neural Systems Research, University of Zurich, Zurich 8006, Switzerland. Department of Economics, Zurich Center for Neuroeconomics, University of Zurich, Zurich 8006, Switzerland. Neuroscience Center Zurich, ETH Zurich and University of Zurich, Zurich 8057, Switzerland.
 Neurology Service, Headache Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Service, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Service, Headache Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Service, Headache Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Department, Hospital de Viladecans-IDIBELL, Viladecans, Barcelona, Spain. Neurology Service, Neurophysiology Department, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Service, Headache Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Service, Multiple Sclerosis Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Service, Headache Unit, Hospital Universitari de Bellvitge-IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain. Neurology Department, Hospital de Viladecans-IDIBELL, Viladecans, Barcelona, Spain.
 Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, Cagliari, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Department of Medical Science and Public Health, University of Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ATS Sardegna, ASSL Cagliari, Cagliari, Italy. Multiple Sclerosis Center, Binaghi Hospital, ATS Sardegna, ASSL Cagliari, Cagliari, Italy. Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, Cagliari, Italy. Intensive Care Unit, "San Francesco" Hospital, Nuoro, Italy. Intensive Care Unit, "San Francesco" Hospital, Nuoro, Italy. Intensive Care Unit, "San Francesco" Hospital, Nuoro, Italy. , Amman, Jordan. Nephrology, Dialysis and Transplantation, University of Cagliari, Cagliari, Italy. Nephrology, Dialysis and Transplantation, University of Cagliari, Cagliari, Italy. Department of Biomedical Sciences, Oncology and Molecular Pathology Unit, University of Cagliari, Cagliari, Italy. Department of Surgical Sciences, University of Cagliari, Cagliari, Italy. Department of Cellular, Computational and Integrative Biology, Center of Medical Sciences (CISMed), University of Trento, Trento, Italy. Clinical-Chemical Analysis and Microbiology Laboratory, "San Francesco" Hospital, Nuoro, Italy. Department of Biomedical Sciences, Clinical Metabolomics Unit, University of Cagliari, Strada Interna Policlinico Universitario, 09042, Monserrato, CA, Italy. latzori@unica.it.
 Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy. jessica.mandrioli@unimore.it. Department of Neurosciences, St. Agostino-Estense Hospital, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. jessica.mandrioli@unimore.it. Unit of Statistical and Methodological Support to Clinical Research, Azienda Ospedaliero-Universitaria, Modena, Italy. Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy. Department of Neurosciences, St. Agostino-Estense Hospital, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. Neurosciences PhD Program, University of Modena and Reggio Emilia, Modena, Italy. Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy. Unit of Statistical and Methodological Support to Clinical Research, Azienda Ospedaliero-Universitaria, Modena, Italy. Department of Neurosciences, St. Agostino-Estense Hospital, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. Clinical and Experimental Medicine PhD Program, University of Modena and Reggio Emilia, Modena, Italy. Department of Neurosciences, St. Agostino-Estense Hospital, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy. Unit of Statistical and Methodological Support to Clinical Research, Azienda Ospedaliero-Universitaria, Modena, Italy. Department of Neurosciences, St. Agostino-Estense Hospital, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy. Department of Neurosciences, St. Agostino-Estense Hospital, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy. Department of Life Sciences, University of Modena and Reggio Emilia, 41125, Modena, Italy. NEuroMuscular Omnicenter, Serena Onlus Foundation, Milan, Italy. Istituto Maugeri IRCCS Milano, Milan, Italy. NEuroMuscular Omnicenter, Serena Onlus Foundation, Milan, Italy. NEuroMuscular Omnicenter, Serena Onlus Foundation, Milan, Italy. ALS Centre, Neurologic Clinic, Maggiore della Carità University Hospital, Novara, Italy. ALS Centre, Neurologic Clinic, Maggiore della Carità University Hospital, Novara, Italy. ALS Centre, Neurologic Clinic, Maggiore della Carità University Hospital, Novara, Italy. Department of Neurosciences, University of Padua, Padua, Italy. Centro Regionale Specializzato Malattie del Motoneurone, Azienda Ospedale Università di Padova, Padua, Italy. Department of Neurosciences, University of Padua, Padua, Italy. 3rd Neurology Unit and ALS Centre, IRCCS 'Carlo Besta' Neurological Institute, Milan, Italy. 3rd Neurology Unit and ALS Centre, IRCCS 'Carlo Besta' Neurological Institute, Milan, Italy. Department of Neurosciences, Rehabilitatioņ Ophthalmology, Genetics, Mother and Child Disease, Ospedale Policlinico San Martino, Genova, Italy. Department of Neurosciences, Rehabilitatioņ Ophthalmology, Genetics, Mother and Child Disease, Ospedale Policlinico San Martino, Genova, Italy. 'Rita Levi Montalcini' Department of Neurosciences, ALS Centre, University of Turin and Azienda Ospedaliero Universitaria Città della Salute e della Scienza, Turin, Italy. 'Rita Levi Montalcini' Department of Neurosciences, ALS Centre, University of Turin and Azienda Ospedaliero Universitaria Città della Salute e della Scienza, Turin, Italy. Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy. National Institute for Cardiovascular Research, via Irnerio 48, 40126, Bologna, Italy.
 Division of Experimental Medicine, McGill University, Montréal, Québec, Canada. Montréal Neurological Institute-Hospital, McGill University Health Centre, McGill University, Montréal, Québec, Canada. Montréal Neurological Institute-Hospital, McGill University Health Centre, McGill University, Montréal, Québec, Canada. Department of Respirology and Thoracic Surgery, University Institute of Cardiology and Respirology of Quebec, University of Laval, Québec, Québec, Canada. Translational Research in Respiratory Diseases Program, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada. Montréal Neurological Institute-Hospital, McGill University Health Centre, McGill University, Montréal, Québec, Canada. Translational Research in Respiratory Diseases Program, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada; Respiratory Division, Sleep Laboratory, McGill University Health Centre, Montréal, Québec, Canada. Translational Research in Respiratory Diseases Program, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada; Respiratory Division, Sleep Laboratory, McGill University Health Centre, Montréal, Québec, Canada. Electronic address: marta.kaminska@mcgill.ca.
 Department of Translantation/Hepatobiliary, The First Hospital of China Medical University, Shenyang, China. Department of Neurosurgery, The First Hospital of China Medical University, Shenyang, China. Department of Ophthalmology, The First Hospital of China Medical University, Shenyang, China. Department of Otorhinolaryngology, The First Hospital of China Medical University, Shenyang, China. Department of Cardiac Surgery, The First Hospital of China Medical University, Shenyang, China. Electronic address: bliu17@cmu.edu.cn. Department of Interventional Radiology, The First Hospital of China Medical University, Shenyang, China. Electronic address: xiayonghui@cmu.edu.cn.

 Laboratory for Molecular Immunology, Department of Biotechnology, University of Rijeka, R. Matejcic 2, 51000 Rijeka, Croatia. Laboratory for Molecular Immunology, Department of Biotechnology, University of Rijeka, R. Matejcic 2, 51000 Rijeka, Croatia. Laboratory for Molecular Immunology, Department of Biotechnology, University of Rijeka, R. Matejcic 2, 51000 Rijeka, Croatia. Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 9RT, UK. Laboratory for Molecular Immunology, Department of Biotechnology, University of Rijeka, R. Matejcic 2, 51000 Rijeka, Croatia. Laboratory for Molecular Immunology, Department of Biotechnology, University of Rijeka, R. Matejcic 2, 51000 Rijeka, Croatia.
 Occidental College, Los Angeles, CA, USA.
 Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, , EC-10 Cleveland Clinic, 9501 Euclid Avenue, Cleveland, OH 44195, USA. Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, , EC-10 Cleveland Clinic, 9501 Euclid Avenue, Cleveland, OH 44195, USA; Kaufman Center for Heart Failure Treatment and Recovery, Heart Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: tangw@ccf.org.
 Department of Pharmacology and Department of Pharmacy of the Second Affiliated Hospital, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University School of Medicine, Hangzhou, China. Department of Pharmacology and Department of Pharmacy of the Second Affiliated Hospital, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University School of Medicine, Hangzhou, China. Key Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China. Department of Pharmacology and Department of Pharmacy of the Second Affiliated Hospital, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University School of Medicine, Hangzhou, China.
 Department of Pharmacy, Wuhan Mental Health Center, Wuhan, China; Department of Pharmacy, Wuhan Hospital for Psychotherapy, Wuhan, China. Tongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Foundational Sciences, Central Michigan University College of Medicine, Mount Pleasant, MI, USA. Department of Pharmacy, The Third Hospital of Wuhan, Tongren Hospital of Wuhan University, Wuhan, China. Electronic address: 2014103060001@whu.edu.cn. Tongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: kunhuang@hust.edu.cn.
 Department of Primary Care Medicine, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia. Department of Primary Care Medicine, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia. Department of Primary Care Medicine, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia. Department of Radiology, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia. Department of Orthopaedic and Traumatology, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia. Department of Primary Care Medicine, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia. Institute of Pathology, Laboratory and Forensic Medicine (I-PPerForM), Universiti Teknologi MARA, Jalan Hospital, Sungai Buloh, Selangor, Malaysia.
 Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, University of New Mexico, Albuquerque, NM, 87131-0001, USA. Department of Neurosurgery, Thomas Jefferson University, 909 Walnut Street, 2nd Floor, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA. Department of Neurosurgery, Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, 909 Walnut St, Philadelphia, PA, 19107, USA.
 Department of Biology, School of Sciences and Humanities, Nazarbayev University, Astana 010000, Kazakhstan. Department of Biology, School of Sciences and Humanities, Nazarbayev University, Astana 010000, Kazakhstan. Center for Life Sciences, National Laboratory Astana, Nazarbayev University, Astana 010000, Kazakhstan. Department of Pediatric Surgery, Children's Hospital, Inselspital Bern, University of Bern, 3010 Bern, Switzerland. Department of Biology, School of Sciences and Humanities, Nazarbayev University, Astana 010000, Kazakhstan. The Environment & Resource Efficiency Cluster (EREC), Nazarbayev University, Astana 010000, Kazakhstan.
 College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA. College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA. Department of Dermatology, University of Arkansas for Medical Sciences, 4301 W. Markham St., Slot #576, Little Rock, AR, 72205, USA. HKWong@uams.edu.
 Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, University College London, London, UK and. UCL Queen Square Motor Neuron Disease Centre, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, University College London, London, UK and. UCL Queen Square Motor Neuron Disease Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
 Functional Genomics Laboratory, Department of Microbiology, School of Life Sciences, Central University of Tamil Nadu, Thiruvarur 610005, Tamil Nadu, India. Apoptosis and Cell Survival Research Laboratory, 412G Pearl Research Park, School of Biosciences and Technology, Vellore Institute of Technology, Vellore 632014, Tamil Nadu, India. Electronic address: priti.t@vit.ac.in. Functional Genomics Laboratory, Department of Microbiology, School of Life Sciences, Central University of Tamil Nadu, Thiruvarur 610005, Tamil Nadu, India. Electronic address: ravanan@cutn.ac.in.
 Department of Dermatology, Medical Center-University of Freiburg, Freiburg, Germany.
 Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France. Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France. Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France. Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France. Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France. Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France. Department of Medical Statistics and Epidemiology, Centre Hospitalier Universitaire Montpellier, University of Montpellier, 34090 Montpellier, France. Department of Medical Statistics and Epidemiology, Centre Hospitalier Universitaire Montpellier, University of Montpellier, 34090 Montpellier, France. Department of Radiology, CHU of Montpellier, Arnaud de Villeneuve Hospital, 34090 Montpellier, France.
 Molecular Modeling and Simulation (MMS) Team, Institute for Quantum Life Science, National Institutes for Quantum Science and Technology (QST), 4-9-1, Anagawa, Inage Ward, Chiba City, Chiba, 263-8555, Japan. Toulouse Biotechnology Institute, TBI, Université de Toulouse, CNRS, INRAE, INSA, 135, Avenue de Rangueil, 31077, Toulouse Cedex 04, France. Molecular Modeling and Simulation (MMS) Team, Institute for Quantum Life Science, National Institutes for Quantum Science and Technology (QST), 4-9-1, Anagawa, Inage Ward, Chiba City, Chiba, 263-8555, Japan. Molecular Modeling and Simulation (MMS) Team, Institute for Quantum Life Science, National Institutes for Quantum Science and Technology (QST), 4-9-1, Anagawa, Inage Ward, Chiba City, Chiba, 263-8555, Japan. kono.hidetoshi@qst.go.jp.

 Department of Respiratory Medicine and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, People's Republic of China. Department of Respiratory Medicine and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, People's Republic of China. Department of Respiratory Medicine and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, People's Republic of China. Department of Intensive Care Medicine, Chengdu Second People's Hospital, ChengDu City, Sichuan Province, 610000, People's Republic of China. Department of Respiratory Medicine, Chengdu Second People's Hospital, ChengDu City, Sichuan Province, 610000, People's Republic of China. Department of Respiratory Medicine, Chengdu Second People's Hospital, ChengDu City, Sichuan Province, 610000, People's Republic of China.
 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 2Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 3Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL 60612, USA. 4Research Center for Human Tissues and Organs Degeneration, Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China. 1Department of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.
 Department of Physiology, Midnapore College, Midnapore, West Bengal, India. Department of Biological Sciences, New York City College of Technology/CUNY, Brooklyn, New York, USA. Department of Biology, College of Arts and Sciences, Adelphi University, Garden City, New York, USA. Department of Psychology, Gordon F. Derner School of Psychology, Adelphi University, Garden City, New York, USA.
 Dr Phillip Frost Department of Dermatology, University of Miami, Miami, Florida, USA. Dr Phillip Frost Department of Dermatology, University of Miami, Miami, Florida, USA. Dr Phillip Frost Department of Dermatology, University of Miami, Miami, Florida, USA. Dr Phillip Frost Department of Dermatology, University of Miami, Miami, Florida, USA. Dr Phillip Frost Department of Dermatology, University of Miami, Miami, Florida, USA. Dr Phillip Frost Department of Dermatology, University of Miami, Miami, Florida, USA.

 ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, 10126 Turin, Italy. SC Neurologia 1U, Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, 10126 Turin, Italy. Institute of Cognitive Sciences and Technologies, National Research Council, 00185 Rome, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, 10126 Turin, Italy. SC Neurologia 1U, Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, 10126 Turin, Italy. Neuroscience Institute of Turin (NIT), Regione Gonzole 10, 10043 Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, 10126 Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, 10126 Turin, Italy. SC Neurologia 1U, Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, 10126 Turin, Italy. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, 10126 Turin, Italy. SC Genetica Medica U, Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, 10126 Turin, Italy. Department of Neurology, Azienda Ospedaliero-Universitaria di Cagliari and University of Cagliari, 09123 Cagliari, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal, and Child Health, University of Genoa, 16132 Genoa, Italy. IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy. Department of Advanced Medical and Surgical Sciences, MRI Research Center SUN-FISM, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. ALS Clinical Research Centre, Department of Biomedicine, Neurosciences and Advanced Diagnostics, University of Palermo, 90129 Palermo, Italy. Intensive Neurorehabilitation Unit, ALS Centre, IRCCS Istituti Clinici Scientifici Maugeri, 98073 Mistretta, Italy. Neurological ALS Tertiary Centre, Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari, 70124 Bari, Italy. "Il Bene" Centre for Immunological and Rare Neurological Diseases at Bellaria Hospital, IRCCS, Istituto Delle Scienze Neurologiche, 40125 Bologna, Italy. Azienda Ospedaliera Ospedali Riuniti Marche Nord, Presidio di Fano, UOC Neurologia, 61032 Fano, Italy. Fondazione IRCCS Istituto Neurologico Carlo Besta, SC Neurologia 3-Neuroalgologia, 20133 Milano, Italy. Neurology Unit, ALS Clinic, San Gerardo Hospital and University of Milano-Bicocca, 20900 Monza, Italy. Department of Medical, Surgical and Neurological Sciences, University of Siena, 53100 Siena, Italy. Neurology Unit, Department of Neuroscience, S. Agostino Estense Hospital, Azienda Ospedaliero Universitaria di Modena, 41125 Modena, Italy. Centre for Neuroscience and Neurotechnology (CfNN), Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41124 Modena, Italy. Division of Neurology, Department of Neurosciences, Santa Chiara Hospital, 38122 Trento, Italy. Department of Medical Sciences, Multiple Sclerosis Centre, University of Cagliari, 09123 Cagliari, Italy. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal, and Child Health, University of Genoa, 16132 Genoa, Italy. IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy. Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy. Institute of Genomic Medicine, Catholic University School of Medicine, 00168 Rome, Italy. Medical Genetics, Policlinico A. Gemelli Foundation, IRCCS, 00168 Rome, Italy. Department of Geriatrics, Neurosciences and Orthopedics, Clinic Center NEMO-Roma, Institute of Neurology, Catholic University School of Medicine, 00168 Rome, Italy. Neurology, Policlinico A. Gemelli Foundation, IRCCS, 00168 Rome, Italy. Neuromuscular Omnicentre (NEMO)-Fondazione Serena Onlus, 20162 Milan, Italy. Istituti Clinici Scientifici Maugeri, IRCCS, 20138 Milan, Italy. ALS Centre, Department of Neurology, Azienda Ospedaliera Universitaria Maggiore della Carità, 28100 Novara, Italy. Department of Health Sciences, Interdisciplinary Research Center of Autoimmune Diseases, School of Medicine, University of Eastern Piedmont Amedeo Avogadro, 28100 Novara, Italy. CRCSLA et Maladie du Neurone Moteur, Service de Neurologie, CHU de Clermont-Ferrand Clermont-Ferrand CEDEX 9 and UMR1107, Neurodol, UCA, 63000 Clermont-Ferrand, France. Hôpital des Peupliers, Ramsay Générale de Santé, 75013 Paris, France. CRCSLA et Maladie du Neurone Moteur, Service de Neurologie, CHU de Clermont-Ferrand Clermont-Ferrand CEDEX 9 and UMR1107, Neurodol, UCA, 63000 Clermont-Ferrand, France. Centre de Référence SLA, CHU and Université de Montpellier, 34295 Montpellier, France. ALS Centre, "Rita Levi Montalcini" Department of Neuroscience, University of Turin, 10126 Turin, Italy. SC Neurologia 1U, Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino, 10126 Turin, Italy. Institute of Cognitive Sciences and Technologies, National Research Council, 00185 Rome, Italy. Neuroscience Institute of Turin (NIT), Regione Gonzole 10, 10043 Turin, Italy.
 Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Department of Neurology, University of Rochester Medical Center, Rochester, NY, USA. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Department of Neurology, University of Rochester Medical Center, Rochester, NY, USA. Radboud University Medical Centre; Donders Institute for Brain, Cognition and Behaviour; Department of Neurology; Centre of Expertise for Parkinson & Movement Disorders; Nijmegen, the Netherlands. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Department of Neurology, University of Rochester Medical Center, Rochester, NY, USA. Center for Health + Technology, University of Rochester Medical Center, Rochester, NY, USA. Department of Neurology, University of Rochester Medical Center, Rochester, NY, USA. Weill Institute for Neurosciences, Department of Neurology, University of California-San Francisco, San Francisco, CA, USA. Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, USA. Division of Occupational and Environmental Medicine, San Francisco Veterans Affairs Health Care System, School of Medicine, University of California-San Francisco, San Francisco, CA, USA. Radboud University Medical Centre; Donders Institute for Brain, Cognition and Behaviour; Department of Neurology; Centre of Expertise for Parkinson & Movement Disorders; Nijmegen, the Netherlands.
 Evidence-based Medicine, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany. Electronic address: mariusgoldkuhle@uk-koeln.de. Department of Health Research Methods, Evidence, and Impact, Michael G DeGroote Cochrane Canada Centre, Cochrane Canada, McMaster GRADE Centre and Department of Medicine, McMaster University, 1280 Main St. W., Hamilton, ON L8S 4K1, Canada. Evidence-based Medicine, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany. Department of Internal Medicine, American University of Beirut, Lebanon, P.O.Box 11-0236 and Department of Health Research Methods, Evidence, and Impact, McMaster University, 1280 Main St. W., Hamilton, ON L8S 4K1, Canada. Minneapolis VA Health Care System, Urology Section 112D, One Veterans Drive, Minneapolis, Minnesota 55417. Princess Máxima Center for Pediatric Oncology, Heidelberglaan 25, 3584CS Utrecht, the Netherlands. Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland; Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB), University Hospital Basel and University of Basel, Basel, Switzerland; Meta-Research Innovation Center at Stanford (METRICS), Stanford University, Stanford, CA, USA; Meta-Research Innovation Center Berlin (METRIC-B), Berlin Institute of Health, Berlin, Germany. Czech National Centre for Evidence-Based Healthcare and Knowledge Translation (Cochrane Czech Republic, Czech EBHC: JBI Centre of Excellence, Masaryk University GRADE Centre), Faculty of Medicine, Masaryk University, 625 00 Brno, Czech Republic; Institute of Health Information and Statistics of the Czech Republic, 100 00 Prague, Czech Republic. Department of Medicine and Population Health, University of Kansas Health System, 3901 Rainbow Blvd, MS3002, Kansas City, KS 66160, USA; Department of Health Research Methods, Evidence, and Impact, McMaster University, 1280 Main St. W., Hamilton, Ontario L8S 4K1, Canada. IRCCS Istituto delle Scienze Neurologiche di Bologna, Unit of Epidemiology and Statistics, Cochrane Review Group Multiple Sclerosis and Rare Diseases of the CNS, Via Altura 3, 40139 Bologna, Italy. Department of Health Research Methods, Evidence, and Impact, Michael G DeGroote Cochrane Canada Centre, Cochrane Canada and McMaster GRADE Centre, McMaster University, Hamilton, Ontario, Canada; Department of Medicine, McMaster University, Hamilton, Ontario, Canada; Department of Biomedical Sciences, Humanitas University, Milan, Italy; Cochrane Canada, Hamilton, Ontario, Canada. Department of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, UK; Department of Population Health, London School of Hygiene and Tropical Medicine, London. Evidence-based Medicine, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany.
 The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast Faculty of Medicine Health and Life Sciences, Belfast, UK. The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast Faculty of Medicine Health and Life Sciences, Belfast, UK. The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast Faculty of Medicine Health and Life Sciences, Belfast, UK. The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast Faculty of Medicine Health and Life Sciences, Belfast, UK. Sarajevo Medical School, Sarajevo School of Science and Technology Sarajevo Medical School, Sarajevo, Bosnia and Herzegovina. National Heart & Lung Institute, Imperial College London, London, UK. The Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast Faculty of Medicine Health and Life Sciences, Belfast, UK b.schock@qub.ac.uk.
 Institute of Brain Science, Shanxi Datong University, Datong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. Research Center of Neurobiology, The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of the State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, China. Research Center of Neurobiology, The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of the State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. Research Center of Neurobiology, The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of the State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, China. Research Center of Neurobiology, The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of the State Administration of Traditional Chinese Medicine, Shanxi University of Chinese Medicine, Jinzhong, China. Department of Physiology, Shanxi Medical University, Taiyuan, China; slj_0354@126.com. Institute of Brain Science, Shanxi Datong University, Datong, China. Department of Neurology, Datong Forth People's Hospital, Datong, China; sxdtyjz2020@163.com.
 Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy. Neurological Clinic and Stroke Unit, Naples, Italy. Neurological Clinic and Stroke Unit, Naples, Italy. Multiple Sclerosis Center, Naples, Italy. Neurology Unit, Department of Neurosciences, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy.
 Danish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. National Centre for Register-Based Research, Department of Economics and Business Economics, Aarhus BSS, Aarhus University, Aarhus, Denmark. Department of Clinical Microbiology, Copenhagen University Hospital- Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Division of Infection Medicine, University of Edinburgh, Edinburgh, United Kingdom. Division of Infection Medicine, University of Edinburgh, Edinburgh, United Kingdom. Danish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
 National Research Centre for the Working Environment, Copenhagen, Denmark. Department of Neurology, The Danish Multiple Sclerosis Registry, Copenhagen University Hospital, Glostrup, Denmark. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. National Research Centre for the Working Environment, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. National Research Centre for the Working Environment, Copenhagen, Denmark. Section of Epidemiology, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
 Universidade de São Paulo, Faculdade de Medicina, Hospital das Clínicas, Departamento de Neurologia, São Paulo SP, Brazil. Universidade de São Paulo, Faculdade de Medicina, Hospital das Clínicas, Departamento de Neurologia, São Paulo SP, Brazil. Universidade de São Paulo, Faculdade de Medicina, Hospital das Clínicas, Departamento de Neurologia, São Paulo SP, Brazil. Universidade de São Paulo, Faculdade de Medicina, Hospital das Clínicas, Departamento de Neurologia, São Paulo SP, Brazil. Universidade de São Paulo, Faculdade de Medicina, Hospital das Clínicas, Departamento de Neurologia, São Paulo SP, Brazil. Pontifícia Universidade Católica do Rio Grande do Sul, Instituto do Cérebro do Rio Grande do Sul, Porto Alegre RS, Brazil.
 Lady Davis Institute of the Jewish General Hospital and McGill University, Montreal, Quebec, Canada. Lady Davis Institute of the Jewish General Hospital and McGill University, Montreal, Quebec, Canada. Lady Davis Institute of the Jewish General Hospital, Montreal, Quebec, Canada. Radboud University Medical Center, Nijmegen, The Netherlands. University of Rhode Island, Kingston, Rhode Island. National Scleroderma Foundation, Tri-State Chapter, Buffalo, New York. National Scleroderma Foundation, Los Angeles, California. Sclérodermie Québec, Longueuil, Quebec, Canada. Scleroderma Australia and Scleroderma Victoria, Melbourne, Victoria, Australia. University of Texas McGovern School of Medicine, Houston. Hôpital Cochin, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France. Western University and Lawson Research Institute, London, Ontario, Canada. Scleroderma Atlantic, Halifax, Nova Scotia, Canada. Scleroderma Society of Ontario and Scleroderma Canada, Hamilton, Ontario, Canada. New York University, New York, New York. San Diego State University and University of California, San Diego. McGill University, Montreal, Quebec, Canada. Jewish General Hospital and McGill University, Montreal, Quebec, Canada.
 Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. yani_liu@hotmail.com. Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. sjshicn@163.com. Union Jiangnan Hospital, Huazhong University of Science and Technology, Wuhan, 430022, China. sjshicn@163.com.
 Department of Nursing, Université du Québec à Trois-Rivières, 555 boul. de l'Université, Drummondville, QC J2C 0R5, Canada. Réseau Québécois de Recherche en Soins Palliatifs et de Fin de Vie (RQSPAL), Quebec, QC, Canada. Centre for Research and Intervention on Suicide, Ethical Issues, and End-of-life Practices (CRISE), Montreal, QC, Canada. Faculty of Nursing, Université de Montréal, Montréal, QC, Canada. Research Chair in Nursing Care for Older People and their Families, Montréal, QC, Canada. Canada Research Chair in Care for Older People, Montréal, QC, Canada. Research Centre of the Institut universitaire de gériatrie de Montréal, Montréal, QC, Canada. Faculty of Nursing, Université de Montréal, Montréal, QC, Canada. Réseau Québécois de Recherche en Soins Palliatifs et de Fin de Vie (RQSPAL), Quebec, QC, Canada. Centre for Research and Intervention on Suicide, Ethical Issues, and End-of-life Practices (CRISE), Montreal, QC, Canada. Department of Nursing, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada. Department of Psychoeducation, Université de Sherbrooke, Longueuil, QC, Canada. Réseau Québécois de Recherche en Soins Palliatifs et de Fin de Vie (RQSPAL), Quebec, QC, Canada. Centre for Research and Intervention on Suicide, Ethical Issues, and End-of-life Practices (CRISE), Montreal, QC, Canada. Centre de Recherche Charles-Le Moyne (CRCLM), Longueuil, QC, Canada. Department of Psychology, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada.
 Department of Chemistry, College of Humanities and Sciences, Virginia Commonwealth University, Richmond, Virginia, USA. Division of Rheumatology, John T. Milliken Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA; Department of Genetics, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA. Scleroderma Program, Feinberg School of Medicine, Northwestern University, Chicago, Ilinois, USA. Division of Rheumatology, Department of Internal Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA. Division of Rheumatology, Department of Internal Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA. Department of Physiology & Biophysics, College of Medicine, University of Illinois at Chicago, Chicago, Ilinois, USA. Department of Physiology & Biophysics, College of Medicine, University of Illinois at Chicago, Chicago, Ilinois, USA. Department of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, Ilinois, USA. Departamento de Bioquímica y Medicina Molecular, Facultad de Medicina, Universidad Autónoma de Nuevo León, Monterrey, México. Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Department of Pediatrics, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; The UPMC Lupus Center of Excellence, Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Department of Computational Medicine and Bioinformatics, University of Michigan Medical School, Ann Arbor, Michigan, USA; Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA. Department of Computational Medicine and Bioinformatics, University of Michigan Medical School, Ann Arbor, Michigan, USA; Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA. Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. Scleroderma Program, Feinberg School of Medicine, Northwestern University, Chicago, Ilinois, USA. Department of Obstetrics & Gynecology, Virginia Commonwealth University, Richmond, Virginia, USA. Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minesota, USA. Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minesota, USA. Department of Biomedical Engineering, College of Engineering, University of Wisconsin-Madison, Madison, Wincosin, USA. Department of Biomedical Engineering, College of Engineering, University of Wisconsin-Madison, Madison, Wincosin, USA. Department of Obstetrics & Gynecology, Virginia Commonwealth University, Richmond, Virginia, USA. Electronic address: maria.teves@vcuhealth.org. Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
 Department of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, MO, USA. Electronic address: jbrazill@wustl.edu. Department of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, MO, USA. Electronic address: mingyu.shin@wustl.edu. Department of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, MO, USA. Electronic address: mkristann@gmail.com. Department of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, MO, USA. Electronic address: anuragm@wustl.edu. Department of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, MO, USA. Electronic address: ivana.shen@wustl.edu. Department of Neuroscience, Washington University, Saint Louis, MO, USA; Center of Regenerative Medicine, Washington University School of Medicine, Saint Louis, MO, USA; Hope Center for Neurological Disorders, Washington University School of Medicine, Saint Louis, MO, USA. Electronic address: cavalli@wustl.edu. Department of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, MO, USA; Center of Regenerative Medicine, Washington University School of Medicine, Saint Louis, MO, USA; Department of Cell Biology and Physiology, Washington University, Saint Louis, MO, USA; Department of Biomedical Engineering, Washington University, Saint Louis, MO, USA. Electronic address: scheller@wustl.edu.
 Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Department of Neurological Surgery, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Jefferson Integrated Magnetic Resonance Imaging Center, Department of Radiology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
 Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
 F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. F.M. Kirby Neurobiology Center, Rosamund Stone Zander Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
 Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China. Department of Plastic Surgery and Regenerative Medicine, Fujian Medical University Union Hospital, Fuzhou, P.R. China. Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China. Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China. Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China. Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China.
 Department of Biosciences, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biosciences, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biosciences, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biosciences, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biosciences, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biotechnology, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biotechnology, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biotechnology, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India. Department of Biosciences, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore, 632014, India.
 Hacettepe University, Department of Oral and Maxillofacial Surgery, Turkey. Electronic address: goknurtopaloglu@gmail.com. Hacettepe University, Department of Oral and Maxillofacial Surgery, Turkey. Hacettepe University, Department of Oral and Maxillofacial Surgery, Turkey. Hacettepe University, Department of Oral and Maxillofacial Surgery, Turkey.
 Department of Surgery, Ophthalmology, Otorhinolaryngology and Physiotherapy, Faculty of Medicine, HVUV, 47003 Valladolid, Spain. Department of Anatomy and Radiology, Faculty of Health Sciences, GIR Physical Exercise and Aging, University of Valladolid, Campus Los Pajaritos, 42004 Soria, Spain. Department of Applied Biology-Nutrition and Institute of Bioengineering, Miguel Hernández University (UMH), 03202 Elche, Spain. Institute for Health and Biomedical Research (ISABIAL), 03010 Alicante, Spain. CIBER Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain. Department of Internal Medicine, University of Alcalá de Henares, 28801 Alcalá de Henares, Spain. Department of Biochemistry, Molecular Biology and Physiology, Faculty of Health Sciences, GIR Physical Exercise and Aging, University of Valladolid, Campus Duques de Soria, 42004 Soria, Spain.
 Department of Obstetrics and Gynecology, Brooke Army Medical Center, Fort Sam Houston, TX 78234, USA. Department of Obstetrics and Gynecology, Brooke Army Medical Center, Fort Sam Houston, TX 78234, USA. Department of Obstetrics and Gynecology, Brooke Army Medical Center, Fort Sam Houston, TX 78234, USA. Department of Obstetrics and Gynecology, Walter Reed National Military Medical Center, Bethesda, MD 20814, USA. Department of Obstetrics and Gynecology, Brooke Army Medical Center, Fort Sam Houston, TX 78234, USA.
 Department of Biochemistry, University of Nebraska-Lincoln, Lincoln, Nebraska, USA. Department of Biochemistry and Nebraska Redox Biology Center, University of Nebraska-Lincoln, Lincoln, Nebraska, USA. Fred & Pamela Buffett Cancer Center, Omaha, Nebraska, USA. Department of Biochemistry, University of Nebraska-Lincoln, Lincoln, Nebraska, USA. Department of Biochemistry and Nebraska Redox Biology Center, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
 Department of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. The Second Clinical Medical College of Nanchang University, Nanchang, Jiangxi, China. Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China. Department of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
 Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", Piazza Lauro de Bosis 6, 00135, Rome, Italy. Laboratory of Molecular and Cellular Neurobiology and of Neurochemistry, Fondazione Santa Lucia IRCCS, Via del Fosso di Fiorano, 64, 00143, Rome, Italy. Laboratory of Molecular and Cellular Neurobiology and of Neurochemistry, Fondazione Santa Lucia IRCCS, Via del Fosso di Fiorano, 64, 00143, Rome, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168, Rome, Italy. Laboratory of Molecular and Cellular Neurobiology and of Neurochemistry, Fondazione Santa Lucia IRCCS, Via del Fosso di Fiorano, 64, 00143, Rome, Italy. Section of Human Anatomy, Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168, Rome, Italy. Fondazione Policlinico Agostino Gemelli IRCCS, 00168, Rome, Italy. Laboratory of Molecular and Cellular Neurobiology and of Neurochemistry, Fondazione Santa Lucia IRCCS, Via del Fosso di Fiorano, 64, 00143, Rome, Italy. Institute of Translational Pharmacology (IFT), Consiglio Nazionale delle Ricerche (CNR), 00133, Rome, Italy. Laboratory of Molecular and Cellular Neurobiology and of Neurochemistry, Fondazione Santa Lucia IRCCS, Via del Fosso di Fiorano, 64, 00143, Rome, Italy. Institute of Translational Pharmacology (IFT), Consiglio Nazionale delle Ricerche (CNR), 00133, Rome, Italy. Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", Piazza Lauro de Bosis 6, 00135, Rome, Italy. mariapaola.paronetto@uniroma4.it. Laboratory of Molecular and Cellular Neurobiology and of Neurochemistry, Fondazione Santa Lucia IRCCS, Via del Fosso di Fiorano, 64, 00143, Rome, Italy. mariapaola.paronetto@uniroma4.it.
 Yatiris, PLADEMA, UNICEN, Tandil, Buenos Aires, Argentina. ddeangeli@pladema.exa.unicen.edu.ar. CONICET, CABA, Argentina. ddeangeli@pladema.exa.unicen.edu.ar. Yatiris, PLADEMA, UNICEN, Tandil, Buenos Aires, Argentina. Yatiris, PLADEMA, UNICEN, Tandil, Buenos Aires, Argentina. CONICET, CABA, Argentina. Yatiris, PLADEMA, UNICEN, Tandil, Buenos Aires, Argentina. CONICET, CABA, Argentina. ENyS, CONICET-HEC-UNAJ, Florencio Varela, Buenos Aires, Argentina. ENyS, CONICET-HEC-UNAJ, Florencio Varela, Buenos Aires, Argentina. Normal Anatomy Department, UBA, CABA, Argentina. CONICET, CABA, Argentina. Laboratorio de Inteligencia Artificial, Universidad Torcuato Di Tella, CABA, Argentina. Yatiris, PLADEMA, UNICEN, Tandil, Buenos Aires, Argentina. CONICET, CABA, Argentina. Yatiris, PLADEMA, UNICEN, Tandil, Buenos Aires, Argentina. CONICET, CABA, Argentina.
 Department of Dermatology, Hospital Universitario San Cecilio, 18016 Granada, Spain. Department of Dermatology, Hospital Universitario San Cecilio, 18016 Granada, Spain. Department of Dermatology, Hospital Universitario San Cecilio, 18016 Granada, Spain.
 Department of Systems and Biomedical Engineering, Faculty of Engineering, Cairo University, Giza, Egypt. Department of Biomedical, Industrial, and Human Factors Engineering, College of Engineering and Computer Science, Wright State University, Dayton, OH, United States. Department of Electrical Power Engineering, Faculty of Engineering, Cairo University, Giza, Egypt. Department of Systems and Biomedical Engineering, Faculty of Engineering, Cairo University, Giza, Egypt. Department of Biomedical, Industrial, and Human Factors Engineering, College of Engineering and Computer Science, Wright State University, Dayton, OH, United States. Department of Neuroscience, Cell Biology and Physiology, Boonshoft School of Medicine and College of Science and Mathematics, Wright State University, Dayton, OH, United States.
 Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Clinical Trial Unit, Department of Clinical Research, University Hospital Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. University Center of Cardiovascular Science & Department of Cardiology, University Heart and Vascular Center Hamburg, Hamburg, Germany. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Cardiovascular Research Institute Basel (CRIB) and Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland.
 Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), University Medical Center Hamburg-Eppendorf, Lübeck-Borstel-Riems, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), University Medical Center Hamburg-Eppendorf, Lübeck-Borstel-Riems, Hamburg, Germany. Institute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), University Medical Center Hamburg-Eppendorf, Lübeck-Borstel-Riems, Hamburg, Germany. Institute of Infection Research and Vaccine Development (IIRVD), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), University Medical Center Hamburg-Eppendorf, Lübeck-Borstel-Riems, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), University Medical Center Hamburg-Eppendorf, Lübeck-Borstel-Riems, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), University Medical Center Hamburg-Eppendorf, Lübeck-Borstel-Riems, Hamburg, Germany.
 Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). Experimental and Clinical Research Center, a joint cooperation of Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). German Centre for Cardiovascular Research, Partner Site Berlin, Germany (H.M., N.W., R.D., D.N.M.). Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). Experimental and Clinical Research Center, a joint cooperation of Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). Experimental and Clinical Research Center, a joint cooperation of Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). German Centre for Cardiovascular Research, Partner Site Berlin, Germany (H.M., N.W., R.D., D.N.M.). Department of Nephrology, Faculty of Medicine, University Hospital, Heinrich-Heine-University, Düsseldorf, Germany (J.S.). CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty and University Hospital, Düsseldorf, Germany (J.S.). Department of Biomedicine, University of Bergen, Norway (H.W.). Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). Experimental and Clinical Research Center, a joint cooperation of Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). German Centre for Cardiovascular Research, Partner Site Berlin, Germany (H.M., N.W., R.D., D.N.M.). HELIOS Clinic, Department of Cardiology and Nephrology, Berlin, Germany (R.D.). Institute of Clinical Microbiology and Hygiene, University Hospital Regensburg and University of Regensburg, Germany (J.J.). Institute for Medical Microbiology, Immunology, and Hygiene, and Center for Molecular Medicine Cologne, University Hospital Cologne and Faculty of Medicine, University of Cologne, Germany (J.J.). VIB Laboratory of Translational Immunomodulation, VIB Center for Inflammation Research, Hasselt University, Diepenbeek, Belgium (M.K.). Department of Immunology, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium (M.K.). University Multiple Sclerosis Center, Hasselt University/Campus Diepenbeek, Belgium (M.K.). Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany (H.M., S.G., F.C.L., N.W., R.D., S.K., D.N.M.). Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Experimental and Clinical Research Center, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). Experimental and Clinical Research Center, a joint cooperation of Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Germany (H.M., F.C.L., N.W., R.D., D.N.M.). German Centre for Cardiovascular Research, Partner Site Berlin, Germany (H.M., N.W., R.D., D.N.M.).
 Neuroscience Research Group (NRG), Universal Scientific Education and Research Network (USERN), Tehran, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Tehran University of Medical Science, Tehran, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. School of Medicine, Tehran University of Medical Science, Tehran, Iran. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
 Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Center for Cell Dynamics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Center for Cell Dynamics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Center for Cell Dynamics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Center for Cell Dynamics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. Department of Biochemistry and Molecular Genetics, University of Colorado-Anschutz Medical Campus, Aurora, CO, 80045, USA. Department of Biochemistry and Molecular Genetics, University of Colorado-Anschutz Medical Campus, Aurora, CO, 80045, USA. Department of Genetics, Stanford University School of Medicine, Stanford, CA, 94305, USA. Center for Cell Dynamics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. Brain Science Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. shuying.sun@jhmi.edu. Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. bwu20@jhmi.edu. Center for Cell Dynamics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. bwu20@jhmi.edu. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. bwu20@jhmi.edu.
 Department of Infectious Diseases, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Infectious Diseases, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Infectious Diseases, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Infectious Diseases, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Infectious Diseases, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital-Rigshospitalet, Glostrup, Denmark. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Hong Kong Center for Neurodegenerative Diseases, Hong Kong Central College, Hong Kong, China. Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK. UK Dementia Research Institute at UCL, London, UK. Department of Infectious Diseases, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
 Neurology Clinic, Diskapi Yildirim Beyazit Training and Research Hospital, Şehit Ömer Halisdemir Street. No: 20 Altındag, 06110, Ankara, Turkey. halilnder@yahoo.com. Department of Radiology, Hacettepe University Medical School, Ankara, Turkey. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, Hacettepe University Medical School, Ankara, Turkey.
 IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia. IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia. Barwon Health, Department of Anaesthesia and Pain, University Hospital Geelong, Geelong, VIC 3220, Australia. Department of Anesthesiology, Weill Cornell Medical College, New York, NY 10065, USA. IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia. Faculty of Health, School of Medicine, Deakin University, Waurn Ponds, VIC 3216, Australia. Geriatrics Section, Department of Internal Medicine, University of Palermo, 90133 Palermo, Italy. IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia. Faculty of Health, School of Psychology, Deakin University, Geelong, VIC 3220, Australia. IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia. IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia. Barwon Health, Department of Anaesthesia and Pain, University Hospital Geelong, Geelong, VIC 3220, Australia. Barwon Health, Department of Anaesthesia and Pain, University Hospital Geelong, Geelong, VIC 3220, Australia. IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia.
 Department of Neuroscience, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Neuroscience, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Neuroscience, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA. Global Head of Neuroscience, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA. Department of Neuroscience, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Center for Neuromuscular Disorders and Center for Multiple Sclerosis and Related Disorders, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus. Department of Neuroscience, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.
 Centre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK. Centre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK. Centre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK. Molecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34139 Trieste, Italy. Department of Medical, Surgical and Health Sciences, University of Trieste, Trieste, Italy. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Barlo Multiple Sclerosis Centre and Keenan Research Institute for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada. Department of Immunology, University of Toronto, Toronto, Ontario, Canada. Great Ormond Street Institute of Child Health, University College London, London, UK. Molecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34139 Trieste, Italy. Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh BioQuarter, Edinburgh, UK. Centre for Discovery Brain Sciences, Chancellor's Building, The University of Edinburgh, Edinburgh, UK. Dementia Research Institute at The University of Edinburgh, Edinburgh, UK. Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Barlo Multiple Sclerosis Centre and Keenan Research Institute for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada. Department of Immunology, University of Toronto, Toronto, Ontario, Canada. Molecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology (ICGEB), 34139 Trieste, Italy. Department of Medical, Surgical and Health Sciences, University of Trieste, Trieste, Italy. British Heart Foundation Centre of Research Excellence, School of Cardiovascular Medicine & Sciences, King's College London, London, UK. Centre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK.
 Department of Neurology, Mayo Clinic, Scottsdale, AZ, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Radiology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Ophthalmology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, University of Florida, Gainesville, FL, USA. Brooke Army Medical Center, San Antonio, TX, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Jacksonville, FL, USA. Department of Neurology, Western University, London, Ontario, Canada. Department of Neurology, University of Sassari, Sassari, Italy. Department of Neurology, Cleveland Clinic, Cleveland, OH, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
 ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. rosario.vasta@unito.it. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Department of Neuroscience "Rita Levi Montalcini", University of Turin, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. International School of Advanced Studies, University of Camerino, Camerino, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Department of Neuromuscular Diseases, Queen Square Institute of Neurology, UCL, London, WC1N 3BG, UK. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Neurology 1, AOU Città della Salute e della Scienza di Torino, Turin, Italy. Institute of Cognitive Science and Technologies, National Research Council, Rome, Italy. ALS Center, Department of Neurology, Azienda Ospedaliero Universitaria Maggiore della Carità, and University of Piemonte Orientale, Novara, Italy. ALS Center, Department of Neurology, Azienda Ospedaliero Universitaria Maggiore della Carità, and University of Piemonte Orientale, Novara, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Neurology 1, AOU Città della Salute e della Scienza di Torino, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Neurology 1, AOU Città della Salute e della Scienza di Torino, Turin, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Neurology 1, AOU Città della Salute e della Scienza di Torino, Turin, Italy. Institute of Cognitive Science and Technologies, National Research Council, Rome, Italy. ALS Center, Department of Neuroscience "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. Neurology 1, AOU Città della Salute e della Scienza di Torino, Turin, Italy.
 Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan. Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan. Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan. Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan. Department of Omics and Systems Biology, Graduate School of Medical and Dental Sciences, Niigata University, 757 Ichibancho, Asahimachi-dori, Chuo-ku, Niigata City, Niigata 951-8510, Japan. Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan.
 Division of Allergy, Pulmonary and Critical Care, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Division of Allergy, Pulmonary and Critical Care, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Department of Microbiology, Pathology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Division of Allergy, Pulmonary and Critical Care, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Department of Microbiology, Pathology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Division of Allergy/Immunology, Department of Medicine, Washington University, St. Louis, MO, USA.
 Beth Israel Lahey Health, Burlington, MA, Unites States. Retired, Greenfield Township, PA, United States. Electronic address: slickstick51@gmail.com.
 Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA MBenatar@med.miami.edu. Neurology, University of Michigan, Ann Arbor, Michigan, USA. Staats Life Sciences Consulting, Los Angeles, California, USA. Neurology, University of Michigan, Ann Arbor, Michigan, USA. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA. ALS Association, Washington, District of Columbia, USA. ALS Association, Washington, District of Columbia, USA. Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King's College London, London, UK.
 Department of Neurology, University of California San Francisco (UCSF), San Francisco, USA. Department of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany. Department of Neuroscience, Neurology Unit, Maurizio Bufalini Hospital, AUSL Romagna, Cesena, Italy. Department of Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Department of Stroke and Neuroscience, Charing Cross Hospital, Imperial College London NHS Healthcare Trust, London, UK. Department of Brain Sciences, Imperial College London, London SW7 2AZ, UK. Neuroimmunological Diseases Section, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD, USA. Neuroimmunological Diseases Section, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD, USA. Department of Neuroscience, Mayo Clinic, Jacksonville, FL, 32224, USA. Neuroscience Graduate Program, Mayo Clinic Graduate School of Biomedical Sciences, Jacksonville, FL, 32224, USA. Department of Neuroscience, Mayo Clinic, Jacksonville, FL, 32224, USA. Neuroscience Graduate Program, Mayo Clinic Graduate School of Biomedical Sciences, Jacksonville, FL, 32224, USA. Department of Neurology, Mayo Clinic, Jacksonville, FL, 32224, USA. Division of Vascular and Endovascular Surgery, Mayo Clinic, Jacksonville, FL, 32224, USA. Institute of Experimental Neurology, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Institute of Experimental Neurology, Division of Neuroscience, Vita e Salute San Raffaele University, Milan, Italy. Division of Immunology, Transplantation and Infectious Diseases, IRCCS Ospedale San Raffaele, Milan, Italy. Institute of Experimental Neurology, Division of Neuroscience, IRCCS Ospedale San Raffaele, Milan, Italy. Department of Acute Medical Care, Intensive Care Unit, University Hospital Basel, Basel, Switzerland. Department of Acute Medical Care, Intensive Care Unit, University Hospital Basel, Basel, Switzerland. Department of Neurology, University Hospital Basel and University of Basel, Basel, Switzerland. Neurology B, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Department of Neurology, Landesklinikum Mistelbach-Gänserndorf, Mistelbach, Austria. Department of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany. Department of Neurology, Oslo University Hospital, Oslo, Norway. Department of Internal Medicine, Drammen Hospital, Vestre Viken Hospital Trust, Drammen, Norway. Department of Clinical Science, Faculty of Medicine, University of Bergen, Bergen, Norway. Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Department of Infectious Diseases, Oslo University Hospital, Oslo, Norway. Department of Medical Sciences, Neurology, Uppsala University, Uppsala, Sweden. Department of Surgical Sciences, Radiology, Uppsala University, Uppsala, Sweden. Department of Medical Sciences, Uppsala University, Neurosurgery,, Sweden. Department of Neuroscience, Karolinska Institute, Stockholm, Sweden. Department of Medical Sciences, Neurology, Uppsala University, Uppsala, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK. UK Dementia Research Institute at UCL, London, UK. Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China. Wisconsin Alzheimer's Disease Research Center, School of Medicine and Public Health, University of Wisconsin, University of Wisconsin-Madison, Madison, WI, USA. Department of Neurology, Ulm University Hospital, Ulm, Germany. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Department of Neurology, University of California San Francisco (UCSF), San Francisco, USA. Department of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany. Department of Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland. Multiple Sclerosis Centre, Department of Neurology, University Hospital and University of Basel, Basel, Switzerland. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. mattfos89@gmail.com. Department of Neuroscience, Neurology Unit, S.Maria Delle Croci Hospital of Ravenna, AUSL Romagna, Ravenna, Italy. mattfos89@gmail.com. Department of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany. samir.aburumeileh@gmail.com.
 Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands. Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands.
 Department of Defense/Uniformed Services University Brain Tissue Repository, Uniformed Services University, Bethesda, MD 20817, USA. Murtha Cancer Center Research Program, Uniformed Services University of the Health Sciences, Bethesda, MD 20817, USA. Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD 20817, USA. Human Oncology and Pathogenesis Program, Sloan Kettering Institute, New York, NY 10065, USA. Neurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA. Department of Neurology, Johns Hopkins University Medical Center, Baltimore, MD 21287, USA.
 Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Jonathan.Zipursky@sunnybrook.ca. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont. Department of Medicine (Zipursky), Sunnybrook Health Sciences Centre; Institute of Health Policy, Management, and Evaluation (Zipursky, Gomes, Paterson, Austin, Mamdani, Ray), University of Toronto; ICES Central (Everett, Gomes, Paterson, Li, Austin, Mamdani, Ray, Zipursky); Keenan Research Centre of the Li Ka Shing Knowledge Institute (Gomes, Mamdani), St. Michael's Hospital; Leslie Dan Faculty of Pharmacy (Gomes, Mamdani), University of Toronto; Sunnybrook Research Institute (Austin, Juurlink, Zipursky); Department of Medicine (Ray), St. Michael's Hospital, Toronto, Ont.
 Rutgers Robert Wood Johnson Medical School, New Brunswick, United States of America. Centrastate Medical Center, Freehold, United States of America. Centrastate Medical Center, Freehold, United States of America.
 Department of Human Pathology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. Department of Human Pathology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Pneumothorax Research Center and Division of Thoracic Surgery, Nissan Tamagawa Hospital, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Pneumothorax Research Center and Division of Thoracic Surgery, Nissan Tamagawa Hospital, Tokyo, Japan. Department of Medical Oncology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan. Department of Pathology, Nissan Tamagawa Hospital, Tokyo, Japan. Department of Human Pathology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan. The Study Group for Pneumothorax and Cystic Lung Diseases, Setagaya-Ku, Tokyo, Japan. Department of Respiratory Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan.
 Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan. Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan. Sunnybrook Health Sciences Centre, Sunnybrook Research Institute, Toronto, ON, Canada. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada. Institute of Medical Sciences, University of Toronto, Toronto, ON, Canada. Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan. Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan. Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore (UOL), Lahore, Pakistan. Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore (UOL), Lahore, Pakistan. Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan. Department of Public Health and Nutrition, The University of Haripur (UOH), Haripur, Pakistan. Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan. Department of Medical Lab Technology, The University of Haripur (UOH), Haripur, Pakistan.

 Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark. Jens.Andersen@sund.ku.dk. Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark. Arne.Schousboe@sund.ku.dk.

 Institute of Anatomy, Kiel University, Kiel, Germany. Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel. Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel. Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel. Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel. Institute of Anatomy, Kiel University, Kiel, Germany. School of Chemistry, Tel Aviv University, Tel Aviv, Israel. Institute for Drug Research, The Hebrew University of Jerusalem, Jerusalem, Israel. School of Mechanical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv, Israel. Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel. Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. The Center for Nanoscience and Nanotechnology, Tel Aviv University, Tel Aviv, Israel.

 Adelaide Dental School, The University of Adelaide, Adelaide, South Australia, Australia. Adelaide Dental School, The University of Adelaide, Adelaide, South Australia, Australia.
 School of Life Sciences, University of Glasgow, Room 341, Sir James Black Building, Glasgow G12 8QQ, UK.


 Department of Neurological Sciences, Larner College of Medicine, University of Vermont, Burlington, VT, USA. adam.sprouse-blum@uvmhealth.org. Department of Neurological Sciences, University of California San Diego, San Diego, CA, USA. Dana Medical Library, University of Vermont, Burlington, VT, USA. Dana Medical Library, University of Vermont, Burlington, VT, USA. Department of Medicine, Larner College of Medicine, University of Vermont, Burlington, VT, USA.
 Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Dicle University School of Medicine, Diyarbakır, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Dicle University School of Medicine, Diyarbakır, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology and Immunology, Sakarya University School of Medicine, Sakarya, Türkiye. Department of Physical Medicine and Rehabilitation, Yüzüncü Yıl University Faculty of Medicine, Van, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Erciyes University Faculty of Medicine, Kayseri, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Erciyes University Faculty of Medicine, Kayseri, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Akdeniz University, Faculty of Medicine, Antalya, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Akdeniz University, Faculty of Medicine, Antalya, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Ankara University Faculty of Medicine, Ankara, Türkiye. Rheumatology Clinic, University of Health Sciences Fatih Sultan Mehmet Training and Research Hospital, Istanbul, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Adnan Menderes University, Faculty of Medicine, Aydın, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Atatürk University Faculty of Medicine, Erzurum, Türkiye. Department of Physical Medicine and Rehabilitation, Kapaklı State Hospital, Tekirdağ, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Marmara University Faculty of Medicine, Istanbul, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Marmara University Faculty of Medicine, Istanbul, Türkiye. Department of Physical Medicine and Rehabilitation, Division of Rheumatology, Necmettin Erbakan University Meram Faculty of Medicine, Konya, Türkiye.
 From the Department of Neurology (N.M.-O., M.T., X.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia. Section of Neuroradiology (D.P., M.A., À.R.), Department of Radiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain deborah.pareto.idi@gencat.cat. Section of Neuroradiology (D.P., M.A., À.R.), Department of Radiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. From the Department of Neurology (N.M.-O., M.T., X.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia. From the Department of Neurology (N.M.-O., M.T., X.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia. Section of Neuroradiology (D.P., M.A., À.R.), Department of Radiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. From the Department of Neurology (N.M.-O., M.T., X.M., J.S.-G.), Multiple Sclerosis Centre of Catalonia.
 Department of Neurology, Tohoku University Graduate School of Medicine. Department of Education and Support for Regional Medicine, Tohoku University Hospital. Department of Neurology, Tohoku University Graduate School of Medicine. Department of Neurology, National Hospital Organization Yonezawa National Hospital. Department of Neurology, Tohoku University Graduate School of Medicine. Multiple Sclerosis Therapeutics, Fukushima Medical University. Department of Neurology, Tohoku Medical and Pharmaceutical University. Department of Neurology, Tohoku University Graduate School of Medicine.
 Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Institute for Experimental Immunology, Affiliated to Euroimmun, Lübeck, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine‑Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, Mainz, Germany. Institute for Experimental Immunology, Affiliated to Euroimmun, Lübeck, Germany. Institute of Neuroimmunology and Multiple Sclerosis Research, University Medical Center, of the Georg August University, Göttingen, Germany. Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine‑Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University, Mainz, Germany. Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, City Campus, Göttingen, Germany. Electronic address: ehrenreich@mpinat.mpg.de.
 Melbourne School of Psychological Sciences, The University of Melbourne, Parkville, Victoria, Australia. Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, Victoria, Australia. Alfred Brain, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Psychiatry, Alfred Health, Melbourne, Victoria, Australia. Alfred Brain, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Psychiatry, Alfred Health, Melbourne, Victoria, Australia. Alfred Brain, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Alfred Brain, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Neuropsychiatry, Royal Melbourne Hospital, Melbourne, Victoria, Australia. Department of Psychiatry, The University of Melbourne, Melbourne, Victoria, Australia. Melbourne School of Psychological Sciences, The University of Melbourne, Parkville, Victoria, Australia. Alfred Brain, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia. Department of Medicine, Austin Hospital, The University of Melbourne, Melbourne, Victoria, Australia. Melbourne School of Psychological Sciences, The University of Melbourne, Parkville, Victoria, Australia. Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, Victoria, Australia. Alfred Brain, Alfred Health, Melbourne, Victoria, Australia. Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
 Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany. Institute for Infection Research and Vaccine Development, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany.
 Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy. nicola.merli@edu.unife.it. Department of Neuroscience and Rehabilitation, S. Anna University Hospital, Ferrara, Italy. Department of Neuroscience and Rehabilitation, S. Anna University Hospital, Ferrara, Italy. Department of Radiology, S. Anna University Hospital, Ferrara, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy. Department of Neuroscience and Rehabilitation, S. Anna University Hospital, Ferrara, Italy. Interdepartmental Research Center for Multiple Sclerosis and Other Inflammatory and Degenerative Disorders of the Nervous System, University of Ferrara, Ferrara, Italy. Neurology Unit, Fondazione IRCCS Casa Sollievo Della Sofferenza, San Giovanni Rotondo, Italy. Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy. Interdepartmental Research Center for Multiple Sclerosis and Other Inflammatory and Degenerative Disorders of the Nervous System, University of Ferrara, Ferrara, Italy.
 Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Mellen Center for Multiple Sclerosis Treatment and Research, Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Twinsburg Family Health and Surgery Center, Internal Medicine and Geriatrics Department, Twinsburg, OH, USA. Family Medicine, Hillcrest Hospital, Cleveland Clinic, Mayfield Heights, OH, USA. Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Qr8 Health, Inc., Cleveland, OH, USA. Qr8 Health, Inc., Cleveland, OH, USA. Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Health and Wellness Center, Cleveland Clinic, Vero Beach, FL, USA.
 Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Clinical Physiology and Nuclear Medicine, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Division of Clinical Neuroscience, Department of Research and Innovation, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Division of Clinical Neuroscience, Department of Research and Innovation, Oslo University Hospital, Oslo, Norway. Department of Neurology, Oslo University Hospital, Oslo, Norway. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Clinical Immunology, Zealand University Hospital, Køge, Denmark. Department of Neurology, Danish Multiple Sclerosis Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Multiple Sclerosis Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Department of Neurology, Danish Headache Centre, Copenhagen University Hospital, Rigshospitalet-Glostrup, Glostrup, Denmark.
 Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland. Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland. Nutrition Unit, Service of Endocrinology, Diabetes, Nutrition and Therapeutic Education, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland. Nutrition Unit, Service of Endocrinology, Diabetes, Nutrition and Therapeutic Education, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland. Institute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland. Nutrition Unit, Service of Endocrinology, Diabetes, Nutrition and Therapeutic Education, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland. Nutrition Unit, Service of Endocrinology, Diabetes, Nutrition and Therapeutic Education, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland. Department of General Internal Medicine, Bern University Hospital, Inselspital, University of Bern, Bern, Switzerland. Institute of Primary Health Care, University of Bern, Bern, Switzerland. Salk Institute for Biological Sciences, La Jolla, California, USA. Interdisciplinary Center for Bone Diseases, Service of Rheumatology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Department of Rheumatology and Immunology, Bern University Hospital, Inselspital, University of Bern, Bern, Switzerland. Interdisciplinary Center for Bone Diseases, Service of Rheumatology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Division of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. Salk Institute for Biological Sciences, La Jolla, California, USA. Department of General Internal Medicine, Bern University Hospital, Inselspital, University of Bern, Bern, Switzerland. Institute of Primary Health Care, University of Bern, Bern, Switzerland. Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland. Nutrition Unit, Service of Endocrinology, Diabetes, Nutrition and Therapeutic Education, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland. Diabetes Centre, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
 Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. Department of Medical, Surgical, and Experimental Sciences, University of Sassari, Sassari, Italy. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Center of Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center of Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Center of Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Center of Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Center of Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA.
 Department of Neurosciences, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia; Department of Neurology, Alfred Health, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia. Electronic address: mastura.monif@monash.edu. Department of Neurosciences, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia; Department of Neurology, Alfred Health, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia. Department of Neurosciences, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia; Department of Neurology, University Hospital of Geelong, Level 2, Kardinia House, Bellerine Street, Geelong, Victoria, 3220, Australia. Department of Immunology and Pathology, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Burnett Building, 89 Commercial Road, Melbourne, Victoria, 3004, Australia. Department of Neurology, Melbourne Health, 300 Grattan Street, Parkville, Victoria, 3050, Australia; Department of Neuroscience, Eastern Health, Level 2, 5 Arnold Street, Box Hill, Victoria, 3128, Australia. Department of Neurosciences, Monash Health, Clayton Road, Clayton, Victoria, 3168, Australia. Department of Neurosciences, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia; Department of Neurology, Alfred Health, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia. Department of Neurosciences, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia; Department of Neurology, Alfred Health, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia. Department of Neurosciences, Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia; Department of Neurology, Alfred Health, Level 6, Alfred Centre, 99 Commercial Road, Melbourne, Victoria, 3004, Australia.
 Department of Internal Medicine, Division of Vascular Medicine, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Internal Medicine, Division of Vascular Medicine, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Laboratory Medicine, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Pathology and Medical Biology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Pulmonary Diseases and Tuberculosis, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Pathology and Medical Biology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Internal Medicine, Division of Vascular Medicine, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands. Department of Internal Medicine, Division of Vascular Medicine, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands.
 Schön Klinik Hamburg Eilbek, Hamburg, Germany. University of Pittsburgh and Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania. Hospital Sant Joan de Déu and Universitat de Barcelona, Barcelona, Spain. Indiana University School of Medicine and Riley Hospital for Children at IU Health, Indianapolis. Semmelweis University, Budapest, Hungary. University of Colorado School of Medicine and Children's Hospital Colorado, Aurora. University of Genoa and IRCCS San Martino Polyclinic Hospital, Genoa, Italy. Royal Free London NHS Foundation Trust, London, UK. Scleroderma & Raynaud's United Kingdom, London, UK. University of Milan, ASST G. Pini, Milan, Italy. Hackensack University Medical Center, Hackensack, New Jersey. Charles University, Prague, Czech Republic. Royal Free London, London, UK. Great Ormond Street Hospital, London, UK. Ghent University, Ghent University Hospital, VIB Inflammation Research Center, and ERN ReCONNET, Ghent, Belgium. Children's Hospital Research Institute and University of Washington, Seattle, and Janssen Pharmaceutical Companies of Johnson & Johnson, Spring House, Pennsylvania. German Rheumatism Research Center, Berlin, Germany. University of Michigan, Ann Arbor. Hospital de Santa Maria, Faculdade de Medicina, and Universidade de Lisboa, Lisbon, Portugal. University of Leeds and Leeds Teaching Hospital Trust, Leeds, UK. Asklepios Klinik Nord-Heidberg, Hamburg, Germany. Cerrahpasa Medical School and Istanbul University-Cerrahpasa, Istanbul, Turkey. Alder Hey Children's Foundation NHS Trust, Liverpool, UK. IRCCSG Istituto G. Gaslini, Genoa, Italy. Chinese Organization for Scleroderma, Chengdu City, Sichuan Province, China. University of California, Los Angeles, University of Washington, Seattle, and University of Florence, Florence, Italy.
 School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. Department of Nuclear Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
 Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Gamma Knife Center Cairo, Nasser Institute Hospital, Cairo, Egypt. Neurosurgery Department, Benha University, Qalubya, Egypt. Gamma Knife Center Cairo, Nasser Institute Hospital, Cairo, Egypt. Neurosurgery Department, Ain Shams University, Cairo, Egypt. Gamma Knife Center Cairo, Nasser Institute Hospital, Cairo, Egypt. Neurosurgery Department, Ain Shams University, Cairo, Egypt. Gamma Knife Center Cairo, Nasser Institute Hospital, Cairo, Egypt. Clinical Oncology Department, Ain Shams University, Cairo, Egypt. Gamma Knife Center Cairo, Nasser Institute Hospital, Cairo, Egypt. Neurosurgery Department, Ain Shams University, Cairo, Egypt. Gamma Knife Center Cairo, Nasser Institute Hospital, Cairo, Egypt. Radiation Oncology Department, National Cancer Institute, Cairo University, Cairo, Egypt. Department of Neurosurgery, Koc University School of Medicine, Istanbul, Turkey. Department of Neurosurgery, Koc University School of Medicine, Istanbul, Turkey. Department of Neurosurgery, Neurological Institute, Taipei Veteran General Hospital, Taipei, Taiwan. School of Medicine, National Yang-Ming University, Taipei, Taiwan. Department of Neurosurgery, Neurological Institute, Taipei Veteran General Hospital, Taipei, Taiwan. School of Medicine, National Yang-Ming University, Taipei, Taiwan. Department of Neurosurgery, Université de Sherbrooke, Centre de recherche du CHUS, Sherbrooke, Quebec, Canada. Department of Neurosurgery, Post Graduate Institute of Medical Education and Research, Chandigarh, India. Department of Neurological Surgery, University of Virginia, Charlottesville, Virginia, USA. Department of Neurological Surgery, University of Virginia, Charlottesville, Virginia, USA. Stereotactic and Radiation Neurosurgery, Na Homolce Hospital, Prague, Czech Republic. Stereotactic and Radiation Neurosurgery, Na Homolce Hospital, Prague, Czech Republic. Department of Neurosurgery, University of Alberta, Edmonton, Canada. Department of Neurosurgery, Allegheny Health Network, Pittsburgh, Pennsylvania, USA. Division of Radiation Oncology, Allegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, Pennsylvania, USA. Department of Neurosurgery, Allegheny Health Network, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Virginia, Charlottesville, Virginia, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA. Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
 Department of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia. Department of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia. Graduate School of Biomedicine, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia. Institute of Neuropathology, RWTH Aachen University Medical School, Aachen, Germany. Institute of Neuropathology, RWTH Aachen University Medical School, Aachen, Germany. Amsterdam UMC location University of Amsterdam, Department of Neuropathology, Amsterdam Neuroscience, Amsterdam, the Netherlands. Institute of Neuropathology, RWTH Aachen University Medical School, Aachen, Germany. Department of Neurology, Center for Motor Neuron Biology and Disease, Columbia University, New York, NY, USA. Department of Neurology, Eleanor and Lou Gherig ALS Center, Columbia University, New York, NY, USA. Department of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia. Faculty of Chemistry and Chemical Technology, University of Ljubljana, Ljubljana, Slovenia.
 CanPharmaConsulting, Nottingham, NG9 3BB, UK. canpharmaconsulting@gmail.com. Fertin Pharma, Dandyvej 19, Vejle, 7100, Denmark. Fertin Pharma, Dandyvej 19, Vejle, 7100, Denmark. Fertin Pharma, Dandyvej 19, Vejle, 7100, Denmark. Vectura Fertin Pharma, Basel, Switzerland. Vectura Fertin Pharma, Basel, Switzerland.
 Liverpool Ocular Oncology Centre, Liverpool University Hospitals Trust, Liverpool, UK. K.McLean@liverpool.ac.uk. Department of Eye and Vision Science, Institute of Life Course and Medical Science, University of Liverpool, Liverpool, UK. K.McLean@liverpool.ac.uk. Liverpool Ocular Oncology Centre, Liverpool University Hospitals Trust, Liverpool, UK. Liverpool Ocular Oncology Research Group, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, UK. Liverpool Ocular Oncology Centre, Liverpool University Hospitals Trust, Liverpool, UK. Liverpool Ocular Oncology Research Group, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, UK.
 Statistical Genetics Lab, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. hanxikun2017@gmail.com. Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia. hanxikun2017@gmail.com. Statistical Genetics Lab, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia. School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia. Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Broad Institute of Harvard and MIT, Cambridge, MA, USA. Statistical Genetics Lab, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia. School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia. Mental Health and Neuroscience Program, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Broad Institute of Harvard and MIT, Cambridge, MA, USA. Genomics and Bioinformatics Hub, Brigham and Women's Hospital, Boston, MA, USA. Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Institute of Human Genetics, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany. Twin Research and Genetic Epidemiology, King's College London, London, UK. Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison, Madison, WI, USA. Twin Research and Genetic Epidemiology, King's College London, London, UK. University Hospital Southampton NHS Foundation Trust, Southampton, UK. Faculty of Medicine, University of Southampton, Southampton, UK. Regeneron Pharmaceuticals, Inc., Tarrytown, NY, USA. Division of Research, Kaiser Permanente Northern California (KPNC), Oakland, CA, USA. Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Department of Medicine, Duke University, Durham, NC, USA. Department of Ophthalmology, Duke University, Durham, NC, USA. Singapore Eye Research Institute, Singapore, Singapore. Duke-NUS Medical School, Singapore, Singapore. Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Cleveland Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Department of Ophthalmology, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Retinal Disease Control, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Advanced Ophthalmic Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Ophthalmic Imaging and Information Analytics, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. Department of Ophthalmology, Tohoku University Graduate School of Medicine, Sendai, Japan. Department of Neuroscience, Université de Montréal, Montréal, Quebec, Canada. Neuroscience Division, Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, Quebec, Canada. 23andMe, Inc., Sunnyvale, CA, USA. 23andMe, Inc., Sunnyvale, CA, USA. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Centre for Eye Research Australia, University of Melbourne, Melbourne, Victoria, Australia. Department of Ophthalmology, Flinders Medical Centre, Flinders University, Bedford Park, South Australia, Australia. Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Centre for Ophthalmology and Visual Science, University of Western Australia, Lions Eye Institute, Perth, Western Australia, Australia. Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Broad Institute of Harvard and MIT, Cambridge, MA, USA. NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, UK. Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Broad Institute of Harvard and MIT, Cambridge, MA, USA. Statistical Genetics Lab, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia.
 School of Kinesiology, University of the Fraser Valley, Chilliwack, BC, Canada. Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada. Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada. Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada. Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. National Scleroderma Foundation, Michigan Chapter, Southfield, MI, USA. Clinical Psychology, Radboud University, Nijmegen, The Netherlands. Department of Medical Psychology, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. IQ Healthcare, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. Department of Psychiatry, Radboudumc Center for Mindfulness, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, QC, Canada. Centre for Prognosis Research, School of Primary, Community and Social Care, Keele University, Staffordshire, UK. Department of Psychology, Université du Québec à Montréal, Montreal, QC, Canada. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. Department of Psychology, McGill University, Montreal, QC, Canada. Department of Psychiatry, McGill University, Montreal, QC, Canada. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. Department of Psychology, McGill University, Montreal, QC, Canada. Department of Applied Human Sciences, Concordia University, Montreal, QC, Canada. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. Department of Psychiatry, McGill University, Montreal, QC, Canada. Department of Applied Human Sciences, Concordia University, Montreal, QC, Canada. Department of Community Health Sciences, University of Calgary, Calgary, AB, Canada. Hotchkiss Brain Institute and O'Brien Institute for Public Health, University of Calgary, Calgary, AB, Canada. Department of Medicine, McGill University, Montreal, QC, Canada. Research Institute, McGill University Health Centre, Montreal, QC, Canada. University of Michigan, Ann Arbor, MI, USA. Service de Médecine Interne, Centre de Référence Maladies Auto-immunes et Systémiques Rares d'Ile de France, Hôpital Cochin, Assistance Publique, Hôpitaux de Paris (APHP), Paris, France. APHP-CUP, Hôpital Cochin, Université de Paris, Paris, France. Department of Biostatistics and Health Informatics, King's College London, London, UK. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada. Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, QC, Canada. Department of Psychology, McGill University, Montreal, QC, Canada. Department of Medicine, McGill University, Montreal, QC, Canada. Biomedical Ethics Unit, McGill University, Montreal, QC, Canada. Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada. Department of Oncology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. Department of Psychosocial Resources, Tom Baker Cancer Centre, Cancer Care, Alberta Health Services, Calgary, AB, Canada.
 From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.). From the Department of Radiology, Royal Melbourne Hospital, 300 Grattan St, Parkville, VIC 3050, Australia (J.S.N.T., J.K.C.L., J.B., W.W., P.S., D.G., J.C., D.M.P., S.B.H., F.G., E.L.); and Department of Radiology, University of Melbourne, Melbourne, Australia (J.K.C.L., J.B., W.W., P.S., D.M.P., S.B.H., F.G., E.L.).
 VIB Laboratory of Translational Immunomodulation, Center for Inflammation Research (IRC), Hasselt University, 3590 Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute (BIOMED), Hasselt University, 3590 Diepenbeek, Belgium. VIB Laboratory of Translational Immunomodulation, Center for Inflammation Research (IRC), Hasselt University, 3590 Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute (BIOMED), Hasselt University, 3590 Diepenbeek, Belgium. VIB Laboratory of Translational Immunomodulation, Center for Inflammation Research (IRC), Hasselt University, 3590 Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute (BIOMED), Hasselt University, 3590 Diepenbeek, Belgium. Environmental Biology, Centre for Environmental Sciences, Hasselt University, Agoralaan Building D, 3590 Diepenbeek, Belgium. Environmental Biology, Centre for Environmental Sciences, Hasselt University, Agoralaan Building D, 3590 Diepenbeek, Belgium. Department of Plant Physiology and Biophysics, Institute of Biological Sciences, Maria Curie-Skłodowska University, 20-033 Lublin, Poland. Experimental and Clinical Research Center, A Joint Cooperation of Max-Delbrück-Center for Molecular Medicine and Charité-Universitätsmedizin, 13125 Berlin, Germany. Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), 13125 Berlin, Germany. Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 13125 Berlin, Germany. Department of Microbiome Research, Friedrich-Alexander-University Erlangen-Nürnberg, 91054 Erlangen, Germany. Department of Medicine II, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany. VIB Laboratory of Translational Immunomodulation, Center for Inflammation Research (IRC), Hasselt University, 3590 Diepenbeek, Belgium. Department of Immunology and Infection, Biomedical Research Institute (BIOMED), Hasselt University, 3590 Diepenbeek, Belgium. University Multiple Sclerosis Center (UMSC), Hasselt University/Campus Diepenbeek, 3590 Diepenbeek, Belgium.
 IRCCS Istituto Ortopedico Galeazzi, Milan, Italy. Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy. Department of Translational Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy. Interdepartmental Research Center for the Study of Multiple Sclerosis and Inflammatory and Degenerative Diseases of the Nervous System, University of Ferrara, Ferrara, Italy. Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy. National Institute of Molecular Genetics "Romeo ed Enrica Invernizzi" (INGM), Milan, Italy. Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy. Department of Chemical Pharmaceutical and Agricultural Sciences, University of Ferrara, Ferrara, Italy. IRCCS Istituto Ortopedico Galeazzi, Milan, Italy. Department of Chemical Pharmaceutical and Agricultural Sciences, University of Ferrara, Ferrara, Italy. Department of Translational Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy. Department of Translational Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy. Biological and Chemical Research Centre (CNBCh UW), University of Warsaw, Warsaw, Poland. Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy. Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.
 Department of Physical Medicine and Rehabilitation, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. johnsoj8@ccf.org. Center for Value-Based Care Research, Cleveland Clinic, Cleveland, OH, USA. johnsoj8@ccf.org. Department of Hospital Medicine, Cleveland Clinic, Cleveland, OH, USA. Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA. Department of Healthcare Delivery and Population Science, University of Massachusetts Medical School-Baystate, Springfield, USA. Department of Healthcare Delivery and Population Science, University of Massachusetts Medical School-Baystate, Springfield, USA. Mellen Center for Treatment and Research in Multiple Sclerosis, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Center for Geriatric Medicine, Cleveland Clinic, Cleveland, OH, USA. Office of Nursing Research and Innovation, and Consultant Staff, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Penn Medicine Lancaster General Hospital, Lancaster, PA, USA. Center for Value-Based Care Research, Cleveland Clinic, Cleveland, OH, USA. Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA. Population Health Research Institute, Case Western Reserve University at MetroHealth System, Cleveland, OH, USA. Center for Value-Based Care Research, Cleveland Clinic, Cleveland, OH, USA. Rehabilitation and Sports Therapy, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA. Center for Value-Based Care Research, Cleveland Clinic, Cleveland, OH, USA.
 Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL. Department of Laboratory Medicine and Pathology (EO, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; Department of Neurology (CV-S, NZ), Mayo Clinic, AZ; Department of Neurology (JB, DD, EPF, AZ, SJP, AM), Mayo Clinic, Rochester, MN; and Department of Neurology (ASL-C), Mayo Clinic, FL.
 Department of Neurology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia. Department of Neurology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia. Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado, Aurora, CO, USA. Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology and Clinical Investigation Center, Strasbourg University Hospital Center, Strasbourg, France. Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Division of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan. Department of Neurology, San Carlos Clinical Hospital, Madrid, Spain. Department of Medicine, Complutense University of Madrid, Madrid, Spain. Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford, UK. Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin, corporate member of Free University of Berlin, Humboldt University of Berlin, and Berlin Institute of Health, Berlin, Germany. Max Delbrück Center for Molecular Medicine, Berlin, Germany. Department of Human Neuroscience, Sapienza University, Rome, Italy. Alexion, AstraZeneca Rare Disease, Boston, MA, USA. Alexion, AstraZeneca Rare Disease, Boston, MA, USA. Alexion, AstraZeneca Rare Disease, Boston, MA, USA. Department of Neurology, National Cancer Center, Goyang, South Korea.
 Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Research Institute of Animuscure INC, Suwon, South Korea. Research Institute of Animuscure INC, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. College of Pharmacy, Sookmyung Women's University, Seoul, South Korea. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, South Korea. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, South Korea.
 Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA, United States. Department of Pathology, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, United States. Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Department of Neuroscience, Baylor College of Medicine, Houston, TX, United States. School of Medicine, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, United States. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Department of Neuroscience, Baylor College of Medicine, Houston, TX, United States. Department of Neurology, Mayo Clinic Foundation, Rochester, MN, United States. Department of Laboratory Medicine and Pathology, Mayo Clinic Foundation, Rochester, MN, United States. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN, United States. Department of Neurology, Mayo Clinic Foundation, Rochester, MN, United States. Department of Laboratory Medicine and Pathology, Mayo Clinic Foundation, Rochester, MN, United States. Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, CA, United States. Chan Zuckerberg Biohub, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States. Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States. Department of Neurology, University of California, San Francisco, San Francisco, CA, United States.
 Department of Neurology, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Arnold-Heller-Str. 3, 24105, Kiel, Germany. n.margraf@neurologie.uni-kiel.de. Institute of Clinical Chemistry, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Kiel, Germany. Department of Neurology, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Arnold-Heller-Str. 3, 24105, Kiel, Germany. Department of Neurology, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Arnold-Heller-Str. 3, 24105, Kiel, Germany. Institute of Clinical Chemistry, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Kiel, Germany. Institute of Epidemiology and Biobank PopGen, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Kiel, Germany. Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel and University Hospital Schleswig-Holstein, Kiel, Germany. Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany. Multiple Sclerosis Centre, Neurology, Departments of Head, Spine and Neuromedicine, Biomedicine and Clinical Research, University Hospital Basel and University of Basel, Basel, Switzerland. Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital and University of Basel, Basel, Switzerland. Department of Neurology, University Hospital Schleswig-Holstein (UKSH), Christian-Albrechts-University (CAU), Arnold-Heller-Str. 3, 24105, Kiel, Germany.
 The Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. National Hospital for Neurology and Neurosurgery, University College London Hospitals Foundation NHS Trust, London, UK. Medical Statistics Department, London School of Hygiene and Tropical Medicine, London, UK. The Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. The Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Department of Medical Physics and Biomedical Engineering, Centre for Medical Image Computing, UCL, London, UK. e-Health Centre, Open University of Catalonia, Barcelona, Spain. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Centre for Medical Image Computing, Department of Computer Science, University College London, London, UK. Radiomics Group, Vall d'Hebron Institute of Oncology, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Department of Medical Physics and Biomedical Engineering, Centre for Medical Image Computing, UCL, London, UK. Oxford Eye Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. Vision and Eye Research Institute, Anglia Ruskin University, Cambridge, UK. Oxford Eye Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. Oxford Eye Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. NIHR Clinical Research Network, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. Gene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, UK. Gene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Brain MRI 3T Research Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. NIHR Clinical Research Network, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. Oxford Centre for Genomic Medicine, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Gene Control Mechanisms and Disease Group, Department of Medicine, Division of Brain Sciences and MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, UK. National Hospital for Neurology and Neurosurgery, University College London Hospitals Foundation NHS Trust, London, UK. The Ataxia Centre, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. National Hospital for Neurology and Neurosurgery, University College London Hospitals Foundation NHS Trust, London, UK.
 Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Section of Molecular Immunology und Gastroenterology, I. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Section of Molecular Immunology und Gastroenterology, I. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Department of Computational Neuroscience, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Department of Computational Neuroscience, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Microscopy Imaging Facility (UMIF), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Centre Göttingen, 37075 Göttingen, Germany. Unité de Chronobiologie Théorique, Faculté des Sciences, CP231, Université Libre de Bruxelles (ULB), B-1050 Brussels, Belgium. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany. Calcium Signalling Group, Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
 Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg (ZMNH), University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg (ZMNH), University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany. Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany. Department of Neurosurgery, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, 20246, Hamburg, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany. n.schweingruber@uke.de.
 Department of Neurology, West China Hospital, Sichuan University, Chengdu, China. Mental Health Center, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, China. University College London Queen Square Institute of Neurology, London, UK. Chalfont Centre for Epilepsy, Chalfont St Peter, UK. Stichting Epilepsie Instellingen Nederland, Heemstede, the Netherlands. Department of Neurology, West China Hospital, Sichuan University, Chengdu, China. Department of Neurology, West China Hospital, Sichuan University, Chengdu, China.
 Department of Pediatric Rheumatology and Nephrology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. RINGGOLD: 71068 Department of Pediatric Rheumatology and Nephrology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. RINGGOLD: 71068 Department of Nephrology, Guangzhou Women and Children's Medical Center, Guangzhou, China. RINGGOLD: 159390 Department of Nephrology, Rheumatology and Immunology, Fujian Children's Hospital, Fuzhou, China. College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, China. Department of Pediatric Rheumatology and Nephrology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. RINGGOLD: 71068 Department of Pediatric Rheumatology and Nephrology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. RINGGOLD: 71068 Department of Pediatric Rheumatology and Nephrology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. RINGGOLD: 71068 Department of Nephrology, Rheumatology and Immunology, Fujian Children's Hospital, Fuzhou, China. College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, China. Department of Nephrology, Guangzhou Women and Children's Medical Center, Guangzhou, China. RINGGOLD: 159390 Department of Pediatric Rheumatology and Nephrology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. RINGGOLD: 71068
 Department of Neuroscience and Experimental Therapeutics, School of Medicine, Texas A&M University Health Science Center, Bryan, TX, USA; Texas A&M Health Institute of Pharmacology and Neurotherapeutics, School of Medicine, Texas A&M University, Bryan, TX, USA; Engineering Medicine, Intercollegiate School of Engineering Medicine, Texas A&M University, Houston, TX, USA; Department of Biomedical Engineering, College of Engineering, Texas A&M University, College Station, TX, USA; Department of Veterinary Integrative Biosciences, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX, USA. Electronic address: sambareddy@tamu.edu.
 Department of Neurology, University of Utah, Salt Lake City, UT. Department of Neurology, University of Utah, Salt Lake City, UT. Department of Neurology, University of Utah, Salt Lake City, UT. Department of Neurology, University of Utah, Salt Lake City, UT. Center for NeuroGenetics and Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL. Center for NeuroGenetics and Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL. Department of Neurology, University of Utah, Salt Lake City, UT. Department of Neurology, University of Utah, Salt Lake City, UT.
 Department of Respiratory Medicine, The First Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. Center of Molecular Diagnosis and Therapy, The Second Hospital of Fujian Medical University, Quanzhou, Fujian Province, China. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. Center of Molecular Diagnosis and Therapy, The Second Hospital of Fujian Medical University, Quanzhou, Fujian Province, China. Center of Molecular Diagnosis and Therapy, The Second Hospital of Fujian Medical University, Quanzhou, Fujian Province, China. zeng_yiming@fjmu.edu.cn. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. wuduojiao@126.com. Department of Respiratory Medicine, The First Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China. wzchencs@163.com. Quzhou Hospital of Wenzhou Medical University, Quzhou, Zhejiang Province, China. wzchencs@163.com. Jinshan Hospital Centre for Tumor Diagnosis and Therapy, Department of Oncology, Fudan University Shanghai Medical College, Shanghai, China. xdwang@fuccb.com. Center of Molecular Diagnosis and Therapy, The Second Hospital of Fujian Medical University, Quanzhou, Fujian Province, China. xdwang@fuccb.com.
 Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil. Department of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil. Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil. Department of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil. Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
 Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Medicine and Women's Guild Lung Institute and. Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
 Graduated, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Biostatistics and Data Science, School of Public Health, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77030, USA. Graduated, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Graduated, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. Girona University, Girona, Spain. Graduated, Faculty of Nursing, Bushehr University of Medical Sciences, Bushehr, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Bone and Joint Diseases Research Center, Department of Orthopedic Surgery, Shiraz University of Medical Sciences, Shiraz, Iran. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. School of Medicine, Jahrom University of Medical Sciences, Jahrom, Iran. School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. Islamic University of Azad Medical Branch, Tehran, Iran. School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Mashhad University of Medical Sciences, Mashhad, Iran. School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran. School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Firoozabadi hospital clinical research development unit (FHCRDU), Department of internal medicine, school of medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Islamic Azad University, Tehran, Iran. Graduated, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Department of Radiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Legal Medicine Research Center, Iranian Legal Medicine Organization, Tehran, Iran. ERIS Research Institute, Tehran, Iran. University of Psychology Sciences, South Azad Tehran, Iran. Dental and Periodontal Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Students Research Committee, Faculty of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran. Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, California, USA. Islamic Azad University of Najafabad, Najafabad, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Department of Orthopedic Surgery, Kerman University of Medical Sciences, Kerman, Iran. School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Department of Clinical Laboratory Sciences, School of Allied Medicine, Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran. ERIS Research Institute, Tehran, Iran.
 Neuroimmunology Clinic and Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Rabin Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Ophthalmology and Neurology, Mayo Clinic, Rochester, MN, USA. Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department of Neurology, Great Ormond Street Hospital for Children, London, UK. Queen Square Multiple Sclerosis Centre, UCL Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK. Department of Neurology, Great Ormond Street Hospital for Children, London, UK. Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. Department of Neurology, Walton Centre NHS Foundation Trust, Liverpool, UK. Department of Neurology, Walton Centre NHS Foundation Trust, Liverpool, UK. Rabin Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Rabin Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Rabin Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Department of Neurology, Mayo Clinic, Rochester, MN, USA. Center for MS and Autoimmune Neurology, Mayo Clinic, Rochester, MN, USA. Neuroimmunology Clinic and Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Neuroimmunology Clinic and Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Neuroimmunology Clinic and Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Neuroimmunology Clinic and Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Experimental and Clinical Research Center, A Cooperation Between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and the Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, NeuroCure Clinical Research Center, Berlin, Germany. Max Delbrueck Center for Molecular Medicine, Experimental and Clinical Research Center, Berlin, Germany. Neuroimmunology Clinic and Research Laboratory, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
 Department of Neurology, Ludwig Maximilians University Munich, Marchioninistr. 15, 81377, Munich, Germany. susanne.schneider@med.uni-muenchen.de. Department of Neurology, Shree Krishna Hospital, Pramukhswami Medical College, Bhaikaka University, Karamsad, Anand, Gujarat, India. Chulalongkorn Centre of Excellence for Parkinson's Disease and Related Disorders, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, 1873 Rama 4 Road, Bangkok, Thailand. Department of Neurology, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania. Chulalongkorn Centre of Excellence for Parkinson's Disease and Related Disorders, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, 1873 Rama 4 Road, Bangkok, Thailand. Departments of Neurology, Neurosurgery, and Medicine Boston University School of Medicine and Boston Medical Center, Boston, USA. Neuroimmunology and Multiple Sclerosis Unit of Girona, University Hospital Dr. Josep Trueta of Girona, Girona, Catalonia, Spain. Movement Disorders Unit, Neurology Service, Internal Medicine Department, UFMG, Belo Horizonte, Brazil. Departments of Neurology, Neurosurgery, and Medicine Boston University School of Medicine and Boston Medical Center, Boston, USA. Department of Neurology, Shree Krishna Hospital, Pramukhswami Medical College, Bhaikaka University, Karamsad, Anand, Gujarat, India. Faculty of Medicine and Health Sciences, Translational Neurosciences, University of Antwerp, Antwerp, Belgium. Department of Neurology, Antwerp University Hospital, Antwerp, Belgium. Faculty of Medicine and Health Sciences, Translational Neurosciences, University of Antwerp, Antwerp, Belgium. Department of Neurology, Antwerp University Hospital, Antwerp, Belgium. Division of Neurology, Edmond J. Safra Program in Parkinson's Disease, Morton and Gloria Shulman Movement Disorders Clinic, Toronto Western Hospital - UHN, University of Toronto, Toronto, ON, Canada. Movement Disorders Unit, Neurology Department, Hospital General Universitario Gregorio Marañón, Madrid, Spain. Institut Fresnel, Nuclear Medicine Department, Aix Marseille Univ, APHM, CNRS, Centrale Marseille, Timone Hospital, CERIMED, Marseille, France. Neurology Department, Hospital 12 de Octubre, Madrid, Spain. Shaheed Zulfiqar Ali Bhutto Medical University, Islamabad, Pakistan. Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA. Division of Neurology, Edmond J. Safra Program in Parkinson's Disease, Morton and Gloria Shulman Movement Disorders Clinic, Toronto Western Hospital - UHN, University of Toronto, Toronto, ON, Canada. Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA. Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy. Department of Neurology, Columbia University Vagelos College of Physicians and Surgeons, New York, USA. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Movement Disorders Unit, Neurology Department, Hospital General Universitario Gregorio Marañón, Madrid, Spain. Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, USA. Neurology Department, Ramon y Cajal University Hospital, Madrid, Spain. Departmemt of Neurology and Neurorehabilitation, Hospital Zum Heiligen Geist, Academic Teaching Hospital of the Heinrich-Heine-University Duesseldorf, Kempen, Germany. Privya Neurology Clinic, Ahmedabad, Gujarat, India. Departmemt of Neurology and Neurorehabilitation, Hospital Zum Heiligen Geist, Academic Teaching Hospital of the Heinrich-Heine-University Duesseldorf, Kempen, Germany. Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, Karnataka, India.
 Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. Institute for Advanced Biosciences, Keio University, Tsuruoka, Japan. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Psychiatry, Hokkaido University Graduate School of Medicine, Hokkaido, Japan. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan. Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan. Hills Joint Research Laboratory for Future Preventive Medicine and Wellness, Keio University School of Medicine, Tokyo, Japan. Departments of Mechanical Engineering and Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA. School of Electrical, Computer and Biomedical Engineering, Southern Illinois University, Carbondale, IL, USA. Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan. Departments of Mechanical Engineering and Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA. Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan. Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL, USA. Institute for Advanced Biosciences, Keio University, Tsuruoka, Japan. Gut Environmental Design Group, Kanagawa Institute of Industrial Science and Technology, Kawasaki, Japan. Transborder Medical Research Center, University of Tsukuba, Tsukuba, Japan. Laboratory for Regenerative Microbiology, Graduate School of Medicine, Juntendo University, Tokyo, Japan. Department of Psychiatry, School of Medicine, Showa University, Tokyo, Japan. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. akamiya1@jhmi.edu.
 Neurologia-Stroke Unit ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy. Stroke Research Centre, Department of Brain Repair and Rehabilitation, Queen Square Institute of Neurology, University College London, and National Hospital for Neurology and Neurosurgery, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Department of Medical Physics and Biomedical Engineering, Centre for Medical Image Computing, UCL, London, UK. National Institute for Health Research, University College London Hospitals, Biomedical Research Centre, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Department of Medical Physics and Biomedical Engineering, Centre for Medical Image Computing, UCL, London, UK. National Institute for Health Research, University College London Hospitals, Biomedical Research Centre, London, UK. E-Health Center, Universitat Oberta de Catalunya, Barcelona, Spain. Stroke Research Centre, Department of Brain Repair and Rehabilitation, Queen Square Institute of Neurology, University College London, and National Hospital for Neurology and Neurosurgery, London, UK. Stroke Research Centre, Department of Brain Repair and Rehabilitation, Queen Square Institute of Neurology, University College London, and National Hospital for Neurology and Neurosurgery, London, UK. Lysholm Department of Neuroradiology and the Neuroradiological Academic Unit, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, Queen Square, London, UK. Department of Statistical Science, University College London, Gower Street, London, UK. NMR Research Unit, Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, University College London (UCL) Queen Square Institute of Neurology, Faculty of Brain Sciences, UCL, London, UK. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Brain Connectivity Center, IRCCS Mondino Foundation, Pavia, Italy. Stroke Research Centre, Department of Brain Repair and Rehabilitation, Queen Square Institute of Neurology, University College London, and National Hospital for Neurology and Neurosurgery, London, UK. d.werring@ucl.ac.uk.
 Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, 20251, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Experimental Immunology; Amsterdam Infection & Immunity Institute, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, 1105 AZ, The Netherlands. Department of Pediatrics, Emma Children's Hospital, Amsterdam University Medical Center, University of Amsterdam and Vrije Universiteit Amsterdam, Amsterdam, 1105 AZ, The Netherlands. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Partner Site Hamburg-Lübeck-Borstel-Riems, German Center for Infection Research (DZIF), Hamburg, 20246, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. University of Bordeaux, Institut National de la Santé et de la Recherche Médicale, Bordeaux Population Health Research Center UMR1219 and INRIA SISTM Team, Bordeaux, 33000, France. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Institute of Anatomy and Experimental Morphology, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Pediatrics, Emma Children's Hospital, Amsterdam University Medical Center, University of Amsterdam and Vrije Universiteit Amsterdam, Amsterdam, 1105 AZ, The Netherlands. Department of Experimental Immunology; Amsterdam Infection & Immunity Institute, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, 1105 AZ, The Netherlands. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. Department of Pathology, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, 1105 AZ, The Netherlands. Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Rheumatology and Clinical Immunology and Department of Experimental Immunology, Amsterdam Infection & Immunity Institute, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, 1007 MB, The Netherlands. Amsterdam Rheumatology & Immunology Center, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, 1105 AZ, The Netherlands. Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Institute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Pediatric Surgery, Altona Children's Hospital, Hamburg, 22763, Germany. Institute of Anatomy and Experimental Morphology, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, 20251, Germany. Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. Department of Virus Immunology, Leibniz Institute of Virology, Hamburg, 20251, Germany. madeleine.bunders@leibniz-liv.de. III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany. madeleine.bunders@leibniz-liv.de.
 RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. Leibniz Group 'Dendritic Organelles and Synaptic Function', Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. Center for Behavioral Brain Sciences, Otto von Guericke University, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. Department of Cellular Neuroscience, Leibniz Institute for Neurobiology, Magdeburg, Germany. German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. Department of Cellular Neuroscience, Leibniz Institute for Neurobiology, Magdeburg, Germany. German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Molecular Imaging in Neurosciences, Paul Flechsig Institute of Brain Research, Leipzig, Germany. Department of Systems Physiology of Learning and Memory, Leibniz Institute for Neurobiology, Magdeburg, Germany. Institute of Neuroimmunology and Multiple Sclerosis, Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Molecular Imaging in Neurosciences, Paul Flechsig Institute of Brain Research, Leipzig, Germany. Department of Biochemistry and Physiology, Faculty of Pharmacy and Food Science, University of Barcelona, Barcelona, Spain. Institut de Neurociències de la Universitat de Barcelona, Barcelona, Spain. Center for Behavioral Brain Sciences, Otto von Guericke University, Magdeburg, Germany. Department of Cellular Neuroscience, Leibniz Institute for Neurobiology, Magdeburg, Germany. German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. Institute of Anatomy and Molecular Neurobiology, Westfälische Wilhelms-University, Münster, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. Center for Behavioral Brain Sciences, Otto von Guericke University, Magdeburg, Germany. RG Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany. Leibniz Group 'Dendritic Organelles and Synaptic Function', Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Center for Behavioral Brain Sciences, Otto von Guericke University, Magdeburg, Germany. German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany.
 Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Mail Stop C238, 12850 E. Montview Blvd., Aurora, CO, 80045, USA. robert.mcqueen@cuanschutz.edu. Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Mail Stop C238, 12850 E. Montview Blvd., Aurora, CO, 80045, USA. Syreon Research Institute, Budapest, Hungary. School of Medicine, Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Mail Stop C238, 12850 E. Montview Blvd., Aurora, CO, 80045, USA. School of Medicine, Department of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Syreon Research Institute, Budapest, Hungary. Syreon Research Institute, Budapest, Hungary. Center for Health Technology Assessment, Semmelweis University, Budapest, Hungary. Syreon Research Institute, Budapest, Hungary. Center for Health Technology Assessment, Semmelweis University, Budapest, Hungary.
 Department of Integrated Program in Neuroscience, McGill University, Montreal, Quebec, Canada. Translational Research in Respiratory Diseases, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada. Department of Medicine and Department of Epidemiology, Biostatistics & Occupational Health, McGill University Health Centre, Montreal, Quebec, Canada. Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada. Montreal Neurological Hospital, McGill University Centre, Montreal, Quebec, Canada. Respiratory Division and Sleep Laboratory, McGill University Health Centre, Montreal, Quebec, Canada. Respiratory Division and Sleep Laboratory, McGill University Health Centre, Montreal, Quebec, Canada. Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada. Respiratory Division and Sleep Laboratory, McGill University Health Centre, Montreal, Quebec, Canada.
 School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, PR China. Electronic address: ls18845611672@163.com. School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, PR China. Electronic address: 957782420@qq.com. School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, PR China. Electronic address: guifangfan99@163.com. School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, PR China. Electronic address: liurunping@bucm.edu.cn.
 Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Shanghai Geriatric Institute of Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200031, China. Electronic address: liute1979@shutcm.edu.cn. Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn.
 Dementia Research Centre, Institute of Neurology, University College London, London, UK. Dementia Research Centre, Institute of Neurology, University College London, London, UK. Dementia Research Centre, Institute of Neurology, University College London, London, UK. National Hospital for Neurology and Neurosurgery, University College London Hospitals, London, UK. Dementia Research Centre, Institute of Neurology, University College London, London, UK. Department of Medical Statistics, London School of Hygiene and Tropical Medicine, London, UK. Moorfields Eye Hospital, London, UK. UCL Queen Square Institute of Neurology, London, UK. UCL Queen Square Institute of Neurology, London, UK. Institute of Ophthalmology, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK. Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, UK. National Institute for Health Research, University College London Hospitals Biomedical Research Centre, London, UK. MRC CTU at UCL, Institute of Clinical Trials and Methodology, University College London, London, UK. Movement Disorders Centre, University College London, London, UK. Dementia Research Centre, Institute of Neurology, University College London, London, UK r.weil@ucl.ac.uk. National Hospital for Neurology and Neurosurgery, University College London Hospitals, London, UK. Movement Disorders Centre, University College London, London, UK. The Wellcome Centre for Human Neuroimaging, Institute of Neurology, University College London, London, UK.
 Department of Neurology and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA. Sorbonne Université, Institut du Cerveau ICM, Paris Brain Institute, Inserm, CNRS, Assistance Publique - Hôpitaux de Paris, Hôpital de la Pitié-Salpêtrière, DMU Neurosciences 6, Paris, France. Assistance Publique - Hôpitaux de Paris, Hôpital de la Pitié-Salpêtrière, DMU Neurosciences 6, Epilepsy Unit and Department of Clinical Neurophysiology, Paris, France. Comprehensive Epilepsy Center, Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA. Universidad Autonoma de Centro America, School of Medicine, San Jose, Costa Rica. Comprehensive Epilepsy Center, Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA. Nebraska Medical Center, Omaha, Nebraska, USA. Comprehensive Epilepsy Center, Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA. Department of (Neuro) Pathology, Amsterdam Neuroscience, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands. Division of Neurology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Epilepsy NeuroGenetics Initiative, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Department of Biomedical and Health Informatics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Division of Neurology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Epilepsy NeuroGenetics Initiative, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Department of Biomedical and Health Informatics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Division of Experimental Neurology, Mayo Clinic, Rochester, Minnesota, USA. Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA. Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA. Department of Pediatrics, Children's Hospital Medical Center, University of Nebraska, Omaha, Nebraska, USA. Sorbonne Université, Institut du Cerveau ICM, Paris Brain Institute, Inserm, CNRS, Assistance Publique - Hôpitaux de Paris, Hôpital de la Pitié-Salpêtrière, DMU Neurosciences 6, Paris, France. Assistance Publique - Hôpitaux de Paris, Hôpital de la Pitié-Salpêtrière, DMU Neurosciences 6, Epilepsy Unit and Department of Clinical Neurophysiology, Paris, France. Department of Neurological Sciences, University of Nebraska Medical Center, Omaha, Nebraska, USA. Department of Acute Brain Injury, Istituto di Recerche Farmacologiche Mario Negri IRCCS, Milan, Italy. Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, California, San Francisco, USA. Division of Neurology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Epilepsy NeuroGenetics Initiative, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Department of Biomedical and Health Informatics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. Comprehensive Epilepsy Center, Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA. Université Libre de Bruxelles, Hôpital Erasme, Brussels, Belgium. Comprehensive Epilepsy Center, Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA.
 Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany carolin.beuker@ukmuenster.de. Institute of Biostatistics and Clinical Research, University of Muenster, Muenster, Germany. Institute of Biostatistics and Clinical Research, University of Muenster, Muenster, Germany. Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany. WIdO, AOK Research Institute, Berlin, Germany. WIdO, AOK Research Institute, Berlin, Germany. WIdO, AOK Research Institute, Berlin, Germany. Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany. Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Muenster, Muenster, Germany. Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany.
 Department of Neurology and Institute of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. Department of Neurology and Institute of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, College of Life Sciences, Shaanxi Normal University, Xi'an, China. Department of Neurology of The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, College of Life Sciences, Shaanxi Normal University, Xi'an, China. Immuno-oncology Branch, Research Institute of the National Cancer Center, Goyang, Korea. Immuno-oncology Branch, Research Institute of the National Cancer Center, Goyang, Korea. Department of Neurology of The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Department of Neurology of The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Department of Neurology of The Second People's Hospital of Zhaoqing, Zhaoqing, China. Department of Neurology and Institute of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. Department of Neurology and Institute of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. Immuno-oncology Branch, Research Institute of the National Cancer Center, Goyang, Korea. Department of Neurology, Hospital of the National Cancer Center, Goyang, Korea. Department of Neurology of The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
 Division of Transfusion Medicine, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA. Division of Transfusion Medicine, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Division of Transfusion Medicine, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA. Division of Transfusion Medicine, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Division of Transfusion Medicine, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA. Division of Transfusion Medicine, Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, School of Medicine, 600 North Wolfe Street, Pathology 627, Baltimore, MD 21287, USA.
 Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland. Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, University College London, London, UK. Department of Neurophysics, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; Felix Bloch Institute for Solid State Physics, Faculty of Physics and Earth Sciences, Leipzig University, Leipzig, Germany. Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland. Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland; Department of Neurophysics, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; Wellcome Trust Centre for Neuroimaging, UCL Queen Square Institute of Neurology, University College London, London, UK. Electronic address: patrick.freund@balgrist.ch.
 Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. INMED, INSERM, Aix Marseille University, 13284 Marseille, France. INMED, INSERM, Aix Marseille University, 13284 Marseille, France. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Janssen Research & Development, LLC, San Diego, California 92121, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. INMED, INSERM, Aix Marseille University, 13284 Marseille, France. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States. Department of Chemistry, Emory University, Atlanta, Georgia 30322, United States. Department of Pharmacology and Chemical Biology, Emory University, Atlanta, Georgia 30322, United States.
 Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California 94158. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Transposon Therapeutics, San Diego, California 92122. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Department of Psychological Science, University of Arkansas, Fayetteville, Arkansas 72701. Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095. Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Global Brain Health Institute, University of California, San Francisco, San Francisco, California 94158, and Trinity College Dublin, Dublin, Ireland. Department of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Global Brain Health Institute, University of California, San Francisco, San Francisco, California 94158, and Trinity College Dublin, Dublin, Ireland. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine of USC, University of Southern California, Los Angeles, California 90033. Department of Genetics, Stanford University School of Medicine, Stanford, California 94305. Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California 94158. Transposon Therapeutics, San Diego, California 92122. Transposon Therapeutics, San Diego, California 92122. Transposon Therapeutics, San Diego, California 92122. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Global Brain Health Institute, University of California, San Francisco, San Francisco, California 94158, and Trinity College Dublin, Dublin, Ireland. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Global Brain Health Institute, University of California, San Francisco, San Francisco, California 94158, and Trinity College Dublin, Dublin, Ireland. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Department of Pathology, University of California, San Francisco, San Francisco, California 94158. Department of Neurosciences, ALS Translational Research, University of California, San Diego, La Jolla, California 92093. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158. Global Brain Health Institute, University of California, San Francisco, San Francisco, California 94158, and Trinity College Dublin, Dublin, Ireland. Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, California 94158 jennifer.yokoyama@ucsf.edu. Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California 94158. Global Brain Health Institute, University of California, San Francisco, San Francisco, California 94158, and Trinity College Dublin, Dublin, Ireland.
 British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Department of Human Genetics, The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1HH, UK. Medical Research Council Biostatistics Unit, University of Cambridge, East Forvie Building, Cambridge Biomedical Campus, Forvie Site, Robinson Way, Cambridge, CB2 0SR, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Department of Human Genetics, The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1HH, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. British Heart Foundation Centre of Research Excellence, University of Cambridge, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, CB2 0BB, UK. Department of Human Genetics, The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1HH, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. Division of Hematology/Oncology, Boston Children's Hospital, Harvard Medical School, 1 Blackfan Circle, Boston, MA, 02115, USA. Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Ave, Boston, MA, 02115, USA. Broad Institute of MIT and Harvard, 415 Main St, Cambridge, MA, 02142, USA. Harvard-MIT Health Sciences and Technology, Harvard Medical School, 77 Massachusetts Ave, Cambridge, MA, 02139, USA. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. Department of Haematology, Barts Health National Health Service Trust, London, E1 1BB, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Institute for Health and Care Research Cambridge BioResource, Box 229, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, CB2 0BB, UK. Wellcome Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SD, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Institute for Health and Care Research Cambridge BioResource, Box 229, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Institute for Health and Care Research Cambridge BioResource, Box 229, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SD, UK. European Molecular Biology Laboratory, Genome Biology Unit, 69117, Heidelberg, Germany. Division of Computational Genomics and Systems Genetics, German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. Division of Hematology/Oncology, Boston Children's Hospital, Harvard Medical School, 1 Blackfan Circle, Boston, MA, 02115, USA. Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Ave, Boston, MA, 02115, USA. Broad Institute of MIT and Harvard, 415 Main St, Cambridge, MA, 02142, USA. Department of Human Genetics, The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1HH, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Department of Human Genetics, The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1HH, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. British Heart Foundation Centre of Research Excellence, University of Cambridge, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, CB2 0BB, UK. Health Data Research UK Cambridge, Wellcome Genome Campus and University of Cambridge, Cambridge, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Nuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, University of Oxford, Headley Way, Headington, Oxford, OX3 9DU, UK. National Institute for Health Research Oxford Biomedical Research Centre-Haematology Theme, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, UK. National Health Service Blood and Transplant, Oxford Centre, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. British Heart Foundation Centre of Research Excellence, University of Cambridge, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, CB2 0BB, UK. Health Data Science Research Centre, Fondazione Human Technopole, Viale Rita Levi Montalcini 1, Milan, 20157, Italy. Division of Hematology/Oncology, Boston Children's Hospital, Harvard Medical School, 1 Blackfan Circle, Boston, MA, 02115, USA. Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Ave, Boston, MA, 02115, USA. Broad Institute of MIT and Harvard, 415 Main St, Cambridge, MA, 02142, USA. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. Department of Clinical and Biomedical Sciences, University of Exeter Medical School, Faculty of Health and Life Sciences, RILD Building, Barrack Road, Exeter, EX2 5DW, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. Medical Research Council Biostatistics Unit, University of Cambridge, East Forvie Building, Cambridge Biomedical Campus, Forvie Site, Robinson Way, Cambridge, CB2 0SR, UK. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, CB2 0BB, UK. Department of Pediatric Immunology, Rheumatology and Infectious Disease, Emma Children's Hospital, Amsterdam University Medical Center, Amsterdam, CB2 0PT, UK. Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Sanquin, University of Amsterdam, Amsterdam, Netherlands. Health Data Research UK Cambridge, Wellcome Genome Campus and University of Cambridge, Cambridge, UK. Department of Immunology and Inflammation, Imperial College London, Commonwealth Building, The Hammersmith Hospital, Du Cane Road, London, W12 0NN, UK. British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. asb38@medschl.cam.ac.uk. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. asb38@medschl.cam.ac.uk. British Heart Foundation Centre of Research Excellence, University of Cambridge, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. asb38@medschl.cam.ac.uk. Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, CB2 0BB, UK. asb38@medschl.cam.ac.uk. Health Data Research UK Cambridge, Wellcome Genome Campus and University of Cambridge, Cambridge, UK. asb38@medschl.cam.ac.uk. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. who1000@cam.ac.uk. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. who1000@cam.ac.uk. Department of Haematology, University College London Hospitals, WC1E 6AS, London, UK. who1000@cam.ac.uk. Department of Human Genetics, The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1HH, UK. ns6@sanger.ac.uk. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. ns6@sanger.ac.uk. Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. ns6@sanger.ac.uk. British Heart Foundation Centre of Research Excellence, University of Cambridge, Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK. ns6@sanger.ac.uk. Genomics Research Centre, Fondazione Human Technopole, Viale Rita Levi Montalcini 1, Milan, 20157, Italy. ns6@sanger.ac.uk. Medical Research Council Biostatistics Unit, University of Cambridge, East Forvie Building, Cambridge Biomedical Campus, Forvie Site, Robinson Way, Cambridge, CB2 0SR, UK. wja24@cam.ac.uk. The National Institute for Health and Care Research Blood and Transplant Unit in Donor Health and Genomics, Strangeways Research Laboratory, Strangeways Research Laboratory, University of Cambridge, Wort's Causeway, Cambridge, CB1 8RN, UK. wja24@cam.ac.uk. National Health Service Blood and Transplant, Cambridge Centre, Cambridge Biomedical Campus, Long Road, Cambridge, CB2 0PT, UK. wja24@cam.ac.uk.
 UK Dementia Research Institute, Basic and Clinical Neuroscience, King's College London, London, UK mark.crook-rumsey@ukdri.ac.uk s.haar@imperial.ac.uk. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Electrical and Electronic Engineering, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Electrical and Electronic Engineering, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Basic and Clinical Neuroscience, King's College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. University of Surrey, United Kingdom Dementia Research Institute, Guildford, UK. National Hospital for Neurology and Neurosurgery, UCLH, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK. Department of Brain Sciences, Imperial College London, London, UK. UK Dementia Research Institute, Care Research and Technology Centre, Imperial College London, London, UK mark.crook-rumsey@ukdri.ac.uk s.haar@imperial.ac.uk. Department of Brain Sciences, Imperial College London, London, UK.
 San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology, San Diego, California. San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology, San Diego, California. Radboud University, Nijmegen, The Netherlands. Jewish General Hospital, Montreal, Quebec, Canada. Jewish General Hospital and McGill University, Montreal, Quebec, Canada. Reference Center for Rare Systemic Autoimmune Diseases of Ile de France, Hôpital Cochin, AP-HP, Université Paris Descartes, Paris, France. San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology and San Diego State University, San Diego, California. Jewish General Hospital and McGill University, Montreal, Quebec, Canada. San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology and San Diego State University, San Diego, California.
 Nephrology Unit, Careggi University Hospital, and. Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy. Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and. Nephrology Unit, Careggi University Hospital, and.
 Centre for Medical Image Computing Department of Medical Physics and Biomedical Engineering and Department of Computer Science, University College London, UK. Department of Neuroimaging Institute of Psychiatry Psychology and Neuroscience, King's College London, UK. Centre for Medical Image Computing Department of Medical Physics and Biomedical Engineering and Department of Computer Science, University College London, UK. Centre for Medical Image Computing Department of Medical Physics and Biomedical Engineering and Department of Computer Science, University College London, UK; Queen Square Institute of Neurology, University College London, UK; Department of Radiology and Nuclear Medicine, Amsterdam University Medical Center, The Netherlands. Centre for Medical Image Computing Department of Medical Physics and Biomedical Engineering and Department of Computer Science, University College London, UK. Centre for Medical Image Computing Department of Medical Physics and Biomedical Engineering and Department of Computer Science, University College London, UK. Electronic address: a.altmann@ucl.ac.uk.
 Department of Neurology, Zealand University Hospital, Roskilde, Denmark. Electronic address: magnus.spangsberg.boesen@regionh.dk. Department of Paediatrics and Adolescent Medicine, Copenhagen University Hospital, Denmark; Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. Electronic address: malene.landbo.02.boerresen@regionh.dk. Department of Neurology, Zealand University Hospital, Roskilde, Denmark. Electronic address: soren.k.chris@gmail.com. Department of Paediatrics and Adolescent Medicine, Copenhagen University Hospital, Denmark. Electronic address: amalie.wandel.klein-petersen.03@regionh.dk. Department of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital Rigshospitalet Glostrup, Denmark. Electronic address: sahla.el.mahdaoui.01@regionh.dk. Department of Neurology, Copenhagen University Hospital, Rigshospitalet Glostrup, Denmark. Electronic address: malini.vendela.sagar@regionh.dk. Department of Neurology, Copenhagen University Hospital, Rigshospitalet Glostrup, Denmark. Electronic address: emilie.schou@regionh.dk. Department of Paediatrics, Herlev University Hospital, Denmark. Electronic address: anna_eltvedt@hotmail.com. Department of Clinical Neurophysiology, Copenhagen University Hospital, Denmark. Electronic address: melita.cacic.hribljan@regionh.dk. Department of Paediatrics and Adolescent Medicine, Copenhagen University Hospital, Denmark. Electronic address: alfred.peter.born@regionh.dk. Department of Paediatrics and Adolescent Medicine, Copenhagen University Hospital, Denmark. Electronic address: Peter.Uldall@regionh.dk. National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark. Electronic address: lct@sdu.dk. Department of Paediatrics, Herlev University Hospital, Denmark. Electronic address: Maria.Jose.Miranda.Gimenez-Rico@regionh.dk.
 Alzheimer Centre, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, De Boelelaan 1118, 1081 HZ, Amsterdam, The Netherlands. j.ebenau@amsterdamumc.nl. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Alzheimer Centre, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, De Boelelaan 1118, 1081 HZ, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. UCL Institutes of Neurology and Healthcare Engineering, London, UK. Alzheimer Centre, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, De Boelelaan 1118, 1081 HZ, Amsterdam, The Netherlands. Alzheimer Centre, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, De Boelelaan 1118, 1081 HZ, Amsterdam, The Netherlands. Brain Research Centre, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Alzheimer Centre, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, De Boelelaan 1118, 1081 HZ, Amsterdam, The Netherlands. Department of Epidemiology & Data Science, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands. Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
 Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Nursing (Serra-Hunter Professor), University of Girona, Girona, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. Neuroimmunology and Multiple Sclerosis Unit, Department of Neurology, Dr. Josep Trueta University Hospital, Girona, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Neuroimmunology and Multiple Sclerosis Unit, Department of Neurology, Dr. Josep Trueta University Hospital, Girona, Spain. Girona Neurodegeneration and Neuroinflammation Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Radiology (IDI), Girona Biomedical Research Institute (IdIBGi), Dr. Josep Trueta University Hospital, Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Biology, University of Barcelona, Barcelona. Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain. Vascular Health Research Group of Girona (ISV-Girona), Jordi Gol Institute for Primary Care Research (Institut Universitari per a la Recerca en Atenció Primària Jordi Gol I Gorina -IDIAPJGol), Girona, Spain. Laboratory of Neuropharmacology-Neurophar, Department of Medicine and Life Sciences, Universitat Pompeu Fabra (UPF), Barcelona, Spain. Hospital del Mar Medical Research Institute (IMIM), Barcelona, Catalonia, Spain. Laboratory of Neuropharmacology-Neurophar, Department of Medicine and Life Sciences, Universitat Pompeu Fabra (UPF), Barcelona, Spain. Hospital del Mar Medical Research Institute (IMIM), Barcelona, Catalonia, Spain. Laboratory of Neuropharmacology-Neurophar, Department of Medicine and Life Sciences, Universitat Pompeu Fabra (UPF), Barcelona, Spain. Hospital del Mar Medical Research Institute (IMIM), Barcelona, Catalonia, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta University Hospital, Girona, Spain. Nutrition, Eumetabolism and Health Group, Girona Biomedical Research Institute (IdibGi), Girona, Spain. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain. Department of Medical Sciences, School of Medicine, University of Girona, Girona, Spain.
 Division of Infection and Immunity, Cardiff University, School of Medicine, Cardiff, UK ShahR45@cardiff.ac.uk. Division of Infection and Immunity, Cardiff University, School of Medicine, Cardiff, UK. School of Life & Medical Sciences, University of Hertfordshire, Hatfield, UK. Institute of Medicines Development, Cardiff, UK. Multiple Sclerosis Society, London, UK. Statistics and Data Management Centre, Perinatal HIV Research Unit, Chris Hani Baragwanath Academic Hospital, University of the Witwatersrand, Johannesburg, South Africa. 6School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. Division of Infection and Immunity, Cardiff University, School of Medicine, Cardiff, UK. Division of Infection and Immunity, Cardiff University, School of Medicine, Cardiff, UK.
 Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany; German Center for Neurodegenerative Diseases, Site Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany. Institute of Laboratory Medicine, University Hospital, LMU Munich, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany. Department of Neurosurgery, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurosurgery, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Institute of Pathology, Technische Universität München, Munich, Germany. German Center for Neurodegenerative Diseases, Site Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Institute of Neuronal Cell Biology, Technical University Munich, 80802, Munich, Germany. Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany; German Center for Neurodegenerative Diseases, Site Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany; German Center for Neurodegenerative Diseases, Site Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany; German Center for Neurodegenerative Diseases, Site Munich, Germany. Institute of Laboratory Medicine, University Hospital, LMU Munich, Munich, Germany. Department of Neurosurgery, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. German Center for Neurodegenerative Diseases, Site Munich, Germany; Neuroproteomics, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. German Center for Neurodegenerative Diseases, Site Munich, Germany; Neuroproteomics, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. German Center for Neurodegenerative Diseases, Site Munich, Germany; Neuroproteomics, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany; Department of Bioinformatics, Wissenschaftszentrum Weihenstephan, Technical University of Munich, Freising, Germany. German Center for Neurodegenerative Diseases, Site Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Neuroproteomics, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. Chair of Proteomics and Bioanalytics, Technical University of Munich, Freising, Germany; German Cancer Consortium (DKTK), Munich Partner Site, Munich, Germany; German Cancer Research Center (DKFZ), Heidelberg, Germany. Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Martinsried, Germany. Protein Analysis Unit, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-University (LMU) Munich, Großhaderner Straße 9, 82152, Martinsried, Germany. Protein Analysis Unit, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-University (LMU) Munich, Großhaderner Straße 9, 82152, Martinsried, Germany. Research Unit Protein Science and Metabolomics and Proteomics Core, Helmholtz Centre Munich, German Research Center for Environmental Health, 85764, Neuherberg, Germany. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK; UK Dementia Research Institute at UCL, London, UK; Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China. Department of Neurology, Halle University Hospital, Martin Luther University Halle/Wittenberg, Saale, Germany. Institute of Pathology, Technische Universität München, Munich, Germany. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany. Electronic address: hemmer@tum.de. Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany; German Center for Neurodegenerative Diseases, Site Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Electronic address: johannes.levin@med.uni-muenchen.de.
 Moorfields Eye Hospital NHS Foundation Trust, NIHR Moorfields Biomedical Research Centre, London, UK p.foster@ucl.ac.uk. Medical School, University of Bristol, Bristol, UK. NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust & UCL Institute of Ophthalmology, London, UK. Faculty of Medicine, University of Southampton, Southampton, UK. Clinical Research Imaging Centre, Queens Medical Research Institution, Edinburgh, UK. Population Health Research Institute, St Georges Medical School, University of London, London, UK. NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust, London, UK. Department of Molecular Neurosciences, Moorfields Eye Hospital and The National Hospital for Neurology and Neurosurgery, Queen Square Institute of Neurology, UCL, London, UK. Departments of Neurology, Ophthalmology and Expertise Center for Neuro-ophthalmology, Amsterdam UMC, Amsterdam, The Netherlands. Population Health Research Institute, St Georges Medical School, University of London, London, UK. Institute of Ophthalmology, University College London, London, UK. UK Biobank, Stockport, UK. UK Biobank, Stockport, UK. Nuffield Department of Population Health, University of Oxford, Oxford, UK.
 IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. School of Psychology, Faculty of Health, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. Melbourne Neuropsychiatry Centre, University of Melbourne, Parkville, VIC 3053, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. School of Biomedical Sciences, UNSW Sydney, Kensington, NSW 2052, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. School of Biomedical Sciences, UNSW Sydney, Kensington, NSW 2052, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. Biostatistics Unit, Faculty of Health, Deakin University, Burwood, VIC 3125, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. Florey Institute for Neuroscience and Mental Health, University of Melbourne, Parkville, VIC 3052, Australia. Orygen, The National Centre of Excellence in Youth Mental Health, Parkville, VIC 3052, Australia. IMPACT, Institute for Innovation in Physical and Mental Health and Clinical Translation, Barwon Health, School of Medicine, Deakin University, Geelong, VIC 3220, Australia. Florey Institute for Neuroscience and Mental Health, University of Melbourne, Parkville, VIC 3052, Australia.
 Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin, United States. Breathing Research and Therapeutics Center, University of Florida, Gainesville, Florida, United States. Department of Physical, Therapy University of Florida, Gainesville, Florida, United States. McKnight Brain Institute, University of Florida, Gainesville, Florida, United States. Breathing Research and Therapeutics Center, University of Florida, Gainesville, Florida, United States. Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States. McKnight Brain Institute, University of Florida, Gainesville, Florida, United States. Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin, United States. Breathing Research and Therapeutics Center, University of Florida, Gainesville, Florida, United States. Department of Physical, Therapy University of Florida, Gainesville, Florida, United States. McKnight Brain Institute, University of Florida, Gainesville, Florida, United States.
 Department of Neurosurgery, Anhui Provincial Hospital, WanNan Medical College, Wuhu, PR China. Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, PR China. Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, PR China. Department of Nerve Electrophysiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, PR China. Department of Nerve Electrophysiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, PR China; Anhui Provincial Institute of Stereotactic Neurosurgery, 9 Lujiang Road, Hefei, Anhui Province 230001, PR China. Department of Neurosurgery, Anhui Provincial Hospital, WanNan Medical College, Wuhu, PR China. Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, PR China. Department of Neurosurgery, Anhui Provincial Hospital, WanNan Medical College, Wuhu, PR China; Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, PR China; Anhui Provincial Institute of Stereotactic Neurosurgery, 9 Lujiang Road, Hefei, Anhui Province 230001, PR China. Electronic address: qianruobing@ustc.edu.cn.
 Marmara University School of Medicine, Dermatology, Istanbul, Turkey. Electronic address: ozlemapti2@gmail.com. Marmara University School of Medicine, Dermatology, Istanbul, Turkey. Marmara University School of Medicine, Cardiology, Istanbul, Turkey. Marmara University School of Medicine, Rheumatology, Istanbul, Turkey.
 From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. From the Department of Epidemiology and Biostatistics (J.H., B.S., V.K., D.G., V.Z., S.P., P.E., K.K.T., M.-r.J., A.D.), School of Public Health, Imperial College London, United Kingdom; Singapore Institute for Clinical Sciences (SICS) (J.H.), Agency for Science, Technology and Research (A*STAR); Center for Life Course Health Research (V.K., S.P., J.A., S.K.-K., M.-r.J.), Faculty of Medicine, Research Unit of Mathematical Sciences (V.K.), University of Oulu, Finland; The Stanley Center for Psychiatric Research (A.A.-O.), Broad Institute of MIT and Harvard, Cambridge, MA; Analytical and Translational Genetics Unit (A.A.-O.), Massachusetts General Hospital, Boston; Institute for Molecular Medicine Finland (A.A.-O.), University of Helsinki; Research Unit of Biomedicine (K.-H.H.), Medical Research Center (MRC), University of Oulu, University Hospital, Finland; Department of Gastroenterology and Metabolism (K.-H.H.), Poznan University of Medical Sciences, Poland; Unit of Primary Care (S.K.-K., M.-r.J.), Oulu University Hospital; Healthcare and Social Services of Selänne (S.K.-K., I.T.), Pyhäjärvi, Finland and City of Oulu; MediCity and Institute of Biomedicine (M.S., S.J.), University of Turku; Department of Clinical Chemistry (T.L.), Fimlab Laboratories, and Finnish Cardiovascular Research Center, Tampere, Faculty of Medicine and Health Technology, Tampere University; Finnish Institute for Health and Welfare (V.S.), Helsinki; Research Centre of Applied and Preventive Cardiovascular Medicine (O.T.R.), University of Turku; Department of Clinical Physiology and Nuclear Medicine (O.T.R.), Turku University Hospital; Centre for Population Health Research (O.T.R.), University of Turku and Turku University Hospital, Finland; Department of Brain Sciences (P.M.M.), Faculty of Medicine, Imperial College London; UK Dementia Research Institute at Imperial College London (P.M.M., P.E.); MRC Centre for Environment and Health (P.E., M.-r.J.), School of Public Health, Imperial College London, United Kingdom; Department of Hygiene and Epidemiology (K.K.T.), University of Ioannina Medical School, Greece; Biocenter Oulu (M.-r.J.), University of Oulu, Finland; and Department of Life Sciences (M.-r.J.), College of Health and Life Sciences, Brunel University London, United Kingdom. a.dehghan@imperial.ac.uk.
 Laboratory of Technological Development in Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Molecular Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Molecular Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Real Time PCR Platform RPT09A, Laboratory of Molecular Biology and Endemic Diseases, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Molecular Virology, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro 21040-900, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. Department of Pharmacology and Psychobiology, Roberto Alcântara Gomes Institute Biology (IBRAG), Rio de Janeiro State University (UERJ), Rio de Janeiro 20551-030, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. Unit of Intensive Treatment, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Unit of Intensive Treatment, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Epidemiology and Evaluation Service, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Post-Graduate Program in Infectious and Parasitic Diseases, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Post-Graduate Program in Infectious and Parasitic Diseases, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Department of Oral Diagnosis, School of Dentistry, State University of Paraíba, Araruna 58429-500, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil. Department of Neurology, Reference and Research Center for Multiple Sclerosis and Other Central Nervous System Idiopathic Demyelinating Inflammatory Diseases, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro 21941-901, Brazil.
 Genentech, Inc, South San Francisco, CA, USA. Genentech, Inc, South San Francisco, CA, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. The Guthy-Jackson Charitable Foundation, Beverly Hills, CA, USA. The Guthy-Jackson Charitable Foundation, Beverly Hills, CA, USA. Departments of Medicine and of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA, USA. University of Michigan Kellogg Eye Center, Ann Arbor, MI, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. Department of Statistics, The Ohio State University, Columbus, OH, USA. University of Utah School of Medicine, Salt Lake City, UT, USA. Geffen School of Medicine at UCLA, Los Angeles, CA, USA. MRYeaman@ucla.edu. Division of Molecular Medicine, David Geffen School of Medicine at UCLA, Institute for Infection and Immunity, Harbor-UCLA Medical Center, Lundquist Institute at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA, 90502, USA. MRYeaman@ucla.edu.
 Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg 20251, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg 20251, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg 20246, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. Department of Occupational Safety and Health, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. Department of Psychosomatic Medicine and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. Department of Psychosomatic Medicine and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg 20246, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg 20246, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. Institute for Infection Research and Vaccine Development, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg 20251, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg 20246, Germany. Institute of Medical Microbiology, Virology and Hygiene, Department for Infection Prevention and Control, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. German Center for Infection Research (DZIF), Partner Site Hamburg-Lübeck-Borstel-Riems, Hamburg 20246, Germany. I. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany. Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg 20251, Germany.
 Department of Neurology, CRC-SEP, Montpellier University Hospital, Montpellier, France/Institute for Neurosciences of Montpellier (INM), INSERM and University of Montpellier, Montpellier, France. Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France/Service de Neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France/Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR 5292, Centre de Recherche en Neurosciences de Lyon, Bron, France/Eugene Devic Edmus Foundation against Multiple Sclerosis, State-Approved Foundation, Bron, France. Department of Neurology, Hospital Fondation Adolphe de Rothschild, Paris, France. Department of Neurology, CRC-SEP, CHU Toulouse, Toulouse, France; Infinity, INSERM IMR1291-CNRS UMR5051, University Toulouse III, Toulouse, France. Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France/Service de Neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France/Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR 5292, Centre de Recherche en Neurosciences de Lyon, Bron, France/Eugene Devic Edmus Foundation against Multiple Sclerosis, State-Approved Foundation, Bron, France. Department of Neurology, Hôpital de la Timone, APHM, Marseille, France. Department of Neurology, CHU Bordeaux, Bordeaux, France. Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Department of Neurology, Pitié-Salpêtrière Hospital, APHP, Paris, France. Department of Neurology, CHU Lille, INSERM U117, University of Lille, Lille, France. Department of Neurology, CHU Nantes, Nantes, France. Service de Neurologie, CRCSEP, Unit de Recherche Clinique Cote d'Azur (UR2CA-URRIS), Centre Hospitalier Universitaire Pasteur 2, Nice, France. Department of Neurology, CHU Rouen, Rouen, France. Institute for Neurosciences of Montpellier (INM), INSERM and University of Montpellier, Montpellier, France. Department of Neurology, CRC-SEP, Montpellier University Hospital, Montpellier, France/Institute for Neurosciences of Montpellier (INM), INSERM and University of Montpellier, Montpellier, France. Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France/Service de Neurologie, sclérose en plaques, pathologies de la myéline et neuro-inflammation, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France/Observatoire Français de la Sclérose en Plaques, INSERM 1028 et CNRS UMR 5292, Centre de Recherche en Neurosciences de Lyon, Bron, France/Eugene Devic Edmus Foundation against Multiple Sclerosis, State-Approved Foundation, Bron, France. Department of Neurology, CRC-SEP, Montpellier University Hospital, Montpellier, France/Institute for Neurosciences of Montpellier (INM), INSERM and University of Montpellier, Montpellier, France. Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro Inflammation, and Centre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France; INSERM 1028 et CNRS UMR5292, Centre des Neurosciences de Lyon -FORGETTING team, Bron, France/Université Claude Bernard Lyon 1, Villeurbanne, France.
 Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. andres.miguez@vhir.org. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. andres.miguez@vhir.org. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. andres.miguez@vhir.org. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. andres.miguez@vhir.org. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. andres.miguez@vhir.org. Neurology-Neuroimmunology Department, Multiple Sclerosis Centre of Catalunya (Cemcat), Vall d'Hebron Research Institute (VHIR), Vall d'Hebron University Hospital, Barcelona, Spain. andres.miguez@vhir.org. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. REMAR-IVECAT Group, Germans Trias i Pujol Health Science Research Institute, Can Ruti Campus, Badalona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Pathophysiology of Neurodegenerative Diseases, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Division of Hematopoietic Innovative Therapies, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas, Madrid, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. ICREC Research Program, Germans Trias i Pujol Health Science Research Institute, Can Ruti Campus, Badalona, Spain. Faculty of Medicine, University of Vic-Central University of Catalonia (UVic-UCC), Vic, Spain. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. Laboratory of Pathophysiology of Neurodegenerative Diseases, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. Division of Hematopoietic Innovative Therapies, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas, Madrid, Spain. Brain Repair Group, School of Biosciences, Cardiff University, Cardiff, UK. REMAR-IVECAT Group, Germans Trias i Pujol Health Science Research Institute, Can Ruti Campus, Badalona, Spain. Nephrology Department, Germans Trias i Pujol Universitary Hospital, Badalona, Spain. Laboratory of Stem Cells and Regenerative Medicine, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. jmcanals@ub.edu. Creatio, Production and Validation Center of Advanced Therapies, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. jmcanals@ub.edu. Institute of Neurosciences, University of Barcelona, Barcelona, Spain. jmcanals@ub.edu. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. jmcanals@ub.edu. Networked Biomedical Research Centre for Neurodegenerative Disorders (CIBERNED), Madrid, Spain. jmcanals@ub.edu.
 Evidence Synthesis, Modeling & Simulation, Evidera, St-Laurent, Quebec, Canada. Evidence Synthesis, Modeling & Simulation, Evidera, St-Laurent, Quebec, Canada. Evidence Synthesis, Modeling & Simulation, Evidera, St-Laurent, Quebec, Canada. Institute of Neurosciences "Federico Olóriz", University of Granada, Granada, Spain. Evidence Synthesis, Modeling & Communication, Evidera, Waltham, Massachusetts, USA. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Department of Rheumatology, Clinical Immunology and Allergy, University of Crete School of Medicine, Crete, Greece. Division of Rheumatology, Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri, USA. First Department of Propaedeutic Internal Medicine, "Laikon" General Hospital, National Kapodistrian University of Athens Medical School, Athens, Greece. Specialty Care, Global Medical Affairs, GSK, Collegeville, Pennsylvania, USA. Value Evidence and Outcomes, GSK, Brentford, UK. Value Evidence and Outcomes, GSK, Collegeville, Pennsylvania, USA nick.g.ballew@gsk.com.
 Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia; Faculty of Medicine, University of Queensland (UQ), Brisbane, QLD, Australia. Electronic address: santiago.diaztorres@qimrberghofer.edu.au. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Nuffield Department of Population Health, Oxford University, Oxford, UK; Medical Scientist Training Program, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia. Departments of Ophthalmology & Twin Research and Genetic Epidemiology, King's College London, London, UK. Departments of Ophthalmology & Twin Research and Genetic Epidemiology, King's College London, London, UK. Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, UK. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia. Centre for Ophthalmology and Visual Science, University of Western Australia, Lions Eye Institute, Australia. Department of Ophthalmology, Harvard Medical School, Boston, 02114, MA, USA. Department of Epidemiology, Erasmus MC Rotterdam, the Netherlands. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia; Faculty of Medicine, University of Queensland (UQ), Brisbane, QLD, Australia. Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia; Faculty of Medicine, University of Queensland (UQ), Brisbane, QLD, Australia; School of Biomedical Sciences, Queensland University of Technology (QUT), Brisbane, Australia. Electronic address: Puya.Gharahkhani@qimrberghofer.edu.au.
 Division of Rheumatology, Department of Medicine, Geneva University Hospitals and University of Geneva, Geneva, Switzerland. Division of Rheumatology, Department of Medicine, Geneva University Hospitals and University of Geneva, Geneva, Switzerland. Department of Rheumatology, Charité University Hospital, Berlin, Germany. Servicio de Reumatología, Hospital 12 de Octubre, Madrid, Spain. Department of Internal Medicine 3, Universitätsklinikum Erlangen, Erlangen, Germany. University Hospital Tuebingen, Center for Interdisciplinary Rheumatology, Immunology and Autoimmune Diseases (INDIRA), Tuebingen, Germany. Rheumatology Unit, Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy. Department of Internal Medicine and Clinical immunology, Referral Centre for Rare Systemic Auto-immune Diseases North and North-West of France, University of Lille, Inserm, CHU Lille, U1286-INFINITE, University of Lille, Lille, France. Unit of Immunology, Rheumatology, Allergy and Rare Diseases (UnIRAR), San Raffaele Hospital-Vita-Salute San Raffaele University, Milan, Italy. Hospital de Clinicas da Universidade Federal do Parana, Curitiba, Brazil. Rheumatology Department, Hospitais da Universidade Coimbra, Coimbra, Portugal. Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. Department of Rheumatology, Santa Casa da Misericórdia do Rio de Janeiro, Rio de Janeiro, Brazil. Rheumatology and Clinical Immunology, Humanitas University, Pieve Emanuele; IRCCS-Humanitas Clinical and Research Center, Rozzano, MI, Italy. Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, MI, Italy. Department of Rheumatology, Rikshospitalet University Hospital, Oslo, Norway. Clinica Medica, Università Politecnica delle Marche & Azienda Ospedali Riuniti, Ancona, Italy. Department of Rheumatology, University Hospital Zürich, Zürich, Switzerland. Division of Rheumatology, Department of Medicine, Geneva University Hospitals and University of Geneva, Geneva, Switzerland.
 From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. mckeon.andrew@mayo.edu. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany. From the Departments of Laboratory Medicine and Pathology and Neurology (A.M., E.P.F., S.J.P., B.Y., A.Z., D.D.); Department of Laboratory Medicine and Pathology (C.L., N.V., M.G., R.L.-C., J.M.); Khon Kaen University (N.V.), Thailand; University of Virginia (M.W.B.); Division of Biomedical Statistics and Informatics (S.D.), Mayo Clinic, Rochester, MN; The Institute for Experimental Immunology (R.M., M.S.), affiliated to Euroimmun AG, Lubeck, Germany.
 Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK. Department of Neurology, Tongji Hospital of Tongji Medical College, Huazhong University of Science of Technology, Wuhan, China. Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK. Department of Neurology, Civil Hospital of Guadalajara, University of Guadalajara, Guadalajara, Mexico. Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN. Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK. Neuroscience Centre, Bangkok International Hospital, Bangkok, Thailand. Department of Neurology, First Affiliated Hospital of Kunming Medical University, Kunming, China. Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK. Neurology Department, Wexham Park Hospital, Frimley Foundation Health Trust, Slough, UK. Department of Paediatric Neurology, Oxford University NHS Foundation Trust, Oxford, UK. Oxford Autoimmune Neurology Diagnostic Laboratory, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Department of Neurology, Division of Psychological Medicine and Clinical Neuroscience, Cardiff University, University Hospital of Wales, Cardiff, UK. Children's Neuroscience Centre, Evelina London Children's Hospital, London, UK. Women and Children's Department, Faculty of Life Sciences and Medicine, King's College London, London, UK. Department of Paediatric Neurology, Birmingham Women and Children's Hospital, Birmingham, UK. Department of Paediatric Neurology, Alder Hey Children's NHS Foundation Trust and Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool, UK. Department of Neurology, Walton Centre NHS Foundation Trust, Liverpool, UK. Department of Neurology, St. George's University Hospitals National Health Service Foundation Trust, London, UK. Department of Neurology, Southampton General Hospital, Southampton, UK. Department of Paediatric Neurology, Great Ormond St. Hospital for Children, London, UK. Department of Ophthalmology, King's College Hospital NHS Foundation Trust, London, UK. Department of Neurology, University Hospitals Plymouth National Health Service Foundation Trust, Devon, UK. Department of Neurosciences, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. Department of Neurology, Gloucestershire Hospitals National Health Service Foundation Trust, Gloucestershire, UK. Preventive Neurology Unit, Queen Mary University London, London, UK. Department of Neurology, University Hospitals Sussex National Health Service Foundation Trust, Brighton, UK. Department of Neurology, King's College Hospital NHS Foundation Trust, London, UK. Department of Neurology, Guy's and St. Thomas' National Health Service Foundation Trust, London, UK. Oxford Autoimmune Neurology Diagnostic Laboratory, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Department of Ophthalmology and Neurology, Mayo Clinic, Rochester, MN. Centre MS and Autoimmune Neurology, Department Neurology, Mayo Clinic, Rochester, MN. MDUK Neuromuscular Centre, Department of Paediatrics, University of Oxford, Oxford, UK. Department of Paediatric Neurology, John Radcliffe Hospital, Oxford, UK. Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK. Departments of Neurology & Laboratory Medicine and Pathology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, MN. Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK. Neurology Department, Wexham Park Hospital, Frimley Foundation Health Trust, Slough, UK. Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, Oxford, UK.
 The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. Huashan Hospital, Fudan University, Shanghai, China. Department of Anatomy and Cell Biology, Department of Neurological Surgery, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. Institute of Brain Science, Shanxi Datong University, Datong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center, Shanxi University of Chinese medicine, Jinzhong, China.
 Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany. Institute of Biometry and Clinical Epidemiology, Charité-Universitätsmedizin Berlin, Berlin, Germany. Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany. Center for Stroke Research Berlin, Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, University of Cologne and University Hospital, Cologne, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. Department of Neurology, Kreiskrankenhaus Oberberg GmbH, Oberberg, Germany. Department of Neurology, LVR Klinik Bonn, Bonn, Germany. Department of Neuropediatric, University of Duisburg-Essen, Essen, Germany. Department of Neuropediatric, University of Duisburg-Essen, Essen, Germany. Department of Neurology, Helios Hospital Erfurt, Erfurt, Germany. Department of Neurology Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, Essen, Germany. Department of Neurology, Sankt Katharinen Krankenhaus GmbH, Frankfurt, Germany. Department of Neurology, Helios Hospital Pforzheim, Pforzheim, Germany. Clinic of Neurology and Neurophysiology, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany. Department of Neurology, Asklepios Hospital Hamburg Barmbek, Hamburg, Germany. Neurological Outpatient Department Neuer Wall, Hamburg, Germany. Department of Neurology, University of Regensburg, Regensburg, Germany. Department of Neurology, University of Regensburg, Regensburg, Germany. Neurological Outpatient Department, Leipzig, Germany. Department of Neurology, University of Münster, Münster, Germany. Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. andreas.meisel@charite.de. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany. andreas.meisel@charite.de. Center for Stroke Research Berlin, Charité - Universitätsmedizin Berlin, Berlin, Germany. andreas.meisel@charite.de.
 Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia. Electronic address: m.lane@deakin.edu.au. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia. Cancer Epidemiology Division, Cancer Council Victoria, 615 St Kilda Rd, Melbourne, VIC 3004, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, VIC, Australia. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia; Centre for Adolescent Health, Murdoch Children's Research Institute, VIC, Australia; Black Dog Institute, NSW, Australia; James Cook University, QLD, Australia. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia. Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, VIC 3220, Australia; Center for Epidemiological Research in Nutrition and Health, University of Sao Paulo, Av. Dr. Arnaldo, 715, Sao Paulo 01246-904, Brazil. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia; Mental Health, Drugs & Alcohol Service, University Hospital Geelong, Barwon Health, VIC 3220, Australia; Department of Psychiatry, University of Melbourne, Parkville, VIC 3050, Australia. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia. Deakin University, IMPACT (the Institute for Mental and Physical Health and Clinical Translation), Food & Mood Centre, School of Medicine, Barwon Health, Geelong, Australia.
 Department of Infectious and Tropical Diseases, Toulouse University Hospital, Toulouse, France. Department of Medical Pharmacology, CIC 1436, Toulouse University Hospital, Toulouse, France. Department of Hematology, Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France. HIV/AIDS Clinical Unit, National Institute for Infectious Disease "L. Spallanzani", Rome, Italy. Department of Neurology, Medical Center, University of Freiburg, Freiburg, Germany. Department of Neurology, University Hospital Bonn, Bonn, Germany. Department of Nephrology and Organ Transplantation, CHU Rangueil, Toulouse, France. Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), INSERM UMR1291, CNRS UMR5051, Toulouse III University, Toulouse, France. Neuroimmunology and Multiple Sclerosis Research Section, Department of Neurology, University Hospital Zurich and University of Zurich, Zurich, Switzerland. Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, Hannover, Germany. Unit of Rehabilitation of Neuroviral Diseases, Bicêtre Hospital, APHP, Le Kremlin-Bicêtre, France. INSERM U1186, Paul Brousse Hospital, Paris Saclay University, Villejuif, France. Department of Neurology, University Hospital of Cologne, Cologne, Germany. Department of Neurology, Institute of Translational Neurology, University Hospital Münster, Münster, Germany. Department of Neurology, Barts Health NHS Trust and Queen Mary University of London, London, UK. Department of Neurology, Technical University of Munich, Munich, Germany. Department of Neurology, University Hospital of Liège, Liège, Belgium. Department of Infectious and Tropical Diseases, Lyon University Hospital, Lyon, France. Amsterdam University Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Department of Neuroscience, Amsterdam University Medical Center, Amsterdam, the Netherlands. Department of Neurology, Washington University in St Louis, St Louis, MO, USA. Department of Medical Pharmacology, CIC 1436, Toulouse University Hospital, Toulouse, France. Experimental Immunotherapeutics Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD. Department of Infectious and Tropical Diseases, Toulouse University Hospital, Toulouse, France. Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), INSERM UMR1291, CNRS UMR5051, Toulouse III University, Toulouse, France. European Society of Clinical Microbiology and Infectious Diseases (ESCMID) Study Group on Infections of the Brain (ESGIB), Basel, Switzerland.
 Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Nova Scotia Health, Halifax, Nova Scotia B3S 0H6, Canada. Department of Medicine (Geriatrics), Dalhousie University, Halifax, Nova Scotia B3H 2Y9, Canada. Department of Psychology and Neuroscience, Dalhousie University, Halifax, Nova Scotia B3H 4R2, Canada. School of Communication Sciences and Disorders, Faculty of Health Sciences, Western University, London, Ontario N6G 1H1, Canada. Canadian Centre for Activity and Aging, Faculty of Health Sciences, Western University, London, Ontario N6G 1H1, Canada. Faculty of Engineering and Applied Science, Queen's University, Kingston Ontario K7L 3N6, Canada. School of Communication Sciences and Disorders, Faculty of Health Sciences, Western University, London, Ontario N6G 1H1, Canada. Department of Computer Science, Western University, London, Ontario N6A 5B7, Canada. Rotman Research Institute, Baycrest Centre, North York, Ontario M6A 2E1, Canada. Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario M5T 3M7, Canada. Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario M5T 3M7, Canada. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre and University of Toronto, Toronto, Ontario M5S 3H2, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario M4N 3M5, Canada. Rotman Research Institute, Baycrest Centre, North York, Ontario M6A 2E1, Canada. Rotman Research Institute, Baycrest Centre, North York, Ontario M6A 2E1, Canada. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre and University of Toronto, Toronto, Ontario M5S 3H2, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario M4N 3M5, Canada. Department of Medicine (Neurology), University of Ottawa, Ottawa, Ontario K1H 8M5, Canada. Ottawa Hospital Research Institute, Ottawa, Ontario K1Y 4E9, Canada. Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 3K7, Canada. Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario M5B 1W8, Canada. Department of Medicine (Neurology), University of Ottawa, Ottawa, Ontario K1H 8M5, Canada. Bruyere Research Institute, Ottawa, Ontario K1R 6M1, Canada. Department of Medicine (Neurology), University of Ottawa, Ottawa, Ontario K1H 8M5, Canada. Ottawa Hospital Research Institute, Ottawa, Ontario K1Y 4E9, Canada. University of Ottawa Brain and Mind Research Institute, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada. Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario M6J 1H4, Canada. Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario M5S 3H2, Canada. Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, Toronto, Ontario M5T 2S8, Canada. Thunder Bay Regional Health Research Institute, Thunder Bay, Ontario P7B 7A5, Canada. Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 3K7, Canada. London Health Sciences Centre, London, Ontario N6A 5W9, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario M5S 3H2, Canada. Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, Toronto, Ontario M5T 2S8, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario M4N 3M5, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario M5S 3H2, Canada. Cognitive and Movement Disorders Clinic, Sunnybrook Health Sciences Centre, Toronto, Ontario M4N 3M5, Canada. Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 3K7, Canada. Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 5B7, Canada. Cognitive Neurology and Alzheimer's Disease Research Centre, Parkwood Institute, St. Joseph's Health Care, London, Ontario N6A 4V2, Canada. Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario M6J 1H4, Canada. Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Toronto Dementia Research Alliance, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario M5S 3H2, Canada. Department of Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 1N4, Canada. Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 3K7, Canada. London Health Sciences Centre, London, Ontario N6A 5W9, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario M5S 3H2, Canada. Division of Neurology, St. Michael's Hospital, Toronto, Ontario M5B 1W8, Canada. Rotman Research Institute, Baycrest Centre, North York, Ontario M6A 2E1, Canada. Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 1L7, Canada. Rotman Research Institute, Baycrest Centre, North York, Ontario M6A 2E1, Canada. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre and University of Toronto, Toronto, Ontario M5S 3H2, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario M4N 3M5, Canada. Rotman Research Institute, Baycrest Centre, North York, Ontario M6A 2E1, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario M5S 3H2, Canada. University Health Network Memory Clinic, Krembil Brain Institute, Toronto Western Hospital, Toronto, Ontario M5T 2S8, Canada. University Health Network Memory Clinic, Krembil Brain Institute, Toronto Western Hospital, Toronto, Ontario M5T 2S8, Canada. Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre and University of Toronto, Toronto, Ontario M5S 3H2, Canada. Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, Ontario M4N 3M5, Canada. Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6Canada. Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada.

 Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. gaoxiukui@zju.edu.cn. International Institutes of Medicine, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu, Zhejiang, China. gaoxiukui@zju.edu.cn. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. gaoxiukui@zju.edu.cn. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of General Intensive Care Unit of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejinag, China. Key Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Pathology of Sir Run Run Shaw Hospital, Center of Cryo-Electron Microscopy, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. lyjlj@zju.edu.cn. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. zhengliling@zju.edu.cn. Department of Biochemistry and Department of General Intensive Care Unit of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejinag, China. zhengliling@zju.edu.cn. Key Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China. zhengliling@zju.edu.cn. Department of Biochemistry and Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. zhouyt@zju.edu.cn. Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang Provincial Key Lab for Tissue Engineering and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. zhouyt@zju.edu.cn. Key Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China. zhouyt@zju.edu.cn. ZJU-UoE Institute, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. zhouyt@zju.edu.cn. Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China. zhouyt@zju.edu.cn. Liangzhu Laboratory, Hangzhou, Zhejiang, China. zhouyt@zju.edu.cn.
 Department of Medicine, Division of Molecular Medicine, University of São Paulo School of Medicine, São Paulo, Brazil; Laboratory of Medical Investigation 29, University of São Paulo School of Medicine, São Paulo, Brazil; Department of Pharmacy and Postgraduate Program of Health and Science, Federal University of Rio Grande do Norte, Natal, Brazil; Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil; Interunit Postgraduate Program on Bioinformatics, Institute of Mathematics and Statistics (IME), University of Sao Paulo (USP), Sao Paulo, Brazil. Electronic address: otavio.cmarques@usp.br. Department of Nephrology and Internal Intensive Care Medicine, Charité University Hospital, Berlin, Germany; BIH Center for Regenerative Therapies (BCRT) and Berlin-Brandenburg School for Regenerative Therapies (BSRT), all Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Berlin, Germany. Department of Nephrology and Internal Intensive Care Medicine, Charité University Hospital, Berlin, Germany. Department of Internal Medicine II, University of Tübingen, Tübingen, Germany. Department of Internal Medicine II, University of Tübingen, Tübingen, Germany. Department of Internal Medicine II, University of Tübingen, Tübingen, Germany. Department of Internal Medicine II, University of Tübingen, Tübingen, Germany. Department of Internal Medicine II, University of Tübingen, Tübingen, Germany. Centre for BioSeparation Technology, Vellore Institute of Technology (VIT), Vellore, Tamil Nadu, India. Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany. Leiden University Medical Center (LUMC), Department of Rheumatology, Leiden, the Netherlands. Department of Ophthalmology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt- Universität zu Berlin, Department of Neurology with Experimental Neurology, Berlin, Germany.; Berlin Institute of Health at Charité - Universitätsmedizin Berlin, BIH Biomedical Innovation Academy, Berlin, Germany; Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, NeuroCure Cluster of Excellence, Berlin, Germany; Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Center for Stroke Research Berlin, Berlin, Germany; German Center for Neurodegenerative Diseases (DZNE), Partner Site Berlin, Germany; German Centre for Cardiovascular Research (DZHK), Partner Site Berlin, Berlin, Germany. Leiden University Medical Center (LUMC), Department of Rheumatology, Leiden, the Netherlands. Leiden University Medical Center (LUMC), Department of Rheumatology, Leiden, the Netherlands. LUMC, Department of Internal Medicine (Nephrology), Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden, the Netherlands. LUMC, Department of Internal Medicine (Nephrology), Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden, the Netherlands. LUMC, Department of Internal Medicine (Nephrology), Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden, the Netherlands. Leiden University Medical Center (LUMC), Department of Rheumatology, Leiden, the Netherlands. Leiden University Medical Center (LUMC), Department of Rheumatology, Leiden, the Netherlands. Institute of Clinical Molecular Biology, Kiel University, Kiel, Germany. Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Interunit Postgraduate Program on Bioinformatics, Institute of Mathematics and Statistics (IME), University of Sao Paulo (USP), Sao Paulo, Brazil. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany. Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany. Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany. Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany. Experimental and Clinical Research Center, A collaboration of Max Delbruck Center for Molecular Medicine and Charité Universitätsmedizin, and HELIOS Clinic, Department of Cardiology and Nephrology, Berlin 13125, Germany. Priority Area Chronic Lung Diseases, Research Center Borstel (RCB), Member of the German Center for Lung Research (DZL), Borstel, Germany. Priority Area Chronic Lung Diseases, Research Center Borstel (RCB), Member of the German Center for Lung Research (DZL), Borstel, Germany. Institute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität Zu Berlin, Berlin, Germany. Laboratory of Chemical Biology and Signal Transduction, The Rockefeller University, New York, NY, USA. University of Washington School of Medicine and Seattle Children's Research Institute, Seattle, WA, USA. CellTrend GmbH, Luckenwalde, Germany. CellTrend GmbH, Luckenwalde, Germany. Institute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität Zu Berlin, Berlin, Germany. Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat-Gan, Israel. Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany. Electronic address: gabriela.riemekasten@uksh.de.
 Laboratory of Molecular Virology and Parasitology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil. Laboratory of Molecular Virology and Parasitology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil. Real Time PCR Platform RPT09A, Fiocruz, Rio de Janeiro 21040-360, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil. Department of Oral Diagnosis, School of Dentistry, State University of Paraíba, Araruna 58429-500, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. Laboratory of Translacional Neurosciences, Biomedical Institute, Federal University of the State of Rio de Janeiro-UNIRIO, Rio de Janeiro 22290-240, Brazil. Department of Neurology, Reference and Research Center for Multiple Sclerosis and Other Central Nervous System Idiopathic Demyelinating Inflammatory Diseases, Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro 21941-617, Brazil. Laboratory of Molecular Virology and Parasitology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil. Laboratory of Technological Development in Virology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro 21040-360, Brazil.
 Lonsdale Medical Centre, London, UK; and Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK. Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK. Institute for Mental and Physical Health and Clinical Translation (IMPACT), Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, Australia. Institute for Mental and Physical Health and Clinical Translation (IMPACT), Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, Australia. Institute for Mental and Physical Health and Clinical Translation (IMPACT), Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, Australia; Department of Psychiatry, Kuopio University Hospital, Kuopio, Finland; and Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK. Institute for Mental and Physical Health and Clinical Translation (IMPACT), Food & Mood Centre, School of Medicine, Barwon Health, Deakin University, Geelong, Australia. Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK; and National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre, South London and Maudsley NHS Foundation Trust, King's College London, London, UK.
 Neurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Computational Biology Group, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, New York, NY, USA. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, New York, NY, USA. Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road South, Jacksonville, FL, USA. Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. Program in Medical and Population Genetics, Broad Institute of Massachusetts Institute of Technology (M.I.T.), Cambridge, MA, USA. Division of Medical Sciences and Department of Medicine, Harvard Medical School, Boston, MA, USA. Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Centre for Alzheimer's and Related Dementias, National Institute on Aging, Bethesda, MD, USA. Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. Program in Medical and Population Genetics, Broad Institute of Massachusetts Institute of Technology (M.I.T.), Cambridge, MA, USA. Division of Medical Sciences and Department of Medicine, Harvard Medical School, Boston, MA, USA. Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. Program in Medical and Population Genetics, Broad Institute of Massachusetts Institute of Technology (M.I.T.), Cambridge, MA, USA. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. Program in Medical and Population Genetics, Broad Institute of Massachusetts Institute of Technology (M.I.T.), Cambridge, MA, USA. Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Neurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. Neurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Centre for Alzheimer's and Related Dementias, National Institute on Aging, Bethesda, MD, USA. Centre for Alzheimer's and Related Dementias, National Institute on Aging, Bethesda, MD, USA. Department of Neurology, Johns Hopkins University Medical Center, Baltimore, MD, USA. Neuroregeneration and Stem Cell Programs, Institute of Cell Engineering, Johns Hopkins University Medical Center, Baltimore, MD, USA. Department of Pharmacology and Molecular Science, Johns Hopkins University Medical Center, Baltimore, MD, USA. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University Medical Center, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University Medical Center, Baltimore, MD, USA. Department of Neurology, Johns Hopkins University Medical Center, Baltimore, MD, USA. Department of Pathology and Anatomical Sciences, Jacobs School of Medicine and Biomedical Sciences, University of Buffalo, Buffalo, NY, USA. Department of Pathology (Neuropathology), Johns Hopkins University Medical Center, Baltimore, MD, USA. Department of Pathology (Neuropathology), Johns Hopkins University Medical Center, Baltimore, MD, USA. Cognitive & Movement Disorders Clinic, Sunnybrook Health Sciences Centre, University of Toronto, 1 King's College Circle, Room 2374, Toronto, ON, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada. Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, 2075 Bayview Avenue, Toronto, ON, Canada. LC Campbell Cognitive Neurology Research Unit, Sunnybrook Research Institute, University of Toronto, 2075 Bayview Avenue, Toronto, ON, Canada. Department of Anatomical Pathology, Sunnybrook Health Sciences Centre, University of Toronto, 1 King's College Circle, Room 2374, Toronto, ON, Canada. Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada. Institute of Medical Science, Faculty of Medicine, University of Toronto, 1 King's College Circle, Room 2374, Toronto, ON, Canada. Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Sunnybrook Health Sciences Centre, University of Toronto, 1 King's College Circle, Room 2374, Toronto, ON, Canada. Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, 2075 Bayview Avenue, Toronto, ON, Canada. LC Campbell Cognitive Neurology Research Unit, Sunnybrook Research Institute, University of Toronto, 2075 Bayview Avenue, Toronto, ON, Canada. Longitudinal Studies Section, National Institute on Aging, Baltimore, MD, USA. Laboratory of Behavioral Neuroscience, National Institute on Aging, Baltimore, MD, USA. Longitudinal Studies Section, National Institute on Aging, Baltimore, MD, USA. Scripps Research Translational Institute, Scripps Research, La Jolla, CA, USA. Scripps Research Translational Institute, Scripps Research, La Jolla, CA, USA. Translational Immunology, Research Programs Unit, University of Helsinki, Helsinki, Finland. Department of Neurology, Helsinki University Hospital, Helsinki, Finland. Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA. Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA. Department of Neurology, University of Massachusetts Medical School, Worcester, MA, USA. Department of Genetics and Genomic Medicine Research & Teaching, UCL GOS Institute of Child Health, University College London, London, UK. Department of Neurodegenerative Disease, Queen Square Institute of Neurology, University College London, London, UK. NIHR Great Ormond Street Hospital Biomedical Research Centre, University College London, London, UK. Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. UCL Movement Disorders Centre, University College London, London, UK. Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. UCL Movement Disorders Centre, University College London, London, UK. UK Dementia Research Institute, Department of Neurogenerative Disease and Reta Lila Weston Institute, London, UK. Institute of Advanced Study, The Hong Kong University of Science and Technology, Hong Kong SAR, China. Maggiore della Carita University Hospital, Novara, Italy. Department of Health Sciences, University of Eastern Piedmont, Novara, Italy. Rita Levi Montalcini Department of Neuroscience, University of Turin, Turin, Italy. Azienda Ospedaliero Universitaria Città, della Salute e della Scienza, Corso Bramante, 88, Turin, Italy. Rita Levi Montalcini Department of Neuroscience, University of Turin, Turin, Italy. Azienda Ospedaliero Universitaria Città, della Salute e della Scienza, Corso Bramante, 88, Turin, Italy. Civin Laboratory for Neuropathology, Banner Sun Health Research Institute, Sun City, AZ, USA. Civin Laboratory for Neuropathology, Banner Sun Health Research Institute, Sun City, AZ, USA. Department of Psychiatry and Psychology, Mayo Clinic, 4500 San Pablo Road South, Jacksonville, FL, USA. Department of Neurology, Mayo Clinic, 4500 San Pablo Road South, Jacksonville, FL, USA. Center for Sleep Medicine, Mayo Clinic, Rochester, MN, USA. Institute of Cognitive Sciences and Technologies, C.N.R., Via S. Martino della Battaglia, 44, Rome, Italy. Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road South, Jacksonville, FL, USA. Rita Levi Montalcini Department of Neuroscience, University of Turin, Turin, Italy. Azienda Ospedaliero Universitaria Città, della Salute e della Scienza, Corso Bramante, 88, Turin, Italy. Institute of Cognitive Sciences and Technologies, C.N.R., Via S. Martino della Battaglia, 44, Rome, Italy. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA. Center for Translational & Computational Neuroimmunology, Department of Neurology, Columbia University Irving Medical Center and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, New York, NY, USA. Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road South, Jacksonville, FL, USA. Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA. The American Genome Center, Collaborative Health Initiative Research Program, Uniformed Services University of the Health Sciences, Bethesda, MD, USA. Computational Biology Group, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Neuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. Department of Neurology, Johns Hopkins University Medical Center, Baltimore, MD, USA. RNA Therapeutics Laboratory, Therapeutics Development Branch, National Center for Advancing Translational Sciences, Rockville, MD, USA. Neurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. Department of Neurology, Johns Hopkins University Medical Center, Baltimore, MD, USA.
 School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China; Laboratory for Space Environment and Physical Science, Harbin Institute of Technology, Harbin 150001, China. Department of Neurology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China; Laboratory for Space Environment and Physical Science, Harbin Institute of Technology, Harbin 150001, China. Beijing Institute for Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing 100069, China; Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China; Laboratory for Space Environment and Physical Science, Harbin Institute of Technology, Harbin 150001, China. Department of Neurology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China; Key Laboratory of Biological Big Data (Harbin Institute of Technology), Ministry of Education, Harbin 150001, China. Electronic address: qhjiang@hit.edu.cn. School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China; Laboratory for Space Environment and Physical Science, Harbin Institute of Technology, Harbin 150001, China. Electronic address: xia.liang@hit.edu.cn.
 Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Pneumology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Pneumology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Rheumatology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Department of Immunology, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. SERGAS (Servizo Galego de Saude) and IDIS (Instituto de Investigación Sanitaria de Santiago), NEIRID Lab. (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, Santiago University Clinical Hospital, 15706 Santiago de Compostela, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Rheumatology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Rheumatology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Department of Rheumatology, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain. Rheumatology Department, Hospital Universitario de la Princesa, IIS-Princesa, Cátedra UAM-ROCHE EPID Futuro, Universidad Autónoma de Madrid, 28006 Madrid, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Pneumology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. School of Medicine, Universidad de Cantabria, 39011 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Rheumatology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, Instituto de Investigación Marqués de Valdecilla, Avenida Cardenal Herrera Oria s/n, Lab. 201/202, 39011 Santander, Spain. Rheumatology Department, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain. Department of Medicine and Psychiatry, Universidad de Cantabria, 39011 Santander, Spain. Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg 2000, South Africa.
 Center for Health + Technology, University of Rochester, CU, Rochester, NY, USA. Center for Health + Technology, University of Rochester, CU, Rochester, NY, USA. Center for Health + Technology, University of Rochester, CU, Rochester, NY, USA. Center for Health + Technology, University of Rochester, CU, Rochester, NY, USA. Center for Health + Technology, University of Rochester, CU, Rochester, NY, USA. Department of Neurology, University of Rochester, Rochester, NY, USA. Pittsford Sutherland High School, Pittsford, NY, USA. Department of Medicine, University of Rochester, Rochester, NY, USA. Department of Medicine, University of Rochester, Rochester, NY, USA. Hospice of Michigan, Ann Arbor, MI, USA. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY, USA. GO2 Foundation for Lung Cancer, Washington, DC, USA. GO2 Foundation for Lung Cancer, Washington, DC, USA. Center for Health + Technology, University of Rochester, CU, Rochester, NY, USA. Department of Neurology, University of Rochester, Rochester, NY, USA.
 From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. simone.beretta@unimib.it. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy. From the Department of Neurology (S.B., C.M.C., C.F.), Fondazione IRCCS San Gerardo dei Tintori, Monza; Department of Medicine and Surgery (S.B., C.M.C., C.F.), University of Milano Bicocca; The Milan Center for Neuroscience (NeuroMI) (S.B., G.G., C.F.); Neurology Unit and Department of Clinical and Experimental Sciences (V.C., S. Gipponi, A. Padovani), University of Brescia; Unit of Neurology and Neurophysiology (G.C., M.G., M.S.), ASST PG23, Bergamo; Santa Maria della Misericordia University Hospital (G.P., M.V.), Udine, Italy; San Marino Neurological Unit (B.V., S. Guttmann), San Marino Hospital; The Mario Negri Institute for Pharmacological Research IRCCS (E. Bianchi, E. Beghi), Milan; Department of Medical Area (DAME) (M.V.), University of Udine; Neurology Unit (M.S.C.), ASST Valcamonica, Esine, Brescia; USL Centro Toscana (P. Palumbo), Neurology Unit, Nuovo Ospedale Santo Stefano, Prato; Department of Neurology and Stroke Unit (G.G., E.C.A.), Niguarda, Milan; Department of Neurology and Department of Clinical Neurophysiology AOU Modena (S. Meletti), University of Modena and Reggio Emilia; Department of Neuroscience, Rehabilitation, Ophtalmology, Genetics, Maternal and Child Health (C.S.), University of Genoa; Ospedale Santa Maria del Carmine di Rovereto (D.O.), Trento; Neurology Unit (M.F.), IRCCS San Raffaele Scientific Institute, Milan; Department of Neurology (A.Z.), Metropolitan Stroke Network, Ospedale Maggiore, Bologna; Department of Neurology (P.B.), Ospedale A. Manzoni ASST Lecco; University of Milan (L.T., L.P., A. Priori); Neurology Unit (L.T., A. Priori), ASST Santi Paolo e Carlo; Aldo Ravelli Center for Neurotechnology and Experimental Brain Therapeutics (L.T.), Milan; IRCCS Institute of Neurological Science of Bologna (P.C.); DIBINEM (P.C.), University of Bologna; UOC Neurology (M.B.), ASST Vimercate; Department of Neurology (V.D.G.), ASST Cremona; Neurophysiopathology Unit, Fondazione Policlinico Universitario A. Gemelli, Rome, Italy; Department of Basic Medical Sciences, Neurosciences and Sense Organs (D.P.), University of Bari; Department of Neurology and Laboratory of Neuroscience (F.V., V.S.), IRCCS Istituto Auxologico Italiano; "Dino Ferrari" Center (F.V., V.S.), Department of Pathophysiology and Transplantation, Università degli Studi di Milano; Neurology Division (S.C.), "S. Maria" University Hospital, Terni; IRCCS Mondino Foundation (A. Pisani), Department of Brain and Behavioral Sciences, University of Pavia; Department of Diagnostic and Therapeutic Services (V.L.R.), IRCCS ISMETT, Palermo; Department of Neurology 2 (L.M.), Careggi University Hospital, Florence; Department of Neurology and Neurosurgery (D.V.R.), ASST di Mantova; Clinical Neurology Unit (P. Manganotti), Cattinara University Hospital, University of Trieste; Department of Neurology (D.L.A.S.), AORN S.Giovanni Moscati, Avellino; Neurology and Stroke Unit (A.F.), Neuroscience Department, ASST-Lecco, Merate; Department of Neurology (M.P.), Ospedale San Filippo Neri, Rome; IRCCS Centro Neurolesi Bonino-Pulejo (S. Marino), Messina; Department of Neurology (P. Polverino), IRCCS Humanitas Research Hospital, Rozzano, Milan; Department of Medical and Surgical Sciences (U.A.), Magna Graecia University of Catanzaro; Department of Biotechnological and Clinical Sciences (R.O.), University of L'Aquila; Department of Neurology (E.P.), Ospedale Valduce, Como; Neurological Clinic (G.S.), University of Pisa; Department of Neurology (P. Merlo), Humanitas Gavazzeni, Bergamo; Department of Neurology (M.C.), S. Luigi Gonzaga Hospital, Orbassano; Ospedale Luigi Sacco (L.P.), Milan; IRCCS Institute of Neurological Science of Bologna (A.L.), UOSI Multiple Sclerosis Rehabilitation; Department of Biomedical Science and Neuromotricity (A.L.), University of Bologna; Department of Neurology (S.A.), Fermo; Department of Neurosciences (A.D.R.), Federico II University, Naples; Neurology Unit and Department of Neurosciences (S. Monaco), University of Verona; IRCCS Fondazione Ospedale Maggiore Policlinico (A. Priori), Milan; and Department of Advanced Medical and Surgical Sciences (G.T.), University of Campania, Naples, Italy.
 Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy. Centre Hospitalier Universitaire de Grenoble, Service de Neurologie, Grenoble Institute of Neurosciences, Grenoble Alpes University, Grenoble, France. Neurology Department, Colentina Clinical Hospital, Bucharest, Romania and Department of Clinical Neurosciences, "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. Neurology Department, Colentina Clinical Hospital, Bucharest, Romania and Department of Clinical Neurosciences, "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. Diomid Gherman Institute of Neurology and Neurosurgery, Chișinău, Moldova. Neurology Unit, Neuromotor and Rehabilitation Department, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy. Neurology Unit ASST Valcamonica, Brescia, Italy. University Clinic for Neurology, Medical Faculty, University "Ss. Cyril and Methodius", Skopje, Macedonia. Department of the Research Centre of Neurology, Moscow, Russia. Semmelweis University Budapest, Budapest, Hungary. Tel Aviv University School of Medicine and Shamir (Assaf Harofeh) Medical Center, Tel Aviv, Israel. Department of Neurology, Specialist Hospital Konskie, Collegium Medicum, Jan Kochanowski University, Kielce, Poland. CEPID BRAINN - Brazilian Institute of Neuroscience and Neurotechnology and University of Campinas, Campinas, Brazil. Neurology Department Hospital Santo António - CHUP, Porto, Portugal. Department of Neurology, UHC Sestre milosrdnice, Zagreb, Croatia. Department of Neurology, Centro Hospitalar Universitário de São João, E.P.E, Porto, Spain. Cardiovascular I&D Unit, Portugal Department of Clinical Neurosciences and Mental Health, Faculty of Medicine University of Porto, Porto, Portugal. Neurology Service, Facultad de Medicina, Universidad Autonoma de San Luis Potosi. Hospital Central, San Luis Potosi, Mexico. Department of Neurology, Oslo University Hospital, Oslo, Norway. Centre Hospitalier Universitaire de Grenoble, Service de Neurologie, Grenoble Institute of Neurosciences, Grenoble Alpes University, Grenoble, France. Department of Neurology and Neurosurgery, Ivano-Frankivsk National Medical University, Ivano-Frankivsk, Ukraine. Selcuk University Faculty of Medicine, Department of Neurology, Konya, Turkey. University of Health Science, Gulhane School of Medicine, Neurology Department, Ankara, Turkey. Department of Neurology, Kepler University Hospital, Linz, Austria. Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy. European Acadmey of Neurology, Vienna, Austria. Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy. Neurocritical Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Neurocritical Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Department of Neurology, University Hospital of Bern, Bern, Switzerland.

 Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY. Center for Health + Technology (CHeT) (JS, SR, AV, JW, CE, BC, EW, CZ, CH); Department of Neurology and Biostatistics (ND), University of Rochester; Pittsford Sutherland High School (JH), NY; Loyola University Chicago Stritch School of Medicine (DA), IL; PepGen Inc. (JL), Boston, MA; Children's Hospital of Philadelphia (CHOP) (DRL, CP, MW), PA; University of Florida College of Medicine (SHS), Gainesville; Friedreich's Ataxia Research Alliance (FARA) (SW), Downingtown, PA; and Department of Neurology (CH), University of Rochester, NY.
 Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota. Center for Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota. Department of Neurology, University of California, San Francisco (UCSF), San Francisco. Department of Neurology, Mayo Clinic, Jacksonville, Florida. Department of Neurology, University of Texas Southwestern Medical Center, Dallas. Autoimmune Neurology Group, West Wing, Level 3, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom. Autoimmune Neurology Group, West Wing, Level 3, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom. Department of Neurology, University of California, San Francisco (UCSF), San Francisco. Movement Disorders Unit, Department of Neurology, Tel Aviv Sourazky Medical Center, Affiliate of Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel. Department of Neurology, University of California, San Francisco (UCSF), San Francisco. Department of Neurology, Mayo Clinic, Jacksonville, Florida. Washington University in St Louis, St Louis, Missouri. Washington University in St Louis, St Louis, Missouri. Department of Neurology, University of Utah, Salt Lake City. Department of Neurology, University of Utah, Salt Lake City. Larner College of Medicine at the University of Vermont, Burlington. Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota. Center for Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota. Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota. Center for Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota. Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota. Center for Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota. Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota. Center for Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota. Center for Multiple Sclerosis and Autoimmune Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota. Graduate School of Health Sciences, Mayo Clinic College of Medicine, Rochester, Minnesota. Department of Neurology, University of Texas Southwestern Medical Center, Dallas. Autoimmune Neurology Group, West Wing, Level 3, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.
 Maastricht University, Department of Psychiatry and Neuropsychology, Alzheimer Centre Limburg, School for Mental Health and Neurosciences, Maastricht, The Netherlands. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Health Economics Group, University of Exeter College of Medicine and Health, University of Exeter, Exeter, UK. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Quantify Research, Hantverkargatan 8, Stockholm, Sweden. RTI Health Solutions, Research Triangle Park, North Carolina, USA. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden. Care Policy Evaluation Centre, London School of Economics, London, UK. Eli Lilly and Company (UK), Bracknell, UK. Erasmus MC University Medical Center, Department of Public Health, Rotterdam, The Netherlands. Medicus Economics LLC, Boston, Massachusetts, USA. University of Southern California, Leonard D. Schaeffer Center for Health Policy & Economics, Los Angeles, California, USA. Department of Health Services, Policy & Practice, Brown University School of Public Health, Providence, Rhode Island, USA. Providence Veterans Affairs (VA) Medical Center, Center of Innovation in Long Term Services and Supports, Providence, Rhode Island, USA. Center for the Evaluation of Value and Risk in Health, Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, Massachusetts, USA. Department of Health Services, Policy & Practice, Brown University School of Public Health, Providence, Rhode Island, USA. Osakidetza Basque Health Service, Debagoiena Integrated Health Organisation, Research Unit, Arrasate-Mondragón, Spain. Biodonostia Health Research Institute, Donostia-San Sebastián, Spain. Department of Health Services, Policy & Practice, Brown University School of Public Health, Providence, Rhode Island, USA. University of Calgary, Department of Community Health Sciences, Calgary, Canada. O'Brien Institute of Public Health, Alberta, Canada. Evidera, Bethesda, Maryland, USA. University of Southern California, Leonard D. Schaeffer Center for Health Policy & Economics, Los Angeles, California, USA. Karolinska Institutet, Department for Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Solna, Sweden. H. Lundbeck A/S, Valby, Denmark. Maastricht University, Department of Psychiatry and Neuropsychology, Alzheimer Centre Limburg, School for Mental Health and Neurosciences, Maastricht, The Netherlands.
 Neurobiology Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, Guangdong 518107, China. Neurobiology Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, Guangdong 518107, China. Neurobiology Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, Guangdong 518107, China. Neurobiology Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, Guangdong 518107, China. Neurobiology Research Center, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, Guangdong 518107, China. APDA Center for Advanced Parkinson Research, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Neurogenomics Lab, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA. APDA Center for Advanced Parkinson Research, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Neurogenomics Lab, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, China. Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, China. Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, China. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Assistance Publique Hôpitaux de Paris, Département de Neurologie et de Génétique, Hôpital Pitié-Salpêtrière, F-75013 Paris, France. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4068 Stavanger, Norway. Department of Chemistry, Bioscience and Environmental Engineering, University of Stavanger, 4021 Stavanger, Norway. Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. Paris-Saclay University, UVSQ, Inserm, Gustave Roussy, 'Exposome and Heredity' Team, CESP, F94805 Villejuif, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Assistance Publique Hôpitaux de Paris, Département de Neurologie et de Génétique, Hôpital Pitié-Salpêtrière, F-75013 Paris, France. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Assistance Publique Hôpitaux de Paris, Département de Neurologie et de Génétique, Hôpital Pitié-Salpêtrière, F-75013 Paris, France. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Praxis Precision Medicines, Cambridge, MA 02142, USA. Department of Neurology, Center for Health and Technology, University of Rochester, Rochester, NY 14642, USA. Department of Neurology and Neurosurgery, Institute of Clinical Medicine, University of Tartu, Tartu 50406, Estonia. Neurology Clinic, Tartu University Hospital, Tartu 50406, Estonia. Centre for Molecular Medicine and Innovative Therapeutics, Murdoch University, Murdoch, Perth, WA 6150, Australia. Perron Institute for Neurological and Translational Science, Nedlands, WA 6009, Australia. Banner Sun Health Research Institute, Sun City, AZ 85351, USA. Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Assistance Publique Hôpitaux de Paris, Département de Neurologie et de Génétique, Hôpital Pitié-Salpêtrière, F-75013 Paris, France. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4068 Stavanger, Norway. Department of Chemistry, Bioscience and Environmental Engineering, University of Stavanger, 4021 Stavanger, Norway. Department of Neurology, Stavanger University Hospital, 4068 Stavanger, Norway. Department of Neurology, Haukeland University Hospital, 5020 Bergen, Norway. Department of Clinical Medicine, University of Bergen, 5020 Bergen, Norway. Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. Departments of Radiology and Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, USA. Program of Physical Therapy and Program of Occupational Therapy, Washington University School of Medicine, St. Louis, MO 63110, USA. German Center for Neurodegenerative diseases (DZNE), 72076 Tübingen, Germany. Department of Neurology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands. John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK. Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK. John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK. APDA Center for Advanced Parkinson Research, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Neurogenomics Lab, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA.
 Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA; Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address: joann.arce@childrens.harvard.edu. Emory School of Medicine, Atlanta, GA 30322, USA. Benaroya Research Institute, University of Washington, Seattle, WA 98101, USA. University of California San Francisco, San Francisco, CA 94115, USA. The University of Texas at Austin, Austin, TX 78712, USA. Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA. University of California San Francisco, San Francisco, CA 94115, USA. Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. University of California San Francisco, San Francisco, CA 94115, USA. Yale School of Medicine, New Haven, CT 06510, USA. Yale School of Medicine, New Haven, CT 06510, USA. Yale School of Public Health, New Haven, CT 06510, USA. Yale School of Medicine, New Haven, CT 06510, USA. Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA. Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA; Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. Yale School of Medicine, New Haven, CT 06510, USA. Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA; Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA. Knocean, Inc., Toronto, ON M6P 2T3, Canada. La Jolla Institute for Immunology, La Jolla, CA 92037, USA. Drexel University, Tower Health Hospital, Philadelphia, PA 19104, USA. Emory School of Medicine, Atlanta, GA 30322, USA. Emory School of Medicine, Atlanta, GA 30322, USA. Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20814, USA. Yale School of Public Health, New Haven, CT 06510, USA. Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. University of California San Francisco, San Francisco, CA 94115, USA. University of California San Francisco, San Francisco, CA 94115, USA. Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. University of California San Francisco, San Francisco, CA 94115, USA. Yale School of Medicine, New Haven, CT 06510, USA; Broad Institute of MIT & Harvard, Cambridge, MA 02142, USA. University of California San Francisco, San Francisco, CA 94115, USA. Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT & Harvard, Cambridge, MA 02142, USA. Benaroya Research Institute, University of Washington, Seattle, WA 98101, USA. Stanford University School of Medicine, Palo Alto, CA 94305, USA. Yale School of Medicine, New Haven, CT 06510, USA. Drexel University, Tower Health Hospital, Philadelphia, PA 19104, USA. Emory School of Medicine, Atlanta, GA 30322, USA. Yale School of Public Health, New Haven, CT 06510, USA. Clinical and Data Coordinating Center, Boston Children's Hospital, Boston, MA 02115, USA; Precision Vaccines Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT & Harvard, Cambridge, MA 02142, USA. National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20814, USA. National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20814, USA. Yale School of Public Health, New Haven, CT 06510, USA. La Jolla Institute for Immunology, La Jolla, CA 92037, USA. Yale School of Medicine, New Haven, CT 06510, USA. Electronic address: steven.kleinstein@yale.edu.
 Center for Genomic and Precision Medicine, College of Medicine, University of Ibadan, Ibadan, Nigeria. mayowaowolabi@yahoo.com. Neurology Unit, Department of Medicine, College of Medicine, University of Ibadan, Ibadan, Nigeria. mayowaowolabi@yahoo.com. African Stroke Organization, Ibadan, Nigeria. mayowaowolabi@yahoo.com. World Federation for Neurorehabilitation, North Shields, UK. mayowaowolabi@yahoo.com. Lebanese American University of Beirut, Beirut, Lebanon. mayowaowolabi@yahoo.com. Blossom Specialist Medical Center, Ibadan, Nigeria. mayowaowolabi@yahoo.com. Neurology, Public Health, Disability Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. Neurology Department Inselspital - University of Bern, Bern, Switzerland. European Academy of Neurology, Vienna, Austria. European Federation of Neurological Associations, Brussels, Belgium. European Federation of Neurological Associations, Brussels, Belgium. Department of Neurology, University College Hospital, Ibadan, Nigeria. Institute of Human Behaviour and Allied Sciences, New Delhi, India. Department of Neurology, Duke University School of Medicine, Durham, NC, USA. John Walton Muscular Dystrophy Research Center, Newcastle University, Newcastle, UK. Faculty of Medicine and Health Sciences, University of East Anglia, Norwich, UK. One Neurology Initiative, Brussels, Belgium. Department of Neurology, Mayo Clinic, Phoenix, AZ, USA. Atria Academy of Science and Medicine, New York, NY, USA. American Brain Foundation, Minneapolis, MN, USA. Tics and Tourette Across the Globe, Hannover, Germany. Australian Clinical Psychology Association, Sydney, New South Wales, Australia. Department of Neurology, Apollo Specialty Hospitals, Nellore, India. Meningitis Research Foundation, Bristol, UK. Alzheimer's Disease International, London, UK. Women's Brain Project, Guntershausen, Switzerland. Women's Brain Project, Guntershausen, Switzerland. Women's Brain Project, Guntershausen, Switzerland. Department of Paediatric Neurology, Erasmus MC University Medical Center, Rotterdam, The Netherlands. European Paediatric Neurology Society, Bolton, UK. Department of Non-Communicable Diseases, Ministry of Health, Nairobi, Kenya. Global Brain Health Institute, San Francisco, CA, USA. Department of Brain and Behavioral Sciences of the University of Pavia, Pavia, Italy. IRCCS C. Mondino Foundation Neurological Institute, Pavia, Italy. International Headache Society, London, UK. University of Kent, Canterbury, UK. International Neuro-Palliative Care Society, Roseville, MN, USA. Department of Neurology, Ludwig-Maximilians University Munich, Klinikum Großhadern, Munich, Germany. International Federation of Clinical Neurophysiology, Milwaukee, WI, USA. Amal Neuro Developmental Centres, Gudalur, India. Al Ameen Educational Trust, Gudalur, India. 37 Military Hospital, Accra, Ghana. African Academy of Neurology, Cape Town, South Africa. European Paediatric Neurology Society, Bolton, UK. Department of Paediatric Neurology, Children's Hospital Datteln, University Witten/Herdecke, Witten, Germany. National Institute for Stroke and Applied Neurosciences, Auckland University of Technology, Auckland, New Zealand. Migraine Association of Ireland, Dublin, Ireland. European Federation of Neurological Associations, Brussels, Belgium. European Federation of Neurological Associations, Brussels, Belgium. European Federation of Neurological Associations, Brussels, Belgium. Department of Paediatric Neurology and Critical Care, University of Pittsburgh Medical Centre Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. Safar Center for Resuscitation Research, University of Pittsburgh Medical Centre Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. Multiple Sclerosis International Federation, London, UK. Multiple Sclerosis International Federation, London, UK. Multiple Sclerosis International Federation, London, UK. National Autonomous University of Honduras, Tegucigalpa, Honduras. Pan-American Federation of Neurological Societies, Santiago de Chile, Chile. HOMI Fundacion Hospital Paediatrico la Misericordia, Bogota, Colombia. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. World Sleep Society, Rochester, MN, USA. World Sleep Society, Rochester, MN, USA. Paracelsus-Elena Hospital, Kassel, Department of Neurosurgery, University Medical Centre, Goettingen, Germany. Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital Neuroscience Institute, University of Cape Town, Cape Town, South Africa. International Child Neurology Association, London, UK. African Stroke Organization, Ibadan, Nigeria. Neuroscience and Ageing Research Unit, Institute for Advanced Medical Research and Training, College of Medicine, University of Ibadan, Ibadan, Nigeria. Department of Neurology, University College Hospital, Ibadan, Nigeria. World Federation for Neurorehabilitation, North Shields, UK. Department of Neurology, Pennsylvania State University College of Medicine, Hershey, PA, USA. World Federation for Neurorehabilitation, North Shields, UK. SRH Neurorehabilitation Hospital Bad Wimpfen, Bad Wimpfen, Germany. European Academy of Neurology, Vienna, Austria. Department of Neurology, Ghent University Hospital, Ghent, Belgium. Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Alberta, Canada. International League Against Epilepsy, Flower Mound, TX, USA. International League Against Epilepsy, Flower Mound, TX, USA. Clinical Neurosciences Section, UCL Institute of Child Health, University College London, London, UK. Cohen Veterans Bioscience, New York, NY, USA. Brain Health Nexus, New York, NY, USA. One Neurology Initiative, Brussels, Belgium. Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy. European Brain Council, Brussels, Belgium. Alzheimer's Disease International, London, UK. World Federation for Neurorehabilitation, North Shields, UK. Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. European Paediatric Neurology Society, Bolton, UK. Paediatric Neurosciences Research Group, School of Health and Wellbeing, University of Glasgow, Glasgow, UK. Department of Medicine, Afe Babalola University, Ado-Ekiti, Nigeria. Federal Teaching Hospital, Ido-Ekiti, Nigeria. College of Medicine, University of Ibadan, Ibadan, Nigeria. Department of Neurosurgery, University of North Carolina at Chapel Hill, North Carolina, NC, USA. World Federation of Neurosurgical Societies, Prague, Czech Republic. Department of Clinical Sciences/Diagnostic Radiology, Lund University, Lund, Sweden. Department of Clinical Sciences/Neurology, Lund University, Lund, Sweden. Clinical Neurotechnology Laboratory, Department of Psychiatry and Neurosciences, Charité Campus Mitte, Charité - Universitätsmedizin Berlin, Berlin, Germany. Department of Neurology, Erasmus MC University Medical Center, Rotterdam, The Netherlands. Peripheral Nerve Society, Roseville, MN, USA. Peripheral Nerve Society, Roseville, MN, USA. Department of Neurology, Cedars Sinai Medical Center, Los Angeles, CA, USA. Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool, UK. Encephalitis Society, Malton, North Yorkshire, UK. World Federation of Neurosurgical Societies, Prague, Czech Republic. Department of Neurosurgery, Humanitas Clinical and Research Center - IRCCS, Humanitas University, Milan, Italy.
 Wolfson Institute for Population Health, Queen Mary University Barts and The London School of Medicine and Dentistry, London, UK. Toronto General Hospital Research Institute, University of Toronto, Toronto, Ontario, Canada. Nuffield Department of Medicine, Oxford University, Oxford, UK. Bristol Medical School, University of Bristol Faculty of Health Sciences, Bristol, UK. Institute for Research and Education to Advance Community Health, Washington State University, Seattle, Washington, USA. The Walton Centre NHS Foundation Trust, Liverpool, UK. Centre for Clinical Brain Sciences, Royal Infirmary, Edinburgh, UK. Department of Psychological Medicine, King's College London Institute of Psychiatry Psychology and Neuroscience, London, UK trudie.chalder@kcl.ac.uk. Departments of Anesthesiology, Medicine and Psychiatry, University of Michigan, Ann Arbor, Michigan, USA. Ashford St Peter's NHS Foundation Trust, Chertsey, St George's University Hospitals, London, UK. Institute of Mental Health, University College London, London, UK. Department of Neurology, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts, USA. Neuroscience Research Centre, St George's University, London, UK. James J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio, USA. Pure Sports Medicine, London, UK. Research Clinic for Functional Disorders, Aarhus University, Aarhus, Denmark. Centre for Epidemic Interventions Research, Division for Health Services, Norwegian Institute of Public Health, Oslo, Norway. Hopital Avicenne, Universite Sorbonne Paris Nord - Campus de Bobigny, Bobigny, France. Centre for Evidence Synthesis in Global Health, Liverpool School of Tropical Medicine, Liverpool, UK. Institute for Evidence-Based Healthcare, Faculty of Health Sciences & Medicine, Bond University, Robina, Queensland, Australia. Institute of Health Research, University of Exeter, Exeter, UK. Psychosomatic Medicine, University Hospital, Technical University Munich, Munich, Germany. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK. Persistent Physical Symptom Service, South London and Maudsley NHS Foundation Trust, London, UK. Department of Neurology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. Department of Medical Psychology, University of Amsterdam, Amsterdam, Netherlands. Regenstrief Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA. Brisbane Clinical Neuroscience Centre, The University of Queensland, Brisbane, Queensland, Australia. Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia, USA. Primary Care Research Centre, Primary Care Population Sciences and Medical Education Unit, Faculty of Medicine, University of Southampton, Southampton, UK. Kirby Institute, University of New South Wales, Sydney, New South Wales, Australia. Faculty of Occupational Medicine, Guy's and St Thomas' NHS Foundation Trust, London, UK. Department of Internal Medicine, Radboud University Medical College, Nijmegen, Netherlands. Department of Medicine, Cumberland Infirmary Carlisle, Carlisle, UK. Department of Infection and Immunity, Barts Health NHS Trust, London, UK. Primary Care & Population Science, University College London, London, UK. Neurology and Psychiatry, Massachusetts General Hospital, Charlestown, Massachusetts, USA. Department of Neurology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. Department of Neuroscience, The Medical School, University of Sheffield, Sheffield, UK. Division of Clinical Psychology and Psychotherapy Clinic, University of Marburg, Marburg, Germany. Persistent Physical Symptom Service, South London and Maudsley NHS Foundation Trust, London, UK. Dept. of Neurology and Center of Clinical Neuroscience, Charles University in Prague, Prague, Czech Republic. Psychological Medicine Research, University of Oxford, Oxford, UK. Department of Neurology, King's College Hospital, London, UK. Centre for Mental Health, University of Toronto, University Health Network, Toronto, Ontario, Canada. Centre for Clinical Brain Sciences, Royal Infirmary, University of Edinburgh, Edinburgh, UK. Department of Neurosciences, Biomedicine and Movement, University of Verona, Verona, Italy. Centre for Movement, Occupational and Rehabilitation Sciences, Oxford Brookes University, Oxford, UK. Psychological Medicine, King's College London Institute of Psychiatry Psychology and Neuroscience, London, UK. Division of Medicine and Laboratory Sciences, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Cognitve Neurology Research Group, University of Exeter Medical School, Exeter, UK.
 Neurology, University of Rochester, Rochester, NY, USA. Neurology, University of Rochester, Rochester, NY, USA. Neurology, University of Rochester, Rochester, NY, USA. Center for Health and Technology, University of Rochester, Rochester, NY, USA. Translational Medicine, Ionis Pharmaceuticals, Carlsbad, CA, USA. Neurology, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Neuroscience Research Program, Houston Methodist Research Institute, Houston, TX, USA. Neuromuscular Medicine, Stanford University, Palo Alto, CA, USA. Neurodegeneration Development Unit, Biogen, Cambridge, MA, USA. Neurology, University of Rochester, Rochester, NY, USA. Neuromuscular Medicine, Stanford University, Palo Alto, CA, USA. Neuromuscular Clinic, Houston Methodist Research Institute, Houston, TX, USA. Neurology, University of Kansas Medical Center, Kansas City, KS, USA. Neurology, University of Utah, Salt Lake City, UT, USA. Neurology, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Neurology, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Center for Genetic Muscle Disorders, Kennedy Krieger Institute, Baltimore, MD, USA. Physical Therapy, University of Florida, Gainesville, FL, USA. Pharmacokinetics and Clinical Pharmacology, Ionis Pharmaceuticals, Carlsbad, CA, USA. Neurology, University of Utah, Salt Lake City, UT, USA. Neuromuscular Clinic, Houston Methodist Research Institute, Houston, TX, USA. Neurology, University of Kansas Medical Center, Kansas City, KS, USA. Center for Genetic Muscle Disorders, Kennedy Krieger Institute, Baltimore, MD, USA. Fixel Institute for Neurological Diseases, University of Florida, Gainesville, FL, USA. Biometrics, Ionis Pharmaceuticals, Carlsbad, CA, USA. Clinical Development, Ionis Pharmaceuticals, Carlsbad, CA, USA. Ionis Pharmaceuticals, Carlsbad, CA, USA. Electronic address: fbennett@ionisph.com.
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 ORCID: 0009-0003-7349-1648 ORCID: 0000-0003-3127-1287 ORCID: 0000-0002-6763-0125 ORCID: 0000-0002-2628-4334


 ORCID: 0000-0003-4987-6313




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 ORCID: 0000-0002-5471-7774 ORCID: 0000-0002-6184-3998



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 ORCID: 0000-0001-8105-9124 ORCID: 0000-0002-7265-5634 ORCID: 0000-0001-6578-8474 ORCID: 0000-0002-5043-5649





 ORCID: 0000-0002-9075-4126






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 ORCID: 0000-0002-5825-8026 ORCID: 0000-0001-6649-1461 ORCID: 0000-0001-8516-9718




 ORCID: 0000-0003-3028-0253 ORCID: 0000-0001-6870-6585 ORCID: 0000-0001-8088-9695 ORCID: 0000-0001-8629-553X ORCID: 0000-0001-7120-130X

 ORCID: 0000-0002-7107-8679




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 ORCID: 0000-0001-6862-5531 ORCID: 0000-0002-7288-6344 ORCID: 0000-0001-6077-0654 ORCID: 0000-0002-2034-8800
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 ORCID: 0000-0002-3952-849X ORCID: 0000-0002-0339-9876 ORCID: 0000-0002-1212-5762

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 ORCID: 0000-0002-2875-124X ORCID: 0000-0003-4274-9258 ORCID: 0000-0003-2784-8207 ORCID: 0000-0003-3198-6063 ORCID: 0000-0001-5744-6466 ORCID: 0000-0002-2169-3788 ORCID: 0000-0003-1026-570X ORCID: 0000-0002-8850-6502


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 ORCID: 0000-0002-8513-5443 ORCID: 0000-0002-6755-496X ORCID: 0009-0002-5395-9963 ORCID: 0009-0001-3119-8203 ORCID: 0000-0003-3459-7741 ORCID: 0000-0002-9860-7657
 ORCID: 0000-0003-3062-5872
 ORCID: 0000-0003-4900-3184






 ORCID: 0000-0002-3903-8343






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 ORCID: 0000-0001-8113-3988 ORCID: 0000-0003-3824-2796 ORCID: 0000-0002-0020-8739
 ORCID: 0000-0002-2347-8096



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 ORCID: 0000-0002-6579-9963


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 ORCID: 0000-0002-6146-068X ORCID: 0000-0001-7224-2189 ORCID: 0000-0002-8997-0307 ORCID: 0000-0002-7311-2615 ORCID: 0000-0002-4633-9195

 ORCID: 0000-0001-8957-661X






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 ORCID: 0000-0003-2320-5095 ORCID: 0000-0001-9268-6270

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 ORCID: 0000-0002-7201-065X ORCID: 0000-0001-5486-6588 ORCID: 0000-0002-1318-4262 ORCID: 0000-0003-4147-0642



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 ORCID: 0000-0002-7328-1427 ORCID: 0000-0003-1457-6222
 ORCID: 0000-0003-1215-3373


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 ORCID: 0000-0002-4808-7008
 ORCID: 0000-0002-7904-8482 ORCID: 0000-0002-1668-5177 ORCID: 0000-0003-4688-8482 ORCID: 0000-0001-8909-1591


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 ORCID: 0000-0002-0406-0460

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 ORCID: 0000-0003-2022-3386 ORCID: 0000-0001-9461-5927 ORCID: 0000-0001-5554-1697 ORCID: 0000-0002-7592-0253
 ORCID: 0000-0003-4570-2252

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 ORCID: 0000-0002-0469-6872

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 ORCID: 0000-0003-0812-676X ORCID: 0000-0001-8617-5052



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 ORCID: 0000-0002-7703-0553 ORCID: 0000-0002-0367-1008
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 ORCID: 0000-0003-2358-4320 ORCID: 0000-0002-9232-8964 ORCID: 0000-0002-6910-0080 ORCID: 0000-0002-1850-1175 ORCID: 0000-0002-7826-0019 ORCID: 0000-0002-4979-613X ORCID: 0000-0001-9227-0240 ORCID: 0000-0001-5390-2655 ORCID: 0000-0002-5485-0479
 ORCID: 0000-0002-4146-5870 ORCID: 0000-0001-5626-1144 ORCID: 0000-0001-5209-6647 ORCID: 0000-0002-0825-0851

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 ORCID: 0000-0003-2793-6303 ORCID: 0000-0003-0997-8817 ORCID: 0000-0001-5528-8070

 ORCID: 0000-0002-8776-0664





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 ORCID: 0000-0002-5863-2452 ORCID: 0000-0002-8333-7738 ORCID: 0000-0001-7689-2533
 ORCID: 0000-0002-3336-4092 ORCID: 0000-0001-8649-6374 ORCID: 0000-0003-2760-5651
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 ORCID: 0000-0002-4051-3500 ORCID: 0000-0002-7400-5686 ORCID: 0000-0003-0704-9387 ORCID: 0000-0003-2871-0672 ORCID: 0000-0003-1220-8354 ORCID: 0000-0001-8143-7893
 ORCID: 0000-0001-6618-7013 ORCID: 0000-0001-6022-7731 ORCID: 0000-0003-4441-3088









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 ORCID: 0000-0002-6612-4749
 ORCID: 0000-0001-5608-2947

 ORCID: 0000-0003-1322-0689
 ORCID: 0000-0002-4493-1347



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 ORCID: 0000-0002-1343-9069 ORCID: 0000-0003-0023-9399

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 ORCID: 0000-0002-7947-9418


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 ORCID: 0000-0003-2455-1432 ORCID: 0000-0001-6892-104X ORCID: 0000-0002-8455-980X ORCID: 0000-0002-1790-2719
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 ORCID: 0000-0003-0680-7828



 ORCID: 0000-0001-6352-8687 ORCID: 0009-0008-4455-436X ORCID: 0000-0002-6809-9401 ORCID: 0000-0002-7133-7378
 ORCID: 0000-0003-3237-6267 ORCID: 0000-0003-0483-4478 ORCID: 0000-0003-2050-2908 ORCID: 0000-0001-9037-7300 ORCID: 0000-0002-3959-4067 ORCID: 0000-0002-3878-8820
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 ORCID: 0000-0002-0256-8930 ORCID: 0000-0001-5899-9097
 ORCID: 0000-0002-3424-5976 ORCID: 0000-0001-6172-801X





 ORCID: 0000-0002-0969-3339

 ORCID: 0000-0002-5789-5162


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 ORCID: 0000-0002-6402-6774 ORCID: 0000-0001-8069-9998 ORCID: 0000-0003-0125-7150



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 ORCID: 0000-0002-5485-0479



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 ORCID: 0000-0002-6735-5768 ORCID: 0000-0002-8725-3654
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 ORCID: 0000-0002-9631-4674 ORCID: 0000-0001-5484-2359

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 ORCID: 0000-0003-0491-3360 ORCID: 0000-0001-5327-5479 ORCID: 0000-0001-6232-9555 ORCID: 0000-0001-8672-711X ORCID: 0000-0002-4918-9276


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 ORCID: 0000-0002-7102-9703 ORCID: 0000-0001-5998-2609 ORCID: 0000-0003-3421-1394 ORCID: 0000-0001-7678-3812 ORCID: 0000-0003-2311-6623 ORCID: 0000-0003-1213-5853 ORCID: 0000-0001-9735-606X ORCID: 0000-0003-3127-1287


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 ORCID: 0000-0002-4910-5204

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 ORCID: 0000-0002-1292-1144






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 ORCID: 0000-0002-3623-7363 ORCID: 0000-0002-8125-8972
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 ORCID: 0000-0001-5510-231X ORCID: 0000-0002-2176-1242 ORCID: 0000-0001-9948-2553


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 ORCID: 0000-0001-9271-346X ORCID: 0000-0002-8225-8747 ORCID: 0000-0002-5093-0754 ORCID: 0000-0001-8143-7893 ORCID: 0000-0002-3760-6634 ORCID: 0000-0002-2838-9148 ORCID: 0000-0003-2871-0672
 ORCID: 0000-0002-2110-9393 ORCID: 0000-0003-2902-5589


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 ORCID: 0000-0001-9658-815X ORCID: 0000-0002-9326-5678 ORCID: 0000-0002-5393-7417 ORCID: 0000-0001-7179-0335
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 ORCID: 0000-0002-9266-2030


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 ORCID: 0000-0002-7796-0064 ORCID: 0000-0002-5597-2670 ORCID: 0000-0001-6695-5684 ORCID: 0000-0002-9751-5881
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 ORCID: 0000-0001-6242-9804


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 ORCID: 0000-0002-2166-4012

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 ORCID: 0000-0001-7360-6853 ORCID: 0000-0002-9593-8231 ORCID: 0000-0002-8468-8513 ORCID: 0000-0002-8575-7824




 ORCID: 0000-0002-2245-039X ORCID: 0000-0001-9540-1859 ORCID: 0000-0003-0355-9443

 ORCID: 0000-0002-7696-1479 ORCID: 0000-0002-7381-2427 ORCID: 0000-0002-5350-3328 ORCID: 0000-0001-7717-6125 ORCID: 0000-0003-4982-4855 ORCID: 0000-0002-5397-5595
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 ORCID: 0000-0001-5982-669X





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 ORCID: 0000-0001-9062-5925

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 ORCID: 0000-0002-3942-4340

 ORCID: 0000-0002-9041-8325 ORCID: 0000-0002-2632-9889 ORCID: 0000-0002-4219-9594 ORCID: 0000-0003-3877-0783


 ORCID: 0000-0001-9415-936X ORCID: 0000-0003-0680-7828


 ORCID: 0000-0002-8722-4255 ORCID: 0000-0001-9900-4295 ORCID: 0000-0001-8372-3615 ORCID: 0000-0002-2399-3020
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 ORCID: 0000-0003-4174-4885 ORCID: 0000-0001-7097-4765 ORCID: 0000-0002-2963-7625 ORCID: 0000-0001-7061-6941 ORCID: 0000-0002-0030-0236 ORCID: 0000-0001-9217-1445 ORCID: 0000-0001-6577-8217 ORCID: 0000-0002-8042-3286 ORCID: 0000-0001-6700-1022

 ORCID: 0000-0002-4851-8277 ORCID: 0000-0001-6914-9987 ORCID: 0000-0002-0399-5344 ORCID: 0000-0001-6842-799X
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 ORCID: 0000-0003-1243-2372 ORCID: 0000-0001-9244-1193


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 ORCID: 0000-0002-8139-6144 ORCID: 0000-0002-8819-1619
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 ORCID: 0000-0001-5464-6518 ORCID: 0000-0001-6041-4588






 ORCID: 0000-0001-5884-9734

 ORCID: 0000-0002-0955-6641

 ORCID: 0000-0003-2755-2043 ORCID: 0000-0001-6909-6109 ORCID: 0000-0002-4664-9310 ORCID: 0000-0001-6183-2394 ORCID: 0000-0003-4541-8841 ORCID: 0000-0002-2833-6337
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 ORCID: 0000-0002-6817-9671
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 ORCID: 0000-0002-5874-4366 ORCID: 0000-0003-3821-6256 ORCID: 0000-0001-7486-0706 ORCID: 0000-0003-1638-7978 ORCID: 0000-0002-7797-2399
 ORCID: 0000-0002-1532-2868

 ORCID: 0000-0001-5878-8687 ORCID: 0000-0003-1284-4350
 ORCID: 0000-0002-2179-4407








 ORCID: 0000-0001-8788-0984 ORCID: 0000-0002-9926-2531

 ORCID: 0000-0002-9568-2790 ORCID: 0000-0001-5689-585X ORCID: 0000-0003-3855-4706 ORCID: 0000-0002-7371-0391 ORCID: 0000-0002-4872-9189 ORCID: 0000-0003-4310-3432 ORCID: 0000-0002-4341-4719

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 ORCID: 0000-0003-2632-5236 ORCID: 0000-0001-7447-344X ORCID: 0000-0002-2786-3434

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 ORCID: 0000-0002-1473-1715 ORCID: 0000-0001-5177-2076 ORCID: 0000-0003-0591-2976 ORCID: 0000-0003-3210-4771
 ORCID: 0000-0002-5398-3632 ORCID: 0000-0002-5418-316X
 ORCID: 0000-0002-1812-9844


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 ORCID: 0000-0002-0156-4719 ORCID: 0000-0003-0079-3445 ORCID: 0000-0002-3988-5673 ORCID: 0000-0002-5070-2567 ORCID: 0000-0002-9532-7051 ORCID: 0000-0001-8502-4455 ORCID: 0000-0002-2151-9413
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 ORCID: 0000-0003-2419-8587
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 ORCID: 0000-0003-3509-5591




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 ORCID: 0000-0002-4175-6053



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 ORCID: 0000-0003-3668-5147
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 ORCID: 0000-0003-2736-3541 ORCID: 0000-0001-6481-0748
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 ORCID: 0000-0003-3644-7528





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 ORCID: 0000-0003-1975-3195 ORCID: 0000-0002-2172-9955 ORCID: 0000-0001-6119-2542 ORCID: 0000-0001-6119-605X

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 ORCID: 0000-0003-1762-5499




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 ORCID: 0000-0002-0217-0324 ORCID: 0000-0002-6041-6759 ORCID: 0000-0003-2565-242X
 ORCID: 0000-0002-8329-6083 ORCID: 0000-0002-6623-0429




 ORCID: 0000-0003-1655-1184
 ORCID: 0000-0001-8767-2675 ORCID: 0000-0001-9600-402X


 ORCID: 0000-0001-7274-2634
 ORCID: 0000-0001-5905-1572 ORCID: 0000-0002-2004-0531
 ORCID: 0000-0002-3389-8713
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 ORCID: 0000-0002-6781-707X
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 ORCID: 0000-0002-2856-1905 ORCID: 0000-0001-8410-3039 ORCID: 0000-0003-2215-8143 ORCID: 0000-0003-2637-1611 ORCID: 0000-0003-1411-1003 ORCID: 0000-0002-0094-4592 ORCID: 0000-0001-9396-8683

 ORCID: 0000-0002-0125-6038 ORCID: 0000-0003-3062-030X ORCID: 0000-0003-4609-1895 ORCID: 0000-0003-4171-8919 ORCID: 0000-0003-2006-3503
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 ORCID: 0000-0003-0116-8035 ORCID: 0000-0002-6661-2910 ORCID: 0000-0002-6140-5584 ORCID: 0000-0002-1960-9065


 ORCID: 0000-0003-0659-5298 ORCID: 0000-0002-1662-143X ORCID: 0000-0002-8792-4219 ORCID: 0000-0002-5396-0932 ORCID: 0000-0003-3975-8938 ORCID: 0000-0002-2954-5755 ORCID: 0000-0003-1412-4453 ORCID: 0000-0002-8528-2283 ORCID: 0000-0002-1125-7720 ORCID: 0000-0001-8407-7782 ORCID: 0000-0001-7857-2373

 ORCID: 0000-0001-9365-4115 ORCID: 0000-0002-9120-5970
 ORCID: 0000-0003-3898-1943
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 ORCID: 0000-0001-9072-8211

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 ORCID: 0000-0001-9547-7757

 ORCID: 0000-0002-9845-3125
 ORCID: 0000-0003-2030-5568

 ORCID: 0000-0001-5179-5016 ORCID: 0000-0002-4508-3829

 ORCID: 0000-0002-4015-9783 ORCID: 0000-0002-8387-6491 ORCID: 0000-0002-6661-2910 ORCID: 0000-0003-0861-2178 ORCID: 0000-0002-7969-8346
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 ORCID: 0000-0003-2733-242X ORCID: 0000-0001-6614-569X ORCID: 0000-0002-4933-8171 ORCID: 0000-0002-8629-6628 ORCID: 0000-0002-5171-3436 ORCID: 0000-0001-5161-9880 ORCID: 0000-0002-3125-7453 ORCID: 0000-0002-7776-6472 ORCID: 0000-0002-4274-5567
 ORCID: 0000-0003-2074-1861
 ORCID: 0000-0002-3495-7201 ORCID: 0000-0001-5948-8109 ORCID: 0000-0003-2254-3025
 ORCID: 0000-0001-8298-176X ORCID: 0000-0001-8566-4284 ORCID: 0000-0002-3746-3282 ORCID: 0000-0003-2077-2537 ORCID: 0000-0002-7996-7673 ORCID: 0000-0002-1306-2708 ORCID: 0000-0002-3817-5186 ORCID: 0000-0002-6986-9914 ORCID: 0000-0001-6380-2420 ORCID: 0000-0002-5496-9971 ORCID: 0000-0001-7423-4764 ORCID: 0000-0003-0575-6950
 ORCID: 0000-0002-4302-2678



 ORCID: 0000-0001-8608-7757 ORCID: 0000-0002-5092-6325
 ORCID: 0000-0002-5912-9998 ORCID: 0000-0001-8486-0558 ORCID: 0000-0002-3889-8739 ORCID: 0000-0003-0077-8114 ORCID: 0000-0003-4848-8909 ORCID: 0000-0003-0573-6175 ORCID: 0000-0003-1148-6723 ORCID: 0000-0002-6333-832X
 ORCID: 0000-0003-3495-0357 ORCID: 0009-0008-1379-431X

 ORCID: 0000-0002-1037-3594 ORCID: 0000-0002-3240-7441

 ORCID: 0000-0001-8846-3349 ORCID: 0000-0002-8162-1559 ORCID: 0000-0002-7736-7113 ORCID: 0000-0002-3750-9615
 ORCID: 0000-0003-3440-8859 ORCID: 0000-0002-1717-298X ORCID: 0000-0002-2152-4220
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 ORCID: 0000-0003-3031-3502 ORCID: 0000-0003-0979-0953 ORCID: 0000-0003-2213-6585
 ORCID: 0000-0002-5140-289X ORCID: 0000-0002-2389-8533 ORCID: 0000-0002-5644-8432 ORCID: 0000-0002-7526-9982



 ORCID: 0000-0001-5447-7224
 ORCID: 0000-0002-7758-3326 ORCID: 0000-0002-6024-8353 ORCID: 0000-0001-5149-2955 ORCID: 0000-0002-7603-1458 ORCID: 0000-0002-9430-371X ORCID: 0000-0002-0394-1223 ORCID: 0000-0002-7817-0814 ORCID: 0000-0001-8725-0739 ORCID: 0000-0003-2927-4008 ORCID: 0000-0002-6999-1004 ORCID: 0000-0002-2883-511X ORCID: 0000-0003-2791-6599 ORCID: 0000-0003-1266-9142 ORCID: 0000-0001-7970-5537 ORCID: 0000-0001-8532-2954 ORCID: 0000-0002-4487-3028 ORCID: 0000-0003-3788-3815 ORCID: 0000-0002-7442-9323
 ORCID: 0000-0001-8158-712X ORCID: 0000-0003-2143-1646 ORCID: 0000-0002-4612-5699 ORCID: 0000-0002-7433-4383 ORCID: 0000-0002-4184-2023 ORCID: 0000-0002-5257-1142

 ORCID: 0000-0002-4755-177X ORCID: 0000-0001-6802-8585 ORCID: 0000-0002-5001-7113 ORCID: 0000-0002-8925-8280
 ORCID: 0000-0002-8825-734X ORCID: 0000-0002-3334-4980 ORCID: 0000-0003-3080-6841 ORCID: 0000-0002-8556-8230 ORCID: 0000-0002-4400-8499 ORCID: 0000-0003-2285-5117 ORCID: 0000-0001-9713-7211 ORCID: 0000-0001-7389-2546 ORCID: 0000-0002-6758-4763 ORCID: 0000-0002-2776-3935
 ORCID: 0000-0002-9909-8858 ORCID: 0000-0002-8489-1861


 ORCID: 0000-0002-3931-5013 ORCID: 0000-0001-7312-7078 ORCID: 0000-0001-9827-1877 ORCID: 0000-0002-1922-9732 ORCID: 0000-0002-2555-4427 ORCID: 0000-0001-7563-5324 ORCID: 0000-0001-9365-3702 ORCID: 0000-0002-1619-8328 ORCID: 0000-0002-7511-5684 ORCID: 0000-0002-4275-9328 ORCID: 0000-0001-6403-016X
 ORCID: 0000-0002-6371-6482 ORCID: 0000-0002-5340-8697 ORCID: 0000-0002-9256-2582 ORCID: 0000-0003-2231-752X ORCID: 0000-0002-5201-0927 ORCID: 0000-0001-8308-9853 ORCID: 0000-0003-4073-3930 ORCID: 0000-0001-7972-9141 ORCID: 0000-0002-1538-6730

 ORCID: 0000-0002-1306-2708 ORCID: 0000-0003-4220-3378 ORCID: 0000-0002-2591-6387 ORCID: 0000-0002-5033-1938 ORCID: 0000-0001-6380-2420
 ORCID: 0000-0002-0985-3662 ORCID: 0000-0002-3386-6308 ORCID: 0000-0001-7337-7122 ORCID: 0000-0002-9860-7657 ORCID: 0000-0002-0020-8739 ORCID: 0000-0001-7699-0328 ORCID: 0000-0003-4074-6125 ORCID: 0000-0002-3985-1297 ORCID: 0000-0003-3834-2981 ORCID: 0000-0002-5967-2800
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 ORCID: 0000-0001-5871-8806 ORCID: 0000-0001-5940-3195 ORCID: 0000-0002-1562-4022 ORCID: 0000-0002-3196-1336 ORCID: 0000-0001-6467-7422 ORCID: 0000-0002-0546-8310 ORCID: 0000-0002-1956-2607
 ORCID: 0009-0008-2812-1214 ORCID: 0000-0002-0751-8967 ORCID: 0009-0008-9849-2782 ORCID: 0000-0002-7972-3556 ORCID: 0000-0002-5656-3270 ORCID: 0009-0001-8292-683X ORCID: 0000-0003-3043-8479
 ORCID: 0000-0002-7974-9051 ORCID: 0000-0002-0206-322X ORCID: 0000-0002-1134-5771 ORCID: 0000-0001-7555-1040 ORCID: 0000-0001-7738-8910 ORCID: 0000-0002-2993-585X ORCID: 0000-0002-6140-5584
 ORCID: 0000-0001-8543-1368
 ORCID: 0000-0001-5306-7880

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 ORCID: 0000-0002-9966-4047 ORCID: 0000-0002-4074-6646 ORCID: 0000-0001-6716-8973 ORCID: 0000-0003-1142-2842 ORCID: 0000-0002-6244-2096 ORCID: 0000-0001-5362-8203
 ORCID: 0000-0003-0094-0900 ORCID: 0000-0002-4691-4524 ORCID: 0000-0003-0123-7934 ORCID: 0000-0002-6623-0429 ORCID: 0000-0002-7697-2776 ORCID: 0000-0002-6985-0658 ORCID: 0000-0002-1058-3831
 ORCID: 0000-0002-6602-0974 ORCID: 0000-0002-2560-3022 ORCID: 0000-0002-4438-5286 ORCID: 0000-0003-4543-3099

 ORCID: 0000-0002-5340-8697 ORCID: 0000-0001-7972-9141 ORCID: 0000-0002-1538-6730
 ORCID: 0000-0002-1245-3352 ORCID: 0000-0001-5834-8307 ORCID: 0000-0003-2091-956X ORCID: 0000-0002-8556-8230 ORCID: 0000-0002-1169-7478 ORCID: 0000-0003-2291-6952 ORCID: 0000-0002-5554-6946 ORCID: 0000-0001-8690-6839


 ORCID: 0000-0002-3534-8467 ORCID: 0000-0003-3612-1448 ORCID: 0000-0003-0548-2689 ORCID: 0000-0002-8161-0462 ORCID: 0000-0002-5241-266X ORCID: 0000-0003-2245-4639 ORCID: 0000-0002-7154-1328 ORCID: 0000-0003-2344-2285 ORCID: 0000-0003-0197-5267 ORCID: 0000-0002-7748-853X ORCID: 0000-0001-7119-0786 ORCID: 0000-0003-4455-7241 ORCID: 0000-0002-7924-7406

 ORCID: 0000-0002-9417-2748 ORCID: 0000-0001-9048-7227 ORCID: 0000-0003-0334-539X ORCID: 0000-0002-5485-0479 ORCID: 0000-0002-3633-8818 ORCID: 0000-0001-8109-1001 ORCID: 0000-0002-8627-9879 ORCID: 0000-0002-5313-5166 ORCID: 0000-0001-9501-4031 ORCID: 0000-0002-6142-2384 ORCID: 0000-0003-2501-2932 ORCID: 0000-0001-7357-8530 ORCID: 0000-0003-2902-5589 ORCID: 0000-0003-2542-0469 ORCID: 0000-0002-0462-0755 ORCID: 0000-0002-0119-3639 ORCID: 0000-0002-1549-3851
 ORCID: 0000-0003-2542-0469 ORCID: 0000-0002-7968-5908 ORCID: 0000-0001-6862-5515 ORCID: 0000-0002-8603-8848 ORCID: 0000-0002-2824-2760 ORCID: 0000-0002-4241-5891 ORCID: 0000-0001-5682-0145 ORCID: 0000-0002-4535-0245
 ORCID: 0000-0002-3870-2804 ORCID: 0000-0002-9527-2011
 ORCID: 0000-0001-7168-214X ORCID: 0000-0002-8052-9240


 ORCID: 0000-0002-1921-9542 ORCID: 0000-0002-8425-2867 ORCID: 0000-0001-9724-5490

 ORCID: 0000-0003-1146-3070 ORCID: 0000-0003-0552-8923 ORCID: 0000-0003-1729-5987 ORCID: 0000-0001-9046-3540 ORCID: 0009-0006-7145-6402 ORCID: 0000-0003-0459-9615 ORCID: 0000-0003-3112-4009 ORCID: 0000-0003-1513-2113 ORCID: 0000-0001-9302-3225 ORCID: 0000-0001-6618-2044 ORCID: 0000-0003-1271-4222 ORCID: 0000-0001-8880-2347 ORCID: 0000-0002-9229-0740 ORCID: 0000-0001-5286-428X ORCID: 0000-0002-1899-0853 ORCID: 0000-0002-6611-2449 ORCID: 0009-0005-0197-0185 ORCID: 0000-0001-9393-5718 ORCID: 0000-0001-9237-1236 ORCID: 0000-0002-8024-5096 ORCID: 0000-0001-7266-6547
 ORCID: 0000-0002-2137-7582 ORCID: 0000-0003-0775-1045 ORCID: 0000-0003-1611-1373 ORCID: 0000-0003-3551-7010 ORCID: 0000-0003-2721-583X ORCID: 0000-0002-4104-6705 ORCID: 0000-0001-6525-3971 ORCID: 0000-0001-9829-8092



























































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































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 Declaration of interests TK received research funding from the German Research Foundation, Interdisciplinary Centre for Clinical Studies (IZKF) Münster, National Multiple Sclerosis Society (USA), European Leukodystrophy Association, Progressive MS Alliance, European Commission (H2020-MSCA-ITN-2018), and Novartis; and received compensation for serving on a scientific advisory board (Novartis) and speaker honoraria from Novartis and Roche. MM has received research grants from MAGNIMS-ECTRIMS, Multiple Sclerosis Society UK, and Merck; consulting fees from Ipsen, BMS Celgene, Biogen, Sanofi-Genzyme, Roche, and Merck; honoraria for lectures from Merck, Roche, and Sanofi-Genzyme; and support for attending meetings from Merck, Biogen, and Sanofi-Genzyme. TC is an employee of the National Multiple Sclerosis Society (USA), which is one of the sponsors of the International Advisory Committee on Clinical Trials in Multiple Sclerosis. JAC has received personal compensation for consulting for Biogen, Bristol-Myers Squibb, Convelo, Genentech, Janssen, NervGen, Novartis, and PSI; for speaking for H3 Communications; and for serving as an editor of the Multiple Sclerosis Journal. JC has received grants or contracts from Biogen, Merck and UC San Francisco; and has received payments or honoraria for lectures, speaker bureaus, or presentations from Biogen, Merck, Sanofi Genzyme, Novartis, Bristol-Myers, and Roche; participation on Data Safety Monitoring Boards or Advisory Boards from Novartis, Merck, Sanofi Genzyme, and Biogen. JG has received grant and contract research support from the National Multiple Sclerosis Society (USA), Biogen, and Octave Biosciences; serves on a steering committee for a trial supported by Novartis; has received speaker fees from Alexion and BMS; and served on an advisory board for Genentech. XM received speaking honoraria and travel expenses for participation in scientific meetings; has been a steering committee member of clinical trials or participated in advisory boards of clinical trials with Abbvie, Actelion, Alexion, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Sandoz, Immunic, Janssen Pharmaceuticals, Medday, Merck, Mylan, Nervgen, Novartis, Sanofi-Genzyme, Teva Pharmaceuticals, TG Therapeutics, Excemed, Multiple Sclerosis International Federation, and National Multiple Sclerosis Society (USA). RAM receives research funding from Biogen Idec and Roche; and is the chair of the Medical Advisory Committee of the Multiple Sclerosis Society of Canada. VWY is funded by research grants from the Multiple Sclerosis Society of Canada, the Canadian Institutes of Health Research, Canadian Cancer Society, and Genentech; has received speaker honoraria from Biogen, EMD Serono, Novartis, Roche, and Sanofi-Genzyme; and is the recipient of unrestricted educational grants from Biogen, EMD Serono, Novartis, Roche, Sanofi-Genzyme, and Teva Canada to support educational activities of the Alberta MS Network, which he directs. AJT reports personal fees as an editorial board member for The Lancet Neurology receiving a free subscription; is Editor-in-Chief for the Multiple Sclerosis Journal receiving an honorarium from SAGE Publications; receives support from the UCLH NIHR Biomedical Research Centre; and receives support for travel as Chair of the Scientific Advisory Committee and International Progressive MS Alliance from the National MS Society (USA) as member, National Multiple Sclerosis Society (USA) Research Programs Advisory Committee, and as a Board member of the European Charcot Foundation; has received payment in the past 36 months (paid to the UCL) from Eisai and from the German Aerospace Centre, Health Research (ERA-NET NEURON); has received fees or support for travel from Hoffman La Roche, Novartis, and CanProCo SAB; had received honoraria or support for travel from EXCEMED and Almirall; has received support for travel to PACTRIMS and has received support for travel to the Multiple Sclerosis Society of Canada; unpaid roles include as a Guarantor of BRAIN, Trustee of the National Brain Appeal (National Hospital for Neurology and Neurosurgery), and as Chair of the Scientific Ambassadors, ‘STOP MS’ Appeal Board (Multiple Sclerosis Society UK). DSR reports personal fees from Bounds Law Group LLC, grants from Vertex, grants from Sanofi-Genzyme, grants from Abata Therapeutics, outside the submitted work; has a patent system and method of automatically detecting tissue abnormalities (US Patent 9,607,392) issued, a patent method of analysing multisequence MRI data for analysing brain abnormalities in a subject (US Patent 9,888,876) issued, a patent Automatic identification of subjects at risk of multiple sclerosis (US Patent application 16/254,710) issued, and a patent high-resolution cerebrospinal fluid-suppressed T2*-weighted magnetic resonance imaging of cortical lesions (US Patent application 62/838,578) pending.
 Declaration of interests No authors received funding for the writing of this manuscript or had direct conflicts of interest with regard to the content of the manuscript. Unrelated to the current work, JSG has received grant or clinical trial funding from the US National Multiple Sclerosis Society (NMSS), University of California San Diego (UCSD), Octave, Biogen, EMD Serono, Novartis, and Sanofi; serves on a steering committee for a clinical trial with Novartis; has served on advisory boards for Genentech and Bayer; and has received educational speaker fees from Alexion. Unrelated to the current work, KMK has received fellowship funding from the NMSS and Biogen; and has received honoraria from Normative, Biogen, Novartis, Roche, and EMD Serono. Unrelated to the current work, MA has received consultancy and speaking honoraria from Sanofi-Genzyme and GlaxoSmithKline (GSK); and has received speaking honoraria from Celgene. Unrelated to the current work, LHH has received honoraria for speaking, consulting, or advisory board activities from Genzyme, Novartis, Genentech, Bristol Myers Squibb, EMD Serono, Horizon Therapeutics, and Greenwich Biosciences; receives research support paid to her institution from Biogen; and receives salary support from the Eric and Sheila Samson Foundation. RJMF has received research support from the Adelson Medical Research Foundation, MS Society UK, and the Wellcome Trust; and participates on a data safety monitoring or advisory board for Biogen and Frequency Therapeutics. Unrelated to the current work, BS has received grant support from the US National Institute of Health and consulting fees from Bloom Burton, Neurodiem, and Senda Biosciences; has received speaking honoraria from Advances Curriculum for Multiple Sclerosis Continuing Medical Education course and PRIME; has a patent optioned by Vaccinex and a second provisional patent that has been filed; and is on a safety monitoring board for Eli Lilly.
 The authors report no competing interests.
 The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of interests GG declares consulting or speaker fees from AbbVie, Aslan, Atara Bio, Biogen, Bristol Myers Squibb–Celgene, GlaxoSmithKline, GW Pharma, Janssen–Actelion, Japanese Tobacco, Jazz Pharmaceuticals, LifNano, Merck & Co, Merck KGaA–EMD Serono, Moderna, Novartis, Sanofi Genzyme, Roche-Genentech, and Teva Pharmaceuticals. MS declares speaking honoraria, research support from, and participation on an advisory board for Biogen, Bristol Myers Squibb, Merck, Novartis, Sanofi, Hoffmann-La Roche, and Viatris, and a patent: Epstein-Barr virus genotypic variants and uses thereof as risk predictors, biomarkers and theraputic targets of multiple sclerosis. FA declares participation on an advisory board for Hoffmann-La Roche.
 Declaration of interests KMK has received grants from the MS Society of Canada; speaking or consulting fees from Biogen, EMD Serono, Novartis, and Roche; and is an advisory board member for Biogen, Novartis, and Roche, outside the submitted work. RD has received payments to her institution, including grants from Biogen, Merck, Celgene, National MS Society, MS Society UK, Horne Family Trust, and the BMA Foundation; honoraria from Biogen, Janssen, Merck, Novartis, Roche, Sanofi, and Teva; participated on an advisory board for Biogen, Janssen, Merck, Novartis, and Roche; and received support for attending meetings or travel from Biogen, Janssen, Merck, Novartis, Roche, and Sanofi, outside the submitted work. MPA received grants for a sponsored statistician from Merck; consulting fees from Almirall, Bayer Schering Pharma, Biogen-Idec, Sanofi Genzyme, Merck-Serono, Novartis, and Roche; honoraria from Almirall, Bayer Schering Pharma, Biogen-Idec, Merck-Serono, Novartis, Roche, and Sanofi-Genzyme; participated on the data safety and monitoring board or advisory board for Merck, Novartis, Roche, and Sanofi Genzyme; and reports a leadership role as president of The European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), outside the submitted work. RB received investigator-initiated grants from Biogen, Novartis, and F Hoffman LaRoche, and sponsored grants from F Hoffman LaRoche; consulting fees from Alexion, Biogen, EMD Serono, Novartis, F Hoffman Laroche, Genzyme Sanofi, TG Therapeutics, and Janssen. AIC received speaker's honoraria from Bayer Healthcare; and support for attending meetings from Teva, outside the submitted work. MM received grants from the Danish MS Society; consulting fees from Merck, Sanofi, Roche, and Novartis; payment or honoraria from Merck, Sanofi, Roche, Novartis, Biogen, and Bristol Myers Squibb; and participated on the data safety and monitoring board or advisory board for Merck, Sanofi, Roche, Novartis, Biogen, and Bristol Myers Squibb, outside the submitted work. ST received speaker honoraria from Bayer Healthcare and Biogen GmbH, and manuscript writing assistance from Hexal AG, outside the submitted work. MT received grants for a sponsored statistician from Biogen; consulting fees from Almirall, Bayer Schering Pharma, Biogen-Idec, Genzyme, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Aventis, Viela Bio, and Teva Pharmaceuticals; honoraria from Almirall, Bayer Schering Pharma, Biogen-Idec, Genzyme, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Aventis, Viela Bio, and Teva Pharmaceuticals; and reports a leadership role as ECTRIMS vice president, outside the submitted work. SV has received payments to her institution including grants from Biogen, Janssen, Merck, Novartis, Roche, and Sanofi; consulting fees from Biogen, Bristol-Myers Squibb, Celgene, Janssen, Merck, Novartis, Roche, and Sanofi; honoraria from Biogen, Merck, Novartis, Roche, Sanofi, and Teva; participated on the data safety and monitoring board or advisory board for Biogen; support for attending meetings or travel from Biogen, Merck, Novartis, and Roche, outside the submitted work. KH received grants or contracts from Almirall, Biogen, Merck, Novartis, Sanofi Genzyme, Roche, and Teva; payment or honoraria from Almirall, Bayer, Biogen, Merck, Novartis, Sanofi Genzyme, Roche, Teva, Janssen, and Bristol-Myers Squibb; support for attending meetings or travel from Bayer, Biogen, Merck, Roche, Sanofi Genzyme, and Teva; participation on a data safety and monitoring board or advisory board from Biogen, Teva, Roche, Novartis, Jansen, and Merck, outside the submitted work. RA, YF, MH, VGJ, AA, VP declare no competing interests.
 Carlo Pozzilli has served on scientific advisory boards for Novartis, Merck, Biogen, Sanofi‐Genzyme, Roche, Janssen, Alexion, has received funding for travel and speaker honoraria from Merck, Serono, Biogen, Sanofi‐Genzyme, Roche, Almirall, Janssen, Alexion and Novartis, and receives research support from Merck, Biogen, Novartis and Almirall. Maura Pugliatti has served on scientific advisory boards for Merck Serono, Biogen and Mylan, has received funding for travel and speaker honoraria from Merck Serono, Biogen, Sanofi‐Genzyme, Teva and Almirall, and has received financial support for research and scientific events from Biogen Idec and Sanofi‐Genzyme. Patrick Vermersch has received honoraria and consulting fees from Biogen, Sanofi‐Genzyme, Novartis, Teva, Merck, Roche, Imcyse, AB Science and Celgene, and research support from Novartis, Sanofi‐Genzyme and Roche. Nikolaos Grigoriadis has received honoraria, travel support, consultancy fees and research grants from Biogen Idec, Biologix, Genesis Pharma, Novartis, TEVA, Bayer, Merck Serono, Sanofi – Genzyme, ROCHE, Celgene and ELPEN. Mona Alkhawajah has received speaker honorarium, consultation fees and/or educational travel support from Roche, Merck, Biogen, Novartis, SAJA, Hikma, Actelion and/or Sanofi. Laura Airas has served on scientific advisory boards for Novartis, Merck Serono, Biogen, Sanofi‐Genzyme and Roche, and has received institutional research support from Merck Serono and Sanofi‐Genzyme. Celia Oreja‐Guevara has received speaker and consultation fees from Biogen Idec, Celgene, Sanofi‐Genzyme, Novartis, Roche, Merck and Teva.
 Disclosure C.A. Pérez received postgraduate fellowship support from Genentech and has participated in advisory boards for Sanofi. F.X. Cuascut received research funding from Genentech and Biogen and has participated in advisory boards for Genentech, Biogen, Horizon, and Pharma Novartis and Horizon. G.J. Hutton received research funding from Biogen, Hoffman-La Roche, Sanofi, MedImmune, and Novartis and has participated in advisory boards for Novartis and Horizon.

 Massimo Filippi is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology, and Associate Editor of Neurological Sciences, received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi, speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Roche, Sanofi, Takeda, and TEVA, participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda, scientific direction of educational evens for Biogen, Bristol-Myers Squibb, Celgene, Lilly, Merck, Novartis, Roche, Sanofi-Genzyme, he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA); Paolo Preziosa received speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb and Genzyme, he has received research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla; Douglas L. Arnold reports consulting fees from Biogen, Celgene, Frequency Therapeutics, Genentech, Merck, Novartis, Race to Erase MS, Roche, and Sanofi-Aventis, Shionogi, Xfacto Communications, grants from Immunotec and Novartis, and an equity interest in NeuroRx; Frederik Barkhof acts in steering committee or iDMC member for Biogen, Merck, Roche, EISAI and Prothena. Consultant for Roche, Biogen, Merck, IXICO, Jansen, Combinostics. Research agreements with Merck, Biogen, GE Healthcare, Roche, Co-founder and shareholder of Queen Square Analytics LTD; Daniel M. Harrison has received consulting fees from Genentech, EMD-Serono, Biogen, and Sanofi-Genzyme, has received research support from EMD-Serono and Genentech, has received royalties and writing fees for UpToDate, Inc. and the American College of Physicians; Pietro Maggi received research support from Fund for Scientific Research (F.R.S, FNRS), Cliniques universitaires Saint-Luc Fonds de Recherche Clinique and Biogen, speaker fees from Sanofi-Genzyme and Biogen; Caterina Mainero has nothing to disclose; Xavier Montalban has received speaking honoraria and travel expenses for participation in scientific meetings, has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Abbvie, Actelion, Alexion, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Immunic, Janssen Pharmaceuticals, Medday, Merck, Mylan, Nervgen, Novartis, Sandoz, Sanofi-Genzyme, Teva Pharmaceutical, TG Therapeutics, Excemed, MSIF and NMSS; Elia Sechi has nothing to disclose; Brian G. Weinshenker reports personal fees from Novartis, MedImmune/VielaBio, Horizon, Alexion, Chugai, Roche, Genentech Mitsubishi-Tanabe and UCB Biosciences, has a patent of NMO-IgG for diagnosis of neuromyelitis optica with royalties paid to RSR Ltd, Oxford University, Hospices Civil de Lyon, and MVZ Labor PD Dr Volkmann und Kollegen GbR; Maria A. Rocca received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche and speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono SpA, Novartis, Roche, and Teva, she receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. She is an Associate Editor for Multiple Sclerosis and Related Disorders.

 Xavier Montalban has received speaking honoraria and travel expenses for participation in scientific meetings, has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Abbvie, Actelion, Alexion, Biogen, Bristol‐Myers Squibb/Celgene, EMD Serono, Genzyme, Hoffmann‐La Roche, Immunic, Janssen Pharmaceuticals, Medday, Merck, Mylan, Nervgen, Novartis, Sandoz, Sanofi‐Genzyme, Teva Pharmaceutical, TG Therapeutics, Excemed, MSIF, and NMSS. Paul Matthews has received consultancy fees from Novartis and Biogen. He has received honoraria or speakers' fees from Novartis and Biogen and has received research or educational funds from Biogen, Novartis, Merck, and Bristol Myers Squibb. Alex Simpson is an employee of F Hoffmann‐La Roche. John Petrie and Cormac Sammon are employees of PHMR Ltd, which received financial support from F Hoffmann‐La Roche for the work, including the development of the literature review and preparation of the manuscript. Sreeram Ramagopalan is an employee of F Hoffmann‐La Roche. Ente Ospedaliero Cantonale (employer) received compensation for Giulio Disanto: financial support for speaking, educational, or travel grants from Biogen Idec, Sanofi Genzyme, Roche, Merck, and Novartis. The submitted work is not related to these agreements. Jens Kuhle received speaker fees, research support, travel support, and/or served on advisory boards by Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Progressive MS Alliance, Bayer, Biogen, Bristol Myers Squibb, Celgene, Merck, Novartis, Octave Bioscience, Roche, and Sanofi.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.




 Declaration of interests R.R. is interim Chief Medical Officer and scientific Co-Founder of Abata Therapeutics, which is developing treatments for autoimmune conditions including progressive MS.
 Competing interests: None declared.
 Competing interests: SB has received honoraria from Biogen Idec, Bristol Meyer Squibbs, Merck Serono, Novartis, Sanofi-Genzyme, Roche and Teva. His research is funded by the Deutsche Forschungsgemeinschaft (DFG) and Hertie Foundation. FL has served on the advisory board of Roche and received travel funding from Teva. AS has received speaker honoraria and/or travel compensation for activities with Bristol Myers Squibb, CSL Behring, Novartis and Roche, and research support by the Swiss MS Society and Baasch Medicus Foundation, not related to this manuscript. LK has received compensation for serving on Scientific Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Genzyme, Horizon, Janssen, Merck Serono, Novartis and Roche. She has received speaker honoraria and travel support from Bayer, Biogen, Bristol-Myers Squibb, Genzyme, Grifols, Merck Serono, Novartis, Roche, Santhera and Teva. She has received research support from the German Research Foundation, the IZKF Münster, IMF Münster, Biogen, Immunic AG, Novartis and Merck Serono. CK has received speaker fees, travel support and/or served on advisory boards by Biogen, Merck, Roche and Sanofi. BW has received grants from the German Ministry of Education and Research, Deutsche Forschungsgemeinschaft, Dietmar Hopp Foundation and Klaus Tschira Foundation, grants and personal fees from Merck, and personal fees from Alexion, Bayer, Biogen, Teva; none related to this work. AB has received personal compensation from Merck Serono, Biogen, Novartis, Teva, Roche, Sanofi/Genzyme, Celgene/BMS and Janssen; he has received grants for congress travel and participation from Biogen, Teva, Novartis, Sanofi/Genzyme, Merck Serono and Celgene. None related to this report. HT has received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Celgene, GSK, Jannssen, Merck, Novartis, Roche, Sanofi Genzyme and Teva. SM has received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, Merck Serono, Novartis, ONO Pharma, Roche and Teva. CT has received honoraria for consultation and expert testimony from Alexion Pharma Germany, Chugai Pharma Germany and Roche Pharma. None of this interfered with the current report. UKZ has received speaking fees, travel support and financial support for research activities from Alexion, Almirall, Bayer, Biogen, Bristol-Myers-Squibb, Janssen, Merck-Serono, Novartis, Octapharm, Roche, Sanofi-Genzyme and Teva as well as EU, BMBF, BMWi. CH has received speaker honoraria from Merck and Roche. He has received grant support from Merck, Novartis and Roche. TK has received speaker honoraria and/or personal fees for advisory boards from Bayer Healthcare, Merck, Novartis Pharma, Sanofi-Aventis/Genzyme, Roche Pharma, Alexion and Biogen as well as grant support from Novartis and Chugai Pharma in the past. None of this interfered with the current report. RG has received speaker and board honoraria from Baxter, Bayer Schering, Biogen Idec, Bristol Meyer Squibb, CSL Behring, Eisai, Genzyme, Janssen, Merck Serono, Novartis, Stendhal, Talecris and Teva. His department has received grant support from Bayer Schering, BiogenIdec, Genzyme, Merck Serono, Novartis and Teva. All of RG’s declarations are unrelated to the content of this manuscript. BH has served on scientific advisory boards for Novartis; he has served as DMSC member for AllergyCare, Polpharma, Sandoz and TG therapeutics; he or his institution has received speaker honoraria from Desitin; his institution has received research grants from Regeneron for multiple sclerosis research. He holds part of two patents: one for the detection of antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis and one for genetic determinants of neutralising antibodies to interferon. FZ has recently received research grants and/or consultation funds from Biogen, Ministry of Education and Research (BMBF), Bristol-Meyers-Squibb, Celgene, German Research Foundation (DFG), Janssen, Max-Planck-Society (MPG), Merck Serono, Novartis, Progressive MS Alliance (PMSA), Roche, Sanofi Genzyme and Sandoz. HW has received honoraria for acting as a member of Scientific Advisory Boards for Janssen, Merck and Novartis as well as speaker honoraria and travel support from Alexion, Amicus Therapeuticus, Biogen, Biologix, Bristol Myers Squibb, Cognomed, F. Hoffmann-La Roche Ltd, Gemeinnützige Hertie-Stiftung, Medison, Merck, Novartis, Roche Pharma AG, Genzyme, Teva and WebMD Global. HW is acting as a paid consultant for Biogen, Bristol Myers Squibb, EMD Serono, Idorsia, Immunic, Novartis, Roche, Sanofi, the Swiss Multiple Sclerosis Society and UCB. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgesellschaft (DFG), Deutsche Myasthenie Gesellschaft e.V., Alexion, Amicus Therapeutics, Argenx, Biogen, CSL Behring, F. Hoffmann - La Roche, Genzyme, Merck KgaA, Novartis Pharma, Roche Pharma and UCB Biopharma. JDL has received speaker fees, research support, travel support, and/or served on advisory boards by Abbvie, Alexion, Argenx, Biogen, Merck, Novartis, Roche, Sanofi and Takeda. JDL has received speaker fees, research support, travel support, and/or served on advisory boards by Abbvie, Alexion, Argenx, Biogen, Merck, Novartis, Roche, Sanofi and Takeda.
 Conflict of Interest Disclosures: Dr Roos reported receiving grants from the National Health and Medical Research Council, MS Australia, and the Trish Multiple Sclerosis Research Foundation and served on scientific advisory boards, received conference travel support and/or speaker honoraria from Roche, Novartis, Merck, and Biogen outside the submitted work. Dr Hughes reported receiving unrestricted educational grants or speaking honoraria from Biogen, Merck Serono, Novartis, Roche, and Sanofi Genzyme. Dr Malpas reported receiving received conference travel support from Merck, Novartis, and Biogen and research support from the National Health and Medical Research Council, Multiple Sclerosis Research Australia, The University of Melbourne, The Royal Melbourne Hospital Neuroscience Foundation, and Dementia Australia. Dr Boz reported receiving conference travel support from Biogen, Novartis, Roche, Bayer-Schering, Merck, and Teva and has participated in clinical trials by Sanofi Aventis, Roche, and Novartis. Dr Alroughani reported receiving honoraria as a speaker and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche, and Sanofi Genzyme outside the submitted work. Dr Buzzard reported receiving grants from CSL and the National Health and Medical Research Council and honoraria and consulting fees from Biogen, Teva, Novartis, Genzyme Sanofi, Roche, Merck, CSL, and Grifols outside the submitted work. Dr Skibina reported receiving honoraria and consulting fees from Bayer Schering, Novartis, Merck, Biogen, and Genzyme companies. Dr Van der Walt reported serving on advisory boards and receiving unrestricted research grants from Novartis, Biogen, Merck, and Roche; grant support from the National Health and Medical Research Council of Australia and MS Research Australia; and speaker honoraria and travel support from Novartis, Roche, and Merck outside the submitted work. Dr Butzkueven reported receiving institutional (Monash University) funding from Biogen, F. Hoffmann-La Roche Ltd, Merck, Alexion, CSL, and Novartis; has carried out contracted research for Novartis, Merck, F. Hoffmann-La Roche Ltd, and Biogen; has taken part in speakers’ bureaus for Biogen, Genzyme, UCB, Novartis, F. Hoffmann-La Roche Ltd, and Merck; and has received personal compensation from Oxford Health Policy Forum for the Brain Health Steering Committee outside the submitted work. Dr Lechner-Scott reported receiving travel compensation from Novartis, Biogen, Roche, and Merck and honoraria for talks and advisory board commitment as well as research grants from Biogen, Merck, Roche, Teva, and Novartis during the conduct of the study. Dr Kuhle reported receiving grants from the Swiss MS Society, Swiss National Research Foundation, Novartis, Roche, Biogen, Merck, and Bristol Myers Squibb outside the submitted work. Dr Terzi reported receiving travel grants from Novartis, Bayer-Schering, Merck, and Teva and has participated in clinical trials by Sanofi Aventis, Roche, and Novartis. Dr Laureys reported receiving travel and/or consultancy compensation and/or research grants from Sanofi Genzyme, Roche, Teva, Merck, Novartis, Celgene, Biogen, and Bristol Myers Squibb outside the submitted work. Dr John reported receiving grants from Sanofi, Novartis, Biogen, and Amicus as a principal investigator for a sponsored study and grants outside the submitted work. Dr Grammond reported receiving advisory board fees from Novartis, EMD Serono, Roche, Biogen, IDEC, Sanofi Genzyme, Pendopharm, and Roche; grant support from Genzyme and Roche; and research grants for his institution from Biogen, IDEC, Sanofi Genzyme, and EMD Serono. Dr Grand-Maison reported receiving reported grants from Roche, Novartis, Alexa, and Biogen and honoraria or research funding from Biogen, Genzyme, Novartis, Teva Neurosciences, and Atara Pharmaceuticals during the conduct of the study. Drs Jensen and Rasmussen reported having served on scientific advisory boards for, served as consultant for, received support for congress participation, or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche, and Sanofi Genzyme. Dr Rasmussen reported receiving advisory board fees from Novartis, Roche, Merck, and Biogen outside the submitted work. Dr Svendsen reported receiving travel grants from Bristol Myers Squibb and research support from Roche outside the submitted work. Dr Stilund reported serving on scientific advisory boards for Sanofi, receiving support for congress participation, or receiving speaker honoraria from Biogen, Teva, Merck, Roche, and Sanofi; grants for his research from Novartis; and being currently engaged in sponsor-initiated research projects by Bayer, Jansen, Shionogi, and Sanofi outside the submitted work. Dr Weglewski reported serving on scientific advisory boards for Merck and Roche; receiving conference travel support from Biogen, Merck, Roche, and Sanofi; and receiving speaker honoraria from Roche, Merck, and Sanofi outside the submitted work. Dr Sellebjerg reported serving on scientific advisory boards, being on the steering committees of clinical trials, serving as a consultant, receiving support for congress participation, receiving speaker honoraria, or receiving research support for his laboratory from Biogen, Merck, Novartis, Roche, Sanofi Genzyme, Bristol Myers Squibb, and Teva outside the submitted work. Dr Gray reported receiving honoraria as consultant on scientific advisory boards for Genzyme, Biogen, Merck, Roche, and Novartis; receiving travel grants from Biogen, Merck, Roche, and Novartis; participating in clinical trials by Biogen and Merck; and receiving research grant support from Biogen outside the submitted work. Dr Magyari reported receiving grants from Roche, Biogen, Novartis, Sanofi, and Merck during the conduct of the study; serving on scientific advisory boards for AbbVie, Biogen, Merck, Novartis, Roche, Sanofi, and Teva; receiving honoraria for lecturing from Biogen, Genzyme, Merck, Novartis, and Sanofi; and receiving support for congress participation from Biogen, Genzyme, Roche, and Teva outside the submitted work. Dr Kalincik reported grants from the National Health and Medical Research Council, MS Australia, Novartis, Biogen, Roche, Merck, and Celgene outside the submitted work; serving on scientific advisory boards for MS International Federation and World Health Organization, BMS, Roche, Sanofi Genzyme, Novartis, Merck, and Biogen; serving on the steering committee for Brain Atrophy Initiative by Sanofi Genzyme; receiving conference travel support and/or speaker honoraria from WebMD Global, Novartis, Biogen, Sanofi Genzyme, Teva, BioCSL, and Merck; and receiving research or educational event support from Biogen, Novartis, Genzyme, Roche, Celgene, and Merck. No other disclosures were reported.

 The authors report no potential conflict of interest.
 Declaration of Competing Interest None.
 The authors declare no conflict of interest.
 Declaration of Competing Interest We wish to confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: M.P.S. has received consulting fees from Biogen, Genzyme, GeNeuro, MedDay, Merck, Novartis, Roche, and Teva. In the last 3 years, J.C. has received support from the Efficacy and Evaluation (EME) Program, a Medical Research Council (MRC) and National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Program (NIHR), the UK MS Society, the US National MS Society, and the Rosetrees Trust. He is supported in part by the NIHR University College London Hospitals (UCLH) Biomedical Research Center, London, UK. He has been a local principal investigator for a trial in MS funded by MS Canada; a local principal investigator for commercial trials funded by Ionis, Novartis, and Roche; and has taken part in advisory boards/consultancy for Azadyne, Biogen, Lucid, Janssen, Merck, NervGen, Novartis, and Roche. In the last 3 years, D.M.K. has received consulting fees from the American Medical Group Association (AMGA) Analytics and the Canadian Stroke Consortium. He has received research funding from the National Institutes of Health (NIH), Patient-Centered Outcomes Research Institute (PCORI), Greenwall Foundation, and W. L. Gore and served on the Scientific Advisory Board for Optum Labs. R.A.M. receives research funding from Canadian Institutes of Health Research, Research Manitoba, MS Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium of MS Centers, the Arthritis Society, and US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution).
 Declaration of Competing Interest The Authors declare that there is no conflict of interest. FFK received travel grants from Merck and Novartis. NM received honoraria for scientific lectures from Novartis, Merck, and Biogen. TW received honoraria as speaker from Roche and Novartis. MS received honoraria as speaker and for consultation from Almirall and AbbVie. KWS reports honoraria for lectures or travel reimbursements for attending meetings from Biogen, Merck, Bavarian Nordic and Bristol-Myers Squibb as well as research support from Bristol-Myers Squibb. MAF received honoraria as speaker and for consultation from Biogen, Lundbeck, Merck KGaA, Novartis and Roche. His research is funded by the Bundesministerium für Bildung und Forschung (BMBF), Deutsche Forschungsgemeinschaft (DFG), Landesforschungsförderung Hamburg, Gemeinnützige Hertie-Stiftung, Else Kröner-Fresenius-Stiftung, Deutsche Multiple Sklerose-Gesellschaft, Fritz Thyssen-Stiftung, Werner Otto-Stiftung, Walter und Ilse Rose-Stiftung, Stiftung zur Bekämpfung neuroviraler Erkrankungen and Research Fund of the University Medical Center Hamburg-Eppendorf. LK received compensation for serving on Scientific Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Genzyme, Horizon, Janssen, Merck Serono, Novartis, Roche and Viatris. She received speaker honoraria and travel support from Argenx, Bayer, Biogen, Bristol-Myers Squibb, Genzyme, Grifols, Merck Serono, Novartis, Roche, Santhera and Teva. She receives research support from the German Research Foundation, the IZKF Münster, IMF Münster, Biogen, Immunic AG, Novartis and Merck Serono. RP received honoraria for lecturing and consulting from Alexion, Bayer Healthcare, Biogen, Bristol-Mayers Squibb, MedDay, Merck Serono, Mylan, Novartis, Roche, Sanofi Genzyme. He received research funds from Teva, Merck Serono, and Novartis. MP received honoraria for lecturing from Argenx, Biogen, Bayer, Novartis, Hexal, Sanofi and Merck. He received research funding from Novartis and Biogen. His research is funded by the German Multiple Sclerosis Society North Rhine-Westphalia (DMSG). CK received honoraria for lecturing and consulting as well as financial research support from Ablynx, Almirall, Amgen, Bayer Vital, Bristol-Mayers Squibb, Biotronik, Boehringer Ingelheim, Biogen, CSL Behring, Daiichi-Sankyo, Desitin, Eisai, Ever Pharma, Sanofi Genzyme, Merck Serono, Mylan, Medday, Novartis, Pfizer, Roche, Siemens, Stago, and Teva. SGM received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Bundesinstitut für Risikobewertung (BfR), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Gemeinsamer Bundesausschuss (G-BA), German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Alexion, Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, HERZ Burgdorf, Merck Serono, Novartis, ONO Pharma, Roche, and Teva. TS reports honoraria for lectures and travel grants from Alexion, Alnylam Pharmaceuticals, argenx, Bayer Vital, Biogen, Celgene, Centogene, CSL Behring, Euroimmun, Janssen, Merck Serono, Novartis, Pfizer, Roche, Sanofi, Siemens, Sobi, Teva. His research is supported by the German Ministry for Education and Research (BMBF), Bristol-Myers Squibb Foundation for Immuno-Oncology, Claudia von Schilling Foundation for Breast Cancer Research, Else Kröner Fresenius Foundation, Hannover Biomedical Research School (HBRS), Alnylam Pharmaceuticals, CSL Behring, Novartis, Sanofi Genzyme, VHV Stiftung.
 The authors declare no competing interest.



 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: R.A.M. received research funding from Canadian Institutes of Health Research, Research Manitoba, MS Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium of MS Centers, the Arthritis Society, and the US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution). M.P.S. has received consulting fees from Biogen, Genzyme, GeNeuro, MedDay, Merck, Novartis, Roche, and Teva. F.B. received research funding from National Multiple Sclerosis Society and consulting fees from Biogen, Eisai, and Chiesi. W.Y.C. research funding from AstraZeneca, Janssen, and Roche. G.R.C. serves on Data and Safety Monitoring Boards for Applied Therapeutics, AI therapeutics, AMO Pharma, AstraZeneca, Avexis Pharmaceuticals, BioLineRx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Pharmaceuticals, Immunic, Karuna Therapeutics, Mapi Pharmaceuticals Ltd, Merck, Mitsubishi Tanabe Pharma Holdings, Opko Biologics, Prothena Biosciences, Novartis, Regeneron, Sanofi-Aventis, Reata Pharmaceuticals, Teva Pharmaceuticals, NHLBI (Protocol Review Committee), University of Texas Southwestern, University of Pennsylvania, Visioneering Technologies, Inc., and consulting or advisory boards for Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions LLC, Entelexo Biotherapeutics, Inc., Genzyme, Genentech, GW Pharmaceuticals, Immunic, Immunosis Pty Ltd, Klein-Buendel Incorporated, Merck/Serono, Novartis, Perception Neurosciences, Protalix Biotherapeutics, Regeneron, Roche, and SAB Biotherapeutics. He is employed by the University of Alabama at Birmingham and President of Pythagoras, Inc. a private consulting company located in Birmingham AL. MW.K. received consulting fees and travel support from Biogen, Novartis, Roche, Sanofi Genzyme and EMD Serono. M.M.C. has no disclosures. E.M.M. has research/grant support from PCORI, National MS Society, National Institutes of Health, the US Department of Defense, Biogen, Teva, and Genentech. She received royalties for editorial duties from UpToDate and consulting fees from BeCareLink, LLC. J.J.H.P. is the founder of Core Clinical Sciences. F.P. has received research grants from Janssen, Merck KGaA and UCB, and fees for serving on DMC in clinical trials with Chugai, Lundbeck and Roche, and preparation of expert witness statement for Novartis. A.S. received research funding from MS Canada, National Multiple Sclerosis Society, CMSC and the US Department of Defence and is a member of editorial board for Neurology. She serves as a consultant for Gryphon Bio, LLC. She is a member of the Data and Safety Monitoring Board for Premature Infants Receiving Milking or Delayed Cord Clamping (PREMOD2), Central Vein Sign: A Diagnostic Biomarker in Multiple Sclerosis (CAVS-MS), and Ocrelizumab for Preventing Clinical Multiple Sclerosis in Individuals With Radiologically Isolated Disease (CELLO). In the last 3 years, J.C. has received support from the Efficacy and Evaluation (EME) Programme, a Medical Research Council (MRC) and National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Programme (NIHR), the UK MS Society, the US National MS Society, and the Rosetrees Trust. He is supported in part by the NIHR University College London Hospitals (UCLH) Biomedical Research Centre, London, UK. He has been a local principal investigator for a trial in MS funded by MS Canada. A local principal investigator for commercial trials funded by Ionis, Novartis, and Roche and has taken part in advisory boards/consultancy for Azadyne, Biogen, Lucid, Janssen, Merck, NervGen, Novartis, and Roche.
 Declaration of Competing Interest “The authors declare no conflict of interest.”

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest Isabel Voigt and Judith Wenk declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Hernan Inojosa received speaker honoraria from Roche and financial support for research activities from Biogen and Alexion. Katja Akgün reports: scientific advisory board and/or consulting for Roche, Sanofi, Alexion, Teva, Biogen, and Celgene. Tjalf Ziemssen reports: scientific advisory board and/or consulting for Biogen, Roche, Novartis, Celgene, and Merck; compensation for serving on speakers bureaus for Roche, Novartis, Merck, Sanofi, Celgene, and Biogen; research support from Biogen, Novartis, Merck, and Sanofi.


 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 Declaration of competing interest The authors declare no funding sources and any other financial conflict of interest.

 Declaration of Competing Interest The authors Guilherme Diogo Silva, Samira Luisa Apóstolos-Pereira, and Dagoberto Callegaro receive regular visits and grants from Biogen, Roche, Merck, Novartis, and EMS.
 Declaration of Competing Interest All authors have participated in (a) conception and design, or analysis and interpretation of the data; (b) drafting the article or revising it critically for important intellectual content; and (c) approval of the final version. This manuscript has not been submitted to, nor is under review at, another journal or other publishing venue. The authors have no affiliation with any organization with a direct or indirect financial interest in the subject matter discussed in the manuscript.
 Declaration of Competing Interest None of the authors declare any potential conflicts of interest.





 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: R.A.M. received research funding from Canadian Institutes of Health Research, Research Manitoba, MS Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium of MS Centers, the Arthritis Society, and the US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution). In the last 3 years, J.C. has received support from the Efficacy and Evaluation (EME) Programme, a Medical Research Council (MRC) and the National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Programme (NIHR), the UK MS Society, the US National MS Society, and the Rosetrees Trust. He is supported in part by the NIHR University College London Hospitals (UCLH) Biomedical Research Centre, London, UK. He has been a local principal investigator for a trial in MS funded by the MS Canada. A local principal investigator for commercial trials funded by Ionis, Novartis, and Roche and has taken part in advisory boards/consultancy for Azadyne, Biogen, Lucid, Janssen, Merck, NervGen, Novartis, and Roche. In the last 3 years, G.P. has worked as an independent contractor with the MS Society (UK) and Bristol-Myers Squibb. M.B. has received support from the NIHR partnership and the HTA Programme (NIHR), the UK MS Society, and the NIHR Local Clinical Network. M.P.S. has received consulting fees from Biogen, Genzyme, GeNeuro, MedDay, Merck, Novartis, Roche, and Teva. E.G., J.R., A.A., S.S., J.B., C.P., and S.P. have nothing to declare.
 Declaration of Competing Interest The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Anneke van der Walt served on advisory boards and receives unrestricted research grants from Novartis, Biogen, Merck, and Roche. She has received speaker’s honoraria and travel support from Novartis, Roche, and Merck. She receives grant support from the National Health and Medical Research Council of Australia and MS Research Australia. Adam Vogel is Chief Science Officer of Redenlab Inc. Gustavo Noffs works in scientific development for Redenlab Inc. Scott Kolbe receives grant income from MS Research Australia and has received honoraria from Novartis, Biogen, and Merck. Helmut Butzkueven’s institution receives compensation for serving on scientific advisory boards and speaker bureaus for Biogen, Novartis, Roche, Merck, and UCB, steering committee duties for trials conducted by Biogen, Merck, Roche, and Novartis and his institution receives research support from Merck, Roche, Novartis, ALexion, and Biogen.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 RM receives research funding from: CIHR, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Research Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and the US Department of Defense, and is a co-investigator on studies receiving funding from Biogen Idec and Roche Canada. She holds the Waugh Family Chair in Multiple Sclerosis. KF is a member of the Data and Safety Monitoring Board for A Trial of Bile Acid Supplementation in Patients With Multiple Sclerosis, Comparative Effectiveness Trial of COVID-19 Testing Modalities; VIRTual vs UsuAL in-office care for MS. KK receives research funding from the CMSC, the Department of Defense Congressionally Directed Medical Research Program, through the Multiple Sclerosis Research Program Award No. W81XWH2010566 and NIMH MH123724, National Institutes of Health NIMH. DR has received research support from the MS Society of Canada, Consortium of Multiple Sclerosis Centers CMSC, and Roche Canada. She has received speaker or consultant fees from Alexion, Biogen, EMD Serono, Novartis, Roche, and Sanofi Aventis. AS receives research funding from Multiple Sclerosis Society of Canada, National Multiple Sclerosis Society, CMSC and the US Department of Defense and is a member of editorial board for Neurology. She serves as a consultant for Gryphon Bio, LLC. She is a member of the Data and Safety Monitoring Board for Premature Infants Receiving Milking or Delayed Cord Clamping PREMOD2, Central Vein Sign: A Diagnostic Biomarker in Multiple Sclerosis CAVS-MS, and Ocrelizumab for Preventing Clinical Multiple Sclerosis in Individuals With Radiologically Isolated Disease CELLO. HT has, in the last five years, received research support from the the National Multiple Sclerosis Society, the Canadian Institutes of Health Research, the Multiple Sclerosis Society of Canada, the Multiple Sclerosis Scientific Research Foundation and the EDMUS Foundation ‘Fondation EDMUS contre la sclérose en plaques’. JF receives research grant support from the Canadian Institutes of Health Research, the National Multiple Sclerosis Society, the Multiple Sclerosis Society of Canada, Crohn’s and Colitis Canada, Research Nova Scotia; consultation and distribution royalties from MAPI Research Trust. CM is supported by a University Research Chair University of Waterloo and has received research funding from the Canadian Institutes of Health Research, the Multiple Sclerosis Society of Canada, the National Multiple Sclerosis Society, Alberta Innovates, CMSC, Ontario Brain Institute Integrated Discovery Program, and the Public Health Agency of Canada.

 Declaration of Competing Interest The authors declare that no conflicting interests exist.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Lucy Meunier: no conflict of interest; Dominique Larrey: Sanofi, TEVA.


 The authors have declared that no competing interests exist.

 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Yi Chao Foong reports a relationship with Biogen that includes: travel reimbursement. Francesca Bridge reports a relationship with Biogen that includes: travel reimbursement. Anneke van der Walt reports a relationship with Novartis Pharmaceuticals Corporation that includes: consulting or advisory, funding grants, speaking and lecture fees, and travel reimbursement. Anneke van der Walt reports a relationship with Biogen that includes: consulting or advisory, funding grants, speaking and lecture fees, and travel reimbursement. Anneke van der Walt reports a relationship with Merck & Co Inc that includes: consulting or advisory, funding grants, speaking and lecture fees, and travel reimbursement. Anneke van der Walt reports a relationship with F Hoffmann-La Roche Ltd that includes: consulting or advisory, funding grants, speaking and lecture fees, and travel reimbursement. Anneke van der Walt reports a relationship with National Health and Medical Research Council that includes: funding grants. Anneke van der Walt reports a relationship with Multiple Sclerosis Research Australia that includes: funding grants. Melissa Gresle reports a relationship with Biogen that includes: funding grants. Melissa Gresle reports a relationship with F Hoffmann-La Roche Ltd that includes: funding grants. Daniel Merlo reports a relationship with Novartis that includes: speaking and lecture fees. Helmut Butzkueven reports a relationship with Novartis that includes: consulting or advisory, funding grants, and speaking and lecture fees. Helmut Butzkueven reports a relationship with Biogen Inc that includes: consulting or advisory, funding grants, and speaking and lecture fees. Helmut Butzkueven reports a relationship with Merck & Co Inc that includes: consulting or advisory, funding grants, and speaking and lecture fees. Helmut Butzkueven reports a relationship with F Hoffmann-La Roche Ltd that includes: consulting or advisory, funding grants, and speaking and lecture fees. Helmut Butzkueven reports a relationship with UCB Pharma SA that includes: consulting or advisory and speaking and lecture fees. Helmut Butzkueven reports a relationship with National Health and Medical Research Council that includes: funding grants. Helmut Butzkueven reports a relationship with Medical Research Future Fund that includes: funding grants. Helmut Butzkueven reports a relationship with Monash partners that includes: funding grants. Helmut Butzkueven reports a relationship with Trish MS research foundation that includes: funding grants. Helmut Butzkueven reports a relationship with Pennycook Foundation that includes: funding grants. Helmut Butzkueven reports a relationship with Multiple Sclerosis Research Australia that includes: funding grants. Helmut Butzkueven reports a relationship with MSBase Foundation that includes: consulting or advisory. Helmut Butzkueven reports a relationship with Oxford Health Policy Forum Brain Health Initiative that includes: consulting or advisory. Yi Chao Foong reports a relationship with National Health and Medical Research Council that includes: funding grants. Yi Chao Foong reports a relationship with Avant Foundation that includes: funding grants. Yi Chao Foong reports a relationship with Multiple Sclerosis Research Australia that includes: funding grants. Yi Chao Foong reports a relationship with Australian and New Zealand Association of Neurologists that includes: funding grants.
 Declaration of Competing Interest Seyed H. Mousavi, MD, Declarations of interest none, John W. Lindsey, MD, Declarations of interest none, Rajesh K. Gupta, MD, Declarations of interest none, Jerry S. Wolinsky, MD, Declarations of interest none, John A. Lincoln, MD, PhD
 Dr. Mariottini reports personal fees from Sanofi, personal fees from Novartis, personal fees from Biogen, non-financial support from Sanofi, non-financial support from Biogen, non-financial support from Janssen Neuroscience and non-financial support from Merck, outside the submitted work. Dr. De Matteis has nothing to disclose. Dr. Cencioni has nothing to disclose. Prof. Muraro reports grants from National Institute of Health Research, non-financial support from National Institute of Health Research and grants from Benaroya Research Institute and National Institute of Allergy and Infectious Diseases of the National Institutes of Health, during the conduct of the study, and personal fees from Jasper Therapeutics, personal fees from Magenta Therapeutics, personal fees from Quell Therapeutics and personal fees from Rubius Therapeutics, outside the submitted work.


 There is no conflict of interest to declare. There was no financial support for this review.


 Declaration of competing interest The authors declare no conflicts of interest.

 Z.M., J.G., O.G., M.S., and J.N. declare no relationships with any companies whose products or services are featured in the subject matter of the article and no relevant financial or non-financial interests to disclose. H.P. is a full-time employee of GE Healthcare. F.P.C. received a Guarantors of Brain fellowship 2017–2020. F.B. is a steering committee and iDMC member for Biogen, Merck, Roche, and EISAI; consultant for Roche, Biogen, Merck, IXICO, Jansen, and Combinostics; and has research agreements with Novartis, Merck, Biogen, GE, and Roche. F.B. is a co-founder and shareholder of Queen Square Analytics Ltd.

 Declaration of interests MG received support and honoraria for research, consultation, lectures, and education from Almirall, Biogen, Celgene/BMS, Horizon, Janssen-Cilag, Merck, Novartis, Roche, Sanofi/Genzyme, and TEVA ratiopharm. TB has participated in meetings sponsored by and received honoraria (lectures, advisory boards, and consultations) from pharmaceutical companies marketing treatments for multiple sclerosis: Almirall, Biogen, Celgene/BMS, Horizon, Janssen-Cilag, Merck, Novartis, Roche, Sandoz, Sanofi/Genzyme, TEVA, and TG Therapeutics. His institution has received financial support in the last 12 months by unrestricted research grants (Biogen, Celgene/BMS, Merck, Novartis, Roche, and Sanofi/Genzyme) and for participation in clinical trials in multiple sclerosis sponsored by Biogen, Celgene/BMS, Merck, Novartis, Roche, and Sanofi/Genzyme.

 The authors report no competing interests.

 The authors declare no conflict of interest.

 Melanie Filser has no conflict of interest. Axel Buchner has no conflict of interest. Gereon R. Fink has no conflict of interest. Stefan M. Gold: Honoraria/speaker fees from Mylan, Almirall, and Celgene. Research grants from Biogen and kind support from the GAIA Group. Iris-Katharina Penner: Honoraria/speaker fees from Adamas Pharma, Almirall, Bayer Pharma, Biogen, BMS, Celgene, Desitin, Genzyme, Janssen, Merck, Roche, Novartis, and Teva. Research support from the German MS Society, Celgene, Teva, Roche, and Novartis. All listed potential conflicts of interest are outside the context of this article’s research, authorship, and publication.

 The authors declare no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Declaration of Competing Interest Lorefice L., Fenu G., Cocco E. received honoraria for consultancy or speaking from Biogen, Novartis, Sanofi Genzyme, Bristol, Merck, Roche. Mellino P received travel grants from Sanofi and Roche.
 The authors declare no conflict of interest.


 Declaration of Competing Interest The authors declare no conflicts of interest.


 The authors declare no conflict of interest.
 The authors declare that they have no conflict of interest.
 MP, MCM, GM, PB, SF, AT, GB, LT, CM: no competing interests are disclaimed. RB has served on scientific advisory boards and received funding for travel, speaker honoraria, research support from Almirall, Bayer, Biogen, Bristol Myers Squibb/Celgene, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Genzyme, Teva.


 Competing interests: MW and MDW declare no financial interests. KEH reports speaker and personal fees from Roche, Merck and Biogen, and travel grants to attend educational meetings from Roche, Novartis, Merck and Biogen. ECT has received honoraria for consulting work from Novartis, Merck, Biogen and Roche, and funding to attend or speak at educational meetings from Biogen, Janssen, Merck, Roche, Takeda and Novartis. TPP reports honoraria from Roche and MedDay Pharma, travel expenses from Sanofi Genzyme and Novartis, and is Treasurer for the BMA. FJ reports honoraria and support to attend educational meetings from Biogen and Teva Pharmaceutical Industries. GI reports payments and honoraria for speaking, travel, and advisory boards from Merck, Sanofi Genzyme, Novartis and Biogen. VT has received honoraria, travel grants and research grant support from Roche, Merck, Biogen, Novartis, Viatris, Bristol Myers Squibb, Almirall, Sanofi.OP reports speaker fees, consultancy fees, and personal fees from Biogen, Sanofi Genzyme, Roche, Merck and Novartis, and grant support from Biogen and Sanofi Genzyme. NPR reports honoraria from Roche, Sanofi Genzyme and Novartis, and research grants from Novartis, Sanofi Genzyme and Biogen.
 The authors declare no competing interests.

 J.S. Wolinsky received compensation for consulting, scientific advisory boards, or other activities with Avotres, Brainstorm Cell Therapeutics, Cleveland Clinic Foundation, EMD Serono, Inmagene, Novartis/Sandoz, Roche/Genentech, Sanofi Genzyme, and the University of Alabama. Royalties are received for out licensed monoclonal antibodies through UTHealth to Millipore (Chemicon International) Corporation. All other authors report no disclosures related to this work. Go to Neurology.org/N for full disclosures.
 We declare no competing interests.
 Declaration of Competing Interest and/or Funding Sources All the authors declare no conflict of interests neither do we have any funding sources for this systemic review and meta-analysis.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.B. completed an internship at F. Hoffmann-La Roche Ltd. while researching the submitted work. During completion of the work related to this manuscript, A.B. was an MSc student at the Ulm University, 89081 Ulm, Germany. M.W. is an employee and shareholder of F. Hoffmann-La Roche Ltd. F.M. is an employee and shareholder of Denali Therapeutics. During completion of the work related to this manuscript, F.M. was an employee of F. Hoffmann-La Roche Ltd. Q.W. is an employee of F. Hoffmann-La Roche Ltd. S.B. is an employee and shareholder of Biogen Inc. During completion of the work related to this manuscript, S.B. was an employee of F. Hoffmann-La Roche Ltd. M.M. is an employee and shareholder of F. Hoffmann-La Roche Ltd. J.L. has received research support from Innosuisse—Swiss Innovation Agency, Biogen, and Novartis; and speaking honoraria and/or fees for serving on advisory boards from Novartis, Roche, and Teva. L.K.s’ institution (University Hospital Basel) has received the following exclusively for research support: steering committee, advisory board, and consultancy fees from: Actelion, Bayer HealthCare, Biogen, BMS, Genzyme, GlaxoSmithKline, Janssen, Japan Tobacco, Merck, Novartis, Roche, Sanofi, Santhera, Shionogi, TG Therapeutics; speaker fees from: Bayer HealthCare, Biogen, Merck, Novartis, Roche, and Sanofi; support of educational activities from: Allergan, Bayer HealthCare, Biogen, CSL Behring, Desitin, Genzyme, Merck, Novartis, Roche, Pfizer, Sanofi, Shire, and Teva; license fees for Neurostatus products and grants from: Bayer HealthCare, Biogen, European Union, InnoSwiss, Merck, Novartis, Roche, Swiss MS Society, and Swiss National Research Foundation. J.B.’s institution has received a research collaboration grant from F. Hoffmann-La Roche Ltd. not related to the current research.
 None declared.

 Conflict of Interest Disclosure: The authors declare no conflict of interest.

 GL declares to be a consultant for Allergan, Almirall, Biogen, Novartis Sanofi, Merck Serono, Bristol, Ipsen, and Bristol Celgene. VBM has received funding for research support and speaker honoraria from Novartis, Roche, Biogen, Teva, Almirall, Sanofi-Genzyme, Merck, Bayer, and Mylan. SB received speaker honoraria and/or advisory board fee from Novartis, Sanofi Genzyme, Merck-Serono, Brystol-Meyers, Biogen-Idec, Viatris, and Roche. AG received personal compensations for speaking or consultancy from Biogen, Bristol Myers Squibb, Merck-Serono, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. GTM received personal compensations from Serono, Biogen, Novartis, Roche, and TEVA for public speaking and advisory boards. FS received public speaking honoraria from Alexion, Argenx, Biogen, Mylan, Novartis, Roche, Sanofi, and Teva; he also received compensation for advisory boards or consultation fees from Alexion, Almirall, Argenx, Avexis, Biogen, Forward Pharma, Lexeo Therapeutics, Merk, Novartis, Novatek, Roche, Sanofi, and Takeda. MB declares fees from Biogen, Sanofi Genzyme, Roche, and Novartis. DM, GS, SC, ES, and LMEG declare no competing interests. MB, LM, and RT declare to be Novartis employees.

 Declaration of Competing Interest All authors (Lingyu Kong, Xinwen Zhang, Lingyue Meng, Hao Xue, Wenlong Zhou, Xin Meng, Qiuxia Zhang, and Jianzhong Shen) declare no conflict of interest. All authors have read and approved the final version of the manuscript (Title: Effects of Music Therapy Intervention on Gait Disorder in Persons with Multiple Sclerosis: A Systematic Review of Clinical Trials).
 Declaration of Competing Interest Nothing to declare.
 Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article.



 Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Sipila JOT reports a relationship with Medaffcon Oy that includes: consulting or advisory. Sipila JOT reports a relationship with Orion Corporation that includes: equity or stocks.
 Conflicts of interest We have no competing interests.
 The authors report no conflicts of interest with direct relevance to this study.
 Declaration of Competing Interest The authors report no competing interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Ruth Ann Marrie receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and the US Department of Defense, and is a co-investigator on studies receiving funding from Biogen Idec and Roche Canada.
 J.A.N.B. reports no competing interests. S.N.H. reports no competing interests. S.P. is supported by a research grant from the Dutch MS Research Foundation. M.M.S. serves on the Editorial Boards of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation, ARSEP, Amsterdam Neuroscience and ZonMW, and has received compensation for consulting services or speaker honoraria from Atara Biotherapeutics, Biogen, Celgene/Bristol Meyers Squibb, Sanofi-Genzyme, MedDay and Merck. B.M.J.U. has received consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche and Teva. L.J.v.R. reports no competing interests. A.P. reports personal fees from Novartis, Heidelberg Engineering and Zeiss, grants from Novartis outside the submitted work, and is part of the steering committee of the OCT multiple sclerosis study, which is sponsored by Novartis and the Angio-OCT steering committee, which is sponsored by Zeiss. He does not receive compensation for these activities
 Prof Maddess has received grant support from Konan Medical USA Inc. and sits on an advisory panel of EyeCo Pty Ltd. Prof Maddess, Dr Carle and Dr van Kleef have patents assigned to Konan Medical USA. The remaining authors have no conflicts of interest.



 Declaration of Competing Interest LH has no conflicts of interest relevant to this study. KC has received honoraria for speaking at meetings, advisory work or support to attend meetings from Merck, Biogen Idec, Sanofi Genzyme and Roche. SM has no conflicts of interest relevant to this study. JF has no conflicts of interest relevant to this study. OC has served as a consultant for Novartis and has received a speaker honorarium from Merck. She has obtained funding from NIHR, UCLH NIHR BRC, National and UK MS Society, PMSA, and MRC. DC is a consultant Hoffmann-La Roche. In the last three years he has been a consultant for Biogen, has received research funding from Hoffmann-La Roche, the International Progressive MS Alliance, the MS Society, and the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre, and a speaker's honorarium from Novartis. He co-supervises a clinical fellowship at the National Hospital for Neurology and Neurosurgery, London, which is supported by Merck. FB is a consultant for Biogen, Bayer, Merck, Roche, Novartis, IXICO and Combinostics; has received funding from European Commission Horizon (2020), UK MS Society, National Institute for Health Research University College London Hospitals Biomedical Research Centre and GE healthcare; and serves on the editorial boards of Radiology, Brain, Neuroradiology, Multiple Sclerosis Journal, and Neurology.
 Declaration of Competing Interest DM reports no disclosures. NB reports no disclosures. CS reports no disclosures. GLM reports no disclosures. AU received grants (to his Institution) from FISM, Biogen, Roche, Alexion, Merck Serono; participated on a Data Safety Monitoring Board or Advisory Board (to his Institution) for BD, Biogen, Iqvia, Sanofi, Roche, Alexion, Bristol Myers Squibb. MI received grants NIH, NMSS, FISM; received fees for consultation from Roche, Genzyme, Merck, Biogen and Novartis. AL received fees for consultation from Roche, Sanofi-Genzyme, Merck, Biogen, Novartis, Bristol-Myers Squibb.
 Declaration of Competing Interest The authors have no conflicts of interest to declare
 Declarations of Competing Interests None.

 The authors declare no competing interests.


 The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare no conflict of interest.

 The authors declare no competing interests.

 Declaration of Competing Interest The authors declare no conflict of interest.
 None
 Declaration of Competing Interest The authors declare no competing interests.
 Declaration of Competing Interest Antonio Carotenuto has received research grants from Almirall; honoraria form Novartis, Merck and Biogen; was supported by MAGNIMS/ECTRIMS research fellowship program. Giuseppe Pontillo was supported by MAGNIMS//ECTRIMS research fellowship program (2020) and ESNR research fellowship program (2021). Marcello Moccia has received research grants from the ECTRIMS-MAGNIMS, the UK MS Society, and Merck, and honoraria from Biogen, BMS Celgene, Ipsen, Merck, Novartis and Roche. Sirio Cocozza discloses Board Membership: Amicus Therapeutics; Payment for Lectures Including Service on Speakers Bureaus: Sanofi; Research Grants: FISM; Telethon. Roberta Lanzillo received personal compensation for speaking or consultancy from Biogen, Teva, Genzyme, Merck, Novartis, and Almirall. Vincenzo Brescia Morra has received honoraria from Almirall, Bayer, Biogen, Merck, Novartis, Roche and Sanofi Genzyme, and research grants from the Italian MS Foundation. Maria Petracca has received travel/meeting expenses from Novartis, Roche and Merck, speaking honoraria from HEALTH&LIFE S.r.l. and honoraria for consulting services from Biogen and research grants from Baroni Foundation. Mario Tranfa, Valentina Iuzzolino, Pierpaolo Perrella, Andrea Elefante and Arturo Brunetti have nothing to disclose.
 Declaration of Competing Interest None.
 The authors report no conflict of interest.

 Declaration of Competing Interest The authors report no disclosures relevant to the manuscript.No targeted funding is reported
 Declaration of Competing Interest The authors have no conflicts of interest to declare.

 A. Pappolla has received speaking honoraria from Novartis, travel expenses by Roche, and has performed an ECTRIMS Clinical Training Fellowship. M. Tintoré has received compensation for consulting services, speaking honoraria and research support from Almirall, Bayer Schering Pharma, Biogen-Idec, Genzyme, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Aventis, Viela Bio and Teva Pharmaceuticals. À. Rovira serves/ed on scientific advisory boards for Novartis, Sanofi-Genzyme, SyntheticMR, Bayer, Roche, Biogen, Icometrix and OLEA Medical, and has received speaker honoraria from Bayer, Sanofi-Genzyme, Bracco, Merck-Serono, Teva Pharmaceutical Industries Ltd., Novartis, Roche and Biogen. The remaining authors declare no conflict of interest.

 Declaration of Competing Interest None.

 The authors have no conflicts of interest to declare.
 Declaration of interests The authors declare no competing interest.


 TVB, PV, and KA hold patents related to ferrostatin-1 analogs (US9862678, WO2016075330, EP3218357, WO2019154795).

 Declaration of Competing Interest None.





 Mark Jenkinson receives royalties from Oxford University Innovations for licensing of the FSL software for commercial, non‐academic use. The remaining authors report no financial interests or potential conflicts of interest for this work.

 Declaration of Competing Interest The authors did not report any conflict of interest in relation to the study.

 Declaration of Competing Interest The authors declare that there is no conflict of interest regarding the publication of this paper.
 Declaration of Competing Interest Marcello Moccia has received research grants from the ECTRIMS-MAGNIMS, the UK MS Society, and Merck; honoraria from Biogen, Ipsen, Merck, Roche, and Sanofi-Genzyme. Vincenzo Brescia Morra has received research grants from the Italian MS Society, and Roche, and honoraria from Bayer, Biogen, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. Raffaele Palladino has received research grants from Sanofi-Genzyme. Other authors have nothing to disclose.


 Declaration of Competing Interest Drs. Vinicius A. Schoeps and Nishita Singh have nothing to disclose. Dr. Emmanuelle Waubant has participated in multicenter clinical trials funded by Genentech, Alexion and Biogen. She has current support from the NIH, NMSS, PCORI, CMSC and Race to Erase MS. She does not receive honorarium from companies.
 The authors declare that they have no conflict of interest.
 Declaration of Competing Interest MD Buron has received speaker honoraria from Novartis. F Sellebjerg has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, H. Lundbeck A/S, Merck, Novartis, Roche and Sanofi Genzyme. His laboratory has received research support from , Merck, Novartis, Roche and Sanofi Genzyme. M Magyari has served in scientific advisory board for Sanofi, Novartis, Merck, and has received honoraria for lecturing from Biogen, Merck, Novartis, Roche, Genzyme, Bristol Myers Squibb. J Romme Christensen has received speaker honoraria from Biogen. PV. Rasmussen has received speaker honoraria from TEVA, Biogen, Roche and Novartis, support for congress participation from Merck, Roche, Sanofi and TEVA, fees for serving on advisory boards from Merck, Roche, Novartis, Biogen, and Sanofi. PS. Sorensen has received personal compensation for serving on advisory boards for Biogen, Merck, Novartis, Teva; on steering committees or independent data monitoring boards in trials sponsored by Merck, and Novartis; and has received speaker honoraria from Biogen, Merck, Teva, BMS/Celgene, and Novartis. H Joensen, M Kant, D Bech and L Pontieri report no disclosures

 Declaration of interests LGe, SS, EDS, EC, NS, and LP have no conflicts of interest to declare. GM received travel grants from Janssen (unrelated to the present work). LGa participated on advisory boards for, and received writing honoraria and travel grants from Almirall, Biogen, Euroimmun, Fujirebio, Merck, Mylan, Novartis, Roche, Sanofi, and Teva. AM received travel grants and writing honoraria from Almirall, Biogen, Merck, Mylan, Novartis, Sanofi Genzyme, and Teva. AT received research support from Lundbeck and served as speaker for Lundbeck and Angelini (unrelated to the present work). MDF participated on advisory boards for and received speaker or writing honoraria, research support and funding for travelling from Bayer, Biogen Idec, Genzyme, Merck, Mylan, Novartis, Roche, Siemens Healthineers, Teva and Viatris.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 Miguel Angel Robles-Sanchez received speaking or consulting honoraria; participated in scientific activities organized by Merck, Teva, Biogen, Viatris, Novartis, Sanofi-Genzyme, Celgene, EXCEMED, and Roche; and was awarded the ECTRIMS MS Nurse Training Fellowship Programme. Xavier Montalban received speaking honoraria and travel expenses for participation in scientific meetings and has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Abbvie, Actelion, Alexion, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Immunic, Janssen Pharmaceuticals, Medday, Merck, Mylan, NervGen, Novartis, Sandoz, Sanofi-Genzyme, Teva Pharmaceutical, TG Therapeutics, Excemed, MSIF, and NMSS. Jaume Sastre-Garriga received speaking or consulting honoraria and attended scientific activities in the last 2 years organized by Merck, Teva, Bial, EXCEMED, Biogen, Celgene, Novartis, Sanofi-Genzyme, and Roche and also serves as the director of Revista de Neurología and as a member of the editorial board of the Multiple Sclerosis Journal . Lluís Ramió-Torrentà has received speaking or consulting honoraria; attended scientific activities organized by Merck, Teva, Biogen, Bayer, Novartis, Sanofi, Roche, Almirall, and Mylan; and participated in advisory boards organized by Sanofi, Merck, Roche, Biogen, Novartis, Almirall, and Mylan. Montse Moharra (the coordinator of the Shared Decision-Making Program), Cristina Bosch-Farré, María José Hernández-Leal (a lecturer in the University of Navarra, with postdoctoral research in the University of La Frontera and Millennium Nucleus on Sociomedicine), and Carme Bertran-Noguer declare no conflicts of interest.
 The authors declare that they have no competing interests.
 Potential Conflicts of Interest The authors have nothing to report.



 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest Mina Stanikić reports employment by Roche branch in Serbia, Roche d.o.o., from February 2019 to February 2020. The employer of Chiara Zecca receives support for advisor activities, speaking or grants from Celgene, Genzyme, Lilly, Merck, Novartis, Roche, and grants from Abbvie, Almirall, Biogen Idec, Celgene, Genzyme, Lilly, Merck, Novartis, Roche, Teva Pharma. Pasquale Calabrese has received honoraria for speaking at scientific meetings, serving at scientific advisory boards and consulting activities from Abbvie, Actelion, Almirall, Bayer-Schering, Biogen, EISAI, Lundbeck, Merck Serono, Novartis, Sanofi-Aventis and Teva. He also receives research grants from the Swiss Multiple Sclerosis Society (SMSG), and the Swiss National Research Foundation. Mathias Mettler, Urban Schwegler, Chloé Sieber, Vladeta Ajdacic-Gross, Stephanie Rodgers, Christina Haag, Susanne Kägi, Irene Rapold and Viktor von Wyl declare no competing interests.
 Declaration of Competing Interest The authors have no competing interests to report.

 The authors declare that they have no competing interests related to this paper.



 The author has no conflicts of interest to disclose.
 The authors declare no conflict of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest None.

 Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest None.
 Declaration of interests The author does not have any conflict of interest to disclose.
 None declared.
 L. Müller-Jensen and P. Huehnchen are participants in the BIH Charité (Junior) Clinician Scientist Program funded by the Charité—Universitätsmedizin Berlin and the Berlin Institute of Health at Charité (BIH). Go to Neurology.org/N for full disclosures.
 Competing interests: AC has received research grants from Almirall, and served on advisory boards for: Merk, Novartis, Roche and Almirall. PV received speaker honoraria from Biogen Idec. PP received speaker honoraria from Biogen, Novartis, Merck Serono, Bristol Myers Squibb and ExceMED. DM has nothing to declare. MF is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology and Associate Editor of Neurological Sciences; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche and Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda and Teva; participation in Advisory Boards for Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme and Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla and ARiSLA (Fondazione Italiana di Ricerca per la SLA). MAR received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen and Roche; and speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono, Novartis, Roche and Teva. She receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders.
 Competing interests: The authors declare that the research will be conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no competing interests.
 Competing interests: TS received compensation for serving on scientific advisory boards, honoraria for consultancy and funding for travel from Biogen. JH has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis and Sandoz and speaker’s fees from Biogen, Novartis, Merck KGaA, Teva and Sanofi-Genzyme; he has served as P.I. for projects, or received unrestricted research support from, Biogen, Celgene, Merck KGaA, Novartis, Roche and Sanofi-Genzyme.
 Declaration of Competing Interest None.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: S.K. reports grants and consulting fees from Roche; grants and consulting fees from Sanofi-Genzyme; consulting fees from Novartis; and grants from Biogen. L.G. was an employee of and shareholder in F. Hoffmann-La Roche Ltd. at the time of the project. She is now an employee of Novartis AG. H-E.A. is an employee of NeuroRx Research. C.B. is a contractor for F. Hoffmann-La Roche Ltd. U.B. is an employee of and shareholder in F. Hoffmann-La Roche Ltd. C.E. is an employee of NeuroRx Research and has received speaker honoraria from EMD Serono. N.H. is an employee of and shareholder in F. Hoffmann-La Roche Ltd. S.M. is an employee of and shareholder in F. Hoffmann-La Roche Ltd. D.L.A. reports consulting fees from Albert Charitable Trust, Alexion Pharma, Biogen, Celgene, Frequency Therapeutics, Genentech, Med-Ex Learning, Merck, Novartis, Population Council, Receptos, Roche, and Sanofi-Aventis; grants from Biogen, Immunotec, and Novartis; and an equity interest in NeuroRx ‘Research’?. A.T. reports grants and personal fees from Roche; grants and personal fees from Sanofi-Genzyme; personal fees from Novartis; and personal fees from EMD Serono outside the submitted work.
 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: CY reports no potential conflicts of interest. CW reports serving as a site principal investigator in clinical trials sponsored by Alexion Pharmaceuticals and Roche, receiving no direct benefit for this participation.

 A.J. Solomon participates in contracted research with Sanofi, Biogen, Novartis, Actelion, and Genentech/Roche, receives research support from Bristol Myers Squibb, personal compensation for consulting for Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, Horizon Therapeutics, TG Therapeutics, and Octave Bioscience, personal compensation nonpromotional speaking for EMD Serono, and provides expert witness testimony. R.A. Marrie receives research funding from CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and US Department of Defense. She is a coinvestigator on a study partially funded by Biogen Idec and Roche (no funds to her or her institution). She is supported by the Waugh Family Chair in Multiple Sclerosis. S. Viswanathan participates in contracted research with Alexion, Novartis, Sanofi, and Roche. J. Correale has received financial compensation for academic presentations, assistance to advisory boards, financial support for clinical and basic research, and travel assistance to congresses from the following companies: Biogen, Merck, Novartis, Roche, Bayer, Sanofi-Genzyme, Gador, Raffo, Bristol Myers Squibb, and Janssen. M. Magyari has served in scientific advisory board for Sanofi, Novartis, and Merck and has received honoraria for lecturing from Biogen, Merck, Novartis, Roche, Genzyme, and Bristol Myers Squibb. N. Robertson has received honoraria and/or support to attend educational meetings from Biogen, Novartis, Janssen, Genzyme, and Roche. His institution has also received research support from Biogen, Novartis, and Sanofi. D. Saylor has received funding from the National Multiple Sclerosis Society. W.E. Kaye receives funding from the Agency for Toxic Substances and Disease Registry, the National Multiple Sclerosis Society, the Association for the Accreditation of Human Research Protection Programs, and Rockefeller University. L. Rechtman and E. Bae have no disclosures to report. R.T. Shinohara receives consulting income from Octave Bioscience and compensation for scientific reviewing from the American Medical Association, the NIH, the Department of Defense, and the Emerson Collective. R. King, J. Laurson-Doube, and A. Helme have no disclosures to report. Go to Neurology.org/N for full disclosures.
 Competing interests: KS: receives funding from the Multiple Sclerosis Society of Canada (MSSOC) and Neurofonden, but reports no conflict of interest or involvement of either foundation with respects to this study. FP: Has received research grants from Genzyme, UCB, and Merck KGaA and fees for serving as DMC in clinical trials with Chugai, Lundbeck and Roche. TO: Has received funding for spasticity research from Almirall and unrestricted MSM research grants and/or honoraria for advisory boards/lectures from Biogen, Novartis, Sanofi, AstraZeneca and Merck. LA: Has received lecture honoraria from Biogen and Teva. JH: Has received honoraria for serving on advisory boards for Sandoz, Biogen, Sanofi-Genzyme, Merch KGaA and Novartis; has received speaker’s fees from Biogen, Merck KGaA, Novartis, Sanofi-Genzyme, and TEVA; has served as principle investigator for projects or received unrestricted research support from Biogen, Merck, Novartis, Roche and Sanofi-Genzyme. IK: Is supported by the Horizon 2020 Multiple MS grant number 733161. PS: Supported by the Margaretha af Ugglas Foundation, and Horizon 2020 Multiple MS grant number 733161. SM: Has received MS research grants and/or honoraria for advisory boards/lectures from Roche, Novartis, AstraZeneca, Merck, Teva and IQVIA.

 Declaration of Competing Interest D. Wagner is Chief Scientific Officer and Co-Founder of Op-T, LLC. No funding from Op-T, LLC was used for this manuscript. All other authors have no declarations of interest to declare.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: M.W. reports personal fees from Novartis, Alnylam, Amicus, Biogen, Bristol Myers Squibb, Pfizer, Bial and other from Boehringer Ingelheim Foundation. C.E.W. reports no disclosures. M.K. reports no disclosures. M.P. has a consultant relationship with Novartis, Merck, Genentech/Roche; has received non-personal, institutional honoraria from Medac, Merck, Novartis, TEVA, Genentech/Roche and has research agreements with Bayer Health Care. L.S. reports no disclosures. H.T. reports funding for research projects, lectures and travel from Alexion, Bayer, Biogen, Celgene/Bristol Myers Squibb, GlaxoSmithKline, Janssen, Merck Serono, Novartis, Roche, Sanofi/Genzyme, Siemens and Teva, and received research support from Chemische Fabrik Karl Bucher GmbH, German Multiple Sclerosis Society (DMSG) and the German Ministry for Education and Research (BMBF). A.G. has received honoraria for lecturing, travel expenses for attending meetings and financial support for research from Bayer Schering, Biogen Idec, Merck Serono, Novartis, TEVA Neurosciences and is member of the Editorial Board of the Journal of Neuroimaging. P.E. has received travel expenses from Bayer Health Care and is member of the Editorial Board of the Journal of Neuroimaging.
 Declaration of Competing Interest None.


 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dr. Dinov reports no financial interests/personal relationships. Dr. Brenton has served as a consultant for Cycle Pharmaceuticals.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that there are no competing interests related to this manuscript.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Antonio Gallo reports a relationship with Biogen that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Antonio Gallo reports a relationship with Merck Serono that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Antonio Gallo reports a relationship with Mylan ITALIA Srl that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Antonio Gallo reports a relationship with Novartis that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Antonio Gallo reports a relationship with Roche that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Antonio Gallo reports a relationship with Sanofi Genzyme that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Antonio Gallo reports a relationship with Teva Health that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Lorena Lorefice reports a relationship with Biogen that includes: consulting or advisory and speaking and lecture fees. Lorena Lorefice reports a relationship with Novartis that includes: consulting or advisory and speaking and lecture fees. Lorena Lorefice reports a relationship with Sanofi that includes: consulting or advisory and speaking and lecture fees. Lorena Lorefice reports a relationship with Sanofi Genzyme that includes: consulting or advisory and speaking and lecture fees. Lorena Lorefice reports a relationship with Merck Serono that includes: consulting or advisory and speaking and lecture fees. Lorena Lorefice reports a relationship with Teva Health that includes: consulting or advisory and speaking and lecture fees. Lorena Lorefice reports a relationship with Almirall Ltd that includes: speaking and lecture fees. Alvino Bisecco reports a relationship with Biogen that includes: consulting or advisory and speaking and lecture fees. Alvino Bisecco reports a relationship with Roche that includes: consulting or advisory and speaking and lecture fees. Alvino Bisecco reports a relationship with Merck & Co Inc that includes: consulting or advisory and speaking and lecture fees. Alvino Bisecco reports a relationship with Celgene Corp Los Angeles that includes: consulting or advisory and speaking and lecture fees. Alvino Bisecco reports a relationship with Sanofi Genzyme that includes: consulting or advisory and speaking and lecture fees. Massimiliano Calabrese reports a relationship with Biogen that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with Bristol Myers Squibb that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with Celgene Corp Los Angeles that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with Sanofi Genzyme that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with Merck Serono that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with Novartis that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with Roche that includes: speaking and lecture fees. Massimiliano Calabrese reports a relationship with International Progressive MS Alliance that includes: funding grants. Massimiliano Calabrese reports a relationship with Ministry of Health that includes: funding grants. Massimiliano Di Filippo reports a relationship with Bayer AG that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Biogen Italy that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Sanofi Genzyme that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Merck & Co Inc that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Mylan ITALIA Srl that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Novartis that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Roche that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Siemens Healthineers that includes: speaking and lecture fees and travel reimbursement. Massimiliano Di Filippo reports a relationship with Teva Health that includes: speaking and lecture fees and travel reimbursement. Gioacchino Tedeschi reports a relationship with Teva Health that includes: board membership. Gioacchino Tedeschi reports a relationship with Roche that includes: board membership. Gioacchino Tedeschi reports a relationship with Eli Lilly Italy that includes: board membership. Gioacchino Tedeschi reports a relationship with Allergan US that includes: board membership. Gioacchino Tedeschi reports a relationship with Sanofi-Aventis US LLC that includes: speaking and lecture fees and travel reimbursement. Gioacchino Tedeschi reports a relationship with Merck Serono Ltd that includes: speaking and lecture fees and travel reimbursement. Gioacchino Tedeschi reports a relationship with Bayer Schering Pharma AG that includes: speaking and lecture fees and travel reimbursement. Gioacchino Tedeschi reports a relationship with Biogen Italy that includes: speaking and lecture fees and travel reimbursement. Gioacchino Tedeschi reports a relationship with Novartis that includes: speaking and lecture fees and travel reimbursement.
 S.J. Baetge has no relevant financial or non-financial interests to disclose. M. Filser has no relevant financial or non-financial interests to disclose. A. Renner has no relevant financial or non-financial interests to disclose. L.M. Raithel has no relevant financial or non-financial interests to disclose. S. Lau reports has no relevant financial or non-financial interests to disclose. J. Pöttgen has no relevant financial or non-financial interests to disclose. I.K. Penner reports to have received honoraria for speaking at scientific meetings, serving at scientific advisory boards and consulting activities from Adamas Pharma, Almirall, Bayer Pharma, Biogen, BMS, Celgene, Genzyme, Janssen, Merck, Novartis, Roche, and Teva. She received research support from the German MS Society, Celgene, Novartis, Roche, and Teva. All payments were transferred to the institution.

 Declaration of Competing Interest The authors declare that there is no conflict of interest.
 The authors declare there are no conflicts of interest – financial or otherwise – related to the material presented herein.


 Declaration of Competing Interest Salma Al-Abri has no conflicts of interests to declare. Abdullah Al-Asmi has received honoraria from Novartis, Sanofi, Biologix, Merck, Roche, Biogen, and Bayer. He serves on the scientific advisory boards of Novartis, Merck, and Roche. Sachin Jose has no conflicts of interests to declare. Arunodaya R Gujjar has no conflicts of interests to declare.

 Declaration of Competing Interest The authors state that there is no conflict of interest.
 Declaration of Competing Interest The authors declare no competing interests.
 UB is an employee of Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: J.A.C. reports personal compensation for consulting for Bio-gen, Bristol—Myers Squibb, Convelo, Genentech, Janssen, NervGen, Novartis, and PSI; speaking for H3 Communications; and serving as an Editor of Multiple Sclerosis Journal. F.L. reports research funding from: Novartis, Actelion, Biogen, Sanofi, NMSS, NIH, Brainstorm Cell Therapeutics; consulting agreements/advisory boards/DSMB activities with: Biogen, EMD Serono, Novartis, Teva, Actelion/Janssen, Sanofi/Genzyme, Acorda, Roche/Genentech, MedImmune/Viela Bio/Horizon Thera-peutics, Receptos/Celgene/BMS, TG Therapeutics, Medday, Atara Biotherapeutics, Mapi Pharma, Apitope, Orion Biotechnology, Brainstorm Cell Therapeutics Jazz Pharmaceuticals, GW Pharma, Mylan, Immunic, Population Council, Avotres, Neurogene, Banner Life Sciences, Labcorp, Entelexo Biotherapeutics, Neuralight; stock Options from Avotres; and speaking for Sanofi (nonpromotional). C.L. reports personal compensation for speaking, advisory boards, or consulting for Biogen, Sanofi, EMD Serono, Alexion Pharmaceuticals, Bristol Myers Squib, Greenwich Biosciences, InterX Inc., and Diagnose Early. D.P. reports consulting compensation for advisory board activities from Biogen, Sanofi/Genzyme, EMD Serono, and Roche/Genentech. T.C. reports personal compensation for consulting for Biogen, Novartis, Genentech, and Sanofi-Genzyme, and research funding from Brainstorm Cell Therapeutics, Novartis and Verily. M.M. is an employee of Tigermed. Y.G. is an employee of Brainstorm Cell Therapeutics. R.A. is an employee of Brainstorm Cell Therapeutics. S.L. is an employee of Brainstorm Cell Therapeutics. C.L. is an employee of Brainstorm Cell Thera-peutics. Y.S.L. is an employee of Brainstorm Cell Therapeutics. A.M.K. reports personal compensation for consulting for Argenix, Atara Biotherapeutics, and Brainstorm Cell Therapeutics. R.K. is an employee of Brainstorm Cell Therapeutics.
 The authors declare that they have no conflict of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.M. is supported by the Margaretha af Ugglas Foundation. M.E.K. is supported by the Michael Smith Foundation for Health Research Scholar award, BC Support Unit’s Real-World Clinical Trials Methods Cluster, Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery grant and Discovery Accelerator Supplements. Over the past 3 years, he has received consulting fees from Biogen Inc. for consulting. J.L. has received travel support and/or lecture honoraria from Biogen, Novartis, Teva, Sanofi, Merck, BMS, Axelion and Roche; has served on scientific advisory boards for Biogen, Novartis, Teva, Sanofi, Merck, BMS, Axelion, and Roche; serves on the editorial board of the Acta Neurologica Scandinavica; and has received unconditional research grants from Biogen, Novartis, and Teva. I.K. has support in the form of research grants from Swedish Brain Foundation, Swedish research council (2020-01638), EU Horizon 2020 (MultipleMS, project nr 733161and EU-STANDS4PM, project no. 825843) and Region Stockholm. T.O. has grant support from the Swedish research council, the Swedish Brain Foundation, and the Wallenberg Foundation. T.O. has received honoraria for advisory boards/lectures and unrestricted MS research grants from Biogen, Novartis, Merck, Sanofi, and Roche. The remaining author declares no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare no conflict of interest in preparing this article.
 Declaration of Competing Interest Authors declare no conflict of interest.
 Declaration of interests F. Piehl reports having received grants from Merck KGaA, Janssen and UCB for different studies, payment from Novartis for expert testimony. He participated on Data safety monitoring board or advisory board for clinical trials with Chugai, Lundbeck and Roche. He is also chairman of the Neuro research committee (a Swedish patient organization), an unpaid role. The other authors report no competing interests.

 The research activities of RC2NB (Research Center for Clinical Neuroimmunology and Neuroscience Basel) are supported by the University Hospital and the University of Basel and by grants from Novartis, Roche and Neurostatus-UHB AG. One of the main projects of RC2NB is the development of a new comprehensive MS Digital solution. This study was performed in collaboration with Healios AG, Basel, Switzerland and received funding from the Swiss Innovation Agency (Innosuisse, project ID 33535.1 IP-ICT). PopReach Incorporated (Peak) provided access to selected cognitive training games without any influence on the study design, analysis, and interpretation. Silvan Pless has nothing to disclose. Tim Woelfle has nothing to disclose. Yvonne Naegelin’s institution (University Hospital Basel) has received financial support for lectures from Teva and Celgene and grant support from Innosuisse (Swiss Innovation Agency). Johannes Lorscheider’s institution has received research grants from Novartis, Biogen and Innosuisse as well as honoraria for advisory boards and/or speaking fees from Novartis, Roche and Teva. Oscar Reyes is Lead Data Scientist of Healios AG. Andrea Wiencierz has nothing to disclose. Pasquale Calabrese has received honoraria for speaking at scientific meetings, serving at scientific advisory boards and consulting activities from: Abbvie, Actelion, Almirall, Bayer-Schering, Biogen Idec, Celgene, EISAI, Genzyme, Lundbeck, Merck Serono, Novartis, Pfizer, Teva, and Sanofi-Aventis. His research is also supported by the Swiss Multiple Sclerosis Society and the Swiss National Research Foundation. Ludwig Kappos has received no personal compensation. His institution (University Hospital Basel/Foundation Clinical Neuroimmunology and Neuroscience Basel) has received the following exclusively for research support: steering committee, advisory board and consultancy fees (Abbvie, Actelion, AurigaVision AG, Biogen, Celgene, Desitin, Eli Lilly, EMD Serono, Genentech, Genzyme, Glaxo Smith Kline, Janssen, Japan Tobacco, Merck, Minoryx, Novartis, Roche, Sanofi, Santhera, Senda, Shionogi, Teva, and Wellmera; speaker fees (Celgene, Janssen, Merck, Novartis, and Roche); support for educational activities (Biogen, Desitin, Novartis, Sanofi and Teva); license fees for Neurostatus products; and grants (European Union, Innosuisse, Novartis, Roche Research Foundation, Swiss MS Society and Swiss National Research Foundation).
 Conflict of interest statement The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Orschiedt (ORCID# 0000-0002-2813-6343) is employed by the Temedica GmbH and the Technical University of Munich. E. Jacyshyn-Owen, M. Eberl, M. Kahn (ORCID# 0000-0002-9596-6339) and B. Friedrich (ORCID# 0000-0002-2198-9925) are employed by the Temedica GmbH. S. Jansen is employed by the Noventi Health SE. N. Joschko is an employee of Roche Pharma AG and shareholder of F. Hoffmann-La Roche Ltd. S. Schneeweiss (ORCID# 0000-0003-2575-467X) is participating in investigator-initiated grants to the Brigham and Women’s Hospital from Boehringer Ingelheim and UCB unrelated to the topic of this study. He is a consultant to Aetion Inc., a software manufacturer of which he owns equity. His interests were declared, reviewed, and approved by the Brigham and Women’s Hospital in accordance with their institutional compliance policies.


 Competing interests: IM has no disclosures to report. EW has participated in multicentre clinical trials funded by Genentech, Alexion and Biogen. She has current support from the NIH, NMSS, PCORI, CMSC and Race to Erase MS. No funding was required for this study. The spouse of author SD is an employee of Genentech.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 BMJ has received speaker honoraria from Biogen & Roche. WB has consulted for/received travel expenses from Roche, Sanofi and Biogen. RD has received speaker honoraria from Biogen Idec, Teva, Merck, Janssen, Roche and Sanofi Genzyme; sat on advisory boards for Roche, Merck, Novartis, Sandoz, Janssen and Biogen; and received research support from Biogen, Merck and Celgene.
 Declaration of competing interest Funding: The authors did not receive support from any organization for the submitted work. Competing interests: S Toscano received travel funding from Biogen, Sanofi-Genzyme, Almirall, Merck Serono and Teva. CG Chisari received research grants from Sanofi, and travel payment and grants for congress participation from Novartis, Biogen, Genzyme, Almirall, Bayer Schering, Merck Serono, and Teva. A Meli has nothing to declare. C. Finocchiaro received travel funding from Mylan. S Lo Fermo received honoraria for scientific lectures from Biogen, Merck Serono, and Teva, travel payment and grants for congress participation from Novartis, Biogen Idec, Genzyme, Almirall, Bayer Schering, Merck Serono and Teva, and served on scientific advisory boards for Biogen, Novartis, and Merck Serono. M. Zappia served on advisory boards for Bayer, Biogen, Celgene, Merck, Novartis, Roche, Sanofi, Teva and Almirall, received compensation for consulting services from Boehringer-Ingerheim, Lundbeck and Union Chimique Belge, and scientific grants from AIFA-Agenzia Italiana del Farmaco, Novartis and Lundbeck, received honoraria for scientific lectures from Biogen, Merck Serono, Teva, Novartis, and Sanofi. F Patti received honoraria for speaking activities by Biogen, Novartis, Teva, Sanofi, Genzyme, Bayer Schering, Merck Serono, Almirall, Roche, and Celgene, and has served as an advisory board member for Bayer Schering, Roche, Biogen, Merck and Novartis. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
 The authors declare that they have no competing interests.


 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: In the last 3 years, RP received support from the UK MS Society. RP has taken part into in consultancy for MSD. RAM receives research funding from Canadian Institutes of Health Research, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium of MS Centers, the Arthritis Society and US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution). In the last 3 years, JC has received support from the Efficacy and Evaluation (EME) Programme, a Medical Research Council (MRC) and National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Programme (NIHR), the UK MS Society, the US National MS Society and the Rosetrees Trust. He is supported in part by the NIHR University College London Hospitals (UCLH) Biomedical Research Centre, London, UK. He has been a local principal investigator for a trial in MS funded by the Canadian MS society. A local principal investigator for commercial trials funded by Ionis, Novartis and Roche, and has taken part in advisory boards/consultancy for Azadyne, Biogen, Lucid, Janssen, Merck, NervGen, Novartis and Roche.

 Friberg is partly funded by an unrestricted research grant from Biogen and has received unrestricted research grants from Celgene/Bristol-Myers Squibb. The data in this project is not publicly available in accordance with the General Data Protection Regulation, the Swedish law SFS 2018:218, the Swedish Data Protection Act, the Swedish Ethical Review Act, and the Public Access to Information and Secrecy Act.

 JL-S received travel compensation from Biogen, Merck, and Novartis and has been involved in clinical trials with Biogen, Merck, Novartis, and Roche; her institution has received honoraria for talks and advisory board service from Biogen, Merck, Novartis, and Roche. VM has accepted honoraria for presentations and research funds from Biogen and Merck. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declared no competing interests for this work.
 The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

 The authors declare no conflicts of interest.


 Declaration of Competing Interest GMzH received compensation for serving on scientific advisory boards (LFB) and speaker honoraria (Alexion). HW is acting as a paid consultant for AbbVie, Actelion, Biogen, IGES, Johnson & Johnson, Novartis, Roche, Sanofi-Aventis, and the Swiss Multiple Sclerosis Society. The remaining authors declare no financial interests or conflicts of interest.


 B. Barrera has nothing to disclose. H. Simpson has nothing to disclose. E. Engebretson has nothing to disclose. S. Sillau has nothing to disclose. B. Valdez has nothing to disclose. J. Parra‐Gonzalez has nothing to disclose. R. C. Winger is an employee of Genentech, Inc, and a shareholder of F. Hoffmann‐La Roche Ltd. L. A. Epperson has nothing to disclose. A. Banks has nothing to disclose. K. Pierce has nothing to disclose. M. Spotts has nothing to disclose. K. O'Gean has nothing to disclose. E. Alvarez has received compensation for activities such as advisory boards, lectures and consultancy from Actelion/Janssen, Alexion, Bayer, Biogen, Celgene/BMS, EMD Serono/Merck, Genentech/Roche, Novartis, Sanofi and TG Therapeutics; and research support from Biogen, Genentech/Roche, Novartis, TG Therapeutics, Patient‐Centered Outcomes Research Initiative, National Multiple Sclerosis Society, National Institutes of Health and Rocky Mountain MS Center. R. Gross has nothing to disclose. A. Piquet reports research support and consulting fees from Genentech. Outside of this work, Dr. Piquet reports grants from the University of Colorado and Rocky Mountain MS Center, consulting fees from Alexion, honorarium from Medlink and publication royalties from Springer as a co‐editor of a textbook. T. Schreiner has received research funding from the National MS Center, Roche, Rocky Mountain MS Center and Biogen; and consultant fees from Roche and MS Focus. J. R. Corboy has received research Support from the National Institutes of Health, Patient‐Centered Outcomes Research Institute, National Multiple Sclerosis Society and Novartis; has served on an advisory committee for Bristol Meyers Squibb and on the editorial board for Annals of Neurology; and is a Medical Director at the Rocky Mountain Multiple Sclerosis Center. J. Pei is an employee of Genentech, Inc, and a shareholder of F. Hoffmann‐La Roche Ltd. T. L. Vollmer has received compensation for lectures and consultancy from Biogen IDEC, Genentech/Roche, Celgene, EMD Serono, Bristol Meyers Squib and Novartis; and has received research support from the Rocky Mountain Multiple Sclerosis Center, Biogen, Actelion, Roche/Genentech, F. Hoffman‐La Roche, Ltd and TG Therapeutics, Inc. K. V. Nair National MS Center has served as a consultant to Bristol Myers Squibb, Novartis, TG Therapeutics and PhRMA Foundation. She serves on the speakers' bureau of Sanofi‐Genzyme and Alexion, and she has received research grants from Genentech, PhRMA Foundation, Bristol Myers Squibb and Novartis.


 Declaration of Competing Interest JL reported receiving honoraria for lectures and for advisory boards from Biogen, Novartis, Merck, Alexion, Roche, Sanofi, and BMS; and unconditional grants from Biogen and Novartis; and is serving on the editorial board of the Acta Neurologica Scandinavica outside the submitted work. LN has received honoraria for lectures from Biogen, Novartis, Teva and Merck, and for advisory boards from Merck, Janssen and Sanofi. MS, EB, MA, JB, IR, SC and MB report no conflicts of interest.
 The authors have no conflicts of interest to declare.
 The authors declare no conflict of interest.
 No potential conflict of interest was reported by the author(s).
 Declaration of Competing Interest F.S. received public speaking honoraria from Alexion, Argenx, Biogen, Mylan, Novartis, Roche, Sanofi, Teva; he also received compensation for Advisory boards or consultation fees from Alexion, Almirall, Argenx, Avexis, Biogen, Forward Pharma, Lexeo Therapeutics, Merk, Novartis, Novatek, Roche, Sanofi, Takeda. The other authors report no conflict of interest.

 Conflict of Interest: No conflict of interest was declared by the authors.

 Declaration of Competing Interest MJ: None declared IL: received consultation and/or speaker fees from: Novartis. GBJ: participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Janssen, Lek, Merck, Novartis, Pliva/Teva, Roche, Sanofi Genzyme, Swixx. MK: Research contracts with Krka, Vizera, Clinres, Phamalinea with the aim of statistical analysis and a grant from AstraZeneca as a support to developments of sustainability and resilience of the healthcare system after COVID-19 pandemic. UR: participated as a clinical investigator and/or received consultation and/or speaker fees from: Bayer, Biogen, Sanofi Genzyme, Merck, Novartis, Pliva/Teva, Roche.
 Competing Interests: The authors have declared that no competing interest exists.



 Declaration of Competing Interest None.

 The authors declare no conflict of interest.

 Conflicts of interest and sources of funding: The authors have no conflicts of interest to declare. This study was funded by the Austrian Science Fund (FWF; KLI 718, P 30701, P 34198).
 Declaration of Competing Interest Jordanne Florio-Smith is a current employee of Roche Products Ltd UK and owns stocks and stock options in Roche Mavis Ayer has received consulting fees and speaker fees from Roche, Novartis, Merck, Janssen, Sanofi, Biogen; support for participating in conferences from Roche, Novartis, Merck, Sanofi, Biogen; participated in advisory boards/data safety monitoring boards with Roche, Novartis, Merck, Janssen, Sanofi, Biogen; equipment and/or services from Biogen and Roche; chair of MMSNA Samantha Colhoun has received speaker fees from Novartis Nicola Daykin has received consulting fees from and participated in advisory boards with Roche; speaker fees from Janssen; payment for manuscript writing from Journal of Prescribing Practice; co-chair and policy advisor of MMSNA Brenda Hamill Ayer has received consulting fees and support for participating in conferences from Roche Xierong Liu – none apart from employee of IPSOS MORI Emma Rogers – none apart from ex-employee of IPSOS MORI Alison Thomson has received speaker fees from Novartis; payment for advisory boards from Novartis, Biogen Roberta Pace Balzan is a current employee of Roche Products Ltd UK and owns stocks and stock options in Roche The study and its publication were funded by Roche Products Ltd, and conducted by Ipsos MORI
 Federico Montini has no potential conflicts of interest and reports no disclosures; Agostino Nozzolillo has no potential conflicts of interest and reports no disclosures; Paola M.V. Rancoita has no potential conflicts of interest and reports no disclosures; Chiara Zanetta has no potential conflicts of interest and reports no disclosures; Lucia Moiola received compensation for speaking activities, and/or consulting services from Merck, Biogen, Novartis, Roche, Sanofi, and TEVA; Federica Cugnata has no potential conflicts of interest and reports no disclosures; Federica Esposito received consulting and speaking fees from Novartis, Sanofi Genzyme; Maria A. Rocca received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from AstraZaneca, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Horizon Therapeutics Italy, Merck Serono SpA, Novartis, Roche, Sanofi and Teva. She receives research support from the MS Society of Canada, the Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders; Vittorio Martinelli received compensation for speaking and/or for consultancy and support for travel expenses and participation in Congresses from Biogen, Merck-Serono, Novartis, Genzyme and Teva Pharmaceutical Industries; Massimo Filippi is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Neurological Sciences, and Radiology; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA).
 David Leppert is Chief Medical Officer of GeNeuro. Tobias Granberg is the recipient of a Multiple Sclerosis Innovation Award from Merck. Fredrik Piehl has received research grants from Janssen, Merck KGaA and UCB, and fees for serving on DMC in clinical trials with Chugai, Lundbeck and Roche, and for preparation of expert witness statement for Novartis. Kamila Zondra Revendova, Chiara Starvaggi Cucuzza, Ali Manouchehrinia, Mohsen Khademi, Michal Bar, Elisabeth Sandberg, and Russell Ouellette declare no conflict of interest.
 The authors declare no competing interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article. AP, AH, APS, MM, CQ, MT, and GRL have nothing to declare. KH reports speaker and personal fees from Roche, Merck, and Biogen, and travel grants to attend educational meetings from Roche, Novartis, Merck, and Biogen. ET reports speaker fees and honoraria from Biogen, Janssen, Merck, Novartis, and Takeda, Roche, and travel expenses to attend educational meetings from Biogen, Merck, and Roche. TA has received speaker fees, support for scientific meetings and honoraria for advisory work from Merck Serono, Novartis, Roche, and Genzyme. G.I has received honoraria and travel expenses from Biogen, Merck, Novartis, and Roche and has served on advisory boards/acted as a speaker for Biogen, Novartis, Merck, and Roche. NE reports speaker fees and honoraria from Biogen, Merck, Novartis, and Roche.

 JL has received lecture honoraria from Biogen, BMS, Celgene, Janssen, Merck, Novartis, Sanofi, Roche and Alexion; has served on scientific advisory boards for Biogen, BMS, Merck, Novartis, Sanofi, Roche and Alexion; serves on the editorial board of the Acta Neurologica Scandinavica; and has received unconditional research grants from Biogen and Novartis. HF and AN: no conflict of interest.



 Declaration of Competing Interest All authors have completed the Unified Competing Interest form at http://www.icmje.org/coi_disclosure.pdf and declare that Ruth Ann Marrie, Lesley Graff, Amber Salter, James Marriott and Charles Bernstein have relationships that could be perceived to constitute a conflict of interest, and all authors have non-financial interests (research funding from government or non-profit sources that may be relevant to the submitted work. Ruth Ann Marrie receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and US Department of Defense. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her/her institution). She is supported by the Waugh Family Chair in Multiple Sclerosis. Lisa Lix receives research funds from CIHR, NSERC, and the Arthritis Society. James Bolton receives research funding from CIHR, Brain and Behavior Research Foundation and the MS Society of Canada. John Fisk receives research funds from CIHR, the MS Society of Canada, Crohn's and Colitis Canada, Research Nova Scotia; consultation and distribution royalties from MAPI Research Trust. Kathryn Fitzgerald receives research funds from NIH, CMSC, US Department of Defense and National MS Society. Lesley Graff receives research funds from CIHR, and Crohn's and Colitis Canada and has consulted to Roche Canada. Carol Hitchon has research funds for unrelated studies from UCB Canada and Pfizer. Kaarina Kowalec receives research funds from the CMSC, US Department of Defense, CIHR, NIH. James Marriott has conducted clinical trials for Biogen Idec and Roche, and receives research funding from the MS Society of Canada. Scott Patten receives research funding from CIHR, the MS Society of Canada, Roche, Biogen and the Government of Alberta. Amber Salter receives research funding from Multiple Sclerosis Society of Canada, National Multiple Sclerosis Society, CMSC and the US Department of Defense. Charles Bernstein has consulted to Abbvie Canada, Amgen Canada, BMS Canada, JAMP Canada, Janssen Canada, Pfizer Canada, Roche Canada, Sandoz Canada, Takeda Canada, and has received unrestricted educational grants from Abbvie Canada, BMS Canada, Janssen Canada, Pfizer Canada and Takeda Canada. He has been on speaker's bureaus of Abbvie Canada and Shire Canada.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest No conflicts of interest noted.
 Declaration of Competing Interest The authors report no disclosures or conflicts of interest relevant to this manuscript.

 Declaration of Competing Interest Tiffany Grezmak, John Lace, and Rachel Galioto declare no conflict(s) of interest. Kunio Nakamura has received personal fee for licensing from Biogen. Daniel Ontaneda has received research support from the National Institutes of Health, National Multiple Sclerosis Society, Patient Centered Outcomes Research Institute, Race to Erase MS Foundation, Genentech, Genzyme, and Novartis, and consulting fees from Biogen Idec, Genentech/Roche, Genzyme, Janssen, Novartis, and Merck.
 Declaration of Competing Interest F. Jespersen has nothing to disclose. S. L. Petersen has served on scientific advisory boards for Janssen-Cilag and Novartis. P. Andersen has nothing to disclose. F. Sellebjerg has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, H. Lundbeck A/S, Merck, Novartis, Roche and Sanofi Genzyme. His-laboratory has received research support from Biogen, Merck, Novartis, Roche and Sanofi Genzyme. M. Magyari has served in scientific advisory board for Sanofi, Novartis, Merck, and has received honoraria for lecturing from Biogen, Merck, Novartis, Roche, Genzyme, Bristol Myers Squibb. P. S. Sørensen has received personal compensation for serving on scientific advisory boards, steering committees, independent data monitoring committees or have received speaker honoraria for Biogen, Merck, Novartis, TEVA and Celgene/BMS. M. Blinkenberg reports personal fees from Biogen, Sanofi Genzyme, Biogen, Merck, Novartis, Bristol-Myers Squibb, Roche and non-financial support from Biogen, Roche and Sanofi Genzyme.
 The authors declare that they have no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest None.


 Patrick Altmann has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Merck, Roche, Sanofi-Genzyme and Teva, and received honoraria for consulting from Biogen. He received a research grant from Quanterix International and was awarded a sponsorship from Biogen, Merck, Sanofi-Genzyme, Roche, and Teva to programme a smartphone application for people with MS. Thomas Berger has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for multiple sclerosis: Almirall, Biogen, Bionorica, Celgene/BMS, GSK, Janssen-Cilag, MedDay, Merck, Novartis, Roche, Sanofi Aventis/Genzyme, TG Therapeutics and TEVA. His institution has received financial support in the last 2 years by unrestricted research grants (Biogen, Celgene/BMS, Novartis, Roche, Sanofi Aventis/Genzyme, TEVA) and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Merck, Novartis, Roche, Sanofi Aventis/Genzyme, TEVA. Gabriel Bsteh has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Celgene/BMS, Lilly, Merck, Novartis, Roche, Sanofi-Genzyme and Teva, and received honoraria for consulting Biogen, Celgene/BMS, Novartis, Roche, Sanofi-Genzyme and Teva. He has received research grants from Celgene/BMS and Novartis. Sarinah Dekany declares no conflict of interest with respect to the study and data presented in this paper. Christian Enzinger received funding for travel and speaker honoraria from Biogen, Bayer, Celgene, Merck, Novartis, Roche, Shire, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis; research support from Merck Serono, Biogen, and Teva Pharmaceutical Industries Ltd./sanofi-aventis; serving on scientific advisory boards for Bayer, Biogen, Celgene, Merck, Novartis, Roche and Teva Pharmaceutical Industries Ltd./sanofi-aventis. Michael Guger received support and honoraria for research, consultation, lectures and education from Almirall, Bayer, Biogen, Celgene, Genzyme, MedDay, Merck, Novartis, Octapharma, Roche, Sanofi Aventis, Shire, and TEVA ratiopharm. Jörg Kraus received consulting and/or research funding and/or educational support from Almirall, Bayer, Biogen, Celgene/ Bristol Myers Squibb, MedDay, Medtronic, Merck, Novartis, Roche, Sanofi-Aventis, Shire, and TEVA ratiopharm. Barbara Kornek has received honoraria for lecturing or consulting from Biogen, BMS-Celgene, Merck, Novartis, Johnson&Johnson, Sanofi-Genzyme, Roche, and Teva. Fritz Leutmezer has participated in meetings sponsored by, received speaker honoraria or travel funding or unrestricted scientific grants from Actelion, Biogen, Celgene, Med Day, Merck, Novartis, Roche, Sanofi-Genzyme, Schering, and Teva. Tobias Monschein has participated in meetings sponsored by or received travel funding from Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme and Teva. Markus Ponleitner has participated in meetings sponsored by or received travel funding from Amicus, Merck, Novartis and Sanofi-Genzyme. Paulus Stefan Rommer received honoraria for lectures or consultancy from AbbVie, Alexion, Allmiral, Biogen, Daiichi-Sankyo, Merck, Novartis, Roche, Sandoz, Sanofi Genzyme, Teva. He received research grants from Amicus, Biogen, Merck, and Roche. Franziska Di Pauli has participated in meetings sponsored by, received honoraria (lectures, advisory boards, consultations) or travel funding from Almirall, Bayer, Biogen, Celgene, Janssen, Merck, Novartis, Sanofi-Genzyme, Roche, and Teva. Her institution has received research grants from Roche. Tobias Zrzavy has participated in meetings sponsored by or received travel funding from Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme and Teva.

 M. Albergoni has nothing to disclose. L. Storelli declared the receipt of grants and contracts from FISM—Fondazione Italiana Sclerosi Multipla—within a fellowship program (cod. 2019/BR/009). P. Preziosa received speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb and Genzyme. He has received research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. M.A. Rocca received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono SpA, Novartis, Roche, and Teva. She receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders. M. Filippi is Editor in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology, and Associate Editor of Neurological Sciences; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA).
 Declaration of Competing Interests The authors report no competing interests.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: MJ Williams has received consulting fees from Alexion, Biogen Idec, Bristol Myers Squibb, EMD Serono, Genentech, Inc., Janssen, Novartis, Sanofi Genzyme and TG Therapeutics and serves on speakers bureaus for Biogen, Bristol Myers Squibb, EMD Serono, Janssen, Genentech and TG Therapeutics. AF Okai has received consulting fees from Alexion, Biogen, Bristol Myers Squibb, EMD Serono, Greenwich Biosciences, Novartis, Roche, Genentech, Inc., Sanofi Genzyme and TG Therapeutics and serves on speakers bureaus for Alexion, Biogen, EMD Serono and Sanofi Genzyme. AH Cross has, in the past year, received fees or honoraria for consulting for Biogen, EMD Serono, F. Hoffmann-La Roche Ltd, Genentech, Inc., Horizon Therapeutics, Janssen Pharmaceuticals, Jazz Pharmaceuticals, Novartis and TG Therapeutics. NL Monson has received consulting fees from EMD Serono and Genentech, Inc.; is a founder of GenRab; and holds patent US 8,394,583 B2 on MSPreciseTM, a diagnostic tool for predicting conversion to multiple sclerosis. T Vartanian reports personal compensation for consulting, speaking or serving on steering committees or advisory boards for Biogen Idec, Novartis, Genentech, Inc., EMD Serono, the National Multiple Sclerosis Society and the National Institutes of Health. BW Thrower serves on speakers bureaus for Biogen, Horizon Therapeutics, Genentech, Inc. and Bristol Myers Squibb. AT Reder has received consulting fees from Bayer, Biogen, F. Hoffmann-La Roche Ltd, Genentech, Inc., Merck Serono, Novartis and TG Therapeutics; is an editor for MedLink; and has received unrestricted research grant support from Bayer, Biogen, F. Hoffmann-La Roche Ltd, Genentech, Inc., Mallinckrodt, Merck Serono and Novartis. JB English has received consulting fees from Biogen, EMD Serono, Sanofi Genzyme, Bristol Myers Squibb and IT Therapeutics, contracted research support from Biogen, EMD Serono, Novartis and Genentech, Inc. and serves on speakers bureaus for Biogen, EMD Serono, Sanofi Genzyme and Bristol Myers Squibb. GF Wu has received honoraria for consulting from Novartis and Genentech, Inc. and research funding from Biogen, EMD Serono and F. Hoffmann-La Roche Ltd. E Bernitsas has received grant support from F. Hoffmann-La Roche Ltd, Genentech, Inc., Sanofi Genzyme, MedImmune, Novartis, EMD Merck Serono, Chugai, Mallinckrodt and TG Therapeutics; is a Chief Editor for the “Brain Sciences” Neuroimaging section; and has received consulting fees/honoraria from Biogen, Merck Serono, Bristol Myers Squibb, Horizon, Janssen Pharmaceuticals and Genentech, Inc. S Yap is an employee of Genentech, Inc., and a shareholder of F. Hoffmann-La Roche Ltd. J Ndrio is an employee of Genentech, Inc., and a shareholder of F. Hoffmann-La Roche Ltd. J Pei is an employee of Genentech, Inc., and a shareholder of F. Hoffmann-La Roche Ltd. EM Mowry has received grant support from Biogen, Genentech and Teva and royalties for editorial duties from UpToDate and has participated in data safety monitoring boards for the NIAID and TRIM trials. F Magrini was an employee of Genentech, Inc., at the time of the study. J Acosta is an employee of Genentech, Inc., and a shareholder of F. Hoffmann-La Roche Ltd. L Amezcua reports personal compensation for consulting or serving on steering committees or advisory boards for Biogen Idec, Novartis, Genentech, Inc. and EMD Serono and has received research support from the National Multiple Sclerosis Society, NIH NINDS and Biogen.

 The authors declare no conflict of interest.

 Declaration of interests JRC declares institutional support from Patient-Centered Outcomes Research Institute (PCORI) and the National Multiple Sclerosis Society (NMSS) for this study; institutional support for research from the National Institutes of Health (NIH), Novartis, and EMD Serono; speaking honorarium from MS Xchange, the University of Chicago, Emory University, The Ohio State University, and the European Committee For Treatment And Research In Multiple Sclerosis (ECTRIMS); a fee for sitting on a Medical Advisory board of Bristol Myers Squib; being Associate Editor for Annals of Neurology and Former Editor in Chief of Neurology: Clinical Practice; and being paid Medical Director of the Rocky Mountain Multiple Sclerosis Center. RJF declares research funding for this trial from PCORI and the NMSS; other research funding from NMSS, the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, Biogen, Novartis, and Sanofi; consulting fees from AGB Science, Biogen, Celgene, EMD Serono, Genentech, Genzyme, Greenwich Biosciences, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; and participation on an advisory board for AB Science. IK declares institutional support for this study from PCORI and NMSS; institutional support for research from Genentech, Biogen, and NMSS; consulting fees from Roche; royalties from Kluwer-Walters; and fees for sitting on an advisory board from Horizon. GRC declares institutional funding from PCORI for this study; fees for consulting or participating in advisory boards for Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions, Entelexo Biotherapeutics, Genzyme, Genentech, GW Pharmaceuticals, Immunic, Klein-Buendel, Merck/Serono, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Protalix Biotherapeutics, Recursion/Cerexis Pharmaceuticals, Regeneron, Roche, and SAB Biotherapeutics, and as President of Pythagoras; travel support from Roche; and participation in Data and Safety Monitoring Boards for Applied Therapeutics, AI Therapeutics, AMO Pharma, Astra-Zeneca, Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Pharmaceuticals, Immunic, Karuna Therapeutics, Mapi Pharmaceuticals, Merck, Mitsubishi Tanabe Pharma Holdings, Opko Biologics, Prothena Biosciences, Novartis, Regeneron, Sanofi-Aventis, Reata Pharmaceuticals, the National Heart, Lung, and Blood Institute (Protocol Review Committee), University of Texas Southwestern, University of Pennsylvania, and Visioneering Technologies; and being an unpaid board member of the Consortium of MS Centers and the Birmingham Jewish Federation. AEM declares institutional research support from Genzyme/Sanofi, Roche/Genentech, Novartis, and MedDay; consulting fees from AbbVie, Accordant Health Services, Adamas, Banner Life Sciences, Biogen Idec, Corevitas, Bristol Myers Squibb, Celgene, Janssen, Mapi Pharma, Novartis, Roche/Genentech, Verana Health, and Viatris/Mylan; speaker fees from Biogen Idec, EMD Serono, Alexion, Genentech, and Horizon Therapeutics; and acting as a medical expert in a legal case. All other authors declare no competing interests.
 Declaration of Competing Interest None.
 Disclosures of Competing Interest Caba, Liu, Jiang, Gafson, Fisher and Belachew are employees and shareholders of Biogen. Cafaro and Lombard are employees and shareholders of Therapanacea. Elliott is an employee of NeuroRx Research. Arnold receives consulting fees from Biogen, Celgene, Frequency Therapeutics, Genentech, Merck, Novartis, Race to Erase MS, Roche, and Sanofi-Aventis, Shionogi, Xfacto Communications, grants from Immunotec and Novartis, and an equity interest in NeuroRx Research. Paragios is an employee of Therapanacea, employee of CentraleSupélec, Université Paris-Saclay, French Ministry of Higher Education and Research; holds stock options in Arterdrone and TheraPanacea; and receives compensation for editorial services from Elsevier.


 The authors have declared that no competing interests exist.

 Declaration of Competing Interest Elyse Swallow, Oscar Patterson-Lomba, Lei Yin, Andres Gomez-Lievano, and Jingyi Liu are employees of Analysis Group, which received funding from Bristol Myers Squibb for the conduct of this study. Timothy Pham and Tom Tencer were employees of Bristol Myers Squibb at the time of this study and may be shareholders of the company. Komal Gupte-Singh is an employee of Bristol Myers Squibb and may be a shareholder of the company.



 Declaration of Competing Interest The Authors declare that there are no conflicts of interest.
 Declaration of interest None.
 The authors declare no conflicts of interest.
 Declaration of Competing Interest None.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The authors have declared that no competing interests exist.
 Declaration of Competing Interest None of the authors has any conflict of interest to disclose.
 Declaration of Competing Interest None.
 Declaration of Competing Interest The Authors declare that there is no conflict of interest.
 The authors declare no competing interests.
 Declaration of Competing Interest WC is the founder of Normin Health Consulting Ltd, which is a contract research organization that received funding from Bristol Myers Squibb to conduct this study. Other authors have none to declare.
 The authors report no conflicts of interest in this work.


 The authors have no conflicts of interest to declare.
 Competing interests: AAT: nothing to disclose. ZLEvK: nothing to disclose. MS: nothing to disclose. JN: nothing to disclose. LGFS: nothing to disclose. GvD: nothing to disclose. CMR: nothing to disclose. EPJA: nothing to disclose. EH: has accepted (speaker and congress) fees from Merck Serono, Biogen Idec, Roche, Novartis, Teva and Sanofi Genzyme. BIL-W: nothing to disclose. BADJ: nothing to disclose. BvO: nothing to disclose. EMS: nothing to disclose. BMJU: received research support and/or consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Teva and Immunic Therapeutics. TR: received funding for research from Genmab; received consulting fees from Novartis. JK: received research grants for multicentre investigator initiated trials DOT-MS trial, ClinicalTrials.gov Identifier: NCT04260711 (ZonMW) and BLOOMS trial (ZonMW and Treatmeds), ClinicalTrials.gov Identifier: NCT05296161); received consulting fees for F. Hoffmann-La Roche, Biogen, Teva, Merck, Novartis and Sanofi/Genzyme (all payments to institution); reports speaker relationships with F. Hoffmann-La Roche, Biogen, Immunic, Teva, Merck, Novartis and Sanofi/Genzyme (all payments to institution); adjudication committee of MS clinical trial of Immunic (payments to institution only).
 Competing interests: None declared.
 Declaration of Competing Interest The authors have no conflicts of interest to report.
 The authors declare that they have no conflicts of interest.

 Competing interests: None declared.
 The authors declare that they have no competing interests.


 I have read the journal’s policy and the authors of this manuscript have the following competing interests: Authors Violaine Harris and Saud Sadiq are listed as inventors on US patent #US 8,642,331, which is related to the study presented in the manuscript. The patent is issued to the Tisch MS Research Center of New York and is considered a non-financial competing interest. This does not alter our adherence to PLOS ONE policies on sharing data or materials. Furthermore, Violaine Harris and Saud Sadiq have no other relevant declarations related to employment, consultancy, products in development, etc. The remaining authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 NG and KH are full-time employees of Sanofi and may own stock or stock options. SQ, FM, MM’H, AL, and AR are employees of Modus Outcomes and were paid consultants to Sanofi in relation to this analysis. DPB was an employee of Sanofi at the time of the study and is now a full-time employee of Novartis.
 Competing interests: BVT has received compensation for consulting, talks, and advisory/steering board activities for Merck, Novartis, Biogen, and Roche. He receives research funding support from MS Research Australia, Medical Research Future Fund Australia and the National Health & Medical Research Council Australia.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: C.E. has received speaker honoraria from EMD Serono and is an employee of NeuroRx Research. D.L.A. has received grants from Biogen, Immunotec, and Novartis and consulting fees from Biogen, Celgene, Frequency Therapeutics, Genentech/Roche, Med-Ex Learning, Merck, Novartis, the Population Council, Queens University and Sanofi Aventis, and has an ownership interest in NeuroRx. D.A. has received personal compensation from NeuroRx Research. Z.T. is an employee of Biogen. B.Z., A.G., S.B., D.P.B., and E.F. are employees and shareholders of Biogen. D.A.R., D.F. and A.M.E. have nothing to disclose.
 Dr. Sadigh receives research support from the National Multiple Sclerosis Society.

 Declaration of Competing Interest Tarunya Arun has nothing to disclose. Carlos Capela has received consulting fees from Janssen, Merck and Roche, has received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Almirall, Biogen, Bristol Myers Squibb, Janssen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva, has received support for attending meetings and/or travel from Almirall, Bayer, Merck, Novartis, Roche, Sanofi-Genzyme and Teva, has participated on a Data Safety Monitoring Board or Advisory Board for Biogen, Janssen, Merck, Novartis, Roche and Sanofi-Genzyme. Guy Laureys and/or his employer (UZ Ghent) have received financial compensation for congress attendance, consultancy, research and education by Almirall, Biogen, Celgene, Bristol Myers Squibb, Novartis, Roche, Sanofi, Teva. Pietro Iaffaldano and/or his institution has received medical writing support for present manuscript from Novartis, has received grants from Novartis, Biogen and Roche; has received consulting fees from Novartis, Biogen, Sanofi, genzyme, BMS, Merck and Roche; has received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Roche, Biogen, Sanofi and Merck; support for attending meetings and/or travel from Biogen, Sanofi and Merck and participated on a data safety monitoring board or advisory board for Novartis, Biogen, Sanofi, Genzyme, BMS, Merck and Roche. Eddie Jones is an employee of Adelphi Real World. Adelphi Real World received funds from Novartis in exchange for access to the MS DSP data set that was used for analysis. Eddie Jones did not receive any funding directly from Novartis. Patricia Dominguez-Castro, and Simone Hiltl are employees of Novartis Pharma AG. Gustavo Seifer was an employee of Novartis Pharma AG at the time of study design, execution, interpretation and submission. Rainel Sanchez-de la Rosa was an employee of Novartis Pharma AG at the time of study design and execution.


 Declaration of Competing Interest Tomas Kalincik served on several advisory boards and received research/educational support from pharma companies, none of which has biased this work. Other authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper: [The authors MSP, MH, JHS, ÖD, FS, EH, and KJW have no relevant disclosures. YY has been supported by travel grants from Novartis and Sanofi Genzyme, has received an honorarium for active participation in an advisory board by Sanofi Genzyme as well as speaking honoraria by Roche, Sanofi Genzyme, TEVA and Bristol Myers Squibb and RG Gesellschaft für Information und Organisation mbH. His research is funded by Deutsche Forschungsgemeinschaft and Heinrich und Erna Schaufler-Stiftung. SB reports receiving honoraria from Biogen Idec, Bristol Meyer Squibbs, Merck Healthcare, Novartis, Roche, Sanofi Genzyme and TEVA. His research is funded by Deutsche Forschungsgemeinschaft (DFG), Hertie foundation and Hermann and Lilly-Schilling foundation. CF reports speaker honoraria and honoraria for participating on advisory boards from Novartis, Teva, Merck, Sanofi Genzyme, Alexion, Bristol-Myers Squibb, and Roche, and has received research support from Sanofi Genzyme and Novartis].
 None.

 Declaration of Competing Interest None.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. E. Le Page received honoraria for consulting or lectures, invitations for national and international congresses from Biogen, Merck, Teva, Sanofi-Genzyme, Novartis, Alexion, Roche; research support from Teva and Biogen; academic research grants from PHRC and LFSEP, and travel grant from ARSEP Foundation. H. Doyen received honoraria for consulting from Biogen. L. Michel received honoraria for consulting from sanofi, roche, Janssen, celgene, Merck and novartis. S. Lamy, D.Veillard, A. Kerbrat, E. Chretien, A. Ousmen and G. Edan reports no disclosures.
 Declaration of Competing Interest AJ has received honorarium and consultations fees from Biogen, Serono, Roche/Genentech, BMS, and TG therapeutics. ATR has received unrestricted grant support from Roche/Genentech. VPC has received compensation for consulting and/or speaking engagements from EMD Serono, Sanofi and Roche/Genentech. AFA: has received fellowship funding from Roche/Genentech SRB and TJC have nothing to disclose.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest FST: funded partly by unrestricted research grant from Biogen and Celgene/Bristol-Myers Squibb. AM: funded partly by unrestricted research grant from Biogen. CM: funded partly by unrestricted research grant from Biogen AH: declares no conflicting interests. KF: received honoraria for serving on advisory boards for Biogen, Merck, Roche and speaker's fees from Merck. HG: was employed by IQVIA; a contract research organization that performs commissioned pharmacoepidemiological studies, and therefore was collaborating with several pharmaceutical companies; previously funded partly by an unrestricted research grant from Biogen. AG: has received research support from Novartis. KA: had unrestricted research grants from Biogen. JH: received honoraria for serving on advisory boards for Biogen and Novartis and speaker's fees from Biogen, Merck-Serono, Bayer-Schering, Teva, and Sanofi-Aventis. He has served as PI for projects sponsored by, or received unrestricted research support from, Biogen, Merck-Serono, TEVA, Novartis, and Bayer-Schering. JH's MS research is also funded by the Swedish Research Council. EF: funded partly by unrestricted research grant from Biogen, and has received unrestricted research grants from Celgene/Bristol-Myers Squibb.
 Conflicts of Interest: The authors report no conflict of interest.

 The authors have no competing interests for this study.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 None of the authors declare any conflicts of interest.

 Declaration of Competing Interest BAS has received personal compensation for consulting, congresses, serving on a scientific advisory board, speaking, or other research activities with Biogen-Idec, Genzyme, Merck-Serono, Novartis, Teva, Roche, Bristol Myers Squibb, LACTRIMS, International Society For Neurochemistry, International Brain and Research Organization. ECC has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen-Idec, Genzyme, Merck-Serono, Novartis, Teva, Roche, LACTRIMS and the Guthy-Jackson Charitable Foundation. RA has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen-Idec, Genzyme, Merck-Serono, Novartis, Bristol Myers Squibb, Janssen, Roche and LACTRIMS. PAL has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen-Idec, Genzyme, Merck-Serono, Novartis, Bristol Myers Squibb, Raffo, Roche, Teva, and LACTRIMS. MFF has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen-Idec, Merck-Serono, Novartis, Teva. MFF is CEO and co-founder of Entelai LLC. OG has received personal compensation for consulting, congresses, serving on a scientific advisory board, speaking, or other research activities with Biogen-Idec, Merck-Serono, Novartis, Roche, Bristol Myers Squibb, LACTRIMS, Synthon Bago, Raffo. Rest of the authors had nothing to disclose.

 The authors declare that they have no competing interests.


 Declaration of Competing Interest Marcello Moccia has received research grants from ECTRIMS-MAGNIMS, UK MS Society, and Merck; and honoraria from Biogen, Merck, Roche, and Sanofi-Genzyme. Raffaele Palladino has received research grants from the UK MS Society, and honoraria from Sanofi. Antonio Carotenuto has received research grants from the ECTRIMS-MAGNIMS and from Almirall, and served on advisory boards for: Merk, Novartis, Roche and Almirall. Maria Petracca discloses travel/meeting expenses from Novartis, Roche and Merck, speaking honoraria from HEALTH&LIFE S.r.l. honoraria for consulting services from Biogen, and research grants from Italian MS Foundation and Baroni Foundation.
 Declaration of Competing Interest XJ, CS, BC, BZ, EF, SB, and ARG are employees of and hold stock/stock options in Biogen. DLA reports consulting fees from Celgene, EMD Serono, Frequency Therapeutics, MedDay, Merck, Novartis, Roche, and Sanofi, and research support from Biogen, Immunotec, and Novartis. CE reports speaker honoraria from EMD Serono and is an employee of NeuroRx.
 Declaration of Competing Interest M.S., M.A., C.L., Mo.M., S.P., Pe.M., S.E., D.M., F.S., B.A. have no conflict to disclose. Ma.M. reports grants and personal fees from Almiral. She was awarded a MAGNIMS-ECTRIMS fellowship in 2020. Pu.M. reports grants from Almirall, Teva, Sanofi Genzyme, Merck Serono, Biogen Italy, Novartis, consultancy for Novartis, Biogen Italy, and Sanofi. G.P. reports grants from Almirall, Teva, Sanofi Genzyme, Merck Serono, Biogen Italy, Novartis, Roche, Bristol Myers Squibb; consultancy for Novartis, Biogen Italy, Sanofi Genzyme, Roche, Bristol Myers Squibb; board membership Sanofi Genzyme, Novartis, Biogen Italy, Roche, Merck Serono, Bristol Myers Squibb.
 Declaration of Competing Interest RMM has received research support from Merck. IB has received research support from Merck, Novartis, Teva, and the Dutch MS Research Foundation. BMJU reports research support and/or consultancy fees from Biogen, Merck, Novartis, Roche, Sanofi, Teva, and Immunic Therapeutics. LK's institution (University Hospital Basel) has received the following exclusively for research support: Steering committee, advisory board, and consultancy fees from Actelion (Janssen/J&J), Bayer, Biogen, BMS, Janssen (J&J), Merck, Novartis, Roche, Sanofi, Santhera, and TG Therapeutics; speaker fees from Bayer, Biogen, Merck, Novartis, Roche, and Sanofi; support of educational activities from Allergan, Bayer, Biogen, CSL Behring, Desitin, Merck, Novartis, Roche, Pfizer, Sanofi, Shire, and Teva; license fees for Neurostatus products; and grants from Bayer, Biogen, European Union, InnoSwiss, Merck, Novartis, Roche, Swiss MS Society, and Swiss National Research Foundation. MSF has received honoraria or consultation fees from Alexion, Atara Biotherapeutics, Bayer, BeiGene, BMS (Celgene), EMD Serono, Janssen (J&J), Merck, Novartis, PendoPharm, Roche, and Sanofi; has been a member of a company advisory board, board of directors, or other similar group for Alexion, Atara Biotherapeutics, Bayer, BeiGene, BMS (Celgene), Clene Nanomedicine, Janssen (J&J), McKesson, Merck, Novartis, Roche, and Sanofi; has participated in a company sponsored speaker’s bureau for EMD Serono and Sanofi; and has been in receipt of research or educational grants from Sanofi. GC has received consulting fees from Bayer, Biogen, Merck, Novartis, Receptos, Roche, Sanofi, and Teva; lecture fees from Bayer, Biogen, Merck, Novartis, Sanofi, Serono Symposia International Foundation, and Teva; and trial grant support from Bayer, Biogen, Merck, Novartis, Receptos, Roche, Sanofi, and Teva. DJ is an employee of Merck Serono Ltd, Feltham, UK (an affiliate of Merck KGaA, Darmstadt, Germany). FB is supported by the NIHR Biomedical Research Centre at UCLH and is a consultant to Biogen, Combinostics, IXICO, Merck, and Roche. NDeS is a consultant for Biogen, Merck, Novartis, Sanofi, Roche, and Teva; has grants or grants pending from FISM and Novartis, is on the speakers’ bureaus of Biogen, Merck, Novartis, Roche, Sanofi, and Teva; and has received travel funds from Merck, Novartis, Roche, Sanofi, and Teva. HV has received research support from Merck, Novartis, Pfizer, and Teva; consulting fees from Merck; and speaker honoraria from Novartis. All funds were paid to his institution. GG, RAvS, JWRT, and MB report no disclosures.
 Declaration of Competing Interest Dr. Barone has received prior consulting and speaking honoraria from Biogen and Sanofi Genzyme, but no personal compensation relative to this research study.

 The authors have no competing interests to declare that are relevant to the content of this article.

 Competing interests: MAR received speakers’ honoraria from Bayer, Biogen Idec, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, Roche and Teva, and receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. PV received speakers’ honoraria from Biogen Idec. AM received speakers’ honoraria from Biogen Idec. Ente Ospedaliero Cantonale (EOC, employer) received compensation for CG’s speaking activities, consulting fees or research grants from AbbVie, Almirall, Biogen Idec, Bristol Myers Squibb, Genzyme, Lundbeck, Merck, Novartis, Teva Pharma, Roche. EOC received compensation for CZ’s speaking activities, consulting fees or research grants from AbbVie, Almirall, Biogen Idec, Bristol Myers Squibb, Genzyme, Lundbeck, Merck, Novartis, Teva Pharma, Roche. CZ holds a grant from EOC for senior researchers. FB serves as an Editorial Board member of Neuroradiology, Neurology, Multiple Sclerosis Journal and Radiology; he has serves as steering committee or IDMC member for Biogen, Merck, Prothena, EISAI accepted consulting fees from Biogen-IDEC, IXICO Ltd, Jansen Merck Serono, Novartis, and Roche. He has received grants from the Amyloid Imaging to Prevent Alzheimer’s Disease Initiative (Innovative Medicines Initiative), the European Progression of Neurological Disease Initiative (H2020), UK MS Society, Dutch MS Society, NIHR University College London Hospital Biomedical Research Centre, the European Committee for Treatment and Research in Multiple Sclerosis and the MRI in MS network. MMS serves on the Editorial Boards of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation, ARSEP, Amsterdam Neuroscience and ZonMW and has received compensation for consulting services or speaker honoraria from Atara Biotherapeutics, Biogen, Celgene/Bristol Myers Squibb, Sanofi-Genzyme, MedDay and Merck. EMS has nothing to disclose. HV has received research grants from Merck Serono, Novartis and Teva, speaker honoraria from Novartis, and consulting fees from Merck Serono; all funds paid directly to his institution. AG received speaker and consulting fees from Biogen, Bristol Myers Squibb, Coloplast, Merck Serono, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. AB received speaker’s honoraria and/or compensation for consulting service and/or speaking activities from Biogen, Roche, Merck, Celgene, Coloplast and Genzyme. OC is NIHR Research Professor (RP-2017-08-ST2-004). She also receives funding from MRC, UK and National MS Society and, NIHR and Rosetrees Trust. MY has nothing to disclose. AR serves on scientific advisory boards for Novartis, Sanofi-Genzyme, SyntheticMR and OLEA Medical, and has received speaker honoraria from Bayer, Sanofi-Genzyme, Merck-Serono, Teva Pharmaceutical Industries, Novartis, Roche, BMS and Biogen Idec. JS-G declares grants and personal fees from Genzyme, Almirall, Biogen, Celgene, Merck, Bayer, Biopass, Bial, Novartis, Roche and Teva, outside the submitted work; JS-G is Associate Editor of Multiple Sclerosis Journal and Scientific Director of Revista de Neurologia. JP has received support for scientific meetings and honoraria for advisory work from Merck Serono, Novartis, Chugai, Alexion, Roche, Medimmune, Argenx, UCB, Mitsubishi, Amplo, Janssen, Sanofi. Grants from Alexion, Roche, Medimmune, Amplo biotechnology and UCB. Patent ref P37347WO and licence agreement Numares multimarker MS diagnostics Shares in AstraZeneca. Acknowledges Partial funding by Highly specialised services NHS England. LM was funded by an MRC fellowship (G0901996). AG has received honoraria for lecturing, travel expenses for attending meetings and financial support for research from Novartis, Biogen, Merck Serono, Sanofi-Genzyme, Roche. PE has received travel expenses from Bayer Health Care and is member of the Editorial Board of the Journal of Neuroimaging. CL received a research grant by the German Federal Ministry for Education and Research, BMBF, German Competence Network Multiple Sclerosis (KKNMS), grant no.01GI1601I, has received consulting and speaker’s honoraria from Biogen Idec, Bayer Schering, Daiichi Sanykyo, Merck Serono, Novartis, Sanofi, Genzyme and TEVA. BB received financial support by the German Federal Ministry for Education and Research, BMBF, German Competence Network Multiple Sclerosis (KKNMS), grant no.01GI1601I. MM reports grants and personal fees from Sanofi Genzyme, Merck Serono, Novartis and Almirall. She was awarded a MAGNIMS-ECTRIMS fellowship in 2020. PP received speakers’ honoraria from Biogen Idec, Novartis, Bristol, Myers Squibb, Genzyme and Excemed and was supported by a senior research fellowship FISM—Fondazione Italiana Sclerosi Multipla—cod. 2019/BS/009 and financed or co-financed with the ‘5 per mille’ public funding. MF is Editor-in-Chief of the Journal of Neurology and Associate Editor of Human Brain Mapping, Neurological Sciences and Radiology; received compensation for consulting services and/or speaking activities from Almirall, Alexion, Bayer, Biogen Idec, Celgene, Eli Lilly, Genzyme, Merck-Serono, Neopharmed Gentili, Novartis, Roche, Sanofi, Takeda and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

 Declaration of Competing Interest The authors have no conflicts of interest to disclose. This study was funded by an unrestricted grant from Mallinckrodt Pharmaceuticals. The funders had no role in the research or preparation of this manuscript.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 Declaration of interests AB-O has received consulting fees from Gossamer, Janssen/Actelion, Atara Biotherapeutics, Biogen, BMS/Celgene/Receptos, F. Hoffmann-La Roche Ltd., Genentech, Inc., MAPI, MedImmune, Merck/EMD Serono, Novartis, Sanofi Genzyme, and GSK; has performed contracted research for Genentech, Inc., Novartis, and Biogen; and receives a salary from the University of Pennsylvania Perelman School of Medicine. G-AT, UB, LG, FM, AS, and HK are employees and shareholders of F. Hoffmann-La Roche Ltd. CH, SF, RH, XJ, and AH are employees of Genentech, Inc., and shareholders of F. Hoffmann-La Roche Ltd. CB has received consulting fees as a contractor for F. Hoffmann-La Roche Ltd. AHC has, in the past year, received fees or honoraria for consulting from Biogen, Celgene, EMD Serono/Merck, F. Hoffmann-La Roche Ltd., Genentech, Inc., Greenwich Biosciences, Janssen Pharmaceuticals, and Novartis. SLH serves on the SAB of Accure, Annexon, and Alector and on the BOD of Neurona, has consulted for NGM Bio, and has received travel reimbursement and writing assistance from F. Hoffmann-La Roche Ltd. and Novartis for CD20-related meetings and presentations. LK’s institution (University Hospital Basel) has received funds in the past 3 years that were exclusively used for research support at the Department, for steering committee and advisory board participation, consultancy services, and participation in educational activities from the following organisations: Actelion, AurigaVision AG, Bayer AG, BMS, Celgene, df-mp Molnia & Pohlman, Eli Lilly, EMD Serono, Genentech, GSK, Janssen LLC, Janssen Pharmaceuticals, Japan Tobacco Inc., Merck, MH Consulting, Merck Healthcare KGaA, Minoryx Therapeutics S.L., Novartis, Novartis Biociências S.A., Österreichische Gesellschaft für Neurologie, Roche, Sanofi, Santhera Pharmaceuticals, Senda Biosciences Inc., Shionogi BV, TG Therapeutics, and Wellmera AG; has served a leadership or fiduciary role for Foundation Clinical Neuroimmunology and Neuroscience Basel, MAGNIMS Steering Committee, European Charcot Foundation, and Neurostatus-UHB AG; the Research of the MS Center in Basel has been supported by grants from Novartis, Innosuisse, and Roche. JK received speaker fees, research support, and travel support and/or served on advisory boards for ECTRIMS, Swiss MS Society, Swiss National Research Foundation (grant no. 320030_189140/1), University of Basel, Bayer, Biogen, Celgene, Genzyme, Merck, Novartis, Roche, Sanofi, and Teva. DL is Chief Medical Officer of GeNeuro and has received travel reimbursement and personal compensation for consulting and speaking from Quanterix, Orion, Novartis, Roche, and Sanofi; has received consulting fees for GeNeuro SA as CMO, Orion, Novartis, Roche, and Sanofi; has received travel support from GeNeuro SA and Sanofi; and holds stock in GeNeuro SA.
 Declaration of Competing Interest This study was funded by Sanofi. Jeffrey Wilken received grants from Biogen; grants and personal fees from Sanofi; consulting fees from Bristol Myers Squibb (BMS); and speaker fees from Biogen, Sanofi, and Serono. Anthony Traboulsee is the MS Society of Canada Research Chair at the University of British Columbia (UBC) supported by the MS/MRI Research Group and received research funding from the MS Society of Canada, Roche, and Sanofi; and also received honoraria or travel support from Consortium of MS Centers, Roche, Sanofi. Flavia Nelson is funded by National Institutes of Health (NIH), the University of Minnesota Institute for translational Neuroscience and is an advisor for Sanofi, Genentech, BMS, Horizon and Novartis. Carolina Ionete reported receiving compensation for advisory board participation for Sanofi, and research support from NIH, National Multiple Sclerosis Society (NMSS), Department of Defense (DOD), Consortium of MS Centers, Dan and Diane Riccio Foundation, Biogen, Roche, and Novartis. Shannon Kolind received research support from Roche, Genzyme, the MS Society of Canada, the Natural Sciences and Engineering Research Council (NSERC), Vancouver Coastal Health Research Institute (VCHRI), Michael Smith Foundation for Health Research (MSFHR), the Canadian Institutes of Health Research (CIHR), Brain Canada, and Milan & Maureen Ilich Foundation, and consulting fees from Novartis. Timothy Fratto has nothing to disclose. Robert Kane has been a consultant for Biogen Idec. Roopali Gandhi, Andreea M. Rawlings, and Nora Roesch are employees of Sanofi and may hold stock and/or stock options in the company. Mark A. Ozog was an employee of Sanofi and may hold stock and/or stock options in the company (at the time of study). John DeLuca reported personal compensation for consulting from Celgene/BMS, Biogen Idec, Novartis, Consortium of MS Centers, and MedRhythms; is a speaker for Sanofi, Biogen IDEC and Excemed; received grant funding from Biogen Idec, EMD Serono, Canadian MS Society, NIH, National Multiple Sclerosis Society, and Consortium of MS Centers.

 All authors are employees of Genentech/Roche and are stockholders of Roche.
 A. Viehöver received lecture honoraria from Roche and Merck. R. Diem received grants from the German Research Foundation (FOR 2289), the Hertie Foundation, and the German Ministry of Education and Research. M. Korporal-Kuhnke reports lecture honoraria from Novartis, BMS and Merck. O. Fösleitner received the Rahel Goetein-Straus stipend grant from the Medical Faculty of the University of Heidelberg. J.M.E. Jende received grants from the German Research Foundation (SFB 1158), and the International Foundation for Research in Paraplegia. S. Heiland received a research grant from the German Research Foundation (SFB 1118). B. Wildemann received grants from the German Ministry of Education and Research, German Research Foundation, Dietmar Hopp Foundation and Klaus Tschira Foundation, grants and personal fees from Merck, Sanofi Genzyme, Novartis, and personal fees from Alexion, Bayer, Biogen, Teva; none related to this work. M. Bendszus reports personal fees from Boehringer Ingelheim, grants and personal fees from Novartis, grants from Siemens, personal fees from Merck, personal fees from Bayer, grants and personal fees from Guerbet, grants from Hopp Foundation, grants from DFG, grants from European Union, grants from Stryker, personal fees from Teva, personal fees from BBraun, personal fees from Vascular Dynamics, personal fees from Grifols, personal fees from Neuroscios. J.C. Hayes received a research grant, personal fees, lecture honoraria and financial support for conference attendance from Alnylam Pharmaceuticals, the Olympia Morata stipend grant from the Medical Faculty of the University of Heidelberg, lecture honoraria and financial support for conference attendance from Pfizer, and advised for Akcea Therapeutics. A.M. Pietsch, M. Weiler, G. Sam and J.M. Hayes declare that they have no competing interests.
 J.Y. Broos, F.C. Loonstra, L.R.J. de Ruiter, E.M.M. Strijbis, and H.E. de Vries report no disclosures. M.M. Schoonheim serves on the editorial board of Frontiers of Neurology and has received research support, compensation for consulting services, or speaker honoraria from the Dutch MS Research Foundation, ARSEP, Eurostars-EUREKA, ZonMW, ExceMed, Amsterdam Neuroscience, Atara, Biogen, Celgene/BMS, Merck, MedDay, and Sanofi-Genzyme. B.M.J. Uitdehaag received consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Teva, and Immunic Therapeutics. J. Killestein has speaker and consultancy relationships with and received research grants from Biogen, Genzyme, Immunic, Merck, Novartis, Roche, Sanofi, and TEVA. M. Giera is a consultant to Boehringer Ingelheim Pharma GmbH&Co.KG. G. Kooij received research grants from Biogen, Merck and Novartis. Go to Neurology.org/N for full disclosures.

 Declarations of Competing Interest The authors declare no relevant conflicts of interest.

 Conflicts of interest and sources of funding: none declared.




 M. Strupp is Joint Chief Editor of the Journal of Neurology, Editor in Chief of Frontiers of Neuro-otology and Section Editor of F1000. He has received speaker’s honoraria from Abbott, Auris Medical, Biogen, Eisai, Grünenthal, GSK, Henning Pharma, Interacoustics, J&J, MSD, NeuroUpdate, Otometrics, Pierre-Fabre, TEVA, UCB, and Viatris. He receives support for clinical studies from Decibel, U.S.A., Cure within Reach, U.S.A. and Heel, Germany. He distributes “M-glasses” and “Positional vertigo App”. He acts as a consultant for Abbott, AurisMedical, Heel, IntraBio and Sensorion. He is a sharholder, investor and chief medical officer of IntraBio. S. Bardins is a shareholder of EyeSeeTec GmbH, manufacturer of the eye-tracking equipment used in the study.
 Amy Perrin Ross has provided consultation to Biogen, Alexion, Genzyme, Genentech, Roche, EMD Serono, Novartis, Viela Bio, and Mallinckrodt. Noreen Barker participated in advisory boards and received support to attend educational meetings from Novartis in the past. Harriet Gaunt has no conflicts of interest. Christian Besser was an employee of Novartis during the analysis of this study until final version of paper development. Shubhanvita Naval and Dee Stoneman are employees of Novartis.





 OS is funded by a Merit Review grant (federal award document number BX005664-01) from the US Department of Veterans Affairs, Biomedical Laboratory Research and Development; is funded by RFA-2203-39314 (principal investigator) and RFA-2203-39305 (co-principal investigator) grants from the National Multiple Sclerosis Society; is a 2021 recipient of a Grant for Multiple Sclerosis Innovation, Merck; serves on the editorial board of Therapeutic Advances in Neurological Disorders; has served on data monitoring committees for Genentech/Roche, Novartis, Pfizer, and TG Therapeutics without monetary compensation; has served on a clinical trial steering committee for EMD Serono without monetary compensation; has advised EMD Serono, Genentech, Genzyme, TG Therapeutics, and VYNE Therapeutics; and received grant support from EMD Serono and Exalys. BT declares no competing interests.


 Conflicts of interest LJ, RD, OG, AL, AG, CP: nothing to disclose. MBM received personal compensation for consulting and travel fees from Biogen and Merck. CB received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Alexion, Biogen, BMS-Celgene, Merck, Novartis, Teva, and Sanofi-Genzyme.
 The authors have no conflicts of interest to report in relation to the current article. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 Declaration of Competing Interest The authors report no financial interests or potential conflict of interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.J.S.: Consulting or Advisory Boards: EMD Serono, Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, TG Therapeutics, Octave Bioscience. Non-Promotional Speaking: EMD Serono. Research Funding: Bristol Myers Squibb and Biogen. Contracted Research: Sanofi, Biogen, Novartis, Actelion, Genentech/Roche. Medicolegal consultations including expert witness testimony. J.O.: Consulting or speaking from Biogen-Idec, BMS, EMD Serono, Novartis, Roche, Sanofi-Genzyme, and Alexion. Research funding: Biogen-Idec, Roche, and EMD-Serono. S.T., M.T., J..C.C., A.H., D.J.M., M.H.: No COI to declare.


 Declaration of interests The authors declare no competing interests.
 Declaration of Competing Interest Melinda Magyari has served on scientific advisory board, as consultant for, received support for congress participation or speaker honoraria from Biogen, Sanofi, Roche, Novartis, Merck, Alexion, Bristol Myers Squibb. The Danish MS Registry received research support from Biogen, Genzyme, Roche, Merck, Novartis. The rest of the authors declare that they have no conflict of interest.
 Declaration of competing interests Rolf Pringler Holm has received speaker honoraria from Novartis. Luigi Poentieri has no conflict of interest. Malthe Faurschou Wandall-Holm has received speaker honoraria from Novartis. Elisabeth Framke has no conflict of interest. Finn Sellebjerg has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, H. Lundbeck A/S, Merck, Novartis, Roche and Sanofi Genzyme. His laboratory has received research support from Biogen, Merck, Novartis, Roche and Sanofi Genzyme. Melinda Magyari has served in scientific advisory board for Sanofi, Novartis, Merck, and has received honoraria for lecturing from Biogen, Merck, Novartis, Roche, Genzyme, Bristol Myers Squibb. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
 Declaration of Competing Interest The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declared potential conflicts of interest with respect to the research, authorship and/or publication of this article as following: P.H. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. O.Z. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. P.H. has nothing to disclose. E.K.H. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. I.W. received compensations for travel from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme and Teva. A.M. has nothing to disclose. J.D. has nothing to disclose. M.L. has nothing to disclose I.S. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. M.V. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. J.L. received compensations for travel and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. P.S. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. J.A. received compensations for travel from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme and Teva. R.A. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. M.V. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. M.D. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. A.M. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. M.P. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. J.M. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag. D.H. received compensations for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Roche, Sanofi Genzyme, Teva and Janssen cilag
 The authors declare no competing interests.
 The authors declare no conflicts of interest related to this study.


 Declaration of Competing Interest The authors have no conflicts of interest to declare. We do not have any financial support for this study.
 The authors declare that they have no conflict of interest.
 JFF reports personal compensation for consulting activities from Biogen and Octave, and compensation (paid to his institution) for data safety monitoring or advisory boards from Biogen, Genentech, and Novartis. NC and GK are employees of and hold stock or stock options in Biogen.

 Declaration of Conflicting Interests The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: S.S. has no financial disclosures. G.C. has participated on data monitoring and safety-monitoring boards for Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, CSL Behring, Galmed Pharmaceuticals, Horizon Pharmaceuticals, Hisun Pharmaceuticals, Mapi Pharmaceuticals, Merck, Merck/Pfizer, Opko Biologics, Neurim, Novartis, Ophazyme, Sanofi-Aventis, Reata Pharmaceuticals, Receptos/Celgene, Teva pharmaceuticals, Vivus, NHLBI (Protocol Review Committee), and NICHD (OPRU oversight committee); participated in consulting or advisory boards for Biogen, Click Therapeutics, Genzyme, Genentech, Gilgamesh Pharmaceuticals, GW Pharmaceuticals, Klein-Buendel Incorporated, Medimmune, Medday, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Recursion Pharmaceuticals, Roche, Somahlution, and TG Therapeutics; and is employed by the University of Alabama at Birmingham and President of Pythagoras, Inc., a private consulting company located in Birmingham AL. S.K. reports consulting or advisory work with Biogen, EMD Serono, Genentech, Genzyme, Mallinckrodt, MedDay, Novartis, Teva, and TG Therapeutics, nonpromotional speaking with Biogen, EMD Serono, Genentech, and Novartis, and grant and research support from Biogen and Novartis. S.C. has received consulting fees for grant reviews from the Department of Defense. J.S.W. received compensation for consulting, scientific advisory boards, or other activities with Avotres, Brainstorm Cell Therapeutics, Cleveland Clinic Foundation, EMD Serono, Inmagene, Novartis/Sandoz, Roche/Genentech, Sanofi Genzyme, and University of Alabama. Royalties are received for out-licensed monoclonal antibodies through UTHealth to Millipore (Chemicon International) Corporation. F.L. reports Sources of Funding for Research: Novartis; Actelion; Biogen; Sanofi, NMSS, NIH; Brainstorm Cell Therapeutics. Consulting Agreements/Advisory Boards/DSMB: Biogen; EMD Serono; Novartis; Teva; Actelion/Janssen; Sanofi/Genzyme; Acorda; Roche/Genentech; MedImmune/Viela Bio; Receptos/Celgene/BMS; TG Therapeutics; Medday; Atara Biotherapeutics; Mapi Pharma; Apitope; Orion Biotechnology; Brainstorm Cell Therapeutics; Jazz Pharmaceuticals; GW Pharma; Mylan; Immunic; Population Council; Avotres; Neurogene; Banner Life Sciences. Stock Options: Avotres. Speaker: Sanofi (nonpromotional); EMD Serono (nonpromotional).
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Henrik Ahvenjärvi reports a relationship with Finnish Cultural Foundation that includes: funding grants. Marja Niiranen reports a relationship with Finnish Medical Foundation that includes: funding grants. Päivi Hämäläinen reports a relationship with Novartis that includes: speaking and lecture fees. Päivi Hämäläinen reports a relationship with Sanofi that includes: speaking and lecture fees. Päivi Hämäläinen reports a relationship with Merck that includes: speaking and lecture fees. Mervi Ryytty reports a relationship with Biogen that includes: consulting or advisory and speaking and lecture fees. Mervi Ryytty reports a relationship with Merck that includes: consulting or advisory. Mervi Ryytty reports a relationship with Novartis that includes: consulting or advisory. Mervi Ryytty reports a relationship with Roche that includes: consulting or advisory. Mervi Ryytty reports a relationship with Sanofi that includes: consulting or advisory. Johanna Krüger reports a relationship with Novartis that includes: consulting or advisory. Johanna Krüger reports a relationship with Roche that includes: consulting or advisory.






 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare no conflict of interest for this study.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.




 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Conflict of Interest Disclosures: Dr. Terry Wahls personally follows and promotes the Wahls™ diet. She has equity interest in the following companies: Terry Wahls LLC; TZ Press LLC; The Wahls Institute, PLC; FBB Biomed Inc; Levels Health Inc., Foogal Inc. and the website http://www.terrywahls.com. She also owns the copyright to the books Minding My Mitochondria (2nd Edition) and The Wahls Protocol, The Wahls Protocol Cooking for Life, and the trademarks The Wahls Protocol® and Wahls™ diet, Wahls Paleo™ diet, and Wahls Paleo Plus™ diets. She has completed grant funding from the National Multiple Sclerosis Society for the Dietary Approaches to Treating Multiple Sclerosis Related Fatigue Study. She has financial relationships with Bio-Ceuticals Ltd., MCG Health LLC, Vibrant America LLC, Standard Process Inc., MasterHealth Technologies Inc., Genova Diagnostics Inc., and the Institute for Functional Medicine. She receives royalty payments from Penguin Random House. Dr Wahls has conflict of interest management plans in place with the University of Iowa and the Iowa City Veteran's Affairs Medical Center. All other authors report no personal or financial conflicts of interest in this work.
 Declaration of Competing Interest A.M. López-Real has received speaker and consultation fees, and congress travel support, from Biogen, Janssen, Merck, Novartis, Roche and Sanofi. I. Gonzalez has received speaker and consultation fees, and congress travel support, from Biogen, Janssen, Merck, Novartis, Roche and Sanofi. D.M. Solar has received speaker and consultation fees, and congress travel support, from Almirall, Biogen, Bristol-Myers Squibb Pharma, Merck, Novartis, Roche, Sanofi and Teva. A. Oterino has received speaker and consultation fees, and congress travel support, from Abbvie, Almirall, Biogen, Janssen, Novartis and Sanofi. E. Costa has received speaker and consultation fees, and congress travel support, from Biogen, Janssen, Merck, Novartis, Roche and Sanofi. A. Pato has received speaker and consultation fees, and congress travel support, from Biogen, Janssen, Merck, Novartis, Roche and Sanofi. M.A. Llaneza has received speaker and consultation fees, and congress travel support, from Almirall, Bayer, Biogen, Bristol-Myers Squibb Pharma, Janssen, Merck, Novartis, Roche, Sanofi and Teva. D.A. García-Estevez has received speaker and consultation fees, and congress travel support, from Bayor,Biogen, Novartis, Roche and Sanofi. A. Rodriguez-Regal has received speaker and consultation fees, and congress travel support, from Biogen, Janssen, Merck, Novartis, Roche and Sanofi. M. Rodríguez has received speaker and consultation fees, and congress travel support, from Biogen, Janssen, Merck, Novartis, Roche and Sanofi. J. Peña has received speaker and consultation fees, and congress travel support, from Almirall, Biogen, Bristol-Myers Squibb Pharma, Janssen, Merck, Novartis, Roche and Sanofi.
 The authors declare no competing interests.

 Declaration of Competing Interest The authors declare that they have no conflict of interest.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: T. Hrnciarova has nothing to disclose. J. Drahota has nothing to disclose. T. Spelman received compensation from serving on scientific advisory boards and steering comittees from Biogen and consultancy fees from Hartmann and Abbvie. J. Hillert received honoraria for serving on advisory boards for Biogen, Bristol-Myers-Squibb/Celgene, Janssen, Merck KGaA, Sandoz and Sanofi-Genzyme and speaker...s fees from Biogen, Janssen, Novartis, Merck, Teva, Sandoz and Sanofi-Genzyme. He has served as P.I. for projects sponsored by, or received unrestricted research support from, Biogen, Bristol-MyersSquibb/Celgene, Janssen, Merck KGaA, Novartis, Roche, and Sanofi-Genzyme. His MS research is funded by the Swedish Research Council and the Swedish Brain foundation. J. Lycke has received travel support and/or lecture honoraria and has served on scientific advisory boards for Alexion, Almirall, Biogen, Bristol Myers Squibb, Celgene, Janssen, Merck, Novartis, Roche and Sanofi; and has received unconditional research grants from Biogen and Novartis, and financial support from Sanofi for an investigator-initiated study. E. Kubala Havrdova has received honoraria/research support from Biogen, Merck Serono, Novartis, Roche, and Teva; has served as a member of advisory boards for Actelion, Biogen, Celgene, Merck Serono, Novartis, and Sanofi Genzyme; has been supported by the Czech Ministry of Education project Cooperatio LF1, research area Neuroscience, and the project National Institute for Neurological Research (Programme EXCELES, ID project No LX22NPO5107) funded by the European Union-Next Generation EU. E. Recmanova has nothing to disclose. J. Adamkova has nothing to disclose. J. Mares has nothing to disclose. J. Libertinova reported receiving grants, personal fees and funding for travel from Merck, Roche, Novartis, Biogen Inc, Sanofi Genzyme. Z. Pavelek reports personal fees from Biogen, Eli Lilly, Genzyme, Merck Serono, Novartis, Pfizer, Roche, and Teva Pharma. P. Hradilek received speakers honoraria and travel compensations from Biogen, Merck, Teva, Sanofi, Roche, Novartis and Janssen Cilag. R. Ampapa received conference travel support from Roche, Sanofi, Biogen and Merck and has participated in clinical trials by Biogen, Novartis, Sanofi, Merck and Roche. I. Stetkarova received compensation for travel and speaker honoraria from Biogen Idec, Merck, and Roche. M. Peterka has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Merck, Novartis, Biogen, Sanofi-Genzyme, Jansse-Cilag, Teva, Roche. A. Martinkova has nothing to disclose. P. Stourac has nothing to disclose. M. Grunermelova has nothing to disclose. M. Vachova received compensation for travel, conference fees, consulting fees and speaker honoraria from Biogen, Lundbeck, Merck, Novartis, Roche, Sanofi, and Teva. M. Dufek has nothing to disclose. D. Horakova was supported by the Charles University: Cooperatio Program in Neuroscience, by the project National Institute for Neurological Research (Programme EXCELES, ID Project No. LX22NPO5107) - Funded by the European Union Next Generation EU, and by General University Hospital in Prague project MH CZ-DRO-VFN64165. She also received compensation for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, and Teva, as well as support for research activities from Biogen Idec.
 Declaration of Competing Interest The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article.
 The authors declare no competing interests.
 Declaration of interests AJS reports grant funding from National Institute of Neurological Disorders and Stroke, National Institutes of Health, and Bristol Myers Squibb; contracted research with Sanofi, Biogen, Novartis, Actelion, and Genentec; personal compensation for consulting from EMD Serono and Octave Bioscience; payment or honoraria for lectures from EMD Serono; expert testimony from The Jacob D Fuchsberg Law Firm and Koskoff Koskoff & Bieder; participation on a Data Safety Monitoring Board for Patient Centered Research Institute and Yale University; participation on an advisory board for Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, TG Therapeutics, and Horizon Therapeutics. AJS is also content Chair for the American Academy of Neurology Institute Multiple Sclerosis Quality Measure Development Work Group and Section Editor for Multiple Sclerosis and Related Disorders. GA reports a grant from FIS PI19/01590 from Instituto de Salud Carlos III, Spain; personal compensation for consulting from Sanofi; payment or honoraria for lectures from Merck, Roche, and Novartis; support for attending meetings or travel from Merck, Novartis, European Committee for Treatment and Research in Multiple Sclerosis, and European Academy of Neurology; participation on a Data Safety Monitoring Board or Advisory Board for Merck, Roche, Horizon Therapeutics. GA is editor for Europe of Multiple Sclerosis Journal—Experimental, Translational and Clinical. GA is also executive committee member of International Women in Multiple Sclerosis network and steering committee member of European Biomarkers in Multiple Sclerosis consortium. WJB reports personal compensation for consulting from Biogen, Jannsen, Merck, Novartis, Roche, Sanofi, and Viatris; and payment or honoraria for lectures from Biogen, Jannsen, Merck, Novartis and Roche. EPF reports grant funding from the National Institutes of Health; personal compensation for consulting from Alexion, Genentech, UCB, and Horizon Therapeutics; and payment or honoraria for lectures from Pharmacy Times. EPF also served as site primary investigator in a randomised clinical trial on inebilizumab in neuromyelitis optica spectrum disorder sponsored by Medimmune/Viela-Bio/Horizon Therapeutics. EPF is also employed at the Mayo Clinic where commercial MOG-IgG, aquaporin-4-IgG and other antibodies are tested but does not receive any royalties from this testing. MPA reports grants or contracts with Biogen, Merck, Sanofi, Genzyme, Roche, Novartis, and Celgene/Bristol Myers Squibb; payment or honoraria for lectures from Biogen, Merck, Sanofi, Genzyme, Roche, Novartis, and Celgene/Bristol Myers Squibb; and participation on a Data Safety Monitoring Board or Advisory Board for Biogen, Merck, Sanofi, Genzyme, Roche, Novartis, and Celgene/Bristol Myers Squibb. BLB reports a grant from the National Multiple Sclerosis Society; personal compensation for consulting from Roche, Sanofi, Novartis, and UCB; and serves on the American Academy of Neurology Board of Directors and the International Medical and Scientific Advisory Board for the Multiple Sclerosis International Federation (MSIF). FB reports a grant from EU-IMI; personal compensation for consulting from Merck, Biogen, Roche, Combinostics, and IXICO; participation on a Data Safety Monitoring Board or Advisory Board for Prothena and EISAI; and stock options for QSA LTD. QSA is a contract research organization that provides imaging analysis services to the pharmaceutical industry. FB notes that his work with QSA has no relationship with his work as a diagnostic neuroradiologist nor with the content of the Personal View. JRC reports grants or contracts from the National Multiple Sclerosis Society, Patient Centered Outcomes Research Institute, EMD Serono, and Med Day; payment or honoraria for lectures from ECTRIMS European Charcot Foundation, Emory University, University of Chicago, MS XChange, and The Ohio State University. JRC also reports expert testimony for Mylan; participation on a Data Safety Monitoring Board or Advisory Board for Bristol Myers Squibb; and serves as Medical Director of Rocky Mountain Multiple sclerosis Center. JC reports grants or contracts from Biogen and Merck; payment or honoraria for lectures from Biogen, Merck, Sanofi, Bristol Myers Squibb, Novartis, Roche, and Jansen; and receipt of equipment, materials, drugs, medical writing, gifts, or other services from Novartis. KF reports grants from Ministry of Education, Culture, Sports, Science and Technology of Japan, and from Ministry of Health, Welfare and Labor of Japan. KF also reports personal compensation for consulting from Merck Biopharma, Japan Tobacco, and Abbvie; payment or honoraria for lectures and presentations from Biogen, Eisai, Mitsubishi Tanabe, Novartis, Chugai/Roche, Alexion, VielaBio/Horizon, Therapeutics, Teijin, Asahi Kasei Medical, Merck, and Takeda; participation on an Advisory Board for Biogen, Mitsubishi Tanabe, Novartis, Chugai/Roche, Alexion, VielaBio/Horizon Therapeutics, and UCB. KF serves as President of Pan-Asian Committee for Treatment and Research in Multiple Sclerosis, President of the Japanese Society of Neuroimmunology, Board Member of Japan Multiple Sclerosis Society and European Charcot Foundation, and Committee and Board member Executive Committee, International Medical and Scientific Board, MSIF. BH reports support from the European Union, Bundesministerium für Bildung und Forschung, and Deutsche Forschungsgemeinschaft; personal compensation for consulting from Sandoz and Biocom; patents for antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis (2012) and genetic determinants of neutralizing antibodies to interferon (filed 2010); and participation on a Data Safety Monitoring Board for TG Therapeutics and Polpharma and an Advisory Board for Novartis. RAM reports grants or contracts from Biogen Idec and Roche. SDN reports grants or contracts from Biogen, Roche, Genentech, National Multiple Sclerosis Society, Department of Defense, and Patient Centered Outcomes Research Institute; personal compensation for consulting from Biogen, Roche, Genentech, Bristol Myers Squibb, EMD Serono, Greenwich Biosciences, Novartis, and Horizon Therapeutics; and participation on a Data Safety Monitoring Board or Advisory Board for MedDay Pharmaceuticals. SDN also reports support from the Stiff Person Syndrome Research Foundation. MAR reports grants or contracts from Multiple Sclerosis Society of Canada and Fondazione Italiana Sclerosi Multipla; personal compensation for consulting from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, and Roche; payment or honoraria for lectures from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono SpA, Novartis, Roche, and Teva. MAR also serves as Associate Editor for Multiple Sclerosis and Related Disorders. BY serves on the MSIF scientific advisory board and as President of MENACTRIMS. BY also reports personal compensation for consulting from Merck, Biogen, Novartis, Roche, Sanofi, and Bayer. JAC reports personal compensation for consulting from Biogen, Convelo, EMD Serono, Gossamer Bio, and PSI; serves as President of the Americas Committee on Treatment and Research in Multiple Sclerosis; and receives personal compensation for working as the Editor of Multiple Sclerosis Journal. All other authors declare no competing interests.
 Conflict-of-interest disclosure: The authors declare no competing financial interests.


 Declaration of Competing Interest Mar Tintoré has received compensation for consulting services, speaking honoraria and research support from Almirall, Bayer Schering Pharma, Biogen-Idec, Genzyme, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Aventis, Viela Bio and Teva Pharmaceuticals. Data Safety Monitoring Board for Parexel and UCB Biopharma


 Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. AHC has performed consulting or contracted research for Biogen, EMD Serono, Genentech, Bristol Myers Squibb, Octave, Novartis, Roche, and TG Therapeutics.
 C.F. has received travel or speaker honoraria from Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, Roche, and Bristol Meyer Squibb. M.C. declares no conflicts of interest. N.M. has received travel grants from Biogen Idec and Sanofi Genzyme. M.L. has received travel grants from Biogen Idec, Sanofi Genzyme, and Merck Serono. Eli. B has received travel grants from Biogen Idec, Sanofi Genzyme, Novartis, and Roche. Ele. B. has received a grant for the organization of a scientific congress from Biogen Idec and has received travel or speaker honoraria from Biogen Idec, Sanofi Genzyme, Merck Serono, and Teva Neurosciences. L.M. and M.V. declare no conflicts of interest. M.P. has participated on advisory boards for Bayer Schering, Genzyme, Biogen, Merck Serono, and Mylan, and has received travel or speaker honoraria from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva Neurosciences, Mylan, Roche, and Bristol Meyer Squibb. The funders had no role in the design of the study; in the collection, analysis, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
 Declaration of Competing Interest Marco Vercellino and Paola Cavalla have received research funding and speaker fees from Merck Serono, Roche, Novartis, Biogen, Sanofi. The other Authors declare that there is no conflict of interest regarding this study.

 Conflicts of Interest: See Disclosures at the end of the article.
 Declaration of Competing Interest L.R., F.L., A.T., E.C., S.N., E.S. report no disclosures. M.M. Schoonheim serves on the editorial board of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation and Amsterdam Neuroscience, and has served as a consultant for or received research support and/or speaker honoraria from Atara Biotherapeutics, Biogen, Celgene, Genzyme, MedDay and Merck. Uitdehaag received consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, and Teva and Immunic Therapeutics.
 Declaration of Competing Interest Bart Van Wijmeersch has received honoraria, travel, and research grants from Almirall, BMS, Biogen, Imcyse, Janssen, Merck Serono, Novartis, Roche, Sanofi Genzyme, and Teva Pharmaceuticals. Veronica Popescu has received honoraria, travel, and research grants from Almirall, Biogen, Medtronic, Merck, Novartis, Roche, Sanofi Genzyme, and Teva Pharmaceuticals. The remaining authors have no disclosures related to this study.


 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Maria-Elizabeth Baeva: has received honoraria and participated in consultant advisory board for Novartis unrelated to this research. Luanne M. Metz: No conflicts. Jamie Greenfield: No conflicts. Carlos R. Camara-Lemarroy: Has received honoraria and participated in consultant advisory board for Novartis, EMD Serono and Sanofi, unrelated to this research.
 Declaration of Competing Interest None.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Jennifer A. McCombe reports a relationship with Roche that includes: consulting or advisory. Jennifer A. McCombe reports a relationship with Novartis that includes: consulting or advisory.

 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Ll. Coll: nothing to disclose. D. Pareto: has received a research contract with Biogen Idec, and a grant from Instituto Salud Carlos III (PI18/00823). P. Carbonell-Mirabent: his yearly salary is supported by a grant from Biogen to Fundació privada Cemcat for statistical analysis. A. Cobo-Calvo: has received grant from Instituto de Salud Carlos III, Spain; JR19/00007. G. Arrambide: has received compensation for consulting services, participation in advisory boards or speaking honoraria from Merck, Roche, and Horizon Therapeutics; and travel support for scientific meetings from Novartis, Roche, and ECTRIMS. G. Arrambide is editor for Europe of the Multiple Sclerosis Journal – Experimental, Translational and Clinical; a member of the executive committee of the International Women in Multiple Sclerosis (iWiMS) network, and a member of the European Biomarkers in MS (BioMS-eu) consortium steering committee. She is a recipient of grants PI19/01590 and PI22/01570, awarded by the Instituto de Salud Carlos III (ISCIII), Ministerio de Ciencia e Innovación de España. Á. Vidal Jordana: has engaged in consulting and/or participated as speaker in events organized by Roche, Novartis, Merck, and Sanofi. M. Comabella: has received compensation for consulting services and speaking honoraria from Bayer Schering Pharma, Merk Serono, Biogen-Idec, Teva Pharmaceuticals, Sanofi-Aventis, and Novartis. J. Castilló: nothing to disclose. B. Rodríguez-Acevedo: has received honoraria for consulting services from Wellspect. A. Zabalza: nothing to disclose. I. Galán: nothing to disclose. L. Midaglia: nothing to disclose. C. Nos: has received funding for travel from Biogen Idec and F. Hoffmann-La Roche, Ltd. and speaker honoraria from Novartis. A. Salerno: nothing to disclose. C. Auger: has received speaking honoraria from Novartis, Biogen and Stendhal. M. Alberich: nothing to disclose. J. Río: has received speaking honoraria and personal compensation for participating on Advisory Boards from Biogen-Idec, Genzyme, Merck- Serono, Mylan, Novartis, Roche, Teva, and Sanofi-Aventis. J. Sastre-Garriga: serves as co-Editor for Europe on the editorial board of Multiple Sclerosis Journal and as Editor-in-Chief in Revista de Neurología, receives research support from Fondo de Investigaciones Sanitarias (19/950) and has served as a consultant/speaker for Biogen, Celgene/Bristol Meyers Squibb, Genzyme, Novartis and Merck. A. Oliver: nothing to disclose. X. Montalban: has received speaking honoraria and travel expenses for participation in scientific meetings, has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Abbvie, Actelion, Alexion, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Immunic, Janssen Pharmaceuticals, Medday, Merck, Mylan, Nervgen, Novartis, Sandoz, Sanofi-Genzyme, Teva Pharmaceutical, TG Therapeutics, Excemed, MSIF and NMSS. A. Rovira: serves on scientific advisory boards for Novartis, Sanofi-Genzyme, Synthetic MR, Roche, Biogen, and OLEA Medical; has received speaker honoraria from Bayer, SanofiGenzyme, Merck-Serono, Teva Pharmaceutical Industries Ltd, Novartis, Roche, and Biogen; and is CMO and co-founder of TensorMedical. M. Tintoré: has received compensation for consulting services and speaking honoraria from Almirall, Bayer Schering Pharma, Biogen-Idec, Genzyme, Merck-Serono, Novartis, Roche, Sanofi-Aventis, and Teva Pharmaceuticals. MT is former co-editor of Multiple Sclerosis Journal. X. Lladó: is currently being supported by the ICREA Academia Program. He has also received support from the DPI2020-114769RBI00 project funded by the Ministerio de Ciencia, Innovación y Universidades. C. Tur: is currently being funded by a Junior Leader La Caixa Fellowship (fellowship code is LCF/BQ/PI20/11760008), awarded by “la Caixa” Foundation (ID 100010434). She has also received the 2021 Merck’s Award for the Investigation in MS, awarded by Fundación Merck Salud (Spain) and a grant awarded by the Instituto de Salud Carlos III (ISCIII), Ministerio de Ciencia e Innovación de España (PI21/01860). In 2015, she received an ECTRIMS Post-doctoral Research Fellowship and has received funding from the UK MS Society. She is a member of the Editorial Board of Neurology. She has also received honoraria from Roche and Novartis and is a steering committee member of the O’HAND trial and of the Consensus group on Follow-on DMTs.

 N. Castrogiovanni and J. Mostert report no disclosures. P. Repovic received consulting and/or speaking honoraria from Alexion, Biogen, Celgene, Roche, Sanofi Genzyme, Viela, and EMD Serono. J.D. Bowen received honoraria from serving on the scientific advisory board and speaker's bureau of Biogen, Celgene, EMD Serono, Genentech, and Novartis. He has received research support from AbbVie Inc, Alexion, Alkermes, Biogen, Celgene, Sanofi Genzyme, Genentech, Novartis, and TG Therapeutics. B. Uitdehaag received consultancy fees and/or research support from Biogen, Sanofi Genzyme, EMD Serono, Novartis, Roche, Teva, and Immunic Therapeutics. E. Strijbis reports no disclosures. G. Cutter served on Data and Safety Monitoring Boards: Applied Therapeutics, AI Therapeutics, AMO Pharma, Astra-Zeneca, Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Pharmaceuticals, Immunic, Karuna Therapeutics, Mapi Pharmaceuticals LTD, Merck, Mitsubishi Tanabe Pharma Holdings, Opko Biologics, Prothena Biosciences, Novartis, Regeneron, Sanofi-Aventis, Reata Pharmaceuticals, Teva Pharmaceuticals, NHLBI (Protocol Review Committee), University of Texas Southwestern, University of Pennsylvania, and Visioneering Technologies, Inc. Consulting or Advisory Boards: Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions LLC, Entelexo Biotherapeutics, Inc., Genzyme, Genentech, GW Pharmaceuticals, Immunic, Immunosis Pty Ltd, Klein Buendel Incorporated, Merck/Serono, Novartis, Perception Neurosciences, Protalix Biotherapeutics, Regeneron, Roche, and SAB Biotherapeutics. Dr. Cutter is employed by the University of Alabama at Birmingham and President of Pythagoras, Inc., a private consulting company located in Birmingham AL. M.W. Koch received consulting fees and travel support from Biogen, Novartis, Roche, Sanofi Genzyme, and EMD Serono. Go to Neurology.org/N for full disclosures.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: M.v.D. is supported by a research grant from BMS. I.M.N. is supported by the Dutch MS Research Foundation, grant nr. 15-911. M.H. is supported by the Dutch MS Research Foundation, grant nr. 16-954b. J.J.G.G. has served as a consultant for or received research support from Biogen, Celgene, Genzyme, MedDay, Merck, Novartis and Teva. B.M.J.U. reports personal fees for consultancies from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, and Teva, outside the submitted work. C.E.T. has a collaboration contract with ADx Neurosciences and Quanterix, performed contract research or received grants from AC-Immune, Axon Neurosciences, Biogen, BioOrchestra, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, Grifols, Novo Nordisk, PeopleBio, Quanterix, Roche, Toyama, Vivoryon. She serves on editorial boards of Alzheimer Research and Therapy, and Neurology. H.E.H. serves on the editorial board of Multiple Sclerosis Journal, receives research support from the Dutch MS Research Foundation and the Dutch Research Council. She has served as a consultant for or received research support from Atara Biotherapeutics, Biogen, Novartis, Celgene/Bristol Meyers Squibb, Sanofi Genzyme, MedDay and Merck BV. B.A.d.J., E.A.W., M.K., B.M., and S.d.G.D. report no disclosures relevant to the manuscript.
 The authors declare no competing interests.


 Competing interests: MM reports grants and personal fees from Almirall. She was awarded a MAGNIMS-ECTRIMS fellowship in 2020. MG has nothing to disclose. AM received speakers’ honoraria from Biogen Idec. EP received speakers’ honoraria from Biogen Idec. LM received personal compensation for consulting, serving on a scientific advisory board, speaking or other activities with Sanofi-Genzyme, Novartis, Teva, Merck Serono, Biogen, Roche, and Excemed. PP received speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb and Genzyme. He has received research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. MF is Editor in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology and Associate Editor of Neurological Sciences; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). MAR received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono SpA, Novartis, Roche and Teva. She receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. She is the Associate Editor for Multiple Sclerosis and Related Disorders.
 Dr. Zanetta received compensation for speaking activities, and/or consulting services from Alexion, Biogen, Merck, Novartis, Roche, Sanofi. Prof. M.A. Rocca received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from AstraZaneca, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Horizon Therapeutics Italy, Merck Serono SpA, Novartis, Roche, Sanofi and Teva. She receives research support from the MS Society of Canada, the Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders. Dr. Meani has nothing to disclose. Dr. Martinelli received compensation for speaking and/or for consultancy and support for travel expenses and participation in Congresses from Biogen, Merck-Serono, Novartis, Genzyme and Teva Pharmaceutical Industries. Dr. Ferrè has nothing to disclose. Dr. Moiola received compensation for speaking activities, and/or consulting servicesfrom Merck, Biogen, Novartis, Roche, Sanofi, and TEVA. Prof. Filippi is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Neurological Sciences, and Radiology; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla.



 Declaration of competing interest None.
 Declaration of Competing Interest The authors report the following disclosures: T.K. has received consulting and advisory board fees from Genentech/ Roche and Novartis, T.F. reports no disclosures B.H has received research support from Analysis Group, Celgene (Bristol-Myers Squibb), Verily Life Sciences, Merck-Serono, Novartis, and Genzyme. M.B reports no disclosures B.G reports no disclosures T.C. has received compensation for consulting from Banner Life Sciences, Biogen, Bristol Myers Squibb, Novartis Pharmaceuticals, Roche Genentech, and Sanofi Genzyme. She has received research support from the National Institutes of Health, National MS Society, US Department of Defense, Sumaira Foundation, Brainstorm Cell Therapeutics, Bristol Myers Squibb, EMD Serono, I-Mab Biopharma, Mallinckrodt ARD, Novartis Pharmaceuticals, Octave Bioscience, Roche Genentech, Sanofi Genzyme, and Tiziana Life Sciences


 Dr. Shiv Saidha is a Professor in the Department of Neurology at the Johns Hopkins University School of Medicine. Dr. Saidha engaged in this research as a private consultant or advisor and not in his capacity as a Johns Hopkins faculty member, and has been compensated for a consulting or advising service by Novartis in income/honorarium. Dr. Saidha has received consulting fees from Medical Logix for the development of CME programs in neurology and has served on scientific advisory boards for Novartis, Biogen, Genentech Corporation, TG therapeutics, and Bristol Myers Squibb. He has performed consulting for Novartis, Genentech Corporation, JuneBrain LLC, and Lapix therapeutics. He is the PI of investigator-initiated studies funded by Genentech Corporation, Novartis, and Biogen. He previously received support from the Race to Erase MS foundation. He has received equity compensation for consulting from JuneBrain LLC and Lapix therapeutics. He was also the site investigator of a trial sponsored by MedDay Pharmaceuticals and is the site investigator of a trial sponsored by Novartis. Eric Maiese, Kerri Wyse, and Qiujun Shao are employees of Novartis Pharmaceuticals Corporation. Judith Bell, Sydney Harold, Jose Marcano Belisario, and Emma Hawe are employees of RTI Health Solutions and worked as consultants to Novartis Pharmaceuticals Corporation.

 Declaration of Competing Interest Unsong Oh has received consulting fees from Horizon Therapeutics and Genentech. E. Woolbright, R. Coleman, M. Conaway declare no conflicts of interest. D. Lehner-Gulotta serves as a consultant for Functional Formularies. M. D. Goldman has served on the DSMB for Anokion SMC and Immunic. She has received consulting fees from Adamas Pharmaceuticals, Biogen IDEC, Brainstorm Cell Therapeutics Ltd, EMD Serono, Genetec, Greenwich Biosciences, Horizons, Immunic, Merck, Novartis, Sanofi, Genzyme, and Vebrilio. J.N. Brenton has received consulting fees from Cycle Pharmaceuticals.
 Nikolaos G. Dimitriou: no conflicts of interest to disclose. Sven G. Meuth: receives honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Healthcare, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS und Teva. His research is funded by the German Ministry for Education and Research (BMBF), Deutschen Forschungsgesellschaft (DFG), Else Kröner Fresenius Foundation, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Almirall, Amicus Therapeutics Germany, Biogen Idec, Diamed, Fresenius Medical Care, Genzyme, Merck Healthcare, Novartis, ONO Pharma, Roche, und Teva. Elena H Martinez-Lapiscina: no conflicts of interest to disclose. The views expressed in this article are the personal views of the author(s) and may not be understood or quoted as being made on behalf of or reflecting the position of the European Medicines Agency or one of its committees or working parties. Til Menge: personal fees from Biogen, BMS, Novartis, Teva, Roche, Merck Serono; non-financial support from Biogen, Merck Serono, Roche. Philipp Albrecht: received grants and non-financial support from Biogen; grants, personal fees and non-financial support from Allergan / Abbvie; personal fees and non-financial support from Bayer; personal fees and non-financial support from Sanofi Genzyme; grants, personal fees and non-financial support from Merck; grants, personal fees and non-financial support from Merz Pharmaceuticals; grants, personal fees and non-financial support from Novartis; grants, personal fees and non-financial support from Roche; grants, personal fees and non-financial support from Teva; and grants, personal fees and non-financial support from Ipsen, outside the submitted work.
 Declaration of Competing Interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare no competing interests.
 Conflict of Interest Disclosures: Dr Henderson reported being an employee of Daiichi Sankyo outside the submitted work. Dr Bhise reported grants from Horizon Blue Cross Blue Shield and Novartis, and personal fees from Biogen and Cycle Pharmaceuticals outside the submitted work. Dr Pal reported grants from the National Institutes of Health and personal fees from Guidepoint and Kyowa Kirin outside the submitted work. No other disclosures were reported.



 Declaration of Competing Interest None.

 Competing interests: EW has current support from the NIH, NMSS, PCORI, CMSC and Race to Erase MS.
 The authors declare no competing interests.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 RdN is an author in one study that was included in this meta-synthesis. All other authors declare that they have no conflicts of interest.
 Declaration of Interest Statement R.K. and F.H. are employees of Cytel Inc. TW is an employee of IPAM e.V. and has received honoraria from several pharmaceutical/consultancy companies (Novo Nordisk, Abbvie, Merck, GSK, BMS, LEO Pharma, Astra Zeneca, Bayer, Boehringer Ingelheim, Pharmerit). UM works for a statutory insurance fund (AOK PLUS), which provided the data used in this study. CC is an employee of F. Hoffmann-La Roche Ltd. EMLR and LC are employees and shareholders of F. Hoffmann-La Roche Ltd.



 Conflict of interests: The authors declare no conflicts of interest.
 J.M.S. reports no relevant disclosures. W.C. reports no relevant disclosures. Y.H.C. reports no relevant disclosures. H.J. reports no relevant disclosures. S.T.K. reports no relevant disclosures. J-K.S. reports no relevant disclosures. J-H.M. has received funding and research support from the National Research Foundation of Korea and SMC Research and Development Grants and has lectured, consulted, and received honoraria from Bayer Schering Pharma, Merck, Biogen Idec, Sanofi, UCB, Samsung Bioepis, Mitsubishi Tanabe, Celltrion, Roche, and Janssen.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The authors declare no conflicts of interest.
 Competing interests: DL is Chief Medical Officer of GeNeuro. MW received speaker honoraria from Novartis Pharma, Chugai Pharmaceutical, Biogen Japan and Alexion. FP has received research grants from Janssen, Merck KGaA and UCB, and fees for serving on DMC in clinical trials with Chugai, Lundbeck and Roche, and preparation of witness report for Novartis. RF has received speaker fees for teaching and workshops from Biogen, Merck, Novartis, Roche, Teva and Alexion. For educational activities, courses or research, he has received unrestricted grants from Biogen, EMD Serono. JL is an employee of Quanterix. BE has received travel grants for ECTRIMS 2018 from Roche. KF has served on advisory boards and received speaker honoraria from Biogen, Roche and Merck and received research funds from Amicus. TM received speaker honoraria from Biogen Japan, Chugai Pharmaceutical, Alexion Pharmaceuticals, Novartis Pharma and Takeda Pharmaceutical. KM received speaker honoraria from Novartis Pharma, Chugai Pharmaceutical and Nihon Pharmaceutical. NI received grant support from Mitsubishi Tanabe Pharma, Osoegawa Neurology Clinic, Bayer Yakuhin and Japan Blood Products Organization and speaker honoraria from Novartis Pharma, Biogen Japan, Alexion, Mitsubishi Tanabe Pharma, Chugai Pharmaceutical, Teijin Pharma and Eisai. J-IK received research funds from Dainippon Sumitomo Pharma, Daiichi Sankyo, Mitsubishi Tanabe Pharma and Kyowa Kensetsukougyo, and consultancy fees, speaking fees and/or honoraria from Novartis Pharma, Mitsubishi Tanabe Pharma, CSL Behring, Biogen Japan, Teijin Health Care, the Takeda Pharmaceutical, Kyowa Kirin, Ono Pharmaceutical, Alexion Pharmaceuticals, Tsumura, Ricoh, EMC and Eisai. JO served on advisory boards for Roche and Merck. JK received speaker fees, research support, travel support and/or served on advisory boards by the Progressive MS Alliance, Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Biogen, Celgene, Merck, Novartis, Octave Bioscience, Roche, Sanofi. No other disclosures were reported.


 Declaration of Competing Interest Andrea I Ciplea has received speaker honoraria from Bayer HealthCare, Biogen GmbH, and Teva, as well as sponsorship for congress participation and travel grants from Teva. Anna Kurzeja is an employee of Teva Pharmaceuticals Europe B.V. Sandra Thiel has received speaker honoraria from Bayer HealthCare and Biogen GmbH, as well as payment for manuscript writing from HEXAL AG. Sabrina Haben has nothing to disclose. Evelyn Adamus has nothing to disclose. K Hellwig has received travel grants from Biogen, Novartis and Merck, and received speaker and research honoraria from Biogen Idec Germany, Teva, Sanofi Genzyme, Novartis, Bayer Health-Care, Merck Serono and Roche.
 The authors have declared that no competing interests exist.
 Declaration of Competing Interest The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: IK, OA, AA, RL, and SR have no competing interests. JL-S: has accepted travel compensation from Novartis, Biogen, and Merck. Her institution received honoraria for talks, advisory board commitment, and research grants from Biogen Idec, Merck, Roche, and Novartis. She is on the board of directors for MS Plus. SC and CP are employers with Olea Medical, La Ciotat, France. PL is an employer with Siemens Healthcare GmbH, Erlangen, Germany.
 The authors declare that they have no competing interests.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.C. receives funding from the MS Society of Canada’s endMS Postdoctoral Fellowship and the Michael Smith Foundation for Health Research Trainee Award. H.S.N. has received funding from the Multiple Sclerosis Society of Canada’s endMS Postdoctoral Fellowship, and the Michael Smith Foundation for Health Research Trainee Award. F.Z. and Y.Z. have no disclosures. H.T. has, in the last 5 years, received research support from the Canada Research Chair Program, the National Multiple Sclerosis Society, the Canadian Institutes of Health Research, the Multiple Sclerosis Society of Canada, and the Multiple Sclerosis Scientific Research Foundation. In addition, in the last 5 years, has had travel expenses or registration fees prepaid or reimbursed to present at CME conferences from the Consortium of MS Centers (2018), National MS Society (2016, 2018), ECTRIMS/ACTRIMS (2015, 2016, 2017, 2018, 2019, 2020, 2021, and 2022), American Academy of Neurology (2015, 2016, and 2019). Speaker honoraria are either declined or donated to an MS charity or to an unrestricted grant for use by HT’s research group.


 11. Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Conflicts of interest and sources of funding: O.F. was supported by the Rahel Goitein-Straus research grant and the Physician-Scientist fellowship of the Medical Faculty of the University of Heidelberg. S.H. (SFB 1118), D.S. (SFB 1118), M.B. (SFB 1158), and B.W. were supported by the German Research Foundation. J.H. received a research grant, personal fees, lecture honoraria and financial support for conference attendance from Alnylam Pharmaceuticals. B.W. received grants from the German Ministry of Education and Research, Dietmar Hopp Foundation, Klaus Tschira Foundation; grants and personal fees from Merck; and personal fees from Alexion, Bayer, Biogen, and Teva, none related to this work. W.W. reports to be inventor and patent-holder on “Peptides for use in treating or diagnosing IDH1R132H positive cancers” (EP2800580B1) and “Cancer therapy with an oncolytic virus combined with a checkpoint inhibitor” (US11027013B2). He consulted for Apogenix, Astra Zeneca, Bayer, Enterome, MSD, and Roche/Genentech with honoraria paid to the Medical Faculty at the University of Heidelberg. L.B.J. and G.S. have nothing to disclose.

 Disclosure of interest The author has no conflict of interest to disclose in relation with this editorial.
 Competing interests: None declared.
 Declaration of Competing Interest The authors have no disclosures related to the current work.


 Declaration of Competing Interest H. Houzen has received funding for travel and/or speaker honoraria from Biogen, Novartis Pharma, Takeda Pharma Corporation, Alexion Pharmaceuticals, Inc., Chugai Pharmaceutical Company, and Mitsubishi Tanabe Pharma Corporation. T. Kano has no potential competing interests to disclose. K. Kondo has no potential competing interests to disclose. T. Takahashi has received research support from Cosmic Corporation. M. Niino has received funding for travel and/or speaker honoraria from Biogen, Mitsubishi Tanabe Pharma Corporation, Chugai Pharmaceutical Company, Alexion Pharmaceuticals, Inc., Takeda Pharma Corporation, and Novartis Pharma.
 The authors declare no conflict of interest.


 Declaration of Competing Interest Per Soelberg Sørensen has received personal compensation for serving on scientific advisory boards, steering committees, independent data monitoring committees or have received honoraria as speaker from Biogen, Merck, Novartis, TEVA, GlaxoSmithKline, Sanofi/Genzyme, and BMS/Celgene. Alex Heick has served on scientific advisory boards for Biogen, Sanofi-Genzyme, Novartis, Janssen and Merck. Honoraria for lecturing has been received from Biogen, Merck, Novartis and Sanofi. Support for congress participation has been received from Biogen, Sanofi-Genzyme, Teva, Roche, Merck, Novartis, Bayer, Schering, Pfizer and Janssen. Peter Vestergaard Rasmussen has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche and Sanofi Genzyme. Jakob Schäfer has served on a scientific advisory board with Sanofi, received speaker honoraria from Novartis and received travel compensation from Merck, Roche, Sanofi. Rikke Ratzer has served on scientific advisory boards, received speaker honoraria and received support for congress participation from Roche, Merck, Sanofi, Medtronic and Ipsen. Finn Sellebjerg holds a professorship at the Faculty of Health Sciences and Medicine, University of Copenhagen, sponsored by the Danish Multiple Sclerosis Society. He has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche and Sanofi Genzyme. His-laboratory has received research support from Biogen, Merck, Novartis, Roche and Sanofi Genzyme. Melinda Magyari has served in scientific advisory board for Sanofi, Novartis, Merck, and has received honoraria for lecturing from Biogen, Merck, Novartis, Roche, Genzyme, Bristol Myers Squibb. Luigi Pontieri, Hanna Joensen, Alex Heick and Caroline Ellinore Pihl has nothing to declare.
 Rosa Cortese was awarded a MAGNIMS‐ECTRIMS fellowship in 2019. Marco Battaglini has nothing to disclose. Maria Pia Sormani has received consulting fees from Biogen, Genzyme, GeNeuro, MedDay, Merck, Novartis, Roche and Teva. Ludovico Luchetti, Giordano Gentile, and Maira Inderyas have nothing to disclose. NA is an employee of Merck Healthcare KGaA, Darmstadt, Germany. Nicola De Stefano is a consultant for Biogen, Merck, Novartis, Sanofi‐Genzyme, Roche and Teva, has grants or grants pending from FISM and Novartis, is on the speakers' bureaus of Biogen, Merck, Novartis, Roche, Sanofi‐Genzyme and Teva, and has received travel funds from Merck, Novartis, Roche, Sanofi‐Genzyme and Teva.

 The authors declare no conflict of interest.
 Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.



 Michael Guger has received support and honoraria for research, consultation, lectures, and education from Alexion, Almirall, Bayer, Biogen, Celgene, Genzyme, Janssen, MedDay, Merck, Novartis, Ratiopharm, Roche, Sanofi Aventis, and Teva. Robert Hatschenberger has received no financial support within the last 3 years. Fritz Leutmezer has received support and honoraria for research, consultation, lectures, and education from Alexion, Almirall, Bayer, Biogen, Celgene, Genzyme, Janssen, MedDay, Merck, Novartis, Octapharm, Ratiopharm, Roche, Sanofi Aventis, and Teva.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest None.
 Declaration of Competing Interest The authors declare no conflicts of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.R.G., X.J., C.S., C.M.S., B.C., E.F., C.d.M., and S.B. are employees of and hold stock/stock options in Biogen. C.T. has a collaboration contract with ADx Neurosciences and Quanterix, and performed contract research for AC-Immune, Axon Neurosciences, Biogen, Brainstorm Therapeutics, Celgene, EIP Pharms, Eisai, PeopleBio, Roche, Toyama, and Vivoryon. M.W. reports no disclosures. H.Z. has served at scientific advisory boards and/or as a consultant for AbbVie, Acumen, Alector, ALZPath, Annexon, Apellis, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, NervGen, Novo Nordisk, Passage Bio, Pinteon Therapeutics, Red Abbey Labs, reMYND, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics, and Wave, has given lectures in symposia sponsored by Cellectricon, Fujirebio, AlzeCure, Biogen, and Roche, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program, outside the submitted work. G.G. has received compensation for serving as a consultant or speaker for or has received research support from AbbVie, Aslan, Atara Bio, Biogen, BMS-Celgene, GlaxoSmithKline, GW Pharma, Janssen/Actelion, Japanese Tobacco, Jazz Pharmaceuticals, LifNano, Merck & Co., Merck KGaA/EMD Serono, Moderna, Novartis, Sanofi-Genzyme, Roche/Genentech, and Teva. C.E. has received speaker honoraria from EMD Serono and is an employee of NeuroRx Research.
 The authors have declared that no competing interests exist.

 The authors declare no conflict of interest.
 Declaration of Competing Interest Jacqueline Nicholas has received research grants from ADAMAS, Biogen Idec, Genentech, Novartis, and PCORI and consulting and/or speaking fees from Alexion, Bristol Myers Squib, EMD Serono, Genetech, Jazz Pharmaceuticals, Inc., Novartis, and Viela Bio. Fred Lublin has consulted for, conducted studies funded by, or received honraria for services provided to Jazz Pharmaceuticals, Inc. Sylvia Klineova has consulted for, conducted studies funded by, or received honraria for services provided to Biogen Idec, Alexion and Jazz pharmaceuticals, Inc. Joris Berwaerts is an employee of Jazz Pharmaceuticals, Inc. Robert Chinnapongse is an employee of Jazz Pharmaceuticals, Inc. Daniel Checketts is an employee of Jazz Pharmaceuticals, Inc. Joshua R. Steinerman is an employee of Jazz Pharmaceuticals, Inc. Sajida Javaid has consulted for, conducted studies funded by, or received honraria for services provided to Jazz Pharmaceuticals, Inc.
 Declaration of Competing Interest None

 MM reports grants and personal fees from Almirall. She was awarded a MAGNIMS-ECTRIMS fellowship in 2020. PP received speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb and Genzyme; he has received research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. MAR received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from AstraZaneca, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Horizon Therapeutics Italy, Merck Serono SpA, Novartis, Roche, Sanofi and Teva. She receives research support from the MS Society of Canada, the Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. She is an Associate Editor for Multiple Sclerosis and Related Disorders. MF is the Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Neurological Sciences, and Radiology; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla.
 D.R. van Nederpelt: has nothing to disclose. H. Amiri: has nothing to disclose. I. Brouwer: has received research support from Merck, Novartis, Teva, and the Dutch MS Research Foundation. S. Noteboom is supported by research grants from Atara, Biotherapeutics, Merck and Biogen. L.B. Mokkink: has nothing to disclose. F. Barkhof serves on the steering committee or iDMC member for Biogen, Merck, Roche, EISAI and Prothena. Consultant for Roche, Biogen, Merck, IXICO, Jansen, Combinostics. Research agreements with Merck, Biogen, GE Healthcare, Roche. Co-founder and shareholder of Queen Square Analytics LTD. Supported by the NIHR biomedical research center at UCLH. H. Vrenken has received research support from Merck, Novartis, Pfizer, and Teva, consulting fees from Merck, and speaker honoraria from Novartis; all funds were paid to his institution. J.P.A. Kuijer has nothing disclose.
 MRB has received fees for consultation from Genentech and EMD Serono. ZL, ML, HK, LL, WD, and JEM have no disclosures. AHC has received fees for consulting or contracted research from Biogen, Brisol Myers Squibb, EMD Soreno (Merck), Genentech, Horizon Therapeutics, Jazz Pharmaceuticals, Novartis, and TG Therapeutics. TLSB has investigator‐initiated research funding from the NIH, the Alzheimer's Association, the Foundation at Barnes‐Jewish Hospital and Avid Radiopharmaceuticals (a wholly owned subsidiary of Eli Lilly and Company). She participates as a site investigator in clinical trials sponsored by Avid Radiopharmaceuticals, Eli Lilly and Company, Biogen, Eisai, Jaansen, and Roche. She serves as an unpaid consultant to Eisai and Siemens, and is on the Speaker's Bureau for Biogen. RTN has consulted for Abata Therapeutics, Banner Life Sciences, BeiGene, Biogen, Bristol Myers Squibb, Genentech, Genzyme, Janssen, GW Therapeutics, Horizon Therapeutics, Lundbeck, NervGen, TG Therapeutics. SC has received consulting fees from Biogen, Novartis, Sanofi Genzyme, BMS and Jansen. SC has received funding for investigator‐initiated research from Biogen, BMS and the BMS foundation.

 Declaration of Competing Interest Juliane Klehmet reports financial support was provided by Biogen GmbH. Juliane Klehmet reports a relationship with Biogen GmbH that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Bristol-Myers Squibb that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Janssen that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Novartis that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Roche that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Bayer that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Merck Serono that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with Sanofi Genzyme that includes: consulting or advisory and speaking and lecture fees. Juliane Klehmet reports a relationship with TEVA Pharmaceuticals that includes: consulting or advisory and speaking and lecture fees. Yvonne Begus-Nahrmann reports financial support was provided by Biogen GmbH. Kirsi Taipale reports a relationship with Biogen GmbH that includes: employment. Gabriele Niemczyk reports a relationship with Biogen GmbH that includes: employment. Karin Rehberg-Weber reports a relationship with Biogen GmbH that includes: employment.
 Declaration of Competing Interest All authors declare that they have no conflicts of interest.




 Competing interests: LB and LP have no conflicts of interest to declare. GM received travel grants from Janssen and Lundbeck (unrelated to the present work). AM received travel grants and writing honoraria from Almirall, Biogen, Merck, Mylan, Novartis, Sanofi Genzyme and Teva. LG participated on advisory boards for, and received writing honoraria and travel grants from Almirall, Biogen, Euroimmun, Fujirebio, Merck, Mylan, Novartis, Roche, Sanofi, Siemens Healthineers and Teva. AT received research support from Lundbeck and served as speaker for Lundbeck and Angelini (unrelated to the present work). MDF participated on advisory boards for and received speaker or writing honoraria, funding for travelling and research support from Alexion, Bayer, Biogen Idec, Sanofi, Siemens Healthineers, Merck, Mylan, Novartis, Roche, Teva and Viatris.

 Declaration of Competing Interest This study is an investigator-initiated study sponsored by Sanofi-Genzyme. QWu, QWang, JY, EAM, PC, AS, CAD, CF, and BK have nothing to disclose. Y Mao-Draayer has served as a consultant and/or received grant support from: Acorda, Bayer Pharmaceutical, Chugai, Biogen Idec, EMD Serono, Sanofi-Genzyme, Genentech, Novartis, Horizon, Janssen, Questor, and Teva Neuroscience. Y Mao-Draayer was supported by grants from NIH NIAID Autoimmune Center of Excellence: UM1-AI110557–05, UM1 AI144298–01, NIH NINDS R01-NS080821, PCORI, Novartis, Sanofi-Genzyme, and Chugai.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interests All authors declare that they have no conflicts of interest to disclose.
 Declaration of Competing Interest Anna A Shah, MD - I have participated in advisory boards through Genentech and TG therapeutics. I have received funding for non-promotional educational programming through NCQA, Novartis and Rocky Mountain MS Center. Brian Callaghan, MD – I receive research contracts and I am on the editorial board for the American Academy of Neurology. I consult for Dynamed. I perform medicolegal consultations including for the Vaccine Injury Compensation Program. Andrew J Solomon, MD - Consulting or Advisory Boards: EMD Serono, Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, TG Therapeutics, Octave Bioscience.  Non-Promotional Speaking: EMD Serono.   Research Funding: Bristol Myers Squibb and Biogen.  Contracted Research:  Sanofi, Biogen, Novartis, Actelion, Genentech/Roche. Medicolegal consultations including expert witness testimony. Colin Lyness, MD, Jessica Piche, MD, and Benjamin Stewart, MD, have no reportable conflicts of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: TT and AB are former employees of Evidera, which was paid by Actelion Pharmaceuticals Ltd, now a Janssen Pharmaceutical Company of Johnson & Johnson, for work on this study. TS, NB, and BH are employees of Actelion Pharmaceuticals Ltd, a Janssen Pharmaceutical company of Johnson & Johnson and may hold stock in Johnson & Johnson. BL and CJ are employees of Janssen Research and Development, LLC. BL, CJ, and NB are stockholders in Johnson & Johnson, and BL and NB have a portfolio that at times includes other pharmaceutical and health care–related companies. APB is a director of Innovus Consulting Ltd and holds a stock portfolio that at times includes pharmaceutical and health care–related companies. RF has received personal consulting fees from AB Science, Biogen, Celgene, EMD Serono, Genentech, Genzyme, Greenwich Biosciences, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics. RF has served on advisory committees for AB Science, Biogen, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics, and received clinical trial contract and research grant funding from Biogen, Novartis, and Sanofi.
 The authors declare no competing interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Omar Abdel-Mannan has nothing to disclose. Olga Ciccarelli received research funding from UCLH NIHR Biomedical Research Centre, UK, and National MS Society, Rosetrees Trust; she is an Associate Editor for Neurology; and she has received honoraria from Merck and Biogen.
 Nothing to report.

 Declaration of Competing Interest Glen M. Doniger is an employee of NeuroTrax Corporation. The authors declare no other potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare no conflict of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: K.F. has received payment for lectures and advisory boards from Roche, Biogen and Merck and received funding from Neuro Sweden, and Neuro Stockholm, the Swedish state under the agreement between the Swedish government and the county councils. A.G., P.A., S.E., S.F. and T.F. report no disclosures relevant to the manuscript. A.M.L-G. receives grant support and awards from the Patient-Centred Outcomes Research Institute and the National MS Society; she has received sponsored and reimbursed travel from ICER and the National Institutes of Health. F.P. has received research grants from Merck KGaA and UCB, fees for serving on DMC in clinical trials with Chugai, Lundbeck and Roche and fee for expert witness report for Novartis. K.M. receives research funding from the Swedish Research Council for Health, Working Life and Welfare (Forte).
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: The authors declare that there is no conflict of interest. A.T. has received research funding from CIHR, MS Society of Canada, Hilton Foundation, Roche, Genzyme, and Clene. He has received honoraria from Roche, Genzyme, Novartis, and Biogen. J.O. holds the Waugh Family Chair in MS Research and has received research funding from the Barford/Love MS Fund of St. Michael’s Hospital, Biogen-Idec, Brain Canada, EMD-Serono, the MS Society of Canada, the National MS Society, the National Institutes of Health, and Roche. She has received compensation for consulting of speaking from Biogen-Idec, BMS, EMD-Serono, Novartis, Roche, and Sanofi-Genzyme.
 Declaration of interests The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Conflict of interest: TEK receives grant support from Novartis.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: M.F. is a co-investigator on projects funded by the Patient-Centered Outcomes Research Institute, the University Hospitals Kingston Foundation and the National Multiple Sclerosis Society. She has received consulting or teaching honoraria from Novartis and Biogen. P.F. received funding from the FWO Flanders, MS Society Flanders, KBS King Baudouin Foundation, MS Canada and Promobilia. Teaching honoraria were received from Roche. U.D. has received research support, travel grants and/or teaching honoraria from Biogen Idec, Merck Serono, Novartis, Bayer Schering and Sanofi Aventis as well as honoraria from serving on scientific advisory boards of Biogen Idec and Genzyme. D.K. has received consultancy or teaching honoraria from Roche, Almirall, Sanofi Genzyme, Biogen, Merck, Novartis and Teva.
 SJL, NS, CY, EH, EF, EM, AG, HR, SJ, PGB are/were employees of Biogen and may hold stocks/stock options in Biogen. AH, XJ and TB are employees of Genentech (a subsidiary of Roche) and may hold stocks/stock options in F. Hoffmann-La Roche Ltd.


 The authors declare no competing interests.

 Declaration of Competing Interest None.

 The authors have declared that no competing interests exist.
 The authors declare that they have no competing interests.
 No potential conflict of interest was reported by the author(s).

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflict of Interest TDR and NCL have nothing to disclose. HW receives honoraria for acting as a member of Scientific Advisory Boards from Abbvie, Alexion, Argenx, Bristol Myers Squibb/Celgene, Janssen, Merck, and Novartis. He receives speaker honoraria and travel support from Alexion, Biogen, Bristol Myers Squibb, F. Hoffmann-La Roche Ltd., Genzyme, Merck, Neurodiem, Novartis, Roche Pharma AG, TEVA, and WebMD Global. He is acting as a paid consultant for Abbvie, Actelion, Argenx, Biogen, Bristol Myers Squibb, EMD Serono, Fondazione Cariplo, Gossamer Bio, Idorsia, Immunic, Immunovant, Janssen, Lundbeck, Merck, NexGen, Novartis, PSI CRO, Roche, Sanofi, Swiss Multiple Sclerosis Society, UCB, and Worldwide Clinical Trials. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgesellschaft (DFG), Deutsche Myasthenie Gesellschaft e.V., Alexion, Amicus Therapeutics Inc., Argenx, Biogen, CSL Behring, F. Hoffmann - La Roche, Genzyme, Merck KgaA, Novartis Pharma, Roche Pharma, UCB Biopharma. SGM receives honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Healthcare, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, Quintiles/MS und Teva. His research is funded by the German Ministry for Education and Research (BMBF), Deutschen Forschungsgesellschaft (DFG), Else Kröner Fresenius Foundation, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Almirall, Amicus Therapeutics Germany, Biogen Idec, Diamed, Fresenius Medical Care, Genzyme, Merck Healthcare, Novartis, ONO Pharma, Roche, und Teva. AJ received honoraria and travel-reimbursements for acting as a speaker for Biogen.
 Declarations of Competing Interest None.


 Dr. Benet first became aware of the success of the methodology reported here while serving as an expert witness in a lawsuit concerning the validity of the fingolimod patent. All other authors declared no competing interests for this work.

 Disclosures of conflicts of interest: P.M.B. Support from Amsterdam UMC – VU University Amsterdam. S.N. No relevant relationships. F.A.N.S. No relevant relationships. E.S.B. Career transition award paid to institution from the National Multiple Sclerosis Society; patent pending for high-resolution cerebrospinal fluid–suppressed T2*-weighted MRI of cortical lesions. G.B. No relevant relationships. M. Castellaro No relevant relationships. M. Calabrese Grants to institution from Roche, Novartis, and Merck Serono; consulting fees from Roche, Novartis, Merck Serono, and Genzyme; payment for lectures from Roche, Novartis, Merck Serono, and Genzyme; support for attending meetings or travel from Roche, Novartis, and Merck Serono. D.T.C. Grants from F. Hoffmann-La Roche, the International Progressive MS Alliance, the MS Society, the Medical Research Council, and the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre; consulting fees from F. Hoffmann-La Roche and Biogen; payment for lectures from Novartis; co-supervisor of a clinical fellowship at the National Hospital for Neurology and Neurosurgery, London, which is supported by Merck. P.E. No relevant relationships. M.F. Grants to institution from Biogen, Merck Serono, Novartis, Roche, the Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA); consulting fees from Alexion, Almirall, Biogen, Merck, Novartis, Roche, and Sanofi; speaker honoraria from Bayer, Biogen, Celgene, Chiesi Italia, Eli Lilly, Genzyme, Janssen, Merck Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and Teva; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol Myers Squibb, Lilly, Novartis, and Sanofi Genzyme; participation on a data safety monitoring board or advisory board for Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi Genzyme, and Takeda; editor in chief of the Journal of Neurology, associate editor of Human Brain Mapping, associate editor of Radiology, and associate editor of Neurological Sciences. M.I. Consulting fees from Novartis, Roche, Merck, Almirall, Biogen, and Janssen; payment for lectures from Novartis, Roche, Merck, Almirall, Biogen, Janssen, and BMS. C.L. Payment for lectures from Novartis; support for attending meetings or travel from Merck and Roche. A.M. No relevant relationships. B.M. No relevant relationships. A.M.P. No relevant relationships. M.M. Grant to institution from the German Research Foundation (DFG SPP2177). P.P. Research support to institution from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla; speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb, and Genzyme. D.S.R. Grants to institution from Abata Therapeutics, Sanofi, and Vertex; payment for expert testimony from Bounds Law Group; patent pending for high-resolution cerebrospinal fluid–suppressed T2*-weighted MRI of cortical lesions and patent issued for automatic identification of subjects at risk of multiple sclerosis. M.A.R. Grants to institution from the MS Society of Canada and the Fondazione Italiana Sclerosi Multipla; consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, and Roche; speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono, Novartis, Roche, and Teva; associate editor for Multiple Sclerosis and Related Disorders. M.M.S. Grants to institution from the Dutch MS Research Foundation, Eurostars-EUREKA, ARSEP, Amsterdam Neuroscience, Magnetic Resonance Imaging in MS (MAGNIMS), ZonMw, Atara Biotherapeutics, Biogen, Celgene/Bristol Myers Squibb, Sanofi Genzyme, and Merck; speaker fees to institution from Excellence in Medical Education and Sanofi Genzyme; unpaid board member of MS Center Amsterdam, head of the International Multiple Sclerosis Cognition Society steering committee, and editorial board member of Neurology, Frontiers in Neurology, and Radiology. J.W.R.T. No relevant relationships. B.W. Grants from the German Research Foundation (DFG) and SPP Radiomics; speaker honorarium from Philips. L.E.J. Grants to institution from the Michael J. Fox Foundation, Alzheimer Nederland Stichting Parkinson Fonds, Health~Holland TKI, and the Alzheimer’s Association; support for travel from the Alzheimer’s Association International Conference. C.R.G.G. No relevant relationships. J.J.G.G. No relevant relationships. M.D.S. No relevant relationships.


 The authors declare that they have no competing interests.
 JG is receiving reagents from Novartis and Roche to study the role of B cells in MS. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 IR has received compensation for lectures from biogen. MA has received compensation for lectures and/or advisory boards from Biogen, Genzyme, and Novartis. LN has received lecture honoraria from Biogen, Novartis, Teva, Sanofi and has served on advisory boards for Merck, Janssen and Sanofi. KB has served as a consultant, at advisory boards, or at data monitoring committees for Abcam, Axon, BioArctic, Biogen, JOMDD/Shimadzu. Julius Clinical, Lilly, MagQu, Novartis, Ono Pharma, Roche Diagnostics, and Siemens Healthineers, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB BBS, which is a part of the GU Ventures Incubator Program, all unrelated to the work presented in this paper. HZ has served at scientific advisory boards and/or as a consultant for Abbvie, Alector, Annexon, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, Nervgen, Novo Nordisk, Pinteon Therapeutics, Red Abbey Labs, Passage Bio, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics, and Wave, has given lectures in symposia sponsored by Cellectricon, Fujirebio, Alzecure, Biogen, and Roche, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB BBS, which is a part of the GU Ventures Incubator Program outside submitted work. JL has received travel support and/or lecture honoraria and has served on scientific advisory boards for Alexion, Almirall, Biogen, Bristol Myers Squibb, Celgene, Janssen, Merck, Novartis, Roche and Sanofi; and has received unconditional research grants from Biogen and Novartis, and financial support from Sanofi for an investigator initiated study. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 F. Sellebjerg has served on scientific advisory boards for, served as a consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Merck, Novartis, Roche, and Sanofi Genzyme. His laboratory has received research support from Biogen, Merck, Novartis, Roche, and Sanofi Genzyme; J. Talbot reports non-financial support from Biogen, non-financial support from Sanofi Genzyme outside the submitted work; H. Højsgaard Chow reports non-financial support from Merck, non-financial support from Teva, nonfinancial support from Biogen, non-financial support from Roche, outside the submitted work; H.R. Siebner has received honoraria as a speaker from Sanofi Genzyme, Denmark; Lundbeck AS, Denmark; and Novartis, Denmark, as a consultant from Sanofi Genzyme, Denmark; Lophora, Denmark; and Lundbeck AS, Denmark, and as an editor-in-chief (Neuroimage Clinical) and a senior editor (NeuroImage) from Elsevier Publishers, Amsterdam, The Netherlands. He has received royalties as a book editor from Springer Publishers, Stuttgart, Germany, and from Gyldendal Publishers, Copenhagen, Denmark; M.R. von Essen, R.H. Hansen, and H. Lundell report no disclosures relevant to the manuscript. Go to Neurology.org/NN for full disclosure.
 Declaration of Competing Interest None.
 F.C. Loonstra, L.R.J. de Ruiter, B. Moraal, E.M.M. Strijbis, B.A. de Jong report no disclosures. M.M. Schoonheim serves on the editorial board of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation and Amsterdam Neuroscience and has served as a consultant for or received research support and/or speaker honoraria from Atara Biotherapeutics, Biogen, Celgene, Genzyme, MedDay and Merck. B.M.J. Uitdehaag received consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Teva and Immunic Therapeutics.

 Declarations of Competing Interest none.
 Declaration of Competing Interest In the last two years, Gavin Giovannoni has received compensation for serving as a consultant or speaker for or have received research support from AbbVie, Aslan, Atara Bio, Biogen, BMS-Celgene, GlaxoSmithKline, Janssens/J&J, Japanese Tobacco, Jazz Pharmaceuticals, LifNano, Merck & Co, Merck KGaA/EMD, Moderna, Serono, Moderna, Novartis, Sandoz, Sanofi and Roche/Genentech.


 Declaration of competing interest Pr Deiva has received personal compensation for speaker activities from Novartis, Alexion, Biogen, Roche and Sanofi. Dr. Maillart has received consulting or travel fees from Alexion, Biogen, Janssen, Novartis, Sanofi, Teva and Merck Serono, and research grant from Biogen, none related to the present work. Other authors report no competing interest.
 Declaration of Competing Interests The authors declare that there is no conflict of interest.

 Declaration of Competing Interest Valentina Torri Clerici has acted as an Advisory Board member for Almirall, Merck, Novartis, Roche and Sanofi; has received funding for traveling and honoraria for speaking or writing from Almirall, Biogen, Bristol-Meyers Squibb, Novartis, Sanofi, and Teva; has received support for research projects from Almirall; is involved as principal investigator in clinical trials for FISM, Merck, Novartis, and Sanofi. Laura Brambilla has received honoraria for speaking from Novartis and Sanofi, and for traveling from Coloplast, Merck, Roche, and Sanofi. She has acted as an Advisory Board member for Biogen, Merck, Novartis, and Sanofi. She is involved as principal investigator in clinical trials for Merck and Roche. Simone Tonietti has received honoraria for lecturing from Sanofi and Teva; for writing from Teva; for participation in advisory boards from Biogen and Merck; and for travel expenses to attend congresses and meetings from Biogen, Merck, Novartis, Sanofi, and Teva. Marco Ronzoni has acted as an Advisory Board member for Biogen, Roche and Sanofi; has received honoraria for speaking from Sanofi and for traveling from Biogen, Mylan and Novartis. Sebastiano Crisafulli has received travel grants from Merck and Novartis. Carlo Antozzi has received honoraria for Advisory Board participation from Momenta Pharmaceuticals, and for meeting participation from Biogen and Sanofi. Paolo Confalonieri has received honoraria for speaking or consultation fees from Biogen, Novartis, and Roche; has received funding for travel to attend scientific events or speaker honoraria from Biogen, Merck, Mylan, Roche, and Teva; has received institutional research support from Merck, Mylan, Novartis, and Roche. He is also involved as principal investigator in clinical trials for Biogen, Merck, and Roche. Paolo Luca Politi, Federica Viggiani, Simone Mercurio, Irene Tramacere and Chiara Redemagni have nothing to disclose.

 Competing interests: None declared.
 Competing interests: Some authors (CC, MS, GS, DC) are employees of MSD. Dr. Eleftherios P. Diamandis declares that he holds an advisory role with Abbott Diagnostics and a consultant role with Imaware Diagnostics. All other authors have nothing to declare.
 Declaration of Competing Interest All authors declare no conflicts of interest.
 Conflict of interests None.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors have no conflict of interest to report.


 The authors have declared that no competing interests exist.

 The authors declare no competing interests.

 The authors declare there is no conflicts of interest.



 The authors declare no conflict of interest.

 J.K. declares that she has received honoraria for lecturing from Biogen, Merck, Mylan, Novartis, Roche, Sanofi and Teva and has received financial research support from Amicus Therapeutics and Sanofi. A.B.-O. declares that he has received grant support to the University of Pennsylvania from Biogen Idec, EMD Serono, Novartis and Roche Genentech. He has participated as a speaker in meetings sponsored by and received consulting fees from Accure, Atara Biotherapeutics, Biogen, Bristol-Myers Squibb, GlaxoSmithKline, Gossamer, Janssen, Medimmune, EMD Serono, Novartis, Roche Genentech and Sanofi. T.J.T. is an employee of and may have ownership interests in Sanofi. H.W. declares that he has acted as a member of the Scientific Advisory Boards of Abbvie, Alexion, Argenx, Bristol Myers Squibb, Janssen, Merck and Novartis. He also declares that he has received speaker’s honoraria and travel support from Alexion, Biogen, Bristol-Myers Squibb, F. Hoffmann-La Roche, Genzyme, Merck, Neurodiem, Novartis, Roche, Teva and WebMD Global and acts as a paid consultant for Abbvie, Actelion, Argenx, Biogen, Bristol-Myers Squibb, EMD Serono, Fondazione Cariplo, Gossamer Bio, Idorsia, Immunic, Immunovant, Janssen, Lundbeck, Merck, NexGen, Novartis, PSI Contract Research Organization, Roche, Sanofi, UCB and Worldwide Clinical Trials. His research is funded by Alexion, Amicus Therapeutics, Argenx, Biogen, CSL Behring, F. Hoffmann-La Roche, Genzyme, Merck, Novartis, Roche and UCB.
 None.

 The authors declare no conflict of interest.





 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 All the authors declare that they have no competing interests.
 Declaration of competing interest The authors declare no competing interests related to the manuscript.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.A. Toorop reports no disclosures relevant to the manuscript; M. Steenhuis reports no disclosures relevant to the manuscript; F.C. Loeff reports no disclosures relevant to the manuscript; S.S. Weijers reports no disclosures relevant to the manuscript; J. Killestein received research grants for multicentre investigator initiated trials (DOT-MS trial, ClinicalTrials.gov Identifier: NCT04260711 (ZonMW) and BLOOMS trial (ZonMW and Treatmeds), ClinicalTrials.gov Identifier: NCT05296161), received consulting fees for F. Hoffmann-La Roche Ltd, Biogen, Teva, Merck, Novartis and Sanofi/Genzyme (all payments to institution), reports speaker relationships with F. Hoffmann-La Roche Ltd, Biogen, Immunic, Teva, Merck, Novartis and Sanofi/Genzyme (all payments to institution) apart from multi-sponsored events, adjudication committee of MS clinical trial of Immunic (payments to institution only); T. Rispens received funding for research from Genmab, received consulting fees from Novartis; Z.L.E. van Kempen reports no disclosures relevant to the manuscript.


 Declaration of Competing Interest The authors report no conflict of interest.
 The authors declare there is no conflict of interest.
 Declaration of Competing Interest The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Conflict of Interest Disclosures: Dr. Terry Wahls personally follows and promotes the Wahls™ diet. She has equity interest in the following companies: Terry Wahls LLC; TZ Press LLC; The Wahls Institute, PLC; FBB Biomed Inc; Levels Health Inc., Foogal Inc. and the website http://www.terrywahls.com. She also owns the copyright to the books Minding My Mitochondria (2nd Edition) and The Wahls Protocol, The Wahls Protocol Cooking for Life, and the trademarks The Wahls Protocol® and Wahls™ diet, Wahls Paleo™ diet, and Wahls Paleo Plus™ diets. She has completed grant funding from the National Multiple Sclerosis Society for the Dietary Approaches to Treating Multiple Sclerosis Related Fatigue Study. She has financial relationships with BioCeuticals Ltd., MCG Health LLC, Vibrant America LLC, Standard Process Inc., MasterHealth Technologies Inc., Foogal Inc., Genova Diagnostics Inc., and the Institute for Functional Medicine. She receives royalty payments from Penguin Random House. Dr Wahls has conflict of interest management plans in place with the University of Iowa and the Iowa City Veteran's Affairs Medical Center. All other authors report no personal or financial conflicts of interest in this work.
 TK: received grant from Italian Ministry of Health. MC: received consulting fees from Zambon, support for attending meetings/travel from Janssen. MF: received part of grant from Italian Ministry of Health. MM: received honoraria for presentation/manuscript writing and support for attending meetings/travel from EISAI. MS: received grant from FISM; speaking honoraria from Merck, Sanofi, Novartis, Roche, Viatris, Biogen, BMS; support for patents IT 1417523 and EP2981625. MI: received consulting fees from Biogen, Novartis Merck, Sanofi, Roche, BMS, Janssen; received honoraria for presentation from Biogen, Novartis Merck, Sanofi, Roche, BMS, Janssen. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 AP declares grant support for remyelination trials in multiple sclerosis to the Amsterdam University Medicam Centre, Department of Neurology, MS Centre (for the RESTORE trial), and University College London (for the RECOVER trial); funding for a trial from Fight for Sight (nimodipine in optic neuritis trial); royalties or licenses from Up-to-Date (Wolters Kluver) on a book chapter; speaker fees from the Heidelberg Academy; participation on advisory boards for SC Zeiss Optical Coherence Tomography Angiorgaphy Angi-Network and the SC Novartis Optical Coherence Tomography in Multiple Sclerosis study; leadership roles for a governing board for International Multiple Sclerosis Visual System Consortium (until December, 2022) and Chairman of European Reference Network for rare Eye Diseases Neuro-ophthalmology (until October, 2020); is a board member of National Dutch Neuro-ophthalmology Association; received equipment from Optical Coherence Tomography Angiorgaphy and Zeiss (Plex Elite); and provided medical writing support to Novartis. YL declares no competing interests.


 Declaration of interests L.K. has received no personal compensation. His institutions (University Hospital Basel/Stiftung Neuroimmunology and Neuroscience Basel) have received the following exclusively for research support: steering committee, advisory board, and consultancy fees (AbbVie, Actelion, Auriga Vision AG, Bayer HealthCare, Biogen, Celgene, df-mp Monia & Pohlmann, Eli Lilly, EMD Serono, Genentech, Genzyme, GlaxoSmithKline, Janssen, Merck, Minoryx, Novartis, Roche, Sanofi, Santhera, Senda Biosciences, Shionogi, and Wellmera AG); speaker fees (Bristol Myers Squibb, Celgene, Janssen, Merck, Novartis, and Roche); support for educational activities (Biogen, Desitin, Novartis, Sanofi, and Teva); license fees for Neurostatus products; and grants (European Union, Innosuisse, Novartis, Roche, Swiss MS Society, and Swiss National Research Foundation).
 Declaration of Competing Interest MRB has received consulting fees from Genentech and EMD Serono. BX has nothing to disclose. JRC has received consulting fees from EMD Serono, Genentech, Janssen Pharmaceuticals and Novartis. SC has received research funding from BMS as well as consulting fees from BMS, Biogen, Novartis, Sanofi Genzyme, and Horizon Therapeutics. GFW is a consultant for Genzyme, Novartis, Sanagamo, Roche, and the US Dept. of Justice and has received grant funding from Biogen, EMD Serono, and Genentech. RTN has consulted for Abata Therapeutics, Alexion Pharmaceuticals, Biogen, BMS, Celltrion, Genentech, Genzyme, Janssen, GW Therapeutics, Horizon Therapeutics, Lundbeck, NervGen, and TG Therapeutics. DY has nothing to disclose. AHC has received consulting fees from Biogen, Bristol Myers Squibb, EMD Serono, Genentech (Roche), Horizon Pharmaceuticals, Janssen (J&J), Greenwich Bioscience, Novartis, and TG Therapeutics. AHC has received support for contracted research from: EMD Serono and Genentech (Roche).
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 VB is working for Biogen since May 2017. RG is working for Sanofi Genzyme since September 2017. The authors declare no conflict of interest related to this study.
 YD received grant support from the National Natural Science Foundation of China and the Department of Science and Technology of Guangxi Zhuang Autonomous Region. WL declares no competing interests. We thank Dev Sooranna (Imperial College London) for English language edits of the letter.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: M.F. is an investigator on projects funded by Multiple Sclerosis Canada, the Patient-Centered Outcomes Research Institute, the University Hospitals Kingston Foundation, and the National Multiple Sclerosis Society. She has received consulting or teaching honoraria from Novartis and Biogen. L.A.-M. and R.S. have no disclosures.

 The authors declare the following competing financial interest(s): N.A. is stock owner of Biosfer Teslab and has a patent of the lipoprotein profiling described in the present manuscript. The rest of the authors declare no conflict of interest.

 Declaration of Competing Interest AP, JN, GT, and MFD are employed by Merck, Sharp, and Dohme, Inc, and may own stock or stock options.

 The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: F. Hoffmann‐La Roche Ltd, Basel, Switzerland, provided financial support for the study and publication of this manuscript. J. S. Graves has received research support from Biogen, EMD Serono, Novartis, and Sanofi; has received speaking honoraria from Bristol Myers Squibb, Bayer, and Alexion; and served on advisory boards for Genentech and Bayer. M. Ganzetti is a contractor for F. Hoffmann‐La Roche Ltd. F. Dondelinger was an employee of and is a shareholder in F. Hoffmann‐La Roche Ltd; he is currently employed by Novartis Institutes for Biomedical Research. F. Lipsmeier is an employee of F. Hoffmann‐La Roche Ltd. S. Belachew was an employee of F. Hoffmann‐La Roche Ltd during the completion of the work related to this manuscript and is now an employee of Biogen (Cambridge, MA), which is not in any way associated with this study. C. Bernasconi is a contractor for F. Hoffmann‐La Roche Ltd. X. Montalban has received speaking honoraria and travel expenses for participation in scientific meetings; has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Actelion, Alexion, Bayer, Biogen, Celgene, EMD Serono, Genzyme, Immunic, MedDay, Merck, Mylan, Nervgen, Novartis, Roche, Sanofi‐Genzyme, Teva Pharmaceuticals, TG Therapeutics, Excemed, MSIF, and NMSS. J. van Beek was an employee of F. Hoffmann‐La Roche Ltd during the completion of the work related to this manuscript and is now an employee of Biogen (Cambridge, MA), which is not in any way associated with this study. M. Baker and C. Gossens are employees of and shareholders in F. Hoffmann‐La Roche Ltd. M. Lindemann is a consultant to F. Hoffmann‐La Roche Ltd via Inovigate.
 MD, NL, MG, SH, NL, SR, BI, EL, CY, DP, AS, SJ, PS, DR No competing interests declared, MJ is a shareholder and employee of Vertex Pharmaceuticals, Inc
 Declaration of Competing Interest None declared.
 Declarations of interest The authors have nothing to declare.
 The authors declare that they have no competing interests.


 Conflict of Interest Disclosures P Dillon was an employee of F. Hoffmann-La Roche Ltd during completion of the work related to this manuscript. A Siadimas is an employee of F. Hoffmann-La Roche Ltd O Fajardo is an employee of F. Hoffmann-La Roche Ltd S Roumpanis is an employee of F. Hoffmann-La Roche Ltd K Fitovksi is an employee of F. Hoffmann-La Roche Ltd N Jessop is an employee of F. Hoffmann-La Roche Ltd L Whitley is a Senior Partner at TranScrip Partners LLP and a consultant to F. Hoffmann-La Roche Ltd E Muros-Le Rouzic is an employee of F. Hoffmann-La Roche Ltd
 Declaration of Competing Interest The authors declare no conflict of interest.

 G. Boffa was supported by a research fellowship FISM - Fondazione Italiana Sclerosi Multipla 2019/BR/016 and financed or cofinanced with the “5 per mille” public funding. A. Signori has nothing to disclose. L. Massacesi received educational grants and/or research funds from Fondazione Cassa di Risparmio di Firenze, Biogen, Merck-Serono, Genzyme, and Roche and received honoraria or consultation fees from Biogen, Roche, Mylan, Merck-Serono, Genzyme, and Novartis. A. Mariottini reports nonfinancial support from Biogen idec, Sanofi Genzyme, Novartis, Teva, and Roche and personal fees from Merck Serono. E. Sbragia has nothing to disclose. S. Cottone received grants and honoraria from Roche, Sanofi, Merck, Biogen, and Novartis. M.P. Amato has served on Scientific Advisory Boards for Biogen, Novartis, Roche, Merck, Sanofi Genzyme, and Teva; received speaker honoraria from Biogen, Merck, Sanofi Genzyme, Roche, Novartis, and Teva; and received research grants for her Institution from Biogen, Merck, Sanofi Genzyme, Novartis, and Roche. C. Gasperini reports fees as invited speaker or travel expenses for attending meeting from Biogen, Merck‐Serono, Teva, Mylan, Sanofi, Novartis, and Genzyme. LP: consulting fees from Biogen, Novartis, and Roche; speaker honoraria from Biogen, Genzyme, Merck Serono, Mylan, Novartis, and Teva; travel grants from Biogen, Genzyme, Novartis, and Teva; and research grants from the Italian MS Society (Associazione Italiana Sclerosi Multipla) and Genzyme. L. Moiola has received speaker's honoraria from the following companies: Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and TEVA. S. Meletti has nothing to disclose. V. Brescia Morra has received funding for research support and speaker honoraria from Novartis, Roche, Biogen, Teva, Almirall, Sanofi-Genzyme, Merk, Bayer, and Mylan. M. Trojano has served on scientific AB for Biogen, Novartis, Roche, Merck, and Genzyme; received speaker honoraria from Biogen, Roche, Sanofi, Merck, Genzyme, and Novartis; and received research grants for her Institution from Biogen, Merck, and Novartis. G. Salemi received grants and honoraria from Roche, Sanofi, Merck, Biogen, and Novartis. F. Patti reports consulting fees from Alexion, Almirall, Bayer, Biogen, Calgene, Merck, Myalin, Novartis, Roche, Sanofi, and TEVA and research grants from Biogen and Merck. M. Filippi is Editor-in-Chief of the Journal of Neurology and Associate Editor of Human Brain Mapping, received compensation for consulting services and/or speaking activities from Almiral, Alexion, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries, and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). G. De Luca reports travel grants and/or speaker honoraria from Merck-Serono, Roche, Sanofi Genzyme, and Biogen. G. Lus has nothing to disclose. M. Zaffaroni received travel support and fees for lecturing or participating in advisory boards from Almirall, Biogen, Merck, Novartis, and Sanofi-Genzyme. P. Sola received travel grants from Teva, Roche, Sanofi, Merck, Biogen, Bristol, and Novartis and fees for consultation from Merck, Biogen, and Sanofi Genzyme. A. Conte received grants from Roche and fees for consultation from Sanofi Genzyme, Merck, Biogen, Almirall, and Novartis. R. Nistri has nothing to disclose. U. Aguglia has nothing to disclose. F. Granella received research grants from Biogen and Roche and fees for consultation from Biogen, Sanofi, Merck Serono, Novartis, and Roche. S. Galgani received fees as invited speaker or travel expenses for attending meeting from Biogen, Merck‐Serono, Teva, Almirall, Sanofi‐Aventis, Novartis, and Genzyme. L.M. Caniatti has nothing to disclose. A. Lugaresi has served as a Biogen, Merck Serono, Novartis, Roche, Sanofi/Genzyme, and Teva Advisory Board Member. She received congress and travel/accommodation expense compensations or speaker honoraria from Biogen, Merck, Mylan, Novartis, Sanofi/Genzyme, Teva, and Fondazione Italiana Sclerosi Multipla (FISM). Her institutions received research grants from Novartis. S. Romano reports fees as speaker and travel expense refunds from Biogen, Novartis, and Roche. P. Iaffaldano has served on scientific advisory boards for Biogen Idec, Bayer, Teva, Roche, Merck Serono, Novartis, and Genzyme and has received funding for travel and/or speaker honoraria from Sanofi Aventis, Genzyme, Biogen Idec, Teva, Merck Serono, and Novartis. R. Saccardi has nothing to disclose. E. Angelucci is DMC member for Celgene and VERTEX-CRISPR-CAS9, Adv board for Novartis, BlueBirdBio, and Gilead. G.L. Mancardi received support from Biogen Idec (honoraria for lecturing, travel expenses for attending meetings, and financial support for research), Genzyme (honorarium for lecturing), Merck Serono, Novartis, Teva (financial support for research), and Sanofi Aventis (honorarium for speaking). M.P. Sormani received consulting fees from Biogen Idec, Merck Serono, Teva, Genzyme, Roche, Novartis, GeNeuro, and Medday. M. Inglese received grants NIH, NMSS, and FISM and received fees for consultation from Roche, Genzyme, Merck, Biogen, and Novartis. Go to Neurology.org/N for full disclosures.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


 Declaration of Competing Interest All authors declare that they have no conflict of interest.

 Declaration of Competing Interest E.T. and S.F. declare that there is no conflict of interest. M.W. was supported by grants from JSPS KAKENHI (Grant Numbers JP19K07995, JP22K07351) and received honoraria for lecturing and interviewing from Novartis Pharma, Chugai Pharmaceutical Co. Ltd., Biogen Japan, and Alexion. M.K. received honoraria for lecturing from Novartis Pharma, Chugai Pharmaceutical Co. Ltd., Alexion, and Nihon Pharmaceutical. R.Y. received honoraria from Teijin Pharma, Ono Pharmaceutical, Takeda Pharmaceutical, Eisai, Novartis, Nihon Pharmaceutical, and CSL Behring. T.M. was supported by grants from JSPS KAKENHI (Gant Number JP20K07869) and received speaker honoraria from Novartis Pharma, Biogen Japan, Alexion, and Chugai Pharmaceutical Co. Ltd. N.I. was supported by grants from JSPS KAKENHI (Grant Number JP21K07464) and AMED Grant Number JP21zf0127004, and received speaker honoraria from Alexion, Novartis Pharma, Biogen Japan, Mitsubishi Tanabe Pharma, Chugai Pharmaceutical Co. Ltd., Teijin Pharma, Takeda Pharmaceutical, CSL Behring, and Eisai.
 Michael Guger received support and honoraria for research, consultation, lectures and education from Alexion, Almirall, Bayer, Biogen, Bristol-Myers-Squibb, Celgene, Genzyme, Horizon, Janssen-Cilag, MedDay, Merck, Novartis, Roche, Sanofi Aventis and TEVA ratiopharm. Christian Enzinger received funding for travel and speaker honoraria from Bayer, Biogen, Genzyme, Merck, Novartis, Roche, Shire, and Teva Pharmaceutical Industries Ltd./sanofi-aventis, research support from Biogen, Merck, and Teva Pharmaceutical Industries Ltd./sanofi-aventis and serving on scientific advisory boards for Bayer, Biogen, Merck, Novartis, Roche and Teva Pharmaceutical Industries Ltd./sanofi- Aventis. Fritz Leutmezer has received funding for travel and speaker honoraria from Actelion, Almirall, Bayer, Biogen, Celgene, Genzyme, MedDay, Merck, Novartis, Pfizer, Octapharm, Roche, Sanofi-Genzyme and Teva. Franziska Di Pauli has participated in meetings sponsored by, received honoraria (lectures, advisory boards, consultations) or travel funding from Almirall, Bayer, Biogen, Merck, Novartis, Sanofi-Genzyme, Teva, Celgene and Roche. Her institution received scientific grants from Roche. Jörg Kraus received consulting and/or research funding and/or educational support from Almirall, Bayer, Biogen, Celgene, MedDay, Medtronic, Merck, Novartis, Roche, Sanofi-Aventis, Shire, TEVA ratiopharm. Stefan Kalcher declares that there is no conflict of interest. Erich Kvas declares that there is no conflict of interest. Thomas Berger has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for multiple sclerosis: Almirall, Bayer, Biogen, Biologix, Bionorica, Bristol-Myers-Squibb, Eisai, GW Pharma, Horizon, Janssen-Cilag, MedDay, Merck, Novartis, Octapharma, Roche, Sandoz, Sanofi/Genzyme, TG Pharmaceuticals, TEVA-ratiopharm and UCB. His institution has received financial support in the last 12 months by unrestricted research grants (Biogen, Bayer, Bristol-Myers-Squibb, Merck, Novartis, Sanofi/Genzyme, and TEVA ratiopharm) and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Bristol-Myers-Squibb, Merck, Novartis, Octapharma, Roche, Sanofi/Genzyme, and TEVA.
 The authors declare a competing interest. N.K., L.S., F.W., D.S., K.K., M.S., M.D., and A.-S.S. have nothing to disclose. C.J. received travel support from Novartis. M. Lindner received research support from the Innovative Medical Research (IMF) program of the University Münster. M. Liebmann received travel support from Biogen and research support from the Innovative Medical Research (IMF) program of the University Münster. M.E. received speaker honoraria and travel support from Sanofi Genzyme. She received research support from the Deutsche Multiple Sklerose Gesellschaft (DMSG) Landesverband Nordrhein-Westfalen (NRW) and the Innovative Medical Research (IMF) program of the University Münster. T.S.-H. received research and travel support from Biogen and Novartis. A.-K.F. received travel support from Novartis. A.S.-M. received travel expenses and research support from Novartis. I.M. reports personal fees from Biogen, Bayer Healthcare, Teva, Serono, Novartis, Genzyme, Roche, and grants from Biogen, Genzyme, Novartis, Niedersachsen Research Network on Neuroinfectiology 2 (N-RENNT), and the Federal Ministry for Economics and Technology. S.G.M. receives honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, Ono Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS und Teva. His research is funded by the German Ministry for Education and Research (BMBF), Deutschen Forschungsgesellschaft (DFG), Else Kröner Fresenius Foundation, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Almirall, Amicus Therapeutics Germany, Biogen Idec, Diamed, Fresenius Medical Care, Genzyme, Merck Serono, Novartis, Ono Pharma, Roche, und Teva. C.C.G. received speaker honoraria from Mylan and Bayer Healthcare, and travel/accommodation/meeting expenses from Bayer Healthcare, Biogen, EUROIMMUN, Novartis, and Sanofi-Genzyme. She also received research support from Biogen, Novartis, and Roche. G.M.z.H. received speaker honoraria and travel support from Alexion and Laboratoire français du Fractionnement et des Biotechnologies (LFB) and is acting as a member of Scientific Advisory Board for Alexion. N.S. received travel support from Biogen and Novartis, as well as research support from Biogen and Roche. T.K. received research funding from the German Research Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Münster, National MS Society, European Leukodystrophy Association, Progressive Multiple Sclerosis Alliance, European Commission (H2020-MSCA-ITN-2018) and Novartis. She received compensation for serving on scientific advisory boards (Frequency Therapeutics, Inc.) and speaker honoraria from Novartis and Roche. H.W. received honoraria for acting as a member of Scientific Advisory Boards Biogen, Evgen, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Roche Pharma, and Sanofi-Aventis, UCB Pharma as well as speaker honoraria and travel support from Alexion, Biogen, Biligix, Cognomed, F. Hoffmann-La Roche Ltd., Gemeinnützige Hertie-Stiftung, Merck Serono, Novartis, Roche Pharma, Genzyme, Teva, and WebMD Global. Prof. Wiendl is acting as a paid consultant for Actelion, Biogen, IGES Pharma, Johnson & Johnson, Novartis, Roche, Sanofi-Aventis, and the Swiss Multiple Sclerosis Society. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Fresenius Foundation, the European Union, Hertie Foundation, NRW Ministry of Education and Research, Interdisciplinary Center for Clinical Studies (IZKF) Muenster and Biogen, GlaxoSmithKline, Roche, Sanofi-Genzyme. L.K. received compensation for serving on Scientific Advisory Boards for Alexion, Genzyme, Janssen, Merck Serono, Novartis and Roche. She received speaker honoraria and travel support from Bayer, Biogen, Celgene, Genzyme, Grifols, Merck Serono, Novartis, Roche, Santhera and Teva. She receives research support from the German Research Foundation, the IZKF Münster, IMF Münster, Biogen, Immunic, Novartis and Merck Serono. The authors have no additional financial interests.

 Anat Achiron served on the scientific advisory board and/or received speaker honoraria/consulting from Biogen, BMS, Merck, Novartis, Roche and Sanofi, received grant/research support from Biogen, BMS, Merck, Roche and Sanofi and received institutional support from Sackler School of Medicine, Tel-Aviv University for Autoimmune Diseases research. All other authors have no competing interests. This does not alter our adherence to PLOS ONE policies on sharing data and materials



 Declaration of Competing Interest Steve Simpson-Yap: nothing to disclose. Duncan Maddox: nothing to disclose. Jeanette Reece: nothing to disclose. Jeannette Lechner-Scott: received travel compensation from Novartis, Biogen, Roche and Merck. Her institution receives the honoraria for talks and advisory board commitment as well as research grants from Biogen, Merck, Roche, TEVA and Novartis. Cameron Shaw: served on scientific advisory boards for Merck, Genzyme, Almirall, and Biogen; received honoraria and travel grants from Sanofi Aventis, Novartis, Biogen, Merck, Genzyme and Teva. Bruce Taylor: received funding for travel and speaker honoraria from Bayer Schering Pharma, CSL Australia, Biogen and Novartis, and has served on advisory boards for Biogen, Novartis, Roche and CSL Australia. Tomas Kalincik: served on scientific advisory boards for MS International Federation and World Health organisation, BMS, Roche, Janssen, Sanofi Genzyme, Novartis, Merck and Biogen, steering committee for Brain Atrophy Initiative by Sanofi Genzyme, received conference travel support and/or speaker honoraria from WebMD Global, Eisai, Novartis, Biogen, Roche, Sanofi-Genzyme, Teva, BioCSL and Merck and received research or educational event support from Biogen, Novartis, Genzyme, Roche, Celgene and Merck. Anneke van der Walt: served on advisory boards for Novartis, Biogen, Merck and Roche and NervGen. She received unrestricted research grants from Novartis, Biogen, Merck and Roche. She is currently a co-Principal investigator on a co-sponsored observational study with Roche, evaluating a Roche-developed smartphone app, Floodlight-MS. She has received speaker's honoraria and travel support from Novartis, Roche, Biogen and Merck. She serves as the Chief operating Officer of the MSBase Foundation (not for profit). Her primary research support is from the National Health and Medical Research Council of Australia and MS Research Australia. Mike Boggild: has received travel sponsorship and honoraria from Sanofi-Genzyme, Teva, Novartis, Biogen Idec and Roche.

 Conflicts of interest and sources of funding: A.M. is an employee of Siemens Healthcare SAS. T.K. is an employee and shareholder of Siemens Healthcare AG and holds patents filed by Siemens Healthcare. For the remaining authors, none were declared. The authors received no financial support for the research, authorship, or publication of this article.

 Declaration of Competing Interest Lorefice L., Fenu G., Cocco E. received honoraria for consultancy or speaking from Biogen, Novartis, Sanofi Genzyme, Serono and Teva and Almirall. Pilotto S received travel grants from Biogen, Teva, Janssen and Bristol Myers Squibb. Zoledziewska M., has nothing to disclose.
 Declaration of Competing Interest None.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest None
 Conflicts of interest and sources of funding: none declared.
 Competing interests The authors declare no competing or financial interests.
 Declaration of Competing Interest The authors have declared that there is no conflict of interest.

 Declaration of Competing Interest The authors declare no conflict of interests.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 The authors declare there are no competing interests.


 Declaration of Conflicting Interests The authors declare no potential conflicts of interest regarding this article's research, authorship, and/or publication.
 MM received personal compensations for advisory boards and travel grants from Novartis and Sanofi-Genzyme. FM received personal compensations for advisory boards from Novartis and Merck Serono. SR received personal compensations for public speaking and travel grants from Sanofi-Genzyme and Merck Serono. MC received personal compensations for advisory boards, public speaking, editorial commitments, or travel grants from Biogen Idec, Merck Serono, Fondazione Serono, Novartis, Pomona, Sanofi-Genzyme, and Teva. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that there is no conflict of interest.



 The authors have organizational affiliations to disclose, H.W. receives honoraria for acting as a member of Scientific Advisory Boards from Abbvie, Alexion, Argenx, Bristol Myers Squibb/Celgene, Janssen, Merck, Novartis, Sandoz, Speaker honoraria and travel support from Alexion, Biogen, Bristol Myers Squibb, Genzyme, Merck, Neurodiem, Novartis, Roche, TEVA, WebMD Global. H.W. is acting as a paid consultant for Abbvie, Actelion, Argenx, BD, Biogen, Bristol Myers Squibb, EMD Serono, Fondazione Cariplo, Gossamer Bio, Idorsia, Immunic, Immunovant, Janssen, Lundbeck, Merck, NexGen, Novartis, PSI CRO, Roche, Sanofi, Swiss MS Society, UCB, Worldwide Clinical Trials. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgesellschaft, Deutsche Myasthenie Gesellschaft e.V., Alexion, Amicus Therapeutics Inc., Argenx, Biogen, CSL Behring, F. Hoffmann-La Roche, Genzyme, Merck KgaA, Novartis, Roche Pharma, UCB Biopharma.




 The authors have no conflicts of interest or any financial and personal relationships with other people or organizations that could inappropriately influence their work to declare.



 SS is a cofounder, stockholder and paid consultant of Gliknik Inc. DB, HO, EM, and SG are Gliknik employees. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest.

 Declaration of Competing Interest Benjamin Greenberg has received consulting fees from Alexion, Novartis, EMD Serono, Horizon Therapeutics, Genentech/Roche, Signant, IQVIA, Sandoz, Genzyme, Immunovant and PRIME Education. He has received grant funding from NIH, Anokion, Clene Nanomedicine, and Regeneron. He serves as an unpaid member of the board of the Siegel Rare Neuroimmune Association. He receives royalties from UpToDate. In the last two years, Gavin Giovannoni has received compensation for serving as a consultant or speaker for, or has received research support from AbbVie, Aslan, Atara Bio, Biogen, BMS-Celgene, GlaxoSmithKline, Janssens/J&J, Japanese Tobacco, Jazz Pharmaceuticals, LifNano, Merck & Co, Merck KGaA/EMD Serono, Moderna, Novartis, Sanofi and Roche/Genentech.

 Declaration of Competing Interest Authors declare no conflicts of interest.
 The authors declare no conflict of interest.
 Disclosure statement No potential conflict of interest was reported by the author(s).
 Declaration of Competing Interest The authors have no competing interests to declare.
 The author declares that they have no competing interests.
 Declaration of Competing Interest None.

 Declaration of Competing Interest Le H Hua has received personal fees for speaking, consulting and advisory board activities from Bristol Myers Squibb, EMD Serono, Genentech, Genzyme, Novartis, TG Therapeutics, Horizon, Greenwich and Alexion, and research support from Biogen paid to her institution. Amit Bar-Or participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from Accure, Atara Biotherapeutics, Biogen, Bristol Myers Squibb/Celgene/Receptos, GlaxoSmithKline, Gossamer, Janssen/Actelion, Medimmune, Merck/EMD Serono, Novartis, Roche/Genentech and Sanofi Genzyme, and has received grant support to the University of Pennsylvania from Biogen Idec, Roche/Genentech, Merck/EMD Serono and Novartis. Stanley L Cohan has received speaker fees from Biogen, Bristol Myers Squibb, Novartis, Roche Genentech and Sanofi Genzyme, and serves on advisory boards or as a consultant to AbbVie, Biogen, Bristol Myers Squibb, EMD Serono, Novartis and Sanofi Genzyme. Institutional research support (the Providence Brain and Spine Institute) was received from AbbVie, Adamas, Biogen, EMD Serono, MedDay, Novartis, Roche Genentech, Sage Bionetworks and Sanofi Genzyme. Fred D Lublin has participated in consulting agreements, advisory boards and Data and Safety Monitoring Board activities for Actelion/Janssen, Acorda, Apitope, Atara Biotherapeutics, Avotres, Banner Life Sciences, Biogen, Brainstorm Cell Therapeutics, EMD Serono, GW Pharma, Immunic, Jazz Pharmaceuticals, Labcorp Entelexo Biotherapeutics, Mapi Pharma, Medday, MedImmune/Viela Bio/Horizon Therapeutics, Mylan, Neuralight, Neurogene, Novartis, Orion Biotechnology, Population Council, Receptos/Celgene/Bristol Myers Squibb, Roche/Genentech, Sanofi/Genzyme, Teva and TG Therapeutics, acted as a speaker (non-promotional) for Sanofi, reports research funding from Actelion, Biogen, Brainstorm Cell Therapeutics, National Institutes of Health, Novartis, National Multiple Sclerosis Society and Sanofi, and has stock options with Avotres and Neuralight. Patricia K Coyle has received consulting fees from Accordant, Alexion, Bayer, Biogen, Celgene, Genentech/Roche, Genzyme/Sanofi, GlaxoSmithKline, Mylan, Novartis, Serono and TG Therapeutics, and research grants from Actelion, Alkermes, Corrona LLC, Genentech/Roche, MedDay, NINDS, Novartis and PCORI. Bruce AC Cree has received personal compensation for consulting from Alexion, Atara, Autobahn, Avotres, Biogen, Boston Pharma, EMD Serono, Gossamer Bio, Hexal/Sandoz, Horizon, Neuron23, Novartis, Sanofi, Siemens, TG Therapeutics and Therini and received research support from Genentech. Xiangyi Meng, Wendy Su and Gina M Cox are employees of Novartis Pharmaceuticals Corporation. Robert J Fox has received personal fees from Actelion, Biogen, Celgene, EMD Serono, Genentech, Immunic, Novartis and Teva, grants from Novartis and other support from Biogen and Novartis (clinical trial contracts).
 The authors declare that they have no conflict of interest.
 Conflict of interest None declared.
 Declaration of Competing Interest The authors declare that they have no conflict of interest.
 Declaration of Competing Interest Kamm CP has received honoraria for lectures as well as research support from Biogen, Novartis, Almirall, Teva, Merck, Sanofi Genzyme, Roche, Janssen, Eli Lilly, Celgene and the Swiss MS Society (SMSG). Sanak L has no disclosures to report. Von Wyl V has no disclosures to report. Chan A has received speakers’/board honoraria from Actelion (Janssen/J&J), Almirall, Bayer, Biogen, Celgene (BMS), Genzyme, Merck KGaA (Darmstadt, Germany), Novartis, Roche, and Teva, all for hospital research funds. He received research support from Biogen, Genzyme, and UCB, the European Union, and the Swiss National Foundation. He serves as associate editor of the European Journal of Neurology, on the editorial board for Clinical and Translational Neuroscience and as topic editor for the Journal of International Medical Research. Stanikic M reports employment by Roche branch in Serbia, Roche d.o.o. from February 2019 to February 2020. Zina-Mary Manjaly has no disclosures to report. Zecca C is recipient of a grant for senior reseachers provided by AFRI (Area Formazione accademica, Ricerca e Innovazione), EOC. Ente Ospedaliero Cantonale (employer) received compensation for C.Z.’s speaking activities, consulting fees, or research grants from Almirall, Biogen Idec, Bristol Meyer Squibb, Lundbeck, Merck, Novartis, Sanofi, Teva Pharma, Roche. Calabrese P. has received speakers’/board honoraria from Almirall, Biogen, Celgene (BMS), Genzyme, Novartis, Roche, Schwabe and Teva.

 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: P.v.O. and F.d.G. are employees of Sherpa BV and Orikami Digital Health Products, respectively (industry partners). B.M.J.U. received consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, and Teva. J.K. has accepted speaker and consultancy fees from Merck, Biogen, Teva, Genzyme, Roche, and Novartis. The remaining authors have no conflicts of interest to declare.
 The authors declare no competing interests.
 Conflict of interest Authors have no relevant conflict of interest, financial or otherwise.
 The authors have no conflict of interest to declare.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The authors declare no competing interests.


 The authors declare no conflict of interests.
 Declaration of Competing Interest The authors declare no competing interests for this work.
 Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Giulia Longoni, Edgar Martinez Chavez, Kimberly Young, Robert A. Brown, Sonya Bells, Dumitru Fetco, Laura Kim, Stephanie A. Grover, Helen M. Branson, Arun Reginald, John G. Sled, and Donald J. Mabbott have nothing to disclose. Fiona Costello has received speaker honoraria for Accure Therapeutics, Novartis, Alexion; and consultant honoraria for Frequency Therapeutics and Alexion. Amit Bar-Or participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from Janssen/Actelion; Atara Biotherapeutics, Biogen Idec, Celgene/Receptos, Roche/Genentech, MAPI, Medimmune, Merck/EMD Serono, Novartis, Sanofi-Genzyme. Ruth Ann Marrie receives research funding from CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC, US Department of Defense and the Arthritis Society. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her/her institution). Douglas L. Arnold has received personal compensation for serving as a Consultant for Alexion, Biogen, Celgene, Eli Lilly, EMD Serono, Frequency Therapeutics, Genentech, Merck, Novartis, Roche, Sanofi, and Shionogi, and holds an equity interest in NeuroRx. Sridar Narayanan has received speaker’s honoraria from Novartis Canada and Roche and is a part-time employee of NeuroRx Research. Brenda L. Banwell serves as a consultant to Novartis, Roche, UCB, Sanofi-Genzyme, Biogen, and UTSW regarding design and safe conduce of clinical trials and as a central reviewer for Novartis and Roche. E. Ann Yeh has received research funding from NMSS, CMSC, CIHR, NIH, OIRM, SCN, CBMH Chase an Idea, SickKids Foundation, Rare Diseases Foundation, MS Scientific Foundation (Canada), McLaughlin Center, Mario Battaglia Foundation. Investigator initiated research funding from Biogen. Scientific advisory: Biogen, Hoffman-LaRoche, Vielabio. Speaker honoraria: Saudi Epilepsy Society, NYU, MS-ATL; ACRS, PRIME.
 Declaration of Competing Interest The authors have no conflicts of interest to report.
 The authors declare no competing interests.


 The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 Competing interests: FB acts as a consultant for Combinostics, Biogen-Idec, Janssen, IXICO, Merck-Serono, Novartis and Roche. He has received grants, or grants are pending, from the Amyloid Imaging to Prevent Alzheimer’s Disease (AMYPAD) initiative, the Biomedical Research Centre at University College London Hospitals, the Dutch MS Society, ECTRIMS–MAGNIMS, EU-H2020, the Dutch Research Council (NWO), the UK MS Society and the National Institute for Health Research, University College London. He has received payments for the development of educational presentations from IXICO and his institution from Biogen-Idec and Merck. He is co-founder of Queen Square Analytics. He is on the editorial board of Radiology, Neuroradiology, Multiple Sclerosis Journal and Neurology. JHC is a scientific consultant to and shareholder in BrainKey and Claritas Healthcare, as has worked as a consultant to Queen Square Analytics.
 This study was supported by a grant from the International Organization of Multiple Sclerosis Nurses and EMD Serono to Mindy Robert, and in part by the Weber State University Sigma Theta Tau Nu Nu Chapter to Mindy Robert. There are no other financial or funding disclosures or conflicts of interest for the remaining authors.
 Amnon Sonnenberg has no conflict of interest to declare.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.
 Thoralf Niendorf is founder and CEO of MRI.TOOLS, Berlin, Germany.


 Competing interests: SA has no conflicts to declare. LAG has consulted to Roche Canada. She receives research funding from CIHR, the Multiple Sclerosis Society of Canada and Crohn’s and Colitis Canada. CNB receives research funding from CIHR, Brain and Behavior Research Foundation, Crohn’s and Colitis Canada and the MS Society of Canada. JDF receives research grant support from the Canadian Institutes of Health Research, the National Multiple Sclerosis Society, the Multiple Sclerosis Society of Canada, Crohn’s and Colitis Canada, Research Nova Scotia; consultation and distribution royalties from MAPI Research Trust. Lisa M Lix receives research funds from CIHR, NSERC and the Arthritis Society. SBP receives research funding from CIHR, the MS Society of Canada, Roche, Biogen and the Government of Alberta. CNB is supported by the Bingham Chair in Gastroenterology. CNB has served on advisory Boards for AbbVie Canada, Amgen Canada, Bristol Myers Squibb Canada, JAMP Pharmaceuticals, Lilly Canada, Roche Canada, Janssen Canada, Sandoz Canada, Takeda Canada and Pfizer Canada; consultant for Mylan Pharmaceuticals and Takeda; educational grants from AbbVie Canada, Pfizer Canada, Takeda Canada and Janssen Canada. Speaker’s panel for AbbVie Canada, Janssen Canada, Pfizer Canada and Takeda Canada. Received research funding from AbbVie Canada, Amgen Canada, Sandoz Canada, Takeda Canada and Pfizer Canada. JJM has conducted trials for Biogen Idec and Roche, and receives research funding from the MS Society of Canada. CAH has served on an Advisory Board for AstraZeneca Canada, and has received unrelated research funding from Pfizer Canada, Public Health Agency of Canada and Health Sciences Centre Foundation. RAM is a co-investigator on a study funded by Biogen Idec and Roche (no funds to her/her institution). RAM receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and the US Department of Defense and is a co-investigator on studies receiving funding from Biogen Idec and Roche Canada. She holds the Waugh Family Chair in Multiple Sclerosis.

 JI reports no conflicts of interest and funding by the Bundesinstitut für Risikobewertung (BfR), LM received honoraria from Biogen and Merck, as well as research funding from the Deutsche Multiple Sklerose Gesellschaft, MP received honoraria for lecturing from Argenx, Alexion, Novartis, Bayer Health Care, Sanofi-Aventis, Biogen and Merck; SS received no financial compensation or support from any organization or entity that may have an interest in the content of this manuscript; MW declares nor conflict of interest and nor funding received for the preparation of this report; OA has received, with approval of the Heinrich Heine University, advisor fees, honoraria, or travel reimbursements from Alexion, Almirall, Biogen, Horizon, MedImmune, Merck, Novartis, Roche, and Teva; research support from the German Science Foundation (DFG), the German Ministry of Education and Research (BMBF), Biogen, and Novartis. He is member of the European Reference Network—Eye Diseases (ERN-EYE) consortium and member of the German Neuromyelitis optica Study Group (NEMOS); SGM received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Bundesinstitut für Risikobewertung (BfR), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Gemeinsamer Bundesausschuss (G-BA), German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Alexion, Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, HERZ Burgdorf, Merck Serono, Novartis, ONO Pharma, Roche, and Teva; PA received research grants from BMS, Celgene, German Research Association, EFRE NRW, Ipsen, Merck, Merz, Novartis and speaker honoraria, travel support and recompensation for serving on advisory boards from Allergan, Abbvie, BMS, Celgene, Ipsen, Hexal, Janssen Cilag, Lilly, Merck, Merz, Novartis, Sanofi, TEVA.
 Alexander Bartnik, Tom A. Fuchs, Kira Ashton, Amy Kuceyeski, Xian Li, Matthew Mallory, Devon Oship, Niels Bergsland, Deepa Ramasamy, and Dejan Jakimovski have nothing to disclose. Ralph H. B. Benedict has received research support from Accorda, Novartis, Genzyme, Biogen Idec, and Mallinkrodt; and is on the speakers’ bureau for EMD Serono; and consults for Biogen Idec, Genentech, Roche, Sanofi/Genzyme, Takeda, NeuroCog Trials, and Novartis. Dr Benedict also receives royalties for Psychological Assessment Resources. Bianca Weinstock-Guttman has participated in speaker’s bureaus and/or served as a consultant for Biogen, Novartis, Genzyme & Sanofi, Genentech, AbbVie, Bayer AG, and Celgene/BMS. Dr Weinstock-Guttman also has received grant/research support from the agencies listed in the previous sentence as well as Mallinckrodt Pharmaceuticals, Inc. She serves in the editorial board for BMJ Neurology, Journal of International MS and CNS Drugs. Robert Zivadinov received personal compensation from Bristol Myer Squibb, EMD Serono, Sanofi, Novartis, and Keystone Heart for speaking and also consultant fees. He received financial support for the research activities from Bristol Myers Squibb, Novartis, Mapi Pharma, Keystone Heart, Genentech, Protembis, V-WAVE Medical, and Boston Scientific. Michael G. Dwyer has received consultant fees from Keystone Heart and research grant support from Novartis, Keystone Heart, and Bristol Myers Squibb.
 The authors have no conflict of interest to declare.



 The authors declare no competing interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Ruth Ann Marrie receives research funding from: Canadian Institutes of Health Research, Research Manitoba, MS Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium of MS Centers, the Arthritis Society, U.S. Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution). In the last 3 years, Jeremy Chataway has received support from the Efficacy and Evaluation (EME) Programme, a Medical Research Council (MRC), and National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Program (NIHR), the UK MS Society, the US National MS Society, and the Rosetrees Trust. He is supported in part by the NIHR University College London Hospitals (UCLH) Biomedical Research Centre, London, UK. He has been a local principal investigator for a trial in MS funded by the MS Canada. He is a local principal investigator for commercial trials funded by Ionis, Novartis, and Roche, and has taken part in advisory boards/consultancy for Azadyne, Biogen, Lucid, Janssen, Merck, NervGen, Novartis, and Roche. Barbara Bierer reports receiving research funding from the National Institutes of Health, US Food and Drug Administration, World Health Organization, Bill & Melinda Gates Foundation, The Greenwall Foundation, and Comprehensive and Integrative Medicine Institute (South Korea). She has served as a consultant on bioethical issues for Merck and Lilly. She serves on the Board of Directors of Clinithink, Edward P. Evans Foundation, Vivli, and North Star Research Board. Marcia Finlayson is a co-investigator on projects funded by the Patient-Centered Outcomes Research Institute, the University Hospitals Kingston Foundation, and the National Multiple Sclerosis Society. She has received consulting/speaker fees from Novartis and Biogen and serves on the editorial board of the IJMSC. Jennifer Panagoulias does not have any disclosures to declare. MP Sormani has received consulting fees from Biogen, Genzyme, GeNeuro, MedDay, Merck, Novartis, Roche, and Teva. Elena Martinez-Lapiscina is an employee of the European Medicines Agency. The views expressed in this article are the personal views of the author(s) and may not be understood or quoted as being made on behalf of or reflecting the position of the European Medicines Agency or one of its committees or working parties. Lilyana Amezcua received personal compensation for consulting, speaking, or serving on steering committees or advisory boards for Biogen Idec, Novartis, Genentech, EMD Serono and research support from the National MS Society, NIH NINDS, Bristol Myer Squibb Foundation, Race to Erase MS and Biogen Idec. She is a local PI for commercial trials funded by Genentech and Sanofi, Genzyme.
 Competing interests: AAT: nothing to disclose. LH: nothing to disclose. KB: nothing to disclose. MK: nothing to disclose. NWMC: nothing to disclose. AW: nothing to disclose. BIL-W: nothing to disclose. EMMS: nothing to disclose. BMJU: received research support and/or consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Teva and Immunic Therapeutics. TR: received funding for research from Genmab; consultancy fees from Novartis. JK: received research grants for multicentre investigator initiated trials DOT-MS trial, ClinicalTrials. gov Identifier: NCT04260711 (ZonMW) and BLOOMS trial (ZonMW and Treatmeds), ClinicalTrials. gov Identifier: NCT05296161); received consulting fees for F. Hoffmann-La Roche, Biogen, Teva, Merck, Novartis and Sanofi/Genzyme (all payments to institution); reports speaker relationships with F. Hoffmann-La Roche, Biogen, Immunic, Teva, Merck, Novartis and Sanofi/Genzyme (all payments to institution); adjudication committee of MS clinical trial of Immunic (payments to institution only). ZLEvK: nothing to disclose.

 A. Gonzalez-Martinez has received education funding from Lilly, Novartis, Roche, TEVA, Abbvie-Allergan, & Daichi. B.C. Healy served on the scientific advisory board for Biogen, Worldwide Medical Biostatistics, Multiple Sclerosis, served on the editorial board for Statistical Methods in Medical Research, received research support from Merck Serono, Genzyme, Novartis, Google Life Sciences, NIH, National Multiple Sclerosis Society. H.L. Weiner has consulted for Genentech, Inc; Tiziana Life Sciences; IM Therapeutics; MedDay Pharmaceuticals; vTv Therapeutics; I-MAB Biopharma and received research support National Institutes of Health; National Multiple Sclerosis Society; Sanofi Genzyme; and Genentech, Inc. T. Chitnis served on clinical trial advisory boards for Novartis Pharmaceuticals, Genzyme-Sanofi, consulted for Biogen Idec, Novartis, Genzyme-Sanofi, Genentech Roche, received research support from EMD Serono, Novartis, Biogen, Verily, National Multiple Sclerosis Society, the Peabody Foundation, the Consortium for MS Centers, Guthy-Jackson Charitable Foundation. R. Patel, H. Lokhande, A. Paul, S. Saxena, and M. Polgar-Turcsanyi have no disclosures.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Competing interests: AS received research support from MSBase. JL received research support from Innosuisse—Swiss Innovation Agency, Biogen and Novartis; he served on advisory boards for Biogen, Novartis, Roche and Teva. SV received consulting and lecture fees, travel grants and research support from Biogen, Celgene, Genentech, Genzyme, Medday Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Aventis and Teva Pharma. MT has served on scientific advisory boards for Biogen, Novartis, Roche and Genzyme; has received speaker honoraria and travel support from Biogen Idec, Sanofi-Aventis, Merck Serono, Teva, Genzyme and Novartis; and has received research grants for her institution from Biogen Idec, Merck Serono and Novartis. JH has received honoraria for serving on advisory boards for Biogen, Sanofi-Genzyme and Novartis; and speaker’s fees from Biogen, Novartis, Merck Serono, Bayer-Schering, Teva and Sanofi-Genzyme. He has served as PI for projects or received unrestricted research support from Biogen Idec, Merck Serono, TEVA, Sanofi-Genzyme and Bayer-Schering; his MS research is funded by the Swedish Research Council and the Swedish Brain Foundation. RH is an employee of Biogen and holds a stock. FP is an employee of Biogen. MM has served on scientific advisory board for Biogen Idec and Teva; and has received honoraria for lecturing from Biogen Idec, Merck Serono, Sanofi-Aventis and Teva. NK-H has received honoraria for lecturing and participating in advisory councils, travel expenses for attending congresses and meetings, and financial support for monitoring the Danish Multiple Sclerosis Treatment Register from Bayer-Schering, Merck Serono, Biogen Idec, Teva, Sanofi-Aventis and Novartis. PSS has served on scientific advisory boards for Merck Serono, Teva, Novartis, Sanofi-Aventis and Biogen Idec; has received research support from Biogen Idec, Novartis and Sanofi-Aventis; and received speaker honoraria from Merck Serono, Novartis, Teva, Sanofi-Aventis, Biogen Idec and Genzyme. TS received compensation for serving on scientific advisory boards, honoraria for consultancy and funding for travel from Biogen; and speaker honoraria from Novartis. AvdW reported receiving grants from National Health and Medical Research Council (NHMRC), Novartis, Roche and MS Research Australia; and personal fees from Biogen, Merck, Novartis and Roche. DH received compensation for travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck Healthcare (Darmstadt, Germany), Bayer, Sanofi, Roche and Teva, as well as support for research activities from Biogen. She was also supported by the Charles University: Cooperation Program in neuroscience. EH received honoraria/research support from Biogen, Merck Serono, Novars, Roche and Teva; has been a member of advisory boards for Actelion, Biogen, Celgene, Merck Serono, Novars and Sanofi Genzyme. MG received consulting fees from Teva Canada Innovation, Biogen, Novartis and Genzyme Sanofi; and lecture payments from Teva Canada Innovation, Novartis and EMD. He has also received a research grant from Canadian Institutes of Health Research. SE received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche and Teva. FG received honoraria or research funding from Biogen, Genzyme, Novartis, Teva Neurosciences, Mitsubishi and ONO Pharmaceuticals. OG has nothing to disclose. MT received travel grants from Novartis, Bayer-Schering, Merck and Teva; and has participated in clinical trials by Sanofi Aventis, Roche and Novartis. SO has nothing to disclose. OS has received honoraria and consulting fees from Bayer Schering, Novartis, Merck, Biogen and Genzyme companies. VVP received travel grants from Merck Healthcare (Darmstadt, Germany), Biogen, Sanofi, Bristol Meyer Squibb, Almirall and Roche. His institution has received research grants and consultancy fees from Roche, Biogen, Sanofi, Merck Healthcare (Darmstadt, Germany), Bristol Meyer Squibb, Janssen, Almirall and Novartis Pharma. MJS received consulting fees, speaker honoraria, and/or travel expenses for scientific meetings from Alexion, Bayer Healthcare, Biogen, Bristol Myers Squibb, Celgene, Janssen, Merck-Serono, Novartis, Roche, Sanofi and Teva. JP accepted travel compensation from Novartis, Biogen, Genzyme and Teva; and speaking honoraria from Biogen, Novartis, Genzyme and Teva. RA received honoraria as a speaker and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche and Sanofi-Genzyme. PAM received speakers fees and travel grants from Novartis, Biogen, T’évalua and Sanofi. RG has nothing to disclose. SM has received a MENACTRIMS clinical fellowship grant (2020). TC-T received speaking/consulting fees and/or travel funding from Bayer, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva. CZ has nothing to disclose. KdG has nothing to disclose. JLS-M accepted travel compensation from Novartis, Merck and Biogen; speaking honoraria from Biogen, Novartis, Sanofi, Merck, Almirall, Bayer and Teva; and has participated in clinical trials by Biogen, Merck and Roche. BY and SK have nothing to disclose. MPS has received consulting fees from Biogen, Merck, Teva, Genzyme, Roche, Novartis, GeNeuro and MedDay. TK reported receiving grants from MS Research Australia and grants, personal fees and non-financial support from Biogen; personal fees and non-financial support from Sanofi Genzyme and Merck; personal fees from Roche, Novartis, WebMD Global, Teva and BioCSL; and grants from NHMRC, MS Research Australia, ARSEP-OFSEP, UK MS Society and Medical Research Future Fund. HB’s institution (Monash University) received compensation for consulting, talks, and advisory/steering board activities from Alfred Health, Biogen, Merck, Novartis, Roche and UCB pharma; research support from Biogen, Merck, Roche, MS Australia, National Health and Medical Research (Australia) and the Medical Research Future Fund (Australia), the Pennycook Foundation, Novartis and Roche. He has received personal compensation for steering group activities from Oxford Health Policy Forum.
 Declaration of Competing Interest On behalf of all authors, the corresponding author states that there is no conflict of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: A.H.H. has no relevant conflicts of interest. A.M. is supported by the Margaretha af Ugglas Foundation. A.G. has received research support from Novartis. O.C. is an NIHR Research Professor and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. She has received research grants from the MS Society of Great Britain & Northern Ireland, National MS Society, NIHR, NIHR UCLH BRC, MRC and Rosetrees Trust. J.H. has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis and Sandoz and speaker’s fees from Biogen, Novartis, Merck KGaA, Teva and Sanofi-Genzyme; he has served as P.I. for projects, or received unrestricted research support from, Biogen, Celgene, Merck KGaA, Novartis, Roche and Sanofi-Genzyme; his MS research was funded by the Swedish Research Council and the Swedish Brain foundation. K.A.M. receives funding from the Swedish Research Council for Health, Working Life and Welfare (Forte).

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: AN: AN is funded by a NMSS Clinician Scientist fellowship. J.S., S.P., A.A.: none. R.A.M.: RAM receives research funding from: Canadian Institutes of Health Research, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium of MS Centers, the Arthritis Society, US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution). H.R.: Research support for clinical trials through the University of California, paid to UCSF: Pfizer, Merck, Novartis, Lilly, Roche, Daiichi, Seattle Genetics, Macrogenics, Sermonix, Polyphor, AstraZeneca, Astellas and Gilead. Honoraria from: Puma, Samsung, Chugai, Blueprint and NAPO. R.B.: R.B. has received research support from NIH, NSF, DOD, NMSS, as well as Biogen, Novartis, and Roche Genentech. She has received consulting or advisory board fees from Alexion, Biogen, EMD Serono, Genzyme Sanofi, Jansen, Novartis, Roche Genentech, TG Therapeutics.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: J.K.: Institution (University Hospital Basel) received and used exclusively for research support; consulting fees (Biogen, Novartis, Protagen AG, Roche, and Teva), speaker fees (Biogen, Novartis, Roche, Sanofi, and Swiss MS Society), travel expenses (Merck Serono, Novartis, and Roche), and grants (Bayer AG, Biogen, Celgene, ECTRIMS Research Fellowship Programme, Merck, Novartis, Roche, Sanofi, Swiss MS Society, Swiss National Research Foundation (320030_160221) and University of Basel). T.C.: Consulting fees (Biogen, Novartis Pharmaceuticals, Roche Genentech, and Sanofi) and research support (National Institutes of Health, National MS Society, U.S. Department of Defense, EMD Serono, I-Mab Biopharma, Novartis Pharmaceuticals, Octave Bioscience, Genentech, Sanofi, and Tiziana Life Sciences). B.B.: Consulting fees (Novartis Pharmaceuticals, Roche, Sanofi, and UCB), nonremunerated advisory input (Biogen, EMD Serono, Novartis Pharmaceuticals, and Teva), and speaker fees (Medscape). M.T.: Research support (Novartis Pharmaceuticals and Sanofi). D.L.A.: Consulting fees (Biogen, Celgene, Frequency Therapeutics, Genentech, Merck, Novartis, Race to Erase MS, Roche, Sanofi, Shionogi, and Xfacto Communications), grants (Immunotec and Novartis), and equity interest (NeuroRx). A.M.R., S.S.G., S.S., and P.T.: Employees of Sanofi, and may hold shares and/or stock options in the company. ALL: Employee of Sanofi and owns shares in Sanofi. L.K.: Institution (University Hospital Basel) has received the following exclusively for research support in the past 3 years: steering committee, advisory board, and consultancy fees (Abbvie, Actelion, AurigaVision AG, Biogen, Celgene, Desitin, Eli Lilly, EMD Serono, Genentech, GlaxoSmithKline, Janssen, Japan Tobacco, Merck, Minoryx, Novartis, Roche, Sanofi, Santhera, Senda, Shionogi, Teva, and Wellmera); speaker fees (Celgene, Janssen, Merck, Novartis, and Roche); support of educational activities (Biogen, Desitin, Novartis, Sanofi, and Teva); license fees for Neurostatus products; and grants (European Union, Innosuisse, Novartis, Roche Research Foundation, Swiss MS Society, and Swiss National Research Foundation).
 The authors declare no conflict of interest.



 J.B.A. has received travel and congress participation funds from Merck. F.S. has served on scientific advisory boards, been on the steering committees of clinical trials, served as a consultant, received support for congress participation, received speaker honoraria, or received research support for his laboratory from Biogen, Merck, Novartis, Roche, Sanofi and Genzyme, and Teva. M.M. has served on scientific advisory board for Biogen, Sanofi, Teva, Roche, Novartis, and Merck; has received honoraria for lecturing from Biogen, Merck, Novartis, Sanofi and Genzyme; and has received research support and support for congress participation from Biogen, Genzyme, Teva, Roche, Merck, and Novartis.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.

 LA discloses travel support and personal compensation for consulting and serving on steering committees or advisory boards for Biogen Idec, EMD Serono, Genentech, and Novartis as well as research support from Biogen Idec, the Bristol Myers Squibb Foundation, the National Institute of Neurological Disorders and Stroke, and the National Multiple Sclerosis Society. NM discloses personal compensation for consulting and serving on steering committee for the CHIMES study sponsored by Genentech and has research support from the National Institute of Neurological Disorders and Stroke. AR discloses serving on steering committee for the CHIMES study sponsored by Genentech. TV reports personal compensation for consulting and serving on steering committees or advisory boards for Biogen Idec, Genentech, TG Therapeutics, and Sanofi/Genzyme, as well as research support from Genentech, the National Institute of Neurological Disorders and Stroke, and the National Multiple Sclerosis Society. Genentech had no part in drafting this article, and no authors have received competing direct financial compensation from Genentech. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors report no disclosures relevant to the manuscript. Go to Neurology.org/NN for full disclosure.
 Disclosure/conflict of interest statement and funding Jalusic K. O. has nothing to disclose. Ellenberger D. has nothing to disclose. Stahmann A. has no personal pecuniary interests to disclose, other than being the lead of the German MS Registry, which receives funding from a range of public and corporate sponsors, recently including The German Innovation Fund (G-BA), The German MS Trust, Biogen, German MS Society, Celgene (BMS), Merck and Novartis. Berger K. received funding from the German Ministry of Education and Research, for a project within the Competence Net Multiple Sclerosis and from the German Innovation Fund (GBA) for the coordination of the VersiMs project (both to the University of Münster).


 Declaration of Competing Interest Lorefice L., Fenu G., Frau J, and Cocco E. received honoraria for consultancy or speaking from Biogen, Novartis, Sanofi, Genzyme, Serono and Teva and Almirall. Caria P., Pilotto S., D'Alterio MN, Fronza M., Murgia F., Dettori T., Frau DV, Atzori L., and Angioni S., have nothing to disclose.
 Declaration of Competing Interest We have no competing interests to declare.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflicts of interest The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosures.


 The authors declare no conflict of interest.

 Declaration of Competing Interest The authors have no competing interests to report.
 I have been supported by a grant from AMED-CREST for basic research on the role of the gut microbiome in multiple sclerosis; received research support from Novartis and Chiome Bioscience; and received speaker honoraria from Novartis, Biogen, Chugai, Alexion, Mitsubishi-Tanabe, and Takeda.

 R.F.N. participates in trials with Sanofi Genzyme and Novartis. None of the other authors has any conflict of interest to disclose.
 Declaration of Competing Interest Authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest The attached manuscript is an unfunded project. The Authors report no significant conflicts of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: VT has received honoraria for consultancy, travel and research grants from Biogen, Merck Serono, Viatris, Allmiral, Bristol Myers Squibb, Novartis, Sanofi. The other authors declare no competing interests.
 Declaration of Competing Interest The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Conflicts of interest: the authors declare there is no conflicts of interest.
 Declaration of Competing Interest None.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Conflict of Interest Statement No conflict of interest exists.

 Declaration of Competing Interest The authors declare no conflict of interest.


 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: I.S. has received honoraria from Merck, Biogen Idec, Neurodiem, Oxford PharmaGenesis and EPG Health.




 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors have no conflicts of interest to disclose.
 The authors have declared that no competing interests exist.


 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Declaration of Competing Interest The authors have no conflict of interest in relation with this work.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 T. Roux déclare des interventions ponctuelles pour Alexion, Biogen, BMS-Celgene, Merck, Novartis, Sanofi Genzyme et avoir été pris en charge à l’occasion de déplacement pour congrès par Biogen, Merck, Teva. E. Maillart et C. Papeix déclarent des interventions ponctuelles pour Biogen, Merck, Novartis, Roche, Teva, Alexion, Sanofi, BMS et avoir été pris en charge à l’occasion de déplacement pour congrès par Biogen, Merck, Novartis, Roche, Teva, Alexion, Sanofi.




 AB declares no competing interests. SG reports honoraria for lectures and travel grants from Alnylam Pharmaceuticals and Merck; and his research is supported by the Deutsche Forschungsgemeinschaft, Else Kröner Fresenius Foundation, Hannover Biomedical Research School, Alnylam Pharmaceuticals, and CSL Behring. KFJ reports travel grants from Merck and Novartis; and his research is supported by the Else Kröner Fresenius Foundation. SGM reports honoraria for lectures and travel grants from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, Teva, and Destitin; and his research is supported by the German Ministry for Education and Research, Bundesinstitut für Risikobewertung, Deutsche Forschungsgemeinschaft, Else Kröner Fresenius Foundation, Gemeinsamer Bundesausschuss, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies Muenster, German Foundation Neurology, Alexion, Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, HERZ Burgdorf, Merck Serono, Novartis, ONO Pharma, Roche, and Teva. TS reports honoraria for lectures and travel grants from Alexion, Alnylam Pharmaceuticals, Argenx, Bayer Vital, Biogen, Celgene, Centogene, CSL Behring, Euroimmun, Janssen, Merck Serono, Novartis, Pfizer, Roche, Sanofi, Siemens, Sobi, and Teva; and his research is supported by the German Ministry for Education and Research, Bristol-Myers Squibb Foundation for Immuno-Oncology, Claudia von Schilling Foundation for Breast Cancer Research, Else Kröner Fresenius Foundation, Hannover Biomedical Research School, Alnylam Pharmaceuticals, CSL Behring, Novartis, Sanofi Genzyme, and VHV Foundation.
 The authors declare that there are no commercial or financial conflict of interest in the context of this work.

 The authors have no conflict of interests to declare.
 SM: received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi- Aventis, Chugai Pharma, QuintilesIMS, and Teva. PA is employed by the Clinic Maria Hilf GmbH, Germany. He received a research grant from Ipsen Pharma to support the analysis of the data of patients with spasticity and a grant from Merz Pharmaceuticals for funding of NAB-testing. Besides this, he reports grants, personal fees and non-financial support from Allergan, Biogen, Ipsen, Merz Pharmaceuticals, Merck, Novartis, and Roche, personal fees and non-financial support from Bayer Healthcare, and non-financial support from Sanofi-Aventis/Genzyme. RM reports personal fees from Actelion, Biogen and Medison Pharma; grants, personal fees and other from Merck Serono and Teva; personal fees and other from Novartis, Roche; other from TG Therapeutics and MAPI-Pharma, outside the submitted work. H-PH: has received fees for consulting, speaking, and serving on steering committees from Bayer HealthCare, Biogen Idec, Celgene Receptos, CSL Behring, GeNeuro, Genzyme, Horizon Therapeutics formerly Viela Bio, MedDay, MedImmune, Merck Serono, Novartis, Roche, Sanofi, and TG Therapeutics with approval by the Rector of Heinrich Heine University Düsseldorf. JM: presentations and participation in Advisory Boards: Biogen, Novartis, Roche, Sanofi, Merck and Teva. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest.
 Competing interests: None declared.


 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of competing interest The Authors have no competing interest to declare.

 The authors declare no conflict of interest.
 S.T. has shares in Tzartos NeuroDiagnostics. All other authors have no potential conflict of interest to report.
 Declaration of Competing Interests KB has participated in meetings sponsored by and received travel funding from Roche, Biogen and Teva. FDP has participated in meetings sponsored by, received honoraria (lectures, advisory boards, consultations) or travel funding from Almirall, Bayer, Biogen, Celgene, Janssen, Merck, Novartis, Sanofi-Genzyme, Roche and Teva. Her institution has received research grants from Roche. MA received speaker honoraria and/or travel grants from Biogen, Merck, Novartis and Sanofi. AZ has participated in meetings sponsored by, received speaking honoraria or travel funding from Biogen, Merck, Sanofi-Genzyme and Teva. JW has nothing to disclose. FD has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Almirall, Alexion, Biogen, Celgene, Genzyme-Sanofi, Merck, Novartis Pharma, Roche, and TEVA ratiopharm. His-institution has received research grants from Biogen and Genzyme Sanofi. He is section editor of the MSARD Journal (Multiple Sclerosis and Related Disorders). HH has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Siemens, Teva, and received honoraria for acting as consultant for Biogen, Celgen, Novartis and Teva.





 Conflicto de intereses: Los autores no tienen ningún conflicto de interés que declarar.
 The authors have no conflicts of interest to report.

 The authors have declared that no conflict of interest exists.
 VG is an employee and shareholder of Hoffmann-La Roche. No specific funding was received for the conduct of this project from Hoffmann-La Roche and the work and ideas presented are the authors alone. KM and DH have no competing interests.



 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest All the authors on this manuscript submission report no disclosures. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
 The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
 Competing interests: All authors (KK, HG, EF, CM, JH, AK, TO, KA) are employed or affiliated at the Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. KK is currently employed by Celgene/Bristol Myers Squibb; she initiated this study while being employed at Karolinska Institutet (employment ended in October 2019); since then, she has received no salary from Karolinska Institutet or other type of funding for this research. HG is currently employed part-time by Statfinn/EPID Research (which is part of IQVIA); both companies are contract research organisations that perform commissioned pharmacoepidemiological studies, and therefore are collaborating with several pharmaceutical companies. CM since submission of this paper has begun employment with Macanda AB. AK is currently also employed by Takeda Pharma AB. JH, KA and EF are collaborating with several pharmaceutical companies; EF has received an unrestricted MS research grant from Celgene/Bristol Myers Squibb. TO has received advisory board and/or lecture honoraria, and unrestricted MS research grants from Biogen, Novartis, Sanofi, Merck and Roche.
 The authors declare no competing interests. The authors declare no competing interests.



 The authors declare no competing interests.

 Conflicts of interest and sources of funding: none declared.
 S. Pfeuffer received travel grants from Sanofi-Aventis and Merck Serono, lecturing honoraria from Sanofi-Aventis, Mylan Healthcare, and Biogen Idec, and research support from Diamed, Merck Serono, and the German Multiple Sclerosis Society North-Rhine-Westphalia. L. Rolfes received travel reimbursements from Merck Serono and Sanofi-Aventis. J. Ingwersen declares no conflicts of interest. R. Pul received honoraria for lecturing and consulting from Alexion, Bayer HealthCare, Biogen Idec, Bristol-Mayers Squibb, MedDay, Merck Serono, Mylan, Novartis, Roche, and Sanofi-Aventis. He received research funding from HERZ Burgdorf, Merck Serono, and Novartis. K. Kleinschnitz, M. Korsen, and S. Räuber declare no conflicts of interest. T. Ruck reports grants from the German Ministry of Education, Science, Research and Technology, grants and personal fees from Sanofi-Aventis and Alexion, personal fees from Biogen Idec, Roche, and Teva, and personal fees and nonfinancial support from Merck Serono, outside the submitted work. S. Schieferdecker and A. Willison declare no conflicts of interest. O. Aktas reports grants from the German Research Foundation, German Ministry of Education and Research, Roche, Novartis, and Biogen and personal fees from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi, Teva, and Viela Bio, outside the submitted work. C. Kleinschnitz received honoraria for lecturing and consulting and financial research support from Ablynx, Almirall, Amgen, Bayer Vital, Bristol-Mayers Squibb, Biotronik, Boehringer Ingelheim, Biogen Idec, CSL Behring, Daiichi-Sankyo, Desitin, Eisai, Ever Pharma, Sanofi-Aventis, Merck Serono, Mylan, MedDay, Novartis, Pfizer, Roche, Siemens, Stago, and Teva. H.-P. Hartung received personal fees for serving on steering and data monitoring committees and lecturing from Bayer HealthCare, Biogen, BMS Celgene, GeNeuro, MedDay, Merck, Novartis, Roche, TG Therapeutics, and Viela Bio. L. Kappos' institution (University Hospital Basel) has received the following exclusively for research support: steering committee, advisory board, and consultancy fees from Actelion, Bayer HealthCare, Biogen, BMS, Genzyme, GlaxoSmithKline, Janssen, Japan Tobacco, Merck, Novartis, Roche, Sanofi, Santhera, Shionogi, and TG Therapeutics, speaker fees from Bayer HealthCare, Biogen, Merck, Novartis, Roche, and Sanofi, support of educational activities from Allergan, Bayer HealthCare, Biogen, CSL Behring, Desitin, Genzyme, Merck, Novartis, Roche, Pfizer, Sanofi, Shire, and Teva, license fees for Neurostatus products, and grants from Bayer HealthCare, Biogen, European Union, InnoSwiss, Merck, Novartis, Roche, Swiss MS Society, and Swiss National Research Foundation. S.G. Meuth received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen Idec, Celgene, Diamed, Sanofi-Aventis, MedDay, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Bundesinstitut für Risikobewertung (BfR), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Gemeinsamer Bundesausschuss (G-BA), German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology, and by Alexion, Almirall, Amicus Therapeutics Germany, Biogen Idec, Diamed, Fresenius Medical Care, Sanofi-Aventis, HERZ Burgdorf, Merck Serono, Novartis, ONO Pharma, Roche, and Teva. Go to Neurology.org/NN for full disclosures.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors report no competing interests.

 Declaration of competing interest The authors have no competing interests to disclose.
 Concerning the topic of the paper, none of the authors have a conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 All authors have seen and approved the manuscript. Work for this study was performed at West China Hospital of Sichuan University, China. Xiangdong Tang was supported by the Ministry of Science and Technology of the People’s Republic of China (2021ZD0201900) and the National Natural Science Foundation of China (82120108002). Ye Zhang was supported by the National Natural Science Foundation of China (82170099). Rong Ren was supported by the National Natural Science Foundation of China (82170100). The authors report no conflicts of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Ms McKenna, Dr Lin, Dr Whittington, Mr Nikitin, Ms Herron-Smith, Dr Campbell, and Dr Peterson report grants from Arnold Ventures, grants from Blue Cross Blue Shield of MA, grants from California Healthcare Foundation, grants from The Commonwealth Fund, and grants from The Peterson Center on Healthcare, during the conduct of the study; other from America’s Health Insurance Plans, other from Anthem, other from AbbVie, other from Alnylam, other from AstraZeneca, other from Biogen, other from Blue Shield of CA, other from CVS, other from Editas, other from Express Scripts, other from Genentech/Roche, other from GlaxoSmithKline, other from Harvard Pilgrim, other from Health Care Service Corporation, other from Kaiser Permanente, other from LEO Pharma, other from Mallinckrodt, other from Merck, other from Novartis, other from National Pharmaceutical Council, other from Premera, other from Prime Therapeutics, other from Regeneron, other from Sanofi, other from United Healthcare, other from HealthFirst, other from Pfizer, other from Boehringer-Ingelheim, other from uniQure, other from Envolve Pharmacy Solutions, other from Humana, and other from Sun Life, outside the submitted work.


 No potential conflict of interest was reported by the author(s).
 The authors have declared that no competing interests exist.
 All authors declare that they have no competing interests.
 Declaration of Competing Interest Dr Spelman has received honoraria for consultancy and funding for travel from Biogen and Novartis. Dr Horakova has received speaker honoraria and consulting fees from Biogen, Merck, Novartis, Roche, Sanofi Genzyme, and Teva, as well as support for research activities from Biogen and the Czech Ministry of Education (project Progres Q27/LF1). Dr Alroughani has received honoraria as a speaker and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche, and Sanofi Genzyme. Dr Kalincik has served on scientific advisory boards for Biogen, Merck, Novartis, Roche, and Sanofi Genzyme and a steering committee for Genzyme's Brain Atrophy Initiative; has received conference travel support and/or speaker honoraria from BioCSL, Biogen, Merck, Novartis, Sanofi Genzyme, Teva, and WebMD Global; and has received research support from Biogen. Dr Terzi has received travel grants from Bayer Schering, Merck, Novartis, and Teva and has participated in clinical trials by Novartis, Roche, and Sanofi. Dr Grammond has served on advisory boards for Biogen, Genzyme, Merck, Novartis, and Teva Neuroscience and as a consultant for Merck; has received payments for lectures from Merck, Teva Neuroscience, and the Canadian Multiple Sclerosis Society; and has received grants for travel from Novartis and Teva Neuroscience. Dr Patti has received speaker honoraria or advisory board fees from Almirall, Bayer, Biogen, Celgene, Merck, Mylan, Novartis, Roche, Sanofi Genzyme, and Teva and research funding from Biogen, Merck, the Italian Ministry of Education, University and Research, and the Italian Multiple Sclerosis Society Foundation. Dr Csepany has received speaker honoraria and/or conference travel support from Bayer Schering, Biogen, Merck, Novartis, Roche, Sanofi, and Teva. Dr Boz has received conference travel support from Bayer Schering, Biogen, Merck, Novartis, and Teva and has participated in clinical trials by Novartis, Roche, and Sanofi. Dr Lechner-Scott has received travel compensation from Biogen, Merck, and Novartis and has been involved in clinical trials with Biogen, Novartis, and Teva. Her institution has received honoraria for talks and advisory board service from Bayer HealthCare, Biogen, Merck, Novartis, Sanofi Genzyme, and Teva. Dr Granella has received research funding from Biogen and Sanofi Genzyme; fees for advisory boards and speaker honoraria from Biogen, Merck Serono, Novartis, Roche, and Sanofi Genzyme; and travel funding from Biogen, Merck Serono, Roche, and Sanofi Genzyme. Dr Grand'Maison has received honoraria or research funding from Biogen, Genzyme, Mitsubishi, Novartis, Ono Pharmaceuticals, and Teva Neuroscience. Dr. van der Walt reports grants from Roche and Novartis; and has served on advisory boards for and received travel support from Merck, Roche, Biogen, Novartis, Alexion, and BMS. Dr Butzkueven has served on scientific advisory boards for Biogen, Novartis, and Sanofi and steering committees for trials conducted by Biogen and Novartis; has received conference travel support from Biogen, Novartis, and Sanofi; and has received research support from Biogen, Merck, and Novartis. Drs Ozakbas, Onofrj, Prat, and Zhu have nothing to disclose.
 Competing interests: RD, DR, KM, SH, ORP, HLF, NB-M, SW and PB are on the steering committee for the UK MS Pregnancy Register, which seeks to improve our understanding of the safety of DMT in pregnancy. RD has received honoraria for sitting on advisory boards from Roche and Novartis. She sits on the steering committee for the MINORE and SOPRANINO studies, which are examining the safety of ocrelizumab in pregnancy and breastfeeding. She receives grant support from the UK MS Society, BMA foundation, NIHR, MRC, NMSS, Horne Family Charitable Trust, Biogen, Celgene, and Merck. She has received honoraria for advisory boards and/or educational activities from Biogen, Teva, Sanofi, Merck, Janssen, Novartis, and Roche. DR has received honoraria for sitting on advisory boards and/or speaker fees from from Biogen, Celgene, Hikma, Janssen, MedDay, Merck Serono, Novartis, Roche, Sanofi, Teva Neuroscience. He is the UK Coordinating Investigator for Tecfidera, Aubagio and Lemtrada pregnancy registries. He has received research support, paid to his institution, from Actelion, Biogen, Janssen, Merck Serono, Mitsubishi, Novartis, Sanofi, Teva Neuroscience, TG Therapeutics. CO consults for Mirum Pharmaceuticals. KM reports honoraria for advisory boards/educational activities from Biogen, Roche, Merck, Teva, Novartis, Sanofi. ORP has received honoraria for advisory boards and/or educational activities from Biogen, Teva, Sanofi, Merck, Janssen, Novartis, and Roche. SH has received unrestricted educational grants or speaking honoraria from Biogen, Merck Serono, Novartis, Roche and Sanofi Genzyme. NB-M has nothing to declareSW reports honoraria for advisory boards and/or educational activities from Biogen, Sanofi, Merck, Janssen, Novartis, Roche and Celgene. CN-P reports speakers fees from UCB, Sanofi, Jansen, and Alexion. PB has received honoraria for advisory boards and/or educational activities from Merck, Biogen, Roche, MS Academy, Janssen, Sanofi-Genzyme, Teva and MedDay Pharmacuticals.
 The authors declare no conflict of interest.


 Declaration of Competing Interest Francesco Patti has received honoraria for speaking activities by Almirall, Bayer Schering, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA; he also served as advisory board member the following companies: Bayer Schering, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA; he was also funded by Pfizer and FISM for epidemiological studies; he received grants for congress participation from Almirall, Bayer Shering, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. Clara G. Chisari has received grants for congress participation from Almirall, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. Simona Toscano declares no conflict of interest. Pietro Annovazzi has received honoraria for lecturing and participation in advisory boards, and/or travel expenses for attending congresses and meetings from Almirall, Biogen Idec, Merck Serono, Mylan, Novartis, Roche, Sanofi Genzyme, and TEVA. Paola Banfi has received support for attendance to scientific meetings from Biogen Idec, Merck Serono, Novartis, and Sanofi Genzyme. Roberto Bergamaschi has received honoraria for lectures, travel and registration coverage for attending several national or international congresses or symposia from Almirall, Bayer Shering, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Aventis, Sanofi Genzyme, and TEVA. Raffaella Clerici has received speaker's honoraria, consulting fees, honoraria in advisory boards, support for attendance of scientific meetings from Meck Serono, Novartis, and Sanofi Genzyme. Marta Zaffira Conti declares there is no conflict of interest. Antonio Cortese has received speaker honoraria, travel grants, advisory boards member honoraria from Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, and TEVA. Roberta Fantozzi has received consulting fees and honoraria for advisory boards from Biogen Idec, Merck Serono, Novartis, Roche, and TEVA Diana Ferraro declares there is no conflict of interest. Mariano Fischetti declares there is no conflict of interest. Maura Frigo declares there is no conflict of interest. Maurizia Gatto declares there is no conflict of interest. Paolo Immovilli has received speaking honoraria, consulting fees, advisory board honoraria from Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. Stefania Leoni declares there is no conflict of interest. Simona Malucchi has received speaker's honoraria and consulting fees, honoraria in advisory boards from Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, and TEVA Giorgia Maniscalco has received honoraria for public speaking and advisory boards from Biogen, Novartis, and Merck Serono. Girolama Alessandra Marfia is an Advisory Board member of Biogen Idec, Sanofi Genzyme, Merck-Serono, Novartis, and TEVA, and received honoraria for speaking or consultation fees from Almirall, Bayer Schering, Biogen Idec, Merck Serono, Novartis, Sanofi-Genzyme, and TEVA. She is the principal investigator in clinical trials for Actelion, Biogen Idec, Merck Serono, Mitsubishi, Novartis, Roche, Sanofi-Genzyme, and TEVA Damiano Paolicelli has received honoraria for consultancy and/or speaking from Almirall, Bayer Shering, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. Paola Perini has received speaker honoraria and consulting fees from Biogen, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. Carlo Serrati declares no conflict of interest. Rocco Totaro has received speaker's honoraria, consulting fee, honoraria for advisory boards, support for attendance of scientific meetings from Alfa Wasserman, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi genzyme, and TEVA. Gabriella Turano has received support for attendance to scientific meetings from Almirall, Biogen Idec, Merck Serono, Novartis, and Sanofi Genzyme. Paola Valentino has received speaker's honoraria and consulting fee, honoraria for advisory boards from Biogen Idec, Novartis, Merck Serono, Sanofi Genzyme, and TEVA. Mauro Zaffaroni has received honoraria for lecturing or participating for advisory boards or travel funding from Almirall, Biogen, Merck Serono, Novartis, Sanofi Genzyme, and TEVA. Cristina Zuliani has received speaker's honoraria and consulting fees, honoraria for advisory boards, support for attendance of scientific meetings from Almirall, Bayer Shering, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. Diego Centonze is an Advisory Board member of Almirall, Bayer Schering, Biogen Idec, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA, and received honoraria for speaking or consultation fees from Almirall, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and TEVA. He is also the principal investigator in clinical trials for Bayer Schering, Biogen, Merck Serono, Mitsubishi, Novartis, Roche, Sanofi Genzyme, and TEVA. His preclinical and clinical research was supported by grants from Bayer Schering, Biogen Idec, Celgene, Merck Serono, Novartis, Roche, Sanofi Genzyme and TEVA.


 Declaration of Competing Interest We report no financial conflicts of interest with the research reported in this paper.
 Declaration of Competing Interest F.S. has served on scientific advisory boards, been on the steering committees of clinical trials, served as a consultant, received support for congress participation, received speaker honoraria, or received research support for his laboratory from Biogen, Merck, Novartis, Roche, Sanofi Genzyme and Teva. P.S.S. has received personal compensation for serving on scientific advisory boards, steering committees, independent data monitoring committees or have received speaker honoraria for Biogen, Merck, Novartis, TEVA, GlaxoSmithKline, and Celgene. KS has served on the scientific advisory board for Biogen Idec, Merck and has received honoraria for lecturing and support for congress participation from Biogen Idec, Genzyme, Teva, Merck, and Novartis. R.R. has had travel expences reimbursed by Roche. M.M. has served on scientific advisory board for Biogen, Sanofi, Roche, Novartis, Merck and AbbVie, has received honoraria for lecturing from Biogen, Merck, Novartis, Sanofi, Genzyme, has received research support and support for congress participation from Biogen, Genzyme, Teva, Roche, Merck, Novartis. H.R.S has received honoraria as speaker from Sanofi Genzyme, Denmark and Novartis, Denmark, as consultant from Sanofi Genzyme, Denmark and Lundbeck AS, Denmark, and as editor-in-chief (Neuroimage Clinical) and senior editor (NeuroImage) from Elsevier Publishers, Amsterdam, The Netherlands. He has received royalties as book editor from Springer Publishers, Stuttgart, Germany and from Gyldendal Publishers, Copenhagen, Denmark. J.R.C has received honoraria for lecturing from Biogen. C.A., T.D., P.I., P.H.J. and L.B. have nothing to declare.
 I have received funding support from the National Institutes of Health, National MS Society, US Department of Defense, Sumaira Foundation, Brainstorm Cell Therapeutics, Bristol Myers Squibb, EMD Serono, I-Mab Biopharma, Novartis Pharmaceuticals, Octave Bioscience, Roche Genentech, Sanofi Genzyme, and Tiziana Life Sciences. I have served as a consultant to Banner Life Sciences, Biogen, Bristol Myers Squibb, Janssen, Novartis Pharmaceuticals, Roche Genentech, Sanofi Genzyme, and UCB Biopharma.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest YY has been supported by travel grants from Novartis and Sanofi Genzyme, has received an honorarium for active participation in an advisory board by Sanofi Genzyme as well as speaking honoraria by Roche, Sanofi Genzyme, TEVA and Bristol Myers Squibb and RG Gesellschaft für Information und organisation mbH. His research is funded by the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG) and Heinrich und Erna Schaufler Foundation. SB has received funding for travel expenses for attending meetings from Merck Serono and honoraria from Biogen Idec, Bristol Meyer Squibb, Merck Serono, Novartis, Roche, Sanofi Genzyme and TEVA. His research is funded by Deutsche Forschungsgemeinschaft (DFG) and Hertie foundation. CF reports speaker honoraria and honoraria for participating in advisory boards from Alexion, Bristol Myers Squibb, Novartis, Teva, Merck, Sanofi-Genzyme, and Roche. CF received research support from Novartis and Sanofi-Genzyme. All other authors report no conflicts of interest.
 N.S. received support from Biogen.



 Declaration of Competing Interest Henry Bailey, Avidesh Panday, Sorita Lucky Samaroo and Anujh Maharajh declare that they have no conflicts of interest.
 The author declares no conflict of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest Simon Englund declare that there is no conflict of interest; Marie Kierkegaard has received honoraria for lectures from Sanofi, Genzyme Roche and Novartis; Joachim Burman declare that there is no conflict of interest; Katharina Fink has received lecture honoraria from Biogen and Merck, has served on scientific advisory boards for Biogen, Roche, Merck and Alexion, has received a research grant from Amicus; Anna Fogdell-Hahn has received unrestricted funding from Biogen Idec, Pfizer, Orion Pharma and Celltrion, speaking honoraria from Merck, and consulting fee from Roche; Martin Gunnarsson declare that there is no conflict of interest; Jan Hillert has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis and Sandoz and speaker's fees from Biogen, Novartis, Merck KGaA, Teva and Sanofi-Genzyme. He has served as P.I. for projects, or received unrestricted research support from, Biogen, Celgene, Merck KGaA, Novartis, Roche and Sanofi-Genzyme. His MS research was funded by the Swedish Research Council and the Swedish Brain foundation; Annette Langer-Gould receives grant support and awards from the Patient Centered Outcomes Research Institute and the National MS Society; she currently serves as a voting member on the California Technology Assessment Forum, a core program of the Institute for Clinical and Economic Review (ICER). She has received sponsored and reimbursed travel from ICER and the National Institutes of Health; Jan Lycke has received travel support and/or lecture honoraria from Biogen, BMS, Novartis, Sanofi, Roche and Alexion, has served on scientific advisory boards for Biogen, BMS, Novartis, Sanofi, Roche and Alexion, serves on the editorial board of the Acta Neurologica Scandinavica, and has received unconditional research grants from Biogen and Novartis. Petra Nilsson has received travel support from Bayer Schering Pharma, Merck Serono, Biogen and Genzyme a Sanofi Company, honoraria for lectures and advisory boards from Merck Serono and Genzyme a Sanofi Company, advisory boards for Novartis and Roche, lectures for Biogen and has received unrestricted grants from Biogen. Jonatan Salzer has received institutional fees from Mabion S.A. for serving as a consultant in a clinical trial. Anders Svenningsson declare that there is no conflict of interest; Johan Mellergård has received honoraria for Advisory boards for Sanofi Genzyme and Merck and lecture honoraria from Merck; Tomas Olsson has received honoraria for lectures/advisory boards, and unrestricted MS research grants from Biogen, Novartis, Sanofi, Merck and Roche; Elisa Longinetti declare that there is no conflict of interest; Thomas Frisell declare that there is no conflict of interest; Fredrik Piehl has received research grants from Janssen, Merck KGaA and UCB, and fees for serving on DMC in clinical trials with Chugai, Lundbeck and Roche, and preparation of expert witness statement for Novartis. There is no commercial entity relevant for potential conflicts.


 The authors declare that they have no competing interests.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no competing interests.

 Declaration of Competing Interest Aurélien Massire is an employee of Siemens Healthcare SAS and Alto Stemmer is an employee of Siemens Healthcare GmbH. The remaining authors of this manuscript declare no relationships with any companies, whose products or services may be related to the subject matter of the article.
 S. Vukusic has received lecturing fees, travel grants, and research support from Biogen, BMS-Celgene, Janssen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. P. Nicolas, H. Marion-Moffet, M. Gossez, G. Monneret, R. Marignier, and F. Venet report no disclosure relevant to the subject of this manuscript.
 The authors declare no competing interests.
 The authors report no financial relationships with commercial interests.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare there is no conflict of interests.
 The author declares no competing interests.
 Competing interests The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: N.G., T.R., J.H.A., A.V., R.M., and E.B. reports no disclosures. K.M.M. reports grants or personal fees from Biogen, Novartis, Roche, Teva and Sanofi, outside the submitted work. E.G.C. reports grants or personal fees from Almirall, Biogen, Merck, Novartis, Roche, Sanofi Genzyme and Teva, outside the submitted work. Ø.T. reports personal fees from Biogen, Merck, Sanofi, Roche, and Teva, outside the submitted work.
 Declaration of Competing Interest The authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest in the subject matter or materials discussed in this manuscript.
 CR was supported by fortüne/PATE grant no 2536-0-0/1 by the medical faculty, University of Tübingen. CK is currently an employee of CureVac AG Tübingen, Germany, not related to this work. SP received research support from BMS/Pfizer, Boehringer-Ingelheim, Daiichi Sankyo, European Union, German Federal Joint Committee Innovation Fund, and German Federal Ministry of Education and Research, Helena Laboratories and Werfen as well as speakers’ honoraria/consulting fees from Alexion, AstraZeneca, Bayer, Boehringer-Ingelheim, BMS/Pfizer, Daiichi Sankyo, Portola, and Werfen all outside the submitted manuscript. MK has served on advisory boards and received speaker fees/travel grants from Merck, Sanofi-Genzyme, Novartis, Biogen, Jansen, Alexion, Celgene/Bristol-Myers Squibb and Roche. MK also received research grants from Merck, Sanofi-Genzyme and Celgene/Bristol-Myers Squibb, Novartis, Janssen. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Maria Petracca has received travel/meeting expenses from Novartis, Roche and Merck, speaking honoraria from HEALTH&LIFE S.r.l., honoraria for consulting services from Biogen and research grants from Baroni Foundation. Raffaele Palladino has nothing to disclose. Amgad Droby has nothing to disclose. Nicole Graziano has nothing to disclose. Katherine Wang has nothing to disclose. Daniel Kurz has nothing to disclose. Claire Riley reports personal fees from Teva Neuroscience, personal fees from Genzyme Sanofi, personal fees from Genentech, personal fees from Celgene, personal fees from Biogen Idec, personal fees from EMD Serono. Jonathan Howard has nothing to disclose. Sylvia Klineova has nothing to disclose. Fred Lublin reports grants and personal fees from Novartis, Biogen Idec, Teva Neuroscience, Sanofi/Genzyme, Celgene, grants from Transparency Life Sciences and personal fees from Bayer Healthcare, EMD Serono, Actelion, Acorda, Questcor/Malinckrodt, Roche/Genentech, Medimmune, Osmotica, Xenoport, Receptos, Forward pharma, BBB Technologies, Akros, TG therapeutics, Abbvie, MedDay and Atara Biotherapeutics. Matilde Inglese received grants NIH, NMSS, FISM; received fees for consultation from Roche, Genzyme, Merck, Biogen and Novartis.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: R.W.T. and N.L. are shareholders in One Health Vaccines, which has an interest in vaccines against Clostridium perfringens epsilon toxin.
 Declaration of Competing Interest The authors have no conflicts of interest to report.
 There are no conflicts of interest to declare.
 Conflicts of interest the authors declare no conflicts of interest.


 Declaration of Competing Interest None.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 C.Y.C. is a founder and is on the scientific advisory board for Delve Bio. C.Y.C. is also an inventor on US patent 11380421, “Pathogen Detection using Next Generation Sequencing,” under which algorithms for taxonomic classification, filtering, and pathogen detection are used by SURPI+ software. M.R.W. is a founder and is on the scientific advisory board for Delve Bio. C.Y.C. The other authors declare no competing interests. Go to Neurology.org/NN for full disclosures.
 Declaration of Competing Interest The authors declare that there are no conflicts of interest regarding the publication of this article.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: Biogen, Merck, Novartis, Roche, Sanofi/Genzyme, Teva all manufacture multiple sclerosis disease-modifying therapies that were used in this study, or which could be affected by the study. The following authors have received speaker fees, consultancy fees and/ or travel expenses to attend educational meetings from one or more of these companies: E.C.T., D.B., R.D., G.I., K.E.H., N.E., G.G., A.S.K., N.P.R., M.W. and K.S. The following authors declare no conflicts of interest: S.A.Z., M.U., C.H.W., A.R., P.T., N.V., V.A., R.C., K.G., A.H., A.S.K., S.L., S.J.M. and S.J.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare no competing interests.
 The authors declare no competing interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: G.G. has received speaker honoraria and consulting fees from AbbVie, Actelion (Janssen/J&J), Atara Bio, Almirall, Bayer, Biogen, Celgene (BMS), FivePrime, GlaxoSmithKline, GW Pharmaceuticals, Ironwood, Merck & Co., Merck, Novartis, Pfizer Inc., Protein Discovery Laboratories, Roche, Sanofi, Teva, UCB, and Vertex Pharmaceuticals, and has received research support unrelated to this study from Biogen, Ironwood, Merck & Co., Merck, Novartis, and Takeda. A.B. has received honoraria as member of working groups, advisory boards and participated in clinical trials supported by Actelion (Janssen/J&J), Bayer, Biocad, Biogen, Generium, Merck, Mylan, Novartis, Roche, Sanofi, and Teva. J.C. is a board member of Merck-Serono Argentina, an affiliate of Merck KGaA, Biogen LATAM, Merck-Serono LATAM, an affiliate of Merck KGaA, and Genzyme Global. Dr J.C. has received reimbursement for developing educational presentations for Merck-Serono Argentina, an affiliate of Merck KGaA, Merck-Serono LATAM, an affiliate of Merck KGaA, Biogen Argentina, Genzyme Argentina, and TEVA Argentina, as well as professional travel/accommodations stipends. G.E. has received consulting fees and research support from Biogen, Merck, Novartis, Roche, Sanofi, and Teva. M.S.F. has received honoraria or consultation fees from Alexion, Apotex, Atara Biotherapeutics, Bayer, BeiGene, BMS (Celgene), EMD Inc., Canada, an affiliate of Merck KGaA, Janssen (J&J), Merck, Novartis, Roche, and Sanofi; has been a member of a company advisory board, board of directors, or other similar group for Alexion, Atara Biotherapeutics, Bayer, BMS (Celgene), Janssen (J&J), McKesson, Merck, Novartis, Roche, and Sanofi; has participated in a company sponsored speaker’s bureau for EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA and Sanofi; and has been in receipt of research or educational grants from Sanofi. X.M. has received speaking honoraria and travel expenses for participation in scientific meetings, and has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Actelion (Janssen/J&J), Alexion, Bayer, Biogen, Celgene (BMS), EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, Immunic, Janssen (J&J), MedDay, Merck, Mylan, NervGen, Novartis, Roche, Sanofi, Teva, TG Therapeutics, Excemed, MSIF, and NMSS. K.R. has received honoraria for lectures and steering committee meetings from Acorda, Biogen, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, Novartis, Roche, Sanofi, and Teva. D.S. has received consulting fees from Acorda, Biogen, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, and Teva, and speaker fees from Acorda, Biogen, Elan, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, and Teva. B.Y. has received honoraria for lectures and advisory boards from Bayer, Biogen, Genpharm, Merck, Novartis, and Sanofi, and has received research grants from Bayer, Biogen, Merck, Novartis, and Pfizer. T.L. has received consultancy fees or clinical research grants from Acorda, Bayer, Biogen, Daiichi Sankyo, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, Novartis, ONO, Pfizer, and Teva. A.A. and E.V.d.C. are employees of EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. L.B. is a medical consultant to Merck Healthcare KGaA, Darmstadt, Germany.
 MH received speaking fees and travel funds from Bayer HealthCare, Biogen, Merck, Novartis and Teva. NB received travel funds from Novartis. IL-P is an employee of Miltenyi Biotec. AW received speaking fees and travel funds from Biogen, GlaxoSmithKline, Merck Serono, Novartis and Sanofi Genzyme. UKZ received research support as well as speaking fees and travel funds from Alexion, Almirall, Bayer HealthCare, Biogen, Bristol Myers Squibb, Janssen, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva as well as EU, BMBF, BMWi and DFG. BF, EP, RE, WB, MM, MS, SM, AD and DK declare that they have no competing interests.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: J.R.H owns controlling interest in Connecting Health Innovations LLC (CHI), a company that has licenced the right to his invention of the dietary inflammatory index (DII(®)) from the University of South Carolina in order to develop computer and smartphone applications for patient counselling and dietary intervention in clinical settings. N.S. is an employee of CHI. J.R.H. and N.S. calculated the DII scores and contributed to the data interpretation and writing of the manuscript, but they had no role in the data analysis.


 Declaration of Competing Interest None.
 Declaration of Competing Interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Declaration of competing interest There are no conflicts of interest to declare.

 Declaration of Competing Interest The author(s) declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Irina Kalatskaya and P. Alexander Rolfe are employees of EMD Serono Research & Development Institute, Inc., Billerica, MA, USA (an affiliate of Merck KGaA). Gavin Giovannoni has received speaker honoraria and consulting fees from AbbVie, Actelion (Janssen/J&J), Atara Bio, Almirall, Bayer, Biogen, Celgene (BMS), FivePrime, GlaxoSmithKline, GW Pharma, Ironwood, Merck, Novartis, Merck & Co., Pfizer Inc., Protein Discovery Laboratories, Roche, Sanofi-Genzyme, Teva Pharmaceutical Industries Ltd, UCB, and Vertex Pharmaceuticals; and has received research support unrelated to this study from Biogen, Ironwood, Merck, Novartis, Merck & Co., and Takeda. Thomas Leist has received consultancy fees or clinical research grants from Acorda, Bayer, Biogen, Daiichi, EMD Serono, Inc. (an affiliate of Merck KGaA), Novartis, ONO, Pfizer, and Teva Neuroscience. Joseph Cerra was affiliated at the time of this analysis to EMD Serono Research & Development Institute, Inc., Billerica, MA, USA (an affiliate of Merck KGaA). Current affiliation: Northeastern University, Boston, MA, USA. Ursula Boschert is an employee of Ares Trading S.A., Eysins, Switzerland (an affiliate of Merck KGaA).
 H.B. has received institutional (Monash University) funding from Biogen, F. Hoffmann-La Roche Ltd., Merck, Alexion, CSL, and Novartis; has carried out contracted research for Novartis, Merck, F. Hoffmann-La Roche Ltd., and Biogen; has taken part in speakers’ bureaus for Biogen, Genzyme, UCB, Novartis, F. Hoffmann-La Roche Ltd., and Merck; has received personal compensation from Oxford Health Policy Forum for the Brain. J.L.-S received travel compensation from Biogen, Merck, and Novartis; has been involved in clinical trials with Biogen, Merck, Novartis, and Roche; her institution has received honoraria for talks and advisory board service from Biogen, Merck, Novartis, and Roche. V.E.M. has accepted honoraria for presentations and research funds from Biogen and Merck.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflicts of interest.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of interests BB has or will potentially receive financial compensation for consultancy effort for Novartis, Roche, UCB, Horizon Therapeutics, Biogen, and Immunic Therapeutics for advice on clinical trial design. BB is funded by the National Multiple Sclerosis Society, National Institute of Health, and has been previously funded by the Canadian Multiple Sclerosis Society. JLB has received research grants from Novartis, Mallinckrodt Pharmaceuticals, Alexion, and the National Institutes of Health, license fees from a US patent (2014/0170140); consulting fees from Horizon Therapeutics, Alexion, BeiGene Chugai Pharmaceutical, Genentech, Genzyme, Mitsubishi-Tanabe Pharma, Reistone Biopharma, Roche, and AbbVie; and serves on Data Safety Monitoring Boards for Roche, Genentech, and Clene Nanomedicine. RM reports personal fees from Horizon Therapeutics, Alexion, Roche, and UCB and non-financial support from Horizon Therapeutics, Merck, Biogen, and Roche, outside the submitted work. HJK received a grant from the National Research Foundation of Korea and research support from Aprilbio and Eisai; received consultancy and speaker fees from Alexion, Aprilbio, Altos Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, Handok, Horizon Therapeutics (formerly Viela Bio), Kolon Life Science, Mdimune, Merck Serono, Mitsubishi Tanabe Pharma, Novartis, Roche, Sanofi Genzyme, Teva-Handok, and UCB; and is a co-editor for the Multiple Sclerosis Journal and an associated editor for the Journal of Clinical Neurology. FB has received research funding from the National Health and Medical Research Council (Australia), Multiple Sclerosis Research Australia, New South Wales Health, Novartis, and the University of Sydney (Sydney, NSW, Australia). She has received speaker honoraria from Novartis, Biogen, Merck, and Limbic Neurology, and has been on advisory boards for Merck and Novartis. She works at the University of Sydney and at the Children's Hospital at Westmead, Westmead, New South Wales, Australia, which offers MOG-IgG testing. EPF has served on advisory boards for Alexion, Genentech, and Horizon Therapeutics. He has received speaker honoraria from Pharmacy Times and royalties from UpToDate for a topic on MOGAD. He was a site primary investigator in a randomised clinical trial on inebilizumab in neuromyelitis optica spectrum disorder run by Horizon Therapeutics. He is principal investigator on an RO1 on MOG-IgG disease. He works at Mayo Clinic, Rochester, MN, USA, which offers commercial MOG-IgG testing but he receives no royalties from such testing. SR has received research funding from the National Health and Medical Research Council (Australia), the Brain Foundation (Australia), the Royal Australasian College of Physicians, and the University of Sydney. She was supported by an National Health and Medicine Research Council Neil Hamilton Fairley Early Career Fellowship (APP1141169) and is currently supported by an NHMRC Emerging Leadership (EL2) Investigator Grant (APP2008339). She serves as a consultant on an advisory board for UCB and Limbic Neurology, and has been an invited speaker for Biogen, Limbic Neurology, and Excemed. PW has received research grants from Euroimmun AG, Commonwealth Serum Laboratories Behring and patent royalties for antibody testing (W02010046716A1). He is the co-director of the Oxford Autoimmune Neurology Diagnostic Laboratory (Oxford University, Oxford, UK) where MOG-IgG1 autoantibodies are tested and both he and the University of Oxford receive royalties (for antibody tests for LGI1 and CASPR2, W02010046716A1). He has received honoraria or consulting fees from Biogen Idec, F Hoffmann La-Roche, Mereo BioPharma, Retrogenix, UBC, Euroimmun AG, University of British Columbia, and Alexion; and travel grants from the Guthy-Jackson Charitable Foundation. Work in the Oxford Autoimmune Neurology Diagnostic Laboratory is supported by the UK National Health Service Commissioning service for NMOSD. ST has received speaker and consulting fees from Biogen-Idec Argentina, Merck SA, Genzyme-Sanofi, Roche, Novartis Argentina, and Novartis Pharma. She serves as a consultant on an advisory board for Genentech-Roche. and Alexion Pharmaceuticals. JSG has grant or contract research support from the National Multiple Sclerosis Society, Biogen, and Octave Biosciences for work unrelated to the present project. She serves on a steering committee for a trial supported by Novartis. She has received speaker fees from Alexion and Bristol Myers Sqiuibb, and served on an advisory board for Genentech. TC has received compensation for consulting from Biogen, Novartis Pharmaceuticals, Roche, Genentech, and Sanofi Genzyme. She has received research support from the National Institutes of Health, National Multiple Sclerosis Society, US Department of Defense, EMD Serono, Guthy-Jackson Charitable Foundation, I-Mab Biopharma, Mallinckrodt Pharmaceuticals, Novartis, Octave Bioscience, Roche Genentech, The Sumaira Foundation, and Tiziana Life Sciences. AUB has received grant support from Moore Foundation, Clinical and Trnaslational Awards Program, German Federal Ministry of Education and Research (BMBF). He has been named as inventor on several patents and patent applications describing multiple sclerosis serological biomarkers, drug targets for remyelination therapy, marker-less motor function analysis, and retinal image analysis methods. He serves on the Observational Study Monitoring Board for CAVS-MS. He is cofounder, board member, and currently serving as secretary treasurer of IMSVISUAL. He is cofounder and holds stocks of technology startups Motognosis GmbH and Nocturne GmbH. Motognosis GmbH develops and sells systems for assessing motor dysfunction in patients with neurological disorders. Nocturne GmbH offers analysis services for retinal optical coherence tomography. Both companies' products and services are relevant for neurology in general, but not specific to MOGAD. CH reports grant support from the Medical Research Council, Multiple Sclerosis Society, and Vasculitis UK. She serves as a consultant to Novartis, Biogen, Roche, UCB, Viela Bio, and Sanofi. She participated on an independent data safety monitoring board for the Wellcome Trust. RN reports grant support from Multiple Sclerosis Research Foundation (Netherlands). He has participated on a data safety monitoring board or advisory board for EXCEL study (neurofibromatosis). He is board member of the Dutch Pediatric Neurology Society. LP has received speaker honoraria and travel grants from Biogen, and has consulted for Biogen, Novartis, and Sanofi. Her university holds a patent for her invention: Live cell based assay for detection of autoantibodies for NMOSD and related disorders (Indian patent number 202141055841). MR is supported by research grants from the Austrian Science Fund (FWF project P32699), the Austrian Research Promotion Agency, Euroimmun, and Roche, and consulting fees and advisory board from Roche (to institution). MR works at the Clinical Department of the Medical University of Innsbruck (Innsbruck, Austria), which offers diagnostic testing for MOG-IgG and other autoantibodies. AS received personal compensation for consulting, serving on a scientific advisory board, speaking activities with Merck, Sanofi, Biogen, Roche, TEVA Pharmaceuticals, Novartis, Alexion, and Janssen. DKS has received research support from National council for Scientific and Technological Development CNPq Brazil (425331/2016-4 and 308636/2019-8), Fundacao de Amparo Pesquisa do Estado do Rio Grande do Sul (17/2551-0001391-3 and 21/2551-0000077-5), TEVA Pharmaceuticals, Merck, Biogen, and Euroimmun AG; speaker honoraria from Biogen, Novartis, Genzyme, TEVA Pharmaceuticals, Merck, Roche, and Bayer; and participates in advisory boards for Biogen, Roche, and Merck. KR has been an invited speaker for Merck and serves as a consultant for an advisory board for Roche. FP has received honoraria and research support from Alexion, Bayer, Biogen, Chugai, MerckSerono, Novartis, Genyzme, MedImmune, Shire, and Teva Pharmaceuticals, and serves on scientific advisory boards for Alexion, MedImmune, Novartis, and UCB. He has received funding from Deutsche Forschungsgemeinschaft (DFG Exc 257), Bundesministerium für Bildung und Forschung (Competence Network Multiple Sclerosis), Guthy-Jackson Charitable Foundation, EU Framework Program 7, and National Multiple Sclerosis Society of the USA. He serves on the steering committee of the N-Momentum study with inebilizumab (Horizon Therapeutics) and the OCTiMS Study (Novartis). He is an associatee editor with Neurology, Neuroimmunology, and Neuroinflammation and academic editor with PloS One. SJP reports grants, personal fees, and non-financial support from Alexion Pharmaceuticals; grants, personal fees, and non-financial support from MedImmune /Viela Bio; and personal fees for consulting from Genentech, Roche, UCB, and Astellas. He has two patents issued (8889102; application 12-678350; Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia; and 9891219B2; application 12-573942; Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 [AQP4]-IgG Autoantibody positive). SJP also has patents pending for IgGs to the following proteins as biomarkers of autoimmune neurological disorders: septin-5, kelch-like protein 11, GFAP, PDE10A, and MAP1B. He works at Mayo Clinic, which offers commercial MOG-IgG testing. He receives no royalties from the sale of tests done at the neuroimmunology Laboratory at Mayo Clinic. KF serves as an advisor or on scientific advisory boards for Biogen, Mitsubishi Tanabe, Novartis, Chugai, Roche, Alexion, VielaBio/Horizon Therapeutics, UCB, Merck Biopharma, Japan Tobacco and Abbvie; has received funding for travel and speaker honoraria from Biogen, Eisai, Mitsubishi Tanabe, Novartis, Chugai, Roche, Alexion, VielaBio, Teijin, Asahi Kasei Medical, Merck, and Takeda; and has received the Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan and the Grants-in-Aid for Scientific Research from the Ministry of Health, Welfare and Labor of Japan. JP has received consulting fees from Merck, Novartis, Roche, Mitsubishi Tnabe Pharma, UCB, Alexion, Vitaccess, and Argenx, and MRI support from Medimmune, Merck, and Roche. She has received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing, or educational events from Merck, VielaBio, Roche and Alexion. She has participated on a data safety monitoring board or advisory board for Novartis, Roche, Argenx, UCB, Alexion, and Sanofi. She is member of the Charcot Foundation Board, Magnetic Resonance in Multiple Sclerosis steering committee, and National Health Service England Intravenous Immune Globulin Committee. She holds stock for AstraZeneca for a product that is not related to MOG-antibody associated disease. She has a patent for Diagnosing Multiple Sclerosis (application no PCT/GB2013/050285, final patent number 13704627.2–1408; client reference 4440; MS reference P37347WO; patent published Sept 13, 2021).

 The authors have declared that no competing interests exist.

 Declaration of Competing Interest The authors claim no commercial interest or conflict of interest for this study.


 Conflict of interest: ATR receives consulting income or unrestricted research funding from Roche/Genentech, Biogen, BMS, and Novartis.



 Competing interests: None declared.
 Declaration of Competing Interest The authors declare that there are no conflicts of interest.

 Competing interests: AG, ACR, CR, JP and LS have nothing to declare. KH reports research support and speaker honoraria from Biogen, Bayer Healthcare, Novartis Pharma, Teva, Sanofi Genzyme, Merck Serono and Roche. SMG reports honoraria from Mylan GmbH, Almirall S.A. and Celgene and research grants from Biogen, outside the submitted work. He receives research funding from the Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung, Bundesministerium für Gesundheit, the National MS Society and the European Commission. TF reports personal fees from Novartis, Bayer, Janssen, Roche, Vifor, BiosenseWebster, CSL Behring, Fresenius Kabi, Coherex Medical, LivaNova, Minoryx, Immunic, Bristol Myers Squibb, Enanta, IQVIA; all outside the submitted work. AS reports grants from the Fondazione Italiana Sclerosi Multipla and the European Academy of Neurology, during the conduct of the study; personal fees from Almirall and Merck Serono. CH received research grants or speaker honoraries from Biogen, Bristol Myers Squibb, Merck, Novartis and Roche.
 SJ reports no conflicts of interest. OA has received speaking honoraria and travel grants from Alexion, Almirall, Biogen, Celgene, Merck, Novartis, Roche, and VielaBio. IA has received speaking honoraria and scientific advisory board compensation from Alexion, Roche, Merck Serono, Santhera, and Sanofi Genzyme and research support from Chugai and Diamed. JBS has received speaking honoraria and travel grants from Bayer Healthcare, sanofi-aventis/Genzyme, and Biogen and compensation for serving on a scientific advisory board from Roche. AB has received consulting and/or speaking fees from Alexion, Bayer Healthcare, Biogen, Celgene, and Roche. His institution has received compensations for clinical trials from Alexion, Biogen, Merck, Novartis, Roche, and Sanofi. VH reports no conflicts of interest. JH reports a grant for OCT research from the Friedrich-Baur-Stiftung, personal fees and non-financial support from Merck, Alexion, Novartis, Roche, Santhera, Biogen, Heidelberg Engineering, and Sanofi Genzyme, and non-financial support from the Guthy-Jackson Charitable Foundation; he is partially funded by the German Federal Ministry of Education and Research [grant numbers 01ZZ1603[A-D] and 01ZZ1804[A-H] (DIFUTURE)]. KH reports no conflicts of interest. MH reports no conflicts of interest. IK has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities from Alexion, Almirall, Bayer, Biogen, Hexal, Horizon, Merck, Neuraxpharm, Sanofi, and Roche/Chugai. LK has received compensation for serving on scientific advisory boards from Alexion, Biogen, BMS, Celgene GmbH, Genzyme, Horizon, Janssen, Merck Serono, Novartis, and Roche. She has received speaker honoraria and travel support from Bayer, Biogen, Celgene GmbH, Genzyme, Grifols, Merck Serono, Novartis, Roche, Santhera, and Teva; she receives research support from German Research Foundation, IZKF Münster, IMF Münster, Biogen, Immunic AG, Novartis, and Merck Serono. MK has received travel funding, speaker honoraria, and research support from Bristol Myers Squibb, Merck, Novartis, and Roche. TK has received speaker honoraria and/or personal fees for advisory boards from Novartis Pharma, Roche Pharma, Alexion/Astra Zeneca and Biogen; the Institution she works for has received grant support for her research from Bayer-Schering AG, Novartis and Chugai Pharma. FP has received grants from Guthy Jackson Charitable Foundation, German Research Foundation, German Federal Ministry of Education and Research, Novartis, Bayer, Biogen Idec, Teva, Alexion, Roche, Horizon, Sanofi-Aventis/Genzyme, Merck Serono, Chugai, German Research Council, Werth Stiftung of the City of Cologne, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, National Multiple Sclerosis (USA), MedImmune, Shire, and Alexion, and has a patent on Foveal Morphometry pending to Nocturne GmbH; he is Academic Editor at PLoS ONE and Associate Editor of Neurology(®) Neuroimmunology & Neuroinflammation. MR has received speaker honoraria from Novartis, Bayer Vital GmbH, Roche, Alexion, and Ipsen and travel reimbursement from Bayer Schering, Biogen Idec, Merz, Genzyme, Teva, Roche, and Merck. KR has received research support from Novartis Pharma, Merck Serono, German Ministry of Education and Research, European Union (821283-2), Stiftung Charité (BIH Clinical Fellow Program) and Arthur Arnstein Foundation, speaker honoraria from Bayer, and travel grants from Guthy Jackson Charitable Foundation. MS has received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Bristol-Myers-Squibb, Merck, Roche, and Sanofi Genzyme. She has received research funding from the Hertha-Nathorff-Program. PS reports no conflict of interest. FTB has received personal compensation for advisory board participation or speaking, and through his institution has received research support for investigator-initiated studies or for attending scientific meetings, from Actelion, Alexion, Bayer-Schering, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, Teva, UCB, German Research Foundation (DFG), and German Federal Ministry of Education and Research (BMBF). HT has received honoraria for consultation and expert testimony from Alexion Pharma, Bayer, Biogen, Janssen, MERCK, Novartis, Roche, Sanofi Genzyme, and Teva. BW has received grants from the German Ministry of Education and Research, German Research Foundation, Dietmar Hopp Stiftung, Klaus Tschira Stiftung, and Merck, and personal fees from Alexion, Bayer, Biogen, Roche. CT has received honoraria for consultation and expert testimony from Alexion Pharma Germany GmbH, Chugai Pharma Germany GmbH, and Roche Pharma GmbH.
 Conflicto de intereses: Los autores declaran no tener conflictos de interés.
 Declaration of Competing Interest Authors declare that there is no conflict of interest(s).
 The authors have no competing interests to declare that are relevant to the content of this article.
 J.K. reported speaking and consulting relationships with Roche, this company manufactures ocrelizumab. Amsterdam UMC, location VUmc, MS Center Amsterdam has received financial support for research activities from Roche.
 The authors declare that they have no conflicts of interest.

 Declaration of Competing Interest Gregory Brusola reports financial support was provided by National Institute of Child Health and Human Development.

 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Competing interests: RAM received research funding from Canadian Institutes of Health Research, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, Consortium JBof MS Centers and the Arthritis Society, US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a coinvestigator on a study funded in part by Biogen Idec and Roche (no funds to her or her institution). RW reports no disclosures. JB received research funding from CIHR, Brain and Behavior Research Foundation and the MS Society of Canada. JS received research funding from the Canadian Institutes of Health Research and holds stocks in Johnson and Johnson. SBP received research funding from Canadian Institutes of Health Research, the MS Society of Canada, Roche, Biogen and the Government of Alberta. AS received financial and in-kind support from an IBM/CIMVHR Advanced Analytics Grant and Calian Inc. LL received research funds from Canadian Institutes of Health Research, NSERC and the Arthritis Society. CH had research funds for unrelated studies from Pfizer and consulted for Astra-Zeneca Canada. RE-G received research funds from Canadian Institutes of Health Research, University of Manitoba Start-Up Funds. AK received research funds from Canadian Institutes of Health Research, the Heart and Stroke Foundation and Research Manitoba. JDF received research grant support from the Canadian Institutes of Health Research, the National Multiple Sclerosis Society, the Multiple Sclerosis Society of Canada, Crohn’s and Colitis Canada and Research Nova Scotia, and consultation and distribution royalties from MAPI Research Trust. JJM conducted clinical trials for Biogen Idec and Roche, and received research funding from the MS Society of Canada, the MS Scientific Foundation and Research Manitoba. CNB consulted with Abbvie Canada, Amgen Canada, BMS Canada, JAMP Canada, Janssen Canada, Pfizer Canada, Roche Canada, Sandoz Canada and Takeda Canada, and received unrestricted educational grants from Abbvie Canada, BMS Canada, Janssen Canada, Pfizer Canada and Takeda Canada. He has been on speaker’s bureaus of Abbvie Canada and Shire Canada. SBP holds the Cuthbertson & Fischer Chair in Pediatric Mental Health at the University of Calgary. The sponsors had no role in the design and conduct of the study; collection, management, analysis and interpretation of the data, and preparation, review or approval of the manuscript.


 Declaration of competing interest The authors declare that they have no known competing financial interests nor personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 TO has received honoraria for advisory boards/lectures from Biogen, Merck, Novartis and Sanofi. The same companies have provided unrestricted MS research grants, none of which has dealt with the current manuscript. TO has grant support from the Swedish research Council, the Swedish Brain foundation, Knut and Alice Wallenbergs foundation and Margaretha af Ugglas foundation.
 JJS reports funding from the National Institute of Health (R21AG073892, R21AG064308-01), National Multiple Sclerosis Society (MB-1807-31633, RG-1701-26862), ownership in Sosnoff Technologies, LLC, speaking fees from BrainWeek, and consulting fees from Xavor, Inc. AM and JMH report have submitted a patent application on the use of virtual reality, the intellectual property rights for which are held by the Tel Aviv Medical Center. None of the other authors have potential conflicts of interest to be disclosed.
 The authors declare that they have no conflicts of interest and no financial interests related to the material of this manuscript.
 Declaration of competing interest All authors disclosed no relevant relationships.
 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 None.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: E.K.H. received honoraria/research support from Biogen, Merck Serono, Novartis, Roche, and Teva; has been member of advisory boards for Actelion, Biogen, Celgene, Merck Serono, Novartis, and Sanofi Genzyme. She was also supported by the Charles University: Cooperatio Program in neuroscience. D.H. received compensation for travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck Healthcare KGaA (Darmstadt, Germany), Bayer, Sanofi, Roche, and Teva, as well as support for research activities from Biogen. She was also supported by the Charles University: Cooperatio Program in neuroscience. R.A. received honoraria as a speaker and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche and Sanofi-Genzyme. C.B. received conference travel support from Biogen, Novartis, Bayer-Schering, Merck and Teva; has participated in clinical trials by Sanofi Aventis, Roche and Novartis. F.P. received speaker honoraria and advisory board fees from Almirall, Bayer, Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme and TEVA. He received research funding from Biogen, Merck, FISM (Fondazione Italiana Sclerosi Multipla), Reload Onlus Association and University of Catania. A.L. has received personal compensation for consulting, serving on a scientific advisory board, speaking or other activities from Biogen, Merck Serono, Mylan, Novartis, Roche, Sanofi/Genzyme and, Teva, and Bristol Myers Squibb. Her institutions have received research grants from Novartis and Sanofi/Genzyme. S.E. received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche and Teva. M.G. received consulting fees from Teva Canada Innovation, Biogen, Novartis and Genzyme Sanofi; lecture payments from Teva Canada Innovation, Novartis and EMD . He has also received a research grant from Canadian Institutes of Health Research. S.J.K. received compensation for scientific advisory board activity from Merck and Roche. A.A. received speaker honoraria from Merck, Alexion; received travel and registration grants from Merck. K.B. received honoraria and consulting fees from Biogen, Teva, Novartis, Genzyme-Sanofi, Roche, Merck, CSL and Grifols. P.G. has served in advisory boards for Novartis, EMD Serono, Roche, Biogen Idec, Sanofi Genzyme, Pendopharm and has received grant support from Genzyme and Roche, has received research grants for his institution from Biogen Idec, Sanofi Genzyme, EMD Serono. A.v.d.W. served on advisory boards and receives unrestricted research grants from Novartis, Biogen, Merck and Roche She has received speaker’s honoraria and travel support from Novartis, Roche, and Merck. She receives grant support from the National Health and Medical Research Council of Australia and MS Research Australia. H.B. received institutional (Monash University) funding from Biogen, F. Hoffmann-La Roche Ltd, Merck, Alexion, CSL, and Novartis; has carried out contracted research for Novartis, Merck, F. Hoffmann-La Roche Ltd and Biogen; has taken part in speakers’ bureaus for Biogen, Genzyme, UCB, Novartis, F. Hoffmann-La Roche Ltd and Merck; has received personal compensation from Oxford Health Policy Forum for the Brain Health Steering Committee. D.M. received speaker honoraria for Advisory Board and travel grants from Almirall, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. J.L-.S. received travel compensation from Novartis, Biogen, Roche and Merck. Her institution receives the honoraria for talks and advisory board commitment as well as research grants from Biogen, Merck, Roche, TEVA and Novartis. N.J. is a local principal investigator on commercial studies funded by Novartis, Biogen, Amicus and Sanofi J.P. accepted travel compensation from Novartis, Biogen, Genzyme, Teva, and speaking honoraria from Biogen, Novartis, Genzyme and Teva. D.S. received honoraria as a consultant on scientific advisory boards by Bayer-Schering, Novartis and Sanofi-Aventis and compensation for travel from Novartis, Biogen, Sanofi Aventis, Teva and Merck. C.R-.T. received research funding, compensation for travel or speaker honoraria from Biogen, Novartis, Genzyme and Almirall. G.I. had travel/accommodations/meeting expenses funded by Bayer Schering, Biogen, Merck, Novartis, Sanofi Aventis, and Teva. R.A. received conference travel support from Novartis, Teva, Biogen, Bayer and Merck and has participated in a clinical trial by Biogen, Novartis, Teva and Actelion. V.v.P. received travel grants from Merck Healthcare KGaA (Darmstadt, Germany), Biogen, Sanofi, Bristol Meyer Squibb, Almirall and Roche. His institution has received research grants and consultancy fees from Roche, Biogen, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), Bristol Meyer Squibb, Janssen, Almirall and Novartis Pharma M.B. served on scientific advisory boards for Biogen, Novartis and Genzyme and has received conference travel support from Biogen and Novartis. He serves on steering committees for trials conducted by Novartis. His institution has received research support from Biogen, Merck and Novartis. M.D. received consultancy and advisory board fees from Roche, Sanofi-Genzyme, Biogen, Merck-Serono, Bayer-Schering, Novartis and Allergan; received congress support from Biogen, Merck-Serono, Teva and Roche. She has also received research support from Novartis, Biogen, Roche, FWO (Research Foundation Flanders) and Fonds D.V. (Ligue Nationale Belge de la Sclerose en Plaques, Fondation Roi Baudouin). J.K. received speaker fees, research support, travel support, and/or served on advisory boards by Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Progressive MS Alliance, Bayer, Biogen, Bristol Myers Squibb, Celgene, Merck, Novartis, Octave Bioscience, Roche, Sanofi. M.J.S. received consulting fees, speaker honoraria, and/or travel expenses for scientific meetings from Alexion, Bayer Healthcare, Biogen, Bristol Myers Squibb, Celgene, Janssen, Merck-Serono, Novartis, Roche, Sanofi and Teva. M.F-.P. received travel compensation from Merck A.K. received speaker honoraria and scientific advisory board fees from Bayer, BioCSL, Biogen, Genzyme, Innate Immunotherapeutics, Merck, Novartis, Sanofi, Sanofi-Aventis, and Teva. S.M. has received a MENACTRIMS clinical fellowship grant (2020). S.H. received honoraria and consulting fees from Novartis, Bayer Schering and Sanofi, and travel grants from Novartis, Biogen Idec and Bayer Schering. G.L. received travel and/or consultancy compensation from Sanofi-Genzyme, Roche, Teva, Merck, Novartis, Celgene, Biogen. C.O-.G. received honoraria as consultant on scientific advisory boards from Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme and TEVA. E.C. received honoraria as consultant on scientific advisory boards by Biogen, Bayer-Schering, Merck, Genzyme and Novartis; has participated in clinical trials/other research projects by Merck, Roche and Novartis. P.M. received speakers fees and travel grants from Novartis, Biogen, T’évalua, Sanofi and Bayer Schering and received honoraria and consulting fees from Novartis, Bayer Schering and Sanofi. J.L.S-.M. accepted travel compensation from Novartis, Merck and Biogen, speaking honoraria from Biogen, Novartis, Sanofi, Merck, Almirall, Bayer and Teva and has participated in clinical trials by Biogen, Merck and Roche B.S. received consultancy honoraria and compensation for travel from Biogen and Merck. S.H. has received unrestricted educational grants or speaking honoraria from Biogen, Merck Serono, Novartis, Roche and Sanofi Genzyme. Y.B. received speaker honoraria from Merck, Biogen, Brystol, Novartis and Sanofi C.S. served on scientific advisory boards for Merck, Genzyme, Almirall, and Biogen; received honoraria and travel grants from Sanofi Aventis, Novartis, Biogen, Merck, Genzyme and Teva. B.T. received funding for travel and speaker honoraria from Bayer Schering Pharma, CSL Australia, Biogen and Novartis, and has served on advisory boards for Biogen, Novartis, Roche and CSL Australia. M.H. participated as a clinical investigator and/or received consultation and/or speaker fees from Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals and TG Pharmaceuticals S.M. received speaker honoraria, advisory board fees and travel grants from Abbvie, Biogen, Bristol Meyrs Squibb, Teva, Merck, Roche, Ipsen, Sanofi-Genzyme Novartis, Boehringer Stada T.C.T. received speaking/consulting fees and/or travel funding from Almirall, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche, Sanofi-Genzyme and Teva. O.G. received honoraria as consultant on scientific advisory boards for Genzyme, Biogen, Merck, Roche and Novartis; has received travel grants from Biogen, Merck, Roche and Novartis; has participated in clinical trials by Biogen and Merck. B.V.W. received research and travel grants, honoraria for MS-Expert advisor and Speaker fees from Almirall, Biogen, BMS, Janssen, Sanofi, Merck, Novartis, Roche and Teva. N.G. received honoraria and travel support, Consultancy fees, Lecture fees from Biogen Idec, Biologix, Novartis, TEVA, Bayer, Merck Serono, Genesis Pharma, Sanofi – Genzyme, ROCHE, ELPEN. Research grants from Biogen Idec, Novartis, TEVA, Merck Serono, Genesis Pharma, Sanofi – Genzyme, ROCHE J.O. has received research funding from the MS Society of Canada, National MS Society, Brain Canada, Biogen, Roche, EMD Serono (an affiliate of Merck KGaA); and personal compensation for consulting or speaking from Alexion, Biogen, Celgene (BMS), EMD Serono (an affiliate of Merck KGaA), Novartis, Roche, and Sanofi-Genzyme. Y.F. received honoraria as a consultant on scientific advisory boards by Novartis, Teva, Roche and Sanofi-Aventis and compensation for travel from Novartis, Biogen, Sanofi Aventis, Teva, Roche and Merck. F.M. participated in clinical trials sponsored by EMD Serono and Novartis. C.S. received travel assistance from Biogen and Novartis. N.S. received travel compensation from Bayer Schering, Novartis, and Biogen Idec. B.W. received honoraria for acting as a member of Scientific Advisory Boards for Almirall, Biogen, Celgene/BMS, Merck Serono, Novartis, Roche, Sanofi-Genzyme and speaker honoraria and travel support from Biogen, Merck Serono, Novartis, Roche, Sanofi-Genzyme; research and/or patient support grants from Roche, Biogen, Merck-Serono, Sanofi-Genzyme; research support from FWO. Honoraria and grants were paid to UZA/UZA Foundation. T.A.H. has received speaking fees or received honoraria for serving on advisory boards for Biogen, Merck, Teva, Novartis, Roche, Bristol Myers Squibb and Sanofi. D.D. received compensation for travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck KGaA, Bayer, Sanofi/Genzyme, Roche and Teva, as well as support for research activities from Biogen, Novartis, Merck, Sanofi, Roche & Teva R.W-.T.’s clinical research fellow grant is co-funded by Novartis. I.R. served on scientific advisory boards, received conference travel support and/or speaker honoraria from Roche, Novartis, Merck and Biogen. Izanne Roos receives research support from Multiple Sclerosis Australia and the Trish Multiple Sclerosis Research Foundation. C.M. has received conference travel support from Merck, Novartis, and Biogen. He has received research support from the National Health and Medical Research Council, Multiple Sclerosis Research Australia, The University of Melbourne, The Royal Melbourne Hospital Neuroscience Foundation, and Dementia Australia. T.K. served on scientific advisory boards for BMS, Roche, Janssen, Sanofi Genzyme, Novartis, Merck and Biogen, steering committee for Brain Atrophy Initiative by Sanofi Genzyme, received conference travel support and/or speaker honoraria from WebMD Global, Eisai, Novartis, Biogen, Sanofi-Genzyme, Teva, BioCSL and Merck and received research or educational event support from Biogen, Novartis, Genzyme, Roche, Celgene and Merck. J.W.L.B. received speaking honoraria and advisory board fees from Biogen, Novartis, Intesso and The Corpus.
 Conflict of Interest All authors declare none.
 Declaration of Competing Interest LC: Nothing to disclose. IA: Participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. MKS: received consultation and/or speaker fees from: Sanofi Genzyme, Roche. MH: Participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals.



 S.L.H. currently serves on the scientific advisory board of Accure, Alector, Annexon, board of directors of Neurona, and has previously consulted for BD, Moderna, and NGM Bio. S.L.H. also has received travel reimbursement and writing support from F. Hoffmann-La Roche and Novartis AG for anti-CD20-theapy-related meetings and presentations. Other authors declare no competing interests.

 The authors declare no competing interests.
 Declaration of interests K.S.L., H.L.L., H.I., N.J., F.F., and M.A.N.’s participation in this project was part of a competitive contract awarded to Data Tecnica International LLC by the National Institutes of Health to support open science research. M.A.N. also currently serves on the scientific advisory board for Clover Therapeutics and is an advisor to Neuron23 Inc.
 Declaration of Competing Interests Lie IA has no disclosures to report. Rød BE has no disclosures to report. Kvistad SS has received unrestricted research grants from Novartis, Biogen. Holmøy T has received speaker honoraria, research support/grants and participated in clinical trials for Biogen, Merck, Sanofi, Bristol Myers Squibb, Roche and Novartis. Myhr KM has received speaker honoraria from Biogen, Sanofi, Novartis, and Roche; and has participated in clinical trials organized by Biogen, Merck, Novartis, Roche, and Sanofi. ØT has received research grants and speaker honoraria from Biogen, Roche, Novartis, Merck, Teva and Sanofi. Wergeland S has received speaker honoraria from and served on scientific advisory boards for Biogen, Janssen-Cilag, Sanofi and Novartis.
 The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare that there is no conflict of interest and competing interests regarding the publication of this article.

 Declaration of Competing Interest All authors declare no conflict of interest.

 J.H. has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis and Sandoz and speaker’s fees from Biogen, Novartis, Merck KGaA, Teva and Sanofi-Genzyme; he has served as principal investigator for projects, or received unrestricted research support from, Biogen, Bristol-Myers-Squibb, Merck KGaA, Novartis, Roche and Sanofi-Genzyme, his MS research is funded by the Swedish Research Council and the Swedish Brain foundation. T.O. has academic grants from the Knut and Alice Wallenberg foundation, the Swedish Research Council and the Swedish Research Council; has received lecture and/or advisory board honoraria, as well as non-restricted MS research grants, from Biogen, Novartis, Sanofi and Merck on projects not related to the one reported here. L.A. reports grants from the Swedish Research Council, grants from the Swedish Research Council for Health Working Life and Welfare and grants from the Swedish Brain Foundation, during the conduct of the study; and personal fees from Teva and Biogene Idec, outside the submitted work.
 The authors declare no conflict of interest.
 The authors declare that they have no conflict of interest.
 A. Gonzalez-Martinez has received education funding from Lilly, Novartis, Roche, TEVA, Abbvie-Allergan, & Daichi. G. Bose has received speaker fees from TEVA, Novartis, and EMD Serono, served on a scientific advisory board from Novartis and EMD Serono, and received research funding from an endMS post-doctoral fellowship award from the Multiple Sclerosis Society of Canada and a TOHAMO innovation fund grant from IFPOC. B. Healy served on the scientific advisory board for Biogen, Worldwide Medical Biostatistics, Multiple Sclerosis, served on the editorial board for Statistical Methods in Medical Research, received research support from Merck Serono, Gen- zyme, Novartis, Google Life Sciences, NIH, National Multiple Sclerosis Society. H. Weiner has consulted for Genentech, Inc; Tiziana Life Sciences; IM Therapeutics; MedDay Pharmaceuticals; vTv Therapeutics; I-MAB Biopharma and received research support National Institutes of Health; National Multiple Sclerosis Society; Sanofi Genzyme; and Genentech, Inc. T. Chitnis served on clinical trial advisory boards for Novartis Pharmaceuticals, Genzyme-Sanofi, consulted for Biogen Idec, Novartis, Genzyme-Sanofi, Genentech Roche, received research support from EMD Serono, Novartis, Biogen, Verily, National Multiple Sclerosis Society, the Peabody Foundation, the Consortium for MS Centers, Guthy-Jackson Charitable Foundation. H. Lokhande, S. Saxena, and M. Polgar-Turcsanyi have no disclosures.

 Declaration of Competing Interest ACR has nothing to disclose. AG has nothing to disclose. AS has received advisory boards and speaker honoraria from Almirall, Merck, and Sanofi Genzyme. CH has received research funds from Genzyme, Roche, Merck, and Bristol-Myers Squibb. JP has nothing to disclose. KH reports research support and speaker honoraria from Biogen, Bayer Healthcare, Novartis Pharma, Teva, Sanofi Genzyme, Merck Serono, and Roche. LS has nothing to disclose. SK has nothing to disclose. SMG has received grants from Biogen and speaker honoraria from Hexal.
 The research was conducted from a medical perspective based on a joint research agreement with Biogen Japan Ltd. TS has served as a medical advisor and has received honoraria for delivering scientific lectures for Alexion Pharmaceuticals Inc., Biogen, Bayer, Eisai Co., Mitsubishi-Tanabe Pharmaceuticals, and Novartis. MK and YT are employees of Biogen and hold stock/stock options in Biogen. QH has nothing to declare.
 The authors declare no conflict of interest.
 F.C. Loonstra, L.R.J. de Ruiter, Eva M.M. Strijbis, H.E. de Vries and M. Rijnsburger report no disclosures. Menno Schoonheim serves on the editorial board of Frontiers of Neurology and has received research support, compensation for consulting services or speaker honoraria from the Dutch MS Research Foundation, ARSEP, Eurostars-EUREKA, ZonMW, ExceMed, Amsterdam Neuroscience, Atara, Biogen, Celgene/BMS, Merck, MedDay and Sanofi-Genzyme. B.M.J. Uitdehaag received consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Teva and Immunic Therapeutics. J. Killestein has speaker and consultancy relationships with and received research grants from Biogen, Genzyme, Immunic, Merck, Novartis, Roche, Sanofi and TEVA.
 Shiv Saidha has received consulting fees from Medical Logix for the development of CME programs in neurology and has served on scientific advisory boards for Biogen, Novartis, Genentech Corporation, TG therapeutics, Rewind therapeutics & Bristol Myers Squibb. He has performed consulting for Novartis, Genentech Corporation, JuneBrain LLC, and Lapix therapeutics. He is the PI of investigator-initiated studies funded by Genentech Corporation, Novartis, and Biogen. He previously received support from the Race to Erase MS foundation. He has received equity compensation for consulting from JuneBrain LLC and Lapix therapeutics. He was also the site investigator of trials sponsored by MedDay Pharmaceuticals, Clene Pharmaceuticals, and is the site investigator of a trial sponsored by Novartis. Dr. Sattarnezhad has received Sylvia Lawry Physician Fellowship award from National Multiple Sclerosis Society (NMSS). Elliot Frohman has received consulting and speaker fees from Biogen, Genzyme, Novartis, Alexion, Horizon, and Janssen. Soheil Mohammadi, Mahdi Gouravani, Mohammad Amin Salehi, J. Fernando Arevalo, Steven L. Galetta, Hamid Harandi, Teresa C Frohman, and Friedemann Paul report no disclosures.

 Conflicts of interest and sources of funding: none declared.

 S.B. and M.S. have nothing to disclose. J.A.G. reports travel expenses and non-financial support from Merck, outside the submitted work. T.K. has received speaker honoraria and/or personal fees for advisory boards from Novartis Pharma, Roche Pharma, Alexion/Astra Zeneca, and Biogen; the institution she works for has received grant support for her research from Bayer-Schering A.G., Novartis, and Chugai Pharma. I.K. has received personal compensation for consulting, serving on a scientific advisory board, speaking, and other activities with Alexion, Almirall, Bayer, Biogen, Hexal, Horizon, Merck, Neuraxpharm, Roche/Chugai, and Sanofi. I.K. is an editorial board member of BMC Neurology, Frontiers in Neurology, and Frontiers in Immunology. J.H. reports grants from Friedrich-Baur-Stiftung, Merck, and Horizon; personal fees and non-financial support from Alexion, Horizon, Roche, Merck, Novartis, Biogen, B.M.S., and Janssen; and non-financial support from the Guthy-Jackson Charitable Foundation and The Sumaira Foundation.


 EM-H, AS, JR, FV, EF, SA-A have nothing to disclose; EL-S and ES received travel reimbursement from Sanofi and ECTRIMS; FP received a Guarantors of Brain fellowship 2017–2020; MS received speaker honoraria from Genzyme, Novartis and Biogen; JMC-M received speaker honoraria from Sanfi; Y.B. received speaking honoraria from Biogen, Novartis and Genzyme; EHM-L received travel support for international and national meetings from Roche and Sanofi-Genzyme, and honoraria for consultancies from Novartis, Roche and Sanofi before joining the European Medicines Agency, where she is currently employed (Human Medicines, since 16 April 2019); however, her contribution to this article is related to her activity at the Hospital Clinic Barcelona/IDIBAPS and therefore does not represent the views of the Agency or its Committees. She is a member of the International Multiple Sclerosis Visual System (IMSVISUAL) Consortium; PV is a shareholder and has received consultancy fees from Accure Therapeutics SL, Attune Neurosciences Inc, QMenta Inc, Spiral Therapeutix Inc, CLight Inc and NeuroPrex Inc, as well as having held grants from the Instituto de Salud Carlos III and the European Commissions; AS received consulting fees and speaker honoraria from Bayer-Schering, Merck-Serono, Biogen-Idec, Sanofi-Aventis, TEVA, Novartis and Roche, Janssen and Horizon Therapeutics; SL received consulting fees and speaker honoraria from Biogen Idec, Novartis, TEVA, Genzyme, Sanofi and Merck.
 J. Ciron: consulting and lecturing fees and travel grants from Biogen, Novartis, Merck, Teva, Sanofi-Genzyme, Roche, BMS-Celgene, and Alexion. J. De Sèze: consulting and lecturing fees, travel grants, and unconditional research support from Biogen, Genzyme, Novartis, Roche, Sanofi Aventis, and Teva Pharma. A. Ruet: consultancy fees, speaker fees, research grants (nonpersonal), or honoraria approved by the institutions from Novartis, Biogen Idec, Genzyme, MedDay, Roche, Teva, and Merck. E. Maillart: consulting and lecturing fees from Alexion, Biogen, BMS, Merck Serono, Novartis, Roche, Sanofi, Teva Pharmaceuticals, and Ad Scientiam and research support from Biogen, Novartis, and Roche. P. Labauge: consulting and lecturing fees, travel grants, and unconditional research support from Biogen, Genzyme, Novartis, Merck Serono, Roche, and Teva Pharma. H. Zephir: consulting or lectures and invitations for national and international congresses from Biogen, Merck, Teva, Sanofi-Genzyme, Novartis, and Bayer, research support from Teva and Roche, and academic research grants from Académie de Médecine, LFSEP, FHU Imminent, and ARSEP Foundation. G. Defer: consulting and lecturing fees for Biogen, BMS, Novartis, Genzyme,Merck Serono, Roche, and Teva; funding for travel from Merck Serono, Biogen, Sanofi-Genzyme, Novartis, and Teva; research support from Merck Serono, Biogen, Genzyme, and Novartis. C. Lebrun-Frénay: fees for consulting or lectures from Novartis, Genzyme, and Roche. T. Moreau: fees as scientific adviser from Biogen, MedDay, Novartis, Genzyme, and Sanofi. D.A. Laplaud: served on the scientific advisory boards for Roche, Sanofi, Novartis, MedDay, Merck, and Biogen; received conference travel support and/or speaker honoraria from Novartis, Biogen, Roche, Sanofi, Celgene, and Merck; and received research support from Fondation ARSEP and Agence Nationale de la Recherche. E. Berger: honoraria and consulting fees from Novartis, Sanofi Aventis, Biogen, Genzyme, Roche, and Teva Pharma. B. Stankoff: consulting and lecturing fees, travel grants from Biogen Idec, Merck Serono, Novartis, and Genzyme, and unconditional research support from Merck Serono, Genzyme, and Roche. P. Clavelou: consulting and lecturing fees, travel grants, and unconditional research support from Actelion, Biogen, Genzyme, Novartis, MedDay, Merck Serono, Roche, and Teva Pharma. E. Thouvenot: consulting and lecturing fees, travel grants, or unconditional research support from the following pharmaceutical companies: Actelion, Biogen, Celgene, Genzyme, Merck Serono, Novartis, Roche, and Teva Pharma; has a patent pending for biomarkers of neurodegeneration and neuroregeneration and a patent pending for a diagnosis method of multiple sclerosis (EP18305630.8); and received academic research support from PHRC and ARSEP Foundation. O. Heinzlef: consulting and lecturing fees from Bayer Schering, Merck, Teva, Genzyme, Novartis, Almirall, and Biogen Idec, travel grants from Novartis, Teva, Genzyme, Merck Serono, and Biogen Idec, and research support from Roche, Merck, and Novartis. J. Pelletier: received fees as scientific adviser from Biogen, Merck Serono, Novartis, travel grants from Biogen, MedDay, Novartis, Genzyme, Roche, Sanofi, and Teva and unconditional research support from Merck Serono and Roche. O. Casez: funding for travel and honoraria from Biogen, Merck Serono, Novartis, Sanofi-Genzyme, and Roche. B. Bourre: served on scientific advisory board for Biogen, Genzyme, Merck Serono, Novartis, and Roche and received funding for travel and honoraria from Biogen Idec, Merck Serono, Novartis, Sanofi-Genzyme, Roche, and Teva. A. Wahab: received expert testimony from Roche and travel grants from Biogen. J.-P. Camdessanché: consulting and lecturing fees from Akcea, Alnylam, Biogen, CSL-Behring, Genzyme, Grifols, Laboratoire Français des Biotechnologies, Natus, Novartis, Pfizer, PharmAlliance, Teva, and SNF-Floerger and travel grants from Biogen, CSL-Behring, Genzyme, Laboratoire Français des Biotechnologies, Merck Serono, Novartis, Pfizer, and Teva. A. Maurousset: received funding for travel from Merck Serono, Teva, Novartis, Sanofi-Genzyme, Biogen, and Roche; served on scientific advisory board for Roche; and received honoraria from Biogen, Novartis, and Roche. N.H. Ben: honoraria and consulting fees from Novartis, Genzyme, and Roche, research support from Biogen and Novartis, and travel grants from Genzyme, Novartis, and Roche. S. Vukusic: grants, personal fees, and nonfinancial support from Biogen, grants and personal fees from GeNeuro, grants, personal fees, and nonfinancial support from Genzyme, grants and personal fees from MedDay, grants, personal fees, and nonfinancial support from Merck Serono, grants, personal fees, and nonfinancial support from Novartis, grants, personal fees, and nonfinancial support from Roche, grants, personal fees, and nonfinancial support from Sanofi, and personal fees from Teva. The other authors report no relevant disclosures. Go to Neurology.org/N for full disclosures.

 Declaration of Competing Interest Dr. Newsome has received consultant fees for scientific advisory boards from Biogen, Genentech, Bristol Myers Squibb, EMD Serono, Greenwich Biosciences, Novartis, and Horizon Therapeutics, is an advisor for Autobahn, is the study lead PI for a Roche clinical trial, was a clinical adjudication committee member for a medDay Pharmaceuticals clinical trial, and has received research funding (paid directly to institution) from Biogen, Roche, Genentech, The Stiff Person Syndrome Research Foundation, National Multiple Sclerosis Society, Department of Defense, and Patient Centered Outcomes Institute.


 Conflicts of Interest and Source of Funding: This article was prepared with the medical writing support of W4Research, financially supported by Merck. Merck had no access to the data or any other role in study design, analysis, or decision to submit for publication. Mónica S., J. Sequeira, P.A., R.G., J.F., F.L., L.L., M.J.S., C.C., and J. de Sá have received honoraria from Merck and others for acting as speakers and for attending scientific meetings. J. Sequeira, P.A., R.G., J.F., F.L., L.L., M.J.S., V.S., C.C., and J. de Sá had also received fees for acting as a consultant and/or for participation in advisory boards from several companies, including Merck. The remaining authors did not receive any financial support and have no conflicts of interest to declare.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors have no funding and conflicts of interest to disclose.
 Declaration of Competing Interest All authors agree with the manuscript content and authorship listing, and each author meets the requirements for authorship. The authors do not have any relevant financial or personal disclosures related to this work.

 Declaration of Competing Interest The authors declare that they have no competing interests.
 Declaration of Competing Interest None.

 Competing interests: JW has nothing to disclose. LA reports grants from Swedish Research Council, grants from Swedish Research Council for Health Working Life and Welfare, grants from Swedish Brain Foundation, during the conduct of the study; personal fees from Teva, personal fees from Biogene Idec, outside the submitted work. TO has received lecture/advisory board honoraria, and unrestricted MS research grants from Biogen, Novartis, Sanofi and Merck. JH has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis and Sandoz and speaker’s fees from Biogen, Novartis, Merck KGaA, Teva and Sanofi-Genzyme. He has served as PI for projects, or received unrestricted research support from, Biogen, Bristol-Myers-Squibb, Merck KGaA, Novartis, Roche and Sanofi-Genzyme. AKH has nothing to disclose.
 The authors have no conflict of interests to declare.


 Declaration of Competing Interest Ilse M. Nauta was supported by the Dutch MS Research Foundation (project number 15–911) and National MS Foundation. Dirk Bertens was partially supported by a grant from the Netherlands Brain Foundation (Hersenstichting, grant number DR.−2019–00,315). Dirk Bertens, Luciano Fasotti and Roy P.C. Kessels were partially supported by a grant from the European Regional Development Fund (ERDF/EFRO, grant number PROJ-00,928). Jay Fieldhouse was supported by Stichting Dioraphte. Bernard M.J. Uitdehaag reported research support and/or consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Teva, and Immunic Therapeutics. Roy P.C. Kessels is associate editor for Neuropsychology Review, member of the editorial board of the Journal of the International Neuropsychological Society, member of the scientific advisor board of Alzheimer Nederland, and chair of the scientific advisory board of the Korsakoff Knowledge Center Netherlands (Korsakov Kenniscentrum). Anne E.M. Speckens reported no disclosures. Brigit A. de Jong reported receiving grants from Dutch MS Research Foundation (project number 15–911) and National MS Foundation. B.A. de Jong is member of the medical advisory board of the Dutch MS Society, chair of the committee for the revision of the guideline on disease modifying therapy and MS for the Netherlands Society of Neurology, and chair of the committee of the Dutch National MS registration of the Netherlands Society of Neurology.

 Declaration of Competing Interest V.O.B. reports no conflicts of interest. S.M. received grant support from Novartis Pharma GmbH. T.K. has served on advisory boards for Roche Pharma and has received personal compensations/speaker honoraria from Bayer Healthcare, Teva Pharma, Merck, Novartis Pharma, Sanofi-Aventis/Genzyme, Roche Pharma, and Biogen and grant support from Novartis and Chugai Pharma in the past. T.K. received speaker honoraria and/or personal fees for advisory boards from Novartis Pharma, Roche Pharma, Alexion/Astra Zeneca, Horizon, Merck, Chugai and Biogen. E.M. received funding for travel or speaker honoraria from Roche, Novartis, Sanofi, Biogen, Teva Pharma, and Merck and research support from Novartis, Sanofi, Merck, GlycoEra, and Roche.
 Declaration of Competing Interest No competing interest to declare.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.






 Competing interests: None declared.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: S. Sen has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. R. Karabudak has received honoraria for giving educational lectures, consultancy fees for participating advisory boards, and travel grants for attending scientific congresses or symposia from Roche, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey, Abdi İbrahim İlac, Deva and ARIS. A. Siva has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi İbrahim İlac. E. Portaccio received compensation for travel grants, participation in advisory board and/or speaking activities from Biogen, Merck Serono, Sanofi, Teva, and Novartis; serves on the editorial board of Frontiers in Neurology and Brain Sciences. M.P. Amato served on scientific advisory boards for and has received speaker honoraria and research support from Biogen Idec, Merck Serono, Bayer Schering Pharma, and Sanofi Aventis, and serves on the editorial board of Multiple Sclerosis Journal and BMC Neurology. M.P. Sormani received consulting fees from Roche, Biogen, Merck, Novartis, Sanofi, Celgene, Immunic, Geneuro, GSK, Medday; received payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Roche, Biogen Merck, Novartis, Sanofi, Celgene; participated on a Data Safety Monitoring Board or Advisory Board for Roche, Sanofi, Novartis, Merck. P. Confalonieri has received honoraria for speaking or consultation fees from Novartis and Biogen, has received funding for travel to attend scientific events or speaker honoraria from Merck Serono, Biogen Idec, Teva, Mylan and Roche. He has also received institutional research support from Merk-Serono, Novartis and Roche. He is also principal investigator in clinical trials for Biogen, Merck Serono, Roche. I. Schiavetti received consulting fees from Hippocrates Research, NovaNeuro, Sakura Italia, ADL Farmaceutici, Associazione Commissione Difesa Vista Onlus. M. Inglese received research grants from NIH, DOD, NMSS, FISM, and Teva Neuroscience; received fees for participating in advisory boards from Roche, Biogen, Merck and Genzyme. M. Radaelli received speaker honoraria from Biogen Idec, Sanofi-Genzyme, Novartis and Merck Serono and funding for travel to scientific meetings from Biogen Idec, Sanofi-Genzyme, Novartis, Merck Serono, Teva and Roche. N. De Rossi received speaker honoraria from Biogen Idec, Genzyme, Novartis, Sanofi-Aventis; received funding for participation in advisory board to Novartis, Biogen and Genzyme-Sanofi and for travel to scientific meetings from Biogen Idec, Teva, Sanofi-Genzyme, Roche, Almirall and Novartis. P. Immovilli reports personal fees from Roche, personal fees from Biogen, personal fees from Merck, outside the submitted work. M. Capobianco reports personal fees and non-financial support from Biogen, personal fees and non-financial support from Merck Serono, personal fees and non-financial support from Roche, personal fees and non-financial support from Novartis, personal fees and non-financial support from Sanofi, personal fees from Almirall, outside the submitted work. M. Trojano reports grants and personal fees from Biogen, grants and personal fees from Novartis, grants and personal fees from Roche, grants and personal fees from Merck, personal fees from Sanofi, personal fees from TEVA, from null, outside the submitted work. G. Comi reports personal fees from Novartis, Teva Pharmaceutical Industries Ltd, Teva Italia Srl, Sanofi Genzyme, Genzyme Corporation, Genzyme Europe, Merck KGgA, Merck Serono SpA, Celgene Group, Biogen Idec, Biogen Italia Srl, F. Hoffman-La Roche, Roche SpA, Almirall SpA, Forward Pharma, Medday, Excemed, outside the submitted work. F. Patti reports grants from Biogen, grants from Merck, grants from FISM, grants from Onlus association, grants from University of Catania, personal fees from Almirall, personal fees from Bayer, personal fees from Biogen, personal fees from Merck, personal fees from Roche, personal fees from Sanofi, personal fees from TEVA, outside the submitted work. M. Salvetti reports grants and personal fees from Biogen, grants and personal fees from Merck, grants and personal fees from Novartis, grants and personal fees from Roche, grants and personal fees from Sanofi, grants and personal fees from Teva, grants from Italian Multiple Sclerosis Foundation, grants from Sapienza University of Rome, outside the submitted work. C. Cordioli received grants or contracts from Roche, Novartis, Merck Serono, Biogen, Celgene; received consulting fees from Biogen. R. Bergamaschi has served on scientific advisory boards for Biogen, Merck-Serono, Novartis, Sanofi-Genzyme; received research support from Almirall, Bayer, Biogen, Merck-Serono, Novartis, Sanofi-Genzyme; received support for travel and congress from Biogen, Roche, Merck-Serono, Sanofi-Genzyme, Teva; received honoraria for speaking engagements from Biogen, Merck-Serono, Novartis, Sanofi-Genzyme. M. Filippi is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology and Associate Editor of Neurological Sciences; received compensation for consulting services and/or speaking activities from Alexion, Almirall, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla and ARiSLA (Fondazione Italiana di Ricerca per la SLA). He received speaker honoraria from the following companies: Biogen, Merck, Novartis, Roche, Sanofi-Genzyme and TEVA. E. Cocco reports grants, personal fees, and non-financial support from Biogen and Merck; personal fees and non-financial support from Novartis; grants from Roche; and personal fees from Genzyme, outside the submitted work. L. Moiola received compensation for consulting services, travel grants, and/or speaking activities from Biogen, Serono, Sanofi, Teva, Roche, and Novartis. P. Perini has received speaker honoraria and consulting fees from Biogen, Merck Serono, Novartis, Roche, Sanofi Genzyme, and TEVA. The remaining authors have nothing to report.
 The authors declare that they have no competing interests.
 The authors declare that they have no conflict of interest. Alexander Wuschek, Matthias Bussas, Malek El Husseini, Laura Harabacz, Viktor Pineker, Isabelle Riederer, and Claus Zimmer have nothing to disclose. Viola Pongratz received research funding from Novartis (Oppenheim Förderpreis 2017). Jan S. Kirschke has received research funding from the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG; project 432290010), the German Federal Ministry of Education and Research (13GW0469D) and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (101045128—iBack-epic—ERC-2021-COG). He is Co-Founder of Bonescreen GmbH. Achim Berthele has received consulting and/or speaker fees from Alexion, Bayer Healthcare, Biogen, Celgene, Novartis, Roche and Sandoz/Hexal. His institution has received compensation for clinical trials from Alexion, Biogen, Merck, Novartis, Roche, and Sanofi Genzyme. Bernhard Hemmer is associated with DIFUTURE (Data Integration for Future Medicine) [BMBF 01ZZ1804[A-I]]. Bernhard Hemmer received funding from the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology [EXC 2145 SyNergy—ID 390857198] and the European Union’s Horizon 2020 Research and Innovation Program [grant MultipleMS, EU RIA 733161]. He has served on scientific advisory boards for Novartis; he has served as DMSC member for AllergyCare, Sandoz, Polpharma and TG therapeutics; he or his institution have received speaker honoraria from Desitin; his institution received research grants from Regeneron for multiple sclerosis research. He holds part of two patents; one for the detection of antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis and one for genetic determinants of neutralizing antibodies to interferon. Mark Mühlau received research support from the Bavarian State Ministry for Science and Art (Collaborative Bilateral Research Program Bavaria—Québec: AI in medicine, Grant F.4-V0134.K5.1/86/34), the German Research Foundation (DFG SPP2177; Radiomics: Next Generation of Biomedical Imaging; project number 428223038); the National Institutes of Health (Grant 1R01NS112161-01); the German Federal Ministry of Education and Research (DIFUTURE: 01ZZ1603[A-D] and 01ZZ1804[A-I]).
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: S.O.R. has received speaking and consulting honoraria from Genzyme, Biogen Idec, Novartis, Roche, Excemed and MSD; as well as research support from Novartis. S.R. has received speaking honoraria or scientific advisory fees from Merck, Novartis and Biogen. M.P.A. has served on Scientific Advisory Boards for Biogen, Novartis, Roche, Merck, Sanofi Genzyme, and Teva; has received speaker honoraria from Biogen, Merck, Sanofi Genzyme, Roche, Novartis, and Teva; has received research grants for her Institution from Biogen, Merck, Sanofi Genzyme, Novartis, and Roche. She is co-editor of the Multiple Sclerosis Journal and Associate Editor of Frontiers in Neurology. M.C. has received compensation for consulting services and speaking honoraria from GSK, Novartis, Sanofi Pasteur, MSD, Pfizer and Sequirus. M.F.F. has received a grant from Biogein Idec Argentina. M.F. is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology, and Associate Editor of Neurological Sciences; received compensation for consulting services and/or speaking activities from Alexion, Almirall, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). B.H. has served on scientific advisory boards for Novartis; he has served as DMSC member for AllergyCare, Polpharma Sandoz and TG therapeutics; he or his institution have received speaker honoraria from Desitin; His institution received research grants from Regeneron for multiple sclerosis research. He holds part of two patents; one for the detection of antibodies against KIR4.1 in a sub-population of patients with multiple sclerosis and one for genetic determinants of neutralizing antibodies to interferon. All conflicts are not relevant to the topic of the study. R.J. has received advisory board honoraria from Bristol-Myers Squibb. M.M. has served on scientific advisory board, received support for congress participation or speaker honoraria from Biogen, Sanofi, Roche, Novartis, Merck, Abbvie, Alexion, BMS. The Danish MS Registry received research support from Biogen, Genzyme, Roche, Merck, Novartis. C.O.G. has received speaking and consulting honoraria from Biogen Idec, Sanofi Genzyme, Novartis, Merck, Teva, Roche, Jannsen and BMS. A.S. has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi İbrahim İlaç. S.V. received grants, personal fees and/or non-financial support from Biogen, BMS-Celgène, Sanofi Genzyme, Merck, Novartis, Roche, Teva. M.T. has received compensation for consulting services and speaking honoraria from Almirall, Bayer Schering Pharma, Biogen Idec, Genzyme, Merck-Serono, Novartis, Roche, Sanofi-Aventis Viela-Bio and Teva Pharmaceuticals M.T. has received compensation for consulting services and speaking honoraria from Almirall, Bayer Schering Pharma, Biogen Idec, Genzyme, Merck-Serono, Novartis, Roche, Sanofi-Aventis Viela-Bio and Teva Pharmaceuticals. C.L.F. and Y.H. report no disclosures.
 Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: HH has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Siemens, Teva, and received honoraria for acting as consultant for Biogen, Celgene, Novartis and Teva. GA has received speaking honoraria and compensation for consulting services or participation in advisory boards from Sanofi, Merck, Roche and Horizon Therapeutics; travel funding from Novartis, Roche and ECTRIMS; is the editor for Europe of Multiple Sclerosis Journal—Experimental, Translational and Clinical; and is a member of the International Women in Multiple Sclerosis (iWiMS) network executive committee. KB has participated in meetings sponsored by, received speaking honoraria or travel funding from Roche, Biogen, Sanofi, and Teva. SG has received speaker honoraria and has been a member of scientific boards for Biogen Idec, Genzyme, Novartis, and Merck and received grant funding from Genzyme, Merck and Takeda. MK has received funding for travel and speaker honoraria from Bayer, Novartis, Merck, Biogen Idec and Teva Pharmaceutical Industries Ltd. and serves on scientific advisory boards for Biogen Idec, Merck Serono, Roche, Novartis and Gilead. CT has a collaboration contract with ADx Neurosciences, Quanterix and Eli Lilly, performed contract research or received grants from AC-Immune, Axon Neurosciences, Bioconnect, Biogen, Biorchestra, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, Novo Nordisk, PeopleBio, Roche, Toyama, and Vivoryon. She serves on editorial boards of Medidact Neurologie/Springer, Alzheimer Research and Therapy, Neurology: Neuroimmunology & Neuroinflammation, and is editor of a Neuromethods book Springer. Research of CET is supported by the European Commission (Marie Curie International Training Network, grant agreement no. 860197 (MIRIADE), Innovative Medicines Initiatives 3TR (Horizon 2020, grant no. 831434) and JPND (bPRIDE), National MS Society (Progressive MS alliance) and Health Holland, the Dutch Research Council (ZonMW), Alzheimer Drug Discovery Foundation, The Selfridges Group Foundation, Alzheimer Netherlands, Alzheimer Association. CT is recipient of ABOARD, which is a public–private partnership receiving funding from ZonMW (#73305095007) and Health~Holland, Topsector Life Sciences & Health (PPP-allowance; #LSHM20106). ABOARD also receives funding from Edwin Bouw Fonds and Gieskes-Strijbisfonds. HT has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Bayer, Biogen, Celgene, Fresenius, Genzyme-Sanofi, Janssen, Merck, Novartis, Roche, Siemens and Teva. LMV has served at scientific advisory boards, participated in meetings sponsored by, received speaking honoraria or travel funding or research grants from Roche, Sanofi, Merck, Biogen, Bristol Myers, and Novartis. MAVW has received research grants from The Binding Site, Siemens Healthineers and Sebia Inc, has participated in an advisory board for Myeloma360. HZ has served in scientific advisory boards and/or as a consultant for Abbvie, Alector, Annexon, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, Nervgen, Novo Nordisk, Pinteon Therapeutics, Red Abbey Labs, Passage Bio, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics, and Wave; has given lectures in symposia sponsored by Cellectricon, Fujirebio, Alzecure, Biogen, and Roche; and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program (outside submitted work). FD has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Almirall, Biogen, Celgene, Genzyme-Sanofi, Merck, Novartis Pharma, Roche, and Teva. His institution has received research grants from Biogen and Genzyme Sanofi. He is section editor of the MSARD Journal (Multiple Sclerosis and Related Disorders). JW, BK, and RS have nothing to disclose.
 Declaration of Competing Interest No authors have any competing interests to declare.

 Declaration of Competing Interest None.

 The authors declare that they have no conflict of interest. AL has received personal compensation for consulting, serving on a scientific advisory board, speaking or other activities from Alexion, Bristol Myers Squib, Janssen, Biogen, Merck Serono, Novartis, Sanofi/Genzyme. Her institutions have received research grants from Novartis.
 Disclosure/Conflict of interest J.W. Lindsey has received personal compensation for speaking or consulting for EMD Serono, Celgene, Mapi Pharmaceuticals, Banner Life Sciences, TG Therapeutics, Genentech, and Genzyme; is participating in clinical trials funded by Genentech, Biogen, Atara, EMD Serono, and AbbVie; and has received research funding from the National MS Society and Genentech. Ms. Pham and Dr. Saroukhani have no conflicts to report.
 HV has received research support from Merck, Novartis, Pfizer, and Teva, consulting fees from Merck, and speaker honoraria from Novartis; all funds were paid to his institution. GJN has received personal compensation for activities with Bayer and research support from Merck. AS is an employee of Merck Healthcare KGaA, Darmstadt, Germany. DJ is an employee of Merck Serono Ltd, Feltham, UK (an affiliate of Merck KGaA). MPS has received consulting fees from Biogen, Genzyme, GeNeuro, MedDay, Merck, Novartis, Roche, and Teva. BMJU has received consultancy fees from Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. AV has received research support from Merck. GC has received consulting fees from Bayer, Biogen, Merck, Novartis, Receptos, Roche/Genentech, Sanofi-Aventis, and Teva Pharmaceutical Industries Ltd; lecture fees from Bayer, Biogen, Merck, Novartis, Sanofi-Aventis, Serono Symposia International Foundation, and Teva Pharmaceutical Industries Ltd; and trial grant support from Bayer, Biogen, Merck, Novartis, Receptos, Roche/Genentech, Sanofi-Aventis, and Teva Pharmaceutical Industries Ltd. LK’s institution (University Hospital Basel, University of Basel) has received in the last 3 years and used exclusively for research support: steering committee, advisory board, and consultancy fees (Actelion [Janssen/JandJ], Addex, Bayer, Biogen, Biotica, Genzyme, Lilly, Merck, Mitsubishi, Novartis, Ono Pharma, Pfizer, Receptos, Sanofi, Santhera, Siemens, Teva, UCB, and Xenoport); speaker fees (Bayer, Biogen, Merck, Novartis, Sanofi, and Teva); support of educational activities (Bayer, Biogen, CSL Behring, Genzyme, Merck, Novartis, Sanofi, and Teva); license fees for Neurostatus products; and grants (Bayer, Biogen, European Union, Merck, Novartis, Roche Research Foundation, Swiss MS Society, and Swiss National Research Foundation). NDeS is a consultant for Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva; has grants or grants pending from FISM and Novartis, is on the speakers’ bureaus of Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva; and has received travel funds from Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. FB is supported by the NIHR Biomedical Research Centre at UCLH and is a consultant to Biogen, Combinostics, IXICO, Merck, and Roche. MB, MLdeV, and BCAT have nothing to disclose.
 Declaration of Competing Interest In the last two years, Gavin Giovannoni has received compensation for serving as a consultant or speaker for or has received research support from AbbVie, Aslan, Atara Bio, Biogen, BMS-Celgene, GlaxoSmithKline, Janssens/J&J, Japanese Tobacco, Jazz Pharmaceuticals, LifNano, Merck & Co, Merck KGaA/EMD, Moderna, Serono, Moderna, Novartis, Sandoz, Sanofi and Roche/Genentech.
 Competing interests: IR served on scientific advisory boards for Novartis and Merck, and received conference travel support and/or speaker honoraria from Roche, Novartis, Biogen, Teva, Sanofi Genzyme, and Merck. A-LN received grants from MS Research Australia; grants, personal fees, and nonfinancial support from Biogen; grants and personal fees from Merck Serono; personal fees from Teva and Novartis; and nonfinancial support from Roche and Sanofi Genzyme. GI received speaking honoraria from Biogen, Novartis, Sanofi, Merck, Roche, Almirall, and Teva. SE received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, and Teva. FP received speaker honoraria and advisory board fees from Almirall, Bayer, Biogen, Celgene, Merck, Novartis, Roche, Sanofi Genzyme, and Teva, and research funding from Biogen, Merck, FISM (Fondazione Italiana Sclerosi Multipla), Reload Onlus Association, and the University of Catania. DH received speaker honoraria and consulting fees from Biogen, Merck, Teva, Roche, Sanofi Genzyme, and Novartis, and support for research activities from Biogen and the Czech Ministry of Education (project PROGRES Q27/LF1). EVH received honoraria or research support from Biogen, Merck Serono, Novartis, Roche, and Teva; has been a member of advisory boards for Actelion, Biogen, Celgene, Merck Serono, Novartis, and Sanofi Genzyme; and received research support from the Czech Ministry of Education (project PROGRES Q27/LF1). MG received consulting fees from Teva Canada Innovation, Biogen, Novartis, and Sanofi Genzyme; lecture payments from Teva Canada Innovation, Novartis, and EMD; and research support from the Canadian Institutes of Health Research. PD served on editorial boards for, and has been supported to attend meetings by, EMD, Biogen, Novartis, Genzyme, and Teva Neuroscience; he holds grants from the Canadian Institutes of Health Research and the MS Society of Canada, and received funding for investigator-initiated trials from Biogen, Novartis, and Genzyme. FG’M received honoraria or research funding from Biogen, Genzyme, Novartis, Teva Neurosciences, Mitsubishi, and ONO Pharmaceuticals. AL received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities from Biogen, Merck Serono, Mylan, Novartis, Roche, Sanofi Genzyme, and Teva; her institutions have received research grants from Novartis (in the past 4 years). PG served on advisory boards for Novartis, EMD Serono, Roche, Biogen Idec, Sanofi Genzyme, and Pendopharm; received grant support from Genzyme and Roche; and received research grants for his institution from Biogen Idec, Sanofi Genzyme, and EMD Serono. MPA received honoraria as a consultant on scientific advisory boards for Biogen, Bayer Schering, Merck, Teva, and Sanofi-Aventis, and received research grants by Biogen, Bayer Schering, Merck, Teva, and Novartis. PS served on scientific advisory boards for Biogen Idec and Teva; received funding for travel and speaker honoraria from Biogen Idec, Merck, Teva, Sanofi Genzyme, Novartis, and Bayer; and received research grants for her institution from Bayer, Biogen, Merck, Novartis, Sanofi, and Teva. DF received travel grants and/or speaker honoraria from Merck, Teva, Novartis, Biogen, and Sanofi Genzyme. KB received honoraria and consulting fees from Biogen, Teva, Novartis, Sanofi Genzyme, Roche, Merck, CSL, and Grifols. JL-S received travel compensation from Novartis, Biogen, Roche, and Merck; her institution received honoraria for talks and advisory board commitments, as well as research grants from Biogen, Merck, Roche, Teva, and Novartis. RA received honoraria as a speaker and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche, and Sanofi Genzyme. CB received conference travel support from Biogen, Novartis, Bayer Schering, Merck, and Teva, and participated in clinical trials by Sanofi-Aventis, Roche, and Novartis. VVP received travel grants from Merck, Biogen, Sanofi, Celgene, Almirall, and Roche; his institution received research grants and consultancy fees from Roche, Biogen, Sanofi, Celgene, Merck, and Novartis Pharma. MT received travel grants from Novartis, Bayer Schering, Merck, and Teva, and participated in clinical trials by Sanofi-Aventis, Roche, and Novartis. DM received speaker honoraria for advisory board service and travel grants from Almirall, Biogen, Merck, Novartis, Roche, Sanofi Genzyme, and Teva. CR-T received research funding, compensation for travel, or speaker honoraria from Biogen, Novartis, Genzyme, and Almirall. DLS received honoraria as a consultant on scientific advisory boards from Bayer Schering, Novartis, and Sanofi-Aventis, and compensation for travel from Novartis, Biogen, Sanofi-Aventis, Teva, and Merck. FG received an institutional research grant from Biogen and Sanofi Genzyme; served on scientific advisory boards for Biogen, Novartis, Merck, Sanofi Genzyme, and Roche; and received funding for travel and speaker honoraria from Biogen, Merck, and Sanofi-Aventis. MS participated in, but did not receive honoraria for, advisory board activity for Biogen, Merck, Bayer Schering, Sanofi-Aventis, and Novartis. RB received speaker honoraria from Bayer Schering, Biogen, Genzyme, Merck, Novartis, Sanofi-Aventis, and Teva; research grants from Bayer Schering, Biogen, Merck, Novartis, Sanofi-Aventis, and Teva; and congress, travel, and accommodation expense compensations from Almirall, Bayer Schering, Biogen, Genzyme, Merck, Novartis, Sanofi-Aventis, and Teva. RA received conference travel support from Novartis, Teva, Biogen, Bayer, and Merck, and participated in clinical trials by Biogen, Novartis, Teva, and Actelion. JLS-M received travel compensation from Novartis and Biogen; received speaking honoraria from Biogen, Novartis, Sanofi, Merck, Almirall, Bayer, and Teva; and participated in a clinical trial by Biogen. JP received travel compensation from Novartis, Biogen, Genzyme, and Teva, and speaking honoraria from Biogen, Novartis, Genzyme and Teva. TC-T received speaking or consulting fees and/or travel funding from Bayer, Biogen, Merck, Novartis, Roche, Sanofi Genzyme, and Teva. GL received travel and/or consultancy compensation from Sanofi Genzyme, Roche, Teva, Merck, Novartis, Celgene, and Biogen. JO received research funding from the MS Society of Canada, the National MS Society, Brain Canada, Biogen Idec, Roche, and EMD Serono, and personal compensation for consulting or speaking from EMD Serono, Sanofi Genzyme, Biogen Idec, Roche, Celgene, and Novartis. AA received personal fees and speaker honoraria from Teva, Merck, Biogen Gen Pharma, Roche, Novartis, Bayer, and Sanofi Genzyme, and received travel and registration grants from Merck, Biogen Gen Pharma, Roche, Sanofi Genzyme, and Bayer. HB received compensation for consulting, talks, and advisory or steering board activities from Biogen, Merck, Novartis, Genzyme, Alfred Health, and Oxford Health Policy Forum, and research support from Novartis, Biogen, Roche, Merck, the National Health and Medical Research Council of Australia, Pennycook Foundation, and MS Research Australia MB served on scientific advisory boards for Biogen, Novartis, and Genzyme, received conference travel support from Biogen and Novartis, and serves on steering committees for trials conducted by Novartis; his institution received research support from Biogen, Merck, and Novartis. EC Cristiano received honoraria as a consultant on scientific advisory boards for Biogen, Bayer Schering, Merck, Genzyme, and Novartis, and participated in clinical trials or other research projects by Merck, Roche, and Novartis. SH received honoraria and consulting fees from Novartis, Bayer Schering, and Sanofi, and travel grants from Novartis, Biogen Idec, and Bayer Schering. GI received compensation for travel, accommodations, and meeting expenses from Bayer Schering, Biogen, Merck, Novartis, Sanofi-Aventis, and Teva. LK received research support from Acorda, Actelion, Allozyne, BaroFold, Bayer HealthCare, Bayer Schering, Bayhill Therapeutics, Biogen, Elan, European Union, Genmab, Gianni Rubatto Foundation, GlaxoSmithKline, Glenmark, MediciNova, Merck, Novartis, Novartis Research Foundation, Roche, Roche Research Foundation, Sanofi-Aventis, Santhera, the Swiss MS Society, the Swiss National Research Foundation, Teva Neuroscience, UCB, and Wyeth. BW-G participated in speakers' bureaus and/or served as a consultant for Biogen, EMD Serono, Novartis, Genentech, Celgene/Bristol Meyers Squibb, Sanofi Genzyme, Bayer, Janssen, and Horizon; received grant/research support from these same agencies; and serves on editorial boards for BMJ Neurology, Children, CNS Drugs, MS International, and Frontiers Epidemiology. BVW received research and travel grants and honoraria for advisory and speaking fees from Bayer Schering, Biogen, Sanofi Genzyme, Merck, Novartis, Roche, and Teva. TK served on scientific advisory boards for BMS, Roche, Sanofi Genzyme, Novartis, Merck, and Biogen, and the steering committee for the Brain Atrophy Initiative by Sanofi Genzyme; received conference travel support and/or speaker honoraria from WebMD Global, Novartis, Biogen, Sanofi Genzyme, Teva, BioCSL, and Merck; and received support for research or educational events from Biogen, Novartis, Genzyme, Roche, Celgene, and Merck.

 None
 ASD, NK, LS, and MG have nothing to disclose. IM reports grants from Novartis Pharma GmbH, during the conduct of the study; personal fees from BiogenIdec, Bayer Healthcare, TEVA, Serono, Novartis Pharma GmbH, Genzyme, Roche, grants from BiogenIdec, Genzyme, outside the submitted work. WB has nothing to disclose related to this work.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare the following conflicts of interest. Chiara Marzi: None. Alessandro d'Ambrosio: None. Stefano Diciotti: None. Alvino Bisecco received speaker's honoraria and/or compensation for consulting service and/or speaking activities from Biogen, Roche, Merck, Celgene and Genzyme. Manuela Altieri: None. Massimo Filippi is Editor‐in‐Chief of the Journal of Neurology and Associate Editor of Human Brain Mapping; received compensation for consulting services and/or speaking activities from Almirall, Alexion, Bayer, Biogen Idec, Celgene, Eli Lilly, Genzyme, Merck‐Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck‐Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). Maria Assunta Rocca received speakers' honoraria from Bayer, Biogen Idec, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, Roche and Teva, and receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. Loredana Storelli: None. Patrizia Pantano has received funding for travel from Novartis, Genzyme, and Bracco and a speaking honorarium from Biogen. She received research support from Italian Ministry of Foreign Affairs and Fondazione Italiana Sclerosi Multipla. Silvia Tommasin: None. Rosa Cortese: None. Nicola De Stefano has received honoraria from Biogen‐Idec, Bristol Myers Squibb, Celgene, Genzyme, Immunic, Merck Serono, Novartis, Roche and Teva for consulting services, speaking, and travel support. He serves on advisory boards for Merck, Novartis, Biogen‐Idec, Roche, and Genzyme, Immunic and he has received research grant support from the Italian MS Society. Gioacchino Tedeschi is speaker, consulting fees and research support from Biogen, Genzyme, Merck Serono, Mylan, Novartis, Roche, Teva, Allergan, Abbvie and Lundbeck. Research support from Fondazione Italiana Sclerosis Multipla. Antonio Gallo received speaker and consulting fees from Biogen, Genzyme, Merck Serono, Mylan, Novartis, Roche, and Teva, and receives research support from Fondazione Italiana Sclerosi Multipla.
 None declared.
 Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: HH has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Siemens, Teva, and received honoraria for acting as consultant for Biogen, Celgene, Novartis and Teva; GA has received speaking honoraria and compensation for consulting services or participation in advisory boards from Sanofi, Merck, Roche and Horizon Therapeutics; travel funding from Novartis, Roche and ECTRIMS; is the editor for Europe of Multiple Sclerosis Journal – Experimental, Translational and Clinical; and is a member of the International Women in Multiple Sclerosis (iWiMS) network executive committee; SG has received speaker honoraria and has been scientific boards from Biogen Idec, Genzyme, Novartis and Merck and grant funding from Genzyme, Merck and Takeda; BK has nothing to disclose; MK has received funding for travel and speaker honoraria from Bayer, Novartis, Merck, Biogen Idec and Teva Pharmaceutical Industries Ltd. and serves on scientific advisory boards for Biogen Idec, Merck Serono, Roche, Novartis and Gilead; RS has nothing to disclose; CT has a collaboration contract with ADx Neurosciences, Quanterix and Eli Lilly, performed contract research or received grants from AC-Immune, Axon Neurosciences, Bioconnect, Biogen, Bioorchestra, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, Novo Nordisk, PeopleBio, Roche, Toyama, Vivoryon. She serves on editorial boards of Medidact Neurologie/Springer, Alzheimer Research and Therapy, Neurology: Neuroimmunology and Neuroinflammation, and is editor of a Neuromethods book Springer. Research of CET is supported by the European Commission (Marie Curie International Training Network, grant agreement No 860197 (MIRIADE), Innovative Medicines Initiatives 3TR (Horizon 2020, grant no 831434) and JPND (bPRIDE), National MS Society (Progressive MS alliance) and Health Holland, the Dutch Research Council (ZonMW), Alzheimer Drug Discovery Foundation, The Selfridges Group Foundation, Alzheimer Netherlands, Alzheimer Association. CT is a recipient of ABOARD, which is a public-private partnership receiving funding from ZonMW (#73305095007) and Health–Holland, Topsector Life Sciences and Health (PPP-allowance; #LSHM20106). ABOARD also receives funding from Edwin Bouw Fonds and Gieskes-Strijbisfonds; HT has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Bayer, Biogen, Celgene, Fresenius, Genzyme-Sanofi, Janssen, Merck, Novartis, Roche, Siemens and Teva; LMV has served at scientific advisory boards, participated in meetings sponsored by, received speaking honoraria or travel funding or research grants from Roche, Sanofi, Merck, Biogen, Bristol Myers and Novartis; MAVW has received research grants from The Binding Site, Siemens Healthineers and Sebia Inc and has participated in an advisory board for Myeloma360; HZ has served at scientific advisory boards and/or as a consultant for Abbvie, Alector, Annexon, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, Nervgen, Novo Nordisk, Pinteon Therapeutics, Red Abbey Labs, Passage Bio, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics and Wave, has given lectures in symposia sponsored by Cellectricon, Fujirebio, Alzecure, Biogen and Roche, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Programme (outside submitted work); FD has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Almirall, Biogen, Celgene, Genzyme-Sanofi, Merck, Novartis Pharma, Roche and Teva. His institution has received research grants from Biogen and Genzyme Sanofi. He is section editor of the MSARD Journal (Multiple Sclerosis and Related Disorders).

 The authors have organizational affiliations to disclose, S.M. is a board member of Hitch Bio and is a shareholder of Hitch Bio. Neha Kapate, Ninad Kumbhojkar, S.P., L.-L.W.W., and S.M. are inventors on patent applications related to the technology described in the manuscript (owned and managed by Harvard University).

 Declaration of competing interest Authors declare no conflict of interest.
 MG is a contractor for F. Hoffmann-La Roche Ltd. JSG over the past year has received grant/contract research support from the National MS Society, Biogen, and Octave Biosciences. She serves on a steering committee for a trial supported by Novartis. She has received honoraria for a non-promotional, educational activity for Sanofi Genzyme. She has received speaker fees from Alexion and BMS and served on an advisory board for Genentech. SPH is a contractor for F. Hoffmann-La Roche Ltd. FD was an employee of and is a shareholder in F. Hoffmann-La Roche Ltd; he is currently employed by Novartis Institutes for Biomedical Research. LM has nothing to disclose. LG is an employee of F. Hoffmann-La Roche Ltd. LC is an employee of and shareholder in F. Hoffmann-La Roche Ltd. FL is an employee of F. Hoffmann-La Roche Ltd. CB is a contractor for F. Hoffmann-La Roche Ltd. XM has received speaking honoraria and travel expenses for participation in scientific meetings; has been a steering committee member of clinical trials; or participated in advisory boards of clinical trials in the past years with Actelion, Alexion, Bayer, Biogen, Celgene, EMD Serono, Genzyme, Immunic, Medday, Merck, Mylan, Nervgen, Novartis, Roche, Sanofi-Genzyme, Teva, TG Therapeutics, Excemed, MSIF, and NMSS. SLH serves on the scientific advisory boards for Alector, Annexon, and Accure; is on the Board of Directors for Neurona Therapeutics; and has received travel reimbursement and writing assistance from F. Hoffmann-La Roche Ltd and Novartis for CD20-related meetings and presentations. ML is a consultant for F. Hoffmann-La Roche Ltd via Inovigate.
 Competing interests: JK reported speaking and consulting relationships with Biogen, Genzyme, Merck, Novartis, Roche, Sanofi and TEVA. Amsterdam UMC, location VUmc, MS Center Amsterdam has received financial support for research activities from Biogen, Celgene, Genzyme, Merck, Novartis, Roche, Sanofi and TEVA. TR reports consulting fees from Novartis. No other disclosures were reported.
 Conflict of Interest Disclosures: Dr Monreal reported receiving research grants, travel support, or honoraria for speaking engagements from Biogen, Sanofi, Merck, Novartis, Almirall, Roche, Bristol Myers Squibb, and Janssen outside the submitted work. Dr Sainz de la Maza reported receiving personal fees from Almirall, Bristol Myers Squibb, and Teva outside the submitted work and receiving compensation for lectures or travel expenses from Merck Serono, Biogen, Sanofi Genzyme, Roche, Janssen, and Novartis. Dr Llufriu reported receiving compensation for consulting services and speaker honoraria from Biogen Idec, Novartis, Teva, Genzyme, Sanofi Genzyme, and Merck. Dr Álvarez-Lafuente reported receiving nonfinancial support for meeting attendance from Biogen, Novartis, and Sanofi Genzyme outside the submitted work. Dr Casanova reported receiving compensation for consulting services and speaker honoraria from Sanofi Genzyme, Roche, Bristol Myers Squibb, Janssen, and Novartis. Dr Ramió-Torrentà reported receiving personal fees from Roche, Janssen, and Bristol Myers Squibb outside the submitted work and receiving compensation for consulting services and speaking honoraria from Biogen, Merck, Novartis, Bayer, Sanofi Genzyme, Teva Pharmaceutical Industries Ltd, Almirall, and Mylan. Dr Martínez-Rodríguez reported participating as a principal investigator in pharmaceutical company-sponsored clinical trials for Novartis, Roche, Merck Serono, Actelion, and Celgene and receiving personal fees for consulting services and lectures from Novartis, Biogen Idec, Sanofi, and Merck Serono. Dr Brieva reported receiving support for research projects from the Neuroimmunology and Multiple Sclerosis Unit, Department of Neurology, Doctor Josep Trueta University Hospital, and receiving speaker and consultancy fees and travel expenses for attending conferences from Bayer, Biogen, Roche, Merck, Novartis, Almirall, and Sanofi. Dr Saiz reported receiving compensation for consulting services and speaker honoraria from Bayer Schering, Merck, Biogen Idec, Sanofi-Aventis, Teva, Novartis, Roche, Janssen, and Horizon Therapeutics. Dr Eichau reported receiving personal fees from Novartis, Biogen, Merck, Roche, Sanofi, Bristol Myers Squibb, and Janssen outside the submitted work and receiving speaker honoraria and fees for consulting from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, and Teva. Dr Cabrera-Maqueda reported receiving speaking honoraria from Sanofi and personal fees from Bristol Myers Squibb outside the submitted work. Dr Pérez-Miralles reported receiving speaking honoraria from Almirall, Biogen, Sanofi Genzyme, Mylan, Novartis, Roche, Sanofi-Aventis, Teva, and Merck Serono; receiving compensation for serving on scientific advisory boards for Roche and Sanofi-Aventis; and being a member of the steering committee for Roche outside the submitted work. Dr Montalbán reported receiving speaking honoraria from Actelion, Alexion, Bayer, Biogen, Bristol Myers Squibb/Celgene, EMD Serono, Exemed, Genzyme, Hoffmann-La Roche, Immunic, Janssen Pharmaceuticals, MedDay, Merck, Mylan, Multiple Sclerosis International Federation, NervGen, Novartis, Sandoz, Sanofi Genzyme, Teva Pharmaceutical, and TG Therapeutics; receiving travel expenses for scientific meeting participation from the National Multiple Sclerosis Society; and being a member of clinical trials of a steering committee or participating on advisory boards of clinical trials in the past 3 years with Biogen, Hoffmann-La Roche, Sanofi Genzyme, Merck, Novartis, and Teva Pharmaceutical outside the submitted work. Dr Tintoré reported receiving personal fees for consulting services and speaking honoraria from Almirall, Bayer Schering Pharma, Biogen Idec, Genzyme, Janssen, Merck Serono, Viatris, Novartis, Roche, Sanofi-Aventis, Vela Bio, and Teva Pharmaceutical and grants from the Carlos III Health Institute, the Genzyme Charitable Foundation, Fundación Salud 2000, Biogen Idec, Novartis, and Biogen Idec during the conduct of the study; receiving personal fees from Almirall, Bayer Schering Pharma, Biogen Idec, Genzyme, Janssen, Merck Serono, Viatris, Novartis, Roche, Sanofi-Aventis, Vela Bio, and Teva Pharmaceutical and grants from the Carlos III Health Institute, Biogen Idec, and Novartis outside the submitted work; and serving as the 2015 to 2021 coeditor of the Multiple Sclerosis Journal–Experimental, Translational and Clinical and 2022 president of the European Committee for Treatment and Research in Multiple Sclerosis. Dr Rodríguez-Jorge reported receiving personal fees from Sanofi outside the submitted work and receiving speaker honoraria from Biogen Idec and Sanofi. Dr Álvarez-Cermeño reported receiving other fees from the Biogen board membership, the Merck Serono board membership, Bayer Healthcare, Sanofi, and Roche for lectures; receiving grants from Novartis; and receiving nonfinancial support from Teva outside the submitted work. Dr Costa-Frossard reported receiving speaker fees and travel support and/or serving on advisory boards for Biogen, Sanofi, Merck, Bayer, Novartis, Roche, Teva, Celgene, Ipsen, Biopas, Bristol Myers Squibb, Janssen, and Almirall. Dr Villar reported receiving grants and personal fees from Merck, Roche, Sanofi Genzyme, Bristol Myers Squibb, Celgene, Biogen, and Novartis outside the submitted work. No other disclosures were reported.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Competing interests: None declared.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 JR, LD, MD, JDK, GF, SVS are inventors on the patent EP2018/084920: A new inflammation associated, low cell count enterotype issued to VIB VZW, Katholieke Universiteit Leuven, KU Leuven and Vrije Universiteit Brussel. JR is inventor on patent EP14184535.4 - 12/09/2014: Biological sampling and storage container, International patent application on 14/09/2015: PCT/EP2015/070977 issued to VIB VZW, Vrije Universiteit Brussel and LRD.
 None.
 Declaration of Competing Interest Authors have no conflicts of interest to disclose.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 Declaration of Competing Interest The authors declare no conflict of interests.
 G.M. is the inventor of patent number EP1904073 (Europe) and US2008274089 (USA) filed on 12 July 2006. The other authors declare no competing interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: M.S. was supported by a research grant from Melbourne University. A.J.C.E., I.D., T.A.A.B. and L.D. report no disclosures. J.K. reports grants from Biogen, Novartis, TEVA, Bayer Schering Pharma, GlaxoSmithKline, Merck, Genzyme and Roche. S.C.K. receives grant income from the National Health and Medical Research Council of Australia and has received honoraria from Novartis and Biogen. J.J.G.G. has served as a consultant for or received research support from Biogen, Celgene, Genzyme, MedDay, Merck, Novartis and Teva. M.M.S. serves on the editorial board of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation, Eurostars-EUREKA, ARSEP, Amsterdam Neuroscience, MAGNIMS and ZonMW and has served as a consultant for or received research support from Atara Biotherapeutics, Biogen, Celgene/Bristol Myers Squibb, Genzyme, MedDay and Merck.


 Declaration of Competing Interest There is no conflict of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: D.L.R. has received research support from the MS Society of Canada, Consortium of Multiple Sclerosis Centers (CMSC) and Roche Canada. She has received speaker or consultant fees from Alexion, Biogen, EMD Serono, Novartis, Roche and Sanofi Aventis. C.W. receives research funding from CIHR, Multiple Sclerosis Society of Canada and the Canada Foundation for Innovation. R.C. is the site investigator for studies funded by Roche, Novartis, Vielo Bio and Serono, and receives research support from Teva Innovation Canada, Roche Canada and Vancouver Coastal Health Research Institute. R.C. has received honoraria from Roche, EMD Serono, Sanofi, Biogen, Novartis and Alexion. M.S.F. has received research or educational grants from Sanofi Genzyme Canada. He has received honoraria or consultation fees from Alexion, Atara Biotherapeutics, Bayer Healthcare, BeiGene, BMS (Celgene), EMD Inc., F. Hoffmann-La Roche, Janssen (J&J), Merck Serono, Novartis, Sanofi Genzyme and Teva Canada Innovation. He has served as a member of an advisory board or board of directors for Alexion, Atara Biotherapeutics, Bayer Healthcare, BeiGene, BMS (Celgene), Celestra, F. Hoffmann-La Roche, Janssen (J&J), McKesson, Merck Serono, Novartis and Sanofi Genzyme. He has participated in a speaker’s bureau for Sanofi Genzyme and EMD Serono. S.A.M. has served as an advisory board member or received consulting fees from Biogen Idec, Bristol Myers Squibb/Celgene, EMD Serono, Novartis, Roche, Sanofi Genzyme and Teva Neuroscience. She has participated in a speaker’s bureau for Biogen Idec, Bristol Myers Squibb/Celgene, EMD Serono, Novartis, Roche and Sanofi Genzyme. She has received research support from Biogen Idec, Novartis, Roche and Sanofi Genzyme. She has participated as a site investigator in clinical trials sponsored by AbbVie, Bristol Myers Squibb/Celgene, EMD Serono, Novartis, Genzyme, Roche and Sanofi Genzyme. L.L. is a site investigator for studies funded by Roche, Novartis and Sanofi Aventis. He has received consultation fees from Alexion, Biogen, Bristol Myers Squibb, EMD Serono, Novartis, Roche and Sanofi Aventis. J.M.B. has received honoraria for speaking engagements and education activities and consultations from Roche, Biogen, Novartis and Prime. She has served as an advisor to CADTH. R.N. has nothing to disclose. A.K. has nothing to disclose. S.M. has nothing to disclose. R.A.M. receives research funding from Canadian Institutes of Health Research (CIHR), Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC and US Department of Defense and the Arthritis Society. She is supported by the Waugh Family Chair in Multiple Sclerosis. She is a co-investigator on a study funded, in part, by Biogen Idec and Roche (no funds to her/her institution).

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. This study was supported by an Independent Investigator –led Grant from Helius Medical, the company that makes the PoNS units. They and their employees had no involvement in the design and conduct of this study. Helius Medical technologies provided the PoNS™ (both TLNS and sham) devices. They have no involvement in data collection, analysis or reporting.

 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 Declaration of Competing Interest The authors declared that there is no conflict of interest.

 None.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest L. Amezcua has consulted for EMD Serono, Biogen, and Novartis; receives research support from NMSS, NIH NINDS, and Bristol Myers Squibb Foundation; and receives clinical trial research support from Genentech. M. J. Williams is an employee of Joi Life Wellness Group, LLC, which received funding from EMD Serono to conduct this study. J. Zhou, B. Hayward, and T. Livingston are employees of EMD Serono. M. Gough was an employee of Ashfield MedComms (Macclesfield, UK), an Ashfield Health company, at the time of manuscript development and was funded by the study sponsor to provide medical writing support.
 Conflicts of interest.—The authors certify that there is no conflict of interest with any financial organisation regarding the material discussed in the manuscript.
 I have read the journal’s policy and the authors of this manuscript have the following competing interests: Carmen Durán has received speaking and/or advisory board honoraria from Sanofi, Novartis, AbbVie, and Bial. Guillermo Navarro has received speaking and/or advisory board honoraria from Biogen, Novartis, Merck, Teva, Sanofi, and Roche. Guillermo Izquierdo Ayuso has received speaking and/or advisory board honoraria from Bayer, Biogen-Idec, Novartis, Sanofi, Merck-Serono, Almirall, and Roche. Anabel Granja Domínguez, Aurora Alemán, Anja Hochsprung, Cristina Páramo, and Ana Venegas have nothing to disclose. Raúl Romero Sevilla and Ana Lladonosa are employees of Novartis, Spain.

 The authors declare no conflict of interest.

 The authors declare no conflict of interest.

 Declaration of Competing Interest HH receives research support from the ZonMW, NWO, ATARA, Biogen, Celgene/BMS, Merck and MedDay and serves as a consultant for Sanofi Genzyme, Merck BV, Biogen Idec, Roche and Novartis, and received honorary from these parties paid to her institution. She serves on the editorial board of Multiple Sclerosis Journal. CT receives research support from the National MS Society (Progressive MS alliance) and Innovative Medicines Initiatives 3TR, has a research contract with Celgene. She serves on editorial boards of Medidact Neurologie/Springer, Neurology: Neuroimmunology & Neuroinflammation. She is editor of a Neuromethods book Springer. VG, HB, AG, EW, BJ declare to have no competing interests.
 The research activities of Tim Woelfle’s institution, RC2NB (Research Center for Clinical Neuroimmunology and Neuroscience Basel), are supported by the University Hospital and the University of Basel and by grants from Novartis and Roche. One of the main projects of RC2NB is the development of a new comprehensive MS Digital solution. Silvan Pless has nothing to disclose. Oscar Reyes is Senior Data Scientist of Healios AG. Andrea Wiencierz has nothing to disclose. Anthony Feinstein has nothing to disclose. Pasquale Calabrese has received honoraria for speaking at scientific meetings, serving at scientific advisory boards and consulting activities from: Abbvie, Actelion, Almirall, Bayer-Schering, Biogen Idec, Celgene, EISAI, Genzyme, Lundbeck, Merck Serono, Novartis, Pfizer, Teva, and Sanofi-Aventis. His research is also supported by the Swiss Multiple Sclerosis Society and the Swiss National Research Foundation. Konstantin Gugleta has nothing to disclose. Ludwig Kappos has received no personal compensation. His institution (University Hospital Basel/Foundation Clinical Neuroimmunology and Neuroscience Basel) has received the following exclusively for research support: steering committee, advisory board and consultancy fees (Abbvie, Actelion, AurigaVision AG, Biogen, Celgene, Desitin, Eli Lilly, EMD Serono, Genentech, Genzyme, Glaxo Smith Kline, Janssen, Japan Tobacco, Merck, Minoryx, Novartis, Roche, Sanofi, Santhera, Senda, Shionogi, Teva, and Wellmera; speaker fees (Celgene, Janssen, Merck, Novartis, and Roche); support for educational activities (Biogen, Desitin, Novartis, Sanofi and Teva); license fees for Neurostatus products; and grants (European Union, Innosuisse, Novartis, Roche Research Foundation, Swiss MS Society and Swiss National Research Foundation). Johannes Lorscheider’s institution has received research grants from Novartis, Biogen and Innosuisse as well as honoraria for advisory boards and/or speaking fees from Novartis, Roche and Teva. Yvonne Naegelin’s institution (University Hospital Basel) has received financial support for lectures from Teva and Celgene and grant support from Innosuisse (Swiss Innovation Agency). The research activities of RC2NB (Research Center for Clinical Neuroimmunology and Neuroscience Basel) are supported by the University Hospital and the University of Basel and by grants from Novartis and Roche. One of the main projects of RC2NB is the development of a new comprehensive MS Digital solution.
 The authors of this manuscript declare relationships with the following companies: Roland Opfer, Julia Krüger, Lothar Spies, and Ann-Christin Ostwaldt are employees of jung diagnostics GmbH, Hamburg, Germany. There is no actual or potential conflict of interest for the other authors.
 The authors declare no conflict of interest.
 Stefan Braune received honoraria from Kassenärztliche Vereinigung Bayerns and health maintenance organisations for patient care, and from Biogen, NeuroTransData, Novartis, and Roche for consulting, project management, clinical studies, and lectures; he also received honoraria and expense compensation as a board member of NeuroTransData. Sandra Bluemich, Carola Bruns and Jeanette Hoffmann are employees of Roche Pharma AG, Grenzach-Wyhlen, Germany. Petra Dirks and Erwan Muros-Le Rouzic are employees of Hoffmann-La Roche Ltd, Basel, Switzerland. Arnfin Bergmann received honoraria from NeuroTransData for project management, clinical studies, and travel expenses from Novartis and Servier; he also received honoraria and expense compensation as a board member of NeuroTransData. Yanic Heer is an employee of PricewaterhouseCoopers (PwC), Zurich, Switzerland.
 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: JMM declares competing interests as principal/sub-Investigator of clinical trials for: Abbvie, Adaptimmune, Agios Pharmaceuticals, Amgen, Astex Pharmaceuticals, Astra Zeneca Ab, Blueprint Medicines, Boehringer Ingelheim, Boston Pharmaceuticals, Bristol Myers Squibb, Ca, Casi Pharmaceuticals, Inc, Celgene Corporation, Cellcentric, Chugai Pharmaceutical Co, Cullinan-Apollo, Curevarc, Daiichi Sankyo, Debiopharm, Eisai, Eisai Limited, Eli Lilly, Forma Tharapeutics, Gamamabs, Genentech, Glaxosmithkline, H3 Biomedicine, Hoffmann La Roche Ag, Imcheck Therapeutics, Incyte Corporation, Innate Pharma, Institut De Recherche Pierre Fabre, Iris Servier, Iteos Belgium SA, Janssen Cilag, Janssen Research Foundation, Janssen R&D LLC, Kura Oncology, Kyowa Kirin Pharm. Dev, Lilly France, Loxo Oncology, Medimmune, Menarini Ricerche, Merck Sharp & Dohme Chibret, Merrimack Pharmaceuticals, Merus, Molecular Partners Ag, Nanobiotix, Nektar Therapeutics, Novartis Pharma, Octimet Oncology Nv, Oncoethix, Oncopeptides, Orion Pharma, Genomics, Ose Pharma, Pfizer, Pharma Mar, Pierre Fabre Medicament, Relay Therapeutics, Inc, Roche, Sanofi Aventis, Seattle Genetics, Sotio A.S, Syros Pharmaceuticals, Taiho Pharma, Tesaro, Transgene S.A, Turning Point Therapeutics, Xencor. The other authors have declared no conflicts of interest.

 The authors declare no competing interests.
 Declaration of Competing Interest We wish to confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: HB has received institutional (Monash University) funding from Biogen, Roche, Merck Healthcare KGaA (Darmstadt, Germany), Alexion, CSL, and Novartis; has carried out contracted research for Novartis, Merck Healthcare KGaA (Darmstadt, Germany), Roche, and Biogen; has taken part in speakers’ bureaus for Biogen, Sanofi, UCB, Novartis, Roche, and Merck; and has received personal compensation from Oxford Health Policy Forum for the Brain Health Steering Committee. TS received compensation for serving on scientific advisory boards, honoraria for consultancy and funding for travel from Biogen, and speaker honoraria from Novartis. SO reports no disclosures. RA has received honoraria as a speaker and scientific advisory board participant, and research grants from Bayer, Biogen, Biologix, Genpharm, GlaxoSmithKline, Lundbeck, Merck Healthcare KGaA (Darmstadt, Germany), Novartis, Roche, and Sanofi. MT received travel grants from Novartis, Bayer, Merck Healthcare KGaA (Darmstadt Germany), and Teva; and has participated in clinical trials by Sanofi, Roche, and Novartis. SH serves on advisory boards for Merck Healthcare KGaA (Darmstadt, Germany), Biogen, Novartis, Sanofi, Roche, and Bayer. She has received money for travel and speaker honorarium from Biogen, Sanofi, Novartis, Merck Healthcare KGaA (Darmstadt, Germany), Roche, and Bayer. GL and/or his institution received speaker honoraria, advisory board fees, research support, or conference travel support from Biogen, BMS/Celgene, Merck Healthcare KGaA (Darmstadt, Germany), Sanofi, Teva, Roche, and Novartis. TK served on scientific advisory boards for BMS/Celgene, Roche, Sanofi, Novartis, Merck Healthcare KGaA (Darmstadt, Germany), and Biogen, a steering committee for Brain Atrophy Initiative by Sanofi; received conference travel support and/or speaker honoraria from WebMD Global, Novartis, Biogen, Sanofi, Teva, BioCSL, and Merck Healthcare KGaA (Darmstadt, Germany); and received research or educational event support from Biogen, Novartis, Sanofi, Roche, BMS/Celgene, and Merck Healthcare KGaA (Darmstadt, Germany). AvdW received travel support, speaker honoraria and served on advisory boards for Biogen, Merck Healthcare KGaA (Darmstadt, Germany), Sanofi, Novartis, and Teva. BY has received honoraria for lectures and advisory boards from Bayer, Biogen, Genpharm, Sanofi, Roche, Merck Healthcare KGaA (Darmstadt, Germany), and Novartis; and has received research grants from Bayer, Biogen, Merck Healthcare KGaA (Darmstadt, Germany), Novartis, and Pfizer. JL-S has accepted travel compensation from Biogen, Merck Healthcare KGaA (Darmstadt, Germany), and Novartis. Her institution receives the honoraria for talks and advisory board commitment as well as research grants from Biogen, BMS/Celgene, Merck Healthcare KGaA (Darmstadt, Germany), Janssen, Novartis, Roche, Sanofi, and Teva. AS reports no disclosures. JK received speaker fees, research support, travel support, and/or served on advisory boards by Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Progressive MS Alliance, Bayer, Biogen, BMS/Celgene, Merck Healthcare KGaA (Darmstadt, Germany), Novartis, Octave Bioscience, Roche, and Sanofi. JLS-M has received travel compensation from Novartis, Merck Healthcare KGaA (Darmstadt, Germany), and Biogen, speaking honoraria from Biogen, Novartis, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), Almirall, Bayer, and Teva; and has participated in clinical trials by Biogen, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), and Roche. YBM reports no disclosures. DLAS has received honoraria as a consultant on scientific advisory boards by Bayer, Novartis, and Sanofi; and compensation for travel from Novartis, Biogen, Sanofi, Teva, and Merck Healthcare KGaA (Darmstadt, Germany). VVP has received travel grants from Merck Healthcare KGaA (Darmstadt, Germany), Biogen, Sanofi, BMS, Almirall, and Roche. His institution has received research grants and consultancy fees from Roche, Biogen, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), BMS, Janssen, Almirall, and Novartis. DH received compensation for travel, speaker honoraria, and consultant fees from Biogen, Novartis, Merck Healthcare KGaA (Darmstadt, Germany), Bayer, Sanofi, Roche, and Teva, as well as support for research activities from Biogen. She was also supported by the Charles University: Cooperation Program in neuroscience. RA received speaker honoraria, advisory board fees, research support, or conference travel support from Biogen, Merck Healthcare KGaA (Darmstadt, Germany), Sanofi, Roche, and Novartis. FP has received personal compensation for serving on advisory boards for Almirall, Alexion, Biogen, BMS, Merck Healthcare KGaA (Darmstadt, Germany), Novartis, and Roche. He has also received research grants from Biogen, Merck Healthcare KGaA (Darmstadt, Germany), and Roche, and from FISM, Reload Association (Onlus), Italian Health Ministry, and University of Catania. RM has received honoraria for attendance at advisory boards and travel sponsorship from Bayer, Biogen, CSL, Merck Healthcare KGaA (Darmstadt, Germany), Novartis, and Sanofi. AA-A has received honoraria for serving on scientific advisory boards from Merck Healthcare KGaA (Darmstadt, Germany), Novartis, Roche, and Sanofi; and also received travel reimbursement from, Biologix, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), Roche, Bayer, and Novartis. OG reports no disclosures. JO has received research funding from the MS Society of Canada, National MS Society, Brain Canada, Biogen, Roche, and EMD Serono Research & Development Institute, Inc., Billerica, MA, USA (an affiliate of Merck KGaA), and personal compensation for consulting or speaking from EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, Sanofi, Biogen, Roche, BMS/Celgene, and Novartis. AA reports no disclosures. NT and SLW are employees of EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA.
 The authors report no relevant disclosures. Go to Neurology.org/N for full disclosures.
 ALM: none known. MRT: none known. RLP: none known. RR: none known.

 Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors report no conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest: Dr. Brenton has served as a consultant for Cycle Pharmaceuticals
 Conflicts of interest None disclosed.
 Financial interests: The authors have no relevant financial interest. Non-financial interest: Dr. Mayfield has an accepted application for the algorithm to be a provisional U.S. patent as of 8/25/2022. Although currently licensed by USF, no financial compensation has been a result of this. The remaining authors have no relevant non-financial interests to disclose.



 Declaration of Competing Interest The authors declared no conflict of interest


 The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosures.
 The authors have no funding or conflicts of interest to disclose.
 The authors declare no competing interests.
 A. Winkelmann reports personal compensation from Bayer Healthcare, Celgene, Merck, Novartis, Sanofi Genzyme, and Teva. C. Metze reports no disclosures. U. K. Zettl received speaking fees, travel support and financial support for research activities from Alexion, Almirall, Bayer, Biogen, Merck Serono, Novartis, Octapharm, Roche, Sanofi Genzyme, Teva and as well as EU, BMBF, BMWi, and DFG. None resulted in a conflict of interest. M. Loebermann reports personal compensation from Gilead, Janssen, Pfizer and Sanofi and research support from Cempra, Correvio, Pfizer, Sanofi, Schering, Seqirus, Themis Bioscience, Valneva and Vectura.
 Declaration of Competing Interest S.Q., M.Y., P.B., J.M. have no conflicts of interest. H.K. has received speaker and travel honoraria from Novartis, Teva, Biogen, and Roche.
 Declaration of Competing Interest EL and SD have no declarations of interest to report. SS has served on scientific advisory boards for Bristol Myers Squibb, F. Hoffmann-La Roche Ltd., Forepont Capital Partners, Genentech, Inc., Horizon Therapeutics plc and TG Therapeutics, Inc., and received research support from BeCare MS Link and MedDay Pharmaceuticals SA. She has also received compensation for consulting services from, served on scientific advisory boards for and received speaker honorarium from Alexion Pharmaceuticals, Inc., Biogen, Inc., Bristol Myers Squibb, EMD Serono, Inc., Horizon Therapeutics, Inc., Novartis AG, Genentech, Inc. and Sanofi Genzyme. She is also CEO of Global Consultant MD. She also serves on the steering committee of Horizon Therapeutics, Inc. and Genentech, Inc.
 L Dumitrescu received support for attending scientific meetings from Stada M&D, Sanofi, AbbVie, Biogen Idec and Teva. R Tanasescu received grant income from UK MRC (CARP MR/T024402/1). R Tanasescu also received support for attending scientific meetings from AbbVie, Biogen Idec, Teva and Genzyme, and consultancy fees from Johnson & Johnson Romania. C Coclitu received support for attending scientific meetings and consultancy fees from Novartis, Merck, and Roche. C S Constantinescu received research grant support, support for attending scientific meetings, and consultancy fees from Biogen Idec, Bayer Schering, Genzyme, Merck Serono, Morphosys, Novartis, Roche, Sanofi Pasteur and Merck Sharp and Dohme. A Garjani’s institution received research support from the UK MS Society and Merck; A Garjani received support for attending scientific meetings from Merck and Novartis, and consultancy fees from the MS Academy and Biogen. N Evangelou has served as a member of advisory boards for Biogen, Merck, Novartis, and Roche, received grant income from the United Kingdom Multiple Sclerosis Society, UK MRC, Patient-Centered Outcomes Research Institute (PCORI), and NIHR. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article.


 Declaration of Competing Interest Jennifer Massey and Ian Sutton have received honoraria from Biogen, Roche, Sanofi Genzyme, Merck, Novartis and Teva.
 Declaration of Competing Interest Pallab K. Bhattacharyya: past salary support from Novartis. Robert J. Fox: personal consulting fees from AB Science, Biogen, Bristol Myers Squibb, EMD Serono, Genentech, Genzyme, Greenwich Biosciences, Immunic, INmune Bio, Janssen, Lily, Novartis, Sanofi, Siemens, and TG Therapeutics, service on advisory committees for AB Science, Biogen, Immunic, Janssen, Novartis, and Sanofi, and clinical trial contract and research grant fundings from Biogen, Novartis, and Sanofi. Ken E. Sakaie: salary support from Novartis and Genzyme, consulting fees from INmune Bio. Tucker Harvey: none. Jim Bena: none. Paola Raska: none. Jian Lin: past salary support from Novartis. Mark J. Lowe: personal consulting fees from INmune Bio.
 Declaration of Competing Interest M.Sa., M.M., M.N. and J.H. have no competing interests. S.L. has received travel honoria from Roche, and research support from Turunmaa Duodecim society, Finnish Brain Foundation and Turku Doctoral Programme in Clinical Research. M.Su. has served on advisory boards for Sanofi-Aventis and Roche and has received speaker honoraria from Merck Serono and travel honoraria from Orion, Roche, Biogen and Sanofi-Aventis and received research support from The Finnish Medical Foundation, The Finnish MS Foundation and from The Finnish Medical Society (Finska Läkaresällskapet). A.V. has received speaker honoraria from Janssen. L.A. has received honoraria from Biogen, Roche, Genzyme, Merck Serono and Novartis, and institutional research grant support from Finnish Academy, Sanofi-Genzyme, and Merck Serono.

 Declaration of Competing Interest All authors wish to declare that have nothing to disclose. There are no competing interest(s) or conflict of interest that may be perceived to influence the results and discussion reported in this paper. All authors or their institutions did not receive payment or services from a third party (government, commercial, or private foundation) for any aspect of the submitted work at any time. The funding for the writing and editing process was carried out and supported by Unidad de Investigación en Salud (UIS). Each author filled and signed an electronic ICMJE form for disclosure of potential conflicts of interest and was responsible for the accuracy and completeness of the submitted information. If editors need to confirm this asseveration, the corresponding author may share this information separately. This document was designed to improve delivering of this information since all electronic ICMJE forms have the statement as “nothing to disclose”.
 The authors declare that they have no competing interests.


 The authors declare no competing interests.

 Declaration of interests PM received consultancy honoraria from Sanofi and Biogen and, research funding from Biogen. VVP received support for attending meetings and/or travel, support for participating in Advisory Board and consulting fees (the latters payed to the institution Cliniques Universitaires Saint-Luc) from Roche, Biogen, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), Bristol Meyer Squibb, Janssen, Almirall, Alexion and Novartis Pharma. PAC Is PI on grants to JHU from Genentech and previously Principia; he has received consulting honoraria for serving on SABs for Nervgen, Idorsia, Biogen, Vaccitech, and Lilly. DSR has received research funding from Abata Therapeutics, Sanofi-Genzyme, and Vertex Pharmaceuticals. MA received consultancy honoraria from Abata Therapeutics, Biogen, Sanofi-Genzyme and GSK.








 I have read the journal’s policy and the authors of this manuscript have the following competing interests: AM and EF were partly funded by research grants from Biogen. EF has received unrestricted researcher-initiated grants from Bristol-Myers Squibb/Celgene. KA has received unrestricted researcher-initiated grants from Biogen. JH received honoraria for serving on advisory boards for Biogen and Novartis and speaker’s fees from Biogen, Merck-Serono, Bayer-Schering, Teva, and Sanofi-Aventis. He has served as P.I. for projects sponsored by or received unrestricted research support from, Biogen, Merck-Serono, TEVA, Novartis, and Bayer-Schering. JH’s MS research is also funded by the Swedish Research Council. Authors AA and EP have non-financial interests to disclose. The authors do have competing interests that alter their adherence to PLOS ONE policies on sharing data and materials.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 MM received personal compensations for advisory boards and travel grants from Novartis, Sanofi-Genzyme; SR received personal compensations for public speaking and travel grants from Sanofi-Genzyme and Merck Serono; MC received personal compensations for advisory boards, public speaking, editorial commitments or travel grants from Biogen Idec, Merck Serono, Fondazione Serono, Novartis, Pomona, Sanofi-Genzyme and Teva. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article.
 The authors declare no conflict of interest.




 Declaration of Competing Interest Y.K. declares no competing financial interests. JC has received grant support from Janssen, Novartis, and Bristol Meyers Squibb.
 Conflicts of interest and sources of funding: This work was financially supported by the European Union’s Seventh Framework Programme (FP7/2007-2013), the Danish Council for Independent Research, the Research Committee of Rigshospitalet, and Desirée and Niels Yde’s foundation. The authors have no conflicts to report.
 The authors declare no competing interests.


 RL has received honoraria from Biogen, Merck, Novartis, Roche, and Teva. MP discloses travel/meeting expenses from Novartis, Roche and Merck, speaking honoraria from HEALTH&LIFE S.r.l. and honoraria for consulting services from Biogen. VBM has received research grants from the Italian MS Society, and Roche, and honoraria from Bayer, Biogen, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. MM has received research grants from the ECTRIMS-MAGNIMS, the UK MS Society, and Merck, and honoraria from Biogen, Merck, Novartis and Roche. Other authors have nothing to disclose.
 The authors declare no conflict of interest.
 Under a license agreement between AxoProtego Therapeutics LLC and the Johns Hopkins University, Dr. Hoke and the University are entitled to royalty distributions related to the technology discussed in this publication related to ethoxyquin derivatives. Dr. Hoke also is a founder and serves as the Chair of AxoProtego Therapeutics LLC's, Scientific Advisory Board. This arrangement has been reviewed and approved by the Johns Hopkins University in accordance with its conflict‐of‐interest policies.
 Declaration of Competing Interest All authors declare no conflict of interest relevant to study.
 Declaration of Competing Interest Dr. Cross has done paid consulting for: Biogen, Celgene, EMD Serono, Genentech/Roche, Greenwich Biosciences, Janssen and Novartis, and has contracted research funded by EMD Serono and Genentech.

 Conflict of interest The authors declare that they have no conflict of interest.
 Declaration of Competing Interest The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: F.B. (Fabio Buttari) acted as Advisory Board members of Teva and Roche and received honoraria for speaking or consultation fees from Merck Serono, Teva, Biogen Idec, Sanofi, and Novartis and non-financial support from Merck Serono, Teva, Biogen Idec, and Sanofi. R.F. received honoraria for serving on scientific advisory boards or as a speaker from Biogen, Novartis, Roche, and Merck and funding for research from Merck. D.C. (Diego Centonze) is an Advisory Board member of Almirall, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva and received honoraria for speaking or consultation fees from Almirall, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Gen-zyme, and Teva. He is also the principal investigator in clinical trials for Bayer Schering, Biogen, Merck Serono, Mitsubishi, Novartis, Roche, Sanofi-Genzyme, and Teva. His preclinical and clinical research was supported by grants from Bayer Schering, Biogen Idec, Celgene, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva. G.M. (Giuseppe Matarese) reports receiving research grant support from Merck, Biogen, and Novartis and advisory board fees from Merck, Biogen, Novartis, and Roche. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results. A.B., E.D., F.A., L.G., E.I., G.G., A.Bo., R.F., A.F., F.C., F.DV., A.Mu., L.Gu., G.M, M.S.B.: nothing to report.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.L.B., C.S., C.G., M.P.S., Y.Y.M.W., E.D.vP. B.L.B., T.M.L., and R.F.N. declared no conflicts of interest. A.B-O. has participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from Accure, Atara Biotherapeutics, Biogen, BMS/Celgene/Receptos, GlaxoSmithKline, Gossamer, Janssen/Actelion, Medimmune, Merck/EMD Serono, Novartis, Roche/Genentech, and Sanofi-Genzyme.

 T.K., F.L., A.Z., C.S. and T.Z. have nothing to disclose. T.B. has received honoraria and consulting fees from Almirall, Bayer, Biogen, Biologix, Bionorica, Celgene/BMS, Genesis, GSK, Horizon, Janssen-Cilag, Jazz, MedDay, Merck, Novartis, Octapharma, Roche, Sandoz, Sanofi-Genzyme, TEVA, TG Therapeutics, and UCB. His institution has received financial support by unrestricted research grants from Almirall, Biogen, Bayer, Celgene/BMS, Merck, Novartis, Roche, Sanofi-Genzyme and TEVA, and honoraria for participation in clinical trials sponsored by Alexion, Bayer, Biogen, Celgene/BMS, Merck, Novartis, Octapharma, Roche, Sanofi, and TEVA. In the past 36 months, E.S. received grants from Roche, Eisai, FFG/AAL, Horizon2020 and the Austrian Alzheimer Association (all to the institution). E.S. received consulting fees from Biogen and received support for attending meetings and/or travel from Roche. E.S. received for lectures, presentations, speakers bureaus, manuscript writing, or educational events payment by Biogen, Roche, Eisai, and Novartis. E. Stögmann participated on an advisory board (Biogen, Roche, Eisai) and held leadership or a fiduciary role in scientific societies (Austrian Alzheimer Association, the EAN scientific panel dementia). The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 Declaration of Competing Interest Authors declare no conflict of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: S.K. reports personal fees from Biogen, Alexion Pharmaceuticals, and EMD Serono, as well as grant funding from Biogen. R.S.F. reports personal fees from Alexion Pharmaceuticals and Genentech as well as grant funding from Novartis, Biogen, and The National MS Society outside the submitted work. T.D. reports personal fees from Biogen Idec and Alexion Pharmaceuticals. T.L. has nothing to disclose. T.S. reports clinical fellowship funding from the National Multiple Sclerosis Society, Biogen, honoraria from the American Academy of Neurology, and research grants to institution from PCORI and Consortium for MS Centers outside the submitted work. R.B. reports personal fees from Biogen Idec and Sanofi Genzyme. L.Z.-R. reports personal fees from Biogen, Genentech and Novartis for work as scientific advisor and research grants to institution from Biogen, Genentech, and Consortium for MS Centers outside the submitted work. A.H. reports personal fees from Teva, Biogen, Alexion, Horizon, and Banner Life Sciences, as well as research grants from Biogen, the National MS Society, and the Consortium for MS Centers outside the submitted work.


 The authors declare no conflict of interest.


 The authors have no conflict of interest to declare.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.T.R. is a consultant for or has received unrestricted research support from Bayer, Biogen, Bristol Myers Squibb, Genentech/Roche, NKMax America, Mallinckrodt, Merck Serono, Novartis, and TG Therapeutics. O.S. serves on the editorial board of Therapeutic Advances in Neurological Disorders and has served on data monitoring committees for Genentech/Roche, Pfizer, Novartis, and TG Therapeutics without monetary compensation. He has advised Celgene, EMD Serono, Genentech, Genzyme, and TG Therapeutics, and currently receives grant support from EMD Serono and Exalys. S.K.T. has no disclosures. T.P.L. serves as site investigator for Biogen, Bristol Myers Squibb, EMD Serono, Genentech/Roche, Janssen, Novartis, and Sanofi. He has advised Biogen, Genentech/Roche, Horizon, Janssen, and Novartis.


 Declaration of Competing Interest The authors have no conflicts to declare.




 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 The authors declare no conflicts of interest.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 No potential conflict of interest was reported by the author(s).
 Declaration of Competing Interest Tanuja Chitnis has received compensation for consulting from Biogen, Novartis Pharmaceuticals, Roche Genentech, and Sanofi Genzyme, and has received research support from the National Institutes of Health, National MS Society, US Department of Defense, EMD Serono, I-Mab Biopharma, Mallinckrodt ARD, Novartis Pharmaceuticals, Octave Bioscience, Inc., Roche Genentech, and Tiziana Life Sciences. This research was conducted in part with the support of the Department of Defense through the Multiple Sclerosis Research Program under Award No. W81XWH-18-1-0648 (to T. Chitnis). John Foley has received research support from Biogen, Novartis, Adamas, Octave Bioscience, Inc., Genentech, and Mallinckrodt, has received speakers' honoraria and acted as a consultant for EMD Serono, Genzyme, Novartis, Biogen, and Genentech, has equity interest in Octave Bioscience, Inc., and is the founder of InterPro Bioscience. Carolina Ionete has received research support from Biogen, Serono, Genentech, NMSS, and the Department of Defense, and received compensation for advisory board activity from Sanofi-Genzyme. Nabil K. El Ayoubi has received support to attend scientific educational courses from Novartis, Merck Serono, Sanofi, Biologix, and has received speaker honoraria for scientific presentations on Multiple Sclerosis from Biologix, Sanofi, Merck Serono, and Novartis. Shrishti Saxena, Patricia Gaitan-Walsh, Anu Paul, and Fermisk Saleh have no disclosures. Hrishikesh Lokhande has received research support from the US Department of Defense and Octave Bioscience, Inc. Howard Weiner has received research support from the Department of Defense, Genentech, Inc., National Institutes of Health, National Multiple Sclerosis Society, Novartis, and Sanofi Genzyme. He has received compensation for consulting from Genentech, Inc., IM Therapeutics, IMAB Biopharma, MedDay Pharmaceuticals, Tiziana Life Sciences, and vTv Therapeutics. Ferhan Qureshi, Anisha Keshavan, Kian Jalaleddini, and Ati Ghoreyshi are employees of Octave Bioscience, Inc. Michael J. Becich, Fatima Rubio da Costa, Victor M. Gehman, and Fujun Zhang were employees of Octave Bioscience, Inc., at the time the study was completed. Samia J. Khoury has received compensation for scientific advisory board activity from Merck and Roche and for serving on IDMC for Biogen.

 JH reports grants for OCT research from the Friedrich-Baur-Stiftung and Merck, personal fees and non-financial support from Celgene, Merck, Alexion, Novartis, Roche, Santhera, Biogen, Heidelberg Engineering, Sanofi Genzyme and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work.Thomas Huber ist neben seiner im Manuskript genannten Affiliation bei der Firma Smart Reporting GmbH beschäftigt.Jan Kirschke ist neben seiner im Manuskript genannten Affiliation Co-Founder der Firma BoneScreen GmbH.
 Declaration of Conflicting Interests: The authors have no potential conflicts of interest relevant to this manuscript.
 The authors declare no competing interests.
 Declaration of Competing Interest None of the authors have a conflict of interest.


 Declaration of interests HH has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Siemens, Teva, and received honoraria for acting as consultant for Biogen, Celgene, Novartis and Teva. He is associate editor of Frontiers in Neurology. KB has participated in meetings sponsored by and received travel funding or speaker honoraria from Roche, Teva, Merck, Biogen, Sanofi. GB has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Celgene, Lilly, Merck, Novartis, Sanofi-Genzyme and Teva, and received honoraria for consulting Biogen, Celgene, Merck, Novartis, Roche and Teva. MA received speaker honoraria and/or travel grants from Biogen, Novartis, Merck and Sanofi. PA has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Merck, Roche, Sanofi-Genzyme and Teva, and received honoraria for consulting from Biogen. He received a research grant from Quanterix International and was awarded a combined sponsorship from Biogen, Merck, Sanofi-Genzyme, Roche, and Teva for a clinical study. FDP has participated in meetings sponsored by, received honoraria (lectures, advisory boards, consultations) or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Roche and Teva. AG has nothing to disclose. DM has participated in meetings sponsored by Siemens. MP has participated in meetings sponsored by, received speaker or consulting honoraria or travel funding from Amicus, Merck, Novartis and Sanofi-Genzyme. PP has nothing to disclose. CS has participated in meetings sponsored by Siemens. SW has participated in meetings sponsored by, received honoraria or travel funding from Allergan, Biogen, Ipsen Pharma, Merck, Novartis, Roche, Sanofi Genzyme, Teva and Bristol Myers Squibb. AZ has participated in meetings sponsored by, received speaking honoraria or travel funding from Biogen, Merck, Novartis, Sanofi-Genzyme and Teva. TB has participated in the last 2 years in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for multiple sclerosis: Almirall, Biogen, Bionorica, BMS/Celgene, Eisai, Horizon, Jazz Pharmaceuticals, Janssen-Cilag, MedDay, Merck, Novartis, Roche, Sanofi Aventis/Genzyme, Sandoz, TG Therapeutics, TEVA and UCB. His institution has received financial support in the last 2 years by unrestricted research grants (Biogen, BMS/Celgene, Novartis, Sanofi Aventis/Genzyme, Roche, TEVA) and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, BMS/Celegen, Merck, Novartis, Roche, Sanofi Aventis/Genzyme, TEVA. JW has nothing to disclose. FD has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Almirall, Biogen, Celgene-BMS, Genzyme-Sanofi, Horizon, Merck, Novartis Pharma, Roche, and Teva. His institution has received research grants from Biogen and Genzyme Sanofi. He is section editor of the MSARD Journal (Multiple Sclerosis and Related Disorders) and review editor of Frontiers Neurology.
 The authors have no conflicts of interest to declare.

 Competing interests: None declared.

 DM, GC, SLM and SC are inventors on patent EI0000273 named ‘enhancement of ARMD response as therapy in multiple sclerosis’.
 Declaration of Competing Interest Francesca Bridge has received travel support from Biogen. Helmut Butzkueven served on scientific advisory boards for Biogen, Novartis and Sanofi-Aventis and received conference travel support from Novartis, Biogen and Sanofi Aventis. He serves on steering committees for trials conducted by Biogen and Novartis received research support from Merck, Novartis and Biogen. Anneke van der Walt has received travel support and served on advisory boards for Novartis, Biogen, Merck Serono, Roche and Teva. She receives grant support from the National Health and Medical Research Council of Australia. Vilija Jokubaitis receives research grant support form F.Hoffmann La-Roche, MS Research Australia and the National Health and Medical Research Council of Australia (NHMRC 1156519).

 Competing interests: XM has received speaking honoraria and/or travel expenses for participation in scientific meetings, and/or has been a steering committee member of clinical trials and/or participated in advisory boards of clinical trials in the past years with Actelion, Alexion, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, Excemed, Genzyme, Hoffmann-La Roche, Immunic, Janssen Pharmaceuticals, Medday, Merck Healthcare KGaA, MSIF, Mylan, Nervgen, NMSS, Novartis, Sandoz, Sanofi-Genzyme, Teva Pharmaceutical and TG Therapeutics. DW has received consultant fees from Amgen, Eli Lilly, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA (an affiliate of Merck KGaA), Merck, Celgene and Janssen. MCG has received personal compensation from AbbVie, Astellas, EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, Galapagos, Genentech/Roche, Gilead, Incyte, Eli Lilly, Pfizer, Sanofi and Vertex. DT is an employee of Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA, and received stock or an ownership interest from Novartis. DP-R was an employee of EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA at the time of the study, and is currently an employee of and has received stock from Pfizer. CLB and HG are employees of Merck Healthcare KGaA, Darmstadt, Germany. AHK is an employee of and received stock or an ownership interest from EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA.

 Alessandro Cagol has nothing to disclose. Nuria Cerdá Fuertes has nothing to disclose. Mark Stössel has nothing to disclose. Muhamed Barakovic is an employee of Hays plc and a consultant for F. Hoffmann-La Roche Ltd. Sabine Schaedelin has nothing to disclose. Marcus D’Souza is CEO of Neurostatus-UHB Ltd. He has received travel support from Bayer AG, Biogen, Teva Pharmaceuticals and Sanofi Genzyme and research support from the University Hospital Basel. Jens Würfel is currently an employee of F. Hoffmann-La Roche Ltd. He served on scientific advisory boards of Actelion, Biogen, Genzyme-Sanofi, Novartis, and Roche. He is or was supported by grants of the EU (Horizon2020), German Federal Ministeries of Education and Research (BMBF) and of Economic Affairs and Energy (BMWI). Alexander Ulrich Brandt is cofounder and shareholder of technology startups Motognosis and Nocturne UG. He is named as inventor on several patent applications describing MS serum biomarkers, perceptive visual computing and retinal image analysis. Ludwig Kappos: Institutional research support: steering committee, advisory board, consultancy fees: Actelion, Bayer HealthCare, Biogen, Bristol Myers Squibb, Genzyme, Janssen, Japan Tobacco, Merck, Novartis, Roche, Sanofi, Santhera, Shionogi, and TG Therapeutics, speaker fees: Bayer HealthCare, Biogen, Merck, Novartis, Roche, and Sanofi; support of educational activities: Allergan, Bayer HealthCare, Biogen, CSL Behring, Desitin, Genzyme, Merck, Novartis, Roche, Pfizer, Sanofi, Shire, and Teva; license fees for Neurostatus products; and grants: Bayer HealthCare, Biogen, European Union, Innosuisse, Merck, Novartis, Roche, Swiss MS Society, and Swiss National Research Foundation. Till Sprenger: Grants from EFIC-Grünenthal, Novartis Pharmaceuticals Switzerland, the Swiss MS Society, and the Swiss National Research Foundation. Institution received payments for steering committee/consultation and speaking activities from Actelion, Biogen Idec, Bristol Myers Squibb, Electrocore, Eli Lilly, Janssen, Merck Serono, Mitsubishi Pharma, Novartis, Roche, Sanofi, and Teva. Yvonne Naegelin’s employer, the University Hospital Basel, received payments for lecturing from Celgene GmbH and Teva Pharma AG that were exclusively used for research support, not related to this study. Jens Kuhle received speaker fees, research support, travel support, and/or served on advisory boards by Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Progressive MS Alliance, Bayer, Biogen, Celgene, Merck, Novartis, Octave Bioscience, Roche, Sanofi. Cristina Granziera: The University Hospital Basel (USB), as the employer of C.G., has received the following fees which were used exclusively for research support: (i) advisory board and consultancy fees from Actelion, Genzyme-Sanofi, Novartis, GeNeuro and Roche; (ii) speaker fees from Genzyme-Sanofi, Novartis, GeNeuro and Roche; (iii) research support from Siemens, GeNeuro, Roche. The University of Basel (USB), as the employer of Athina Papadopoulou has received speaker-fees from Sanofi-Genzyme, Eli Lilly and Teva and fees for advisory boards (Lundbeck Schweiz AG, AbbVie AG). Athina Papadopoulou has received travel support from Bayer AG, Teva, Lilly and F. Hoffmann-La Roche. Her research was/is being supported by the University and the University Hospital of Basel, the Swiss Multiple Sclerosis Society, the ‘Stiftung zur Förderung der gastroenterologischen und allgemeinen klinischen Forschung sowie der medizinischen Bildauswertung’, the "Freie Akademische Gesellschaft" Basel and the Swiss National Science Foundation (Project number: P300PB_174480).
 The authors declare no competing interests.

 The authors declare no conflict of interest.


 Disclosures of conflicts of interest: M.A.R. Grants from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla; consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; speaker honoraria from AstraZeneca, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Horizon Therapeutics Italy, Merck Serono, Novartis, Roche, Sanofi, and Teva. M.M. Grants and personal fees from Almiral; MAGNIMS-ECTRIMS fellowship in 2020; speaker honoraria from Sanofi Genzyme, Merck-Serono, and Novartis; travel grants from Novartis and Sanofi Genzyme. M.B. Teacher at the International MRIlab—A Journey From The Basics To Advanced Methodologies of MRI; co-founder and CEO of SIENA Imaging SRL. A.E. research grants from the UK Medical Research Council (MRC), Innovate UK, Biogen, Merck, and Roche; consulting fees from Biogen, Merck, and Roche; honoraria from Roche and Biogen; support for attending meetings and travel from the National MS Society; on the board of the Journal of the American Academy of Neurology; founder and stake holder in Queen Square Analytics. J.I. grants from National Institutes of Health, National Institute on Aging, U.S. Department of Veteran's Affairs and U.S. Department of Defense; Chair for the Scientific Advisory Board of Applied Cognition; holds equity stake in and receives consulting fees from Applied Cognition. E.P. honorarium from Biogen. P.P. Research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla; honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb, and Genzyme. L.S. No relevant relationships. T.T. Grant from Canon Medical Systems. P.V. Honoraria from Biogen. M.F. Grants from Biogen, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla; consulting fees from Alexion, Almirall, Biogen, Merck, Novartis, Roche, and Sanofi; honoraria from Bayer, Biogen, Celgene, Chiesi Italia, Eli Lilly, Genzyme, Janssen, Merck Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and Teva; participation on a DataSafety monitoring board or advisory board for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, and Takeda; associate editor of Radiology.




 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could influence the study presented in this manuscript.

 JS has received fees for serving on scientific advisory boards andconsulting, and research support from Novartis and Roche. EM has received research support from Fondation ARSEP and Biogen Idec, travel funding and/or consulting fees from Alexion, Biogen Idec, BMS, Merck, Novartis, Roche, Sanofi-Genzyme and Teva. AG has received personal compensation for consulting, lecturing and congress participation from Novartis, Alexon, AEI/Roche andNovartis. DL has received fees for board membership and consultancy and grants from Alexion, Actelion, BMS, Biogen,Merck, Novartis, Roche, Sanofi and Teva. LM has received consulting fees from Biogen, Novartis Pharma, Teva, BMS, Roche,Sanofi-Genzyme and Janssen Cilag. ET has received honoraria, travel grants, or research grants from the following pharmaceutical companies: Actelion, Biogen, Bristol Myers Squibb/Celgene, Merck, Novartis, Roche, Teva. HZ has received personal fees from Novartisrelated to this work and consulting fees from Biogen, Roche,Alexion, Roche, BMS, Novartis and Merck, unrelated to this work. DB has received personal compensation for consulting,serving on a scientific advisory board, speaking, or other activities with Biogen, Novartis, Merck, Sanofi-Genzyme, Roche, Celgene-BMS and Alexion. RL has received consultancy and speaker honoraria from Biogen, Sanofi-Genzyme, Merck-Serono,Novartis, Orion and GSK, and research grants from GSK, Population Bio and Roche. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declarations of Competing Interest Paul M. Matthews has received consultancy fees from Novartis, Biogen, Nodthera, and Rejuveron Therapeutics; honoraria or speakers’ fees from Novartis, Biogen and Redburn Investing; research or educational funds from Biogen, Novartis, Merck and Bristol Myers Squibb; and institutional grants from UK Dementia Research Institute, NERC and NIHR Biomedical Research Centre at Imperial College London. Kevin G. Pollock, Vishal Sharma and Nathan Hill are employees of Bristol-Myers Squibb and hold stock in the company. Digant Gupta and Deepali Mittal are employees of Bridge Medical Consulting, which was contracted by Bristol-Myers Squibb to conduct this research. Antonio Scalfari and Wenjia Bai have no disclosures in relation to this work.
 E.S. Frisch and D. Häusler report no disclosures. M.S. Weber is serving as an editor for PLoS One and received travel funding and/or speaker honoraria from Biogen-Idec, Merck Serono, Novartis, Roche, TEVA, Bayer, and Genzyme. Go to Neurology.org/NN for full disclosures.
 Conflict of Interest Disclosures: Mr Hittle reported grants from the National Institutes of Health (NIH) and personal fees from Institute for Clinical Research during the conduct of the study. Dr Culpepper reported grants from National Multiple Sclerosis Society (NMSS) during the conduct of the study, support from the Veterans Health Administration MS Center of Excellence, and being a member of the NMSS Health Care Delivery and Policy Research study section. Dr Langer-Gould reported being principal investigator for 2 industry-sponsored phase 3 clinical trials (Biogen Idec, Hoffmann-LaRoche) and 1 industry-sponsored observation study (Biogen Idec) and grant support from the NIH, National Institute of Neurological Disorders and Stroke (NINDS), Patient-Centered Outcomes Research Institute, and NMSS. Dr Marrie reported being co-investigator on trials sponsored by Roche and Biogen outside the submitted work; support from the Waugh Family Chair in Multiple Sclerosis; research funding from Canadian Institutes of Health Research, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Consortium of MS Centers, and NMSS; and serving on the editorial board of Neurology. Dr Cutter reported being a member of data and safety monitoring boards for Applied Therapeutics, AI Therapeutics, AstraZeneca, Avexis Pharmaceuticals, AMO Pharmaceuticals, Apotek, Biolinerx, Brainstorm Cell Therapeutics, Bristol Myers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Pharmaceuticals, Immunic, Karuna Therapeutics, Mapi Pharmaceuticals, Modigenetech/Prolor, Merck, Merck/Pfizer, Mitsubishi Tanabe Pharma Holdings, Opko Biologics, Prothena Biosciences, Novartis, Regeneron, Neurim, Sanofi-Aventis, Reata Pharmaceuticals, Receptos/Celgene, Teva Pharmaceuticals, National Heart, Lung, and Blood Institute (protocol review committee), Eunice Kennedy Shriver National Institute of Child Health and Human Development (Obstetric-Fetal Pharmacology Research Center oversight committee), University of Texas Southwestern, University of Pennsylvania, and Visioneering Technologies; being a member of consulting or advisory boards for Atara Biotherapeutics, Argenix, Bioeq, Consortium of MS Centers (grant), Genzyme, Genentech, Innate Therapeutics, Klein-Buendel Incorporated, Medimmune, Medday, Novartis, Opexa Therapeutics, Roche, Savara, Somahlution, Teva Pharmaceuticals, Transparency Life Sciences, and TG Therapeutics; receiving personal fees from Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions, Entelexo Biotherapeutics, Genzyme, Genentech, GW Pharmaceuticals, Immunic, Immunosis, Klein-Buendel Incorporated, Merck/Serono, Novartis, Perception Neurosciences, Protalix Biotherapeutics, Regeneron, Roche, and SAB Biotherapeutics; and receiving personal fees from Pythagoras (company owned for consulting) outside the submitted work. Dr Kaye reported funding from the Agency for Toxic Substances and Disease Registry, NMSS, and Association for the Accreditation of Human Research Protection Programs. Dr Wagner reported funding from the Agency for Toxic Substances and Disease Registry and NMSS. Dr LaRocca reported being previously employed full-time by the NMSS. Dr Nelson reported grants from the Centers for Disease Control and Prevention, NIH, and NMSS; contracts from the Agency for Toxic Substances and Diseases Registry; compensation for serving as a consultant to Acumen; and being on a data monitoring committee for Neuropace. Dr Wallin reported serving on data safety monitoring boards for the NIH NINDS; being a member of the NMSS Health Care Delivery and Policy Research study section; and receiving funding support from the NMSS and Department of Veterans Affairs Merit Review Research Program. No other disclosures were reported.


 H.V.K., M.R.R., A.Z., and W.L. are AbbVie employees and may hold stock or options. T.P.M. was an AbbVie employee at the time this work was conducted and may hold stock or options. B.A.C.C. has received personal compensation for consulting from Alexion, Atara, Autobahn, Avotres, Biogen, EMD Serono, Gossamer Bio, Horizon, Neuron23, Novartis, Sanofi, TG Therapeutics, and Therini and has received research support from Genentech.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 None of the authors has any proprietary interests or conflicts of interest related to this submission. This submission has not been previously published anywhere, and it is not simultaneously being considered for any other publication.
 R. d. N. is the Chair of the NIHR Research for Patient Benefit East Midlands Research Advisory Committee; he has received funding to prepare and deliver lectures on cognitive rehabilitation in multiple sclerosis from Novartis and Biogen. N. E. is a member of the advisory board for Biogen, Merck, Novartis and Roche; he has received grant income from the MS Society, MRC, PCORI and NIHR. The remaining authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest. GB and MC are serving as the Editorial Board members of this journal. GB served as Guest Editor of Special issue ”Vitamin D and the Nervous System”. We declare that GB and MC had no involvement in the peer review of this article and has no access to information regarding its peer review. Full responsibility for the editorial process for this article was delegated to GR.

 Declaration of Competing Interest The authors have no conflict of interest.
 PV holds a patent covering the composition of matter and uses of BN201. PV is a founder, holds stocks in Bionure SL, which has licensed the patent rights to Oculis SL and serves on its scientific advisory board, having been compensated by such activities. MM and SP were employees of Accure Therapeutics (formerly Bionure SL), and SH and AK were employees of Simbec-Orion.
 YJ-L: has received grants from Merck. MM: has received travel grants or speaking fees from Merck, Sanofi-Genzyme and Biogen. JRS: has received grants from Merck. MD-A: has received travel grants or speaking fess from Merck, Novartis and Sanofi-Genzyme. JR: has received speaking/consulting fees and/or travel funding from Merck, Sanofi-Genzyme, Roche, Biogen, Novartis, BMS, Jannsen and Teva. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 GM, VS and ADL are actually working at Movendo Technology that developed hunova®. Other authors declare that they have no competing interests.



 Competing interests: TÅ has been supported by Tercentenary fund of Bank of Sweden, AFA Insurance and European Aviation Safety Authority. LA reports grants from Swedish Research Council, grants from Swedish Research Council for Health Working Life and Welfare, grants from Swedish Brain Foundation, during the conduct of the study; personal fees from Teva, personal fees from Biogene Idec, outside the submitted work. TO has received lecture/advisory board honoraria, and unrestricted MS research grants from Biogen, Novartis, Sanofi and Merck.
 The authors have no conflict of interest.
 The authors declare that they have no competing interests.


 The authors declare no conflict of interest.
 The authors declare no conflicts of interest.
 GAJ is the author of “Overcoming Multiple Sclerosis”. GAJ and SN are co-editors of “Overcoming Multiple Sclerosis Handbook. Roadmap to Good Health”, and facilitators of past residential lifestyle modification workshops. PJ is a contributor to “Overcoming Multiple Sclerosis Handbook. Roadmap to Good Health”. The other authors declare no competing interests.


 Declaration of Competing Interest Medical writing support was provided by Biogen. S. Batagelj is an employee of Biogen. All other authors have no conflict of interests to report. The authors were not paid for their work developing the manuscript. Views and opinions expressed in this manuscript are solely those of the authors.
 The authors declare no conflicts of interest
 Declaration of Competing Interest The authors declare no competing interests.



 All authors were Novartis employees at the time of the studies.
 Mona Ramezani, Fatemeh Ehsani, Cyrus Taghizadeh Delkhosh, Nooshin Masoudian, and Shapour Jaberzadeh declare that they have no conflicts of interest.


 G. Bsteh has participated in meetings sponsored by, received speaker honoraria from, or travel funding from Biogen, Celgene/BMS, Lilly, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva and received honoraria for consulting Biogen, Celgene/BMS, Novartis, Roche, Sanofi-Genzyme, and Teva. He has received unrestricted research grants from Celgene/BMS and Novartis. H. Hegen has participated in meetings sponsored by, received speaker honoraria from, or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Siemens, and Teva and received honoraria for consulting Biogen, Celgene, Novartis, and Teva. P. Altmann has participated in meetings sponsored by, received speaker honoraria from, or travel funding from Biogen, Merck, Roche, Sanofi-Genzyme, and Teva and received honoraria for consulting from Biogen. He received a research grant from Quanterix International and was awarded a combined sponsorship from Biogen, Merck, Sanofi-Genzyme, Roche, and Teva for a clinical study. M. Auer received speaker honoraria and/or travel grants from Biogen, Merck, Novartis, and Sanofi-Genzyme. K. Berek has participated in meetings sponsored by and received travel funding from Biogen, Roche, Sanofi-Genzyme, and Teva. F. Di Pauli has participated in meetings sponsored by, received honoraria from (lectures, advisory boards, consultations), or travel funding from Biogen, Celgene BMS, Horizon, Johnson&Johnson, Merck, Novartis, Sanofi-Genzyme, Teva, and Roche. Her institution has received research grants from Roche. B. Kornek has received honoraria for speaking and for consulting from Biogen, BMS-Celgene, Johnson&Johnson, Merck, Novartis, Roche, Teva, and Sanofi-Genzyme outside of the submitted work. No conflict of interest with respect to the present study. N. Krajnc has participated in meetings sponsored by, received speaker honoraria from, or travel funding from BMS/Celgene, Janssen-Cilag, Merck, Novartis, Roche, and Sanofi-Genzyme and held a grant for a Multiple Sclerosis Clinical Training Fellowship Programme from the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS). F. Leutmezer has participated in meetings sponsored by, received speaker honoraria from, or travel funding from Actelion, Almirall, Biogen, Celgene, Johnson&Johnson, MedDay, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva and received honoraria for consulting Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. S. Macher declares no conflict of interest relevant to this study P. Rommer has received honoraria for consultancy/speaking from AbbVie, Allmiral, Alexion, Biogen, Merck, Novartis, Roche, Sandoz, Sanofi-Genzyme and has received research grants from Amicus, Biogen, Merck, Roche. K. Zebenholzer received speaking honoraria or travel grants from Biogen, Novartis, and Sanofi-Genzyme. G. Zulehner has participated in meetings sponsored by or received travel funding from Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. T. Zrzavy has participated in meetings sponsored by or received travel funding from Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. F. Deisenhammer has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Almirall, Biogen, Celgene, Merck, Novartis, Roche, and Sanofi-Genzyme. His institution received scientific grants from Biogen and Sanofi-Genzyme. B. Pemp has received honoraria for consulting from Novartis, has received honoraria for advisory boards/consulting from Chiesi and GenSight, and has received speaker honoraria from Chiesi and Santen. T. Berger has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for MS: Allergan, Bayer, Biogen, Bionorica, BMS/Celgene, Genesis, GSK, GW/Jazz Pharma, Horizon, Janssen-Cilag, MedDay, Merck, Novartis, Octapharma, Roche, Sandoz, Sanofi-Genzyme, Teva, and UCB. His institution has received financial support in the past 12 months by unrestricted research grants (Biogen, Bayer, BMS/Celgene, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Merck, Novartis, Octapharma, Roche, Sanofi-Genzyme, and Teva). Go to Neurology.org/N for full disclosures.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: C.O., T.S., L.M.J., M.L.S., F.W., F.P., P.S., M.N., A.K., R.R., and C.D. declare no disclosures relevant to the manuscript. V.M.C. is named together with Euroimmun GmbH on a patent application filed recently regarding the diagnostic of SARS-CoV-2 by antibody testing. K.R. is site principal investigator in clinical trials sponsored by Roche, the manufacturer of ocrelizumab and rituximab, and received research support from Novartis Pharma, Merck Serono, German Ministry of Education and Research, European Union (821283-2), Stiftung Charité, and Arthur Arnstein Foundation, and travel grants from Guthy Jackson Charitable Foundation.

 This study has no conflict of interest.
 Declaration of competing interest The authors report no conflict of interest.
 Declaration of Conflicting Interests The Authors declare no conflict of interest.
 Declaration of interests The authors declare no relevant conflicts of interest.
 The authors declare that they have no competing interests.
 Declaration of Competing Interest The authors of this manuscript declare no relationships with any companies, whose products or services may be related to the subject matter of the article.
 EH, RC, MS, DH, CM, KM, JG, DB, PC No competing interests declared
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.B. received speaker’s honoraria and compensation for consulting service and speaking activities from Biogen, Roche, Merck, Celgene, and Genzyme. V.N. received speaker and consulting fees from Biogen, Bayer, Merck Serono, Genzyme, Mylan, Novartis, Roche, Celgene, and Teva. An.G. received speaker and consulting fees from Biogen, Genzyme, Merck Serono, Mylan, Novartis, Roche, and Teva, and receives research support from Fondazione Italiana Sclerosi Multipla. The remaining authors have nothing to disclose.
 The authors have no relevant financial or non-financial interests to disclose.


 The authors declare no conflict of interest.

 Competing interests: JS-G declares fees from Sanofi, Biogen, Celgene, Merck, Biopass, Novartis and Roche, outside the submitted work. AR serves on scientific advisory boards for Novartis, Sanofi-Genzyme, Synthetic MR, TensorMedical, Roche, Biogen and OLEA Medical, and has received speaker honoraria from Bayer, Sanofi-Genzyme, Merck-Serono, Teva Pharmaceutical Industries Ltd, Novartis, Roche and Biogen. He is also member of the editorial board of Neurology and Neuroradiology, and member of the executive committee of the International Society of Radiology (ISR) and of MAGNIMS. AG-V has nothing to disclose. PC-M has nothing to disclose. MA has nothing to disclose. AV-J has received support has received support for contracts Juan Rodes (JR16/00024) and from Fondo de Investigación en Salud (PI17/02162) from Instituto de Salud Carlos III, Spain, and has engaged in consulting and/or participated as speaker in events organised by Roche, Novartis, Merck and Sanofi. CA declares that she has no conflict of interest. MT reports personal fees from Almirall, Bayer Healthcare, Biogen Idec, Merck-Serono, Novartis, Roche, Viela-Bio, Sanofi–Genzyme and Teva, grants from Sanofi-Genzyme, and other competing interests related to Biogen Idec, outside the submitted work. XMo reports personal fees from and other competing interests related to Actelion, Alexion, Biogen, Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Immunic, Medday, Merck, Mylan, Nervgen, Novartis, Sanofi-Genzyme, Teva Pharmaceutical and TG Therapeutics and grants received through the institutions from AbbVie, Biogen, Hoffmann-La Roche, Medday, Merck, Novartis, Sanofi-Genzyme and Teva Pharmaceutical, outside the submitted work. DP reports personal fees from Novartis and Sanofi-Genzyme, outside the submitted work.

 Competing interests: MSa has received support for attending meetings and/or travel from Turku University Foundation, the InFLAMES Flagship Programme of the Academy of Finland and Merck. MM has no competing interests. AV has received a personal grants from Päivikki and Sakari Sohlberg Foundation and Janssen Pharmaceutica. SL has received research support from the Turunmaa Duodecim Society, Finnish Brain Foundation and Turku Doctoral Programme in Clinical Research, and travel honoraria from Turku University Foundation and Turku Doctoral Programme in Clinical Research. MSu has received research support from The Finnish Medical Foundation, The Finnish MS Foundation and from The Finnish Medical Society. DL is chief medical officer of GeNeuro. JK has received speaker fees, research support, travel support and/or served on advisory boards by the Progressive MS Alliance, Swiss MS Society, Swiss National Research Foundation (320030_189140 / 1), University of Basel, Biogen, Celgene, Merck, Novartis, Octave Bioscience, Roche, Sanofi. LA has received institutional research support (grants) from the Academy of Finland, Sigrid Juselius Foundation, Sanofi-Genzyme, Merck and Novartis and honoraria for lectures and/or for advising from Novartis, Sanofi Genzyme, Janssen, Merck and ParadigMS Foundation, and has participated on Novartis scientific advisory board.
 Conflict of Interest Disclosures: Dr Kalincik reports grants from National Health and Medical Research Council during the conduct of the study; personal fees from WebMD Global, Eisai, Novartis, Biogen, Merck, Roche, Sanofi Genzyme, Teva, and BioCSL outside the submitted work; grants from Novartis, Biogen, Roche, Merck, and Celgene outside the submitted work; served on scientific advisory boards for MS International Federation and World Health Organization, Bristol Myers Squibb, Roche, Janssen, Sanofi Genzyme, Novartis, Merck, and Biogen; and served on the steering committee for Brain Atrophy Initiative by Sanofi Genzyme. Dr Roos reports personal fees from Novartis, Merck, Roche, and Biogen outside the submitted work; grants from Trish Multiple Sclerosis and Multiple Sclerosis Australia outside the submitted work; served on scientific advisory boards/steering committees for Novartis and Merck; and received conference travel support and/or speaker honoraria from Roche, Novartis, Biogen, Teva, Sanofi-Genzyme, and Merck. Dr Freedman reports grants from Multiple Sclerosis Australia during the conduct of the study; research/educational grants from Sanofi-Genzyme Canada; honoraria/consultation fees from Alexion, Atara Biotherapeutics, Bayer Healthcare, Beigene, BMS (Celgene), EMD Inc, Hoffmann-La Roche, Janssen, Merck Serono, Quanterix, Novartis, Sanofi-Genzyme, and Teva Canada Innovation; serving as a member of company advisory boards or boards of directors for Alexion, Atara Biotherapeutics, Bayer Healthcare, Beigene, BMS (Celgene), Celestra Health, Hoffmann-La Roche, Janssen, McKesson, Merck Serono, Novartis, and Sanofi-Genzyme; and participated in company-sponsored speaker’s bureau for Sanofi-Genzyme and EMD Serono. Dr Massey reports personal fees from Roche, Biogen, Novartis, and Merck during the conduct of the study and serving on the scientific advisory board for Roche. Dr Sutton reports personal fees from Biogen for educational activities, and personal fees for serving on advisory boards of Merck, Bristol Myers Squibb, and Roche outside the submitted work. Dr Macdonell received compensation for traveling, conference fees, and consulting fees from Merck, Teva, Sanofi Genzyme, Biogen Idec, Novartis, Roche, Bristol Myers Squibb, and Celgene. Dr Torkildsen received speaker honoraria from and served on scientific advisory boards for Biogen, Sanofi-Aventis, Merck, and Novartis. Dr Bø received speaker honoraria from Novartis and consultant fees from Viatris. Dr Havrdova reports personal fees from Biogen, Merck trials, Novartis, Roche, Teva, and Czech Ministry of Education outside the submitted work and has been member of advisory boards for Actelion, Biogen, Celgene, Merck Serono, Novartis, and Sanofi Genzyme. Dr Trněný received honoraria from Janssen, Gilead Sciences, Bristol-Myers Squibb, Takeda, Amgen, AbbVie, Roche, MorphoSys, and Novartis; served as an advisor to Takeda, Bristol-Myers Squibb, Incyte, AbbVie, Amgen, Roche, Gilead Sciences, Janssen, MorphoSys, and Novartis; received conference travel support from Gilead Sciences, Takeda, Bristol-Myers Squibb, Roche, Janssen, and AbbVie; and received personal fees from Roche, Gilead Sciences, Novartis, Incyte, Morphosys, Janssen, Takeda, and AstraZeneca outside the submitted work. Dr Kozak reports personal fees from Amgen Czechia, Sobi Czechia, Novartis Czechia, and AbbVie Czechia outside the submitted work. Dr Van der Walt reports grants from the National Health and Medical Research Council of Australia; personal fees from Roche, Merck, Novartis, and Bristol Myers Squibb outside the submitted work; serving on advisory boards and receiving unrestricted research grants from Novartis, Biogen, Merck, and Roche; and receiving speaker’s honoraria and travel support from Novartis, Roche, and Merck. Dr Butzkueven reports grants from Biogen, Roche, Merck, Novartis, Alexion, and CSL to their institution; has carried out contracted research for Novartis, Merck, Roche, and Biogen; has taken part in speakers’ bureaus for Biogen, Genzyme, UCB, Novartis, Roche, and Merck; has received personal compensation from Oxford Health Policy Forum for the Brain Health Steering Committee; travel support from Merck, and is the managing director of the MSBase Foundation and leads the administrative team running this registry from which much of the dataset is extracted. Dr McCombe received speaker fees and travel grants from Novartis, Biogen, T’évalua, Sanofi. Dr Lechner-Scott reports grants from Novartis and Biogen during the conduct of the study; travel compensation from Novartis, Biogen, Roche, and Merck; and her institution receives the honoraria for talks and advisory board commitment as well as research grants from Biogen, Merck, Roche, Teva Pharmaceuticals, and Novartis. Dr Willekens reports consulting/speaker fees paid to their institution from Almirall, BMS-Celgene, Janssen, Merck, Roche, Sanofi-Genzyme, Novartis, and Biogen; grants from Janssen, Roche, Sanofi-Genzyme, Novartis, FWO-TBM, Belgian Charcot Foundation, and Queen Elisabeth Medical Foundation; nonfinancial support from Biogen, Merck, Roche, Sanofi-Genzyme, and Novartis outside the submitted work. Dr Alroughani reports honoraria for speaking and for serving in scientific advisory board from Biogen, Merck, Novartis, Roche, Sanofi, Bayer, and GSK outside the submitted work. Dr Kuhle reports grants from Swiss National Research Foundation, Progressive MS Alliance, Biogen, Bristol Myers Squibb, Celgene, Merck, Novartis, Octave Bioscience, Roche, and Novartis outside the submitted work and speaker fees, research support, or travel support and/or served on advisory boards by Swiss MS Society, Bayer, and Sanofi. Dr Patti reports grants from Biogen, Novartis, and Roche; personal fees from Novartis; speaker honoraria and advisory board fees from Almirall, Bayer, Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva Pharmaceuticals, and research funding from Biogen, Merck, Fondazione Italiana Sclerosi Multipla, Reload Onlus Association, and University of Catania. Dr Duquette served on editorial boards and has been supported to attend meetings by EMD, Biogen, Novartis, Genzyme, and Teva Neuroscience, reports grants from the Canadian Institutes of Health Research, and reports funding for investigator-initiated trials from Biogen, Novartis, and Genzyme. Dr Lugaresi reports personal fees from Alexion, Biogen, Bristol Myers Squibb, Merck Serono, Novartis, Roche, and Sanofi/Genzyme; grants from Novartis and Sanofi/Genzyme; personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities from Roche, Biogen, Bristol Myers Squibb, Merck Serono, Mylan, Novartis, Roche, Sanofi/Genzyme, and Teva; and research grants from Novartis and Sanofi paid to their institution. Dr Khoury reports personal fees from Merck and Novartis outside the submitted work and compensation for serving on scientific advisory boards from Roche and Merck. Dr Slee has participated in, but not received honoraria for, advisory board activity for Biogen, Merck, Bayer Schering, Sanofi Aventis, and Novartis. Dr Hodgkinson reports grants from Merck; clinical trials with Roche, Atara, Biogen, and Novartis during the conduct of the study; personal fees from Novartis (advisory board); personal fees from Merck (advisory boards and speaking tours); grants and travel support for conference attendance from Merck outside the submitted work; honoraria and consulting fees from Novartis, Bayer Schering, and Sanofi; and travel grants from Novartis, Biogen Idec, and Bayer Schering. Dr John reports grants from Biogen and Sanofi, both paid to Monash Health outside the submitted work and is a local principal investigator on commercial studies funded by Novartis, Biogen, Amicus, and Sanofi. Dr Maimone received speaker honoraria for advisory board and travel grants from Almirall, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. Dr van Pesch reports travel grants, research grant, and consultancy paid to their institution from Biogen and Roche; consultancy paid to their institution from Novartis Pharma during the conduct of the study; consultancy paid to their institution from Merck, Sanofi, BMS, Janssen, and Almirall outside the submitted work; and travel grants from Merck Healthcare KGaA (Darmstadt, Germany), Biogen, Sanofi, Bristol Myers Squibb, Almirall, and Roche. Dr Laureys reports compensation for travel, advisory boards, and consultancy paid to their institution from Sanofi-Genzyme, Roche, Teva, Merck, Novartis, Celgene, Biogen, and BMS outside the submitted work. Dr Karabudak reports honoraria or consultancy fees for participating in advisory boards, giving educational lectures, and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, and Biogen Idec/Gen Pharma. Dr La Spitaleri received honoraria as a consultant on scientific advisory boards by Bayer-Schering, Novartis, and Sanofi-Aventis and compensation for travel from Novartis, Biogen, Sanofi Aventis, Teva, and Merck. Dr Csepany received speaker honoraria/ conference travel support from Bayer Schering, Biogen, Merck, Novartis, Roche, Sanofi-Aventis, and Teva. Dr Gouider reports grants from Menactrims and personal fees from Biogen, Hikma, Merck, Roche, and Sanofi outside the submitted work. Dr Mrabet reports grants from Menactrims outside the submitted work. Dr Castillo-Trivino reports personal fees from Almirall, Biogen, Bristol Myers Squibb, Janssen, Merck, Novartis, Roche, and Sanofi-Genzyme outside the submitted work and speaking/consulting fees and/or travel funding from Bayer and Teva. Dr Garber has received research funding from Roche and travel grants and/or honoraria from Merck, Biogen, Roche, and Novartis. Dr Sanchez-Menoyo reports personal fees for speaking honoraria and/or advisory board from Biogen, Merck, Sanofi, Novartis, Almirall, Bayer, Teva, and Sociedad Vasca de Neurologia; travel compensation from Biogen, Novartis, and Merck outside the submitted work. Dr Blanco received speaking/consulting fees from Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Sandoz. Dr Weinstock-Guttman reports personal fees from Biogen, Horizon, Sanofi, Labcorp, EMD Serono, and MAPA outside the submitted work and has participated in speaker's bureaus and/or served as a consultant for Novartis, Genentech, Celgene/Bristol Myers Squibb, Sanofi Genzyme, Bayer, Janssen, and Horizon. Dr Taylor reports funding for travel and speaker honoraria from Bayer Schering Pharma, CSL Australia, Biogen, and Novartis and has served on advisory boards for Biogen, Novartis, Roche, and CSL Australia. Dr Fragoso received honoraria as a consultant on scientific advisory boards by Novartis, Teva, Roche, and Sanofi-Aventis and compensation for travel from Novartis, Biogen, Sanofi Aventis, Teva, Roche, and Merck. Dr de Gans reports serving on scientific advisory boards for Roche, Janssen, Sanofi-Genzyme, Novartis, and Merck; received conference fees and travel support from Novartis, Biogen, Sanofi-Genzyme, Teva, AbbVie, and Merck; and received educational event support from Novartis. Dr Kermode received speaker honoraria and scientific advisory board fees from Bayer, BioCSL, Biogen, Genzyme, Innate Immunotherapeutics, Merck, Novartis, Sanofi, Sanofi-Aventis, and Teva. Dr Snowden reports personal fees from Novartis, Jazz, Gilead, Janssen, Medac, and Kiadis Pharma outside the submitted work. No other disclosures were reported.

 The authors declare no competing interests.
 CONFLICT OF INTEREST Dr. Raji consults for Brainreader ApS, Icometrix, Neurevolution LLC, and AHNP Precision Health. Dr. Raji is an Editorial Board Member of this journal but was not involved in the peer-review process nor had access to any information regarding its peer-review.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that they have no competing interests.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 The authors declare no conflict of interest.
 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Allison Osen- Reports no disclosure. Tyler Kaplan- Reports no disclosure. Thomas Shoemaker- Reports no disclosure. Dusan Stefoski- Reports no disclosure. Fabian Sierra Morales- Reports no disclosure.
 RW, MR, PR, and CR have nothing to disclose. CF received speaker honoraria and/or travel compensation for activities with Biogen, Sanofi Genzyme, Novartis, and Merck and research support from Chiesi, not related to this work. He reports no conflict of interest related to this manuscript. LD has received travel grants from Bayer, Biogen, Roche, and Merck as well as speaker honoraria from Merck and Biogen, not related to this work. AC has served on advisory boards for and received funding for travel or speaker honoraria from Actelion‐Janssen, Almirall, Bayer, Biogen, Celgene, Sanofi Genzyme, Merck, Novartis, Roche, and Teva, all for hospital research funds; and research support from Biogen, Genzyme, and UCB. Chan A is an associate editor of the European Journal of Neurology and serves on the editorial board for Clinical and Translational Neuroscience and as a topic editor for the Journal of International Medical Research. AS received speaker honoraria and/or travel compensation for activities with Bristol Myers Squibb, CSL Behring, Novartis, Roche, and research support by Baasch Medicus Foundation, the Medical Faculty of the University of Bern, and the Swiss MS Society. She serves on the Editorial Board of Frontiers in Neurology—Multiple Sclerosis and Neuroimmunology. All are not related to this work. RH received speaker/advisor honoraria from Merck, Novartis, Roche, Biogen, Alexion, Sanofi, Janssen, Bristol‐Myers Squibb, and Almirall. He has received research support within the last 5 years from Roche, Merck, Sanofi, Biogen, Chiesi, and Bristol‐Myers Squibb. He has also received research grants from the Swiss MS Society. He also serves as an associate editor for the Journal of Central Nervous System Disease. None of these are related to this work.
 The authors have no duality or conflicts of interest to declare.
 The authors declare no conflict of interest.
 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: M.C. has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Ad Scientiam, Biogen, Merck, Sanofi-Genzyme, Roche, Celgene/Bristol Myers Squibb (BMS), Alexion, Horizon Therapeutics, none related to this study. O.T-R. has nothing to disclose. A.S. reported serving on the steering committee for the ARISE and Teriflunomide in Radiologically Isolated Syndrome (TERIS) studies. D.T.O. received personal compensation for consulting and advisory services from Alexion, Biogen, Celgene/BMS, EMD Serono, Genentech, Genzyme, Janssen Pharmaceuticals, Novartis, Osmotica Pharmaceuticals, RVL Pharmaceuticals, Inc., TG Therapeutics, Viela Bio, Inc., and research support from Biogen and EMD Serono/Merck; he has issued national and international patents and pending patents related to developed technologies; he is the Founder of Revert, a corporation involved in healthcare; he also received royalties for intellectual property licensed by The Board of Regents of The University of Texas System; and he is the Principal Investigator of the ARISE study. R.K., H.E., and M.T. have nothing to disclose. C.C-D. has received travel grants and personal compensation for consulting, serving on a scientific advisory board, and speaking with Biogen, Novartis, Merck, Sanofi-Genzyme, and Roche. F.D-D. and E.T. have nothing to disclose. J.C. has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen, Novartis, Merck, Sanofi-Genzyme, Roche, Celgene-BMS, and Alexion, none related to this study. H.Z. has nothing to disclose. B.B. serves on the scientific advisory board and has received funding for travel and research funding from Alexion, BMS, Biogen, Merck, Novartis, Sanofi Roche, and Teva. O.C. has received travel grants, personal compensation for serving on a scientific advisory board, and lecturing fees from Biogen, Novartis, Merck, Sanofi-Genzyme, Roche, and Celgene-BMS. J.D.S. and T.M. have nothing to disclose. J-P.N. has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen, Novartis, Sanofi-Genzyme, Roche, and Alexion, but none related to this study. D.P. and O.K. reported serving on the steering committee for the ARISE and TERIS studies. Me.T. has nothing to disclose. N.D. reported receiving personal fees from Biogen, Novartis, Merck, and Roche outside the submitted work. C.B. has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Alexion, Biogen, BMS-Celgene, Merck, Novartis, Teva, and Sanofi-Genzyme. C.L. has received travel grants and personal compensation for consulting or speaking from Biogen, Novartis, Merck, Sanofi-Genzyme, and Roche, none related to this study. J.B. and C.L-C. have nothing to disclose. C.L-F. reported serving as the Principal Investigator of the TERIS study, on the steering committee for the ARISE study, and as co-president of the Observatoire Français de la Sclérose En Plaques (OFSEP) scientific committee, without honoraria.

 Declaration of Competing Interest Itay Lotan – no conflict of interest related to the study. Thibo Billiet- an employee of icometrix. Annemie Ribbens- an employee of icometrix. Win Van Hecke- founder of icometrix. Benny Huang- no conflict of interest related to the study. Ilya Kister- Ilya Kister reports he served on advisory boards for Biogen, Genentech, and Horizon and received research support for investigator-initiated grants from Genentech, Sanofi Genzyme, Biogen, EMD Serono, National MS Society, and Guthy Jackson Charitable Foundation. He received royalties from Walters-Kluwer for 'Top 100 Diagnosis in Neurology'. Eyal Lotan- no conflict of interest related to the study.


 Declaration of Competing Interest Valentino Paola received speaker honoraria from Roche, research support from Merck and grant support from Quanterix. Malucchi Simona received speaker honoraria from Biogen and Roche. Bava Cecilia Irene: nothing to discose Martire Serena: nothing to discose Capobianco Marco served on the scientific advisory board of Biogen, Sanofi Genzyme, Novartis, Roche, Becton-Dickinson, Alexion and Horizon and received speaker honoraria from Almirall, Biogen, Novartis, Sanofi Genzyme. Malentacchi Maria: nothing to discose Sperli Francesca: nothing to discose Oggero Alessandra: nothing to discose Di Sapio Alessia received personal compensation for speaking and consulting by Biogen, Novartis, Roche, Sanofi and Alexion and has been reimbursed by Merck, Biogen, Genzyme and Roche for attending several conferences. Bertolotto Antonio served on the scientific advisory board of Almirall, Bayer, Biogen, and Genzyme; received speaker honoraria from Biogen, Novartis and Sanofi and grant support from Almiral, Biogen, Associazione San Luigi Gonzaga ONLUS, Fondazione per la Ricerca Biomedica ONLUS, Mylan, Novartis and the Italian Multiple sclerosis Society.
 Competing interests: None declared.
 No conflicts of interest, financial or otherwise, are declared by the authors.
 The authors declare that they have no competing interests.
 The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosures.

 The authors declare no conflict of interest.
 Declaration of Competing Interest There is no conflict of interest.

 Competing interests: CT and CG received honoraria for speaking, manuscript writing or educational events from Merck, Biogen, Roche, Novartis Sanofi, Celgene, and Almirall. LP (Luca Prosperini) received consulting fees and/or speaker honoraria from Biogen, Celgene, Genzyme, Merck-Serono, Novartis and Teva, travel grants from Biogen, Genzyme, Novartis and Teva, research grants from the Italian MS Society (Associazione Italiana Sclerosi Multipla) and Genzyme. SH received travel funding and/or speaker honoraria from Biogen, Roche, Genzyme, Novartis and CSL Behring. SG received honoraria for speaking and travel grants from Biogen, Sanofi-Aventis, Merck Serono, Bayer-Schering, Teva, Genzyme, Almirall and Novartis. SR has received honoraria from Biogen, Merck Serono, Novartis and Teva for consulting services, speaking and/or travel support. EN participates on a data safety monitoring board or advisory board and receives fees for educational training from Gilead, Eli Lilly, GS, SOBI and Roche. EN has a patent pending for raloxifene use in COVID-19 with Dompè Pharmaceutical. DG is a member of the advisory board of Biomerieux and Eli Lilly and received fees for educational training or consultancy from Almirall, Biogen, Celgene, Diasorin, Janssen, Qiagen and Quidel. All the other authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: L.B. received funding from NIH, Harvard Medical School Shore grant, ROHHAD Fight, Inc. She received honoraria from Novartis. She participated in clinical trials with Biogen, Alexion, and Genentech/Roche. She is a consultant to the National Vaccine Injury Compensation Program and the Massachusetts Department of Public Health. T.C.C. receives research funding from Hoffman-La Roche, Ltd. T.C. has served as a consultant for Biogen, Novartis, Genentech-Roche, and Tiziana Life Sciences; clinical trial advisory boards and/or clinical trial participation: Novartis, Sanofi, and Genentech-Roche; received research support from Bristol Myers Squibb, Octave Bioscience, Novartis, Sanofi, and Tiziana Life Sciences. M.G. received research funding from Pfizer and Roche. L.K., over the last 3 years, has received research or programmatic funding, or has received compensation for consulting, speaking, travel and meal allowances, or serving on dSMB committees from Biogen, Novartis, Eisai, Roche, Gerson Lehrman, Janssen, Medscape, NeuroLive, Peer View, WebMD, Bristol Myers Squibb, CME Outfitters, General Dynamics Information, At the Limits, Cambridge Medical Technologies, and Medergy Marketing. She is also a non-compensated consultant and/or advisory board member with Novartis and Celgene. L.K. receives royalties for use of the Fatigue Severity Scale by various biopharmaceutical entities. M.R. disclosures include the following: Advisory Board or panel: Serono, Biogen, Horizon, TG, Novartis; Board Member: Chagrin Falls Educational Foundation, Ohio NMSS, IConquer MS; Consultant: Biogen, Genentech, Improve Consulting, Kijia, Novartis, BMS; Grants/Research support: she has received commercial research support from Medimmune, Novartis, Biogen (MS Paths), Roche-Genentech, and CBF Foundation. She has received foundation/society research support from the National Multiple Sclerosis Society. She has received educational grants from Genzyme and CBJ Foundation. Speaker’s Bureau: Genzyme, Biogen, and Multiple Sclerosis Association of America; IDMC member: Biogen; Owner: Brain Fresh (Professional development educational support) and Brain Ops Group (Joint Venture with Healthy Hostess DBA Kijia for Professional development through brain-based tools). J.R. received research funding from NMSS, GJCF, NIH, Biogen, and VA. T.S. participates in research funded by Roche and National MS Society. She is on the Data Safety Monitoring board for Biogen studies of pediatric MS. She has received speakers’ fees from Roche and Cycle Pharmaceuticals. E.W. has participated in multicenter clinical trials funded by Genentech, Alexion, and Biogen. She has current support from the NIH, NMSS, PCORI, CMSC, and Race to Erase MS. She has received honoraria for a talk for CMSC and for consulting for Emerald Pharmaceuticals. R.C., S.M., N.S., M.R., J.-M.T., M.W., M.W.-M., and Y.W. declare no conflicts of interest.

 The authors have no conflict of interest to declare.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Gabriele Di Sante reports financial support was provided by Fondazione Cassa di Risparmio di Perugia. Francesco Ria reports financial support was provided by Italian Multiple Sclerosis Association. Maurizio Fraziano reports financial support was provided by Italian Multiple Sclerosis Association. Francesco Ria reports financial support was provided by Università Cattolica del Sacro Cuore.

 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest Authors report no conflict of interest relevant to the study.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Dr V.J.B. is funded by the National MS Society Career Transition Award. Ms S.C., Mr J.J., Ms G.K., Mrs A.M.A., Mr M.K., Mr A.A., and Mr W.A.S. have no relevant disclosures. Drs R.C., E.C., M.J.P., J.E.O., and G.M.M. have no relevant disclosures. Dr N.P. has received research support to UCSF from the Race to Erase MS Foundation and from the National Center for Advancing Translational Sciences, National Institutes of Health, through a UCSF-CTSI Grant. Dr S.L.H. currently serves on the scientific advisory board of Accure, Annexon, Alector, board of directors of Neurona, and has previously consulted for NGM Bio and Moderna. Dr S.L.H. also has received travel reimbursement and writing assistance from Roche and Novartis for CD20-related meetings and presentations. Dr J.M.G. has received research support to UCSF from Genentech/Roche and Vigil Neuroscience, and consulting fees from Biogen. Dr R.B. is funded by the NMSS Harry Weaver Award, NIH, DOD, NSF as well as Biogen, Novartis, and Roche Genentech. She has received personal fees for consulting from Alexion, EMD Serono, Horizon, Jansen, Genzyme Sanofi, and TG Therapeutics. Dr B.A.C.C. has received personal compensation for consulting from Alexion, Atara, Biogen, EMD Serono, Novartis, Sanofi, and TG Therapeutics. Dr R.G.H. has received consulting fees from Roche/Genentech, Sanofi/Genzyme, Novartis, Celgene, Atara Bio, QIA Consulting, Boston Pharma, and Neurona Therapeutic. Grants from Roche/Genentech and Atara Bio.
 Declaration of Competing Interest None of the authors has any financial disclosure or competing interest.
 Declaration of interests F.Z. has recently received research grants and/or consultation funds from Biogen, Ministry of Education and Research (BMBF), Bristol-Meyers-Squibb, Celgene, German Research Foundation (DFG), Janssen, Max-Planck-Society (MPG), Merck Serono, Novartis, Progressive MS Alliance (PMSA), Roche, Sanofi Genzyme, and Sandoz. S.B. has received honoraria and compensation for travel from Biogen Idec, Bristol Meyer Squibbs, Merck Serono, Novartis, Sanofi-Genzyme, Roche, and Teva.
 KB has participated in meetings sponsored by, received travel funding from, or received honoraria for acting as an advisor/speaker for Roche, Biogen, TEVA, Sanofi-Genzyme, Merck, and Novartis. AB was an employee of VASCage – Research Centre on Vascular Ageing and Stroke and has participated in meetings sponsored by or received travel funding from Novartis, Sanofi-Genzyme, Merck, Almirall, and Biogen. DR was an employee of VASCage – Research Centre on Vascular Ageing and Stroke. MA received speaker honoraria and/or travel grants from Biogen, Merck, Novartis, and Sanofi. RB has participated in meetings sponsored by and received travel grants from Biogen, Novartis, and Sanofi. AZ has participated in meetings sponsored by and received speaking honoraria or travel funding from Biogen, Merck, Sanofi-Genzyme and Teva. SW has participated in meetings sponsored by and received honoraria or travel funding from Allergan, Biogen, Ipsen Pharma, Merck, Novartis, Roche, Sanofi Genzyme, Teva, and Bristol Myers Squibb. TB has participated in meetings sponsored by and received honoraria lectures, advisory boards, and consultations from pharmaceutical companies marketing treatments for MS: Allergan, Bayer, Biogen, Bionorica, BMS/Celgene, GSK, GW/Jazz Pharma, Horizon, Janssen-Cilag, MedDay, Merck, Novartis, Octapharma, Roche, Sandoz, Sanofi-Genzyme, Teva, and UCB. FP has participated in meetings sponsored by and received honoraria lectures, advisory boards, consultations or travel funding from Bayer, Biogen, Merck, Novartis, Sanofi-Genzyme, Teva, Celgene, and Roche. Her institution has received research grants from Roche. FD has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Almirall, Alexion, Biogen, Celgene, Genzyme-Sanofi, Horizon, Janssen, Merck, Novartis Pharma, Roche, and TEVA ratiopharm. His institution has received research grants from Biogen and Genzyme Sanofi. He is a section editor of the MSARD Journal Multiple Sclerosis and Related Disorders and a review editor of Frontiers Neurology. HH has participated in meetings sponsored by and received speaker honoraria or travel funding from Bayer, Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme, Siemens, and Teva, and received honoraria for acting as consultant for Biogen, Celgene, Novartis, and Teva. MR was supported by a research support from Euroimmun and Roche. The University Hospital and Medical University of Innsbruck Austria, employer of Dr. Reindl receives payments for antibody assays MOG, AQP4, and other autoantibodies and for MOG and AQP4 antibody validation experiments organized by Euroimmun Lübeck, Germany. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no competing interests.
 The authors declare the following financial interests/personal relationships which may be considered potential competing interests: Miriam Fedičová has received personal compensation for speaking or other activities from Biogen, Merck, Roche, Novartis and Teva. Mgr. Pavol Mikula has no potential conflict of interest. Marianna Vitková received personal compensation for speaking or other activities from Biogen, Merck, Novartis, Roche and Teva. Norbert Žilka has no potential conflict of interest. Eng. Jozef Hanes has no potential conflict of interest. Lýdia Frigová has no potential conflict of interest. Zuzana Gdovinová has received personal compensation for consulting, serving on a scientific board from Biogen, Boehringer-Ingelheim, Merck, MSD, Novartis, Pfizer, Takeda, and Schwabe. Jarmila Szilasiová received personal compensation for consulting or other activities, with received compensation for serving on a scientific advisory board from Biogen, Teva, Novartis, SwixxBiopharm, Roche, and Merck.
 The authors declare no conflict of interest.
 Declaration of Competing Interest There were no conflicts of interest in this study.
 Authors have no conflicts of interests specific to these studies to report. KSS reports the following financial relations not related to the current studies: intellectual property related to SIRT1 gene therapy; grant funding from Gyroscope Therapeutics; and Scientific Advisory Board membership, consulting fees, equity options, and grant funding from Noveome Biotherapeutics.


 Author RC received funding from the Deutsche Forschungsgemeinschaft DFG, German Research Foundation under Germany’s Excellence Strategy – EXC2151 – 390873048. Author SK reports funding from the DFG, Novartis, F. Hoffmann-La Roche and Sanofi; and speaker fees and consultancy honoraria from Novartis, F. Hoffmann-La Roche, Sanofi, and Teva outside the submitted work. Author SK is also supported by the DFG IRTG 2168, grant no. 272482170 and is a member of the Excellence Cluster “ImmunoSensation2” EXC2151 – 390873048. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest Dr. Raskin is the developer of the Memory for Intentions Test (MIST). The authors have no other competing interests to declare. There has been no significant financial support for this work that could have influenced its outcome.
 Declaration of interests M.M.v.L. received research support from EMD Serono, Merck, GSK and Idorsia Pharmaceutical Ltd. J.S. received lecture and/or consultancy fees from Biogen, Merck, Novartis and Sanofi-Genzyme. The remaining authors declare no competing interests.
 Author PA is employed by Maria Hilf Clinics GmbH, Mönchengladbach. The following financial disclosures are unrelated to the work: SM received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology, and by Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, Merck Serono, Novartis, ONO Pharma, Roche, and Teva. MD received speaker honoraria from Merck and Novartis. PA is employed by Maria Hilf Clinics GmbH, Mönchengladbach. He received compensation for serving on Scientific Advisory Boards for Ipsen, Novartis, Biogen; he received speaker honoraria and travel support from Novartis, Teva, Biogen, Merz Pharmaceuticals, Ipsen, Allergan, Bayer Healthcare, Esai, UCB and Glaxo Smith Kline; he received research support from Novartis, Biogen, Teva, Merz Pharmaceuticals, Ipsen, Bristol-Myers Squibb and Roche. TR reports grants from German Ministry of Education, Science, Research and Technology, during the conduct of the study; grants and personal fees from Sanofi-Genzyme; personal fees from Biogen; personal fees and non-financial support from Merck Serono; personal fees from Roche, Teva, Alexion, Argenx, UCB, and BMS outside the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.The work was funded by a research grant from Celgene / Bristol Myers Squibb to PA.

 Declaration of Competing Interest JS is a co-inventor in the patent # US 9,248,128.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Matilde Inglese received grants NIH, NMSS, FISM; received fees for consultation from Roche, Genzyme, Merck, Biogen and Novartis. Matteo Bassetti received research grants, advisory board and/or speaker honoraria from Msd, Pfizer, Menarini, Shionogi, Sobi, Cidara, Angelini.



 Declaration of Competing Interest The authors declare no conflict of interest.

 The authors declare no conflict of interest.

 All authors have no financial interests or potential conflicts of interest to report with regards to the current study.
 Declaration of Competing Interest Dr. Koch received consulting fees and travel support from Biogen, Novartis, Roche, Sanofi Genzyme and EMD Serono. Dr. Repovic received consulting and/or speaking honoraria from Alexion, Biogen, Celgene, Roche, Sanofi Genzyme, Viela and EMD Serono. Dr. Mostert reports no disclosures. Dr. Bowen received honoraria from serving on the scientific advisory board and speaker's bureau of Biogen, Celgene, EMD Serono, Genentech and Novartis. He has received research support from AbbVie Inc, Alexion, Alkermes, Biogen, Celgene, Sanofi Genzyme, Genentech, Novartis and TG Therapeutics. Dr. Comtois reports no disclosures. Dr. Strijbis reports no disclosures. Prof. Uitdehaag received consultancy fees and/or research support from Biogen, Sanofi Genzyme, EMD Serono, Novartis, Roche, Teva, and Immunic Therapeutics. Prof. Cutter served on Data and Safety Monitoring Boards: Astra-Zeneca, Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Horizon Pharmaceuticals, Hisun Pharmaceuticals, Mapi Pharmaceuticals LTD, Merck, Merck/Pfizer, Opko Biologics, OncoImmune, Neurim, Novartis, Ophazyme, Sanofi-Aventis, Reata Pharmaceuticals, Teva Pharmaceuticals, VielaBio Inc, Vivus, NHLBI (Protocol Review Committee), NICHD (OPRU oversight committee). Consulting or Advisory Boards: Biodelivery Sciences International, Biogen, Click Therapeutics, Genzyme, Genentech, GW Pharmaceuticals, Immunic, Klein-Buendel Incorporated, Medimmune, Medday, Neurogenesis LTD, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Recursion/Cerexis Pharmaceuticals, Roche, TG Therapeutics. Dr. Cutter is employed by the University of Alabama at Birmingham and President of Pythagoras, Inc. a private consulting company located in Birmingham AL.

 Mathias Due Buron has received speaker honoraria from Novartis.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors do not have competing financial interests concerning the work described. T. Mak owns equity in Treadwell Therapeutics Inc. and Agios Pharmaceuticals and is a consultant for AstraZeneca and Tessa Therapeutics.


 Conflict of interests None declared.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors Suzi Claflin, Julie A Campbell, Richard Norman, Deborah F. Mason, Tomas Kalincik, Steve Simpson-Yap, Helmut Butzkueven, William M. Carroll, Andrew J. Palmer, C. Leigh Blizzard, Ingrid van der Mei, Glen J Henson and Bruce V. Taylor report no conflicts of interest.
 Declaration of interests The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.
 The research was conducted by Adelphi Values Patient-Centered Outcomes who received funding from Novartis Pharma AG to complete this work. Some of the authors are salaried employees of Novartis Pharma AG.

 The authors declare to not have any potential conflict of interest.

 CR participated as clinical investigator and/or received consultation and/or speaker fees and/or conference travel grants from: Biogen, Merck, Novartis, Sanofi Genzyme, Roche, Teva. IZ has served on scientific advisory boards, received support for congress participation, speaker honoraria, or for being member of clinical endpoint committees in clinical trials, and received research support for his laboratory from Biogen, Merck, Roche, Sanofi Genzyme, Novartis, Alexion, and Bristol Myers Squibb. CsR received speaker fees, conference honoraria from Biogen, Novartis, Merck, Roche, Sanofi. AM participated as clinical investigator and/or received consultation and/or speaker fees and/or conference travel grants from Biogen, Merck, Novartis, Sanofi Genzyme, Roche, Teva. GL received speaker fees and honoraria form Biogen, Novartis, Merck, Roche, Sanofi. ZM received speaker fees and conference/travel grants from: Biogen, Merck, Novartis, Roche and Sanofi Genzyme. ÁP received received investigator and speaker fees from: Sanofi Genzyme, Roche. GJ, GR, AT, KM and ID reported no conflict of interest. MS participated as clinical investigator and received consultation / speaker fees and conference travel grants from: Biogen, Merck, Novartis, Sanofi Genzyme, Roche, Teva. ZJ received consultation fees, speaker fees and conference travel grants from: Biogen, Merck, Novartis, Sanofi Genzyme, Roche. ZB received congress support from Biogen, Merck, Novartis, Sanofi-Genzyme and Roche. IP participated as clinical investigator, and received consultation, and speaker fees, and conference travel grants from: Biogen, Merck, Novartis, Sanofi Genzyme. TC has received personal honoraria for speaking, advisory boards and travel expenses from Biogen, Novartis, Roche, Sanofi-Genzyme, Teva.




 The authors declare no conflict of interest.
 Conflicts of interest.—The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript.

 Declaration of Competing Interest The authors declare that they have no competing interests.


 MS receives research support and has received fees as speaker from Sanofi, Biogen, Roche, Novartis, Bayer Schering, and Merck Serono. VR, GB and GR declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. AA and CR are employees of Merck Serono S.p.A., Rome, Italy, an affiliate of Merck KGaA, Darmstadt, Germany.
 Conflict of Interest Disclosures: Dr Tur reported receiving grants from “La Caixa” Foundation Junior Leader incoming fellowship, Fundación Merck Salud (Spain) 2021 Merck’s Award for the Investigation in MS, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación de España Proyecto de Investigación, ECTRIMS 2015 ECTRIMS postdoctoral research fellowship, and the UK MS Society; speaker honoraria from Roche and Novartis; nonfinancial support from Biogen; being a steering committee member of the O’HAND trial and the Consensus Group on Follow-on DMTs; and being a member of the editorial board of Neurology. Dr Carbonell-Mirabent reported receiving grants from Biogen to Fundació Privada Cemcat for statistical analysis. Dr Cobo Calvo reported receiving grants from Instituto de Salud Carlos III, Spain; JR19/00007 during the conduct of the study. Dr Otero-Romero reported receiving a grant from Instituto de Salud Carlos III, Spain. Dr Arrambide reported receiving personal fees from Sanofi, Merck, and Horizon Therapeutics; nonfinancial support from Roche and Novartis; a research grant from Instituto de Salud Carlos III, Spain; travel support for scientific meetings from Novartis, Roche, and ECTRIMS; working as an editor for Europe of the Multiple Sclerosis Journal – Experimental, Translational and Clinical; working as a member of the International Women in Multiple Sclerosis Network executive committee; and working as a member of the European Biomarkers in MS Consortium steering committee. Dr Vidal-Jordana reported receiving grants from Fondo de Investigaciones Sanitarias, Instituto de Salud Carlos III, Spain; personal fees from Novartis, Roche, Merck, and Sanofi; and speaking honoraria and travel expenses from Novartis, Roche, Teva, Biogen, and Sanofi Genzyme. Dr Rodríguez-Acevedo reported receiving honoraria for consulting services from Wellspect. Dr Nos reported receiving steering committee fees from Hoffmann-La Roche; consulting fees from Sanofi; travel fees from Biogen Idec and F. Hoffmann-La Roche; speaker honoraria from Novartis; and funding from Novartis for registration for scientific meeting outside the submitted work. Dr Pareto reported receiving grants from Biogen Idec; speaking honoraria from Novartis and Sanofi Genzyme; and having a research contract with Biogen Idec. Dr Comabella reported receiving compensation for consulting services and speaking honoraria from Bayer Schering Pharma, Merck Serono, Biogen-Idec, Teva Pharmaceuticals, Sanofi-Aventis, and Novartis. Dr Río reported receiving speaking honoraria and personal compensation for participating on advisory boards from Biogen-Idec, Genzyme, Merck-Serono, Mylan, Novartis, Teva, Sanofi-Aventis, Roche, and Janssen. Dr Sastre-Garriga reported receiving personal fees for advisory board participation, speaking honoraria, and travel expenses from Novartis, Biogen, Sanofi, Celgene-BMS, Merck, Bial, Teva, Almirall, Genzyme, and Roche outside the submitted work. Dr Rovira reported receiving advisory board fees and/or speaker honoraria from Novartis, Synthetic MRI, Biogen, Bayer, Merck-Serono, Bristol Myers, OLEA Medical, Roche, TensorMedical, Sanofi Genzyme, and Teva Pharmaceuticals and being a shareholder in TensorMedical. Dr Tintoré reported receiving consulting and/or speaking honoraria from Almirall, Bayer, Schering Pharma, Biogen-Idec, Genzyme, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Aventis, Viela Bio, and Teva Pharmaceuticals and being a co-editor of Multiple Sclerosis Journal – Experimental, Translational and Clinical. Dr Montalban reported received speaking honoraria, travel expenses for participation in scientific meetings, and/or being a steering committee member of or participated in advisory boards for Actelion, Alexion, Almirall, Bayer, Biogen, Bristol Myers Squibb, Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Immunic, Janssen, Medday, Merck, Mylan, Nervgen, Novartis, Oryzon Genomics, Sanofi-Genzyme, Sandoz, Teva Pharmaceuticals, TG Therapeutics, and NMSS outside the submitted work. No other disclosures were reported.
 P.M.L. founded and is an adviser to Vironika LLC. P.M.L. is named on a patent for inhibitors of EBNA1. S.S.S. declares no competing interests.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Laure Michel reports a relationship with Biogen that includes: consulting or advisory. Laure Michel reports a relationship with Teva Health that includes: consulting or advisory. Laure Michel reports a relationship with Roche that includes: consulting or advisory. Laure Michel reports a relationship with Sanofi Genzyme that includes: consulting or advisory. Laure Michel reports a relationship with Janssen Pharmaceuticals Inc that includes: consulting or advisory. Laure Michel reports a relationship with Novartis that includes: consulting or advisory. Laure Michel reports a relationship with Merck & Co Inc that includes: consulting or advisory. Eric Thouvenot reports a relationship with Actelion Ltd that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Eric Thouvenot reports a relationship with Biogen that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Eric Thouvenot reports a relationship with Bristol Myers Squibb Co that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Eric Thouvenot reports a relationship with Merck & Co Inc that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Eric Thouvenot reports a relationship with Novartis that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Eric Thouvenot reports a relationship with Roche that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Sandra Vukusic reports a relationship with Biogen Inc that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Bristol Myers Squibb Co that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Janssen Pharmaceuticals Inc that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Merck & Co Inc that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Novartis that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Roche that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Sandoz Inc that includes: speaking and lecture fees and travel reimbursement. Sandra Vukusic reports a relationship with Sanofi Genzyme that includes: speaking and lecture fees and travel reimbursement. Helene Zephir reports a relationship with Alexion that includes: consulting or advisory. Helene Zephir reports a relationship with Biogen Inc that includes: consulting or advisory. Helene Zephir reports a relationship with Horizon Therapeutics plc that includes: consulting or advisory. Helene Zephir reports a relationship with Merck & Co Inc that includes: consulting or advisory. Helene Zephir reports a relationship with Novartis that includes: consulting or advisory. Helene Zephir reports a relationship with Sanofi that includes: consulting or advisory. Helene Zephir reports a relationship with Roche that includes: consulting or advisory and funding grants. Helene Zephir reports a relationship with Foundation for Help in Research of Multiple Sclerosis that includes: funding grants.
 The author(s) declared the following potential conflict of interest with respect to the research, authorship, and/or publication of this article: S.N.B. and N.J.F. report no disclosures. C.S.M. has received speaker honoraria from Biogen, EMD Serono and Genzyme-Sanofi.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as potential conflict of interest.
 The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosures.
 Declaration of Competing Interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest None.
 Leoni Rolfes: received travel reimbursements from Merck Serono and Sanofi Genzyme and research support from Diamed, Merck Serono, and Novartis. Her research is funded by the Interdisciplinary Center for Clinical Studies (IZKF) Muenster. Steffen Pfeuffer: received travel grants from Sanofi Genzyme and Merck Serono, lecturing honoraria from Sanofi Genzyme, Mylan Healthcare, and Biogen, and research support from Diamed, Merck Serono, and the German Multiple Sclerosis Society Northrhine-Westphalia. Jelena Skuljec: received research funding from the University Medicine Essen Foundation. She was financially supported by a “Welcome Back” grant from the Medical Faculty of the University Duisburg-Essen, Germany. Xia He: nothing to declare. Chuanxin Su: nothing to declare. Sinem Özalp: nothing to declare. Marc Pawlitzki: received research funding from Novartis. His research is founded by the German Multiple Sclerosis Society North Rhine-Westphalia (DMSG) and the program “Innovative Medizinische Forschung” (IMF) of the Medical Faculty of the University of Muenster. Tobias Ruck: reports grants from the German Ministry of Education, Science, Research and Technology, grants, and personal fees from Sanofi-Genzyme and Alexion; personal fees from Biogen, Roche, and Teva; personal fees and nonfinancial support from Merck Serono, outside the submitted work. Melanie Korsen: nothing to declare. Derya Aslan: nothing to declare. Tim Hagenacker: received honoraria and consulting from Alexion, Novartis, Biogen, Sanofi-Genzyme, Argenxy, Hormosan, and Roche, as well as financial research support from Biogen, Roche, Novartis, and Sanofi-Genzyme. Christoph Kleinschnitz: received honoraria for lecturing and consulting as well as financial research support from Ablynx, Almirall, Amgen, Bayer Vital, Bristol-Mayers Squibb, Biotronik, Boehringer Ingelheim, Biogen, CSL Behring, Daiichi-Sankyo, Desitin, Eisai, Ever Pharma, Sanofi Genzyme, Merck Serono, Mylan, Medday, Novartis, Pfizer, Roche, Siemens, Stago, and Teva. Sven G. Meuth: received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology, and by Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, Merck Serono, Novartis, ONO Pharma, Roche, and Teva. Refik Pul: received honoraria for lecturing and consulting from Alexion, Bayer Healthcare, Biogen, Squibb/Celgene, Horizon, MedDay, Merck Serono, Mylan, Novartis, Roche, and Sanofi Genzyme. He received research funds from Teva, Merck Serono, and Novartis.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 V. E. Maltby: has received honoraria for presentations from Biogen and Merck Healthcare Pty Ltd. She received research funding from Merck KGgA and Biogen. B. Taylor: has received travel assistance from Merck KGaA, Novartis, and Biogen IDEC and served on Ad Boards for Merck, Sanofi, Novartis, and Biogen. H.Butzkueven: has received institutional (Monash University) funding from Biogen, F. Hoffmann-La Roche Ltd, Merck, Alexion, CSL, and Novartis; has performed contracted research for Novartis, Merck, F. Hoffmann-La Roche Ltd, and Biogen; has taken part in speakers' bureaus for Biogen, Genzyme, UCB, Novartis, F. Hoffmann-La Roche Ltd, and Merck; and has received personal compensation from Oxford Health Policy Forum for the Brain Health Steering Committee. J. Lechner-Scott's institution receives nondirected funding and honoraria for presentations and membership on advisory boards from Sanofi Genzyme, Biogen, Merck KGaA, Teva, Roche, and Novartis Australia. All other authors have nothing to disclose. Go to Neurology.org/N for full disclosures.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 No potential conflict of interest was reported by the author(s). The authors do not have competing financial interests in relation to the work. Of note, author (HLG) and the SCI Guiding Principles Consensus Panel play a leadership role within the SCI Research System.


 The authors declare no conflict of interest.

 Competing interests: None declared.
 The authors of this manuscript declare no relationships with any companies, whose products or services may be related to the subject matter of the article.


 The authors have no ethical statement, funding and conflicts of interest to disclose.
 Pierre Denys: Consultancy: Allergan, Taris, Medtronic, Coloplast. Grant research study: Ipsen and Allergan. Juan Carlos Castaño Botero: Astellas (consultant and lecturer fees), Boston Scientific (consultant and lecturer fees) Medtronic (consultant fees, trial investigator), Ipsen (trial investigator). Ricardo Luis Vita Nunes: Grant/Research study: Ipsen; Consultancy: Astellas Pharma, Zambon; Lectures: Astellas, Zambon, Zodiac, Aché, Coloplast. Barton Wachs: Nothing to disclose. Cristiano Mendes Gomes: Grant/Research study: Ipsen; Consultancy: Astellas Pharma, Boston Scientific; Lectures: Astellas, Boston Scientific, Zodiac. Grigory Krivoborodov: Lectures: Astellas, Coloplast, Pierre Fabre, Braun, Medtronic. Le Mai Tu: Consultancy and Lectures: Astellas Pharma, Pfizer. Giulio Del‐Popolo: Grant/Research study: Ipsen, Wellspect, B Braun, Hollister; Consultant: Coloplast, Wellspect, Pierre Fabre, Braun. Catherine Thompson: Employee of June Pharma under contract by Ipsen. Claire Vilain and Magali Volteau: Employee of Ipsen. Michael Kennelly: Research Grants: Allergan, Amphora, Axonics, Boston Scientific, Coloplast, Cook Myosite, Dignify Therapeutics, Ipsen, Taris, Uro1, FemPulse, EBT Medical; Consultancy Fees: Allergan, Boston Scientific, Coloplast, Laborie, Urovant.

 The authors declare no competing interests.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 K. Hellwig has received speaker honoraria and research support from Bayer, Biogen, Merck, Novartis, Sanofi-Genzyme, Roche, and Teva; has received support for congress participation from Bayer, Biogen, Merck, Roche, Sanofi-Genzyme, and Teva; and has served on scientific advisory boards for Bayer, Biogen, Sanofi, Teva, Roche, Novartis, and Merck. M. Tokic is employed in a project funded by a grant from the Innovation Fund of the Federal Joint Committee. S. Thiel received speakers honoraria from Bayer Healthcare and Biogen GmbH as well as payment for manuscript writing from HEXAL AG. S. Hemat reports no disclosures relevant to the manuscript. N. Timmesfeld has received a grant from the Innovation Fund of the Federal Joint Committee. A.I. Ciplea has received speaker honoraria from Bayer Healthcare, sponsorship for congress participation from Teva, and travel grants from Teva and Novartis. R. Gold has received speaker honoraria and research support from Bayer-Schering Healthcare, Biogen-Idec Germany, Chugai, Eisai, Merck Serono, Nikkiso Pharma, Novartis, Roche, Sanofi-Genzyme, and TEVA; has received consulting honoraria from CSL Behring, Baxter, Janssen, and Talecris; and has stock options in Bayer, Merck, and Roche. A. Langer-Gould reports no disclosures relevant to the manuscript. Go to Neurology.org/NN for full disclosure.
 Conflicts of Interest: None declared.

 The authors declare no conflict of interest.
 Declaration of Competing Interest None.


 Declaration of competing interest YGY, NC, and RH are employees of Bristol Myers Squibb. JVS and KP were employees of Bristol Myers Squibb at the time of this study.

 The authors declare no competing interests.

 The authors declare no conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Grace Gombolay receives part time salary support from the Centers for Disease Control and Prevention for acute flaccid myelitis case reviews and surveillance. Jamika Hallman-Cooper has nothing to disclose.

 Declaration of Competing Interest Ulrik Dalgas has received research support, travel grants, and/or teaching honoraria from Biogen Idec, Bristol Myers Squibb, Merck Serono, Novartis, Bayer Schering, and Sanofi Aventis, as well as honoraria from serving on the scientific advisory boards of Biogen Idec and Genzyme. All other authors declare no conflict of interest.

 The authors report no competing interests.

 The authors declare no conflict of interest.

 The authors declare that they have no competing interests.
 The authors declare no competing interests.

 The authors have no conflicts of interest to disclose.
 We have no conflicts of interest to declare.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest O.A.A. has received speaker's honorarium from Janssen, Sunovion and Lundbeck and is a consultant for cortechs.ai, Milken and Biogen. Dr. Dale is a Founder of and holds equity in CorTechs Labs, Inc., and serves on its Scientific Advisory Board. He is a member of the Scientific Advisory Board of Human Longevity, Inc. and receives funding through research agreements with General Electric Healthcare and Medtronic, Inc. The terms of these arrangements have been reviewed and approved by UCSD in accordance with its conflict of interest policies. Geir Selbæk has received honoraria as a participant at advisory board meetings for Roche and Biogen. Remaining authors have no conflicts of interest to declare.

 The authors declare no competing interests.
 Conflict of Interest No conflict of interest was declared by the authors.
 Declaration of Competing Interest SN is a co-editor of Overcoming Multiple Sclerosis Handbook: Roadmap to Good Health. SN is a facilitator of Overcoming MS educational workshops for people with MS.
 AM-V, PAP, IL, LB, EM, AM-Y, SM-Y, and LR-P received honoraria compensation to participate in advisory boards, collaborations as a consultant, and scientific communications, and received research support and funding for travel and congress expenses from Biogen Idec, Novartis, TEVA, BMS, Horizon, Merck Serono, Genzyme, Almirall, Bial, Kern Pharma, Lilly, Sanofi, Bayer, and Roche.
 Declaration of Competing Interest None.
 The author(s) declare no potential competing interests with respect to the research, authorship, and/or publication of this article.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 Conflicts of interest.—The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript.
 S.R. has received honoraria from Biogen, Merck Serono, Novartis and Teva for consulting services, speaking and/or travel support. C.T. and C.G. received honoraria for speaking, manuscript writing or educational events from Merck, Biogen, Roche, Novartis Sanofi, Celgene, and Almirall. L.P. received consulting fees and/or speaker honoraria from Biogen, Celgene, Genzyme, Merck-Serono, Novartis and Teva, travel grants from Biogen, Genzyme, Novartis and Teva, and research grants from the Italian MS Society (Associazione Italiana Sclerosi Multipla) and Genzyme. S.H. received travel funding and/or speaker honoraria from Biogen, Roche, Genzyme, Novartis and CSL Behring. S.G. received honoraria for speaking and travel grants from Biogen, Sanofi-Aventis, Merck Serono, Bayer-Schering, Teva, Genzyme, Almirall and Novartis. E.N. participates on a data safety monitoring board or advisory board and receives fees for educational training from Gilead, Eli Lilly, G.S., SOBI and Roche, and he has a patent pending for raloxifene use in COVID-19 with Dompè Pharmaceutical. DG is a member of the advisory board of Biomerieux and Eli Lilly and received fees for educational training or consultancy from Almirall, Biogen, Celgene, Diasorin, Janssen, Qiagen and Quidel. All the other authors declare that they have no conflict of interest. The funders had no role in the design of the study, in the collection, analyses or interpretation of data, in the writing of the manuscript or in the decision to publish the results.

 Declaration of Competing Interest The authors have no conflicting financial interests.
 Conflict of interests J.R. Karlowicz report no disclosures relevant to the manuscript. M. Klakegg report no disclosures relevant to the manuscript. J.H. Aarseth report no disclosures relevant to the manuscript. L. Bø has received unrestricted research grants to his institution and/or scientific advisory board or speakers honoraria from Biogen, Genzyme, Merck, NOvartis, Roche, and Teva, and has participated in clinical trials organized by Biogen, Merck, Novartis and Roche. H. Torgauten report no disclosures relevant to the manuscript. Ø. Torkildsen has received speaker honoraria from and served on scientific advisory boards for Biogen, Sanofi-Aventis, Merck and Novartis. K-M. Myhr has received unrestricted research grants to his institution, scientific advisory board or speaker honoraria from Biogen, Novartis, and Sanofi, and has participated in clinical trials organized by Biogen, Merck, Novartis, Roche and Sanofi. S. Wergeland has received honoraria for lecturing and advice from Biogen, Janssen and Sanofi.His department has received unrestricted institutional grants from Biogen, Merck and Novartis. He is currently collaborating on research projects funded by Merck and EMD Serono.
 GJ receives royalties for his books, Overcoming Multiple Sclerosis and Recovering from Multiple Sclerosis and GJ and SN receive royalties from their book, Overcoming Multiple Sclerosis: Roadmap to Good Health and have previously received remuneration for conducting educational workshops for people with MS.



 The authors have no funding and conflicts of interest to disclose.
 The authors declare that they do not have any conflicts of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest The authors declare no conflict of interest.
 Declarations of Competing Interest None.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no competing interests.
 Declaration of Competing Interest No potential conflict of interest was reported by the authors
 Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht.

 The authors declare that they have no competing interests.
 Declaration of Competing Interest The authors declare that they have no conflict of interest, and no funding has been used for the manuscript.

 The authors declare that they have no competing interests.

 The authors have declared that no competing interests exist.
 R.C., C.L., N.A. and A.P. are inventors on patents and patent applications related to MCAM modulation and uses thereof (CA2676962C, AU2009212789B2, US8293468B2 and US9017682B2). A.P. is an inventor on patents and patent applications related to DICAM-specific antibodies and uses thereof (US10428144B2, WO2016095046A1, EP3233919B1 and CA2971364A1). E.P. is currently an employee of Immunic AG and owns stock options of the parent company of Immunic AG.
 Declaration of competing interest MT and CDS declares no conflict of interest. LHF, KLL and AHL have an ongoing patent application in USA for the speckle tracking ultrasonography method used in the present study: Patent application no. 16/482,550. HHN and HBJ have received financial compensation for travels, consultations, and advisory boards from Biogen Idec, Roche, Sanofi Genzyme, Merck & Co Inc., Novartis, and Teva.
 S. Küchlin: doctoral fellowship with funding from the University of Freiburg and the Else Kröner-Fresenius Foundation. G. Ihorst: funding from Novartis and Janssen Pharmaceuticals. B. Grotejohann and F. Beisse: nothing to report. S.P. Heinrich: funding from the DFG, German Federal Institute for Sport Science, and German Ophthalmologic Society. P. Albrecht: grant and personal fees and nonfinancial support from Allergan, Biogen, Celgene, Ipsen, Janssen Cilag, Merck, Merz Pharmaceuticals, Novartis, Roche, and Teva, outside the submitted work. J. Ungewiss: employee at the Aalen University of Applied Sciences, employee at Carl Zeiss Vision International GmbH, doctoral fellowship with funding from the Ministry of Science Research and Arts Baden-Wuerttemberg as part of the HAW-Prom program, speakers' honorary from AMO Ireland (affiliated to Johnson & Johnson Vision), and coinventor of patents/patent applications with the numbers 10 2017 126 741, WO 2020/089284 A1, and 20 174 551.0. M. Wörner is a managing partner of Blickshift GmbH and coinventor of patent applications WO 2020/089284 A1 and 20 174 551.0. M.J. Hug: grants from Bristol-Myers Squibb and speaker's honoraria from Amgen, Baxter Deutschland, CSL Behring, Biotest Pharma, Fresenius Kabi, Leo Pharma, Merck Serono, Novartis Pharma, Pfizer, Roche Pharma, and Sun Pharmaceuticals Industries. S. Wolf has served as a consultant for Bayer, Novartis, Chengdu Kanghong Biotech, Zeiss, and Roche; has received grant support from Zeiss; and has received grant support from Heidelberg Engineering. W.A. Lagrèze has received grants from the German Federal Ministry for Education and Research (BMBF), grants from the German Research Foundation (DFG), and speakers' honoraria from and worked on advisory boards for Alcon, Allergan, Santhera, Boehringer Ingelheim, and Merz Pharma. Go to Neurology.org/NN for full disclosure.
 Disclosures: L. Steinman reported a patent to „GlialCAM tolerizing therapies and uses thereof” pending (Pasithea Therapeutics). No other disclosures were reported.
 The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosures.

 Competing interests The authors declare no competing interests.
 The authors declare no competing interests.



 Conflict of interest There is nothing to declare as competing interest for any of the authors including the corresponding author.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: J.O’.M. received funding from the Multiple Sclerosis Scientific Research Foundation. B.B. serves as a consultant to Novartis, Sanofi-Genzyme, Roche and UCB, and has received grant support from the Canadian Multiple Sclerosis Society and Foundation, National Multiple Sclerosis Society, and the National Institutes of Health. E.A.Y. has received research support in the last 3 years from the National MS Society, Canadian Institutes of Health Research, National Institutes of Health, Ontario Institute of Regenerative Medicine, Stem Cell Network, SickKids Foundation, Peterson Foundation, MS Society of Canada, and the MS Scientific Research Foundation. She has received funding for investigator-initiated research from Biogen and has served on scientific advisory boards for Biogen, Alexion and Hoffman-LaRoche. A.B.-O. is funded by the NIH, ITN, NMSS, and MSSOC, and has participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from: Janssen/Actelion; Atara Biotherapeutics, Biogen Idec, Celgene/Receptos, Roche/Genentech, Medimmune, Merck/EMD Serono, Novartis, Sanofi-Genzyme. R.A.M. receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC, Biogen, Roche, the Government of Alberta, the Arthritis Society, and the US Department of Defense. She is supported by the Waugh Family Chair in Multiple Sclerosis. The remaining authors have no relevant conflicts of interest to disclose.

 Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.



 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: A.G. has received research support from the UK MS Society, speaker honorarium and travel support to attend an educational meeting from the MS Academy, speaker honorarium from Biogen and travel support to attend educational meetings from Novartis and Merck. B.J.L. declares no conflicts of interest. C.M.A. has received speaker honorarium from the MS Academy. DDG has book royalty agreement with Taylor & Francis Publishing. S.W.G. declares no conflicts of interest. S.M.P. has received research funding from Guthy Jackson Charitable Foundation. R.d.N. is the Chair of the National Institute for Health Research (NIHR) for Patient Benefit East Midlands Research Advisory Committee and has received funding for trials from the NIHR. He has received funding to prepare and deliver lectures (speakers’ bureau) on cognitive rehabilitation in MS from Novartis, Merck and Biogen. In the last 3 years, JC has received support from the Efficacy and Evaluation (EME) Programme, a Medical Research Council (MRC) and National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Programme (NIHR), the UK MS Society, the US National MS Society and the Rosetrees Trust. He is supported, in part, by the NIHR University College London Hospitals (UCLH) Biomedical Research Centre, London, UK. He has been a local principal investigator for a trial in MS funded by the Canadian MS society. A local principal investigator for commercial trials funded by Actelion, Novartis and Roche; and has taken part in advisory boards/consultancy for Azadyne, Janssen, Merck, NervGen, Novartis and Roche. ECT has received honoraria/speaker fees/travel expenses to attend educational meetings from Biogen, Janssen, Merck, Novartis, Roche and Takeda. DO has received research support from the National Institutes of Health, National MS Society, Patient-Centered Outcomes Research Institute (PCORI), Race to Erase MS Foundation, Genentech, Genzyme and Novartis. Consulting fees obtained from Biogen Idec, Genentech/Roche, Genzyme, Janssen, Novartis and Merck. N.E. has served as a member of advisory boards for Biogen, Merck, Novartis and Roche, received grant income from the UK MS Society, MRC, PCORI and NIHR.
 SB, EP and CD have declared that no competing interests exist. AL has the following competing interests: has served as a Biogen, Bristol Myers Squibb, Merck Serono, Novartis, Roche, Sanofi/ Genzyme and Teva Advisory Board Member. She received congress and travel/accommodation expense compensations or speaker honoraria from Alexion, Biogen, Merck Serono, Mylan, Novartis, Roche, Sanofi/Genzyme, Teva and Fondazione Italiana Sclerosi Multipla (FISM). Her institutions received research grants from Novartis and Sanofi/Genzyme.

 Declaration of Competing Interests The Authors declare that there is no conflict of interest.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 L. Cacciaguerra received speaker and consultant honoraria from ACCMED, Roche, BMS Celgene, and Sanofi. P. Morris reports no disclosures. W.O. Tobin has received research funding from Mallinckrodt Inc., the Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology, and the NIH (grant R01NS113803 and R01NS121928) outside the submitted work; he has received honoraria from Neurology Live and has coedited Mayo Clinic Cases in Neuroimmunology. J.J. Chen served as consultant for Roche and UCB. S.A. Banks, P. Elsbernd, and V. Redenbaugh report no disclosures. J.-M. Tillema is associate editor for the Journal of Child Neurology. F. Montini and E. Sechi report no disclosures. A.S. Lopez-Chiriboga has served on advisory boards for Genentech and Horizon Therapeutics. N.L. Zalewski and Y. Guo report no disclosures. M. Assunta Rocca received speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, Roche, and Teva and receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. M. Filippi is editor-in-chief of the Journal of Neurology, associate editor of Human Brain Mapping, associate editor of Radiology, and associate editor of Neurological Sciences; received compensation for consulting services and/or speaking activities from Almiral, Alexion, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). S.J. Pittock reports grants, personal fees, and nonfinancial support from Alexion Pharmaceuticals, Inc.; grants, personal fees, nonfinancial support, and other support from MedImmune, Inc./Viela Bio, Inc.; and personal fees for consulting from Genentech/Roche; he has a patent, patent # 8,889,102 (application #12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia)—issued and a patent, patent # 9,891,219B2 (application #12-573942, Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 [AQP4]–IgG Autoantibody positive)—issued. C.F. Lucchinetti received grants from the National Institute of Health, National Multiple Sclerosis Society, National Institute of Neurological Disorders and Stroke, Kingsland Foundation, Biogen Idec. E.P. Flanagan has served on advisory boards for Alexion, Genentech, and Horizon Therapeutics, has received speaker honoraria from Pharmacy Times, and received royalties from UpToDate. Dr. Flanagan was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics, has received funding from the NIH (R01NS113828), and is a member of the medical advisory board of the MOG project. Dr. Flanagan is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports, and a patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity. Go to Neurology.org/N for full disclosures.
 G. Fadda, A.C. de la Parra, and J. O'Mahony report no disclosures relevant to the manuscript; P. Waters and the University of Oxford hold patents for antibody assays and receive royalties, he has received speaker honoraria from Alexion, Roche, and UBC, he is codirector of Oxford Autoimmune Diagnostic Laboratory where MOG antibody testing is performed; E.A. Yeh reports personal fees for consulting from Biogen, Hoffmann-Laroche, and Alexion; grants from Biogen, Ontario Institute for Regenerative Medicine, Stem Cell Network, Center for Brain and Mental Health, The Peterson Foundation, National MS Society, MS Scientific Foundation, NIH, and Canadian Institutes of Health Research and Consortium of MS Centers; ABO participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from: Janssen/Actelion; Atara Biotherapeutics, Biogen Idec, Celgene/Receptos, Roche/Genentech, Medimmune, Merck/EMD Serono, Novartis, and Sanofi-Genzyme; R.A. Marrie receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, and The Arthritis Society, and she is supported by the Waugh Family Chair in Multiple Sclerosis; S. Narayanan has received research funding from the Canadian Institutes of Health Research, the International Progressive MS Alliance, the Myelin Repair Foundation and Immunotec, honoraria/travel support from Genentech and MedDay, and personal compensation from NeuroRx Research; DLA reports personal fees for consulting from Acorda, Biogen, Celgene, F. Hoffmann-La Roche, Frequency Therapeutics, GeNeuro, MedImmune, Merck-Serono, Novartis, and Sanofi-Aventis, grants from Biogen, Immunotec, and Novartis, and equity interest in NeuroRx Research; D.L. Collins reports grants from Canadian Institute of Health Research, during the conduct of the study, and personal fees from NeuroRx Inc., outside the submitted work; B. Banwell receives funding from the Multiple Sclerosis Scientific Foundation and the National Multiple Sclerosis Society, she has received consultancy fees from Novartis, UCB pharmaceuticals, and Medscape, and she serves as a nonremunerated advisor on clinical trial design for Novartis, Biogen, Teva Neuroscience, Roche, and Sanofi-Aventis. Go to Neurology.org/N for full disclosures.

 NO authors have competing interests.
 Declaration of Competing Interest Mina Stanikić reports employment by Roche branch in Serbia, Roche d.o.o., from February 2019 to February 2020. Christian P Kamm has received honoraria for lectures as well as research support from Biogen, Novartis, Almirall, Teva, Merck, Sanofi Genzyme, Roche, Janssen, Eli Lilly, Celgene and the Swiss MS Society. Ente Ospedaliero Cantonale (employer) received compensation for Chiara Zecca's speaking activities, consulting fees, or research grants from Almirall, Biogen Idec, Bristol Meyer Squibb, Lundbeck, Merck, Novartis, Sanofi, Teva Pharma, Roche. Chiara Zecca is recipient of a grant for senior researchers provided by AFRI (Area Formazione accademica, Ricerca e Innovazione), EOC. Ente Ospedaliero Cantonale (employer) received compensation for Claudio Gobbi's speaking activities, consulting fees, or research grants from Almirall, Biogen Idec, Bristol Meyer Squibb, Lundbeck, Merck, Novartis, Sanofi, Teva Pharma, Roche. Anke Salmen has received speaker honoraria and/or travel compensation for activities with Bristol Myers Squibb, Novartis, Roche and research support of Baasch Medicus Foundation and the Swiss MS society, not related to this work. Andrew Chan has served on advisory boards for, and received funding for travel or speaker honoraria from Actelion-Janssen, Almirall, Bayer, Biogen, Celgene, Sanofi-Genzyme, Merck, Novartis, Roche and Teva, all for hospital research funds; and research support from Biogen, Genzyme and UCB. Eric Twomey, Milo A. Puhan, Vladeta Ajdacic-Gross and Viktor von Wyl declare no competing interests.


 Declaration of competing interest The authors have no competing financial interest to declare in relation to the content of this article.
 JS-M and IM-T have received funding for research projects and conference fees, mentoring, and assistance for conference attendance from Teva, Merck, Biogen, Roche, Novartis, and Sanofi. AG-M has received compensation for travel expenses, speaking honoraria and consultation fees from Bayer, Merck, Teva, Biogen Idec, Novartis, Roche, Almirall and Sanofi-Genzyme. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling Editor L.O declared a shared parent affiliation with the authors A.S, J.S, A.G, E.R, O.R.LF, B.B, R.G, A.J.S, A.G at the time of review.
 The authors declare no competing interests.


 KA received personal compensation for consulting services and speaker honoraria from Roche, Novartis, Merck, Sanofi, Teva, BMS, Biogen, and Celgene. TZ received personal compensation for consulting services and speaker honoraria from Biogen Idec, Bayer, Novartis, Sanofi, Teva, and Synthon. TZ received additional financial support for research activities from Bayer, Biogen Idec, Novartis, Teva, and Sanofi Aventis. CW received travel support from Novartis. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have no potential conflicts of interest to disclose.
 Declaration of competing interest The other authors declare no competing interests.
 The authors report no competing interests relevant to this study. E. Polvinen, M. Matilainen, and M. Nylund report no disclosures; M. Sucksdorff has received research support from the Finnish Medical Foundation, the Finnish MS Foundation, and the Finnish Medical Society (Finska Läkaresällskapet); L. Airas has received honoraria from F. Hoffmann-La Roche Ltd., Genzyme, Janssen, and Merck Serono and institutional research grant support from Academy of Finland, Genzyme, Merck Serono, and Novartis. Go to Neurology.org/NN for full disclosure.
 D.B. is a consultant for Ipsen, Merz, Allergan, and Medtronic. P.K. is a consultant for Ipsen. A.F. and J.Y.L. are Ipsen employees. J.L. is a consultant for Ipsen, Allergan, and Medtronic.
 Declarations of Competing Interest None.

 The authors declare no conflict of interest.
 Competing interests: ARL research fundings from Sanofi. SW has received speaker honoraria from and served on scientific advisory boards for Biogen, Janssen-Cilag, Sanofi and Novartis. ØT has received speaker honoraria from and served on scientific advisory boards for Biogen, BMS, Jansen, Sanofi, Merck and Novartis. TH has received speaker honoraria and/or unrestricted research grants from Biogen, Merck, Roche, Novartis, Sanofi and Bristol-Myers Squibb, and participated in clinical trials organised by Merck, Sanofi and Roche. TB has received unrestricted research grants from Biogen Idec and Sanofi Genzyme. MK-M has received unrestricted research grants to his institution; scientific advisory board and speaker honoraria from Biogen, Merck, Novartis, Roche and Sanofi, and has participated in clinical trials organised by Biogen, Merck, Novartis, Roche and Sanofi. HFH has received honoraria for lecturing or advice from Biogen, Merck, Roche, Novartis and Sanofi. AS is shareholder of Age Labs, a molecular diagnostics company that discovers, develops and commercialises diagnostic tests for the early detection of age-related diseases. EGC has received honoraria for lecturing and advice from Biogen, BMS, Janssen, Merck, Novartis, Roche and Sanofi.
 LP receives support from Alector. AHC has received fees for consulting or participating in advisory boards for: Biogen, Bristol-Myers Squibb, EMD Serono (affiliate of Merck KgaA), Genentech (Roche), Horizon Pharmaceuticals, Janssen (J&J), Jazz Pharmaceuticals, Novartis, Octave, and TG Therapeutics and AHC serves on scientific advisory boards for EMD Serono, Novartis and Genentech. AHC was supported by The Manny & Rosalyn Rosenthal - Dr. John L. Trotter MS Center Chair in Neuroimmunology of The Foundation for Barnes-Jewish Hospital. BDT was supported by the NIH grant R35NS09730; LG was supported by the NMSS post-doctoral fellowship FG-1907-34474.
 CMJ has an equity position with Vaccitech plc. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 None.
 Declaration of Competing Interest Authors declare no conflict of interst.
 T.V., K.R.R., and V.A.F. are the inventors of US patent No. 9758573.
 The authors have declared that no competing interests exist.

 Declaration of Competing Interest None.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 LP: consulting fees and/or speaker honoraria from Biogen, Celgene, Genzyme, Merck Serono, Novartis, and Teva; travel grants from Biogen, Genzyme, Novartis, and Teva; research grants from the Italian MS Society (Associazione Italiana Sclerosi Multipla) and Genzyme. CT: honoraria for speaking and travel grants from Biogen, Sanofi-Aventis, Merck Serono, Bayer-Schering, Teva, Genzyme, Almirall, and Novartis. SH: travel funding and/or speaker honoraria from Biogen, Roche, Genzyme, Novartis, CSL Behring. SR: personal fees and non-financial support from Biogen, Genzyme, Merck Serono, Novartis, and Teva. CG: fees as invited speaker or travel expenses for attending meeting from Biogen, Merck-Serono, Teva, Sanofi, Novartis, Genzyme.
 The authors declare no conflict of interest.
 Competing Interests: The authors have declared that no competing interest exists.
 Declaration of Competing Interest None
 Conflicto de intereses: Ninguno.


 The authors declare that they have no competing interests.
 MS received travel support from Biogen, Merck, Bristol-Myers Squibb, Sanofi, Roche, Teva and Novartis. JF received travel support and honoraria for presentations from Biogen, Merck, Roche and Sanofi. MK has received speaker honoraria from Bayer, Novartis, Merck, Biogen Idec and Teva Pharmaceutical Industries Ltd. and serves on scientific advisory boards for Biogen Idec, Merck Serono, Roche, Novartis, Bristol-Myers Squibb and Gilead. He received research grants from Teva Pharmaceutical Industries, Ltd., Biogen and Novartis. ET has received consultation fees and/or speakers’ honoraria from Arvelle, Argenx, Angellini, Bial, Biogen-Idec, Boehringer Ingelheim, Eisai, Epilog, GL Pharma, Jazz/GW Pharmaceuticals, Ever Pharma, Hikma, LivaNova, Marinus, Medtronics, Newbridge, Novartis, Sanofi, Genzyme, and UCB Pharma. PW has received consultation fees and/or speakers’ honoraria from Bayer, Biogen Idec, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi Genzyme, Teva Pharmaceutical Industries Ltd. He received research grants from Biogen Idec and Merck. TM received travel support, honoraria for presentations or participation on advisory boards from Biogen Idec, Celgene, Novartis, Roche, Sanofi, Merck and Teva. AB has nothing to disclose. She was trained within the frame of the PhD Program Molecular Medicine of the Medical University of Graz. PH, WH, LM and AH have nothing to disclose. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript.
 Dr. Chia has no conflicts of interest to report. Dr. Redenbaugh has no conflicts of interest to report. Dr. Chen is a consultant to UCB and Roche. Dr. Pittock reports grants, personal fees and non-financial support from Alexion Pharmaceuticals, Inc.; grants, personal fees, non-financial support and other support from MedImmune, Inc/Viela Bio.; personal fees for consulting from Genentech/Roche; has a patent, Patent# 8,889,102 (Application#12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia) – issued; a patent, Patent# 9,891,219B2 (Application#12-573942,Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)-IgG Autoantibody positive) – issued. Dr. Flanagan has served on advisory boards for Alexion, Genentech and Horizon Therapeutics; has received research support from UCB; has received speaker honoraria from Pharmacy Times; has received royalties from UpToDate; was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics; has received funding from the NIH (R01NS113828); is a member of the medical advisory board of the MOG project; is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports; has a patent submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity.

 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 Conflict of Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 MH, CN, GS, LW, AA, VJ, XY, SW, FB, SG, DK, WF, SB No competing interests declared, GG, MG I acknowledge that I have significant ownership in Autoimmunity Biologic Solutions, Inc (Galveston, TX), which is commercializing therapies that target the IL7R pathway in autoimmune diseases. While I do not believe this represents a conflict of interest it can lead to the perception of said conflict

 The authors declare that they have no competing interests.
 Declaration of competing interest The authors have no competing interests to declare.
 Competing interests: GG received funding through an HEE/NIHR ICA Internship (November 2020–April 2021).

 This research was funded in part, by a pilot grant program supported by the Consortium for Multiple Sclerosis Centers and EMD Serono Inc. awarded to Dr. Silveira. Dr. Cutter reports personal fees from Pythagoras Board membership, personal fees from Brainstorm Cell Therapeutics, personal fees from Teva Neuroscience, personal fees from EMD Serono, personal fees from Novartis, personal fees from CSL Behring, personal fees from Avexis Pharmaceuticals, personal fees from Genzyme, personal fees from Medimmune/Viela Bio, personal fees from Receptos/celgene, personal fees from Biolinerx, personal fees from Sanofi-Aventis, personal fees from Galmed, personal fees from Opko, personal fees from NHLBI, personal fees from NICHD, personal fees from Vivus, personal fees from Genentech, personal fees from Reata Pharmaceuticals, personal fees from GW Pharmaceuticals, personal fees from Roche, personal fees from Orphazyme, personal fees from Horizon Pharmaceuticals, personal fees from Merck/Pfizer, personal fees from Klein-Buendel, personal fees from TG Therapeutics, personal fees from Celgene/BMS, personal fees from Recursion Pharmaceuticals, personal fees from Antisense Therapeutics, personal fees from AMO Pharmaceuticals, personal fees from Astra Zeneca, personal fees from Regeneron, personal fees from Mitsubishi Tanabe Pharma, personal fees from Immunic, personal fees from Protalix Biotherapeutics, personal fees from Alexion, personal fees from Clinical Trial Solutions LLC, personal fees from Green Valley Pharmaceuticals, personal fees from Mapi Pharmaceuticals, personal fees from AI Therapeutics, personal fees from SAB Biotherapeutics, personal fees from Avexis, personal fees from Brainstorm Therapeutics, personal fees from Applied Therapeutics, outside the submitted work. The other authors have nothing to disclose.
 Declaration of Competing Interest Nothing.
 Declaration of Competing Interest This statement is to certify that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 None


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 JAG reports no disclosures. RW received a research grant from the medical faculty of the TUM. BH served on scientific advisory boards for Novartis; he has served as DMSC member for AllergyCare, Polpharma, Sandoz; Biocon and TG therapeutics; he or his institution have received speaker honoraria from Desitin; his institution received research grants from Regeneron for MS research. He holds part of two patents, one for the detection of antibodies against KIR4.1 in a subpopulation of patients with MS and one for genetic determinants of neutralizing antibodies to interferon. All conflicts are not relevant to the topic of the study. BH received funding for the study by the European Union’s Horizon 2020 Research and Innovation Program (grant MultipleMS, EU RIA 733161) and the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy—ID 390857198). TK has received speaker honoraria and/or personal fees for advisory boards from Bayer Healthcare, Teva Pharma, Merck, Novartis Pharma, Sanofi-Aventis/Genzyme, Roche Pharma and Biogen as well as grant support from Novartis and Chugai Pharma in the past. BK is funded by the Else Kröner-Fresenius Stiftung and the Gemeinnützige Hertie-Stiftung and was awarded with the Oppenheim award granted by Novartis. He received travel support and a research grant from Novartis which are both outside the submitted work. JH reports grants for OCT research from the Friedrich-Baur-Stiftung and Merck, personal fees and non-financial support from Celgene, Janssen, Bayer, Merck, Alexion, Novartis, Roche, Biogen and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work. JH is partially funded by the German Federal Ministry of Education and Research ((DIFUTURE), Grant Numbers 01ZZ1603[A-D] and 01ZZ1804[A-H]).


 The authors declare no conflict of interest.



 The authors declare no conflict of interest.

 Declaration of Competing Interest M.Tutuncu, S. Demir, S. Sen, T. Gunduz, C Uzunköprü, H Gumus have received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and regis- tration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. Asli Tuncer has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. Serkan Ozakbas has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. H. Efendi has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi Ibrahim Rana Karabudak has received honoraria for giving educational lectures, consultancy fees for participating advisory boards, and travel grants for attending scientific congresses or symposia from Roche, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey, Abdi Ibrahim Ilac, Deva and ARIS. Aksel Siva has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi Ibrahim Ilac. The rest of authors declare no conflict of interest with the study project.
 Declaration of Competing Interest There are no conflicts of interest for any of the authors of this paper.

 Declaration of Competing Interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article.
 The authors have declared that no competing interests exist.

 The authors declare no competing interests.
 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 The authors report no conflicts of interest.


 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: KC, AJV, AM, and GS declare that they have no conflict of interest with respect to this article. FP is an employee of and holds stocks/stock options in Biogen. The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: KC, AM, and GS are funded by the European Union’s Horizon 2020 research and innovation program under grant agreement No. 825162. The HTx project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No. 825162. This dissemination reflects only the author’s view, and the Commission is not responsible for any use that may be made of the information it contains. AJV is funded in part by a Cancer Center Support Grant from the National Cancer Institute made to Memorial Sloan Kettering Cancer Center (P30-CA008748) and a SPORE grant from the National Cancer Institute to Dr. H. Scher (P50-CA092629). The data that support the findings of this study were made available from Biogen International GmbH. Restrictions apply to the availability of these data, which were used under license for this study.

 PN has received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Roche, and financial support for research activities from Roche and Merck. DS has received financial support for conference travel and/or speaker honoraria from Novartis, Biogen, Merck, Sanofi, and Janssen-Cilag. DH received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck Serono, Teva, and Bayer Schering and financial support for research activities from Biogen Idec. MT has received speaker honoraria and consultant fees from Biogen Idec, Sanofi, Teva, Merck, Medion Pharma, UCB, and Astra Zeneca. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors P.M. and E.M. are inventors of the patent “Method for obtaining of oleacein and oleomissional secoiridoids and method of producing pharmaceutical preparations thereof” WO/2020/165613.

 Declaration of Competing Interest None.
 A.P. De Rosa, F. Esposito, P. Valsasina, A. d’Ambrosio, A. Bisecco, S. Tommasin, M. Battaglini, P. Pantano, M. Cirillo, and A. Gallo have nothing to disclose. M.A. Rocca received speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, Roche, and Teva and research support from the Canadian MS Society and Fondazione Italiana Sclerosi Multipla. M. Filippi is the Editor-in-Chief of the Journal of Neurology and Associate Editor of Human Brain Mapping, Neurological Sciences, and Radiology, received compensation for consulting services and/or speaking activities from Alexion, Almirall, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries, and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, the Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). G. Tedeschi received funding for travel, speaking honorarium, consulting service, and research projects from Novartis, Genzyme, Teva, Merck, Biogen, Roche, Allergan, Abbvie, Lilly, and Mylan. N. De Stefano has received honoraria from Biogen-Idec, Celgene, Immunic, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva for consulting services, speaking, and travel support. N. De Stefano serves on advisory boards for Biogen-Idec, Immunic, Merck Serono, Novartis, Roche, and Sanofi-Genzyme. N. De Stefano has received research grant support from the Italian Multiple Sclerosis Society.

 JH reports a grant for OCT research from the Friedrich‐Baur‐Stiftung and Merck, personal fees and non‐financial support from Alexion, Bayer HealthCare Pharmaceuticals, Biogen, Celgene, F. Hoffman‐La Roche, Janssen Biotech, Merck, Novartis, and Sanofi Genzyme and non‐financial support from the Guthy‐Jackson Charitable Foundation, all outside the submitted work. UH received financial compensation once for a lecture organised by CSL Behring, after submission of the manuscript, and outside the submitted work. BIO has provided consultancy to Roche once on a topic outside the submitted work. KAR, JB, MG, AA, ZA, AG, HS, UM: nothing to declare.

 The authors declare no conflict of interest.
 The authors have no conflict of interest to declare.
 The authors declare no conflict of interest.
 M.S.W. received travel funding and/or speaker honoraria from Biogen-Idec, Merck Serono, Novartis, Roche, TEVA, Bayer, and Genzyme. The other authors declare that they have no competing interests.
 The authors declare no conflict of interest.




 Declaration of Competing Interest Dr. Hashimoto is the inventor of filed patent applications on “The use of R-Ketamine in the treatment of psychiatric diseases”, “(S)-norketamine and salt thereof as pharmaceutical”, “R-Ketamine and derivative thereof as prophylactic or therapeutic agent for neurodegeneration disease or recognition function disorder”, “Preventive or therapeutic agent and pharmaceutical composition for inflammatory diseases or bone diseases”, “R-Ketamine and its derivatives as a preventive or therapeutic agent for a neurodevelopmental disorder”, and “Preventive or therapeutic agent and pharmaceutical composition for inflammatory diseases” by the Chiba University. Dr. K. Hashimoto has also received speakers' honoraria, consultant fee, or research support from Abbott, Boehringer Ingelheim, Daiichi-Sankyo, Meiji Seika Pharma, Seikagaku Corporation, Sumitomo-Pharma, Taisho, Otsuka, Murakami Farm and Perception Neuroscience. Other authors declare no conflict of interest.
 The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. R.C.A. is a consultant for Progentec Diagnostics. G.K. declares no conflict of interest.
 R.N. and S.K. are employees of Daiichi Sankyo Co., Ltd. Other authors have no conflicts of interest with the material presented in this manuscript, and specifically no financial interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest The authors declared no potential conflicts of interests with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest There is no conflicts of interest in this article.
 Declaration of interests JLB reports payment for consultation from MedImmune/Viela Bio/Horizon Therapeutics, Alexion, Chugai, Clene Nanomedicine, Genentech, Genzyme, Mitsubishi Tanabe Pharma, Reistone Biopharma, Beigene, and Roche; personal fees from AbbVie; grants from Novartis, Mallinckrodt, and Alexion; data safety monitoring board work for Roche–Genentech and Clene Nanomedicine; and has a patent for aquaporumab issued. FC reports payment for consultation from Roche, Alexion, and Frequency Therapeutics, and speakers' fees from Accure Therapeutics, Alexion, Neurodiem, and the Sumaira Foundation. JJC reports payment for consultation from UCB, Horizon, and Roche. AP received grant support for remyelination trials in multiple sclerosis for the Amsterdam University Medicam Centre, Department of Neurology, Multiple Sclerosis Centre (RESTORE trial), University College London (RECOVER trial), and Fight for Sight (nimodipine in optic neuritis trial); received royalties or licences from Up-to-Date (Wolters Kluver) on a book chapter; received speaker fees for the Heidelberg Academy; participates on advisory board for SC Zeiss OCTA Angi-Network, Novartis OCTiMS study; holds leadership roles for governing board IMSVISUAL; is chairman of ERN-EYE Neuro-ophthalmology (until October, 2020), board member of National Dutch Neuro-ophthalmology Association; received equipment from OCT angiography from Zeiss (Plex Elite); and received medical writing support from Novartis for a manuscript. SLG reports payment for consultation from Biogen and Genentech. VB is a consultant for GenSight Biologics and Neurophoenix, and receives research support from GenSight Biologics and Santhera/Chiesi. NJN is a consultant for GenSight Biologics, Santhera/Chiesi, Stealth Biotherapeutics, and Neurophoenix; receives research support from GenSight Biologics and Santhera/Chiesi; is a participant in educational webinars sponsored by WebMD-Global Medscape and First Class; and is a medical-legal consultant in matters not related to this work.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 None declared.
 Declaration of interests B.P.K. is an inventor on patents and/or patent applications filed by Mass General Brigham that describe genome engineering technologies. B.P.K. is a consultant for EcoR1 capital and is an advisor to Acrigen Biosciences, Life Edit Therapeutics, and Prime Medicine.
 Competing Interests The authors declare that they have no conflicts of interest.
 Declaration of interests AA has received research funding from DMSG, AMSEL, the Bavarian MS Trust, and UCSF Weill Institute for Neurosciences. JO has received research support from the Swiss MS Society and served on advisory boards for Roche and Merck. CGo's employer (Ente Ospedaliero Cantonale) has received compensation for CG's speaking activities, consulting fees, or research grants from Almirall, Biogen Idec, Bristol Myers Squibb, Lundbeck, Merck, Novartis, Sanofi, Teva Pharma, and Roche. CZ is recipient of a grant for senior researchers provided by AFRI (l'Area Formazione Accademica, Ricerca e Innovazione). HT has received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Celgene, GlaxoSmithKline, Janssen, Merck, Novartis, Roche, Sanofi Genzyme, and Teva. HW has received honoraria and consultation fees from Bayer Healthcare, Biogen, Fresenius Medical Care, GlaxoSmithKline, GW Pharmaceuticals, Merck Serono, Novartis, Sanofi Genzyme, and Teva. CGr's employer (University Hospital Basel) has received the following fees which were used exclusively for research support: advisory boards and consultancy fees from Actelion, Novartis, Genzyme-Sanofi, GeNeuro, Hoffmann La Roche, and Siemens Healthineers; speaker fees from Biogen, Hoffmann La Roche, Teva, Novartis, Janssen, and Genzyme-Sanofi; and research grants from Hoffmann La Roche, GeNeuro, Genzyme, and Biogen. LK's institutions (University Hospital Basel and the Research Center for Clinical Neuroimmunology and Neuroscience Basel) have received and dedicated to research support: payments for steering committee and advisory board participation, consultancy services, and participation in educational activities from Actelion, Bayer, Bristol Myers Squibb, df-mp (Dörries Frank Molnia & Pohlman), Celgene, Eli Lilly, EMD Serono, Genentech, GlaxoSmithKline, Janssen, Japan Tabacco, Merck, MH Consulting, Minoryx, Novartis, Hoffmann-La Roche, Senda Biosciences, Sanofi, Santhera, Shionogi, TG Therapeutics, and Wellmera; license fees for Neurostatus-UHB products; and grants from Novartis, Innosuisse and Roche. DL has received grants from Progressive MS Alliance and is Chief Medical Officer of GeNeuro. SW is Chief Medical Officer and co-founder of Neopredix, a spin-off company of the University of Basel. JK has received speaker fees, research support and/or travel support from, and/or served on advisory boards for, the Swiss MS Society, the Swiss National Research Foundation (grant number 320030_189140/1), the University of Basel, the Progressive MS Alliance, Alnylam, Bayer, Biogen, Bristol Myers Squibb, Celgene, Immunic, Merck, Neurogenesis, Novartis, Octave Bioscience, Quanterix, Roche, Sanofi, and Stata DX. All other authors declare no competing interests.


 T.H., G.G., and D.P.M. are full-time employees of Novartis Pharma AG, Basel, Switzerland. K.S.N., M.B., and O.P. are full-time employees of Novartis Institutes for Biomedical Research, Basel, Switzerland. M.d.M. and R.T. are full-time employees of Novartis Farma S.p.A., Origgio, Italy. V.B. and F.N. have no declaration of interest to declare. F.D. is an ex-employee of Novartis Pharma AG, Basel, Switzerland.
 Julie A Campbell declares that she has no conflict of interest. Hasnat Ahmad declares that he has no conflict of interest. Gang Chen declares that he has no conflict of interest. Ingrid van der Mei declares that she has no conflict of interest. Bruce Taylor declares that he has no conflict of interest. Suzi Claflin declares that she has no conflict of interest. Glen J Henson declares that he has no conflict of interest. Steve Simpson-Yap declares that he has no conflict of interest. Laura Laslett declares that she has no conflict of interest. Kirsty Hawkes declares that she has no conflict of interest. Carol Hurst declares that she has no conflict of interest. Hilary Waugh declares that she has no conflict of interest. Andrew J Palmer declares that he has no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.



 Declaration of Competing Interest We all authors declare we have no competing interests in relation to their work (financial and non-financial). All the authors listed have approved the manuscript.



 The authors declare no competing interests relevant to this study.

 The authors have declared that no competing interests exist.
 The authors declare no competing interests.
 Declaration of Competing Interest Alessandra Angelucci, Andrea Aliverti and Marina Scarlato are co-inventors of an industrial design application on the graphic test described in the paper.
 Declarations of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. There is no conflict of interest to list for any of the authors.

 Declaration of interests The authors declare no competing interests.
 Declaration of Competing Interest Glen M. Doniger is an employee of NeuroTrax Corporation. The authors declare no other potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest None of the authors of this manuscript have any conflict of interest in this subject.
 Authors BP and Yoe-SB are preparing patent applications. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflicts of Interest: A.K.M. is one of the inventors of a technology claiming the use of Prevotella histicola to treat autoimmune diseases. A.K.M. received royalties from Mayo Clinic (paid by Evelo Biosciences). However, no funds or products from the patent were used in the present study. All other authors declare no commercial or financial relationships that could be a potential conflict of interest.

 A patent application covering the use of flow cytometry for diagnostic purposes of neurological involvement in rheumatic disorders has been requested by GMzH, MH, and HW. All the remaining authors have no competing interests.
 The authors declare no competing interests.
 Conflict of Interest: The authors declare no competing financial interests.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare no conflict of interest.


 J.D. serves on scientific advisory boards for AstraZeneca, Novartis and UK Biobank, and has received multiple grants from academic, charitable and industry sources outside of the submitted work. A.S.B. has received grants unrelated to this work from AstraZeneca, Bayer, Biogen, BioMarin, Bioverativ, Novartis and Sanofi. J.E.P. has received hospitality and travel expenses to speak at Olink-sponsored academic meetings (none within the past 5 years). During the drafting of the manuscript, D.S.P. became a full-time employee of AstraZeneca and P.S. became a full-time employee of GlaxoSmithKline. M.L. has received lecture honoraria from Lundbeck pharmaceutical. The other authors declare no competing interests.

 Declaration of Competing Interest No other disclosures were reported.

 The authors declare no competing interest.
 The authors declare no competing interests.

 Declaration of Competing Interest I. Schiavetti has acted as a paid consultant to Associazione Commissione Difesa Vista, Eye Pharma, Hippocrates Research, and D.M.G Italia. L. Barcellini: no disclosures. C. Lapucci has received Travel grant from Novartis, Roche and Merck. F. Tazza(:) no disclosures. M. Cellerino reports no disclosures. E. Capello reports no disclosures. D. Franciotta received personal honoraria from Merck, Biogen, Sanofi-Genzyme, Roche. M. Inglese received grants NIH, NMSS, FISM; received fees for consultation from Roche, Genzyme, Merck, Biogen and Novartis. M. P. Sormani, received consulting fees from Merck, Biogen, Novartis, Sanofi, Roche, Geneuro, GSK, Medday, and Immunic. A. Uccelli, received grants (to his Institution) from FISM, Biogen, Roche, Alexion, Merck Serono; participated on a Data Safety Monitoring Board or Advisory Board (to his Institution) for BD, Biogen, Iqvia, Sanofi, Roche, Alexion, Bristol Myers Squibb. A. Laroni received fees for consultation from Roche, Genzyme, Merck, Biogen, Novartis, Bristol-Myers Squibb.
 The author declares no competing interests.
 Conflicts of Interest The authors have declared that no conflicts of interest exist.

 K. Fujihara received speaker honoraria and travel funding from Bayer, Biogen Japan, Eisai, Mitsubishi Tanabe, Novartis, Astellas, Takeda, Asahi Kasei Medical, Daiichi Sankyo, and Nihon Pharmaceutical and received research support from Bayer, Biogen, Asahi Kasei Medical, The Chemo-Sero-Therapeutic Research Institute, Teva, Mitsubishi Tanabe Pharma, Teijin, Chugai, Ono, Nihon Pharmaceutical, and Genzyme. I. Nakashima received speaker honoraria and travel funding from Mitsubishi Tanabe Pharma, Biogen Japan, and Novartis Pharmaceuticals and received research support from LSI Medience Corporation. The other authors declare no competing interests.

 T. Armangué received speaker honoraria from Biogen, Sanofi-Aventis, and Novartis not related to this manuscript; A. Saiz reports compensation for consulting services and speaker honoraria from Merck-Serono, Biogen-Idec, Sanofi-Aventis, Teva Pharmaceutical Industries Ltd, Novartis, Roche, Alexion, and Janssen; C. Lechner has served as a consultant for Roche but has no conflict of interest with this manuscript; I. Ayzenberg served on scientific advisory boards for Roche, Merck, and Alexion and received research support from Diamed, none related to this article; M. Sepulveda has received speaker honoraria from Biogen and Roche Pharma; E. Martínez-Hernández has received speaker honoraria from Biogen; G. Arrambide has received speaking honoraria and compensation for consulting services or participation in advisory boards from Sanofi, Merck, and Roche; travel expenses for scientific meetings from Novartis, Roche, Stendhal, and ECTRIMS; is editor for Europe of the Multiple Sclerosis Journal – Experimental, Translational, and Clinical; and is a member of the International Women in Multiple Sclerosis (iWiMS) network executive committee. F. Brilot has received research funding from the National Health and Medical Research Council (Australia), Multiple Sclerosis Research Australia, NSW Health, Novartis, and the University of Sydney. She has received speaker honoraria from Novartis, Biogen, Merck, and Limbic Neurology, has been on advisory boards for Merck and Novartis. and is a member of the International Women in Multiple Sclerosis (iWiMS) network executive committee. S. Ramanathan has received research funding from the National Health and Medical Research Council (Australia), the Brain Foundation (Australia), the Royal Australasian College of Physicians, and the University of Sydney. She is supported by an NHMRC Neil Hamilton Fairley Early Career Fellowship (APP1141169). She serves as a consultant on an advisory board for UCB and Limbic Neurology, and has been an invited speaker for Biogen, EXCEMED, and Limbic Neurology. S. Ferrari received support for attending scientific meetings by Shire, Sanofi-Genzyme, Roche, and Euroimmun; E. P. Flanagan has served on advisory boards for Alexion, Genentech, and Horizon Therapeutics. He has received speaker honoraria from Pharmacy Times. He received royalties from UpToDate. He was a site primary investigator in a randomized clinical trial on inebilizumab in neuromyelitis optica spectrum disorder run by MedImmune/Viela-Bio/Horizon Therapeutics. He has received funding from the NIH (R01NS113828). He is a member of the medical advisory board of the MOG project. He is an editorial board member of the Journal of the Neurologic Sciences and Neuroimmunology Reports. A patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity. M. Reindl is supported by research grants from the Austrian Science Fund (FWF project P32699), the Austrian Research Promotion Agency, Euroimmun, and Roche; consulting fees and advisory board from Roche (to institution) and payments for antibody assays (MOG, AQP4, and other autoantibodies) to institution (University Hospital and Medical University of Innsbruck, Austria). R. Marignier serves on scientific advisory board for Alexion, Horizon Therapeutics, Roche, and UCB; has received honoraria from Alexion, Biogen, Merck, Novartis, and Roche. S. Mariotto received support for attending scientific meetings by Merck and Euroimmun and received speaker honoraria from Biogen. The other authors report no relevant disclosures. Go to Neurology.org/N for full disclosures.

 Declaration of Competing Interest No disclosure relevant to the manuscript.

 The authors declare no conflict of interest.


 Conflict of Interests and Disclosures None
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 F.C. Oertel reports grants from National Multiple Sclerosis Society, grants from American Academy of Neurology, grants from Deutsche Gesellschaft für Neurologie, all outside the submitted work. J. Krämer received honoraria for lecturing for Biogen, Novartis, Mylan, Teva, Roche, Sanofi, and Genzyme and financial research support from Sanofi, Genzyme, Roche, and American Therapeutics. S. Motamedi has nothing to disclose. A. Keihani has nothing to disclose. H. Zimmermann reports grants from Novartis and personal fees from Bayer Healthcare, all outside the submitted work. N.G. Dimitriou has nothing to disclose. S. Condor-Montes has nothing to disclose. C. Bereuter has nothing to disclose. C. Cordano has nothing to disclose. A.C. Abdelhak has nothing to disclose. A. Trip has nothing to disclose. O. Aktas reports honoraria for lectures and support for attending meetings by Alexion, Bayer, Biogen, Novartis, Roche, and Sanofi, all outside the submitted work. S.G. Meuth has nothing to disclose. H. Wiendl reports personal fees from Biogen, Genzyme, Merck Serono, Novartis, Roche Pharma AG, Sanofi-Aventis, UCB, Alexion, Biologix, Cognomed, F. Hoffmann-La Roche Ltd, Gemeinnützige Hertie-Stiftung, TEVA, WebMD Global, Actelion, IGES, Johnson & Johnson, and Swiss Multiple Sclerosis Society, grants from German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Fresenius Foundation, European Union, Hertie Foundation, NRW Ministry of Education and Research, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, and GlaxoSmithKline, all outside the submitted work. K. Ruprecht reports grants from Novartis Pharma, Merck Serono, German Ministry of Education and Research, European Union (821,283-2), Stiftung Charité, and Arthur Arnstein Foundation and other from Guthy Jackson Charitable Foundation, all outside the submitted work. J. Bellmann-Strobl reports personal fees and nonfinancial support from Sanofi-Aventis GmbH, personal fees and nonfinancial support from Roche Pharma AG, personal fees and nonfinancial support from Bayer AG, and personal fees from Merck Serono GmbH, al outside the submitted work. F. Paul reports research support from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Alexion, and Merck Serono and research support from the German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Guthy-Jackson Charitable Foundation, and NMSS. He also reports consulting fees as an associate editor for Neurology, Neuroimmunology & Neuroinflammation and as an academic editor for PloS ONE and consultant fees for Sanofi Genzyme, Biogen, MedImmune, Shire, and Alexion. He also reports speaker honoraria from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire. He is advisory board member for Novartis and MedImmune Scientific and holds stocks of Nocturne GmbH—all outside the submitted work. A. Petzold reports personal fees from Novartis, Heidelberg Engineering, and Zeiss, reports grants from Novartis, outside the submitted work; and is part of the steering committee of the OCTiMS study that is sponsored by Novartis and the Angio-OCT steering committee, which is sponsored by Zeiss. He does not receive compensation for these activities. AS reports compensation for consulting services and speaker honoraria from Merck-Serono, Biogen-Idec, Sanofi, Novartis, Roche, Janssen, and Alexion. A.U. Brandt reports grants from Deutsche Forschungsgemeinschaft, during the conduct of the study; shares from Nocturne GmbH, and shares from Motognosis GmbH, outside the submitted work; In addition, A.U. Brandt has multiple patents regarding retinal image analysis technology owned by Charite and UCI and licensed to Nocturne GmbH. A.J. Green reports other from Bionure, grants, personal fees, and other from Inception Sciences, grants from Sherak Foundation, personal fees and other from Pipeline Pharmaceuticals, grants from Hilton Foundation, grants from Adelson Foundation, grants from National MS Society, personal fees from JAMA Neurology, personal fees and other from Mediimmune/Viela, outside the submitted work; In addition, A.J. Green has a patent small molecule drug for remyelination pending and has worked on testing off-label compounds for remyelination. Go to Neurology.org/NN for full disclosures.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of competing interest The authors declare that they have no competing interests.
 The authors have organizational affiliations to disclose. J.L.B. has received personal fees and nonfinancial support from Chugai Pharmaceutical, Viela Bio/Horizon Therapeutics, Equillium, Frequency Therapeutics, Mitsubishi-Tanabe, Reistone Bio, Abbvie, Clene Neuroscience, Alexion, Genentech, and Roche; and grants from Mallinckrodt and Novartis. H.-C.v.B. is an employee of F. Hoffmann-La Roche Ltd. R.C. is Site Investigator for studies funded by Roche, Novartis, MedImmune, and EMD Serono and has received honoraria from Roche, EMD 75 Serono, Sanofi, Biogen, Novartis, and Teva. K.R.E. has received research/grant support from Biogen, Sanofi Genzyme, F. Hoffmann-La Roche Ltd., Genentech, Inc., and Novartis. R.F. has nothing to declare. P.S.G. has received honoraria for speaking, advisory boards or consultation fees from Actelion, Alexion, Biogen, Bristol Myers Squibb-Celgene, EMD Serono, Sanofi Genzyme, Innodem Neurosciences, McKesson, Novartis, Pendopharm, F. Hoffmann-La Roche Ltd., and Teva Neuroscience. He also serves as a scientific advisor for Innodem Neurosciences. B.M.G. has received consulting fees from Alexion, Novartis, EMD Serono, Viela Bio, Genentech/Roche, Greenwhich Biosciences, Axon Advisors, Rubin Anders, ABCAM, Signant, IQVIA, Sandoz, DruggabilityTechnologies, Genzyme, Immunovant, and PRIME Education. He has received grant funding from PCORI, NIH, NMSS, The Siegel Rare Neuroimmune Association, Clene Nanomedicine, and the Guthy Jackson Charitable Foundation for NMO. He serves as an unpaid member of the board of the Siegel Rare Neuroimmune Association. He receives royalties from UpToDate. D.A.H. has in the past 10 y consulted for the following companies: Bayer, Biohaven Pharmaceuticals, Bristol-Myers Squibb, Compass Therapeutics, Eisai, EMD Serono, Genentech, Inc., Juno Therapeutics, McKinsey & Co., MedImmune/AstraZeneca, Mylan Pharmaceuticals, Neurophage Pharmaceuticals, NKT Therapeutics, Novartis, Proclara Biosciences, Questcor Pharmaceuticals, F. Hoffmann-La Roche Ltd., Sage Therapeutics, Sanofi Genzyme, Toray Industries, and Versant Venture. C.I. has received consulting fees from EMD Serono and Sanofi Genzyme. C.B.L. has served on scientific advisory boards or as a speaker for Biogen, Sanofi, EMD Serono, Alexion, and Bristol-Myers Squibb and has done consulting for InterX, Inc. and Diagnose Early. E.E.L. has received honoraria for consulting from Genentech, Inc., Genzyme, EMD Serono, Bristol Myers Squibb, TG Therapeutics, NGM Bio, Janssen, and Biogen. G.P. has served on advisory boards and/or speaker bureaus for Biogen, Celgene/Bristol Myers Squibb, EMD Serono, Genentech, Inc., F. Hoffmann-La Roche Ltd., Novartis, Sanofi Genzyme, Greenwich Biosciences, Teva, and VielaBio/Horizon. F.P. has received fees for serving on DMC in clinical trials with Chugai, Lundbeck and Roche, and preparation of expert witness statement for Novartis. M.S.W. is serving as an editor for PLoS One and has received travel funding and/or speaker honoraria from Biogen, Merck Serono, Novartis, F. Hoffmann-La Roche Ltd., Teva, Bayer, and Genzyme. T.Z. received personal compensation from Almirall, Biogen, Bayer, Celgene, Novartis, Roche, Sanofi, and Teva for the consulting services. D.J. received consulting fees and/or research support from: Biogen, Genentech, Novartis, EMD Serono, Banner Life Sciences, Bristol Myers Squibb, Horizon, and Sanofi Genzyme. J.M.G. has received consulting fees from Biogen. A.H.C. has received fees or honoraria for consulting for Biogen, Celgene/Bristol Myers Squibb, EMD Serono, F. Hoffmann-La Roche Ltd., Genentech, Inc., and Novartis, and TG Therapeutics and received fees for serving on scientific advisory boards and reviewing grants for the Conrad N. Hilton Foundation and Race to Erase MS. B.C., B.M., R.C.W., X.J., C.T.H., and A.H. are employees of Genentech, Inc. A.B.-O. has participated as a speaker in meetings sponsored by and received consulting fees from Janssen Pharmaceuticals/Actelion, Atara Biotherapeutics, Biogen Idec, Celgene/Receptos, Roche/Genentech, Mapi Pharma, MedImmune, Merck/EMD Serono, Novartis, and Sanofi Genzyme. Yes, the authors have stock ownership to disclose. B.C., B.M., R.C.W., X.J., C.T.H., and A.H. are shareholders of F. Hoffmann-La Roche Ltd. R. Yes, the authors have research support to disclose. J.L.B. has received personal fees and nonfinancial support from Chugai Pharmaceutical, Viela Bio/Horizon Therapeutics, Equillium, Frequency Therapeutics, Mitsubishi-Tanabe, Reistone Bio, Abbvie, Clene Neuroscience, Alexion, Genentech, and Roche and grants from Mallinckrodt and Novartis. R.C. receives research support from Teva Innovation Canada, Roche Canada, and Vancouver Coastal Health Research Institute. K.R.E. has received research/grant support from Biogen, Sanofi Genzyme, F. Hoffmann-La Roche Ltd., Genentech, Inc., and Novartis. P.S.G. has received research or educational grant from Biogen, EMD Serono, Genzyme-Sanofi, Hoffmann-La Roche, and Teva Innovation Canada. He has received honoraria for speaking and advisory board participation from Actelion, Allergan, Biogen Idec, EMD Serono, Sanofi Genzyme, Merz, Novartis, Pendopharm, F. Hoffmann-La Roche Ltd., and Teva Neuroscience. D.A.H. has received generous support by grants from the National Institutes of Health (U10 AI089992, R25 NS079193, P01 AI073748, U24 AI11867, R01 AI22220, UM 1HG009390, P01 AI039671, P50 CA121974, and R01 CA227473) and the National Multiple Sclerosis Society (CA 1061-A-18, RG-1802-30153); is also supported by grants from the National Institute of Neurological Disorders and Stroke and the Nancy Taylor Foundation for Chronic Diseases; and has received funding for his laboratory from Bristol-Myers Squibb, Genentech, Inc., Novartis Questcor, Sanofi Genzyme, and Race to Erase MS. C.I. has received search support from F. Hoffmann-La Roche Ltd, Genentech, Inc., Biogen, and Sanofi Genzyme. E.E.L. has received research funding from Genentech, Inc. and Biogen. F.P. has received research grants from Janssen, Merck KGaA, and UCB. M.S.W. receives research support from the Deutsche Forschungsgemeinschaft (WE 3547/5-1), Novartis, Teva, Biogen Idec, F. Hoffmann-La Roche Ltd., Merck, and the ProFutura Programm of the Universitätsmedizin Göttingen. T. Ziemssen received additional financial support for the research activities from Biogen, Novartis, Teva, and Sanofi. D.J. received consulting fees and/or research support from Biogen, Genentech, Novartis, EMD Serono, Banner Life Sciences, Bristol Myers Squibb, Horizon, and Sanofi Genzyme. J.M.G. has received research support to UCSF from Roche/Genentech and Vigil Neurosciences for clinical trials. A.B.-O. has received grant support from Biogen Idec, Roche/Genentech, Merck/EMD Serono, Novartis, and Sanofi-Genzyme.
 The authors have declared that no competing interests exist.
 K.P. and R.E.K. are named inventors on a patent covering the TNFR1 antagonist; K.P., R.F. and R.E.K. are named inventors on a patent covering the TNFR2 agonist. R.E.K. is a consultant for Immatics, Roche, SunRock and Oncomatryx. K.P. is a consultant for SunRock and Oncomatryx.
 SE, EE, JH and FS declare no competing interests. TU received grants from advanceCOR, grants from Else Kröner-Fresenius Stiftung (2018_EKMS.21), personal fees from Merck Serono, personal fees from Pfizer. FZ has recently received research grants and/or consultation funds from Biogen, Ministry of Education and Research (BMBF), Bristol-Meyers-Squibb, Celgene, German Research Foundation (DFG), Janssen, Max-Planck-Society (MPG), Merck Serono, Novartis, Progressive MS Alliance (PMSA), Roche, Sanofi Genzyme, and Sandoz. SB has received funding for travel expenses for attending meetings from Merck Serono and honoraria from Biogen Idec, Bristol Meyer Squibbs, Merck Serono, Novartis, Roche, Sanofi Genzyme and TEVA. His research is funded by Deutsche Forschungsgemeinschaft (DFG) and Hertie foundation. FL received consultancy fees from Roche and support with travel costs from Teva Pharma.
 Partial funding for the study was provided by an investigator-initiated grant to Dr. Makar from Teva Neuroscience, Inc. which markets glatiramer acetate as a treatment for multiple sclerosis. Guda declares no competing interests. Ray declares no competing interests. Andhavarapu declares no competing interests. Keledjian declares no competing interests. Gerzanich declares no competing interests. Simard declares no competing interests. Nimmagadda declares no competing interests. Bever declares no competing interests.


 Conflict of Interest Disclosures: Dr Januel reported receiving personal fees and reimbursement for conference registration fees, travel expenses, and accommodation from Sanofi-Genzyme outside the submitted work. Dr Maillart reported receiving research support from Fondation ARSEP and Biogen Idec and travel funding and/or consulting fees from Alexion, Biogen Idec, Bristol Myers Squibb (BMS), Janssen, Merck, Novartis, Roche, Sanofi-Genzyme, Cellgène, and Teva. Prof Zephir reported receiving consulting fees from Biogen Idec, Sanofi, Merck, Novartis, Roche, Horizon Therapeutics, Alexion, and BMS; grant research support from Roche; and nonfinancial support from BMS, Alexion, and Biogen Idec outside the submitted work. Dr Guilloton reported receiving consulting and/or lecture fees and/or travel funding from Novartis, Merck, Sanofi, BMS, and Biogen and grants from Novartis, Aguettant, Biogen, Merck, Sanofi, and BMS outside the submitted work. Dr Bensa reported receiving consulting honoraria from Alexion, Sanofi, Merck, Biogen, BMS, Novartis, Roche, and Teva. Dr Heinzlef reported receiving consulting and lecture fees from Bayer Schering, Merck, Teva, Genzyme, Novartis, Almirall, and Biogen Idec; travel grants from Novartis, Teva, Genzyme, Merck Serono, and Biogen Idec; and research support from Roche, Merck, and Novartis. Dr Casez reported receiving personal fees from Biogen, Roche, Merck, Novartis, Janssen, and Sanofi and nonfinancial support from Roche, Merck, and Novartis outside the submitted work. Dr Bourre reported serving on scientific advisory boards for and/or receiving funding for travel and honoraria from Alexion, Biogen, BMS, Janssen, Merck, Novartis, Sanofi, Roche, and Teva; receiving grants from Alexion, Merck, and Novartis; and receiving personal fees from Biogen, Roche, Janssen, and BMS outside the submitted work. Prof Vukusic reported receiving lecturing fees, travel grants, and research support from Biogen, BMS-Celgene, Janssen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. Dr Maurousset reported receiving personal fees from Merck, Biogen, Roche, Teva, and Alexion outside the submitted work. Dr Berger reported receiving honoraria and consulting fees from Alexion, Novartis, Sanofi-Aventis, Biogen Idec, Genzyme, Merck, Roche, and Teva. Dr Laplaud reported receiving grants from Roche, Sanofi, the ARSEP Foundation, the EDMUS Foundation, and the National Agency of Research and receiving personal fees from Biogen, Novartis, Alexion, Merck, and MSD outside the submitted work. Dr Dubessy reported participating in paid advisory boards for Merck and Novartis and receiving personal fees from Merck outside the submitted work. Dr Branger reported receiving personal fees from Novartis, Biogen, Merck, BMS, Alexion, and Sanofi outside the submitted work. Prof Thouvenot reported receiving personal fees from Biogen, BMS, Janssen, Horizon, Merck, Novartis, and Sanofi outside the submitted work. Prof Clavelou reported receiving personal fees for board participation from Janssen and Novartis and for board participation and travel from Sanofi and Merck outside the submitted work. Dr Moreau reported receiving travel grants and fees for advisory boards from Biogen, Roche, Novartis, Sanofi, and Teva outside the submitted work. Dr Papeix reported receiving honoraria and consulting fees from Alexion, Biogen, Merck, Horizon, and Roche outside the submitted work and serving as president of the Francophone Multiple Sclerosis Society from 2021 to 2024. Prof Tubach reported being head of the Centre de Pharmacoépidémiologie (Cephepi) of the Assistance Publique–Hôpitaux de Paris and of the Clinical Research Unit of Pitié-Salpêtrière Hospital, both of which have received unrestricted research funding and grants for the research projects handled and fees for consultant activities from a large number of pharmaceutical companies that have contributed indiscriminately to the salaries of the employees; Prof Tubach is not employed by these companies and did not receive any personal remuneration from them. Dr Louapre reported receiving consulting or travel fees from Biogen, Novartis, Roche, Sanofi, Teva, and Merck Serono and a research grant from Biogen. No other disclosures were reported.

 S.K. (Susumu Kusunoki) received honoraria for lectures from CSL Behring, Nihon Pharmaceutical CO., Ltd., and Japan Blood Products Organization, and is a member of Data Safety Monitoring Board of Argenx. The other authors have no conflict of interest.
 Conflict of interest disclosure: ONW currently has consulting, equity, and/or board relationships with Kronos Biosciences, Sofie Biosciences, Breakthrough Properties, Vida Ventures, Nammi Therapeutics, Two River, Iconovir, Appia BioSciences, Neogene Therapeutics, 76Bio, and Allogene Therapeutics. None of these companies contributed to or directed any of the research reported in this article. ONW, JC, and CGR are inventors on patents that disclose [(18)F]FAC. JC, CGR, and DAN are inventors on patents that disclose TRE-515. PMC, ONW, DAN, JC, CGR, and KAS hold stock shares of Trethera Corporation, which is developing TRE-515. HMS and LS are paid members of the Trethera Corporation Scientific Advisory Board. KAS is an employee of Trethera Corporation.
 Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose.

 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 Declaration of Competing Interest The authors have no duality or conflicts of interest to declare.

 Tianrong Yeo has received honoraria from ASNA, Edanz Pharma, Euroimmun AG, Merck, Novartis, Terumo BCT for consulting services and speaker’s fees, and research grants from the National Medical Research Council (NMRC Singapore) and Roche. He has also received travel grants from UCB, Merck and PACTRIMS, and travel awards from ACTRIMS, ECTRIMS and Orebro University. Kevin Tan has received travel grants and compensation from Novartis, Merck, Sanofi, Eisai, Viela Bio and Roche for consulting services. Rachel Wan En Siew, Muhammad Yaaseen Gulam, Janis Siew Noi Tye, Amelia Yun Yi Aw, Thanushiree Sivalingam, Xuejuan Peng, Kok Pin Yong, Seyed Ehsan Saffari, and Yinxia Chao report no competing interests.
 Declaration of competing interest The authors have no conflicts of interest to declare.
 Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose.
 The authors declare no conflict of interest.
 C.-A. Sirbu has received speaker honoraria; consulting fees; and travel, research, and educational grants from Bayer, Novartis, Merck, Schering, Ever Pharma, Roche, Janssen, and Teva. The remaining authors have no conflicts of interest.
 S.A. Laurent reports no disclosures. During the conduct of this study, N.B.S. was a student at the University of California, San Francisco, and had no disclosures. After the completion of this study, N.B.S. became an employee of Genentech, Inc., and a shareholder of F. Hoffmann-La Roche Ltd. E.L. Eggers, H. Wu, B. Michel, and S. Demuth report no disclosures. A. Palanichamy is currently an employee of Spark Therapeutics, a subsidiary of F. Hoffmann-La Roche, Ltd. M.R. Wilson reports receiving grants from Roche/Genentech, during the conduct of the study. M. Sirota reports a financial relationship with TwoXAR for working as a Scientific Advisor outside the submitted work. R.D. Hernandez reports no disclosures. In the past 36 months, B.A.C. Cree has received personal compensation for consulting from Alexion, Atara, Autobahn, Avotres, Biogen, Boston Pharma, EMD Serono, Gossamer Bio, Hexal/Sandoz, Horizon, Immunic, Neuron23, Novartis, Sanofi, Siemens, TG Therapeutics, and Therini and received research support from Genentech. A.E. Herman is an employee of Genentech, Inc., and a shareholder of F. Hoffmann-La Roche Ltd. H.-C. von Büdingen reports receiving grants, personal fees, and nonfinancial reports from F. Hoffmann-La Roche Ltd during the conduct of this study; during the planning, initiation, and conduct of this study, he was employed by University of California, San Francisco, and received personal fees from F. Hoffmann-La Roche Ltd to participate in advisory boards. H.-C.v.B. is an employee and a shareholder of F. Hoffmann-La Roche Ltd. Go to Neurology.org/NN for full disclosure.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors have also declared that no competing interests exist.
 There is no conflict of interest to declare.
 The authors declare no competing interests.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The Authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.
 Declaration of Competing Interest Per Magne Ueland is a paid employee at Bevital AS; Adrian McCann is a paid employee at Bevital AS. Bevital AS is owned by a not-for-profit foundation established to promote research into functional B-vitamin deficiency. Marie Kupjetz: none, Nadine Patt: none, Niklas Joisten: none, Roman Gonzenbach: none, Jens Bansi: none, Philipp Zimmer: none.

 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare that they have no competing interests.
 Conflict of Interest Disclosures: Dr Ayroza Galvão Ribeiro Gomes reported grants from Roche during the conduct of the study. Dr de Moura Brasil Matos reported grants from Hoffmann La Roche outside the submitted work. Dr Pereira reported grants from CNPq–Conselho Nacional de Desenvolvimento Científico e Tecnológico (308172/2018-3) during the conduct of the study. Dr Ribeiro Monteiro reported grants from CNPq–Conselho Nacional de Desenvolvimento Científico e Tecnológico during the conduct of the study. Dr Schindler reported nonfinancial support from UCB Pharma outside the submitted work. Dr Chien reported grants from Novartis and Alexion during the conduct of the study and nonfinancial support as a member from the Canadian Institutes of Health Research Standing Committee on Science outside the submitted work. Dr Schwake reported speaker honoraria from Alexion and travel support from Novartis and UCB outside the submitted work. Dr Schneider reported research grant support from Novartis and speaker honoraria from Roche and Alexion outside the submitted work. Dr Aktas reported personal fees from Alexion, Almirall, Horizon, Novartis, and Roche outside the submitted work and serving as steering committee member and co-coordinator of the German Neuromyelitis Optica Study Group (NEMOS). Dr Fischer reported grants to their institution from Medtronic, Stryker, Rapid Medical, Penumbra, and Phenox; consultant fees paid to their institution from Medtronic, Stryker, and CSL Behring outside the submitted work; participation in an advisory board for Alexion/Portola, Boehringer Ingelheim, Biogen, and Acthera (fees paid to institution); member of a clinical event committee of the COATING study (Phenox); member of the data and safety monitoring committee of the TITAN, LATE_MT, and IN EXTREMIS trials; and vice-presidency of the Swiss Neurological Society. Dr Mehling reported grants from the Swiss National Science Foundation, Roche, and Merck and fees for advisory board activities paid to their institution from Merck, Roche, Novartis, and Biogen outside the submitted work. Dr Derfuss reported grants from Alexion, Novartis, and Roche and fees paid to their institution for membership in advisory boards, data and safety monitoring boards, and/or steering committees from Actelion, Biogen, Celgene, Sanofi, GeNeuro, Merck, MedDay, Roche, Alexion, and Novartis outside the submitted work. Dr Kappos reported consultant, speaking, advisory board, and/or steering committee fees from Bayer, Biogen, Bristol Myers Squibb, Celltrion, df-mp Molnia & Pohlman, Eli Lilly (Suisse), EMD Serono, F&U confirm, Genentech, GlaxoSmithKline, Janssen, Japan Tobacco, Merck (Schweiz), Minoryx Therapeutics, Novartis, Roche, Santhera Pharmaceuticals, Shionogi, and Wellmera, grants from the European Union, Innosuisse, and Swiss National Science Foundation; and product license fees from Neurostatus outside the submitted work. Dr Ayzenberg reported personal fees from Roche, Alexion, Merck, Horison, and Sanofi and grants from Diamed from outside the submitted work. Dr Ringelstein reported personal fees from Alexion, Horizon, Roche, and Biogen outside the submitted work. Dr Callegaro reported being on the board of BCTRIMS, the Brazilian commitment for treatment and research in multiple sclerosis and related diseases, and serving as coordinator of the Neuroimmunology Center, Hospital das Clínicas, São Paulo University. Dr Kuhle reported grants from the Swiss MS Society, Swiss National Science Foundation, Novartis, Biogen, Merck, Bristol Myers Squibb, and Roche outside the submitted work. Dr Papadopoulou reported grants from University of Basel, grants from University Hospital of Basel, and grants from Swiss Multiple Sclerosis Society during the conduct of the study; advisory board and/or speaking fees to their institution from AbbVie, Eli Lilly, Lundbeck, and TEVA and conference travel support from TEVA outside the submitted work. Dr Pröbstel reported advisory board and/or consultant fees from Roche, Biogen, and Novartis outside the submitted work. No other disclosures were reported.
 Declaration of Competing Interest None.

 M.E., A.W., R.C., Y.A., F.B., A.F., C.B., A.E., E.N., and B.O. declare no conflict of interest. S.K. reports receiving funding from the Deutsche Forschungsgemeinschaft (DFG), Novartis, F. Hoffmann-La Roche, and Sanofi, and also receiving speaker fees and consultancy honoraria from Novartis, F. Hoffmann-La Roche, Sanofi, and Teva (outside the submitted work).
 Declaration of Competing Interest Although considered to be irrelevant, EF, GP, LKJ and ASK have nothing relevant to declare. In the past 3 years DB has received honoraria for teaching and consultancy, unrelated to this work from inMuneBio, Merck Serono, Novartis, Roche, Teva. GG has received honoraria and meeting support from AbbVie Biotherapeutics, Biogen, Novartis, Merck Sharp Dome, Merck Serono, Roche, Sanofi Genzyme, Synthon, Teva. He also serves as chief editor for Multiple Sclerosis and Related Disorders and has been an academic director of the Neurology Academy, supported by Roche. KS has received research support from: Biogen, Merck KGaA, and Novartis and speaking/consultancy honoraria from: Biogen, EMD Serono, Medscape; Merck KGaA, Novartis, Roche, Sanofi-Genzyme, and Teva
 The authors declare no conflict of interest.
 The authors declare no competing interests.
 The Wistar Institute, on behalf of the authors T.E.M. and P.M.L., has filed patents covering composition of matter and their use on the small molecule disclosed here for the treatment of human cancer and other diseases (patent number WO2015073864, “EBNA1 Inhibitors and Their Method of Use”; WO2016183534, “EBNA1 Inhibitors and Methods using Same”). P.M.L. has an ownership interest in Vironika, LLC. Go to Neurology.org/NN for full disclosures.
 Competing Interest Statement The authors declare no competing interests.



 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The corresponding author, on behalf of the others, declares no conflict of interest. All aspects of human research are considered by the authors.
 Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no competing interests.

 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: The authors declare no conflict of interest.

 S. Malhotra reports no disclosures relevant to the manuscript; L. Hurtado-Navarro is a cofounder of Viva In Vitro Diagnostics SL but declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest; A. Pappolla, L.M. Villar, J. Río, X. Montalban, and M. Comabella report no disclosures relevant to the manuscript; P. Pelegrin is a cofounder of Viva In Vitro Diagnostics SL but declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Go to Neurology.org/NN for full disclosures.
 The authors declare no conflict of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: MWH reports no disclosures relevant to the manuscript. CSt reports no disclosures relevant to the manuscript. FP receives honoraria for lecturing, and travel expenses for attending meetings from Guthy Jackson Foundation, Sanofi Genzyme, Novartis, Alexion, Viela Bio, Roche, UCB, Mitsubishi Tanabe, and Celgene. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Einstein Foundation, Guthy Jackson Charitable Foundation, EU FP7 Framework Program, Biogen, Genzyme, Merck Serono, Novartis, Bayer, Teva, Alexion, Roche, Parexel, Viela Bio, and Almirall. FP serves on advisory boards and steering committees for Novartis and Viela Bio and is Associate Editor of Neurology, Neuroimmunology & Neuroinflammation and Academic Editor for PLoS ONE. AD reports no disclosures relevant to the manuscript. JBS has received travel grants and speaking honoraria from Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi Genzyme, Teva Pharmaceuticals, Roche, and Novartis all unrelated to this work. IA received personal fees from Roche, Alexion, and Merck and received research support from Diamed, none related to this manuscript. CSc reports no disclosures relevant to the manuscript. IK has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Alexion, Biogen, Celgene, Hexal, Horizon, Merck, and Roche/Chugai. KH received consultant and speaker honoraria from Bayer, Biogen, Merck, Novartis, Sanofi Genzyme, Roche, and Teva. SJ reports no disclosures relevant to the manuscript. BW received grants from the German Ministry of Education and Research, Deutsche Forschungsgemeinschaft, Dietmar Hopp Foundation, and Klaus Tschira Foundation, grants and personal fees from Merck, Novartis, and personal fees from Roche; none related to this work. MS has received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Merck, Roche, and Sanofi Genzyme. She has received research funding from the Hertha-Nathorff-Program. None of this interfered with the current report. AB received speaker and consulting honoraria from Alexion, Biogen, Bayer Healthcare, Celgene, Merck, Novartis Pharma, and Roche; all outside the submitted work. KG reports no disclosures relevant to the manuscript. FL received consultancy fees from Roche and support with travel cost from Teva Pharma. MG received honoraria and travel reimbursements for attending meetings from Biogen, Celgene, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva and research grants from the German Ministry for Education and Research (BMBF), Merck Serono, and Novartis. None of this interfered with the current report. LK received compensation for serving on Scientific Advisory Boards for Alexion, Biogen, Celgene GmbH, Genzyme, Horizon, Janssen, Merck Serono, Novartis, and Roche. She received speaker honoraria and travel support from Bayer, Biogen, Celgene GmbH, Genzyme, Grifols, Merck Serono, Novartis, Roche, Santhera, and Teva. She receives research support from the German Research Foundation, the IZKF Münster, IMF Münster, Biogen, Immunic AG, Novartis, and Merck Serono. RS reports no disclosures relevant to the manuscript. SG has received speaker honoraria from Alnylam, not related to this manuscript. JHF reports no disclosures relevant to the manuscript. AW received speaker honoraria and meeting expenses from Novartis, Bayer, Biogen, Sanofi Genzyme, Teva, Roche, and Merck. CW has received institutional honoraria and/or grant support from Novartis, Sanofi-Genzyme, Alexion, Janssen, Merck, Biogen, and Roche. FTB has received honoraria for speaking and advisory board consultation from Alexion, Roche, and Horizon Therapeutics; none of these had an impact on this manuscript. OA has received personal fees from Alexion, Bayer Healthcare, Biogen, Celgene, Merck Serono, MedImmune, Novartis, Roche, Teva, and Zambon, outside of the submitted work. MR received speaker honoraria from Novartis, Bayer Vital GmbH, Roche, Alexion, and Ipsen and travel reimbursement from Bayer Schering, Biogen Idec, Merz, Genzyme, Teva, Roche, and Merck, none related to this study. JPS reports no disclosures relevant to the manuscript. VH reports no disclosures relevant to the manuscript. JH reports personal fees, research grants and non-financial support from Merck, Novartis, Roche, Santhera, Biogen, Alexion, Celgene, Janssen; and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work. J.H. is (partially) funded by the German Federal Ministry of Education and Research [Grant Numbers 01ZZ1603[A-D] and 01ZZ1804[A-H] (DIFUTURE)]. HP received honoraria for lectures from Bayer Health Care, Biogen Idec, and Teva Pharma and travel reimbursement from Novartis. TK has received speaker honoraria and/or personal fees for advisory boards from Bayer Healthcare, Teva Pharma, Merck, Novartis Pharma, Sanofi-Aventis/Genzyme, Roche Pharma, Alexion, and Biogen as well as grant support from Novartis and Chugai Pharma in the past. None of this interfered with the current report. BK reports no disclosures relevant to the manuscript. CT has received honoraria for consultation and expert testimony from Alexion Pharma Germany GmbH, Biogen Idec/GmbH, Chugai Pharma Germany GmbH, MERCK, Novartis Pharma GmbH and Roche Pharma GmbH. None of this interfered with the current report.
 Declaration of Competing Interest None of the authors report any conflicts of interest.
 Y. Blanco received speaker honoraria from Novartis, Roche, Sanofi, Merck, and Biogen; S. Llufriu received compensation for consulting services and speaker honoraria from Biogen Idec, Novartis, TEVA, Genzyme, Sanofi, Merck, and Bristol-Myers Squibb and holds grants from the Instituto de Salud Carlos III; M. Artola received financial honoraria for presentations and attendance at conferences by Almirall, Biogen idec, Sanofi, Novartis, and Merck; J.M. Cabrera-Maqueda received speaking honoraria and travel expenses for participation in scientific meetings from Sanofi. A. Hernando received financial speaker honoraria from Merck and attendance at conferences by Almirall, Bayer, Biogen, Novartis, Roche, Sanofi, and Teva. J. López-Contreras has received grants from Instituto de Salud Carlos III - Ministry of Economy and Innovation (Spain)and Fundació La Marató, speaking honoraria from Pfizer, MSD, Astra-Zeneca, Guerbet, and Hartmann, funding for clinical trials from Pfizer, Shionogi, MSD, Arsanis, Summit, GSK, Actelion, and Angelini, and for educational activities from MSD, Pfizer, Angelini, Gilead, and Guerbet; L. Martín-Aguilar received speaking honoraria from Roche; E. Martinez-Hernandez received speaking compensation from Biogen; M. Sepulveda received speaking honoraria from Roche, Biogen, and UCB Pharma and travel reimbursement from Biogen, Sanofi, Merck, and Roche for national and international meetings. E. Solana received travel reimbursement and congress assistance from Sanofi and Merck and reports personal fees from Roche Spain; T. Armangué received personal compensation for speaking fees from Sanofi and Roche. J.O. Dalmau holds patents for the use of NMDAR, GABAaR, GABAbR, DPPX, and IgLON5 as autoantibody tests and receives royalties related to autoantibody tests from Athena Diagnostics and Euroimmun Inc. L. Querol received research grants from Instituto de Salud Carlos III - Ministry of Economy and Innovation (Spain), CIBERER, Fundació La Marató, GBS-CIDP Foundation International, UCB, and Grifols, received speaker or expert testimony honoraria from CSL Behring, Novartis, Sanofi-Genzyme, Merck, Annexon, Alnylam, Biogen, Janssen, Lundbeck, ArgenX, UCB, LFB, Octapharma, and Roche, serves at Clinical Trial Steering Committee for Sanofi Genzyme and Roche, and is Principal Investigator for UCB's CIDP01 trial. A. Saiz received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Merck, Sanofi, Biogen, Roche, Novartis, Janssen, and Horizon Therapeutics. The other authors report no disclosures. Go to Neurology.org/NN for full disclosures.

 Declaration of interests The authors declare no competing interests.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Conflict of Interest Disclosures: Dr Kalincik reported receiving advisory board fees from MS International Federation, World Health Organization, BMS, WebMD Global, Eisai, Novartis, Biogen, Roche, Janssen, Sanofi Genzyme, Teva, BioCSL, and Merck; grants from Novartis, Biogen, Roche, Merck, and Celgene outside the submitted work; steering committee fees for Brain Atrophy Initiative by Sanofi Genzyme; conference travel support and/or speaker honoraria from WebMD Global, Eisai, Novartis, Biogen, Sanofi Genzyme, Teva, BioCSL, and Merck; and research or educational event support from Biogen, Novartis, Genzyme, Roche, Celgene, and Merck outside the submitted work. Dr Horakova reported receiving speaker honoraria, travel compensation, and consultant fees from Biogen, Merck, Teva, Roche, Sanofi Genyzme, and Novartis; grants from Charles University in Prague Cooperation Program in Neuroscience and General University Hospital in Prague; and support for research activities from Biogen and Czech Ministry of Education outside the submitted work. Dr Buzzard reported receiving advisory board and speaker honoraria from Roche, Biogen, Sanofi Genzyme, Teva, Novartis, Merck Serono, Alexion, BioCSL, and Grifols outside the submitted work. Dr Alroughani reported receiving speaker honoraria and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche, and Sanofi Genzyme outside the submitted work. Dr Izquierdo reported receiving grants from Novartis and Sanofi Genzyme and speaker honoraria from Biogen, Merck Serono, Teva, Roche, Novartis, Sanofi Genzyme, and Almirall outside the submitted work. Dr Eichau reported receiving speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, Teva, Bristol Myers Squibb, Janssen, and Almirall outside the submitted work. Dr Kuhle reported receiving grants from Swiss MS Society, Swiss National Science Foundation, Roche, Novartis, Merck, Biogen, and Bristol Myers Squibb outside the submitted work. Dr Patti reported receiving speaker honoraria and advisory board fees from Almirall, Bayer, Biogen, Celgene, Merck, Novartis, Roche, Sanofi Genzyme, Teva, and Bristol Myers Squibb; grants from Merck, Novartis, Roche, Alexion, and Biogen; and research funding from Biogen, Merck, FISM (Fondazione Italiana Sclerosi Multipla), Reload Onlus Association, and University of Catania outside the submitted work. Dr Grand’Maison reported receiving honoraria or research funding from Biogen, Genzyme, Novartis, Teva Neurosciences, Mitsubishi, and ONO Pharmaceuticals and grants from Atara, Biogen, Novartis, Genzyme, and Roche outside the submitted work. Dr Hodgkinson reported receiving grants from Novartis, Biogen, Atara, and Roche; honoraria and consulting fees from Novartis, Bayer Schering, and Sanofi; and travel grants from Novartis, Biogen Idec, and Bayer Schering outside the submitted work. Dr Grammond reported serving on advisory boards for Novartis, EMD Serono, Roche, Biogen Idec, Sanofi Genzyme, and Pendopharm and receiving grant support from Genzyme, Roche, Biogen Idec, Sanofi Genzyme, and EMD Serono outside the submitted work. Dr Lechner-Scott reported receiving travel compensation from Novartis, Biogen, Roche, and Merck and speaker honoraria, advisory board fees, and research grants from Biogen, Merck, Roche, Teva, and Novartis during the conduct of the study. Dr Girard reported receiving consulting fees from Teva Canada Innovation, Biogen, Novartis, and Genzyme Sanofi; lecture payments from Teva Canada Innovation, Novartis, and EMD; and a research grant from Canadian Institutes of Health Research. Dr Duquette reported serving on the editorial boards of and has been supported to attend meetings by EMD, Biogen, Novartis, Genzyme, and Teva Neuroscience; received grants from the CIHR and the MS Society of Canada; and received funding for investigator-initiated trials from Biogen, Novartis, and Genzyme. Dr Macdonell reported receiving grants from Biogen, Novartis, and Roche outside the submitted work. Dr Weinstock-Guttman reported receiving grants from Biogen and Novartis and personal fees from Horizon, Sanofi Genzyme, Bayer, Mylan, and Labcorp outside the submitted work. Dr Slee reported participating in, but not receiving honoraria for, advisory board activity for Biogen, Merck, Bayer Schering, Sanofi-Aventis, and Novartis. Dr Van Pesch reported receiving travel grants from Merck Healthcare KGaA (Darmstadt, Germany), Biogen, Sanofi, Bristol Myers Squibb, Almirall, and Roche and research grants and consultancy fees from Roche, Biogen, Sanofi, Merck Healthcare KGaA (Darmstadt, Germany), Bristol Myers Squibb, Janssen, Almirall, and Novartis Pharma outside the submitted work. Dr Barnett reported serving on scientific advisory boards for Biogen, Novartis, and Genzyme; receiving conference travel support from Biogen and Novartis; receiving research support from Biogen, Merck, and Novartis; receiving grants from Biogen, Bristol Myers Squibb, Roche, Novartis, and Merck; and consultant fees from Sydney Neuroimaging Analysis Centre and RxPx Corporation outside the submitted work. Dr Van Wijmeersch reported receiving research and travel grants and MS expert advisor and speaker fees from Almirall, Bayer-Schering, Biogen, Bristol Myers Squibb, Janssen, Viatris, Sanofi Genzyme, Merck, Novartis, Roche, and Teva outside the submitted work. Dr Prevost reported receiving travel fees from Novartis, Biogen, Genzyme and Teva and speaker fees from Biogen, Novartis, Genzyme, and Teva. Dr Terzi reported receiving travel grants from Novartis, Bayer-Schering, Merck, and Teva and participating in clinical trials by Sanofi-Aventis, Roche, and Novartis outside the submitted work. Dr Boz reported receiving conference travel support from Biogen, Novartis, Bayer-Schering, Merck, Roche, and Teva and participating in clinical trials by Sanofi-Aventis, Roche, and Novartis outside the submitted work. Dr Laureys reported receiving travel and/or consultant fees from Sanofi Genzyme, Roche, Teva, Merck, Novartis, Celgene, and Biogen outside the submitted work. Dr Kermode reported receiving speaker honoraria and scientific advisory board fees from Bayer, BioCSL, Biogen, Genzyme, Innate Immunotherapeutics, Merck, Novartis, Sanofi, Sanofi-Aventis, and Teva. Dr Garber reported receiving personal fees from Biogen, Merck, and Novartis outside the submitted work. Dr Yamout reported receiving grants from Merck and Novartis and speaker fees from Sanofi, Roche, Biogen, and Janssen outside the submitted work. Dr Khoury reported receiving scientific advisory board fees from Merck and Roche. Dr Merlo reported receiving personal fees from Novartis Australia outside the submitted work. Dr Monif reported serving on the advisory board for Merck; receiving speaker honoraria from Merck and Biogen; and receiving funding from Merck, the Australian National Health Medical Research Council, Brain Foundation, Charles and Sylvia Viertel Foundation, Bethlehem Griffith Foundation, and MS Research Australia. Dr Jokubaitis reported receiving grants from Roche; conference travel support from Merck and Roche; speakers honoraria from Biogen and Roche; and research support from the Australian National Health and Medical Research Grant and MS Research Australia outside the submitted work. Dr van der Walt reported receiving grants from Novartis, Roche, the National Health and Medical Research Council of Australia, and MS Research Australia and research grants and advisory board fees from Novartis, Roche, Biogen, Merck outside the submitted work. Dr Butzkueven has reported receiving grants from National Health and Medical Research Council, Biogen, Roche, Novartis, and Merck; travel support from Merck; speaker fees from UCB; funding from Biogen, F. Hoffmann-La Roche Ltd, Merck, Alexion, CSL, and Novartis; performed contracted research for Novartis, Merck, F. Hoffmann-La Roche Ltd and Biogen; received speakers fees from Biogen, Genzyme, UCB, Novartis, F. Hoffmann-La Roche Ltd, and Merck; and received personal compensation from Oxford Health Policy Forum for the Brain Health Steering Committee. No other disclosures were reported.
 Declartion of Competing Interest The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare that they have no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor DL declared a shared parent affiliation with some of the authors RM, PP at the time of review.
 KPf, FR and REK are named inventors on a patent covering the TNFR1 antagonist. KPf, RFi and REK are named inventors on a patent covering the TNFR2 agonist. KPf and REK received funding from Baliopharm, a company which has licensed the TNFR1 technology. REK and RFi received funding from Resano, a company which has licensed the TNFR2 technology.
 Conflict of Interest The authors declare no conflicts of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors have declared that no competing interests exist.

 In the last 5 years JC has received financial compensation for academic presentations, participation in advisory councils, research grants and assistance to attend congresses from the following companies: Biogen, Merck, Novartis, Roche, Bayer, Sanofi-Genzyme, Gador, Raffo, Bristol Myers Squibb, and Janssen. CR served as a consultant for Sanofi Genzyme and has received personal compensation for speaking engagements for EMD Serono, Inc., the Multiple sclerosis Society of Canada, and Teva Pharmaceutical Industries Ltd. AB has received personal compensation and research grants from Novartis, Sanofi, Roche, Teva, Biogen, Merck, BMS, Synthon-Bago, and Gador.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 R.N. received support from advisory boards and travel from Novartis, Roche and Biogen. He has grant support from the UK Multiple Sclerosis Society and is a member of a National Institute for Health and Care Excellence Health Technology Assessment committee. All other authors report no competing interests.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: CNB is supported by the Bingham Chair in Gastroenterology. CNB has served on advisory Boards for AbbVie Canada, Amgen Canada, Bristol Myers Squibb Canada, JAMP Pharmaceuticals, Lilly Canada, Roche Canada, Janssen Canada, Sandoz Canada, Takeda Canada, and Pfizer Canada; Consultant for Mylan Pharmaceuticals and Takeda; Educational grants from Abbvie Canada, Pfizer Canada, Takeda Canada, and Janssen Canada. Speaker's panel for Abbvie Canada, Janssen Canada, Pfizer Canada, and Takeda Canada. Received research funding from Abbvie Canada, Amgen Canada, Sandoz Canada, Takeda Canada and Pfizer Canada. LAG has consulted for Roche Canada. She receives research funding from CIHR, the Multiple Sclerosis Society of Canada and Crohn's and Colitis Canada. JMB receives research funding from CIHR, Brain and Behavior Research Foundation, Crohn's and Colitis Canada and the MS Society of Canada. JDF receives research grant support from the Canadian Institutes of Health Research, the National Multiple Sclerosis Society, the Multiple Sclerosis Society of Canada, Crohn's and Colitis Canada, Research Nova Scotia; consultation and distribution royalties from MAPI Research Trust. CH receives research funding from CIHR, unrelated grant funding from Pfizer; Advisory board for Astra-Zeneca Canada for unrelated product, unrelated research funds from Research Manitoba, Health Sciences Center foundation, International League of Associations for Rheumatology, unrelated educational funds from the Royal College of Physicians and Surgeons of Canada. SBP receives research funding from CIHR, the MS Society of Canada, Roche, Biogen and the Government of Alberta. JJM has conducted trials for Biogen Idec and Roche, and receives research funding from the MS Society of Canada. RAM is a co-investigator on a study funded by Biogen Idec and Roche (no funds to her/her institution). Ruth Ann Marrie receives research funding from CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and the US Department of Defense, and is a co-investigator on studies receiving funding from Biogen Idec and Roche Canada. She holds the Waugh Family Chair in Multiple Sclerosis. DJ has no disclosures to report.


 None
 M. Huiskamp receives research support from the Dutch MS Research Foundation. Prof. Dr. Killestein reports speaker and consulting fees and grants from Biogen, Celgene, Genzyme, Immunic, Merck, Novartis, Roche, Sanofi and Teva. Prof. Dr. van Berckel has received research support from EU-FP7, CTMM, ZonMw, NWO and Alzheimer Nederland. BvB has performed contract research for Rodin, IONIS, AVID, Eli Lilly, UCB, DIAN-TUI and Janssen. BvB was a speaker at a symposium organized by Springer Healthcare. BvB has a consultancy agreement with IXICO for the reading of PET scans. BvB is a trainer for GE. BvB only receives financial compensation from Amsterdam UMC. Prof. Dr. Geurts has served as a consultant for Merck-Serono, Biogen, Novartis, Genzyme and Teva Pharmaceuticals; he has received research support from the Dutch MS Research Foundation, Ammodo, Eurostars-EUREKA, Biogen, Celgene/BMS, Merck, MedDay and Novartis. Prof. Dr. Hulst receives research support from Dutch MS Research Foundation, ZonMW, NWO, ATARA, Biogen, Celgene/BMS, Merck and Medday, serves as a consultant for Sanofi Genzyme, Merck BV, Biogen Idec, Roche and Novartis and is on the editorial board of Multiple Sclerosis Journal. Other authors report no conflicts of interest.
 Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-21-3073/coif). The series “Laboratory Investigations in Neuroimmunological Diseases and Their Clinical Significance” was commissioned by the editorial office without any funding or sponsorship. The authors have no other conflicts of interest to declare.

 None


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors report no conflict of interest.
 The authors report no competing interests.
 The authors declare no conflict of interest.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


 None
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Amber Salter reports honoraria for consulting for Gryphon Bio, LLC and research funding from Multiple Sclerosis Society of Canada, National Multiple Sclerosis Society, Consortium of MS Centers and the US Department of Defense. She is a member of the Editorial Board for Neurology. Dr Salter is a member of the Data and Safety Monitoring Board for Premature Infants Receiving Milking or Delayed Cord Clamping (PREMOD2), Central Vein Sign: A Diagnostic Biomarker in Multiple Sclerosis (CAVS-MS), Ocrelizumab for Preventing Clinical Multiple Sclerosis in Individuals With Radiologically Isolated Disease (CELLO), and Video Telehealth Pulmonary Rehabilitation to Reduce Hospital Readmission in Chronic Obstructive Pulmonary Disease (Tele-COPD). Gary Cutter data/safety monitoring committees for AMO, BioLineRx, BrainStorm Cell Therapeutics, Galmed, Horizon, Hisun, Merck, Merck/Pfizer, OPKO Biologics, Neurim, Novartis, Orphazyme, Sanofi, Reata, Receptos/Celgene, Teva, NHLBI (Protocol Review Committee), NICHD (OPRU oversight committee); consulting/advisory boards for Biogen, Click Therapeutics, Genzyme, Genentech, GW, Klein Buendel, MedImmune, MedDay, Novartis, Osmotica, Perception Neuroscience, Recursion, Roche, Somahlution, and TG Therapeutics Robert J Fox has received personal consulting fees from AB Science, Biogen, Celgene, EMD Serono, Genentech, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; has served on advisory committees for AB Science, Biogen, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; and received a clinical trial contract and research grant funding from Biogen, Novartis, and Sanofi. Ruth Ann Marrie receives research funding from CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society, and US Department of Defense. She is a co-investigator on a study funded in part by Biogen Idec and Roche (no funds to her/her institution). She is supported by the Waugh Family Chair in Multiple Sclerosis. Samantha Lancia has nothing to disclose. Alexander Keenan, Hoa H Le, Kavita Gandhi, and Maria Ait-Tihyaty are employees of Janssen Pharmaceuticals and may own stock in Johnson & Johnson.
 Dr Esposito has served as a speaker/board member for Abbvie, Almirall, Biogen, Celgene, Eli Lilly, Janssen, Leo Pharma, Novartis. Dr Fargnoli has served on advisory boards, received honoraria for lectures and research grants from AMGEN, Almirall, Abbvie, BMS, Galderma, Kyowa Kyrin, Leo Pharma, Pierre Fabre, UCB, Lilly, Pfizer, Janssen, MSD, Novartis, Sanofi-Regeneron, Sunpharma. Drs De Berardinis and Totaro have no conflict of interest to declare.

 None
 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 T.V. discloses personal compensation for consulting and serving on steering committees or advisory boards for Biogen Idec, Genentech. N.M. discloses personal compensation for consulting and serving on steering committees for the CHIMES study sponsored by Genentech. The other authors report no competing interests.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Competing interests: None declared.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 E.A.K., A.W.R., E.S.K., H.L. and F.L.C. report no conflicts of interest. M.M.S. serves on the editorial board of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation, Eurostars-EUREKA, ARSEP, Amsterdam Neuroscience, MAGNIMS and ZonMW and has served as a consultant for or received research support from Atara Biotherapeutics, Biogen, Celgene/Bristol Meyers Squibb, Genzyme, MedDay and Merck. S.Y.H. has received consulting fees and research grants from Siemens Healthineers. E.C.K. has received consulting fees from Banner Life Sciences, Galen/Atlantica, Genentech, Greenwich Biosciences and OM1, and research funds from Abbvie, Biogen and Genentech.

 The authors declare no conflict of interest.
 L.Q. received research grants from Instituto de Salud Carlos III—Ministry of Economy and Innovation (Spain), CIBERER, Fundació La Marató, GBS-CIDP Foundation International, UCB and Grifols, received speaker or expert testimony honoraria from CSL Behring, Novartis, Sanofi-Genzyme, Merck, Annexon, Alnylam, Biogen, Janssen, Lundbeck, ArgenX, UCB, LFB, Octapharma and Roche, serves at Clinical Trial Steering Committee for Sanofi-Genzyme and Roche and is Principal Investigator for UCB’s CIDP01 trial.
 The authors declare no conflict of interest.



 Declaration of Competing Interest There are no financial or personal interests (across any/all authors) that would affect author objectivity regarding this manuscript.
 The author(s)declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article:M.K. and B.S. are employees of Novartis. J.V. was an employee of Novartis Pharma AG during the development of the tool and the usability testing until the final version of the manuscript development. G.G. received consulting fees from AbbVie, Actelion, Atara Bio, Biogen, Celgene, Sanofi-Genzyme, Genentech, GlaxoSmithKline, Merck-Serono, Novartis, Roche and Teva, for research from Biogen, Roche, Merck, Merck-Serono, Novartis, Sanofi-Genzyme, and Takeda. E.A. received compensation for consulting from Actelion/Janssen, Alexion, Bayer, Biogen, Celgene/BMS, EMD Serono/Merck, Genentech/Roche, Genzyme, Novartis, Sanofi, and TG Therapeutics, and for research from Biogen, Genentech/Roche, Novartis, TG Therapeutics, Patient-Centered Outcomes Research Initiative, National Multiple Sclerosis Society, National Institutes of Health, and Rocky Mountain MS Center. O.H. received consulting fees from Biogen, Celgene, Janssen, Merck, Novartis, Roche, and Sanofi; funding for research from Biogen, Novartis, and Sanofi; and as a speaker from Merck, Novartis, Roche, and Sanofi. C.O.G. received consulting fees from Novartis, Alexion, and Roche; compensation for research from Alexion; and as a speaker from Novartis and Roche. P.V. has received compensation for consulting and/or research and registration, travel, and accommodation for meetings from Biogen, Roche, Novartis, Sanofi, Teva, Merck, AB Science, Imcyse and Celgene. T.Z. has received compensation for consulting and lecturing from Alexion, Biogen, Celgene, Novartis, Roche, Sanofi, and Teva and for research from Biogen, Novartis, Roche, Teva, and Sanofi. Y.X. has nothing to disclose. R.R.C. has received compensation for consulting services and speaking fees from Biogen, Roche, Novartis, Bayer, Merck, Sanofi, Genzyme, Teva Pharmaceutical Industries Ltd, and Almirall. M.T. has received compensation for consulting from Novartis, Biogen, Merck, Roche, and Sanofi, and her institution received support for research from Biogen, Merck, Novartis, and Roche. R.G. has received compensation for serving as a consultant or speaker from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis and Teva Neuroscience. He, or the institution he works for, has received research support from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis and Teva Neuroscience. He has also received honoraria as a Journal Editor from SAGE and Thieme Verlag. E.T. has received compensation for consulting from Novartis, Biogen, and Sanofi/Genzyme Europe B.V.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors report no conflict of interest in this work.
 The authors have no conflict of interest to declare.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest There are no conflicts of interest regarding this article.
 The authors have declared that no competing interests exist.


 The authors declare no conflict of interest.
 Disclosure: James Flynn declares no relevant financial relationships with ineligible companies. Disclosure: Valerie Gerriets declares no relevant financial relationships with ineligible companies.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 RM receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, the Arthritis Society and the US Department of Defense, and is a co-investigator on studies receiving funding from Biogen Idec and Roche Canada. LK declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. GC reports that he has served on data/safety monitoring committees for Applied Therapeutics, AI therapeutics, AMO Pharma, Astra-Zeneca, Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Pharmaceuticals, Immunic, Karuna Therapeutics, Mapi Pharmaceuticals Ltd, Merck, Mitsubishi Tanabe Pharma Holdings, Opko Biologics, Prothena Biosciences, Novartis, Regeneron, SanofiAventis, Reata Pharmaceuticals, NHLBI (Protocol Review Committee), University of Texas Southwestern, University of Pennsylvania, Visioneering Technologies, Inc. and on consulting/advisory boards for Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions LLC, Entelexo Biotherapeutics, Inc., Genzyme, Genentech, GW Pharmaceuticals, Immunic, Klein-Buendel Incorporated, Merck/Serono, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Protalix Biotherapeutics, Recursion/Cerexis Pharmaceuticals, Regeneron, Roche, SAB Biotherapeutics. RF has received personal consulting fees from AB Science, Biogen, Celgene, EMD Serono, Genentech, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; has served on advisory committees for AB Science, Biogen, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; and received clinical trial contract and research grant funding from Biogen, Novartis, and Sanofi. Amber Salter reports honoraria for consulting for Gryphon Bio, LLC and research funding from Multiple Sclerosis Society of Canada, National Multiple Sclerosis Society, Consortium of MS Centers and the US Department of Defense. She is a member of the Editorial Board for Neurology. AS was a member of the Data and Safety Monitoring Board for Premature Infants Receiving Milking or Delayed Cord Clamping (PREMOD2), Central Vein Sign: A Diagnostic Biomarker in Multiple Sclerosis (CAVS-MS), Ocrelizumab for Preventing Clinical Multiple Sclerosis in Individuals With Radiologically Isolated Disease (CELLO), and Video Telehealth Pulmonary Rehabilitation to Reduce Hospital Readmission in Chronic Obstructive Pulmonary Disease (Tele-COPD).
 The authors have declared that no competing interests exist.
 H.P. declares no conflict of interest. D.L. has received speaker bureau fees/consultancy/research grants from Merck, Novartis, BMS, Bayer, Sanofi, Roche, Biogen.

 The authors declare no competing interests.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Dr Terry Wahls has equity interest in the following companies: Terry Wahls LLC; TZ Press LLC; The Wahls Institute, PLC; FBB Biomed Inc; and the website http://www.terry-wahls.com. She also owns the copyright to the books Minding My Mitochondria (2nd Edition) and The Wahls Protocol, The Wahls Protocol Cooking for Life, and the trademarks The Wahls Protocol and Wahls diet, Wahls Paleo diet, and Wahls Paleo Plus diets. She has completed grant funding from the National Multiple Sclerosis Society for the Dietary Approaches to Treating Multiple Sclerosis Related Fatigue Study. She has financial relationships with BioCeuticals Ltd., MCG Health LLC, Vibrant America LLC, Standard Process Inc., MasterHealth Technologies Inc., Foogal Inc., Genova Diagnostics Inc., and the Institute for Functional Medicine. She receives royalty payments from Penguin Random House. Dr Wahls has conflict of interest management plans in place with the University of Iowa and the Iowa City Veteran’s Affairs Medical Center. All other authors report no personal or financial conflicts of interest in this work.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors had no conflicts of interest.
 Disclosure: Arezou Babaesfahani declares no relevant financial relationships with ineligible companies. Disclosure: Niloufar Khanna declares no relevant financial relationships with ineligible companies. Disclosure: Brianne Kuns declares no relevant financial relationships with ineligible companies.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 None.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 This study received funding from Novartis and Sanofi Genzyme. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 None

 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.
 The authors report no conflicts of interest in this work.
 None

 FINANCIAL DISCLOSURES: Dr Montalban has received speaking honoraria and/or travel expenses for participation in scientific meetings and/or has been a steering committee member of clinical trials and/or participated in advisory boards of clinical trials in past years with Actelion, Alexion, Bayer, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono, Excemed, Genzyme, Hoffmann-La Roche, Immunic Therapeutics, Janssen Pharmaceuticals, MedDay, Merck, Multiple Sclerosis International Federation, Mylan, National Multiple Sclerosis Society, NervGen Pharma, Novartis, Sanofi-Genzyme, Teva Pharmaceuticals, and TG Therapeutics. Dr Sastre-Garriga has received personal fees from Biogen, Biopass Medical Systems, Celgene, Merck, Orchid Pharma, and Sanofi. He is a member of the Editorial Committee of Multiple Sclerosis Journal and director of the Scientific Committee of Revista de Neurologia. The other authors declare no conflicts of interest.
 CMD has received compensation for serving on an advisory board and/or speaking fees (Sanofi). BL has nothing to disclose. IM has received honoraria and travel expenses for lecturing (Sanofi). SG has nothing to disclose. SFH has received consulting agreements, speaker honoraria, and grant/research financial support (AbbVie, Acorda, Actelion, Adamas, Avanir, Bayer, Biogen, Novartis, Osmotica, Questcor, Roche, Sanofi, Synthon, and Teva). KWS has received consulting and/or speaking fees (Biogen, Merck, Novartis, Roche, Sanofi, and Synthon). H-PH has received consulting and/or speaking fees (Bayer, Biogen, BMS Celgene, CSL Behring, GeNeuro, Horizon Therapeutics, Merck Serono, Novartis, Octapharma, Roche, Sanofi, and TG Therapeutics). EKH has received honoraria and grant support (Actelion, Biogen, Merck Serono, Novartis, Receptos, Roche, Sanofi, and Teva), and support (Ministry of Education of Czech Republic [PROGRES Q27/LF1]). CCL has received compensation for consulting (Acorda Therapeutics, Bayer, Biogen, Cephalon, EMD Serono, Novartis, Pfizer, Questcor, Sanofi, Strativa, Teva, and UCB). TZ has received consulting and/or speaking fees (Almirall, Bayer, Biogen, Merck, Novartis, Roche, Sanofi, and Teva) and grant/research support (Biogen, Novartis, Sanofi, and Teva). BVW has received advisory board and/or speaking fees (Almirall, Biogen, Merck, Novartis, Roche, and Sanofi); research support (Biogen, Merck, Novartis, and Sanofi), and contracted research (PI) (Biogen, Merck, Sanofi, Novartis, and Roche). SGM has received honoraria for lecturing, travel expenses for attending meetings, and financial research support (Almirall, Amicus Therapeutics, Bayer HealthCare, Biogen, Celgene, Diamed, HERZ Burgdorf, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi, and Teva). DHM and EMP were employees of Sanofi during study conduct and analysis, and may hold shares and/or stock options in the company. DPB is an employee of Sanofi and may hold shares and/or stock options in the company. PAS has received grant research support (Novo Nordisk). The adjudicators (CMD, BL, and PAS), and IM and SG who assisted CMD), received no compensation for review of the cases reported in this study.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 FINANCIAL DISCLOSURE: The authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest SEM reports non-financial support from Merck for congress participation. SRH, SB, MRM, MBH and SC have nothing to disclose. MRvE has received speaker honoraria from Merck. FS has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche and Sanofi Genzyme. His laboratory has received research support from Biogen, Merck, Novartis, Roche and Sanofi Genzyme. JRC has received speaker honoraria from Biogen.
 The authors declare that they have no conflict of interest.
 Disclosure: Sreelakshmi Panginikkod declares no relevant financial relationships with ineligible companies. Disclosure: Appaji Rayi declares no relevant financial relationships with ineligible companies. Disclosure: Franklyn Rocha Cabrero declares no relevant financial relationships with ineligible companies. Disclosure: Lokesh Rukmangadachar declares no relevant financial relationships with ineligible companies.

 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer MF declared a past co-authorship with the author EC to the handling editor AF-C.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare that they have no competing interests.
 All authors do not have any conflict of interest.Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article
 AR is a Chief Science Officer for Cognitive Leap, a virtual reality company. NC is on an Advisory Board for Akili Interactive and is a member of the Editorial Boards of Multiple Sclerosis Journal and Frontiers in NeuroTrauma. JD is an Associate Editor of the Archives of Physical Medicine and Rehabilitation; received compensation for consulting services and/or speaking activities from Biogen Idec, Bristol Myers Squibb, MedRhythms, and Novartis; and receives research support from Biogen Idec, the National Multiple Sclerosis Society, Consortium of Multiple Sclerosis Centers, Bristol Myers Squibb, Roche Genentech, The National MS Society of Canada and the National Institutes of Health. AG is co-founder, shareholder, BOD member, and advisor for Akili Interactive. RB is the recipient of a National Multiple Sclerosis Society Harry Weaver Award. She has received research support from the National Multiple Sclerosis Society, the National Science Foundation, the NIH, and DOD. She has also received research support from Biogen, Novartis, and Roche Genentech. She has received personal compensation for consulting from Alexion, Biogen, EMD Serono, Jansen, Novartis, Roche Genentech, Sanofi Genzyme, and TG Therapeutics. Cognitive Leap Inc. provided the Virtual Reality Attention Tracker (VRAT) system used during the study. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 No potential conflict of interest relevant to this article was reported.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: MAT received research funding support from Biogen; consulting fees for medical advisory boards from Alexion, Biogen, Genentech, and TG Therapeutics; and speaker fees from Genentech. SV received lecturing fees, travel grants, and research support from Biogen, BMS-Celgene, Janssen, Merck, Novartis, Roche, Sandoz, Sanofi-Genzyme, and Teva. MS and AG employees of and held stock/stock options in Biogen at the time of this work. IB and SL are employees of and hold stock/stock options in Biogen. PW received funding for travel and honoraria (for lectures and advisory boards) from Biogen, Celgene/BMS, Janssen-Cilag, Merck, Novartis, Roche, Sandoz, Sanofi-Genzyme, and Teva.
 The authors declare no conflict of interest.

 None



 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: We declare that we have financial and personal relationships with other people or organizations that can inappropriately influence our work, there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of, the manuscript entitled, “Managing cognitive impairment and its impact in multiple sclerosis: An Australian multidisciplinary perspective”

 No potential conflict of interest was reported by the authors.
 The authors have declared that no competing interests exist.

 The authors have declared that no competing interests exist.
 Sarah A. Morrow has served as an advisory board member or received consulting fees from Biogen Idec, Bristol Myers Squibb/Celgene, EMD Serono, Novartis, Roche, Sanofi Genzyme and Teva Neurosciences; has participated in a speaker’s bureau for Biogen Idec, Bristol Myers Squibb/Celgene, EMD Serono, Novartis, Roche and Sanofi Genzyme; has received research support from Biogen Idec, EMD Serono, Novartis, Roche and Sanofi Genzyme; and has participated as a site investigator in clinical trials sponsored by Bristol Myers Squibb/Celgene, EMD Serono, Novartis, Roche and Sanofi Genzyme. Nektaria Alexandri is an employee of the healthcare business of Merck KGaA, Darmstadt, Germany. Paola Kruger has received honoraria for advisory boards and/or speaker honoraria from the healthcare business of Merck KGaA, Darmstadt, Germany and Roche. Dawn Langdon has participated in speaker bureau for Almirall, Bayer, Biogen, Excemed, the healthcare business of Merck KGaA, Darmstadt, Germany, Novartis, Roche, Sanofi and TEVA; has had consultancy from Bayer, Biogen, the healthcare business of Merck KGaA, Darmstadt, Germany, Novartis, Sanofi and TEVA; has had research grants from Bayer, Biogen, the healthcare business of Merck KGaA, Darmstadt, Germany and Novartis. The authors report no other potential conflicts of interest for this work.
 MB is a certified MS specialist RDN and has a private practice providing nutrition education for people living with MS. AO reports that he received personal compensation for participation in scientific advisory boards, steering committees, and/or for speaking engagements from Alexion Pharmaceuticals, Banner Life Sciences, Biogen, Biologix, Bristol Myers Squibb, Celgene, EMD Serono, Genentech, GW Pharma, Horizon therapeutics, Jazz Pharma, Novartis (local and global), Sanofi/Genzyme, Sandoz pharmaceuticals, TG therapeutics, and Viela Bio. Consultant fee for serving as a scientific reviewer for Exploration-Hypothesis Development Award (EHDA) peer review panel of the 2020 Multiple Sclerosis Research Program (MSRP) for the Department of Defense Congressionally Directed Medical Research Programs (CDMRP). Honoraria from CMSC, Medscape, WebMD, and MJH Life Sciences for Educational Activities. AO serves as a site PI for studies funded (directly paid to MCW) by National MS Society/PCORI; Atara biotherapeutics, Biogen, Bristol Myers Squibb, Celgene, CorEvitas, LLC, EMD Serono, Genentech, GW pharma, Immunic, Sanofi/Genzyme, Novartis, Roche. AO received research funds from Central for Immunology, Research Affairs Committee, Neuroscience Research Center, Clinical and Translational Science Institute (CTSI), and the National Institutes of Health. AO serves on the editorial board of the International Journal of MS Care. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Dr. Wilson received funding from the National Multiple Sclerosis Society for a clinical fellowship in multiple sclerosis. Dr. Howard received funding from the National Multiple Sclerosis Society for a clinical fellowship in multiple sclerosis and has received funding from Novartis and Genentech. Dr. Dennis has no relevant disclosures. Ms. Taylor has no relevant disclosures. Dr. Gorman has received institutional funding for POMS clinical trials from Biogen and Roche / Genentech and institutional funding for research unrelated to POMS from Pfizer. Dr. Benson received funding from NIH, Harvard Medical School Shore grant, ROHHAD Fight, Inc. She received honoraria from Novartis. She participated in clinical trials with Biogen, Alexion and Genentech/Roche.

 The authors declare that they have no competing interests.
 The authors report no competing interests.
 The authors declare no conflict of interest.
 The other authors report no conflicts of interest related to the contents of the manuscript.

 The authors declare that they have no conflicts of interest.
 The authors report no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.
 Competing interests: None declared.

 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article
 Sarah Wilson, Fabien Rollot, Mathieu Fauvernier, Laurent Remontet, Laure Tron, Marc Debouverie, Jérôme de Sèze, Thibault Moreau, Christine Lebrun Frenay, Pierre Labauge, Jean Pelletier and Olivier Dejardin report no disclosures. Floriane Calocer: received funding for the present research from the ARSEP foundation for a Postdoctoral Fellowship (payment to the institution), from the “Réseau Bas-Normand pour la SEP” for a Postdoctoral Fellowship (payment to the institution), from the Regional Council of Normandy (payment to the institution), from the Ecole Doctorale of Caen University for a training in LSHTD to conduct this research (payment to the institution). She received support for attending meetings and/or travel from the ARSEP Foundation (paid directly to herself, unrelated to this work). Sandra Vukusic: received grants or contracts (paid to her university hospital) from Biogen, BMS-Celgene, Janssen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva; received consulting fees from Biogen, BMS-Celgene, Janssen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva (paid to her university hospital); received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Biogen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva (paid to her university hospital); received support for attending meetings and/or travel from Biogen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva, participated on a Data Safety Monitoring Board or Advisory Board for Biogen (contracts with her university hospital), all of the above unrelated to this work. Emmanuelle Le Page: received payment or honoraria for consulting or lectures from Biogen, Merck, Teva, Sanofi-Genzyme, Novartis Alexion; received research support from Teva and Biogen, and received academic research grants from PHRC and LFSEP, and a travel grant from the ARSEP Foundation; received payment for consulting from Biogen, Merck, Sanofi-Genzyme, and Novartis; received invitations for national and international congresses from Biogen, Merck, Sanofi-Genzyme, Novartis Alexion, all of the above unrelated to this work. Jonathan Ciron: participated on a Data Safety Monitory Board of Advisory Board with Biogen, Novartis, Merck, Sanofi, Roche, Alexion and BMS-Celgene (all unrelated to this work). Aurélie Ruet: Consultancy fees from Roche and Biogen, payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Merck, Roche, Biogen, research grants (paid to the institution) from Roche, Biogen and Sanofi-Genzyme, and support for attending meetings and/or travel from Biogen, Novartis and Alexion, all of the above unrelated to this work. Hélène Zephir: received research support for one PhD student from Roche, and research support for one MD student from FHU Imminent, consulting fees from Biogen IDEC (Symposium Biogen Idec in ISNI congress); received payment or honoraria for lectures from Merck, received payment or honoraria for lectures and boards from Novartis, all of the above unrelated to this work. David-Axel Laplaud: received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Biogen, Merck, Alexion, BMS, Roche and Novartis, all of the above unrelated to this work. Pierre Clavelou: received consulting fees from Biogen, Janssen, Medday, Merck, Novartis, Roche, Sanofi-Genzyme and Teva Pharma; and support for attending meetings and/or travel from Sanofi-Genzyme, and participated on a Data Safety Monitoring Board or Advisory Board for Medday, Merck and Novartis. All of the above unrelated to this work. Eric Berger: received consulting fees from Novartis, Sanofi Aventis, Biogen, Genzyme, Roche and Teva Pharma; received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Novartis, Sanofi Aventis, Biogen, Genyme, Roche and Teva Pharma (all of the above unrelated to this work). Olivier Heinzlef: consulting fees from Bayer Schering, Merck, Teva, Genzyme, Novartis, Almirall and BiogenIdec, support for attending meetings and/or travel grants from Novartis, Teva, Genzyme, Merck Serono and Biogen Idec and other financial or non-financial interests from Novartis, Teva, Genzyme, Merck Serono and BiogenIdec (all of the above unrelated to this work). Eric Thouvenot: received grants or contracts from Novartis and Biogen (paid to the institution), consulting fees from Merck, Novartis, Biogen and Celgene (paid directly to himself); received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Merck, Novartis, Biogen, Celgene (paid directly to himself). All of the above unrelated to this work. Jean Philippe Camdessanché: received grants or contracts from CSL-Behring, Grifols, Laboratoire Français des Biotechnologies, consulting fees from Akcea, Alexion, Alnylam, Argenx, Bristol Myers Squibb, Laboratoire Français des Biotechnologies, Pfizer, UCB Pharma, SNF-Floeger, received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Akcea, Alexion, Alnylam, Argenx, Biogen, CSL-Behring, Genzyme, Grifols, Laboratoire Français des Biotechnologies, Merck-Serono, Natus, Novartis, Pfizer, UCB Pharma and Teva. Received support for attending meetings and/or travel from Akcea, Alexion, Alnylam, Argenx, Biogen, CSL-Behring, Genzyme, Grifols, Laboratoire Français des Biotechnologies, Merck-Serono, Natus, Novartis, Pfizer, Teva, SNF-Floeger, all of the above unrelated to this work. Emmanuelle Leray: received consulting fees from Alexion, Merck, Novartis, Roche and Biogen, received payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Sanofi Genzyme, and received support for attending meetings and/or travel from Sanofi Genzyme, all of the above unrelated to this work. Gilles Defer Received research grants (paid to institution) from Biogen, Merck Serono, Novartis, Sanofi Genzyme; payment for speaker honoraria from Biogen, Merck Serono, Novartis, Sanofi Genzyme, Teva Pharmaceuticals, BMS; funding for travel from Biogen, Merck Serono, Novartis, Sanofi Genzyme, Teva Pharmaceuticals; and personal compensation for scientific advisory boards from Biogen, Merck Serono, Novartis, Sanofi Genzyme, Teva Pharmaceuticals, and BMS. All of the above unrelated to this work.
 DO received personal compensation for consulting and advisory services from Alexion, Biogen, Celgene/Bristol Myers Squibb, EMD Serono, Genentech, Genzyme, Janssen Pharmaceuticals, Novartis, Osmotica Pharmaceuticals, RVL Pharmaceuticals, Inc., TG Therapeutics, and research support from Biogen, Novartis, and EMD Serono/Merck. DO has issued national and international patents along with pending patents related to other developed technologies. DO received royalties for intellectual property licensed by The Board of Regents of The University of Texas System. BZ receives research funding from the NIH (U54 AG044170) and is supported by the Mayo Clinic Eugene and Marcia Applebaum Award. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Maya Zeineddine has received honororia for lectures from Biologix, Biogen, Janssen, Hikma Pharmaceuticals, Novartis, Merck, Roche and Sanofi-Genyme. She received travel grants from Novartis, Merck and Roche and a research grant from Biogen. She has no conflict of interest related to this study. Amal Al-Hajje declares that there is no conflict of interest. Pascale Salameh declares that there is no conflict of interest. Anne Helme and Michael Gunnar Thor declare the following: Multiple Sclerosis International Federation (MSIF) is an alliance of national multiple sclerosis (MS) organizations. MSIF receives income from a wide range of sources, including healthcare and other companies, individuals, member organizations, campaigns, foundations and trusts. Over the last 5 years, MSIF received funding from the following companies: Biogen, BristolMyersSquibb, Coloplast, Janssen, Merck, Mylan, Novartis, Roche and Sanofi – all of which is publicly disclosed. MSIF has not received any funding from industry for its access to medicines work in 2019, 2020, 2021 or 2022. Farid Boumediene declares that there is no conflict of interest. Bassem Yamout has received speaker honoraria from Bayer, Biogen, Merck, Novartis, Roche and Sanofi; research grants from Bayer, Biogen, Merck, Novartis and Pfizer; and advisory board honoraria from Bayer, Biogen, Merck, Novartis, Roche and Sanofi. He has no conflict of interest related to this study.


 The authors declare no conflict of interest.

 The authors declare that they have no financial conflict of interest with regard to the content of this report.
 Conflict of interest: The authors declared that there is no conflict of interest.
 Declaration of Competing Interest There is no conflicts of interest.


 No conflict of interest was declared by the authors.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: C.V.B. declared leadership position with University of South Florida, patents holder and patent applications on stem cell biology and its therapeutic applications, consultant to a number of stem cell–based companies, and research funding from the NIH. All the other authors declared no potential conflicts of interest.

 CC has received honoraria for speaking from Bayer and research funding from Novartis and Alexion, unrelated to this study. CC is a member of the Standing Committee on Science for the Canadian Institutes of Health Research (CIHR). The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Cortnee Roman and Denise Bruen have consulted for Novartis Pharmaceuticals Corporation.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 FB has received travel support from Biogen and a travel grant from the European Committee for Treatment and Research in Multiple Sclerosis. YF has received travel support from Biogen and receives grant support from MS Research Australia, National Health and Medical Research Council of Australia, Australia and New Zealand Association of Neurologists, and Avant Foundation. HB served on scientific advisory boards for Biogen, Novartis and Sanofi-Aventis and received conference travel support from Novartis, Biogen and Sanofi Aventis, and serves on steering committees for trials conducted by Biogen and Novartis received research support from Merck, Novartis, and Biogen. VJ receives research grant support from MS Research Australia and the National Health and Medical Research Council of Australia (NHMRC 1156519). AV has received travel support and served on advisory boards for Novartis, Biogen, Merck Serono, Roche and Teva, and receives grant support from the National Health and Medical Research Council of Australia. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.

 CS and RK hold international patents on work discussed in this manuscript. This work has been licensed to ATARA Biotherapeutics. They consult to ATARA Biotherapeutics on their EBV T‐cell immunotherapy programme. RK is also appointed to the Scientific Advisory Board of Atara Biotherapeutics.
 UP received speaker fee from Merck, Biogen and Bayer and personal compensation from Biogen and Roche for consulting service. RH has received travel compensation from Celgene and Sanofi. HI received speaker fee from Roche. TZ reports consulting or serving on speaker bureaus for Biogen, Celgene, Roche, Novartis, Celgene Merck and Sanofi as well as research support from Biogen, Novartis, Merck and Sanofi. KA reports consulting or serving on speaker bureaus for Roche, Sanofi, Merck, Alexion, Teva, Biogen, BMS and Celgene for consulting service. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Disclosure: Arezou Babaesfahani declares no relevant financial relationships with ineligible companies. Disclosure: Tushar Bajaj declares no relevant financial relationships with ineligible companies.
 The authors declare no conflict of interest.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest All authors have declared no competing financial interests.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.






 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: C.C.N. received personal fees for scientific oral communications and participated in trials with Novartis, Biogen, and Sanofi. I.M. has participated in trials with Roche, Janssen, Novartis, and Merck, and received conference sponsorship from Sanofi and other Multiple Sclerosis companies. The remaining authors have no potential conflicts of interest to declare.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict-of-interest statement: Vesic K, Gavrilovic A, Mijailović RN declare no conflict of interest. Borovcanin MM has received research funding from Ministry of Science and Technological Development of the Republic of Serbia (No. 175069).
 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer OS declared a past co-authorship with the author GFW to the handling editor.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 None declared.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: AB: personal compensation from Merck Serono, Biogen, Novartis, TEVA, Roche, Sanofi/Genzyme, Celgene/Bristol Myers Squibb, Janssen, Sandoz/HEXAL; grants for congress travel and participation from Biogen, TEVA, Novartis, Sanofi/Genzyme, Merck Serono, Celgene, Janssen. MC declares that there is no conflict of interest. SF: speaker’s and/or scientific board honoraria and/or travel grants from Biogen, Bristol Myers Squibb, Celgene, Janssen, Merck, Novartis, and Roche. His research is funded by Ruhr-University Bochum, Deutsche Multiple Sklerose Gesellschaft, Stiftung für therapeutische Forschung, Lead Discovery Center GmbH, and Novartis. JK: personal compensation from Merck Serono, Biogen, Novartis, TEVA, Roche, Sanofi/Genzyme, Celgene/Bristol Myers Squibb, and Janssen. RP: honoraria for lectures and travel grants from Alexion, Bayer Healthcare, Biogen, Bristol Myers Squibb/Celgene, Horizon, Janssen-Cilag, MedDay Pharmaceuticals, Merck, Novartis, Roche, Sanofi Genzyme, Sanofi-Aventis, and Teva. He received research funding from HERZ Burgdorf, Merck, and Novartis. TS: honoraria for lectures and travel grants from Alexion, Alnylam Pharmaceuticals, Bayer Vital, Biogen, Celgene, Centogene, CSL Behring, Euroimmun, Janssen, Merck Serono, Novartis, Pfizer, Roche, Sanofi, Siemens, Sobi, and Teva. His research is funded by Alnylam Pharmaceuticals, Bristol Myers Squibb Foundation for Immuno-Oncology, Claudia von Schilling Foundation, CSL Behring, Else Kröner Fresenius Foundation, Hannover Biomedical Research School (HBRS), Internal funding of the MHH (HilF), Novartis, Sanofi Genzyme, VHF Stiftung. SGM: Honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer Health Care, Biogen, Bristol Myers Squibb/Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, Ono Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research, Bundesinstitut für Risikobewertung, Deutsche Forschungsgemeinschaft, Else Kröner Fresenius Foundation, Gemeinsamer Bundesausschuss, German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Research Muenster, German Foundation Neurology, and Alexion, Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, HERZ Burgdorf, Merck Serono, Novartis, Ono Pharma, Roche, and Teva.


 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


 The authors have no conflict of interest to declare.
 The authors declare there is no conflict of interest.
 All enrolled authors had no conflict of interest.
 The authors declare no conflict of interest.

 The authors have declared no competing or potential conflicts of interest



 Conflict of interest None.

 Declaration of Competing Interest Glen M. Doniger is an employee of NeuroTrax Corporation. The authors declare no other potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest None.
 M.G., E.Z., A.F. and U.M. declare no conflict of interest except those that may potentially be related to their employer. A.D. has received personal compensation and travel grants from Biogen, Celgene, Janssen, Roche and Sanofi for speaker activity. T.W. has received honoraria from several pharmaceutical/consultancy firms, e.g., Novo Nordisk, Roche, Abbvie, Merck, GSK, BMS, Bayer, and Boehringer Ingelheim. T.Z. has received consulting fees, grants, and research support from various pharmaceutical companies, e.g., Almirall, Bayer, Biogen, Genzyme, Merck, Novartis, Roche, Sanofi, and Teva.
 Conflict of Interest: The authors stated that they have no conflicts of interest regarding the publication of this article.
 D.B., G.P. and D.L.S. have filed patents on VSN16, and related compounds, in relation to symptomatic and neuroprotective activities in MS and other diseases. Although not considered relevant, G.G. and D.B. have received funds for meetings presentations and as consultants for most companies within the MS-related disease modifying drugs, including Abbvie, Bayer, Biogen, Johnson & Johnson, Merck, Novartis, Roche, Sanofi-Genzyme, Siphon, Teva.
 The authors declare no conflict of interest.


 D.J. and N.B. have nothing to disclose. F.Q., V.G., A.K. and K.L. are employees of Octave Bioscience. M.R. received research funding from the National Multiple Sclerosis Society, Department of Defense and National Institute of Neurological Diseases and Stroke. M.G.D. received compensation from Keystone Heart for consultant fees. He received financial support for research activities from Bristol Myers Squibb, Mapi Pharma, Keystone Heart, Protembis and V-WAVE Medical. B.W.-G. received honoraria for serving in advisory boards and educational programmes from Biogen Idec, Novartis, Genentech, Genzyme and Sanofi, Janssen, Abbvie and Bayer. She also received support for research activities from the National Institutes of Health, National Multiple Sclerosis Society, Department of Defense, Biogen Idec, Novartis, Genentech, Genzyme and Sanofi. R.Z. has received personal compensation from Bristol Myers Squibb, EMD Serono, Sanofi, Keystone Heart, Protembis and Novartis for speaking and consultant fees. He received financial support for research activities from Sanofi, Novartis, Bristol Myers Squibb, Octave, Mapi Pharma, Keystone Heart, Protembis and V-WAVE Medical.
 The author declares no conflict of interest.



 The authors declare that they have no conflict of interest.
 Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 P.G. declares no conflict of interest. R.D. has received payments to her institution, including grants from Biogen, Merck, Celgene, National MS Society, MS Society UK, Horne Family Trust, and the BMA Foundation and honoraria from Biogen, Janssen, Merck, Novartis, Roche, Sanofi, and Teva; she has participated on an advisory board for Biogen, Janssen, Merck, Novartis, and Roche and received support for attending meetings or travel from Biogen, Janssen, Merck, Novartis, Roche, and Sanofi, outside the submitted work.
 The authors declare no conflict of interest.
 No conflict of interest was declared by the authors.
 The authors declare that they have no competing interests.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.

 The authors declare no conflict of interest.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.



 Conflict of interests The authors have declared that no competing interests exist
 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 The authors declare the following competing interests: Ellen Skorve has received initial funding for this study through an unrestricted research grant from Novartis (project planning and inclusion phase). Øivind Torkildsen has received speaker honoraria from and served on scientific advisory boards for Biogen, Sanofi-Aventis, Merck, and Novartis. Kjell-Morten Myhr has received unrestricted research grants to his institution, scientific advisory board or speaker honoraria from Biogen, Merck, Novartis, Roche, and Sanofi; and has participated in clinical trials organized by Biogen, Merck, Novartis, Roche, and Sanofi. All other authors report no competing interests.

 MB has received speaker honoraria from Novartis. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 GJ is the data custodian for HOLISM study, and the author of “Overcoming Multiple Sclerosis” and co-editor of “Overcoming Multiple Sclerosis Handbook. Roadmap to Good Health”. SN is a co-editor of “Overcoming Multiple Sclerosis Handbook. Roadmap to Good Health”. GJ and SN receive royalties from aforementioned authored publications, have previously received remuneration from facilitation of Overcoming MS residential workshops. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare that they have no financial conflict of interest.Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
 FINANCIAL DISCLOSURE: The authors declare no conflicts of interest.

 The authors declare no conflict of interest.
 Competing interests: LA has received speaker honoraria and/or travel compensation for activities with Biogen, Novartis, Bayer Schweiz AG, Teva, Merck, Sanofi Genzyme, Roche, Celgene and the Swiss MS Society (SMSG). CZ received honoraria for speaking, consulting fees, grants or travel compensation from Abbvie, Almirall, Biogen Idec, Celgene, Genzyme, Lilly, Merck Serono, Novartis, Roche, Teva Pharma. OF has received honoraria for lectures and advisory boards as well as research and travel support from Biogen, Novartis, Almirall, Bayer Schweiz AG, Teva, Merck, Sanofi Genzyme, Roche and the Swiss MS Society (SMSG). CPK has received honoraria for lectures as well as research support from Biogen, Novartis, Almirall, Bayer Schweiz AG, Teva, Merck, Sanofi Genzyme, Roche, Celgene and the Swiss MS Society (SMSG). SM received speaker honoraria and/or travel compensation for activities with Bayer Schweiz AG, Biogen, Celgene, Teva, Merck-Serono, Sanofi Genzyme, Novartis, Roche and Almirall and the Swiss MS Society (SMSG).J. Kuhle received speaker fees, research support, travel support from, and/or served on advisory boards for Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Progressive MS Alliance, Bayer, Biogen, Bristol Myers Squibb, Celgene, Merck, Novartis, Octave Bioscience, Roche, and Sanofi. AL received financial compensation and/or travel support for lectures and advice from Almirall, Biogen Idec, Bayer, Celgene, Genzyme, Merck Serono, Novartis, Roche Teva. A Lutterotti is a co-founder of Cellerys and co-inventor on a patent held by the University of Zurich on the use of peptide-coupled cells for treatment of MS.C. Gobbi received honoraria for speaking, consulting fees, grants or travel compensation from Abbvie, Almirall, Biogen Idec, Celgene, Genzyme, Lilly, Merck Serono, Novartis, Roche, Teva Pharma. CV was an employee of Biogen Switzerland at the time of the study. EV-B is an employee of Biogen International. KN has served on advisory boards for Biogen, Novartis, Bayer Schweiz AG, Teva, Merck, Sanofi Genzyme, Roche, Celgene and the Swiss MS Society (SMSG).
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare they have no conflict of interest.

 Declaration of interests The authors declare no competing interests.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 There are no conflicts of interest.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 Declaration of Competing Interest Statistical support was funded by Sanofi. No other conflict of interest relating to this manuscript.

 Jennifer Massey and Ian Sutton have received honoraria from Biogen, Roche, Sanofi Genzyme, Merck and Teva.
 The authors declare no conflict of interest.
 Competing interests: None declared.


 Conflict of interest The authors declare that there are no conflicts of interest.
 Disclosure: Dac Teoli declares no relevant financial relationships with ineligible companies. Disclosure: Franklyn Rocha Cabrero declares no relevant financial relationships with ineligible companies. Disclosure: Travis Smith declares no relevant financial relationships with ineligible companies. Disclosure: Sassan Ghassemzadeh declares no relevant financial relationships with ineligible companies.
 The authors declare no conflict of interest.



 Absent.

 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Conflicts of Interest No potential conflict of interest relevant to this article was reported.
 Conflict of interestThe authors have no conflicts of interest to disclose.
 Elena Grebenciucova: Advisory board member for Alexion, Genentech, Horizon Therapeutics, Prevail Therapeutics; research support from F. Hoffman-La Roche Ltd. Thomas Shoemaker: Advisory board member for Genentech and Genzyme, Speakers bureau for Biogen and Genentech. Edith Graham: Advisory board member for EMD Serono, Genentech, Horizon Therapeutics, and Novartis; research support from F. Hoffman-La Roche Ltd. Archit Baskaran has no disclosures.
 Conflicts of Interests: The Authors declare that there are no competing interests.
 Jussi Sipilä has received consultancy fees (Medaffcon) and holds shares (Orion Corporation).
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Dr Ralf Gold has received research support and speaker’s honoraria from Bayer Schering, Biogen, Bristol Myers Squibb, Chugai, Eisai, Janssen, Merck Serono, Nikkiso Pharma, Novartis, Roche, Sanofi Genzyme and TEVA; and consulting honoraria from ZLB Behring, Baxter, Merck, MIMS and Talecris. He holds personal stock options in Bayer, Merck, Novartis and Roche. Dr Michael Barnett has received institutional support for research or speaking from Alexion, Biogen, Merck, Roche, BMS and Sanofi Genzyme; is Research Director, Sydney Neuroimaging Analysis Centre and Research Consultant, RxMx. Dr Andrew Chan has received speakers’/board honoraria from Actelion (Janssen/Johnson & Johnson), Alexion, Almirall, Bayer, Biogen, Bristol Myers Squibb (Celgene), Genzyme, Merck KGaA (Darmstadt, Germany), Novartis, Roche and Teva, all for hospital research funds. Beyond this project, Dr Huiyu Feng has no further disclosures. Dr Kazuo Fujihara serves as an advisor or on scientific advisory boards for Biogen, Mitsubishi Tanabe, Novartis, Chugai/Roche, Alexion, VielaBio/Horizon Therapeutics, UCB, Merck Biopharma, Japan Tobacco and AbbVie; has received funding for travel and speaker honoraria from Biogen, Eisai, Mitsubishi Tanabe, Novartis, Chugai, Roche, Alexion, VielaBio, Teijin, Asahi Kasei Medical, Merck and Takeda and has received the Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan and the Grants-in-Aid for Scientific Research from the Ministry of Health, Welfare and Labour of Japan. In the last 2 years, Dr Gavin Giovannoni has received compensation for serving as a consultant or speaker for or has received research support from AbbVie, Aslan, Atara Bio, Biogen, Bristol Myers Squibb (Celgene), GlaxoSmithKline, Janssen/J&J, Japan Tobacco, Jazz Pharmaceuticals, LifNano, Merck & Co, Merck KGaA/EMD Serono, Moderna, Novartis, Sanofi and Roche/Genentech. In the last 5 years, Dr Giovannoni has received grant support for research from Biogen, Merck KGaA/EMD Serono, Novartis, Sanofi, Roche/Genentech and Takeda. Dr Xavier Montalbán has received speaking honoraria and travel expenses for participation in scientific meetings, has been a Steering Committee member of clinical trials or participated in advisory boards of clinical trials in the past years with AbbVie, Actelion, Alexion, Biogen, Bristol Myers Squibb (Celgene), EMD Serono, Genzyme, Hoffmann-La Roche, Immunic Therapeutics, Janssen, MedDay, Merck, Mylan, Nervgen, Novartis, Sandoz, Sanofi Genzyme, Teva Pharmaceuticals, TG Therapeutics, Excemed, Multiple Sclerosis International Federation and National Multiple Sclerosis Society. Beyond this project, Dr Fu-Dong Shi has no further disclosures. Dr Mar Tintoré has received compensation for consulting services, speaking honoraria and research support from Almirall, Bayer Schering Pharma, Biogen-Idec, Genzyme, Janssen, Merck Serono, Novartis, Roche, Sanofi-Aventis, Viela Bio and Teva Pharmaceuticals and participates on the Data Safety Monitoring Boards for Parexel and UCB Biopharma. Beyond this project, Dr Qun Xue has no further disclosures. Beyond this project, Dr Chunsheng Yang has no further disclosures. Beyond this project, Dr Hongyu Zhou has no further disclosures.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 We have no competing interests to declare.
 The authors declare no conflict of interest.

 GM has served on advisory boards for Genentech-Roche, Novartis, Mercks, and Biologix, received speaker fees from Biologix, Mercks, and Novartis, and participated in educational activities for Neurology Live and John Hopkin’s e-Litterature Review. CL has served on scientific advisory boards and/or as speaker for EMD-Serono, Biogen, Bristol-Myers Squibb, Roche, Novartis, Actelion, FindTx and Sanofi-Genzyme and has received a Grant for Multiple Sclerosis Innovation from Merck/EMD-Serono. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The other authors declare no conflicts of interest.

 Declaration of Competing Interest A/Prof Yasmine Probst is a person living with MS and is funded by Multiple Sclerosis Australia for a research fellowship. Miss Sarah Manche has no declarations of interest.
 James Close has nothing to disclose. Jo Vandercappellen and Miriam King were employees of Novartis Pharma AG at the time of manuscript preparation. Jeremy Hobart has received consulting fees, honoraria, support to attend meetings or research support from Acorda, Asubio, Bayer Schering, Biogen Idec, F. Hoffmann-La Roche, Genzyme, Merck Serono, Novartis, Oxford PharmaGenesis, and Teva.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest None.

 The authors declare no conflict of interest.
 The authors have declared that no competing interests exist.



 The authors declare no competing interests.
 Competing interests: None declared.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of competing interest None of the authors has anything to declare.
 Declaration of Competing Interest None.



 There are no conflicts of interest.
 The authors declare that the research will be conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflicts of interest.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.

 The authors have declared that no competing interests exist.
 FINANCIAL DISCLOSURES: The other authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.

 There are no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest None declared.
 Declaration of Competing Interest The authors declare that there is no conflict of interest.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors declare that there are no conflicts of interest, financial or otherwise.
 Alice Laroni has received personal compensation for public speaking and advisory boards from F. Hoffman-La Roche and Bristol-Myers Squibb. Trishna Bharadia has also recieved honoraria from Blue Latitude Health, Curatio, University College London, MS International Federation, Future Science Group, Savvy Cooperative, WEGO Health, Prime Global, Eyeforpharma, Professional Record Standards Body, DOD D&I, Queen Mary University London, Merck, The Method, Clara Health, The Conference Forum, Greenphire, Hollister, Medable, Oxford Health Polict Forum, College of Contemporary Health, Pfizer, Bristol-Myers Squibb, UCB, Medidata, Talking Medicines, Pivot Digital, NHS England and Sandoz; and Pieter van Galen has received honoraria from Johnson & Johnson.
 EK is employed by NVIDIA Corporation, Singapore. DW, GZ, YL, KK, LL, JY, C-CS, AN, and CW are employees at Sydney Neuroimaging Analysis Centre. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 There are no conflicts of interest.



 AI has received consultancy honoraria from Janssen. CP has served on scientific advisory boards for Novartis, Merck, Biogen, Sanofi, Genzyme, Teva, and Actelion; received funding for travel and speaker honoraria from Biogen, Teva, Sanofi Genzyme, Actelion, and Novartis; received research support from Biogen, Teva, Novartis, and Genzyme. SR has received honoraria from Biogen, Merck Serono, Novartis, Roche, Bristol Myers Squibb, Sanofi Genzyme, Viatris for consulting services, speaking and/or travel support. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 Competing interests: AIC: received speaker honoraria from Bayer Healthcare, Biogen and Teva and sponsorship for congress participation and travel grants from Teva; MT: is employed in a project funded by a grant from the Innovation Fund of the Federal Joint Committee, NT: has received a grant from the Innovation Fund of the Federal Joint Committee; ST: received speakers honoraria from Bayer Healthcare and Biogen as well as payment for manuscript writing from HEXAL AG; RG: has received speaker honoraria and research support from Bayer-Schering Healthcare, Biogen-Idec Germany, Chugai, Eisai, Merck Serono, Nikkiso Pharma, Novartis, Roche, Sanofi-Genzyme, and TEVA, has received consulting honoraria from CSL Behring, Baxter, Janssen and Talecris and has stock options in Bayer, Merck and Roche; KH: has received speaker honoraria and research support from Bayer, Biogen, Merck, Novartis, Sanofi-Genzyme, Roche and Teva, has received support for congress participation from Bayer, Biogen, Merck, Roche, Sanofi Genzyme and Teva, and has served on scientific advisory boards for Bayer, Biogen, Sanofi, Teva, Roche, Novartis, Merck.
 O.S. declares the following potential conflict of interest with respect to the research, authorship and/or publication of the article: O.S. has received in the past 3 years fees from F. Hoffmann-La Roche, Merck, Sanofi, Celgene/Receptos, Immunic, Roche/Genentech, Teva Pharmaceuticals and a personal compensation fee for lectures from Novartis, Immunic, Sanofi Genzyme, F. Hoffmann-La Roche, EMD Serono. A.C. and O.K. declare no conflict of interest.

 Conflict of interest: The authors declare that there are no conflicts of interest.
 The Authors declare that there is no conflict of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that there is no conflict of interest.
 Declaration of Competing Interest The authors have no conflicts of interest to declare.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 MB and JB were employed by Sigmovir Biosystems, Inc. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors declare no conflict of interest.
 All authors have no potential conflict of interest to report.
 FINANCIAL DISCLOSURES: Dr Fritz serves on the MS scientific advisory board for Helius Medical. The other authors declare no conflicts of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.

 The authors report no conflicts of interest in this work.
 FINANCIAL DISCLOSURES: Dr Villwock has a patent pending for olfactory testing and training methods (AROMA, Affordable Rapid Olfaction Measurement Array). The other authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 The authors have declared that no competing interests exist.
 There are no conflicts of interest.
 Declaration of Competing Interest LB has received unrestricted research grants from Sanofi, and advisory board honoraria from Sanofi, Merck and Biogen CSS has received unrestricted research grants from Sanofi and Novartis, and advisory board and/or speaker honoraria from Sanofi, Merck, BMS, Novartis and Biogen HØF has received unrestricted research grants from Biogen and Novartis, and advisory board and/or speaker honoraria Sanofi, Merck and Biogen PBH has received funding for travel or speaker's fees from Novartis, UCB, Biogen, Teva and Sanofi. HO has no conflicts of interest. CB has no conflicts of interest. EGC has received unrestricted research grants from Sanofi, and advisory board and/or speaker honoraria from Biogen, BMS, Janssen, Merck, Novartis, Roche, Sanofi and Teva.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Declaration of Competing Interest The author(s) declared no potential conflicts of interest concerning the research, authorship, and publication of this article.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.





 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.

 H.K. is affiliated with Orchid Pharmed Company, which is a partner of NanoAlvand Company in conducting clinical trials. However, H.K.’s contribution to this study was independent and not influenced by any potential conflicts of interest. The remaining authors declare no conflicts of interest.
 The authors declare no conflict of interest. G.T.M. received personal compensation from Serono, Biogen, Novartis, Roche, and TEVA for public speaking and advisory boards.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: TT and AB were employees of Evidera, who were paid by Actelion Pharmaceuticals Ltd, now a Janssen Pharmaceutical Company of Johnson & Johnson, for work on this study. TS is employee of Actelion Pharmaceuticals Ltd, a Janssen Pharmaceutical company of Johnson & Johnson, and may hold stock in Johnson & Johnson. NB and BH are employees of Actelion Pharmaceuticals Ltd, a Janssen Pharmaceutical company of Johnson & Johnson. BL is an employee of Janssen Research and Development, LLC. BL, BH, and NB are stockholders in Johnson & Johnson and have a portfolio that at times includes other pharmaceutical and healthcare-related companies. APB is a director of Innovus Consulting Ltd and holds a stock portfolio that at times includes pharmaceutical and healthcare-related companies. RF has received personal consulting fees from AB Science, Biogen, Celgene, EMD Serono, Genentech, Genzyme, Greenwich Biosciences, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics. RF has served on advisory committees for AB Science, Biogen, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics, and received a clinical trial contract and research grant funding from Biogen, Novartis, and Sanofi.
 The authors declare no conflict of interest.
 The author(s) declared the following potential conflicts of interest: CC-M has received support for attending congresses from Bristol Myers Squibb Sanofi, Merck, and Novartis. MP has received academic funding support from Merck. RR-C has received compensation for consulting services and speaking fees from Biogen, Novartis, Bayer, Merck, Sanofi, Genzyme, Teva, and Almirall. GÁ-B has received academic support from Merck, Sanofi, Biogen, Teva, and Novartis. LR-T has received compensation for consulting services and speaking fees from Biogen, Novartis, Bayer, Merck, Sanofi, Genzyme, Roche, Bristol Myers Squibb, Teva, and Almirall. JG has received speaking fees from Novartis, Teva, Sanofi, and Merck. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no competing interests.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 FINANCIAL DISCLOSURES: Dr Weiss was an employee of Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA, during the development of this article. Dr Su is an employee of Novartis. Ms Fleming has received consultancy fees from Novartis (independent of the submitted work). Messrs Leong and Sweitzer declare no conflicts of interest.
 Declaration of Competing Interest The authors declare that there are no conflicts of interest.
 Conflict of interest The authors declared no conflict of interest.
 The authors declare that M. Filippi is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Associate Editor of Radiology, and Associate Editor of Neurological Sciences; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bris-tol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Bio-gen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. M.A. Rocca received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono SpA, Novartis, Roche, and Teva. She receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders. The other authors have no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors report no conflicts of interest.
 Declaration of Competing Interest None.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.
 Declaration of Competing Interest None.
 F.P. has received honoraria and research support from Alexion, Bayer, Biogen, Chugai, MerckSerono, Novartis, Genzyme, MedImmune, Shire, Teva and serves on scientific advisory boards for Alexion, MedImmune and Novartis. M.M.S. serves on the editorial board of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation, Eurostars-EUREKA, ARSEP, Amsterdam Neuroscience, MAGNIMS and ZonMW and has served as a consultant for or received research support from Atara Biotherapeutics, Biogen, Celgene/Bristol Meyers Squibb, Genzyme, MedDay and Merck. N.S., S.K., S.P.K., T.B., D.S.B., D.L.S. and C.F. have no competing interests.
 RL and MC received financial compensation for attendance to expert meetings as part of an educational programme by Merck Serono S.p.A., Rome, Italy, an affiliate of Merck. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest All authors have no conflict of interest to report.
 The authors declare that they have no competing interests.
 The researchers declare that there was no conflict of interest in the process of implementation, extraction and report of the findings of the present study.



 AK, MF, FH, and HM have no competing interests. AB has received consulting and/or speaker fees from Alexion, Bayer Healthcare, Biogen, Celgene, Novartis, Roche, and Sandoz/Hexal and his institution has received compensation for clinical trials from Alexion, Biogen, Merck, Novartis, Roche, and Sanofi Genzyme; all outside the presented work. BH has served on scientific advisory boards for Novartis; he has served as DMSC member or consultant for AllergyCare, Allergy Therapeutics, Polpharma, Sandoz, Biocon, and TG therapeutics; he or his institution has received speaker honoraria from Desitin; his institution received research grants from Regeneron for multiple sclerosis research. He holds part of two patents; one for the detection of antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis and one for genetic determinants of neutralizing antibodies to interferon.
 The authors declare no conflict of interest.
 WW and MP were employed by BD Center Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.





 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 FINANCIAL DISCLOSURES: Dr Wawrzyniak has participated in a focus group discussion with Alexion. The other authors declare no conflicts of interest.
 The authors have no conflicts of interest to disclose.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest None.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Conflict of Interest: The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 No potential conflict of interest was reported by the authors.

 The authors declare no conflict of interest.
 Conflict of Interest: The authors declared that there is no conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 AB received personal compensation from Merck Serono, Biogen, Novartis, TEVA, Roche, Sanofi/Genzyme, Celgene/Bristol Myers Squibb, Janssen, and Sandoz/HEXAL. He received grants for congress travel and participation from Biogen, TEVA, Novartis, Sanofi/Genzyme, Merck Serono, Celgene and Janssen. KS was employee of Novartis Pharma GmbH. The authors declare that this study received funding from Novartis Pharma GmbH. The funder was involved in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing financial interest or personal relationships that could have appeared to influence the work reported in this paper. This research did not receive any specific grants from funding agencies in the areas of public, commercial or charitable purposes.
 The authors declare that there is no conflict of interest.

 Conflict of Interest: The authors have no potential conflicts of interest to disclose.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 FINANCIAL DISCLOSURES: Ms McCormack is a speaker for EMD Serono, Biogen, and Genentech. Dr Mechtler has received personal compensation for consulting, serving on a scientific advisory board, speaking, research affiliation, or other activities from Alder Pharmaceuticals, Allergan, Amgen, Avanir, Biohaven, Boston Biomedical, Inc, CellDex, DelMar Pharmaceuticals, electroCore, Jushi, Novartis, Orbis Pharmaceuticals, Promius, and Teva Pharmaceuticals. Dr Mechtler also has a financial interest in Jushi. No Jushi products were used by patients in this study. The other authors declare no conflicts of interest.
 The authors certify that there are no conflict of interest with any financial organisation regarding the material discussed in the manuscript.
 The authors declare they have no conflict of interest.


 Declaration of Competing Interest The authors declare that they have no competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Jai Perumal has received fees from Acorda, Biogen, Genzyme, and Teva. Roumen Balabanov has received consulting fees from Biogen, Sanofi, and Teva and grant/research support from Biogen. Laura Balcer has received consulting fees from Biogen and Genzyme. Steven Galetta has received consulting fees from Biogen. Zhaonan Sun, Hanyue Li, Danette Rutledge, and Robin L. Avila are employees of and may hold stock and/or stock options in Biogen. Robert J. Fox has received personal consulting fees from AB Science, Biogen, Bristol Myers Squib, EMD Serono, Genentech, Genzyme, Greenwich Biosciences, Immunic, Janssen, Novartis, Sanofi, Siemens, and TG Therapeutics; has served on advisory committees for AB Science, Biogen, Immunic, Janssen, Novartis, and Sanofi; and received clinical trial contract and research grant funding from Biogen, Novartis, and Sanofi.
 MR-S received speaking or consulting honoraria, participated in scientific activities organized by Merck, Teva, Biogen, Novartis, Sanofi-Genzyme, Celgene, EXCEMED, and Roche, and was awarded the ECTRIMS MS Nurse Training Fellowship Programme and the Strategic Plan for Research and Innovation in Health 2016–2020 (PERIS). CC-M has received support for attending congresses from sanofi, merk, teva and novartis and is funded by a fellowship from the Departament de Salut de la Generalitat de Catalunya [SLT017/20/000115, 2021]. MA received speaking or consulting honoraria, participated in scientific activities in the last 2 years organized by Bristol-Myers Squibb/Celgene. XM received speaking honoraria and travel expenses for participation in scientific meetings, has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past years with Abbvie, Actelion, Alexion, Biogen, Bristol-Myers Squibb/Celgene, EMD Serono, Genzyme, Hoffmann-La Roche, Immunic, Janssen Pharmaceuticals, Medday, Merck, Mylan, Nervgen, Novartis, Sandoz, Sanofi-Genzyme, Teva Pharmaceutical, TG Therapeutics, Excemed, MSIF and NMSS. JS-G received speaking or consulting honoraria and attended scientific activities in the last 2 years organized by Merck, Teva, Bial, EXCEMED, Biogen, Celgene, Novartis, Sanofi-Genzyme, and Roche; and is the director of the “Revista de Neurologia” (Neurology Journal) and an editorial board member of the Multiple Sclerosis Journal. LR-T has received speaking or consulting honoraria, attended scientific activities organized by Merck, Teva, Biogen, Novartis, Sanofi, Roche, Bristol-Myers-Squibb, Almirall, and Mylan, and participated in advisory boards organized by Sanofi, Merck, Roche, Biogen, Novartis, Bristol-Myers-Squibb, and Almirall. PA-B, the coordinator of the Expert Patient Program Catalunya. CC-M has received support for attending congresses from Bristol Myers Squibb, Sanofi, Merck, and Novartis and is funded by a fellowship from the Departament de Salut de la Generalitat de Catalunya [SLT017/20/000115, 2021]. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors report no conflicts of interest in this work. Eleonora Cocco reports grants, personal fees, and non-financial support from Biogen and Merck; personal fees and non-financial support from Novartis; grants from Roche; and personal fees from Genzyme, outside the submitted work.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Dr Mette Louise Andersen reports grants from the Region of Southern Denmark, grants from the Jascha Foundation, and grants from the Consultant Schous Foundation, during the conduct of the study. The authors declare no competing interests.
 The authors declare that this study received funding from Merck KGaA. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Dr. Nawfal M. Sheaheed received speaker honoraria from Eli Lilly, Bayer, Merck, and Biologix FZCO. Dr. Murad Al-Naqshbandi is an employee of Merck KGaA Middle East Ltd., an affiliate of Merck KGaA, Darmstadt, Germany. Prof. Rieckmann has received honoraria for lectures from Allmiral, Apple Healthcare, Bayer, Biogen, Boehringer-Ingelheim, Celgene, Daiichi Sankyo, Genpharm, Medtronic, Merck-Serono, NeuroPlasticity Consulting, Novartis, Pfizer, Roche, Sanofi, Siemens AG, and Teva; research grants from Teva, Oberfranken-Stiftung, German Neurology Foundation, Red Bull, and hpCosmos; and advisory board or steering committee fees from Bayer Biogen Novartis, Merck-Serono, Teva, German Multiple Sclerosis Society, and Canada Drug Review.
 None
 Declaration of Competing Interest The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Lawrence Steinman has issued patents and an ongoing application on DNA vaccines for tolerance to myelin antigens, including GlialCAM. Lawrence Steinman also has patent filings regarding antivirals for the treatment of MS. Lawrence Steinman is the principal investigator at Stanford University in the ATA188 trial with a cell‐based therapy for progressive MS. William Robinson and Tobias Lanz have patent filings relevant to these studies.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 None.

 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: N.F. received travel funds for research meetings from Novartis. M.H. received speaking fees and travel funds from Bayer HealthCare, Biogen, Merck Serono, Novartis and Teva. U.K.Z. received speaking fees, travel support and financial support for research activities from Alexion, Almirall, Bayer, Biogen, Bristol Myers Squibb, Janssen, Merck Serono, Novartis, Octapharma, Roche, Sanofi Genzyme, Teva and EU, BMBF, BMWi and DFG. M-C.H., S.E.L., P.M., J.L.D., B.S., J.B. and F.H. declare no competing interests.

 Declaration of Competing Interest The authors declare no conflicts of interest with the manuscript. The funding source had no influence on the study design, collection, analysis, and data interpretation. The funding source was not involved in the decision to publish.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Shin Yee Chey, Niamh-Anna O'Sullivan, Trevor Beer, and Wai K Leong have no disclosures. Allan Kermode has in recent times received speaker honoraria and Scientific Advisory Board fees from Bayer, BioCSL, Biogen-Idec, Merck, Novartis, Roche, Sanofi-Aventis, Sanofi-Genzyme, Teva, NeuroScientific Biopharmaceuticals, Innate Immunotherapeutics, and Mitsubishi Tanabe Pharma.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 None

 Competing interests: VP has received research funding from Novartis (Oppenheim Förderpreis 2017). AB has received consulting and/or speaker fees from Alexion, Biogen, Celgene, Horizon, Novartis, Roche and Sandoz/Hexal. His institution has received compensation for clinical trials from Alexion, Biogen, Merck, Novartis, Roche, and Sanofi Genzyme. JSK has received research funding from the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG; project 432290010), the German Federal Ministry of Education and Research (13GW0469D) and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (101045128—iBack-epic—ERC-2021-COG). He is Co-Founder of Bonescreen. BH has served on scientific advisory boards for Novartis; he has served as DMSC member for AllergyCare, Sandoz, Polpharma, Biocon and TG therapeutics; his institution received research grants from Roche for multiple sclerosis research. He has received honoraria for counseling (Gerson Lehrmann Group). He holds part of two patents; one for the detection of antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis and one for genetic determinants of neutralising antibodies to interferon.
 The authors declare no conflict of interest.

 The authors have declared no conflict of interest.

 Competing interests: HMB, ACN, K-EB, ISJ, CN, DKH, MVMH, KM and WR have nothing to disclose. RB received research support from Biogen, Roche Genentech and Novartis; personal consulting fees from Alexion, Biogen, EMD Serono, Novartis, Roche Genentech and Sanofi Genentech; and funding from Harry Weaver Award from the National Multiple Sclerosis Society and the National Institutes of Health. SZ received consulting honoraria from Alexion, Biogen-Idec, EMD-Serono, Genzyme, Novartis, Roche/Genentech and Teva Pharmaceuticals, Inc, and served on data safety monitoring boards for Lilly, BioMS, Teva and Therapeutics. JJS received research support from Novartis. TS received travel grants from Biogen, Merck, Novartis and Roche, and research grants from Biogen, and served on advisory boards for Biogen, Merck and Novartis. FN served on advisory boards for Sanofi and received travel grants from Sanofi and Merck.
 The authors declare no competing interests.

 The authors declare no conflict of interest.

 None declared.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.

 The authors declare that they have no competing interests.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.




 Declaration of Competing Interest Ichiro Nakashima has received speaker honoraria and travel funding from Novartis Pharmaceuticals, Mitsubishi Tanabe Pharma, Biogen Japan, and received research support from LSI Medience Corporation.
 The authors report no conflicts of interest.

 The authors declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: A.H., B.I.O., M.M., A.Be., U.M., A.W., M.Bu., M.Bo., K.K., I.G., H.S., B.W., L.G. and D.S. declare that there is no conflict of interest. J.S.K. is Co-Founder of Bonescreen GmbH. C.G. reports funding from the German Research Foundation (Deutsche Forschungsgesellschaft DFG), the Hertie Foundation, the Hans and Klementia Langmatz and the German Federal Ministry of Education and Research, all of which are not related to this study. A.Ba. reports personal compensation from Merck Serono, Biogen, Novartis, TEVA, Roche, Sanofi/Genzyme, Celgene/Bristol Myers Squibb, Janssen, Sandoz/HEXAL; grants for congress travel and participation from Biogen, TEVA, Novartis, Sanofi/Genzyme, Merck Serono, Celgene and Janssen. None related to this report. M.S. has received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Bristol Myers Squibb, Merck, Roche and Sanofi Genzyme. She has received travel support from Celgene and TEVA. She has received research funding from the Hertha-Nathorff-Program. None of this related to this study. M.C.K. has served on advisory boards and received speaker fees/travel grants from Merck, Sanofi/Genzyme, Novartis, Biogen, Jansen, Alexion, Celgene/Bristol Myers Squibb and Roche. M.K. also received research grants from Merck, Sanofi/Genzyme and Celgene/Bristol Myers Squibb, Novartis and Janssen, all not related to this study. J.H. reports grants for OCT research from the Friedrich-Baur-Stiftung and Merck, personal fees and nonfinancial support from Celgene, Horizon, Janssen, Bayer, Merck, Alexion, Novartis, Roche, Biogen and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work. J.H. is partially funded by the German Federal Ministry of Education and Research [(DIFUTURE), grant numbers 01ZZ1603[A-D] and 01ZZ1804[A-H]]. B.H. has served on scientific advisory boards for Novartis; he has served as DMSC member for AllergyCare, Polpharma, Sandoz and TG therapeutics; he or his institution have received speaker honoraria from Desitin; his institution received research grants from Regeneron for multiple sclerosis research. B.H. holds part of two patents; one for the detection of antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis and one for genetic determinants of neutralizing antibodies to interferon. All of B.H.’s conflicts are not relevant to the topic of the study. B.H. received funding from the Multiple MS EU consortium, the Clinspect-M consortium funded by the Bundesministerium für Bildung und Forschung and the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy – ID 390857198).
 The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Absent.

 The authors declare no conflict of interest.
 The authors declare no conflict of interest.




 Declaration of Competing Interest The authors have no conflicts of interest to disclose.
 Dr. Aparasu has received research funding from Astellas Inc., Incyte Corp., Gilead, and Novartis Inc. for projects unrelated to the current work. Dr. Hutton reports grants from Biogen, Novartis, MedImmune, Hoffman-LaRoche, E.M.D. Serono, Sanofi, and personal fees from Novartis, Sanofi, Celgene outside the submitted work. The other authors declare no conflicts of interest for this article.
 The authors declare no conflict of interest. The funder of the project (Research Administration, Kuwait university) had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results, however funder of APC is the corresponding author.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare that there is no conflict of interest and competing interests regarding the publication of this article.

 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 There are no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Authors declare that they have no conflicts of interest
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest Dr. Huang owns stock in Longeviti. Dr. Bettegowda is a consultant for DePuy-Synthes, Bionaut Labs, Galectin Therapeutics, Privo Technologies, and Haystack Oncology; and is the co-founder of OrisDX. Dr. Lim is a consultant for Tocagen, VBI, InCephalo Therapeutics, Pyramid Bio, Merck, BMS, Insightec, Biohaven, Sanianoia, Hemispherian, Black Diamond Therapeutics, Novocure, Noxxon, and Stryker; receives research support from Arbor, BMS, Accuray, Tocagen, Biohaven, Kyrin-Kyowa, and Urogen; and owns stock in Egret Therapeutics.




 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.




 There are no conflicts of interest.
 FINANCIAL DISCLOSURE: The authors declare no conflicts of interest.

 HT and HH have filed an international patent application on “Polysialic acid and derivatives thereof, pharmaceutical composition and method of producing Polysialic acid,” WO2020025653A2. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 MK has received consulting fees from Biogen Idec, Genentech, Janssen Pharmaceuticals, Novartis, OptumRx, and TG Therapeutics on topics unrelated to this manuscript. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest Authors declare no conflict of interest.



 The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.
 The authors declare no conflict of interest.
 The authors declare no competing interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 L.B. has received payment for teaching qigong since 2005 but was not an instructor in this trial. The other authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: I.C.G. became employed by Biogen following her contributions to this research. S.Y.H. has received consulting fees and research grants from Siemens Healthineers. E.C.K. has received consulting fees from Banner Life Sciences, Galen/Atlantica, Genentech, Greenwich Biosciences and OM1, and research funds from Abbvie, Biogen, and Genentech. Other authors report no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Declaration of Competing Interest None.

 Conflict of interest The authors declare that they have no competing interest.
 The authors declare no conflict of interest.
 The authors have no conflicts of interests to declare.


 The authors declare no conflict of interest.


 LL, GF, JF, GC, and EC received honoraria for consultancy or speaking from Biogen, Novartis, Sanofi, Genzyme, Serono and Teva and Almirall. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no conflicts of interest.
 The authors declare no conflict of interest.
 TW personally follows and promotes the Wahls™ diet. She has equity interest in the following companies: Terry Wahls LLC; TZ Press LLC; The Wahls Institute, PLC; FBB Biomed Inc; and the website: http://www.terrywahls.com. She also owns the copyright to the books Minding My Mitochondria (2nd Edition) and The Wahls Protocol, The Wahls Protocol Cooking for Life, and the trademarks The Wahls Protocol® and Wahls™ diet, Wahls Paleo™ diet, and Wahls Paleo Plus™ diets. She has completed grant funding from the National Multiple Sclerosis Society for the Dietary Approaches to Treating Multiple Sclerosis Related Fatigue Study. She has financial relationships with BioCeuticals Ltd., MCG Health LLC, Vibrant America LLC, Standard Process Inc., MasterHealth Technologies Inc., Foogal Inc., Genova Diagnostics Inc., and the Institute for Functional Medicine. She receives royalty payments from Penguin Random House. TW has conflict of interest management plans in place with the University of Iowa and the Iowa City Veteran's Affairs Medical Center. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Competing interests: K-MM received speaker honoraria from Biogen, Novartis, Roche and Sanofi, and has participated in clinical trials organised by Biogen, Merck, Novartis, Roche and Sanofi.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Competing Interests: The authors have declared that no competing interest exists.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationshipsthat could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest MP discloses travel/meeting expenses from Novartis, Roche and Merck, speaking honoraria from HEALTH&LIFE S.r.l., honoraria for consulting services from Biogen and research grants from Baroni Foundation. A. Carotenuto has received research grants from ALMIRALL, and honoraria from Novartis, Merck and Biogen. M. Moccia has received research grants from the ECTRIMS-MAGNIMS, the UK MS Society, and Merck, and honoraria from Biogen, Merck, Novartis and Roche. S. Bucello has served on scientific advisory boards for Biogen Idec, Roche, Merck Serono, Novartis, Celgene and Sanofi-Genzyme and has received funding for travel and/or speaker honoraria from Sanofi-Genzyme, Biogen Idec, Teva, Merck Serono and Novartis. MI received compensation for consulting services and/or speaking activities from Biogen Idec, Merck-Serono, Novartis, Roche, Sanofi Genzyme; received research support from NIH, NMSS, the MS Society of Canada, the Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, H2020 EU Call. M. Clerico received personal compensations for advisory boards, public speaking, editorial commitments or travel grants from Biogen Idec, Merck Serono, Fondazione Serono, Novartis, Roche, Sanofi-Genzyme and Teva. LM received personal compensations for speaking in scientific meeting and for advisory boards and for travel grants from Celgene, Novartis, Biogen, Merck, Roche and Sanofi. LL received speaker honoraria and travel grants from Teva, Merck, Sanofi, Novartis, Biogen, Roche and Bayer. MF is Editor-in-Chief of the Journal of Neurology, has received compensation for consulting services and/ or speaking activities from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries, and receives research support from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla and ARiSLA (Fondazione Italiana di Ricerca per la SLA). GB received fees for consultation and Advisory board from Biogen, Almirall, Novartis, Merck, Teva, Roche and Sanofi Genzyme. CP received consulting and lecture fees and research funding and travel grants from Almirall, Bayer, Biogen, Gen- zyme, Merck Serono, Novartis, Roche and Teva. VBM has received research grants from the Italian MS Society, and Roche, and honoraria from Bayer, Biogen, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. RL has received honoraria from Biogen, Merck, Novartis, Roche, and Teva. Other authors have nothing to disclose.

 Competing Interests: The authors have no potential conflict of interest, financial or otherwise, to disclose.

 SD Cassard, SE Emrich, and D Pelletier have nothing to disclose. KC Fitzgerald reports research funding from NIH, NMSS, and the DoD. She has served on Data and Safety Monitoring Boards for trials funded by the NIH and NMSS, and has received honorarium for serving as an external thesis committee reviewer. P Qian reports research funding for this clinical trial. She has served on a Data and Safety Monitoring Board for a trial funded by Janssen and has received speaking honorariums from Biogen and Bristol Myers Squibb. EA Sugar reports receiving salary support from NIH funds for statistical assistance with the design, execution and analysis of this project. CJ Azevedo has received personal compensation for participation on advisory boards or data and safety monitoring boards for Horizon Therapeutics, Genentech, Sanofi Genzyme, and TG Therapeutics; she has received honoraria for participation in CME activities from Catamount Medical Education, American Academy of Neurology, Spire Learning, and Efficient LLC,; she has received payment for serving on a grant review committee from the Department of Defense and for serving on a data and safety monitoring board from Genentech; she receives grant support from the National Multiple Sclerosis Society and the National Institutes of Health. AD Goodman has received personal compensation for consulting from Genentech-Roche, Janssen, TG Therapeutics, Novartis, payment for expert testimony from EMD Serono, support for attending meetings from Biogen, payment for participation on a data and safety monitoring board from IMCYSE, and research support from Atara, Biogen, EMD Serono, and Sanofi Genzyme. E Waubant has participated in multicentre clinical trials funded by Genentech, Alexion and Biogen; she has current support from the NIH, NMSS, PCORI, CMSC and Race to Erase MS. She has received consulting fees from Emerald Pharmaceuticals, payments from Neurology Live and Yoga Moves MS, had support for attending the ACTRIMS 2022 and ECTRIMS 2022 conferences, volunteered on a data and safety monitoring board for a Novartis trial, chaired the International Women in Multiple Sclerosis (iWiMS) network (unpaid), and served as President-elect of ACTRIMS forum (unpaid). EM Mowry has received grant or research support from the National MS Society, Biogen, Genentech and Teva Neuroscience, has served on a data and safety monitoring board for an NIH trial and receives honoraria from UpToDate (editorial duties) and consulting fees from BeCare Link LLC.

 GSa received grants outside of this study, for speaking or consultancies from: Almirall, Biogen, Merck, Novartis, Roche, and Sanofi Genzyme. PR received grants outside of this study for speaking or consultancies from: Biogen, Bristoll-Myers-Squibb, Merck, Novartis, Roche, and Sanofi Genzyme. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Authors hold no conflict of interest and no grant was taken for the present study. Institutional ethical approval was obtained before carrying out the study.
 Conflicto de interés: Ninguno.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Declaration of Competing Interest A. Moreau reports no disclosure relevant to the manuscript; I. Kolitsi reports no disclosure relevant to the manuscript; L. Kremer reports no disclosure relevant to the manuscript; M.-C. Fleury reports no disclosure relevant to the manuscript; L. Lanotte reports no disclosure relevant to the manuscript; F. Sellal reports no disclosure relevant to the manuscript; C. Gaultier reports no disclosure relevant to the manuscript; G. Ahle reports grants from Biogen, grants from Novartis, grants from Roche, grants from Sanofi, grants from Abbvie, grants from Pfizer, grants from CSL Behring, outside the submitted work; S. Courtois reports no disclosure relevant to the manuscript; A. Fickl reports no disclosure relevant to the manuscript; S. Mostoufizadeh reports no disclosure relevant to the manuscript; C. Dentel reports no disclosure relevant to the manuscript; N. Collongues reports no disclosure relevant to the manuscript; J. de Seze reports no disclosure relevant to the manuscript; K. Bigaut has received lecturing fees and travel grants from Biogen, Celgene-BMS, Novartis, Roche, and Sanofi-Genzyme.


 Declaration of Competing Interest None.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Lasse Skovgaard has nothing to disclose. Philipp Trénel has nothing to disclose. Katrine Westergaard has nothing to disclose. Astrid Karnøe Knudsen has nothing to disclose.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Financial Disclosures: The authors declare no conflicts of interest.
 Declaration of Competing Interests The authors declare no conflict of interests
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.

 Declaration of Competing Interest This manuscript has not been published or presented elsewhere in part or in entirety, and is not under consideration by another journal. All study participants provided informed consent, and the appropriate ethics review boards approved the study design. All the authors have approved the manuscript and agree with submission to your esteemed journal and were fully involved in the study and preparation of the manuscript. There are no conflicts of interest to declare. This study is not funded by any institution or organization. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


 DM: Nothing to disclose. BB: Participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals. KL: Nothing to disclose. SL: Nothing to disclose. IA: Participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. TG: Participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals. MKS: received consultation and/or speaker fees from: Sanofi Genzyme, Roche. MH: Participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest The authors declared no potential conflicts of interest with respect to the research, authorship, and publication of this article.
 The authors declare no conflict of interest. A.M.L. has taken part in advisory boards for Sanofi, Merck, Novartis, and Biogen and has contributed with lectures or in pharmaceutical studies/received grants from Teva, Serono, Merck, and Novartis.

 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Dr. Pablo Herrero is the creator of the DNHS technique and teaches courses about this technique. The authors report no other conflicts of interest in this work.

 The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 Declaration of Competing Interest There is no conflict of interest
 Declaration of Competing Interest Authors declare that they have no conflict of interest.

 Competing interests: PP received speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb and Genzyme. He has received research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. MM reports grants and personal fees from Almiral. She was awarded a MAGNIMS-ECTRIMS fellowship in 2020. MF is Editor-in-Chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Neurological Sciences and Radiology; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. MAR received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from AstraZeneca, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Horizon Therapeutics Italy, Merck Serono SpA, Novartis, Roche, Sanofi and Teva. She receives research support from the MS Society of Canada, the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Daniel Kreiter, Audrey Merry, Romy Spee and Oliver Gerlach have nothing to disclose; Raymond Hupperts received institutional research grants and fees for lectures and advisory boards from Biogen, Merck and Genzyme-Sanofi.

 Declaration of Competing Interest Pr. S.P receive fees from Medtronic. CC, MBV, SF, SC-C and JPN have no conflicts to disclose.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: FC has received travel grants and/or speaking honoraria from Biogen, Merck, Sanofi-Genzyme, and Roche and research grants from Merck. The other authors have no conflicting interests to declare.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The authors declare no conflict of interest.

 The authors declare no conflict of interest.
 AZ, LS, PO, and RM were employed by Klinikum Bayreuth GmbH. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer GP declared a past co-authorship with the authors SS and MI to the handling editor.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 JH owns controlling interest in Connecting Health Innovations LLC (CHI), a company that has licensed the right to his invention of the dietary inflammatory index (DII®) from the University of South Carolina in order to develop computer and smart phone applications for patient counseling and dietary intervention in clinical settings. NS was employed by CHI. The subject matter of this manuscript will not have any direct bearing on that work, nor has that activity exerted any influence on this project. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 MW-H has served on scientific advisory board for Sanofi and has received honoraria for lecturing for Novartis and Sanofi. RH has served on scientific advisory board for Novartis and has received honoraria for lecturing for Novartis and Sanofi. FS has served on scientific advisory boards for, served as consultant for, received support for congress participation or received speaker honoraria from Alexion, Biogen, Bristol Myers Squibb, H. Lundbeck A/S, Merck, Novartis, Roche and Sanofi Genzyme. His laboratory has received research support from Merck, Novartis, Roche, and Sanofi Genzyme. MM has served in scientific advisory board for Sanofi, Novartis, Merck, and has received honoraria for lecturing from Biogen, Merck, Novartis, Roche, Sanofi Genzyme, and Bristol Myers Squibb. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Elisabetta Signoriello received personal compensation from Almirall, Biogen, Genzyme, Novartis, and Teva for traveling and advisory boards. Giacomo Lus received personal compensation for activities with Biogen Idec, Merck Serono, Novartis, Sanofi-Aventis Pharmaceuticals, and Teva neuroscience as a consultant and speaker and received research support from Biogen Idec, Merck Serono, and Novartis. Matteo Foschi published opinions in a medical journal on other pharmaceuticals and received financial support for travel and meeting attendance from Biogen, Merck, Roche and Sanofi-Genzyme. Simona Bonavita received honoraria for public speaking and/or for advisory boards from Roche, Novartis, Teva, Sanofi-Genzyme, Merck Serono, and Biogen. Francesco Saccà received honoraria for public speaking and/or for advisory boards from Alexion, Almirall, Argenx, Avexis, Biogen, Forward Pharma, Merck, Mylan, Novartis, Pomona, Sanofi, Roche, and Teva. Maria Pia Sormani has received consulting fees from Biogen, Merck, Teva, Genzyme, Roche, Novartis, GeNeuro, and Medday. Alessio Signori received teaching honoraria from Novartis outside this work.
 Competing interests: EMS, EC, JC, JM and ZLEvK report no disclosures. JK received grants from Biogen, Novartis, TEVA, Bayer Schering Pharma, GlaxoSmithKline, Merck, Genzyme and Roche. PR received consulting and/or speaking honoraria from Alexion, Biogen, Celgene, Roche, Sanofi Genzyme, Viela and EMD Serono. JDB received honoraria from serving on the scientific advisory board and speaker’s bureau of Biogen, Celgene, EMD Serono, Genentech and Novartis. He has received research support from AbbVie, Alexion, Alkermes, Biogen, Celgene, Sanofi Genzyme, Genentech, Novartis and TG Therapeutics. GC served on data and safety monitoring boards: AstraZeneca, Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Horizon Pharmaceuticals, Hisun Pharmaceuticals, Mapi Pharmaceuticals, Merck, Merck/Pfizer, Opko Biologics, OncoImmune, Neurim, Novartis, Ophazyme, Sanofi-Aventis, Reata Pharmaceuticals, Teva Pharmaceuticals, VielaBio, Vivus, NHLBI (Protocol Review Committee), NICHD (OPRU oversight committee); consulting or advisory boards: Biodelivery Sciences International, Biogen, Click Therapeutics, Genzyme, Genentech, GW Pharmaceuticals, Immunic, Klein-Buendel Incorporated, Medimmune, Medday, Neurogenesis, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Recursion/Cerexis Pharmaceuticals, Roche, TG Therapeutics. GC is employed by the University of Alabama at Birmingham and President of Pythagoras, a private consulting company located in Birmingham, Alabama, USA. MK received consulting fees and travel support from Biogen, Novartis, Roche, Sanofi Genzyme and EMD Serono.
 JLMA was employed by Sanofi and hold shares and/or stock options in the company. SE received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi, Roche and Teva. RLR received speaker honoraria and/or consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi, Roche and Mylan. MÁC received speaker honoraria, research fundings and consultant fees from Biogen Idec, Novartis, Merck, Mylan, Bayer, Sanofi, Roche and Teva. JD received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, UCB, Sanofi, Roche, Almirall and Teva. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: MPA has served on Scientific Advisory Boards for Biogen, Novartis, Roche, Merck, Sanofi-Genzyme, and Teva; has received speaker honoraria from Biogen, Merck, Sanofi-Genzyme, Roche, Novartis, and Teva; has received research grants for her Institution from Biogen, Merck, Sanofi-Genzyme, Novartis, and Roche. She is a co-editor of the Multiple Sclerosis Journal and associate editor of Frontiers in Neurology. VBM has received honoraria from Almirall, Bayer, Biogen, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. DC is an advisory board member or has given advice to Almiral, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva; has received honoraria for speaking or consultation fees from Almiral, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva; is the principal investigator in clinical trials for Bayer Schering, Biogen, Merck Serono, Mitsubishi, Novartis, Roche, Sanofi-Genzyme, and Teva. His preclinical and clinical research was supported by grants from Bayer Schering, Biogen Idec, Celgene, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva. EC has served on scientific advisory boards from Bayer, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. NDS declares no conflict of interest. MF is the Editor-in-Chief of the Journal of Neurology and associate editor of Radiology, Human Brain Mapping and Neurological Sciences; received compensation for consulting services and/or speaking activities from Almiral, Alexion, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck Serono, Novartis, Roche, Sanofi, Almiral, Eli Lilly, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). CG has served on scientific advisory boards for Biogen, Novartis, Roche, Merck, and Sanofi-Genzyme and has received speaker honoraria from Biogen, Merck, Bayer, Sanofi-Genzyme, Roche, Novartis, Almiral, and Mylan. PG has been a consultant and member of advisory board for Biogen Italy, Sanofi, Merck, Almiral, Roche, and Novartis; has received funding for travel and speaker honoraria from Merck Serono, Biogen Idec, Sanofi, Novartis-Pharma, and Roche; has received research support from Bayer, Biogen Italy, Merk, Sanofi, Roche, and Novartis. CP is involved in scientific advisory boards for Alexion, Biogen, Roche, Merck, Novartis, Janssen, and Almiral; receives consulting and/or speaking fees from Alexion, Almiral, Biogen, Bristol Myers, Janssen, Roche, Merck, Novartis, and Biogen; and research support from Merck, Roche, Novartis, Biogen, Bristol Myers, and Almiral. MT has served on the scientific AB for Biogen, Novartis, Roche, Merck, BMS, and Genzyme; has received speaker honoraria from Biogen, Roche, Sanofi, Merck, Genzyme, Janssen, and Novartis; and has received research grants for her institution from Biogen, Merck, Novartis, and Roche.
 B.E.H. hold patents related to AAV gene therapy. All other authors declare no competing financial interest.
 There are no conflicts of interest.

 XF has received unrestricted research support from Bayer, Biogen, BMS, Mallinckrodt, Merck-Serono, and Novartis, which produce drugs for the treatment of MS, some of which are anti-CD20 therapies, and Roche-Genentech, which produces rituximab and ocrelizumab studied in this paper. AR has received unrestricted research support from Bayer, Biogen, BMS, Roche-Genentech, Mallinckrodt, Merck-Serono, and Novartis, and is a consultant for Bayer, Biogen, Merck-Serono, Novartis, Roche-Genentech, and TG therapeutics. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer DM declared a shared parent affiliation with the authors SB, AD, SaS to the handling editor at the time of review.



 Declaration of Competing Interest The authors declare that they have no competing interests.
 MM declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. ELP received honoraria for lectures or consulting from Biogen Idec, Merck Serono, Novartis, SanofiAventis, TEVA, Roche, Alexion. LM has received personal compensation for consulting, speaking or other activities with Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, Teva and BMS. EL has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Alexion, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme.

 Nicholas Young and Niels Bergsland have nothing to disclose. Robert Zivadinov has received personal compensation from Bristol Myers Squibb, EMD Serono, Sanofi, Keystone Heart, Protembis, and Novartis for speaking and consultant fees. He received financial support for research activities from Sanofi, Novartis, Bristol Myers Squibb, Octave, Mapi Pharma, Keystone Heart, Protembis, and V-WAVE Medical. None of the aforementioned interest had any role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. Michael G. Dwyer received compensation from Keystone Heart for consultant fees. He received financial support for research activities from Bristol Myers Squibb, Mapi Pharma, Keystone Heart, Protembis, and V-WAVE Medical. Bianca Weinstock-Guttman received honoraria for serving in advisory boards and educational programs from Biogen Idec, Novartis, Genentech, Genzyme and Sanofi, Janssen, Abbvie, and Bayer. She also received support for research activities from the National Institutes of Health, National Multiple Sclerosis Society, Department of Defense, and Biogen Idec, Novartis, Genentech, Genzyme, and Sanofi. Dejan Jakimovski and Niels Bergsland have nothing to disclose.
 SG-P has received speaker honoraria from Sanofi, Roche, Merck, and Biogen and has participated on Merck and Bristol Myers Squibb advisory boards. PN has receiver speaker and advising honoraria from MSD, Abbvie, Pfizer, Takeda, Janssen, Kern, Faes, Ferring, Tillots, Otsuka. The other authors have nothing to disclose. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors have nothing to declare.
 Declaration of Competing Interest The authors declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article. MLE is grateful for financial support from Lundbeckfonden (R347-2020-2454). TS has received travel grants from Biogen, Merck, Novartis, and Roche, has received research grants from Biogen and Roche, has served on advisory boards for Biogen, Merck, Novartis and Roche. ZI is grateful for financial support from Biogen (DK-BGT-11542), from Scleroseforeningen (A25341, A29926, A31829, A33600), University of Southern Denmark (14/24200), Odense University Hospital (5798002573633).
 The reviewer JB declared a shared affiliation, with no collaboration, with one of the authors, DB, to the handling editor at the time of the review. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Declaration of Competing Interest Q.A. and S.K are inventors of an Indian patent application “Cocrystals of dimethylfumarate with enhanced physio-chemical stability and biological activity” (Ref.No:202211055785, 28th September 2022). All other authors declare no conflict of interest.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 SS has received compensation for lectures and/or advisory board membership from Merck. LN has received honoraria for lectures and/or advisory board membership from Biogen, Novartis, Merck, and Teva. MA has received compensation for lectures and/or an advisory board membership from Biogen, Genzyme, and Novartis. IK was supported by a Horizon 2020 Multiple MS grant (No. 733161). TO has received unrestricted MS research grants, and/or lecture advisory board honoraria from Biogen, Novartis, Sanofi, and Roche. CM has received honoraria for lectures and advisory board memberships from Biogen, Merck, Novartis, and SanofiAventis. JL has received travel support and/or lecture honoraria from Biogen, Novartis, Teva, and Genzyme/ SanofiAventis; has served on scientific advisory boards for Almirall, Teva, Biogen, Novartis, and Genzyme/ SanofiAventis; serves on the editorial board of the Acta Neurologica Scandinavica; and has received unconditional research grants from Biogen, Novartis, and Teva. FA declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.





 Competing interests: WD has nothing to declare. SS has nothing to declare. FP received speaker honoraria and advisory board fees from Almirall, Bayer, Biogen, Celgene, Merck, Novartis, Roche, Sanofi-Genzyme and TEVA. He received research funding from Biogen, Merck, FISM (Fondazione Italiana Sclerosi Multipla), Reload Onlus Association and University of Catania. GI received speaking honoraria from Biogen, Novartis, Sanofi, Merck, Roche, Almirall and Teva. SE received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche and Teva. AP has nothing to declare. MG received consulting fees from Teva Canada Innovation, Biogen, Novartis and Genzyme Sanofi; lecture payments from Teva Canada Innovation, Novartis and EMD. He has also received a research grant from Canadian Institutes of Health Research. PD served on editorial boards and has been supported to attend meetings by EMD, Biogen, Novartis, Genzyme, and TEVA Neuroscience. He holds grants from the CIHR and the MS Society of Canada and has received funding for investigator-initiated trials from Biogen, Novartis, and Genzyme. MO has nothing to declare. AL has received personal compensation for consulting, serving on a scientific advisory board, speaking or other activities from Biogen, Merck Serono, Mylan, Novartis, Roche, Sanofi/Genzyme, Teva. Her institutions have receved research grants from Novartis [last 4 yrs]. SO has nothing to declare. OG has nothing to declare. CB received conference travel support from Biogen, Novartis, Bayer-Schering, Merck and Teva; has participated in clinical trials by Sanofi Aventis, Roche and Novartis. PG has served in advisory boards for Novartis, EMD Serono, Roche, Biogen idec, Sanofi Genzyme, Pendopharm and has received grant support from Genzyme and Roche, has received research grants for his institution from Biogen idec, Sanofi Genzyme, EMD Serono. MT received travel grants from Novartis, Bayer-Schering, Merck and Teva; has participated in clinical trials by Sanofi Aventis, Roche and Novartis. MPA received honoraria as consultant on scientific advisory boards by Biogen, Bayer-Schering, Merck, Teva and Sanofi-Aventis; has received research grants by Biogen, Bayer-Schering, Merck, Teva and Novartis. DS received honoraria as a consultant on scientific advisory boards by Bayer-Schering, Novartis and Sanofi-Aventis and compensation for travel from Novartis, Biogen, Sanofi Aventis, Teva and Merck. CR-T received research funding, compensation for travel or speaker honoraria from Biogen, Novartis, Genzyme and Almirall. DM received speaker honoraria for Advisory Board and travel grants from Almirall, Biogen, Merck, Novartis, Roche, Sanofi-Genzyme, and Teva. EC has nothing to declare. TK served on scientific advisory boards for BMS, Roche, Sanofi Genzyme, Novartis, Merck and Biogen, steering committee for Brain Atrophy Initiative by Sanofi Genzyme, received conference travel support and/or speaker honoraria from WebMD Global, Eisai, Novartis, Biogen, Sanofi-Genzyme, Teva, BioCSL and Merck and received research or educational event support from Biogen, Novartis, Genzyme, Roche, Celgene and Merck. KB received honoraria and consulting fees from Biogen, Teva, Novartis, Genzyme-Sanofi, Roche, Merck, CSL and Grifols. OS has nothing to declare. AvdW has nothing to declare. HB Institution (Monash university) has received compensation for consulting, talks, advisory/steering board activities from Biogen, Merck, Novartis, Genzyme, Alfred Health; research support from Novartis, Biogen, Roche, Merck, NHMRC, Pennycook Foundation, MSRA. HB has received compensation for same activities from Oxford Health Policy Forum, Merck, Biogen, Novartis. GI had travel/accommodations/meeting expenses funded by Bayer Schering, Biogen, Merck, Novartis, Sanofi Aventis, and Teva. AS has nothing to declare.
 Competing interests: The authors have no competing interests with respect to this research. The full disclosure statement is as follows: DLA reports consulting fees from Albert Charitable Trust, Alexion Pharma, Biogen, Celgene, Frequency Therapautics, Genentech, Med-Ex Learning, Merck, Novartis, Population Council, Receptos, Roche and Sanofi-Aventis, grants from Biogen, Immunotec and Novartis and an equity interest in NeuroRx. FB has received compensation for consulting services and/or speaking activities from Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, Genzyme, Synthon BV, Roche, Teva, Jansen Research and IXICO and is supported by the NIHR Biomedical Research Centre at UCLH. OC has received research grants from the MS Society of Great Britain & Northern Ireland, National Institute for Health Research (NIHR) University College London Hospitals Biomedical Research Centre, EUH2020, Spinal Cord Research Foundation and Rosetrees Trust. She serves as a consultant for Novartis, Teva and Roche and has received an honorarium from the American Academy of Neurology as Associate Editor of Neurology and serves on the Editorial Board of Multiple Sclerosis Journal. DC is a consultant for Hoffmann-La Roche. In the last 3 years, he has been a consultant for Biogen, has received research funding from Hoffmann-La Roche, the International Progressive MS Alliance, the MS Society, the Medical Research Council and the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre and a speaker’s honorarium from Novartis. He co-supervises a clinical fellowship at the National Hospital for Neurology and Neurosurgery, London, which is supported by Merck. AE has received speaker’s honoraria from Biogen and At The Limits educational programme. AE has received research grants from Medical Research Council, UK Research and Innovation’s Innovate UK, Biogen, UCL Innovation and Enterprise, Roche and Merck. AE serves on the Editorial Board of Neurology. He has received travel support from the National Multiple Sclerosis Society and honorarium from the Journal of Neurology, Neurosurgery and Psychiatry for Editorial Commentaries. AE and FB have equity stake in Queen Square Analytics. FP was funded by a Guarantors of Brain non-clinical Postdoctoral Fellowship. EC and JS have nothing to disclose.

 The authors report no conflicts of interest in this work.
 Yao-Chen Zhang, Ke-Yi Fan, Qi Wang, Jing-Xi Hu, Qian Wang, He-Yi Zhang, Shan Song, Rong Zhao, Jun Qiao, and Sheng-Xiao Zhang has nothing to disclose.
 Disclosure: Mari Ogino declares no relevant financial relationships with ineligible companies. Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.
 The authors declare that they have no competing interests.
 AS contracted Research with Sanofi, Biogen, Novartis, Actelion, Genentech/Roche. Consulting fees from Octave Bioscience. Research support from Bristol Myers Squibb. Personal compensation for consulting for Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, TG Therapeutics and OctavemBioscience. Personal compensation non-promotional speaking for EMD Serono. Participationin ma Data Safety and Monitoring Board for NCT03073603, and NCT04877457. MF received a grant from Sanofi-Genzyme Canada. Honoraria or consultation fees from Alexion/Astra Zeneca, BiogenIdec, EMD Inc./EMD Serono/Merck Serono, Find Therapeutics, Hoffman La-Roche, Novartis, Quanterix, Sanofi-Genzyme, Teva Canada Innovation. Member of a company advisory board or board of directors for Alexion/Astra Zeneca, Atara Biotherapeutics, Bayer Healthcare, Celestra Health, EMD Inc./Merck Serono, Find Therapeutics, Hoffman La-Roche, Actelion/Janssen (J&J), Novartis, Sanofi-Genzyme, Setpoint Medical. Participation in a company sponsored speaker's bureau: Sanofi-Genzyme, EMD Serono. PR contracted research with Biogen, Genentech, Novartis, Sanofi. Consulting honoraria: Banner, BristolMyersSquibb, EMD Serono, Genentech, Novartis, Sanofi, TG therapeutics. Speaker honoraria: Biogen, BristolMyersSquibb, Genentech, Novartis, Sanofi, TG therapeutics. OS serves on the editorial boards of Therapeutic Advances in Neurological Disorders, has served on data monitoring committees for Genentech-Roche, Pfizer, Novartis, and TG Therapeutics without monetary compensation, has advised EMD Serono, Novartis, and VYNE, receives grant support from EMD Serono, is a 2021 recipient of a Grant for Multiple Sclerosis Innovation (GMSI), Merck KGaA, is funded by a Merit Review grant (federal award document number (FAIN) BX005664-01 from the United States (U.S.) Department of Veterans Affairs, Biomedical Laboratory Research and Development, is funded by RFA-2203-39314 (PI) and RFA-2203-39305 (co-PI) grants from the National Multiple Sclerosis Society (NMSS). The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest: The authors declared that there is no conflict of interest.
 Competing interests: MaM has received research grants from the ECTRIMS-MAGNIMS, the UK MS Society and Merck; honoraria from Biogen, Ipsen, Merck, Roche and Sanofi-Genzyme. AC has received research grants from Almirall, research grants from ECTRIMS-MAGNIMS and honoraria from Almirall, Biogen, Roche Sanofi-Genzyme and Novartis. MP has received research grants from Italian MS Foundation and Baroni Foundation, honoraria from HEALTH&LIFE S.r.l. and Biogen and sponsorship for travel/meeting expenses from Novartis, Roche and Merck. RL has received honoraria from Biogen, Merck, Novartis, Roche and Teva. VBM has received research grants from the Italian MS Society, and Roche, and honoraria from Bayer, Biogen, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme and Teva.
 Lilyana Amezcua: advisory/consulting fees from EMD Serono, Genzyme, and Novartis; research support from Biogen and MedDay. Yang Mao-Draayer: consulting fees from Biogen, Celgene, EMD Serono, Genzyme, Novartis, Janssen, Horizon, and Roche-Genentech; contracted research for NIH NINDS R01-NS080821, NIAID Autoimmune Center of Excellence UM1-AI110557, Biogen, Chugai, Novartis, and Sanofi-Genzyme; speaker bureaus for Biogen and Teva. Wendy S. Vargas: advisory/consulting fees from Alexion, Biogen, Genentech, and Octapharma; research support from Teva. Rebecca Farber: Consulting fees for Alexion and Genentech; research grants from Novartis and Biogen; research support from NIH, grant number 2U19AI128949-06. Sara Schaefer: Consulting/advisory fees from Novartis, Biogen, and Genzyme; speaking fees from Biogen. Filipe Branco, Sarah M. England, Nicholas Belviso, James B. Lewin, Jason P. Mendoza, and Sai L. Shankar are employees and stockholders of Biogen.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Competing interests: AF-H has received unrestricted funding from Biogen Idec, Pfizer, Orion Pharma and Celltrion, speaking honoraria from Merck and consulting fee from Roche and AstraZeneca. KF has received honoraria for serving on advisory boards for Biogen and Merck KGaA, and speaker’s fees from Biogen, Novartis and Merck KGaA. JH has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis and Sandoz, and speaker’s fees from Biogen, Novartis, Merck, KGaA, Teva and Sanofi-Genzyme, and he has served as PI for projects, or received unrestricted research support from, Biogen, Celgene, Merck KGaA, Novartis, Roche and Sanofi-Genzyme. AML-G receives grant support and awards from the Patient Centered Outcomes Research Institute and the National MS Society; she currently serves as a voting member on the California Technology Assessment Forum, a core program of the Institute for Clinical and Economic Review (ICER); she has received sponsored and reimbursed travel from ICER and the National Institutes of Health. PN has received travel support from Bayer Schering Pharma, Merck Serono, Biogen and Genzyme a Sanofi Company, honoraria for lectures and advisory boards from Merck Serono and Genzyme a Sanofi Company, advisory boards for Novartis and Roche, lectures for Biogen and has received unrestricted grants from Biogen. JL has received travel support and/or lecture honoraria from Biogen, Novartis, Merck, Alexion, BMS, Celgene, Janssen and Sanofi Genzyme; has served on scientific advisory boards for Almirall, Teva, Biogen, Novartis, Merck, Roche, Sanofi Genzyme and BMS; serves on the editorial board of the Acta Neurologica Scandinavica; and has received unconditional research grants from Biogen and Novartis, and financial support from Sanofi for an investigator-initiated study. JS has received consultancy fees paid to the institution by Mabion S.A. FP has received research grants from Janssen, Merck KGaA and UCB, and fees for serving as Chair of DMC in clinical trials with Chugai, Lundbeck and Roche, and preparation of witness statement for Novartis. TO has received compensation for advisory boards/lectures and unrestricted MS research grants from Biogen, Merck, Novartis and Sanofi.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper
 The authors have no potential conflicts of interest to disclose.


 The authors declare no conflict of interest.
 V.C. has nothing to declare; M.M. has served on scientific advisory boards for Bayer Schering, Biogen, Sanofi-Genzyme, Merck Serono, Novartis, Teva, Mylan, Almirall, and has received consulting and/or speaking fees, research support, or travel grants from Alexion, Almirall, Bayer Schering, Biogen, Bristol-Myers-Squibb, Janssen, Sanofi-Genzyme, Merck, Novartis, Teva, and Roche; M.L. has received honoraria from Biogen, Merck Serono, Novartis, Roche, Sanofi-Genzyme, Almirall, Bristol-Myers-Squibb, and Bayer for consulting services, speaking fees, and/or travel support.

 Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-22-1317/coif). JD serves as an unpaid editorial board member of Quantitative Imaging in Medicine and Surgery. The other authors have no conflicts of interest to declare.
 Lita Araujo, Keiko Higuchi, and Nupur Greene are employees of Sanofi and may hold stock or stock options. Kristen G Bzdek was an employee of Sanofi at the time of the study. Srikanth Kyatham was an employee of Axtria at the time the study was conducted. Axtria was a paid consultant to Sanofi in relation to this project.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Jai Perumal has received fees from Acorda, Biogen, Genzyme, and Teva. Roumen Balabanov has received consulting fees from Biogen, Sanofi, and Teva and grant/research support from Biogen. Ray Su and Roger Chang were employees of Biogen at the time of these analyses and may hold stock and/or stock options in Biogen. Robin L. Avila, and Danette Rutledge are employees of and may hold stock and/or stock options in Biogen. Laura Balcer is editor-in-chief of the Journal of Neuro-Ophthalmology. Steven Galetta has received consulting fees from Biogen and Genentech. Robert J. Fox has received personal consulting fees from AB Science, Biogen, Celgene, EMD Serono, Genentech, Genzyme, Greenwich Biosciences, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; has served on advisory committees for AB Science, Biogen, Genzyme, Immunic, Janssen, Novartis, Sanofi, and TG Therapeutics; and has received clinical trial contract and research grant funding from Biogen, Novartis, and Sanofi.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors have no conflict of interest to declare.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Dr Peter Joseph Jongen reports he was a member of the Scientific Advisory Board of the Dutch National MS Foundation at the time of the study. Miss Petra Prinssen reports a grant from the Dutch National MS Foundation, during the conduct of the study. The authors have no other conflicting interests to declare that are relevant to this article.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Lisa Grech, Ernest Butler, and Michelle Allan received a research grant from Merck Pharmaceuticals, outside of the submitted work.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Brittney Lager and Jacob Liseno are employees of AcariaHealth. Ivan Božin, Sarah M. England, Sai L. Shankar, Jason P. Mendoza, and James B. Lewin are employees of and hold stock/stock options in Biogen.
 The authors declare no conflict of interest.


 The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare no conflicts of interest regarding the publication of this manuscript. This research was conducted in an ethical and responsible manner, and all potential conflicts of interest have been disclosed.
 The authors declare no conflict of interest.
 All coauthors are employees of Genentech, Inc., and shareholders of F. Hoffmann-La Roche Ltd.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Daniel Kantor has received consulting fees from Biogen, Bristol Myers Squibb, and Janssen. He has received research support from Bristol Myers Squibb. Timothy Pham, now employed at GSK, was an employee of Bristol Myers Squibb when the study was conducted and may be a shareholder in the company. Oscar Patterson-Lomba, Elyse Swallow, and Akanksha Dua are employees of Analysis Group, Inc., a consulting firm that received funding from Bristol Myers Squibb to conduct this research. Komal Gupte-Singh is an employee of Bristol Myers Squibb and may be a shareholder in the company.

 Declaration of Competing Interest M.H. participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. T.G. participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. G.L. declares that he is the founder and owner of Genos Glycoscience Ltd., which offers commercial service of glycomic analysis and has several patents in this field. I.G. is an employee of Genos Glycoscience Ltd. The other authors declare that there is no conflict of interest.
 Declaration of Competing Interest No competing interest.
 Paul Dillon was an employee of F. Hoffmann-La Roche Ltd, Basel, Switzerland during completion of the work related to this manuscript and has shares/ownership of F. Hoffmann-La Roche Ltd. Yanic Heer was an employee of PricewaterhouseCoopers (PwC), Zurich, Switzerland during completion of the work related to this manuscript. Eleni Karamasioti was an employee of PricewaterhouseCoopers (PwC), Zurich, Switzerland during completion of the work related to this manuscript. Erwan Muros-Le Rouzic is an employee of and shareholder in F. Hoffmann-La Roche Ltd, Basel, Switzerland. Giuseppe Marcelli is an employee of F. Hoffmann-La Roche Ltd, Basel, Switzerland. Danilo Di Maio is an employee of F. Hoffmann-La Roche Ltd, Basel, Switzerland. Stefan Braune received honoraria from Kassenärztliche Vereinigung Bayerns and health maintenance organizations for patient care, and from Biogen, Merck, NeuroTransData, Novartis, and Roche for consulting, project management, clinical studies, and lectures; he also received honoraria and expense compensation as a board member of NeuroTransData. Gisela Kobelt is president of EHE International GmbHan and employee of European Health Economics, Mulhouse, France. Jürgen Wasem is a professor for health services management at University Duisburg-Essen, Germany. He has received an honorarium for consulting study concept and quality assurance of data calculations.

 I have received research support from the National Institutes of Health, National MS Society, US Department of Defense, Sumaira Foundation, Brainstorm Cell Therapeutics, Bristol Myers Squibb, EMD Serono, I-Mab Biopharma, Mallinckrodt ARD, Novartis Pharmaceuticals, Octave Bioscience, Roche Genentech, Sanofi Genzyme, and Tiziana Life Sciences. I have also received consulting fees from Banner Life Sciences, Biogen, Bristol Myers Squibb, Janssen, Novartis Pharmaceuticals, Roche Genentech, Sanofi Genzyme, and UCB Biopharma.

 Competing interestsThere is no competing interest.

 The authors declare that they have no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 William L. Conte has received research funding from Novartis and Sanofi; consulting fees from AstraZeneca, Banner, Bayer, Biogen, Bristol Myers Squib, Genentech, Novartis, and Sanofi; and speaker fees from AbbVie, Alexion, Biogen, Bristol Myers Squib, EMD Serono, Genentech, Horizon, Janssen, Novartis, and Sanofi. Mark Cascione has received consulting fees from Biogen, EMD Serono, Genentech, Novartis, and Sanofi Genzyme; speaker fees from Acorda, Biogen, EMD Serono, Novartis, and Sanofi Genzyme; and grant support from Adamas, Biogen, Genentech, Novartis, and Sanofi Genzyme. Amy B. Sullivan has received consulting and speaker fees from Biogen, Bristol Myers Squibb, Genentech, and Novartis.
 Declaration of Competing Interest The authors declare no competing interests.
 The authors declare that they have no competing interest.

 Declaration of Competing Interest The authors declare that they have no conflicts of interest.
 Declaration of interests L.C. and J.H. are co-shareholders of Reelin Therapeutics, Inc. and coinventors of a patent related to anti-Reelin strategies (application 15/763,047 and publication 20180273637).

 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Declaration of Competing Interest The authors declare that they have no competing interests or conflicts of interest related to the content of this work. All authors have participated in the development and execution of the research and have contributed to the preparation and revision of the manuscript.

 Conflict of interest The authors declare no conflicts of interest with the contents of this article.
 The authors declare no conflict of interest.
 Declaration of competing interest The authors have no relevant conflict of interest to disclose.
 None
 C.C.H., J.H.E., A.J., and P.D.M. declare that they have no competing interests. I.H., J.S., and J.H. obtained financial support from Biogen for conducting this study. J.Z., B.Z., and M.M. are employees of Biogen and hold stocks from the company.
 Anza B. Memon M.D. has received an honorarium from Horizon Therapeutics for advisory board participation for management of Neuromyelitis Optica Spectrum Disorder.



 The authors declare no conflict of interest.
 The authors declare no competing financial interest.

 The authors declare no competing interests.



 Marc Bigaud, Pamela Ramseier, Sarah Tisserand, Meike Lang, Beatrice Urban, Christian Beerli and Goril Karlsson are employees of Novartis, except for Christian Beerli who has since retired, and all author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 JI is employed by Omnion Research International Ltd The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Competing interests: None declared.



 The authors declare no competing interests.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest No authors report conflicts of interest.

 The authors declare no competing interests.
 Declaration of Competing Interest The authors have no conflicts of interest to declare.
 The authors declare no competing interests.
 No potential conflict of interest was reported by the authors.
 Disclosure: Shirin Ghanavatian declares no relevant financial relationships with ineligible companies. Disclosure: Armen Derian declares no relevant financial relationships with ineligible companies.

 The authors declare no conflict of interest.
 Competing interests: MD has financial and intellectual property interests in and holds employment by Adaptive Sensory Technology. MAF has received honoraria as speaker and for consultation from Biogen, Lundbeck, Merck KGaA, Novartis and Roche. His research is funded by the Bundesministerium für Bildung und Forschung (BMBF), Deutsche Forschungsgemeinschaft (DFG), Landesforschungsförderung Hamburg, Gemeinnützige Hertie-Stiftung, Else Kröner-Fresenius-Stiftung, Fritz Thyssen-Stiftung, Werner Otto-Stiftung and Deutsche Multiple Sklerose-Gesellschaft. HZ received speaking honoraria from Bayer Healthcare and Novartis and research grants from Novartis.
 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors report no conflicts of interest.

 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.



 The authors declare no conflict of interest.

 Declaration of Competing Interest Synne Brune-Ingebretsen has received honoraria for lecturing from Biogen and Novartis. Einar Høgestøl received honoraria for lecturing and advisory board activity from Biogen, Merck and Sanofi-Genzyme and unrestricted research grant from Merck. Nicole Kerlero de Rosbo reports no disclosures. Pål Berg-Hansen has received advisory board and/or speaker honoraria from Novartis, UCB, Sanofi, Merck and Biogen Idec. Cathrine Brunborg reports no disclosures. Kaj Blennow has served as a consultant, at advisory boards, or at data monitoring committees for Abcam, Axon, Biogen, JOMDD/Shimadzu. Julius Clinical, Lilly, MagQu, Novartis, Roche Diagnostics, and Siemens Healthineers, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program. Henrik Zetterberg has served at scientific advisory boards and/or as a consultant for Abbvie, Acumen, Alector, Alzinova, ALZPath, Annexon, Apellis, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, Nervgen, Novo Nordisk, Optoceutics, Passage Bio, Pinteon Therapeutics, Prothena, Red Abbey Labs, reMYND, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics, and Wave, has given lectures in symposia sponsored by Cellectricon, Fujirebio, Alzecure, Biogen, and Roche, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program (outside submitted work). Friedemann Paul received honoraria and research support from Alexion, Bayer, Biogen. Antonio Uccelli has received personal compensation from Novartis, Biogen, Merck, Roche and Sanofi Genzyme for public speaking and advisory boards. AU received funding for research by Fondazione Italiana Sclerosi Multipla, the Italian Ministry of Health and Banco San Paolo. Pablo Villoslada received consultancy fees and hold stocks from Accure Therapeutics SL, Spiral Therapeutics Inc., Clight Inc., Neuroprex Inc., QMenta Inc. and Attune Neurosciences Inc. Hanne F. Harbo reports no disclosures. Tone Berge has received unrestricted research grants from Biogen and Sanofi-Genzyme.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declared no conflict of interest.
 Declaration of Competing Interest The authors declare no conflict of interest.
 FB, DR, AH, JD, and VK report no conflict of interest. MSe has received consulting and/or speaker honoraria from Alexion, Bayer, Biogen, Bristol-Myers-Squibb, Merck, Roche, and Sanofi Genzyme. She has received travel support from Celgene, and TEVA. She has received research funding from the Hertha-Nathorff-Program. MSue reports personal fees and grants from Merck Healthcare Deutschland and Bayer Vital GmbH and grant support from the University of Greifswald (Gerhard-Domagk fellowship). KHS has received personal fees and travel grants from Bayer, Biogen, MerckSerono and Genzyme. FL received speaker fees, travel compensation and serves on advisory boards for/from Alexion, Bayer, Biogen, Fresenius, Merck-Serono, Novartis, Roche, Teva. His research is funded by German Federal Ministry of Education and Research (BMBF) and Deutsche Forschungsgesellschaft (DFG) and European Union (EU), outside the submitted work. HT reports funding for research projects, lectures and travel from Alexion, Bayer, Biogen, Celgene, Sanofi-Genzyme, Fresenius, Merck, Mylan, Novartis, Roche, Siemens Health Diagnostics, and Teva, and received research support from DMSG, DMS Stiftung, AMSEL-Stiftung Ursula Späth, Bayerische DMSG-Stiftung, Ministry of Science and Art of the State Baden-Württemberg (MWK-BW), and German Federal Ministry of Education and Research (BMBF). JL received speaker fees or travel compensation from UCB, Bayer, Roche, Teva and the Cure Huntington’s Disease Initiative (CHDI). His institution has been reimbursed for his role as a principal investigator in trials for UCB and CHDI. His research is funded by the European Huntington’s Disease Initiative and Ministry for Education and Research Baden-Württemberg outside the submitted work, as well as the German Federal Ministry of Education and Research (BMBF).
 The authors declare no conflict of interest.
 The authors declare that they have no competing interests.
 Conflict of interest statement The authors declare that there is no type of conflict of interest with this research or its publication.


 No competing interests declared.


 Disclosure: Antonio Ocejo declares no relevant financial relationships with ineligible companies. Disclosure: Ricardo Correa declares no relevant financial relationships with ineligible companies.
 Declaration of competing interest The authors involved in this publication declared no conflicts of interest.
 Competing interests: OH has competing interests with Bayer Schering, Merck, Teva, Genzyme, Novartis and BiogenIdec (support for attending meeting or travel, and consulting fees). The other authors have no competing interests.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Pierre Clavelou has received honoraria, and contributions to meeting from Almirall, Biogen, Janssen, Merck, Novartis, Roche, Sanofi-Genzyme and Teva. Giovanni Castelnovo received fees for consulting and speaking from Biogen, Abbvie, Merck, Novartis, Roche, Sanofi Genzyme, Merz and Celgene BMS. Jerome De Sèze has received fees for consultancy, advisory board and clinical trials from UCB, Novartis, Biogen, Merck, Teva, Genzyme/ Sanofi, Roche, Alexion, BMS/Celegene, Janssen and Horizon Therapeutics. Gilles Defer has received personal compensation for scientific advisory boards for Biogen, Novartis, BMS, Genzyme, Merck Serono, Roche and Teva and has received speaker honoraria and travel grants from Merck Serono, Biogen, Novartis, BMS, Roche, Genzyme and Teva. Valérie Pourcher has received fees for consultancy, advisory board and speaking trials from Novartis, Biogen, Merck and Roche. Patrick Vermersch received honoraria for contributions to meetings from Biogen, Sanofi-Genzyme, Novartis, Teva, Merck, Roche, Imcyse, AB Science, Almirall and BMS-Celgene and research support from Novartis, Sanofi-Genzyme and Merck. Ali-Frederic Ben-Amor is an employee of Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA, Darmstadt, Germany. Carine Savarin is an employee of Merck Santé, Lyon, France, an affiliate of Merck KGaA, Darmstadt, Germany.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
 ZS was employed by Philips Healthcare. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer YM declared a past co-authorship with the author ZS to the handling editor.
 Ferdinando Clarelli, Beatrice Pignolet, Elisabetta Mascia, Marco Frasca, Santoro Silvia, Sorosina Melissa, Florence Bucciarelli and Giorgio Valentini have nothing to disclose. Laura Ferrè received compensation for speaking activities from Novartis. Lucia Moiola received compensation for consulting services, travel grants, and/or speaking activities from Biogen, Serono, Sanofi, Teva, Roche, and Novartis. Vittorio Martinelli has received compensations for consulting services and/or speaking activities from Novartis, Genzyme, Almirall, TEVA, Biogen, and Merck-Serono. Giancarlo Comi has received personal compensation for consulting and speaking activities from F. Hoffmann-La Roche Ltd., Roche SpA, Novartis, Teva Pharmaceutical Industries Ltd, Teva Italia Srl, Sanofi Genzyme, Genzyme Corporation, Genzyme Europe, Merck KGgA, Merck Serono SpA, Celgene Group, Biogen Idec, Biogen Italia Srl, Almirall SpA, Forward Pharma, Medday, and Excemed. Roland Liblau received grant support from Pierre Fabre, GlaxoSmithKline, and BMS. He received speaker or scientific board honoraria from Biogen, Servier, Novartis, and Sanofi-Genzyme. Massimo Filippi is Editor-in-Chief of the Journal of Neurology; received compensation for consulting services and/or speaking activities from Bayer, Biogen Idec, Merck-Serono, Novartis, Roche, Sanofi Genzyme, Takeda, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). Federica Esposito has received compensation for consulting services and/or speaking activities from Novartis, Sanofi Genzyme, Almirall, TEVA, and Merck-Serono.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 J.J.E., G.D. and R.S. report no conflict of interest. The employer of C.G. and C.Z. received research grants or honoraria for speaking and consulting fees from Almirall, Biogen Idec, Celgene, Merck, Novartis, Roche, Sanofi and Teva Pharma.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors have declared that no competing interests exist.
 Conflict of interest: The authors have no competing interests to declare that are relevant to the content of this article.


 HT has received consulting fees from EMD Serono outside of the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest and Funding Source: This research was funded by an IDEXLYON fellowship. The authors have no conflicts of interest to declare. The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. The results of the present study do not constitute endorsement by the American College of Sports Medicine.

 The authors declare that there are no conflicts of interest related to this article.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors confirmed that the research was conducted in the absence of any financial or commercial relationships that could be considered as a potential conflict of interest.
 PM, BV and JF are employed by Exigo Consultores. The study sponsor contracted with Exigo Consultores for the development of the research project. Exigo Consultores provided support in the form of salaries for authors but did not have any additional role in the study design, data collection and analysis, or preparation of the manuscript. CC has received compensation for advisory board/consulting services to Biogen, Janssen, Merck, Novartis, Roche, and Sanofi, and has been on the speakers’ bureau for Almirall, Biogen, BMS, Janssen, Merck, Novartis, Roche, and Sanofi. JC has received compensation for activity with Almirall, Biogen, Bristol-Myers-Squibb, Janssen, Merck, Novartis, Roche, Sanofi, and Zambon. AS has received compensation for activity with Astra Zeneca, Biogen, Merck, Novartis, Roche, and Sanofi. DF and IM are employees of Roche Farmacêutica e Química, Lda., Portugal.
 Declaration of Competing Interest Irrestrictive research grants from Biogen Argentina, Genzyme Argentina, Merck Argentina, Novartis Argentina, and Roche Argentina allowed the development and implementation of the RELEVAREM Registry. Those grants did not interfere in the development plan, variables, PI selection, patient information nor other aspects of the Registry. Authors declare no conflict of interest with the research done.
 Conflict of Interest Disclosures: Dr Oechtering reported receiving travel grants from Biogen Idec, Novartis, and Bayer; grants from Swiss MS Society; and serving on an advisory board by Roche outside the submitted work. Dr Lorscheider reported receiving grants from Novartis and Biogen; personal fees from Novartis, Roche, and Teva; serving on the advisory boards for Roche and Teva and receiving grants from Innosuisse Innovation Agency outside the submitted work. Dr Cagol reported receiving grant support from the Horizon 2020 Eurostar program. Dr Barro reported receiving travel support from Novartis and Teva. Dr Abdelhak reported receiving research grants from the German Multiple Sclerosis Society, Roche, and Denali Therapeutics outside the submitted work. Dr Achtnichts reported serving on the scientific advisory boards for Celgene, Novartis Pharmaceuticals, Merck, Biogen, Sanofi Genzyme, Roche and Bayer; receiving funding for travel and/or speaker honoraria from Celgene, Biogen, Sanofi Genzyme, Novartis, Merck Serono, Roche, Teva and the Swiss Multiple Sclerosis Society; and research support from Biogen, Sanofi Genzyme, and Novartis. Dr. Lalive reported receiving speaker honoraria from Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi Aventis, and Teva; consulting fees from Biogen Idec, Geneuro, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, and Teva; and research grants from Biogen Idec, Merck Serono, Novartis. Dr Müller reported receiving honoraria for travel, honoraria for lectures/consulting, and/or grants for studies from Almirall, Biogen, Celgene, Novartis, Teva, Merck Serono, Genzyme, Roche, and Bayer Schweiz. Dr Pot reported receiving consulting fees and/or travel compensation, used exclusively for research support, for activities with Biogen, Merck, Novartis, Roche, and Sanofi Genzyme. Dr Salmen reported receiving speaker honoraria and/or travel compensation for activities with Almirall Hermal GmbH, Biogen, Merck, Novartis, Roche, and Sanofi Genzyme; personal fees from Bristol Myers Squibb, CSL Behring, Novartis, and Roche; and grants from Baasch Medicus Foundation, Medical Faculty of the University of Bern, and the Swiss Multiple Sclerosis Society outside the submitted work. Dr Zecca reported receiving honoraria for speaking/consulting fees or grants from Abbvie, Almirall, Biogen Idec, Celgene, Janssen, Genzyme, Lilly, Merck Serono, Novartis, Roche, Sanofi, and Teva Pharma outside the submitted work. Dr Khalil reported receiving funding for travel and speaker honoraria from Bayer, Novartis, Merck, Biogen Idec, and Teva Pharmaceutical Industries; serving on scientific advisory boards for Biogen Idec, Merck, Roche, Novartis, Bristol Myers Squibb, and Gilead; and receiving grants from Teva Pharmaceutical Industries, Biogen, and Novartis. Dr Yaldizli reported receiving grants from European Committee for Treatment and Research in Multiple Sclerosis/European Magnetic Resonance Imaging in Multiple Sclerosis network, University of Basel, Pro Patient Stiftung University Hospital Basel, Free Academy Basel, Swiss Multiple Sclerosis Society and advisory board/lecture and consultancy fees from Roche, Sanofi Genzyme, Almirall, Biogen, and Novartis. Dr Derfuss reported receiving speaker fees, research support, travel support, and/or served on advisory boards, data safety monitoring boards, or Steering Committees of Actelion, Alexion, Celgene, Polyneuron, Novartis Pharma, Merck Serono, Sanofi, Biogen, Teva, Bayer-Schering, GeNeuro, Mitsubishi Pharma, MedDay, Roche, and Genzyme. Dr Berger reported receiving a grant from the German Ministry of Education and Research (within the German Competence Net Multiple Sclerosis) plus additional funds from Biogen, all to the University of Münster, for an investigator-initiated adverse event registry for patients with multiple sclerosis. Dr Wiendl reported receiving honoraria for acting as a member of scientific advisory boards from Abbvie, Alexion, Argenx, Bristol Myers Squibb/Celgene, Janssen, Merck, and Novartis; speaker honoraria and travel support from Alexion, Biogen, Bristol Myers Squibb, F. Hoffmann-La Roche Ltd, Genzyme, Merck, Neurodiem, Novartis, Roche Pharma AG, Teva Pharma, and WebMD Global; consultant fees from Abbvie, Actelion, Argenx, Biogen, Bristol Myers Squibb, EMD Serono, Fondazione Cariplo, Gossamer Bio, Idorsia, Immunic, Immunovant, Janssen, Lundbeck, Merck, NexGen, Novartis, PSI CRO, Roche, Sanofi, Swiss Multiple Sclerosis Society, UCB, and Worldwide Clinical Trials; and research funding from the German Ministry for Education and Research, Deutsche Forschungsgesellschaft, Deutsche Myasthenie Gesellschaft e.V., Alexion, Amicus Therapeutics Inc, Argenx, Biogen, CSL Behring, F. Hoffmann - La Roche, Genzyme, Merck KgaA, Novartis Pharma, Roche Pharma, and UCB Biopharma. Dr Piehl reported receiving grants from Merck KGaA and UCB; data safety monitoring board member fees from Chugai, Lundbeck, and Roche; and fees for the preparation of expert witness statement from Novartis outside the submitted work. Dr Fischer reported receiving grants from the Swiss National Science Foundation, Medtronic, Stryker, Penumbra, Phenox, Rapid Medical; consultant fees from Medtronic, CSL Behring, and Stryker; and fees for participation in an advisory board from Alexion/Portola and Boehringer Ingelheim; being a member of a clinical event committee of the COATING study (Phenox) and of the data and safety monitoring committee of the TITAN, LATE MT and IN EXTREMIS trials; and serving as vice presidency of the Swiss Neurological Society. Dr Kappos’ employer (University Hospital Basel) has received and dedicated to research support fees for board membership, consultancy or speaking, or grants in the past 3 years from Abbvie, Actelion, Advancell, Allozyne, Auriga Vision AG, Bayer, Bayhill, Biogen Idec, BioMarin, Celgene, CSL Behring, df-mp Molnia & Pohlman, Eisai, Eli Lilly EU, EMD Serono, Genentech, Genmab, GeNeuro SA, Genzyme, Gianni Rubatto Foundation, Glaxo Smith Kline, Glenmark, Innosuisse, Janssen, Japan Tobacco, Merck Serono, MediciNova, Minoryx Therapeutics, Mitsubishi Pharma, MH Consulting, Neurostatus-UHB AG, Novartis, Novartis Research Foundation, Novo Nordisk, Österreichische Gesellschaft für Neurologie, Peptimmune, Roche, Roche Research Foundation, Santhera, Sanofi-Aventis, Senda Biosciences Inc, Swiss MS Society, Swiss National Research Foundation, Teva Pharmaceutical Industries Ltd, TG Therapeutics, UCB, Wellmera AG, and Wyeth; and Dr Kappos reported having a patent for Neurostatus UHB-AG with royalties paid Payments made to institution (University Hospital Basel); being CEO (employment by University Hospital Basel)MAGNIMS Steering Committee) and a board member of the European Charcot Foundation. Dr Gobbi reported receiving honoraria for speaking/consulting or grants from Abbvie, Almirall, Biogen Idec, Celgene, Genzyme, Merck Serono, Novartis, Roche, Teva Pharma. Dr Granziera reported The University Hospital Basel (USB), as the employer of C.G., has received the following fees which were used exclusively for research support: (1) advisory boards and consultancy fees from Actelion, Novartis, Genzyme-Sanofi, GeNeuro, Hoffmann La Roche and Siemens Healthineers; (2) speaker fees from Biogen, Hoffmann La Roche, Teva, Novartis, Janssen and Genzyme-Sanofi; and (3) research grants from Hoffmann La Roche, GeNeuro, Genzyme, Biogen. Dr Bridel reported serving on scientific advisory boards for Biogen, Novartis, and BMS. Dr Leppert reported receiving grants from Progressive MS Alliance outside the submitted work; and being chief medical officer of GeNeuro. Dr Kuhle reported receiving grants from Swiss National Science Foundation, Swiss MS Society, Biogen, Celgene, Merck, Novartis, Roche, Sanofi, Progressive MS Alliance, University of Basel, Octave Bioscience. No other disclosures were reported.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: GC has served on data and safety monitoring boards for AstraZeneca, AveXis, BioLineRx, BrainStorm Cell Therapeutics, Bristol Myers Squibb/Celgene, CSL Behring, Galmed, HISUN USA, Horizon Pharmaceuticals, Mapi Pharma, Merck, Merck/Pfizer, Neurim, Novartis, OncoImmune, OPKO Biologics, Orphazyme, Reata, Sanofi, Teva, Viela Bio, VIVUS, the National Heart, Lung, and Blood Institute (Protocol Review Committee), and the National Institute of Child Health and Human Development (Obstetric Pharmacology Research Unit oversight committee) and has received compensation for consulting or advisory board service from BioDelivery Sciences International, Biogen, Click Therapeutics, Genentech, Genzyme, GW Pharmaceuticals, Klein-Buendel, MedDay, MedImmune, NeuroGenesis, Novartis, Osmotica, Perception Neurosciences, Recursion/CereXis, Roche, and TG Therapeutics. Dr Cutter is employed by the University of Alabama at Birmingham and is president of Pythagoras, Inc., a private consulting company located in Birmingham, AL, USA. RAR and MLN were employees of Biogen at the time of these analyses and may hold stock and/or stock options in Biogen. CdM, CMS, EF, and TK are employees of and hold stock and/or stock options in Biogen. FDL has received compensation for consulting and advisory board work from Acorda, Actelion/Janssen, Apitope, Atara Biotherapeutics, Avotres, Banner Life Sciences, Biogen, Brainstorm Cell Therapeutics, EMD Serono, Entelexo Biotherapeutics, GW Pharma, Immunic, Jazz Pharmaceuticals, Labcorp, Mapi Pharma, Medday, MedImmune/Viela Bio/Horizon Therapeutics, Mylan, Neuralight, Neurogene, Novartis, Orion Biotechnology, Population Council, Receptos/Celgene/BMS, Roche/Genentech, Sanofi Genzyme, Teva, and TG Therapeutics; has received research funding from Actelion, Biogen, Brainstorm Cell Therapeutics, Novartis, Sanofi, the National Institutes of Health, and the National Multiple Sclerosis Society; has received speaker honoraria from Sanofi; and holds stock options in Avotres and Neuralight. JSW has served on advisory boards and data monitoring or steering committees for, has consulting agreements with, or has received speaker honoraria from Avotres, BrainStorm Cell Therapeutics, Cleveland Clinic Foundation, EMD Serono, MedDay, NervGen, Novartis, Roche/Genentech, Sanofi Genzyme, and the University of Alabama at Birmingham, and has received royalties for out-licensed monoclonal antibodies through UTHealth from MilliporeSigma. HM and SJ have not declared any conflicts of interest.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: JM, NM, and RGB are employees of Roche Pharma Spain. SSM received payment for lecturing or travel expenses from Merck-Serono, Biogen, Sanofi-Genzyme, Roche, and Novartis. JMM has served on scientific advisory boards and/or has received speaking honoraria, research funding, and support to attend scientific meetings from Biogen, Merck, Novartis, Roche and Teva. JS has received speaking honoraria, compensation for consulting services and support to attend scientific meetings from Almirall, Bayer, Biogen, Merck, Novartis, Sanofi, Roche, and Teva. AA has received compensation for consulting services from Biogen, BMS, Sanofi, Roche, Janssen, and Novartis; and speaking honoraria from Biogen, BMS, Sanofi, Roche, Janssen, Merck, Almirall, and Novartis. ABC has received courses and honoraria for her participation as speaker/meeting moderator/symposia organizer from Alter, Almirall, Bayer, Bial, Biogen, Bristol-Myers-Squibb, Lilly, Merck-Serono, Mylan, Novartis, Roche, Sanofi-Genzyme, Teva, and UCB; and support to attend scientific meetings from Biogen, Bial, Merck-Serono, Novartis, Roche, Sanofi-Genzyme, and Teva. JLSM has received support to attend scientific meetings from Novartis, Merck, and Biogen; speaking honoraria from Biogen, Novartis, Sanofi, Merck, Almirall, Bayer, and Teva; and has participated in clinical trials from Biogen, Merck, and Roche. FJBH has received compensation for consulting services and speaking honoraria from Almirall, Biogen, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, and Teva. CC has received compensation for consulting services, speaking honoraria and support to attend scientific meetings and courses from Merck, Teva, Sanofi-Genzyme, Novartis, Biogen, Roche, and Bristol-Myers-Squibb. LB has received compensation for consulting services, speaking honoraria and support to attend scientific meetings from Bayer, Celgene, Biogen, Genzyme, Merck, Novartis, Roche, Almirall, and Teva. JDGS has received compensation for consulting services and speaking honoraria from Biogen, Novartis, Merck, UCB, Sanofi-Genzyme, Roche, Almirall, and Teva. MCA has received compensation for consulting services from Genzyme, Roche, Novartis, Sanofi, and Biogen. LNC has received compensations from Sanofi-Genzyme, Merk, Biogen, and Roche. EA has received speaking honoraria from Roche, Novartis, Merck, Sanofi, and Biogen. MGR has received speaking honoraria from Biogen, Sanofi, Almirall, and Novartis. OC has participated in studies and has received speaking honoraria from Roche, Merck, Biogen, and Novartis. LGT has received speaking honoraria from Biogen, Novartis, Merck, Bayer, Sanofi-Genzyme, Almirall, Roche, and Teva. MH has participated in observational studies and has received compensation for consulting services and speaking honoraria from Roche, Merck, Sanofi, Biogen, Novartis, and Bayer. The rest of the authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of interests The authors declare no competing interests.



 The authors declare that they have no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work presented in this review.
 All authors declare no conflict of interests.
 The authors declare no conflict of interest.
 Declaration of interests The authors declare no competing interests.

 Declaration of conflicting interest C.K. and M.M. having nothing to declare. G.Y.G. receives part time salary support from the Centers for Disease Control and Prevention for acute flaccid myelitis surveillance and an honorarium as a Media Editor of Pediatric Neurology.






 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest relevant to this review.
 All authors are employees of Mallinckrodt Pharmaceuticals, the manufacturer of Acthar Gel. The authors report no other conflicts of interest in this work.
 The authors declare no conflict of interest.

 DR received research support, travel grants, consultancy fees and speaker fees from Bayer Healthcare, Biogen, Celgene, Lilly, Merck, Novartis, Roche, Sanofi Genzyme, Teva and Zambon. SE received speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, Almirall and Teva. GB received consultant fee and grant for trip and Congress registration from Almirall, Biogen, Merck, Novartis, Roche, Teva, Sanofi Genzyme. JC has received compensation for participation in clinical trials, presence in advisory boards and as a speaker from Roche, Novartis, Sanofi, Almirall, Zambon, Biogen, Janssen, Merck and Bristol-Myers-Squibb and research funding from Biogen, Merck, Roche and Fundação BIAL. CW is an employee of Novartis.
 The authors declare no conflict of interest.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.

 Competing interests: FB has received travel funding from Biogen.
 Declaration of Competing Interest Priyanka Algu reports no disclosures. Natasha Hameed reports no disclosures. Tracy DeAngelis reports personal fees from Biogen Inc and Alexion Pharmaceuticals. Joel Stern reports no disclosures. Asaff Harel reports personal fees from Teva, Biogen Inc, Alexion, Horizon, and Banner Life Sciences, as well as research grants from the National MS Society, Biogen, and the Consortium for MS Centers.
 The authors declare no competing financial interest.




 The authors declare no conflict of interest.
 Competing interests: ES and EL-S received travel reimbursement from Sanofi and ECTRIMS; AC received support from the ECTRIMS-MAGNIMS fellowship (2018) and, was granted a postdoctoral fellowship from ECTRIMS in 2022; AS received compensation for consulting services and speaker honoraria from Merck, Biogen-Idec, Sanofi, Novartis, Roche, Janssen and Horizon Therapeutics; YB received speaking honoraria from Biogen, Novartis and Genzyme; SL received compensation for consulting services and speaker honoraria from Biogen Idec, Novartis, TEVA, Genzyme, Sanofi and Merck. MMS serves on the editorial board of Neurology and Frontiers in Neurology, receives research support from the Dutch MS Research Foundation, Eurostars-EUREKA, ARSEP, Amsterdam Neuroscience, MAGNIMS and ZonMW and has served as a consultant for or received research support from Atara Biotherapeutics, Biogen, Celgene/Bristol Meyers Squibb, Genzyme, MedDay and Merck. HV has received research grants from Pfizer, Merck Serono, Novartis. and Teva; speaker honoraria from Novartis; and consulting fees from Merck Serono, all paid directly to his institution. FB: Steering committee and iDMC member for Biogen, Merck, Roche, EISAI. Consultant for Roche, Biogen, Merck, IXICO, Jansen, Combinostics. Research agreements with Novartis, Merck, Biogen, GE, Roche. Co-founder and shareholder of Queen Square Analytics LTD. MAR received speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, Roche, and Teva and research support from the Canadian MS Society and Fondazione Italiana Sclerosi Multipla. MF is editor-in-chief of the Journal of Neurology and Associate Editor of Human Brain Mapping, Neurological Sciences, and Radiology, received compensation for consulting services and/or speaking activities from Alexion, Almirall, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries, and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, the Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). BB received financial support by the German Federal Ministry for Education and Research, BMBF, German Competence Network Multiple Sclerosis (KKNMS), grant no.01GI1601I. CL received a research grant by the German Federal Ministry for Education and Research, BMBF, German Competence Network Multiple Sclerosis (KKNMS), grant no.01GI1601I, has received consulting and speaker’s honoraria from Biogen Idec, Bayer Schering, Daiichi Sanykyo, Merck Serono, Novartis, Sanofi, Genzyme and TEVA. AR serves on scientific advisory boards for Novartis, Sanofi-Genzyme, Synthetic MR, TensorMedical, Roche, Biogen, and OLEA Medical, and has received speaker honoraria from Bayer, Sanofi-Genzyme, Merck-Serono, Teva Pharmaceutical Industries, Novartis, Roche, Bristol-Myers and Biogen. JS-G serves as co-editor for Europe on the editorial board of Multiple Sclerosis Journal and as editor-in-chief in Revista de Neurología, receives research support from Fondo de Investigaciones Sanitarias (19/950) and has served as a consultant/speaker for Biogen, Celgene/Bristol Meyers Squibb, Genzyme, Novartis, Merck and Roche. AT has been supported by grants from MRC (MR/S026088/1), NIHR BRC (541/CAP/OC/818837) and RoseTrees Trust (A1332 and PGL21/10079), has had meeting expenses from Merck, Biomedia and Biogen Idec and was UK PI for two clinical trials sponsored by MEDDAY (MS-ON-NCT02220244 and MS-SPI2-NCT02220244). OC acts as a consultant for Novartis and Merck, and has received research funding from: NIHR, UK MS Society, NIHR UCLH BRC, MRC, Rosetrees Trust.
 Conflict of Interest Disclosures: Dr Siva reported receiving consultancy, travel, and registration coverage from F. Hoffmann-La Roche Ltd, Merck-Serono, and Sanofi-Genzyme; consultancy fees from Alexion; and grants from the Turkish Multiple Sclerosis Society outside the submitted work. Dr Sormani reported receiving personal fees from Biogen, Merck, Novartis, Roche, Sanofi, Alexion, and Immunic outside the submitted work. Dr Bovis reported receiving grants from National MS Society 2022 Biostatistic/Informatics Junior Faculty Award outside the submitted work. Dr Vermersch reported receiving personal fees from AB Science, Imcyse, Sanofi-Genzyme, Merck, Novartis, Celgene-BMS, Roche, and Teva and grants from Sanofi-Genzyme, Merck, and Roche outside the submitted work. Dr Thouvenot reported receiving personal fees from Actelion and Teva and grants from Biogen, Merck-Serono, Novartis, and Roche outside the submitted work. Dr Efendi reported receiving personal fees from Sanofi outside the submitted work. Dr Le Page reported receiving personal fees from Biogen Idec, Novartis, Merck, Alexion, and Sanofi outside the submitted work. Dr Derache reported receiving personal fees from Biogen and Sanofi, speaker fees from Janssen, and expert advice from Merck and Novartis outside the submitted work. Dr Hoepner reported receiving speaker honoraria from Merck, Novartis, Roche, Biogen, Alexion, Sanofi, Janssen, Bristol Myers Squibb, Teva, and Almirall; grants from Roche, Merck, Sanofi, Bristol Myers Squibb, Biogen, Chiesi, Swiss MS Society, and SISF University Bern outside the submitted work. Dr De Seze reported receiving personal fees from Sanofi during the conduct of the study. Dr Ciron reported receiving advisory board fees from Biogen, Novartis, Merck, Sanofi, and Roche outside the submitted work. Dr Clavelou reported receiving advisory board and travel fees from Sanofi and Janssen and advisory board fees from Merck during the conduct of the study. Dr Wiertlewski reported receiving advisory board fees from Sanofi outside the submitted work. Dr Cohen reported receiving advisory board fees from Biogen, Merck, Sanofi, Roche, Celgene-BMS, Alexion, Horizon Therapeutics, and Ad Scientiam outside the submitted work. Dr Azevedo reported receiving grants from the National Multiple Sclerosis Society and the National Institutes of Health; personal fees from Horizon Therapeutics, Genentech, Sanofi Genzyme, TG Therapeutics, and EMD Serono; grant review from the Department of Defense and the National Institutes of Health; and continuing medical education activity fees from Efficient LLC, American Academy of Neurology, Spire Learning, and Catamount Medical Education outside the submitted work. Dr Kantarci reported receiving grants from the National Institutes of Health outside the submitted work. Dr Okuda reported receiving personal fees from Alexion, Celgene/Bristol Myers Squibb, Genentech, Genzyme/Sanofi, Janssen Pharmaceuticals, Novartis, Osmotica Pharmaceuticals, RVL Pharmaceuticals, TG Therapeutics, and Viela Bio Inc and grants from Biogen and EMD Serono/Merck outside the submitted work. No other disclosures were reported.
 The authors declare no conflict of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest WB has received honoraria from Biogen, Celgene (BMS), Merck, Mylan, Novartis, Roche, Sanofi and Viatris. AA, LA and AH are employees of Merck Serono Ltd., Feltham, UK, an affiliate of Merck KGaA.

 Declaration of Competing Interest Marko Andabaka nothing to declare. Tatjana Pekmezovic has been an advisor or speaker for Sanofi-Genzyme, Medis, Hemofarm, Merck, Teva, and Roche. Luka Crnosija nothing to declare. Nikola Veselinovic has been a speaker for Medis, Merck, Teva, Hemofarm, Novartis and Roche. Anmari Junakovic nothing to declare Olivera Tamas has been a speaker for Medis, Merck, Teva, Hemofarm, Novartis and Roche. Maja Budimkic Stefanovic has been a speaker for Medis, Merck, Hemofarm, Novartis and Roche. Vanja Jovicevic nothing to declare. Nikola Momcilovic nothing to declare. Milovan Roganovic nothing to declare. Gorica Maric nothing to declare. Aleksa Jovanovic nothing to declare. Tereza Gabevic participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. Magdalena Krbot Skoric participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. Sarlota Mesaros has been an advisor or speaker for Medis, Merck, Teva, Hemofarm, Novartis, and Roche. Ljiljana Radulovic has been an advisor or speaker for Medis, Merck, Novartis, and Roche. Mario Habek participated as a clinical investigator and/or received consultation and/or speaker fees from: Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. Jelena Drulovic has been an advisor or speaker for Bayer HealthCare, Sanofi-Genzyme, Medis, Merck, Teva, Novartis, Biogen, Hemofarm, Pharma Swiss, Amicus, and Roche.

 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors have declared that no competing interests exist.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The Authors declare that there is no conflict of interest relevant to the study.


 The authors declare no conflict of interest.
 Dejan Jakimovski serves as Associate Editor of Clinical Neurology and Neurosurgery and compensated by Elsevier B.V. Taylor Wicks and Niels Bergsland have nothing to disclose. Michael G. Dwyer received compensation from Keystone Heart for consultant fees. He received financial support for research activities from Bristol Myers Squibb, Novartis, Merck Serono, Mapi Pharma, Keystone Heart, Protembis and V-WAVE Medical. Bianca Weinstock-Guttman received honoraria as a speaker and/or as a consultant for Biogen Idec, Teva Pharmaceuticals, EMD Serono, Genzyme, Sanofi, Genentech, Novartis, Celgene/BMS, Janssen, Labcorp, TG therapeutics, and Horizon. Dr Weinstock-Guttman received research funds from Biogen Idec, EMD Serono, Genzyme, Genentech, Sanofi, Novartis. Robert Zivadinov has received personal compensation from Bristol Myers Squibb, EMD Serono, Sanofi, Protembis, Janssen, 415 Capital, and Novartis for speaking and consultant fees. He received financial support for research activities from Sanofi, Novartis, Bristol Myers Squibb, Octave, Mapi Pharma, CorEvitas, Protembis and V-WAVE Medical. The authors report no other conflicts of interest in this work.
 Y-TL is an employee of Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA. TW and PB are employees of Emergo by UL, Utrecht, The Netherlands, which received funding from Merck for this study. CW is an employee of Emergo by UL, Cambridge, UK, which received funding from Merck for this study. DJ is an employee of Merck Serono Ltd., Feltham, UK, an affiliate of Merck KGaA. MK is a former employee of Ares Trading SA, Eysins, Switzerland, an affiliate of Merck KGaA; current affiliation: EMD Serono, Inc., Rockland, MA, USA, an affiliate of Merck KGaA. The authors report no other conflicts of interest in this work.



 Aparajita Chatterjee and Ambar Chakravarty each declare no potential conflicts of interest.
 None.





 Declaration of Interests P.J.T. and B.L.L.C. are listed as inventors on issued and pending patent claims covering compositions and methods of enhancing glial cell function. P.J.T. is a co-founder and consultant for Convelo Therapeutics, which has licensed some of these claims and patents from Case Western Reserve University (CWRU). P.J.T. and CWRU retain equity in Convelo Therapeutics. V.F. and L.B. are listed as inventors on issued and pending patent claims covering glial cell generation methods.
 G.E. McIntosh, E.S. Liu, and M. Allan report no disclosures relevant to the manuscript. L.B. Grech receives a salary partly funded by MS Australia (20-206). Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp. TAKE-HOME POINTS → Depression in people with MS is frequently undiagnosed, untreated, or undertreated leading to an increased morbidity and mortality.→ Our search found a significant lack in the number of high-quality guidelines and consensus statements to guide clinicians managing people with comorbid MS and depression.→ The complexity in diagnosis and barriers to effective treatment of depression in MS highlight the need for specific and updated guideline development in this area.
 The authors declare there are no conflicts of interest.
 Declaration of Competing Interest The authors declare no competing interest.
 The authors declare that they have no conflict of interest.


 Declaration of Competing Interest The authors have no conflicts of interest to declare.
 Tjalf Ziemssen has received personal compensation for participating in advisory boards, trial steering committees, and data and safety monitoring committees, as well as for scientific talks and project support from Almirall, Bayer, BAT, Biogen, Celgene, Sanofi Genzyme, Merck, Novartis, Roche, Vitaccess and Teva. Eugen Schlegel has received research support, consulting fees and honoraria for lectures from Biogen, Lilly, Merck and Novartis. Marie Groth and Benjamin Ettle are employees of Novartis Pharma GmbH, Nuremberg, Germany. Tobias Bopp has received consulting fees and honoraria for lectures from Biogen, Celgene, Merck, Novartis, Pathios Therapeutics, Roche, Sanofi Genzyme and Teva.
 None.

 CONFLICTS OF INTEREST No potential conflict of interest relevant to this article was reported.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 FUNDING/SUPPORT: Funding for this research was provided by EMD Serono, (CrossRef Funder ID: 10.13039/100004755) through the Multiple Sclerosis Leadership and Innovation Network, a scientific consortium created to advance MS science by generating actionable real-world data and patient-centered solutions to improve patient outcomes. The authors had full control of the manuscript and provided their final approval of all content.
 The authors have no conflicts of interest to disclose.
 Conflicts of Interest: The authors have no competing interests to declare.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor AL declared a past co-authorship with the author MI.


 IY, WP, ZN, and LC are employees and stockholders of Gossamer Bio.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest CWK received travel support from UCB and Alexion. JDL received speaker fees, research support, travel support, and/or served on advisory boards by Abbvie, Alexion, Argenx, Biogen, Merck, Novartis, Roche, Sanofi, Takeda. IEA received speaker fees, research support, and/or served on advisory boards by Novartis, Pfizer, Merck, Abbvie, and Tanabe.
 The authors report no conflicts of interest in this work.
 David Ellenberger, Firas Fneish, Sarah Schilling, and Melanie Peters had no personal financial interests to disclose other than being employees of the German MS Registry. Niklas Frahm is an employee of the MSFP. Moreover, he is an employee of Rostock’s University Medical Center and received travel funds for research meetings from Novartis. Judith Haas has no personal pecuniary interests to disclose, other than being the President of the German MS Society federal association, which receives funding from a range of public and corporate sponsors, recently including BMG, G-BA, The German MS Trust, Biogen, Bristol Myers Squibb, Merck Serono, Novartis, Roche, Sanofi, and Viatris (former Mylan). Micha Löbermann received speaker honoraria from Sanofi, AbbVie, and Pfizer; he served as investigator in vaccine studies sponsored by Janssen, GSK, and Novartis. Friedemann Paul has received speaking fees, travel support, honoraria from advisory boards, and/or financial support for research activities from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, Shire, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA. He serves as academic editor for PLoS ONE and associate editor for Neurology, Neuroimmunology, and Neuroinflammation. Dieter Pöhlau received speaking fees, travel support, and financial support for research projects from Allmirall, Bayer, Biogen-Idec, Merck-Serono, Octapharm, Novartis, Roche, Sanofi-Aventis, and Teva. Anna-Lena Röper is an employee of the MSFP and Germany MS society, which is funded by many public and corporate sponsors. She received travel funds from Novartis. None resulted in a conflict of interest. Alexander Stahmann has no personal financial interests to disclose, other than being the leader of the German MS Registry, which receives funding from a range of public and corporate sponsors, recently including G-BA, The German MS Trust, German MS Society, Biogen, Bristol Myers Squibb, Merck, Novartis, Roche, and Sanofi. Herbert Temmes has no personal pecuniary interests to disclose, other than being the Secretary General of the German MS Society federal association, which receives funding from a range of public and corporate sponsors, recently including Bundesgesundheitsministerium (BMG), The German Innovation Fund (G-BA), The German MS Trust, Biogen, Bristol Myers Squibb, Merck Serono, Novartis, Roche, Sanofi, and Viatris (former Mylan). Uwe K. Zettl has received speaking fees, travel support, and/or financial support for research activities from Alexion, Almirall, Bayer, Biogen, Bristol-Myers-Squibb, Janssen, Merck Serono, Novartis, Octapharm, Roche, Sanofi Genzyme, and Teva as well as EU, BMBF, BMWi, and DFG.
 The authors declare that they have no competing interests.
 Declaration of Competing Interest The authors report no conflicts of interest.
 The authors declare no potential conflict of interest.
 The authors declare no conflict of interest.
 J-HM has lectured, consulted, and received Honoria from Bayer, Merck, Biogen Idec, Sanofi Genzyme, Teva-Handok, UCB, Samsung Bioepis, Mitsubishi Tanabe Pharma, Roche, and Janssen; received grants from the National Research Foundation of Korea and SMC Research and Development Grant. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 V.C. has received grant from European Charcot Foundation for the present work and received support for scientific meeting from Janssen. R.M. has no conflicts of interest to be reported. S.M. has received support for scientific meetings from Roche. R.M. has no conflicts of interest to be reported. L.G. has no conflicts of interest to be reported. M.R. has no conflicts of interest to be reported. M.I.L. has no conflicts of interest to be reported. S.M. has no conflicts of interest to be reported. M.C. received speaker honoraria from Biogen, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, and Roche and receives research support from the Progressive MS Alliance and Italian Minister of Health. R.G. has no conflicts of interest to be reported. J.P. has received support for scientific meetings and honorariums for advisory work from Merck Serono, Novartis, Chugai, Alexion, Roche, Medimmune, Argenx, UCB, Mitsubishi, Amplo, Janssen and Sanofi. Grants from Alexion, Roche, Medimmune, UCB, Amplo Biotechnology. Patent ref P37347WO and licence agreement Numares multimarker MS diagnostics Shares in AstraZeneca; acknowledges partial funding by highly specialized services NHS England.
 The authors declare no conflict of interest.



 Disclosure: Hillary Ramroop declares no relevant financial relationships with ineligible companies. Disclosure: Ricardo Cruz declares no relevant financial relationships with ineligible companies.
 The authors declare that there is no conflict of interests with respect to the research, authorship, and/or publication of this article.

 Declaration of Competing Interest Thomas P. Leist has received compensation for consulting from Biogen, Genentech, Novartis, Sanofi, Horizon, TG Pharma, Bristol Myers Squibb (BMS); as a speaker from Biogen, Genentech, Horizon, and Alexion; and for research from Genentech, Biogen, BMS, Anokion. Michele Cole is a former employee of Janssen Scientific Affairs, LLC and shareholder Johnson & Johnson, Inc. Sumit Verma is an employee of STATinMED, which was contracted by Janssen Scientific Affairs, LLC for work on this study. Hoa H. Le and Alex Keenan are employees of Janssen Scientific Affairs, LLC and shareholders of Johnson & Johnson, Inc.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 None



 Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Disclosure: Niloufar Khanna declares no relevant financial relationships with ineligible companies. Disclosure: Valerie Gerriets declares no relevant financial relationships with ineligible companies.
 FAAG has received travel grants from Genzyme, Biogen, Pfizer, Teva, Novartis, Roche, and Ipsen to attend scientific meetings. The other authors report no conflicts of interest.
 GZ, DW, KK, and CW are a part-time employee at the Sydney Neuroimaging Analysis Centre. MB has received institutional support for research, speaking and/or participation in advisory boards for Biogen, Merck, Novartis, Roche, and Sanofi Genzyme, and is a research consultant to RxPx and research director for the Sydney Neuroimaging Analysis Centre. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Lars Forsberg has nothing to disclose. Tim Spelman has received compensation for serving on the scientific advisory board for Biogen and speaker honoraria from Novartis. Pernilla Klyve has nothing to disclose. Ali Manouchehrinia is supported by the Margaretha af Ugglas Foundation. Ryan Ramanujam has nothing to disclose. Elena Mouresan has nothing to disclose. Jiri Drahota has nothing to disclose. Dana Horakova was supported by the Czech Ministry of Education (project Cooperatio LF1, research area Neuroscience). She also received compensation for travel, speaker honoraria, and consultant fees from Biogen Idec, Novartis, Merck, Sanofi, Roche, and Teva, as well as support for research activities from Biogen Idec. Hanna Joensen has received honoraria for an advisory board from Biogen. Luigi Pontieri has nothing to disclose. Melinda Magyari has served on the scientific advisory board, served as a consultant for, received support for congress participation, and received speaker honoraria from Biogen, Sanofi, Roche, Novartis, Merck, Abbvie, and Alexion. The Danish MR Registry received research support from Biogen, Genzyme, Roche, Merck, and Novartis. David Ellenberger has nothing to disclose. Alexander Stahmann has no personal pecuniary interests to disclose, other than being the lead of the German MS Registry, which receives funding from a range of public and corporate sponsors, recently including The German Innovation Fund (G-BA), The German MS Trust, German MS Society, Biogen, Celgene (Bristol-Myers Squibb), Merck, Novartis, Roche, and Sanofi. None resulted in a conflict of interest. Jeff Rodgers has nothing to disclose. The UK MS Register is funded by the MS Society. James Witts has nothing to disclose. The UK MS Register is funded by the MS Society. Rod Middleton has nothing to disclose. The UK MS Register is funded by the MS Society. Richard Nicholas has received support from advisory boards from Roche and Biogen. He has grant support from the UK MS Society and Berkeley Foundation and is a vice chair of a NICE HTA committee. Vladimir Bezlyak is an employee of Novartis Pharma AG. Nicholas Adlard is an employee of Novartis Pharma AG. Thomas Hach is an employee of Novartis Pharma AG. Carol Lines is an employee of Novartis Pharma AG. Sandra Vukusic has received grants, personal fees, unrestricted research grants, and nonfinancial support from Biogen, BMS-Celgene, Genzyme, Janssen, Merck Serono, Novartis, Roche, Sanofi, and Teva. Merja Soilu-Hanninen has received congress fee covering and lecture and consultation fees by Biogen, Celgene, Merck, Novartis, Roche, Sanofi, and Teva. Anneke van der Walt served on advisory boards and receives unrestricted research grants from Novartis, Biogen, Merck, Alexion, NervGen, and Roche. She has received speaker's honoraria and travel support from Novartis, Roche, Biogen, and Merck. She receives grant support from the National Health and Medical Research Council of Australia and MS Research Australia. Helmut Butzkueven's institution (Monash University) has received compensation for his services on scientific advisory boards and as a speaker from Biogen, Novartis, Roche, Merck, and UCB. He serves on steering committees for trials conducted by Biogen, Merck, and Novartis, and his institution has received research support from Roche, Merck, Novartis, and Biogen. Pietro Iaffaldano has received advisory board membership, speaker honoraria, and travel support from Almirall, Bayer Shering, Biogen, Genzyme, Merck, Novartis, Sanofi, Roche, Teva, and their local affiliates. Maria Trojano received advisory board membership, speaker honoraria, travel support and research grant from Almirall, Bayer Shering, Biogen, Genzyme, Merck, Novartis, Sanofi, Roche, Teva, and their local affiliates. Anna Glaser has received research support from Novartis. Jan Hillert has received honoraria for serving on advisory boards for Biogen, Celgene, Sanofi-Genzyme, Merck KGaA, Novartis, and Sandoz and speaker's fees from Biogen, Novartis, Merck KGaA, Teva, and Sanofi-Genzyme. He has served as PI for projects or received unrestricted research support from Biogen, Celgene, Merck KGaA, Novartis, Roche, and Sanofi-Genzyme. His MS research was funded by the Swedish Research Council and the Swedish Brain foundation.


 The authors declare no competing interests.



 Competing interests The authors report no competing interests. Conflict of interest statement The authors have declared that no conflict of interest exists.

 Competing Interests: The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare that they have no conflict of interests.

 Competing interests The authors declare no competing financial interests relative to the present study.

 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest Dr. Coyle's disclosures for the past 24 months: • Consulting & Nonbranded Speaker Fees: Accordant, Biogen, Bristol Myers Squibb, GlaxoSmithKline, Genentech, Horizon Therapeutics, LabCorp, Eli Lilly and Company, Mylan, Novartis, Sanofi Genzyme, TG Therapeutics • Research support: Actelion, Alkermes, Celgene, CorEvitas LLC, Genentech/Roche, Janssen, MedDay, NINDS, Novartis, Sanofi Genzyme
 The authors declare that there is no conflict of interest regarding the publication of this paper.
 The authors declare no conflict of interest.
 Declaration of Competing Interest WJB, AH, NW, SK, ZK, JD, and SM received consulting fees for model development from EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA. SK was an employee of ICON plc, Ontario, Canada at the time the study was conducted, and is currently an employee of AstraZeneca, Mississauga, Canada. ZK was employed by ICON plc at the time this study was conducted. BH was an employee of EMD Serono Research & Development Institute, Inc., Billerica, MA, USA, an affiliate of Merck KGaA, at the time the study was conducted. GTH is an employee of Merck Healthcare KGaA, Darmstadt, Germany. SM was an employee of ICON plc, Blue Bell, PA, USA at the time the study was conducted, and is currently an employee of Unlearn.AI, San Francisco, CA, USA



 The authors declare no conflict of interest.
 The authors declare that they have no competing interests.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: N.C.-F. was awarded with an ECTRIMS Clinical Training Fellowship Program in 2017–2018. S.N. has nothing to disclose. S.S. has nothing to disclose. T.S. is an employee at the MIAC in Basel. In the last 3 years, he has received travel support from Roche and Actelion. E.R. has nothing to disclose. A.P. has consulted for Teva and received speaker-fee from Sanofi Genzyme and travel support from Bayer AG, Teva, UCB-Pharma AG, and Hoffmann La Roche. Her research was/is being supported by the University of Basel, the University Hospital of Basel, the Swiss MS Society, the Swiss National Science Foundation, and the ‘Stiftung zur Förderung der gastroenterologischen und allgemeinen klinischen Forschung sowie der medizinischen Bildauswertung’. J.W. declares employment with Medical Image Analysis Center, scientific advisory board membership for Biogen, Genzyme, Novartis, Teva, and Roche; personal fees from Bayer, Novartis, and Roche; and grants from the European Union (Horizon 2020), German Federal Ministries of Education and Research (BMBF), and Economic Affairs and Energy (BMWI). J.K. received speaker fees, research support, travel support, and served on advisory boards by the Progressive MS Alliance, Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Biogen, Celgene, Merck, Novartis, Octave Bioscience, Roche, and Sanofi. Ö.Y. received advisory board/lecture and consultancy fees from Roche, Sanofi Genzyme, Biogen, and Novartis. L.K. received institutional research support from steering committee and advisory board; consultancy fees from Actelion, Bayer HealthCare, Biogen, Bristol Myers Squibb, Genzyme, Janssen, Japan Tobacco, Merck, Novartis, Roche, Sanofi, Santhera, Shionogi, and TG Therapeutics; speaker fees from Bayer HealthCare, Biogen, Merck, Novartis, Roche, and Sanofi; support of educational activities from Allergan, Bayer HealthCare, Biogen, CSL Behring, Desitin, Genzyme, Merck, Novartis, Roche, Pfizer, Sanofi, Shire, and Teva; license fees for Neurostatus products; and grants from Bayer HealthCare, Biogen, European Union, Innosuisse, Merck, Novartis, Roche, Swiss MS Society, and Swiss National Research Foundation. T.D. received speaker fees, research support, travel support and served on Advisory Boards, data safety monitoring boards, or Steering Committees of Actelion, Alexion, Celgene, Polyneuron, Novartis Pharma, Merck Serono, Biogen, Teva, Bayer-Schering, GeNeuro, Mitsubishi Pharma, MedDay, Roche, and Genzyme. B.F.-D. received travel support and fees from advisory boards and for consultations and speaker fees from Almirall, Biogen, Celgene, Merck, Novartis, Sanofi Genzyme, Roche, and Teva.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 PM, TG, PP, Ad'E, MP, MAB, VL declared no conflicts of interest; AMP received compensation for grants, participation in advisory board/data safety monitoring board and/or speaking activities from Biogen, Merck Serono, Roche, Novartis, Sanofi Genzyme, BMS SQUIBB, Janssen; RB received compensation for travel, grants, participation in advisory board/data safety monitoring board and/or speaking activities from Biogen, Merck Serono, Roche, Novartis, Celgene, Janssen, Sanofi Genzyme, Teva, Almirall; MC received compensation for consulting fee and/or speaking activities from Alexion, Biogen, Merck Serono, Roche, Novartis, Beckton-Dickinson; GC received compensation for consulting fee, grants, travel, participation in advisory board/data safety monitoring board and/or speaking activities from Merck Serono, Novartis, Sanofi Genzyme, Genzyme Corporation, Merck KGgA, Celgene, F. Hoffman-La Roche, Almirall, Janssen, BMS SQUIBB, BMS; CG received compensation for participation in advisory board/data safety monitoring board and/or speaking activities from Almirall, Jansen, Bayer, Biogen, Celgene, Merck, Mylan, Novartis, Roche, Sanofi and TEVA; FP received compensation for consulting fee, grants, travel, participation in advisory board/data safety monitoring board and/or speaking activities from FISM, RELOAD Onlus, Roche Biogen, Almirall, Bayer, Bristol Myers and Squibb, Merk, Novartis, Roche, Janssen, Sanofi, Alexion; MPu received compensation for consulting fee, grants, travel, participation in advisory board/data safety monitoring board and/or speaking activities from Janssen Cilag, Merck Serono, Sanofi Genzyme, Novartis, Biogen, Bristol Myers and Squibb; MU received compensation for travel, participation in advisory board/data safety monitoring board and/or speaking activities from Roche, Biogen, Sanofi Genzyme, Merck Serono; MT received compensation for grants, travel, participation in advisory board/data safety monitoring board and/or speaking activities from Biogen, Merck, Novartis, Roche, Janssen, Sanofi, Alexion, BMS.
 FINANCIAL DISCLOSURES: The authors declare no conflicts of interest.
 The authors have declared that no competing interests exist.
 I. Kister served on the scientific advisory board for Biogen Idec, Genentech, Alexion, Horizon, and EMD Serono; received consulting fees from Roche; and received research support from the Guthy-Jackson Charitable Foundation, National Multiple Sclerosis Society, Biogen Idec, Serono, Genzyme, and Genentech/Roche; he receives royalties from Wolters Kluwer for Top 100 Diagnoses in Neurology (co-written with Jose Biller). J. Katz served on the scientific advisory board for Genentech, EMD Serono, and Novartis and received speaker fees from Biogen, Genentech, EMD Serono, Novartis, and TG Therapeutics. A. Bouley served on the scientific advisory board for Banner, Genentech, and EMD Serono; received consulting fees from Novartis; and received speaker fees from Biogen, Genentech, and EMD Serono. E.H. Parrotta has served on advisory boards for Genentech and Novartis. T.E. Bacon, E.A. Douglas, I.L. O'Shea, and C. Oh have nothing to disclose. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.
 Mitzi J. Williams received advisory/consulting fees from Biogen, Celgene, EMD Serono, Genentech, Sanofi Genzyme, and Teva Neuroscience; speaker fees from Biogen, Genentech, Sanofi Genzyme, and Teva. Lilyana Amezcua received advisory/consulting fees from EMD Serono, Genzyme, and Novartis; research support from Biogen and MedDay. Angel Chinea received advisory/consulting fees from Biogen, Genentech, Novartis, Sanofi Genzyme, and Teva Neuroscience; research support from Biogen, Novartis, and Sanofi Genzyme; speaker fees from Biogen, Genentech, Novartis, Sanofi Genzyme, and Teva. Stanley Cohan advisory/consulting fees from Biogen, Celgene, Novartis, Pear Therapeutics, Roche Genentech, Sage Therapeutics, and Sanofi Genzyme; research support from AbbVie, Adamas, Alithios, Biogen, EMD Serono, MedDay, Novartis, Roche Genentech, and Sanofi Genzyme; speaker fees from Biogen, Roche Genentech, and Sanofi Genzyme. Annette Okai received advisory/consulting fees from Biogen, Celgene, EMD Serono, Genentech, Novartis, and Sanofi Genzyme; research support from Biogen, Novartis, Sanofi Genzyme, and TG Therapeutics; speaker fees from Biogen, Genentech, Novartis, Sanofi Genzyme, and Teva. Darin T. Okuda received personal compensation for consulting and advisory services from Alexion, Biogen, Celgene/Bristol Myers Squibb, EMD Serono, Genentech, Genzyme, Janssen, Novartis, Osmotica, RVL, TG Therapeutics, and Viela Bio; research support from Biogen and EMD Serono/Merck; has issued national and international patents along with pending patents related to other developed technologies; received royalties for intellectual property licensed by The Board of Regents of The University of Texas System. Wendy Vargas received advisory/consulting fees from Alexion, Biogen, Genentech, and Octapharma; research support from Teva. Nick Belviso, Ivan Božin, Xiaotong Jiang, James B. Lewin, Jennifer Lyons, Changyu Shen and Sarah M. England are employees of and hold stock/stock options in Biogen. Nydjie Grimes was an employee of Biogen at the time of analysis.
 Ahmed Shatila received honoraria for lectures (Sanofi-Genzyme, Merck, Genpharm, Roche, Novartis, Boehringeringer Ingelheim, Biologix) and for advisory boards (Sanofi-Genzyme, Roche, Novartis, Pfizer, Biologix); educational conferences travel and registration and hotel accommodation has been sponsored by Sanofi-Genzyme, Merck, Genpharm, Roche, Novartis, Biologix. Raed Alroughani received honoraria as a speaker and for serving in scientific advisory boards from Bayer, Biogen, Merck, Novartis, Roche, and Sanofi. Taoufik Alsaadi Alsaadi received consulting fees, honoraria, and research grants from Novartis, GlaxoSmithKline, Merck, Pfizer, and Hekma. Jihad Inshasi and Samar Farouk received honoraria as a speaker and for serving in scientific advisory boards from Bayer, Biogen, Merck, Novartis, Roche, and Sanofi. Victoria Mifsud received honoraria for participation in Advisory boards from Merck, Roche and Novartis. Amir Boshra and Shatha Sayegh are employees of Merck Serono Middle East FZ-Ltd. Mona Thakre, Abubaker Almadani, Beatrice Benedetti, Deeb Kayed, Derk Krieger, Miklos Szolics, Anu Jacob and Ali Hassan have nothing to disclose beyond the current work.
 The authors declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: Drs Ioannis N. Petropoulos, Fatima Al-Shibani, Gulfidan Bitirgen, Georgios Ponirakis, Adnan Khan, Hoda Gad, Ziyad R. Mahfoud, Heba Altarawneh, Muhammad Hassan Rehman, Karen John, Dhabia Al-Merekhi, Pooja George, Ali Ulvi Uca, Ahmet Ozkagnici, Faiza Ibrahim, Reny Francis, Beatriz Canibano, Dirk Deleu, Ahmed El-Sotouhy, Surjith Vattoth, Ahmed Own, Ashfaq Shuaib, Naveed Akhtar and Saadat Kamran declare no conflict of interest. Dr. Rayaz A. Malik is a principal investigator on grants from Proctor and Gamble and Pfizer and has received consulting honoraria for serving on advisory boards for Novo Nordisk, Aventis Pharma, and Proctor and Gamble.

 Declaration of interests H.T. and L.Z. received consulting fees from EMD Serono outside of the submitted work. D.J. has received consulting fees from Biogen, Genentech, Novartis, EMD Serono, Banner Life Sciences, Bristol Meyers Squibb, Horizon, Cycle and Sanofi Genzyme outside of the submitted work. A.BO. has received fees for advisory board participation and/or consulting from Abata, Accure, Atara Biotherapeutics, Biogen, BMS/Celgene/Receptos, GlaxoSmithKline, Gossamer, Immunic, Janssen/Actelion, Medimmune, Merck/EMD Serono, Novartis, Roche/Genentech, Sangamo, Sanofi-Genzyme, Viracta; and has received grant support to the University of Pennsylvania from Biogen Idec, Roche/Genentech, Merck/EMD Serono and Novartis. L.P. has recived grant support from Alector on projects not related to this work.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.
 O.S. serves on the editorial boards of Therapeutic Advances in Neurological Disorders; has served on data-monitoring committees for Genentech-Roche, Pfizer, Novartis, and TG Therapeutics without monetary compensation; has advised EMD Serono, Genentech, Genzyme, Novartis, TG Therapeutics, and VYNE; currently receives grant support from EMD Serono and Exalys; is a 2021 recipient of a Grant for Multiple Sclerosis Innovation (GMSI), Merck KGaA; is funded by a Merit Review grant [federal award document number (FAIN) BX005664-01] from the US Department of Veterans Affairs, Biomedical Laboratory Research and Development; and is funded by RFA-2203-39314 (PI) and RFA-2203-39305 (co-PI) grants from the National Multiple Sclerosis Society (NMSS).
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 DISCLOSURES: Ms Yaeger serves as a statistical editor for Circulation: Cardiovascular Imaging. Ms McFadyen and Dr Salter declare no conflicts of interest.
 The authors declare no conflicts of interest.

 Federico Carlini and Valeria Lusi report no conflicts of interest. Alice Laroni received fees for consultation from Roche, Genzyme, Merck, Biogen, Novartis, Bristol-Myers Squibb. Caterina Rizzi and Francesco Assogna are employees of Merck Serono S.p.A., Italy, an affiliate of Merck KGaA.
 The authors declare no conflict of interest.
 The authors declare no competing interests.



 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 D.L.K. and J.T. are inventors of GABA-related patents. D.L.K. is an inventor of GAD-related patents and serves on the Scientific Advisory Board of Diamyd Medical.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest Helga Taylor, Saleh Alhasan, Maha Saleem(,) Shane Poole, Fei Jiang report no disclosures. Erin E. Longbrake has received research support from Genetech, NIH. She has received consulting or advisory board fees from Genentech, Janssen, TG Therapeutics, NGM Bio, Bristol Myers Squibb, EMD Serono and Genzyme. Riley Bove is supported by a National Multiple Sclerosis Society Harry Weaver Award. She receives research support from NIH, NSF, Department of Defense, National Multiple Sclerosis Society, as well as from Biogen, Novartis and Roche Genentech. She also reports scientific advisory board and consulting fees from Alexion, EMD Serono, Horizon, Genzyme Sanofi, Janssen, and TG Therapeutics.


 Disclosure: Naimah Dease declares no relevant financial relationships with ineligible companies. Disclosure: Emily Kershner declares no relevant financial relationships with ineligible companies. Disclosure: Brandon Wills declares no relevant financial relationships with ineligible companies.
 Disclosure: Franklyn Rocha Cabrero declares no relevant financial relationships with ineligible companies. Disclosure: Elizabeth Morrison declares no relevant financial relationships with ineligible companies.
 The authors declare no conflict of interest.
 Declaration of Competing Interest None.

 The authors declare no competing interests.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: AB-Z received consulting fees from Biogen, EMD Serono, Greenwich Biosciences, TG Therapeutics, and Genentech. She received educational grants from Biogen and Greenwich Biosciences. J-ML received consulting and speaking fees from Biogen, Sanofi Genzyme, and Novartis. JK is owner of BPS International and IHS International, which have received consulting fees from Greenwich Biosciences and Vertex Pharmaceuticals. No funding was received for authorship of this article. BL has no financial conflicts to disclose.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 All other authors listed declare no competing financial and/or non-financial interests in relation to the work described.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: LM received personal fees from Biogen and Merck. SR declares no conflict of interest, CBS declares no conflict of interest. SL has received speakeŕs honoraria and honoraria for attendance at advisory boards from Alexion and Argenx. TZ personal compensation and project support from Alexion, Almirall, Biogen, Bristol Myers Squibb, Janssen, Novartis, Roche, Sanofi, and Teva. TR reports grants from German Ministry of Education, Science, Research and Technology, grants and personal fees from Sanofi-Aventis and Alexion; personal fees from Biogen Idec, Roche and Teva; personal fees and nonfinancial support from Merck Serono, outside the submitted work. SGM received honoraria for lecturing and travel expenses for attending meetings from Almirall, Amicus Therapeutics Germany, Bayer HealthCare, Biogen, Celgene, Diamed, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Novo Nordisk, ONO Pharma, Roche, Sanofi-Aventis, Chugai Pharma, QuintilesIMS, and Teva. His research is funded by the German Ministry for Education and Research (BMBF), Bundesinstitut für Risikobewertung (BfR), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Gemeinsamer Bundesausschuss (G-BA), German Academic Exchange Service, Hertie Foundation, Interdisciplinary Center for Clinical Studies (IZKF) Muenster, German Foundation Neurology and by Alexion, Almirall, Amicus Therapeutics Germany, Biogen, Diamed, Fresenius Medical Care, Genzyme, HERZ Burgdorf, Merck Serono, Novartis, ONO Pharma, Roche, and Teva. MP received honoraria for lecturing from Argenx, Biogen and Merck. He received research funding from Novartis. His research is funded by the German Multiple Sclerosis Society North Rhine-Westphalia (DMSG) and the programme ‘Innovative Medizinische Forschung’ (IMF) of the Medical Faculty of the University of Muenster.
 Declaration of Competing Interest Shamik Bhattacharyya has received research support from National Institute of Health, Alexion Pharmaceuticals, UCB, and Judy Pauline Staples Aull Research Award; consulting fees from Alexion Pharmaceuticals, Teladoc Health; publishing honorarium from UpToDate and American Academy of Neurology. Kristin Galetta has received consulting fees from Glaxo Smith Kline. Landon Oetjen has nothing to report.
 S.S.M. received research grants, travel support or honoraria for speaking engagements from Almirall, Biogen, Bristol Myers Squibb, Janssen, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme, and Teva. E.M. received research grants, travel support or honoraria for speaking engagements from Almirall, Biogen, Janssen, Merck, Novartis, Roche, and Sanofi-Genzyme. L.C.-F. received speaker fees and travel support from, and/or served on advisory boards by, Almirall, Bayer, Biogen, Biopas, Bristol Myers Squibb, Celgene, Ipsen, Janssen, Merck, Novartis, Roche, Sanofi and Teva. L.V. received research grants, travel support or honoraria for speaking engagements from Biogen, Bristol Myers Squibb, Merck, Novartis, Roche and Sanofi-Genzyme. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of interests The authors declare no competing interests.
 Competing interests: MM reports grants and personal fees from Almirall. She was awarded a MAGNIMS-ECTRIMS fellowship in 2020. PP received speaker honoraria from Roche, Biogen, Novartis, Merck Serono, Bristol Myers Squibb and Genzyme. He has received research support from Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. LS declared the receipt of grants and contracts from FISM within a fellowship program and received speakers’ honoraria from Biogen Idec. MG has nothing to disclose. LM received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Sanofi-Genzyme, Novartis, Teva, Merck Serono, Biogen, Roche, and Excemed. MF is editor-in-chief of the Journal of Neurology, Associate Editor of Human Brain Mapping, Neurological Sciences, and Radiology; received compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA; participation in Advisory Boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Lilly, Novartis, Sanofi-Genzyme; he receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. MAR received consulting fees from Biogen, Bristol Myers Squibb, Eli Lilly, Janssen, Roche; and speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Bromatech, Celgene, Genzyme, Merck Healthcare Germany, Merck Serono SpA, Novartis, Roche, and Teva. She receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. She is Associate Editor for Multiple Sclerosis and Related Disorders.
 None
 Disclosure: Donavon Johnson declares no relevant financial relationships with ineligible companies. Disclosure: Michael Lopez declares no relevant financial relationships with ineligible companies. Disclosure: Brendan Kelley declares no relevant financial relationships with ineligible companies.


 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of interests The authors declare no competing interests.
 The authors declare no conflict of interest.
 Conflict of Interest Disclosures: Dr Hemmer reported personal fees from Polpharma and Sandoz during the conduct of the study; personal fees from Novartis, Biocom, and TG Therapeutics outside the submitted work; a patent for genetic determinants of antibodies against interferon-beta issued and a patent for KIR4.1 antibodies in multiple sclerosis issued; served on scientific advisory boards for Novartis; served as data monitoring and safety committee member for AllergyCare, Polpharma Biologics SA, Sandoz, and TG therapeutics; speaker honoraria from Desitin paid to himself and his institution; grants from Regeneron for multiple sclerosis research paid to his institution; funding from the Multiple MS EU consortium, the Clinspect-M consortium funded by the Bundesministerium für Bildung und Forschung, and the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy; ID 390857198). Dr Wiendl reported honoraria for serving on scientific advisory boards, speaker honoraria, and travel support from AbbVie, Actelion, Alexion, Amicus Therapeutics Inc, Argenx, Biogen, BMS/Celgene, Bristows, CSL Behring, Deutsche Forschungsgesellschaft (DFG), Deutsche Myasthenie Gesellschaft eV, EMD Serono, F. Hoffmann-La Roche Ltd, Fondazione Cariplo, Genzyme, German Ministry for Education and Research (BMBF), Gossamer Bio, Idorsia, IGES, Immunic, Immunovant, Janssen, Johnson & Johnson, Lundbeck, Merck, Neurodiem, NexGen, Novartis, PSI CRO, Sanofi, Swiss Multiple Sclerosis Society, Teva Pharmaceuticals, UCB Biopharma, WebMD Global, and Worldwide Clinical Trials and research support from Biogen, Merck, Novartis, Hoffmann LaRoche, Deutsche Forschungsgemeinschaft, and the Federal Government of Germany paid to their institution. Dr Selmaj reported personal fees from Polpharma Biologics SA during the conduct of the study; personal fees from Roche, Biogen, Novartis, BMS, TG Therapeutics, Sanofi, Celgene, and Merck outside the submitted work; in addition, Dr Selmaj had a patent for myelin patches issued. No other disclosures were reported.

 Competing interests O.A.A. has received speaker’s honorarium from Lundbeck, Sunovion and Janssen and is a consultant for Cortechs.ai. A.M.D. is a founder of and holds equity interest in CorTechs Labs and serves on its scientific advisory board. He is also a member of the Scientific Advisory Board of Healthlytix and receives research funding from General Electric Healthcare (GEHC). The terms of these arrangements have been reviewed and approved by the University of California, San Diego in accordance with its conflict of interest policies. Remaining authors have nothing to disclose.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have no disclosures.
 Declaration of Competing Interest The authors report no conflict of interest.




 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 Disclosure: Dawood Tafti declares no relevant financial relationships with ineligible companies. Disclosure: Moavia Ehsan declares no relevant financial relationships with ineligible companies. Disclosure: Kathryn Xixis declares no relevant financial relationships with ineligible companies.

 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

 There are no competing interests.
 Conflict of interests The authors declare no competing interests.

 AL was a cofounder of KeyWise AI, currently a consultant for Otsuka US, and on the medical board of Buoy Health. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of interests The authors declare no competing interests.


 The authors declare no competing interests.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of interest The authors declare no conflicts of interest.
 The authors declare no conflict of interest.

 Conflict of Interest: S. Şen, M. Tütüncü, S. Demir, T. Gündüz, C. Uzunköprü, H. Gümüş have received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. Aslı Tuncer has received honoraria or consultancy fees for partici- pating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. Serkan Özakbaş has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck- Serono, Novartis, Teva, Biogen Idec/Gen Pharma. H. Efendi has received honoraria or consultancy fees for partici- pating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi Ibrahim Rana Karabudak has received honoraria for giving educational lec- tures, consultancy fees for participating advisory boards, and travel grants for attending scientific congresses or symposia from Roche, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey, Abdi Ibrahim Ilac, Deva and ARIS. Aksel Siva has received honoraria or consultancy fees for partici- pating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi Ibrahim Ilac. The rest of authors declare no conflict of interest with the study project.
 Declaration of Competing Interest The authors declare that there is no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 No potential conflict of interest was reported by the author(s).
 HI received speaker honoraria from Roche and financial support for research activities from Teva, Biogen and Alexion. SG has or has had consulting relationships with Una Health GmbH, Lindus Health Ltd.; Flo Health Ltd, and Thymia Ltd., FORUM Institut für Management GmbH, High-Tech Gründerfonds Management GmbH, Ada Health GmbH and holds share options in Ada Health GmbH. JNK reports consulting services for Owkin, France, Panakeia, UK and DoMore Diagnostics, Norway and has received honoraria for lectures by MSD, Eisai and Fresenius. UP received personal compensation from Bayer, Biogen and Roche for the consulting service. KA received personal compensation from Novartis, Biogen Idec, Teva, Sanofi and Roche for the consulting service. TZ reports scientific advisory board and/or consulting for Biogen, Roche, Novartis, Celgene, and Merck; compensation for serving on speakers bureaus for Roche, Novartis, Merck, Sanofi, Celgene, and Biogen; research support from Biogen, Novartis, Merck, and Sanofi.
 Disclosure: Anu Saji declares no relevant financial relationships with ineligible companies. Disclosure: Vikas Gupta declares no relevant financial relationships with ineligible companies.
 Disclosure: Shirin Ghanavatian declares no relevant financial relationships with ineligible companies. Disclosure: Armen Derian declares no relevant financial relationships with ineligible companies.
 Disclosure: Wael Ibrahim declares no relevant financial relationships with ineligible companies. Disclosure: Nowera Zafar declares no relevant financial relationships with ineligible companies. Disclosure: Sandeep Sharma declares no relevant financial relationships with ineligible companies.
 Disclosure: Natalia Miranda-Cantellops declares no relevant financial relationships with ineligible companies. Disclosure: Timothy Tiu declares no relevant financial relationships with ineligible companies.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Disclosures SG reports past consultancy or advisory roles for Merck and OncoMed; research funding from Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Genentech, EMD Serono, Pfizer, Regeneron Pharmaceuticals, and Takeda, all unrelated to the current work. The Icahn School of Medicine at Mount Sinai has filed patent applications relating to SARS-CoV-2 serological assays and NDV-based SARS-CoV-2 vaccines which list Florian Krammer as co-inventor. Mount Sinai has spun out a company, Kantaro, to market serological tests for SARS-CoV-2. Florian Krammer has consulted for Merck and Pfizer (before 2020), and is currently consulting for Pfizer, Seqirus, 3rd Rock Ventures and Avimex. The Krammer laboratory is also collaborating with Pfizer on animal models of SARS-CoV-2.


 Kyong Jin Shin, a contributing editor of the Journal of Clinical Neurology, was not involved in the editorial evaluation or decision to publish this article. All remaining authors have declared no conflicts of interest.

 The authors declare no conflict of interest.
 Competing interests: PE has no conflicts of interests or financial disclosures to declare regarding this submission. LC received speaker and consultant honoraria from Biomedia, ACCMED, Roche, BMS Celgene and Sanofi. KNK and DG reports no disclosures. JJC has received consulting fees from Roche, UCB and Horizon. ASL-C has served on advisory boards for Genentech and Horizon Therapeutics. ES, VR and PPM reports no disclosures. JLC has received research support from Roche and Genentech for an MS clinical trial, and serves as chair of the DMSC for several migraine clinical trials. DMW has received consulting fees from Alexion, Roche, Genentech, Horizon Therapeutics, Imcyse, Bristol Myers Squibb and Reistone, serves on an attack adjudication committee for a MOGAD clinical trial funded by UCB Pharma and is co-editor in chief of the neurologist. J-MT is associate editor for Journal of Child Neurology. CV-S and ST no disclosures. SJP reports grants, personal fees and non-financial support from Alexion Pharmaceuticals; grants, personal fees, non-financial support and other support from MedImmune, Inc/Viela Bio.; personal fees for consulting from Genentech/Roche. He has a patent, Patent# 8889102 (application#12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia)—issued; a patent, Patent# 9891219B2 (application#12-573942, Methods for Treating Neuromyelitis Optica (NMO) by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)-IgG Autoantibody positive)—issued. EPF has served on advisory boards for Alexion, Genentech, Horizon Therapeutics and UCB. He has received research support from UCB. He has received speaker honoraria from Pharmacy Times. He received royalties from UpToDate. EPF was a site primary investigator in a randomised clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics. EPF has received funding from the NIH (R01NS113828). EPF is a member of the medical advisory board of the MOG project. EPF is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports. A patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity.
 M.H.: Participated as a clinical investigator and/or received consultation and/or speaker fees from Biogen, Sanofi Genzyme, Merck, Bayer, Novartis, Pliva/Teva, Roche, Alvogen, Actelion, Alexion Pharmaceuticals, TG Pharmaceuticals. Other authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest. Figures were created using BioRender software(©) (biorender.com, accessed on 7 November 2022).


 Declaration of Competing Interest All authors declare that there are no conflicts of interest.
 The authors disclose no conflict of interest regarding this article.
 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
 The authors report no conflicts of interest.



 The authors declare no conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor declared a past co-authorship/collaboration (DOI: 10.1159/000524587) with the author BM.
 Disclosure of competing interests The authors declare that they have no competing interest.


 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 X Jiang, G Simoneau, A Harrington, W Castro-Borrero, C de Moor, F Pellegrini are employees and former employees of and hold stock/stock options in Biogen. L Tian received consulting fees from Biogen. M Zuercher, P van Hoevell, and Y Heer are employees of Rewoso AG, Zürich, Switzerland. A Bergmann has received consulting fees from advisory board, speaker, and other activities for NeuroTransData; project management and clinical studies for and travel expenses from Novartis and Servier. S Braune has received honoraria from Kassenaerztliche Vereinigung Bayern and health maintenance organizations for patient care; honoraria for consulting, project management, clinical studies, and lectures and from Biogen, Eli Lilly, Merck, NeuroTransData, Novartis, Roche, and Thieme Verlag; honoraria and expense compensation as board member of NeuroTransData.
 The authors declare no conflict of interest.

 The authors report no conflicts of interest in this work.
 None declared.



 The authors declare no competing interests.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 SL has nothing to disclose. AML received consulting fees for ADC therapeutics SA not related to this study. PHL received honoraria for speaking for Biogen-Idec, CSL Behring, Merck Serono, Novartis, Sanofi-Aventis, TEVA, Roche; consulting fees from Biogen-Idec, Geneuro, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, TEVA; research grants from Biogen-Idec, Merck Serono, Novartis nonrelated to this study.

 Stephen L. Hauser has received personal compensation from Annexon, Alector, Accure, and Neurona; he has also received travel reimbursement from F. Hoffmann-La Roche Ltd and Novartis for CD20-related meetings and presentations. Ludwig Kappos has received no personal compensation. His institutions (University Hospital Basel/Stiftung Neuroimmunology and Neuroscience Basel) have received the following exclusively for research support: steering committee, advisory board and consultancy fees (Abbvie, Actelion, Auriga Vision AG, Bayer HealthCare, Biogen, Celgene, df-mp [Dörries Frank-Molnia & Pohlman], Eli Lilly, EMD Serono, Genentech, Genzyme, Glaxo Smith Kline, Janssen, Merck, Minoryx, Novartis, Roche, Sanofi, Santhera, Senda Biosciences, Shionogi and Wellmera AG); speaker fees (Bristol Myrers Squibb, Celgene, Janssen, Merck, Novartis, and Roche); support for educational activities (Biogen, Desitin, Novartis, Sanofi and Teva); license fees for Neurostatus products; and grants (European Union, Innosuisse, Novartis, Roche, Swiss MS Society and Swiss National Research Foundation). Amit Bar-Or has participated as a speaker in meetings sponsored by, and received consulting fees and/or grant support from, Accure, Atara Biotherapeutics, Biogen, BMS/Celgene/Receptos, GlaxoSmithKline, Gossamer, Janssen/Actelion, Medimmune, Merck/EMD Serono, Novartis, Roche/Genentech, Sanofi Genzyme. Heinz Wiendl has received honoraria for acting as a member of scientific advisory boards for Biogen, Evgen, Genzyme, MedDay Pharmaceuticals, Merck Serono, Novartis, Roche Pharma AG, and Sanofi-Aventis, as well as speaker honoraria and travel support from Alexion, Biogen, Cognomed, F. Hoffmann-La Roche Ltd., Gemeinnützige Hertie-Stiftung, Merck Serono, Novartis, Roche Pharma AG, Genzyme, Teva, and WebMD Global. Heinz Wiendl is acting as a paid consultant for AbbVie, Actelion, Biogen, IGES, Johnson & Johnson, Novartis, Roche, Sanofi-Aventis, and the Swiss Multiple Sclerosis Society. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Fresenius Foundation, the European Union, Hertie Foundation, NRW Ministry of Education and Research, Interdisciplinary Center for Clinical Studies (IZKF) Muenster and RE Children’s Foundation, Biogen, GlaxoSmithKline GmbH, Roche Pharma AG, and Sanofi-Genzyme. David Paling has participated as a speaker in meetings sponsored by, and received consulting fees from, Biogen, Celgene, Janssen, MedDay, Merck, Novartis, Sanofi Genzyme and Roche. Mitzi J. Williams has received consulting fees from EMD Serono, Horizon, Novartis, Alexion, Biogen, Sanofi, Genentech, Octave Biosciences, TG Therapeutics, Janssen, and Bristol Myers Squibb; and speaking fees from Genentech, Biogen, EMD Serono and TG Therapeutics. Ralf Gold has received compensation for serving as a consultant or speaker from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis and Teva Neuroscience. He, or the institution he works for, has received research support from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis and Teva Neuroscience. He has also received honoraria as a Journal Editor from SAGE and Thieme Verlag. Andrew Chan has received speakers’/board honoraria from Actelion (Janssen/J&J), Alexion, Almirall, Bayer, Biogen, Celgene (BMS), Merck KgaA, Novartis, Roche, Sanofi, and Teva, all for hospital research funds. He received research support from Biogen, Roche, Sanofi and UCB. Ron Milo has received research support from Bayer, Medison, Merck, Novartis and Teva; and honoraria or consulting fees from Actelion, Bayer, Biogen, Genzyme, Medison, Merck, Neopharm, Novartis, Roche, Sanofi, Teva and TG-Therapeutics. Patrick Vermersch has received honoraria and consulting fees from Biogen, Sanofi, Teva, Novartis, Merck, Imcyse, Roche and AB Science, and research support from Biogen, Sanofi and Merck. Ayan Das Gupta, Goeril Karlsson, Roseanne Sullivan, Gordon Graham, Martin Merschhemke and Dieter A. Häring are employees of Novartis.
 Disclosure: Frederick Chu declares no relevant financial relationships with ineligible companies. Disclosure: Marco Cascella declares no relevant financial relationships with ineligible companies.

 The authors declare that they have no competing interests.

 Disclosure: Yana Puckett declares no relevant financial relationships with ineligible companies. Disclosure: Aishah Gabbar declares no relevant financial relationships with ineligible companies. Disclosure: Abdullah Bokhari declares no relevant financial relationships with ineligible companies.

 Disclosure: Franklyn Rocha Cabrero declares no relevant financial relationships with ineligible companies. Disclosure: Orlando De Jesus declares no relevant financial relationships with ineligible companies.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Disclosure: Kaberi Feroze declares no relevant financial relationships with ineligible companies. Disclosure: Jim Wang declares no relevant financial relationships with ineligible companies.
 Conflict of Interest Disclosures: Dr. Baller reported receiving grants from the National Institutes of Health (NIH) during the conduct of the study. Dr. Shinohara reported receiving grants from the NIH and the Multiple Sclerosis Society during the conduct of the study. Dr. Shinohara receives consulting income from Octave Bioscience, and compensation for scientific reviewing from the American Medical Association. Dr. Satterthwaite reported receiving grants from the NIH during the conduct of the study.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 Disclosure: Jeevan Gautam declares no relevant financial relationships with ineligible companies. Disclosure: Conrad Krawiec declares no relevant financial relationships with ineligible companies.

 None to declare.
 IP is one of the founders of the Neuroaspis PLP10(®) intervention formula and a director of the company that owns the rights of the intellectual property of the product. The remaining authors have no conflict of interest.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest The authors have no competing interests to declare relevant to the content of this work.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflict of interest None
 The authors have no conflict of interest to report.
 The authors declare no conflict of interest.

 The authors declare no conflict of interest.
 Ü.K., S.H., K.K. and S.D. have nothing to declare. R.G. received speaker’s and board honoraria from Baxter, Bayer Schering, Biogen Idec, CLB Behring, Genzyme, Merck Serono, Novartis, Stendhal, Talecris and Teva. His department received grant support from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis and Teva. All are not related to the content of this manuscript. SF received speaker’s and/or scientific board honoraria and/or support for the attendance of scientific meetings from Biogen, BMS, Celgene, Genesis Pharma, Janssen, Novartis and Roche and grant support from Ruhr-University Bochum, DMSG, Stiftung für therapeutische Forschung, Lead Discovery Center GmbH and Novartis. All are not related to the content of this manuscript.
 Declaration of Competing Interest Jeremy Hobart has received consulting fees, honoraria, support to attend meetings or research support from Acorda, Asubio, Bayer Schering, Biogen Idec, F. Hoffmann-La Roche, Genzyme, Merck Serono, Novartis, Oxford PharmaGenesis and Teva. Disclosures do not show a conflict with the work being presented. Tanuja Chitnis has received compensation for consulting from Biogen, Novartis Pharmaceuticals, Roche Genentech, and Sanofi Genzyme. She has received research support from Brainstorm Cell Therapeutics, EMD Serono, I-Mab Biopharma, Mallinckrodt ARD, the National Institutes of Health, National MS Society, Novartis Pharmaceuticals, Octave Bioscience, Roche Genentech, Sumaira Foundation, Tiziana Life Sciences, and US Department of Defense. Disclosures do not conflict with the work being presented. Jiwon Oh has received research support from Biogen-Idec, Eli-Lilly, EMD-Serono, and Roche; and fees for consulting or speaking from Biogen-Idec, Bristol Myers Squibb, EMD-Serono, Novartis, Roche, and Sanofi-Genzyme. Laurie Burke has past and ongoing research support and contracts from various non-profit organisations and for-profit companies that do not conflict with this work. Andrew Lloyd works for and holds stock in Acaster Lloyd Consulting Ltd which has received fees from Novartis. Disclosures do not show a conflict with the work being presented. Pamela Vo is an employee of Novartis Pharma AG. Miriam King and Jo Vandercappellen were employees of Novartis Pharma AG during the analysis of this study and manuscript development.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflicts of interest and sources of funding: T.S. has received research support from Novartis Pharmaceuticals and Genzyme-Sanofi, consulting fees from Novartis pharmaceuticals, speaking fee from Tiziana Life Sciences, and research funding from Nancy Davis Foundation’s “Race to Erase MS” program, Ann Romney Center for Neurologic Diseases, Harvard Neuro-Discovery Center, National Multiple Sclerosis Society, Department of Defense, and Water Cove Charitable Foundation. H.L.W. has received research support from Cure Alzheimer’s Fund, EMD Serono, Inc, Genentech, Inc, National Institutes of Health, National Multiple Sclerosis Society, Genzyme-Sanofi, and Verily Life Sciences, and payment for consulting from Genentech, Inc, IM Therapeutics, I-MAB Biopharma, MedDay Pharmaceuticals, Tiziana Life Sciences, and vTv Therapeutics. The other authors have nothing to disclose.
 Disclosure: Irim Salik declares no relevant financial relationships with ineligible companies. Disclosure: Ryan Winters declares no relevant financial relationships with ineligible companies.
 The author declares no conflict of interest.
 Conflict of interest Authors have no conflict of interests to disclose.
 D.V. is an owner and CEO of Driatec srl. The remaining authors declare no conflict of interest.


 Declaration of Competing Interest The authors report no conflicts of interest and certify that no funding has been received for this study and/or preparation of this manuscript.
 Competing interests: None declared.
 Competing interests: None declared.
 Declaration of Competing Interest The authors declare that there were no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest Statement PML is an advisor and has ownership interest in Vironika, LLC.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 Disclosure The authors have nothing to disclose.
 The authors have declared that no competing interests exist.

 Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflicts of Interest No potential conflict of interest relevant to this article was reported.
 The authors declare no conflict of interest.




 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Disclosure: Christopher Simone declares no relevant financial relationships with ineligible companies. Disclosure: Prabhu Emmady declares no relevant financial relationships with ineligible companies.
 Disclosure: Hillary Moss declares no relevant financial relationships with ineligible companies. Disclosure: Jonathan Weil declares no relevant financial relationships with ineligible companies. Disclosure: Pinaki Mukherji declares no relevant financial relationships with ineligible companies.
 C.K.N. has no conflict of interest to declare. M.A.G.-B. is founder and has significant ownership of Autoimmunity Biologic Solutions, Inc., which is commercializing therapeutic approaches that target the alternative splicing of IL7R transcripts. This ownership and associated intellectual property could constitute or be perceived as constituting a conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.




 Declaration of Competing Interest None. The authors declare no competing interests. This work was supported by a research grant from 100 Talent Grant of the Province of Shandong, China, to L.S.C., and C.B. and by a Deutsche Forschungsgemeinschaft (DFG), SFB 940.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.

 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: The authors are affiliated with BIOLONG. Roman R Rodriguez Martin is the discoverer and lead developer of Biomodulina T® and InmunyVital® and the Founder of the Laboratory of Biomodulators and the Founder and President of BIOLONG, the company commercializing InmunyVital® (Biomodulina T®).
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Susana Sainz de la Maza received payment for lecturing or travel expenses from Merck, Biogen, Sanofi- Genzyme, Roche, and Novartis. Ana María Alonso Torres received compensation for consulting services from Biogen, BMS, Sanofi, Roche, Janssen and Novartis; and speaking honoraria from Biogen, BMS, Sanofi, Roche, Janssen, Merck, Almirall and Novartis. Ana B Caminero received courses and honoraria for her participation as speaker/meeting moderator/symposia organizer from Alter, Almirall, Bayer, Bial, Biogen, Bristol-Myers-Squibb, Lilly, Merck, Mylan, Novartis, Roche, Sanofi-Genzyme, Teva and UCB; and support to attend scientific meetings from Biogen, Bial, Merck-Serono, Novartis, Roche, Sanofi-Genzyme and Teva. Laura Borrega received compensation for consulting services, speaking honoraria and support to attend scientific meetings from Bayer, Celgene, Biogen, Genzyme, Merck, Novartis, Roche, Almirall and Teva. José L Sánchez-Menoyo received support to attend scientific meetings from Novartis, Merck, and Biogen; speaking honoraria from Biogen, Novartis, Sanofi, Merck, Almirall, Bayer and Teva; and participated in clinical trials from Biogen, Merck, and Roche. Francisco J Barrero-Hernández received compensation for consulting services and speaking honoraria from Almirall, Biogen, Genzyme, Merck, Novartis, Roche, Sanofi and Teva. Carmen Calles received compensation for consulting services, speaking honoraria and support to attend scientific meetings and courses from Merck, Teva, Sanofi-Genzyme, Novartis, Biogen, Roche, and Bristol-Myers-Squibb. Julio Dotor García-Soto received compensation for consulting services and speaking honoraria from Biogen, Novartis, Merck, UCB, Sanofi-Genzyme, Roche, Almirall and Teva. Laura Navarro-Cantó received compensations from Sanofi-Genzyme, Merk, Biogen and Roche. Eduardo Agüera-Morales received speaking honoraria from Roche, Novartis, Merck, Sanofi and Biogen. Moisés Garcés has received speaking honoraria from Biogen, Sanofi, Almirall and Novartis. Laura Gabaldón-Torres received speaking honoraria from Biogen, Novartis, Merck, Bayer, Sanofi-Genzyme, Almirall, Roche and Teva. Mariona Hervás participated in observational studies and received compensation for consulting services and speaking honoraria from Roche, Merck, Sanofi, Biogen, Novartis and Bayer. Jorge Maurino and Rocío Gómez-Ballesteros are employees of Roche Farma Spain. Tamara Castillo-Triviño reports personal fees from Almirall, Biogen, Bristol Myers Squibb, Janssen, Merck, Novartis, Roche, and Sanofi-Genzyme, outside the submitted work. The rest of the authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest The authors declare that they have no conflict of interest.
 We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. Multiple sclerosis (MS) is the most common debilitating neurological disease among adults. MS is an autoimmune central nervous system disorder characterised by demyelination and neurodegeneration that leads to physical disability. Previous researches examined nutritional strategies that are potentially effective for MS management.(,) Given the important role of inflammation, oxidative stress and mitochondrial dysfunction in MS development, treatments with anti-inflammatory and antioxidant supplements have received growing attention.(,) Among them, coenzyme Q10 (CoQ10) is considered a promising therapeutic agent in neurodegenerative diseases. The administration of CoQ10 alone or in combination with other substances in mice with induced-neurodegenerative disease provided neuroprotective effects such as decreased brain oxidative stress and damage, as well as increased neurotrophic factors (e.g., BDNF).(,) CoQ10 supplementation might be of potential interest due to its anti-inflammatory and antioxidant effects in MS patients, as well as its positive effects on fatigue and depressive symptoms. Physical exercise is also a potential therapeutic strategy for managing MS, and is considered safe and effective, with positive effects in fitness, functional capacity and quality of life. Exercise exerts its positive therapeutic effects through different pathways. It increases regeneration of sensory neurons after axonal injury, stimulates the expression of genes associated with axon growth and regeneration, and improves nerve function.(,) Physical exercise can also reduce MS symptoms by improving motor coordination, aerobic capacity and muscle strength. Moreover, physical exercise has been shown to increase the expression of neurotrophic factors such as brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF).(,) Although many different strategies have been used, the combination of resistance and aerobic training, known as concurrent training (CT), has been shown to be particularly beneficial for people with MS.(,) Considering the potential benefits of CoQ10 supplementation in MS, it is plausible to suggest that it might exert additional effects when combined with CT. Therefore, the aim of the present study was to investigate the effects of eight weeks of a CT and CoQ10 supplementation on physical function, serum BDNF and NGF levels in people with MS. Our hypothesis is that CT would promote improvements in the studied outcomes with higher results for the combination of CT and CoQ10.
 Declaration of competing interest The authors declare no competing interest.
 The authors declare no conflicts of interest.
 The authors declare no conflict of interest.
 The authors declare no competing interests.


 Declaration of competing interest None.
 Declaration of Competing Interest The authors have no conflict of interests to disclose.





 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors have declared that no competing interests exist.


 The authors have no conflict of interest associated with the submitted article.




 The authors declare no conflict of interest.

 The authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Competing interests: CL has received consulting or travel fees from Biogen, Novartis, Roche, Sanofi, Teva and Merck Serono, and research grant from Biogen, none related to the present work. EM has received consulting or travel fees from Alexion, Biogen, Horizon, Janssen, Merck, Novartis, Sanofi and Teva, and research grant from Biogen, none related to the present work. VP has received consulting or travel fees from Gilead, ViiV, MSD, Biogen, Novartis, Roche and Merck Serono, none related to the present work. LJ, BA, CS, DS, YB, AH, LB and A-GM have no competing interest to declare.

 Declaration of Competing Interest Two authors (WLS & KRL) are among the co-founders of S1P Therapeutics Inc, which was created to commercialize S1P-related discoveries (including S1P transport inhibitors) from their laboratories.
 The authors have declared that no competing interests exist.
 The authors have declared that no competing interests exist.
 Declaration of Competing Interest The authors declare that they have no conflict of interest.
 The authors declare no competing interests.
 Disclosure: Andrew Harb declares no relevant financial relationships with ineligible companies. Disclosure: Stephen Kishner declares no relevant financial relationships with ineligible companies.

 There are no conflicts of interest.





 This work has been filed as an international patent WO 2022/023773 A1.
 Disclosure: Caleb Shumway declares no relevant financial relationships with ineligible companies. Disclosure: Bhupendra Patel declares no relevant financial relationships with ineligible companies. Disclosure: Orlando De Jesus declares no relevant financial relationships with ineligible companies.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Competing interests: CAH: unrelated grant funding from Pfizer; advisory board for AstraZeneca Canada for unrelated product; unrelated research funds from Research Manitoba, Health Science Center Foundation and International League of Associations for Rheumatology; and unrelated educational funds from the Royal College of Physicians and Surgeons of Canada. RAM: receives research funding from CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn’s and Colitis Canada, National Multiple Sclerosis Society, CMSC, Arthritis Society, Brain Canada, and US Department of Defense; coinvestigator on a study funded in part by Biogen Idec and Roche Canada; and supported by the Waugh Family Chair in Multiple Sclerosis. CNB: supported by the Bingham Chair in Gastroenterology; has served on advisory boards for AbbVie Canada, Amgen Canada, Bristol Myers Squibb Canada, Roche Canada, Janssen Canada, Sandoz Canada, Takeda Canada and Pfizer Canada; consultant for Mylan Pharmaceuticals and Takeda; educational grants from AbbVie Canada, Pfizer Canada, Takeda Canada and Janssen Canada; speaker’s panel for AbbVie Canada, Janssen Canada, Pfizer Canada and Takeda Canada; and received research funding from AbbVie Canada, Bristol Myers Squibb Canada, Sandoz Canada and Pfizer Canada. CC: receives grant funding from PHAC and CITF through internal research funding streams at PHAC. JK: receives grant funding from PHAC through internal research funding streams at PHAC.
 A. Jarocki, L. A. Gonzalez, C. A. Andrews, and K. A. Kerber: no conflicts of interest to disclose; E. Benard-Seguin: Neuro Nexus Hackathon Grant and Fighting Blindness Canada received from University of Calgary; F. Costello: consulting fees received from Accure Therapeutics and Frequency Therapeutics. Payment for lectures received from Novartis and Alexion; L. B. De Lott: funding received from K23EY027849 grant and North American Neuro-Ophthalmology Society Pilot Grant. Payment for lectures received from the American Academy of Neurology.
 The authors declare that they have no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.




 Declaration of Competing Interest No potential conflict of interest was reported by the authors.




 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Conflicts of Interest All authors declare that this study has no commercial or financial relationships that could be construed as a potential conflict of interest.
 Competing Interests The authors report there are no competing interests to declare.
 Competing interests: The authors report the following relationships: speaker honoraria, advisory board or steering committee fees, research support and/or conference travel support from Acthelion (EKH, RA), Almirall (MT, FG, RB, CRT, JLS-M), Bayer (MT, AL, PS, RA, MT, CB, JL-S, EP, VVP, RB, DS, RA, JO, JLSM, SH, CR, AGK, TC, NS, BT, MS, CAS), BioCSL (TK, AGK, BT), Biogen (TK, TS, DH, EKH, MT, GI, AL, MG, PD, PG, VJ, AVW, FG, PS, DF, RA, RH, CB, JLS, EP, VVP, FG, RB, RA, CRT, JP, JO, MB, JLSM, SH, CR, CSh, OGerlach, AGK, TC, BS, NS, BT, MS, HB), Biologix (RA), BMS/Celgene (EKH, AL), Genpharm (RA), Genzyme-Sanofi (TK, EKH, MT, GI, AL, MG, PD, PG, AVW, FG, PS, DF, RA, RH, MT, CB, JLS, EP, EP, VVP, FG, RB, RB, DS, CRT, JP, JO, MB, JLSM, SH, O Gerlach, AGK, HB), GSK (RA), Innate Immunotherapeutics (AGK), Lundbeck (EP), Merck / EMD (TK, DH, EKH, MT, GI, AL(Merck Serono), MG, PD, PG, VJ, AVW, PS, DF, RA, RH, MT, CB, JLS, EP, VVP, FG, RB, DS, RA, JO, MB, JLSM, CR, FM, O Gerlach, AGK, TC, BS, MS, HB), Mitsubishi (FG),Novartis (TK, TS, DH, EKH, MT, GI, AL, MG, PD, PG, VJ, AVW, FG, PS, DF, RA, RH, MT, CB, JLS, EP, VVP, FG, RB, DS, RA, CRT, JP, JO, MB, JLSM, SH, CR, FM, CSh, OG, AGK, TC, NS, BT, MS, HB), ONO Pharmaceuticals (FG), Roche (TK, EKH, AL, MT, CB, VVP, BT), Teva (TK, DH, EKH, MT, GI, AL, MG, PD, PG, VJ, FG, PS, DF, RH, MT, CB, JLS, VVP, RB, DS, RA, JP, JO, JLSM, CR, AGK, TC, MS, CAS), WebMD (TK), UCB (EP).


 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Competing interests The authors declare no competing financial interests.




 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: LK received honoraria for lecturing and travel expenses for attending meetings from Alexion, Biogen, Janssen, Merck, Sanofi Genzyme, Novartis, Teva, Viatris, and Roche; her research is funded by the Deutsche Forschungsgemeinschaft (DFG), Interdisciplinary Center for Clinical Studies (IZKF) Muenster, Biogen, Merck, and Novartis. ME received speaker honoraria and travel support from Sanofi Genzyme; she received research support from the Deutsche Multiple Sklerose Gesellschaft (DMSG) Landesverband, Nordrhein-Westfalen (NRW), and the Innovative Medical Research (IMF) program of the University Münster. SB has received honoraria and compensation for travel from Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, and Roche. FZ has recently received research grants and consultation funds from DFG, BMBF, PMSA, MPG, Genzyme, Merck Serono, Roche, Novartis, Sanofi-Aventis, Celgene, ONO, and Octapharma. DS consults for, advises for, received grants from, and holds intellectual property rights with NorthSea; he consults for, advises for, and received grants from Boehringer Ingelheim; and consults for and advises for Pliant, UCB, Inversago, and Prometik. FL received consultancy fees from Roche and support with travel cost from Teva Pharma. The remaining authors have nothing to disclose.
 Declaration of Competing Interest We declare no conflict of interest.
 Competing interests: None declared.
 Declaration of Competing Interest Authors have no competing interests to disclose.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare no competing interests.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.





 AKM is one of the inventors of a technology claiming the use of Prevotella histicola to treat autoimmune diseases. AKM received royalties from Mayo Clinic (paid by Evelo Biosciences). However, no fund or product from the patent were used in the present study. All other authors declare no commercial or financial relationships that could be a potential conflict of interest.
 The authors report no conflicts of interest.
 Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Jerry Prince, Aaron Carass, Peter Calabresi reports financial support was provided by National Institutes of Health. Ellen Mowry, Scott Newsome, Jerry Prince, Aaron Carass reports financial support was provided by Patient-Centered Outcomes Research Institute. Jerry Prince, Aaron Carass reports financial support was provided by US Office of Congressionally Directed Medical Research Programs. Blake Dewey reports financial support was provided by National Multiple Sclerosis Society. Jerry Prince reports a relationship with Sonavex that includes: board membership, consulting or advisory, and equity or stocks.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: EC received the ECTRIMS Clinical Fellowship (2013–2014), ECTRIMS travel grant awards, and academic travel support from Novartis, Genzyme, Merck, Biogen and Roche, has been a member of advisory boards at Genzyme, Biogen, Merck and Novartis, has received sub-investigator fees from the ISS “Social Cognition in MS” project at Teva. BS received academic travel support from Novartis, Teva, Merck and Biogen RUSM received academic travel support from Novartis, Genzyme, Merck, Biogen and Roche, and has been a member of advisory boards at Genzyme, Biogen, Merck and Novartis. LJ, IG, KK, AR, SBG, JPC nothing to disclose CC received academic travel support from Novartis, Genzyme, Merck, Biogen and Roche, and has been a member of advisory boards at Genzyme, Biogen, Merck and Novartis, has received PI fees from the ISS “Social Cognition in MS” project at Teva.
 The authors declare that they have no competing interests.

 The authors declare no competing interests.
 Maria Luisa Torre is a co-founder and member of the advisory board of Pharmaexceed S.r.l.
 Declaration of competing interest The authors declare no conflict of interest.

 Conflicts of Interest: None declared.

 No conflict of interest has been reported.
 Competing interest The authors declare that they have no conflicts of interest.

 Conflict of interests Authors declare no conflict of interests.
 None
 The authors declare that they have no conflicts of interest.


 The authors declare no competing interests.
 Declaration of Competing Interest MN has received consultant fees from Biogen; and travel and/or speaker honoraria from Biogen, Takeda, Mitsubishi Tanabe, Chugai, Alexion, and Novartis, YM has nothing to disclose, AA and ME were former employees of Biogen, NB, MK, IC, CdM, and JRW are employees of and may hold stock/stock options in Biogen, SMR has authored IP around the MS PATHS software; is a stockholder and scientific officer of Qr8 Health; and has received royalties and grant funding from Biogen, National MS Society, Department of Defense, and NIH.
 K. Toljan, A. Mahadeen, and M. Amin report no disclosures relevant to the manuscript. M. Rensel reports research funding (PPD, Biogen, Genentech, CBJ Foundation and NMSS), reports patient education funds (Genzyme) serving on DSMC for Biogen, was a speaker or consultant for (Serono, Novartis, Genentech, Genzyme, Horizon, TG, Improve Consulting, Kijia and MSAA), and is a founder of Brain Fresh. S.E. Jones reports no disclosures relevant to the manuscript. D. Ontaneda reports research support from the NIH, National Multiple Sclerosis Society, Patient-Centered Outcomes Research Institute, Race to Erase MS Foundation. A. Kunchok has received compensation as an assistant editor for the Neurology journal. Go to Neurology.org/N for full disclosures.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer NH declared a shared affiliation with the author MS to the handling editor at the time of review.

 The authors declare no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest None.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Dr. Saraceni and Dr. Santamato are part of the Scientific Direction of “Filippo Turati” Foundation who financed 1 year scholarship of the first author of this study. The other authors declare no competing interests.
 The authors declare no competing interest.
 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare no conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Disclosure: Fatima Saleem declares no relevant financial relationships with ineligible companies. Disclosure: Michael Soos declares no relevant financial relationships with ineligible companies.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no competing interests.
 The authors declare no competing interests.

 Declaration of Competing Interest All author's have no financial/personal interest.

 The authors have declared that no competing interests exist.

 Competing interests: Authors declare no competing interests.
 SA has received speaker honoraria from Alexion, Bayer, and Roche. JB reports payment for consultation from Horizon Therapeutics, Alexion, Antigenomycs, BeiGene, Chugai, Clene Nanomedicine, Genentech, Reistone Bio, Roche, Imcyse, and TG; grants from Alexion, Novartis, and the National Institutes of Health. In addition, JB has a patent on Compositions and methods for the treatment of neuromyelitis optica. YB has received speaker honoraria from Novartis, Roche, Genzyme-Sanofi, Merck, and Biogen. EC has received reimbursement for developing educational presentations, educational and research grants, consultation fees, and/or travel stipends from Biogen Argentina, Genzyme Argentina, Merck Argentina and LATAM, Roche Argentina and LATAM, Raffo, Novartis Argentina, LACTRIMS, and The Guthy-Jackson Charitable Foundation. JC has served on advisory boards for Horizon, Roche, and UCB. CC has received honoraria for speaking from Bayer and research funding from Novartis. JD has received royalties from Wolters Kluwer, Neurology—UpToDate and from Medlink Neurology as contributing author, from Athena Diagnostics for the use of Ma2 as an autoantibody test, and from Euroimmun for the use of NMDA-receptor, GABA(B)-receptor, GABA(A)-receptor, DPPX, and IgLON5 as autoantibody tests and has received research support from Advance Medical (allosteric modulation of NMDAR) SAGE Therapeutics, Instituto Carlos III/FEDER (FIS PI20/00197, CIBERER CB15/00010, Proyectos Integrados de Excelencia, PIE 16/00014 and AC18/00009), Agencia de Gestio d'Ajuts Universitaris i de Recerca (AGAUR), CERCA Programme Generalitat de Catalunya, ERA-NET NEURON, La Caixa Foundation Health Research Award, Pablove Foundation Childhood Cancer Grant, Safra Foundation, Sage therapeutics, Cellex Foundation, and La Caixa Health Foundation. EF has served on advisory boards for Alexion, Genentech, Horizon Therapeutics, and UCB. He has received speaker honoraria from Pharmacy Times. He received royalties from up-to-date. EF was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics. EF has received funding from the NIH (R01NS113828). EF is a member of the medical advisory board of the MOG project. EF is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports. A patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity. CF participates in a regional medical board advisory of Alexion. CG-A has received grants from Biogen Colombia. JH reports grants for OCT research from the Friedrich-Baur-Stiftung and Merck, personal fees, and non-financial support from Celgene, Janssen, Bayer, Merck, Alexion, Horizon, Novartis, Roche, Biogen, and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work. JH was partially funded by the German Federal Ministry of Education and Research [(DIFUTURE), Grant Numbers 01ZZ1603[A-D] and 01ZZ1804[A-H]]. HK has received a grant from the National Research Foundation of Korea; consultancy/speaker fees or research support from Alexion, Aprilbio, Altos Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, Handok, Horizon Therapeutics (formerly Viela Bio), Kolon Life Science, MDimune, Mitsubishi Tanabe Pharma, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok, and UCB; and is a coeditor for the Multiple Sclerosis Journal and an associated editor for the Journal of Clinical Neurology. CLM reports consultancy fees for Chiesi Farmaceutici, Regulatory PharmaNet, and Thenewway Srl and received speaker honoraria and/or travel support for meetings from Santhera Pharmaceuticals, Chiesi Farmaceutici, Regulatory Pharma Net, Thenewway Srl, First Class Srl, and Biologix. ML-P has received funding for travel and speaker honoraria from Novartis, Biogen, and Roche. MLei was funded by NHS (Myasthenia and Related Disorders Service and National Specialized Commissioning Group for Neuromyelitis Optica, UK) and by the University of Oxford, UK. She has been awarded research grants from the UK association for patients with myasthenia—Myaware and the University of Oxford. She has received speaker honoraria or travel grants from Biogen Idec, Novartis, Argenx, UCB, and the Guthy–Jackson Charitable Foundation. MLei serves on scientific or educational advisory boards for UCB Pharma, Argenx, and Viela/Horizon. SL has received consulting fees and speaker honoraria from Biogen, Novartis, TEVA, Genzyme, Sanofy, and Merck. PL has received reimbursement for developing educational presentations, educational and research grants, consultation fees, and/or travel stipends from Biogen Argentina and LATAM, Genzyme Argentina, Merck Argentina, Roche Argentina, Novartis Argentina, and LACTRIMS. AL has served as a Biogen, Bristol Myers Squibb, Merck Serono, Novartis, Roche, Sanofi/Genzyme, and Teva Advisory Board Member, has received congress and travel/accommodation expense compensations, or speaker honoraria from Biogen, Merck Serono, Mylan, Novartis, Roche, Sanofi/Genzyme, Teva, and Fondazione Italiana Sclerosi Multipla (FISM), her institutions received research grants from Novartis and Sanofi/Genzyme. SMo reports consultancy fees (Invex Therapeutics); advisory board fees (Invex therapeutics, Gensight); and speaker fees (Heidelberg engineering, Chugai-Roche Ltd., Allergan, Santen, Chiesi, and Santhera), all outside the submitted work. RM serves on scientific advisory boards for Alexion, Horizon Therapeutics, Roche, and UCB has received speaker honoraria from Alexion, Biogen, Horizon Therapeutics, Novartis, Roche, and Sanofi Genzyme, has received support for attending scientific meetings by Merck and Euroimmun, has received speaker honoraria from Biogen and Novartis. SMa received speaker honoraria for presenting at scientific meetings by Novartis and Biogen. SMo reports consultancy fees (Invex Therapeutics); advisory board fees (Invex therapeutics, Gensight); and speaker fees (Heidelberg engineering, Chugai-Roche Ltd., Allergan, Santen, Chiesi, and Santhera). All outside the submitted work. FC receives ongoing research support from the National Multiple Sclerosis Society (NMSS), the American Academy of Neurology (AAN), and Deutsche Gesellschaft für Neurologie (DGN). JPa has received support for scientific meetings and honorariums for advisory work from Merck Serono, Novartis, Chugai, Alexion, Roche, Medimmune, Argenx, UCB, Mitsubishi, Amplo, Janssen, and Sanofi. Grants from Alexion, Roche, Medimmune, UCB, and Amplo biotechnology. Patent ref P37347WO and license agreement Numares multimarker MS diagnostics Shares in AstraZeneca. Acknowledges Partial funding by Highly specialized services NHS England. SP is a named inventor on filed patents that relate to functional AQP4/NMO-IgG assays and NMO-IgG as a cancer marker, was consulted for Alexion and MedImmune, has received research support from Grifols, MedImmune, and Alexion, all compensation for consulting activities is paid directly to Mayo Clinic. SR has received research funding from the National Health and Medical Research Council (Australia), the Petre Foundation, the Brain Foundation (Australia), the Royal Australasian College of Physicians, and the University of Sydney. She was supported by an NHMRC Investigator Grant (GNT2008339). She serves as a consultant on an advisory board for UCB and Limbic Neurology and has been an invited speaker for Biogen, Excemed, and Limbic Neurology. AS received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Merck-Serono, Sanofi, Biogen, Roche, Novartis, Alexion, Janssen, and Horizon Therapeutics. DS received a grant from the National Multiple Sclerosis Society and serves on several advisory committees for the Multiple Sclerosis International Federation in unpaid roles. MS received speaker honoraria from Teva Pharmaceuticals and has received funding from the German Research Foundation, Federal Ministry of Education and Research and Federal Ministry for Economic Affairs and Energy, Volkswagen Stiftung, and Berlin Institute of Health. He is holding patents for the 3D printing of computed tomography models and is a shareholder of PhantomX and MSC3D. All unrelated to this work. PSu has served on advisory boards for Horizon Therapeutics, Viridian Therapeutics, Invex Therapeutics, Kriya Therapeutics, and GenSight Biologics. He receives research support from the NIH, DOD, Horizon, Invex, and Viridian. AM has received a grant for Biopas Laboratories and reports speaking fees from Chiesi. HZ received research grants from Novartis and speaking fees from Bayer Healthcare, unrelated to this project. FP served on the scientific advisory boards of Novartis and MedImmune; received travel funding and/or speaker honoraria from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an associate editor of Neurology: Neuroimmunology & Neuroinflammation; is an academic editor of PLoS ONE; consulted for Sanofi Genzyme, Biogen, MedImmune, Shire, and Alexion; received research support from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Geynzme, Alexion, and Merck Serono; and received research support from the German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy-Jackson Charitable Foundation, and NMSS. HS-K received speaker honoraria from Roche. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Dr. Chien reports personal fees from Bayer, grants from Novartis, outside the submitted work. Dr. Bellmann-Strobl reports personal fees from Bayer Healthcare, personal fees from sanofi-aventis/Genzyme, personal fees from Roche, outside the submitted work. Dr. Paul reports personal fees and non-financial support from SanofiGenzyme, personal fees, non-financial support and other from BiogenIdec, personal fees and non-financial support from MedImmune, personal fees and non-financial support from Shire, personal fees and non-financial support from Alexion, grants, personal fees and non-financial support from Bayer, grants and personal fees from Novartis, grants and personal fees from Teva, grants and personal fees from Merck Serono, personal fees from Actelion, personal fees from Chugai, personal fees from Roche, personal fees from Celgene, grants from Sanofi-Aventis/Genzyme, grants from Alexion, grants from German Research Council (DFG Exc 257), grants from Werth Stiftung of the City of Cologne, grants from German Ministry of Education and Research (BMBF Competence Network Multiple Sclerosis), grants from Arthur Arnstein Stiftung Berlin, grants from EU FP7 Framework Program (combims.eu), grants from Guthy Jackson Charitable Foundation, grants from National Multiple Sclerosis Society of the USA, outside the submitted work. All other authors declare no competing interests.
 The authors have no conflicts of interest to declare.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that they have no conflict of interest.

 The authors declare no conflict of interest.

 Declaration of Competing Interest The author declares no conflicts of interest.


 Declaration of Competing Interest D.T.O. received personal compensation for consulting and advisory services from Alexion, Biogen, Celgene/Bristol Myers Squibb, EMD Serono, Genentech, Genzyme, Janssen Pharmaceuticals, Novartis, Osmotica Pharmaceuticals, RVL Pharmaceuticals, Inc., TG Therapeutics, Viela Bio, Inc., and research support from Biogen and EMD Serono/Merck. D.T.O. has issued national and international patents along with pending patents related to this current work and other developed technologies and has received royalties for intellectual property licensed by The Board of Regents of The University of Texas System. A.S, T.M, K.B, and M.M. report no disclosures.


 Conflict of interest E. Wetmore reports no disclosures relevant to the manuscript. D. Lehner-Gulotta is a consultant for Functional Formularies. B. Florenzo has no disclosures relevant to the manuscript. B. Banwell serves as a consultant to Novartis, Roche, UCB, Teva Neuroscience, Biogen, and Sanofi. AGC Bergqvist serves as a paid speaker for Nutricia North America. R. Coleman reports no disclosures relevant to the manuscript. M. Conaway reports no disclosures relevant to the manuscript. M.D. Goldman has served on the DSMB for Anokion SMC and Immunic. She has received consulting fees from Adamas Pharmaceuticals, Biogen IDEC, Brainstorm Cell Therapeutics Ltd, EMD Serono, Genetec, Greenwich Biosciences, Horizons, Immunic, Merck, Novartis, Sanofi Genzyme, and Vebrilio. J.N. Brenton has served as a consultant to Cycle Pharmaceuticals. JNB's research is funded by the NIH and the National Institute of Neurological Disorders and Stroke (grant number: K23NS116225) and by the iTHRIV Scholars Program through the National Center for Advancing Translational Sciences of the NIH under award numbers UL1TR003015 and KL2TR003016.

 F.B. acted as Advisory Board members of Teva and Roche and received honoraria for speaking or consultation fees from Merck Serono, Teva, Biogen Idec, Sanofi, and Novartis and non-financial support from Merck Serono, Teva, Biogen Idec, and Sanofi. R.F. received honoraria for serving on scientific advisory boards or as a speaker from Biogen, Novartis, Roche, and Merck and funding for research from Merck. D.C. is an Advisory Board member of Almirall, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva and received honoraria for speaking or consultation fees from Almirall, Bayer Schering, Biogen, GW Pharmaceuticals, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva. He is also the principal investigator in clinical trials for Bayer Schering, Biogen, Merck Serono, Mitsubishi, Novartis, Roche, Sanofi-Genzyme, and Teva. His preclinical and clinical research was supported by grants from Bayer Schering, Biogen Idec, Celgene, Merck Serono, Novartis, Roche, Sanofi-Genzyme, and Teva. G.Mat. reports receiving research grant support from Merck, Biogen, and Novartis and advisory board fees from Merck, Biogen, Novartis, and Roche. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results. M.S.B., L.G., E.I., F.C., T.M., G.G., E.D., F.A., A.Br., A.Bo., G.Man., V.R., M.S., A.F.: nothing to report.





 The authors declare no competing financial interest.


 LM reports personal fees from Biogen and Merck, both outside the scope of this study, PG reports personal fees for activities as a patient consultant from Novartis, WJG reports consulting income from Novocardia Inc., and Great Point Ventures, outside the scope of this work, SGM reports no conflict of interest related to this study, ADS declares that she serves as a member of the Scientific Advisory Board of the German Society for Digital Medicine and the Strategic Advisory Board of HumanFirst.

 Disclosure: Daniel Scura declares no relevant financial relationships with ineligible companies. Disclosure: Sunil Munakomi declares no relevant financial relationships with ineligible companies.

 Disclosure: Divy Mehra declares no relevant financial relationships with ineligible companies. Disclosure: Majid Moshirfar declares no relevant financial relationships with ineligible companies.
 Conflict of interest The authors declared no conflict of interest.

 The authors declare no conflict of interest.



 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no conflicts of interest.

 Competing interests: None declared.
 The authors declare no competing interests.



 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of interests The authors declare that they have no conflict of interest related to this study. PLX5622 was provided by Plexxikon Inc. under a material transfer agreement between Stanford University and Plexxikon Inc.
 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Tjalf Ziemssen has received personal compensation for participating on advisory boards, trial steering committees, and data and safety monitoring committees, as well as for scientific talks and project support from Almirall, Bayer, BAT, Biogen, Celgene, Sanofi Genzyme, Merck, Novartis, Roche, Vitaccess, and Teva. Marie Groth and Veronika Eva Winkelmann are employees of Novartis Pharma GmbH, Nuremberg, Germany. Tobias Bopp has received a consulting fee and honoraria for lectures from AstraZeneca, Biogen, Celgene, Merck, Novartis, Pathios Therapeutics, Roche, Sanofi Genzyme, and Teva.
 The authors declare no conflict of interest.


 Conflict of interest statement The authors declared no conflict of interest.
 The authors declare that they have no conflicts of interest.
 Conflict of interest: The authors declare no conflicts of interest.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no competing interests.

 Declaration of Competing Interest H.R.M., M.P., E.J.D., M.M., R.C., R.A., and R.S.P. have no conflicts of interest to disclose. J.A.N. has received research grants from Biogen Idec, Genzyme, Novartis, PCORI, ADAMAS, and Alexion. She has received consulting fees and honoraria from Biogen, Genentech, GW Pharmaceuticals, EMD Serono, Bristol Myers Squib, Novartis, Alexion, Viela Bio, and the American Academy of Neurology.
 The authors declare no conflict of interest.


 The authors declare no conflict of interest.
 All participants provided written informed consent. Participants have declared that no competing interest exists.
 Declaration of Competing Interest This statement is to certify that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Disclosure: Freddie Rodriguez-Beato declares no relevant financial relationships with ineligible companies. Disclosure: Orlando De Jesus declares no relevant financial relationships with ineligible companies.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors report no conflicts of interest.
 Competing interests: OA reports grants from the German Ministry of Education and Research (BMBF) and the German Research Foundation (DFG); grants and personal fees from Biogen and Novartis; and travel support and personal fees from Alexion, Almirall, MedImmune, Merck Serono, Roche, Sanofi, Viela Bio/Horizon Therapeutics and Zambon. OA is a member of the European Reference Network for Rare Eye Diseases (ERN-EYE), co-funded by the Health Program of the European Union under the Framework Partnership Agreement No 739534 'ERN-EYE. H-PH has received fees for consulting, speaking and serving on steering committees from Bayer Healthcare, Biogen Idec, Celgene Receptos, CSL Behring, GeNeuro, Genzyme, MedDay, MedImmune, Merck Serono, Novartis, Roche, Sanofi, TG Therapeutics and Viela Bio/Horizon Therapeutics, with approval by the Rector of Heinrich Heine University Düsseldorf. KF has received fees for consulting, speaking and serving on steering committees from AbbVie, Alexion, Asahi Kasei Medical, Biogen, Chugai/Roche, Eisai, Japan Tobacco, MedImmune/Viela Bio, Merck, Merck Biopharma, Mitsubishi-Tanabe, Novartis, Takeda, Teijin and UCB, and has received Grant-in-Aid for Scientific Research from the Ministry of Health, Welfare and Labor of Japan. FP has received research support, speaker fees and travel reimbursement from Bayer, Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme and Teva; is supported by the German Competence Network for Multiple Sclerosis and the German Research Council (DFG Exc 257); has received travel reimbursement from the Guthy–Jackson Charitable Foundation; and serves on the steering committee of the OCTIMS study sponsored by Novartis. RM serves on scientific advisory boards for Alexion, Roche and Viela Bio/Horizon Therapeutics; and has received funding for travel and fees from Alexion, Biogen, Merck, Novartis, Roche and Viela Bio/Horizon Therapeutics. JLB reports payment for study design/consultation from MedImmune/Viela Bio/Horizon Therapeutics; reports personal fees from AbbVie, Alexion, Beigene, Chugai, Clene Nanomedicine, Genentech, Genzyme, Mitsubishi Tanabe Pharma, Reistone Biopharma and Roche; reports grants and personal fees from EMD Serono and Novartis; reports grants from Alexion, Mallinckrodt and the National Institutes of Health; and has a patent for Aquaporumab issued. HJK has received a grant from the National Research Foundation of Korea; consultancy/speaker fees or research support from Alexion, AprilBio, ALTOS Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, Handok, Horizon Therapeutics (formerly Viela Bio), Kolon Life Science, MDimune, Mitsubishi Tanabe Pharma, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok and UCB; and is a co-editor for the Multiple Sclerosis Journal and an associated editor for the Journal of Clinical Neurology. BGW receives payments for serving as chair of attack adjudication committees for clinical trials in NMOSD for Alexion, MedImmune, UCB Bioscience and Viela Bio/Horizon Therapeutics; has consulted with Chugai, Genentech, Horizon Pharmaceuticals, Mitsubishi Tanabe Pharma and Roche; has received payments for speaking for Genentech and Roche; and has a patent for NMO-IgG for diagnosis of neuromyelitis optica, with royalties paid by Hospices Civils de Lyon, MVZ Labor PD Dr Volkmann und Kollegen GbR, RSR and the University of Oxford. SJP has received personal compensation for serving as a consultant for Astellas, Genentech and Sage Therapeutics; has received personal compensation for serving on scientific advisory boards or data safety monitoring boards for F. Hoffman-La Roche AG, Genentech and UCB; has received research support from Alexion, Roche/Genentech and Viela Bio/MedImmune/Horizon; has a Patent# 8,889,102 (Application#12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia)—issued; has a patent, Patent# 9,891,219B2 (Application#12-573942, Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)-IgG Autoantibody positive)—issued; and his institution has received compensation for serving as a consultant for Alexion, Astellas and Viela Bio/MedImmune/Horizon. DMW reports personal fees from Biogen, Genentech, Horizon, Mitsubishi Tanabe, Roche, UCB Pharma and Viela Bio; and research support paid to Mayo Clinic by Alexion Pharmaceuticals. GC has received personal fees for participation on data and safety monitoring boards from AI Therapeutics, AMO Pharma, AstraZeneca, Avexis Pharmaceuticals, Biolinerx, Brainstorm Cell Therapeutics, Bristol Meyers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Pharmaceuticals, Immunic, Karuna Therapeutics, Mapi Pharmaceuticals, Merck, Mitsubishi Tanabe Pharma Holdings, NHLBI (Protocol Review Committee), Novartis, Opko Biologics, Prothena Biosciences, Regeneron, Sanofi-Aventis, Reata Pharmaceuticals, University of Texas Southwestern, University of Pennsylvania and Visioneering Technologies; has received personal fees for consulting or advisory board participation from Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions, Entelexo Biotherapeutics, Genentech, Genzyme, GW Pharmaceuticals, Immunic, Klein-Buendel Incorporated, Merck/Serono, Novartis, Osmotica Pharmaceuticals, Perception Neurosciences, Protalix Biotherapeutics, Recursion/Cerexis Pharmaceuticals, Regeneron, Roche, SAB Biotherapeutics; and is employed by the University of Alabama at Birmingham and President of Pythagoras, a private consulting company located in Birmingham, Alabama. BAC reports personal compensation for consulting from Alexion, Atara Biotherapeutics, Autobahn, Avotres, Biogen, EMD Serono, Gossamer Bio, Horizon, Neuron23, Novartis, Sanofi, TG Therapeutics and Therini Bio; and has received research support from Genentech. MAS, WAR, DS and DC are employees of Horizon Therapeutics and own stock. MG and EK are former employees of Horizon Therapeutics and own stock.
 Conflict of Interest Disclosures: Dr Buchard reported that he is the Lead AI Scientist at [RE]MEDs, a research company involved in the conduct of the study. [RE]MEDs received no funds from the pharmaceutical industry or any party interested in vaccines. Dr Moride reported being President of YolaRX Consultants, which provides consultancy services to the pharmaceutical industry. YolaRX Consultants had no part in this study. Dr Duchemin reported being an employee of [RE]MEDs. Dr Abenhaim reported having a patent pending for a [RE]MEDs search engine and being the founder and owner of [RE]MEDs and of LASER Core. Until 2018, LASER Core conducted studies supported by vaccine manufacturers, but has not conducted manufacturer-supported studies since then. No other disclosures were reported.
 None

 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationship that could be construed as a potential conflict of interest.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.



 Conflict of interest: the authors declare no potential conflict of interest.


 Ali Motahharynia, Ghazaal Alavi Tabatabaei, Reza Sarrafi, Saba Naghavi, and Iman Adibi announce that there is no conflict of interest to declare.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 Disclosure: Carol Le declares no relevant financial relationships with ineligible companies. Disclosure: Phillip Nahirniak declares no relevant financial relationships with ineligible companies. Disclosure: Sachit Anand declares no relevant financial relationships with ineligible companies. Disclosure: Wantzy Cooper declares no relevant financial relationships with ineligible companies.



 The authors declare that they have no competing interests.
 The authors declare no conflict of interest.

 Competing interestsBeate Bittner is employee of F. Hoffmann-La Roche and owns stock in Roche.
 Declaration of Competing Interest The authors declare no competing interests.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Competing InterestsThe authors declare no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of Interest.
 Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 None
 Declaration of Competing Interest S. Sen and A. Tuncer has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma. R. Karabudak has received honoraria for giving educational lectures, consultancy fees for participating advisory boards, and travel grants for attending scientific congresses or symposia from Roche, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey, Abdi İbrahim İlac, Deva and ARIS. H. Efendi has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi İbrahim İlac. A Siva has received honoraria or consultancy fees for participating to advisory boards, giving educational lectures and/or travel and registration coverage for attending scientific congresses or symposia from F. Hoffmann-La Roche Ltd, Sanofi-Genzyme, Merck-Serono, Novartis, Teva, Biogen Idec/Gen Pharma of Turkey and Abdi İbrahim İlac. The rest of authors declares no conflict of interest with the study project.
 P.W. has received consultation fees and/or speakers’ honoraria from Bayer, Biogen Idec, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi Genzyme, and Teva Pharmaceutical Industries Ltd. He received research grants from Biogen Idec and Merck. E.T. has received consultation fees and/or speakers’ honoraria from Arvelle, Argenx, Angellini, Bial, Biogen-Idec, Boehringer Ingelheim, Eisai, Epilog, GL Pharma, Jazz/GW Pharmaceuticals, Ever Pharma, Hikma, LivaNova, Marinus, Medtronics, Newbridge, Novartis, Sanofi, Genzyme, and UCB Pharma. T.M. has received travel support, honoraria for presentations or participation on advisory boards from Biogen Idec, Celgene, Novartis, Roche, Sanofi, Merck and Teva. The remaining authors have nothing to disclose.

 Y.E.O., J.V.d.B., N.C. and I.W. declare no conflict of interest. B.W. received honoraria for acting as a member of Scientific Advisory Boards for Almirall, Biogen, Celgene/BMS, Merck, Janssen, Novartis, Roche, Sandoz, Sanofi-Genzyme and speaker honoraria and travel support from Biogen, Celgene/BMS, Merck, Novartis, Roche, Sanofi-Genzyme; research and/or patient support grants from Biogen, Janssen, Merck, Sanofi-Genzyme., Roche. Honoraria and grants were paid to UZA/UZA Foundation.
 Declaration of competing interest The authors do not have any conflicts of interest to disclose.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest We declared that all authors have no conflict of interest.
 The authors declare no conflict of interest.
 Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.

 Conflicts of interest The authors declare they have no conflicts of interest.
 J.P. Briggs reports Advisory or Leadership Role: peer review editor for PCORI (paid honorarium) and JASN EIC. P.B. Imrey reports Consultancy: Colgate Palmolive.


 Authors declare no conflict of interest.

 The authors are inventors on several patents relevant to the subject of this review.

 The authors declare that they have no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 LJB is editor-in-chief of the Journal of Neuro-Ophthalmology. The remaining authors have no disclosures.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of interests We declare no competing interests.

 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 None declared.


 Mana Kameyama is an employee of Asahi Kasei Medical Co., Ltd. The remaining authors declare no conflict of interest.
 Declaration of Competing Interest In the last two years, Professor Giovannonu has received compensation for serving as a consultant or speaker for or has received research support from AbbVie, Aslan, Atara Bio, Biogen, BMS-Celgene, GlaxoSmithKline, Janssens/J&J, Japanese Tobacco, Jazz Pharmaceuticals, Merck & Co, Merck KGaA/EMD, Moderna, Serono, Moderna, Novartis, Sandoz, Sanofi and Roche/Genentech. In addition, he has received research funding from Merck KGaA/EMD Serono, Novartis, Sanofi, Roche/Genentech and Takeda.
 There are no conflicts of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.




 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 Declaration of interests K.M. is an employee of Miyarisan Pharmaceutical. This study has partially supported the finance for the collaboration study from Miyarisan Pharmaceutical.
 Declaration of Competing Interest None.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Paul Lang, PhD reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Paul Lang, PhD reports a relationship with Sanofi that includes: employment. Svend S. Geertsen, PhD reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Svend S. Geertsen, PhD reports a relationship with Sanofi that includes: employment. Alex L. Lublin, PhD reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Alex L. Lublin, PhD reports a relationship with Sanofi that includes: employment. Michelle C. Potter, PhD reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Michelle C. Potter, PhD reports a relationship with Sanofi that includes: employment. Tatiana Gladysheva reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Tatiana Gladysheva reports a relationship with Sanofi that includes: employment. Jill S. Gregory reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Jill S. Gregory reports a relationship with Sanofi that includes: employment. Pascal Rufi, MD reports writing assistance was provided by Elevate Scientific Affairs, Envision Pharma Group. Pascal Rufi, MD reports a relationship with Sanofi that includes: employment.
 MC is Director of the Birmingham Health Partners Centre for Regulatory Science and Innovation, Director of the Centre for the Centre for Patient Reported Outcomes Research and is a National Institute for Health and Care Research (NIHR) Senior Investigator. MC receives funding from the NIHR Birmingham Biomedical Research Centre, NIHR Surgical Reconstruction and Microbiology Research Centre, NIHR Birmingham-Oxford Blood and Transplant Research Unit (BTRU) in Precision Transplant and Cellular Therapeutics, and NIHR ARC West Midlands at the University of Birmingham and University Hospitals Birmingham NHS Foundation Trust, Health Data Research UK, Innovate UK (part of UK Research and Innovation), Macmillan Cancer Support, SPINE UK,UKRI, UCB Pharma, Janssen, GSK and Gilead. MC has received personal fees from Astellas, Aparito Ltd, CIS Oncology, Takeda, Merck, Daiichi Sankyo, Glaukos, GSK and the Patient-Centered Outcomes Research Institute (PCORI) outside the submitted work. OLA receives funding from the NIHR Birmingham Biomedical Research Centre (BRC), NIHR Applied Research Collaboration (ARC), West Midlands, NIHR Birmingham-Oxford Blood and Transplant Research Unit (BTRU) in Precision Transplant and Cellular Therapeutics at the University of Birmingham and University Hospitals Birmingham NHS Foundation, Innovate UK (part of UK Research and Innovation), Gilead Sciences Ltd, Janssen pharmaceuticals, Inc, and Sarcoma UK. OLA declares personal fees from Gilead Sciences Ltd, GlaxoSmithKline (GSK) and Merck outside the submitted work. The authors have no competing interests



 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 None.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: David Pau, Marie Lotz, Gaelle Grandclaude and Alexandre Civet are employees of Roche SAS. Romain Jegou is an employee of Keyrus Life Science.
 The author (V.D.M.) was employed by Exagen Inc. and declares that the research was conducted in the absence of financial relationships that could be construed as a potential conflict of interest. There is an overlap of scientific work with the author’s commercial role, as she previously worked in a commercial institution that provides diagnostics and prognostics for patients with SLE.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest The authors confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome.




 Declaration of Competing Interest The authors state that this study was conducted without any commercial or financial relationship that could be interpreted as a potential conflict of interest. The authors declare no competing financial interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interests.
 Declaration of competing interest I am a member of the Scientific Advisory Board at Convelo Therapeutics and have equity interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflicts of Interests: The Authors declare that there are no competing interests.



 Conflicts of interest CMJ is an employee of the VA Maryland Health Care System. The views reported here do not reflect the views of the VA or United States Government. CMJ has an equity position with Vaccitech plc. Beyond these declarations, there are no other conflicts of interests to report. The review was conducted in the absence of any commercial or financial relationships.
 The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 All authors declare that they have no conflict of interest concerning the research related to the manuscript.
 The authors declare no conflict of interest.



 The authors declare no conflict of interest.
 The authors declare that they have no conflict of interest.
 The authors declare that they have no conflict of interest.

 The authors have declared that no competing interests exist.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Declaration of interests M.C. is a member of the scientific advisory board of Vigil, receives research support from Vigil, and is a consultant for CST.
 The authors declare no conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.




 The authors have no conflicts of interest. COMPETING INTERESTS BP is an inventor on US Patent #10,905,663 entitled “Treatment of Demyelinating Disorders” that describes a small molecule approach to enhancing the ISR as a therapeutic approach for demyelinating disorders. The structure of Sephin1 is included in the molecules covered. BP is also member of the scientific advisory board of Inflectis Bioscience. JRC has received personal compensation for consulting from Inception Sciences (Inception 5) and Pipeline Therapeutics Inc, and has contributed to and received personal compensation for a US Provisional Patent Application concerning the use of BZA as a remyelination therapy (US Provisional Patent Application Serial Number 62/374,270 (issued 08/12/2016)).
 Appendix D. Conflicts of interest Besides above mentioned funding, none of the authors have any financial interests to disclose.
 Conflict of interest The authors declare that there is no conflict of interest.
 The authors declare that they have no competing interests.
 The authors declare no commercial or financial conflict of interest.




 Declaration of Competing Interest The authors declare that they have no financial or personal conflicts of interest.

 There are no conflicts of interest.
 None declared.

 The authors declare no conflict of interest.
 Disclosure: Raffaela Di Napoli declares no relevant financial relationships with ineligible companies. Disclosure: Gennaro Esposito declares no relevant financial relationships with ineligible companies. Disclosure: Marco Cascella declares no relevant financial relationships with ineligible companies.


 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 U.P. received speaker fees from Merck, Biogen and Bayer and personal compensation from Biogen and Roche for consulting services. R.H. has received travel compensation from Celgene and Sanofi. H.I. received speaker fees from Roche. T.Z. reports consulting or serving on speaker bureaus for Biogen, Celgene, Roche, Novartis, Celgene Merck and Sanofi as well as research support from Biogen, Novartis, Merck and Sanofi. K.A. received personal compensation from Roche, Sanofi, Alexion, Teva, Biogen and Celgene for consulting services. P.S.A. and P.A. have nothing to disclose.
 The authors declare that they have no competing interests.




 The authors declare no conflict of interest.
 The authors declare no competing interests.
 Declaration of Competing Interest We confirm that there are no known conflicts of interest associated with the publication and that there is no significant financial support for the work that could affect its outcome.
 FR and FB are listed as inventors for an early patent application family designation relative to the synergic use of arsenic salts and metallic ions for the treatment of autoimmune diseases. DR-G and FR are currently employees of MEDSENIC SAS. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest.
 Elias Sotirchos reports: scientific advisory board and/or consulting for Alexion, Viela Bio, Horizon Therapeutics, Genentech, and Ad Scientiam; speaking honoraria from Alexion, Viela Bio, and Biogen. Kathryn Fitzgerald, Matthew Smith, Maria Reyes‐Mantilla, Ryan Canissario, Min Qiao, and Sarah Simmons have nothing to disclose. Carol Singh and Elizabeth Fisher are employees of Biogen and hold stock/stock options in the company. Carrie Hersh reports: scientific advisory board and/or consulting for Biogen, Novartis, Genentech, Genzyme, EMD Serono, TG Therapeutics, and Bristol‐Myers Squibb; compensation for serving on speakers bureaus for Genzyme and Biogen; research support from Biogen, Novartis, and Genentech. Megan Hyland reports: research support from Biogen. Georgina Arrambide reports: consulting services or participation in advisory boards from Sanofi, Merck and Roche; travel expenses for scientific meetings from Novartis, Roche, Stendhal and ECTRIMS; speaking honoraria from Sanofi, Roche, and Merck. Xavier Montalban reports: speaking honoraria and travel expenses for scientific meetings, has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past 3 years with Actelion, Alexion, Biogen, Celgene, EMD Serono, Genzyme, Immunic, Medday, Merck, Mylan, Novartis, Roche, Sanofi‐Genzyme, and Teva Pharmaceutical. Manuel Comabella reports: compensation for consulting services and speaking honoraria from Bayer Schering Pharma, Merk Serono, Biogen‐Idec, Teva Pharmaceuticals, Sanofi‐Aventis, and Novartis. Robert Naismith reports: scientific advisory board and/or consulting for Abata Therapeutics, Banner Life Sciences, BeiGene, Biogen, Bristol Myers Squibb, Genentech, Genzyme, Janssen, GW Therapeutics, Horizon Therapeutics, Lundbeck, NervGen, TG Therapeutics. Lauren Krupp reports: scientific advisory board and/or consulting for Biogen, Novartis, Janssen, Gerson Lehrman, Sanofi, and Biogen; research support from Biogen. Jacqueline Nicholas reports: scientific advisory board and/or consulting for Novartis, Genentech, Greenwich Biosciences, Biogen, EMD Serono, and TG Therapeutics; compensation for serving on speakers bureaus for EMD Serono, Alexion, Viela Bio, and Bristol Myers Squibb; research support from Novartis, Biogen, and Genentech. Katja Akgün reports: scientific advisory board and/or consulting for Roche, Sanofi, Alexion, Teva, Biogen, and Celgene. Tjalf Ziemssen reports: scientific advisory board and/or consulting for Biogen, Roche, Novartis, Celgene, and Merck; compensation for serving on speakers bureaus for Roche, Novartis, Merck, Sanofi, Celgene, and Biogen; research support from Biogen, Novartis, Merck, and Sanofi. Richard Rudick is a former Biogen employee and holds stock in the company. Robert Bermel reports: scientific advisory board and/or consulting for Astra Zeneca, Biogen, EMD Serono, Genzyme, Genentech, Novartis, and VielaBio, research support from Biogen, Genentech, and Novartis, and shared rights to intellectual property underlying the Multiple Sclerosis Performance Test, currently licensed to Qr8 Health and Biogen. Ellen Mowry reports: research support from Biogen, Teva, and Genentech, and royalties for editorial duties from UpToDate. Peter Calabresi reports: consulting fees from Biogen, Nervgen, Idorsia, Avidea (now Vaccitech), and Disarm Therapeutics (now Lilly); research support from Principia and Genentech.
 All authors are employees of, and may hold stock in, Sanofi.
 Die Autor*innen geben an, dass kein Interessenkonflikt besteht. MS und PZ sind Mitarbeitende der Deutschen Rentenversicherung Bund, die medizinische Rehabilitationsleistungen finanziert.
 Competing Interests NV and ET are employees of Aronora, Inc. and Oregon Health Science University (OHSU). This potential conflict of interest has been reviewed and managed by the OHSU Conflict of Interest in Research Committee. The remaining authors declare no competing financial interests.
 The authors declare no competing interests.
 Declaration of competing interest The authors declare that there are no conflicts of interest.

 Declaration of Competing Interest The authors have no conflicts of interest to disclose.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 PB has a financial interest in the Fuzionaire Diagnostics and the University of Chicago. PB is a named inventor of patents related to [(18)F]3F4AP owned by the University of Chicago and licensed to the Fuzionaire Diagnostics. PB’s interests were reviewed and are managed by the MGH and Mass General Brigham in accordance with their conflict of interest policies. The other authors declare no competing interests.

 Competing interests: MG has received honoraria as a speaker and for the partecipation to Advisory boards from Roche, UCB and Alexion.
 Ana María Alonso Torres has received compensation for serving on advisory boards for Biogen Spain S.L.U., Bristol Myers Squibb (BMS), Janssen, Novartis, Roche, and Sanofi; speaker honoraria from Almirall, Biogen Spain S.L.U., BMS, Janssen, Merck, Novartis, Roche, and Sanofi. Ángel Guillermo Arévalo Bernabé has received compensation for serving on advisory boards for Biogen Spain S.L.U. and Merck. Noelia Becerril Ríos has received compensation for serving on advisory boards and speaker fees from Almirall, Bayer, Biogen Spain S.L.U., BMS, Janssen, Merck, Novartis, and Sanofi. María Fuensanta Hellín Gil has received compensation for serving on advisory boards and a speaker event for Biogen Spain S.L.U. José Manuel Martínez Sesmero has received compensation for serving on advisory boards for Biogen Spain S.L.U., Merck, Roche, and Teva Pharmaceutical. Virginia Meca Lallana has received compensation for serving on scientific advisory boards and has received speaker honoraria from Almirall, Biogen Spain S.L.U., BMS, Genzyme, Janssen, Merck-Serono, Novartis, Roche, Sanofi-Aventis, Terumo, and Teva Pharmaceutical. Lluís Ramió-Torrentá has received compensation for serving on advisory boards and speaker honoraria from Almirall, Biogen Spain S.L.U., BMS, Merck, Novartis, Roche, Sanofi, and Teva Pharmaceutical. Alfredo Rodriguez-Antigüedad Zarranz has received compensation for serving on advisory boards or speaker honoraria from Biogen, BMS, Janssen, Merck‐Serono, Novartis, Roche, and Sanofi. Laura Gómez Maldonado and Inés Triana Junco are employees of Biogen Spain S.L.U. and hold shares or stocks as part of their remuneration. Manuel Gómez-Barrera, Nataly Espinoza Cámac, and Itziar Oyagüez work for Pharmacoeconomics & Outcomes Research Iberia (PORIB), an independent research organisation, which received funding pursuant to a contract with Biogen Spain S.L.U.

 The authors declare that there is no conflict of interests regarding the publication of this paper.
 SV: Abbvie-Allergan, Apellis, Bayer, Novartis, Roche SPA: Advisory Board participation MMP: none MEH: This work was supported by the National Institutes of Health EY014800 and an Unrestricted Grant from Research to Prevent Blindness, Inc., New York, NY, to the Department of Ophthalmology & Visual Sciences, University of Utah; and the National Institutes of Health R01EY015130 and R01EY017011 to MEH. LO’T: Bayer and Novartis: Advisory Board participation. AN: none. Celeste Limoli: none. EV: Allergan: Consultant/Advisor, Lecture fees, Grant support (AAO Financial Disclosure and First-slide Policy 2021); FB Vision and Santen: Consultant/Advisor, Lecture fees; Bruschettini, Oftagest, Sooft, Thea and Visufarma: Lecture fees; Alfa intes, OffHealth, Servimed and Shire: Grant support (AAO Financial Disclosure and First-slide Policy 2021). PN: none.

 Declaration of competing interest The authors declare that they have no conflicts of interest.
 The authors declare no conflict of interest.

 Competing interests: None declared.

 The authors declare no conflict of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Conflicts of interest The authors declare no conflicts of interest.


 Declaration of Competing Interest The authors declare no conflict of interest, financial or otherwise.
 The authors declare no conflict of interest.

 None



 Declaration of Competing Interest The authors have no conflicts of interest to declare.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.











 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 No potential conflict of interest was reported by the authors.

 The authors report no conflicts of interest.
 The authors declare no conflict of interest.

 The authors declare no conflict of interest.
 C.A.G. is a cofounder of TEGA Therapeutics, Inc. and hold equity positions in the company. C.A.G., B.E.T., and C.C. is an employee of TEGA Therapeutics, Inc. and own stock or stock options.

 The authors declare no competing interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest SK, HW and TB received research funding from Biogen. HW receives speaker honoraria and travel support from Biogen and is acting as a paid consultant for Biogen.
 The authors declare no competing interests.


 Declaration of competing interest None declared.




 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

 The authors declare that there are no competing interests associated with the manuscript.



 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: FK reports no potential competing interests. MCD has received consultancy fees from Baxter (data and safety monitoring board and lecture fees); Grifols/Talecris, Novartis, Octapharma (lecture fees and serving on DSMB); Alexion, Argenx and Dysimmune Diseases Foundation (consulting fees). He serves as an Associate Editor for Neurology (N2) and TAND. HCL received honoraria for speaking and advisory board engagement or academic research support by Akcea, Alnylam, Biogen, Celgene, CSL Behring, Grifols, Gruenenthal, LFB Pharma, Takeda and UCB.

 The authors have no financial or academic conflicts of interest to disclose. We did not receive any funding to complete this study from National Institutes of Health (NIH), Wellcome Trust, and Howard Hughes Medical Institute (HHMI).

 The authors report no competing interests relevant to the specific content of this article.
 Disclosure: Kristen Ashby declares no relevant financial relationships with ineligible companies. Disclosure: Brooke Adams declares no relevant financial relationships with ineligible companies. Disclosure: Mrin Shetty declares no relevant financial relationships with ineligible companies.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 FC, SF, RR, MMC, AM, GC, AC, and VC have nothing to declare. AB has served on advisory boards and/or has received travel grants and/or speaker honoraria from Merck, Biogen, Almirall, Novartis, and Sanofi-Genzyme. ML has served on advisory boards and/or has received travel grants and/or speaker honoraria from Merck, Biogen, Almirall, Novartis, and Sanofi-Genzyme. MM: scientific advisory board membership of Bayer Schering, Biogen, Sanofi-Genzyme, Merck, Novartis, Teva; consulting and/or speaking fees, research support or travel grants from Almirall, Bayer Schering, Biogen, CSL Behring, Sanofi-Genzyme, Merck, Novartis, Teva, Roche, Ultragenix; principal investigator in clinical trials for Biogen, Merck, Novartis, Roche, Sanofi Genzyme, Teva, Ultragenix, and CSL Behring. PC has no conflict of interest regarding this article.
 The coauthors have no competing financial interests.
 A.S. reports grants from the Italian Multiple Sclerosis Foundation (FISM) and the European Academy of Neurology, during the conduct of the study; she serves as board member for Merck Serono, and received personal fees from Almirall and Merck Serono, outside the submitted work. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

 The coauthors have no competing financial interests.
 Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-22-6515/coif). The authors have no conflicts of interest to declare.
 The authors declare no conflict of interest.
 Declaration of Competing Interest None.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no conflict of interest exists.
 The authors declare no conflict of interest.
 R.C. was involved in the collection of the data at the site and was not involved in the analysis. No other authors have any conflict of interest to disclose.

 Conflict of Interest PB has a financial interest in Fuzionaire Diagnostics and the University of Chicago. PB is a named inventor on patents related to [(18)F]3F4AP owned by the University of Chicago and licensed to Fuzionaire Diagnostics. Dr. Brugarolas’ interests were reviewed and are managed by MGH and Mass General Brigham in accordance with their conflict-of-interest policies. A provisional patent application related to 5Me3F4AP has been filed. PB, JESR, YS and SRR are listed as inventors on this provisional patent. The other authors declare no conflict of interests.
 Competing interests: None declared.
 J.W.C. has a financial interest in Silverier, a parent company for biotech-focused start-up companies that is currently focused on translating PET and MRI imaging agents that target myeloperoxidase. J.W.C.’s interests were reviewed and are managed by Massachusetts General Hospital and Mass General Brigham in accordance with their conflict of interest policies. C.W. has a financial interest in Einsenca, a company focused on translating PET and MRI imaging agents targeting myeloperoxidase. C.W.’s interests were reviewed and are managed by MGH and Mass General Brigham in accordance with their conflict of interest policies. Other authors have reported that they have no relationship relevant to the contents of this paper to disclose.
 SMG reports honoraria from Hexal and STREAMED UP and grant funding from the European Commission, German Federal Ministry of Health, German Research Foundation, and National Multiple Sclerosis Society, USA. MJL reports grant support from Bill & Melinda Gates Foundation, Wellcome Trust, Novartis, Boehringer Ingelheim, Merck, Sanofi, Regeneron, Moderna, Schmidt Futures, Google Ventures, Flu Lab, National Health Service England, UK National Institute for Health and Care Research, and UK Medical Research Council; an unpaid advisorship for the European Society of Cardiology; and receipt of drugs for clinical trials from Roche, AbbVie, Regeneron, GlaxoSmithKline, Vir Biotechnology, and Boehringer Ingelheim. NM reports grant support from Bill & Melinda Gates Foundation and Wellcome Trust and unpaid board membership for Cystic Fibrosis Europe. CO reports grant funding from the European Commission, German Federal Ministry of Research and Education, German Research Foundation, and Berlin Institute of Health; consulting fees from Janssen, Peak Profile, LIMES Schlosskliniken; honoraria from Janssen, Neuraxpharm, Fortbildungskolleg, and LIMES Schlosskliniken; participation in the Data and Safety Monitoring Board for the Central Institute of Mental Health Mannheim; and unpaid consultancy for the German National Guidelines for Depression.
 There are no conflicts of interest.
 The authors declare no conflict of interest.

 The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
 Declaration of Competing Interest The authors declare that there are no conflicts of interest.
 Declaration of Competing Interest The authors declare no conflict of interests
 CONFLICTS OF INTEREST: Dr KPS Nair received funding from GWS Pharma and Pharma Olan for drug trials on spasticity in multiple sclerosis. He also received funding from the National Institute of Health and Care Research UK, Medical Research Council UK, and the MS Society UK. The other authors declare that there are no competing financial interests in relation to the work described.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: B.G.W. receives payments for serving as chair of attack adjudication committees for clinical trials in NMOSD for Alexion, MedImmune, UCB Biosciences, and Viela Bio/Horizon Therapeutics; has consulted with Chugai, Genentech, Mitsubishi Tanabe Pharma, and Roche Pharmaceuticals regarding clinical trial design for NMOSD; has received speaking fees from Genentech, Horizon Therapeutics, and Roche; and has a patent for NMO-IgG for diagnosis of neuromyelitis optica, with royalties paid by Hospices Civils de Lyon, MVZ Labor PD Dr. Volkmann und Kollegen GbR, Oxford University, and RSR. D.M.W. reports personal fees from Arcus Medica, Biogen, Celgene, Genentech, MedImmune, Novartis, Reistone, TG Therapeutics, and Third Rock Ventures; research support paid to Mayo Clinic by Alexion Pharmaceuticals and Terumo BCT; and serves on a clinical trial adjudication committee for MedImmune and Viela Bio. A.J.G. reports grants from Conrad N. Hilton Foundation and Tom Sherak MS Hope Foundation; other financial relationships (for activities as expert witness, associate editor, advisory board/steering committee participation, and endpoint adjudication) with Bionure, Inception Sciences, JAMA Neurology, MedImmune/Viela Bio, Mylan, Synthon, and Trims Pharma; and personal fees from and other financial relationships with Pipeline Therapeutics. J.L.B. reports payment for study design/consultation from MedImmune/Viela Bio; personal fees from AbbVie, Alexion, Antigenomycs, BeiGene, Chugai, Clene Nanomedicine, EMD Serono, Genentech, Genzyme, Mitsubishi Tanabe Pharma, Novartis, Reistone Bio, Roche, and TG Therapeutics; grants from the National Institutes of Health, Novartis, and Mallinckrodt; and has a patent for Aquaporumab issued. H.J.K. has received a grant from the National Research Foundation of Korea; and consultancy/speaker fees from Alexion, Celltrion, Eisai, HanAll BioPharma, Merck Serono, Novartis, Sanofi Genzyme, Teva-Handok, and Viela Bio; serves on a steering committee for MedImmune/Viela Bio; and is a co-editor for the Multiple Sclerosis Journal and an associate editor for the Journal of Clinical Neurology. S.J.P. reports grants, personal fees, and non-financial support from Alexion Pharmaceuticals, Inc.; grants from Autoimmune Encephalitis Alliance, Grifols; grants, personal fees, non-financial support, and other from MedImmune and Viela Bio; consulting support from Astellas; personal fees for consulting services from UCB; and has a patent # 9,891,219 (Application#12-573942) “Methods for Treating Neuromyelitis Optica (NMO) by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)-IgG Autoantibody positive.” K.F. serves on scientific advisory boards for Alexion, Bayer Schering, Biogen Idec, Chugai, MedImmune, Merck Serono, Mitsubishi Tanabe Pharma, Nihon Pharmaceutical, Novartis, Ono, and Viela Bio; has received funding for travel and speaker honoraria from Asahi Kasei Medical, Astellas, Bayer Schering, Biogen Idec, Daiichi Sankyo, Dainippon Sumitomo, Eisai, Mitsubishi Tanabe Pharma, Nihon Pharmaceutical, Novartis, and Takeda; and research support from Asahi Kasei Medical, Bayer Schering, Biogen Idec, Chemo-Sero-Therapeutic Research Institute, Chugai, Genzyme Japan, the Ministry of Education, Culture, Sports, Science and Technology of Japan, the Ministry of Health, Welfare and Labor of Japan, Mitsubishi Tanabe Pharma, Nihon Pharmaceutical, Ono, Teijin, and Teva. F.P. has received research support, speaker honoraria, and travel reimbursement from Bayer, Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, and Teva; is supported by the German Competence Network for Multiple Sclerosis and the German Research Council (DFG Exc 257); received travel reimbursement from the Guthy–Jackson Charitable Foundation; and serves on the steering committee of the OCTIMS study sponsored by Novartis. G.C. has received personal fees for participation on Data and Safety Monitoring Boards from AI therapeutics, AMO Pharma, Applied Therapeutics, AstraZeneca, AveXis Pharmaceuticals, BioLineRx, Brainstorm Cell Therapeutics, Bristol Myers Squibb/Celgene, CSL Behring, Galmed Pharmaceuticals, Green Valley Pharma, Horizon Therapeutics, Immunic, Karuna Therapeutics, Mapi Pharma Ltd., Merck, Mitsubishi Tanabe Pharma Holdings, NHLBI (Protocol Review Committee), Novartis, Opko Biologics, Prothena Biosciences, Reata Pharmaceuticals, Regeneron, Sanofi-Aventis, Teva Pharmaceuticals, University of Pennsylvania, University of Texas Southwestern, and Visioneering Technologies, Inc.; personal fees for consulting or advisory board participation from Alexion, Antisense Therapeutics, Biogen, Clinical Trial Solutions LLC, Entelexo Biotherapeutics, Inc., Genentech, Genzyme, GW Pharmaceuticals, Immunosis Pty Ltd, Immunic, Klein-Buendel Incorporated, Merck/Serono, Novartis, Perception Neurosciences, Protalix Biotherapeutics, Regeneron, Roche, and SAB Biotherapeutics; is employed by the University of Alabama at Birmingham; and is President of Pythagoras, Inc., AL, USA. R.M. serves on scientific advisory boards for MedImmune and Viela Bio; and has received funding for travel and honoraria from Biogen Idec, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva, and Viela Bio. O.A. reports grants from the German Ministry of Education and Research (BMBF) and the German Research Foundation (DFG); grants and personal fees from Biogen, Genzyme, Novartis, and Teva; and personal fees from Alexion, Almirall, Horizon Therapeutics, Merck Serono, and Roche, and is a member of the European Reference Network for Rare Eye Diseases (ERN-EYE), co-funded by the Health Program of the European Union under the Framework Partnership Agreement No 739534 `ERN-EYE’. H.-P.H. has received fees for consulting, speaking, and serving on steering committees from Bayer Healthcare, Biogen Idec, Celgene Receptos, CSL Behring, GeNeuro, Genzyme, Horizon Therapeutics (formerly Viela Bio) MedDay, MedImmune, Merck Serono, Novartis, Roche, Sanofi, and TG Therapeutics, with approval by the Rector of Heinrich Heine University Düsseldorf. D.S., M.S., W.R., K.P., and D.C. are employees of Horizon Therapeutics (formerly Viela Bio) and own stock. E.K. is a former employee of Horizon Therapeutics and owns stock. B.A.C.C. reports personal fees for consulting from Alexion, Atara, Autobahn, Avotres, Biogen, Boston Pharma, EMD Serono, Gossamer Bio, Hexal/Sandoz, Horizon, Neuron23, Novartis, Sanofi, Siemens, TG Therapeutics, and Therini, and received research support from Genentech.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Competing interests: HI has received grants from Dokkyo Medical University (Young Investigator Award 2021-19). TK has received AMED (grant nos. JP19dm0908001, JP20dm0107162 and JP21zf0127005), and JSPS KAKENHI (Grant-in-Aid for Scientific Research (C) 19K08037). KTa has received payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Sumitomo Pharma and EUROIMMUN Japan in the past 36 months.
 Dr. Nicolò Bruschi has nothing to disclose. Dr. Maria Malentacchi received fees from Novartis and Biogen Idec for speaking in scientific meetings. Dr. Simona Malucchi received fees from Merck Serono, Biogen Idec, Novartis and Bristol Meyers for participation in advisory boards and for speaking in scientific meetings. Dr. Francesca Sperli received fees from Merck Serono, Biogen Idec, Novartis and Sanofi for participation in advisory boards and for speaking in scientific meetings. Dr. Arianna Sala has nothing to disclose. Dr. Paola Valentino received speaker honoraria from Roche, Biogen and Novartis,research support from Merck and grant support from Quanterix. Dr. Serena Martire has nothing to disclose. Dr. Antonio Bertolotto received honoraria for contribution in research, consultancy activity and activity of lectures from Almirall, Bayer, Biogen, Genzyme, Merck, Sanofi, Novartis, FISM, TEVA. Dr. Marisa Pautasso has nothing to disclose. Dr. Marco Alfonso Capobianco served on advisory board for Merck Serono, Biogen, Sanofi Genzyme, Roche, Novartis. Received honoraria from Almirall, Biogen, Novartis, Merck Serono, TEVA, Sanofi Genzyme.
 Competing interests: JO and DEG report a US patent application. SK, FF, JYP, YX, EKW and DEG report a US patent application (62/654,025).
 The authors report no conflicts of interest in this work.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 There are no conflicts of interest.
 The authors declare that they have no competing interests pertaining to this manuscript.
 All authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest or non-financial interest in the subject matter or materials discussed in this manuscript.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Competing interestsThe authors declare no competing interests.
 Declaration of competing interest The authors declare that they have no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 D.J.Z. and X.C. are inventors on an intellectual property disclosure related to the technology described in the manuscript that has been filed with Johns Hopkins University, which seeks to license the technology.




 Author SL is employed by Agilent Technologies Sweden AB. Author KH is employed by Agilent Technologies Deutschland GmbH. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.
 Domenico Zacà is an employee of Siemens Healthcare, Italy. Other authors declare no conflict of interest.
 Declaration of Competing Interest None.
 L. von Baumgarten, H.J. Stauss, and J.D. Lünemann report no disclosures relevant to the manuscript. Go to Neurology.org/NN for full disclosures.
 SF, GP, SB, and RD’A have financial and/or business interests in HealthTech Connex, which may be affected by the research reported in this manuscript. JV was employed by company Healthcode. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest The authors declare no conflict of interest regarding this manuscript.
 No potential conflict of interest was reported by the author(s).

 BK received independent (investigator initiated, project leader) grants from Siemens and Nutricia; is a member of an Astra Zeneca advisory board working on standard use of a new therapy for anticoagulant associated intracranial haemorrhage; provided content-independent lectures funded by Astra Zeneca, Biogen, Novartis, Medtronic, Boehringer Ingelheim, Servier, Angels Initiative; and was/is an investigator in clinical trials founded by Baxalta, Roche, Novartis, Astra Zeneca. MC was an investigator in clinical trials founded by Novartis, Teva, Biogen, Sanofi, and Serono. The authors JK and AW declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 There are no conflicts of interest.


 Declaration of Competing Interest None of the authors of this paper has a financial or personal relationship with other people or organizations that could inappropriately influence or bias the content of the paper.
 Declaration of Competing Interest M.M.v.L. received research support from EMD Serono, Merck, GSK and Idorsia Pharmaceutical Ltd. J.S. received lecture and/or consultancy fees from Biogen, Merck, Novartis and Sanofi-Genzyme. The remaining authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no competing interests.

 The authors declare no competing interests.
 The authors declare no conflict of interest.



 None.
 Declaration of competing interest M.V.-P. is co-founder and CSO of Ahead Therapeutics SL. L.A.-F., S.R.-F., B.B. and S.R.-V., M.S., and M.D. are employees by this company. J.V. and M.V.-P. hold a patent that relate to liposome immunotherapy for autoimmune diseases, licensed to Ahead Therapeuthics SL. This work was partially funded by Ahead Therapeutics SL. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of competing interest None.
 None






 Disclosure: Joseph Dougherty declares no relevant financial relationships with ineligible companies. Disclosure: Michael Carney declares no relevant financial relationships with ineligible companies. Disclosure: Marc Hohman declares no relevant financial relationships with ineligible companies. Disclosure: Prabhu Emmady declares no relevant financial relationships with ineligible companies.



 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Alina Zorn reports financial support was provided by Medical Research Council. Professor George Baillie is the Editor in Chief of Cellular Signalling.


 The authors declare no conflict of interest.
 The authors declare no conflict of interest.



 The author declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
 The authors declare no competing interests.
 The authors declare no competing interests.
 Conflict of interest: None declared.
 The authors declare no conflict of interests.

 There is no conflict of interest to declare.
 The authors declare no conflict of interest.
 Conflicts of Interest: None.
 Declaration of Competing Interest The authors declare that no conflict of interest could be perceived as prejudicing the impartiality of the research reported.



 J.S.H., J.R.H., C.A., M.K., H.R., A.O., H.H.N., E.A.S., N.A. and F.B.-S. declare no conflicts of interest. S.G. has received support for congress participation from Merck. H.K. has served on scientific advisory boards for Lundbeck A/S and Novartis and has received travel grants from IPSEN and Merck. K.B.S. has served as a consultant for Takeda Pharma A/S and received travel grants from TEVA, Biogen, Merck, and Novartis. N.B.F. has received consultancy fees from Almirall, NeuroPN, Vertex, Nanobiotix, and Novartis Pharma, and has undertaken consultancy work for Aarhus University with remunerated work for Biogen, Merz, and Confo Therapeutics. She has received grants from IMI2PainCare, an EU IMI 2 (Innovative Medicines Initiative) public-private consortium, and the companies involved are Grunenthal, Bayer, Eli Lilly, Esteve, and Teva. P.V.R. has received speaker honoraria from Biogen, Roche, Merck, Alexion, and Novartis; support for congress participation from Merck, Roche, and Sanofi; and fees for serving on advisory boards from Bristol–Myers–Squibb, Merck, Roche, Novartis, Biogen, Sanofi, and Alexion. H.H.C. reports non-financial support from Merck, non-financial support from Teva, non-financial support from Biogen, and non-financial support from Roche, outside the submitted work. F.S. has served on scientific advisory boards, as a consultant for, supported congress participation, or received speaker honoraria from Alexion, Biogen, Bristol–Myers–Squibb, H. Lundbeck A/S, Merck, Novartis, Roche, and Sanofi Genzyme. His laboratory has received research support from Biogen, Merck, Novartis, Roche, and Sanofi Genzyme. RMH has received support for congress participation from Merck, Ipsen, and speaker honoraria from AbbVie. ABO has served on scientific advisory boards for Biogen Idec, Novartis, and Sanofi Genzyme; has received research support from Novartis; has received speaker honoraria from Biogen, Novartis, and TEVA; and has received support for congress participation from Merck, TEVA, Biogen, Roche, Novartis, and Sanofi Genzyme. T.P. has received research support for the MS clinic at Aarhus University Hospital from Merck, Alexion, Roche, Biogen, Novartis, and Sanofi.
 Severa M, Rizzo F, Ricci D, Etna MP, Sinigaglia A, Buscarinu MC, Valdarchi C, Piubelli C, Gobbi F, Ristori G, Riccetti S, Cola G, Palmerini P, Rosato A, Balducci S, Barzon L and Coccia EM declare no conflict of interest. Salvetti M received research support and consulting fees from Biogen, Merck, Novartis, Roche, Sanofi, Teva. Landi D received travel funding from Biogen, Merck Serono, Sanofi‐Genzyme and Teva, honoraria for speaking from Sanofi‐Genzyme and Teva, and consultation fees from Merck Serono and Teva. She is sub‐investigator in clinical trials being conducted for Biogen, Merck Serono, Novartis, Roche and Teva. Girolama MA is an Advisory Board member of Biogen Idec, Genzyme, Merck‐Serono, Novartis, Teva and received honoraria for speaking or consultation fees from Almirall, Bayer Schering, Biogen Idec, Merck Serono, Novartis, Sanofi‐Genzyme, Roche, Mylan, Teva. She is the principal investigator in clinical trials for Actelion, Biogen Idec, Merck Serono, Mitsubishi, Novartis, Roche, Sanofi‐Genzyme, Merck Serono and Teva.
 The authors have no competing interests to declare.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 L.K.M., M.P.S., A.J., L.M.S., E.P., J.Z., C.M.H., and P.C.D. are current or past employees of Elicio Therapeutics and as such receive salary and benefits, including ownership of stock and stock options from the company. L.K.M., M.P.S., L.M.S., J.Z., C.M.H., and P.C.D. have Amphiphile patents pending to Elicio Therapeutics. V.D. and R.K. hold international patents on EBV vaccine and immunotherapy; R.K. acts as a consultant for Atara Biotherapeutics. R.K. is on the Scientific Advisory Board of Atara Biotherapeutics. K.B., M.S., G.A., T.T.L., A.P., and C.S. declare no financial or non-financial competing interests. The authors have no other financial or non-financial competing interests including relevant affiliations or financial involvement with any organization or entity with a financial interest in, or financial conflict with the subject matter or materials discussed in the manuscript, apart from those disclosed.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that they have no competing interest.
 The authors declare no competing interest.


 The authors declare no competing interests.

 The authors declare no competing interests.

 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Competing interestsThe authors declare that they have no competing interests.


 The authors declare no conflict of interest.
 Conflict of interest The authors declare no potential conflict of interest.




 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 CJ and RO are employees of the VA Maryland Health Care System. The reviews reported here do not reflect the views of the VA or the United States Government. CJ has an equity position with Cartesian Therapeutics. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of competing interest Authors declared no declaration of interest statement.
 The authors declare no competing interests.
 No conflicts of interest reported by any of the authors in this work.
 The authors declare no competing interests.
 The authors declare that they have no competing interests.
 We declare no conflicts of interest.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no competing interests.
 The authors declare that there are no conflicts of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors have no conflict of interest to report.
 The authors declare no conflict of interest.

 The authors declare no competing interests.

 Conflict of Interest and Funding Source: This work was supported by the National Institute of Neurological Disorders and Stroke under Award Number R01 NS060910. Dr. Crainiceanu is consulting with Bayer, Johnson and Johnson, and Cytel on methods development for wearable devices in clinical trials. The details of the contracts are disclosed through the Johns Hopkins University eDisclose system and have no direct or apparent relationship with the current paper. The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
 Declaration of Competing Interest The authors declare no conflict of interest.
 Declaration of Competing Interest S.M.K has lectured, consulted, and received honoraria from Bayer Schering Pharma, Genzyme, Merck Serono, and UCB; received a grant from the National Research Foundation of Korea and the Korea Health Industry Development Institute Research; is an Associate Editor of the Journal of Clinical Neurology. S.M.K and Seoul National University Hospital have transferred the technology of flow cytometric autoantibody assay to EONE Laboratory, Korea. The remaining authors declare no competing interests.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare that they have no competing interests.
 The authors have declared that no competing interests exist.

 Declaration of Competing Interest The authors declare no conflict of interest or competing financial interest affecting this work.
 The authors declare no conflict of interest.
 The authors declare no conflict of interest.

 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 B.B and A.L are cofounders and shareholders of SYMBYX Pty Ltd., a med tech company developing protocols targeting the microbiome to address metabolic and neurodegenerative diseases.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have no conflicts of interest to disclose.
 The authors declare no competing financial interest.
 Declaration of Competing Interest The authors have no conflict of interests to declare.

 F. Paul served on the scientific advisory boards of Novartis and MedImmune; received travel funding and/or speaker honoraria from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an associate editor of Neurology: Neuroimmunology & Neuroinflammation; is an academic editor of PLoS ONE; consulted for Sanofi Genzyme, Biogen, MedImmune, Shire, and Alexion; received research support from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Geynzme, Alexion, and Merck Serono; and received research support from the German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy-Jackson Charitable Foundation, and NMSS; J. Palace has received support for scientific meetings and honorariums for advisory work From Merck Serono, Novartis, Chugai, Alexion, Roche, Medimmune, Argenx, UCB, Mitsubishi, Amplo, Janssen, Sanofi. Grants from Alexion, Roche, Medimmune, UCB, and Amplo biotechnology; has patent ref P37347WO and licence agreement Numares multimarker MS diagnostics Shares in AstraZenica; and acknowledges partial funding by highly specialised services NHS England; R. Marignier reports personal fees from Viela Bio, Roche, and UCB and nonfinancial support from Viela Bio, Merck, Biogen, and Roche, outside the submitted work. AC-C reports funding from the Instituto de Salud Carlos III (Spain) JR19/00007; S. Ramanathan has received research funding from the National Health and Medical Research Council (Australia), the Petre Foundation, the Brain Foundation (Australia), the Royal Australasian College of Physicians, and the University of Sydney. She is supported by an NHMRC Investigator Grant (GNT2008339). She serves as a consultant on an advisory board for UCB and Limbic Neurology and has been an invited speaker for Biogen, Excemed, and Limbic Neurology; M. Lana-Peixoto reports no disclosures relevant to the manuscript; L. Law is an employee of Oxford PharmaGenesis; D.K. Sato reports grants from Conselho Nacional de Desenvolvimento Científico e Tecnológico, Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul, TEVA, and Merck and personal fees from TEVA, Merck, Biogen, Roche, and Viela Bio, outside the submitted work. KS reports personal fees from Biogen, Novartis, Merck, Roche, Celgene, and TG Therapeutics and grants from Merck and Roche, outside the submitted work; C. Quan received travel funding and/or speaker honoraria from Sanofi Genzyme, Novatis, Roche, Biogen, and Bristol Myers Squibb; is on the editorial board for Neuroimmunology Reports; and received research support from Novatis; N. Asgari reports no disclosures; J. De Seze has done some consulting and served on the board for Roche; I. Kleiter has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Alexion, Almirall, Biogen, Celgene, Hexal, Horizon, Merck, and Roche/Chugai; L. Pandit has received Speaker honorarium from Biogen and consulted for Biogen, Novartis, and Sanofi. She is listed as an inventor of a live cell-based assay for AQP4-IgG for which her university (Nitte university) holds a patent (No: 202141055841A); A. Vaknin-Dembinsky reported grants from F. Hoffmann-La Roche Ltd; personal fees from Roche, Biogen, Genzyme Sanofi, Merck, and Novartis; and grants from Merck and the Ministry of Health of Israel outside the submitted work. No other disclosures were reported; K. Fujihara serves on scientific advisory boards or as a consultant for Biogen, Mitsubishi-Tanabe, Novartis, Chugai, Roche, Alexion, VielaBio/Horizon Therapeutics, UCB, Merck Biopharma, Japan Tobacco, Argenx, and Abbvie; has received funding for travel or speaker honoraria from Chugai, Roche, Biogen, Novartis, Alexion, Teijin, Mitsubishi-Tanabe, AsahiKasei, Eisai, Takeda, and Bayer; serves on editorial boards of Clinical and Experimental Neuroimmunology, Frontiers in Neurology, Neurology: Neuroimmunology and Neuroinflammation, MS, MS and Related Disorders and Neuroimmunology Reports and advisory board of Sri Lanka journal of Neurology; and has been funded by the Grants-in-Aid for Scientific Research from the Ministry of Education, Science and Technology of Japan and by the Grants-in-Aid for Scientific Research from the Ministry of Health, Welfare and Labor of Japan; S. Kuwabara reports no disclosures relevant to the manuscript; N. Kissani reports no disclosures relevant to the manuscript; H.J. Kim received a grant from the National Research Foundation of Korea and research support from Aprilbio and Eisai; received consultancy/speaker fees from Alexion, Aprilbio, Altos Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, Handok, Horizon Therapeutics (formerly Viela Bio), Kolon Life Science, MDimune, Mitsubishi Tanabe Pharma, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok, and UCB; is a coeditor for the MS Journal; and an associated editor for the Journal of Clinical Neurology; A. Saiz received compensation for consulting services and speaker honoraria from Merck, Biogen, Sanofi, Novartis, Roche, Janssen, Alexion, and Horizon Therapeutics; R. Hornby is an employee of Oxford PharmaGenesis; G. Arrambide has received speaking honoraria, compensation for consulting services, or participation in advisory boards from Sanofi, Merck, Roche, and Horizon Therapeutics and travel support for scientific meetings from Novartis, Roche, and ECTRIMS; is the editor for Europe of the MS Journal—Experimental, Translational and Clinical, and is a member of the International Women in MS (iWiMS) Network executive committee and of the European Biomarkers in MS (BioMS-eu) Consortium steering committee; S. Huda reports no disclosures relevant to the manuscript; M.I. Leite is funded by the NHS (Myasthenia and Related Disorders Service and National Specialised Commissioning Group for Neuromyelitis Optica, UK) and by the University of Oxford, UK. She has been awarded research grants from the UK association for patients with myasthenia—Myaware and the University of Oxford. She has received speaker honoraria or travel grants from Biogen Idec, Novartis, UCB, and the Guthy-Jackson Charitable Foundation and serves on scientific or educational advisory boards for UCB Pharma, Argenx, and Viela/Horizon; J. Bennett has received grant support from Mallinckrodt Pharmaceuticals, Novartis, Alexion, NIH, and Guthy Jackson Charitable Foundation; received consulting fees from Alexion, Horizon Therapeutics, Reistone-Bio, Mitsubishi Tanabe, Sanofi-Genzyme, Antigenomycs, Beigene, Genentech-Roche, TG Therapeutics, and Chugai; and provides services on Independent Data Safety Monitoring Boards for Clene Nanomedicine and Roche. He provides editorial assistance to the Journal of Neuro-Ophthalmology, MS Journal, Neurology: Neuroimmunology & Neuroinflammation, and Frontiers in Ophthalmology. In the past 36 months, B. Cree has received personal compensation for consulting from Alexion, Atara, Autobahn, Avotres, Biogen, EMD Serono, Gossamer Bio, Horizon, Neuron23, Novartis, Sanofi, TG Therapeutics, and Therini and received research support from Genentech; D. Rotstein has received research support from the MS Society of Canada, Consortium of MS Centers (CMSC), University of Toronto Division of Neurology, and Roche Canada. She has received speaker's or consultant's fees from Alexion, Biogen, EMD Serono, Novartis, Roche, and Sanofi-Genzyme; S. Pittock has received personal compensation for serving as a consultant for Genentech, Sage Therapeutics, Astellas, and UCB. He's received personal compensation for serving on scientific advisory boards or data safety monitoring boards for F. Hoffman-LaRoche AG, Genentech, and UCB. His institution has received compensation for serving as a consultant for Astellas, Alexion, and Viela Bio/MedImmune. All compensation is paid to Mayo Clinic. He has received research support from Alexion, Grifols, NIH, Viela Bio/MedImmune, F. Hoffman-LaRoche AG/Roche/Genentech, and NovelMed. All compensation is paid to Mayo Clinic. He has a patent, Patent# 8,889,102 (Application#12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia)—issued; a patent, Patent# 9,891,219B2 (Application#12-573942, Methods for Treating Neuromyelitis Optica (NMO) by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)–IgG Autoantibody positive)—issued; Patents for Kelch11, LUZP4, Septin, MAP1b Abs, GFAP-IgG, and PDE10A pending. Go to Neurology.org/NN for full disclosures.
 Conflict of Interest All authors declare no conflict of interest.





 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 None declared.


 Disclosures Dr Saylor reports grants from National Institute of Mental Health; grants from National Multiple Sclerosis Society; grants from Fogarty International Center; grants from American Academy of Neurology; grants from National Institute of Aging; and grants from National Institute of Neurological Disorders and Stroke.
 The authors declare no conflict of interest.
 Declaration of competing interest The authors declare no competing interests.
 JLB reports payment for study design/consultation from MedImmune/Viela Bio; personal fees from AbbVie, Antigenomycs, Alexion, Chugai, Clene Nanomedicine, Genentech, Genzyme, Mitsubishi-Tanabe, Reistone Bio, Beigene, TG Therapeutics, Novartis, and Roche; grants from Novartis, Mallinckrodt, and the National Institutes of Health; and has a patent for Aquaporumab issued. KF serves as an advisor or on scientific advisory boards for Biogen, Mitsubishi Tanabe, Novartis, Chugai/Roche, Alexion, Viela Bio/Horizon Therapeutics, UCB, Merck Biopharma, Japan Tobacco, and AbbVie; has received funding for travel and speaker honoraria from Biogen, Eisai, Mitsubishi Tanabe, Novartis, Chugai, Roche, Alexion, Viela Bio, Teijin, Asahi Kasei Medical, Merck, and Takeda; and has received the Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan and the Grants-in-Aid for Scientific Research from the Ministry of Health, Welfare and Labor of Japan. HJK has received a grant from the National Research Foundation of Korea and research support from Aprilbio and Eisai; received consultancy/speaker fees from Alexion, Aprilbio, Altos Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, Handok, Horizon Therapeutics (formerly Viela Bio), MDimune, Mitsubishi Tanabe Pharma, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok, and UCB; is a co-editor for the Multiple Sclerosis Journal and an associate editor for the Journal of Clinical Neurology. RM serves on scientific advisory boards for Viela Bio/Horizon Therapeutics, Roche, Alexion, UCB; and has received funding for travel and fees from Alexion, Biogen, Merck, Novartis, Roche, and Viela Bio/Horizon Therapeutics. KCO'C has received research support from Alexion, now part of AstraZeneca, and Viela Bio, now part of Horizon Therapeutics, Cabaletta Bio, and Argenx. He is a consultant and equity shareholder of Cabaletta Bio. During the last 2 years, he has served as consultant/advisor for Alexion Pharmaceuticals, now part of AstraZeneca, and for Roche. RCS has been a consultant to Roche Pharmaceuticals and directs the William H. Annesley EyeBrain Center, including the OCT reading center at Thomas Jefferson University partnered with Wills Eye Hospital. AT is the MS Society of Canada Research Chair at UBC, with support from the MSMRI Research Group. He has research funding from Hilton Foundation, Roche, and Biogen; and receives honoraria from Roche, Sanofi Genzyme, and Biogen. HW receives honoraria for acting as a member of scientific advisory boards for AbbVie, Alexion, Argenx, Bristol Myers Squibb/Celgene, Janssen, Merck, Novartis, and Sandoz, as well as speaker honoraria and travel support from Alexion, Biogen, Bristol Myers Squibb, Genzyme, Merck, Neurodiem, Novartis, Roche, TEVA, and WebMD Global. He is acting as a paid consultant for AbbVie, Actelion, Argenx, Beckton Dickinson, Biogen, Bristol Myers Squibb, EMD Serono, Fondazione Cariplo, Gossamer Bio, Idorsia, Immunic, Immunovant, Janssen, Lundbeck, Merck, NexGen, Novartis, PSI CRO, Roche, Sanofi, Swiss Multiple Sclerosis Society, UCB, and Worldwide Clinical Trials. His research was funded by the German Federal Ministry for Education and Research (BMBF), Deutsche Forschungsgesellschaft (DFG), Deutsche Myasthenie Gesellschaft e.V., Alexion, Amicus, Therapeutics Inc., Argenx, Biogen, CSL Behring, F. Hoffmann-La Roche, Genzyme, Merck KgaA, Novartis, Roche Pharma, and UCB Biopharma. JW, RB, and TK are employees of F. Hoffmann-La Roche Ltd. SSZ has served, or serves, as a consultant and received honoraria from Alexion, Biogen, EMD-Serono, Horizon, Novartis, Roche/Genentech, Sanofi-Genzyme, and Teva Pharmaceuticals, Inc., and has served on Data Safety Monitoring Boards for Lilly, BioMS, Teva, and Opexa Therapeutics. VGA is an employee of Genentech, Inc. ANL is an employee of Genentech, Inc., and stockholder of Genentech, Inc., and F. Hoffmann-La Roche Ltd. SL-C is an employee of Roche Products Ltd. SJP has received personal compensation for serving as a consultant for Genentech/Roche, Sage Therapeutics, and Astellas. He has received personal compensation for serving on scientific advisory boards or data safety monitoring boards for F. Hoffmann-La Roche AG, Genentech, and UCB. His institution has received compensation for serving as a consultant for Astellas, Alexion, and Viela Bio/MedImmune. All compensation is paid to Mayo Clinic. He has received research support from Alexion, Viela Bio/MedImmune, and Roche/Genentech. He has two patents issued: Patent# 8,889,102 (Application#12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia); Patent# 9,891,219B2 (Application#12-573942, Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 [AQP4]-IgG Autoantibody positive). The authors declare that this study is funded by F. Hoffmann-La Roche Ltd. F. Hoffmann-La Roche Ltd. contributed to the study design and writing of this article. All authors, including those employed by Roche, had final responsibility for the decision to submit for publication and will be involved in future collection, analysis, and interpretation of data.

 The authors have no relevant financial or non-financial interests to disclose.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors report no relevant disclosures. Go to Neurology.org/NN for full disclosure.
 A Armuzzi has received consulting fees from: AbbVie, Allergan, Amgen, Arena, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Eli-Lilly, Ferring, Galapagos, Gilead, Janssen, MSD, Mylan, Pfizer, Protagonist Therapeutics, Roche, Samsung Bioepis, Sandoz, and Takeda; speaker’s fees from: AbbVie, Amgen, Arena, Biogen, Bristol-Myers Squibb, Eli-Lilly, Ferring, Galapagos, Gilead, Janssen, MSD, Novartis, Pfizer, Roche, Samsung Bioepis, Sandoz, Takeda, and Tigenix; and research support from: MSD, Takeda, Pfizer, and Biogen. R Gabbiadini has received speaker’s fees from Pfizer. A Dal Buono has received speaker’s fees from Abbvie. A Repici received consultancy fees from Medtronic and Fujifilm. B Bartocci, A Busacca, E Mencaglia, A Quadarella, and L Gasparini declare no conflicts of interest.
 Declaration of Competing Interest The authors report no competing interest.
 The authors have no conflict of interest to disclose.

 Declaration of interests CJC has received research grants from the National Institutes of Health and is secretary for the International Neuropalliative Care Society. RG has received honoraria from Abbott Laboratories and travel support from Sun Pharma and Intas Pharma, and is a board member for the International Neuropalliative Care Society. LCH receives funding from the National Institute on Aging, Centers for Medicare and Medicaid Services Civil Monetary Penalty Fund, National Institute for Nursing Research, and the Patient Centered Outcomes Research Institute. BMK has received research grants from the National Institutes of Health and the Patient Centered Outcomes Research Institute; has received honoraria from the Parkinson Foundation and International Movement and Parkinson Disease Society, Davis Phinney Foundation, and American Academy of Neurology; has received royalties from Elsevier; and is President of the International Neuropalliative Care Society. JM has received research grants from the Patient Centered Outcomes Research Institute, Canadian Open Parkinson Network, Brain Canada, the Canadian Consortium on Neurodegeneration in Aging, the National Institutes of Health, and University Hospital Foundation; has received royalties from Elsevier; and is American Academy of Neurology Vice President, US delegate for Oxford University Press, and on the board of directors of the Parkinson Foundation, and on the board of directors of the International Neuropalliative Care Society (20192–021). DJO has received royalties from Oxford University Press and Springer, and is a board member for the International Neuropalliative Care Society. SZP has received support from the Gordon and Betty Moore Foundation, American Academy of Hospice and Palliative Medicine, Palliative Care Quality Collaborative, Cambia Foundation, Hellman Foundation, Alafi Family Foundation, Stupski Foundation, Archstone Foundation, and Unihealth Foundation; has received received royalties from McGraw Hill Publishers; and is President of Palliative Care Quality Collaborative, on the board of directors of By the Bay Health, and advisory board Chair for Sojourns Scholar Leadership Program. PH is a board member for the International Neuropalliative Care Society. MS is on the membership committee for the International Neuropalliative Care Society. All other authors declare no competing interests. LCH (R01-AG065394) and BMK (K02 AG062745) received support from the National Institute of Aging for this work.

 The authors declare no conflict of interest.
 The authors declare no conflict of interest.

 Competing interests The authors declare no competing or financial interests.
 Declaration of Competing Interest The authors declared no competing interests.
 The authors declare that there is no conflict of interest regarding the publication of this article.
 The authors declare no competing interest.
 The authors have no conflict of interest to report.
 The authors declare no conflict of interest.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflict of interests: The authors whose names are listed certify that they have NO affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers’ bureaus; membership, employment, consultancies, stock ownership, or other equity interest; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affi liations, knowledge or beliefs) in the subject matter or materials discussed in this manuscript.
 The authors declare no conflict of interest.

 The authors have declared that no competing interests exist.
 Declaration of Competing Interest None.


 Authors Hannah Foote, Audrey Bowen and Emma Patchwood are also affiliated at Division of Psychology and Mental Health, University of Manchester, Manchester, UK. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of competing interest The authors declares that they have no relevant or material financial interests that relate to the research described in this paper.

 Nabiximols and placebo sprays were donated by GW Pharmaceuticals. GW Pharmaceuticals did not play any other role in this study apart from providing in-kind contribution of the study medication (Nabiximols and placebo sprays). Dr. Bernard Le Foll has obtained funding from Pfizer Inc. (GRAND Awards, including salary support) for investigator-initiated projects. Dr. Le Foll has obtained funding from Indivior for a clinical trial sponsored by Indivior. Dr. Le Foll has in-kind donations of cannabis products from Aurora Cannabis Enterprises Inc. and study medication donations from Pfizer Inc. (varenicline for smoking cessation) and Bioprojet Pharma. He was also provided a coil for a Transcranial magnetic stimulation (TMS) study from Brainsway. Dr. Le Foll has obtained industry funding from Canopy Growth Corporation (through research grants handled by the Centre for Addiction and Mental Health and the University of Toronto), Bioprojet Pharma, Alcohol Countermeasure Systems (ACS), Alkermes and Universal Ibogaine. Lastly, Dr. Le Foll has received in kind donations of nabiximols from GW Pharmaceuticals for past studies funded by CIHR and NIH. He has participated in a session of a National Advisory Board Meeting (Emerging Trends BUP-XR) for Indivior Canada and is part of Steering Board for a clinical trial for Indivior. He has been consultant for Shinogi. He is supported by CAMH, Waypoint Centre for Mental Health Care, a clinician-scientist award from the department of Family and Community Medicine of the University of Toronto and a Chair in Addiction Psychiatry from the department of Psychiatry of University of Toronto.
 The authors declare no conflict of interest.
 The authors declare that they have no competing interests
 Competing interests: NB is a paid consultant for Mymee and has ownership in the company. MDJ is paid as an independent contractor by Mymee. ML is a salaried employee of Mymee. LC serves on the Board of Scientific Advisors for Mymee. MD is employed by Mymee and has ownership in the company. There are no other competing interests to disclose. NB is the guarator for this paper.

 The authors declare no conflict of interest.
 The authors declare no competing interests.
 Declaration of Competing Interest The authors declare that there are no conflicts of interest.

 The authors declare no competing interests.


 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that they have no competing interests.

 The authors declare no competing interests.
 Declaration of Competing Interest ASM, LMM, SH, and GMzH have nothing to disclose. BZ is a current employee and shareholder of F. Hoffmann- La Roche Ltd. HW received honoraria for acting as a member of Scientific Advisory Boards for Janssen, Merck, and Novartis as well as speaker honoraria and travel support from Alexion, Amicus Therapeuticus, Biogen, Biologix, Bristol Myers Squibb, Cognomed, F. Hoffmann-La Roche Ltd., Gemeinnützige Hertie-Stiftung, Medison, Merck, Novartis, Roche Pharma AG, Genzyme, TEVA, and WebMD Global. Heinz Wiendl is acting as a paid consultant for Biogen, Bristol Myers Squibb, EMD Serono, Idorsia, Immunic, Novartis, Roche, Sanofi, the Swiss Multiple Sclerosis Society, and UCB. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgesellschaft (DFG), Deutsche Myasthenie Gesellschaft e.V., Alexion, Amicus Therapeutics Inc., Argenx, Biogen, CSL Behring, F. Hoffmann - La Roche, Genzyme, Merck KgaA, Novartis Pharma, Roche Pharma, and UCB Biopharma. CCG received speaker honoraria from MyLan and DIU Dresden International University GmbH, and travel expenses for attending meetings from Biogen, Euroimmun, MyLan, and Novartis Pharma. Her research is funded by the German Research Foundation (DFG), the German Ministry for Education and Research (BMBF), the European Union (Horizon2020), the IZKF Münster, Biogen, Roche, and Novartis.
 The authors have declared that no competing interests exist.
 The authors declare no conflict of interest.
 Declaration of Competing Interest None.

 Conflict of Interest A Benussi was partially supported by the Airalzh-AGYR2020, by Fondazione Cariplo (grant n° 2021–1516), and by the Fondation pour la Recherche sur Alzheimer. M. Hallett is an inventor of a patent held by NIH for the H-coil for magnetic stimulation for which he receives license fee payments from the NIH (from Brainsway). He is on the Medical Advisory Board of Brainsway (unpaid position). S. Kreig reports being a consultant for Brainlab and receiving honorarium for lectures provided for Nexstim and Inomed. M Massimini is a co-founder and shareholder of Intrinsic Powers, a spin-off of the University of Milan, Milan, Italy. T. Picht served as a consultant for the TMS system manufacturer Nexstim Oy, Helsinki, Finland. U. Ziemann reports receiving a grant from Takeda Pharmaceutical Company Ltd., and consulting fees CorTec GmbH. The other authors have no potential conflicts of interest to disclose.
 This study is funded by PTC Therapeutics, Inc. All authors are employees and stock owners of PTC Therapeutics, Inc.

 Conflicts of interest and sources of funding: A.F.M., S.C.S., F.T., and G.V. are Bracco Imaging SpA employees. A.M. received a PhD fellowship from Bracco Imaging SpA. D.B. is a Bracco Imaging SpA consultant. M.A. is a consultant of Bracco Imaging SpA and of Centro Diagnostico Italiano; he receives consultancy fees/salary in light of these consultancies. S.P. is a consultant of Centro Diagnostico Italiano. M.S. is a professor and radiologist at the Erasmus Medical Center and at the Medical Delta; she received fees paid by GE Healthcare (speaker fees), AuntMinnie (speaker fees), and Bracco Imaging SpA (consultancy fees). A.B. is a professor at Università degli Studi di Torino and a consultant of Bracco Imaging SpA.

 Declaration of interests WJJ receives grant support from the National Institutes of Health (NIH), the Alzheimer's Association, and Roche/Genentech; has received consulting fees from Eli Lilly, Biogen, Bioclinica, Eisai, and Prothena; and holds stock options in Optoceutics. CET receives grant support from the EU/European Federation of Pharmaceutical Industries Associations Innovative Medicines Initiative Joint Undertaking. CET's research is supported by the European Commission (Marie Curie International Training Network, Multi-omics Interdisciplinary Research Integration to Address Dementia Diagnosis grant agreement number 860197, and the EU Joint Programme—Neurodegenerative Disease Research), Health Holland, the Dutch Research Council (ZonMW), the Alzheimer Drug Discovery Foundation, the Selfridges Group Foundation, Alzheimer Netherlands, the Alzheimer Association, the Foundation of Multiple Sclerosis (MS) Research, and the National MS Foundation. CET is a recipient of funding from ABOARD, which is a public–private partnership (PPP) receiving funding from ZonMW (grant number 73305095007), and Health~Holland/Topsector Life Sciences & Health (PPP allowance; grant number LSHM20106). CET performed contract research or consulted for ADx Neurosciences, AC-Immune, Axon Neurosciences, Biogen, Brainstorm Therapeutics, Celgene, Denali, EIP Pharma, Eisai, Fujirebio, Merck, Novo Nordisk, PeopleBio, Quanterix, Roche, Toyama, and Vivoryon. CET is editor for Alzheimer Research and Therapy and serves on editorial boards for Medidact Neurologie/Springer, and Neurology: Neuroimmunology & Neuroinflammation. CD receives grant support from the NIH and has received consulting fees from Eisai, Novartis, and Nova Nordisc.
 The Authors have no conflicts of interest and received no additional funding for this work.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors have declared that no competing interests exist.
 The authors declare no conflict of interest.

 The authors declare that they have no competing interests.

 Declaration of Competing Interest All the authors declare they have no conflicts of interest.





 Declaration of Competing Interest The authors have no conflicts of interest to declare.
 The authors declare no competing interests.
 The authors declare no competing interests.
 Authors declare that no competing interests exist.



 All authors report no conflicts of interest in this work.




 The authors declare that they have no competing interests.
 Dejan Jakimovski, Svetlana P Eckert, Omid Mirmosayyeb, Sangharsha Thapa, and Penny Pennington have nothing to disclose. David Hojnacki has received speaker honoraria and consultant fees from Biogen Idec, Teva Pharmaceutical Industries Ltd., EMD Serono, Pfizer Inc, and Novartis. Bianca Weinstock-Guttman received honoraria for serving in advisory boards and educational programs from Biogen Idec, Novartis, Genentech, Genzyme and Sanofi, Janssen, Abbvie and Bayer. She also received support for research activities from the National Institutes of Health, National Multiple Sclerosis Society, Department of Defense, and Biogen Idec, Novartis, Genentech, Genzyme and Sanofi.
 LP, AT, AZ, KF, YU, LS, CT No competing interests declared, YZ consulted for Ono Pharmaceutical


 Yuxiong Jiang, Youdong Chen, Qian Yu, and Yuling Shi have no conflicts of interest that are directly relevant to the content of this article.

 I.E.L. and M.H. have received grants from the Swedish Research Council. M.H. is a member of the medical advisory board of the Myositis Association. The other authors declare no conflict of interest.
 Declaration of Competing Interest This statement is to certify that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare no competing interests.
 Conflict of interest statement The authors declare that they have no competing interests.
 The authors declare no conflict of interest.

 Declaration of competing interest The authors declare that they have no conflict of interest to disclose.
 All authors declare no conflicts of interest.

 Declaration of Competing Interest There are no other conflicts related with this work.




 Disclosure: Ryan Brotman declares no relevant financial relationships with ineligible companies. Disclosure: Maria Moreno-Escobar declares no relevant financial relationships with ineligible companies. Disclosure: Joe Joseph declares no relevant financial relationships with ineligible companies. Disclosure: Gauri Pawar declares no relevant financial relationships with ineligible companies.
 None disclosed.

 None.

 M.Av.Es. consulted for Biogen, and has received travel grants from Shire (formerly Baxalta), performs work as a medical monitor for an ongoing trial from Ferrer (NCT05178810).
 R.T. Benson serves as a voluntary member of the AAN Registry Subcommittee and has nothing to disclose. The views expressed are the authors' own and do not necessarily reflect those of the National Institutes of Health, the Department of Health and Human Services, or the United States Government. S.M. Benish serves as voluntary Chair of the AAN Registry Subcommittee and Member of the AAN Quality Committee and on the AAN Board of Directors and has nothing to disclose. G.J. Esper has received personal compensation in the range of $500–$4,999 for serving as a consultant for NeuroOne Technology Corporation, has received personal compensation in the range of $500–$4,999 for serving as a consultant for Pfizer, has received personal compensation in the range of $500–$4,999 for serving as an Expert Witness for Mitchell Law Group, and reports no other disclosures that are relevant to this manuscript. The institution of B.M. Kissela has received research support from the NIH/NINDS and NCATS. B.M. Kissela reports no other disclosures that are relevant to this manuscript. N. Rosendale has received personal compensation in the range of $500–$4,999 for serving as an Editor Associate Editor or Editorial Advisory Board Member for Neurology. The institution of N. Rosendale has received research support from the UCSF Academy of Medical Educators. N. Rosendale reports no other disclosures that are relevant to this manuscript. E.T. Marulanda-Londono and O.A. Hope have nothing to disclose. T.T.A. Pham is a member of the AAN Registry Subcommittee. T.T.A. Pham has nothing to disclose. M. Roe, A. Torres, A. Lien, and S. Kauwe are employees of Verana Health and have nothing to disclose. K.B. Lundgren and A. Mante are employees of the American Academy and have nothing to disclose. B. Schierman is an employee of the American Academy and has nothing to disclose. L.K. Jones has received publishing royalties from a publication relating to health care and serves as a voluntary member of the Board of Directors with the Mayo Clinic ACO and American Academy of Neurology Institute. L.K. Jones reports no other disclosures that are relevant to this manuscript. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.
 The authors declare no competing interests.
 Conflict of Interest Disclosures: Dr Waters reported receiving grants from UK Research and Innovation. The Innovate UK grant was received by his supervisor and funded his Research Associate position during the conduct of the study. Dr Marshall reported receiving grants from Tom and Sheila Springer Charity and grants from Barts Charity during the conduct of the study; grants from the National Institute for Health and Care Research (NIHR), grants from Innovate UK, grants from the Michael J. Fox Foundation, and grants from Alzheimer’s Research UK outside the submitted work. Dr Dobson reported grants from the Multiple Sclerosis Society of Great Britain and Northern Ireland, grants from the National Multiple Sclerosis Society, grants from the BMA Foundation, grants from the Horne Family Charitable Trust, grants from the Medical Research Council, grants from the NIHR, grants from Biogen, grants from Merck, grants from Celgene (now Bristol Myers Squibb), and personal fees from Novartis, Janssen Biogen, Merck, Teva, and Roche. Dr Noyce reported receiving grants from Barts Charity, Parkinson’s UK, Cure Parkinson’s, the Michael J. Fox Foundation, Innovate UK, Solvemed, and Alchemab and personal fees from AstraZeneca, AbbVie, Zambon, BIAL, uMedeor, Alchemab, Britannia, and Charco Neurotech outside the submitted work. No other disclosures were reported.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Disclosure: Kevin Moriles declares no relevant financial relationships with ineligible companies. Disclosure: Muhammad Hashmi declares no relevant financial relationships with ineligible companies.

 There are no conflicts of interest among the authors to disclose.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The authors have no potential conflicts of interest to disclose.
 The authors report no disclosures relevant to the manuscript. Go to Neurology.org/N for full disclosures.

 Declaration of Competing Interest None.
 The authors declares no conflict of interests.
 The authors declare no conflict of interest.

 Declaration of interests B.E.G. receives support from an Abbvie-Harvard grant for research unrelated to these studies.
 None declared.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 S Irani is a coapplicant and receives royalties on a licensed patent application WO/210/046716 (U.K. patent no., PCT/GB2009/051441) entitled “Neurological Autoimmune Disorders” and has filed “Diagnostic Strategy to improve specificity of CASPR2 antibody detection (PCT/G82019 /051257); he has received honoraria and research support from UCB, Immunovant, MedImmun, Roche, Cerebral therapeutics, ADC therapeutics, CSL Behring and ONO Pharma; A.McKeon has received royalties pertaining to the commercialization of septin-5 and MAP1B antibodies for diagnosis of autoimmune neurological diseases, has patents pending for neural IgGs as biomarkers for diagnosis and treatment of autoimmune neurological disorders, and has received research support from Euroimmun AG; APi served in the advisory board of Z-cube (technology division of Zambon pharmaceuticals), he received honoraria from Z-cube s.r.l., Biomarin, Zambon, Abbvie, Nutricia and Chiesi pharmaceuticals. He received research support from Vitaflo Germany and Zambon Italy; APa is consultant and served on the scientific advisory board of GE Healthcare, Eli-Lilly and Actelion Ltd Pharmaceuticals, received speaker honoraria from Nutricia, PIAM, Lansgstone Technology, GE Healthcare, Lilly, UCB Pharma and Chiesi Pharmaceuticals, he is funded by Grant of Ministry of University (MURST); the other authors report no disclosures relevant to the manuscript. S Mariotto is associate editor of Immunologic Research.
 None.
 Competing interests: WG is employed by Utrecht University and conducts research under the umbrella of the Utrecht-WHO Collaborating Centre for Pharmaceutical Policy and Regulation. The Centre has received unrestricted research funding from public sources, eg, WHO, the Netherlands Organisation for Health Research and Development (ZonMW), the Dutch National Health Care Institute (ZIN), EC Horizon 2020, the Dutch Medicines Evaluation Board (MEB) and the Dutch Ministry of Health. None of the abovementioned public funding sources had any involvement in the current study. WG is also employed by the National Health Care Institute.At the time of the project, MLDB was employed by Copenhagen Centre for Regulatory Sciences (CORS). CORS is a cross-faculty university anchored institution involving various public (Danish Medicines Agency, Copenhagen University) and private (Novo Nordisk, Lundbeck, Ferring Pharmaceuticals, LEO Pharma) stakeholders as well as patient organisations (Rare Diseases Denmark). The Centre is purely devoted to the scientific aspects of the regulatory field and with a patient-oriented focus and the research is not company-specific product or directly company related. In the past 5 years, CORS has received funding from Novo Nordisk, Lundbeck, Ferring Pharmaceuticals and LEO Pharma for projects not related to this study. Currently, MLDB is employed by Utrecht University and conducts research under the umbrella of the Utrecht-WHO Collaborating Centre for Pharmaceutical Policy and Regulation. This Centre receives no direct funding or donations from private parties, including the pharmaceutical industry. Research funding from public–private partnerships, eg, IMI, and The Escher Project (http://escher.lygature.org/) is accepted under the condition that no company-specific product or company-related study is conducted. The Centre has received unrestricted research funding from public sources, e.g. World Health Organisation (WHO), the Netherlands Organisation for Health Research and Development (ZonMW), the Dutch National Health Care Institute (ZIN), EC Horizon 2020, the Dutch Medicines Evaluation Board (MEB) and the Dutch Ministry of Health. None of the abovementioned companies had any involvement in the current study.The other authors declare no competing interests.



 The authors have declared that no competing interest exists.
 GB: has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Celgene/BMS, Lilly, Merck, Novartis, Roche, Sanofi-Genzyme and Teva, and received honoraria for consulting Biogen, Celgene/BMS, Novartis, Roche, Sanofi-Genzyme and Teva. He has received unrestricted research grants from Celgene/BMS and Novartis. WM: declares no conflict of interest relevant to this study. SM: declares no conflict of interest relevant to this study. VS: declares no conflict of interest relevant to this study/ NK: has participated in meetings sponsored by, received speaker honoraria or travel funding from BMS/Celgene, Janssen-Cilag, Merck, Novartis, Roche and Sanofi-Genzyme and held a grant for a Multiple Sclerosis Clinical Training Fellowship Programme from the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS). PP: declares no conflict of interest relevant to this study. CM: declares no conflict of interest relevant to this study. KN: declares no conflict of interest relevant to this study. CW: has received honoraria consultancy/speaking from Apomedica, Curelator, Eli Lilly, Grünenthal, Hermes, Novartis, Pfizer, Ratiopharm/Teva, and Stada. BP: declares no conflict of interest relevant to this study.

 Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dariush Hinderberger reports financial support was provided by German Research Foundation. George Harauz reports financial support was provided by Natural Sciences and Engineering Research Council of Canada.



 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest None.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflicts of interest and sources of funding: This work was supported by the 234 Discipline Climbing Plan of the First Affiliated Hospital of Naval Medical University (grants 2019YPT002 and 2020YPT002). The authors have no conflicts to report.
 Declaration of interests The authors declare no competing interests.
 The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.


 Declaration of competing interest F Eftimov and T Kuijpers report (governmental) grants from ZonMw to study immune response after SARS-Cov-2 vaccination in auto-immune diseases. F Eftimov also reports grants from Prinses Beatrix Spierfonds, CSL Behring, Kedrion, Terumo BCT, Grifols, Takeda Pharmaceutical Company, and GBS-CIDP Foundation; consulting fees from UCB Pharma and CSL Behring; honoraria from Grifols. AJ van der Kooi reports grants from CSL Behring and participation on an advisory board for Argen-X. M Löwenberg reports a grant from Galapagos not related to this study, and honoraria from Bristol Myers Squibb, Pfizer, Takeda, and Tillotts. Ph I Spuls is involved in performing clinical trials with many pharmaceutical industries that manufacture drugs used for the treatment of e.g. psoriasis and atopic dermatitis, for which financial compensation is paid to the department/hospital and is a chief investigator of the TREAT NL registry taskforce and SECURE-AD registry. M.W. Bekkenk is a secretary for Dutch Experimental Dermatology Board and head of the pigmentary disorders group within the Dutch Dermatology Board, and reports honoraria from Pfizer, Sanofi, Novartis and Fondation René Touraine. J Killestein has speaking relationships with Merck Serono, Biogen Idec, TEVA, Sanofi, Genzyme, Roche and Novartis; Amsterdam UMC, location VUmc, MS Center Amsterdam has received financial support for research activities from Merck Serono, Bayer Shcering Pharma, Biogen Idec, GlaxoSmithKline, Roche, Teva, Sanofi, Genzyme, GlaxoSmithKline, and Novartis. B Horváth reports unpaid positions as medical advisor for several patient groups, a board position for ERN-SKIN, and associate editor for The British Journal of Dermatology; reports grants from Abbvie, Akari Therapeutics, Celgene, and Novartis; consulting fees from UCB Pharma, Novartis and Janssen-Cilag; honoraria from Abbvie. J.J.G.M. Verschuuren reports consulting fees from Argenx, Alexion and NMD Pharma; is coinventor on patent applications based on MuSK-related research. DJ Hijnen reports grants from Abbvie, AstraZeneca, Janssen, LEO Pharma and UCB Pharma, and honoraria from Abbvie, Galderma, Janssen, Lilly, Pfizer, Sanofi and UCB Pharma, and a paid position in an advisory board for BIOMAP IMI. P.A. van Doorn participated on an advisory board for Octapharma. P. van Paassen reports grants from Alexion Pharma and GSK; and participation on GSK and Vifor Pharma advisory boards. G.R.A.M. D'Haens reports consulting fees from Abbvie, Agomab, AstraZeneca, AM Pharma, AMT, Arena Pharmaceuticals, Bristol Meiers Squibb, Boehringer Ingelheim, Celltrion, Eli Lilly, Exeliom Biosciences, Exo Biologics, Galapagos, Index Pharmaceuticals, Kaleido, Roche, Gilead, Glaxo Smith Kline, Gossamerbio, Pfizer, Immunic, Johnson and Johnson, Origo, Polpharma, Procise Diagnostics, Prometheus laboratories, Prometheus Biosciences, Progenity, and Protagonist; honoraria from Abbvie, Arena, Galapagos, Gilead, Pfizer, BMS, Takeda; participation on advisory boards for Abbvie, Seres Health, Galapagos, and AstraZeneca. R.B. Takkenberg reports honoraria from Sobi and Norgine and participation in an advisory board for Norgine. SH Goedee is a board member of the Dutch Society of Clinical Neurophysiology (unpaid), reports grants from Prinses Beatrix Spierfonds, and received speaker fees from Shire/Takeda. AH Zwinderman reports paid data safety monitoring board positions for Torrent Ltd and Foresee Pharmaceuticals Co. No other disclosures were reported. Bar plot showing proportions of self-reported increased disease activity (with corresponding 95% CI's), physician confirmed increased disease activity, and treatment intensification, within each IMID group at 60 days after start of primary immunization. IBD: inflammatory bowel disease; IMID: immune-mediated inflammatory disease; ISP: immunosuppressant; MS: multiple sclerosis; NMO: neuromyelitis optica; SLE: systemic lupus erythematosus. Bar plot showing incidence of self-reported increased disease activity at different timepoints. A) self-reported increased disease activity within 60 days after vaccination: at 60 days after start of primary immunization (prim. imm.), seven to 60 days after first additional vaccination (add. vacc.), and at other follow-up moments within seven to 60 days after a vaccination other than the moments mentioned before (e.g. second vaccination of primary immunization or second additional vaccination). B) self-reported increased disease activity not within 60 days after vaccination, in the two-monthly follow-up surveys starting at first vaccination. Figure showing the results of the multivariate mixed model on determinants of self-reported increased disease activity. RR's with corresponding 95% CI for age, female sex, BMI, IMID group (with gastro-intestinal disease as reference group), recent increased disease activity (self-reported increased disease activity in the three months preceding enrollment), ISP use, and any SARS-CoV-2 vaccination in 60 days before the survey. BMI: body mass index; CI: confidence interval; IMID: immune-mediated inflammatory disease; ISP: immunosuppressant; MS: multiple sclerosis; NMO: neuromyelitis optica; RR: relative risk; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Dr. Bernstein is supported in part by the Bingham Chair in Gastroenterology. Dr. Bernstein has consulted to Abbvie Canada, Amgen Canada, Bristol Myers Squibb Canada, Janssen Canada, Pfizer Canada, Roche Canada, Sandoz Canada, Takeda Canada, and has received unrestricted educational grants from Abbvie Canada, Janssen Canada, Pfizer Canada, and Takeda Canada. He has consulted to Takeda and Mylan Pharmaceuticals. He has been on the speaker’s bureau of Abbvie Canada, Janssen Canada, Medtronic Canada and Takeda Canada. He has received a research grant from Abbvie Canada and contract grants from Abbvie, Janssen, Pfizer, Roche, Boeringher Ingelheim. Dr Graff has consulted to Roche Canada. All other authors do not possess any competing interest.
 The authors have declared that no competing interests exist.
 The authors declare no competing interests.
 Disclosure of Interest: None of the following authors have any proprietary interests or conflicts of interest related to this submission
 Declaration of competing interest Eduardo Muñoz is a Scientific Advisor of Emerald Health Pharmaceuticals. The rest of the authors declare no competing financial interests.
 The authors have additional information to disclose. T.G. received compensation for activities with Biogen Idec. S.D. received compensation for activities with Sanofi Genzyme. A.H. has received speaker’s fees from Bayer Healthcare, Biogen, Celgene, Genzyme, Merck, Novartis, and Teva. A.L.F. received research funding by Georgius Agricola Stiftung Ruhr; received honoraria and travel grants from Novartis AG, Sanofi, and Eisai GmbH, none related to this work; and owns shares of Fresenius SE & Co., Gilead Sciences, Medtronic PLC, and Novartis AG. J.M. received travel grants from Biogen Idec, Novartis AG, Teva, and Eisai GmbH, and his research is funded by Klaus Tschira Foundation and Ruhr-University, Bochum (FoRUM-program), none related to this work. R.G. received speaker’s and board honoraria from Baxter, Bayer Schering, Biogen Idec, CLB Behring, Genzyme, Merck Serono, Novartis, Stendhal, Talecris, and TEVA, all not related to this manuscript. His department received grant support from Bayer Schering, BiogenIdec, Genzyme, Merck Serono, Novartis, and TEVA, all not related to this manuscript. K.P. received travel grants and speaker’s honoraria from Biogen Idec and Bayer Schering, Novartis, and Grifols, all not related to this manuscript. All other authors have nothing to declare.
 Declaration of competing interest The authors declare no conflict of interest. Hans Knoop receives royalties for a published manual of CBT for CFS/ME.

 Michael Hull, Vamshi Ruthwik Anupindi, and Mitchell DeKoven are employees of IQVIA, contracted by Ipsen to conduct this study; Jing He is a former employee of IQVIA, contracted by Ipsen to conduct this study; Jonathan Bouchard is an employee of Ipsen.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no competing interests.

 We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of, the manuscript entitled.
 E.A.T., D.B., Y.H., C.-Y.C., Z.O., E.E.M., M.I.Z. and H.R. are full-time employees and hold stock options at Biogen. The remaining authors declare no competing interests.
 The authors have declared that no competing interests exist.

 Competing interests: In the last 3 years, JC has received support from the Efficacy and Evaluation (EME) Programme, a Medical Research Council (MRC) and National Institute for Health Research (NIHR) partnership and the Health Technology Assessment (HTA) Programme (NIHR), the UK MS Society, the US National MS Society and the Rosetrees Trust. He is supported in part by the NIHR University College London Hospitals (UCLH) Biomedical Research Centre, London, UK. He has been a local principal investigator for a trial in MS funded by the Canadian MS society. A local principal investigator for commercial trials funded by: Actelion, Novartis and Roche; and has taken part in advisory boards/consultancy for Azadyne, Janssen, Merck, NervGen, Novartis and Roche.
 Declaration of Competing Interest CVV consults for Amylyx Pharmaceuticals and Bridge Bio. HF has no conflicts to declare.
 M.M. and C.B. are employed at Werfen, a company that sells autoimmune diagnostic tests. The rest of the authors declare no conflict of interest.
 There are no conflicts of interest.
 The authors declare that they have no competing interests.
 The authors declare no competing interests.
 The authors declare that this study was funded in its entirety by UCB Biopharma SRL. The funder had the following involvement in the study: all authors were employees of UCB at the time of execution of the study. The funder was involved in the funding of the study in its entirety, as well study design, collection, analysis, interpretation of data, the writing of this article, and the decision to submit it for publication.
 The authors declare that they have no competing interests and the research is not funded by any funding agency.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The following authors have no financial disclosures: S.H.A., A.A.A., K.A., and F.P.
 The authors report no competing interests.
 Declaration of competing interest The authors state that they are aware of no personal or financial conflicts that might have appeared to have an effect on the case reported.

 Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-22-1267/coif). The authors have no conflicts of interest to declare.


 Declaration of Competing Interest The authors declare no conflict of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: S.A.A. serves as a consultant for Teleflex, Inc. M.D.M. has no conflicts of interest for the data presented in this manuscript. She is a Clinical Trial Investigator with Mitsubishi-Tanabe, Boehringer-Ingelheim, EICOS, Corbus, Prometheus and Horizon. She is also a member and on the Scientific Advisory Board for Mitsubishi-Tanabe and Boehringer-Ingelheim. She is a Grant reviewer for the Young Investigator Program for Actelion Pharma and is a conference speaker on autoantibodies for Medtelligence. The other authors have no conflicts of interest to declare; there are no other commercial sources for the work reported on in the manuscript, or any other financial interests that any of the authors may have, which could create a potential conflict of interest or the appearance of a conflict of interest regarding the work.
 Competing interests: The author reports no conflicts of interest.

 The authors declare no conflict of interest.
 Declaration of Competing Interest No conflict of interest.




 Declaration of Competing Interest A Signori received consulting fees from Horizon, Chiesi and Sanofi-Genzyme outside of this work, F Bovis, I Schiavetti and M Ponzano have nothing to disclose. MS Freedman received research/educational grants from Sanof-Genzyme; received  honoraria/consultation fees from Alexion, Atara Biotherapeutics, Bayer Healthcare, Beigene, BMS (Celgene), EMD, Hofman La-Roche, Janssen (J&J), Merck Serono, Novartis, Quanterix, Sanof-Genzyme, and Teva Canada Innovation; served on advisory boards/boards of directors for Alexion, Atara Biotherapeutics, Bayer  Healthcare, Beigene, BMS (Celgene), Celestra, Hofman La-Roche, Janssen (J&J), McKesson, Merck Serono, Novartis, and Sanofi-Genzyme; and participated in speakers bureau for Sanof-Genzyme and EMD Serono.K Marhardt is an employee of Merck Gesellschaft mbH, Vienna, Austria, an affiliate of Merck KGaA; N Alexandri is an employee of Merck Healthcare KGaA, Darmstadt, Germany. MP Sormani has received consulting fees from Biogen, GeNeuro, MedDay, Merck, Novartis, Roche, Sanofi and Teva.
 Declaration of interests SR is a founder of Mestag, a scientific advisor for Rheos Medicines, serves on the advisory boards for Janssen and Pfizer, and is a consultant for Sanofi. The remaining authors have no declarations of interests.

 The authors declare the following competing financial interest(s): S.P.N., S.L. and O.T.P. own stocks in Aurlide Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflicts of interest and sources of funding: F.P. was supported by a Physician-Scientist Fellowship of the Medical Faculty of the University of Heidelberg. S.H. (SFB 1118), D.S. (SFB 1118), and M.B. (SFB 1158) were supported by the German Research Foundation. F.C. is an employee of Siemens Healthcare GmbH and was involved in the technical development of the TSE SMS sequence prototype. T.H. is supported in part by the Dietmar Hopp Foundation (project no. 1DH2011152). For the remaining authors, none were declared.

 Declaration of Competing Interest G. Gao is a cofounder of biopharmaceutical companies, Voyager Therapeutics & ASPA Therapeutics and holds equities in the companies. G. Gao is an inventor on patents with potential royalties licensed to Voyager, ASPA, and other biopharmaceutical companies. D.J. Gessler is a cofounder of ASPA Therapeutics and holds equity in the company. G. Gao and D.J. Gessler are inventors on a pending patent (PCT/US2016/058197) that is relevant to the content of this manuscript, which may result in potential royalties if granted and licensed.
 Declaration of competing interest The authors do not have any conflicts of interest related to this work.
 The authors declare that they have no affiliations with or involvement in any organization or entity with any financial interest in the subject matter or materials discussed in this manuscript.

 K.A. is the scientific founder, advisor and shareholder of Therini Bio, Inc. Her interests are managed by Gladstone Institutes according to its conflict of interest policy. The Krogan Laboratory has received research support from Vir Biotechnology, F. Hoffmann-La Roche and Rezo Therapeutics. N.J.K. has financially compensated consulting agreements with the Icahn School of Medicine at Mount Sinai, New York, Maze Therapeutics, Interline Therapeutics, Rezo Therapeutics, GEn1E Lifesciences, Inc. and Twist Bioscience Corp. He is on the Board of Directors of Rezo Therapeutics and is a shareholder in Tenaya Therapeutics, Maze Therapeutics, Rezo Therapeutics and Interline Therapeutics.
 Declaration of Competing Interest Marco A. Lana-Peixoto has received research support, teaching compensation and travel grants from Roche; and travel grants from Novartis and Biogen. Natalia C. Talim, Dagoberto Callegaro, Vanessa Daccath Marques, Vinicius A. Schoeps, and Marcus Vinicius M. Gonçalves declare no conflict of interest. Alfredo Damasceno has received advisory board compensation from Horizon, Janssen, and Alexion; and travel grants from Biogen, Serono and Roche. Jefferson Becker has received advisory board compensation from Horizon, teaching compensation and travel grants travel grants from Biogen, EMS, Janssen, Sanofi-Genzyme, Merck Serono, Novartis, Roche and Teva.
 Conflict of interest All authors declare that they have no competing interest with respect to the contents of this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 Declaration of Competing Interest Thomas W. Lategan, Tiffany N. Sprague, and Franck S. Rousseau are employees of Banner Life Sciences. Laurene Wang is a paid consultant to Banner Life Sciences. Regina Berkovich – served as a consultant for ANI, Alexion, BMS, Banner Life Sciences, Biogen, EMD Serono, Horizon, Mallinckrodt, Novartis, and Sanofi.


 Declaration of Competing Interest Nil.



 Conflict of interest: No potential conflict of interest relevant to this article was reported.
 Conflict of interest: None declared
 None declared.
 Declaration of interests ERV has received grant and research support to her institution from Boehringer Ingelheim, Forbius, Kadmon, and Horizon, and consulting and speaking fees from Boehringer Ingelheim (payments made to herself). KA has received grant and research support to his institution from Ulla och Roland Gustafssons Donationsfond and the Swedish Medical Society. VS has received grant and research support to her institution from the Research Foundation Flanders, Belgian Fund for Scientific Research in Rheumatic Diseases, Janssen-Cilag, and Boehringer Ingelheim, consulting fees from Boehringer Ingelheim (payments made to herself and her institution) and Janssen-Cilag (payments made to institution), speaker fees from UCB (payments made to her institution), Boehringer Ingelheim (payments made to self and her institution), and Janssen-Cilag (payments made to her institution), and support for attending meetings or travel expenses from Boehringer Ingelheim (payments made to her institution).
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 There are no conflicts of interest.
 The authors declare no conflict of interest.


 Disclosure: Edgar Zamora declares no relevant financial relationships with ineligible companies. Disclosure: Narothama Aeddula declares no relevant financial relationships with ineligible companies.


 Dr Jurriaan Peters is the site PI on the Marinus TrustTSC Trial, a phase III study of ganaxolone in refractory epilepsy in TSC. He is a speaker and consultant for Jazz Pharmaceuticals, SK Life Sciences, and Neurelis. The authors report no other conflicts of interest in this work.
 The authors declare no competing interests.
 The authors declare no competing financial interest.

 Declaration of Competing Interest The authors declare no conflict of interest.

 E.C., M.R., B.D., C.K., M.P.-G., M.D., R.L.McL., C.McH., S.A., and M.H. have no conflicts of interest to declare. N.P. serves as the associate editor of the International Journal of Neuroscience and has received speaker honoraria from Novartis. O.H. has received speaking honoraria from Janssen Cilag, Biogen Idec, Sanofi Aventis, Novartis and MerckSerono. She has been a member of advisory panels for Biogen Idec, Allergen, Ono Pharmaceuticals, Novartis, Cytokinetics and Sanofi Aventis. She serves as the editor-in-chief of the journal Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.
 The authors declare no conflict of interest.

 The authors declare no conflict of interest.
 Laynie Dratch receives consulting fees from Passage Bio and has received honoraria from the Muscular Dystrophy Association (MDA) and NSGC. Cynthia Clyburn has received honoraria from the MDA. Tanya Bardakjian is employed by Sarepta, a gene therapy company, and has financial relationships with Novartis, Invitae, Vigil Therapeutics, and Genome Medical. Murray Grossman participates in treatment trials sponsored by Passage Bio, Alector, and Prevail, and is a member of the Medical and Scientific Advisory Board of AFTD; he also receives funding from NIH and Department of Defense. Brianna Morgan receives funding support from the NIH and P.E.O. International. David J. Irwin is on the scientific advisory board of Denali Therapeutics. None of these sources of funding represent a conflict of interest. Katheryn A. Q. Cousins, Weiyi Mu, Elisabeth McCarty Wood, and Lauren Massimo declare no conflicts of interest.
 Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/disclosure-of-interest/ and declare: MS received honoraria/has been a consultant for AbbVie, Angelini, Lundbeck, Otsuka. DC has received grant monies for research from Eli Lilly, Janssen Cilag, Roche, Allergen, Bristol-Myers Squibb, Pfizer, Lundbeck, Astra Zeneca, Hospira; Travel Support and Honoraria for Talks and Consultancy from Eli Lilly, Bristol-Myers Squibb, Astra Zeneca, Lundbeck, Janssen Cilag, Pfizer, Organon, Sanofi-Aventis, Wyeth, Hospira, Servier, Seqirus; and is a current or past Advisory Board Member for Lu AA21004: Lundbeck; Varenicline: Pfizer; Asenapine: Lundbeck; Aripiprazole LAI: Lundbeck; Lisdexamfetamine: Shire; Lurasidone: Servier; Brexpiprazole: Lundbeck; Treatment Resistant Depression: LivaNova; Cariprazine: Seqirus. He is founder of the Optimal Health Program, currently operating as Optimal Health Australia; and is part owner of Clarity Healthcare. He is on the scientific advisory of The Mental Health Foundation of Australia. He does not knowingly have stocks or shares in any pharmaceutical company. EV has received grants and served as consultant, advisor or CME speaker for the following entities: AB-Biotics, AbbVie, Angelini, Biogen, Boehringer-Ingelheim, Celon Pharma, Dainippon Sumitomo Pharma, Ferrer, Gedeon Richter, GH Research, Glaxo-Smith Kline, Janssen, Lundbeck, Novartis, Orion Corporation, Organon, Otsuka, Sage, Sanofi-Aventis, Sunovion, Takeda, and Viatris, outside of the submitted work. CUC has been a consultant or advisor to or have received honoraria from: AbbVie, Acadia, Alkermes, Allergan, Angelini, Aristo, Boehringer-Ingelheim, Cardio Diagnostics, Cerevel, CNX Therapeutics, Compass Pathways, Darnitsa, Gedeon Richter, Hikma, Holmusk, IntraCellular Therapies, Janssen/Johnson & Johnson, Karuna, LB Pharma, Lundbeck, MedAvante-ProPhase, MedInCell, Merck, Mindpax, Mitsubishi Tanabe Pharma, Mylan, Neurocrine, Newron, Noven, Otsuka, Pharmabrain, PPD Biotech, Recordati, Relmada, Reviva, Rovi, Seqirus, SK Life Science, Sunovion, Sun Pharma, Supernus, Takeda, Teva, and Viatris. He provided expert testimony for Janssen and Otsuka. He served on a Data Safety Monitoring Board for Lundbeck, Relmada, Reviva, Rovi, Supernus, and Teva. He has received grant support from Janssen and Takeda. He received royalties from UpToDate and is also a stock option holder of Cardio Diagnostics, Mindpax, and LB Pharma.
 The authors have declared that no competing interests exist.
 The authors declare no conflict of interest.
 Conflict of Interest None declared.

 Declaration of Competing Interest The authors declare no competing financial interest.


 Three of the authors (J.-P.G., A.S.K., T.A.B.) have received speaker honoraria from Siemens Healthineers outside of the presented work within the last three years. One author (S.H.) is an employee of Fraunhofer MEVIS. The other authors of this manuscript declare no relationships with any companies, whose products or services may be related to the subject matter of this article.

 The authors report no competing interests.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare they have no conflicts of interest to disclose.


 AH is owner and director of Future Cognition LTD and H2 Cognitive Designs LTD, which support online studies and develop custom cognitive assessment software, respectively. PH is owner and director of H2 Cognitive Designs LTD and reports personal fees from H2 Cognitive Designs LTD outside the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest None.
 GMzH received compensation for serving on scientific advisory boards (LFB) and speaker honoraria (Alexion). HW is acting as a paid consultant for AbbVie, Actelion, Biogen, IGES, Johnson & Johnson, Novartis, Roche, Sanofi-Aventis, and the Swiss Multiple Sclerosis Society. CCG received speaker honoraria from the DIU Dresden and research funding from Biogen and Roche. The remaining authors declare no financial interests or conflicts of interest.
 Authors CO, TO, EK, KY, and NG are employed by the company ProteoBridge Corporation. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors report no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The not-for-profit research institute Brain Chemistry Labs has applied for a patent on the use of this biomarker.


 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that they have no competing interests.

 V. S. received compensation for consulting services and/or speaking activities from AveXis, Cytokinetics, Italfarmaco, Liquidweb S.r.l. and Novartis Pharma AG, receives or has received research support from the Italian Ministry of Health, AriSLA and E‐Rare Joint Transnational Call. He is on the Editorial Board of Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, European Neurology, American Journal of Neurodegenerative Diseases, Frontiers in Neurology. B.P. received compensation for consulting services and/or speaking activities from Liquidweb S.r.l. N. T. received compensation for consulting services from Amylyx Pharmaceuticals and Zambon Biotech SA. He is Associate Editor for Frontiers in Aging Neuroscience.
 Competing interests: The authors have stated explicitly that there are no conflicts of interest in connection with this article.



 Nik Krajnc: has participated in meetings sponsored by, received speaker honoraria or travel funding from BMS/Celgene, Janssen-Cilag, Merck, Novartis, Roche and Sanofi-Genzyme and held a grant for a Multiple Sclerosis Clinical Training Fellowship Programme from the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS). Bianca Itariu: declares no conflict of interest relevant to this study. Stefan Macher: declares no conflict of interest relevant to this study. Wolfgang Marik: declares no conflict of interest relevant to this study. Jürgen Harreiter: has participated in meetings sponsored by, received speaker/consultancy honoraria or travel funding from Novo Nordisk, Sanofi, Novartis, Eli Lilly, Boehringer-Ingelheim. He has received unrestricted research grants from Bayer and Astra Zeneca. Martin Michl: declares no conflict of interest relevant to this study. Klaus Novak: declares no conflict of interest relevant to this study. Christian Wöber: has received honoraria consultancy/speaking from Apomedica, Curelator, Eli Lilly, Grünenthal, Hermes, Lundbeck, Novartis, Pfizer, Ratiopharm/Teva, and Stada. Berthold Pemp: declares no conflict of interest relevant to this study. Gabriel Bsteh: has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Celgene/BMS, Lilly, Merck, Novartis, Roche, Sanofi-Genzyme and Teva, and received honoraria for consulting Biogen, Celgene/BMS, Novartis, Roche, Sanofi-Genzyme and Teva. He has received unrestricted research grants from Celgene/BMS and Novartis.


 T. Lee reports consultancy: BD Bard Consultant, Boston Scientific, Venostent, Xeltis and advisory or leadership role: Associate Editor, Kidney360. G.R. Cutter reports consultancy: AI thera, AMO, Astra-Zeneca, Avexis, BMS/Celgene, CSL Behring, DSMB ApplThera, Horizon, Immunic, Karunar, Kezar, Mapi, Merck, Mitsubishi Tanabe, Novartis, Opko Biologics, Prothena, Reata, Regeneron, Sanofi-Aventis, Teva, University of Texas Southwestern, University of Pennsylvania, Visioneering Technologies, Inc.; ownership interest: Pythagoras, Inc. a private consulting company; advisory or leadership role: JASN Statistical editor, Multiple Sclerosis Journal Editorial board, Multiple Sclerosis and Related Diseases Editorial Board, Neurology Clinical Practice Contributing Statistical Editor; and other interests or relationships: Consulting or Advisory Boards: Alexion, Antisense Therapeutics, Avotres, Biogen, Clene Nanomedicine, Clinical Trial Solutions LLC, Entelexo Biotherapeutics, Inc., Genentech, Genzyme, GW Pharmaceuticals, Hoya Corporation, Immunic, Immunosis Pty Ltd, Klein-Buendel Incorporated, Linical, Merck/Serono, Novartis, Perception Neurosciences, Protalix Biotherapeutics, Regeneron, Roche, SAB Biotherapeutics. M. Allon is Editor-in-Chief, Kidney360. All remaining authors have nothing to disclose.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Dr. Krishnaswamy is on the scientific advisory board of KovaDx and AI Therapeutics. Dr. Hafler receives research funding from Nayan Therapeutics and Hoffmann-La Roche Pharmaceutical. Dr. Hafler is on the scientific advisory board of Carmine Therapeutics. All other authors declare no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


 The authors declare no conflict of interest.

 AM and FK are employees of, and may hold stock in, Novartis. BME reports consulting activities with adidas AG, Siemens AG, SiemensHealthineers AG, WSAudiology GmbH outside of the study. He is a shareholder in Portabiles HealthCare Technologies GmbH. In addition, BME holds a patent related to gait assessment. LP and LC are co-founders and own shares of mHealth Technologies (https://mhealthtechnologies.it/). LS and CB are consultants of Philipps Healthcare, Bosch Healthcare, Eli Lilly, Gait-up. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Yue Wang reports no disclosures relevant to the manuscript. J. Liang was supported by grants from the Natural Science Foundation of Hubei Province (No. 2020CFB226). Y. Fang, D. Yao, L. Zhang, Y. Zhou, Yajuan Wang, L. Hu, and Z. Lu report no disclosures relevant to the manuscript. Yilong Wang was supported by grants from the National Natural Science Foundation of China (No. 81825007), the National Natural Science Foundation Beijing Outstanding Young Scientist Program (No. BJJWZYJH01201910025030), Youth Beijing Scholar Program (No.010), Beijing Talent Project-Class A: Innovation and Development (No. 2018A12), “National Ten-Thousand Talent Plan”-Leadership of Scientific and Technological Innovation; and National Key R&D Program of China (No. 2017YFC1307900, 2017YFC1307905). Z. Xiao was supported by grants from the National Natural Science Foundation of China (No. 81971055, 81471133, 82101292), the Interdisciplinary Innovative Talents Foundation from Renmin Hospital of Wuhan University (JCRCYG-2022-006) and Buchang Zhiyuan Public Welfare Projects for Heart and Brain Health (HIGHER2022094). Go to Neurology.org/N for full disclosures.





 The final author serves as a member of the Board of Directors for IDDSI, the International Dysphagia Diet Standardization Initiative. (IDDSI). IDDSI was not involved in the design, conduct or analysis of this study. The final author serves on the board of the Dysphagia Research Society. All other authors have no funding or financial relationships to disclose.

 ACal received research grant from Cytokinetics. ACh served on scientific advisory boards for Mitsubishi Tanabe, Roche, Biogen, Denali Pharma, AC Immune, Biogen, Lilly, and Cytokinetics. The sponsor organizations had no role in data collection and analysis and did not participate to writing and approving the manuscript. The information reported in the manuscript has never been reported elsewhere. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that they have no financial conflict of interest with regard to the content of this report.
 A.S. and M.C. declare the unconditioned research grant to the University of Genova from Laboratori Baldacci for laboratory investigations. E.G., S.S., E.H., G.P., C.P. and S.P. have no competing interests.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: GM served on advisory boards for Genentech-Roche, Novartis, Mercks, and Biologix, received speaker fees from Biologix, Mercks, and Novartis, and participated in educational activities for Neurology Live and John Hopkin's e-Litterature Review.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors report no relevant disclosures. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 The authors declare no conflict of interest.
 Conflict of Interest: The authors have no financial conflicts of interest.

 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Disclosure: Amal Chamli declares no relevant financial relationships with ineligible companies. Disclosure: Asmahane Souissi declares no relevant financial relationships with ineligible companies.
 Declaration of interest: The authors have no conflicts of interest to declare.
 The authors declare no competing interests.
 Disclosure: Sharmila Sarkar declares no relevant financial relationships with ineligible companies. Disclosure: Waqas Siddiqui declares no relevant financial relationships with ineligible companies.






 The authors declare that there is no conflict of interest

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.





 The authors declare no competing interests.



 Declaration of Competing Interest All authors declare no conflict of interest.

 Declaration of Competing Interest None.

 All authors declare no competing interests.

 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Disclosure: Angela Macri declares no relevant financial relationships with ineligible companies. Disclosure: Eddie Kwan declares no relevant financial relationships with ineligible companies. Disclosure: Laura Tanner declares no relevant financial relationships with ineligible companies.

 GWD is the inventor on multiple patents awarded and pending describing therapeutic use of mitofusin activators in neurodegenerative disease. He is the founder and a consultant for Mitochondria in Motion, Inc. and Mitochondria Emotion Inc., and may benefit financially if mitofusin activators are approved for human use.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-22-514/coif). The authors have no conflicts of interest to declare.
 The authors declare that there are no conflicts of interest present.
 Declarations of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors report no relevant disclosures. Go to Neurology.org/N for full disclosures.
 R.J.M. is cofounder of and holds shares in Keapstone Therapeutics, collaborates and receives funding from BenevolentAI, Quell Therapeutics, Sosei Heptares and MSD, is a consultant to Aclipse Therapeutics, has shares in Aclipse One Inc and is an inventor on patents related to M102. N.S. is an employee and shareholder of Aclipse Therapeutics. H.J.R. is the chairman of the Board of Aclipse Therapeutics. F.M. is an employee and shareholder of Merck and Co. P.J.S. is an advisory board member and consultant for Biogen, Aclipse Therapeutics, Quell Therapeutics, BenevolentAI, QurAlis, Astex, GeniUS and Eli Lilly and collaborates with and receives research funding from Quell Therapeutics, Aclipse Therapeutics, Pfizer and SwanBio. She is a cofounder of and holds shares in Keapstone Therapeutics and holds shares in Aclipse One Inc. She is an inventor on patents related to low-dose IL-2, SRSF1 and M102. Support for clinical trials participation in the last five years has been received from Biogen, Alexion, Orion Pharma, WAVE, the EU Horizon 2020 programme and UK NIHR.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Ichiro Nakashima reports personal fees from Alexion Pharma GK, Chugai, Biogen Japan, Mitsubishi Tanabe Pharma, and Novartis, and grants from LSI Medience, the Ministry of Education, Science and Technology of Japan, and the Ministry of Health, Labor and Welfare of Japan (MHLW). Jin Nakahara reports personal fees from AbbVie, Alexion Pharma GK, Asahi Kasei Medical, Biogen, Bristol Myers Squibb, Chugai, CSL Behring, Daiichi Sankyo, Eisai, Kyorin, Mitsubishi Tanabe Pharma, Novartis, Otsuka, Roche, Takeda, and Teijin Pharma; research scholarships from AbbVie, Boehringer Ingelheim, Chugai, Daiichi Sankyo, EA Pharma, Eisai, JB, Mitsubishi Tanabe Pharma, Otsuka, Shionogi, Sumitomo Pharma, Teijin Pharma, and Tsumura; and grants from the Ministry of Education, Science and Technology of Japan, the MHLW, and Biogen. Hiroaki Yokote reports personal fees from Biogen Japan, Mitsubishi Tanabe Pharma, Novartis, Chugai Pharma, and Alexion Pharma GK; and grants from the MHLW. Yasuhiro Manabe declared no potential conflicts of interest with respect to this work. Kazumi Okamura and Kou Hasegawa are employees of, and hold stock in, Alexion Pharma GK, AstraZeneca Rare Disease. Kazuo Fujihara has received personal fees and other support from AbbVie, Asahi Kasei Medical, Biogen, Chugai, Eisai, Merck Group, Mitsubishi Tanabe Pharma, Novartis, Ono, Roche, Sumitomo Dainippon, Takeda, Teijin Pharma, UCB, and Viela Bio (formerly MedImmune); and grants from the Ministry of Education, Science and Technology of Japan and the MHLW.
 Declaration of Competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflicts of Interest: The study is funded by the pharmaceutical company Vayamed. Vayamed GmbH is not involved in the planning, design, conduct, analysis, and publication of this investigator-initiated study and will not have special or privileged access to study data at any stage. The study is entirely conducted by an established public research department at Charité—Universitätsmedizin Berlin. Financial dependencies with the funder do not exist. MK has received speaker honoraria from the Federal Association of Pharmaceutical Cannabinoid Companies Demecan, EVER Pharma, Grunenthal, Hormosan, IUVO Therapeutics, Lilly, the Medical Service of the Health Insurance Funds, Novartis, Stadapharm, Teva, and Tilray. He has received consultancy fees from Almirall. He has received expert opinion fees from several local and social courts. He is member of the ad hoc commission cannabis in medicine of the German Pain Society and the Science Network Cannabinoids in Medicine (Wissenschaftsnetzwerk Cannabinoide in der Medizin). CSK has received consultancy and speaker fees from Pedanios GmbH and Deutsches Institut für Medizinalcannabis more than 3 years ago. He is part of the Science Network Cannabinoids in Medicine (Wissenschaftsnetzwerk Cannabinoide in der Medizin). No further conflicts of interest related to this manuscript were declared.
 Competing interests: BD: partly employed by the ARTIS national safety monitoring system (AbbVie, AstraZeneca, BMS, Eli Lilly, Galapagos, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi and UCB). TIK: has received congress participation support from Biogen and advisory board fee for Novartis. KH: clinical assessor at the Swedish Product Agency. SAP: grants and support for attending meeting from Boehringer Ingelheim. HR: consultant and lecture fees for AbbVie, Pfizer, UCB and Viatris. BG: consultant and lecturer fee for Novartis and Nordic Pharma. LD: grant from BMS outside the present work; support for attending meetings from Galderma, AbbVie, Eli Lilly and Janssen. JA: grants from AbbVie, AstraZeneca, BMS, Eli Lilly, Galapagos, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi and UCB; AbbVie, AstraZeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi and UCB have entered into agreements with Karolinska Institutet with JA as the principal investigator, mainly in the context of safety monitoring of biologics via the ARTIS national safety monitoring system.
 The authors declare no competing interests.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest Disclosures: Dr Köhler-Forsberg reported personal fees from WCG Clinical and Lundbeck Pharma A/S outside the submitted work. Dr Gamradt reported personal fees from Abcam for giving a webinar presentation outside the submitted work. Dr Chae reported receiving research funding from the Deutsche Forschungsgemeinschaft outside the submitted work. Prof Correll reported receiving personal fees from AbbVie Inc outside the submitted work and consulting, advising, or receiving honoraria from Acadia Pharmaceuticals, Alkermes PLC, Allergan PLC, Angelini Pharma, Aristo Pharma GmbH, Biogen Inc, Boehringer Ingelheim, Cardio Diagnostics, Cerevel Therapeutics, LLC, CNX Therapeutics Ltd, COMPASS Pathways PLC, Darnitsa, Denovo, Gedeon Richter PLC, Hikma Pharmaceuticals PLC, Holmusk, Intra-Cellular Therapies, Janssen/Johnson & Johnson, Karuna Therapeutics, LB Pharmaceuticals, Lundbeck, MedAvante-ProPhase Inc, Medincell, Merck & Co, MindPax, Mitsubishi Tanabe Pharma Corporation, Mylan NV, Neurocrine Biosciences, Inc, Neurelis Inc, Newron Pharmaceuticals SpA, Noven, Novo Nordisk A/S, Otsuka Pharmaceutical Co, Ltd, Pharmabrain GmbH, PPD Biotech, Recordati, Relmada Therapeutics, Inc, Reviva Labs, Laboratorios Farmaceuticos ROVI, Seqirus Limited, SK Life Science Inc, Sunovion Pharmaceutical Inc, Sun Pharmaceutical Industries Ltd, Supernus Pharmaceuticals, Takeda Pharmaceuticals International, Teva Pharmaceutical Industries Ltd, and Viatris Inc; providing expert testimony for Janssen Pharmaceuticals and Otsuka Pharmaceutical Co, Ltd; serving on a data safety monitoring board for COMPASS Pathways PCL, Denovo, Lundbeck, Relmada Therapeutics, Inc, Reviva Labs, Laboratorios Farmaceuticos ROVI, Sage Therapeutics, Supernus Pharmaceuticals, and Teva Pharmaceutical Industries Ltd; receiving grant support from Janssen Pharmaceuticals and Takeda Pharmaceuticals International; receiving royalties from UpToDate; and holding a stock option in Cardio Diagnostics, MindPax, LB Pharmaceuticals, and The Quantic Group. Prof Gold reported receiving personal fees from Hexal AG and Streamed Up and grants from the National Multiple Sclerosis Society, Deutsche Forschungsgemeinschaft DFG, Bundesministerium für Gesundheit, Bundesministerium für Bildung und Forschung, and the European Commission outside the submitted work. Dr Otte reported receiving personal fees from Fortbildungskolleg, Janssen Pharmaceuticals, Lundbeck, Neuraxpharm, PeakProfiling GmbH, and LIMES Klinikgruppe and grants from the German Research Foundation, German Federal Ministry of Education and Research, European Union, and Berlin Institute of Health outside the submitted work. No other disclosures were reported.
 CJW is a member of the independent data monitoring committee for a trial of masitinib in ALS, for which his institution receives funding from AB Science. The other authors declare that they have no competing interests.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest None.

 In accordance with Taylor & Francis policy, authors have the following disclosures: D.C. is an independent consultant and a contract consultant with Janssen Scientific Affairs, LLC, and has been diagnosed with multiple sclerosis; B.D., G.G., A.P., S.Z., and L.S., are employees of Janssen Scientific Affairs, LLC. W.P. is an employee of CorEvitas, LLC, which derives its profits from interactions with pharmaceutical sponsors.
 I have read the journal’s policy and the authors of this manuscript have the following competing interests: CGWK is a shareholder in Queen Square Analytics Ltd.
 Declaration of Competing Interest J.S, SY.X, DC.T, YY.D, XL.X, S.L, GM.C, FD.S, ZZ.Z, XH.Z and Y.L declared there is no conflict of interest. D.C. is a consultant for Biogen and Hoffmann-La Roche. In the last three years he has received research funding from Hoffmann-La Roche, the International Progressive MS Alliance, the MS Society, and the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research center, and a speaker's honorarium from Novartis. He co-supervises a clinical fellowship at the National Hospital for Neurology and Neurosurgery, London, which is supported by Merck. F.B acts as a consultant for Bayer-Schering, Biogen-Idec, GeNeuro, Ixico, Merck-Serono, Novartis and Roche. He has received grants, or grants are pending, from the Amyloid Imaging to Prevent Alzheimer's Disease (AMYPAD) initiative, the Biomedical Research center at University College London Hospitals, the Dutch MS Society, ECTRIMS–MAGNIMS, EU-H2020, the Dutch Research Council (NWO), the UK MS Society, and the National Institute for Health Research, University College London. He has received payments for the development of educational presentations from Ixico and his institution from Biogen-Idec and Merck. He is on the editorial board of Radiology, Neuroradiology, Multiple Sclerosis Journal and Neurology.
 The authors declare no conflict of interest.
 G.S. Perez reports no disclosures relevant to the manuscript; L. Singer reports no disclosures relevant to the manuscript; T. Cao reports no disclosures relevant to the manuscript; P. Jamshidi reports no disclosures relevant to the manuscript; K. Dixit reports no disclosures relevant to the manuscript; M. Kontzialis reports no disclosures relevant to the manuscript; R. Castellani reports no disclosures relevant to the manuscript; P. Pytel reports no disclosures relevant to the manuscript; N. Anadani reports no disclosures relevant to the manuscript; C. Bevan has participated in an ad board for Genentech; E. Grebenciucova reports no disclosures relevant to the manuscript; R. Balabanov received honoraria from Biogen, Sanofi, Alexion, and Teva Pharmaceutical and research support from the National Multiple Sclerosis Society, National Institute of Health, Nextcure, and Biogen; B. Cohen reports no disclosures relevant to the manuscript. E. Graham received consulting and advisory board fees from Novartis, Atara Biotherapeutics, Tavistock Life Sciences, Horizon Therapeutics, Roche Genentech. She receives research support from F. Hoffman-La Roche Ltd. She received compensation for question writing from ACP MKSAP. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 There are no conflicts of interest.
 Declaration of Competing Interest The authors declare that there are no relevant financial or non-financial competing interests to report.
 Declaration of interests RM reports personal fees from Eli Lilly, Lunbeck, and Bromatech for participation on advisory boards and for speaker activities. MAR received consulting fees from Biogen, Bristol-Myers Squibb, Eli Lilly, Janssen, and Roche; speaker honoraria from AstraZeneca, Biogen, Bristol-Myers Squibb, Bromatech, Celgene, Genzyme, Horizon Therapeutics Italy, Merck-Serono, Novartis, Roche, Sanofi, and Teva Pharmaceuticals; and research support from the Multiple Sclerosis Society of Canada, the Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla. PJG reports grants and personal fees from Eli Lilly; a grant from Celgene; personal fees from Aeon Biopharma, Allergan/AbbVie, Biohaven Pharmaceuticals, CoolTech, Dr Reddys, Epalex, Impel Neuropharma, Lundbeck, Novartis, Praxis, Sanofi, Satsuma, and Teva Pharmaceuticals; personal fees for advice through Gerson Lehrman Group, Guidepoint, SAI Med Partners, and Vector Metric; fees for educational materials from CME Outfitters, Omnia Education, and WebMD; publishing royalties or fees from Massachusetts Medical Society, Oxford University Press, UptoDate, and Wolters Kluwer; payment for medicolegal advice in headache; and a patent on magnetic stimulation for headache (number WO2016090333 A1) assigned to eNeura without fee. MF reports compensation for consulting services from Alexion, Almirall, Biogen, Merck, Novartis, Roche, and Sanofi; speaking activities from Bayer, Biogen, Celgene, Chiesi Italia, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and Teva; participation in advisory boards for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, and Takeda; scientific direction of educational events for Biogen, Merck, Roche, Celgene, Bristol-Myers Squibb, Eli Lilly, Novartis, and Sanofi-Genzyme; and research support from Biogen Idec, Merck-Serono, Novartis, Roche, Italian Ministry of Health, and Fondazione Italiana Sclerosi Multipla.

 H.O. is a founding scientist and scientific advisor of SanBio Co. Ltd., and K Pharma Inc. T. Kondo, I.E., H.T., Y.N. and T. Komiya are employed by Ono Pharmaceutical Co., Ltd. H.O. received research funding from Ono Pharmaceutical Co., Ltd. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. The other authors indicate no potential conflict of interest.
 G.W.D. is an inventor on multiple patents owned by Washington University and other entities that cover the use of small molecule mitofusin activators to treat neurodegenerative diseases. G.W.D. is the founder of Mitochondria in Motion, Inc., a Saint Louis based biotech R&D company that aims to enhance mitochondrial trafficking and fitness in neurodegenerative diseases. The other authors declare no competing interests. Studies with MiM111 and CPR1 were performed under terms of an MTA between Mitochondria in Motion, Inc. and Washington University in St. Louis.
 The authors declare no conflict of interest.

 LP is the head of PNI Europe and teaches about this research line. The remaining authors are also part of the PNI Europe team. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.




 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 The authors declare no conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no competing interests.
 Conflict of InterestNo potential conflict of interest was reported by the author(s).


 Dr. Polimanti is paid for his editorial work on the journal Complex Psychiatry and received a research grant from Alkermes. The other authors reported no biomedical financial interests or potential conflicts of interest.

 Declaration of Interests: J.A.S.: Scientific Advisory Board/Consultant: AVID radiopharmaceuticals (subsidiary of Lilly), Alnylam Pharmaceuticals, Apellis Pharmaceuticals, Takeda Pharmaceuticals, National Hockey League. No other authors have conflicts to disclose.
 There is no conflict of interest to declare.

 Declaration of interests J.K.I. and S.-T.A. are co-founders of AcuraStem, Inc. S.-T.A., W.-H.C., S.M., and S.H. are employees of AcuraStem, Inc. J.K.I. is a co-founder of Modulo Bio, serves on the scientific advisory boards of AcuraStem, Spinogenix, Synapticure, and Vesalius Therapeutics, and is employed at BioMarin Pharmaceutical. B.V.Z. is a co-founder of ZZ Biotech and chairman of its scientific advisory board. J.A.P. is a co-founder of Modelis. F.-B.G. receives research funding from Stealth BioTherapeutics.
 All the authors declare no conflicts of interest.

 The authors report no competing interests.
 The authors declare that they have no competing interests.
 C.M.B. reports Shire (grant recipient, Scientific Advisory Board member); Lundbeckfonden (grant recipient); Pearson (author, royalty recipient); Equip Health Inc. (Clinical Advisory Board). The remaining authors declare no competing interests.
 Author VN-C has served as a speaker, consultant, and/or instructor for: AbbVie, Eli Lilly and Company, Galapagos, Janssen, Moonlake, Novartis, Pfizer, and UCB Pharma; and has received grant and/or research support from AbbVie and Novartis. Author LP has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Almirall, Amgen, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Janssen, LEO Pharma, Lilly, Novartis, Pfizer, Sandoz, Sanofi, and UCB. Author SV has received speaker’s honoraria and participated in projects sponsored by Bayer, Janssen, LEO Pharma, Lilly, Novartis, Pfizer, Roche, Sanofi and UCB. Author JR has received consultancy and/or speaker’s honoraria from Abbvie, UCB, Janssen, Novartis, Pfizer, Amgen and Lilly and/or participated in clinical trials and/or research projects sponsored by Pfizer, Novartis and Janssen. Author ML-V has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Almirall, Amgen, Boehringer Ingelheim, Celgene, Janssen, Kyowa Kirian, LEO Pharma, Lilly, Novartis, and UCB. Author CF-C has received consultancy and/or speaker’s honoraria and participated in clinical trials and/or research projects sponsored by AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, the Spanish Society of Rheumatology and UCB. Author RA has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Almirall, Amgen, Galápagos, Gebro, Janssen, Lilly, MSD, Nordimet, Novartis, Pfizer and UCB. Author JP has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by Janssen, Novartis, Pfizer, MSD, Lilly, Amgen, BMS, AbbVie, and UCB. Author EG-A has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, MSD, Roche, Amgen, Janssen, Lilly, Novartis, Pfizer and UCB. Author PZ has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Celgene, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer and UCB. Author BJ has received consultancy fees from Amgen, UCB and Janssen; has received speaker’s honoraria from Lilly, Abbvie and Janssen; has participated in clinical trials and/or research projects sponsored by Janssen, Lilly, Bristol Myers Squibb, Abbvie; has received support for attending congress from Novartis, Pfizer, UCB. Author JG has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by Novartis, UCB, Pfizer, BMS, MSD, AbbVie, Lilly, Janssen, AstraZeneca and Galápagos. Author XJ has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Lilly, MSD, Nordic Pharma, Novartis, Pfizer and UCB. Author RB has received grants/research supports from Abbvie, MSD, and Roche, and had consultation fees/participation in company-sponsored speaker´s bureau from Abbvie, Pfizer, Roche, Bristol-Myers, Lilly, Janssen, and MSD. Author SA has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Almirall, Janssen, LEO Pharma, Lilly, Novartis and UCB. Author JS has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, UCB, Novartis, Amgen, Pfizer and Janssen-Cilag. Author RQ has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by Novartis, Janssen, UCB, Pfizer, Amgen, MSD, Eli-Lilly and AbbVie. Author JC has received consultancy and/or speaker’s honoraria from and/or participated in clinical trials and/or research projects sponsored by AbbVie, Almirall, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Fresenius, Janssen, Lilly, Novartis, Pfizer, Sandoz and UCB.


 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 Declaration of Competing Interest Vincent COTTIN has no conflict of interest to disclose in relation with the content of the manuscript. Elodie BLANCHARD has no conflict of interest to disclose in relation with the content of the manuscript. Mallorie KERJOUAN declares research fees paid by Pfizer and Novartis to her institution. Romain LAZOR has no conflict of interest to disclose in relation with the content of the manuscript. Martine REYNAUD-GAUBERT has no conflict of interest to disclose in relation with the content of the manuscript. Romain LAZOR has no conflict of interest to disclose in relation with the content of the manuscript. Camille TAILLE declares consulting fees paid to her by Novartis. Yurdagül UZUNHAN has no conflict of interest to disclose in relation with the content of the manuscript. Lidwine WEMEAU has no conflict of interest to disclose in relation with the content of the manuscript. Claire ANDREJAK has no conflict of interest to disclose in relation with the content of the manuscript. Dany BAUD has no conflict of interest to disclose in relation with the content of the manuscript. Philippe BONNIAUD has no conflict of interest to disclose in relation with the content of the manuscript. Pierre-Yves BRILLET has no conflict of interest to disclose in relation with the content of the manuscript. Alain CALENDER has no conflict of interest to disclose in relation with the content of the manuscript. Lara CHALABREYSSE has no conflict of interest to disclose in relation with the content of the manuscript. Isabelle COURT-FORTUNE has no conflict of interest to disclose in relation with the content of the manuscript. Nicolas DESBAILLETS has no conflict of interest to disclose in relation with the content of the manuscript. Gilbert FERRETTI has no conflict of interest to disclose in relation with the content of the manuscript. Anne GUILLEMOT has no conflict of interest to disclose in relation with the content of the manuscript. Laurane HARDELIN has no conflict of interest to disclose in relation with the content of the manuscript. Marianne KAMBOUCHNER has no conflict of interest to disclose in relation with the content of the manuscript. Violette LECLERC (deceased). Mathieu LEDERLIN has no conflict of interest to disclose in relation with the content of the manuscript. Marie-Claire MALINGE has no conflict of interest to disclose in relation with the content of the manuscript. Alain MANCEL has no conflict of interest to disclose in relation with the content of the manuscript. Sylvain MARCHAND-ADAM declares consulting fees paid by Novartis. Jean-Michel MAURY has no conflict of interest to disclose in relation with the content of the manuscript. Jean-Marc NACCACHE has no conflict of interest to disclose in relation with the content of the manuscript. Mouhamad NASSER has no conflict of interest to disclose in relation with the content of the manuscript. Hilario NUNES has no conflict of interest to disclose in relation with the content of the manuscript. Gaële PAGNOUX has no conflict of interest to disclose in relation with the content of the manuscript. Grégoire PRÉVOT has no conflict of interest to disclose in relation with the content of the manuscript. Christine ROUSSET-JABLONSKI has no conflict of interest to disclose in relation with the content of the manuscript. Olivier ROUVIERE has no conflict of interest to disclose in relation with the content of the manuscript. Salim SI-MOHAMED has no conflict of interest to disclose in relation with the content of the manuscript. Renaud TOURAINE has no conflict of interest to disclose in relation with the content of the manuscript. Julie TRACLET has no conflict of interest to disclose in relation with the content of the manuscript. Ségolène TURQUIER has no conflict of interest to disclose in relation with the content of the manuscript. Stéphane VAGNARELLI has no conflict of interest to disclose in relation with the content of the manuscript. Kaïs AHMAD has no conflict of interest to disclose in relation with the content of the manuscript.
 Declaration of Competing Interest Sinem Nihal Esatoglu has received honorariums for presentations from UCB Pharma, Roche, Pfizer, and Merck Sharp Dohme. Gulen Hatemi has received grant/research support from Celgene and has served as a speaker for AbbVie, Celgene, Novartis, and UCB Pharma. Emire Seyahi has received honorariums for presentations from Novartis, Pfizer, and AbbVie. No other disclosures were reported.
 J-YN, SC, TL, YS, and KK are employees of CORESTEMCHEMON Inc. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Declaration of Competing Interest The authors declare that they have no competing interests.
 Declaration of Competing Interest T.A., T.S. and T.Z. are coinventors on a patent application, publication number WO2020/234473 entitled “ANTI-TDP-43 BINDING MOLECULES AND USES THEREOF.” T.A., T.S., E.C., A.E., L.M. M.A., R.M., R.O., K.P., M.C., C.D., A.B.S., V.E., O.A., A.P. and M.K are employees of AC Immune and entitled to options and/or shares. A.B., J.S. A.E., and T.Z. were employees of AC Immune at the time of this study. M.N., V.L. and S.P. received research funding from AC Immune. The other authors declare no competing interests.
 Declaration of interests NC is funded by a personal fellowship from the Research Foundation Flanders (grant number 12ZU922N) and declares royalties from Oxford University Innovation. SM is funded by a Wellcome Trust Career Development Award (223024/Z/21/Z) and is supported by the NIHR Imperial Biomedical Research Centre. IBM declares honoraria from AbbVie; grant support paid to his university from AstraZeneca and Eli Lilly; participation on data safety monitoring boards or advisory boards of AstraZeneca, Bristol Myers Squibb, Eli Lilly, Novartis, Janssen, GlaxoSmithKline, AbbVie, Cabaletta, Compugen, Causeway, Gilead, Moonlake, Reflexion, UCB, and XinThera; patents from Novartis; leadership roles with Evelo, Versus Arthritis, and Greater Glasgow and Clyde Health Board; and stock or stock options with Evelo, Compugen, and Cabaletta. JJVM has received funding to his institution from Amgen and Cytokinetics for his participation in the Steering Committee for the ATOMIC-HF, COSMIC-HF, and GALACTIC-HF trials and meetings and other activities related to these trials; has received payments through Glasgow University from work on clinical trials, consulting, and other activities from Alnylam, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cardurion, Dal-Cor, GlaxoSmithKline, Ionis, KBP Biosciences, Novartis, Pfizer, and Theracos; and has received personal lecture fees from the Corpus, Abbott, Hikma, Sun Pharmaceuticals, Medscape/Heart.Org, Radcliffe Cardiology, Alkem Metabolics, Eris Lifesciences, Lupin, ProAdWise Communications, Servier Director, and Global Clinical Trial Partners. NS declares consulting fees or speaker honoraria, or both, from Abbott Laboratories, Afimmune, Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Hanmi Pharmaceuticals, Janssen, Merck Sharp & Dohme, Novartis, Novo Nordisk, Pfizer, Roche Diagnostics, and Sanofi; and grant support paid to his university from AstraZeneca, Boehringer Ingelheim, Novartis, and Roche Diagnostics. KK is supported by the National Institute for Health Research (NIHR) Applied Research Collaboration East Midlands and the NIHR Leicester Biomedical Research Centre. KK has also acted as a consultant, speaker, or received grants for investigator-initiated studies for AstraZeneca, Abbott, Amgen, Napp, Bayer, Novartis, Novo Nordisk, Sanofi-Aventis, Lilly, Merck Sharp & Dohme, Boehringer Ingelheim, Oramed Pharmaceuticals, and Applied Therapeutics. PNT declares personal consulting fees from Immunovant and leadership roles in the Society for Endocrinology and British Thyroid Association. All other authors declare no competing interests. The views expressed are those of the authors and not necessarily those of the funder.


 The authors have declared that no competing interests exist.
 Declaration of interests The authors declare no competing interests.

 D.M., D.C., C.R., L.C., and J.B. are full-time employees of F. Hoffmann-La Roche. D.M. was employed by F. Hoffmann-La Roche when the study was completed and the manuscript submitted. D.M. moved to Biogen while the manuscript was under review.


 Competing interests: CM has received conference travel support and/or speaker fees from Merck, Novartis and Biogen. He has received research support from the National Health and Medical Research Council, Multiple Sclerosis Research Australia, The University of Melbourne, The Royal Melbourne Hospital Neuroscience Foundation, and Dementia Australia. MN: I have received honoraria and consultancy fees from Abcuro, Sanofi-Genyzme, Roche, Biogen and CSL-BehringTomas Kalincik has served on scientific advisory boards for Roche, Sanofi-Genzyme, Novartis, Merck and Biogen, steering committee for Brain Atrophy Initiative by Sanofi-Genzyme, received conference travel support and/or speaker honoraria from WebMD Global, Novartis, Biogen, Sanofi-Genzyme, Teva, BioCSL and Merck and received research support from Biogen. Other authors have no conflicts of interest to report.




 The authors have declared that no competing interests exist.
 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

 The authors declare no competing financial interests.
 All authors declare no competing financial interest.


 Declaration of interests J.K.I. and S.A. are co-founders of AcuraStem, Inc. S.A., W.-H.C., S.M., and S.H. are employees of AcuraStem, Inc. J.K.I. is a co-founder of Modulo Bio, serves on the scientific advisory boards of AcuraStem, Spinogenix, Synapticure, and Vesalius Therapeutics, and is employed by BioMarin Pharmaceutical. H.G. is a co-founder of Exai Bio and Vevo Therapeutics and serves on the scientific advisory boards of Exai Bio and Verge Genomics. J.K.I. and G.R.L. are inventors on a patent application (PCT/US2021/014541) that has been filed related to this work.

 The authors declare no conflicts of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors have declared that no competing interests exist.
 On behalf of all authors, the corresponding author states that there is no conflict of interest.
 MOVR Data used in this article were captured by MDA’s MOVR Data Hub. As such, principal investigators who contributed to MOVR and/or participated in the design and implementation of MOVR did not provide any work to analyze or write this report. The authors have no conflict of interest to report.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 The authors declare no competing interests.
 Megan T. Lynch, Margaret A. Taub, Jose Farfel, Jingyun Yang, Peter Abadir, Philip L DeJager, Francine Grodstein, David A. Bennett, and Rasika Mathias declare that they have no conflict of interest.


 XL received research grants from the Research Fund Secretariat of the Food and Health Bureau (HMRF, HKSAR), Research Grants Council Early Career Scheme (RGC/ECS, HKSAR), Research Grants Council Research Impact Fund (RGC/RIF, HKSAR), Janssen and Pfizer; internal funding from the 10.13039/501100003803University of Hong Kong; consultancy fee from Merck Sharp & Dohme and Pfizer, unrelated to this work. SCWC has received traveling support from Novartis and GSK. EYFW has received research grants from the Food and Health Bureau of the Government of the Hong Kong SAR, 10.13039/501100001809National Natural Science Foundation of China, and the Hong Kong Research Grants Council, outside the submitted work. CSLC has received grants from the Food and Health Bureau of the Hong Kong Government, Hong Kong Research Grant Council, Hong Kong Innovation and Technology Commission, Pfizer, IQVIA, and Amgen; personal fees from Primevigilance Ltd.; outside the submitted work. FTTL has been supported by the RGC Postdoctoral Fellowship under the Hong Kong Research Grants Council and has received research grants from Food and Health Bureau of the Government of the Hong Kong SAR, outside the submitted work. CKHW reports receipt of research funding from the EuroQoL Group Research Foundation, the Hong Kong Research Grants Council, the Hong Kong Health and Medical Research Fund, AstraZeneca, and Boehringer Ingelheim; all of which are outside this work. EWC reports grants from the 10.13039/501100005407Food and Health Bureau (Hong Kong), the Research Grants Council (RGC, Hong Kong), 10.13039/501100001809National Natural Science Fund of China, Bayer, AstraZeneca, Novartis, RGA Reinsurance Company, Pfizer, Narcotics Division of the Security Bureau of HKSAR; Consulting fee from Pfizer, Novartis, and AstraZeneca; honorarium from Hospital Authority (Hong Kong), Pfizer, Novartis, and AstraZeneca, outside the submitted work. WKL received speaker fees from Ferring, Janssen, Takeda and Daiichi Sankyo. He has also participated on the Data Safety Advisory Board of AstraZeneca and Pfizer. All outside the submitted work. CSL reports payment of speaker fees from AbbVie, AstraZeneca, GSK, Janssen, Pfizer and Roche. He has also participated on the AstraZeneca Data Safety Advisory Board. All outside the submitted work. ICKW receives research funding outside the submitted work from Amgen, Bristol Myers Squibb, Pfizer, Janssen, Bayer, GSK, Novartis, Takeda, the Hong Kong Research Grants Council, the Health Bureau of the Government of the Hong Kong Special Administrative Region, National Institute for Health Research in England, 10.13039/501100000780European Commission, and the 10.13039/501100000925National Health and Medical Research Council in Australia; has received consultancy fee from the World Health Organization and IQVIA, and is a non-executive director of Jacobson Medical in Hong Kong. All other authors report no conflicts of interest.
 A. Mueller and F. Kluge are employees of, and may hold stock in, Novartis. B. Eskofier reports consulting activities with adidas AG, Siemens AG, Siemens Healthineers AG, WSAudiology GmbH outside of the study. He is a shareholder in Portabiles HealthCare Technologies GmbH. In addition, Dr. Eskofier holds a patent related to gait assessment. H. Sillén is an employee of, and may hold stock in, AstraZeneca. M. Froelich is an employee of Grunenthal. L. Palmerini and L. Chiari are co-founders and own shares of mHealth Technologies (https://mhealthtechnologies.it/). L. Schwickert and C. Becker are consultants of Philipps Healthcare, Bosch Healthcare, Eli Lilly, Gait-up. M. Niessen is an employee of McRoberts. Jeff Hausdorff reports having submitted a patent for assessment of mobility using wearable sensors in 400 PD.

 The authors declare no competing interests.

 The authors declare that there are no conflicts of interest present.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflict of Interest None declared.
 Declaration of competing interest None.


 The authors declare no competing interests.

 Declaration of Competing Interest A. Stein: Reported that he is a speaker and consultant with Abbvie, and a speaker for Pfizer and Takeda, but has no conflicts related to this manuscript M Helmick: Reported no conflicts of interest S. Jia: Reported research grants from the University of Michigan, The Cystic Fibrosis Foundation, INSMED, and honoraria from UpToDate J. Fulton: Reported no conflicts of interest E. Reid: Reported honoraria from the Cystic Fibrosis Foundation A. Bruce: Reported research support from the NIH, National Multiple Sclerosis Society and CF Foundation. M. Litvin: Reported no conflicts of interest J. Bailey: Reported no conflicts of interest S. Sankararaman: Reported no conflicts of interest E. Dimango: Reported serving as an investigator for Vertex A. Leonard: Reported no conflicts of interest C. Clemm: Reported employment by the Cystic Fibrosis Foundation K Reno: Reported employment by the Cystic Fibrosis Foundation S. Hempstead: Reported employment by the Cystic Fibrosis Foundation
 AC declares Ad-Board participation fee from Biogen, Sanofi, Merck and speaking honoraria from Sanofi, Merck, Biogen, Allmiral, Novartis, and Bristol-Myers Squibb. CG declares speaker honoraria and travel expenses for attending meetings from Bayer Schering Pharma, Sanofi-Aventis, Merck, Biogen, Novartis, and Almirall. VAS provides intellectual and scientific advice for Novartis, Roche, Biogen, Lupin, PTC, Santhera and receives honoraria to participate in Ad-Boards. OC, MM, MAB, GB declare no conflict of interest.

 Ki Hoon Kim reports no financial disclosures. Jae-Won Hyun has received grants from the National Cancer Center and National Research Foundation of Korea. Su-Hyun Kim has lectured, consulted, and received honoraria from Bayer Schering Pharma, Biogen, Genzyme, Merck Serono, and UCB, and received a grant from the National Research Foundation of Korea. Ho Jin Kim has received a grant from the National Research Foundation of Korea, research support from Aprilbio and Eisai, consultancy/speaker fees from Alexion, Aprilbio, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, MDimune, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok, UCB, and Viela Bio, and is a co-editor for the Multiple Sclerosis Journal and an associated editor for the Journal of Clinical Neurology.
 The authors declare no conflict of interest.


 Declaration of interests T.L.S.-J. is on the Scientific Advisory Board of Cognition Therapeutics and Scottish Brain Sciences and receives collaborative grant funding from two industry partners. None of these had any influence over the current paper.
 Conflict of interest CO reports honoraria for lectures and/or scientific advice from Ferring, Janssen, Lundbeck, SAGE Therapeutics, Fortbildungskolleg, Limes Klinikgruppe, and Medical Tribune. SMG reports honoraria from Celgene and Hexal and research funding from Biogen. All other authors declare no potential conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 BH received funding from Regeneron Pharmaceuticals for genetic research in Multiple Sclerosis. The other authors declare that they have no conflict of interest.
 The authors declare no competing interest.

 The authors declare no competing interests.
 J.M. reports receiving advisory board fees from Biogen, Amylix and Italfarmaco, grant support from Roche, and grant support from Pfizer (active study drug for this study by grant number Wi211892 to J.M.). ACh received consulting fees from Biogen, Cytokinetics, Amylyx. ACa reports receiving advisory board fees from Biogen and Amylix, and grant support from Cytokinetics. GL reports scientific advisory for CSL Behring, Biogen Inc, Vertex Pharmaceuticals Incorporated, Chromocell Corporation, Janssen Pharmaceuticals, Inc, Lilly, and the Bracco Group. C.L. has served as a scientific consultant for Mitsubishi Tanabe Pharma Europe, Cytokinetics, Neuraltus, and Italfarmaco. R.D.A., E.Z., S.D.B., F.B., I.M., C.S., D.L.T., R.V., N.F., G.G., M.P., F.G., C.T., L.M., F.D.M., A.S., G.S., A.F., E.D.B., C.C., G.M., A.Co. declare no competing interests. Disclosure forms provided by the authors are available with the full text of this article.
 Declaration of competing interest JY: Student Award from the Faculty of Medicine, McGill University; FM: Postdoctoral Fellowship from the Fonds de recherche du Quebec – Santé; AD: Unrestricted research grant from the Canadian Institutes for Health Research; EO: none; AL: research support Fondation de l’IUCPQ, Fonds de recherche en apnée du sommeil (Alphonse l’Espérance), Reseau de recherche en santé respiratoire du Quebec, consulting fee from Institut national de l'excellence en santé et en services sociaux du Québec and Jazz Pharmaceuticals; TG: none; JK: research support from CIHR, Fonds de recherche du Quebec – Santé, Multiple Sclerosis Society of Canada, Signifier Medical, consulting fees from Powell-Mansfield Inc and Esai Inc, DSMB for Bresotec Inc; MK: Research support including equipment from CIHR, Weston Brain Foundation, Fisher Paykel, Philips, Vitalaire, The Chest Foundation, Adviory Board for Biron Soins du sommeil; Honorarium for a lecture for eMedEvents; Advisory Pannel for Jazz Pharmaceuticals.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.
 I have no conflicts of interest to disclose.
 Disclosure Dr. A.A. Zagouras has no relationships to disclose. Dr. W.H.W. Tang is partially supported by grants from the National Institutes of Health (R01HL126827, R01HL146754), and has served as a consultant for Sequana Medical A.G., Owkin Inc, Relypsa Inc, preCARDIA Inc, Cardiol Therapeutics Inc, Genomics plc, and has received honorarium from Springer Nature for authorship/editorship and American Board of Internal Medicine for exam writing committee participation–all unrelated to the subject and contents of this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Conflict of interest: None declared
 Arichena R Manmatharayan, MBBS, MD: No disclosure. Michael Kogan, MD, PhD: No disclosure Caio Matias, MD, PhD: No disclosure India Shelley, BA: No disclosure Amar Chinni, BA: No disclosure Kichang Kang, BA: No disclosure Kiran Talekar, MD: No disclosure Scott Faro, MD: No disclosure Feroze B. Mohamed, Ph. D: No disclosure Ashwini Sharan, MD: No disclosure Chengyuan Wu, MD, MSBmE: No disclosure Mahdi Alizadeh, PhD: No disclosure.
 The authors declare no conflict of interest.
 Henry Wong, Dmitry Nedosekin, and Sophia Ly have no conflicts of interest to declare.

 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.
 The authors declare no competing interests.

 The authors declare that they have no competing interests in this work.
 Conflicts of Interest The authors declare that they have no competing financial interests.



 Antonio Canosa serves on the Editorial Board of Biomedicines and serves as Guest Editor for the Special Issues &lsquo;Recent Advances in Amyotrophic Lateral Sclerosis Genetics and Pathophysiology&rsquo; and &lsquo;Recent Advances in Amyotrophic Lateral Sclerosis Genetics and Pathophysiology 2.0&prime; of Biomedicines. Andrea Calvo received a research grant from Cytokinetics. Adriano Chi&ograve; serves on scientific advisory boards for Mitsubishi Tanabe, Roche, Biogen, Cytokinetics, Denali, and AveXis, and received a research grant from Italfarmaco. Jessica Mandrioli received research support from Pfizer. The other authors have no conflict of interest relevant for the manuscript.
 Dr. Dorsey has received honoraria for speaking at American Academy of Neurology, American Neurological Association, Excellus BlueCross BlueShield, International Parkinson’s and Movement Disorders Society, National Multiple Sclerosis Society, Northwestern University, Physicians Education Resource, LLC, PRIME Education, LLC, Stanford University, Texas Neurological Society, and Weill Cornell; received compensation for consulting services from Abbott, Abbvie, Acadia, Acorda, Bial-Biotech Investments, Inc., Biogen, Boehringer Ingelheim, California Pacific Medical Center, Caraway Therapeutics, Curasen Therapeutics, Denali Therapeutics, Eli Lilly, Genentech/Roche, Grand Rounds, Huntington Study Group, Informa Pharma Consulting, Karger Publications, LifeSciences Consultants, MCM Education, Mediflix, Medopad, MedRhythms, Merck, Michael J. Fox Foundation, NACCME, Neurocrine, NeuroDerm, NIH, Novartis, Origent Data Sciences, Otsuka, Physician’s Education Resource, Praxis, PRIME Education, Roach, Brown, McCarthy & Gruber, Sanofi, Seminal Healthcare, Spark, Springer Healthcare, Sunovion Pharma, Theravance, Voyager and WebMD; research support from Biogen, Biosensics, Burroughs Wellcome Fund, CuraSen, Greater Rochester Health Foundation, Huntington Study Group, Michael J. Fox Foundation, National Institutes of Health, Patient-Centered Outcomes Research Institute, Pfizer, PhotoPharmics, Safra Foundation, and Wave Life Sciences; editorial services for Karger Publications; stock in Included Health, stock in Mediflix and ownership interests in SemCap. Dr. Schneider has received compensation for consulting services from Escape Bio and Parkinson’s Foundation; research support from Acadia Pharmaceuticals, Biohaven Pharmaceuticals, the Michael J. Fox Foundation for Parkinson’s Research, National Institutes of Health, Parkinson Study Group, and CHDI Foundation. Dr. Kieburtz has research support from NIH (NINDS, NCATS) and the Michael J Fox Foundation. He is paid to serve on DSMBs of studies for Janssen, Lilly, and Roche/Genentech. He receives payments from Hoover Brown LLC and Clintrex Research Corp, and has equity interests in both. He also has equity interests in Biohaven, Inhibikase, Modality.AI and Safe Therapeutics LLC. Dr. Tanner has received has received grant support from the NIH, the Michael J Fox Foundation, the Department of Defense, the Parkinson Foundation, the Marcus Program in Precision Medicine, Gateway LLC, Roche-Genentech, Biogen, Bioelectron Technology Corporation; personal compensation as a consultant/scientific advisory board /data & safety monitoring board member for CNS Ratings, Cadent, Adamas, Biogen, Neurocrine, Kyowa Kirin, Jazz/Cavion, Lundbeck and the Australian Parkinson’s Mission. Dr. De Miranda is funded by the National Institutes for Environmental Health Sciences (R00ES029986). Dr. Goldman has received research support from the Michael J. Fox Foundation, the National Institutes of Health, the Agency for Toxic Substances and Disease Registry (ATSDR), the Health Resources and Services Administration (HRSA), the US Department of Defense, and the Veterans Health Administration. Prof. Bloem currently serves as co-Editor in Chief for the Journal of Parkinson’s Disease but was not involved in any way in the peer review process of this editorial. He serves on the editorial board of Practical Neurology and Digital Biomarkers, has received honoraria from serving on the scientific advisory board for Abbvie, Biogen and UCB, has received fees for speaking at conferences from AbbVie, Zambon, Roche, GE Healthcare and Bial, and has received research support from the Netherlands Organization for Scientific Research, the Michael J Fox Foundation, UCB, Not Impossible, the Hersenstichting Nederland, the Parkinson’s Foundation, Verily Life Sciences, Horizon 2020 and the Parkinson Vereniging (all paid to the institute).

 Competing interests: None declared.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 Conflict of Interest Disclosures: Dr Magyari reported receiving grants and personal fees from Biogen, Roche, Novartis, Merck, and Sanofi and nonfinancial support from Merck (funding of conference participation) outside the submitted work. No other disclosures were reported.

 The authors declare that there are no conflicts of interest related to this study. RBP: reports grants from Roche and Merck and speaker honoraria from Novartis, outside the submitted work; JAP: nothing to disclose; SLAP: reports grants, preceptorships and research support from Genzyme, Roche, Novartis, Merck-Serono, and Biogen, outside the submitted work; CMR: reports speaker honoraria from Roche and the Brazilian Committee for Treatment and Research of Multiple Sclerosis, outside the submitted work; DC: reports grants, preceptorships, and research support from Genzyme, Roche, Novartis, Merck-Serono, Teva and Biogen, outside the submitted work; DKS: reports grants from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) – Brazil (425331/2016–4), grants from Fundação e Amparo à Pesquisa do Estado do Rio Grande do Sul (FAPERGS) – Brazil, grants and personal fees from TEVA and Merck, personal fees from Biogen, Roche, and Viela Bio, outside the submitted work.


 The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
 CONFLICT OF INTEREST The authors declare that Drs. Naba, Varga and Teves receive research support unrelated to this work from Boehringer-Ingelheim.
 Conflict of interest The authors have no conflict of interest to declare.





 Declaration of competing interest The authors declare no competing interests.
 The authors declare no conflict of interest.

 The authors declare no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 The authors declare no conflict of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare no conflict of interest.


 The authors declare no competing interests.


 The authors declare no conflict of interest. NT has received funding from Deakin University for an Executive Dean’s Post-Doctoral Fellowship. MB is supported by a NHMRC Senior Principal Research Fellowship (1156072). DRS is a current investigator with the NHMRC Medical Research Future Fund (APP1200214). MML is supported by a Deakin University Scholarship and has received research funding support from Be Fit Foods. LE is CIA and is partially supported by a NHMRC Boosting Dementia Project Grant (APP1171174). NV has not COI to declare for this work. WM is currently funded by an NHMRC Investigator Grant (#2008971) and a Multiple Sclerosis Research Australia early-career fellowship. WM has previously received funding from the Cancer Council Queensland and university grants/fellowships from La Trobe University, Deakin University, University of Queensland, and Bond University. WM has received industry funding and/or has attended events funded by Cobram Estate Pty. Ltd. and Bega Dairy and Drinks Pty Ltd. WM has received travel funding from the Nutrition Society of Australia. WM has received consultancy funding from Nutrition Research Australia and ParachuteBH. WM has received speakers honoraria from The Cancer Council Queensland and the Princess Alexandra Research Foundation. SAS is supported by a Mentored Research Training Grant (MRTG) from the Foundation for Anesthesia Education and Research (FAER).


 C.V.‐S., Y.G., E.S., M.M., K.N.K., P.M.E., V.R., J.‐M.T., A.B., C.F.L., report no conflicts of interest. J.J.C. has served as a consultant for Roche and UCB, which have upcoming treatment trials in MOGAD. S.L.‐C. and A.K. have served on an advisory board for Genentech/Roche, which has an upcoming treatment trial in MOGAD. D.D. has consulted for UCB, which has an upcoming treatment trial in MOGAD. S.J.P. reports grants, personal fees, and nonfinancial support from Roche/Genentech, and personal fees for consulting services from UCB, which have upcoming treatment trials in MOGAD. E.P.F. has participated in advisory boards for Roche and UCB who have upcoming treatment trials in MOGAD. E.P.F. has received funding from the NIH (R01NS113828). Mayo Clinic Laboratories offer commercial testing for MOG‐IgG, but none of the authors receive financial compensation for this.




 Competing interests: MB reports grants from the National Institutes of Health (R01-NS105479) and the Muscular Dystrophy Association; as well as consulting fees from Alector, Annexon, Biogen, Denali, Novartis, Orphazyme, Sanofi and UniQure. The University of Miami has licensed intellectual property to Biogen to support design of the ATLAS study. SAG reports grants from National Institutes of Health, Centers for Disease Control and Prevention (CDC/ATSDR), and the ALS Association, as well as consulting fees from Structure Films. He is listed as inventor on patent held by University of Michigan for the treatment of ALS and reports the participation on a Data Safety Monitoring Board or Advisory Board for Watermark. KAS reports consulting fees from the ALS Association. ELF reports grants from the National Institutes of Health, Centers for Disease Control and Prevention (CDC/ATSDR), the Novo Nordisk Foundation, and the Juvenile Diabetes Research Foundation. She is named as inventor on a patent held by University of Michigan titled 'Methods For Treating Amyotrophic Lateral Sclerosis' for treating ALS using JAK/STAT inhibitors and reports multiple positions on Data Safety Monitoring Boards, Advisory Boards or or other boards, as well as multiple editorial positions. MW reports grants from the National Institutes of Health and the Centers for Disease Control and Prevention, as well as consulting fees from the Spaulding Rehabilitation. He additionally reports membership on a Data Safety Monitoring Board or Advisory Board for Biogen, a leadership role for the International Society for Environmental Epidemiology, and an editorial position with Springer. ET reports a position in the Pa Rare Disease Task Force. KDD reports the support of the preparation of this manuscript from the ALS Association and the ASTDR’s National ALS Registry. NMT reports the support of the preparation of this manuscript from the ALS Association and the ASTDR’s National ALS Registry. AA-C reports consultancies or advisory boards for Amylyx, Apellis, Biogen, Brainstorm, Cytokinetics, GenieUs, GSK, Lilly, Mitsubishi Tanabe Pharma, Novartis, OrionPharma, Quralis and Wave Pharmaceuticals.
 AA received 2 research grants from UCSF Weill Institute for Neurosciences and from The German Multiple Sclerosis Society, all unrelated to the work presented in this paper. JK received 4 speaker fees, research support, travel support and/or served on advisory boards of the Swiss 5 MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, 6 Progressive MS Alliance, Bayer, Biogen, Celgene, Merck, Novartis, Roche and Sanofi, all unrelated to the work presented in this paper. KB has served as a 13 consultant, at advisory boards, or at data monitoring committees for Abcam, Axon, Biogen, 14 JOMDD/Shimadzu. Julius Clinical, Lilly, MagQu, Novartis, Roche Diagnostics, and Siemens 15 Healthineers, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), 16 which is a part of the GU Ventures Incubator Program, all unrelated to the work presented in this paper. SS reports personal fees as speaker or advisor from Abbott, Allergan-Abbvie, AstraZeneca, Eli Lilly, Lundbeck, Novartis, NovoNordisk, Pfizer, Teva; 3 research grants from Allergan, Novartis, Uriach, all unrelated to the work presented in this paper. She is President elect of the European Stroke Organisation, second vice president of the European Headache Federation and a member of the Women Initiative for Stroke in Europe. HT reports 8 lectures and travel from Alexion, Bayer, Biogen, Celgene/Bristol-Myers-Squibb, 9 GlaxoSmithKline, Janssen, Genzyme, Merck Serono, Novartis, Roche, Sanofi/Genzyme, 10 Siemens and Teva, and received research support from Chemische Fabrik Karl Bucher 11 GmbH, German Multiple Sclerosis Society (DMSG) and the German Ministry for Education 12 and Research (BMBF), all unrelated to the work presented in this paper. AHA received 2 research grants from Medtronic and Boehringer Ingelheim, honoraria for advice or lecturing from Bayer, BMS, Pfizer, MSD, Boehringer Ingelheim, Abbvie, Teva, Novartis, Roche, Lundbeck and participated on a data safety monitoring for Lundbeck, all unrelated to the work presented in this paper. MO gave scientific advice to Axon, Biogen Idec, Fujirebio and Roche, all unrelated to the work presented in this paper. AMD-R received 3 grants from Norvegian Research Council, EU Horizon 2020, Hesle Sør-øst and participated on a data safety monitoring from EU Horizon 2020, all unrelated to the work presented in this paper. HZ served at scientific advisory boards and/or as a consultant for Abbvie, Acumen, Alector, Alzinova, ALZPath, Annexon, Apellis, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, Nervgen, Novo Nordisk, Optoceutics, Passage Bio, Pinteon Therapeutics, Prothena, Red Abbey Labs, reMYND, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics, and Wave, has given lectures in symposia sponsored by Cellectricon, Fujirebio, Alzecure, Biogen, and Roche, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program, all unrelated to the work presented in this paper. DM received support for attending meetings and/or travel from Novartis, Biogen, Sanofi and Merck, participated on a scientific advisory board for Merck, consulting fees and payment for presentations from Roche and Novartis, all unrelated to the work presented in this paper. MF received support for attending meetings and/or travel from Biogen, Roche, Novartis, Merck and Sanofi, all unrelated to the work presented in this paper. SAR received support from the Medical Faculty of Martin-Luther-University Halle-Wittenberg (Clinician Scientist-Programm No. CS22/06), unrelated to the work presented in this paper. Other authors report no competing interests.

 S.W.S. serves on the Scientific Advisory Council of the Lewy Body Dementia Association and the Multiple System Atrophy Coalition. S.W.S. receives research support from Cerevel Therapeutics. S.W.S. is an editorial board member of the Journal of Parkinson’s Disease and JAMA Neurology. The views expressed in this article are those of the authors and do not necessarily reflect the views or policies of the Uniformed Services University, the United States Department of Defense, the United States government, or the Henry M. Jackson Foundation for the Advancement of Military Medicine.
 Competing interests: Jonathan Zipursky has received payments from private law firms for medicolegal opinions on the safety and effectiveness of analgesics, including opioids. Dr. Zipursky is supported by the University of Toronto Department of Medicine Clinician Scientist Training Program and a Canadian Institutes of Health Research (CIHR) Banting and Best Doctoral Award. David Juurlink reports receiving payment for expert testimony from multiple law firms related to analgesics, including opioids; an honorarium for a lecture on pain management from Texas Tech University Health Sciences Center; and reimbursement for travel costs for presentations and scientific meetings from CIHR, Stanford University and Texas Tech University Health Sciences Center. Dr. Juurlink is an unpaid member of Physicians for Responsible Opioid Prescribing (PROP), a nongovernmental organization with the goal of promoting opioid stewardship. Tara Gomes reports receiving grant and contract funding from the Ontario Ministry of Health, the Public Health Agency of Canada, the Ontario College of Pharmacists and the Government of Canada (paid to institution in support of Dr. Gomes’ research program). A Tier 2 Canada Research Chair supports Dr. Gomes’ salary. Dr. Gomes has also received payment for travel and a stipend for participating in the Drugs and Therapeutics Advisory Committee from Indigenous Services Canada. Muhammad Mamdani reports receiving grant funding from Roche, examining drug use for multiple sclerosis. Dr. Mamdani has also received honoraria as a member of the scientific advisory board of SaNotize. No other competing interests were declared.

 Conflicts of Interest and Source of Funding: The authors have disclosed that they have no significant relationships with, or financial interest in, any commercial companies pertaining to this article.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor JW declared a shared parent affiliation with the author BY at the time of review.
 Competing Interests The authors declare that they have no competing interests.


 No competing financial interests exist.
 Conflict of Interest Statement The authors report no competing interests related to this paper.

 Over the past 36 months, Dr Sills has received consultancy and/or speaker fees for projects and presentations related to the experimental and clinical pharmacology of antiseizure drugs from Angelini Pharma, Arvelle Therapeutics GmbH, Bial Pharma UK Ltd, Desitin Pharma Ltd, Eisai Ltd, UCB Pharma Ltd and Zogenix International Ltd.
 Declaration of Interests CXA, DV, KL, HLL, FF, and MAN declare that they are consultants employed by Data Tecnica International, whose participation in this is part of a consulting agreement between the US National Institutes of Health and said company. MAN also an advisor to Neuron23 Inc and Character Biosciences.
 CONFLICT OF INTERESTS T.R.P. is the founder of BIOIO, a St. Louis-based biotech company specializing in drug target identification. BIOIO-1001 and related compounds are BIOIO assets. Conflicts of interest for T.M.M. are Ionis, licensing agreement; Consulting for Ionis, Biogen, Cytokinetics, Disarm Therapeutics, BIOIO; UCB, advisory board; Honorarium for Regeneron and Denali.

 Conflict of Interest: The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.


 Declaration of Competing Interest Winfried Stöcker is head and Bianca Teegen full-time employee of a diagnostic reference laboratory, integrated into patient care, collaborating with the company Euroimmun, nowadays PerkinElmer. All other authors declare no subject-related conflict of interest.
 Ms. Yang reports no disclosures. Dr. Roberts reports no disclosures. Dr. Winton‐Brown reports no disclosures. Dr. Lloyd reports no disclosures. Prof. Velakoulis reports no disclosures. Prof. Terence O′Brien's institution has received grant funding from the National Health and Medical Research Council (NHMRC) (Investigator Grant APP1176426), Medical Research Future Fund (MRFF), National Institutes of Health (NIH), and US Department of Defense (DOD). His institution has also received research and/or consulting fees from Industry, including Eisai, UCB, Biogen, Supernus, Praxis Pharmaceuticals, ES Therapeutics, and Epidarex. Prof. Kwan is supported by a Practitioner Fellowship (MRF1136427) from the MRFF. Dr Rayner is supported in part by the Australian Epilepsy Research Fund and has received funding from the NHMRC (Investigator grant APP2008737). This funding is unrelated to this study. Associate Professor Charles Malpas has received conference travel support and/or speaker Merck and has received research support from the NHMRC, Multiple Sclerosis Research Australia, The University of Melbourne, The Royal Melbourne Hospital Neuroscience Foundation, and Dementia Australia.

 The authors declare no competing interests.
 Dr. Rao, Dr. Alberts, and Mr. Schindler have coauthored IP around the C3B software, for which they have received royalties from the Cleveland Clinic. Dr. Rao and Dr. Alberts are stockholders and scientific officers of Qr8 Health. Dr. Rao is an Editorial Board Member of this journal but was not involved in the peer-review process nor had access to any information regarding its peer-review. Dr. Posk is a paid consultant of Qr8 Health and may be granted stock options. Mr. Schindler and Mr. Blum are Qr8 Health employees. Dr. Galioto, Ms. Sokolowski, Ms. Pierce, Ms. Penn, Ms. Sturtevant, Dr. Skugor, Dr. Anstead, and Dr. Leverenz report no conflicts of interest. Dr. Rao, Dr. Alberts, and Mr. Schindler have coauthored IP around the C3B software, for which they have received royalties from the Cleveland Clinic.

 Emmanuel Biver has received fees from Nestlé for advisory boards outside the submitted work. Daniel Aeberli has received funds from Alfred und Anneliese Sutter‐Stöttner Stiftung, 6302 Zug Switzerland. Satchidananda Panda is the author of the books “The Circadian Code” and “The Circadian Diabetes Code.” Tinh‐Hai Collet's research is supported by grants from the Leenaards Foundation, the Vontobel Foundation, the SwissLife Jubiläumsstiftung Foundation, the Medical Board of the Geneva University Hospitals (HUG), the Nutrition 2000plus Foundation, and the Swiss Multiple Sclerosis Society. The other authors declared no conflict of interest.

 Declaration of competing interest Prof Helmut Butzkueven's institution receives funding from Biogen, Roche, Merck and Novartis for speaker engagements, study steering and advisory committee service. He is on the editorial board of Multiple Sclerosis and Related Disorders and the Steering committee of the Brain Health Initiative (Oxford Health Policy Forum). Prof Terence J. O'Brien receives research funding from Biogen, UCB Pharma, Eisai Pharma, Anavex Pharmaceuticals, Zynerba Pharmaceuticals, and serves on the scientific advisory boards for UCB Pharma, Eisai Pharmaceuticals, Zynerba Pharmaceuticals, ESTherapeutics, Seqirus Pharmaceuticals. Dr Mastura Monif's has served on advisory board for Merck and has received speaker honoraria from Merck and Biogen. Her institution receives funding from Merck, Australian.National Health Medical Research Council, Brain Foundation, Charles and Sylvia.Viertel Foundation, and MS Research Australia. The remaining authors report no conflicts of interest.
 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


 Saoirse Elizabeth O’Sullivan is a paid consultant to Vectura Fertin Pharma, Switzerland, and a paid employee of Artelo Biosceince, USA. Sanne Skov Jensen(,) Gitte Nykjær Nikolajsen and Heidi Ziegler Bruun are paid employees of Fertin Pharma, Denmark. Rhenu Bhuller and Julia Hoeng are paid employees of Vectura Fertin Pharma, Switzerland.
 The authors declare no competing interests.
 L.R.P. is a consultant to Eyenovia, Twenty Twenty and Skye Bioscience. S.M., J.E.C. and A.W.H. are co-founders of and hold stock in Seonix Pty Ltd. Z.L.F. and X.W. are employed by and hold stock or stock options in 23andMe, Inc. A.P.K. has acted as a paid consultant or lecturer to Abbvie, Aerie, Allergan, Google Health, Heidelberg Engineering, Novartis, Reichert, Santen and Thea. The other authors declare no competing interests.

 Disclosures of conflicts of interest: J.S.N.T. Consultant for Annalise.ai. J.K.C.L. No relevant relationships. J.B. No relevant relationships. W.W. No relevant relationships. P.S. No relevant relationships. D.G. No relevant relationships. J.C. No relevant relationships. D.M.P. No relevant relationships. S.B.H. No relevant relationships. F.G. Investigator-initiated research grant for CAD software in multiple sclerosis; director, founder, and CEO of Radiopaedia Australia and Radiopaedia Events. E.L. Advisory committee member of the Royal Australian and New Zealand College of Radiologists Artificial Intelligence Advisory Committee.
 The authors declare no conflict of interest.

 The authors declare that they have no competing interests
 E. Orozco and C. Valencia-Sanchez report no disclosures relevant to the manuscript; J.W. Britton has consulted for UCB pharmaceuticals; D. Dubey has research support from the Department of Defence (CA210208), Centers of Multiple Sclerosis and Autoimmune Neurology and Clinical and Translational Science, Mayo Clinic, and Grifols pharmaceuticals, has consulted for UCB, Immunovant, Argenx, and Astellas pharmaceuticals (compensation for consulting activities paid directly to Mayo Clinic), and has patents pending for KLHL11-IgG, LUZP4-IgG, and cavin-4-IgG as markers of neurologic autoimmunity; E.P. Flanagan has funding from NIH (R01NS113828), has served on advisory boards for Alexion, Genentech, Horizon Therapeutics, and UCB, has received honoraria from Pharmacy Times and UpToDate, and has a patent pending for DACH1-IgG as a biomarker of paraneoplastic autoimmunity; A.S. Lopez-Chiriboga has consulted for Horizon Therapeutics and Genentech; N. Zalewski reports no disclosures relevant to the manuscript. A. Zekeridou has patent applications pending on PDE10A-IgG and DACH1-IgG as biomarkers of paraneoplastic neurologic autoimmunity and has received research funding from Genentech; S.J. Pittock is a named inventor on filed patents that relate to functional AQP4/NMO-IgG assays and NMO-IgG as a cancer marker, has patents pending for KLHL11-IgG and Septin-5-IgG and issued for MAP1B-IgG as markers of neurologic autoimmunity and paraneoplastic disorders, has consulted for Alexion and Medimmune, and has received research support from Genentech, Grifols, Medimmune, and Alexion; A. McKeon reports research funding from the NIH (NIH: RO1NS126227, U01NS120901), patents issued for GFAP and MAP1B-IgGs and patents pending for PDE10A, Septins-5 and Septins-7, and KLCHL11-IgGs, and has consulted for Janssen and Roche pharmaceuticals, without personal compensation. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.


 CB owns shares in NowRx Inc. JG has received unrelated clinical trial support through UCSF from Roche/Genentech and Vigil Neurosciences, personal fees for consulting from Biogen, and personal fees for medical-legal consulting. FC has received personal fees for medical-legal consulting. SS has received personal compensation for serving on medical advisory boards for Alexion Pharmaceuticals, and Horizon Therapeutics. DD has patents pending for KLHL11-IgG, LUZP4-IgG, and cavin-4-IgG as markers of neurological autoimmunity. DD has also received funding from the US Department of Defense (DOD) (CA210208). DD has consulted for UCB, Immunovant, Argenx, and Astellas. All compensation for consulting activities is paid directly to Mayo Clinic. SeP has received personal compensation for serving as a consultant for Genentech, Sage Therapeutics, and Astellas. He's received personal compensation for serving on scientific advisory boards or data safety monitoring boards for F. Hoffman-LaRoche AG, Genentech, and UCB. His institution has received compensation for serving as a consultant for Astellas, Alexion, and Viela Bio/MedImmune. All compensation is paid to Mayo Clinic. He has received research support from Alexion, Viela Bio/MedImmune, Roche/Genentech. He has a patent, Patent# 8,889,102 (Application#12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia)—issued; a patent, Patent# 9,891,219B2 (Application#12-573942, Methods for Treating Neuromyelitis Optica (NMO) by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)-IgG Autoantibody positive)—issued. JD has received grants from the Chan Zuckerberg Biohub, personal fees from the Public Health Company and from Allen & Company. MW has received unrelated grants from Roche/Genentech and Novartis as well as speaking honoraria from Novartis, Takeda, WebMD and Genentech. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
 NGM received travel grants from Eisai Pharma and Angelini Pharma. Lecture fees were given by Jazz Pharma and Angelini Pharma. Research support was granted by Jazz Pharma, Angelini Pharma, Eisai Pharma, UCB Pharma, LivaNova and Desitin Pharma. He also receives funding from the Ministry of Health (Schleswig–Holstein) and the German Research Council (DFG). Non-financial interests: none. JD has no relevant financial or non-financial interests to disclose. ET has no relevant financial or non-financial interests to disclose. FL reports having received speaker’s honoraria from Grifols, Biogen, Novartis, Roche, Alexion, serving on advisory boards for Roche and Biogen and receiving research funding from the German Ministry of Education and Research, the German Society for Laboratory Medicine (DGKL) and the German Research Council (DFG). He works for an academic institution offering commercial autoantibody testing. Non-financial interests: none. WL has no relevant financial or non-financial interests to disclose. AF has no relevant financial or non-financial interests to disclose. KB receives for the MEMO Study funding by the German Research Society (Deutsche Forschungsgemeinschaft DFG, grant: BE1996/1-1). The measurement of NfL was done through funds from the Institute of Epidemiology and Social Medicine, University of Muenster. The BiDirect Study is supported by grants of the German Ministry of Research and Education (BMBF) to the University of Muenster (01ER0816 and 01ER1506). Non-financial interests: none. JK received speaker fees, research support, travel support, and/or served on advisory boards by Swiss MS Society, Swiss National Research Foundation (320030_189140/1), University of Basel, Progressive MS Alliance, Bayer, Biogen, Bristol Myers Squibb, Celgene, Merck, Novartis, Octave Bioscience, Roche, Sanofi. Non-financial interests: none. GK receives non-project-related financial support from the BMBF project CONNECT-GENERATE: Genetics of autoimmune encephalitis. Non-financial interests: none. The authors declare that they have no conflict of interest concerning this work.


 G.T. is an editorial board member of NRP. M.F. receives financial support from the External Research Program, Medtronic GmbH, unrelated to this work. C.G. reports personal fees from Amgen, personal fees from Boehringer Ingelheim, personal fees from Daiichi Sankyo, personal fees from Abbott, personal fees from Prediction Biosciences, personal fees from Novartis, and personal fees from Bayer outside the submitted work.


 Declaration of Competing Interest The author declares no competing interests.
 Potential Conflicts of Interest Nothing to report.



 None.

 None of the authors report any conflicts of interest.

 DJW received funding from the Stroke Foundation/British Heart Foundation. RS, FP and BK received funding from UCLH/UCL BRC. The remaining authors declare no financial or other conflicts of interest.
 The authors declare no competing interests.

 R. Brett McQueen, Nicholas D. Mendola, and Kavita V. Nair received funding for this work through the PhRMA Foundation Center of Excellence Grant—Center for Pharmaceutical Value (pValue), paid for by the University of Colorado. R. Brett McQueen received a grant paid to the University of Colorado by Eli Lilly and consulting fees from the Monument Analytics and Institute for Clinical and Economic Review. Kavita V. Nair received grants through the University of Colorado by Genentech, Biogen, Novartis, Gilead Sciences, Bristol Meyers Squibb, and Rocky Mountain MS Center, received consulting fees from Biogen, Novartis, and Celgene, honoraria from Sanofi, and support for attending meetings from the American Academy of Neurology and Consortium of Multiple Sclerosis Centers. Kavita V. Nair reports a leadership role as the Vice Chair at Payment, Policy and Coding Subcommittee, American Academy of Neurology. Ivett Jakab, Bertalan Németh, András Inotai, and Zoltán Kaló are employed by Syreon Research Institute. Syreon Research Institute received funding from the University of Colorado for this work. Ivett Jakab reports leadership positions as a member of the Board of Trustees, European Patients’ Academy on Therapeutic Innovation Foundation, and the President of European Patients’ Forum Youth Group. Jeffrey Bennett received institutional grants or contracts from Novartis, Mallinckrodt, Alexion, and the National Institutes of Health. Jeffrey Bennett reports both institutional and personal royalties or licenses and a patent of Aquaporumab, and consulting fees from MedImmune/Viela Bio/Horizon Therapeutics, Alexion, Chugai, Genentech, Genzyme, Mitsubishi-Tanabe, Reistone Biopharma, Roche, Beigene, and Abbvie. Jeffrey Bennett reports participation on a data safety monitoring board/advisory board of Roche/Genentech and Clene Nanomedicine.
 All authors have seen and approved the manuscript. The work was performed at the McGill University Health Centre. The study was funded by the Research Institute of the McGill University Health Centre (MUHC), the Department of Medicine of the MUHC and the American Thoracic Society Foundation, with support from the Canadian Sleep and Circadian Network. Andrea Benedetti reports research grants from the Canadian Institutes of Health Research and salary support from Fonds de Recherche du Québec–Santé chercheur boursier, served on Advisory Boards (Abbvie, Sunovion, and Paladin). Richard John Kimoff reports research grants from the Canadian Institutes of Health Research, The Multiple Sclerosis Society of Canada, Fonds de Recherche du Quebec–Santé, Philips-Respironics Inc., ResMed Inc., and VitalAire Inc. Marta Kaminska reports research grants and in-kind support from Philips, VitalAire Inc., the American Thoracic Society Foundation, Canadian Institutes for Health Research, and Weston Brain Institute; Advisory Committee for Biron Soins du Sommeil; Advisory Board for Jazz Pharmaceuticals. The other authors report no conflicts of interest.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Competing interests: RSW has received honoraria from GE Healthcare and Britannia, as well as speaking honoraria from the Shirley Ryan Ability Lab. PAK has received honoraria from Alimera, AbbVie, Apellis, Boehringer-Ingleheim, Thea, Bayer and Gyroscope, as well as consulting fees from DeepMind. PAK participates on data safety monitoring /advisory boards for RetinAI, Novartis, Roche, AbbVie, Boehringer-Ingleheim and Apellis. PAK also holds stock with Big Medical Picture, stock options with Bitfount, and holds a patent: Google US10198832B2.

 Competing interests: CB has received speaking fees from Chugai Pharma. HW receives honoraria for acting as a member of Scientific Advisory Boards from Abbvie, Alexion, Argenx, Bristol Myers Squibb/Celgene, Janssen, Merck, Novartis and Sandoz. Speaker honoraria and travel support from Alexion, Biogen, Bristol Myers Squibb, Genzyme, Merck, Neurodiem, Novartis, Ology, Roche, TEVA and WebMD Global. HW is acting as a paid consultant for Abbvie, Actelion, Argenx, BD, Biogen, Bristol Myers Squibb, EMD Serono, Fondazione Cariplo, Gossamer Bio, Idorsia, Immunic, Immunovant. Janssen. Lundbeck, Merck, NexGen, Novartis, PSI CROl, Roche, Sanofi, Swiss Multiple Sclerosis Society, UCB and Worldwide Clinical Trials. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgesellschaft (DFG), Deutsche Myasthenie Gesellschaft e.V., Alexion. Amicus Therapeutics Inc., Argenx, Biogen, CSL Behring, F. Hoffmann - La Roche, Genzyme, Merck KgaA, Novartis, Roche Pharma and UCB Biopharma. HR received Consulting fees from PLURISTEM, NEOVASC; Payment honoraria for lectures, presentations from DAICHI SANKYIO, DIAPLAN, MEDUPDATE, STREAMEDUP, CORVIA; Participation in Advisory Boards from BMS, PFIZER, NOVONORDISK; the department received research grants from BARD, PFIZER, BMS. JM has received grants from Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung (BMBF), Else Kröner-Fresenius-Stiftung, EVER Pharma Jena, and Ferrer International, travel grants from Boehringer Ingelheim, and speaking fees from Bayer Vital and Chugai Pharma.
 Conflict of Interest Disclosures: Dr H. J. Kim reported receiving grants from the National Research Foundation of Korea; receiving personal fees from APRILBIO and Eisai; receiving consulting or speaker fees from or serving on a steering or scientific committee for Alexion, APRILBIO, ALTOS Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, Handok, Horizon Therapeutics (formerly Viela Bio), Kaigene, Kolon Life Science, MDimune, Mitsubishi Tanabe Pharma, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok, and UCB outside the submitted work; and serving as coeditor for the Multiple Sclerosis Journal and associate editor for the Journal of Clinical Neurology. No other disclosures were reported.
 The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Yujie Wang, MD: Research funding from Genentech. Scott D. Newsome, DO: None relevant to this manuscript. Has received consultant fees for scientific advisory boards from Biogen, Genentech, Bristol Myers Squibb, EMD Serono, Greenwich Biosciences, Novartis, TG Therapeutics, and Horizon Therapeutics; is the study lead PI for a Roche clinical trial; was a clinical adjudication committee member for a medDay Pharmaceuticals clinical trial; and has received research funding (paid directly to institution) from Biogen, Roche, Genentech, The Stiff Person Syndrome Research Foundation, National Multiple Sclerosis Society, Department of Defense, and Patient Centered Outcomes Research Institute.
 Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: SS reports no conflicts of interest. GD reports no conflicts of interest. TME reports no conflicts of interest. CA reports no conflicts of interest. AT reports personal fees paid to his institution from Eisai ltd and fees and support for travel from Hoffmann-La Roche outside the submitted work, and Editorial Board member, The Lancet Neurology, receiving free subscription, Editor-in-Chief, Multiple Sclerosis Journal, honorarium from SAGE Publications, support for travel as Chair, Scientific Advisory Committee, International Progressive MS Alliance, and member, National MS Society (USA), Research Programs Advisory Committee, Received honoraria and support for travel for lecturing from EXCEMED and Almirall. He acknowledges also support from the UCL/UCLH NIHR Biomedical Research Centre. NW reports that the Max Planck Institute for Human Cognitive and Brain Sciences has an institutional research agreement with Siemens Healthcare, that he holds a patent on acquisition of MRI data during spoiler gradients (US 10,401,453 B2) and that he was a speaker at an event organized by Siemens Healthcare and was reimbursed for the travel expenses. AC reports no conflicts of interest. PF reports no conflicts of interest.
 The authors declare the following competing financial interest(s): S.F.T. is a member of the medical advisory boards for the CureGRIN Foundation and the GRIN2B Foundation, is a member of the scientific advisory boards for Sage Therapeutics and Eumentis Therapeutics, is a Senior Advisor for GRIN Therapeutics, is a consultant for Neurocrine, is a cofounder of NeurOp, Inc. and AgriThera, Inc., and is on the Board of Directors for NeurOp Inc. D.C.L. is on the Board of Directors for NeurOp Inc. Multiple authors are coinventors on Emory-owned IP involving NMDA receptor modulators (M.P.D., P.M., Y.J., D.S.M., P.J.A., R.G.F., N.S.A., H.Y., S.F.T., and D.C.L.). H.Y. is PI on a grant from Sage Therapeutics to Emory. K.C. is an employee of Janssen Research and Development. The other authors declare no competing financial interest.

 P.A. is an employee of Regeneron Pharmaceuticals and receives salary from and owns options and/or stock of the company. The remaining authors declare no competing interests.
 Competing interests: None declared.

 The authors have no conflict of interest to declare. Figure 1.Light microscopy of patient A. Two glomeruli show segmentary sclerosis of the flocculus. Focal aspect of collapse of glomerular capillaries is shown in a glomerulus with some hyperplastic epithelial cells containing drops of protein reabsorption (collapsing lesion). No signs of endocapillary hypercellularity or glomerulitis.Figure 2.Clinical course after transplantation. eGFR = estimated glomerular filtration rate; KTx = kidney transplantation; RBx = renal biopsy.
 Declaration of Competing Interest F.B acts as a consultant for Biogen-Idec, IXICO, Merck-Serono, Novartis, Combinostics and Roche. He has received grants, or grants are pending, from the Amyloid Imaging to Prevent Alzheimer's Disease (AMYPAD) initiative, the Biomedical Research Centre at University College London Hospitals, the Dutch MS Society, ECTRIMS–MAGNIMS, EU-H2020, the Dutch Research Council (NWO), the UK MS Society, and the National Institute for Health Research, University College London. He has received payments for the development of educational presentations from Ixico and his institution from Biogen-Idec and Merck. He is on the editorial board of Radiology, European Neuroradiology, Multiple Sclerosis Journal and Neurology. F.B. and D.C.A. are on the board of directors of Queen Square Analytics.
 Declaration of competing interest MB has served on a scientific advisory board for Teva and has received speaker honoraria for lecturing from Novartis and Roche, and support for congress participation from Teva, Novartis and Roche. PB has received speaker honoraria from Novartis and has served on an advisory board for Biogen. MH, SC, AP, SM, MS, ES, AE, MB, MM, AB, and LCT report no disclosures.
 Jarith Ebenau reports no disclosures relevant to the manuscript. Denise Visser reports no disclosures relevant to the manuscript. Sander Verfaillie reports no disclosures relevant to the manuscript. Tessa Timmers reports no disclosures relevant to the manuscript. Mardou van Leeuwenstijn reports no disclosures relevant to the manuscript. Mara ten Kate reports no disclosures relevant to the manuscript. Frederik Barkhof is a consultant for Biogen-Idec, Bayer-Schering, Merck-Serono, Roche, NovartisIXICO, and Combinostics; has received sponsoring from European Commission-Horizon 2020, National Institute for Health Research-University College London Hospitals Biomedical Research Centre, TEVA, Novartis, and Biogen; and serves on the editorial boards of Radiology, Brain, Neuroradiology, Multiple Sclerosis Journal, and Neurology. Philip Scheltens has acquired grant support (for the institution) from Biogen. In the past two years, he has received consultancy/speaker fees (paid to the institution) from Probiodrug Biogen, EIP Pharma, Merck AG. Niels Prins is consultant to Boehringer Ingelheim, Aribio, and Amylyx. He is co-PI of a study with Fuji Film Toyama Chemical. He serves on the DSMB of Abbvie’s M15-566 trial. NP has received a speaker fee from Biogen. Payments were made to his company. He is CEO and co-owner of the Brain Research Centre, The Netherlands. Ronald Boellaard reports no disclosures relevant to the manuscript. Bert Windhorst reports no disclosures relevant to the manuscript. Wiesje van der Flier Research programs have been funded by ZonMW, NWO, EU-FP7, EU-JPND, Alzheimer Nederland, CardioVascular Onderzoek Nederland, Health ~ Holland, Topsector Life Sciences & Health, stichting Dioraphte, Gieskes-Strijbis fonds, stichting Equilibrio, Pasman stichting, Biogen MA Inc, Boehringer Ingelheim, Life-MI, AVID, Roche BV, Fujifilm, Combinostics. WF is recipient of a grant for the Heart-Brain Connection crossroads (HBCx) consortium of the Dutch CardioVascular Alliance (DCVA). This work was supported by the Dutch Heart Foundation [#2018–28]. WF holds the Pasman chair. WF has performed contract research for Biogen MA Inc and Boehringer Ingelheim. WF has been an invited speaker at Boehringer Ingelheim, Biogen MA Inc, Danone, Eisai and WebMD Neurology (Medscape). WF is consultant to Oxford Health Policy Forum CIC, Roche, and Biogen MA Inc. WF was associate editor at Alzheimer’s Research & Therapy (2020–2021); She is associate editor of Brain (2021–). All funding is paid to her institution. Bart van Berckel has received research support from EU-FP7, CTMM, ZonMw, NWO, and Alzheimer Nederland. BvB has performed contract research for Rodin, IONIS, AVID, Eli Lilly, UCB, DIAN-TUI, and Janssen. BvB was a speaker at a symposium organized by Springer Healthcare. BvB has a consultancy agreement with IXICO for the reading of PET scans. BvB is a trainer for GE. BvB only receives financial compensation from Amsterdam UMC.

 Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf and declare: no support from any organisation for the submitted work; RS, FMA, KO and SJN declared no competing interest; AYF is joint copyright holder of FROM-16 and of the Dermatology Life Quality Index (DLQI). Cardiff University receives royalties from their use: AYF receives a share of these under standard university policy; SMS receives unrestricted educational grant from the European Hematology Association, Unrestricted educational grant from 'The Centre for Innovative Regulatory Science', Travel grant from Merck, Novo Nordisk and Dr August Wollf. SMS is joint copyright holder for FROM-16 and Cardiff University receives royalty from its commercial use; JRI receives a stipend as Editor-in-Chief of the British Journal of Dermatology and an authorship honorarium from UpToDate. He is a consultant for Boehringer Ingelheim, ChemoCentryx, Novartis and UCB Pharma and has served on advisory boards for Insmed, Kymera Therapeutics and Viela Bio, all in the field of hidradenitis suppurativa (HS). He is co-copyright holder of HiSQOL, Investigator Global Assessment and Patient Global Assessment instruments for HS. His department receives income from copyright of the Family Reported Outcome Measure (FROM-16), DLQI and related instruments.
 Declaration of interests Johannes Levin reports part-time employment by MODAG GmbH and a grant of the Michael J Fox Foundation for Parkinson's Research. In addition, he reports speaker fees from Bayer Vital, Biogen and Roche, consulting fees from Axon Neuroscience and Biogen, author fees from Thieme medical publishers and W. Kohlhammer GmbH medical publishers, all outside the submitted work. He is a member of the advisory board of Biogen and a member of the Data Safety Monitoring Board of Axon Neuroscience. He is beneficiary of the phantom share program of MODAG GmbH. In addition, he is inventor in a patent “Pharmaceutical Composition and Methods of Use” (EP 22 159 408.8) filed by MODAG GmbH. Bernhard Hemmer received funding by the European Union's Horizon 2020 Research and Innovation Program and the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy within the framework of the Munich Cluster for Systems Neurology and Roche. He holds part of two patents: one for the detection of antibodies against KIR4.1 in a subpopulation of patients with multiple sclerosis and one for genetic determinants of neutralizing antibodies to interferon. Wilko Weichert reports research funding from Roche, MSD, BMS and AstraZeneca. He has attended and given talks at Advisory Boards, gave advice to and served as speaker on national and international conferences for Roche, MSD, BMS, AstraZeneca, Pfizer, Merck, Lilly, Boehringer, Novartis, Takeda, Bayer, Amgen, Astellas, Eisai, Johnson and Johnson, Janssen, Illumina, Siemens, Agilent, ADC, GSK and Molecular Health. Stefan F. Lichtenthaler reports research funding from Shionogi and Novartis. Steffen Tiedt reports consulting fees from Alpha Apollo Inc. Christiane Gasperi reports funding from the Hertie Foundation, the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) and the Hans and Klementia Langmatz Stiftung. Carla Palleis reports funding from the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy within the framework of the Munich Cluster for Systems Neurology. No other disclosures were reported.
 Competing interests: PJF reports personal fees from Allergan, Carl Zeiss, Google/DeepMind and Santen, a grant from Alcon, outside the submitted work. PJP reports grants from Topcon Inc, outside the scope of the current report. AK reports personal fees from Abbvie, Aerie, Google Health, Novartis, Reichert, Santen and Thea, outside the submitted work. AP reports grant support for remyelination trials in multiple sclerosis to the Amsterdam University Medicam Centre, Department of Neurology, MS Centre (RESTORE trial) and UCL, London RECOVER trial; Fight for Sight (nimodipine in optic neuritis trial); royalties or licenses from Up-to-Date (Wolters Kluver) on a book chapter; speaker fees for the Heidelberg Academy; participation on Advisory Board SC Zeiss OCTA Angi-Network, SC Novartis OCTiMS study; equipment: OCTA from Zeiss (Plex Elite).
 O.M.D. has received grant/research support from the Brain and Behavior Foundation, Simons Autism Foundation, Stanley Medical Research Institute, Deakin University, Lilly, NHMRC, and the Australasian Society for Bipolar and Depressive Disorders (ASBDD)/Servier. O.M.D. has also received in-kind support from BioMedica Nutraceuticals, NutritionCare, and Bioceuticals. W.M. has previously received funding from the Cancer Council Queensland and university grants/fellowships from La Trobe University, Deakin University, University of Queensland, and Bond University. W.M. has received industry funding and/or has attended events funded by Cobram Estate Pty. Ltd. and Bega Dairy and Drinks Pty Ltd. W.M. has received travel funding from the Nutrition Society of Australia. W.M. has received consultancy funding from Nutrition Research Australia and ParachuteBH. W.M. has received speakers’ honoraria from The Cancer Council Queensland and the Princess Alexandra Research Foundation.
 No conflicts of interest, financial or otherwise, are declared by the authors.
 Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
 Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

 The authors declare no conflict of interest.
 S Gholizadeh is an employee of Genentech, Inc., and shareholder of F. Hoffmann-La Roche Ltd. A Exuzides was an employee of Genentech, Inc., at the time of this study and manuscript preparation and is a shareholder of F. Hoffmann-La Roche Ltd. KE Lewis, C Palmer, M Waltz, and AM Jolley declare that they have nothing to disclose. JW Rose has received research support from the National Multiple Sclerosis Society, Guthy-Jackson Charitable Foundation, National Institutes of Health (NIH), Friends of MS and Biogen. He has received intellectual property interests from a discovery or technology relating to health care. JM Behne has received personal compensation as Executive Director of the Guthy-Jackson Charitable Foundation. MK Behne has received personal compensation for serving as an independent contractor with the Guthy-Jackson Charitable Foundation. TF Blaschke has received personal compensation for serving as a consultant for Merck, the Guthy-Jackson Charitable Foundation, and the Bill and Melinda Gates Foundation. He has received personal compensation for serving as an officer or member of the board of directors for Durect. He has received personal compensation for serving as an editor, associate editor, or editorial advisory board member for Annual Reviews. He has received stock or ownership interest from Durect. He has received research support from the Bill and Melinda Gates Foundation. TJ Smith has received personal compensation as an advisor to the Guthy-Jackson Charitable Foundation. He has received personal compensation for serving as a consultant for Horizon and Immunovant. He has received personal compensation for serving on a scientific advisory or data safety monitoring board for Horizon. He has received intellectual property interests from discoveries and technologies relating to health care. J Sinnott has received research support from the Guthy-Jackson Charitable Foundation and the NIH. LJ Cook has received research support from the Centers for Disease Control and Prevention, Guthy-Jackson Charitable Foundation, Utah Highway Safety Office and NIH. MR Yeaman has received personal compensation as an advisor to the Guthy-Jackson Charitable Foundation. He has received personal compensation for serving on a scientific advisory board for Genentech. He has received honoraria from Roche, Horizon and Alexion for scientific presentations pertaining to NMOSD. He has received research support from the NIH (National Institute of Allergy and Infectious Disease) and the US Department of Defense. He holds numerous patents and has received intellectual property interests from discoveries and technologies relating to health care.
 The authors declare no competing interests and no conflict of interest. MAF received honoraria for consultation and travel expenses from Biogen, Merck KGaA, Novartis and Roche unrelated to this work.

 The authors declare no conflicts of interest.
 Competing interests: BN, PS, MS and AM are employees of Evidera, a part of Thermo Fisher Scientific. MP has received grant/research support from AstraZeneca, Aurinia, Eli Lilly, Exagen, GSK, Janssen and Thermo Fisher. MP has also received consulting fees from the BPR Scientific Advisory Committee, Alexion, Amgen, AnaptysBio, Argenx, AstraZeneca, Aurinia, AxDev, Biogen, Boston Pharmaceuticals, Caribou Biosciences, CVS Health, Eli Lilly, Gilead Biosciences, GSK, Idorsia Pharmaceuticals, Janssen, Kezar Life Sciences, Kira Pharmaceuticals, Momenta Pharmaceuticals, Nimbus Lakshmi, Proviant, Sanofi, SinoMab and UCB. MP has received speakers’ fees from Aurinia, MedShr and Arthros-FocusMedEd, and has received consulting fees for participation in a data safety monitoring board or advisory board for EMD Serono, Emergent Biosolutions, IQVIA and PPD Development. GKB has received consulting fees from Pfizer, Lilly and Novartis, and has received honorary fees from GSK, AstraZeneca, Pfizer, Novartis, Aenorasis, AbbVie and Lilly. GKB has also received a research grant from Pfizer. AHJK has received research support to Washington University from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant number P30 AR073752), National Center for Advancing Translational Sciences (grant number UL1 TR002345), Leona M. and Harry B. Helmsley Charitable Trust, Rheumatology Research Foundation, and National Multiple Sclerosis Society, GSK, and Foghorn Therapeutics. AHJK has performed consultancy for Alexion Pharmaceuticals, ANI Pharmaceuticals, AstraZeneca, Aurinia Pharmaceuticals, Exagen Diagnostics, GSK, Kypha and Pfizer unrelated to this work. AHJK has received payment or honoraria (for lectures, presentations, speakers bureaus, manuscript writing or educational events) from AstraZeneca, Aurinia Pharmaceuticals, Exagen Diagnostics and GSK. AHJK has participated on a data safety monitoring board or advisory board for National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases. AHJK has been a board member for the Rheumatology Research Foundation Scientific Advisory Board and the Lupus Foundation of America-Heartland Chapter, and president of the St Louis Rheumatology Association. AHJK is the inventor of patent number 11029318 with Kypha unrelated to this work. The funders had no role in the decision to publish or preparation of this manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of Washington University, its affiliated academic health care centers, or the National Institutes of Health. AF has received honoraria and consulting fees from GSK, Aenorasis and AstraZeneca. AF has been a paid speaker for AbbVie, Amgen, Pfizer, Lilly, Genesis-Pharma, Novartis, UCB and Boehringer-Ingelheim. RAL, DC and NB are employees of GSK and hold stocks and shares in GSK.
 Declaration of interests J.W. is a consultant for Allergan, Editas, Maze, Regenxbio and has received sponsored research support from Aerpio Pharmaceuticals Inc. L.R.P. is a consultant for Eyenovia, Twenty, and CharacterBio. A.P.K. is a consultant to Aerie, Allergan, Google Health, Novartis, Reichert, Santen and Thea. S.M. hold stock at Seonix Bio Ltd. S.D.T is supported by the QIMR Statistical Genetics PhD scholarship. All remaining authors declare no competing interests.

 A. McKeon reports research funding from NIH (NIH: RO1NS126227, U01NS120901), patents issued for GFAP and MAP1B-IgGs and patents pending for PDE10A, Septins-5 and -7, and KLCHL11-IgGs, and has consulted for Janssen and Roche pharmaceuticals, without personal compensation. C. Lesnick reports no disclosures relevant to the manuscript. N. Vorasoot reports no disclosures relevant to the manuscript. M.W. Buckley reports no disclosures relevant to the manuscript. S. Dasari reports no disclosures relevant to the manuscript. E.P. Flanagan has funding from NIH (R01NS113828), has served on advisory boards for Alexion, Genentech, Horizon Therapeutics and UCB, has received honoraria from Pharmacy Times and UpToDate, and has a patent pending for DACH1-IgG as a biomarker of paraneoplastic autoimmunity; M. Gilligan reports no disclosures relevant to the manuscript. R. Lafrance Corey reports no disclosures relevant to the manuscript. R. Miske is employed by Euroimmun. S.J. Pittock is a named inventor on filed patents that relate to functional AQP4/NMO-IgG assays and NMO-IgG as a cancer marker, has patents pending for KLHL11-IgG and Septin-5-IgG, and issued for MAP1B-IgG as markers of neurologic autoimmunity and paraneoplastic disorders, has consulted for Alexion and Medimmune; and has received research support from Genentech, Grifols, Medimmune, and Alexion; M Scharf is employed by Euroimmun. B. Yang reports no disclosures relevant to this manuscript. A. Zekeridou has patent applications pending on PDE10A-IgG and DACH1-IgG as biomarkers of paraneoplastic neurologic autoimmunity and has received research funding from Genentech; D. Dubey has research support from Department of Defence (CA210208), Centers of Multiple Sclerosis and Autoimmune Neurology, and Clinical and Translational Science, Mayo Clinic, and Grifols pharmaceuticals, has consulted for UCB, Immunovant, Argenx and Astellas pharmaceuticals (compensation for consulting activities paid directly to Mayo Clinic), and has patents pending for KLHL11-IgG, LUZP4-IgG, and cavin-4-IgG as markers of neurologic autoimmunity; J Mills reports no disclosures relevant to the manuscript. Go to Neurology.org/NN for full disclosures.


 F. Stascheit received speaker honoraria from Alexion. U. Grittner reports no conflict of interest, S. Hoffmann received speaker honoraria from Alexion. P. Mergenthaler receives funding from the Einstein Foundation Berlin, and is supported by grants from the Bundesministerium für Bildung und Forschung, the Volkswagen Foundation, and the Else Kröner Fresenius Stiftung, and is on the board of HealthNextGen Inc. and has equity interest in the company. M. Schroeter reports speaker honoraria from Argenx, Bayer, Biogen, Datamed, Grifols, Merck, Roche, Sanofi. He received consulting fees from Alexion, Biogen, Argenx/Efran MG, Gilead, and Roche. T. Ruck reports grants from German Ministry of Education, Science, Research and Technology, grants and personal fees from Sanofi-Genzyme, Novartis and Alexion; personal fees from Abbott, argenx, Biogen, Bristol-Myers Squibb, Roche and Teva; personal fees and nonfinancial support from Merck Serono, outside the submitted work. F. Blaes received speaker honoraria from UCB, Argenx, Alexion and Grifols. J. Kaiser reports no conflicts of interests. U. Schara received speaker honoria from Alexion and Biogen. A. D. Marina reports no conflicts of interests. A. Thieme reports no conflicts of interests. T. Hagenacker reports speaker honoraria from Alexion, argenx and Hormosan, Biogen, Roche Sanofi Genzyme and Novartis Gene Therapies. He received consulting fees from Biogen, Roche, Sanofi Genzyme, Alexion, argenx, Hormsosan and Alnylam and research support from Sanofi Genzyme, Roche, Biogen and Novartis. C. Jacobi reports speaker honoraria from Alexion, CSL Behring, TEVA and Sanofi Genzyme. He received consulting fees from Alexion, Roche, Merck Serono and Novartis. P. P. Urban received speaker honoraria from Alexion. B. Berger received travel grants and/or training expenses from Bayer Vital GmbH, Ipsen Pharma GmbH, Norvartis, Biogen GmbH and Genzyme, as well as lecture fees from Ipsen Pharma GmbH, Alexion Pharma GmbH, Merck, Sanofi Genzyme and Roche. K. C. Knop received speaker honoraria from Alexion, Bayer, Biogen, Grifols, Hormosan, Novartis, Sanofi Genzyme, Roche and consulting fees from Hormosan, Merck, Sanofi Genzyme and Sarepta. B. Schalke received consulting fees from argnx. D.J. Lee received speaking honoria from Alexion, Anylam, Biogen, Janssen, Merck, Novartis, Roche and Sanofi. P. Kalischewski received speaker honoraria, consulting fees and NIS from Biogen, Sanofi, Teva, Merck, Roche, Novartis and Biogen. M. Pawlitzki received speaker honoraria and travel/accommodation/meeting expenses from Novartis. H. Wiendl is acting as a paid consultant for Abbvie, Actelion, Biogen, IGES, Johnson & Johnson, Novartis, Roche, Sanofi-Aventis, and the Swiss Multiple Sclerosis Society. His research is funded by the German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Else Kröner Fresenius Foundation, Fresenius Foundation, the European Union, Hertie Foundation, NRW Ministry of Education and Research, Interdisciplinary Center for Clinical Studies (IZKF) Muenster and RE Children’s Foundation, Biogen, GlaxoSmithKline GmbH, Roche Pharma AG, Sanofi-Genzyme. A. Meisel received speaker honoraria, consulting fees or financial research support from Alexion, argnx, Grifols, Hormosan, Janssen, Octapharmam UCB and Vitaccess for consulting services and financial research support from Octapharma and Alexion. He serves as chairman of the medical advisory board of the German Myasthenia Gravis Society.
 Declaration of competing interest The Food & Mood Centre has received Grant/Research support from Fernwood Foundation, Wilson Foundation, the A2 Milk Company, and Be Fit Foods. MML is supported by a Deakin University Scholarship and has received research funding support from Be Fit Foods. ML is currently funded by an Alfred Deakin Postdoctoral Research Fellowship. MF is supported by a Deakin University Scholarship and has received grants and fellowships from Avant Mutual, the Royal Australian and New Zealand College of Psychiatrists (RANZCP) and the National Health and Medical Research Council (NHMRC). TR has received grants, fellowships and research support from University of the Sunshine Coast, Australian Postgraduate Awards, Fernwood Foundation, Roberts Family Foundation and Be Fit Food. TR received consultancy, honoraria and travel funds from Oxford University Press, the University of Melbourne, the University of Sydney, Bond University, University of Southern Queensland, Dietitians Association of Australia, Nutrition Society of Australia, The Royal Australian and New Zealand College of Psychiatrists, Academy of Nutrition and Dietetics, Black Dog Institute, Australian Rotary Health, Australian Disease Management Association, Department of Health and Human Services, Primary Health Networks, Barwon Health, West Gippsland Healthcare Group, Central West Gippsland Primary Care Partnership, Parkdale College, City of Greater Geelong and Global Age. AO is supported by an NHMRC Emerging Leader 2 Fellowship (2009295). She has received research funding from National Health & Medical Research Council, Australian Research Council, University of Melbourne, Deakin University, Sanofi, Meat and Livestock Australia and Woolworths Limited and Honoraria from Novartis. FNJ has received Grant/Research support from the Brain and Behaviour Research Institute, the National Health and Medical Research Council (NHMRC), Australian Rotary Health, the Geelong Medical Research Foundation, the Ian Potter Foundation, Eli Lilly, Meat and Livestock Australia, Woolworths Limited, the Fernwood Foundation, Wilson Foundation, the A2 Milk Company, Be Fit Foods, and The University of Melbourne, and has received speakers honoraria from Sanofi-Synthelabo, Janssen Cilag, Servier, Pfizer, Health Ed, Network Nutrition, Angelini Farmaceutica, Eli Lilly and Metagenics. FNJ has written two books for commercial publication and has a personal belief that good diet quality is important for mental and brain health. DNA is supported by funds from an NHMRC Emerging Leader 2 Fellowship (2009295). WM is currently funded by an Alfred Deakin Postdoctoral Research Fellowship and a Multiple Sclerosis Research Australia early-career fellowship. WM has previously received funding from the Cancer Council Queensland and university grants/fellowships from La Trobe University, Deakin University, University of Queensland, and Bond University. WM has received industry funding and has attended events funded by Cobram Estate Pty. Ltd. WM has received travel funding from Nutrition Society of Australia. WM has received consultancy funding from Nutrition Research Australia and ParachuteBH. WM has received speakers' honoraria from The Cancer Council Queensland and the Princess Alexandra Research Foundation.
 Nothing to report.
 S.R.A. has consulted for Indoc Research Canada. C.E.F. receives commercial grant support from Vielight Inc. and Hoffman La Roche. S.K. has received research support from Brain and Behavior Foundation, National Institute on Ageing, BrightFocus Foundation, Brain Canada, Canadian Institute of Health Research, Canadian Consortium on Neurodegeneration in Aging, Centre for Ageing and Brain Health Innovation, Centre for Addiction and Mental Health; an Academic Scholars Award from the Department of Psychiatry, University of Toronto; and has received equipment support from Soterix Medical. S.H.P. has received research funding from Zywie Bio LLC. B.G.P. receives research support from the Peter & Shelagh Godsoe Endowed Chair in Late-Life Mental Health, CAMH Foundation, and Discovery Fund, National Institute of Aging, Brain Canada, the Canadian Institutes of Health Research, the Alzheimer’s Drug Discovery Foundation, the Ontario Brain Institute, the Centre for Aging and Brain Health Innovation, the Bright Focus Foundation, the Alzheimer’s Society of Canada, the W. Garfield Weston Foundation, the Weston Brain Institute, the Canadian Consortium on Neurodegeneration in Aging and Genome Canada; receives honoraria from the American Geriatrics Society for book authorship; and is listed on United States Provisional Patent Nos. 6/490,680 and 17/396030 and Canadian Provisional Patent No. 3054093 for a cell-based assay and kits for assessing serum anticholinergic activity. T.K.R. has received research support from Brain Canada, Brain and Behavior Research Foundation, BrightFocus Foundation, Canada Foundation for Innovation, Canada Research Chair, Canadian Institutes of Health Research, Centre for Aging and Brain Health Innovation, National Institutes of Health, Ontario Ministry of Health and Long-Term Care, Ontario Ministry of Research and Innovation, and the Weston Brain Institute; received for an investigator-initiated study in-kind equipment support from Newronika; in-kind research online accounts from Scientific Brain Training Pro; participated in 2021 in one advisory board meeting for Biogen Canada Inc; and is listed on United States Provisional Patent No. 17/396030 that describes cell-based assays and kits for assessing serum cholinergic receptor activity. D.P.S. receives research funding from CIHR, Alzheimer’s Association, University of Calgary, and Hotchkiss Brain Institute. M.C.T. receives grant support from NIH and CIHR and is a clinical trial investigator for Biogen, Janssen, Anavex, Green Valley and Roche. All other authors report no competing interests.
 M.A.N. and S.W.S.’s participation in this project was part of a competitive contract awarded to Data Tecnica International LLC by the National Institutes of Health to support open science research. M.A.N. also currently serves on the scientific advisory board for Character Bio Inc. and Neuron23 Inc. S.W.S. serves on the scientific advisory board of the Lewy Body Dementia Association and the Multiple System Atrophy Coalition. S.W.S. is an editorial board member for the Journal of Parkinson’s Disease and JAMA Neurology. S.W.S. receives research support from Cerevel Therapeutics.
 The authors declare no competing interests.

 The authors declare no conflict of interest.
 D.M.D. is a GP Partner in the National Health Service (NHS); he has received fees for presentations, including Royal College of Psychiatrists International Congress Edinburgh 2013 (travel and accommodation only), webinars for general practitioners, PRIMHE (Primary care Mental Health & Education), Network Locums and BMJ Masterclasses; he received an honorarium from Lundbeck for a symposium presentation at the British Association of Psychopharmacology 2019 Summer Meeting on ‘The primary/secondary care interface for treating depression: challenges and future perspectives’, which covered practical ways to improve to help patient care and there was no endorsement of any pharmaceutical treatment or product. J.K.-G. owns shares in AstraZeneca and GSK plc. M.H. is supported by an Australian Rotary Health PhD Scholarship. W.M. is currently funded by an NHMRC (National Health and Medical Research Council) Investigator Grant (#2008971) and a Multiple Sclerosis Research Australia early-career fellowship and has previously received funding from the Cancer Council Queensland and university grants/fellowships from La Trobe University, Deakin University, University of Queensland, and Bond University; he has received industry funding and has attended events funded by Cobram Estate Pty. Ltd., has received travel funding from Nutrition Society of Australia, and consultancy funding from Nutrition Research Australia and ParachuteBH; he has received speakers honoraria from The Cancer Council Queensland and the Princess Alexandra Research Foundation. A.H.Y. is Deputy Editor of BJPsych Open and did not take part in the review or decision-making process of this paper; he is employed by King's College London, is an Honorary Consultant at SLaM (South London and Maudsley) (NHS UK); his independent research is funded by the National Institute for Health and Care Research (NIHR) Maudsley Biomedical Research Centre at SLaM NHS Foundation Trust and King's College London; he has given paid lectures and advisory boards for the following companies with drugs used in affective and related disorders: Astrazenaca, Boehringer Ingelheim, Eli Lilly, LivaNova, Lundbeck, Sunovion, Servier, Livanova, Janssen, Allegan, Bionomics, Sumitomo Dainippon Pharma, COMPASS, Sage, Novartis, Neurocentrx; he is Principal Investigator in the Restore-Life VNS (vagus nerve stimulation) registry study funded by LivaNova, Principal Investigator on ESKETINTRD3004: ‘An Open-label, Long-term, Safety and Efficacy Study of Intranasal Esketamine in Treatment-resistant Depression’, Principal Investigator on ‘The Effects of Psilocybin on Cognitive Function in Healthy Participants’, Principal Investigator on ‘The Safety and Efficacy of Psilocybin in Participants with Treatment-Resistant Depression (P-TRD)’, UK Chief Investigator for Compass; COMP006 & COMP007 studies, UK Chief Investigator for Novartis MDD (Major Depressive Disorder) study MIJ821A12201; grant funding (past and present): NIMH (National Institute of Mental Health) (USA); CIHR (Canadian Institutes of Health Research) (Canada); NARSAD (National Alliance for Research in Schizophrenia and Affective Disorders) (USA); Stanley Medical Research Institute (USA); MRC (Medical Research Council) (UK); Wellcome Trust (UK); Royal College of Physicians (Edin); BMA (British Medical Association) (UK); UBC-VGH (University of British Colombia - Vancouver General Hospital) Foundation (Canada); WEDC (Western Economic Diversification Canada) (Canada); MSFHR (Michael Smith Health Research) (Canada); NIHR (National Institute for Health Research) (UK); Janssen (UK) EU Horizon 2020. M.B. is supported by a NHMRC Senior Principal Research Fellowship and Leadership 3 Investigator grant (1156072 and 2017131); he has received grant/research support from National Health and Medical Research Council, Wellcome Trust, Medical Research Future Fund, Victorian Medical Research Acceleration Fund, Centre for Research Excellence CRE, Victorian Government Department of Jobs, Precincts and Regions and Victorian COVID-19 Research Fund; he received honoraria from Springer, Oxford University Press, Cambridge University Press, Allen and Unwin, Lundbeck, Controversias Barcelona, Servier, Medisquire, HealthEd, ANZJP, EPA, Janssen, Medplan, Milken Institute, RANZCP, Abbott India, ASCP, Headspace and Sandoz (past 3 years). V.M. has received research funding from Johnson & Johnson, a pharmaceutical company interested in the development of anti-inflammatory strategies for depression, but the research described in this paper is unrelated to this funding. V.M. is supported by MQ Brighter Futures grants (MQBF/1 IDEA) and (MQBF/4), by the Medical Research Foundation (Grant: MRF-160-0005-ELP-MONDE) and by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London. The views expressed are those of the authors and not necessarily those of the funders, the NHS, the NIHR or the Department of Health and Social Care.
 S.W.S. serves on the Scientific Advisory Council of the Lewy Body Dementia Association and the Multiple System Atrophy Coalition. S.W.S. and B.J.T. receive research support from Cerevel Therapeutics. B.J.T. holds patents on the clinical testing and therapeutic implications of the C9orf72 repeat expansion. H.R.M. is employed by the University College London. In the last 12 months, he reports paid consultancy from Roche and Amylyx; lecture fees/honoraria from BMJ, Kyowa Kirin, and Movement Disorders Society; and research grants from Parkinson’s UK, Cure Parkinson’s Trust, PSP Association, Medical Research Council, and the Michael J Fox Foundation. H.R.M. is a co-applicant on a patent application related to C9orf72 “method for diagnosing a neurodegenerative disease” (PCT/GB2012/052140).
 Declaration of Competing Interest All authors report no competing interests except the Alzheimer's Disease Neuroimaging Initiative: Dr. Petersen serves on scientific advisory boards for Elan Corporation, Wyeth, and GE Healthcare; receives royalties from the publication of Mild Cognitive Impairment (Oxford University Press, 2003); and receives research support from the NIH/NIA (U01 AG06786 [PI], P50 AG16574 [PI], U01 AG 024904 [Subcontract PI], and R01 AG11378 [Co-I]). Dr. Aisen serves on a scientific advisory board for NeuroPhage; serves as a consultant to Elan Corporation, Wyeth, Eisai Inc., Neurochem Inc., Schering-Plough Corp., Bristol-Myers Squibb, Eli Lilly and Company, NeuroPhage, Merck & Co., Roche, Amgen, Genentech, Inc., Abbott, Pfizer Inc, Novartis, and Medivation, Inc.; receives research support from Pfizer Inc, Baxter International Inc., Neuro-Hitech, Abbott, Martek, and the NIH (NIA U01-AG10483 [PI], NIA U01-AG024904 [Coordinating Center Director], NIA R01-AG030048 [PI], and R01-AG16381 [Co-I]); and has received stock options from Medivation, Inc. and NeuroPhage. Dr. Beckett received funding for travel to attend a conference not funded by industry; and receives research support from the NIH (2 P30 AG10129 [Director of Biostatistics Core], 2 P30 CA93373 [Director of Biostatistics Shared Resource], 1 U01 AG24904 [PI, UC Davis site; Biostatistics Team Leader], 1KL2RR024144-01 [Director of Biostatistics Core], 5R01EB002138-07 [Co-I], and 1RC2AG036535-01 [PI, UC Davis site]). Dr. Donohue receives research support from the NIH (AG010483 [Statistician] and AG024904 [Statistician]), the General Clinical Research Center, UCSD, National Center for Research Resources, and from the United States Public Health Service. Dr. Gamst served on an expert review board for Neurochem Inc; and receives research support as an investigator from the NIH [MH22005, CA104573, AG024904, MH062512, DK075128, AG010483, MH079752AG031224, MH083552, MH083506, HL095089], and the National Science Foundation. Dr. Harvey serves as an Associate Editor of Statistics for Alzheimer Disease and Associated Disorders; and receives research support from the NIH (NIA 2P30AG10129 [Biostatistician], NIA R01AG029672 [Biostatistician], NIA 1U01AG24904 [Member of Biostatistics Core], NRCC RL1NS062412 [Biostatistician], NIA R01AG031252 [Biostatistician], 1RC2AG036535– 01 [Member of Biostatistics Team]) and from the Hillblom Foundation, 2007A005NET (Biostatistician). Dr. Jack served on a scientific advisory board for Elan Corporation; receives research support from Pfizer Inc, the NIH (NIA AG11378 [PI], P50-AG16574 [Co-I], and U01 AG024904 [Co-I]) and from the Mayo U of MN Biotechnology Partnership; and holds stock in GE Healthcare. Dr. Jagust has served on a scientific advisory boards for Genentech, Inc.; has served as a consultant for Synarc, Elan Corporation, Genentech, Inc., Ceregene, Schering Plough, and Merck & Co; and receives research support from the NIH (AG027859 [PI], AG027984 [PI], and AG 024904 [Co-I]) and from the Alzheimer’s Association. Dr. Shaw has received funding for travel and speaker honoraria from Pfizer Inc; serves on the editorial board of Therapeutic Drug Monitoring; may potentially receive revenue for patent pending (application 10/192,193): O-methylated rapamycin derivatives for alleviation and inhibition of lymphoproliferative disorders, licensed by the University of Pennsylvania to Novartis; receives royalties from publication of Applied Pharmacokinetics and Pharmacodynamics: Principles of Therapeutic Drug Monitoring, Wolters Kluwer/Lippincott Williams & Wilkins, 2005; receives research support from the NIH (AG024904 [Co-PI Biomarker Core Laboratory]); and receives board of directors’ compensation and holds stock options in Saladax Biomedical. Dr. Toga received a speaker honorarium from St. Jude Children’s Hospital; serves in an editorial capacity for NeuroImage, InSight, The Cerebellum, Neuroimaging, Neuroinformatics, Anatomy & Embryology, Current Medical Imaging Reviews, Biology Image Library, Biomedical Computation Review, Brain Structure and Function, and Journal of Neural Regeneration Research; has served on scientific and/or external advisory boards for Wellcome Trust, Allen Institute for Brain Science, University of Texas at Austin, Oklahoma IDeA Network for Biomedical Research Excellence, Takeda Global Research & Development Center, and the University of Pittsburgh; and has received/receives research support from the NIH (1R01 HD053893-01 [Co-I], NIBIB 2 R01 LM005639 [Co-I], NCRR 5 P41 RR013642 [PI], R01 HD050735-01 [Co-I], 1 R01 NS049194 [Co-I], 1 R01 EB 006266-01 [Subcontract PI], NIMH/UCI, R24 RR021992 [Subcontract PI], 2P50AG005133 [Consultant: Core-Neuroimaging], NCRR 5 U24 RR021760 [PI], NIMH 2 P50 AG016570 [Co-I], NIMH 1R01MH072641-01A1 [Co-I], NIMH 5 R01 MH071940 [PI], NIMH/NIA 1 U01 AG024904 [Subcontract PI], NIMH/MGH, R24 RR021382 [Subcontract PI], NIBIB/BWH 1 U54 EB05149 [Subcontract PI], 1 R01 DA017830 [Co-I], NCRR 5 U54 RR021813 [PI], R01 MH069259 [Subcontract PI], 1 R01 NS050792 [Subcontract PI], MH069433 [Co-I], NIMH 9 P01 EB 001955-11 [CoPI]), 2005 Equipment Grant, and an Academic Excellence Grant–SUN Microsystems, and from High-Q Foundation and the National Multiple Sclerosis Society. Dr. Trojanowski has received funding for travel and honoraria from Takeda Pharmaceutical Company Ltd. and to attend numerous conferences not funded by industry; serves as an Associate Editor of Alzheimer’s & Dementia; holds 14 patents that may accrue revenue: US Patent 5,281,521, issued 25 Jan 1994: Modified Avidin-Biotin Technique; US Patent 5,580,898, issued 3 Dec 1996: Method of Stabilizing Microtubules to Treat Alzheimer’s Disease; US Patent 5,601,985, issued 11 Feb 1997: Method of Detecting Abnormally Phosphorylated Tau; US Patent 5,733,734, issued 31 Mar 1998: Method of Screening for Alzheimer’s Disease or Disease Associated with the Accumulation of Paired Helical Filaments; US Patent 5,792,900, issued 11 Aug 1998: Compositions and Methods for Producing and Using Homogeneous Neuronal Cell Transplants; US Patent 5,849,988, issued 15 Dec 1998: Rat Comprising Straight Filaments in Its Brain; US Patent 6,214,334, issued 10 Apr 2001: Compositions And Methods for Producing and Using Homogeneous Neuronal Cell Transplants to Treat Neurodegenerative Disorders and Brain and Spinal Cord Injuries; US Patent 6,358,681, issued 19 Mar 2002: Diagnostic Methods for Alzheimer’s Disease by Detection of Multiple MRNAs; US Patent 6,727,075, issued 27 Mar 2004: Methods and Compositions for Determining Lipid Peroxidation Levels in OxidantStress Syndromes and Diseases; US Patent 7,011,827, issued 14 Mar 2006: Compositions and Methods for Producing and Using Homogenous Neuronal Cell Transplants; Penn 0652, K1828, filed 5 Aug 1998: Method of Identifying, Diagnosing and Treating Alpha-synuclein Positive Neurodegenerative Disorders; Penn L1986, Filed 13 Nov 1998: Mutation-specific Functional Impairments in Distinct Tau Isoforms of Hereditary Frontotemporal Dementia and Parkinsonism Linked to Chromosome-17: Genotype Predicts Phenotype; Penn R3868 (UPN-4439), filed 28 Feb 2005: Microtubule Stabilizing Therapies for Neurodegenerative Disorders; and Penn S-4018, DB&R 46406-217282, filed 22 Nov 2005: Treatment of Alzheimer’s and Related Diseases with an Antibody; and receives research support from the NIH (NIA P01 AG 09215-20 [PI], NIA P30 AG 10124-18 [PI], NIA PO1 AG 17586-10 [Project 4 Leader], NIA 1PO1 AG-19724-07 [Core C Leader], NIA 1 U01 AG 024904-05 [Co-PI Biomarker Core Laboratory], NINDS P50 NS053488-02 [PI], NIA UO1 AG029213-01 [Co-I]; RC2NS069368 [PI], RC1AG035427 [PI], and NIA P30AG036468 [PI]), and from the Marian S. Ware Alzheimer Program. Dr. Weiner serves on scientific advisory boards for Bayer Schering Pharma, Eli Lilly and Company, CoMentis, Inc., Neurochem Inc, Eisai Inc., Avid Radiopharmaceuticals Inc., Aegis Therapies, Genentech, Inc., Allergan, Inc., Lippincott Williams & Wilkins, Bristol-Myers Squibb, Forest Laboratories, Inc., Pfizer Inc, McKinsey & Company, Mitsubishi Tanabe Pharma Corporation, and Novartis; has received funding for travel from Nestle´ and Kenes International and to attend conferences not funded by industry; serves on the editorial board of Alzheimer’s & Dementia; has received honoraria from the Rotman Research Institute and BOLT International; serves as a consultant for Elan Corporation; receives research support from Merck & Co., Radiopharmaceuticals Inc., the NIH (U01AG024904 [PI], P41 RR023953 [PI], R01 AG10897 [PI], P01AG19724 [Co-I], P50AG23501 [Co-I], R24 RR021992 [Co-I], R01 NS031966 [Co-I], and P01AG012435 [Co-I]), the US Department of Defense (DAMD17- 01-1-0764 [PI]), the Veterans Administration (MIRECC VISN 21 [Core PI]), and from the State of California; and holds stock in Synarc and Elan Corporation.
 The authors declare no conflict of interest.
 Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form. (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-22-831/coif). CH is the recipient of the grant award from URVentures that funded this research. He receives royalties for the use of multiple disease specific instruments. He has provided consultation to Biogen Idec, Ionis Pharmaceuticals, aTyr Pharma, AMO Pharma, Acceleron Pharma, Cytokinetics, Expansion Therapeutics, Harmony Biosciences, Regeneron Pharmaceuticals, Astellas Pharmaceuticals, AveXis, Recursion Pharmaceuticals, IRIS Medicine, Inc., Takeda Pharmaceutical Company, Scholar Rock, Avidity Biosciences, Novartis Pharmaceuticals Corporation, SwanBio Therapeutics, and the Marigold Foundation. He receives grant support from the Department of Defense, Duchenne UK, Parent Project Muscular Dystrophy, Recursion Pharmaceuticals, Swan Bio Therapeutics, Neurocrine Biosciences, the National Institute of Neurological Disorders and Stroke, the Muscular Dystrophy Association, the Friedreich’s Ataxia Research Alliance, Cure Spinal Muscular Atrophy, and the Amyotrophic Lateral Sclerosis Association. He is the director of the University of Rochester’s Center for Health + Technology. JCK has provided consultation/participated on advisory boards for Amgen, Boehringer Ingelheim, Bristol Myers Squibb, and EQRX. She has received support from Amgen, Bristol Myers Squibb, Foundation Medicine, Genentech, Lung Ambition Alliance, Mirati, Novartis, and Takeda, paid to GO2 Foundation for Lung Cancer. She is the PI on a research project unrelated to this work, funded by Bristol Myers Squibb and Genentech and paid to GO2 Foundation for Lung Cancer. Jacinta Wiens is now an employee of Merck but was employed at GO2 Foundation for Lung Cancer during her participation on this study. The other authors have no conflicts of interest to declare.

 Ettore Beghi reports grants from the Italian Ministry of Health, grants from SOBI, personal fees from Arvelle Therapeutics, and grants from American ALS Association, outside the submitted work. Elena Krehan, Eugenia Bianchi, Maria Lolichand, Victoria Gryb, Verena Rass, Rafael Avalos‐Pavon, Oxana Grosu, M. Meoni, Mafalda Maria Laracho de Seabra, Maria Sofia, Cotelli, Raimund Helbok, Claudio Bassetti, Eugenia Irene Davidescu, Bogdan Ovidiu Popescu, Maurizio Leone, Franco Valzania, Anne Hege Aamodt and Gordana Kiteva‐Trenchevska have nothing to report. Maria Zakharova reports payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Johnson and Johnson (Janssen), and has supported webinars/lections dedicated to the COVID‐19 pandemic: February 26, 2021 – webinar – “COVID‐19 pandemic: new challenges for MS therapy” (taught in Russian); May 28, 2021 ‐ conference, “Management of MS patients in the COVID‐19 era” (taught in Russian); and December 3, 2021 – webinar “СOVID‐19: updated data from multiple sclerosis patient registries” (taught in Russian). Tibor Kovács reports consulting fees from Richter Ltd, Pfizer Hungary, Biogen Hungary and Ipsen, payment or honoraria for lectures, presentations, speaker bureaus, manuscript writing or educational events from Richter Ltd, Pfizer Hungary, Biogen Hungary and Ipsen, support for attending meetings and/or travel from Richter Ltd, Pfizer Hungary and Medis Hungary, and participation on a Data Safety Monitoring Board or Advisory Board for Novo Nordisk and Biogen. Arijana Lovrencic‐Huzjan reports payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from TEVA, Krka and Novartis, and is President of the Ethics Committee of UHC Sestre milosrdnice. Due to the conflict of interest, she did not participate in the discussion or decision‐making on the proposed research. Elena Moro reports grants or contracts from any entity (if not indicated in item #1 above) as follows: research grant from Ipsen; honoraria for consulting from Medtronic, Abbott and Kyowa; and participation on a data safety monitoring board or advisory board for Newronika. Clarissa Lin Yasuda reports support for the present manuscript from FAPESP2013/07559–3; FAPESP 2019/11457–8, and payment or honoraria for lectures, presentations, speaker bureaus, manuscript writing or educational events from UCB, ZODIAC and TORRENT. Carmel Armon reports royalties or licenses: UpToDate co‐author on two chapters, payment for expert testimony as a neurology consultant to Inbal, Inc. and the Israeli government insurance company. Luís Maia reports support for the present manuscript from Research4COVID – FCT grant n°229 Project grant for institution, and Bial Foundation Grant Project grant for institution. Waldemar Brola reports payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Biogen, Merck, Novartis, Sanofi Genzyme and Roche, and support for attending meetings and/or travel from Biogen, Sanofi and Roche.

 J. Seabury reports no disclosures relevant to the manuscript; D. Alexandrou reports no disclosures relevant to the manuscript; C. Engebrecht reports no disclosures relevant to the manuscript; N. Dilek reports no disclosures relevant to the manuscript; B. Greco reports no disclosures relevant to the manuscript; J. Heatwole reports no disclosures relevant to the manuscript; J. Larkindale is a paid employee of PepGen Inc.; D.R. Lynch receives grant support from the NIH, FDA, Friedreichs Ataxia Research Alliance, Reata Pharmaceuticals, Retrotope, PTC Therapeutics, Design Pharmaceuticals; C. Park reports no disclosures relevant to the manuscript; S. Rosero reports no disclosures relevant to the manuscript; S. Subramony receives research support from the NIH, FDA, Wyck, Friedreichs Ataxia Research Alliance, Muscular Dystrophy Association, Facioscapulohumeral Muscular Dystrophy Society, National Ataxia Foundation, Reata, PTC, Retrotope, Biohaven, Takeda, Acceleron, Pharnext, Avidity, and Reneo. He has provided consultation or served on advisory boards for Dyne, Avidity, Reata, and Avexis; A. Varma reports no disclosures relevant to the manuscript; E. Wagner reports no disclosures relevant to the manuscript; S. Walther reports no disclosures relevant to the manuscript; J. Weinstein reports no disclosures relevant to the manuscript; M. Wells reports no disclosures relevant to the manuscript; C. Zizzi has provided consultation to Recursion Pharmaceuticals; C. Heatwole receives royalties for the use of multiple disease-specific instruments. He has provided consultation to Biogen Idec, Ionis Pharmaceuticals, aTyr Pharma, AMO Pharma, Acceleron Pharma, Cytokinetics, Expansion Therapeutics, Harmony Biosciences, Regeneron Pharmaceuticals, Astellas Pharmaceuticals, AveXis, Recursion Pharmaceuticals, IRIS Medicine, Inc., Takeda Pharmaceutical Company, Scholar Rock, Avidity Biosciences, Novartis Pharmaceuticals Corporation, SwanBio Therapeutics, and the Marigold Foundation. He receives grant support from the Department of Defense, Duchenne UK, Parent Project Muscular Dystrophy, Recursion Pharmaceuticals, SwanBio Therapeutics, the National Institute of Neurological Disorders and Stroke, the Muscular Dystrophy Association, the Friedreichs Ataxia Research Alliance, Cure Spinal Muscular Atrophy, and the Amyotrophic Lateral Sclerosis Association. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.
 Conflict of Interest Disclosures: Dr Flanagan has served on advisory boards for Alexion, Genentech, UCB, and Horizon Therapeutics outside the submitted work; has a patent for DACH1-IgG as a biomarker of paraneoplastic autoimmunity pending; has received speaker honoraria from Pharmacy Times; has received royalties from UpToDate; was a site primary investigator in a randomized clinical trial on inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics; has received funding from the National Institutes of Health (grant R01NS113828); is a member of the medical advisory board of the MOG project; and is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports. Dr Geschwind reported grants from the National Institute on Aging (grants R01 AG031189, R56 AG055619, and R01 AG062562) and research support from Michael J. Homer Family Fund during the conduct of the study; personal fees from MedConnect Pro LLC Medical Legal, Clarion, Blade Therapeutics, Clearview Healthcare Partners, LifeSci Capital LLC, Ascel Health LLC, Teledoc Health Inc, Microvention Terumo, Reata Pharmaceuticals, Wolters Kluwer, Maupin Cox, Wallace & Milsap LLC, Trinity Partners LLC, Anderson Boutwell Traylor, and Adept Field; nonfinancial support from Ionis Pharmaceuticals; has consulted for Best Doctors Inc, Biohaven Pharma Inc, Bioscience Pharma Partners, LLC, First Thought Consulting, Grand Rounds Inc/UCSF Second Opinion Inc, Quest Diagnostics, and Smith & Hennessey LLC; has received speaking honoraria from Oakstone Publishing; has received research support from Alliance Biosecure, CurePSP, the Tau Consortium, Quest Diagnostics, and the National Institutes of Health; and serves on the board of directors for San Francisco Bay Area Physicians for Social Responsibility and on the editorial board of Dementia & Neuropsychologia. Dr Lopez-Chiriboga has served on advisory boards for Genentech and Horizon Therapeutics. Dr Blackburn reported personal fees from Genentech, grants from Siegel Rare Neuroimmune Association outside the submitted work. Dr Binks reported grants from Wellcome Trust during the conduct of the study and had a patent for Ref. JA94536P.GBA pending (diagnostic strategy to improve specificity of CASPR2 antibody detection). Dr Gelfand reported grants from Genentech/Roche for research support to University of California, San Francisco for clinical trials; service on trial steering committees and grants from Vigil Neuroscience for research support to University of California, San Francisco for clinical research study; and personal fees from Biogen for consulting outside the submitted work. Dr Day reported grants from National Institute on Aging (grant K23AG064029) during the conduct of the study; personal fees from PeerView Media, Continuing Education, DynaMed, and Parabon Nanolabs outside the submitted work; is co–principal investigator of the ExTINGUISH Trial (1U01NS120901); owns stock (>$10 000) in ANI Pharmaceuticals; and is the clinical director of the Anti-NMDA Receptor Encephalitis Foundation (uncompensated). Dr Clardy reported being site investigator for an Alexion clinical trial; grants from National Institute of Neurological Disorders and Stroke for the ExTINGUISH Trial, Western Institute for Veteran Research, and Sumaira Foundation for NMO; research support from Siegel Rare Neuroimmune Association Funding and Barbara Gural Steinmetz Foundation Funding; personal fees from American Academy of Neurology (section editor, Neurology Podcast and Neurology Minute), from Alexion, VielaBio/Horizon, Genentech/Roche, Guidepoint, ExpertConnect, and Clarion Healthcare (majority fees to University of Utah); and funding from Viela Bio/Horizon and Alexion/AstraZeneca outside the submitted work. Dr Solomon reported research funding from Bristol Myers Squibb; consulting and nonpromotional speaking for EMD Serono; personal fees from Genentech, Biogen, Alexion, Celgene, Greenwich Bioscience, and Octave Biosciences; expert witness testimony for Jacob D. Fuchsberg Law Firm and Koskoff, Koskoff, and Bieder; served on advisory board of Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, and TG Therapeutics; and conducted contract research for Sanofi, Biogen, Novartis, Actelion, and Genetech outside the submitted work. Dr Pittock reported grants, personal fees, and nonfinancial support from Alexion and MedImmune/Viela Bio/Horizon (all compensation is paid directly to the Mayo Clinic); grants from the National Institutes of Health, Grifols, NovelMed, and F. Hoffmann-LaRoche/Roche/Genentech (all compensation is paid directly to Mayo Clinic); consulting for Astellas (compensation to Mayo Clinic and personal compensation); personal fees from Sage Therapeutics, UCB, and F. Hoffmann-LaRoche/Roche/Genentech; and had patent #8,889,102 issued, patent #9,891,219B2 issued, and a patent for GFAP-IgG; Septin-5-IgG; MAP1B-IgG; Kelch-like protein 11; PDE10A pending. Dr McKeon reported grants from the National Institutes of Health (grants RO1NS126227 and U01NS120901) during the conduct of the study; consulting fees from Janssen and Roche (all paid to Mayo Clinic) outside the submitted work; and had a patent for MAP1B antibody issued, a patent for Septins 5, 7, GFAP, PDE10A, KLCHL11 antibodies pending, a patent for Septin antibodies licensed, and a patent for MAP1B antibodies with royalties paid. Dr Dubey reported a patent for KLHL11 pending, a patent for LUZP4 pending, and a patent for CAVIN4 pending; and has consulted for UCB, Astellas, Argenx, Immunovant and Arialys pharmaceuticals (all compensation paid directly to Mayo Clinic). Dr Zekeridou reported grants from Roche/Genentech outside the submitted work and had a patent for DACH1-IgG as biomarker of neurological autoimmunity pending and a patent for PDE10A-IgG as biomarker of neurological autoimmunity pending. Dr Vernino has served as a consultant for Alterity, Argenx, Catalyst, Genentech, and Sage Therapeutics and has received research support from Dysautonomia International, BioHaven, Grifols, and Quest Diagnostics (through a licensing contract). Dr Irani reported grants from UCB, CSL Behring, and ONO Pharmaceuticals outside the submitted work; had a patent for LGI1/Caspr2 antibodies with royalties paid from EIAG, a patent for Autoantibody diagnostics issued, and a patent for Relapse predictions pending; and honoraria/research support from UCB, Immunovant, MedImmun, Roche, Janssen, Cerebral therapeutics, ADC therapeutics, Brain, CSL Behring, and ONO Pharmaceuticals. No other disclosures were reported.
 A.G.: Anders Gustavsson is a partner of Quantify Research, providing consultancy services to pharmaceutical companies and other private and public organizations and institutions. A.G. reports the following in the past 3 years outside this work: stock or stock options in Mindmore AB. A.K.: From January 2021 Andreas Karlsson has been a full-time employee of Swedbank, Sweden. A.S.: Anders Sköldunger reports no conflicts of interest. A.T.: Ali Tafazzoli is an employee of Evidera, which provides consulting and other research services to pharmaceutical, medical device, and related organizations. Data collection and sharing for Alzheimer’s Disease Archimedes condition event simulator (ADACE) was funded in part by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). Jorgen Moller and Weicheng Ye contributed to the design of the workshop scenarios. A.W.: Anders Wimo reports the following to conduct this study: grants from ELI-LILLY European Union Innovative Medicines Initiative 2 (IMI2) project grant. Anders Wimo reports the following outside this study: consulting fees from Biogen, consulting fees from EISAI, grants from MSD (research grant, payment to my institution – Karolinska Institutet, Sweden), grants from World Health Organization (WHO) (payment to my institution – Karolinska Institutet, Sweden), grants from Swedish Government – Swedish Study on Aging and Care (SNAC) project (payment to my institution – Karolinska Institutet, Sweden), grants from H2020 EU project Alzheimer’s Disease Archimedes condition event simulator (PRODEMOS): (payment to my institution - Karolinska Institutet, Sweden), grants from Merck; license/royalty from Resource Use in Dementia (RUD) Instrument. SveDem is supported by the Swedish Associations of Local Authorities and Regions, the Swedish Research Council (grant # 2016-02317), FORTE (grant# 2017-0164),Svenska Sällskapet för Medicinsk Forskning, the Swedish Order of St John, the Swedish Stroke Association, and grants from the Regional Agreement on Medical Training and Clinical Research (ALF) between Stockholm County Council and Karolinska Institutet. B.T.: The contributions of Bryan Tysinger and Jakub Hlávka were supported by the National Institute on Aging of the National Institutes of Health under Award Numbers R01AG062277, P30AG024968, and P30AG066589. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. B.T. reports the following in the past 3 years outside the submitted work: participation in the International Microsimulation Association (no payments are involved). B.W.: Bengt Winblad was supported by grant from the Swedish Research Council (2018-02843) and Margaretha af Ugglas’ foundation. B.W. reports participation in SAB for Alzhemed, Axon Neuroscience, Biogen, and Resverlogix. B.W. reports no conflicts of interest. C.B.: Chiara Brück is supported by funding from the Dutch Research Council (grant number 016.Veni.198.020). Chiara Brück reports no competing interest. C.G.: From November 2020 Colin Green has been a full-time employee of Biogen Idec, United Kingdom (UK). C.G. reports the following in the past 3 years outside this study: grants from Institutional funding/grant – To University of Exeter, UK – from the UK Multiple Sclerosis Society, through their open competitive grant funding scheme; consulting fees from payments from Shift Health (Canada) for methods advice on research related to Huntington’s disease; support for attending meetings and/or travel from Gates Foundation for travel/accommodation expenses to attend Expert Advisory Committee Meeting on Alzheimers Disease. E.J.: Dr. Jutkowitz is supported by grants from the National Institute on Aging (1R21AG059623, 1R01AG060871, RF1AG069771). E.J. reports the following in the past 3 years outside this study: Grants to my institution (1R21AG059623, 1R01AG060871, and RF1AG069771) and funding from the Veterans Affairs (VA) National Center on Homelessness Among Veterans; participation in Data Safety Monitoring Board for a National Institute on Aging study awarded to the Indiana University School of Nursing. E.S.: Eldon Spackman reports no competing interest. E.S. reports the following in the past 3 years outside this work: grants from Canadian Institute of Health Research (payment to institution), Alberta Health Services (payment to institution); Alberta Innovates (payment to institution); consulting fees from Canadian Agency for Drugs and Technologies in Health – payment to me Institute for Clinical and Economic Review (payment to me); participation in data safety advisory board GSK (fees payment to me). J.H.: The contributions of Bryan Tysinger and Jakub Hlavka were supported by the National Institute on Aging of the National Institutes of Health under Award Numbers R01AG062277, P30AG024968, and P30AG066589. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. In the past 3 years, J.P.H. has received speaker fees from FTI Consulting and Alzheimer Foundation Czech Republic. J.M.: Basque dementia model project was supported by an unrestricted grant from Nutricia. J.M. reports the following in the past 3 years outside this work: Member of the Board of Spanish Public Health Society. L.J.: Linus Jönsson is an employee of H. Lundbeck A/S, Valby, Denmark, a pharmaceutical company that develops and markets treatments for Alzheimer’s disease and other conditions. L.J. Linus Jönsson reports the following in the past 3 years outside the submitted work: grants from FORTE (research Grant to Karolinska Institutet); license/royalty from Resource Use in Dementia (RUD) instrument license fees (to own company EPS AB); honoraria for lecture Karolinska Institutet Biogen AB (paid to me); board membership of Institute for Health Economics Bengt Jönssons foundation for Health economics research. M.B.: Mark Belger is an employee and minor shareholder in Eli Lilly. M.L.M.: Mauricio Lopez Mendez reports no competing interest. P.L.: Pei-Jung Lin is supported by a grant from the National Institutes of Health (R01AG060165). P.L. Pei-Jung Lin reports the following in the last 3 years outside this work: Research funding support from Alzheimer’s Association, Genentech, and Janssen to Tufts Medical Center. P.S.: Peter Shewmaker reports no competing interest. R.A.: Care Policy Evaluation Centre (CPEC) study was funded by Alzheimer’s Research UK. Robert Anderson reports the following in the past 3 years to conduct this study: payments from Care Policy Evaluation Centre, London School of Economics. R.A. reports the following in the past 3 years outside this study: payments from Nuffield Department of Primary Care Health Sciences, University of Oxford. R.E.: Development of an earlier version of the DAVIS model was supported by funding from Takeda Pharmaceuticals International; no funding was provided for the adaptation presented here. R.H.: Ron Handels reports the following to conduct the study: financial support from the Dutch Alzheimer’s Association, ‘Alzheimer Nederland’, grant number WE.15-2016-09. The funding bodies had no role in the design of the analysis, interpretation of data, and in writing the manuscript. R.H. reports the following in the past 3 years outside this study: consulting fees from Biogen, Eisai, and Erasmus University Rotterdam; public and private-public grants from international frameworks (H2020, Joint Programming Neurodegenerative Diseases (JPND), IMI), national frameworks (Netherlands: ZonMw; Sweden: SNAC and SveDem), and patient organizations (Alzheimer Netherlands). W.H.: William L Herring is an employee of RTI Health Solutions (RTI-HS), an independent nonprofit research organization. Model development and workshop participation were funded in part through research contracts with Janssen Global Services, LLC and Janssen Scientific Affairs, LLC. Josephine Mauskopf of RTI-HS and Alex Keenan and Frank Wiegand of Janssen Global Services, LLC contributed to the model development. Cheryl Neslusan of Janssen Scientific Affairs, LLC contributed to the design of the workshop scenarios. Author disclosures are available in the supporting information.
 Outside this work, C.R.S. has served as consultant, scientific collaborator or on scientific advisory boards for Sanofi, Berg Health, Pfizer and Biogen and has received grants from NIH, U.S. Department of Defense, American Parkinson Disease Association, and the Michael J Fox Foundation (MJFF). C.R.S. is named as co-inventor on U.S. patent applications held by Brigham and Women’s Hospital relating to therapeutics; biomarkers; and polygenic scores for neurodegenerative diseases. M.A.S. has no conflict of interest related to this work. Outside this work, M.A.S. has received grants from NINDS, DoD, MJFF, the Parkinson’s Foundation and Farmer Family Foundation and has served as a consultant to commercial programs: Eli Lilly & Co (data monitoring committee), Prevail Therapeutics (scientific advisory board) and Denali Therapeutics (scientific advisory board); and via the Parkinson Study Group to nQ Medical (scientific advisory board), Chase Therapeutics (scientific advisory board) and Partner Therapeutics (scientific advisory board). A.-M.W. has received research funding from the ALS Association, the Parkinson's Foundation, has participated in clinical trials funded by Acorda, Biogen, Bristol-Myers Squibb, Sanofi/Genzyme, Pfizer and Abbvie and received consultant payments from Mitsubishi Tanabe and Accordant. J.-C.C. has no conflict of interest related to this work. Outside this work, J.C.C. has received honoraria for consulting in advisory boards for Abbvie, Actelion, Air Liquide, Biogen, BMS, BrainEver, Clevexel, Denali, Pfizer, Theranexus and Zambon. B.R. is an employee of and holds equity in Praxis Precision Medicines and is an advisor for Caraway Therapeutics and Brain Neurotherapy Bio. I.S. is the Principal Investigator of a MJFF Computational Science Grant (2017–19). S.K. is supported by Multiple Sclerosis of Western-Australia (MSWA) and the Perron Institute. P.H. is a Scientific Advisor of Neuron23. T.G.B has no conflict of interest related to this work. Outside this work, T.G.B. has received grants from NIA, NINDS, MJFF and the State of Arizona, has served as a scientific advisory board member (with stock options) and consultant to Vivid Genomics, Inc. and has received honoraria from the World PD Coalition. J.J.v.H. has no conflict of interest related to this work. Outside this work, J.J.v.H. has received grants from the Alkemade-Keuls Foundation, Stichting Parkinson Fonds, Parkinson Vereniging, The Netherlands Organisation for Health Research and Development, The Netherlands Organisation for Scientific Research, Hersenstichting, AbbVie, MJFF and research support from Hoffmann-La-Roche, Lundbeck and the Centre of Human Drug Research. R.A.B. has no conflict of interest related to this work. Outside this work, R.A.B. received consultancy monies from LCT, FCDI, Novo Nordisk, Cellino, Sana, UCB; received royalties from Wiley and Springer-Nature; grant funding from CPT, NIHR Cambridge Biomedical Research Centre (146281), MRC, Wellcome (203151/Z/16/Z) and Rosetrees Trust (A1519 M654). C.H.W.-G. has no conflict of interest related to this work. C.H.W.-G. is supported by a RCUK/UKRI Research Innovation Fellowship awarded by the Medical Research Council (MR/R007446/1) and the NIHR Cambridge Biomedical Research Centre and received grant support from MJFF, the Evelyn Trust, the Cure Parkinson’s Trust, Parkinson’s UK, the Rosetrees Trust and the Cambridge Centre for Parkinson-Plus. C.H.W.-G. has received honoraria from Lundbeck and Profile Pharma Ltd and consultancy payments from Modus Outcomes and Evidera. The other authors report no competing interests.
 Declaration of interests The Icahn School of Medicine at Mount Sinai has filed patent applications relating to SARS-CoV-2 serological assays and NDV-based SARS-CoV-2 vaccines, which list F.K. as co-inventor. Mount Sinai has spun out a company, Kantaro, to market serological tests for SARS-CoV-2. F.K. has consulted for Merck and Pfizer (before 2020) and is currently consulting for Pfizer, Seqirus, Third Rock Ventures, Merck, and Avimex. The Krammer laboratory is also collaborating with Pfizer on animal models of SARS-CoV-2. Viviana Simon is a co-inventor on a patent filed relating to SARS-CoV-2 serological assays (the “Serology Assays”). O.L. is a named inventor on patents held by Boston Children’s Hospital relating to vaccine adjuvants and human in vitro platforms that model vaccine action. His laboratory has received research support from GlaxoSmithKline (GSK). C.B.C. serves as a consultant to bioMerieux and is funded for a grant from the Bill & Melinda Gates Foundation. J.A.O. is a consultant at Knocean, Inc. J.L.-S. serves as a scientific advisor of Precion, Inc. S.R.H., G.M., and K.W. are employees of Metabolon, Inc. V.S.-M. is a current employee of MyOwnMed. N.R. reports contracts with Lilly and Sanofi for COVID-19 clinical trials and serves as a consultant for ICON EMMES for consulting on safety for COVID19 clinical trials. A. Rahman is a current employee of Immunai, Inc. S.H.K. is a consultant related to ImmPort data repository for Peraton. N.D.G. is a consultant for Tempus Labs and the National Basketball Association. Akiko Iwasaki is a consultant for 4BIO, Blue Willow Biologics, Revelar Biotherapeutics, RIGImmune, Xanadu Bio, and Paratus Sciences. M. Kraft receives research funds paid to her institution from NIH and ALA and from Sanofi and Astra-Zeneca for work in asthma; serves as a consultant for Astra-Zeneca, Sanofi, Chiesi, and GSK for severe asthma; and is a co-founder and CMO for RaeSedo, Inc., a company created to develop peptidomimetics for treatment of inflammatory lung disease. E. Melamed received research funding from Babson Diagnostics and honorarium from Multiple Sclerosis Association of America and has served on the advisory boards of Genentech, Horizon, Teva, and Viela Bio.
 All authors declare no competing interests.
 Competing interests: PW was a coauthor of trials of both graded exercise therapy and cognitive behaviour therapy, including the PACE trial, is a trustee of the Voluntary Hospital of St Bartholomew’s Charity, was a previous member of Independent Medical Experts Group, which advises the UK MoD on its Armed Forces Compensation Scheme, and receives personal consultancy fees from Swiss Re reinsurance company. BA was a centre leader in the PACE trial. AJC reports grants from NIHR (Physio 4 FMD) and CSO (Long Covid Cognitive phenotyping). AJC is a paid associate editor of JNNP and unpaid president elect of the Functional Neurological Disorders Society (FNDS), he gives expert testimony in court on a range of neuropsychiatric topics on a 50% claimant 50%: defender basis. He is the author of a self-help book based on CBT principles for treatment of FND (no royalties taken). DJC declares grants from Pfizer and Aptinyx; consulting fees from AbbVie, Allergan Sales, Heron Therapeutics, Eli Lilly and Company, Aptinyx, H. Lundbeck A/S, Neumentum, Pfizer, Regeneron Pharmaceuticals, Samumed, Swing Therapeutics, Tonix Pharmaceuticals, Virios Therapeutics. Fees from Fasken Martineau DuMoulin, Kellogg, Hansen, Todd, Figel & Frederick, PLLC, Marks & Clerk Law, Nix Patterson, Pfizer, Zuber Lawler & Del Duca. JC reports consulting fees from Bial, and honoraria from Janssen, Bial and Brittania. BAD reports NIH R13 infrastructure grant for 2022 Functional Neurological Disorders Society meeting in Boston. TC was co-investigator of several trials of behavioural interventions for CFS/ME, including the PACE trial, has received royalties for several books and book chapters on CFS/ME and received payments for workshops on CBT for CFS/ME. BAD is on the board of directors of the FNDS and receives royalties from Oxford University Press for 'Psychogenic Nonepileptic Seizures: Towards the Integration of Care'. She does paid consultancy for Bioserenity (EEG interpretations) and Best Doctors (clinical consultations). She received support to attend the American Epilepsy Society Board of Directors meeting in 2021. She chairs the data safety monitoring board of the DSMB NIH-ESETT trial 2015–2019, and received travel expenses to attend the American Epilepsy Society Board of Directors FNDS meeting and Epilepsy Foundation of New England PAB. MJE reports royalties from Oxford University Press for the book 'The Oxford Specialist Handbook of Movement Disorders', consulting fees from UCB (personal) and Merz Pharma (to his institution), honoraria from the International Parkinson’s Disease and Movement Disorder Society, medicolegal fees for personal injury and clinical negligence cases, support to attend meetings from the FNDS, leadership roles in International Parkinson’s Disease and Movement Disorder Society and Dystonia UK, and is a medical board member of FND Action and FND Hope, and board member of the FNDS. JE was the President of the Faculty of Sport and Exercise Medicine at the time of the Royal College of Physicians’ review of this guideline and submitted comments on behalf of the Faculty. He is Medical Director of a company which occasionally manages patients with CFS/ME. AJE has received grant support from the NIH and the Michael J Fox Foundation, personal compensation as a consultant/scientific advisory board member for Neuroderm, Neurocrine, Amneal, Acadia, Acorda, Bexion, Kyowa Kirin, Sunovion, Supernus (formerly, USWorldMeds), Avion Pharmaceuticals, and Herantis Pharma, and publishing royalties from Lippincott Williams & Wilkins, Cambridge University Press, and Springer. He received an honorarium from Avion. He cofounded REGAIN Therapeutics (a biotech start-up developing nonaggregating peptide analogues as replacement therapies for neurodegenerative diseases) and is co-owner of a patent that covers synthetic soluble nonaggregating peptide analogues as replacement treatments in proteinopathies. PF declares consulting fees from FADL Forlag, Munksgaard, Ny Nordisk Forlag and Arnold Busk, an honorarium from Lundbeck Pharma,and medicolegal fees from Retslægerådet. SF was a co-founding member of the GRADE working group and a member of the GRADE guidance group. She has been engaged in debates related to the evidence regarding CFS/ME for many years from a biopsychosocial perspective. PGlasziou declares an NHMRC Investigator Award: 'Neglected Problems in Health Care' supporting his salary; grants from the National Heart Foundation, Commonwealth Department of Health and WHO for work unconnected to this paper, and is a board member (unpaid) for Therapeutic Guidelines. IH has an NRS Fellowship from CSO, has been paid for medicolegal consultations, receives travel expenses for attending medical conferences and one honorarium from Bristol NHS Neurology Department, and is on the board of Fowler’s syndrome UK Charity. WH was a member of the 2007 NICE Guideline Development Group, and is Chief Medical Officer of LV=, an insurance company. PH was part of the steering committee of the German clinical practice guideline on functional somatic symptoms. MH reports fees for medicolegal expert court reports (none concern CFS/ME). HK reports grants from ZonMw, Stichting NKCV, MS Research, and Dutch Cancer Society, was coauthor of trials of cognitive behaviour therapy, reports royalties for a published treatment manual for CBT for fatigue in CFS/ME, and an honorarium for a lecture from Intercept Pharma Deutschland. A Lehn is an unpaid director of the FNDS. AL reports grants for investigator initiated research grants from Gilead Sciences, AbbVie and Sequiris. AM has been on a trial steering committee for a trial of graded exercise therapy, was formerly the Chair of the British Association for CFS and ME (BACME) and Principal Medical Adviser for Action for ME. IM has been paid honoraria by The@WorkPartnership for lectures on the occupational health management approach to managing long-term conditions (including CFS/ME) in the workplace, is the Academic Dean of the Faculty of Occupational Medicine and commented on the NICE guidelines on the management of CFS/ME on behalf of the Faculty. MM received an honorarium for a lecture in 2020 for ViiV, received financial support to attend the EACS 2021 conference (virtual) and ViiV EACS 2019 conference, and was a centre co-lead for the PACE trial. IN reports research grants received from NIHR and MRC to conduct clinical trials on complex interventions, not specific to CFS/ME, has served on several Data Safety Committee as an independent member for trials on complex interventions, one of which related to CFS/ME, and is Co-Chair of Wellcome Trust/Indian Alliance DBT Team Science Grant and Clinical and Public Health Research Centers Grants Committee. DLP reports grants from the National Institutes of Health and Sidney R. Baer Jr. Foundation for work unrelated to this paper, has received honoraria for continuing medical education lectures at Harvard Medical School and the American Academy of Neurology, royalties from Springer Nature for a textbook on Functional Movement Disorder, is a member of the Board of Directors of the FNDS, senior (paid) editor of Brain and Behavior and is an Editorial Board Member of Epilepsy & Behavior. WP reports occasional paid lectures pertaining to FND (most payments donated to charity), has received fees for expert testimony in court on a range of neurological topics including FND, is a board member of FND Hope and FND Action, and is on the board of directors of the BNPA. MR reports a grant from Elsevier, royalties from Oxford University Press, honoraria from UCB Pharma, LivaNova, Eisai, and Angellini and sits on a data safety monitoring board for IqVia Medtech. WR reports grants from the German Research Foundation, royalties from books and fees for German legal opinions. AS was a member of the 2007 NICE Guideline Development Group for CFS/ME (CG53)]. TS reports being a member of the Board of Directors and Membership and Liaisons Committee of the FNDS and being a member of the Functional Movement Disorders Study Group (Movement Disorders Society). MS was a co-principal investigator for the PACE trial and has led a trial of CBT for CFS/ME. He is current President of the European Association of Psychosomatic Medicine Current (unpaid) and was the previous President of the Academy of Consultation Liaison Psychiatry (unpaid). BS is a Council Member of the Association of British Neurologists and Medical Expert Committee member of FND Hope UK. JS reports grants from Scottish Government and NIHR; royalties from UptoDate, the Donald Baxter Lecture Award, Montreal, titled 'Multiple Sclerosis at the limits', personal fees from expert witness work, Secretary FNDS, Medical Advisor FND Hope, Medical Advisor FND Action, running a self-help website for patients with FND. DTW reports consulting fees for expert opinions on patients in a prolonged disorder of consciousness, fees for occasional medicolegal and personal injury cases, member of NIHR grant Programme Supervisory Committee of a trial of vocational rehabilitation after head injury, Deputy Secretary to British Society of Physical and Rehabilitation Medicine (unpaid) and is employed at a nursing home where he sees 2-3 patients with functional disorders. SCW reports honoraria from two talks on psychological impacts of COVID to Swiss Re during the pandemic, but neither covered CFS nor Long Covid. He is on the Board of the ESRC and am also a member of the Judicial Appointments Commission for which he receives renumeration. None are relevant to this paper. SCW is also on the Board of the South London and Maudsley Foundation NHS Trust for which he receives no renumeration. SCW reports receiving grants to research CFS and has published over 150 papers on this subject, including being an author on several RCTs relevant to this submission, but none within the last 36 months. VW is Head of the Collaborative on Fatigue Following Infection (COFFI) (unpaid). AZ reports fees for expert witness medicolegal reports, but not in cases specifically focused on CFS/ME. No other authors declared any relevant competing interests.
 Declaration of interests CFB, LM, DAN, and SX are employees of Ionis Pharmaceuticals, which funded the trial, and own stock options in Ionis Pharmaceuticals. CAT received support from Ionis Pharmaceuticals for consultation and sponsored research and carried out collaborative research with CFB under National Institutes of Health (NIH) grant U01NS072323; provides consulting to Biogen, Vertex, Entrada, and Avidity Biosciences; received honoraria from Sanofi; served on scientific advisory boards for Dyne and Pepgen; and serves on the Myotonic Dystrophy Foundation Board. KE received consulting fees from Ionis Pharmaceuticals, Avidity, and Dyne Therapeutics; and received honoraria from the Myotonic Dystrophy Foundation and the Muscular Dystrophy Association. CH receives royalties for the use of multiple disease specific instruments; provided consultation to Biogen, Ionis Pharmaceuticals, aTyr Pharma, AMO Pharma, Acceleron Pharma, Cytokinetics, Expansion Therapeutics, Harmony Biosciences, Regeneron Pharmaceuticals, Astellas Pharmaceuticals, AveXis, Recursion Pharmaceuticals, IRIS Medicine, Takeda Pharmaceutical Company, Scholar Rock, Avidity Biosciences, Novartis Pharmaceuticals Corporation, SwanBio Therapeutics, and the Marigold Foundation; and receives grant support from the Department of Defense, Duchenne UK, Parent Project Muscular Dystrophy, Recursion Pharmaceuticals, Swan Bio Therapeutics, Neurocrine Biosciences, the National Institute of Neurological Disorders and Stroke, the Muscular Dystrophy Association, the Friedreich's Ataxia Research Alliance, Cure Spinal Muscular Atrophy, and the Amyotrophic Lateral Sclerosis Association. WDA received a consulting fee and grant funding from Avidity Biosciences and a consulting fee from Dyne Therapeutics. TA received a grant or contract from the Myotonic Dystrophy Foundation and was on the Myotonic Dystrophy Foundation scientific advisory board. JWD received consulting fees from Affinia Therapeutics and Shift Therapeutics; honoraria from Biogen and Roche Pharmaceuticals; participated in advisory boards for AMO Pharmaceuticals, Avidity Biosciences, Biogen, Cytokinetics, Epirium Bio, Ionis Pharmaceuticals, Kate Therapeutics, Novartis Gene Therapies, Roche/Genentech Pharmaceuticals, Sarepta Therapeutics, Scholar Rock, Shift Therapeutics, and Vertex Pharmaceuticals; has leadership roles for Muscular Dystrophy Association, Myotonic Dystrophy Foundation, and Cure Congenital Muscular Dystrophy. GD is an employee of Biogen and owns stock options in Biogen. TD received consulting fees from Dyne, Roche/Genentech Pharmaceuticals, Biogen, Trinds, and ATOM; speaking honoraria for Genentech, Biogen, Roche, and Sarepta; has served on Advisory boards for Novartis, Pfizer, Actigraph, Scholar Rock, Sarepta, Sanofi Genzyme, and Cytokinetics; has unpaid leadership roles for myotonic dystrophy exercise recommendations and physical therapy guidance and the CureSMA Medical Advisory Council. NEJ received royalties or licenses from University of Rochester; received consulting fees from AMO Pharma Fulcrum Therapeutics, Avidity Biosciences, Dyne, Vertex, Arthex, and Entrada; participated in a Data Safety Monitoring Board for Biogen; and owns stock or stock options in ML Bio Solutions. DJL received funding from the DuchenneXchange Advisory Council, Cure Duchenne. JMS received consulting fees from Dyne Therapeutics, Roche, Avidity, ML Bio, Fulcrum Therapeutics, MT Pharma, Sarepta, and Amylyx; payment or honorarium from MDA; and stock or stock options from Dyne Therapeutics. SHS received consulting fees from Reata Pharmaceuticals, Avidity Biosciences, and Dyne therapeutics. KMB was an employee of Ionis Pharmaceuticals at the time the trial was conducted; is a current employee of and owns stock options in Acadia Pharmaceuticals; is an advisor to non-profit organisations Myotonic Dystrophy Foundation and SMA Foundation; and is a Board Member of DTx Pharma. CFB is a Board member of Flamingo Therapeutics and Hereditary Disease Foundation. RM is the chair of three clinical trials in Duchenne muscular dystrophy funded by TRiNDS. All other authors declare no competing interests.




























































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 20230311
 20230222
 20230515
 20220921

 20230818
 20230130
 20230101
 20220831
 20230307
 20230630
 20230207
 20230610
 20230418
 20220917

 20230107
 20221031
 20230510
 20230320
 20221109
 20221128
 20221117

 20221103
 20230208
 20230103
 20230608

 20221117
 20220930

 20230302
 20230519
 20230703
 20220917
 20221008
 20230321
 20230304


 20220905

 20221021
 20221119
 20221105
 20230417
 20230426

 20220913
 20220531

 20221209
 20230703
 20221209
 20230729
 20221229
 20230315
 20230213
 20230717
 20230418
 20230104

 20230605
 20230407
 20221117
 20221018
 20230118
 20221211

 20230310
 20230629
 20221128
 20230530

 20230621
 20230212
 20220712
 20230701
 20220327
 20230610
 20221207
 20230615
 20230306
 20230417
 20230705
 20230804
 20221123
 20221205
 20230321


 20221001
 20210709
 20230802
 20230627
 20230620
 20230623
 20221028
 20230220
 20230221
 20221105
 20221205
 20230425
 20230409

 20221124
 20221130
 20221207
 20230203
 20230718
 20221222
 20230808
 20230404
 20221022
 20230329
 20230814
 20230323

 20221124
 20221109
 20230520
 20230329
 20230425


 20220927
 20230802
 20220712
 20221205
 20221222
 20230311
 20230203
 20221031
 20230707
 20221125
 20221220
 20221013
 20230714
 20230704
 20221207
 20230403
 20230224
 20230506
 20230608
 20230310
 20230518
 20230505
 20230615
 20221220
 20230321
 20221207
 20230216
 20230219
 20230409
 20220901

 20230425
 20221103
 20230313
 20230202
 20230206
 20230714
 20230225
 20230214
 20230312
 20230210
 20230426
 20230130
 20230425
 20230608
 20221205
 20230620
 20230725
 20210801


 20220914
 20230228
 20221224
 20230215
 20230407
 20230705
 20230705
 20230528

 20230323
 20221216
 20230413
 20230220
 20221117
 20230214
 20221209
 20230213
 20230524
 20230120
 20230331
 20230130
 20230309
 20230407
 20230131
 20230518
 20221206
 20230530
 20230301
 20221128
 20221011
 20221229
 20230523
 20220924
 20230411
 20230427
 20230629
 20230222
 20230329
 20230701
 20230405
 20230503
 20230112

 20230417
 20220616

 20230720
 20230315
 20230205
 20220916
 20221101
 20230201
 20230328
 20221118
 20230604
 20221205
 20220828
 20230509
 20230216
 20221227
 20230213
 20230520
 20220425
 20230202
 20230219
 20220818
 20221129
 20230615
 20230125
 20230428
 20230312
 20210911
 20230214
 20230613
 20230714
 20230511
 20230615
 20221110
 20230323
 20230221
 20230419
 20221017
 20221212
 20230205
 20230609
 20221222
 20230329
 20230213

 20230720
 20221205
 20220424
 20220211
 20230412
 20230318
 20230206
 20220317
 20221127
 20221130
 20230501
 20230126
 20230602
 20230321
 20230213

 20221025
 20230721
 20230326
 20230513
 20220312
 20221102
 20230321
 20230125
 20230303
 20230508
 20210617
 20230113
 20220921
 20230424
 20230407

 20230517
 20230120
 20230118

 20230811
 20230705
 20230521
 20230625
 20230704
 20230202
 20230410
 20221109
 20230720
 20230526
 20230802
 20220829
 20230223
 20230731
 20221107
 20221002
 20230310
 20230323
 20230116
 20230518
 20221018
 20230712
 20230217
 20221114
 20221209
 20221102
 20230526
 20221031
 20230129
 20221112
 20221121
 20221223
 20230620
 20211104
 20230306


 20221121
 20230702
 20230704
 20230405
 20230716
 20221212
 20230610

 20220928
 20211227
 20230330
 20230107
 20230407
 20220707

 20230622
 20230327
 20230717
 20230313
 20221020
 20230608
 20230725
 20221124
 20230420
 20230418
 20230529
 20230409
 20221221

 20230427
 20230227
 20230306


 20230325
 20230324



 20230513
 20230312
 20230429
 20230126

 20221104

 20230702
 20230203
 20230624
 20221206
 20230616
 20230322
 20221224
 20230205
 20230218
 20221221
 20221013

 20230306

 20230704
 20220915
 20221105
 20221117
 20230725
 20220826
 20230522
 20230725
 20230213
 20230123
 20221107
 20221128
 20230424
 20230725
 20230526
 20230505
 20230620
 20230527
 20230306
 20230627
 20230513
 20230731
 20221113
 20230610
 20230612
 20230510
 20230427



 20221113
 20230417
 20211024

 20230518
 20230201
 20230410
 20230323
 20230320
 20230212
 20230425
 20221209
 20221130
 20230616
 20230403
 20221117
 20230324
 20230526
 20230221
 20230315
 20221014
 20230418
 20230427
 20230714
 20230219

 20221109
 20230407
 20230221
 20230629
 20230322
 20230209
 20230326
 20230412
 20230719
 20230117
 20221115
 20230325
 20230104
 20221218
 20220621
 20221005

 20230605

 20221122
 20230429
 20230515
 20230201
 20221019
 20221108

 20230124
 20230828
 20220307
 20230221

 20230607
 20221105

 20230719
 20220804
 20230526

 20230521
 20230419
 20230510
 20220305
 20230522
 20230628
 20230613
 20230202

 20221027
 20230126
 20221228
 20230526

 20220815

 20230523
 20230628
 20230202
 20230331

 20230402
 20230624
 20230331
 20220409
 20221228
 20221011
 20210625
 20230101
 20220913
 20221201
 20230113

 20230319
 20230707
 20230411
 20221219
 20230123
 20230615
 20230302
 20221018
 20230705
 20230501
 20230625

 20230719
 20230801
 20230429
 20221110
 20230624
 20230505
 20230418
 20220419
 20230122
 20220810
 20230118
 20230630
 20230416
 20221025


 20230202
 20221217
 20221205
 20230224
 20230629
 20221222
 20230508

 20221213
 20221207
 20221014
 20221113
 20230503
 20230522
 20230418
 20230415

 20230826
 20230618
 20230209
 20230403
 20221215

 20230831
 20221128

 20230405
 20221006
 20230510

 20230728
 20230316
 20230109
 20221117
 20230516
 20230103
 20221109
 20221214
 20230302
 20221123
 20230213
 20230207
 20221213
 20221019
 20230210
 20230803
 20221121
 20230703
 20230120
 20230627
 20230717
 20230708
 20230528
 20230113
 20230601

 20221210
 20230511
 20230125
 20230822
 20230409
 20221227
 20230328
 20230215
 20230201
 20230502
 20230406
 20221125
 20230420
 20221209
 20230620
 20230408
 20230707
 20221125
 20230111
 20220924
 20220830
 20230201
 20230111
 20220924
 20230413
 20220929

 20230529

 20221130
 20211101
 20230418
 20230818
 20230713
 20230126
 20230524
 20221130
 20221022
 20220809
 20221123
 20210811
 20230501
 20230731

 20230623
 20230219

 20230323
 20230810
 20230428

 20230424


 20230131

 20221128
 20220915
 20221223
 20230421
 20230212
 20230212
 20230426
 20221215
 20221028
 20230111
 20230321
 20230709
 20221221
 20210806
 20221026
 20230629
 20230221
 20230221
 20230110
 20230302
 20221227
 20230813
 20230207
 20221213
 20230611
 20220131
 20230628
 20230304
 20221110
 20230129
 20230326
 20221115
 20230331
 20221223
 20221209
 20221208
 20230306
 20221213
 20220504
 20230607
 20230610
 20230602
 20230630
 20230428
 20230119
 20221121
 20230202
 20230525
 20230114
 20221130
 20220615
 20221221
 20230131
 20230422
 20221027

 20230702
 20230324
 20230703
 20221108
 20221012
 20230811
 20220805
 20230619
 20220325
 20230323
 20230102
 20220124
 20230124
 20230302
 20221223
 20230607
 20230516
 20221129
 20221129
 20230305
 20221205
 20230502
 20230812
 20230208
 20230417
 20230314
 20230628
 20221117


 20230411
 20230315

 20230130
 20230428
 20221222
 20230506
 20230530
 20220810

 20230612
 20220919
 20221010

 20230428
 20230414
 20230705
 20230131
 20230228
 20220811
 20230609
 20230517
 20230911

 20230509
 20220727
 20220905

 20230526

 20230124
 20230518
 20230530

 20230413
 20230105

 20220928
 20221115
 20220915
 20230630
 20221130
 20230608
 20230112
 20230704
 20221222
 20221222
 20230414
 20221001
 20230526
 20230726

 20230505
 20230613
 20221119
 20230626
 20221001
 20230620
 20230113
 20230307
 20221221
 20230518
 20230906
 20230128
 20220317
 20230508
 20230620
 20230512
 20221118
 20221026
 20221012
 20230205
 20230516
 20230615
 20230310
 20220907
 20221205
 20230814
 20230402
 20230119

 20230110
 20221117
 20230104
 20230201
 20230501
 20230522


 20230509
 20221116
 20230601
 20230416
 20230713
 20230707
 20230302

 20230524
 20230210
 20221114
 20230602
 20230121

 20230130
 20230522
 20221008
 20221224

 20230129
 20220305
 20230322
 20230309
 20210915

 20221122

 20230126
 20230216
 20230506
 20230628
 20221117
 20221206
 20221202
 20221221
 20230623
 20221021


 20230622
 20221212
 20230822
 20230530
 20230205
 20230130
 20230315
 20230104
 20230127
 20230516
 20230317
 20230605
 20230207
 20221003
 20230201
 20230503
 20220916
 20230411
 20230417
 20230309
 20220210
 20230525
 20230721
 20221213
 20230104
 20230522
 20221124

 20220410
 20221221
 20221111


 20230118

 20230803
 20230323
 20221223
 20220708
 20230726

 20221101
 20221219
 20230609
 20221219
 20221216
 20230629

 20221218
 20230603
 20230212
 20230630
 20220425
 20230105
 20230205
 20230604
 20230113
 20230829
 20221223
 20221230
 20221212
 20230620
 20230804
 20230211
 20230214
 20230514
 20230506
 20220912
 20230711
 20230214
 20210819
 20230707
 20230629
 20221110
 20221117
 20230217
 20230307
 20221113
 20230722
 20230312
 20230111

 20230310
 20230103
 20230516
 20230210
 20230403

 20230810
 20230624

 20220929

 20230324
 20220324
 20230403
 20230802
 20220426
 20230506
 20230731
 20230201
 20230217
 20221216
 20230122
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 20230228
 20230409
 20230518
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 20230206
 20230220
 20230317
 20230414
 20230501
 20230206
 20220516
 20220130
 20230103
 20230215
 20220924
 20230220
 20230406

 20230316
 20221121
 20221102
 20230221
 20230405
 20230221

 20230418
 20230628
 20220826
 20230302
 20220927
 20221118
 20230117
 20230427
 20221111
 20230501
 20230125
 20230228
 20230704

 20230219
 20230401
 20221226
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 20230414
 20230718
 20230227
 20230708
 20230324


 20221122
 20230330
 20230725
 20221013
 20230119
 20230121
 20230130
 20230320
 20230501

 20230219
 20230529



 20230601

 20230604
 20230829
 20221229
 20221223
 20230327
 20230317
 20221114
 20230420
 20230817
 20210127

 20230302
 20221223
 20230306
 20230213
 20230118
 20230217
 20230411
 20230703

 20230506
 20230621
 20230509
 20221215
 20221026
 20230331
 20230314
 20221201
 20230524
 20230120
 20230329
 20230425
 20230511

 20230526
 20230725
 20230903

 20221118
 20230126

 20230323

 20221130
 20230330
 20230526
 20230422
 20221007
 20230609
 20221201
 20230428

 20230505
 20220516
 20230625
 20230102
 20230201
 20230819
 20230417
 20230224

 20221113
 20221228
 20221217
 20221018
 20230116
 20221217
 20220321
 20230419
 20230509
 20230417
 20221205
 20221223

 20230323
 20230707
 20230323
 20230325
 20230226
 20230307
 20230710
 20230721
 20230325
 20230208

 20230717
 20230806
 20230330
 20230120
 20220209
 20221213
 20230417
 20221112
 20230109
 20220930
 20221015
 20220926
 20230103
 20230220
 20230218
 20220817
 20230305

 20230630
 20230118
 20221220

 20220928
 20230221
 20230701
 20230309
 20230209
 20221223
 20230608

 20230706
 20230307
 20221228
 20220830
 20221020
 20230330
 20230705
 20230705
 20230613
 20230530
 20230306
 20230103
 20230211
 20221126
 20230111
 20230605

 20230625
 20230403
 20230328
 20230209
 20230425
 20230213
 20230417


 20230301
 20230331

 20230213
 20230807
 20211001
 20230527
 20230902
 20230207
 20230215
 20230322
 20221223
 20230224
 20220912
 20230405
 20230724
 20230801
 20230510

 20230508
 20230628
 20220812
 20221227
 20230904
 20230622
 20230710
 20230104
 20221028

 20230403


 20220520
 20221013
 20230802
 20230126
 20230619
 20230214
 20230104
 20230622
 20221029
 20230119
 20230107
 20230328
 20230113



 20230504
 20230617
 20230429

 20230713
 20220901
 20230113
 20221227
 20230203
 20230618
 20230105
 20220915
 20230124
 20220924
 20221124
 20230709

 20230123
 20230318

 20230301
 20221114
 20230103
 20230322
 20221214
 20230414
 20221128
 20230104
 20230519
 20230524
 20220824
 20230519
 20230208
 20230215
 20230407
 20221020


 20230628
 20220721
 20230204
 20220707

 20230704
 20230519
 20220729
 20221013
 20230208
 20230403
 20230619

 20230420

 20230811
 20221107

 20221007
 20230523
 20230306
 20221123
 20230616
 20230110
 20230113
 20230501
 20230414

 20230602

 20221220
 20230215
 20221128

 20230701
 20220406
 20230323
 20230409
 20230418

 20221118
 20230522
 20221130
 20220903
 20230322
 20230123
 20230317

 20221222
 20230106
 20230329
 20230201
 20221103
 20230726

 20221228
 20230816
 20230123
 20220827
 20230426
 20220913
 20230525
 20230429
 20230603
 20230629
 20220804
 20230416
 20221209

 20221215
 20230228
 20230124

 20230826
 20230131
 20230729
 20221001
 20230703
 20230328
 20230301
 20230724
 20230311
 20230112
 20221217
 20230130
 20230114
 20230414
 20230511
 20230609
 20221018

 20230306
 20230310
 20230123
 20220517
 20230502

 20220215
 20230718

 20221217
 20221122
 20230609
 20211105
 20230211
 20230406
 20230503
 20230421
 20230207
 20230120
 20230707
 20230217
 20230529
 20221207

 20230210
 20230724
 20230817
 20220907
 20230201
 20230203
 20230615

 20221128
 20230512
 20230130
 20230716
 20220926
 20230308
 20230105
 20230821
 20230324
 20230505
 20230624
 20221119
 20221215
 20220720
 20230323

 20230810
 20230623
 20221224
 20221129
 20230406
 20230225
 20230609
 20230220
 20221229
 20221227
 20230618
 20230525
 20230613
 20230203
 20221010
 20230429
 20230221
 20230105
 20230509
 20230602
 20220606
 20230710
 20221130
 20230216
 20221129
 20230424
 20230107
 20230214
 20230809

 20230825
 20230110
 20230705
 20230126
 20230316
 20220628
 20220328
 20230528
 20220427
 20230621

 20230227

 20230209
 20221124
 20230323
 20230629
 20230612
 20221217
 20221110
 20221025
 20230131
 20221123
 20230727
 20221215
 20230528
 20230512
 20220923
 20230608
 20230725
 20230405
 20220614
 20230327
 20220921
 20230707

 20230911
 20230117
 20221004
 20230113
 20221202
 20221116
 20221206
 20230726
 20230413
 20230602

 20220805
 20230707
 20230801
 20230630
 20230404
 20230818
 20230828
 20230331
 20230312
 20230425
 20221028
 20230804
 20230112
 20230601
 20220309
 20230215
 20230405
 20230413
 20220420
 20230630
 20221014
 20230523
 20221129

 20221102
 20221116
 20230108
 20220824
 20230221
 20230522
 20230727
 20230527
 20230525
 20221209
 20221123
 20220709
 20221205
 20221212
 20230609
 20230815
 20230512
 20230224
 20230510
 20230330
 20221113
 20230426


 20230214
 20230526
 20230819
 20230112
 20230125

 20230318
 20230131
 20221219
 20230605
 20230122
 20230112
 20230423
 20230104
 20230313
 20230320
 20230411
 20230519
 20230608
 20230118
 20220725
 20230528
 20230905
 20230320
 20230510
 20230104
 20230212
 20230211
 20230223

 20221118
 20201201

 20230215
 20230307
 20230515
 20230106
 20230120
 20230713
 20230629
 20230211
 20221214
 20230518
 20230607
 20230602
 20230104
 20230821
 20230123
 20230629

 20221224
 20230424
 20230118
 20230518
 20230406
 20230104
 20230628
 20230331
 20221020
 20230608
 20230222
 20230119
 20221205
 20230315
 20221214
 20230519
 20221121
 20230404
 20230117
 20220623
 20230417
 20221207
 20230114

 20221230
 20230130
 20230123
 20230531
 20230602
 20230216
 20230407
 20230317
 20221114
 20221130
 20230707
 20230710
 20221115
 20230120
 20230720
 20230313
 20230728
 20230622
 20230412
 20221213

 20230131
 20211020
 20230306
 20230206
 20230517
 20230609
 20221104
 20230629
 20230323
 20230206
 20230215
 20230307
 20230102
 20230218
 20230801
 20230705
 20230619
 20221223

 20220801

 20230901
 20230217
 20230124
 20230611
 20230825
 20230312
 20230603

 20230601
 20221003
 20230330
 20221223
 20230308
 20221229
 20230114
 20230331
 20230322

 20221212
 20221216
 20230601
 20230503
 20230628
 20221016
 20221121
 20221028
 20230808
 20230524
 20221224
 20221214

 20230529
 20230510
 20221209
 20230517
 20230305
 20230114
 20230331
 20230129
 20230213
 20230609
 20221214
 20230619
 20230618
 20221213
 20230625
 20230616
 20230104
 20221214
 20230304

 20230516
 20221109
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 20230717
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 20230228
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 20230524
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 20220520
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 20230404
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 20230429
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 20230522
 20230606
 20230405
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 20230127
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 20230519
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 20230324
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 20230123
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 20230825
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 20230526
 20230525
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 20230823
 20230113
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 20230713

 20230504


 20230612
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 20230428
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 20230611
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 20230703
 20230818
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 20221028
 20230629
 20230310

 20230217
 20230620
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 20221118
 20230330
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 20230713
 20230626
 20230318

 20230728
 20230514
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 20230822
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 20230610
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 20230113
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 20221018
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 20230130
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 20220830
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 20230625
 20230519
 20230123
 20230904
 20230906
 20230726
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 20230901
 20230908


 20230807
 20221003


 20230717

 20230725
 20230104
 20230814
 20230728
 20230412
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 20230608
 20230628
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 20230101
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 20230717
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 20230101

 20230420

 20230830
 20230508
 20230307
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 20230912
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 20230706
 20230522
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 20230312
 20230203
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 20230816
 20230714
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 20230804
 20230801
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 20230503
 20221020
 20230828
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 20221225
 20230706
 20230508
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 20220311
 20230523
 20230804
 20230104
 20230523
 20230905

 20230416
 20230713
 20230824


 20230811
 20230717
 20230530
 20221227
 20220907
 20230801
 20230704
 20230327
 20230308
 20230308

 20221110

 20230726
 20230710
 20230601
 20230403
 20230314
 20230322
 20230123
 20230116
 20220908
 20230623
 20230602
 20230524
 20230503
 20230301
 20221228
 20230613
 20230519
 20230314
 20230120
 20230829


 20230825
 20230331
 20220908
 20230215
 20230515
 20230223
 20230407
 20230625

 20230417


 20230908
 20230601
 20230728
 20230728
 20230629

 20230517
 20230220
 20230809
 20230620
 20230404
 20230217
 20230126
 20230110
 20221102
 20230418
 20230728
 20230623
 20230613
 20230227

 20220717
 20230727
 20230626
 20230804
 20230523
 20230414
 20220505
 20230129
 20230208
 20230821
 20230818
 20230119
 20211213
 20201013
 20230621
 20230302
 20230120
 20220304
 20230816
 20230826
 20221209
 20230713
 20221123
 20230317
 20230724
 20230120
 20221208
 20230601
 20230905
 20230620
 20230707

 20230424
 20230323

 20230317
 20230312
 20230309
 20230223
 20230105
 20230203
 20221228
 20220809
 20230809
 20230819
 20230815
 20230728
 20230430
 20230624
 20230516
 20230411
 20230428

 20230407
 20230129
 20230216
 20230204
 20230204
 20230116
 20230119
 20221219
 20221120
 20230701
 20230726
 20230902
 20230823
 20230628
 20230712
 20230725

 20230628
 20230602
 20230606
 20230327
 20230311
 20230321
 20230306
 20230303
 20230307

 20230210
 20230207
 20230123
 20230120
 20230118
 20230105
 20221116
 20220826

 20220127
 20230829
 20230901
 20230826
 20230627
 20230718
 20230724
 20230703


 20230403
 20230317
 20230228
 20230131
 20230210
 20230125
 20230126
 20230209
 20230125
 20230205
 20230104

 20230910
 20230830
 20230723
 20230201
 20220628
 20230817
 20230703
 20230531
 20230909
 20221130
 20230330
 20221125
 20230829
 20220309
 20230417
 20230527
 20221217
 20230504
 20230901
 20230622
 20221005
 20221228
 20221202
 20230221
 20230106
 20230208
 20220415

 20230816
 20230704
 20230711
 20230705
 20230612
 20230511
 20230409
 20230308
 20230316
 20230301
 20230105
 20221212
 20221026
 20221017
 20230628
 20230731
 20230717
 20230728

 20230724
 20230711
 20230624
 20230425
 20230330
 20220802
 20230404
 20230301
 20230210
 20221223
 20221205
 20221107
 20221123
 20220509
 20211231
 20210827
 20230914
 20230710
 20230828
 20230710
 20230711
 20230201
 20230621
 20230614
 20230510
 20230417
 20230322
 20230304
 20230316
 20230313
 20230308
 20230203
 20230112
 20221213
 20220916
 20220916
 20220617
 20230717
 20230811
 20230805
 20230723

 20230601
 20230601

 20230301
 20230214
 20230110
 20230102
 20230102

 20221129


 20221109
 20221012
 20230512
 20230323
 20230623
 20230327

 20230820
 20230620
 20230524
 20230712
 20230128
 20230213
 20220911
 20230809
 20230419
 20230316
 20230405
 20230331
 20230323
 20230809
 20230107
 20230308
 20230211
 20230114
 20230606
 20230423
 20230628
 20230621
 20230511

 20230825
 20230802
 20230414
 20230611
 20230504
 20230406
 20230328
 20230405
 20230315
 20230216
 20230227
 20230208
 20230103

 20220826
 20220808
 20230824
 20230720
 20230725
 20230717
 20230714
 20230629
 20230609
 20230426
 20230414
 20230315
 20230306
 20230201
 20230110
 20221215
 20221208
 20220627
 20230831
 20230902

 20230828
 20230801
 20230713
 20230710
 20230711
 20230630
 20230626
 20230528
 20230424
 20230408

 20221126
 20221205
 20221128
 20221103

 20220701
 20220330
 20230822

 20230804
 20230725


 20230512
 20230504
 20230428

 20230420
 20230315
 20230220
 20230203
 20230201
 20221201
 20221010
 20220920
 20230905

 20230419
 20230407
 20221026
 20230308

 20230131
 20230808
 20230419

 20230728
 20230323
 20230413

 20230323
 20230426
 20230808
 20221029
 20230719
 20230526
 20230814
 20230526
 20230630
 20230607
 20230425
 20230504
 20230413
 20230201
 20230326
 20230206

 20230208
 20230110
 20221223

 20210513
 20230904
 20230914
 20230809
 20230726
 20230627
 20230703
 20230629
 20230614
 20230617
 20230616
 20230526
 20221127
 20230521
 20230418
 20230429
 20230414
 20230329
 20230214
 20230206
 20230218
 20220825
 20230914
 20230728
 20230721
 20230704

 20230520
 20230418
 20230413
 20230411
 20230408
 20230304
 20230201
 20221226
 20221130
 20230821

 20230620
 20230531
 20230514
 20230328
 20230217

 20230104
 20221019
 20230910
 20230531

 20221130
 20230811

 20230222
 20221117
 20230418
 20221102
 20221225
 20230131
 20230602
 20230214
 20230822
 20230217
 20230813
 20230613
 20230623
 20230607
 20230425
 20230330
 20230124
 20230103
 20221026


 20230715
 20230608
 20230601
 20230627
 20230117
 20230106
 20221220
 20230804
 20230810

 20230808
 20230630
 20230722
 20230715
 20230512
 20230321

 20230117
 20221220
 20221119
 20221130
 20230815
 20230804
 20230601

 20230504
 20230412
 20230403
 20230324
 20230325
 20230208
 20230125
 20230123
 20221219
 20221214
 20221102
 20230606
 20230328

 20230505
 20230120
 20230301
 20230707
 20230516
 20221226
 20230329
 20221214
 20221205
 20230628
 20230908
 20230713

 20230829
 20230901
 20230811
 20230707
 20230424
 20230417
 20230401
 20230216
 20230130
 20230123
 20221114
 20220609
 20220214
 20230911
 20230907
 20230729
 20230809
 20230627
 20230325

 20221123
 20230804
 20230626
 20230616
 20230525
 20230530
 20230602
 20230325
 20230203
 20230213
 20230426
 20230112
 20230102
 20221101
 20221010
 20230811
 20230715
 20230426
 20230503
 20230329
 20230117

 20230218
 20230203
 20230201
 20230106

 20221011
 20220822
 20221116

 20230219

 20230601

 20230614
 20230301
 20230515

 20230404
 20230221


 20230207
 20230313
 20230131
 20230720

 20230404
 20220317
 20230317
 20230208
 20230729
 20230614
 20230612

 20230130
 20221205
 20221021
 20230802
 20230607
 20230512
 20230830
 20230828
 20230619
 20230327
 20230326

 20230728
 20230728
 20230525
 20230412

 20230621
 20230526
 20230806
 20230221
 20230606
 20230503
 20230824
 20210531
 20230516
 20230619
 20230102
 20230512
 20230323
 20230501
 20230315
 20230131
 20230210
 20220216
 20230228
 20230120
 20221215
 20230907
 20230707
 20230522
 20230311
 20230814
 20220828
 20230602
 20230223
 20230301
 20230515
 20230201
 20230531
 20230203

 20230908
 20230705
 20230727
 20230610
 20230525
 20230221
 20230913
 20230707
 20230728
 20230818
 20220810
 20230519
 20230207

 20230716
 20220915
 20230101
 20230624
 20230421
 20230713
 20230703
 20230519

 20230824
 20230820
 20230428
 20230101
 20230413
 20221209
 20230617
 20230504
 20230803
 20230110
 20230724
 20230608
 20230424
 20230214
 20230125
 20230104
 20230103
 20221005
 20220913
 20230324
 20230324
 20230223
 20221010
 20230731
 20230508
 20230423
 20221125
 20230411
 20230504
 20230423
 20230714
 20230502


 20230214
 20230405
 20230329
 20230822
 20230708
 20230114

 20230519
 20230407
 20230515
 20230212
 20221124
 20230830
 20230406
 20230617
 20221124
 20230712
 20230518
 20230111
 20230719
 20230807


 20230202
 20230706
 20230214
 20220720
 20220526
 20230503
 20230719
 20221101
 20230901
 20230816
 20230828
 20230828


 20230209
 20230210

 20230517

 20220115
 20230426
 20230823
 20220830
 20230130
 20221105
 20221211
 20230221
 20230531
 20230331
 20220412
 20230718
 20221112
 20230804
 20230704
 20230603
 20230505
 20230414
 20230828
 20230724
 20230820
 20230712
 20230421
 20230508
 20230404
 20230714
 20230509
 20230908
 20230803
 20230613
 20230202
 20230831
 20230524
 20230403
 20230410
 20230808
 20230103
 20230622
 20230531
 20230427

 20230701
 20230621
 20230530
 20230607


 20230616

 20220905
 20230120
 20221129
 20230624
 20230427
 20230525
 20230315
 20230422
 20230809

 20220624
 20230823
 20230524
 20230314
 20220601
 20220928
 20221228
 20220805
 20230312
 20230823
 20230630
 20230819
 20230719
 20230221
 20230615
 20230220
 20230320
 20230712

 20221114
 20230419
 20230622
 20230316
 20221117
 20230608
 20230419
 20221124

 20230119

 20230612
 20221221
 20230630
 20230507
 20230321

 20230228
 20230228
 20230213
 20230906
 20230116
 20230812
 20230528

 20230907
 20230901
 20230505
 20230203
 20230830
 20230728
 20230630
 20230527
 20230824
 20230718
 20230705
 20230410

 20230418
 20220117
 20230425
 20230801
 20230707
 20230315
 20230815
 20230616
 20230430
 20221008
 20230531
 20230307
 20221103
 20230527
 20230212
 20230807
 20221126
 20230211
 20221013
 20221214
 20230830
 20230519
 20230207
 20230605
 20221221
 20230331
 20230825
 20230215
 20230804
 20230424
 20230805
 20230509
 20230324
 20230329
 20230412
 20221209
 20230202
 20230220
 20230505
 20230804
 20230709
 20230414
 20230110
 20230215
 20230714
 20230412
 20220603
 20230427
 20230211
 20230208
 20230516
 20230607
 20230519
 20230209
 20230217
 20230105
 20230703
 20230220



 20230317
 20230702
 20230629
 20230404
 20230307

 20230309
 20230314
 20230504
 20230907
 20230724
 20230905
 20230816
 20230614
 20221121
 20221214
 20230309
 20230606
 20230310
 20230603
 20230106
 20221117
 20230701
 20230404
 20221218
 20230622
 20230523
 20230505
 20230109
 20221210
 20230225
 20221212
 20221211
 20230825
 20230324
 20230227
 20221121
 20230828
 20230410
 20221202
 20230817
 20230131
 20230602
 20230628
 20230203
 20220504

 20230525
 20230226
 20230730
 20230513
 20230321
 20230111
 20230725
 20230708
 20230608
 20230510
 20230830
 20230505
 20230412
 20230401
 20230515
 20221026
 20230822
 20230224

 20230503
 20221019

 20230609
 20230905

 20230322
 20230502
 20221207
 20230428
 20220915
 20221228
 20230222

 20230806

 20230404
 20230816
 20230526

 20230105
 20230703
 20230731
 20230629
 20230228
 20230216
 20230212
 20221208
 20230907
 20230521
 20230911
 20230224
 20230307
 20230217
 20230606

 20221202
 20230725

 20221106

 20230123
 20230515
 20230525



 20230821
 20230116
 20230117
 20221102
 20230823
 20230420
 20230803
 20230309
 20230830
 20230714
 20230119
 20230307
 20221111
 20230608
 20230420
 20221030
 20221107
 20230525
 20230404

 20230302
 20221014
 20230518
 20230206
 20230620
 20230618
 20230608
 20230815
 20230418
 20230613
 20221012
 20230629

 20230322
 20230323
 20230215
 20230724
 20230425
 20230405
 20230809
 20230123
 20230109
 20221125
 20230620
 20230504
 20221226
 20230413
 20221004
 20221027
 20220725


 20230716
 20230710
 20230321
 20230320
 20230219
 20230105
 20230103
 20221101

 20221102
 20230428
 20230420
 20230411
 20230331
 20230905
 20230724
 20230201
 20230811
 20221129
 20230818
 20230803
 20230320
 20230419
 20230311
 20221224
 20220908
 20230811
 20230323
 20230204
 20230623
 20230309
 20230125
 20221205
 20230804
 20221116
 20230329
 20221224
 20230325
 20221201
 20230803

 20230516

 20230807
 20230712
 20230521
 20220927
 20230504
 20221017
 20230302
 20230801
 20230801
 20230310
 20230707
 20230417
 20230504
 20221229
 20230109
 20230711
 20230706
 20221207
 20230816
 20230828

 20221025

 20230523
 20230519
 20230710

 2023 Jan
 2023 Jan
 2023 Aug 1
 2023 Feb
 2023 Jan
 2023 Jul
 2023 Apr
 2023 Apr
 2023 Jan
 2023 Feb
 2023 Mar
 2023 Mar
 2023 Sep
 2023 Mar
 2023
 2023 May
 2023 Sep
 2023 Jul
 2023 Mar
 2023 Jun 1
 2023 Apr
 2023 Aug
 2023 Jan
 2023 Aug 1
 2023 Aug
 2023 Mar
 2023 Jun
 2023 May 4
 2023 Jul
 2023 Sep
 2023 Aug
 2023 May
 2023 Apr 4
 2023 Apr
 2023 Jul
 2023 Feb
 2023 Aug
 2023 Mar
 2023 Jun 29
 2023 Sep
 2023 Aug
 2023 Jun
 2023 Jun
 2023 Jul 17
 2023 Mar
 2023 Mar
 2023 Mar
 2023 Jul
 2023 Aug
 2023 Feb
 2023 Feb
 2023 May
 2023 Mar 6
 2023 Jun 8
 2023 Aug
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 2023
 2023 Aug
 2023 Jul
 2023
 2023 Apr
 2023 Jan
 2023 Feb
 2023
 2023
 2023 Feb
 2023 Mar
 2023 Jan 3
 2023 May 2
 2023 Jun
 2023
 2023 Dec
 2023 May
 2023 Jun
 2023 Sep
 2023 Aug
 2023 Feb 1
 2023 Jun
 2023 Jul
 2023 Feb 28
 2023 Apr 15
 2023 Aug 28
 2023 Jan
 2023
 2023 Jan 21
 2023 Jun
 2023 May 2
 2023 Jul
 2023 Feb 22
 2023 May
 2023 Jan
 2023 Jul 1
 2023 Aug 18
 2023
 2023 Mar
 2023 Jun
 2023 Apr
 2023 Aug 8
 2023 Apr
 2023 Aug
 2023 Apr 18
 2023 Jan
 2023 Aug
 2023 Feb
 2023 Feb
 2023 Jul
 2023 Mar 20
 2023 Feb
 2023 Mar
 2023 Mar
 2023 Jan
 2023 Apr
 2023 Feb 8
 2023
 2023 Aug 1
 2023 Apr
 2023 Jan
 2023 Jan
 2023 Jul 25
 2023 Jun
 2023 Jun 1
 2023 Aug
 2023 Jan
 2023 Jan
 2023 May
 2023 Apr
 2023 Apr 26
 2023 Jan
 2023 Jan
 2023 Jan
 2023 Jan 15
 2023 Jan
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 2023 Aug
 2023 Jun 1
 2023 Jan
 2023 May
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 2023 Jan
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 2023 Feb 13
 2023 Sep 5
 2023 Jul 4
 2023 Jan 4
 2023 Jul 1
 2023 Aug
 2023 May 15
 2023 Feb
 2023 Feb
 2023 Mar
 2023 Jan 15
 2023 May-Jun
 2023 Apr
 2023 Aug
 2023 Jan
 2023 May 30
 2023 Apr 1
 2023 Aug
 2023 Mar
 2023 Mar
 2023 Jul 1
 2023 Feb
 2023 Aug
 2023 Apr
 2023 Jul
 2023 Mar 16
 2023 Aug
 2023 May
 2023 Sep
 2023 Jan
 2023 Jan
 2023 May
 2023 Jul 25
 2023 Apr
 2023 Jan
 2023 Feb
 2023 Oct 1
 2023 Aug
 2023 Sep
 2023 Sep
 2023 Jan
 2023 Mar
 2023 Sep
 2023 Feb
 2023 Jan
 2023 Apr
 2023 Jun
 2023
 2023 Jan
 2023 Feb
 2023
 2023 Mar 1
 2023 Aug
 2023 Apr
 2023 Oct 1
 2023 Apr 4
 2023 Jan
 2023 Aug
 2023
 2023 Mar
 2023 Jul-Aug 01
 2023 Jan
 2023 Jan
 2023 Oct
 2023 Mar 29
 2023 Aug
 2023 Aug 1
 2023 Sep
 2023 Feb 1
 2023 Aug 2
 2023 Jul
 2023 Jan
 2023 May
 2023 Apr
 2023 Mar
 2023 Jan
 2023 Aug
 2023 Jan
 2023 Apr 4
 2023 Feb
 2023 Jul 14
 2023 Jul 4
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 2023 Jun
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 2023 Jun 8
 2023
 2023 Apr
 2023
 2023 Aug 8
 2023 May
 2023 Apr
 2023 Jan 15
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 2023 Apr
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 2023 Mar
 2023 Jul 1
 2023 Jul
 2023 Jan 21
 2023 Jul-Sep
 2023 Mar
 2023 Mar
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 2023 May
 2023 Apr
 2023 Feb 10
 2023 Sep
 2023 Jun 3
 2023 Jul
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 2023
 2023 Jun
 2023 Jun 29
 2023 Jun 29
 2023 Jan
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 2023 Feb
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 2023 Sep
 2023 Jun
 2023 May 31
 2023 Jul
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 2023 Jun 1
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 2023 May 24
 2023 Feb
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 2023 May-Jun
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 2023
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 2023
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 2023 Jan 3
 2023 Feb 1
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 2023 May 15
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 2023
 2023 Jan 12
 2023 Dec
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 2023 Jun 21
 2023 Oct
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 2023
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 2023 Jan
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 2023 May
 2023 Jan 15
 2023 Jun 4
 2023
 2023 Feb 1
 2023 Jul
 2023 Apr
 2023 Jan
 2023 Feb 13
 2023 Oct
 2023 Mar
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 2023 Sep
 2023
 2023 Aug
 2023 May
 2023 Jul-Aug
 2023 Mar
 2023 Aug
 2023 Jul 14
 2023 Jul
 2023 Jul
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 2023 Mar
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 2023 Feb 15
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 2023 Mar
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 2023
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 2023
 2023
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 2023
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 2023 Jan-Feb
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 2023 May
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 2023 Mar
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 2023 Jul-Aug 01
 2023 Jun
 2023 May
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 2023
 2023 Jan 21
 2023 May 17
 2023 Jan 20
 2023 May
 2023 Apr 10
 2023
 2023 Sep 12
 2023 Aug
 2023 Aug
 2023 Jul 4
 2023 Jul
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 2023
 2023 Feb
 2023 Jan
 2023 Jan
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 2023 Feb 15
 2023 Aug
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 2023 Mar 6
 2023
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 2023 Aug 1
 2023 Jul 25
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 2023
 2023 Jun
 2023 Feb 28
 2023 Jan-Dec
 2023 Aug
 2023 Feb 27
 2023 Jun
 2023
 2023 Aug 31
 2023 Mar 29
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 2023 Jun 1
 2023 Jul 15
 2023 Jun
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 2023
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 2023 Mar 22
 2023 Apr
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 Pratt VM Scott SA Pirmohamed M Esquivel B Kattman BL Malheiro AJ












































































































































































































 Adam MP Mirzaa GM Pagon RA Wallace SE Bean LJH Gripp KW Amemiya A























































































































































 Adam MP Mirzaa GM Pagon RA Wallace SE Bean LJH Gripp KW Amemiya A
















































































































































































































































































































































































































































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 Sepulveda-Falla, Diego Villegas Lanau, Carlos Andrés White, Charles Serrano, Geidy E Acosta-Uribe, Juliana Mejía-Cupajita, Barbara Villalba-Moreno, Nelson David Lu, Pinzhang Glatzel, Markus Kofler, Julia K Ghetti, Bernardino Frosch, Matthew P Lopera Restrepo, Francisco Kosik, Kenneth S Beach, Thomas G
 Seabury, Jamison Rosero, Spencer Varma, Anika Weinstein, Jennifer Engebrecht, Charlotte Dilek, Nuran Heatwole, John Alexandrou, Danae Cohen, Brittany Larkindale, Jane Lynch, David R Park, Courtney Subramony, Sub H Wagner, Ellen Walther, Susan Wells, McKenzie Zizzi, Christine Heatwole, Chad
 Flanagan, Eoin P Geschwind, Michael D Lopez-Chiriboga, A Sebastian Blackburn, Kyle M Turaga, Sanchit Binks, Sophie Zitser, Jennifer Gelfand, Jeffrey M Day, Gregory S Dunham, S Richard Rodenbeck, Stefanie J Clardy, Stacey L Solomon, Andrew J Pittock, Sean J McKeon, Andrew Dubey, Divyanshu Zekeridou, Anastasia Toledano, Michel Turner, Lindsey E Vernino, Steven Irani, Sarosh R
 Handels, Ron L H Green, Colin Gustavsson, Anders Herring, William L Winblad, Bengt Wimo, Anders Sköldunger, Anders Karlsson, Andreas Anderson, Robert Belger, Mark Brück, Chiara Espinosa, Robert Hlávka, Jakub P Jutkowitz, Eric Lin, Pei-Jung Mendez, Mauricio Lopez Mar, Javier Shewmaker, Peter Spackman, Eldon Tafazzoli, Ali Tysinger, Bryan Jönsson, Linus
 Liu, Ganqiang Ni, Chunming Zhan, Jiamin Li, Weimin Luo, Junfeng Liao, Zhixiang Locascio, Joseph J Xian, Wenbiao Chen, Ling Pei, Zhong Corvol, Jean-Christophe Maple-Grødem, Jodi Campbell, Meghan C Elbaz, Alexis Lesage, Suzanne Brice, Alexis Hung, Albert Y Schwarzschild, Michael A Hayes, Michael T Wills, Anne-Marie Ravina, Bernard Shoulson, Ira Taba, Pille Kõks, Sulev Beach, Thomas G Cormier-Dequaire, Florence Alves, Guido Tysnes, Ole-Bjørn Perlmutter, Joel S Heutink, Peter van Hilten, Jacobus J Barker, Roger A Williams-Gray, Caroline H Scherzer, Clemens R
 Diray-Arce, Joann Fourati, Slim Doni Jayavelu, Naresh Patel, Ravi Maguire, Cole Chang, Ana C Dandekar, Ravi Qi, Jingjing Lee, Brian H van Zalm, Patrick Schroeder, Andrew Chen, Ernie Konstorum, Anna Brito, Anderson Gygi, Jeremy P Kho, Alvin Chen, Jing Pawar, Shrikant Gonzalez-Reiche, Ana Silvia Hoch, Annmarie Milliren, Carly E Overton, James A Westendorf, Kerstin Cairns, Charles B Rouphael, Nadine Bosinger, Steven E Kim-Schulze, Seunghee Krammer, Florian Rosen, Lindsey Grubaugh, Nathan D van Bakel, Harm Wilson, Michael Rajan, Jayant Steen, Hanno Eckalbar, Walter Cotsapas, Chris Langelier, Charles R Levy, Ofer Altman, Matthew C Maecker, Holden Montgomery, Ruth R Haddad, Elias K Sekaly, Rafick P Esserman, Denise Ozonoff, Al Becker, Patrice M Augustine, Alison D Guan, Leying Peters, Bjoern Kleinstein, Steven H
 Owolabi, Mayowa O Leonardi, Matilde Bassetti, Claudio Jaarsma, Joke Hawrot, Tadeusz Makanjuola, Akintomiwa I Dhamija, Rajinder K Feng, Wuwei Straub, Volker Camaradou, Jennifer Dodick, David W Sunna, Rosita Menon, Bindu Wright, Claire Lynch, Chris Chadha, Antonella Santuccione Ferretti, Maria Teresa Dé, Anna Catsman-Berrevoets, Coriene E Gichu, Muthoni Tassorelli, Cristina Oliver, David Paulus, Walter Mohammed, Ramla K Charway-Felli, Augustina Rostasy, Kevin Feigin, Valery Craven, Audrey Cunningham, Elizabeth Galvin, Orla Perry, Alexandra Heumber Fink, Ericka L Baneke, Peer Helme, Anne Laurson-Doube, Joanna Medina, Marco T Roa, Juan David Hogl, Birgit O'Bryan, Allan Trenkwalder, Claudia Wilmshurst, Jo Akinyemi, Rufus O Yaria, Joseph O Good, David C Hoemberg, Volker Boon, Paul Wiebe, Samuel Cross, J Helen Haas, Magali Jabalpurwala, Inez Mojasevic, Marijeta DiLuca, Monica Barbarino, Paola Clarke, Stephanie Zuberi, Sameer M Olowoyo, Paul Owolabi, Ayomide Oyesiku, Nelson Maly-Sundgren, Pia C Norrving, Bo Soekadar, Surjo R van Doorn, Pieter A Lewis, Richard Solomon, Tom Servadei, Franco
 White, Peter Abbey, Susan Angus, Brian Ball, Harriet A Buchwald, Dedra S Burness, Christine Carson, Alan J Chalder, Trudie Clauw, Daniel J Coebergh, Jan David, Anthony S Dworetzky, Barbara A Edwards, Mark J Espay, Alberto J Etherington, John Fink, Per Flottorp, Signe Garcin, Béatrice Garner, Paul Glasziou, Paul Hamilton, Willie Henningsen, Peter Hoeritzauer, Ingrid Husain, Mujtaba Huys, Anne-Catherine M L Knoop, Hans Kroenke, Kurt Lehn, Alexander Levenson, James L Little, Paul Lloyd, Andrew Madan, Ira van der Meer, Jos W M Miller, Alastair Murphy, Maurice Nazareth, Irwin Perez, David L Phillips, Wendy Reuber, Markus Rief, Winfried Santhouse, Alastair Serranova, Tereza Sharpe, Michael Stanton, Biba Stewart, Donna E Stone, Jon Tinazzi, Michele Wade, Derick T Wessely, Simon C Wyller, Vegard Zeman, Adam
 Thornton, Charles A Moxley, Richard Thomas 3rd Eichinger, Katy Heatwole, Chad Mignon, Laurence Arnold, W David Ashizawa, Tetsuo Day, John W Dent, Gersham Tanner, Matthew K Duong, Tina Greene, Ericka P Herbelin, Laura Johnson, Nicholas E King, Wendy Kissel, John T Leung, Doris G Lott, Donovan J Norris, Daniel A Pucillo, Evan M Schell, Wendy Statland, Jeffrey M Stinson, Nikia Subramony, Sub H Xia, Shuting Bishop, Kathie M Bennett, C Frank


































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































 Pratt, Victoria M Scott, Stuart A Pirmohamed, Munir Esquivel, Bernard Kattman, Brandi L Malheiro, Adriana J












































































































































































































 Adam, Margaret P Mirzaa, Ghayda M Pagon, Roberta A Wallace, Stephanie E Bean, Lora JH Gripp, Karen W Amemiya, Anne























































































































































 Adam, Margaret P Mirzaa, Ghayda M Pagon, Roberta A Wallace, Stephanie E Bean, Lora JH Gripp, Karen W Amemiya, Anne
















































































































































































































































































































































































































































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 Harroud, Adil Stridh, Pernilla McCauley, Jacob L Saarela, Janna van den Bosch, Aletta M R Engelenburg, Hendrik J Beecham, Ashley H Alfredsson, Lars Alikhani, Katayoun Amezcua, Lilyana Andlauer, Till F M Ban, Maria Barcellos, Lisa F Barizzone, Nadia Berge, Tone Berthele, Achim Bittner, Stefan Bos, Steffan D Briggs, Farren B S Caillier, Stacy J Calabresi, Peter A Caputo, Domenico Carmona-Burgos, David X Cavalla, Paola Celius, Elisabeth G Cerono, Gabriel Chinea, Angel R Chitnis, Tanuja Clarelli, Ferdinando Comabella, Manuel Comi, Giancarlo Cotsapas, Chris Cree, Bruce C A D'Alfonso, Sandra Dardiotis, Efthimios De Jager, Philip L Delgado, Silvia R Dubois, Bénédicte Engel, Sinah Esposito, Federica Fabis-Pedrini, Marzena J Filippi, Massimo Fitzgerald, Kathryn C Gasperi, Christiane Gomez, Lissette Gomez, Refujia Hadjigeorgiou, Georgios Hamann, Jörg Held, Friederike Henry, Roland G Hillert, Jan Huang, Jesse Huitinga, Inge Islam, Talat Isobe, Noriko Jagodic, Maja Kermode, Allan G Khalil, Michael Kilpatrick, Trevor J Konidari, Ioanna Kreft, Karim L Lechner-Scott, Jeannette Leone, Maurizio Luessi, Felix Malhotra, Sunny Manouchehrinia, Ali Manrique, Clara P Martinelli-Boneschi, Filippo Martinez, Andrea C Martinez-Maldonado, Viviana Mascia, Elisabetta Metz, Luanne M Midaglia, Luciana Montalban, Xavier Oksenberg, Jorge R Olsson, Tomas Oturai, Annette Pääkkönen, Kimmo Parnell, Grant P Patsopoulos, Nikolaos A Pericak-Vance, Margaret A Piehl, Fredrik Rubio, Justin P Santaniello, Adam Santoro, Silvia Schaefer, Catherine Sellebjerg, Finn Shams, Hengameh Shchetynsky, Klementy Silva, Claudia Siokas, Vasileios Søndergaard, Helle B Sorosina, Melissa Taylor, Bruce Vandebergh, Marijne Vasileiou, Elena S Vecchio, Domizia Voortman, Margarete M Weiner, Howard L Wever, Dennis Yong, V Wee Hafler, David A Stewart, Graeme J Compston, Alastair Zipp, Frauke Harbo, Hanne F Hemmer, Bernhard Goris, An Smolders, Joost Hauser, Stephen L Kockum, Ingrid Sawcer, Stephen J Baranzini, Sergio E Harroud, Adil Jónsdóttir, Ingileif Blanco, Yolanda Llufriu, Sara Madireddy, Lohith Saiz, Albert Villoslada, Pablo Stefánsson, Kári





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 Bourdette, Dennis Yadav, Vijayshree Goodman, Andrew Racke, Michael Fallis, Robert Tornatore, Carlo Goldman, Myla Kannan, Meena Sriram, Subramaniam Berger, Joseph Cross, Anne Rammohan, Kottil Xia, Zongqi Leist, Thomas Lynch, Sharon Klawiter, Eric Amezcua, Lilyana Bowen, James



























 Arnoldus, Epj Barkhof, F Bouvy, W H van Dijk, G W van Eijk, Jjj Eurelings, M van Genugten, J Hoitsma, E Hoogervorst, Elj de Jong, B A Kalkers, N F van Kempen, Zle Killestein, J Kloosterziel, M E Kragt, J J Lierop, Zygj van Lissenberg-Witte, B I Moraal, B Mostert, J P van Munster, Cep Nielsen, J van Oosten, B W Rispens, T van Rooij, L C Roosendaal, C M Sinnige, Lgf Strijbis, Emm Toorop, A A Uitdehaag, Bmj Vennegoor, A Wokke, Bha Zeinstra, Empe













 Dear, Keith Dwyer, Terry Blizzard, Leigh Lucas, Robyn M Kilpatrick, Trevor Williams, David Lechner-Scott, Jeanette Shaw, Cameron Chapman, Caron Coulthard, Alan Pender, Michael P Valery, Patricia







































 Barkhof, Frederik Ciccarelli, Olga Stefano, Nicola de Enzinger, Christian Filippi, Massimo Gasperini, Claudio Kappos, Ludwig Palace, Jacqueline Rocca, Maria A Rovira, Àlex Sastre-Garriga, Jaume Vrenken, Hugo

















































































































































































































































































































 Fraser, Clare Abegg, Mathias Alroughani, Raed Alshowaeir, Daniah Alvarenga, Regina Andris, Cécile Asgari, Nasrin Barnett, Yael Battistella, Roberto Behbehani, Raed Berger, Thomas Bikbov, Mukharram M Biotti, Damien Biousse, Valerie Boschi, Antonella Brazdil, Milan Brezhnev, Andrei Calabresi, Peter Cordonnier, Monique Costello, Fiona Cruz, Franz Marie Cunha, Leonardo Provetti Daoudi, Smail Deschamps, Romain DeSeze, Jerome Diem, Ricarda Etemadifar, Masoud Flores-Rivera, Jose Fonseca, Pedro Frederiksen, Jette Frohman, Elliot Frohman, Teresa FromentTilikete, Caroline Fujihara, Kazuo Gálvez, Alberto Gouider, Riadh Gracia, Fernando Grigoriadis, Nikolaos Guajardo, José Manuel Habek, Mario Hawlina, Marko Hernández-Martínez de Lapiscina, Elena Hooker, Juzar Hor, Jyh Yung Howlett, William Huang-Link, Yumin Idrissova, Zhannat Illes, Zsolt Jancic, Jasna Jindahra, Panitha Karussis, Dimitrios Kerty, Emilia Kim, Ho Jin Lagrèze, Wolf Leocani, Letizia Levin, Netta Liskova, Petra Maiga, Youssoufa Marignier, Romain McGuigan, Chris Meira, Dália Merle, Harold Monteiro, Mário L R Moodley, Anand Moura, Frederico Muñoz, Silvia Mustafa, Sharik Nakashima, Ichiro Noval, Susana Oehninger, Carlos Ogun, Olufunmilola Omoti, Afekhide Pandit, Lekha Paul, Friedemann Rebolleda, Gema Reddel, Stephen Rejdak, Konrad Rejdak, Robert Rodriguez-Morales, Alfonso Rougier, Marie-Bénédicte Sa, Maria Jose Sanchez-Dalmau, Bernardo Saylor, Deanna Shatriah, Ismail Siva, Aksel Stiebel-Kalish, Hadas Szatmary, Gabriella Ta, Linh Tenembaum, Sylvia Tran, Huy Trufanov, Yevgen VanPesch, Vincent Wang, An-Guor Wattjes, Mike P Willoughby, Ernie Zakaria, Magd Zvornicanin, Jasmin Balcer, Laura Plant, Gordon T






















































































































 Bolton, James M Sareen, Jitender Singer, Alexander Lix, Lisa M El-Gabalawy, Renée Katz, Alan Berrigan, Lindsay Peschken, Christine Kowalec, Kaarina







































































































 Brownlee, Wallace Wynne, Megan Hockey, Leanne Parker, Josephine Flight, Jennifer Frost, Chris Nicholas, Jennifer Nixon, Stuart Beveridge, Judy Chandran, Siddharthan Connick, Peter Lyle, Dawn Galea, Ian Jarman, Elisabeth Ford, Helen Fernandes, Linford Vinjam, Maruthi Pavitt, Sue Sharrack, Basil Paling, David Shehu, Abdullah Arun, Tarunya Belhag, Mohamed Pearson, Owen Ingram, Gillian Rickards, Christopher McDonnell, Gavin Hughes, Stella Spilker, Cord Fisniku, Leonora Aram, Julia Rice, Claire Pluchino, Stefano Peruzzotti-Jametti, Luca Harikrishnan, Sreedharan Guck, Nikki Robertson, Neil Tallantyre, Emma Harrower, Timothy Gallagher, Paul Ahmed, Fayyaz Young, Carolyn Arndt, Heike Silber, Eli Nicholas, Richard Duddy, Martin Lee, Martin Evangelou, Nikos Allen, Christopher Craner, Matthew Geraldes, Ruth Hobart, Jeremy Hillier, Charles Chhetri, Suresh Mattoscio, Miriam Chaudhuri, Abhijit Kalra, Seema Straukiene, Agne Rog, David





































































































 Lucas, Robyn M Dear, Keith Dwyer, Terry Broadley, Simon Kilpatrick, Trevor Williams, David Shaw, Cameron Chapman, Caron Coulthard, Alan Pender, Michael P Valery, Patricia



 Huseyinsinoglu, Burcu Ersoz Ben-Zacharia, Aliza Bitton Cohen, E T Gonçalves, Paulo Jorge Correia Kragt, J Jolijn Hynes, Sinéad M Marron, Frances Elizabeth
















































 van der Mei, Ingrid Broadley, Simon Ponsonby, Anne-Louise Dear, Keith Dwyer, Terry Blizzard, Leigh Lucas, Robyn M Kilpatrick, Trevor Williams, David Lechner-Scott, Jeanette Shaw, Cameron Chapman, Caron Coulthard, Alan Pender, Michael P





































































































 Vd Kooi, A J Raaphorst, J Koos Zwinderman, A H Löwenberg, M Volkers, A G D'Haens, G R A M Takkenberg, R B Tas, S W Spuls, P I Bekkenk, M W Musters, A H Post, N F Bosma, A L Hilhorst, M L Vegting, Y Bemelman, F J Verstegen, N J M Fernandez, L Keijzer, S Keijser, J B D Cristianawati, O Voskuyl, A E Broens, B Sanchez, A P Nejentsev, S Mirfazeli, E S Wolbink, G J Boekel, L Rutgers, B A de Leeuw, K Horváth, B Verschuuren, J J G M Ruiter, A M van Ouwerkerk, L van der Woude, D Allaart, Rcf Teng, Yko Busch, M H Brusse, E van Doorn, P A Baars, Mae Hijnen, D J Schreurs, Crg van der Pol, W L Goedee, H S van Els, C A C M de Wit, J






 Pearson, John F Clarke, Glynnis Abernethy, David A Willoughby, Ernest Sabel, Clive E









































 Albrecht, Walter Bischof, Felix Bittkau, Foroogh Bittkau, Simon Bohr, Kin-Arno Borries, Bettina Brockmeier, Bernd Brummer, Dagmar Bühler, Bernhard Butz, Wolfgang Cepek, Lukas Claassen, Lars Dee, Jürgen Dieterle, Lienhard Drees, Eckehard Engelmann, Christoph Ernst, Michael Fasold, Oliver Fischer, Johannes Flach, Michael Fleischer, Robert Friedrich, Lea Friedrich, Anke Fritzinger, Michael Gehring, Klaus Gierer, Stephanie Gierer, Stephan Gößling, Jens Grips, Eva Haldenwanger, Andreas Hans-Joachim Harth, Andreas Hartmann, Rolf Helm, Roland Herbst, Heinz-Peter Hofer, Christian Hofmann, Werner Erwin Hoge, Alexander Hummel, Sibylla Ikenberg, Benno Israel-Willner, Heike Jankovits, Ralf Kallmann, Boris-Alexander Kausch, Ulrich Keppler, Marc Kessler, Kirn Kirchhöfer, Ulrike Kirchmeier, Jürgen Knoblich, Rupert Knoll, Thomas Knorn, Philipp Köchling, Monika Kornhuber, Anselm Wolfgang Kramer, Bernd Krause, Michaela Krauß, Martin Kubalek, Ralf Kunz, Jürgen Landefeld, Harald Lange, Thomas Lehmann-Horn, Klaus Lippert, Esther Lippmann, Karla Maier-Janson, Walter Märkl, Martin Masri, Said Moser, Christof Neusch, Clemens Niemann, Julius Paschke, Tilmann Peikert, Anna Sybilla Peikert, Andreas Peters, Henning Pfister, Robert Reifschneider, Gerd Ries, Stefan Rieth, Christoph Roick, Holger Roth, Gerhard Dieter Roth, Roland Safavi, Ali Saur, Joachim Schmitt-Roth, Brigitte Scholz, Erich Franz Schreiber, Herbert Schreiber, Klaus Schrey, Christoph Schumann, Carsten Seiler, Martin Sigel, Karl-Otto Sikora, Viola Sotiriadis, Nikolaos Spiegel, Stefanie Städt, Detlef Sühnel, Torsten Tiel-Wilck, Klaus Ulzheimer, Jochen Christoph Unsorg, Barbara Sofie Voith, Silvia Wannenmacher, Achim Stephan Weber, Hildegund Weih, Markus Wendtland, Bernd Wiborg, Andreas Wimmer, Martin Winker, Thomas Wontroba, Isaak Wüstenhagen, Monika























































































































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 Horakova, Dana Buzzard, Katherine Terzi, Murat Prat, Alexandre Girard, Marc Grammond, Pierre Barnett, Michael Stewart, Grace Onofrj, Marco Izquierdo, Guillermo Eichau, Sara Grand'Maison, Francois Prevost, Julie Van Wijmeersch, Bart Amato, Maria Pia Shaygannejad, Vahid Boz, Cavit Bolaños, Ricardo Fernandez Soysal, Aysun Ramo-Tello, Cristina Solaro, Claudio Gobbi, Claudio Cabrera-Gomez, Jose Antonio Roullet, Etienne Zwanikken, Cees Den Braber-Moerland, Leontien Deri, Norma Saladino, Maria Laura Cristiano, Edgardo Rojas, Juan Ignacio Vrech, Carlos Shaw, Cameron Shuey, Neil Boggild, Mike Tan, Ik Lin Hardy, Todd Decoo, Danny Moore, Fraser Oh, Jiwon Lalive, Patrice Ampapa, Radek Petersen, Thor Oreja-Guevara, Celia Perez Sempere, Angel Dominguez, Jose Andres Besora, Sarah Hughes, Stella Gray, Orla Grigoriadis, Nikolaos Piroska, Imre Rozsa, Csilla Kasa, Krisztian Simo, Magdolna Kovacs, Krisztina Sas, Attila Dobos, Eniko Rajda, Cecilia McGuigan, Chris Mason, Deborah Schepel, Jan Alkhaboori, Jabir Rio, Maria Edite Mihaela, Simu Al-Harbi, Talal Altintas, Ayse Kister, Ilya Marriott, Mark Kilpatrick, Trevor King, John Nguyen, Ai-Lan Dwyer, Chris Monif, Mastura Roos, Izanne Taylor, Lisa Diamanti, Matteo Chisari, Clara Toscano, Simona Salvatore, Lo Fermo Larochelle, Catherine De Luca, Giovanna Di Tommaso, Valeria Travaglini, Daniela Pietrolongo, Erika di Ioia, Maria Farina, Deborah Mancinelli, Luca Hupperts, Raymond Olascoaga, Javier Saiz, Albert Zivadinov, Robert Benedict, Ralph Verheul, Freek Fabis-Pedrini, Marzena











































































































 Barkhof, F de Stefano, N Sastre-Garriga, J Ciccarelli, O Enzinger, C Filippi, M Gasperini, C Kappos, L Palace, J Vrenken, H Rovira, À Rocca, M A Yousry, T
















































































 Maglione, Alessandro Di Sapio, Alessia Laroni, Alice Iovino, Aniello Mannironi, Antonio Uccelli, Antonio Nucciarone, Barbara Serrati, Carlo Nicoletti, Carolina Gabri Lapucci, Caterina Mancinelli, Chiara Rosa Cordioli, Cinzia Bezzini, Daiana Carmagnini, Daniele Brogi, Davide Nicola, De Stefano Landi, Doriana Nobile Orazio, Eduardo Cocco, Eleonora Signoriello, Elisabetta Nako, Enri Assandri, Ester Marinelli, Fabiana Baldi, Federica Caleri, Francesca Siciliano, Gabriele Cola, Gaia Perego, Germana Lus, Giacomo Brichetto, Giampaolo Bellucci, Gianmarco Da Rin, Giorgio Marfia, Girolama Alessandra Vazzoler, Giulia Liberatore, Giuseppe Trivelli, Giuseppe Callari, Graziella Gandoglia, Ilaria Schiavetti, Irene Frau, Jessica Pasquali, Livia Petrucci, Loredana Lorefice, Lorena Ruggiero, Lucia Salvetti, Marco Monti Bragadin, Margherita Buscarinu, Maria Chiara Gagliardi, Maria Sormani, Maria Pia Ferrò, Maria Teresa Rilla, Maria Teresa Clerico, Marinella Battaglia, Mario Alberto Fronza, Marzia Del Sette, Massimo Inglese, Matilde Scialabba, Matteo Bedognetti, Michele Ulivelli, Monica De Rossi, Nicola Gazzola, Paola Bigi, Rachele Dubbioso, Raffaele Reniè, Roberta Iodice, Rosa Fabbri, Sabrina Rasia, Sarah Parodi, Sergio Rolla, Simona Platzgummer, Stefan Maria Laura, Stromillo Tassinari, Tiziana Carlini, Valentina





























 Moln Ar, Fanni Eszter Rauer, Sebastian Wabbels, Bettina Noll, Marion M Uller, Marcus Guthoff, Tanja Guthoff, Rainer Aktas, Orhan Kruse, Freidrich E Huhn, Konstantin Nickel, Florian T Linker, Ralf A Fitzner, Dirk Hein, Katharina van Oterendorp, Christian Zipp, Frauke Uphaus, Timo Fleischer, Vinzenz Siller, Nelly Lorenz, Katrin Beck, Anna Pitz, Susanna Elflein, Heike Hartmann, Kathrin K Umpfel, Tanja Mulazzani, Elisabeth Wilhelm, Helmut Zielmann, Ulf Heesen, Christoph Stellmann, Patrick Rosenkranz, Sina





















































































 Abad, S Bayen, M Bielefeld, P Chalumeau, M Chiquet, C Cohen, J-D Despert, V Devilliers, H Fardeau, C Georgin-Lavialle, S Guex-Crosier, Y Guillaume Czitrom, S Heron, E Hofer, M Agbo Kpati, K P Labalette, P Lemelle, I Nouar, D Pugnet, G Sellam, J Sene, D Terrier, B Trad, G S






























 Altieri, Manuela Borgo, Riccardo Capuano, Rocco Storelli, Loredana Pagani, Elisabetta Sibilia, Mauro Piervincenzi, Claudia Ruggieri, Serena Petsas, Nikolaos Cortese, Rosa Stromillo, Maria Laura































































 Metspalu, Andres Milani, Lili Mägi, Reedik Nelis, Mari Hudjašov, Georgi












































 Chapman, Caron Coulthard, Alan Dear, Keith Dwyer, Terry Kilpatrick, Trevor Lucas, Robyn McMichael, Tony Ponsonby, Anne-Louise Taylor, Bruce Valery, Patricia van der Mei, Ingrid Williams, David
























































 Leist, Thomas P Habib, Lily Udugama, Paarami Gray, Orla Horakova, Dana Sartori, Charlotte More, Rein Siddiqui, Ana Farr, Pamela Stupar, Dusko Tang, Cynthia Le, Alison Smirnova, Sonya Palshetkar, Gaurang Spelman, Tim

 Ferrari, Raffaele Hernandez, Dena G Nalls, Michael A Rohrer, Jonathan D Ramasamy, Adaikalavan Kwok, John B J Dobson-Stone, Carol Brooks, William S Schofield, Peter R Halliday, Glenda M Hodges, John R Piguet, Olivier Bartley, Lauren Thompson, Elizabeth Haan, Eric Hernández, Isabel Ruiz, Agustín Boada, Mercè Borroni, Barbara Padovani, Alessandro Cruchaga, Carlos Cairns, Nigel J Benussi, Luisa Binetti, Giuliano Ghidoni, Roberta Forloni, Gianluigi Galimberti, Daniela Fenoglio, Chiara Serpente, Maria Scarpini, Elio Clarimón, Jordi Lleó, Alberto Blesa, Rafael Waldö, Maria Landqvist Nilsson, Karin Nilsson, Christer Mackenzie, Ian R A Hsiung, Ging-Yuek R Mann, David M A Grafman, Jordan Morris, Christopher M Attems, Johannes Griffiths, Timothy D McKeith, Ian G Thomas, Alan J Pietrini, P Huey, Edward D Wassermann, Eric M Baborie, Atik Jaros, Evelyn Tierney, Michael C Pastor, Pau Razquin, Cristina Ortega-Cubero, Sara Alonso, Elena Perneczky, Robert Diehl-Schmid, Janine Alexopoulos, Panagiotis Kurz, Alexander Rainero, Innocenzo Rubino, Elisa Pinessi, Lorenzo Rogaeva, Ekaterina St George-Hyslop, Peter Rossi, Giacomina Tagliavini, Fabrizio Giaccone, Giorgio Rowe, James B Schlachetzki, Johannes C M Uphill, James Collinge, John Mead, Simon Danek, Adrian Van Deerlin, Vivianna M Grossman, Murray Trojanowski, John Q van der Zee, Julie Deschamps, William Van Langenhove, Tim Cruts, Marc Van Broeckhoven, Christine Cappa, Stefano F Le Ber, Isabelle Hannequin, Didier Golfier, Véronique Vercelletto, Martine Brice, Alexis Nacmias, Benedetta Sorbi, Sandro Bagnoli, Silvia Piaceri, Irene Nielsen, Jørgen E Hjermind, Lena E Riemenschneider, Matthias Mayhaus, Manuel Ibach, Bernd Gasparoni, Gilles Pichler, Sabrina Gu, Wei Rossor, Martin N Fox, Nick C Warren, Jason D Spillantini, Maria Grazia Morris, Huw R Rizzu, Patrizia Heutink, Peter Snowden, Julie S Rollinson, Sara Richardson, Anna Gerhard, Alexander Bruni, Amalia C Maletta, Raffaele Frangipane, Francesca Cupidi, Chiara Bernardi, Livia Anfossi, Maria Gallo, Maura Conidi, Maria Elena Smirne, Nicoletta Rademakers, Rosa Baker, Matt Dickson, Dennis W Graff-Radford, Neill R Petersen, Ronald C Knopman, David Josephs, Keith A Boeve, Bradley F Parisi, Joseph E Seeley, William W Miller, Bruce L Karydas, Anna M Rosen, Howard van Swieten, John C Dopper, Elise G P Seelaar, Harro Pijnenburg, Yolande A L Scheltens, Philip Logroscino, Giancarlo Capozzo, Rosa Novelli, Valeria Puca, Annibale A Franceschi, Massimo Postiglione, Alfredo Milan, Graziella Sorrentino, Paolo Kristiansen, Mark Chiang, Huei-Hsin Graff, Caroline Pasquier, Florence Rollin, Adeline Deramecourt, Vincent Lebert, Florence Kapogiannis, Dimitrios Ferrucci, Luigi Pickering-Brown, Stuart Singleton, Andrew B Hardy, John Momeni, Parastoo











 Coles, Alasdair Chataway, Jeremy Duddy, Martin Emsley, Hedley Ford, Helen Fisniku, Leonora Galea, Ian Harrower, Timothy Hobart, Jeremy Huseyin, Huseyin Kipps, Christopher M Marta, Monica McDonnell, Gavin V McLean, Brendan Pearson, Owen R Rog, David Schmierer, Klaus Sharrack, Basil Straukiene, Agne Ford, David V









































































































































 Akhtar, Shaheen Anwar, Mohammad Arciero, Elena Asgar, Omar Ashraf, Samina Breen, Gerome Chung, Raymond Curtis, Charles J Chaudhary, Shabana Chowdhury, Maharun Colligan, Grainne Deloukas, Panos Durham, Ceri Durrani, Faiza Eto, Fabiola Finer, Sarah Garcia, Ana Angel Griffiths, Chris Harvey, Joanne Heng, Teng Huang, Qin Qin Hurles, Matt Hunt, Karen A Hussain, Shapna Islam, Kamrul Jacobs, Benjamin M Khan, Ahsan Khan, Amara Lavery, Cath Lee, Sang Hyuck Lerner, Robin MacArthur, Daniel Malawsky, Daniel Martin, Hilary Mason, Dan Mazid, Mohammed Bodrul McDermott, John McSweeney, Sanam Miah, Shefa Munir, Sabrina Newman, Bill Owor, Elizabeth Qureshi, Asma Rahman, Samiha Safa, Nishat Solly, John Tahmasebi, Farah Trembath, Richard C Tricker, Karen Uddin, Nasir van Heel, David A Winckley, Caroline Wright, John
















































































































































































































































































































































































































































































































































































































































 Lucas, Robyn Dear, Keith Ponsonby, Anne-Louise van der Mei, Ingrid Blizzard, Leigh Simpson-Yap, Steve Taylor, Bruce V Broadley, Simon Kilpatrick, Trevor Williams, David Lechner-Scott, Jeannette Shaw, Cameron Chapman, Caron Coulthard, Alan Valery, Patricia








































































































































































































 Branger, Pierre Abrous, Mouloud Zéphir, Hélène Petit, Julie Vukusic, Sandra Gelet, Céline Carra-Dallière, Clarisse Ayrignac, Xavier Russello, Mélanie Laplaud, David Gaultier, Alina Le Frère, Fabienne Callier, Céline Caillon, Cynthia Gueydan, Eglantine Louapre, Céline Galanaud, Damien Ungureanu, Aurelian Coudoin, Sylvie Hebant, Benjamin Gerard, Emmanuel Vimont, Christine Biotti, Damien Bonneville, Fabrice Freitas, Noellie Duman, Taskin Kilic, Erhan Tutuncu, Melih Uygunoglu, Ugur Destan, Sena Sen, Sedat Friedli, Christoph Wagner, Franca Weber, Lea Tchoubar, Annaig Dumont, Emilie Eryilmaz, Asli Roman, Tanguy Pelletreau, Christopher Grateau, Aurélie Mathieu, Yanica Yaiche, Sarhan Rintelen, Felix Firmino, Isabel De Chastenier, Aymeric Gheribenblidia, Amel Zeydan, Burcu










































































































 Aguglia, U Amato, M P Ancona, A L Ardito, B Avolio, C Balgera, R Banfi, P Barcella, V Barone, P Bellantonio, P Berardinelli, A Bergamaschi, R Bertora, P Bianchi, M Bramanti, P Brescia Morra, V Brichetto, G Brioschi, A M Buccafusca, M Bucello, S Busillo, V Calchetti, B Cantello, R Capobianco, M Capone, F Capone, L Cargnelutti, D Carozzi, M Cartechini, E Cavaletti, G Cavalla, P Celani, M G Clerici, R Clerico, M Cocco, E Torri Clerici, V Coniglio, M G Conte, A Corea, F Cottone, S Crociani, P D'Andrea, F Danni, M C De Luca, G de Pascalis, D De Riz, M De Robertis, F De Rosa, G De Stefano, N Della Corte, M Di Sapio, A Docimo, R Falcini, M Falcone, N Fermi, S Ferraro, E Ferrò, M T Fortunato, M Foschi, M Gajofatto, A Gallo, A Gallo, P Gatto, M Gazzola, P Giordano, A Granella, F Grasso, M G Grimaldi, Lme Iaffaldano, P Immovilli, P Imperiale, D Inglese, M Iodice, R Leva, S Leuzzi, V Lugaresi, A Lus, G Maimone, D Mancinelli, L Maniscalco, G T Marfia, G A Margari, L Marinelli, F Marini, B Marson, A Mascoli, N Massacesi, L Melani, F Merello, M Fioretti, C Mirabella, M Montepietra, S Nasuelli, D Nicolao, P Pasquali, L Passantino, F Patti, F Pecori, C Peresson, M Pesci, I Piantadosi, C Piras, M L Pizzorno, M Plewnia, K Pozzilli, C Protti, A Quatrale, R Realmuto, S Ribizzi, G Rinalduzzi, S Rini, A Romano, S Filippi, M Ronzoni, M Rossi, P Rovaris, M Salemi, G Santangelo, G Santangelo, M Leone, A Sarchielli, P Sinisi, L Ferraro, D Solaro, C Spitaleri, D Strumia, S Tassinari, T Santuccio, G Tortorella, C Totaro, R Tozzo, A Trivelli, G Turano, G Ulivelli, M Valentino, P Venturi, S Vianello, M Zaffaroni, M Zarbo, R




























































































































































































































































































































 Altieri, Manuela Borgo, Riccardo Capuano, Rocco Storelli, Loredana Pagani, Elisabetta Sibilia, Mauro Piervincenzi, Claudia Ruggieri, Serena Petsas, Nikolaos Cortese, Rosa Stromillo, Maria Laura



















































































































































































































































































































































 Rossi, Francesca Luigi, Zulliani Mampreso, Edoardo Gambara, Silvia Squilini, Sabrina Matricardi, Sara Clerici, Valentina Torri Polito, Anna Nunzia Rosa, Gabriella Di Bedin, Roberta Vitetta, Francesca Varone, Antonio Maimone, Davide Bisecco, Alvino Sabatino, Elena Di Scannapieco, Sara Papi, Claudia Guerrieri, Simone Pisani, Francesco Praticò, Andrea Po, Chiara Grazian, Luisa Passarini, Alice Bergamoni, Stefania Rasia, Sasha Bergamaschi, Roberto Marchioni, Enrico































































































































































































































































































































 Chapman, Caron Coulthard, Alan Dear, Keith Dwyer, Terry Kilpatrick, Trevor Lucas, Robyn McMichael, Tony Ponsonby, Anne-Louise Taylor, Bruce Valery, Patricia van der Mei, Ingrid A F Williams, David










































































































 Chow, Nancy Sealey, Rob Balneaves, Lynda





















 Bolton, James Graff, Lesley Kornelsen, Jennifer Mazerolle, Erin Patel, Ronak Figley, Teresa D Helmick, Carl A


























































































































 Aini, I Albertelli, M Alessi, Y Altieri, B Antonini, S Barrea, L Birtolo, F Campolo, F Cannavale, G Cantone, C Carra, S Centello, R Cozzolino, A Molfetta, S Vito, V Fanciulli, G Feola, T Ferraù, F Gay, S Giannetta, E Grillo, F Grossrubatscher, E Guarnotta, V Salvia, A Laffi, A Lania, A Liccardi, A Malandrino, P Mazzilli, R Messina, E Mikovic, N Minotta, R Modica, R Muscogiuri, G Pandozzi, C Pugliese, G Puliani, G Ragni, A Rubino, M Russo, F Sesti, F Verde, L Veresani, A Vetrani, C Vitale, G Zamponi, V Zanata, I

















































 Danel-Brunaud, Veronique Moreau, Caroline Perez, Thierry Dumont Dujardin, K Delval, Arnaud Gelé, Patrick Pleuvret, Marie Santraine, Valerie Niset, Francine Dumont, Julien Laugeais, Victor Bon, Mathilde Ouk, Thavarak Potey, Camille Leclercq, Celine Gers, Elise Salachas, Francois Bruneteau, Gaelle Lacomblez, Lucette Socha, Julie Pineau, Fanny Lenglet, Timothee Folhinha, Patricia Doucelance Stéphanie Bordet, Amandine Royer, Hugo Osman, Nadia Khelifa, Sabah Ait Corcia, Philippe Beltran, Stephane Carmier, Delphine Barantin, Laurent Blasco, Hélène Bakkouche, Salah Eddine Mouzouri, Mohad Antoine, Jean-Christophe Camdessanché, Jean-Philippe Dimier, Nathalie Kaminsky, Anne-Laure Court-Fortune, Isabelle Boutet, Claire Gonzalo, Philippe Visneux, Vincent Ferraud, Karine Berlier, Georgette Genestet, Steeve Gut-Gobert, Christophe Salem, Douraied Ben Nicolas, Pauline Larvor, Sabine Mouly, Kevin Roux, Liana Le Postec, Kevin Bezeazux, Camille Rosec, Sylvain Fortin-Prunier, Hélène Novert, Gaelle Menanteau, Elsa Postec, Kevin Denizot, Magali Bernard, Emilien Vial, Christophe Broussole, Emmanuel Svahn, Juliette Cam, Pierre Le Berthezene, Yves Combet, Philippe Jacqueline, Sophie Neuillet, Camille Mansuy, Adeline Camu, William Juntas-Morates Pageot Esselin Champfleur Roy-Bellina Lehmann, Sylvain Alphandry, Sebastien Labar, Laura Baudesson, Leandra Attarian, Sharam Grapperon, Aude-Marie Pouget, Jean Verschueren, Annie Bas, Jaochim Finet-Monnier, Armelle Belingher, Carole Diallo, Saran Heddadji, Nacime Alphandery, Sebastien Baudesson, Leandra Reginensi, Pascale Desnuelle, Claude Soriani, Marie-Hélene Chanalet, S Mondot, Lydiane Puma Pruvost, Isabelle Barré, Carole Cintas, Pascal Bes, Marie-Christine Arne Acket, Blandine Pariente, Jérémie Guilbaud, Isabelle Bonneville, Fabrice Causse, E Lagarde, Thierry Geffroy, Jeremy Centelles, Magali Hermet-Douard, Véronique Pittion-Vouyovitch, Sophie Michon, Maud Meyer, Mylène Lomazzi, Sandra Hossu, Gabriella Chatelain, Anne Couratier, Philippe Lautrette, Geraldine Vincent, Francois Antonini, Larie-Therese Favard, Florent Boncoeur-Martel, M L Arie-Paule Chouly, Marianne Desport, Jean-Claude Jesus, Pierre Fayemendy, Phillipe Labetoulle, Clémence Catteau, Julie Villeneuve, Olivier Machat, Selam Guy, Nathalie Clavelou, Pierre Greil, Anick Duclos, M Jean, Betty Chassain, Carine Tsoutsos, Camille Speziale, Claudine Cladiere, Aurélie Bouteloup, C Farigon, N Argondo, Sophia Sickout Dumont, Emilie Rouvet, Sandrine Viader, Fausto Lefilliatre, Mathilde Mouton, Philippe Mondou, A Allouche, Stephane Bari-Makouri, Rachida Kolev, Ivan Pihan, Morgane Ho, Helene Le Catroux, Bertrand Castel, Maela Rigal, Marine Bellot, Catherine Vomscheid, Maelle Hervé, Marie-Cécile Duban, Marie-Pierre Vieillart, Anne Cassereau, Julien Codron, Philippe Pautot, Vivien Meslier, Nicole Trzepizur, Wojciech Tanguy, J Y Allain, Philippe Thiery, Cecile Reynier, Pascal Barbe, Tiphaine Vialle-Soubranne Vienne, Nathalie Olivier, Audrey Miller, Jeanne Bost, Marie Fournier Gay, David Bonicel, Robin El Mountassir, Fouzia Fischer, Clara Mangin, Jean-François Chupin, Marie Cointepas, Yann Accart, Bertrand Gelé, Patrick Fievet, Florine Chabel, Matthieu Derenaucourt, Virginie Facon, Loïc Njosse, Yanick Tchantchou Hisbergues, Michael Deplanque Tabuenca, Christine Cazalère, Marie-France Couratier, Philippe Camu, William Corcia, Philippe Desnuelle, Claude Caillier, Maxime Danel, Véronique Morerau, Caroline Laugeais, Victor Lecocq, Amelie Potin, Nathalie Frisch, Marie Léon, Marie Devos, David Salachas, François Pradat, Pierre-Francois Lacomblez, Lucette Camdessanché, Jean-Philippe Attarian, Sharam Langlet, Timothée Blasco, Hélène Dupuis, Luc Bon, Mathilde Bernard, Emilien Cassereau, Julien Soriani, Marie-Hélène Raoul, Cedric Lehman, Sylvain Turgeman, Sabine Goutines, Valérie





































































































































 Fortuné, Catherine Gietzen, Amy Hudson, Marie Lawrie-Jones, Amanda Mayes, Maureen D Nielson, Warren R Sauvé, Maureen Wojeck, Robyn K Adams, Claire Elizabeth Henry, Richard S Assassi, Shervin Benedetti, Andrea El-Baalbaki, Ghassan Fligelstone, Kim Frech, Tracy Hinchcliff, Monique Johnson, Sindhu R Larche, Maggie Leite, Catarina Nguyen, Christelle Nielsen, Karen Pope, Janet Rannou, François Rodriguez-Reyna, Tatiana Sofia Schouffoer, Anne A Suarez-Almazor, Maria E Agard, Christian André, Marc Bernstein, Elana J Berthier, Sabine Bissonnette, Lyne Bruns, Alessandra Cacciatore, Carlotta Carreira, Patricia Casadevall, Marion Chaigne, Benjamin Chung, Lorinda Crichi, Benjamin Domsic, Robyn Dunne, James V Dunogue, Bertrand Fare, Regina Farge-Bancel, Dominique Fortin, Paul R Gordon, Jessica Granel-Rey, Brigitte Guffroy, Aurélien Gyger, Genevieve Hachulla, Eric Hoa, Sabrina Ikic, Alena Jones, Niall Khalidi, Nader Lakin, Kimberly Lambert, Marc Launay, David Lee, Yvonne C Maillard, Hélène Maltez, Nancy Manning, Joanne Marie, Isabelle Lopez, Maria Martin Martin, Thierry Masetto, Ariel Maurier, François Mekinian, Arsene Díaz, Sheila Melchor Nikpour, Mandana Olagne, Louis Poindron, Vincent Proudman, Susanna Régent, Alexis Rivière, Sébastien Robinson, David Almazar, Esther Rodríguez Roux, Sophie Smets, Perrine Sobanski, Vincent Spiera, Robert Steen, Virginia Sutton, Evelyn Thorne, Carter Wilcox, Pearce Ayala, Mara Cañedo Cook, Vanessa Hu, Sophie Matthews, Bianca Nassar, Elsa-Lynn Neyer, Marieke A Nordlund, Julia Provencher, Sabrina














 Macklin, Eric Hayden, Douglas Lai, PoYing Donahue, Rachel Marion, Joseph Alameda, Gustavo Mathai, Nithya Ho, Doreen McCaffrey, Alexandra Berry, James Babu, Suma Scalia, Jennifer Freeman, Marlene Tourenne, Clotilde Lagier Sadri-Vakili, Ghazaleh Quick, Adam Kolb, Stephen Heintzman, Sarah Heitzman, Daragh Martin, Alan Ajroud-Driss, Senda Sufit, Robert Szymanski, April Appel, Stanley H Greene, Ericka Simpson Thonhoff, Jason Shroff, Sheetal Liao, Bing Katz, Jonathan Jenkins, Liberty Felice, Kevin Whitaker, Charles Maragakis, Nicholas J Clawson, Lora L Uchil, Alpa Riley, Kristen Arneklev, JinAe Simmons, Zachary Grogan, James Su, Xiaowei Mamarabadi, Mansoureh Goutman, Stephen A Feldman, Eva Olney, Nicholas Bazan, Tracy Miller, Timothy Malcolm, Amber Fernandes, Joseph Americo M Piccione, Ezequiel Thaisetthawatkul, Pariwat Ilieva, Hristelina Pasinelli, Piera Jawdat, Omar Farmakidis, Constantine Jabari, Duaa Statland, Jeffrey Pasnoor, Mamatha Dimachkie, Mazen Weiss, Michael D Rad, Nassim Wang, Leo H Foster, Laura Vu, Tuan Suresh, Niraja Farias, Jerrica Ladha, Shafeeq Jacobsen, Bill Milliard, Jourdan Bowser, Robert Owegi, Margaret Ayo Brown, Robert H Jr Ghasemi, Mehdi Houmani, Hajar Douthwright, Catherine Newman, Daniel S Arcila-Londono, Ximena Steijlen, Kara Yasek, Julia Hams, Matthew Jackson, Carlayne Bhavaraju-Sanka, Ratna Swenson, Andrea Nance, Christopher Gutmann, Ludwig Heiman-Patterson, Terry Deboo, Anahita Caress, Jim Cartwright, Michael Fee, Dominic Shrilla, David Peltier, Amanda Lewis, Richard Burford, Matthew Diaz, Frank Rosenfeld, Jeffrey Borg, David Bhuvaneswaran, Karthikeyan Walk, David Maiser, Sam Johnson, Kristin Rao, Pooja Elliott, Matthew Rakocevic, Goran Jones, Sarah Solorzano, Guillermo Kasarskis, Edward J Mahuwala, Zabeen Mathur Kumaraswamy, Vishakhadatta Vish Rutkove, Seward McIlduff, Courtney Bedlack, Richard Li, Xiaoyan Parker, Sarah Elman, Lauren Quinn, Colin Goyal, Namita A Habib, Ali A Mozaffar, Tahseen Korb, Manisha Kak Mullen, Jeffrey Rezania, Kourosh Soliven, Betty Roos, Raymond Twydell, Paul Mundwiler, Andrew Young, Eufrosina Meyer, Jenny A Benatar, Michael Glass, Jonathan Fournier, Christina Cohen, Jeffrey A Stommel, Elijah Robbins, Nathaniel M Jones, Vovanti Zilliox, Lindsay Diaz-Abad, Montserrat Jin, Peter Chauhan, Chandana Wymer, James P Chuquilin, Miguel Subramony, S H McNeely, Whitney Beydoun, Said R Darki, Leila Rodriguez, Rodrigo Shah, Jaimin Oskarsson, Bjorn Pattee, Gary L Bobenhouse, James Hayat, Ghazala Al-Dahhak, Roula Kafaie, Jafar Martinez-Thompson, Jennifer Staff, Nathan Nayar, Shakti Kuenzler, Rebecca Bayat, Elham Rosow, Laura Bodkin, Cynthia Gursoy, Nurcan Al-Lahham, Tawfiq Lacomis, David Gibson, Summer Rivner, Michael Kushlaf, Hani A Gwathmey, Kelly G Elliott, Michael McKinnon, Johnathan Wu, Abel Walsh, Alison Whitesell, Jackie Erickson, Amber Locatelli, Eduardo Connors, Robert McCluskey, Leo Usman, Uzma Kovvuru, Sukanthi Sherman, Alex Hasenoehrl, Meredith Dagostino, Derek Faulconer, Kenneth Kharakozova, Olga Korin, Alexander Tarasenko, Natalia Vigneswaran, Prasha Katsovskiy, Igor Whitworth, Isaac Wahab, Yusra Novak, Ilya Tustison, Eric Jentoft, Katie Ostrow, Joe Changkuon, Genevive La, Thuong Deignan, Christina Li, Haining Patel, Payal Phan, Minh Hurwitz, Samuel Estes, Michaela Palillo, Jack Thomas, Mirna De Mattos, Annette Patterson, Janae Figueroa-Szostek, Precious Jean, Sandra Louis Pothier, Lindsay Harkey, Brittney DiStefano, Sofia Bailey, Abbey Jordan, Boglarka Pagliaro, Jaclyn Wright, Spencer Abu-Hamdan, Natalie Igne, Courtney Kolvek, Taylor Bailey, Jesse Barlow, Victoria Arroyave, Luisa Henrique, Jennifer Proeung, Serena Rosenthal, Jesse Gladden, Catherine Cirino, Melissa Henrique, Natalie Deirmendjian, Emma Small, Catherine Bulat, Allison Hurwitz, Samuel Popel, Najla Irwin, Liam Hall, Meghan Connolly, Mariah Kittle, Gale Hamilton, Jenny De Santiago, Diana Felix, Adrian Lovett, Marlee Nelson, Linda Martin, Ashley Garrett, Karly Garcia, Abigail De La Rosa Rede, Diana Pabon, Marissa Khan, Kamran Fetouh, Ahmed Woodcook, Joan Kamp, Cornelia Kennedy, Julie McGarry, Andrew Torti, Margherita















































 Fortuné, Catherine Hudson, Marie Benedetti, Andrea Hummers, Laura K Adams, Claire Elizabeth Ayala, Mara Cañedo Cook, Vanessa Hu, Sophie Matthews, Bianca Nassar, Elsa-Lynn Nordlund, Julia Provencher, Sabrina Assassi, Shervin El-Baalbaki, Ghassan Fligelstone, Kim Frech, Tracy Hinchcliff, Monique Johnson, Sindhu R Larche, Maggie Khalidi, Nader Leite, Catarina Nguyen, Christelle Rannou, François Nielsen, Karen Pope, Janet Rodriguez-Reyna, Tatiana Sofia Schouffoer, Anne A Suarez-Almazor, Maria E Agard, Christian André, Marc Olagne, Louis Bernstein, Elana J Berthier, Sabine Bissonnette, Lyne Bruns, Alessandra Masetto, Ariel Roux, Sophie Cacciatore, Carlotta Crichi, Benjamin Farge-Bancel, Dominique Carreira, Patricia Fare, Regina Lopez, Maria Martin Díaz, Sheila Melchor Almazar, Esther Rodríguez Casadevall, Marion Chaigne, Benjamin Dunogue, Bertrand Régent, Alexis Chung, Lorinda Domsic, Robyn Dunne, James V Wilcox, Pearce Fortin, Paul R Ikic, Alena Gordon, Jessica Lakin, Kimberly Spiera, Robert Granel-Rey, Brigitte Guffroy, Aurélien Martin, Thierry Poindron, Vincent Gyger, Genevieve Hachulla, Eric Hoa, Sabrina Jones, Niall Lambert, Marc Launay, David Maillard, Hélène Sobanski, Vincent Lee, Yvonne C Maltez, Nancy Manning, Joanne Marie, Isabelle Maurier, François Mekinian, Arsene Rivière, Sébastien Nikpour, Mandana Proudman, Susanna Robinson, David Smets, Perrine Steen, Virginia Sutton, Evelyn Thorne, Carter
















































































































 Fortuné, Catherine Gietzen, Amy Guillot, Geneviève Lewis, Nancy Nielsen, Karen Sauvé, Maureen Richard, Michelle Welling, Joep Varga, John Adams, Claire E Ayala, Mara Cañedo Cook, Vanessa Hu, Sophie Nassar, Elsa-Lynn Neyer, Marieke Alexandra Nordlund, Julia Provencher, Sabrina Bartlett, Susan J Hudson, Marie Benedetti, Andrea Gottesman, Karen Hummers, Laura K Lawrie-Jones, Amanda Mayes, Maureen D Assassi, Shervin Nielson, Warren R El-Baalbaki, Ghassan van den Ende, Cornelia Fligelstone, Kim Frech, Tracy Harel, Daphna Hinchcliff, Monique Johnson, Sindhu R Larche, Maggie Khalidi, Nader Leite, Catarina Nguyen, Christelle Rannou, François Pope, Janet Reyna, Tatiana Sofia Rodriguez Schouffoer, Anne A Suarez-Almazor, Maria E Agard, Christian Abdallah, Nassim Ait Crichi, Benjamin Farge-Bancel, Dominique André, Marc Olagne, Louis Smets, Perrine Bernstein, Elana J Berthier, Sabine Bissonnette, Lyne Bruns, Alessandra Masetto, Ariel Roux, Sophie Carreira, Patricia Fare, Regina Martin, Maria Díaz, Sheila Melchor Almazar, Esther Rodríguez Casadevall, Marion Chaigne, Benjamin Dunogue, Bertrand Régent, Alexis Chung, Lorinda Denton, Christopher Domsic, Robyn Dunne, James V Wilcox, Pearce Fortin, Paul R Ikic, Alena Gordon, Jessica Lakin, Kimberly Spiera, Robert Granel-Rey, Brigitte Guffroy, Aurélien Martin, Thierry Poindron, Vincent Gyger, Genevieve Hachulla, Eric Lambert, Marc Launay, David Maillard, Hélène Sobanski, Vincent Hoa, Sabrina Jones, Niall Kafaja, Suzanne Lee, Yvonne C Maltez, Nancy Manning, Joanne Marie, Isabelle Maurier, François Mekinian, Arsene Rivière, Sébastien Nikpour, Mandana Proudman, Susanna Robinson, David Steen, Virginia Sutton, Evelyn Thorne, Carter Varga, John







 Allen, Naomi Aslam, Tariq Atan, Denize Balaskas, Konstantinos Barman, Sarah Barrett, Jenny Bishop, Paul Black, Graeme Braithwaite, Tasanee Carare, Roxana Chakravarthy, Usha Chan, Michelle Chua, Sharon Day, Alexander Desai, Parul Dhillon, Bal Dick, Andrew Doney, Alexander Egan, Cathy Ennis, Sarah Foster, Paul Fruttiger, Marcus Gallacher, John Garway-Heath, David Gibson, Jane Guggenheim, Jeremy Hammond, Chris Hardcastle, Alison Harding, Simon Hogg, Ruth Hysi, Pirro Keane, Pearse Khaw, Peng Tee Khawaja, Anthony Lascaratos, Gerassimos Littlejohns, Thomas Lotery, Andrew Luben, Robert Luthert, Phil Macgillivray, Tom Mackie, Sarah Madhusudhan, Savita Mcguinness, Bernadette Mckay, Gareth Mckibbin, Martin Moore, Tony Morgan, James O'sullivan, Eoin Oram, Richard Owen, Chris Patel, Praveen Paterson, Euan






 Aguerre, Ines Amezcua, Lilyana Chitnis, Tanuja Lewis, Jessica Coleman Engel, Casey Han, May H Klawiter, Eric C Kocsik, Alexandra Kruse-Hoyer, Mason Levine, Libby Levy, Michael Marcille, Melanie Mealy, Maureen A Moore, Stephanie Mullin, Devin S Nelson, Katherine E Onomichi, Kaho B Planchon, Sarah M Pruitt, Ana Repovic, Pavle Riley, Claire S Rimler, Zoe Russo, Andrew W Ocampo, Collin Tanchanco Tomczak, Anna J





 Cuomo, Giovanna Moroncini, Gianluca Stork, Jiri Iannone, Fiorenzo Walker, Ulrich Bertoldo, Eugenia Krasowska, Dorota Salvador, Maria João Tikly, Mohammed Riccieri, Valeria Sha, Ami Gheorghiu, Ana Maria Sunderkötter, Cord Ingegnoli, Francesca Mouthon, Luc Smith, Vanessa Cantatore, Francesco Paolo Eyerich, Kilian Wiland, Piotr Vanthuyne, Marie Anic, Branimir Üprus, Maria Granel, Brigitte Vacca, Alessandra Tanaseanu, Cristina-Mihaela Lefebvre, Paloma García de la Peña Sibilia, Jean Litinsky, Ira Saketkoo, Lesley Ann Kerzberg, Eduardo Limonta, Massimiliano Rimar, Doron Sfikakis, Petros Cutolo, Maurizio Foti, Rosario Novak, Srdan Radic, Mislav Pellerito, Raffaele Rozzano, Carlo Francesco Selmi Ananieva, Lidia P Szűcs, Gabriela de la Puente, Carlos Ionescu, Ruxandra Maria Pozzi, Maria Rosa Alegre-Sancho, Juan Jose Herrmann, Kristine De Langhe, Ellen Altunizade, Sule Yavuz Agachi, Svetlana Veale, Douglas Loyo, Esthela Li, Mengtao Rosato, Edoardo Maurer, Britta Castellví, Iván Spertini, François Solanki, Kamal Del Papa, Nicoletta Espinosa, Gerard Czirják, László Coleiro, Bernard Bancel, Dominique Farge Pellerito, Raffaele Denton, Christopher Damjanov, Nemanja Granollers, Vera Ortiz Santamaria Kohm, Michaela Stamenkovic, Bojana Allanore, Yannick Airo', Paolo Balbir-Gurman, Alexandra Cerinic, Marco Matucci Riemekasten, Gabriela Heitmann, Stefan Hunzelmann, Nicolas Montecucco, Carlomaurizio Morovic-Vergles, Jadranka Ribi, Camillo





 Grimbacher, Bodo Warnke, Clemens Wicklein, Rebecca Wijburg, Martijn Brouwer, Matthijs Lambert, Nicolas Engalenc, Xavier Gaudin, Marion Küpper, Clemens Aouba, Achille Manda, Victoria Brousse, Xavier Ducours, Maïlys Duffau, Pierre Ouallet, Jean‐Christophe Mrabet, Hela Gourdon, Florence Le Maréchal, Marion Bernard‐Valnet, Raphael Delobel, Pierre Lajaunie, Rebecca Treiner, Emmanuel Lhomme, Sebastien Bonneville, Fabrice Ribaute, Carole Ciron, Jonathan Biotti, Damien Kamar, Nassim Weiss, Nicolas Pourcher, Valérie Rakotoarison, Juliette Leveneur, Yann De Menibus, Laurence Grassl, Niklas Lifermann, Francois Cohen‐Aubart, Fleur Ney, Douglas Kapadia, Ronak Dinur‐Schejter, Yael Shifman, Tzlil Shamriz, Oded Berger, Joseph Lambotte, Olivier Perpoint, Thomas Harel, Asaff Wyplosz, Benjamin
 Adamo, Sabrina Bartha, Rob Berezuk, Courtney Black, Alanna Borrie, Michael Bronskill, Susan Bulman, Dennis Casaubon, Leanne Cornish, Ben Defrawy, Sherif Dilliott, Allison Dixon, Roger A Farhan, Sali Faria, Frederico Fraser, Julia Freedman, Morris Ghani, Mahdi Greenberg, Barry Haddad, Hassan Hassan, Ayman Hatch, Wendy Hegele, Rob Holmes, Melissa Hudson, Chris Jog, Mandar Kleinstiver, Peter Kwan, Donna Leontieva, Elena Levine, Brian Mandelcorn, Efrem Margolin, Ed McIlroy, Bill Montero-Odasso, Manuel Munoz, David Nanayakkara, Nuwan Ozzoude, Miracle Ramirez, Joel Rashkovan, Natalie Robinson, John Rogaeva, Ekaterina Adamson, Yanina Sarquis Scott, Christopher Strong, Michael Sujanthan, Sujeevini Symons, Sean Theyers, Athena Troyer, Angela Van Ooteghem, Karen Woulfe, John Zamyadi, Mojdeh





 Soltis, Anthony R Viollet, Coralie Sukumar, Gauthaman Alba, Camille Lott, Nathaniel McGrath Martinez, Elisa Tuck, Meila Singh, Jatinder Bacikova, Dagmar Zhang, Xijun Hupalo, Daniel N Adeleye, Adelani Wilkerson, Matthew D Pollard, Harvey B Dalgard, Clifton L Black, Sandra E Gan-Or, Ziv Keith, Julia Masellis, Mario Rogaeva, Ekaterina Brice, Alexis Lesage, Suzanne Xiromerisiou, Georgia Calvo, Andrea Canosa, Antonio Chio, Adriano Logroscino, Giancarlo Mora, Gabriele Krüger, Reijko May, Patrick Alcolea, Daniel Clarimon, Jordi Fortea, Juan Gonzalez-Aramburu, Isabel Infante, Jon Lage, Carmen Lleó, Alberto Pastor, Pau Sanchez-Juan, Pascual Brett, Francesca Aarsland, Dag Al-Sarraj, Safa Attems, Johannes Gentleman, Steve Hardy, John A Hodges, Angela K Love, Seth McKeith, Ian G Morris, Christopher M Morris, Huw R Palmer, Laura Pickering-Brown, Stuart Ryten, Mina Thomas, Alan J Troakes, Claire Albert, Marilyn S Barrett, Matthew J Beach, Thomas G Bekris, Lynn M Bennett, David A Boeve, Bradley F Dalgard, Clifton L Dawson, Ted M Dickson, Dennis W Faber, Kelley Ferman, Tanis Ferrucci, Luigi Flanagan, Margaret E Foroud, Tatiana M Ghetti, Bernardino Gibbs, J Raphael Goate, Alison Goldstein, David S Graff-Radford, Neill R Kaufmann, Horacio Kukull, Walter A Leverenz, James B Lopez, Grisel Mao, Qinwen Masliah, Eliezer Monuki, Edwin Newell, Kathy L Palma, Jose-Alberto Perkins, Matthew Pletnikova, Olga Renton, Alan E Resnick, Susan M Rosenthal, Liana S Ross, Owen A Scherzer, Clemens R Serrano, Geidy E Shakkottai, Vikram G Sidransky, Ellen Tanaka, Toshiko Tayebi, Nahid Topol, Eric Torkamani, Ali Troncoso, Juan C Woltjer, Randy Wszolek, Zbigniew K Scholz, Sonja W Baloh, Robert H Bowser, Robert Brice, Alexis Broach, James Camu, William Chiò, Adriano Cooper-Knock, John Drepper, Carsten Drory, Vivian E Dunckley, Travis L Feldman, Eva Fratta, Pietro Gerhard, Glenn Gibson, Summer B Glass, Jonathan D Hardy, John A Harms, Matthew B Heiman-Patterson, Terry D Jansson, Lilja Kirby, Janine Kwan, Justin Laaksovirta, Hannu Landers, John E Landi, Francesco Le Ber, Isabelle Lumbroso, Serge MacGowan, Daniel Jl Maragakis, Nicholas J Mouzat, Kevin Myllykangas, Liisa Orrell, Richard W Ostrow, Lyle W Pamphlett, Roger Pioro, Erik Pulst, Stefan M Ravits, John M Robberecht, Wim Rogaeva, Ekaterina Rothstein, Jeffrey D Sendtner, Michael Shaw, Pamela J Sidle, Katie C Simmons, Zachary Stein, Thor Stone, David J Tienari, Pentti J Traynor, Bryan J Troncoso, Juan C Valori, Miko Van Damme, Philip Van Deerlin, Vivianna M Van Den Bosch, Ludo Zinman, Lorne



 Pilotto, Andrea Piccinelli, Stefano Cotti Lazzari, Susanna Negro, Giulia Cereda, Giulia Sofia Infante, Roberto Giovannelli, Ginevra Cutellè, Claudia Tinti, Lorenzo Diamanti, Susanna Fanella, Gaia Rifino, Nicola Tremolizzo, Lucio Ermanis, Giovanni Kuris, Fedra Sartor, Roberto Bax, Francesco Gigli, Gian Luigi Barvas, Edoardo Volpini, Mirco Frusciante, Roberto Bernardi, Mariaeva Turla, Marinella Valenti, Raffaella Valenti, Raffaella Kiferle, Lorenzo Pradella, Silvia Innocenti, Alessandro Ciolli, Ludovico Orlandi, Niccolò Vandelli, Gabriele Mazzoli, Marco Benedetti, Luana Pardini, Matteo Grisanti, Stefano Biassoni, Erica Cabona, Corrado Schenone, Angelo Boso, Federica Agosta, Federica Orrico, Mario Roveri, Luisa Sferruzza, Giacomo Gentile, Mauro Piccolo, Laura Merli, Elena Salmaggi, Andrea Bocci, Tommaso Ferrucci, Roberta Dini, Michelangelo Guarino, Maria Nicodemo, Marianna Beretta, Sandro Giossi, Alessia Campana, Chiara Censori, Bruno Primiano, Guido Troiano, Maria Bollo, Luca Calcagno, Narghes Trogu, Francesca Morelli, Claudia Colosimo, Carlo Di Schino, Chiara Costantini, Franco Cosentino, Giuseppe Marchioni, Enrico Avorio, Federica Russelli, Giovanna Panarello, Giovanna Carlucci, Giovanna Azzolini, Federica Lotti, Antonio Ciccone, Alfonso Furlanis, Giovanni Giometto, Bruno Bellavita, Giulia Valentina, Scarano Lorusso, Lorenzo Altavista, Maria Concetta Brigandì, Amelia Sorbera, Chiara Gatto, Lucia Sacco, Simona Clerici, Raffaella Schirinzi, Erika Bonanni, Enrica Merico, Elena Beretta, Natascia Gallo, Giuseppe Sciolla, Chiara Bertolotto, Antonio Pomati, Simone Masserini, Federico Camilli, Federico Panzera, Ivan Cardinali, Patrizio Cristina Acciarri, Maria De Michele, Giovanna Perillo, Sandra Palmieri, Gianluigi Rosalio Cuomo, Nunzia Giglio, Augusta
 Ivan, Paula Andreea Sandu, Georgiana Odajiu, Irina Dragoș Sandu, Constantin Vitalie, Lisnic Mikhail, Gavriliuc Olesea, Odainic Cavallieri, Francesco Toschi, Giulia Zedde, Marialuisa Turla, Marinella Bianchi, Marta Civelli, Patrizia Cvetkovska, Emilija Barbov, Ivan Babunovska, Marija Kozlova, Alexandra Abramova, Anna Daria, Eliseeva Dobronyi, Levente Dénes, Kitti Bereczki, Dániel Agajany, Netta Geva, Matan Kindl, Philipp Kosno, Krystian Michał, Lipowski Silva, Lucas Scardua Batista João, Rafael Jung, Simon Müller, Madlaine Aires, Elaine Vinski, Ivana Lisak, Marijana Marjiana, Lesiv Ural, Onur Kara, Iskender Öztürk, Bilgin Caldeiras, Ana Catarina Oliveira Rodriguez-Leyva, Ildefonso Boldingh, Marion von Oertzen, Tim Jenkins, Thomas M Riahi, Anis Taba, Pille Azzam, Ahmed Y Wojtecki, Lars Sellner, Johan Castillo, Sergio Bušková, Jitka Novotny, Vojtech Jelcic, Ilijas Dafea, Ahmed Medina, Marco T Flemen, Heidi Øyen Elbahnasawy, Mohamed Gamal Kohler, Edith Farmen, Annette Huuse




 Liu, Ganqiang Valentino, Rebecca R Peng, Jiajie Liao, Zhixiang Locascio, Joseph J Corvol, Jean-Christophe Dong, Xianjun Maple-Grødem, Jodi Campbell, Meghan C Elbaz, Alexis Lesage, Suzanne Brice, Alexis Mangone, Graziella Growdon, John H Hung, Albert Y Schwarzchild, Michael A Hayes, Michael T Wills, Anne-Marie Herrington, Todd M Ravian, Bernard Shoulson, Ira Taba, Pille Kõks, Sulev Beach, Thomas G Cormier-Dequaire, Florence Alves, Guido Tysnes, Ole-Bjørn Perlmutter, Joel S Heutink, Peter van Hilten, Jacobus J Kasten, Meike Mollenhauer, Brit Trenkwalder, Claudia Klein, Christine Barker, Roger A Williams-Gray, Caroline H Marinus, Johan Scherzer, Clemens R
 Abraham, James Adkisson, Michael Albert, Marisa Altamirano, Luz Torres Alvarenga, Bonny Anderson, Matthew L Anderson, Evan J Arnett, Azlann Asashima, Hiromitsu Atkinson, Mark A Baden, Lindsey R Barton, Brenda Beach, Katherine Beagle, Elizabeth Becker, Patrice M Bell, Matthew R Bernui, Mariana Bime, Christian Boddapati, Arun Kumar Booth, J Leland Borresen, Brittney Brakenridge, Scott C Bristow, Laurel Bryant, Robert Calfee, Carolyn S Carreño, Juan Manuel Carrillo, Sidney Chak, Suzanna Chang, Iris Connors, Jennifer Conway, Michelle Corry, David B Cowan, David Croen, Brett Dela Cruz, Charles S Cusimano, Gina Eaker, Lily Edwards, Carolyn Ehrlich, Lauren I R Elashoff, David Erickson, Heidi Erle, David J Farhadian, Shelli Farrugia, Keith Fatou, Benoit Fernandes, Andrea Fernandez-Sesma, Ana Fragiadakis, Gabriela K Furukawa, Sara Geltman, Janelle N Ghale, Rajani Bermúdez González, Maria Carolina Goonewardene, I Michael Guerrero, Estella Sanchez Guirgis, Faheem W Hafler, David A Hamilton, Sydney Harris, Paul Hayati, Arash Nemati Hendrickson, Carolyn M Agudelo Higuita, Nelson I Hodder, Thomas Holland, Steven M Hough, Catherine L Huerta, Christopher Hurley, Kerin C Hutton, Scott R Iwasaki, Akiko Jauregui, Alejandra Jha, Meenakshi Johnson, Brandi Joyner, David Kangelaris, Kirsten N Kelly, Geoffrey Khalil, Zain Khan, Zenab Kheradmand, Farrah Kim, James N Kimura, Hiroki Ko, Albert I Kohr, Bernard Kraft, Monica Krummel, Matthew Kutzler, Michele A Lasky-Su, Jessica Lee, Serena Lee, Deanna Leipold, Michael Lentucci, Claudia Leroux, Carolyn Lin, Edward Liu, Shanshan Love, Christina Lu, Zhengchun Maliskova, Lenka Manning, Brittany Roth Manohar, Monali Martens, Mark McComsey, Grace A McEnaney, Kerry McLin, Renee Melamed, Esther Melnyk, Nataliya Mendez, Kevin Messer, William B Metcalf, Jordan P Michelotti, Gregory Mick, Eran Mohanty, Subhasis Mosier, Jarrod Mulder, Lubbertus C F Murphy, Maimouna Nadeau, Kari R C Nelson, Ebony Nelson, Allison Nguyen, Viet Oberhaus, Jordan Panganiban, Bernadine Pellegrini, Kathryn L Pickering, Harry C Powell, Debra L Presnell, Scott Pulendran, Bali Rahman, Adeeb H Rashid, Ahmad Sadeed Raskin, Ariel Reed, Elaine F Ribeiro, Susan Pereira Rivera, Adreanne M Rogers, Jacob E Rogers, Angela Rogowski, Brandon Rooks, Rebecca Rosenberg-Hasson, Yael Rothman, Jessica Rousseau, Justin F Salehi-Rad, Ramin Saluvan, Mehmet Samaha, Hady Schaenman, Joanna Schunk, Ron Semenza, Nicholas C Sen, Subha Sevransky, Jonathan Seyfert-Margolis, Vicki Shaheen, Tanzia Shaw, Albert C Sieg, Scott Siegel, Sarah A R Sigal, Natalia Siles, Nadia Simmons, Brent Simon, Viviana Singh, Gagandeep Sinko, Lauren Smith, Cecilia M Smolen, Kinga K Song, Li-Zhen Srivastava, Komal Sullivan, Peter Syphurs, Caitlin Tcheou, Johnstone Tegos, George P Tharp, Greg K Tong, Alexandra Tsitsiklis, Alexandra Ungaro, Ricardo F Vaysman, Tatyana Viode, Arthur Vita, Randi Wang, Xiaomei Ward, Alyssa Ward, Dawn C Willmore, Andrew Woloszczuk, Kyra Wong, Kari Woodruff, Prescott G Xu, Leqi van Haren, Simon van de Guchte, Adriana Zhao, 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 R01 NS110949/NS/NINDS NIH HHS/United States





 UM1 AI109565/AI/NIAID NIH HHS/United States DH_/Department of Health/United Kingdom





 U18 TR003807/TR/NCATS NIH HHS/United States UG3 TR002884/TR/NCATS NIH HHS/United States UH3 TR002884/TR/NCATS NIH HHS/United States K12 NS098482/NS/NINDS NIH HHS/United States






 RC-2773803/Ministero della Salute/
 510/17.01.2022/University of Medicine and Pharmacy, Science and Technology George Emil Palade Targu Mures/















 MR/T024402/1/MRC_/Medical Research Council/United Kingdom



 2017/R/4/Fondazione Italiana Sclerosi Multipla/


 MR/L010305/1/MRC_/Medical Research Council/United Kingdom


 THC-135234/CIHR/Canada



 University of Geneva/
 2022YFC3600201/National Key R&D Program of China/ 2022QN015/Chinese Universities Scientific Fund/

 U54 AG044170/AG/NIA NIH HHS/United States










 MC_PC_17228/MRC_/Medical Research Council/United Kingdom MC_QA137853/MRC_/Medical Research Council/United Kingdom MR/V028766/1/MRC_/Medical Research Council/United Kingdom 88/MSS_/Multiple Sclerosis Society/United Kingdom



 BTBR100196/MTPConnect/ 1/CX/CSRD VA/United States 1/CX/CSRD VA/United States











 075-15-2020-784/Ministry of Science and Higher Education of the Russian Federation/
























 R01 NS076511/NS/NINDS NIH HHS/United States














 20FC1030/Ministry of Health, Labor, and Welfare of Japan/









 CSTC2021 jscx-gksb-N0008/Key Project of Technological Innovation and Application Development of Chongqing Science and Technology Bureau/

 96-02-53-34905/Tehran University of Medical Sciences and Health Services/
 R01 NS082347/NS/NINDS NIH HHS/United States R01 EY032284/EY/NEI NIH HHS/United States




















 R01 NS112161/NS/NINDS NIH HHS/United States















 R01 DK131196/DK/NIDDK NIH HHS/United States R41 AI113977/AI/NIAID NIH HHS/United States R41 AI129571/AI/NIAID NIH HHS/United States





 K23 NS116225/NS/NINDS NIH HHS/United States




































 MR/V028766/1/MRC_/Medical Research Council/United Kingdom


 R01 NS112274/NS/NINDS NIH HHS/United States


 W81XWH2210793/U.S. Department of Defense/








 FISM2018/S/3/Fondazione Italiana Sclerosi Multipla/



 KL2 TR002534/NH/NIH HHS/United States TLI TR002533/NH/NIH HHS/United States UL1 TR002535/NH/NIH HHS/United States




 2018-203-001/Valencia Catholic University Saint Vincent Martyr/














 KLI 718/FWF_/Austrian Science Fund FWF/Austria

 FISM2021/C19-R-Single/005/Fondazione Italiana Sclerosi Multipla/
 CZ.02.2.69/0.0/0.0/16_018/0002635/University of Ostrava/ GeNeuro GNC-401/EudraCT number:/GeNeuro S.A/ 2019-004822-15/GeNeuro S.A/ 2020-02700/Swedish MRC/ FO2021-0277/ Hjärnfonden/

 donation #Jan2021-002/Roche Products/



 W81XWH-17-l-0089/U.S. Department of Defense/
 BEK-2017-26529/Istanbul Üniversitesi-Cerrahpasa/
 THC-135234/CIHR/Canada














 GR-2019-12369599/Ministero della Salute/
 R01 HD082176/HD/NICHD NIH HHS/United States










 EGID3185/Multiple Sclerosis Society of Canada/


 #EGID3185/Multiple Sclerosis Society of Canada/



 2021YFS0173/Department of Science and Technology of Sichuan Province/ 2022YFS0315/Department of Science and Technology of Sichuan Province/ ZYGX2021YGCX005/Medico-Engineering Cooperation Funds from University of Electronic Science and Technology of China/ ZYGX2021YGCX005/Medico-Engineering Cooperation Funds from University of Electronic Science and Technology of China/ 21HXFH041/1·3·5 project for disciplines of excellence-Clinical Research Incubation Project/



















 MR/V028766/1/MRC_/Medical Research Council/United Kingdom
 DIFA-FA-2018-027/HRBI_/Health Research Board/Ireland COVID-19 Related Research Costed Extension/Higher Education Authority/

 2018126/Jordan University of Science and Technology/














 Australian Research Council/ Metro South Health Research Support Scheme./










 K23 DK118209/DK/NIDDK NIH HHS/United States R03 DK126994/DK/NIDDK NIH HHS/United States
 ZONMW_/ZonMw/Netherlands
 320030_166346/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung/


 U01 AG024904/AG/NIA NIH HHS/United States CIHR/Canada

























 SFB 1158/Deutsche Forschungsgemeinschaft/ SFB 1118/Deutsche Forschungsgemeinschaft/ Olympia Morata/Medizinischen Fakultät Heidelberg, Universität Heidelberg/ Rahel Goetein-Straus/Medizinischen Fakultät Heidelberg, Universität Heidelberg/


 MC_EX_MR/N50192X/1/MRC_/Medical Research Council/United Kingdom R380R/1114/DMT_/The Dunhill Medical Trust/United Kingdom

















 R01NS109023/NS/NINDS NIH HHS/United States R01NS109023/NS/NINDS NIH HHS/United States

 GSD164127/CIHR/Canada









 MR/T024402/1/MRC_/Medical Research Council/United Kingdom CARP/T024402/1/MRC_/Medical Research Council/United Kingdom






 U01 NS045719/NS/NINDS NIH HHS/United States








 Research Roche-Italia/Roche-Italia/ Preclinical Research Grant F. Hoffmann-La Roche-Basel/F. Hoffmann-La Roche-Basel/








 PG2020710/Rebecca L. Cooper Medical Research Foundation/

















 2019-PR-Single-024/Multiple Sclerosis Italian Foundation (FISM)/ University of Ferrara/University of Ferrara/































 K23 NS116225/NS/NINDS NIH HHS/United States KL2 TR003016/TR/NCATS NIH HHS/United States UL1 TR003015/TR/NCATS NIH HHS/United States









 R21 EB027852/EB/NIBIB NIH HHS/United States
 R01 NS071463/NS/NINDS NIH HHS/United States



 K01 MH121582/MH/NIMH NIH HHS/United States









 R01 NS086981/NS/NINDS NIH HHS/United States R21 NS121806/NS/NINDS NIH HHS/United States F31 NS105387/NS/NINDS NIH HHS/United States C06 RR012169/RR/NCRR NIH HHS/United States C06 RR015431/RR/NCRR NIH HHS/United States S10 OD011939/OD/NIH HHS/United States

 T32 NR016914/NR/NINR NIH HHS/United States
 FC001030/ARC_/Arthritis Research UK/United Kingdom





 #0000201382/Sanofi/ #18499/University Hospital Foundation (University of Alberta)/
 MR/S026088/1/MRC_/Medical Research Council/United Kingdom
 PJT-156363/CIHR/Canada FDN-159934/CIHR/Canada

 337530/Academy of Finland/










 FPU 19/00167/Spanish Ministry of Education, Culture and Sport/ 2020-PREDUCLM-16704/Universidad de Castilla-La Mancha/ 2020-PREDUCLM-15596/Universidad de Castilla-La Mancha/


















 212-058/MS Australia/





 2R25NS090978-06/NH/NIH HHS/United States K01 MH122741/MH/NIMH NIH HHS/United States R01AG052550/NH/NIH HHS/United States KL2TR002346/NH/NIH HHS/United States KL2 TR002346/TR/NCATS NIH HHS/United States R01 AG052550/AG/NIA NIH HHS/United States K01MH122741/NH/NIH HHS/United States R25 NS090978/NS/NINDS NIH HHS/United States



 30/MSS_/Multiple Sclerosis Society/United Kingdom C57775/A22182/CRUK_/Cancer Research UK/United Kingdom DH_/Department of Health/United Kingdom






















 R21 NS118320/NS/NINDS NIH HHS/United States


 R01 MH130458/MH/NIMH NIH HHS/United States R01 NS102807/NS/NINDS NIH HHS/United States R01 AI126880/AI/NIAID NIH HHS/United States F32 NS101790/NS/NINDS NIH HHS/United States R01 ES029136/ES/NIEHS NIH HHS/United States R00 NS114111/NS/NINDS NIH HHS/United States T32 CA207021/CA/NCI NIH HHS/United States







 R01 NS082347/NS/NINDS NIH HHS/United States


 FISM2019/BS/009/Fondazione Italiana Sclerosi Multipla/ FISM2018/R/16/Fondazione Italiana Sclerosi Multipla/
 K12 HD055931/HD/NICHD NIH HHS/United States KL2 TR000143/TR/NCATS NIH HHS/United States KL2 TR001432/TR/NCATS NIH HHS/United States UL1 TR001409/TR/NCATS NIH HHS/United States

 SMS_IC010/CSO_/Chief Scientist Office/United Kingdom MMPP/01/CSO_/Chief Scientist Office/United Kingdom 215621/Z/19/Z/WT_/Wellcome Trust/United Kingdom MRC_/Medical Research Council/United Kingdom 104916/Z/14/Z/WT_/Wellcome Trust/United Kingdom







 NMSS RG-1802-30468/NMSS/ 1R21NS123419-01/GF/NIH HHS/United States
 P30 DK026743/GF/NIH HHS/United States












 ANR-16-RHUS-0001/ANR/






 Novartis Canada/



 U24 AI118660/AI/NIAID NIH HHS/United States


 21775/Shiraz University of Medical Sciences/











 Current research fund 2022/Ministero della Salute/
 MR/T020296/2/UK Research and Innovation/







 R01 NS109023/NS/NINDS NIH HHS/United States

















 R01 ES025530/NH/NIH HHS/United States









 R21 OD030163/OD/NIH HHS/United States


 81701191/National Natural Science Foundation of China/





























 Tisch MS Research Center of New York/





 NRC-9625/Ahvaz Jundishapur University of Medical Sciences/














 Physical activity/French Physical and Rehabilitation Medicine Society/









 UL1 TR001082/TR/NCATS NIH HHS/United States UL1 TR002535/TR/NCATS NIH HHS/United States









 R21 EB027852/EB/NIBIB NIH HHS/United States
 NMSS PP-2103-37382/MSS_/Multiple Sclerosis Society/United Kingdom





 R01 DE030122/DE/NIDCR NIH HHS/United States R01 LM012806/LM/NLM NIH HHS/United States T15 LM007093/LM/NLM NIH HHS/United States R01 DE029818/DE/NIDCR NIH HHS/United States




 31871026/National Natural Science Foundation of China/ 32100935/National Natural Science Foundation of China/ 31771129/National Natural Science Foundation of China/ 2019M663982/Postdoctoral Research Foundation of China/ 2019QH001/Foundation of Naval Medical University/ WF510105001/Foundation of Center of Hydrogen Science/




 R01 EY025687/EY/NEI NIH HHS/United States R01 EY032342/EY/NEI NIH HHS/United States
 PP1829/National Multiple Sclerosis Society/
 MH CZ-DRO, General University Hospital in Prague-VFN, 00064165/Ministry of Health of the Czech Republic/ NV18-08-00062/Ministry of Health of the Czech Republi/ Cooperatio, Medical Diagnostics and Basic Medical Sciences, Neuroscience/Charles University in Prague/ National Institute for Neurological Research, Programme EXCELES, ID Project No. LX22NPO5107/European Union/ reg. no. LM2023033/BBMRI.cz/ n/A/Roche/

 U01 AG024904/AG/NIA NIH HHS/United States CIHR/Canada


 427572/CIHR/Canada 440476/CIHR/Canada


 HI20C1073/Korea Health Industry Development Institute/Republic of Korea




 UL1 TR001412/TR/NCATS NIH HHS/United States


 R01 AT011005/AT/NCCIH NIH HHS/United States




 UC2 AR081033/AR/NIAMS NIH HHS/United States K01 AR072129/AR/NIAMS NIH HHS/United States P30 AR075043/AR/NIAMS NIH HHS/United States R01 AR042742/AR/NIAMS NIH HHS/United States R01 AR050511/AR/NIAMS NIH HHS/United States R01 AR054966/AR/NIAMS NIH HHS/United States R01 AR063611/AR/NIAMS NIH HHS/United States R01 AR065183/AR/NIAMS NIH HHS/United States
 UH3TR000890/NH/NIH HHS/United States











 DH2-21182/Hitchcock Foundation/ MHMH Fund 23042/Edgerton Fund:/ NA/Bornstein Research Fund/ NA/Diamond Endowment/





 PM-ID: 7644/Fresenius Kabi Austria GmbH/

 TL1 TR002386/TR/NCATS NIH HHS/United States R21 AI144819/AI/NIAID NIH HHS/United States R01 NS102417/NS/NINDS NIH HHS/United States R01 NS123398/NS/NINDS NIH HHS/United States K22 NS123508/NS/NINDS NIH HHS/United States

















 ZONMW_/ZonMw/Netherlands




 WT_/Wellcome Trust/United Kingdom 220575/Z/20/Z/WT_/Wellcome Trust/United Kingdom 104943/Z/14/Z/WT_/Wellcome Trust/United Kingdom



 R01 AI133623/AI/NIAID NIH HHS/United States R21 NS123596/NS/NINDS NIH HHS/United States


 00064173/Ministerstvo Zdravotnictví Ceské Republiky/ 00023752/Ministerstvo Zdravotnictví Ceské Republiky/ 00023001/Ministerstvo Zdravotnictví Ceské Republiky/ 112616/GAUK/2016/Grantová Agentura, Univerzita Karlova/ 260388/SVV/2019/Grantová Agentura, Univerzita Karlova/ Q35/Grantová Agentura, Univerzita Karlova/ Q37/Grantová Agentura, Univerzita Karlova/ Q41/Grantová Agentura, Univerzita Karlova/ SGS19/169/OHK3/3T/13/České Vysoké Učení Technické v Praze/ 13-23940S/Grantová Agentura České Republiky/ NU21-08-00432/Agentura Pro Zdravotnický Výzkum České Republiky/


 T1EDK-01859/Operational Program Competitiveness, Entrepreneurship and Innovation/



 R01 NS114227/NS/NINDS NIH HHS/United States UL1 TR001412/TR/NCATS NIH HHS/United States






 PREDOC//22/UJI/ UJI B-02/MCI/AEI/




 F32 HD101214/HD/NICHD NIH HHS/United States



 F31 NS122411/NS/NINDS NIH HHS/United States 1F31NS122411-01/NS/NINDS NIH HHS/United States DP5-OD-021352-01/NH/NIH HHS/United States R01-DC-16800-01A1/NH/NIH HHS/United States R01-DC-014960-01A1/NH/NIH HHS/United States R01-AG-059763/NH/NIH HHS/United States













 The Cyprus Institute of Neurology and Genetics/The Cyprus Institute of Neurology and Genetics/




 MSS_/Multiple Sclerosis Society/United Kingdom DH_/Department of Health/United Kingdom
















 MR/S026088/1/MRC_/Medical Research Council/United Kingdom










 259639/University of Guadalajara/
 Ciencia de Frontera-2019-552265/Consejo Nacional de Ciencia y Tecnología/













 962667/National Institute for Medical Research Development/




 James Cook University/












 Ricerca Corrente 2022/Ministero della Salute/ RF-2016-02361294/Ministero della Salute/ PE00000006-B43D22000650006/Ministero della Salute/ 2023/Fondazione Alessandro e Vincenzo Negroni Prati Morosini/ 2023/Fondazione Romeo ed Enrica Invernizzi/






 22080/Vice-Chancellor for Research, Shiraz University of Medical Sciences/












 R01 NS100811/NS/NINDS NIH HHS/United States






























 18-0424/MS Australia/ APP1127819/National Health and Medical Research Council/ RG-1803-30499/National Multiple Sclerosis Society/


 2011/B/7/Italian MS Foundation/ 10-723/Stichting MS Research/ 16-947/Stichting MS Research/


 MR/T024437/1/MRC_/Medical Research Council/United Kingdom


 RG-1501-03141/MSS_/Multiple Sclerosis Society/United Kingdom







 K23 HD101667/HD/NICHD NIH HHS/United States UL1 TR002369/TR/NCATS NIH HHS/United States












 2018/29/B/NZ3/02380/National Science Center/

 THC-135234/CIHR/Canada 333252/CIHR/Canada




 F2018-0052/Neuroförbundet/ FORSS-315121/Forskningsrådet i Sydöstra Sverige/ SB16-0011/Stiftelsen för Strategisk Forskning/ 2018-02776/Vetenskapsrådet/
 RG-1507-05433/National Multiple Sclerosis Society/




 MRC_/Medical Research Council/United Kingdom













 R35 NS111644/NS/NINDS NIH HHS/United States


 MC_PC_17228/MRC_/Medical Research Council/United Kingdom Z99 AG999999/ImNIH/Intramural NIH HHS/United States








 U54 MD007597/MD/NIMHD NIH HHS/United States

 UH3TR000890/NH/NIH HHS/United States


 N/A/Biogen Japan Ltd./

 10.13039/100009945/GMSI/

 R01 DC004689/DC/NIDCD NIH HHS/United States


















 SCG grant NV18-04-00168/Grantová Agentura České Republiky/ GA UK 154218/Univerzita Karlova v Praze/ PROGRES-Q27/LF1/Univerzita Karlova v Praze/



 Consejería de Educación, Cultura y Deportes-JCCM and FEDER funds/ Universidad de Castilla-La Mancha/



 R35 GM143060/GM/NIGMS NIH HHS/United States



 PP-1708-29077/National Multiple Sclerosis Society/ NA/Dana Foundation/










 F.4-V0134.K5.1/86/34/Bayerisches Staatsministerium für Wissenschaft und Kunst/ KKF 2020/Faculty of Medicine, Munich University of Technology/











 WT_/Wellcome Trust/United Kingdom



 399831/Isfahan University of Medical Sciences/












 101017558/European Union/








 RG 5184A2/1/National Multiple Sclerosis Society/














 K23 NS107624/NS/NINDS NIH HHS/United States R01 MH123550/MH/NIMH NIH HHS/United States R01 NS112274/NS/NINDS NIH HHS/United States UL1 TR001863/TR/NCATS NIH HHS/United States


 no number/Alberta Multiple Sclerosis Network/


 R03NR014515/NR/NINR NIH HHS/United States








 APVV-15-0228/Slovak Research and Development Agency/ APVV-21-0261/Slovak Research and Development Agency/
 UL1 TR000448/TR/NCATS NIH HHS/United States UL1 TR002345/TR/NCATS NIH HHS/United States P30 CA091842/CA/NCI NIH HHS/United States UL1 TR000448/TR/NCATS NIH HHS/United States P30 CA091842/CA/NCI NIH HHS/United States



 n/a/Merck (Germany)/



 WT_/Wellcome Trust/United Kingdom WT200804/WT_/Wellcome Trust/United Kingdom




 F31 NS108668/NS/NINDS NIH HHS/United States R01 ES017080/ES/NIEHS NIH HHS/United States RC2 AG036607/AG/NIA NIH HHS/United States R01 NR017431/NR/NINR NIH HHS/United States






 K23 NS116225/NS/NINDS NIH HHS/United States
 K23 AR078930/AR/NIAMS NIH HHS/United States












 UL1 TR001863/TR/NCATS NIH HHS/United States
 MR/T024402/1/MRC_/Medical Research Council/United Kingdom















 Canadian Institute for Health Research/





 779312/h2020 european research council/







 81473577/Innovative Research Group Project of the National Natural Science Foundation of China/ 82004028/Innovative Research Group Project of the National Natural Science Foundation of China/ 81903596/National Natural Science Foundation of China/ 201803D421073/ShanXi Science and Technology Department/ 201901D211538/Shanxi Provincial Key Research and Development Project/


 SFB/CRC-TR 128/Deutsche Forschungsgemeinschaft/
 Mashhad University of Medical Sciences/



 R01 NS103940/NS/NINDS NIH HHS/United States





 2021-022/Dr. Rolf M. Schwiete Stiftung/ FOR2289/Deutsche Forschungsgemeinschaft/













 AG/NIA NIH HHS/United States EY/NEI NIH HHS/United States

 Governo Italiano: Ricerca Corrente/ Fondazione Alessandro e Vincenzo Negroni Prati Morosini/ Fondazione Romeo ed Enrica Invernizzi/









 RC2 AG036607/AG/NIA NIH HHS/United States R01 AI076544/AI/NIAID NIH HHS/United States R01 NS049510/NS/NINDS NIH HHS/United States F31 NS108668/NS/NINDS NIH HHS/United States R01 ES017080/ES/NIEHS NIH HHS/United States R01 NS071463/NS/NINDS NIH HHS/United States




 2007-0481/European Leukodystrophy Association/ INSERM-DHOS/ Programme Hospitalier de Recherche Clinique/ MNP2008-007125/Agence nationale de la Recherche/ Fondation pour la recherche médicale/ Commissariat aux energies atomique/ ARSEP/ ECTRIMS/ Assistance Publique des Hôpitaux de Paris/ ANR-10-IAIHU-06/Investissements d'avenir/



 DMM1SAT18/Almirall S.L./


 FDN 167270/CIHR/Canada

 K01 MH121582/MH/NIMH NIH HHS/United States R01 HD082176/HD/NICHD NIH HHS/United States
 INFRA-P (n.378-35)/Regione Piemonte/




 R35 NS111644/NS/NINDS NIH HHS/United States R01 NS049510/NS/NINDS NIH HHS/United States TL1 TR001871/TR/NCATS NIH HHS/United States R01 ES017080/ES/NIEHS NIH HHS/United States MC_QA137853/MRC_/Medical Research Council/United Kingdom MC_PC_17228/MRC_/Medical Research Council/United Kingdom R01 NS099240/NS/NINDS NIH HHS/United States R01 AI076544/AI/NIAID NIH HHS/United States R35NS111644/NH/NIH HHS/United States


 R01 AI121945/AI/NIAID NIH HHS/United States R56 AI121945/AI/NIAID NIH HHS/United States T32 NS082174/NS/NINDS NIH HHS/United States
 MR/R001162/1/MRC_/Medical Research Council/United Kingdom National Multiple Sclerosis Society/ National Institute of Health/ International Progressive MS Alliance/ MEHTA/JUL17/948-795/MNDA_/Motor Neurone Disease Association/United Kingdom MC_EX_MR/N50192X/1/MRC_/Medical Research Council/United Kingdom MSS_/Multiple Sclerosis Society/United Kingdom




 E!113682 HORIZON2020/Eurostars/
 143279/CIHR/Canada







 3031/MSS_/Multiple Sclerosis Society/United Kingdom






 UL1 TR001085/TR/NCATS NIH HHS/United States

 R03 HS028502/HS/AHRQ HHS/United States




 PCN-2-117/N/0/K/Medical University of Silesia/

 81971542, 82171771, 82271854/National Natural Science Foundation of China/



 R01 DK131417/DK/NIDDK NIH HHS/United States















 RF1 AG071996/AG/NIA NIH HHS/United States













 F31 AG067717/AG/NIA NIH HHS/United States T32 HL110952/HL/NHLBI NIH HHS/United States UL1 TR002240/TR/NCATS NIH HHS/United States



 R01 AG072305/AG/NIA NIH HHS/United States R01 NS041435/NS/NINDS NIH HHS/United States S10 OD026859/OD/NIH HHS/United States












 RF1 AG072637/AG/NIA NIH HHS/United States UL1 TR002345/TR/NCATS NIH HHS/United States

 National Research Foundation (NRF) of Korea/ NRF-2021R1A2B5B03002123/Ministry of Science and ICT, Republic of Korea/ NRF-2018R1A5A2024425/Ministry of Science and ICT, Republic of Korea/ NRF-2021K2A9A2A06037695/Ministry of Science and ICT, Republic of Korea/ NRF-2022M3E5F1017919/Ministry of Science and ICT, Republic of Korea/ HI19C0664/Korean Health Technology R&D Project/ Ministry of Health & Welfare, Republic of Korea/ KEIT 20018560/Alchemist Project of the Korea Evaluation Institute of Industrial Technology/ NTIS 1415180625/Alchemist Project of the Korea Evaluation Institute of Industrial Technology/ Ministry of Trade, Industry & Energy, Republic of Korea/
 TG01010108/Technology Agency of the Czech Republic/



 MOP-142238/CIHR/Canada


 075-15-2020-795/Ministry of Science and Higher Education of the Russian Federation/




 F32 CA090073/CA/NCI NIH HHS/United States









 R01 NS113828/NS/NINDS NIH HHS/United States



 1R01NS096083/NH/NIH HHS/United States










 NKFIH K138125/National Research, Development, and Innovation Office/








 R35 NS111644/NS/NINDS NIH HHS/United States



 82173763/National Natural Science Foundation of China/ 91842305/National Natural Science Foundation of China/ 81771686/National Natural Science Foundation of China/ 52161145501/ISF-NSFC Joint Scientific Research Program/ 2020QNQT003/Funds for Youth Interdisciplinary and Innovation Research Groups of Shandong University/ ZR202206110012/Fundamental Research Funds of Shandong Province/ 2021CXGC010515/Shandong Provincial Key Research and Development Program (Major Scientific and Technological Innovation Project)/ 2019JZZY011127/Shandong Provincial Key Research and Development Program (Major Scientific and Technological Innovation Project)/ 2019JZZY021013/Shandong Provincial Key Research and Development Program (Major Scientific and Technological Innovation Project)/ ZR2020MH260/Shandong Provincial Natural Science Foundation/

 VEGA 1/0481/23/Scientific Grant Agency of the Ministry of Education of the Slovak Republic/


 EY019014/GF/NIH HHS/United States











 R01 NS119517/NS/NINDS NIH HHS/United States R03 NS126993/NS/NINDS NIH HHS/United States






 R01NS041435/NS/NINDS NIH HHS/United States R01NS082347/NS/NINDS NIH HHS/United States


 IK6 BX004982/BX/BLRD VA/United States R01 AT010980/AT/NCCIH NIH HHS/United States


 KL2 TR000136/TR/NCATS NIH HHS/United States

 National Multiple Sclerosis Society/ National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR)/




 PJT-156363/CIHR/Canada FDN-159934/CIHR/Canada

 K01 MH121582/MH/NIMH NIH HHS/United States THC-135234/CIHR/Canada


 RG-1707-28657/MSS_/Multiple Sclerosis Society/United Kingdom JF-1808-32223/MSS_/Multiple Sclerosis Society/United Kingdom



 PJT-168830/CIHR/Canada


 E63C22002080006/This research was founded by PNRR: "Health Extended ALliance for Innovative Therapies, Advanced Lab-research, and Integrated Approaches of Precision"/











 01.16.0078.00/FINEP/ 440779/2016-2/RENEZIKA/ 88887.130752/2016- 00/CAPES/




 PJT155933/CIHR/Canada


 CB06/05/0076/Biomedical Research Networking Center on Neurodegenerative Diseases/











 DS 466/Medical University of Lublin/







 2017/68/TUBAP/





 WT_/Wellcome Trust/United Kingdom


 P20 GM103408/GM/NIGMS NIH HHS/United States P20 GM109095/GM/NIGMS NIH HHS/United States R15 NS107743/NS/NINDS NIH HHS/United States



 JP 19K07515/Japan Society for the Promotion of Science/ S1411007/Ministry of Education, Culture, Sports, Science and Technology/

 2021ZD0201600/STI 2030-Major Projects/ 2020M672994/Chinese Postdoctoral Science Foundation/ 2020A1515010053/Natural Science Foundation of Guangdong Province/ 32070962/NSFC/ 81771300/NSFC/ 81971140/NSFC/ 82001284/NSFC/ 82101418/NSFC/

 KL2 TR002381/TR/NCATS NIH HHS/United States UL1 TR002378/TR/NCATS NIH HHS/United States




 Doctoral School in Health Care Sciences, Karolinska Institutet/ F2019-0056/NEURO Sweden/ 19115/Promobilia Foundation/ SLL20180182/Stockholm Region/




















 ID: 9910096961/Hamadan University of Medical Sciences/

 R-8676/Charcot research foundation/ R-6832/Charcot research foundation/ G099618N/Research Foundation Flanders/ EURLIPIDS EMR23/Interreg V-A EMR program/

 Ricerca Corrente on emerging infections/Ministero della Salute/ 848096/European Project SHARP/ resolution number 395 on 25 May 2021/Camera di Commercio, Industria e Artigianato di Roma/









 K12 HD055931/HD/NICHD NIH HHS/United States UL1 TR001082/TR/NCATS NIH HHS/United States UL1 TR002535/TR/NCATS NIH HHS/United States







 Fondazione Italiana Sclerosi Multipla (FISM)/
 1S25119N/Fonds Wetenschappelijk Onderzoek/










 R01 NS114066/NS/NINDS NIH HHS/United States
 R01 MH130458/MH/NIMH NIH HHS/United States R01 ES032323/ES/NIEHS NIH HHS/United States K99 NS114111/NS/NINDS NIH HHS/United States R01 AI126880/AI/NIAID NIH HHS/United States DP2 AI154435/AI/NIAID NIH HHS/United States F32 NS101790/NS/NINDS NIH HHS/United States UM1 AI126611/AI/NIAID NIH HHS/United States WT_/Wellcome Trust/United Kingdom U01 AI129206/AI/NIAID NIH HHS/United States R00 NS114111/NS/NINDS NIH HHS/United States K22 AI152644/AI/NIAID NIH HHS/United States R01 ES025530/ES/NIEHS NIH HHS/United States R01 AI149699/AI/NIAID NIH HHS/United States R21 NS087867/NS/NINDS NIH HHS/United States







 IK2 RX002826/RX/RRD VA/United States IK6 HX003156/HX/HSRD VA/United States
 F31 HD101281/HD/NICHD NIH HHS/United States
 DP2 GM146322/GM/NIGMS NIH HHS/United States R01 NS034939/NS/NINDS NIH HHS/United States

 2009/R/12/FISM - Italian Foundation Multiple Sclerosis/





 P01 NS031492/NS/NINDS NIH HHS/United States R01 AG043540/AG/NIA NIH HHS/United States P01 MH064570/MH/NIMH NIH HHS/United States P01 DA028555/DA/NIDA NIH HHS/United States P30 MH062261/MH/NIMH NIH HHS/United States P01 NS043985/NS/NINDS NIH HHS/United States R01 NS034239/NS/NINDS NIH HHS/United States R01 NS036126/NS/NINDS NIH HHS/United States P20 GM103427/GM/NIGMS NIH HHS/United States
 R35 NS111644/NS/NINDS NIH HHS/United States

 R01 NS113828/NS/NINDS NIH HHS/United States

 CIHR/Canada


 KL2 TR002381/TR/NCATS NIH HHS/United States UL1 TR002378/TR/NCATS NIH HHS/United States
 400000308/Baqiyatallah University of Medical Sciences/


 TRR 274/1/Deutsche Forschungsgemeinschaft (German Research Foundation)/ CRC870 A11-ID 118803580, Mi 694/8-1, Mi 694/9-1 A03-ID 428663564, FOR Immunostroke/Deutsche Forschungsgemeinschaft (German Research Foundation)/ INST95/1755-1 FUGG, ID 518284373/Deutsche Forschungsgemeinschaft (German Research Foundation)/ TRR128, Project B10 and B13/Deutsche Forschungsgemeinschaft (German Research Foundation)/ FP/2007-2013; ERC Grant Agreement n. 616791/EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013))/ FP/2007-2013; ERC Grant Agreement n. 310932/EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013))/

 R01 NS114220/NS/NINDS NIH HHS/United States









 R35 NS097303/NS/NINDS NIH HHS/United States
 R01 AI144667/AI/NIAID NIH HHS/United States F32 AI172499/AI/NIAID NIH HHS/United States I01 BX003690/BX/BLRD VA/United States R01 AI169686/AI/NIAID NIH HHS/United States R01 EB027143/EB/NIBIB NIH HHS/United States

 TA-2104-37423/National Multiple Sclerosis Society/ W81XWH-19-1-0622/U.S. Department of Defense/









 451-03-47/2023-01/200007/Ministry of Science, Technological Development and Innovation of Republic of Serbia/ 451-03-47/2023-01/200178/Ministry of Science, Technological Development and Innovation of Republic of Serbia/ 451-03-47/2023-01/200053/Ministry of Science, Technological Development and Innovation of Republic of Serbia/ 101079355/Horizon - EU grant/





 #FPU20-03072/"Agencia Estatal de Investigación-Ministerio de Ciencia, Innovación y Universidades"; FPU fellowship/ PID2022-1427850B-I00/"Fondo Europeo de Desarrollo Regional" (FEDER)-UE "A way to build Europe" from the "Ministerio de Economía y Competitividad/ PDC2022-133987-I00/"Fondo Europeo de Desarrollo Regional" (FEDER)-UE "A way to build Europe" from the "Ministerio de Economía y Competitividad/ PY20_00958/"Consejería de Transformación Económica, Industria, Conocimiento y Universidad, Junta de Andalucía"/ CTS-510/"Consejería de Transformación Económica, Industria, Conocimiento y Universidad, Junta de Andalucía"/ CEIJ-003/CEIMAR/

 R01 NS113828/NS/NINDS NIH HHS/United States

 2021.0347 (G.D.S.)/Fondazione Cassa di Risparmio di Perugia/



 F32 NS087899/NS/NINDS NIH HHS/United States KL2 TR001441/TR/NCATS NIH HHS/United States R21 AI133305/AI/NIAID NIH HHS/United States R01 CA204806/CA/NCI NIH HHS/United States P01 AI150585/NH/NIH HHS/United States

 18/CRT/6214/SFI_/Science Foundation Ireland/Ireland



 F32 HD101214/HD/NICHD NIH HHS/United States F31 HD101281/HD/NICHD NIH HHS/United States







 R21 NS109783/NS/NINDS NIH HHS/United States







 SWH2012LC02/Southwest Hospital/









 JF-1907-34355/National Multiple Sclerosis Society/



 P30 CA008748/CA/NCI NIH HHS/United States P50 CA092629/CA/NCI NIH HHS/United States




 PID2019-111788RB-I00/Ministerio de Ciencia e Innovación/






 R01 AG034924/AG/NIA NIH HHS/United States R01 AG066165/AG/NIA NIH HHS/United States P30CA013330/CA/NCI NIH HHS/United States NS116526/NH/NIH HHS/United States

 16-18-0001/Israeli Ministry of Agriculture and Rural Development/



 R01 NS071463/NS/NINDS NIH HHS/United States



 R01AI137047/National Institutes of Health/ R01EY027346/National Institutes of Health/ RG-1602-07722/National Multiple Sclerosis Society/


 R01 NS107523/NS/NINDS NIH HHS/United States

 R01 EY022936/EY/NEI NIH HHS/United States R01 NS115488/NS/NINDS NIH HHS/United States DH_/Department of Health/United Kingdom


 P01 HL142494/HL/NHLBI NIH HHS/United States R01 AG065582/AG/NIA NIH HHS/United States R01 AG067025/AG/NIA NIH HHS/United States R01 NS108419/NS/NINDS NIH HHS/United States F31 HL147364/HL/NHLBI NIH HHS/United States R35 HL139598/HL/NHLBI NIH HHS/United States R01 NS127808/NS/NINDS NIH HHS/United States R01 AG067025/AG/NIA NIH HHS/United States R01 AG050986/AG/NIA NIH HHS/United States UL1 TR001873/TR/NCATS NIH HHS/United States R35 HL135752/HL/NHLBI NIH HHS/United States P01 HL131478/HL/NHLBI NIH HHS/United States K99 HL151750/HL/NHLBI NIH HHS/United States R00 HL151750/HL/NHLBI NIH HHS/United States R01 HL158534/HL/NHLBI NIH HHS/United States
 AI07290/AI/NIAID NIH HHS/United States T32 AI007290/AI/NIAID NIH HHS/United States T32 AR050942/AR/NIAMS NIH HHS/United States T32 AI 7290-32/NH/NIH HHS/United States




 19-0702/Multiple Sclerosis Research Australia/


 FOR2289/Deutsche Forschungsgemeinschaft/
 U01 CA275310/CA/NCI NIH HHS/United States U01CA275310/NH/NIH HHS/United States
 2018/Rita Levi Montalcini Prize/


















 T32 AI007485/AI/NIAID NIH HHS/United States I01 CX002212/CX/CSRD VA/United States R01 AI137075/AI/NIAID NIH HHS/United States T90 DE023520/DE/NIDCR NIH HHS/United States P30 ES005605/ES/NIEHS NIH HHS/United States

 SEED/016/21/Interdisziplinäres Zentrum für Klinische Forschung, Münster/ MzH3/020/030/Interdisziplinäres Zentrum für Klinische Forschung, Münster/ HiGHmed 01ZZ1802V/Bundesministerium für Bildung und Forschung/ ME4050/12-1/Deutsche Forschungsgemeinschaft/
 R01 GM130791/GM/NIGMS NIH HHS/United States R01 AR076516/AR/NIAMS NIH HHS/United States S10 RR025141/RR/NCRR NIH HHS/United States UL1 TR002243/TR/NCATS NIH HHS/United States UL1 TR000445/TR/NCATS NIH HHS/United States UL1 RR024975/RR/NCRR NIH HHS/United States U01 HG004798/HG/NHGRI NIH HHS/United States R01 NS032830/NS/NINDS NIH HHS/United States RC2 GM092618/GM/NIGMS NIH HHS/United States P50 GM115305/GM/NIGMS NIH HHS/United States U01 HG006378/HG/NHGRI NIH HHS/United States U19 HL065962/HL/NHLBI NIH HHS/United States R01 HD074711/HD/NICHD NIH HHS/United States HHSN268201100005C/HL/NHLBI NIH HHS/United States HHSN268201100006C/HL/NHLBI NIH HHS/United States HHSN268201100007C/HL/NHLBI NIH HHS/United States HHSN268201100008C/HL/NHLBI NIH HHS/United States HHSN268201100009C/HL/NHLBI NIH HHS/United States HHSN268201100010C/HL/NHLBI NIH HHS/United States HHSN268201100011C/HL/NHLBI NIH HHS/United States HHSN268201100012C/HL/NHLBI NIH HHS/United States
 R01 NS104021/NS/NINDS NIH HHS/United States UL1 TR001412/TR/NCATS NIH HHS/United States
 #88882.428089/2019-01/Coordenação de Aperfeicoamento de Pessoal de Nível Superior/ #88887.374020/2019-00/Programa Institucional de Internacionalização/ #303531/2020-7/National Council for Scientific and Technological Development/ 2016/L'ORÉAL - ABC - UNESCO Para Mulheres na Ciência/ #23038.006930/2014/59/Prêmio Capes de Teses - Ciências Biológicas II, CAPES, 2014/ #21/2551-0001935-2/Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul (FAPERGS)/ #835286/European Research Council (ERC) under the European Union's Horizon 2020/





 R01 NS113828/NS/NINDS NIH HHS/United States R01 NS071463/NS/NINDS NIH HHS/United States
 WT_/Wellcome Trust/United Kingdom
 202846/Z/16/Z/WT_/Wellcome Trust/United Kingdom

 CIHR/Canada




 R21 MH118174/MH/NIMH NIH HHS/United States R33 MH118174/MH/NIMH NIH HHS/United States P30 CA046934/CA/NCI NIH HHS/United States P30 NS048154/NS/NINDS NIH HHS/United States P30 DK116073/DK/NIDDK NIH HHS/United States
 R01 AI125247/AI/NIAID NIH HHS/United States R01 CA068782/CA/NCI NIH HHS/United States R01 NS123532/NS/NINDS NIH HHS/United States

 FC001030/ARC_/Arthritis Research UK/United Kingdom





 R01-CA068782/HHS | National Institutes of Health (NIH)/


 P41 EB030006/EB/NIBIB NIH HHS/United States




 R21 AI156123/AI/NIAID NIH HHS/United States

 R35 NS111644/NS/NINDS NIH HHS/United States R01 AI165771/AI/NIAID NIH HHS/United States R21 AI171994/AI/NIAID NIH HHS/United States
 R01 AG059718/AG/NIA NIH HHS/United States R01 AI131624/AI/NIAID NIH HHS/United States I01 BX005396/BX/BLRD VA/United States R35 GM137921/GM/NIGMS NIH HHS/United States R01 AG052606/AG/NIA NIH HHS/United States R01 AG050676/AG/NIA NIH HHS/United States R03 CA262044/CA/NCI NIH HHS/United States
 R01 CA227473/CA/NCI NIH HHS/United States UL1 TR001863/TR/NCATS NIH HHS/United States UM1 AI144288/AI/NIAID NIH HHS/United States P01 AI039671/AI/NIAID NIH HHS/United States R25 NS079193/NS/NINDS NIH HHS/United States P50 CA121974/CA/NCI NIH HHS/United States U19 AI089992/AI/NIAID NIH HHS/United States P01 AI073748/AI/NIAID NIH HHS/United States
 R33 MH108156/MH/NIMH NIH HHS/United States T32 NS115657/NS/NINDS NIH HHS/United States T32 GM008136/GM/NIGMS NIH HHS/United States
 15-898 MS/Stichting MS Research/
 CRC-TR-128/German Research Council (DFG)/ CRC-TR-128/German Research Council (DFG)/ CRC-TR-128/German Research Council (DFG)/ CRC-TR-128/German Research Council (DFG)/


 19K07953/Japan Society for the Promotion of Science (JSPS) KAKENHI/ Ministry of Education, Culture, Sports, Science and Technology/ Ministry of Health, Labour and Welfare of Japan/


 JP22K07527/Japan Society for the Promotion of Science/ JP23K06493/Japan Society for the Promotion of Science/ JP21K0287/Japan Society for the Promotion of Science/ JP20K07894/Japan Society for the Promotion of Science/ JP20K07455/Japan Society for the Promotion of Science/ JP22K18378/Japan Society for the Promotion of Science/ Kindai University Research Enhancement Grant KD2303/Kindai University/ All-Kindai University support project against COVID-19/Kindai University/
 R01 NS112287/NS/NINDS NIH HHS/United States P30 AI028697/AI/NIAID NIH HHS/United States P30 CA016042/CA/NCI NIH HHS/United States R21 AI119916/AI/NIAID NIH HHS/United States





 MSS_/Multiple Sclerosis Society/United Kingdom
 MOH-TA20nov-002/National Medical Research Council/ CSAINV20nov-0015/National Medical Research Council/ OFLCG18May-0026/National Medical Research Council/
 R35 GM138283/GM/NIGMS NIH HHS/United States ZIA DK075149/ImNIH/Intramural NIH HHS/United States P30 CA023168/CA/NCI NIH HHS/United States

 22-15-00103/Russian Science Foundation/

 K02 NS072288/NS/NINDS NIH HHS/United States R01 NS092835/NS/NINDS NIH HHS/United States







 G0601744/MRC_/Medical Research Council/United Kingdom G0802545/MRC_/Medical Research Council/United Kingdom
 TL1 TR002493/TR/NCATS NIH HHS/United States UL1 TR002494/TR/NCATS NIH HHS/United States





 R01 NS103212/NS/NINDS NIH HHS/United States RF1 NS122174/NS/NINDS NIH HHS/United States




 R35 NS111644/NS/NINDS NIH HHS/United States




 270949263/GRK2162/Deutsche Forschungsgemeinschaft/



 R01 CA093606/CA/NCI NIH HHS/United States R01 AI153508/AI/NIAID NIH HHS/United States R01 CA259171/CA/NCI NIH HHS/United States R01 DE017336/DE/NIDCR NIH HHS/United States P30 CA010815/CA/NCI NIH HHS/United States
 P01 AI102853/AI/NIAID NIH HHS/United States ZIA DK075149/ImNIH/Intramural NIH HHS/United States ZIA AI001175/ImNIH/Intramural NIH HHS/United States ZIA BC011765/ImNIH/Intramural NIH HHS/United States
 R01 AG079477/AG/NIA NIH HHS/United States T32 NS115664/NS/NINDS NIH HHS/United States

 P41 EB028239/EB/NIBIB NIH HHS/United States R01 EB029455/EB/NIBIB NIH HHS/United States R21 AI160738/AI/NIAID NIH HHS/United States



 FG-2108-38348/MSS_/Multiple Sclerosis Society/United Kingdom RG-1901-33219/MSS_/Multiple Sclerosis Society/United Kingdom
 R01 ES032323/ES/NIEHS NIH HHS/United States R01 AI126880/AI/NIAID NIH HHS/United States R01 ES025530/ES/NIEHS NIH HHS/United States R01 AI149699/AI/NIAID NIH HHS/United States R21 NS087867/NS/NINDS NIH HHS/United States




 Research Group no KSRG 2022-053/King Salman Center for Disability Research/




 R24 OD031447/OD/NIH HHS/United States P40 OD018537/OD/NIH HHS/United States R01 NS110859/NS/NINDS NIH HHS/United States R24 OD022005/OD/NIH HHS/United States U54 HD083092/HD/NICHD NIH HHS/United States U54 NS093793/NS/NINDS NIH HHS/United States P50 HD103555/HD/NICHD NIH HHS/United States




 MC_UU_00005/12/MRC_/Medical Research Council/United Kingdom MR/T033371/1/MRC_/Medical Research Council/United Kingdom MR/M008983/1/MRC_/Medical Research Council/United Kingdom MR/M008525/1/MRC_/Medical Research Council/United Kingdom MC_UU_00030/14/MRC_/Medical Research Council/United Kingdom MR/T046015/1/MRC_/Medical Research Council/United Kingdom MC_U105597119/MRC_/Medical Research Council/United Kingdom MR/L023784/2/MRC_/Medical Research Council/United Kingdom MR/M023664/1/MRC_/Medical Research Council/United Kingdom G0301152/MRC_/Medical Research Council/United Kingdom


 FOR2289/Deutsche Forschungsgemeinschaft/



 P30 CA033572/CA/NCI NIH HHS/United States U01 NS122101/NS/NINDS NIH HHS/United States



















































 L30 CA220897/CA/NCI NIH HHS/United States

























 University of Social Welfare and Rehabilitation Sciences/


























 4001854/National Institute for Medical Research Development (NIMAD)/











 Novartis Pharma GmbH, Nuremberg, Germany/
 Iran National Science Foundation/

































 U54 AG044170/AG/NIA NIH HHS/United States








 R25 NS113757/NS/NINDS NIH HHS/United States










 SL43058/Roche Italia/










































 Swiss Multiple Sclerosis Society/Swiss Multiple Sclerosis Society/





 FF-1602-07939/FastForward at the National Multiple Sclerosis Society/ 1858/1859/Fight for Sight/ 206020/Z/16/Z/The Wellcome Trust/ 25036-166159/the Technology Strategy Board/Innovate UK/
 DST-SERB, CRG (Core Research Grant), Grant Number: CRG/2021/001009./Daejeon Institute of Science and Technology/

 R01 NS111105/NS/NINDS NIH HHS/United States

 NS053956/NH/NIH HHS/United States


 PP1829/National Multiple Sclerosis Society/ Functional Brain Mechanisms Underlying Depression in MS/











 MR/S026088/1/MRC_/Medical Research Council/United Kingdom













 288164/Norges Forskningsråd (Research Council of Norway)/


 Project number (RSPD2023R798),/Researchers Supporting Project number (RSPD2023R798), King Saud University, Riyadh, Saudi Arabia/

 BC Children's Hospital Research Institute/ 950-230363/Canada Research Chairs/ RN382474-418628/CAPMC/CIHR/Canada 237961/Consejo Nacional de Ciencia y Tecnología/ Milan and Maureen Ilich Foundation/ EGID 2002/Multiple Sclerosis Society of Canada/ RG-1507-05301/National Multiple Sclerosis Society/ 2016-05371/Natural Sciences and Engineering Research Council of Canada/ 402039-2011/Natural Sciences and Engineering Research Council of Canada/




























 FRGS/1/2020/STG03/UM/02/7/FRGS/







 CSTC2021 jscx-gksb-N0008/the Key Project of Technological Innovation and Application Development of Chongqing Science and Technology Bureau/















 MSCA-ITN-ETN H2020-860563/EU-project euSNN European School of Network Neuroscience/





























 Margarita Salas call is fro Laura Diaz-Marugan/ Biostime Institute Nutrition & Care (BINC)-Geneva grant/ Novartis Grant/ FISM-Fondazione Italiana Sclerosi Multipla-Cod.:2020/R-Single/029 and financed or co-financed with the '5 per mille' public funding/ Helmut Horten Fundation Grant/



















 52103191/National Natural Science Foundation of China/ 2019ZY1007/Scientific Research project of Traditional Chinese Medicine in Henan Province/ 32340144/Start-up Grant/

 P30 DK056336/DK/NIDDK NIH HHS/United States













 R01 HL149409/HL/NHLBI NIH HHS/United States R01 NS121928/NS/NINDS NIH HHS/United States R56 NR019306/NR/NINR NIH HHS/United States





 None./





 Intramural Grant/American University in Cairo/
 Telethon 2017/The Cyprus Muscular Dystrophy Association/


 SUBK.D150.22.027/Wroclaw Medical University/

























 Multiple Sclerosis Ltd./






























 KKF 8700000708/Department of Surgery/
 9910096961/Hamadan University of Medical Sciences/
 iStar/Gemeinnützige Hertie-Stiftung/









 GRS 2448/A/21/Gerencia regional de salud de Castilla y Léon/
 DMR-109-189/China Medical University Hospital/





































 2022/King Juan Carlos University/


 CAPMC/CIHR/Canada






































 C009-16.1/MSS_/Multiple Sclerosis Society/United Kingdom


 19-0702/Multiple Sclerosis Research Australia/
 28277_138_02_95/Iran University of Medical Sciences/
 NV18-08-00062/Ministerstvo Zdravotnictví Ceské Republiky/ RVO VFN 64165/Ministerstvo Zdravotnictví Ceské Republiky/ project Cooperatio LF1, research area Neuroscience/Ministerstvo Školství, Mládeže a Tělovýchovy/ Programme EXCELES, ID project No LX22NPO5107/European Commission/ 1154218/Grantová Agentura, Univerzita Karlova/








 3-16013/This study was supported by the Ministry of Science and Technology, Israel, and The Ministry of Foreign Affairs and International Cooperation, General Directorate for Country Promotion, Italian Republic./
 Virginia Commonwealth University; College of Health Professions/











 Biogen Switzerland AG/




 AGAPAO study/University of Campania "Luigi Vanvitelli"/







 MM03/09/Kuwait University/

















 ANR-18-CE45-0013/French National Research Agency/ ANR-10-LABX-57/Laboratory of Excellence TRAIL/ ANR-10-IDEX-03-02/IdEx Bordeaux/ French Ministry of Education and Research/ Centre national de la recherche scientifique/ PID2020-118608RB-I00/Spanish Ministerio de Ciencia e Innovación/ University of Bordeaux's France 2030 program / RRI "IMPACT"/


 OPUS 2016/23/B/NZ6/02541/Narodowe Centrum Nauki/ OPUS 2020/01/0/NZ6/00072/Narodowe Centrum Nauki/










 LTGY23H090006/Zhejiang Basic Public Welfare Research Project/ 2022489445/Zhejiang Medical and Health Science and Technology Plan Project/
 PI17/01726/Instituto de Salud Carlos III/ BES-2017-080384/Ministerio de Ciencia, Innovación y Universidades/ DPI 2016-79302-R/Ministerio de Economía y Competitividad/

 RF-2016-02361294/Ministero della Salute/



 K24 AT011568/AT/NCCIH NIH HHS/United States


 Majmaah University/ Saudi Arabian Cultural Mission/ The University of Queensland/ 2009957/National Health and Medical Research Council/



















 Conselho Nacional de Desenvolvimento Científico e Tecnológico/ Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/




























 5016-00143B/Innovationsfonden/






















 MR/T024402/1/MRC_/Medical Research Council/United Kingdom




 VIDI grant 09150172010056/ZONMW_/ZonMw/Netherlands


 1395/Semnan University of Medical Sciences/





 202102010263/Guangzhou Science and Technology Plan Project/ A20220136/Medical Science and Technology Foundation of Guangdong/





 POIR.04.01.04-00-0118/17/National Centre for Research and Development/

 R01 AG034676/AG/NIA NIH HHS/United States R01 AG052425/AG/NIA NIH HHS/United States U54 AG044170/AG/NIA NIH HHS/United States

 E65E22000370002/Regione Campania/






 R01 AI128074/AI/NIAID NIH HHS/United States





































 APP316901/The National Health and Medical Research Council of Australia/ 224215/The National Health and Medical Research Council of Australia/ 1127819/The National Health and Medical Research Council of Australia/ RG3364A1/2/The National Multiple Sclerosis Society of the United States of America/

 No. 82001740/National Natural Science Foundation of China/ 21BTQ050/Innovative Research Group Project of the National Natural Science Foundation of China/


 I01 RX002682/RX/RRD VA/United States






 2022CXZX-169/Education and Technology Innovation Project in Gansu Province/China 2021-1-177/Science and Technology Department of Gansu Province/China CY2021-MS-A06/Second Hospital of Lanzhou University/China 2022-77-6/Diagnosis and Treatment network platform/China

 Biogen/ Carl Tryggers Stiftelse för Vetenskaplig Forskning/ Vetenskapsrådet/
 JP 23K14675/Japanese Society for the promotion of Science/ 22/Regione Autonoma della Sardegna Legge Regionale 12/12/2022/

 MH CZ-DRO-VFN64165/Všeobecná Fakultní Nemocnice v Praze/ MH CZ-DRO-VFN64165/Všeobecná Fakultní Nemocnice v Praze/ MH CZ-DRO-VFN64165/Všeobecná Fakultní Nemocnice v Praze/ NU22-04-00193/Ministerstvo Zdravotnictví Ceské Republiky/












 138125/NKFIH/ 0/ELKH-SZTE Neuroscience Research Group/ 22-3/ÚNKP/ 3.6.3-VEKOP-16-2017-00009/EFOP/




 Vrije Universiteit Brussel/ Belgian Charcot Foundation/ Genzyme-Sanofi/ Innoviris/ Fonds Wetenschappelijk Onderzoek (FWO)/

 2022/003/the German charity fund ´Förderverein zur Kontinenzforschung und Kontinenzaufklärung e. V. ', Karmeliterhöfe, Karmeliterstr, 10, 52064 Aachen, Germany./
 Merck KGaA, Darmstadt, Germany/

















 R01 AI043496/AI/NIAID NIH HHS/United States U19 AI046374/AI/NIAID NIH HHS/United States


 KU2760/4-1/Deutsche Forschungsgemeinschaft/


 R01 HL063762/HL/NHLBI NIH HHS/United States R01 NS093382/NS/NINDS NIH HHS/United States RF1 AG053391/AG/NIA NIH HHS/United States
 None/














 R01AT007452/AT/NCCIH NIH HHS/United States





 31870334/National Natural Science Foundation of China/




 6602c-TF/19-345/Bozok Üniversitesi/







 R01 GM143362/GM/NIGMS NIH HHS/United States R01 GM132672/GM/NIGMS NIH HHS/United States




 R01 AI080769/AI/NIAID NIH HHS/United States R01 AI074745/AI/NIAID NIH HHS/United States R21 AI148898/AI/NIAID NIH HHS/United States R01 AI121302/AI/NIAID NIH HHS/United States





 HN21C1058/Korea Drug Development Fund funded by the Ministry of Science and ICT; Ministry of Trade, Industry, and Energy; and Ministry of Health and Welfare/ 2022M3A9G1014520, 2023R1A2C2003034, 2019M3D1A1078940, and 2019R1A6A1A11051471/National Research Foundation of Korea/







 801790/ERC_/European Research Council/International






 960037/Mashhad University of Medical Sciences/



 F2019-0056/Neuroförbundet/ 19115/Stiftelsen Promobilia/ CIMED, SLL20190446/Center for Innovative Medicine/ ALF, SLL20180182/Stockholms Läns Landsting/












 FPU 17/04240/Spanish Ministry of Education, Culture and Sports under University Professor Training Program Grant/ US-1379382/European Regional Development Fund (ERDF) and the Regional Ministry for Economy Transfor-mation, Industry, Knowledge, and Universities of the Junta de Andalucía [Andalusian Regional Govt.], under Operational Program ERDF 2014-2020/

 project 2013/R/13/Fondazione Italiana Sclerosi Multipla/







 P20 GM103436/GM/NIGMS NIH HHS/United States P20 GM135004/GM/NIGMS NIH HHS/United States


 T32 GM007367/GM/NIGMS NIH HHS/United States


 R01 EY024655/EY/NEI NIH HHS/United States R01 EY032284/EY/NEI NIH HHS/United States R01 NS082347/NS/NINDS NIH HHS/United States

 grant agreement n°115014/Innovative Medicines Initiative Joint Undertaking (European Union's Seventh Framework Programme (FP7/2007-2013))/








 GR-2008-1138784/Ministero della Salute/






 KL2 TR002381/TR/NCATS NIH HHS/United States UL1 TR002378/TR/NCATS NIH HHS/United States

 Cooperatio Program/Charles University in Prague, Czech Republic/ research area NEUR/Charles University in Prague, Czech Republic/ FN HK 00179906/grant projects of the Ministry of Health of the Czech Republic/
 NS112727/RG/CSR NIH HHS/United States AI144004/RG/CSR NIH HHS/United States




































 R01NS085211/NS/NINDS NIH HHS/United States R01NS112274/NS/NINDS NIH HHS/United States R01NS060910/NS/NINDS NIH HHS/United States R01MH123550/MH/NIMH NIH HHS/United States
 1K23NS072366-01A1/NS/NINDS NIH HHS/United States 1R01NS104403-01/NS/NINDS NIH HHS/United States








 K23MH120510/MH/NIMH NIH HHS/United States R21MH126271/MH/NIMH NIH HHS/United States R56 AG069086/MH/NIMH NIH HHS/United States R01MH113929/MH/NIMH NIH HHS/United States R01MH115949/MH/NIMH NIH HHS/United States R56AG069086/AG/NIA NIH HHS/United States R01AG060987/AG/NIA NIH HHS/United States










 RF1 AG061729/AG/NIA NIH HHS/United States R21 NS122152/NS/NINDS NIH HHS/United States P30 CA016059/CA/NCI NIH HHS/United States

 not applicable/Novartis Pharma GmbH, Germany/











 A20H4b0141/Agency for Science, Technology and Research/ NRF2019-THE002-0006/National Research Foundation Singapore/ NRF-CRP24-2020-0001/National Research Foundation Singapore/ CG/C010A/2017_SERI/National Medical Research Council/ OFLCG/004c/2018-00/National Medical Research Council/ MOH-000249-00/National Medical Research Council/ MOH-000647-00/National Medical Research Council/ MOH-001001-00/National Medical Research Council/ MOH-001015-00/National Medical Research Council/ MOH-000500-00/National Medical Research Council/ MOH-000707-00/National Medical Research Council/ MOH-001072-06/National Medical Research Council/ MOH-001286-00/National Medical Research Council/
 grant number: 70831/Student Research Committee, Tabriz University of Medical Sciences/





 KU 3791/4-1/Deutsche Forschungsgemeinschaft/ FI 1543/4-1/Deutsche Forschungsgemeinschaft/ 65-0021/Von-Behring-Röntgen-Stiftung/


 2017/20032-5/Fundação de Amparo à Pesquisa do Estado de São Paulo/ 2018/18078-0/Fundação de Amparo à Pesquisa do Estado de São Paulo/



 82030096/National Natural Science Foundation of China/ 82173410/National Natural Science Foundation of China/ 82230105/National Natural Science Foundation of China/
 None/













 CNPq/Conselho Nacional de Desenvolvimento Científico e Tecnológico/Brazil UFC/Universidade Federal do Ceará/Brazil


 Social Sciences and Humanities Research Council of Canada/ Brock University/
 Tabriz University of Medical Sciences, Tabriz, Iran/

 R01 NS102417/NS/NINDS NIH HHS/United States
 Aston University/




 National Institutes of Health; National Institute on Aging/ National Institutes of Health; National Center for Medical Rehabilitation Research/


 K01 AG030514/AG/NIA NIH HHS/United States P30 AG010129/AG/NIA NIH HHS/United States R01 AG032306/AG/NIA NIH HHS/United States U01 AG024904/AG/NIA NIH HHS/United States







 ALFGBG-722081/Swedish State Support for Clinical Research/ ALFGBG-71320/Swedish State Support for Clinical Research/ ALFGBG-71320/Swedish State Support for Clinical Research/ #2022-01018/Vetenskapsrådet/ #2019-02397/Vetenskapsrådet/ 101053962/European Union's Horizon Europe research and innovation programme/ 201809-2016862/Alzheimer's Drug Discovery Foundation/ ADSF-21-831376-C/AD Strategic Fund and the Alzheimer's Association/ ADSF-21-831381-C/AD Strategic Fund and the Alzheimer's Association/ ADSF-21-831377-C/AD Strategic Fund and the Alzheimer's Association/ JPND2021-00694/), the European Union Joint Programme - Neurodegenerative Disease Research/ UKDRI-1003/UK Dementia Research Institute at UCL/


 16154/Nasjonalforeningen for Folkehelsen/ 263024513, 466106904, 446812474, 504079349/Deutsche Forschungsgemeinschaft/ 2019054, 2019055, 2022046/Southern and Eastern Norway Regional Health Authority/ 19008/Barnekreftforeningen Norge/ TO01000078/Technology Agency of the Czech Republic/ 295910, 327571/The Research Council of Norway/ 882717/Austrian Research Promotion Agency/ 8F21002/Ministry of Education Youth and Sports/ 01ED2106/Federal Ministry of Education and Research/ ES 518 RTD/2020/26/State Education Development Agency/ 20-JPW2-0002-04/Agence Nationale de la Recherche/ 2020-02905/Swedish Research Council/










 FISM2019/S/3/Fondazione Italiana Sclerosi Multipla/ FISM 2019/BR/009/Fondazione Italiana Sclerosi Multipla/ 5 per mille/





 R21 DA055427/DA/NIDA NIH HHS/United States R21 DA055426/DA/NIDA NIH HHS/United States




 BX002565 (JLD)/veterans affairs merit award/ NS122152/National Institute of Neurologic Disease and Stroke R21/ AG061872 (XH)/National Institute on Aging RF1/ AG061729 (XH)/National Institute on Aging RF1/ AG066546-02 (Biomarker Core, XH/National Institute on Aging P30/ JPP/San Antonio Claude D. Pepper Center RL5/ 5P30NS047463/NIH-NINDS Center core grant/
 2018/02/X/NZ5/01487/Narodowe Centrum Nauki/ Operational Programme "Innovative Economy" for 2007-2013/European Regional Development Fund/




 UL1 TR001881/TR/NCATS NIH HHS/United States
 P30 EY021725/EY/NEI NIH HHS/United States R01 EY033782/EY/NEI NIH HHS/United States








 R21AI153749/U.S. Department of Health & Human Services | NIH | Center for Information Technology (Center for Information Technology, National Institutes of Health)/ K99AI159380/U.S. Department of Health & Human Services | NIH | Center for Information Technology (Center for Information Technology, National Institutes of Health)/ R01NS102156/U.S. Department of Health & Human Services | NIH | Center for Information Technology (Center for Information Technology, National Institutes of Health)/ R21AI153749/U.S. Department of Health & Human Services | NIH | Center for Information Technology (Center for Information Technology, National Institutes of Health)/ FG-1507-05297/National Multiple Sclerosis Society (National MS Society)/ RG-1701-26630/National Multiple Sclerosis Society (National MS Society)/ #17319/Conrad N. Hilton Foundation (CNHF)/







 R01 AI113903/AI/NIAID NIH HHS/United States

 R01 NS107569/NS/NINDS NIH HHS/United States





 PG/17/26/32881/BHF_/British Heart Foundation/United Kingdom


 R01 EB000790/EB/NIBIB NIH HHS/United States R01 NS057198/NS/NINDS NIH HHS/United States R01 MH124839/MH/NIMH NIH HHS/United States RF1 AG073593/AG/NIA NIH HHS/United States R01 MH120219/MH/NIMH NIH HHS/United States
 KYSQ 2020-092-01/Beijing Tiantan Hospital of Capital Medical University/ ZYLX202108/Beijing Hospital Authority Clinical Medicine Development of Special Funding/









 1I01CX002212/National Institutes of Health/NIAID 1R01AI137075 (AKM)/ NIH P30 ES005605/University of Iowa Environmental Health Sciences Research Center/ Gift from P. Heppelmann and M. Wacek/ T32AI007260/NIH: Interdisciplinary Immunology Postdoctoral Training Program/

 2020Y9128/Joint Funds for the Innovation of Science and Technology, Fujian Province(CN)/ 2019J01311/Natural Science Foundation of Fujian Province/





 PS 166120/CIHR/Canada NEURON 161466/CIHR/Canada





 SYLYC2022138, SYL20060187, and SYL20060189/Postgraduate Cultivating Innovation and Quality Improvement Action Plan of Henan University/ SYLYC2022138, SYL20060187, and SYL20060189/Postgraduate Cultivating Innovation and Quality Improvement Action Plan of Henan University/ 21A310005/Key Project of Henan Education Committee/ U2004104/National Natural Science Foundation of China/



















 2022JH2/101500024/Application and Base Research Joint Program of Liaoning Province/ 201602768/Project of Natural Science Foundation of Liaoning Province/ 20-205-4-044/Project of Natural Science Foundation of Shenyang/




 108-1081874-1988/Ministry of Science and Education, Croatia/
 21-1-079/Multiple Sclerosis Research Australia/
 KSRG 2022-053/King Salman Center for Disability Research/


 No.yzjj2018rc03/Presidential Foundation of Zhujiang Hospital of Southern Medical University/



 5/3/8/1/ITR-F/2020/Indian Council of Medical Research/
 259373024 - CRC/TRR 167 (B05)./Deutsche Forschungsgemeinschaft/ 069032/State of Berlin, Germany, Elsa-Neumann Ph.D. scholarship/ 821283-2/European Union/ The publication of this article was funded by Freie Universität Berli/Freie Universität Berlin/
 21PJ023/Health Commission of Sichuan Province/ 2022M710101/Postdoctoral Research Foundation of China/




 203930/B/16/Z/WT_/Wellcome Trust/United Kingdom














 R21AG082327/National Institute of Health/

 R01NS12646801/NH/NIH HHS/United States DMS-166172/National Science Foundation/ N/A/Bryon Riesch Paralysis Foundation/


 82101419/National Natural Science Foundation of China: Role and Mechanism of Akkermansia-Mediated Activation of Microglia NLRP3 Inflammasome in Multiple Sclerosis/ 20212BAB216024/Jiangxi Provincial Natural Science Foundation: the Role and Mechanism of p38 MAPK Signaling Pathway Induced by Intestinal Flora Change in EAE Mice/ 2021B660/Jiangxi Science and Technology Project of Chinese Medicine: Study on the Role and Mechanism of CGAS-STING Signaling Pathway in Microglia Mediated by Rhodiola Sachalinensis in Multiple Sclerosis/ 2022B1007/Jiangxi Science and Technology Project of Chinese Medicine: Study on the Role and Mechanism of CGAS-STING Signaling Pathway in Microglia Mediated by Rhodiola Sachalinensis in Multiple Sclerosis/ 202210392/Jiangxi Science and Technology Program of Health Commission: the Role and Mechanism of Intestinal Flora Changes in Mediating the Activation of NLRP3 Inflammasome in Microglia in Multiple Sclerosis/ GJJ200215/Science and Technology Research Project of Jiangxi Education: Study on the Role and Mechanism of p38 MAPK Signaling Pathway Induced by Intestinal Flora Changes in EAE Mice/ YFYPY202021/Scientific Research and Development Project of the First Affiliated Hospital of Nanchang University: Effects of Exercise Training on Intestinal Flora of Multiple Sclerosis Model Rats and Its Mechanism/















 R01 MH123550/MH/NIMH NIH HHS/United States R01 MH120482/MH/NIMH NIH HHS/United States K23 MH133118/MH/NIMH NIH HHS/United States R01 MH113550/MH/NIMH NIH HHS/United States R01 NS085211/NS/NINDS NIH HHS/United States K99 MH127293/MH/NIMH NIH HHS/United States R21 AG070434/AG/NIA NIH HHS/United States T32 MH019112/MH/NIMH NIH HHS/United States R01 NS112274/NS/NINDS NIH HHS/United States R01 MH112847/MH/NIMH NIH HHS/United States


 2022/Krembil Foundation/





 22K15711/Japan Society for the Promotion of Science/ 310030_189080/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung/




 9390BN0 (to KS)/National Institute for Occupational Safety and Health/ 9390KK9 (to KS)/National Institute for Occupational Safety and Health/










 K23 AG058806/AG/NIA NIH HHS/United States R01 AG075507/AG/NIA NIH HHS/United States R01 MH112829/MH/NIMH NIH HHS/United States

 KL2TR001879/NH/NIH HHS/United States R01NS112274/NH/NIH HHS/United States






 R01 DE017336/DE/NIDCR NIH HHS/United States R01 CA093606/CA/NCI NIH HHS/United States P30 CA010815/CA/NCI NIH HHS/United States R50 CA211199/CA/NCI NIH HHS/United States R01 AI153508/AI/NIAID NIH HHS/United States


 A-2081-20210327/Welch Foundation/







 N/a/Eastern Virginia Medical School/







 P01 AI150585/AI/NIAID NIH HHS/United States


 Amity University/
 Mason2210/Judith Jane Mason and Harold Stannett Williams Memorial Foundation/ BGRF 2207/Bethlehem Griffiths Research Foundation/











 101010/WT_/Wellcome Trust/United Kingdom

 DL57/2016/CP1334/CT0006/Fundação para a Ciência e Tecnologia/ UIDP/04378/2020 and UIDB/04378/2020/Fundação para a Ciência e Tecnologia/

 7005433/City University of Hong Kong/ 7005626/City University of Hong Kong/ 9667198/City University of Hong Kong/ 9609307/City University of Hong Kong/ 9610560/City University of Hong Kong/ Hong Kong Centre for Cerebro-cardiovascular Health Engineering/ 81871409/National Natural Science Foundation of China/ 11102218/Research Grants Council/ 11200422/Research Grants Council/ RFS2223-1S02/Research Grants Council/ PDFS2122-1S01/Research Grants Council/ C1134-20G/Research Grants Council/ Tung Biomedical Sciences Centre/











 TRR128/Deutsche Forschungsgemeinschaft (German Research Foundation)/ TRR 274/1, TRR 152/Deutsche Forschungsgemeinschaft (German Research Foundation)/
 Bristol Myers Squibb/
 64.310/436/2565/Chulalongkorn University/
 R01 AR059775/AR/NIAMS NIH HHS/United States R01 AR060574/AR/NIAMS NIH HHS/United States R01 AR070854/AR/NIAMS NIH HHS/United States R01 CA138962/CA/NCI NIH HHS/United States U01 CA138962/CA/NCI NIH HHS/United States NS/NINDS NIH HHS/United States AT/NCCIH NIH HHS/United States








 F31 HL162467/HL/NHLBI NIH HHS/United States R21 AI148409/AI/NIAID NIH HHS/United States 1F31HL162467-01A1/HL/NHLBI NIH HHS/United States R01HL101972/HL/NHLBI NIH HHS/United States


 P30 AG021342/AG/NIA NIH HHS/United States U19 AI089992/AI/NIAID NIH HHS/United States K24 AG042489/AG/NIA NIH HHS/United States 75N93019C00065/AI/NIAID NIH HHS/United States U01 CA260507/CA/NCI NIH HHS/United States R01 CA227473/CA/NCI NIH HHS/United States P50 CA121974/CA/NCI NIH HHS/United States P01 AI039671/AI/NIAID NIH HHS/United States UM1 HG009390/HG/NHGRI NIH HHS/United States R01 AI122220/AI/NIAID NIH HHS/United States P01 AI073748/AI/NIAID NIH HHS/United States R25 NS079193/NS/NINDS NIH HHS/United States















 RRZD/029/Wellcome Trust (WT)/ MS50/Multiple Sclerosis Society (MS Society)/ 203151/Z/16/Z/Wellcome Trust (WT)/






 Ricerca Corrente 2023/Ministero della Salute/ Fondazione Alessandro and Vincenzo Negroni Prati Morosini/ Fondazione Romeo and Enrica Invernizzi/


 AES, ISCIII P121/00242./Instituto de Salud Carlos III/








 DIP-265/Defence Research and Development Organisation/



 P30 NS076408/NS/NINDS NIH HHS/United States P41 EB027061/EB/NIBIB NIH HHS/United States R01 GM130622/GM/NIGMS NIH HHS/United States






























 I01 CX002212/CX/CSRD VA/United States P30 ES005605/ES/NIEHS NIH HHS/United States R01 AI137075/AI/NIAID NIH HHS/United States T90 DE023520/DE/NIDCR NIH HHS/United States




 222102310340/the 2022 Key Scientific and Technological Project of Henan Science and Technology Department/ 22A310015/2022 Key Scientific Research Project of Universities of Henan Education Department/ B2021-68/Doctoral Fund Project of Henan Polytechnic University/ 81803399/2022 Innovative Research Team of Henan Polytechnic University/ T2022-3/2022 Innovative Research Team of Henan Polytechnic University/ 2020GGJS054/2020 Henan Provincial Colleges and Universities Youth Backbone Training Plan/ 82171451/National Natural Science Foundation of China/ 212102310774/2021 Key Scientific and Technological Project of Henan Science and Technology Department/ NSFRF220416/the Fundamental Research Funds for the Universities of Henan Province/ H20-523/College of Medicine-Beijing Bencaoyuan Pharmaceutical Co., Ltd Joint Scientific Research Project/ LHGJ20200829/2020 Joint Project of Henan Medical Science and Technology Research Program/ 81803399/the National Natural Science Foundation of China/
 MR/M020827/1/MRC_/Medical Research Council/United Kingdom




 R01 EB017230/EB/NIBIB NIH HHS/United States I01 CX002160/CX/CSRD VA/United States K01 EB032898/EB/NIBIB NIH HHS/United States S10 OD021771/OD/NIH HHS/United States R21 NS116434/NS/NINDS NIH HHS/United States R01 EB027585/EB/NIBIB NIH HHS/United States R01 NS117816/NS/NINDS NIH HHS/United States P50 HD103537/HD/NICHD NIH HHS/United States UL1 RR024975/RR/NCRR NIH HHS/United States R01 NS109114/NS/NINDS NIH HHS/United States K01 EB030039/EB/NIBIB NIH HHS/United States KL2 TR002245/TR/NCATS NIH HHS/United States R01 EY023240/EY/NEI NIH HHS/United States






 62877/Tabriz University of Medical Sciences/
 ME Association/








 P2022/BMD-7209-INTEGRAMUNE-CM/Comunidad de Madrid/ PI22/01759/Instituto de Salud Carlos III/ CEX2020-001041-S/Ministerio de Ciencia e Innovación/ FPU20/05176/Formación de Profesorado Universitario/ Pro CNIC Foundation/



 R01 AI131238/AI/NIAID NIH HHS/United States R01 AI029564/AI/NIAID NIH HHS/United States











 17K14961/JSPS KAKENHI/ 18H05121/JSPS KAKENHI/ 22gm1310008, CREST/AMED-CREST/ GLIA Center Grant/University of Yamanashi/
 81974206/Innovative Research Group Project of the National Natural Science Foundation of China/

 PS 168843/CAPMC/CIHR/Canada MSS_/Multiple Sclerosis Society/United Kingdom









 2021-ZZ-JC030/Project of Shaanxi Provincial Administration of Traditional Chinese Medicine/ 82204425/National Natural Science Foundation of China/ 32241007/National Natural Science Foundation of China/



 MR/V00381X/1/MRC_/Medical Research Council/United Kingdom
 MOP-324604/CIHR/Canada



 KL2 TR003016/TR/NCATS NIH HHS/United States UL1 TR003015/TR/NCATS NIH HHS/United States

 Diego Centonze and Georgia Mandolesi RF-2018-12366144/Ministero della Salute (Ministry of Health, Italy)/ Fabio Buttari GR-2018-12366154/Ministero della Salute (Ministry of Health, Italy)/ Progetto Ricerca Corrente to IRCCS Neuromed/Ministero della Salute (Ministry of Health, Italy)/ Progetto Ricerca Corrente to IRCCS San Raffaele; Georgia Mandolesi/Ministero della Salute (Ministry of Health, Italy)/ Diego Centonze cod. 2019/S/1 and financed or co-financed with the '5 per mille' public funding/Fondazione Italiana Sclerosi Multipla (FISM)/ Mario Stampanoni Bassi cod. 2020/R-Multi/018 and financed or co-financed with the '5 per mille' public funding/Fondazione Italiana Sclerosi Multipla (FISM)/ Project 'Nuovi Biomarker Diagnostici e Terapeutici delle Malattie Neurodegenerative' - ADOPT co-funded by FOE 2020/funding from CNR to Diego Centonze/ Giuseppe Matarese 2018/S/5/Fondazione Italiana Sclerosi Multipla (FISM)/ Giuseppe Matarese grant 2017 K55HLC 001/Progetti di Rilevante Interesse Nazionale (PRIN)/ Giuseppe Matarese RF-2019-12371111/Ministero della Salute (Ministry of Health, Italy)/ FISM/Fondazione Italiana Sclerosi Multipla (FISM)/

 23081.052442/2020-36/Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/ 303531/2020-7/Conselho Nacional de Desenvolvimento Científico e Tecnológico/ 21/2551-0001935-2/Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul/






























 not applicable/Novartis Pharma GmbH/










 22-15-00103/the Russian Science Foundation/

 K24 AG075234/AG/NIA NIH HHS/United States













 81903294/National Natural Science Foundation of China/ 202102020120/Guangzhou Basic and Applied Basic Research Foundation/ A2022080/Medical Scientific Research Foundation of Guangdong Province of China/
 R35 ES030443/ES/NIEHS NIH HHS/United States



 22-14-00245/Russian Science Foundation/


 R01 AG057671/AG/NIA NIH HHS/United States P30 AG024827/AG/NIA NIH HHS/United States











 ESO.0423006/Roche Hellas/
 BU1019/16-1/Deutsche Forschungsgemeinschaft/ GRK2515/1-1/Deutsche Forschungsgemeinschaft/ INST 2105/27-1 FUGG/Deutsche Forschungsgemeinschaft/ JU 2966/2-1/Deutsche Forschungsgemeinschaft/







 BONFOR/Rheinische Friedrich-Wilhelms-Universität Bonn/



 R01 ES033692/ES/NIEHS NIH HHS/United States R21 ES029624/ES/NIEHS NIH HHS/United States ES028244/ES/NIEHS NIH HHS/United States ES028288/ES/NIEHS NIH HHS/United States R01 ES029136/ES/NIEHS NIH HHS/United States

 21K07541/Japan society for the promotion of science　Grants-in-Aid for Scientific Research/





 DOCPRO42551/Intern funding of the University of Antwerp: DOCPRO4 BOF PhD fellowship at the University of Antwerp/






 LF-OC-21-000665/LEO Foundation/ NEA21-ECRG156/National Eczema Association/











 R01 DK100256/DK/NIDDK NIH HHS/United States R01 AI139475/AI/NIAID NIH HHS/United States R01 AI141631/AI/NIAID NIH HHS/United States R21 AI115752/AI/NIAID NIH HHS/United States




















 APP160100627/Australian Research Council/ 204-0000000057/Multiple Sclerosis Research Australia/Incubator/




 R01 NS112161/NS/NINDS NIH HHS/United States





 1R01NS121928/NS/NINDS NIH HHS/United States








 2042022005/Huanggang Normal University/










 GR-2018-12366005/Ministero della Salute/




 P400PM_199310/SNSF_/Swiss National Science Foundation/Switzerland







 I01 BX003690/BX/BLRD VA/United States R01 AI144667/AI/NIAID NIH HHS/United States R01 AI169686/AI/NIAID NIH HHS/United States R01 EB027143/EB/NIBIB NIH HHS/United States




 Regione Sardegna (Legge Regionale 7/2007 annualità 2016)/










 R01 NS115180/NS/NINDS NIH HHS/United States
 AR077890/NH/NIH HHS/United States




 RGPIN-2020-05087/Natural Sciences and Engineering Research Council/

 SRG/2022/000961/Science and Engineering Research Board/



 R01 NS034939/NS/NINDS NIH HHS/United States
 F30 AG077794/AG/NIA NIH HHS/United States












 SR-Tiget Core Grant, Tele21-A5/Telethon Foundation/ EKFP2020/Else Kröner Fresenius Prize for Medical Research 2020/

 P20 GM103418/GM/NIGMS NIH HHS/United States
 R01 AI144026/AI/NIAID NIH HHS/United States
 PJ015726/Cooperative Research Program for Agriculture Science and Technology Development/

 I01 BX005002/BX/BLRD VA/United States IK6 BX004982/BX/BLRD VA/United States R01 AT010980/AT/NCCIH NIH HHS/United States










 32102749/National Natural Science Foundation of China/ 32122086/National Natural Science Foundation of China/ 2022M721277/China Postdoctoral Science Foundation/ 2021YFD1800800/National Key Research and Development Program of China/ 2021CFA016/Natural Science Foundation of Hubei Province/ 2662023PY005/Fundamental Research Funds for the Central Universities/



 pdjh2023b0107/Special Fund Project for Science and Technology Innovation Strategy of Guangdong Province/ 202212121008/National College Students Innovation and Entrepreneurship Training Program/




 K23 NS117883/NS/NINDS NIH HHS/United States K23NS117883/NH/NIH HHS/United States U01NS111678/NH/NIH HHS/United States K01MH121582/NH/NIH HHS/United States


 P51 OD011092/OD/NIH HHS/United States





 P41 EB022544/EB/NIBIB NIH HHS/United States R01NS114066/NS/NINDS NIH HHS/United States S10 OD026987/OD/NIH HHS/United States P41EB022544/EB/NIBIB NIH HHS/United States S10OD026987/NIH Office of the Director/ R01 NS114066/NS/NINDS NIH HHS/United States





 R01 EY015130/EY/NEI NIH HHS/United States R01 EY017011/EY/NEI NIH HHS/United States







 Not applicable/University of Western Australia/ Not applicable/Perron Institute for Neurological and Translational Science/ Not applicable/Multiple Sclerosis Western Australia (MSWA)/






 3123/Mazandaran University of Medical Sciences/






 Association of Chartered Physiotherapists in Neurology/ Physiotherapy Network Fund/
 82270562/National Natural Science Foundation of China/ 81901655/National Natural Science Foundation of China/ tsqn202103190/Tai Shan Young Scholar Foundation of Shandong Province/ Q-2022134/TCM science and technology development plan of Shandong Province/ 2021YXNS045/Key research and development plan in Jining City/ JYFY303574/Postdoctoral Fund of the Affiliated Hospital of Jining Medical University/


 R01 NS125016/NS/NINDS NIH HHS/United States

 pdjh2023b0107/Special Fund Project for Science and Technology Innovation Strategy of Guangdong Province/ 202212121008/National College Students Innovation and Entrepreneurship Training Program/
 MR/N013700/1/MRC_/Medical Research Council/United Kingdom MR/S003045/1/MRC_/Medical Research Council/United Kingdom
 R01 CA169519/CA/NCI NIH HHS/United States R21 DA023056/DA/NIDA NIH HHS/United States R01 DA043543/DA/NIDA NIH HHS/United States R21 DA040305/DA/NIDA NIH HHS/United States R01 CA261979/CA/NCI NIH HHS/United States






 Royal Melbourne Hospital Neuroscience Foundation/
 20210312/Medical Research Project of Hebei Province/








 82130030,81920108011,82171115 and 81770982/National Natural Science Foundation of China/
 56/MSS_/Multiple Sclerosis Society/United Kingdom MR/V00381X/1/MRC_/Medical Research Council/United Kingdom N/A/SPRINT-MND/MS/
 R01 NS103988/NS/NINDS NIH HHS/United States









 19K07511/Japan Society for the Promotion of Science KAKENHI/ 19K06471/Japan Society for the Promotion of Science KAKENHI/ 16K09703/Japan Society for the Promotion of Science KAKENHI/ 20K09719/Japan Society for the Promotion of Science KAKENHI/

 WT_/Wellcome Trust/United Kingdom FP7/2007-2013/ERC_/European Research Council/International 100/MSS_/Multiple Sclerosis Society/United Kingdom

 919888/Multiple Sclerosis Society of Canada/ 201600031/Alberta Innovates/













 22-15-00103./Russian Science Foundation,/
 K24 AG054415/AG/NIA NIH HHS/United States
 Research Credit Tax/Centre for Risk Research Inc. Montreal/
 22-15-00103/Russian Science Foundation,/










 R01NS103998/NH/NIH HHS/United States K25HL150305/National Institute of Health/ RG-1902-33633/National Multiple Sclerosis Society/ N/A/Pfizer/




 LA/P/0045/2020 (ALiCE)/Fundação para a Ciência e Tecnologia/ UIDB/00511/2020/Fundação para a Ciência e Tecnologia/ UIDP/00511/2020/Fundação para a Ciência e Tecnologia/ NORTE-01-0145-FEDER-000054/European Regional Development Fund/ EXPL/NAN-MAT/0209/2021/Fundação para a Ciência e Tecnologia/ UI/BD/150946/2021/Fundação para a Ciência e Tecnologia/ SFRH/BD/040932/2020/Fundação para a Ciência e Tecnologia/ CEEC-IND/01741/2021/Fundação para a Ciência e Tecnologia/ CEEC-INST/00049/2018/Fundação para a Ciência e Tecnologia/








 P30 CA142543/CA/NCI NIH HHS/United States P50 CA070907/CA/NCI NIH HHS/United States R38 HL150214/HL/NHLBI NIH HHS/United States U01 AI156189/AI/NIAID NIH HHS/United States














 2020YFC2004202/National Key R&D Program of China/











 SUB/2/DN/22/004/2211/Medical University of Białystok/








 724133976/Babol University of Medical Sciences/



 POS_2021_0008/Hezkuntza, Hizkuntza Politika Eta Kultura Saila, Eusko Jaurlaritza/



 I01 BX000136/BX/BLRD VA/United States R01 DK044234/DK/NIDDK NIH HHS/United States R01 DK080684/DK/NIDDK NIH HHS/United States
 MR/S005528/1/MRC_/Medical Research Council/United Kingdom RG81529/MSS_/Multiple Sclerosis Society/United Kingdom DH_/Department of Health/United Kingdom



 U01 AG024904/AG/NIA NIH HHS/United States






 20K11548/Scientific Research Programfor the Promotion of Sciences/




 NVTX2022: TX2022-20a-1/Vietnam National University Ho Chi Minh City (VNU-HCM)/
 MR/W006804/1/MRC_/Medical Research Council/United Kingdom










 MC_PC_17228/MRC_/Medical Research Council/United Kingdom WT_/Wellcome Trust/United Kingdom DH_/Department of Health/United Kingdom BHF_/British Heart Foundation/United Kingdom DUK_/Diabetes UK/United Kingdom

 U54 MH091657/MH/NIMH NIH HHS/United States


 R01 AG042178/AG/NIA NIH HHS/United States R01 AG069333/AG/NIA NIH HHS/United States R56 AG060767/AG/NIA NIH HHS/United States RF1 AG079264/AG/NIA NIH HHS/United States R56 AG066347/AG/NIA NIH HHS/United States R01 AG047812/AG/NIA NIH HHS/United States R01 NS105473/NS/NINDS NIH HHS/United States




 The Danish Ministry of Helath/ The Danish Multiple Sclerosis Society/ Bdr Hartmanns Foundation/ Karen A Tolstrup Foundation/ Direktør Ejnar Jonasson kaldet Johnsen og hustrus mindelegat/ Foundation for Reserach in Neurology/ Lykfeldts Fond/ Familien Hede Nielsens Fond/




 P41 EB031771/EB/NIBIB NIH HHS/United States




 2021-09/Schweizerische Multiple Sklerose Gesellschaft (Swiss Multiple Sclerosis Society)/ KFS-4962-02-2020/Krebsliga Schweiz (Swiss Cancer League)/ 310030_204470/1/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF)/ 310030L_197952/1/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF)/ CRSII5_180323/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF)/ 310030_184781/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF)/
















 31171348/National Natural Science Foundation of China (National Science Foundation of China)/ 32070768/National Natural Science Foundation of China (National Science Foundation of China)/ 32270754/National Natural Science Foundation of China (National Science Foundation of China)/ 31871404/National Natural Science Foundation of China (National Science Foundation of China)/




 2010778/National Science Foundation (NSF)/ H22P0M0007/Agency for Science, Technology and Research (A*STAR)/

 19/2551-0001-873-8/Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul/ 303263/2018-0/Coordenação de Aperfeiçoamento de Pessoal de Nível Superior/
 cx2021094/College Students' Innovative Entrepreneurial Training Plan Program of Jining Medical University/ cx2021011/College Students' Innovative Entrepreneurial Training Plan Program of Jining Medical University/ 2017WS143/Shandong Province Medicine and Health Science and Technology Development Plan Project/ 2019WS368/Shandong Province Medicine and Health Science and Technology Development Plan Project/ 2017JYQD23/Doctoral Setup Foundation of Jining Medical University/ ZR2020MH070/Natural Science Foundation of Shandong Province/ ZR2020MH078/Natural Science Foundation of Shandong Province/


 MSS_/Multiple Sclerosis Society/United Kingdom





 Young Investigator grant to H.-F. C./Saarland University/













 17H06400/Japan Society for the Promotion of Science/ 17H06404/Japan Society for the Promotion of Science/ 22K07527/Japan Society for the Promotion of Science/ 20K07433/Japan Society for the Promotion of Science/ 20K07455/Japan Society for the Promotion of Science/ 22K18378/Japan Society for the Promotion of Science/
 G03152021115804390/Sigma Xi Grants in Aid of Research (GIAR) program/ 2017YFB0403801/National Key Research and Development Program of China/ 31971096/National Natural Science Foundation of China/ 31771256/National Natural Science Foundation of China/ 31971099/National Natural Science Foundation of China/ 32100918/National Natural Science Foundation of China/ 2021M690060/Postdoctoral Research Foundation of China/ 2022T150227/Postdoctoral Research Foundation of China/



 R01 DA044999/DA/NIDA NIH HHS/United States


 K99 EB033407/EB/NIBIB NIH HHS/United States R01 NS114066/NS/NINDS NIH HHS/United States




 Azrieli Foundation/ Canada Research Chairs Program/ Canada Foundation for Innovation/ Ontario Research Fund/

 K01 DA023503/DA/NIDA NIH HHS/United States R21 DA044886/GM/NIGMS NIH HHS/United States R21 DA044886/DA/NIDA NIH HHS/United States R21 NS066130/NS/NINDS NIH HHS/United States P20 GM103643/GM/NIGMS NIH HHS/United States T32 AI07363-15/AI/NIAID NIH HHS/United States R01 DA11276/NH/NIH HHS/United States R01 NS098426/GM/NIGMS NIH HHS/United States R01 DA011276/DA/NIDA NIH HHS/United States R01 NS098426/NS/NINDS NIH HHS/United States T32 AI007363/AI/NIAID NIH HHS/United States
 K99 DK129785/DK/NIDDK NIH HHS/United States P30 DK020572/DK/NIDDK NIH HHS/United States
 3030277001/Excellence 2025 Talent Cultivation Program at Fudan University/ 82071201/National Natural Science Foundation of China/ 81971032/National Natural Science Foundation of China/ 92249305/National Natural Science Foundation of China/ 2022QD002/Research Start-up Fund of Huashan Hospital/ 2022ZD0211600/Science and Technology Innovation 2030 Major Projects/ 2018SHZDZX01/Shanghai Municipal Science and Technology Major Project/ 2019074/Shanghai Talent Development Funding for The Project/ ZHANGJIANG LAB, Tianqiao and Chrissy Chen Institute, and the State Key Laboratory of Neurobiology and Frontiers Center for Brain Science of Ministry of Education, Fudan University/

 The HTx project has received funding from the European Union's Horizon 2020 research and innovation programme under grant agreement Nº 825162. This dissemination reflects only the author's view and the Commission is not responsible for any use that may be made of the information it contains./






 P01 CA019014/CA/NCI NIH HHS/United States P30 CA016086/CA/NCI NIH HHS/United States P30 AI050410/AI/NIAID NIH HHS/United States


 2018B030337001/Guangzhou Science and Technology Research Project, China/ 2022A1515110993/Guangzhou Science and Technology Research Project, China/ JCYJ20210324115008022/Basic Research of Shenzhen Science and Technology Project, China/ JCYJ20220530144211024/Basic Research of Shenzhen Science and Technology Project, China/ FTWS2021069/Health Public Welfare Scientific Research Projects of Futian, China/ FTWS2022010/Health Public Welfare Scientific Research Projects of Futian, China/





 U01 AG068057/AG/NIA NIH HHS/United States R01 MH112070/MH/NIMH NIH HHS/United States HHSN271201300284P/DA/NIDA NIH HHS/United States RF1 AG054409/AG/NIA NIH HHS/United States S10 OD023495/OD/NIH HHS/United States R01 NS042645/NS/NINDS NIH HHS/United States R01 CA269948/CA/NCI NIH HHS/United States

 Canadian Occupational Therapy Foundation/ REA Foundation/ Ordre des ergothérapeutes du Québec/ Centre for Interdisciplinary Research in Rehabilitation of Greater Montreal/ Université de Montréal's Faculty of Medicine and School of Rehabilitation/ Fonds de recherche du Québec-Santé/ CIHR/Canada CIHR/Canada





 P30 CA042014/CA/NCI NIH HHS/United States R01 GM088040/GM/NIGMS NIH HHS/United States T32 HG008962/HG/NHGRI NIH HHS/United States T32 HL007208/HL/NHLBI NIH HHS/United States


 #9127045/ZONMW_/ZonMw/Netherlands #9127045/ZONMW_/ZonMw/Netherlands

 PID2019-109033RB-I00/Spanish Ministry of Science and Innovation/ n/a/Centro de Investigación Biomédica en Red de Salud Mental/



 2023A1515010641/Guangdong Province Natural Science Foundation/ N/A/Vincent & Lily Woo Foundation/










 PDAMP3_137087/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung,Switzerland/ PDAMP3_137087/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung,Switzerland/ JPJSJRP20221507/JSPS under the Joint Research Program implemented in association with SNSF (JRPs)/ 22K15711/JSPS/ PDFMP3_137127/Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung/




 R01 AG058621/AG/NIA NIH HHS/United States R01 MH113535/MH/NIMH NIH HHS/United States RF1 NS076815/NS/NINDS NIH HHS/United States





 R01 ES025748/ES/NIEHS NIH HHS/United States










 Z99 NS999999/ImNIH/Intramural NIH HHS/United States



 R21 AI144193/AI/NIAID NIH HHS/United States R21 AI164107/AI/NIAID NIH HHS/United States T32 CA009592/CA/NCI NIH HHS/United States



 R01NS090464/Foundation for the National Institutes of Health/ R01NS105144/Foundation for the National Institutes of Health/ S10OD021782/Foundation for the National Institutes of Health/ RG-1602-07671/National Multiple Sclerosis Society/

 PRIN 2017TSHBXZ_003/Ministry of Education, Universities and Research/ 2020FR7TCL/Ministry of Education, Universities and Research/

 PI21/00770, PI21/00140, PI17-00232/Instituto de Salud Carlos III/ (303/C/2016) (201602.30.31)/Fundació La Marató de TV3 2016/ PID2019-106209RB-I00/Ministerio de Ciencia e Innovación (MICINN)/ CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM)/

 2020R1A2C2007148/National Research Foundation of Korea/ 2016R1A5A1010148/National Research Foundation of Korea/ 2019M3E5D3073106/National Research Foundation of Korea/ 2018R1C1B6008884/National Research Foundation of Korea/





 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ 712965/EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/







 Ricerca Corrente/Ministero della Salute (Ministry of Health, Italy)/





 81671597/National Natural Science Foundation of China/ 82271258/National Natural Science Foundation of China/ 82074538/National Natural Science Foundation of China/ 2018SHZDZX01/Shanghai Municipal Science and Technology Major Project/ 21DZ2271800/Shanghai Key Laboratory for Acupuncture Mechanism and Acupoint Function/

 R01 NS109025/NS/NINDS NIH HHS/United States UL1 TR001881/TR/NCATS NIH HHS/United States P50 HD103557/HD/NICHD NIH HHS/United States R00 NS089780/NS/NINDS NIH HHS/United States R03 AG065772/AG/NIA NIH HHS/United States R01 NS099102/NS/NINDS NIH HHS/United States DP2 MH129988/MH/NIMH NIH HHS/United States


 81872522/National Natural Science Foundation of China/ 82073429/National Natural Science Foundation of China/ No. 81903205/National Natural Science Foundation of China/ No.2019-01-07-00-07-E00046/Innovation Program of Shanghai Municipal Education Commission/ No. SHDC2020CR1014B/Clinical Research Plan of SHDC/ No. 20XD1403300/Program of Shanghai Academic Research Leader/ 22PJD058/Shanghai Pujiang Program/
 UM1 CA186107/NH/NIH HHS/United States UM1 CA186107/NH/NIH HHS/United States UM1 CA186107/NH/NIH HHS/United States




 31800899/National Natural Science Foundation of China/ 2019YFS0212/Sichuan Province Science and Technology Support Program/ Z2021LC001/West China Hospital, Sichuan University/ ZYYC20009/West China Hospital, Sichuan University/

 11201141/Agencia Nacional de Investigación y Desarrollo/ RCFP44842-212-2018/Colciencias/ CVTUCH 2022-2/Concurso de Validación Tecnológica de la Universidad de Chile 2022/


 MC_UU_00007/10/MRC_/Medical Research Council/United Kingdom C8781/A13174/CRUK_/Cancer Research UK/United Kingdom MR/R008345/1/MRC_/Medical Research Council/United Kingdom U. MC_UU_00007/10/MRC Human Genetics Unit/



 TDK-2019-9670/Bilimsel Araştırma Projeleri, Erciyes Üniversitesi/
 14588/MSS_/Multiple Sclerosis Society/United Kingdom









 MC_PC_17228/MRC_/Medical Research Council/United Kingdom MR/V028766/1/MRC_/Medical Research Council/United Kingdom
 U1804186 and 81671619/National Science Foundation of China/ 202300410307, 212102310893, 212102310611, 22A180009 and 22A320043/Henan province Foundation/ GG2020009/Xinxiang City Foundation/






 No.81703978/This study was supported by the National Natural Science Foundation of China/ No.〔2022〕256/the National Young Qihuang Scholars Training Program/ No.〔2019〕35/the Outstanding Youth Talents Program of Shanxi Province/ (No.20210302124293/the Natural Science Foundation of Shanxi Province/ No.2021-142/the Research Project supported by Shanxi Scholarship Council of China/ No.Y213004/the Key science and technology R&D project of Jinzhong/ No.2020PY-JC-03, No.2021PY-QN-03, No.2022PY-TH-16, No.2022TD1013)/National Defense Science and Technology Innovation Fund of the Chinese Academy of Sciences/ No.202204041101002/the Key National Science and Technology Cooperation Project of Shanxi Province/
 2019R1A2C2002393/National Research Foundation of Korea/Korea




 MOE-112-S-023-A/the Higher Education Sprout Project by the Ministry of Education in Taiwan/ NA/the donation of TE Health Consultant Company Limited/

 R01 AI164709/AI/NIAID NIH HHS/United States R01 HG010730/HG/NHGRI NIH HHS/United States U01 CA275301/CA/NCI NIH HHS/United States WT_/Wellcome Trust/United Kingdom R01 CA228700/CA/NCI NIH HHS/United States R01 AI137337/AI/NIAID NIH HHS/United States

 PP00P3-157476/SNSF_/Swiss National Science Foundation/Switzerland 310030-192738/SNSF_/Swiss National Science Foundation/Switzerland 323630-183987/SNSF_/Swiss National Science Foundation/Switzerland









 826254/AHA/American Heart Association-American Stroke Association/United States R01 EB025220/EB/NIBIB NIH HHS/United States


 81870255/National Natural Science Foundation of China/ LY21H020001/Science Fund for Distinguished Young Scholars of Zhejiang Province/ 2021KY306/Medical Science and Technology Project of Zhejiang Province/ 2021J296/Natural Science Foundation of Ningbo Municipality/








 U01 HL131022/HL/NHLBI NIH HHS/United States






 DFJH201923/Climbing Program of Introduced Talents and High-level Hospital Construction Project of Guangdong Provincial People's Hospital/ DFJH201803/Climbing Program of Introduced Talents and High-level Hospital Construction Project of Guangdong Provincial People's Hospital/ KJ012019099/Climbing Program of Introduced Talents and High-level Hospital Construction Project of Guangdong Provincial People's Hospital/ KJ012021143/Climbing Program of Introduced Talents and High-level Hospital Construction Project of Guangdong Provincial People's Hospital/ KD0120220129/Foreign Distinguished Teacher Program of Guangdong Science and Technology Department/ 2022A1515012081/Guangdong Basic and Applied Basic Research Foundation/ 82171698/National Natural Science Foundation of China/ 82170561/National Natural Science Foundation of China/ 81300279/National Natural Science Foundation of China/ 81741067/National Natural Science Foundation of China/ 82100238/National Natural Science Foundation of China/ 2021B1515020003/Natural Science Foundation for Distinguished Young Scholars of Guangdong Province/ G2022030047L/Program for High-level Foreign Expert Introduction of China/ FWL/VA Clinical Merit and ASGE clinical research funds/
 K23 AI163359/AI/NIAID NIH HHS/United States EAIN-21038/PCORI/Patient-Centered Outcomes Research Institute/United States
 THC-135234/CIHR/Canada


 K23 EY027849/EY/NEI NIH HHS/United States KL2 TR002241/TR/NCATS NIH HHS/United States R01 AG059733/AG/NIA NIH HHS/United States R01 MD008879/MD/NIMHD NIH HHS/United States



 A136717/Genentech/

 R01 NS057563/NS/NINDS NIH HHS/United States R01 CA194414/CA/NCI NIH HHS/United States P30 AR048311/AR/NIAMS NIH HHS/United States P30 AI027767/AI/NIAID NIH HHS/United States




 MC_UU_00011/4/MRC_/Medical Research Council/United Kingdom


 MC_EX_MR/N50192X/1/MRC_/Medical Research Council/United Kingdom MR/R001162/1/MRC_/Medical Research Council/United Kingdom 217ARF R45951/Chief Scientist Office [UK]/



 PKU2022LCXQ034/Clinical Medicine Plus X-Young Scholars Project of Peking University/


























 0068926/Novo Nordisk Foundation/ 0075825/Novo Nordisk Foundation/ 337530/Academy of Finland/ 315492/Academy of Finland/


 UH3 HL147367/HL/NHLBI NIH HHS/United States UG3 HL147367/HL/NHLBI NIH HHS/United States R01 HL097088/HL/NHLBI NIH HHS/United States P01 HL131471/HL/NHLBI NIH HHS/United States U19 AI149646/AI/NIAID NIH HHS/United States P01 AI100263/AI/NIAID NIH HHS/United States P01 HL158506/HL/NHLBI NIH HHS/United States R21 AR077557/AR/NIAMS NIH HHS/United States R01 AI121135/AI/NIAID NIH HHS/United States R01 NS076991/NS/NINDS NIH HHS/United States R21 EB015684/EB/NIBIB NIH HHS/United States R01 HL152723/HL/NHLBI NIH HHS/United States



 K99 AI163868/AI/NIAID NIH HHS/United States T32 AI007334/AI/NIAID NIH HHS/United States R35 NS097976/NS/NINDS NIH HHS/United States RF1 AG064926/AG/NIA NIH HHS/United States K99 NS126707/NS/NINDS NIH HHS/United States C06 RR018928/RR/NCRR NIH HHS/United States



 PN-III-P2-2.1-PED-2019-3022/546PED/2020/Romanian Ministry of Research and Innovation CCCDI-UEFISCDI/

 Science and Technology Department of Zhejiang Province/ 2022C03096/Key Technologies R &amp; D Program of Zhejiang Province/ Hangzhou Municipal Health Commission, Project for Hangzhou Medical Disciplines of Excellence &amp; Key Project for Hangzhou Medical Disciplines/ LY22H090009/Natural Science Foundation of Zhejiang Province/ 81920108018/National Natural Science Foundation of China/ 82001412/National Natural Science Foundation of China/ 81901356/National Natural Science Foundation of China/


 R01 AG055425/AG/NIA NIH HHS/United States R56 AG055425/AG/NIA NIH HHS/United States UL1 TR001422/TR/NCATS NIH HHS/United States

 UIDP/04378/2020/Fundação de Apoio à Pesquisa e à Inovação Tecnológica do Estado de Sergipe/ UIDB/04378/2020/Fundação de Apoio à Pesquisa e à Inovação Tecnológica do Estado de Sergipe/



 K23 HL150237/HL/NHLBI NIH HHS/United States



 R01 NS126227/NS/NINDS NIH HHS/United States


 K24 AR080217/AR/NIAMS NIH HHS/United States R01 AR080356/AR/NIAMS NIH HHS/United States
 MR/S006591/1/MRC_/Medical Research Council/United Kingdom









 № 122041400080-0./Ministry of Science and Higher Education of the Russian Federation/



 (K.T.)/The Nancy Taylor Foundation for Chronic Diseases/

 81971574/National Natural Science Foundation of China/ 2021A1515220060/Basic and Applied Basic Research Foundation of Guangdong Province/ 202201020376/Special Fund for the Construction of High-level Key Clinical Specialty (Medical Imaging) in Guangzhou, Guangzhou Key Laboratory of Molecular Imaging and Clinical Translational Medicine/ R01-NS047592/National Institutes of Health (US)/ P01-NS059560/National Institutes of Health (US)/ U01-EY025500/National Institutes of Health (US)/ RG 1701-26617/National Multiple Sclerosis Society (US)/



 Z-3BC/02/Interdisciplinary Center of Clinical Research Würzburg/ JU 426/10-1/Deutsche Forschungsgemeinschaft/ JU 426/11-1/Deutsche Forschungsgemeinschaft/

 BRC-1215-20017/DH_/Department of Health/United Kingdom 216596/Z/19/Z/WT_/Wellcome Trust/United Kingdom NF-SI-0617-10077/DH_/Department of Health/United Kingdom



 101250/Nordisk Ministerråd/







 2021YFS0248/Key R & D Projects of Science and Technology Department of Sichuan Province/ 2020HXBH163/Postdoctoral Foundation of West China Hospital/ 20221174L/College Students' innovation and entrepreneurship training program/

 P01 AG066597/AG/NIA NIH HHS/United States P30 AG072979/AG/NIA NIH HHS/United States R01 NS115139/NS/NINDS NIH HHS/United States U19 AG062418/AG/NIA NIH HHS/United States

 UIDB/04501/2020 and UIDP/04501/2020/Fundação para a Ciência e Tecnologia/ SFRH/BD/144706/2019/Fundação para a Ciência e Tecnologia/



 81402442/National Natural Science Foundation of China/







 R01 AI155869/AI/NIAID NIH HHS/United States
 National Institute of Pharmaceutical Education and Research, S A S Nagar/




 1R011AG071803/AG/NIA NIH HHS/United States 1R01MD013818-01/MD/NIMHD NIH HHS/United States R01 MD013818/MD/NIMHD NIH HHS/United States R01 AG071803/AG/NIA NIH HHS/United States K23 DK123319/DK/NIDDK NIH HHS/United States

 P30 EY026878/EY/NEI NIH HHS/United States R01 EY034234/EY/NEI NIH HHS/United States K08 EY026652/EY/NEI NIH HHS/United States



 Research reported in this publication was funded by Novartis Pharma AG. The research was supported in part by the National Center for Advancing Translational Sciences of the National Institutes of Health under award number UL1TR001412. The content is sole/Novartis (Netherlands)/






 2019-0369/Shandong Provincial Traditional Chinese Medicine Science and Technology Development Plan Project/ 2019GSF108008, 2019GSF108033/Key research and development program of Shandong Province (public welfare)/ QYPY2019NSFC0616/National Natural Science Foundation of China Incubation Fund/ 2021BJ000005/Shandong Provincial Medical and Health Science and Technology Development Program (Healthcare Project)/

 P50 AR080612/AR/NIAMS NIH HHS/United States
 R01 AG077481/AG/NIA NIH HHS/United States R01 DC011020/DC/NIDCD NIH HHS/United States R01 NS100859/NS/NINDS NIH HHS/United States






























 UL1TR002541/NH/NIH HHS/United States U54NS092090/NR/NINR NIH HHS/United States U54HD090255/NH/NIH HHS/United States R01EB019483/NH/NIH HHS/United States R01NS079788/NH/NIH HHS/United States UL1TR002541/NH/NIH HHS/United States U54NS092090/NR/NINR NIH HHS/United States U54HD090255/NH/NIH HHS/United States R01EB019483/NH/NIH HHS/United States R01NS079788/NH/NIH HHS/United States




 R01 NS100859/NS/NINDS NIH HHS/United States T32HL134621/NH/NIH HHS/United States 1R01 NS100859/NS/NINDS NIH HHS/United States




 P30 AG019610/AG/NIA NIH HHS/United States P30 AG072980/AG/NIA NIH HHS/United States U24 NS072026/NS/NINDS NIH HHS/United States
 K23 NS117883/NS/NINDS NIH HHS/United States P30 EY026877/EY/NEI NIH HHS/United States R01 NS113828/NS/NINDS NIH HHS/United States
 HI22C1314/The Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea/





 R42 NS113642/NH/NIH HHS/United States R42 NS115184/NH/NIH HHS/United States R35 HL135736/NH/NIH HHS/United States


 AL-CHALABI/APR15/844-791/MNDA_/Motor Neurone Disease Association/United Kingdom ALCHALABI-DOBSON/APR14/829-791/MNDA_/Motor Neurone Disease Association/United Kingdom MR/R024804/1/MRC_/Medical Research Council/United Kingdom




 T32 EB025816/EB/NIBIB NIH HHS/United States


 MR/V027735/1/MRC_/Medical Research Council/United Kingdom

 I01 BX005180/BX/BLRD VA/United States I21 BX004957/BX/BLRD VA/United States RF1 AG056032/AG/NIA NIH HHS/United States


 2019YFA0801800/National Basic Research Program of China/ 2018YFA0107000/National Basic Research Program of China/ 81825001/National Natural Science Foundation of China/ 32030030/National Natural Science Foundation of China/ 81900147/National Natural Science Foundation of China/ 31971052/National Natural Science Foundation of China/ 82000147/National Natural Science Foundation of China/ 32100906/National Natural Science Foundation of China/ 82170175/National Natural Science Foundation of China/ 81721004/Innovative Research Group Project of the National Natural Science Foundation of China/ 20ZR1430900/Shanghai Science and Technology Commission/ 19XD1422100/Shanghai Science and Technology Commission/ 20JC1410100/Shanghai Science and Technology Commission/ 20204Y0008/Shanghai Science and Technology Commission/ 2019-I2M-5-051/CAMS Innovation fund for Medical Sciences/



 MC_EX_MR/N50192X/1/MRC_/Medical Research Council/United Kingdom DOD/14/15/My Name'5 Doddie Foundation/ MC_UU_00004/07/MRC_/Medical Research Council/United Kingdom

 MR/T001712/1/MRC_/Medical Research Council/United Kingdom












 JP22bm0804003/Japan Agency for Medical Research and Development/ JP22bm0804023/Japan Agency for Medical Research and Development/ JP17K10083/Japan Society for the Promotion of Science/ JP20H03567/Japan Society for the Promotion of Science/ JP22K18388/Japan Society for the Promotion of Science/
 R42 NS113642/NS/NINDS NIH HHS/United States R35 HL135736/HL/NHLBI NIH HHS/United States R42 NS115184/NS/NINDS NIH HHS/United States

 81922059/National Natural Science Foundation of China/ xzy022019006/Fundamental Research Funds for the Central Universities/

 2021YFC2501200/National Key Research and Development Program of China/ 2021YJ0415/Sichuan Science and Technology Program/ 2022ZDZX0023/Sichuan Science and Technology Program/
 451-03-47/2023-01/200042/Ministry of Education, Science, and Technological Development, Republic of Serbia/

 R21 MH119803/MH/NIMH NIH HHS/United States R01 NS083706/NS/NINDS NIH HHS/United States R01 NS088321/NS/NINDS NIH HHS/United States R01 AG076154/AG/NIA NIH HHS/United States R01 AG066447/AG/NIA NIH HHS/United States R01 AG074609/AG/NIA NIH HHS/United States T32 NS007224/NS/NINDS NIH HHS/United States

 R01 DC017291/DC/NIDCD NIH HHS/United States
 HHSN268201600018C/HL/NHLBI NIH HHS/United States HHSN268201600001C/HL/NHLBI NIH HHS/United States HHSN268201600004C/HL/NHLBI NIH HHS/United States HHSN268201600003C/HL/NHLBI NIH HHS/United States HHSN268201600002C/HL/NHLBI NIH HHS/United States
 NIHR301592/National Institute for Health and Care Research/





 MR/M008525/1/MRC_/Medical Research Council/United Kingdom MR/M023664/1/MRC_/Medical Research Council/United Kingdom MR/T046015/1/MRC_/Medical Research Council/United Kingdom
 R21 DC018098/DC/NIDCD NIH HHS/United States R33 DA047527/DA/NIDA NIH HHS/United States RF1 MH132337/MH/NIMH NIH HHS/United States T32 MH014276/MH/NIMH NIH HHS/United States
 108890/Z/15/Z/Wellcome Trust/United Kingdom
 P30 AG072975/AG/NIA NIH HHS/United States RF1 AG054617/AG/NIA NIH HHS/United States T32 AG000247/AG/NIA NIH HHS/United States R01 AG017917/AG/NIA NIH HHS/United States P30 AG010161/AG/NIA NIH HHS/United States K99 AG065501/AG/NIA NIH HHS/United States R01 NS017950/NS/NINDS NIH HHS/United States UF1 NS125513/NS/NINDS NIH HHS/United States R01 AG059727/AG/NIA NIH HHS/United States R01 AG072475/AG/NIA NIH HHS/United States P30 AG066546/AG/NIA NIH HHS/United States R01 AG022018/AG/NIA NIH HHS/United States R13 AG030995/AG/NIA NIH HHS/United States R01 AG015819/AG/NIA NIH HHS/United States F31 AG074599/AG/NIA NIH HHS/United States


 R01 NS131409/NS/NINDS NIH HHS/United States R01 NS097850/NS/NINDS NIH HHS/United States UM1 HG006493/HG/NHGRI NIH HHS/United States U24 HG008956/HG/NHGRI NIH HHS/United States R44 NS097094/NS/NINDS NIH HHS/United States S10 OD021553/OD/NIH HHS/United States R01 DC015530/DC/NIDCD NIH HHS/United States R00 NS077435/NS/NINDS NIH HHS/United States

 T32 AG044402/AG/NIA NIH HHS/United States

 R21 AG072078/AG/NIA NIH HHS/United States R21AG072078/AG/NIA NIH HHS/United States RF1NS113820/NS/NINDS NIH HHS/United States R01 NS107347/NS/NINDS NIH HHS/United States RF1AG078948/AG/NIA NIH HHS/United States RF1 NS127925/NS/NINDS NIH HHS/United States RF1NS127925/NS/NINDS NIH HHS/United States R01 AG078948/AG/NIA NIH HHS/United States R01NS107347/NS/NINDS NIH HHS/United States
 R01 MH120170/MH/NIMH NIH HHS/United States R01 MH124871/MH/NIMH NIH HHS/United States R01 MH118278/MH/NIMH NIH HHS/United States R01 MH119084/MH/NIMH NIH HHS/United States R01 MH124871/MH/NIMH NIH HHS/United States R01 MH120170/MH/NIMH NIH HHS/United States

 73305095007/ZONMW_/ZonMw/Netherlands







 P01 AG019724/AG/NIA NIH HHS/United States P50 AG023501/AG/NIA NIH HHS/United States





 K08 NS094744/NS/NINDS NIH HHS/United States R01 NS122907/NS/NINDS NIH HHS/United States
 K23 NS105935/NS/NINDS NIH HHS/United States P30 AG066462/AG/NIA NIH HHS/United States






 FKZ-01ER0816/Bundesministerium für Bildung und Forschung/ FKZ-01ER1506/Bundesministerium für Bildung und Forschung/ FKZ-01ER1205/Bundesministerium für Bildung und Forschung/





 F31 DC020108/DC/NIDCD NIH HHS/United States R01 DC009890/DC/NIDCD NIH HHS/United States R15 DC018944/DC/NIDCD NIH HHS/United States R01 DC017291/DC/NIDCD NIH HHS/United States K24 DC016312/DC/NIDCD NIH HHS/United States
 R01 AG021055/AG/NIA NIH HHS/United States UF1 AG057707/AG/NIA NIH HHS/United States P30 AG066519/AG/NIA NIH HHS/United States
 R01 NS131409/NS/NINDS NIH HHS/United States R01 NS097850/NS/NINDS NIH HHS/United States K99 NS077435/NS/NINDS NIH HHS/United States R44 NS097094/NS/NINDS NIH HHS/United States R01 DC015530/DC/NIDCD NIH HHS/United States R00 NS077435/NS/NINDS NIH HHS/United States
 2021JJ31083/the Natural Science Foundation of Hunan Province/
 1140386/National Health and Medical Research Council/








 U01 AG046152/AG/NIA NIH HHS/United States U01 AG061356/AG/NIA NIH HHS/United States R01 AG017917/AG/NIA NIH HHS/United States T32 AG058527/AG/NIA NIH HHS/United States R01 AG015819/AG/NIA NIH HHS/United States P30 AG072975/AG/NIA NIH HHS/United States P30 AG010161/AG/NIA NIH HHS/United States R01 AG069904/AG/NIA NIH HHS/United States

 K08 AR077689/AR/NIAMS NIH HHS/United States UL1 TR001863/TR/NCATS NIH HHS/United States R21 AI159580/AI/NIAID NIH HHS/United States

 DH_/Department of Health/United Kingdom
 MR/T024402/1/MRC_/Medical Research Council/United Kingdom
 WT_/Wellcome Trust/United Kingdom MR/M019969/1/MRC_/Medical Research Council/United Kingdom MR/M020827/1/MRC_/Medical Research Council/United Kingdom MR/V031260/1/MRC_/Medical Research Council/United Kingdom
 R01 MH130458/MH/NIMH NIH HHS/United States P01 AI056299/AI/NIAID NIH HHS/United States K99 NS114111/NS/NINDS NIH HHS/United States DP2 AI154435/AI/NIAID NIH HHS/United States F32 NS101790/NS/NINDS NIH HHS/United States K12 CA090354/CA/NCI NIH HHS/United States R00 NS114111/NS/NINDS NIH HHS/United States
 R43 AG061978/AG/NIA NIH HHS/United States





 P40 OD018537/OD/NIH HHS/United States R01 NS117461/NS/NINDS NIH HHS/United States



 PRO4ALL/Roche Italia/

 2211610/National Cancer Center, Korea/
 2020-FAR.L-CF_003; 2021-FAR.L-CF_002; FAR2057432; FIR2030548; 2020-FAR.L-PA_001/University of Ferrara/ PRIN 2019-PRA.A-PA_001/MIUR/






 100014_165884/SNSF_/Swiss National Science Foundation/Switzerland 100019_176016/SNSF_/Swiss National Science Foundation/Switzerland CRSII5_177277/SNSF_/Swiss National Science Foundation/Switzerland 10001C_188878/SNSF_/Swiss National Science Foundation/Switzerland



 MC_PC_17228/MRC_/Medical Research Council/United Kingdom MC_QA137853/MRC_/Medical Research Council/United Kingdom


 IP-2018-01-8563/Croatian Science Foundation/ 18-211-1369/University of Rijeka/

 R01 HL126827/HL/NHLBI NIH HHS/United States R01 HL146754/HL/NHLBI NIH HHS/United States
















 K08 NS101118/NS/NINDS NIH HHS/United States R35 GM128772/GM/NIGMS NIH HHS/United States
 RF-2016-02362405/Ministero della Salute/ FP7/2007-2013 under grant agreement 259867/European Commission/ Joint Programme - Neurodegenerative Disease Research (Strength, ALS-Care and Brain-Mend projects)/Ministero dell'Istruzione, dell'Università e della Ricerca/ PRIN, grant 2017SNW5MB/Ministero dell'Istruzione, dell'Università e della Ricerca/ Department of Excellence grant/Ministero dell'Istruzione, dell'Università e della Ricerca/
 R00 ES029986/ES/NIEHS NIH HHS/United States










 UL1 TR001422/TR/NCATS NIH HHS/United States UL1 TR002003/TR/NCATS NIH HHS/United States R01 AI097134/AI/NIAID NIH HHS/United States R01 AR073284/AR/NIAMS NIH HHS/United States P30 AR075043/AR/NIAMS NIH HHS/United States P30 AR073752/AR/NIAMS NIH HHS/United States S10 OD027016/OD/NIH HHS/United States R01 HD037416/HD/NICHD NIH HHS/United States L40 AR076139/AR/NIAMS NIH HHS/United States UL1 TR000448/TR/NCATS NIH HHS/United States
 T32 AR060719/AR/NIAMS NIH HHS/United States R56 AR081251/AR/NIAMS NIH HHS/United States P30 AR074992/AR/NIAMS NIH HHS/United States P30 DK020579/DK/NIDDK NIH HHS/United States


 P50HD105351/NH/NIH HHS/United States

 VIT SEED Grant - RGEMS Fund (Sanction Order No. SG20220054)/Vellore Institute of Technology, Vellore/



 R35 GM131701/GM/NIGMS NIH HHS/United States R01 GM132640/GM/NIGMS NIH HHS/United States

 IG21877/Associazione Italiana per la Ricerca sul Cancro/







 R01 GM136897/GM/NIGMS NIH HHS/United States R21 AG072078/AG/NIA NIH HHS/United States T32 GM007445/GM/NIGMS NIH HHS/United States R01 NS107347/NS/NINDS NIH HHS/United States RF1 NS113820/NS/NINDS NIH HHS/United States RF1 NS127925/NS/NINDS NIH HHS/United States T32 GM008403/GM/NIGMS NIH HHS/United States
 R01 AG068398/AG/NIA NIH HHS/United States



 MR/N026063/1/MRC_/Medical Research Council/United Kingdom MR/V031260/1/MRC_/Medical Research Council/United Kingdom MR/S025065/1/MRC_/Medical Research Council/United Kingdom
 R01NS113828/NS/NINDS NIH HHS/United States
 grant RF-2016-02362405/Ministero della Salute/ FP7/2007-2013 under grant agreement 259867/Seventh Framework Programme/ PRIN/Ministero dell'Istruzione, dell'Università e della Ricerca/ grant 2017SNW5MB/Ministero dell'Istruzione, dell'Università e della Ricerca/ Brainteaser Project/European Union's Horizon 2020 research and innovation programme/ grant GA101017598/European Union's Horizon 2020 research and innovation programme/

 KL2 TR002245/TR/NCATS NIH HHS/United States P30 DK058404/DK/NIDDK NIH HHS/United States T32 AR059039/AR/NIAMS NIH HHS/United States P30 CA068485/CA/NCI NIH HHS/United States T32 HL087738/HL/NHLBI NIH HHS/United States UL1 TR002243/TR/NCATS NIH HHS/United States I01 BX002882/BX/BLRD VA/United States R01 DK084246/DK/NIDDK NIH HHS/United States

 AL-CHALABI/APR15/844-791/MNDA_/Motor Neurone Disease Association/United Kingdom ALCHALABI-TALBOT/APR14/926-794/MNDA_/Motor Neurone Disease Association/United Kingdom MR/R024804/1/MRC_/Medical Research Council/United Kingdom ALCHALABI-DOBSON/APR14/829-791/MNDA_/Motor Neurone Disease Association/United Kingdom R01 NS105479/NS/NINDS NIH HHS/United States
 R35 NS097273/NS/NINDS NIH HHS/United States

 ZIA NS003154/ImNIH/Intramural NIH HHS/United States





 n/a/SSADH Association/ n/a/Hørslev Foundation/


 K01 AG070376/AG/NIA NIH HHS/United States R01 AG058233/AG/NIA NIH HHS/United States T32 AG058529/AG/NIA NIH HHS/United States
 University of Adelide/

 Z01 AG000949/ImNIH/Intramural NIH HHS/United States ZIA AG000534/ImNIH/Intramural NIH HHS/United States ZIA NS003154/ImNIH/Intramural NIH HHS/United States









 P30 AG062428/AG/NIA NIH HHS/United States


 R01 NS113828/NS/NINDS NIH HHS/United States








 P30 EY016665/EY/NEI NIH HHS/United States R01 EY027004/EY/NEI NIH HHS/United States R01 EY022305/EY/NEI NIH HHS/United States R01 EY015473/EY/NEI NIH HHS/United States R01 EY031424/EY/NEI NIH HHS/United States P30 EY014104/EY/NEI NIH HHS/United States R01 EY032559/EY/NEI NIH HHS/United States
 MS1-173066/CAPMC/CIHR/Canada MS1-173066/CAPMC/CIHR/Canada

 640116/ERC_/European Research Council/International
 The National Psoriasis Foundation-NPF/ 2020-FAR.L-CF_003/University of Ferrara/ 2021-FAR.L-CF_002/University of Ferrara/
 1R01AG073278-01A1/AG/NIA NIH HHS/United States


 NRF-2016R1A5A2945889/National Research Foundation Grant funded by the Korean Government (MSIP)/ NRF-2022R1A2B5B02001482/National Research Foundation Grant funded by the Korean Government (MSIP)/
 K08 NS126573/NS/NINDS NIH HHS/United States R01 MH119435/MH/NIMH NIH HHS/United States R01 MH122471/MH/NIMH NIH HHS/United States R25 MH060482/MH/NIMH NIH HHS/United States

 MR/S026088/1/MRC_/Medical Research Council/United Kingdom


 2019YFH0145/the Science &amp; Technology Department of Sichuan Province/ 2019YFH0196/the Science &amp; Technology Department of Sichuan Province/ 81571272/National Natural Science Foundation of China/ 8187017/National Natural Science Foundation of China/ ZYJC21001/the 1.3.5 project for disciplines of excellence and Brain Science project of West China Hospital, Sichuan University/


 R35 NS127253/NS/NINDS NIH HHS/United States R61 NS124965/NS/NINDS NIH HHS/United States R56 NS033123/NS/NINDS NIH HHS/United States R01 NS097903/NS/NINDS NIH HHS/United States R21 NS103009/NS/NINDS NIH HHS/United States R37 NS033123/NS/NINDS NIH HHS/United States

 APQ-01532-18, APQ-02559-17/FAPEMIG, Fundação de Amparo à Pesquisa do Estado de Minas Gerais/ 140585/2019-2, 310347/2018-1/Conselho Nacional de Desenvolvimento Científico e Tecnológico- CNPq/ 001/Coordenação de Aperfeicoamento de Pessoal de Nivel Superior, Brazil (CAPES)/
 R01 AI052201/AI/NIAID NIH HHS/United States R35-HL150829/NH/NIH HHS/United States P01 HL108793/HL/NHLBI NIH HHS/United States P01-HL108793/NH/NIH HHS/United States R35 HL150829/HL/NHLBI NIH HHS/United States R01-AI052201/NH/NIH HHS/United States

 R01 NS113828/NS/NINDS NIH HHS/United States

 K01 AT010984/AT/NCCIH NIH HHS/United States


 289581/MCCC_/Marie Curie/United Kingdom

 CIHR/Canada


 WT_/Wellcome Trust/United Kingdom 205167/Z/16/Z/WT_/Wellcome Trust/United Kingdom MR/TR000953/1/MRC_/Medical Research Council/United Kingdom MR/T019050/1/MRC_/Medical Research Council/United Kingdom MR/S026088/1/MRC_/Medical Research Council/United Kingdom 541/CAP/OC/818837/DH_/Department of Health/United Kingdom



 F31 DA054849/DA/NIDA NIH HHS/United States

 R01 AG075444/AG/NIA NIH HHS/United States R21 NS128635/NS/NINDS NIH HHS/United States R01 HD082373/HD/NICHD NIH HHS/United States R01 AG079956/AG/NIA NIH HHS/United States R01 NS105804/NS/NINDS NIH HHS/United States RF1 AG081401/AG/NIA NIH HHS/United States R35 NS111619/NS/NINDS NIH HHS/United States
 R01 AG071756/AG/NIA NIH HHS/United States K24 AG045333/AG/NIA NIH HHS/United States R01 AG057234/AG/NIA NIH HHS/United States U19 AG063911/AG/NIA NIH HHS/United States P30 AG062422/AG/NIA NIH HHS/United States R01 AG052496/AG/NIA NIH HHS/United States P01 AG019724/AG/NIA NIH HHS/United States R01 AG038791/AG/NIA NIH HHS/United States K01 AG049152/AG/NIA NIH HHS/United States U01 AG045390/AG/NIA NIH HHS/United States R01 AG062588/AG/NIA NIH HHS/United States R01 AG058233/AG/NIA NIH HHS/United States R01 AG073482/AG/NIA NIH HHS/United States U54 NS123985/NS/NINDS NIH HHS/United States
 R01 HL146500/HL/NHLBI NIH HHS/United States R01 CA265726/CA/NCI NIH HHS/United States R01 DK103794/DK/NIDDK NIH HHS/United States BHF_/British Heart Foundation/United Kingdom WT_/Wellcome Trust/United Kingdom

 VR4-172745/CAPMC/CIHR/Canada GA4-177764/CAPMC/CIHR/Canada

 MR/S03546X/1/MRC_/Medical Research Council/United Kingdom MR/T027800/1/MRC_/Medical Research Council/United Kingdom MR/T046422/1/MRC_/Medical Research Council/United Kingdom DH_/Department of Health/United Kingdom MR/L016311/1/MRC_/Medical Research Council/United Kingdom





 WT_/Wellcome Trust/United Kingdom

 HL111598/HL/NHLBI NIH HHS/United States HL149800/HL/NHLBI NIH HHS/United States







 SAF2017-88076-R/Ministerio de Ciencia, Innovación y Universidades/ RTI2018-099001-B-I00/Ministerio de Ciencia, Innovación y Universidades/ PID2021-126961OB-I00/Ministerio de Ciencia, Innovación y Universidades/ CIBERNED/Instituto de Salud Carlos III/ RD16/0011/0012/Instituto de Salud Carlos III/ RD16/0011/0011/Instituto de Salud Carlos III/ RD16/0011/0006/Instituto de Salud Carlos III/ 2017SGR-1095/Departament de Salut, Generalitat de Catalunya/ 2017SGR-1408/Departament de Salut, Generalitat de Catalunya/ A12076/CHDI Foundation/ LCF/PR/HR21-00622/"la Caixa" Foundation/
 P30 AR073752/AR/NIAMS NIH HHS/United States UL1 TR002345/TR/NCATS NIH HHS/United States


 R01 NS126227/NS/NINDS NIH HHS/United States

 81102552/National Natural Science Foundation of China/ 81703978/National Natural Science Foundation of China/ YDZX20201400001483/Central Government Guided Local Funding Projects for Science and Technology Development/ 〔2019〕35/Outstanding Youth Talents Program of Shanxi Province/ 20210302124293/Natural Science Foundation of Shanxi Province/ 201901D111334/Natural Science Foundation of Shanxi Province/ 20200026/Returned Chinese Scholars Technology Activities Preferred Project, Shanxi Province of China/ 2021-142/Research project supported by Shanxi Scholarship Council of China/ Y213004/Key Science and Technology R&D Project of Jinzhong/ 2021PY-QN-03/Young Scientist Cultivation Program Project, Shanxi University of Chinese Medicine/ 2021CX016/Graduate Innovation and Entrepreneurship Program of Shanxi University of Chinese Medicine/
 NUM-COVID 19 - Organo-Strat 01KX2021/Bundesministerium für Bildung und Forschung/ 16GW0191/Einstein Stiftung Berlin/




 32270720/National Natural Science Foundation of China (National Science Foundation of China)/ 91954121/National Natural Science Foundation of China (National Science Foundation of China)/ T2121004/National Natural Science Foundation of China (National Science Foundation of China)/ 32100671/National Natural Science Foundation of China (National Science Foundation of China)/ 82072201/National Natural Science Foundation of China (National Science Foundation of China)/ 2021M702848/China Postdoctoral Science Foundation/

 E-26/201.406/2021/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ VPPCB-005-FIO-20-2-56/Oswaldo Cruz Foundation/ E-26/210.254/2020/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ E-26/210.657/2021/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ E-26/210.273/2018/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ E-26/201.040/2021/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ E-26/210.817/2021/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/ 403008/2021-2/National Council for Scientific and Technological Development/ 00/Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro/

 U01 AG061356/AG/NIA NIH HHS/United States P30 AG072980/AG/NIA NIH HHS/United States ZIA AG000935/ImNIH/Intramural NIH HHS/United States RF1 AG057473/AG/NIA NIH HHS/United States ZIA NS003154/ImNIH/Intramural NIH HHS/United States P50 NS038377/NS/NINDS NIH HHS/United States U24 NS072026/NS/NINDS NIH HHS/United States P30 AG019610/AG/NIA NIH HHS/United States
 U01 AG016976/AG/NIA NIH HHS/United States
 FUAM 20/32/Fundación Universidad Autónoma de Madrid/ SEPAR 474-2017/Sociedad Española de Neumología y Cirugía Torácica/ PI18/00042/Instituto de Salud Carlos III/ RD21/0002/0025/Instituto de Salud Carlos III/ PI18/00042/European Regional Development Fund/ RD21/0002/0025/European Union/ CPII21/00004/Instituto de Salud Carlos III/ CPII21/00004/European Social Fund/ RD16/0012/0009/Instituto de Salud Carlos III/ RD16/0012/0009/European Regional Development Fund/ RD16/0012/0014/Instituto de Salud Carlos III/ RD16/0012/0014/European Regional Development Fund/



 P20 AG068053/AG/NIA NIH HHS/United States P30 AG066515/AG/NIA NIH HHS/United States P30 AG062421/AG/NIA NIH HHS/United States P30 AG066508/AG/NIA NIH HHS/United States RF1 NS110048/NS/NINDS NIH HHS/United States P30 AG066519/AG/NIA NIH HHS/United States P30 AG072973/AG/NIA NIH HHS/United States P30 AG066530/AG/NIA NIH HHS/United States P30 AG066509/AG/NIA NIH HHS/United States P20 AG068077/AG/NIA NIH HHS/United States P30 AG066546/AG/NIA NIH HHS/United States P30 AG072972/AG/NIA NIH HHS/United States P20 AG068082/AG/NIA NIH HHS/United States P30 AG072975/AG/NIA NIH HHS/United States P30 AG066444/AG/NIA NIH HHS/United States P30 AG066507/AG/NIA NIH HHS/United States P30 AG072946/AG/NIA NIH HHS/United States P30 AG066511/AG/NIA NIH HHS/United States R56 AG062479/AG/NIA NIH HHS/United States P30 AG066512/AG/NIA NIH HHS/United States P30 AG062422/AG/NIA NIH HHS/United States R01 AG079280/AG/NIA NIH HHS/United States P30 AG072977/AG/NIA NIH HHS/United States P30 AG062677/AG/NIA NIH HHS/United States P20 AG068024/AG/NIA NIH HHS/United States P30 AG072958/AG/NIA NIH HHS/United States P30 AG062715/AG/NIA NIH HHS/United States P30 AG066506/AG/NIA NIH HHS/United States P30 AG066468/AG/NIA NIH HHS/United States P30 AG072976/AG/NIA NIH HHS/United States RF1 AG062479/AG/NIA NIH HHS/United States P30 AG072931/AG/NIA NIH HHS/United States P30 AG066514/AG/NIA NIH HHS/United States P30 AG072959/AG/NIA NIH HHS/United States

 R01 NS126227/NS/NINDS NIH HHS/United States R56 AG055619/AG/NIA NIH HHS/United States DH_/Department of Health/United Kingdom R01 AG062562/AG/NIA NIH HHS/United States 104079/Z/14/Z/WT_/Wellcome Trust/United Kingdom MR/V007173/1/MRC_/Medical Research Council/United Kingdom K23 AG064029/AG/NIA NIH HHS/United States R01 AG031189/AG/NIA NIH HHS/United States
 R01 AG060871/AG/NIA NIH HHS/United States P30 AG066589/AG/NIA NIH HHS/United States RF1 AG069771/AG/NIA NIH HHS/United States P30 AG024968/AG/NIA NIH HHS/United States R01 AG062277/AG/NIA NIH HHS/United States R21 AG059623/AG/NIA NIH HHS/United States R01 AG060165/AG/NIA NIH HHS/United States U01 AG024904/AG/NIA NIH HHS/United States
 MC_PC_17230/MRC_/Medical Research Council/United Kingdom R01 NS115144/NS/NINDS NIH HHS/United States U01 NS100603/NS/NINDS NIH HHS/United States U01 NS095736/NS/NINDS NIH HHS/United States
 U19 AI090023/AI/NIAID NIH HHS/United States U19 AI118608/AI/NIAID NIH HHS/United States U54 AI142766/AI/NIAID NIH HHS/United States U19 AI057229/AI/NIAID NIH HHS/United States U19 AI062629/AI/NIAID NIH HHS/United States U19 AI118610/AI/NIAID NIH HHS/United States U19 AI128910/AI/NIAID NIH HHS/United States R01 AI104870/AI/NIAID NIH HHS/United States U19 AI125357/AI/NIAID NIH HHS/United States R01 AI145835/AI/NIAID NIH HHS/United States U19 AI128913/AI/NIAID NIH HHS/United States R01 AI122220/AI/NIAID NIH HHS/United States U19 AI077439/AI/NIAID NIH HHS/United States R01 AI135803/AI/NIAID NIH HHS/United States U19 AI089992/AI/NIAID NIH HHS/United States


 U01 NS072323/NS/NINDS NIH HHS/United States P50 NS048843/NS/NINDS NIH HHS/United States
























































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































 1
 1
 8
 1
 1

 4
 4
 1
 1
 3
 3
 9
 3


 9
 7969
 873
 3
 4
 4
 1
 8
 8
 3

 9

 9
 9
 5
 14
 4
 7

 9

 8

 8
 7
 7
 14

 3



 2
 3-4
 6
 1671
 23
 9

 1
 4


 4-5

 2

 1

 2
 1
 5
 2
 7
 9


 9
 9
 2
 6

 9

 6
 1
 3
 10372
 3
 5
 7
 5
 5
 1
 7
 1

 4
 6

 6
 2

 8
 1
 8

 2
 7
 3
 2
 3
 3
 1
 4
 1
 2
 5
 4

 1
 5
 6
 6
 9
 1
 1


 824
 1
 1
 7944
 Pt 1

 2

 9
 6
 1
 2
 3
 8


 9

 11-12
 1
 10
 1
 2
 7


 2
 2


 3



 6
 4


 1
 4
 2

 2
 6
 3
 8
 4
 9


 5
 4
 8
 1
 1
 14
 9

 9


 3
 2

 4

 3

 2

 3
 4
 4
 5
 1
 1
 8

 873
 4


 10
 1
 8
 3
 7
 1
 8
 4

 6




 1
 14
 2
 7
 1
 4

 6
 6
 6
 3
 5
 3
 6
 5
 4-5

 4
 4-5

 3
 7


 3



 6
 2

 1
 9
 4-6

 9



 6


 1
 1
 2
 4-5




 2
 7


 8
 3


 4
 1

 1
 3
 7
 6
 4
 5
 3

 5
 1
 1
 1
 8
 1

 7
 4
 4
 9
 9

 2
 2
 1

 5
 3
 10

 4
 1
 1
 4


 6
 1
 2

 4
 1
 1
 10
 3
 2
 5
 1
 3




 4


 1

 8

 873
 8
 8
 3
 3


 6
 7
 3
 7


 7
 2
 4
 6

 5
 3
 2


 1


 7. Vyp. 2
 2
 7


 1
 2

 1
 3
 5
 4
 6
 5


 1
 5
 1
 5
 2
 8
 11
 8
 8
 1
 7
 6
 2
 9

 10
 1


 1
 2



 9



 2

 1
 8
 2


 3
 8

 1
 1
 7. Vyp. 2
 3





 6
 8
 3
 1
 3

 4

 1
 4


 10
 1
 2
 5
 4

 5
 10


 9
 1
 8
 1
 3
 7. Vyp. 2
 4
 3

 3
 1
 3

 6

 4-5
 7. Vyp. 2
 3
 3





 1
 4



 2
 3
 4-5
 4-5

 1

 4
 9
 1
 7
 9
 4


 1

 9
 7
 3
 9
 11



 1
 3



 9
 8
 11
 4
 2

 1
 9

 3

 6
 6


 1
 1



 873

 6

 1
 1
 8
 1
 4-5
 2
 3
 7
 8
 9
 5



 10
 5
 2

 1

 13
 2
 8
 9
 5
 1


 7
 2
 4-5
 1
 7

 5


 4
 2
 10
 1

 8
 7. Vyp. 2
 7
 9
 6
 4

 6

 1
 12
 1
 2
 4

 4
 2
 3. Vyp. 2
 9
 6


 7

 13
 4
 3

 1
 1
 1
 1
 6

 7. Vyp. 2
 4



 6
 9
 3
 4
 13



 1
 10
 6
 1


 5
 4
 1
 5
 5
 7

 1
 7
 1





 3
 20
 7. Vyp. 2
 3
 1
 4-5


 7
 6
 7
 7


 3
 7
 5
 9
 1
 3
 2
 1
 2

 1
 7
 6
 3

 6


 2
 6
 3
 7
 2
 3
 1
 1

 1
 8

 5

 8
 9


 7. Vyp. 2
 3


 9

 7
 8
 3


 5

 5
 2
 6
 9
 1
 1
 6
 1
 1
 5
 2
 1
 5
 1
 7. Vyp. 2
 7
 1
 3
 1
 4
 9

 1

 3
 3
 2

 1


 5
 9

 6


 9
 5
 8
 9
 7. Vyp. 2
 3
 6

 20
 2



 1
 2
 6


 10
 11
 4
 1
 9

 3

 6
 1
 8-9
 2
 8
 7
 5

 4
 5
 4


 8


 5
 3

 6


 9
 3


 1



 2
 3
 2
 6

 2
 1
 3
 7
 13
 1
 20

 8

 5

 1
 5

 1

 6

 3
 1



 16
 4-5
 9

 6

 6
 9
 1
 3
 7. Vyp. 2
 1

 2

 1
 1
 2
 12
 2
 1
 2
 5

 1
 1
 5
 3
 6
 2
 1
 10
 4
 1
 4
 1
 1
 9
 6
 2
 1
 5
 4

 9
 1

 20
 9
 9
 8
 3
 13
 1
 1
 9
 1
 6
 15
 1

 5

 4
 1



 3

 6
 3
 5
 9
 9

 1
 2
 2


 6

 1

 8


 1

 1

 6
 10
 7
 1
 1
 8
 3
 11

 7
 10
 4
 5


 3
 7

 1
 3
 7
 2
 1
 5
 3
 3
 2

 3
 2



 3
 9
 13


 4
 9
 9
 1
 s01
 4
 4
 3
 1
 10
 3
 6


 2
 5
 1-2
 4-5
 2
 3
 1
 7
 3
 3
 8

 3

 1

 2
 10

 2
 2

 1
 7
 3

 1
 8
 1

 1
 15
 5
 1

 8
 2


 1



 13
 3
 4
 4

 2
 17

 3
 2
 1
 7

 1
 4
 9
 1
 1
 3
 5


 1




 9

 1
 2
 5
 3


 4

 5

 8
 2
 2
 1
 1
 6
 1
 3
 8
 10
 4


 7

 3

 1
 16
 2
 9
 3
 12
 3
 3
 5
 8
 2

 7
 5
 9
 5
 5
 1
 1

 2
 9
 7
 1

 7
 1



 8
 8

 2
 2
 4
 Pt 2
 3
 1
 3
 6

 1

 6
 3
 5
 3
 9
 4

 5
 7
 5
 2
 4
 7. Vyp. 2
 1
 1
 15
 4
 7

 3
 3

 5

 8
 3
 1
 25
 1


 1
 2
 4
 1
 8S
 5
 4
 16
 5
 7
 1
 12
 6

 1
 3
 3

 23

 2


 4
 8
 1
 2
 10

 873


 1

 4
 17
 8
 3
 2
 2
 873
 4
 6
 873
 9
 1
 2
 8
 2

 2

 3
 1

 4

 9
 5
 3
 3

 2
 1
 1
 2
 2
 17
 4

 3
 4
 4
 873

 7
 8

 7
 8


 4
 1
 5

 7

 1
 2
 3

 1
 1
 3
 1

 1
 4-5
 1

 3
 13
 1

 3
 1


 2
 2
 5
 12
 13
 13
 6

 1
 3
 7
 1
 1

 8
 1


 2
 13
 6
 5


 4

 3-4
 6
 4
 1
 3-4
 4

 8
 3
 5
 5
 1
 1


 4

 4
 1
 5



 6

 1
 2
 4
 1
 12

 2
 2
 6
 7
 8
 4
 2
 1
 8



 3

 1
 4
 2
 7
 3

 7. Vyp. 2
 5

 8
 1
 7. Vyp. 2

 1
 2
 2


 4


 1
 1
 14
 15

 2
 8
 2
 2
 1
 7
 3
 3
 6
 6
 7

 1
 10
 4-5
 6

 1
 1
 1
 4
 4

 13-14
 1

 25
 2
 2
 2

 3
 9

 2
 32
 3
 11
 1
 8

 1
 4
 4
 1
 9
 8
 4
 6
 5
 3

 2
 7
 7
 8


 4
 7
 3
 6
 2
 3
 1
 2
 6
 1
 3

 1


 1
 1
 5
 17
 5
 2

 1
 6
 9
 4
 1
 1
 8

 1

 3
 2

 1
 8
 8
 1
 8
 7
 5
 1

 3

 1


 7
 9
 4
 1
 5
 5
 7
 10
 9
 7
 4
 1
 1

 1
 1
 1


 8
 6
 6
 3



 2
 8
 4

 16
 1
 4-5
 4
 9
 3


 2

 2
 4
 1
 5

 9

 1
 4
 8
 4-5
 2
 16
 7


 9
 3

 4

 3

 6

 11
 1
 5
 5

 4
 8
 12

 2
 4

 8



 4

 5

 3
 4
 3
 7
 8
 2

 2
 5
 10
 3

 2
 13

 2
 2
 3

 1

 4
 8

 6

 1
 4
 2
 7
 2
 1
 6
 38
 4
 1
 2
 1
 3

 9
 8

 2
 1

 8
 3
 8
 16
 6


 9

 7
 4

 4
 2
 8
 8
 8
 6
 3
 7
 1
 5
 1
 2
 1
 18

 4

 2
 11


 1

 4
 1
 10
 20


 9

 3
 6
 8
 4
 3
 1
 1
 5
 1
 5

 2

 3
 1


 5

 1
 7
 12
 2
 3
 8
 37
 2
 10
 1


 7
 7. Vyp. 2
 4
 3
 1

 3




 7

 1
 3
 2

 1

 2
 6
 4

 4
 2
 4
 1
 7947
 1
 3
 2
 13
 1
 3
 1
 8
 2
 9
 1
 7
 2
 3
 4
 3

 2
 2

 13
 4
 7
 2


 2


 8
 2
 191

 10

 5
 4

 4
 2
 1
 6

 20
 4

 7
 3
 6

 17-18

 1
 5
 13
 11

 12
 1
 3
 1
 4
 6
 9
 17

 9
 4

 20
 1

 3
 1
 4

 6
 3
 3
 2

 5
 702
 2
 3
 6
 5
 8

 3
 2
 2


 7


 3
 1
 6
 12
 4
 3
 3
 3
 9

 2
 2
 5
 4
 8
 2
 2
 9
 5
 13
 9
 2
 4
 7
 10
 8
 3
 1

 3
 9



 1

 2
 7
 3
 9
 5
 10
 6
 2

 4
 3
 4
 7
 4
 4

 5
 6
 2
 1-2

 1
 1



 7
 11



 3
 1
 1
 1
 4
 11

 2
 9
 2
 1
 2
 9
 4

 2
 13
 5
 1

 4
 6
 8
 1
 5
 11
 10

 1
 8
 5
 6
 2


 3
 1
 6

 2

 3
 2
 1
 1
 1
 5
 9
 6
 17
 16
 1

 3
 8
 2

 9
 6


 3
 3
 4
 4
 6
 5
 2
 4
 12
 1

 3
 3

 7

 4
 1

 1




 9

 1
 4

 1
 4
 5
 8
 7

 22



 4
 1


 1
 3
 3
 7

 6
 5
 5
 3
 3
 7

 9
 8

 1

 10

 23
 7
 1


 4
 3


 10
 3
 7

 12

 2

 3
 2
 4
 1
 2


 1
 2


 2


 4






 3

 5
 2
 5
 5
 192
 1




 4
 1




 8


 7





 9
 2

 1
 2
 3


 1





 5






 7





 2

 3
 1




 3





 7






 8
 9



 1
 3
 10

 4
 8

 2
 3



 6

 6
 5



 5
 2
 9
 4


 2

 3

 1
 2
 1
 3



 10

 6

 5
 3

 10

 3



 3
 4




 3




 3



 14


 1








 4



 1




 1

 2
 1
 3
 11
 4
 3
 2


 4


 3

 4
 1
 7
 13


 3
 7



 2-3



 5
 4
 2
 2
 873
 7


 3
 2
 3
 2
 2

 10
 2
 1



 2
 1


 11



 9
 4

 2
 1

 5





 2


 1

 2
 16







 2
 4


 8


 2



 1

 2
 2
 2
 2
 3
 3
 2



 4





 5


 4


 5




 10
 17
 7



 2



 17





 2


 6
 5

 1
 1

 13



 3

 4
 6
 5

 3
 3

 2
 3
 4
 3
 8

 8

 1

 2


 10









 4
 3
 4
 3
 2
 2
 8

 4


 3

 3

 1
 5
 2
 1


 7
 7




 6
 7
 10




 1

 15
 13
 1
 17

 2
 1
 1
 10
 4

 1
 4


 1


 3


 1

 3

 2

 1
 9




 9




 9

 11
 11
 2
 2
 1


 1
 1




 3

 6
 2


 1

 1


 16


 2


 3
 10
 3





 13

 3



 2


 3

 1


 6



 2
 12




 2

 3
 3



 3




 6

 2
 10

 9


 4

 1


 6
 5
 6

 4


 9

 2


 2

 10


 1

 9



 2

 6
 10


 10



 7

 7
 2

 1



 1
 1
 2

 3






 6

 Suppl 1
 1
 2

 10
 8
 8






 5
 8


 1

 1
 10

 1
 2

 2

 3
 3

 9

 2
 11



 5

 3


 3


 1







 1







 1
 10





 3
 4

 2
 2
 1





 3




 14


 2



 3














 6
 5
 4



 2






 5
 10



 1
 9



 5




 3
 4





 2

 6




 1


 1


 1
 1







 3

 6

 1
 9
 3
 Pt A

 6
 4


 7
 7

 7


 1
 3
 3
 1




 6
 3
 2

 1
 6


 8


 7
 5



 3
 1


 3

 8

 1



 5

 7
 7-8

 6



 2
 3



 6
 3

 2
 1
 9

 1

 5
 3
 6
 1



 4

 2
 10



 1



 4



 4

 1
 4

 3
 9

 6



 9




 1
 1


 7


 6
 1

 7
 2
 1






 5
 12
 10

 1


 17



 5





 2
 5

 8
 2

 3
 2
 2




 8

 3
 5
 3
 1

 10



 3



 6
 7

 6

 1
 2
 1
 S1
 1

 8


 2
 5
 6


 5

 1





 4
 5




 7





 1


 9
 7



 3




 9

 5
 1

 4




 2
 29




 1


 1
 11
 1

 15
 7

 3
 13




 1



 6
 8
 3




 3

 1


 1










 10
 2
 2


 7




 7
 1



 2
 1
 5
 5
 4





 2
 6

 1
 7

 5
 5
 1
 13-15
 4
 11

 2



 5


 1


 1

 2
 2


 4
 2
 2
 10
 4

 8
 873

 9
 7
 3


 9




 15
 10








 4-5

 3
 2
 3

 6
 2





 14
 2
 3



 1
 1









 2

 1

 8
 12
 3
 9
 6
 3
 4


 4
 1


 10








 3



 4
 3
 4

 1
 8

 6


 4



 Sup16b
 5


 2





 5


 5

 6


 1
 13

 1



 s1
 3

 6
 4




 7

 12
 4
 7

 3








 9
 5
 1
 6
 5
 N° 809-10

 3
 7


 1
 5



 14
 13
 3
 2




 7
 14





 2
 6
 2
 17
 6




 8




 5

 8


 7

 4
 10

 6
 8

 10
 1


 2
 16

 4

 7
 7

 5


 1

 4


 12
 35


 5

 1

 7
 3
 2
 11


 7
 873

 1
 7

 1



 2


 5
 8



 10
 7
 1


 1




 4
 4
 2

 Pt A
 5
 N° 809-10

 3

 3

 21




 1

 1


 1


 6
 3
 3

 1



 1

 6








 3
 26
 6



 5
 2




 1
 4
 2


 3
 11




 5

 9
 6
 9


 7
 1

 2

 8
 2
 1


 1


 29

 14
 1




 1
 7
 2


 5


 3

 3


 21


 2


 8
 7

 9
 4


 1
 3
 1

 5
 1
 4
 7
 9
 3

 2


 1
 9

 5
 3
 7
 17
 8
 6
 10
 7
 11

 4

 2


 3





 3
 5
 6
 6
 1

 1

 6
 6


 1


 6

 17
 6
 6

 7
 2
 4



 3
 22

 7
 3


 17
 8







 12


 1
 4
 15

 2

 19
 1

 3
 9


 2
 2



 3
 2
 3
 13


 2
 8





 10
 3
 2
 11
 10
 5

 2


 Supplement

 3

 6


 3
 1
 3



 9


 5

 2
 4
 3

 4
 4
 2
 4
 2
 3
 4
 9


 6




 6

 7
 6
 4
 5


 1





 1
 1
 1
 1
 2



 2
 1

 13

 4
 8
 3

 1

 2



 5
 3
 6

 17
 1
 5
 3
 17

 11
 1


 1
 8
 1

 1

 8


 2
 3
 3
 3
 5

 2
 3

 13

 3

 5
 8

 6


 4
 Suppl 1
 2


 7

 1








 6
 2
 4
 12
 3
 1
 4
 1

 5
 Pt A


 3


 5

 6
 3
 7
 8

 2


 1
 1
 12





 11

 2
 6
 4
 2

 2
 2
 3
 5


 2
 10
 3

 7
 3
 16


 1
 2
 4
 2

 4
 6
 6
 2
 7

 1

 5

 8


 1
 4
 8


 1
 1
 1


 7



 3
 1
 8
 5
 14

 1
 15
 13

 5

 6
 7

 5



 7
 14

 3
 5




 1
 2
 1
 11
 7
 8
 3


 2

 4
 1
 9





 5-6
 195
 6

 1
 3
 3
 2

 2

 4
 1

 3
 4

 1
 3
 1


 7

 8
 3
 1
 4
 4

 1

 10
 11
 34
 8
 5
 7
 2
 1
 7

 6
 1
 1
 2
 1

 1
 2

 9

 4


 1

 1
 1
 7
 2
 8

 1
 1

 1
 4

 1





 6
 1
 4
 2

 3
 3
 4
 5

 5

 11
 9


 5
 1


 4
 4
 9

 8
 2
 3

 2
 3
 1
 7
 2



 12


 4
 4

 1
 2
 7
 S1
 3


 7


 3
 1
 16
 15

 2
 14

 5


 3
 6

 1
 8
 15
 1
 2
 5
 4
 5

 3
 5
 3
 2
 2


 10
 1
 6
 6

 3


 1

 2
 2

 9
 9
 1



 7
 4
 8
 3
 1
 3

 1
 5
 3



 1
 1
 1
 2
 2



 2
 4
 8
 1
 2

 4
 3
 1
 4
 2
 10


 4

 2
 6

 1
 2

 10
 5
 4
 10


 2
 262

 4
 2
 1
 2
 1


 3
 2

 3

 2
 2
 2
 5
 2
 8

 13
 1
 3

 1

 22

 1
 8


 7
 9
 1

 7
 3
 3




 8
 6

 1
 8
 25


 6
 6
 1
 1
 2
 1

 4


 9


 1
 2
 6
 3
 3
 2
 2

 1
 2
 1
 1

 7
 7


 1
 4

 2
 7

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 9
 8

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 1



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 8
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 8




 7



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 5

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 10373

 6
 5
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 4
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 678

 15

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 5
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 9

 5




 1
 6

 2
 8

 1
 3
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 3
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 7
 698
 7
 3
 1
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 86
 9

 1
 3

 11
 16


 7
 21


 1


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 8

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 1


 3

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 10


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 1

 6

 1
 2
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 2
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 3

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 8
 8
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 4

 2
 6
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 1
 1
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 1


 1
 1
 9

 3
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 9

 8
 7
 8
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 13

 16


 Pt 1
 4
 5
 5
 1
 2

 1
 8
 1
 6
 8
 10
 4
 7
 6
 5
 1
 1







 1


 10391


 4
 1

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 6
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 37

 1
 1
 7942
 6636



 2


 17
 2
 3

 8
 4
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 3
 36
 4
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 2
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 1




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 2
 10
 1


 2

 2

 3
 2

 8
 1

 9
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 2

 2

 3
 9

 8
 5

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 9-10
 13-15

 8
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 1
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 4
 4
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 2

 2
 4

 5
 7
 1
 7
 29
 4



 4

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 6



 6
 1
 7
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 8
 7
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 Suppl 1
 8






 1
 5
 7
 7
 3
 7
 4
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 6


 4
 6
 790
 1
 2
 6

 2
 4
 2
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 9
 5
 4
 5
 2
 4
 2
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 Pt A

 9
 6
 8



 17
 2
 1
 8




 2
 32
 3

 6
 6
 2


 6
 7
 4
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 2
 8
 1

 4
 5
 3
 5
 1

 2
 2

 1
 5
 13
 3
 6

 2
 7
 9
 2

 5
 1
 5
 1
 6
 6

 3
 Amato MP Banwell B Barkhof F Chataway J Chitnis T Comi G Derfuss T Finlayson M Goldman M Green A Hellwig K Kos D Miller A Mowry E Oh J Salter A Sormani MP Tintore M Tremlett H Trojano M van der Walt A Vukusic S Waubant E
















 Harroud A Stridh P McCauley JL Saarela J van den Bosch AMR Engelenburg HJ Beecham AH Alfredsson L Alikhani K Amezcua L Andlauer TFM Ban M Barcellos LF Barizzone N Berge T Berthele A Bittner S Bos SD Briggs FBS Caillier SJ Calabresi PA Caputo D Carmona-Burgos DX Cavalla P Celius EG Cerono G Chinea AR Chitnis T Clarelli F Comabella M Comi G Cotsapas C Cree BCA D'Alfonso S Dardiotis E De Jager PL Delgado SR Dubois B Engel S Esposito F Fabis-Pedrini MJ Filippi M Fitzgerald KC Gasperi C Gomez L Gomez R Hadjigeorgiou G Hamann J Held F Henry RG Hillert J Huang J Huitinga I Islam T Isobe N Jagodic M Kermode AG Khalil M Kilpatrick TJ Konidari I Kreft KL Lechner-Scott J Leone M Luessi F Malhotra S Manouchehrinia A Manrique CP Martinelli-Boneschi F Martinez AC Martinez-Maldonado V Mascia E Metz LM Midaglia L Montalban X Oksenberg JR Olsson T Oturai A Pääkkönen K Parnell GP Patsopoulos NA Pericak-Vance MA Piehl F Rubio JP Santaniello A Santoro S Schaefer C Sellebjerg F Shams H Shchetynsky K Silva C Siokas V Søndergaard HB Sorosina M Taylor B Vandebergh M Vasileiou ES Vecchio D Voortman MM Weiner HL Wever D Yong VW Hafler DA Stewart GJ Compston A Zipp F Harbo HF Hemmer B Goris A Smolders J Hauser SL Kockum I Sawcer SJ Baranzini SE Harroud A Jónsdóttir I Blanco Y Llufriu S Madireddy L Saiz A Villoslada P Stefánsson K





 Cabrera-Gomez JA Roullet E Zwanikken C Den Braber-Moerland L Barnett M Hodgkinson S Garber J Slee M McCombe P Taylor B MacDonell R Massey J Van Pesch V Decoo D Willekens B Fragoso Y Prevost J Prat A Girard M Grammond P Larochelle C Oh J Lalive P Gobbi C Horakova D Havrdova E Ampapa R Izquierdo G Eichau S Sanchez-Menoyo JL Ramo-Tello C Blanco Y Saiz A Besora S Shaygannejad V Cartechini E Diamanti M Amato MP Spitaleri D Patti F Chisari C D'Amico E Salvatore LF Yamout B Khoury SJ Al-Asmi A Jose Sa M Al-Harbi T Karabudak R Turkoglu R Kilpatrick T King J Nguyen AL Dwyer C Monif M Taylor L Baker J
















































































































































































































































































 Valsasina P Sibilia M Preziosa P Bisecco A d'Ambrosio A Altieri M Capuano R Tommasin S Ruggieri S Piervincenzi C Gianni C Stromillo ML Cortese R Zaratin P























































 Bourdette D Yadav V Goodman A Racke M Fallis R Tornatore C Goldman M Kannan M Sriram S Berger J Cross A Rammohan K Xia Z Leist T Lynch S Klawiter E Amezcua L Bowen J



























 Arnoldus E Barkhof F Bouvy WH van Dijk GW van Eijk J Eurelings M van Genugten J Hoitsma E Hoogervorst E de Jong BA Kalkers NF van Kempen Z Killestein J Kloosterziel ME Kragt JJ Lierop ZV Lissenberg-Witte BI Moraal B Mostert JP van Munster C Nielsen J van Oosten BW Rispens T van Rooij LC Roosendaal CM Sinnige L Strijbis E Toorop AA Uitdehaag B Vennegoor A Wokke B Zeinstra E













 Dear K Dwyer T Blizzard L Lucas RM Kilpatrick T Williams D Lechner-Scott J Shaw C Chapman C Coulthard A Pender MP Valery P







































 Barkhof F Ciccarelli O Stefano N Enzinger C Filippi M Gasperini C Kappos L Palace J Rocca MA Rovira À Sastre-Garriga J Vrenken H

















































































































































































































































































































 Fraser C Abegg M Alroughani R Alshowaeir D Alvarenga R Andris C Asgari N Barnett Y Battistella R Behbehani R Berger T Bikbov MM Biotti D Biousse V Boschi A Brazdil M Brezhnev A Calabresi P Cordonnier M Costello F Cruz FM Cunha LP Daoudi S Deschamps R DeSeze J Diem R Etemadifar M Flores-Rivera J Fonseca P Frederiksen J Frohman E Frohman T FromentTilikete C Fujihara K Gálvez A Gouider R Gracia F Grigoriadis N Guajardo JM Habek M Hawlina M Hernández-Martínez de Lapiscina E Hooker J Hor JY Howlett W Huang-Link Y Idrissova Z Illes Z Jancic J Jindahra P Karussis D Kerty E Kim HJ Lagrèze W Leocani L Levin N Liskova P Maiga Y Marignier R McGuigan C Meira D Merle H Monteiro MLR Moodley A Moura F Muñoz S Mustafa S Nakashima I Noval S Oehninger C Ogun O Omoti A Pandit L Paul F Rebolleda G Reddel S Rejdak K Rejdak R Rodriguez-Morales A Rougier MB Sa MJ Sanchez-Dalmau B Saylor D Shatriah I Siva A Stiebel-Kalish H Szatmary G Ta L Tenembaum S Tran H Trufanov Y VanPesch V Wang AG Wattjes MP Willoughby E Zakaria M Zvornicanin J Balcer L Plant GT






















































































































 Bolton JM Sareen J Singer A Lix LM El-Gabalawy R Katz A Berrigan L Peschken C Kowalec K







































































































 Brownlee W Wynne M Hockey L Parker J Flight J Frost C Nicholas J Nixon S Beveridge J Chandran S Connick P Lyle D Galea I Jarman E Ford H Fernandes L Vinjam M Pavitt S Sharrack B Paling D Shehu A Arun T Belhag M Pearson O Ingram G Rickards C McDonnell G Hughes S Spilker C Fisniku L Aram J Rice C Pluchino S Peruzzotti-Jametti L Harikrishnan S Guck N Robertson N Tallantyre E Harrower T Gallagher P Ahmed F Young C Arndt H Silber E Nicholas R Duddy M Lee M Evangelou N Allen C Craner M Geraldes R Hobart J Hillier C Chhetri S Mattoscio M Chaudhuri A Kalra S Straukiene A Rog D





































































































 Lucas RM Dear K Dwyer T Broadley S Kilpatrick T Williams D Shaw C Chapman C Coulthard A Pender MP Valery P



 Huseyinsinoglu BE Ben-Zacharia AB Cohen ET Gonçalves PJC Kragt JJ Hynes SM Marron FE
















































 van der Mei I Broadley S Ponsonby AL Dear K Dwyer T Blizzard L Lucas RM Kilpatrick T Williams D Lechner-Scott J Shaw C Chapman C Coulthard A Pender MP





































































































 Vd Kooi AJ Raaphorst J Koos Zwinderman AH Löwenberg M Volkers AG D'Haens GRAM Takkenberg RB Tas SW Spuls PI Bekkenk MW Musters AH Post NF Bosma AL Hilhorst ML Vegting Y Bemelman FJ Verstegen NJM Fernandez L Keijzer S Keijser JBD Cristianawati O Voskuyl AE Broens B Sanchez AP Nejentsev S Mirfazeli ES Wolbink GJ Boekel L Rutgers BA de Leeuw K Horváth B Verschuuren JJGM Ruiter AM van Ouwerkerk L van der Woude D Allaart R Teng Y Busch MH Brusse E van Doorn PA Baars M Hijnen DJ Schreurs C van der Pol WL Goedee HS van Els CACM de Wit J






 Pearson JF Clarke G Abernethy DA Willoughby E Sabel CE









































 Albrecht W Bischof F Bittkau F Bittkau S Bohr KA Borries B Brockmeier B Brummer D Bühler B Butz W Cepek L Claassen L Dee J Dieterle L Drees E Engelmann C Ernst M Fasold O Fischer J Flach M Fleischer R Friedrich L Friedrich A Fritzinger M Gehring K Gierer S Gierer S Gößling J Grips E Haldenwanger AH Harth A Hartmann R Helm R Herbst HP Hofer C Hofmann WE Hoge A Hummel S Ikenberg B Israel-Willner H Jankovits R Kallmann BA Kausch U Keppler M Kessler K Kirchhöfer U Kirchmeier J Knoblich R Knoll T Knorn P Köchling M Kornhuber AW Kramer B Krause M Krauß M Kubalek R Kunz J Landefeld H Lange T Lehmann-Horn K Lippert E Lippmann K Maier-Janson W Märkl M Masri S Moser C Neusch C Niemann J Paschke T Peikert AS Peikert A Peters H Pfister R Reifschneider G Ries S Rieth C Roick H Roth GD Roth R Safavi A Saur J Schmitt-Roth B Scholz EF Schreiber H Schreiber K Schrey C Schumann C Seiler M Sigel KO Sikora V Sotiriadis N Spiegel S Städt D Sühnel T Tiel-Wilck K Ulzheimer JC Unsorg BS Voith S Wannenmacher AS Weber H Weih M Wendtland B Wiborg A Wimmer M Winker T Wontroba I Wüstenhagen M























































































































 Alexander J Bove R Baranzini S Cree BAC Caverzasi E Cuneo R Caillier SJ Cooper T Green AJ Guo CY Gelfand JM Gomez-O'shea R Gupta S Hollenbach J Harms M Henry RG Hauser SL Mendoza M Oksenberg JR Papinutto N Pleasure S Powers K Renschen A Santaniello A Sabatino JJ Stern WA Wilson MR Zamvil SS

















































































 Horakova D Buzzard K Terzi M Prat A Girard M Grammond P Barnett M Stewart G Onofrj M Izquierdo G Eichau S Grand'Maison F Prevost J Van Wijmeersch B Amato MP Shaygannejad V Boz C Bolaños RF Soysal A Ramo-Tello C Solaro C Gobbi C Cabrera-Gomez JA Roullet E Zwanikken C Den Braber-Moerland L Deri N Saladino ML Cristiano E Rojas JI Vrech C Shaw C Shuey N Boggild M Tan IL Hardy T Decoo D Moore F Oh J Lalive P Ampapa R Petersen T Oreja-Guevara C Perez Sempere A Dominguez JA Besora S Hughes S Gray O Grigoriadis N Piroska I Rozsa C Kasa K Simo M Kovacs K Sas A Dobos E Rajda C McGuigan C Mason D Schepel J Alkhaboori J Rio ME Mihaela S Al-Harbi T Altintas A Kister I Marriott M Kilpatrick T King J Nguyen AL Dwyer C Monif M Roos I Taylor L Diamanti M Chisari C Toscano S Salvatore LF Larochelle C De Luca G Di Tommaso V Travaglini D Pietrolongo E di Ioia M Farina D Mancinelli L Hupperts R Olascoaga J Saiz A Zivadinov R Benedict R Verheul F Fabis-Pedrini M











































































































 Barkhof F de Stefano N Sastre-Garriga J Ciccarelli O Enzinger C Filippi M Gasperini C Kappos L Palace J Vrenken H Rovira À Rocca MA Yousry T
















































































 Maglione A Di Sapio A Laroni A Iovino A Mannironi A Uccelli A Nucciarone B Serrati C Nicoletti CG Lapucci C Mancinelli CR Cordioli C Bezzini D Carmagnini D Brogi D Nicola S Landi D Nobile Orazio E Cocco E Signoriello E Nako E Assandri E Marinelli F Baldi F Caleri F Siciliano G Cola G Perego G Lus G Brichetto G Bellucci G Da Rin G Marfia GA Vazzoler G Liberatore G Trivelli G Callari G Gandoglia I Schiavetti I Frau J Pasquali L Petrucci L Lorefice L Ruggiero L Salvetti M Monti Bragadin M Buscarinu MC Gagliardi M Sormani MP Ferrò MT Rilla MT Clerico M Battaglia MA Fronza M Del Sette M Inglese M Scialabba M Bedognetti M Ulivelli M De Rossi N Gazzola P Bigi R Dubbioso R Reniè R Iodice R Fabbri S Rasia S Parodi S Rolla S Platzgummer S Maria Laura S Tassinari T Carlini V





























 Moln Ar FE Rauer S Wabbels B Noll M M Uller M Guthoff T Guthoff R Aktas O Kruse FE Huhn K Nickel FT Linker RA Fitzner D Hein K van Oterendorp C Zipp F Uphaus T Fleischer V Siller N Lorenz K Beck A Pitz S Elflein H Hartmann K K Umpfel T Mulazzani E Wilhelm H Zielmann U Heesen C Stellmann P Rosenkranz S





















































































 Abad S Bayen M Bielefeld P Chalumeau M Chiquet C Cohen JD Despert V Devilliers H Fardeau C Georgin-Lavialle S Guex-Crosier Y Guillaume Czitrom S Heron E Hofer M Agbo Kpati KP Labalette P Lemelle I Nouar D Pugnet G Sellam J Sene D Terrier B Trad GS






























 Altieri M Borgo R Capuano R Storelli L Pagani E Sibilia M Piervincenzi C Ruggieri S Petsas N Cortese R Stromillo ML































































 Metspalu A Milani L Mägi R Nelis M Hudjašov G












































 Chapman C Coulthard A Dear K Dwyer T Kilpatrick T Lucas R McMichael T Ponsonby AL Taylor B Valery P van der Mei I Williams D
























































 Leist TP Habib L Udugama P Gray O Horakova D Sartori C More R Siddiqui A Farr P Stupar D Tang C Le A Smirnova S Palshetkar G Spelman T

 Ferrari R Hernandez DG Nalls MA Rohrer JD Ramasamy A Kwok JBJ Dobson-Stone C Brooks WS Schofield PR Halliday GM Hodges JR Piguet O Bartley L Thompson E Haan E Hernández I Ruiz A Boada M Borroni B Padovani A Cruchaga C Cairns NJ Benussi L Binetti G Ghidoni R Forloni G Galimberti D Fenoglio C Serpente M Scarpini E Clarimón J Lleó A Blesa R Waldö ML Nilsson K Nilsson C Mackenzie IRA Hsiung GR Mann DMA Grafman J Morris CM Attems J Griffiths TD McKeith IG Thomas AJ Pietrini P Huey ED Wassermann EM Baborie A Jaros E Tierney MC Pastor P Razquin C Ortega-Cubero S Alonso E Perneczky R Diehl-Schmid J Alexopoulos P Kurz A Rainero I Rubino E Pinessi L Rogaeva E St George-Hyslop P Rossi G Tagliavini F Giaccone G Rowe JB Schlachetzki JCM Uphill J Collinge J Mead S Danek A Van Deerlin VM Grossman M Trojanowski JQ van der Zee J Deschamps W Van Langenhove T Cruts M Van Broeckhoven C Cappa SF Le Ber I Hannequin D Golfier V Vercelletto M Brice A Nacmias B Sorbi S Bagnoli S Piaceri I Nielsen JE Hjermind LE Riemenschneider M Mayhaus M Ibach B Gasparoni G Pichler S Gu W Rossor MN Fox NC Warren JD Spillantini MG Morris HR Rizzu P Heutink P Snowden JS Rollinson S Richardson A Gerhard A Bruni AC Maletta R Frangipane F Cupidi C Bernardi L Anfossi M Gallo M Conidi ME Smirne N Rademakers R Baker M Dickson DW Graff-Radford NR Petersen RC Knopman D Josephs KA Boeve BF Parisi JE Seeley WW Miller BL Karydas AM Rosen H van Swieten JC Dopper EGP Seelaar H Pijnenburg YAL Scheltens P Logroscino G Capozzo R Novelli V Puca AA Franceschi M Postiglione A Milan G Sorrentino P Kristiansen M Chiang HH Graff C Pasquier F Rollin A Deramecourt V Lebert F Kapogiannis D Ferrucci L Pickering-Brown S Singleton AB Hardy J Momeni P











 Coles A Chataway J Duddy M Emsley H Ford H Fisniku L Galea I Harrower T Hobart J Huseyin H Kipps CM Marta M McDonnell GV McLean B Pearson OR Rog D Schmierer K Sharrack B Straukiene A Ford DV









































































































































 Akhtar S Anwar M Arciero E Asgar O Ashraf S Breen G Chung R Curtis CJ Chaudhary S Chowdhury M Colligan G Deloukas P Durham C Durrani F Eto F Finer S Garcia AA Griffiths C Harvey J Heng T Huang QQ Hurles M Hunt KA Hussain S Islam K Jacobs BM Khan A Khan A Lavery C Lee SH Lerner R MacArthur D Malawsky D Martin H Mason D Mazid MB McDermott J McSweeney S Miah S Munir S Newman B Owor E Qureshi A Rahman S Safa N Solly J Tahmasebi F Trembath RC Tricker K Uddin N van Heel DA Winckley C Wright J
















































































































































































































































































































































































































































































































































































































































 Lucas R Dear K Ponsonby AL van der Mei I Blizzard L Simpson-Yap S Taylor BV Broadley S Kilpatrick T Williams D Lechner-Scott J Shaw C Chapman C Coulthard A Valery P








































































































































































































 Branger P Abrous M Zéphir H Petit J Vukusic S Gelet C Carra-Dallière C Ayrignac X Russello M Laplaud D Gaultier A Le Frère F Callier C Caillon C Gueydan E Louapre C Galanaud D Ungureanu A Coudoin S Hebant B Gerard E Vimont C Biotti D Bonneville F Freitas N Duman T Kilic E Tutuncu M Uygunoglu U Destan S Sen S Friedli C Wagner F Weber L Tchoubar A Dumont E Eryilmaz A Roman T Pelletreau C Grateau A Mathieu Y Yaiche S Rintelen F Firmino I De Chastenier A Gheribenblidia A Zeydan B










































































































 Aguglia U Amato MP Ancona AL Ardito B Avolio C Balgera R Banfi P Barcella V Barone P Bellantonio P Berardinelli A Bergamaschi R Bertora P Bianchi M Bramanti P Brescia Morra V Brichetto G Brioschi AM Buccafusca M Bucello S Busillo V Calchetti B Cantello R Capobianco M Capone F Capone L Cargnelutti D Carozzi M Cartechini E Cavaletti G Cavalla P Celani MG Clerici R Clerico M Cocco E Torri Clerici V Coniglio MG Conte A Corea F Cottone S Crociani P D'Andrea F Danni MC De Luca G de Pascalis D De Riz M De Robertis F De Rosa G De Stefano N Della Corte M Di Sapio A Docimo R Falcini M Falcone N Fermi S Ferraro E Ferrò MT Fortunato M Foschi M Gajofatto A Gallo A Gallo P Gatto M Gazzola P Giordano A Granella F Grasso MG Grimaldi L Iaffaldano P Immovilli P Imperiale D Inglese M Iodice R Leva S Leuzzi V Lugaresi A Lus G Maimone D Mancinelli L Maniscalco GT Marfia GA Margari L Marinelli F Marini B Marson A Mascoli N Massacesi L Melani F Merello M Fioretti C Mirabella M Montepietra S Nasuelli D Nicolao P Pasquali L Passantino F Patti F Pecori C Peresson M Pesci I Piantadosi C Piras ML Pizzorno M Plewnia K Pozzilli C Protti A Quatrale R Realmuto S Ribizzi G Rinalduzzi S Rini A Romano S Filippi M Ronzoni M Rossi P Rovaris M Salemi G Santangelo G Santangelo M Leone A Sarchielli P Sinisi L Ferraro D Solaro C Spitaleri D Strumia S Tassinari T Santuccio G Tortorella C Totaro R Tozzo A Trivelli G Turano G Ulivelli M Valentino P Venturi S Vianello M Zaffaroni M Zarbo R




























































































































































































































































































































 Altieri M Borgo R Capuano R Storelli L Pagani E Sibilia M Piervincenzi C Ruggieri S Petsas N Cortese R Stromillo ML



















































































































































































































































































































































 Rossi F Luigi Z Mampreso E Gambara S Squilini S Matricardi S Clerici VT Polito AN Rosa GD Bedin R Vitetta F Varone A Maimone D Bisecco A Sabatino ED Scannapieco S Papi C Guerrieri S Pisani F Praticò A Po C Grazian L Passarini A Bergamoni S Rasia S Bergamaschi R Marchioni E































































































































































































































































































































 Chapman C Coulthard A Dear K Dwyer T Kilpatrick T Lucas R McMichael T Ponsonby AL Taylor B Valery P van der Mei IAF Williams D










































































































 Chow N Sealey R Balneaves L





















 Bolton J Graff L Kornelsen J Mazerolle E Patel R Figley TD Helmick CA


























































































































 Aini I Albertelli M Alessi Y Altieri B Antonini S Barrea L Birtolo F Campolo F Cannavale G Cantone C Carra S Centello R Cozzolino A Molfetta S Vito V Fanciulli G Feola T Ferraù F Gay S Giannetta E Grillo F Grossrubatscher E Guarnotta V Salvia A Laffi A Lania A Liccardi A Malandrino P Mazzilli R Messina E Mikovic N Minotta R Modica R Muscogiuri G Pandozzi C Pugliese G Puliani G Ragni A Rubino M Russo F Sesti F Verde L Veresani A Vetrani C Vitale G Zamponi V Zanata I

















































 Danel-Brunaud V Moreau C Perez T Dumont Dujardin K Delval A Gelé P Pleuvret M Santraine V Niset F Dumont J Laugeais V Bon M Ouk T Potey C Leclercq C Gers E Salachas F Bruneteau G Lacomblez L Socha J Pineau F Lenglet T Folhinha PDS Bordet A Royer H Osman N Khelifa SA Corcia P Beltran S Carmier D Barantin L Blasco H Bakkouche SE Mouzouri M Antoine JC Camdessanché JP Dimier N Kaminsky AL Court-Fortune I Boutet C Gonzalo P Visneux V Ferraud K Berlier G Genestet S Gut-Gobert C Salem DB Nicolas P Larvor S Mouly K Roux LL Postec K Bezeazux C Rosec S Fortin-Prunier H Novert G Menanteau E Postec K Denizot M Bernard E Vial C Broussole E Svahn J Cam PL Berthezene Y Combet P Jacqueline S Neuillet C Mansuy A Camu W Juntas-Morates Pageot Esselin Champfleur Roy-Bellina Lehmann S Alphandry S Labar L Baudesson L Attarian S Grapperon AM Pouget J Verschueren A Bas J Finet-Monnier A Belingher C Diallo S Heddadji N Alphandery S Baudesson L Reginensi P Desnuelle C Soriani MH Chanalet S Mondot L Puma Pruvost I Barré C Cintas P Bes MA Acket B Pariente J Guilbaud I Bonneville F Causse E Lagarde T Geffroy J Centelles M Hermet-Douard V Pittion-Vouyovitch S Michon M Meyer M Lomazzi S Hossu G Chatelain A Couratier P Lautrette G Vincent F Antonini LT Favard F Boncoeur-Martel MLA Chouly M Desport JC Jesus P Fayemendy P Labetoulle C Catteau J Villeneuve O Machat S Guy N Clavelou P Greil A Duclos M Jean B Chassain C Tsoutsos C Speziale C Cladiere A Bouteloup C Farigon N Argondo SS Dumont E Rouvet S Viader F Lefilliatre M Mouton P Mondou A Allouche S Bari-Makouri R Kolev I Pihan M Ho HL Catroux B Castel M Rigal M Bellot C Vomscheid M Hervé MC Duban MP Vieillart A Cassereau J Codron P Pautot V Meslier N Trzepizur W Tanguy JY Allain P Thiery C Reynier P Barbe T Vialle-Soubranne Vienne N Olivier A Miller J Bost M Fournier Gay D Bonicel R El Mountassir F Fischer C Mangin JF Chupin M Cointepas Y Accart B Gelé P Fievet F Chabel M Derenaucourt V Facon L Njosse YT Hisbergues M Deplanque Tabuenca C Cazalère MF Couratier P Camu W Corcia P Desnuelle C Caillier M Danel V Morerau C Laugeais V Lecocq A Potin N Frisch M Léon M Devos D Salachas F Pradat PF Lacomblez L Camdessanché JP Attarian S Langlet T Blasco H Dupuis L Bon M Bernard E Cassereau J Soriani MH Raoul C Lehman S Turgeman S Goutines V





































































































































 Fortuné C Gietzen A Hudson M Lawrie-Jones A Mayes MD Nielson WR Sauvé M Wojeck RK Adams CE Henry RS Assassi S Benedetti A El-Baalbaki G Fligelstone K Frech T Hinchcliff M Johnson SR Larche M Leite C Nguyen C Nielsen K Pope J Rannou F Rodriguez-Reyna TS Schouffoer AA Suarez-Almazor ME Agard C André M Bernstein EJ Berthier S Bissonnette L Bruns A Cacciatore C Carreira P Casadevall M Chaigne B Chung L Crichi B Domsic R Dunne JV Dunogue B Fare R Farge-Bancel D Fortin PR Gordon J Granel-Rey B Guffroy A Gyger G Hachulla E Hoa S Ikic A Jones N Khalidi N Lakin K Lambert M Launay D Lee YC Maillard H Maltez N Manning J Marie I Lopez MM Martin T Masetto A Maurier F Mekinian A Díaz SM Nikpour M Olagne L Poindron V Proudman S Régent A Rivière S Robinson D Almazar ER Roux S Smets P Sobanski V Spiera R Steen V Sutton E Thorne C Wilcox P Ayala MC Cook V Hu S Matthews B Nassar EL Neyer MA Nordlund J Provencher S














 Macklin E Hayden D Lai P Donahue R Marion J Alameda G Mathai N Ho D McCaffrey A Berry J Babu S Scalia J Freeman M Tourenne CL Sadri-Vakili G Quick A Kolb S Heintzman S Heitzman D Martin A Ajroud-Driss S Sufit R Szymanski A Appel SH Greene ES Thonhoff J Shroff S Liao B Katz J Jenkins L Felice K Whitaker C Maragakis NJ Clawson LL Uchil A Riley K Arneklev J Simmons Z Grogan J Su X Mamarabadi M Goutman SA Feldman E Olney N Bazan T Miller T Malcolm A Fernandes JAM Piccione E Thaisetthawatkul P Ilieva H Pasinelli P Jawdat O Farmakidis C Jabari D Statland J Pasnoor M Dimachkie M Weiss MD Rad N Wang LH Foster L Vu T Suresh N Farias J Ladha S Jacobsen B Milliard J Bowser R Owegi MA Brown RH Jr Ghasemi M Houmani H Douthwright C Newman DS Arcila-Londono X Steijlen K Yasek J Hams M Jackson C Bhavaraju-Sanka R Swenson A Nance C Gutmann L Heiman-Patterson T Deboo A Caress J Cartwright M Fee D Shrilla D Peltier A Lewis R Burford M Diaz F Rosenfeld J Borg D Bhuvaneswaran K Walk D Maiser S Johnson K Rao P Elliott M Rakocevic G Jones S Solorzano G Kasarskis EJ Mahuwala Z Mathur Kumaraswamy VV Rutkove S McIlduff C Bedlack R Li X Parker S Elman L Quinn C Goyal NA Habib AA Mozaffar T Korb MK Mullen J Rezania K Soliven B Roos R Twydell P Mundwiler A Young E Meyer JA Benatar M Glass J Fournier C Cohen JA Stommel E Robbins NM Jones V Zilliox L Diaz-Abad M Jin P Chauhan C Wymer JP Chuquilin M Subramony SH McNeely W Beydoun SR Darki L Rodriguez R Shah J Oskarsson B Pattee GL Bobenhouse J Hayat G Al-Dahhak R Kafaie J Martinez-Thompson J Staff N Nayar S Kuenzler R Bayat E Rosow L Bodkin C Gursoy N Al-Lahham T Lacomis D Gibson S Rivner M Kushlaf HA Gwathmey KG Elliott M McKinnon J Wu A Walsh A Whitesell J Erickson A Locatelli E Connors R McCluskey L Usman U Kovvuru S Sherman A Hasenoehrl M Dagostino D Faulconer K Kharakozova O Korin A Tarasenko N Vigneswaran P Katsovskiy I Whitworth I Wahab Y Novak I Tustison E Jentoft K Ostrow J Changkuon G La T Deignan C Li H Patel P Phan M Hurwitz S Estes M Palillo J Thomas M De Mattos A Patterson J Figueroa-Szostek P Jean SL Pothier L Harkey B DiStefano S Bailey A Jordan B Pagliaro J Wright S Abu-Hamdan N Igne C Kolvek T Bailey J Barlow V Arroyave L Henrique J Proeung S Rosenthal J Gladden C Cirino M Henrique N Deirmendjian E Small C Bulat A Hurwitz S Popel N Irwin L Hall M Connolly M Kittle G Hamilton J De Santiago D Felix A Lovett M Nelson L Martin A Garrett K Garcia AR Rede D Pabon M Khan K Fetouh A Woodcook J Kamp C Kennedy J McGarry A Torti M















































 Fortuné C Hudson M Benedetti A Hummers LK Adams CE Ayala MC Cook V Hu S Matthews B Nassar EL Nordlund J Provencher S Assassi S El-Baalbaki G Fligelstone K Frech T Hinchcliff M Johnson SR Larche M Khalidi N Leite C Nguyen C Rannou F Nielsen K Pope J Rodriguez-Reyna TS Schouffoer AA Suarez-Almazor ME Agard C André M Olagne L Bernstein EJ Berthier S Bissonnette L Bruns A Masetto A Roux S Cacciatore C Crichi B Farge-Bancel D Carreira P Fare R Lopez MM Díaz SM Almazar ER Casadevall M Chaigne B Dunogue B Régent A Chung L Domsic R Dunne JV Wilcox P Fortin PR Ikic A Gordon J Lakin K Spiera R Granel-Rey B Guffroy A Martin T Poindron V Gyger G Hachulla E Hoa S Jones N Lambert M Launay D Maillard H Sobanski V Lee YC Maltez N Manning J Marie I Maurier F Mekinian A Rivière S Nikpour M Proudman S Robinson D Smets P Steen V Sutton E Thorne C
















































































































 Fortuné C Gietzen A Guillot G Lewis N Nielsen K Sauvé M Richard M Welling J Varga J Adams CE Ayala MC Cook V Hu S Nassar EL Neyer MA Nordlund J Provencher S Bartlett SJ Hudson M Benedetti A Gottesman K Hummers LK Lawrie-Jones A Mayes MD Assassi S Nielson WR El-Baalbaki G van den Ende C Fligelstone K Frech T Harel D Hinchcliff M Johnson SR Larche M Khalidi N Leite C Nguyen C Rannou F Pope J Reyna TSR Schouffoer AA Suarez-Almazor ME Agard C Abdallah NA Crichi B Farge-Bancel D André M Olagne L Smets P Bernstein EJ Berthier S Bissonnette L Bruns A Masetto A Roux S Carreira P Fare R Martin M Díaz SM Almazar ER Casadevall M Chaigne B Dunogue B Régent A Chung L Denton C Domsic R Dunne JV Wilcox P Fortin PR Ikic A Gordon J Lakin K Spiera R Granel-Rey B Guffroy A Martin T Poindron V Gyger G Hachulla E Lambert M Launay D Maillard H Sobanski V Hoa S Jones N Kafaja S Lee YC Maltez N Manning J Marie I Maurier F Mekinian A Rivière S Nikpour M Proudman S Robinson D Steen V Sutton E Thorne C Varga J







 Allen N Aslam T Atan D Balaskas K Barman S Barrett J Bishop P Black G Braithwaite T Carare R Chakravarthy U Chan M Chua S Day A Desai P Dhillon B Dick A Doney A Egan C Ennis S Foster P Fruttiger M Gallacher J Garway-Heath D Gibson J Guggenheim J Hammond C Hardcastle A Harding S Hogg R Hysi P Keane P Khaw PT Khawaja A Lascaratos G Littlejohns T Lotery A Luben R Luthert P Macgillivray T Mackie S Madhusudhan S Mcguinness B Mckay G Mckibbin M Moore T Morgan J O'sullivan E Oram R Owen C Patel P Paterson E






 Aguerre I Amezcua L Chitnis T Lewis JC Engel C Han MH Klawiter EC Kocsik A Kruse-Hoyer M Levine L Levy M Marcille M Mealy MA Moore S Mullin DS Nelson KE Onomichi KB Planchon SM Pruitt A Repovic P Riley CS Rimler Z Russo AW Ocampo CT Tomczak AJ





 Cuomo G Moroncini G Stork J Iannone F Walker U Bertoldo E Krasowska D Salvador MJ Tikly M Riccieri V Sha A Gheorghiu AM Sunderkötter C Ingegnoli F Mouthon L Smith V Cantatore FP Eyerich K Wiland P Vanthuyne M Anic B Üprus M Granel B Vacca A Tanaseanu CM Lefebvre PGP Sibilia J Litinsky I Saketkoo LA Kerzberg E Limonta M Rimar D Sfikakis P Cutolo M Foti R Novak S Radic M Pellerito R Rozzano CFS Ananieva LP Szűcs G de la Puente C Ionescu RM Pozzi MR Alegre-Sancho JJ Herrmann K De Langhe E Altunizade SY Agachi S Veale D Loyo E Li M Rosato E Maurer B Castellví I Spertini F Solanki K Del Papa N Espinosa G Czirják L Coleiro B Bancel DF Pellerito R Denton C Damjanov N Granollers VOS Kohm M Stamenkovic B Allanore Y Airo' P Balbir-Gurman A Cerinic MM Riemekasten G Heitmann S Hunzelmann N Montecucco C Morovic-Vergles J Ribi C





 Grimbacher B Warnke C Wicklein R Wijburg M Brouwer M Lambert N Engalenc X Gaudin M Küpper C Aouba A Manda V Brousse X Ducours M Duffau P Ouallet J Mrabet H Gourdon F Le Maréchal M Bernard‐Valnet R Delobel P Lajaunie R Treiner E Lhomme S Bonneville F Ribaute C Ciron J Biotti D Kamar N Weiss N Pourcher V Rakotoarison J Leveneur Y De Menibus L Grassl N Lifermann F Cohen‐Aubart F Ney D Kapadia R Dinur‐Schejter Y Shifman T Shamriz O Berger J Lambotte O Perpoint T Harel A Wyplosz B
 Adamo S Bartha R Berezuk C Black A Borrie M Bronskill S Bulman D Casaubon L Cornish B Defrawy S Dilliott A Dixon RA Farhan S Faria F Fraser J Freedman M Ghani M Greenberg B Haddad H Hassan A Hatch W Hegele R Holmes M Hudson C Jog M Kleinstiver P Kwan D Leontieva E Levine B Mandelcorn E Margolin E McIlroy B Montero-Odasso M Munoz D Nanayakkara N Ozzoude M Ramirez J Rashkovan N Robinson J Rogaeva E Adamson YS Scott C Strong M Sujanthan S Symons S Theyers A Troyer A Van Ooteghem K Woulfe J Zamyadi M





 Soltis AR Viollet C Sukumar G Alba C Lott N McGrath Martinez E Tuck M Singh J Bacikova D Zhang X Hupalo DN Adeleye A Wilkerson MD Pollard HB Dalgard CL Black SE Gan-Or Z Keith J Masellis M Rogaeva E Brice A Lesage S Xiromerisiou G Calvo A Canosa A Chio A Logroscino G Mora G Krüger R May P Alcolea D Clarimon J Fortea J Gonzalez-Aramburu I Infante J Lage C Lleó A Pastor P Sanchez-Juan P Brett F Aarsland D Al-Sarraj S Attems J Gentleman S Hardy JA Hodges AK Love S McKeith IG Morris CM Morris HR Palmer L Pickering-Brown S Ryten M Thomas AJ Troakes C Albert MS Barrett MJ Beach TG Bekris LM Bennett DA Boeve BF Dalgard CL Dawson TM Dickson DW Faber K Ferman T Ferrucci L Flanagan ME Foroud TM Ghetti B Gibbs JR Goate A Goldstein DS Graff-Radford NR Kaufmann H Kukull WA Leverenz JB Lopez G Mao Q Masliah E Monuki E Newell KL Palma JA Perkins M Pletnikova O Renton AE Resnick SM Rosenthal LS Ross OA Scherzer CR Serrano GE Shakkottai VG Sidransky E Tanaka T Tayebi N Topol E Torkamani A Troncoso JC Woltjer R Wszolek ZK Scholz SW Baloh RH Bowser R Brice A Broach J Camu W Chiò A Cooper-Knock J Drepper C Drory VE Dunckley TL Feldman E Fratta P Gerhard G Gibson SB Glass JD Hardy JA Harms MB Heiman-Patterson TD Jansson L Kirby J Kwan J Laaksovirta H Landers JE Landi F Le Ber I Lumbroso S MacGowan DJ Maragakis NJ Mouzat K Myllykangas L Orrell RW Ostrow LW Pamphlett R Pioro E Pulst SM Ravits JM Robberecht W Rogaeva E Rothstein JD Sendtner M Shaw PJ Sidle KC Simmons Z Stein T Stone DJ Tienari PJ Traynor BJ Troncoso JC Valori M Van Damme P Van Deerlin VM Van Den Bosch L Zinman L



 Pilotto A Piccinelli SC Lazzari S Negro G Cereda GS Infante R Giovannelli G Cutellè C Tinti L Diamanti S Fanella G Rifino N Tremolizzo L Ermanis G Kuris F Sartor R Bax F Gigli GL Barvas E Volpini M Frusciante R Bernardi M Turla M Valenti R Valenti R Kiferle L Pradella S Innocenti A Ciolli L Orlandi N Vandelli G Mazzoli M Benedetti L Pardini M Grisanti S Biassoni E Cabona C Schenone A Boso F Agosta F Orrico M Roveri L Sferruzza G Gentile M Piccolo L Merli E Salmaggi A Bocci T Ferrucci R Dini M Guarino M Nicodemo M Beretta S Giossi A Campana C Censori B Primiano G Troiano M Bollo L Calcagno N Trogu F Morelli C Colosimo C Di Schino C Costantini F Cosentino G Marchioni E Avorio F Russelli G Panarello G Carlucci G Azzolini F Lotti A Ciccone A Furlanis G Giometto B Bellavita G Valentina S Lorusso L Altavista MC Brigandì A Sorbera C Gatto L Sacco S Clerici R Schirinzi E Bonanni E Merico E Beretta N Gallo G Sciolla C Bertolotto A Pomati S Masserini F Camilli F Panzera I Cardinali P Cristina Acciarri M De Michele G Perillo S Palmieri GR Cuomo N Giglio A
 Ivan PA Sandu G Odajiu I Dragoș Sandu C Vitalie L Mikhail G Olesea O Cavallieri F Toschi G Zedde M Turla M Bianchi M Civelli P Cvetkovska E Barbov I Babunovska M Kozlova A Abramova A Daria E Dobronyi L Dénes K Bereczki D Agajany N Geva M Kindl P Kosno K Michał L Silva LS Batista João R Jung S Müller M Aires E Vinski I Lisak M Marjiana L Ural O Kara I Öztürk B Caldeiras ACO Rodriguez-Leyva I Boldingh M von Oertzen T Jenkins TM Riahi A Taba P Azzam AY Wojtecki L Sellner J Castillo S Bušková J Novotny V Jelcic I Dafea A Medina MT Flemen HØ Elbahnasawy MG Kohler E Farmen AH




 Liu G Valentino RR Peng J Liao Z Locascio JJ Corvol JC Dong X Maple-Grødem J Campbell MC Elbaz A Lesage S Brice A Mangone G Growdon JH Hung AY Schwarzchild MA Hayes MT Wills AM Herrington TM Ravian B Shoulson I Taba P Kõks S Beach TG Cormier-Dequaire F Alves G Tysnes OB Perlmutter JS Heutink P van Hilten JJ Kasten M Mollenhauer B Trenkwalder C Klein C Barker RA Williams-Gray CH Marinus J Scherzer CR
 Abraham J Adkisson M Albert M Altamirano LT Alvarenga B Anderson ML Anderson EJ Arnett A Asashima H Atkinson MA Baden LR Barton B Beach K Beagle E Becker PM Bell MR Bernui M Bime C Boddapati AK Booth JL Borresen B Brakenridge SC Bristow L Bryant R Calfee CS Carreño JM Carrillo S Chak S Chang I Connors J Conway M Corry DB Cowan D Croen B Dela Cruz CS Cusimano G Eaker L Edwards C Ehrlich LIR Elashoff D Erickson H Erle DJ Farhadian S Farrugia K Fatou B Fernandes A Fernandez-Sesma A Fragiadakis GK Furukawa S Geltman JN Ghale R Bermúdez González MC Goonewardene IM Guerrero ES Guirgis FW Hafler DA Hamilton S Harris P Hayati AN Hendrickson CM Agudelo Higuita NI Hodder T Holland SM Hough CL Huerta C Hurley KC Hutton SR Iwasaki A Jauregui A Jha M Johnson B Joyner D Kangelaris KN Kelly G Khalil Z Khan Z Kheradmand F Kim JN Kimura H Ko AI Kohr B Kraft M Krummel M Kutzler MA Lasky-Su J Lee S Lee D Leipold M Lentucci C Leroux C Lin E Liu S Love C Lu Z Maliskova L Manning BR Manohar M Martens M McComsey GA McEnaney K McLin R Melamed E Melnyk N Mendez K Messer WB Metcalf JP Michelotti G Mick E Mohanty S Mosier J Mulder LCF Murphy M Nadeau KRC Nelson E Nelson A Nguyen V Oberhaus J Panganiban B Pellegrini KL Pickering HC Powell DL Presnell S Pulendran B Rahman AH Rashid AS Raskin A Reed EF Ribeiro SP Rivera AM Rogers JE Rogers A Rogowski B Rooks R Rosenberg-Hasson Y Rothman J Rousseau JF Salehi-Rad R Saluvan M Samaha H Schaenman J Schunk R Semenza NC Sen S Sevransky J Seyfert-Margolis V Shaheen T Shaw AC Sieg S Siegel SAR Sigal N Siles N Simmons B Simon V Singh G Sinko L Smith CM Smolen KK Song LZ Srivastava K Sullivan P Syphurs C Tcheou J Tegos GP Tharp GK Tong A Tsitsiklis A Ungaro RF Vaysman T Viode A Vita R Wang X Ward A Ward DC Willmore A Woloszczuk K Wong K Woodruff PG Xu L van Haren S van de Guchte A Zhao Y



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 The Lancet. Neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 Journal of neurology
 Optometry and vision science : official publication of the American Academy of Optometry
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Revue medicale suisse
 Nature medicine
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Nature
 The Science of the total environment
 Multiple sclerosis and related disorders
 Journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Brain : a journal of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Sleep & breathing = Schlaf & Atmung
 Nature reviews. Neurology
 Telemedicine journal and e-health : the official journal of the American Telemedicine Association
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
 Multiple sclerosis and related disorders
 Wiener medizinische Wochenschrift (1946)
 BMC neurology
 Neurology
 Neurology
 International journal of molecular sciences
 JAMA neurology
 Multiple sclerosis and related disorders
 Journal of neuroimmunology
 European journal of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Contemporary clinical trials
 Journal of the neurological sciences
 Neurology India
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Medicina (Kaunas, Lithuania)
 JAMA otolaryngology-- head & neck surgery
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of neuropsychology
 The neurologist
 The Clinical neuropsychologist
 Multiple sclerosis and related disorders
 Journal of digital imaging
 United European gastroenterology journal
 Cell chemical biology
 Journal of neurology
 Journal of clinical and experimental neuropsychology
 Cell death and differentiation
 Clinical neurology and neurosurgery
 Multiple sclerosis and related disorders
 Annals of neurology
 JAMA
 European review for medical and pharmacological sciences
 European journal of neurology
 Archives of disease in childhood. Education and practice edition
 Human brain mapping
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 European journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of magnetic resonance imaging : JMRI
 Journal of neurology
 Multiple sclerosis and related disorders
 Klinische Monatsblatter fur Augenheilkunde
 Multiple sclerosis and related disorders
 Gaceta medica de Mexico
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 NeuroImage. Clinical
 Acta medica portuguesa
 The European journal of neuroscience
 European radiology
 The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses
 BMC research notes
 Annals of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society
 Soins; la revue de reference infirmiere
 Holistic nursing practice
 Multiple sclerosis and related disorders
 Journal of psychosomatic research
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 BMC neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Revista de neurologia
 Neurologia
 Journal of hospice and palliative nursing : JHPN : the official journal of the Hospice and Palliative Nurses Association
 Genes
 European journal of ophthalmology
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 EBioMedicine
 Annals of clinical and translational neurology
 Neurology
 Journal of neurology, neurosurgery, and psychiatry
 BMJ open
 BMC women's health
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis and related disorders
 Revue neurologique
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Genes
 ORL; journal for oto-rhino-laryngology and its related specialties
 Journal of child neurology
 Neurologia i neurochirurgia polska
 Neurology
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroimmunology
 European journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 JAMA neurology
 Seminars in pediatric neurology
 Journal of theoretical biology
 Home health care services quarterly
 International immunopharmacology
 Neurobiology of disease
 Multiple sclerosis and related disorders
 Journal of neurology
 Neurologic clinics
 Multiple sclerosis and related disorders
 BMC neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Clinical linguistics & phonetics
 Multiple sclerosis and related disorders
 European journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Frontiers in immunology
 The International journal of neuroscience
 Studies in health technology and informatics
 Studies in health technology and informatics
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Archives of Razi Institute
 Fertility and sterility
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 EBioMedicine
 Acta biochimica Polonica
 Journal of neurology
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 Neuroscience
 Naunyn-Schmiedeberg's archives of pharmacology
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Revue neurologique
 Scientific reports
 Multiple sclerosis and related disorders
 BMC neurology
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Progres en urologie : journal de l'Association francaise d'urologie et de la Societe francaise d'urologie
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Scandinavian journal of immunology
 PloS one
 Internal and emergency medicine
 Frontiers in immunology
 Clinical and translational science
 Journal of comparative effectiveness research
 Neurology
 The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses
 European journal of neurology
 Journal of neurology
 Journal of neuroimmunology
 Neurologia
 Neurodegenerative disease management
 Annals of clinical and translational neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 European journal of neurology
 Multiple sclerosis and related disorders
 Medical principles and practice : international journal of the Kuwait University, Health Science Centre
 International journal of environmental research and public health
 The Libyan journal of medicine
 Multiple sclerosis and related disorders
 Ocular immunology and inflammation
 Turkish journal of ophthalmology
 European journal of neurology
 Multiple sclerosis and related disorders
 Theranostics
 Journal of neurology
 Molecular biology reports
 Acupuncture in medicine : journal of the British Medical Acupuncture Society
 Multiple sclerosis and related disorders
 Journal of the neurological sciences
 Medicina (Kaunas, Lithuania)
 European neurology
 Investigative radiology
 Multiple sclerosis and related disorders
 Journal of neurology
 Brain and behavior
 Scientific reports
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Journal of the International Neuropsychological Society : JINS
 CNS drugs
 European journal of neurology
 Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Journal of psychosomatic research
 Frontiers in immunology
 Pediatric neurology
 Multiple sclerosis and related disorders
 Applied neuropsychology. Adult
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 BMC psychology
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Soins; la revue de reference infirmiere
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology
 Human brain mapping
 Journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of molecular sciences
 Cognitive neuropsychiatry
 The Lancet. Neurology
 Multiple sclerosis and related disorders
 NeuroImage
 International journal of audiology
 Acta neurologica Belgica
 PloS one
 Journal of neurology
 Multiple sclerosis and related disorders
 Neuropsychological rehabilitation
 Journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of neuroinflammation
 Multiple sclerosis and related disorders
 NeuroImage. Clinical
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Disability and health journal
 PloS one
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Explore (New York, N.Y.)
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis and related disorders
 Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
 Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
 CNS drugs
 American journal of therapeutics
 Journal of neurology, neurosurgery, and psychiatry
 Journal of clinical pathology
 Multiple sclerosis and related disorders
 Journal of immunology research
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 BMJ open
 Trials
 Journal of clinical psychology
 The International journal of pharmacy practice
 PloS one
 Neurology
 European journal of neurology
 The Journal of nutrition
 Journal of patient-reported outcomes
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of digital imaging
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 European journal of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Gait & posture
 European journal of radiology
 Journal of oral rehabilitation
 Neurological research
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of neurology
 Magnetic resonance imaging
 Multiple sclerosis and related disorders
 Frontiers in immunology
 Journal of neurology
 Multiple sclerosis and related disorders
 Neurourology and urodynamics
 European journal of neurology
 Journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Human brain mapping
 European radiology
 Multiple sclerosis and related disorders
 Ocular immunology and inflammation
 Journal of medical case reports
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 NeuroImage. Clinical
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neuroradiology
 La Clinica terapeutica
 Journal of neurology, neurosurgery, and psychiatry
 Journal of pharmacy practice
 Multiple sclerosis and related disorders
 Acta neurologica Belgica
 Multiple sclerosis and related disorders
 European journal of ophthalmology
 Cerebral cortex (New York, N.Y. : 1991)
 EBioMedicine
 Multiple sclerosis and related disorders
 Neurology
 Scientific reports
 Clinical neuroradiology
 Neurology
 The primary care companion for CNS disorders
 Multiple sclerosis and related disorders
 Brain and behavior
 Investigative radiology
 Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
 Multiple sclerosis and related disorders
 Neurology
 Journal of medical economics
 Journal of neurology
 BMC neurology
 Acta neurologica Belgica
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Folia medica
 Rinsho shinkeigaku = Clinical neurology
 European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society
 The Lancet. Neurology
 Nature reviews. Neurology
 Continuum (Minneapolis, Minn.)
 Journal of the neurological sciences
 Journal of neurology
 Progress in neurobiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Cell reports. Medicine
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Nature communications
 Journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of neurology
 The Lancet. Neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 The neuroradiology journal
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of molecular sciences
 Clinical neurology and neurosurgery
 Multiple sclerosis and related disorders
 Forensic science, medicine, and pathology
 Clinical biochemistry
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurologia i neurochirurgia polska
 European journal of neurology
 International journal of molecular sciences
 NeuroImage. Clinical
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 BMC neurology
 Magnetic resonance in medicine
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 The Lancet. Neurology
 Blood advances
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Journal of neurology
 Multiple sclerosis and related disorders
 Acta neurologica Belgica
 Nature reviews. Neurology
 Multiple sclerosis and related disorders
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Anesthesia and analgesia
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Frontiers in immunology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Soins; la revue de reference infirmiere
 Journal of neuroimmunology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 NeuroImage. Clinical
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurology
 Journal of neurology
 Scientific reports
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of Alzheimer's disease : JAD
 Journal of neurology, neurosurgery, and psychiatry
 Journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 European journal of neurology
 Annales pharmaceutiques francaises
 Immunology letters
 Multiple sclerosis and related disorders
 Value in health regional issues
 European journal of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 European journal of neurology
 Multiple sclerosis and related disorders
 CNS drugs
 Multiple sclerosis and related disorders
 Disability and rehabilitation
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 JAMA neurology
 European journal of neurology
 Drugs
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society
 Journal of neurology, neurosurgery, and psychiatry
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Current reviews in clinical and experimental pharmacology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of pharmaceutics
 Disability and rehabilitation
 Multiple sclerosis and related disorders
 Acta neurologica Taiwanica
 Neurodegenerative disease management
 Rehabilitacion
 Revista de neurologia
 Scientific reports
 Talanta
 Laboratory investigation; a journal of technical methods and pathology
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Brain and behavior
 Journal of neurology, neurosurgery, and psychiatry
 Seminars in ophthalmology
 Neurologia
 Multiple sclerosis and related disorders
 PloS one
 Magnetic resonance imaging
 BMC neurology
 Cerebral cortex (New York, N.Y. : 1991)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 AJNR. American journal of neuroradiology
 Journal of neurology
 Brain research
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Investigative radiology
 Vestnik oftalmologii
 Diagnostic and interventional imaging
 BMJ open
 Contemporary clinical trials
 Multiple sclerosis and related disorders
 Current protein & peptide science
 Multiple sclerosis and related disorders
 Nutrients
 The European journal of health economics : HEPAC : health economics in prevention and care
 Acta neurologica Belgica
 Multiple sclerosis and related disorders
 European journal of neurology
 Journal of pharmacy practice
 The neurologist
 American journal of physical medicine & rehabilitation
 Der Nervenarzt
 Multiple sclerosis and related disorders
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Brain and behavior
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 PloS one
 Neurology
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Handbook of clinical neurology
 Translational psychiatry
 Neuroradiology
 Annals of clinical and translational neurology
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 The patient
 Hip international : the journal of clinical and experimental research on hip pathology and therapy
 The Australasian journal of dermatology
 Medicina clinica
 Journal of neurology, neurosurgery, and psychiatry
 IEEE journal of biomedical and health informatics
 Multiple sclerosis and related disorders
 European journal of neurology
 CNS & neurological disorders drug targets
 The Egyptian journal of immunology
 International immunopharmacology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Brain and cognition
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Proceedings of the National Academy of Sciences of the United States of America
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Annals of clinical and translational neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Journal of the neurological sciences
 Brain and behavior
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Cell
 International journal of pharmaceutics
 Multiple sclerosis and related disorders
 Journal francais d'ophtalmologie
 The Journal of clinical investigation
 Neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Scientific reports
 Current eye research
 Neurosciences (Riyadh, Saudi Arabia)
 Scientific reports
 Journal of neurology
 Multiple sclerosis and related disorders
 Brain : a journal of neurology
 PloS one
 CNS neuroscience & therapeutics
 The journal of spinal cord medicine
 Multiple sclerosis and related disorders
 Infectious diseases now
 Neuroscience and biobehavioral reviews
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology
 Clinical and translational science
 Neurological research
 Radiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroscience research
 Clinical epigenetics
 Frontiers in immunology
 Neurology(R) neuroimmunology & neuroinflammation
 Neurology
 Frontiers in immunology
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Annals of clinical and translational neurology
 Journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Annals of neurology
 European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society
 Multiple sclerosis and related disorders
 Journal of comparative effectiveness research
 Multiple sclerosis and related disorders
 Acta radiologica (Stockholm, Sweden : 1987)
 Journal of neurology, neurosurgery, and psychiatry
 Diagnosis (Berlin, Germany)
 Neurobiology of disease
 Evaluation and program planning
 Molecular biology reports
 Multiple sclerosis and related disorders
 Metabolomics : Official journal of the Metabolomic Society
 Journal of magnetic resonance imaging : JMRI
 PloS one
 Archives of physical medicine and rehabilitation
 Lipids in health and disease
 Neurologia i neurochirurgia polska
 Human brain mapping
 Clinical nursing research
 Hormone molecular biology and clinical investigation
 Neuroradiology
 International journal of molecular sciences
 Journal of neurology
 Nature reviews. Neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Brain and behavior
 Journal of medical economics
 Annals of physical and rehabilitation medicine
 Acta neurologica Belgica
 Neurorehabilitation and neural repair
 Urologie (Heidelberg, Germany)
 Frontiers in public health
 BMC neurology
 Journal of autoimmunity
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International ophthalmology
 Multiple sclerosis and related disorders
 Acta neurologica Belgica
 Multiple sclerosis and related disorders
 Frontiers in immunology
 The Lancet. Neurology
 European journal of neurology
 Multiple sclerosis and related disorders
 Med (New York, N.Y.)
 Multiple sclerosis and related disorders
 Frontiers in immunology
 International journal of molecular sciences
 The Lancet. Neurology
 Food & function
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Journal of proteome research
 Brain : a journal of neurology
 Multiple sclerosis and related disorders
 Disability and rehabilitation
 Annals of clinical and translational neurology
 eLife
 Multiple sclerosis and related disorders
 Patient education and counseling
 BMC neurology
 Journal of medical imaging and radiation sciences
 Neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 European journal of neurology
 Neurology
 Journal of health psychology
 Neurodegenerative disease management
 European journal of neurology
 Multiple sclerosis and related disorders
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Journal of neurology
 Proceedings of the National Academy of Sciences of the United States of America
 Journal of child neurology
 PloS one
 The Annals of pharmacotherapy
 Statistical methods in medical research
 Physiotherapy theory and practice
 Multiple sclerosis and related disorders
 European neurology
 Investigative radiology
 European journal of neurology
 Multiple sclerosis and related disorders
 Clinical neurology and neurosurgery
 Journal of neuroscience research
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Investigative radiology
 Biology open
 Multiple sclerosis and related disorders
 Neuropsychological rehabilitation
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Biochimica et biophysica acta. General subjects
 Neuropsychopharmacology reports
 PeerJ
 Journal of the neurological sciences
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Frontiers in immunology
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Applied neuropsychology. Child
 Neurology(R) neuroimmunology & neuroinflammation
 Proceedings of the National Academy of Sciences of the United States of America
 Journal of neuroimmunology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Hematology (Amsterdam, Netherlands)
 Journal of thrombosis and thrombolysis
 Sensors (Basel, Switzerland)
 The Journal of clinical investigation
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Disability and rehabilitation
 Frontiers in immunology
 Neuropsychological rehabilitation
 Multiple sclerosis and related disorders
 Neuropsychological rehabilitation
 Multiple sclerosis and related disorders
 Sensors (Basel, Switzerland)
 Physiotherapy theory and practice
 Multiple sclerosis and related disorders
 European journal of medical research
 Multiple sclerosis and related disorders
 Expert opinion on drug delivery
 Multiple sclerosis and related disorders
 Journal of neurology
 Annals of physical and rehabilitation medicine
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society
 International journal of environmental research and public health
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Clinical neurology and neurosurgery
 Arquivos de neuro-psiquiatria
 Journal of pharmaceutical and biomedical analysis
 Human molecular genetics
 The journal of sexual medicine
 Scientific reports
 Neurology(R) neuroimmunology & neuroinflammation
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Journal of neuroinflammation
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 BMC public health
 WIREs mechanisms of disease
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 International journal of molecular sciences
 Brain connectivity
 Journal of neurology, neurosurgery, and psychiatry
 Holistic nursing practice
 United European gastroenterology journal
 Frontiers in immunology
 Acta neuropathologica communications
 Tomography (Ann Arbor, Mich.)
 Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA
 Multiple sclerosis (Houndmills, Basingstoke, England)
 BMJ open
 Personalized medicine
 Scientific reports
 Cerebral cortex (New York, N.Y. : 1991)
 Arquivos de neuro-psiquiatria
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of the International Neuropsychological Society : JINS
 Current drug safety
 BMC health services research
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology, neurosurgery, and psychiatry
 Annals of neurology
 Journal of neuroinflammation
 Physical therapy
 Cannabis and cannabinoid research
 NeuroImage. Clinical
 Brain and nerve = Shinkei kenkyu no shinpo
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis and related disorders
 Disability and rehabilitation
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of molecular sciences
 Neurodegenerative disease management
 ACS chemical neuroscience
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 European journal of neurology
 Medicina (Kaunas, Lithuania)
 Nutrients
 Nature reviews. Neurology
 Frontiers in immunology
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Therapeutic delivery
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroimmunology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Disability and health journal
 International immunopharmacology
 Neurology(R) neuroimmunology & neuroinflammation
 Journal of magnetic resonance imaging : JMRI
 Scandinavian journal of occupational therapy
 International journal of molecular sciences
 European journal of neurology
 Journal of psychosomatic research
 The Lancet. Neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 European journal of neurology
 Multiple sclerosis and related disorders
 Frontiers in immunology
 Journal of neuroendocrinology
 Multiple sclerosis and related disorders
 Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
 Multiple sclerosis and related disorders
 Revista da Associacao Medica Brasileira (1992)
 Multiple sclerosis and related disorders
 Biomaterials
 Medicina
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 Brain imaging and behavior
 Multiple sclerosis and related disorders
 Neurochemical research
 Journal of peptide science : an official publication of the European Peptide Society
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Revista de neurologia
 Continuum (Minneapolis, Minn.)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurochemical research
 Sensors (Basel, Switzerland)
 Multiple sclerosis and related disorders
 PloS one
 European journal of neurology
 AJNR. American journal of neuroradiology
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 Transplant immunology
 Multiple sclerosis and related disorders
 NMR in biomedicine
 Journal of comparative effectiveness research
 Evaluation and program planning
 La Revue du praticien
 Clinical pharmacology and therapeutics
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuropsychology
 Rinsho shinkeigaku = Clinical neurology
 The Lancet. Neurology
 Cells
 Neurologia
 Arquivos de neuro-psiquiatria
 Frontiers in immunology
 Journal of clinical pathology
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Multiple sclerosis and related disorders
 Inquiry : a journal of medical care organization, provision and financing
 Journal of neuroimmunology
 Breastfeeding medicine : the official journal of the Academy of Breastfeeding Medicine
 Sensors (Basel, Switzerland)
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Neurobiology of disease
 Biological chemistry
 Neurology
 European journal of neurology
 Neurology(R) neuroimmunology & neuroinflammation
 Revista de neurologia
 Nursing research
 Neurodegenerative disease management
 CEN case reports
 European journal of medical research
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Human brain mapping
 Frontiers in endocrinology
 Multiple sclerosis and related disorders
 Journal of comparative effectiveness research
 BMJ open
 Transgenic research
 Expert opinion on therapeutic targets
 Radiology
 Neurology
 Scientific reports
 Advanced biology
 Investigative radiology
 Neurology(R) neuroimmunology & neuroinflammation
 International journal of molecular sciences
 Neurobiology of disease
 Nutritional neuroscience
 Pediatric neurology
 European psychiatry : the journal of the Association of European Psychiatrists
 Computerized medical imaging and graphics : the official journal of the Computerized Medical Imaging Society
 International journal of molecular sciences
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine
 The Clinical neuropsychologist
 International journal of medical informatics
 Journal of integrative and complementary medicine
 Journal of managed care & specialty pharmacy
 Neurologia
 American journal of ophthalmology
 Prion
 PloS one
 Journal of health, population, and nutrition
 Multiple sclerosis and related disorders
 Practical neurology
 Nutrients
 Brain and nerve = Shinkei kenkyu no shinpo
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 European journal of neurology
 Physiotherapy research international : the journal for researchers and clinicians in physical therapy
 Contemporary clinical trials
 Multiple sclerosis and related disorders
 The Lancet. Neurology
 Multiple sclerosis and related disorders
 Mutation research. Genetic toxicology and environmental mutagenesis
 Multiple sclerosis and related disorders
 Cells
 Journal of the International Neuropsychological Society : JINS
 Journal of neuroscience research
 European journal of neurology
 Multiple sclerosis and related disorders
 International journal of molecular sciences
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Molecular biology reports
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Acta neuropathologica communications
 Neurology
 Multiple sclerosis and related disorders
 BMC neurology
 Mucosal immunology
 Diagnostic and interventional imaging
 Journal of neurology
 BMC neurology
 The Journal of neuropsychiatry and clinical neurosciences
 Applied neuropsychology. Adult
 International journal of medical informatics
 Multiple sclerosis and related disorders
 Cellular & molecular immunology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Frontiers in immunology
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Stem cell research & therapy
 The British journal of dermatology
 Advances in therapy
 Metabolic brain disease
 Multiple sclerosis and related disorders
 Microbial pathogenesis
 Cleveland Clinic journal of medicine
 JCO precision oncology
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Clinical rehabilitation
 Work (Reading, Mass.)
 BMC neurology
 International journal of behavioral medicine
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroinflammation
 Journal of the International Neuropsychological Society : JINS
 Multiple sclerosis (Houndmills, Basingstoke, England)
 European journal of neurology
 ACS chemical neuroscience
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurochemistry international
 Expert review of medical devices
 Multiple sclerosis and related disorders
 Scientific reports
 International journal of molecular sciences
 Annals of neurology
 Autoimmunity reviews
 Glia
 Disability and rehabilitation
 Multiple sclerosis (Houndmills, Basingstoke, England)
 The Lancet. Neurology
 Scandinavian journal of occupational therapy
 PloS one
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Nature reviews. Neurology
 The Journal of clinical investigation
 Molecular neurobiology
 Psychology, health & medicine
 Irish journal of medical science
 BMJ open
 Pharmacology & therapeutics
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology, neurosurgery, and psychiatry
 Journal of neurology
 Revista de neurologia
 Multiple sclerosis and related disorders
 Molecular and cellular biochemistry
 Annals of neurology
 Computational intelligence and neuroscience
 Neurobiology of disease
 Multiple sclerosis and related disorders
 JAMA neurology
 International journal of molecular sciences
 Frontiers in immunology
 Journal of neurology, neurosurgery, and psychiatry
 Neurosurgery
 Digestive diseases and sciences
 The Science of the total environment
 International journal of molecular sciences
 Journal of neuroinflammation
 Journal of neurology
 Brain and behavior
 Computers in biology and medicine
 Scientific reports
 Multiple sclerosis and related disorders
 Brain : a journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Experimental brain research
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 The Journal of dermatology
 Endocrine, metabolic & immune disorders drug targets
 Frontiers in immunology
 Biomedical physics & engineering express
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Archives of medical research
 Neurophysiologie clinique = Clinical neurophysiology
 Alternative therapies in health and medicine
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Radiology
 Communications biology
 Journal of medicinal chemistry
 Acta pharmacologica Sinica
 Neuron
 Multiple sclerosis and related disorders
 Cells
 Proteomics. Clinical applications
 Multiple sclerosis and related disorders
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Multiple sclerosis and related disorders
 European journal of neurology
 International journal of epidemiology
 Journal of medical virology
 Medicine
 Journal of neuroinflammation
 Handbook of clinical neurology
 Multiple sclerosis and related disorders
 BMC neurology
 Brain and behavior
 Journal of neurology
 Journal of neuroinflammation
 Journal of speech, language, and hearing research : JSLHR
 Investigative radiology
 Neurorehabilitation and neural repair
 International journal of molecular sciences
 Disability and rehabilitation. Assistive technology
 Nature reviews. Neurology
 Scientific reports
 Neurology
 European journal of neurology
 Multiple sclerosis and related disorders
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Neurology(R) neuroimmunology & neuroinflammation
 Clinical neuropharmacology
 Brain, behavior, and immunity
 Medicine
 Multiple sclerosis and related disorders
 The European journal of neuroscience
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Dysphagia
 Journal of neurology, neurosurgery, and psychiatry
 Arquivos de neuro-psiquiatria
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Scandinavian journal of medicine & science in sports
 Multiple sclerosis and related disorders
 Soins; la revue de reference infirmiere
 Multiple sclerosis and related disorders
 Journal of neuroimmunology
 Therapeutic drug monitoring
 International immunopharmacology
 Neurologia i neurochirurgia polska
 Sensors (Basel, Switzerland)
 Nature metabolism
 Journal of occupational rehabilitation
 Neurology(R) neuroimmunology & neuroinflammation
 Revista de neurologia
 Soins; la revue de reference infirmiere
 NeuroRehabilitation
 Journal of neurology, neurosurgery, and psychiatry
 Soins; la revue de reference infirmiere
 Multiple sclerosis (Houndmills, Basingstoke, England)
 BMC neurology
 Journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Folia neuropathologica
 Journal of neuroimmunology
 The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
 Health and quality of life outcomes
 Multiple sclerosis and related disorders
 Journal of neurology
 Multiple sclerosis and related disorders
 Journal of neurology, neurosurgery, and psychiatry
 European journal of neurology
 Neurology India
 Journal of neurology
 International immunopharmacology
 Molecular biology reports
 Human brain mapping
 Neuropediatrics
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Acta radiologica (Stockholm, Sweden : 1987)
 Proceedings of the National Academy of Sciences of the United States of America
 Inflammopharmacology
 Journal of bodywork and movement therapies
 Journal of neurology
 Journal of neurology, neurosurgery, and psychiatry
 JAMA neurology
 Soins; la revue de reference infirmiere
 Multiple sclerosis and related disorders
 Sensors (Basel, Switzerland)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Journal of neurology, neurosurgery, and psychiatry
 Nature reviews. Neurology
 Journal of molecular graphics & modelling
 Journal of neuroimmunology
 European journal of neurology
 Gut microbes
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Gait & posture
 European journal of neurology
 Frontiers in immunology
 PM & R : the journal of injury, function, and rehabilitation
 Thyroid : official journal of the American Thyroid Association
 Current opinion in neurology
 Multiple sclerosis and related disorders
 Nature medicine
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroscience research
 Multiple sclerosis and related disorders
 Iranian journal of allergy, asthma, and immunology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 AJR. American journal of roentgenology
 Contemporary clinical trials
 Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
 Nutrients
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Multiple sclerosis and related disorders
 Annals of behavioral medicine : a publication of the Society of Behavioral Medicine
 European journal of neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 European journal of physical and rehabilitation medicine
 PloS one
 British journal of clinical pharmacology
 International journal of molecular sciences
 European review for medical and pharmacological sciences
 International journal of molecular sciences
 Journal of neurology
 Multiple sclerosis and related disorders
 Journal of neurology
 European radiology
 International journal of molecular sciences
 BMC neurology
 BMC neurology
 European journal of cancer (Oxford, England : 1990)
 European journal of neurology
 BMC neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurology
 The Cochrane database of systematic reviews
 Brain : a journal of neurology
 Multiple sclerosis and related disorders
 Physiology & behavior
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Frontiers in immunology
 Journal of child neurology
 Journal of the American Academy of Dermatology
 Journal of digital imaging
 American family physician
 Military medicine
 Expert review of pharmacoeconomics & outcomes research
 Multiple sclerosis and related disorders
 Nature medicine
 Neurodegenerative disease management
 Neurology(R) neuroimmunology & neuroinflammation
 Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society
 Journal of translational medicine
 Scientific reports
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Expert opinion on pharmacotherapy
 Multiple sclerosis and related disorders
 The Journal of biological chemistry
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Seminars in ultrasound, CT, and MR
 Clinical immunology (Orlando, Fla.)
 Magnetic resonance imaging
 Multiple sclerosis and related disorders
 JAMA neurology
 Multiple sclerosis and related disorders
 Journal of medical case reports
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Prosthetics and orthotics international
 BMC neurology
 JCI insight
 EBioMedicine
 WIREs mechanisms of disease
 Immunological medicine
 Nature immunology
 The Journal of clinical investigation
 Brain : a journal of neurology
 Pharmaceutical medicine
 The European journal of health economics : HEPAC : health economics in prevention and care
 Rehabilitation psychology
 PloS one
 Frontiers in immunology
 Frontiers in immunology
 Frontiers in immunology
 Human immunology
 Journal of pharmaceutical and biomedical analysis
 Molecular biology reports
 Molecular psychiatry
 The Journal of biological chemistry
 International journal of molecular sciences
 BioFactors (Oxford, England)
 Current topics in behavioral neurosciences
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Cephalalgia : an international journal of headache
 Pharmacology & therapeutics
 Clinical nuclear medicine
 BMC neurology
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Neurobiology of disease
 Journal of neurology
 International journal of molecular sciences
 Annals of clinical and translational neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Annals of neurology
 Physiotherapy
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurologia i neurochirurgia polska
 International journal of molecular sciences
 MMW Fortschritte der Medizin
 Neurobiology of disease
 Journal of neurovirology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Immunology
 OTJR : occupation, participation and health
 International journal of molecular sciences
 Molecular neurobiology
 Journal of endodontics
 Arquivos de neuro-psiquiatria
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurological research
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Phytotherapy research : PTR
 International journal of pharmaceutics
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Journal of medical economics
 Brain : a journal of neurology
 The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses
 The European journal of health economics : HEPAC : health economics in prevention and care
 European journal of medicinal chemistry
 Journal of clinical nursing
 International journal of qualitative studies on health and well-being
 Clinical immunology (Orlando, Fla.)
 The Journal of neuroscience : the official journal of the Society for Neuroscience
 RoFo : Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Cell and tissue research
 Multiple sclerosis and related disorders
 Turkish journal of medical sciences
 Nature reviews. Neurology
 EBioMedicine
 Brain : a journal of neurology
 Science advances
 Journal of neurology, neurosurgery, and psychiatry
 Journal of immunology (Baltimore, Md. : 1950)
 Neuropathology and applied neurobiology
 Autoimmunity reviews
 Multiple sclerosis and related disorders
 Journal of neurology, neurosurgery, and psychiatry
 Acta neurologica Belgica
 Journal of neurology
 Experimental & molecular medicine
 The Journal of clinical investigation
 International journal of molecular sciences
 Nature reviews. Neurology
 Clinical nursing research
 Radiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Rheumatology (Oxford, England)
 Biochimica et biophysica acta. Molecular basis of disease
 Disability and rehabilitation
 Frontiers in immunology
 Multiple sclerosis and related disorders
 Neurology(R) neuroimmunology & neuroinflammation
 JAMA neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Pharmacotherapy
 Annals of neurology
 The neuroradiology journal
 Orphanet journal of rare diseases
 Health expectations : an international journal of public participation in health care and health policy
 Nutrients
 Journal of integrative neuroscience
 Inflammation research : official journal of the European Histamine Research Society ... [et al.]
 Multiple sclerosis and related disorders
 Scientific reports
 Frontiers in immunology
 Biosensors & bioelectronics
 European journal of medical research
 Tuberkuloz ve toraks
 Microbes and infection
 ACS chemical neuroscience
 Journal of neurology, neurosurgery, and psychiatry
 Nursing open
 PeerJ
 Journal of the European Academy of Dermatology and Venereology : JEADV
 Journal of neurochemistry
 Nutrients
 The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses
 BMC neurology
 Journal of aging and physical activity
 Neurological research
 Multiple sclerosis and related disorders
 Clinical and translational medicine
 Journal of controlled release : official journal of the Controlled Release Society
 Neuroscience bulletin
 CNS drugs
 Methods in molecular biology (Clifton, N.J.)
 Journal of neuroinflammation
 International urogynecology journal
 Journal of comparative effectiveness research
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 European journal of neurology
 European journal of medical research
 International journal of psychophysiology : official journal of the International Organization of Psychophysiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 EBioMedicine
 Journal of neuroinflammation
 Multiple sclerosis and related disorders
 eLife
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology
 Neurology
 FASEB journal : official publication of the Federation of American Societies for Experimental Biology
 International journal of environmental research and public health
 Neurorehabilitation and neural repair
 Journal of neurology, neurosurgery, and psychiatry
 Disability and rehabilitation
 Journal of neurology, neurosurgery, and psychiatry
 JAMA neurology
 Disability and rehabilitation
 Scientific reports
 Journal of Alzheimer's disease : JAD
 Biochemical and biophysical research communications
 Advanced materials (Deerfield Beach, Fla.)
 Journal of neuroengineering and rehabilitation
 Physiotherapy theory and practice
 Journal of biomechanics
 Frontiers in immunology
 Glia
 Journal of molecular medicine (Berlin, Germany)
 Journal of neuroscience research
 International journal of molecular sciences
 Frontiers in immunology
 Frontiers in public health
 Journal of the neurological sciences
 CNS neuroscience & therapeutics
 Journal of neuropathology and experimental neurology
 International journal of molecular sciences
 Frontiers in immunology
 Cells
 AJR. American journal of roentgenology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Acta physiologica (Oxford, England)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Revista de neurologia
 Multiple sclerosis and related disorders
 Journal of the neurological sciences
 Journal of the experimental analysis of behavior
 Multiple sclerosis and related disorders
 Practical neurology
 Journal of neurophysiology
 Genome medicine
 Neurology(R) neuroimmunology & neuroinflammation
 Journal of proteomics
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Clinical pharmacology and therapeutics
 Journal of neurology, neurosurgery, and psychiatry
 Neuropsychological rehabilitation
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurosciences (Riyadh, Saudi Arabia)
 International journal of molecular sciences
 Genes
 Multiple sclerosis and related disorders
 Biomaterials
 Clinical chemistry and laboratory medicine
 Journal of neurologic physical therapy : JNPT
 International immunopharmacology
 Molecular psychiatry
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Med (New York, N.Y.)
 Frontiers in immunology
 Advanced materials (Deerfield Beach, Fla.)
 Molecular neurobiology
 Medicina (Kaunas, Lithuania)
 Cells
 Multiple sclerosis and related disorders
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Disability and rehabilitation
 Frontiers in immunology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 European journal of neurology
 Toxicology and applied pharmacology
 Journal of neurology
 Multiple sclerosis and related disorders
 EBioMedicine
 Frontiers in immunology
 Bioinformatics (Oxford, England)
 Experimental neurology
 Glia
 Clinica chimica acta; international journal of clinical chemistry
 European journal of clinical pharmacology
 Environmental monitoring and assessment
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Disability and rehabilitation
 European journal of immunology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroimmunology
 Journal of immunology (Baltimore, Md. : 1950)
 International journal of environmental research and public health
 CNS & neurological disorders drug targets
 Annals of clinical and translational neurology
 Multiple sclerosis and related disorders
 Rehabilitation psychology
 Sensors (Basel, Switzerland)
 Frontiers in immunology
 Cell death and differentiation
 Journal of neurology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neuroimmunology
 Neurology(R) neuroimmunology & neuroinflammation
 Frontiers in immunology
 Journal of neurology
 European journal of neurology
 Frontiers in immunology
 The European journal of health economics : HEPAC : health economics in prevention and care
 EBioMedicine
 Acta neuropathologica communications
 The patient
 Acta neurologica Belgica
 International journal of molecular sciences
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Orphanet journal of rare diseases
 Brain : a journal of neurology
 Proceedings of the National Academy of Sciences of the United States of America
 Revue neurologique
 Archives of physical medicine and rehabilitation
 Health expectations : an international journal of public participation in health care and health policy
 European journal of physical and rehabilitation medicine
 Glia
 Neurobiology of disease
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Molecular neurobiology
 Frontiers in immunology
 JAMA neurology
 Nature reviews. Microbiology
 Multiple sclerosis and related disorders
 Biomolecules
 Problemy endokrinologii
 Journal of neural transmission (Vienna, Austria : 1996)
 International journal of molecular sciences
 Neurology(R) neuroimmunology & neuroinflammation
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Cells
 Neuroscience letters
 Neurology
 European journal of clinical nutrition
 Cytokine
 The journal of spinal cord medicine
 Neurology(R) neuroimmunology & neuroinflammation
 Glia
 International journal of molecular sciences
 Disability and rehabilitation
 BMJ open
 European radiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurology(R) neuroimmunology & neuroinflammation
 Medicine
 Neurourology and urodynamics
 Molecular neurobiology
 Scientific reports
 Disability and rehabilitation
 Frontiers in immunology
 Neurology(R) neuroimmunology & neuroinflammation
 Journal of medical Internet research
 Acta neuropathologica
 International journal of molecular sciences
 Journal of the neurological sciences
 Journal of autoimmunity
 Chinese journal of integrative medicine
 European journal of pharmacology
 Statistics in medicine
 Scientific reports
 Neurological research
 Advanced science (Weinheim, Baden-Wurttemberg, Germany)
 Biochemical and biophysical research communications
 Seminars in pediatric neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis and related disorders
 Motor control
 Brain : a journal of neurology
 Physical therapy
 Nutrients
 Annals of neurology
 Journal of neuroengineering and rehabilitation
 Scientific reports
 The journal of allergy and clinical immunology. In practice
 Neuropathology and applied neurobiology
 Journal of neurology
 Brain research
 Neurology(R) neuroimmunology & neuroinflammation
 Neurobiology of disease
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Cell death & disease
 Clinical neurology and neurosurgery
 Multiple sclerosis and related disorders
 Journal of neurology
 Multiple sclerosis and related disorders
 Journal of neuroengineering and rehabilitation
 Molecular biology reports
 Journal of medicinal chemistry
 Immunobiology
 Irish journal of medical science
 European journal of neurology
 Proceedings of the National Academy of Sciences of the United States of America
 European journal of physical and rehabilitation medicine
 International journal of molecular sciences
 Science advances
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Archives of physical medicine and rehabilitation
 Disability and rehabilitation. Assistive technology
 Medicine
 International journal of public health
 Journal of neurologic physical therapy : JNPT
 Multiple sclerosis and related disorders
 Journal of autoimmunity
 Multiple sclerosis and related disorders
 Frontiers in immunology
 Nature neuroscience
 Multiple sclerosis and related disorders
 Die Rehabilitation
 Rehabilitation psychology
 Acta neuropathologica
 Multiple sclerosis and related disorders
 IEEE journal of biomedical and health informatics
 PeerJ
 Food & function
 PloS one
 Brain : a journal of neurology
 Multiple sclerosis and related disorders
 Neurology(R) neuroimmunology & neuroinflammation
 The Journal of experimental medicine
 Neurology(R) neuroimmunology & neuroinflammation
 The Journal of pharmacology and experimental therapeutics
 Nature
 Scientific reports
 Neurologia i neurochirurgia polska
 Journal of dental research
 ACS chemical neuroscience
 Turkish journal of medical sciences
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Current opinion in neurology
 American journal of physical medicine & rehabilitation
 International journal of obesity (2005)
 Glia
 Neurology(R) neuroimmunology & neuroinflammation
 International journal of molecular sciences
 Radiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 PloS one
 Revue neurologique
 Multiple sclerosis and related disorders
 Clinical and experimental immunology
 Neurology(R) neuroimmunology & neuroinflammation
 Biochemical pharmacology
 Neurology
 Neurology
 Nature reviews. Neuroscience
 PloS one
 Multiple sclerosis and related disorders
 Pediatric neurology
 Fundamental & clinical pharmacology
 Biochemical and biophysical research communications
 Frontiers in immunology
 Nature metabolism
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of visualized experiments : JoVE
 Frontiers in immunology
 Journal of Korean medical science
 Molecular metabolism
 Neurology(R) neuroimmunology & neuroinflammation
 Toxins
 Multiple sclerosis and related disorders
 Continuum (Minneapolis, Minn.)
 Journal of neurologic physical therapy : JNPT
 Journal of neurology, neurosurgery, and psychiatry
 Laboratory investigation; a journal of technical methods and pathology
 Frontiers in immunology
 Science advances
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Experimental neurology
 Toxins
 PloS one
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis and related disorders
 Journal of clinical nursing
 Cellular immunology
 Scientific reports
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Cells
 Theranostics
 Multiple sclerosis and related disorders
 Revista de neurologia
 Journal of the American Pharmacists Association : JAPhA
 Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova
 Journal of neuroinflammation
 International journal of molecular sciences
 Multiple sclerosis (Houndmills, Basingstoke, England)
 European journal of neurology
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 European journal of neurology
 JAMA neurology
 eLife
 Disability and rehabilitation
 Human genomics
 Microbial pathogenesis
 BMJ open
 Journal of speech, language, and hearing research : JSLHR
 Archives of physical medicine and rehabilitation
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 Autoimmunity reviews
 Neurology India
 Naunyn-Schmiedeberg's archives of pharmacology
 Somatosensory & motor research
 International immunopharmacology
 La Revue de medecine interne
 Science translational medicine
 Journal of neurology
 Journal of nephrology
 Neurology
 Molecular diagnosis & therapy
 European journal of neurology
 Cortex; a journal devoted to the study of the nervous system and behavior
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of integrative neuroscience
 Iranian journal of immunology : IJI
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 PloS one
 Expert review of medical devices
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Sensors (Basel, Switzerland)
 Professional case management
 Turkish journal of medical sciences
 Journal of neurochemistry
 Medical decision making : an international journal of the Society for Medical Decision Making
 European journal of neurology
 Frontiers in immunology
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Neurology(R) neuroimmunology & neuroinflammation
 International journal of molecular sciences
 FASEB journal : official publication of the Federation of American Societies for Experimental Biology
 Autoimmunity reviews
 Journal of neurology
 Cellular and molecular neurobiology
 The Cochrane database of systematic reviews
 Seminars in ultrasound, CT, and MR
 Cells
 Brain and behavior
 Biomolecules
 Acta neuropathologica
 Viruses
 Molecular neurobiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Neurology(R) neuroimmunology & neuroinflammation
 Journal of geriatric physical therapy (2001)
 Neurobiology of disease
 International journal of molecular sciences
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Neurochemistry international
 Multiple sclerosis and related disorders
 The Lancet. Neurology
 Frontiers in immunology
 Seminars in neurology
 Immunity
 Cellular and molecular neurobiology
 The Lancet. Neurology
 European journal of neurology
 Molecular neurobiology
 Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
 Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
 Frontiers in immunology
 Autoimmunity reviews
 International journal of molecular sciences
 Viruses
 Journal of peptide science : an official publication of the European Peptide Society
 Laboratory medicine
 Glia
 Phytomedicine : international journal of phytotherapy and phytopharmacology
 The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
 Drug discovery today
 Proceedings of the Institution of Mechanical Engineers. Part H, Journal of engineering in medicine
 Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
 Journal of autoimmunity
 PloS one
 Acta neuropathologica communications
 Computer methods and programs in biomedicine
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Current molecular medicine
 Neuron
 Multiple sclerosis and related disorders
 Phytomedicine : international journal of phytotherapy and phytopharmacology
 Frontiers in immunology
 ImmunoHorizons
 Neurology(R) neuroimmunology & neuroinflammation
 Journal of neuroinflammation
 Scientific reports
 Glia
 Cells
 Frontiers in immunology
 Neurology(R) neuroimmunology & neuroinflammation
 Neurochemical research
 International journal of molecular sciences
 Neurology(R) neuroimmunology & neuroinflammation
 Annals of neurology
 Nature immunology
 Mucosal immunology
 Experimental neurology
 Arthritis care & research
 Proceedings of the National Academy of Sciences of the United States of America
 Molecular neurobiology
 Drug delivery
 Multiple sclerosis and related disorders
 Cell death & disease
 Journal of immunology (Baltimore, Md. : 1950)
 Nature reviews. Neurology
 Scientific reports
 Neurourology and urodynamics
 Neurology
 European journal of neurology
 Multiple sclerosis and related disorders
 Molecular biology reports
 Journal of virology
 Journal of medical virology
 Current stem cell research & therapy
 Academic radiology
 European journal of pharmacology
 Journal of controlled release : official journal of the Controlled Release Society
 Neurology(R) neuroimmunology & neuroinflammation
 Clinical and experimental immunology
 Journal of immunology (Baltimore, Md. : 1950)
 Multiple sclerosis and related disorders
 Neurology(R) neuroimmunology & neuroinflammation
 Redox biology
 Proceedings of the National Academy of Sciences of the United States of America
 PLoS biology
 Journal of neuroinflammation
 Fluids and barriers of the CNS
 Scientific reports
 AJNR. American journal of neuroradiology
 Brain : a journal of neurology
 JAMA network open
 Neurology
 International journal of molecular sciences
 Immunology
 Journal of neuroimmunology
 Medicina
 Biomolecules
 The Journal of clinical endocrinology and metabolism
 Multiple sclerosis and related disorders
 European journal of neurology
 Journal of neurology
 Journal of autoimmunity
 Multiple sclerosis and related disorders
 Molecules (Basel, Switzerland)
 American journal of therapeutics
 Neurology(R) neuroimmunology & neuroinflammation
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 ACS chemical neuroscience
 Vaccine
 PloS one
 Arquivos de neuro-psiquiatria
 Eye (London, England)
 Neurology(R) neuroimmunology & neuroinflammation
 Brain, behavior, and immunity
 Journal of neurosurgery
 In vivo (Athens, Greece)
 Multiple sclerosis and related disorders
 Cells
 Multiple sclerosis and related disorders
 Glia
 Nature communications
 International immunopharmacology
 Neurology(R) neuroimmunology & neuroinflammation
 International immunopharmacology
 International journal of biological macromolecules
 Multiple sclerosis and related disorders
 Immunology letters
 JAMA neurology
 Brain research bulletin
 Neurology(R) neuroimmunology & neuroinflammation
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Immunity, inflammation and disease
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Neurology(R) neuroimmunology & neuroinflammation
 Nature immunology
 Journal of immunology (Baltimore, Md. : 1950)
 Pediatric neurology
 Science advances
 Frontiers in cellular and infection microbiology
 Multiple sclerosis and related disorders
 European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society
 Immunology and cell biology
 Nature communications
 Journal of immunological methods
 Multiple sclerosis and related disorders
 Journal of immunology (Baltimore, Md. : 1950)
 Neurology(R) neuroimmunology & neuroinflammation
 Nutrients
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 Neurology(R) neuroimmunology & neuroinflammation
 Neurological research
 Cell metabolism
 Frontiers in bioscience (Landmark edition)
 Viruses
 JAMA neurology
 Multiple sclerosis and related disorders
 Biological psychiatry
 Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
 Frontiers in immunology
 Journal of neuroinflammation
 Brain research bulletin
 Molecular neurobiology
 Frontiers in cellular and infection microbiology
 Advanced science (Weinheim, Baden-Wurttemberg, Germany)
 Cureus
 Brain communications
 Frontiers in neurology
 SAGE open medicine
 Brain communications
 Multiple sclerosis journal - experimental, translational and clinical
 Clinical and experimental medicine
 Cardiology in the young
 Neural regeneration research
 Brain communications
 Annals of translational medicine
 Occupational therapy in health care
 Neural regeneration research
 Journal of neurology
 Radiology case reports
 Frontiers in nutrition
 Brain communications
 Brain communications
 Biomedicines
 ACG case reports journal
 American journal of lifestyle medicine
 The International journal of neuroscience
 Current opinion in hematology
 Neural regeneration research
 Multiple sclerosis journal - experimental, translational and clinical
 JAAD case reports
 Ocular immunology and inflammation
 Neural regeneration research
 Frontiers in neurology
 Frontiers in molecular neuroscience
 Brain communications
 Journal of neurology
 Sleep medicine reviews
 Frontiers in digital health
 Practical neurology
 Frontiers in genetics
 Frontiers in neurology
 Brain communications
 Frontiers in neurology
 Journal of clinical medicine
 Brain communications
 Behavioral sciences (Basel, Switzerland)
 Heliyon
 Journal of visualized experiments : JoVE
 Neurology and therapy
 Multiple sclerosis and related disorders
 Digital health
 SAGE open medicine
 Patient preference and adherence
 Clinical case reports
 Brain communications
 Frontiers in neurology
 Frontiers in neurology
 Neurology and therapy
 Multiple sclerosis and related disorders
 Cureus
 Acta neurologica Belgica
 Frontiers in neurology
 Health science reports

 Brain pathology (Zurich, Switzerland)
 Frontiers in neurology
 Adapted physical activity quarterly : APAQ
 Frontiers in neurology
 Cureus
 Journal of clinical medicine
 Frontiers in psychology
 Journal of ophthalmic inflammation and infection
 Immunometabolism (Cobham, Surrey)
 The Neurohospitalist
 Frontiers in molecular neuroscience
 Ear, nose, & throat journal
 Caspian journal of internal medicine

 Neurology and therapy
 Frontiers in neurology
 Brain : a journal of neurology
 Australian occupational therapy journal
 Clinical case reports
 Frontiers in neurology
 Frontiers in genetics
 Frontiers in cellular neuroscience
 Frontiers in genetics
 Acta neurologica Belgica
 Neurology and therapy
 Neural regeneration research
 Assessment
 Epilepsy & behavior reports
 Disability and rehabilitation
 Computational and structural biotechnology journal
 Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
 Neural regeneration research
 Nutritional neuroscience
 International journal of MS care
 Multiple sclerosis journal - experimental, translational and clinical
 The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
 Frontiers in neurology
 Free neuropathology
 Expert review of neurotherapeutics
 International journal of MS care
 Frontiers in neurology
 Journal of neuroimmunology
 Zeitschrift fur Gastroenterologie

 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Cureus
 Frontiers in neurology
 Frontiers in neuroinformatics
 CNS & neurological disorders drug targets
 Frontiers in psychology
 The Journal of clinical investigation
 Neurology and therapy
 Royal Society open science
 Annals of medicine and surgery (2012)
 Frontiers in human neuroscience
 Frontiers in neurology
 British journal of pharmacology
 Ultrasonography (Seoul, Korea)
 Multiple sclerosis journal - experimental, translational and clinical
 Journal of clinical medicine
 The Journal of clinical investigation
 Journal of biomedical physics & engineering
 The Nurse practitioner
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Romanian journal of ophthalmology
 Multiple sclerosis journal - experimental, translational and clinical
 Multiple sclerosis and related disorders
 Archives of biochemistry and biophysics
 Health psychology research
 Cureus
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Cureus
 Neurology and therapy
 Frontiers in neurology
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Medicine international
 Brain communications
 Health science reports
 Brain communications
 Current neuropharmacology
 Acta neurologica Belgica
 Brain communications
 Frontiers in neuroinformatics
 Cureus
 Frontiers in neurology
 Annals of general psychiatry
 BMJ neurology open
 Multiple sclerosis journal - experimental, translational and clinical
 Multiple sclerosis journal - experimental, translational and clinical
 The Lancet regional health. Europe
 Frontiers in neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of speech-language pathology
 Journal of clinical medicine
 Nutritional neuroscience
 Annals of medicine and surgery (2012)
 Noro psikiyatri arsivi
 Multiple sclerosis and related disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Internal medicine (Tokyo, Japan)
 Northern clinics of Istanbul
 Cell transplantation
 Urologia
 Frontiers in human neuroscience
 Neurology and therapy
 International journal of MS care
 Frontiers in neurology
 Frontiers in neurology
 European journal of radiology open
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Clinical & translational immunology
 Frontiers in neurology
 Frontiers in human neuroscience
 Applied neuropsychology. Adult

 Biomedicines
 Degenerative neurological and neuromuscular disease
 Frontiers in neurology
 Free radical biology & medicine
 Journal of clinical medicine
 Frontiers in neurology
 Clinical and experimental immunology
 Network neuroscience (Cambridge, Mass.)
 Journal of palliative medicine
 Disability and rehabilitation
 Revue neurologique
 Expert opinion on drug safety
 Frontiers in neurology
 Brain and neuroscience advances
 Technology and health care : official journal of the European Society for Engineering and Medicine
 Frontiers in cellular neuroscience
 World journal of psychiatry
 Frontiers in molecular neuroscience
 Methods in molecular biology (Clifton, N.J.)
 Frontiers in neuroscience
 Materia socio-medica
 Therapeutic advances in neurological disorders
 Archives of physical medicine and rehabilitation
 International journal of psychiatry in medicine
 Therapeutic advances in neurological disorders
 Brain communications
 European neurology
 Hepatology forum
 Caspian journal of internal medicine
 Caspian journal of internal medicine
 Healthcare (Basel, Switzerland)
 Farmacia hospitalaria : organo oficial de expresion cientifica de la Sociedad Espanola de Farmacia Hospitalaria
 Iranian journal of child neurology
 Network neuroscience (Cambridge, Mass.)
 Disability and rehabilitation
 Revue neurologique
 Farmacia hospitalaria : organo oficial de expresion cientifica de la Sociedad Espanola de Farmacia Hospitalaria
 European radiology
 Multiple sclerosis and related disorders
 Multiple sclerosis journal - experimental, translational and clinical
 Multiple sclerosis and related disorders
 Journal of clinical medicine
 Journal of medical biochemistry
 Pharmaceuticals (Basel, Switzerland)
 Journal of clinical medicine
 Brain : a journal of neurology
 Psychology, health & medicine
 Brain communications
 Bioengineering (Basel, Switzerland)
 Applied neuropsychology. Adult
 Qualitative health research
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 Clinical hematology international
 Journal of neuroimmunology
 Clinical linguistics & phonetics
 Frontiers in molecular neuroscience
 Pharmaceuticals (Basel, Switzerland)
 Brain sciences
 Northern clinics of Istanbul
 Oncology letters
 Soins; la revue de reference infirmiere
 Expert opinion on therapeutic targets
 Frontiers in cellular neuroscience
 Frontiers in neurology
 International journal of MS care
 Annals of palliative medicine
 Metabolites
 International journal of MS care
 Cell journal
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Iranian journal of public health
 Heliyon
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 Applied neuropsychology. Adult
 Journal of neurology
 Oman medical journal
 Communications medicine
 Psychiatrike = Psychiatriki
 Frontiers in physiology
 Healthcare (Basel, Switzerland)
 Frontiers in nutrition
 Brain pathology (Zurich, Switzerland)
 Current neuropharmacology
 Annals of medicine and surgery (2012)
 International journal of MS care
 Journal of neurology
 Journal of clinical medicine
 BMJ neurology open
 Ageing research reviews
 Medicina clinica (English ed.)
 Journal of chemical neuroanatomy
 The Lancet. Neurology
 Trends in neurosciences
 Applied neuropsychology. Adult
 Archives of physical medicine and rehabilitation
 Brain communications
 NeuroImage. Clinical
 Frontiers in neurology
 Multiple sclerosis journal - experimental, translational and clinical
 Disability and rehabilitation
 Journal of neurosciences in rural practice
 Diagnostics (Basel, Switzerland)
 Frontiers in neurology
 Frontiers in neuroscience
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Nutritional neuroscience
 Therapeutic advances in neurological disorders
 Multiple sclerosis and related disorders
 Disability and rehabilitation
 Clinical & translational immunology
 Journal of clinical medicine
 Practical neurology
 Pharmacotherapy
 The Lancet. Neurology
 Clinical neurology and neurosurgery

 Life (Basel, Switzerland)
 Nature
 European radiology
 Archives of physical medicine and rehabilitation
 Postepy psychiatrii neurologii
 Health (London, England : 1997)
 Brain sciences
 Biomedicines
 Encephalitis (Seoul, Korea)
 Sexuality and disability
 Journal of clinical neurology (Seoul, Korea)
 European journal of case reports in internal medicine
 Journal of clinical medicine
 Therapeutic advances in neurological disorders
 Journal of neurology
 Frontiers in medical technology
 International journal of MS care
 Frontiers in pharmacology
 Journal of magnetic resonance imaging : JMRI
 Frontiers in neurology
 The Journal of pharmacology and experimental therapeutics
 IBRO neuroscience reports
 Microorganisms
 Neuropsychological rehabilitation
 Frontiers in neurology
 International journal of MS care
 International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics
 Multiple sclerosis and related disorders
 Neurology and therapy
 CNS & neurological disorders drug targets
 Frontiers in neurology
 Frontiers in neurology
 Journal of the neurological sciences
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of clinical medicine
 Cureus
 Future medicinal chemistry
 Neurodegenerative disease management
 European radiology
 Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
 Practical neurology
 Frontiers in neurology
 Frontiers in immunology
 ChemMedChem
 Journal of autoimmunity
 Multiple sclerosis and related disorders
 Journal of neuroscience research
 Current drug safety
 European journal of immunology
 Journal of medical signals and sensors
 Frontiers in rehabilitation sciences
 IJID regions
 Heliyon
 Clinical & translational immunology
 Journal of the International Neuropsychological Society : JINS
 Cureus
 International journal of MS care
 Frontiers in nutrition
 Journal of clinical medicine
 European journal of microbiology & immunology
 Surgical neurology international
 Frontiers in neuroscience
 Global medical genetics
 Multiple sclerosis and related disorders
 International journal of MS care
 Annals of medicine and surgery (2012)
 Neurology and therapy
 Frontiers in neuroscience
 Pharmaceutics
 Brain sciences
 Frontiers in neurology
 Journal of clinical medicine
 Journal of advanced pharmaceutical technology & research
 Journal of immunoassay & immunochemistry
 Neurology(R) neuroimmunology & neuroinflammation
 Emerging infectious diseases
 Frontiers in neurology
 Cureus
 Journal of neurology, neurosurgery, and psychiatry
 Postepy psychiatrii neurologii
 Disability and rehabilitation
 AIMS neuroscience
 Acta neurologica Belgica
 Clinical and experimental medicine
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Frontiers in neurology
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Current neuropharmacology
 Multiple sclerosis and related disorders
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Frontiers in computational neuroscience
 Frontiers in neurology
 Frontiers in aging neuroscience
 Neurologia i neurochirurgia polska
 International journal of MS care
 Pharmaceutics
 Biomedicines
 International journal of MS care
 Brain sciences
 Antioxidants (Basel, Switzerland)
 Multiple sclerosis and related disorders
 Micromachines
 Physiotherapy theory and practice
 Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
 International journal of MS care
 Frontiers in psychology
 Cureus
 Frontiers in neurology
 Chronic diseases and translational medicine
 Journal of clinical medicine
 Current issues in molecular biology
 Neurodegenerative disease management
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Frontiers in neuroscience
 Cureus
 Cureus
 Journal of education and health promotion
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Children (Basel, Switzerland)
 International journal of molecular sciences
 Neurology
 Journal of physiotherapy
 Progress in molecular biology and translational science
 Health promotion journal of Australia : official journal of Australian Association of Health Promotion Professionals
 Frontiers in cellular neuroscience
 International journal of MS care
 Current medical research and opinion
 Journal of clinical medicine
 Journal of clinical medicine
 Multiple sclerosis journal - experimental, translational and clinical
 Healthcare (Basel, Switzerland)
 Frontiers in psychology
 Neural regeneration research
 Clinical proteomics
 Multiple sclerosis journal - experimental, translational and clinical
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of MS care
 Multiple sclerosis and related disorders
 Basic and clinical neuroscience
 Journal of cardiovascular development and disease
 Frontiers in neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Immunological investigations
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Journal of neuroimmunology
 Journal of geriatric physical therapy (2001)
 Frontiers in neuroscience
 Frontiers in neural circuits
 Archives of public health = Archives belges de sante publique
 Journal of neuroimmunology
 Brain communications
 Frontiers in neurology
 Neurology and therapy
 Clinical neurology and neurosurgery
 Insights into imaging
 Nursing open
 Journal of neurology
 Disability and rehabilitation
 Disability and rehabilitation
 Therapeutic advances in neurological disorders
 Journal of clinical medicine
 Frontiers in neurology
 Expert review of pharmacoeconomics & outcomes research
 Immunologic research
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Neuroradiology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Healthcare (Basel, Switzerland)
 Diagnostics (Basel, Switzerland)
 International journal of MS care
 Journal of imaging
 Advanced pharmaceutical bulletin
 Frontiers in neuroscience
 International journal of surgery case reports
 Multiple sclerosis journal - experimental, translational and clinical
 Turkish journal of physical medicine and rehabilitation
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Journal of neurology
 Frontiers in neurology
 Journal of neurogastroenterology and motility
 Neuro-ophthalmology (Aeolus Press)
 Canadian Association of Radiologists journal = Journal l'Association canadienne des radiologistes
 Clinical & translational immunology
 Noro psikiyatri arsivi
 Annals of clinical biochemistry
 Frontiers in neurology
 Balkan journal of medical genetics : BJMG
 Frontiers in neurology
 Neurology and therapy
 Frontiers in psychology
 Frontiers in neurology
 Journal of clinical medicine
 Therapeutic advances in neurological disorders
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Brain & NeuroRehabilitation
 NeuroImage. Clinical
 Frontiers in cellular neuroscience
 International journal of MS care
 Healthcare (Basel, Switzerland)
 Non-coding RNA research
 Sleep & breathing = Schlaf & Atmung
 Applied neuropsychology. Adult
 Clinical neurology and neurosurgery
 Frontiers in neurology
 Telemedicine journal and e-health : the official journal of the American Telemedicine Association
 Diagnostics (Basel, Switzerland)
 Frontiers in neurology
 International journal of MS care
 NMR in biomedicine
 Frontiers in physiology
 Der Nervenarzt
 Neurology and therapy
 Frontiers in molecular neuroscience
 Clinical neurology and neurosurgery
 Neurology and therapy
 Frontiers in neurology
 Multiple sclerosis journal - experimental, translational and clinical
 Canadian journal of ophthalmology. Journal canadien d'ophtalmologie
 International journal of women's health
 Brain sciences
 Multiple sclerosis and related disorders
 Clinical epidemiology
 Frontiers in molecular neuroscience
 Heliyon
 Neural regeneration research
 Multiple sclerosis and related disorders
 Neurologia i neurochirurgia polska
 Frontiers in neuroscience
 Journal of health psychology
 Clinical & translational immunology
 Frontiers in molecular neuroscience
 Journal of Ayurveda and integrative medicine
 Health (London, England : 1997)
 Therapeutic advances in drug safety
 Disability and rehabilitation
 Journal of neuroimmunology
 Multiple sclerosis journal - experimental, translational and clinical
 Revue neurologique
 Biostatistics (Oxford, England)
 Frontiers in neurology
 Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy
 Clinical case reports
 Frontiers in cell and developmental biology
 Advances in radiation oncology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Nature reviews. Neurology
 Neural regeneration research
 Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
 Journal of neurology, neurosurgery, and psychiatry
 Brain sciences
 Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
 Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology
 Acta neurologica Belgica
 Journal of neurology, neurosurgery, and psychiatry
 iScience
 Neuro endocrinology letters
 Life (Basel, Switzerland)
 Folia phoniatrica et logopaedica : official organ of the International Association of Logopedics and Phoniatrics (IALP)
 Seminars in neurology
 Frontiers in molecular neuroscience
 Journal of patient experience
 Journal of clinical medicine
 Rehabilitation psychology
 Medicine international
 Exploratory research in clinical and social pharmacy
 Neurology
 Biomolecules & biomedicine
 Acta neurologica Belgica
 Disability and rehabilitation
 Journal of the neurological sciences
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Neural regeneration research
 Therapeutic advances in neurological disorders
 Health science reports
 European journal of neurology
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Postepy psychiatrii neurologii
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Biomedicines
 Journal of clinical medicine
 Current neuropharmacology
 Expert review of clinical immunology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology
 Multiple sclerosis and related disorders
 Exploratory research in clinical and social pharmacy
 Biomedicines
 Multiple sclerosis and related disorders
 Movement disorders clinical practice
 Multiple sclerosis journal - experimental, translational and clinical
 Frontiers in neuroinformatics
 BMC nursing
 Frontiers in neuroscience
 Frontiers in neurology
 Frontiers in digital health
 Iranian journal of child neurology
 International journal of MS care
 Journal of clinical medicine
 Clinical neurology and neurosurgery
 Neurologia
 Methods in molecular biology (Clifton, N.J.)
 Clinical immunology (Orlando, Fla.)
 Neurological research
 Contemporary clinical trials
 Human brain mapping
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Viral immunology
 Medicinal research reviews
 Annals of Indian Academy of Neurology
 International journal of MS care
 Neurology and therapy
 Frontiers in cellular neuroscience
 Multiple sclerosis (Houndmills, Basingstoke, England)
 JGH open : an open access journal of gastroenterology and hepatology
 Expert review of neurotherapeutics
 Frontiers in neurology
 Nanomedicine : nanotechnology, biology, and medicine
 European journal of neurology
 Acta neurologica Belgica
 Acta ophthalmologica
 Therapeutic advances in urology
 Life (Basel, Switzerland)
 Diagnostics (Basel, Switzerland)
 Frontiers in neurology
 Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine
 Integrative medicine reports
 Frontiers in neuroscience
 Multiple sclerosis journal - experimental, translational and clinical
 NMR in biomedicine
 Neurobiology of disease
 Neurology and therapy
 Iranian journal of parasitology
 Journal of neurologic physical therapy : JNPT
 Caspian journal of internal medicine
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Nutrition and health
 Hong Kong medical journal = Xianggang yi xue za zhi
 Journal of neurology
 Neurology
 Frontiers in neurology
 Biomedicines
 International journal of molecular sciences
 Frontiers in neurology
 Journal of neurology, neurosurgery, and psychiatry
 Frontiers in neurology
 Biomolecules
 Diagnostic and interventional imaging
 International journal of biological sciences
 Journal of neurochemistry
 Multiple sclerosis and related disorders
 Regenerative medicine
 Multiple sclerosis and related disorders
 Journal of neurology
 BJR case reports
 Journal of neuropathology and experimental neurology
 EClinicalMedicine
 European radiology
 Frontiers in neuroscience
 Frontiers in pharmacology
 Current medicinal chemistry
 eNeurologicalSci
 Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina)
 Frontiers in neuroscience
 Frontiers in immunology
 European radiology
 Journal of magnetic resonance imaging : JMRI
 Frontiers in physiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Frontiers in immunology
 Immunological investigations
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Multiple sclerosis and related disorders
 European journal of neurology
 American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
 Journal of neuroimmunology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Multiple sclerosis journal - experimental, translational and clinical
 Neurology and therapy
 Frontiers in medicine
 International journal of MS care
 Current research in translational medicine
 International journal of MS care
 Neurologia
 Multiple sclerosis and related disorders
 International ophthalmology
 Neuroscience bulletin
 Acta neurologica Belgica
 Ophthalmology science
 Frontiers in cardiovascular medicine
 Frontiers in neurology
 The Clinical neuropsychologist
 Multiple sclerosis and related disorders
 Journal of clinical medicine
 Neurochemical research
 Therapeutic advances in neurological disorders
 Multiple sclerosis journal - experimental, translational and clinical
 Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists
 International medical case reports journal
 Acta radiologica (Stockholm, Sweden : 1987)
 Journal of clinical medicine
 The neuroradiology journal
 Photodiagnosis and photodynamic therapy
 Multiple sclerosis and related disorders
 Neuropathology and applied neurobiology
 Journal of neurology, neurosurgery, and psychiatry
 Journal of neurology
 Frontiers in neurology
 Multiple sclerosis and related disorders
 Molecular biology reports
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Disability and rehabilitation
 Acta neurologica Belgica
 Brain sciences
 Cell journal
 Brain sciences
 Frontiers in neurology
 Medical journal of the Islamic Republic of Iran
 Frontiers in neuroscience
 Biomedicines
 Journal of neuroradiology = Journal de neuroradiologie
 Climacteric : the journal of the International Menopause Society
 Frontiers in nutrition
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Therapeutic advances in neurological disorders
 Frontiers in neurology
 Journal of clinical medicine
 Journal of neurology, neurosurgery, and psychiatry
 Frontiers in neurology
 Therapeutic advances in neurological disorders
 Molecular therapy. Methods & clinical development
 Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological Society
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Frontiers in neurology
 Archives of physical medicine and rehabilitation
 Frontiers in neuroscience
 Journal of the Academy of Consultation-Liaison Psychiatry
 Journal of magnetic resonance imaging : JMRI
 The Journal of urology
 Multiple sclerosis and related disorders
 Frontiers in neurology
 European radiology
 Diagnostics (Basel, Switzerland)
 Frontiers in pharmacology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Infection and drug resistance
 Journal of neuroimmunology
 Frontiers in immunology
 Biochimica et biophysica acta. Molecular basis of disease
 Medicinal research reviews
 Cells
 Frontiers in immunology
 Actas dermo-sifiliograficas
 medRxiv : the preprint server for health sciences
 Journal of pharmaceutical sciences
 Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society
 Frontiers in immunology
 Handbook of clinical neurology
 Multiple sclerosis journal - experimental, translational and clinical
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Frontiers in neurology
 BMC neurology
 Neural regeneration research
 Neurology
 Journal of neurology
 Biological research for nursing
 Journal of neurology, neurosurgery, and psychiatry
 Journal of neurology, neurosurgery, and psychiatry
 European journal of neurology
 Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
 Neurology and therapy

 Cellular and molecular neurobiology
 Frontiers in neurology
 Noro psikiyatri arsivi
 Journal of neurology, neurosurgery, and psychiatry
 Neurology and therapy
 International immunopharmacology
 Journal of neurology, neurosurgery, and psychiatry
 Heliyon
 Journal of clinical neurology (Seoul, Korea)
 Journal of neurology
 European journal of neurology
 Life (Basel, Switzerland)
 Bioengineering (Basel, Switzerland)
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Quantitative imaging in medicine and surgery
 ClinicoEconomics and outcomes research : CEOR
 Frontiers in neuroscience
 Multiple sclerosis journal - experimental, translational and clinical
 CNS drugs
 Journal of clinical medicine
 Health science reports
 Multiple sclerosis and related disorders
 Journal of central nervous system disease
 Current neuropharmacology
 Degenerative neurological and neuromuscular disease
 Journal of clinical medicine
 Biomedicines
 Vaccines
 Frontiers in nutrition
 Neurology and therapy
 Journal of clinical medicine
 Human brain mapping
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Biomedicines
 Pharmacoepidemiology and drug safety
 Multiple sclerosis and related disorders
 Brain sciences
 Neurology and therapy
 Frontiers in neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Disability and rehabilitation. Assistive technology
 Neurology and therapy
 Neurology and therapy
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Multiple sclerosis journal - experimental, translational and clinical
 CNS & neurological disorders drug targets
 The Lancet. Neurology
 Acta neurologica Belgica
 The Egyptian journal of neurology, psychiatry and neurosurgery
 Multiple sclerosis (Houndmills, Basingstoke, England)
 IBRO neuroscience reports
 Frontiers in cellular neuroscience
 Neurology and therapy
 Brain research bulletin
 Biomedicines
 Ideggyogyaszati szemle
 Journal of neuroimmunology
 Cell reports
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Frontiers in neuroscience
 CNS & neurological disorders drug targets
 Autoimmunity reviews
 Multiple sclerosis journal - experimental, translational and clinical
 Clinical and experimental immunology
 Multiple sclerosis and related disorders
 Revue neurologique
 The Journal of biological chemistry
 Viruses
 International journal of surgery case reports
 Indian journal of ophthalmology
 iScience
 Cureus
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Journal of neuroinflammation
 Journal of neurology
 International journal of molecular sciences
 Cells
 Archives of physical medicine and rehabilitation
 Journal of neuroinflammation
 Molecular neurobiology
 Explore (New York, N.Y.)
 International ophthalmology
 Neurology and therapy
 Frontiers in bioengineering and biotechnology
 Journal of biochemical and molecular toxicology
 Journal of neurology, neurosurgery, and psychiatry
 IEEE transactions on medical imaging
 Advances in experimental medicine and biology
 Journal of neurology
 BMC neurology
 Research square
 Aging and disease
 Frontiers in immunology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Frontiers in neuroscience
 Multiple sclerosis and related disorders
 Der Nervenarzt
 Cellular & molecular immunology
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Neuro-ophthalmology (Aeolus Press)

 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 International journal of molecular sciences
 Journal of neurology, neurosurgery, and psychiatry
 Cureus
 Frontiers in molecular neuroscience
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Revue neurologique
 iScience
 Multiple sclerosis and related disorders
 Disability and rehabilitation
 Neurologia i neurochirurgia polska
 Journal of integrative and complementary medicine
 Pathophysiology : the official journal of the International Society for Pathophysiology
 Neurology and therapy
 Journal of neuroimmunology
 Frontiers in neurology
 Brain sciences
 Multiple sclerosis and related disorders
 Frontiers in neurology
 International journal of environmental research and public health
 Pilot and feasibility studies
 Complementary therapies in medicine
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Neurology and therapy
 Cureus
 Urologia
 Mini reviews in medicinal chemistry

 Complementary therapies in clinical practice
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis and related disorders
 Neurology and therapy
 Diagnostics (Basel, Switzerland)
 Healthcare (Basel, Switzerland)
 Frontiers in neuroscience
 Journal of personalized medicine
 Frontiers in neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Journal of clinical medicine
 Multiple sclerosis and related disorders
 Frontiers in cellular neuroscience
 Current neuropharmacology
 Cureus
 Research square
 Health care for women international
 Ophthalmic surgery, lasers & imaging retina
 Frontiers in immunology
 Medicine and science in sports and exercise
 Maedica
 Biomedical optics express
 NeuroImage. Clinical
 Pharmaceuticals (Basel, Switzerland)
 PharmacoEconomics - open
 Multiple sclerosis and related disorders
 JAMA neurology
 Multiple sclerosis journal - experimental, translational and clinical
 Multiple sclerosis journal - experimental, translational and clinical
 Neuron
 Journal of chromatographic science
 European journal of neurology
 Journal of neurology
 Acta biochimica et biophysica Sinica
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 BJUI compass
 International journal of molecular sciences
 Cell reports
 Multiple sclerosis journal - experimental, translational and clinical
 European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Drugs in R&D
 Molecular neurobiology
 Glia
 Multiple sclerosis journal - experimental, translational and clinical
 Journal of neuropsychology
 Frontiers in cellular neuroscience
 Frontiers in molecular biosciences
 Neurochemical research
 Viruses
 ClinicoEconomics and outcomes research : CEOR
 Clinical case reports
 Digital health
 BMC neurology
 Biomedicines
 International journal of MS care
 Acta bio-medica : Atenei Parmensis
 BMJ case reports
 Multiple sclerosis and related disorders
 ACS medicinal chemistry letters
 Annals of hematology
 Ear, nose, & throat journal
 Experimental & molecular medicine
 Harvard review of psychiatry
 Clinical & translational immunology
 Journal of neurology, neurosurgery, and psychiatry
 JAMA neurology
 Brain sciences
 European radiology
 Journal of health economics and outcomes research
 Frontiers in psychiatry
 Multiple sclerosis and related disorders
 Applied neuropsychology. Adult
 Multiple sclerosis and related disorders
 PM & R : the journal of injury, function, and rehabilitation
 International journal of MS care
 Cureus
 Multiple sclerosis and related disorders
 Multiple sclerosis and related disorders
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Journal of magnetic resonance imaging : JMRI
 Journal of clinical medicine
 Degenerative neurological and neuromuscular disease
 Patient preference and adherence
 Basic & clinical pharmacology & toxicology
 Journal of clinical psychology in medical settings
 Journal of neurology
 Current neurology and neuroscience reports
 eNeurologicalSci
 Journal of neurology
 Experimental brain research
 Mayo Clinic proceedings
 Studies in health technology and informatics
 Journal of the neurological sciences
 bioRxiv : the preprint server for biology
 Neurology. Clinical practice
 Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society
 Phytomedicine : international journal of phytotherapy and phytopharmacology
 RoFo : Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin
 The journal of pain
 Glia
 Molecular immunology
 Vaccines
 Iranian journal of psychiatry
 Current stem cell research & therapy
 Gut and liver
 Nanomedicine : nanotechnology, biology, and medicine
 CNS drugs
 Radiologie (Heidelberg, Germany)
 Journal of investigative medicine high impact case reports
 International journal of MS care
 Medicine
 American journal of physical medicine & rehabilitation
 Frontiers in neurology
 Annals of the New York Academy of Sciences
 Inflammopharmacology
 Acta neuropathologica communications
 International immunopharmacology
 Journal of autoimmunity
 Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
 Journal of clinical medicine
 Journal of biomedical science
 Multiple sclerosis and related disorders
 Journal of clinical medicine
 Biomedicines
 Frontiers in neuroscience
 Brain communications
 Journal of clinical medicine
 Experimental dermatology
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Explore (New York, N.Y.)

 International journal of retina and vitreous
 Journal of autoimmunity
 Multiple sclerosis and related disorders
 Frontiers in neurology
 Cureus
 Neural regeneration research
 Archives of medical research
 Urologie (Heidelberg, Germany)
 Journal of neuroimmunology
 Journal of neuroimmunology

 Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999)
 Frontiers in neuroscience
 Multiple sclerosis journal - experimental, translational and clinical
 Rehabilitation psychology
 Cell biochemistry and function
 Scientific reports
 Journal of immunological methods
 Neuropsychology
 IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society
 bioRxiv : the preprint server for biology
 The journal of pain
 American journal of physical medicine & rehabilitation
 Neuropsychology
 Preventive medicine
 medRxiv : the preprint server for health sciences
 bioRxiv : the preprint server for biology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 International journal of MS care
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 Multiple sclerosis international
 Life (Basel, Switzerland)
 Multiple sclerosis and related disorders
 Journal of neurology
 Pediatric neurology
 Journal of magnetic resonance imaging : JMRI
 Biology
 Experimental and therapeutic medicine
 Therapeutic advances in neurological disorders
 Frontiers in neuroscience
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 International journal of MS care
 PLOS digital health
 Neurology. Clinical practice
 Neurology and therapy
 Neurology and therapy
 Therapeutic advances in neurological disorders
 Journal of magnetic resonance imaging : JMRI
 EBioMedicine
 Frontiers in neurology
 CNS & neurological disorders drug targets
 Heliyon
 Proceedings of the National Academy of Sciences of the United States of America
 Journal of the neurological sciences
 International journal of MS care
 Biomedical optics express
 Neuropsychology review
 Neurology and therapy
 Biomedicines
 Archivum immunologiae et therapiae experimentalis
 Antioxidants & redox signaling
 Archives of physical medicine and rehabilitation
 Glia
 Frontiers in immunology
 Biomedicines
 Frontiers in neurology
 Multiple sclerosis and related disorders
 Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco
 Neurology


 Vision (Basel, Switzerland)
 Multiple sclerosis and related disorders
 Archivos de bronconeumologia
 Communications medicine
 Therapeutic advances in chronic disease
 Multiple sclerosis journal - experimental, translational and clinical
 Brain communications
 Digital health
 Multiple sclerosis and related disorders
 Vaccines
 Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience
 Trends in immunology
 Journal of neurology, neurosurgery, and psychiatry
 Neural regeneration research

 Journal of neurology
 Soins; la revue de reference infirmiere
 Therapeutic advances in neurological disorders
 Immunity
 Frontiers in bioscience (Landmark edition)
 JAMA neurology
 Clinical chemistry and laboratory medicine
 medRxiv : the preprint server for health sciences
 Diagnostics (Basel, Switzerland)
 Frontiers in immunology
 Multiple sclerosis international
 Multiple sclerosis and related disorders
 Behavioral sleep medicine
 Food & function
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Annals of neurology
 Multiple sclerosis and related disorders
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 European journal of immunology

 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Current research in food science
 International immunopharmacology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Cannabis and cannabinoid research
 Acta neuropathologica
 Stem cell reports
 Magnetic resonance in medicine
 Frontiers in medicine
 Cell reports
 Current Alzheimer research
 Archives of dermatological research
 Inflammation
 Archives of physical medicine and rehabilitation
 Frontiers in public health
 Journal of affective disorders
 Cells
 Archivos de la Sociedad Espanola de Oftalmologia
 Noro psikiyatri arsivi
 Multiple sclerosis and related disorders
 Frontiers in sports and active living
 Frontiers in neuroscience
 Animal cells and systems
 Neurological research and practice




 Current molecular medicine
 Frontiers in immunology
 Multiple sclerosis and related disorders
 Brain : a journal of neurology
 Journal of magnetic resonance imaging : JMRI
 Journal of clinical neurology (Seoul, Korea)
 World neurosurgery
 Life (Basel, Switzerland)
 Journal of neurology, neurosurgery, and psychiatry
 Biomedicines
 Molecules (Basel, Switzerland)
 Pharmaceuticals (Basel, Switzerland)
 Journal of clinical medicine
 Cells
 International journal of molecular sciences
 Neurology
 Therapeutic innovation & regulatory science
 Multiple sclerosis and related disorders
 Pharmaceutics
 Current issues in molecular biology
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 PM & R : the journal of injury, function, and rehabilitation
 Multiple sclerosis (Houndmills, Basingstoke, England)
 American journal of audiology
 Journal of neurologic physical therapy : JNPT
 Radiography (London, England : 1995)
 Frontiers in cellular neuroscience
 bioRxiv : the preprint server for biology
 Annals of neurology
 Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
 Journal of molecular graphics & modelling
 Multiple sclerosis journal - experimental, translational and clinical
 Journal of neurologic physical therapy : JNPT
 medRxiv : the preprint server for health sciences
 Patient preference and adherence
 Seminars in neurology
 Integrative medicine research
 Recent patents on anti-cancer drug discovery
 Nature reviews. Immunology
 BMC neurology
 Biomedicines
 Frontiers in immunology
 International journal of molecular sciences
 Frontiers in neuroscience
 Handbook of clinical neurology
 Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan
 Current stem cell research & therapy
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 eNeurologicalSci
 British journal of nursing (Mark Allen Publishing)
 Neurology and therapy

 ArXiv
 Experimental and therapeutic medicine
 Molecular psychiatry

 Journal of binocular vision and ocular motility

 Seminars in pediatric neurology
 Brain and nerve = Shinkei kenkyu no shinpo

 medRxiv : the preprint server for health sciences
 Neuropsychological rehabilitation
 Frontiers in behavioral neuroscience
 Brain sciences

 Biomedical journal
 BMC neurology
 International journal of molecular sciences
 NeuroImage. Clinical
 Journal of neuroinflammation
 Journal of the neurological sciences
 International immunopharmacology
 Clinical neurology and neurosurgery
 Journal of Alzheimer's disease : JAD
 International journal of molecular sciences
 European radiology
 Biomedicines
 Cells
 Multiple sclerosis and related disorders
 International immunopharmacology
 Handbook of clinical neurology
 Frontiers in immunology
 Clinical nuclear medicine

 Journal of clinical medicine
 Journal of the American Geriatrics Society
 Antioxidants (Basel, Switzerland)
 Annals of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Clinical neurology and neurosurgery
 Gut
 Journal of neurology, neurosurgery, and psychiatry
 Multiple sclerosis and related disorders
 Frontiers in integrative neuroscience
 Research square
 Frontiers in genetics
 Biotechnology progress
 Nature chemistry
 Molecular neurobiology
 The Medical clinics of North America
 Cureus
 Archives of physical medicine and rehabilitation
 Revue medicale suisse
 Frontiers in medicine
 Encephalitis (Seoul, Korea)
 Cancers
 Research square

 Annals of the New York Academy of Sciences
 Current problems in diagnostic radiology
 Frontiers in chemistry


 International journal of molecular sciences
 Sensors (Basel, Switzerland)
 Viruses
 Recent advances in anti-infective drug discovery
 Molecular neurobiology
 Photodiagnosis and photodynamic therapy
 European journal of immunology
 Ageing research reviews
 Pharmaceutics
 Cells
 Expert opinion on drug safety
 International immunopharmacology
 Frontiers in immunology
 Patient preference and adherence
 Multiple sclerosis and related disorders
 European journal of translational myology
 Biochimica et biophysica acta. Molecular cell research
 Vaccines
 International journal of molecular sciences
 Cellular & molecular immunology
 NMR in biomedicine
 Annals of neurology
 Life sciences
 Progress in neurobiology
 Human genetics
 Neuroimmunomodulation
 IEEE journal of biomedical and health informatics
 Journal of neurology
 Mini reviews in medicinal chemistry
 Biomedicines
 Brain, behavior, and immunity
 PLOS digital health
 Nature neuroscience
 Annals of clinical and translational neurology
 Brain sciences
 Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
 Journal of neurosurgical sciences
 Physiotherapy theory and practice
 Der Nervenarzt
 Journal of virology
 Journal of speech, language, and hearing research : JSLHR
 Frontiers in immunology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 The Neurohospitalist
 Metabolic brain disease
 Frontiers in cellular neuroscience
 Neurology and therapy
 JCI insight
 Journal of neurology, neurosurgery, and psychiatry
 Radiologia
 SLAS discovery : advancing life sciences R & D
 Cureus
 Cureus
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 iScience

 Current molecular medicine
 Journal of neurosciences in rural practice
 Multiple sclerosis and related disorders
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Annals of palliative medicine

 Neurology
 Proceedings of the National Academy of Sciences of the United States of America

 Brain, behavior, and immunity
 BMJ open
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Health and quality of life outcomes
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 Biology
 Diagnostics (Basel, Switzerland)
 Multiple sclerosis journal - experimental, translational and clinical
 Cells
 Arthroplasty today
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Expert opinion on biological therapy
 Soins; la revue de reference infirmiere
 Multiple sclerosis and related disorders
 Journal of medical virology
 Cellular and molecular neurobiology
 The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
 Applied microbiology and biotechnology
 Neuroscience
 Journal of neurology
 Clinical neurology and neurosurgery
 Journal of computational and graphical statistics : a joint publication of American Statistical Association, Institute of Mathematical Statistics, Interface Foundation of North America
 Journal of neurology, neurosurgery, and psychiatry
 Pharmacological reports : PR
 Metabolic brain disease
 Biomolecules
 Journal of chemical neuroanatomy
 Advances in immunology
 Molecular neurobiology
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Clinical chemistry and laboratory medicine
 Neuroendocrinology
 Therapeutic advances in neurological disorders
 Immunology letters
 BMJ case reports
 Clinical immunology (Orlando, Fla.)
 Current neurology and neuroscience reports
 Frontiers in cell and developmental biology
 SAGE open medical case reports
 iScience
 Drug discovery today
 Journal of neurology
 bioRxiv : the preprint server for biology
 International immunopharmacology
 Journal of neurology
 Revue medicale suisse
 Frontiers in cellular neuroscience
 Neurology
 Methods in molecular biology (Clifton, N.J.)
 Anti-cancer agents in medicinal chemistry
 Molecular neurobiology
 Current medicinal chemistry
 bioRxiv : the preprint server for biology
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Computerized medical imaging and graphics : the official journal of the Computerized Medical Imaging Society
 Multiple sclerosis and related disorders
 BMC neurology
 Molecular neurobiology
 Nature communications
 Bioactive materials
 European journal of pharmacology
 Neurologia
 Journal of medical Internet research
 NeuroImage
 Clinical case reports
 Aging and disease
 Neurological research
 Pathology, research and practice
 Neural regeneration research
 The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale
 Neuromolecular medicine
 Advanced science (Weinheim, Baden-Wurttemberg, Germany)
 BMC genomic data
 Clinical neurology and neurosurgery
 Neurology
 Frontiers in neurology
 Frontiers in psychology
 Progress in molecular biology and translational science
 Molecular therapy. Nucleic acids
 Frontiers in cellular neuroscience
 British journal of pharmacology
 Immunology letters
 Frontiers in neuroscience
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Proceedings of the National Academy of Sciences of the United States of America
 Cureus
 Frontiers in immunology
 Experimental and clinical psychopharmacology
 bioRxiv : the preprint server for biology
 Biomedicines
 Otolaryngologia polska = The Polish otolaryngology
 Frontiers in medicine
 The neuroradiology journal

 European journal of medicinal chemistry
 iScience
 Neurochemical research
 European journal of nutrition
 Clinical neurology and neurosurgery
 Journal of cellular and molecular medicine
 Cureus
 FEBS letters
 bioRxiv : the preprint server for biology
 Frontiers in neurology
 Scandinavian journal of public health
 EClinicalMedicine
 CNS drugs
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 Journal of neurology
 Journal of neurochemistry
 International journal of molecular sciences
 Research square
 Pharmacology & therapeutics
 Glia
 Immunology and cell biology
 Multiple sclerosis and related disorders
 Current medical research and opinion
 Investigative radiology
 Clinical nutrition (Edinburgh, Scotland)
 Journal of dietary supplements
 Biomedicines
 Neurology
 Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
 Radiology case reports
 Parkinsonism & related disorders
 Handbook of clinical neurology
 ACS omega
 The American journal of pathology
 Food & function
 NPJ digital medicine
 bioRxiv : the preprint server for biology



 Basic and clinical neuroscience
 Journal of neurology
 Antibodies (Basel, Switzerland)

 Journal of fluorescence
 Expert opinion on biological therapy
 Frontiers in pharmacology
 Case reports in rheumatology
 Neuroscience bulletin
 Stroke and vascular neurology
 Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]
 Methods in molecular biology (Clifton, N.J.)
 Case reports in women's health
 Journal of neurosurgery. Case lessons
 Frontiers in immunology
 bioRxiv : the preprint server for biology
 Cureus
 Frontiers in rehabilitation sciences
 Journal of neuroimmunology
 Vaccines
 Biology
 Multiple sclerosis and related disorders
 Nature reviews. Rheumatology
 Aging and disease
 Evidence-based complementary and alternative medicine : eCAM
 Spine
 Journal of King Saud University. Science
 Journal of physiology and biochemistry
 Clinical rehabilitation
 Multiple sclerosis and related disorders
 International journal of molecular sciences
 British medical bulletin
 Annals of neurology
 PloS one
 International journal of molecular sciences
 Autoimmunity reviews

 Critical reviews in microbiology
 Journal of ethnopharmacology
 Frontiers in neuroscience
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Journal of neurology, neurosurgery, and psychiatry
 JAMA neurology
 Neural regeneration research
 Journal of neurochemistry
 Heliyon
 Nutrients
 FASEB journal : official publication of the Federation of American Societies for Experimental Biology
 Sleep
 Autoimmunity reviews
 Expert opinion on therapeutic targets
 International journal of molecular sciences
 Pediatric neurology
 Journal of religion and health
 Aging clinical and experimental research
 Research in psychotherapy (Milano)
 The neuroradiology journal
 Current medicinal chemistry
 Neurology and therapy
 Integrative cancer therapies
 European journal of internal medicine

 Current pharmaceutical biotechnology
 Cellular & molecular immunology
 Xenobiotica; the fate of foreign compounds in biological systems
 Experimental and therapeutic medicine
 Journal of clinical medicine
 Archiv der Pharmazie
 AAPS open
 Pharmacology & therapeutics
 Annals of biomedical engineering
 Frontiers in medicine
 Cureus
 Life (Basel, Switzerland)
 Frontiers in cellular neuroscience
 Neuromolecular medicine
 SN comprehensive clinical medicine
 Frontiers in immunology
 Frontiers in neuroscience
 International journal of molecular sciences
 Multiple sclerosis and related disorders
 International journal of molecular sciences
 Journal of medicine and life
 Neural regeneration research
 Multiple sclerosis and related disorders
 International journal of molecular sciences
 Acta ophthalmologica
 International journal of molecular sciences
 Sleep medicine reviews
 Biochemical pharmacology
 Ageing research reviews
 Diseases (Basel, Switzerland)
 World journal of gastroenterology
 medRxiv : the preprint server for health sciences
 Clinical and experimental dermatology
 Journal of the American Society of Nephrology : JASN
 Therapeutic advances in neurological disorders
 Brain : a journal of neurology
 Nanoscale advances
 CNS drugs
 Frontiers in rehabilitation sciences

 Journal of immunology research
 Frontiers in immunology
 Biochemical pharmacology
 Substance abuse : research and treatment
 Frontiers in immunology
 Eye (London, England)
 Frontiers in rehabilitation sciences
 European journal of medicinal chemistry
 The lancet. Gastroenterology & hepatology
 Current opinion in ophthalmology
 Sensors (Basel, Switzerland)
 Frontiers in neuroscience
 Seminars in neurology
 bioRxiv : the preprint server for biology
 Current topics in medicinal chemistry
 Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy
 Multiple sclerosis and related disorders
 Perspectives in clinical research
 Current neurology and neuroscience reports
 International immunopharmacology
 Frontiers in neuroscience
 American journal of lifestyle medicine
 Bioengineering (Basel, Switzerland)
 International immunopharmacology
 Cellular and molecular neurobiology
 European journal of immunology
 PharmacoEconomics
 Scandinavian journal of public health
 Archives of medical science : AMS
 International journal of molecular sciences
 NeuroImage. Clinical
 Critical reviews in food science and nutrition
 Neurologia
 Cell reports
 Multiple sclerosis and related disorders
 International immunopharmacology
 Annals of clinical and translational neurology
 Biochemistry and biophysics reports
 Eye (London, England)
 European journal of neurology
 Journal of magnetic resonance imaging : JMRI
 Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
 International journal of molecular sciences
 Autoimmunity reviews
 Immunobiology
 Molecular diversity
 Iranian journal of psychiatry
 Frontiers in aging neuroscience
 Frontiers in molecular neuroscience
 Neurology India
 Contemporary clinical trials communications
 Biomedicines
 Frontiers in endocrinology
 Operative neurosurgery (Hagerstown, Md.)
 Pesticide biochemistry and physiology
 Antioxidants & redox signaling
 Journal of neurology
 Nature reviews. Gastroenterology & hepatology
 Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions
 Cellular signalling
 International immunopharmacology
 European journal of immunology
 Nutrients
 Experimental eye research
 Cellular immunology
 European journal of case reports in internal medicine
 Critical reviews in food science and nutrition
 Vestnik oftalmologii
 Expert review of neurotherapeutics
 Advanced nanobiomed research
 Frontiers in immunology
 International journal of molecular sciences
 International journal of molecular sciences
 International journal of molecular sciences
 Wiley interdisciplinary reviews. RNA
 Applied health economics and health policy
 The Journal of foot and ankle surgery : official publication of the American College of Foot and Ankle Surgeons
 The neurologist
 Food science & nutrition
 Canadian journal of physiology and pharmacology
 Nucleosides, nucleotides & nucleic acids
 Cureus
 Frontiers in immunology
 Neurologia medico-chirurgica
 Advances in experimental medicine and biology
 AJR. American journal of roentgenology
 Biomedicines
 Frontiers in immunology
 Diagnostics (Basel, Switzerland)
 Cells
 Cell reports
 Sensors (Basel, Switzerland)
 European journal of medicinal chemistry
 European journal of neurology
 Australian journal of primary health
 Reviews in the neurosciences
 Translational stroke research
 bioRxiv : the preprint server for biology
 ArXiv
 Ageing research reviews
 The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology
 European journal of immunology
 NMR in biomedicine
 Arquivos brasileiros de oftalmologia
 Disability and rehabilitation
 bioRxiv : the preprint server for biology
 Journal of the neurological sciences
 bioRxiv : the preprint server for biology
 Oman journal of ophthalmology
 Immunotherapy advances
 Pain practice : the official journal of World Institute of Pain
 Cells

 ImmunoHorizons
 Journal of medicinal chemistry
 Metabolites
 Frontiers in neurology
 Journal of clinical & experimental immunology
 Frontiers in immunology
 Biomedicines
 Frontiers in cellular neuroscience
 Environmental research
 Frontiers in immunology
 Cell biology international
 Medical & biological engineering & computing
 CNS & neurological disorders drug targets
 Vaccine
 International journal of molecular sciences
 Journal of neuroinflammation
 Respiration; international review of thoracic diseases
 Reviews on environmental health
 ACS chemical neuroscience
 Clinical and experimental medicine
 International journal of molecular sciences
 Journal of translational medicine
 Phytomedicine : international journal of phytotherapy and phytopharmacology
 Frontiers in immunology
 Annals of clinical and translational neurology
 Clinical drug investigation
 Die Rehabilitation
 Research square
 Scientific reports
 Life sciences
 Glia
 Multiple sclerosis and related disorders
 Frontiers in neurology
 European journal of nuclear medicine and molecular imaging
 Metabolic brain disease
 Journal of neurology, neurosurgery, and psychiatry
 PharmacoEconomics - open
 Chinese journal of integrative medicine
 Mediators of inflammation
 Eye (London, England)
 Brain and nerve = Shinkei kenkyu no shinpo
 Journal of autoimmunity
 International journal of molecular sciences
 Immunogenetics
 The Canadian journal of hospital pharmacy
 Neurosurgery
 Journal of personalized medicine
 International journal of molecular sciences
 International immunopharmacology
 Nutrients
 Paediatrics and international child health
 Frontiers in pharmacology
 Operative neurosurgery (Hagerstown, Md.)
 Jornal de pediatria
 Inflammation
 Histochemistry and cell biology
 Ageing research reviews
 Life (Basel, Switzerland)
 Clinical rehabilitation
 Neural regeneration research
 Neurology
 Artificial organs
 Inflammation
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 Frontiers in human neuroscience
 Bioactive materials
 International immunopharmacology
 Clinical and experimental medicine
 Glia
 The Journal of experimental medicine
 Naunyn-Schmiedeberg's archives of pharmacology
 The Journal of physiology
 NMR in biomedicine
 Nature reviews. Immunology
 Journal of biomolecular structure & dynamics
 International reviews of immunology
 European journal of neurology
 International journal of experimental pathology
 International immunopharmacology
 Frontiers in cellular and infection microbiology
 Operative neurosurgery (Hagerstown, Md.)
 Neuro-ophthalmology (Aeolus Press)
 The journal of pain
 Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
 Medicina (Kaunas, Lithuania)
 Recent patents on anti-cancer drug discovery
 Journal of clinical medicine
 Biology
 Journal of medicinal chemistry
 CNS neuroscience & therapeutics
 Brain research
 Pharmaceutics
 International journal of biological macromolecules
 Free radical biology & medicine
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Neurochemical research
 Journal of biomolecular structure & dynamics
 Computers in biology and medicine
 European journal of immunology
 Molecular neurobiology
 Advanced science (Weinheim, Baden-Wurttemberg, Germany)

 Molecules (Basel, Switzerland)
 Rheumatology (Oxford, England)
 Biochemical Society transactions
 European journal of neurology
 Immunology and cell biology
 British journal of health psychology
 Therapeutic advances in neurological disorders
 Nutrition and health
 The Journal of the American Academy of Orthopaedic Surgeons
 Clinical rehabilitation
 Brain : a journal of neurology

 Gene
 Journal of neurology
 International journal of molecular sciences
 PloS one
 Journal of neurology
 Molecules (Basel, Switzerland)
 Annals of translational medicine
 International journal of molecular sciences
 Journal of neuroimmunology
 Frontiers in immunology
 Molecular brain
 Life (Basel, Switzerland)
 Journal of clinical medicine
 Neuropathology : official journal of the Japanese Society of Neuropathology
 bioRxiv : the preprint server for biology
 BMJ open
 International journal of molecular sciences
 The lancet. Psychiatry
 Journal of neurosciences in rural practice
 Cells
 medRxiv : the preprint server for health sciences
 Pharmaceutics
 Pharmacology & therapeutics
 Autoimmunity reviews
 Progress in rehabilitation medicine
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of ethnopharmacology
 Neurochemistry international
 BMJ neurology open
 Neurology and therapy
 Journal for immunotherapy of cancer
 Clinical epidemiology
 Computerized medical imaging and graphics : the official journal of the Computerized Medical Imaging Society
 Journal of pharmacy & bioallied sciences
 Journal of medical case reports
 Stem cell research & therapy
 Frontiers in neuroscience
 Frontiers in pharmacology
 Bio-protocol
 Neuropharmacology
 Frontiers in neurology
 Life sciences
 iScience
 The primary care companion for CNS disorders
 Current diabetes reviews
 Cerebellum (London, England)
 Journal of biomolecular structure & dynamics
 Frontiers in immunology
 Hematology/oncology and stem cell therapy
 Healthcare (Basel, Switzerland)
 Human brain mapping
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 Neurology(R) neuroimmunology & neuroinflammation
 Frontiers in human neuroscience
 Journal of neurophysiology
 Progres en urologie : journal de l'Association francaise d'urologie et de la Societe francaise d'urologie
 International immunopharmacology
 Molecules (Basel, Switzerland)
 Frontiers in pharmacology
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 Journal of autoimmunity
 Cell cycle (Georgetown, Tex.)
 Disability and rehabilitation
 Multiple sclerosis international
 Indian journal of palliative care
 In vivo (Athens, Greece)
 Molecular neurobiology
 Veterinary journal (London, England : 1997)
 Immunology letters
 International immunopharmacology
 Immunity & ageing : I & A
 Biomedica : revista del Instituto Nacional de Salud
 Molecular medicine (Cambridge, Mass.)
 Nutrients
 Neurogastroenterology and motility
 Glia
 JPMA. The Journal of the Pakistan Medical Association
 IBRO neuroscience reports
 Nanomedicine : nanotechnology, biology, and medicine
 Statistics in medicine
 Neuropharmacology
 Neural regeneration research
 Reviews in the neurosciences
 Physiotherapy theory and practice
 Journal of palliative medicine
 Advances in experimental medicine and biology
 Human cell
 Urologia

 Ideggyogyaszati szemle
 Journal of visualized experiments : JoVE
 Amino acids
 Cellular signalling
 Folia neuropathologica
 Rehabilitation psychology
 Brain sciences
 Pharmaceutics
 Journal of electrocardiology
 Journal of neuropsychology
 Redox biology
 Human brain mapping
 Cell biology and toxicology
 The Journal of neuroscience : the official journal of the Society for Neuroscience
 Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
 Biomolecules
 Magnetic resonance imaging
 Applied health economics and health policy
 Brain sciences
 Current protocols
 Phytomedicine : international journal of phytotherapy and phytopharmacology
 Frontiers in cellular neuroscience
 European journal of neurology

 Pharmaceuticals (Basel, Switzerland)
 Clinical & translational immunology
 Journal of the Belgian Society of Radiology
 JPMA. The Journal of the Pakistan Medical Association
 Regenerative medicine
 Medical image analysis
 Nature communications
 Colloids and surfaces. B, Biointerfaces
 European journal of neurology
 Cancers
 Proceedings of the National Academy of Sciences of the United States of America
 European journal of neurology
 The American journal of Chinese medicine
 Acta neurochirurgica
 Acta physiologica (Oxford, England)
 Translational psychiatry
 Journal of neurology
 Preventive medicine reports
 European journal of neurology
 The Egyptian journal of neurology, psychiatry and neurosurgery
 Age and ageing
 Expert review of clinical pharmacology
 Pharmaceutics
 Clinical neurology and neurosurgery
 Recenti progressi in medicina
 Applied neuropsychology. Adult
 Current pharmaceutical design
 Cell death & disease
 European journal of medicinal chemistry
 Journal of neurochemistry
 Frontiers in bioengineering and biotechnology
 Computers in biology and medicine
 Translational psychiatry
 Journal of pain research
 Scientific reports
 Discover. Oncology
 Aging cell
 BioImpacts : BI
 European journal of neurology
 Frontiers in immunology
 Journal of neuroengineering and rehabilitation
 BMC complementary medicine and therapies
 Journal of central nervous system disease
 Journal of Alzheimer's disease reports
 International journal of molecular sciences
 bioRxiv : the preprint server for biology
 Inflammation
 The Journal of clinical endocrinology and metabolism
 Medicine and science in sports and exercise
 Pathology, research and practice
 Clinical immunology (Orlando, Fla.)
 Cell transplantation
 Current neurology and neuroscience reports
 Journal of neuroengineering and rehabilitation
 PloS one
 Operative neurosurgery (Hagerstown, Md.)
 Pharmacology & therapeutics
 Medicina (Kaunas, Lithuania)
 International journal of molecular sciences
 Molecular neurobiology
 Acta radiologica (Stockholm, Sweden : 1987)
 Journal of psychosomatic research
 Allergy and asthma proceedings
 Biochemical pharmacology
 International journal of molecular sciences
 Journal of neuroscience research
 bioRxiv : the preprint server for biology
 Frontiers in neurology
 Medicine
 Journal of natural products
 Journal of neuroscience methods
 Journal of labelled compounds & radiopharmaceuticals
 Neurology(R) neuroimmunology & neuroinflammation
 Current protocols
 Neurology
 Journal of neurochemistry
 Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
 Research synthesis methods
 Glia
 International immunopharmacology
 European journal of neurology
 Radiology case reports
 Scientific reports
 Stroke
 mBio
 Neuropharmacology
 Frontiers in neurology
 Journal of neurology
 Nutrients
 Irish journal of medical science
 Brain research
 Neurology(R) neuroimmunology & neuroinflammation
 Medicina (Kaunas, Lithuania)
 NeuroImage
 Journal of neuro-oncology
 Australian occupational therapy journal
 The Lancet. Neurology
 Medicine
 Acta neuropathologica
 Mediators of inflammation
 Artificial organs
 Disease models & mechanisms
 Ageing research reviews
 Journal of immunology research
 Human genetics
 Journal of Alzheimer's disease reports
 International journal of molecular sciences
 European review for medical and pharmacological sciences
 Redox biology
 Discoveries (Craiova, Romania)
 International journal of molecular sciences
 Clinical rheumatology
 Cureus
 Multiple sclerosis and related disorders

 European journal of gastroenterology & hepatology
 Clinical rehabilitation
 International journal of biological macromolecules
 Expert review of clinical immunology
 American journal of translational research
 Sensors (Basel, Switzerland)
 Fluids and barriers of the CNS
 RMD open
 Journal of natural products
 Biology
 European journal of clinical pharmacology
 Pharmacology & therapeutics
 Rinsho shinkeigaku = Clinical neurology
 European journal of clinical nutrition
 Neurourology and urodynamics
 British journal of health psychology
 Immunobiology
 Free radical biology & medicine
 Colloids and surfaces. B, Biointerfaces
 IUBMB life
 Journal of translational medicine
 Nature reviews. Immunology
 iScience
 Journal of immunological methods
 Cureus
 The neurologist
 Journal of neuroimmunology
 Brain communications
 Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
 Clinical pharmacology in drug development
 Journal of the American Medical Directors Association
 Investigative radiology
 Cancer research communications
 The Lancet. Neurology
 Cancer genomics & proteomics
 Multiple sclerosis and related disorders
 Magnetic resonance in medicine
 Frontiers in public health
 Pharmaceuticals (Basel, Switzerland)
 Cureus
 International journal of molecular sciences
 Inflammopharmacology
 Biomaterials research
 Immunologic research
 Comprehensive psychiatry
 European journal of neurology
 Neurology
 Nutritional neuroscience
 Nature protocols
 Public health
 Multiple sclerosis and related disorders
 Cell death discovery
 BMC nephrology
 Virology journal
 Journal of infusion nursing : the official publication of the Infusion Nurses Society
 Journal of biochemical and molecular toxicology
 Molecular psychiatry
 Drug design, development and therapy
 Translational stroke research
 Noro psikiyatri arsivi
 Pharmaceutical medicine
 European journal of neurology
 Journal of neuroinflammation
 Vaccines
 eLife
 Environmental science. Processes & impacts
 EMBO reports
 BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy
 Archives of dermatological research
 Journal of internal medicine
 Autoimmunity reviews
 Hematological oncology
 medRxiv : the preprint server for health sciences
 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
 Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
 Antioxidants (Basel, Switzerland)
 Integrative medicine (Encinitas, Calif.)
 Schizophrenia research
 BMC infectious diseases
 Pharmacology
 Computer methods and programs in biomedicine
 Human molecular genetics
 Cellular and molecular neurobiology
 Journal of magnetic resonance imaging : JMRI
 Neurology

 JAAD case reports
 Pakistan journal of medical sciences
 JNMA; journal of the Nepal Medical Association

 Current opinion in neurology
 Neurology. Clinical practice
 Cell communication and signaling : CCS
 JAMA neurology
 Histochemistry and cell biology
 Frontiers in medicine

 Journal of neuropathology and experimental neurology
 Annals of medicine and surgery (2012)
 Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
 CASE (Philadelphia, Pa.)
 Metabolic brain disease
 Yonsei medical journal
 Neurology
 The Annals of thoracic surgery
 Neuromuscular disorders : NMD
 Clinical case reports
 Pathogens (Basel, Switzerland)
 Annals of neurology
 Molecular cell
 Materia socio-medica
 EMBO reports
 Multiple sclerosis and related disorders
 Urologie (Heidelberg, Germany)
 Frontiers in pharmacology
 Organic & biomolecular chemistry
 Immunologic research
 European journal of medical research
 BMJ open
 Neurology
 Cannabis and cannabinoid research
 Journal of neuroscience research
 Protein science : a publication of the Protein Society
 The journal of headache and pain
 Clinical rheumatology
 Biochimica et biophysica acta. Biomembranes
 Neuroepidemiology
 The Turkish journal of pediatrics
 The journal of obstetrics and gynaecology research
 Stem cell research
 Pharmacological research
 Frontiers in neuroscience
 Clinical nuclear medicine
 American journal of human genetics
 American journal of ophthalmology case reports
 Hand (New York, N.Y.)
 The Journal of hand surgery
 Journal of neurosurgery. Case lessons
 Journal of autoimmunity
 Frontiers in immunology
 Movement disorders : official journal of the Movement Disorder Society
 ACR open rheumatology
 Scientific reports
 Cureus
 Cell death & disease
 Ophthalmic epidemiology
 Neurochemistry international
 Proceedings of the National Academy of Sciences of the United States of America
 Behaviour research and therapy
 Annals of clinical and translational neurology
 Advances in therapy
 Frontiers in immunology
 International journal of pharmaceutics
 Arthritis research & therapy
 International urology and nephrology
 Heliyon
 Nature genetics
 Cureus
 The Journal of pharmacology and experimental therapeutics
 BMJ open
 Seminars in cell & developmental biology
 Antibodies (Basel, Switzerland)
 Indian journal of dermatology
 BMC medicine
 Scientific reports
 Frontiers in immunology
 Annals of medicine and surgery (2012)
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Frontiers in neurology
 Clinical rheumatology
 Case reports in ophthalmology
 Brain communications
 International journal of surgery case reports
 Acta pharmaceutica Sinica. B
 Quantitative imaging in medicine and surgery
 Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine
 Current gene therapy
 Cellular signalling
 Journal of scleroderma and related disorders
 Journal of the American Association of Nurse Practitioners
 The Journal of molecular diagnostics : JMD
 International journal of molecular sciences
 European journal of internal medicine
 Glia
 Journal of endodontics
 The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians
 Current neuropharmacology
 Multiple sclerosis and related disorders
 EBioMedicine
 International journal of exercise science
 Molecules (Basel, Switzerland)
 Investigative radiology
 FASEB bioAdvances
 Progress in neurobiology
 Pediatric neurology
 Computational and structural biotechnology journal
 Neurology
 Nature immunology
 Multiple sclerosis and related disorders
 Pharmacological research
 Frontiers in immunology
 Journal of clinical medicine
 Multiple sclerosis and related disorders
 British journal of pharmacology
 Journal of magnetic resonance imaging : JMRI
 Multiple sclerosis and related disorders
 Gerontology
 Journal of aerosol medicine and pulmonary drug delivery
 Archives of toxicology
 Rambam Maimonides medical journal
 The American journal of case reports
 Clinical case reports
 Lancet (London, England)
 NeuroImage. Clinical
 Annals of medicine and surgery (2012)
 Biomedicines
 Annals of neurology
 Rheumatic diseases clinics of North America

 Rheumatic diseases clinics of North America
 Medicinal research reviews
 Neuropsychiatric disease and treatment
 Molecular neurobiology
 ACS chemical neuroscience
 Sleep & breathing = Schlaf & Atmung
 Autoimmunity reviews
 Modern rheumatology case reports
 Brain communications
 Current issues in molecular biology
 The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
 Life (Basel, Switzerland)
 PEC innovation
 BMJ (Clinical research ed.)
 Cureus
 Diagnostics (Basel, Switzerland)
 The Indian journal of radiology & imaging
 European radiology
 Journal of proteomics
 Science translational medicine
 Neurology
 Cancers

 Brain : a journal of neurology
 International journal of oral and maxillofacial surgery
 Sleep medicine
 Journal of intellectual disability research : JIDR
 International archives of occupational and environmental health
 Amyotrophic lateral sclerosis & frontotemporal degeneration
 Clinical pharmacology in drug development
 Frontiers in psychology
 European journal of ophthalmology
 Journal of the neurological sciences
 Therapeutic advances in neurological disorders
 Frontiers in immunology
 Molecular neurobiology
 Croatian medical journal
 Brain : a journal of neurology
 Frontiers in aging neuroscience
 Biology
 Iranian journal of basic medical sciences
 Frontiers in pharmacology
 RNA biology
 Clinical reviews in allergy & immunology
 Expert opinion on biological therapy
 Frontiers in aging neuroscience
 Journal of endocrinological investigation
 GMS ophthalmology cases
 Journal of the European Academy of Dermatology and Venereology : JEADV
 European journal of neurology
 Journal of neurology, neurosurgery, and psychiatry
 Science translational medicine
 Journal of biochemical and molecular toxicology
 Cerebellum (London, England)
 The journal of headache and pain
 Chinese journal of integrative medicine
 Science immunology
 Journal of the American Society of Nephrology : JASN
 International immunopharmacology
 Nature communications
 Immunobiology
 medRxiv : the preprint server for health sciences
 Neurology
 International journal of molecular sciences
 Brain : a journal of neurology
 Frontiers in bioengineering and biotechnology
 Movement disorders : official journal of the Movement Disorder Society
 Neurology
 The Journal of investigative dermatology
 Research (Washington, D.C.)
 Italian journal of pediatrics
 Inflammopharmacology
 Rheumatology (Oxford, England)
 Laryngoscope investigative otolaryngology
 Kardiologiia
 Frontiers in aging neuroscience
 Annals of medicine and surgery (2012)
 Pharmaceuticals (Basel, Switzerland)
 Frontiers in molecular biosciences
 Multiple sclerosis journal - experimental, translational and clinical
 Frontiers in molecular biosciences
 Frontiers in neuroscience
 Neurology. Clinical practice
 Journal of investigative medicine high impact case reports
 Bioengineering (Basel, Switzerland)
 Korean journal of neurotrauma
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Cytokine

 Journal of wound care
 Alzheimer's research & therapy

 Journal of the International Neuropsychological Society : JINS
 Brain research bulletin
 Neurology(R) neuroimmunology & neuroinflammation
 Virchows Archiv : an international journal of pathology
 Journal of neurology
 Skeletal radiology
 Iranian journal of child neurology
 Muscle & nerve
 Frontiers in pharmacology
 Neuropathology and applied neurobiology
 Clinical reviews in allergy & immunology
 Epilepsia
 Journal of autism and developmental disorders
 Neurologia i neurochirurgia polska
 Clinical reviews in allergy & immunology
 Archives of physical medicine and rehabilitation
 Amyotrophic lateral sclerosis & frontotemporal degeneration
 Dysphagia
 Autoimmunity reviews
 Current neurovascular research
 Neurobiology of disease
 Journal of cutaneous pathology
 Acta neuropathologica
 American journal of ophthalmology
 International journal of molecular sciences
 Frontiers in molecular biosciences
 Antioxidants (Basel, Switzerland)
 Frontiers in immunology

 Endocrinologia, diabetes y nutricion
 Cells
 Clinical and experimental rheumatology
 Brain stimulation
 Neurobiology of aging
 Translational pediatrics
 microPublication biology
 Journal of autoimmunity
 Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
 Frontiers in neuroscience
 Journal of back and musculoskeletal rehabilitation
 Neurology
 Nature reviews. Drug discovery
 Therapeutic advances in neurological disorders
 Neurotoxicology
 JMIR research protocols
 RMD open
 Cell & bioscience
 Journal of radiology case reports
 Frontiers in aging
 JAMA psychiatry
 Trials
 NeuroImage
 Multiple sclerosis and related disorders
 Cephalalgia : an international journal of headache
 Journal of market access & health policy
 PLoS computational biology
 Multiple sclerosis and related disorders
 International journal of molecular sciences
 Neurology. Clinical practice
 Frontiers in aging neuroscience
 Network neuroscience (Cambridge, Mass.)
 International journal of preventive medicine
 NeuroImage
 The Lancet. Neurology
 Archives of dermatological research
 International journal of molecular sciences
 Human molecular genetics
 Journal of clinical medicine
 Cellular and molecular neurobiology
 Frontiers in physiology
 Annals of neurology
 International journal of molecular sciences
 Journal of the European Academy of Dermatology and Venereology : JEADV
 The Journal of clinical investigation
 Brain : a journal of neurology
 Clinical linguistics & phonetics
 Environmental research
 Health expectations : an international journal of public participation in health care and health policy
 Autoimmunity reviews
 Cellular and molecular neurobiology
 Scientific reports
 Phenomics (Cham, Switzerland)
 Biochimie
 Brain communications
 Human genetics
 The journal of pathology. Clinical research
 Alzheimer's & dementia : the journal of the Alzheimer's Association
 Arquivos de neuro-psiquiatria
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Cell
 Annals of medicine and surgery (2012)
 Alzheimer's & dementia : the journal of the Alzheimer's Association
 Annals of clinical and translational neurology
 Molecular neurodegeneration
 Nature communications
 Frontiers in immunology
 Alzheimer's & dementia : the journal of the Alzheimer's Association
 Rheumatology international
 Therapeutic advances in musculoskeletal disease
 Respiratory medicine and research
 Seminars in arthritis and rheumatism
 Frontiers in aging neuroscience
 The European journal of neuroscience
 Neurobiology of disease
 Neurobiology of disease
 Lancet (London, England)
 Cerebellum (London, England)
 Neurologia
 PloS one
 Cell reports
 bioRxiv : the preprint server for biology
 Cell reports methods
 Journal of internal medicine
 Cells, tissues, organs
 BMJ neurology open
 Revue neurologique
 JPEN. Journal of parenteral and enteral nutrition
 ACS chemical neuroscience
 GeroScience
 PloS one
 International journal of tryptophan research : IJTR
 Journal of neurochemistry
 eNeuro
 Bone & joint research
 Journal of speech, language, and hearing research : JSLHR
 Journal of Alzheimer's disease : JAD
 Cell stem cell
 Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
 Cellular and molecular life sciences : CMLS
 Clinical rheumatology
 Frontiers in cellular neuroscience
 Cureus
 Cells
 Journal of neuromuscular diseases
 Frontiers in psychology
 Frontiers in neurology
 Cell research
 Scientific reports
 Arthritis care & research
 Proceedings of the National Academy of Sciences of the United States of America
 EClinicalMedicine
 Journal of neuroengineering and rehabilitation
 Neurology(R) neuroimmunology & neuroinflammation
 Nature
 Science (New York, N.Y.)
 microPublication biology
 Frontiers in cell and developmental biology
 European journal of radiology
 The Indian journal of radiology & imaging
 Bone
 medRxiv : the preprint server for health sciences
 The Journal of neuroscience : the official journal of the Society for Neuroscience
 Human cell
 Annals of neurology
 Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Stem cell reviews and reports
 Journal of cancer research and clinical oncology
 Biology
 IBRO neuroscience reports
 Journal of the peripheral nervous system : JPNS
 Cell reports. Medicine
 European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
 Frontiers in cardiovascular medicine
 Journal of neurology
 Proceedings of the National Academy of Sciences of the United States of America
 Headache
 Clinical and experimental medicine
 Nature communications
 Sleep medicine
 Pharmacological research
 medRxiv : the preprint server for health sciences
 Biology
 Epilepsia open
 Rheumatic diseases clinics of North America
 Frontiers in cell and developmental biology
 Biophysical chemistry
 The American journal of case reports
 World neurosurgery: X
 Toxins
 American journal of clinical dermatology
 Amyotrophic lateral sclerosis & frontotemporal degeneration
 Life sciences
 American journal of medical genetics. Part C, Seminars in medical genetics
 Journal of clinical medicine
 Scientific reports
 bioRxiv : the preprint server for biology
 Infection and drug resistance
 Aging and disease
 Journal of the American Nutrition Association
 Journal of the European Academy of Dermatology and Venereology : JEADV
 Research square
 Biomedicines
 Journal of Parkinson's disease
 Journal of clinical epidemiology
 Thorax
 Acta neurobiologiae experimentalis
 Frontiers in neurology
 JAMA network open
 European journal of public health
 Arquivos de neuro-psiquiatria
 Arthritis care & research
 Advances in therapy
 Palliative care and social practice
 The Journal of investigative dermatology
 Molecular metabolism
 Journal of neuroimaging : official journal of the American Society of Neuroimaging
 Rheumatology (Oxford, England)
 Annals of clinical and translational neurology
 FASEB journal : official publication of the Federation of American Societies for Experimental Biology
 Phytotherapy research : PTR
 Journal of cranio-maxillo-facial surgery : official publication of the European Association for Cranio-Maxillo-Facial Surgery
 Journal of clinical medicine
 Military medicine
 Antioxidants & redox signaling
 Frontiers in immunology
 Cellular and molecular life sciences : CMLS
 Brain topography
 Life (Basel, Switzerland)
 Frontiers in cellular neuroscience
 Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
 Microbiology spectrum
 Hypertension (Dallas, Tex. : 1979)
 European journal of neurology
 Nature communications
 European journal of neurology
 Journal of neural transmission (Vienna, Austria : 1996)
 Journal of clinical medicine
 Journal of the peripheral nervous system : JPNS
 Brain : a journal of neurology
 Annals of neurology
 Journal of neurology
 Journal of biochemistry
 Cytometry. Part A : the journal of the International Society for Analytical Cytology
 Handbook of clinical neurology
 Journal of neurology, neurosurgery, and psychiatry
 Journal of neurology
 American journal of physiology. Renal physiology
 Brain : a journal of neurology
 CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
 Folia medica
 The American journal of surgical pathology
 Frontiers in molecular neuroscience
 Research square
 Neurochemical research
 medRxiv : the preprint server for health sciences
 Neurotrauma reports
 bioRxiv : the preprint server for biology
 Journal of oral rehabilitation
 Therapeutic advances in neurological disorders
 medRxiv : the preprint server for health sciences
 bioRxiv : the preprint server for biology
 Journal of neurology
 Archives of rheumatology
 AJNR. American journal of neuroradiology
 The Tohoku journal of experimental medicine
 Brain, behavior, and immunity
 Epilepsia
 European journal of neurology
 Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
 Journal of Alzheimer's disease : JAD
 European journal of neurology
 Obesity (Silver Spring, Md.)
 European journal of neurology
 Journal of autoimmunity
 Frontiers in immunology
 Arthritis care & research
 Frontiers in neuroscience
 Neurosurgery
 Brain : a journal of neurology
 Journal of cannabis research
 Eye (London, England)
 Nature genetics
 Translational behavioral medicine
 Radiology. Artificial intelligence
 Nutrients
 European journal of immunology
 Trials
 Neurology. Clinical practice
 Annals of neurology
 Journal of cachexia, sarcopenia and muscle
 Frontiers in neurology
 Journal of neurology
 Movement disorders : official journal of the Movement Disorder Society
 Science signaling
 Neurological research and practice
 Epilepsia
 Lupus
 Experimental neurology
 Annals of neurology
 Cell biology and toxicology
 Current neuropharmacology
 American journal of respiratory cell and molecular biology
 Archives of academic emergency medicine
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Journal of neurology
 Nature immunology
 Journal of neurology
 Cellular & molecular immunology
 The EMBO journal
 PharmacoEconomics - open
 Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine
 Journal of ethnopharmacology
 International immunopharmacology
 Journal of neurology, neurosurgery, and psychiatry
 Epilepsia
 Journal of neurology, neurosurgery, and psychiatry
 JAMA neurology
 Therapeutic advances in neurological disorders
 NeuroImage. Clinical
 ACS chemical neuroscience
 The Journal of neuroscience : the official journal of the Society for Neuroscience
 Nature communications
 BMJ open
 Arthritis care & research
 Clinical nephrology. Case studies
 NeuroImage
 European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society
 European journal of nuclear medicine and molecular imaging
 Science advances
 BMJ open
 EBioMedicine
 BMJ open
 International journal of molecular sciences
 Journal of neurophysiology
 Epilepsy & behavior : E&B
 Microvascular research
 Neurology
 Journal of clinical medicine
 Journal of neurology
 Brain communications
 Multiple sclerosis (Houndmills, Basingstoke, England)
 Cellular and molecular life sciences : CMLS
 Lupus science & medicine
 EBioMedicine
 Rheumatology (Oxford, England)
 Neurology(R) neuroimmunology & neuroinflammation
 Annals of neurology
 International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
 Journal of neurology
 Journal of affective disorders
 Annals of neurology
 Brain communications
 bioRxiv : the preprint server for biology
 Cell discovery
 Autoimmunity reviews
 International journal of molecular sciences
 BJPsych open
 Cell genomics
 Neurobiology of disease
 International journal of molecular sciences
 Translational lung cancer research
 Neurology
 European journal of neurology
 medRxiv : the preprint server for health sciences
 Neurology. Clinical practice
 JAMA neurology
 Alzheimer's & dementia : the journal of the Alzheimer's Association
 Brain : a journal of neurology
 Cell reports. Medicine
 Nature reviews. Neurology
 Journal of neurology, neurosurgery, and psychiatry
 The Lancet. Neurology
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 20230528
 20230501
 20230601
 20230220
 20230517
 20230405
 20230224
 20230203
 20230202
 20230911
 20230909
 20230810
 20230812
 20230703
 20230505
 20230822
 20230213
 20230804
 20230705
 20230616
 20230608
 20230710
 20230718
 20230329
 20230301
 20230818
 20230428
 20230322
 20230116
 20230412
 20230415
 20230816
 20230715
 20230517
 20230830
 20230519
 20230228
 20230224
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 20230307
 20230222
 20230509
 20230626
 20230315
 20230914

 20230322
 20230324
 20230721

 20230719
 20230418
 20230529
 20230322
 20230705
 20230311

 20230309
 20230228
 20230411
 20230418
 20230720
 20230215
 20230719
 20230206
 20230604
 20230217
 20230829
 20230705
 20230729
 20230426
 20230322
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 20230201
 20230823
 20230608
 20230515
 20230902
 20230901
 20230619
 20230327
 20230616
 20230911
 20230801
 20230728
 20230814
 20230822
 20230705
 20230621
 20230625
 20230911
 20230311
 20230703
 20230612
 20230905
 20230210
 20230807
 20230626
 20230404
 20230601
 20230721
 20230801
 20230418
 20230307
 20230324
 20230516
 20230421
 20230721
 20230214
 20230907
 20230822
 20230611
 20230404
 20230829
 20230202
 20230725
 20230416
 20230405
 20230719
 20230308
 20230602
 20230224
 20230607
 20230911
 20230718
 20230817
 20230718
 20230619
 20230311
 20230913
 20230725
 20230815
 20230905
 20230307
 20230718
 20230208
 20230321
 20230829
 20230412
 20230111
 20230824
 20230501
 20230715
 20230807
 20230718
 20230411
 20230825
 20230831
 20230619
 20230430
 20230501
 20230515
 20230810
 20230712
 20230827
 20230216
 20230724
 20230717
 20230619
 20230315
 20230307
 20230201
 20230314
 20230210
 20230622
 20230619
 20230807
 20230517
 20230118
 20230811
 20230515
 20230428
 20230203
 20230619
 20230701
 20230530
 20230905
 20230620

 20230411
 20230608
 20230413
 20230713
 20230911
 20230708
 20230322
 20230111
 20230610
 20230517
 20230608
 20230301
 20230523
 20230905
 20230514
 20230701
 20230302
 20230712
 20230616
 20230222
 20230719
 20230814

 20230503
 20230204
 20230815
 20230622
 20230213
 20230202
 20230906
 20230805
 20230831
 20230913
 20230823
 20230914
 20230828
 20230323
 20230728
 20230228
 20230228
 20230718
 20230604
 20230421
 20230510
 20230501
 20230910
 20230202
 20230307
 20230215
 20230419
 20230704
 20230604
 20230721
 20230426
 20230720
 20221223
 20230811
 20230908
 20230616
 20230717
 20230615
 20230911
 20230913
 20230829
 20230712
 20230523
 20230731
 20230605
 20230715
 20230528
 20230911
 20230803
 20230829
 20230727
 20230912
 20230612
 20230530
 20230501
 20230825
 20230115
 20230718
 20230619
 20230502
 20230614
 20230731
 20230718
 20230912
 20230811

 20230911
 20230619

 20230619
 20230315
 20221229
 20230810
 20230718
 20230525
 20230602
 20230908
 20230826
 20230501
 20230510
 20230823
 20230525
 20230501
 20230511
 20230202
 20230718
 20230421
 20230530
 20230824
 20230807
 20230819
 20230817
 20230724
 20230701
 20230310
 20230331
 20230828

 20230321
 20230519
 20230804
 20230509
 20230322
 20230718
 20230511
 20230224
 20230819
 20230308
 20230328
 20230816
 20230819
 20230718
 20230712
 20230428
 20230310
 20230330
 20230529
 20230721
 20230909
 20230308
 20230905
 20230721
 20230208
 20230913
 20230914
 20230619
 20230214
 20230905
 20230815
 20230704
 20230701
 20230830
 20230821
 20230705
 20230501
 20230330
 20230501
 20230111
 20230516
 20230814
 20230718
 20230330
 20230819
 20230616
 20230527
 20230130
 20230718
 20230425
 20230626
 20230602
 20230519
 20230816
 20230315
 20230903
 20230213
 20230727
 20230905
 20230912
 20230608
 20230718
 20230627
 20230519
 20230913
 20230310
 20230828
 20230424
 20230805
 20230517
 20230609
 20230502
 20230502
 20230201
 20230223
 20230412
 20230605
 20230804
 20230803
 20230419
 20230314
 20230502
 20230805
 20230620
 20230726
 20230704
 20230616
 20230331
 20230615
 20230607
 20230605
 20230218
 20230612
 20230317
 20230705
 20230902
 20230526
 20230331
 20230818
 20230418
 20230702
 20230824
 20230509
 20230426
 20230523
 20230328
 20230401
 20230704
 20230913
 20230725
 20230907
 20230829
 20230626
 20230222
 20230724
 20230818
 20230705
 20230328
 20230721
 20230502
 20230213
 20230821
 20230623
 20230328
 20230906
 20230525
 20230718
 20230603
 20230722
 20230331
 20230103
 20230307
 20230831
 20230531
 20230316
 20230302
 20230909
 20230601
 20230801
 20230910
 20230802
 20230625
 20230718
 20230228
 20230526
 20230201
 20230613
 20230409
 20230804
 20230613
 20230410
 20230328
 20230725
 20230724
 20230622
 20230530
 20230902
 20230522
 20230421
 20230404
 20230522
 20230117
 20230913
 20230331
 20230331
 20230912
 20230821
 20230424
 20230701
 20230910
 20230619
 20230406
 20230607
 20230225
 20230509
 20230804
 20230313
 20230616
 20230912
 20230807
 20230727
 20230511
 20230821
 20230612
 20230831
 20230513
 20230803
 20230814
 20230814
 20230331
 20230307
 20230503
 20230412
 20230912
 20230911
 20230914
 20230406
 20230331
 20230301
 20230908
 20230328
 20230419
 20230726
 20230206
 20230414
 20230111
 20230614
 20230617
 20230627
 20230705
 20230804
 20230904
 20230821
 20230203
 20230214
 20230323
 20230829
 20230426
 20230818
 20230504
 20230902
 20230801
 20230209
 20230518
 20230528
 20230726
 20230718
 20230202
 20230415
 20230718
 20230613
 20230517
 20230406
 20230415
 20230718
 20230404
 20230718
 20230912
 20230701
 20230815
 20230418
 20230616
 20230614
 20230913
 20230704
 20230612
 20230415
 20230417
 20230727
 20230502
 20230612
 20230810
 20230226
 20230322
 20230824
 20230627
 20230507
 20230324
 20230517
 20221228
 20230803
 20230820
 20230310
 20230708
 20230824
 20230810
 20230428
 20230519
 20230524
 20230206
 20230322
 20230330
 20230214
 20221201
 20230613
 20230830
 20230605
 20230723
 20230908
 20230830
 20230413
 20230911
 20230318
 20230910
 20230808
 20230515
 20230430
 20230412
 20230214
 20230111
 20230814
 20230328
 20230314
 20230704
 20230331
 20230224
 20230322
 20230913
 20230306
 20230415
 20230322
 20230412
 20230309
 20230814
 20230706
 20230619
 20230803
 20230830
 20230905
 20230804
 20230111
 20230623
 20230415
 20230328
 20230824
 20230804
 20230425
 20230718
 20230429
 20230703
 20230328
 20230124
 20230815
 20230912
 20230323
 20230905
 20230831
 20230223
 20230621
 20230701
 20230723
 20230613
 20230712
 20230301
 Humans *Multiple Sclerosis/therapy Aging Inflammation Disease Progression *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis, Relapsing-Remitting/pathology
 Humans *Multiple Sclerosis/therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy Aging *Disabled Persons Disease Progression
 Humans *Mendelian Randomization Analysis Genome-Wide Association Study *Multiple Sclerosis/drug therapy/genetics Bayes Theorem Phenotype Polymorphism, Single Nucleotide/genetics
 Humans *Multiple Sclerosis/drug therapy *Hematopoietic Stem Cell Transplantation Transplantation, Autologous *Multiple Sclerosis, Chronic Progressive Neuroprotection *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Chickenpox/epidemiology *Multiple Sclerosis/epidemiology/genetics Mendelian Randomization Analysis Genome-Wide Association Study Herpesvirus 3, Human/genetics Polymorphism, Single Nucleotide
 Child Humans Age of Onset Magnetic Resonance Imaging *Multiple Sclerosis/diagnostic imaging/therapy Guidelines as Topic
 Humans Herpesvirus 4, Human/genetics *Multiple Sclerosis/etiology/prevention & control *Epstein-Barr Virus Infections/complications/therapy Longitudinal Studies
 Pregnancy Child Infant, Newborn Humans Female *Multiple Sclerosis/therapy Family Planning Services Pregnancy Outcome Recurrence *Multiple Sclerosis, Relapsing-Remitting/complications
 Humans *Multiple Sclerosis/diagnostic imaging/therapy *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/therapy Disease Progression Longitudinal Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Young Adult Humans *Multiple Sclerosis/therapy/drug therapy
 Humans Herpesvirus 4, Human *Epstein-Barr Virus Infections/complications *Multiple Sclerosis/epidemiology/etiology Longitudinal Studies Antibodies, Viral
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Artificial Intelligence Reproducibility of Results *Demyelinating Diseases Magnetic Resonance Imaging/methods
 Humans *Multiple Sclerosis/drug therapy/etiology *Epstein-Barr Virus Infections/pathology Herpesvirus 4, Human
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunologic Factors/pharmacology/therapeutic use *Multiple Sclerosis, Chronic Progressive/drug therapy Recurrence
 Humans *Palliative Care/methods/psychology Quality of Life *Multiple Sclerosis/complications/therapy Pain Management Death
 Adult Humans *Multiple Sclerosis/complications/therapy Quality of Life Exercise Exercise Therapy Anxiety Disorders/therapy Anxiety/etiology/therapy
 Humans Inappropriate Prescribing *Deprescriptions Polypharmacy Prevalence *Multiple Sclerosis/drug therapy/epidemiology
 Humans Young Adult Aging *Brain/immunology/pathology/physiopathology Brain Stem/immunology/pathology/physiopathology Case-Control Studies *Cognitive Reserve Disease Progression *Educational Status *Genome-Wide Association Study Homozygote Mobility Limitation *Multiple Sclerosis/genetics/immunology/physiopathology/psychology *Protective Factors Time Factors
 Humans *Multiple Sclerosis/therapy
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Cerebral Cortex/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Disease Progression Prognosis
 Humans *Multiple Sclerosis/complications Meninges/pathology Disease Progression *Multiple Sclerosis, Relapsing-Remitting/complications/pathology
 Humans Sclerosis *Multiple Sclerosis/diagnostic imaging
 Humans *Multiple Sclerosis/complications/epidemiology/therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Longitudinal Studies Magnetic Resonance Imaging Obesity/complications/epidemiology Recurrence Disease Progression
 Humans Female *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Rituximab/therapeutic use Cohort Studies Neoplasm Recurrence, Local
 Humans *Multiple Sclerosis/complications/therapy/diagnosis *Autonomic Nervous System Diseases/diagnosis/etiology Autonomic Nervous System Central Nervous System
 Humans *Multiple Sclerosis/complications/therapy/psychology *Sexual Dysfunction, Physiological/therapy/complications Sildenafil Citrate Pain/complications Exercise Therapy/methods
 Humans *Multiple Sclerosis/epidemiology/therapy *Epstein-Barr Virus Infections *Migraine Disorders/therapy
 Adolescent Adult Humans Child Young Adult *Multiple Sclerosis/therapy/drug therapy *Neurodegenerative Diseases/diagnosis Central Nervous System Risk Factors Diagnosis, Differential
 Humans *Anti-Bacterial Agents/adverse effects *Multiple Sclerosis/drug therapy/epidemiology Penicillins Odds Ratio
 Humans *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods *Multiple Sclerosis, Chronic Progressive Brain/diagnostic imaging Positron-Emission Tomography
 Humans *Multiple Sclerosis/drug therapy Clinical Trials as Topic
 Humans *Multiple Sclerosis/complications/drug therapy/epidemiology Autoimmunity *Autoimmune Diseases/complications/drug therapy *Arthritis, Rheumatoid *Lupus Erythematosus, Systemic
 Humans Vitamin D *Multiple Sclerosis/drug therapy/epidemiology *Melatonin/therapeutic use Vitamins *Vitamin D Deficiency/epidemiology
 Humans *Multiple Sclerosis/diagnosis/epidemiology/therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Crotonates/adverse effects Toluidines/adverse effects Hydroxybutyrates/therapeutic use
 Humans *Multiple Sclerosis/drug therapy Immunosuppressive Agents/therapeutic use Disease Progression *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis/complications/drug therapy *Depressive Disorder, Major/drug therapy/epidemiology/psychology Depression Comorbidity Antidepressive Agents/therapeutic use
 Child Humans Bayes Theorem *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Sample Size Clinical Trials as Topic
 Humans *Multiple Sclerosis/etiology/metabolism Central Nervous System *Extracellular Vesicles/metabolism Blood-Brain Barrier
 Humans *Multiple Sclerosis/epidemiology/etiology/therapy *Neurodegenerative Diseases *COVID-19 Mathematical Concepts Models, Biological *Autoimmune Diseases
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Cross-Sectional Studies *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Magnetic Resonance Imaging Thalamus/diagnostic imaging Atrophy/pathology *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/pathology Brain/pathology
 Humans *Multiple Sclerosis/therapy/drug therapy Artificial Intelligence
 Adolescent Adult Humans Child *Multiple Sclerosis/drug therapy
 Humans *Multiple Sclerosis Depression/etiology *Multiple Sclerosis, Relapsing-Remitting Quality of Life
 Young Adult Humans *Multiple Sclerosis/therapy Brain-Gut Axis *Multiple Sclerosis, Chronic Progressive/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Gastrointestinal Microbiome
 Adult Humans Child *Multiple Sclerosis/diagnostic imaging/drug therapy *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Antibodies, Monoclonal, Humanized/therapeutic use Treatment Outcome Recurrence Immunologic Factors/therapeutic use
 Humans *Multiple Sclerosis/drug therapy Health Services Accessibility
 Adult Humans *Multiple Sclerosis/drug therapy/chemically induced Immunosuppressive Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab/therapeutic use Cladribine/therapeutic use
 Humans *Neural Networks, Computer Artificial Intelligence *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Image Interpretation, Computer-Assisted/methods Image Processing, Computer-Assisted/methods
 Female Humans *Brain Neoplasms *Breast Neoplasms *Lung Neoplasms/complications Mendelian Randomization Analysis *Multiple Sclerosis/complications/epidemiology *Ovarian Neoplasms/etiology
 Humans *Multiple Sclerosis/diagnosis/pathology Central Nervous System/pathology Magnetic Resonance Imaging/methods Diagnostic Errors/prevention & control Documentation
 Humans *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive/diagnosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis Prognosis Uncertainty
 Humans *Multiple Sclerosis/complications/drug therapy/chemically induced Network Meta-Analysis Bayes Theorem Seizures/drug therapy/etiology Cladribine/adverse effects Anticonvulsants
 Humans *Multiple Sclerosis/diagnosis/drug therapy Antibodies, Monoclonal
 Humans *Multiple Sclerosis/drug therapy
 Humans *Multiple Sclerosis/therapy Clinical Trials as Topic *Multiple Sclerosis, Chronic Progressive Patient Selection Patient Participation
 Humans *Tuberous Sclerosis/complications/diagnosis/genetics *Multiple Sclerosis/complications/diagnosis/genetics Genetic Testing
 Humans *COVID-19 COVID-19 Vaccines/therapeutic use *Multiple Sclerosis/complications/therapy Pandemics SARS-CoV-2 Disease Progression
 Humans *Multiple Sclerosis/complications/diagnostic imaging Quality of Life Cerebellum/diagnostic imaging *Cerebellar Diseases Gait
 Humans Child *Multiple Sclerosis/diagnostic imaging/epidemiology Magnetic Resonance Imaging/methods *Demyelinating Diseases/diagnostic imaging Biomarkers *Pediatrics
 Humans *Multiple Sclerosis/epidemiology/therapy Quality of Life Comorbidity *Cerebrovascular Disorders/epidemiology *Peripheral Vascular Diseases
 Humans *Multiple Sclerosis/psychology *Multiple Sclerosis, Relapsing-Remitting/psychology *Multiple Sclerosis, Chronic Progressive/psychology Cognition Phenotype Neuropsychological Tests *Cognitive Dysfunction/diagnosis/etiology/psychology
 Humans *Multiple Sclerosis/epidemiology/therapy Europe/epidemiology Czech Republic Surveys and Questionnaires *Neurology
 Humans Pregnancy Female *Multiple Sclerosis/diagnosis/epidemiology/etiology Reproductive Techniques, Assisted/adverse effects Pregnancy, Multiple
 Animals Humans *Multiple Sclerosis/etiology/therapy *Encephalomyelitis, Autoimmune, Experimental T-Lymphocytes Cytokines
 Humans *Gastrointestinal Microbiome/physiology Brain/physiology *Multiple Sclerosis, Relapsing-Remitting/metabolism *Multiple Sclerosis/metabolism Central Nervous System
 Humans *Multiple Sclerosis/complications/epidemiology *Deglutition Disorders/epidemiology/etiology Prevalence Bibliometrics
 Humans *Multiple Sclerosis/complications/diagnosis/psychology Quality of Life *Cognition Disorders/diagnosis/etiology/psychology Neuropsychological Tests Self Report Cognition
 Humans *Hepatitis, Autoimmune *Multiple Sclerosis/diagnosis/drug therapy/genetics *Drug-Related Side Effects and Adverse Reactions *Chemical and Drug Induced Liver Injury/etiology/genetics Genotype
 Humans *Multiple Sclerosis/cerebrospinal fluid *Multiple Sclerosis, Chronic Progressive/cerebrospinal fluid *Multiple Sclerosis, Relapsing-Remitting/cerebrospinal fluid Immunoglobulin G
 Humans Child *Multiple Sclerosis/complications/psychology Cognition Intelligence Tests Neuropsychological Tests Memory
 Humans *Yoga/psychology *Multiple Sclerosis/therapy/psychology Exercise *Meditation Emotions
 Humans *Multiple Sclerosis/therapy/etiology *Mesenchymal Stem Cell Transplantation/methods *Mesenchymal Stem Cells/physiology Neuroprotection
 Humans *Smartphone Reproducibility of Results *Multiple Sclerosis/complications/diagnosis Cross-Sectional Studies Cognition
 Humans *Trigeminal Neuralgia/complications/diagnostic imaging Retrospective Studies *Multiple Sclerosis/complications/diagnostic imaging *Radiosurgery Treatment Outcome Pain/complications *Multiple Sclerosis, Relapsing-Remitting/complications
 Humans *Multiple Sclerosis/therapy Retrospective Studies *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis, Relapsing-Remitting *Hematopoietic Stem Cell Transplantation
 Humans *Multiple Sclerosis/etiology/prevention & control *Diet, Mediterranean *Cardiovascular Diseases
 Humans *Multiple Sclerosis/diagnosis
 Humans *Multiple Sclerosis/complications/psychology *Cognition Disorders/complications *Neurodegenerative Diseases/complications Cognition *Cognitive Dysfunction/etiology/complications Neuropsychological Tests
 Child Humans *Multiple Sclerosis/diagnosis/drug therapy Disease Progression Age of Onset
 Humans *Multiple Sclerosis/epidemiology/therapy Health Care Costs
 Humans *Multiple Sclerosis/diagnosis/therapy *Extracellular Vesicles Central Nervous System Biomarkers Cell Communication
 Animals Humans *Multiple Sclerosis/therapy/metabolism *Mesenchymal Stem Cell Transplantation/methods *Mesenchymal Stem Cells/metabolism
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Brain/pathology Clinical Decision-Making Cost-Benefit Analysis
 Humans *Multiple Sclerosis/genetics/therapy *Epstein-Barr Virus Infections/genetics Herpesvirus 4, Human Epigenesis, Genetic DNA Methylation
 Humans *Multiple Sclerosis/complications/diagnosis Brain/diagnostic imaging *Aphasia/etiology Paresis/etiology Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/complications/diagnosis *Apraxias/diagnosis/etiology *Eyelid Diseases/diagnosis/etiology
 Mice Animals Humans *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive/pathology *Disabled Persons *Motor Disorders *Multiple Sclerosis, Relapsing-Remitting/pathology Immunoglobulin G Disease Progression Cerebrospinal Fluid
 Child Humans *Multiple Sclerosis/complications/therapy/chemically induced Immunosuppressive Agents/therapeutic use Immunologic Factors/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Sleep
 Humans *Multiple Sclerosis/diagnosis Retrospective Studies *Multiple Sclerosis, Chronic Progressive/diagnosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis Biomarkers/cerebrospinal fluid Disease Progression
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Neurodegenerative Diseases Treatment Outcome Risk Assessment
 Humans Affective Symptoms/diagnosis/etiology/psychology *Multiple Sclerosis/complications/diagnosis/psychology Quality of Life *Bipolar Disorder/diagnosis Anxiety/diagnosis/etiology/psychology
 Humans *Ethnicity *Multiple Sclerosis/epidemiology/ethnology Prevalence United States/epidemiology Racial Groups
 Humans Female *Multiple Sclerosis/complications/diagnostic imaging Neuroimaging Magnetic Resonance Imaging *Migraine Disorders/diagnostic imaging Brain/diagnostic imaging
 Humans Male *Anti-N-Methyl-D-Aspartate Receptor Encephalitis/diagnosis/drug therapy/complications *Multiple Sclerosis/complications/diagnosis/drug therapy Autoantibodies Receptors, N-Methyl-D-Aspartate China
 Adult Humans *Multiple Sclerosis/complications/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Cognitive Dysfunction/drug therapy/etiology/prevention & control Cognition 4-Aminopyridine/therapeutic use
 Humans Male Female Adult *Multiple Sclerosis/epidemiology Australia/epidemiology *Multiple Sclerosis, Relapsing-Remitting/epidemiology Epidemiologic Studies
 Humans Caregivers Cross-Sectional Studies Health Services Needs and Demand *Multiple Sclerosis/therapy *Multiple Sclerosis, Chronic Progressive/therapy Referral and Consultation
 Humans *Multiple Sclerosis/diagnosis/epidemiology Cost-Benefit Analysis *Multiple Sclerosis, Relapsing-Remitting
 Humans *Alarmins/metabolism *Autoimmune Diseases/metabolism/pathology Cell Death Inflammation *Multiple Sclerosis/metabolism/pathology
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis/drug therapy *Multiple Sclerosis, Chronic Progressive/diagnosis/drug therapy Recurrence Disease Progression
 Humans *Vitamins Vitamin D/therapeutic use *Multiple Sclerosis/diagnostic imaging/drug therapy/chemically induced Dietary Supplements Recurrence
 Female Humans Male *Multiple Sclerosis/complications/epidemiology Prevalence *Sexual Dysfunction, Physiological/epidemiology/etiology *Sexual Dysfunctions, Psychological Sexual Behavior
 Humans Pakistan/epidemiology *Multiple Sclerosis/epidemiology/therapy
 Male Humans Female *Multiple Sclerosis/diagnosis Retrospective Studies Portugal Age of Onset Disease Progression *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis/diagnosis/genetics *B-Lymphocyte Subsets Risk Factors
 Humans *Obesity, Morbid/surgery *Multiple Sclerosis/complications/surgery Obesity/surgery *Bariatric Surgery Weight Loss Disease Progression
 Pregnancy Child Female Humans *Breast Feeding *Multiple Sclerosis/prevention & control/diagnosis Prospective Studies Perimenopause Hormone Replacement Therapy
 Humans *Mindfulness Comorbidity Quality of Life *Multiple Sclerosis/complications/therapy Bias
 Humans *Multiple Sclerosis/epidemiology/therapy Quality of Life Retrospective Studies Comorbidity Cost of Illness Health Care Costs
 Humans Adult *Multiple Sclerosis/complications/diagnostic imaging Nerve Fibers Tomography, Optical Coherence/methods Retina Cognition
 Humans *Multiple Sclerosis/drug therapy/pathology *Remyelination/physiology Myelin Sheath/pathology Inflammation/drug therapy Homeostasis
 Humans Female Male *Multiple Sclerosis/epidemiology Wales/epidemiology Disease Progression *Disabled Persons Disability Evaluation *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Female Humans Young Adult Adult Male *Multiple Sclerosis/diagnosis Delayed Diagnosis Egypt Disability Evaluation Recurrence *Multiple Sclerosis, Relapsing-Remitting
 Female Humans Middle Aged Adult *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis/pathology Magnetic Resonance Imaging Spinal Cord Brain/pathology Disease Progression
 Humans Causality Comorbidity Health Status *Multiple Sclerosis/complications/epidemiology/genetics Risk Factors Male Female
 Pregnancy Female Humans *Multiple Sclerosis/therapy *Pregnancy Complications/epidemiology/therapy
 Humans *Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/diagnostic imaging/drug therapy Prognosis Intermediate Filaments Biomarkers
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy Models, Statistical Recurrence Disease Progression *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Female Humans Adult *Multiple Sclerosis/complications Neuropsychological Tests Personality *Multiple Sclerosis, Relapsing-Remitting Personality Disorders/diagnosis/etiology
 Humans *Multiple Sclerosis/complications/therapy Randomized Controlled Trials as Topic Exercise Exercise Therapy Cognition
 Male Humans Adult *Multiple Sclerosis/complications/diagnosis Diplopia/diagnosis/etiology *Nystagmus, Pathologic/diagnosis/etiology Cerebellum/pathology Ataxia/pathology
 *Multiple Sclerosis/complications/diagnosis/genetics/pathology *Spinocerebellar Degenerations/complications/diagnosis/genetics/pathology Humans Male Adult Ataxia/genetics/pathology Brain/pathology Spinal Cord
 Humans *Multiple Sclerosis/drug therapy Quality of Life Disease Progression Neoplasm Recurrence, Local *Multiple Sclerosis, Chronic Progressive/diagnosis *Multiple Sclerosis, Relapsing-Remitting Italy Atrophy Delivery of Health Care
 Humans Female *Multiple Sclerosis/complications/diagnostic imaging/psychology *Cognitive Dysfunction Memory Disorders Chronic Disease Recurrence Cognition Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/complications/therapy *Music Therapy Gait *Music *Gait Disorders, Neurologic/etiology/therapy *Movement Disorders
 Humans *Multiple Sclerosis/complications/pathology Skin/pathology *Neuralgia Nerve Fibers, Unmyelinated/pathology Longitudinal Studies
 Humans *Multiple Sclerosis/complications/diagnosis Quality of Life *Multiple Sclerosis, Relapsing-Remitting/diagnosis/psychology *Cognitive Dysfunction/diagnosis/etiology *Cognition Disorders/diagnosis Neuropsychological Tests
 Humans *Multiple Sclerosis/therapy *Multiple Sclerosis, Chronic Progressive/therapy Stem Cell Transplantation *Neural Stem Cells
 Humans Male Female *Restless Legs Syndrome/epidemiology Prevalence *Multiple Sclerosis/complications/epidemiology Motivation
 Humans *Multiple Sclerosis/therapy Neurons Stem Cells *Amyotrophic Lateral Sclerosis
 Humans *Multiple Sclerosis/epidemiology Finland
 Adult Humans *Multiple Sclerosis/complications/epidemiology *Epilepsy/epidemiology Seizures Risk Factors Incidence
 Humans Vitamin D *Multiple Sclerosis/epidemiology/genetics *Vitamin D Deficiency Dietary Supplements Risk Factors
 Humans *Multiple Sclerosis/diagnostic imaging Retinal Ganglion Cells Artificial Intelligence Tomography, Optical Coherence Retina/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging
 Humans *Multiple Sclerosis/epidemiology/therapy Quality of Life Comorbidity Disease Progression
 Female Male Humans *Multiple Sclerosis/pathology Evoked Potentials, Visual Cross-Sectional Studies *Multiple Sclerosis, Relapsing-Remitting/pathology Saccades Atrophy/complications
 Humans *Multiple Sclerosis/complications/diagnosis Pupil/physiology Visual Field Tests/methods Visual Fields *Multiple Sclerosis, Chronic Progressive/diagnosis
 Humans *Multiple Sclerosis/complications/diagnosis Fatigue *Sleep Wake Disorders/diagnosis/epidemiology Sleep
 Humans *Multiple Sclerosis/prevention & control
 Humans Young Adult Adult *Multiple Sclerosis/epidemiology/therapy Pandemics *COVID-19/epidemiology *Telemedicine Health Facilities
 Humans Adult *Multiple Sclerosis/complications/diagnostic imaging *Sarcopenia *Demyelinating Diseases Magnetic Resonance Imaging Linear Models *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging Disability Evaluation Disease Progression *Multiple Sclerosis, Chronic Progressive
 Humans Aged *Multiple Sclerosis/diagnosis/epidemiology Cross-Sectional Studies Aging
 Adult Humans *Hemorrhagic Stroke/complications Retrospective Studies *Multiple Sclerosis/complications/diagnosis/epidemiology *Brain Edema Length of Stay Hospitals *Stroke/diagnosis/epidemiology/therapy
 Adult Humans Male Female *Multiple Sclerosis/epidemiology Iran Cross-Sectional Studies Age of Onset Disease Progression Demography *Multiple Sclerosis, Relapsing-Remitting *Multiple Sclerosis, Chronic Progressive
 Female Humans Dimethyl Fumarate/adverse effects *Multiple Sclerosis/drug therapy/chemically induced Immunosuppressive Agents/adverse effects Alopecia/chemically induced *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced
 Humans Male Female *Multiple Sclerosis/drug therapy Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Disease Progression Recurrence
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Tomography, Optical Coherence/methods *Multiple Sclerosis, Chronic Progressive/pathology *Retinal Degeneration/diagnostic imaging/pathology Atrophy/pathology Retina/diagnostic imaging/pathology
 Humans *Multiple Sclerosis/diagnosis/psychology Cognition
 Humans *Multiple Sclerosis/drug therapy/genetics Drug Repositioning Leukocytes, Mononuclear/metabolism Reproducibility of Results Single-Cell Gene Expression Analysis RNA/metabolism
 Humans *Multiple Sclerosis/therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Treatment Outcome *Hematopoietic Stem Cell Transplantation Transplantation, Autologous
 Male Humans Female *Multiple Sclerosis/drug therapy/epidemiology Immunosuppressive Agents/therapeutic use Interferon beta-1a/therapeutic use Cross-Sectional Studies *COVID-19 *Multiple Sclerosis, Relapsing-Remitting/drug therapy Glatiramer Acetate/therapeutic use Fingolimod Hydrochloride/therapeutic use Lebanon/epidemiology
 Humans *Multiple Sclerosis/drug therapy/chemically induced *Gastrointestinal Microbiome Crotonates/therapeutic use Interferon beta-1a
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Interferon-beta/adverse effects Cohort Studies Prospective Studies Spinal Cord/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Atrophy/pathology
 Humans Adult Middle Aged *Multiple Sclerosis/drug therapy/epidemiology SARS-CoV-2 COVID-19 Vaccines Iran/epidemiology *COVID-19
 Humans Black or African American *Exercise Therapy/psychology *Multiple Sclerosis/therapy/psychology Quality of Life *Resistance Training Randomized Controlled Trials as Topic Walking
 Humans *Transcranial Direct Current Stimulation/methods *Multiple Sclerosis/complications/therapy Quality of Life Evoked Potentials, Motor Brain Transcranial Magnetic Stimulation
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy/chemically induced Immunosuppressive Agents/adverse effects *Melanoma/drug therapy
 Humans *Multiple Sclerosis/epidemiology/therapy Iran/epidemiology Registries Neurologists
 Humans *Multiple Sclerosis/complications/diagnostic imaging *Disabled Persons *Motor Disorders Linear Models Surveys and Questionnaires
 Adult Humans *Multiple Sclerosis/diagnosis Disease Progression Recurrence *Disabled Persons *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis/complications/epidemiology/diagnosis Lithuania/epidemiology Oligoclonal Bands Optic Nerve Recurrence
 Humans *Facial Paralysis/diagnosis/etiology *Multiple Sclerosis/complications/diagnosis
 Humans *Multiple Sclerosis/complications/diagnosis Prospective Studies Longitudinal Studies Cognition *Cognitive Dysfunction/diagnosis/etiology
 Humans *Multiple Sclerosis/diagnosis/epidemiology/therapy *Demyelinating Diseases/diagnosis/pathology Follow-Up Studies Oligoclonal Bands Chronic Disease *Spinal Cord Diseases Magnetic Resonance Imaging
 Humans Middle Aged *Multiple Sclerosis/complications/psychology Social Cognition Cognition *Cognition Disorders/complications Neuropsychological Tests
 Male Humans Middle Aged Alemtuzumab/adverse effects *Multiple Sclerosis/diagnosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy/diagnosis Diagnosis, Differential Immunosuppression Therapy
 Adult Humans Middle Aged Aged *Multiple Sclerosis/complications/psychology *Memory, Episodic Neuropsychological Tests Cognition Executive Function/physiology Memory Disorders/diagnosis/etiology
 Humans *Multiple Sclerosis/therapy
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Brain Algorithms Head Image Enhancement
 Humans *Multiple Sclerosis/epidemiology/etiology *Hodgkin Disease/etiology *Inflammatory Bowel Diseases/epidemiology/etiology *Colitis, Ulcerative
 Animals Humans *Multiple Sclerosis/metabolism/pathology RNA, Messenger/genetics/metabolism Neurons/metabolism Brain/metabolism RNA/metabolism Acetyltransferases/metabolism
 Adult Aged Female Humans Male Middle Aged Cross-Sectional Studies Longitudinal Studies Magnetic Resonance Imaging *Multiple Sclerosis/complications/diagnostic imaging/pathology *Optic Neuritis/complications/diagnostic imaging/pathology Retina/diagnostic imaging/pathology Retinal Ganglion Cells Tomography, Optical Coherence *Cerebral Cortical Thinning/pathology *Retrograde Degeneration
 Humans *Multiple Sclerosis/complications/psychology Reproducibility of Results Neuropsychological Tests *Cognitive Dysfunction/etiology/complications Cognition Memory, Short-Term
 Humans *Multiple Sclerosis/drug therapy *Ferroptosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy/cerebrospinal fluid Disease Progression Axons/metabolism Chronic Disease
 Adult Humans *Multiple Sclerosis/complications/diagnostic imaging/epidemiology Retrospective Studies Age of Onset Disease Progression *Spinal Cord Diseases *Optic Nerve Diseases Disability Evaluation Recurrence *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/epidemiology
 Humans Female *Multiple Sclerosis/drug therapy Immunologic Factors/adverse effects *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/drug therapy Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced *Drug-Related Side Effects and Adverse Reactions/drug therapy Recurrence
 Humans *Multiple Sclerosis/complications Cognition Neuropsychological Tests *Cognitive Dysfunction/etiology
 Humans Disability Evaluation *Disabled Persons Disease Progression *Multiple Sclerosis/complications/genetics Multiple Sclerosis, Relapsing-Remitting Mutation
 Adult Humans Female Pregnancy *Multiple Sclerosis/diagnosis/epidemiology Cross-Sectional Studies *Multiple Sclerosis, Relapsing-Remitting/diagnosis/epidemiology Surveys and Questionnaires Contraceptives, Oral
 Humans Brain Diseases *Conversion Disorder *Multiple Sclerosis/diagnosis/therapy Nervous System Diseases/diagnosis/therapy Prospective Studies
 Child Humans *Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/diagnostic imaging/drug therapy Magnetic Resonance Imaging Treatment Outcome Immunosuppressive Agents/therapeutic use
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *White Matter/diagnostic imaging/pathology Algorithms
 Humans *Multiple Sclerosis/epidemiology/etiology/prevention & control *Diet, Mediterranean Risk Factors Case-Control Studies Diet Alcohol Drinking
 Humans *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/drug therapy *Multiple Sclerosis/psychology Prospective Studies *Cognitive Dysfunction/etiology Neuropsychological Tests Magnetic Resonance Imaging Cognition
 Humans Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy Recurrence Immunosuppressive Agents/therapeutic use
 Female Humans Adult Middle Aged Male *Metabolic Syndrome/epidemiology/complications *Multiple Sclerosis/complications/diagnostic imaging/epidemiology Cross-Sectional Studies Portugal/epidemiology Cholesterol, HDL
 Humans Incidence *Multiple Sclerosis/epidemiology/diagnosis Bayes Theorem Prevalence Italy/epidemiology Algorithms
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology Magnetic Resonance Imaging Brain/diagnostic imaging/pathology *Nervous System Diseases/pathology Software
 Humans *Multiple Sclerosis/complications/psychology Quality of Life/psychology East Asian People Disability Evaluation Depression/diagnosis Fatigue/diagnosis Surveys and Questionnaires
 Humans *Brain Ischemia/complications/diagnosis/therapy *Multiple Sclerosis/epidemiology/therapy/complications Treatment Outcome *Stroke/epidemiology/therapy *Ischemic Stroke/complications
 Humans Male Female *Multiple Sclerosis/complications/diagnosis Retina *Phlebitis/etiology/complications *Retinal Vein
 Humans Natalizumab/adverse effects *Multiple Sclerosis/diagnostic imaging/drug therapy/chemically induced Cohort Studies Follow-Up Studies Treatment Outcome Antibodies Denmark/epidemiology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Immunologic Factors/adverse effects
 Humans Rituximab/therapeutic use *Multiple Sclerosis/drug therapy Immunologic Factors/therapeutic use Mexico Tertiary Care Centers *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced
 Humans Female *Multiple Sclerosis/complications/epidemiology/psychology Depression/complications Quality of Life Anxiety/complications Anxiety Disorders/complications
 Humans *Multiple Sclerosis/drug therapy Models, Statistical Prognosis Disease Progression *Multiple Sclerosis, Chronic Progressive/drug therapy Recurrence *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Caudate Nucleus Feedback Magnetic Resonance Imaging/methods *Multiple Sclerosis/complications/diagnostic imaging Prefrontal Cortex Reward *Ventral Striatum
 Humans *Multiple Sclerosis, Chronic Progressive/diagnosis *Multiple Sclerosis Portugal Disease Progression Biomarkers
 Adult Humans *Mendelian Randomization Analysis/methods *Multiple Sclerosis/epidemiology/genetics Genome-Wide Association Study/methods Risk Factors Causality Polymorphism, Single Nucleotide
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Choroid Plexus/diagnostic imaging Magnetic Resonance Imaging Brain/pathology *Neuromyelitis Optica/pathology Atrophy/pathology *Neurodegenerative Diseases/pathology
 Humans Decision Support Techniques *Multiple Sclerosis/therapy Patient Participation Qualitative Research *Multiple Sclerosis, Relapsing-Remitting Decision Making
 Humans Female Adult *Multiple Sclerosis/diagnosis/therapy Prospective Studies Walking Disability Evaluation Physical Therapy Modalities
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Retrograde Degeneration/pathology *Optic Neuritis/diagnostic imaging/etiology Retina/diagnostic imaging/pathology Magnetic Resonance Imaging Tomography, Optical Coherence Atrophy/pathology
 Female Humans Child, Preschool Natalizumab/therapeutic use *Multiple Sclerosis/complications/drug therapy Immunologic Factors/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Speech Phonetics *Multiple Sclerosis/diagnosis/complications Speech Acoustics Dysarthria/diagnosis/etiology
 Humans *Multiple Sclerosis/diagnosis/drug therapy Inflammation
 Humans *Acupressure/methods *Multiple Sclerosis/complications/therapy Renal Dialysis/adverse effects Fatigue/etiology/therapy Surveys and Questionnaires
 Humans Switzerland/epidemiology *Multiple Sclerosis/epidemiology/therapy Cross-Sectional Studies Activities of Daily Living Mental Health
 Humans *Multiple Sclerosis/complications/psychology Reproducibility of Results Anxiety Chronic Disease Adaptation, Psychological
 Child Humans *Multiple Sclerosis/psychology *Multiple Sclerosis, Chronic Progressive/complications/diagnostic imaging Follow-Up Studies Magnetic Resonance Imaging Cognition Disease Progression
 Male Humans *Multiple Sclerosis/diagnostic imaging/drug therapy *Cannabidiol/therapeutic use Dronabinol/therapeutic use *Cannabinoids Drug Combinations Muscle Spasticity/diagnostic imaging/drug therapy
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy Immunologic Factors/adverse effects Antibodies, Monoclonal, Humanized/adverse effects *Pericarditis/chemically induced/diagnostic imaging/drug therapy
 Male Female Humans *Nicolau Syndrome/etiology/pathology/therapy *Multiple Sclerosis/drug therapy/complications Retrospective Studies Glatiramer Acetate/adverse effects Skin
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive Rituximab/adverse effects *Neutropenia
 Humans Palliative Care/methods *Multiple Sclerosis/complications/therapy Quality of Life *Terminal Care *Hospice and Palliative Care Nursing
 Humans *Extended Family Bayes Theorem *Multiple Sclerosis/epidemiology/genetics Climate Environmental Exposure
 Adolescent Humans Male *Multiple Sclerosis/complications/diagnosis *COVID-19 Magnetic Resonance Imaging/methods Paralysis/complications *Strabismus
 Humans *Multiple Sclerosis/complications Emotions *Demyelinating Diseases Fixation, Ocular Eye Movements *Autoimmune Diseases of the Nervous System *Multiple Sclerosis, Chronic Progressive
 Humans *Multiple Sclerosis/diagnosis/therapy Retrospective Studies New York *Disabled Persons
 Humans *Multiple Sclerosis/epidemiology/therapy Europe/epidemiology France/epidemiology Caribbean Region/epidemiology Ethnicity
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *Cervical Cord/diagnostic imaging/pathology Spinal Cord/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Disease Progression Atrophy/pathology *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology
 Humans *Multiple Sclerosis/complications/diagnosis Apolipoprotein A-I Cholesterol, LDL Cross-Sectional Studies Cholesterol Cholesterol, HDL Apolipoproteins B Apolipoproteins E Biomarkers Apolipoproteins C
 Humans *Glymphatic System *Multiple Sclerosis/diagnosis/etiology Brain Basal Ganglia Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology Disease Progression Brain/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/complications/drug therapy *Monkeypox/complications Immunosuppressive Agents/adverse effects *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy
 Male Humans Female Adult Middle Aged *Multiple Sclerosis/complications/diagnostic imaging/pathology Brain Mapping/methods Depression/diagnostic imaging/etiology Dopamine Prospective Studies Serotonin Magnetic Resonance Imaging/methods Brain/pathology Fatigue/etiology
 Humans *Multiple Sclerosis/psychology Neoplasm Recurrence, Local Systematic Reviews as Topic Meta-Analysis as Topic *Multiple Sclerosis, Chronic Progressive/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging
 Female Humans Prevalence Sclerosis *Sexual Dysfunction, Physiological/epidemiology/etiology *Multiple Sclerosis/complications/epidemiology *Sexual Dysfunctions, Psychological/epidemiology/etiology
 Adult Humans Female Male *Multiple Sclerosis/drug therapy/psychology Cohort Studies Quality of Life Patient Reported Outcome Measures
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy Disease Progression Chronic Disease Magnetic Resonance Imaging Recurrence *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Retrospective Studies
 Humans Female Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy/epidemiology *Multiple Sclerosis, Relapsing-Remitting/drug therapy/epidemiology Cohort Studies Natalizumab/adverse effects Recurrence Immunosuppressive Agents/adverse effects
 Humans *Multiple Sclerosis/chemically induced Immunologic Factors/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Healthy Aging Magnetic Resonance Imaging Recurrence Inflammation *Multiple Sclerosis, Chronic Progressive
 Humans *Multiple Sclerosis/drug therapy/genetics/pathology Up-Regulation Cholecalciferol Leukocytes, Mononuclear/pathology *MicroRNAs/genetics Dietary Supplements
 Adult Humans *Multiple Sclerosis/complications/diagnosis/pathology *Vestibular Evoked Myogenic Potentials/physiology *Vestibule, Labyrinth Patient Acuity Head Impulse Test
 Child Humans Young Adult Adult *Immunosuppressive Agents/therapeutic use *Multiple Sclerosis/drug therapy/epidemiology Alberta/epidemiology Fingolimod Hydrochloride/therapeutic use Retrospective Studies
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology *Multiple Sclerosis, Chronic Progressive/diagnosis/pathology Brain/diagnostic imaging/pathology Atrophy/pathology Recurrence *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Magnetic Resonance Imaging Disease Progression
 Humans *Multiple Sclerosis/diagnosis/epidemiology Delivery of Health Care Health Personnel Health Care Costs Neurologists
 Humans *Multiple Sclerosis/complications/drug therapy Baclofen/therapeutic use Cohort Studies Sweden/epidemiology Muscle Spasticity/drug therapy/etiology *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/diagnosis/genetics/cerebrospinal fluid Argentina Magnetic Resonance Imaging Asia Oligoclonal Bands/cerebrospinal fluid
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy Biomarkers Inflammation *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/therapy *Multiple Sclerosis, Chronic Progressive Immunotherapy Proportional Hazards Models Recurrence *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis/complications/diagnostic imaging/cerebrospinal fluid Iron Magnetic Resonance Imaging Immunoglobulin G Inflammation/pathology Brain/pathology
 Female Humans Male Alemtuzumab/adverse effects *Multiple Sclerosis/diagnostic imaging/drug therapy/chemically induced Kuwait *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/psychology *Cognitive Dysfunction *Cognition Disorders Cognition Neuropsychological Tests
 Humans *Multiple Sclerosis/diagnostic imaging Veins Magnetic Resonance Imaging
 Adult Pregnancy Female Child Humans *Multiple Sclerosis/epidemiology/etiology Risk Factors Environmental Exposure/adverse effects Disease Progression
 Humans *Multiple Sclerosis/complications/diagnostic imaging *Brain Injuries Atrophy *Neurodegenerative Diseases Brain/diagnostic imaging
 Humans *Multiple Sclerosis/complications/therapy/psychology Health Personnel Social Support Qualitative Research Social Workers
 Humans Forkhead Transcription Factors/genetics/metabolism Gene Expression Leukocytes, Mononuclear/metabolism *Multiple Sclerosis/genetics/metabolism *Multiple Sclerosis, Chronic Progressive/genetics/metabolism T-Lymphocytes, Regulatory
 Humans *Multiple Sclerosis/diagnosis Brain-Derived Neurotrophic Factor Interleukin-10 Prognosis Nerve Growth Factor Core Binding Factor Alpha 2 Subunit/genetics *RNA, Long Noncoding *Multiple Sclerosis, Relapsing-Remitting/diagnosis RNA, Messenger *Multiple Sclerosis, Chronic Progressive
 Humans Female Male *COVID-19 *Multiple Sclerosis/epidemiology/therapy Pandemics Nerve Tissue Proteins Patient-Centered Care Quality of Health Care
 Humans *Multiple Sclerosis/complications/therapy/diagnosis *Mindfulness Retrospective Studies Brain Fatigue/etiology/therapy Neuropsychological Tests
 Pregnancy Humans Female Autoantibodies *Neuromyelitis Optica/complications *Multiple Sclerosis/diagnosis/drug therapy Rituximab Recurrence
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Cross-Sectional Studies Retina/diagnostic imaging *Retinal Diseases Tomography, Optical Coherence
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Biomarkers Lymphocytes/pathology Blood Platelets Neutrophils Retrospective Studies Inflammation
 Humans *Multiple Sclerosis/diagnosis/diagnostic imaging Brain Paralysis
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis/psychology *Multiple Sclerosis Speech Cognition Memory, Short-Term
 Humans Female Young Adult Adult Male *Multiple Sclerosis/diagnostic imaging/epidemiology/drug therapy Immunosuppressive Agents/therapeutic use Immunologic Factors/therapeutic use Retrospective Studies Oman/epidemiology *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis, Chronic Progressive/complications/diagnostic imaging/pathology *Multiple Sclerosis/complications *Multiparametric Magnetic Resonance Imaging *Cognition Disorders/psychology Cognition Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/complications/diagnosis Quality of Life *Cognition Disorders/etiology Executive Function Cognition Neuropsychological Tests *Cognitive Dysfunction/etiology/complications
 Humans *Multiple Sclerosis/complications/diagnostic imaging *Cerebral Veins/diagnostic imaging/physiology Dilatation Fatigue/etiology
 Humans Cladribine/pharmacology/therapeutic use *Multiple Sclerosis/drug therapy/genetics/metabolism Leukocytes, Mononuclear/metabolism Proteomics *MicroRNAs/metabolism Biomarkers
 Humans *Multiple Sclerosis/complications Visual Perception Space Perception Cognition Neuropsychological Tests
 Humans *Learning Health System *Multiple Sclerosis/diagnosis/therapy *Neurodegenerative Diseases Retrospective Studies Algorithms
 Humans Adult *Multiple Sclerosis/therapy Czech Republic *Mobile Applications Life Style Healthy Lifestyle
 Humans *Multiple Sclerosis/diagnosis *Multiple Sclerosis, Chronic Progressive/therapy Nerve Growth Factors *Mesenchymal Stem Cells Biomarkers
 Male Animals Mice Mice, Inbred C57BL Antioxidants/pharmacology *Multiple Sclerosis/drug therapy/veterinary Cuprizone Glutathione Peroxidase Superoxide Dismutase *Rodent Diseases
 Male Female Pregnancy Humans Cohort Studies *Multiple Sclerosis/diagnosis/epidemiology/therapy Pregnancy Rate Semen Reproductive Techniques, Assisted/adverse effects Fertilization in Vitro/adverse effects Denmark/epidemiology
 Humans Antibodies, Monoclonal Cognition Cohort Studies Immunologic Factors/therapeutic use *Multiple Sclerosis/complications/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab/therapeutic use
 Humans *Multiple Sclerosis/complications/epidemiology *Cardiovascular Diseases/complications/epidemiology Cognition *Cognitive Dysfunction/epidemiology/etiology/diagnosis Comorbidity Neuropsychological Tests
 Humans Male *Multiple Sclerosis Antioxidants Oxidative Stress Disease Progression Central Nervous System *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis, Relapsing-Remitting
 Male Humans Female Adult Middle Aged *Multiple Sclerosis/drug therapy/chemically induced Immunosuppressive Agents/therapeutic use Fingolimod Hydrochloride/therapeutic use Glatiramer Acetate/therapeutic use Dimethyl Fumarate/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *Glymphatic System/diagnostic imaging Cohort Studies Brain/pathology *Vascular Diseases
 Humans Nutritional Status Prevalence *Multiple Sclerosis/complications/epidemiology *Malnutrition/diagnosis/epidemiology Obesity
 Female Humans Adult Middle Aged Male *Multiple Sclerosis/complications/diagnosis/psychology Feasibility Studies Smartphone Quality of Life Cognition
 Humans Pandemics *Multiple Sclerosis/drug therapy/epidemiology *COVID-19/epidemiology Communicable Disease Control Drug Prescriptions
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Neurons/physiology Cerebellum Cellular Senescence *Alzheimer Disease/pathology
 Animals Male Mice Antioxidants/pharmacology/therapeutic use *Cuprizone/toxicity Disease Models, Animal Mice, Inbred C57BL *Multiple Sclerosis/chemically induced/drug therapy/prevention & control
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology *Trigeminal Neuralgia/etiology/complications Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging *Multiple Sclerosis, Chronic Progressive Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/therapy/psychology Cross-Sectional Studies Psychotherapy *Cognitive Behavioral Therapy Counseling
 Humans Dimethyl Fumarate/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy Diffusion Tensor Imaging *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Adult Middle Aged *Multiple Sclerosis/complications/diagnosis/epidemiology Quality of Life Nutritional Status *Deglutition Disorders Cross-Sectional Studies Disability Evaluation Fatigue/diagnosis/epidemiology/etiology Depression/diagnosis/epidemiology/etiology *Malnutrition/diagnosis/epidemiology/etiology
 Humans *Depression/epidemiology *Multiple Sclerosis/complications/epidemiology Anxiety/epidemiology Anxiety Disorders United Kingdom/epidemiology
 Pregnancy Female Humans *Multiple Sclerosis/drug therapy Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence
 Young Adult Humans Male Female Adult *Multiple Sclerosis/drug therapy/epidemiology Saudi Arabia/epidemiology *Multiple Sclerosis, Relapsing-Remitting/drug therapy/epidemiology *Physicians *Multiple Sclerosis, Chronic Progressive/drug therapy
 Adult Humans *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods
 Humans Prospective Studies Reproducibility of Results Quality of Life Pilot Projects *Multiple Sclerosis/complications/diagnosis *Rectal Diseases Surveys and Questionnaires Psychometrics/methods
 Humans *Multiple Sclerosis/diagnosis/drug therapy/epidemiology *Diabetes Mellitus, Type 2 Antihypertensive Agents/therapeutic use *Hypertension/diagnosis/drug therapy/epidemiology Hypoglycemic Agents Lipids
 Humans *Multiple Sclerosis/etiology/therapy Central Nervous System Immune System/metabolism Immune Tolerance
 Humans Activities of Daily Living *Multiple Sclerosis/epidemiology/therapy Sweden/epidemiology Cross-Sectional Studies Income *Disabled Persons
 Humans *Multiple Sclerosis/complications/diagnosis *Central Nervous System Vascular Malformations
 Humans *Interferon-beta/pharmacology *Multiple Sclerosis/drug therapy/genetics/chemically induced Treatment Outcome
 Humans *Technology Assessment, Biomedical *Multiple Sclerosis/diagnosis/drug therapy Cost-Benefit Analysis European Union Netherlands
 Humans Female Adult Middle Aged *Multiple Sclerosis/drug therapy Alemtuzumab/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Retrospective Studies Cost-Benefit Analysis
 Humans *Multiple Sclerosis/complications/diagnostic imaging/drug therapy Topiramate/therapeutic use *Nystagmus, Pathologic/drug therapy/etiology Eye Movements
 Young Adult Humans *Affective Symptoms/diagnosis/etiology/psychology *Multiple Sclerosis/complications/psychology Cross-Sectional Studies Adaptation, Psychological Emotions
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy/metabolism *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Microglia/metabolism/pathology Brain/pathology *White Matter/pathology Magnetic Resonance Imaging Inflammation/pathology Iron/metabolism Receptors, GABA/metabolism
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Central Nervous System Diseases/pathology Atrophy/pathology
 Humans Alemtuzumab/adverse effects *Multiple Sclerosis/drug therapy/chemically induced *Multiple Sclerosis, Relapsing-Remitting Central Nervous System
 Humans *Multiple Sclerosis/diagnostic imaging/therapy *Neurology Magnetic Resonance Imaging/methods Communication Consensus
 Pregnancy Female Humans Glatiramer Acetate/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence Bridge Therapy Immunosuppressive Agents/therapeutic use
 Adult Female Humans Male Antibodies, Monoclonal, Humanized Infusions, Intravenous *Multiple Sclerosis/drug therapy/etiology Patient Outcome Assessment
 Humans *Multiple Sclerosis *Chitinases Biomarkers *Multiple Sclerosis, Chronic Progressive/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting Disease Progression
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology *Cognition Disorders/psychology Processing Speed Cognition/physiology Magnetoencephalography/methods Magnetic Resonance Imaging Neuropsychological Tests Brain/pathology
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis/cerebrospinal fluid *Multiple Sclerosis/diagnosis Sulfoglycosphingolipids/cerebrospinal fluid/chemistry Cross-Sectional Studies *Multiple Sclerosis, Chronic Progressive/diagnosis/cerebrospinal fluid Biomarkers/cerebrospinal fluid Protein Isoforms
 Humans Female Adult Male *Multiple Sclerosis/complications/drug therapy Rituximab *COVID-19/complications *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy SARS-CoV-2
 Male Humans Female *Multiple Sclerosis/complications/psychology Cross-Sectional Studies *Motor Disorders *Neurodegenerative Diseases Depression/epidemiology/psychology Cognition
 Humans *Multiple Sclerosis/epidemiology/etiology *Epstein-Barr Virus Infections/complications Quality of Life Moon Herpesvirus 4, Human Recurrence
 Humans *Multiple Sclerosis/complications/diagnosis/psychology Reproducibility of Results Neuropsychological Tests *Cognitive Dysfunction/diagnosis/etiology Cognition
 Male Humans Young Adult Adult Vitreous Body/surgery CD8-Positive T-Lymphocytes *Multiple Sclerosis/complications/diagnosis *Uveitis/diagnosis/etiology/drug therapy Vitrectomy Inflammation
 Humans *Multiple Sclerosis/complications/diagnosis Retinal Ganglion Cells Retrospective Studies Cross-Sectional Studies Tomography, Optical Coherence *Optic Neuritis/diagnosis/etiology
 Humans *Multiple Sclerosis/epidemiology/complications Prospective Studies Diet Life Style Surveys and Questionnaires
 Humans Female Male Adult Dimethyl Fumarate/adverse effects *Multiple Sclerosis/diagnostic imaging/drug therapy/chemically induced Immunosuppressive Agents/therapeutic use Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Medication Adherence Recurrence Outcome Assessment, Health Care
 Animals Mice *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology *Fluorine-19 Magnetic Resonance Imaging Pharmaceutical Preparations *Multiple Sclerosis, Chronic Progressive Magnetic Resonance Imaging/methods Sphingosine-1-Phosphate Receptors
 Middle Aged Humans *Multiple Sclerosis/diagnostic imaging/drug therapy Fingolimod Hydrochloride/therapeutic use Natalizumab/therapeutic use *Multiple Sclerosis, Relapsing-Remitting Retrospective Studies Recurrence Immunosuppressive Agents/therapeutic use
 Humans *Multiple Sclerosis/genetics/metabolism Leukocytes, Mononuclear/metabolism Iran *MicroRNAs/metabolism *Multiple Sclerosis, Relapsing-Remitting/genetics
 Humans *Multiple Sclerosis, Relapsing-Remitting/complications/therapy *Multiple Sclerosis/etiology Quality of Life *Acupuncture Therapy/adverse effects Fatigue/etiology/therapy Amantadine
 Male Adult Humans Female Middle Aged *Multiple Sclerosis/diagnosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis Reproducibility of Results Pandemics *COVID-19/diagnosis
 Adult Humans Middle Aged Atrophy/drug therapy/pathology Brain/drug effects/pathology Glatiramer Acetate/therapeutic use/pharmacology Glia Maturation Factor/pharmacology *Gray Matter/drug effects/pathology Magnetic Resonance Imaging Multiple Sclerosis/diagnostic imaging/drug therapy/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/pathology Pilot Projects
 Female Humans Adult Male *Multiple Sclerosis/diagnostic imaging Retrospective Studies Follow-Up Studies *Multiple Sclerosis, Chronic Progressive Brain *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging Magnetic Resonance Imaging Disability Evaluation Disease Progression
 Humans Female Male *Multiple Sclerosis, Relapsing-Remitting/complications/epidemiology *Multiple Sclerosis/diagnosis Retrospective Studies *Cardiovascular Diseases/epidemiology/etiology Disease Progression Risk Factors *Multiple Sclerosis, Chronic Progressive Heart Disease Risk Factors
 Humans Male Female Adult Middle Aged *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Brain/metabolism Magnetic Resonance Spectroscopy Receptors, Antigen, T-Cell/metabolism
 Humans Adolescent Adult *Multiple Sclerosis/therapy Quality of Life *Multiple Sclerosis, Relapsing-Remitting/therapy Palliative Care Surveys and Questionnaires
 Humans *COVID-19 *Multiple Sclerosis/complications/epidemiology/drug therapy Case-Control Studies Retrospective Studies Bayes Theorem Vitamin D/therapeutic use Risk Factors
 Humans Female *Multiple Sclerosis/diagnostic imaging Intermediate Filaments/pathology Biomarkers/cerebrospinal fluid Magnetic Resonance Imaging Demography *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis/blood/diagnosis Multivariate Analysis *Plasma/chemistry *Spectroscopy, Fourier Transform Infrared/methods Biomarkers/blood
 Adult Humans Female Male *Multiple Sclerosis/drug therapy/epidemiology Retrospective Studies Cohort Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy/epidemiology Recurrence Chronic Disease United Kingdom/epidemiology
 Humans *Multiple Sclerosis/complications/psychology Processing Speed Neuropsychological Tests Fatigue/diagnosis/etiology *Cognition Disorders/diagnosis
 Adult Child Humans Crotonates/therapeutic use Immunosuppressive Agents/therapeutic use *Multiple Sclerosis/drug therapy/chemically induced *Multiple Sclerosis, Relapsing-Remitting/drug therapy Toluidines/therapeutic use
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology *Cognitive Dysfunction/etiology/complications Gray Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Neuropsychological Tests Cerebral Cortex/pathology Brain/pathology
 Humans *Multiple Sclerosis/complications/psychology Quality of Life/psychology Longitudinal Studies Anxiety/etiology Fatigue/psychology
 Humans Child *Multiple Sclerosis/complications/diagnosis/psychology Case-Control Studies Cognition *Cognitive Dysfunction/etiology/complications Fatigue/etiology/complications Neuropsychological Tests
 Humans *Depression/diagnosis Patient Health Questionnaire *Multiple Sclerosis/complications/psychology Surveys and Questionnaires Patient Reported Outcome Measures Psychometrics
 Humans Biomarkers *Multiple Sclerosis/diagnosis Phenotype
 Adult Humans Child Adolescent *Immunosuppressive Agents/therapeutic use *Multiple Sclerosis/diagnostic imaging/drug therapy/epidemiology Fingolimod Hydrochloride/therapeutic use Recurrence Disease Progression Demography
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Pyramidal Tracts/diagnostic imaging Retrospective Studies Disease Progression Spinal Cord/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Spinal Cord Diseases/diagnostic imaging/pathology
 Humans *Multiple Sclerosis/complications Neuropsychological Tests
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Neuropsychological Tests Magnetic Resonance Imaging Tongue
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/etiology Retrospective Studies Treatment Outcome *Hematopoietic Stem Cell Transplantation Denmark
 Adult Humans Cognition Depression/psychology Fatigue/psychology *Multiple Sclerosis/complications/psychology Neuropsychological Tests Perception Processing Speed Middle Aged
 Humans *Multiple Sclerosis/drug therapy Immunologic Factors/therapeutic use *Multiple Sclerosis, Chronic Progressive/drug therapy Interferon beta-1a/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Antibodies, Monoclonal, Humanized/adverse effects Immunologic Factors/adverse effects *Leukoencephalopathy, Progressive Multifocal/chemically induced *Multiple Sclerosis/drug therapy/chemically induced *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Natalizumab/adverse effects Adolescent Young Adult Adult Middle Aged Aged
 Humans Female Bupropion/adverse effects *Multiple Sclerosis/complications/drug therapy/chemically induced Quality of Life *Sexual Dysfunction, Physiological/drug therapy/etiology Fatigue/drug therapy/etiology Double-Blind Method
 Humans *Multiple Sclerosis/diagnosis/psychology/rehabilitation *Cognition Disorders Hospitals Patients
 Humans *Multiple Sclerosis/diagnosis/psychology *Cognitive Dysfunction/diagnosis/etiology/psychology *Cognition Disorders Cognition Phenotype Neuropsychological Tests
 Humans Female Male Natalizumab/adverse effects *Multiple Sclerosis/drug therapy/epidemiology/chemically induced Austria/epidemiology *Multiple Sclerosis, Relapsing-Remitting/drug therapy/epidemiology/chemically induced *Leukoencephalopathy, Progressive Multifocal Registries Immunologic Factors/adverse effects
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Retrospective Studies Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Atrophy/pathology *Multiple Sclerosis, Relapsing-Remitting/pathology
 Humans *Multiple Sclerosis/diagnostic imaging/therapy/complications Brain/pathology Gray Matter/pathology Cerebral Cortex/pathology Walking Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/diagnosis *Cognition Disorders Neuropsychological Tests
 Humans Black or African American Demography Hispanic or Latino *Multiple Sclerosis/diagnosis/drug therapy/epidemiology/ethnology *Multiple Sclerosis, Relapsing-Remitting/drug therapy Adolescent Young Adult Adult Middle Aged Aged
 Humans *Cervical Cord/diagnostic imaging/pathology *Multiple Sclerosis/pathology Spinal Cord/diagnostic imaging/pathology *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology Gray Matter/pathology Magnetic Resonance Imaging Atrophy/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis/genetics *Multiple Sclerosis *Ferroptosis/genetics *Neurodegenerative Diseases Protein Serine-Threonine Kinases
 Humans *Multiple Sclerosis/complications/diagnosis/psychology Social Cognition Cognition Fatigue/diagnosis/etiology/psychology Neuropsychological Tests *Stroke/complications
 Young Adult Humans Aged *Multiple Sclerosis/diagnostic imaging/drug therapy Single-Blind Method Magnetic Resonance Imaging Neuroimaging Treatment Outcome Double-Blind Method
 Humans *Multiple Sclerosis/complications/diagnostic imaging Lower Extremity Gray Matter *Mobile Applications Neuroimaging
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *Neurodegenerative Diseases/pathology Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology Machine Learning
 Humans *Vestibular Evoked Myogenic Potentials/physiology *Multiple Sclerosis/diagnosis/pathology Brain Stem Magnetic Resonance Imaging
 Humans *Stuttering/diagnostic imaging/etiology *Multiple Sclerosis/complications/diagnostic imaging Frontal Lobe/diagnostic imaging Language Recurrence
 Pregnancy Animals Rabbits Female Male *Multiple Sclerosis/therapy/etiology Anti-Mullerian Hormone *Hematopoietic Stem Cell Transplantation/adverse effects Cyclophosphamide Ovary Transplantation, Autologous
 Humans *Multiple Sclerosis/complications *Cardiorespiratory Fitness Thalamus *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology Magnetic Resonance Imaging Atrophy/pathology
 Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy/pathology Recurrence
 Humans *Multiple Sclerosis/complications/psychology Reproducibility of Results Pandemics *COVID-19/complications *Cognitive Dysfunction/diagnosis/etiology Neuropsychological Tests Cognition
 Humans *Multiple Sclerosis/complications Task Performance and Analysis Brain/pathology Brain Mapping *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/complications/drug therapy *Leukoencephalopathy, Progressive Multifocal/drug therapy/etiology Immune Checkpoint Inhibitors/therapeutic use Natalizumab/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy *JC Virus
 Adult Humans Middle Aged *Chronic Pain/drug therapy/epidemiology/complications *Cannabis *Medical Marijuana/therapeutic use *Multiple Sclerosis/complications/epidemiology/drug therapy *Neuralgia/complications
 Humans *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis NK Cell Lectin-Like Receptor Subfamily K/metabolism CD8-Positive T-Lymphocytes *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis/diagnosis Granzymes *Multiple Sclerosis, Chronic Progressive/diagnosis CD8-Positive T-Lymphocytes T-Lymphocyte Subsets *Multiple Sclerosis, Relapsing-Remitting/diagnosis
 Humans Female Middle Aged Male *Multiple Sclerosis/complications/epidemiology Quality of Life Cross-Sectional Studies Fear *Wheelchairs
 Humans *Multiple Sclerosis/pathology *Multiple Sclerosis, Chronic Progressive/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods
 Male Humans Female *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive Knee Joint Gait Range of Motion, Articular *Multiple Sclerosis, Relapsing-Remitting
 Humans Female Middle Aged *Multiple Sclerosis/complications/epidemiology Quality of Life *Disabled Persons Exercise Comorbidity Disease Progression Fatigue/etiology
 Humans *Multiple Sclerosis/therapy/psychology Psychosocial Intervention Quality of Life Feasibility Studies Anxiety/therapy/psychology
 Humans Rituximab/therapeutic use *Multiple Sclerosis/diagnostic imaging/drug therapy Quality of Life Immunologic Factors/therapeutic use Prospective Studies *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Costs and Cost Analysis Salaries and Fringe Benefits
 Humans *Multiple Sclerosis/complications/psychology Feedback Motivation *Cognitive Dysfunction/complications Fatigue/complications Cognition/physiology
 Humans Female *Multiple Sclerosis, Relapsing-Remitting/therapy/psychology *Multiple Sclerosis/complications/therapy Quality of Life *Acupressure Cognition
 Humans Adult *Multiple Sclerosis/diagnosis/therapy/epidemiology Consensus Pandemics *COVID-19 *Telemedicine Recurrence
 Humans Cost of Illness East Asian People *Multiple Sclerosis, Chronic Progressive/complications/epidemiology *Multiple Sclerosis, Relapsing-Remitting/complications/epidemiology
 Humans Female Adult Male *Multiple Sclerosis/diagnosis/cerebrospinal fluid Prospective Studies Intermediate Filaments Biomarkers/cerebrospinal fluid *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/cerebrospinal fluid Disease Progression Recurrence Chemokine CXCL13
 Humans *Multiple Sclerosis/drug therapy/genetics Leukocytes, Mononuclear Interferon beta-1a/pharmacology Antiviral Agents/pharmacology Signal Transduction
 Humans Dimethyl Fumarate/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy/pathology Recurrence
 Humans *Glomerulosclerosis, Focal Segmental/complications/diagnosis/drug therapy *Multiple Sclerosis/complications/diagnosis/drug therapy Kidney Biopsy/adverse effects
 Humans Administration, Intravenous *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab/therapeutic use
 Humans *Multiple Sclerosis/diagnosis/cerebrospinal fluid Oligoclonal Bands/cerebrospinal fluid Immunoglobulin G Immunoglobulin kappa-Chains Immunoblotting Isoelectric Focusing
 Humans *Quality of Life Cross-Sectional Studies *Multiple Sclerosis/epidemiology/therapy/complications Delivery of Health Care Patient Acceptance of Health Care
 Humans *Multiple Sclerosis/diagnosis/drug therapy Fingolimod Hydrochloride/therapeutic use Interferon-gamma Enzyme-Linked Immunosorbent Assay Immune System *Multiple Sclerosis, Relapsing-Remitting
 Humans Female Adult *Multiple Sclerosis/complications/psychology *Cognition Disorders/diagnosis/etiology/psychology Trail Making Test Neuropsychological Tests *Cognitive Dysfunction/diagnosis/etiology Cognition
 Adult Humans Female Middle Aged Male *Multiple Sclerosis/genetics *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis, Relapsing-Remitting Genetic Association Studies United Kingdom
 Humans *Multiple Sclerosis/diagnosis/therapy Feasibility Studies Quality of Life Single-Blind Method *COVID-19 Cognition Occupations Randomized Controlled Trials as Topic
 Humans Cross-Sectional Studies Affective Symptoms/epidemiology/psychology *Multiple Sclerosis/epidemiology/psychology Anxiety/epidemiology/psychology *Neuralgia/epidemiology Cognition
 Humans Female Adult Male *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Cross-Sectional Studies Jordan Medication Adherence
 Humans *Multiple Sclerosis/genetics/therapy/metabolism Signal Transduction *Mesenchymal Stem Cells Cell Differentiation
 Adult Humans *Multiple Sclerosis/diagnosis/diagnostic imaging Magnetic Resonance Imaging Mutation *Leukoencephalopathies/diagnostic imaging/genetics Receptor Protein-Tyrosine Kinases Spinal Cord/pathology
 Humans *Multiple Sclerosis/diagnostic imaging/epidemiology Cohort Studies Retrospective Studies Magnetic Resonance Imaging/methods *Demyelinating Diseases/diagnostic imaging/epidemiology/pathology
 Adult Humans Lutein Single-Blind Method *Multiple Sclerosis/complications/drug therapy Zeaxanthins Dietary Supplements Cognition *Macular Pigment
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Quality of Life Research Design Patient Reported Outcome Measures
 Humans *Multiple Sclerosis/diagnosis/genetics Causality Metabolomics *Disabled Persons Biomarkers Disease Progression
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging Longitudinal Studies
 Humans Female Infant *Multiple Sclerosis/diagnostic imaging/pathology Imaging, Three-Dimensional/methods Magnetic Resonance Imaging/methods Image Enhancement Neuroimaging
 Humans *Multiple Sclerosis/diagnosis Diagnosis, Differential Consensus
 Humans *Multiple Sclerosis/drug therapy Retrospective Studies *Physicians Perception *Multiple Sclerosis, Relapsing-Remitting
 Female Humans *Multiple Sclerosis/complications/therapy Pandemics *Multiple Sclerosis, Relapsing-Remitting/therapy Treatment Outcome *COVID-19 SARS-CoV-2 *Hematopoietic Stem Cell Transplantation/adverse effects
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/complications/drug therapy/pathology Immunosuppressive Agents/adverse effects *Lymphoma/chemically induced/complications/drug therapy Central Nervous System/pathology
 Humans *Multiple Sclerosis/complications/diagnosis Gait Walking Movement Postural Balance
 Humans *Multiple Sclerosis/diagnostic imaging Intermediate Filaments *Multiple Sclerosis, Relapsing-Remitting Biomarkers Magnetic Resonance Imaging
 Middle Aged Humans Oral Health Quality of Life/psychology *Multiple Sclerosis, Relapsing-Remitting/complications Mental Health *Multiple Sclerosis/complications Surveys and Questionnaires
 Male Humans *Multiple Sclerosis/drug therapy Argentina/epidemiology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/pathology Registries Recurrence
 Humans *Multiple Sclerosis/complications/therapy Postural Balance Gait Exercise Therapy
 Humans Natalizumab/adverse effects *Multiple Sclerosis/drug therapy/epidemiology Prospective Studies Immunologic Factors/adverse effects Quality of Life Pandemics *COVID-19 *Multiple Sclerosis, Relapsing-Remitting/drug therapy Patient Outcome Assessment Hospitals
 Female Humans *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Retrospective Studies Magnetic Resonance Imaging Outcome Assessment, Health Care Vitamin D
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Longitudinal Studies Brain Mapping Brain/pathology Magnetic Resonance Imaging *Cognitive Dysfunction/diagnostic imaging/etiology/pathology Cognition Atrophy/pathology
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Iron Brain/pathology *White Matter/pathology Magnetic Resonance Imaging/methods
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy Immunosuppressive Agents/therapeutic use Retrospective Studies Patient Reported Outcome Measures *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy
 Humans Egypt *Genome-Wide Association Study *Multiple Sclerosis/drug therapy/genetics Pharmacogenetics Pharmacogenomic Testing Polymorphism, Single Nucleotide Disease Progression
 Humans *Multiple Sclerosis/complications/diagnostic imaging/therapy Brain/pathology *Central Nervous System Diseases/pathology Magnetic Resonance Imaging Atrophy/pathology
 Humans *Multiple Sclerosis/drug therapy/epidemiology Pensions Prospective Studies Sweden/epidemiology
 Humans Female *White Matter/diagnostic imaging *Multiple Sclerosis/complications/diagnostic imaging Urinary Bladder/diagnostic imaging Diffusion Tensor Imaging/methods Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Follow-Up Studies Disease Progression Magnetic Resonance Imaging/methods Chronic Disease Recurrence
 Humans *Multiple Sclerosis/complications/diagnostic imaging *Ocular Motility Disorders/diagnostic imaging/etiology Magnetic Resonance Imaging *Ophthalmoplegia
 Humans *Transcutaneous Electric Nerve Stimulation/methods Quality of Life Activities of Daily Living *Multiple Sclerosis/complications/therapy *Neuralgia Treatment Outcome
 Humans *Multiple Sclerosis/complications Memory, Short-Term Case-Control Studies *Multiple Sclerosis, Chronic Progressive Phenotype *Multiple Sclerosis, Relapsing-Remitting/complications
 Humans *Multiple Sclerosis/complications/diagnostic imaging Diffusion Tensor Imaging Postural Balance Cerebral Cortical Thinning Time and Motion Studies Gait Walking
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Demyelinating Diseases Neuroimaging Brain/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/pathology
 Humans *Multiple Sclerosis/complications/drug therapy/diagnosis Consensus Latin America/epidemiology *COVID-19 Neurologists
 Female Humans Adult *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/complications/diagnosis/drug therapy *Uveitis *Panuveitis/diagnosis/drug therapy/etiology
 Humans Male Young Adult Adult *Multiple Sclerosis/complications/diagnosis Eye *Facial Paralysis/etiology Brain Stem Diagnosis, Differential
 Male Humans Female *Multiple Sclerosis/complications/diagnosis/cerebrospinal fluid Prospective Studies *Brain Contusion Retrospective Studies *Brain Injuries, Traumatic/complications/diagnosis *Multiple Sclerosis, Relapsing-Remitting *Brain Concussion
 Humans *Exercise Behavior Therapy/methods Outcome Assessment, Health Care Research Design *Multiple Sclerosis/therapy/psychology
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy Retrospective Studies Immunosuppressive Agents/therapeutic use Gadolinium Glatiramer Acetate Interferon-beta Magnetic Resonance Imaging Brain/diagnostic imaging Spinal Cord/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting
 Humans Dimethyl Fumarate/pharmacology Immunosuppressive Agents/pharmacology Magnetic Resonance Imaging/methods *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/drug therapy *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/pathology Natalizumab/pharmacology Precision Medicine
 Humans *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/pathology *Multiple Sclerosis/complications/diagnostic imaging/pathology Retrograde Degeneration/pathology Geniculate Bodies/diagnostic imaging/pathology Retina/diagnostic imaging/pathology *Optic Neuritis/diagnostic imaging/pathology Tomography, Optical Coherence
 Humans *Multiple Sclerosis/complications/diagnostic imaging/drug therapy Brain/diagnostic imaging/pathology Interferon beta-1a/therapeutic use Magnetic Resonance Imaging/methods Atrophy/pathology Disease Progression
 Humans Middle Aged *Multiple Sclerosis/complications/diagnosis Knee Foot Hand Strength Fibrinogen
 Humans *Cervical Cord/pathology *Multiple Sclerosis/diagnostic imaging/pathology Black or African American Spinal Cord/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Brain Stem/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting/pathology
 Humans *Multiple Sclerosis/complications/diagnostic imaging Depression/diagnostic imaging Brain/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting Fatigue Magnetic Resonance Imaging
 Male Humans Middle Aged *Multiple Sclerosis, Chronic Progressive/therapy *Multiple Sclerosis/therapy/drug therapy Quality of Life Hydrodynamics Surveys and Questionnaires
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology Atrophy/pathology *Spinal Cord Diseases/pathology Brain/diagnostic imaging/pathology Recurrence *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology Spinal Cord/diagnostic imaging/pathology Disability Evaluation
 Female Humans Middle Aged Carbapenems/adverse effects Anti-Bacterial Agents *Multiple Sclerosis/drug therapy/chemically induced beta-Lactams/adverse effects *Brain Diseases/chemically induced/drug therapy
 Humans *Multiple Sclerosis/diagnostic imaging/therapy Plasma Exchange/methods *Neuromyelitis Optica/therapy Retrospective Studies Spinal Cord
 Humans *Multiple Sclerosis/complications/psychology Exercise Therapy Walking Physical Therapy Modalities Cognition
 Humans *Processing Speed Feasibility Studies Exercise *Multiple Sclerosis/complications/therapy/psychology Walking Exercise Therapy/methods
 Humans *Multiple Sclerosis/complications/diagnosis Tomography, Optical Coherence/methods Pilot Projects Retinal Ganglion Cells Cross-Sectional Studies Case-Control Studies *Optic Neuritis/diagnosis
 Rats Animals *Multiple Sclerosis/diagnostic imaging/therapy/pathology *Demyelinating Diseases/chemically induced/diagnostic imaging/therapy Lysophosphatidylcholines/toxicity *Remyelination Models, Animal Myelin Sheath Disease Models, Animal
 Humans Acute Disease Disease Progression Intermediate Filaments *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/diagnosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Recurrence
 Humans *Multiple Sclerosis/complications Alemtuzumab/adverse effects *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/drug therapy Prospective Studies Fatigue/complications Neuropsychological Tests
 Humans *Multiple Sclerosis/complications/diagnostic imaging/drug therapy *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/drug therapy/pathology Retina/pathology *Retinal Degeneration/diagnostic imaging/drug therapy/pathology Pyridines/therapeutic use Tomography, Optical Coherence/methods Atrophy/drug therapy/pathology
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging *Biological Phenomena Disease Progression Generalization, Psychological Recurrence
 Humans Magnetic Resonance Imaging/methods *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Multiple Sclerosis/pathology Tibial Nerve/diagnostic imaging Peripheral Nerves
 Humans Middle Aged *Multiple Sclerosis/pathology Arachidonic Acid Cross-Sectional Studies *Multiple Sclerosis, Chronic Progressive *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging Patient Acuity
 Humans *Multiple Sclerosis/complications/drug therapy/diagnosis *Psychotic Disorders/complications/drug therapy Adrenal Cortex Hormones Patients
 Humans *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/psychology *Multiple Sclerosis/complications Depression/etiology Brain/diagnostic imaging Fatigue/psychology
 Humans Adult *Multiple Sclerosis/diagnostic imaging/pathology Longitudinal Studies Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Brain Injuries
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Sodium Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Sexually Transmitted Diseases/pathology
 Humans *Transcranial Magnetic Stimulation *Multiple Sclerosis/complications/therapy
 Humans Artificial Intelligence Atrophy Magnetic Resonance Imaging *Multiple Sclerosis/diagnostic imaging/therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Retrospective Studies Longitudinal Studies Choroid Plexus/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/pathology Brain/pathology Disease Progression Atrophy/pathology
 Humans *Multiple Sclerosis/drug therapy Spain *Multiple Sclerosis, Relapsing-Remitting/drug therapy Nitriles/therapeutic use Recurrence
 Humans *Multiple Sclerosis/complications/drug therapy Memantine/therapeutic use *Nystagmus, Pathologic/drug therapy/etiology Eye Movements
 Humans *Multiple Sclerosis/drug therapy/epidemiology France Germany/epidemiology Injections, Subcutaneous Italy
 Humans Female Adult Middle Aged Male *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging *Multiple Sclerosis/psychology Cross-Sectional Studies Quality of Life *Cognitive Dysfunction/etiology/complications Magnetic Resonance Imaging Neurologic Examination
 Humans *Multiple Sclerosis/diagnostic imaging/drug therapy Antibodies, Monoclonal *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab/therapeutic use
 Humans *Multiple Sclerosis, Relapsing-Remitting *Multiple Sclerosis Patients Axons Cytokines
 Male Humans Adult *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/complications/drug therapy/psychology Antibodies, Monoclonal *Cognitive Dysfunction/drug therapy/etiology *Antineoplastic Agents/therapeutic use
 Humans Child Antibodies, Monoclonal, Humanized/adverse effects *Multiple Sclerosis/complications/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunologic Factors/adverse effects
 Humans Natalizumab/therapeutic use *Multiple Sclerosis/drug therapy *Leukoencephalopathy, Progressive Multifocal Immunologic Factors/therapeutic use *Multiple Sclerosis, Relapsing-Remitting
 Humans Biomarkers *Multiple Sclerosis/diagnosis
 Pregnancy Female Humans *Multiple Sclerosis/complications/drug therapy Breast Feeding Fingolimod Hydrochloride *Hypertension
 Adult Humans Immunologic Factors/therapeutic use Magnetic Resonance Imaging *Multiple Sclerosis/diagnostic imaging/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab/therapeutic use Retrospective Studies
 Humans Aged Middle Aged *Multiple Sclerosis/diagnostic imaging/psychology *Cognitive Reserve Magnetic Resonance Imaging Neuropsychological Tests Aging Atrophy
 Humans *Remyelination/physiology Myelin Sheath/physiology Oligodendroglia/physiology *Multiple Sclerosis/therapy/metabolism Cell Differentiation/physiology
 Humans *Trigeminal Neuralgia/diagnosis/pathology *Demyelinating Diseases/diagnostic imaging *Multiple Sclerosis/diagnosis/diagnostic imaging Magnetic Resonance Imaging/methods
 Humans Male Female *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Prospective Studies
 Humans Natalizumab/adverse effects Immunologic Factors/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy/complications *Multiple Sclerosis/complications
 Humans Neuroprotection *Multiple Sclerosis/therapy *Multiple Sclerosis, Chronic Progressive/therapy Gray Matter *Neural Stem Cells
 Child Pregnancy Female Child, Preschool Humans Cohort Studies Retrospective Studies *Mothers Anti-Bacterial Agents *Multiple Sclerosis/drug therapy/epidemiology/chemically induced Denmark/epidemiology Registries
 Humans *Multiple Sclerosis, Chronic Progressive/diagnosis Uncertainty *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis Denmark Disease Progression
 Humans *Multiple Sclerosis, Chronic Progressive Bibliometrics *Multiple Sclerosis/drug therapy *Neurology Databases, Factual
 Humans *Multiple Sclerosis/complications/psychology Reaction Time Exercise Attention Brain/diagnostic imaging
 Pregnancy Humans Female Czech Republic/epidemiology *Multiple Sclerosis/drug therapy/epidemiology Disease Progression Recurrence Breast Feeding *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Animals Mice Female Male *Androgens Disease Models, Animal Myelin Sheath/physiology *Multiple Sclerosis/genetics/pathology Neurons/pathology
 Female Humans Adult Disease Progression *Multiple Sclerosis/diagnosis Prognosis *Multiple Sclerosis, Chronic Progressive Leukocytosis
 Humans *Quality of Life Prospective Studies *Multiple Sclerosis/complications/diagnostic imaging Magnetic Resonance Imaging Cognition Patient Reported Outcome Measures Fatigue/complications
 Humans Child *Multiple Sclerosis/diagnostic imaging/epidemiology *Demyelinating Diseases/diagnostic imaging/epidemiology Disease Progression Magnetic Resonance Imaging Retrospective Studies *Autoimmune Diseases of the Nervous System
 Humans Adult Male Child Adolescent *Multiple Sclerosis/diagnostic imaging/epidemiology Retrospective Studies Cognition Age of Onset Magnetic Resonance Imaging Disease Progression
 Humans Natalizumab/adverse effects SARS-CoV-2 Immunologic Factors/adverse effects Pandemics *COVID-19 *Multiple Sclerosis, Relapsing-Remitting/chemically induced *Multiple Sclerosis/drug therapy/epidemiology/chemically induced
 Humans Natalizumab/therapeutic use *Multiple Sclerosis/drug therapy *Leukoencephalopathy, Progressive Multifocal Immunologic Factors *Multiple Sclerosis, Relapsing-Remitting
 Humans Choroid Plexus/diagnostic imaging *Demyelinating Diseases/diagnostic imaging/pathology Brain/pathology *Optic Neuritis/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Inflammation/pathology *Multiple Sclerosis/pathology
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis/drug therapy Chronic Disease *Multiple Sclerosis Disease Progression
 Humans Quality of Life/psychology Retrospective Studies Cross-Sectional Studies *Multiple Sclerosis/complications *Multiple Sclerosis, Relapsing-Remitting/complications/epidemiology/drug therapy Fatigue/etiology/complications Disease Progression
 Humans Retrospective Studies *Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Meninges/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Immunotherapy
 Humans *Cognition Disorders/diagnosis Correlation of Data *Cognitive Dysfunction/diagnostic imaging/etiology *Multiple Sclerosis/complications/diagnostic imaging Brain/diagnostic imaging/pathology Cognition Neuropsychological Tests Magnetic Resonance Imaging
 Humans Fingolimod Hydrochloride/therapeutic use/pharmacology Dimethyl Fumarate/therapeutic use/pharmacology Benchmarking *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Brain/diagnostic imaging/pathology *White Matter/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/pathology
 Humans Quality of Life *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents *Multiple Sclerosis/drug therapy
 Humans Cross-Sectional Studies Retina/diagnostic imaging/pathology Optic Nerve/diagnostic imaging/pathology *Multiple Sclerosis/complications/diagnostic imaging/pathology *Optic Neuritis/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Cognition Tomography, Optical Coherence/methods
 Humans *Demyelinating Diseases/diagnostic imaging *Multiple Sclerosis/diagnostic imaging/drug therapy *Autoimmune Diseases of the Nervous System Magnetic Resonance Imaging
 Humans Quality of Life *Multiple Sclerosis, Relapsing-Remitting Immunosuppressive Agents *Multiple Sclerosis/drug therapy
 Humans Biomarkers *Inflammation/blood/cerebrospinal fluid/metabolism *Multiple Sclerosis/diagnosis/immunology/metabolism Oligoclonal Bands/cerebrospinal fluid
 Aged Female Humans Male Middle Aged Chronic Disease Disease Progression *Multiple Sclerosis/diagnosis/drug therapy Multiple Sclerosis, Relapsing-Remitting/drug therapy/diagnosis Recurrence Retrospective Studies *Immunomodulating Agents/administration & dosage/therapeutic use Immunomodulation *Withholding Treatment
 Humans Follow-Up Studies Cognition *Cognition Disorders/diagnosis Memory Neuropsychological Tests *Multiple Sclerosis, Relapsing-Remitting/complications/diagnosis/psychology *Multiple Sclerosis/diagnosis
 Child Humans Female Adult *Multiple Sclerosis/diagnosis/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging Brain Stem/pathology *Vasculitis/pathology
 Humans Laboratories, Clinical Canada Oligoclonal Bands *Multiple Sclerosis/diagnosis/cerebrospinal fluid *Paraproteinemias *Monoclonal Gammopathy of Undetermined Significance
 Humans Quality of Life Immunosuppressive Agents *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy
 Humans United States *Multiple Sclerosis/drug therapy Crotonates/therapeutic use Toluidines/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Disease Progression
 Male Humans Female *Multiple Sclerosis, Relapsing-Remitting/complications/epidemiology *Multiple Sclerosis/complications Prognosis Prodromal Symptoms Prevalence Pain/complications Fatigue/etiology/complications Disease Progression
 Humans *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive/diagnosis/drug therapy Walking Research Design *Disabled Persons Disability Evaluation
 Humans *Multiple Sclerosis/genetics/metabolism Gene Expression Profiling/methods Brain/metabolism Microarray Analysis Central Nervous System/metabolism Computational Biology/methods Gene Regulatory Networks
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Parkinson Disease/pathology Choroid/pathology Image Processing, Computer-Assisted/methods
 Humans *Multiple Sclerosis/complications/therapy Quality of Life *Self-Management Fatigue/etiology/therapy/psychology Internet
 Humans Female Male Alemtuzumab/adverse effects Retrospective Studies *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced Recurrence
 Female Humans Adult *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive Sphingosine-1-Phosphate Receptors/therapeutic use *Macular Edema/chemically induced/drug therapy
 Humans *Sodium *Multiple Sclerosis/diagnostic imaging/pathology Reproducibility of Results Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology Image Processing, Computer-Assisted/methods
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced *Multiple Sclerosis/chemically induced Heart Arrhythmias, Cardiac/chemically induced Electrocardiography Heart Rate/physiology
 Adult Humans *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy/epidemiology Sweden/epidemiology Czech Republic/epidemiology Registries Recurrence
 Female Humans Male *Multiple Sclerosis/complications/diagnosis Walking/physiology Lower Extremity Postural Balance/physiology
 Humans *White Matter/diagnostic imaging Diffusion Tensor Imaging/methods *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/complications Processing Speed *Multiple Sclerosis/complications Quality of Life Brain/diagnostic imaging
 Humans *Multiple Sclerosis/diagnosis Diagnosis, Differential Consensus Magnetic Resonance Imaging Syndrome
 Humans Alemtuzumab/adverse effects *Multiple Sclerosis/complications/drug therapy *Anemia, Hemolytic, Autoimmune/chemically induced Antibodies, Monoclonal
 Humans Delusions/diagnosis Hallucinations/diagnosis/etiology *Multiple Sclerosis/complications/diagnosis *Psychotic Disorders/diagnosis *Schizophrenia/complications/diagnosis/drug therapy Syndrome
 Humans Prognosis Tomography, Optical Coherence/methods *Clinical Deterioration Cross-Sectional Studies *Multiple Sclerosis/diagnostic imaging/complications *Retinal Degeneration *Macular Degeneration Atrophy/complications
 Humans *Deglutition Disorders/etiology/complications *Multiple Sclerosis/complications/diagnosis Reproducibility of Results Pilot Projects Surveys and Questionnaires Psychometrics
 Humans *Multiple Sclerosis/drug therapy Alemtuzumab/adverse effects Fibrin Fibrinogen Degradation Products *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunologic Factors
 Humans *Multiple Sclerosis/etiology Diet
 Child, Preschool Humans *Gastrointestinal Microbiome *Multiple Sclerosis/etiology/complications Obesity/complications/epidemiology *Microbiota Risk Factors
 Humans Dimethyl Fumarate/adverse effects *Multiple Sclerosis/drug therapy/microbiology *Gastrointestinal Microbiome *Gastrointestinal Diseases/drug therapy Bacteroidetes *Drug-Related Side Effects and Adverse Reactions/drug therapy Immunosuppressive Agents/therapeutic use
 Humans Adult Middle Aged *Multiple Sclerosis/diagnostic imaging/epidemiology/drug therapy SARS-CoV-2 COVID-19 Vaccines Case-Control Studies *COVID-19/epidemiology Prospective Studies Pandemics Propensity Score RNA, Viral/therapeutic use Recurrence
 Humans Child *Multiple Sclerosis/drug therapy Intermediate Filaments *Multiple Sclerosis, Relapsing-Remitting/drug therapy Crotonates/therapeutic use Toluidines/therapeutic use Neurofilament Proteins
 Humans *Arthroplasty, Replacement, Hip/adverse effects *Arthroplasty, Replacement, Knee/adverse effects Retrospective Studies *Multiple Sclerosis/complications/diagnosis/surgery Anesthesia, General/adverse effects Treatment Outcome *Myasthenia Gravis/diagnosis/surgery Postoperative Complications/etiology/epidemiology
 Humans Female Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Gray Matter/pathology *Multiple Sclerosis, Chronic Progressive/pathology Brain/diagnostic imaging/pathology Disability Evaluation Atrophy/pathology
 Adult Female Humans Male Cladribine/adverse effects Immunosuppressive Agents/adverse effects *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Recurrence Retrospective Studies Tablets Middle Aged
 Humans Biomarkers/blood/cerebrospinal fluid Cross-Sectional Studies *MicroRNAs/blood/cerebrospinal fluid/genetics *Multiple Sclerosis/blood/cerebrospinal fluid/genetics *Multiple Sclerosis, Chronic Progressive/blood/cerebrospinal fluid/genetics Recurrence
 Humans *Multiple Sclerosis/psychology *Self Concept
 Humans Lymphocytic choriomeningitis virus *Multiple Sclerosis/etiology *Lymphocytic Choriomeningitis CD8-Positive T-Lymphocytes
 Humans Dimethyl Fumarate/adverse effects Immunosuppressive Agents/adverse effects Retrospective Studies *Lymphopenia/chemically induced *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced *Leukopenia Lymphocyte Count *Drug-Related Side Effects and Adverse Reactions/drug therapy *Thrombocytopenia/chemically induced *Multiple Sclerosis/drug therapy
 Humans Female Male Levamisole/adverse effects Brain/diagnostic imaging/pathology *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Retrospective Studies *Encephalomyelitis, Acute Disseminated/pathology Magnetic Resonance Imaging
 Humans Male Female *Multiple Sclerosis/therapy Patient Compliance
 Humans Glatiramer Acetate/therapeutic use *Multiple Sclerosis/complications *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy/pathology *Urticaria/chemically induced/drug therapy/complications *Vasculitis/chemically induced/complications/drug therapy Immunosuppressive Agents/adverse effects
 Humans Male *Methanol/toxicity *Multiple Sclerosis/etiology
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *Deep Learning Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology Attention Blindness/pathology
 Humans *Multiple Sclerosis/drug therapy Polypharmacy
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/complications Cross-Sectional Studies *Cognitive Dysfunction/etiology Neuropsychological Tests
 Female Humans *Multiple Sclerosis/complications/diagnostic imaging Glial Fibrillary Acidic Protein Intermediate Filaments Prospective Studies Neurofilament Proteins Biomarkers Cognition Magnetic Resonance Imaging
 Humans Young Adult Adult *White Matter/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/pathology Magnetic Resonance Imaging Brain/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Atrophy/pathology *Multiple Sclerosis/pathology
 Humans *Multiple Sclerosis/diagnosis Interleukin-8/genetics *Multiple Sclerosis, Relapsing-Remitting/diagnosis Cytokines Magnetic Resonance Imaging
 Humans *Alzheimer Disease/diagnosis *Dementia/psychology *Parkinson Disease/complications/diagnosis *Multiple Sclerosis/complications/diagnosis *Cognitive Dysfunction/diagnosis Neuropsychological Tests Cognition
 Adult Child Humans Male Female *Multiple Sclerosis/diagnostic imaging/complications Choroid Plexus/diagnostic imaging Retrospective Studies Clinical Relevance Brain Magnetic Resonance Imaging
 Humans Cladribine/adverse effects *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Immunosuppressive Agents/adverse effects *Multiple Sclerosis/drug therapy *Drug-Related Side Effects and Adverse Reactions *Lymphopenia/chemically induced Recurrence
 Humans *Multiple Sclerosis/diagnosis Cognition
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy Chronic Disease Recurrence
 Humans *Multiple Sclerosis/drug therapy *Plants, Medicinal Adjuvants, Immunologic
 Humans *Multiple Sclerosis Immunoglobulin G Antibodies, Viral *Multiple Sclerosis, Relapsing-Remitting *Optic Neuritis Antigens, Viral
 Humans Male Female Adult Middle Aged Quality of Life/psychology Cross-Sectional Studies Sex Characteristics *Multiple Sclerosis/complications/epidemiology Fatigue/etiology/complications *Sexual Dysfunction, Physiological/epidemiology/etiology
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy Cost-Benefit Analysis Immunosuppressive Agents/therapeutic use Rituximab/therapeutic use Colombia *Multiple Sclerosis/drug therapy
 Female Humans Adult *Multiple Sclerosis/diagnostic imaging/genetics *White Matter/diagnostic imaging/pathology Canada Brain/diagnostic imaging/pathology Brain Stem Magnetic Resonance Imaging *Cerebellar Ataxia
 Humans *Multiple Sclerosis/drug therapy Antibodies, Monoclonal/therapeutic use *Antineoplastic Agents/therapeutic use Immunoglobulin G *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/complications Fingolimod Hydrochloride/therapeutic use Nerve Fibers/pathology Retina/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Disease Progression Tomography, Optical Coherence/methods
 Humans *Multiple Sclerosis *Diet, Ketogenic Intermediate Filaments *Multiple Sclerosis, Relapsing-Remitting Biomarkers
 Humans Interferon beta-1a/therapeutic use Interferon-beta/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence Randomized Controlled Trials as Topic Clinical Trials, Phase III as Topic
 Humans Qualitative Research *Delivery of Health Care Health Personnel *Multiple Sclerosis/diagnosis Communication
 Adult Humans *Multiple Sclerosis, Relapsing-Remitting *Multiple Sclerosis Exercise Qualitative Research Motivation
 Humans Child Child, Preschool *Multiple Sclerosis/drug therapy Greece/epidemiology Immunomodulating Agents Retrospective Studies Treatment Failure *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Adult Child Female Middle Aged Adolescent *Multiple Sclerosis/drug therapy/epidemiology Immunosuppressive Agents Cross-Sectional Studies Fingolimod Hydrochloride Interferon-beta
 Humans *Multiple Sclerosis/drug therapy SARS-CoV-2 Pandemics Retrospective Studies Prospective Studies Immunologic Factors/therapeutic use/adverse effects *COVID-19 *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy
 Adult Humans *Antibodies, Monoclonal/therapeutic use Antineoplastic Agents/therapeutic use *Multiple Sclerosis/drug therapy Multiple Sclerosis, Relapsing-Remitting/drug therapy Neoplasm Recurrence, Local/drug therapy
 Humans *Multiple Sclerosis, Chronic Progressive/diagnosis/drug therapy Prognosis *Multiple Sclerosis Retrospective Studies Prospective Studies
 Humans *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/pathology *Multiple Sclerosis/complications Gray Matter/diagnostic imaging/pathology Iron Choroid Plexus/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Atrophy/pathology
 Humans *Multiple Sclerosis/diagnosis Fatigue Standing Position Accelerometry
 Child Humans *Gene-Environment Interaction *Multiple Sclerosis/chemically induced/epidemiology/genetics Genetic Predisposition to Disease/genetics Interleukin-6 HLA-DRB1 Chains/genetics Risk Factors Genotype HLA Antigens Case-Control Studies Proto-Oncogene Proteins c-bcl-2/genetics
 Female Humans Male *Activities of Daily Living Biomechanical Phenomena *Multiple Sclerosis/complications/drug therapy Muscle Spasticity/drug therapy/etiology Pilot Projects Upper Extremity
 Humans *Prodromal Symptoms *Multiple Sclerosis/diagnosis
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Glatiramer Acetate/therapeutic use Natalizumab/therapeutic use Cladribine/therapeutic use
 Female Male Humans *Multiple Sclerosis/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Depression/etiology Magnetic Resonance Imaging Brain/diagnostic imaging/pathology Atrophy/pathology
 Animals Swine *Baclofen *Multiple Sclerosis/drug therapy Skin Drug Delivery Systems Half-Life
 Humans Adaptation, Psychological Anthropology, Cultural Emotions *Multiple Sclerosis/diagnosis Qualitative Research
 Female Humans Male Comorbidity Data Analysis Germany/epidemiology *Multiple Sclerosis/epidemiology/drug therapy Retrospective Studies
 Humans Young Adult Adult 4-Aminopyridine/adverse effects *Multiple Sclerosis/complications/drug therapy Valproic Acid *Status Epilepticus/chemically induced/drug therapy *Epilepsy Sodium
 Humans Cladribine/therapeutic use *Multiple Sclerosis/drug therapy Immunosuppressive Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Tablets Registries
 Humans *Multiple Sclerosis/complications Fatigue/etiology Quality of Life
 Humans Female Adult Dimethyl Fumarate/adverse effects *Antipsychotic Agents/therapeutic use *Eosinophilia/chemically induced/complications/diagnosis *Multiple Sclerosis/drug therapy/complications
 Humans *Neuromyelitis Optica/diagnostic imaging *Multiple Sclerosis/diagnostic imaging/pathology *Deep Learning Brain/pathology Magnetic Resonance Imaging/methods Aquaporin 4
 Humans *Multiple Sclerosis/diagnosis *Biosensing Techniques/methods Biomarkers/analysis Magnetic Resonance Imaging
 Pregnancy Female Mice Animals Neuroprotection *Encephalomyelitis, Autoimmune, Experimental/drug therapy *Multiple Sclerosis/drug therapy/metabolism/pathology Estriol/pharmacology/therapeutic use Cerebral Cortex/metabolism *Neurodegenerative Diseases Atrophy/drug therapy/pathology Mice, Inbred C57BL
 Humans *Evoked Potentials, Visual *Multiple Sclerosis/diagnosis
 Adolescent Adult Humans Female Middle Aged Male *Multiple Sclerosis/epidemiology Longevity Cross-Sectional Studies *COVID-19 *Multiple Sclerosis, Relapsing-Remitting/epidemiology Chronic Disease Recurrence
 Humans *Multiple Sclerosis/diagnosis Tissue Inhibitor of Metalloproteinase-1 *Neuromyelitis Optica/pathology Aquaporin 4 Inflammation *Multiple Sclerosis, Relapsing-Remitting/diagnosis/cerebrospinal fluid Biomarkers/cerebrospinal fluid
 Humans Myelin-Oligodendrocyte Glycoprotein *Optic Neuritis/diagnosis/therapy *Neuromyelitis Optica/diagnosis/therapy *Multiple Sclerosis/complications/therapy Autoantibodies
 Humans Aged *Immunosenescence/physiology *Multiple Sclerosis/therapy Aging Immune System Brain
 Pregnancy Humans Female Glatiramer Acetate/adverse effects *Multiple Sclerosis/chemically induced Breast Feeding Immunosuppressive Agents/adverse effects Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced Mothers Recurrence
 Male Humans Female Risk Factors *Multiple Sclerosis/etiology/genetics Cross-Sectional Studies Canada/epidemiology Genetic Predisposition to Disease
 Male Female Humans *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Cerebral Cortex Amides Protons
 Humans *Multiple Sclerosis/complications/psychology Depression/epidemiology/etiology/therapy Anxiety/therapy Anxiety Disorders Patient Reported Outcome Measures Randomized Controlled Trials as Topic
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Brain Magnetic Resonance Imaging/methods Brain Mapping/methods *Cognitive Dysfunction/diagnostic imaging/etiology/pathology
 Humans Female Aged Aged, 80 and over Middle Aged Male Polypharmacy *Multiple Sclerosis/drug therapy/epidemiology Anticonvulsants Antidepressive Agents/therapeutic use *Peptic Ulcer/drug therapy
 Humans *Multiple Sclerosis/complications/diagnostic imaging/pathology Reproducibility of Results Spinal Cord/diagnostic imaging/pathology Gray Matter/pathology Magnetic Resonance Imaging/methods
 Female Humans Middle Aged Rituximab/therapeutic use/pharmacology Brain/metabolism *White Matter/pathology Magnetic Resonance Imaging Positron-Emission Tomography Immunity, Innate *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/drug therapy/pathology *Multiple Sclerosis/pathology
 Humans *Multiple Sclerosis/genetics *RNA, Long Noncoding/genetics Amyloid Precursor Protein Secretases/genetics Aspartic Acid Endopeptidases/genetics *Multiple Sclerosis, Chronic Progressive/complications/genetics *Multiple Sclerosis, Relapsing-Remitting/genetics Cognition Gene Expression Profiling
 Adult Humans *Multiple Sclerosis/drug therapy Antibodies, Monoclonal *Antineoplastic Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Infusions, Intravenous Double-Blind Method Magnetic Resonance Imaging Treatment Outcome
 Humans Female Young Adult Adult *Multiple Sclerosis/diagnostic imaging/pathology Prospective Studies Peripheral Nerves Magnetic Resonance Imaging/methods Biomarkers Immunoglobulins
 Humans *Optic Nerve Diseases/diagnosis/etiology/therapy *Optic Neuritis/diagnosis/etiology/therapy *Neuromyelitis Optica/diagnosis/therapy/complications *Multiple Sclerosis/diagnosis/therapy/complications Optic Nerve
 Humans *Multiple Sclerosis/diagnostic imaging Image Processing, Computer-Assisted Image Enhancement Patient Outcome Assessment Magnetic Resonance Imaging Brain
 Humans MEDLINE *Multiple Sclerosis/complications *Nervous System Diseases *Vascular Diseases *Venous Insufficiency/complications
 Adult Humans *Ketamine *Multiple Sclerosis/complications/drug therapy Midazolam/therapeutic use Double-Blind Method Fatigue/etiology/chemically induced Treatment Outcome Randomized Controlled Trials as Topic Clinical Trials, Phase II as Topic
 Humans Female Middle Aged Male *Multiple Sclerosis/diagnostic imaging/pathology Cross-Sectional Studies Quality of Life Brain/diagnostic imaging/pathology *Multiple Sclerosis, Chronic Progressive/pathology Magnetic Resonance Imaging/methods Disease Progression Phosphates Atrophy/pathology *Vascular Diseases Risk Factors
 Humans *Multiple Sclerosis/genetics Myelin Proteins Central Nervous System *Autoimmune Diseases Spinal Cord Antigens
 Male Female Humans *Multiple Sclerosis/epidemiology Prevalence Incidence Japan/epidemiology *Multiple Sclerosis, Chronic Progressive/epidemiology
 Adult Female Humans *Dietary Supplements Fatigue/drug therapy/etiology *Multiple Sclerosis/complications/drug therapy Vitamin D/therapeutic use Male
 Humans Cost-Benefit Analysis *Multiple Sclerosis/drug therapy Economics, Medical Health Care Costs
 Male Female Humans Adult Middle Aged *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Multiple Sclerosis/pathology Gadolinium Prospective Studies *White Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Brain/pathology Contrast Media
 Male Humans Female Adult Cladribine/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents/therapeutic use *Multiple Sclerosis/drug therapy Tablets Denmark
 Humans Cladribine/adverse effects Gray Matter/diagnostic imaging/pathology *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging/drug therapy Disease Progression Atrophy/pathology Brain/pathology Magnetic Resonance Imaging Tablets/pharmacology/therapeutic use
 Humans Alemtuzumab/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/chemically induced/drug therapy Antibodies, Monoclonal, Humanized/adverse effects *Neutropenia/chemically induced/diagnosis/drug therapy *Thrombocytopenia/chemically induced/diagnosis
 Humans Female Young Adult Adult Male Plasma Exchange/adverse effects *Multiple Sclerosis/complications/therapy *Hypokalemia/etiology/therapy Retrospective Studies Plasmapheresis Recurrence Steroids
 Humans *Cannabinoids/therapeutic use *Cannabis *Multiple Sclerosis/drug therapy
 Humans *Magnetic Resonance Imaging *Multiple Sclerosis/diagnosis Oligoclonal Bands
 Humans *Multiple Sclerosis/epidemiology Risk *Neoplasms
 Humans *Multiple Sclerosis/drug therapy Neuroinflammatory Diseases Cladribine/therapeutic use Neuroimaging Brain/diagnostic imaging Tablets/therapeutic use Immunosuppressive Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/complications/drug therapy Prospective Studies Austria Muscle Spasticity/drug therapy/etiology Pain Spasm/complications
 Adult Humans *Chronic Periodontitis/complications/epidemiology *Multiple Sclerosis/epidemiology/complications Reproducibility of Results *Autoimmune Diseases/complications Chronic Disease
 Female Humans Pregnancy Cryopreservation/methods *Fertility Preservation/methods *Hematopoietic Stem Cell Transplantation *Multiple Sclerosis/therapy/complications *Primary Ovarian Insufficiency/etiology Retrospective Studies Stem Cell Transplantation/adverse effects
 Humans Male Female Young Adult Adult *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Brain/pathology *Multiple Sclerosis, Relapsing-Remitting/pathology *White Matter/pathology Atrophy/pathology Gray Matter
 Humans Fingolimod Hydrochloride/therapeutic use Natalizumab/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy *Multiple Sclerosis/drug therapy Treatment Outcome Recurrence Immunosuppressive Agents/therapeutic use Immunologic Factors/adverse effects
 Humans *Multiple Sclerosis/diagnosis Glial Fibrillary Acidic Protein Intermediate Filaments/metabolism Cross-Sectional Studies Retrospective Studies *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/metabolism Biomarkers Inflammation/metabolism
 Humans *Multiple Sclerosis, Relapsing-Remitting *Multiple Sclerosis *Neurodegenerative Diseases Exercise Exercise Therapy
 Humans *Multiple Sclerosis/etiology Diet Food
 Humans *Multiple Sclerosis/pathology Neoplasm Recurrence, Local *Multiple Sclerosis, Chronic Progressive/pathology Central Nervous System/pathology Gray Matter/diagnostic imaging/pathology
 Humans *Cannabidiol/therapeutic use Dronabinol/therapeutic use Drug Combinations *Multiple Sclerosis/complications/drug therapy Muscle Spasticity/drug therapy/etiology Muscle Tonus Randomized Controlled Trials as Topic Spasm/drug therapy
 Humans *Multiple Sclerosis Brain *Multiple Sclerosis, Relapsing-Remitting/drug therapy Double-Blind Method Treatment Outcome
 Humans *Multiple Sclerosis/diagnosis Prognosis Magnetic Resonance Imaging Treatment Outcome Immunotherapy
 Humans Depression/etiology *Multiple Sclerosis/complications/therapy Quality of Life/psychology Anxiety/complications/psychology *Cognitive Dysfunction/therapy/complications
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Gray Matter/pathology Cross-Sectional Studies Reproducibility of Results Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Atrophy/pathology Software
 Humans *Multiple Sclerosis/diagnostic imaging/pathology *Aging, Premature/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Aging Disease Progression Biomarkers
 Humans Female *Multiple Sclerosis/complications/diagnosis/drug therapy Magnetic Resonance Imaging *Optic Neuritis/diagnosis/drug therapy *Neuromyelitis Optica/complications/diagnosis/drug therapy Optic Nerve/pathology
 Adult Female Humans Infant, Newborn Male Pregnancy Child Development Interferon beta-1a/therapeutic use Interferon-beta/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced Prospective Studies Infant Child, Preschool
 Humans *Multiple Sclerosis/drug therapy Transplantation, Autologous/methods Treatment Outcome Immunosuppressive Agents/therapeutic use *Hematopoietic Stem Cell Transplantation/methods *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis Treatment Outcome *Drug-Related Side Effects and Adverse Reactions Decision Making
 Humans *Arthroplasty, Replacement, Hip/adverse effects Retrospective Studies *Multiple Sclerosis/complications/surgery Patient Readmission Postoperative Complications/epidemiology/etiology Risk Factors Length of Stay
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/complications/drug therapy Antibodies, Monoclonal, Humanized/adverse effects *Psoriasis/drug therapy/complications Treatment Outcome Severity of Illness Index
 Humans *Multiple Sclerosis/diagnostic imaging Case-Control Studies *COVID-19/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging Magnetic Resonance Imaging Recurrence Disease Progression
 Humans *Multiple Sclerosis/pathology *Mental Disorders Inflammation/pathology
 Humans *Multiple Sclerosis/diagnosis Smartphone Gait
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting Immunosuppressive Agents/adverse effects Nitriles
 Humans Biomarkers Glial Fibrillary Acidic Protein Hydroxychloroquine/therapeutic use Intermediate Filaments *Multiple Sclerosis/diagnosis *Multiple Sclerosis, Chronic Progressive/drug therapy Neurofilament Proteins Clinical Trials, Phase II as Topic
 Humans *Multiple Sclerosis Dimethyl Fumarate/therapeutic use Actigraphy Sleep *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy *Sleep Wake Disorders/drug therapy/etiology
 Male Female Humans Young Adult Adult Middle Aged *Multiple Sclerosis, Relapsing-Remitting/diagnosis *Multiple Sclerosis/diagnosis Oligoclonal Bands Biomarkers *Chitinases/cerebrospinal fluid Cross-Sectional Studies
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental *Neuroprotective Agents/therapeutic use/metabolism Toll-Like Receptor 7/metabolism Spinal Cord Inflammation/metabolism *Multiple Sclerosis/drug therapy/metabolism Mice, Inbred C57BL
 Humans *Multiple Sclerosis/complications/diagnostic imaging Case-Control Studies Prospective Studies Severity of Illness Index Pituitary Gland/diagnostic imaging Fatigue/diagnostic imaging/etiology Disability Evaluation
 Humans *Multiple Sclerosis/diagnosis Retrospective Studies Delayed Diagnosis Radiography
 Humans *Multiple Sclerosis/psychology *Cognition Disorders *Cognitive Dysfunction/diagnosis Neuropsychological Tests Cognition
 Humans *Multiple Sclerosis/epidemiology/complications Prospective Studies *Chlamydia Infections/complications/epidemiology *Pneumonia *Chlamydia
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis Patient Preference Chronic Disease Recurrence
 Humans Corpus Callosum/diagnostic imaging/pathology *Remyelination *Multiple Sclerosis/diagnostic imaging/drug therapy/pathology Brain/pathology Myelin Sheath/pathology *White Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Water Biomarkers
 Humans *Multiple Sclerosis/complications Retrospective Studies *Venous Insufficiency Veins Cerebrovascular Circulation
 Child Humans *Multiple Sclerosis/diagnosis Veins Brain Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/genetics/pathology Proteome/genetics Bayes Theorem Brain/pathology Gray Matter/pathology
 Humans *Multiple Sclerosis/diagnosis Neuropsychological Tests *Cognitive Dysfunction/diagnosis/etiology Phenotype Processing Speed Cognition
 Humans Female Young Adult Adult Middle Aged Aged Aged, 80 and over Male *Multiple Sclerosis/complications/psychology *Cognitive Dysfunction/diagnosis/etiology *Cognition Disorders/diagnosis/etiology Fatigue/diagnosis/etiology/psychology Perception
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Retinal Ganglion Cells/pathology Prospective Studies Tomography, Optical Coherence/methods Optic Nerve/diagnostic imaging *Optic Neuritis/diagnostic imaging
 Humans Female Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology Prospective Studies *Lymphatic Vessels/diagnostic imaging/metabolism Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology
 Pregnancy Child Infant, Newborn Female Humans Retrospective Studies *Premature Birth/epidemiology Cohort Studies Pharmaceutical Preparations *Multiple Sclerosis/drug therapy/epidemiology Placenta Pregnancy Outcome/epidemiology
 Humans *Multiple Sclerosis/psychology Prospective Studies Canada Employment Unemployment
 Humans *Multiple Sclerosis/drug therapy Central Nervous System Neuroglia Cell Physiological Phenomena Inflammation/pathology
 Animals Mice *Multiple Sclerosis/drug therapy *Chitosan Brain Disease Models, Animal
 Adult Humans Accidental Falls/prevention & control Fatigue/epidemiology/etiology Fear *Multiple Sclerosis/complications/epidemiology Postural Balance/physiology Quality of Life
 Female Humans Glatiramer Acetate/adverse effects *Multiple Sclerosis/complications/drug therapy *Retinal Vein Occlusion/chemically induced/diagnosis/drug therapy Dimethyl Fumarate/therapeutic use Risk Factors Immunosuppressive Agents/adverse effects
 Animals *Multiple Sclerosis/drug therapy Neuroprotection Oligodendroglia Neurons Inflammation *Encephalomyelitis, Autoimmune, Experimental
 Humans Quality of Life Vision, Ocular Tomography, Optical Coherence *Multiple Sclerosis/complications/diagnostic imaging *Brain Concussion Vision Disorders/diagnosis
 Humans Disability Evaluation *Disabled Persons/rehabilitation *Multiple Sclerosis/rehabilitation Clinical Trials as Topic
 Humans *Brain/diagnostic imaging Cost of Illness *Genome-Wide Association Study *Multiple Sclerosis/diagnostic imaging/genetics Neuroimaging Randomized Controlled Trials as Topic Disease Progression
 Humans Tomography, Optical Coherence/methods *Multiple Sclerosis/diagnosis/complications Cross-Sectional Studies Retinal Ganglion Cells/pathology Nerve Fibers/pathology *Myopia/pathology
 Male Humans Adult *Multiple Sclerosis/complications/drug therapy Baclofen/therapeutic use *Muscle Relaxants, Central/therapeutic use Tremor/drug therapy/etiology Injections, Spinal Muscle Spasticity/drug therapy/etiology
 Humans *Multiple Sclerosis/pathology Optic Nerve Brain/pathology *Optic Neuritis/pathology *Multiple Sclerosis, Relapsing-Remitting/pathology Atrophy/pathology Magnetic Resonance Imaging
 Humans Gray Matter/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology *Multiple Sclerosis/complications/diagnostic imaging/pathology Neurites/pathology Magnetic Resonance Imaging/methods *Cognitive Dysfunction/diagnostic imaging/etiology/pathology Atrophy/pathology Brain/diagnostic imaging/pathology
 Humans Female Adult Middle Aged Male *Multiple Sclerosis/complications/diagnostic imaging Cross-Sectional Studies Muscle Strength/physiology Quadriceps Muscle/diagnostic imaging Ultrasonography Muscle, Skeletal
 Humans *Multiple Sclerosis/complications Myelin Sheath *Remyelination Myelin Basic Protein
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Multiple Sclerosis/pathology Brain/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Central Nervous System Diseases/pathology Atrophy/pathology
 Animals *Multiple Sclerosis/metabolism Oligodendroglia/metabolism Fibroblast Growth Factors/metabolism Cell Differentiation Central Nervous System/metabolism
 Humans Female *Multiple Sclerosis/complications Intermittent Fasting *Veterans *Spinal Cord Injuries *Cardiovascular Diseases Fasting
 Humans *Multiple Sclerosis/therapy Ireland Surveys and Questionnaires Employment
 Humans *Multiple Sclerosis/drug therapy *Epstein-Barr Virus Infections/diagnosis Herpesvirus 4, Human
 Humans *Multiple Sclerosis/psychology Biomarkers *Cognitive Dysfunction/psychology Cognition Vitamin D
 Humans *Apraxia, Ideomotor *Apraxias/therapy/rehabilitation *Multiple Sclerosis/complications/therapy Neuropsychology Quality of Life Recovery of Function *Stroke *Stroke Rehabilitation *Virtual Reality
 Humans *Multiple Sclerosis Immunologic Factors *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Microglia Myelin Sheath Magnetic Resonance Imaging *White Matter/diagnostic imaging/pathology Positron-Emission Tomography/methods Brain/diagnostic imaging
 Humans Animals Mice Rats *Multiple Sclerosis/drug therapy Immunosuppressive Agents Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Dimethyl Fumarate/therapeutic use
 Humans *Multiple Sclerosis, Relapsing-Remitting *Multiple Sclerosis Postural Balance Case-Control Studies Time and Motion Studies
 Humans Female Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology Artificial Intelligence Retrospective Studies Reproducibility of Results Magnetic Resonance Imaging/methods
 Adult Child Humans *Multiple Sclerosis/pathology Veins Magnetic Resonance Imaging Brain/pathology
 Humans *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging Diffusion Tensor Imaging *Multiple Sclerosis Brain Mapping Cross-Sectional Studies Neuropsychological Tests Brain/diagnostic imaging Cognition Magnetic Resonance Imaging Neural Pathways/diagnostic imaging
 Pregnancy Humans Female *DNA Methylation *Multiple Sclerosis/genetics/metabolism Parity CD8-Positive T-Lymphocytes/metabolism Neuronal Plasticity Membrane Proteins/genetics
 Animals *Interleukin-10 Neuroinflammatory Diseases B-Lymphocytes Central Nervous System *Multiple Sclerosis/etiology Receptors, Interleukin-10
 Humans Rituximab/adverse effects *Multiple Sclerosis/drug therapy Prospective Studies Immunologic Factors/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced Recurrence Chronic Disease
 Humans *Multiple Sclerosis/diagnosis Optic Nerve/diagnostic imaging *Optic Neuritis/diagnosis
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis *Multiple Sclerosis/diagnosis Cohort Studies Immunoglobulin kappa-Chains/cerebrospinal fluid *Cognitive Dysfunction/diagnosis
 Humans Case-Control Studies CD8-Positive T-Lymphocytes Dimethyl Fumarate/pharmacology/therapeutic use *Multiple Sclerosis/pathology *Multiple Sclerosis, Chronic Progressive/drug therapy/pathology Myelin Basic Protein T-Lymphocytes
 Humans *Multiple Sclerosis/psychology *Mentalization *Theory of Mind/physiology Emotions/physiology Social Perception Neuropsychological Tests
 Animals Humans Middle Aged *Multiple Sclerosis/diagnostic imaging/etiology Retrospective Studies Diet/adverse effects Fruit Vegetables
 Female Humans Double-Blind Method Interleukin-2/therapeutic use *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Treatment Outcome Male Adult
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis *Multiple Sclerosis/drug therapy *Selenium/therapeutic use Coffee *Paullinia Pilot Projects Carnitine/therapeutic use Nutrigenomics Cytokines
 Humans *Multiple Sclerosis/drug therapy Antigens, CD CD40 Ligand B-Lymphocytes
 Humans *Multiple Sclerosis *Epstein-Barr Virus Infections Herpesvirus 4, Human *Multiple Sclerosis, Chronic Progressive Central Nervous System
 Humans Dimethyl Fumarate/therapeutic use *Multiple Sclerosis/drug therapy Immunosuppressive Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Magnetic Resonance Imaging Double-Blind Method
 Child Humans Adolescent *Multiple Sclerosis Follow-Up Studies Interferon beta-1a Natalizumab Retrospective Studies Gadolinium *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Immunosuppressive Agents
 Humans *COVID-19 *Multiple Sclerosis/therapy Pandemics Cross-Sectional Studies Physical Therapy Modalities
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab/therapeutic use Canada Disease Progression
 Humans *Multiple Sclerosis/complications/drug therapy Prospective Studies Quality of Life Urinary Bladder Longitudinal Studies Muscle Spasticity/etiology/complications
 Humans *Multiple Sclerosis/diagnostic imaging Bayes Theorem Magnetic Resonance Imaging/methods
 Humans Publication Bias *Multiple Sclerosis/drug therapy Research Design
 Humans *Multiple Sclerosis/diagnosis Intermediate Filaments Ambulatory Care Facilities Hospitals Patients
 Young Adult Humans Adolescent *Multiple Sclerosis/pathology Endothelial Cells Blood-Brain Barrier/metabolism Central Nervous System/metabolism Disease Progression
 Humans *Multiple Sclerosis/therapy *Self-Management *Rehabilitation Nursing Program Evaluation Self Efficacy
 Humans *Multiple Sclerosis/drug therapy Central Nervous System Blood Platelets Blood-Brain Barrier Inflammation
 Humans *Motivation *Multiple Sclerosis/diagnosis Motor Activity Exercise Self Efficacy
 Humans *Multiple Sclerosis Follow-Up Studies Cohort Studies Metabolomics *Multiple Sclerosis, Chronic Progressive
 Male Humans Prospective Studies Sensitivity and Specificity *Magnetic Resonance Imaging/methods *Multiple Sclerosis/diagnostic imaging/pathology Computers Brain/diagnostic imaging/pathology Retrospective Studies
 Humans *Multiple Sclerosis/diagnostic imaging/cerebrospinal fluid Prognosis Prospective Studies *Optic Neuritis/pathology Optic Nerve/pathology Magnetic Resonance Imaging/methods Disease Progression
 Humans *Multiple Sclerosis Cross-Sectional Studies Postural Balance Gait *Multiple Sclerosis, Relapsing-Remitting
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy/etiology *Multiple Sclerosis Treatment Outcome *Hematopoietic Stem Cell Transplantation/adverse effects/methods Transplantation, Autologous/methods
 Humans COVID-19 Vaccines/therapeutic use *Multiple Sclerosis/drug therapy *COVID-19 Immunity
 Humans *Myelin Sheath Protons Magnetic Resonance Imaging/methods Phantoms, Imaging *Multiple Sclerosis/diagnostic imaging/pathology Water Magnetic Resonance Spectroscopy Imaging, Three-Dimensional/methods
 Humans *Multiple Sclerosis/complications Life Change Events Muscle Spasticity/psychology Adaptation, Psychological Qualitative Research
 Humans Female *Complement Factor D *Multiple Sclerosis/therapy Depression/etiology Lipoproteins Anxiety/etiology
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Multiple Sclerosis Cross-Sectional Studies Magnetic Resonance Imaging/methods Hypothalamus/diagnostic imaging/pathology
 Humans *Transcriptome *Multiple Sclerosis/genetics Gene Expression Profiling RNA-Seq
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Neurites/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *White Matter/diagnostic imaging/pathology
 Humans *Multiple Sclerosis Tyrosine Protein Kinase Inhibitors Central Nervous System/pathology *Multiple Sclerosis, Chronic Progressive Signal Transduction
 Male Humans Child Child, Preschool *Multiple Sclerosis/diagnostic imaging/drug therapy *Diffuse Cerebral Sclerosis of Schilder/diagnostic imaging/drug therapy Neoplasm Recurrence, Local/pathology *Brain Neoplasms/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging
 Humans Syndrome Surveys and Questionnaires *Multiple Sclerosis/diagnosis Language Russia Disability Evaluation
 Humans *Quality of Life *Multiple Sclerosis/therapy Qualitative Research Sweden
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis State Medicine Dimethyl Fumarate/therapeutic use Disease Progression Immunosuppressive Agents
 Humans *Multiple Sclerosis/complications *Virtual Reality Cognition Neuropsychological Tests *Cognitive Dysfunction/etiology
 Humans *Liver Cirrhosis, Biliary/complications *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive Syndrome Necrosis
 Humans Female Aged Aged, 80 and over Middle Aged *Multiple Sclerosis/complications/diagnostic imaging Brain/pathology Magnetic Resonance Imaging/methods Gray Matter/pathology *White Matter/diagnostic imaging/pathology Anisotropy
 Humans Ataxia *Multiple Sclerosis/diagnosis *Nervous System Diseases/diagnosis *Neurology *Urology
 Humans *Caregivers Quality of Life Caregiver Burden *Multiple Sclerosis/therapy Mental Health
 Humans Male Female *Multiple Sclerosis/complications Quality of Life Outcome Assessment, Health Care Chronic Disease
 Humans *Autoimmunity/genetics Gene Expression Regulation Gene Regulatory Networks *Hepatocyte Nuclear Factor 4/genetics/metabolism *Multiple Sclerosis/genetics/immunology Transcriptome Genes, myc
 Humans Natalizumab/therapeutic use Cross-Sectional Studies *Multiple Sclerosis/drug therapy Risk Factors Administration, Intravenous Immunologic Factors/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Infant, Newborn Pregnancy Female Humans Cladribine *Multiple Sclerosis Cohort Studies Pregnancy Outcome Recurrence *Multiple Sclerosis, Relapsing-Remitting Immunosuppressive Agents
 Humans *Multiple Sclerosis/diagnosis Nerve Fibers *Corneal Injuries Cornea Microscopy, Confocal
 Humans *RNA, Circular/genetics/metabolism Leukocytes, Mononuclear/metabolism *Multiple Sclerosis/genetics/metabolism RNA/genetics/metabolism DNA Methylation
 Humans *Multiple Sclerosis/diagnostic imaging *COVID-19/prevention & control
 Humans Vitamin B 12 Folic Acid *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting Vitamins
 Adult Humans Middle Aged Gadolinium/therapeutic use *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence Thromboplastin
 Humans *Optic Neuritis/diagnosis *Multiple Sclerosis/diagnosis
 Humans Male *Multiple Sclerosis/diagnosis *Demyelinating Diseases/pathology Magnetic Resonance Imaging/methods Brain/pathology Prognosis
 Humans *White Matter/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/pathology *Multiple Sclerosis/pathology Retrospective Studies Diffusion Tensor Imaging/methods Diffusion Magnetic Resonance Imaging Brain/diagnostic imaging/pathology
 Humans *Multiple Sclerosis/therapy B-Lymphocytes Immunosuppressive Agents/therapeutic use
 Humans Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology *Multiple Sclerosis/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology *Central Nervous System Diseases/pathology
 Humans *Multiple Sclerosis/diagnosis B-Lymphocytes Central Nervous System Autoantibodies Biomarkers
 Humans Cells, Cultured Cytokines/metabolism Dendritic Cells *Interleukin-27/metabolism Leukocytes, Mononuclear/metabolism *Multiple Sclerosis/genetics/metabolism T-Lymphocytes/metabolism
 Humans *Optic Neuritis/diagnosis *Multiple Sclerosis/diagnosis
 Humans *Multiple Sclerosis/drug therapy *Ginger Quality of Life Matrix Metalloproteinase 9 Interleukin-17 *Multiple Sclerosis, Relapsing-Remitting/drug therapy Dietary Supplements Double-Blind Method
 Humans *Multiple Sclerosis/rehabilitation Randomized Controlled Trials as Topic *Patient Selection
 Adult Humans *Multiple Sclerosis/drug therapy Antibodies, Monoclonal/adverse effects *Antineoplastic Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Double-Blind Method Treatment Outcome
 Humans *Multiple Sclerosis, Chronic Progressive/cerebrospinal fluid *Multiple Sclerosis/cerebrospinal fluid Ascorbic Acid Central Nervous System Metals Biomarkers/cerebrospinal fluid
 Male Female Humans *Multiple Sclerosis/genetics Genome-Wide Association Study Neoplasm Recurrence, Local Prognosis Immune System
 Humans *Mobile Applications *Multiple Sclerosis/therapy *Self-Management *Telemedicine Qualitative Research
 Humans Female Male *Multiple Sclerosis/psychology Qualitative Research Self Concept Emotional Adjustment Disease Progression
 Humans *Multiple Sclerosis/diagnostic imaging Upper Extremity Magnetic Resonance Imaging Smartphone Brain
 Animals *Multiple Sclerosis/diagnostic imaging/pathology *Remyelination Magnetic Resonance Imaging/methods *Encephalomyelitis, Autoimmune, Experimental/pathology Callithrix Disease Models, Animal Myelin Sheath
 Humans Fingolimod Hydrochloride/adverse effects Natalizumab/adverse effects *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Rituximab/adverse effects *Multiple Sclerosis/drug therapy Immunologic Factors/adverse effects Retrospective Studies Treatment Outcome Recurrence Immunosuppressive Agents/therapeutic use
 Pregnancy Humans Male Female *Family Planning Services *Multiple Sclerosis/therapy Australia Qualitative Research Patient Outcome Assessment
 Humans Female Adult Hydroxychloroquine/adverse effects *Multiple Sclerosis/complications/drug therapy Leflunomide/adverse effects *Lupus Erythematosus, Cutaneous/chemically induced/diagnosis/drug therapy
 Humans *Carotid Intima-Media Thickness *Multiple Sclerosis/diagnostic imaging
 Humans *Multiple Sclerosis/drug therapy Tumor Necrosis Factor-alpha Canada Research
 Humans Male *Multiple Sclerosis/drug therapy/epidemiology *COVID-19/epidemiology Electronic Health Records Retrospective Studies COVID-19 Testing Pandemics Dimethyl Fumarate Hospitalization
 Adult Humans *Mobile Applications *Multiple Sclerosis/therapy Chronic Disease Exercise *Self-Management
 Humans *Quality of Life *Multiple Sclerosis/therapy Healthy Lifestyle Life Style Vitamin D Vitamins
 Humans *Multiple Sclerosis, Chronic Progressive/drug therapy *Multiple Sclerosis Glatiramer Acetate *Hematopoietic Stem Cell Transplantation Fingolimod Hydrochloride *Multiple Sclerosis, Relapsing-Remitting/therapy
 Humans *Problem Solving *Multiple Sclerosis/therapy Patient Participation Qualitative Research
 Humans Natalizumab/therapeutic use *Multiple Sclerosis Immunologic Factors/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Autoantibodies *Parkinson Disease/diagnosis *Multiple Sclerosis/diagnosis Diagnostic Errors
 Humans *Multiple Sclerosis/therapy Activities of Daily Living *Stroke Rehabilitation
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Leukocytes, Mononuclear Antibodies, Monoclonal, Humanized/therapeutic use
 Humans Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy Dimethyl Fumarate/therapeutic use Immunosuppressive Agents/therapeutic use Retrospective Studies Smoking *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy Austria *Multiple Sclerosis/drug therapy Treatment Outcome Fingolimod Hydrochloride/therapeutic use Recurrence Immunosuppressive Agents/therapeutic use Immunologic Factors/pharmacology/therapeutic use
 Animals Mice Natalizumab/pharmacology/therapeutic use *Th17 Cells Virulence *Multiple Sclerosis/drug therapy/cerebrospinal fluid Brain
 Female Child Humans Male *Encephalomyelitis, Acute Disseminated/diagnostic imaging/therapy Follow-Up Studies Syndrome Central Nervous System *Multiple Sclerosis/diagnostic imaging/epidemiology Recurrence Observational Studies as Topic Multicenter Studies as Topic
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy Retrospective Studies Ethnicity Neurons Disease Progression Disability Evaluation
 Humans *Multiple Sclerosis/drug therapy Sphingosine-1-Phosphate Receptors/therapeutic use Immunologic Factors/adverse effects Thiazoles/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy Sphingosine/therapeutic use
 Humans *Multiple Sclerosis/drug therapy Research Design Data Interpretation, Statistical Computer Simulation
 Humans *Multiple Sclerosis/therapy Exercise Social Support Exercise Therapy Cognition
 Female Humans Middle Aged *Multiple Sclerosis/epidemiology Australia/epidemiology Queensland/epidemiology *Multiple Sclerosis, Relapsing-Remitting/epidemiology Prevalence Incidence
 Humans COVID-19 Vaccines/adverse effects *Multiple Sclerosis/complications/drug therapy *COVID-19/prevention & control SARS-CoV-2 Vaccination/adverse effects
 Humans Female Adult Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology Retrospective Studies Prospective Studies Brain/pathology Magnetic Resonance Imaging/methods
 Humans Retinal Ganglion Cells/pathology *Multiple Sclerosis, Relapsing-Remitting/pathology *Multiple Sclerosis/pathology Retina/pathology Cohort Studies Tomography, Optical Coherence/methods
 Humans *Multiple Sclerosis/drug therapy Immunosuppressive Agents Fingolimod Hydrochloride/pharmacology/therapeutic use Glatiramer Acetate/therapeutic use Natalizumab *Gastrointestinal Microbiome Dimethyl Fumarate/pharmacology/therapeutic use *Multiple Sclerosis, Relapsing-Remitting
 Humans Cytokines/cerebrospinal fluid/chemistry Interleukin-10 Interleukin-13 Interleukin-17/cerebrospinal fluid Interleukin-2 Interleukin-4/cerebrospinal fluid Interleukin-5 Interleukin-9 Interleukins/cerebrospinal fluid/chemistry *Multiple Sclerosis/cerebrospinal fluid/diagnosis *Multiple Sclerosis, Relapsing-Remitting/cerebrospinal fluid/diagnosis
 Mice Humans Animals *Multiple Sclerosis/etiology *Encephalomyelitis, Autoimmune, Experimental Disease Models, Animal Magnetic Resonance Imaging Atrophy
 Humans Adult Middle Aged Aged *Cognitive Reserve *Multiple Sclerosis/psychology Cognition Memory Neuropsychological Tests
 Humans *Multiple Sclerosis/therapy Exercise Therapy Physical Therapy Modalities Cognition Gait
 Humans Female Adult Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology Prospective Studies Contrast Media Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology Imaging, Three-Dimensional/methods
 Humans *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive/genetics Stem Cells Cell Differentiation Organoids Oligodendroglia
 Humans *Multiple Sclerosis/drug therapy Walking Double-Blind Method
 Humans *Multiple Sclerosis/complications/psychology Hydrocortisone *COVID-19/epidemiology Quality of Life/psychology Pandemics Depression/epidemiology/psychology Fatigue/epidemiology/etiology/psychology
 Humans *Multiple Sclerosis/drug therapy Quality of Life *Neurodegenerative Diseases Chronic Disease Tea
 Humans Aged *COVID-19/complications *Multiple Sclerosis/epidemiology/complications Pandemics SARS-CoV-2 Depression/epidemiology/psychology Anxiety/epidemiology Stress, Psychological/epidemiology
 Humans *Spectrum Analysis, Raman/methods *Multiple Sclerosis/diagnostic imaging Pilot Projects Spectroscopy, Fourier Transform Infrared
 Humans *Acetylcysteine/therapeutic use/pharmacology Anxiety/drug therapy/etiology Biomarkers Depression/drug therapy/etiology Glutathione/metabolism/pharmacology *Multiple Sclerosis/complications/drug therapy Oxidative Stress
 Humans Male Female *Quality of Life Cross-Cultural Comparison *Multiple Sclerosis/complications Sexuality Surveys and Questionnaires Follicle Stimulating Hormone
 Humans Female Adult Male *Multiple Sclerosis, Relapsing-Remitting/pathology Retinal Ganglion Cells/pathology Prospective Studies *Multiple Sclerosis/complications Atrophy/pathology Tomography, Optical Coherence/methods
 Humans Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents/therapeutic use Dimethyl Fumarate/pharmacology/therapeutic use Chemokine CXCL13
 Animals *Multiple Sclerosis/drug therapy Brain-Gut Axis Dysbiosis/therapy *Encephalomyelitis, Autoimmune, Experimental *Probiotics/therapeutic use
 Humans Animals *Multiple Sclerosis/therapy *Gastrointestinal Microbiome *Encephalomyelitis, Autoimmune, Experimental *Microbiota Central Nervous System
 Female Humans Adolescent Young Adult Adult Male *Multiple Sclerosis, Relapsing-Remitting/drug therapy Rituximab/therapeutic use *Multiple Sclerosis/drug therapy Retrospective Studies Immunologic Factors/therapeutic use Off-Label Use
 Humans *Multiple Sclerosis/pathology Glial Fibrillary Acidic Protein *Multiple Sclerosis, Chronic Progressive/complications Neurons/pathology *Cognitive Dysfunction/etiology/complications Neurofilament Proteins Biomarkers
 Child Humans Adolescent Body Mass Index *Multiple Sclerosis/complications Intelligence Intelligence Tests Obesity
 Humans *Multiple Sclerosis/diagnostic imaging Cross-Sectional Studies Neurofilament Proteins *Multiple Sclerosis, Chronic Progressive/diagnostic imaging Biomarkers Contactins
 Humans *Multiple Sclerosis/drug therapy Antigens, CD20 Antibodies, Monoclonal, Humanized Learning
 Humans Immunoglobulin kappa-Chains/cerebrospinal fluid Immunoglobulin Light Chains *Multiple Sclerosis/diagnosis/cerebrospinal fluid Biomarkers/cerebrospinal fluid *Central Nervous System Diseases/diagnosis Oligoclonal Bands/cerebrospinal fluid
 Humans *Artificial Intelligence *Multiple Sclerosis/diagnostic imaging Area Under Curve Databases, Factual
 Adult Humans *COVID-19 SARS-CoV-2 *Multiple Sclerosis/therapy Autografts Cyclophosphamide
 Humans *Venous Thromboembolism/etiology/complications *Venous Thrombosis/epidemiology/etiology Incidence *Multiple Sclerosis/complications/epidemiology *Pulmonary Embolism/etiology/complications Risk Factors
 Humans Walk Test *Walking *Multiple Sclerosis/diagnosis Health Status Mobility Limitation
 Humans Coculture Techniques *Induced Pluripotent Stem Cells Interleukin-17/metabolism *Multiple Sclerosis/genetics/metabolism Astrocytes/metabolism Tumor Necrosis Factor-alpha/metabolism Neurons/metabolism *Central Nervous System Diseases Intercellular Signaling Peptides and Proteins/metabolism Central Nervous System Cells, Cultured
 Pregnancy Humans Female *Neuromyelitis Optica/diagnosis/therapy *Multiple Sclerosis/diagnosis/therapy Vaccination Postpartum Period Recurrence
 Humans *Multiple Sclerosis/diagnosis Croatia Psychometrics Reproducibility of Results Cross-Sectional Studies Quality of Life Walking Language
 Animals Mice *Multiple Sclerosis/drug therapy Disease Models, Animal *Neurodegenerative Diseases Receptors, IgG *Encephalomyelitis, Autoimmune, Experimental
 Humans Exergaming Exercise Therapy Employment *Virtual Reality *Multiple Sclerosis/rehabilitation
 Humans *Biosimilar Pharmaceuticals/therapeutic use *Multiple Sclerosis/drug therapy Treatment Outcome Europe
 Humans *Multiple Sclerosis/complications Feedback Australia Self Efficacy *Cognitive Dysfunction/etiology
 Adult Female Humans Middle Aged Male *Multiple Sclerosis/therapy Upper Extremity Physical Therapy Modalities *Stroke Rehabilitation
 Humans *Evoked Potentials, Motor/physiology *Multiple Sclerosis/diagnosis Electromyography Transcranial Magnetic Stimulation/methods Magnetic Resonance Imaging
 Humans Range of Motion, Articular/physiology Reproducibility of Results *Multiple Sclerosis/diagnosis Physical Examination Hip
 Humans *Multiple Sclerosis/therapy *COVID-19 Australia Health Personnel Health Services Accessibility
 Humans *Multiple Sclerosis/complications Cross-Sectional Studies *Cognitive Dysfunction/etiology Movement Ataxia
 Humans Male Female Rituximab/therapeutic use *Multiple Sclerosis/drug therapy *Pyoderma Gangrenosum/diagnosis/drug therapy/etiology *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunoglobulins, Intravenous/therapeutic use
 Female Humans Male Adolescent Young Adult Adult Middle Aged Aged Aged, 80 and over Interferon beta-1a/therapeutic use *Multiple Sclerosis/drug therapy Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Injections Injections, Subcutaneous
 Humans *Azetidines/adverse effects Benzyl Compounds/adverse effects *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy
 Humans Concept Formation *Empathy Health Personnel *Multiple Sclerosis/therapy Quality of Life
 Humans Female Middle Aged Male *Intermittent Urethral Catheterization *Multiple Sclerosis/complications Retrospective Studies Functional Status Cognition
 Humans *Ethnicity *Multiple Sclerosis/psychology Rehabilitation Research Exercise White
 Humans *Multiple Sclerosis/complications Switzerland/epidemiology Cross-Sectional Studies Educational Status Registries
 Humans *Multiple Sclerosis/diagnosis Postural Balance Biomechanical Phenomena Posture *Wearable Electronic Devices
 Humans Feasibility Studies *Multiple Sclerosis/therapy Quality of Life *COVID-19 Physical Therapy Modalities
 Humans *Multiple Sclerosis/diagnosis Smartphone Walk Test Walking Disability Evaluation
 Humans Cladribine/adverse effects *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents/adverse effects
 Humans Alemtuzumab/adverse effects *Multiple Sclerosis/chemically induced *Lymphohistiocytosis, Hemophagocytic/chemically induced Antibodies, Monoclonal, Humanized/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/complications Quality of Life *Cognitive Dysfunction/etiology Cognition *Primary Dysautonomias
 Humans Chromatography, Liquid/methods *Tandem Mass Spectrometry/methods Chromatography, High Pressure Liquid/methods *Multiple Sclerosis/drug therapy
 Humans *Epigenesis, Genetic/genetics Gene Regulatory Networks Genome-Wide Association Study *Multiple Sclerosis/drug therapy/genetics DNA Methylation/genetics Quantitative Trait Loci/genetics
 Humans Female *Urinary Bladder, Overactive *Multiple Sclerosis/complications Sexual Behavior Sexuality Qualitative Research
 Humans Bayes Theorem *Fatigue/diagnosis/etiology/physiopathology/therapy *Multiple Sclerosis/complications/physiopathology Quality of Life *Transcranial Direct Current Stimulation/methods Single-Blind Method Dorsolateral Prefrontal Cortex Task Performance and Analysis Reaction Time
 Pregnancy Female Humans *Multiple Sclerosis/drug therapy/etiology Retrospective Studies Fertilization in Vitro/adverse effects Ovulation Induction/methods Incidence
 Humans Bashkiria/epidemiology Follow-Up Studies *Multiple Sclerosis/epidemiology/genetics Genome-Wide Association Study Prospective Studies Alleles Genetic Predisposition to Disease Polymorphism, Single Nucleotide Glypicans/genetics
 Mice Animals *Multiple Sclerosis/complications/drug therapy Microglia/physiology Depression/drug therapy/etiology Quality of Life *Encephalomyelitis, Autoimmune, Experimental/drug therapy Oxidative Stress Anxiety/drug therapy/etiology Mice, Inbred C57BL
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis *Multiple Sclerosis Retrospective Studies Prospective Studies Quality of Life Exercise
 Adolescent Child Humans *Multiple Sclerosis/complications/diagnostic imaging *Optic Nerve Injuries/complications Evoked Potentials, Visual Optic Nerve/diagnostic imaging *Optic Neuritis Magnetic Resonance Imaging/methods Tomography, Optical Coherence/methods
 Male Humans *Multiple Sclerosis/therapy Quality of Life Mental Processes Communication Risk Factors
 Humans Iran *Multiple Sclerosis/drug therapy Theory of Planned Behavior Surveys and Questionnaires Medication Adherence
 Animals *Multiple Sclerosis/therapy *Neurodegenerative Diseases/etiology Central Nervous System/pathology Axons/pathology Disease Progression
 Humans *Multiple Sclerosis/complications Depression/psychology Neuropsychological Tests *Cognitive Dysfunction/psychology *Cognition Disorders/diagnosis Cognition
 Humans Prospective Studies Longitudinal Studies Iron Brain/diagnostic imaging/pathology *Multiple Sclerosis/diagnostic imaging/pathology *Central Nervous System Diseases/pathology Magnetic Resonance Imaging/methods Oxidative Stress Atrophy/pathology Gray Matter/pathology
 Humans Brain/diagnostic imaging *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging *Multiple Sclerosis Magnetic Resonance Imaging/methods *Connectome/methods
 Humans *Neuromyelitis Optica/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Retrospective Studies Cohort Studies *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging Brain/diagnostic imaging
 Humans *Yoga Pilot Projects Quality of Life *Multiple Sclerosis/therapy *Meditation Feasibility Studies
 Humans Child, Preschool Adolescent *Hodgkin Disease/epidemiology/complications *Multiple Sclerosis/epidemiology/complications Cross-Sectional Studies *Inflammatory Bowel Diseases/complications *Colitis, Ulcerative/epidemiology/etiology *Crohn Disease/etiology
 Animals Female Humans Male *Multiple Sclerosis/pathology Sex Characteristics Brain/pathology Central Nervous System/pathology Iron
 Humans *Multiple Sclerosis/pathology Reactive Oxygen Species/metabolism Oligodendroglia/pathology Cell Death *Multiple Sclerosis, Chronic Progressive/pathology Adenosine Triphosphate/metabolism
 Humans *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Brain Phantoms, Imaging
 Humans *Neuromyelitis Optica/complications/epidemiology Cohort Studies *Multiple Sclerosis/complications/epidemiology Retrospective Studies Magnetic Resonance Imaging *Fractures, Bone
 Humans Aged *Multiple Sclerosis/drug therapy Immune Checkpoint Inhibitors/therapeutic use Retrospective Studies *Nervous System Diseases *Neoplasms/complications/drug therapy
 Adult Humans Manitoba/epidemiology Mental Health Cross-Sectional Studies Cohort Studies *Multiple Sclerosis/complications/epidemiology *Arthritis, Rheumatoid/epidemiology/psychology *Inflammatory Bowel Diseases/epidemiology Canada/epidemiology Pain
 Humans *Multiple Sclerosis/genetics Life Style Genetic Testing
 Humans *Multiple Sclerosis Cross-Sectional Studies Retrospective Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Chronic Disease
 Humans *Brain/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods Diffusion Magnetic Resonance Imaging
 Male Humans Female Brazil/epidemiology *Multiple Sclerosis/complications Patients Universities
 Humans *Multiple Sclerosis/chemically induced Cladribine/therapeutic use Immunosuppressive Agents/therapeutic use Immunologic Factors Fingolimod Hydrochloride *Multiple Sclerosis, Relapsing-Remitting/drug therapy Natalizumab Chronic Disease Recurrence
 Humans Female *Multiple Sclerosis/complications Rehabilitation, Vocational/methods *Cognitive Dysfunction Employment
 Humans Epitopes, T-Lymphocyte/chemistry/genetics *Multiple Sclerosis/therapy *Vaccines/therapeutic use
 Female Humans Natalizumab/therapeutic use Rituximab/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunologic Factors/therapeutic use *Multiple Sclerosis/drug therapy Retrospective Studies Cost-Benefit Analysis Saudi Arabia Disease Progression
 Humans Ethnicity *Multiple Sclerosis/therapy Research Design Surveys and Questionnaires Clinical Trials as Topic
 Humans *Multiple Sclerosis/drug therapy Immunologic Factors/adverse effects Prospective Studies Antibodies, Monoclonal, Humanized/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Diabetes Mellitus, Type 2/complications Genome-Wide Association Study Interleukin-17/genetics Mendelian Randomization Analysis *Multiple Sclerosis/epidemiology/genetics/complications Polymorphism, Single Nucleotide/genetics *Psoriasis/epidemiology/genetics Risk Factors Janus Kinases/metabolism STAT Transcription Factors/metabolism
 Humans Adolescent Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis *MicroRNAs *Multiple Sclerosis, Relapsing-Remitting/drug therapy Biomarkers *Autoimmune Diseases
 Humans Female Middle Aged Male Aged *Multiple Sclerosis *Frailty Walking *Multiple Sclerosis, Relapsing-Remitting Exercise Frail Elderly
 Humans *Cannabinoids/adverse effects Quality of Life Dronabinol/adverse effects Activities of Daily Living *Multiple Sclerosis/complications/drug therapy Muscle Spasticity/drug therapy/etiology *Cannabidiol/adverse effects *Cannabis
 Humans *Multiple Sclerosis/pathology Gadolinium Contrast Media Magnetic Resonance Imaging Neuroimaging Brain
 Female Pregnancy Humans Family Planning Services *Multiple Sclerosis/therapy *Neuromyelitis Optica/therapy *Autoimmune Diseases Central Nervous System
 Humans Latent Class Analysis Disease Progression *Multiple Sclerosis, Chronic Progressive/drug therapy *Disabled Persons Registries *Multiple Sclerosis/drug therapy
 Humans *Depression *Multiple Sclerosis/complications Diet Kidney Anxiety/etiology
 Humans *Shoes *Multiple Sclerosis/rehabilitation Walking Gait Postural Balance
 Adult Humans *Multiple Sclerosis/therapy Cohort Studies Magnetic Resonance Imaging Disease Progression Registries
 Young Adult Humans Female Middle Aged Male British Columbia/epidemiology Cohort Studies Retrospective Studies *Multiple Sclerosis/therapy/drug therapy Quality of Life Health Care Costs Drug Costs
 Humans Female Middle Aged *Multiple Sclerosis/drug therapy *Breast Neoplasms/therapy Neoplasm Recurrence, Local Disease Progression Patient Outcome Assessment
 Adult Humans Female Child Adolescent Male *Multiple Sclerosis, Relapsing-Remitting/drug therapy Intermediate Filaments *Multiple Sclerosis/drug therapy Crotonates/therapeutic use Toluidines/therapeutic use
 Humans Follow-Up Studies Magnetic Resonance Imaging *Multiple Sclerosis/diagnosis *Demyelinating Diseases Biomarkers Disease Progression Chemokine CXCL13
 Humans Cladribine/therapeutic use *Multiple Sclerosis/drug therapy Herpesvirus 3, Human *Influenza Vaccines/therapeutic use Immunosuppressive Agents/therapeutic use *Chickenpox/drug therapy *Influenza, Human/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Tablets/therapeutic use
 Animals Mice *Multiple Sclerosis/drug therapy/metabolism Glia Maturation Factor/metabolism Cytokines/metabolism Methanol Molecular Docking Simulation *Encephalomyelitis, Autoimmune, Experimental/drug therapy Neuroglia/metabolism Mice, Inbred C57BL
 Humans Adult Middle Aged *Multiple Sclerosis/complications/drug therapy Treatment Outcome 4-Aminopyridine/therapeutic use/pharmacology Potassium Channel Blockers/therapeutic use/pharmacology Gait/physiology Walking/physiology
 Pregnancy Infant, Newborn Humans Female Pregnancy Outcome/epidemiology Natalizumab/adverse effects Dimethyl Fumarate/adverse effects *Multiple Sclerosis/drug therapy/epidemiology *Premature Birth/epidemiology Denmark/epidemiology
 Humans *Multiple Sclerosis/cerebrospinal fluid Oligoclonal Bands Retrospective Studies Lithuania Radiography
 Male Rats Animals Vitamin D Antioxidants/pharmacology *Multiple Sclerosis/drug therapy Vitamins/pharmacology/therapeutic use *Multiple Sclerosis, Chronic Progressive/drug therapy Models, Animal
 Humans *Cholesterol/metabolism *Multiple Sclerosis/metabolism Disability Evaluation
 Humans Ethnicity *Hispanic or Latino *Immunity, Humoral *Multiple Sclerosis/immunology White *Black or African American
 Male Humans Female *Multiple Sclerosis Prospective Studies *Multiple Sclerosis, Relapsing-Remitting/therapy *Hematopoietic Stem Cell Transplantation Transplantation, Autologous Chemokine CXCL13
 Humans Disease Progression *Prospective Studies Pharmacoepidemiology *Multiple Sclerosis/drug therapy Drug Approval
 Humans *Multiple Sclerosis/drug therapy *Antibodies, Monoclonal, Humanized/administration & dosage *Self Administration/instrumentation
 Adult Humans Child *Cognition Disorders/psychology *Multiple Sclerosis/diagnosis Cognition Neuropsychological Tests Memory and Learning Tests *Cognitive Dysfunction/diagnosis/etiology
 Pregnancy Female Humans *Multiple Sclerosis/genetics In Situ Hybridization, Fluorescence Postpartum Period Leukocytes Telomere
 Humans *Multiple Sclerosis/complications Hot Temperature Exercise/physiology Fatigue/complications Prescriptions
 Humans Quality of Life/psychology Self Efficacy *Emotional Regulation Cross-Sectional Studies *Multiple Sclerosis/psychology
 Humans Adult *Multiple Sclerosis/psychology *Disabled Persons Exercise Therapy/psychology Exercise/psychology Physical Therapy Modalities Qualitative Research
 Humans Antibodies, Monoclonal/adverse effects Rituximab/therapeutic use Natalizumab/therapeutic use Alemtuzumab *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Female Adult *Multiple Sclerosis/diagnostic imaging Biopsy Immunosuppression Therapy Magnetic Resonance Imaging
 Male Humans Adult Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology Cohort Studies Retrospective Studies Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology
 Humans *Multiple Sclerosis/complications Goals Motivation Leisure Activities Fatigue/etiology/therapy
 Humans Brain-Derived Neurotrophic Factor *Multiple Sclerosis/pathology Neuroinflammatory Diseases Inflammation/pathology *Neuroprotective Agents
 Male Humans Female *COVID-19 Cause of Death Sclerosis Causality *Multiple Sclerosis/complications
 Humans *Multiple Sclerosis/psychology Quality of Life/psychology Adaptation, Psychological Anxiety/psychology Social Support Stress, Psychological/psychology
 Humans *Multiple Sclerosis
 Humans Aged *Multiple Sclerosis/diagnosis Blood Pressure Cross-Sectional Studies Neuropsychological Tests Cognition
 Child, Preschool Child Humans *Multiple Sclerosis/epidemiology/genetics *Epstein-Barr Virus Infections Herpesvirus 4, Human B-Lymphocytes Genotype HLA-DRB1 Chains/genetics Genetic Predisposition to Disease/genetics
 Humans *Multiple Sclerosis/complications Walking Physical Therapy Modalities Mobility Limitation Lower Extremity Disability Evaluation
 Humans Neuroglia *Central Nervous System Diseases/metabolism *Multiple Sclerosis/metabolism Central Nervous System Microglia/metabolism
 Humans *Multiple Sclerosis/complications Cross-Sectional Studies *Insulin Resistance *Neurodegenerative Diseases *Cognitive Dysfunction/etiology Cognition *Insulins Neuropsychological Tests
 United States Humans *Multiple Sclerosis/epidemiology Incidence Canada Prevalence Indigenous Peoples
 Humans *Multiple Sclerosis/diagnostic imaging Oxygen Magnetic Resonance Imaging Brain/diagnostic imaging
 Humans *Multiple Sclerosis/therapy Activities of Daily Living Task Performance and Analysis Biomechanical Phenomena Cross-Over Studies Mouth *Virtual Reality
 Humans *Multiple Sclerosis/drug therapy Cross-Sectional Studies Neural Conduction/physiology *Peripheral Nervous System Diseases/diagnosis
 Humans Female Adult Male *Multiple Sclerosis/diagnosis Retrospective Studies Prospective Studies Glial Fibrillary Acidic Protein Intermediate Filaments/metabolism/pathology *Multiple Sclerosis, Chronic Progressive/metabolism Biomarkers
 Mice Animals *Multiple Sclerosis/therapy Granulocyte-Macrophage Colony-Stimulating Factor Antigens *Autoimmune Diseases T-Lymphocytes *Encephalomyelitis, Autoimmune, Experimental
 Humans *Multiple Sclerosis/complications *COVID-19 Prospective Studies Argentina/epidemiology
 Animals Humans *Multiple Sclerosis/drug therapy Central Nervous System Immunity *Probiotics/pharmacology/therapeutic use Cytokines
 Humans *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods *Disabled Persons *Motor Disorders Neuroimaging Brain/diagnostic imaging Machine Learning
 Humans *Multiple Sclerosis/complications Tomography, Optical Coherence Retina *Optic Neuritis/complications Angiography Retinal Vessels Fluorescein Angiography/methods
 Animals *Multiple Sclerosis/drug therapy Caloric Restriction Central Nervous System *Remyelination Disease Models, Animal Myelin Sheath/physiology
 Animals Mice Encephalomyelitis, Autoimmune, Experimental/metabolism/therapy Enzyme-Linked Immunosorbent Assay *Immunodominant Epitopes/analysis Mannans/chemistry Mice, Inbred C57BL *Myelin-Oligodendrocyte Glycoprotein/analysis *Peptide Fragments/analysis *Multiple Sclerosis/metabolism/therapy
 Humans *Demyelinating Diseases/diagnostic imaging *Multiple Sclerosis/diagnostic imaging *Autoimmune Diseases of the Nervous System Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/diagnosis Central Nervous System Biomarkers Inflammation Disease Progression
 Humans Myelin-Oligodendrocyte Glycoprotein Syndrome *Multiple Sclerosis/diagnostic imaging *Central Nervous System Diseases Central Nervous System/pathology Autoantibodies
 Humans Incidence *Multiple Sclerosis, Relapsing-Remitting/pathology Chronic Disease Recurrence Cognition Magnetic Resonance Imaging *Multiple Sclerosis Brain/pathology
 Humans *Antioxidants/pharmacology *Multiple Sclerosis/drug therapy Drug Repositioning Oxidative Stress Anti-Inflammatory Agents/therapeutic use/pharmacology
 Humans *Proteomics/methods *Multiple Sclerosis/diagnosis Tears/chemistry Mass Spectrometry Chromatography, Liquid
 Humans *Self-Management/methods *Text Messaging *Multiple Sclerosis/therapy *Telemedicine Fatigue
 Humans *Multiple Sclerosis/diagnostic imaging Retinal Ganglion Cells Nerve Fibers Tomography, Optical Coherence/methods Retina
 Humans *Endocannabinoids/genetics/metabolism/therapeutic use *Multiple Sclerosis/drug therapy Inflammation Mass Spectrometry Biomarkers
 Humans *Multiple Sclerosis/complications/diagnostic imaging Gadolinium Retrospective Studies Cerebellar Nuclei Magnetic Resonance Imaging/methods Contrast Media Cognition Gadolinium DTPA *Organometallic Compounds
 Humans *Multiple Sclerosis/psychology Depression/complications/diagnosis Chicago Neuropsychological Tests Reproducibility of Results
 Humans Female *Multiple Sclerosis/therapy Siblings *Hematopoietic Stem Cell Transplantation *Red-Cell Aplasia, Pure/therapy *Graft vs Host Disease/therapy
 Humans Rituximab/adverse effects *Neuromyelitis Optica/drug therapy/chemically induced *Multiple Sclerosis/drug therapy/chemically induced Immunologic Factors/adverse effects Retrospective Studies
 Humans *Multiple Sclerosis/diagnostic imaging/pathology Cerebral Cortex/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Gray Matter/diagnostic imaging/pathology Myelin Sheath/pathology Brain/pathology
 Humans *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy Alemtuzumab/therapeutic use Network Meta-Analysis Bayes Theorem Recurrence
 Adult Humans *Multiple Sclerosis/therapy Cross-Sectional Studies Program Evaluation Exercise *Wheelchairs
 Humans *Neuromyelitis Optica Autoantibodies/therapeutic use *Multiple Sclerosis/complications
 Humans Heart Rate *Receptors, Lysosphingolipid *Multiple Sclerosis/drug therapy Thiazoles
 Humans *Demyelinating Diseases/diagnostic imaging *Multiple Sclerosis/diagnostic imaging *Autoimmune Diseases of the Nervous System Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/psychology Reaction Time Reward Fatigue/complications Cognition
 Male Humans Middle Aged *Multiple Sclerosis/diagnosis Fingolimod Hydrochloride/adverse effects Contrast Media *Decompressive Craniectomy Gadolinium Magnetic Resonance Imaging
 Humans *Optic Neuritis/diagnosis *Multiple Sclerosis/diagnosis
 Humans CD8-Positive T-Lymphocytes Memory T Cells Cross-Sectional Studies *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive HLA-DR Antigens
 Young Adult Humans *Multiple Sclerosis/diagnosis Quality of Life *Sexual Dysfunction, Physiological/etiology/epidemiology/psychology Central Nervous System Brain
 Humans *Multiple Sclerosis Longitudinal Studies *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging Magnetic Resonance Imaging *White Matter Chronic Disease Brain/diagnostic imaging
 Humans Autoantibodies *Autoimmune Diseases/drug therapy Central Nervous System *Multiple Sclerosis/drug therapy B-Lymphocytes
 Humans Female *Oligoclonal Bands/cerebrospinal fluid *Multiple Sclerosis/cerebrospinal fluid/diagnosis Retrospective Studies Immunoglobulin G Albumins
 Humans Double-Blind Method *Interferon beta-1a/administration & dosage/adverse effects/therapeutic use Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy Recurrence Treatment Outcome Adolescent Young Adult Adult Middle Aged
 Humans Adult Middle Aged *Multiple Sclerosis/complications Exercise Therapy *Neurological Rehabilitation Randomized Controlled Trials as Topic
 Humans Female *Multiple Sclerosis/epidemiology *Neurodegenerative Diseases Risk Factors *Air Pollution/adverse effects Particulate Matter/adverse effects
 Humans Herpesvirus 4, Human *Multiple Sclerosis/pathology *Epstein-Barr Virus Infections Memory T Cells Brain/pathology CD8-Positive T-Lymphocytes
 Female Humans Pregnancy *Breast Feeding *Multiple Sclerosis/epidemiology Mothers/education Weaning Parturition
 Humans *Exercise Therapy/methods *Multiple Sclerosis/diagnostic imaging Exercise Neuroimaging Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/diagnosis Intermediate Filaments/chemistry Enzyme-Linked Immunosorbent Assay Axons Neurofilament Proteins Biomarkers
 Humans *Multiple Sclerosis/cerebrospinal fluid Spinal Puncture Leukocyte Count *Nervous System Diseases Inflammation
 Adult Child Female Humans Male Adolescent Young Adult *Multiple Sclerosis/genetics Leukocytes, Mononuclear Age of Onset Disease Progression Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/pathology Brain/pathology Inflammation Ion Channels Cytokines
 Humans *Choroid Plexus/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging
 Humans Middle Aged *Multiple Sclerosis/pathology *Multiple Sclerosis, Chronic Progressive/diagnostic imaging/pathology *Cardiovascular Diseases/diagnostic imaging/epidemiology/etiology Cross-Sectional Studies Risk Factors Brain/diagnostic imaging/pathology Magnetic Resonance Imaging/methods Memory, Short-Term Heart Disease Risk Factors Atrophy/pathology Disability Evaluation Disease Progression STAT2 Transcription Factor
 Humans Adolescent Female Middle Aged *Neuromyelitis Optica Aquaporin 4 *Multiple Sclerosis/diagnosis/complications Oligoclonal Bands *Myelitis, Transverse/diagnosis/complications Immunoglobulin G
 Adult Humans Female Male Dimethyl Fumarate/therapeutic use/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents/therapeutic use/adverse effects *Multiple Sclerosis/drug therapy Pandemics Prospective Studies *COVID-19
 Female Humans Male Aging/psychology Longitudinal Studies *Multiple Sclerosis/diagnosis Surveys and Questionnaires Middle Aged
 Humans *Multiple Sclerosis/drug therapy Pyrimidines/therapeutic use *Lupus Erythematosus, Systemic/drug therapy *Arthritis, Rheumatoid/drug therapy
 Female Humans Adult *Glomerulonephritis, Membranoproliferative/pathology *Multiple Sclerosis/complications/drug therapy Interferons/therapeutic use Proteinuria/complications *Glomerulonephritis, IGA/complications/diagnosis/drug therapy Immunoglobulin A
 Humans Adult *Multiple Sclerosis/therapy Central Nervous System Quality of Life Exercise Randomized Controlled Trials as Topic
 Humans Cladribine/adverse effects *Multiple Sclerosis/drug therapy Eyebrows Immunosuppressive Agents/adverse effects Alopecia/chemically induced/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Pregnancy Child Humans Female *Multiple Sclerosis/therapy Breast Feeding Consensus Delphi Technique Muscle Spasticity
 Humans *Multiple Sclerosis/diagnostic imaging Brain Mapping Artificial Intelligence Magnetic Resonance Imaging Neural Pathways/diagnostic imaging Brain/diagnostic imaging Phenotype
 Humans *Lewy Body Disease *Parkinson Disease/complications/epidemiology Hydrocortisone *Multiple Sclerosis/epidemiology/genetics Mendelian Randomization Analysis Genome-Wide Association Study *Alzheimer Disease/epidemiology *Epilepsy/epidemiology/genetics
 Humans Infant Child, Preschool *Multiple Sclerosis/complications *Cognition Disorders/diagnosis *Cognitive Dysfunction/complications Cognition Electroencephalography Neuropsychological Tests
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy Dimethyl Fumarate/therapeutic use Cladribine/therapeutic use Immunosuppressive Agents/therapeutic use Cost-Benefit Analysis *Multiple Sclerosis Spain
 Humans Glatiramer Acetate/therapeutic use *Multiple Sclerosis/drug therapy Natalizumab/therapeutic use Interferons/therapeutic use Interferon-beta/therapeutic use Cohort Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Cost of Illness Immunosuppressive Agents/therapeutic use
 Mice Humans Animals *Cyclotides/genetics/chemistry/metabolism *Multiple Sclerosis/drug therapy/genetics Australia Tobacco/genetics/metabolism Plant Proteins/metabolism
 Humans *Multiple Sclerosis/drug therapy Agammaglobulinaemia Tyrosine Kinase B-Lymphocytes Inflammation/drug therapy Macrophages Protein Kinase Inhibitors/pharmacology
 Humans *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Cerebral Cortex/pathology Artificial Intelligence
 Humans *Neuromyelitis Optica *Multiple Sclerosis/diagnostic imaging Aquaporin 4 Myelin-Oligodendrocyte Glycoprotein Retina/pathology *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging Autoantibodies
 Humans *Multiple Sclerosis/diagnosis Smartphone Patient Acuity Self Report Disability Evaluation
 Animals *Multiple Sclerosis/pathology Central Nervous System/pathology Inflammation/pathology Axons/pathology Dendritic Cells/pathology
 Humans Female Adult Contrast Media Gadolinium *Multiple Sclerosis/diagnostic imaging/pathology Scalp Cerebellar Nuclei/diagnostic imaging/pathology *Organometallic Compounds Retrospective Studies Magnetic Resonance Imaging/methods Gadolinium DTPA
 Humans Male United States Adult Female *Multiple Sclerosis, Relapsing-Remitting/drug therapy Prospective Studies *Multiple Sclerosis/drug therapy Treatment Outcome Antilymphocyte Serum Recurrence
 Humans Herpesvirus 4, Human/physiology *Epstein-Barr Virus Infections *Multiple Sclerosis/pathology Risk Factors Molecular Mimicry
 Humans *Transcranial Magnetic Stimulation/methods *Multiple Sclerosis/complications Electroencephalography Evoked Potentials Evoked Potentials, Motor
 Female Male Humans *Multiple Sclerosis/complications *Diet, Mediterranean Cross-Sectional Studies Nutritional Status Fatigue/complications
 Humans *Multiple Sclerosis/diagnostic imaging Myelin-Oligodendrocyte Glycoprotein Reproducibility of Results Brain/diagnostic imaging Databases, Factual Autoantibodies
 Humans *Schizophrenia/diagnosis *Multiple Sclerosis/diagnosis Reproducibility of Results *Psychotic Disorders/psychology *Neurosciences Biomarkers
 Humans *White Matter/diagnostic imaging/pathology *Deep Learning Reproducibility of Results Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology *Multiple Sclerosis/diagnostic imaging/pathology Image Processing, Computer-Assisted/methods
 Humans *Multiple Sclerosis, Relapsing-Remitting/genetics *Multiple Sclerosis/genetics DNA, Mitochondrial/genetics DNA Copy Number Variations Leukocytes Telomere/genetics
 Humans Glatiramer Acetate/therapeutic use Interferon-beta/therapeutic use Leukocytes, Mononuclear DNA Methylation *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans Male Female Walk Test *Multiple Sclerosis/diagnosis Postural Balance Reproducibility of Results Time and Motion Studies Walking *Disabled Persons
 Humans Polysomnography *Multiple Sclerosis/complications Sleep Sleep Stages *Sleep Wake Disorders/complications *Disorders of Excessive Somnolence
 Humans *Memory, Episodic *Multiple Sclerosis/complications Intention Neuropsychological Tests Memory Disorders/diagnosis/etiology
 Humans *Neural Networks, Computer *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods Brain/diagnostic imaging Image Processing, Computer-Assisted/methods
 Humans *Acupuncture Therapy/adverse effects/methods Gait/physiology *Multiple Sclerosis/physiopathology/therapy Muscle Spasticity/physiopathology/therapy Pilot Projects Treatment Outcome Feasibility Studies Muscle Strength/physiology Sensation/physiology Postural Balance/physiology Cross-Over Studies
 Humans *Multiple Sclerosis/drug therapy Antibodies, Monoclonal Treatment Outcome Cost-Benefit Analysis
 Humans *Multiple Sclerosis/epidemiology Incidence Prevalence Asia/epidemiology China/epidemiology
 Humans Prospective Studies *Multiple Sclerosis/diagnosis Cross-Sectional Studies Cornea/innervation Microscopy, Confocal
 Humans *Multiple System Atrophy/genetics/metabolism alpha-Synuclein/genetics/metabolism beta-Synuclein/metabolism *Multiple Sclerosis/genetics/metabolism Brain/metabolism Amyloidogenic Proteins/genetics/metabolism
 Humans *Multiple Sclerosis/diagnosis alpha-Synuclein Leukocytes, Mononuclear Case-Control Studies Interleukin-6 Biomarkers
 Humans Adult Middle Aged Animals *Coffee/adverse effects Case-Control Studies Iran/epidemiology *Multiple Sclerosis/epidemiology/etiology Beverages/adverse effects Tea/adverse effects Milk
 Adult Humans Fingolimod Hydrochloride Immunologic Factors Immunosuppressive Agents *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting Natalizumab Recurrence Treatment Outcome Comparative Effectiveness Research
 Pregnancy Female Humans *Breast Feeding *Multiple Sclerosis/drug therapy Antigens, CD20/therapeutic use
 Animals Male Female Case-Control Studies *Multiple Sclerosis/metabolism Diet Kidney/metabolism Energy Intake Acids/metabolism
 Humans *Multiple Sclerosis/drug therapy Immunosuppressive Agents/adverse effects Glatiramer Acetate/therapeutic use Fingolimod Hydrochloride/therapeutic use Natalizumab/therapeutic use
 Pregnancy Humans Female *Multiple Sclerosis/therapy Postpartum Period Vaccination *Pregnancy Complications/therapy Recurrence
 Humans Female Adult Middle Aged Male *Multiple Sclerosis/psychology Cross-Sectional Studies Decision Making Patient Preference Italy
 Pregnancy Female Humans Child Aged *Multiple Sclerosis/therapy Consensus Immunization Vaccination *Neurology
 Humans *Multiple Sclerosis/rehabilitation Feasibility Studies Exercise Therapy/methods Exercise Surveys and Questionnaires
 Humans *Multiple Sclerosis/complications Behavior Therapy Exercise Quality of Life Fatigue/therapy/psychology
 Humans *Multiple Sclerosis/pathology Diffusion Tensor Imaging Glial Fibrillary Acidic Protein Intermediate Filaments/pathology *Multiple Sclerosis, Chronic Progressive/pathology Gray Matter/diagnostic imaging/pathology Biomarkers Brain/diagnostic imaging/pathology
 Humans *Multiple Sclerosis
 Adult Humans Aged Middle Aged *Multiple Sclerosis/drug therapy Retrospective Studies Crotonates/therapeutic use Toluidines/therapeutic use Recurrence *Lymphopenia/chemically induced *Leukopenia *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/drug therapy/genetics *Multiple Sclerosis/drug therapy/genetics Mice, Inbred Strains *Antineoplastic Agents/therapeutic use Signal Transduction DNA Repair DNA Mice, Inbred C57BL
 Humans *Multiple Sclerosis Pilot Projects Prospective Studies Brain-Derived Neurotrophic Factor *Multiple Sclerosis, Relapsing-Remitting/cerebrospinal fluid Biomarkers Cognition
 Humans *Multiple Sclerosis/therapy *Gastrointestinal Microbiome *Neuromyelitis Optica *Vitamin D Deficiency/complications Inflammation/complications
 Humans *Gait Depression/etiology *Multiple Sclerosis/psychology Self Efficacy Walking/psychology Cognition
 Humans *Multiple Sclerosis/complications Biomarkers Fingolimod Hydrochloride Disulfides Sulfhydryl Compounds Serum Albumin Homeostasis Neuropsychological Tests
 Humans Male Female *Multiple Sclerosis/complications Quality of Life Depression/epidemiology *Sexual Dysfunction, Physiological/epidemiology Sexual Behavior
 Humans Female Male *Quality of Life/psychology Trinidad and Tobago/epidemiology Surveys and Questionnaires Mental Health *Multiple Sclerosis/epidemiology
 Humans *Multiple Sclerosis/metabolism Axons/metabolism Cell Death
 Humans *Receptors, Calcitriol/genetics *Multiple Sclerosis/genetics Patients Polymorphism, Single Nucleotide
 Humans *Multiple Sclerosis/psychology Quality of Life Cross-Sectional Studies Fatigue/psychology Patient Reported Outcome Measures
 Humans Biomarkers Blood Cells Case-Control Studies *Multiple Sclerosis/genetics *Neurodegenerative Diseases *RNA, Long Noncoding/genetics
 Humans *Multiple Sclerosis/pathology *Cervical Cord/pathology Spinal Cord/pathology Magnetic Resonance Imaging/methods Brain/pathology
 Humans *Multiple Sclerosis/pathology *White Matter/pathology Cross-Sectional Studies Axons/pathology *Multiple Sclerosis, Chronic Progressive/pathology Myelin Sheath/pathology Brain/pathology
 Humans *Multiple Sclerosis Aging Sclerosis
 Humans Natalizumab/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced *Multiple Sclerosis/drug therapy Immunologic Factors/therapeutic use Quality of Life Treatment Outcome *Leukoencephalopathy, Progressive Multifocal/chemically induced Patient Reported Outcome Measures
 Humans *Multiple Sclerosis/complications Self Efficacy Sleep Quality Nurse's Role Fatigue/etiology/therapy Quality of Life
 Humans *T-Lymphocytes, Regulatory Administration, Intranasal Cholera Toxin CD4-Positive T-Lymphocytes *Multiple Sclerosis/drug therapy
 Male Humans Female Adult Middle Aged *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods Neuroimaging Algorithms Consensus
 Humans *COVID-19 *Multiple Sclerosis/drug therapy Antibodies, Viral
 Humans *Sleep Initiation and Maintenance Disorders/therapy *Meditation *Mindfulness *Multiple Sclerosis/complications Pilot Projects Quality of Life
 Humans *Multiple Sclerosis/complications Retrospective Studies Depression/etiology/psychology *Cognitive Dysfunction Fatigue/etiology
 Adult Humans *Multiple Sclerosis/psychology Accidental Falls Case-Control Studies Postural Balance Artificial Intelligence Time and Motion Studies Cognition Cerebellum/diagnostic imaging Magnetic Resonance Imaging
 Humans *Multiple Sclerosis/complications Cross-Sectional Studies Smartphone Gait Cognition
 Humans *Cannabis/adverse effects *Multiple Sclerosis/complications Pain/etiology Dronabinol
 Humans *Multiple Sclerosis *Ferroptosis
 Humans Female Cohort Studies *Multiple Sclerosis/complications *Breast Neoplasms/complications Proportional Hazards Models Registries
 Humans Male Female Incidence Prevalence *Multiple Sclerosis/epidemiology Iran/epidemiology Longitudinal Studies
 Humans *Cladribine/therapeutic use/adverse effects *Multiple Sclerosis/drug therapy/genetics Memory B Cells Proteome Immunoglobulin Heavy Chains/genetics/therapeutic use Clone Cells
 Humans *Multiple Sclerosis/complications Cross-Sectional Studies Black or African American Fingers White Motor Skills
 Humans *Multiple Sclerosis/metabolism Clostridium perfringens Central Nervous System Brain Myelin Sheath/metabolism
 Humans *Multiple Sclerosis/therapy Longitudinal Studies Quality of Life Patient Acceptance of Health Care Surveys and Questionnaires
 Cats Animals *Multiple Sclerosis/therapy Stromal Vascular Fraction *Spinal Cord Injuries/therapy Adipose Tissue Stromal Cells
 Humans *Pemphigus, Benign Familial/drug therapy *Multiple Sclerosis/drug therapy Antibodies, Monoclonal, Humanized/therapeutic use *Pemphigus
 Humans Female Adult Middle Aged Male Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy Greece Quality of Life Immunosuppressive Agents/adverse effects Prospective Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence Treatment Outcome
 Humans *Multiple Sclerosis/metabolism Gonadal Steroid Hormones/metabolism/pharmacology *Neuroprotective Agents/pharmacology *Melatonin/therapeutic use Oxidative Stress
 Humans Cross-Sectional Studies Foot *Multiple Sclerosis/complications Vibration Walking Male Female
 Humans *Multiple Sclerosis/epidemiology *Epstein-Barr Virus Infections Herpesvirus 4, Human Simplexvirus *Herpesviridae Infections/epidemiology Herpesvirus 3, Human *Viruses
 Pregnancy Young Adult Humans Female *Multiple Sclerosis/drug therapy *Pregnancy Complications/drug therapy Family Planning Services/methods Prenatal Care Breast Feeding
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy/genetics *Mycosis Fungoides/drug therapy/genetics *Skin Neoplasms/drug therapy/genetics High-Throughput Nucleotide Sequencing
 Humans Female Male *West Nile Fever/complications/drug therapy *West Nile virus *Multiple Sclerosis/drug therapy/complications Antibodies, Viral Immunoglobulin M
 Humans *Multiple Sclerosis/diagnostic imaging Tomography, Optical Coherence Artificial Intelligence Cross-Sectional Studies *Sexually Transmitted Diseases
 Female Humans Male Middle Aged *COVID-19/epidemiology/prevention & control *COVID-19 Vaccines/adverse effects Hospitalization *Multiple Sclerosis/drug therapy/epidemiology Vaccination
 Humans *Multiple Sclerosis *Self-Management
 Adult Humans Middle Aged *Multiple Sclerosis/complications Employment Logistic Models Rehabilitation, Vocational *Disabled Persons/rehabilitation
 Humans *Multiple Sclerosis/diagnosis Reproducibility of Results Gait Walking
 Humans *Depression/psychology Motivation *Multiple Sclerosis/complications Social Stigma Shame Anxiety/psychology Patient Acceptance of Health Care/psychology
 Humans Cladribine/adverse effects *Multiple Sclerosis/drug therapy Immunosuppressive Agents/adverse effects Follow-Up Studies *Multiple Sclerosis, Relapsing-Remitting/drug therapy Neoplasm Recurrence, Local Tablets/therapeutic use
 Humans *Multiple Sclerosis Cladribine/adverse effects Transcriptome Alemtuzumab/therapeutic use *Immune Reconstitution *Neurodegenerative Diseases/chemically induced *Multiple Sclerosis, Relapsing-Remitting/drug therapy/genetics RNA-Binding Proteins Ubiquitin-Protein Ligases
 Humans *Multiple Sclerosis/psychology *Cognition Disorders/diagnosis/etiology *Cognitive Dysfunction/etiology/complications Neuropsychological Tests Self Report Cognition
 Humans *Multiple Sclerosis/diagnostic imaging Prospective Studies Diet Chronic Disease Inflammation/diagnostic imaging Magnetic Resonance Imaging Recurrence
 Humans *Leukoencephalopathy, Progressive Multifocal/chemically induced/complications *Multiple Sclerosis/complications Natalizumab/adverse effects Antibodies, Monoclonal, Humanized/adverse effects *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy *Brain Diseases Immunologic Factors/adverse effects
 Humans *Multiple Sclerosis/metabolism *Neurodegenerative Diseases Inflammation/metabolism Neurotransmitter Agents Glutamic Acid/metabolism
 Adult Humans Middle Aged Activities of Daily Living *Multiple Sclerosis/therapy Physical Therapy Modalities *Stroke *Stroke Rehabilitation
 Humans *Quality of Life *Multiple Sclerosis/therapy Outcome Assessment, Health Care/methods Treatment Outcome Patient-Centered Care
 Humans *Multiple Sclerosis/drug therapy Antibodies, Monoclonal, Humanized/pharmacology/therapeutic use B-Lymphocytes Biomarkers
 Humans *Multiple Sclerosis/drug therapy Myelin Sheath/metabolism Central Nervous System Oligodendroglia/metabolism Brain Cell Differentiation/physiology
 Humans *Encephalitis/cerebrospinal fluid *Nervous System Diseases *Multiple Sclerosis/therapy Aging *Hashimoto Disease
 Adult Humans Exercise Exercise Therapy Fatigue/etiology/therapy Gait *Multiple Sclerosis/rehabilitation Quality of Life
 Humans Cladribine/therapeutic use/pharmacology Immunosuppressive Agents/therapeutic use/pharmacology CD8-Positive T-Lymphocytes *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Tablets/therapeutic use Algorithms
 Humans *Monocytes DNA Methylation *Multiple Sclerosis/genetics B-Lymphocytes Epigenesis, Genetic
 Humans *Multiple Sclerosis/pathology *White Matter/pathology Positron-Emission Tomography Magnetic Resonance Imaging/methods Inflammation/metabolism Disease Progression Atrophy/pathology Brain/pathology *Multiple Sclerosis, Relapsing-Remitting/pathology
 Pregnancy Humans Female *Multiple Sclerosis/genetics Incidence *Autoimmune Diseases/genetics DNA Methylation
 Mice Animals *Multiple Sclerosis/genetics Microglia/metabolism *Multiple Sclerosis, Chronic Progressive/genetics *Neurodegenerative Diseases Mice, Biozzi *Encephalomyelitis, Autoimmune, Experimental/metabolism Gene Expression Disease Models, Animal
 Humans *Multiple Sclerosis/complications *Peroneal Neuropathies *Stroke/complications/therapy *Electric Stimulation Therapy Qualitative Research
 Humans *Multiple Sclerosis/pathology Retrospective Studies Magnetic Resonance Imaging/methods Brain/pathology
 Humans Myelin-Oligodendrocyte Glycoprotein *Neuromyelitis Optica *Optic Neuritis Aquaporin 4 *Multiple Sclerosis/diagnosis Immunoglobulin G Autoantibodies
 Humans *Multiple Sclerosis/complications Outcome Assessment, Health Care Learning Fatigue/etiology Occupational Therapists
 Humans *Multiple Sclerosis/diagnostic imaging Retinal Ganglion Cells Artificial Intelligence Tomography, Optical Coherence/methods Nerve Fibers
 Humans *Multiple Sclerosis/drug therapy Retrospective Studies Cross-Sectional Studies *Anti-Anxiety Agents/therapeutic use Brain Modafinil/therapeutic use
 Humans *Neutrophils Retrospective Studies Lymphocytes Biomarkers *Multiple Sclerosis/diagnosis Prognosis
 Humans Natalizumab/therapeutic use *Multiple Sclerosis/diagnosis/diagnostic imaging *HIV Infections/complications/drug therapy Antibodies, Monoclonal, Humanized/therapeutic use *Leukoencephalopathy, Progressive Multifocal/diagnosis/diagnostic imaging HIV Immunologic Factors/therapeutic use
 Animals Humans *Multiple Sclerosis/drug therapy *Remyelination Myelin Sheath Oligodendroglia Disease Models, Animal Inflammation Disease Progression
 Humans Mice Animals *Multiple Sclerosis/pathology Endothelial Cells Brain/pathology Clostridium perfringens/metabolism Blood-Brain Barrier
 Humans Female *Saliva Acetylcholinesterase *Multiple Sclerosis Inflammation
 Humans Female Middle Aged Male *Quality of Life/psychology *Multiple Sclerosis/psychology Adaptation, Psychological Surveys and Questionnaires Social Support
 Humans *Kinesiophobia Reproducibility of Results Quality of Life *Multiple Sclerosis/complications Surveys and Questionnaires Psychometrics Fatigue/diagnosis/etiology
 Humans *Multiple Sclerosis/therapy Exercise Therapy/methods *Remyelination Single-Blind Method Exercise Randomized Controlled Trials as Topic
 Female Male Rats Animals *Multiple Sclerosis/drug therapy/pathology Propranolol/therapeutic use *Epstein-Barr Virus Infections Herpesvirus 4, Human *Encephalomyelitis, Autoimmune, Experimental/drug therapy/pathology Norepinephrine Receptors, Adrenergic/therapeutic use Microglia
 Humans Female *Spouse Abuse/psychology Retrospective Studies Emotional Abuse *Multiple Sclerosis/epidemiology Prospective Studies Prevalence
 Pregnancy Female Humans *Multiple Sclerosis/complications *Pregnancy Complications/epidemiology Postpartum Period Cohort Studies Chronic Disease Recurrence
 Humans *Neuromyelitis Optica/diagnosis/therapy Diagnosis, Differential Myelin-Oligodendrocyte Glycoprotein Aquaporin 4 *Multiple Sclerosis/diagnosis/therapy Immunoglobulin G Autoantibodies
 Infant Infant, Newborn Pregnancy Humans Female *Breast Feeding *Multiple Sclerosis/drug therapy Glatiramer Acetate/therapeutic use Interferon-beta/therapeutic use
 Humans *Multiple Sclerosis/drug therapy Lurasidone Hydrochloride Molecular Docking Simulation Clopenthixol Drug Repositioning/methods *Neurodegenerative Diseases
 Humans *COVID-19/complications SARS-CoV-2 *Multiple Sclerosis/complications Risk Factors Exercise
 Humans *Multiple Sclerosis/drug therapy *COVID-19 COVID-19 Vaccines SARS-CoV-2 Antibodies, Viral
 Humans *Multiple Sclerosis/diagnostic imaging Head Brain/diagnostic imaging Algorithms Cluster Analysis
 Humans Male Female *Transcriptome *Multiple Sclerosis/genetics Sex Characteristics Gene Expression Profiling Central Nervous System Carrier Proteins Cell Cycle Proteins
 Humans Adult Middle Aged *Multiple Sclerosis/complications Palliative Care Qualitative Research
 Humans *Multiple Sclerosis *B-Lymphocytes
 Humans Astrocytes/metabolism *Exosomes/metabolism *Multiple Sclerosis/metabolism Central Nervous System Immunity
 Humans Prospective Studies Interleukin-2 *Multiple Sclerosis/drug therapy *COVID-19 SARS-CoV-2 Antibodies
 Humans Analgesics, Opioid/adverse effects *Multiple Sclerosis/drug therapy *Opioid-Related Disorders/drug therapy Prescriptions *Prescription Drug Misuse
 Humans *Trigeminal Neuralgia/diagnostic imaging/etiology/surgery *Radiosurgery/adverse effects Retrospective Studies Treatment Outcome Case-Control Studies *Multiple Sclerosis/complications/surgery Pain/surgery Follow-Up Studies
 Humans *Epstein-Barr Virus Infections/epidemiology *Hodgkin Disease/epidemiology/complications/pathology *Multiple Sclerosis/epidemiology/complications Herpesvirus 4, Human *Inflammatory Bowel Diseases/complications *Colitis, Ulcerative/epidemiology *Crohn Disease/complications
 Humans *Multiple Sclerosis Finland
 Humans Microglia *Multiple Sclerosis/pathology Macrophages Anti-Inflammatory Agents/pharmacology Cytokines/genetics *Neurotoxicity Syndromes
 Pregnancy Humans Female *Multiple Sclerosis/pathology CD8-Positive T-Lymphocytes Transcriptome CD4-Positive T-Lymphocytes Epigenesis, Genetic Inflammation/metabolism
 Humans Gait Cognition *Multiple Sclerosis/complications Walking Speed *Virtual Reality Exercise Therapy/methods
 Adult Humans Female Child *Adverse Childhood Experiences Quality of Life *Multiple Sclerosis/epidemiology *Child Abuse Life Change Events
 Humans *Glioblastoma Brain/diagnostic imaging Magnetic Resonance Imaging/methods Cerebral Infarction *Multiple Sclerosis/diagnostic imaging Image Processing, Computer-Assisted/methods
 Humans *Multiple Sclerosis/diagnosis Fibronectins Leptin Health Status Healthy Volunteers Ubiquitin Thiolesterase
 Male Child Humans Aged Cross-Sectional Studies *Multiple Sclerosis/epidemiology Leisure Activities/psychology Social Support Denmark/epidemiology
 Humans *Multiple Sclerosis/genetics Genome-Wide Association Study Biomarkers Blood Proteins/genetics Brain Immunoglobulins/genetics Membrane Proteins/genetics
 Humans Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy Natalizumab/therapeutic use Immunosuppressive Agents/therapeutic use Immunologic Factors/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Treatment Outcome Propensity Score Recurrence
 Humans Acoustic Stimulation/methods *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging *Multiple Sclerosis Auditory Perception/physiology Evoked Potentials/physiology Electroencephalography/methods Evoked Potentials, Auditory/physiology
 Humans Communication *COVID-19/prevention & control COVID-19 Vaccines/therapeutic use *Multiple Sclerosis/complications *Vaccination Hesitancy
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy *Psoriasis/diagnosis/drug therapy *Etretinate *Skin Diseases, Vesiculobullous Chronic Disease
 Humans *Autoimmune Diseases CD4-Positive T-Lymphocytes Inflammation *Multiple Sclerosis/drug therapy Neoplasms Phosphofructokinase-2/metabolism
 Female Humans Middle Aged Fingolimod Hydrochloride/adverse effects *Neuromyelitis Optica/diagnosis/drug therapy/pathology *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Immunologic Factors/therapeutic use
 Humans Adolescent Bayes Theorem *Multiple Sclerosis/diagnostic imaging ROC Curve Retrospective Studies Magnetic Resonance Imaging/methods
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis Prognosis Recurrence
 Humans *Multiple Sclerosis/diagnosis Prospective Studies Mexico/epidemiology Disease Progression *Demyelinating Diseases/diagnosis/complications/pathology Magnetic Resonance Imaging/methods
 Humans *Multiple Sclerosis/complications Autonomic Nervous System *Autonomic Nervous System Diseases/diagnosis/etiology Valsalva Maneuver Blood Pressure/physiology Heart Rate/physiology
 Adult Humans *Chronic Pain/therapy Quality of Life/psychology *Multiple Sclerosis/therapy *Hypnosis Fatigue/etiology/therapy
 Humans *Multiple Sclerosis/genetics DNA Methylation Leukocytes, Mononuclear/pathology *Multiple Sclerosis, Relapsing-Remitting/genetics Chronic Disease DNA Recurrence Butyrophilins/genetics GTPase-Activating Proteins/genetics Kruppel-Like Transcription Factors/genetics
 Male Humans Female Adult Middle Aged *Multiple Sclerosis/diagnostic imaging/pathology *Neuromyelitis Optica/diagnostic imaging/pathology Prospective Studies Magnetic Resonance Imaging/methods Myelin Sheath/pathology
 Humans *Genome-Wide Association Study *Multiple Sclerosis/genetics Genetic Profile Risk Factors Epigenesis, Genetic
 Humans *Multiple Sclerosis/drug therapy/metabolism Sphingosine-1-Phosphate Receptors Bradycardia/chemically induced Receptors, Lysosphingolipid/agonists/metabolism/therapeutic use Fingolimod Hydrochloride/pharmacology/therapeutic use *Tetrahydroisoquinolines/therapeutic use Sphingosine/metabolism
 Animals Humans Mice Cuprizone *Demyelinating Diseases/chemically induced/drug therapy Disease Models, Animal Mice, Inbred C57BL Microglia/metabolism *Multiple Sclerosis/drug therapy/metabolism Myelin Sheath/metabolism TRPV Cation Channels Capsaicin/pharmacology
 Humans *Neurodegenerative Diseases/epidemiology Cross-Sectional Studies Biological Specimen Banks *Epstein-Barr Virus Infections Herpesvirus 4, Human *Alzheimer Disease *Multiple Sclerosis/epidemiology
 Humans *Multiple Sclerosis/pathology Herpesvirus 4, Human Interferon beta-1a *Epstein-Barr Virus Infections Epstein-Barr Virus Nuclear Antigens Antigens, Viral Antibodies, Viral Immunoglobulin G Antiviral Agents
 Humans Mice Animals *Glucocorticoids/therapeutic use Dexamethasone/pharmacology T-Lymphocytes *Multiple Sclerosis/drug therapy Energy Metabolism
 Humans *Multiple Sclerosis Blood Proteins Biomarkers
 Adult Female Humans Male *Exercise Quality of Life Health Status Exercise Therapy/methods *Multiple Sclerosis/therapy
 Humans Alleles *Brain-Derived Neurotrophic Factor/genetics Genotype *Multiple Sclerosis/genetics
 Adult Humans *Multiple Sclerosis/complications Pain/complications Fatigue/complications Cognition Anxiety
 Humans *Multiple Sclerosis/diagnostic imaging Gadolinium Prospective Studies Biological Specimen Banks Contrast Media Biomarkers Glial Fibrillary Acidic Protein Neurofilament Proteins
 Humans *Air Pollutants/adverse effects/analysis *Multiple Sclerosis/etiology/genetics HLA-DRB1 Chains/genetics *Air Pollution/adverse effects/analysis Lung Environmental Exposure/adverse effects/analysis Particulate Matter/adverse effects/analysis
 Humans *COVID-19/complications/epidemiology/genetics Kelch-Like ECH-Associated Protein 1 Genome-Wide Association Study *Multiple Sclerosis/complications/genetics SARS-CoV-2/genetics NF-E2-Related Factor 2 Polymorphism, Single Nucleotide
 Female Humans Adolescent Young Adult Adult *Multiple Sclerosis/complications/drug therapy *Venous Thrombosis/chemically induced/drug therapy/diagnosis *Intracranial Thrombosis/chemically induced/diagnostic imaging/drug therapy Headache/etiology Steroids/therapeutic use Anticoagulants/adverse effects
 Humans Female Adult Male *MicroRNAs/genetics *Multiple Sclerosis/genetics Cohort Studies Brain Biomarkers
 Humans *Multiple Sclerosis *Disabled Persons *Motor Disorders Central Nervous System Inflammation
 Child Pregnancy Humans Female Adult *Multiple Sclerosis Cross-Sectional Studies *Multiple Sclerosis, Relapsing-Remitting Anxiety Patient Reported Outcome Measures Surveys and Questionnaires Reproducibility of Results Psychometrics
 Female Humans Male East Asian People Magnetic Resonance Imaging *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy *Natalizumab/therapeutic use Retrospective Studies Adult Middle Aged
 Female Cattle Rats Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy/pathology Cytokines/metabolism *Multiple Sclerosis/drug therapy/pathology Interleukin-10/metabolism Spinal Cord Interleukin-6 Anti-Inflammatory Agents/therapeutic use Mice, Inbred C57BL
 Female Humans Male *Adipokines Leptin Resistin Adiponectin *Multiple Sclerosis/diagnostic imaging Cross-Sectional Studies
 Humans Tomography, Optical Coherence/methods *Multiple Sclerosis/diagnostic imaging Retina Angiography Retinal Vessels/diagnostic imaging *Optic Neuritis Fluorescein Angiography/methods
 Humans Speech Intelligibility *Parkinson Disease/complications *Multiple Sclerosis/complications Speech Acoustics Speech Production Measurement
 Humans *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Disease Progression Contrast Media Brain/diagnostic imaging/pathology
 Humans *Multiple Sclerosis/complications *Robotics Randomized Controlled Trials as Topic Walking Gait
 Humans *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive/diagnostic imaging Retrospective Studies Retina/diagnostic imaging Walking *Retinal Degeneration/diagnostic imaging Atrophy
 Humans Activities of Daily Living *Exoskeleton Device Lower Extremity *Multiple Sclerosis/rehabilitation Walking Cross-Over Studies
 Humans *Multiple Sclerosis Autoimmunity *alpha-Crystallins Autoantigens
 Humans Female Male *Diffusion Tensor Imaging *Multiple Sclerosis/diagnostic imaging Cerebral Cortex Frontal Lobe Anisotropy
 Pregnancy Humans Female *Multiple Sclerosis/epidemiology Cohort Studies Probability *Disabled Persons Recurrence *Multiple Sclerosis, Relapsing-Remitting Disease Progression
 Humans *Automobile Driving *Parkinson Disease/epidemiology Retrospective Studies *Multiple Sclerosis/epidemiology Automobiles Sweden/epidemiology Accidents, Traffic
 Adult Humans *Multiple Sclerosis/drug therapy Pandemics *COVID-19 Glatiramer Acetate/therapeutic use Interferon-beta/therapeutic use
 Humans Doxycycline Ethnicity Genetic Therapy *Graves Ophthalmopathy *Multiple Sclerosis/diagnosis *Optic Atrophy, Hereditary, Leber
 Humans Male *Multiple Sclerosis/epidemiology COVID-19 Testing *COVID-19 *Disabled Persons Disease Progression
 Humans Female Male Cladribine/adverse effects *Multiple Sclerosis/drug therapy Immunosuppressive Agents/adverse effects Portugal/epidemiology Retrospective Studies Tertiary Care Centers *Drug-Related Side Effects and Adverse Reactions Recurrence *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/metabolism Proteomics Brain/pathology *Extracellular Vesicles/metabolism Immune System Extracellular Matrix Biomarkers
 Humans Female Young Adult Adult Middle Aged Male *Multiple Sclerosis/epidemiology Case-Control Studies Retrospective Studies *Myasthenia Gravis
 Humans *Multiple Sclerosis/therapy Exercise/physiology Exercise Therapy/methods Walking *Resistance Training
 Humans *Metacognition Awareness/physiology *Multiple Sclerosis/complications Quality of Life Brain/physiology Heart Rate/physiology
 Humans *Deep Learning *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods Positron-Emission Tomography Disease Progression Chronic Disease Retrospective Studies
 Male Female Humans Incidence Longitudinal Studies Bayes Theorem *Multiple Sclerosis/epidemiology Iran/epidemiology
 Humans *Deglutition Disorders/diagnosis/etiology *Multiple Sclerosis/complications Czech Republic Surveys and Questionnaires Patient Reported Outcome Measures Reproducibility of Results
 Humans *Multiple Sclerosis/complications *Tobacco, Smokeless *Smoking Cessation *Tobacco Smoke Pollution Quality of Life Disease Progression Tobacco Use Cessation Devices Smoking/adverse effects/epidemiology
 Male Humans Female *Multiple Sclerosis Retrospective Studies Disability Evaluation Spinal Cord Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology *Multiple Sclerosis, Relapsing-Remitting
 Humans Aquaporin 4 Brain/pathology *Diagnostic Errors Latin America/epidemiology Magnetic Resonance Imaging/methods *Multiple Sclerosis/diagnostic imaging/epidemiology *Neuromyelitis Optica/diagnostic imaging/epidemiology Retrospective Studies
 Humans Network Meta-Analysis *Exercise Exercise Therapy Physical Fitness *Multiple Sclerosis/therapy
 Humans *Mindfulness/methods *Multiple Sclerosis/complications Cognitive Training *Cognitive Behavioral Therapy/methods Cognition Treatment Outcome
 Humans *Multiple Sclerosis, Relapsing-Remitting/diagnosis *Symptom Flare Up
 Humans *Multiple Sclerosis/drug therapy Antigens, CD20 Antibodies, Monoclonal/therapeutic use Rituximab/therapeutic use *Antineoplastic Agents/therapeutic use
 Humans *Acetoacetates Acetone Genome-Wide Association Study Lysine Mendelian Randomization Analysis *Multiple Sclerosis/genetics Metabolome/genetics Serine Polymorphism, Single Nucleotide
 Humans *Leukoencephalopathy, Progressive Multifocal/therapy *Multiple Sclerosis/drug therapy Natalizumab/therapeutic use Peptides/therapeutic use
 Rats Animals *Toxoplasma Ethidium/pharmacology/therapeutic use *Multiple Sclerosis/drug therapy *Neurodegenerative Diseases *Toxoplasmosis/drug therapy Cytokines/therapeutic use
 Adult Humans Cladribine/therapeutic use Cohort Studies *COVID-19 Immunosuppressive Agents/therapeutic use *Lymphopenia/drug therapy *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Pandemics Poland/epidemiology Retrospective Studies Tablets/therapeutic use
 Humans *Neuroanatomy *Multiple Sclerosis Neurophysiology Acclimatization Electromyography
 Humans *Multiple Sclerosis Citric Acid Cycle
 Humans *Multiple Sclerosis Workplace
 Humans *Multiple Sclerosis/drug therapy Transmembrane Activator and CAML Interactor Protein B-Lymphocytes Cytokines
 Pregnancy Female Humans Aged *Multiple Sclerosis/drug therapy *Hematopoietic Stem Cell Transplantation *Cognitive Dysfunction Forecasting
 Humans *Multiple Sclerosis *Occupational Health Health Personnel
 Humans Activities of Daily Living Memory Disorders/etiology/rehabilitation *Multiple Sclerosis/rehabilitation Outcome Assessment, Health Care Quality of Life
 Humans *Neuromyelitis Optica/epidemiology Japan/epidemiology Prevalence Incidence *Multiple Sclerosis/epidemiology
 Female Humans *Multiple Sclerosis Middle Aged
 Pregnancy Humans Female *COVID-19 RNA, Viral Pregnant Women SARS-CoV-2 *Multiple Sclerosis/epidemiology *Pregnancy Complications, Infectious/epidemiology Pregnancy Outcome
 Humans *Multiple Sclerosis Quality of Life *Multiple Sclerosis, Chronic Progressive/therapy *High-Intensity Interval Training/methods Bicycling Single-Blind Method Exercise Therapy/methods Randomized Controlled Trials as Topic
 Humans *Multiple Sclerosis/diagnosis Retrospective Studies Brain/pathology Magnetic Resonance Imaging/methods Evoked Potentials, Somatosensory/physiology Biomarkers Disability Evaluation Evoked Potentials
 Aged Child Female Humans Pregnancy Consensus Evidence-Based Medicine Immunization *Multiple Sclerosis/drug therapy Vaccination
 Humans *Multiple Sclerosis/diagnosis/cerebrospinal fluid Immunoglobulin kappa-Chains/cerebrospinal fluid Oligoclonal Bands/cerebrospinal fluid Immunoglobulin G/cerebrospinal fluid *Demyelinating Diseases Biomarkers/cerebrospinal fluid
 Humans Immunosuppressive Agents/therapeutic use Medication Adherence *Multiple Sclerosis/drug therapy Prospective Studies Retrospective Studies
 Animals Mice Disease Models, Animal *Encephalomyelitis, Autoimmune, Experimental/drug therapy Interleukin-17 *Multiple Sclerosis/drug therapy Osteopontin
 Female Humans Adult *Familial Mediterranean Fever/complications/drug therapy/diagnosis *Multiple Sclerosis/diagnosis Antibodies, Monoclonal, Humanized/therapeutic use Colchicine *Demyelinating Diseases/complications
 Humans *Multiple Sclerosis/drug therapy Rituximab/therapeutic use B-Lymphocytes/metabolism Cytokines Autoantibodies
 *Computerized Adaptive Testing/methods Computer Simulation *Multiple Sclerosis/diagnosis *Quality of Life Surveys and Questionnaires Humans Adolescent Adult Middle Aged Aged Aged, 80 and over Psychometrics
 Humans Herpesvirus 4, Human *Epstein-Barr Virus Infections/complications Septins Antibodies, Viral Epstein-Barr Virus Nuclear Antigens *Multiple Sclerosis/complications
 Humans Adjuvants, Immunologic/adverse effects Atrophy/drug therapy/pathology Brain/diagnostic imaging/pathology Interferon beta-1a/therapeutic use *Magnetic Resonance Imaging *Multiple Sclerosis, Relapsing-Remitting/diagnostic imaging/drug therapy/chemically induced Treatment Outcome
 Humans *Multiple Sclerosis, Chronic Progressive Central Nervous System Disease Progression
 Humans *Multiple Sclerosis, Chronic Progressive/drug therapy *Multiple Sclerosis Disease Progression Proportional Hazards Models *Disabled Persons
 Humans *Fatigue Syndrome, Chronic/complications *Nervous System Diseases/complications Brain *Parkinson Disease *Multiple Sclerosis/complications
 Humans Rivastigmine/therapeutic use *Multiple Sclerosis/complications Prospective Studies *Cognitive Dysfunction/etiology/complications *Cognition Disorders
 Humans *Intermediate Filaments *Multiple Sclerosis/pathology Biomarkers Axons/pathology Longitudinal Studies Neurofilament Proteins Recurrence
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/pathology *Multiple Sclerosis/drug therapy/pathology Proto-Oncogene Proteins c-akt/metabolism Glycogen Synthase Kinase 3 beta/metabolism Signal Transduction Phosphatidylinositol 3-Kinases/metabolism Glucagon-Like Peptide 1 *Neuroprotective Agents/therapeutic use/pharmacology *Neurodegenerative Diseases Mice, Inbred C57BL
 Animals Humans Mice beta Catenin/metabolism Cell Differentiation Disease Models, Animal Glycogen Synthase Kinase 3/metabolism Lithium/pharmacology Lithium Chloride/pharmacology Mice, Inbred C57BL *Multiple Sclerosis/drug therapy/metabolism Oligodendroglia/metabolism Stem Cells/metabolism Tolonium Chloride/metabolism/pharmacology Enzyme Inhibitors/pharmacology
 Humans *Multiple Sclerosis/pathology Processing Speed Magnetic Resonance Imaging/methods *Cognition Disorders/pathology Machine Learning Neuropsychological Tests
 Child Humans Male Female Adolescent *Multiple Sclerosis/diagnostic imaging Tertiary Care Centers Brain Interferon-beta/therapeutic use Brain Stem
 Humans *Multiple Sclerosis/diagnosis/cerebrospinal fluid Immunoglobulin kappa-Chains/cerebrospinal fluid Immunoglobulin G/cerebrospinal fluid Biomarkers/cerebrospinal fluid Sensitivity and Specificity Oligoclonal Bands/cerebrospinal fluid
 Humans *Multiple Sclerosis/diagnostic imaging Brain/pathology Feasibility Studies Contrast Media Magnetic Resonance Imaging/methods
 Mice Animals *Multiple Sclerosis/therapy Myeloid Cells *Encephalomyelitis, Autoimmune, Experimental Central Nervous System Monocytes Mice, Inbred C57BL
 Humans *Multiple Sclerosis/drug therapy *Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology/therapeutic use Central Nervous System/metabolism Inflammation/drug therapy Anti-Inflammatory Agents/therapeutic use
 Humans Male Female Cholecalciferol/therapeutic use/pharmacology Ultraviolet Rays *Multiple Sclerosis, Relapsing-Remitting/drug therapy Cognition Research Design *Multiple Sclerosis
 Humans *Multiple Sclerosis/complications Smartphone Feasibility Studies Magnetic Resonance Imaging Brain/pathology
 Humans *COVID-19 SARS-CoV-2 *Multiple Sclerosis/complications Breakthrough Infections Prospective Studies *Sphingosine 1 Phosphate Receptor Modulators Antibodies, Viral
 Humans Female Adult *Multiple Sclerosis/drug therapy Cohort Studies Intermediate Filaments Treatment Outcome Neurofilament Proteins Biomarkers
 Humans *Multiple Sclerosis Patients
 Humans Female Male Nutrition Surveys Cross-Sectional Studies Pilot Projects Prospective Studies *Multiple Sclerosis/complications Aging
 Humans *Mobile Applications Quality of Life *Multiple Sclerosis/therapy *Parkinson Disease/therapy *Stroke/therapy
 Humans Male Female Adult Middle Aged Aged *Cognition Disorders/diagnosis/etiology Cognitive Dysfunction *Multiple Sclerosis/complications Magnetic Resonance Imaging Magnetoencephalography Neuropsychological Tests *Brain/diagnostic imaging
 Humans Male Middle Aged Aged Female *Quality of Life/psychology Depression/psychology Anxiety/psychology Mental Health Anxiety Disorders *Multiple Sclerosis/complications
 Humans Aged Child *Multiple Sclerosis/epidemiology Prospective Studies New Zealand/epidemiology Survival Analysis Cause of Death
 Humans *Multiple Sclerosis/drug therapy Neurons/physiology Disease Progression Cytokines Inflammation/pathology
 Humans *Multiple Sclerosis *Intrinsically Disordered Proteins Myelin Proteins Membrane Proteins
 Humans *Multiple Sclerosis/drug therapy Immunosuppressive Agents/therapeutic use Retrospective Studies Kinetics Fingolimod Hydrochloride/therapeutic use Natalizumab/therapeutic use
 Humans *Multiple Sclerosis/epidemiology Sweden/epidemiology Case-Control Studies Social Class Life Style Registries Socioeconomic Factors Risk Factors
 Humans *Multiple Sclerosis *Gastrointestinal Microbiome
 Female Humans Male Central Nervous System *Multiple Sclerosis/drug therapy Oligodendroglia/physiology Proteomics *Triiodothyronine/adverse effects Middle Aged
 Humans *Multiple Sclerosis/complications Biomechanical Phenomena/physiology Postural Balance/physiology Walking/physiology Movement
 Humans Self Report *Multiple Sclerosis/diagnosis Cross-Sectional Studies Sweden/epidemiology Fatigue/etiology/complications
 Humans *Multiple Sclerosis *Epstein-Barr Virus Infections Herpesvirus 4, Human Immunity
 Humans *Vibration/therapeutic use *Multiple Sclerosis/complications Walking/physiology Toes Muscles Gait/physiology Biomechanical Phenomena
 Humans *Multiple Sclerosis/drug therapy *Graves Disease/drug therapy Antithyroid Agents Antibodies, Monoclonal, Humanized/adverse effects
 Child Humans *Multiple Sclerosis/pathology Brain Blood-Brain Barrier/diagnostic imaging/pathology Inflammation/pathology Choroid/pathology
 Humans *Resistance Training Quality of Life *Multiple Sclerosis/complications Exercise/physiology Pain/complications
 Adolescent Adult Humans Middle Aged Young Adult *Hematopoietic Stem Cell Transplantation *Multiple Sclerosis/therapy *Neural Stem Cells Prospective Studies Stem Cell Transplantation/methods
 Humans *Multiple Sclerosis/diagnostic imaging Gray Matter Cerebral Cortex Upper Extremity Magnetic Resonance Imaging/methods Lower Extremity/diagnostic imaging
 Humans *Multiple Sclerosis Case-Control Studies Seasons
 Humans Adult Myelin Sheath/physiology *Multiple Sclerosis/metabolism *Remyelination/physiology Oligodendroglia/metabolism Neuroglia
 Humans *Neuromyelitis Optica *Multiple Sclerosis/diagnosis Retrospective Studies Evoked Potentials, Somatosensory/physiology Tibial Nerve/pathology Aquaporin 4
 Humans CD4-Positive T-Lymphocytes *Lactobacillus plantarum/metabolism *Lacticaseibacillus paracasei *Multiple Sclerosis/diagnosis/therapy Interleukin-17/metabolism Cytokines/metabolism Lactobacillus/metabolism Interferon-gamma/metabolism Th1 Cells Transforming Growth Factor beta/metabolism *Probiotics/therapeutic use/pharmacology
 Humans Female Male *Neuromyelitis Optica Case-Control Studies Canada/epidemiology Aquaporin 4 *Multiple Sclerosis/complications Demography Autoantibodies
 Adult Male Humans Female Middle Aged *Multiple Sclerosis/diagnostic imaging Contrast Media Prospective Studies Pilot Projects Magnetic Resonance Imaging/methods *Vascular Diseases Brain/pathology
 Humans *Multiple Sclerosis/rehabilitation Quality of Life Neoplasm Recurrence, Local Walking Physical Therapy Modalities Exercise Therapy/methods Randomized Controlled Trials as Topic
 Humans *Antibodies, Monoclonal, Humanized/therapeutic use Nucleosides *Multiple Sclerosis/complications *Virus Activation Hepatitis B Antibodies *Hepatitis B/complications
 Humans *Vitamin D/pharmacology/therapeutic use/metabolism *Multiple Sclerosis/drug therapy Neuroprotection Vitamins/pharmacology Nerve Growth Factors
 Animals *Multiple Sclerosis/diagnostic imaging *Neurodegenerative Diseases *Encephalomyelitis, Autoimmune, Experimental/diagnostic imaging *White Matter/diagnostic imaging Neuroimaging Disease Models, Animal
 Humans Female Child, Preschool Child Adolescent *Multiple Sclerosis/diagnosis Depression *Urinary Bladder, Overactive Neuropsychological Tests *Cognitive Dysfunction/diagnosis Anxiety *Running
 Adult Humans *Multiple Sclerosis/complications Adaptation, Psychological Pain/complications Fatigue/complications Self Report
 Adolescent Adult Female Humans Middle Aged Activities of Daily Living Cross-Sectional Studies Disability Evaluation Hand Strength *Multiple Sclerosis/diagnosis Patient Reported Outcome Measures Upper Extremity
 Humans *Sleep Initiation and Maintenance Disorders/complications/diagnosis Self Report *Multiple Sclerosis/complications Sleep *Cognitive Dysfunction Fatigue/diagnosis/etiology
 Humans *Multiple Sclerosis/psychology Retrospective Studies Insurance Claim Review Cross-Sectional Studies Recurrence
 Adult Humans Cross-Sectional Studies Electromyography/methods *Multiple Sclerosis/complications Muscle Contraction/physiology *Muscle Fatigue/physiology Muscle, Skeletal/physiology
 Humans Female Male *Multiple Sclerosis/complications Cross-Sectional Studies Prospective Studies Gait Walking
 Male Humans Adult Interferon-beta/adverse effects *Multiple Sclerosis/drug therapy *Thrombotic Microangiopathies/chemically induced *Renal Insufficiency/complications
 Humans Dimethyl Fumarate/pharmacology/therapeutic use *Multiple Sclerosis/drug therapy *Colitis, Ulcerative/drug therapy Anti-Inflammatory Agents/therapeutic use Intestines
 Humans Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy *Sleep Initiation and Maintenance Disorders Anxiety/epidemiology Outcome Assessment, Health Care
 Humans *Multiple Sclerosis/drug therapy Antioxidants Prospective Studies Cholesterol, LDL Lipoproteins *Hyperemia Oxidation-Reduction Glucagon-Like Peptide 1 Lipoproteins, LDL
 Humans Processing Speed *Multiple Sclerosis Cognition Walking *Cognitive Dysfunction/etiology *Multiple Sclerosis, Chronic Progressive/complications Retinoids Gait
 Female Humans Male Middle Aged Biomarkers Brain-Derived Neurotrophic Factor Glial Fibrillary Acidic Protein Intermediate Filaments/pathology *Multiple Sclerosis/pathology *Neuroprotective Agents
 Adolescent Adult Aged Female Humans Male Middle Aged Young Adult Feasibility Studies *Mobile Applications *Multiple Sclerosis/diagnosis Reproducibility of Results Smartphone
 Humans *Image Processing, Computer-Assisted/methods Neural Networks, Computer Magnetic Resonance Imaging/methods *Multiple Sclerosis/diagnostic imaging Thalamus/diagnostic imaging Atrophy
 Humans *Monocytes Cladribine/pharmacology/therapeutic use *Multiple Sclerosis/drug therapy Blood-Brain Barrier Leukocytes, Mononuclear
 Humans Female Middle Aged Male Retrospective Studies *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive/epidemiology Cross-Sectional Studies Quality of Life Disease Progression Registries
 Humans Child Kuwait/epidemiology *Multiple Sclerosis/epidemiology Incidence Registries Gulf War
 Humans Immune Checkpoint Inhibitors/adverse effects *Multiple Sclerosis/drug therapy *Neoplasms/drug therapy *Antineoplastic Agents, Immunological/adverse effects
 Humans *Multiple Sclerosis/complications Brain/diagnostic imaging/pathology Gray Matter/pathology Magnetic Resonance Imaging/methods *White Matter/pathology
 Humans *Emotions Qualitative Research Data Collection Fear *Multiple Sclerosis
 Male Humans *Multiple Sclerosis/rehabilitation *Telerehabilitation Activities of Daily Living Argentina Quality of Life *Virtual Reality
 Case-Control Studies *Gray Matter/diagnostic imaging/pathology *Atrophy Magnetic Resonance Imaging *Multiple Sclerosis, Relapsing-Remitting/complications/diagnostic imaging *Processing Speed Humans Male Female Adult Middle Aged
 Humans *Multiple Sclerosis/drug therapy Cladribine/therapeutic use Fingolimod Hydrochloride/therapeutic use Immunosuppressive Agents/therapeutic use Dimethyl Fumarate/therapeutic use Retrospective Studies Registries Tablets/therapeutic use Recurrence *Multiple Sclerosis, Relapsing-Remitting/drug therapy
 Humans *Multiple Sclerosis/epidemiology/genetics Genome-Wide Association Study Mendelian Randomization Analysis Case-Control Studies Quality of Life Risk Factors *Migraine Disorders/epidemiology/genetics/complications Polymorphism, Single Nucleotide/genetics
 Adult Humans Alemtuzumab/adverse effects Interferon beta-1a/adverse effects *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Neoplasm Recurrence, Local/drug therapy
 Child Adolescent Humans *Epstein-Barr Virus Infections/complications *Infectious Mononucleosis/complications Siblings Herpesvirus 4, Human Retrospective Studies *Multiple Sclerosis/complications
 Humans *Ethnicity *Multiple Sclerosis/complications Pilot Projects Walking Speed Cognition Accidental Falls
 Male Female Humans Adult Middle Aged Temperature *Body Temperature *Multiple Sclerosis/complications Cold Temperature Hot Temperature Fatigue Skin Temperature Body Temperature Regulation/physiology
 Humans *Multiple Sclerosis/pathology *Cervical Cord/diagnostic imaging/pathology Retrospective Studies Magnetic Resonance Imaging/methods Spinal Cord/diagnostic imaging/pathology
 Humans *Diabetes Mellitus, Type 1/complications Mendelian Randomization Analysis/methods Genome-Wide Association Study *Amyotrophic Lateral Sclerosis *Chronic Pain/epidemiology/genetics/complications Polymorphism, Single Nucleotide *Arthritis, Rheumatoid/epidemiology/genetics/complications *Lupus Erythematosus, Systemic/etiology *Multiple Sclerosis/epidemiology/genetics/complications *Psoriasis/complications *Inflammatory Bowel Diseases/epidemiology/genetics/complications
 Humans Antibodies Aquaporin 4 *Autoantibodies Epstein-Barr Virus Infections *Immune System Diseases *Multiple Sclerosis/diagnosis Oligoclonal Bands Retrospective Studies *Myelin-Oligodendrocyte Glycoprotein/immunology
 Humans Isotretinoin/adverse effects *Multiple Sclerosis/epidemiology/drug therapy Retrospective Studies *Fibromyalgia/chemically induced/epidemiology/drug therapy *Acne Vulgaris/drug therapy/epidemiology/chemically induced Anti-Bacterial Agents/therapeutic use *Peripheral Nervous System Diseases/chemically induced *Migraine Disorders/drug therapy/epidemiology *Dermatologic Agents/adverse effects
 Humans *Multiple Sclerosis/diagnostic imaging Retrospective Studies Algorithms Tomography, X-Ray Computed/methods Magnetic Resonance Imaging/methods Signal-To-Noise Ratio Image Processing, Computer-Assisted/methods
 Male Humans *Spermatic Cord Torsion *Anemia, Iron-Deficiency *Multiple Sclerosis *Diverticulitis
 Male Female Humans *Military Personnel Incidence Retrospective Studies *Multiple Sclerosis/epidemiology *Optic Neuritis/epidemiology/etiology
 Female Humans Adult Male *Multiple Sclerosis/therapy Cross-Sectional Studies Cost of Illness Lebanon Surveys and Questionnaires Health Care Costs Severity of Illness Index Quality of Life
 Humans Adult Middle Aged *Fingolimod Hydrochloride/adverse effects Immunosuppressive Agents/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced Drugs, Generic/adverse effects Recurrence Treatment Outcome
 Humans *CD40 Ligand *Multiple Sclerosis Brain/pathology
 Humans Interferon beta-1a/therapeutic use *Interferon-beta/therapeutic use Retrospective Studies *Multiple Sclerosis/drug therapy Patient Reported Outcome Measures Fatigue/drug therapy Disability Evaluation
 Pregnancy Infant, Newborn Humans Female Natalizumab/adverse effects Rituximab/adverse effects Retrospective Studies *Abortion, Spontaneous *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy Recurrence
 Humans Electromyography *Neck Reflex/physiology Neck Muscles/physiology *Multiple Sclerosis/diagnostic imaging Receptors, Antigen, T-Cell
 Humans *Multiple Sclerosis/diagnostic imaging/genetics *Neuromyelitis Optica/diagnostic imaging/genetics/pathology *Connectome Brain/diagnostic imaging/pathology Magnetic Resonance Imaging Cerebellum/diagnostic imaging/pathology
 Female Humans Male *Drug-Related Side Effects and Adverse Reactions *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting Prospective Studies Tetanus Toxoid Vaccination/adverse effects
 Humans Gray Matter/diagnostic imaging/pathology Pilot Projects *Multiple Sclerosis/diagnosis Magnetic Resonance Imaging/methods *White Matter/diagnostic imaging/pathology
 Humans *COVID-19 COVID-19 Vaccines Retrospective Studies SARS-CoV-2 *Multiple Sclerosis/drug therapy Seroconversion Antibodies, Viral *Drug-Related Side Effects and Adverse Reactions Vaccination
 Humans *Multiple Sclerosis/drug therapy *Sphingosine 1 Phosphate Receptor Modulators/pharmacology/therapeutic use Sphingosine-1-Phosphate Receptors/metabolism Pandemics *COVID-19 Recurrence
 Female Humans Adult Middle Aged *Muscle Fatigue *Multiple Sclerosis/complications Walking/physiology Gait/physiology Walk Test/methods
 Animals Humans Mice Amyloid Amyloidogenic Proteins Autoantigens/genetics *Encephalomyelitis, Autoimmune, Experimental/genetics/chemically induced Mice, Inbred C57BL *Multiple Sclerosis/genetics/metabolism *Myelin-Oligodendrocyte Glycoprotein/genetics/chemistry Peptide Fragments/chemistry *Citrullination
 Humans *Multiple Sclerosis/complications/drug therapy *Myelitis, Transverse/complications/drug therapy/chemically induced 4-Aminopyridine/therapeutic use Potassium Channel Blockers/therapeutic use Treatment Outcome Methylprednisolone/therapeutic use Double-Blind Method
 Humans *Spinal Cord Diseases *Myelitis/diagnosis *Multiple Sclerosis/diagnostic imaging *Neuromyelitis Optica/diagnostic imaging Magnetic Resonance Imaging
 Humans Herpesvirus 4, Human T-Lymphocytes, Cytotoxic *Epstein-Barr Virus Infections *Multiple Sclerosis/therapy Leukocytes, Mononuclear *Hematopoietic Stem Cell Transplantation/adverse effects
 Humans Female Adult Middle Aged *Multiple Sclerosis/diagnostic imaging Diffusion Tensor Imaging/methods Longitudinal Studies Magnetic Resonance Imaging Disease Progression Brain/diagnostic imaging
 Humans *Multiple Sclerosis/pathology Microglia/metabolism Receptors, GABA/metabolism Positron-Emission Tomography Brain/pathology Magnetic Resonance Imaging Immunoglobulin G
 Humans *Intermediate Filaments Biomarkers *Multiple Sclerosis Neurofilament Proteins
 Humans Mexico/epidemiology Cross-Sectional Studies *Neuromyelitis Optica/complications *Multiple Sclerosis/complications Inflammation/complications
 Male Humans Middle Aged Biotin/adverse effects *Hyperthyroidism/chemically induced/diagnosis/drug therapy Thyroid Function Tests Hormones/therapeutic use *Multiple Sclerosis/drug therapy
 Humans *Multiple Sclerosis/diagnostic imaging Thalamic Nuclei/diagnostic imaging Thalamus/diagnostic imaging Magnetic Resonance Imaging/methods *White Matter/diagnostic imaging
 Humans *Foot Orthoses Ankle *Multiple Sclerosis/therapy *Peroneal Neuropathies/therapy *Electric Stimulation Therapy Peroneal Nerve/physiology Gait/physiology Electric Stimulation *Gait Disorders, Neurologic/etiology/therapy *Stroke
 Humans Female *Multiple Sclerosis Menopause Patients Chronic Disease
 Humans COVID-19 Vaccines Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy Pandemics Rituximab SARS-CoV-2 *COVID-19 Vaccination
 Adult Humans *Multiple Sclerosis/metabolism B-Lymphocytes Blood-Brain Barrier/metabolism Magnetic Resonance Imaging Iron
 Animals *Multiple Sclerosis/genetics Microglia/metabolism Astrocytes/metabolism *White Matter/metabolism Inflammation/genetics RNA/metabolism Oligodendroglia/metabolism
 Humans *Polymorphism, Single Nucleotide *Multiple Sclerosis/genetics Programmed Cell Death 1 Receptor/genetics Case-Control Studies Genetic Predisposition to Disease
 Humans *Interleukin-3 *Multiple Sclerosis
 Mice Animals Humans Ranvier's Nodes/metabolism Potassium/metabolism Neurons/metabolism Oligodendroglia/metabolism *Encephalomyelitis, Autoimmune, Experimental/genetics/metabolism *Multiple Sclerosis/genetics/metabolism
 Humans Female Adult Middle Aged Male Disease Progression *Demyelinating Diseases/pathology *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging Risk Factors
 United States Humans *Neurology *Multiple Sclerosis
 Humans Cost-Benefit Analysis *Multiple Sclerosis Delivery of Health Care Patient Care Cost-Effectiveness Analysis
 Middle Aged Humans Female *Multiple Sclerosis/psychology Quality of Life/psychology Retrospective Studies Depression/psychology Cross-Sectional Studies Cognition Neuropsychological Tests
 Male Child Humans Female Cohort Studies Sex Factors *Multiple Sclerosis/epidemiology Income Pensions Sick Leave Occupations *Disabled Persons Sweden/epidemiology
 Central Nervous System *Central Nervous System Diseases/drug therapy *Multiple Sclerosis *Neurodegenerative Diseases Fungi Inflammation
 Humans Antibodies, Neutralizing *Multiple Sclerosis/drug therapy *COVID-19/prevention & control Leukocytes, Mononuclear SARS-CoV-2 Breakthrough Infections
 Humans *Monocytes *Multiple Sclerosis/diagnosis Retrospective Studies Lymphocytes Glucocorticoids Immunosuppressive Agents
 Animals Humans *CD4-Positive T-Lymphocytes Encephalomyelitis, Autoimmune, Experimental *Interleukin-17/metabolism Interleukin-23/metabolism *Multiple Sclerosis/metabolism Th17 Cells
 Humans Natalizumab/therapeutic use Chromatography, Liquid/methods *Multiple Sclerosis/drug therapy Tandem Mass Spectrometry/methods Antibodies, Monoclonal, Humanized/therapeutic use Peptides/therapeutic use Chromatography, High Pressure Liquid/methods
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy *Multiple Sclerosis/drug therapy Microglia Phagocytosis Macrophages Mice, Inbred C57BL
 Humans *Multiple Sclerosis/pathology Gray Matter/pathology Magnetic Resonance Imaging Atrophy/pathology Neurotransmitter Agents Cholinergic Agents Brain/pathology
 Animals Mice *Docosahexaenoic Acids/metabolism/pharmacology *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism Endocannabinoids/metabolism Mice, Inbred C57BL Multiple Sclerosis/drug therapy/metabolism Recurrence Disease Progression T-Lymphocytes/cytology/drug effects Cell Differentiation/drug effects
 Humans *Multiple Sclerosis/metabolism *Remyelination/physiology Central Nervous System/metabolism Oligodendroglia/metabolism Neurons/metabolism Myelin Sheath/metabolism
 Humans *Cannabinoids/therapeutic use/pharmacology *Multiple Sclerosis/drug therapy Neuroinflammatory Diseases *Alzheimer Disease/drug therapy *Parkinson Disease/drug therapy Endocannabinoids Receptors, Cannabinoid
 Female Male Mice Animals *Multiple Sclerosis/pathology *Encephalomyelitis, Autoimmune, Experimental/pathology Immunity, Innate Sexism Lymphocytes/pathology Disease Models, Animal
 Humans *Multiple Sclerosis/drug therapy Interleukin-17 Fluoxetine/pharmacology/therapeutic use Interleukin-6 Neuroimmunomodulation Th1 Cells Cytokines Interferon-gamma
 Humans *Trigeminal Neuralgia/diagnostic imaging/etiology/surgery Prospective Studies *Multiple Sclerosis/complications *Microvascular Decompression Surgery/methods Magnetic Resonance Imaging Treatment Outcome
 Humans *Multiple Sclerosis/drug therapy Fingolimod Hydrochloride/pharmacology/therapeutic use *Sphingosine 1 Phosphate Receptor Modulators/therapeutic use Sphingosine-1-Phosphate Receptors Antibodies, Monoclonal/therapeutic use
 Humans *Multiple Sclerosis/diagnostic imaging *Glioblastoma/diagnostic imaging/metabolism Receptors, GABA/metabolism Protein Transport Positron-Emission Tomography/methods
 Humans Quality of Life Hand Strength *Neuromyelitis Optica/diagnosis *Multiple Sclerosis/psychology *Central Nervous System Diseases/complications Cognition Gait Analysis Fatigue Central Nervous System
 Humans *Optic Nerve Diseases/complications *Optic Atrophy, Hereditary, Leber/complications/diagnosis/genetics *Optic Neuritis/etiology/genetics *Multiple Sclerosis/complications/genetics Central Nervous System DNA, Mitochondrial/genetics Autoantibodies
 Mice Animals Humans Female *Multiple Sclerosis/pathology Disease Models, Animal *Encephalomyelitis, Autoimmune, Experimental/pathology Central Nervous System/pathology Mice, Transgenic
 Adult Female Humans Middle Aged Antibodies, Monoclonal/therapeutic use Antibodies, Monoclonal, Humanized/pharmacology/therapeutic use *Antineoplastic Agents/therapeutic use Immunity, Cellular *Multiple Sclerosis/drug therapy Male
 Humans *Multiple Sclerosis Neuroinflammatory Diseases Brain Synapses *White Matter
 Animals Mice Armadillo Domain Proteins/genetics/metabolism Axons/pathology Cytoskeletal Proteins/genetics/metabolism Disease Models, Animal Down-Regulation *Encephalomyelitis, Autoimmune, Experimental/pathology *Multiple Sclerosis/genetics/pathology *Retinal Ganglion Cells/metabolism/pathology *RNA Splicing Factors/genetics
 Humans Aged *COVID-19/prevention & control RNA, Viral SARS-CoV-2 *Multiple Sclerosis/complications Rituximab *Vaccines Breakthrough Infections
 Humans *Myeloid-Derived Suppressor Cells/metabolism *Multiple Sclerosis/metabolism Cytokines/metabolism CD4-Positive T-Lymphocytes/metabolism Immunosuppressive Agents *MicroRNAs/metabolism
 Humans *Multiple Sclerosis/complications Myelin Sheath Axons Brain *White Matter Inflammation/complications Disease Progression Magnetic Resonance Imaging
 Humans *Multiple Sclerosis Cross-Sectional Studies Imagery, Psychotherapy
 Humans Amyloid beta-Peptides/cerebrospinal fluid *Multiple Sclerosis, Relapsing-Remitting/complications *Multiple Sclerosis Amyloid Precursor Protein Secretases Bayes Theorem Prospective Studies Aspartic Acid Endopeptidases Inflammation
 Humans Child Child, Preschool *Multiple Sclerosis/cerebrospinal fluid Proteome/metabolism Prospective Studies Canada Central Nervous System/metabolism Syndrome Cerebrospinal Fluid Proteins/metabolism
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy SARS-CoV-2 *Multiple Sclerosis *COVID-19 Glatiramer Acetate/therapeutic use Dimethyl Fumarate/therapeutic use Interferon-beta N,N-Dimethyltryptamine Immunoglobulin A Immunoglobulin G Antibodies, Viral
 Humans Amyotrophic Lateral Sclerosis/genetics Austria *C9orf72 Protein/genetics Frontotemporal Dementia/genetics *Multiple Sclerosis/genetics Multiple Sclerosis, Chronic Progressive/genetics Retrospective Studies
 Humans *Multiple Sclerosis *Vaccination
 Mice Female Animals *Multiple Sclerosis/pathology Hydrogen Peroxide/metabolism Mice, Inbred NOD *Encephalomyelitis, Autoimmune, Experimental/pathology Spinal Cord/pathology *Multiple Sclerosis, Relapsing-Remitting/metabolism Axons/pathology Mitochondria/metabolism DNA, Mitochondrial/metabolism
 Humans DNA, Viral/genetics *Epstein-Barr Virus Infections/complications/genetics Herpesvirus 4, Human/genetics Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting *Toll-Like Receptor 10 Viral Load
 Humans *COVID-19/prevention & control SARS-CoV-2 *Multiple Sclerosis/drug therapy COVID-19 Vaccines Cohort Studies New York Prospective Studies *Vaccines
 Humans Herpesvirus 4, Human/genetics *Multiple Sclerosis/genetics *Epstein-Barr Virus Infections/genetics Antigens, Viral Antibodies, Viral
 Humans *Yoga *Occupational Therapy *Multiple Sclerosis Qualitative Research
 Humans Biomarkers/metabolism *Extracellular Vesicles/metabolism *Multiple Sclerosis, Chronic Progressive/diagnosis *Multiple Sclerosis, Relapsing-Remitting/diagnosis *Myelin Basic Protein/metabolism Myelin-Oligodendrocyte Glycoprotein/metabolism Oligodendroglia/metabolism Pilot Projects Prognosis
 Humans *Paraparesis, Tropical Spastic/complications *Human T-lymphotropic virus 1 *Multiple Sclerosis/complications Th17 Cells/pathology Interleukin-17
 Male Female Humans Herpesvirus 4, Human *Epstein-Barr Virus Infections/complications/epidemiology *Multiple Sclerosis/etiology *Periapical Abscess/complications Cross-Sectional Studies Acute Disease
 Humans Central Nervous System/pathology *Central Nervous System Diseases/therapy *Multiple Sclerosis/therapy *Neuromyelitis Optica/therapy Plasma Exchange/methods
 Humans *COVID-19/prevention & control SARS-CoV-2 T-Lymphocytes *Multiple Sclerosis/drug therapy COVID-19 Vaccines Vaccination Antibodies, Viral
 Humans *Multiple Sclerosis/drug therapy/genetics Leukocytes, Mononuclear Docosahexaenoic Acids/pharmacology/therapeutic use Interleukin-2/genetics/pharmacology Interleukin-4/pharmacology Tretinoin/pharmacology/therapeutic use Cytokines GATA3 Transcription Factor/genetics
 Humans *Multiple Sclerosis/pathology Processing Speed Retrospective Studies *Cigarette Smoking Cross-Sectional Studies Glia Maturation Factor Brain/diagnostic imaging/pathology *Central Nervous System Diseases Magnetic Resonance Imaging/methods Atrophy/pathology
 Male Humans Female Aged *Multiple Sclerosis/complications Cross-Sectional Studies Prospective Studies Quality of Life Lower Extremity Muscle, Skeletal Muscle Weakness Muscle Strength/physiology
 Humans *Motor Disorders Disease Progression Disability Evaluation Neoplasm Recurrence, Local/pathology Spinal Cord/diagnostic imaging/pathology Brain/pathology Magnetic Resonance Imaging/methods *Demyelinating Diseases/diagnostic imaging/pathology *Multiple Sclerosis/pathology
 Humans *Multiple Sclerosis/diagnosis *Deglutition Disorders/diagnosis/etiology/epidemiology Reproducibility of Results Quality of Life Cross-Cultural Comparison Croatia Self-Assessment Surveys and Questionnaires Language
 Child Adult Humans *Multiple Sclerosis/genetics HLA-DRB1 Chains/genetics Alleles Genotype Genetic Predisposition to Disease
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy *Multiple Sclerosis/drug therapy NF-kappa B NF-E2-Related Factor 2 bcl-2-Associated X Protein Mice, Inbred C57BL
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/drug therapy *Multiple Sclerosis/drug therapy Micelles Nasal Sprays Brain/pathology Mice, Inbred C57BL Disease Models, Animal
 Humans Male Female Middle Aged *Multiple Sclerosis/pathology Myelin Sheath/pathology Water Walking Pyramidal Tracts/pathology
 Adult Humans *Multiple Sclerosis/drug therapy Retrospective Studies Natalizumab/therapeutic use Drug Costs Alemtuzumab/therapeutic use
 Humans *Multiple Sclerosis/pathology *Remyelination Thiazoles Aniline Compounds Brain/pathology Myelin Sheath/metabolism Magnetic Resonance Imaging/methods *White Matter/pathology
 Male Humans Female *Multiple Sclerosis Health Status Employment
 Humans Cost-Benefit Analysis *Multiple Sclerosis
 Humans *Multiple Sclerosis/drug therapy Fingolimod Hydrochloride/pharmacology/therapeutic use/chemistry Structure-Activity Relationship Antibodies Receptors, Lysosphingolipid Sphingosine-1-Phosphate Receptors
 *Multiple Sclerosis/complications *Muscle Spasticity Nurses Activities of Daily Living Quality of Life Humans Male Female Adolescent Middle Aged Spain Adult Aged Cross-Sectional Studies *Nurse Specialists
 Humans *Multiple Sclerosis *Parkinson Disease Books Communication Emotions
 Humans *Multiple Sclerosis Magnetic Resonance Imaging Blood Proteins Gadolinium Algorithms
 Male Female Mice Animals *Multiple Sclerosis/pathology Galectin 3/genetics Phosphatidylcholines *Encephalomyelitis, Autoimmune, Experimental/pathology Spinal Cord Microglia/physiology
 Young Adult Humans *Multiple Sclerosis/diagnostic imaging Consensus *Neurodegenerative Diseases Brain/diagnostic imaging Magnetic Resonance Imaging/methods Spinal Cord/diagnostic imaging
 Humans *Multiple Sclerosis *Diet, Mediterranean Smoking Social Class
 Male Pregnancy Animals Female Mice *Encephalomyelitis, Autoimmune, Experimental *Multiple Sclerosis/chemically induced Estrogens Benzhydryl Compounds/toxicity *Endocrine Disruptors/toxicity
 Humans *Intermediate Filaments Antibodies Axons Biological Assay Healthy Volunteers *Multiple Sclerosis/diagnostic imaging Biomarkers
 Humans *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents/adverse effects *Multiple Sclerosis Retrospective Studies Universities Fingolimod Hydrochloride/adverse effects Dimethyl Fumarate/adverse effects Recurrence
 Humans *Multiple Sclerosis Consensus Vaccination
 Humans Female Young Adult Adult Male *Multiple Sclerosis/diagnostic imaging Cohort Studies Intermediate Filaments Immunoglobulin kappa-Chains/cerebrospinal fluid Neurofilament Proteins Biomarkers
 Humans *Genome-Wide Association Study Multifactorial Inheritance/genetics *Multiple Sclerosis/genetics Epigenesis, Genetic European People Risk Factors Genetic Predisposition to Disease/genetics Phenotype
 Humans *Myelin Sheath/pathology *Multiple Sclerosis/diagnostic imaging Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology Magnetic Resonance Spectroscopy
 Humans *Multiple Sclerosis/complications Cytomegalovirus *Epstein-Barr Virus Infections/complications Herpesvirus 4, Human Antibodies, Viral Immunoglobulin G Epstein-Barr Virus Nuclear Antigens Prognosis Immunity, Humoral Inflammation/complications Recurrence
 Humans Mice Animals T-Lymphocytes, Regulatory CD4-Positive T-Lymphocytes *Multiple Sclerosis/therapy Lymphocyte Activation *Neural Stem Cells Forkhead Transcription Factors CD4 Antigens
 Animals *Multiple Sclerosis/pathology Axons/pathology *Encephalomyelitis, Autoimmune, Experimental/pathology Neurons/pathology Mitochondria/pathology
 Female Humans *Multiple Sclerosis Quality of Life Menopause Gonadal Steroid Hormones Estrogens
 Mice Animals *Multiple Sclerosis/pathology Blood-Brain Barrier/pathology *Encephalomyelitis, Autoimmune, Experimental Inflammation/pathology Permeability Obesity/complications Mice, Inbred C57BL
 Humans *Multiple Sclerosis/drug therapy Dose-Response Relationship, Drug *Arthritis, Rheumatoid/drug therapy *Lupus Erythematosus, Systemic/drug therapy Double-Blind Method Treatment Outcome
 Humans Adult Middle Aged Aged Aged, 80 and over *Parkinson Disease/diagnosis Reproducibility of Results Postural Balance Disability Evaluation Psychometrics *Stroke/diagnosis *Multiple Sclerosis/diagnosis
 Humans *Multiple Sclerosis/complications Retinal Ganglion Cells/pathology Gray Matter/diagnostic imaging Tomography, Optical Coherence/methods Cerebral Cortex
 Animals Mice Cell Differentiation *Demyelinating Diseases/immunology/metabolism Disease Models, Animal Hydrocortisone *Melatonin/pharmacology Mice, Inbred C57BL *Monocytes/immunology/metabolism *Multiple Sclerosis/immunology/metabolism *Phagocytosis/immunology Receptors, Melatonin *Myelin Sheath/metabolism
 Animals Humans Clostridium perfringens/genetics *Multiple Sclerosis/genetics *Gastrointestinal Microbiome Immune Privilege Lymphocytes *Encephalomyelitis, Autoimmune, Experimental
 Animals Humans *Curcumin/pharmacology *Multiple Sclerosis/drug therapy Polyphenols/pharmacology/therapeutic use Antioxidants/pharmacology Anti-Inflammatory Agents *Microbiota
 Humans T-Lymphocytes *Microbiota *Multiple Sclerosis
 Female Humans Pregnancy Emotions Mothers *Multiple Sclerosis Parturition Postpartum Period Qualitative Research
 Humans *Multiple Sclerosis/pathology Magnetic Resonance Imaging/methods Brain/diagnostic imaging/pathology Neuroimaging Atrophy/pathology
 Humans Female Adult Male *Multiple Sclerosis/pathology Retrospective Studies Cross-Sectional Studies Nerve Fibers/pathology Retina/pathology *Retinal Degeneration/pathology Tomography, Optical Coherence/methods
 Male Humans Adolescent Child Young Adult Adult Middle Aged Aged Cohort Studies *Multiple Sclerosis/epidemiology Risk Factors Incidence *Myopia/epidemiology/etiology Sweden/epidemiology
 Humans *Multiple Sclerosis/pathology Myelin Sheath/pathology *White Matter/pathology Magnetic Resonance Imaging/methods Water Brain/pathology
 Adult Humans *Arthritis, Rheumatoid/drug therapy *Multiple Sclerosis/drug therapy Tumor Necrosis Factor-alpha *Antirheumatic Agents/therapeutic use *Rheumatic Fever/drug therapy Tumor Necrosis Factor Inhibitors/therapeutic use Randomized Controlled Trials as Topic
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/pathology *Multiple Sclerosis/pathology Intermediate Filaments/pathology Optic Nerve/pathology Inflammation/metabolism
 Humans *Quality of Life *Multiple Sclerosis Psychometrics Reproducibility of Results Surveys and Questionnaires
 Humans *Antigens, CD20/immunology B-Lymphocytes/drug effects/immunology *Multiple Sclerosis/drug therapy/immunology Recurrence Rituximab/therapeutic use/pharmacology *Immunologic Factors/pharmacology/therapeutic use Antibodies, Monoclonal/pharmacology/therapeutic use T-Lymphocytes/drug effects/immunology
 Humans *Multiple Sclerosis/drug therapy Retrospective Studies Cross-Sectional Studies Prospective Studies Magnetic Resonance Imaging Brain/diagnostic imaging/pathology Atrophy/pathology
 Humans Natalizumab/pharmacology *Multiple Sclerosis/drug therapy Integrin alpha4beta1/metabolism Monocytes
 Adult Humans Male Female Aged United States/epidemiology Middle Aged *Ethnicity Prevalence *Multiple Sclerosis/epidemiology Medicare Hispanic or Latino
 Humans *Multiple Sclerosis/pathology HLA-DRB1 Chains/genetics Neoplasm Recurrence, Local *Demyelinating Diseases Magnetic Resonance Imaging Chronic Disease Genetic Predisposition to Disease
 Adult Humans *Multiple Sclerosis/drug therapy Retrospective Studies Fingolimod Hydrochloride/therapeutic use Crotonates/therapeutic use Dimethyl Fumarate/therapeutic use Immunosuppressive Agents/therapeutic use Medication Adherence
 Adult Male Humans Female *Antibodies, Monoclonal/therapeutic use Interleukin-10 *Multiple Sclerosis/drug therapy Administration, Intravenous Healthy Volunteers Double-Blind Method Area Under Curve Dose-Response Relationship, Drug
 Female Male Humans *Neuromyelitis Optica/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Myelin-Oligodendrocyte Glycoprotein Retrospective Studies *Optic Neuritis/diagnostic imaging Magnetic Resonance Imaging/methods Autoantibodies
 Humans Sirtuin 1/genetics *Multiple Sclerosis/genetics Polymorphism, Single Nucleotide/genetics Genotype *Optic Neuritis/genetics
 Humans *Critical Pathways *Multiple Sclerosis Stakeholder Participation Family Patient Care
 Humans *Vitamin D Prospective Studies Vitamins *Multiple Sclerosis Dietary Supplements
 Humans Vitamin D *Epstein-Barr Virus Infections/complications *Multiple Sclerosis Herpesvirus 4, Human
 Humans Sclerosis/pathology *Multiple Sclerosis Central Nervous System Microglia Macrophages Chronic Disease
 Humans Feedback *Multiple Sclerosis Magnetic Resonance Imaging/methods Brain Brain Mapping
 Humans Area Under Curve Dose-Response Relationship, Drug Double-Blind Method Electrocardiography, Ambulatory Healthy Volunteers *Multiple Sclerosis/drug therapy *Peptidomimetics/therapeutic use
 Humans Natalizumab/therapeutic use *Leukoencephalopathy, Progressive Multifocal Pilot Projects Follow-Up Studies Retrospective Studies Immunologic Factors/therapeutic use *Multiple Sclerosis/drug therapy
 Humans *Biosensing Techniques Plasma *Multiple Sclerosis Metabolome *Biomedical Research
 Humans *Multiple Sclerosis *Robotic Surgical Procedures Postural Balance Activities of Daily Living
 Female Humans Adult *Multiple Sclerosis *Organizing Pneumonia Immunologic Factors Antibodies, Monoclonal, Humanized *Pneumonia
 Humans *Herpesvirus 1, Human *Multiple Sclerosis *Virus Diseases DNA, Viral *Epstein-Barr Virus Infections *Herpes Simplex
 Male Mice Animals *Hydrogen Sulfide/pharmacology *Multiple Sclerosis/drug therapy NF-kappa B/metabolism Cuprizone Inflammation *MicroRNAs Mice, Inbred C57BL
 Humans Adolescent *Sleep Deprivation/complications/epidemiology *Multiple Sclerosis/epidemiology Case-Control Studies Sweden/epidemiology Sleep
 Humans Reproducibility of Results *Multiple Sclerosis Sexual Behavior Sexuality Language Surveys and Questionnaires Personal Satisfaction
 Animals Mice *Gray Matter *Multiple Sclerosis Cerebral Cortex Central Nervous System Algorithms
 Humans *Quality of Life Cross-Sectional Studies *Multiple Sclerosis/complications Severity of Illness Index Pruritus/epidemiology/etiology/diagnosis
 Humans *Ferroptosis *Multiple Sclerosis *Central Nervous System Diseases *Neuromyelitis Optica Central Nervous System *Iron Overload
 Humans Zinc *Central Nervous System Diseases *Trace Elements *Multiple Sclerosis Central Nervous System
 Young Adult Humans *Power, Psychological Self Efficacy *Multiple Sclerosis Empowerment Patients
 Humans Australia *Life Style Quality of Life Anxiety *Multiple Sclerosis Randomized Controlled Trials as Topic
 Humans Aged *Multiple Sclerosis Depression Exercise Anxiety Self Report
 Humans Genetic Predisposition to Disease/genetics Receptors, Progesterone/genetics Iran *Neurodegenerative Diseases Genotype Polymorphism, Single Nucleotide/genetics *Multiple Sclerosis/genetics Case-Control Studies
 Humans Consensus *Decision Making, Shared Decision Making *Multiple Sclerosis Patient Preference
 Humans *Alzheimer Disease *Multiple Sclerosis Microglia Signal Transduction Brain Syk Kinase
 Mice Animals Microglia Resveratrol/therapeutic use/metabolism *Multiple Sclerosis/drug therapy *Exosomes/metabolism Macrophages
 Humans *Multiple Sclerosis Neuroglia Inflammation/pathology Brain/pathology Spinal Cord/pathology
 Humans *Multiple Sclerosis *Gastrointestinal Microbiome Dysbiosis/microbiology Brain
 Animals Mice *Multiple Sclerosis Neuroinflammatory Diseases *Autoimmune Diseases Central Nervous System Disease Models, Animal Inflammation Pathogen-Associated Molecular Pattern Molecules
 Humans Animals Mice *Multiple Sclerosis/drug therapy Neuroinflammatory Diseases Myeloid Cells *Encephalomyelitis, Autoimmune, Experimental/drug therapy Agammaglobulinaemia Tyrosine Kinase Antigen-Antibody Complex Anti-Inflammatory Agents
 Humans Female Pelvic Floor *Multiple Sclerosis/complications *Transcranial Direct Current Stimulation Exercise Therapy *Urinary Incontinence/etiology/therapy Treatment Outcome *Urinary Incontinence, Stress
 Humans *Multiple Sclerosis Bayes Theorem Network Meta-Analysis Recurrence
 Humans Adult Contrast Media/adverse effects Gadolinium/adverse effects *Multiple Sclerosis/diagnostic imaging Cross-Sectional Studies *Organometallic Compounds Retrospective Studies Magnetic Resonance Imaging/methods Processing Speed Gadolinium DTPA
 Humans Female Adult Male *Multiple Sclerosis/diagnostic imaging Prospective Studies Tomography, Optical Coherence/methods Optic Nerve/diagnostic imaging *Optic Neuritis/diagnostic imaging
 Humans Immunity, Humoral *COVID-19/prevention & control COVID-19 Vaccines *Multiple Sclerosis/drug therapy SARS-CoV-2 Antibodies, Viral Immunoglobulin G Vaccination
 Humans Female Adult Male *Multiple Sclerosis/pathology Cross-Sectional Studies Intermediate Filaments Brain/diagnostic imaging/pathology *Central Nervous System Diseases Biomarkers Neurofilament Proteins Atrophy/pathology *Neurodegenerative Diseases/pathology
 Humans *Multiple Sclerosis Speech Quality of Life *Autoimmune Diseases *Cognition Disorders
 Humans *Multiple Sclerosis Lutein Retina Cognition *Macular Pigment
 Humans Female *Sleep Initiation and Maintenance Disorders/complications Sleepiness *Multiple Sclerosis/complications *Sleep Apnea, Obstructive/complications/diagnosis Cognition *Sleep Wake Disorders/complications *Nurses
 Humans COVID-19 Vaccines SARS-CoV-2 Cross-Sectional Studies *Multiple Sclerosis/drug therapy Prospective Studies RNA, Viral *COVID-19 Vaccination Antibodies, Viral
 Mice Animals *Multiple Sclerosis/pathology Ligands *Encephalomyelitis, Autoimmune, Experimental/pathology Chemokines Cytokines Chemokines, CXC Receptors, Chemokine
 Humans *Neuromyelitis Optica *Multiple Sclerosis Brain Magnetic Resonance Imaging/methods
 Mice Animals *Multiple Sclerosis/metabolism *Demyelinating Diseases/metabolism Oligodendroglia/metabolism Mice, Transgenic Myelin Sheath/metabolism
 Humans *Multiple Sclerosis/drug therapy *COVID-19/prevention & control COVID-19 Vaccines SARS-CoV-2 Natalizumab/therapeutic use Fingolimod Hydrochloride RNA, Messenger
 Humans *Multiple Sclerosis Disability Evaluation Upper Extremity *Disabled Persons Patient Reported Outcome Measures
 Adult Humans *Quality of Life *Multiple Sclerosis/complications Network Meta-Analysis Randomized Controlled Trials as Topic Diet Fatigue/etiology
 Humans *Multiple Sclerosis Inflammasomes NLR Family, Pyrin Domain-Containing 3 Protein Brain-Gut Axis Depression/etiology *Depressive Disorder, Major
 Humans Female Adolescent Dysbiosis/microbiology *Neurodegenerative Diseases Sclerosis *Microbiota Fatty Acids, Volatile *Multiple Sclerosis Bacteria
 Humans *Multiple Sclerosis Exercise Therapy Cognition/physiology Exercise/physiology Fatigue
 Humans Female Middle Aged Male *Multiple Sclerosis/pathology Cross-Sectional Studies Magnetic Resonance Imaging/methods Spinal Cord/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Atrophy/pathology Disability Evaluation
 Humans *Resistance Training/methods *Multiple Sclerosis/complications Postural Balance Muscle Strength Time and Motion Studies Fatigue/etiology Health Status Perception
 Humans Biomarkers Brain/pathology Intermediate Filaments/metabolism Microglia/metabolism *Multiple Sclerosis/metabolism Neurofilament Proteins Positron-Emission Tomography Receptors, GABA/metabolism
 Female Humans Adult *Multiple Sclerosis Natalizumab/therapeutic use *Multiple Sclerosis, Relapsing-Remitting/drug therapy Fingolimod Hydrochloride/therapeutic use *Hematopoietic Stem Cell Transplantation
 Humans *COVID-19 Pandemics *Multiple Sclerosis Australia Smoke
 Humans Longitudinal Studies Disease Progression *Multiple Sclerosis/drug therapy Cohort Studies Chronic Disease Recurrence
 Humans *Alzheimer Disease/pathology Brain/diagnostic imaging/pathology Caloric Restriction Magnetic Resonance Imaging/methods *Multiple Sclerosis/pathology Neuroinflammatory Diseases Pilot Projects
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/metabolism CD8-Positive T-Lymphocytes Central Nervous System/metabolism *Multiple Sclerosis/pathology CD4-Positive T-Lymphocytes Mice, Inbred C57BL
 Animals Mice *Encephalomyelitis/immunology/prevention & control *Encephalomyelitis, Autoimmune, Experimental/immunology/prevention & control Mice, Inbred C57BL *Myelin-Oligodendrocyte Glycoprotein/immunology/therapeutic use Peptide Fragments/therapeutic use Peptides/therapeutic use Tissue Distribution Vaccines Nanoparticles/therapeutic use Multiple Sclerosis/immunology/therapy
 Male Humans Female *Multiple Sclerosis Eye-Tracking Technology Eye Movements *Disabled Persons Surveys and Questionnaires
 Adult Humans *Multiple Sclerosis Reproducibility of Results Exercise Surveys and Questionnaires Psychometrics
 Humans *Multiple Sclerosis Gait Upper Extremity Movement Postural Balance
 Humans *Transcranial Direct Current Stimulation *Multiple Sclerosis *Telerehabilitation Ataxia Gait
 Female Mice Animals *Encephalomyelitis, Autoimmune, Experimental/pathology *Remyelination/physiology Mice, Inbred C57BL *Multiple Sclerosis/pathology Inflammation Hypoxia Oxygen Disease Models, Animal
 Humans *Multiple Sclerosis/drug therapy *Remyelination Oligodendroglia/metabolism/pathology *Neurodegenerative Diseases/metabolism Myelin Sheath/metabolism/pathology
 Humans *Remyelination Cellular Reprogramming Oligodendroglia/metabolism Myelin Sheath/metabolism *Demyelinating Diseases/therapy/metabolism *Spinal Cord Injuries/metabolism *Multiple Sclerosis/metabolism Cell Differentiation/physiology
 Animals Humans *Myelin Basic Protein/metabolism Proteasome Endopeptidase Complex Ligands Peptide Fragments Peptides/chemistry *Multiple Sclerosis/genetics Immunodominant Epitopes HLA-A Antigens Mammals/metabolism
 Humans *Tumor Necrosis Factor-alpha Tumor Necrosis Factor Inhibitors Central Nervous System Cytokines *Multiple Sclerosis
 Humans *Global Burden of Disease *Multiple Sclerosis Europe Income North America
 Humans Retrospective Studies Cyclophosphamide/therapeutic use/adverse effects *Multiple Sclerosis/drug therapy Treatment Outcome *Central Nervous System Diseases/diagnostic imaging/drug therapy/chemically induced Central Nervous System
 Humans *Multiple Sclerosis/diagnostic imaging SARS-CoV-2 Retrospective Studies *COVID-19/diagnostic imaging/pathology Brain/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Magnetic Resonance Imaging/methods *Central Nervous System Diseases/pathology Atrophy/pathology *Multiple Sclerosis, Relapsing-Remitting
 Humans Microglia/pathology *Multiple Sclerosis/pathology Phagocytes/pathology Myelin Sheath/pathology Monocytes/pathology *Nervous System Diseases/pathology
 Humans *Multiple Sclerosis Seasons Cytokines Chronic Disease Recurrence
 Humans *Epstein-Barr Virus Infections Herpesvirus 4, Human *Multiple Sclerosis Risk Factors Gene-Environment Interaction Genetic Predisposition to Disease
 Animals Mice *Multiple Sclerosis/genetics Myelin Proteins/genetics *Encephalomyelitis, Autoimmune, Experimental/genetics Autopsy Oligodendroglia
 Humans *Contrast Media Gadolinium *Multiple Sclerosis Magnetic Resonance Imaging Brain
 Adult Humans *COVID-19/prevention & control COVID-19 Vaccines/adverse effects *Multiple Sclerosis/complications SARS-CoV-2 Vaccination
 Animals Humans *Multiple Sclerosis *Neurodegenerative Diseases Circadian Rhythm/physiology Diet *Circadian Clocks/physiology
 Humans *Autoimmune Diseases of the Nervous System/diagnostic imaging/epidemiology *COVID-19/complications/prevention & control COVID-19 Vaccines *Demyelinating Diseases/diagnostic imaging/epidemiology *Multiple Sclerosis/diagnostic imaging/epidemiology Vaccination
 Humans *Neurology *Multiple Sclerosis *Epilepsy Telephone *Parkinson Disease
 Humans Aquaporin 4 Autoantibodies Brain/diagnostic imaging Cross-Sectional Studies Gray Matter Hippocampus *Multiple Sclerosis/diagnostic imaging *Neuromyelitis Optica/diagnostic imaging Retrospective Studies
 Humans Aquaporin 4 Myelin-Oligodendrocyte Glycoprotein *Myelitis/diagnostic imaging *Neuromyelitis Optica/complications *Multiple Sclerosis/complications Autoantibodies
 Humans *Delay Discounting *Multiple Sclerosis Medication Adherence *Substance-Related Disorders Obesity
 Humans *Leukoencephalopathy, Progressive Multifocal/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Retrospective Studies Intermediate Filaments Natalizumab/therapeutic use Biomarkers
 Humans *Multiple Sclerosis *Nervous System Diseases/therapy/etiology *Hematopoietic Stem Cell Transplantation
 Humans *Multiple Sclerosis Arm Walking Movement Adaptation, Physiological
 Young Adult Humans *Multiple Sclerosis *Gastrointestinal Microbiome Inflammation *Microbiota Feces/microbiology Bacteria Cytokines
 Adult Humans B-Lymphocytes Memory B Cells *Multiple Sclerosis/drug therapy Prospective Studies Rituximab/pharmacology Middle Aged
 Humans *Systems Biology Gene Expression Profiling/methods Drug Repositioning *Multiple Sclerosis Computational Biology/methods Biomarkers
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/metabolism Nerve Growth Factor/genetics Axons/metabolism Nerve Regeneration *Multiple Sclerosis/pathology *Encephalomyelitis Mice, Inbred C57BL
 Humans *Leukoencephalopathy, Progressive Multifocal/diagnostic imaging Natalizumab/therapeutic use *Immune Reconstitution Inflammatory Syndrome *Multiple Sclerosis/drug therapy Early Diagnosis *JC Virus
 Humans Interferon-beta/therapeutic use *Biosimilar Pharmaceuticals/therapeutic use Proteomics Interferon beta-1a/therapeutic use *Multiple Sclerosis/drug therapy Biomarkers
 Humans COVID-19 Vaccines/therapeutic use *Multiple Sclerosis/drug therapy T-Lymphocytes Fingolimod Hydrochloride/therapeutic use *COVID-19 Cytokines RNA, Messenger Immunoglobulin G Antibodies, Viral
 Humans *Spouses/psychology Judgment Social Support Personality *Multiple Sclerosis
 Humans SARS-CoV-2 *COVID-19/epidemiology *Multiple Sclerosis/epidemiology B-Lymphocytes *Neuromyelitis Optica Myelin-Oligodendrocyte Glycoprotein Autoantibodies Aquaporin 4
 Humans Female Young Adult Adult Middle Aged Male *COVID-19/epidemiology COVID-19 Vaccines Saudi Arabia/epidemiology Cross-Sectional Studies *Multiple Sclerosis/epidemiology Pandemics Anxiety/epidemiology
 Humans Microglia *Neurodegenerative Diseases *Multiple Sclerosis Lymphocytes Glutamic Acid Inflammation
 Humans *Multiple Sclerosis/pathology *Neuromyelitis Optica/genetics/pathology Central Nervous System/pathology Myelin Sheath Diagnosis, Differential
 Humans Female Adult Male *COVID-19/epidemiology *Multiple Sclerosis/epidemiology Mental Health Quality of Life/psychology Pandemics Anxiety/epidemiology Depression/epidemiology
 Humans *Multiple Sclerosis/drug therapy Liposomes/metabolism Phosphatidylserines Macrophages/metabolism Phenotype *Nanoparticles
 Humans *Immunoglobulin kappa-Chains Immunoglobulin lambda-Chains *Multiple Sclerosis/diagnosis Immunoglobulin Light Chains Enzyme-Linked Immunosorbent Assay Albumins
 Humans Randomized Controlled Trials as Topic *Multiple Sclerosis Checklist
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Carboplatin/adverse effects/metabolism Proteomics *Multiple Sclerosis/pathology Apoptosis Mice, Inbred C57BL Th17 Cells Th1 Cells
 Humans Male Female Adult *Multiple Sclerosis/pathology Gray Matter/pathology *White Matter/pathology Magnetic Resonance Imaging Cognition Atrophy/pathology Brain/pathology
 Adult Humans *Multiple Sclerosis *Neuromyelitis Optica Cross-Sectional Studies Intelligence Tests Intelligence
 Adult Humans Middle Aged *Multiple Sclerosis/pathology *Cervical Cord/pathology *Disabled Persons *Motor Disorders Spinal Cord/pathology Brain/pathology Magnetic Resonance Imaging Walking Disability Evaluation Atrophy/pathology
 Humans Aquaporin 4 Myelin-Oligodendrocyte Glycoprotein *Hiccup *Neuromyelitis Optica/diagnostic imaging *Multiple Sclerosis/diagnosis Brain Stem/diagnostic imaging Immunoglobulin G Autoantibodies
 Humans *Multiple Sclerosis/drug therapy *Agammaglobulinemia/chemically induced/drug therapy Pilot Projects Antibodies, Monoclonal, Humanized/adverse effects Immunoglobulin M/therapeutic use
 Humans Cytokines *Multiple Sclerosis Chemokines *Body Fluids Disease Progression Pokeweed Mitogens
 Mice Animals *Multiple Sclerosis/drug therapy T-Lymphocytes, Regulatory/metabolism Th17 Cells/metabolism *Nanocapsules Phenotype
 Humans Biomarkers/cerebrospinal fluid *Chemokine CXCL13/cerebrospinal fluid Disease Progression *Multiple Sclerosis/diagnosis Recurrence *Chitinase-3-Like Protein 1/cerebrospinal fluid
 Female Humans Adult Male *Multiple Sclerosis Intermediate Filaments Biomarkers Magnetic Resonance Imaging Disability Evaluation
 Animals *COVID-19 SARS-CoV-2 *Multiple Sclerosis *Epstein-Barr Virus Infections Herpesvirus 4, Human Vitamin D
 Humans *COVID-19 *Multiple Sclerosis Pandemics Self Care *Telenursing
 Mice Animals Resveratrol *Neuroprotective Agents/therapeutic use *Optic Neuritis Solubility Mice, Inbred C57BL *Encephalomyelitis, Autoimmune, Experimental/drug therapy *Multiple Sclerosis/drug therapy Inflammation/drug therapy Disease Models, Animal
 Humans *Botulinum Toxins, Type A/adverse effects *Urinary Bladder, Overactive/etiology/complications *Neuromuscular Agents/adverse effects Administration, Intravesical Retrospective Studies *Multiple Sclerosis/complications/chemically induced *Urology *Urinary Bladder, Neurogenic/drug therapy/etiology Treatment Outcome
 Humans Australia Exercise Longitudinal Studies *Multiple Sclerosis Rural Population
 Animals Female Cattle *Multiple Sclerosis Milk Immunoglobulin G Prevalence Allergens
 Male Humans Middle Aged *Leukoencephalopathy, Progressive Multifocal/chemically induced/diagnostic imaging/drug therapy Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy *Multiple Sclerosis/drug therapy *JC Virus Magnetic Resonance Imaging Natalizumab/adverse effects
 Humans Female Adult Child Male *Multiple Sclerosis/complications Retinal Ganglion Cells/pathology Retina/pathology Prospective Studies Nerve Fibers/pathology Tomography, Optical Coherence/methods
 Animals Mice CD8-Positive T-Lymphocytes Dihydroorotate Dehydrogenase Disease Models, Animal *Drug Repositioning *Encephalomyelitis, Autoimmune, Experimental/drug therapy Mice, Inbred C57BL Molecular Docking Simulation *Multiple Sclerosis/drug therapy Oxidative Stress/drug effects Inflammation/drug therapy
 Humans *Multiple Sclerosis/pathology Brain/diagnostic imaging/pathology Magnetic Resonance Imaging *White Matter/diagnostic imaging/pathology Chronic Disease Atrophy/pathology Gray Matter/diagnostic imaging/pathology
 Humans *Multiple Sclerosis Cross-Sectional Studies Ambulatory Care Facilities *No-Show Patients Appointments and Schedules
 Humans *Multiple Sclerosis/metabolism Brain/pathology Antibody-Producing Cells/metabolism/pathology *White Matter/pathology Immunoglobulin G/metabolism
 Animals Mice *Central Nervous System Diseases *Multiple Sclerosis Axons Immunomodulation Central Nervous System
 Humans *Multiple Sclerosis Leukocytes, Mononuclear Oligodendroglia/physiology Neurons Myelin Sheath
 Humans Animals Hedgehogs *Neurodegenerative Diseases/genetics Disease Progression Memory *Multiple Sclerosis
 Animals Mice Humans Microglia/physiology *Remyelination Neuroprotection *Multiple Sclerosis/drug therapy Myelin Sheath Mice, Knockout Mice, Inbred C57BL Membrane Glycoproteins/genetics Receptors, Immunologic/genetics
 Humans *Multiple Sclerosis/cerebrospinal fluid Biomarkers Oligoclonal Bands/cerebrospinal fluid Immunoglobulin Light Chains Immunoglobulin kappa-Chains/cerebrospinal fluid
 Humans *Cannabidiol Dronabinol Drug Combinations *Cannabis *Multiple Sclerosis Cognition
 Humans Dust/analysis *Multiple Sclerosis/epidemiology Prevalence Lead/analysis Environmental Monitoring/methods *Metals, Heavy/analysis Steel/analysis Risk Assessment Cities China
 Humans *COVID-19 *Multiple Sclerosis Antibodies, Monoclonal Antibodies, Viral
 Humans *Physical Therapists *Multiple Sclerosis Physical Therapy Modalities Exercise Exercise Therapy
 Humans *Multiple Sclerosis/diagnostic imaging Biomarkers Prognosis Magnetic Resonance Imaging/methods Neurofilament Proteins/cerebrospinal fluid Glial Fibrillary Acidic Protein/cerebrospinal fluid
 Humans Corpus Callosum/pathology *Multiple Sclerosis *Leukoencephalopathies/pathology Cognition *Cognitive Dysfunction
 Humans Neutrophils Reactive Oxygen Species *Neutropenia *Central Nervous System Diseases *Multiple Sclerosis Central Nervous System
 Humans Mice Animals *Encephalomyelitis, Autoimmune, Experimental *PPAR-beta/therapeutic use *Multiple Sclerosis/drug therapy Valerates/therapeutic use Mice, Inbred C57BL
 Humans *Multiple Sclerosis Retrospective Studies Saudi Arabia Brain Machine Learning
 Mice Rats Animals *Multiple Sclerosis/drug therapy *Encephalomyelitis, Autoimmune, Experimental/drug therapy Central Nervous System GABA Agonists/therapeutic use gamma-Aminobutyric Acid Mice, Inbred C57BL
 Humans Middle Aged *Multiple Sclerosis/diagnosis Magnetic Resonance Imaging/methods Central Nervous System Cognition
 Humans Hand *Multiple Sclerosis, Chronic Progressive/diagnosis Outcome Assessment, Health Care *Upper Extremity
 Adult Humans *Multiple Sclerosis Self Efficacy Health Status *Self-Management *Disabled Persons
 Humans *Multiple Sclerosis Walking Walk Test Fatigue
 Humans Genome-Wide Association Study *Diabetes Mellitus, Type 1/genetics Genetic Predisposition to Disease *Autoimmune Diseases/genetics *Arthritis, Rheumatoid/genetics Genetic Loci *Multiple Sclerosis/genetics *Inflammatory Bowel Diseases/genetics
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Th17 Cells Virulence Cholinergic Agents *Multiple Sclerosis/genetics Acetylcholine/metabolism Mice, Inbred C57BL Cell Differentiation
 Humans *Neuromyelitis Optica/diagnostic imaging Immunoglobulin G Aquaporin 4 Tomography, Optical Coherence Retina *Optic Neuritis *Multiple Sclerosis/diagnostic imaging Autoantibodies Myelin-Oligodendrocyte Glycoprotein
 Humans *Low Socioeconomic Status *Multiple Sclerosis Social Class Proportional Hazards Models
 Female Humans Middle Aged Interferon-beta *Multiple Sclerosis Interferon beta-1a Polyethylene Glycols *Brain Diseases
 Humans *Multiple Sclerosis/genetics Genome-Wide Association Study Vitamin D Brain Risk Factors
 Humans BNT162 Vaccine Rituximab/therapeutic use SARS-CoV-2 *Multiple Sclerosis/drug therapy *COVID-19/prevention & control Vaccination Antibodies Immunity RNA, Messenger
 Humans *Multiple Sclerosis Prognosis Intermediate Filaments Biomarkers Neurofilament Proteins Disease Progression
 Humans Vitamin D3 24-Hydroxylase/genetics/metabolism *Multiple Sclerosis/genetics Interferon-gamma Macrophage Colony-Stimulating Factor Vitamin D Vitamins
 Humans Animals Mice *Multiple Sclerosis/genetics *Carcinoma, Non-Small-Cell Lung/genetics *Lung Neoplasms/genetics Cyclic Nucleotide Phosphodiesterases, Type 4 Gene Expression Profiling Tumor Microenvironment/genetics
 Humans Female Middle Aged Male Australia/epidemiology *Multiple Sclerosis/drug therapy New Zealand/epidemiology Quality of Life Policy Surveys and Questionnaires Health Status
 Humans *Genome-Wide Association Study *Multiple Sclerosis/genetics Genetic Predisposition to Disease Obesity/genetics Risk Factors Polymorphism, Single Nucleotide Mendelian Randomization Analysis
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/pathology *Ferroptosis Antioxidants Iron/metabolism Ferritins/metabolism *Multiple Sclerosis *Multiple Sclerosis, Chronic Progressive Glutathione/metabolism
 Humans *Multiple Sclerosis Decision Making Individuality Qualitative Research Patient Outcome Assessment
 Humans *Myasthenia Gravis/complications *Neuromyelitis Optica/complications *Pigmentation Disorders/complications *Multiple Sclerosis/complications Central Nervous System
 Humans *Neurodegenerative Diseases *Chitinases/genetics Neuroinflammatory Diseases Biomarkers *Multiple Sclerosis
 Humans Diet *Multiple Sclerosis *Disabled Persons Quality of Life Disability Evaluation
 Aged Pregnancy Female Humans *Multiple Sclerosis Hungary Quality of Life Consensus
 Female Humans *Neuromyelitis Optica/pathology Retrospective Studies Myelin-Oligodendrocyte Glycoprotein Cross-Sectional Studies Aquaporin 4 *Multiple Sclerosis/diagnostic imaging Autoantibodies Magnetic Resonance Imaging
 Humans Animals Mice *Endogenous Retroviruses/genetics Neuroglia Animals, Genetically Modified Myelin Sheath *Multiple Sclerosis/genetics
 Humans *COVID-19/prevention & control/complications *COVID-19 Vaccines/adverse effects *Multiple Sclerosis/etiology *Neuromyelitis Optica/etiology Pandemics/prevention & control Neuroinflammatory Diseases/etiology
 Humans Adult Middle Aged *Multiple Sclerosis Fear Exercise Exercise Therapy Muscle Spasticity Postural Balance
 Humans Caregivers/psychology Australia *Multiple Sclerosis Pandemics *COVID-19
 Adult Male Humans Female *Multiple Sclerosis Case-Control Studies Walking Exercise Test Energy Metabolism
 Animals Mice Heterogeneous Nuclear Ribonucleoprotein A1/genetics/metabolism *Multiple Sclerosis/pathology RNA-Binding Proteins/metabolism *Encephalomyelitis, Autoimmune, Experimental RNA, Small Interfering
 Humans *Multiple Sclerosis Quality of Life *Cognition Disorders Sensory Gating Cognition
 Humans *Multiple Sclerosis Activities of Daily Living Neuropsychological Tests *Cognitive Dysfunction/etiology/diagnosis Self Report
 Humans *Zika Virus Infection/complications/genetics *Zika Virus/genetics Transcription Factor AP-1/genetics *Multiple Sclerosis/genetics Inflammation Phenotype
 Humans Interferon-beta/therapeutic use *Multiple Sclerosis/drug therapy *COVID-19 *Epstein-Barr Virus Infections/complications SARS-CoV-2 Pandemics Post-Acute COVID-19 Syndrome Herpesvirus 4, Human Interferons/therapeutic use/pharmacology Antiviral Agents/therapeutic use/pharmacology
 Humans Female Adult *Multiple Sclerosis Cohort Studies Chronic Disease Prognosis Recurrence
 Humans Herpesvirus 4, Human *Epstein-Barr Virus Infections/complications *Multiple Sclerosis *Neurodegenerative Diseases *Neoplasms
 Humans *Multiple Sclerosis Registries
 Humans *Multiple Sclerosis Central Nervous System Cell Count Enzyme-Linked Immunosorbent Assay Flow Cytometry Chemokine CXCL10
 Humans Alemtuzumab/adverse effects Iodine Radioisotopes/adverse effects Neoplasm Recurrence, Local *Graves Disease/drug therapy *Multiple Sclerosis/drug therapy
 Mice Animals Humans Aged Fingolimod Hydrochloride/pharmacology/therapeutic use *Alzheimer Disease/drug therapy Drug Repositioning Sclerosis *Multiple Sclerosis/drug therapy Inflammation/drug therapy/metabolism
 Humans *Myelin Sheath *Multiple Sclerosis Quality of Life Oligodendroglia Energy Metabolism Glucose
 Female Humans Adult Male Syndrome Immunoglobulin kappa-Chains *Demyelinating Diseases/diagnostic imaging *Autoimmune Diseases of the Nervous System *Multiple Sclerosis/diagnostic imaging Disease Progression
 Middle Aged Humans Male Female Aged Adolescent Young Adult Adult Iran/epidemiology Retrospective Studies *Hypercholesterolemia/epidemiology *Multiple Sclerosis/diagnosis Prevalence Comorbidity *Hypertension/epidemiology *Diabetes Mellitus/epidemiology *Hypothyroidism
 Female Humans RNA Alemtuzumab/therapeutic use COVID-19 Vaccines BNT162 Vaccine *Multiple Sclerosis/drug therapy *COVID-19/prevention & control SARS-CoV-2 Vaccination Immunity, Cellular Antibodies, Viral
 Humans *Influenza, Human/drug therapy/prevention & control Cladribine/therapeutic use *Multiple Sclerosis/drug therapy Influenza A Virus, H3N2 Subtype *Influenza A Virus, H1N1 Subtype Seasons *Influenza Vaccines Antibody Formation Vaccination
 Animals Mice Female *Cuprizone/toxicity Myelin Sheath/metabolism Mice, Inbred C57BL *Multiple Sclerosis/metabolism Hippocampus Walking Disease Models, Animal
 Humans *Multiple Sclerosis/genetics Case-Control Studies Aging/genetics Epigenesis, Genetic DNA Methylation
 Humans *Calcium Genome-Wide Association Study/methods *Multiple Sclerosis/genetics Mendelian Randomization Analysis/methods Vitamin D Calcium, Dietary Calcifediol Polymorphism, Single Nucleotide
 Animals *Gene Expression Profiling/methods Tumor Necrosis Factor-alpha/genetics *Multiple Sclerosis/genetics Reproducibility of Results Prospective Studies Signal Transduction/genetics Cytokines/genetics Computational Biology/methods
 Humans *Cerebral Palsy *Parkinson Disease *Spinal Cord Injuries *Multiple Sclerosis
 Humans Antibodies, Monoclonal, Humanized/adverse effects Immunologic Factors/adverse effects Interferon beta-1a/therapeutic use *Multiple Sclerosis/drug therapy Recurrence
 Mice Animals *Oligodendroglia/metabolism Cell Differentiation/physiology Neuroglia/metabolism *Multiple Sclerosis/metabolism Stem Cells/metabolism Myelin Sheath/metabolism
 Humans Aluminum/toxicity *Autism Spectrum Disorder/pathology Brain/pathology *Alzheimer Disease/pathology Central Nervous System/pathology *Parkinson Disease/pathology *Multiple Sclerosis/pathology
 Humans *Exergaming *Multiple Sclerosis Cognition/physiology Exercise Exercise Therapy
 Humans Female Middle Aged Aged *Caregivers Cross-Sectional Studies Psychometrics *Multiple Sclerosis Reproducibility of Results Surveys and Questionnaires
 Humans *Multiple Sclerosis/pathology Myelin Sheath Cross-Sectional Studies Iron *Disabled Persons *Motor Disorders/complications/pathology Brain/diagnostic imaging/pathology Gray Matter/diagnostic imaging/pathology Magnetic Resonance Imaging *Brain Diseases/pathology Atrophy/pathology
 Humans Myelin-Oligodendrocyte Glycoprotein Autoantibodies *Multiple Sclerosis/diagnostic imaging *Neuromyelitis Optica/diagnostic imaging/pathology Aquaporin 4 Magnetic Resonance Imaging
 Humans Animals Mice *Encephalomyelitis, Autoimmune, Experimental/genetics Transcriptome *Neurodegenerative Diseases *Encephalitis *Multiple Sclerosis/genetics Brain Endothelium
 Humans *Multiple Sclerosis Quality of Life Pain
 Humans *Botulinum Toxins, Type A/adverse effects *Multiple Sclerosis/complications/drug therapy *Neuromuscular Agents/therapeutic use Quality of Life *Spinal Cord Injuries/complications/drug therapy Treatment Outcome *Urinary Bladder, Neurogenic/drug therapy/etiology *Urinary Bladder, Overactive/drug therapy/etiology *Urinary Incontinence/etiology/complications
 Humans Copper *RNA, Small Untranslated *Alzheimer Disease/diagnosis/genetics *Multiple Sclerosis/genetics *MicroRNAs/genetics Biomarkers Zinc Iron
 Humans SARS-CoV-2 *Multiple Sclerosis *COVID-19 T-Lymphocytes Nucleocapsid Proteins Nucleocapsid
 Humans *Multiple Sclerosis Feasibility Studies Cross-Over Studies Gait Walking Orthotic Devices
 Humans COVID-19 Vaccines/adverse effects Pilot Projects Fingolimod Hydrochloride/adverse effects *Multiple Sclerosis/drug therapy *COVID-19/prevention & control Antibodies, Viral Immunoglobulin G Vaccines, Inactivated/adverse effects
 Pregnancy Female Humans Adult *Multiple Sclerosis/drug therapy Fingolimod Hydrochloride/adverse effects Postpartum Period Recurrence Registries
 Humans Reproducibility of Results Sclerosis *Wearable Electronic Devices Gait Exercise *Multiple Sclerosis
 Animals Mice *Multiple Sclerosis/pathology *Myeloid-Derived Suppressor Cells/pathology Retrospective Studies *Encephalomyelitis, Autoimmune, Experimental/pathology Disease Progression Mice, Inbred C57BL
 Humans *COVID-19 Immunity, Cellular *Multiple Sclerosis SARS-CoV-2 Vaccination
 Humans COVID-19 Vaccines COVID-19 Drug Treatment Cohort Studies Fingolimod Hydrochloride/therapeutic use *Multiple Sclerosis/drug therapy *COVID-19/prevention & control SARS-CoV-2 *Vaccines Vaccination
 Animals *Multiple Sclerosis *Gastrointestinal Microbiome *Autoimmune Diseases/metabolism Central Nervous System Autoimmunity Immunomodulation Inflammation
 Animals Humans Astragalus propinquus/chemistry *Multiple Sclerosis/drug therapy *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism *Drugs, Chinese Herbal/pharmacology/therapeutic use/chemistry Polysaccharides
 Adult Animals Cricetinae Humans Sphingosine-1-Phosphate Receptors/metabolism *Colitis, Ulcerative/drug therapy CHO Cells Cricetulus Indans/pharmacology/therapeutic use Oxadiazoles/pharmacology Sphingosine *Multiple Sclerosis/drug therapy
 Humans *Gait Analysis *Multiple Sclerosis Time Factors Gait Walking
 Mice Animals *Remyelination Oligodendroglia/pathology Cuprizone/pharmacology Cell Differentiation Immunoglobulins/pharmacology *Multiple Sclerosis/pathology Mice, Inbred C57BL Myelin Sheath/physiology Disease Models, Animal
 Humans *Genetic Predisposition to Disease/genetics HLA-DRB1 Chains/genetics *Multiple Sclerosis/genetics Gene Frequency Polymorphism, Single Nucleotide/genetics Genotype Alleles Receptors, Calcitriol
 Animals Humans Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy Fingolimod Hydrochloride/therapeutic use Immunosuppressive Agents/therapeutic use L-Selectin Lymph Nodes Lymphocytes *Multiple Sclerosis/drug therapy Pharmaceutical Preparations Sphingosine/metabolism
 Mice Animals *Multiple Sclerosis Potassium Channels Neuroinflammatory Diseases Cuprizone 4-Aminopyridine/pharmacology Inflammation Models, Theoretical
 Child Humans Pandemics Myelin-Oligodendrocyte Glycoprotein *COVID-19/epidemiology SARS-CoV-2 *Multiple Sclerosis/therapy *Neuromyelitis Optica/therapy Autoantibodies
 Humans *Multiple Sclerosis Quality of Life Fear Cognition Fatigue Postural Balance/physiology
 Humans Exercise Therapy Gait *Multiple Sclerosis Postural Balance Walking
 Humans *Multiple Sclerosis Walking Gait Attention Cognition
 Animals *Multiple Sclerosis/pathology Oligodendroglia/pathology *Remyelination/physiology Optic Nerve/pathology Disease Models, Animal Xenopus laevis Myelin Sheath/pathology
 Humans Female Adult Middle Aged *Multiple Sclerosis Quality of Life Qualitative Research *Movement Disorders Activities of Daily Living
 Humans *Gastrointestinal Microbiome *Multiple Sclerosis *Microbiota Intestines Inflammation Dysbiosis *Probiotics/therapeutic use
 Humans *Cladribine/adverse effects *Multiple Sclerosis/drug therapy T-Lymphocytes/pathology Immunosuppressive Agents/pharmacology/therapeutic use Cross-Sectional Studies Guanine Nucleotide Exchange Factors/pharmacology
 Humans *Forearm Activities of Daily Living Hand Strength *Multiple Sclerosis Quality of Life Upper Extremity Fatigue
 Humans *Multiple Sclerosis Bismuth Silver Aluminum Paraffin *Mercury Brain Hazardous Substances
 Humans Dimethyl Fumarate/adverse effects Immunosuppressive Agents *Multiple Sclerosis, Relapsing-Remitting *Hypersensitivity, Delayed/diagnosis
 Rats Animals Mice *Multiple Sclerosis/metabolism *Encephalomyelitis, Autoimmune, Experimental Spinal Cord/metabolism Hypoxia/metabolism Oxygen/metabolism/therapeutic use Disease Models, Animal Mice, Inbred C57BL
 Humans *Multiple Sclerosis/drug therapy Natalizumab/therapeutic use COVID-19 Vaccines Prospective Studies Cladribine Fingolimod Hydrochloride/therapeutic use *COVID-19/prevention & control SARS-CoV-2 Vaccination Immunity, Cellular Antibodies, Viral
 Mice Animals *Multiple Sclerosis/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism Inflammasomes/metabolism Molecular Docking Simulation *Encephalomyelitis, Autoimmune, Experimental/pathology *White Matter/pathology Microglia/metabolism Mice, Inbred C57BL Disease Models, Animal
 Humans CD28 Antigens *CD8-Positive T-Lymphocytes *Fingolimod Hydrochloride/therapeutic use Immunosuppressive Agents/therapeutic use Leukocytes, Mononuclear *Multiple Sclerosis/drug therapy *T-Lymphocytes, Regulatory
 Humans *Multiple Sclerosis/genetics *Alzheimer Disease/genetics Genome-Wide Association Study Genetic Predisposition to Disease/genetics Immune System Genetic Loci Inflammation/genetics Polymorphism, Single Nucleotide
 Pregnancy Female Humans *Abortion, Spontaneous/epidemiology Pregnancy Trimester, First *Multiple Sclerosis Prospective Studies Canada
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Microglia/metabolism Macrophages/metabolism *Multiple Sclerosis/metabolism Spinal Cord/pathology Mice, Inbred C57BL
 Humans Adult Middle Aged *Multiple Sclerosis Quality of Life Cognition Fatigue/complications *Olfaction Disorders/etiology
 Humans *Depression/epidemiology *Multiple Sclerosis Cross-Sectional Studies Prospective Studies Tobacco Smoking
 Humans Natalizumab/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy/chemically induced *JC Virus Risk Assessment Immunologic Factors/adverse effects *Leukoencephalopathy, Progressive Multifocal/diagnosis/etiology
 Humans Aged Adult *Longevity Cross-Sectional Studies *Multiple Sclerosis Aging Physical Functional Performance
 Humans Accidental Falls/prevention & control Randomized Controlled Trials as Topic Physical Therapy Modalities *Multiple Sclerosis *Virtual Reality
 Animals Cicatrix *Multiple Sclerosis/genetics Protein Isoforms/genetics *Transforming Growth Factor beta/genetics/metabolism Transforming Growth Factor beta1/metabolism Transforming Growth Factor beta3/genetics Humans
 Rats Humans Animals *Myelin Sheath/metabolism Tissue Distribution Positron-Emission Tomography/methods Brain/diagnostic imaging/metabolism *Multiple Sclerosis/metabolism Radiopharmaceuticals Fluorine Radioisotopes/chemistry
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Mice, Inbred C57BL *Multiple Sclerosis Central Nervous System Spinal Cord
 Humans Activities of Daily Living Quality of Life *Multiple Sclerosis Goals Pandemics *COVID-19 *Nursing Process
 Humans COVID-19 Vaccines Antibody Formation Fingolimod Hydrochloride *Multiple Sclerosis/drug therapy Prospective Studies Rituximab/therapeutic use *COVID-19/prevention & control SARS-CoV-2 Antibodies, Viral Vaccination
 Animals Mice Adipogenesis Disease Models, Animal Fatty Acids Fatty Acids, Monounsaturated Foam Cells *Multiple Sclerosis *Remyelination
 Adult Humans Female Male *Multiple Sclerosis Case-Control Studies Walking Hemodynamics Cognition Gait
 Humans COVID-19 Vaccines T-Lymphocytes *COVID-19/prevention & control *Multiple Sclerosis/drug therapy SARS-CoV-2 RNA, Messenger Immunity mRNA Vaccines Immunoglobulin G Antibodies, Viral Vaccination
 Humans *Epstein-Barr Virus Infections Herpesvirus 4, Human Neuroinflammatory Diseases Antiviral Agents *Multiple Sclerosis
 Humans Ceramides Autoimmunity *Demyelinating Diseases Immunoglobulin G *Multiple Sclerosis
 Humans Rituximab/adverse effects Retrospective Studies *Agammaglobulinemia/chemically induced/epidemiology/drug therapy *Multiple Sclerosis/drug therapy *Multiple Sclerosis, Chronic Progressive/drug therapy *Neutropenia/chemically induced/epidemiology/drug therapy *Lymphopenia/chemically induced/epidemiology Hospitalization Immunologic Factors/adverse effects
 Humans *Quality of Life/psychology Cohort Studies *Multiple Sclerosis Diet Surveys and Questionnaires
 Humans *COVID-19/prevention & control *Multiple Sclerosis Vaccination Fear Patients
 Humans *Multiple Sclerosis Exercise Therapy/methods Walking Muscle, Skeletal Fatigue/etiology
 Humans *Multiple Sclerosis Cognitive Training Pilot Projects *Cognitive Dysfunction/rehabilitation *Cognition Disorders/rehabilitation
 Humans Alanine Biomarkers *Galectin 3/chemistry Mammals *Multiple Sclerosis Transaminases
 Male Humans Female *Quality of Life *Multiple Sclerosis Health Status Pain Case-Control Studies
 Humans *Multiple Sclerosis Reproducibility of Results Goals Outcome Assessment, Health Care Walk Test Disability Evaluation
 Humans Antibodies, Monoclonal/adverse effects Rituximab/adverse effects *Antineoplastic Agents/therapeutic use B-Lymphocytes *Colitis/chemically induced/drug therapy *Multiple Sclerosis/drug therapy
 Humans Proteomics *Encephalitis Proteins Autoantibodies *Multiple Sclerosis, Relapsing-Remitting
 Humans Adult Middle Aged *Multiple Sclerosis Activities of Daily Living Quality of Life Prospective Studies Feasibility Studies *Virtual Reality
 Humans Aged *Alzheimer Disease Biomarkers/cerebrospinal fluid Disease Progression *Multiple Sclerosis
 Mice Animals Humans Myelin Sheath/metabolism Axons/metabolism *Multiple Sclerosis/pathology *Encephalomyelitis, Autoimmune, Experimental/pathology Risk Factors
 Humans *Telerehabilitation Upper Extremity *Multiple Sclerosis Ataxia *Virtual Reality
 Humans Psychometrics/methods *Multiple Sclerosis Reproducibility of Results Germany Language Fatigue/diagnosis Surveys and Questionnaires
 Male Humans Female Adult *Sense of Coherence *Multiple Sclerosis Cross-Sectional Studies Adaptation, Psychological Emotions Caregivers/psychology Surveys and Questionnaires
 Humans *Multiple Sclerosis/pathology Epigenomics Transcriptome Oligodendroglia/metabolism Cell Differentiation DNA Methylation Myelin Sheath/pathology Mixed Function Oxygenases/metabolism/pharmacology Proto-Oncogene Proteins
 Adolescent Adult Female Humans Male Young Adult Chronic Disease Herpesvirus 3, Human Iran *Multiple Sclerosis/drug therapy Natalizumab Recurrence Retrospective Studies Vaccination/adverse effects Vaccines, Attenuated/adverse effects *Chickenpox Vaccine/adverse effects
 Humans Aged *Deep Learning *Parkinson Disease *Multiple Sclerosis Gait Walking
 Male Animals Mice Mice, Inbred C57BL Chromatography, Liquid *Tandem Mass Spectrometry Central Nervous System *Multiple Sclerosis Disease Models, Animal Peptides/genetics
 Humans Coconut Oil Gait/physiology *Multiple Sclerosis *Neurodegenerative Diseases Pilot Projects
 Humans Aged *Parkinson Disease *Multiple Sclerosis Cross-Over Studies Masks Walking
 Animals Humans *Encephalomyelitis, Autoimmune, Experimental/pathology Endothelial Cells/metabolism Neuroinflammatory Diseases Brain/pathology *Multiple Sclerosis/pathology Blood-Brain Barrier/pathology CD4-Positive T-Lymphocytes/metabolism Endothelium/metabolism/pathology CD146 Antigen/metabolism
 Humans *Multiple Sclerosis Walking/physiology Cross-Sectional Studies Muscle, Skeletal Foot Reproducibility of Results
 Humans Follow-Up Studies Quality of Life Visual Acuity *Erythropoietin/therapeutic use Methylprednisolone/therapeutic use *Optic Neuritis *Multiple Sclerosis/drug therapy
 Animals *Smallpox *Epstein-Barr Virus Infections Herpesvirus 4, Human *Encephalomyelitis *Encephalomyelitis, Autoimmune, Experimental *Viruses *Multiple Sclerosis Disease Models, Animal
 Female Humans *Epilepsia Partialis Continua/etiology/therapy Alemtuzumab/adverse effects Receptors, GABA-A *Status Epilepticus *Encephalitis *Multiple Sclerosis/complications
 Humans Mice Animals Cytochrome P-450 CYP2E1 *Isoflurane Positron-Emission Tomography/methods Cytochrome P-450 Enzyme System/metabolism 4-Aminopyridine *Multiple Sclerosis/diagnostic imaging Oxides
 Animals Humans Mice *Astrocytes/metabolism/pathology *Encephalomyelitis, Autoimmune, Experimental Gene Expression Regulation Mice, Knockout *Multiple Sclerosis/pathology *Microfluidics/methods *Single-Cell Gene Expression Analysis/methods *Nucleic Acids/analysis Gene Editing
 Humans Cross-Sectional Studies *Multiple Sclerosis Gait Walking Gait Analysis
 Humans Antigens, CD20 B-Lymphocytes Lymphocytes *Multiple Sclerosis Rituximab/therapeutic use *Antineoplastic Agents, Immunological/therapeutic use
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental *Multiple Sclerosis Mice, Inbred C57BL Th17 Cells
 Humans Herpesvirus 4, Human/physiology *Epstein-Barr Virus Infections/complications *Multiple Sclerosis Peptides Glycoproteins
 Humans *Fingolimod Hydrochloride/therapeutic use Retrospective Studies Glatiramer Acetate/therapeutic use Immunosuppressive Agents/therapeutic use Turkey *Multiple Sclerosis/drug therapy Interferon-beta/therapeutic use Recurrence
 Child Humans *Quality of Life Surveys and Questionnaires Family Health Prospective Studies *Multiple Sclerosis Canada Employment Parents
 Humans *Neuromyelitis Optica/complications/diagnosis/therapy Aquaporin 4 Myelin-Oligodendrocyte Glycoprotein Autoantibodies *Optic Neuritis/diagnosis/therapy *Multiple Sclerosis/diagnosis Inflammation
 Adult Male Humans Female *Urinary Bladder, Neurogenic/diagnosis/etiology *Parkinson Disease Retrospective Studies *Spinal Cord Injuries/complications *Urinary Tract Infections/diagnosis *Multiple Sclerosis/complications Patient Reported Outcome Measures
 Humans *Multiple Sclerosis Cross-Sectional Studies Walking Body Composition Bone Density
 Mice Animals *Remyelination/physiology Oligodendroglia/physiology *Multiple Sclerosis Cell Differentiation Inflammation Mice, Inbred C57BL
 Humans *Cladribine/pharmacology Leukocytes, Mononuclear CD8-Positive T-Lymphocytes *Multiple Sclerosis/drug therapy Tablets Antigens, CD20 Antigens, CD19 Immunoglobulin G Immunoglobulin M
 Humans *Vitamin D/pharmacology Vitamins/pharmacology *Multiple Sclerosis Cytokines Chemokines
 Male Humans Female Adult Prospective Studies Magnetic Resonance Imaging/methods Cerebellum/diagnostic imaging *White Matter/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Brain/anatomy & histology
 Humans *COVID-19/epidemiology *Multiple Sclerosis *Telemedicine
 Humans *Caregivers/psychology Quality of Life *Multiple Sclerosis Stress, Psychological/psychology Family/psychology Qualitative Research
 Humans COVID-19 Vaccines Fingolimod Hydrochloride *Multiple Sclerosis *COVID-19 *Vaccines Vaccination
 Humans *Robotics/methods *Multiple Sclerosis Reproducibility of Results *Robotic Surgical Procedures Proprioception/physiology
 Humans *T-Lymphocytes, Regulatory *Multiple Sclerosis Immune Tolerance Inflammation/pathology
 Humans *Multiple Sclerosis Prospective Studies Cross-Sectional Studies Pandemics *COVID-19
 Rats Animals Inflammasomes/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism Clemastine/pharmacology NF-E2-Related Factor 2 Pyroptosis NLR Proteins Neuroinflammatory Diseases p38 Mitogen-Activated Protein Kinases Heme Oxygenase-1 *Multiple Sclerosis/metabolism
 Humans *Neuromyelitis Optica/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Immunoglobulin G Retrospective Studies Sleepiness Aquaporin 4 Myelin-Oligodendrocyte Glycoprotein Recurrence Autoantibodies
 Humans Prospective Studies Gray Matter/pathology Canada *Multiple Sclerosis/pathology Myelin-Oligodendrocyte Glycoprotein Brain/pathology Aquaporin 4 Chronic Disease Immunoglobulin G Autoantibodies *Neuromyelitis Optica/pathology
 Animals *Multiple Sclerosis Microglia/physiology Macrophages Axons/pathology Inflammation/pathology Disease Models, Animal
 Humans Bayes Theorem *Multiple Sclerosis Retrospective Studies *Suicidal Ideation Suicide, Attempted
 Adult Humans *COVID-19/prevention & control COVID-19 Vaccines/adverse effects Cross-Sectional Studies *Multiple Sclerosis/epidemiology Switzerland/epidemiology Vaccination/adverse effects *Drug-Related Side Effects and Adverse Reactions Registries
 Humans Child *Neuromyelitis Optica/diagnostic imaging/complications Neutrophils/pathology Monocytes/pathology *Multiple Sclerosis/diagnostic imaging Retrospective Studies Lymphocytes/pathology
 Humans Mice Animals *Encephalomyelitis, Autoimmune, Experimental/therapy *Multiple Sclerosis/therapy Myelin-Oligodendrocyte Glycoprotein/adverse effects Anti-Inflammatory Agents Macrophages/metabolism Mice, Inbred C57BL Peptide Fragments/adverse effects
 Animals Mice Central Nervous System/metabolism Chemokines/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism Mice, Inbred C57BL Mice, Knockout *Multiple Sclerosis/pathology Receptors, CCR6/genetics/metabolism
 Humans *Dimethyl Fumarate/therapeutic use *Multiple Sclerosis Immunosuppressive Agents/therapeutic use Leukocytes, Mononuclear Killer Cells, Natural Biomarkers
 Animals Mice *Neuroinflammatory Diseases Axons/pathology *Multiple Sclerosis/pathology Neurons/pathology Inflammation/pathology
 Humans Natalizumab/therapeutic use *Multiple Sclerosis Retrospective Studies Intermediate Filaments Biomarkers Neurofilament Proteins
 Mice Animals Humans *Encephalomyelitis, Autoimmune, Experimental Central Nervous System/metabolism Spinal Cord/metabolism *Multiple Sclerosis/diagnostic imaging Positron-Emission Tomography/methods Myelin-Oligodendrocyte Glycoprotein/metabolism B-Lymphocytes Mice, Inbred C57BL
 Humans Adult Middle Aged COVID-19 Vaccines Ad26COVS1 BNT162 Vaccine ChAdOx1 nCoV-19 Longitudinal Studies *Multiple Sclerosis/drug therapy Prospective Studies *COVID-19/prevention & control SARS-CoV-2 *Viral Vaccines Immunoglobulin G Antibodies, Viral Immunity, Cellular
 Humans Male Young Adult *COVID-19/complications COVID-19 Vaccines/adverse effects Death, Sudden/etiology *Epilepsy/complications *Multiple Sclerosis/complications Seizures/complications Vaccination/adverse effects Fatal Outcome
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/pathology Lipocalin-2/genetics Macrophages *Multiple Sclerosis/pathology Central Nervous System
 Humans *Multiple Sclerosis Brain/pathology Chronic Disease Magnetic Resonance Imaging Disease Progression Receptors, GABA
 Humans Retrospective Studies *Urinary Bladder, Neurogenic/drug therapy *Multiple Sclerosis/drug therapy Treatment Outcome *Botulinum Toxins, Type A/therapeutic use *Urinary Bladder, Overactive/drug therapy Muscle Spasticity/drug therapy *Neuromuscular Agents/therapeutic use Urodynamics
 Humans *MicroRNAs/genetics/metabolism Down-Regulation *Multiple Sclerosis/genetics rhoA GTP-Binding Protein/genetics rho-Associated Kinases/genetics
 Humans *Neurodegenerative Diseases *Sleep Wake Disorders/complications/diagnosis *Parkinson Disease *Multiple Sclerosis *Stroke
 Humans Pandemics *Multiple Sclerosis Quality of Life *COVID-19/prevention & control Exercise
 Humans Immunization, Secondary Immunity, Humoral Rituximab/therapeutic use *Multiple Sclerosis/drug therapy Fingolimod Hydrochloride/therapeutic use COVID-19 Vaccines/therapeutic use Pandemics SARS-CoV-2 *COVID-19/prevention & control Vaccination Antibodies, Viral Immunoglobulin G RNA, Messenger
 Humans *Multiple Sclerosis/pathology *Remyelination Schwann Cells/metabolism Central Nervous System/metabolism/pathology Myelin Sheath/metabolism/pathology Spinal Cord/pathology Glial Fibrillary Acidic Protein/metabolism
 Humans *Multiple Sclerosis Myelin-Oligodendrocyte Glycoprotein Autoantigens Central Nervous System T-Lymphocytes, Regulatory
 Animals Mice *Epstein-Barr Virus Infections/complications Herpesvirus 4, Human *Multiple Sclerosis *alpha-Crystallins
 Mice Animals Cuprizone/toxicity Glucagon-Like Peptide-1 Receptor/metabolism *Demyelinating Diseases/chemically induced/drug therapy *Remyelination Myelin Sheath *Multiple Sclerosis/metabolism Disease Models, Animal Mice, Inbred C57BL
 Mice Animals Lysophosphatidylcholines/toxicity *Demyelinating Diseases/chemically induced/drug therapy/metabolism Optic Chiasm/metabolism/pathology Evoked Potentials, Visual Myelin Sheath/pathology *Multiple Sclerosis/pathology
 Humans Clostridium perfringens/metabolism Lymphocytes Central Nervous System *Bacterial Toxins/metabolism *Multiple Sclerosis
 Humans Male *COVID-19/epidemiology/prevention & control *COVID-19 Vaccines/administration & dosage *Drug-Related Side Effects and Adverse Reactions Iran/epidemiology *Multiple Sclerosis/epidemiology Retrospective Studies Vaccination/adverse effects
 Male Female Humans *Neuromyelitis Optica/epidemiology/diagnosis Prevalence *Multiple Sclerosis/epidemiology Central Nervous System Incidence
 Humans *Multiple Sclerosis Cross-Sectional Studies Cognition/physiology *Cognitive Dysfunction/etiology/complications *Cognition Disorders/etiology/diagnosis Neuropsychological Tests
 Humans *Multiple Sclerosis *Cannabis Cross-Sectional Studies *Cannabinoids/therapeutic use Pain/complications
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental *Lactococcus lactis Mice, Inbred C57BL Spinal Cord *Multiple Sclerosis
 Humans Drug Evaluation, Preclinical Workflow *Myelin Sheath Algorithms Axons *Multiple Sclerosis
 Humans *Dimethyl Fumarate/adverse effects *Immunosuppressive Agents/adverse effects *Multiple Sclerosis, Relapsing-Remitting/drug therapy Recurrence
 Animals *Encephalomyelitis, Autoimmune, Experimental Astrocytes Receptors, Purinergic P2X7 Integrin beta3 Calcium *Multiple Sclerosis Cell Communication
 Mice Animals Autoimmunity Ubiquitination *Encephalomyelitis, Autoimmune, Experimental/metabolism *Multiple Sclerosis/metabolism Ubiquitin-Protein Ligases/genetics/metabolism Cell Differentiation Mice, Knockout CD4-Positive T-Lymphocytes Ubiquitins/metabolism Mice, Inbred C57BL
 Humans Brazil *Neuromyelitis Optica Prevalence Antibodies *Multiple Sclerosis Aquaporin 4 Autoantibodies
 Child Infant Male Infant, Newborn Pregnancy Humans Female *Family Planning Services *Multiple Sclerosis Prospective Studies Registries Breast Feeding
 United States Adult Female Humans Male Alemtuzumab Network Meta-Analysis *Multiple Sclerosis Chronic Disease Recurrence
 Humans Natalizumab/adverse effects *Leukoencephalopathy, Progressive Multifocal/diagnosis/diagnostic imaging Diagnosis, Differential *Immune Reconstitution Inflammatory Syndrome/diagnosis/drug therapy/etiology Antibodies, Monoclonal, Humanized/therapeutic use *Multiple Sclerosis/diagnosis
 Animals Mice *Multiple Sclerosis Locus Coeruleus *Encephalomyelitis, Autoimmune, Experimental *Adrenergic Neurons Norepinephrine
 Humans *Multiple Sclerosis Cladribine Prospective Studies Intermediate Filaments Neurofilament Proteins Biomarkers Recurrence
 Humans *Neuromyelitis Optica/diagnostic imaging/pathology *Multiple Sclerosis/diagnostic imaging Corpus Callosum/diagnostic imaging/pathology Myelin-Oligodendrocyte Glycoprotein Autoantibodies Aquaporin 4 Immunoglobulin G *Leukoencephalopathies
 Humans Female Adult Middle Aged Male Exercise Test/methods Retrospective Studies *Multiple Sclerosis Cross-Sectional Studies *Cardiorespiratory Fitness
 Humans Animals Mice *Multiple Sclerosis/genetics Beclin-1/genetics Proto-Oncogene Proteins c-akt Autophagy *Encephalomyelitis, Autoimmune, Experimental/genetics Biomarkers Hippocampus Inflammation
 Animals Dogs *Core Stability Smartphone *Multiple Sclerosis Reproducibility of Results Disease Progression Accelerometry Postural Balance
 Humans Myelin-Oligodendrocyte Glycoprotein Myelin Sheath Aquaporin 4 *Neuromyelitis Optica/diagnostic imaging *Multiple Sclerosis/diagnostic imaging Autoantibodies Immunoglobulin G
 Humans *Tyrosine Protein Kinase Inhibitors Microglia *Multiple Sclerosis B-Lymphocytes/metabolism Macrophages
 Humans *T-Lymphocytes, Regulatory RNA Splicing Gene Expression Regulation *Multiple Sclerosis/genetics DEAD-box RNA Helicases/genetics/metabolism Forkhead Transcription Factors/genetics/metabolism
 Humans Cross-Over Studies *Multiple Sclerosis Blood Glucose Exercise/physiology Lipids Insulin *Cardiovascular Diseases
 Humans *MicroRNAs/genetics/metabolism Genome-Wide Association Study 3' Untranslated Regions/genetics *Multiple Sclerosis/genetics Binding Sites/genetics Polymorphism, Single Nucleotide/genetics
 Humans *Paraparesis, Tropical Spastic *Multiple Sclerosis *Human T-lymphotropic virus 1/genetics Biomarkers Central Nervous System Viral Load *Chemokines, C
 Humans *Telerehabilitation *Multiple Sclerosis *COVID-19 SARS-CoV-2 Systematic Reviews as Topic Research Design Review Literature as Topic
 Humans Adult *Speech *Multiple Sclerosis Pilot Projects Cross-Sectional Studies Communication Cognition Social Networking Fatigue
 Humans Female Middle Aged Aged Quality of Life *Multiple Sclerosis Exercise Risk Factors Diet Fatigue *Wheelchairs
 Humans *Microbiota *Autoimmune Diseases *Gastrointestinal Microbiome/physiology *Multiple Sclerosis Fatty Acids, Volatile/metabolism
 Humans Life Expectancy Quality-Adjusted Life Years Global Burden of Disease Risk Factors *Arthritis, Rheumatoid/epidemiology *Multiple Sclerosis/epidemiology Global Health
 Humans Magnetic Resonance Imaging *Glioma/diagnostic imaging/pathology *Multiple Sclerosis
 Humans *Neurodegenerative Diseases *Alzheimer Disease *Amyotrophic Lateral Sclerosis Interleukin-17 Leukocytes, Mononuclear *Parkinson Disease Cytokines *Multiple Sclerosis
 Humans Reproducibility of Results *Multiple Sclerosis Muscle Strength/physiology *Stroke Lower Extremity/physiology Postural Balance/physiology
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental STAT5 Transcription Factor/metabolism Janus Kinase 2/metabolism Spinal Cord/pathology *Multiple Sclerosis/pathology Mice, Transgenic Mice, Inbred C57BL Th17 Cells Th1 Cells
 Adult Humans Child *Uveitis/diagnosis/epidemiology/etiology *Behcet Syndrome/complications Adrenal Cortex Hormones/therapeutic use Immunosuppressive Agents/therapeutic use *Multiple Sclerosis/complications
 Mice Animals *Multiple Sclerosis/diagnostic imaging Triggering Receptor Expressed on Myeloid Cells-1 Quality of Life Central Nervous System/diagnostic imaging *Encephalomyelitis, Autoimmune, Experimental/drug therapy Myeloid Cells Carrier Proteins Positron-Emission Tomography/methods Mice, Inbred C57BL
 Humans *Neuromyelitis Optica/diagnostic imaging Aquaporin 4 Retrospective Studies Cross-Sectional Studies Myelin-Oligodendrocyte Glycoprotein *Multiple Sclerosis/diagnostic imaging *Retinal Degeneration Immunoglobulin G Autoantibodies
 *Glomerulosclerosis, Focal Segmental/complications *Multiple Sclerosis/drug therapy *Immunosuppressive Agents/adverse effects/therapeutic use *Antibodies, Monoclonal, Humanized/adverse effects/therapeutic use Humans Male Adult Edema/chemically induced Albuminuria/chemically induced Treatment Outcome
 Adult Female Humans Male Middle Aged Canada/epidemiology Case-Control Studies *Inflammatory Bowel Diseases/drug therapy/epidemiology *Multiple Sclerosis/epidemiology Necrosis *Tumor Necrosis Factor Inhibitors/adverse effects/therapeutic use
 Humans *Neurodegenerative Diseases/diagnosis/genetics Brain/metabolism *Huntington Disease *Multiple Sclerosis
 Humans Female Male *Multiple Sclerosis Follow-Up Studies Antioxidants Cholesterol, LDL Aryldialkylphosphatase Apolipoprotein A-II Apolipoproteins C
 Humans Speech *Multiple Sclerosis Auditory Perception *Sound Localization/physiology Noise *Speech Perception/physiology Perceptual Masking
 Humans *Multiple Sclerosis Genetic Predisposition to Disease HLA-DRB1 Chains/genetics HLA Antigens
 Male Animals Mice Myelin Sheath/metabolism Cuprizone/toxicity *Demyelinating Diseases/chemically induced/therapy/metabolism Mice, Inbred C57BL *Multiple Sclerosis/metabolism *Mesenchymal Stem Cells Disease Models, Animal
 Animals Female Mice *Multiple Sclerosis/drug therapy Nitric Oxide Mice, Inbred C57BL *Encephalomyelitis, Autoimmune, Experimental/drug therapy/pathology Cytokines/metabolism Interferon-gamma/metabolism Anti-Inflammatory Agents/therapeutic use Disease Models, Animal
 Female Humans Male COVID-19 Vaccines/therapeutic use *COVID-19/prevention & control *Multiple Sclerosis/drug therapy Cladribine RNA, Messenger Cross-Sectional Studies Fingolimod Hydrochloride Prospective Studies SARS-CoV-2 Antibodies, Viral Vaccination
 Adult Humans Middle Aged *Sedentary Behavior *Multiple Sclerosis Longitudinal Studies Cross-Sectional Studies Pilot Projects Reproducibility of Results Accelerometry Exercise
 Humans Cognition *Cognitive Dysfunction/complications Memory, Short-Term *Multiple Sclerosis Neuropsychological Tests *Sleep Apnea Syndromes/complications/diagnosis
 Humans Aged *Frailty Frail Elderly Follow-Up Studies Cross-Sectional Studies *Multiple Sclerosis Geriatric Assessment/methods Chronic Disease Longitudinal Studies
 Humans Adult Middle Aged Aged Walk Test/methods *Multiple Sclerosis Reproducibility of Results Respiratory Function Tests Walking/physiology Exercise Test
 Humans Oligoclonal Bands/cerebrospinal fluid Retrospective Studies *Ischemic Stroke/complications *Central Nervous System Diseases *Multiple Sclerosis/complications *Stroke/complications Immunoglobulin G
 Humans *Stroke Rehabilitation/methods *Multiple Sclerosis Feedback *Robotic Surgical Procedures Recovery of Function Upper Extremity *Stroke
 Female Humans Male *Neuromyelitis Optica/drug therapy COVID-19 Vaccines/adverse effects *COVID-19/prevention & control *Multiple Sclerosis/drug therapy *Myelitis Aquaporin 4 Autoantibodies Myelin-Oligodendrocyte Glycoprotein
 Humans *Multiple Sclerosis *Neurodegenerative Diseases Gait/physiology Adaptation, Physiological/physiology Acclimatization Exercise Test/methods Walking/physiology
 Humans *Multiple Sclerosis Caregivers Case Management Health Personnel Long-Term Care
 Humans Male Escherichia coli *Escherichia coli Infections/microbiology *Multiple Sclerosis *Multiple Sclerosis, Relapsing-Remitting/complications Universities Drug Resistance, Multiple, Bacterial *Urinary Tract Infections/drug therapy/epidemiology *Community-Acquired Infections/drug therapy/epidemiology/microbiology Klebsiella Anti-Bacterial Agents/therapeutic use/pharmacology Microbial Sensitivity Tests
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/metabolism *Multiple Sclerosis/metabolism Aspartic Acid/cerebrospinal fluid D-Aspartic Acid/metabolism Spinal Cord/metabolism Brain/metabolism Synaptic Transmission Excitatory Amino Acids/metabolism Glutamic Acid/metabolism Cytokines/metabolism
 Humans *Precision Medicine Natalizumab *Multiple Sclerosis, Relapsing-Remitting/drug therapy Dimethyl Fumarate/therapeutic use Clinical Decision-Making Randomized Controlled Trials as Topic
 Humans Fingolimod Hydrochloride/therapeutic use COVID-19 Vaccines/therapeutic use *Multiple Sclerosis/drug therapy BNT162 Vaccine Seroconversion Longitudinal Studies Prospective Studies *COVID-19/prevention & control SARS-CoV-2 Immunosuppressive Agents/therapeutic use Antibodies, Viral RNA, Messenger Antibodies, Neutralizing Vaccination
 Humans COVID-19 Vaccines Rituximab/therapeutic use SARS-CoV-2 Spike Glycoprotein, Coronavirus BNT162 Vaccine *COVID-19 *Autoimmune Diseases of the Nervous System Antibodies, Monoclonal, Humanized/therapeutic use Vaccination *Multiple Sclerosis/drug therapy *Myasthenia Gravis Antibodies, Viral
 Male Female Humans *Multiple Sclerosis Gadolinium Retrospective Studies Magnetic Resonance Imaging/methods Contrast Media Brain Gadolinium DTPA Cerebellar Nuclei
 Humans Myelin-Oligodendrocyte Glycoprotein *Multiple Sclerosis *Thymus Hyperplasia/diagnosis Autoantibodies *Optic Neuritis *Immune System Diseases
 Animals Humans Mice Caco-2 Cells *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism Inflammation/metabolism *Iridoids/therapeutic use Mice, Inbred C57BL Multiple Sclerosis/metabolism *Olea
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/metabolism Choroid Plexus/metabolism/pathology Central Nervous System/metabolism *Multiple Sclerosis/metabolism Interferon-gamma/metabolism Mice, Inbred C57BL
 Humans Prevalence Global Burden of Disease Risk Factors *Arthritis, Rheumatoid/epidemiology *Multiple Sclerosis/epidemiology *Inflammatory Bowel Diseases/epidemiology Global Health Incidence
 Humans *Multiple Sclerosis Brain/pathology Brain Mapping/methods Data Accuracy Neuroimaging Magnetic Resonance Imaging/methods Italy
 Humans Neuroinflammatory Diseases *Parkinson Disease/metabolism *Multiple Sclerosis *Epilepsy *MicroRNAs/physiology
 Adult Humans Prognosis *Multiple Sclerosis Reproducibility of Results Systematic Reviews as Topic Disease Progression
 Humans Spinal Cord/diagnostic imaging Magnetic Resonance Imaging/methods *Spastic Paraplegia, Hereditary/pathology *Multiple Sclerosis
 Mice Animals *Multiple Sclerosis *Encephalomyelitis, Autoimmune, Experimental Spinal Cord/metabolism Myelin-Oligodendrocyte Glycoprotein/metabolism Lipids/adverse effects
 Animals Mice Cuprizone Tumor Necrosis Factor-alpha *Demyelinating Diseases/chemically induced/drug therapy *Neuroprotective Agents/therapeutic use Brain-Derived Neurotrophic Factor/therapeutic use *Chalcones/adverse effects Disease Models, Animal Mice, Inbred C57BL *Multiple Sclerosis/drug therapy
 Mice Animals Microglia/metabolism *Multiple Sclerosis/metabolism *Neurodegenerative Diseases/metabolism Nitric Oxide/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism Cytokines/metabolism Tumor Necrosis Factor-alpha/metabolism Lipopolysaccharides/pharmacology
 Animals Mice Autoimmunity Central Nervous System *Encephalomyelitis, Autoimmune, Experimental Interleukin-10/therapeutic use Macrophages Mice, Inbred C57BL Microglia *Multiple Sclerosis
 Humans *COVID-19/prevention & control *COVID-19 Vaccines/adverse effects *Multiple Sclerosis SARS-CoV-2 Viral Vaccines
 Mice Animals Cuprizone/toxicity *Demyelinating Diseases/pathology Disease Models, Animal Mice, Inbred C57BL Myelin Sheath/metabolism Oligodendroglia/metabolism *Multiple Sclerosis/pathology Hippocampus/metabolism Receptors, Purinergic P1/metabolism
 Child Humans *Multiple Sclerosis Cross-Sectional Studies Prospective Studies Chronic Disease Fatty Acids, Unsaturated Recurrence Disability Evaluation Disease Progression
 Humans *Epstein-Barr Virus Infections Herpesvirus 4, Human HLA-DRB1 Chains/genetics *Multiple Sclerosis/genetics Receptors, Antigen, T-Cell/genetics T-Lymphocytes HLA Antigens/genetics
 Humans Postural Balance *Parkinson Disease Prospective Studies *Multiple Sclerosis Retrospective Studies *Stroke
 Animals Mice Brain/metabolism Cuprizone/toxicity *Demyelinating Diseases/chemically induced/metabolism Disease Models, Animal Mice, Inbred C57BL *Microbiota Microglia/metabolism *Multiple Sclerosis/metabolism Vagus Nerve/metabolism
 Humans *Multiple Sclerosis B-Lymphocytes *B-Lymphocyte Subsets/metabolism Cytokines/therapeutic use B-Cell Activating Factor/metabolism
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/pathology Myelin Basic Protein Myelin Proteolipid Protein Neoplasm Recurrence, Local/pathology Spinal Cord/pathology *Multiple Sclerosis/pathology Mice, Inbred Strains Chronic Disease Inflammation/pathology Brain/pathology Protein Isoforms
 Humans Rituximab/adverse effects *Multiple Sclerosis *Biosimilar Pharmaceuticals/adverse effects Antibodies, Monoclonal/therapeutic use *Antineoplastic Agents/therapeutic use
 Mice Animals *Remyelination *Demyelinating Diseases/chemically induced Lysophosphatidylcholines Clemastine/adverse effects Internal Capsule/pathology Myelin Sheath/pathology *Multiple Sclerosis/pathology Oligodendroglia Mice, Inbred C57BL Disease Models, Animal Cuprizone/pharmacology
 Animals Humans *Tryptophan Kynurenine/metabolism *Multiple Sclerosis Kynurenic Acid/metabolism Quinolinic Acid Mammals/metabolism
 Humans Autoantibodies *Optic Neuritis/diagnosis/therapy Myelin-Oligodendrocyte Glycoprotein *Optic Nerve Diseases *Neuromyelitis Optica *Multiple Sclerosis Aquaporin 4
 Humans *Multiple Sclerosis CD8-Positive T-Lymphocytes Granzymes Programmed Cell Death 1 Receptor Memory T Cells Perforin Myelin-Oligodendrocyte Glycoprotein Cytokines
 Humans *COVID-19/complications Neuroinflammatory Diseases SARS-CoV-2 *Multiple Sclerosis Central Nervous System Autoantibodies
 Mice Animals Humans *Multiple Sclerosis Interleukin-3 Neuroglia/metabolism Central Nervous System Microglia
 Mice Animals Sphingosine-1-Phosphate Receptors/metabolism/therapeutic use Cuprizone *Remyelination Receptors, Lysosphingolipid/metabolism/therapeutic use Central Nervous System/metabolism *Multiple Sclerosis/metabolism Oligodendroglia/metabolism beta-Arrestins/metabolism/therapeutic use Mice, Inbred C57BL
 Humans Retrospective Studies Intermediate Filaments Biomarkers *COVID-19 SARS-CoV-2 *Multiple Sclerosis Neurofilament Proteins
 Humans Adult Middle Aged Austria/epidemiology Cross-Sectional Studies *Multiple Sclerosis Prospective Studies *COVID-19 SARS-CoV-2 Vaccination
 Female Mice Animals *Encephalomyelitis, Autoimmune, Experimental Interleukin-17 *Remyelination Mice, Inbred C57BL Inflammation/drug therapy Cytokines/metabolism *Multiple Sclerosis/drug therapy Anti-Inflammatory Agents/pharmacology *Artemisinins/pharmacology/therapeutic use RNA, Messenger/genetics
 Humans Fingolimod Hydrochloride/pharmacology/therapeutic use Sphingosine-1-Phosphate Receptors *COVID-19 *Sphingosine 1 Phosphate Receptor Modulators/pharmacology/therapeutic use SARS-CoV-2/metabolism Sphingosine/metabolism/pharmacology *Multiple Sclerosis/metabolism
 Humans Female Middle Aged Male Quality of Life/psychology Surveys and Questionnaires *Multiple Sclerosis Longitudinal Studies *Neurodegenerative Diseases Australia Psychometrics/methods
 Mice Animals *Multiple Sclerosis CD28 Antigens/genetics Disease Models, Animal Mice, Knockout Mice, Inbred C57BL
 Humans *Arthritis, Rheumatoid/drug therapy *Autoimmune Diseases Immunity, Innate *Lupus Erythematosus, Systemic *Multiple Sclerosis
 Humans Animals Mice *Multiple Sclerosis Neurons/metabolism Mitochondria/metabolism Lymphocytes/metabolism Anti-Inflammatory Agents/therapeutic use Chronic Disease
 Humans Herpesvirus 4, Human *Epstein-Barr Virus Infections/complications *Multiple Sclerosis *COVID-19/complications SARS-CoV-2 Inflammation/complications Disease Progression
 Humans *Multiple Sclerosis Autoantigens Adhesins, Bacterial Myelin Sheath/metabolism Haemophilus influenzae Autoantibodies Myelin Proteins Peptides Myelin-Oligodendrocyte Glycoprotein
 Humans *Oligoclonal Bands/cerebrospinal fluid Retrospective Studies *Multiple Sclerosis/cerebrospinal fluid Immunoglobulin G Isoelectric Focusing/methods
 Animals Mice Axons Corpus Callosum/metabolism Cuprizone/toxicity *Demyelinating Diseases/metabolism/pathology Disease Models, Animal Mice, Inbred C57BL *Multiple Sclerosis/metabolism Myelin Sheath/physiology Oligodendroglia/metabolism *Remyelination/immunology T-Lymphocytes/metabolism/pathology
 Mice Animals *Multiple Sclerosis/drug therapy Th17 Cells Interleukin-17/metabolism CD8-Positive T-Lymphocytes/metabolism Molecular Docking Simulation *Encephalomyelitis, Autoimmune, Experimental/drug therapy STAT3 Transcription Factor/metabolism Cell Differentiation Cytokines/metabolism Mice, Inbred C57BL Th1 Cells
 Humans *Myoclonus *Huntington Disease Reflex/physiology *Multiple Sclerosis *Neurology Reaction Time/physiology Electromyography
 Humans Receptors, Tumor Necrosis Factor, Type I/therapeutic use Cytokines *Autoimmune Diseases/drug therapy Tumor Necrosis Factor-alpha *Arthritis, Rheumatoid *Multiple Sclerosis
 Humans *Multiple Sclerosis Cross-Sectional Studies Postural Balance/physiology Walking/physiology Gait/physiology
 Humans *Cytokines Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology Tumor Necrosis Factor-alpha Interleukin-10 *Multiple Sclerosis Interleukin-17 Interferon-gamma/pharmacology Neurons
 Humans Citrullination *Multiple Sclerosis Myelin Basic Protein Th17 Cells/metabolism Tumor Necrosis Factor-alpha/metabolism
 Humans Dogs Animals Oligoclonal Bands/cerebrospinal fluid Prospective Studies *Multiple Sclerosis/diagnosis *Meningoencephalitis/veterinary *Meningitis/veterinary Immunoglobulin G/cerebrospinal fluid *Arteritis/veterinary *Brain Neoplasms
 Animals Mice *Central Nervous System/metabolism/pathology Encephalomyelitis, Autoimmune, Experimental/metabolism/pathology *Insulin-Like Growth Factor I/metabolism *Macrophages/metabolism Mice, Inbred C57BL Microglia/metabolism Multiple Sclerosis/pathology Neuroinflammatory Diseases
 Male Humans Adult Middle Aged Aged *Parkinson Disease *Multiple Sclerosis Outcome Assessment, Health Care Disease Progression Hand
 Humans Exergaming *Restless Legs Syndrome/epidemiology *Multiple Sclerosis Quality of Life Single-Blind Method Fatigue Severity of Illness Index
 Humans *COVID-19/epidemiology/prevention & control COVID-19 Vaccines/adverse effects 2019-nCoV Vaccine mRNA-1273 Ad26COVS1 BNT162 Vaccine Incidence Cohort Studies *Multiple Sclerosis/epidemiology Retrospective Studies SARS-CoV-2 Vaccination/adverse effects *Drug-Related Side Effects and Adverse Reactions
 Animals Mice *Multiple Sclerosis/genetics *MicroRNAs/genetics/metabolism CD4-Positive T-Lymphocytes *Encephalomyelitis, Autoimmune, Experimental/genetics/pathology Cell Differentiation/genetics Th17 Cells Oligodendroglia/metabolism Dendritic Cells/metabolism Mice, Inbred C57BL
 Mice Animals *Remyelination Oligodendroglia/pathology Myelin Sheath/pathology *Multiple Sclerosis Axons/pathology Mammals
 Male Female Humans Middle Aged *Multiple Sclerosis Depression/etiology/psychology *Cognitive Dysfunction/diagnosis/etiology Fatigue/diagnosis/etiology Cognition
 Mice Animals Humans *Encephalomyelitis, Autoimmune, Experimental/drug therapy *Neuroprotective Agents/pharmacology/therapeutic use Blood-Brain Barrier *Disabled Persons *Motor Disorders/complications/drug therapy/pathology *Multiple Sclerosis/drug therapy Anti-Inflammatory Agents/pharmacology/therapeutic use
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Lipopolysaccharides/adverse effects Spinal Cord/pathology *Multiple Sclerosis Cell Differentiation
 Mice Animals *Multiple Sclerosis *Gastrointestinal Microbiome Mice, Inbred C57BL *Encephalomyelitis, Autoimmune, Experimental Diet/adverse effects Immunomodulation
 Humans Glial Fibrillary Acidic Protein *Multiple Sclerosis Intermediate Filaments Body Mass Index Overweight Biomarkers Blood Volume Obesity
 Humans Flow Cytometry Diagnosis, Differential Retrospective Studies *Connective Tissue Diseases/diagnosis *Lupus Erythematosus, Systemic *Multiple Sclerosis
 Female Humans Genetic Predisposition to Disease Genome-Wide Association Study Leukocyte Count *Autoimmune Diseases/genetics *Arthritis, Rheumatoid *Multiple Sclerosis
 Adult Animals Mice Rabbits Cell Differentiation/physiology *Demyelinating Diseases/pathology Homeodomain Proteins/metabolism *Multiple Sclerosis/pathology Myelin Sheath/metabolism/pathology Nerve Regeneration/physiology *Oligodendrocyte Precursor Cells/metabolism Oligodendroglia/metabolism Stem Cells/metabolism
 Female Animals Mice *Multiple Sclerosis/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism TRPA1 Cation Channel/metabolism Hyperalgesia/drug therapy Nociception *Transient Receptor Potential Channels/metabolism Neuroinflammatory Diseases Spinal Cord/metabolism *Neuralgia/drug therapy
 Adult Female Male Humans *Nasal Polyps/epidemiology *Arthritis, Rheumatoid *Diabetes Mellitus, Type 1 *Multiple Sclerosis *Arthritis, Juvenile
 Humans *Multiple Sclerosis CD8-Positive T-Lymphocytes Herpesvirus 4, Human *Epstein-Barr Virus Infections/metabolism Longitudinal Studies Phenotype
 Animals Mice *White Matter/metabolism Lipopolysaccharides/toxicity Oligodendroglia/metabolism Myelin Sheath/metabolism Spinal Cord/metabolism Axons/metabolism *Multiple Sclerosis/metabolism Inflammation/metabolism Kallikreins/metabolism
 Humans *Multiple Sclerosis Herpesvirus 4, Human *Epstein-Barr Virus Infections Antigens, Viral Pilot Projects Dimethyl Fumarate/pharmacology/therapeutic use Capsid Antibody Formation Immunoglobulin G Antibodies, Viral Capsid Proteins
 Humans *Intermediate Filaments *Multiple Sclerosis Prospective Studies Axons Cohort Studies
 Female Humans *Multiple Sclerosis Myelin-Oligodendrocyte Glycoprotein Case-Control Studies *Epstein-Barr Virus Infections Herpesvirus 4, Human Aquaporin 4 Autoantibodies Immunoglobulin G *Neuromyelitis Optica
 Humans Genome-Wide Association Study *Inflammatory Bowel Diseases/genetics Quantitative Trait Loci *Colitis, Ulcerative/drug therapy/genetics Inflammation/genetics *Multiple Sclerosis/genetics Polymorphism, Single Nucleotide
 Mice Humans Animals Granulocyte-Macrophage Colony-Stimulating Factor Moraxella catarrhalis Klebsiella pneumoniae Myelin Sheath/pathology Th17 Cells Virulence *Encephalomyelitis, Autoimmune, Experimental/pathology *Multiple Sclerosis/pathology Respiratory System Mice, Inbred C57BL Th1 Cells
 Mice Animals Microglia/metabolism *Encephalomyelitis, Autoimmune, Experimental/therapy/metabolism Pyroptosis *Mesenchymal Stem Cells/metabolism Inflammation/metabolism *Multiple Sclerosis/therapy *MicroRNAs/genetics/metabolism
 Adult Humans SARS-CoV-2 Cohort Studies COVID-19 Testing *Iritis Immunomodulating Agents *COVID-19/diagnosis/epidemiology *Arthritis, Rheumatoid/epidemiology *Inflammatory Bowel Diseases *Multiple Sclerosis/epidemiology Ontario/epidemiology
 Animals Humans Myelin-Oligodendrocyte Glycoprotein Autoantibodies Receptors, Fc *Multiple Sclerosis *Encephalomyelitis, Autoimmune, Experimental Complement System Proteins Antibodies, Monoclonal
 Animals Mice Disease Models, Animal ELAV Proteins/metabolism *Encephalomyelitis, Autoimmune, Experimental/drug therapy Gene Expression Regulation Mice, Inbred C57BL *Multiple Sclerosis/drug therapy Myelin Sheath/metabolism *Neuralgia/genetics/metabolism Spinal Cord/metabolism
 Rats Animals Rabbits N-Formylmethionine Leucyl-Phenylalanine/chemistry/pharmacology *Multiple Sclerosis/drug therapy Liposomes Angiopoietin-1/therapeutic use Rats, Inbred Lew *Encephalomyelitis, Autoimmune, Experimental/drug therapy/pathology Inflammation/drug therapy
 Adult Humans *COVID-19 COVID-19 Vaccines Fingolimod Hydrochloride *Multiple Sclerosis Prospective Studies SARS-CoV-2 B-Lymphocytes Adaptor Proteins, Signal Transducing Antibodies, Viral Vaccination
 Animals Mice Infant, Newborn Humans *Multiple Sclerosis Immunoglobulin G/metabolism *Neuroblastoma Complement System Proteins/metabolism Apoptosis
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental Inflammation Mice, Inbred C57BL Microglia *Multiple Sclerosis Myeloid Cells Tetratricopeptide Repeat Interferons/pharmacology
 Humans *Multiple Sclerosis Gray Matter/metabolism/pathology Cerebral Cortex/pathology Meninges/metabolism/pathology Inflammation Disease Progression
 Humans Aquaporin 4 Autoantibodies Leukocyte Count *Multiple Sclerosis Myelin-Oligodendrocyte Glycoprotein *Neuromyelitis Optica Oligodendroglia
 Humans Quality of Life *Urinary Bladder, Neurogenic/diagnosis/etiology Reproducibility of Results Cross-Cultural Comparison Language *Urinary Incontinence *Lower Urinary Tract Symptoms/diagnosis Surveys and Questionnaires *Spinal Cord Injuries/complications/epidemiology *Multiple Sclerosis/complications Psychometrics
 Female Male Humans Myelin-Oligodendrocyte Glycoprotein *Aquaporin 4 Retrospective Studies Autoantibodies *Multiple Sclerosis
 Humans Biomarkers Glial Fibrillary Acidic Protein Intermediate Filaments/metabolism *Multiple Sclerosis/diagnosis Neurofilament Proteins Recurrence *Susac Syndrome/metabolism
 Humans Prospective Studies *Optic Neuritis/diagnostic imaging/etiology Optic Nerve/pathology Myelin-Oligodendrocyte Glycoprotein *Multiple Sclerosis Tomography, Optical Coherence Vision Disorders
 Humans *Neurodegenerative Diseases/drug therapy *Alzheimer Disease/drug therapy *Parkinson Disease/drug therapy Vitamin K/therapeutic use *Multiple Sclerosis
 Mice Humans Animals *White Matter/pathology *Murine hepatitis virus/physiology Myelin Sheath Interferons Proteins/genetics Spinal Cord/pathology *Multiple Sclerosis/pathology Mice, Inbred C57BL *Coronavirus Infections RNA-Binding Proteins/genetics Apoptosis Regulatory Proteins/genetics
 Humans *Epstein-Barr Virus Infections/diagnosis/drug therapy/complications Herpesvirus 4, Human Antibodies, Viral *Autoimmune Diseases/complications Antiviral Agents/therapeutic use *Multiple Sclerosis
 Humans *Mesenchymal Stem Cell Transplantation/adverse effects/methods *Multiple Sclerosis *Mesenchymal Stem Cells Injections, Spinal Adipose Tissue *Spinal Cord Injuries/therapy
 Humans Outpatients Pandemics *COVID-19 Magnetic Resonance Imaging/methods Neuroimaging/methods Brain/diagnostic imaging *Multiple Sclerosis
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy T-Lymphocytes *Proanthocyanidins/pharmacology/therapeutic use *Multiple Sclerosis/drug therapy Cytokines/metabolism CD4-Positive T-Lymphocytes Glycolysis Administration, Oral Mice, Inbred C57BL
 Animals Mice *Demyelinating Diseases/chemically induced/drug therapy/metabolism *Nanocapsules/therapeutic use Tretinoin/pharmacology Endothelial Cells/metabolism *Multiple Sclerosis/drug therapy Myelin Sheath Inflammation/drug therapy Oligodendroglia Cell Differentiation *Neurodegenerative Diseases/drug therapy Lipids/pharmacology Mice, Inbred C57BL
 Humans Male Evoked Potentials *Multiple Sclerosis *Optic Neuritis Prognosis Retina Retinal Ganglion Cells Female Adult Middle Aged
 Female Mice Animals *Encephalomyelitis, Autoimmune, Experimental BCG Vaccine Neuroprotection Tokyo Mice, Inbred C57BL *Multiple Sclerosis Myelin-Oligodendrocyte Glycoprotein Mice, Transgenic *Mycobacterium bovis Peptides Peptide Fragments
 Mice Animals *Multiple Sclerosis Antigen Presentation Myelin-Oligodendrocyte Glycoprotein *Encephalomyelitis, Autoimmune, Experimental CD4-Positive T-Lymphocytes Myelin Proteolipid Protein Antibodies/metabolism
 Humans *Cladribine/adverse effects *Multiple Sclerosis Expert Testimony Lymphocytes Tablets/pharmacology Recurrence Immunosuppressive Agents/adverse effects
 Animals Humans Mice Antibodies, Monoclonal Antigens, CD19 Autoimmunity Central Nervous System *Encephalomyelitis, Autoimmune, Experimental/drug therapy Mice, Inbred C57BL Multiple Sclerosis/drug therapy Myelin-Oligodendrocyte Glycoprotein T-Lymphocytes B-Lymphocytes *Immunotherapy, Adoptive
 Mice Animals *Neurodegenerative Diseases *Multiple Sclerosis Mitochondria Superoxide Dismutase/genetics Motor Neurons Superoxide Dismutase-1/genetics Phenotype Paralysis/genetics Inflammation/genetics
 Humans *CD8-Positive T-Lymphocytes Leukocytes, Mononuclear *Multiple Sclerosis Flow Cytometry Recurrence Antigens, CD20
 Mice Animals Autoimmunity T-Lymphocytes Neuroinflammatory Diseases Receptors, Aryl Hydrocarbon/genetics/metabolism *Autoimmune Diseases *Multiple Sclerosis
 Animals Humans Mice Central Nervous System/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism Inflammation *Multiple Sclerosis/metabolism *Receptors, Tumor Necrosis Factor, Type I/agonists *Receptors, Tumor Necrosis Factor, Type II/agonists Tumor Necrosis Factor-alpha/metabolism
 Humans Biomarkers/blood/cerebrospinal fluid Intermediate Filaments Multiple Sclerosis/cerebrospinal fluid *Neurofilament Proteins/cerebrospinal fluid *Pseudotumor Cerebri/blood/cerebrospinal fluid Spinal Puncture
 Mice Animals Glatiramer Acetate/pharmacology/therapeutic use *Encephalomyelitis, Autoimmune, Experimental Peptides/pharmacology *Multiple Sclerosis Immunomodulation Endoplasmic Reticulum Stress Mitochondria/metabolism Mice, Inbred C57BL Disease Models, Animal
 Humans *Multiple Sclerosis Spinal Cord/diagnostic imaging *Cervical Cord Magnetic Resonance Imaging/methods Brain/diagnostic imaging
 Humans Aquaporin 4 Autoantibodies Cross-Sectional Studies *Encephalitis *Immunoglobulin G/blood/cerebrospinal fluid *Multiple Sclerosis/diagnosis *Myelin-Oligodendrocyte Glycoprotein/blood/cerebrospinal fluid *Myelitis *Neuromyelitis Optica *Optic Neuritis
 Humans Female Adult Middle Aged Male *Multiple Sclerosis Cohort Studies Retrospective Studies COVID-19 Vaccines *COVID-19
 Humans Aged United States Patient Readmission Retrospective Studies Coma Medicare Social Class Socioeconomic Factors *Stroke *Multiple Sclerosis Residence Characteristics
 Animals Mice Mice, Inbred C57BL *Multiple Sclerosis *Encephalomyelitis, Autoimmune, Experimental *Theilovirus Sulfoglycosphingolipids Neoplasm Recurrence, Local Antibodies Myelin-Oligodendrocyte Glycoprotein Glycolipids
 Animals Mice *Multiple Sclerosis Deoxycytidine Kinase/genetics *Encephalomyelitis, Autoimmune, Experimental Lymphocytes/metabolism Disease Models, Animal Mice, Inbred C57BL
 Animals Mice Cell Differentiation Central Nervous System/pathology Cytokines *Encephalomyelitis, Autoimmune, Experimental Mice, Inbred C57BL *MicroRNAs *Multiple Sclerosis Th17 Cells STAT3 Transcription Factor
 Humans Adult Middle Aged COVID-19 Vaccines *Multiple Sclerosis Argentina/epidemiology Prospective Studies *COVID-19/prevention & control SARS-CoV-2 Antibodies, Neutralizing Vaccination Antibodies, Viral
 Adult Humans *Amyotrophic Lateral Sclerosis *Mesenchymal Stem Cells *Adult Stem Cells *Alzheimer Disease *Extracellular Vesicles *Huntington Disease *Multiple Sclerosis *Parkinson Disease/diagnosis/therapy
 Male Humans Intermediate Filaments Nutrition Surveys Biomarkers *Peripheral Nervous System Diseases *Diabetes Mellitus/epidemiology *Multiple Sclerosis
 Female Rats Animals Mice Interleukin-17 *Multiple Sclerosis/pathology Tumor Necrosis Factor-alpha NF-kappa B/metabolism/pharmacology/therapeutic use Rats, Inbred Lew *Encephalomyelitis, Autoimmune, Experimental/drug therapy Spinal Cord/pathology Interleukin-1/metabolism/pharmacology/therapeutic use Mice, Inbred C57BL
 Humans Herpesvirus 4, Human *Epstein-Barr Virus Infections/complications Case-Control Studies *Herpesvirus 6, Human/genetics *Multiple Sclerosis Herpesvirus 3, Human/genetics *Cytomegalovirus Infections Immunoglobulin G Central Nervous System
 Humans *Multiple Sclerosis Singapore/epidemiology SARS-CoV-2 *COVID-19/prevention & control Antibodies, Viral *Neuromyelitis Optica Vaccination Myelin-Oligodendrocyte Glycoprotein
 Humans Autoimmunity/genetics RNA, Untranslated/genetics/metabolism *Autoimmune Diseases/diagnosis/genetics *Arthritis, Rheumatoid *Multiple Sclerosis
 Child Humans *Neuromyelitis Optica/epidemiology *Multiple Sclerosis Retrospective Studies Thailand Myelin-Oligodendrocyte Glycoprotein Autoantibodies Aquaporin 4
 Animals Humans Mice *Antibodies, Catalytic Autoantibodies Catalase DNA *Encephalomyelitis, Autoimmune, Experimental Histones Hydrogen Peroxide Mice, Inbred C57BL *Multiple Sclerosis Myelin-Oligodendrocyte Glycoprotein
 Humans Animals Mice *Cannabinoids/adverse effects *Cannabis *Multiple Sclerosis/drug therapy *Encephalomyelitis, Autoimmune, Experimental/drug therapy/chemically induced/complications Cannabinoid Receptor Agonists *Neuralgia/drug therapy/etiology Muscle Spasticity/drug therapy/etiology Models, Theoretical
 Humans *Multiple Sclerosis Immunologic Factors/pharmacology Antibodies, Monoclonal, Humanized/pharmacology Recurrence Receptors, Antigen, T-Cell
 Male Female Humans alpha-Galactosidase/genetics *Fabry Disease/diagnostic imaging/genetics/complications *White Matter/pathology Retrospective Studies Follow-Up Studies *Multiple Sclerosis/complications Magnetic Resonance Imaging Brain/pathology
 Humans *MicroRNAs/genetics/metabolism Proto-Oncogene Proteins c-akt/metabolism *Multiple Sclerosis/genetics Biomarkers Cell Proliferation Cell Line, Tumor Gene Expression Regulation, Neoplastic PTEN Phosphohydrolase/genetics/metabolism Adaptor Proteins, Signal Transducing/genetics/metabolism Guanylate Kinases/genetics/metabolism
 Adult Female Humans Male ChAdOx1 nCoV-19 *COVID-19/prevention & control *COVID-19 Vaccines/adverse effects *Demyelinating Diseases *Multiple Sclerosis Retrospective Studies SARS-CoV-2 Vaccines, Inactivated/adverse effects
 Humans Reaction Time Muscle, Skeletal/physiology Electromyography/methods *Robotic Surgical Procedures *Robotics Posture/physiology Postural Balance/physiology Muscle Contraction/physiology *Multiple Sclerosis
 Humans Epitopes Molecular Mimicry *Zika Virus Autoantigens *Zika Virus Infection Retrospective Studies Brazil *Central Nervous System Diseases *Multiple Sclerosis Central Nervous System
 Humans *Neuromyelitis Optica/complications/diagnosis Myelin-Oligodendrocyte Glycoprotein Aquaporin 4 *Optic Neuritis/diagnosis/etiology *Multiple Sclerosis Autoantibodies
 Humans SARS-CoV-2 *COVID-19/prevention & control *Multiple Sclerosis Immunoglobulin G Cladribine Leukocytes, Mononuclear Prospective Studies Antigens, CD20 RNA, Messenger
 Humans Mice Animals Myelin Sheath/metabolism *Multiple Sclerosis/metabolism Cyclic Nucleotide Phosphodiesterases, Type 4/metabolism/pharmacology/therapeutic use Evoked Potentials, Visual Oligodendroglia/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism Cell Differentiation *Phosphodiesterase 4 Inhibitors/pharmacology/therapeutic use Anti-Inflammatory Agents/pharmacology Mice, Inbred C57BL
 Humans Rhizotomy *Trigeminal Neuralgia/surgery Retrospective Studies Temperature Treatment Outcome Prospective Studies Hypesthesia Pain/surgery *Multiple Sclerosis
 Animals Dogs Brain/pathology *Meningoencephalitis/veterinary/metabolism/pathology Microtubules/metabolism *Multiple Sclerosis Phosphorylation tau Proteins/metabolism
 Adult Aged Female Humans Middle Aged Young Adult *COVID-19/prevention & control *COVID-19 Vaccines/administration & dosage/adverse effects *Multiple Sclerosis Retrospective Studies RNA, Messenger SARS-CoV-2 Vaccination
 Male Rats Female Animals *Encephalomyelitis, Autoimmune, Experimental Gonadal Steroid Hormones/metabolism Ovary/metabolism *Multiple Sclerosis Testosterone/metabolism Estradiol/metabolism
 Humans Female Male *Kynurenine/metabolism Overweight/complications *Multiple Sclerosis Cross-Sectional Studies Chromatography, Liquid Tandem Mass Spectrometry Tryptophan/metabolism Obesity/complications Metabolome
 Animals Mice *Demyelinating Diseases/pathology Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Multiple Sclerosis/pathology Myelin Sheath/metabolism/pathology Nerve Tissue Proteins/metabolism *Oligodendroglia/metabolism/pathology Receptors, G-Protein-Coupled/metabolism *tau Proteins/genetics/metabolism
 Humans *Blood-Brain Barrier/metabolism CD8-Positive T-Lymphocytes Endothelial Cells/metabolism Central Nervous System/metabolism *Multiple Sclerosis Histocompatibility Antigens Class I/metabolism
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental Chemokines, CXC/metabolism Th1 Cells *Multiple Sclerosis Cell Differentiation Immunoglobulin G/therapeutic use Th17 Cells Mice, Inbred C57BL Receptors, CXCR6/metabolism
 Humans Biomarkers/blood *Glial Fibrillary Acidic Protein/blood Magnetic Resonance Imaging *Multiple Sclerosis, Chronic Progressive/diagnostic imaging Disease Progression *Neurofilament Proteins/blood
 Rats Animals Mice Cuprizone/toxicity *Demyelinating Diseases/chemically induced/drug therapy/metabolism *Thioctic Acid/therapeutic use Carvedilol/therapeutic use *Neurodegenerative Diseases *Multiple Sclerosis Mice, Inbred C57BL Disease Models, Animal
 Mice Animals Hyaluronic Acid/pharmacology Glycosaminoglycans/metabolism *Multiple Sclerosis *Encephalomyelitis, Autoimmune, Experimental/genetics *Encephalitis Chondroitin Sulfates/metabolism
 Humans Immunity, Humoral *Sphingosine 1 Phosphate Receptor Modulators COVID-19 Vaccines Sphingosine-1-Phosphate Receptors SARS-CoV-2 Longitudinal Studies Pandemics *COVID-19 Vaccination Antibodies, Monoclonal Immunoglobulin G *Multiple Sclerosis Antibodies, Viral
 Mice Animals Humans *Encephalomyelitis, Autoimmune, Experimental Th17 Cells *Multiple Sclerosis Central Nervous System/metabolism/pathology Cell Differentiation Mice, Inbred C57BL Th1 Cells
 Humans Female Male Myelin-Oligodendrocyte Glycoprotein Longitudinal Studies *Neuromyelitis Optica/diagnosis Aquaporin 4 Brain Stem *Multiple Sclerosis Autoantibodies Immunoglobulin G Immunoglobulin A Immunoglobulin M
 Animals Rats Male Female Mice *Demyelinating Diseases/chemically induced/pathology Cuprizone Rats, Wistar *Multiple Sclerosis Brain Stem Receptors, Muscarinic Vagus Nerve Mice, Inbred C57BL Disease Models, Animal Myelin Sheath/pathology
 Female Humans *Multiple Sclerosis Immunoglobulin kappa-Chains Oligoclonal Bands *Demyelinating Diseases/diagnosis Biomarkers Cohort Studies *Central Nervous System Diseases
 Animals Mice Nimodipine/pharmacology Calcium Channel Blockers/pharmacology *Oligodendrocyte Precursor Cells/metabolism Zebrafish/genetics Myelin Sheath/metabolism Oligodendroglia/metabolism *Encephalomyelitis, Autoimmune, Experimental/metabolism *Multiple Sclerosis/metabolism Calcium Channels, L-Type/metabolism *MicroRNAs/metabolism Cell Differentiation
 Humans Fingolimod Hydrochloride/pharmacology/therapeutic use *Sphingosine 1 Phosphate Receptor Modulators/therapeutic use *COVID-19/prevention & control COVID-19 Vaccines SARS-CoV-2 Sphingosine-1-Phosphate Receptors/therapeutic use Sphingosine *Multiple Sclerosis Vaccination
 Animals Mice Anti-Inflammatory Agents/pharmacology/therapeutic use *Berberine/pharmacology/therapeutic use Cytokines/metabolism *Encephalomyelitis, Autoimmune, Experimental/drug therapy Mice, Inbred C57BL Multiple Sclerosis Neuroinflammatory Diseases *T-Lymphocytes, Regulatory *Th2 Cells Transcription Factors
 Humans Chronic Disease *COVID-19/prevention & control COVID-19 Testing *COVID-19 Vaccines/adverse effects *Leukoencephalopathy, Progressive Multifocal/diagnostic imaging/etiology *Multiple Sclerosis Natalizumab
 Humans Cell Line Cell Proliferation Cladribine/pharmacology *Epstein-Barr Virus Infections/complications/drug therapy/genetics Epstein-Barr Virus Nuclear Antigens Herpesvirus 4, Human *Multiple Sclerosis Case-Control Studies
 Animals Mice Cell Differentiation Central Nervous System *Encephalomyelitis, Autoimmune, Experimental Mice, Inbred C57BL *Multiple Sclerosis Neuroinflammatory Diseases Th1 Cells Th17 Cells Transcription Factors Virulence Humans
 Animals Mice Neuroinflammatory Diseases Th17 Cells/metabolism *Encephalomyelitis, Autoimmune, Experimental Brain/pathology *Multiple Sclerosis *MicroRNAs Mice, Inbred C57BL Mice, Knockout
 Humans Child Adolescent Child, Preschool Immunity, Humoral *COVID-19/prevention & control COVID-19 Vaccines/adverse effects *Multiple Sclerosis Retrospective Studies SARS-CoV-2 Vaccination/adverse effects Antibodies, Viral N,N-Dimethyltryptamine RNA, Messenger
 Animals Mice *Multiple Sclerosis T-Lymphocytes, Regulatory Myelin-Oligodendrocyte Glycoprotein Myelin Sheath *Encephalomyelitis, Autoimmune, Experimental/metabolism Histocompatibility Antigens Class II/metabolism Mice, Inbred C57BL
 Humans Dysbiosis/complications *Autoimmune Diseases/complications *Sjogren's Syndrome/complications/epidemiology *Arthritis, Rheumatoid/complications *Lupus Erythematosus, Systemic/complications/epidemiology *Multiple Sclerosis
 Humans Child Adult Middle Aged *Neuromyelitis Optica/diagnostic imaging/epidemiology Follow-Up Studies Aquaporin 4 Iran/epidemiology *Myelitis *Multiple Sclerosis *Brain Diseases Disease Progression Recurrence Autoantibodies/therapeutic use Retrospective Studies
 Adult Adolescent Humans Child Child, Preschool Prospective Studies Cross-Sectional Studies Intermediate Filaments Biomarkers *Seizures, Febrile *Multiple Sclerosis
 Animals Mice *Ataxin-1/genetics Central Nervous System *Encephalomyelitis, Autoimmune, Experimental/genetics *Multiple Sclerosis *Spinocerebellar Ataxias/genetics/metabolism
 Animals Mice *Microglia Astrocytes Neuroinflammatory Diseases Programmed Cell Death 1 Receptor/genetics B7-H1 Antigen/genetics Inflammation *Multiple Sclerosis
 Humans Myosin Type I/chemistry/metabolism Serum/metabolism *COVID-19/diagnosis *Autoimmune Diseases *Multiple Sclerosis
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy T-Lymphocytes, Regulatory/metabolism Interleukin-10/metabolism/pharmacology/therapeutic use Transforming Growth Factor beta1/metabolism/pharmacology/therapeutic use Interleukin-17 Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism/therapeutic use *Multiple Sclerosis/metabolism Disease Models, Animal RNA, Messenger/metabolism Forkhead Transcription Factors/metabolism Th17 Cells Mice, Inbred C57BL Th1 Cells/physiology
 Mice Animals Granulocyte-Macrophage Colony-Stimulating Factor/metabolism Neuroinflammatory Diseases Endothelial Cells/metabolism Central Nervous System *Encephalomyelitis, Autoimmune, Experimental *Multiple Sclerosis Pain/metabolism Myeloid Cells Recurrence
 Humans *Inflammasomes/genetics/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/genetics *Multiple Sclerosis Fingolimod Hydrochloride/pharmacology/therapeutic use Pyroptosis Leukocytes, Mononuclear/metabolism Galectin 3 Tumor Necrosis Factor-alpha
 Animals Mice Anti-Inflammatory Agents/therapeutic use *Bacillus amyloliquefaciens/metabolism Camelus Cytokines/metabolism *Encephalomyelitis, Autoimmune, Experimental/drug therapy Mice, Inbred C57BL *Milk Multiple Sclerosis Myelin-Oligodendrocyte Glycoprotein Neuroinflammatory Diseases *Probiotics
 Humans *Neuromyelitis Optica/complications/epidemiology Prospective Studies Aquaporin 4 Cognition *Multiple Sclerosis Immunoglobulin G Autoantibodies
 Female Humans Adult Male *Multiple Sclerosis Oligoclonal Bands/cerebrospinal fluid Case-Control Studies Immunoglobulin kappa-Chains/cerebrospinal fluid Prospective Studies Immunoglobulin Light Chains/cerebrospinal fluid Immunoglobulin lambda-Chains/cerebrospinal fluid Biomarkers
 Adolescent Adult Humans Female Male *Multiple Sclerosis COVID-19 Vaccines/adverse effects Antibody Formation Prospective Studies *COVID-19/prevention & control SARS-CoV-2 Vaccination *Autoimmune Diseases Autoantibodies
 Humans *Neurodegenerative Diseases/genetics *Frontotemporal Dementia *Amyotrophic Lateral Sclerosis/genetics Mendelian Randomization Analysis *Alzheimer Disease *Parkinson Disease *Multiple Sclerosis *Renal Insufficiency, Chronic/genetics Kidney/physiology Genome-Wide Association Study Polymorphism, Single Nucleotide
 Mice Animals Fingolimod Hydrochloride/pharmacology/therapeutic use Immunosuppressive Agents/pharmacology Neuroinflammatory Diseases Bezafibrate Propylene Glycols/pharmacology *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism *Multiple Sclerosis Neuroglia/metabolism Fatty Acids
 Humans Amino Acid Transport System X-AG *Amyotrophic Lateral Sclerosis Cystine/metabolism *Parkinson Disease *Alzheimer Disease Antioxidants Glutamic Acid/metabolism Microglia/metabolism *Multiple Sclerosis *Glioma Amino Acid Transport System y+/genetics/metabolism
 Female Humans Infant, Newborn Pregnancy *Endogenous Retroviruses/genetics Genes, env *Histone-Lysine N-Methyltransferase/genetics/metabolism Mothers *Multiple Sclerosis RNA, Messenger *Tripartite Motif-Containing Protein 28/genetics/metabolism Epigenesis, Genetic *Pregnancy Complications
 Humans Female Adult *Fingolimod Hydrochloride/therapeutic use Natalizumab/adverse effects Dimethyl Fumarate/adverse effects Neoplasm Recurrence, Local/drug therapy *Multiple Sclerosis, Relapsing-Remitting/drug therapy Immunosuppressive Agents/adverse effects Immunologic Factors/adverse effects Recurrence
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Fibronectins/adverse effects Receptor, Platelet-Derived Growth Factor beta/genetics Myelin-Oligodendrocyte Glycoprotein Pericytes/metabolism/pathology *Multiple Sclerosis Mice, Inbred C57BL Disease Models, Animal
 Humans *Neurodegenerative Diseases/drug therapy/genetics/metabolism *Alzheimer Disease/drug therapy/genetics/metabolism *Parkinson Disease/metabolism *Amyotrophic Lateral Sclerosis/genetics/metabolism Genome-Wide Association Study Proteomics Brain/metabolism *Multiple Sclerosis/metabolism Sodium-Phosphate Cotransporter Proteins, Type III/genetics/metabolism Membrane Glycoproteins/metabolism 17-Hydroxysteroid Dehydrogenases/metabolism
 Humans *Multiple Sclerosis Cerebral Infarction/diagnostic imaging/genetics/pathology *Leukoencephalopathies/diagnostic imaging/genetics *Cerebrovascular Disorders/genetics Alopecia/diagnosis/genetics Mutation *Cerebral Arterial Diseases High-Temperature Requirement A Serine Peptidase 1/genetics
 Humans BNT162 Vaccine *COVID-19/prevention & control *COVID-19 Vaccines/adverse effects/therapeutic use *Drug-Related Side Effects and Adverse Reactions Fatigue Fever Immunosuppressive Agents *Multiple Sclerosis *Neuromyelitis Optica Pain Retrospective Studies RNA, Viral SARS-CoV-2 Steroids Vaccination/adverse effects Demyelinating Diseases
 Mice Humans Animals Receptors, Tumor Necrosis Factor, Type I/genetics/metabolism Receptors, Tumor Necrosis Factor, Type II/genetics/metabolism *Multiple Sclerosis Tumor Necrosis Factor Inhibitors *Encephalomyelitis, Autoimmune, Experimental/metabolism Tumor Necrosis Factor-alpha/metabolism Antibodies/therapeutic use
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism NF-kappa B/metabolism Granulocyte-Macrophage Colony-Stimulating Factor/therapeutic use NF-KappaB Inhibitor alpha Tumor Necrosis Factor-alpha/metabolism Interleukin-6 Mice, Inbred Strains *Multiple Sclerosis Protein Kinase Inhibitors Mitogen-Activated Protein Kinases/metabolism RNA, Messenger/metabolism B-Lymphocytes/metabolism
 Animals Mice *Multiple Sclerosis *MicroRNAs/genetics/metabolism Nuclear Receptor Subfamily 1, Group F, Member 3/genetics Vitamins Vitamin A/pharmacology/therapeutic use Disease Models, Animal Neuroinflammatory Diseases Mice, Inbred C57BL *Encephalomyelitis, Autoimmune, Experimental/metabolism Vitamin K Th17 Cells/metabolism
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy/pathology Blood-Brain Barrier/pathology *Gastrointestinal Microbiome/physiology Dysbiosis/drug therapy RNA, Ribosomal, 16S/genetics Tandem Mass Spectrometry *Multiple Sclerosis Sulfadiazine/pharmacology/therapeutic use Homeostasis Mice, Inbred C57BL
 Humans Mice Animals Myelin Sheath/metabolism/pathology *Induced Pluripotent Stem Cells/pathology *Oligodendrocyte Precursor Cells/pathology Oligodendroglia/metabolism *Multiple Sclerosis *Canavan Disease/genetics/metabolism/pathology



































































































































































































 Humans *Cytokines/cerebrospinal fluid *Amyotrophic Lateral Sclerosis Intercellular Signaling Peptides and Proteins Enzyme-Linked Immunosorbent Assay/methods Biomarkers/cerebrospinal fluid









































 Humans *Emotions *Caregivers/psychology




 Humans *Tai Ji Quality of Life


























































































 Humans *Empyema, Subdural/etiology SARS-CoV-2 *COVID-19/complications Tomography, X-Ray Computed Diagnosis, Differential *Empyema/etiology



 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy RNA, Transfer Structure-Activity Relationship Pentosyltransferases/metabolism
 Child Adolescent Humans Female Pregnancy *Diabetes Mellitus, Type 1 Pregnant Women *Autoimmune Diseases *Arthritis, Rheumatoid/complications *Virus Diseases/complications/epidemiology






























 Humans *Medical Tourism *Meningitis/drug therapy *Mycobacterium abscessus/physiology *Mycobacterium Infections, Nontuberculous/diagnosis/etiology/drug therapy Stem Cells














































 Male Female Humans *Neurodegenerative Diseases/therapy/pathology Sex Factors Sex Characteristics *Parkinson Disease/pathology Neurons/pathology


 Humans *Nervous System Diseases/genetics Epigenesis, Genetic *Parkinson Disease/genetics DNA Methylation/genetics Chromatin
























 Mice Animals Humans *CA2 Region, Hippocampal/physiology *Autism Spectrum Disorder Hippocampus Interneurons/physiology Neuronal Plasticity/physiology




















































































 Humans *Syndemic *Mental Disorders Mental Health Social Stigma



































 Adult Humans *Cognitive Behavioral Therapy *Mindfulness
 Humans *Diffuse Cerebral Sclerosis of Schilder/diagnostic imaging/drug therapy/pathology Antibodies, Monoclonal, Humanized/adverse effects Magnetic Resonance Imaging Brain/pathology






























 Humans *Neurodegenerative Diseases Brain Executive Function Cognition Basal Ganglia
 Humans Animals Mice *Blood-Brain Barrier *T-Lymphocytes Protein Transport Cell Culture Techniques Cell Movement















 Humans *Gold Myelin Sheath *Metal Nanoparticles Peptides/pharmacology



















 Humans *Neuromyelitis Optica/diagnosis

 Female Male Humans *Neuromyelitis Optica Aquaporin 4 Rituximab/therapeutic use Azathioprine/therapeutic use Retrospective Studies Immunoglobulins, Intravenous/therapeutic use Immunoglobulin G Autoantibodies Immunosuppressive Agents/therapeutic use Enzyme Inhibitors/therapeutic use Recurrence Myelin-Oligodendrocyte Glycoprotein


 Humans *Diabetes Mellitus, Type 2 *COVID-19 SARS-CoV-2 Immunoglobulin Light Chains Immunoglobulin lambda-Chains Biomarkers Inflammation



 Humans Central Nervous System/metabolism Mitochondria/metabolism *Neurodegenerative Diseases/metabolism *Parkinson Disease/metabolism *Sirtuin 3/metabolism

 Humans *Extracellular Vesicles *Exosomes *Alzheimer Disease *Parkinson Disease Blood-Brain Barrier


 Microglia Culture Media, Conditioned/pharmacology *Mesenchymal Stem Cells *Neural Stem Cells Stem Cell Transplantation










 Child Humans *Demyelinating Diseases

 Humans *T-Lymphocytes, Regulatory *Autoimmune Diseases Th17 Cells




 Humans *White Matter Brain *Neuromyelitis Optica *Nervous System Diseases











 Humans *Calreticulin/genetics Calnexin/genetics/chemistry/metabolism Calcium-Binding Proteins/genetics/metabolism Ribonucleoproteins/genetics/metabolism *Neoplasms



































































 Humans Cytokines *Neurodegenerative Diseases *Alzheimer Disease Inflammation Brain
 *Gene Editing/methods *CRISPR-Cas Systems Genome-Wide Association Study Autoimmunity Polymorphism, Single Nucleotide

 Animals *Microglia/metabolism *Encephalomyelitis, Autoimmune, Experimental/pathology Central Nervous System/metabolism T-Lymphocytes, Helper-Inducer/metabolism
 Humans Neuroinflammatory Diseases *Neurodegenerative Diseases/diagnosis/metabolism *Extracellular Vesicles/metabolism Complement System Proteins/metabolism Biomarkers/metabolism




 Animals *Limosilactobacillus reuteri Immunomodulation Anti-Bacterial Agents Antibodies Antioxidants
 Humans Palliative Care Caregivers *Nervous System Diseases/therapy Quality of Life *Parkinson Disease *Terminal Care














 Animals Humans *Neurodegenerative Diseases/therapy *Amyotrophic Lateral Sclerosis/therapy Stem Cells *Huntington Disease/pathology/therapy *Alzheimer Disease *Parkinson Disease/therapy























































 Adolescent Adult Female Humans Male Young Adult Mutation *Neurofibromatosis 1/genetics/diagnosis





 Female Humans Middle Aged *Graves Disease/complications/drug therapy Autoantibodies *Graves Ophthalmopathy *Thyroiditis, Autoimmune *Hyperthyroidism




 Animals Mice Receptors, Cell Surface/metabolism *Semaphorins/metabolism Signal Transduction *Single-Domain Antibodies *Cell Adhesion Molecules/metabolism
 Humans *Epstein-Barr Virus Infections Herpesvirus 4, Human/genetics *Lymphoma *Lymphoproliferative Disorders/complications *Nasopharyngeal Neoplasms

 Adult Humans Child Female Prospective Studies Retrospective Studies *Optic Neuritis/diagnosis/epidemiology Optic Nerve *Optic Nerve Diseases





 *Membrane Proteins/metabolism Myelin Sheath/metabolism Nerve Tissue Proteins/metabolism *Nogo Proteins/metabolism Oligodendroglia/metabolism *Remyelination Humans
 Humans Adipose Tissue *Arthritis, Rheumatoid Obesity/pathology Immunomodulation *Mesenchymal Stem Cells
 Humans *Activities of Daily Living/psychology Quality of Life Cognition *Occupational Therapy Processing Speed
 *Myelin Sheath/metabolism *Oligodendroglia/metabolism Crotonates/pharmacology/therapeutic use Hydroxybutyrates/metabolism/pharmacology Cell Differentiation





 Humans *Ischemic Stroke *Neurodegenerative Diseases Peptides Transcription Factors


 Animals Humans *Neurodegenerative Diseases/genetics Neuroinflammatory Diseases Genome-Wide Association Study Inflammation

 Humans *Virus Diseases *Autoimmune Diseases *Nervous System Diseases Autoimmunity Autoantibodies


 Humans *Neuroimmunomodulation *Inflammation
 Humans Female Middle Aged *Paraparesis, Spastic Cognition Magnetic Resonance Imaging



 Humans Autoimmunity *Gastrointestinal Microbiome *Autoimmune Diseases Dietary Fiber Immune Tolerance Fatty Acids, Volatile/metabolism

 Humans *Autonomic Nervous System Heart Rate/physiology *Vagus Nerve Fatigue/etiology Inflammation/metabolism



 Humans *Neuroinflammatory Diseases Interleukin-17 Interleukin-6 Interleukins Inflammation/drug therapy Cytokines Th17 Cells Interleukin-1/therapeutic use *Autoimmune Diseases

















 Humans *COVID-19/epidemiology Cross-Sectional Studies Pandemics Adaptation, Psychological Chronic Disease

 Adult Humans Female Middle Aged Male Prevalence Cross-Sectional Studies Retrospective Studies *Complementary Therapies/methods *Nervous System Diseases/epidemiology/therapy *Stroke
























 *Autoimmunity Autoimmune Diseases Humans Animals Longevity Diet Microbiota Vitamin D/metabolism














 Animals Mice *Encephalomyelitis, Autoimmune, Experimental Inflammation/drug therapy/metabolism *Macrophage Migration-Inhibitory Factors/metabolism Mice, Inbred C57BL Microglia/metabolism Molecular Docking Simulation
 Humans Quality of Life *Vitamin D Deficiency/complications Vitamin D *Alzheimer Disease/etiology Vitamins *Neurodegenerative Diseases/complications

 Humans Vitamin D/physiology *Graves Disease/epidemiology *Autoimmune Diseases Vitamins *Hashimoto Disease
 Humans Dendritic Cells/metabolism Immune Tolerance *Interleukin-10/metabolism Monocytes/metabolism *Receptors, Aryl Hydrocarbon/genetics/metabolism










 Animals Humans Mice Immunoglobulin M Myelin Sheath/metabolism Oligodendroglia/metabolism *Remyelination Sulfoglycosphingolipids/metabolism Lipids/immunology
 Humans Central Nervous System *Leukoencephalopathy, Progressive Multifocal *Cytomegalovirus Infections *Opportunistic Infections *Central Nervous System Diseases/therapy Antiviral Agents/therapeutic use Cell- and Tissue-Based Therapy



 Humans *Antibodies, Monoclonal/therapeutic use Pandemics *COVID-19 Europe/epidemiology Personal Satisfaction Surveys and Questionnaires



 Humans *Pontine Tegmentum Eye Movements *Demyelinating Diseases/diagnosis





























 Humans *COVID-19/complications/epidemiology/prevention & control *COVID-19 Vaccines/adverse effects *Guillain-Barre Syndrome/epidemiology/etiology *Myelitis, Transverse Pandemics Vaccination/adverse effects *Venous Thrombosis



 Humans Autoimmunity Cell Adhesion Molecules, Neuronal Dyspnea Muscle Weakness Paralysis *Respiration Disorders *Respiratory Paralysis/diagnosis/etiology
 Humans *Employment *Workplace Health Personnel Knowledge




 Humans *Cannabidiol/pharmacology PPAR gamma/metabolism Sclerosis *Cannabis Seizures


 Mice Animals *Myelin Sheath/pathology *Sulfoglycosphingolipids Mice, Knockout Axons/physiology Neurons Mice, Transgenic
 Animals Mice Autophagy *Encephalomyelitis, Autoimmune, Experimental Inflammation/pathology Mice, Inbred C57BL Mice, Knockout Microglia/metabolism Phosphatidylinositol 3-Kinases/metabolism Proto-Oncogene Proteins c-akt/metabolism Signal Transduction TOR Serine-Threonine Kinases/metabolism *Axl Receptor Tyrosine Kinase/metabolism



 Humans *Neurodegenerative Diseases Retrospective Studies *Inflammatory Bowel Diseases/complications Inflammation Comorbidity
 Female Pregnancy Mice Animals *Nanocapsules *Preimplantation Diagnosis Anti-Inflammatory Agents/pharmacology Lipopolysaccharides/pharmacology Brain Cytokines


 Female Humans COVID-19 Vaccines/adverse effects Pandemics *COVID-19/complications *Diabetes Insipidus/etiology *Hypophysitis *Optic Neuritis *Diabetes Mellitus






 Animals Mice Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors *Encephalomyelitis, Autoimmune, Experimental/drug therapy Fingolimod Hydrochloride/therapeutic use Mice, Biozzi Myeloid Cells
 Humans Mice Animals *Platelet Activation Fibrinolytic Agents Dimethyl Fumarate/pharmacology/therapeutic use/metabolism Thrombin/metabolism/pharmacology Platelet Aggregation Blood Platelets/metabolism *Thrombosis/drug therapy/etiology/metabolism
 Animals *Autoimmune Diseases/therapy Autophagy *Lupus Erythematosus, Systemic/therapy *Arthritis, Rheumatoid Histocompatibility Antigens Class II/metabolism Autoantigens
 Mice Animals Receptors, Galanin/genetics/metabolism *Galanin/genetics/metabolism *Encephalomyelitis, Autoimmune, Experimental Endothelial Cells Receptor, Galanin, Type 2/genetics/metabolism RNA, Messenger/metabolism Spinal Cord/metabolism

 Humans *Nucleic Acids/metabolism Neuroinflammatory Diseases Brain/metabolism *MicroRNAs/genetics Alarmins/metabolism *Neurodegenerative Diseases/genetics
 Humans *Hepatitis B virus Hepatitis B Vaccines/therapeutic use Cohort Studies *Hepatitis B/drug therapy/prevention & control Hepatitis B Antibodies










 Animals *Autoimmunity T-Lymphocytes *Encephalomyelitis, Autoimmune, Experimental Antigens Receptors, Antigen, T-Cell/genetics






 Humans Female Middle Aged Male Rituximab/adverse effects Retrospective Studies *Agammaglobulinemia/chemically induced/epidemiology/complications Immunoglobulin G Immunoglobulin A *Lymphopenia/chemically induced/epidemiology




















 Humans Fecal Microbiota Transplantation *Neurodegenerative Diseases/therapy *Gastrointestinal Microbiome *Microbiota *Clostridium Infections/therapy Dysbiosis/therapy























 Mice Humans Animals *Microglia/metabolism Bone Marrow/metabolism Autoimmunity/genetics Transcriptome Epigenomics Mice, Inbred C57BL Central Nervous System *Encephalomyelitis, Autoimmune, Experimental Myeloid Cells/metabolism
 Humans *Reaction Time/physiology Neuropsychological Tests





 Rats Animals Mice *Encephalomyelitis, Autoimmune, Experimental/therapy Microglia/metabolism Phenotype Cyclophosphamide/therapeutic use *Hematopoietic Stem Cell Transplantation Mice, Inbred C57BL
 Animals Humans Inflammation Kelch-Like ECH-Associated Protein 1/genetics/metabolism *Neurodegenerative Diseases *NF-E2-Related Factor 2/genetics/metabolism Oxidative Stress Ubiquitin-Protein Ligases/genetics
 Humans Adult Prospective Studies Surveys and Questionnaires Fear *Spinal Cord Injuries *Wheelchairs
 Mice Animals *Cuprizone/toxicity Astrocytes/metabolism *Demyelinating Diseases/pathology Neuroglia/metabolism Corpus Callosum/pathology Disease Models, Animal Mice, Inbred C57BL Myelin Sheath/metabolism Oligodendroglia/metabolism
 Humans *Antibodies Biological Assay *Biological Products Enzyme-Linked Immunosorbent Assay Natalizumab/adverse effects Disease Progression


 Female Humans *Contraception *Contraceptives, Oral Fatigue Menstrual Cycle Pilot Projects Adult





 Humans Cohort Studies Taiwan/epidemiology *Autoantibodies Aquaporin 4 Myelin-Oligodendrocyte Glycoprotein *Optic Neuritis/diagnostic imaging/epidemiology/drug therapy Prognosis






 Humans *Myeloid Differentiation Factor 88/genetics Autoimmunity/genetics Polymerase Chain Reaction Mutation *Neoplasms


 Humans *Immune Tolerance *Dendritic Cells




 Humans Male Female *Disabled Persons Social Support Caregivers







 Animals Cell Differentiation Cyclic AMP *Encephalomyelitis, Autoimmune, Experimental/genetics *Receptors, G-Protein-Coupled/genetics/agonists T-Lymphocytes, Regulatory Humans












 Humans *Chemokines, CXC Receptors, Scavenger CD8-Positive T-Lymphocytes Endothelial Cells Receptors, CXCR6 Receptors, Virus Chemokine CXCL16 *Autoimmune Diseases
 Female Humans Male COVID-19 Vaccines/adverse effects Retrospective Studies *COVID-19/prevention & control Neoplasm Recurrence, Local Central Nervous System *Neuromyelitis Optica Cohort Studies Inflammation/etiology Vaccination/adverse effects Myelin-Oligodendrocyte Glycoprotein

 Mice Animals *Autoantigens *Antibody-Producing Cells B-Lymphocytes Lymphocytic choriomeningitis virus Brain
 Mice Animals *Remyelination *Demyelinating Diseases Chemokine CX3CL1 Oligodendroglia/physiology Myelin Sheath Disease Models, Animal Cell Differentiation/physiology Mice, Inbred C57BL
 Humans *Myelin Sheath Magnetic Resonance Imaging/methods Reproducibility of Results Brain/diagnostic imaging/pathology *White Matter/diagnostic imaging/pathology


 Mice Humans Animals *4-Aminopyridine/toxicity/therapeutic use Amyloid Precursor Protein Secretases/metabolism *Alzheimer Disease/drug therapy Peptides/pharmacology Cell Line, Tumor



 Humans Child Artificial Intelligence *Autism Spectrum Disorder *Disabled Persons *Motor Disorders *Virtual Reality *Nervous System Diseases
 Mice Animals Astrocytes Depression/therapy *Depressive Disorder, Major/metabolism Anxiety *Autoimmune Diseases of the Nervous System/metabolism/pathology
 Humans Liquid Biopsy/methods *Cell-Free Nucleic Acids *MicroRNAs *Central Nervous System Neoplasms Biomarkers
 Male Child Humans *Encephalomyelitis, Acute Disseminated/diagnostic imaging/etiology Adenoviridae Brain/pathology Magnetic Resonance Imaging/methods *Adenoviridae Infections *Encephalomyelitis/pathology











 Humans *Interferon Type I/metabolism *Nervous System Diseases Brain/metabolism *Autoimmune Diseases Microglia/metabolism *Neurotoxicity Syndromes
 Humans *COVID-19 Vaccines Sphingosine *COVID-19 SARS-CoV-2 Antibodies, Neutralizing Antibodies, Viral Vaccination







 *Proline/pharmacology/chemistry *Microglia Azetidinecarboxylic Acid/pharmacology/chemistry Amino Acids Endoplasmic Reticulum Stress


 *Biotin *Myelin Basic Protein/metabolism Myelin Sheath/metabolism Proteins *Proteomics/methods Protein Interaction Maps
 Humans Lung *Lung Diseases Bacteria *Microbiota *Brain Diseases
 Humans *Neuromyelitis Optica/therapy Autoantibodies Aquaporin 4









 Humans *Artificial Intelligence *Radiology/methods Radiologists Delivery of Health Care Stakeholder Participation











 Humans *Mitogen-Activated Protein Kinase 14/metabolism *COVID-19 Benzamides Protein Kinase Inhibitors/therapeutic use *Neoplasms/drug therapy Pharmaceutical Preparations

 Humans Neurologists Physician-Patient Relations Emotions *Physicians *Neurodegenerative Diseases/diagnosis

 Humans *Oligoclonal Bands Myelin-Oligodendrocyte Glycoprotein Chronic Disease *Central Nervous System Immunoglobulin G
 Humans Microglia/metabolism Macrophages/metabolism *Central Nervous System Diseases/metabolism Phagocytosis/physiology *Neurodegenerative Diseases/metabolism

 Humans *Extracellular Vesicles/metabolism Brain *Mesenchymal Stem Cells/metabolism Drug Delivery Systems/methods *Neurodegenerative Diseases/therapy/metabolism
 Mice Animals Granulocyte-Macrophage Colony-Stimulating Factor/therapeutic use RNA, Ribosomal, 16S *Encephalomyelitis, Autoimmune, Experimental/drug therapy/genetics Spinal Cord/pathology *Encephalomyelitis/pathology Mice, Inbred C57BL

 Humans *HMGB1 Protein/metabolism *Brain Injuries, Traumatic *Amyotrophic Lateral Sclerosis *Parkinson Disease Inflammation Neuroinflammatory Diseases










 Adolescent Humans Adult Child *Patient Transfer *Transition to Adult Care Chronic Disease
 Humans *Muscular Atrophy, Spinal *Amyloid Neuropathies, Familial/drug therapy Disease Progression *Alzheimer Disease


 Female Humans Cross-Sectional Studies *Alzheimer Disease Emotions *Stroke/complications/psychology *Cognitive Dysfunction




 Humans Male *Amyotrophic Lateral Sclerosis/complications Disease Progression Killer Cells, Natural
 Humans Eicosapentaenoic Acid/pharmacology Docosahexaenoic Acids/therapeutic use/metabolism *Neurodegenerative Diseases/drug therapy *Fatty Acids, Omega-3/therapeutic use Fatty Acids, Unsaturated/metabolism Arachidonic Acid/metabolism Linoleic Acids Inflammation/drug therapy

 Humans Natalizumab *T-Lymphocytes *Blood-Brain Barrier Intercellular Adhesion Molecule-1 Integrin alpha4 CD4-Positive T-Lymphocytes
 Humans Retrospective Studies Positron Emission Tomography Computed Tomography/adverse effects Myelin-Oligodendrocyte Glycoprotein Autoantibodies *Myelitis/diagnostic imaging/etiology *Neuromyelitis Optica/complications/diagnostic imaging *Spinal Cord Diseases/etiology/complications Aquaporin 4 Immunoglobulin G
 Animals *Neuromyelitis Optica/diagnosis Aquaporin 4/analysis Chromatography, Liquid Tandem Mass Spectrometry Biomarkers Autoantibodies Immunoglobulin G Myelin-Oligodendrocyte Glycoprotein

 Humans *Neurodegenerative Diseases/pathology Interferon-alpha/therapeutic use Cytokines Databases, Factual
 Humans *Occupational Injuries Neuroinflammatory Diseases Gliosis/metabolism Central Nervous System/metabolism *Neurodegenerative Diseases/metabolism Microglia/metabolism


 Mice Animals Glatiramer Acetate/therapeutic use *Encephalomyelitis, Autoimmune, Experimental/pathology Peptides/pharmacology Inflammation/drug therapy Mice, Transgenic *Encephalomyelitis/drug therapy Disease Progression

 Humans *Hepatitis A Virus Cellular Receptor 2 Ligands Mucins Membrane Proteins *Autoimmune Diseases T-Lymphocytes Inflammation Immunoglobulins
 Humans Child *Myelitis, Transverse/diagnosis/etiology *Spinal Cord Diseases Antibodies *Autonomic Nervous System Diseases
 Humans *T-Lymphocytes, Regulatory T Follicular Helper Cells T-Lymphocytes, Helper-Inducer Cytokines *Autoimmune Diseases
 Female Humans Aged *Alzheimer Disease/diagnostic imaging/metabolism Microglia Activities of Daily Living Positron-Emission Tomography/methods Brain/diagnostic imaging/metabolism


 Aged Humans United States *Long-Term Care Medicare Nursing Homes Skilled Nursing Facilities *Medicine













 Humans Anxiety *Mental Disorders *Microbiota Anxiety Disorders *Gastrointestinal Microbiome


 Humans Rilpivirine/therapeutic use *Anti-HIV Agents/therapeutic use *HIV Infections/prevention & control Pyridones/therapeutic use *COVID-19/prevention & control SARS-CoV-2 *Vaccines





 Humans *Myelin Sheath *Demyelinating Diseases Neuroglia Central Nervous System/physiology Nerve Regeneration Oligodendroglia/physiology




 Humans RNA Splicing/genetics Spliceosomes/genetics/metabolism *Muscular Dystrophy, Duchenne/genetics/therapy/metabolism *Muscular Atrophy, Spinal/genetics/metabolism RNA Precursors/metabolism
 Humans *Music Therapy/methods Acoustic Stimulation/methods *Music Gait/physiology *Parkinson Disease/rehabilitation *Wearable Electronic Devices
 Humans *COVID-19/complications *Autoimmune Diseases/epidemiology/genetics *Virus Diseases/complications/epidemiology Autoimmunity Autoantigens
 Female Humans *Gastrointestinal Microbiome *COVID-19 Lactobacillus *Autoimmune Diseases *Probiotics/therapeutic use

 Middle Aged Female Humans Spectroscopy, Fourier Transform Infrared Quality of Life *Photochemotherapy/methods Photosensitizing Agents *Autoimmune Diseases/diagnosis/therapy

 Humans *Longevity Intermediate Filaments *Cognitive Dysfunction Cognition Dopamine Inflammation

 Mice Animals *Aspartic Acid/pharmacology *Histone Deacetylases/metabolism Myelin Sheath/metabolism Cell Differentiation

 Male Child Humans Aged Thymus Gland T-Lymphocytes Aging Immunologic Factors/pharmacology/therapeutic use Adjuvants, Immunologic *Autoimmune Diseases *Neoplasms Inflammation
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Microglia/metabolism Interferon-gamma/metabolism B7-H1 Antigen/metabolism Central Nervous System



 Rats Animals *T-Lymphocytes 2-Methoxyestradiol *Encephalomyelitis, Autoimmune, Experimental/drug therapy Rats, Inbred Lew Pharmaceutical Preparations

 Male Animals Mice *Mitoxantrone Metabolomics Glutathione Brain *Chemotherapy-Related Cognitive Impairment Metabolic Networks and Pathways Lipids
 Animals *Stearoyl-CoA Desaturase/genetics/metabolism Autoimmunity Fatty Acids/metabolism Cell Differentiation *Autoimmune Diseases


 Humans *Neurodegenerative Diseases Brain-Gut Axis *Parkinson Disease/therapy *Gastrointestinal Microbiome/physiology *Probiotics/therapeutic use Brain

 Mice Animals *Amyloid beta-Peptides Cellular Senescence/genetics *Alzheimer Disease/genetics Aging/physiology














 Humans *Endogenous Retroviruses/genetics/metabolism Immunoglobulins/genetics *Neoplasms/genetics/therapy/virology Databases, Genetic RNA, Viral
 Humans Dysarthria/etiology Speech/physiology *Cerebellar Ataxia *Parkinson Disease/complications Articulation Disorders Atrophy Speech Acoustics Speech Intelligibility
 Humans *CD8-Positive T-Lymphocytes Cytokines Central Nervous System *Amyotrophic Lateral Sclerosis





 Humans Aged *Antibody Formation SARS-CoV-2 BNT162 Vaccine *COVID-19/prevention & control Vaccination Antibodies, Monoclonal Antilymphocyte Serum RNA, Messenger





 Humans Resveratrol/pharmacology *Cytokines/metabolism *Neuroinflammatory Diseases Neuroglia/metabolism Microglia Astrocytes Inflammation/metabolism





 Humans *Niacin/therapeutic use/metabolism Amyloid beta-Peptides *Pellagra/metabolism *Nervous System Diseases *Alzheimer Disease *Neurology


 Humans *Deep Learning Algorithms Brain/diagnostic imaging Head
 *Dependovirus/genetics *Microglia Capsid Transgenes Macrophages

 Humans *Endogenous Retroviruses/genetics *Mental Disorders/genetics
 Humans Female Middle Aged COVID-19 Vaccines BNT162 Vaccine Immunomodulating Agents Prospective Studies *COVID-19/prevention & control SARS-CoV-2 *Arthritis, Rheumatoid Antibodies, Viral

 Humans Quality of Life Accidental Falls *Robotics Fear *Stroke/psychology *Stroke Rehabilitation/methods *Virtual Reality




 Humans *Methylprednisolone/pharmacology *Oligodendroglia Myelin Sheath Axons Cell Differentiation


 Humans Antibodies, Monoclonal/adverse effects Blood-Brain Barrier Central Nervous System *Brain Neoplasms/drug therapy *Alzheimer Disease/drug therapy
 Female Humans *Critical Pathways *Nurse Specialists
 Female Humans Middle Aged Male *Quality of Life/psychology Cross-Sectional Studies *Social Support Patients Germany
 Humans *Epstein-Barr Virus Infections Herpesvirus 4, Human/genetics Virus Latency/genetics *Autoimmune Diseases B-Lymphocytes Epstein-Barr Virus Nuclear Antigens
 Humans *Neurodegenerative Diseases/metabolism Microglia/metabolism Brain/pathology Up-Regulation

 Animals Rats Humans *Altitude Sickness Rats, Sprague-Dawley Verrucomicrobia *Gastrointestinal Diseases Hypoxia






 *Alkaloids/pharmacology/therapeutic use/chemistry *Neuroprotective Agents/pharmacology/therapeutic use Matrines Signal Transduction Brain
 Humans *Schizophrenia Toll-Like Receptors Central Nervous System Inflammation Brain Cytokines

 Humans CD8-Positive T-Lymphocytes *Alzheimer Disease *Neurodegenerative Diseases *Infectious Encephalitis *Encephalitis Cerebral Infarction Inflammation


 Humans Laboratories, Clinical Intermediate Filaments Neurofilament Proteins *Alzheimer Disease Biomarkers *Nervous System Diseases/diagnosis
 Female Humans *Progestins/pharmacology/therapeutic use/metabolism Progesterone/pharmacology/therapeutic use/metabolism Neuroprotection *Alzheimer Disease/metabolism Neurons/metabolism

 Humans Rituximab/therapeutic use *Autoimmune Diseases/drug therapy *Arthritis, Rheumatoid Autoimmunity B-Lymphocytes
 Humans Vitamin D/therapeutic use *Hypercalcemia/chemically induced Vitamins/therapeutic use *Sarcoidosis/drug therapy *Acute Kidney Injury Calcium/therapeutic use





 Humans Interleukin-17 Neuroinflammatory Diseases *Neurodegenerative Diseases Cytokines *Autoimmune Diseases




 Humans Cohort Studies *Myasthenia Gravis *Cerebrovascular Disorders *Stroke Thrombectomy *Neurology *Epilepsy Treatment Outcome

 Humans Brain/diagnostic imaging *Aphasia, Primary Progressive/diagnostic imaging *Cognitive Dysfunction/diagnosis Neuropsychological Tests
 Animals Axons/metabolism *Demyelinating Diseases/metabolism Disease Models, Animal Histidine/metabolism Humans Myelin Proteins/metabolism Myelin Sheath/metabolism Oligodendroglia/metabolism *Remyelination
 Humans *Neoplasms/drug therapy Apoptosis Epithelial-Mesenchymal Transition Hydrolases

 Humans Neuropharmacology Antioxidants/pharmacology/therapeutic use/chemistry *Mental Disorders/drug therapy *Organoselenium Compounds/pharmacology/therapeutic use/chemistry




 Humans Pandemics *COVID-19/epidemiology *Sleep Initiation and Maintenance Disorders/epidemiology Quality of Life Cross-Sectional Studies *Sleep Wake Disorders/epidemiology *Parkinson Disease/complications/epidemiology *Demyelinating Diseases Depression/epidemiology

 Male Mice Animals Humans *Astrocytes/metabolism *NF-E2-Related Factor 2/genetics/metabolism Central Nervous System/metabolism Oligodendroglia/metabolism Myelin Sheath/metabolism Nerve Regeneration/physiology Cholesterol/metabolism

 Humans Cholesterol 24-Hydroxylase/metabolism *Cholesterol/metabolism *Alzheimer Disease/metabolism Brain/metabolism
 Humans *Suicide/psychology Suicidal Ideation Suicide Prevention *Parkinson Disease/psychology *Epilepsy/psychology
 Humans *Parkinson Disease/complications Smartphone Gait Walking *Stroke/complications Back Pain
 Humans *Cervical Cord/diagnostic imaging Reproducibility of Results Diffusion Magnetic Resonance Imaging/methods Spinal Cord/diagnostic imaging Signal-To-Noise Ratio Algorithms


 Humans *MicroRNAs/genetics/therapeutic use/metabolism *Neurodegenerative Diseases/diagnosis/genetics/therapy *Alzheimer Disease/metabolism *Huntington Disease Biomarkers/metabolism
 Humans Prospective Studies *Neurodegenerative Diseases/metabolism/therapy *Mesenchymal Stem Cells/metabolism *Parkinson Disease *Alzheimer Disease/metabolism




 Humans *Sulfatases/genetics *COVID-19/genetics Polymorphism, Genetic Oxidoreductases Acting on Sulfur Group Donors/genetics
 Adult Aged Humans Middle Aged Young Adult Cognition *East Asian People Healthy Volunteers Japan Neuropsychological Tests *Processing Speed United States
 Humans Female *COVID-19/complications SARS-CoV-2 *Myelitis/diagnostic imaging/etiology Magnetic Resonance Imaging Hemorrhage/etiology/complications


 Humans *Receptors, AMPA/metabolism *Nervous System Diseases Synaptic Transmission Glutamic Acid/physiology Endocytosis



 Animals Humans Mice Basic Helix-Loop-Helix Transcription Factors *Colitis/chemically induced/genetics Colon/pathology Dextran Sulfate Disease Models, Animal Disease Progression *Encephalomyelitis, Autoimmune, Experimental/genetics/pathology Mice, Inbred C57BL *Microbiota Th17 Cells

 Humans Cognition/physiology *Cognitive Dysfunction/etiology/rehabilitation Exercise Therapy Memory/physiology Treatment Outcome
 Animals Mice *Inflammasomes/metabolism Monocytes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism Leukocytes, Mononuclear/metabolism Interleukin-11/genetics/metabolism Central Nervous System/metabolism *Encephalomyelitis, Autoimmune, Experimental Cell Movement

 Humans *Chemokines, CC *Monocyte Chemoattractant Proteins



 Humans Adult *Susac Syndrome/diagnosis/drug therapy/pathology Magnetic Resonance Imaging Brain/pathology *Hearing Loss, Sensorineural/diagnosis/etiology Prognosis Diagnosis, Differential



 Humans *Peroxidase/metabolism *Halogenation Imidazoles Benzimidazoles/pharmacology

 Humans *Microglia/pathology Brain/physiology Central Nervous System Macrophages *Brain Diseases/pathology
 Animals Humans *Caloric Restriction Diet *Stroke Longevity



 Humans *Arrestin/metabolism *Receptors, G-Protein-Coupled/metabolism beta-Arrestins/metabolism Dynamins/metabolism Endocytosis/physiology Clathrin/metabolism Caveolins/metabolism Receptors, Peptide/metabolism




 Humans *Receptors, sigma/metabolism/therapeutic use *Amyotrophic Lateral Sclerosis Neurons/metabolism *Huntington Disease *Neurodevelopmental Disorders/drug therapy/metabolism
 Humans *Neuromyelitis Optica/surgery *Hematopoietic Stem Cell Transplantation Aquaporin 4 Transplantation, Autologous
 Humans *Amyotrophic Lateral Sclerosis/complications/diagnostic imaging/pathology Longitudinal Studies *Bulbo-Spinal Atrophy, X-Linked Retina/diagnostic imaging/pathology *Motor Neuron Disease/pathology *Retinal Degeneration/diagnostic imaging/etiology/pathology Tomography, Optical Coherence/methods Atrophy/pathology Motor Neurons/pathology
 Humans Chitinase-3-Like Protein 1/metabolism Astrocytes/metabolism *Chitinases/metabolism *Neurodegenerative Diseases/metabolism Synapsins/metabolism *Brain Neoplasms/metabolism
 Humans Cytokines/metabolism *Neurodegenerative Diseases/metabolism Neuroinflammatory Diseases Chemokine CX3CL1/metabolism Central Nervous System/metabolism *Alzheimer Disease/metabolism Microglia/metabolism

 Animals Humans *Fingolimod Hydrochloride *Sphingosine/metabolism Brain/metabolism Lysophospholipids/metabolism Sphingolipids Receptors, Lysosphingolipid/metabolism Mammals/metabolism
 Animals Mice Cuprizone/toxicity Sulfates/adverse effects Oligodendroglia/pathology *Encephalomyelitis, Autoimmune, Experimental/chemically induced/drug therapy/pathology Corpus Callosum/pathology *Central Nervous System Diseases/pathology Heparitin Sulfate/therapeutic use Mice, Inbred C57BL Disease Models, Animal Myelin Sheath/pathology
 Humans *Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology Interleukin-15 *Interleukin-27 Macrophages/metabolism T-Lymphocytes/metabolism Tumor Necrosis Factor-alpha
 Humans Female *Neuromyelitis Optica/complications Retrospective Studies Autoantibodies Aquaporin 4 Immunoglobulin G Diagnostic Errors
 Humans *Cost-Effectiveness Analysis State Medicine Cost-Benefit Analysis Urinary Catheters *Urinary Tract Infections/epidemiology/prevention & control United Kingdom Quality-Adjusted Life Years


 Humans Blood-Brain Barrier/metabolism *Parkinson Disease Lactoferrin/metabolism/therapeutic use *Neuroprotective Agents/pharmacology/therapeutic use *Alzheimer Disease/drug therapy Mental Health Endothelial Cells/metabolism *COVID-19 SARS-CoV-2/metabolism Iron/metabolism/therapeutic use *Neurodegenerative Diseases/drug therapy Oxidation-Reduction




 Humans Autoantibodies *Encephalitis/diagnosis/therapy *Hashimoto Disease/diagnosis/therapy *Autoimmune Diseases of the Nervous System
 Humans *Paraparesis, Tropical Spastic Ataxia *Cartilage Diseases


 Animals Female Pregnancy Humans *Vitamin D Deficiency/epidemiology Vitamin D Vitamins *Autistic Disorder Brain










 Adult Humans *COVID-19 Interferon Lambda SARS-CoV-2 Interferons/therapeutic use *Virus Diseases Antiviral Agents/adverse effects


 Humans *Myelin Sheath Astrocytes Oligodendroglia Brain *Brain Diseases

 Humans *Plants, Medicinal Donepezil/metabolism Rivastigmine/metabolism Endophytes/metabolism Fungi/metabolism *Central Nervous System Diseases
 Humans *Inflammasomes/metabolism Immunohistochemistry Immunity, Innate *Central Nervous System Diseases Brain/metabolism Caspase 1/metabolism Interleukin-1beta NLR Family, Pyrin Domain-Containing 3 Protein


 Humans *Immunomodulating Agents *Receptor, Nerve Growth Factor/metabolism






 Aged Female Young Adult Humans Male *Osteoporosis/diagnosis/epidemiology/etiology Bone Density *Fractures, Bone Risk Factors Glucocorticoids/therapeutic use
 Humans *Receptors, Tumor Necrosis Factor, Type II Receptors, Tumor Necrosis Factor, Type I Tumor Necrosis Factor-alpha/physiology Cytokines *Rheumatic Diseases/drug therapy




 Animals Mice *Cuprizone/toxicity *Demyelinating Diseases/chemically induced/drug therapy Resveratrol/pharmacology Myelin Sheath/metabolism Autophagy Mice, Inbred C57BL Disease Models, Animal
 Adult Humans Independent Living *Telemedicine Postural Balance Physical Therapy Modalities *Nervous System Diseases Randomized Controlled Trials as Topic

 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Histones/metabolism Mice, Inbred C57BL Myelin-Oligodendrocyte Glycoprotein *MicroRNAs *Antibodies, Catalytic DNA
 Humans *Fatigue Syndrome, Chronic/therapy Cryotherapy Chronic Disease Treatment Outcome Inflammation/metabolism
 Humans United States/epidemiology Seasons *Hospitalization Cerebral Hemorrhage *Subarachnoid Hemorrhage Risk Factors
 United States Female Humans Risk Evaluation and Mitigation Risk Assessment *Sodium Oxybate Natalizumab Vigabatrin Pharmaceutical Preparations *Physicians United States Food and Drug Administration
 Humans Rats Animals *Astrocytes/pathology Neuroglia/pathology Neurons/pathology Microglia/physiology *Alzheimer Disease/pathology
 Humans *Exosomes *Autoimmune Diseases/diagnosis/therapy/etiology *Sjogren's Syndrome *Arthritis, Rheumatoid Biomarkers/metabolism

 *Verrucomicrobia/metabolism Akkermansia *Probiotics/therapeutic use Brain
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism Interleukin-17/metabolism *Gastrointestinal Microbiome Tumor Necrosis Factor-alpha/metabolism Interleukin-6/metabolism NF-kappa B/metabolism Lipopolysaccharides Myeloid Differentiation Factor 88/metabolism Toll-Like Receptor 4/metabolism Cytokines/metabolism Inflammation/pathology Myelin-Oligodendrocyte Glycoprotein/metabolism/therapeutic use Forkhead Transcription Factors/metabolism RNA, Messenger Mice, Inbred C57BL

 Child, Preschool Female Humans Infant Male Abducens Nerve *Abducens Nerve Diseases/diagnosis/etiology/drug therapy Bone Marrow *Esotropia *Lymphohistiocytosis, Hemophagocytic/complications/diagnosis/drug therapy
 Humans *Neuromyelitis Optica Intermediate Filaments Aquaporin 4 Immunoglobulin G/therapeutic use Biomarkers Autoantibodies


 Animals Mice *Astrocytes/metabolism Brain/metabolism Cuprizone/toxicity/metabolism *Demyelinating Diseases/chemically induced/genetics Disease Models, Animal Glycosylation Mice, Inbred C57BL Polysaccharides/metabolism Protein Tyrosine Phosphatases/metabolism

 Humans *Selenium *Neurodegenerative Diseases *Alzheimer Disease *Amyotrophic Lateral Sclerosis Databases, Factual
 Humans *Cytokines/metabolism Interleukin-17 Dimethyl Fumarate Leukocytes, Mononuclear/metabolism *Amyotrophic Lateral Sclerosis/drug therapy Granzymes Inflammation/drug therapy Nucleotidyltransferases
 Humans *Prostaglandin-Endoperoxide Synthases *Endocannabinoids Pain Sleep


 Animals Humans Orexins *Wakefulness/physiology Sleep/physiology Circadian Rhythm/physiology Signal Transduction *Sleep Wake Disorders ErbB Receptors Mammals
 Humans *Arnold-Chiari Malformation/complications Cross-Sectional Studies Cerebellum *Syringomyelia/complications *Peripheral Nervous System Diseases/complications Pruritus






 Child Humans *Diet, Ketogenic/adverse effects *Neuroblastoma Combined Modality Therapy Treatment Outcome
 Humans SARS-CoV-2 Pandemics *COVID-19/diagnosis Antibodies, Viral *Arthritis, Rheumatoid Vaccination



 Humans *Dimethyl Fumarate/therapeutic use *Xenobiotics Biotransformation Acetylcysteine Metabolic Networks and Pathways Immunosuppressive Agents/therapeutic use


 *Potassium Channels *Cyclic Nucleotide-Gated Cation Channels/metabolism Structure-Activity Relationship Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels Neurons/metabolism

 Animals *Asthma/drug therapy Cytokines *Dermatitis, Atopic/drug therapy Interleukin-33 Interleukin-4/therapeutic use Humans
 Animals Humans *Cloud Computing Computer Simulation *Delivery of Health Care






 Humans Animals Rats *Autoantibodies HEK293 Cells *Lupus Vasculitis, Central Nervous System Brain Autoantigens Immunoglobulin G

 Humans Receptors, Aryl Hydrocarbon/metabolism Universities *Autoimmune Diseases *Neoplasms/drug therapy/metabolism Diet
 Rats Animals Mice *Encephalomyelitis, Autoimmune, Experimental Interleukin-10/metabolism Interleukin-17 Rats, Sprague-Dawley Inflammation Transforming Growth Factor beta/metabolism Hippocampus Interleukin-23 Mice, Inbred C57BL
 Animals Mice Humans Myelin-Oligodendrocyte Glycoprotein *Optic Neuritis/therapy Binding Sites Autoantibodies Epitopes
 Humans *Stroke/diagnostic imaging/etiology *Ischemic Stroke Middle Cerebral Artery


 Humans *Plasma Exchange Pilot Projects Interleukin-6 Plasmapheresis *Nervous System Diseases/therapy Retrospective Studies
 Humans Retrospective Studies *Retina/diagnostic imaging *Diabetic Retinopathy/diagnosis Tomography, Optical Coherence/methods
 Humans *Neurodegenerative Diseases/metabolism Nerve Growth Factors/metabolism *Parkinson Disease/metabolism Central Nervous System/metabolism *Alzheimer Disease
 Humans *Neurodegenerative Diseases Proteomics *Parkinson Disease/metabolism *Alzheimer Disease *Chronobiology Disorders Circadian Rhythm/genetics
 Humans *Myelin Proteins/genetics/metabolism Nogo Proteins Nerve Regeneration/physiology Nerve Growth Factors *Neurodegenerative Diseases Nogo Receptors
 Humans *Neurodegenerative Diseases/metabolism *Alzheimer Disease/metabolism *Parkinson Disease/metabolism Ion Channels/metabolism/therapeutic use Homeostasis

 Humans *Diabetic Neuropathies Liver Cirrhosis Risk Factors Abdominal Pain Autonomic Nervous System

 Animals Humans Male Sodium Skin *Hypertension *Diabetes Mellitus Pharmaceutical Preparations




 Humans Naltrexone/therapeutic use/pharmacology *Chronic Pain/drug therapy Analgesics, Opioid/therapeutic use Narcotic Antagonists/therapeutic use/pharmacology *Opioid-Related Disorders/drug therapy Chronic Disease Recurrence


 Mice Animals Protein Phosphatase 2/genetics/metabolism *Encephalomyelitis, Autoimmune, Experimental Th1 Cells/metabolism Th2 Cells *Lupus Erythematosus, Systemic/genetics
 Humans Autoimmunity/genetics Gene Expression Regulation *Autoimmune Diseases *MicroRNAs/metabolism *Lupus Erythematosus, Systemic
 Humans Nucleosides/pharmacology/therapeutic use *Antineoplastic Agents/pharmacology/therapeutic use *Neoplasms/drug therapy Drug Resistance Membrane Transport Proteins Antimetabolites/pharmacology

 Animals *Inflammasomes *Autoimmune Diseases Autoimmunity Inflammation Self Tolerance
 Humans *Craniocerebral Trauma *Brain Concussion/diagnosis Vision Disorders/diagnosis/etiology Eye Movements Saccades

 *Receptor, trkB/metabolism *Brain-Derived Neurotrophic Factor/physiology Benzamides Signal Transduction
 Humans *Autism Spectrum Disorder Central Nervous System *Gastrointestinal Microbiome/physiology *Intestinal Diseases
 Humans Tomography, Optical Coherence/methods *Ophthalmology Angiography/methods Retina *Retinal Diseases/diagnostic imaging Fluorescein Angiography/methods Retinal Vessels
 Humans *Biosensing Techniques/methods Pandemics Immunoassay/methods *COVID-19/diagnosis Biomarkers/analysis *Autoimmune Diseases/diagnosis Autoantibodies Electrochemical Techniques/methods

 Humans Myelin-Oligodendrocyte Glycoprotein Retrospective Studies *COVID-19/complications *Optic Neuritis/diagnosis/etiology/therapy Vision Disorders/diagnosis/etiology Autoantibodies

 Humans Receptors, Cannabinoid/metabolism/therapeutic use Molecular Docking Simulation *Cannabinoids/therapeutic use Cannabinoid Receptor Antagonists Obesity/drug therapy
 Humans Japan Plasmapheresis/methods Plasma Exchange *Myasthenia Gravis/therapy *Nervous System Diseases/therapy *Neuromyelitis Optica/therapy


 Humans *Neuromyelitis Optica/diagnosis/drug therapy RNA, Viral/therapeutic use *COVID-19/complications SARS-CoV-2 Immunotherapy Aquaporin 4
 Animals Saccharomyces cerevisiae *COVID-19 Interferons/therapeutic use Immunity, Innate *Communicable Diseases/drug therapy Mammals



 Humans *Extracellular Traps *Autoimmune Diseases *Lupus Erythematosus, Systemic Neutrophils Autoantigens *Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis


 Female Humans Cost-Benefit Analysis *Endometriosis Omalizumab *Asthma/drug therapy Cost-Effectiveness Analysis Quality-Adjusted Life Years
 Humans Iceland *International Classification of Diseases Predictive Value of Tests Registries *Health Facilities

 Animals Humans *Cannabinoids/therapeutic use Zebrafish Endocannabinoids *Cannabis Models, Animal Receptors, Cannabinoid
 Humans *White Matter/diagnostic imaging/pathology Reproducibility of Results Cross-Sectional Studies Brain/pathology Magnetic Resonance Imaging/methods Image Processing, Computer-Assisted

 Female Humans Age of Onset *ATP Binding Cassette Transporter, Subfamily B, Member 1/genetics *Demyelinating Diseases/epidemiology/genetics Genotype Risk Factors
 Animals *Gastrointestinal Microbiome Kynurenic Acid Tryptophan *Encephalitis *Encephalomyelitis, Autoimmune, Experimental Macrophages

 Animals Rats *Fibrinogen/metabolism *Myelitis Signal Transduction *Toll-Like Receptor 9/metabolism



 Humans *Susac Syndrome/diagnosis Magnetic Resonance Imaging Biomarkers Glial Fibrillary Acidic Protein
 Humans *Deep Learning *Glioma/diagnostic imaging/genetics *Brain Neoplasms/diagnostic imaging/genetics Magnetic Resonance Imaging Mutation
 Humans *Liraglutide/therapeutic use *Amyloidosis/diagnosis/drug therapy
 Humans Iron/metabolism *Alzheimer Disease/metabolism *Ferroptosis *Neurodegenerative Diseases/metabolism *Cognitive Dysfunction/drug therapy/etiology/metabolism

 Humans Autoimmunity Receptor, Anaphylatoxin C5a *Autoimmune Diseases *Arthritis, Rheumatoid Inflammation




 Humans Aged *Parkinson Disease/surgery *Radiosurgery/methods *Dystonia/therapy *Essential Tremor Tremor/etiology/surgery *Dystonic Disorders/etiology *Deep Brain Stimulation/methods


 Humans Aged *Pituitary Adenylate Cyclase-Activating Polypeptide Prognosis *Brain Injuries, Traumatic Aging Biomarkers
 Female Humans Middle Aged *Trigeminal Neuralgia/diagnostic imaging/surgery *Augmented Reality Rhizotomy/methods Trigeminal Nerve/surgery Tomography, X-Ray Computed/methods
 Humans Mice Animals *Paraquat/toxicity *Antioxidants/pharmacology/metabolism Dimethyl Fumarate/pharmacology Lung Oxidative Stress Fibrosis Inflammation/chemically induced/drug therapy

 Humans *Neurodegenerative Diseases/complications/diagnostic imaging Postural Balance *Parkinson Disease/complications/diagnostic imaging Gait Magnetic Resonance Imaging *Gait Disorders, Neurologic/diagnostic imaging/etiology
 Humans *Immunomodulating Agents Inflammation *Inflammatory Bowel Diseases/therapy Liver
 Humans Female Aged *Acute Coronary Syndrome/diagnostic imaging/etiology/therapy Coronary Vessels *Drug-Eluting Stents Treatment Outcome *Diverticulitis



 Humans *Quality of Life *Nutrients Vitamins Vitamin A Vitamin K Mental Fatigue
 Mice Animals *Retina Optic Nerve Retinal Ganglion Cells Axons Oligodendroglia *Demyelinating Diseases
 Humans T-Lymphocytes *Diabetes Mellitus, Type 1 *Arthritis, Rheumatoid HLA-DR Antigens Peptides Epitopes


 Humans *Neuromyelitis Optica/diagnosis/therapy Aquaporin 4 *Optic Neuritis/diagnosis/etiology Optic Nerve/diagnostic imaging Phenotype
 Humans *Myelitis, Transverse/diagnosis/therapy Autoantibodies Myelin-Oligodendrocyte Glycoprotein *Neuromyelitis Optica/diagnosis/therapy Aquaporin 4

 Child Humans Carrier Proteins Interleukin-18 *COVID-19 Antibodies, Monoclonal *Arthritis, Rheumatoid
 United States Humans Mice Rats Animals Guinea Pigs *Cannabidiol/pharmacology Clinical Relevance *COVID-19 SARS-CoV-2 *Cannabis Inflammation/drug therapy Immunity, Innate
 Humans *Guillain-Barre Syndrome/pathology Hypoxia/pathology Hypoxia-Inducible Factor 1, alpha Subunit *Neuroinflammatory Diseases Th17 Cells
 Humans *Gastrointestinal Microbiome/physiology T-Lymphocytes, Regulatory *Microbiota Immune System
 Humans *Autoimmunity/genetics *Autoimmune Diseases/genetics RNA RNA-Binding Proteins/genetics Molecular Biology RNA, Messenger
 Humans *Technology Assessment, Biomedical/methods Uncertainty Netherlands Canada Pharmaceutical Preparations
 Male Female Humans Adult Adolescent *Hemangioendothelioma/diagnostic imaging/surgery Hyperplasia/surgery/pathology Foot/diagnostic imaging/surgery/pathology *Vascular Neoplasms/pathology *Vascular Malformations/diagnosis/pathology Diagnosis, Differential
 Female Humans Young Adult Adult Corpus Callosum/diagnostic imaging/pathology *COVID-19/complications *Brain Diseases Infarction/pathology Magnetic Resonance Imaging




 Humans *Neurodegenerative Diseases/therapy *Neuralgia/therapy *Alzheimer Disease *Parkinson Disease Bibliometrics

 Bees Animals *COVID-19 Fatty Acids/metabolism Anti-Bacterial Agents Biomarkers


 Humans *Neuromyelitis Optica Central Nervous System Azathioprine Bibliometrics Databases, Factual

 Humans Acrolein/toxicity *Tobacco Smoke Pollution *Electronic Nicotine Delivery Systems Lung *Pulmonary Disease, Chronic Obstructive/etiology *Neoplasms/chemically induced

 Humans Torque *Lower Extremity Bicycling/physiology Foot Biomechanical Phenomena *Self-Help Devices Muscle, Skeletal/physiology
 Animals *Neuralgia Structure-Activity Relationship Macrophages Monocytes Receptors, Purinergic P2X7 Purinergic P2X Receptor Antagonists/pharmacology






 Humans *Protein Kinases/metabolism Necroptosis/physiology Glycogen Synthase Kinase 3 beta Phosphatidylinositol 3-Kinases *Nervous System Diseases Apoptosis

 Humans Plasma Cells *Autoimmune Diseases/therapy B-Lymphocytes Autoimmunity *Arthritis, Rheumatoid Autoantibodies
 Humans *Brain/diagnostic imaging
 Humans Myelin-Oligodendrocyte Glycoprotein *Research Design *Optic Neuritis/drug therapy Immunoglobulin G
 Adult Humans *Brain Injuries Peer Group *Spinal Cord Injuries *Stroke/therapy






 Humans Inflammasomes/metabolism *Autoimmune Diseases Immunity, Innate *Arthritis, Rheumatoid Inflammation

 Animals *Antioxidants Kelch-Like ECH-Associated Protein 1/metabolism Reactive Oxygen Species/metabolism *NF-E2-Related Factor 2/metabolism Oxidative Stress Mammals/metabolism
 Animals Mice Rats Anion Transport Proteins/physiology *Lymphocytes *Lysophospholipids Sphingosine Sphingosine-1-Phosphate Receptors



 Humans Child *Vagus Nerve Stimulation/methods *Drug Resistant Epilepsy/therapy Blood Glucose Leukocytes, Mononuclear *Epilepsy/therapy Anti-Inflammatory Agents


 Humans Ultraviolet Rays Nitric Oxide *Air Pollution *Air Pollutants Particulate Matter *Autoimmune Diseases/etiology Vitamin D
 Animals Mice *Helminth Proteins *Fasciola hepatica Macrophages Peptides/metabolism Inflammation
 Child Humans *COVID-19 SARS-CoV-2 Cytokines *Autoimmune Diseases
 Humans *Neurodegenerative Diseases/diagnostic imaging/pathology Brain/physiology *Alzheimer Disease *Parkinson Disease Fractals
 Humans *Antioxidants/therapeutic use Brain Flavonoids/pharmacology/therapeutic use/chemistry *Brain Injuries, Traumatic/drug therapy

 *Lymphocytes Cell Count Flow Cytometry *Health Status Immunomodulation
 Humans Astrocytes Microglia Neuroinflammatory Diseases *RNA, Long Noncoding/genetics *MicroRNAs
 Humans Adult Middle Aged *Cough *Insufflation Cross-Sectional Studies Switzerland Respiration, Artificial
 Male Humans *Air Pollutants/toxicity/analysis Environmental Exposure/analysis *Air Pollution/analysis *Brain Neoplasms/chemically induced/epidemiology *Environmental Pollutants Particulate Matter/analysis
 Humans *Alzheimer Disease *Epstein-Barr Virus Infections Glycogen Synthase Kinase 3 Phosphatidylinositol 3-Kinases *Zika Virus Infection Herpesvirus 4, Human *Zika Virus *Nervous System Diseases

 Humans Biomarkers/metabolism *Nervous System Diseases *Parkinson Disease/metabolism *S100 Calcium Binding Protein beta Subunit
 Humans Mitochondria *Neurodegenerative Diseases/therapy *Alzheimer Disease *Parkinson Disease Central Nervous System
 Humans *Neurodegenerative Diseases/drug therapy/metabolism NF-E2-Related Factor 2/metabolism *Alzheimer Disease/drug therapy *Parkinson Disease Signal Transduction Antioxidants/pharmacology/therapeutic use
 Humans Animals Mice Arsenic Trioxide *Copper Reactive Oxygen Species/metabolism Autoimmunity Hydrogen Peroxide/metabolism *Scleroderma, Systemic/chemically induced/drug therapy/metabolism Fibrosis
 Humans Male Biomarkers *Brain/diagnostic imaging/pathology Atrophy/pathology Europe
 Humans Male Agammaglobulinaemia Tyrosine Kinase Administration, Oral Feces *Protein Kinase Inhibitors/pharmacology Chromatography, Liquid
 Humans Female Middle Aged Male Germany/epidemiology *Insurance Occupations Pensions Employment Sick Leave

 Humans Gait Walking Locomotion *Parkinson Disease *Stroke Postural Balance
 Humans *Receptor, Bradykinin B2 Pain/drug therapy Receptor, Bradykinin B1 Peptides *Fibromyalgia
 Animals Mice *Astrocytes/metabolism Neuroinflammatory Diseases Vascular Endothelial Growth Factor A/genetics/metabolism Hypoxia-Inducible Factor-Proline Dioxygenases/genetics/metabolism Hypoxia/metabolism Prolyl Hydroxylases/metabolism Procollagen-Proline Dioxygenase/metabolism *Encephalomyelitis, Autoimmune, Experimental/genetics/metabolism Hypoxia-Inducible Factor 1, alpha Subunit/genetics/metabolism


 Male Female Animals Humans Tissue Distribution *Radiometry/methods Positron-Emission Tomography/adverse effects/methods Radiopharmaceuticals *Demyelinating Diseases
 Humans Animals Mice *Neuroprotective Agents/pharmacology/therapeutic use Dopamine/metabolism Proto-Oncogene Proteins c-akt/metabolism *Neurodegenerative Diseases/metabolism Hydrogen Peroxide/pharmacology *Neuroblastoma/metabolism Dopaminergic Neurons Mice, Inbred C57BL 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology/metabolism Disease Models, Animal
 Humans Retrospective Studies Prognosis Myelin-Oligodendrocyte Glycoprotein Cohort Studies *Autoantibodies Chronic Disease *Immunoglobulin G Recurrence

 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/drug therapy/pathology *Grape Seed Extract/pharmacology/therapeutic use Interleukin-17 Interleukin-1beta Tumor Necrosis Factor-alpha/metabolism Interleukin-6/metabolism Th1 Cells Mice, Inbred C57BL Interferon-gamma/metabolism/pharmacology/therapeutic use Th17 Cells/metabolism Interleukin-12/pharmacology/therapeutic use Cytokines/metabolism
 Humans *Gastrointestinal Microbiome *Depressive Disorder, Major *Autism Spectrum Disorder/microbiology Bacteria Firmicutes Bacteroidetes Clostridiales
 Adult Humans Child *Tomography, Optical Coherence/methods Retinal Ganglion Cells Neuroinflammatory Diseases Retina/diagnostic imaging *Neuromyelitis Optica/diagnosis Biomarkers
 Humans *Fatigue Syndrome, Chronic/diagnosis/therapy *Encephalitis Myalgia
 Animals Mice *Diet, High-Fat/adverse effects Liver Inflammation Adipose Tissue *Autoimmune Diseases Obesity
 Animals Mice *Neuroprotective Agents/pharmacology/therapeutic use/chemistry Australia *Neurodegenerative Diseases/drug therapy Brain Anti-Inflammatory Agents, Non-Steroidal/pharmacology/therapeutic use




 Mice Animals *Cues *Brain Mapping Ephrins/metabolism Brain/metabolism Disease Models, Animal
 Humans *Inflammatory Bowel Diseases/drug therapy Inflammation/drug therapy Cytokines Anti-Inflammatory Agents/therapeutic use Interleukins/genetics/therapeutic use
 Humans Diet Vitamins *Diet, Mediterranean *Alzheimer Disease Brain Vegetables Inflammation


 Humans *Trigeminal Neuralgia/diagnostic imaging/surgery Retrospective Studies Treatment Outcome Hypesthesia Pain, Postoperative
 Child Humans BCG Vaccine/therapeutic use *Tuberculosis/prevention & control Immunity, Innate *Urinary Bladder Neoplasms/drug therapy
 Humans *Synoviocytes/metabolism Dimethyl Fumarate/pharmacology/therapeutic use Matrix Metalloproteinase 3 Interleukin-6/metabolism *Arthritis, Rheumatoid/metabolism Synovial Membrane/metabolism Inflammation/metabolism Fibroblasts/metabolism Cell Proliferation Cells, Cultured

 Humans *Ion Channels/metabolism Endothelial Cells/metabolism Mechanotransduction, Cellular/physiology Central Nervous System/metabolism *Neural Stem Cells






 Humans *Fatty Acids, Volatile/metabolism *Autoimmune Diseases/drug therapy Butyrates Propionates Acetates


 Humans *Autoimmune Diseases/drug therapy/metabolism Receptor-Interacting Protein Serine-Threonine Kinase 2/metabolism Inflammation/drug therapy Immunity, Innate *Arthritis, Rheumatoid Signal Transduction

 Humans *Ankyrins/metabolism Myelin Sheath/metabolism *Demyelinating Diseases/chemically induced/drug therapy/metabolism Oligodendroglia/metabolism Neuroglia/metabolism TRPA1 Cation Channel/metabolism
 Animals *Analgesics, Opioid/adverse effects Neuroinflammatory Diseases *Neuralgia/drug therapy/chemically induced Sphingosine/pharmacology Lysophospholipids Receptors, Lysosphingolipid
 Humans *Neuroprotective Agents/pharmacology/therapeutic use/chemistry Proto-Oncogene Proteins c-akt/metabolism Phosphatidylinositol 3-Kinases/metabolism Neuroinflammatory Diseases Signal Transduction *Neurodegenerative Diseases/drug therapy *Artemisinins/pharmacology/therapeutic use
 Adult Humans Aged Fingers Hand Strength *Motor Disorders Motor Skills/physiology Aging/physiology *Stroke Upper Extremity
 Humans Brain/diagnostic imaging Magnetic Resonance Imaging/methods Image Processing, Computer-Assisted/methods *Deep Learning Brain Mapping/methods *Calcinosis Algorithms
 Animals Humans *Gastrointestinal Microbiome *Autoimmune Diseases *Lupus Erythematosus, Systemic/etiology/therapy *Diabetes Mellitus, Type 1 Risk Factors *Intestinal Diseases Dysbiosis
 Humans *Polymorphism, Single Nucleotide/genetics Retinoid X Receptors/genetics Models, Molecular Mutation *Mutation, Missense Computational Biology/methods
 Animals Mice Humans Epigenesis, Genetic Autoimmunity *Autoimmune Diseases *Lupus Erythematosus, Systemic/genetics *Arthritis, Rheumatoid



 Humans *Verrucomicrobia/physiology Akkermansia *Gastrointestinal Microbiome Inflammation




 Humans *Amyloid beta-Peptides *Magnetic Resonance Imaging/methods Aging Basal Ganglia/pathology Arteries



 Animals Humans Sphingosine-1-Phosphate Receptors *Positron-Emission Tomography/methods *Brain/diagnostic imaging Fluorine Radioisotopes/pharmacokinetics Radiopharmaceuticals/chemistry Macaca
 Animals Mice Axons Cytokines Inflammation Microglia Nerve Regeneration Recovery of Function Spinal Cord *Spinal Cord Injuries *T-Lymphocytes, Regulatory *STAT3 Transcription Factor/metabolism
 Mice Male Female Animals *Anxiety/psychology *Fear/physiology Brain Anxiety Disorders/genetics Mice, Knockout Behavior, Animal Maze Learning/physiology

 Lactobacillus acidophilus Carboxymethylcellulose Sodium Glatiramer Acetate *Nanoparticles/chemistry *Cerium/chemistry
 *Antioxidants/pharmacology Reactive Oxygen Species/metabolism NAD Proteomics *Neuroprotective Agents/pharmacology/therapeutic use NF-E2-Related Factor 2/metabolism
 Humans Neoplasm Recurrence, Local/complications/drug therapy Nivolumab/adverse effects *Myasthenia Gravis/drug therapy Immunotherapy/adverse effects *Neurology
 Humans *Neurodegenerative Diseases Stem Cells *Parkinson Disease/drug therapy Central Nervous System *Biological Products/therapeutic use
 Humans *NF-E2-Related Factor 2/genetics Chlorhexidine/pharmacology Kelch-Like ECH-Associated Protein 1/metabolism *Parkinson Disease/drug therapy Oxidative Stress Reactive Oxygen Species/metabolism
 Humans *Rare Diseases/drug therapy *Drug Repositioning Pattern Recognition, Automated Software Knowledge Bases




 Mice Animals Spectrometry, Fluorescence *Alzheimer Disease/metabolism Amyloidogenic Proteins/metabolism Amyloid Amyloid beta-Peptides/metabolism Plaque, Amyloid/metabolism Mice, Transgenic

 Humans Blood-Brain Barrier/physiology *Brain Ischemia Endothelial Cells *Stroke *Nervous System Diseases Inflammation
 Humans Vertigo/complications *Stroke/complications/diagnostic imaging Cerebellum *Brain Stem Infarctions Ataxia *Nystagmus, Pathologic/etiology/diagnosis
 Animals Mice *Cytokines/immunology *Encephalitis/immunology/virology Immunity Semliki forest virus Signal Transduction *Suppressor of Cytokine Signaling Proteins/genetics/metabolism
 Humans Attitude *Physicians Health Personnel Self Report *Conversion Disorder

 Humans *Fibromyalgia/etiology/prevention & control Vitamin D/therapeutic use Vitamins/therapeutic use *Vitamin D Deficiency/complications/drug therapy Pain/complications
 Humans United States *Radiculopathy/diagnostic imaging Neck Pain/diagnostic imaging/etiology/therapy Magnetic Resonance Imaging *Spinal Cord Diseases Neck Cervical Vertebrae/diagnostic imaging
 Humans Checklist/methods Reproducibility of Results *Alzheimer Disease *Telerehabilitation *Nervous System Diseases/diagnosis *Stroke Outcome Assessment, Health Care Psychometrics
 Pregnancy Female Humans *Cell-Free Nucleic Acids/genetics Biomarkers, Tumor/genetics Liquid Biopsy/methods Mutation *Neurology

 Humans *Genetic Predisposition to Disease Genome-Wide Association Study/methods Polymorphism, Single Nucleotide Phenotype *Autoimmune Diseases/genetics
 Humans *COVID-19/prevention & control *COVID-19 Vaccines/adverse effects Magnetic Resonance Imaging RNA, Messenger *Susac Syndrome/etiology
 Animals Mice *Histones/metabolism Hydrolysis Myelin Basic Protein/metabolism Mice, Inbred C57BL *Encephalomyelitis, Autoimmune, Experimental DNA/metabolism Autoantibodies/metabolism
 Humans *Cross-Cultural Comparison Communication *Advance Care Planning Surveys and Questionnaires Italy Psychometrics

 Animals Mice Histones/metabolism Hydrolysis *Encephalomyelitis, Autoimmune, Experimental Myelin Basic Protein/metabolism Mice, Inbred C57BL DNA/metabolism Myelin-Oligodendrocyte Glycoprotein *Antibodies, Catalytic/metabolism Immunoglobulin G

 Animals Mice Granulocyte-Macrophage Colony-Stimulating Factor *Encephalomyelitis, Autoimmune, Experimental/drug therapy Interleukin-6 Receptors, Histamine H4 Tumor Necrosis Factor-alpha NF-kappa B *Neurodegenerative Diseases Adaptor Proteins, Signal Transducing Inflammation/drug therapy Antigens, CD19 Disease Progression

 Humans Mice Animals CD8-Positive T-Lymphocytes *Theilovirus Ovalbumin *Demyelinating Diseases/pathology Mice, Inbred C57BL CD4-Positive T-Lymphocytes
 Animals Mice *Fingolimod Hydrochloride/pharmacology/therapeutic use Cuprizone Microglia Neuroinflammatory Diseases *Psychotic Disorders


 Female Humans Adolescent *Vasculitis, Central Nervous System/drug therapy Central Nervous System/pathology Immunosuppressive Agents/therapeutic use Prednisolone/therapeutic use Magnetic Resonance Imaging

 Humans Retrospective Studies *Disabled Persons Victoria Information Storage and Retrieval Primary Health Care
 Humans *Peroxidase/metabolism *Myocardial Infarction/diagnostic imaging/drug therapy/metabolism Positron-Emission Tomography
 Humans *Mental Health Clinical Trials as Topic

 Animals Humans *Fingolimod Hydrochloride/pharmacology Phosphorylation Proto-Oncogene Proteins c-akt/metabolism Receptors, Lysosphingolipid/metabolism *Sphingosine-1-Phosphate Receptors/metabolism Threonine *Triple Negative Breast Neoplasms/drug therapy Zebrafish/metabolism


 Humans Cell Death/physiology *Ferroptosis Reactive Oxygen Species/metabolism Lipid Peroxidation *Brain Diseases/drug therapy
 Adult Humans Leukocyte L1 Antigen Complex *Graves Ophthalmopathy *Autoimmune Diseases/diagnosis Inflammation *Arthritis, Juvenile Calgranulin A Calgranulin B *Rheumatic Diseases/diagnosis *Lupus Erythematosus, Systemic Biomarkers Chronic Disease

 *Neuromyelitis Optica/drug therapy Humans Magnetic Resonance Imaging Biomarkers/blood Glial Fibrillary Acidic Protein/blood *Antibodies, Monoclonal, Humanized/therapeutic use Retrospective Studies
 Mice Animals *Proto-Oncogene Proteins c-akt/metabolism Phosphatidylinositol 3-Kinases/metabolism Ellagic Acid/pharmacology *Neural Tube Defects/chemically induced/prevention & control/metabolism Oxidative Stress Tretinoin/adverse effects/metabolism
 Humans Mice Animals *Inflammasomes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism *Shock, Septic/chemically induced/drug therapy NF-kappa B/metabolism Signal Transduction Disease Models, Animal


 Humans CTLA-4 Antigen T-Lymphocytes *Neoplasms *Immune System Diseases *Autoimmune Diseases

 *Myelin Sheath/pathology *Water Brain/diagnostic imaging Magnetic Resonance Imaging/methods Neural Networks, Computer

 Male Humans Middle Aged Baclofen/adverse effects *Muscle Relaxants, Central *Spinal Stenosis/complications/surgery Injections, Spinal Muscle Spasticity/etiology/chemically induced Decompression/adverse effects Catheters/adverse effects
 Humans *Neurodegenerative Diseases/therapy Secretome *Parkinson Disease *Mesenchymal Stem Cells *Mesenchymal Stem Cell Transplantation/methods



 Animals Humans *Ischemic Stroke Brain-Gut Axis Interleukin-17 *Encephalomyelitis, Autoimmune, Experimental Brain *Central Nervous System Diseases Interleukin-23

 Humans *COVID-19/complications SARS-CoV-2 Cytokines Inflammation *Autoimmune Diseases/complications/drug therapy Autoantibodies

 Humans *Chronic Pain Comorbidity Depression/complications/epidemiology/therapy *Depressive Disorder, Major/complications/epidemiology/therapy Systematic Reviews as Topic
 Humans *Alzheimer Disease/complications *Diabetes Mellitus, Type 2/complications Insulin/metabolism *Insulin Resistance/physiology *Parkinson Disease *Metabolic Syndrome/complications
 Humans Transcranial Magnetic Stimulation/methods Cerebellum/physiology *Essential Tremor *Parkinson Disease *Stroke

 Humans *Epigenesis, Genetic *DNA Histocompatibility Antigens Class II/genetics DNA Methylation Protein Processing, Post-Translational Mutant Proteins
 Adult Aged Humans Middle Aged Young Adult *Autoimmune Diseases/etiology Blood Glucose Creatinine Cyclophosphamide/therapeutic use *Hematopoietic Stem Cell Transplantation/methods *Hyponatremia/chemically induced Prospective Studies Transplantation Conditioning/methods Transplantation, Autologous Uric Acid

 Humans *Neurites Reproducibility of Results Benchmarking Brain/diagnostic imaging Diffusion Magnetic Resonance Imaging/methods *White Matter/diagnostic imaging Water
 Humans Anti-Inflammatory Agents/pharmacology/therapeutic use Inflammation/drug therapy/pathology *Naphthoquinones/pharmacology/therapeutic use *Autoimmune Diseases/drug therapy
 Humans *Artificial Cells *Nervous System Diseases/therapy Immunotherapy *Brain Diseases Autoantibodies

 Humans Aged Pursuit, Smooth Eye Movements Psychomotor Performance/physiology Hand/physiology *Nervous System Diseases *Motion Perception/physiology
 Humans *Urology Magnetic Resonance Imaging Urinary Bladder Urination/physiology *Lower Urinary Tract Symptoms/diagnostic imaging/etiology/therapy
 Animals Humans Mice Actins/metabolism Fibrosis *Fingolimod Hydrochloride/pharmacology/therapeutic use *Graft vs Host Disease Macrophages rho-Associated Kinases/genetics/metabolism rhoA GTP-Binding Protein/metabolism Transcriptome
 Humans Agammaglobulinaemia Tyrosine Kinase/metabolism *Autoimmune Diseases/drug therapy Signal Transduction *Tyrosine Protein Kinase Inhibitors/pharmacology *Neoplasms/drug therapy

 Humans *Trigeminal Neuralgia/surgery *Microvascular Decompression Surgery/methods Treatment Outcome Pain/surgery *Balloon Occlusion/methods Retrospective Studies
 Humans *Immunity, Innate Autoimmunity Trained Immunity Macrophages Adaptive Immunity *Autoimmune Diseases
 Mice Animals *Dimethyl Fumarate/pharmacology/therapeutic use/metabolism NF-E2-Related Factor 2/metabolism Signal Transduction Liver/metabolism *Reperfusion Injury/metabolism
 Humans Aged *Oral Health Retrospective Studies Toothbrushing Oral Hygiene *Cerebrovascular Disorders





 Humans Herpesvirus 4, Human/genetics *Epstein-Barr Virus Infections *Autoimmune Diseases Risk Factors *Lupus Erythematosus, Systemic
 Humans *Extracellular Vesicles/metabolism *Autoimmune Diseases/therapy/metabolism *Osteoarthritis/metabolism *Mesenchymal Stem Cells/metabolism Cytokines/metabolism

 Humans *Copper Research Ataxia Colombia/epidemiology *Spinal Cord Diseases
 *COP9 Signalosome Complex/genetics *Intracellular Signaling Peptides and Proteins/genetics *Peptide Hydrolases/genetics/metabolism Humans
 Humans *Nervous System Diseases/prevention & control/metabolism Diet Brain/metabolism Cognition/physiology Nutritional Status
 Humans *Irritable Bowel Syndrome *Enteric Nervous System/metabolism Neuroglia/metabolism *Gastrointestinal Diseases *Inflammatory Bowel Diseases/metabolism Interferons/metabolism
 Rats Animals Humans *Transcription Factors/genetics/metabolism Astrocytes/metabolism Gene Expression Regulation *Neural Stem Cells/metabolism Transcriptome Cell Differentiation/physiology
 Male Female Humans Young Adult Adult Middle Aged *Restless Legs Syndrome/epidemiology Prevalence Cross-Sectional Studies *Spinal Cord Injuries/complications/epidemiology *Neuromyelitis Optica/complications Spinal Cord

 Humans Autoantigens Liposomes *Autoimmune Diseases/drug therapy Immune Tolerance *Diabetes Mellitus, Type 1
 Humans *Neurodegenerative Diseases/diagnostic imaging Bayes Theorem Neural Networks, Computer Magnetic Resonance Imaging *Alzheimer Disease/diagnostic imaging/pathology
 Mice Animals Spinal Cord/metabolism *Spinal Cord Injuries/metabolism *Neural Stem Cells/metabolism gamma-Aminobutyric Acid/metabolism Cell Proliferation/physiology Receptors, GABA/metabolism

 Humans *Dipeptidyl-Peptidase IV Inhibitors/pharmacology/therapeutic use Dipeptidyl Peptidase 4/metabolism *Diabetes Mellitus, Type 2 Glucagon *COVID-19 *Alzheimer Disease
 Adult Humans Adolescent Young Adult Middle Aged Aged *Resistance Training Exercise Therapy Walking Exercise *Stroke

 Adult Humans Cross-Sectional Studies Chronic Disease *Neoplasms/epidemiology/therapy *Pulmonary Disease, Chronic Obstructive/therapy Anxiety Caregivers/psychology Health Services Needs and Demand



 Male Humans Adult Middle Aged *Migraine Disorders/epidemiology/diagnosis Headache/epidemiology/etiology/diagnosis *Epilepsy Pain Measurement Registries
 Mice Humans Animals *Encephalomyelitis, Autoimmune, Experimental/etiology *Mycobacterium avium subsp. paratuberculosis Autoantigens *Paratuberculosis/complications Mice, Inbred C57BL Adjuvants, Immunologic Myelin-Oligodendrocyte Glycoprotein Peptides
 *Cyclotides/pharmacology/therapeutic use/chemistry Amino Acid Sequence Plants/metabolism Cysteine Structure-Activity Relationship
 Humans *Cyclic Nucleotide Phosphodiesterases, Type 7 *Phosphodiesterase Inhibitors/pharmacology 3',5'-Cyclic-AMP Phosphodiesterases/metabolism Nucleotides, Cyclic
 Rats Animals Antioxidants/pharmacology *Alzheimer Disease/drug therapy *Trifolium/metabolism *Neuroprotective Agents/pharmacology/therapeutic use Amyloid beta-Peptides/metabolism Plant Extracts/pharmacology Hippocampus/metabolism Superoxide Dismutase/metabolism Disease Models, Animal Maze Learning
 Humans Anxiety *Cognitive Behavioral Therapy Depression Mental Health *Psychotherapy, Group


 Humans Adult Middle Aged Electrocardiography *Cortisone Pilot Projects *Long QT Syndrome/chemically induced/diagnosis/drug therapy Arrhythmias, Cardiac/chemically induced/drug therapy Heart Rate
 Humans Male Female *Cognitive Dysfunction/diagnosis *Alzheimer Disease/diagnosis Cognition Neuropsychological Tests Disease Progression
 Humans *Dimethyl Fumarate/pharmacology Kelch-Like ECH-Associated Protein 1 *Galectin 1 Proteomics NF-E2-Related Factor 2
 Humans *White Matter/diagnostic imaging Magnetic Resonance Imaging/methods Neuroimaging *Alzheimer Disease Skull Image Processing, Computer-Assisted/methods Brain/diagnostic imaging
 Animals Humans Prospective Studies *MicroRNAs/genetics/metabolism *Neurodegenerative Diseases/genetics/drug therapy/metabolism *Parkinson Disease/genetics Biomarkers Mammals/genetics/metabolism

 Male Humans Female Middle Aged *Atrial Fibrillation/diagnosis/epidemiology *Crohn Disease *Colitis, Ulcerative *Rheumatic Fever Biological Specimen Banks *Autoimmune Diseases/diagnosis/epidemiology Inflammation *Scleroderma, Systemic United Kingdom/epidemiology Risk Factors Incidence
 Animals Humans Mice Alzheimer Disease/metabolism *Astrocytes/metabolism Gene Expression Profiling Proteomics Single-Cell Gene Expression Analysis *Transcriptome RNA-Seq *Central Nervous System Diseases/genetics/metabolism
 Humans *Diffusion Magnetic Resonance Imaging/methods *Brain/diagnostic imaging Neurites Image Processing, Computer-Assisted/methods Algorithms Neural Networks, Computer
 Humans Lebanon *Pandemics Reproducibility of Results *COVID-19 Economics, Medical

 Animals Humans Mice Aging *Alzheimer Disease/genetics/metabolism Amyloid beta-Protein Precursor/genetics/metabolism Mitochondria tau Proteins
 Humans *Neurodegenerative Diseases/drug therapy/metabolism Phosphatidylinositol 3-Kinases/metabolism Janus Kinases/metabolism Phosphatidylinositol 3-Kinase/metabolism Polyphenols/pharmacology Signal Transduction *Alkaloids/pharmacology *Biological Products

 Humans *Amyotrophic Lateral Sclerosis/diagnosis Intermediate Filaments Prognosis Biomarkers Neurofilament Proteins Body Mass Index




 Humans *Lymphangioleiomyomatosis/diagnosis/diagnostic imaging *Tuberous Sclerosis/complications/diagnostic imaging *Lung Neoplasms/diagnosis/diagnostic imaging Lung/pathology *Pneumothorax/diagnostic imaging/etiology
 *Nerve Growth Factors/metabolism/pharmacology Secretome *Mesenchymal Stem Cells/metabolism Neurons/metabolism Signal Transduction
 Humans *Diffusion Tensor Imaging/methods Brain/diagnostic imaging *White Matter/diagnostic imaging Brain Mapping/methods Image Enhancement/methods Algorithms Image Processing, Computer-Assisted/methods
 Mice Animals *Herpesvirus 4, Human *Epstein-Barr Virus Infections/prevention & control CD8-Positive T-Lymphocytes Epitopes, T-Lymphocyte Lymph Nodes Vaccines, Subunit
 Humans *Spike Glycoprotein, Coronavirus/genetics SARS-CoV-2 *COVID-19 Antibodies, Monoclonal Edible Grain
 Humans Female Male *Neuromyelitis Optica/diagnosis Contrast Media Myelin-Oligodendrocyte Glycoprotein Autoantibodies Gadolinium Aquaporin 4 *Spinal Cord Diseases/complications Immunoglobulin G

 Humans *Capsid/metabolism Herpesvirus 4, Human/genetics/metabolism Viral Envelope/metabolism *Epstein-Barr Virus Infections/metabolism Capsid Proteins/genetics/metabolism
 Humans Female Young Adult Adult Middle Aged Aged Aged, 80 and over *Myelitis, Transverse/diagnostic imaging *Neuromyelitis Optica/diagnostic imaging Retrospective Studies Neoplasm Recurrence, Local Aquaporin 4 Immunoglobulin G Autoantibodies
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism T-Lymphocytes, Regulatory Flavonoids/pharmacology/therapeutic use Th17 Cells Signal Transduction Th1 Cells Cell Differentiation Mice, Inbred C57BL
 Humans *Trigeminal Neuralgia/surgery Treatment Outcome Retrospective Studies Follow-Up Studies Prospective Studies Pain Electrocoagulation/methods
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental/metabolism/pathology NF-kappa B/metabolism Nestin Neuroinflammatory Diseases Cytokines/metabolism Mice, Inbred C57BL Cytoskeletal Proteins/genetics Armadillo Domain Proteins/genetics
 Humans *Gene Regulatory Networks *Schizophrenia/genetics/metabolism Genome-Wide Association Study Transcriptome Gene Expression Profiling Brain/metabolism
 Humans Female *Neuromyelitis Optica/diagnostic imaging/drug therapy Retrospective Studies Aquaporin 4 Treatment Outcome Azathioprine/therapeutic use

 Humans Autoantibodies *Cerebellar Diseases/complications Nerve Tissue Proteins *Paraneoplastic Cerebellar Degeneration/diagnosis/complications Recombinant Proteins

 Humans Qualitative Research *Anthropology, Cultural/methods *Walking
 Humans Memantine/pharmacology/therapeutic use Post-Acute COVID-19 Syndrome *Alzheimer Disease/drug therapy *Parkinson Disease/drug therapy *COVID-19 Amantadine/pharmacology/therapeutic use

 Humans *Dystonia/etiology Retrospective Studies *Deep Brain Stimulation/adverse effects *Parkinson Disease/surgery/complications Tremor/complications *Essential Tremor/surgery/complications *Dystonic Disorders/complications *Tourette Syndrome/surgery/complications Postoperative Complications/epidemiology/etiology
 Humans *Critical Pathways *State Medicine Italy Delivery of Health Care Chronic Disease
 Adult Humans Middle Aged Aged Aged, 80 and over Neuropsychological Tests Portugal *Alzheimer Disease Psychometrics Educational Status Reference Values


 Humans *Inflammasomes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism Glycogen Synthase Kinase 3 beta Neuroinflammatory Diseases *Brain Injuries, Traumatic/drug therapy/metabolism
 Humans *Hyaluronic Acid/metabolism Extracellular Matrix Proteins/metabolism Extracellular Matrix/metabolism Collagen/metabolism *Glioma/metabolism Central Nervous System/metabolism Tumor Microenvironment

 Humans Molecular Docking Simulation *Interleukin-6 Inhibitors *Methotrexate Interleukin-6 Molecular Dynamics Simulation Inflammation
 Humans Middle Aged Aged Infant *Neurodegenerative Diseases/diagnostic imaging Biological Specimen Banks *Stroke/diagnostic imaging Brain/diagnostic imaging *Metabolic Syndrome/diagnostic imaging Obesity/complications Aging United Kingdom

 Animals *Cannabis/chemistry Aluminum Antioxidants Acetylcholinesterase Zebrafish *Cannabidiol/pharmacology Oils Dronabinol/pharmacology

 Humans Mendelian Randomization Analysis/methods *Arthritis, Rheumatoid *Glioma *Hypertension Telomere/genetics Genome-Wide Association Study Polymorphism, Single Nucleotide

 Humans Female Male *Stiff-Person Syndrome/complications/diagnosis/epidemiology Phenotype Prevalence
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Th17 Cells Neuroinflammatory Diseases Spinal Cord/pathology Integrins/metabolism Integrin alpha4
 Humans Gait Outcome Assessment, Health Care *Spinal Cord Injuries/rehabilitation *Walking Walking Speed
 Animals Mice Cyclooxygenase 2 *Ferroptosis Administration, Oral Ethanol *Cation Transport Proteins


 Mice Animals *CD8-Positive T-Lymphocytes *Neurons/metabolism Brain/metabolism Inflammation Cytokines/metabolism Cell Communication

 Humans *Inflammasomes/metabolism *Alzheimer Disease/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism Amyloid beta-Peptides Cytokines/metabolism Caspases


 Mice Animals *Autoimmune Diseases/genetics *MicroRNAs/genetics/metabolism Autoimmunity/genetics *Inflammatory Bowel Diseases/genetics Biomarkers

 Humans HLA-DRB1 Chains/genetics Mutation *Arthritis, Rheumatoid *Biomedical Research *Lupus Erythematosus, Systemic
 Humans Delayed Diagnosis *Histiocytosis, Langerhans-Cell/complications/diagnosis/genetics *Erdheim-Chester Disease/complications/diagnosis/genetics *Histiocytosis, Sinus/diagnosis/pathology/therapy Prognosis
 Humans *Exoskeleton Device Quality of Life Gait *Spinal Cord Injuries/complications *Stroke Personal Satisfaction
 Humans Prospective Studies *Technology *Biomedical Technology Chronic Disease Surveys and Questionnaires
 Humans *Trigeminal Neuralgia/diagnostic imaging/etiology/surgery Treatment Outcome Retrospective Studies Trigeminal Ganglion Rhizotomy/methods *Radiosurgery/methods
 Humans *Th17 Cells/metabolism Lipid Metabolism Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism Cell Differentiation *Autoimmune Diseases/metabolism Lipids
 Humans *Alzheimer Disease/complications *Helicobacter pylori *Helicobacter Infections/complications *Hyperhomocysteinemia/complications *Neurodegenerative Diseases/complications
 Mice Animals *Dysbiosis/chemically induced/microbiology RNA, Ribosomal, 16S/genetics Antibody Formation Adjuvants, Immunologic/pharmacology Bacteria/genetics Feces/microbiology Freund's Adjuvant/pharmacology Ileum/microbiology Anti-Bacterial Agents/pharmacology *Gastrointestinal Microbiome Immunoglobulin G/pharmacology
 Infant, Newborn Humans Antioxidants/pharmacology Oxidative Stress *Alzheimer Disease/drug therapy Anti-Inflammatory Agents/pharmacology *Ischemic Stroke/drug therapy Hydrogen/pharmacology/therapeutic use
 Humans *COVID-19/complications SARS-CoV-2 Retrospective Studies *Ischemic Stroke *Encephalitis Observational Studies as Topic

 Adult Humans *Common Variable Immunodeficiency/diagnosis/epidemiology Retrospective Studies *Autoimmune Diseases/diagnosis/epidemiology Autoimmunity Immunoglobulin E
 Animals Female Humans Male *Cannabinoids/pharmacology/therapeutic use Dronabinol/therapeutic use Muscle Spasticity/drug therapy Cannabinoid Receptor Agonists Signal Transduction/physiology Receptors, Cannabinoid Receptor, Cannabinoid, CB1
 Animals Humans Brain-Gut Axis *Neurodegenerative Diseases/metabolism *Autism Spectrum Disorder/metabolism Dysbiosis/metabolism Post-Acute COVID-19 Syndrome *COVID-19/metabolism *Microbiota Brain/metabolism
 Animals Dimethyl Fumarate/pharmacology/therapeutic use *Ischemic Stroke/drug therapy *Stroke/drug therapy Blood-Brain Barrier/metabolism Inflammation/drug therapy NF-E2-Related Factor 2/metabolism


 Humans Male Female *Uric Acid Antioxidants Cross-Sectional Studies Prospective Studies *Migraine Disorders Headache
 Mice Animals Humans *Encephalomyelitis, Autoimmune, Experimental/drug therapy Mice, Inbred C57BL Inflammation/drug therapy Cytokines/metabolism Anti-Inflammatory Agents/pharmacology/therapeutic use
 Humans *Contrast Media Magnetic Resonance Imaging/methods Tomography, X-Ray Computed Gadolinium Phagocytes *Nervous System Diseases/diagnostic imaging

 Humans Aquaporin 4 Consensus Delphi Technique Immunoglobulin G *Neuromyelitis Optica/drug therapy
 Animals Mice *Cell Culture Techniques Microglia/metabolism/pathology *Neuralgia/etiology/metabolism/pathology *Neuroglia/metabolism/pathology Peripheral Nerve Injuries/complications/metabolism/pathology *Spinal Cord/metabolism/pathology Cells, Cultured Clinical Protocols Disease Models, Animal *Nervous System Diseases/complications/metabolism/pathology
 Humans Costs and Cost Analysis Health Expenditures Pharmaceutical Preparations *Nervous System Diseases *Parkinson Disease *Central Nervous System Depressants Retrospective Studies Health Care Costs

 Animals Mice *Alzheimer Disease/genetics/metabolism/pathology Amyloid beta-Peptides/genetics/metabolism Amyloid beta-Protein Precursor Apoptosis/genetics bcl-2-Associated X Protein Caspase 3 Cognition Disease Models, Animal Mice, Inbred C57BL Mice, Transgenic Mitochondrial Dynamics/genetics
 Humans Bias *Antidepressive Agents/therapeutic use *Research Design Network Meta-Analysis
 Animals Mice Cuprizone *Encephalomyelitis, Autoimmune, Experimental/metabolism *Insulin-Like Growth Factor I/metabolism Mice, Inbred C57BL Myelin Sheath/metabolism Neuroinflammatory Diseases Oligodendroglia/metabolism *Receptor, IGF Type 1/metabolism
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental Nuclear Receptor Subfamily 1, Group F, Member 3/genetics/metabolism T-Lymphocytes, Regulatory Cytokines/metabolism Inflammation/drug therapy Anti-Inflammatory Agents/therapeutic use Th17 Cells Mice, Inbred C57BL
 Humans Follow-Up Studies SARS-CoV-2 *Peripheral Nervous System Diseases BNT162 Vaccine *Giant Cell Arteritis *Limbic Encephalitis *COVID-19/prevention & control Neoplasm Recurrence, Local *Autoimmune Diseases/etiology *Nervous System Diseases Vaccination/adverse effects


 Humans *Mentors Surveys and Questionnaires
 Mice Animals Herpesvirus 4, Human/physiology *Epstein-Barr Virus Infections *Lymphoma/complications/pathology *Lymphoma, B-Cell/complications Cell Death Immunity Adenosine Triphosphate Tumor Microenvironment
 Humans *Brain-Gut Axis Tryptophan *Gastrointestinal Microbiome Indoles Inflammation


 Humans *Diet, Ketogenic *Gastrointestinal Microbiome Weight Loss Obesity/metabolism Body Weight Carbohydrates

 Pregnancy Female Rats Male Animals Humans Valproic Acid/adverse effects *Autism Spectrum Disorder/chemically induced/drug therapy Interleukin-6 Tumor Necrosis Factor-alpha/pharmacology Rats, Wistar Phosphodiesterase Inhibitors/adverse effects Social Behavior Behavior, Animal *Prenatal Exposure Delayed Effects/drug therapy Disease Models, Animal
 Male Humans *Giant Cell Arteritis/complications/diagnosis/drug therapy Area Postrema/pathology *Neuromyelitis Optica/pathology Vomiting/complications/pathology Nausea/complications/pathology
 Male Humans Female Quality of Life/psychology *Inflammatory Bowel Diseases/complications/epidemiology Comorbidity Anxiety/epidemiology *Cognition Disorders/epidemiology Depression/epidemiology
 Humans Neuroimaging *Neurosciences Aging *Alzheimer Disease Brain
 Adult Humans *Glioblastoma/pathology SARS-CoV-2 *COVID-19 RNA, Viral/metabolism/therapeutic use Endothelial Cells/metabolism Organoids/metabolism/pathology Tumor Microenvironment
 Child Female Humans Child, Preschool Parenting *Occupational Therapy Parents/education *Disabled Persons Mothers
 Adult Humans *Palliative Care Quality of Life Long-Term Care Caregivers *Dementia
 Humans *Urinary Bladder, Overactive/complications/drug therapy *Botulinum Toxins, Type A Quality of Life *Urinary Bladder, Neurogenic/etiology/complications Treatment Outcome *Urinary Incontinence/etiology *Urinary Tract Infections/complications Urodynamics *Spinal Cord Injuries/complications/drug therapy Cholinergic Antagonists/therapeutic use
 Humans *COVID-19/complications SARS-CoV-2 Post-Acute COVID-19 Syndrome RNA, Viral Endothelial Cells Inflammation *Primary Dysautonomias/etiology Vagus Nerve
 Humans Macrophages/metabolism Inflammation/metabolism *Lupus Nephritis/metabolism *Arthritis, Rheumatoid/metabolism *Lupus Erythematosus, Systemic/metabolism Macrophage Activation/physiology

 Animals Sphingomyelin Phosphodiesterase/genetics Zebrafish/metabolism Saposins/genetics *Sphingolipidoses *Lysosomal Storage Diseases Mechanistic Target of Rapamycin Complex 1
 Humans *Neurodegenerative Diseases/pathology Brain-Gut Axis Ecosystem *Parkinson Disease *Gastrointestinal Microbiome/physiology Brain/pathology
 Animals Mice *Bone Resorption/drug therapy/metabolism Fingolimod Hydrochloride/pharmacology/therapeutic use Histone Deacetylases/metabolism Lipopolysaccharides Mice, Inbred C57BL NF-kappa B/metabolism Osteoclasts Osteogenesis *Osteolysis/drug therapy/chemically induced RANK Ligand/metabolism Repressor Proteins/metabolism
 Animals Humans *Actins DNA-Binding Proteins/metabolism Endosomes/genetics/metabolism HEK293 Cells Lectins, C-Type/genetics/chemistry/metabolism Membrane Proteins/metabolism Monosaccharide Transport Proteins/chemistry/genetics/metabolism Nuclear Proteins/metabolism Protein Transport Transcription Factors/metabolism Ubiquitin-Protein Ligases/genetics Ubiquitins/metabolism *Zebrafish/genetics/metabolism

 Humans *Immune System *Mental Disorders/drug therapy Sphingosine Brain
 Humans *Autoimmune Diseases/drug therapy *COVID-19 Disease Progression *Fatty Acids, Omega-3/pharmacology Inflammation/drug therapy
 Mice Animals *Microglia/metabolism *Encephalomyelitis, Autoimmune, Experimental/genetics/metabolism NF-E2-Related Factor 2/genetics/metabolism Pyruvaldehyde/metabolism Magnesium Oxide/metabolism Mice, Inbred C57BL Cytokines/metabolism

 Humans Neuroinflammatory Diseases *Neurodegenerative Diseases/drug therapy/pathology *Parkinson Disease *Alzheimer Disease/drug therapy Brain/pathology Oligonucleotides/therapeutic use


 Humans Adult *Neuromyelitis Optica/epidemiology/genetics Retrospective Studies Autoantibodies Neoplasm Recurrence, Local Aquaporin 4

 Humans Female *Crohn Disease/diagnosis/epidemiology/pathology Incidence Cohort Studies *Infectious Mononucleosis/epidemiology Retrospective Studies Outpatients *Colitis, Ulcerative/diagnosis/epidemiology/pathology *Inflammatory Bowel Diseases *Epstein-Barr Virus Infections/complications/epidemiology Germany/epidemiology
 Humans Adult *Quality of Life *Acceptance and Commitment Therapy Outcome Assessment, Health Care Anxiety/therapy Health Status
 Animals Humans *RNA, Circular/genetics/metabolism RNA/metabolism *Neurodegenerative Diseases/genetics RNA Splicing Brain/metabolism
 Humans *Neuromyelitis Optica/diagnosis/complications Glial Fibrillary Acidic Protein/cerebrospinal fluid Aquaporin 4 Biomarkers Autoantibodies Immunoglobulin G

 Humans *Gait/physiology *Walking/physiology Lower Extremity Knee Knee Joint Biomechanical Phenomena
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental Choroid Plexus/physiology Neuroinflammatory Diseases Brain Central Nervous System Mice, Inbred C57BL
 Humans Adult Adolescent Young Adult Middle Aged Aged Aged, 80 and over Quality of Life Retrospective Studies Post-Acute COVID-19 Syndrome *COVID-19/epidemiology *Arthritis, Rheumatoid/epidemiology/therapy
 Humans *Dendrobium/chemistry Leukocytes, Mononuclear Monocytes *Phenanthrenes/pharmacology/chemistry T-Lymphocytes Tetradecanoylphorbol Acetate/pharmacology Fluorenes/chemistry/pharmacology

 Humans Male Female Aged Adult Middle Aged Pharmacovigilance Hot Temperature *Drug-Related Side Effects and Adverse Reactions Databases, Factual Adverse Drug Reaction Reporting Systems *Stroke/chemically induced/epidemiology
 Animals Endocannabinoids/metabolism *Neurodegenerative Diseases/drug therapy Neuroinflammatory Diseases *Neuroprotective Agents/pharmacology/therapeutic use
 Humans COVID-19 Vaccines Antibody Formation *COVID-19/prevention & control SARS-CoV-2 Immunotherapy *Neuromuscular Diseases Antibodies Antibodies, Viral
 Adult Humans *Food, Processed Case-Control Studies Australia/epidemiology Diet/adverse effects Energy Intake *Demyelinating Diseases/epidemiology/etiology Central Nervous System Fast Foods/adverse effects Food Handling
 Humans Cystectomy/adverse effects *Urinary Diversion/adverse effects *Robotics Retrospective Studies Quality of Life *Urinary Bladder Neoplasms/surgery Urinary Bladder/surgery *Laparoscopy/adverse effects Postoperative Complications/etiology/surgery Treatment Outcome
 Humans Reproducibility of Results Surveys and Questionnaires *Fear *Cognition Psychometrics
 Rats Animals Guinea Pigs Mice *Encephalomyelitis, Autoimmune, Experimental Connexin 43/metabolism/therapeutic use *Paeonia/chemistry Interleukin-6 Glucosides/pharmacology CD8-Positive T-Lymphocytes/metabolism Interleukin-2/therapeutic use Mice, Inbred C57BL
 Animals Humans *Zebrafish/genetics *Dimethyl Fumarate/pharmacology NF-E2-Related Factor 2/genetics/metabolism Zebrafish Proteins/genetics/metabolism Antioxidants/pharmacology Oxidative Stress
 Humans Blood-Brain Barrier Ligands *Nanoparticles *Alzheimer Disease Lipids
 Animals Inflammasomes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/genetics/metabolism *Exosomes/metabolism *Central Nervous System Diseases Models, Animal *Mesenchymal Stem Cells
 Animals Male Rats Blood-Brain Barrier/pathology Molecular Weight Myelin Sheath *Neuroinflammatory Diseases Oxidative Stress Rats, Sprague-Dawley Reactive Oxygen Species/metabolism *Stroke/metabolism
 Humans *Sodium Chloride/pharmacology Signal Transduction *Hypertension

 *Leukocytes *Cerebrospinal Fluid


 Humans Child *Anti-N-Methyl-D-Aspartate Receptor Encephalitis/diagnosis Siblings *Hashimoto Disease/diagnosis/genetics Cognition

 Humans Transcranial Magnetic Stimulation/methods *Nervous System Diseases *Amyotrophic Lateral Sclerosis *Alzheimer Disease Evoked Potentials, Motor/physiology
 Humans *Amyotrophic Lateral Sclerosis/drug therapy Area Under Curve Half-Life Double-Blind Method Kinetics
 Adult Humans Aged *Palliative Care *Quality of Life Caregivers Patient Satisfaction Caregiver Burden

 Humans Animals Mice Immunotherapy Immunization *Nucleic Acids RNA, Double-Stranded *Melanoma/genetics
 Humans *Alzheimer Disease/pathology Amyloid Amyloid beta-Peptides/metabolism Brain/pathology Cognition *Cognitive Dysfunction/drug therapy/etiology/metabolism
 Female Humans *Carcinoma, Renal Cell/genetics *Deoxyribonuclease (Pyrimidine Dimer)/genetics *Kidney Neoplasms/genetics *Polycystic Kidney, Autosomal Dominant/genetics RNA, Messenger/genetics *Tuberous Sclerosis Complex 2 Protein/genetics Tumor Suppressor Proteins/genetics *TRPP Cation Channels/genetics


 Adult Humans Cross-Sectional Studies Vietnam/epidemiology Quality of Life *Neuralgia/epidemiology *Osteoarthritis


 Rats Humans Animals *Sphingosine *Fingolimod Hydrochloride/pharmacology Propylene Glycols/pharmacology Ligands Receptors, Lysosphingolipid/metabolism Sphingosine-1-Phosphate Receptors/metabolism Mitochondria/metabolism Adenosine Triphosphate Immunosuppressive Agents/pharmacology STAT3 Transcription Factor/metabolism
 Humans *Esters/pharmacology *Leukocytes, Mononuclear Interleukin-6 Tumor Necrosis Factor-alpha Dimethyl Fumarate/pharmacology Glutathione

 Animals *Sjogren's Syndrome *Melatonin/therapeutic use Salivary Glands/pathology *Autoimmune Diseases/pathology Autoantibodies
 Humans *Schizophrenia Cohort Studies *Autoimmune Diseases of the Nervous System
 Humans *Telemedicine Quality of Life *Stroke/therapy Executive Function *Brain Injuries
 Male Child Humans Female United States Cross-Sectional Studies *Neurology Neurologists *Physicians, Women Academies and Institutes Authorship
 Male Pregnancy Female Humans Adolescent *Vitamin B Complex/therapeutic use Randomized Controlled Trials as Topic Anxiety Disorders/drug therapy Vitamin D/therapeutic use *Depressive Disorder, Major/drug therapy




 Male Humans Vitamin D *Diabetic Nephropathies/epidemiology/genetics/complications *Diabetes Mellitus, Type 2/epidemiology/genetics/complications Mendelian Randomization Analysis Creatinine Vitamins Polymorphism, Single Nucleotide
 Animals Mice *Demyelinating Diseases/pathology/virology Membrane Glycoproteins Mice, Inbred C57BL *Murine hepatitis virus/metabolism Neuroinflammatory Diseases *Nitric Oxide Synthase Type II/genetics/metabolism Receptors, Immunologic *Coronavirus Infections/pathology
 United States Humans *COVID-19 Pandemics Quality Improvement Retrospective Studies Review Literature as Topic
 Humans *Butyrylcholinesterase/chemistry *Acetylcholinesterase/metabolism Cholinesterase Inhibitors/pharmacology/chemistry Enzyme Inhibitors Glutathione Transferase Piperazines/pharmacology

 Female Humans *Metformin/pharmacology/therapeutic use *Diabetes Mellitus, Type 2/drug therapy Hypoglycemic Agents/pharmacology/therapeutic use *Neoplasms/drug therapy Glucose/metabolism AMP-Activated Protein Kinases/metabolism


 Humans *HIV Infections Leadership *Non-alcoholic Fatty Liver Disease
 Child Humans *Myelitis, Transverse/diagnosis *Enterovirus Infections/complications/diagnosis *Neuromuscular Diseases/diagnosis *Myelitis/diagnosis *Central Nervous System Viral Diseases/diagnosis/complications
 Animals Mice Corpus Callosum/metabolism Cuprizone/toxicity *Demyelinating Diseases/drug therapy Disease Models, Animal Mice, Inbred C57BL Microglia/metabolism Myelin Sheath/metabolism *Receptors, Aryl Hydrocarbon/genetics/metabolism *Remyelination/physiology

 Animals Mice *Oligodendroglia/metabolism *Myelin Sheath/metabolism Neurogenesis/physiology Exocytosis Cell Differentiation/physiology
 Humans Particulate Matter/analysis *Air Pollutants/analysis *Air Pollution/adverse effects/analysis *Environmental Pollutants Nervous System/chemistry Particle Size
 Mice Animals *Estrogen Receptor alpha/genetics/metabolism Lymphotoxin beta Receptor/genetics/metabolism TNF Receptor-Associated Factor 3/genetics/metabolism *Encephalomyelitis, Autoimmune, Experimental Estrogens/pharmacology Phenotype Dendritic Cells/metabolism Mice, Inbred C57BL
 Humans Tumor Necrosis Factor-alpha Interleukin-17 *Psoriasis/drug therapy Biological Factors *Inflammatory Bowel Diseases/drug therapy *Biological Products/therapeutic use
 Humans Female Prospective Studies *Alopecia Areata/epidemiology Risk Factors *Graves Disease
 Humans Autoimmunity/genetics Genetic Predisposition to Disease *Autoimmune Diseases/epidemiology/genetics *Myositis/epidemiology/genetics *Rheumatic Diseases *Celiac Disease *Inflammatory Bowel Diseases



 Animals Mice Apoptosis Dopaminergic Neurons/metabolism Lipids Mice, Inbred C57BL *Parkinson Disease/metabolism *Parkinsonian Disorders/metabolism Phenotype Reactive Oxygen Species/metabolism Humans
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/metabolism *Enhancer of Zeste Homolog 2 Protein/metabolism *Ferroptosis *Mesenchymal Stem Cells/metabolism Microglia/metabolism *MicroRNAs/metabolism


 Humans *Schizophrenia/etiology Risperidone/therapeutic use *Antipsychotic Agents/adverse effects Fingolimod Hydrochloride/adverse effects Treatment Outcome Drug Therapy, Combination Double-Blind Method
 Adult Aged Humans Middle Aged *Epstein-Barr Virus Infections/genetics/prevention & control/epidemiology Genome-Wide Association Study Herpesvirus 4, Human/genetics Vaccination *Vaccines Mendelian Randomization Analysis
 Rats Animals *Dimethyl Fumarate/metabolism/pharmacology *Microglia/metabolism Astrocytes Connexin 43/metabolism/pharmacology Coculture Techniques Inflammation/metabolism
 Humans *Image Processing, Computer-Assisted/methods Brain/diagnostic imaging Diffusion Magnetic Resonance Imaging/methods *White Matter/diagnostic imaging Gray Matter/diagnostic imaging
 Child Humans Animals Female *Autism Spectrum Disorder/etiology Chromatin/genetics Alternative Splicing/genetics Valproic Acid/adverse effects RNA, Messenger/metabolism Disease Models, Animal *Prenatal Exposure Delayed Effects
 Humans Animals Mice *Myasthenia Gravis Crotonates/pharmacology/therapeutic use Hydroxybutyrates Nitriles
 Female Humans Adult Reproducibility of Results Prospective Studies *Contrast Media/pharmacokinetics *Brain Magnetic Resonance Imaging/methods Perfusion
 Humans Climate Change Biodiversity Temperature *Air Pollution/adverse effects *Environmental Pollutants *Stroke *Dementia



 Female Humans Infant *Tuberous Sclerosis/complications/diagnosis/genetics Tumor Suppressor Proteins/genetics *Angiofibroma/diagnosis/etiology/metabolism Sirolimus Seizures/etiology

 Humans *Amyotrophic Lateral Sclerosis/therapy/drug therapy Genes, Modifier Superoxide Dismutase-1/genetics/therapeutic use Motor Neurons Mutation

 Humans *COVID-19 SARS-CoV-2 Angiotensin-Converting Enzyme 2/metabolism COVID-19 Drug Treatment Peptidyl-Dipeptidase A/chemistry/metabolism Protein Binding
 Male Humans Aged Adult Middle Aged Female Anticonvulsants/adverse effects Longitudinal Studies *Parkinson Disease/drug therapy/epidemiology Case-Control Studies *Epilepsy/drug therapy/epidemiology
 Animals Mice Antigens, CD34/metabolism Cell Adhesion Molecules/metabolism *Encephalomyelitis, Autoimmune, Experimental/pathology Endothelial Cells/metabolism *Pluripotent Stem Cells/metabolism Spleen Stromal Cells/metabolism *Telocytes/metabolism/pathology Tryptases/metabolism Vimentin/metabolism


 Humans *Amyotrophic Lateral Sclerosis/pathology Heterogeneous-Nuclear Ribonucleoproteins/genetics/metabolism Inclusion Bodies/pathology Mutation/genetics *RNA-Binding Protein FUS/genetics/metabolism RNA-Binding Proteins/genetics/metabolism

 Humans *Epilepsy, Temporal Lobe Retrospective Studies *Hippocampal Sclerosis Hippocampus/surgery/pathology Anterior Temporal Lobectomy/adverse effects Treatment Outcome Postoperative Complications/surgery Sclerosis/surgery/pathology


 Humans *Epilepsy/genetics Genotype *Hamartoma *Intellectual Disability Mutation *Refractive Errors Retrospective Studies *Tuberous Sclerosis/complications/genetics Tuberous Sclerosis Complex 1 Protein/genetics Tuberous Sclerosis Complex 2 Protein/genetics Tumor Suppressor Proteins/genetics
 Humans Child *Tumor Suppressor Proteins/genetics Mutation/genetics *Tuberous Sclerosis/complications/diagnostic imaging/genetics Tuberous Sclerosis Complex 1 Protein/genetics Tuberous Sclerosis Complex 2 Protein/genetics DNA Copy Number Variations Ras Homolog Enriched in Brain Protein/genetics
 Male Humans Child, Preschool *Aortic Aneurysm, Thoracic/complications/diagnosis *Aortic Aneurysm, Thoracoabdominal *Tuberous Sclerosis/complications/surgery *Blood Vessel Prosthesis Implantation Aorta, Abdominal/surgery *Aortic Aneurysm, Abdominal/surgery *Endovascular Procedures Treatment Outcome Postoperative Complications/surgery Retrospective Studies
 Female Humans Middle Aged Sclerosis *Myositis *Autoimmune Diseases Autoantibodies *Connective Tissue Diseases RNA, Transfer *Lupus Erythematosus, Systemic/complications



 Humans *Herpesvirus 4, Human/genetics *Epstein-Barr Virus Infections/genetics Inflammasomes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/genetics/metabolism Protein Interaction Maps

 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Endothelial Cells/metabolism *Oxysterols/metabolism Neuroinflammatory Diseases Central Nervous System/metabolism Mice, Inbred C57BL
 Female Male Humans Retrospective Studies Prospective Studies Rituximab Chile/epidemiology Myelin-Oligodendrocyte Glycoprotein *Neuromyelitis Optica Aquaporin 4 *Encephalitis Seizures Autoantibodies Immunoglobulin G Oligodendroglia
 Infant, Newborn Child Humans Child, Preschool Aged *Urinary Bladder, Neurogenic/drug therapy Muscarinic Antagonists/therapeutic use Urinary Bladder *Urinary Bladder, Overactive/drug therapy *Urinary Tract *Autonomic Nervous System Diseases *Drug-Related Side Effects and Adverse Reactions

 Molecular Docking Simulation *Cannabinoids/pharmacology Molecular Conformation Quantitative Structure-Activity Relationship

 Humans *SARS-CoV-2 *COVID-19/complications Central Nervous System Brain Blood-Brain Barrier
 Humans Focus Groups *Technology Assessment, Biomedical Qualitative Research *Communication Geography


 Humans Male *Adrenoleukodystrophy/drug therapy Brain/diagnostic imaging/blood supply Cerebrovascular Circulation/physiology Spin Labels Vitamin D Dietary Supplements Magnetic Resonance Imaging
 Mice Animals *Immunotoxins/genetics/therapeutic use Diphtheria Toxin/genetics T-Lymphocytes Cell Line
 Humans Female Adult Male *Pseudotumor Cerebri Magnetic Resonance Imaging Optic Nerve Headache/diagnostic imaging/etiology Vision Disorders/diagnostic imaging/etiology

 Adult Humans Adolescent *Myelin Sheath/metabolism *Myelin Basic Protein/chemistry Unilamellar Liposomes/chemistry Lipids Cholesterol/metabolism
 Humans *COVID-19/epidemiology Pandemics *Parkinson Disease/epidemiology Prevalence *Nervous System Diseases/epidemiology *Stroke/epidemiology *Dementia/epidemiology
 Child Pregnancy Female Humans Adult Everolimus/adverse effects *Rhabdomyoma/drug therapy/complications/diagnosis *Tuberous Sclerosis/complications/drug therapy/diagnosis Retrospective Studies *Heart Neoplasms/drug therapy/diagnosis *Cardiomyopathies Disease Progression

 Humans Codon, Nonsense *Tuberous Sclerosis/genetics/pathology Tumor Suppressor Proteins/genetics *Induced Pluripotent Stem Cells/pathology Tuberous Sclerosis Complex 2 Protein/genetics Leukocytes, Mononuclear/pathology Tuberous Sclerosis Complex 1 Protein/genetics Mutation/genetics
 Humans *Everolimus/therapeutic use *Tuberous Sclerosis/drug therapy/metabolism Sirolimus/therapeutic use Mechanistic Target of Rapamycin Complex 1

 Humans *Angiomyolipoma/complications/diagnostic imaging *Tuberous Sclerosis/complications/diagnostic imaging *Kidney Neoplasms/complications/diagnostic imaging *Retroperitoneal Neoplasms/pathology Positron-Emission Tomography Magnetic Resonance Imaging
 Humans *Tumor Suppressor Proteins/genetics *Tuberous Sclerosis/genetics/pathology Tuberous Sclerosis Complex 2 Protein/genetics Mutation Tuberous Sclerosis Complex 1 Protein/genetics Phenotype

 Humans *Hand/surgery *Scleroderma, Systemic/complications/surgery
 Humans *Amyotrophic Lateral Sclerosis/diagnosis/surgery Referral and Consultation *Cubital Tunnel Syndrome Diagnostic Errors Neurosurgical Procedures

 Humans Female Middle Aged Male *COVID-19 Vaccines SARS-CoV-2 Immunomodulating Agents Prospective Studies *COVID-19 Immunosuppressive Agents
 Humans *Extracellular Vesicles Immunomodulation *Scleroderma, Systemic/therapy Fibrosis *Mesenchymal Stem Cells


 Female Humans Middle Aged Male Longitudinal Studies *Inflammatory Bowel Diseases/complications/epidemiology Cognition Comorbidity *Colitis, Ulcerative/epidemiology

 Animals Mice *Encephalomyelitis, Autoimmune, Experimental *Inflammasomes/metabolism Interleukin-1 Receptor-Associated Kinases/genetics/metabolism Microglia/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/genetics/metabolism Phosphorylation Pyroptosis
 Adult Humans Female United States/epidemiology Adolescent Young Adult Middle Aged Male *Glucocorticoids/therapeutic use Longitudinal Studies Retrospective Studies Prednisone/therapeutic use *Optic Neuritis/drug therapy/epidemiology
 Mice Animals Male *Cannabidiol/pharmacology/therapeutic use Neuroprotection PPAR gamma/metabolism *Ischemic Stroke/drug therapy Mice, Inbred C57BL *Brain Ischemia/metabolism *Stroke/drug therapy/metabolism *Neuroprotective Agents/pharmacology/therapeutic use Infarction, Middle Cerebral Artery/drug therapy Disease Models, Animal
 Humans *Propionates/pharmacology *Histones/metabolism Receptors, G-Protein-Coupled/metabolism Neuroprotection Hydrogen Peroxide/pharmacology/metabolism Ganglia, Spinal/metabolism
 Humans *Cognitive Behavioral Therapy *Fatigue Syndrome, Chronic/therapy/psychology Treatment Outcome Surveys and Questionnaires Cognition

 Adult Humans Child *Torticollis/drug therapy/complications *Neuromuscular Agents/therapeutic use Retrospective Studies *Botulinum Toxins, Type A/therapeutic use Muscle Spasticity/drug therapy/etiology Health Care Costs Treatment Outcome
 Mice Animals Dextran Sulfate/toxicity Janus Kinases/metabolism Signal Transduction STAT Transcription Factors/metabolism *Colitis Suppressor of Cytokine Signaling Proteins/genetics *Inflammatory Bowel Diseases Myeloid Cells/metabolism Suppressor of Cytokine Signaling 3 Protein/genetics/metabolism
 Animals Mice *Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism Fingolimod Hydrochloride/therapeutic use *Chitosan/therapeutic use T-Lymphocytes/metabolism *Nanoparticles Mice, Inbred C57BL
 Humans *Arthritis, Rheumatoid/chemically induced Genome-Wide Association Study *Lupus Erythematosus, Systemic/complications Mendelian Randomization Analysis Proprotein Convertase 9/genetics *PCSK9 Inhibitors/adverse effects/therapeutic use *Asthma/chemically induced
 Humans Female Adolescent Young Adult Adult Middle Aged *Tuberous Sclerosis/complications/epidemiology MTOR Inhibitors Retrospective Studies *Hamartoma/complications *Kidney Failure, Chronic/etiology/complications *Angiomyolipoma/complications/pathology *Skin Diseases *Renal Insufficiency, Chronic/complications/epidemiology

 Humans *Quantitative Trait Loci/genetics Genome-Wide Association Study Gene Regulatory Networks/genetics Brain Phenotype *Brain Diseases/genetics Polymorphism, Single Nucleotide/genetics

 Animals Humans Rabbits *Tumor Necrosis Factor-alpha *Corneal Neovascularization Retina Neovascularization, Pathologic Human Umbilical Vein Endothelial Cells Cells, Cultured
 Humans Consensus Induced Pluripotent Stem Cells *Motor Neuron Disease/drug therapy Randomized Controlled Trials as Topic



 Female Pregnancy Humans *Siblings Cesarean Section Delivery, Obstetric *Asthma Outcome Assessment, Health Care
 Humans Adalimumab/adverse effects *Antibodies, Monoclonal/therapeutic use *Biological Products/adverse effects Insulin Glargine Trastuzumab Interferons
 Mice Animals Humans Inflammasomes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism *Amyotrophic Lateral Sclerosis/drug therapy/metabolism *Neurodegenerative Diseases NLR Proteins

 Child Humans Infant *Neuromyelitis Optica/diagnosis Aquaporin 4 *Leigh Disease/diagnosis Myelin-Oligodendrocyte Glycoprotein Autoantibodies Syndrome








 Humans *Amyotrophic Lateral Sclerosis/genetics *Neurodegenerative Diseases Mutation
 Humans Animals *Amyotrophic Lateral Sclerosis/metabolism Wnt Signaling Pathway Motor Neurons/metabolism Oxidative Stress Nerve Degeneration/metabolism/pathology Disease Models, Animal

 Humans DNA, Mitochondrial/genetics Mitochondria/genetics *Mitochondrial Diseases/genetics Mutation/genetics *Optic Atrophy, Autosomal Dominant/genetics *Diffuse Cerebral Sclerosis of Schilder/genetics
 Humans *Mosaicism Tuberous Sclerosis Complex 2 Protein/genetics Tuberous Sclerosis Complex 1 Protein/genetics Mutation *Tuberous Sclerosis/diagnosis/genetics
 Humans Adult *Amyotrophic Lateral Sclerosis/metabolism Protein Deglycase DJ-1/genetics/metabolism Motor Neurons/metabolism Mutation Oxidative Stress/physiology

 Mice Animals *Amyotrophic Lateral Sclerosis Astrocytes Superoxide Dismutase-1 Motor Neurons/physiology Spinal Cord Disease Models, Animal Disease Progression Mice, Transgenic Superoxide Dismutase
 Humans Female Middle Aged Tooth Cervix/pathology *Tooth/pathology Cone-Beam Computed Tomography/methods Tomography, X-Ray Computed/adverse effects/methods *Scleroderma, Systemic/complications/diagnostic imaging *Root Resorption/etiology
 Infant Infant, Newborn Humans Pregnancy Child Female *Rhabdomyoma/diagnostic imaging/genetics/complications Everolimus Cesarean Section Ultrasonography *Tuberous Sclerosis/complications/diagnostic imaging/genetics *Heart Neoplasms/diagnostic imaging/therapy/complications


 Humans *Genetic Predisposition to Disease Genotype *Arthritis, Rheumatoid/diagnosis/genetics Risk Factors Phenotype HLA Antigens/genetics Histocompatibility Antigens Class II/genetics HLA-DRB1 Chains/genetics Alleles

 Molecular Docking Simulation *Nuclear Receptor Subfamily 1, Group F, Member 3 *Drug Discovery Transcription Factors Receptors, Retinoic Acid Tretinoin Ligands
 Humans Young Adult Adult Reproducibility of Results Feasibility Studies Prospective Studies *Magnetic Resonance Imaging/methods Magnetic Resonance Spectroscopy

 Mice Animals *Canavan Disease/genetics/metabolism Cell Lineage Epigenesis, Genetic Central Nervous System/metabolism Oligodendroglia Myelin Sheath/metabolism Mammals



 Mice Animals *Microglia/metabolism Multiomics Blood-Brain Barrier/metabolism *Alzheimer Disease/genetics Fibrinogen
 Child Humans Female Male *Neuromyelitis Optica/diagnosis/epidemiology Aquaporin 4 *Myelitis Brain Stem Immunoglobulin G Retrospective Studies Autoantibodies
 Mice Animals *Tumor Necrosis Factor-alpha/metabolism *Protein Kinases/metabolism Dimethyl Fumarate Necroptosis Receptor-Interacting Protein Serine-Threonine Kinases/metabolism Systemic Inflammatory Response Syndrome Oxidative Phosphorylation Apoptosis
 Humans *Parkinson Disease/epidemiology Prospective Studies Retrospective Studies *Autoimmune Diseases/complications/epidemiology *Sjogren's Syndrome/epidemiology

 Adult Humans Male Female Biological Availability Cross-Over Studies *Fumarates Administration, Oral
 Animals Rats Male Phencyclidine/toxicity *Schizophrenia/chemically induced/drug therapy/metabolism Fingolimod Hydrochloride/pharmacology/therapeutic use Brain-Derived Neurotrophic Factor Rats, Sprague-Dawley *Cognitive Dysfunction/chemically induced/drug therapy Cytokines Disease Models, Animal
 Adult Aged Humans Middle Aged Young Adult *Brain/pathology Cross-Sectional Studies *Magnetic Resonance Imaging/methods Magnetic Resonance Spectroscopy Prospective Studies
 Female Humans *Neuromyelitis Optica Pakistan Aquaporin 4 Retrospective Studies Myelin-Oligodendrocyte Glycoprotein Neoplasm Recurrence, Local Autoantibodies Immunoglobulin G
 Humans Aged *Dementia/therapy *Neurodegenerative Diseases Quality of Life Goals *Cognitive Dysfunction/therapy
 Humans Administration, Inhalation *Interferon-beta/pharmacology/therapeutic use Respiratory Aerosols and Droplets Nebulizers and Vaporizers Drug Delivery Systems *Idiopathic Pulmonary Fibrosis/drug therapy Transforming Growth Factor beta/therapeutic use Particle Size
 Male Humans *Mitoxantrone/toxicity Cardiotoxicity *Antineoplastic Agents/pharmacology Autophagy Cytochrome P-450 Enzyme System/metabolism

 Male Humans Middle Aged *Amyotrophic Lateral Sclerosis/complications/diagnosis/epidemiology Comorbidity Syndrome Muscle Weakness

 Humans *Scleroderma, Systemic/diagnosis/therapy Fibrosis *Vascular Diseases Disease Progression *Autoimmune Diseases/complications
 Humans *Amyotrophic Lateral Sclerosis/diagnostic imaging/genetics/pathology C9orf72 Protein/genetics Magnetic Resonance Imaging Mutation/genetics Atrophy


 Male Humans Aged *Tremor Autoimmunity *Autoimmune Diseases Autoantibodies Immunotherapy
 Humans Diagnosis, Differential *Vasculitis, Central Nervous System/etiology/complications Central Nervous System *Systemic Vasculitis/etiology/complications

 Humans *Quality of Life *Scleroderma, Systemic/complications Fibrosis Autoimmunity Vaccination/adverse effects
 Humans *Amyotrophic Lateral Sclerosis/genetics/therapy *Neurodegenerative Diseases Genetic Therapy Dependovirus/genetics

 Humans *Amyotrophic Lateral Sclerosis/genetics/metabolism *Neurodegenerative Diseases/genetics RNA-Binding Proteins/genetics Motor Neurons/metabolism DNA Damage RNA-Binding Protein FUS/genetics Fragile X Mental Retardation Protein/genetics
 Humans *Amyotrophic Lateral Sclerosis Copper Manganese *Neurodegenerative Diseases Metabolome Mutation

 Humans *Janus Kinase Inhibitors/pharmacology/therapeutic use *Autoimmune Diseases/drug therapy *Arthritis, Rheumatoid/drug therapy *Lupus Erythematosus, Systemic/drug therapy Immunity, Innate Janus Kinases
 Female Humans Adult Everolimus/therapeutic use *Lupus Nephritis/complications/diagnosis/drug therapy Mycophenolic Acid/therapeutic use Tacrolimus/therapeutic use *Angiomyolipoma/chemically induced/complications/drug therapy *Tuberous Sclerosis/complications/diagnosis/drug therapy *Lupus Erythematosus, Systemic/complications TOR Serine-Threonine Kinases/therapeutic use





 Adolescent Adult Female Humans Infant, Newborn Pregnancy *Cannabidiol Cannabinoid Receptor Agonists *Cannabis *Chronic Pain *Hallucinogens Randomized Controlled Trials as Topic Risk Assessment Sleepiness Systematic Reviews as Topic Meta-Analysis as Topic Observational Studies as Topic




 Mice Humans Animals *Tuberous Sclerosis/genetics/metabolism/pathology Tuberous Sclerosis Complex 1 Protein/metabolism Proteomics Tandem Mass Spectrometry *Neural Stem Cells/metabolism/pathology TOR Serine-Threonine Kinases/metabolism
 Animals Mice *Anemia, Aplastic/metabolism Antibodies, Monoclonal/metabolism Cytokines/metabolism *Graft vs Host Disease/metabolism Signal Transduction *T-Lymphocytes/metabolism/pathology *Interleukin Receptor Common gamma Subunit/antagonists & inhibitors/metabolism Primates



 Humans Male Female *Amyotrophic Lateral Sclerosis/drug therapy *Motor Neuron Disease/drug therapy Exercise Risk Factors

 Humans *Amyotrophic Lateral Sclerosis/diagnostic imaging *White Matter/diagnostic imaging Diffusion Tensor Imaging/methods Extremities *Sleep Initiation and Maintenance Disorders/complications
 Humans Child *Cognition Disorders/complications South Africa/epidemiology *Tuberous Sclerosis/complications/psychology *Cognitive Dysfunction/complications Cognition/physiology Neuropsychological Tests
 Humans Female Longitudinal Studies *Unemployment *Occupations Anxiety Disorders/epidemiology Denmark/epidemiology Sick Leave
 Humans *Amyotrophic Lateral Sclerosis/genetics Genome-Wide Association Study *Neurodegenerative Diseases HLA Antigens Motor Neurons
 Adult Humans *Cannabidiol/adverse effects Everolimus/adverse effects Healthy Volunteers Sirolimus/adverse effects Drug Interactions

 Humans Retrospective Studies Myelin-Oligodendrocyte Glycoprotein Autoantibodies *COVID-19 SARS-CoV-2 *Optic Neuritis/diagnosis/drug therapy/etiology Immunoglobulin G


 Humans Autoantibodies Autoimmunity Protein Array Analysis *Autoimmune Diseases *Scleroderma, Systemic *Dermatomyositis

 Humans Male Middle Aged Aged Female *Antibodies, Antineutrophil Cytoplasmic Retrospective Studies Sclerosis *Glomerulonephritis Prognosis
 Humans *Alzheimer Disease/genetics/pathology *Lewy Body Disease/pathology *Amyotrophic Lateral Sclerosis/pathology Retrospective Studies *Multiple System Atrophy




 Humans *MicroRNAs/genetics *Neural Cell Adhesion Molecule L1/metabolism *Amyotrophic Lateral Sclerosis/metabolism Reproducibility of Results *Extracellular Vesicles/metabolism
 Humans *Scleroderma, Systemic/therapy *Autoimmune Diseases Immunosuppression Therapy Immunomodulation *Mesenchymal Stem Cells *Mesenchymal Stem Cell Transplantation
 Humans Rituximab/therapeutic use *Scleroderma, Systemic/drug therapy/complications *Lung Diseases, Interstitial/drug therapy/etiology Fibrosis Inflammation/drug therapy

 Humans Syndrome *Neuroendocrine Tumors/drug therapy/genetics *Antineoplastic Agents/therapeutic use *von Hippel-Lindau Disease/genetics/therapy Everolimus *Multiple Endocrine Neoplasia Type 1/complications Somatostatin/therapeutic use *Pancreatic Neoplasms/drug therapy/genetics

 Humans Sirolimus/therapeutic use MTOR Inhibitors *Tuberous Sclerosis/complications/drug therapy Ointments/therapeutic use *Angiofibroma/complications/drug therapy *Facial Neoplasms/complications/drug therapy Immunosuppressive Agents/therapeutic use TOR Serine-Threonine Kinases
 Humans *Amyotrophic Lateral Sclerosis/complications/epidemiology/psychology Prevalence Neuropsychological Tests *Cognitive Dysfunction/etiology/complications *Language Development Disorders Cognition
 Humans *Neuromyelitis Optica/diagnosis Retrospective Studies Benchmarking *Optic Neuritis/diagnosis Tomography, Optical Coherence/methods Autoantibodies *Aquaporins Aquaporin 4
 Animals Humans *Encephalomyelitis, Autoimmune, Experimental/therapy Inflammation/therapy *Interleukin 1 Receptor Antagonist Protein Interleukin-1 Lentivirus Quality of Life Mice
 Rats Animals Inflammasomes/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism Glyburide/pharmacology Dimethyl Fumarate/pharmacology/therapeutic use NF-E2-Related Factor 2/metabolism *Diabetes Mellitus, Type 2/drug therapy *Non-alcoholic Fatty Liver Disease/drug therapy Antioxidants/metabolism *Diabetes Mellitus, Experimental/drug therapy/metabolism Inflammation/drug therapy Oxidative Stress
 Humans Gait Ataxia/etiology *Essential Tremor Tremor Consensus *Cerebellar Ataxia/complications Ataxia/complications *Cerebellar Diseases/complications Gait/physiology
 Humans Female Adult Male *Pseudotumor Cerebri/complications/drug therapy Glucagon-Like Peptide-1 Receptor/agonists Acetazolamide Pilot Projects Glucagon-Like Peptide 1 Headache/complications Weight Loss
 Mice Male Animals *Parkinson Disease/drug therapy/metabolism Endoribonucleases/metabolism Endoplasmic Reticulum Chaperone BiP Caspase 12/metabolism Protein Serine-Threonine Kinases/metabolism Mice, Inbred C57BL Endoplasmic Reticulum Stress Unfolded Protein Response *Neuroprotective Agents/pharmacology/therapeutic use Disease Models, Animal
 Mice Animals *Nuclear Receptor Subfamily 1, Group F, Member 3/genetics Cell Differentiation *Encephalomyelitis, Autoimmune, Experimental Lipids
 Humans *Kidney Failure, Chronic/therapy *Arteriovenous Shunt, Surgical/methods Retrospective Studies Renal Dialysis/methods *Arteriovenous Fistula Treatment Outcome
 Humans Rituximab/adverse effects Retrospective Studies *Agammaglobulinemia/drug therapy/epidemiology/chemically induced *Autoimmune Diseases/drug therapy/chemically induced *Arthritis, Rheumatoid/drug therapy *Infections/chemically induced
 Humans Mice Animals *Macular Degeneration/metabolism Retina/metabolism Neuroglia/metabolism *Neurodegenerative Diseases/metabolism Single-Cell Analysis
 Mice Animals *Encephalomyelitis, Autoimmune, Experimental Astrocytes/metabolism/pathology Taurochenodeoxycholic Acid/metabolism/pharmacology Neuroinflammatory Diseases Proto-Oncogene Proteins c-akt/metabolism Lipopolysaccharides/pharmacology Cyclooxygenase 2/metabolism/pharmacology NF-kappa B/metabolism RNA, Messenger/genetics Mice, Inbred C57BL Receptors, G-Protein-Coupled/metabolism

 Child Humans United States/epidemiology Aged Cross-Sectional Studies Retrospective Studies *Neurology *Nervous System Diseases/epidemiology/therapy Health Care Surveys Registries *Dementia Ambulatory Care
 Animals Mice *Theilovirus Neuroinflammatory Diseases Brain/diagnostic imaging Spinal Cord/diagnostic imaging Atrophy Disease Models, Animal *Demyelinating Diseases


 Humans *Parkinson Disease/genetics Syndrome Biomarkers Forecasting Central Nervous System/pathology
 Humans Male Female Global Burden of Disease Quality-Adjusted Life Years Risk Factors *Nervous System Diseases/epidemiology *Stroke *Alzheimer Disease Prevalence Global Health


 Female Humans Adolescent *Tuberous Sclerosis/complications/diagnosis/therapy *Encephalitis Hospitals Physical Examination *Pneumonia, Mycoplasma



 Humans Child Female Infant Child, Preschool Adolescent *Rhabdomyoma/diagnostic imaging *Tuberous Sclerosis Heart Myocardium Heart Ventricles *Heart Neoplasms/complications/diagnosis








 Female Humans Portal Vein/pathology *Pancytopenia/etiology *Hypertension, Portal/etiology/complications Liver Cirrhosis/complications *Vascular Diseases *Scleroderma, Systemic/complications/diagnosis


 Humans Pandemics *COVID-19 Neuropsychological Tests Educational Status *Cognitive Reserve
 Humans *COVID-19 Prolactin SARS-CoV-2 RNA, Viral Immune System Anti-Inflammatory Agents

 Humans Sclerotherapy *Hypertension *Leg Ulcer/etiology/therapy Skin *Varicose Ulcer/therapy
 Humans *Alzheimer Disease/genetics *Parkinson Disease/genetics *Amyotrophic Lateral Sclerosis/genetics Genome-Wide Association Study Genetic Predisposition to Disease/genetics *Neurodegenerative Diseases/genetics Polymorphism, Single Nucleotide/genetics

 Adult Humans Male Aged Female Intracellular Signaling Peptides and Proteins Leucine Retrospective Studies *Encephalitis/complications/diagnosis *Cognitive Dysfunction/etiology Cognition *Epilepsy, Temporal Lobe Neuropsychological Tests
 Animals Humans *Amyotrophic Lateral Sclerosis/metabolism *Neurodegenerative Diseases/metabolism Motor Neurons/metabolism Stem Cell Transplantation/methods Disease Models, Animal
 Humans Retrospective Studies *Immunotherapy *Immunologic Factors Disease Progression Adrenal Cortex Hormones/therapeutic use Recurrence
 Male Female Humans Adult Middle Aged Aged *Neuroendocrine Tumors/genetics/pathology *Tuberous Sclerosis/genetics/pathology Capecitabine Retrospective Studies Temozolomide Mutation/genetics *Kidney Neoplasms/pathology *Pancreatic Neoplasms/genetics/therapy/pathology
 Humans *Amyotrophic Lateral Sclerosis/diagnosis Cohort Studies Prospective Studies Magnetic Resonance Imaging/methods Pyramidal Tracts


 Humans *Amyotrophic Lateral Sclerosis/diagnosis Motor Neurons/physiology Action Potentials/physiology Muscle, Skeletal/physiology Reproducibility of Results

 Humans Animals Mice Infant *Amyotrophic Lateral Sclerosis/pathology *Frontotemporal Dementia/pathology Motor Neurons/pathology Mutation DNA-Binding Proteins/metabolism Cyclins/genetics/metabolism
 Animals Mice Humans *Sjogren's Syndrome/genetics *Arthritis, Rheumatoid/genetics *Lupus Erythematosus, Systemic/genetics *Autoimmune Diseases HLA Antigens/genetics Histocompatibility Antigens Class II *Rheumatic Diseases *Scleroderma, Systemic/genetics Interferon Regulatory Factors


 Humans Quality of Life Prevalence *Neuralgia/epidemiology/etiology *Polyneuropathies/epidemiology/etiology *Scleroderma, Systemic/complications/epidemiology
 Humans *Hypertension, Renal/drug therapy/etiology *Acute Kidney Injury/diagnosis/etiology/therapy Angiotensin-Converting Enzyme Inhibitors/therapeutic use *Scleroderma, Systemic/complications/diagnosis/therapy *Scleroderma, Localized
 Male Humans Aged Prospective Studies *Motor Neuron Disease *Amyotrophic Lateral Sclerosis Exercise Physical Therapy Modalities
 Humans *Motor Neuron Disease/diagnosis *Amyotrophic Lateral Sclerosis/diagnosis/epidemiology/therapy Prospective Studies Pandemics *COVID-19
 Humans *Amyotrophic Lateral Sclerosis/complications/physiopathology Exhalation *Cough/etiology Spirometry Linear Models Severity of Illness Index
 Humans Precision Medicine *Scleroderma, Systemic/therapy/drug therapy Fibrosis Autoantibodies/therapeutic use *Autoimmune Diseases

 Humans *Amyotrophic Lateral Sclerosis/metabolism Superoxide Dismutase-1/metabolism Protein Aggregates C9orf72 Protein/genetics DNA-Binding Proteins/genetics/metabolism

 Humans *Amyotrophic Lateral Sclerosis/genetics/pathology *Frontotemporal Dementia/genetics/pathology C9orf72 Protein/genetics/metabolism Transcriptome *Pick Disease of the Brain/genetics DNA-Binding Proteins/genetics/metabolism Exons Sequence Analysis, RNA
 Humans Female Male Plasma Exchange Retrospective Studies Myelin-Oligodendrocyte Glycoprotein *Optic Neuritis/therapy *Neuromyelitis Optica Vision Disorders/therapy Autoantibodies
 Humans *Mesenchymal Stem Cell Transplantation *Autoimmune Diseases/therapy *Lupus Erythematosus, Systemic *Mesenchymal Stem Cells *Rheumatic Diseases/therapy


 *Scleroderma, Localized *Scleredema Adultorum *Skin Diseases/etiology *Scleroderma, Systemic Skin *Basidiomycota

 Humans *Neuroendocrine Tumors/genetics/pathology *Pancreatic Neoplasms/genetics *Stomach Neoplasms *Intestinal Neoplasms/genetics *Multiple Endocrine Neoplasia Type 1/genetics
 Mice Animals *Amyotrophic Lateral Sclerosis/metabolism Mitochondria/metabolism Apoptosis *Neurodegenerative Diseases/metabolism Mitochondrial Dynamics/physiology
 Humans Immunosuppressive Agents/adverse effects *Lung Diseases, Interstitial/diagnosis/drug therapy/etiology Cyclophosphamide/therapeutic use *Scleroderma, Systemic/complications/drug therapy Patient Care Lung
 Mice Animals *Amyotrophic Lateral Sclerosis/diagnostic imaging/drug therapy Superoxide Dismutase-1/metabolism Edaravone/metabolism Neuroinflammatory Diseases *Neurodegenerative Diseases Pilot Projects Superoxide Dismutase/genetics/metabolism Motor Neurons Mice, Transgenic Brain/metabolism Disease Progression Disease Models, Animal
 Humans *Amyotrophic Lateral Sclerosis/genetics Twins, Monozygotic/genetics *Neurodegenerative Diseases Mutation/genetics Whole Genome Sequencing


 Humans Antigen-Antibody Complex *Scleroderma, Systemic *Autoimmune Diseases Antigens *Lupus Erythematosus, Systemic
 Humans *Fingers/blood supply Skin Nails/diagnostic imaging/blood supply Microcirculation *Scleroderma, Systemic/complications/diagnostic imaging

 Humans Female *Quality of Life Activities of Daily Living Hand Strength Longitudinal Studies Disability Evaluation *Scleroderma, Systemic/diagnosis
 Humans United States *Amyotrophic Lateral Sclerosis/epidemiology Prevalence Incidence Cost of Illness Registries
 Humans *Amyotrophic Lateral Sclerosis/drug therapy Motor Neurons Drug Discovery/methods Biomarkers

 Animals Male Mice Amnesia/metabolism Disease Models, Animal *Fingolimod Hydrochloride/therapeutic use/metabolism/pharmacology Gulf War Memory Disorders/chemically induced/drug therapy/metabolism Mice, Inbred C57BL Microglia Neuroinflammatory Diseases NF-kappa B/metabolism *Persian Gulf Syndrome/chemically induced/drug therapy/metabolism Protein Kinases/metabolism/pharmacology/therapeutic use Pyridostigmine Bromide/therapeutic use/pharmacology

 Humans Tumor Necrosis Factor Inhibitors/adverse effects Etanercept/adverse effects *Rheumatology *Arthritis, Rheumatoid/complications/drug therapy/epidemiology *Arthritis, Psoriatic/complications/drug therapy/epidemiology Antibodies, Monoclonal

 Male Humans Adult *Hodgkin Disease Positron Emission Tomography Computed Tomography *Lymphoma Breast Mammography


 Humans *Amyotrophic Lateral Sclerosis/diagnosis/drug therapy *Motor Neuron Disease/diagnosis/drug therapy Therapies, Investigational Transcranial Magnetic Stimulation Treatment Outcome Randomized Controlled Trials as Topic Multicenter Studies as Topic
 Humans *Depressive Disorder, Major/diagnostic imaging/genetics *Cardiovascular Diseases/diagnostic imaging/genetics Genome-Wide Association Study/methods *Autism Spectrum Disorder/diagnostic imaging/genetics *Amyotrophic Lateral Sclerosis Mendelian Randomization Analysis/methods Phenotype *Brain Diseases/diagnostic imaging/genetics *Hypertension Neuroimaging

 Humans *Cluster Headache/therapy Cross-Sectional Studies


 Humans *Magnetic Resonance Imaging *White Matter
 Female Humans Adult Fluphenazine/adverse effects *Parkinsonian Disorders *Parkinson Disease, Secondary/chemically induced *Antipsychotic Agents/adverse effects Amnesia Memory Disorders/chemically induced





 Humans *Migraine Disorders/diagnosis Brain Neuroimaging Headache Pain

 Humans *Amyotrophic Lateral Sclerosis/metabolism *Induced Pluripotent Stem Cells Motor Neurons/metabolism Superoxide Dismutase-1/metabolism Mutation Phenotype Superoxide Dismutase/metabolism
 Mice Animals *Amyotrophic Lateral Sclerosis/drug therapy/genetics/pathology Superoxide Dismutase-1/genetics/metabolism Superoxides/metabolism Superoxide Dismutase/genetics/metabolism Mice, Transgenic Motor Neurons/metabolism Mitochondria/genetics/pathology Disease Progression Disease Models, Animal

 Humans *Transcriptome/genetics RNA, Messenger/genetics/metabolism Gene Expression Profiling Genome-Wide Association Study *Amyotrophic Lateral Sclerosis/genetics Genetic Predisposition to Disease Quantitative Trait Loci


 Humans Lung *Lung Diseases, Interstitial/etiology *Scleroderma, Systemic/complications Fibrosis *Autoimmune Diseases/complications Autophagy

 Animals Mice *Amyotrophic Lateral Sclerosis/metabolism DNA-Binding Proteins/genetics/metabolism Lysosomes/metabolism *Neurodegenerative Diseases/genetics Humans


 Female Humans *Amyotrophic Lateral Sclerosis/epidemiology *Air Pollutants/toxicity/analysis Case-Control Studies *Air Pollution/adverse effects/analysis Particulate Matter/toxicity/analysis Environmental Exposure/adverse effects/analysis Women's Health
 Humans *Gastrostomy/psychology Quality of Life *Motor Neuron Disease/therapy/complications/psychology Health Personnel Caregivers/psychology
 Humans *Connective Tissue Diseases/complications *Myositis *Autoimmune Diseases/complications *Muscular Diseases/etiology *Lupus Erythematosus, Systemic/complications *Arthritis, Rheumatoid/complications Muscle, Skeletal/pathology *Scleroderma, Systemic/complications
 Humans Mitophagy/physiology *Neurodegenerative Diseases/metabolism Mitochondria/metabolism *Parkinson Disease/metabolism Autophagy/physiology
 Humans *Lung Diseases, Interstitial/complications *Scleroderma, Systemic Immunosuppressive Agents/therapeutic use Biomarkers Disease Progression Lung



 Humans *Amyotrophic Lateral Sclerosis/genetics Genome-Wide Association Study *Duodenitis Phenotype *Gastritis Mendelian Randomization Analysis
 Humans *Amyotrophic Lateral Sclerosis/genetics Endothelial Cells
 Male Humans Female *Apolipoprotein E4/genetics Amyloid beta-Peptides/metabolism Apolipoprotein E2/genetics *Alzheimer Disease/genetics/pathology Apolipoproteins E/genetics Genotype Cognition
 Humans *Amyotrophic Lateral Sclerosis/diagnosis/therapy Brazil *Laughter Consensus Crying *Motor Neuron Disease *Neurology
 Humans *Amyotrophic Lateral Sclerosis/epidemiology/genetics/diagnosis Syndrome Delayed Diagnosis *Cognitive Dysfunction/epidemiology/genetics *Cognition Disorders/diagnosis
 Animals *Amyotrophic Lateral Sclerosis/drug therapy/genetics/metabolism Motor Neurons Mutation RNA-Binding Protein FUS/metabolism *Phosphatidylinositol 3-Kinases/metabolism Disease Models, Animal

 Humans *Neurodegenerative Diseases/genetics/pathology *Alzheimer Disease/genetics Gene Expression Regulation Mitochondria/genetics RNA/genetics
 Humans United States/epidemiology Cause of Death *Amyotrophic Lateral Sclerosis *Cardiovascular Diseases/epidemiology Causality
 Humans *Neurodegenerative Diseases/genetics *Amyotrophic Lateral Sclerosis/genetics Nerve Degeneration Homeostasis RNA
 Infant, Newborn Humans *Vitamin D-Binding Protein/genetics *Genome-Wide Association Study Vitamin D/genetics Calcifediol Vitamins Polymorphism, Single Nucleotide Pore Forming Cytotoxic Proteins/genetics
 Humans *Arthritis, Psoriatic Chronic Disease *Hidradenitis Suppurativa Immunity, Innate Inflammation *Interleukin-17 Interleukin-23 Lymphocytes *Psoriasis



 Humans *Lymphangioleiomyomatosis/diagnosis/therapy *Lung Neoplasms/diagnosis/therapy/genetics *Tuberous Sclerosis/diagnosis/therapy/genetics Lung *Angiomyolipoma/drug therapy
 Humans Retrospective Studies *Scleroderma, Systemic Autoantibodies *Lung Diseases, Interstitial/complications *Scleroderma, Localized Phenotype

 Rats Animals *Autism Spectrum Disorder/genetics/metabolism Mechanistic Target of Rapamycin Complex 1/metabolism Pyramidal Cells/metabolism Hippocampus/metabolism Neuronal Plasticity Disease Models, Animal
 Humans *Amyotrophic Lateral Sclerosis/genetics beta Catenin/metabolism Cell Line, Tumor Cell Movement Cell Proliferation/genetics Gene Expression Regulation, Neoplastic Leukocytes, Mononuclear/metabolism *MicroRNAs/genetics/metabolism *Neuroblastoma *RNA, Long Noncoding/genetics/metabolism Zinc Finger E-box-Binding Homeobox 1/genetics/metabolism
 Mice Animals *Amyotrophic Lateral Sclerosis/genetics *Frontotemporal Dementia/genetics *Alzheimer Disease/genetics Neuroprotection DNA-Binding Proteins/metabolism *Pick Disease of the Brain Immunotherapy
 Humans Male Female Child Middle Aged Incidence *Sjogren's Syndrome Cohort Studies *Diabetes Mellitus, Type 1/complications Prevalence *Anemia, Pernicious/complications *Celiac Disease/epidemiology/complications *Autoimmune Diseases/epidemiology/complications Social Class *Graves Disease/complications *Lupus Erythematosus, Systemic England *Thyroiditis/complications


 Humans *Magnetic Resonance Imaging/methods Neuroimaging Imaging, Three-Dimensional/methods Brain *Nervous System Diseases
 Pregnancy Female Humans Pregnancy Trimester, First/physiology *Decidua/metabolism *Trophoblasts/metabolism Phenotype Macrophages/metabolism

 Humans *Transcriptome/genetics *Cryopreservation/methods Gene Expression Profiling/methods B-Lymphocytes
 Humans *Anaplasmataceae Infections/diagnosis/drug therapy *Anaplasmataceae/genetics *Tick-Borne Diseases/diagnosis/drug therapy Real-Time Polymerase Chain Reaction Immunocompromised Host
 Mice Animals Fibrosis *Cadherins/metabolism Cell Adhesion *Liver/metabolism

 Humans *Neuromyelitis Optica/diagnosis/therapy/complications *Encephalitis/complications Myelin-Oligodendrocyte Glycoprotein *Meningitis, Aseptic/etiology/complications *Meningoencephalitis/diagnosis/etiology Autoantibodies
 Humans Child *Gastrostomy/adverse effects Cohort Studies *Bone Marrow Transplantation Retrospective Studies Enteral Nutrition/methods
 Humans *Frontotemporal Dementia/genetics/metabolism Mitochondrial Proteins/chemistry Mitochondria/metabolism Mutation/genetics *Amyotrophic Lateral Sclerosis/metabolism

 Humans *COVID-19 Artificial Intelligence Pandemics ROC Curve Hospitalization Retrospective Studies

 Humans *Neuromyelitis Optica Kynurenine Tryptophan Pilot Projects Tandem Mass Spectrometry Autoantibodies Aquaporin 4 Immunoglobulin G
 Rats Animals *Ganglia, Spinal/metabolism Proteomics Rats, Sprague-Dawley Cells, Cultured Axons/metabolism Nerve Regeneration/physiology Sensory Receptor Cells/physiology *Peripheral Nerve Injuries/metabolism

 Humans Adult Middle Aged Aged *Dysphonia/diagnosis/etiology *Amyotrophic Lateral Sclerosis/complications Speech Acoustics Voice Quality Acoustics Speech Production Measurement/methods
 Humans Aged, 80 and over *Alzheimer Disease/pathology Cognition Brain/pathology *Lewy Body Disease/pathology
 Mice Animals *Amyotrophic Lateral Sclerosis/genetics Motor Neurons *Neurodegenerative Diseases Mutation DNA-Binding Proteins/genetics
 Humans *DNA Methylation *Transcriptome beta Catenin Leukocytes, Mononuclear Ligands DNA RNA, Messenger/genetics
 Humans *Amyotrophic Lateral Sclerosis/metabolism Cell Nucleus/metabolism Cytoplasm/metabolism DNA-Binding Proteins/genetics/metabolism *Frontotemporal Dementia/genetics/metabolism



 Humans *DNA Repeat Expansion/genetics Mutation Proteins/genetics *Neuromuscular Diseases/genetics RNA/genetics Nucleotides
 Humans *Muscular Dystrophies/diagnosis *Neuromuscular Diseases/diagnosis/therapy Rare Diseases *Glycogen Storage Disease Type II Registries


 Animals Mice *Amyotrophic Lateral Sclerosis/genetics/pathology Biological Transport Chloride Channels/genetics/metabolism Endoplasmic Reticulum/metabolism Homeostasis Mitochondrial Proteins/metabolism Mutation/genetics
 Humans *Alzheimer Disease/genetics Genomics Brain DNA, Mitochondrial Aging/genetics *Hippocampal Sclerosis

 Humans Animals Mice *Scleroderma, Localized Interleukin-6 Endothelial Cells Skin Disease Models, Animal *Basidiomycota

 Humans Aged *Digital Technology Gait Walking Walking Speed Physical Therapy Modalities *Proximal Femoral Fractures
 Female Humans Myelin-Oligodendrocyte Glycoprotein Aquaporin 4 *Myelitis, Transverse/etiology COVID-19 Vaccines/adverse effects SARS-CoV-2 BNT162 Vaccine *COVID-19/prevention & control *Neuromyelitis Optica *Optic Neuritis Central Nervous System *Encephalomyelitis, Acute Disseminated/etiology Vaccination/adverse effects Inflammation
 Adult Animals Humans Mice Axons/metabolism *Central Nervous System/cytology/metabolism/pathology *Microglia/cytology/metabolism/pathology *Myelin Sheath/metabolism/pathology Neurodegenerative Diseases/metabolism/pathology Oligodendroglia/metabolism/pathology Cognition Transforming Growth Factor beta1/metabolism Receptor, Transforming Growth Factor-beta Type I/metabolism Lipid Metabolism Aging/metabolism/pathology
 *Astrocytes/physiology *Genetic Testing/methods High-Throughput Screening Assays *Microfluidic Analytical Techniques/methods *Microglia/physiology *Amphiregulin/genetics *Autocrine Communication/genetics Gene Expression Humans




 Humans *Osteopetrosis/diagnostic imaging/genetics *Osteosclerosis/diagnostic imaging/genetics *Osteochondrodysplasias/genetics Mutation/genetics *Vacuolar Proton-Translocating ATPases/genetics Nucleoside Transport Proteins/genetics

 Female Humans Male *Amyotrophic Lateral Sclerosis/genetics/metabolism C9orf72 Protein/genetics Dipeptides/genetics/metabolism DNA Helicases/metabolism *Frontotemporal Dementia/genetics/metabolism Histones JNK Mitogen-Activated Protein Kinases/metabolism Poly-ADP-Ribose Binding Proteins RNA Helicases/metabolism RNA Recognition Motif Proteins Stress Granules Drosophila melanogaster Animals
 Humans *COVID-19 *MicroRNAs/genetics RNA-Binding Proteins/genetics *Nervous System Diseases *Neoplasms
 Humans *Amyotrophic Lateral Sclerosis/drug therapy Bayes Theorem Disease Progression Time Factors Clinical Trials as Topic

 Humans *Drug Approval/methods Europe Cross-Sectional Studies *Patient Reported Outcome Measures
 Mice Animals *Lateral Ventricles *Transcriptome/genetics Brain Neurons Cell Differentiation/genetics Fibroblast Growth Factors Mammals



 Humans Middle Aged *Intermediate Filaments Prealbumin Switzerland *Amyloid Neuropathies, Familial/diagnosis Biomarkers Neurofilament Proteins

 Adult Humans *Depressive Disorder, Major/diagnosis Depression *Sleep Initiation and Maintenance Disorders/epidemiology *Metabolic Syndrome/metabolism *Insulins

 Humans Male Middle Aged *CADASIL/diagnostic imaging/genetics *Stroke, Lacunar/genetics *Ischemic Stroke/genetics *Fabry Disease/genetics Exome Receptor, Notch3/genetics *Stroke/diagnostic imaging/genetics Receptors, Notch/genetics Magnetic Resonance Imaging Mutation/genetics
 Humans *Acetylcholine *Methylphenidate Nicotine/pharmacology Norepinephrine Reboxetine Double-Blind Method
 Humans Female Middle Aged Male *Trigeminal Neuralgia/drug therapy Retrospective Studies Lacosamide/therapeutic use Cohort Studies Treatment Outcome Pain
 Humans *COVID-19 SARS-CoV-2 Pandemics *Coinfection Intensive Care Units
 Humans *Amyotrophic Lateral Sclerosis/drug therapy/genetics Interleukin-18 Quality of Life Ribosomal Proteins Autophagy
 Male Humans Aged Middle Aged Female Snoring/pathology Biological Specimen Banks Brain/diagnostic imaging/pathology Cognition Sleep Magnetic Resonance Imaging *Disorders of Excessive Somnolence/pathology Obesity/complications/pathology *Cardiovascular Diseases/epidemiology United Kingdom/epidemiology
 Humans *Antioxidants/pharmacology/therapeutic use/metabolism Phosphatidylinositol 3-Kinases/metabolism Ultraviolet Rays Oxidative Stress Phenols/pharmacology/therapeutic use *Neoplasms/drug therapy Polyphenols/pharmacology Free Radicals/metabolism Inflammation/drug therapy Anti-Inflammatory Agents/pharmacology/therapeutic use/chemistry


 Animals *Status Epilepticus Seizures *Seizures, Febrile Brain Disease Models, Animal
 Humans *Churg-Strauss Syndrome *Granulomatosis with Polyangiitis *Sarcoidosis *Arthritis, Rheumatoid Disease Progression

 Humans Amyloidogenic Proteins/metabolism *Diabetes Mellitus, Type 2/metabolism *Alzheimer Disease/metabolism *Parkinson Disease
 Female Humans Young Adult Adult *Low Back Pain/etiology *Tarlov Cysts/complications/diagnosis/therapy Activities of Daily Living *Cysts Primary Health Care

 Animals Humans Cyanobacteria Toxins *Neurodegenerative Diseases Ecosystem *Amino Acids, Diamino/metabolism Fresh Water/microbiology Amino Acids/metabolism *Cyanobacteria/metabolism Mammals
 Humans Rituximab *Biosimilar Pharmaceuticals/therapeutic use Antibodies, Monoclonal, Murine-Derived/therapeutic use *Autoimmune Diseases Immunosuppressive Agents/therapeutic use *Antineoplastic Agents/therapeutic use *Immune System Diseases

 Humans Microglia/metabolism *Neurodegenerative Diseases/metabolism Central Nervous System/metabolism *Alzheimer Disease/metabolism *Parkinson Disease/metabolism
 Humans Child *Carcinoma, Adenoid Cystic Mosaicism Inheritance Patterns Phenotype

 Humans Benchmarking *Amyotrophic Lateral Sclerosis *Intrinsically Disordered Proteins Water RNA-Binding Protein FUS




 Humans Skin *Psoriasis Inflammation/complications *Skin Neoplasms *Hidradenitis Suppurativa Chronic Disease


 Animals *Trichloroethylene/toxicity/analysis *Parkinson Disease/epidemiology/etiology Solvents/toxicity Risk Factors
 Humans *Bias *Randomized Controlled Trials as Topic *Evidence-Based Medicine
 Adult Humans *Lung Diseases, Interstitial/diagnosis/etiology Interleukin-8 Pulmonary Surfactant-Associated Protein D *Scleroderma, Systemic/complications/diagnosis Biomarkers Lung
 Rats Animals Rats, Sprague-Dawley NF-kappa B/metabolism/pharmacology/therapeutic use Toll-Like Receptor 4/metabolism/therapeutic use *Brain Ischemia/drug therapy Inflammation/drug therapy/metabolism Nerve Growth Factors/pharmacology Microglia/metabolism Infarction, Middle Cerebral Artery/complications/drug therapy *Reperfusion Injury/drug therapy/metabolism

 Male Female Humans Aged Incidence Cohort Studies *HIV Infections *Autoimmune Diseases/epidemiology *Cross Infection Inflammation *Dementia/diagnosis/epidemiology Hospitals
 Male Humans Female Prospective Studies Cohort Studies Sweden/epidemiology *Emotions Occupations *Musculoskeletal Diseases/epidemiology Sick Leave
 Female Humans *Neuromyelitis Optica/diagnosis/drug therapy Immunoglobulin G Autoantibodies Myelin-Oligodendrocyte Glycoprotein Central Nervous System

 Humans Male Drug Interactions *Pyridones *Volunteers Healthy Volunteers Area Under Curve Cross-Over Studies

 Animals Humans Mice Cells, Cultured Collagen/metabolism Endothelial Cells/metabolism Fibroblasts/metabolism Fibrosis Microtubule Proteins/metabolism *Myofibroblasts/pathology *Scleroderma, Systemic/pathology Skin/pathology
 Animals Female Humans Male Mice Diet, High-Fat/adverse effects Mammals/metabolism Mice, Knockout Neurons/metabolism Obesity/metabolism TOR Serine-Threonine Kinases/metabolism *Tuberous Sclerosis/complications Weight Gain
 Humans *Insular Cortex Magnetic Resonance Imaging/methods Algorithms Brain/pathology *Epilepsy/pathology Image Processing, Computer-Assisted/methods
 Humans Immunoglobulins, Intravenous/therapeutic use Retrospective Studies *Scleroderma, Systemic/complications/drug therapy *Gastrointestinal Diseases/drug therapy/etiology *Intestinal Pseudo-Obstruction/drug therapy/etiology

 Animals Mice *Adipogenesis *Scleroderma, Localized Adiposity Obesity Subcutaneous Fat
 Animals *Neurodegenerative Diseases/drug therapy *Alzheimer Disease/drug therapy Neuroprotection Cinnamates/pharmacology/therapeutic use/metabolism *Neuroprotective Agents/pharmacology/therapeutic use


 Pregnancy Female Humans Adult *Hodgkin Disease/diagnosis/complications/drug therapy Pregnancy Trimester, Second Bleomycin/therapeutic use Doxorubicin/therapeutic use Vinblastine/therapeutic use
 Humans Mitochondria/metabolism Oxidative Stress/physiology Aging/physiology *Glaucoma/metabolism *Neurodegenerative Diseases/metabolism
 Humans *Glomerulonephritis, IGA/pathology *Glomerulosclerosis, Focal Segmental/pathology Prognosis Macrophages/metabolism Cytokines

 Humans *Cognitive Dysfunction Hippocampus/diagnostic imaging Magnetic Resonance Imaging/methods *Alzheimer Disease/diagnostic imaging Biomarkers


 Humans Female Aged Male *Coronary Artery Disease *Ischemic Attack, Transient Prospective Studies Intermediate Filaments Prognosis *Stroke/diagnosis *Myocardial Infarction
 Humans *SARS-CoV-2 Retrospective Studies Propensity Score *COVID-19 Antibodies, Neutralizing

 Male Humans Female *Parkinson Disease/complications/epidemiology Cross-Sectional Studies *Myocardial Infarction/epidemiology Risk Factors Prevalence
 Humans *Frontotemporal Dementia/genetics *Amyotrophic Lateral Sclerosis/genetics C9orf72 Protein/genetics RNA/genetics Single Molecule Imaging Dipeptides Carrier Proteins
 Humans Infant *Lyme Neuroborreliosis/drug therapy/complications/diagnosis Prospective Studies Retrospective Studies Intermediate Filaments Anti-Bacterial Agents/therapeutic use Biomarkers
 Humans Diffusion Tensor Imaging/adverse effects *Parkinson Disease/complications/diagnostic imaging/pathology *Gait Disorders, Neurologic/diagnostic imaging/etiology *Parkinsonian Disorders/complications/diagnostic imaging Gait/physiology Cognition

 Humans Mitochondrial Dynamics *Neuroblastoma/metabolism Mitochondria/genetics/metabolism Mutation GTP Phosphohydrolases/genetics Mitochondrial Proteins/genetics *Charcot-Marie-Tooth Disease/genetics
 Pregnancy Female Humans *COVID-19 SARS-CoV-2/physiology Spike Glycoprotein, Coronavirus Hemorrhage *Pregnancy Complications, Infectious
 Humans Myelin-Oligodendrocyte Glycoprotein Retrospective Studies *Encephalitis/diagnostic imaging Autoantibodies Magnetic Resonance Imaging

 Mechanistic Target of Rapamycin Complex 1/metabolism *Glycogen Synthase Kinase 3/metabolism *Signal Transduction TOR Serine-Threonine Kinases/metabolism Phosphorylation Protein Phosphatase 1/metabolism
 Humans Algorithms *B-Lymphocyte Subsets *B-Lymphocytes Flow Cytometry Healthy Volunteers Receptors, Complement 3d
 Humans *Terminal Care Palliative Care Death *Neurology *Suicide, Assisted Ethics, Medical
 Humans *Amyotrophic Lateral Sclerosis/prevention & control
 Adult Male Humans Middle Aged Aged Aged, 80 and over Female Prognosis *COVID-19 Biomarkers Intermediate Filaments Central Nervous System Neurofilament Proteins
 Rats Female Male Animals *Heart Failure Stroke Volume/physiology Kidney/physiology Obesity/complications *Hypertension/complications *Renal Insufficiency, Chronic Proteinuria Hypertrophy Disease Models, Animal
 Humans Artificial Intelligence *TDP-43 Proteinopathies/pathology *Amyotrophic Lateral Sclerosis/pathology *Nervous System Diseases
 Pregnancy Female Infant, Newborn Humans *Codeine/adverse effects Oxycodone/adverse effects Analgesics, Opioid/adverse effects Cohort Studies Retrospective Studies *Opioid-Related Disorders/epidemiology/drug therapy Drug Prescriptions
 Female Humans Aged *Gastric Antral Vascular Ectasia/complications/diagnosis/therapy Gastrointestinal Hemorrhage/etiology/therapy *Cocaine Risk Factors *Anemia, Iron-Deficiency/etiology/therapy



 *Glutamine/metabolism *Glutamic Acid/metabolism Astrocytes/metabolism Homeostasis/physiology Neurotransmitter Agents/metabolism gamma-Aminobutyric Acid/metabolism



 Humans *Temporomandibular Joint Disorders/diagnostic imaging Magnetic Resonance Imaging/methods Radiography Machine Learning Automation Temporomandibular Joint/diagnostic imaging



 Humans Quality of Life *Migraine Disorders Functional Laterality/physiology *Headache Disorders Headache

 Humans Spinal Cord Magnetic Resonance Imaging *Cervical Cord/diagnostic imaging Algorithms *Spinal Cord Injuries/diagnostic imaging Spinal Canal
 Humans *Neuromyelitis Optica/epidemiology Aquaporin 4 Antibodies, Antinuclear *Sjogren's Syndrome Immunoglobulin G Autoantibodies
 Female Humans Male Apolipoprotein E4 *Autoantibodies *Autoimmunity Cross-Sectional Studies Immunoglobulin Isotypes Immunoglobulin M Membrane Proteins Nerve Tissue Proteins Seroepidemiologic Studies Adult Middle Aged
 Humans *Adverse Childhood Experiences/statistics & numerical data *Epilepsy/complications/epidemiology Prospective Studies Retrospective Studies *Seizures/epidemiology
 Humans Retrospective Studies *COVID-19/complications/epidemiology SARS-CoV-2 *Cerebrovascular Disorders/epidemiology *Myocardial Infarction
 Middle Aged Female Humans Vasoconstriction/physiology Magnetic Resonance Angiography/adverse effects *Cerebrovascular Disorders/diagnosis *Headache Disorders, Primary/diagnostic imaging Ultrasonography, Doppler, Transcranial/methods Headache/complications Early Diagnosis Excipients *Vasospasm, Intracranial/diagnostic imaging/complications
 Aged Aged, 80 and over Humans Cognition *Cognitive Dysfunction/diagnosis/psychology Neuropsychological Tests Primary Health Care Reproducibility of Results Adolescent Young Adult Adult Middle Aged
 Humans *Cytochrome P-450 CYP3A/genetics Genome-Wide Association Study *Cluster Headache/drug therapy/genetics Tryptamines Verapamil/therapeutic use
 Adult Humans Female Middle Aged Male *Bone Density/physiology *Bone and Bones Absorptiometry, Photon Weight Loss
 Humans Female Adult Middle Aged Aged Male Autoimmunity Immune Checkpoint Inhibitors/therapeutic use Retrospective Studies *Neoplasms/drug therapy Autoantibodies *Encephalitis Central Nervous System
 Humans *Monocytes Interleukin-6 Cross-Sectional Studies Cytokines Biomarkers *Autoimmune Diseases of the Nervous System Receptors, IgG
 *Pulmonary Arterial Hypertension/blood/drug therapy/mortality/pathology Humans Retrospective Studies Male Female Middle Aged *Receptor for Advanced Glycation End Products/blood *Scleroderma, Systemic/complications Lung Diseases, Interstitial/drug therapy/pathology HMGB1 Protein/blood





 Humans Retrospective Studies Retina/diagnostic imaging/pathology *Hamartoma/pathology Tomography, Optical Coherence/methods *Retinal Neoplasms/diagnostic imaging/pathology *Astrocytoma/diagnostic imaging/pathology Fluorescein Angiography/methods
 Humans Genome-Wide Association Study *Glaucoma, Open-Angle/genetics *Glaucoma/genetics Intraocular Pressure/genetics Optic Nerve Polymorphism, Single Nucleotide/genetics Genetic Predisposition to Disease
 Humans *COVID-19 Follow-Up Studies Qualitative Research *Scleroderma, Systemic/therapy Videoconferencing

 Mice Humans Animals Bacteria/genetics Diet *Gastrointestinal Microbiome *Microbiota Feeding Behavior Firmicutes Clostridiales/genetics RNA, Ribosomal, 16S/genetics Mammals
 Humans Mice Animals *Arthritis, Psoriatic CD8-Positive T-Lymphocytes Imiquimod Mice, Inbred C57BL *Psoriasis *Skin Diseases Inflammation Receptors, Antigen, T-Cell/genetics Receptors, CCR4
 United States Humans Aged *Inpatients Single-Blind Method *Walking Hospitalization Outcome Assessment, Health Care Randomized Controlled Trials as Topic Multicenter Studies as Topic

 Adult Humans *Neuromyelitis Optica/drug therapy Aquaporin 4 Complement Inactivating Agents/therapeutic use Recurrence


 Humans Aged Retrospective Studies *Intermediate Filaments Neurofilament Proteins Biomarkers Immunoenzyme Techniques *Status Epilepticus/diagnosis
 Humans Visual Pathways/diagnostic imaging *Friedreich Ataxia/genetics Visual Acuity Retina/diagnostic imaging *Optic Nerve Diseases Tomography, Optical Coherence/methods
 Mice Animals *Endothelial Cells *Extracellular Matrix Proteins/metabolism T-Lymphocytes/metabolism Receptors, Antigen, T-Cell/metabolism Collagen/metabolism

 Adult Humans *Medically Unexplained Symptoms Cohort Studies Quality of Life Surveys and Questionnaires *Epilepsy/epidemiology Somatoform Disorders/epidemiology
 Adult Child Humans Adolescent *Lupus Nephritis/pathology Retrospective Studies Antibodies, Antineutrophil Cytoplasmic *Lupus Erythematosus, Systemic Kidney/pathology Hematuria
 Child Adult Humans *Cannabidiol/therapeutic use/pharmacology *Drug Resistant Epilepsy/drug therapy Anticonvulsants/therapeutic use/pharmacology *Lennox Gastaut Syndrome/drug therapy Seizures/drug therapy/chemically induced *Epilepsies, Myoclonic/drug therapy *Epilepsy/drug therapy/chemically induced *Cannabinoids/pharmacology
 Humans Mice Animals C9orf72 Protein HEK293 Cells *TOR Serine-Threonine Kinases/metabolism *Spinocerebellar Ataxias Mice, Transgenic Autophagy RNA, Messenger Sirolimus Cytoskeletal Proteins/genetics RNA-Binding Proteins/metabolism
 Humans *Phosphatidylinositol 3-Kinases/metabolism *Epithelial Cells/metabolism Lung/metabolism Acetyltransferases/metabolism/pharmacology A549 Cells N-Terminal Acetyltransferases/metabolism
 Humans *Alzheimer Disease Amyloid beta-Peptides Glycation End Products, Advanced/metabolism *Neurodegenerative Diseases Receptor for Advanced Glycation End Products/metabolism
 Humans Mice Animals *COVID-19/metabolism Fibroblasts/metabolism Lung/pathology *Idiopathic Pulmonary Fibrosis/pathology Fibrosis Membrane Proteins/metabolism

 Female Male Humans Immunoglobulins, Intravenous/therapeutic use Myelin-Oligodendrocyte Glycoprotein Autoantibodies *Myelitis, Transverse *Encephalomyelitis, Acute Disseminated/drug therapy Retrospective Studies *Neuromyelitis Optica
 Male Female Humans Aged *COVID-19/complications Follow-Up Studies *Movement Disorders/etiology Risk Factors Tremor/complications
 *Lectins, C-Type *Intestines Colon Signal Transduction Receptors, Antigen, T-Cell, gamma-delta
 Humans *Diffusion Tensor Imaging/methods Retrospective Studies Brain/diagnostic imaging Cerebral Hemorrhage/diagnostic imaging *White Matter/diagnostic imaging
 Adult Child Humans Infant B-Lymphocytes *Programmed Cell Death 1 Receptor Receptors, CXCR5 *T-Lymphocytes, Helper-Inducer *CD4-Positive T-Lymphocytes/immunology
 Animals Mice *Alzheimer Disease/genetics/metabolism Amyloid beta-Peptides/metabolism Mice, Transgenic Neurons/metabolism Synapses/metabolism

 Humans Male Middle Aged Female Cohort Studies Snoring/diagnosis *Parkinson Disease/complications Goals Sleepiness Surveys and Questionnaires *Sleep Apnea, Obstructive/complications/diagnosis/epidemiology Mass Screening
 Mice Animals *Paeonia/chemistry Glucosides/pharmacology/therapeutic use *Interferon Type I/therapeutic use Cytokines/metabolism *Autoimmune Diseases/drug therapy Bleomycin *Scleroderma, Systemic/drug therapy
 Animals Mice Cell Line Dopaminergic Neurons/metabolism Inflammation/chemically induced/drug therapy/metabolism Lipopolysaccharides Microglia Neuroinflammatory Diseases *NF-kappa B/metabolism NLR Family, Pyrin Domain-Containing 3 Protein/metabolism *Signal Transduction *Thymopentin/therapeutic use
 Humans *Parkinson Disease/complications Retina/diagnostic imaging Vision Disorders/etiology *Dementia/complications *Cognitive Dysfunction/etiology
 Humans Biological Specimen Banks *Status Epilepticus/drug therapy Seizures/complications *Drug Resistant Epilepsy/therapy *Encephalitis/complications Biomarkers
 Aged Humans Female Male *Stroke/epidemiology/surgery/etiology *Brain Ischemia/complications/surgery Retrospective Studies Treatment Outcome *Ischemic Stroke/etiology Thrombectomy/adverse effects


 Humans Longitudinal Studies *Retrograde Degeneration/complications/pathology *Spinal Cord Injuries/pathology Spinal Cord/pathology Pyramidal Tracts/pathology Atrophy/pathology
 Mice Animals *Receptors, N-Methyl-D-Aspartate/metabolism Structure-Activity Relationship *Synaptic Transmission/physiology Glutamic Acid/pharmacology Brain/metabolism
 Humans Male Female *Amyotrophic Lateral Sclerosis/genetics *Frontotemporal Dementia/diagnostic imaging/genetics/pathology C9orf72 Protein/genetics DNA Transposable Elements Atrophy
 *Genome-Wide Association Study *Proteomics Microscopy Transcription Factors Causality
 Humans Cross-Sectional Studies Activities of Daily Living *Neurodegenerative Diseases/diagnosis *Cognitive Dysfunction/psychology Cognition Biomarkers Observational Studies as Topic


 Humans *Alzheimer Disease/pathology Neuroimaging/methods Brain/pathology Atrophy/pathology Biomarkers Disease Progression Magnetic Resonance Imaging/methods
 Child Humans Child, Preschool Cohort Studies *Epilepsy, Absence/epidemiology Comorbidity *Epilepsy, Generalized Denmark/epidemiology
 Humans Cross-Sectional Studies Amyloid beta-Peptides/metabolism Positron-Emission Tomography/methods Cognition/physiology *Alzheimer Disease/metabolism *Cognitive Dysfunction/metabolism Amyloid/metabolism Cerebrovascular Circulation
 Humans Animals Mice *Obesity/metabolism *Cognition Brain/metabolism Drosophila/genetics Adipose Tissue/metabolism
 Humans Male Female Adolescent Adult Cross-Sectional Studies *Quality of Life *Family Wales Patient Reported Outcome Measures
 Humans Biomarkers *Nervous System Diseases Proteomics/methods Mass Spectrometry Neuroimaging
 Humans Prospective Studies Biological Specimen Banks Retina/diagnostic imaging *Eye Diseases *Dementia/diagnostic imaging United Kingdom/epidemiology
 Humans Minocycline/therapeutic use *Schizophrenia/drug therapy *Bipolar Disorder/drug therapy *Obsessive-Compulsive Disorder Anti-Inflammatory Agents/therapeutic use
 Rats Animals Rats, Sprague-Dawley *Spinal Cord/physiology *Brain-Derived Neurotrophic Factor/pharmacology/metabolism Proto-Oncogene Proteins c-akt/metabolism Phosphatidylinositol 3-Kinases/metabolism Lipopolysaccharides Hypoxia/metabolism Extracellular Signal-Regulated MAP Kinases/metabolism Inflammation/metabolism Mitogen-Activated Protein Kinase Kinases/metabolism/pharmacology Phrenic Nerve/physiology Neuronal Plasticity
 Humans *Epilepsy, Temporal Lobe/diagnostic imaging/surgery Retrospective Studies Positron Emission Tomography Computed Tomography *Epilepsy/surgery *Drug Resistant Epilepsy/diagnostic imaging/surgery Seizures *Epilepsies, Partial Electroencephalography Treatment Outcome Magnetic Resonance Imaging
 Humans *Livedo Reticularis Plasminogen Activator Inhibitor 1 Thrombomodulin Case-Control Studies Factor XIII Carotid Intima-Media Thickness Microcirculation Microscopic Angioscopy *Thrombophilia/diagnosis *Livedoid Vasculopathy Antithrombins
 Humans *Alzheimer Disease/epidemiology/genetics Genome-Wide Association Study Mendelian Randomization Analysis *Crohn Disease Polymorphism, Single Nucleotide/genetics Biomarkers

 Humans *Neuromyelitis Optica/drug therapy/epidemiology Quality of Life Neoplasm Recurrence, Local Spinal Cord Longitudinal Studies Aquaporin 4 Retrospective Studies Autoantibodies

 Pregnancy Humans Female Myelin-Oligodendrocyte Glycoprotein Retrospective Studies Prospective Studies *Postpartum Period Recurrence *Autoantibodies
 Humans Animals Mice *Huntington Disease/metabolism Neurons/metabolism *Neural Stem Cells/metabolism Corpus Striatum/metabolism Cell Differentiation Huntingtin Protein/genetics/metabolism Disease Models, Animal
 Humans Adult *Lupus Erythematosus, Systemic/drug therapy Severity of Illness Index Antibodies, Monoclonal, Humanized/therapeutic use
 Humans *Glaucoma, Open-Angle/genetics/pathology Genome-Wide Association Study *Parkinson Disease/pathology *Alzheimer Disease/genetics/pathology *Neurodegenerative Diseases/genetics/pathology *Glaucoma/genetics Brain/diagnostic imaging/pathology Nerve Degeneration/genetics/pathology
 Male Female Humans Middle Aged *Glucocorticoids/therapeutic use *Scleroderma, Systemic/drug therapy/complications Databases, Factual Data Collection
 Humans Protein Array Analysis *Cerebellar Ataxia Antibodies *Autoimmune Diseases of the Nervous System/diagnosis Epitopes *RGS Proteins
 Humans Retrospective Studies Chronic Disease Recurrence Myelin-Oligodendrocyte Glycoprotein *Autoantibodies
 Mice Animals Cricetinae *Proto-Oncogene Proteins c-akt/metabolism Phosphatidylinositol 3-Kinases/metabolism/pharmacology Phosphatidylinositol 3-Kinase/metabolism/pharmacology Antioxidants/pharmacology/therapeutic use CHO Cells Cricetulus Signal Transduction Tretinoin/pharmacology *Neural Tube Defects/chemically induced/prevention & control Oxidative Stress
 Humans Middle Aged *COVID-19/complications SARS-CoV-2 Cohort Studies *Myasthenia Gravis/drug therapy Risk Factors Immunosuppressive Agents/therapeutic use
 Humans Adult Cohort Studies *Diet *Energy Intake Food, Processed Depression/epidemiology Fast Foods
 Humans *Leukoencephalopathy, Progressive Multifocal/drug therapy Immune Checkpoint Inhibitors/adverse effects Retrospective Studies *JC Virus *Immune Reconstitution Inflammatory Syndrome/drug therapy



 Humans Autoantibodies Autoimmunity *COVID-19 *Autoimmune Diseases Receptors, G-Protein-Coupled/metabolism
 Humans *Herpesvirus 6, Human/genetics *MicroRNAs/genetics SARS-CoV-2/genetics *COVID-19/complications *Herpesviridae/genetics Real-Time Polymerase Chain Reaction Biomarkers DNA, Viral/genetics


 Humans *Alzheimer Disease/diagnostic imaging/genetics/metabolism *Basal Forebrain/pathology Basal Nucleus of Meynert/metabolism *Cognitive Dysfunction/diagnostic imaging/genetics/metabolism Amyloid beta-Peptides/metabolism
 Humans Endothelin-1 *Lung Diseases, Interstitial/complications/diagnosis *Idiopathic Pulmonary Fibrosis/complications/diagnosis *Autoimmune Diseases/complications/diagnosis *Arthritis, Rheumatoid/complications/diagnosis Biomarkers

 Humans Cohort Studies Incidence *Ischemic Stroke Prospective Studies *COVID-19/complications SARS-CoV-2 *Nervous System Diseases/epidemiology *Stroke/epidemiology
 Female Humans *COVID-19/complications/epidemiology Retrospective Studies SARS-CoV-2 Pandemics Prospective Studies *Nervous System Diseases/epidemiology/etiology/diagnosis Seizures/complications


 Female Humans Adult Adolescent Middle Aged Male *Neurodegenerative Diseases Retrospective Studies *Encephalitis/diagnosis Diagnostic Errors *Autoimmune Diseases of the Nervous System
 Humans *Alzheimer Disease/therapy Cost-Benefit Analysis Economics, Pharmaceutical *Dementia *Cognitive Dysfunction Disease Progression
 Humans *Parkinson Disease/genetics/epidemiology Haplotypes Mitochondria/genetics DNA, Mitochondrial/genetics Disease Progression Cognition
 Humans *COVID-19 SARS-CoV-2 Longitudinal Studies Multiomics Disease Progression
 Humans *Nervous System Diseases/epidemiology Brain Global Health

 Adult Humans Double-Blind Method *Myotonic Dystrophy/drug therapy/genetics Myotonin-Protein Kinase *Oligonucleotides, Antisense/pharmacology/therapeutic use RNA RNA, Messenger/metabolism Treatment Outcome
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 The range of treatment options available for multiple sclerosis (MS) is growing, with the aim of developing safer and more effective therapies. There are ongoing efforts to discover additional mechanisms of MS and create drugs that can target these pathways. A more tailored approach will allow better personalization of drug selection for patients. There is currently a special focus on identifying treatment targets for progressive MS, where there are only a limited number of therapeutic options available to date. In addition, there is ongoing research aimed at developing stem cell therapies, drugs that provide neuroprotection and agents that can potentially reverse the damage caused by MS through remyelination. In this review, these topics are summarized.





























































































































































 This case report describes a case of a man in his 30s who presented with episodic right lower facial paresis for 10 days and was diagnosede with an episodic, transient pattern of unilateral facial palsy associated with relapsing remitting multiple sclerosis.

















































































 This Viewpoint discusses incorporating the central vein sign into the diagnostic criteria for multiple sclerosis.























































 When women with relapsing multiple sclerosis (RMS) plan a pregnancy, doctors must think about the possible effects of medicines. Patients can take medicines with a well-defined safety profile to reduce the risk of attacks after stopping strong treatments. In this study, women stopped taking their RMS medicines and either: took well-defined RMS medicines, glatiramer acetate (GA) or IFN-β; or stopped all RMS medicines. The rate of attacks (in a year) was lower in patients who started taking GA/IFN a while after stopping their previous RMS medicines compared with patients who took no more medication. Women with low RMS activity in the year before stopping RMS treatment because of pregnancy planning may benefit from GA/IFN treatment prior to conception.


























































































































































 The therapeutic benefits of ofatumumab in relapsing multiple sclerosis (RMS) patients have been reported in the ASCLEPIOS I and II trials. Using an Expanded Disability Status Scale-based Markov model, this study aimed to assess the impact of early (i.e. at first-line, as the first treatment after diagnosis) vs delayed (i.e. 3-year delay) ofatumumab initiation in RMS patients from a Spanish societal perspective. In addition, the long-term clinical, societal, and economic outcomes of ofatumumab vs teriflunomide treatment were assessed. Evidence from this study suggests that early initiation of a high-efficacy therapy such as ofatumumab, compared with its delayed initiation, is an effective and cost-saving strategy for improving outcomes in RMS patients. Furthermore, patients receiving ofatumumab for 10 years are projected to experience comparatively better outcomes (clinical, societal, and economic) than those receiving teriflunomide.

















































































































































































































































































































































































 It is important for people living with multiple sclerosis (MS) to take their medication regularly – and to keep doing so – in order to control their symptoms. Some people with MS receive a medication called interferon beta-1a (Rebif®) as a subcutaneous injection (given just under the skin), and the RebiSmart® electromechanical autoinjector was designed to help them to self-inject such medication. This study aimed to find out whether people were using the RebiSmart® device as often as they should be, and how long they continued to use it for. Information was taken from the MSdialog database, which recorded peoples' use of the RebiSmart® device between January 2014 and November 2019. Records for 2644 people using the device were analyzed. Results showed that the RebiSmart® device was used most of the time (around 91.7%). On average, people kept using the device for around a year and 4 months before stopping. This duration was generally longer for men compared with women, and longer for older people than younger people. These results increase our understanding of how people are using the RebiSmart® device to treat their MS symptoms.



































 This study investigated the role of a genetic variant that increases saturated fat absorption and may make people with multiple sclerosis (MS) more susceptible to disability progression. Of 51 people with MS, 19 had followed a program which includes normalization of blood test results and daily intake of unsaturated fatty acids for more than 10 years, while the others had not. The latter group had significantly greater disability than the people who had followed the program, suggesting that the unsaturated fatty acids modulated the effect of the genetic variant. Six MS cases are presented as examples, including a marathon athlete (Case 1) and a patient who showed a dramatic decrease in disability from being wheelchair-bound for 15 years to walking freely (Case 2).









































































































































































































































































































































































































 People with multiple sclerosis (MS) commonly experience fluctuations in pain and fatigue severity. These fluctuations correspond with changes in physical, social, and psychological functioning. It is thus important to identify ways of reducing the impact of MS symptom exacerbations on daily functioning, such as by modifying individuals’ use of coping strategies. We tested whether the relationships between fluctuations in pain/fatigue severity and same-day functioning in MS differ based on coping tendencies. Individuals with MS completed a questionnaire about how they generally cope with stress. They also provided ratings of their pain and fatigue severity 5 times daily for 7 days using a wrist-worn electronic diary, and they completed end-of-day questionnaires about their same-day functioning and emotional health. The results showed that coping tendencies influence the relationships between fluctuations in symptom severity and same-day pain interference and positive emotions/moods and well-being. Specifically, avoidant coping, like disengagement and denial, was related to worse outcomes, whereas approach coping, like problem-solving and seeking social support, was associated with better outcomes. These findings suggest that reducing frequency of avoidant coping and fostering use of approach coping strategies related to pain and fatigue might reduce the impact of these symptoms on functioning and quality of life in MS.





































 A large retrospective study was carried out on people with multiple sclerosis (PwMS) being treated with intramuscular interferon-β medication from the New York State Multiple Sclerosis Consortium. The aim of the study was to look at whether patient-reported and clinical measures could be used early on to predict whether PwMS have worsening of their disease. The study demonstrated that patient-reported levels of limitations in multiple physical and mental symptoms can predict future worsening in objectively quantified disability in PwMS who take intramuscular interferon-β medication. Reported limitations in lower extremities and fatigue were the most predictive of future disability worsening.














 This Viewpoint describes the benefits and limitations of using neurofilament light chain (NfL) as a marker of real-time disease activity and treatment response in multiple sclerosis.

































































 Ocrelizumab (OCR), natalizumab (NTZ), and alemtuzumab (ATZ) are infusible drugs to treat patients with multiple sclerosis (MS). We did a study to understand the costs of these infusible MS drugs in real-world settings by analyzing a patients’ pharmacy and medical claims database. A total of 1,058 patients were included. We found that the annual total costs increased substantially after patients started to use these infusible MS drugs. Specifically, the average first- and second-year total costs for patients were $125,597 and $109,618 for OCR, $117,033 and $106,626 for NTZ, and $179,809 and $108,636 for ATZ, respectively. We also found that the cost of the drug itself is the main driver for the overall healthcare spending, accounting for >78% of the total costs. Additionally, we found that the cost varies depending on where patients receive these infusible MS drugs, and generally speaking, infusions received from hospital outpatient settings would be more expensive than received from home settings. In summary, this study showed that the real-world costs of these infusible MS drugs are very high. Shifting patients away from more costly hospital outpatient departments or using MS drugs that do not require infusion resources (e.g. oral/self-injectable) may help reduce the overall healthcare spending on MS.























































































 Nerve cells in the brain and spinal cord are surrounded by a layer of insulation called myelin that allows cells to transmit messages to each other more quickly and efficiently. This protective sheath is produced by cells called oligodendrocytes which together with their immature counterparts can also repair damage caused to myelin. In the inflammatory disease multiple sclerosis (MS), this insulation is disrupted and oligodendroglia fail to repair breaks in the myelin sheath, leaving nerves vulnerable to further damage. Recently it was discovered that mature and immature oligodendrocytes (which are collectively known as oligodendroglia) sometimes express proteins normally restricted to the immune system called major histocompatibility complexes (or MHCs for short). Researchers believe that MHC expression may allow oligodendroglia to interact with immune cells, potentially leading to the removal of oligodendroglia by the immune system as well as inflammation that exacerbates damage to nerves and hinders myelin repair. Knowing when oligodendroglia start producing MHCs and where these MHC-expressing cells are located is therefore important for understanding their role in MS. However, it is difficult to identify the location of MHC-expressing oligodendroglia using methods that are currently available. To address this, Harrington, Catenacci et al. created a genetically engineered mouse model in which the MHC-expressing oligodendroglia also generated a red fluorescent protein that could be detected under a microscope. This revealed that only a small number of oligodendroglia in the nervous system had MHCs, but these cells were located in areas of the brain and spinal cord with the highest inflammatory activity. Further microscopy studies in mice that developed MS-like symptoms revealed that MHC production in oligodendroglia increased compared with healthy animals, and that the proportion of oligodendroglia that produced MHC was highest in mice with the most severe symptoms. MHC-expressing oligodendroglia also congregated in the most damaged areas of the brain and spinal cord. These results suggest that MHC expression may contribute to inflammation and impact the function of oligodendroglia that have these molecules. In the future, Harrington et al. hope that their new mouse model will help researchers study the role of MHC expression in different diseases, and in the case of MS, aid the development of new treatments.





















































































































































































































































































































































































































































































































































































 Multiple sclerosis is more common in women than men, and many women with multiple sclerosis have not completed their families when they are diagnosed. This means that they face complicated decisions around using disease-modifying therapies, many of which have limited evidence for use in pregnancy. Conversations between clinicians and women with multiple sclerosis around pregnancy do not always address all of the issues that women face, partly because not all of the needed information is available. Consensus guidelines have recently been developed, and both experience and opinion have been used to inform these. This paper provides a practical overview of the use of treatments for MS and its symptoms.























































































 Multiple sclerosis is a long-term condition which affects the brain and nervous system. Multiple sclerosis care has often focused more on the physical aspects of the disease than its mental challenges. Examples of mental challenges are brain fog, which can make it hard to organise thoughts, and memory problems. In 2020, the Multiple Sclerosis in the 21st Century group held a meeting at a medical conference called the European Charcot Foundation. In this conference, a patient expert living with multiple sclerosis, together with a neuropsychologist and neurologist both specialising in multiple sclerosis, discussed its mental symptoms and why they are not always recognised and addressed by people with multiple sclerosis and their healthcare teams. The group emphasised that these symptoms can considerably affect the day-to-day lives of people who experience them, stressing that this is a key reason why mental symptoms need to be better prioritised in care. The group advocated for early and frequent cognition testing to be a part of the standard care approach, as is the case with physical symptoms. They also urged healthcare professionals to promote a ‘brain-healthy’ lifestyle to their patients with multiple sclerosis and to encourage participation in cognitive rehabilitation programmes to maintain their mental abilities in the long run. Finally, the group discussed that more drug development studies that specifically assess how a treatment can reduce mental symptoms are needed: in this way, research and healthcare approaches can better prioritise mental symptoms.





















































 For persons living with advanced MS:Physical exertion has the potential to enhance sense of self through regaining a lost, or creating a new identity.Physical exertion can enhance bodily consciousness and cause individuals to dwell on inability, consequently health care professionals should consider how their language and therapy focus may intensify this.Attempting to meet societally accepted standards of normal had a shaping influence on the exertional experience.The meaning of physical exertion is influenced by an individual’s preconceptions and healthcare professionals should take time to understanding these, in order to optimise engagement in physical exertion.



































































 Signals between the brain and spinal cord are disrupted in people with Multiple Sclerosis. For those with relapsing-remitting Multiple Sclerosis (RRMS), symptoms get periodically better and worse over time. We looked at whether changes in the brain of people with RRMS were associated with changes in their mood over time. People who had more changes in certain areas of the brain at the start of the study were more likely to have symptoms of depression later. This work suggests that early changes in the brain may be linked to increased symptoms of depression over time in people with RRMS. We believe this could be an opportunity to provide care to those suffering from RRMS to lessen the impact of severe depression symptoms before they arise.































 Many people with multiple sclerosis (MS) have spasticity, generally in the lower limbs, but this symptom is complex and multidimensional and therefore difficult to characterize.MS spasticity may be influenced by moderators, triggers, modifiers, and treatment, all of which can affect objective measures and the subjective experience of spasticity.MS spasticity can have physical, functional, social, and emotional/psychological impacts as well as long-term consequences that can affect rehabilitation and ultimately reduce health-related quality of life for people with MS.Given that people with MS may view spasticity differently than their rehabilitation providers, providers should ask patients about their spasticity, including their moderators, triggers, modifiers, experience, impacts, long-term consequences, and effects on quality of life.This conceptual model provides a framework to improve clinician-patient dialogue, research, and rehabilitation for MS spasticity.



































 In MS clinical trials, impacts such as fatigue, walking ability, and quality of life, are measured using questionnaires—called patient-reported outcome measures—completed by people living with MS. The quality of these measures is fundamentally important. If poor quality patient-reported outcome measures are used, treatment benefits are easily missed or underestimated.We studied the quality of 18 fatigue patient-reported outcome measures previously used in MS studies. Specifically, we studied how the questionnaire questions were developed and scored them against recognised quality control standards. In general, the patient-reported outcome measures were poor. Only two scored reasonably well. One common weakness was that people living with MS were not involved during patient-reported outcome measure development. We also conducted novel examinations that went beyond the quality control standards. These test how well the questions relate back to the MS impacts they claim to measure. We found even the two best patient-reported outcome measures were poor.Our study had two findings. First, patient-reported outcome measures of MS fatigue are poor. Second, current standards for testing patient-reported outcome measure development are too easy to satisfy, overestimate patient-reported outcome measure quality, and need updating. Therefore, the ways we measure MS fatigue, one of the most common and burdensome MS symptoms, are scientifically weak. Measuring fatigue in multiple sclerosis: there may be trouble ahead—a video abstract (MP4 125165 KB).



































































































































 People with moderate or severe anomia after stroke not only exhibit more severe symptoms of word-finding difficulties but also manifest a wide variety of such symptoms, compared to people with Parkinson’s disease or multiple sclerosis.The present findings underscore the need to ask patients about their self-perceived word-finding difficulties.Regardless of the degree of difficulties or the underlying condition, self-perceived word-finding difficulties can have a negative impact on communicative participation and should therefore be appropriately addressed.An assessment comprising aspects such as verbal fluency, connected-speech tasks and the measurement of response times in naming tasks may serve to affirm the self-reported word-finding difficulties.

































































































































































































 Multiple sclerosis (MS) is a chronic inflammatory disease of the brain and spinal cord that leads to neuronal damage and neurological disability. A novel cell therapy has been developed aiming to slow or reverse neurological disability in patients with MS. The treatment approach utilizes bone marrow cells called mesenchymal stem cell-derived neural progenitors (MSC-NPs) that are injected into the spinal fluid of the patient. Microglia are an innate immune cell in the brain known to contribute to MS disease progression. This study explores whether microglia might be a therapeutic target of MSC-NP therapy. We found that MSC-NPs inhibited the inflammatory activation of microglia and increased proregenerative markers in microglia. These effects were mediated by the factors secreted by MSC-NPs, possibly including a secreted protein called TGF-β. Overall, this study highlights a potential therapeutic mechanism of MSC-NP therapy in MS.





























































 Cognitive difficulties associated with multiple sclerosis (MS) impact on daily life activities and are considered invisible MS symptoms. This invisibility and the lack of acknowledgement of such symptoms often adds to the distress experienced by people with MS.Occupational therapists are well-placed to address the daily-life impacts of cognitive difficulties in MS.The COB-MS is an occupation-focused intervention that aims to enhance daily function.The intervention was found to be well-accepted well by people with MS and occupational therapists and can feasibly be delivered in clinical practice.































































































































































































































































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 Magnetic resonance imaging (MRI) is widely used in the clinic to diagnose multiple sclerosis (MS), which affects the central nervous system and leads to a range of disabling symptoms. However, MRI is often not capable of detecting how well a patient responds to therapies, in particular those targeting the immune system. We questioned whether an advanced MRI method called hyperpolarized (13)C MRS could help. Using a mouse model for MS, we showed that hyperpolarized (13)C MRS can detect response to two therapies used in the clinic, namely fingolimod and dimethyl fumarate when conventional MRI could not. We also showed that this method is sensitive to the immune response. As hyperpolarized (13)C MRS is becoming available in many centers worldwide, it could be used to evaluate existing and new treatments for people living with MS, improving care and quality of life.
 Shared decision-making among people with Multiple Sclerosis (MS) and their healthcare providers in the management of the physical symptoms of MS. Shared decision-making is suggested to be a key mechanism in promoting optimal symptomatic care related to Multiple Sclerosis (MS). Shared decision-making is mostly done and studied in relation to choosing therapies that may slow disease progression but not usually for symptomatic care. There are a few studies highlighting the effect of utilizing shared decision-making in symptomatic care of MS. We performed this study to identify all the published data about using shared decision-making in symptomatic care in MS to answer the research question: What is the evidence on shared decision-making in managing physical MS symptoms? We performed a systematic search for all the related published study results in four large literature databases. We found 15 studies on the use of shared decision-making in the management of MS-related symptoms. We synthesized the study results relating to the use of shared decision-making in symptomatic care of MS. The studies used several different designs and included a wide range of study rigor and quality. The results of our systematic review are: All the studies were consistent in their conclusions that shared decision-making is important for effective MS-related symptom management.Several studies found that symptomatic care is of the highest priority to people with MS, but not often a priority to their health care providers.The use of a shared decision-making model can promote discussion of symptoms in clinical consultations and align the goals of people with MS and their health care providers.Education of people with MS regarding their symptoms and available treatments will promote effective shared decision-making discussions. The available evidence supports that the use of shared decision-making is beneficial to the management of physical symptoms of MS. Further studies using a randomized controlled study design are required to establish the degree of benefit of utilizing shared decision-making associated with MS symptomatic care.

































































































































































































































































































































































 A new economic model was developed from a United Kingdom National Health Service perspective, to explore whether hydrophilic-coated intermittent catheters would be “worth” introducing for intermittent catheter users with either a spinal cord injury or multiple sclerosis. More specifically, costs were analyzed alongside clinical evidence and health-related quality-of-life data to investigate whether hydrophilic-coated intermittent catheters would offer a notable health benefit when compared with uncoated intermittent catheters for the assessed population, whilst keeping costs to the National Health Service sufficiently low. Model inputs were sourced from published evidence where possible, and experts were consulted otherwise. The results showed that, whilst lifetime use of hydrophilic-coated intermittent catheters is £3,183 more expensive than use of uncoated intermittent catheters per patient, the health benefit with hydrophilic-coated intermittent catheters offsets these costs, by definition a cost-effective result. This means that hydrophilic-coated intermittent catheters are likely to be a cost-effective alternative to uncoated intermittent catheters. Their adoption across clinical practice could avoid a substantial number of infections, thereby freeing up healthcare resources in the National Health Service and reducing antibiotic use in urinary catheter users.















































































































































































































































































































































































































































































 Endoplasmic reticulum (ER) stress-mediated accumulation of misfolded protein is one of the causes involved in the onset of several neurodegenerative diseases (ND). Under physiological conditions, ER stress activates the unfolded protein response (UPR) that repairs the misfolded proteins. However, if the ER stress becomes chronic, the UPR fails to repair the misfolded proteins leading to disease conditions such as Parkinson's disease, Alzheimer's disease, multiple sclerosis, etc. Most in vitro systems are based on the infliction of acute ER stress on the target cells, which kills them, and thus, are not physiologically relevant models, as their neuro-regeneration is not possible. Here, we have developed a physiologically relevant in vitro model system, wherein we exposed Neuro-2a cells to an ER stress inducer which significantly affected their neuro-regenesis without killing them. These dysfunctional cells were then used to assess the effect of secretome (conditioned medium, CM) derived from mesenchymal stromal cells (MSCs) primed or not with neurotrophic factors. We found that priming of MSCs with neurotrophic factors enhances their neuroprotective potential. We demonstrate that when primed CM is given either as a single dose or in multiple doses, it restores neuro-regenesis and protects the stressed Neuro-2a cells from cell death. More importantly, the restoration of neuro-regenesis by primed CM is significantly higher as compared with the naive CM. These results clearly underscore the importance of priming the MSCs with neurotrophic factors for developing more effective therapeutic strategies to combat ND.
















 The drugs amantadine and memantine are known as aminoadamantanes. Amantadine improves motor skills in patients with Parkinson’s disease. It also reduces fatigue in individuals suffering from multiple sclerosis. Memantine improves memory dysfunction linked to Alzheimer’s disease. Aminoadamantanes affect communication between nerve cells by supporting neurotransmission of monoamines. Clinical studies have found that these drugs benefit patients with chronic neurodegenerative diseases, who have depression, fatigue, loss of attention or concentration deficits. These brain function problems may also appear to some extent due to COVID-19 infection. We suggest that aminoadamantanes could improve these problems in COVID-19 patients in both the short and long term. Clinical research is needed to confirm this hypothesis.

































































































































































































 [Figure: see text]

















































 Spasticity is an abnormal, involuntary muscle tightness due to extended muscle contraction. This resistance in movement can be caused by stroke, multiple sclerosis, or traumatic injuries to the brain or spinal cord. Cervical dystonia is a form of sustained involuntary muscle contractions that result in abnormal or repetitive muscle movements in the neck and upper shoulders. Spasticity and cervical dystonia are both associated with significant decrease in quality of life and work productivity as well as significant economic burden. It is therefore important to understand how disease management impacts these patients. Many studies have shown that botulinum toxins type A (BoNT-As) are safe and effective in reducing muscle tightness and improving normal range of motion. This study was conducted to better understand BoNT-A injection patterns, use of healthcare services, and the resulting costs in patients with spasticity or cervical dystonia.

















































































































































































































































































































































































































































 The Scleroderma Patient-centered Intervention Network COVID-19 Home-isolation Activities Together (SPIN-CHAT) Program, a videoconference-based supportive care program, was designed to protect and enhance mental health in individuals affected by systemic sclerosis (commonly known as scleroderma) with at least mild anxiety symptoms during the COVID-19 pandemic. A trial was conducted to evaluate the SPIN-CHAT Program, and results were generally positive. However, important gaps in knowledge remained. Specifically, research team members’ and participants’ perceptions of SPIN-CHAT Trial acceptability (including satisfaction) and factors impacting implementation of the SPIN-CHAT Program had not yet been explored. To fill this gap, we conducted one-on-one, videoconference-based, semi-structured interviewed with 22 research team members and 30 purposefully recruited trial participants. Interviews sought to gain insights into research team members’ and trial participants’ experiences within the SPIN-CHAT Program, delivery preferences, and aspects that were/were not beneficial. Findings suggest research team members and participants valued the SPIN-CHAT Program and found the trial to be acceptable. Results also highlight important factors to consider when designing, developing, and/or refining videoconference-based supportive care programs.




























































































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 Avonex IFN-β-1a PEG-IFN-β-1a Plegridy multiple sclerosis priming


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 biochemistry immunoglobulins multiple sclerosis


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 GENETICS Multiple sclerosis Neurology
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 Multiple Sclerosis Treatment Adherence Questionnaire (MS-TAQ) disease-modifying therapy (DMT) medication adherence multiple sclerosis relapsing-remitting


 RIS demyelination epidemiology incidental finding multiple sclerosis
 carotenoids cognition lutein macular pigment multiple sclerosis
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 genetics multiple sclerosis
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 multiple sclerosis neurological disorder oral health oral health-related quality of life well-being
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 cognitive-motor interference dynamic balance control gait disturbance multiple sclerosis the timed up and go test
 Brain Follow-up studies Magnetic resonance imaging Multiple sclerosis White matter
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 brain contusion cerebrospinal fluid concussion multiple sclerosis traumatic brain injury
 Multiple sclerosis behavior change e-learning physical activity theory
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 MRI MULTIPLE SCLEROSIS
 carbapenem case report encephalopathy multiple sclerosis spasticity
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 Balance Cognition Dual-task Multiple sclerosis Walking
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 Alemtuzumab Cognition Disease-modifying therapy MS-COG composite score Multiple sclerosis Real-world evidence


 Magnetic resonance neurography Peripheral nervous system Proton spin density Quantitative imaging markers T2-relaxometry



 longitudinal analysis multiple sclerosis quantitative MRI relaxometry




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 cytokines multiple sclerosis
 anti-CD20 monoclonal antibody cognitive impairment poor prognosis predictors primary progressive multiple sclerosis




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 MRI Trigeminal neuralgia clinically isolated syndrome diagnosis diagnostic criteria lesion multiple sclerosis
 clinical features disease-modifying drugs multiple sclerosis treatment response


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 Diagnostic uncertainty Objective classifiers Registry data SPMS

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 Breastfeeding Czech national multiple sclerosis patient registry ReMuS EDSS Multiple sclerosis Relapses

 Cerebrospinal fluid Multiple sclerosis Pleocytosis Prognosis
 Cognition MSIS Patient-reported outcomes Secondary progressive multiple sclerosis
 Demyelination Disease progression MRI Pediatric multiple sclerosis Radiologically isolated syndrome Risk factors
 Adult-onset Multiple sclerosis Paediatric-onset Treatment
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 Choroid plexus clinically isolated syndrome (CIS) multiple sclerosis optic neuritis
 Progressive clinical trial multiple sclerosis
 Fatigue Multiple sclerosis Quality of life
 LME MRI Multiple sclerosis biomarker immunotherapy
 BICAMS Brain volume Cognition MRI Multiple sclerosis Neuropsychology
 Clinical parameters Diffusion tensor imaging (DTI) Multiple Sclerosis (MS) White Matter (WM) disease-modifying therapies (DMTs)

 BICAMS Brain MRI Cognition Multiple sclerosis Optic nerve MRI Optical coherence tomography


 CSF and serum biomarkers inflammation multiple sclerosis
 Disease Modifying therapy discontinuation Immunosenescence Multiple sclerosis
 Cognition Disease progression Multiple sclerosis Outcome assessment Prognosis
 Case report Demyelinating disease Multiple sclerosis Rapidly progressive Vasculitis
 Cerebrospinal fluid IgG index Multiple sclerosis Oligoclonal banding

 Multiple sclerosis disease course disease-modifying therapy
 RIS disease predictors multiple sclerosis preclinical phase prodromes
 multiple sclerosis nine-hole peg test outcome measure primary progressive multiple sclerosis timed 25-foot walk
 microarray meta-analysis multiple sclerosis white matter
 Choroid plexus Deep learning Multiple sclerosis Radiologically isolated syndrome Segmentation
 Fatigue Multiple sclerosis Quality of life Web-based program Wellness
 Alemtuzumab Effectiveness Multiple sclerosis Observational prospective study Safety
 Case report Macular edema Multiple sclerosis Siponimod Sphingosine 1-phosphate
 X-nuclei MRI anatomical prior information compressed sensing (CS) lesion classification multiple sclerosis (MS) sodium (23Na)
 Arrhythmia Electrophysiology Fingolimod Multiple sclerosis
 Escalation strategy High-efficacy DMT Multiple sclerosis Registry study
 Explosive muscle strength Falls Multiple sclerosis Neuromuscular function
 Cognition Diffusion tensor imaging (DTI) Diffusion-weighted (DW) Information processing speed (IPS) MRI Multiple sclerosis (MS) TRACULA (TRActs Constrained by UnderLying Anatomy) Tractography


 comorbidity multiple sclerosis psychosis schizophrenia
 Disease progression Multiple sclerosis (MS) Optical coherence tomography (OCT) Prognosis Retinal layer measurement
 Dysphagia Multiple sclerosis Screening questionnaire Validation


 Gut microbiota Multiple sclerosis Neuroinflammation Obesity
 Clostridium dimethyl fumarate flushing gastrointestinal side effects gut microbiota multiple sclerosis
 COVID-19 Disease activity Infections Multiple sclerosis NEDA Virus


 Atrophy Disability MRI Multiple sclerosis
 Cladribine tablets Multiple sclerosis NEDA-3 Real-world Safety

 MSer Person with MS identity-first language person-first language respect
 lymphocytic choriomeningitis virus multiple sclerosis myeloid dendritic cells regulatory T cells toll-like receptor 8 (TLR8)
 Adverse events Complete blood count Dimethyl fumarate Disease activity Eosinophils Lymphocytes Lymphopenia Monocytes Multiple sclerosis Relapsing-remitting multiple sclerosis Tecfidera
 ADEM Demyelinating disorders Levamisole Levamisole-associated multifocal inflammatory encephalopathy Multiple sclerosis Neuroinflammation
 bilan éducatif partagé care compliance démarche éducative educational approach grossesse observance pregnancy shared educational assessment soin therapeutic education éducation thérapeutique
 Glatiramer acetate Multiple sclerosis Urticarial vasculitis

 Attention maps Deep learning Disability Multiple sclerosis Structural MRI


 CSF Cognition GFAP MRI Multiple sclerosis Neurofilament light Serum

 IL-8 cytokine inflammation multiple sclerosis neurodegeneration rs2227306
 Alzheimer’s disease Parkinson’s disease RUDAS cognitive screening test multiple sclerosis
 MRI MULTIPLE SCLEROSIS PAEDIATRIC
 Cladribine tablets Effectiveness Observational study Real-world data Relapsing–remitting multiple sclerosis Safety

 clinical neurology multiple sclerosis
 Curcumin Curcumine Cytokines Encéphalomyélite auto-immune expérimentale Experimental autoimmune encephalomyelitis Gingembre Ginger Multiple sclerosis Sclérose en plaques
 Antibodies Antibody correlations Antibody index Multiple sclerosis Optic neuritis Virus antigens
 Depression Fatigue MSQOL-54 questionnaire Multiple sclerosis Quality of life Sexual dysfunction Sexual function Sexual satisfaction
 cost-utility analysis incremental cost-effectiveness ratio multiple sclerosis relapsing-remitting ocrelizumab quality-adjusted life-years rituximab
 TUFM mitochondrial diseases multiple sclerosis white matter abnormalities
 Anti-CD20 monoclonal antibodies Immunoglobulin Infection Multiple Sclerosis Systematic literature review
 disease progression optical coherence tomography predictor relapsing-remitting multiple sclerosis retinal nerve fiber layer thickness
 Diet Ketogenic Multiple sclerosis Neurodegeneration Neurofilament light chain

 Diagnosis Experience Multiple sclerosis Systematic review
 Multiple sclerosis exacerbation exercise physical activity relapse
 1st line DMTs HLA Injectables Oral Outcome Pediatric-onset multiple sclerosis (POMS)

 SARS-CoV-2 extended-interval dosing multiple sclerosis ocrelizumab


 Brain atrophy Choroid plexus (CP) Iron rim lesions (IRLs) Relapsing-remitting multiple sclerosis (RRMS) White matter lesions (WMLs)

 genetics multiple sclerosis paediatric neurology
 Dexterity Hand to mouth Kinematics Multiple sclerosis (MS) Nabiximols Spasticity Upper limb
 Multiple sclerosis biomarkers epidemiology
 DMAMS DMT Disease-modifying treatments adverse events monitoring multiple sclerosis safety
 Multiple sclerosis neuroimaging
 Drug delivery Multiple sclerosis Muscle spasticity Nanosuspension Transdermal
 Diagnosis emotional adjustment emotions multiple sclerosis psychological adaptation qualitative research systematic review
 Claims data Germany Incidence rate Multiple sclerosis Propensity score matching Serious infections
 Status epilepticus; intoxication; dalfampridine; multiple sclerosis.
 cladribine tablets dimethyl fumarate (Tecfidera®) fingolimod (Gilenya®) lay summary multiple sclerosis relapses teriflunomide (Aubagio®) treatment options



 Biomarker Biosensor Disease management Disease monitoring Multiple sclerosis Patient-centered healthcare Personalized medicine
 estrogen experimental autoimmune encephalomyelitis multiple sclerosis neurodegeneration neuroprotection
 multiple sclerosis patterns sensitivity visual evoked potentials
 disability multiple sclerosis relapses traumatic stress
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 Atypical optic neuritis optic neuritis optic neuropathy typical optic neuritis
 Ageing Envejecimiento Esclerosis múltiple Esclerosis múltiple de comienzo tardío Immunosenescence Inmunosenescencia Late-onset multiple sclerosis Multiple sclerosis
 Breastfeeding Disease-modifying therapies Glatiramer acetate Offspring safety Relapsing-remitting multiple sclerosis

 Amide proton transfer Chemical exchange saturation transfer Molecular imaging Multiple sclerosis
 Anxiety Depression HADS Healthcare delivery Multiple sclerosis Patient satisfaction Patient-reported outcome measures
 MRI The Virtual Brain functional connectivity multiple sclerosis structural connectivity
 MS pharmacoepidemiology polypharmacy population-based data prescription medication use

 Case report Microglia Multiple sclerosis PET Rituximab
 BACE1-AS BC200/BCYRN1 Cognitive impairment Multiple Sclerosis Synaptic plasticity
 B-lymphocytes CD19+ B-cells CD20+ B-cells anti-CD20 monoclonal antibody divozilimab multiple sclerosis

 MOG-associated disease hereditary optic neuropathy ischemic optic neuropathy neuromyelitis optica spectrum disorder optic neuritis optic neuropathy
 Double inversion recovery Magnetic resonance imaging Multiple sclerosis
 multiple sclerosis neurosurgery ultrasound
 Fatigue Ketamine Multiple sclerosis Randomized controlled trial
 Comorbidities Magnetic resonance imaging Mitochondrial function Multiple sclerosis Vascular risk
 MAG MBP MOBP Multiple sclerosis PLP demyelination
 Epidemiology Incidence Japanese Multiple sclerosis Prevalence
 calciferol cholecalciferol disability neurological disorders supplements tiredness
 H1
 3 T magnet Acute black holes Magnetic resonance imaging Multiple sclerosis Proton density T1-weighted
 Cladribine Cladribine tablets Disease-modifying treatment Multiple sclerosis Relapsing-remitting multiple sclerosis
 brain atrophy cladribine tablets grey matter multiple sclerosis white matter
 alemtuzumab multiple sclerosis neutropenia thrombocytopenia


 Cerebrospinal fluid Diagnostic criteria Multiple sclerosis Oligoclonal bands Review

 Cladribine tablets PET SPECT local immunity multiple sclerosis
 multiple sclerosis nabiximols observational study spasticity-associated symptoms
 Chronic periodontitis Meta-analysis Multiple sclerosis Systematic review
 Cryopreservation Fertility preservation Multiple sclerosis Ovary Stem cell transplantation
 Brain Morphometry Multiple sclerosis (MS)
 Comparative effectiveness Fingolimod High-efficacy treatment Multiple sclerosis Natalizumab Ocrelizumab
 Multiple sclerosis biomarker disability progression glial fibrillary acidic protein neurofilament light chain non-inflammatory


 biomarkers imaging diagnostics inflammation macrophage microglia multiple sclerosis myelination oligodendrocyte
 CBD Multiple sclerosis Nabiximols Sativex Spasticity THC

 Biomarkers Cerebrospinal fluid Disease-modifying treatments Inflammation MRI Machine learning Multiple sclerosis Omics Personalized medicine Rehabilitation

 Brain volumetry Multiple sclerosis Reliability Segmentation


 Breastfeeding Child development Interferon Multiple sclerosis Pregnancy
 Disease Modifying Therapies Multiple Sclerosis Transplant Results

 Epidemiology multiple sclerosis outcomes total hip arthroplasty
 fingolimod multiple sclerosis psoriasis real-life experience secukinumab
 COVID-19 EDSS Enhancing lesions Esclerosis múltiple Multiple sclerosis Progresión Progression Realce de lesiones Recaída Relapse
 MULTIPLE SCLEROSIS NEUROIMMUNOLOGY PSYCHIATRY

 Adaptive immunity Aubagio Innate immunity Multiple sclerosis Teriflunomide
 GFAP HCQ NfL PPMS multiple sclerosis
 Sleep actigraphy dimethylfumarate disease-modifying treatment multiple sclerosis sleep disorders

 Autophagy EAE Inflammation Microglia Multiple sclerosis Vesatolimod
 Disability Fatigue Multiple sclerosis Pituitary gland
 Differential diagnosis False positives Mimics Misdiagnosis Multiple sclerosis Multiple sclerosis mimics Serologic testing Serum testing
 Cognitive reserve Cognitive skill learning Multiple sclerosis Neuropsychology Processing speed
 Multiple sclerosis, Chlamydia pneumoniae association meta-analysis
 Multiple sclerosis discrete choice experiment fatigue patient preference patient-focused drug development patient-reported outcome
 MRI multiple sclerosis myelin water fraction remyelination
 cerebral hypoperfusion chronic cerebrospinal venous insufficiency multiple sclerosis vein venous circulation


 Cognitive phenotypes IC-CoDiMS cognition cognitive impairment executive functions memory multiple sclerosis neuropsychology processing speed
 Cognitive function Computerized cognitive assessment Multiple sclerosis Subjective cognitive impairment
 Multiple sclerosis (MS) Optic neuritis Optical coherence tomography (OCT) Peripapillary retinal nerve fiber layer Vision
 cerebrospinal fluid dural lymphatic vessels dynamic contrast-enhanced MRI gadolinium-based contrast agents glymphatic function multiple sclerosis
 Disease-modifying therapies epidemiology multiple sclerosis pregnancy
 Employment status multiple sclerosis productivity loss
 B cells T cells astrocytes autoimmunity glia microglia multiple sclerosis neuroimmunology progressive MS
 Astragaloside IV Intranasal delivery Multiple sclerosis Remyelination β-asarone
 Balance Falls Fatigue Gait Multiple sclerosis
 Acétate de Glatiramère Central retinal vein occlusion Glatiramer Acetate Multiple sclerosis Occlusion de la veine centrale de la rétine Sclérose en plaques


 Disability and Health International Classification of Functioning Multiple sclerosis clinical trial functional status outcome measure rehabilitation

 Myopia multiple sclerosis optical coherence tomography refractive error


 Cognitive impairment GM atrophy MRI Multiple sclerosis NODDI
 Mobility Multiple sclerosis Muscle morphology Muscle performance Sarcopenia Ultrasound


 fibroblast growth factor receptors fibroblast growth factors inflammation multiple sclerosis remyelination
 Intermittent fasting Multiple sclerosis Obesity Time restricted eating Weight loss
 Casework Community care Multiple sclerosis Needs Service evaluation Support

 Cognitive impairment Meta-analysis Molecular biomarkers Multiple sclerosis Neurofilament light chain Systematic review Vitamin D
 Apraxia Cognitive rehabilitation Multiple sclerosis Upper limb Virtual reality
 Epidemiology multiple sclerosis second-line treatment treatment response
 Activated microglia Demyelination MRI PET Synthetic MRI

 Multiple sclerosis core stability functional mobility lumbopelvic stability respiratory function respiratory muscle strength

 MRI Paediatric-onset multiple sclerosis SWI central vein sign gradient echo plural contrast imaging relapsing remitting multiple sclerosis
 aging cognition connectivity maladaption/adaption relapsing remitting multiple sclerosis
 Birth Epigenetics Neurodegeneration Neuroplasticity Pregnancy
 B cells IL-10 IL-10R central nervous system environmental factors experimental autoimmune encephalomyelitis multiple sclerosis


 biomarkers cognitive impairment (CI) kappa free light chains multiple sclerosis symbol digit modalities test (SDMT)

 Assessment Cognitive functions Disability Multiple sclerosis Social cognition Theory of mind

 Immunoregulation Immunosuppression Immunotherapy Neurodegeneration Neuroinflammation Tolerance
 Autoimmune disease Cytokines Food supplement Inflammation Neuroprotection Oxidative stress
 B-cells CD40 CD40-ligand Costimulation T-cells multiple sclerosis
 cerebrospinal fluid microbiota microbiotic markers multiple sclerosis polymicrobial infection

 Disease modifying treatments Multiple sclerosis Natalizumab Paediatric neurology Paediatric onset multiple sclerosis
 Continuity of care Physiotherapy service Teleneurology Telerehabilitation
 Canada cost-consequence disease-modifying therapy multiple sclerosis ofatumumab
 Multiple sclerosis spasticity Nabiximols Urinary disturbances Urodynamic evaluation
 Bayesian approach Magnetic resonance imaging contrast media multiple sclerosis susceptibility-weighted imaging
 multiple sclerosis randomised trials
 R-PLEX Simoa cerebrospinal fluid electrochemiluminescence multiple sclerosis neurofilament light serum
 Astrocytes Endothelial cells Multiple sclerosis Neurovascular unit Pericytes
 Complex intervention Multiple sclerosis Nursing counselling Programme theory Rehabilitation Self-management
 BBB CNS Inflammation Multiple sclerosis Platelet, Platelet-based drug delivery system
 Behavior change Capability-Opportunity-Motivation-Behavior (COM-B) model Multiple sclerosis Newly diagnosed MS Physical activity
 Amino acids Lipids Metabolomics Multiple sclerosis Pathways
 computer-aided diagnosis deep learning multiple sclerosis psychophysics

 Balance Falls Multiple sclerosis Posture Rehabilitation
 Autologous hematopoietic stem cell transplantation Ceramides Lipidomics Metabolomics Relapsing-remitting multiple sclerosis

 3D Cramér-Rao lower bound magnetic resonance fingerprinting myelin tissue fraction mapping myelin-proton ultrashort echo time
 clinical research areas diseases life experience multiple sclerosis qualitative study spasticity
 adipsin combined exercise lipid profile mental function multiple sclerosis
 Brain atrophy Freesurfer Hypothalamus Relapsing remitting multiple sclerosis
 RNA-seq human analysis multiple sclerosis non-coding RNAs spatial transcriptomics transcriptomic analysis
 MRI Multiple sclerosis Soma and neurite density imaging (SANDI)

 Baló concentric sclerosis Fingolimod Pediatric multiple sclerosis Tumefactive Multiple sclerosis
 EDSS multiple sclerosis scales for assessing the severity of neurological disorders symptoms and syndromes
 coproduction multiple sclerosis care patient experience quality improvement
 C C6 C63 I I1 I19 Multiple sclerosis dimethyl fumarate discrete event simulation disease progression ofatumumab relapses relapsing-remitting multiple sclerosis
 Cognition Ecological evaluation Multiple sclerosis Neurotechnology Real-world assessment Virtual reality

 diffusion tensor imaging fronto-striatal gait mobility impairment motor control older persons with multiple sclerosis
 Detrusor sphincter dyssynergia Low compliance bladder Neurourology Overactive detrusor function Underactive detrusor function
 caregiver burden family caregivers family-centered empowerment model multiple sclerosis nursing care
 Intervention Multiple sclerosis PRECEDE-PROCEED model Quality of life
 C -myc CNS autoimmunity Cigarette smoke EAE HNF4α Immune activation Master regulator Multiple sclerosis SP1 Vitamin D
 Multiple sclerosis capillary extended interval dosing fingerprick natalizumab
 Multiple sclerosis cladribine pregnancy
 Corneal nerve branch density Corneal nerve fiber density Corneal nerve fiber tortuosity In vivo confocal microscopy Multiple sclerosis
 Biomarkers Circular RNAs DNA methylation Multiple sclerosis eQTL

 Depression Homocysteine Low-saturated fat diet Modified Paleolithic elimination diet Multiple sclerosis Vitamin B(12)
 biomarker coagulation multiple sclerosis relapse tissue factor

 T2*-weighted images central vein sign magnetic resonance imaging multiple sclerosis paramagnetic rim sign radiologically isolated syndrome


 Multiple sclerosis Myelin oligodendrocyte glycoprotein antibody-associated disease Quantitative gradient recalled echo imaging qGRE
 demyelination extracellular vesicles multiple sclerosis myelin antibodies serum diagnostic biomarkers
 IL-27 Programmed Death 1 receptor (PD1) Programmed Death Ligand 2 (PD-L2) innate immune response lymphoproliferative assay myeloid dendritic cells (mDCs) relapsing-remitting multiple sclerosis (RRMS)


 Rehabilitation diversity equity health equity inclusion patient selection review selection bias social determinants of health
 B-lymphocytes anti-CD20 monoclonal antibody divozilimab multiple sclerosis
 NMR; metabolomics; metallomics copper lead magnesium multiple sclerosis oxidative stress; antioxidant vitamin C
 disease severity genetics machine learning multiple sclerosis prognostics
 Data visualization Digital health Graphs Multiple sclerosis Self-management mHealth
 Multiple sclerosis qualitative research self-concept self-views thematic analysis

 EAE MRI histopathology marmoset neuroscience primate remyelination
 Fingolimod withdrawal Natalizumab withdrawal RRMS Relapsing-remitting multiple sclerosis Rituximab
 Decision making Family planning Multiple sclerosis Pregnancy Qualitative research
 Autoimmune diathesis Case report Leflunomide Multiple sclerosis Subacute cutaneous lupus erythematosus Teriflunomide
 Disability Lifestyle factors Multiple sclerosis Vascular ultrasound

 COVID-19 Electronic health record Methodology Multiple sclerosis Risk factors
 Apps Multiple sclerosis Persuasive technology Scoping review mHealth
 health behaviour lifestyle longitudinal study multiple sclerosis quality of life

 cognitive occupation-based programme for people living with multiple sclerosis (COB-MS) decliner patient & public involvement recruitment study-within-a-trial
 disease-modifying therapy feel-good experience multiple sclerosis natalizumab patient management patient-reported outcomes quality-of-life real-world evidence
 amyotrophic lateral sclerosis atypical parkinsonism and Parkinson disease autoantibodies autoimmune encephalitis multiple sclerosis
 Activities of daily living Home-based programming Multiple Sclerosis Nontraditional Occupational therapy

 Dimethyl fumarate Fingolimod Multiple sclerosis Oral disease-modifying drug Relapse Smoking
 Escalation Horizontal Multiple sclerosis Switch Vertical
 Th17 cells disease rebound multiple sclerosis natalizumab pathogenicity
 children disability multiple sclerosis

 brain immune lymphocytes multiple myelin sclerosis
 Clustered data comparative effectiveness confirmed disability progression longitudinal data multiple imputation multiple sclerosis real-world data
 Behavior change intervention multiple sclerosis physical activity qualitative
 Epidemiology Incidence Mortality Multiple sclerosis Prevalence
 COVID-19 Disease-modifying therapy Multiple sclerosis SARS-CoV-2 Vaccine

 disability multiple sclerosis optical coherence tomography prognosis
 Disease-modifying treatments Gut microbiota Multiple sclerosis
 Cytokines Immune Response Inflammation Interleukin Multiple Sclerosis
 EAE MRI TMEV-IDD cuprizone multiple sclerosis neurodegeneration
 Aging CR Cognition Disease burden Multiple sclerosis
 Functional therapy Multiple sclerosis Occupational therapy Physical therapy Rehabilitation

 Cell cycle Cerebral organoids Multiple sclerosis Pluripotent stem cells
 MS14 Multiple sclerosis Natural product Persian medicine Physical activity
 Coronavirus disease Cortisol Mental health Multiple sclerosis Psychological status
 Cannabis Disease-modifying therapy Fatigue Multiple sclerosis Symptomatic treatment
 Anxiety COVID-19 Depression Multiple sclerosis Pandemic Stress
 Chemometrics Diagnosis Multiple sclerosis Plasma Raman spectroscopy Serum
 N-acetylcysteine antioxidant anxiety depression glutathione multiple sclerosis oxidative stress
 MSISQ-15 Multiple sclerosis Neurology Sexuality
 MS rate of progression Multiple sclerosis OCT as biomarker OCT correlation with retinal atrophy Ocular coherence tomography Retinal atrophy

 Cytokines Demyelination Gut dysbiosis Multiple sclerosis Probiotics
 diet gut microbiota immune system multiple sclerosis postbiotics prebiotics probiotics
 Efficacy Multiple sclerosis Relapsing-remitting MS Rituximab Safety
 Progressive MS cognition glial fibrillary acidic protein neurofilament
 Body mass index intelligence quotient score pediatric multiple sclerosis


 Diagnostic performance FLC index IgG-index Multiple sclerosis Oligoclonal bands
 Artificial intelligence Diagnosis Machine learning Multiple sclerosis
 Respiratory distress syndrome SARS-CoV2 autoimmune disease autologous hematopoietic stem cell transplantation multiple sclerosis
 Deep vein thrombosis Multiple sclerosis Vein thrombosis Venous thromboembolism
 6 min walk test Multiple Sclerosis physical adaptation spatio-temporal parameters walking
 Inflammation Multiple sclerosis Neurodegeneration Stem cells iPS cells
 Neuromyelitis optica breastfeeding disease modifying treatments pregnancy reproductive assistance
 Anxiety Depression Multiple Sclerosis Impact Scale-29 Multiple Sclerosis Walking Scale-12 Multiple sclerosis and Stress Scale-21 psychometrics
 EAE FC autoimmunity multiple sclerosis therapeutic
 Conventional exercise Multiple sclerosis Physical and cognitive abilities Rehabilitation VR-exergaming
 Access Biologic Biosimilar Costs Multiple sclerosis Patient care
 Intervention Outcomes Multiple Sclerosis Neuropsychological Assessment Patient Feedback Psycho-Education RCT
 Meta-analysis Multiple sclerosis Systematic review Task-oriented training Upper limb function
 MEP TMS e-field navigation evoked potentials line navigation motor evoked potentials multiple sclerosis navigated TMS
 Multiple sclerosis Trendelenburg hip abduction strength pelvis psychometrics
 Bushfire COVID-19 pandemic Healthcare access Multiple sclerosis Public health Qualitative research (mixed-methods)
 Cognitive impairment Motor dysfunction Multiple sclerosis Risk of fall
 Disease modifying therapies – risk management
 Adherence RebiSmart® device interferon beta-1a multiple sclerosis persistence
 Active disease Adverse events Age subgroups S1P modulator Secondary progressive multiple sclerosis Siponimod
 Compassion Multiple sclerosis Scoping review
 Clean intermittent catheterization Disability Functional independence measure Multiple sclerosis Neurogenic lower urinary tract dysfunction
 Diversity Ethnicity Multiple sclerosis Race Rehabilitation trials Review
 Cross-sectional analysis Finances Material deprivation Registry Relapsing-remitting multiple sclerosis Switzerland

 disabled persons exercise feasibility study multiple sclerosis
 Multiple sclerosis ambulatory function digital technology outpatient monitoring patient-specific modeling smartphone
 Cladribine Disease-modifying therapies Efficacy Multiple sclerosis Safety
 Alemtuzumab Hemophagocytic lymphohistiocytosis Multiple sclerosis Neuroimmunology Side effect

 Free teriflunomide Liquid chromatography Mass spectrometry Multiple sclerosis Total teriflunomide

 multiple sclerosis overactive bladder qualitative study sexuality women


 genome-wide association signals human leukocyte antigen major histocompatibility region multiple sclerosis
 Anxiety Depression EAE MgH2 Microglial polarization Multiple sclerosis Neuroinflammation
 Disability assessment Disability progression Multiple sclerosis PROMs PROs
 Pediatric MS magnetization transfer optic nerve optical coherence tomography quantitative MRI visual functions
 Communication confidence Health education Health literacy Knowledge Multiple sclerosis
 Educational intervention Multiple sclerosis Randomized controlled trial Theory of planned behavior Treatment adherence drugs
 axonal injury demyelinating diseases multiple sclerosis neurodegeneration neuroinflammation
 Anxiety CNS Cognition Cognitive Testing Comorbidity Demyelinating autoimmune diseases Depression Fatigue
 cerebrospinal fluid iron magnetic resonance imaging multiple sclerosis oxidative stress susceptibility
 MVPA functional connectivity multiple sclerosis resting state networks
 MRI multiple sclerosis neuroimmunology neuroradiology

 Crohn's disease Epstein-Barr virus Hodgkin lymphoma death rates environmental risk factors epidemiology of IBD multiple sclerosis ulcerative colitis vital statistics
 T cells glia microbiota mitochondria multiple sclerosis neurodegeneration sex difference
 Cell survival Demyelination Myelin Neurodegeneration Neurodegenerative disease
 MRI brain compressed sensing multiple sclerosis parametric mapping transversal relaxation time
 Asia Fracture risk Multiple sclerosis Neuromyelitis optica spectrum disorder
 Multiple sclerosis immunology
 depression & mood disorders inflammatory bowel disease mental health multiple sclerosis rheumatology
 EDSS FABP2 genetic variant disability multiple sclerosis pathology-supported genetic testing personalized medicine unsaturated fatty acids vascular ultrasound

 connectome functional connectivity multiple sclerosis resting-state network structural connectivity

 Disease-modifying therapies cladribine outcome measurement second-line treatment
 cognitive impairment depression employment intervention fatigue multiple sclerosis neuropsychology treatment adherence vocational rehabilitation
 CNS Multi-epitope vaccine bioinformatics aided design multiple sclerosis tregitope vasoactive intestinal peptide
 Cost effectiveness Evidence based practice Multiple sclerosis Natalizumab Ocrelizumab Relapsing-remitting Rituximab
 Multiple sclerosis clinical trials diversity social determinants of health
 MULTIPLE SCLEROSIS

 Biomarker Disability EDSS Long-term Multiple sclerosis NEDA-3 RRMS miR-548a-3p miRNA
 Disability Frailty Gait Multiple Sclerosis Physical Activity Walking
 cannabinoids central nervous system multiple sclerosis spasticity
 Demyelinating diseases Magnetic resonance imaging Multiple sclerosis White matter lesion

 MULTIPLE SCLEROSIS STATISTICS
 Anxiety Depression Diet Fatigue Multiple sclerosis Potential renal acid load score and net endogenous acid production (NEAP)
 Balance cutaneous sensation gait multiple sclerosis orthotic devices
 Multiple sclerosis evidence-based healthcare patient-reported outcome measures quality of care

 Multiple sclerosis breast neoplasms comorbidity immunosuppression therapy prognosis qualitative research retrospective studies
 Neurofilament light chain pediatric MS teriflunomide
 B cell CXCL13 clinically isolated syndrome initial clinical demyelinating event multiple sclerosis radiologically isolated syndrome biomarker
 chickenpox vaccine cladribine tablets flu vaccine lay summary multiple sclerosis plain language summary
 EAE reversal GMF-β GMFBI.1 gut dysbiosis gut−brain multiple sclerosis
 Fampridine Gait Multiple sclerosis
 adverse pregnancy outcomes fetal exposure multiple sclerosis
 expanded disability status scale magnetic resonance imaging multiple sclerosis oligoclonal bands
 animal model neuroprotection progressive multiple sclerosis vitamin D

 B cell autoimmunity ethnicity humoral response multiple sclerosis

 Drug approval Drug safety Generalizability Multiple sclerosis Multiple sclerosis disease therapy Pharmacoepidemiology Registry phase III clinical trials
 Sensoready® autoinjector human factors ofatumumab relapsing multiple sclerosis summative evaluation
 BICAMS Cogstate Pediatric MS adult MS cognition cognitive screening
 Multiple sclerosis Pregnancy Puerperium Reproductive biological phases Telomere
 Exercise Heat sensitivity Multiple sclerosis Transcranial magnetic stimulation Uhthoff phenomenon
 Difficulties in emotion regulation Distress Multiple sclerosis Quality of life Self-efficacy
 Exercise Multiple sclerosis Qualitative evaluation Telehealth
 Monoclonal antibody Natalizumab, Rituximab Ocrelizumab Progressive multiple sclerosis Systematic review

 lesion activity lesion segmentation longitudinal analysis longitudinal lesion segmentation multiple sclerosis white matter lesions
 Coaching secondary analysis self-management
 CNS inflammation MS brain-derived neurotrophic factor demyelinating diseases neuroprotection neurotrophin
 COVID-19 epidemiology mortality multiple sclerosis population-based study
 Anxiety Coping Functionality Multiple sclerosis Social support Stress

 Aging Blood pressure Cognition Multiple sclerosis
 B-lymphocytes genetic association studies multiple sclerosis
 Multiple sclerosis Muscle strength Physical functional Sit-to-stand test Validity
 NMOSD astrocyte demyelinating diseases disease modifying therapies glia multiple sclerosis neuroinflammation synaptopathy
 cognition executive function insulin resistance memory multiple sclerosis
 Health Equity Indigenous Peoples Multiple Sclerosis
 Multiple sclerosis cerebral blood flow cerebral oxygen consumption disability neurodegeneration
 Hand to mouth Kinematics Multiple Sclerosis (MS) Upper limb Virtual reality (VR)

 Biomarkers Glial fibrillary acidic protein Multiple sclerosis Neurofilament Outcomes Predictive models
 3–7 keywords Autoimmunity Immune engineering Immunotherapies Multiple sclerosis No full stop Not capitalized Particles Plural Separated by commas
 COVID-19 disease-modifying treatments multiple sclerosis
 Chronic inflammatory disease Microbiota Multiple sclerosis Probiotics
 MRI Machine learning Multimodal analysis Multiple sclerosis Prediction
 Microcirculation Multiple sclerosis Optic neuritis Optical coherence tomography angiography Retina
 Calorie restriction Demyelination Dietary restriction Multiple sclerosis Remyelination
 competitive ELISA mannan multiple sclerosis myelin oligodendrocyte glycoprotein



 Paramagnetic rim lesion cognitive recovery multiple sclerosis quantitative susceptibility mapping (QSM) relapse susceptibility weighted imaging (SWI)
 Antioxidant bioactive compounds Antioxidant drugs Inflammation Multiple sclerosis Neurodegeneration Oxidative stress
 Raman spectroscopy atomic force microscopy infrared spectroscopy multiple sclerosis proteomics tear fluid
 Fatigue management Multiple sclerosis Self-management mHealth

 2-AG AEA anandamide biomarker endocannabinoid multiple sclerosis

 Assessment Cognition Depression Fatigue Multiple sclerosis
 ABO-mismatch transplantation Delayed erythroid engraftment Graft versus host disease Hematopoietic stem cell transplantation Pure red cell aplasia
 Multiple sclerosis Myelin oligodendrocyte glycoprotein-antibody associated disease Neuromyelitis optica spectrum disorders Rituximab
 cortical pathology multiple sclerosis quantitative MRI quantitative susceptibility mapping relaxometry ultra-high field
 disease-modifying therapy indirect treatment comparison network meta-analysis relapsing multiple sclerosis systematic literature review
 Behavior change Focus group Physical activity



 cognitive fatigue effort multiple sclerosis reward
 brain biopsy decompressive craniotomy fingolimod multiple sclerosis tumefactive demyelinating lesion

 B cell NK cell NKT cell T cell primary progressive multiple sclerosis regulatory T cell (Treg)
 Calidad de vida Depresión Depression Disability Discapacidad Disfunción sexual Esclerosis múltiple Función urodinámica Multiple sclerosis Quality of life Sexual dysfunction Urodynamic function

 B cell depletion autoimmune disease of the central nervous system multiple sclerosis (MS) myelin oligodendrocyte glycoprotein associated autoimmune disease (MOGAD) neuromyelitisoptica spectrum disorders (NMOSD)
 antibodies autoimmunity diagnosis evidence-based practice immunoglobulins
 multiple sclerosis pegylated IFN-β relapsing-remitting multiple sclerosis sampeginterferon-β1a
 Balance Mobility Multiple sclerosis Neurological disorders Rehabilitation
 PM2.5 ecological study environmental risk factors multiple sclerosis temperature
 B-cell follicles Epstein-Barr virus Immunopathology Multiple sclerosis Tissue-resident memory T cells
 breastfeeding exclusive multiple sclerosis nursing rate relapse weaning
 MRI brain exercise multiple sclerosis rehabilitation
 enzyme-linked immunosorbent assay multiple sclerosis neurofilament light chain single molecular array advanced technology
 Cerebrospinal fluid Cytology Ghost cells Multiple sclerosis Shadow cells
 Gene expression Pediatric multiple sclerosis Peripheral blood mononuclear cells
 cytokines demyelination ion channels neuroinflammatory diseases thalamic neurons thalamus

 cardiovascular risk comorbidity multiple sclerosis progressive multiple sclerosis secondary progressive multiple sclerosis



 clinical trials immunology multiple sclerosis rheumatology systemic lupus erythematosus
 Interferon-β Membranoproliferative glomerulonephritis Multiple sclerosis Nephrotic-range proteinuria
 Behavioral interventions Meta-analysis Multiple sclerosis Non-pharmacological therapies Physical activity Psychological interventions Quality of life Systematic review

 Multiple sclerosis pregnancy symptomatic treatment
 Connectomics Riemannian manifold functional connectivity geodesic clustering multiple sclerosis
 Mendelian randomization dementia epilepsy multiple sclerosis plasma cortisol
 Electroencephalography Multiple sclerosis Neurocognitive disorders Neuropsychological tests
 cladribine tablets cost–effectiveness dimethyl fumarate multiple sclerosis relapsing-remitting multiple sclerosis
 health economics multiple sclerosis
 Asparaginyl endopeptidases Cyclotide Multiple sclerosis Nicotiana benthamiana Peptide Plant molecular farming Recombinant
 Bruton’s tyrosine kinase Btki evobrutinib experimental autoimmune encephalomyelitis microglia multiple sclerosis



 central nervous systems dendritic cells experimental autoimmune encephalomyelitis multiple sclerosis


 B cells EBV latency programs Epstein Barr-Virus acute infectious mononucleosis chronic EBV infection genomic studies immune response molecular mimicry multiple sclerosis predictive biomarkers serum neurofilament light chain protein
 Corticospinal tract Motor cortex Motor fatigue Neuromuscular assessment Transcranial magnetic stimulation-electroencephalography
 Mediterranean diet Multiple sclerosis fatigue fish nutrition omega-3 red meat symptom
 Central vein MOG MS Myelin oligodendrocyte glycoprotein Pediatric multiple sclerosis
 diagnosis dimension multiple sclerosis neurology psychiatry psychopathology reliability schizophrenia validity
 Brain tissue segmentation Brain volumetry Deep learning Lesion inpainting Magnetic resonance imaging White matter lesions
 aging disability leukocyte telomere length mitochondrial DNA relapsing-remittent multiple sclerosis
 DNA hydromethylation DNA methylation Glatiramer Acetate (GA) treatment Interferon beta (IFN-β) treatment epigenetic histone acetylation multiple sclerosis (MS)
 Balance Figure of 8 walk test Multiple sclerosis Reliability Validity Walking
 meta-analysis multiple sclerosis polysomnography sleep
 Memory for Intentions Test Multiple sclerosis appointment attendance cognitive screening functional outcomes prospective memory
 Convolutional neural networks Deep learning MRI MS lesion segmentation Multiple sclerosis (MS) Residual blocks U-net
 acupuncture mobility multiple sclerosis sensorimotor function

 Asia Chinese Chino Esclerosis múltiple Multiple sclerosis Prevalence Prevalencia
 In vivo corneal confocal microscopy Inflammation Multiple sclerosis Neurodegeneration Neuroregeneration Relapse
 Multiple sclerosis (MS) amyloidogenic evolvability (aEVO) amyloidogenic proteins (APs) antagonistic pleiotropy multiple system atrophy (MSA) oligodendrocytes (OLs) prion α-synuclein (αS) β-amyloid (aβ) β-synuclein (βS)

 Beverages Black tea Carbonated beverages Coffee Green tea Multiple sclerosis
 Real-world evidence Relapsing-remitting multiple sclerosis Treatment outcome
 MULTIPLE SCLEROSIS
 animal-based protein case–control study dietary acid load multiple sclerosis net endogenous acid production plant-based protein potential renal acid load

 Multiple sclerosis breastfeeding disease-modifying treatments pregnancy reproductive assistance
 Cognition Control preference scale Multiple sclerosis Switching therapy
 consensus disease-modifying therapy infections multiple sclerosis vaccination
 behaviour change techniques cytokines exercise multiple sclerosis
 Behavior change E-learning Multiple sclerosis Physical activity Theory
 Diffusion tensor imaging Glial fibrillary acidic protein Magnetic resonance imaging Multiple sclerosis Neurofilament light chain

 Aged, Lymphopenia Relapsing remitting multiple sclerosis Secondary progressive multiple sclerosis Teriflunomide
 DNA damage Erk1/2 inhibitor PD98059 Modified comet assay Multiple sclerosis pathology Oxidative stress
 Brain-derived neurotrophic factor Cerebrospinal fluid Cognition EDSS Multiple sclerosis Serum
 brain-gut axis gut microbiome multiple sclerosis neuromyelitis spectrum disorders
 Cognition Depression Dual-task walking Multiple sclerosis Self-efficacy
 BICAMS Brief Visuospatial Memory Test California Verbal Learning Test EDSS MSSS Symbol Digit Modalities Test biomarker oxidative stress
 Expanded Disability Status Scale depression disability hormonal status multiple sclerosis sexual dysfunction
 EQ-5D-5L MSQOL-54 Multiple sclerosis Quality of life Trinidad and Tobago

 multidisciplinary rehabilitation multiple sclerosis vitamin D receptor SNPs
 Cohort studies Comorbidity Fatigue Health-related quality of life Multiple sclerosis Quality of life
 Biomarker Expression level Multiple sclerosis Real-time PCR lncRNA
 MRI T1/T2w ratio chronic active lesions iron rim lesions multiple sclerosis spinal cord
 Electron microscopy Human brain (bank) Mitochondria Multiple sclerosis Myelin Nanotomy Ultrastructure g-ratio

 Cognitive processing speed Manual dexterity Patient-reported outcomes Q6W dosing Walking speed
 Fatigue Multiple sclerosis Nursing care Patient care management Self efficacy Sleep quality Telenursing

 Double inversion recovery Iterative denoising Juxtacortical lesions Magnetic resonance imaging Multiple sclerosis

 Fatigue Insomnia Mindfulness Multiple Sclerosis Sleep Hygiene Sleep Quality
 Anxiety Cognitive dysfunction Depression Disease duration Fatigue Multiple sclerosis
 Balance cerebellum falls gait multiple sclerosis
 Cognition Gait MS Smartphone sensor
 Cannabis France Inhalation Multiple sclerosis Pain

 Cancer Cohort study Mortality Multiple sclerosis
 Epidemiology Incidence Iran Multiple sclerosis Prevalence
 B cells cladribine immunoglobulin proteome analysis immunoglobulin repertoire multiple sclerosis next generation sequencing
 African American Cognition Multiple sclerosis Physical functional performance Population heterogeneity Social determinants of health
 Clostridium perfringens epsilon toxin multiple sclerosis

 Flow cytometry Immunohistochemistry MRI Mesenchymal stem cells Multiple sclerosis Stromal vascular fraction TEM

 Effectiveness Fingolimod Greece Multiple sclerosis Patient-reported outcomes Quality of life Real-world Safety Satisfaction
 Melatonin Multiple sclerosis Steroid hormone Thyroid hormone
 Gait Plantar pressure Somatosensory impairment Vibration perception
 EBV HSV Human herpes viruses Multiple sclerosis



 Generalizable Interpretable artificial intelligence Multiple sclerosis Optical coherence tomography Patient-wise cross-validation
 COVID-19 Multiple sclerosis (MS) disease-modifying therapies (DMTs) immune response vaccination
 Behaviour decision making education falls intervention
 Positive psychology vocational rehabilitation work
 6-min walk EDSS Gait Inertial sensors MS Reliability
 Anxiety Autonomous motivation Depression Multiple sclerosis Psychological help-seeking attitudes Shame Stigma
 CLARITY CLARITY Extension Cladribine tablets Expanded Disability Status Scale disability disease-modifying therapy employment multiple sclerosis
 B cells Biomarker identification Gene interaction network analysis Immune reconstitution therapy Multiple sclerosis Peripheral blood Transcriptome profiling
 CNS cognition cognitive symptoms cognitive testing demyelinating autoimmune diseases self-report
 Diet EDSS MRI dietary inflammatory index inflammation multiple sclerosis time to relapse and conversion to MS
 multiple sclerosis ocrelizumab pembrolizumab progressive multifocal leukoencephalopathy
 ACh MS glutamate neurotransmitter receptors nitric oxide
 Activities of daily living Constraint induced movement therapy Multiple sclerosis Neurodegeneration Quality of life
 Benchmark Core outcomes Multiple sclerosis Outcome indicator Outcome set PROM Patient-reported outcomes Value-based healthcare
 Multiple sclerosis biomarker ocrelizumab
 Central nervous system Cholesterol metabolism Multiple sclerosis Myelin
 Bacterial meningitis CSF filtration Guillain–barré cerebrospinal fluid encephalitis fungal meningitis liquorpheresis meningeal carcinomatosis subarachnoid hemorrhage viral meningitis
 Exercise Online training Pediatric-onset multiple sclerosis Physical activity Rehabilitation

 cell deconvolution epigenetics epigenome-wide association studies genetic risk methylation multiple sclerosis

 Birth DNA methylation Epigenetics Immune system Neurobiology Parity
 RNA sequencing experimental autoimmune encephalitis microglia secondary progressive MS
 Foot drop electrical stimulator barriers facilitators neurological conditions users’ experience
 Chronic active lesions multiple sclerosis paramagnetic rim lesions (PRLs) slowly expanding lesions (SELs) susceptibility-weighted imaging (SWI) volumetric MRI

 Occupational therapy group intervention occupations self-management

 brain MRI fatigue fractional anisotropy multiple sclerosis treatment resistance
 Monocyte to lymphocyte ratio (MLR) Multiple sclerosis (MS) Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) Neutrophil to lymphocyte ratio (NLR) Platelet to lymphocyte ratio (PLR)
 HIV Multiple sclerosis Natalizumab


 Cholinesterase Multiple sclerosis Saliva Serum
 Multiple sclerosis coping strategies health-related quality of life risk and protective factors social support
 Fatigue Kinesiophobia Multiple sclerosis Tampa Scale of Kinesiophobia-Fatigue
 Multiple sclerosis REHABILITATION MEDICINE SPORTS MEDICINE
 Beta-adrenoceptor blockade Microglia activation/polarization Multiple sclerosis Primary autoimmune response Sympathetic nervous system activation Th17-cell reactivation
 #MeToo Multiple sclerosis emotional abuse physical abuse sexual abuse
 META-ANALYSIS MULTIPLE SCLEROSIS NEUROIMMUNOLOGY
 Aquaporin-4 (AQP4) Autoantibodies Cerebrospinal fluid (CSF) Clinical presentation Diagnosis Diagnostic criteria Differential diagnosis MOG antibody-associated disease (MOGAD) MOG antibody-associated encephalomyelitis (MOG-EM) Magnetic resonance imaging (MRI) Myelin oligodendrocyte glycoprotein (MOG) Myelitis Neuromyelitis optica (NMO) Neuromyelitis optica spectrum disorders (NMOSD) Optic coherence tomography (OCT) Optic neuritis Serology

 Antipsychotics Docking Enzyme MS Molecular dynamics
 COVID-19 Exercise training Immune system Multiple sclerosis Renin–angiotensin system Respiratory system


 Biomarkers Functional profiling Meta-analysis Multiple sclerosis Neurodegeneration Sex-based differences
 Early diagnosis Exercise Rehabilitation Therapy

 T-cells astrocytes exosomes multiple sclerosis
 B-cell depletion COVID-19 vaccination SARS-CoV-2 infection T-cell response anti-CD20 therapy anti-RBD antibody titer multiple sclerosis omicron
 EPIDEMIOLOGY MULTIPLE SCLEROSIS

 Birth-cohort analysis Epidemiology of IBD Epstein-Barr virus Etiology of IBD Vital statistics

 cytokines disease-modifying therapies microglia multiple sclerosis neuroimmunology
 CD4+ CD8+ Methylation Modules Multiple sclerosis Networks Pregnancy T cells Transcriptomics
 Dual task Gait Multiple sclerosis Treadmill training Virtual reality
 abuse autoimmune disorders emotional neurological disorder physical sexual
 Anomaly detection Autoencoder Brain MRI Unsupervised learning

 Aging Leisure activities Multiple sclerosis Social relations Wellbeing
 biomarkers multiple sclerosis proteomics transcriptomics
 Observational causal inference multiple sclerosis
 Electroencephalography (EEG) Event-related potential Mismatch negativity (MMN) Multi-feature paradigm Multiple sclerosis Sensory processing
 COVID-19 Health behavior Mistrust Multiple sclerosis Observational study Vaccine hesitancy
 S1P1 receptor antagonist etretinate fingolimod generalized pustular psoriasis multiple sclerosis
 Multiple sclerosis PFFKB3 TH17 cells autoimmunity glycolysis inflammation
 aquaporin-4 antibody fingolimod rebound syndrome fingolimod withdrawal syndrome neuromyelitis optica spectrum disorder relapse-remitting multiple sclerosis
 MRI active plaque machine learning multiple sclerosis radiomics
 Multiple sclerosis prognosis
 Clinical Definite Multiple Sclerosis Clinically Isolated Syndrome Conversion predictors Conversion risk Prospective cohort study
 Autonomic nervous system Cardiovascular Multiple sclerosis Thermoregulatory

 DNA methylation epigenetics genome-wide analysis multiple sclerosis relapse remission



 TRPV1 capsaicin microglia phagocytosis remyelination
 Alzheimer’s disease Parkinson’s disease amyotrophic lateral sclerosis encephalitis generalized dementia influenza multiple sclerosis varicella-zoster vascular dementia viral exposure
 EBNA-1 Epstein-Barr virus Herpesviridae Interferons Multiple sclerosis
 T cells glucocorticoids metabolism multiple sclerosis
 analytical characterization analytical validation biomarker multiple sclerosis proximity extension assay
 Exercise training Health outcomes Health-related quality of life Multiple sclerosis Neurological disease Rehabilitation
 BDNF genes multiple sclerosis polymorphisms
 Multiple sclerosis Pain cognition
 biomarker contrast enhancement gadolinium multiple sclerosis neurofilament light chain
 HLA-DRB1*15:01 Multiple sclerosis air pollution nitrogen oxides smoking
 COVID-19 Mendelian randomization multiple sclerosis

 Biomarker Disability EDSS Long-term Multiple sclerosis RRMS SPMS miR-25-3p miR-320b miRNA
 Disease-modifying therapy MRI Motor dysfunction Multiple sclerosis Neural plasticity Oligoclonal bands
 Motherhood Multiple sclerosis Needs assessment Patient-reported outcome Pregnancy
 Annual Relapse Rate Japanese Magnetic resonance imaging Natalizumab Relapsing-remitting multiple sclerosis
 EAE cytokines multiple sclerosis  Antigen B
 Adipokines BMI MRI Disability Multiple sclerosis
 MS Meta-analysis Multiple sclerosis OCT OCT-A Optical coherence tomography Optical coherence tomography angiography Perfusion density Retina Vascular density


 gait meta-analysis multiple sclerosis robotic-assisted gait training systematic review
 ambulatory functional score multiple sclerosis (MS) optical coherence tomography (OCT) primary progressive multiple sclerosis (PPMS) relapsing–remitting multiple sclerosis (RRMS)
 Health-related quality of life ambulatory aid mobility assist neurological disorder powered exoskeleton



 Parkinson's disease accidents automobile driving multiple sclerosis traffic
 COVID-19 Disease modifying therapies Multiple sclerosis



 Biomarkers Blood Exosomes Extracellular Vesicles Multiple Sclerosis Proteomic Analysis, Rheumatoid Arthritis Subcortical Stroke

 Balance Gait HIT Mobility Postural control Walking
 allostatic self-efficacy computational psychiatry confidence fatigue interoception metacognition multiple sclerosis perceptual decision-making
 Deep learning Multiple sclerosis PET/MRI Radiomics
 Incidence Iran, Empirical Bayesian Multiple sclerosis Time trends
 DYMUS Dysphagia Multiple sclerosis Reliability Validity
 MULTIPLE SCLEROSIS QUALITY OF LIFE

 Latin American NMOSD misdiagnosis treatment
 CRF physical activity physiotherapy rehabilitation strength
 Cognitive complaints Cognitive impairment Cognitive rehabilitation Mindfulness Multiple sclerosis
 accompagnement accompaniment corticosteroid corticoïde flare-up poussée pseudo-flare-up pseudo-poussée symptom symptôme traitement treatment

 Mendelian randomization Metabolites Metabolome Multiple sclerosis

 Demyelination MS Multiple sclerosis Toxoplasma gondii
 COVID-19 cladribine efficacy relapsing-remitting multiple sclerosis safety
 MRI TMS inhibition motor cortex multiple sclerosis turning

 Demyelinating diseases Employment Multiple sclerosis Vocational rehabilitation Work


 disability dismissal désinsertion professionnelle handicap inaptitude licenciement médecine du travail occupational medicine professional reinsertion reclassement reclassification unfitness
 Multiple sclerosis health outcomes memory rehabilitation
 EPIDEMIOLOGY MULTIPLE SCLEROSIS
 accompagnement disability grossesse handicap insertion professionnelle pregnancy professional integration support traitement treatment
 COVID-19 COVID-19 outcomes Multiple sclerosis SARS-CoV-2 infection pregnancy risk factors
 Cardiorespiratory fitness Glial fibrillary acidic protein High-intensity interval training Kynurenine pathway Multiple sclerosis Physical fitness Primary progressive multiple sclerosis Serum neurofilament light chain
 Evoked potentials MRI Multiple sclerosis
 Multiple sclerosis consensus disease-modifying therapy infections vaccination
 Cerebrospinal fluid biomarker clinically isolated syndrome diagnosis index intrathecal fraction kappa free light chains meta-analysis multiple sclerosis systematic review
 Adherence Disease modifying therapy Medication switches Multiple sclerosis Persistence Specialty pharmacy
 experimental autoimmune encephalomyelitis (EAE) inflammation multiple sclerosis oligodendrocytes osteopontin
 Comorbidity Familial Mediterranean Fever Magnetic resonance imaging Multiple sclerosis Ocrelizumab Risk factor
 B cells CD19 CD20 Monoclonal antibodies Multiple sclerosis
 Bifactor model Health-related quality of life Item response theory MSQOL-54 Multidimensional computerized adaptive test Multiple sclerosis
 B cell depletion Epstein-Barr virus Multiple sclerosis Ocrelizumab antibody response
 Black-hole lesions Brain atrophy First clinical demyelinating event Interferon β-1a Lesion evolution White matter tracts

 multiple sclerosis
 attention fatigue sensory attenuation
 Multiple sclerosis Rivastigmine Wechsler memory scale
 Axonal damage Early multiple sclerosis Neurofilament light chains
 BDNF EAE GSK-3β Multiple sclerosis PI3K/Akt Semaglutide
 Cuprizone Lithium chloride Multiple sclerosis Myelination Stem cell
 MRI artificial intelligence cognitive performance information processing speed machine learning multiple sclerosis symbol digit modalities test

 Cerebrospinal fluid biomarker clinically isolated syndrome consensus diagnosis disease activity index kappa-free light chains multiple sclerosis prediction
 Magnetic resonance imaging adults brain/brain stem imaging sequences intravenous contrast agents
 CNS Immunoengineering macrophages myeloid phenotype
 Dyslipidemia Multiple sclerosis Statins
 Cognitive dysfunction Postural control Relapsing-remitting multiple sclerosis Ultraviolet radiation Vitamin D(3)
 Digital health technology tools MRI Multiple sclerosis Neural correlates Smartphone sensor
 COVID-19 MULTIPLE SCLEROSIS


 Aging Biomarkers Multiple sclerosis
 Parkinson’s disease mobile apps multiple sclerosis neurological diseases review stroke
 Multiple sclerosis cognitive impairment functional connectivity oscillatory activity performance validity
 Anxiety Depression Multiple sclerosis Quality of life Stigma
 epidemiology multiple sclerosis

 Moonlighting intrinsically disordered protein Multiple sclerosis Myelin basic protein Myelin sheath Myelin-associated oligodendrocyte basic protein NAMD
 Disease modifying therapies Multiple sclerosis Ocrelizumab Switch Treatment response
 education income lifestyle multiple sclerosis socioeconomic status
 Bacteroides 2 EDSS-Plus gut microbiome long-term disability worsening multiple sclerosis neurofilament light chain
 Clinical trial Multiple sclerosis Remyelination Thyroid hormone
 Gait Multiple sclerosis Sensors Turning Vestibular disorder
 family fatigue friends leisure work
 Epstein - Barr virus environmental factors hormones immunology multiple sclerosis



 Disease-modifying therapies Immune system Multiple sclerosis Resistance training Strength training

 Functional magnetic resonance imaging disability progression longitudinal network dynamics network efficiency upper and lower limbs
 Multiple sclerosis month of birth risk factors seasons sunlight ultraviolet rays
 MS onset myelin repair oligodendrocyte precursor cells stem cells therapy
 Anti-aquaporin-4 antibody Multiple sclerosis Neuromyelitis optica spectrum disorders Somatosensory evoked potentials Tibial nerve
 Immunoregulation Lactobacillus paracasei Lactobacillus plantarum Multiple sclerosis Probiotics
 NMOSD aquaporin-4 epidemiology risk factors
 FLAIR* central vein sign gadolinium multiple sclerosis
 Balance Gait Multiple sclerosis Neuromodulation Physical therapy Rehabilitation Translingual Walking
 immunosuppressive therapy HBV reactivation Multiple Sclerosis Ocrelizumab therapy anti-HBc antibodies
 1,25(OH)2D3 multiple sclerosis neurodegeneration neuroprotection vitamin D
 Animal models Intravital imaging Multimodal microscopy Multiple sclerosis Neurodegenerative disease
 BICAMS Cognitive function Multiple sclerosis Overactive bladder
 Coping Ecological momentary assessment Fatigue Multiple sclerosis Pain
 multiple sclerosis objective measures subjective measures upper limb
 Cognitive behavioral therapy Insomnia Multiple sclerosis Sleep quality
 Adherence Claims data Disability progression Disease-modifying therapy Relapse


 alternative complement pathway atypical haemolytic uremic syndrome complement factor I interferon-beta multiple sclerosis thrombotic microangiopathy
 Crohn’s disease Nrf2 celiac disease dimethyl fumarate gut disorders inflammation inflammatory bowel diseases intestine repurposing ulcerative colitis

 GLP-1 agonists endothelial dysfunction lipoprotein subfractions multiple sclerosis redox balance
 Cognitive–motor interference Dual task Gait Multiple sclerosis Progressive
 Brain-derived neurotrophic factor Exercise Glial fibrillary acidic protein Multiple sclerosis Neurofilament proteins Neuroprotection
 Digital biomarkers Mobile health Multiple sclerosis Smartphone Smartwatch
 Magnetic resonance imaging Multiple sclerosis Neural networks Thalamus
 blood-brain barrier cladribine dendritic cells monocytes multiple sclerosis spectral flow cytometry trans-endothelial migration
 Cohort studies Natural history Primary progressive multiple sclerosis Quality of life Retrospective study
 First Gulf War Impact assessment Interrupted time series design Kuwait Multiple sclerosis Risk

 arterial spin labeling MRI cerebral blood flow hypoperfusion multiple sclerosis neurodegeneration white matter lesions
 Multiple sclerosis Psychosocial factors Qualitative study
 Argentina Multiple sclerosis Neurorehabilitation Tele rehabilitation Virtual reality
 Brain MRI Information processing speed Multiple sclerosis RRMS Thalamus atrophy
 MS disability discontinuation real-world data registry relapse switching


 Epstein–Barr virus delayed infection infectious mononucleosis intra-family contagion multiple sclerosis
 Cognitive function Diversity Fall prevention Physical function Race
 Body temperature regulation Cold Heat Multiple Sclerosis Thermal comfort
 MRI cervical spine double inversion recovery multiple sclerosis
 Mendelian autoimmune diseases causal effect mediators multisite chronic pain
 autoimmune multiple sclerosis neuroimmunology pediatric risk factors
 adverse event doxycycline fibromyalgia isotretinoin migraine minocycline multiple sclerosis neurologic tetracycline
 Computer vision Denoising MRI Multiple sclerosis (MS) Orthogonal matching pursuit (OMP) Sparse representation


 Lebanon cost-of-illness economic burden healthcare consumption multiple sclerosis productivity losses
 Fingolimod Generic Multiple sclerosis

 fatigue intramuscular interferon-β lower limb limitation multiple sclerosis patient-reported outcomes


 Cerebellum Genetic correlates Multiple sclerosis Neuromyelitis optica spectrum disorder Structural and functional MRI

 Cortical lesions MRI Multiple sclerosis Neuropathology
 Anti-CD20 therapy COVID-19 Disease-modifying therapy Multiple sclerosis Seroconversion Vaccination
 Fingolimod multiple sclerosis ozanimod ponesimod siponimod sphingosine 1-phosphate receptor modulators
 Cost of walking Energy metabolism Fatigue Gait Multiple sclerosis Muscle fatigue
 amyloid animal model antigen processing citrullination multiple sclerosis peptide chemical synthesis
 Acute transverse myelitis Barthel index Fampridine Multiple sclerosis

 Cytotoxic T cells Epstein-Barr virus Multiple sclerosis Stem cell transplant
 Clinical trial Diffusion tensor imaging Functional connectivity Multiple sclerosis Structural and functional connectivity index
 Immunoglobulin G index Microglia Positron-emission tomography Progressive multiple sclerosis T2-lesion TSPO

 Demyelinating diseases Epidemiology Multiple sclerosis Neuromyelitis optica spectrum disorder Optic neuritis Transverse myelitis
 Awareness Biochemical hyperthyroidism Biotin Biotin interference Biotin/streptavidin immunoassay Misdiagnosis
 MRI differential vulnerability segmentation thalamic nuclei thalamus volumetry

 Menopause Multiple sclerosis Systematic review
 COVID-19 Cellular immune response Immunology Multiple sclerosis T cells
 Anti-CD20 treatment Machine learning Paramagnetic rims Single cell RNA sequencing Susceptibility-based MRI
 RNA-sequencing astrocyte microglia multiple sclerosis oligodendrocyte
 Multiple sclerosis association polymorphism programmed cell death protein 1

 Inflammation Multiple sclerosis Neurodegeneration Neuroscience Potassium channels
 MRI diagnostic criteria multiple sclerosis prognosis radiologically isolated syndrome

 Cost-effectiveness Cost-utility Economic evaluation Health technology assessment Informal care Multiple sclerosis Productivity losses Social costs Societal perspective


 brain disorders disease fungus multiple sclerosis signaling
 COVID-19 T-cell response anti-SARS-CoV-2 vaccination disease modifying therapies multiple sclerosis neutralizing antibodies
 area under the curve infection lymphocyte monocyte predictive factor
 Bystander-activation IL-17A Multiple sclerosis
 Antibodies Liquid chromatography Mass spectrometry Multiple sclerosis Natalizumab Serum
 Experimental autoimmune encephalomyelitis Microglia Multiple sclerosis Myelin debris Phagocytosis Polarization

 T-cell cannabinoid endocannabinoid experimental autoimmune encephalomyelitis multiple sclerosis
 epigenetics immune cells multiple sclerosis oligodendrocytes remyelination transcription factors
 Alzheimers disease (AD) Parkinsons disease (PD) cannabinoids endocannabinoids inflammation multiple sclerosis (MS)
 Autoimmunity Experimental autoimmune encephalomyelitis Multiple sclerosis Sex chromosomes Sex differences Sex hormones T helper cell
 Th17- and Th1-cells fluoxetine macrophages multiple sclerosis neuroimmune interaction
 Microvascular decompression balloon compression glycerol rhizolysis secondary trigeminal neuralgia
 Bioactive lipids Demyelination G protein-coupled receptors (GPCRs) Inflammation Neuroimmunology Neurology

 Cognitive function Gait Gait analysis Multiple sclerosis Neuromyelitis optica
 DNAJC30 gene Leber’s hereditary optic neuropathy antibodies to aquaporin-4 antibodies to myelin oligodendrocyte glycoprotein autosomal recessive optic neuropathy demyelinating diseases mitochondrial diseases multiple sclerosis
 EAE Multiple sclerosis animal models cortical lesions cuprizone demyelinating disease progression ethidium bromide in vitro models lysolecithin neurodegeneration plaques transgenic animal models white matter lesions
 Immunoglobulins Lymphocytes Multiple sclerosis Ocrelizumab
 astrocyte glutamate glutamate excitotoxicity ionotropic glutamate receptors microglia multiple sclerosis synapse synaptopathy

 BBIBP-CorV COVID-19 Multiple sclerosis SARS-CoV-2 Vaccine
 Glucocorticoids Multiple sclerosis Myeloid-derived suppressor cells Neuroinflammation miR-223

 Aptitude Cognition Cues Motor Imagery Multiple Sclerosis Physical Therapy
 BACE1 Multiple sclerosis Neurodegeneration, CSF Neuroinflammation
 Cerebrospinal fluid immune system mass spectrometry multiple sclerosis neurons pediatrics proteins proteomics
 COVID-19 SARS-CoV-2 antibodies disease-modifying therapies multiple sclerosis serology vaccines
 C9orf72 repeat expansion disease heterogeneity frontotemporal dementia (FTD) genetic variants intermediate repeat length multiple sclerosis (MS)

 Bioenergetics Mitochondria Progressive EAE Relapsing-remitting EAE
 Epstein-Barr virus Relapsing–remitting multiple sclerosis Toll-like receptor 10 Viral load
 Disease-modifying therapies immunology multiple sclerosis
 EBV GM allotypes MS latent allotypes
 intervention multiple sclerosis occupational therapy qualitative research
 MBP MOG biomarkers exosomes extracellular vesicles multiple sclerosis oligodendrocytes primary progressive multiple sclerosis
 HTLV-1 HTLV-1-associated myelopathy/tropical spastic paraparesis IL-17 Multiple sclerosis Th17 cells Th17-related cytokines
 Apical disease Epstein-Barr virus multiple sclerosis periapical abscess

 COVID-19 SARS-CoV-2 T cell disease-modifying therapy multiple sclerosis
 Multiple sclerosis all-trans retinoic acid docosahexaenoic acid genes peripheral blood mononuclear cells
 Multiple sclerosis processing speed test quantitative MRI smoking
 Lower limb Multiple sclerosis Muscle strength Normative data
 Multiple sclerosis cervicomedullary junction demyelinating disease disability motor impairment progressive multiple sclerosis
 DYMUS questionnaire Dysphagia Multiple Sclerosis Reliability Swallowing Validation
 GWAS Multiple sclerosis POMS pediatric-onset rare variants
 Ajugarin-I Bcl2/Caspase-3 EAE MAPK/NF-κB Nrf2/Keap-1 multiple sclerosis
 Biosurfactant Ibudilast Intranasal delivery Multiple sclerosis Polydopamine Surfactin micelles
 corticospinal tract falls gait multiple sclerosis myelin water imaging superior cerebellar peduncle
 Claim database analysis I I1 I11 I12 Lemtradai Ocrevusii Tysabriiii healthcare expenditure site of case
 cerebrospinal fluid choroid plexus multiple sclerosis neurodegeneration positron emission tomography remyelination

 D61 D81 H83 I1 I15 I18
 Bradycardia Functional antagonists Lymphopenia Structure-activity relationship Three dimensional structural features
 limiting symptoms multiple sclerosis quality of life spasticity specialist nurses
 Multiple Sclerosis Parkinson’s disease chronic illness dance inclusive dance lived experience participatory health research
 Clinical validation Gadolinium-positive lesion MS disease activity Multiple sclerosis
 aging galectin 3 microglia multiple sclerosis neurodegeneration oxidized phosphatidylcholine

 Mediterranean Multiple sclerosis depression diet disability
 BPA BPS Endocrine-disrupting chemicals Environmental risk factor Experimental autoimmune encephalomyelitis
 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) Pediatric-onset MS (POMS) Serum neurofilament light chain (sNfL) Single-molecule array (Simoa)
 Multiple sclerosis adverse event disease-modifying therapies treatment adherence treatment drop-out

 Cerebrospinal fluid Disease activity Kappa free light chain Multiple sclerosis Neurofilament light Prediction
 multiple sclerosis pathway-specific risk score phenotype association polygenic risk score

 multiple sclerosis

 axon injury complex IV experimental demyelination mitochondria multiple sclerosis and neuroprotection
 Disease activity Menopause Multiple sclerosis Perimenopause Sex hormones
 BBB Diabetes EAE Inflammation Microglia Multiple sclerosis Obesity
 IMMUNOLOGY MULTIPLE SCLEROSIS RHEUMATOLOGY SLE
 Balance Mini-BESTest Neurological Turkish Validity
 Brain atrophy Ganglion cells MRI MS Neurodegeneration OCT

 Autoimmunity Demyelinating disorders Microbiology Multiple sclerosis Toxins/drugs/xenobiotics
 curcumin epigallocatechin gallate hydroxytyrosol luteolin microbiome multiple sclerosis neuroprotection polyphenols quercetin resveratrol

 motherhood multiple sclerosis pregnancy qualitative research women

 GCIPL INL Multiple sclerosis disease progression optical coherence tomography pRNFL paramagnetic rim lesion
 Adolescence Multiple sclerosis Myopia Vision Vitamin D
 MRI demyelination disability multiple sclerosis myelin water imaging neuroimaging
 PsA RA TNF inhibitor bDMARD multiple sclerosis spondyloarthritis
 Atomic force microscopy EAE Multiple sclerosis Neurofilament light chain Optic nerve Stiffness
 Multiple sclerosis Turkey Turkish health-related quality of life patient outcome assessments
 anti-CD20 multiple sclerosis ocrelizumab ofatumumab rituximab ublituximab
 Brain atrophy Brain volume loss Expanded disability status scale Multiple sclerosis Physical disability progression Systematic review


 Clinically isolated syndrome genetics multiple sclerosis prognosis
 adherence multiple sclerosis real-world evidence treatment pattern

 MRI anti-myelin oligodendrocyte glycoprotein multiple sclerosis neuromyelitis optica optic neuritis
 Multiple sclerosis Optic neuritis SIRT1 ELISA SIRT1 SNP
 diagnosis emotional support multiple sclerosis peer support qualitative stakeholder engagement
 multiple sclerosis vitamin D vitamin D supplementation
 Epstein Barr Virus Immune response Inflammation Multiple Sclerosis Vitamin D
 CNS autoimmune disease Microglia Multiple sclerosis Tissue-resident immune cells Tissue-resident memory T cells
 Amplitude of low-frequency fluctuations Feedback Learning Multiple sclerosis Resting state

 PML - progressive multifocal leukoencephalopathy extended interval dosing multiple sclerosis natalizumab ocrelizumab
 Lipidomics Magnetic levitation Metabolomics Multiple sclerosis Plasma biomolecules Proteomics
 Balance EquiTest® Hunova® Multiple sclerosis Posturography

 Blood–brain barrier (BBB) Epstein–barr virus (EBV) Experimental autoimmune encephalomyelitis (EAE) Herpes simplex virus (HSV-1) Multiple sclerosis (MS) Neurodegeneration
 NF-κB NaHS cuprizone demyelination miR-146a
 epidemiology multiple sclerosis sleep
 French Multiple Sclerosis Intimacy and Sexuality Questionnaire 15 (MSISQ-15) multiple sclerosis neurology nursing sexual health
 Diagnosis Grey matter lesion Immune infiltration Multiple sclerosis

 cell death demyelinating diseases iron balance disorder iron overload multiple sclerosis oxidative stress
 Alzheimer’s disease Parkinson’s disease central nervous system depression multiple sclerosis neurodegeneration zinc

 Behaviour change Health-related quality of life Lifestyle Multiple sclerosis Multiple sclerosis online course Randomised controlled trial
 intensity movement senescence wellbeing
 RRMS neurodegenerative disease progesterone receptor rs1042838 sex hormone
 Adherence Multiple sclerosis Patient-centered care Shared decision making Treatment
 Alzheimer's disease amyloid beta microglia multiple sclerosis myelin debris neurodegenerative disease neuroimmunology
 Click chemistry Exosomes Multiple sclerosis Resveratrol Sialic acid
 Glial cells Inflammation Multiple sclerosis Neurodegeneration

 Autoimmune disease Demyelination EAE Multiple sclerosis Toll-like receptors
 Autoimmunity BTK LOU064 Multiple sclerosis Neuroinflammation Remibrutinib
 Multiple sclerosis Pelvic floor muscle Primary motor cortex Training Transcranial direct current stimulation Ultrasonography
 dimethyl fumarate disease-modifying therapies multiple sclerosis network meta-analysis real-world evidence
 gadolinium-based contrast agent magnetic resonance imaging multiple sclerosis

 COVID Multiple sclerosis SARS-CoV-2 disease-modifying therapies immunology vaccine
 atrophy disability multiple sclerosis neurodegeneration neurofilament
 Articulation system Dysarthria Dysphonia Multiple sclerosis Phonation system Prosody Speech deficits
 Carotenoids Cognitive function Event-related potentials Macular pigment optical density Multiple sclerosis Optical coherence tomography
 Multiple sclerosis cognitive impairment insomnia sleep sleep apnea sleepiness
 Anti-CD20 Disease-modifying therapy S1P-Modulators SARS-CoV-2 vaccination titre
 B cell aggregates CSF Chemokines EAE MP4
 Magnetic resonance imaging Multiple sclerosis Neuromyelitis optica spectrum disorders Structural covariance
 immunology inflammation major histocompatibility complex mouse multiple sclerosis neuroscience oligodendrocytes
 COVID-19 course COVID-19 outcomes fingolimod multiple sclerosis ocrelizumab third booster vaccine dose
 9-Hole Peg Test Meta-analysis Multiple sclerosis Patient-Reported Outcome Measures Upper limb function

 NLRP3 inflammasome dysbiosis gut-brain axis major depressive disorders multiple sclerosis
 gut microbiota microbiome: short-chain fatty acid multiple sclerosis
 cognition early therapy exercise multiple sclerosis physical functional performance
 image analysis multiple sclerosis
 Resistance training exercise nervous system diseases neurological disorder
 Microglia Multiple Sclerosis Neurofilament light PET TSPO

 Australia COVID 19 Multiple sclerosis bushfire environmental research health services research public health

 Alzheimer’s disease arterial spin labeling caloric restriction diffusion basis spectrum imaging multiple sclerosis neuroinflammation prevention relative cerebral blood flow
 CD4(+) T cells Experimental autoimmune encephalomyelitis Ferroptosis GPX4 Multiple sclerosis
 autoimmune diseases experimental-autoimmune encephalomyelitis immune microenvironment multiple sclerosis tolerogenic nanovaccines
 Assistive technologies BCI EDSS Eye-tracking Fully adjustable electric bed Multiple sclerosis
 Exercise multiple sclerosis physical activity reproducibility of results validation studies
 Balance disorders Multiple sclerosis Tandem gait Upper limbs
 assessment multiple sclerosis new technique pathogenesis and rehabilitation mechanism progress
 axon protection macrophage microglia multiple sclerosis myelination oligodendrocyte oligodendrocyte precursor cell
 AKT/mTOR LINGO1 Multiple sclerosis Notch Nrf2 RXR-γ Remyelination Wnt/β Catenin
 cell-based remyelination therapy demyelination disease modeling induced pluripotent stem cells multiple sclerosis oligodendrocyte oligodendrocyte precursor cells organoids reprogramming spinal cord injury
 HLA class I HTBH IFNγ biotin carboxyl carrier domain immunoproteasome multiple sclerosis myelin basic protein negative stain electron microscopy proteasome sodium dodecyl sulfate
 Neuro-Behcet’s disease TNF-a central nervous system cytokines microglia multiple sclerosis neuroinflammation neurosarcoidosis
 age-period-cohort effects burden global multiple sclerosis national regional
 Cyclophosphamide Encephalitis Multiple sclerosis Neuroinflammatory disorders Vasculitis
 COVID FreeSurfer brain atrophy gray matter volumetry
 Microglia nodules Monocyte encephalopathy Phagocytes Río Hortega Secondary progressive multiple sclerosis Wall microglia
 autoimmune diseases metabolites multiple sclerosis serum
 Epstein-Barr virus human leukocyte antigen infectious mononucleosis multiple sclerosis obesity smoking sun exposure vitamin D
 CMTM5 cuprizone demyelination endoplasmic reticulum stress experimental autoimmune encephalomyelitis multiple sclerosis

 COVID-vaccines adverse events inactivated virus mRNA vaccines multiple sclerosis relapse viral-vector vaccines
 chrononutrition circadian clock immunity metabolism multiple sclerosis retino-hypothalamic tract time-restricted eating
 COVID-19 Radiologically isolated syndrome vaccines

 Brain atrophy Cross-sectional Longitudinal MOGAD MRI Multiple sclerosis NMOSD
 Bright spotty Central canal MOG Multiple sclerosis Neuromyelitis optica spectrum disorder myelin oligodendrocyte glycoprotein myelin oligodendrocyte glycoprotein antibody-associated disease
 delay discounting demand multiple sclerosis probability discounting reinforcer pathology
 Multiple Sclerosis Natalizumab Neurofilament light chain Progressive multifocal leukoencephalopathy
 multiple sclerosis myasthenia neuroimmunology neuropathy stiff man syndrome
 effort energetics locomotion motor control vigor
 Faecalibacterium prausnitzii Gordonibacter urolithinfaciens Gut microbiota Multiple sclerosis Shotgun sequencing

 Drug repurposing MS pathogenesis Multiple sclerosis Protein-protein interaction networks Systems biology
 ADMSC MOG NGF artificial microvesicles astrocytes cytochalasin B cytokines demyelination experimental autoimmune encephalomyelitis (EAE) lentivirus multiple sclerosis neurodegeneration
 John Cunningham virus (JCV) Natalizumab (NTZ) PML immune reconstitution inflammatory syndrome (IRIS) Progressive multifocal leukoencephalopathy (PML)

 COVID-19 immunology infectious diseases interferon multiple sclerosis
 Multiple sclerosis anxiety depression expressed emotion personality social support
 Multiple sclerosis demyelination disease-modifying therapies neuromyelitis optica outcome measurement

 glutamate excitotoxicity lymphocyte microglia mitochondrial dysfunction multiple sclerosis neurodegeneration neuroinflammation oxidative stress slowly expanding lesion smouldering lesion
 genes genetic basis inflammatory demyelinating disease multiple sclerosis neuromyelitis optica spectrum disorders
 Anxiety COVID-19 Depression Multiple Sclerosis (MS) Quality of Life

 ELISA antibodies cerebrospinal fluid free light chains intrathecal synthesis

 Carboplatin Experimental autoimmune encephalomyelitis Multiple sclerosis T cell apoptosis

 Cognition Intelligence quotient Multiple sclerosis Nueromyelitis optica Wechsler adult intelligence scale
 Fitbit Multiple sclerosis activity level brain MRI cervical MRI remote monitoring spinal cord gray matter area
 Brainstem Demyelinating diseases Multiple sclerosis (MS) Myelin oligodendrocyte glycoprotein (MOG) Neuromyelitis optica spectrum disorder (NMOSD)
 B cell depletion Translation to patients anti-CD20 therapy extended interval dosing hypogammaglobulinemia multiple sclerosis ocrelizumab personalized dosing
 biomarker chemokine cytokine multiple sclerosis prognosis
 CNS inflammation Th17 cells Treg cells cellular combination delivery systems drug delivery multiple sclerosis
 APRIL BAFF Biomarker CCL2 CNS CSF CXC13 CXCL10 CXCL12 CXCL8 Chemokine Chitinase 3-like1 Multiple sclerosis
 NEDA disease activity multiple sclerosis neurofilament dynamics neurofilament light chain
 COVID-19 SARS-CoV-2 immunopathogenesis multiple sclerosis vitamin D
 COVID-19 pandemic Education Health-promoting behaviors Multiple sclerosis Self-care Telenursing
 Multiple sclerosis Neuroprotection Optic neuritis Resveratrol
 Symptomatic treatment detrusor overactivity neurogenic bladder self-catheterization urology
 Multiple sclerosis epidemiology physical activity rural population social determinants urban population
 animal-sourced milk cross-reactivity milk proteins multiple sclerosis myelin antigens personalized diet plant-based milk
 MRI Multiple sclerosis fingolimod pembrolizumab progressive multifocal leukencephalopathy
 biomarker disability multiple sclerosis optical coherence tomography predictor retina
 DHODH Drug Repurposing Ilepcimide Multiple Sclerosis NRF2
 Atrophy Intracellular volume fraction MRI Magnetization transfer ratio Multiple sclerosis Quantitative susceptibility mapping T1-weighted/T2-weighted ratio
 Cancellations Depression Missed appointments Multiple sclerosis Neuroticism No shows Prospective memory
 B-cell maturation CXCR3 Central nervous system Immunoglobulins T cells White matter lesions
 CX3CR1 RP-101074 S1PR-1 S1PR-5 microglia multiple sclerosis neuroprotection

 Aberrant myelin Demyelination Neurodegeneration Neuronal cell death Progressive multiple sclerosis Remyelination
 TREM2 axon degeneration demyelination microglia multiple sclerosis oligodendrocytes remyelination
 CSF biomarkers Kappa free light chains Multiple sclerosis Neurofilaments Oligoclonal bands
 Cannabidiol Cannabinoid Multiple sclerosis Nabiximols Sativex
 Enrichment factor Fingernail Industrial pollution Steel plants

 Telerehabilitation exercise internet-based intervention multiple sclerosis (MS) patient preference physiotherapy
 Central vein sign Glial fibrillary acidic protein Neurofilament light chain Optical coherence tomography Paramagnetic rim lesion
 Multiple sclerosis cognitive impairment connectivity corpus callosum disconnection syndrome “callosal disconnection syndrome”
 Multiple sclerosis NET formation NMODS Neutrophils Rituximab

 explainable artificial intelligence local interpretable model-agnostic explanations machine learning multiple sclerosis pre-emptive diagnosis shapley additive explanation
 CNS EAE GABA GABAergic MS immunomodulatory neuroinflammation

 Clinical trial Multiple sclerosis Outcome measurement Progressive MS

 accelerometer sensor disability level fatigue severity walk tests wearable device
 association studies autoimmune diseases cross-trait rheumatoid arthritis shared genes

 Neuromyelitis optica spectrum disorders Optical coherence tomography Retina Serostatus
 Multiple sclerosis mortality risk population-based study socioeconomic disparities socioeconomic status
 Confusion Encephalopathy Multiple sclerosis Seizures beta-interferon

 B cell immunology COVID-19 multiple sclerosis rituximab vaccination
 Assay standardisation Axonal injury Blood-based biomarker Cerebrospinal fluid MS prognosis Neurodegeneration Neurofilament Neuroinflammation Treatment response
 1,25-dihydroxyvitamin D 25-hydroxyvitamin D CYP24A1 multiple sclerosis
 molecular mechanisms multiple sclerosis non-small cell lung cancer shared gene signature shared local immune environment
 Cost-effectiveness analysis Cost-utility analysis Health technology assessment Multi-attribute utility instrument Quality of life
 Body mass index Multiple sclerosis Obesity Shared genetic architecture
 Antioxidants Experimental autoimmune encephalomyelitis Iron toxicity Lipid peroxidation NCOA4 Secondary progressive MS


 Alzheimer’s disease Chitotriosidase Parkinson’s disease amyotrophic lateral sclerosis chitinase-3-like 1 glycohydrolase family 18 multiple sclerosis neuroinflammation

 Consensus Multiple sclerosis Recommendation Treatment
 aquaporin 4-antibody positive neuromyelitis optica spectrum disorder differential diagnosis imaging multiple sclerosis myelin oligodendrocyte glycoprotein antibody-associated disease
 endogenous retrovirus glia multiple sclerosis myelin repair neurodegeneration
 COVID-19 vaccines MS Multiple Sclerosis NMOSD
 Balance Core stability Dynamic neuromuscular stabilization Falling Or Falls OrAccidental fall Multiple sclerosis Spasticity Trunk impairment
 COVID-19 carers multiple sclerosis qualitative resilience stress

 RNA binding protein hnRNP A1 multiple sclerosis oligodendrocyte
 Fatigability Fatigue MS Objective measurement P50 Prepulse inhibition Sensory gating
 Cognitive disorder activities of daily living cognitive rehabilitation functional cognition functional status multiple sclerosis outcome assessment
 AP-1 signaling Gene enrichment analysis Inflammatory demyelinating diseases (IDD) Multiple sclerosis Protein-protein interaction (PPI) Zika virus (ZIKV)
 Epstein-Barr virus SARS-CoV-2 immune cells interferon β multiple Sclerosis


 Biobank Database Multiple sclerosis Quality Registry Sample
 CXCL10 cerebrospinal fluid biomarker immune cell profiling immune cell trafficking multiple sclerosis

 APP/PS1 Aducanumab Alzheimer’s disease Astrogliosis BDNF Dementia Drug repurposing, fingolimod FTY720 Gantenerumab Hippocampus LTP Learning and memory Lecanemab Microglia Neurodegenerative disease Neuroinflammation Ozanimod Siponimod Spatial memory Sphingosine-1-phosphate receptor Spines
 axonal damage demyelination dysmyelination lipids mitochondria neurodegeneration progressive multiple sclerosis remyelination repair

 Administrative data Comorbidities Disease modifying therapies Multiple sclerosis
 COVID-19m-RNA vaccination Cellular immune responses Humoral immune response Multiple sclerosis Teriflunomide alemtuzumab
 cladribine immunization influenza multiple sclerosis vaccination
 Aerobic exercise Hippocampus Multiple sclerosis Myelin


 Cuprizone EAE Multiple Sclerosis Neuroinflammation Oligodendrocytes
 Collaborative research Integrated knowledge translation Knowledge syntheses Principles and strategies Research partnership Spinal cord injury Stakeholder engagement

 HMG Sox Sry glia myelin oligodendrocyte
 Alzheimer’s disease Parkinson’s disease alcohol use disorder aluminium autism spectrum disorder dialysis encephalopathy human brain multiple sclerosis
 Exergame cognition multiple sclerosis rehabilitation virtual reality
 caregivers knowledge multiple sclerosis questionnaire validation
 Atrophy Magnetic resonance imaging Multiple sclerosis Quantitative susceptibility Relaxometry
 MOG Multiple sclerosis aquaporin-4 myelin oligodendrocyte antibody-associated disease myelin oligodendrocyte glyco protein neuromyelitis optica (NMO)


 AbobotulinumtoxinA Botulinum toxin multiple sclerosis neurogenic detrusor overactivity incontinence spinal cord injury
 Atomic Bioinformatic analysis MicroRNAs Multiple sclerosis Spectrophotometry Trace elements

 Orthotic shorts acceptability dynamic elastomeric fabric orthoses gait variability multiple sclerosis walking
 BBIBP-CorV COVID-19 disease-modifying therapies (DMTs) multiple sclerosis vaccine immunogenicity

 accelerometry actigraphy digital biomarkers digital health technologies digital mobility outcomes inertial motion unit multiple sclerosis review sensors wearables
 Biomarker EAE Histopathology Myelin PBMCs Regulatory cells
 COVID-19 SARS-CoV-2 antibodies immune response multiple sclerosis vaccination
 COVID-19 vaccines Disease-modifying therapies Multiple sclerosis SARS-CoV-2
 CNS inflammatory Demyelination Gut microbiota Immunomodulation Microbiome Microbiota interventions Neuroinflammation
 Astragalus membranaceus chemical components experimental autoimmune encephalomyelitis immunoregulation multiple sclerosis
 Binding site Mechanism of action Multiple sclerosis Pharmacology Sphingosine 1-phosphate receptor Ulcerative colitis
 human gait analysis quaternion time series semi-supervised clustering wearable sensors

 Cdx-2 (rs11568820) HLA-DRB1*15:01 Multiple sclerosis disability progression gene polymorphism susceptibility vitamin D receptor
 CD4+ T lymphocytes CD47 FTY720 L-selectin ketogenic diet lymph nodes multiple sclerosis
 Multiple sclerosis Myelination Neuroinflammation Potassium channels

 Accidental Falls Cognitive Dysfunction Multiple Sclerosis Neurologic Gait Dysfunctions Postural Balance
 Balance control Balance training Multiple sclerosis Physiotherapy Systematic review
 biomechanics dual-task gait analysis
 Xenopus myelin optic nerve regeneration visual system
 Balance Control Balance Impairment Content Analysis Multiple Sclerosis Qualitative Research
 diet dysbiosis gut microbiota multiple sclerosis probiotics

 MYO Armband Multiple sclerosis Rehabilitation Serious games Strength Upper limb Virtual reality


 EAE hypoxia integrated stress response neuroinflammation oxidative damage oxygen treatment
 Booster revaccination COVID-19 vaccines Cellular immune response Immunomodulating drugs Multiple sclerosis
 Behavioral deficits Icariin Multiple sclerosis Neuropathology

 Alzheimer's disease Dementia Genetic overlap Multiple sclerosis Neurodegeneration Neuroinflammation Pleiotropy
 Multiple sclerosis first-trimester miscarriage pregnancy

 Cognition Disability Multiple sclerosis Olfactory dysfunction Quality of life
 Depression, anxiety Multiple sclerosis Systematic review Tobacco smoking
 JC virus Natalizumab Natural experiment Ocrelizumab Pseudo-randomization Switching
 Aging Health behavior Lifespan Multiple sclerosis Physical activity
 Fear of falling Gait speed Multiple sclerosis Postural balance Postural control Virtual reality
 Molecular Multiple sclerosis (MS) TGF-β TGF-β1

 Anxiety-like behavior Experimental autoimmune encephalomyelitis Intestinal inflammation Multiple sclerosis Osteoporosis
 COVID-19 Clinical trial Goals Multiple sclerosis Nursing process
 COVID-19 SARS-CoV-2 vaccine anti-CD20 booster dose fingolimod multiple sclerosis
 fatty acid metabolism macrophage multiple sclerosis remyelination

 COVID-19 SARS-CoV-2 T-cell response antibody response mRNA vaccines multiple sclerosis

 Antibodies Ceramide Cerebrospinal fluid Multiple sclerosis Serum
 Hospitalization Hypogammaglobulinemia Multiple sclerosis Rituximab Serious infections
 Diet Epidemiology Health state utility Multiple sclerosis
 COVID-19 adherence multiple sclerosis vaccination
 Autoimmune disease Exercise Metabolism Rehabilitation Walking
 Cognitive rehabilitation computerised tools disease-specific software experimentation home-based cognitive rehabilitation multiple sclerosis

 foot care foot health foot health status questionnaire multiple sclerosis quality of life

 CD-20 Colitis Ocrelizumab Rituximab Ulcerative colitis
 5 in alphabetical order): autoimmune encephalitis Cerebrospinal fluid Immune system Neuronal dysfunction Proteomics
 Feasibility Hand and arm function Home-based training Manual dexterity Multiple sclerosis Rehabilitation Virtual reality
 Alzheimer’s disease (AD) biomarkers disease progression inflammation multiple scleorsis (MS)

 Kinematics Mobile app Task oriented circuit training Telerehabilitation inertial sensors serious gaming virtual reality


 Epigenetic editing Epigenetics Oligodendrocyte Progressive MS
 Highly active MS Multiple sclerosis Natalizumab VZV vaccine

 Central nervous system Demyelinating injury MBP Multiple sclerosis Peptides


 BBB endothelial cells CNS infiltration MCAM blood–brain barrier experimental autoimmune encephalomyelitis multiple sclerosis
 Criterion validity Multiple sclerosis Muscle function Skeletal muscle Speckle tracking ultrasonography






 extended interval dosing multiple sclerosis ocrelizumab ofatumumab rituximab targeting CD20 ublituximab
 T helper cells experimental autoimmune encephalomyelitis gut oral microbiota periodontitis spleen
 APP Alzheimer’s disease EBV MBP gM multiple sclerosis
 Fingolimod beta interferon disease modifying treatment glatiramer acetate treatment switch
 Pediatric caregiver demyelination health-related quality of life multiple sclerosis parent quality of life



 integrated stress response multiple sclerosis remyelination

 chemokine cytokine immune pathophysiology modifiable environmental factor monocyte-derived dendritic cell multiple sclerosis type I IFN vitamin D

 Decentralised clinical trial digital multiple sclerosis randomised controlled trial remote

 COVID-19 Fingolimod Multiple sclerosis Serology
 Assessment Multiple sclerosis Proprioception Rehabilitation Somatosensory function
 autoimmunity inflammation neurodegenerative disease neuroimmunology regulatory T cells

 Clemastine Experimental autoimmune encephalomyelitis Multiple sclerosis NLRP3 inflammasome Neuroinflammation Pyroptosis




 Covid-19 Multiple sclerosis Side effects Vaccination Vaccine hesitancy
 MS Multiple sclerosis NMO NMOSD Neuromyelitis optica Neuromyelitis optica spectrum disorder Neutrophil-to-lymphocyte ratio Pediatric multiple sclerosis
 EAE autoimmune cell therapy encephalomyelitis experimental macrophage M2 meta-analysis multiple sclerosis systematic review
 Autoimmune disease CCL20 CCR6 Experimental autoimmune encephalomyelitis (EAE) Multiple sclerosis
 NEDA biomarker dimethyl fumarate disease-modifying therapies immunophenotype multiple sclerosis transcriptome treatment response

 Biomarkers disease-modifying therapy extended interval dosing natalizumab neurofilament light chain real-world evidence

 NVX-CoV2373 SARS-CoV-2 vaccination anti-CD20 therapy humoral and T cellular vaccination response immunomodulation multiple sclerosis sphingosine-1phosphate receptor modulators
 Autopsy COVID-19 Multiple Sclerosis Vaccine
 Adipocyte Adipose tissue Cachexia Immune cells Lipid metabolism Macrophages Mitochondria

 France botulinum toxin multiple sclerosis neurogenic detrusor overactivity spasticity
 Multiple sclerosis ROCK1 RhoA miR-193a


 COVID-19 immunology multiple sclerosis
 Schwann cells demyelination multiple sclerosis oligodendrocytes remyelination
 cross-linking immunotherapy layer-by-layer self-assembly microparticle and nanoparticle polyelectrolyte multilayer vaccine

 Cuprizone GLP-1R MS Myelin NLY01 Oligodendrocytes
 Axonopathy Cis-phosphorylated tau Inflammation Lysolecithin-induced demyelination Multiple sclerosis Myelin Optic chiasm
 B cells CD19+ cells CD4+ cells CD8+ cells ETX MAL T cells clostridium perfringens epsilon toxin lymphocytes myelin and lymphocyte protein

 Incidence NMO NMOSD Neuromyelitis optica spectrum disorder Prevalence
 Arterial stiffness Augmentation index Cognitive function Multiple sclerosis Pulse wave velocity
 cannabis multiple sclerosis patient-reported outcomes symptom management
 Cell migration Experimental autoimmune encephalomyelitis Hsp65 Lactococcus lactis Regulatory T cells

 Dimethyl fumarate Disease-modifying treatments Head-to-head study Multiple sclerosis Teriflunomide
 astrocytes calcium signaling central nervous system autoimmune disease hemichannel immune cell integrin multiple sclerosis purinergic receptors
 CD4+ T cells HDAC1 Multiple sclerosis RNF157 Ubiquitination



 discontinuation of natalizumab therapy immune reconstitution inflammatory syndrome (IRIS) multiple sclerosis progressive multifocal leukoencephalopathy (PML)
 Experimental autoimmune encephalomyelitis Locus coeruleus Multiple sclerosis Noradrenaline Spinal cord
 NfL biomarkers disease activity immune reconstitution multiple sclerosis treatment response
 Myelin oligodendrocyte glycoprotein aquaporin 4 corpus callosum magnetic resonance imaging multiple sclerosis neuromyelitis optica
 ACSM criteria cardiopulmonary exercise testing cardiorespiratory fitness maximal oxygen consumption multiple sclerosis
 autophagy experimental autoimmune encephalomyelitis hippocampus mouse neurons
 Core stability exercises Exercise progressions Multiple sclerosis Postural control Smartphone accelerometry
 aquaporin-4 cerebrospinal fluid free light chains kappa index myelin oligodendrocyte glycoprotein neuromyelitis optica

 DDX39B FOXP3 RNA helicase RNA splicing autoimmunity biochemistry chemical biology human immunology inflammation multiple sclerosis
 Sedentary behaviour cardiometabolic health light-intensity physical activity multiple sclerosis structured exercise
 3′UTR binding sites Common variants GWAS Non-coding RNA Seed microRNA microRNA–target prediction
 Central nervous system HTLV-1-Associated myelopathy Human T-lymphotropic virus 1 Inflammation Multiple sclerosis XCL1
 Multiple sclerosis REHABILITATION MEDICINE Telemedicine

 Health behaviors Multiple sclerosis Quality of life Rehabilitation Risk factors Wheelchairs
 GPCRs HDAC Microbiota SCFAs, Autoimmune diseases
 ADs Autoimmune diseases Disability-adjusted life-years (DALYs) GBD Health inequality

 Alzheimer’s disease Biomarkers IL-17 Neuroinflammation Proinflammatory cytokine
 Five Times-Sit-to-Stand Test Multiple sclerosis reliability
 Experimental Autoimmune Encephalomyelitis JAK2 Multiple Sclerosis STAT5 T cell T(H)1
 Anti TNFa Behçet Behçet's Biotherapies Biothérapies Sarcoidose Sarcoidosis Uveitis Uvéite Vascularites Vasculitis

 Demyelinating disease MOGAD NMOSD OCT PHOMS



 antioxidant enzymes cholesterol multiple sclerosis
 Central auditory processing Cognitive impairment Multiple sclerosis Spatial processing Speech-in-noise perception

 BM-MSCs Cuprizone demyelination monoamine neurotransmitters multiple sclerosis remyelination
 Cytokine Experimental Autoimmune Encephalomyelitis Ginger Multiple Sclerosis
 COVID-19 Humoral response Inactivated virus vaccine Multiple sclerosis mRNA vaccine
 Accelerometer Control Moderate to vigorous physical activity (MVPA) Multiple sclerosis (MS) Sedentary
 Multiple sclerosis cognitive dysfunction sleep apnea sleep disorders
 Aging Frailty Immunosenescence Multiple sclerosis Neurodegeneration
 Functional capacity Multiple sclerosis Reliability Validity Walk test

 Serious game engagement neuroplasticity sensorimotor learning
 COVID-19 MOGAD MS NMOSD SARS-CoV-2 Vaccination
 adaptation gait asymmetry locomotion multiple sclerosis sensorimotor control split-belt treadmill

 Community-acquired infection multidrug resistance quinolone resistance urinary tract infections
 NMDA receptors aspartate cerebrospinal fluid inflammation multiple sclerosis
 clinical usefulness decision curve analysis net benefit network meta-analysis prediction model
 BNT162b2 COVID-19 SARS-CoV-2 variants immunosuppressant multiple sclerosis
 IFN gamma release assay SARS-CoV-2 SARS-CoV-2 mRNA vaccine humoral immune response multiple sclerosis myasthenia gravis neuromyelitis optica spectrum disorder
 gadolinium deposition gadolinium retention gadolinium-based contrast agents magnetic resonance imaging magnetization transfer multiple sclerosis

 EAE inflammation intestinal permeability multiple sclerosis oleacein
 CNS immune cell infiltration IFN-γ IFN-γR1 choroid plexus experimental autoimmune encephalomyelitis
 Autoimmune diseases Global burden of diseases, injuries, and risk factors study Joinpoint regression analysis Prevalence Trends
 Functional connectivity Functional magnetic resonance imaging MRI MS Multiple sclerosis Quality control
 Brain malignancies Epilepsy MicroRNA-155 Neurodegenerative diseases Stroke, RNA therapeutics


 TMEM106B demyelination lipids multiple sclerosis (MS) myelin oligodendrocyte glycoprotein (MOG)-induced EAE
 Chalcones from Ashitaba brain-derived neurotrophic factor demyelination tumor necrosis factor α
 EAE cannabigerol lipopolysaccharide neuroinflammation microglia nitric oxide
 Experimental autoimmune encephalomyelitis Interleukin-10 Microglia Multiple sclerosis Myeloid cells Regulatory B cells
 CNS dysimmune disorders COVID-19 SARS-CoV-2 multiple sclerosis myelitis vaccines
 Adenosine receptor Hippocampus Multiple sclerosis Myelin Oligodendrocyte
 EDSS Pediatric onset MS lipidomics relapse rate


 Demyelination Gut–microbiota Microglia Subdiaphragmatic vagus nerve
 B cells disease-modifying therapies multiple sclerosis
 ER stress MBP myelin morphology relapse relapsing–remitting EAE
 Biosimilar Multiple sclerosis Rituximab
 Asymmetric motor deficit Clemastine Demyelination Internal capsule Lysophosphatidylcholine Remyelination
 EDSS Kynurenine Multiple sclerosis Tryptophan

 memory T cells multiple sclerosis oligodendrocyte glycoprotein pentamer peripheral blood mononuclear cells

 astrocyte chemokine interleukin-3 microglia monocyte multiple sclerosis neuroinflammation recruitment
 Demyelination GFP reporter mice Multiple sclerosis Oligodendrocyte Sphingosine-1-phosphate receptor 1

 hepatitis B immunity immunization multiple sclerosis vaccination vaccine varicella zoster
 Artemisinin Cytokine Inflammation Myelin Myelin basic protein T cell TAM receptor Tehranolide
 cytokine suppression fingolimod immune response siponimod
 AQoL-8D Australian MS Longitudinal Study Cost-utility analysis EQ-5D-5L EQ-5D-5L-Psychosocial Multi-attribute utility instrument Multiple sclerosis Sleep
 Theiler’s murine encephalomyelitis virus (TMEV) conditional CD28-knockout conventional CD28-knockout immunology & infectious diseases multiple sclerosis (MS) disease neuroimmunology and neuropathology
 Autoimmune diseases Autoimmunity CD38
 autoimmunity glycolysis lymphocytes metabolism mitochondria multiple sclerosis oxidative stress peripheral blood mononuclear cells
 COVID-19 Epstein–Barr virus PASC inflammation multiple sclerosis post-acute sequelae of COVID-19 infection
 autoantibodies autoantigens glucopeptides molecular mimicry multiple sclerosis
 immunofixation electrophoresis isoelectric focusing electrophoresis mirror pattern bands oligoclonal bands
 EAE cortical demyelination cuprizone inflammation multiple sclerosis remyelination
 Magnolol Multiple sclerosis (MS) Rorγt Signal transducer and activators of transcription 3 (stat3) Th17
 C-reflex Clinical neurophysiology Electromyography Long latency reflexes Long loop reflexes Movement disorders
 inflammatory diseases small molecules tumor necrosis factor tumor necrosis factor receptors
 Dynamic balance assessment gait gait analysis multiple sclerosis rehabilitation
 Cytokine Multiple Sclerosis Neurodegeneration Neuron Stem Cell Derived
 Antigen presentation Citrullination Multiple sclerosis Myelin basic protein Th17 cells

 Border associated macrophages Experimental autoimmune encephalomyelitis IGF-1 IGF-1R Microglia Multiple sclerosis
 Digital health Dominant hand Hand dexterity NHPT Neurodegenerative disorders
 Exergaming Multiple sclerosis Rehabilitation Restless legs syndrome Sleep disorders
 Multiple Sclerosis Pseudo-relapse Relapse SARS-CoV-2 Vaccine
 Oligodendrocytes T-regulatory cells Th1 cells Th17 cells dendritic cells microRNAs.
 CLEM demyelination in vivo microscopy multiple sclerosis myelin oligodendrocyte precursor cell oligodendrocytes remyelination

 Anti-inflammation Blood-brain-barrier Bornyl acetate Experimental autoimmune encephalomyelitis
 S1PR3 experimental autoimmune encephalomyelitis multiple sclerosis plasma cells sphingosylphosphorylcholine


 Cerebrospinal fluid Connective tissue disease Flow cytometry Systemic lupus erythematosus

 CNS myelin models multiple sclerosis oligodendrocyte remyelination
 allodynia astrocyte microglia neuroinflammation oligodendrocyte pain
 adult-onset Still’s disease autoimmune diseases nasal polyps rheumatoid arthritis two-sample Mendelian randomization

 KLK6 Microglia Oligodendrocyte Spinal cord Systemic inflammation
 Epstein–Barr virus antibody avidity dimethyl fumarate multiple sclerosis




 Bone mesenchymal stem cells Exosome Experimental autoimmune encephalomyelitis NEK7 Pyroptosis microRNA-23b-3p

 Autoimmunity demyelination effector mechanisms inflammation neuroimmunology
 ELAV RNA binding protein Experimental autoimmune encephalomyelitis (EAE) HuD HuR Microglia Myelin Neuropathic pain
 C16 peptide and ang-1 EAE Neurodegenerative diseases fMLP-modified nano-carriers inflammation
 B lymphocytes COVID-19 vaccination Fingolimod Multiple sclerosis anti-SARS-CoV2 antibodies




 Arabic validation NBSS-SF questionnaire neurogenic bladder quality of life reliability validity

 biomarkers inflammation neuro-ophthalmology neuro-otology
 Aquaporin-4 Multiple sclerosis Myelin oligodendrocyte glycoprotein Optic neuritis Optical coherence tomography
 Alzheimer’s disease Neurodegenerative disease Parkinson’s disease Vitamin K
 Ifit2 coronavirus demyelination interferon-gamma microglia
 Epstein-Barr virus (EBV) antibodies multiple sclerosis (MS) prognosis virus neutralization
 Mesenchymal stem cell bone marrow neurological diseases serious adverse events stem cell umbilical cord
 Accelerated MRI COVID-19 SMS Wave-CAIPI neuroimaging patient access throughput
 Cytokine Experimental autoimmune encephalomyelitis Glycolysis Procyanidin B2 gallate T cell
 Dual therapy Myelination Nanoparticles Neurodegeneration

 Bacillus Calmette–Guérin Tokyo-172 MOG-induced EAE neuroprotection spontaneous EAE

 Cladribine tablets Disease-modifying therapy Expert opinion Real-world evidence Relapsing multiple sclerosis Systematic literature review

 Demyelination Inflammation Mitochondria Mn superoxide dismutase Multiple sclerosis Necroptosis Neurons
 CD20-expressing T cells CD20dim T cells CD20dimCD8+ T cells anti-CD20 therapy ocrelizumab

 EAE MS Neuroinflammation TNF TNFR1 antagonist TNFR2 agonist



 MOG-antibody-associated disease aquaporin 4 IgG cerebrospinal fluid myelin oligodendrocyte glycoprotein IgG neuromyelitis optica spectrum disorder


 CNS demyelinating diseases Picornaviridae infections animal models autoimmunity cytokines enzyme-linked immunosorbent assay neuroimmunology neuroinflammatory diseases neurovirology
 EAE/MS autoimmunity imaging nucleotide metabolism
 Experimental autoimmune encephalomyelitis MicroRNA STAT3 Th17
 Argentina COVID-19 DMTs multiple sclerosis serological response vaccines
 MSCs-based therapy extracellular vesicles mesenchymal cell neurodegenerative diseases treatment
 diabetes epidemiology neurologic disorders serum neurofilament
 Carvacrol Experimental autoimmune encephalomyelitis Inflammation MS Remyelination
 case-control human herpesviruses multiple sclerosis viral infections
 AQP4 COVID Infection MOGAD Multiple Sclerosis Vaccination
 Autoimmunity Circular RNA Enhancer RNA Non-coding RNA Psoriasis Rheumatoid arthritis Single cell RNA-Sequencing
 COVID-19 Demyelinating diseases Neuroimmunology Optic neuritis Transverse myelitis
 C57BL/6 mice EAE model catalase activity catalytic antibodies


 D313Y variant Enzyme replacement therapy Fabry disease LysoGb3 Multiple sclerosis White matter lesions
 MAGI2-AS3 diagnosis long noncoding RNAs miR-374b-5P microRNAs multiple sclerosis
 COVID-19 vaccine Demyelinating disease Multiple sclerosis NMOSD Neuromyelitis Optica spectrum disorders Vaccination




 Multiple sclerosis Neuroinflammation Phosphodiesterases Remyelination
 functional neurosurgery lesioning parameters pain percutaneous radiofrequency rhizotomy trigeminal neuralgia
 Meningoencephalitis of unknown etiology S396 p-tau microtubules multiple sclerosis phosphorylated tau tau protein
 Booster COVID-19 Multiple sclerosis SARS-CoV-2 Vaccine mRNA
 EAE multiple sclerosis ovaries progesterone steroidogenesis testosterone
 Kynurenine pathway Metabolomics Multiple sclerosis Obesity Overweight
 Tau cytoskeleton demyelination myelin oligodendrocyte

 Baicalein CXCR6 Experimental Autoimmune Encephalomyelitis Multiple Sclerosis Th17 cells

 Alpha lipoic acid Carvedilol Cuprizone Demyelination Multiple sclerosis Myelin basic protein
 Chondroitin sulfate Experimental autoimmune encephalomyelitis Extracellular matrix Glycosaminoglycans Hyaluronic acid Multiple sclerosis
 COVID-19 Disease modifying therapy Multiple sclerosis SARS-COV-2 Vaccine
 Butyrophilin 2A2 Cytokine Experimental autoimmune encephalomyelitis Pathogenic Th17 cell Treg

 Cuprizone Multiple sclerosis Muscarinic acetylcholine receptor Potassium channel

 MS OPC Oli-Neu dihydropyridines myelination neuroprotection nimodipine zebrafish
 COVID-19 Fingolimod Multiple sclerosis Ozanimod Ponesimod SARS-CoV-2 Siponimod Sphingosine-one-phosphate modulators Vaccines
 Berberine experimental autoimmune encephalomyelitis multiple sclerosis myelin oligodendrocyte glycoprotein




 COVID-19 Immune response Infection Multiple sclerosis Pediatric Pediatric-onset SARS-CoV-2 Vaccination

 Sjögren’s syndrome autoimmunity gut dysbiosis multiple sclerosis rheumatoid arthritis systemic lupus erythematosus
 Cervical MRI Multiple sclerosis Neuromyelitis optica Relapse rate Rituximab
 Children Epilepsy Febrile seizures Neurofilament NfL Tumor
 Ataxin-1 B cells autoimmunity multiple sclerosis noncoding RNAs

 Autoimmunity Blood serum COVID-19 Human patients Truncated (48 kDa) form of protein Unconventional myosin 1C
 Eae Multiple sclerosis Stat3 inhibitor Th1/Th17/Treg Therapeutic potential


 Bacillus amyloliquifaciens VCAM signals fermented camel's milk multiple sclerosis probiotics
 Neuromyelitis optica spectrum disorders cognition cognitive neuropsychology neuroimmunology
 CSF kappa free light chains Multiple sclerosis Oligoclonal banding

 Mendelian randomization blood urea nitrogen chronic kidney disease estimated glomerular filtration rate neurodegenerative diseases
 NF-κB activation VLCFA β-oxidation fingolimod lipid metabolism multiple sclerosis myelin lipid neurodegeneration neuroinflammation sphingolipid sphingosine 1-phosphate
 Alzheimer's disease GLAST GLT-1 Parkinson's disease SLC7A11 amyotrophic lateral sclerosis glioma neuroinflammation
 SETDB1 TRIM28 human endogenous retroviruses multiple sclerosis pregnancy

 EAE Fibrosis MOG Multiple Sclerosis NG2 PDGFRB PLP Pericytes Perivascular
 Drug discovery Genetics Mendelian randomization Neurodegenerative disease Omics Proteomics
 Autosomal recessive CARASIL HTRA1 Multiple sclerosis
 COVID-19 vaccination MOGAD NMOSD SARS-CoV2 multiple sclerosis safety
 EAE Neuroinflammation Neuroprotection TNFR1 TNFR2
 CD45R lymphocytes Experimental autoimmune encephalomyelitis GM-CSF MAP kinase inhibitor Multiple sclerosis NF-κB
 Experimental autoimmune encephalomyelitis Inflammation Th17 Vitamin A Vitamin D miRNAs
 brain-gut axis experimental autoimmune encephalomyelitis gut microbiota oxymatrine short-chain fatty acids
 Canavan disease allogeneic cell therapy demyelinating diseases iPSCs off-the-shelf cell therapy oligodendrocyte progenitor cells (OPC) universal donor
 diagnosis of multiple sclerosis high-dose corticosteroids intravenous immunoglobulins (ivig) multiple sclerosis flare-up tumefactive sclerosis
 CSF autologous haematopoietic stem cell transplantation cytokines multiple sclerosis rituximab
 aggressive multiple sclerosis highly active multiple sclerosis multiple sclerosis treatment of aggressive MS treatment of highly active MS
 POMS effectiveness fingolimod safety treatment
 multiple sclerosis online registry patient-reported outcomes
 Multiple sclerosis pain interference pain severity participation social activities
 Autoimmune hepatitis Liver Multiple sclerosis Primary biliary cholangitis
 Fingolimod atrioventricular heart block multiple sclerosis
 blood-brain barrier brain delivery exosomes extracellular matrix fibronectin fibronectin aggregates intestinal flora multiple sclerosis remyelination remyelination failure
 GABA-receptor cognition magnetic resonance spectroscopy multiple sclerosis positron emission tomography
 Blood brain barrier permeability intrathecal synthesis multiple sclerosis oligoclonal bands
 Multiple sclerosis occupational performance sensory processing skills
 CDP-choline astrocytes cuprizone microglia multiple sclerosis oligodendrocytes
 CPRD Epidemiology Ethnicity Multiple sclerosis Risk factors
 Atypical inflammatory demyelinating disorders CT, Computed Tomography MRI, Magnetic Resonance Imaging MS, Multiple Sclerosis Magnetic resonance imaging Megacystic Multiple sclerosis NAA, N-Acetyl Aspartate
 EAE diet dietary factors dietary interventions gut dysbiosis gut microbiome multiple sclerosis
 antibodies cell-based ELISA cell-lines immunoglobulins multiple sclerosis
 Nurr1 lymphocyte inflammation multiple sclerosis neuronal loss
 DMT—disease modifying therapies EDSS—Expanded Disability Severity Scale MS—multiple sclerosis SDOH—social determinants of health SES—socioeconomic status nSES—neighborhood socioeconomic status pwMS—persons with multiple sclerosis
 multiple sclerosis oral small molecules ulcerative colitis
 disease-modifying therapy lifestyle multiple sclerosis whole food plant-based diet
 Neuro-Behcet’s disease misdiagnosis multiple sclerosis

 anxiety cognitive deficit depression experimental autoimmune encephalomyelitis motor disability neurological disorder pain pathophysiology preclinical study sensory impairments
 Multiple sclerosis North American Research Committee on Multiple Sclerosis fatigue
 AD, atopic dermatitis BSA, body surface area EASI, eczema area and severity index IGA, investigator's global assessment IL, interleukin Ig, immunoglobulin MS, multiple sclerosis VAS, visual analog scale atopic dermatitis dupilumab multiple sclerosis
 Cystoid macular edema intermediate uveitis multiple sclerosis sarcoidosis uveitis
 COVID-19 SARS-CoV-2 multiple sclerosis vaccination vaccine
 autoimmune encephalitis autoimmunity biomarkers central nervous system clinical outcomes multiple sclerosis
 OPC demyelination multiple sclerosis oligodendrocyte remyelination
 B cell autoreactive antibodies ethnicity multiple sclerosis natalizumab
 Blood biomarker Meta-analysis Multiple sclerosis Neurofilament light chains Pediatric
 Insomnia Multiple sclerosis Sleep Sleep initiation and maintenance disorder
 communities feature reduction modularity multiple sclerosis network analysis phenotype subsumption subtype
 hallucinations multiple sclerosis
 disease-modifying treatments efficacy genomics metabolomics multiple sclerosis proteomics safety transcriptomics
 MOGAD NMOSD autoimmune encephalitis family planning global epidemiology multiple sclerosis
 advanced diffusion imaging grey matter multiple sclerosis neurodegeneration
 cognition glucocorticoids methylprednisolone multiple sclerosis pituitary-adrenal axis
 BDNF brain plasticity multiple sclerosis neuroplasticity biomarkers neurorehabilitation rehabilitation virtual reality
 antigens autoantibodies multiple sclerosis
 Multiple Sclerosis cognitive abilities depression executive functions self-perception sexual dysfunction
 Disease activity MRI Magnetic resonance imaging Multiple sclerosis Vitamin D

 Disease-modifying therapy Multiple sclerosis Pregnancy Symptomatic treatment
 Discrimination Health disparities Multiple sclerosis Well-being
 Patient-completed tool monitoring multiple sclerosis people living with MS telemedicine < General
 LUTS Multiple sclerosis lower urinary tract symptoms urologic evaluation
 adherence exercise self-efficacy fatigue home-based exercise multiple sclerosis
 Fingolimod bladder lymphoma multiple sclerosis
 BICAMS high-density EEG microstates multiple sclerosis
 glutathione magnetic resonance imaging magnetic resonance spectroscopy oxidative stress positron emission tomography progressive multiple sclerosis
 depression fatigability fatigue monitoring multiple sclerosis neuroimaging pathophysiology
 Active and nonactive multiple sclerosis Disability progression Disease-modifying therapy Multiple sclerosis Primary progressive multiple sclerosis Secondary progressive multiple sclerosis Survey Treatment patterns Unmet need
 Aggressive multiple sclerosis Disease-modifying therapy Hematopoietic stem cell transplantation Multiple sclerosis Treatment-naïve
 adverse effects immunomodulatory treatments multiple sclerosis palmoplantar pustular psoriasis teriflunamide
 Case report Demyelinating disease Multiple sclerosis Paroxysmal dystonia
 B cell T cell TLR anti-CD20 therapy multiple sclerosis ocrelizumab
 disease‐modifying therapy multiple sclerosis ocrelizumab primary‐progressive multiple sclerosis relapsing‐remitting multiple sclerosis

 MRI/pathology correlation multiple sclerosis myelin post-mortem quantitative MRI remyelination
 aging experimental autoimmune encephalomyelitis progressive multiple sclerosis relapsing-remitting multiple sclerosis sex
 attention fall risk multitasking social implications
 attitudes brain donation cross-sectional study multiple sclerosis survey
 disability edss familial disease ms disability multiple sclerosis types of multiple sclerosis
 BICAMS Brief International Cognitive Assessment for Multiple Sclerosis cognition meta-analysis multiple sclerosis systematic review
 case report communication language multiple sclerosis pragmatic impairment pragmatics
 Exudative retinal detachment Intermediate uveitis MS associated uveitis
 diet experimental autoimmune encephalomyelitis multiple sclerosis nutrition optic nerve optic neuritis
 Cryptococcus neoformans meningitis multiple sclerosis
 animal models autoimmunity demyelination multiple sclerosis neurodegeneration neuroinflammation remyelination
 clinically isolated syndrome conjugate eye movement multiple sclerosis nerve palsy
 Disease-Modifying Therapies Multiple sclerosis Satisfaction

 Biomarkers Diagnosis Multiple sclerosis Neurofilament Pediatric multiple sclerosis Prognosis Treatment response
 SDMT brain atrophy cognitive functions disease modifying therapies multiple sclerosis
 disease-modifying therapy geography health expenditure latitude secondary progressive multiple sclerosis
 CO-OP cognition executive function multiple sclerosis problem solving rehabilitation
 carbamazepine dysphagia oropharyngeal primary progressive multiple sclerosis
 biomarkers disease progression frailty multiple sclerosis neurophysiology transcranial magnetic stimulation
 disease-modifying treatments efficacy genomics metabolomics multiple sclerosis proteomics safety transcriptomics
 B cells IgG cerebrospinal fluid multiple sclerosis oligoclonal bands (OCB) plasmablasts
 chorea chorea (non-Huntington’s) cognitive decline multiple sclerosis neuroinflammation
 Kikuchi-Fujimoto Multiple Sclerosis Neuroinflammation
 Adherence Dimethyl fumarate Diroximel fumarate Gastrointestinal side effects Multiple sclerosis Real-world treatment Tolerability
 NLRP3 inflammasome PGC-1α SIRT1 demyelination emodin experimental autoimmune encephalomyelitis microglia multiple sclerosis neuroinflammation pyroptosis
 domain/modality specificity multiple sclerosis neuropsychological assessment performance validity
 Anti-N-Methyl-D-Aspartate Receptor Encephalitis Autoimmune encephalitis Demyelinating disease Multiple Sclerosis NMDAR encephalitis
 Multiple sclerosis caregiver intervention occupational therapy online
 Clinical decision support systems Digital twins In silico trials Modelling and simulation Multiple sclerosis Validation
 I-FABP claudin-3 clinically isolated syndrome intestinal permeability multiple sclerosis
 astrocytes colony-stimulating factor-1 receptor inhibition cuprizone demyelination microglia multiple sclerosis neurodegeneration
 Multiple sclerosis Relapsing remitting multiple sclerosis adolescence age of onset childhood obesity population-based primary progressive multiple sclerosis
 exercise gait multiple sclerosis nordic walking quality of life rehabilitation
 Alemtuzumab Graves’ disease Hashimoto's disease disease-modifying therapy multiple sclerosis thyroid
 Multiple sclerosis Videoconferencing
 demyelination microglia multiple sclerosis remyelination signal transduction
 EBV Multiple sclerosis Remyelination Slowly expanding lesions Spatial transcriptomics
 Multiple sclerosis anti-inflammatory fecal microbiota transplantation microbiome short-chain fatty acids
 complementary and alternative medicine conventional health care system disease management holistic approach multiple sclerosis
 disease severity fatigue multiple sclerosis physical activity relapsing remitting multiple sclerosis
 CSF Intrathecal inflammation Lymphocytes RRMS sBCMA sCD27


 Epidemiology Incidence Iran Multiple Sclerosis Prevalence Tehran
 fatigue fatigue scales heat sensitivity multiple sclerosis temperature uhthoff's phenomenon
 connectivity magnetic resonance imaging multiple sclerosis neurodegeneration optical coherence tomography radiologically isolated syndrome
 decision trees human leukocyte antigen immunogenetic risk markers likelihood of multiple sclerosis development machine learning multiple classifier multiple sclerosis
 benign multiple sclerosis chitinase 3-like-1 cytokine evolution inflammation interferon beta-1b multiple sclerosis
 daily activities depression mental health multiple sclerosis nursing quality of life
 Antigen Autoimmunity Immunoglobulins Multiple sclerosis Neuroscience
 Adherence Dimethyl fumarate Diroximel fumarate Incremental innovation Multiple sclerosis Persistence Real-world evidence Tolerability
 biomarker multiple sclerosis urine proteome
 cognitive dysfunction disease-modifying therapy juvenile multiple sclerosis pediatric multiple sclerosis
 cognition cognitive assessment digital health multiple sclerosis virtual reality
 empowerment multiple sclerosis patient information risk communication shared decision making
 Experimental autoimmune encephalomyelitis FGFR infigratinib multiple sclerosis neuroinflammation remyelination
 Chronic cerebrospinal venous insufficiency Common carotid artery Image processing Internal jugular vein Multiple sclerosis disease Ultrasonography
 COVID-19 vaccines Multiple sclerosis dimethyl fumarate diroximel fumarate fumarates
 body image disability multiple sclerosis neuropsychiatric symptoms self-esteem
 Immunology Multiple sclerosis Neurological disorders Neuroscience T cells
 Autoimmune Disease Disability Human Multiple Sclerosis Radiotherapy

 Multiple sclerosis attention cognition memory neurological rehabilitation neuropsychology
 multiple sclerosis optical coherence tomography optical coherence tomography angiography
 multiple sclerosis spasticity
 Cognition management Cognitive impairment Cognitive screening Progressive multiple sclerosis
 Blood-brain barrier EAE Multiple sclerosis Peroxiredoxin 6 Thymulin
 Diabetes Multiple Sclerosis Psychological Resilience Rheumatism Social and Professional functioning
 cadasil demyelinating disease multiple sclerosis small vessel disease stroke
 Multiple sclerosis clinical course progression progressive multiple sclerosis relapses relapsing multiple sclerosis
 diroximel fumarate relapsing-remitting multiple sclerosis (rrms) vaginal fungal infections varicella-zoster virus vumerity
 Cognition Cognition screening Cognitive impairment Cognitive rehabilitation Multiple sclerosis Patient-centric care Quality of life
 diet food literacy multiple sclerosis opinion registered dietitian nutritionist

 Charcot, Jean Martin Classification History of neurology Multiple sclerosis Symptoms
 antioxidants molecular pathways multiple sclerosis naturally occurring molecules neurodegenerative diseases therapeutic approaches
 Alzheimer’s disease Parkinson’s disease infections multiple sclerosis
 Multiple Sclerosis Self‐Management Scale‐Revised multiple sclerosis psychometric evaluation reliability self‐management validity
 PBMCs autoimmunity checkpoint co-regulation neuroinflammation
 Bifidobacteria Lactobacilli Parkinson’s disease hepatic encephalopathy motor coordination. multiple sclerosis
 Half-dose Multiple sclerosis Ocrelizumab Personalized
 ethnicity genetics multiple sclerosis
 Mendelian randomization breast cancer genetic variants meta-analysis multiple sclerosis
 bilateral internuclear ophthalmoplegia binocular diplopia demyelinating disease multiple sclerosis webino
 Multiple Sclerosis neurological rehabilitation (MeSH) outcome assessment (health care) postural balance [MeSH] psychometrics
 Coping strategies Multiple Sclerosis Sexual intimacy Sexual satisfaction Women
 liver disease multiple sclerosis steroids
 Dimethyl fumarate relapsing remitting multiple sclerosis sleep wearable tracker
 Connectome Fingerprinting functional connectome multiple sclerosis normative variation resting state fMRII
 AIC, Akaike Information Criteria CI, confidence interval DMT, disease modifying therapy EDR, excess death rate Excess mortality Flexible model MS, multiple sclerosis Multiple sclerosis Net survival OFSEP, Observatoire Français de la Sclérose en Plaques Observational cohort study PPMS, primary progressive multiple sclerosis R-MS, relapsing onset multiple sclerosis SES, socio-economic status Socio-economic status
 African American Latin American ethnicity magnetic resonance imaging multiple sclerosis neuroimaging race
 Access Barriers Disease-modifying therapies MENA Multiple sclerosis Treatment
 Multiple sclerosis cognitive impairment neuropsychological assessment teleneuropsychology
 language multiple sclerosis speech swallowing validation
 benign multiple sclerosis biomarker ganglion cell complex multiple sclerosis neural biomarker optical coherence tomography retinal ganglion cell retinal nerve fiber layer
 EDSS Mediterranean Multiple sclerosis dietary habits diet‌ disability nutrition quality of life
 Africa multiple sclerosis neurology
 COVID-19 SARS-CoV-2 longitudinally extended transverse myelitis magnetic resonance imaging multiple sclerosis tumefactive demyelinating lesion
 Fatigue Multiple sclerosis Restless Legs Syndrome Sleep disorders Sleep quality
 Multiple sclerosis health disparity health equity minority and vulnerable populations neighborhood characteristics social determinants of health
 disintegrin-like and metalloprotease with thrombospondin type 1 motifs 13 (ADAMTS13) interferon-β (IFN-β) long-term treatment multiple sclerosis thrombotic microangiopathy (TMA)
 C-X-C motif chemokine 5 fingolimod multiple sclerosis neuromyelitis optica spectrum disorder
 ischemic stroke multiple sclerosis neuroinflammation stem cells
 Urology fertility multiple sclerosis quality of life sexual dysfunction
 depression magnetic resonance imaging (MRI) mental health multiple sclerosis neuroinflammation
 Communication techniques Multiple sclerosis Patient–provider communication Shared decision-making
 disability mood multiple sclerosis pain rest-activity rhythm
 fatigue multiple sclerosis prevalence restless leg syndrome (RLS) in multiple sclerosis sleep disturbance
 autoimmune disease (AID) cervical cancer disease modifying therapy (DMT) human papilloma virus (HPV) multiple sclerosis (MS)
 AD, Axial Diffusivities Basal ganglia Diffusion Tensor Imaging FA, Fractional anisotropy MD, Mean Diffusivities MS, Multiple sclerosis Multiple sclerosis RD, Radial Diffusivity RRMS, relapsing-remitting MS Thalamus
 Efficacy Multiple sclerosis Ocrelizumab Primary progressive multiple sclerosis
 Epstein–Barr virus T cells immunotherapy multiple sclerosis
 cell deformability disease modifying treatment exercise leukocytosis lymphocytes multiple sclerosis real-time-deformability cytometry
 cognitive deficit cognitive disorder cognitive impairment digital twin dual-task metaverse multiple sclerosis telerehabilitation
 Cognition multiple sclerosis neuromyielitis optica psychological symptoms

 assessment countermovement jump jump analysis motor deficits multiple sclerosis
 dry needling multiple sclerosis percutaneous neuromodulation physiotherapy
 biomechanics inertial measurement units multiple sclerosis single leg stance test wearable sensors
 Autophagy Mitophagy Multiple sclerosis Reactive nitrogen species Therapeutic compounds

 anti-CD20 monoclonal antibody multiple sclerosis progressive multiple sclerosis relapsing-remitting multiple sclerosis rituximab treatment
 EBV MOG multiple sclerosis B-crystallin
 Cognition Diffusion MRI Graph theory Multiple sclerosis Remodeling
 multiple sclerosis nonpharmacological management palliative care pharmacological management prognostic uncertainty psychological distress
 Interpretive phenomenology advanced multiple sclerosis embodiment hermeneutic stories identity lived experience physical exertion
 EDS Hypersomnia Multiple sclerosis Neurological Disorders Parkinson
 Anti-CD20 alemtuzumab monoclonal antibodies multiple sclerosis natalizumab
 COVID-19 SARS-CoV-2 autoimmune condition case report multiple sclerosis vaccination
 Relapsing–remitting multiple sclerosis anxiety compliance patient-reported outcomes persistence real-world evidence satisfaction teriflunomide
 Development hand and arm function immersive manual dexterity multiple sclerosis training intervention virtual reality
 Nogo receptor 1 Nogo receptor 1-dependent axonopathy Nogo-A myelin debris oligodendrocyte progressive multiple sclerosis remyelination
 Antipsychotics Corticosteroids Multiple sclerosis Psychosis Schizophrenia
 animal model cerebrospinal fluid experimental autoimmune encephalomyelitis multiple sclerosis neuroimmunology
 Amyotrophic lateral sclerosis (ALS) Biomarkers Cerebrospinal fluid samples (CSFs) Cytokines Growth factors Multiple sclerosis (MS) Multiplex array Sandwich ELISA
 arginine vasopressin hormone arginine vasopressin receptors blockers autoimmune disease experimental autoimmune encephalomyelitis immune system multiple sclerosis
 Multiple sclerosis clinical characteristics cognitive functions
 disease modifying treatment multiple sclerosis relapsing-remitting multiple sclerosis review secondary progressive
 Early MS Multiple sclerosis Physical activity/exercise Quality of life Rehabilitation
 anxiety depression dysmenorrhoea fingolimod insomnia multiple sclerosis
 annual relapse rate disease-modifying treatment multiple sclerosis teriflunomide
 arbaclofen baclofen extended-release multiple sclerosis spasticity

 Acute liver failure drug-induced liver injury fingolimod liver transplantation multiple sclerosis
 Axonal damage Multiple sclerosis Optic neuritis Vitamin A
 Anxiety. Magnetic resonance imaging Multiple sclerosis
 astrocytes disease-modulating therapies functional subsets multiple sclerosis multiple sclerosis therapies myelination reactive astrocytes reactivity transcriptional subsets
 Drug interactions Esclerosis múltiple España Interacciones medicamentosas Multimorbidity Multimorbilidad Multiple Sclerosis Polifarmacia Polypharmacy Spain
 Children Epidemiology Incidence Multiple sclerosis Pediatric Pediatric-onset multiple sclerosis Prevalence.
 Brain activity dynamics Entropy Multiple sclerosis Network control theory
 Parkinson’s disease core outcome set falls multiple sclerosis qualitative study stroke
 Alzheimer disease Amyotrophic lateral sclerosis Multiple sclerosis Neuromyelitis optica spectrum disorder Parkinson disease Prodrome
 Esclerosis múltiple España Multiple Sclerosis Polypharmacy Spain drug interactions interacciones medicamentosas multimorbidity multimorbilidad polifarmacia
 Balanced steady-state free precession Diffusion tensor imaging Magnetization transfer ratio Multiple sclerosis Quantitative magnetization transfer
 Cognition Multiple sclerosis Patients Quality of life
 (Medical subject headings): sleep initiation and maintenance arousal fatigue multiple sclerosis sleep apnea syndromes sleep latency sleep-wake disorders
 Anxiety Depression Multiple sclerosis
 administrative claims electronic medical records linked database multiple sclerosis real-world evidence
 8-dihydro-2'-deoxyguanosine 8-oxo-7 multiple sclerosis oxidative stress oxidative stress index total antioxidant status total oxidative status
 BK channel autoimmunity experimental autoimmune encephalomyelitis multiple sclerosis neuroprotection
 autoimmune reactions biomarkers disease-modifying agents multiple sclerosis neurodegeneration
 ALCAM MCAM Th17 cells multiple sclerosis oligodendrocytes
 Myalgic encephalomyelitis/chronic fatigue syndrome auditory hypersensitivity light sensitivity multiple sclerosis
 axonal injury diffusion tensor imaging multiple sclerosis proteomics
 APOE-ε4 COVID-19 FoxO SIRT1 apoptosis autophagy dementia mTOR multiple sclerosis nicotinamide
 cognitive rehabilitation relapsing-remitting multiple sclerosis systematic review
 adjustment barriers content analysis facilitators multiple sclerosis
 Depression Everyday functioning Intelligence Multiple sclerosis Quality of life
 Allogeneic Hematopoietic Stem Cell transplantation Conditioning regiment and stem cell boost Multiple Sclerosis Severe aplastic anemia
 Acetyl-CoA-carboxylase Coenzyme A Cytokines Fatty acid metabolism Multiple sclerosis Soraphen A Th17 cells Treg
 Relapsing-remitting multiple sclerosis disfluencies filled pause silent pause
 demyelination miRNA microRNA multiple sclerosis myelin oligodendrocyte oligodendrocyte precursor cells remyelination
 breastfeeding disease-modifying therapies monoclonal antibodies multiple sclerosis pregnancy review
 axonal diameter measurement diffusion kurtosis imaging diffusion tensor imaging magnetic resonance imaging multiple sclerosis neurite orientation dispersion and density imaging normal-appearing white matter
 Expanded disability status scale multiple sclerosis time perspective
 meta-analysis multiple sclerosis prostate cancer
 accompagnement accompaniment ligne d’écoute téléphonique multiple sclerosis psychological support quality of life qualité de vie sclérose en plaques soutien psychologique telephone hotline
 CNS repair Multiple sclerosis Regulatory T cells cuprizone-induced demyelination experimental autoimmune encephalomyelitis polarization of immune response preclinical models remyelination
 T helper cells adhesion molecules blood–brain barrier choroid plexus meningeal inflammation multiple sclerosis neuroinflammation
 breastfeeding drug therapy immune system multiple sclerosis pregnancy
 health-related quality of life multiple sclerosis social support
 Rehabilitation Tai Chi embodied self-knowledge exercise self-efficacy multiple sclerosis (MS)
 Fingolimod treatment aminoacids metabolism energy homeostasis metabolomics multiple sclerosis nuclear magnetic resonance
 children multiple sclerosis parents psychosocial impact systematic review
 Prednisolone Quercetin Th17 Cells multiple sclerosis
 Executive functions Learning and memory Multiple sclerosis Neuroimaging (structural)
 Biomarkers genetics immunology multiple sclerosis
 Economic burden Iran Medication costs Multiple sclerosis (MS)
 AD, Alzheimer’s disease Alzheimer’s disease MS, multiple sclerosis Multiple sclerosis Neurodegenerative disease PD, Parkinson’s disease Parkinson’s disease SVD, small vessel disease VDBP, vitamin D binding protein VDR, vitamin D receptors VaD, vascular dementia Vitamin D
 Balance Kinect® Multiple Sclerosis (MS) Virtual therapy
 Multiple sclerosis neuropsychology non-pharmacological intervention progressive disease course rehabilitation
 Cerebral lesions Neurosarcoidosis Sarcoidosis Voxel-based lesion symptom mapping
 Family Support Iran Morality Multiple Sclerosis Psychosocial Functioning Social Support Spiritual Experiences

 Multiple sclerosis defense mechanisms depression family environment quality of life
 ECG-derived respiration autonomic nervous system disability fatigue heart rate variability relapsing-remitting multiple sclerosis secondary progressive multiple sclerosis walking capacity
 disability functional ability multiple sclerosis outcome measures reliability and validity
 depression diet adherence disability fatigue health outcomes multiple sclerosis prospective observational study
 MRI MTR histopathology iron multiple sclerosis remyelination
 Multiple sclerosis cladribine disease modifying therapies moderately active treatment. switching therapies
 environmental factors gut bacteria lifestyle factors multiple sclerosis remyelination
 incontinence multiple sclerosis quality of life sacral neuromodulation
 Cladribine tablets Disease activity Multiple sclerosis
 Big Five Conscientiousness Openness multiple sclerosis personality
 COGNITION MOTOR CONTROL MULTIPLE SCLEROSIS QUALITY OF LIFE
 Alzheimer’s disease Amyotrophic lateral sclerosis Ferroptosis Huntington’s disease Multiple sclerosis Neurodegenerative diseases Parkinson’s disease Therapy
 COVID-19 EDSS Enhancing lesions Multiple sclerosis Progression Relapse
 Aquaporin 4 Inflammasome Multiple sclerosis TGN-020

 AIM2 Alzheimer’s disease NLRC4 NLRP1 NLRP3 Parkinson’s disease amyotrophic lateral sclerosis frontotemporal dementia multiple sclerosis
 Anxiety attention cognitive impairment depression fatigue inhibitory control multiple sclerosis

 EAE Kir4.1 antibody autoimmunity glia glycosylation
 7 Tesla Fumarate Glutathione Magnetic resonance spectroscopy Multiple sclerosis Prefrontal cortex
 Alzheimer disease Parkinson disease amyotrophic lateral sclerosis astrocytes locus ceruleus multiple sclerosis oligodendrocytes toxic metals
 Disease-modifying therapies Multiple sclerosis Treatment response
 Multiple sclerosis depression fatigue physical activity sedentary behavior
 Aneurysm Multiple sclerosis Subarachnoid hemorrhage Systemic lupus erythematosus
 biomarker choroid plexus magnetic resonance multiple sclerosis
 Bobath concept multiple sclerosis neurorehabilitation physiotherapy reflex locomotion
 MOG antibody-associated disease (MOGAD) acquired demyelinating syndrome (ADS) multiple sclerosis (MS) myelin oligodendrocyte glycoprotein (MOG) neuromyelitis optica spectrum disorder (NMOSD) pediatric onset multiple sclerosis (POMS)
 Cognitive flexibility Emotional adaptability Multiple sclerosis Psycho-social adaptability
 Anthropometry B‌ody Composition B‌ody Mass Index Diet Fatigue Multiple sclerosis Nutrients Quality of life
 Natalizumab breastfeeding cerebrospinal fluid milk multiple sclerosis
 Discontinuation Disease-modifying therapies Observational study Relapsing-remitting multiple sclerosis Treatment persistence
 Multiple sclerosis conceptual model interviews muscle spasticity qualitative research
 Epstein–Barr virus disease‐modifying therapy multiple sclerosis translational immunology
 Pilates QoL cortisol depression mental health multiple sclerosis prolactin tele-exercise walking yoga
 CEREBELLAR DISEASE MRI MULTIPLE SCLEROSIS TOXICOLOGY


 Inflammatory markers MicroRNAs Multiple sclerosis (MS) Receiver operating characteristics

 EEG neurofeedback cognitive deficits memory rehabilitation
 Brain Genetics Medical research
 Atrophy Cognitive dysfunction Diffusion magnetic resonance imaging Multiple sclerosis
 Comorbidity Exercise Hypertension Multiple sclerosis Occupational therapy Osteoarthritis Rehabilitation
 MS dietary patterns multiple sclerosis nutrition
 digital self-monitoring lifeworld multiple sclerosis patient participation technology assessment
 cortical atrophy explainability leukocortical lesions machine learning multiple sclerosis rim lesions
 B-lymphocytes NK cells T-lymphocytes albumins globulins immunophenotyping multiple sclerosis ocrelizumab
 Biomarkers Cerebrospinal fluid Intermediate filaments Multiple sclerosis
 Greece Multiple sclerosis PLISSIT Satisfaction Sexual dysfunction Sexual rehabilitation
 autoimmune neurology multiple sclerosis neuroimmunology review
 Hereditary angioedema autoimmunity multiple sclerosis teriflunomide
 adverse effects disease modifying therapies escalation therapy immunomodulation multiple sclerosis pharmaceutical preparations therapeutics
 China Delphi method dimethyl fumarate multiple sclerosis review
 Cognition Multiple sclerosis No Evidence of Disease Activity Observational Teriflunomide
 3D bioprinting brain delivery gene therapy hydrogels multiple sclerosis
 dance dance for health dance therapy multiple sclerosis review
 access added therapeutic benefit drug value health technology assessment multiple sclerosis
 NODDI biomarker diffusion imaging intracellular diffusivity multiple sclerosis
 Parkinson's disease cellular process multiple sclerosis natural products neuroinflammation oxidative stress
 Neuroinflammation autoimmune disorders immune complexes inflammation macrophages multiple sclerosis
 Aging Cardiorespiratory fitness Multiple sclerosis, Cognitive impairment, Processing speed, Transcranial magnetic stimulation, Exercise Physical activity
 Epstein-Barr virus autoimmunity infection multiple sclerosis
 Multiple sclerosis cognitive functioning rehabilitation visual complaints visual impairment
 aging comorbidity multiple sclerosis (MS) treatment discontinuation treatment efficacy and safety
 comorbidity multiple sclerosis olypharmacy pharmacoepidemiology quality of life
 anti-Müllerian hormone antral follicle count infertility multiple sclerosis ovarian reserve
 Behaviour change Lifestyle factors Multiple sclerosis Scoping review Self-management Socio-ecological model
 COSMIN criteria Content validity Fatigue Fatigue measurement Measurement Multiple sclerosis Patient reported outcomes
 Cognition antidepressants depression fatigue multiple sclerosis vortioxetine
 acute disseminated encephalomyelitis antibody confluent demyelination multiple sclerosis lesion pattern-II myelin oligodendrocyte glycoprotein perivenous demyelination
 NOVA classification dietary habits disability multiple sclerosis multiple sclerosis severity ultra-processed food
 Costs Misdiagnosis Multiple sclerosis Testing Utilization
 Multiple sclerosis familial risk heritability primary progressive relapsing onset
 COVID-19 SARS-CoV-2 infection multiple sclerosis vaccination
 exercises fatigue ksa multiple sclerosis patients with multiple sclerosis
 Alzheimer's disease PTP1B Parkinson's disease amyotrophic lateral sclerosis multiple sclerosis neurodegenerative diseases
 cladribine tablets (Mavenclad®) lay summary mobility multiple sclerosis relapses
 Biomarkers Magnetic resonance imaging Multiple sclerosis Phase-rim lesions Susceptibility-weighted imaging
 Brain Complication Demyelination Multiple sclerosis SARS-CoV-2 Subdural empyema
 MULTIPLE SCLEROSIS NEUROIMMUNOLOGY
 immunogenetics multiple sclerosis natalizumab progressive multifocal leucoencephalopathy (PML) risk factors
 immune system balance multiple sclerosis myasthenia (myasthenia gravis - MG) narcolepsy type I neuroimmunology
 RNA modifications experimental autoimmune encephalomyelitis multiple sclerosis queuine transfer RNA
 Atopic dermatitis Autoimmune disease Childhood Multiple sclerosis Thyroiditis Type 1 diabetes Viruses
 Female Motivation Multiple sclerosis Physiological sexual dysfunction Quality of life Questionnaire
 cerebellar ataxia multiple sclerosis physiotherapy rehabilitation
 anti-TNF-alpha causal directed acyclic graphs collider confounding mediation multiple sclerosis
 Acute stroke Diet Gut-brain axis Microbiota Multiple sclerosis
 Baropodometry electromyography multiple sclerosis muscle fatigue sample entropy
 hand functions multiple sclerosis myelin sheath development rehabilitation transcranial direct current simulation
 DNA bovine leukemia virus multiple sclerosis peripheral blood mononuclear cells
 Coefficient of variation Elevation Latitude Month-of-birth Month-of-conception Multiple sclerosis Sunspot number Ultraviolet radiation
 Epstein–Barr virus autoimmunity infectious mononucleosis molecular mimicry multiple sclerosis neuroinflammation
 automatic-controlled processing executive functions information processing speed multiple sclerosis phonemic fluency semantic fluency
 cns disease-modifying therapies ms multiple sclerosis pathogenesis
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 anxiety depression glutamate ketogenic diets multiple sclerosis obesity
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 Ketogenic diet cuprizone (CPZ) model demyelinating autoimmune diseases in CNS experimental autoimmune encephalomyelitis (EAE) model multiple sclerosis neuroprotective effects
 Lumbar spine fusion Multiple sclerosis Nationwide outcomes Patient characteristics Spinal deformity Surgical complications
 EAE cuprizone demyelination inflammation mitochondria multiple sclerosis myelin remyelination
 ADAR interferon-β multiple sclerosis rs2229857
 Multiple sclerosis Progression independent of relapse activity Relapse-free Silent progression
 climate change cyclonic storms multiple sclerosis natural disasters
 chronic fatigue syndrome multiple sclerosis myalgic encephalomyelitis restless leg syndrome sleep disorders
 Caregivers Family Multiple sclerosis Shared decision-making
 MRI deep learning federated learning multiple sclerosis segmentation
 B cells T cells immunotherapy innate immune cells multiple sclerosis
 apathy behavioral disorders cognitive dysfunctions multiple sclerosis
 diet intermittent fasting multiple sclerosis patient-reported outcomes time-restricted eating
 Israel MS fatigue happiness multiple sclerosis psychological well-being resilience satisfaction with life sleep stress
 Fatigue L-carnitine modafinil multiple sclerosis


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 RIS children multiple sclerosis pediatric radiologically isolated syndrome treatment
 anti-cd20 monoclonal antibodies coronavirus disease 2019 (covid-19) high fever immunocompromised patient kesimpta ofatumumab paxlovid relapsing-remitting multiple sclerosis (rrms) sars-cov-2 sars-cov-2 infection
 multiple sclerosis
 Bruton’s tyrosine kinase inhibitors clinical trials multiple sclerosis
 Vocational rehabilitation employment job retention multiple sclerosis
 MAGiC multiple sclerosis myelin loss synthetic MRI white matter fraction
 MSQOL-29 Multiple sclerosis Persian Quality of life Validation
 Alemtuzumab Autoimmune thyroid disease Multiple sclerosis
 Multiple sclerosis latent class growth analysis natural history timed 25-foot walk trajectories walking speed
 CSF Parkinson’s disease headache inner ear multiple sclerosis neuroinflammation
 Factor analysis Multiple sclerosis Psychology Psychosocial functioning Self-concept
 Alertness Fitness to drive Multiple sclerosis Sleep
 Ofatumumab anti-CD20. b-cells immunological cells subset immunophenotype multiple sclerosis
 Aging Cognition Multiple sclerosis Social support
 MRI brain atrophy multiple sclerosis
 chaos complexity analysis electroencephalogram multiple sclerosis nonlinear dynamics
 aging brain magnetic resonance imaging multiple sclerosis systematic review
 Alzheimer’s disease HSV-1 demyelination multiple sclerosis trigger vDENT viral
 autoimmune disease comorbidity multiple sclerosis prevalence
 caregivers distress thermometer multiple sclerosis psychometric properties
 acetylcholine autoimmune disease cannabinoids cannabis central nervous system endocannabinoid system experimental autoimmune encephalomyelitis multiple sclerosis tetrahydrocannabinol
 Luminex xMAP technology antibodies astrocytes coagulation inflammation multiple sclerosis signalling pathways
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 brain connectivity functional magnetic resonance imaging (fMRI) graph theory multiple sclerosis (MS) network analysis neuroimaging
 antioxidants oxidative stress relapsing–remitting multiple sclerosis
 Bowel symptoms Constipation Fecal incontinence Management Multiple sclerosis Neurogenic bowel dysfunction
 artificial neural network deep learning multiple sclerosis
 Multiple Sclerosis balance fear of falling participation walking capacity
 autologous hematopoietic stem cell transplantation immunoablative therapy multiple sclerosis
 multiple sclerosis odor discrimination odor threshold olfactory dysfunction
 Iran multiple sclerosis quality of life sexual satisfaction spouses
 case control study covid-19 vaccines multiple sclerosis nervous system neuromyelitis
 Bayesian network Cytoscape multiple sclerosis (MS) qPCR transcriptome
 multiple sclerosis neurodegenerative disorders stem cells
 autoimmune disease endometriosis multiple sclerosis pathogenesis
 autoimmunity mitochondrial dysfunction multiple sclerosis neurodegeneration
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 Multiple sclerosis diagnosis diagnostic errors misdiagnosis
 Alzheimer’s disease Mendelian randomization diabetes mellitus genome-wide association study migraine multiple sclerosis
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 Cohort study Disease activity Disease modifying treatment Fatigue Multiple sclerosis
 Backward walking training Balance Functional mobility Gait Multiple sclerosis
 Balance Fullerton advanced balance scale Multiple sclerosis Reliability Validity
 blood-brain barrier diet gut microbiota gut-brain axis multiple sclerosis nutrition pediatric-onset multiple sclerosis polyunsaturated fatty acids vitamin D
 Alzheimer’s disease Parkinson’s disease amyotrophic lateral sclerosis autoimmunity disease heterogeneity multiple sclerosis neurodegenerative diseases sex/gender differences spinal muscular atrophy


 ALS (amyotrophic lateral sclerosis) Alzheimer's Epigenetics Epilepsy Histone modifications Huntington Methylation Multiple sclerosis Non-coding RNAs Parkinson
 eHealth health behaviour change health education health promotion multiple sclerosis
 Siglec-E immunomodulation microglia multiple sclerosis neuroinflammation organotypic cerebellar slice culture polysialic acid (polySia) remyelination
 multiple sclerosis resilience test construction test-retest reliability
 EU PAS Register number EUPAS24484 cladribine tablets fingolimod relapsing multiple sclerosis safety
 Zadiva® dimethyl fumarate multiple sclerosis real-world practice safety tolerability
 AEFI COVID-19 mRNA-based vaccine multiple sclerosis observational study safety three doses
 Multiple sclerosis discrete choice experiment disease progression disease-modifying therapies fatigue patient preference relapsing-remitting
 Choquet integral fuzzy algorithm health insurance multiple sclerosis risk factor
 cognition cognitive impairment deficit awareness metacognitive knowledge multiple sclerosis

 Biomarkers Brain-specific proteins CSF Multiple sclerosis
 Intravenous immunoglobulins Multiple sclerosis Post-partum Pregnancy Relapse
 Employment MSPT SDMT digital assessment multiple sclerosis processing speed
 multiple sclerosis music therapy physical therapy rehabilitation telerehabilitation
 Body fat Mendelian randomization Multiple sclerosis Risk
 Cyclohexanes Exercise Lactobacillus plantarum Multiple sclerosis Myelination
 autoimmunity autonomic dysfunction cardiovascular disease drug toxicity multiple sclerosis myocarditis
 Alzheimer’s disease—AD multiple sclerosis vascular dementia vascular dysfunction white matter dementia
 Multiple sclerosis Oceania Prevalence


 Astrocytes EAE JNK3 Microglia Multiple sclerosis Spinal cord

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 22q11.2DS Alzheimer’s disease autism spectrum disorder epilepsy hippocampal area CA2 inhibitory transmission multiple sclerosis schizophrenia
 Macronutrients Micronutrients Multiple sclerosis Nutrition counseling Overweight/obesity Randomized controlled clinical trial
 AQP4 MOG MOGAD Multiple sclerosis NMOSD Optic neuritis
 EDSS functional reorganization temporal core–periphery time-varying functional connectivity
 aging engagement immunosenescence late-onset multiple sclerosis pediatric-onset risk factors unmet need
 COVID-19 Dimethyl fumarate Interferon beta Multiple sclerosis Natalizumab Ocrelizumab Vaccine response
 Cigarette smoking Function recovery Passive smoking Relapsing-remitting multiple sclerosis Water Pipe smoking
 Artificial intelligence Clinical decision support Contrast-enhancing lesions Magnetic resonance imaging Multiple sclerosis
 decision-making multiple sclerosis nurse-patient relationship patient-centred care
 Connectivity Disability Exercising Fitness MRI Multiple Sclerosis
 Parkinson’s disease Word-finding difficulties anomia assessment multiple sclerosis self-reports stroke
 Multiple sclerosis Pilates balance core stability fatigue quality of life telerehabilitation
 disease-modifying therapy hypogammaglobulinemia immunoglobulins multiple sclerosis
 comorbidity mTOR multiple sclerosis tuberous sclerosis complex
 age dysarthria multiple sclerosis objective tool sex speech
 Multiple sclerosis (MS) cost-effectiveness cost-utility economic evaluation rehabilitation
 Galectin-3 Galectins Multiple sclerosis
 Cellular components Drug delivery Extracellular matrix Lesion classification, Targeting peptides Multiple sclerosis
 Cortical thickness Local gyrification index Multiple sclerosis Sulcal depth Surface-based morphometry
 Multiple sclerosis Neurodegeneration Neurofilaments Physical exercise Strength exercise training
 Taiwan cause of death cohort study multiple sclerosis survival
 diagnostic imaging disease progression iron multiple sclerosis
 multidisciplinary team multiple sclerosis pneumococcal vaccine vaccination
 MRI McDonald criteria (2017) Thai multiple sclerosis
 Drug repurposing Molecular dynamics simulations Multiple sclerosis S1P agonists Similarity network analysis
 meta-analysis microvasculature multiple sclerosis optic neuritis retina
 Case report Central dilated vascular structure Ectopic germinoma Multiple sclerosis Primary frontal germinoma
 Corticospinal excitability motor evoked potential multiple sclerosis pain transcranial magnetic stimulation
 Multiple sclerosis neuropathic pain pain quality of life.
 Autonomic nervous system Biofeedback Fatigue Heart rate variability Multiple sclerosis Progressive muscle relaxation
 Clinically isolated syndrome Diagnosis McDonald criteria Multiple sclerosis Oligoclonal bands
 brain MRI gray-level co-occurrence matrix lesion severity multiple sclerosis percentile thresholding sex difference texture analysis
 Achalasia Database analysis Diffuse esophageal spasm Esophageal dysphagia Multiple sclerosis
 All of Us Optic neuritis barriers to care multiple sclerosis risk factors
 degenerative disc disease demyelinating disease multiple sclerosis spinal cord plaque spine MRI spondylosis
 EBNA2 EBV GWAS RNA therapeutics targeting EBV multiple sclerosis risk genetic variation
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 McDonald criteria Multiple sclerosis immunoglobulin G index oligoclonal bands
 IgG antibodies SARS-CoV-2 disease-modifying treatments multiple sclerosis vaccines
 Multiple Sclerosis Polymorphism VitD Receptor
 digital technology magnetic resonance imaging multiple sclerosis patient communication survey
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 Multiple Sclerosis ToM rehabilitation rehabilitation training social cognition
 Sjogren's syndrome autoimmunity demyelinating diseases multiple sclerosis (MS) neuromyelitis optica (NMO) systemic lupus erythematosus (SLE) type I interferon (IFN)
 anxiety comorbidity depression multiple sclerosis polypharmacy therapy switches
 IgM Tysabri® biomarkers diagnosis interferon-β multiple sclerosis phosphatidylcholine prognosis
 Dimethyl fumarate disease-modifying therapies immunology multiple sclerosis
 Multiple Sclerosis Muscle Spasticity Spinal Cord Stimulation
 Brain connectivity Connectome EDSS Fatigue Fingerprint Multiple sclerosis
 experimental autoimmune encephalomyelitis intracortical connection multiple sclerosis neurophysiology non-invasive visual evoked potentials
 cannabis medical marijuana multiple sclerosis spasticity
 6MWT fatigue multiple sclerosis physical training walking ability
 HCG11 Multiple sclerosis NORAD RAD51-AS1 ZNRD1ASP lncRNA
 Hypersomnia Multiple sclerosis Neuromyelitis optic spectrum disorder Restless legs syndrome Sleep Willis-Ekbom disease
 BICAMS aMACFIMS cognitive impairment functional outcomes multiple sclerosis
 Anxiety COVID-19 Depression Flu like syndrome Interferon-ß Multiple Sclerosis
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 MRI clinical prediction label uncertainty machine learning missing labels multiple sclerosis noisy labels
 DESDE-LTC health care system multiple sclerosis service mapping
 T2 mapping atrophy demyelination diffusion tensor imaging hippocampus inflammation multiple sclerosis
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 Anti-CD20-Therapy Immunotherapy Kesimpta Multiple sclerosis Patient reported outcomes
 Assisted reproductive technology GnRH antagonists Multiple sclerosis Oocyte cryopreservation Preconception counselling
 Arhgef9 Sam68 alternative splicing experimental autoimmune encephalomyelitis hippocampus multiple sclerosis neuroinflammation parvalbumin
 Depression Fatigue Multıple sclerosis Quality of life Sleep disorders
 African American Cognitive processing speed Hispanic Natalizumab No evidence of disease activity Patient-reported outcome Relapsing–remitting multiple sclerosis
 clinical research protocol health education health literacy multiple sclerosis patient empowerment peer group quality of life


 aging best practice hormone therapy menopause multiple sclerosis
 Alzheimer disease Cd Cu Fe Parkinson disease Zn amyotrophic lateral sclerosis multiple sclerosis neurodegenerative diseases
 Accelerometer Disability Fatigue Multiple sclerosis Physical activity Relapsing-remitting multiple sclerosis
 long-term health outcomes multiple sclerosis neonatal outcomes pregnancy reproduction
 cognitive impairment (CI) immune cell response multiple sclerosis peripheral-CNS interplay white and gray matter damage
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 amino acid biomarker disability metabolomics multiple sclerosis
 basal ganglia fatigue functional connectivity multiple sclerosis neuroimaging
 acceptance and commitment therapy multiple sclerosis psychological distress psychological flexibility quality of life resilience
 Epstein–Barr virus GlialCAM molecular mimicry multiple sclerosis
 ALS DNA-binding proteins MS RNA-binding proteins TDP-43 autoimmunity neurodegeneration
 Acute disseminated encephalomyelitis Ayurveda COVID-19 vaccination Multiple sclerosis
 chronic disease depression exercise interventions exercise is medicine mental illness multiple sclerosis social determinants of health syndemics
 adverse drug effects contraception fertile age foetal development multiple sclerosis pharmacotherapy women
 Co-design cognitive interviews mixed-methods research nutrition education participatory research
 Alemtuzumab K-deleting recombination excision circles (KRECs) Multiple sclerosis T-cell receptor excision circles (TRECs)
 Fingolimod central nervous system cryptococcal infection cryptococcal meningitis cutaneous cryptococcal infection multiple sclerosis
 DMTs’ switches Fingolimod Multiple Sclerosis Ocrelizumab
 Continuous-time Markov model Multiple sclerosis Multistate model Padé Scalable optimization approximation
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 Guillain-Barré syndrome experience multiple sclerosis myasthenia gravis plasma exchange
 Sarcoidosis multiple sclerosis neuro sarcoidosis
 Alzheimer NMMHC IIA Parkinson autoimmune autoimmune myocardioptis multiple sclerosis myosin




 Assessment Disability Multiple sclerosis Patient reported outcome measure Rasch Trajectories of Outcome in Neurological Conditions (TONiC) World Health Organization Disability Assessment Schedule 2.0
 MRI clinical neurology image analysis multiple sclerosis
 corticospinal tract multiple sclerosis (MS) precision medicine transcranial direct-current stimulation (tDCS) transcranial electric stimulation (tES) transcranial magnetic stimulation (TMS)
 AQoL-8D Cost–utility analysis Disutility of relapse EQ-5D-5L-psychosocial Health-related quality of life Multi-attribute utility instrument Multiple sclerosis SF-6D
 CD134 Multiple sclerosis Neuromyelitis optica OX40 T cell
 Brain atrophy Cognition Lesion volume MRI Multiple sclerosis Sex
 IMMUNOLOGY MULTIPLE SCLEROSIS
 Health technology Neuroscience

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 Balance Brain reserve Cognitive reserve Multiple sclerosis
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 Multiple sclerosis biological marker. experimental autoimmune encephalomyelitis microRNA neuroinflammation synaptopathy
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 Machine learning Multiple sclerosis Real-world evidence Treatment switching
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 ELISA: Multiple sclerosis Toxoplasma gondii Toxoplasma-IgG Toxoplasma-IgM
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 Multiple sclerosis epidemiology mortality standardized mortality ratio survival
 MRI diffusion machine learning multi-modal multiple sclerosis quantitative random forest sodium
 Burden Caregiver Iranian Multiple sclerosis Reliability Validity
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 Canada models of care multidisciplinary multiple sclerosis qualitative team-based care
 adherence chronic disease fitbit lessons learned mobile health (mHealth) multiple sclerosis scalability wearable
 Adolescence Childhood Epidemiology Multiple sclerosis Natural history studies
 clinical assessment multiple sclerosis rehabilitation upper extremity function video-assisted
 biomarkers cognition disability predictors multiple sclerosis neurodegeneration progression
 Microvascular decompression Multiple sclerosis Progressive Relapsing-remitting Trigeminal neuralgia
 Alzheimer disease Attention Network Test Demencia por cuerpos de Lewy Enfermedad de Alzheimer Enfermedad de Parkinson Epilepsia Epilepsy Esclerosis múltiple Lewy body dementia Multiple sclerosis Parkinson’s disease
 Experimental Autoimmune Encephalomyelitis In vitro model of blood–brain barrier Multiple Sclerosis T-cell trafficking Toll-like receptors
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 Multiple sclerosis epidemiology quality of life
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 Siglec-E immunomodulation microglia multiple sclerosis neuroinflammation organotypic cerebellar slice culture polysialic acid (polySia) remyelination
 Multiple sclerosis aging apathy caudate magnetic resonance imaging
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 Demyelination Efficacy Pediatric MS Relapsing-remitting course Safety Teriflunomide
 GAPDH experimental autoimmune encephalomyelitis multiple sclerosis neuroinflammation neuroprotection nitric oxide nitrosylation
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 McDonald criteria diagnosis primary progressive multiple sclerosis
 MEF2C MEF2D Multiple sclerosis Single nucleotide polymorphism
 deep learning multiple sclerosis optical coherence tomography retinal ganglion cell layer
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 COVID-19 health care multiple sclerosis outcome assessment
 FOXP3 NLRP3-inflammasome SNHG1 lincRNA-Cox2 lnc-EGFR relapsing–remitting multiple sclerosis
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 Optic neuritis diffusion magnetic resonance imaging diffusion tractography multiple sclerosis optical coherence tomography white matter
 diffusion-weighted magnetic resonance imaging experimental autoimmune encephalomyelitis mouse spinal cord, multiple sclerosis
 Astrocyte B cells Blood-brain barrier EAE Microglia Multiple sclerosis Myelin
 Biomarker Ofatumumab Relapsing multiple sclerosis Serum neurofilament light chain Subclinical disease activity
 Case-control study Iran Multiple sclerosis Seroprevalence Toxoplasma gondii

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 Multiple sclerosis demyelinating disease dietary patterns
 Dysuria Multiple sclerosis Neuromyelitis optica
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 25-hydroxyvitamin D BMD bone-turnover cytokines glucocorticoids multiple sclerosis osteoporosis periostin
 biomarker cancer cardiovascular disorders diabetes free light chains inflammation multiple sclerosis rheumatic disease viral infections κ λ
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 cognition function meta-analysis motor function multiple sclerosis non-invasive brain stimulation
 Alzheimer’s disease Huntington’s disease Parkinson’s disease Sirtuin 3 amyotrophic lateral sclerosis mitochondrial function multiple sclerosis neurodegenerative diseases
 Detection Magnetic resonance imaging Multiple sclerosis Post-processing Reproducibility
 Alzheimer's disease Exosomes Parkinson's disease extracellular vesicles glioblastoma multiple sclerosis, amyotrophic lateral sclerosis neurodegenerative diseases
 Alzheimer's disease Huntington's disease amyotrophic lateral sclerosis multiple sclerosis spinocerebellar ataxia synucleinopathies
 EBV HHV6 Multiple sclerosis PPMS RRMS SPMS
 CCL2 MSC-NP TGF-β cell therapy mesenchymal stem cell microglia multiple sclerosis
 Cognition MSISQ-19 Multiple sclerosis Outcome measurement Quality of life Sexual dysfunction


 Alzheimer disease Multiple sclerosis Neurodegenerative diseases Parkinson disease Protein tyrosine kinases Protein tyrosine phosphatases Tyrosine phosphorylation
 Disease activity Relapsing-remitting multiple sclerosis Vitamin D supplementation
 Gadolinium Magnetic resonance imaging Multiple sclerosis Practice guideline Safety
 magnetic resonance imaging microchimerism multiple sclerosis pregnancy regional volumes sex of offspring sexual chromosomes
 Alzheimer’s disease Bryostatin-1 fragile X syndrome multiple sclerosis protein kinase C stroke traumatic brain injury
 Alzheimer's disease Parkinson's disease astrocytes microglia multiple Sclerosis neuroinflammation
 Multiple sclerosis Myelin oligodendrocyte glycoprotein NMO spectrum disorders Neuromyelitis optica Optic neuritis Optical coherence tomography
 Multiple Sclerosis Pediatrics Acute Transverse Myelitis in Demyelinating Disease of the Central Nervous System
 Alzheimer's disease Electroencephalography (EEG) acute ischaemic stroke (AIS) artificial intelligence brain disorders convolutional neural network (CNN) multiple sclerosis schizophrenia
 Th17 cells autoimmune diseases immune homeostasis multiple sclerosis psoriasis vulgaris regulatory T cells rheumatoid arthritis type 1 diabetes


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 Multiple sclerosis biomarker blood–CSF-barrier compartmentalised inflammation cytokine granulocyte-macrophage colony stimulating factor
 cerebral small vessel disease (CSVD) immune mechanisms ishcemic stroke microglia multiple sclerosis neuromyelitis optica spectrum disorder (NMOsd) white matter lesions (WMLs)

 MRI Pseudocystic lesions atypical inflammatory demyelinating lesions histopathology multiple sclerosis tumefactive demyelinating lesions
 Multiple sclerosis Observational study Pediatrics Survival analysis Therapeutics Treatment Outcome
 Expanded Disability Status Scale Patient-Determined Disease Steps multiple sclerosis patient-reported outcomes validity
 disease management hospital pharmacy service multiple sclerosis/drug therapy patient-reported outcome measures specialty pharmacy pharmacists
 Cladribine Multiple sclerosis Real-world data
 Antibodies Covid-19 Evusheld Multiple sclerosis Tixagevimab-cilgavimab
 Ulcerative colitis comorbidity demyelination multiple sclerosis systematic review
 Cluster analysis Diet Digital data collection Lifestyle interventions Multiple sclerosis Observational data Self-monitoring Symptom management
 EAE model exercise training motor function multiple sclerosis neurotrophin
 accidental falls multiple sclerosis telehealth wheelchair
 Antibody cross-reactivity Calnexin Calreticulin Mutated calreticulin Myeloproliferative neoplasm Relapsing remitting multiple sclerosis
 fatigue multiple sclerosis prognostic factors speech therapy voice disorders
 Alemtuzumab Esclerosis múltiple Estudio observacional Multiple sclerosis Observational study
 Early assessment Multiple Sclerosis Patient-reported outcome Preventive rehabilitation Rehabilitation assessment Upper limb function
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 Experimental autoimmune encephalomyelitis Multiple sclerosis T helper 17 Triggering receptor expressed on myeloid cells 2
 COVID-19 Multiple sclerosis Vaccination
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 Multiple sclerosis cognition cognitive performance depression meta-analysis
 Complication Hip, Knee Multiple sclerosis Postoperative outcome Total joint arthroplasty
 differential diagnosis multiple sclerosis oligoclonal bands
 Demyelination Metformin Multiple sclerosis Oxidative stress
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 Multiple sclerosis United Kingdom biomedical cost-benefit analysis patient-reported outcome measures quality of life technology assessment
 Alertness Depression Fatigability Fatigue Multiple sclerosis Rehabilitation
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 Multiple sclerosis cerebral small vessel disease diffusion-weighted imaging magnetic resonance imaging
 infections multiple sclerosis relapses
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 Ageing DNA methylation Epigenetic clocks Inflammation Lung alveolar macrophages Multiple Sclerosis Smoking
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 MRI multiple sclerosis
 Atrophy Cognition Disability MRI Multiple sclerosis
 MRZ reaction blood-CSF barrier dysfunction cerebrospinal fluid multiple sclerosis neurosarcoidosis oligoclonal bands pleocytosis
 Disease-modifying treatment Multiple sclerosis Spinal cord
 Curcumin Experimental autoimmune encephalomyelitis Multiple sclerosis Myelin oligodendrocyte glycoprotein
 Deep-brain stimulation Long-term efficacy Multiple sclerosis Tremor Ventral intermediate nucleus
 Biofeedback devices EEG Mindfulness Multiple Sclerosis Rumination mHealth
 Behavior change E-learning Multiple sclerosis Physical activity Theory
 Multiple sclerosis cognition occupational therapy public and patient involvement (PPI)
 Anti-CD20 Efficacy Multiple sclerosis Rituximab Safety
 cerebrospinal fluid chloride multiple sclerosis relapse
 Apigenin Apoptosis Multiple Sclerosis Proliferation Th1
 GCIPL disability progression multiple sclerosis optical coherence tomography pRNFL
 different walking speeds gait-parameter multiple sclerosis (MS) three-dimensional gait analysis walking human wearable sensors
 Bipolar Disorder Caregiver Multiple Sclerosis PTSD Traumatic Events
 microstructural damage multiple sclerosis neurogenesis neuroprotection remyelination subventricular zone
 cerebrospinal fluid differential diagnosis interleukin 6 multiple sclerosis neurofilaments light chain oligoclonal bands osteopontin
 Late-onset multiple sclerosis Lesions Magnetic resonance imaging Systematic review
 Multiple sclerosis menopause onset progression smoking
 dietary inflammatory index (DII) macronutrients micronutrients multiple sclerosis nutrition
 COVID-19 DMTs Epidemiology Healthcare Multiple sclerosis Pandemic Recovery
 OCH Treg cells clinical trial iNKT cells multiple sclerosis
 aging education family income multiple sclerosis (MS) patient—centered care socioeconomics
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 MRI MULTIPLE SCLEROSIS
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 Multiple sclerosis Optic neuritis Retrospective analysis Southern India

 B cell T cell TLR anti-CD20 therapy multiple sclerosis ocrelizumab
 Multiple sclerosis Opioid Pain Rehabilitation
 connectomics information processing speed multiple sclerosis (MS) neuropsychological test structural connectivity



 Autoimmune thyroid disease Comorbidty Drug GWAS Multiple sclerosis Transcriptome
 administrative data healthcare utilization multiple sclerosis pregnancy prenatal care recommendations

 cardiovascular multiple sclerosis optical coherence tomography retinal nerve fiber layer retinal vessels vessel diameter
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 Carotid-femoral pulse wave velocity cardiorespiratory fitness vascular stiffness
 Epstein-Barr virus central nervous system disease infectious mononucleosis multiple sclerosis treatment vaccination
 Dimethyl-fumarate (DMF) Multiple sclerosis NF-kB Neurofilament light chain (NFL) miRNA
 Alzheimer’s disease IL-1 family cytokines IL-1 family receptors multiple sclerosis neurodegeneration neuroinflammation
 Asthma CRISPR/Cas9 genome editing Inflammatory bowel disease Multiple sclerosis Post-GWAS SNP
 Alzheimer's disease Huntington's disease Parkinson's disease antiplatelet drugs multiple sclerosis natural phytochemicals
 microglia neurodegeneration progressive multiple sclerosis
 Alzheimer’s disease biomarker complement extracellular vesicle (EV) multiple sclerosis neuroinflammation


 Cocrystals DSC-TGA Dimethyl fumarate Molecular docking Molecular dynamics Multiple sclerosis PXRD Pharmacokinetics
 Demyelination Multiple sclerosis Neurodegeneration Optic Neuritis Retinopathy
 Limosilactobacillus reuteri asthma atopic dermatitis (AD) immune system disease multiple sclerosis necrotizing enterocolitis (NEC) rheumatoid arthritis systemic lupus erythematosus (SLE)
 Brain tumors Community Dementia Home visits Motor neuron disease Multiple sclerosis Neurodegenerative Nursing homes Palliative care Parkinson's disease
 Multiple sclerosis and expanded disability status scale new algorithmic approach
 Bruton’s tyrosine kinase COVID-19 Evobrutinib SARS-CoV-2 multiple sclerosis vaccines
 Graves' disease alemtuzumab (Lemtrada) autoimmune antibodies autoimmune thyroid disease (AITD) multiple sclerosis secondary autoimmunity




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 brain mapping image analysis multiple sclerosis neural networks
 disease progression employment longitudinal studies multiple sclerosis risk factors
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 Mendelian randomization analysis Molecular epidemiology Multiple sclerosis mTOR-associated protein

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 Efficacy fingolimod multiple sclerosis safety
 MULTIPLE SCLEROSIS
 DMT Dimethyl fumarate Efficacy Multiple sclerosis Safety Young adults
 Anti-inflammation Experimental autoimmune encephalomyelitis Hydroxyfasudil Immunomodulation Multiple sclerosis
 cognition epidemiology multiple sclerosis
 Glatiramer acetate Inteferon beta Interleukin-23 Interleukin-27 Multiple sclerosis Polymorphism
 COVID-19 disease-modifying therapies multiple sclerosis prognosis
 Biomarkers Case–control study Diagnosis Multiple sclerosis Oligoclonal bands κ free light chain
 SARS-CoV-2 cellular immunity humoral immunity multiple sclerosis vaccination
 IgG4 experimental autoimmune encephalomyelitis heath shock protein 70 multiple sclerosis mycobacteria
 BICAMS Brief International Cognitive Assessment for MS PASAT SDMT cladribine cognitive impairment dimethyl fumarate fingolimod magnetic resonance imaging (MRI) multiple sclerosis neuropsychological assessment ozanimod paced auditory serial addition task siponimod symbol digit modality test teriflunomide
 A variant of unknown significance Differential diagnosis Fabry disease Misdiagnosis Multiple sclerosis Screening
 Multiple sclerosis brain diagnostics magnetic resonance imaging (MRI) white matter
 DMTs healthcare costs healthcare resource utilization prescription relapsing–remitting multiple sclerosis
 anxiety meta-analysis multiple sclerosis prevalence risk factor
 Multiple sclerosis excessive daytime sleepiness ipRGC optic neuritis outcome measurement symptomatic treatment

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 ginger interleukin‐17 matrix metalloproteinase‐9 multiple sclerosis neurofilament protein L nitric oxide
 Autoantibody Chloride intracellular channel protein-1 Multiple sclerosis Myelitis Optic neuritis
 Multiple sclerosis natalizumab resting-state functional imaging
 Nabiximols Sativex THC/CBD meta-analysis. multiple sclerosis resistant spasticity spasticity numerical rating scale systematic review
 YSEX questionnaire importance of sex multiple sclerosis reasons to have sex sexual motivation sexual motive
 P100 latency disability outcome multiple sclerosis non-neuritic eye prognosis visual evoked potentials
 PPMS SPMS animal model cuprizone demyelination kynurenine multiple sclerosis remyelination translational tryptophan
 COVID-19 disease-related beliefs multiple sclerosis vaccine hesitancy vaccine intent
 calcium intake coaching/accompaniment dietary advice multiple sclerosis personalized medicine
 Adherence Dimethyl fumarate Diroximel fumarate Gastrointestinal side effects Multiple sclerosis Real-world treatment Tolerability
 depression illness perception multiple sclerosis severity sexuality
 1/f spectral slope aperiodic aperiodic exponent excitation/inhibition balance magnetoencephalography resting state spectral power
 Disparities access to care insurance multiple sclerosis quality of life social determinants of health
 bladder diary (BD) depression fatigue multiple sclerosis (MS) neuro-urology neurogenic lower urinary tract symptoms (LUTS)
 cancer immunomodulator immunosuppressant multiple sclerosis nested case-control study
 Diet Diet index Diet quality Food index Lesion MRI Multiple sclerosis
 biological products demyelinating diseases multiple sclerosis oral manifestations oral medicine trigeminal neuralgia
 Claims database Disease-modifying therapies Early treatment Healthcare costs Healthcare resource use Multiple sclerosis Ocrelizumab Real-world evidence Relapse
 dysarthria multiple sclerosis speech acoustics speech disorder speech therapy assessment
 Annualized relapse rate Magnetic resonance imaging Multiple sclerosis Post-partum relapses Pregnancy Relapse
 Assistive technology co-design custom assistive devices multiple sclerosis
 Cost-effectiveness analysis Disease-modifying therapies Ozanimod Relapsing–remitting multiple sclerosis
 Fingolimod Inflammation Melanoma cell lines Multiple sclerosis Ozanimod Ponesimod Siponimod Sphingosine-1 phosphate
 Autoimmune diseases Demyelinating diseases Immunoglobulin G Multiple sclerosis N-glycosylation
 Effectiveness Multiple sclerosis Ocrelizumab Real-world Safety
 Multiple sclerosis disease progression economic burden of disease quality of life
 Alpha calcitonin gene related peptide Biomarker Expanded Disability Status Scale Multiple sclerosis Neuropeptide y Progressive MS Relapsing-remitting MS Substance P



 CSF MS cytokines neuroinflammation relapse vaccine
 A-H, Alpers-Huttenlocher syndrome AD, Alzheimer’s disease ALS, Amyotrophic lateral sclerosis BBB, blood-brain barrier C. elegans,, Caenorhabditis elegans CJD, Creutzfeldt-Jakob disease CMT, Charcot–Marie–Tooth disease CS, Cockayne syndrome Ech A, Echinochrome A FDA, Food and Drug Administration FRDA, Friedreich’s ataxia FTD, Frontotemporal dementia HD, Huntington’s disease Hsp, Heat shock protein LSD, Lysosomal storage diseases MS, Multiple sclerosis MSA, Multiple system atrophy MSP, Multisystem proteinopathy Medicinal plant ND, neurodegenerative disease NPC, Neimann-Pick disease type C NSC, neural stem cells Neuro-inflammation Neurodegeneration Neurogenesis PC, pharmacological chaperone PD, Parkinson’s disease Protein misfolding SMA, Spinal muscular atrophy VD, Vascular dementia prion dis, prion diseases α-syn, alpha-synuclein
 STAT1 Sox9 experimental autoimmune encephalomyelitis interferons multiple sclerosis neural stem cells subventricular zone
 Access to care LGBTQ+ Multiple sclerosis Patient–provider communication
 Experimental autoimmune encephalomyelitis KDM5c KDM6A Multiple sclerosis Sex differences Th17 cell
 B cells aggregation central nervous system multiple sclerosis osteopontin
 CMT1A moya-moya multiple sclerosis neurofibromatosis novel mutations
 DNA methylation Differentially methylated genes Experimental autoimmune encephalomyelitis Multiple sclerosis mtDNA methylation
 Alzheimer’s disease ApoER2 CP: Cancer CP: Immunology JAK/STAT NF-κB PI3K/AKT Reelin VLDR arthritis atherosclerosis cancer coagulation immune system inflammation intestine kidney leukocyte liver lymphatic circulation multiple sclerosis vascular system
 11C-methionine-PET glioblastoma metastatic brain tumor primary central nervous lymphoma radiation necrosis tumefactive multiple sclerosis
 Alzheimer’s disease Multiple sclerosis Parkinson’s disease amantadine memantine neurodegenerative diseases traumatic brain injury
 Alzheimer’s disease Anticonvulsant Embellin Natural treatment Neurological disorder multiple sclerosis
 Graves' disease Graves' ophthalmopathy IFN-β Multiple sclerosis Th1 chemokines
 Multiple sclerosis cognitive training transfer effects brain atrophy treatment response working memory
 T-cells autoimmune inflammatory bowel disease integrins multiple sclerosis psoriasis
 Activities of daily living Daytime sleepiness Disease-modifying therapy Multiple sclerosis Sleep quality Social functioning
 Home-treatment Multiple sclerosis Natalizumab Progressive multifocal leukoencephalopathy Risk
 cancer multiple sclerosis phage display semaphorin single-domain antibody (sdAb, nanobody, VHH)
 EBV DNA Epstein–Barr virus biomarkers infectious mononucleosis lymphoma multiple sclerosis nasopharyngeal carcinoma post-transplant lymphoproliferative disorders serology
 Multiple sclerosis (MS) Nissen fundoplication Small bowel obstruction Superior mesenteric artery syndrome (SMAS)
 Demyelination Indian population multiple sclerosis optic neuritis pediatric optic neuritis
 Molecular neuroscience Neuroscience Omics Transcriptomics
 disease-modifying therapies leflunomide multiple sclerosis peripheral neuropathy teriflunomide

 Chronic-active brain inflammation Multiple sclerosis N-acetylglucosamine N-glycan branching
 Chronic relapsing inflammatory optic neuropathy MOG antibody-associated disease Multiple sclerosis Neuro-ophthalmology Neuromyelitis optica spectrum disorder Optic neuritis
 LINGO-1 Nogo-A demyelination multiple sclerosis regeneration remyelination
 Crohn’s disease IL-17 secreting cells Th17 adipose tissue-derived mesenchymal stem cells cancer chronic inflammatory disease mesenchymal stem cells multiple sclerosis obesity plasticity psoriasis rheumatoid arthritis
 Activities of daily living Clinical trial Cognition Cognitive training Multiple sclerosis Quality of life Rehabilitation Treatment outcome
 Multiple sclerosis Neuroregeneration Oligodendrocyte Remyelination Teriflunomide
 16S rRNA Gut microbiota Matrine Multiple sclerosis Short chain fatty acids
 Gait Metacognition Multiple sclerosis Pilates suspension Self – awareness
 Intermediate uveitis Multiple sclerosis Non-pars planitis Pars planitis SUN classification
 CNS penetration Fingolimod Multiple sclerosis Siponimod
 Alzheimer’s disease Parkinson’s disease ischemic stroke mesenchymal stem cells multiple sclerosis neurological disorders stem cell therapy
 Alzheimer's disease MOTS-c Parkinson's diseases acute stroke adropin multiple sclerosis
 MRI multiple sclerosis neuroimmunology

 Alzheimer’s disease Amyotrophic lateral sclerosis Immune system Multiple sclerosis Neurodegeneration Neuroinflammation Parkinson’s disease Pro-inflammatory

 Autoimmune reaction Autoimmunity Multiple sclerosis Viral infections


 aquaporin2 (AQP2) carotid body (CB) checkpoint inhibition cytokine signaling microglia multiple sclerosis and neuroimmunology pancreatitis vagus nerve
 Cognitive dysfunction Differential diagnosis Multiple sclerosis Neurodegeneration
 MRI deep learning image processing neurodegenerative diseases neurology - clinical
 Social support cognition cognitive decline multiple sclerosis social network

 Diabetes mellitus Immune tolerance Lupus Multiple sclerosis Rheumatoid arthritis Short-chain fatty acids
 Cognitive reserve Multiple sclerosis Racial health disparities
 Autonomic nervous system Fatigue Heart rate variability Multiple sclerosis Neuroinflammatory reflex Parasympathetic modulation Sympathetic modulation Vagus nerve



 Alzheimer disease amyotrophic lateral sclerosis autoimmune encephalitis epidemiology interleukins multiple sclerosis neuromyelitis optica
 MRI multiple sclerosis neuroimmunology neuroophthalmology
 adherence medication neurological conditions quality of life saudi arabia
 Alzheimer’s disease COVID-19 Parkinson’s disease biomarker miRNA neurodegeneration neuroinflammation


 Age Machine learning Neural networks Neuroscience
 Emotional competencies Fatigue Insomnia Multiple sclerosis Paresthesia Symptoms of depression
 Scoping review alzheimer’s disease experiences ischaemic heart disease multiple sclerosis physical activity
 antineutrophil autoantibodies antinuclear autoantibodies autoimmunity multiple sclerosis
 Persian medicine complementary therapies diet therapy randomized controlled trial secondary-progressive multiple sclerosis
 Mongolia depression disability epidemiology multiple sclerosis
 COVID-19 Multiple sclerosis Neuromyelitis optica spectrum disorder
 Biomarkers Disease worsening Immune cell subset frequencies Multiple sclerosis Serum neurofilament light chain
 bicaudate ratio multiple sclerosis neurofilament light chain predictive factors third ventricle width
 EAE Multiple Sclerosis cannabinoid receptor lymphocytes microglia β-Caryophyllene
 Accidental falls Fatigue Multiple sclerosis Rehabilitation Wounds and injuries
 MRZ reaction autoimmue disease multiple sclerosis neuroinflammation polyspecific intrathecal immune response
 COVID-19 SARS-CoV-2 chronic diseases chronic kidney disease coping multiple sclerosis pandemic psoriasis psychopathology
 Balance control Balance training Dual-task Feasibility Highly challenging Intervention development Multiple sclerosis Outcome response Progression criteria Stakeholder involvement
 Complementary and alternative medicine Multiple sclerosis Neurological disorders Stroke Systematic review




 Astrocytes cells Curcumin Neurodegenerative Conditions; Huntington’s disease; Amyotrophic lateral sclerosis; Multiple sclerosis; Alzheimer’s disease; Parkinson’s disease

 Anti-inflammatory agents Fatigue Pain Progressive multiple sclerosis Randomized controlled trial Synbiotics
 cognitive neuropsychology multiple sclerosis psychology randomised trials
 Cell therapy MSCs in MS Mesenchymal stromal cells Multiple sclerosis Regenerative medicine
 Cladribine tablets Disease-modifying therapy Drug safety Immune reconstitution therapy Multiple sclerosis
 clinically isolated syndrome ganglion cell layer macular retinal segmentation multiple sclerosis neurodegeneration optical coherence tomography posterior pole analysis retinal fiber layers
 caregivers coping strategies mental health multiple sclerosis post-traumatic growth
 amide proton transfer chemical exchange saturation transfer molecular imaging multiple sclerosis neuroinflammation
 fingolimod genetic markers machine learning multiple sclerosis precision medicine predictive model
 DMT EDSS MRI NEDA multiple sclerosis relapse second-line treatment
 Deep gray matter FEV1 FVC Multiple sclerosis T2-FLAIR
 COVID-19 outcome SARS-CoV-2 vaccines SARS-CoV-2 variants disease-modifying treatment multiple sclerosis
 Anticipatory postural adjustments Center of pressure Gait initiation Multiple sclerosis Spatiotemporal parameters
 NPC OPC immunomodulatory multiple sclerosis neuroinflammation neuroprotection regeneration remyelination
 Alzheimer ́s disease Huntington ́s disease Nanobody Parkinson ́s disease antibody fragment immunotherapy. intrabody
 air pollution central nervous system disorder neuroinflammation neuropathology stroke



 Alopecia Areata diet multiple sclerosis systemic lupus erythematosus therapeutic strategies vitamin D



 Cortical thickness Multiple Sclerosis Neuromyelitis optica spectrum disorders Person-based similarity index Subcortical volume
 EudraVigilance adverse drug reactions cladribine hepatic safety multiple sclerosis

 Disease modifying therapy High efficacy Multiple sclerosis Relapsing remmiting

 Multiple sclerosis beta-interferon biomarkers disease-modifying therapies glatiramer acetate treatment response
 Relapsing-remitting multiple sclerosis disability progression early-stage patient-reported outcomes
 BMAL1 OPC circadian demyelination multiple sclerosis myelin oligodendrocyte sleep
 Dried Blood Spot Fampridine Multiple Sclerosis Pharmacokinetic study Potassium channel blocker UPLC
 glatiramer acetate low birth weight major congenital malformation multiple sclerosis pregnancy outcome preterm birth safety trimester
 Fatigue Functional connectivity Monoamine Multiple sclerosis Treatment
 5-hydroxymethyl-2-furfural M2 polarization experimental autoimmune encephalomyelitis inflammation multiple sclerosis
 Alzheimer’s disease Epilepsy Multiple Sclerosis Neurological disorders Parkinson’s disease Pathophysiology Risk factor Vitamin D deficiency
 brain connectivity functional MRI machine learning multiple sclerosis neurogenic bladder voiding dysfunction
 autoimmune diseases autoimmune thyroid disorders immune cells multiple sclerosis vitamin D vitiligo
 CP: Immunology DC-10 Tr1 cells aryl hydrocarbon receptor chromatin accessibility immune tolerance interleukin-10 multiple sclerosis regulatory type 1 T cells tolerogenic DC transcriptome
 cladribine immunoglobulin A immunoglobulin G immunoglobulin M multiple sclerosis natalizumab ocrelizumab
 COVID-19 Multiple sclerosis Neuromyelitis optica spectrum disorder Pediatric SARS-CoV-2 Vaccination
 Multiple sclerosis colitis ocrelizumab

 Metabolism Multiple sclerosis OPC maturation Oligodendrocytes Pdh Pdhk1
 EAE OPC microglia multiple sclerosis oligodendrocyte remyelination
 Multiple sclerosis anti-CD20 monoclonal antibodies cost-effectiveness research disease-modifying treatment net health benefit quality-adjusted life years
 cognitive assessment cognitive impairment fatigue mood multiple sclerosis premorbid cognitive functioning self-reported cognitive difficulties
 Axonal-glia interaction axonal damage chronic demyelination cuprizone motor function multiple sclerosis myelin repair remyelination
 Alzheimer’s disease CSF GFAP biomarker blood microfluidic assay multiple sclerosis
 Glycerophospholipids Multiple sclerosis Remyelination Sphingolipids Sulfatide rHIgM22
 T-cell transfer adenovirus cellular therapy central nervous system cytomegalovirus encephalitis immune therapy multiple sclerosis progressive multifocal leukoencephalopathy viral infections virus-specific T-cells
 dermatomyositis and polymyositis multiple sclerosis relapse nephrotic syndrome rheumatoid arthritis sarcoidosis systemic lupus erythematosus
 COVID‐19 Pneumocystis jirovecii pneumonia SARS‐CoV‐2 infection multiple sclerosis rituximab
 BRISA digital health multiple sclerosis questionnaire symptoms
 Convenience Multiple sclerosis Ofatumumab Pre-filled syringe Self-medication Treatment satisfaction
 EDSS plus RRMS biomarkers multiple sclerosis neurofilaments
 dexterity fine motor skills grasp pediatrics rehabilitation

 Anklosing spondylitis Biological agents Brain stem / cerebellum Drugs: CNS (not psychiatric) Multiple sclerosis
 COVID-19 Multiple sclerosis T cell repertoires






 MULTIPLE SCLEROSIS NEUROIMMUNOLOGY

 cigarette smoke multiple sclerosis neuroinflammation oxidative stress smoking uric acid
 Contrast media Gadolinium Magnetic resonance imaging Multiple sclerosis
 care partner cost employee multiple sclerosis severity
 autoimmune disease central nervous system generalized anxiety disorder major depression multiple sclerosis psychiatric disorder
 Cladribine tablets Disease-modifying therapy Real-world evidence Relapsing multiple sclerosis
 Assessment everyday memory multiple sclerosis questionnaire reliability translation validity
 Autonomic nervous system dysfunction COMPASS-31 Multiple sclerosis Neuromyelitis optica spectrum disorder Quality of life

 community mobility participation quality of life self-efficacy
 aquaporins-4 azathioprine devic's neuromyelitis optica magnetic resonance imaging ( mri ) transverse myelitis
 Inflammatory demyelinating disorders Stroke mimic Tumefactive demyelinating disorders Tumefactive multiple scleorosis
 COVID-19 Hospitalization Mortality Multiple sclerosis SARS-CoV-2
 MRI multiple sclerosis white matter lesions
 disease progression multiple sclerosis paramagnetic rim lesion ultra-high field MRI
 EDSS depression fatigue multiple sclerosis rTMS sham condition
 MRI deep gray matter multiple sclerosis patient-reported outcomes
 RebiSmart electromechanical autoinjector adherence interferon beta-1a multiple sclerosis


 Aging Cognitive impairment Cortical thinning Language impairment Multiple sclerosis Processing speed
 COVID-19 vaccination Cortical sinus venous thrombosis Guillain–Barré syndrome Multiple sclerosis (MS) Neurological complications Transverse myelitis (TM)
 Adolescent Multiple sclerosis (MS) Myelin oligodendrocyte glycoprotein-immunoglobulin G-associated disease (MOGAD) Neuromyelitis optica spectrum disorder (NMOSD) Ofatumumab
 Lesion network mapping Memory Multiple sclerosis White matter lesion fMRI


 MS toolkit Multiple sclerosis dashboard employment prediction screening




 Cannabidiol Cannabis sativa, PPARγ Phytocannabinoids

 Multiple sclerosis electrophysiology motor-evoked potential pain sensory-evoked potentials
 axon degeneration multiple sclerosis myelin sulfatide
 AXL receptor tyrosine kinase Autophagy Experimental autoimmune encephalomyelitis (EAE) Multiple sclerosis
 COVID-19 vaccination T-cell responses neutralizing antibodies ofatumumab relapsing multiple sclerosis
 Anger Case-Control Study Iran Multiple Sclerosis Object Relations
 Cuprizone Inflammatory cytokines Mesenchymal Stem Cell Multiple Sclerosis
 Dementia Gut-brain axis Inflammatory bowel diseases Multiple sclerosis Parkinson disease
 Bioactive lipids Lipid nanoparticles Multiple sclerosis Nasal administration Neuroinflammation

 7 Tesla Multiple sclerosis Sodium imaging Spectroscopic imaging Susceptibility weighted imaging
 COVID-19 mRNA vaccine diabetes insipidus lymphocytic hypophysitis multiple sclerosis optic neuritis
 aging disability elderly infections malignancy


 MRI central vein sign comorbidities diffusion multiple sclerosis
 capillary density macular ganglion cell and inner plexiform layer macular ganglion cell complex optical coherence tomography optical coherence tomography angiography peripapillary retinal nerve fiber layer relapsing-remitting multiple sclerosis
 Melatonin Multiple sclerosis Systematic review
 B cells Demyelination Experimental autoimmune encephalomyelitis Microglia Multiple sclerosis Myeloid cells Secondary progressive
 Dimethyl fumarate Hemostasis Multiple sclerosis Platelets Thrombosis
 Antigen presentation Autoimmunity Autophagy Multiple sclerosis Rheumatoid arthritis Systemic lupus erythematosus
 GalR1 GalR2 GalR3 experimental autoimmune encephalomyelitis galanin immunohistochemistry mRNA multiple sclerosis
 COVID-19 SARS-CoV-2 multiple sclerosis relapse vaccination
 Alzheimer's disease Danger associated molecular patterns Extracellular mitochondrial DNA Extracellular ribosomal RNA Multiple sclerosis Neutrophil extracellular traps Non-coding RNAs Parkinson's disease Pattern recognition receptors Stroke
 Anti-CD20 HBV Infection prevention Multiple sclerosis Seroprotection VZV
 autoimmune disorders diabetes mellitus II multiple sclerosis vascular comorbidity
 attention biomarkers blood cognition memory metal multiple sclerosis nanoparticles neuropsychological tests processing speed of information
 dementia multiple sclerosis neuromyelitis optica spectrum disorders population risk
 MOG-antibody disease aquaporin-4 neuromyelitis optica spectrum disorders fatigue multiple sclerosis resting-state functional MRI
 Fahn tremor rating scale cooling functional performance intention tremor multiple sclerosis upper limb
 Alzheimer's disease Mendelian randomization Parkinson's disease bullous pemphigoid multiple sclerosis stroke
 MOGAD MRI MS NMOSD typical lesions
 Balance Multiple sclerosis Non-pharmacological interventions Physical therapy Posturography Tai chi Chuan

 Age-related macular degeneration Color vision Cone contrast threshold testing (CCT) Epiretinal membrane Multiple sclerosis Optic neuritis Retinal vein occlusion
 Brain Eye Multiple sclerosis T cells Uveitis
 Fatigue Multiple sclerosis Quality of life
 anxiety body mass index depression fatigue multiple sclerosis physical activity
 bladder mass mimicking neoplasm neurosarcoidosis nodular leptomeningeal enhancement


 Bladder Cystoscopy Melanosis Neurogenic voiding dysfunction Urgency
 Hypogammaglobulinemia Infection Multiple sclerosis Nmosd Rituximab, ocrelizumab
 Cladribine and pregnancy Disease modifying therapy Fingolimod and pregnancy MS and pregnancy


 MRI atrophy measurement brain volume change deep learning longitudinal analysis multiple sclerosis
 Multiple sclerosis SPMS disease course disease-modifying treatments progression

 Nf-kB PI3K/Akt/mTOR autophagy curcumin mitochondria

 Antibody antigen interaction Antibody isolation CDR3 charge Neuronal binding



 Trigeminal neuralgia demyelinating disease disease modifying therapies inflammation vascular compression


 Cognitive function Correlation HDL cholesterol Metabolic syndrome Schizophrenia


 Antimicrobial agent aetiology autoimmune diseases microbiota risk factor
 backwards walking balance gait lower limb strength muliple sclerosis
 Alzheimer’s disease Parkinson’s disease amyotrophic lateral sclerosis fecal microbiota transplant gut microbiome multiple sclerosis neurodegenerative disease
 Anti-CD20 human MAb DMT-naïve Disease-modifying therapies Drug utilization Relapsing multiple sclerosis

 central nervous system multiple sclerosis physical therapy quality of life
 Chart review Cladribine tablets Disability Fingolimod Real-world data Relapse Relapsing-remitting multiple sclerosis
 Biomarkers Cerebrospinal fluid Kappa free light chain index Multiple sclerosis Prognosis
 ADEM MOGAD Multiple sclerosis Neuroimmunology Outcomes Pediatric
 automatic segmentation choroid plexuses inflammation multiple sclerosis
 ABC transporter ABCC1 AD mouse model Alzheimer’s disease BBB DMF blood–brain barrier dimethyl fumarate drug repurposing fingolimod multiple sclerosis
 clinically isolated syndrome multiple sclerosis normal-appearing grey/white matter proton magnetic resonance spectroscopy treatment effect
 discontinuation disease activity fingolimod multiple sclerosis rebound switch
 inflammation iron magnetic resonance imaging multiple sclerosis oxidative stress
 Multiple sclerosis Quality control Quality indicators Real world data Register
 emotional susceptibility fatigue interoceptive awareness phsyical activity


 Dimethyl fumarate Minority populations Multiple sclerosis Safety and effectiveness
 Cladribine tablets Disease-modifying therapy Multiple sclerosis Patient-reported outcomes
 axonal loss biomarker corneal confocal microscopy multiple sclerosis neurodegeneration
 Italian Neuroimaging Network Initiative atrophy pipelines brain atrophy multiple sclerosis
 CNS-compartmentalized inflammation Human B cells Human macrophage Human microglia Multiple sclerosis
 NA-AION multiple sclerosis myopic/tilted optic discs optic disc drusen optic neuritis papilledema peripapillary hyper-reflective ovoid mass-like structures
 ALS mitochondria neurologic disease oxidative stress physiopathology treatment
 Acute disseminated encephalomyelitis Anti-myelin oligodendrocyte glycoprotein-IgG associated disorders CNS, central nervous system Case report Inflammatory demyelinating disease M. pneumoniae infection MOGAD, Anti-myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G associated disorders MS, multiple sclerosis NMOSD, neuromyelitis optica spectrum disorder T2WI, T2 weighted images
 experimental autoimmune encephalomyelitis microglia multiple sclerosis myeloid cells transcriptomics
 Cognitive decline Cogstate IIV Intra-individual variability Multiple sclerosis Progressive neurological diseases
 Patient Determined Disease Steps multiple sclerosis reliability systematic review validity

 Alzheimer’s disease Financial performance Mild cognitive impairment Multiple sclerosis Neurodegenerative diseases Parkinson’s disease
 COVID-19 Cladribine Multiple sclerosis
 lipid rafts multiple sclerosis myelin sphingolipid sulfatide
 Cyclophosphamide Experimental allergic encephalomyelitis Hematopoietic stem cells Microglia Multiple sclerosis
 Alzheimer's disease KEAP1 NRF2 Parkinson's disease multiple sclerosis neurodegenerative disease
 Fear Multiple sclerosis Rehabilitation Spinal cord injuries Wheelchairs
 RiboTag astrocyte cuprizone demyelination multiple sclerosis remyelination
 adverse events anti-drug antibodies exacerbations immunogenicity multiple sclerosis natalizumab
 COVID-19 GABA GABAA-receptor GABAB-receptor SARS-CoV-2 cancer homotaurine long COVID multiple sclerosis type 1 diabetes
 experimental autoimmune encephalomyelitis ketogenic diet multiple sclerosis optic nerve optic neuritis retinal ganglion cells
 Contraception Estrogen Hormone Menstrual cycle Multiple sclerosis Symptom




 multiple sclerosis neuromyelitis optica spectrum disorder optic neuritis visual acuity
 Aquaporin-4 MRI Multiple sclerosis Myelin oligodendrocyte glycoprotein Optic neuritis Optical coherence tomography


 MS SDM balance fatigue gait disorders neurogenic bladder pain spasms
 COVID-19 Multiple sclerosis T cell response disease modifying therapies mRNA vaccine
 Nogo receptor-Fc axonal regeneration experimental autoimmune encephalomyelitis haematopoietic stem cells remyelination
 Digital health care access connected care geography multiple sclerosis myasthenia gravis myositis neurology remote patient monitoring specialised care networks

 COVID19 SARS-CoV-2 vaccination disease-modifying therapies immune response multiple sclerosis
 Multiple Sclerosis (MS) animal research central nervous system (CNS) demyelination ethics green fluorescent protein (GFP) molecular physiology macrophages oligodendrocytes parabiosis remyelination
 BTLA TNFα Treg cells activation autoimmunity dendritic cell maturation multiple sclerosis programmed cell death tolerance tolerogenic dendritic cells
 MRI PAEDIATRIC
 HCAR2; lupus; neuroinflammation; neuropathic; niacin; nociception; synaptic β-hydroxybutyrate; cytokines


 aide humaine aide sociale disability droit financial benefit handicap human assistance invalidité prestation financière right social assistance vie professionnelle working life


 Alzheimer's disease cancer chronic obstructive pulmonary disease cyclic AMP drug target inflammation multiple sclerosis phosphodiesterase short isoform traumatic brain injury

 digital immunoassay multiple sclerosis neuronal injury validation

 IGFBP7 LAMP2 MS NMOSD diagnosis prediction
 FRET GPCR T cells cAMP experimental autoimmune encephalomyelitis multiple sclerosis

 COVID-19 pandemic Disability Exercise Online exercise


 Asian Indian MS NMOSD ancestry race

 Antioxidants Dietary iron Immune cells Iron chelators Magnetic resonance imaging Oxidative stress
 Cognitive assessment Cognitive impairment Cognitive screening MSNQ Neuropsychology
 Diet MS Microbial dysbiosis Microbiota Phytoestrogen

 Macroprolactin Multiple sclerosis Myelin oligodendrocyte glycoprotein antibody–associated diseases Neuromyelitis optica spectrum disorders Prolactin
 Cell cycle EGCG Molecular docking Network pharmacology T cell-mediated autoimmune diseases multiple sclerosis
 Autoimmune diseases Autoimmune hepatitis CXCL16 CXCR6 Iinflammatory bowel diseases Multiple sclerosis Psoriasis Rheumatoid arthritis
 COVID-19 central nervous system demyelinating diseases multiple sclerosis neuroinflammatory diseases vaccination
 cannabidiol experimental autoimmune encephalomyelitis leukocyte recruitment multiple sclerosis
 Antibody-secreting cells Autoimmunity CNS tolerance Multiple sclerosis Viral infection
 CX3CL1 CX3CR1 NG2 OPC chemokine differentiation multiple sclerosis myelination neuron-glia regeneration
 CS-SENSE (compressed sensing sensitivity encoding) multiple sclerosis myelin quantitative magnetization transfer (QMT) selective inversion recovery (SIR)
 anxiety cognitive impairment depression experience sampling fatigue multiple sclerosis (MS) pain sleep
 CP: Immunology CP: Neuroscience TREM2 experimental autoimmune encephalomyelitis macrophage microglia monocyte multiple sclerosis phenotype spinal cord injury
 4-Aminopyridine Alzheimer's disease cytotoxicity multiple sclerosis toxicity
 Atopic dermatitis Autoimmune illness Autoimmune illnesses Crohn’s disease Cytomegalovirus Disease associations Eczema Epidemiology Epstein-Barr virus Herpes virus Multiple sclerosis Rheumatoid arthritis Ulcerative colitis
 CD4+ T cell subsets. T cells autoimmune diseases ivermectin multiple sclerosis
 Cardiorespiratory fitness Exercise Functional electrical stimulation Multiple sclerosis Rehabilitation Spinal cord injury
 Alzheimer age-related macular degeneration amblyopia epilepsy multiple sclerosis myopia presbyopia virtual reality
 Astrocyte Depression Glial fibrillary acidic protein Multiple sclerosis Repetitive transcranial magnetic stimulation
 cfDNA liquid biopsy microRNA neurological diseases
 Acute disseminated encephalomyelitis Adenovirus Eight-and-a-half syndrome Encefalomielitis diseminada aguda Esclerosis múltiple Internuclear ophthalmoplegia Multiple sclerosis Oftalmoplejía internuclear Síndrome del ocho y medio
 COVID-19 disease modifying therapy multiple sclerosis smoking vaccine
 Fatigue Motor performance Multiple sclerosis Non-invasive brain stimulation Pain Spasticity
 exercise multiple sclerosis physical activity physiotherapy steps-count
 AD CNS MS fibrin fibrinogen neurodegenerative disease
 Glucose metabolic reprogramming autoimmune diseases glucose transporter glycolysis metformin





 Adrenoleukodystrophy Alzheimer’s disease Multiple Sclerosis Omega-9 fatty acid Parkinson’s disease
 Aicardi-Goutières syndrome aging cerebral interferonopathies multiple sclerosis neurodegenerative diseases neurotoxin traumatic brain injury type I interferons
 Booster Covid-19 Multiple sclerosis SARS-CoV-2 Vaccine
 EDSS progression in MS brain network measures graph theory relapsing-remitting multiple sclerosis structural covariance


 Microvascular decompression Tic douloureux Trigeminal neuralgia
 COVID-19 PASC SARS-CoV-2 TDM anosmia disease-modifying therapy hyposmia interferon long COVID long-haul COVID multiple sclerosis neuroinflammation olfaction olfactory olfactory training post-acute sequelae of SARS-CoV-2 infection smell smell disorders threshold detection identification
 MRI MULTIPLE SCLEROSIS NEUROIMMUNOLOGY
 genome-wide expression analysis multiple sclerosis optic neuritis
 L-proline azetidine-2-carboxylic acid endoplasmic reticulum microglia multiple sclerosis neuroinflammation unfolded protein response
 Bacillus SOX5 autoimmune disorder fermented camel’s milk multiple sclerosis myelin-binding protein
 Multiple Sclerosis Parkinson disease chronic neurological diseases neurorehabilitation telerehabilitation
 immunoprecipitation membrane multiple sclerosis myelin basic protein proximity labeling proteomics
 chronic lung diseases lung cancer lung microbiome lung–brain axis multiple sclerosis

 Data quality control Grand mean Monitoring Multicenter clinical trials Registry data
 Biogenic amines Experimental autoimmune encephalomyelitis Monocytes Multiple sclerosis Neuroinflammation
 cuprizone model intranasal delivery route miR-155-antagomir multiple sclerosis teriflunomide
 Alzheimer cerebrospinal fluid glycolysis metabolism metabolites monocytes multiple sclerosis neuroinflammation tricarboxylic acid cycle


 MS-related fatigue cognitive behavioural therapy e-health rehabilitation medicine symptom management


 Artificial Intelligence Multiple sclerosis Open innovation Patient and public involvement
 complement demyelination inflammation leptomeninges microglia



 Density functional theory Dimethyl fumarate Diroximel fumarate Drug delivery G-C(3)N(4) Mono methyl fumarate
 Dimethyl fumarate comparative effectiveness precision medicine propensity score real-world data teriflunomide treatment effect heterogeneity


 adherence disease-modifying therapy medication belief quality of life

 Alzheimer's disease Curcumin Inflammation Neurological disorders Parkinson's disease
 COVID-19 N-Phenyl benzamide cancer inflammatory pain p-38 MAPK rheumatoid arthritis

 Breaking bad news Doctor-patient communication Huntington’s disease Interpretative phenomenological analysis Motor neurone disease Multiple sclerosis Neurodegenerative conditions Parkinson’s disease
 Alzheimer’s disease D-serine L-serine Parkinson’s disease brain injury metabolism multiple sclerosis neuroinflammation
 IgG index multiple sclerosis myelin oligodendrocyte glycoprotein antibody-associated disease oligoclonal bands relapse rate
 Alzheimer’s disease Parkinson’s disease immune response macrophage microglia multiple sclerosis spinal cord injury traumatic brain injury
 HAM/TSP pathogenesis HTLV-1 Nipah virus (NiV) encephalitis measles virus multiple sclerosis neuro-infection
 Alzheimer disease Bioengineered EVs Drug delivery Extracellular vesicles MSC-derived EVs Multiple sclerosis Neurodegenerative disorders Parkinson disease
 Heshouwu (Radix Polygoni Multiflori) T cell response encephalomyelitis, autoimmune, experimental gastrointestinal microbiome
 Addiction Alzheimer’s disease Exosome Huntington’s disease Multiple sclerosis Parkinson’s disease
 High mobility group box 1 Neuroinflammation Receptor for advanced glycation endproducts Toll-like receptor 4
 AQP4 Area postrema syndrome Case report Central nervous system Longitudinal extensive transverse myelitis Magnetic resonance imaging Multiple sclerosis NMOSD Spinal movement disorder Tonic seizures autoimmune

 ALITHIOS ASCLEPIOS I/II Anti-CD20 monoclonal antibody Benefit-risk Ofatumumab Relapsing multiple sclerosis Self-administration Subcutaneous


 autoimmune disease ferroptosis immune system therapeutic target


 Diplopia bilateral internuclear ophthalmoplegia dengue hemorrhagic encephalitis pontine and midbrain hemorrhage





 Correlate Emotionalism Neurological disorders Predictor Systematic review
 cuprizone microglia markers multiple scleorsis remyelination siponimod vitamin D3
 Alzheimer’s disease dementia depression indoleamine 2,3-dioxygenase neuroinflammation tryptophan


 Amyotrophic Lateral Sclerosis Biomarker Circulating blood lymphocytes Disease progression NK lymphocytes
 Alzheimer’s disease EPA/DHA/LA/GLA Huntington’s disease PUFA Parkinson’s disease amyotrophic lateral sclerosis clinical trials multiple sclerosis omega-3 omega-6 polyunsaturated
 Lesion detection Lesion segmentation MRI Multiple sclerosis Systematic review
 Blood–brain barrier Brain microvascular endothelial cells Central nervous system Extended interval dosing Intercellular adhesion molecule-1 Multiple sclerosis Natalizumab Progressive multifocal leukoencephalopathy Standard interval dosing Vascular cell-adhesion molecule-1
 Autoimmune myelitis Clinically isolated syndrome Differential diagnosis Idiopathic Mimics Multiple sclerosis Myelin oligodendrocyte glycoprotein antibody associated disorder Myelopathies Neuromyelitis optica spectrum disorder Spinal cord infarction
 Aquaporin-4 immunoglobulin G Glial fibrillary acidic protein Multiple sclerosis Neurofilament light chain protein Neuromyelitis optica spectrum disorder Ubiquitin C-terminal hydrolase L1
 Burden Comorbidity Epidemiology Multiple sclerosis Secondary conditions
 Alzheimer’s disease HIV-associated neurocognitive disorder Huntington’s disease Parkinson’s disease amyotrophic lateral sclerosis dementia interferon-alpha multiple sclerosis
 Alzheimer’s disease Parkinson’s disease amyotrophic lateral sclerosis astrocytes cell signaling gliosis hydrocarbons immune response inflammation metals microglia multiple sclerosis nanoparticles neurodegenerative diseases neuroinflammation neurological disorders occupational injury traumatic brain injury workplace toxicants
 Algorithms Deep learning Magnetic resonance imaging Multiple sclerosis White matter
 B lymphocytes CCR5 antagonist EAE NF-κB/IκB-α Notch signaling multiple sclerosis
 NMOSD OSE chronic inflammatory CNS disorders immunomodulation progressive multiple sclerosis
 Clinical assessment Clinical measurement Clinical outcome assessment Clinical trial Cost effectiveness research Medical decision-making Multiple sclerosis PRO measure Patient-reported outcome (PRO)
 Autoimmune diseases Inflammation Ligand Multiple sclerosis Rheumatoid arthritis Systemic lupus erythematosus T cell immunoglobulin and mucin domain-containing protein 3 T cells
 Age Autoimmune inflammatory demyelination Infectious myelitis Multiple sclerosis Pediatric Transverse myelitis
 Sjögren’s syndrome T follicular helper cells (TFH cells) T follicular regulatory cells (TFR) autoimmune diseases multiple sclerosis rheumatoid arthritis systemic lupus erythematosus type 1 diabetes


 epidemiology incidence prevalence regional differences registry
 long-term care nursing home outpatient skilled nursing facility specialist
 EDTA EPR ROS cytokines neurodegeneration neurotoxicity oxidative damage thiols’ redox status


 Balance Falling Performance tests Step reaction time Walking
 autoimmunity brain/gut interaction gluten free diet nutrition small intestine

 Cooling Exercise Garment Physical function Vest
 MS OCT electroretinography (ERG) mfPERG mfPhNR optic neuritis (ON)

 african American biomarker black dimethyl fumarate epigenetics hispanic latino
 gene therapy mesenchymal stem cell (MSC) miRNA neurogenesis neurological diseases


 Anxiety Gut–brain axis Microbiome PANS
 autonomic dysfunction postural orthostatic tachycardia syndrome pots sci spinal cord injury syncope tachycardia


 Alzheimer’s disease blood-brain barrier neurodegeneration neuroinflammation neutrophil extracellular traps neutrophils (PMNs) stroke traumatic brain injury
 Optic neuritis Status epilepticus Encephalitis
 EBV cancer latent proteins lymphoma treatment

 Gammaglobulin Immunoglobulin Sandoglobulin Vivaglobin Carimune Gammagard Privigen Cuvitru Gamunex gamma-Globulins Immune globulin Gamma globulin gamma-Globulin Gamimune N Globulin, immune Immune endoglobulin Globulins, gamma- IVIG Human immune globulin g Globulin, Immune [USP] EINECS 232-706-1 9007-83-4 Immune globulin subcutaneous (human)-hipp Cutaquig
 aging astrocyte microglia myelin oligodendrocyte progenitor remyelination

 glia lipid membrane myelin myelin protein myelination


 Alzheimer’s diseases cancer commitment complex multiple sclerosis pre-spliceosome complex splicing
 Parkinson’s disease multiple sclerosis music-based therapy rhythmic auditory stimulation (RAS) spinal cord injuries stroke wearables
 COVID-19 autoimmunity bystander activation central tolerance epitope spreading molecular mimicry multiple sclerosis peripheral tolerance rheumatoid arthritis systemic lupus erythematosus type 1 diabetes
 Bifidobacterium FMT Lactobacillus Probiotics VMT genitourinary tract gut microbiota therapeutics vaginal dysbiosis
 Astrocyte Glial cells Microglia Multiple sclerosis Neuron Sphingosine 1-phosphate Sphingosine 1-phosphate lyase
 Autoimmune diseases Diagnosis Fourier-transform infrared spectroscopy Inflammatory bowel disease Multiple sclerosis Psoriasis Rheumatoid arthritis Type 1 diabetes mellitus
 IL-10 microbiome multiple sclerosis neuroinflammation regulatory B cells (Bregs)
 Aging Cognition Cytokines DTI Depression Dopamine Inflammaging Inflammation Multiple sclerosis Neurofilaments
 Alzheimer’s disease Canavan disease Parkinson’s disease blood–brain barrier central nervous system drug delivery system glioblastoma multiforme multiple sclerosis viral vector virus-like particles
 N-acetylaspartate (NAA) Oli-neuM epigenetics histone deacetylases (HDACs) multiple sclerosis (MS) neurodegeneration remyelination
 extended interval dosing multiple sclerosis natalizumab progressive multifocal leukoencephalopathy standard interval dosing
 Biomodulina T COVID-19 Immunomodulation Immunosenescence Immunotherapy InmunyVital Multiple sclerosis T cells Thymic factor Thymus factor
 experimental autoimmune encephalomyelitis immune tolerance. interferon-gamma microglia multiple sclerosis myeloid cells neurodegenerative disease neuroinflammation
 depressive symptoms hopelessness relapsing-remitting multiple sclerosis suicide workplace difficulties
 Energy management education Fatigue Health-related quality of life High-intensity interval training Multidisciplinary rehabilitation Multiple sclerosis

 Calcium signaling Experimental autoimmune encephalomyelitis Store-operated calcium entry
 COVID-19 cancer chronic illness diabetes health belief model multiple sclerosis qualitative analysis vaccine hesitancy
 adverse outcome pathways cancer chemotherapy metabolomics approach multiple sclerosis topoisomerase inhibitors
 Autoimmunity Fatty acid metabolism Multiple sclerosis Regulatory T cells Stearoyl-CoA desaturase-1
 amide chemical exchange saturation transfer multiple sclerosis myelin relayed nuclear Overhauser effect

 Brain Gut Microbiome Neurodegeneration Neuroinflammation
 Chemokine Nerve injury Neutrophil Neutrophil extracellular trap Phagocytosis Polymorphonuclear leukocyte Wallerian degeneration



 Anti-CD20 antibodies Hepatitis B Multiple Sclerosis Ocrelizumab Reactivation Rituximab
 Alzheimer’s disease Boswellic acid Natural products Neurodegenerative disease Neuroprotective Parkinson's disease
 cGAS cerebral endothelial cells cortical neurons neuroinflammation palmitic acid
 Alzheimer’s disease Brain imaging Depression Meta-analysis Microglia Multiple sclerosis Neuroinflammation Parkinson’s disease Schizophrenia TSPO PET



 chronic fatigue syndrome cytokines depression mood disorders neuroimmune neuroinflammation
 MENDELIAN RANDOMIZATION RANDOMIZED CONTROLLED TRIALS VITAMIN D

 Chair stand test concurrent validity known-group validity minimal detectable change reliability
 Follow-up Guideline Harmonization Imaging Sequences
 CancerHERVdb HERV cancer database expression human endogenous retrovirus

 CD8+ T lymphocytes cytotoxicity neurodegenerative diseases neurotoxicity tissue resident memory CD8+ T cells
 MRI volumetrics Multiple scleroris disability-progression glial-fibrillary-acidic-protein natalizumab neurofilament light
 demyelinating disease drug adverse effects encephalitis fungal infection ocrelizumab
 EAE Factor XI Multiple sclerosis Thrombin
 age bone marrow brain neurons and neuroinflammatory cells cuprizone melatonin multiple sclerosis oxidative stress thymus
 Extended interval dosing Multiple sclerosis Natalizumab Real-world evidence
 Autoimmune diseases Autoimmunity COVID-19 Multiple sclerosis
 COVID-19 IMMUNOLOGY MULTIPLE SCLEROSIS
 Cerebral hemorrhage Cerebral microbleeds Hemorragia cerebral Magnetic resonance imaging Microhemorragias cerebrales Multiecho gradient recalled echo Resonancia magnética Secuencia de eco gradiente Secuencias de susceptibilidad magnética Susceptibility weighted imaging
 S1P Sphingosine-1-phosphate assay spinster homology 2 spns2 transporter inhibitor
 acute pancreatitis cannabinoid receptor 1 cannabinoid receptor 2 cannabinoids cannabis use gastroesophageal reflux disorder (gerd) peptic ulcer diseases
 catatonia electroconvulsive therapy (ect) inflammatory and demyelinating disease recurrent catatonia schizoaffective disorder
 Astrocytes ECM proteins Microglia Neurodegenerative diseases Neuroinflammation TNFα
 Cell biology Cellular neuroscience Immunology Neuroscience

 Alzheimer’s disease Epilepsy Flavonoid Hesperidin Neuroprotection Parkinson’s disease
 Adverse reaction COVID-19 SARS-CoV-2 Side effect Vaccination

 Hydroxycarboxylic acid receptor (Hcar)2 Immunomodulation NAD+/NADP Neurological diseases Niacin treatment Phagocytosis
 Prognosis communication mortality narrative review neurologic disease
 Cladribine 2-Chloro-2'-deoxyadenosine Leustatin MAVENCLAD 2-Chlorodeoxyadenosine Cladarabine Chlorodeoxyadenosine 4291-63-8 2-CdA 2-Chloro-2'-deoxy-beta-adenosine ADENOSINE, 2-CHLORO-2'-DEOXY- UNII-47M74X9YT5 CCRIS 9374 RWJ 26251 HSDB 7564 NSC 105014-F 47M74X9YT5 Cladribine [USAN:USP:INN:BAN] NSC 105014 BRN 0624220 2-Chloro-6-amino-9-(2-deoxy-beta-D-erythropentofuranosyl)purine

 AAV brain gene therapy microglia

 ERVs Epigenetics Glial cells Immune cells Infection Inflammation Neurodegeneration Neurodevelopmental disorders Neurological diseases
 COVID-19 GASTROENTEROLOGY IMMUNOLOGY NEUROLOGY RHEUMATOLOGY

 Health-related quality of life Neurorehabilitation Robot-assisted therapy Systematic review Virtual reality
 Carbamazepine Multiple sclerosis Myelitis Pain Symptomatic
 ApaI BsmI FokI SNP TaqI VDR Vitamin D autoimmunity multiple sclerosis systemic lupus erythematosus
 blood-derived CSF molecules cerebrospinal fluid (CSF) analysis hyperbolic function intrathecal synthesis markers multiple sclerosis (MS) oligoclonal bands (OCBs)
 B cell depletion anti-CD20 monoclonal antibodies hypogammaglobulinemia multiple sclerosis neuroimmunology neuromyelitis optica
 HOG cells corticosteroids demyelination multiple sclerosis oligodendrocyte precursor cells oligodendrocytes remyelination
 Cerebral palsy Multiple sclerosis Parkinson’s disease Poliomyelitis Total hip arthroplasty Total hip replacement
 Depression Neuromyelitis optica Sexual dysfunction
 Alzheimer’s disease bispecific antibodies blood-brain barrier brain drug delivery central nervous system disorders molecular trojan horse multiple sclerosis recombinant monoclonal antibodies
 announcement consultation care pathway consultation d’annonce coordination infirmière spécialisée sclérose en plaques multi-professional team multiple sclerosis nurse specialist parcours de soins therapeutic education éducation thérapeutique équipe pluriprofessionnelle
 Multiple sclerosis (MS) Psychosocial difficulties Quality of life Social relations
 Epstein Barr virus autoimmune diseases initiator latency lupus multiple sclerosis promoter
 Alzheimer's disease Metabolic reprogramming Microglia Multiple sclerosis Parkinson's disease
 Child health Encephalitis Immunotherapy Multiple sclerosis
 Akkermansia muciniphila Gut inflammation Hypobaric hypoxia Multiple sclerosis Obesity Probiotics
 S-allylcysteine experimental autoimmune encephalomyelitis extra virgin olive oil oxidative stress transcranial magnetic stimulation
 Asymptomatic lesions Disability accrual Spinal cord MRI Treatment optimization
 Cladribine Real-world evidence Treatment response
 Distance weighted discrimination Multiway Classification Sparsity Tensors
 MULTIPLE SCLEROSIS STATISTICS
 CREB Dephosphorylation Neurodegeneration diseases Neuronal survival Phosphorylation Synaptic plasticity
 Demyelination Matrine Neurodegeneration Neuroinflammation Neuroprotection
 Toll-like receptor cognition inflammation schizophrenia
 Brain development Energy metabolism Glia Mitochondria Neurologic disorders Neuron Neurotransmission Prohibitin 1 Prohibitin 2 Psychiatric disorders
 Adaptive immunity Cytotoxic T cells Neurodegenerative disease Regulatory T cells Stroke
 Central nervous system Citrullination Disease Peptidylarginine deiminase 4

 analytical phase biomarkers blood cerebrospinal fluid neurodegeneration neurofilament light chain neurological disease post-analytical phase pre-analytical phase
 Allopregnanolone Neurodegenerative disease Neuroprotection Progesterone
 adaptive immune system amylase–trypsin inhibitors autoimmunity gluten inflammation innate immune system non-celiac wheat sensitivity quality of life
 Antigen-specific Autoantibody Autoimmunity Autoreactivity B cells Tolerance
 Calcium and bone Respiratory system
 Brain EAE Farnesol Isoprenoids Transcriptomics
 Autoimmune disease Autoimmune neurological disease Sleep Sleep disturbances Video-polysomnography
 molecular mechanism neuronal activity oligodendrocytes remyelination therapeutic advances
 Painful tonic spasms myelitis neuromyelitis optica spectrum disorder
 Biological sciences Cellular neuroscience Neuroscience
 Neuroinflammation Th-17 cells cytokines interleukin-17 interleukins neurodegenerative diseases


 Neurodegeneration Neuroinflammation Nuclear receptors Orphan receptors


 behavior homeostasis meningeal T cells meningeal immunity meningeal lymphatic vessels neurodegenerative diseases neuroimmunology

 C13-histidine Demyelinating disease EAE mouse model Isobaric labeling Mass spectrometry Proteomics Remyelination
 EMT NETs PADI4 apoptosis cancer citrullination
 Drug repurposing Micro RNAs Microbiota-gut-brain axis Natural compounds Neurodegenerative diseases Neuropsychiatric disorders Post-translational modifications
 Selenium mood neurodegeneration neuroprotection pharmacology therapeutic agents


 Attention Contrastive learning Disentanglement Harmonization MRI Standardization Synthesis
 Disability Disease-modifying therapy Health care access Health policies Multiple sclerosis Socioeconomic condition Socioeconomic indicator Socioeconomic status
 Alzheimer disease COVID-19 Meta-analysis Multiple sclerosis Parkinson disease Systematic review
 Astrocyte Experimental autoimmune encephalomyelitis Microglia Multiple sclerosis NLRP3

 Brain regeneration Exosomes Mesenchymal stem cells Microvesicles Secretome Secretome formulation
 CYP46A1 Cholesterol Cholesterol 24-hydroxylase Neurodegenerative disorders Soticlestat
 Enfermedades neurodegenerativas Enfermedades neurológicas Factor de riesgo Neurodegenerative diseases Neurological diseases Prevención Prevention Risk factor Suicide Suicidio
 Parkinson Parkinson disease balance biomechanics dual task dual task cost fall gait kinesiology low back pain movement multiple sclerosis neurological neurology smartphone stroke turning turning coordination walk
 Diffusion MRI Diffusion tensor imaging Image denoising Multiple sclerosis Spinal cord
 leucine physical activity protein rehabilitation sarcopenia

 Neurodegenerative disease biomarker drug delivery exosomal miRNA exosome
 AD ALS MS MSCs Neurodegenerative disorders PD
 AL-8810 axon brain central nervous system cyclooxygenase inhibitors neuron neuroprotection ocular polyunsaturated fatty acids prostaglandins

 Cerebrospinal Fluid (CSF) Exosome MicroRNA (miRNA) Relapsing Remitting MS (RRMS) Serum U6
 Raman microspectroscopy machine learning mitochondria multiple sclerosis myalgic encephalomyelitis/chronic fatigue syndrome peripheral blood mononuclear cells single cell
 COVID-19 Multiple sclerosis SUMF1 rs794185
 Cognition Japanese Multiple sclerosis PST Z-score

 Parkinson's disease multiple sclerosis neurologic disease sexuality stroke
 assistive devices cerebral palsy educational level multiple sclerosis physical activity quality of life
 AMPA receptor trafficking Alzheimer's disease Attention-deficit/hyperactivity disorder (ADHD) Autism spectrum disorder Endocytosis Epilepsy Glioblastoma Huntington's disease Ischemic stroke Multiple sclerosis Parkinson's disease Traumatic brain injury
 MT: Oligonucleotides: Therapies and Applications arginase-2 inflammation macrophages miR-155 microRNA multiple sclerosis target site blockers
 complement immunity neurodegeneration neuroinflammation therapy
 Alzheimer's disease Parkinson's disease T cells cognitive impairment inflammageing ischemic stroke multiple sclerosis
 Colitis DSS EAE IL-2 Inflammation Microbiota Multiple sclerosis Musculin Th17
 Alzheimer’s disease dementia exercise intervention neurodegeneration neurofilament light
 Cognitive impairment Cognitive rehabilitation Motor rehabilitation Multiple sclerosis
 EAE IL-11 NLRP3 inflammasome monocyte multiple sclerosis
 aging alzheimer’s disease dementia klotho neuroprotection
 CCL13 MCP-4 NF-κB Th2 cytokines human diseases type 2 immunity


 Alzheimer’s Disease NRF-2 dimethyl fumarate heme oxygenase microglia
 Susac syndrome autoimmune vasculopathy encephalopathy hearing loss retinal occlusions
 COVID-19 clinical trials coronavirus interferons—pharmacology mode of administration
 Adalimumab central nervous system drug-induced demyelination rheumatoid arthritis

 Amide Benzimidazoline-2-thione Crystal structure Hydrazide Inflammatory diseases Myeloperoxidase
 Computational bioinformatics Microbiome
 Microglia depletion Microglia replacement Microglia repopulation Microglia transplantation
 Dietary restriction Epilepsy Intermittent fasting Ischemic stroke Neurodegenerative disease Special diet mimetic
 Olfaction Olfactory dysfunction Sniffin' sticks Susac syndrome

 cerebral vasculitis hemorrhage imaging ischemia neurosarcoidosis sarcoidosis
 GPR15 GRKs caveolin clathrin dynamin internalization

 Aquaporin-4-IgG (AQP4-IgG) MOG-IgG associated disorders (MOGAD) clinically isolated syndrome (CIS) multiple sclerosis (MS) neuromyelitis optica spectrum disorders (NMOSD) optic neuritis (ON)
 Economic burden cost of illness economic impact healthcare cost productivity loss systematic review
 Basal ganglia COVID-19 Fatigue Neuroimaging Post-COVID syndrome Thalamus


 Amyotrophic lateral sclerosis Biomarker Kennedy’s disease Motoneuron disease Neurodegeneration Optical coherence tomography
 astrocyte chitinase-3-like protein 1 glioma ischemic stroke neurodegeneration traumatic brain injury
 ADAM’s CX3CL1 Fraktaline MMP’s neurodegeneration

 Fingolimod/FTY720 Neurodegeneration S1P-lyase (SGPL1) Sphingosine 1-phosphate (S1P) Sphingosine 1-phosphate receptor (S1P(1-5)) Sphingosine kinase
 CNS repair EAE cuprizone heparan sulfate multiple sclerosis myelination
 CD8+ T lymphocytes GM-CSF chemokine cytokine macrophage microglia
 Aquaporin 4-IgG Factors Misdiagnosis Neuroimmunologist Neuromyelitis optica spectrum disorder
 Economic evaluation catheter neurogenic bladder spinal cord urinary tract infection

 Autoimmune Dietary Modified atkins Neuroimmunology Obesity
 Alzheimer’s disease COVID-19 Lactoferrin Neuro-COVID-19 Parkinson’s Disease Redox SARS-CoV-2 blood-brain barrier brain tumor mental health neurological symptoms
 IL-6 cytokines inflammation multiple sclerosis osteopontin relapses

 Elevated plus maze test GFAP IBA MOG35 − 55 TNF-α Tail suspension test
 ADC, apparent diffusion coefficient CBF, cerebral blood flow CLIPPERS CNS, central nervous system CSF, cerebrospinal fluid DOT, density of tracts DTI, diffusion tensor imaging DWI, diffusion-weighted imaging Diffusion tensor imaging FLAIR, fluid attenuated inversion recovery ITC, International Tomography Center MPF, macromolecular proton fraction MS, multiple sclerosis Macromolecular proton fraction mapping PWI, perfusion-weighted imaging Perfusion-weighted imaging Quantitative MRI SWI, susceptibility-weighted imaging WI, weighted image

 Acute tropical myeloneuropathy Beriberi HTLV-1 Retroviral myelopathies Strachan syndrome Toxic neuropathy Transverse myelitis Tropical spastic paraparesis Vitamin deficiencies






 Plegridy PEG IFN-beta-1a BIIB017 PEGINTERFERON BETA-1A BIIB 017 UNII-I8309403R0 Peginterferon beta-1a [USAN:INN] Polyethylene glycol-interferon beta-1a I8309403R0 1211327-92-2 N2.1-((2RS)-2-Methyl-3-(alpha-methylpoly(oxyethylene)oxy)propyl)human interferon beta (fibroblast interferon, IFN-beta) glycosylated expressed in mammalian cells Poly(oxy-1,2-ethanediyl), alpha-methyl-omega-hydroxy-, 1-ether with N-(3-hydroxy-2-methylpropyl)interferon beta-1a (human)

 Alzheimer's disease Autism spectrum disorder Brain-gut axis Microbiota Nervous system diseases Parkinson disease

 CCR6 GPCRs Th17 cells antibody immune system inflammation therapy
 Alemtuzumab Lemtrada Campath Campath 1H Campath-1H Campath 1H/LDP03 UNII-3A189DH42V Alemtuzumab [USAN:INN:BAN] LDP-03 HSDB 8177 3A189DH42V 216503-57-0 Immunoglobulin G 1 (human-rat monoclonal CAMPATH-1H gamma1-chain anti-human antigen CD52), disulfide with human-rat monoclonal CAMPATH-1H light chain, dimer. Molecular weight is approximately 150,000 daltons Immunoglobulin G1, anti-(human CD52 (antigen)) (human-rat monoclonalCAMPATH-1H gamma1-chain), disulfide with human-rat monoclonal CAMPATH-1H light chain, dimer
 Absorption spectroscopy Cationic/anionic interactions Electron transfer reactions Emission spectroscopy Hydrophobic interactions Solubility Surfactant Voltammetry
 COVID-19 Interferons SARS-CoV-2 antiviral cytokines type III interferons
 PK/PD PROTACS RIPK2 SBDD inflammatory diseases kinase inhibitors

 Astrocyte Glial network Myelination Neuroinflammation Oligodendroglia Synaptogenesis
 Cerebrovascular Disorders Inflammation Magnetic Resonance Imaging
 Alzheimer’s disease Cell lines Endophytic fungi Excitotoxicity Neurodegeneration
 Caspase-1 Immunoblot Immunofluorescence Immunohistochemistry Inflammasome Interleukin-1β Western blot
 Abducens nerve palsy Pregnancy Sixth cranial nerve palsy
 electrodiagnostic studies electromyography nerve conduction studies neurology neurosurgery spastic foot drop
 ProBDNF immune-mediated inflammatory diseases metabolism mitochondria p75NTR sortilin

 acute disseminated encephalomyelitis covid-19 pneumonia edema glasgow coma scale sars-cov-2
 clinical practice guidelines functional electrical stimulation neurorehabilitation rehabilitation upper motor neuron conditions
 B-cell depletion COVID Multiple sclerosis Ocrelizumab Rituximab Vaccination
 COVID-19 vaccination T-cell response disease-modifying therapy neutralizing antibodies secondary progressive multiple sclerosis
 5-hydroxytryptamine type 3 (5-HT3) Alzheimer’s disease (AD) Ataxia telangiectasia and Rad3-related (ATR) FK506 binding protein (FKBP) Interleukin-2 inducible T-cell kinase (Itk) Parkinson’s disease (PD) Protein Interactor with NIMA1 (Pin1) autoimmune disease cancer cyclophilin cyclosporin hepatitis B virus (HBV) hepatitis C virus (HCV) human immunodeficiency virus 1 (HIV-1) infectious disease multiple sclerosis (MS) neurodegenerative disease parvulin post-translation modifications proline isomerase proline isomerization sanglifehrin systemic lupus erythematosus (SLE)
 Bone fracture Bone mineral density Disability EDSS Glucocorticoid Multiple sclerosis Osteoporosis Risk score Vitamin D




 COVID-19 Coronavirus Main protease inhibitors Masitinib Masitinib analogues Molecular dynamics simulations N-methylpiperazine SARS-CoV-2
 FoxO1 LC3-II/LC3-I MBP Multiple sclerosis SIRT1 SQSTM1/p62
 Parkinson's disease Telemedicine falls prevention multiple sclerosis neurological rehabilitation postural balance stroke videoconference
 Cognition Processing speed Verbal memory Visual memory Working memory
 C57BL/6 mice EAE model of human multiple sclerosis catalytic antibodies hydrolysis of RNAs and micro-RNAs immunization with MOG
 chronic inflammation cognitive function cryotherapy metabolic disorders neurodegenerative disorders neuropsychiatric disorders obesity


 astrocytes inflammation learning memory neurodegeneration neurodevelopment diseases neurons oxidative stress sleep disorders
 Autoimmune diseases Exosomes Immunomodulatory Therapy

 Akkermansia muciniphila gut-brain axis neuropsychiatric disorders probiotic therapeutic target
 Experimental autoimmune encephalomyelitis Gut microbiota Multiple sclerosis Neuroinflammation Panax japonicus Saponins
 gut dysbiosis gut-brain axis microbiota neurological disorders signaling pathways

 CLINICAL NEUROLOGY RANDOMISED TRIALS

 Alzheimer’s disease amyloid biomarker central nervous system cytokines diabetes inflammation microglia neuroinflammation phagocytosis tau
 Astrocytes Demyelination GnT-IX HNK-1-O-Man PTPRZ multiple sclerosis
 Cytomegalovirus Enzyme-linked immunosorbent assay Epstein-barr virus Herpes simplex virus-1 and -2 Human herpesvirus-6 SuperLearner United Kingdom ME/CFS biobank Varicella-zoster virus
 meta-analysis neurodegenerative disease selenium selenoprotein systematic review
 IFNγ IL-17B IL-1β TNFα H-151 autoimmunity cGAS-STING pathway dimethyl fumarate sporadic amyotrophic lateral sclerosis

 Autoimmune diseases Gut microbiota Inflammatory markers Intermittent fasting Metabolic health Weight loss
 ABCA1 Alzheimer’s disease apoptosis neuroinflammation neurological disorders stroke
 EGFR ErbB neurotransmitters orexins sleep zebrafish

 Chronic illness Existential communication Patients’ perspectives Religion Spirituality
 Accelerometry Accessibility Balance Fall risk

 7T cortical microhemorrhage transient ischemic attack ultra-high field MRI
 Central nervous system Neurodegeneration Pleiotropic effect Statins inflammation plasma cholesterol
 Demyelination Familial Mediterranean fever Rituximab Transverse myelitis
 Neuroblastoma Warburg Effect adjuvant therapy childhood malignancies ketogenic diet nutritional therapy


 Astrocytes Glutamate MSG SOD-1 TDP43 convulsions epileptic dementia neurodegeneration
 Meningeal immunity Neuroimmunology Type 2 immunity
 Biotransformation dimethyl fumarate mass balance metabolism pharmacokinetics
 Alzheimer's disease Crocus sativus L Parkinson's disease crocin neurodegenerative disease safranal
 CNS DMTs ageing immunosenescence inflammageing plasticity
 EC18 HCN channel HCN4 iPSC ion channels
 Customer centricity Flexible care setting Oral Parenteral Product optimization Subcutaneous
 Central nervous system Interleukin-4 Neuroprotection and -repair Translation Type 2 inflammation
 In Silico trials Machine learning Modeling and simulation Virtual cohorts Virtual patient
 PET/MRI SLE biomarker imaging - computed tomography organ specific systemic lupus erythematosus transcriptomics (RNA-Seq) urine biomarker
 cryoglobulinemia hepatitis c incontinence transverse myelitis vasculitis
 Akkermansia muciniphila IBD PCOS benefits endometriosis harms microbiota
 MMP-9 MMP-9-1562C/T polymorphism brain brain diseases rs3918242
 CNS EAE IL-17A Interleukin-17 Neuroinflammation Pertussis
 COVID-19 Case report Driving Hemiplegic migraine
 autoantibodies brain immunofluorescence neurons neuropsychiatric syndromes systemic lupus erythematosus
 automatic segmentation algorithm clinical applicability clinical dataset heterogeneous dataset multi-scanner multiple sclerosis white matter lesions (WML)
 AHR structure Ah receptor OCT4 aryl hydrocarbon receptor cancer clinical trials hematopoiesis immune checkpoint inhibitor intestinal bowel disease microbiome multiple sclerosis skin barrier steatosis
 Aerobic training Anxiety Depression Inflammation Multiple sclerosis Royal jelly
 animal model antibody-binding epitope autoantibody myelin oligodendrocyte glycoprotein optic neuritis
 ACA - anterior cerebral artery BMT - best medical treatment CAS - carotid artery stentings CBF - cerebral blood flow CBV - cerebral blood volume CBZ - cortical border-zone CEA - carotid endarterectomy CT - computer tomography DWI - diffusion-weighted imaging ECST - European Carotid Surgery Trial FLAIR - fluid attenuation inversion recovery IBZ - internal border-zone ICA - internal carotid artery LVO - large vessel oclussion MCA - middle cerebral artery MRI - magnetic resonance imaging MS - multiple sclerosis NIHSS - National Institute of Health Stroke Scale PCA - posterior cerebral artery PET - positron emission tomography SPECT - single photon emission tomography TIA - transient ischemic attack TOF - time of flight WI - Watershed infarcts Watershed infarcts carotid stenosis hypoperfusion ischemic stroke
 Personalized Adoptive Neuro-Immunotherapy T cells aging dopamine glutamate nerve-driven immunity neurological diseases neuropeptides neurotransmitters
 Aquaporin-4 (AQP4) Coronavirus Disease modifying treatment Disease reactivation Disease severity Eculizumab Multiple sclerosis Neuromyelitis optica spectrum disorders (NMOSD)
 antibody titers cytokines interleukin mode of action multiple sclerosis plasma separation
 convolutional neural network hyperreflective foci optical coherence tomography outer nuclear layer of the retina
 neurodegenerative diseases neurotrophic factors regenerative therapy
 Biomarker Circadian rhythm disorder Neurodegenerative diseases Proteomics Sleep disruption
 Demyelination Neurodegenerative diseases Neuroregeneration Nogo protein Nogo receptor Oligodendrocytes Reticulon-4
 Metal ion channels Metal ion modulators Metal ions Neurodegenerative diseases Neurotoxicity
 WNT homeostasis neurodegenerative diseases neurogenesis β-catenin
 Breath test Gut microbiota Gut-liver axis Hydrogen Lactulose Methane



 CIS MRI MS clinically isolated syndrome cohort study depression neuropsychological symptoms relapse sex smoking vitamin D



 H-reflex conditioning heksor neurorehabilitation paired-pulse facilitation sensorimotor rhythms skilled behavior spinal cord injury targeted plasticity
 Neoferon Interferon beta 1a Interferon beta-1a UNII-XRO4566Q4R XRO4566Q4R HSDB 8135 Recombinant human interferon beta 1a Interferon beta1 (human fibroblast protein moiety) Betaferon Betaseron Extavia Plegridy Interferon-1b Interferon beta-1b IFN-beta (sub ser) UNII-TTD90R31WZ TTD90R31WZ HSDB 8136 DRG-0054 BAY86-5046 BAY 86-5046 Interferon beta1, 17-L-serine-, (2S-(2R*,5R*))- 17-L-Serine-2-166-interferon beta1 (human fibroblast reduced) 2-166-Interferon beta1 (human fibroblast reduced), 17-L-serine- 145155-23-3

 autoimmune autoinflammatory diseases epigenetic regulation immunity miR-183/96/182 cluster microRNA
 ABC transporters Cancer Cancer therapy Drug resistance Metabolism Nucleosides SLC transporters
 Marijuana benefits cannabis education attainment harmful human body legislation social impacts
 autoimmunity immunoregulation inflammasomes inflammation self-tolerance

 acceptability chronic low back pain neurological desorder satisfaction tele rehabilitation
 Activators Neurite differentiation Neurotrophins Physicochemical properties TrkB receptor


 autoantibodies autoimmune diseases immunosensors inflammation patients’ biological fluids protein-biomarkers
 Alzheimer's disease Parkinson's disease depression epilepsy neurological disorder


 Antagonists Cancer Cannabinoid Docking Heterocycles Obesity
 autoimmune neurological diseases double filtration immunoadsorption plasma exchange plasmapheresis
 Clinical trials Ethics Teriflunomide
 Cannabis ethics research
 Disease-modifying therapy NMO NMOSD Neuromyelitis optica spectrum disorder
 Comparative overview Innate immune response Production systems Recombinant nucleic acid technology Therapeutic applications
 MRI anatomical atlas energy image segmentation lesions filling
 instrument neurology quality of life well-being
 Behcet autoimmune diseases of the nervous system hematopoietic stem cell transplantation myasthenia gravis myopathies nervous system diseases neuromyelitis optica polyneuropathy vasculitis
 Autoimmune disease NETosis Neutrophil extracellular trap (NET)
 BDNF Biosensors Brain CNS Neurological diseases NfL Ultra-sensitive
 Experimental autoimmune encephalomyelitis GPR109A Regulatory T cell Thymic medullary epithelial cell Treg development

 Chronic diseases Iceland comorbidity data accuracy registries validation study
 acute disseminated encephalomyelitis adult clinical characteristics recurrence factors
 Danio rerio animal model cannabinoids endocannabinoids system zebrafish
 FreeSurfer Generative models Lesion segmentation Longitudinal segmentation Whole-brain segmentation
 Bioactivity Camellia sinensis chemical composition scoby toxicity
 ABCB1 gene Análisis de asociación Análisis de haplotipos Association analysis Demyelinating disease Enfermedad desmielinizante Esclerosis múltiple Gen ABCB1 Glicoproteína P Haplotype analysis Multiple sclerosis P-glycoprotein
 CD4(+) T cells CP: Immunology CP: Microbiology GPR35 encephalomyelitis gut microbes immune system kynurenic acid macrophages multiple sclerosis spinal cord tryptophan metabolites
 Multiple sclerosis Pediatric Radiologically isolated syndrome
 Autoimmune myelitis Fibrinogen-like protein 2 Multiple sclerosis Toll-like receptor 9

 Antiviral CC50, 50% cytotoxic concentration COVID-19 COVID-19, coronavirus disease 2019 CPE, cytopathic effect Coronavirus EC50, 50% effective concentration HCoV, human coronavirus Human cell line MS, multiple sclerosis SARS-CoV-2 SARS-CoV-2, severe acute respiratory syndrome coronavirus-2 TCID50, 50% tissue culture infective dose Teriflunomide qPCR, quantitative real-time polymerase chain reaction

 BEE syndrome GFAP RED-M SICRET brain-eye-ear endotheliopathy glial fibrillary acidic protein retinocochleocerebral vasculopathy sNfL serum neurofilament light vasculitis


 Alzheimer’s disease T2DM blood–brain barrier chelators cognitive decline ferroptosis iron reactive oxygen species (ROS)
 Anti-laminin-332 mucous membrane pemphigoid Autoantibodies Autoimmune diseases Cancer biomarkers Laminin-332 Malignancy

 Machine learning Multinomial NLRP3 inhibitors QSAR
 Acceptance and Commitment Therapy Anxiety Depression Systematic Review
 aging behavior cell survival hippocampus lipocalin-2
 ATF3 activating transcription factor 3 adaptive stress response central nervous system innate immune system microglia
 Dystonia Parkinson's disease functional neurosurgery obsessive compulsive disorder radiosurgery tremors
 Clinical trial Interactive data visualization R shiny Statistical monitoring
 IFN-I IFN-α-inducible genes IFNα autoantibodies autoimmune disease diagnostics gene expression immunopathogenesis inflammation monitoring disease activity
 PACAP aging biomarker body fluids diseases endocrine

 Dimethyl fumarate Mice Oxidative stress Paraquat Pulmonary fibrosis

 Balance Functional MRI Gait Neurodegenerative diseases Postural instability Structural MRI

 ACS-ACS/NSTEMI acute coronary syndrome (ACS) angiography (ANCO) congenital heart disease in adults (CHDA) coronary coronary anomaly (CORA) coronary artery disease (CAD)
 Autoimmune Bibliometrics Inflammation Rho GTPases VOSviewer
 AP1 Experimental autoimmune encephalomyelitis TPN10518 Th1/Th17 cells
 CNS resident MUs EAE MS Microglia Myeloid cells
 fatigue fatigue symptoms nootropic nutrient therapy supplementation vitamin supplementation
 Displaced amacrine cell Myelination Nerve conduction Oligodendrocyte loss Retinal ganglion cell
 Autoimmunity HLA motif Inflammatory stress Neoantigen Post-translational modification
 Spinal dural arterio-venous fistula demyelinating disease dilated perimedullary veins myelopathy spinal cord oedema
 Signal transduction anti-inflammation lipid mobilization neurological disease very-long-chain fatty acid
 Devic’s disease aquaporin-4 demyelination neuroophthalmology optical neuritis
 AQP4 MOGAD autoimmune neurology biologics monoclonal antibody myelopathy neuromyelitis optica sarcoidosis transverse myelitis treatment

 COVID 19 Enbrel® IFNAR2 IL-18BP Rebif® TBPII Tadekinig alfa TM ligand affinity chromatography
 PMN cannabidiol innate immunity
 HIF-1α Th17 autoimmune diseases hypoxia neuroinflammation
 Th17 cells Treg cells choline immune regulation indole polyamines secondary bile acids short-chain fatty acids
 RBPs autoimmune diseases genetic variability posttranscriptional regulation

 benign soft tissue masses intravascular endothelial hyperplasia tumors

 calcium metabolic disorders polycystic ovary syndrome vitamin D deficiency
 NLRP3 dimethyl fumarate glibenclamide liver fibrosis thioacetamide
 EAE NRON TUG1 activated macrophages inflammatory cytokine
 anti-aqp4 autoantibody mimic disease myelin-oligodendrocyte glycoprotein (mog) neuromyelitis optica spectrum disorder neuromyelitis optica spectrum disorder (nmosd) stroke systematic literature review
 bibliometric microglia neurodegenerative diseases neuroinflammation neuropathic pain (NP)
 microvascular decompression numbness postoperative pain solitary pontine lesion trigeminal neuralgia
 10-hydroxy-2-decenoic acid Antioxidant Antiviral COVID-19 Major royal jelly protein Royal jelly

 arthritis cartilage naltrexone opiate osteoarthritis pain regenerative medicine
 Citespace NMOSD VOSviewer bibliometric neuromyelitis optica spectrum disorder
 BERT health informatics natural language processing text classification
 COPD DNA adducts acrolein cell signalling inflammation lung cancer oxidative stress respiratory toxicity tobacco smoke α,β-unsaturated aldehydes
 CP: Neuroscience IL-33 MAFB TREM2 astrocytes cuprizone demyelination microglia oligodendrocytes remyelination single-nucleus RNA-seq
 cycling ergometer electric bicycle kinematics knee rehabilitation
 Amide Antagonist P2X7 receptor Structure design Structure-activity relationship
 antiepileptic drugs epilepsy faecal matter transplantation gut microbiota gut-brain axis hypothalamic-pituitary axis probiotic short-chain fatty acids

 brain gut-axis cognition gastrointestinal tract inflammatory bowel disease microbiota neurodegeneration
 Outcome Sphingosine-1-phosphate Sphingosine-1-phosphate receptor modulators Subarachnoid haemorrhage


 Axonal degeneration Natural compounds Necroptosis Neurodegenerative disease Neurological disease Post-translational modification
 Atherosclerosis Cancer Cardiovascular diseases Pleotropic effects Statins
 B cells autoantibodies autoimmune diseases plasma cells rheumatic diseases
 PD-T2 T2 mapping dual echo inline qMRI quantitative imaging reconstruction relaxation

 Peer support intervention models neurological condition peer coach peer mentor

 Antineutrophil cytoplasmic antibody Cranial nerve VIII neuropathy Hypertrophic pachymeningitis IgG4 Thickened dura mater

 Bibliometrics neuromyelitis optica spectrum disorder scientific production
 autoimmunity cell therapy immune tolerance route of administration tolerogenic dendritic cells
 autonomic nerve blocks cancer pain disorder sympathetic ganglia
 autoimmune autoinflammatory inflammasome interleukin 1 neuroinflammatory and neurogenerative disorders pyroptosis



 Cannabis sativa L. biosynthesis pathways industrial application phytocannabinoids structural activity
 MOG (myelin oligodendrocyte glycoprotein) MOG-IgG MOGAD T cells autoantibodies blood brain barrier (BBB) pathophysiology-contemporary knowledge

 blood glucose cytokines insulin neuroimmune peripheral blood monocytes cells seizure tumor necrosis factor vagus nerve stimulation
 cost-effectiveness efficacy immune-mediated neurological disorders nanomembrane neuroregeneration oxidative stress therapeutic plasma exchange
 cuprizone demyelination neural stem cells oligodendrocyte progenitor cells remyelination sub-ventricular zone
 Autoimmunity Ecotoxicology Environmental medicine Epidemiology Immunology Risk factors
 Fasciola hepatica alpha-ketoglutarate (α-KG) fatty acid oxidation (FAO) glutaminolysis helminth defence molecule immune regulation immunometabolism macrophage
 COVID-19 SARS-CoV-2 autoantibody autoimmune diseases autoimmunity
 Approximate entropy Correlation dimension Fractal dimension Largest Lyapunov exponent
 Alzheimer’s disease Chrysin Parkinson’s disease depression epilepsy flavonoid
 4p14 4p16.1 6q23.3 Anti-lipopolysaccharide antibody response Cholera vaccine Genome-wide association study TBC1D1 TBC1D14 TNFAIP3 Vibrio cholerae
 autoimmune diseases flowcytometry lymphocytes pre-analytic conditions storage temperature storage time
 Astrocytes Microglia Neuroinflammation circRNAs lncRNAs miRNAs
 Cough Cough assistance Mechanical insufflation-exsufflation Neurological disease Neuromuscular disease
 brain tumors long-term exposure risk of malignant toxic air pollutants
 EGCG inhibition neurological diseases neurotropic viruses
 Autoimmune diseases COVID-19 Frontiers Hotspots Keywords analysis
 S100B protein pathogenic factor

 Neurodegenerative diseases Nrf2 Nrf2 activators Oxidative stress Phytochemical ingredients
 ATO Nrf2 ROS arsenic trioxide copper fenton-like reaction fibrosis systemic sclerosis





 Bradykinin Cancer Fibromyalgia Inflammatory pain Neuropathic pain Nociplastic pain
 PHD2/PHD3 astrocyte experimental autoimmune encephalomyelitis hypoxia multiple sclerosis neuroprotection
 Glial fibrillary acidic protein Multiple sclerosis Myelin oligodendrocyte glycoprotein antibody-associated disease Neurofilament Neuromyelitis optica spectrum disorder Transverse myelitis
 COVID-19 COVID-19 vaccine neuromyelitis optica outcomes severe acute respiratory syndrome coronavirus 2
 4-Aminopyridine Biodistribution Demyelination First in human Fluorine-18 IND Multiple sclerosis PET Radiation dosimetry Voltage-gated potassium channels [18F]3F4AP
 Akt signal Dopaminergic neurons Hyperoside Neuroprotective Parkinson’s disease SH-SY5Y cells
 MULTIPLE SCLEROSIS MYELIN MYELOPATHY

 demyelination experimental autoimmune encephalomyelitis grape seed extract inflammatory cell inflammatory factor



 Autoimmune diseases Chronic inflammation Mitochondrial translation NADH homeostasis Obesity
 Alzheimer’s disease anti-inflammatory drugs drug discovery metabolites neuroinflammation pre-clinical drug discovery
 CD4+ T cells Paracellular TCR repertoire Th17 Transcellular Treg
 Sativex nabiximols pediatric

 epidemiology oral health oral-systemic disease periodontal disease tooth loss
 ephrin neuronal activity neuroplasticity rTMS sensory systems topography
 IL-35 IL-37 Inflammatory bowel disease MAPK MicroRNA NF-κB
 anti-inflammatory diet inflammation mental disorders neurodegenerative diseases neurological diseases nutrition intervention
 25-hydroxyvitamin D COVID-19 CYP27B1 metabolism respiratory rickets vitamin D receptor
 Moringa oleifera anti-neuroinflammatory mechanisms neurodegenerative neuropharmacological properties phytochemicals

 Autoimmune diseases BCG Cancer Heterologous protection Trained immunity
 dimethyl fumarate. fibroblast like synoviocyte inflammation rheumatoid arthritis
 3βHSD Aromatase Estrogen receptor Experimental autoimmune encephalomyelitis Naringenin
 Brain Central nervous system disorders Glia cell Mechanotransduction Neuron Piezo1 channel
 anti-inflammatory activity anticancer potential antioxidant activity biological activity natural products royal jelly
 Neurological conditions outcomes participation rehabilitation
 Parkinson’s disease glial cell line-derived neurotrophic factor (GDNF) glutamate neurological disorders neuroprotection preclinical studies rasagiline safinamide selegiline type-B monoamine oxidase (MAOB) inhibitors
 JCV PML biomarker clinical studies diagnostics risk stratification
 Delphi study; drop foot functional electric stimulation (FES) person-centered upper motor neuron lesions
 SGK1 diagnostic target immune diseases inflammatory diseases therapeutic target.
 Acetate Autoimmune disease Autoimmunity Butyrate Propionate Short-chain fatty acid
 behavior data cognitive processing speed dual-task evaluation machine learning virtual reality
 3D microcarriers Cargo profile Extracellular vesicles Human mesenchymal stromal cells Shear stress Vertical-Wheel bioreactor
 Autoimmune diseases Inflammation Receptor interacting serine/threonine kinase 2 Therapeutic target
 Autoimmune diseases Frontiers Gut microbiota Hot spots Keywords analysis Visual analysis
 TRPA1 demyelination myelination oligodendrocytes organotypic cortical brain slices

 Artemisinin Excitotoxicity Inflammation Neurodegeneration Neurotransmitters PI3k/Akt
 ageing movement disorders upper limb
 data-driven deep learning quantitative susceptibility mapping single-step susceptibility quantification

 Glaucoma RXRs SNPs genotype–phenotype correlations homology modelling retinoids

 COVID-19 JC virus natalizumab seroconversion
 bioinformatics differentially expressed genes experimental autoimmune encephalomyelitis mRNA splenocytes
 Electroacupuncture Experimental autoimmune encephalomyelitis Hematopoietic stem cells Mesenchymal stem cells Neural stem cells
 Akkermansia muciniphila Alzheimer’s disease depression microbiota-gut-brain axis neuropsychiatric disorders

 Optic Neuritis myelin oligodendrocyte glycoprotein neuromyelitis optica spectrum disorder paracentral acute middle maculopathy retinal ischemia
 Chronic pain Cognitive therapy Hypnosis Low back pain Moderators

 CADISIL brain MRI capillary rarefaction cerebral small vessel disease enlarged perivascular spaces glymphatic system impaired cognition lacunes neurodegeneration white matter hyperintensities
 Anticancer agents Cancer De novo pyrimidine synthesis Human dihydroorotate dehydrogenase (hDHODH) hDHODH inhibitors
 biomarker inflammation osteopontin pathogenesis therapeutic target
 CNS repair heparan sulphate neurite outgrowth recombinant heparin mimetics remyelination

 STAT3 Treg injured microenvironment microglia neuroinflammation spinal cord injury
 Anxiety disorders Elevated-plus maze Light–dark test Tyro3 White matter
 CCR2 CCR3 G protein-coupled receptors Glide LightGBM TensorFlow cheminformatics chemokine receptors drug discovery gradient-boosting machine machine learning molecular docking neural network virtual screening
 Carboxymethylcellulose Cerium (III) nitrate hexahydrate salt Cubosomes Glatiramer acetate Lactobacillus acidophilus
 Glycolysis Hyperexcitability Metabolism Monomethyl fumarate (MMF) Neuroprotection Nrf2 Oxidative stress
 Cancer immunotherapy Demyelinating disorders Meningoencephalitis Myelitis NAEs Neurological complications
 Central nervous system Combination therapy Natural products Neurodegenerative diseases Phytopharmaceuticals Stem cells
 DrugBank Keap1 Nrf2 inhibitor Pharmacophore chlorhexidine repurposable β-propeller domain
 Clinical trials Drug repurposing Knowledge graph reasoning Multimodal data fusion Rare disease
 Integrin Sialic acid TMEV pDC
 Excitotoxicity Glaucoma Glia Inflammasome NMDA Neuroinflammation Siponimod Sphingosine-1-phosphate
 astrocyte calcium electrophysiology gap junction syncytium
 Glatiramer Glat copolymer Tgal copolymer Copolymer i COP 1 Synthetic peptide copolymer I Copolymer I (synthetic peptide) (T,G)-A-L UNII-U782C039QP Multideterminant antigen (T,G)-A-L U782C039QP Poly-L-(tyr,glu)-poly-DL-ala-poly-L-lys (Tyr-tyr-glu-glu)-poly(DL-ala)-poly(lys) (L-Tyrosine-L-glutamic acid)-poly(DL-alanine)-poly(L-lysine) 28704-27-0 L-Glutamic acid, polymer with L-alanine, L-lysine and L-tyrosine Glatiramer acetate Copaxone Copolymer 1 Copolymer-1 Protiramer Glatopa COP-1 UNII-5M691HL4BO Glatiramer acetate [USAN:BAN] 147245-92-9 5M691HL4BO TV 5010 L-Glutamic acid peptide with L-alanine, L-lysine and L-tyrosine, acetate (salt) L-Glutamic acid polymer with L-alanine, L-lysine and L-tyrosine, acetate (salt)
 Alzheimer’s disease Thioflavin-S amyloid fluorescence spectroscopy
 Clinical inertia Clinical vignettes Medical education Psoriatic arthritis Recommendations Therapeutic inertia Treat-to-target Uncertainty
 Blood–brain barrier SARS-CoV-2 cerebral ischaemia flow disturbances inflammation neurological disorders
 acute truncal ataxia acute vestibular syndrome ataxia cerebellar nystagmus stroke
 Semliki Forest virus brain immunology encephalitis suppressors of cytokine signaling
 bias functional neurological disorder implicit attitudes referral decisions
 CIDP MS NMOSD anti complement autoimmune neuropathies demyelinating diseases drug repurposing
 Fibromyalgia syndrome Vitamin D epidemiology generalized pain prevention

 Neurological rehabilitation reliability systematic review telerehabilitation validity
 cfDNA epigenetics liquid biopsy methylation neurology

 Autoimmune diseases GWAS Pleiotropic gene SPU tests

 C57BL/6 mice EAE model of human multiple sclerosis catalytic antibodies cross-complexation and catalytic cross-reactivity hydrolysis of histones and myelin basic protein immunization mice with MOG and DNA–histone complex

 Case-referent study Central demyelination Multiple sclerosis Vaccines
 C57BL/6 mice EAE model of human multiple sclerosis catalytic antibodies cross-complexation and catalytic cross-reactivity hydrolysis of histones and myelin basic protein immunization mice with MOG and DNA-histone complex
 Fish consumption health meta-analysis systematic review umbrella review
 EAE flow cytometry histamine H4 receptor agonist inflammatory mediators multiple sclerosis
 Multiple sclerosis Optic neuritis Optic neuritis classification Optic neuritis diagnostic criteria Optic neuropathy
 OT mice OVA-specific CD4+ T cells OVA-specific CD8+ T cells T cell dependent susceptibility Theiler’s murine encephalomyelitis virus (TMEV) central nervous system microgliosis neuroimmunology
 Fingolimod Microglial activation Neuroinflammation Psychosis Short-term cuprizone exposure
 CNN brain tumor MRI images deep learning healthcare image processing
 conditions indications medicinal cannabis non-cancer pain retrospective review symptoms
 juvenile central nervous system vasculitis lymphocytic inflammation primary angiitis of the central nervous system suspected weighted image unilateral relapsing primary angiitis of the CNS

 neurological injury primary care quality in health care
 18F-MAPP MPO inhibitor PET imaging damaging inflammation intracellular and extracellular MPO myeloperoxidase myocardial infarction

 Aquaporin 4 antibody Myelin oligodendrocyte glycoprotein antibody Neuromyelitis optica spectrum disorders Optic neuritis Transverse myelitis
 FTY720 MK2206 invasiveness sphingosine 1-phosphate receptor 1 threonine 236 phosphorylation triple-negative breast cancer zebrafish

 clinical study cognitive function dietary supplement human study natural product
 Brain diseases Ferroptosis Ferroptosis inducers, Ferroptosis inhibitors Ferroptosis mechanisms
 Biomarker Inflammation NON rheumatic diseases Rheumatic diseases cCLP
 cognition quality of life spinal cord injury
 Biomarkers GFAP inebilizumab magnetic resonance imaging myelitis neuromyelitis optica spectrum disorder optic neuritis serum glial fibrillary acidic protein
 Neural tube defects Orthogonal design PI3K/Akt signaling pathway Wuzi Yanzong Pill
 D359-0396 Inflammation Multiple sclerosis Pyroptosis Sepsis
 CSF MRI multiple sclerosis sleep disorders
 CD27-positive B-cell MOG-associated diseases Neuromyelitis optica spectrum disorder Rituximab
 Autoimmunity Immune Tolerance Immunotherapy T-Lymphocytes Translational Medical Research
 Mendelian randomization appendicular lean mass autoimmune disease grip strength rheumatoid arthritis sarcopenia
 BMC-mcDESPOT Machine Learning Myelin water imaging
 Meta-analysis neurological disorders odds ratio oral antispasticity drugs spasticity
 Baclofen Decompression Intrathecal catheter Lumbar spinal stenosis
 Cell-free therapy Culture media Exosomes Mesenchymal stem cell Neurodegenerative disorders Secretome
 MLR NMOSD PLR hemocyte relapse
 AKT/mTOR and CREB/BDNF/TrkB ER stress/oxidative stress apoptosis dopamine miR-634 unfolded protein response
 Au13 nanoclusters CD4+ T cells CUBIC Experimental autoimmune encephalomyelitis (EAE) Gateway reflex Microinflammation Myelin oligodendrocyte glycoprotein (MOG)
 Gut microbiota Gut-brain axis IL-17 IL-17(+)T cells IL-23 Ischemic stroke
 MS NMOSD anti-SSA/Ro antibody anti-SSB/La antibody primary Sjögren's syndrome salivary gland biopsy sicca
 Autoimmune diseases B-cell tolerance and T-cell tolerance Covid-19 Cytokine storm Immunological reaction Inflammatory reaction Therapeutic protocols
 Cell biology Neuroscience Stem cells research

 Amyloid beta proteins antihyperglycaemic agent cognitive impairment dysmetabolism lipid dysmetabolism tau phosphorylation
 Cerebellum Motor dysfunction Neurological disorders Neuromodulation Randomized controlled trial Transcranial magnetic stimulation
 ADMET Marine Natural Products (MNP) RIPK in silico molecular dynamics necroptosis neurodegeneration virtual screening
 DNA methylation DNA variance HLA/MHC antigen presentation immune regulation

 demyelination drug-induced metabolic nutritional paraneoplastic postinfectious radiation-induced
 diffusion MRI gray matter human brain microstructure white matter
 Anti-inflammation and immune regulation Immune-associated inflammatory diseases Shikonin Traditional Chinese medicine

 EEG ERP attention cognition cranial nerve stimulation neuromodulation neuroplasticity
 extraretinal force impulse interception motion processing visuomotor
 Bas appareil urinaire Bladder Brain mapping Cartographie cérébrale Functional MRI IRM fonctionnelle Lower urinary tract Neuro-urology Vessie
 Fibrosis Fingolimod Macrophage Rezurock Transcriptome Y27632
 Bruton’s tyrosine kinase Bruton’s tyrosine kinase inhibitors autoimmune disease cancer solid tumor
 IκBζ Nrf2 anti-inflammation dimethyl fumarate macrophage
 Balloon compression Microvascular decompression Neuropathic pain Trigeminal neuralgia
 Autoimmune diseases Autoimmunity Cellular reprogramming Innate immune system Trained immunity
 Dimethyl fumarate NRF2 SLC7A11 ferroptosis ischemia-reperfusion injury
 Dental status disability gerodontology neurological disease oral health special care dentistry

 Carers Chronic diseases Long-term care networks Needs
 FTY720 MUE S1PR modulator S1PR1 meningoencephalitis of unknown etiology sphingosine-1-phosphate receptor 1
 Bifidobacterium breve Corpus callosum Demyelination Lactobacillus casei Oxidative stress Probiotic
 Fibrinolysis Granulomatous meningoencephalitis Immunohistochemistry Necrotizing encephalitis Thrombi
 Autoimmune disease B-cell differentiation Epstein–Barr virus Genetic susceptibility Pathogenic T-bet(+) B cells
 Autoimmune disease Exosome Extracellular vesicle MSCs Microvesicle
 Biomarker Circular RNA Frailty
 Spinal cord diseases malabsorption syndromes ataxins anemia leukopenia copper
 COP9 signalosome Neurodevelopment Neurological disorders Regulatory mechanisms c-Jun activation domain binding protein-1
 brain health neurological disorders neuronutrients neuronutrition
 ENS STING glia inflammation neurodegeneration
 astrocytes human induced pluripotent stem cells reprogramming transcription factors transplantation
 Restless leg syndrome, Spinal cord injury, Leg pain syndrome.
 Age-related neurological disorders Juglans spp. Walnut
 Autoimmune diseases Immunotherapy Myasthenia gravis Nanomedicine Preclinical mouse models Rheumatoid arthritis
 Bayesian inference classification deep learning magnetic resonance imaging neurodegenerative diseases spatial information
 Astrocyte Cell proliferation Diazepam binding inhibitor Differentiation Ependymal Ethynyl-2′-deoxyuridine Neural stem cell Oligodendrocyte Spinal cord γ-aminobutyric acid
 glaucoma intraocular pressure neurodegeneration neuroprotection optic nerve injury retinal ganglion cells siponimod sphingosine-1-phosphate
 CD26 SARS-CoV-2 and MERS-CoV infection cancer central nervous system enzyme inhibition neurological and psychiatric disorders
 Ballistic Gait home care services neurological Rehabilitation resistance training
 neuroinflammatory demyelinating and degenerative diseases palliative care patients' PC knowledge and attitudes
 Chronic diseases Long-term care networks Needs Patients
 2ccPA Depression Microglia NPSLE Neuroinflammation
 Acute urinary retention benign prostate hyperplasia postoperative complication transurethral resection of prostate urethral catheterization

 experiences headache migraine registry

 Chemical synthesis Cyclotides In-planta expression Recombinant expression
 Drug development Neurodegenerative disease PDE7 Phosphodiesterase 7 cAMP cancer
 SOD Trifolium resupinatum amyloid peptide spatial memory Alzheimer's disease

 amitriptyline astrocyte–microglia co-culture model depression doxepin inflammation interferon-β
 Alzheimer’s disease Parkinson’s disease immunotherapy molecular farming neurodegenerative disorders novel therapeutic strategies plant-based vaccines
 Cortisone Effect Methylprednisolone QT-interval QTc interval
 cognitive decline longitudinal data neuropsychology prediction modelling real world data
 Click chemistry Dimethylfumarate Electrophile Galectin Michael adduct Unsaturated carbonyls
 brain MRI convolutional neural networks deep learning segmentation semisupervised learning small vessel diseases white matter hyperintensities
 Mechanisms MicroRNAs Neurodegenerative diseases Small RNA

 Atrial fibrillation Autoimmune disease Inflammation Risk factors Sex differences
 CNS disorder astrocytes cell–cell communications scRNA-seq spatial transcriptomics transcriptomic modules
 Brain microstructure Convolutional neural network High angular resolution diffusion imaging Multilayer perceptron Neurite orientation dispersion and density imaging

 carotenoids neurodegeneration neuroinflammation oxidative stress reactive oxygen species
 Alzheimer's disease fluorescence microscopy mitochondria mitochondrial function
 Alkaloids Insulin receptor substrate Janus kinase Neurodegenerative diseases Phosphoinositide 3-kinase Polyphenols
 aging anti-complement component 5 astrogliosis brain neurodegeneration neuroinflammation obesity
 ALS diagnosis neurofilament prognosis

 cannabidiol (CBD) cannabis-based medicine (CBM) delta-9-tetrahydrocannabinol (THC) neuropathic pain (NP) spasticity
 SARS‐CoV‐2 humoral response innate immunity mRNA vaccine
 MMPH Multiple micronodular pneumocyte hyperplasia TSC Tuberous sclerosis complex ground glass nodule
 Tuberous sclerosis, (Lymphangioleio-myomatosis), Cysticlungdisease, (Pneumothorax), Genetics.
 endoplasmic reticulum stress mesenchymal stromal cells-derived secretome neurodegenerative diseases neurotrophic factors priming
 Deep learning Dipole inversion Fiber pathways Fiber tractography In vivo human brain Myelin imaging Proximal learning Susceptibility tensor imaging

 COVID-19 Coarse-grain simulation Constant-pH Monte Carlo Electrostatic interactions Molecular dynamics Multiscale protocol
 differential diagnosis false positivity mimickers misdiagnosis neuromyelitis optica spectrum disorder
 immune-mediated disease inflammatory biomarkers inflammatory cytokines liver cancer
 EBV autophagy viral capsid assembly viral envelope xenophagy
 aquaporin 4 myelitis neuromyelitis optica transverse
 Astragalus Differentiation Th1 Cells Th17 Cells Total Flavonoids Treg Cells
 Ablative procedures Facial pain Outcome analysis Percutaneous balloon compression Radiofrequency-thermocoagulation Trigeminal neuralgia
 EAE IGFBP2 SARM1 neuroinflammation neurons

 High-efficacy MRI Neuromyelitis optica spectrum disorder Progression Treatment
 Afghanistan War Health promotion Healthy People 2020 Iraq War Physical health Veterans Women
 anti-Yo cell-based assay cerebellar degeneration-related proteins paraneoplastic cerebellar degeneration
 Anti-oxidant Coronavirus disease 2019 Inflammation Neurological disorder Vitamin D3
 ageing chronic condition frailty older people qualitative research walking
 Alzheimer’s disease amantadine cognition long-covid 19 syndrome memantine parkinson’s disease
 auto-immune diseases autoimmunity curcumin curcumin-based nanomedicines delivery systems inflammation inflammatory diseases nanomedicines
 Complications Deep brain stimulation Dystonia Infection Parkinson`s disease

 Healthy adults normative scores processing speed psychometric tests selective/sustained attention
 CD4+ IL-17 T cell Th17 autoimmune disease

 Alzheimer's disease GSK3β Inflammation NLRP3 inflammasome Parkinson disease TBI
 CNS/PNS HABPs SPACRCAN extracellular matrix glioma hyaluronan
 antigen-specificity autoimmunity biomaterial immunotherapy mTOR microparticle and nanoparticle tolerance vaccine
 Decagonal Indane 1,3 dione Interleukin-6 Molecular docking Molecular dynamics Precision

 chronic pain low-dose naltrexone non-opioid analgesia

 Biomarker Molecular mechanism Placenta Signal pathway Syncytin-1
 Mendelian randomization health-related outcomes leukocyte telomere length meta-analysis systematic review
 Fingolimod Human serum albumin Lipid-like drug Molecular modeling Spectroscopic Techniques pH-dependent solubility
 respiratory compromise spasms stiff person syndrome stiff person syndrome spectrum disorders
 Th1 cells Th17 cells alpha4 beta7 integrin experimental autoimmune encephalomyelitis intravital microscopy leptomeninges
 Digital health Gait analysis Inertial sensors Rehabilitation Spinal cord injury
 ACSL4 Ethanol Ferroptosis Gastric mucosal lesions Prevotella histicola System Xc-/GPX4 axis VDAC
 COVID-19 MOGAD SARS-CoV-2 myelin oligodendrocyte glycoprotein
 COVID-19 Cognitive impairment dementia post-COVID-19
 T cell migration T cell–neuron co-culture acute brain slice autoimmune disease cortical culture cytokine cytotoxic CD8+ T cells inflammation neurodegeneration neuron

 Alzheimer’s disease Inflammasome Inflammation NLRP3


 Autoimmunity Biomarker Inflammation MiR-128 Neuroimmune disorders
 AXL(+)SIGLEC6(+) dendritic cell Inflammatory demyelinating disease Single-cell RNA sequencing
 HLA-DRB1 gene HLA-DRB1 variants SNPs and Indels SNVs in silico analysis inflammatory and autoimmune diseases organ transplantation single-nucleotide variants
 Erdheim-Chester disease Histiocytosis Langerhans cell histiocytosis Rosai-Dorfman disease
 Neurology Overground exoskeleton Rehabilitation Satisfaction


 Lipid metabolism Nuclear receptor RORγt Th17 cells
 Alzheimer’s disease H. pylori brain cortical thinning hyperhomocysteinemia neurodegeneration
 Mycobacterium tuberculosis adjuvant animal model antibody isotype bioinformatics experimental autoimmune encephalomyelitis pattern matching
 Alzheimer’s disease Brain disorders Hydrogen Medical gas Neuroinflammation Oxidative stress
 COVID-19 brain neuroradiology spine stroke
 Anxiety Depression Fatigue Immune-mediated inflammatory disease Pain Work impairment

 Cannabinoid Cannabis use disorder Desensitization Downregulation THC Tolerance
 Alzheimer’s disease Parkinson’s disease autism spectrum disorder faecal microbiome transplants microbiome neurodegenerative disease neurodevelopmental disease photobiomodulation
 Nrf2 blood pressure dimethyl fumarate ischemic stroke

 Saudi Arabia neurological assessment neurologists neurology tele-neurology virtual clinic


 Computed tomography Contrast agents Magnetic resonance imaging Metal-based nanoparticles Neurological diseases Phagocytic cells
 BTK COVID-19 LPS PET SARS-CoV-2 cancer carbon-11 evobrutinib

 adult glia mouse rodent spinal cord

 amino acids mendelian randomization neurodegenerative disorders

 observational studies randomized controlled trials real-world evidence risk of bias
 EAE demyelination insulin-like growth factor 1 multiple sclerosis neuroinflammation oligodendrocyte
 EAE Multiple sclerosis STA-21 STAT3
 COVID-19 Guillain-Barré syndrome autoimmune cerebral venous sinus thrombosis multiple sclerosis myelitis myositis


 early career failures mentorship set backs stroke career
 EBV ectonucleotidase immune evasion lymphoma
 Gut microbiota Indoles Microbiota-gut-brain axis Neurological diseases Neuropsychiatric diseases
 biomarkers magnetic resonance imaging (MRI) neuromyelitis optica spectrum disorder (NMOSD) optical coherence tomography (OCT) relapse satralizumab
 ADEM CNS complications COVID-19 Demyelination Encephalitis MOG MS
 nutrition obesity very-low-calorie ketogenic diet weight loss
 Acute myocardial infarction Anxiety and depression Cognitive-behavioral stress management Percutaneous coronary intervention Quality of life
 Animal models Autism spectrum disorder Ibudilast Neuroinflammation Neuronal loss Oxidative stress Valproic acid

 anxiety disability inflammatory bowel disease mental illnesses quality of life
 GAN Generative adversarial network Neuroimaging Pathology Review
 Brain Glioblastoma Human Organoids SARS-CoV2 Stem cells iPSC
 assessment occupational therapy parenting with a disability physical disability scoping review


 COVID-19 Dysautonomia Neuroinflammation Vagus nerve

 functional electrical stimulation lower limb impairment overview of systematic review systematic review upper motor neuron lesions walking
 Lipidomics Lysosomal storage disease Zebrafish
 Gut-brain axis Immunity Intestinal microbiota Neurodegenerative diseases


 Alzheimer’s disease Mendelian randomization causality neurological disorders plasma proteins
 barrier function blood–brain barrier immune system inflammation intestinal barrier psychiatric diseases sphingosine-1-phosphate

 Experimental autoimmune encephalomyelitis (EAE) Methylglyoxal Microglia Nuclear factor erythroid 2-related factor 2 (NRF2)
 Alcohol abuse Corticosteroids Marchiafava-Bignami Neuroimaging Thiamine Wernicke encephalopathy
 alzheimer’s disease aptamer microglia neurodegeneration neuroinflammation parkinson’s disease
 Adverse consequences Antiphospholipid syndrome Diagnostic delay Misdiagnosis Thrombotic antiphospholipid syndrome
 neurology no-show risk factors telehealth teleneurology
 AQP4-IgG Aquaporin-4 Demyelinating disease Familial Genetic NMOSD Neuromyelitis optica spectrum disorders


 Acceptance and Commitment Therapy (ACT) Neurological conditions outcomes processes of change scoping review
 Brain development Circular RNA Neurodegenerative disease
 Glial fibrillary acidic protein (GFAP) Myelitis aquaporin-4 antibodies biomarker disease activity myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) neuromyelitis optica spectrum disorder (NMOSD) optic neuritis
 Nabiximols blood marker cannabis use disorder treatment
 3D cameras gait analysis gait kinematics inertial sensors neurological disorders
 CCL20 Choroid plexus Experimental autoimmune encephalomyelitis T cell trafficking Th17 cells
 Autoimmune Diseases COVID-19 Patient Reported Outcome Measures

 APRIL BAFF CD40L DMTs anti-CD20 infectious risk ocrelizumab pwMS
 Climate change Heat waves Pharmaceuticals Pharmacovigilance Thermoregulation
 2-Arachidonoylglycerol Alzheimer’s disease Endocannabinoid Monoacylglycerol lipase Neurodegenerative disease Traumatic brain injury
 COVID-19 antibody reaction immune-mediated neuromuscular disease immunosuppressive therapy vaccination

 cystectomy ileal conduit neurogenic bladder robotic surgical procedures urinary diversion
 CBRQ cognitive factor analysis psychometrics reliability symptoms transdiagnostic validity
 Adhesion molecule Connexin Cytokine Experimental autoimmune encephalomyelitis Total glucosides of white paeony
 Danio rerio Developmental toxicity Dimethyl fumarate (DMF) Glutathionylation Nrf2
 Blood-brain barrier (BBB) Central nervous system (CNS) Lipid nanoparticles Neurodegeneration Surface modification Targeting
 CNS diseases NLRP3 exosomes inflammasomes mesenchymal stem cells neuroinflammation
 Blood–brain barrier Cognitive impairment Immunoproteasome Neuroinflammation Oxidative stress

 Clinical neuroscience Drugs Molecular medicine

 cisplatin mtor multifocal micronodular pneumocyte hyperplasia multiple sclerotic bone lesions tuberous sclerosis complex

 Anti-NMDAR Autoimmune encephalitis Pediatric Siblings Treatment
 amyotrophic lateral sclerosis biomarkers lipidomics
 Motor evoked potential Neurological disorders Short interval intracortical inhibition Transcranial magnetic stimulation
 15-lipooxygenase inhibitor ALS amyotrophic lateral sclerosis pharmacokinetic utreloxastat (PTC857)
 Palliative care meta-analysis neurologic disease neuropalliative care progressive neurologic disease systematic review



 NTHL1 PKD1 TSC2 autosomal dominant polycystic kidney disease renal cell carcinoma tuberous sclerosis
 Demyelinating disorders Eye-tracking Optic neuritis Pupil dynamics
 learned acquisition and reconstruction optimization multi-contrast pulse sequence quantitative multi-parametric mapping
 industrial workers neuropathic pain occupational osteoarthritis pain spinal pain work environment
 diabetic retinopathy dimethyl fumarate heme oxygenase-1 retina streptozotocin
 accuracy diagnosis non-compressive myelopathy spine mri sseps
 ATP DRP1 S616 FTY720-P S1PR STAT3 TFAM cardiomyocytes metabolism mitochondria nucleoids
 Fumarates GPR109A Lysosomal Trapping Macrolides Psoriasis
 Brain-derived blood exosome Extracellular vesicle Liquid chromatography − mass spectrometry Magnetic nanoparticle Neurological disease
 Antioxidant Apoptosis Autophagy Immunity Melatonin Primary Sjögren’s syndrome
 autoimmune disease autoimmune diseases of the nervous system cohort study meta-analysis schizophrenia
 effectiveness meta-analysis neurological diseases safety telemedicine teleneurology

 B vitamins Homocysteine L-methylfolate generalized anxiety disorder major depressive disorder thiamine vitamin B12 vitamin D

 Adverse events Background rates COVID-19 vaccination SARS-CoV-2 Vaccine safety Vaccine surveillance
 Optic neuritis myelin oligodendrocyte glycoprotein antibody-related disease neuromyelitis optica spectrum disorder subclinical visual outcomes

 Diabetic nephropathy Mendelian randomization Vitamin D
 Arg1 CD206 Demyelination Mouse Hepatitis Virus (MHV) NOS2 Neuroinflammation Phagocytic MG/Mφ RSA59 TREM2

 acetylcholinesterase butyrylcholinesterase glutathione S-transferase inhibitor piperazine

 Prediabetes cancer cardiovascular diabetes metformin neuroprotection pleotropic effect
 Acute ischemic stroke Cerebroprotection Elezanumab MCAO RGMa Rabbit


 acute flaccid myelitis acute flaccid paralysis enterovirus D68 transverse myelitis
 AhR Microglia Phagocytosis Remyelination SYK
 COVID-19 Evusheld Omicron breakthrough infection persons with neuroinflammatory diseases tixagevimab and cilgavimab
 L-type prostaglandin D synthase development developmental biology exocytosis mouse myelin neuroscience oligodendrocyte precursor cells oligodendrocytes

 CNS neurodegenerative estrogen extragonadal organ membrane lymphotoxin phenotype change

 Alopecia areata Autoimmune skin diseases Comorbidities Epidemiology Immune-mediated diseases Nurses’ Health Study
 autoimmune diseases familial autoimmunity idiopathic inflammatory myopathies shared familial susceptibility shared genetic susceptibility
 ADs Autoimmune diseases GBD Incidence Prediction Trends
 B cell malignancies B cell targeting therapies COVID-19 persistent SARS-CoV-2 infection viral infections in the hematological patient

 ACSL4 Ferroptosis Lipid peroxidation Neuroprotection Parkinson’s disease
 Bone mesenchymal stem cells EZH2 Exosome Experimental autoimmune encephalomyelitis Ferroptosis MicroRNA-367–3p SLC7A11
 Parkinson’s disease clinical trials iron dyshomeostasis multifunctional drugs

 Antipsychotic agents Clinical trial Fingolimod Schizophrenia White matter
 Epidemiology Epstein–Barr virus Mendelian randomization Public health Vaccination
 Aquaporin 4 Astrocyte-microglia co-culture model Connexin 43 Dimethyl fumarate Monomethyl fumarate
 Deep learning Diffusion MRI Multi-shell HARDI Single-shell HARDI Spherical harmonics fODF

 Anti-acetylcholine receptor antibodies Cytokines Lymphocytes Myasthenia gravis Teriflunomide
 DCE MRI MRI blood-brain barrier perfusion MRI


 AF, angiofibroma BHD, Birt-Hogg-Dube Birt-Hogg-Dube syndrome FCCH, folliculocystic and collagen hamartoma FCP, fibrous cephalic plaque TSC, tuberous sclerosis complex angiofibroma fibrofolliculoma fibrous cephalic plaque mTOR mTORC1, mammalian target of rapamycin complex 1 tuberous sclerosis
 Joint deformities Pachydermodactyly Rheumatoid arthritis Tuberous sclerosis

 Late-Onset Multiple Carboxylase Deficiency Late-Onset Multiple Carboxylase Deficiency Biotinidase BTD Biotinidase Deficiency


 COVID-19 Non-structural proteins SARS-CoV-2 Structural proteins Vaccine

 EAE Haematopoietic stem cells Macrophages Spleen Telocytes Tissue repair and regeneration
 TSC2/PKD1 contiguous gene deletions polycystic kidney disease pregnant woman prenatal diagnosis renal angiomyolipoma tuberous sclerosis

 Amyotrophic lateral sclerosis (ALS) Fused in sarcoma (FUS) PCBP2 TDP43 hnRNP
 angiomyolipomas cortical tubers facial angiofibromas lymphangioleiomyomatosis subependymal tubers tuberous sclerosis
 Anterior temporal lobectomy Multiple hippocampal transection Temporal lobe epilepsy
 Cardio-oncology Dizygotic Rhabdomyomas Tuberous sclerosis complex Twins
 Microglia NLRP3 inflammasome Parkinson disease Wuzi Yanzong Pill
 Tuberous sclerosis genotype hamartoma phenotype


 Aminoacyl transfer-RNA synthetase Antisynthetase syndrome Overlap myositis RNA immunoprecipitation
 angiofibroma angiomyolipoma hematuria radial migration lines subependymal nodules tuberous sclerosis complex


 MAVS NLRP3 inflammasome UFMylation antiviral defense gamma-herpesvirus herpesvirus interactome mitochondrial-derived vesicles viral evasion virus/host interaction
 Neuropathic pain pregabalin treatment
 cholesterol-25-hydroxylase endothelial cells experimental autoimmune encephalomyelitis oxysterols polymorphonuclear myeloid-derived suppressor cells
 Demyelinating disease MOG MOGAD MRI Myelin Oligodendrocyte Glycoprotein NMDAR NMOSD Relapse Rituximab Satralizumab
 Antimuscarinic therapy Botulinum neurotoxins Detrusor sphincter dyssynergia Neurogenic detrusor overactivity Neurogenic detrusor underactivity
 AlCl3 JAK-2/STAT-3 Lactobacillus rhamnosus PPAR-γ Wnt/β-catenin/GSK-3β neurotoxicity probiotic sesamol

 Demyelinating disorders Encephalitis SARS-CoV-2 Viral trigger
 ACE-2 Blood–brain barrier COVID Central nervous system Cerebrovascular disease Neuroinvasion SARS-CoV-2
 Decision Making Health Equity Health policy Organisational development PUBLIC HEALTH QUALITATIVE RESEARCH

 cannabinoid-based medicines cannabinoids cannabis chronic pain marijuana sleep disorders
 adrenoleukodystrophy arterial spin labeling cerebral blood flow perfusion vitamin D
 PD-1 autoimmune diseases cancer diphtheria toxin-derived immunotoxin programmed death-1 cells protein therapeutics yeast
 Empty sella Idiopathic intracranial hypertension Magnetic resonance imaging Optic nerve tortuosity Perioptic subarachnoid space distension Posterior globe flattening Transverse sinus stenosis Visual outcome
 Immune-mediated inflammatory diseases Mendelian randomization Rheumatoid arthritis Systemic lupus erythematosus Valvular heart disease
 Dynamic light scattering Electron paramagnetic resonance Intrinsically disordered protein (IDP) Transmission electron microscopy
 COVID-19 Central nervous system diseases Mortality Prevalence
 cardiac tumor everolimus rhabdomyoma tuberous sclerosis complex
 case reports signet ring cell carcinoma squamous cell carcinoma systemic scleroderma uterine cervical neoplasms

 Angiomyolipoma Astrocytomas Cardiac rhabdomyomas Everolimus MTOR inibitors Tuberous sclerosis complex
 FUS SOD1 TDP-43 amyotrophic lateral sclerosis biomarkers micro RNAs regulators of gene expression

 TSC angiofibroma TSC angiomyolipoma TSC1 TSC2 low-level mosaicism massively parallel sequencing tuberous sclerosis complex variant detection
 Branch retinal vein occlusion Retinal astrocytic hamartoma Tuberous sclerosis complex
 Raynaud phenomenon calcinosis hand surgery joint contracture scleroderma systemic sclerosis
 ALS amyotrophic lateral sclerosis carpal tunnel syndrome compressive neuropathy misdiagnosis
 astrocytomas subependymal giant cell astrocytoma tuberous sclerosis complex tumor
 Autoimmune disease COVID-19 Disease activity Flare SARS-CoV-2 Vaccination
 extracellular vesicle fibrosis mesenchymal stem cell systemic sclerosis vascular injury
 Mendelian randomization Parkinson's disease inflammatory bowel disease neurodegenerative disease


 disabilities information neurological diseases online health information seeking saudi arabia

 Optic neuritis glucocorticoids prescribing utilization
 Blood-brain barrier Cannabinoids Ischemic stroke Neuroinflammation VCE-004.8
 FFAR3 Schwann cells chronic inflammatory demyelinating polyneuropathy dorsal root ganglia propionate
 Chronic fatigue Cognitive behavioural therapy Long term conditions Transdiagnostic

 Botulinum toxin A Cervical dystonia Healthcare resource utilization Spasticity Treatment patterns
 inflammatory bowel diseases (IBDs) myeloid cells neutrophils suppressors of cytokine signaling (SOCS) ulcerative colitis (uc)
 CDX Chitosan nanoparticles Encephalomyelitis Experimental autoimmune Fingolimod Targeted delivery
 Autoimmune disease Drug-target Mendelian randomization HMGCR Immune regulation PCSK9
 Chronic kidney disease Retinal hamartoma Skin lesions TSC
 Fetal cardiac tumor Fetal cranial MRI Fetal echocardiography Genetic testing Termination of pregnancy Tuberous sclerosis complex

 anti-nuclear antibody interstitial lung disease raynaud’s phenomenon scleroderma renal crisis systemic sclerosis

 Adult neurology Clinical trials Motor neurone disease NEUROLOGY THERAPEUTICS
 Amyotrophic lateral sclerosis Cajal bodies FUS Neurodegeneration Nucleolus Paraspeckles Phase separation TDP-43 Transport granules
 PMAT RuvBL1/2 autoantibodies idiopathic inflammatory myopathy particle multiple analyte technology polymyositis scleromyositis speckled pattern systemic sclerosis
 Angiofibroma ash leaf macules rhabdomyoma
 Caesarean delivery Cohort Meta-analysis Offspring health outcomes Sibling comparison Simulation Systemic review

 ALS MCC950 MEFV NLRC4 NLRP1 NLRP3 iPSC-derived microglia inflammasomes
 Lebanon covid-19 haemorrhagic ischaemic neurologic complications stroke
 Neuromyelitis optica spectrum disorder acquired demyelinating syndromes mitochondrial diseases neurogenetics
 CXCL10 JAK inhibition TREX1 brain vascular disorder hereditary autoinflammatory diseases immunosuppression
 Esophageal motility Hematopoietic stem cell transplant Peristalsis Systemic sclerosis
 Orbital perivascular epithelioid cell tumor Retinal astrocytic hamartoma Tuberous sclerosis
 amyotrophic lateral sclerosis biomarker cholesterol motor neurone disease pre-symptomatic
 Case report Foreign-body granuloma Oil injection Penis Sclerosis
 Amyotrophic lateral sclerosis Glutathione Honokiol Mitochondrial biogenesis Mitochondrial dynamics NRF2 Oxidative stress SOD1-G93A
 Ultrasound evaluation shear wave elastography (SWE) systemic sclerosis (SSc)
 blood oxygenation level-dependent cortex glomerulonephritis medulla spin relaxation rate value
 ALS C9ORF72 FUS SOD1 TDP-43 mutations putative targets suppressor
 Amyotrophic lateral sclerosis Autophagy Mitochondrial dynamics Oxidative stress Wnt Ca(2+) Wnt β-catenin
 Raynaud’s phenomenon Systemic sclerosis angioplasty digital ischemi digital ulcers


 DJ-1 amyotrophic lateral sclerosis (ALS) hypoxia metabolism mitochondria oxidative stress
 Anti synthetase antibodies Interstitial lung disease Myositis antibodies Systemic sclerosis
 K+ spatial buffering SOD1 amyotrophic lateral sclerosis astrocytes excitability
 External cervical resorption connective tissue disorders scleroderma systemic sclerosis
 Heart Tuberous Sclerosis congenital heart disease echocardiography fetal tumor rhabdomyoma
 Amyotrophic lateral sclerosis (ALS) RNA modification. epigenetics gene environment interaction heterogeneity metabolism motor neuron disease pathophysiology
 Disability improvement EDSS Interferon beta-1a Long term Prevalence
 Genetic architecture Genetic risk scores Phenome-wide association study Rheumatoid arthritis Risk calibration Vasculitis
 Negatives cannabinoids inflammatory cytokine sport recovery
 brute force negative image-based optimization (BR-NiB) docking rescoring inflammation molecular docking negative image-based rescoring (R-NiB) pharmacophore (PHA) filtering retinoic acid receptor-related orphan receptor gamma t (RORγt) virtual screening (VS)

 RNA‐sequencing myelin oligodendrocytes osteopontin isoforms
 AAV CNS Canavan disease Demyelination Gene therapy N-acetylaspartate Neurodegeneration Neurons Oligodendrocytes
 Angiofibromas Sclerotic bone lesions Tuberous sclerosis complex Variant of uncertain significance
 682YENPTY687 motif Amyloid precursor protein Amyotrophic lateral sclerosis Neurodegeneration
 Abatacept CTLA4 Neuroinflammatory disorders Primary Immune Regulatory Disorders

 Annualized relapsing rate Benign neuromyelitis optica spectrum disorders Good outcome course Myelitis Predictive factors
 Antimycin A (PubChem CID: 14957) Dimethyl fumarate Dimethyl fumarate (PubChem CID: 637568) Dimethyl malonate (PubChem CID: 7943) Dimethyl succinate (PubChem CID: 7820) GSK′872 (PubChem CID: 54674134) MLKL Monomethyl fumarate (PubChem CID: 5369209) N-acetyl-L-cysteine (PubChem CID: 12035) Necroptosis Necrostatin-1 (PubChem CID: 2828334) RIPK3 Reverse electron transport Rotenone (PubChem CID: 6758) Systemic inflammatory response syndrome
 Crohn ‘s disease Parkinson’s disease autoimmune disease bullous pemphigoid comorbidity inflammatory bowel disease ulcerative colitis
 NeuroAssist system electromyography motor recovery neurorobotics robot-assisted therapies upper limb rehabilitation

 cognitive function fingolimod schizophrenia
 MR-STAT diagnostic accuracy diagnostic quality magnetic resonance imaging quantitative MRI synthetic MRI
 MOG antibody disease Neuromyelitis optica Neuromyelitis optica spectrum disorder Optic neuritis Serum antibody against aquaporin 4 (AQP4) Transverse myelitis
 Dementia Goal Attainment Scaling Meta-analysis Neurodegenerative disease Systematic review
 human lung fibroblast (HLF) idiopathic pulmonary fibrosis interferon beta (IFN-β) mesh nebulizer
 Autophagy Cardiotoxicity Differentiated AC16 cardiac cells Metabolism Mitoxantrone Naphthoquinoxaline metabolite


 amyotrophic lateral sclerosis muscular dystrophy polymyositis spondylotic myelopathy

 Amyotrophic Lateral Sclerosis C9orf72 mutation MRI fMRI
 case reports diffuse interstitial lung disease systemic sclerosis
 amyotrophic lateral sclerosis biomarker cerebrospinal fluid mass spectrometry proteomics

 ABRA CNSV PACNS Vasculitis

 Preventative medicine Prevention SARS-CoV-2 Scleroderma Systemic sclerosis Vaccination Vaccines
 RNA binding proteins adeno-associated virus amyotrophic lateral sclerosis gene therapy proteostasis
 epilepsy surgery infantile spasms neurodevelopment vigabatrin
 Amyotrophic lateral sclerosis ALS FMR1 FMRP FXR1 FXR1P FXR2 FXR2P Neurodegenerative disease Protein aggregation
 amyotrophic lateral sclerosis brain steroids disease-related mutations metabolomics metallomics
 Amyotrophic lateral sclerosis Multiple system atrophy Nocturnal hypercapnia Nocturnal hypoventilation Sleep breathing disorders Transcutaneous carbon dioxide monitoring
 Dermatomyositis JAK Janus kinase Primary Sjogren's syndrome Rheumatoid arthritis STAT Systemic lupus erythematosus Systemic sclerosis Vasculitis tsDMARD
 SLE everolimus lupus nephritis mTOR tuberous sclerosis
 amyotrophic lateral sclerosis cognition endophenotype
 amyotrophic lateral sclerosis and neuroinflammation excitotoxicity neurodegeneration oxidative stress superoxide dismutase (SOD1)
 Amyotrophic lateral sclerosis Fasciculation Split phenomenon
 amyotrophic lateral sclerosis (ALS) enzymes of sphingolipids metabolism lipids models of ALS sphingolipids
 Amyotrophic lateral sclerosis (ALS) At-risk Community Education Frontotemporal degeneration (FTD) Genetic counseling

 computer inhalant abuse diffuse sclerosis secondary hyperparathyroidism skeletal fluorosis substance use disorder
 childhood lung disease esophageal abnormalities high-resolution computed tomography scan (HRCT) interstitial lung disease (ILD) juvenile systemic sclerosis pulmonary nodules
 magnetic resonance imaging prenatal diagnosis tuberous sclerosis complex ultrasound
 Diffusion tensor imaging Diffusion-weighted MRI Parkinson’s disease Substantia nigra White matter
 Neural stem progenitor cells Protein biomarkers Proteomics Tuberous sclerosis complex


 bone remineralization computed tomography multiple myeloma whole-body imaging
 Horan-Beighton Syndrome OS-CS AMER1-Related Osteopathia Striata with Cranial Sclerosis Horan-Beighton Syndrome OS-CS APC membrane recruitment protein 1 AMER1 Osteopathia Striata with Cranial Sclerosis
 amyotrophic lateral sclerosis environmental risk factor motor neuron disease strenuous physical activity
 Ankylosis Cone-beam computed tomography Hemarthrosis Infection Temporomandibular joint
 Diffusion tensor imaging Pathophysiology Sleep disorder Sporadic amyotrophic lateral sclerosis White-matter integrity
 LMICs South Africa cognition low-resource setting neuropsychology tuberous sclerosis complex
 Mental disorders Multi-state Sickness absence Unemployment Work
 Aamyotrophic lateral sclerosis human leukocyte antigen serotype
 P-glycoprotein antiseizure medication epilepsy mTOR inhibitor tuberous sclerosis complex
 COVID-19 behaviour compliance natural language processing topic modelling
 immunology < IMMUNOLOGY infections disease/aids < NEURO OPHTHALMOLOGY neuro imaging < NEURO OPHTHALMOLOGY optic neuritis < NEURO OPHTHALMOLOGY optic neuropathy < NEURO OPHTHALMOLOGY
 Myasthenia gravis Myotonia Orbicularis oculi Orbital portion Pre-septal portion Pre-tarsal portion
 CASPR2 case report flow cytometry multifocal motor neuropathy
 autoantibody dermatomyositis polymyositis proteomics systemic sclerosis
 Amyotrophic lateral sclerosis (ALS) Differential expression analysis Protein quantitative trait loci (pQTL) Proteome-wide association study

 Alzheimer’s disease Lewy body disease frontotemporal lobar degeneration neurodegenerative disease tauopathy
 TP73 amyotrophic lateral sclerosis clinical characteristic gene mutation neurodegenerative disease phenotype–genotype association
 CXCL4 ER stress autoimmunity fibrosis plasmacytoid dendritic cells systemic sclerosis type I IFN
 Amyotrophic lateral sclerosis Clinical trial Mesenchymal stem cells Motor neurons Neurological disease
 baicalein chronic kidney disease encapsulating peritoneal sclerosis peritoneal dialysis peritoneal fibrosis
 Exosome L1CAM amyotrophic lateral sclerosis (ALS) biomarker neural-enriched reproducibility
 Autoimmune disease Extracellular vesicles Immunomodulation Mesenchymal stem cells Systemic sclerosis
 biologic therapy precision medicine rituximab systemic sclerosis (SSc) targeted therapy tocilizumab
 Alzheimer’s disease Parkinson’ s disease ageing amyotrophic lateral sclerosis autophagy ketogenic diet (KD) medium chain fatty acid (MCFA) mitochondria
 MEN1 MEN4 Neuroendocrine neoplasms Neurofibromatosis 1 (NF-1) Targeted therapies Tuberous sclerosis (TSC) Von Hippel–Lindau (VHL) syndrome
 astrocytic hamartoma multicolor imaging retinitis pigmentosa

 Edinburgh Cognitive and Behavioural ALS Screen amyotrophic lateral sclerosis frontotemporal degeneration language primary progressive aphasia
 neuroimmunology neuroophthalmology vision

 NLRP3 Nrf2/ARE high-fat diet nonalcoholic fatty liver disease type II diabetes
 Cerebellar ataxia Cerebellum Gait Posture Rehabilitation Therapies
 Glucagon-like peptide-1 Headache Idiopathic intracranial hypertension Visual worsening Weight loss
 Parkinson’s disease Wuzi Yanzong Pill apoptosis dopaminergic neurons endoplasmic reticulum stress


 Hypogammaglobulinemia Infectious risk Rituximab

 Astrocyte Experimental autoimmune encephalomyelitis G-protein coupled bile acid receptor Gpbar1 Neuroinflammation Taurochenodeoxycholic acid


 MRI TMEV brain atrophy siponimod spinal cord
 Guillain-Barré syndrome axon biomarker neuropathy peripheral nervous system peripherin
 IMU distance sensors ecological conditions gait analysis pressure insoles spatial-temporal gait parameters wearable sensors
 Lewy body Parkinson's disease biological definition biomarker diagnostic criteria neurodegeneration neuropathology



 Case report Clinical manifestations Misdiagnosis and overtreatment Neuroimaging manifestations Tuberous sclerosis complex
 Adverse effects Idiopathic pulmonary fibrosis Management strategies Nintedanib Safety Systemic sclerosis
 Alveolar epithelial cells Amphiregulin Basal cells Epithelial Growth Factor Receptor Interstitial lung disease Natural killer cells Scleroderma Systemic sclerosis T cells
 amyotrophic lateral sclerosis deglutition deglutition disorders Parkinson disease

 amyotrophic lateral sclerosis non-invasive ventilation respiratory failure serum chloride survival
 case report de novo missense mutation of TSC2 gene tuberous sclerosis complex–associated neuropsychiatric disorders whole-exome sequencing
 Aminaphtone Raynaud’s phenomenon blood perfusion systemic sclerosis vascular molecules
 alcohol binge drinking cell deformability cell mechanics ethanol immune system leukocytes real-time deformability cytometry
 MOG-IgG associated disorders demyelinating disease encephalomyelitis fever rhombencephalitis
 RNA oligonucleotide RNA-protein interaction hnRNPA1 optogenetics stress granules
 New-York Cognition Questionnaire functional connectivity functional near infrared spectroscopy resting-state time-of-day

 Raynaud phenomenon elastography idiopathic non-cirrhotic portal hypertension systemic sclerosis
 gait kinematics spinocerebellar ataxia 38 (SCA 38)
 Angiotensin Brain injury Renin-angiotensin system Traumatic brain injury
 Cognitive reserve Cognitive screening Normative data Regression-based norms Tele-neuropsychology
 COVID-19 Immunomodulatory effects Prolactin SARS-CoV-2 Severity

 ablation therapy leg ulcer sclerotherapy treatment wound wound care wound dressing wound healing
 Alzheimer’s disease Amyotrophic lateral sclerosis Genome-wide association studies Parkinson’s disease Pleiotropy

 autoimmune encephalitis cognitive assessment cognitive outcomes leucine-rich glioma inactived 1 mild cognitive impairment neuropsychological profile temporal lobe epilepsy
 Bone marrow stem cells Clinical trials Hematopoietic stem cells Mesenchymal stem cells Neural stem cells SOD1G93A transgenic rodents Umbilical cord blood stem cells

 Carcinoid Eosinophilic variant Neuroendocrine neoplasms Neuroendocrine tumors Survival Tuberous sclerosis complex
 Amyotrophic lateral sclerosis Biomarkers Disease progression rate Motor neuron disorder Spinal cord MRI
 Bone brown tumor Bone scan Primary hyperparathyroidism SPECT/CT
 Efficacy Rapamycin Safety Tuberous Sclerosis
 ALS CMAP MUNE far-field potential inter-rater reproducibility
 amyotrophic lateral sclerosis clobazam pharmacokinetics riluzole ultraperformance liquid chromatography-tandem mass spectrometry
 TDP-43 amyotrophic lateral sclerosis cyclin F frontotemporal dementia mouse models ubiquitination
 Autoimmunity Common variation Genome-wide association study Rheumatoid arthritis Systemic lupus erythematosus Systemic sclerosis
 Hippocampal sclerosis Histopathology Outcomes Surgery Temporal lobe epilepsy
 Autism spectrum disorders Brain morphology Language Structural MRI Tuberous sclerosis complex
 anxiety health-related quality of life large fibre neuropathy neuropathic pain small fibre neuropathy systemic sclerosis
 Acute kidney injury Complement Scleroderma renal crisis Systemic sclerosis Thrombotic microangiopathy
 ALS Amyotrophic lateral sclerosis Exercise MND Motor neuron disease Physical activity Rehabilitation
 PLS Functional Rating Scale (PLSFRS) Primary lateral sclerosis (PLS) clinical trials motor neuron disease (MND) natural history study
 Airway protection Cough Deglutition Neurodegenerative
 Autologous hematopoietic stem cell transplantation Intrinsic subsets Machine learning RNA gene expression Systemic sclerosis
 ALS SOD1G93A low-copy exercise home cage monitoring mouse behavior neuromuscular junction functionality physical activity wheel running
 ALS Cell-to-cell propagation Endocytosis Extracellular-vesicles Oligomerization
 interstitial infiltration morphea mycosis fungoides
 Amyotrophic lateral sclerosis (ALS) C9ORF72 Cryptic exon (CE) Frontotemporal dementia (FTD) Single nuclei RNA sequencing TAR DNA-binding protein 43 (TDP-43)

 mesenchymal stem/stromal cells rheumatoid arthritis systemic lupus erythematosus systemic rheumatic diseases systemic sclerosis
 UPLC-MS everolimus metabolomics proteomics tuberous sclerosis complex
 Alzheimer’s disease Parkinson’s disease amyotrophic lateral sclerosis neurodegenerative disorders nitric oxide nitric oxide synthase superoxide dismutase 1
 immunological skin conditions lichen sclerosus (balanitis xerotica obliterans) scleredema Burschke scleroatrophic lichen scleromyxedema systemic sclerosis

 Bronchial carcinoids Carcinoides bronquiales Carcinoides tímicos Gastro-entero-pancreatic neuroendocrine tumours Multiple endocrine neoplasia syndrome type 1 Neuroendocrine tumours Síndrome de Von Hippel Lindau Síndrome de neoplasia endocrina múltiple tipo 1 Thymic carcinoids Tumores neuroendocrinos Tumores neuroendocrinos gastro entero-pancreáticos Von Hippel Lindau syndrome
 mitochondrial fission mitochondrial fusion mitochondrial transport mitophagy

 Amyotrophic lateral sclerosis Blood-brain barrier Edaravone delivery to the brain Focused ultrasound with microbubbles Motor function SOD1 transgenic mice
 Amyotrophic Lateral Sclerosis Genetic modifiers Post-zygotic mutations Repeat expansions
 Tuberous sclerosis complex (TSC) bioinformatics analysis complement C3 immune injury

 Immune complexes Immune complexome analysis Mediator of RNA polymerase II transcription Subunit 30 Systemic sclerosis Vascular endothelial dysfunction
 Microcirculation Superb microvascular imaging Systemic sclerosis
 Amyotrophic Lateral Sclerosis (ALS) SOD1 SOD1 G93A mouse motoneuron disease mouse model neuromuscular pharmacology
 Systemic sclerosis exercise functional capacity rehabilitation


 aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder eculizumab post-marketing surveillance real-world evidence relapse prevention
 Cognition Fingolimod GWI Integrated stress response Microglia activation Neuroinflammation PKR
 cannabinoids cannabis mixed methods pain representative survey
 Arthritis, Psoriatic Arthritis, Rheumatoid Spondylitis, Ankylosing Tumor Necrosis Factor Inhibitors
 ANGPTL2 Differentiation Fyn MAG MYRF Myelination Oligodendrocyte
 Axillary Breast Hodgkin Lymphoma Lymphoproliferative MRI Mammography Ultrasound
 COVID-19 SARS-CoV-2 Severe COVID-19 immunosenescence and exhaustion immunosenescence and inflammaging

 MAMS trial Motor neuron disease Multi-arm Platform trial Statistical analysis plan
 Brain disorders Brain imaging-derived phenotypes Cardiovascular diseases Causal relationships Genetic correlation
 Acute disseminated encephalomyelitis Demyelinating disease Immunotherapy Neurofilament light chain Neuroinflammatory disease Post infectious neurological syndrome
 Natural history chronic cluster headache episodic cluster headache predictors
 Accumulator copay assistance programs insurance design maximizer out-of-pocket healthcare costs prescription drug patient assistance programs


 Fluphenazine extrapyramidal syndrome memory loss neuroleptics neurotoxicity parkinsonism

 Alzheimer’s disease brain dynamics excitatory/inhibitory balance frontotemporal dementia resting-state networks virtual brain modeling
 Cerebellum Cerebral cortex Diffusion Dual-task Parallel fMRI
 Inflammatory bowel disease migraine disorders prevalence
 Cognitive functions Manual dexterity Prefrontal cortex Sensorimotor functions fNIRS

 Autoimmune Emergency department Inpatient Systemic disorders Vitiligo
 amyotrophic lateral sclerosis (ALS) autophagy degenerative motor neuron diseases hyperexcitation induced pluripotent stem cells (iPSCs) motor neurons protein accumulation

 ALS mimic syndrome Chiari 1 malformation adult amyotrophic lateral sclerosis cerebrospinal fluid differential diagnosis related disorder syringomyelia
 Amyotrophic lateral sclerosis (ALS) Sporadic Amyotrophic lateral sclerosis (sALS) Transcriptome-wide association study (TWAS) mRNA expression profile
 hormesis mitochondria mitochondrial dysfunction mitochondrial hormesis mitochondrial metabolism

 SSc SSc-ILD apoptosis autophagy skin fibrosis

 Genetics Lysosomes Mouse models Neurodegeneration Neuroscience
 denervation energy metabolism mouse models neuromuscular junction neurophysiology
 Phonemic analysis intelligibility neurodegenerative disease speech impairment
 Air pollution Amyotrophic lateral sclerosis Mortality Particulate matter Women's health initiative
 amyotrophic lateral sclerosis decision-making gastrostomy motor neuron disease qualitative ventilation
 Myalgia Myopathy Myositis Rheumatoid arthritis Systemic lupus erythematosus Systemic sclerosis
 Alzheimer’s disease Amyotrophic lateral sclerosis Autophagy Huntington’s disease Mitochondrial damage Mitophagy Neurodegeneration Oxidative stress Parkinson’s disease

 Amyotrophic lateral sclerosis Oligogenic inheritance Optineurin Superoxide dismutase 1 Survival TANK-binding kinase 1
 Genome stability Neurodegenerative diseases R-loops RNA helicases Senataxin Transcription termination
 disease progression frontotemporal dementia frontotemporal lobar degeneration neurofilament light trial stratification

 ALS TDP-43 gastrointestinal tract human tissue non-CNS tissue pathology
 APOE aging amyloid causal mediation cognition dementia multiple pathologies neuropathology tau

 ALS-plus syndrome Cognitive impairment Extrapyramidal impairment Neurodegenerative disease Rare damage variants
 ALS PIKFYVE neurodegeneration
 chimeric antigen receptor T cell therapy rheumatoid arthritis systemic lupus erythematosus systemic rheumatic diseases systemic sclerosis
 Alzheimer's disease Friedreich's ataxia Huntington's disease Lou Gehrig's disease Parkinson's disease amyotrophic lateral sclerosis frontotemporal dementia machine learning pathway analysis random forest classification whole blood RNA

 ALS Frameshifting Localized translation Neurodegeneration RAN translation RNA binding protein Repeat expansion Ribosome quality control Translation elongation Translation initiation Translation regulation

 IL-17A IL-17F IL-23 MAIT cells Th17 cells psoriasis spondyloarthritis γδ T cells

 Esophageal motility disorders Pulmonary fibrosis Systemic sclerosis
 diagnostic management interstitial lung disease systemic sclerosis therapeutic management
 Angiomyolipoma Lymphangioleiomyomatosis Pneumothorax Sirolimus Tuberous sclerosis
 Adult-onset scleroderma Cardiac disease Interstitial lung disease Juvenile-onset scleroderma Systemic sclerosis
 amyotrophic lateral sclerosis lenzumestrocel mesenchymal stem cell stem cell therapy survival analysis
 Eker rats animal models of autism cingulate gyrus dendritic spine enriched environment open field test tuberous sclerosis complex
 Amyotrophic Lateral Sclerosis Long non-coding RNA Neurodegeneration Neuronal differentiation ZEB1-AS1 cancer hsa-miR-200c β-Catenin
 Amyotrophic lateral sclerosis (ALS) Frontotemporal dementia (FTD) Immunotherapy Microglia TDP-43

 Cerebellar transcranial direct current stimulation (tDCS) Gait analysis Non-invasive brain stimulation (NIBS) Spinocerebellar ataxia 38 (SCA 38)
 Bell palsy COVID-19 vaccines Incidence Incidencia Parálisis de Bell Vacunas COVID-19

 CP: Immunology antigen-presenting cell decidua basalis decidua parietalis extravillous trophoblast human placentation immune cell distribution macrophage pregnancy

 BCR sequencing TCR sequencing cerebrospinal fluid cryopreservation immune cells single-cell RNA-seq
 Neoehrlichia mikurensis hemophagocytic lymphohistiocytosis hyperinflammation immune suppression neoehrlichiosis opportunistic infection tick-borne disease
 Cadherin-11 Epithelial-to-mesenchymal transition Fibroblasts Fibrosis Macrophages
 epidemiology neuroepidemiology statistics
 Anti-N-Methyl-D-Aspartate Receptor Encephalitis Aseptic Meningitis CNS Demyelinating Autoimmune Diseases Meningoencephalitis Neuromyelitis Optica
 enteral access enteral nutrition hematopoietic/stem cell transplant microbiome oncology pediatrics
 CHCHD10 G58R bioinformatics genetics mitochondrial myopathy multiple-run molecular dynamics simulations structural properties
 Age Aging Diffusion tensor imaging Fractional anisotropy Neurofilament light White matter lesions

 CNS immunity Indoleamine-2,3-dioxygenase-1 (IDO1) glioma tumor vasculature
 AQP4 Cerebrospinal fluid Kynurenine NMOSD NMOSD-IgG Relapse Tryptophan metabolism
 MANF dorsal root ganglia neurite outgrowth peripheral nerve injury priming proteomics


 Alzheimer’s disease cognitive aging neurodegenerative disease oldest-old successful aging vascular
 SYF2 TDP-43 amyotrophic lateral sclerosis androgens connectivity map drug screen induced pluripotent stem cells nineteen complex norgestrel spliceosome
 Wnt/β-catenin signaling pathway chemokine signaling pathway genome-wide DNA methylation interstitial lung disease peripheral blood mononuclear cells systemic sclerosis transcriptome expression profiles
 Acetylated TDP-43 Endogenous gene tagging LLPS Motor neuron disease TDP-43 loss of function
 Anti-Ku antibody Children Idiopathic inflammatory myopathies Systemic sclerosis
 aging anti-complement component 5 astrogliosis brain neurodegeneration neuroinflammation obesity
 atopic dermatitis autoimmune hepatitis cat eye syndrome chatgpt livedo racemosa primary biliary sclerosis psoriasis schmid-fraccaro syndrome
 FAME1 NIID RNA-binding protein RNA/protein aggregates SCA37 frontotemporal dementia/amyotrophic lateral sclerosis liquid/liquid phase separation polyalanine polyglutamine spinocerebellar ataxia
 Becker muscular dystrophy Duchenne muscular dystrophy Neuromuscular diseases Pompe disease amyotrophic lateral sclerosis facioscapulohumeral muscular dystrophy limb girdle muscular dystrophy muscular dystrophies registries spinal muscular atrophy
 corporate digital entrepreneurship digital capability entrepreneurial culture institutional support organizational inertia strategic alliance
 SQSTM1 frameshift mutation multisystem proteinopathy myopathy rimmed vacuoles



 fibrosis humanized mice interleukin 6 scleroderma systemic sclerosis
 Autoimmune disorders COVID-19 vaccine SARS-CoV-2
 Accelerometer Algorithms Cadence DMOs Digital health Real-world gait SL Validation Walking Wearable sensor




 autophagy mitochondria mitostasis neurodegeneration oxidative stress proteasome
 Cone beam computed tomography Jaw metastatic disease Medication related osteonecrosis of the jaw Osteomyelitis Osteoradionecrosis
 bone cartilage knee joints osteoarthritis simultaneous PET/MRI
 Bone fractures Brain abnormalities CSF1R Dementia Dysosteosclerosis Jaw necrosis LRRK1 Leukoencephalopathy Metaphyseal osteosclerosis Neurodegeneration Optic atrophy Osteopenia Osteopetrosis Osteosclerosis Osteosclerotic metaphyseal dysplasia Pyle disease SLC29A3 TCIRG1 TNFRSF11A TNFSF11

 C9orf72 ER stress G3BP1 H3S10 JNK stress granules
 Cancer Neurodegenerative diseases Post-transcriptional gene regulation RNA RNA processing RNA-binding proteins Viral infection

 Cystic fibrosis Eating behavior Food Insecurity Nutrition Pancreatic enzymes Sodium Weight management
 European Medicines Agency Patient-reported outcomes
 NG2 NPC NSC Neural Stem Cell Neuroglia Neurosphere Oligodendrocyte Regeneration
 Adverse event Cancer Immune checkpoint inhibitor Neuromuscular
 FACS adult neurogenesis dopamine gene expression olfactory bulb
 ADHD Alzheimer’s DNA methylation Depression Neurological disorders Rett syndrome
 ATTR amyloidosis biomarker disease severity neurofilament light chain
 Alzheimer’s disease MFGE8 astrocytes microglia synapse loss synapses
 Depressive symptoms Inflammation Major depressive disorder Metabolic syndrome
 RNA sequencing STAT proteins co-operative DNA binding inflammation myocardial infarction
 Gene panel Ischemic stroke Juvenile stroke Stroke etiology Whole-exome sequencing
 cognitive enhancers exploration marginal value theorem stay-or-switch value-based decision-making
 lacosamide neuropathic pain trigeminal neuralgia
 Blood chemistry parameters COVID-19 Clinical outcome Microbiological data SARS-COV-2 infection Secondary infections

 Cognition Magnetic resonance imaging (MRI) Obesity Sleep disturbances UK Biobank White matter hyperintensities (WMH)
 Anti-inflammatory Natural product Oxidative Phenolic metabolites Tumor treatment

 ageing inflammation neurodegeneration optineurin phagocytosis
 development neurodegeneration seizures status epilepticus
 Cardiomyopathy Coronary microvascular dysfunction Myocarditis Systemic autoimmune rheumatic diseases
 cortex disease occurrence febrile seizures hippocampus neurodevelopment
 Amyloidogenic proteins Detecting Interaction Membrane Therapeutic strategies

 Amygdala nuclei Hippocampal subfields Temporal lobe epilepsy Thalamic nuclei Volumes
 Alzheimer’s disease BMAA Parkinson’s disease amyotrophic lateral sclerosis cyanopeptides cyanotoxins gut-brain axis harmful algal blooms microcystin mistranslation neurodegenerative disease non-proteogenic amino acids

 Motor neuron disease (MND) amyloid precursor protein (APP) amyotrophic lateral sclerosis (ALS) cholesterol sequestration cyclodextrin dyslipidaemia
 ABI3 APOE Inflammasomes Natural compounds Nrf2 RIDD pathway TREM2
 autosomal dominant skin disorders early loss of heterozygosity precursor of disseminated biallelic disorders pronounced segmental manifestation simple segmental versus superimposed mosaicism superimposed mosaicism in newborns or infants
 ONYX Transcatheter embolization angiomyolipoma ethylene vinyl alcohol (EVOH) copolymer hemorrhage outcome renal


 Chlamydia psittaci lower extremity atherosclerotic occlusive disease
 Pip5k1c aging articular chondrocytes osteoarthritis
 Neurodegenerative diseases antioxidants flavonoids oxidative stress reactive oxygen species


 HFE SOD1 amyotrophic lateral sclerosis p.H63D survival
 Air pollution Parkinson’s disease chemical water pollution environment indoor air pollution solvents tetrachloroethylene trichloroethylene water pollution
 Applicability Certainty of evidence Cross-over External validity GRADE Treatment switching
 Interstitial Fibrosis Rheumatoid lung disease Systemic disease and lungs

 cancer immune checkpoint inhibitors myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) paraneoplastic neurological syndrome tumor




 Antifibrosis Drug–drug interactions Entecavir Hydronidone Pharmacokinetics
 Lou Gehrig’s disease case study end-of-life nursing palliative care qualitative research

 Anxiety Bone High fat diet Itch Nav1.8 Neurometabolism Normal weight obesity Sensory nerve Skinny fat mTOR
 image registration insula neuroimaging temporal lobe epilepsy
 gastrointestinal immunotherapy scleroderma and related disorders soft tissue rheumatism systematic review

 adipose organoid adipose transplantation localized scleroderma microvascular fragments skin fibrosis
 amyloid-beta antidepressant antiepileptic cognitive dysfunction neuropathic pain tau
 Condylar degeneration Disc displacement Disc morphology Magnetic resonance imaging (MRI) Temporomandibular joint disorders (TMD)
 cartilage chondrocytes collagen cytokines joint pedaling

 ISR UPRmt mitochondria mitochondrial dynamics protein homeostasis quality control
 IgA nephrology M1 macrophage M2 macrophage mononuclear phagocyte system pathogenesis
 ALS Alternative splicing Neural progenitor cells
 Hippocampus Machine learning Normal asymmetries Novelty detection
 UVA1 atopic dermatitis cutaneous T cell lymphoma inflammatory keloids low dose morphea phototherapy satisfaction sclerotic ultraviolet A1
 ALS XPPAUT bifurcation excitability modeling motoneuron
 CAD cardiac marker clinical-utility risk-stratification sNfL
 COVID-19 Omicron Omicron variant SARS-CoV-2 monoclonal antibodies remdesivir sotrovimab
 T lymphocytes macrophages mitochondria salts sodium
 Parkinson's disease STEMI cardiovascular disorders myocardial infarction

 Lyme neuroborreliosis biomarker neurofilament light chain neuroinflammation persistent symptoms
 Diffusion tensor imaging Freezing of gait Neuropsychological assessments PPN Parkinson’s disease Pathophysiology Progressive supranuclear palsy
 cognition cognitive dysfunction meta-review neuroscience peri-operative neurocognitive disorder post-operative psychiatry risk factors surgery
 Charcot-Marie-Tooth type 2A Mitofusin 1 Mitofusin 2
 SARS-CoV-2 brain development haemorrhage human foetal cortex

 Amyotrophic lateral sclerosis Environment Epidemiology Etiology Geoepidemiology Spatial epidemiology
 glycogen synthase kinase 3 (GSK3) Abbreviations: DAPI, 4′,6-diamidino-2-phenylindole; DMSO, dimethyl sulfoxide; ERK, extracellular signal–regulated kinase; FOXK1, forkhead box K1; GSK3, glycogen synthase kinase 3; HA, hemagglutinin; LARP1, La-related protein 1; MEK, ERK kinase; mTORC1, mechanistic target of rapamycin complex 1; PBS, phosphate-buffered saline; PBX2, pre–B cell leukemia transcription factor 2; PI3K, phosphoinositide 3-kinase; PDK1, phosphoinositide-dependent protein kinase 1; PP1, protein phosphatase 1; PP2A, protein phosphatase 2A; RAG, RAS-related GTP-binding protein; RHEB, Ras homolog enriched in Brain; shRNA, short hairpin RNA; siRNA, small interfering RNA; TBC1D7, TBC1 (TRE2-BUB2-CDC16) domain family member 7; TSC2, tuberous sclerosis complex 2; WT, wild-type mechanistic target of rapamycin complex 1 (mTORC1) phosphorylation pre–B cell leukemia transcription factor 2 (PBX2) protein phosphatase 1 (PP1)
 CD21lo B cells autoreactive B cells flow cytometry systemic sclerosis
 Amyotrophic lateral sclerosis Artificial nutrition and hydration Chronic impairments of consciousness Death by circulatory criteria Death by neurological criteria/brain death Decision-making capacity Declaration of death by neurological criteria/brain death Determination and declaration of death by neurological criteria/brain death End-of-life Involuntary euthanasia Lawful physician-hastened death Medical/physician orders for life-sustaining treatment Oregon Death with Dignity Act Organ-sustaining technology Palliative care Palliative sedation Physician-assisted suicide Physician-hastened death (either PAS or VE) Supreme Court of the United States Tracheostomy-assisted mechanical ventilation Uniform Determination of Death Act Voluntary active euthanasia Voluntary passive euthanasia Withholding, withdrawing, or limiting life-sustaining treatment
 ALS
 Biomarker COVID-19 NfL Prognosis
 chronic kidney disease heart failure with preserved ejection fraction hypertension obesity


 anemia blood loss endoscopy substance-induced gastropathy watermelon stomach

 autophagy circRNAs nervous system neurodegeneration therapeutics

 Astrocytes Brain energy and neurotransmitter metabolism GABA-glutamine cycle Glutamate-glutamine cycle Glutamine transporters Neurodegenerative diseases Oligodendrocytes

 3D printing in vitro model platform development traumatic brain injury

 CBCT MRI artificial intelligence computer-assisted image interpretation derangement osteoarthritis
 antiseizure medication cannabidiol developmental and epileptic encephalopathies epilepsy fenfluramine ganaxolone rufinamide stiripentol


 Headache Laterality Left-sided Migraine Right-sided Unilateral
 Disability pain quality of life systemic sclerosis.

 Sjögren syndrome anti-Ro/SSA and anti-La/SSB antibodies anti-aquaporin-4 antibodies (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) sicca symptoms
 APOE4 Age Brain injury GWAS Gender Genetic predisposition Immune check-point genotypes NMDAR1-AB
 childhood trauma dissociative seizures epilepsy functional neurological disorders psychogenic seizures
 COVID-19 dementia omicron stroke
 Cerebrovascular diseases Reversible cerebral vasoconstriction syndrome Thunderclap headache Transcranial color-coded Doppler
 Cognitive Assessment Screening Instrument Mini-Cog mild cognitive impairment neuropsychological testing primary health care regression analysis test-retest reliability
 cluster headache cytochrome P450 3A oxygen polygenetic risk score sumatriptan verapamil

 encephalitis immune checkpoint inhibitors paraneoplastic neurologic syndromes
 Autoimmune encephalitis Cytokines Innate immunity LGI-1 Monocytes
 ILD PAH SSc predictability sRAGE scleroderma

 MTLE PET/MR default mode network (DMN) epileptogenic network fractional amplitude of low-frequency fluctuation (fALFF) standardized uptake value ratio (SUVR)

 FTLD FUS c-Abl c-Src cytoplasmic aggregates phosphorylation
 CBD Cannabidiol Cannabinoid Clinical trial Evidence Neurology


 Experiences Qualitative Remote Scleroderma Virtual
 Artificial Intelligence Chest Radiograph Conventional Radiography Lung Nodule Mass Detection
 high-salt diet immunity microbiome wildling
 Chemokine receptors Clonal expansion Psoriasis and psoriatic arthritis Self-reactive CD8 T cells T-cell recirculation
 Activity Ambulation Geriatrics Hospital Inpatient Mobility Older adults


 Amyotrophic lateral sclerosis Cdon Motor neuron Muscle atrophy Neuromuscular junction
 ANK3 ankyrinG autoantibody autoimmune axon initial segment (AIS) human immunodeficiency virus (HIV) meningoencephalitis node of Ranvier
 Biomarker Cerebrospinal fluid (CSF) Neurodestruction Neurofilament light (NfL) Status epilepticus (SE)
 Friedreich's ataxia MRI OCT biomarkers frataxin

 Autonomic regulation Dysautonomia Heart rate variability Intensive care unit SARS-CoV-2
 comorbidity mental health seizure somatoform disorder
 Antineutrophil cytoplasmic antibody children clinicopathologic features lupus nephritis
 Anandamide CBD, Epilepsy Cannabidiol Cannabis Marijuana Refractory seizure THC

 Epithelial cells LPS Lung diseases N-acetyltransferase 10 Smoking Transcriptomics
 AGEs Alzheimer's disease Parkinson's disease RAGE drug development neurodegeneration neuroinflammation oxidative stress
 cell surface marker extracellular matrix fibroblast subtype pulmonary fibrosis single-cell RNA-sequencing
 Abscess cellulitis diagnostic imaging meta-analysis ultrasonography
 IVIG MOGAD acute treatment effectiveness outcomes safety
 COVID Long covid Movement disorder Myoclonus ataxia Outcome Parkinsonism Sars-CoV2

 Fractional anisotropy ICH score Intracerebral haemorrhage Mean diffusivity Outcome prediction Whole-brain approach
 Antibodies B cells Intestine Pediatrics TFH cells
 Alzheimer's disease Amyloid pathology CREB Jacob early synaptic dysfunction

 Parkinson aging obstructive sleep apnea questionnaire screening validation
 M2 macrophages Systemic scleroderma T lymphocytes TGP Type I interferons
 NF-κB NLRP3 Neurodegenerative disease Neuroinflammation thymopentin (TP-5)
 Parkinson's disease cognition dementia vision
 biomarkers biospecimens new onset refractory status epilepticus standard operating procedures
 cerebrovascular disease stroke

 GAD65 stiff person syndrome therapeutic plasma exchange
 Biomarker Demyelination Neurodegeneration Quantitative MRI Spinal cord injury
 NR2C NR2D blood–brain barrier epilepsy seizure tuberous sclerosis complex
 C9orf72 dementia neurodegeneration radiogenomics thalamus transposable elements

 dementia neurology neuropathology neurophysiology protocols & guidelines telemedicine

 collapsing glomerulopathy focal segmental glomerulosclerosis graft kidney transplantation proteinuria
 Alzheimer's disease Early risk factors Modelling Subtypes
 ADHD Childhood absence epilepsy Prognosis Psychiatric comorbidity School
 Alzheimer’s disease Amyloid Cerebral blood flow PET R 1

 HEALTH SERVICES ADMINISTRATION & MANAGEMENT QUALITATIVE RESEARCH Quality in health care STATISTICS & RESEARCH METHODS
 Analytical validity Biomarker Clinical utility Neurology Protein Proteomics
 dementia epidemiology ophthalmology
 adjunctive treatment meta-analysis minocycline neurology psychiatry
 brain-derived neurotrophic factor cell signaling inflammation phrenic motor neuron plasticity
 Aura Drug-resistant Epilepsy Seizure Stereoelectroencephalography Temporal Lobe Epilepsy Treatment Outcome
 Capillaroscopy Coagulopathy Endothelial dysfunction Livedo Livedoid vasculopathy Microcirculation

 COVID-19 epidemic waves epidemiology risk factors
 AQP4 Demographics Neuromyelitis optica spectrum disorder Relapse Treatment
 Long COVID Omicron SARS-CoV-2 breakthrough infection neuropsychiatric deficits
 MOGAD postpartum pregnancy relapse rate
 Cell transplantation Disease modelling Extracellular vesicles Induced pluripotent stem cells Neurodegeneration Oligomers
 Antirheumatic Agents Biological Products Outcome Assessment, Health Care Therapeutics
 Brain morphology Dementia Genetics Glaucoma MAPT Neurodegenerative disorders
 SSc epidemiology glucocorticoids


 PI3K/Akt signaling pathway Wuzi Yanzong Pill cell apoptosis neural tube defects
 COVID-19 German myasthenia gravis registry Immunosuppressive therapies Myasthenia gravis Outcome
 Diet Major depressive disorder NOVA Nutritional psychiatry Psychological distress Ultra-processed food

 antisaccade cognitive impairment dementia neurodegenerative disease prosaccade


 Anti-GPCR autoantibodies Autoimmune diseases COVID-19 Post-COVID Rheumatic diseases
 human herpesviruses 6 microRNA neurological manifestation
 Ketogenic diet anxiety disorders low carbohydrate diet mood disorders nutritional psychiatry
 Lewy body dementia amyotrophic lateral sclerosis case-control study frontotemporal dementia genome-wide association study non–Alzheimer's dementia resource structural variant
 Basal forebrain Functional connectivity Mild cognitive impairment Nucleus basalis of Meynert Tissue-specific geneset risk score Transcriptional vulnerability
 biomarker endothelin-1 idiopathic pulmonary fibrosis interstitial lung disease interstitial lung disease associated with autoimmune diseases
 Lung cancer (LC) cross-sectional study patient-reported qualitative research quality of life

 COVID-19 coronavirus neurological complications neurology



 Alzheimer's disease cross-comparison decision-analytic modeling dementia economic evaluation model validation
 Parkinson’s disease cognitive progression mitochondrial haplogroups
 COVID-19 SARS-CoV-2 immunophenotyping longitudinal modeling multi-omics systems immunology

 CHRONIC FATIGUE SYNDROME RANDOMISED TRIALS REHABILITATION



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 1040-1042
 2736-2744
 775-789
 54-64
 104672
 83-91
 3400-3403
 1515-1532
 443-452
 104670
 69-92
 104473
 2095-2106
 693-701
 860-867
 2859-2864
 455-459

 104740
 2279-2286
 518-525
 685-691
 502-504
 39-50
 809-818
 123352
 772-783
 104583
 37-41
 215-221
 100747
 337-339
 11625
 123794
 100189
 88-95
 e3073
 726-737
 511-514
 284-290
 104771
 e0285599
 212-221
 53
 7322-7334
 107-118
 218-227
 2329-2332
 148424
 37-47
 173-179
 63-70
 389-390
 e072319
 107106
 104675
 579-588
 104696

 663-672
 831-838
 104491
 179-186
 168-172
 1-4
 83-84
 538-545
 104519
 8-14
 e2947
 104874
 104716
 104475
 2121-2129
 1070-1079
 e0272114
 167-168

 104745
 104850
 293-311
 264
 1459-1472
 990-1001

 104844
 104744
 457-471
 604-610
 e100-e102
 187-192
 389-395
 3633-3644
 104719
 187-194
 1102-1108
 42-48
 109717
 104470
 104443
 105959
 104862
 427-435
 e2217635120
 22-28
 479-480
 58-69
 615-627
 104410
 120669
 e3042
 731-740
 866-874
 1309-1327
 123351
 104838
 235-238

 244-253
 1186-1194
 14313
 312-319
 148-150
 5578
 810-823
 104759
 10-12
 e0288967
 1497-1511
 525-527
 104419
 104723
 105035
 104405
 236-247
 3091-3102
 467-477
 619-626
 e221425
 475-478
 143-161
 20
 1188750

 335-336
 1106028

 104894
 1268-1283
 4403-4414
 104515
 104786
 96-102
 604-614
 22-28
 104520
 e220175
 104711
 2313-2320
 597-604
 275-280
 106028
 102302
 4675-4686
 104432
 44
 642-649
 e0287463
 1456-1464
 97
 11-13
 2209-2223
 49-59
 45-51
 899-905

 433-445
 289-304
 343-345
 133-135
 e3104
 139-148
 101677
 283-285
 205-217
 965-975
 1115311
 42
 103053
 457-460
 461-465
 503-509
 104426
 253-254
 104743
 1226616
 376-377
 2912-2918
 104572
 344-346
 104659
 1224217

 375
 3701-3711
 1149-1157
 43-52
 743-757
 2316-2331
 104435
 3262-3271
 166-180

 104564
 107673
 168
 247-256
 267-268
 104512
 104628
 3190-3199
 e1109-e1122
 374-387
 23-34
 2602-2610
 104576

 104513
 3103-3111
 e2209944120
 537-549
 e0280515
 956-965
 1284-1299
 954-962
 104845
 263-276
 337-345
 982-990
 104671
 107522
 1259-1274
 104482
 104460
 314-319

 104467
 1120-1143
 104799
 104825
 130395
 382-390
 e15138
 120552

 104547
 1176016
 104518
 206-211
 227-234

 e2221544120
 578091
 499-517
 2164443
 463-473


 37-51
 3373-3378
 1199747
 1430-1455
 104841
 764-793
 104625

 1016-1023
 104531
 110
 104483
 863-870
 104766
 1300-1322
 101636
 104606
 104438
 2132-2139

 606-614
 3045-3057
 107675
 585-596
 115173
 998-1009
 1172-1179
 5878

 34-42
 16
 104731
 212-220
 104751
 999
 e1583
 169-181

 89-96
 31-37
 62-70
 423-430
 1175874
 108
 299-314
 925-933
 471-474
 e073782
 107-130
 15003
 6090-6102
 350-356
 119-129
 388-396
 79-92
 552
 1174-1185
 487-493
 384-397
 131

 580-588
 103311
 1005-1014
 23-30
 104415
 3379-3387
 1126-1135
 e899-e910
 967-978
 385-394

 15-21
 72-86
 3059-3069
 162-171


 3
 1172993

 104422
 259-268
 140-149
 578137
 104514
 104608
 101437
 110266

 864-876
 684-692

 2870-2873
 111375
 6-8
 677-683
 434-442
 104552
 1135540
 e13288
 104612
 115-128
 104455
 e20221514
 104695
 122001
 59-64
 114195
 18-34
 104505
 1597-1610
 e3493
 795-797
 19-30
 292-323
 1033-1038
 725-744

 104720
 e0288581
 3212-3220
 396-402
 724-738
 101863
 104563
 e4847
 e230016
 102243
 79-83
 692-703
 797-798
 364-381
 37-44
 375-376

 197-205
 164-172
 1129906
 166-171
 52-59
 104424
 469580231171018
 578036
 241-245


 104420
 105953
 303-310
 405-406
 2769-2780

 S1-S6
 281-291
 207-213
 275-280
 294
 3735-3736
 395-406
 2294-2306
 1107780
 104502
 e220193
 e067516
 121-133
 347-359
 e223244
 e308-e323
 1871
 e2300073
 223-230


 106073
 228-234
 21-25
 e58
 102157


 104430
 253-265
 371-386
 104965
 42-49
 857-861
 159-172
 138-148
 29-34
 e0285022
 22
 104477
 6-14

 485-490
 11-36
 104474
 2144-2176
 e1988
 107056
 104854
 19-21
 104472
 503650
 104567

 274-282
 508-523
 991-1000
 104795


 104481
 2391-2398
 240-246
 100
 285-286
 104561
 71
 486-498
 401-409
 32-36
 263
 250-255
 535-545
 105145
 104863
 112-113
 104417
 104557
 1133967
 104413
 1057-1063
 104621
 6
 232-234
 2217-2233
 739-747
 104767
 106031
 235-243
 e2200501

 104846
 979-989
 162-176
 531-538
 120
 133-145
 719-730
 181
 266-273
 1012-1023
 3357-3361
 527-553
 104569
 104461
 779-788
 105501
 199-207
 104710
 8067

 366-383
 103388
 588-601
 1923-1932
 352-362
 268-282
 693-702
 e0289495
 269-278
 104570
 2305-2309
 305-320

 2884-2888
 1167-1180
 285-290
 e061539
 108358
 287-294
 718-725
 3341-3368
 21-30
 104622
 1533-1559
 103-108
 4776770
 106113
 104589
 775-777

 1194671
 167-169
 453-461
 1455-1463
 160367

 98
 1388-1401
 e3024
 106610
 3423
 104878
 2464-2475
 326-332
 1319-1327
 803-808
 e295-e296
 417-422
 1115120

 875-883
 102843
 102854
 266-269
 60-64
 e220941
 342
 10381-10412
 766-779
 1086-1093.e2
 104530

 e2200018
 104746
 160-164
 104584
 2393-2400
 703-714
 e28431
 e34142
 136
 119-147
 104789
 311
 e2874
 2018-2030
 85
 3115-3131
 320-326
 228-239

 475-482
 387
 3565
 e1296-e1308
 1631-1638
 104575
 e26-e36

 105-111
 44-55
 e33906
 104748
 2603-2622
 104750
 104469
 1087-1095
 589-596
 55-61
 277-286
 1916-1928
 104529
 32-34
 104733
 578105
 55-60
 110379
 371-378

 1258-1259
 450-462

 47-60
 39-41
 663-666
 494-495
 45-46
 1090-1098
 162
 824-830
 904-925
 169-181
 104738
 129-137
 578099
 355-364
 61
 104497
 2271-2282
 104937
 707-717
 1453-1458
 514-521
 1416-1429
 109647
 1617-1625
 186-202
 58-63
 182-195
 719-724
 e2221535120
 1671-1682
 49-56
 1624-1636
 280-283
 397-403
 13-53
 104859

 1001-1011
 104591
 511-517
 477-488
 108572
 578072
 1001-1013
 2180316
 1263-1274
 132-138
 1843-1853
 1141014
 131-133
 267-269
 214-221
 104401
 75-85
 81-91
 343-351
 86-111
 104503
 34-45
 521-529
 115-125
 107142
 189-193

 22-38
 104476
 249-259
 172-178
 104588
 104866
 152-163
 e0272596
 1682-1685

 6018-6026

 3120-3128
 104489
 262-271
 1852-1861

 258
 259
 112928
 2348-2356
 98
 104499
 104560
 221-235
 e1353-e1362
 CD011203
 1993-2002
 104857
 114179
 521-526
 1077088
 178-185
 1390-1392
 1877-1884
 22
 e697-e702
 419-430
 104692
 1882-1883
 151-159

 456-461
 352
 14480
 104555
 104574
 495-509
 104479
 103065
 393-396
 469-488
 109709
 185-191
 104755
 542-543
 104753
 266
 295-300
 358-367
 316

 104701
 e1594
 69-76
 886

 3431-3443
 331-334
 247-277
 43-52
 e0288998
 1077335
 1205879
 1133444
 241-246
 115542
 749-759
 1770-1782
 102886

 560-583
 333-373
 65-71
 3331024231167130
 108432
 e403-e404
 177
 122-132
 106230
 272-282

 246-265
 104548
 104839
 856-870
 64-78
 104528
 52-62
 121-130

 11
 106015
 203-210
 990-1000
 242-244
 313-321

 3839-3854
 262-266
 296-307
 648-656
 510-519
 846-855
 104772
 74-80
 3637-3645
 505-511
 2326-2343
 122936
 94-101
 494-502
 182-194
 131-135
 661-662
 115182
 3496-3503
 2143611
 109688
 4725-4737
 135-138
 248-260
 467-480
 104704
 771-779
 509-510
 104573
 645-656
 eadi0611
 173-180
 1677-1686
 e12851
 103363
 104605
 1-9
 1519-1525
 2139-2148
 215-227


 195
 954-970
 e221512
 374-384
 104577
 227-234
 2352-2359
 166796
 1412-1418
 1004795
 104714

 693-701
 333-342
 473-484
 285-296
 267-272
 64
 858-868

 7
 363-372
 104510
 5099
 1086028
 114862
 254
 107-111
 105084
 3047-3058
 331-336
 570-578
 e15299
 154-159
 759-771

 143-147
 249
 128-134
 725-729
 104465
 e1178
 675-684
 466-478
 117-132
 229-247
 194
 1771-1779
 e220132
 85-93
 e784-e793
 884-888
 1389-1399
 252
 24-32
 436-446
 104411
 18
 104516

 856-865
 4179-4191
 e357-e366
 e22687

 288-297
 502-510
 1595-1607
 698-706
 702-713
 630-643
 11584
 263-273
 57-65
 e2202670
 75
 137-153
 111492
 1168821
 2045-2066
 637-644
 1000-1028

 1213448
 1073278
 120693
 538-543
 674-694

 1212676

 125
 585-594
 e13939
 1099-1106
 67-73
 104436
 120687
 275-285
 104893
 139-145
 819-832
 1

 104890

 104830
 98-107
 290-299
 1384-1410
 576-584
 108-115


 104487
 121930
 1623-1629
 164-173
 110458
 1783-1792
 104492
 363-373
 104797
 361-372.e3
 1200146
 e2210262
 36-50


 104507
 1138-1153
 1024-1032
 1969-1974
 1202006
 301-306
 1025-1034
 116328
 3839-3850
 104509
 104465
 1234984

 114520
 1247-1258
 117471
 371-381
 471
 481-482
 1147-1153
 e2250228
 160-168
 578136
 187-198

 1439-1452
 339-352
 104433
 204-211

 1160397
 407-416
 759-768
 466-470
 578037

 1219560
 1908-1930
 2401-2410
 1180449
 939-950
 104647
 121
 345-357
 367-374

 157-159
 183
 2489-2501
 e2308187120
 265-281
 90-101
 785-794
 25-31
 633-647
 105950
 1107-1117
 4184-4205
 1161849
 151-160
 51-64
 104872

 51-57
 1003-1012


 104693
 104616

 136936
 e679-e689
 481-489
 156235
 614-631

 1890-1905

 1343-1351
 e071657
 2185-2194
 799-808

 e32661
 153-167
 875-883
 389
 3000-3011
 952911

 e44428
 263-282

 120518
 102957
 89-95
 175442
 433-456
 9394
 912-918
 e2300738
 140-146
 101055
 3233-3242
 104412
 545-558
 2453-2463


 518-530
 110
 655
 1562-1563.e2
 e12868
 2380-2391
 148267

 106174
 407-414
 16
 107739
 104501
 2559-2566
 104624
 42
 6121-6131
 8030-8042
 152341
 1361-1369
 2357-2364
 e2301030120
 164-173

 eabq6978
 104565
 104556
 1883-1896
 29-33
 694-706
 313-326
 e32621
 1605593
 139-145
 104763
 102985
 104525
 1162340
 1218-1228
 104558
 31-39
 289-300
 283-299
 104793
 190-201
 e15846
 1062-1071
 e0286402
 1483-1495
 104478



 93-101
 326-333
 10465
 235-242
 217-226
 2450-2460
 323-332
 447-456
 10-18
 663-669
 138-143
 2180-2195


 e220989
 317-325
 e0265297
 223-229
 104521
 108-121

 115435
 e1418-e1432
 e425-e437
 397-415
 e0277483
 104707
 84-88
 215-225
 123-131
 1209923
 1364-1381
 196-205

 1081933
 e78
 101783


 104468
 1188-1204
 112-121
 19-22
 100128
 1079910
 eadg3032
 1229-1240
 114262

 e0283538
 1905-1915
 104578
 6460-6473
 104661
 2883
 1275-1283

 3509-3523
 104488
 377-383
 8-22.e23
 116-121
 198

 748-752
 2726-2735

 104618
 2865-2869
 404-414

 3293-3302
 31
 105962
 e062548
 163-177
 590-596.e1
 114620
 103326
 572-573
 577-588
 72-77
 110382
 227-252
 eabm6267
 1135-1140
 659-661
 e558-e567
 553-561
 2338-2347
 217-232
 314-316
 40
 211-218
 104761
 104462
 832-845
 104603
 104522
 e0283476
 35-44
 1841-1848

 183-193
 780-790
 534-546
 337-349
 2781-2792
 1149629
 247-255


 e22833
 103359
 1047-1066
 455-467
 CD013606
 464-468

 e3144

 461-477

 5878-5890
 936-944

 36-45
 105951


 104729
 105505
 104898
 89-100
 1110672
 229-250
 1502-1514.e8
 1219-1236
 826-833
 1400-1408
 5975-5986
 246-256
 553-568
 1105432
 103289


 e3475
 380-387
 991-1001
 154917
 751-763
 103575
 199-208
 145-159
 103092
 e0280864
 35
 107621
 104480
 104865
 630-647
 1748-1759.e8
 104630
 154569
 1151511
 213-227

 46
 5852
 1018-1035

 1228226

 2645-2659


 271-284
 1540-1551
 399-407
 114374
 317-325
 e2300648120
 2661-2677
 2241664
 104494
 254
 721-731
 461-476
 6481
 1152-1161
 e1095-e1108
 3256-3264
 104764
 815-828
 e0074923
 e28793
 829-833
 341-348
 175879
 43-58

 70-80
 944-953
 104459

 102550
 e2207291120
 e3002000
 106
 3
 5635
 569-573
 3938-3948
 e2319766
 e1776-e1786

 152-169
 578100
 358-365

 361-367
 104471
 2752-2760
 2817-2825
 102982
 104511

 e220-e231

 1375-1381
 1107-1118
 1003-1008
 e0280505
 357-368
 2391-2398

 1-22
 625-632
 1065-1076
 104582

 104592
 1002-1017
 3106
 109562

 110125
 123214
 104484
 58-67
 989-995
 13-30


 104425
 e766
 1141-1146

 1331-1344
 926-934
 19-25
 eadd8693
 1157918
 104852
 9-13
 358-367
 5555
 113437
 104658
 34-42


 819-831
 104717

 456-464
 855-874.e5
 57

 739-748
 104428
 770-779
 107225
 1106472
 100
 45-53
 5853-5865
 1095053
 e2206910
 e41845
 fcad011
 1132170
 20503121231171996
 fcad199
 20552173231188469

 1-3
 2147-2155
 fcad140
 282
 1-14
 2599-2605

 515-518
 1146748
 fcad164
 fcad072

 e00955
 206-212
 1-5

 84-91
 20552173231167079
 1-5
 1-3
 284-288
 1251877
 1207007
 fcad218

 101842
 1063264

 1169919
 1148659
 fcad153
 1213956

 fcad109

 e15754

 1-10
 104914
 20552076231173531
 20503121231178047
 1441-1449
 e7280
 fcac255
 1025659
 1150717

 104932
 e42845

 1245622
 e1422

 e13209
 1104552
 1-16
 1115303
 e44504

 1137717
 13
 e00022
 325-327
 1229625
 1455613221148310
 89-93


 1222574


 e7185
 1138600
 1076421
 1189709
 1129289


 1535-1541
 10731911231178289
 100618
 1-7
 3081-3090

 267-272
 1-7
 118-123
 20552173221142741
 1-4
 1157287

 1-11
 104-110
 1217000
 578128



 e42146
 1172807
 1248632

 1068421


 230118
 4433-4441
 1139316
 1222433

 100-110
 20552173231191170


 317-322
 38-47
 13524585231189470
 107-110
 20552173231186512
 104952
 109729
 73350
 e40986
 13524585231196786
 e40689
 1419-1429
 1068358
 104970

 42
 fcad065
 e1515
 fcad206

 1-4
 fcad041
 1154916
 e36835
 1171163
 22
 e000481
 20552173221144229
 20552173231195879
 100542
 1215774
 104959
 1337-1339
 1-9

 1-9
 1774-1779
 223-230
 104946
 1304-1315

 341-344
 9636897231184596
 3915603231183751
 1151531
 711-719
 157-162
 1194212
 1119660
 100465

 e1444
 1148106
 1130231
 1-7


 15-20
 1227374
 37-51

 1060696

 148-159

 1-11


 1097799
 23982128231185290

 1197492
 161-170
 1143498
 157-168
 1138627
 23-27
 17562864221146836

 912174231190455
 17562864231181170
 fcad026

 74-77
 23-30
 449-453

 155-160
 109-119
 539-556
 1-13

 T155-T160

 104966
 20552173231194352
 104922

 1-8



 1-12
 fcad183

 1-9
 10497323231196521

 61-64
 578135
 1-13
 1199313


 248-254
 83
 47-49
 553-574
 1101379
 1090133
 99-103
 265-268

 63-70
 110-117

 1204-1205
 407-419
 e12877
 104-111
 1-13

 e479
 90

 1145818

 979380
 e13150

 4417-4424
 163-167


 e000304
 102035
 187-192
 102306


 1-8

 fcad044
 103495
 1173779
 20552173231154712
 1-6
 374-376

 1209477
 1205065

 1-8
 17562864221150040
 104909
 1-11
 e1437



 655
 107873





 49-58
 13634593231175321


 54-63
 289-305
 217-229
 003693

 17562864231180734

 1130414
 176-185
 1169400

 1149963

 131-142

 1-24
 1197212
 140-144

 104958
 1649-1668

 1209749
 1086720
 120781
 1209-1215

 e42061



 317-318

 1146027
 1236217
 e202300207
 102977
 104950


 e2250229
 153-159
 1053577
 233-236
 e16954
 e1451
 1-5
 e33242
 35-42
 1227431


 247
 1144896
 164-171
 104899
 152-156
 2821-2832
 1431-1434
 1167612


 1087126

 226-228
 360

 1655-1658
 1145260
 e43274

 23-30
 1-12
 144-153
 1-11

 1282-1295
 1204132
 104955
 104930

 104913

 1207067
 1207626
 1204852
 344-351
 93-98


 51-55


 104919

 1-7

 131-136
 1110884
 e36323
 1090631
 39-43

 1443-1470
 5-13
 13524585231196795
 1233601
 e41650
 e41520
 29
 104993
 104961
 104980


 496

 165-184

 1275048
 15-19
 1-16


 20552173221150370

 1163112
 276
 33
 20552173221151127
 1327-1336
 168-175
 104964
 73-86

 1199491

 134

 578152
 182
 1153422
 1181032
 11
 578130
 fcad143
 1207617
 687-700
 107846
 123
 6435-6444

 1-23
 1-8
 17562864231162661

 1225754
 1-9


 1405-1413



 71-74

 113-122
 1121899
 107884
 20552173221143398
 31-39


 1213377

 136-144
 8465371231180815
 e1454
 104-109
 45632231179618
 1092999
 41-50
 1093352
 25-37
 1198018
 1178980

 17562864231189919
 13524585231189641
 e19
 103464
 1186110
 111-117

 335-339

 1-11
 107892
 1224748


 1165267
 124-130
 e4952
 1153469

 427-439
 1073627
 107888
 833-848
 1172640
 20552173231160312

 103-109

 104908
 375-389
 1087745
 e13350
 2682-2684
 104851

 1194859
 13591053231182364
 e1438
 1193636
 100737
 323-344
 20420986221143830
 1-10
 578170
 20552173231197132


 1108738

 e7605
 1220672
 101150
 1344-1345

 1950-1951




 19


 106906
 283-289


 598-608
 1125115
 23743735231151550


 20
 100282

 351

 1720-1735
 120694

 133-134
 17562864231161892
 e1536

 104924

 59-67




 1-17
 1257-1265

 104936
 100307

 104871
 1099-1106
 20552173231169467
 1060511
 97
 1145251
 1101521
 1006932
 91-98
 26-29

 107967
 206-217
 199-219
 109733
 1-9
 107320

 13524585231190771
 368-377

 S10-S14
 8-14
 351-369
 1207540
 1266-1274
 591-593
 681-687
 979659
 102609



 17562872231177779


 1077838

 26-34
 1107886
 20552173221147620
 e4964
 106290
 303-317
 165-171

 257-266
 13524585231195346
 531-539
 259-261

 e985-e994
 1251667


 1022728

 1091252


 721-743

 104747
 259-273
 104907

 20220138

 101957

 1091955
 1187411

 100464
 52-54
 1241926
 1151836


 1148932
 13524585231195861
 1149625
 I-IX
 1340-1344
 104942


 578164

 20552173231186516
 1335-1357
 1143766
 82-90
 103380
 1-7

 104944


 1-7
 100308
 1175644
 1133390
 1-21
 104956


 17562864231180719
 20552173231178441

 293-302
 2841851231155608

 19714009221150853
 103802
 104991
 e12935


 1135392
 104994

 104928
 104931
 104933
 1-11


 307-316

 1164001
 4
 1112199


 1-5
 1098883

 17562864231162153
 1214897

 792-799
 1112193
 17562864231183221
 177-189
 20-24
 3369
 1158487

 1007580
 480-481

 101097JU0000000000003114
 104903
 1129117
 2277

 1186016
 13524585231199030
 4599-4620
 578145
 1128190
 166599


 1055050



 147-153
 1228754
 49-66
 20552173231155055
 13524585231192460
 1137665
 61
 127-128


 10998004231194954




 751-762

 2643-2673
 1188124
 23-27
 689-697
 883-897
 110791

 e17427
 381-391





 4171-4180
 361-373
 1120541
 20552173231159560
 275-289

 e1004
 104940
 11795735231195775

 33-44



 919336
 145-159


 13524585231197275


 104925

 1709-1728
 1075736

 1-9
 849-861
 289-302
 104921
 104941
 20552173231187810

 649-651

 9
 13524585231197928
 210-234
 1156802
 1399-1407
 110748

 270-274
 578134
 112669

 1128157

 103238
 20552173231196990

 104902

 104740

 107958
 637-642
 105785
 e45079

 209



 925-931
 7



 1187-1203
 1139359
 e23246
 786-791

 39-70

 201


 1201669
 1471-1473
 1176625
 104882
 1-3
 341-350
 104916
 83-98
 230-231

 1137


 e40508
 1123955


 107679
 104896
 1-10


 15-26
 319-327
 578175
 1223220

 104910
 1193015

 41
 102932
 2633
 701
 c88
 3915603231199529


 101794

 104895
 1457-1476


 1137176

 1187851


 104990
 1130205

 e38927

 1-17
 1-3
 1147447

 216-221
 1874-1893
 103454

 229-241
 104935
 287-97
 20552173231169463
 20552173231169475




 1222-1233
 114718
 277-284

 112193
 20552173221149688
 30-34
 1275-1281



 20552173231189398

 1169786
 1175230
 1783-1797

 499-512
 e7455
 20552076231173520
 147

 30-34
 e2023128

 104965
 1033-1034

 1455613231184149
 485-486
 242-247
 e1457




 91-101
 1195101
 104951
 1-9
 104953

 145-151
 e38945
 104792
 104947



 21-32
 1923-1933



 1-14
 100461

 2393
 958-959
 160-167
 120695

 e200154

 154771


 2285-2303
 15-27

 18-25

 495-504
 102633


 23247096231186046
 56-62
 e34205

 1084661


 115
 110381
 103030
 36-42

 64
 104490


 1214652
 fcad107





 9
 102942
 104917
 1126215
 e40865
 1717-1718
 275

 578066
 578178

 299-300
 1196087
 20552173231153557


 13045
 113535






 107586


 1296-1303
 45-50

 104881
 1121051

 104791




 349
 17562864221150312
 1105376
 1-11
 75-81
 e0000171
 e200185
 1669-1682
 1309-1318
 17562864221118731

 104789
 1190279

 e13470
 e2212696120
 120586
 20-25
 3190-3202

 1477-1490

 10
 974-988
 690-693
 2573-2590
 1242508

 1113954
 104864

 197-198



 104739

 71
 20406223231172920
 20552173231165196
 fcad108
 20552076231152989
 104868

 R1-R4
 110-118
 873-876
 763-768

 3787
 35-38
 17562864231154653
 1977-1980
 133
 298-307



 1113348
 5582242
 104901
 1-16
 7247-7269
 1216-1228

 104934

 e2250236


 100537
 110530
 595-605

 335-355
 519-533
 1041-1054
 1049686
 112629
 120-129

 1-13

 1143947
 352-361

 116-120
 252-256
 104927
 1162278
 1197094
 149-158
 48





 1110593
 104486


 201-203
 100-101








 153-154

 104920

 765-781


 1316-1326
 1-12

 S103-S111
 1094106


 e12776
 108605
 20552173231194353


 679-688
 518-529
 100968
 549-551

 178

 1211776

 1108212
 243-266
 676-685

 114541
 100443
 S1-S9
 1491-1515


 368


 1-3

 101052
 411-417


 945-987
 1068736


 100635
 222

 103491
 123
 120677
 109761
 107851
 S45-S66




 104788
 110418
 101-117
 1178792
 643-644


 1058-1067


 1135
 107872


 104912
 1158148

 1058817
 e3383
 1262-1266
 2969
 73-83
 e41124
 842
 66-73
 1083242
 94-96



 34-45
 322-326
 1041961





 120-147

 103606
 e2250033
 102037


 1-8
 110167
 1191838
 1431-1439
 104929

 119485


 666-679
 e4937

 122022
 102488
 1247-1262





 415-431
 e0000305




 523-528
 2189-2195

 e0005923
 2600-2621
 1233870
 1229-1239
 96-102

 1131130
 529-542


 362-375

 e41825
 e41656
 114814
 106588


 154-155
 104549
 1037-1054


 549-550
 e2302997120

 242-252
 e071397

 18
 32-36


 20552173231182534

 101068

 603-618
 19-22
 104604
 e28363
 3191-3210
 1-7
 1-8
 116-128

 107885
 730-743


 1471-1499

 102321
 29-58

 1201-1203
 1140-1149
 14-35
 17562864231170928
 37-45

 109752

 1221890
 2050313X231167937
 106358
 103517
 1120-1126

 110845
 2815
 42-45
 1181071
 111-112
 169-175
 256-265

 2357-2395


 102285
 104918
 150

 3372
 16-35
 175726
 41-46
 e41082
 119826
 e7548
 858-878
 191-199
 154541
 5-17
 5602401

 e2302146
 34
 107790
 e672-e676
 1083864
 1072709
 59-97
 941-959
 1268023

 21-31
 1108191
 1109-1118
 e2221007120
 e40043
 1176639



 1-5
 1198576
 19714009231173102

 115083
 105868
 1066-1076
 573-588
 107909

 e36968
 1528-1540

 1102353
 14034948231153025
 101874
 399-440
 166
 4478-4486
 772-790


 108381
 1683-1698
 65-77
 104498
 319-328

 1427-1435
 218-253



 368-376
 105278
 149-156
 26218-26230

 6290-6301
 23




 167-170
 3565-3566



 389-394
 1127722
 6005531
 541-552

 1479-1499
 223-238
 e00527

 1155333

 e34615
 1062356
 578192


 104726
 576-591
 1349-1359
 5583996

 102397
 583-596
 17-46
 104963

 43-72
 743-751
 e0288008

 103260

 151-176
 116681
 1225875
 137-140
 757-768

 947-954
 547-559
 e18250

 e23068

 103408
 531-552

 65-67
 2375-2390


 19714009231166089

 1007-1013
 15347354221150787
 7-16



 163-172
 235

 e2200665
 3
 108348
 125-136
 1183535
 e39887

 1110967

 41
 1157149
 1177540

 104527

 842-850
 1165-1178
 104949

 200-206

 101789
 115461
 101931

 3400-3421

 733-743
 359-360
 17562864231197309

 4354-4367
 663-670
 1198679

 4522053
 1134634
 115741
 11782218231182553
 1154552
 2385-2390
 1108087
 115111
 66-80
 354-360

 1188839
 268-285

 1807-1834
 123-135
 104911
 146-151
 489-506
 110340
 1175451
 299-316

 109843

 e2350521
 321-327
 173-178
 687-693

 103354
 1-18
 65-74
 113005
 104948
 109539

 101395
 1-11
 2953-2954
 862-863
 244-245

 103444
 152413

 248-257
 1179302
 1150296
 S49-S58
 101101

 1118927
 665-669
 105336

 1798-1807
 50-64
 499-502
 110855
 110787
 e2250234

 109540
 104729
 003861
 1-20
 61-67
 389-411

 1151620



 e1772
 305-314
 458-464
 244-246
 5004-5027

 1-10
 e41099
 1182411

 443-455


 1177127


 112293

 115234

 99




 101855
 1
 e2149675
 e4811
 83-92
 344-375

 120780

 293-297
 ltad012



 288-298
 5873-5891

 1137998
 520-529
 1093574

 1114781
 115449
 1018076
 848-858
 773-784
 789-800


 173
 341-350
 519-530
 2968-2980


 613
 154582
 1149869
 84-97
 653-665
 22-30

 8640
 121302
 2024-2044
 104957
 1099758
 344-351
 1035-1050
 201-210
 431-441
 394-404
 5127157
 203-219
 217-225
 103091


 216-220



 109932

 1-11
 1035220
 377-382
 S22-S27
 612-622

 102026

 2692155231191383
 16-21



 114763
 1158650
 732-747
 110128

 1402-1413

 593-605
 2251-2262
 e4849
 9-23
 1458-1478
 1-25

 247-257
 110856
 1224155

 156-163






 4671-4688
 2129-2144
 148319

 123215
 337-346
 137-148
 39-53
 5367-5381
 107262
 e2350452

 e2301756



 613-626
 1785-1790
 333-344
 604-618
 17562864221137129
 223-229
 64-70
 415-435
 1758-1774

 147036
 614-617

 e0282960


 152

 578140
 1194842
 59


 158-163

 e068059

 376-378
 313-319



 108373
 103295
 20230001
 945-955
 116540
 105565
 e000428
 1375-1383

 901-910
 102282
 1-8
 239
 122
 1097490
 1133863
 e4644
 109505
 1128315
 121531
 106156

 e020123212333
 954-972
 6502-6517
 1251772
 29-36

 4792-4811
 115138

 1209480
 1293-1309
 349-356
 110017

 1114897
 11-20
 102956
 818-828
 2316-2324
 4130557
 285-291
 2128-2133

 106018
 66-74
 110531
 33
 171-180
 80

 e14603
 1870-1889
 471-475
 1-20
 102635
 105-121
 109326
 840-848
 1-24
 2015-2024

 429-435

 3915603231189627

 205-211

 713-729
 110689
 37-46
 235-260


 44-48
 302-318
 102560
 1344-1358
 53-83

 804-811

 9-19
 31-38

 e631
 154686
 1267913
 1919-1927


 e1434
 29
 908-911
 329-346
 102829
 4371
 112986
 3367-3376

 e2211281120
 2534-2538
 1233-1248
 1943-1954
 e13974
 144
 3595-3602
 102122
 1727-1733
 18

 101-107

 107571
 792-801
 169-175

 608
 115718
 637-653
 1184938
 107231
 233
 1993-1998
 9813
 104
 e13874
 109-121
 2498-2505
 1071553
 55
 118
 11795735231167869
 119-128


 56-87


 154705
 109686
 9636897231184473
 277-286
 47
 e0284477
 142-149
 108411


 1749-1765
 1950-1957
 111473
 e11-e16
 115665

 1433-1446

 1111254
 e32810
 103-118
 109729


 e743
 e884-e898

 701-707
 283-300
 616-632
 110160
 463-473
 1380
 1781
 e303-e305
 e0345922
 109690
 1114667



 148443


 119898
 67-76
 257-300
 619-631
 e32377
 387-394
 8821610


 101857
 8571649
 379-397
 811-822

 7380-7400
 102843
 e168


 e38947
 104627

 255-260
 808-835
 1038-1048
 71-91
 5228-5238

 39

 1294-1306

 679-685
 108394
 145-151
 611-614
 586-596
 619-638
 152313
 284-297
 112999
 794-810
 226
 341-342
 106814
 113428
 e35659

 578107
 fcac340
 131-175
 141-151
 171-184

 1800-1809
 847-857
 40-50
 104969

 1007483

 e38051

 1223-1239
 12
 373-387
 152370
 241-254
 e465-e472
 187-207

 1-7
 104923
 290
 192
 51
 78-86
 e23259

 1907-1932

 190
 319-329
 2430-2441
 83


 704-726
 e54228
 35-55
 807-813
 200-211
 103407


 1154-1166
 114593

 16-20
 92-98
 65
 188-198
 107339
 1634-1646
 2071-2087
 1229-1240
 474-483

 36-39
 624-627
 562-565

 365-370
 e200132
 110
 183-187
 11-25
 1101079

 231-241
 203-207
 16-21
 109-112

 133-138
 78-82
 e49-e51
 405-409
 e6913


 2367-2386.e15
 42-47
 e55328
 104442
 41-52
 1208252
 4683-4693
 1-8
 307
 e072309


 1086-1097
 e4741
 97

 184179
 129-147
 479-488

 103129
 106884
 1131758
 729-731
 979-988
 101920
 32-39
 822-826

 102984
 1125257
 1082-1088
 290-297
 4317
 e34460
 103
 88-94
 105508
 e2216941120
 104243

 3986-4003
 1163987
 122815
 148
 477-482
 e16980
 377-388
 e35663
 224-241
 e064169


 200-204
 348
 10878
 1190219
 3701-3708
 889-892
 1118369

 282-287
 fcad211
 108673
 577-597
 4405-4414

 148-162
 110807
 36-42
 2-4
 692-701


 2456-2472
 915-919
 2197099

 104945
 104581
 109-117

 363-371
 336-353
 102460
 14-16
 923-930

 1173-1187
 104730
 106697
 1103053

 104500
 161-173
 1451-1461
 104656
 1002-1013
 55-64
 201-216

 e939035
 e7247
 304-318
 103400
 3043-3046

 502-507
 603-616

 401-410
 829-854
 733-748
 3898-3910
 3035-3046

 103276
 47-51
 fcad166
 3315-3332
 1-9

 100108
 e072348
 e37229

 113-116

 104928
 eabo0205



 1745-1757

 170-180
 427-446
 93-104
 24-32
 911-919
 1183789
 NP87-NP90
 120783
 17562864231189323
 1255540

 37-44
 2557-2569
 1114022

 872-881
 1153503
 140-148
 284-320
 325-339
 1230467
 213-234
 Doc01
 474-487
 606-611
 560-566
 eade3856
 e23357
 394-430
 89
 19-27
 eadd4346
 1589-1600
 110342
 2589
 152388

 e1167-e1177


 1143248
 1127-1142
 e2141-e2154

 0141
 116


 466-477
 68-72
 1188827
 2102-2107

 1243155
 20552173221148911
 1178439
 1192674
 e200161
 23247096231171251

 195-203
 3499-3508
 156253

 S16-S20
 113

 541-550
 64-81

 167-175
 3885-3895

 19-29
 257-263
 1227354
 e12902
 392-411


 206-211
 378-391
 102-107
 394-404
 719-725
 103314

 106218

 433-450
 213-224

 1000248

 1180221

 63-73

 1704-1712
 628-641
 76-87
 1098-1109

 102954
 636-640
 1111763
 455-463
 e613-e623
 185-212
 17562864231181177
 197-206
 e38814

 42
 1-8
 1108149

 29
 120325
 104781
 3331024221128287
 2254586
 e1011434
 104732

 e200182
 1204134
 844-863
 66
 120348
 834-846


 1208-1222

 327-338
 1114231





 1-22
 114510
 1418-1435
 103311
 1849-1865
 8645
 167-181

 fcac310
 1173-1183
 44-55
 2508-2519
 764-775
 3557-3566
 786-802.e28
 3512-3518
 2618-2632
 757-764
 58
 852
 1191782


 1759720X231159712
 101010
 152197
 1148444
 17-31
 106030
 106050
 1878-1890


 e0284440
 111977

 100533
 782-790
 293-303
 e000407
 533-547
 390-398
 2134-2145

 e0283469
 11786469231153111
 259-267

 397-411
 872-887
 561-575
 171-187.e14
 829-836
 95

 1205261
 e37142

 365-380
 1130801
 1043136
 497-515
 14747

 e2306965120
 102154
 78

 120-129
 1023-1030

 1146564
 110916
 173-182
 116615

 3186-3197
 493-514
 547-560

 2933-2937
 983-1000
 5583-5589

 28-37
 86-97
 101175
 25-40
 975012
 1501-1511
 e2305596120
 559-564
 1251-1263
 4970
 41-50
 106812


 S110-S116
 45-66
 1186050
 106984
 e940600
 100212

 247-273
 1-7
 121920
 109-115

 14226

 2141-2145
 502-514
 1-13
 231-242


 203-218
 40-48
 799-807
 97-110
 1193211
 e2332635
 435-441
 201-211

 658-670
 26323524231170881
 284-293
 101664
 446-454
 3139-3145

 e23076
 2119-2143


 e3256-e3260
 896-919
 1192941
 236
 644-660

 1093199
 341-351
 e0410322

 2557-2569
 5581
 1371-1377
 521-535

 329-340
 1175-1185
 297-302

 129-138
 283-294
 235-257
 399-402
 3315-3328
 F73-F86
 2666-2668
 E973-E983
 681-685

 1078441

 1100-1128

 255-266

 501-521
 17562864231191000


 2938-2949
 9-21
 867-872
 215-221
 135-147
 184-195
 2297-2304
 2541-2545
 1051-1066
 1425-1434
 85-95
 2418-2429
 103000
 1189257

 1165982


 21
 1019-1025
 1116-1125
 442-452
 e220079

 e2149702
 471
 e200151
 1053-1068

 1102484
 2128-2138
 959-969
 eabn9405
 17
 320-334
 791-798
 114237
 398-416
 1237-1256
 219-234
 45-56
 e49
 1080-1089
 2409-2415
 625-636
 2640-2648
 201-213
 e112453
 217-228
 45-54
 115897
 110109
 742-750
 1444-1457
 631-637

 17562864231180736
 103339
 3059-3076
 333-345
 5023
 e072094

 66-71
 120005
 75-81
 410-422
 eadg4017
 e066168
 104456
 e069258

 455-464
 108981
 104591
 e568-e581

 2048-2058
 fcad092
 270-276
 238

 104615
 1559-1567

 508-517
 417-430
 1-12
 57-66
 257-270
 fcad049

 83
 103310

 e70
 100316
 105983

 1391-1413
 e892-e903
 413-433

 e200180
 30-39
 1800-1820
 42-49
 101079
 371-383

 218-228
 2021/11/18 00:00 [received] 2022/05/29 00:00 [revised] 2022/06/29 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/11/22 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/11/21 19:03 [entrez]
 2021/08/23 00:00 [received] 2022/03/09 00:00 [revised] 2022/04/20 00:00 [accepted] 2022/10/11 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/10/10 19:03 [entrez]
 2022/06/03 00:00 [received] 2023/01/25 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/08/03 06:43 [medline] 2023/03/04 06:00 [pubmed] 2023/03/03 01:03 [entrez]
 2022/11/01 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/10/31 08:53 [entrez]
 2022/10/17 00:00 [revised] 2022/09/06 00:00 [received] 2022/11/13 00:00 [accepted] 2022/11/17 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/11/16 00:52 [entrez]
 2023/02/16 00:00 [received] 2023/05/07 00:00 [revised] 2023/05/07 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 20:55 [entrez]
 2022/08/31 00:00 [received] 2022/10/27 00:00 [revised] 2022/11/04 00:00 [accepted] 2023/02/11 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/02/10 18:53 [entrez]
 2022/07/08 00:00 [received] 2022/09/16 00:00 [revised] 2022/10/07 00:00 [accepted] 2023/03/17 22:01 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2022/08/05 00:00 [revised] 2022/04/26 00:00 [received] 2022/09/14 00:00 [accepted] 2022/10/10 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/10/09 14:05 [entrez]
 2022/11/18 21:08 [entrez] 2022/11/19 06:00 [pubmed] 2022/11/23 06:00 [medline]
 2023/01/11 00:00 [accepted] 2023/02/10 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/02/09 23:56 [entrez]
 2022/10/25 00:00 [received] 2022/11/10 00:00 [accepted] 2022/11/09 00:00 [revised] 2022/11/26 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/25 11:12 [entrez]
 2023/06/06 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/07/04 13:08 [pubmed] 2023/07/04 11:09 [entrez]
 2022/12/19 00:00 [revised] 2022/09/21 00:00 [received] 2022/12/19 00:00 [accepted] 2023/02/03 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/02/02 08:46 [entrez]
 2023/01/04 20:54 [entrez] 2023/01/05 06:00 [pubmed] 2023/01/07 06:00 [medline]
 2022/07/27 00:00 [received] 2023/03/22 00:00 [revised] 2023/04/02 00:00 [accepted] 2023/06/05 06:43 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 18:05 [entrez]
 2023/07/18 00:00 [accepted] 2023/08/31 06:42 [medline] 2023/07/31 13:08 [pubmed] 2023/07/31 11:14 [entrez]
 2022/06/03 00:00 [received] 2023/05/23 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/06/29 01:08 [pubmed] 2023/06/28 23:24 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/05/05 06:42 [medline] 2023/04/20 13:41 [pubmed] 2023/04/20 08:32 [entrez]
 2023/01/09 00:00 [received] 2023/02/08 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/04 06:00 [pubmed] 2023/03/03 22:09 [entrez]
 2023/04/08 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/04/27 00:42 [pubmed] 2023/04/26 21:22 [entrez]
 2022/05/25 00:00 [received] 2022/09/23 00:00 [accepted] 2022/11/02 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/11/01 21:42 [entrez]
 2024/06/12 00:00 [pmc-release] 2023/08/15 06:42 [medline] 2023/06/12 13:07 [pubmed] 2023/06/12 11:34 [entrez]
 2023/01/13 00:00 [received] 2023/04/12 00:00 [accepted] 2023/04/11 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/21 18:43 [pubmed] 2023/04/21 15:07 [entrez]
 2022/06/28 00:00 [received] 2022/12/19 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/30 23:42 [entrez]
 2023/06/19 13:08 [medline] 2023/06/05 00:42 [pubmed] 2023/06/04 18:02 [entrez]
 2023/03/30 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/01 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:30 [entrez]
 2023/02/13 00:00 [received] 2023/04/16 00:00 [revised] 2023/05/14 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/21 01:05 [pubmed] 2023/05/20 18:03 [entrez]
 2023/06/28 00:00 [accepted] 2023/08/31 06:41 [medline] 2023/07/07 13:05 [pubmed] 2023/07/07 11:19 [entrez]
 2023/08/10 06:42 [medline] 2023/08/09 12:56 [pubmed] 2023/08/09 06:43 [entrez]
 2023/02/15 00:00 [received] 2023/03/09 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/03/17 06:00 [pubmed] 2023/03/16 20:33 [entrez]
 2023/09/27 00:00 [pmc-release] 2023/03/29 06:05 [medline] 2023/03/27 15:33 [entrez] 2023/03/28 06:00 [pubmed]
 2022/07/29 00:00 [received] 2022/09/19 00:00 [revised] 2022/09/23 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/01/10 06:00 [pubmed] 2023/01/09 04:50 [entrez]
 2023/05/04 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 20:57 [entrez]
 2022/05/23 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/01/22 06:00 [pubmed] 2023/02/01 06:00 [medline] 2023/01/21 18:03 [entrez]
 2023/08/10 06:42 [medline] 2023/08/09 12:56 [pubmed] 2023/08/09 06:43 [entrez]
 2022/12/20 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/04 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/27 06:00 [pubmed] 2023/02/26 18:23 [entrez]
 2023/03/26 00:00 [received] 2023/06/19 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:07 [entrez]
 2023/04/04 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/22 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/21 01:12 [pubmed] 2023/07/20 18:05 [entrez]
 2023/04/27 00:00 [received] 2023/05/09 00:00 [accepted] 2023/07/28 06:43 [medline] 2023/05/14 01:07 [pubmed] 2023/05/13 19:29 [entrez]
 2023/06/19 13:09 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 06:33 [entrez]
 2023/06/19 13:08 [medline] 2023/01/13 06:00 [pubmed] 2023/01/12 07:32 [entrez]
 2023/05/23 00:00 [received] 2023/07/14 00:00 [revised] 2023/07/15 00:00 [accepted] 2023/07/31 11:42 [medline] 2023/07/29 11:47 [pubmed] 2023/07/29 01:07 [entrez]
 2022/07/29 00:00 [received] 2022/12/09 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 18:16 [entrez]
 2023/02/21 18:36 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2022/11/02 00:00 [received] 2023/02/07 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 18:39 [entrez]
 2023/01/19 00:00 [received] 2023/04/11 00:00 [revised] 2023/05/05 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/05/23 01:06 [pubmed] 2023/05/22 18:05 [entrez]
 2023/01/29 00:00 [received] 2023/05/13 00:00 [revised] 2023/06/03 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/15 01:08 [pubmed] 2023/06/14 18:06 [entrez]
 2022/12/01 00:00 [accepted] 2023/01/20 06:00 [pubmed] 2023/02/03 06:00 [medline] 2023/01/19 23:22 [entrez]
 2021/09/15 00:00 [accepted] 2021/10/14 06:00 [pubmed] 2023/01/17 06:00 [medline] 2021/10/13 07:27 [entrez]
 2023/05/12 07:06 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 17:39 [entrez]
 2023/03/06 11:15 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/09 06:00 [medline]
 2023/06/09 06:42 [medline] 2023/06/07 19:42 [pubmed] 2023/06/07 15:43 [entrez]
 2023/08/10 06:42 [medline] 2023/08/09 12:55 [pubmed] 2023/08/09 06:43 [entrez]
 2022/12/07 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 18:05 [entrez]
 2022/12/21 00:00 [received] 2023/01/09 00:00 [accepted] 2023/01/07 00:00 [revised] 2023/02/03 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/02/02 05:23 [entrez]
 2022/06/15 00:00 [accepted] 2023/06/30 06:42 [medline] 2022/06/28 06:00 [pubmed] 2022/06/27 23:35 [entrez]
 2023/02/22 00:00 [received] 2023/05/05 00:00 [revised] 2023/05/07 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 20:55 [entrez]
 2023/03/30 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:27 [entrez]
 2023/05/01 06:42 [medline] 2022/12/15 06:00 [pubmed] 2022/12/14 07:43 [entrez]
 2022/04/27 00:00 [received] 2022/10/25 00:00 [revised] 2022/11/07 00:00 [accepted] 2022/11/23 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/22 18:25 [entrez]
 2022/12/05 00:00 [received] 2022/12/05 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/02/08 06:00 [medline] 2022/12/12 08:57 [entrez]
 2023/01/04 00:00 [received] 2023/02/21 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/04/03 03:45 [entrez] 2023/04/04 06:00 [pubmed]
 2023/01/31 08:22 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/02 06:00 [medline]
 2022/08/13 00:00 [received] 2022/12/23 00:00 [revised] 2023/01/06 00:00 [accepted] 2023/01/12 06:00 [pubmed] 2023/01/25 06:00 [medline] 2023/01/11 18:12 [entrez]
 2023/06/13 06:42 [medline] 2023/06/05 13:05 [pubmed] 2023/06/05 10:24 [entrez]
 2022/10/18 00:00 [received] 2022/12/23 00:00 [revised] 2022/12/27 00:00 [accepted] 2023/01/08 01:26 [entrez] 2023/01/09 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2023/03/27 00:00 [received] 2023/03/27 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/04/04 06:00 [pubmed] 2023/04/03 02:52 [entrez]
 2021/10/15 00:00 [received] 2022/05/24 00:00 [accepted] 2023/05/01 06:41 [medline] 2022/07/09 06:00 [pubmed] 2022/07/08 11:19 [entrez]
 2022/12/15 00:00 [received] 2023/06/25 00:00 [accepted] 2023/07/21 06:42 [medline] 2023/07/19 19:07 [pubmed] 2023/07/19 13:36 [entrez]
 2023/08/10 06:42 [medline] 2022/05/18 06:00 [pubmed] 2022/05/17 08:43 [entrez]
 2022/10/16 00:00 [received] 2023/01/30 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:09 [entrez]
 2023/02/08 00:00 [received] 2023/03/18 00:00 [revised] 2023/04/16 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2023/07/18 00:00 [accepted] 2023/08/31 06:42 [medline] 2023/08/17 12:41 [pubmed] 2023/08/17 11:14 [entrez]
 2023/08/10 06:43 [medline] 2023/07/29 21:46 [pubmed] 2023/07/29 06:41 [entrez]
 2022/12/20 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/19 11:32 [entrez]
 2023/03/27 00:00 [revised] 2023/01/27 00:00 [received] 2023/03/29 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 02:23 [entrez]
 2023/07/24 06:42 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 22:00 [entrez]
 2022/12/24 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/23 21:44 [entrez]
 2022/10/25 00:00 [received] 2023/02/06 00:00 [revised] 2023/03/05 00:00 [accepted] 2024/04/15 00:00 [pmc-release] 2023/04/04 06:42 [medline] 2023/03/20 06:00 [pubmed] 2023/03/19 19:02 [entrez]
 2022/08/10 00:00 [received] 2022/11/18 00:00 [accepted] 2023/08/04 06:43 [medline] 2022/12/11 06:00 [pubmed] 2022/12/10 23:02 [entrez]
 2022/06/13 00:00 [received] 2022/09/29 00:00 [accepted] 2022/11/05 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/11/04 12:13 [entrez]
 2021/08/26 00:00 [received] 2021/11/26 00:00 [revised] 2021/12/02 00:00 [accepted] 2022/01/20 06:00 [pubmed] 2023/03/17 06:00 [medline] 2022/01/19 08:47 [entrez]
 2022/06/10 00:00 [received] 2022/09/23 00:00 [revised] 2022/11/03 00:00 [accepted] 2023/01/21 20:57 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/06/03 00:00 [received] 2022/08/22 00:00 [revised] 2022/10/02 00:00 [accepted] 2023/05/08 10:17 [medline] 2022/10/23 06:00 [pubmed] 2022/10/22 19:22 [entrez]
 2022/08/10 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 22:32 [entrez]
 2023/01/23 00:00 [received] 2023/02/28 00:00 [accepted] 2023/02/27 00:00 [revised] 2023/06/16 06:42 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 11:12 [entrez]
 2022/11/18 00:00 [received] 2023/02/12 00:00 [revised] 2023/02/15 00:00 [accepted] 2023/03/11 01:15 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2023/05/22 06:42 [medline] 2023/05/02 12:43 [pubmed] 2023/05/02 08:34 [entrez]
 2022/05/21 00:00 [received] 2022/08/29 00:00 [accepted] 2022/08/27 00:00 [revised] 2022/09/22 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/21 11:15 [entrez]
 2023/07/14 13:08 [medline] 2023/05/15 13:05 [pubmed] 2023/05/15 11:34 [entrez]
 2023/07/20 00:00 [received] 2023/08/04 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 23:35 [entrez]
 2022/11/03 00:00 [received] 2023/01/11 00:00 [accepted] 2023/02/16 02:20 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/18 06:00 [medline]
 2023/03/29 06:04 [medline] 2022/12/22 06:00 [pubmed] 2022/12/21 14:23 [entrez]
 2022/01/03 00:00 [revised] 2021/11/05 00:00 [received] 2022/01/22 00:00 [accepted] 2023/06/26 06:41 [medline] 2022/02/04 06:00 [pubmed] 2022/02/03 08:41 [entrez]
 2022/10/10 00:00 [received] 2023/02/18 00:00 [revised] 2023/03/05 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/21 06:00 [pubmed] 2023/03/20 19:05 [entrez]
 2023/04/19 00:00 [received] 2023/05/03 00:00 [accepted] 2023/08/09 06:43 [medline] 2023/07/03 19:08 [pubmed] 2023/07/03 15:13 [entrez]
 2022/10/12 00:00 [received] 2023/01/23 00:00 [accepted] 2023/01/06 00:00 [revised] 2023/04/19 06:41 [medline] 2023/02/09 06:00 [pubmed] 2023/02/08 00:06 [entrez]
 2023/04/30 00:00 [received] 2023/06/04 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/17 05:11 [pubmed] 2023/06/16 18:05 [entrez]
 2023/03/20 00:00 [received] 2023/04/14 00:00 [revised] 2023/04/17 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:44 [entrez]
 2022/08/08 00:00 [received] 2022/09/12 00:00 [accepted] 2022/09/17 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/16 23:33 [entrez]
 2023/09/13 06:41 [medline] 2023/09/12 06:41 [pubmed] 2023/09/12 02:53 [entrez]
 2022/03/10 00:00 [received] 2023/01/02 00:00 [revised] 2023/01/03 00:00 [accepted] 2023/01/14 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/13 18:22 [entrez]
 2022/10/11 00:00 [received] 2022/10/12 00:00 [accepted] 2022/10/21 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/10/20 03:33 [entrez]
 2023/03/18 00:00 [received] 2023/05/04 00:00 [accepted] 2023/05/03 00:00 [revised] 2023/06/26 06:41 [medline] 2023/05/10 12:42 [pubmed] 2023/05/10 11:15 [entrez]
 2022/12/31 00:00 [received] 2023/03/04 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:50 [entrez] 2023/03/30 06:00 [pubmed]
 2022/09/19 00:00 [received] 2022/10/21 00:00 [accepted] 2022/10/20 00:00 [revised] 2022/11/09 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/08 23:36 [entrez]
 2022/11/05 00:00 [received] 2022/11/17 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/11/28 11:19 [entrez]
 2022/08/09 00:00 [received] 2022/10/22 00:00 [accepted] 2022/10/21 00:00 [revised] 2022/11/18 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/17 23:46 [entrez]
 2023/02/01 21:03 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2022/07/25 00:00 [received] 2022/10/20 00:00 [accepted] 2022/11/04 06:00 [pubmed] 2023/03/17 06:00 [medline] 2022/11/03 21:22 [entrez]
 2022/09/21 00:00 [received] 2023/01/25 00:00 [accepted] 2023/02/08 23:32 [entrez] 2023/02/09 06:00 [pubmed] 2023/02/11 06:00 [medline]
 2022/07/03 00:00 [received] 2022/10/10 00:00 [accepted] 2023/01/04 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/03 18:23 [entrez]
 2022/08/12 00:00 [received] 2023/04/13 00:00 [accepted] 2023/08/02 06:43 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 21:53 [entrez]
 2023/01/30 00:00 [received] 2023/02/07 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/03/17 22:01 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2022/10/10 00:00 [received] 2022/11/11 00:00 [revised] 2022/11/14 00:00 [accepted] 2022/12/11 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/10 18:33 [entrez]
 2022/10/01 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/09/30 05:43 [entrez]
 2023/01/10 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/02/11 06:00 [pubmed] 2023/02/10 19:32 [entrez]
 2023/01/23 00:00 [received] 2023/02/23 00:00 [accepted] 2023/02/22 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 23:26 [entrez]
 2023/06/29 06:43 [medline] 2023/05/18 19:12 [pubmed] 2023/05/18 12:43 [entrez]
 2024/08/01 00:00 [pmc-release] 2023/08/10 06:42 [medline] 2023/07/04 06:42 [pubmed] 2023/07/04 02:15 [entrez]
 2022/06/08 00:00 [received] 2022/09/09 00:00 [accepted] 2022/09/18 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/17 11:18 [entrez]
 2022/08/25 00:00 [received] 2022/10/02 00:00 [accepted] 2022/10/08 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/10/07 23:43 [entrez]
 2022/10/24 00:00 [received] 2023/03/15 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 19:03 [entrez]
 2022/06/01 00:00 [received] 2023/02/14 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 18:07 [entrez]
 2023/05/05 06:42 [medline] 2023/05/03 12:42 [pubmed] 2023/05/03 12:02 [entrez]
 2023/01/14 06:00 [pubmed] 2023/01/27 06:00 [medline] 2023/01/13 23:25 [entrez]
 2022/04/27 00:00 [received] 2022/08/20 00:00 [accepted] 2022/09/05 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/04 23:16 [entrez]
 2023/01/13 06:00 [pubmed] 2023/01/20 06:00 [medline] 2023/01/12 23:26 [entrez]
 2022/09/20 00:00 [received] 2022/10/16 00:00 [revised] 2022/10/17 00:00 [accepted] 2022/10/25 06:00 [pubmed] 2022/11/24 06:00 [medline] 2022/10/24 19:26 [entrez]
 2022/08/15 00:00 [received] 2022/10/17 00:00 [revised] 2022/11/17 00:00 [accepted] 2022/11/27 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/26 18:19 [entrez]
 2022/08/10 00:00 [received] 2022/10/30 00:00 [accepted] 2022/10/25 00:00 [revised] 2022/11/06 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/05 12:24 [entrez]
 2023/02/16 00:00 [received] 2023/03/15 00:00 [revised] 2023/04/16 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2023/08/10 06:42 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:59 [entrez]
 2022/08/05 00:00 [received] 2022/11/04 00:00 [revised] 2022/11/22 00:00 [accepted] 2023/06/02 06:42 [medline] 2022/12/20 06:00 [pubmed] 2022/12/19 22:42 [entrez]
 2022/06/21 00:00 [received] 2022/08/31 00:00 [accepted] 2022/09/14 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/13 11:19 [entrez]
 2022/04/19 00:00 [received] 2022/05/23 00:00 [accepted] 2022/05/19 00:00 [revised] 2023/05/29 06:42 [medline] 2022/06/01 06:00 [pubmed] 2022/05/31 15:38 [entrez]
 2023/01/06 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/01/05 23:32 [entrez]
 2023/08/16 06:42 [medline] 2022/12/10 06:00 [pubmed] 2022/12/09 16:32 [entrez]
 2023/05/23 00:00 [received] 2023/06/22 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/14 13:06 [pubmed] 2023/07/13 18:11 [entrez]
 2022/07/21 00:00 [received] 2022/11/07 00:00 [revised] 2022/12/07 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/15 18:29 [entrez]
 2023/03/06 00:00 [received] 2023/07/20 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/08/01 01:08 [pubmed] 2023/07/31 18:04 [entrez]
 2022/08/15 00:00 [received] 2022/12/26 00:00 [revised] 2022/12/28 00:00 [accepted] 2023/01/14 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/13 18:22 [entrez]
 2022/11/03 00:00 [received] 2023/02/03 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/03/16 06:00 [pubmed] 2023/03/15 12:17 [entrez]
 2022/06/13 00:00 [received] 2023/02/07 00:00 [accepted] 2023/02/14 00:09 [entrez] 2023/02/15 06:00 [pubmed] 2023/02/16 06:00 [medline]
 2023/05/07 00:00 [received] 2023/05/17 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/07/18 01:09 [pubmed] 2023/07/17 21:23 [entrez]
 2023/03/16 00:00 [received] 2023/04/04 00:00 [accepted] 2023/07/05 06:42 [medline] 2023/04/19 06:00 [pubmed] 2023/04/18 06:00 [entrez]
 2022/12/07 00:00 [received] 2022/12/22 00:00 [revised] 2022/12/24 00:00 [accepted] 2023/01/21 01:24 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2023/07/14 13:08 [medline] 2023/05/15 13:06 [pubmed] 2023/05/15 11:33 [entrez]
 2022/12/19 00:00 [received] 2023/05/10 00:00 [revised] 2023/06/04 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/12 19:12 [pubmed] 2023/06/12 18:04 [entrez]
 2023/02/05 00:00 [received] 2023/03/24 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/05/08 06:41 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 18:02 [entrez]
 2022/10/10 00:00 [received] 2022/10/26 00:00 [accepted] 2022/11/02 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/11/01 12:02 [entrez]
 2022/07/12 00:00 [received] 2022/10/06 00:00 [accepted] 2022/10/18 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/17 23:33 [entrez]
 2022/10/18 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/21 06:00 [pubmed] 2023/03/11 06:00 [medline] 2023/01/20 19:26 [entrez]
 2022/10/05 00:00 [received] 2022/12/06 00:00 [accepted] 2022/12/19 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/12/18 18:16 [entrez]
 2023/06/19 13:08 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 00:24 [entrez]
 2023/01/10 00:00 [received] 2023/02/26 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 19:04 [entrez]
 2023/04/25 00:00 [received] 2023/06/07 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/02 01:10 [pubmed] 2023/07/01 18:08 [entrez]
 2022/08/03 00:00 [received] 2022/11/24 00:00 [revised] 2022/11/27 00:00 [accepted] 2022/12/05 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/04 18:13 [entrez]
 2023/03/12 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/29 06:42 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:25 [entrez]
 2023/04/17 06:41 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 11:33 [entrez]
 2023/03/11 00:00 [received] 2023/05/25 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/26 00:41 [pubmed] 2023/06/25 18:05 [entrez]
 2022/12/25 00:00 [received] 2023/02/05 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:23 [entrez]
 2021/11/23 00:00 [received] 2022/03/29 00:00 [accepted] 2022/07/14 06:00 [pubmed] 2023/03/14 06:00 [medline] 2022/07/13 03:03 [entrez]
 2023/07/10 06:42 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 09:33 [entrez]
 2022/03/29 06:00 [pubmed] 2023/01/28 06:00 [medline] 2022/03/28 08:53 [entrez]
 2023/05/05 00:00 [received] 2023/06/02 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/18 19:17 [pubmed] 2023/06/18 18:02 [entrez]
 2022/02/20 00:00 [received] 2022/10/24 00:00 [accepted] 2022/08/19 00:00 [revised] 2024/04/01 00:00 [pmc-release] 2023/03/28 19:06 [medline] 2022/12/09 06:00 [pubmed] 2022/12/08 12:50 [entrez]
 2023/07/14 13:08 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 01:02 [entrez]
 2022/01/22 00:00 [received] 2022/12/31 00:00 [revised] 2023/02/10 00:00 [accepted] 2023/03/08 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/03/07 18:42 [entrez]
 2023/02/17 00:00 [received] 2023/04/05 00:00 [accepted] 2023/03/31 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 11:15 [entrez]
 2023/09/05 06:41 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 10:51 [entrez]
 2023/04/19 00:00 [received] 2023/07/14 00:00 [accepted] 2023/07/03 00:00 [revised] 2023/09/08 06:42 [medline] 2023/08/05 05:42 [pubmed] 2023/08/04 23:21 [entrez]
 2022/01/20 00:00 [received] 2022/09/29 00:00 [revised] 2022/11/16 00:00 [accepted] 2023/05/22 06:42 [medline] 2022/11/30 06:00 [pubmed] 2022/11/29 18:19 [entrez]
 2022/09/29 00:00 [received] 2022/11/11 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/09 18:17 [entrez]
 2022/12/04 00:00 [received] 2022/12/30 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/03/10 06:00 [pubmed] 2023/03/09 02:52 [entrez]
 2023/07/26 06:42 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 11:33 [entrez]
 2023/05/08 10:17 [medline] 2023/05/04 12:41 [pubmed] 2023/05/04 09:43 [entrez]
 2022/07/29 00:00 [revised] 2022/02/20 00:00 [received] 2022/08/12 00:00 [accepted] 2022/09/23 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/22 08:52 [entrez]
 2021/07/11 06:00 [pubmed] 2023/01/24 06:00 [medline] 2021/07/10 05:40 [entrez]
 2023/05/20 00:00 [revised] 2022/05/26 00:00 [received] 2023/07/06 00:00 [accepted] 2023/09/04 06:44 [medline] 2023/08/02 13:08 [pubmed] 2023/08/02 09:43 [entrez]
 2023/08/10 06:42 [medline] 2023/06/27 13:10 [pubmed] 2023/06/27 07:52 [entrez]
 2023/03/29 00:00 [received] 2023/05/20 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/01 11:41 [pubmed] 2023/06/30 18:06 [entrez]
 2023/05/25 00:00 [revised] 2022/12/06 00:00 [received] 2023/06/05 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/10 23:42 [pubmed] 2023/06/10 13:13 [entrez]
 2022/05/04 00:00 [received] 2022/05/31 00:00 [revised] 2022/10/21 00:00 [accepted] 2022/11/20 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/19 18:19 [entrez]
 2022/10/18 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 18:35 [entrez]
 2022/12/19 00:00 [received] 2022/12/19 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 15:23 [entrez]
 2022/08/18 00:00 [received] 2022/10/25 00:00 [accepted] 2022/10/24 00:00 [revised] 2022/11/06 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/05 12:24 [entrez]
 2022/08/08 00:00 [received] 2022/10/15 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/09 18:17 [entrez]
 2023/05/12 07:06 [medline] 2023/05/11 00:42 [pubmed] 2023/05/10 20:42 [entrez]
 2023/01/11 00:00 [received] 2023/03/29 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 18:00 [entrez]
 2023/07/28 06:43 [medline] 2023/07/26 19:11 [pubmed] 2023/07/26 17:33 [entrez]
 2022/08/29 00:00 [received] 2022/11/01 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/05 18:26 [entrez]
 2022/12/01 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/30 08:23 [entrez]
 2022/05/16 00:00 [received] 2022/12/01 00:00 [revised] 2022/12/06 00:00 [accepted] 2022/12/15 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/14 18:33 [entrez]
 2022/05/10 00:00 [received] 2022/08/24 00:00 [accepted] 2023/02/04 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/03 13:53 [entrez]
 2023/05/31 00:00 [revised] 2023/04/03 00:00 [received] 2023/06/26 00:00 [accepted] 2023/08/16 06:42 [medline] 2023/07/19 01:06 [pubmed] 2023/07/18 21:12 [entrez]
 2022/06/04 00:00 [received] 2022/10/28 00:00 [accepted] 2022/08/26 00:00 [revised] 2022/12/23 06:00 [pubmed] 2023/03/21 06:00 [medline] 2022/12/22 11:13 [entrez]
 2023/09/04 06:43 [medline] 2023/08/02 01:07 [pubmed] 2023/08/01 21:23 [entrez]
 2022/05/17 00:00 [received] 2023/03/20 00:00 [accepted] 2023/04/06 10:16 [medline] 2023/04/04 23:52 [entrez] 2023/04/05 06:00 [pubmed]
 2022/10/07 00:00 [revised] 2021/07/29 00:00 [received] 2022/10/07 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/10/12 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/10/11 07:02 [entrez]
 2023/02/27 00:00 [received] 2023/03/24 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 23:26 [entrez]
 2023/08/16 06:43 [medline] 2023/08/07 19:10 [pubmed] 2023/08/07 13:03 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/06/21 06:42 [medline] 2023/06/19 13:09 [pubmed] 2023/06/19 09:13 [entrez]
 2022/09/13 00:00 [received] 2022/11/10 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/05 18:26 [entrez]
 2022/06/25 00:00 [received] 2022/10/26 00:00 [revised] 2022/10/29 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/01/13 06:00 [medline] 2022/11/29 18:13 [entrez]
 2023/04/19 00:00 [received] 2023/05/17 00:00 [accepted] 2023/09/12 06:42 [medline] 2023/05/20 19:13 [pubmed] 2023/05/20 14:57 [entrez]
 2021/11/09 00:00 [received] 2023/03/17 00:00 [accepted] 2023/03/31 06:41 [medline] 2023/03/29 23:45 [entrez] 2023/03/30 06:00 [pubmed]
 2023/02/03 00:00 [received] 2023/03/23 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/04/25 00:41 [pubmed] 2023/04/24 11:31 [entrez]
 2023/07/21 06:43 [medline] 2023/07/19 13:06 [pubmed] 2023/07/19 06:43 [entrez]
 2020/10/01 00:00 [received] 2021/01/01 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/09/03 00:41 [pubmed] 2023/09/02 21:00 [entrez]
 2022/09/27 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/09/26 18:44 [entrez]
 2023/07/04 00:00 [received] 2023/07/26 00:00 [revised] 2023/07/31 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:46 [pubmed] 2023/08/26 01:13 [entrez]
 2023/07/10 06:42 [medline] 2022/07/13 06:00 [pubmed] 2022/07/12 05:43 [entrez]
 2022/10/20 00:00 [received] 2022/11/18 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/17 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/16 18:28 [entrez]
 2023/05/12 07:06 [medline] 2022/12/23 06:00 [pubmed] 2022/12/22 04:33 [entrez]
 2022/08/29 00:00 [received] 2023/02/02 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/17 06:00 [pubmed] 2023/03/16 19:21 [entrez]
 2022/12/09 00:00 [received] 2023/01/21 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 18:19 [entrez]
 2022/05/05 00:00 [received] 2022/10/03 00:00 [revised] 2022/10/23 00:00 [accepted] 2022/11/21 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/20 18:12 [entrez]
 2023/06/27 00:00 [received] 2023/06/27 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/07/10 00:42 [pubmed] 2023/07/09 18:03 [entrez]
 2022/09/24 00:00 [revised] 2022/06/21 00:00 [received] 2022/11/02 00:00 [accepted] 2022/11/26 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/11/25 13:33 [entrez]
 2022/08/27 00:00 [received] 2022/11/15 00:00 [accepted] 2023/04/05 06:42 [medline] 2022/12/21 06:00 [pubmed] 2022/12/20 21:23 [entrez]
 2022/08/05 00:00 [received] 2022/10/01 00:00 [accepted] 2022/10/14 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/10/13 21:22 [entrez]
 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 20:53 [entrez]
 2023/01/19 00:00 [received] 2023/06/22 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/07/05 01:06 [pubmed] 2023/07/04 23:37 [entrez]
 2022/08/23 00:00 [received] 2022/11/28 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/01/05 01:33 [entrez]
 2023/02/07 00:00 [received] 2023/03/22 00:00 [revised] 2023/04/02 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 18:02 [entrez]
 2022/07/06 00:00 [received] 2022/10/21 00:00 [revised] 2022/11/17 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/02/26 06:00 [pubmed] 2023/02/25 22:02 [entrez]
 2023/05/12 07:06 [medline] 2023/05/06 19:41 [pubmed] 2023/05/06 07:53 [entrez]
 2023/05/10 00:00 [received] 2023/06/05 00:00 [revised] 2023/06/06 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:12 [entrez]
 2022/09/05 00:00 [received] 2023/01/31 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 19:22 [entrez]
 2023/07/12 06:42 [medline] 2023/05/19 06:42 [pubmed] 2023/05/19 03:37 [entrez]
 2023/03/11 00:00 [received] 2023/04/03 00:00 [accepted] 2023/04/01 00:00 [revised] 2023/07/04 06:42 [medline] 2023/05/05 12:42 [pubmed] 2023/05/05 09:13 [entrez]
 2022/09/22 00:00 [received] 2023/04/18 00:00 [accepted] 2023/08/09 06:42 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 21:43 [entrez]
 2022/06/27 00:00 [received] 2022/12/04 00:00 [accepted] 2023/04/17 06:41 [medline] 2022/12/21 06:00 [pubmed] 2022/12/20 21:12 [entrez]
 2023/05/01 06:42 [medline] 2023/03/22 06:00 [pubmed] 2023/03/21 09:03 [entrez]
 2022/06/21 00:00 [received] 2022/08/16 00:00 [revised] 2022/11/30 00:00 [accepted] 2024/01/15 00:00 [pmc-release] 2022/12/20 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/12/19 18:29 [entrez]
 2023/01/16 00:00 [revised] 2022/07/01 00:00 [received] 2023/01/18 00:00 [accepted] 2023/01/25 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/24 11:42 [entrez]
 2023/05/01 06:41 [medline] 2023/04/29 19:44 [pubmed] 2023/04/29 14:43 [entrez]
 2022/11/19 00:00 [received] 2023/03/25 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/14 06:00 [pubmed] 2023/04/13 18:05 [entrez]
 2022/09/02 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/09/01 03:34 [entrez]
 2023/07/14 13:06 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 11:33 [entrez]
 2023/02/15 00:00 [received] 2023/04/21 00:00 [revised] 2023/04/23 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 20:55 [entrez]
 2022/08/01 00:00 [received] 2022/10/21 00:00 [revised] 2022/10/28 00:00 [accepted] 2022/11/07 06:00 [pubmed] 2022/11/23 06:00 [medline] 2022/11/06 19:32 [entrez]
 2023/06/19 13:09 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 19:15 [entrez]
 2022/11/12 00:00 [received] 2023/01/24 00:00 [revised] 2023/01/25 00:00 [accepted] 2023/02/05 06:00 [pubmed] 2023/03/09 06:00 [medline] 2023/02/04 18:17 [entrez]
 2022/11/14 00:00 [received] 2023/01/31 00:00 [revised] 2023/02/01 00:00 [accepted] 2023/02/09 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/02/08 19:25 [entrez]
 2022/11/16 00:00 [received] 2023/06/28 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/17 00:42 [pubmed] 2023/07/16 18:06 [entrez]
 2022/11/10 00:00 [received] 2023/02/08 00:00 [accepted] 2023/02/08 00:00 [revised] 2023/05/18 06:42 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 23:31 [entrez]
 2023/04/11 06:42 [medline] 2023/04/08 21:00 [entrez] 2023/04/09 06:00 [pubmed]
 2022/12/15 00:00 [received] 2023/02/20 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/21 06:00 [pubmed] 2023/03/20 19:05 [entrez]
 2022/07/07 00:00 [received] 2023/01/31 00:00 [accepted] 2023/02/11 00:01 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/02/09 00:00 [received] 2023/04/03 00:00 [accepted] 2023/08/11 06:42 [medline] 2023/04/26 12:41 [pubmed] 2023/04/26 11:19 [entrez]
 2023/05/22 06:42 [medline] 2023/01/31 06:00 [pubmed] 2023/01/30 08:32 [entrez]
 2022/12/24 00:00 [received] 2023/04/10 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/08 00:41 [pubmed] 2023/05/07 18:06 [entrez]
 2023/05/08 00:00 [revised] 2022/12/12 00:00 [received] 2023/05/25 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/05/29 06:42 [pubmed] 2023/05/29 03:45 [entrez]
 2022/10/08 00:00 [received] 2022/11/17 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/11 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/10 18:33 [entrez]
 2023/02/24 00:00 [received] 2023/05/26 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/26 00:41 [pubmed] 2023/06/25 18:05 [entrez]
 2023/06/02 00:00 [received] 2023/07/07 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/08/10 06:43 [pubmed] 2023/08/10 04:00 [entrez]
 2023/04/14 06:41 [medline] 2021/07/14 06:00 [pubmed] 2021/07/13 05:31 [entrez]
 2023/07/03 06:41 [medline] 2023/06/30 06:42 [pubmed] 2023/06/30 04:23 [entrez]
 2023/07/03 06:41 [medline] 2023/06/30 06:42 [pubmed] 2023/06/30 04:24 [entrez]
 2022/09/17 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/09/16 18:13 [entrez]
 2022/09/06 00:00 [received] 2022/10/01 00:00 [accepted] 2023/06/15 06:42 [medline] 2023/06/14 06:42 [pubmed] 2023/06/14 03:47 [entrez]
 2022/05/04 00:00 [received] 2022/09/24 00:00 [revised] 2022/10/14 00:00 [accepted] 2022/12/27 06:00 [pubmed] 2023/02/08 06:00 [medline] 2022/12/26 21:55 [entrez]
 2023/05/01 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 05:52 [entrez]
 2023/02/13 00:00 [received] 2023/03/30 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 18:07 [entrez]
 2023/05/25 00:00 [received] 2023/06/24 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/17 00:42 [pubmed] 2023/07/16 18:06 [entrez]
 2023/06/07 00:00 [received] 2023/06/27 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/10 00:41 [pubmed] 2023/07/09 18:06 [entrez]
 2022/12/12 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 18:02 [entrez]
 2022/12/11 00:00 [received] 2023/02/27 00:00 [accepted] 2023/06/20 06:42 [medline] 2023/05/31 19:16 [pubmed] 2023/05/31 17:03 [entrez]
 2023/01/19 00:00 [received] 2023/03/15 00:00 [accepted] 2023/03/14 00:00 [revised] 2023/06/16 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 12:15 [entrez]
 2022/09/01 00:00 [received] 2022/12/05 00:00 [revised] 2022/12/12 00:00 [accepted] 2022/12/18 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/12/17 18:21 [entrez]
 2022/12/19 00:00 [received] 2023/03/10 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/05/23 06:42 [medline] 2023/04/16 06:00 [pubmed] 2023/04/15 19:29 [entrez]
 2022/11/17 00:00 [received] 2023/02/09 00:00 [accepted] 2023/07/14 13:06 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 10:02 [entrez]
 2022/08/16 00:00 [received] 2022/10/25 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/11/17 21:48 [entrez]
 2022/11/25 00:00 [received] 2023/01/13 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 18:24 [entrez]
 2022/11/16 00:00 [received] 2022/12/02 00:00 [revised] 2022/12/07 00:00 [accepted] 2023/01/01 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/31 18:17 [entrez]
 2022/08/05 00:00 [received] 2022/09/30 00:00 [revised] 2022/10/03 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 22:00 [entrez]
 2023/03/03 00:00 [received] 2023/05/03 00:00 [accepted] 2023/05/26 06:42 [medline] 2023/05/25 01:07 [pubmed] 2023/05/24 23:22 [entrez]
 2022/11/22 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/23 18:11 [entrez]
 2022/11/08 00:00 [received] 2023/03/26 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/04/02 00:25 [entrez] 2023/04/03 06:00 [pubmed]
 2023/01/11 00:00 [revised] 2022/09/15 00:00 [received] 2023/01/12 00:00 [accepted] 2024/05/01 00:00 [pmc-release] 2023/05/12 07:06 [medline] 2023/01/31 06:00 [pubmed] 2023/01/30 08:32 [entrez]
 2022/12/09 00:00 [received] 2023/02/16 00:00 [revised] 2023/02/19 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 22:04 [entrez]
 2023/05/12 07:06 [medline] 2023/04/09 06:00 [pubmed] 2023/04/08 01:52 [entrez]
 2022/12/04 00:00 [revised] 2022/08/08 00:00 [received] 2023/01/18 00:00 [accepted] 2023/01/22 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/01/21 02:42 [entrez]
 2023/01/13 00:00 [received] 2023/05/05 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/05/18 19:12 [pubmed] 2023/05/18 13:44 [entrez]
 2022/08/02 00:00 [received] 2022/11/22 00:00 [accepted] 2023/04/11 06:42 [medline] 2022/12/07 06:00 [pubmed] 2022/12/06 23:42 [entrez]
 2023/02/10 00:00 [received] 2023/05/12 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:27 [entrez]
 2023/01/24 00:00 [revised] 2022/10/07 00:00 [received] 2023/01/26 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/03/02 06:00 [pubmed] 2023/03/01 03:44 [entrez]
 2022/11/29 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/11/28 05:32 [entrez]
 2022/05/24 00:00 [received] 2022/09/08 00:00 [accepted] 2022/10/12 06:00 [pubmed] 2022/12/29 06:00 [medline] 2022/10/11 21:48 [entrez]
 2022/12/30 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/12/29 09:02 [entrez]
 2023/03/15 00:00 [revised] 2022/10/14 00:00 [received] 2023/05/01 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 13:42 [pubmed] 2023/05/08 07:43 [entrez]
 2022/08/03 00:00 [received] 2022/09/16 00:00 [accepted] 2022/09/15 00:00 [revised] 2022/09/25 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/24 11:23 [entrez]
 2023/02/21 00:00 [received] 2023/04/03 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 18:05 [entrez]
 2020/12/23 00:00 [received] 2021/01/01 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/04/30 00:42 [pubmed] 2023/04/29 19:29 [entrez]
 2023/07/10 06:42 [medline] 2023/06/29 06:43 [pubmed] 2023/06/29 05:43 [entrez]
 2023/01/30 00:00 [revised] 2022/10/18 00:00 [received] 2023/01/31 00:00 [accepted] 2023/04/19 06:41 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 15:38 [entrez]
 2022/12/02 00:00 [received] 2023/03/16 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 11:17 [entrez]
 2023/06/08 00:00 [revised] 2023/02/12 00:00 [received] 2023/06/12 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/16 13:10 [pubmed] 2023/06/16 06:38 [entrez]
 2023/03/24 00:00 [received] 2023/04/02 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/16 06:00 [pubmed] 2023/04/15 18:09 [entrez]
 2022/09/28 00:00 [received] 2023/04/18 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/05/26 06:42 [pubmed] 2023/05/26 03:53 [entrez]
 2022/11/25 00:00 [received] 2023/01/09 00:00 [revised] 2023/01/10 00:00 [accepted] 2023/01/21 01:22 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2023/07/27 06:42 [medline] 2023/07/21 06:44 [pubmed] 2023/07/21 04:33 [entrez]
 2023/01/20 00:00 [received] 2023/04/02 00:00 [revised] 2023/04/16 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2023/06/28 06:42 [medline] 2022/06/17 06:00 [pubmed] 2022/06/16 09:04 [entrez]
 2023/06/23 06:42 [medline] 2023/06/22 06:42 [pubmed] 2023/06/22 02:28 [entrez]
 2023/06/23 00:00 [revised] 2023/04/11 00:00 [received] 2023/07/06 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 20:13 [entrez]
 2023/01/09 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/03/19 06:00 [pubmed] 2023/03/18 19:02 [entrez]
 2022/07/11 00:00 [received] 2023/01/10 00:00 [accepted] 2023/03/16 02:24 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/21 06:00 [medline]
 2022/07/13 00:00 [received] 2022/08/17 00:00 [accepted] 2022/08/09 00:00 [revised] 2022/09/20 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/19 11:18 [entrez]
 2022/03/25 00:00 [received] 2022/08/31 00:00 [accepted] 2022/08/09 00:00 [revised] 2022/11/03 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/02 00:31 [entrez]
 2023/07/12 06:42 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 06:12 [entrez]
 2022/08/23 00:00 [received] 2023/03/14 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/16 06:00 [pubmed] 2023/04/15 18:03 [entrez]
 2022/06/13 00:00 [received] 2022/11/14 00:00 [revised] 2022/11/15 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/12/08 23:43 [entrez]
 2023/04/22 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/02 00:00 [accepted] 2023/06/29 06:42 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:25 [entrez]
 2022/06/09 00:00 [received] 2022/10/10 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/02/04 06:00 [medline] 2022/12/05 18:29 [entrez]
 2022/09/13 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/09/12 12:00 [entrez]
 2022/11/30 00:00 [received] 2023/04/12 00:00 [revised] 2023/05/08 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/22 00:41 [pubmed] 2023/05/21 18:11 [entrez]
 2022/12/21 00:00 [received] 2023/02/08 00:00 [accepted] 2023/02/08 00:00 [revised] 2023/02/17 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/02/16 11:05 [entrez]
 2022/11/07 00:00 [revised] 2022/09/21 00:00 [received] 2022/12/13 00:00 [accepted] 2022/12/28 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/12/27 08:23 [entrez]
 2022/11/23 00:00 [received] 2023/02/07 00:00 [accepted] 2023/02/14 00:02 [entrez] 2023/02/15 06:00 [pubmed] 2023/02/16 06:00 [medline]
 2023/02/02 00:00 [received] 2023/05/02 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 23:30 [entrez]
 2022/04/26 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/04/25 05:55 [entrez]
 2023/01/10 00:00 [accepted] 2023/02/03 06:00 [pubmed] 2023/02/14 06:00 [medline] 2023/02/02 11:20 [entrez]
 2022/12/05 00:00 [revised] 2022/10/28 00:00 [received] 2023/01/18 00:00 [accepted] 2023/04/06 06:42 [medline] 2023/01/25 06:00 [pubmed] 2023/01/24 11:23 [entrez]
 2022/07/14 00:00 [accepted] 2022/08/19 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/08/18 23:28 [entrez]
 2022/07/15 00:00 [received] 2022/11/20 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/11/28 23:45 [entrez]
 2022/07/04 00:00 [received] 2023/05/15 00:00 [revised] 2023/06/13 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/06/19 00:42 [pubmed] 2023/06/18 18:10 [entrez]
 2022/10/16 00:00 [received] 2023/01/03 00:00 [accepted] 2023/02/10 03:12 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2022/09/20 00:00 [received] 2023/03/09 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 18:03 [entrez]
 2023/01/17 00:00 [received] 2023/02/24 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/23 06:00 [pubmed] 2023/03/22 19:09 [entrez]
 2023/04/25 06:42 [medline] 2021/09/14 06:00 [pubmed] 2021/09/13 08:58 [entrez]
 2022/09/09 00:00 [received] 2023/01/25 00:00 [revised] 2023/02/13 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:23 [entrez]
 2023/04/01 00:00 [received] 2023/05/28 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/27 01:07 [pubmed] 2023/06/26 18:03 [entrez]
 2023/02/24 00:00 [received] 2023/06/22 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 23:38 [entrez]
 2023/01/11 00:00 [received] 2023/03/25 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/14 01:07 [pubmed] 2023/05/13 18:07 [entrez]
 2023/07/12 06:42 [medline] 2023/06/15 06:41 [pubmed] 2023/06/15 05:31 [entrez]
 2022/06/16 00:00 [received] 2022/10/08 00:00 [revised] 2022/11/03 00:00 [accepted] 2022/11/22 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/21 18:28 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/07/12 06:42 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 17:43 [entrez]
 2022/11/29 00:00 [received] 2023/03/24 00:00 [accepted] 2023/03/23 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/19 12:41 [pubmed] 2023/04/19 11:13 [entrez]
 2022/08/12 00:00 [revised] 2022/06/03 00:00 [received] 2022/09/26 00:00 [accepted] 2022/10/18 06:00 [pubmed] 2023/01/28 06:00 [medline] 2022/10/17 09:03 [entrez]
 2022/09/14 00:00 [received] 2022/12/01 00:00 [accepted] 2022/11/30 00:00 [revised] 2022/12/13 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/12 23:37 [entrez]
 2022/12/05 00:00 [received] 2023/01/17 00:00 [revised] 2023/02/04 00:00 [accepted] 2024/03/01 00:00 [pmc-release] 2023/04/04 06:42 [medline] 2023/02/11 06:00 [pubmed] 2023/02/10 18:22 [entrez]
 2022/11/07 00:00 [received] 2023/05/22 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/26 00:42 [pubmed] 2023/06/25 18:05 [entrez]
 2023/05/12 07:06 [medline] 2022/12/24 06:00 [pubmed] 2022/12/23 00:12 [entrez]
 2023/02/17 00:00 [received] 2023/03/25 00:00 [revised] 2023/03/27 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/13 01:11 [entrez] 2023/04/14 06:00 [pubmed]
 2023/05/31 06:42 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 00:52 [entrez]
 2022/11/10 00:00 [received] 2023/03/15 00:00 [revised] 2023/04/14 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 20:57 [entrez]
 2023/03/01 00:00 [received] 2023/05/24 00:00 [revised] 2023/07/18 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/23 01:11 [pubmed] 2023/07/22 18:06 [entrez]
 2022/09/20 00:00 [received] 2022/11/16 00:00 [revised] 2022/12/02 00:00 [accepted] 2022/12/07 06:00 [pubmed] 2023/01/04 06:00 [medline] 2022/12/06 19:25 [entrez]
 2023/07/04 06:42 [medline] 2023/07/03 00:41 [pubmed] 2023/07/02 19:03 [entrez]
 2021/12/12 00:00 [received] 2022/02/05 00:00 [accepted] 2023/04/28 06:42 [medline] 2022/02/13 06:00 [pubmed] 2022/02/12 05:38 [entrez]
 2022/12/21 00:00 [received] 2023/03/28 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/12 13:44 [entrez] 2023/04/13 06:00 [pubmed]
 2022/12/12 00:00 [received] 2023/03/09 00:00 [accepted] 2023/03/08 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/19 06:00 [pubmed] 2023/03/18 12:13 [entrez]
 2022/09/23 00:00 [received] 2023/01/10 00:00 [revised] 2023/02/03 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 18:14 [entrez]
 2023/06/02 06:42 [medline] 2022/03/18 06:00 [pubmed] 2022/03/17 12:12 [entrez]
 2022/09/28 00:00 [received] 2022/11/10 00:00 [accepted] 2022/11/09 00:00 [revised] 2022/11/28 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/27 14:04 [entrez]
 2022/12/02 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/01 01:53 [entrez]
 2022/12/01 00:00 [received] 2023/04/02 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/08 18:42 [pubmed] 2023/05/08 18:00 [entrez]
 2022/10/07 00:00 [received] 2023/01/19 00:00 [revised] 2023/01/25 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/01/31 06:00 [pubmed] 2023/01/30 18:08 [entrez]
 2022/09/07 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/06/03 11:42 [pubmed] 2023/06/02 23:35 [entrez]
 2022/12/14 00:00 [received] 2023/03/03 00:00 [revised] 2023/03/19 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 19:03 [entrez]
 2022/10/01 00:00 [received] 2023/02/08 00:00 [revised] 2023/02/10 00:00 [accepted] 2023/02/22 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/02/21 16:29 [entrez]
 2023/08/11 06:42 [medline] 2023/08/10 12:43 [pubmed] 2023/08/10 07:24 [entrez]
 2022/07/12 00:00 [received] 2022/09/30 00:00 [revised] 2022/10/19 00:00 [accepted] 2023/04/05 06:42 [medline] 2022/11/20 06:00 [pubmed] 2022/11/19 22:08 [entrez]
 2022/12/20 00:00 [received] 2023/06/08 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/21 19:10 [pubmed] 2023/07/21 13:35 [entrez]
 2022/12/26 00:00 [received] 2023/03/20 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:09 [entrez]
 2023/01/10 00:00 [received] 2023/04/20 00:00 [revised] 2023/05/07 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/24 01:06 [pubmed] 2023/05/23 18:02 [entrez]
 2021/12/13 00:00 [received] 2022/03/08 00:00 [revised] 2022/03/10 00:00 [accepted] 2022/03/31 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/03/30 05:38 [entrez]
 2022/09/09 00:00 [received] 2022/10/20 00:00 [accepted] 2022/11/03 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/11/02 00:40 [entrez]
 2022/10/11 00:00 [received] 2023/02/02 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 19:05 [entrez]
 2022/10/25 00:00 [received] 2023/01/05 00:00 [accepted] 2023/01/26 06:00 [pubmed] 2023/03/21 06:00 [medline] 2023/01/25 08:34 [entrez]
 2023/03/04 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/03/03 10:53 [entrez]
 2023/04/05 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/08 13:41 [pubmed] 2023/05/08 11:23 [entrez]
 2023/07/17 06:42 [medline] 2022/01/11 06:00 [pubmed] 2022/01/10 15:07 [entrez]
 2022/09/27 00:00 [received] 2023/01/04 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/01/14 06:00 [pubmed] 2023/01/13 21:22 [entrez]
 2022/04/22 00:00 [received] 2022/09/15 00:00 [accepted] 2023/04/21 06:41 [medline] 2022/09/22 06:00 [pubmed] 2022/09/21 21:02 [entrez]
 2022/12/21 00:00 [received] 2023/04/18 00:00 [revised] 2023/04/22 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/01 00:42 [pubmed] 2023/04/30 18:04 [entrez]
 2022/11/18 00:00 [received] 2023/02/19 00:00 [revised] 2023/02/28 00:00 [accepted] 2023/04/18 10:16 [medline] 2023/04/17 03:37 [entrez] 2023/04/18 06:00 [pubmed]
 2022/07/05 00:00 [accepted] 2022/07/29 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/07/28 16:32 [entrez]
 2023/05/19 06:41 [medline] 2023/05/18 01:07 [pubmed] 2023/05/17 20:52 [entrez]
 2022/12/01 00:00 [received] 2023/01/05 00:00 [accepted] 2023/01/20 23:40 [entrez] 2023/01/21 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/10/06 00:00 [revised] 2022/05/23 00:00 [received] 2023/01/02 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/01/19 06:00 [pubmed] 2023/01/18 04:33 [entrez]
 2022/01/12 00:00 [received] 2022/10/03 00:00 [accepted] 2023/04/12 06:41 [medline] 2023/02/05 06:00 [pubmed] 2023/02/04 07:13 [entrez]
 2023/02/10 00:00 [received] 2023/08/01 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/08/11 18:42 [pubmed] 2023/08/11 13:34 [entrez]
 2023/01/10 00:00 [received] 2023/04/21 00:00 [accepted] 2023/09/13 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 21:23 [entrez]
 2023/04/10 00:00 [revised] 2023/02/02 00:00 [received] 2023/04/25 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/09 13:42 [pubmed] 2023/05/09 06:53 [entrez]
 2023/04/26 00:00 [received] 2023/06/15 00:00 [revised] 2023/06/21 00:00 [accepted] 2024/06/25 00:00 [pmc-release] 2023/08/11 06:43 [medline] 2023/06/27 01:06 [pubmed] 2023/06/26 19:19 [entrez]
 2022/11/30 00:00 [received] 2023/05/22 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/07/04 13:09 [pubmed] 2023/07/04 11:10 [entrez]
 2022/08/24 00:00 [received] 2023/01/19 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 21:23 [entrez]
 2023/05/12 07:06 [medline] 2023/04/11 06:00 [pubmed] 2023/04/10 08:23 [entrez]
 2022/03/10 00:00 [received] 2022/11/02 00:00 [accepted] 2022/11/01 00:00 [revised] 2024/04/01 00:00 [pmc-release] 2023/03/28 19:06 [medline] 2022/11/10 06:00 [pubmed] 2022/11/09 23:45 [entrez]
 2023/08/10 06:43 [medline] 2023/07/20 13:06 [pubmed] 2023/07/20 06:59 [entrez]
 2022/10/10 00:00 [received] 2023/05/11 00:00 [revised] 2023/05/19 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/12 19:12 [pubmed] 2023/06/12 18:04 [entrez]
 2023/07/09 00:00 [revised] 2023/04/20 00:00 [received] 2023/07/17 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/07/24 06:43 [pubmed] 2023/07/24 04:25 [entrez]
 2022/06/27 00:00 [received] 2022/08/24 00:00 [accepted] 2022/08/29 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/08/28 23:17 [entrez]
 2022/09/20 00:00 [received] 2022/12/18 00:00 [revised] 2023/02/13 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 18:14 [entrez]
 2023/01/11 00:00 [received] 2023/03/24 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/08 00:42 [pubmed] 2023/08/07 18:06 [entrez]
 2022/08/25 00:00 [revised] 2022/05/30 00:00 [received] 2022/10/17 00:00 [accepted] 2022/10/28 06:00 [pubmed] 2022/12/20 06:00 [medline] 2022/10/27 10:33 [entrez]
 2022/10/03 06:00 [pubmed] 2023/01/17 06:00 [medline] 2022/10/02 20:52 [entrez]
 2022/11/15 00:00 [received] 2023/02/26 00:00 [revised] 2023/03/04 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/03 06:00 [pubmed] 2023/04/02 18:01 [entrez]
 2023/02/09 00:00 [received] 2023/03/15 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:09 [entrez]
 2022/11/14 00:00 [received] 2022/12/14 00:00 [revised] 2023/01/15 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/12 06:00 [pubmed] 2023/02/11 18:18 [entrez]
 2023/03/20 00:00 [received] 2023/05/11 00:00 [accepted] 2023/05/08 00:00 [revised] 2023/08/14 06:42 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 23:25 [entrez]
 2022/08/05 00:00 [received] 2022/10/11 00:00 [revised] 2022/10/14 00:00 [accepted] 2022/10/22 06:00 [pubmed] 2022/11/24 06:00 [medline] 2022/10/21 19:24 [entrez]
 2023/05/03 00:00 [received] 2023/06/19 00:00 [revised] 2023/07/09 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/17 19:08 [pubmed] 2023/07/17 18:02 [entrez]
 2022/11/02 00:00 [received] 2023/01/26 00:00 [accepted] 2023/03/08 01:45 [entrez] 2023/03/09 06:00 [pubmed] 2023/03/10 06:00 [medline]
 2022/06/22 00:00 [received] 2022/09/27 00:00 [accepted] 2022/09/26 00:00 [revised] 2022/11/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/15 00:02 [entrez]
 2022/08/29 00:00 [received] 2022/11/07 00:00 [revised] 2022/12/03 00:00 [accepted] 2022/12/19 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/18 18:27 [entrez]
 2022/09/19 00:00 [revised] 2022/04/10 00:00 [received] 2022/10/16 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/11/03 06:00 [pubmed] 2023/01/03 06:00 [medline] 2022/11/02 08:42 [entrez]
 2023/03/28 00:00 [revised] 2023/01/27 00:00 [received] 2023/05/09 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/12 07:06 [pubmed] 2023/05/12 05:27 [entrez]
 2022/08/31 00:00 [received] 2022/10/14 00:00 [accepted] 2022/10/13 00:00 [revised] 2022/11/01 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/10/31 12:13 [entrez]
 2022/11/29 00:00 [received] 2023/01/19 00:00 [revised] 2023/01/24 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/05 06:00 [pubmed] 2023/02/04 18:18 [entrez]
 2022/08/15 00:00 [received] 2022/10/24 00:00 [revised] 2022/11/11 00:00 [accepted] 2022/11/28 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/27 18:16 [entrez]
 2022/10/08 00:00 [revised] 2022/07/05 00:00 [received] 2022/11/01 00:00 [accepted] 2022/11/22 06:00 [pubmed] 2023/01/28 06:00 [medline] 2022/11/21 13:44 [entrez]
 2022/04/13 00:00 [received] 2022/11/29 00:00 [accepted] 2022/10/03 00:00 [revised] 2023/07/10 06:42 [medline] 2022/12/24 06:00 [pubmed] 2022/12/23 11:12 [entrez]
 2023/01/08 00:00 [received] 2023/05/14 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 18:03 [entrez]
 2021/11/05 06:00 [pubmed] 2023/01/27 06:00 [medline] 2021/11/04 17:18 [entrez]
 2022/09/14 00:00 [received] 2022/11/29 00:00 [accepted] 2023/03/06 23:31 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/09 06:00 [medline]
 2023/08/11 06:42 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/02/27 03:05 [entrez] 2023/02/28 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/09/05 00:00 [received] 2022/10/29 00:00 [revised] 2022/11/19 00:00 [accepted] 2022/11/28 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/27 18:16 [entrez]
 2023/03/31 00:00 [received] 2023/06/16 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/17 19:08 [pubmed] 2023/07/17 18:02 [entrez]
 2023/04/28 00:00 [received] 2023/06/07 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/17 00:42 [pubmed] 2023/07/16 18:06 [entrez]
 2022/12/22 00:00 [received] 2023/03/30 00:00 [revised] 2023/04/02 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2023/03/14 00:00 [received] 2023/07/01 00:00 [revised] 2023/07/15 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/24 00:41 [pubmed] 2023/07/23 18:01 [entrez]
 2023/05/12 07:06 [medline] 2022/12/13 06:00 [pubmed] 2022/12/12 11:46 [entrez]
 2023/03/24 00:00 [received] 2023/06/04 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 23:03 [entrez]
 2023/05/19 06:42 [medline] 2023/05/18 13:09 [pubmed] 2023/05/18 07:23 [entrez]
 2022/06/24 00:00 [received] 2022/09/05 00:00 [accepted] 2022/09/29 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/28 21:41 [entrez]
 2023/05/17 06:42 [medline] 2021/12/28 06:00 [pubmed] 2021/12/27 17:09 [entrez]
 2022/11/28 00:00 [received] 2023/02/24 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/06 06:00 [pubmed] 2023/04/05 18:08 [entrez]
 2022/09/01 00:00 [received] 2022/12/31 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/01/08 06:00 [pubmed] 2023/01/07 16:56 [entrez]
 2022/12/23 00:00 [received] 2023/03/26 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2022/07/09 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/07/08 01:53 [entrez]
 2022/03/08 00:00 [received] 2022/03/22 00:00 [revised] 2022/03/23 00:00 [accepted] 2022/04/04 06:00 [pubmed] 2023/02/18 06:00 [medline] 2022/04/03 20:33 [entrez]
 2023/03/09 00:00 [received] 2023/05/25 00:00 [revised] 2023/06/03 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/06/24 21:05 [pubmed] 2023/06/24 18:00 [entrez]
 2022/12/21 00:00 [received] 2023/02/21 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/06/05 06:43 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 18:07 [entrez]
 2022/06/09 00:00 [received] 2023/05/08 00:00 [accepted] 2024/09/05 00:00 [pmc-release] 2023/09/06 06:42 [medline] 2023/07/18 01:09 [pubmed] 2023/07/17 21:23 [entrez]
 2022/11/08 00:00 [received] 2023/03/08 00:00 [accepted] 2023/03/14 00:39 [entrez] 2023/03/15 06:00 [pubmed] 2023/03/16 06:00 [medline]
 2022/03/17 00:00 [received] 2022/09/14 00:00 [accepted] 2023/05/29 06:41 [medline] 2022/10/21 06:00 [pubmed] 2022/10/20 11:15 [entrez]
 2022/10/14 00:00 [received] 2023/04/13 00:00 [accepted] 2023/08/07 06:41 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 21:53 [entrez]
 2023/07/31 06:43 [medline] 2023/07/28 19:11 [pubmed] 2023/07/28 17:42 [entrez]
 2022/09/02 00:00 [received] 2022/10/26 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/09 18:18 [entrez]
 2022/08/31 00:00 [revised] 2022/05/19 00:00 [received] 2023/02/04 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/04/20 06:42 [pubmed] 2023/04/20 05:53 [entrez]
 2023/09/11 06:42 [medline] 2023/05/15 19:12 [pubmed] 2023/05/15 13:51 [entrez]
 2023/02/17 00:00 [received] 2023/04/15 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/31 13:12 [pubmed] 2023/05/31 07:53 [entrez]
 2022/12/07 00:00 [received] 2023/03/27 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/21 18:43 [pubmed] 2023/04/21 18:02 [entrez]
 2022/03/29 00:00 [received] 2022/10/11 00:00 [accepted] 2022/12/22 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/21 21:23 [entrez]
 2022/12/07 06:00 [pubmed] 2022/12/16 06:00 [medline] 2022/12/06 04:02 [entrez]
 2023/03/12 00:00 [received] 2023/04/13 00:00 [accepted] 2023/04/12 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/28 00:42 [pubmed] 2023/04/27 23:31 [entrez]
 2022/06/30 00:00 [received] 2023/01/31 00:00 [accepted] 2023/02/28 00:55 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/10/04 00:00 [received] 2023/02/23 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/07 06:00 [pubmed] 2023/03/06 11:17 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2022/05/15 00:00 [received] 2022/10/25 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/01 06:43 [pubmed] 2023/09/01 04:13 [entrez]
 2023/03/31 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 00:39 [entrez]
 2023/04/11 06:42 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 22:09 [entrez]
 2022/06/19 00:00 [received] 2022/12/19 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/21 18:37 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2022/12/09 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/12/08 11:46 [entrez]
 2023/06/22 06:41 [medline] 2023/06/21 13:04 [pubmed] 2023/06/21 07:43 [entrez]
 2023/03/23 00:00 [received] 2023/05/01 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/22 00:41 [pubmed] 2023/05/21 18:09 [entrez]
 2022/12/11 00:00 [received] 2023/02/28 00:00 [accepted] 2023/02/12 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/13 06:00 [pubmed] 2023/03/11 23:25 [entrez]
 2023/02/06 00:00 [received] 2023/04/06 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/05/02 00:42 [pubmed] 2023/05/01 19:22 [entrez]
 2023/05/01 06:41 [medline] 2023/01/28 06:00 [pubmed] 2023/01/27 00:22 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2022/10/08 00:00 [received] 2022/10/27 00:00 [accepted] 2022/11/05 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/11/04 12:17 [entrez]
 2023/03/22 19:17 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2023/05/02 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/10 00:42 [pubmed] 2023/07/09 18:06 [entrez]
 2022/10/11 00:00 [received] 2023/01/19 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/11 06:00 [pubmed] 2023/02/10 18:22 [entrez]
 2023/05/04 00:00 [received] 2023/05/26 00:00 [revised] 2023/06/22 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 18:06 [entrez]
 2022/10/04 00:00 [received] 2022/11/22 00:00 [revised] 2022/12/05 00:00 [accepted] 2022/12/14 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/13 18:22 [entrez]
 2023/02/22 00:00 [received] 2023/05/18 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 18:07 [entrez]
 2022/03/03 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/23 00:15 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2022/11/27 00:00 [received] 2022/12/06 00:00 [accepted] 2022/12/25 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/24 11:14 [entrez]
 2022/10/20 00:00 [received] 2023/01/03 00:00 [revised] 2023/02/02 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/27 06:00 [pubmed] 2023/02/26 18:23 [entrez]
 2022/11/08 00:00 [received] 2023/01/29 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/06 06:00 [pubmed] 2023/03/05 18:09 [entrez]
 2022/06/08 00:00 [received] 2022/08/24 00:00 [revised] 2022/12/07 00:00 [accepted] 2022/12/24 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/23 18:20 [entrez]
 2022/07/08 00:00 [received] 2022/09/27 00:00 [accepted] 2022/09/26 00:00 [revised] 2022/10/14 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/10/13 23:35 [entrez]
 2022/10/11 00:00 [received] 2022/11/23 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/21 18:37 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/05/01 06:41 [medline] 2023/03/07 06:00 [pubmed] 2023/03/06 05:43 [entrez]
 2023/05/01 06:42 [medline] 2023/04/29 19:44 [pubmed] 2023/04/29 14:43 [entrez]
 2023/01/05 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/14 13:07 [pubmed] 2023/07/13 18:11 [entrez]
 2022/09/17 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/09/16 17:32 [entrez]
 2021/12/27 00:00 [received] 2022/08/04 00:00 [revised] 2022/11/03 00:00 [accepted] 2022/12/04 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/03 18:26 [entrez]
 2023/07/19 06:42 [medline] 2022/11/18 06:00 [pubmed] 2022/11/17 18:02 [entrez]
 2023/08/10 06:43 [medline] 2023/07/25 06:43 [pubmed] 2023/07/25 05:43 [entrez]
 2022/07/05 00:00 [received] 2022/08/17 00:00 [accepted] 2022/08/16 00:00 [revised] 2022/08/27 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/08/26 11:15 [entrez]
 2023/06/19 13:08 [medline] 2023/05/22 06:41 [pubmed] 2023/05/22 05:54 [entrez]
 2023/08/10 06:43 [medline] 2023/07/25 06:43 [pubmed] 2023/07/25 05:43 [entrez]
 2022/12/29 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/02/25 02:47 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2021/08/15 00:00 [received] 2022/11/28 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/01/26 18:11 [entrez]
 2022/08/19 00:00 [received] 2022/09/24 00:00 [revised] 2022/11/05 00:00 [accepted] 2022/11/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/15 18:26 [entrez]
 2022/11/17 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2023/03/17 06:00 [medline] 2022/11/28 11:23 [entrez]
 2022/12/20 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/17 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/04/27 00:42 [pubmed] 2023/04/26 19:24 [entrez]
 2023/08/10 06:42 [medline] 2023/07/25 13:08 [pubmed] 2023/07/25 08:13 [entrez]
 2023/06/19 13:09 [medline] 2023/05/26 13:10 [pubmed] 2023/05/26 08:03 [entrez]
 2023/02/10 00:00 [received] 2023/04/07 00:00 [accepted] 2023/07/04 06:42 [medline] 2023/05/05 12:42 [pubmed] 2023/05/05 09:13 [entrez]
 2023/04/11 00:00 [revised] 2023/02/14 00:00 [received] 2023/06/08 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/12 13:06 [pubmed] 2023/06/12 09:53 [entrez]
 2023/04/02 00:00 [received] 2023/05/11 00:00 [revised] 2023/05/25 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:11 [entrez]
 2022/12/12 00:00 [received] 2023/02/10 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 19:14 [entrez]
 2023/04/10 00:00 [received] 2023/05/22 00:00 [revised] 2023/06/24 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 18:03 [entrez]
 2022/11/23 00:00 [received] 2023/04/23 00:00 [revised] 2023/05/10 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 18:00 [entrez]
 2023/02/10 00:00 [received] 2023/07/15 00:00 [accepted] 2023/08/02 06:42 [medline] 2023/08/01 01:08 [pubmed] 2023/07/31 23:36 [entrez]
 2022/08/21 00:00 [revised] 2022/03/24 00:00 [received] 2022/09/14 00:00 [accepted] 2022/11/15 06:00 [pubmed] 2022/12/29 06:00 [medline] 2022/11/14 02:03 [entrez]
 2023/05/02 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/18 19:18 [pubmed] 2023/06/18 18:02 [entrez]
 2023/04/07 00:00 [received] 2023/05/23 00:00 [revised] 2023/06/05 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/18 01:07 [pubmed] 2023/06/17 18:07 [entrez]
 2023/01/19 00:00 [received] 2023/04/18 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/16 19:10 [pubmed] 2023/05/16 18:02 [entrez]
 2022/10/18 00:00 [received] 2023/04/12 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/04/27 12:41 [pubmed] 2023/04/27 11:08 [entrez]
 2022/10/12 00:00 [received] 2023/03/14 00:00 [revised] 2023/03/31 00:00 [accepted] 2023/08/11 06:42 [medline] 2023/07/22 10:42 [pubmed] 2023/07/21 21:00 [entrez]
 2022/11/12 00:00 [accepted] 2022/09/19 00:00 [received] 2023/06/05 06:42 [medline] 2022/11/15 06:00 [pubmed] 2022/11/14 15:02 [entrez]
 2023/04/25 06:42 [medline] 2023/04/21 18:42 [pubmed] 2023/04/21 16:42 [entrez]
 2022/10/05 00:00 [received] 2022/10/30 00:00 [accepted] 2022/11/15 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/14 00:03 [entrez]
 2023/02/08 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/16 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2021/08/04 00:00 [received] 2021/10/08 00:00 [accepted] 2021/10/26 06:00 [pubmed] 2023/02/25 06:00 [medline] 2021/10/25 06:54 [entrez]
 2023/08/31 06:42 [medline] 2023/08/09 01:05 [pubmed] 2023/08/08 23:20 [entrez]
 2023/04/30 00:00 [received] 2023/05/16 00:00 [revised] 2023/05/17 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/04 01:08 [pubmed] 2023/06/03 18:03 [entrez]
 2022/12/30 00:00 [received] 2023/01/24 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/02/11 01:23 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2022/11/27 00:00 [received] 2023/03/05 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 18:00 [entrez]
 2023/05/12 07:06 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 02:32 [entrez]
 2023/05/22 06:42 [medline] 2023/03/21 06:00 [pubmed] 2023/03/20 08:22 [entrez]
 2022/10/13 00:00 [received] 2023/01/20 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:23 [entrez]
 2023/03/03 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/16 19:10 [pubmed] 2023/05/16 18:02 [entrez]
 2022/05/19 00:00 [received] 2022/10/11 00:00 [accepted] 2023/02/01 13:43 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2022/12/01 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/30 03:43 [entrez]
 2023/05/04 00:00 [received] 2023/06/06 00:00 [accepted] 2023/07/05 06:42 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:49 [entrez]
 2022/12/18 00:00 [received] 2023/03/28 00:00 [revised] 2023/04/02 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 18:04 [entrez]
 2022/10/02 00:00 [received] 2022/11/12 00:00 [revised] 2022/11/15 00:00 [accepted] 2022/12/01 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/30 18:03 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/03/21 00:00 [received] 2023/05/10 00:00 [revised] 2023/05/21 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/06/03 11:42 [pubmed] 2023/06/02 18:02 [entrez]
 2023/01/08 00:00 [received] 2023/02/13 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 13:47 [entrez]
 2022/12/14 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/03/21 06:00 [pubmed] 2023/03/20 19:05 [entrez]
 2022/10/15 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/10/14 05:03 [entrez]
 2022/08/16 00:00 [received] 2023/03/02 00:00 [accepted] 2024/07/04 00:00 [pmc-release] 2023/07/05 06:42 [medline] 2023/04/19 06:00 [pubmed] 2023/04/18 06:00 [entrez]
 2022/12/23 00:00 [received] 2023/03/17 00:00 [accepted] 2023/03/16 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/27 00:42 [pubmed] 2023/04/26 23:33 [entrez]
 2022/10/30 00:00 [received] 2023/07/07 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 23:18 [entrez]
 2023/05/01 06:42 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 17:52 [entrez]
 2022/12/12 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/12/11 04:42 [entrez]
 2022/09/05 00:00 [received] 2022/10/18 00:00 [accepted] 2022/11/10 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/11/09 21:22 [entrez]
 2023/02/16 00:00 [received] 2023/03/30 00:00 [accepted] 2023/03/29 00:00 [revised] 2023/06/16 06:42 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 11:13 [entrez]
 2023/07/12 06:42 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 17:39 [entrez]
 2023/05/27 00:00 [revised] 2022/12/01 00:00 [received] 2023/06/05 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/09 19:42 [pubmed] 2023/06/09 17:25 [entrez]
 2022/03/06 00:00 [received] 2023/03/15 00:00 [revised] 2023/03/20 00:00 [accepted] 2023/08/25 06:42 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 20:31 [entrez]
 2021/09/15 00:00 [received] 2023/01/12 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/02/11 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/10 19:29 [entrez]
 2022/09/23 00:00 [received] 2023/02/04 00:00 [revised] 2023/03/25 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 18:04 [entrez]
 2022/08/31 00:00 [received] 2022/12/14 00:00 [revised] 2023/02/28 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 18:04 [entrez]
 2023/06/21 00:00 [revised] 2023/01/02 00:00 [received] 2023/07/06 00:00 [accepted] 2023/09/08 06:42 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 20:33 [entrez]
 2022/09/01 00:00 [received] 2022/12/21 00:00 [accepted] 2023/04/17 06:41 [medline] 2023/01/18 06:00 [pubmed] 2023/01/17 11:17 [entrez]
 2022/10/13 00:00 [revised] 2022/08/01 00:00 [received] 2022/10/20 00:00 [accepted] 2022/10/27 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/10/26 09:24 [entrez]
 2022/11/23 00:00 [received] 2023/03/22 00:00 [revised] 2023/03/25 00:00 [accepted] 2024/05/01 00:00 [pmc-release] 2023/06/05 06:42 [medline] 2023/03/31 06:00 [pubmed] 2023/03/30 18:06 [entrez]
 2022/11/16 00:00 [accepted] 2023/01/05 06:00 [pubmed] 2023/01/12 06:00 [medline] 2023/01/04 11:23 [entrez]
 2022/07/27 00:00 [received] 2022/12/13 00:00 [revised] 2022/12/17 00:00 [accepted] 2022/12/23 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/22 18:10 [entrez]
 2023/06/15 06:42 [medline] 2022/06/22 06:00 [pubmed] 2022/06/21 14:53 [entrez]
 2022/07/29 00:00 [received] 2022/09/26 00:00 [accepted] 2022/10/06 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/05 11:27 [entrez]
 2024/07/10 00:00 [pmc-release] 2023/08/15 06:42 [medline] 2023/07/10 13:05 [pubmed] 2023/07/10 11:33 [entrez]
 2023/05/10 00:00 [revised] 2023/02/23 00:00 [received] 2023/05/21 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 12:52 [entrez]
 2023/03/29 06:05 [medline] 2023/03/16 06:00 [pubmed] 2023/03/15 12:19 [entrez]
 2022/04/05 00:00 [received] 2022/09/30 00:00 [accepted] 2022/11/22 21:43 [entrez] 2022/11/23 06:00 [pubmed] 2022/11/25 06:00 [medline]
 2023/03/21 00:00 [received] 2023/04/24 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 18:03 [entrez]
 2023/05/17 06:42 [medline] 2023/04/28 18:43 [pubmed] 2023/04/28 13:53 [entrez]
 2022/11/08 00:00 [received] 2023/01/13 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 21:42 [entrez]
 2022/09/09 00:00 [received] 2022/10/11 00:00 [accepted] 2022/10/20 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/19 11:19 [entrez]
 2023/05/01 06:42 [medline] 2022/11/09 06:00 [pubmed] 2022/11/08 08:02 [entrez]
 2021/06/15 00:00 [received] 2022/01/08 00:00 [revised] 2022/01/27 00:00 [accepted] 2022/04/15 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/04/14 05:17 [entrez]
 2023/06/19 13:08 [medline] 2023/01/25 06:00 [pubmed] 2023/01/24 03:43 [entrez]
 2023/05/25 00:00 [received] 2023/08/25 00:00 [revised] 2023/08/26 00:00 [accepted] 2023/09/12 06:42 [medline] 2023/08/31 00:41 [pubmed] 2023/08/30 19:20 [entrez]
 2022/03/08 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/03/07 12:16 [entrez]
 2022/12/05 00:00 [received] 2023/02/07 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 18:13 [entrez]
 2022/12/07 01:52 [entrez] 2022/12/08 06:00 [pubmed] 2022/12/15 06:00 [medline]
 2023/07/10 06:42 [medline] 2023/06/08 06:42 [pubmed] 2023/06/08 03:45 [entrez]
 2022/04/25 00:00 [received] 2022/05/03 00:00 [accepted] 2023/04/05 06:42 [medline] 2022/11/09 06:00 [pubmed] 2022/11/08 22:03 [entrez]
 2023/05/12 07:06 [medline] 2023/05/11 06:42 [pubmed] 2023/05/11 00:33 [entrez]
 2023/01/23 00:00 [received] 2023/07/06 00:00 [accepted] 2023/07/21 06:43 [medline] 2023/07/20 01:06 [pubmed] 2023/07/19 23:22 [entrez]
 2021/12/21 00:00 [received] 2022/07/20 00:00 [revised] 2022/07/26 00:00 [accepted] 2022/08/29 06:00 [pubmed] 2022/11/11 06:00 [medline] 2022/08/28 18:20 [entrez]
 2023/03/06 00:00 [received] 2023/05/12 00:00 [revised] 2023/05/19 00:00 [accepted] 2023/08/18 06:42 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 19:28 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/05/03 00:00 [revised] 2023/03/28 00:00 [received] 2023/05/04 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/05/22 06:41 [pubmed] 2023/05/22 03:50 [entrez]
 2022/11/18 00:00 [received] 2023/03/21 00:00 [accepted] 2023/08/16 06:42 [medline] 2023/04/20 00:41 [pubmed] 2023/04/19 21:23 [entrez]
 2023/07/05 06:42 [medline] 2023/05/10 12:42 [pubmed] 2023/05/10 09:23 [entrez]
 2020/04/21 00:00 [received] 2020/05/11 00:00 [accepted] 2023/05/15 06:42 [medline] 2022/03/10 06:00 [pubmed] 2022/03/09 05:33 [entrez]
 2023/02/22 00:00 [received] 2023/05/05 00:00 [revised] 2023/05/21 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 18:04 [entrez]
 2022/11/16 00:00 [received] 2023/04/27 00:00 [accepted] 2023/06/30 06:42 [medline] 2023/06/28 19:15 [pubmed] 2023/06/28 16:12 [entrez]
 2022/12/17 00:00 [received] 2023/03/09 00:00 [revised] 2023/06/12 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 19:14 [entrez]
 2022/10/03 00:00 [received] 2023/01/25 00:00 [accepted] 2023/02/02 23:57 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/07 06:00 [medline]
 2022/10/18 00:00 [received] 2023/01/25 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 21:03 [entrez]
 2022/10/28 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/10/27 12:02 [entrez]
 2022/01/05 00:00 [received] 2022/12/05 00:00 [accepted] 2024/02/01 00:00 [pmc-release] 2023/01/27 06:00 [pubmed] 2023/02/04 06:00 [medline] 2023/01/26 20:33 [entrez]
 2022/11/30 00:00 [received] 2022/12/16 00:00 [accepted] 2022/12/15 00:00 [revised] 2022/12/29 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/28 11:15 [entrez]
 2023/03/23 00:00 [received] 2023/05/19 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 19:24 [entrez]
 2023/04/25 10:20 [medline] 2023/04/21 18:42 [pubmed] 2023/04/21 16:42 [entrez]
 2022/08/18 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/08/17 12:32 [entrez]
 2023/05/08 06:41 [medline] 2023/05/05 06:42 [pubmed] 2023/05/05 04:51 [entrez]
 2023/05/12 00:00 [received] 2023/05/12 00:00 [accepted] 2023/08/29 12:44 [medline] 2023/05/26 01:05 [pubmed] 2023/05/25 22:00 [entrez]
 2023/06/30 06:42 [medline] 2023/06/29 01:08 [pubmed] 2023/06/28 20:44 [entrez]
 2022/10/22 00:00 [received] 2023/01/24 00:00 [accepted] 2023/02/05 06:00 [pubmed] 2023/03/11 06:00 [medline] 2023/02/04 19:25 [entrez]
 2023/01/05 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/01 00:41 [pubmed] 2023/04/30 18:08 [entrez]
 2023/04/27 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/18 06:42 [pubmed] 2023/07/18 03:14 [entrez]
 2023/02/04 00:00 [received] 2023/03/27 00:00 [revised] 2023/04/01 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 18:07 [entrez]
 2023/06/02 00:00 [received] 2023/06/21 00:00 [revised] 2023/06/22 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:21 [entrez]
 2023/01/13 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 11:20 [entrez]
 2021/08/07 00:00 [received] 2022/03/20 00:00 [accepted] 2023/06/05 06:42 [medline] 2022/04/10 06:00 [pubmed] 2022/04/09 12:03 [entrez]
 2022/11/07 00:00 [received] 2022/12/20 00:00 [revised] 2022/12/26 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/09 18:10 [entrez]
 2022/07/01 00:00 [received] 2022/09/15 00:00 [accepted] 2022/09/29 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/28 03:02 [entrez]
 2021/06/26 06:00 [pubmed] 2023/02/04 06:00 [medline] 2021/06/25 08:38 [entrez]
 2022/03/19 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/03/18 08:40 [entrez]
 2022/09/14 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/13 17:12 [entrez]
 2022/10/13 00:00 [accepted] 2023/06/12 06:42 [medline] 2022/12/02 06:00 [pubmed] 2022/12/01 11:13 [entrez]
 2023/01/26 06:00 [pubmed] 2023/02/02 06:00 [medline] 2023/01/25 18:02 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/02/10 00:00 [revised] 2022/11/07 00:00 [received] 2023/02/17 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/03/20 06:00 [pubmed] 2023/03/19 16:54 [entrez]
 2023/05/17 00:00 [received] 2023/06/23 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/22 10:41 [pubmed] 2023/07/21 18:06 [entrez]
 2022/04/27 00:00 [received] 2022/10/12 00:00 [revised] 2023/04/10 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/24 00:41 [pubmed] 2023/04/23 18:09 [entrez]
 2022/01/20 00:00 [received] 2022/12/05 00:00 [revised] 2022/12/18 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/30 18:19 [entrez]
 2022/06/26 00:00 [received] 2023/01/08 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 11:15 [entrez]
 2023/08/10 06:42 [medline] 2023/06/15 06:42 [pubmed] 2023/06/15 05:32 [entrez]
 2022/07/12 00:00 [received] 2023/01/24 00:00 [accepted] 2023/03/02 13:43 [entrez] 2023/03/03 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2022/09/04 00:00 [received] 2022/09/28 00:00 [accepted] 2022/10/19 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/10/18 20:52 [entrez]
 2023/05/18 00:00 [received] 2023/06/21 00:00 [revised] 2023/06/30 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:16 [entrez]
 2022/12/13 00:00 [received] 2023/04/03 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/21 01:05 [pubmed] 2023/05/20 18:03 [entrez]
 2023/06/13 00:00 [received] 2023/06/19 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/10 00:41 [pubmed] 2023/07/09 18:06 [entrez]
 2023/02/21 18:22 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/02/15 00:00 [received] 2023/06/30 00:00 [accepted] 2023/06/28 00:00 [revised] 2023/07/21 06:44 [medline] 2023/07/20 01:07 [pubmed] 2023/07/19 23:14 [entrez]
 2023/04/04 00:00 [received] 2023/06/20 00:00 [accepted] 2023/09/13 06:41 [medline] 2023/08/01 13:08 [pubmed] 2023/08/01 11:03 [entrez]
 2023/03/17 00:00 [revised] 2023/01/09 00:00 [received] 2023/04/10 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/29 19:44 [pubmed] 2023/04/29 14:56 [entrez]
 2022/05/12 00:00 [received] 2022/09/12 00:00 [accepted] 2022/11/10 21:57 [entrez] 2022/11/11 06:00 [pubmed] 2022/11/15 06:00 [medline]
 2023/03/22 00:00 [received] 2023/05/26 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/03 00:41 [pubmed] 2023/07/02 18:07 [entrez]
 2023/01/27 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/14 01:07 [pubmed] 2023/05/13 18:05 [entrez]
 2023/03/05 00:00 [accepted] 2023/08/09 06:43 [medline] 2023/04/19 00:41 [pubmed] 2023/04/18 23:31 [entrez]
 2023/07/11 06:42 [medline] 2022/04/20 06:00 [pubmed] 2022/04/19 05:41 [entrez]
 2022/11/30 00:00 [revised] 2022/08/22 00:00 [received] 2023/01/12 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/02/17 06:00 [medline] 2023/01/23 02:02 [entrez]
 2022/04/10 00:00 [received] 2022/06/20 00:00 [revised] 2022/06/22 00:00 [accepted] 2022/09/12 06:00 [pubmed] 2023/03/07 06:00 [medline] 2022/09/11 22:03 [entrez]
 2022/06/15 00:00 [received] 2022/12/30 00:00 [accepted] 2023/04/17 06:41 [medline] 2023/01/19 06:00 [pubmed] 2023/01/18 21:22 [entrez]
 2023/07/03 06:41 [medline] 2023/05/03 18:41 [pubmed] 2023/05/03 13:23 [entrez]
 2023/01/30 00:00 [received] 2023/04/02 00:00 [revised] 2023/04/15 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/12 19:07 [pubmed] 2023/05/12 18:01 [entrez]
 2022/08/02 00:00 [revised] 2022/05/11 00:00 [received] 2022/09/29 00:00 [accepted] 2022/10/11 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/10/10 09:23 [entrez]
 2021/10/14 00:00 [received] 2022/02/22 00:00 [revised] 2022/03/03 00:00 [accepted] 2023/05/17 06:42 [medline] 2022/05/17 06:00 [pubmed] 2022/05/16 02:43 [entrez]
 2023/01/02 07:33 [entrez] 2023/01/03 06:00 [pubmed] 2023/01/04 06:00 [medline]
 2022/10/14 00:00 [received] 2022/12/27 00:00 [revised] 2023/01/08 00:00 [accepted] 2023/02/05 06:00 [pubmed] 2023/03/09 06:00 [medline] 2023/02/04 18:17 [entrez]
 2022/03/31 00:00 [received] 2022/12/04 00:00 [revised] 2022/12/15 00:00 [accepted] 2022/12/23 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/22 18:10 [entrez]
 2022/09/08 00:00 [received] 2022/11/14 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/15 18:29 [entrez]
 2022/08/15 00:00 [received] 2023/01/31 00:00 [revised] 2023/02/02 00:00 [accepted] 2023/02/27 06:00 [pubmed] 2023/03/21 06:00 [medline] 2023/02/26 18:18 [entrez]
 2023/01/22 00:00 [received] 2023/06/04 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/13 18:11 [entrez]
 2022/12/24 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/23 00:22 [entrez]
 2023/05/10 06:42 [medline] 2023/05/08 18:41 [pubmed] 2023/05/08 15:23 [entrez]
 2023/08/11 06:42 [medline] 2023/08/10 12:41 [pubmed] 2023/08/10 07:24 [entrez]
 2022/12/15 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/14 01:32 [entrez]
 2022/10/28 00:00 [revised] 2022/08/26 00:00 [received] 2022/11/02 00:00 [accepted] 2022/12/08 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/12/07 03:13 [entrez]
 2023/05/01 06:42 [medline] 2022/10/15 06:00 [pubmed] 2022/10/14 04:23 [entrez]
 2022/08/17 00:00 [received] 2022/10/10 00:00 [revised] 2022/11/10 00:00 [accepted] 2022/11/19 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/18 18:26 [entrez]
 2023/01/09 00:00 [received] 2023/04/27 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/05/16 06:42 [medline] 2023/05/11 19:13 [pubmed] 2023/05/11 18:00 [entrez]
 2023/04/09 00:00 [revised] 2022/10/28 00:00 [received] 2023/04/19 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/05/23 06:42 [pubmed] 2023/05/23 03:47 [entrez]
 2023/05/12 07:06 [medline] 2023/04/19 06:41 [pubmed] 2023/04/19 02:53 [entrez]
 2023/06/19 13:09 [medline] 2023/04/16 06:00 [pubmed] 2023/04/15 03:32 [entrez]
 2022/10/31 00:00 [received] 2023/01/23 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/31 18:16 [entrez] 2023/04/01 06:00 [pubmed]
 2023/04/29 00:00 [received] 2023/07/29 00:00 [revised] 2023/08/25 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/08/29 00:42 [pubmed] 2023/08/28 19:20 [entrez]
 2023/02/26 00:00 [received] 2023/05/12 00:00 [revised] 2023/06/14 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/01 11:41 [pubmed] 2023/06/30 18:09 [entrez]
 2022/06/19 00:00 [received] 2022/09/26 00:00 [revised] 2022/09/28 00:00 [accepted] 2023/02/12 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/02/11 22:05 [entrez]
 2023/04/04 06:42 [medline] 2023/04/03 06:05 [entrez] 2023/04/04 06:00 [pubmed]
 2022/04/26 00:00 [received] 2022/09/14 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/15 21:44 [entrez]
 2023/08/10 06:43 [medline] 2023/08/09 12:55 [pubmed] 2023/08/09 06:43 [entrez]
 2023/03/07 00:00 [received] 2023/08/22 00:00 [accepted] 2023/09/04 06:44 [medline] 2023/09/01 00:41 [pubmed] 2023/08/31 23:22 [entrez]
 2022/11/29 06:00 [pubmed] 2023/03/14 06:00 [medline] 2022/11/28 04:59 [entrez]
 2022/12/26 00:00 [received] 2023/03/15 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/12 20:43 [entrez] 2023/04/13 06:00 [pubmed]
 2022/08/05 00:00 [received] 2023/03/16 00:00 [accepted] 2023/04/07 06:42 [medline] 2023/04/05 23:19 [entrez] 2023/04/06 06:00 [pubmed]
 2022/08/16 00:00 [received] 2022/09/30 00:00 [accepted] 2022/09/29 00:00 [revised] 2022/10/07 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/10/06 11:13 [entrez]
 2023/03/08 00:00 [received] 2023/04/27 00:00 [revised] 2023/05/09 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/06/19 13:08 [medline] 2023/05/16 19:10 [pubmed] 2023/05/16 18:02 [entrez]
 2022/11/23 00:00 [received] 2022/11/23 00:00 [accepted] 2022/12/01 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/11/30 02:33 [entrez]
 2022/11/07 00:00 [received] 2023/07/07 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/07/28 19:11 [pubmed] 2023/07/28 13:34 [entrez]
 2023/03/01 00:00 [revised] 2022/06/20 00:00 [received] 2023/03/02 00:00 [accepted] 2023/05/12 07:06 [medline] 2023/03/17 06:00 [pubmed] 2023/03/16 05:43 [entrez]
 2024/01/09 00:00 [pmc-release] 2023/04/19 06:41 [medline] 2023/01/10 06:00 [pubmed] 2023/01/09 10:51 [entrez]
 2022/01/27 00:00 [received] 2022/11/11 00:00 [revised] 2022/11/15 00:00 [accepted] 2022/11/23 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/22 18:25 [entrez]
 2023/02/03 00:00 [received] 2023/03/09 00:00 [revised] 2023/05/10 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 19:28 [entrez]
 2022/10/12 00:00 [received] 2022/12/20 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/07 16:06 [entrez]
 2021/08/20 00:00 [received] 2022/11/02 00:00 [revised] 2022/11/07 00:00 [accepted] 2022/11/24 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/23 18:18 [entrez]
 2022/12/15 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/14 07:43 [entrez]
 2022/12/09 00:00 [received] 2023/02/08 00:00 [accepted] 2023/02/07 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/02 06:00 [pubmed] 2023/03/01 23:55 [entrez]
 2022/11/02 00:00 [revised] 2022/07/31 00:00 [received] 2022/11/04 00:00 [accepted] 2022/11/25 06:00 [pubmed] 2023/03/17 06:00 [medline] 2022/11/24 01:43 [entrez]
 2023/06/01 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 14:04 [entrez]
 2024/04/01 00:00 [pmc-release] 2023/04/12 06:42 [medline] 2023/02/08 06:00 [pubmed] 2023/02/07 10:06 [entrez]
 2022/12/15 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/14 01:33 [entrez]
 2022/09/28 00:00 [revised] 2021/10/18 00:00 [received] 2022/10/05 00:00 [accepted] 2022/10/21 06:00 [pubmed] 2022/11/25 06:00 [medline] 2022/10/20 03:07 [entrez]
 2022/04/11 00:00 [received] 2023/02/05 00:00 [accepted] 2023/02/11 00:08 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/03/17 00:00 [received] 2023/07/12 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 04:50 [entrez]
 2022/05/10 00:00 [received] 2022/09/16 00:00 [accepted] 2022/11/21 21:43 [entrez] 2022/11/22 06:00 [pubmed] 2022/11/24 06:00 [medline]
 2023/04/27 00:00 [received] 2023/05/23 00:00 [accepted] 2023/08/23 06:42 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 21:12 [entrez]
 2022/11/23 00:00 [received] 2023/01/04 00:00 [accepted] 2023/02/06 03:43 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2022/11/16 00:00 [received] 2023/05/15 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 01:06 [pubmed] 2023/06/27 21:42 [entrez]
 2023/05/19 00:00 [received] 2023/07/06 00:00 [revised] 2023/07/13 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/26 01:06 [pubmed] 2023/07/25 18:01 [entrez]
 2023/04/17 00:00 [revised] 2023/02/21 00:00 [received] 2023/04/27 00:00 [accepted] 2023/08/15 06:42 [medline] 2023/07/08 19:42 [pubmed] 2023/07/08 06:34 [entrez]
 2023/02/13 00:00 [received] 2023/03/26 00:00 [accepted] 2023/03/24 00:00 [revised] 2023/08/14 06:42 [medline] 2023/05/28 13:09 [pubmed] 2023/05/28 11:05 [entrez]
 2022/08/24 00:00 [received] 2022/12/22 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/04 06:00 [pubmed] 2023/02/03 18:04 [entrez]
 2023/06/19 13:08 [medline] 2023/06/10 15:13 [pubmed] 2023/06/09 18:08 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2022/11/14 00:00 [revised] 2022/09/20 00:00 [received] 2022/11/17 00:00 [accepted] 2022/11/20 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/19 00:14 [entrez]
 2023/01/29 00:00 [received] 2023/05/01 00:00 [revised] 2023/05/02 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 18:08 [entrez]
 2022/11/22 00:00 [received] 2023/01/04 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 18:13 [entrez]
 2023/09/01 06:42 [medline] 2023/08/22 13:42 [pubmed] 2023/08/22 11:34 [entrez]
 2023/02/14 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 18:06 [entrez]
 2023/06/26 06:41 [medline] 2022/12/29 06:00 [pubmed] 2022/12/28 00:23 [entrez]
 2023/01/19 00:00 [received] 2023/03/14 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/03/29 06:00 [pubmed] 2023/03/28 20:52 [entrez]
 2022/11/19 00:00 [received] 2023/02/05 00:00 [accepted] 2023/08/15 06:42 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 22:42 [entrez]
 2022/07/06 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/02/04 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/02/03 19:33 [entrez]
 2022/05/23 00:00 [received] 2023/03/07 00:00 [revised] 2023/04/29 00:00 [accepted] 2023/06/15 06:42 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 18:05 [entrez]
 2022/09/12 00:00 [received] 2023/02/02 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/07 06:00 [pubmed] 2023/04/06 11:24 [entrez]
 2022/06/28 00:00 [received] 2022/11/03 00:00 [revised] 2022/11/23 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/05 18:26 [entrez]
 2022/12/13 00:00 [received] 2023/04/11 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/20 13:41 [pubmed] 2023/04/20 11:23 [entrez]
 2022/11/25 00:00 [revised] 2022/08/30 00:00 [received] 2022/11/28 00:00 [accepted] 2023/07/11 06:42 [medline] 2022/12/11 06:00 [pubmed] 2022/12/10 01:52 [entrez]
 2023/01/18 00:00 [received] 2023/06/06 00:00 [accepted] 2023/06/22 06:42 [medline] 2023/06/20 19:14 [pubmed] 2023/06/20 13:33 [entrez]
 2022/06/28 00:00 [received] 2023/01/27 00:00 [revised] 2023/02/24 00:00 [accepted] 2023/09/05 06:41 [medline] 2023/04/11 06:00 [pubmed] 2023/04/10 19:20 [entrez]
 2023/01/05 00:00 [received] 2023/06/26 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 23:36 [entrez]
 2022/11/09 00:00 [received] 2022/11/14 00:00 [accepted] 2022/11/26 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/25 09:22 [entrez]
 2022/12/12 00:00 [revised] 2022/08/04 00:00 [received] 2023/01/01 00:00 [accepted] 2023/01/12 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/01/11 08:03 [entrez]
 2022/09/27 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/09/26 14:43 [entrez]
 2022/03/04 00:00 [received] 2022/07/20 00:00 [accepted] 2023/03/31 06:42 [medline] 2022/08/31 06:00 [pubmed] 2022/08/30 03:03 [entrez]
 2022/12/15 00:00 [received] 2023/01/20 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/02/01 06:00 [pubmed] 2023/01/31 23:14 [entrez]
 2022/11/14 00:00 [received] 2022/12/29 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/21 01:27 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/07/25 00:00 [received] 2022/09/13 00:00 [accepted] 2022/09/12 00:00 [revised] 2022/09/25 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/24 23:28 [entrez]
 2023/03/09 00:00 [accepted] 2023/05/05 06:42 [medline] 2023/04/14 06:00 [pubmed] 2023/04/13 23:27 [entrez]
 2022/07/08 00:00 [received] 2022/09/06 00:00 [accepted] 2022/09/29 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/28 23:40 [entrez]
 2023/08/11 06:42 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/04/04 00:00 [revised] 2023/02/09 00:00 [received] 2023/05/18 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/05/29 06:41 [pubmed] 2023/05/29 03:45 [entrez]
 2022/12/23 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/12/22 08:03 [entrez]
 2021/06/17 00:00 [received] 2022/04/25 00:00 [revised] 2022/05/07 00:00 [accepted] 2023/05/09 06:42 [medline] 2022/06/07 06:00 [pubmed] 2022/06/06 19:27 [entrez]
 2021/07/10 00:00 [received] 2021/10/24 00:00 [accepted] 2021/11/02 06:00 [pubmed] 2023/02/25 06:00 [medline] 2021/11/01 16:56 [entrez]
 2023/05/01 06:42 [medline] 2023/04/19 06:00 [pubmed] 2023/04/18 07:53 [entrez]
 2023/07/19 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/18 12:42 [pubmed] 2023/08/18 11:07 [entrez]
 2022/12/03 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/02 06:42 [medline] 2023/07/31 06:43 [pubmed] 2023/07/31 05:16 [entrez]
 2022/06/01 00:00 [received] 2023/01/17 00:00 [accepted] 2023/01/26 23:31 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/31 06:00 [medline]
 2022/09/23 00:00 [received] 2023/03/06 00:00 [revised] 2023/05/03 00:00 [accepted] 2023/06/15 06:41 [medline] 2023/05/27 09:42 [pubmed] 2023/05/26 18:09 [entrez]
 2022/12/01 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/30 08:23 [entrez]
 2022/10/25 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/10/24 04:50 [entrez]
 2022/04/15 00:00 [received] 2022/07/31 00:00 [accepted] 2022/08/10 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/08/09 23:28 [entrez]
 2022/09/01 00:00 [received] 2022/11/16 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/29 18:13 [entrez]
 2021/05/05 00:00 [received] 2021/08/03 00:00 [accepted] 2021/08/13 06:00 [pubmed] 2023/02/25 06:00 [medline] 2021/08/12 06:47 [entrez]
 2023/02/02 00:00 [received] 2023/04/16 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/06 19:42 [pubmed] 2023/05/06 18:00 [entrez]
 2023/05/21 00:00 [received] 2023/07/10 00:00 [accepted] 2023/08/17 06:43 [medline] 2023/08/16 06:42 [pubmed] 2023/08/16 03:51 [entrez]
 2023/01/30 00:00 [received] 2023/02/17 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/04/18 06:41 [medline] 2023/04/14 20:58 [entrez] 2023/04/15 06:00 [pubmed]
 2023/06/02 00:00 [revised] 2023/03/26 00:00 [received] 2023/06/07 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 06:35 [entrez]
 2022/11/16 00:00 [received] 2023/01/29 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 18:24 [entrez]
 2023/06/12 06:42 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 18:16 [entrez]
 2022/11/21 00:00 [received] 2023/03/19 00:00 [revised] 2023/03/22 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/03 06:00 [pubmed] 2023/04/02 18:01 [entrez]
 2023/05/17 00:00 [received] 2023/07/10 00:00 [accepted] 2023/08/29 12:42 [medline] 2023/08/28 06:43 [pubmed] 2023/08/28 04:58 [entrez]
 2023/02/09 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:28 [entrez]
 2022/10/07 00:00 [received] 2023/02/12 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/04/18 06:41 [medline] 2023/04/14 20:58 [entrez] 2023/04/15 06:00 [pubmed]
 2023/04/25 10:20 [medline] 2023/03/29 06:00 [pubmed] 2023/03/28 05:12 [entrez]
 2023/08/10 06:43 [medline] 2023/08/09 12:56 [pubmed] 2023/08/09 06:43 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/02/01 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/01/31 20:02 [entrez]
 2022/07/13 00:00 [received] 2022/10/07 00:00 [revised] 2022/11/06 00:00 [accepted] 2023/06/02 06:43 [medline] 2022/12/01 06:00 [pubmed] 2022/11/30 03:23 [entrez]
 2022/01/04 00:00 [received] 2022/11/21 00:00 [revised] 2022/11/25 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/09 18:18 [entrez]
 2023/09/14 06:42 [medline] 2022/09/16 06:00 [pubmed] 2022/09/15 09:03 [entrez]
 2022/10/15 00:00 [revised] 2022/06/23 00:00 [received] 2022/11/05 00:00 [accepted] 2022/12/24 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/23 13:53 [entrez]
 2021/09/10 00:00 [received] 2023/04/12 00:00 [accepted] 2023/05/12 07:06 [medline] 2023/04/21 18:42 [pubmed] 2023/04/21 14:39 [entrez]
 2022/03/24 00:00 [received] 2023/02/06 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 18:04 [entrez]
 2022/08/31 00:00 [received] 2023/01/17 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/03/28 17:14 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 18:09 [entrez]
 2022/09/20 00:00 [received] 2023/02/27 00:00 [accepted] 2023/04/28 06:41 [medline] 2023/04/27 00:42 [pubmed] 2023/04/26 23:44 [entrez]
 2022/08/21 00:00 [received] 2022/10/28 00:00 [revised] 2022/11/29 00:00 [accepted] 2023/05/19 06:42 [medline] 2022/12/18 06:00 [pubmed] 2022/12/17 22:07 [entrez]
 2022/09/27 00:00 [received] 2022/10/17 00:00 [accepted] 2022/10/29 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/10/28 21:43 [entrez]
 2022/10/07 00:00 [received] 2022/12/12 00:00 [revised] 2023/01/07 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/01/31 06:00 [pubmed] 2023/01/30 18:08 [entrez]
 2022/11/15 00:00 [received] 2023/03/17 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/02 06:00 [pubmed] 2023/04/01 18:01 [entrez]
 2023/02/27 00:00 [revised] 2022/12/02 00:00 [received] 2023/06/16 00:00 [accepted] 2023/09/08 06:42 [medline] 2023/06/20 13:10 [pubmed] 2023/06/20 08:13 [entrez]
 2022/03/13 00:00 [received] 2022/11/15 00:00 [accepted] 2022/12/22 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/12/21 21:23 [entrez]
 2021/08/07 06:00 [pubmed] 2023/03/22 06:00 [medline] 2021/08/06 08:40 [entrez]
 2022/10/27 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/10/26 06:06 [entrez]
 2023/05/30 00:00 [revised] 2023/02/07 00:00 [received] 2023/06/08 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/14 06:42 [pubmed] 2023/06/14 03:45 [entrez]
 2022/12/08 00:00 [received] 2023/01/20 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/27 06:00 [pubmed] 2023/02/26 18:23 [entrez]
 2022/06/17 00:00 [received] 2022/12/12 00:00 [accepted] 2023/02/22 14:27 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2022/06/15 00:00 [received] 2022/11/22 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/23 18:11 [entrez]
 2023/01/24 00:00 [received] 2023/02/22 00:00 [accepted] 2023/02/21 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 11:03 [entrez]
 2022/12/27 16:22 [entrez] 2022/12/28 06:00 [pubmed] 2022/12/30 06:00 [medline]
 2023/09/11 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 01:43 [entrez]
 2022/03/14 00:00 [received] 2022/12/29 00:00 [accepted] 2023/02/07 13:43 [entrez] 2023/02/08 06:00 [pubmed] 2023/02/10 06:00 [medline]
 2023/07/10 06:42 [medline] 2022/12/15 06:00 [pubmed] 2022/12/14 01:42 [entrez]
 2023/09/14 06:42 [medline] 2023/06/12 06:43 [pubmed] 2023/06/12 01:03 [entrez]
 2023/05/22 06:42 [medline] 2022/02/01 06:00 [pubmed] 2022/01/31 05:33 [entrez]
 2023/04/03 00:00 [received] 2023/05/23 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/14 13:08 [pubmed] 2023/07/13 18:11 [entrez]
 2022/07/26 00:00 [received] 2023/02/08 00:00 [accepted] 2023/09/05 06:41 [medline] 2023/03/06 06:00 [pubmed] 2023/03/05 18:24 [entrez]
 2023/04/18 10:16 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 15:13 [entrez]
 2022/10/03 00:00 [revised] 2022/08/08 00:00 [received] 2022/12/29 00:00 [accepted] 2023/01/13 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/12 22:13 [entrez]
 2023/01/31 00:00 [received] 2023/03/16 00:00 [revised] 2023/03/25 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:09 [entrez]
 2022/04/13 00:00 [received] 2022/10/31 00:00 [revised] 2022/11/04 00:00 [accepted] 2023/01/28 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/01/27 18:20 [entrez]
 2023/01/30 00:00 [revised] 2022/06/22 00:00 [received] 2023/03/10 00:00 [accepted] 2023/06/23 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 21:41 [entrez]
 2022/06/27 00:00 [received] 2022/12/13 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2022/09/14 00:00 [received] 2022/11/18 00:00 [revised] 2022/12/07 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/19 18:28 [entrez]
 2023/04/18 10:16 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 12:33 [entrez]
 2023/01/23 00:00 [received] 2023/01/30 00:00 [accepted] 2023/02/07 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/06 08:53 [entrez]
 2022/02/22 00:00 [received] 2022/12/03 00:00 [revised] 2022/12/12 00:00 [accepted] 2022/12/19 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/18 18:27 [entrez]
 2023/06/21 06:42 [medline] 2022/05/05 06:00 [pubmed] 2022/05/04 12:03 [entrez]
 2022/12/11 00:00 [received] 2023/06/03 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/10 23:42 [pubmed] 2023/06/10 18:01 [entrez]
 2023/01/30 00:00 [received] 2023/06/03 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 18:02 [entrez]
 2023/01/20 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/29 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/06/05 00:41 [pubmed] 2023/06/04 19:27 [entrez]
 2023/05/18 00:00 [revised] 2023/03/16 00:00 [received] 2023/06/11 00:00 [accepted] 2023/09/13 06:41 [medline] 2023/06/30 06:42 [pubmed] 2023/06/30 03:32 [entrez]
 2022/12/30 00:00 [received] 2023/03/07 00:00 [accepted] 2023/05/05 06:42 [medline] 2023/05/04 06:42 [pubmed] 2023/05/04 02:08 [entrez]
 2022/10/12 00:00 [received] 2022/12/30 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/02/13 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/12 18:10 [entrez]
 2022/06/29 00:00 [received] 2022/09/07 00:00 [accepted] 2022/11/21 21:43 [entrez] 2022/11/22 06:00 [pubmed] 2022/11/24 06:00 [medline]
 2022/09/09 00:00 [received] 2023/01/16 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:23 [entrez]
 2023/02/28 00:00 [received] 2023/05/02 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 04:06 [entrez]
 2022/10/19 00:00 [received] 2023/01/09 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/20 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/19 18:15 [entrez]
 2022/12/01 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/30 03:53 [entrez]
 2023/06/15 06:42 [medline] 2022/06/16 06:00 [pubmed] 2022/06/15 21:12 [entrez]
 2022/07/21 00:00 [received] 2022/11/01 00:00 [accepted] 2022/12/21 21:22 [entrez] 2022/12/22 06:00 [pubmed] 2022/12/24 06:00 [medline]
 2023/01/31 13:43 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/03 06:00 [medline]
 2022/09/13 00:00 [received] 2023/02/20 00:00 [revised] 2023/04/20 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/22 00:41 [pubmed] 2023/05/21 18:05 [entrez]
 2022/08/10 00:00 [received] 2022/10/17 00:00 [accepted] 2022/10/28 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/27 23:59 [entrez]
 2023/01/10 05:53 [entrez] 2023/01/11 06:00 [pubmed] 2023/01/12 06:00 [medline]
 2023/06/08 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/07/03 00:41 [pubmed] 2023/07/02 23:37 [entrez]
 2022/11/16 00:00 [received] 2023/02/04 00:00 [revised] 2023/03/20 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:30 [entrez] 2023/04/14 06:00 [pubmed]
 2022/08/19 00:00 [received] 2023/05/19 00:00 [accepted] 2023/07/04 06:42 [medline] 2023/05/23 13:05 [pubmed] 2023/05/23 12:02 [entrez]
 2022/11/09 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/08 05:12 [entrez]
 2023/09/14 06:42 [medline] 2022/10/13 06:00 [pubmed] 2022/10/12 09:13 [entrez]
 2023/04/03 00:00 [received] 2023/07/25 00:00 [accepted] 2023/08/29 12:44 [medline] 2023/08/28 06:41 [pubmed] 2023/08/28 04:58 [entrez]
 2023/08/21 06:43 [medline] 2022/08/06 06:00 [pubmed] 2022/08/05 10:43 [entrez]
 2023/04/01 00:00 [received] 2023/06/02 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/19 19:08 [pubmed] 2023/07/19 18:00 [entrez]
 2023/06/02 06:42 [medline] 2022/03/26 06:00 [pubmed] 2022/03/25 08:37 [entrez]
 2022/12/25 00:00 [received] 2023/03/10 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:09 [entrez]
 2022/12/07 00:00 [received] 2022/12/28 00:00 [revised] 2022/12/29 00:00 [accepted] 2023/01/08 01:45 [entrez] 2023/01/09 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2024/05/01 00:00 [pmc-release] 2023/05/22 06:42 [medline] 2022/01/26 06:00 [pubmed] 2022/01/25 05:36 [entrez]
 2022/06/17 00:00 [received] 2022/09/20 00:00 [revised] 2023/01/22 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/01/30 06:00 [pubmed] 2023/01/29 18:07 [entrez]
 2022/09/24 00:00 [received] 2023/02/24 00:00 [accepted] 2023/03/02 23:38 [entrez] 2023/03/03 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2022/08/23 00:00 [received] 2022/12/08 00:00 [revised] 2022/12/22 00:00 [accepted] 2022/12/30 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/29 18:17 [entrez]
 2023/06/23 06:42 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:22 [entrez]
 2022/09/15 00:00 [received] 2023/05/11 00:00 [revised] 2023/05/15 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 18:04 [entrez]
 2022/11/01 00:00 [received] 2022/11/18 00:00 [accepted] 2022/11/16 00:00 [revised] 2022/11/30 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/29 11:18 [entrez]
 2021/06/13 00:00 [received] 2021/12/05 00:00 [revised] 2021/12/07 00:00 [accepted] 2022/01/30 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/01/29 05:36 [entrez]
 2022/11/21 00:00 [received] 2023/01/16 00:00 [revised] 2023/03/04 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 19:04 [entrez]
 2022/07/14 00:00 [received] 2022/11/24 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/11 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/10 18:33 [entrez]
 2023/05/04 12:42 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 12:43 [entrez]
 2023/05/09 00:00 [received] 2023/07/31 00:00 [revised] 2023/08/07 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/25 12:42 [pubmed] 2023/08/25 08:54 [entrez]
 2023/05/01 06:42 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 01:06 [entrez]
 2022/11/26 00:00 [received] 2023/04/05 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 23:14 [entrez]
 2022/10/06 00:00 [received] 2023/02/05 00:00 [revised] 2023/03/13 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/03/26 06:00 [pubmed] 2023/03/25 19:09 [entrez]
 2023/06/30 06:42 [medline] 2023/06/29 01:08 [pubmed] 2023/06/28 19:03 [entrez]
 2022/09/29 00:00 [received] 2022/11/08 00:00 [revised] 2022/11/16 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/11/29 18:19 [entrez]
 2022/08/29 00:00 [received] 2022/10/14 00:00 [revised] 2022/10/20 00:00 [accepted] 2023/10/25 00:00 [pmc-release] 2022/10/26 06:00 [pubmed] 2023/03/10 06:00 [medline] 2022/10/25 11:43 [entrez]
 2023/02/18 00:00 [received] 2023/06/25 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/08/11 06:43 [pubmed] 2023/08/11 02:02 [entrez]
 2022/08/01 00:00 [received] 2023/04/02 00:00 [accepted] 2023/04/13 06:42 [medline] 2023/04/11 23:17 [entrez] 2023/04/12 06:00 [pubmed]
 2022/11/09 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/15 21:43 [entrez] 2023/03/16 06:00 [pubmed] 2023/03/21 06:00 [medline]
 2023/08/11 06:43 [medline] 2023/08/10 12:41 [pubmed] 2023/08/10 07:24 [entrez]
 2022/05/06 00:00 [received] 2023/01/11 00:00 [accepted] 2023/01/30 00:01 [entrez] 2023/01/31 06:00 [pubmed] 2023/02/01 06:00 [medline]
 2023/01/13 00:00 [received] 2023/03/18 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/11 00:42 [pubmed] 2023/05/10 18:02 [entrez]
 2022/12/23 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/22 04:32 [entrez]
 2022/11/23 00:00 [received] 2023/04/18 00:00 [revised] 2023/05/06 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 18:02 [entrez]
 2022/10/15 00:00 [received] 2023/05/16 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 23:37 [entrez]
 2022/06/28 00:00 [revised] 2022/04/22 00:00 [received] 2022/07/11 00:00 [accepted] 2022/08/11 06:00 [pubmed] 2023/01/17 06:00 [medline] 2022/08/10 21:02 [entrez]
 2022/10/10 00:00 [accepted] 2022/11/03 06:00 [pubmed] 2023/02/25 06:00 [medline] 2022/11/02 04:03 [entrez]
 2023/04/25 00:00 [received] 2023/05/27 00:00 [revised] 2023/06/08 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:18 [entrez]
 2022/08/26 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/08/25 10:43 [entrez]
 2022/06/27 00:00 [received] 2022/09/12 00:00 [accepted] 2022/10/11 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/10/10 21:04 [entrez]
 2023/02/15 10:53 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/18 06:00 [medline]
 2023/02/16 00:00 [received] 2023/04/10 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 05:25 [entrez]
 2023/02/28 00:00 [received] 2023/04/03 00:00 [accepted] 2023/05/02 06:42 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:21 [entrez]
 2023/06/06 00:00 [received] 2023/06/07 00:00 [accepted] 2023/07/07 06:43 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 23:45 [entrez]
 2022/11/16 00:00 [received] 2023/01/26 00:00 [revised] 2023/01/27 00:00 [accepted] 2023/02/24 19:34 [entrez] 2023/02/25 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/08/29 00:00 [received] 2023/02/21 00:00 [accepted] 2023/04/18 06:41 [medline] 2023/03/01 06:00 [pubmed] 2023/02/28 23:44 [entrez]
 2022/08/13 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/08/12 02:23 [entrez]
 2023/06/12 06:42 [medline] 2023/06/10 15:14 [pubmed] 2023/06/09 20:53 [entrez]
 2023/08/07 06:42 [medline] 2023/05/17 13:10 [pubmed] 2023/05/17 07:32 [entrez]
 2023/05/11 00:00 [received] 2023/08/18 00:00 [accepted] 2023/09/13 06:42 [medline] 2023/09/12 00:42 [pubmed] 2023/09/11 23:22 [entrez]
 2022/07/15 00:00 [received] 2022/11/15 00:00 [revised] 2022/11/17 00:00 [accepted] 2023/05/16 06:42 [medline] 2023/01/01 06:00 [pubmed] 2022/12/31 01:12 [entrez]
 2023/05/11 06:42 [medline] 2023/05/10 00:41 [pubmed] 2023/05/09 19:03 [entrez]
 2022/07/28 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/07/27 07:22 [entrez]
 2023/04/17 06:41 [medline] 2022/09/06 06:00 [pubmed] 2022/09/05 05:54 [entrez]
 2021/06/26 00:00 [received] 2022/02/24 00:00 [revised] 2022/03/17 00:00 [accepted] 2022/05/05 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/05/04 15:24 [entrez]
 2022/06/25 00:00 [received] 2023/04/27 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/27 09:42 [pubmed] 2023/05/26 23:31 [entrez]
 2023/08/10 06:42 [medline] 2023/08/09 12:55 [pubmed] 2023/08/09 06:43 [entrez]
 2022/11/18 00:00 [received] 2023/01/10 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/01/25 06:00 [pubmed] 2023/01/24 21:23 [entrez]
 2023/04/24 00:00 [revised] 2022/04/26 00:00 [received] 2023/04/27 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/05/02 06:41 [pubmed] 2023/05/02 00:23 [entrez]
 2023/03/03 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 23:39 [entrez]
 2022/05/10 00:00 [received] 2022/11/07 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 10:43 [entrez]
 2023/08/16 06:43 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 09:32 [entrez]
 2022/06/09 00:00 [received] 2022/12/03 00:00 [revised] 2022/12/30 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/01/09 18:06 [entrez]
 2023/09/12 06:42 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 00:53 [entrez]
 2022/07/18 00:00 [received] 2022/09/12 00:00 [accepted] 2022/09/29 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/28 21:41 [entrez]
 2022/05/22 00:00 [received] 2022/10/17 00:00 [revised] 2022/11/13 00:00 [accepted] 2022/11/27 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/26 18:19 [entrez]
 2023/09/14 06:42 [medline] 2022/09/16 06:00 [pubmed] 2022/09/15 13:53 [entrez]
 2023/08/10 06:43 [medline] 2023/07/01 11:42 [pubmed] 2023/07/01 02:53 [entrez]
 2022/03/10 00:00 [received] 2022/10/18 00:00 [accepted] 2022/12/01 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/30 21:41 [entrez]
 2023/07/12 06:42 [medline] 2023/06/09 06:41 [pubmed] 2023/06/09 03:55 [entrez]
 2023/01/13 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/12 04:43 [entrez]
 2023/06/07 00:00 [received] 2023/06/22 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:16 [entrez]
 2022/12/23 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/12/22 04:23 [entrez]
 2022/12/23 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/12/22 13:53 [entrez]
 2022/12/01 00:00 [received] 2023/04/05 00:00 [accepted] 2023/08/11 06:42 [medline] 2023/04/14 06:00 [pubmed] 2023/04/13 23:32 [entrez]
 2022/05/29 00:00 [revised] 2022/02/27 00:00 [received] 2022/09/06 00:00 [accepted] 2022/09/14 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/13 11:23 [entrez]
 2023/04/03 00:00 [received] 2023/05/23 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 06:43 [pubmed] 2023/06/28 01:25 [entrez]
 2023/06/27 00:00 [received] 2023/07/21 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/08/12 10:52 [pubmed] 2023/08/12 01:21 [entrez]
 2022/12/09 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/12/08 11:46 [entrez]
 2023/02/24 00:00 [received] 2023/04/20 00:00 [accepted] 2023/05/24 06:42 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 12:20 [entrez]
 2022/12/23 00:00 [received] 2023/05/01 00:00 [accepted] 2023/06/15 06:42 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 21:22 [entrez]
 2021/11/16 00:00 [received] 2022/11/16 00:00 [revised] 2022/11/18 00:00 [accepted] 2022/12/02 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/01 18:25 [entrez]
 2023/07/13 06:42 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 04:05 [entrez]
 2022/10/04 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/10/03 06:10 [entrez]
 2023/04/06 00:00 [received] 2023/05/26 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/08/02 06:42 [medline] 2023/06/26 00:41 [pubmed] 2023/06/25 18:09 [entrez]
 2022/09/13 00:00 [received] 2022/12/28 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/01/21 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/20 18:04 [entrez]
 2023/01/13 00:00 [received] 2023/02/25 00:00 [revised] 2023/03/05 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 19:03 [entrez]
 2022/07/01 00:00 [received] 2022/12/13 00:00 [revised] 2022/12/15 00:00 [accepted] 2023/06/30 06:42 [medline] 2023/01/20 06:00 [pubmed] 2023/01/19 22:02 [entrez]
 2023/02/14 00:00 [received] 2023/04/17 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/05/21 01:05 [pubmed] 2023/05/20 18:04 [entrez]
 2023/05/08 00:00 [received] 2023/07/10 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/09/07 00:41 [pubmed] 2023/09/06 21:23 [entrez]
 2023/01/13 00:00 [revised] 2022/10/24 00:00 [received] 2023/01/14 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/01/29 06:00 [pubmed] 2023/01/28 06:32 [entrez]
 2023/06/06 06:42 [medline] 2022/03/18 06:00 [pubmed] 2022/03/17 17:17 [entrez]
 2023/03/22 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/01 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:31 [entrez]
 2023/05/26 00:00 [revised] 2022/11/09 00:00 [received] 2023/06/05 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/12 13:07 [pubmed] 2023/06/12 09:53 [entrez]
 2023/01/03 00:00 [received] 2023/03/27 00:00 [revised] 2023/05/10 00:00 [accepted] 2023/06/06 06:42 [medline] 2023/05/18 01:07 [pubmed] 2023/05/17 18:09 [entrez]
 2022/09/22 00:00 [received] 2022/11/03 00:00 [revised] 2022/11/03 00:00 [accepted] 2022/11/22 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/11/21 19:03 [entrez]
 2022/05/11 00:00 [received] 2022/10/18 00:00 [accepted] 2022/10/27 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/26 11:16 [entrez]
 2022/07/09 00:00 [revised] 2022/02/19 00:00 [received] 2022/09/23 00:00 [accepted] 2022/09/29 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/28 10:23 [entrez]
 2022/10/31 00:00 [received] 2023/01/12 00:00 [revised] 2023/02/03 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/13 06:00 [pubmed] 2023/02/12 18:16 [entrez]
 2023/01/01 00:00 [received] 2023/04/28 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/06/01 13:09 [pubmed] 2023/06/01 10:40 [entrez]
 2023/04/17 00:00 [revised] 2022/12/08 00:00 [received] 2023/05/03 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/15 06:42 [pubmed] 2023/06/15 04:43 [entrez]
 2022/08/09 00:00 [received] 2023/01/25 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 19:04 [entrez]
 2022/09/09 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/09/08 01:32 [entrez]
 2022/09/14 00:00 [received] 2022/11/08 00:00 [revised] 2022/12/03 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/12 18:23 [entrez]
 2023/05/17 00:00 [received] 2023/05/21 00:00 [accepted] 2023/08/18 06:42 [medline] 2023/08/16 18:42 [pubmed] 2023/08/16 16:04 [entrez]
 2022/12/14 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/31 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/16 06:00 [pubmed] 2023/04/15 18:09 [entrez]
 2022/09/07 00:00 [received] 2023/01/06 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/31 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/01/30 18:08 [entrez]
 2023/02/12 14:06 [entrez] 2023/02/13 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2022/10/26 00:00 [received] 2022/12/10 00:00 [revised] 2022/12/28 00:00 [accepted] 2023/01/12 06:00 [pubmed] 2023/02/08 06:00 [medline] 2023/01/11 18:13 [entrez]
 2022/10/07 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/17 23:52 [entrez]
 2022/05/14 00:00 [received] 2022/10/21 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/09 04:37 [entrez]
 2022/09/28 00:00 [received] 2023/01/21 00:00 [accepted] 2023/01/19 00:00 [revised] 2023/04/24 06:41 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 11:16 [entrez]
 2023/04/02 00:00 [revised] 2023/01/18 00:00 [received] 2023/04/05 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/04/12 06:00 [pubmed] 2023/04/11 22:53 [entrez]
 2023/06/19 13:08 [medline] 2023/05/22 06:42 [pubmed] 2023/05/22 05:53 [entrez]
 2023/06/28 06:42 [medline] 2023/06/27 06:42 [pubmed] 2023/06/27 00:32 [entrez]
 2023/02/16 14:13 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/22 06:00 [medline]
 2023/07/12 06:42 [medline] 2023/05/10 06:42 [pubmed] 2023/05/10 03:48 [entrez]
 2022/08/02 00:00 [received] 2022/11/09 00:00 [accepted] 2022/10/20 00:00 [revised] 2022/11/18 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/17 10:39 [entrez]
 2023/05/10 00:00 [received] 2023/05/26 00:00 [revised] 2023/05/29 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:21 [entrez]
 2023/02/09 00:00 [received] 2023/03/30 00:00 [revised] 2023/04/15 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/21 18:43 [pubmed] 2023/04/21 18:02 [entrez]
 2021/03/09 00:00 [received] 2023/06/30 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/13 19:15 [pubmed] 2023/07/13 13:35 [entrez]
 2023/05/11 00:00 [revised] 2023/03/20 00:00 [received] 2023/06/12 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/06/20 06:42 [pubmed] 2023/06/20 04:23 [entrez]
 2022/09/06 00:00 [received] 2023/02/04 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/04/12 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 21:02 [entrez]
 2022/11/02 00:00 [accepted] 2023/07/27 06:43 [medline] 2022/12/10 06:00 [pubmed] 2022/12/09 05:33 [entrez]
 2022/10/27 00:00 [received] 2023/04/13 00:00 [revised] 2023/05/21 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/27 09:42 [pubmed] 2023/05/26 19:28 [entrez]
 2022/12/29 00:00 [received] 2023/01/31 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 18:14 [entrez]
 2022/10/08 00:00 [revised] 2022/04/12 00:00 [received] 2022/10/12 00:00 [accepted] 2022/10/20 06:00 [pubmed] 2023/02/07 06:00 [medline] 2022/10/19 04:03 [entrez]
 2023/07/03 06:41 [medline] 2023/06/02 13:15 [pubmed] 2023/06/02 06:53 [entrez]
 2021/11/18 00:00 [received] 2022/12/19 00:00 [revised] 2023/01/19 00:00 [accepted] 2023/04/21 06:41 [medline] 2023/01/26 06:00 [pubmed] 2023/01/25 18:19 [entrez]
 2023/02/23 10:38 [entrez] 2023/02/24 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/02/18 00:00 [received] 2022/12/07 00:00 [accepted] 2022/12/17 06:00 [pubmed] 2023/02/22 06:00 [medline] 2022/12/16 03:12 [entrez]
 2023/06/19 13:08 [medline] 2023/05/22 06:42 [pubmed] 2023/05/22 05:54 [entrez]
 2022/08/24 00:00 [revised] 2022/06/02 00:00 [received] 2022/09/10 00:00 [accepted] 2023/06/09 06:42 [medline] 2022/10/09 06:00 [pubmed] 2022/10/08 13:12 [entrez]
 2022/12/26 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/12/25 21:02 [entrez]
 2023/01/18 00:00 [received] 2023/02/13 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/04/14 20:58 [entrez] 2023/04/15 06:00 [pubmed]
 2022/11/21 00:00 [received] 2023/01/13 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/02/11 01:09 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2020/01/04 00:00 [received] 2020/04/15 00:00 [accepted] 2023/04/18 10:16 [medline] 2022/03/10 06:00 [pubmed] 2022/03/09 05:33 [entrez]
 2023/03/22 19:42 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2022/12/22 00:00 [received] 2023/02/23 00:00 [accepted] 2023/03/28 19:06 [medline] 2023/03/27 03:34 [entrez] 2023/03/28 06:00 [pubmed]
 2021/06/14 00:00 [received] 2021/08/29 00:00 [accepted] 2021/09/17 06:00 [pubmed] 2023/02/25 06:00 [medline] 2021/09/16 06:06 [entrez]
 2023/02/27 03:06 [entrez] 2023/02/28 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/07/11 00:00 [received] 2022/11/16 00:00 [revised] 2022/11/20 00:00 [accepted] 2022/12/07 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/06 18:13 [entrez]
 2023/05/29 06:42 [medline] 2023/05/26 13:09 [pubmed] 2023/05/26 06:23 [entrez]
 2022/11/17 00:00 [received] 2023/01/23 00:00 [revised] 2023/01/23 00:00 [accepted] 2023/02/09 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/08 18:05 [entrez]
 2023/02/17 06:00 [pubmed] 2023/03/21 06:00 [medline] 2023/02/16 16:12 [entrez]
 2023/04/14 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/03 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:40 [entrez]
 2023/06/06 00:00 [received] 2023/06/26 00:00 [revised] 2023/06/26 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:14 [entrez]
 2022/10/16 00:00 [received] 2022/11/14 00:00 [revised] 2022/11/16 00:00 [accepted] 2022/11/27 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/26 18:19 [entrez]
 2022/05/19 00:00 [received] 2022/12/04 00:00 [revised] 2022/12/05 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2022/12/28 06:00 [medline] 2022/12/09 19:35 [entrez]
 2022/06/29 00:00 [received] 2022/11/12 00:00 [accepted] 2022/12/02 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/12/01 09:43 [entrez]
 2022/11/02 00:00 [received] 2022/11/29 00:00 [accepted] 2022/12/22 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/21 21:23 [entrez]
 2023/05/31 00:00 [revised] 2023/03/29 00:00 [received] 2023/06/05 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/15 19:14 [pubmed] 2023/06/15 12:27 [entrez]
 2022/06/21 00:00 [received] 2022/08/12 00:00 [accepted] 2023/10/21 00:00 [pmc-release] 2022/10/21 22:09 [entrez] 2022/10/22 06:00 [pubmed] 2022/10/26 06:00 [medline]
 2023/01/23 00:33 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2023/06/26 06:41 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 09:46 [entrez]
 2023/07/10 06:42 [medline] 2023/06/22 13:09 [pubmed] 2023/06/22 06:41 [entrez]
 2022/08/24 00:00 [received] 2022/11/07 00:00 [accepted] 2023/08/04 06:43 [medline] 2022/12/13 06:00 [pubmed] 2022/12/12 12:04 [entrez]
 2022/06/10 00:00 [received] 2023/06/22 00:00 [accepted] 2023/08/24 06:42 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 00:34 [entrez]
 2023/03/29 00:00 [received] 2023/05/23 00:00 [accepted] 2023/09/12 06:42 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:07 [entrez]
 2023/02/07 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/02/06 01:22 [entrez]
 2022/12/14 00:00 [revised] 2022/06/20 00:00 [received] 2023/01/02 00:00 [accepted] 2023/01/31 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/01/30 07:03 [entrez]
 2022/11/25 00:00 [received] 2023/02/28 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/04/03 04:20 [entrez] 2023/04/04 06:00 [pubmed]
 2022/10/10 00:00 [received] 2022/11/11 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/20 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/19 18:15 [entrez]
 2023/01/28 06:00 [pubmed] 2023/02/03 06:00 [medline] 2023/01/27 05:43 [entrez]
 2023/05/18 06:42 [medline] 2023/05/17 01:07 [pubmed] 2023/05/16 21:03 [entrez]
 2023/01/30 00:00 [received] 2023/02/24 00:00 [accepted] 2023/04/17 06:41 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 12:03 [entrez]
 2023/06/14 06:42 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 07:03 [entrez]
 2023/04/12 06:41 [medline] 2023/02/08 06:00 [pubmed] 2023/02/07 10:06 [entrez]
 2022/01/18 00:00 [received] 2022/09/09 00:00 [accepted] 2022/10/04 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/03 21:52 [entrez]
 2022/11/30 00:00 [received] 2023/01/27 00:00 [accepted] 2023/02/01 23:55 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2023/04/13 00:00 [revised] 2023/02/12 00:00 [received] 2023/07/19 06:43 [medline] 2023/05/03 12:42 [pubmed] 2023/05/03 11:35 [entrez]
 2023/02/03 06:00 [pubmed] 2023/02/15 06:00 [medline] 2023/02/02 11:26 [entrez]
 2022/05/27 00:00 [received] 2023/01/27 00:00 [accepted] 2023/04/13 06:42 [medline] 2023/04/11 21:22 [entrez] 2023/04/12 06:00 [pubmed]
 2023/01/14 00:00 [received] 2023/04/06 00:00 [revised] 2023/04/13 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:28 [entrez]
 2022/12/13 00:00 [received] 2023/02/28 00:00 [revised] 2023/03/07 00:00 [accepted] 2023/04/18 06:41 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 19:28 [entrez]
 2022/02/11 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/02/10 17:14 [entrez]
 2022/10/27 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/18 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 18:02 [entrez]
 2023/08/08 06:42 [medline] 2023/07/21 06:44 [pubmed] 2023/07/21 05:26 [entrez]
 2022/05/27 00:00 [received] 2022/12/02 00:00 [revised] 2022/12/02 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/12/19 18:24 [entrez]
 2022/10/21 00:00 [received] 2022/12/12 00:00 [revised] 2022/12/21 00:00 [accepted] 2023/01/21 01:24 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2023/03/26 00:00 [received] 2023/04/15 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:17 [entrez]
 2022/10/20 00:00 [received] 2022/11/01 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/12/07 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/06 18:13 [entrez]
 2024/02/01 00:00 [pmc-release] 2022/09/20 06:00 [pubmed] 2023/02/04 06:00 [medline] 2022/09/19 03:12 [entrez]
 2022/04/12 06:00 [pubmed] 2023/01/28 06:00 [medline] 2022/04/11 08:44 [entrez]
 2022/12/06 00:00 [received] 2022/12/08 00:00 [accepted] 2022/12/30 06:00 [pubmed] 2023/01/18 06:00 [medline] 2022/12/29 18:12 [entrez]
 2022/11/12 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/11/11 15:23 [entrez]
 2023/07/07 06:42 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 09:32 [entrez]
 2020/06/23 00:00 [received] 2020/07/19 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/04/14 21:00 [entrez] 2023/04/15 06:00 [pubmed]
 2022/07/12 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/05/12 07:06 [medline] 2023/01/21 06:00 [pubmed] 2023/01/20 19:23 [entrez]
 2023/02/14 01:26 [entrez] 2023/02/15 06:00 [pubmed] 2023/02/16 06:00 [medline]
 2023/02/13 00:00 [received] 2023/04/13 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/08/03 19:14 [pubmed] 2023/08/03 13:35 [entrez]
 2022/05/07 00:00 [received] 2023/03/16 00:00 [accepted] 2023/03/24 00:40 [entrez] 2023/03/25 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2022/09/28 00:00 [received] 2022/12/01 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/02/07 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/06 18:11 [entrez]
 2022/06/13 00:00 [accepted] 2022/07/09 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/07/08 21:41 [entrez]
 2023/06/07 00:00 [received] 2023/07/18 00:00 [revised] 2023/07/18 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/08/12 10:51 [pubmed] 2023/08/12 01:21 [entrez]
 2023/05/18 06:42 [medline] 2023/05/17 06:42 [pubmed] 2023/05/17 04:33 [entrez]
 2022/11/02 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/01 04:52 [entrez]
 2022/09/27 00:00 [received] 2022/12/14 00:00 [revised] 2022/12/18 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/30 18:19 [entrez]
 2023/03/28 00:00 [received] 2023/03/28 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/06/09 13:42 [pubmed] 2023/06/09 06:04 [entrez]
 2022/07/07 00:00 [revised] 2022/01/27 00:00 [received] 2022/12/12 00:00 [accepted] 2023/04/07 10:18 [medline] 2022/12/21 06:00 [pubmed] 2022/12/20 00:33 [entrez]
 2022/10/06 00:00 [received] 2022/12/09 00:00 [revised] 2022/12/14 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/19 19:27 [entrez]
 2023/01/03 00:00 [received] 2023/06/04 00:00 [revised] 2023/06/22 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 18:05 [entrez]
 2022/11/14 00:00 [received] 2022/11/18 00:00 [accepted] 2022/12/14 21:05 [entrez] 2022/12/15 06:00 [pubmed] 2022/12/17 06:00 [medline]
 2022/09/20 00:00 [received] 2022/12/05 00:00 [revised] 2022/12/17 00:00 [accepted] 2022/12/26 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/25 18:22 [entrez]
 2022/05/30 00:00 [received] 2023/05/23 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/07/27 06:43 [medline] 2023/07/26 01:06 [pubmed] 2023/07/25 20:53 [entrez]
 2023/01/05 00:00 [received] 2023/02/05 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:23 [entrez]
 2023/05/02 00:00 [received] 2023/06/15 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:02 [entrez]
 2022/04/26 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/04/25 05:55 [entrez]
 2022/12/05 00:00 [revised] 2022/06/17 00:00 [received] 2022/12/15 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/02/18 06:00 [medline] 2023/01/05 08:42 [entrez]
 2022/12/30 00:00 [revised] 2022/10/04 00:00 [received] 2023/01/19 00:00 [accepted] 2023/01/26 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/25 00:03 [entrez]
 2023/02/21 00:00 [received] 2023/05/01 00:00 [revised] 2023/06/03 00:00 [accepted] 2023/07/24 06:41 [medline] 2023/06/17 05:11 [pubmed] 2023/06/16 18:05 [entrez]
 2022/12/09 00:00 [received] 2022/12/14 00:00 [accepted] 2023/01/21 01:28 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2023/07/17 00:00 [received] 2023/08/25 00:00 [revised] 2023/08/27 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/09 11:46 [pubmed] 2023/09/09 01:12 [entrez]
 2022/04/05 00:00 [received] 2022/11/30 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2022/10/24 00:00 [received] 2022/12/06 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/12/30 11:14 [entrez]
 2022/11/27 00:00 [revised] 2022/10/12 00:00 [received] 2022/11/29 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/12 10:24 [entrez]
 2023/04/17 00:00 [received] 2023/06/02 00:00 [accepted] 2023/06/22 06:42 [medline] 2023/06/21 01:07 [pubmed] 2023/06/20 23:44 [entrez]
 2023/05/10 00:00 [received] 2023/06/06 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/08/05 05:41 [pubmed] 2023/08/04 21:54 [entrez]
 2023/01/27 00:00 [received] 2023/02/09 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 19:04 [entrez]
 2022/08/18 00:00 [received] 2023/02/09 00:00 [accepted] 2023/02/15 00:22 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/17 06:00 [medline]
 2023/04/19 00:00 [received] 2023/05/05 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/05/17 01:07 [pubmed] 2023/05/16 19:14 [entrez]
 2023/02/24 00:00 [received] 2023/04/13 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/08/29 12:42 [medline] 2023/05/09 00:42 [pubmed] 2023/05/08 21:58 [entrez]
 2022/07/15 00:00 [received] 2022/08/22 00:00 [accepted] 2022/08/21 00:00 [revised] 2022/09/13 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/12 11:48 [entrez]
 2022/12/30 00:00 [received] 2023/06/27 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 23:36 [entrez]
 2023/07/17 06:42 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 03:03 [entrez]
 2023/07/19 06:42 [medline] 2021/08/20 06:00 [pubmed] 2021/08/19 17:21 [entrez]
 2022/11/29 00:00 [received] 2023/07/02 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/07/21 01:11 [pubmed] 2023/07/20 18:08 [entrez]
 2023/06/27 00:00 [received] 2023/06/29 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/12 19:07 [pubmed] 2023/07/12 18:00 [entrez]
 2022/10/14 00:00 [received] 2022/10/18 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/11/11 06:00 [pubmed] 2022/12/30 06:00 [medline] 2022/11/10 23:44 [entrez]
 2022/09/09 00:00 [received] 2022/10/27 00:00 [revised] 2022/11/15 00:00 [accepted] 2022/11/25 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/24 18:21 [entrez]
 2022/05/30 00:00 [received] 2023/01/09 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/02 06:00 [pubmed] 2023/03/01 18:06 [entrez]
 2022/12/29 00:00 [received] 2023/02/13 00:00 [accepted] 2023/03/24 02:19 [entrez] 2023/03/25 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2022/07/21 00:00 [received] 2022/09/28 00:00 [revised] 2022/11/11 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/11/19 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/18 18:26 [entrez]
 2023/08/10 06:43 [medline] 2023/07/22 11:41 [pubmed] 2023/07/22 05:32 [entrez]
 2022/09/21 00:00 [received] 2023/02/27 00:00 [revised] 2023/03/11 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/26 06:00 [pubmed] 2023/03/25 19:01 [entrez]
 2022/07/28 00:00 [received] 2022/12/14 00:00 [accepted] 2023/01/10 23:36 [entrez] 2023/01/11 06:00 [pubmed] 2023/01/13 06:00 [medline]
 2022/12/21 00:00 [received] 2023/03/25 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/07/19 06:42 [medline] 2023/04/02 06:00 [pubmed] 2023/04/01 04:32 [entrez]
 2022/06/06 00:00 [received] 2022/11/24 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/03/11 06:00 [pubmed] 2023/03/10 11:23 [entrez]
 2022/07/22 00:00 [received] 2022/11/30 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/01/04 06:00 [pubmed] 2023/01/03 11:20 [entrez]
 2022/11/25 00:00 [received] 2023/04/05 00:00 [revised] 2023/05/15 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/23 01:06 [pubmed] 2023/05/22 18:08 [entrez]
 2022/11/23 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/13 06:00 [pubmed] 2023/02/12 19:27 [entrez]
 2023/04/05 06:42 [medline] 2023/04/03 20:53 [entrez] 2023/04/04 06:00 [pubmed]
 2023/02/01 16:03 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2023/04/05 00:00 [received] 2023/06/30 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 21:37 [entrez]
 2023/05/22 00:00 [received] 2023/06/19 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 18:06 [entrez]
 2023/07/12 06:42 [medline] 2023/07/11 06:42 [pubmed] 2023/07/11 04:23 [entrez]
 2022/10/01 06:00 [pubmed] 2022/12/22 06:00 [medline] 2022/09/30 02:51 [entrez]
 2022/10/25 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/10/24 04:53 [entrez]
 2022/11/04 00:00 [received] 2023/03/15 00:00 [accepted] 2023/03/28 19:06 [medline] 2023/03/25 00:32 [entrez] 2023/03/26 06:00 [pubmed]
 2022/03/07 00:00 [accepted] 2022/03/25 06:00 [pubmed] 2023/01/31 06:00 [medline] 2022/03/24 17:27 [entrez]
 2023/05/12 07:06 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 01:56 [entrez]
 2022/10/12 00:00 [received] 2023/07/25 00:00 [accepted] 2023/08/04 06:43 [medline] 2023/08/03 01:06 [pubmed] 2023/08/02 23:37 [entrez]
 2022/04/27 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/04/26 05:54 [entrez]
 2023/07/12 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/06 05:53 [entrez]
 2023/06/03 00:00 [revised] 2023/04/25 00:00 [received] 2023/07/14 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 05:52 [entrez]
 2023/02/02 06:00 [pubmed] 2023/02/17 06:00 [medline] 2023/02/01 13:22 [entrez]
 2022/11/09 00:00 [received] 2023/01/09 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 18:39 [entrez]
 2021/07/15 00:00 [received] 2022/11/15 00:00 [revised] 2022/12/07 00:00 [accepted] 2022/12/24 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/23 18:20 [entrez]
 2023/06/19 13:08 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 00:53 [entrez]
 2022/09/30 00:00 [received] 2023/01/26 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/02/22 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/21 18:17 [entrez]
 2023/02/18 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/02/17 09:53 [entrez]
 2023/01/23 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:06 [entrez]
 2022/09/06 00:00 [received] 2023/04/28 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 23:19 [entrez]
 2023/05/22 00:00 [received] 2023/07/20 00:00 [revised] 2023/08/02 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:43 [pubmed] 2023/08/26 01:14 [entrez]
 2023/03/29 00:00 [revised] 2022/12/05 00:00 [received] 2023/04/03 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/04/12 06:00 [pubmed] 2023/04/11 06:34 [entrez]
 2023/05/31 00:00 [received] 2023/06/18 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 19:12 [entrez]
 2022/09/30 00:00 [revised] 2022/03/16 00:00 [received] 2022/10/26 00:00 [accepted] 2022/11/16 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/11/15 06:03 [entrez]
 2023/06/05 06:42 [medline] 2022/05/25 06:00 [pubmed] 2022/05/24 16:13 [entrez]
 2022/12/15 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/14 08:42 [entrez]
 2021/12/30 00:00 [received] 2022/09/07 00:00 [revised] 2022/10/13 00:00 [accepted] 2023/01/28 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/27 18:53 [entrez]
 2023/06/06 06:42 [medline] 2021/04/17 06:00 [pubmed] 2021/04/16 12:10 [entrez]
 2023/02/21 00:00 [received] 2023/07/19 00:00 [accepted] 2023/08/09 06:43 [medline] 2023/08/07 19:10 [pubmed] 2023/08/07 13:34 [entrez]
 2022/12/12 00:00 [revised] 2022/10/20 00:00 [received] 2022/12/28 00:00 [accepted] 2023/02/07 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/06 21:43 [entrez]
 2022/05/25 00:00 [received] 2022/10/19 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 18:35 [entrez]
 2023/02/04 00:00 [received] 2023/03/01 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 12:21 [entrez]
 2023/03/15 00:00 [accepted] 2023/05/05 06:42 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 23:17 [entrez]
 2023/05/01 06:42 [medline] 2023/04/28 18:42 [pubmed] 2023/04/28 12:43 [entrez]
 2022/05/06 00:00 [received] 2022/12/23 00:00 [accepted] 2023/03/28 17:13 [medline] 2023/02/07 06:00 [pubmed] 2023/02/06 23:15 [entrez]
 2023/05/03 06:42 [medline] 2022/05/17 06:00 [pubmed] 2022/05/16 03:27 [entrez]
 2021/11/23 00:00 [received] 2021/12/17 00:00 [accepted] 2022/01/31 06:00 [pubmed] 2023/02/04 06:00 [medline] 2022/01/30 20:37 [entrez]
 2023/01/03 21:02 [entrez] 2023/01/04 06:00 [pubmed] 2023/01/06 06:00 [medline]
 2022/09/30 00:00 [received] 2023/02/03 00:00 [revised] 2023/02/13 00:00 [accepted] 2023/02/23 06:00 [pubmed] 2023/03/11 06:00 [medline] 2023/02/22 08:44 [entrez]
 2022/09/27 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/09/26 14:50 [entrez]
 2022/10/07 00:00 [received] 2023/02/07 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 11:18 [entrez]
 2022/10/21 00:00 [received] 2023/02/18 00:00 [accepted] 2023/02/17 00:00 [revised] 2023/06/16 06:42 [medline] 2023/04/07 06:00 [pubmed] 2023/04/06 11:18 [entrez]
 2022/12/22 01:33 [entrez] 2022/12/23 06:00 [pubmed] 2022/12/24 06:00 [medline]
 2022/03/28 00:00 [received] 2023/02/10 00:00 [revised] 2023/03/14 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 19:06 [entrez]
 2022/01/27 00:00 [received] 2022/11/04 00:00 [accepted] 2023/05/26 06:42 [medline] 2022/11/22 06:00 [pubmed] 2022/11/21 23:36 [entrez]
 2022/10/03 00:00 [revised] 2022/08/10 00:00 [received] 2022/10/10 00:00 [accepted] 2022/10/18 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/10/17 09:32 [entrez]
 2022/05/24 00:00 [received] 2022/07/31 00:00 [revised] 2022/08/16 00:00 [accepted] 2023/03/03 02:25 [entrez] 2023/03/04 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2022/12/07 00:00 [received] 2023/03/17 00:00 [revised] 2023/03/30 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/04/07 06:00 [pubmed] 2023/04/06 19:23 [entrez]
 2022/09/29 00:00 [received] 2022/12/29 00:00 [revised] 2023/02/19 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/26 06:00 [pubmed] 2023/02/25 18:46 [entrez]
 2023/08/15 06:42 [medline] 2023/06/12 13:07 [pubmed] 2023/06/12 11:33 [entrez]
 2023/03/18 00:00 [received] 2023/04/07 00:00 [revised] 2023/04/13 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:29 [entrez]
 2023/03/27 00:00 [received] 2023/06/06 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 03:59 [entrez]
 2022/06/28 00:00 [received] 2022/08/17 00:00 [accepted] 2022/08/27 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/08/26 21:13 [entrez]
 2022/07/29 00:00 [received] 2023/01/09 00:00 [accepted] 2023/07/19 06:43 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 09:05 [entrez]
 2022/06/26 00:00 [received] 2022/09/19 00:00 [accepted] 2023/04/17 06:41 [medline] 2022/09/29 06:00 [pubmed] 2022/09/28 00:12 [entrez]
 2022/11/29 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/11/28 18:14 [entrez]
 2022/12/12 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/02/11 01:18 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2022/10/17 00:00 [received] 2023/04/17 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 00:42 [pubmed] 2023/04/27 23:40 [entrez]
 2022/08/02 00:00 [received] 2022/11/01 00:00 [accepted] 2022/10/31 00:00 [revised] 2022/11/11 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/10 23:52 [entrez]
 2023/03/12 00:00 [revised] 2023/01/07 00:00 [received] 2023/04/10 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/02 06:41 [pubmed] 2023/05/02 01:23 [entrez]
 2022/08/05 00:00 [received] 2023/01/20 00:00 [revised] 2023/01/22 00:00 [accepted] 2023/01/29 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/28 18:08 [entrez]
 2022/11/08 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/01 00:15 [entrez] 2023/03/02 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/02/18 00:00 [received] 2023/06/27 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/10 19:08 [pubmed] 2023/07/10 18:03 [entrez]
 2022/01/26 00:00 [received] 2022/10/03 00:00 [revised] 2022/10/21 00:00 [accepted] 2023/06/02 06:42 [medline] 2022/11/09 06:00 [pubmed] 2022/11/08 08:03 [entrez]
 2023/02/22 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/02/21 16:01 [entrez]
 2022/10/11 00:00 [received] 2023/03/05 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/04/03 06:00 [pubmed] 2023/04/02 18:53 [entrez]
 2022/09/11 00:00 [received] 2022/12/13 00:00 [accepted] 2022/12/26 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/25 23:20 [entrez]
 2023/03/10 00:00 [revised] 2023/01/11 00:00 [received] 2023/03/24 00:00 [accepted] 2023/09/05 06:41 [medline] 2023/04/06 06:00 [pubmed] 2023/04/05 09:22 [entrez]
 2022/04/23 00:00 [received] 2022/07/02 00:00 [revised] 2022/08/01 00:00 [accepted] 2023/05/22 06:42 [medline] 2022/09/27 06:00 [pubmed] 2022/09/26 14:54 [entrez]
 2022/12/03 00:00 [received] 2023/04/03 00:00 [accepted] 2023/05/02 06:42 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:21 [entrez]
 2023/03/18 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/19 06:42 [medline] 2023/06/29 01:08 [pubmed] 2023/06/28 18:23 [entrez]
 2023/06/19 13:08 [medline] 2023/03/01 06:00 [pubmed] 2023/02/28 02:04 [entrez]
 2022/08/26 00:00 [received] 2023/05/13 00:00 [revised] 2023/06/27 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 21:55 [entrez]
 2023/01/27 00:00 [received] 2023/02/27 00:00 [revised] 2023/03/01 00:00 [accepted] 2023/04/18 10:16 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 19:08 [entrez]
 2023/05/12 07:06 [medline] 2022/02/19 06:00 [pubmed] 2022/02/18 17:08 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/03/29 06:05 [medline] 2022/11/23 06:00 [pubmed] 2022/11/22 10:07 [entrez]
 2022/11/02 00:00 [received] 2023/03/14 00:00 [accepted] 2023/04/03 06:42 [medline] 2023/03/30 23:21 [entrez] 2023/03/31 06:00 [pubmed]
 2023/08/11 06:43 [medline] 2023/07/25 13:08 [pubmed] 2023/07/25 08:12 [entrez]
 2022/03/27 00:00 [received] 2022/09/12 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/03/29 06:05 [medline] 2022/10/14 06:00 [pubmed] 2022/10/13 23:28 [entrez]
 2022/08/08 00:00 [received] 2022/10/07 00:00 [revised] 2022/12/22 00:00 [accepted] 2024/04/05 00:00 [pmc-release] 2023/04/10 06:42 [medline] 2023/01/21 06:00 [pubmed] 2023/01/20 18:41 [entrez]
 2022/12/19 00:00 [received] 2023/01/18 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/26 18:08 [entrez]
 2022/12/27 00:00 [received] 2023/01/24 00:00 [revised] 2023/01/29 00:00 [accepted] 2023/02/11 01:09 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/01/24 00:00 [revised] 2022/02/17 00:00 [received] 2023/02/22 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 01:00 [entrez]
 2023/01/23 00:00 [received] 2023/03/30 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/12 19:06 [pubmed] 2023/05/12 18:01 [entrez]
 2023/06/16 06:42 [medline] 2023/06/14 19:10 [pubmed] 2023/06/14 15:59 [entrez]
 2022/12/18 00:00 [received] 2023/02/08 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/06 06:00 [pubmed] 2023/03/05 18:09 [entrez]
 2023/05/12 00:00 [revised] 2023/01/30 00:00 [received] 2023/05/12 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/15 06:42 [pubmed] 2023/05/15 03:44 [entrez]
 2022/04/28 00:00 [received] 2022/12/16 00:00 [accepted] 2023/06/08 06:42 [medline] 2023/01/12 06:00 [pubmed] 2023/01/11 09:33 [entrez]
 2022/11/28 00:00 [revised] 2022/10/21 00:00 [received] 2022/12/22 00:00 [accepted] 2022/12/27 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/12/26 06:33 [entrez]
 2023/06/26 06:42 [medline] 2023/06/23 19:11 [pubmed] 2023/06/23 12:33 [entrez]
 2023/03/03 00:00 [received] 2023/05/22 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/06/02 01:07 [pubmed] 2023/06/01 23:43 [entrez]
 2023/08/28 06:42 [medline] 2023/08/25 00:42 [pubmed] 2023/08/24 20:57 [entrez]
 2023/02/11 00:00 [received] 2023/05/19 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/06/17 05:11 [pubmed] 2023/06/16 18:05 [entrez]
 2022/12/14 00:00 [received] 2023/06/20 00:00 [accepted] 2023/08/31 06:41 [medline] 2023/08/30 00:41 [pubmed] 2023/08/29 23:44 [entrez]
 2021/12/13 00:00 [revised] 2021/10/18 00:00 [received] 2022/01/22 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/30 00:22 [entrez]
 2022/10/09 00:00 [received] 2022/12/03 00:00 [accepted] 2022/12/02 00:00 [revised] 2022/12/24 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/23 11:15 [entrez]
 2022/11/18 00:00 [received] 2023/03/11 00:00 [accepted] 2023/03/29 06:05 [medline] 2023/03/27 23:37 [entrez] 2023/03/28 06:00 [pubmed]
 2023/08/18 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 19:03 [entrez]
 2023/04/18 06:42 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 14:54 [entrez]
 2023/05/01 06:42 [medline] 2023/04/20 13:41 [pubmed] 2023/04/20 08:23 [entrez]
 2023/07/20 00:00 [received] 2023/08/09 00:00 [revised] 2023/08/13 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:43 [pubmed] 2023/08/26 01:16 [entrez]
 2023/06/29 06:43 [medline] 2021/01/28 06:00 [pubmed] 2021/01/27 20:06 [entrez]
 2023/07/03 06:41 [medline] 2023/06/07 01:07 [pubmed] 2023/06/06 23:21 [entrez]
 2022/08/31 00:00 [received] 2023/02/24 00:00 [accepted] 2023/03/02 23:19 [entrez] 2023/03/03 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2022/04/28 00:00 [received] 2022/11/17 00:00 [accepted] 2022/12/24 06:00 [pubmed] 2023/03/23 06:00 [medline] 2022/12/23 21:44 [entrez]
 2023/02/13 00:00 [revised] 2022/10/17 00:00 [received] 2023/02/16 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 13:55 [entrez]
 2022/11/18 00:00 [received] 2023/01/08 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/02 06:00 [pubmed] 2023/03/01 18:06 [entrez]
 2023/08/28 06:42 [medline] 2023/08/26 05:41 [pubmed] 2023/08/25 22:13 [entrez]
 2022/08/29 00:00 [received] 2022/12/09 00:00 [accepted] 2023/02/22 11:19 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/05/18 06:42 [medline] 2023/05/16 13:10 [pubmed] 2023/05/16 10:10 [entrez]
 2022/12/27 00:00 [received] 2023/05/24 00:00 [revised] 2023/06/27 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 19:31 [entrez]
 2023/06/21 06:42 [medline] 2023/06/19 13:08 [pubmed] 2023/06/19 12:03 [entrez]
 2022/12/23 00:00 [received] 2023/04/23 00:00 [revised] 2023/05/04 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/14 01:07 [pubmed] 2023/05/13 18:05 [entrez]
 2023/04/28 00:00 [revised] 2023/01/31 00:00 [received] 2023/05/15 00:00 [accepted] 2023/07/21 06:44 [medline] 2023/05/20 09:43 [pubmed] 2023/05/20 03:41 [entrez]
 2023/01/18 00:00 [received] 2023/04/03 00:00 [revised] 2023/05/06 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/18 01:07 [pubmed] 2023/05/17 18:01 [entrez]
 2022/09/20 00:00 [received] 2022/11/05 00:00 [revised] 2022/12/14 00:00 [accepted] 2023/01/02 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/01 18:08 [entrez]
 2020/08/03 00:00 [received] 2022/09/28 00:00 [accepted] 2023/07/10 06:42 [medline] 2022/10/27 06:00 [pubmed] 2022/10/26 23:13 [entrez]
 2022/11/28 00:00 [received] 2023/02/13 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 21:12 [entrez]
 2023/03/14 19:52 [entrez] 2023/03/15 06:00 [pubmed] 2023/03/17 06:00 [medline]
 2022/12/02 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/01 06:53 [entrez]
 2023/05/11 00:00 [revised] 2022/11/08 00:00 [received] 2023/05/16 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/05/25 06:42 [pubmed] 2023/05/25 01:13 [entrez]
 2022/05/24 00:00 [received] 2023/01/04 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/04 06:00 [pubmed] 2023/02/03 18:04 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/03/02 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/08 18:42 [pubmed] 2023/05/08 18:00 [entrez]
 2022/12/15 00:00 [received] 2023/03/13 00:00 [revised] 2023/05/10 00:00 [accepted] 2024/06/15 00:00 [pmc-release] 2023/05/29 06:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 18:02 [entrez]
 2022/10/07 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/10/06 17:52 [entrez]
 2023/03/21 00:00 [received] 2023/05/13 00:00 [revised] 2023/05/20 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 18:02 [entrez]
 2023/03/01 00:00 [received] 2023/05/11 00:00 [accepted] 2023/05/01 00:00 [revised] 2023/09/04 06:43 [medline] 2023/07/25 19:15 [pubmed] 2023/07/25 12:22 [entrez]
 2023/07/11 00:00 [received] 2023/08/14 00:00 [revised] 2023/08/31 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/09 11:47 [pubmed] 2023/09/09 01:24 [entrez]
 2023/08/25 06:42 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 23:28 [entrez]
 2022/10/31 00:00 [accepted] 2023/09/13 06:41 [medline] 2022/11/19 06:00 [pubmed] 2022/11/18 11:17 [entrez]
 2022/06/10 00:00 [received] 2022/11/22 00:00 [accepted] 2023/01/26 20:52 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/31 06:00 [medline]
 2023/07/06 06:42 [medline] 2023/07/05 06:42 [pubmed] 2023/07/05 00:22 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/06/20 06:42 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 05:28 [entrez]
 2022/09/02 00:00 [received] 2022/11/16 00:00 [accepted] 2023/05/17 06:42 [medline] 2022/12/01 06:00 [pubmed] 2022/11/30 21:13 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/08/10 06:43 [medline] 2023/05/26 06:42 [pubmed] 2023/05/26 05:53 [entrez]
 2023/03/04 00:00 [received] 2023/03/27 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 23:13 [entrez]
 2022/05/31 00:00 [received] 2022/09/27 00:00 [accepted] 2022/09/26 00:00 [revised] 2022/10/08 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/10/07 11:08 [entrez]
 2023/07/12 06:42 [medline] 2023/06/09 13:42 [pubmed] 2023/06/09 06:03 [entrez]
 2022/12/02 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/01 04:12 [entrez]
 2022/12/30 00:00 [received] 2023/04/19 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/15 00:42 [pubmed] 2023/05/14 18:09 [entrez]
 2023/08/18 06:42 [medline] 2023/08/17 06:43 [pubmed] 2023/08/17 03:46 [entrez]
 2023/03/11 00:00 [received] 2023/03/25 00:00 [revised] 2023/05/02 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/12 19:06 [pubmed] 2023/05/12 18:01 [entrez]
 2023/05/17 06:42 [medline] 2022/05/17 06:00 [pubmed] 2022/05/16 03:19 [entrez]
 2022/09/23 00:00 [received] 2023/06/15 00:00 [accepted] 2023/06/27 06:42 [medline] 2023/06/26 00:41 [pubmed] 2023/06/25 23:14 [entrez]
 2022/10/20 00:00 [received] 2022/12/04 00:00 [revised] 2023/01/01 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2021/12/09 00:00 [received] 2022/12/27 00:00 [accepted] 2022/12/23 00:00 [revised] 2023/02/02 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/02/01 11:14 [entrez]
 2023/09/11 06:43 [medline] 2023/08/27 18:41 [pubmed] 2023/08/27 18:00 [entrez]
 2022/11/09 00:00 [received] 2023/03/29 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 21:22 [entrez]
 2023/02/03 00:00 [revised] 2022/11/16 00:00 [received] 2023/02/06 00:00 [accepted] 2023/04/06 06:41 [medline] 2023/02/12 06:00 [pubmed] 2023/02/11 09:03 [entrez]
 2023/06/19 13:09 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 00:24 [entrez]
 2022/09/19 00:00 [received] 2022/10/31 00:00 [accepted] 2022/10/29 00:00 [revised] 2022/11/15 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/14 00:03 [entrez]
 2022/11/13 00:00 [received] 2022/12/17 00:00 [revised] 2022/12/24 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/12/30 18:12 [entrez]
 2022/10/15 00:00 [received] 2022/12/06 00:00 [accepted] 2022/12/17 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/12/16 23:38 [entrez]
 2022/06/02 00:00 [revised] 2022/01/26 00:00 [received] 2022/09/24 00:00 [accepted] 2022/10/19 06:00 [pubmed] 2022/12/27 06:00 [medline] 2022/10/18 08:43 [entrez]
 2023/01/16 18:53 [entrez] 2023/01/17 06:00 [pubmed] 2023/01/19 06:00 [medline]
 2022/12/18 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/17 07:42 [entrez]
 2022/03/22 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/03/21 05:29 [entrez]
 2023/10/19 00:00 [pmc-release] 2023/04/21 06:41 [medline] 2023/04/19 18:42 [pubmed] 2023/04/19 13:43 [entrez]
 2023/04/20 00:00 [received] 2023/04/21 00:00 [accepted] 2023/07/19 06:42 [medline] 2023/05/10 00:41 [pubmed] 2023/05/09 22:48 [entrez]
 2021/09/12 00:00 [received] 2023/03/20 00:00 [revised] 2023/04/15 00:00 [accepted] 2023/06/19 16:16 [medline] 2023/06/18 13:11 [pubmed] 2023/06/18 10:58 [entrez]
 2022/06/20 00:00 [received] 2022/11/17 00:00 [accepted] 2022/11/15 00:00 [revised] 2022/12/06 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/05 11:14 [entrez]
 2022/08/03 00:00 [received] 2022/11/06 00:00 [accepted] 2022/12/24 06:00 [pubmed] 2023/03/17 06:00 [medline] 2022/12/23 21:23 [entrez]
 2024/02/27 00:00 [pmc-release] 2023/04/12 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 11:56 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2022/12/08 00:00 [received] 2023/05/16 00:00 [revised] 2023/06/26 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/21 01:11 [pubmed] 2023/07/20 18:05 [entrez]
 2023/01/30 00:00 [received] 2023/03/19 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:30 [entrez] 2023/04/14 06:00 [pubmed]
 2023/07/12 06:42 [medline] 2023/03/26 06:00 [pubmed] 2023/03/25 06:32 [entrez]
 2022/10/30 00:00 [received] 2023/02/13 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 19:08 [entrez]
 2022/10/18 00:00 [received] 2023/02/07 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 20:53 [entrez]
 2023/06/08 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/11 01:08 [pubmed] 2023/07/10 23:29 [entrez]
 2023/06/20 00:00 [received] 2023/07/19 00:00 [revised] 2023/07/20 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/07/27 01:09 [pubmed] 2023/07/26 18:05 [entrez]
 2023/02/03 00:00 [received] 2023/03/06 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/05/08 06:41 [medline] 2023/03/31 06:00 [pubmed] 2023/03/30 18:05 [entrez]
 2022/11/24 00:00 [revised] 2022/08/31 00:00 [received] 2022/12/22 00:00 [accepted] 2023/01/25 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/24 11:43 [entrez]
 2023/02/21 18:14 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/06/13 00:00 [accepted] 2023/09/07 06:42 [medline] 2023/07/18 01:09 [pubmed] 2023/07/17 23:30 [entrez]
 2022/12/26 00:00 [received] 2023/07/11 00:00 [revised] 2023/08/03 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 18:02 [entrez]
 2023/03/06 00:00 [revised] 2022/10/21 00:00 [received] 2023/03/09 00:00 [accepted] 2023/06/06 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 09:57 [entrez]
 2023/01/09 00:00 [received] 2023/01/11 00:00 [accepted] 2023/02/16 02:20 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/18 06:00 [medline]
 2021/11/04 00:00 [revised] 2021/08/18 00:00 [received] 2021/12/02 00:00 [accepted] 2022/01/12 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/01/11 07:15 [entrez]
 2022/11/24 06:00 [pubmed] 2023/02/22 06:00 [medline] 2022/11/23 05:53 [entrez]
 2023/05/05 06:42 [medline] 2023/04/20 13:41 [pubmed] 2023/04/20 08:33 [entrez]
 2022/09/08 00:00 [received] 2022/11/02 00:00 [revised] 2022/11/05 00:00 [accepted] 2022/11/21 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/20 18:12 [entrez]
 2022/06/01 00:00 [received] 2022/10/17 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/01/27 06:00 [medline] 2023/01/09 23:25 [entrez]
 2022/10/01 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/09/30 05:32 [entrez]
 2022/10/18 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/10/17 06:33 [entrez]
 2022/08/21 00:00 [revised] 2022/05/15 00:00 [received] 2022/09/09 00:00 [accepted] 2022/09/28 06:00 [pubmed] 2022/11/25 06:00 [medline] 2022/09/27 02:43 [entrez]
 2022/09/08 00:00 [received] 2022/12/24 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/07 18:22 [entrez]
 2021/10/27 00:00 [received] 2022/11/24 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/04/01 02:17 [entrez] 2023/04/02 06:00 [pubmed]
 2023/05/01 06:41 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 17:52 [entrez]
 2024/01/01 00:00 [pmc-release] 2022/08/18 06:00 [pubmed] 2022/12/24 06:00 [medline] 2022/08/17 07:42 [entrez]
 2022/10/21 00:00 [received] 2023/02/21 00:00 [revised] 2023/03/01 00:00 [accepted] 2023/04/03 06:42 [medline] 2023/03/07 06:00 [pubmed] 2023/03/06 19:25 [entrez]
 2023/08/18 06:42 [medline] 2023/08/17 06:43 [pubmed] 2023/08/17 04:43 [entrez]
 2023/06/10 00:00 [received] 2023/06/27 00:00 [revised] 2023/06/28 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:22 [entrez]
 2022/10/23 00:00 [accepted] 2023/04/24 06:41 [medline] 2023/01/19 06:00 [pubmed] 2023/01/18 23:28 [entrez]
 2022/05/13 00:00 [received] 2022/12/15 00:00 [revised] 2022/12/19 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2024/01/02 00:00 [pmc-release] 2023/04/06 06:41 [medline] 2023/01/03 06:00 [pubmed] 2023/01/02 05:22 [entrez]
 2022/07/14 00:00 [revised] 2022/03/04 00:00 [received] 2022/09/04 00:00 [accepted] 2022/09/11 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/10 06:12 [entrez]
 2022/09/09 00:00 [received] 2023/02/03 00:00 [revised] 2023/02/19 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/26 06:00 [pubmed] 2023/02/25 18:46 [entrez]
 2022/10/06 00:00 [received] 2023/06/16 00:00 [revised] 2023/06/30 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/25 01:09 [pubmed] 2023/07/24 18:04 [entrez]
 2023/04/21 06:41 [medline] 2023/03/10 06:00 [pubmed] 2023/03/09 10:25 [entrez]
 2022/01/28 00:00 [received] 2022/07/23 00:00 [accepted] 2023/02/09 14:06 [entrez] 2023/02/10 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2022/11/20 00:00 [revised] 2022/07/13 00:00 [received] 2022/11/29 00:00 [accepted] 2023/04/14 06:41 [medline] 2022/12/09 06:00 [pubmed] 2022/12/08 15:42 [entrez]
 2023/05/20 00:00 [received] 2023/06/04 00:00 [revised] 2023/06/06 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:17 [entrez]
 2023/07/19 06:43 [medline] 2023/07/17 15:08 [pubmed] 2023/07/17 10:13 [entrez]
 2023/05/26 00:00 [received] 2023/06/30 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:16 [entrez]
 2022/11/14 00:00 [received] 2023/02/19 00:00 [accepted] 2023/02/15 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 11:14 [entrez]
 2022/12/21 00:00 [received] 2022/12/26 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/09 04:37 [entrez]
 2022/05/26 00:00 [received] 2022/07/21 00:00 [accepted] 2022/07/21 00:00 [revised] 2022/08/31 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/08/30 23:12 [entrez]
 2022/03/30 00:00 [received] 2022/09/13 00:00 [accepted] 2022/07/28 00:00 [revised] 2022/10/21 06:00 [pubmed] 2023/02/22 06:00 [medline] 2022/10/20 11:13 [entrez]
 2023/02/22 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:12 [entrez] 2023/04/14 06:00 [pubmed]
 2023/02/24 00:00 [received] 2023/06/02 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 23:38 [entrez]
 2022/12/14 00:00 [received] 2023/06/20 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 23:38 [entrez]
 2023/04/23 00:00 [received] 2023/05/14 00:00 [revised] 2023/05/16 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 18:02 [entrez]
 2023/03/10 00:00 [revised] 2022/12/23 00:00 [received] 2023/05/01 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 13:42 [pubmed] 2023/05/08 07:04 [entrez]
 2022/12/10 00:00 [received] 2023/03/03 00:00 [accepted] 2023/03/06 23:29 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/09 06:00 [medline]
 2022/04/12 00:00 [received] 2022/12/29 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/17 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/16 18:07 [entrez]
 2022/12/31 00:00 [received] 2023/01/27 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 10:17 [entrez]
 2022/11/27 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/26 05:42 [entrez]
 2022/06/28 00:00 [received] 2022/11/21 00:00 [accepted] 2023/03/29 06:05 [medline] 2023/01/12 06:00 [pubmed] 2023/01/11 21:42 [entrez]
 2024/06/05 00:00 [pmc-release] 2023/06/06 06:42 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 07:13 [entrez]
 2022/02/11 00:00 [received] 2022/09/22 00:00 [revised] 2022/10/02 00:00 [accepted] 2023/05/03 06:42 [medline] 2022/11/02 06:00 [pubmed] 2022/11/01 04:13 [entrez]
 2023/04/04 00:00 [received] 2023/06/02 00:00 [revised] 2023/06/24 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/01 11:41 [pubmed] 2023/06/30 18:06 [entrez]
 2023/01/25 00:00 [received] 2023/03/22 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/04/06 06:00 [pubmed] 2023/04/05 19:25 [entrez]
 2023/02/20 00:00 [revised] 2023/01/19 00:00 [received] 2023/03/06 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 00:23 [entrez]
 2022/10/22 00:00 [received] 2023/02/01 00:00 [accepted] 2023/02/27 04:55 [entrez] 2023/02/28 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/05/26 06:42 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 02:12 [entrez]
 2023/01/19 00:00 [received] 2023/01/30 00:00 [revised] 2023/02/04 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/06/05 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 19:21 [entrez]
 2022/09/14 00:00 [received] 2023/03/13 00:00 [accepted] 2023/03/11 00:00 [revised] 2024/08/01 00:00 [pmc-release] 2023/08/09 06:43 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 23:30 [entrez]
 2023/01/23 18:33 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/26 06:00 [medline]
 2021/03/22 00:00 [received] 2021/06/21 00:00 [revised] 2021/08/12 00:00 [accepted] 2021/08/22 06:00 [pubmed] 2023/03/23 06:00 [medline] 2021/08/21 08:33 [entrez]
 2023/02/24 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/02/23 10:42 [entrez]
 2022/12/20 00:00 [received] 2023/03/22 00:00 [revised] 2023/03/30 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/27 00:42 [pubmed] 2023/04/26 18:01 [entrez]
 2023/08/17 06:43 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 23:35 [entrez]
 2023/06/21 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 04:43 [entrez]
 2023/03/22 00:00 [received] 2023/06/29 00:00 [accepted] 2023/08/09 06:42 [medline] 2023/08/08 00:42 [pubmed] 2023/08/07 21:23 [entrez]
 2023/07/05 06:42 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:58 [entrez]
 2023/01/10 00:00 [received] 2023/04/26 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/28 01:07 [pubmed] 2023/05/27 23:27 [entrez]
 2023/05/07 00:00 [received] 2023/08/24 00:00 [accepted] 2023/09/04 06:44 [medline] 2023/09/03 00:41 [pubmed] 2023/09/02 23:34 [entrez]
 2022/12/09 00:00 [received] 2023/01/06 00:00 [revised] 2023/02/05 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/05 06:00 [pubmed] 2023/03/04 18:20 [entrez]
 2022/09/02 00:00 [received] 2023/01/24 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 18:35 [entrez]
 2023/03/29 06:04 [medline] 2023/03/23 06:00 [pubmed] 2023/03/22 09:32 [entrez]
 2022/11/08 00:00 [received] 2022/12/07 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/07 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/06 18:16 [entrez]
 2023/01/08 00:00 [received] 2023/02/15 00:00 [revised] 2023/02/18 00:00 [accepted] 2023/04/28 06:41 [medline] 2023/02/26 06:00 [pubmed] 2023/02/25 19:35 [entrez]
 2022/04/07 00:00 [received] 2022/09/01 00:00 [accepted] 2022/09/13 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/12 11:56 [entrez]
 2023/09/12 06:41 [medline] 2023/08/09 12:55 [pubmed] 2023/08/09 09:08 [entrez]
 2023/06/05 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/23 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/07/27 01:09 [pubmed] 2023/07/26 19:20 [entrez]
 2023/04/13 00:00 [received] 2023/07/27 00:00 [revised] 2023/07/31 00:00 [accepted] 2023/09/14 06:42 [medline] 2023/08/04 01:08 [pubmed] 2023/08/03 19:18 [entrez]
 2022/12/11 00:00 [received] 2023/04/24 00:00 [revised] 2023/05/08 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/23 01:06 [pubmed] 2023/05/22 18:08 [entrez]
 2023/06/14 06:42 [medline] 2023/04/04 06:00 [pubmed] 2023/04/03 11:33 [entrez]
 2022/11/28 00:00 [received] 2023/04/20 00:00 [revised] 2023/05/07 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/15 00:42 [pubmed] 2023/05/14 18:09 [entrez]
 2022/09/26 00:00 [received] 2023/05/22 00:00 [accepted] 2023/06/29 06:42 [medline] 2023/06/28 01:06 [pubmed] 2023/06/27 23:46 [entrez]
 2022/08/13 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/08/12 05:43 [entrez]
 2021/10/28 00:00 [received] 2022/08/17 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/01/27 06:00 [pubmed] 2023/01/26 12:02 [entrez]
 2023/02/17 00:00 [received] 2023/07/15 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/09/05 00:41 [pubmed] 2023/09/04 23:40 [entrez]
 2022/09/06 00:00 [received] 2023/05/04 00:00 [accepted] 2023/06/23 06:42 [medline] 2023/05/09 13:42 [pubmed] 2023/05/09 12:04 [entrez]
 2023/01/23 00:00 [received] 2023/06/23 00:00 [revised] 2023/06/23 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/07/12 19:07 [pubmed] 2023/07/12 18:00 [entrez]
 2022/09/25 00:00 [revised] 2022/06/20 00:00 [received] 2022/12/14 00:00 [accepted] 2023/01/05 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/01/04 23:53 [entrez]
 2023/05/18 06:42 [medline] 2022/10/30 06:00 [pubmed] 2022/10/29 02:22 [entrez]
 2023/06/02 06:42 [medline] 2023/05/23 01:06 [pubmed] 2023/05/22 23:29 [entrez]
 2022/08/09 00:00 [received] 2023/01/27 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/01 06:00 [pubmed] 2023/01/31 12:02 [entrez]
 2022/11/06 00:00 [received] 2023/01/26 00:00 [revised] 2023/02/05 00:00 [accepted] 2023/08/03 06:42 [medline] 2023/03/04 06:00 [pubmed] 2023/03/03 01:03 [entrez]
 2023/07/03 06:41 [medline] 2023/06/01 01:08 [pubmed] 2023/05/31 23:30 [entrez]
 2021/06/21 00:00 [received] 2022/04/19 00:00 [accepted] 2022/05/21 06:00 [pubmed] 2023/03/08 06:00 [medline] 2022/05/20 23:33 [entrez]
 2022/10/14 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/10/13 11:12 [entrez]
 2022/11/29 00:00 [received] 2023/07/07 00:00 [accepted] 2023/08/04 06:43 [medline] 2023/08/02 19:15 [pubmed] 2023/08/02 13:33 [entrez]
 2022/10/22 00:00 [received] 2022/12/30 00:00 [accepted] 2023/02/13 03:18 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/04/14 00:00 [received] 2023/05/30 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 04:21 [entrez]
 2022/12/29 00:00 [received] 2023/01/27 00:00 [accepted] 2023/03/03 02:32 [entrez] 2023/03/04 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2022/10/10 00:00 [received] 2022/12/05 00:00 [revised] 2022/12/26 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/03/04 06:00 [medline] 2023/01/07 16:14 [entrez]
 2023/02/16 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/20 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/06/27 01:06 [pubmed] 2023/06/26 18:07 [entrez]
 2022/04/11 00:00 [received] 2022/09/21 00:00 [accepted] 2022/10/31 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/10/30 00:54 [entrez]
 2022/06/09 00:00 [received] 2023/01/06 00:00 [accepted] 2022/12/29 00:00 [revised] 2023/05/26 06:42 [medline] 2023/01/20 06:00 [pubmed] 2023/01/19 23:25 [entrez]
 2022/04/14 00:00 [received] 2022/12/26 00:00 [revised] 2022/12/29 00:00 [accepted] 2023/01/11 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/10 19:19 [entrez]
 2023/02/25 00:00 [received] 2023/03/19 00:00 [revised] 2023/03/25 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/13 01:11 [entrez] 2023/04/14 06:00 [pubmed]
 2022/09/12 00:00 [received] 2022/12/29 00:00 [accepted] 2023/06/08 06:42 [medline] 2023/01/14 06:00 [pubmed] 2023/01/13 11:53 [entrez]
 2022/04/26 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/04/25 12:10 [entrez]
 2023/08/11 06:43 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2023/04/20 10:17 [medline] 2023/04/19 06:41 [pubmed] 2023/04/19 00:32 [entrez]
 2023/02/17 00:00 [received] 2023/04/25 00:00 [revised] 2023/05/02 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/07 00:42 [pubmed] 2023/05/06 19:30 [entrez]
 2023/07/03 06:41 [medline] 2023/06/14 13:07 [pubmed] 2023/06/14 11:15 [entrez]
 2022/09/03 00:00 [received] 2023/04/14 00:00 [accepted] 2023/05/01 10:17 [medline] 2023/04/30 00:42 [pubmed] 2023/04/29 23:19 [entrez]
 2023/08/11 06:42 [medline] 2023/08/10 12:41 [pubmed] 2023/08/10 07:24 [entrez]
 2023/03/26 00:00 [received] 2023/07/01 00:00 [revised] 2023/07/12 00:00 [accepted] 2023/08/07 06:41 [medline] 2023/07/16 01:07 [pubmed] 2023/07/15 19:23 [entrez]
 2022/05/07 00:00 [received] 2022/08/21 00:00 [accepted] 2022/08/18 00:00 [revised] 2022/09/02 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/01 11:16 [entrez]
 2022/12/22 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/01/21 01:28 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/11/21 00:00 [revised] 2022/10/03 00:00 [received] 2022/11/21 00:00 [accepted] 2022/12/28 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/27 11:33 [entrez]
 2022/11/16 00:00 [received] 2023/01/08 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 18:35 [entrez]
 2023/01/04 00:00 [received] 2023/06/16 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/27 01:06 [pubmed] 2023/06/26 18:03 [entrez]
 2022/12/13 00:00 [revised] 2022/09/29 00:00 [received] 2022/12/17 00:00 [accepted] 2023/03/29 06:05 [medline] 2022/12/25 06:00 [pubmed] 2022/12/24 07:42 [entrez]
 2021/09/11 00:00 [received] 2022/07/03 00:00 [revised] 2022/09/13 00:00 [accepted] 2022/10/03 06:00 [pubmed] 2023/02/04 06:00 [medline] 2022/10/02 22:03 [entrez]
 2022/12/17 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/01/30 06:00 [pubmed] 2023/01/29 18:07 [entrez]
 2022/09/27 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/09/26 14:59 [entrez]
 2022/08/29 00:00 [received] 2022/10/19 00:00 [accepted] 2022/10/10 00:00 [revised] 2022/11/25 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/24 09:33 [entrez]
 2023/06/09 00:00 [received] 2023/07/03 00:00 [revised] 2023/07/06 00:00 [accepted] 2023/07/31 11:42 [medline] 2023/07/29 11:43 [pubmed] 2023/07/29 01:21 [entrez]
 2023/09/04 06:42 [medline] 2023/09/01 00:41 [pubmed] 2023/08/31 23:40 [entrez]
 2022/07/21 00:00 [received] 2023/01/18 00:00 [revised] 2023/01/22 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/01/26 19:24 [entrez]
 2022/05/31 00:00 [received] 2023/03/05 00:00 [accepted] 2023/02/18 00:00 [revised] 2023/05/17 06:42 [medline] 2023/03/20 06:00 [pubmed] 2023/03/19 00:19 [entrez]
 2023/07/12 06:42 [medline] 2023/07/11 06:42 [pubmed] 2023/07/11 04:23 [entrez]
 2022/08/04 00:00 [received] 2023/01/13 00:00 [accepted] 2023/05/19 06:42 [medline] 2023/01/21 06:00 [pubmed] 2023/01/20 01:53 [entrez]
 2022/11/16 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/11/15 01:34 [entrez]
 2022/11/28 00:00 [received] 2022/12/28 00:00 [revised] 2022/12/30 00:00 [accepted] 2023/01/08 01:27 [entrez] 2023/01/09 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2022/11/30 00:00 [received] 2023/03/06 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/03/23 06:00 [pubmed] 2023/03/22 12:20 [entrez]
 2022/10/14 00:00 [received] 2022/12/04 00:00 [revised] 2022/12/05 00:00 [accepted] 2022/12/17 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/16 19:26 [entrez]
 2023/04/18 06:42 [medline] 2023/04/14 20:02 [entrez] 2023/04/15 06:00 [pubmed]
 2023/05/12 07:06 [medline] 2022/11/29 06:00 [pubmed] 2022/11/28 07:52 [entrez]
 2023/05/05 06:42 [medline] 2023/01/05 06:00 [pubmed] 2023/01/04 14:03 [entrez]
 2023/06/19 13:08 [medline] 2023/05/19 13:05 [pubmed] 2023/05/19 08:53 [entrez]
 2023/02/07 00:00 [received] 2023/04/20 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/30 01:06 [pubmed] 2023/05/29 18:01 [entrez]
 2022/08/25 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/08/24 05:43 [entrez]
 2022/12/04 00:00 [received] 2023/05/09 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/05/19 13:05 [pubmed] 2023/05/19 11:10 [entrez]
 2023/05/01 06:42 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 01:06 [entrez]
 2022/12/13 00:00 [revised] 2022/03/30 00:00 [received] 2023/01/21 00:00 [accepted] 2023/06/07 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 05:33 [entrez]
 2022/11/26 00:00 [received] 2023/03/23 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/05/08 06:41 [medline] 2023/04/09 06:00 [pubmed] 2023/04/08 19:31 [entrez]
 2022/09/26 00:00 [revised] 2022/07/25 00:00 [received] 2022/10/08 00:00 [accepted] 2022/10/22 06:00 [pubmed] 2023/01/17 06:00 [medline] 2022/10/21 00:53 [entrez]
 2023/04/05 06:42 [medline] 2023/03/28 06:00 [pubmed] 2023/03/27 03:58 [entrez]
 2022/04/02 00:00 [received] 2022/07/26 00:00 [revised] 2022/08/18 00:00 [accepted] 2022/09/14 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/09/13 00:22 [entrez]
 2023/07/12 06:42 [medline] 2023/06/29 06:43 [pubmed] 2023/06/29 00:53 [entrez]
 2022/05/25 00:00 [received] 2022/07/06 00:00 [accepted] 2023/05/15 06:42 [medline] 2022/07/22 06:00 [pubmed] 2022/07/21 11:18 [entrez]
 2023/01/10 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/01 00:00 [accepted] 2023/02/10 06:00 [pubmed] 2023/03/16 06:00 [medline] 2023/02/09 18:09 [entrez]
 2022/04/14 00:00 [revised] 2021/11/11 00:00 [received] 2022/06/01 00:00 [accepted] 2023/06/08 06:42 [medline] 2022/07/09 06:00 [pubmed] 2022/07/08 01:22 [entrez]
 2022/12/02 07:22 [entrez] 2022/12/03 06:00 [pubmed] 2022/12/06 06:00 [medline]
 2023/04/20 00:00 [received] 2023/06/30 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 19:29 [entrez]
 2022/12/19 00:00 [received] 2023/04/25 00:00 [revised] 2023/05/05 00:00 [accepted] 2023/12/21 00:00 [pmc-release] 2023/06/23 06:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 21:39 [entrez]
 2022/08/02 06:00 [pubmed] 2023/02/04 06:00 [medline] 2022/08/01 08:03 [entrez]
 2022/10/14 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/10/13 09:04 [entrez]
 2022/06/23 00:00 [received] 2023/01/23 00:00 [accepted] 2023/05/12 07:06 [medline] 2023/02/08 06:00 [pubmed] 2023/02/07 23:14 [entrez]
 2022/06/10 00:00 [received] 2023/03/23 00:00 [revised] 2023/04/02 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 18:04 [entrez]
 2022/01/17 00:00 [received] 2023/02/01 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/21 06:44 [pubmed] 2023/07/21 04:13 [entrez]
 2023/08/31 06:42 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 00:05 [entrez]
 2023/01/05 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/31 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:07 [entrez]
 2021/11/23 00:00 [received] 2022/01/29 00:00 [revised] 2022/02/15 00:00 [accepted] 2022/03/08 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/03/07 08:48 [entrez]
 2023/08/14 06:41 [medline] 2023/08/11 18:42 [pubmed] 2023/08/11 14:03 [entrez]
 2022/08/17 00:00 [received] 2022/10/14 00:00 [accepted] 2022/11/08 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/11/07 21:42 [entrez]
 2022/10/28 00:00 [received] 2023/03/30 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/05/17 06:42 [medline] 2023/04/21 18:43 [pubmed] 2023/04/21 14:46 [entrez]
 2022/07/26 00:00 [revised] 2021/12/14 00:00 [received] 2022/08/21 00:00 [accepted] 2022/10/02 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/10/01 01:42 [entrez]
 2023/05/03 00:00 [received] 2023/05/21 00:00 [accepted] 2023/07/28 06:43 [medline] 2023/05/26 01:05 [pubmed] 2023/05/25 19:27 [entrez]
 2022/10/13 00:00 [received] 2023/01/30 00:00 [revised] 2023/03/04 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 19:17 [entrez]
 2022/01/05 00:00 [received] 2022/08/11 00:00 [accepted] 2022/11/24 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/11/23 21:22 [entrez]
 2022/08/25 00:00 [received] 2023/05/31 00:00 [accepted] 2023/07/14 13:05 [medline] 2023/06/16 13:10 [pubmed] 2023/06/16 11:14 [entrez]
 2022/11/13 00:00 [received] 2022/12/13 00:00 [accepted] 2022/12/12 00:00 [revised] 2023/01/11 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/01/10 11:14 [entrez]
 2022/05/18 00:00 [received] 2022/11/21 00:00 [accepted] 2022/11/09 00:00 [revised] 2023/01/13 06:00 [pubmed] 2023/02/08 06:00 [medline] 2023/01/12 23:22 [entrez]
 2022/07/13 00:00 [received] 2023/02/23 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/03/01 06:00 [pubmed] 2023/02/28 12:02 [entrez]
 2023/03/03 00:00 [received] 2023/04/04 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:27 [entrez]
 2023/04/04 06:42 [medline] 2023/03/11 06:00 [pubmed] 2023/03/10 23:20 [entrez]
 2023/06/14 06:42 [medline] 2023/06/02 06:42 [pubmed] 2023/06/02 04:43 [entrez]
 2024/06/01 00:00 [pmc-release] 2023/06/08 06:42 [medline] 2023/06/06 13:09 [pubmed] 2023/06/06 10:03 [entrez]
 2022/12/21 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/20 07:53 [entrez]
 2022/09/03 00:00 [received] 2023/01/27 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 18:04 [entrez]
 2022/11/04 00:00 [revised] 2022/06/16 00:00 [received] 2022/11/08 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/11/29 00:52 [entrez]
 2022/08/10 00:00 [received] 2022/11/19 00:00 [accepted] 2023/07/07 06:42 [medline] 2022/11/29 06:00 [pubmed] 2022/11/28 08:25 [entrez]
 2023/04/01 00:00 [received] 2023/06/23 00:00 [revised] 2023/06/23 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 19:22 [entrez]
 2022/04/08 06:00 [pubmed] 2023/03/25 06:00 [medline] 2022/04/07 05:26 [entrez]
 2022/07/27 00:00 [received] 2023/02/13 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/04/10 04:00 [entrez] 2023/04/11 06:00 [pubmed]
 2022/12/19 00:00 [received] 2023/03/23 00:00 [revised] 2023/04/08 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 18:02 [entrez]
 2022/11/14 00:00 [received] 2023/02/16 00:00 [accepted] 2023/04/20 06:42 [medline] 2023/04/19 06:00 [pubmed] 2023/04/18 06:00 [entrez]
 2023/07/14 13:06 [medline] 2023/05/15 13:06 [pubmed] 2023/05/15 11:33 [entrez]
 2022/11/19 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/18 04:22 [entrez]
 2023/02/20 00:00 [revised] 2022/09/19 00:00 [received] 2023/03/15 00:00 [accepted] 2023/06/22 06:42 [medline] 2023/05/09 06:42 [pubmed] 2023/05/09 00:23 [entrez]
 2022/08/01 00:00 [revised] 2022/04/21 00:00 [received] 2022/09/06 00:00 [accepted] 2022/09/13 06:00 [pubmed] 2023/01/31 06:00 [medline] 2022/09/12 04:42 [entrez]
 2024/06/01 00:00 [pmc-release] 2023/06/02 06:43 [medline] 2022/09/06 06:00 [pubmed] 2022/09/05 05:03 [entrez]
 2022/05/09 00:00 [received] 2023/03/11 00:00 [accepted] 2023/03/23 00:38 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2022/11/08 00:00 [revised] 2022/09/02 00:00 [received] 2023/01/11 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/23 06:44 [entrez]
 2023/02/18 00:00 [received] 2023/03/12 00:00 [revised] 2023/03/16 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 02:00 [entrez] 2023/03/30 06:00 [pubmed]
 2022/08/03 00:00 [received] 2022/08/12 00:00 [revised] 2022/08/17 00:00 [accepted] 2023/02/01 04:07 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/03 06:00 [medline]
 2022/10/31 00:00 [received] 2022/12/12 00:00 [accepted] 2022/12/06 00:00 [revised] 2022/12/23 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/22 11:13 [entrez]
 2022/07/14 00:00 [received] 2022/12/06 00:00 [revised] 2023/01/05 00:00 [accepted] 2023/01/28 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/27 18:03 [entrez]
 2022/12/30 00:00 [received] 2023/03/25 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/03/29 23:23 [entrez] 2023/03/30 06:00 [pubmed]
 2022/10/31 00:00 [received] 2023/01/23 00:00 [accepted] 2023/02/23 09:36 [entrez] 2023/02/24 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/08/10 00:00 [received] 2022/10/12 00:00 [revised] 2022/10/24 00:00 [accepted] 2022/11/21 06:00 [pubmed] 2022/12/06 06:00 [medline] 2022/11/20 18:20 [entrez]
 2022/09/28 00:00 [received] 2023/07/12 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/07/26 01:06 [pubmed] 2023/07/25 23:38 [entrez]
 2023/03/13 07:47 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/09/05 00:00 [received] 2022/12/15 00:00 [revised] 2022/12/21 00:00 [accepted] 2023/06/05 06:43 [medline] 2023/01/01 06:00 [pubmed] 2022/12/31 19:12 [entrez]
 2023/09/07 06:42 [medline] 2023/08/16 18:42 [pubmed] 2023/08/16 14:43 [entrez]
 2022/08/16 00:00 [received] 2022/12/04 00:00 [accepted] 2023/04/17 06:41 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 21:22 [entrez]
 2021/11/30 00:00 [revised] 2021/05/09 00:00 [received] 2022/07/29 00:00 [accepted] 2022/09/03 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/09/02 14:45 [entrez]
 2023/01/17 00:00 [received] 2023/04/05 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/05/02 06:41 [pubmed] 2023/05/02 01:54 [entrez]
 2022/06/16 00:00 [received] 2022/08/18 00:00 [accepted] 2022/08/27 06:00 [pubmed] 2022/12/16 06:00 [medline] 2022/08/26 05:38 [entrez]
 2023/03/01 00:00 [revised] 2022/11/06 00:00 [received] 2023/04/06 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/04/25 06:42 [pubmed] 2023/04/25 12:42 [entrez]
 2023/03/26 00:00 [received] 2023/04/26 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/07/11 13:10 [pubmed] 2023/07/11 10:43 [entrez]
 2023/07/12 06:42 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 16:13 [entrez]
 2023/04/19 00:00 [received] 2023/06/20 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 23:37 [entrez]
 2021/11/04 00:00 [received] 2022/03/28 00:00 [revised] 2022/06/09 00:00 [accepted] 2022/08/05 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/08/04 20:02 [entrez]
 2023/07/28 06:42 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 14:14 [entrez]
 2022/08/31 00:00 [received] 2022/11/09 00:00 [revised] 2022/12/07 00:00 [accepted] 2022/12/25 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/24 18:12 [entrez]
 2022/12/29 00:00 [received] 2023/01/03 00:00 [accepted] 2023/01/11 06:13 [entrez] 2023/01/12 06:00 [pubmed] 2023/01/13 06:00 [medline]
 2022/03/30 00:00 [received] 2022/11/01 00:00 [revised] 2022/12/10 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/12/15 19:26 [entrez]
 2022/06/27 00:00 [received] 2023/01/27 00:00 [accepted] 2024/03/01 00:00 [pmc-release] 2023/03/29 06:05 [medline] 2023/03/01 06:00 [pubmed] 2023/02/28 11:39 [entrez]
 2023/01/12 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/02/14 06:00 [medline] 2023/01/23 23:22 [entrez]
 2023/08/22 06:42 [medline] 2023/08/21 12:42 [pubmed] 2023/08/21 11:09 [entrez]
 2023/02/03 00:00 [received] 2023/08/18 00:00 [accepted] 2023/08/28 06:41 [medline] 2023/08/27 05:43 [pubmed] 2023/08/26 23:15 [entrez]
 2022/08/02 00:00 [received] 2022/11/23 00:00 [accepted] 2023/08/11 06:42 [medline] 2023/02/01 06:00 [pubmed] 2023/01/31 11:13 [entrez]
 2023/08/17 06:42 [medline] 2023/07/29 21:45 [pubmed] 2023/07/29 06:53 [entrez]
 2022/09/14 00:00 [revised] 2022/07/07 00:00 [received] 2022/09/14 00:00 [accepted] 2022/10/02 06:00 [pubmed] 2023/01/17 06:00 [medline] 2022/10/01 11:22 [entrez]
 2022/11/02 00:00 [received] 2023/04/24 00:00 [accepted] 2023/08/23 06:42 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 21:12 [entrez]
 2023/06/19 13:08 [medline] 2023/03/29 06:00 [pubmed] 2023/03/28 06:33 [entrez]
 2022/12/23 00:00 [revised] 2022/11/01 00:00 [received] 2023/02/02 00:00 [accepted] 2023/04/06 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 09:52 [entrez]
 2023/06/02 00:00 [received] 2023/07/15 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/07/25 01:09 [pubmed] 2023/07/24 23:48 [entrez]
 2022/09/18 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/07 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 20:32 [entrez]
 2023/01/13 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/12 07:22 [entrez]
 2022/08/16 00:00 [received] 2022/11/28 00:00 [revised] 2022/11/28 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/12/19 18:15 [entrez]
 2022/09/28 00:00 [received] 2023/01/11 00:00 [accepted] 2023/01/31 00:05 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/02 06:00 [medline]
 2022/08/27 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/21 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/20 18:04 [entrez]
 2022/08/24 00:00 [received] 2023/04/13 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/04/15 06:00 [pubmed] 2023/04/14 08:53 [entrez]
 2023/06/19 13:08 [medline] 2023/05/11 06:42 [pubmed] 2023/05/11 05:43 [entrez]
 2023/03/21 00:00 [received] 2023/05/30 00:00 [accepted] 2023/05/30 00:00 [revised] 2023/08/14 06:43 [medline] 2023/06/09 13:42 [pubmed] 2023/06/09 11:04 [entrez]
 2022/04/05 00:00 [received] 2022/08/23 00:00 [accepted] 2022/10/19 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/10/18 20:52 [entrez]
 2022/11/03 00:00 [revised] 2022/08/16 00:00 [received] 2022/11/21 00:00 [accepted] 2022/12/02 11:33 [entrez] 2022/12/03 06:00 [pubmed] 2022/12/07 06:00 [medline]
 2023/01/24 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/03/11 01:14 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2023/06/14 06:42 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 01:43 [entrez]
 2022/10/25 00:00 [received] 2023/01/10 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 21:22 [entrez]
 2023/05/08 06:42 [medline] 2022/05/18 06:00 [pubmed] 2022/05/17 10:02 [entrez]
 2023/01/04 00:00 [received] 2023/04/09 00:00 [accepted] 2023/08/28 06:41 [medline] 2023/05/03 00:41 [pubmed] 2023/05/02 21:40 [entrez]
 2024/05/15 00:00 [pmc-release] 2023/07/14 13:07 [medline] 2023/07/12 19:07 [pubmed] 2023/07/12 16:22 [entrez]
 2022/02/16 06:00 [pubmed] 2023/01/26 06:00 [medline] 2022/02/15 12:16 [entrez]
 2023/01/21 00:00 [received] 2023/07/07 00:00 [accepted] 2023/07/21 06:44 [medline] 2023/07/19 01:06 [pubmed] 2023/07/18 23:18 [entrez]
 2023/05/09 06:42 [medline] 2023/04/04 06:00 [pubmed] 2023/04/03 02:33 [entrez]
 2022/11/30 00:00 [received] 2022/12/11 00:00 [accepted] 2022/12/25 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/12/24 18:14 [entrez]
 2022/09/23 00:00 [revised] 2022/03/22 00:00 [received] 2022/10/09 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/10/08 05:03 [entrez]
 2022/11/04 00:00 [received] 2023/05/10 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/09 23:38 [entrez]
 2021/11/06 06:00 [pubmed] 2022/12/16 06:00 [medline] 2021/11/05 08:38 [entrez]
 2022/10/06 00:00 [received] 2022/12/12 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/02/26 06:00 [pubmed] 2023/03/09 06:00 [medline] 2023/02/25 18:54 [entrez]
 2023/02/18 00:00 [received] 2023/03/27 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:45 [entrez]
 2023/04/09 00:00 [revised] 2022/08/23 00:00 [received] 2023/04/15 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 05:33 [entrez]
 2022/05/14 00:00 [received] 2023/03/28 00:00 [accepted] 2023/02/22 00:00 [revised] 2023/06/05 06:42 [medline] 2023/04/21 18:43 [pubmed] 2023/04/21 15:03 [entrez]
 2023/01/19 00:00 [revised] 2022/10/18 00:00 [received] 2023/01/20 00:00 [accepted] 2023/04/20 06:42 [medline] 2023/02/08 06:00 [pubmed] 2023/02/07 15:23 [entrez]
 2022/12/08 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/11 01:19 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/04/28 00:00 [received] 2023/06/14 00:00 [accepted] 2023/07/25 06:42 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:32 [entrez]
 2022/10/18 00:00 [received] 2023/01/16 00:00 [accepted] 2023/03/06 04:09 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/08 06:00 [medline]
 2022/12/21 00:00 [received] 2023/04/20 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/08/04 06:43 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 18:02 [entrez]
 2022/11/20 00:00 [revised] 2022/06/27 00:00 [received] 2022/11/22 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/01/27 06:00 [medline] 2022/12/08 14:25 [entrez]
 2023/07/21 06:44 [medline] 2023/06/22 01:07 [pubmed] 2023/06/21 21:13 [entrez]
 2022/12/26 00:00 [received] 2023/01/27 00:00 [revised] 2023/02/06 00:00 [accepted] 2023/02/25 02:43 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/04/26 00:00 [received] 2023/06/26 00:00 [accepted] 2023/08/10 06:43 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 03:58 [entrez]
 2023/07/15 00:00 [received] 2023/08/12 00:00 [revised] 2023/08/16 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/26 10:43 [pubmed] 2023/08/26 01:02 [entrez]
 2022/09/08 06:00 [pubmed] 2022/12/24 06:00 [medline] 2022/09/07 08:22 [entrez]
 2023/05/01 06:42 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 03:43 [entrez]
 2022/12/15 00:00 [revised] 2022/09/17 00:00 [received] 2023/01/24 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/03/28 06:00 [medline] 2023/01/26 03:43 [entrez]
 2023/08/10 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 03:44 [entrez]
 2023/07/21 06:42 [medline] 2023/07/19 13:06 [pubmed] 2023/07/19 06:43 [entrez]
 2022/10/07 00:00 [received] 2022/11/02 00:00 [revised] 2022/11/25 00:00 [accepted] 2022/12/14 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/13 18:22 [entrez]
 2023/02/25 00:00 [received] 2023/05/07 00:00 [revised] 2023/05/10 00:00 [accepted] 2024/07/15 00:00 [pmc-release] 2023/06/13 06:42 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 18:02 [entrez]
 2021/06/15 00:00 [received] 2022/12/17 00:00 [accepted] 2023/01/31 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/01/30 03:22 [entrez]
 2023/05/16 00:00 [received] 2023/07/13 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/24 00:41 [pubmed] 2023/07/23 18:01 [entrez]
 2022/08/26 00:00 [accepted] 2022/09/27 06:00 [pubmed] 2023/03/23 06:00 [medline] 2022/09/26 20:42 [entrez]
 2024/04/01 00:00 [pmc-release] 2023/04/06 06:41 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 08:12 [entrez]
 2022/05/23 00:00 [received] 2022/12/07 00:00 [accepted] 2023/01/05 23:43 [entrez] 2023/01/06 06:00 [pubmed] 2023/01/10 06:00 [medline]
 2023/01/23 00:00 [received] 2023/07/05 00:00 [accepted] 2023/08/23 06:42 [medline] 2023/08/22 00:41 [pubmed] 2023/08/21 21:38 [entrez]
 2022/09/03 00:00 [received] 2023/02/14 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/04/26 06:41 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 20:26 [entrez]
 2023/04/17 00:00 [received] 2023/04/27 00:00 [revised] 2023/05/02 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:30 [entrez]
 2023/03/29 00:00 [received] 2023/05/22 00:00 [revised] 2023/06/11 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 18:05 [entrez]
 2022/08/15 00:00 [received] 2022/10/18 00:00 [accepted] 2022/10/30 06:00 [pubmed] 2022/12/24 06:00 [medline] 2022/10/29 05:02 [entrez]
 2022/08/19 00:00 [received] 2022/12/01 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/03/17 06:00 [medline] 2022/12/15 21:22 [entrez]
 2023/08/21 06:41 [medline] 2022/07/21 06:00 [pubmed] 2022/07/20 13:13 [entrez]
 2023/05/01 06:42 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 02:32 [entrez]
 2022/09/04 00:00 [received] 2023/01/25 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/12 20:43 [entrez] 2023/04/13 06:00 [pubmed]
 2023/07/18 00:00 [received] 2023/08/05 00:00 [revised] 2023/08/07 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:41 [pubmed] 2023/08/26 01:14 [entrez]
 2023/05/10 00:00 [received] 2023/06/15 00:00 [revised] 2023/06/20 00:00 [accepted] 2023/07/31 11:43 [medline] 2023/07/29 11:51 [pubmed] 2023/07/29 01:16 [entrez]
 2022/06/21 00:00 [received] 2022/11/16 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/15 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/14 18:11 [entrez]
 2022/07/02 00:00 [received] 2022/11/19 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2022/12/21 06:00 [medline] 2022/12/09 18:31 [entrez]
 2022/06/22 00:00 [received] 2023/03/20 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 16:42 [entrez]
 2023/07/05 06:42 [medline] 2023/03/01 06:00 [pubmed] 2023/02/28 10:54 [entrez]
 2023/01/24 00:00 [received] 2023/05/27 00:00 [revised] 2023/06/03 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/06/12 00:42 [pubmed] 2023/06/11 18:08 [entrez]
 2022/08/29 00:00 [received] 2023/02/09 00:00 [accepted] 2023/02/08 00:00 [revised] 2023/05/26 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 10:39 [entrez]
 2022/09/04 00:00 [received] 2022/12/05 00:00 [revised] 2022/12/27 00:00 [accepted] 2023/01/02 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/01 18:08 [entrez]
 2022/12/28 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/27 06:42 [entrez]
 2023/02/24 00:00 [received] 2023/04/28 00:00 [revised] 2023/06/03 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/05 01:06 [pubmed] 2023/07/04 18:01 [entrez]
 2023/01/17 00:00 [received] 2023/04/17 00:00 [revised] 2023/05/02 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/05/27 09:42 [pubmed] 2023/05/26 18:42 [entrez]
 2023/04/04 00:00 [received] 2023/05/22 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:47 [entrez]
 2022/12/19 00:00 [revised] 2022/11/06 00:00 [received] 2022/12/28 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/27 23:52 [entrez]
 2021/08/31 00:00 [received] 2022/10/03 00:00 [accepted] 2022/10/11 06:00 [pubmed] 2022/12/21 06:00 [medline] 2022/10/10 11:21 [entrez]
 2023/02/18 00:00 [received] 2023/04/16 00:00 [revised] 2023/04/26 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:21 [entrez]
 2022/12/31 00:00 [received] 2023/01/21 00:00 [revised] 2023/02/08 00:00 [accepted] 2023/03/11 01:03 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/06/20 00:00 [received] 2023/01/01 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/01/23 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/22 18:14 [entrez]
 2023/04/05 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/08/28 06:43 [medline] 2023/05/10 00:41 [pubmed] 2023/05/09 22:48 [entrez]
 2023/07/12 06:42 [medline] 2023/06/02 06:42 [pubmed] 2023/06/02 05:43 [entrez]
 2023/06/05 06:42 [medline] 2022/06/07 06:00 [pubmed] 2022/06/06 15:56 [entrez]
 2023/04/07 00:00 [received] 2023/06/21 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/07/26 06:42 [pubmed] 2023/07/26 03:54 [entrez]
 2022/12/02 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/01 01:53 [entrez]
 2023/01/23 00:00 [revised] 2022/09/12 00:00 [received] 2023/01/24 00:00 [accepted] 2023/02/01 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/31 08:53 [entrez]
 2022/06/19 00:00 [received] 2022/11/22 00:00 [revised] 2022/11/24 00:00 [accepted] 2022/12/02 06:00 [pubmed] 2022/12/21 06:00 [medline] 2022/12/01 19:23 [entrez]
 2023/03/02 00:00 [received] 2023/04/17 00:00 [accepted] 2023/04/17 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/24 12:41 [pubmed] 2023/04/24 11:19 [entrez]
 2022/09/30 00:00 [received] 2022/12/28 00:00 [revised] 2023/01/05 00:00 [accepted] 2023/01/14 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/13 18:22 [entrez]
 2022/10/31 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/23 00:00 [accepted] 2023/02/17 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/16 18:14 [entrez]
 2023/06/05 00:00 [received] 2023/07/18 00:00 [accepted] 2023/08/29 12:42 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 04:58 [entrez]
 2022/10/26 00:00 [received] 2023/02/01 00:00 [revised] 2023/03/24 00:00 [accepted] 2023/04/21 06:41 [medline] 2023/04/06 06:00 [pubmed] 2023/04/05 13:13 [entrez]
 2023/07/13 00:00 [received] 2023/08/10 00:00 [revised] 2023/08/24 00:00 [accepted] 2023/09/08 06:42 [medline] 2023/08/28 00:41 [pubmed] 2023/08/27 19:25 [entrez]
 2022/12/23 00:00 [revised] 2022/05/09 00:00 [received] 2022/12/27 00:00 [accepted] 2023/01/11 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/01/10 03:13 [entrez]
 2023/04/10 00:00 [received] 2023/07/04 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 19:26 [entrez]
 2022/10/14 00:00 [received] 2023/01/13 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/26 11:15 [entrez]
 2022/08/12 00:00 [received] 2023/02/10 00:00 [accepted] 2023/03/17 09:54 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2022/06/29 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/06/28 03:13 [entrez]
 2022/03/29 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/03/28 05:25 [entrez]
 2023/04/10 00:00 [revised] 2023/02/15 00:00 [received] 2023/05/12 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/05/17 06:42 [pubmed] 2023/05/17 03:53 [entrez]
 2022/04/28 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/04/27 08:33 [entrez]
 2023/04/10 00:00 [received] 2023/05/29 00:00 [revised] 2023/06/18 00:00 [accepted] 2023/08/02 06:42 [medline] 2023/06/27 01:06 [pubmed] 2023/06/26 18:09 [entrez]
 2022/04/08 00:00 [received] 2023/03/20 00:00 [accepted] 2024/07/15 00:00 [pmc-release] 2023/07/05 06:42 [medline] 2023/06/14 13:07 [pubmed] 2023/06/14 10:42 [entrez]
 2023/01/27 00:00 [received] 2023/02/22 00:00 [revised] 2023/02/24 00:00 [accepted] 2023/03/11 01:12 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/04/22 00:00 [received] 2022/08/19 00:00 [revised] 2022/08/29 00:00 [accepted] 2023/08/29 12:42 [medline] 2022/10/07 06:00 [pubmed] 2022/10/06 02:53 [entrez]
 2022/12/03 00:00 [received] 2022/12/16 00:00 [accepted] 2023/02/10 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/02/09 23:16 [entrez]
 2022/07/30 00:00 [received] 2022/11/07 00:00 [revised] 2022/11/23 00:00 [accepted] 2022/12/04 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/03 18:26 [entrez]
 2023/05/15 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 11:04 [entrez]
 2023/05/01 00:00 [received] 2023/05/29 00:00 [revised] 2023/06/10 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:05 [pubmed] 2023/07/14 01:25 [entrez]
 2023/02/09 00:00 [received] 2023/05/29 00:00 [accepted] 2023/06/30 06:42 [medline] 2023/06/28 13:09 [pubmed] 2023/06/28 09:25 [entrez]
 2022/01/07 00:00 [received] 2022/11/11 00:00 [accepted] 2022/11/03 00:00 [revised] 2024/02/01 00:00 [pmc-release] 2022/12/18 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/17 23:40 [entrez]
 2022/09/03 00:00 [received] 2022/11/05 00:00 [accepted] 2022/11/04 00:00 [revised] 2022/11/11 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/10 11:15 [entrez]
 2022/10/26 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/10/25 06:12 [entrez]
 2022/09/08 00:00 [received] 2022/12/19 00:00 [revised] 2023/01/27 00:00 [accepted] 2023/02/04 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/03 18:03 [entrez]
 2022/07/17 00:00 [received] 2022/09/26 00:00 [accepted] 2022/11/23 21:41 [entrez] 2022/11/24 06:00 [pubmed] 2022/11/26 06:00 [medline]
 2023/05/09 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/15 06:42 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:27 [entrez]
 2022/06/24 00:00 [received] 2022/11/25 00:00 [accepted] 2022/11/24 00:00 [revised] 2022/12/16 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/15 11:16 [entrez]
 2023/05/10 00:00 [revised] 2023/02/20 00:00 [received] 2023/05/11 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/15 06:42 [pubmed] 2023/05/15 03:47 [entrez]
 2023/03/06 00:00 [received] 2023/04/28 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:36 [entrez]
 2021/11/07 00:00 [received] 2022/08/16 00:00 [accepted] 2023/06/26 06:42 [medline] 2022/09/24 06:00 [pubmed] 2022/09/23 11:23 [entrez]
 2023/02/19 00:00 [received] 2023/05/22 00:00 [revised] 2023/05/25 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 18:01 [entrez]
 2023/07/05 00:00 [received] 2023/07/07 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/07/26 01:06 [pubmed] 2023/07/25 23:37 [entrez]
 2023/01/30 00:00 [accepted] 2023/06/26 06:42 [medline] 2023/04/06 06:00 [pubmed] 2023/04/05 11:21 [entrez]
 2021/07/06 00:00 [received] 2022/03/14 00:00 [accepted] 2023/04/28 06:42 [medline] 2022/06/15 06:00 [pubmed] 2022/06/14 11:20 [entrez]
 2023/02/27 00:00 [received] 2023/03/23 00:00 [revised] 2023/03/24 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:11 [entrez] 2023/04/14 06:00 [pubmed]
 2022/09/22 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/09/21 03:23 [entrez]
 2023/04/04 00:00 [received] 2023/06/18 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 23:39 [entrez]
 2022/04/18 00:00 [received] 2022/11/14 00:00 [revised] 2022/11/24 00:00 [accepted] 2023/06/02 06:43 [medline] 2022/12/15 06:00 [pubmed] 2022/12/14 10:23 [entrez]
 2023/09/13 06:42 [medline] 2023/09/11 18:41 [pubmed] 2023/09/11 15:13 [entrez]
 2022/04/01 00:00 [received] 2022/11/01 00:00 [revised] 2022/11/14 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/01/20 06:00 [pubmed] 2023/01/19 22:01 [entrez]
 2022/05/06 00:00 [received] 2022/09/01 00:00 [revised] 2022/09/19 00:00 [accepted] 2022/10/08 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/10/07 19:13 [entrez]
 2022/11/29 00:00 [revised] 2022/07/16 00:00 [received] 2022/12/23 00:00 [accepted] 2023/01/15 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/14 02:02 [entrez]
 2022/12/03 06:00 [pubmed] 2023/03/07 06:00 [medline] 2022/12/02 04:03 [entrez]
 2022/10/25 00:00 [revised] 2022/07/13 00:00 [received] 2022/10/26 00:00 [accepted] 2022/11/17 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/11/16 04:42 [entrez]
 2022/10/26 00:00 [received] 2022/11/29 00:00 [revised] 2022/12/05 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2022/12/28 06:00 [medline] 2022/12/09 19:35 [entrez]
 2023/08/10 06:42 [medline] 2023/07/27 06:42 [pubmed] 2023/07/27 02:32 [entrez]
 2022/07/29 00:00 [received] 2023/03/08 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/04/13 06:00 [pubmed] 2023/04/12 23:31 [entrez]
 2023/02/10 00:00 [received] 2023/05/24 00:00 [accepted] 2023/06/20 06:42 [medline] 2023/06/19 06:42 [pubmed] 2023/06/19 03:06 [entrez]
 2022/12/20 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/19 11:33 [entrez]
 2022/06/27 00:00 [accepted] 2022/08/06 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/08/05 23:25 [entrez]
 2023/04/25 00:00 [received] 2023/06/28 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/16 01:06 [pubmed] 2023/07/15 18:05 [entrez]
 2023/05/10 00:00 [received] 2023/07/26 00:00 [revised] 2023/07/29 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:46 [pubmed] 2023/08/26 01:05 [entrez]
 2023/01/25 00:00 [received] 2023/02/26 00:00 [accepted] 2023/02/23 00:00 [revised] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 02:53 [entrez]
 2022/11/06 00:00 [received] 2023/03/02 00:00 [accepted] 2023/07/31 11:43 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 11:14 [entrez]
 2023/07/27 00:00 [received] 2023/08/11 00:00 [revised] 2023/08/12 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:44 [pubmed] 2023/08/26 01:16 [entrez]
 2022/10/31 00:00 [received] 2023/07/19 00:00 [accepted] 2023/08/31 06:41 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 21:43 [entrez]
 2022/08/18 00:00 [received] 2023/02/27 00:00 [revised] 2023/03/30 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 18:04 [entrez]
 2023/02/04 00:00 [received] 2023/02/25 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/19 06:00 [pubmed] 2023/03/18 19:02 [entrez]
 2023/03/06 00:00 [received] 2023/04/17 00:00 [revised] 2023/04/22 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:22 [entrez]
 2022/09/28 00:00 [received] 2022/10/19 00:00 [revised] 2022/10/21 00:00 [accepted] 2022/11/08 06:00 [pubmed] 2022/11/30 06:00 [medline] 2022/11/07 06:33 [entrez]
 2022/12/08 00:00 [received] 2023/04/20 00:00 [accepted] 2023/08/16 06:42 [medline] 2023/08/05 05:42 [pubmed] 2023/08/04 21:54 [entrez]
 2022/05/05 00:00 [received] 2023/01/05 00:00 [accepted] 2022/12/22 00:00 [revised] 2023/04/21 06:41 [medline] 2023/01/13 06:00 [pubmed] 2023/01/12 23:19 [entrez]
 2022/12/24 00:00 [received] 2023/05/07 00:00 [revised] 2023/05/16 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/06/03 11:42 [pubmed] 2023/06/02 18:01 [entrez]
 2023/06/19 13:08 [medline] 2022/03/10 06:00 [pubmed] 2022/03/09 12:23 [entrez]
 2022/06/13 00:00 [received] 2022/12/19 00:00 [accepted] 2023/02/15 21:42 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/18 06:00 [medline]
 2023/03/20 00:00 [revised] 2022/12/21 00:00 [received] 2023/03/24 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/04/06 06:00 [pubmed] 2023/04/05 06:12 [entrez]
 2023/02/24 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:27 [entrez]
 2022/04/22 06:00 [pubmed] 2023/03/25 06:00 [medline] 2022/04/21 05:21 [entrez]
 2023/07/05 06:42 [medline] 2023/07/03 19:08 [pubmed] 2023/07/03 15:13 [entrez]
 2021/12/04 00:00 [received] 2022/05/13 00:00 [accepted] 2022/04/07 00:00 [revised] 2022/10/15 06:00 [pubmed] 2023/02/22 06:00 [medline] 2022/10/14 23:39 [entrez]
 2023/06/19 13:08 [medline] 2023/05/23 06:42 [pubmed] 2023/05/23 04:43 [entrez]
 2022/05/06 00:00 [received] 2022/08/31 00:00 [accepted] 2022/11/29 21:44 [entrez] 2022/11/30 06:00 [pubmed] 2022/12/02 06:00 [medline]
 2023/02/08 06:00 [pubmed] 2023/02/10 06:00 [medline] 2023/02/07 10:07 [entrez]
 2022/10/03 00:00 [revised] 2022/08/25 00:00 [received] 2022/10/09 00:00 [accepted] 2022/11/03 06:00 [pubmed] 2023/01/03 06:00 [medline] 2022/11/02 08:44 [entrez]
 2022/09/17 00:00 [received] 2022/11/08 00:00 [accepted] 2022/11/17 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/11/16 11:18 [entrez]
 2022/05/19 00:00 [received] 2022/12/30 00:00 [accepted] 2023/01/08 23:19 [entrez] 2023/01/09 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2023/08/18 06:42 [medline] 2022/08/25 06:00 [pubmed] 2022/08/24 08:53 [entrez]
 2022/05/25 00:00 [received] 2023/01/30 00:00 [accepted] 2023/03/10 02:30 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/14 06:00 [medline]
 2022/09/13 00:00 [received] 2023/02/08 00:00 [accepted] 2023/05/24 06:42 [medline] 2023/05/23 01:06 [pubmed] 2023/05/22 21:43 [entrez]
 2022/11/18 00:00 [received] 2023/05/04 00:00 [accepted] 2022/12/19 00:00 [revised] 2023/07/28 06:43 [medline] 2023/07/27 13:10 [pubmed] 2023/07/27 11:54 [entrez]
 2023/01/05 00:00 [received] 2023/05/21 00:00 [accepted] 2023/05/10 00:00 [revised] 2023/07/10 06:42 [medline] 2023/05/27 19:14 [pubmed] 2023/05/27 14:57 [entrez]
 2023/04/17 00:00 [received] 2023/05/16 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:11 [entrez]
 2022/10/16 00:00 [received] 2022/12/01 00:00 [revised] 2022/12/06 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/12/15 18:13 [entrez]
 2022/11/10 00:00 [received] 2022/11/14 00:00 [accepted] 2024/05/01 00:00 [pmc-release] 2023/06/19 13:08 [medline] 2022/11/27 06:00 [pubmed] 2022/11/26 22:15 [entrez]
 2022/02/08 00:00 [accepted] 2022/07/10 06:00 [pubmed] 2022/12/24 06:00 [medline] 2022/07/09 11:16 [entrez]
 2022/08/24 00:00 [received] 2022/11/08 00:00 [revised] 2022/11/29 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/12/05 19:33 [entrez]
 2022/09/02 00:00 [revised] 2021/06/10 00:00 [received] 2022/11/24 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/12/12 19:42 [entrez]
 2023/02/10 00:00 [received] 2023/06/05 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/06/10 15:13 [pubmed] 2023/06/09 23:28 [entrez]
 2023/09/08 06:43 [medline] 2023/08/15 06:42 [pubmed] 2023/08/15 05:28 [entrez]
 2023/04/18 00:00 [revised] 2023/02/02 00:00 [received] 2023/07/27 06:43 [medline] 2023/05/12 07:06 [pubmed] 2023/05/12 04:02 [entrez]
 2023/01/30 00:00 [received] 2023/02/16 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/03/05 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/03/04 18:13 [entrez]
 2023/02/01 00:00 [received] 2023/05/05 00:00 [revised] 2023/05/07 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 20:55 [entrez]
 2022/09/28 00:00 [received] 2023/03/20 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/03/31 06:00 [pubmed] 2023/03/30 23:27 [entrez]
 2022/09/24 00:00 [received] 2022/10/26 00:00 [revised] 2022/11/11 00:00 [accepted] 2022/11/19 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/18 18:26 [entrez]
 2022/07/14 00:00 [received] 2022/12/30 00:00 [revised] 2023/01/08 00:00 [accepted] 2023/06/28 06:42 [medline] 2023/04/27 00:42 [pubmed] 2023/04/26 19:52 [entrez]
 2022/04/04 00:00 [received] 2022/12/15 00:00 [revised] 2023/01/22 00:00 [accepted] 2023/06/02 06:42 [medline] 2023/03/31 06:00 [pubmed] 2023/03/30 13:03 [entrez]
 2022/11/02 00:00 [received] 2023/02/09 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/09/05 06:41 [medline] 2023/06/20 13:10 [pubmed] 2023/06/20 08:23 [entrez]
 2023/01/11 00:00 [received] 2023/02/06 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/02/25 04:08 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/04/21 00:00 [revised] 2022/07/21 00:00 [received] 2023/05/08 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/05/16 13:10 [pubmed] 2023/05/16 06:13 [entrez]
 2023/06/20 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/20 00:41 [pubmed] 2023/08/19 23:16 [entrez]
 2022/11/08 00:00 [received] 2022/12/26 00:00 [accepted] 2023/01/12 23:24 [entrez] 2023/01/13 06:00 [pubmed] 2023/01/17 06:00 [medline]
 2022/07/29 00:00 [received] 2022/11/12 00:00 [revised] 2022/12/27 00:00 [accepted] 2023/05/09 10:16 [medline] 2023/01/28 06:00 [pubmed] 2023/01/27 19:25 [entrez]
 2022/11/07 00:00 [revised] 2022/03/22 00:00 [received] 2022/12/11 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/15 13:13 [entrez]
 2022/10/27 00:00 [received] 2023/01/13 00:00 [accepted] 2023/01/12 00:00 [revised] 2023/04/27 06:42 [medline] 2023/03/19 06:00 [pubmed] 2023/03/18 12:13 [entrez]
 2022/10/18 00:00 [received] 2023/01/18 00:00 [revised] 2023/01/27 00:00 [accepted] 2023/02/03 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/02/02 19:26 [entrez]
 2022/06/09 00:00 [received] 2022/10/20 00:00 [accepted] 2022/12/19 21:12 [entrez] 2022/12/20 06:00 [pubmed] 2022/12/22 06:00 [medline]
 2023/03/02 00:00 [received] 2023/04/27 00:00 [revised] 2023/05/26 00:00 [accepted] 2023/06/21 06:42 [medline] 2023/06/08 01:08 [pubmed] 2023/06/07 19:29 [entrez]
 2023/01/24 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/23 02:12 [entrez]
 2022/07/08 00:00 [received] 2023/01/03 00:00 [accepted] 2022/12/20 00:00 [revised] 2023/01/12 23:12 [entrez] 2023/01/13 06:00 [pubmed] 2023/01/17 06:00 [medline]
 2023/03/29 00:00 [received] 2023/04/18 00:00 [revised] 2023/04/20 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 18:01 [entrez]
 2022/10/13 00:00 [received] 2022/11/18 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/09 04:37 [entrez]
 2022/12/13 00:00 [received] 2023/01/12 00:00 [accepted] 2023/01/12 00:00 [revised] 2023/04/27 06:42 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 12:20 [entrez]
 2022/10/03 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/17 00:00 [accepted] 2023/06/05 06:43 [medline] 2023/04/03 06:00 [pubmed] 2023/04/02 18:01 [entrez]
 2021/12/14 00:00 [received] 2023/04/03 00:00 [accepted] 2023/04/13 06:42 [medline] 2023/04/11 23:36 [entrez] 2023/04/12 06:00 [pubmed]
 2022/11/16 00:00 [received] 2023/03/30 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/05/19 13:04 [pubmed] 2023/05/19 11:09 [entrez]
 2023/06/23 06:42 [medline] 2023/06/08 13:07 [pubmed] 2023/06/08 06:52 [entrez]
 2022/10/04 00:00 [received] 2022/12/25 00:00 [revised] 2023/01/16 00:00 [accepted] 2023/01/22 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/21 18:14 [entrez]
 2021/12/24 00:00 [received] 2022/07/18 00:00 [accepted] 2023/06/12 06:42 [medline] 2022/07/26 06:00 [pubmed] 2022/07/25 11:21 [entrez]
 2023/04/21 00:00 [revised] 2023/02/10 00:00 [received] 2023/04/28 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 13:42 [pubmed] 2023/05/08 07:43 [entrez]
 2023/09/07 06:42 [medline] 2023/09/05 18:41 [pubmed] 2023/09/05 14:03 [entrez]
 2023/04/21 06:41 [medline] 2023/03/21 06:00 [pubmed] 2023/03/20 13:20 [entrez]
 2023/04/20 00:00 [received] 2023/05/05 00:00 [revised] 2023/05/08 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:13 [entrez]
 2023/01/04 14:03 [entrez] 2023/01/05 06:00 [pubmed] 2023/01/07 06:00 [medline]
 2022/11/30 00:00 [received] 2023/02/03 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 18:24 [entrez]
 2022/09/09 00:00 [received] 2022/12/30 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/27 06:00 [pubmed] 2023/02/26 18:23 [entrez]
 2023/01/30 00:00 [accepted] 2023/06/07 06:42 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 11:33 [entrez]
 2023/08/11 06:42 [medline] 2023/08/10 12:42 [pubmed] 2023/08/10 07:24 [entrez]
 2022/01/05 00:00 [received] 2022/10/19 00:00 [revised] 2022/10/25 00:00 [accepted] 2023/04/04 06:42 [medline] 2022/11/21 06:00 [pubmed] 2022/11/20 19:25 [entrez]
 2023/04/03 06:41 [medline] 2020/12/02 06:00 [pubmed] 2020/12/01 17:08 [entrez]
 2023/01/06 13:33 [entrez] 2023/01/07 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2022/11/15 00:00 [received] 2023/02/07 00:00 [accepted] 2023/03/06 03:52 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/08 06:00 [medline]
 2024/07/01 00:00 [pmc-release] 2023/07/05 06:42 [medline] 2023/03/11 06:00 [pubmed] 2023/03/10 09:53 [entrez]
 2023/01/15 00:00 [received] 2023/05/04 00:00 [revised] 2023/05/14 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 18:00 [entrez]
 2022/10/15 00:00 [received] 2022/12/15 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/09 04:37 [entrez]
 2022/10/14 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/05 06:00 [pubmed] 2023/02/04 18:18 [entrez]
 2023/02/09 00:00 [received] 2023/06/12 00:00 [accepted] 2023/08/02 06:42 [medline] 2023/07/31 06:43 [pubmed] 2023/07/31 04:53 [entrez]
 2021/11/10 00:00 [received] 2023/05/17 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 23:25 [entrez]
 2022/12/22 00:00 [received] 2023/01/20 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 18:06 [entrez]
 2022/12/15 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/14 19:32 [entrez]
 2023/07/28 06:42 [medline] 2023/05/18 13:09 [pubmed] 2023/05/18 11:17 [entrez]
 2023/03/06 00:00 [received] 2023/06/01 00:00 [accepted] 2023/06/01 00:00 [revised] 2023/07/10 06:42 [medline] 2023/06/08 01:08 [pubmed] 2023/06/07 23:26 [entrez]
 2022/11/02 00:00 [received] 2023/03/26 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 18:06 [entrez]
 2023/04/07 06:42 [medline] 2022/09/21 06:00 [pubmed] 2022/09/20 13:34 [entrez]
 2023/04/19 00:00 [received] 2023/07/14 00:00 [accepted] 2023/08/29 12:45 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 04:44 [entrez]
 2023/01/04 06:00 [pubmed] 2023/01/26 06:00 [medline] 2023/01/03 04:03 [entrez]
 2022/10/24 00:00 [received] 2023/03/27 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/29 19:11 [pubmed] 2023/06/29 14:04 [entrez]
 2022/03/15 00:00 [received] 2022/09/12 00:00 [revised] 2022/10/01 00:00 [accepted] 2023/04/21 06:41 [medline] 2022/11/02 06:00 [pubmed] 2022/11/01 23:12 [entrez]
 2022/10/27 00:00 [received] 2022/12/12 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2022/02/04 00:00 [received] 2022/10/10 00:00 [accepted] 2023/04/26 06:41 [medline] 2023/04/25 00:41 [pubmed] 2023/04/24 09:42 [entrez]
 2022/08/11 00:00 [received] 2022/09/28 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/01/18 11:29 [entrez] 2023/01/19 06:00 [pubmed] 2023/01/21 06:00 [medline]
 2022/10/18 00:00 [received] 2023/03/20 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 21:37 [entrez]
 2022/09/29 00:00 [received] 2023/03/23 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/06/19 13:08 [medline] 2023/04/07 06:00 [pubmed] 2023/04/06 20:52 [entrez]
 2022/03/21 00:00 [received] 2022/11/30 00:00 [accepted] 2023/01/05 06:00 [pubmed] 2023/02/11 06:00 [medline] 2023/01/04 19:02 [entrez]
 2023/01/13 00:00 [received] 2023/06/12 00:00 [accepted] 2023/06/30 06:42 [medline] 2023/06/29 01:08 [pubmed] 2023/06/28 23:21 [entrez]
 2022/08/30 00:00 [received] 2023/01/27 00:00 [accepted] 2023/01/20 00:00 [revised] 2023/07/04 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 04:32 [entrez]
 2022/10/22 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/10/21 01:43 [entrez]
 2023/07/06 06:42 [medline] 2023/06/08 19:14 [pubmed] 2023/06/08 16:53 [entrez]
 2022/07/06 00:00 [received] 2022/11/30 00:00 [accepted] 2023/03/22 03:43 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/24 06:00 [medline]
 2023/01/20 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/19 07:32 [entrez]
 2023/01/11 12:13 [entrez] 2023/01/12 06:00 [pubmed] 2023/01/14 06:00 [medline]
 2024/08/01 00:00 [pmc-release] 2023/07/21 06:43 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 08:37 [entrez]
 2022/07/05 00:00 [received] 2022/11/23 00:00 [accepted] 2022/11/21 00:00 [revised] 2022/12/15 06:00 [pubmed] 2023/02/25 06:00 [medline] 2022/12/14 23:26 [entrez]
 2023/04/24 00:00 [revised] 2023/02/04 00:00 [received] 2023/05/05 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/19 06:42 [pubmed] 2023/05/19 03:44 [entrez]
 2022/01/28 00:00 [received] 2022/09/06 00:00 [accepted] 2022/11/21 21:43 [entrez] 2022/11/22 06:00 [pubmed] 2022/11/24 06:00 [medline]
 2023/02/15 00:00 [received] 2023/03/22 00:00 [revised] 2023/03/30 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:13 [entrez] 2023/04/14 06:00 [pubmed]
 2023/04/12 06:42 [medline] 2023/01/18 06:00 [pubmed] 2023/01/17 10:05 [entrez]
 2022/06/24 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/06/23 05:03 [entrez]
 2022/02/27 00:00 [received] 2023/03/27 00:00 [accepted] 2023/04/19 06:41 [medline] 2023/04/17 13:43 [entrez] 2023/04/18 06:00 [pubmed]
 2022/06/12 00:00 [received] 2022/11/04 00:00 [revised] 2022/11/17 00:00 [accepted] 2022/12/11 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/10 22:03 [entrez]
 2022/01/03 00:00 [received] 2022/12/31 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/26 18:08 [entrez]
 2022/05/18 00:00 [received] 2022/07/28 00:00 [revised] 2022/08/30 00:00 [accepted] 2022/08/31 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/08/30 18:43 [entrez]
 2022/05/07 00:00 [received] 2022/04/10 00:00 [accepted] 2022/12/30 21:43 [entrez] 2022/12/31 06:00 [pubmed] 2023/01/04 06:00 [medline]
 2022/12/03 00:00 [received] 2023/01/23 00:00 [revised] 2023/01/23 00:00 [accepted] 2023/02/01 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/31 19:21 [entrez]
 2022/05/26 00:00 [received] 2022/12/02 00:00 [accepted] 2023/03/29 06:05 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 21:46 [entrez]
 2022/11/26 00:00 [received] 2023/04/04 00:00 [accepted] 2024/07/25 00:00 [pmc-release] 2023/07/26 06:42 [medline] 2023/06/01 01:08 [pubmed] 2023/05/31 21:53 [entrez]
 2023/04/28 00:00 [accepted] 2023/06/22 06:42 [medline] 2023/06/03 11:42 [pubmed] 2023/06/02 23:28 [entrez]
 2021/12/21 00:00 [received] 2022/10/28 00:00 [accepted] 2023/02/16 13:43 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/22 06:00 [medline]
 2022/12/20 00:00 [received] 2023/02/03 00:00 [revised] 2023/04/05 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 18:02 [entrez]
 2022/08/29 00:00 [received] 2023/03/03 00:00 [revised] 2023/03/14 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/05/22 06:42 [medline] 2023/04/13 06:00 [pubmed] 2023/04/12 18:09 [entrez]
 2022/10/02 00:00 [revised] 2022/09/07 00:00 [received] 2022/10/17 00:00 [accepted] 2022/10/28 06:00 [pubmed] 2023/03/07 06:00 [medline] 2022/10/27 06:32 [entrez]
 2022/11/22 00:00 [received] 2022/11/27 00:00 [accepted] 2022/12/18 06:00 [pubmed] 2023/01/13 06:00 [medline] 2022/12/17 18:13 [entrez]
 2023/04/21 00:00 [received] 2023/06/20 00:00 [accepted] 2023/07/26 06:42 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:33 [entrez]
 2022/03/19 00:00 [received] 2023/06/05 00:00 [accepted] 2023/08/25 06:42 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 23:28 [entrez]
 2022/11/16 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/15 07:12 [entrez]
 2023/02/06 08:03 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2022/10/27 00:00 [received] 2023/07/03 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/08/07 06:42 [pubmed] 2023/08/07 04:25 [entrez]
 2022/09/20 00:00 [received] 2022/11/30 00:00 [accepted] 2023/03/14 20:12 [entrez] 2023/03/15 06:00 [pubmed] 2023/03/17 06:00 [medline]
 2023/05/26 00:00 [received] 2023/07/24 00:00 [revised] 2023/07/26 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/31 00:42 [pubmed] 2023/07/30 19:14 [entrez]
 2022/10/09 00:00 [received] 2023/04/21 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 21:12 [entrez]
 2023/02/23 00:00 [received] 2023/04/03 00:00 [revised] 2023/04/07 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/27 18:41 [pubmed] 2023/04/27 13:23 [entrez]
 2022/05/02 00:00 [received] 2022/11/30 00:00 [revised] 2022/12/12 00:00 [accepted] 2022/12/19 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/18 18:27 [entrez]
 2023/08/21 06:42 [medline] 2023/08/17 18:42 [pubmed] 2023/08/17 15:43 [entrez]
 2023/02/09 06:00 [pubmed] 2023/03/24 06:00 [medline] 2023/02/08 13:12 [entrez]
 2021/07/14 00:00 [received] 2021/09/26 00:00 [accepted] 2021/10/22 06:00 [pubmed] 2022/12/17 06:00 [medline] 2021/10/21 05:43 [entrez]
 2022/10/10 00:00 [received] 2023/02/22 00:00 [revised] 2023/02/22 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/06/26 06:41 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 19:32 [entrez]
 2022/10/28 00:00 [received] 2023/01/19 00:00 [accepted] 2023/02/23 02:12 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/05/19 06:42 [medline] 2023/05/17 19:12 [pubmed] 2023/05/17 14:03 [entrez]
 2023/05/13 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/08/28 06:42 [medline] 2023/06/10 15:13 [pubmed] 2023/06/09 23:31 [entrez]
 2022/07/29 00:00 [received] 2022/10/21 00:00 [revised] 2022/10/31 00:00 [accepted] 2022/11/08 06:00 [pubmed] 2022/12/06 06:00 [medline] 2022/11/07 19:23 [entrez]
 2023/03/31 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/07 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/28 13:11 [pubmed] 2023/07/28 11:43 [entrez]
 2022/08/14 00:00 [received] 2023/03/10 00:00 [accepted] 2023/03/23 14:24 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2022/10/06 00:00 [received] 2023/01/10 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/02/07 06:00 [pubmed] 2023/02/06 11:20 [entrez]
 2022/12/22 00:00 [received] 2023/01/25 00:00 [revised] 2023/02/13 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:23 [entrez]
 2023/02/08 00:00 [revised] 2022/12/01 00:00 [received] 2023/02/20 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 03:53 [entrez]
 2022/10/25 00:00 [received] 2022/12/19 00:00 [revised] 2022/12/29 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/02/08 06:00 [medline] 2023/01/09 04:33 [entrez]
 2022/04/25 00:00 [received] 2023/02/02 00:00 [accepted] 2023/02/22 09:56 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/07/23 00:00 [accepted] 2024/09/01 00:00 [pmc-release] 2023/09/07 06:42 [medline] 2023/08/02 01:07 [pubmed] 2023/08/01 23:30 [entrez]
 2023/04/12 00:00 [received] 2023/06/23 00:00 [revised] 2023/06/30 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:02 [entrez]
 2023/05/18 00:00 [received] 2023/06/12 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/13 19:15 [pubmed] 2023/07/13 15:31 [entrez]
 2022/09/02 00:00 [received] 2022/11/25 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/07 18:22 [entrez]
 2023/06/13 06:42 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 00:22 [entrez]
 2022/05/07 00:00 [received] 2022/07/20 00:00 [revised] 2022/07/21 00:00 [accepted] 2022/09/03 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/09/02 22:07 [entrez]
 2023/03/22 07:08 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/24 06:00 [medline]
 2023/06/06 00:00 [received] 2023/07/30 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 23:44 [entrez]
 2022/12/19 00:00 [received] 2023/01/20 00:00 [revised] 2023/01/23 00:00 [accepted] 2023/02/25 02:53 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/05/12 07:06 [medline] 2023/01/25 06:00 [pubmed] 2023/01/24 03:43 [entrez]
 2023/04/19 00:00 [revised] 2022/11/08 00:00 [received] 2023/05/17 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/05/20 19:13 [pubmed] 2023/05/20 15:01 [entrez]
 2023/07/27 00:00 [received] 2023/08/14 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/09 11:44 [pubmed] 2023/09/09 01:11 [entrez]
 2022/11/10 00:00 [received] 2023/02/10 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 19:04 [entrez]
 2023/05/23 00:00 [revised] 2023/03/16 00:00 [received] 2023/05/24 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/05/27 19:14 [pubmed] 2023/05/27 15:10 [entrez]
 2023/04/12 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 11:33 [entrez]
 2022/01/10 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/06/01 23:42 [pubmed] 2023/06/01 12:52 [entrez]
 2023/09/14 06:42 [medline] 2022/10/04 06:00 [pubmed] 2022/10/03 07:53 [entrez]
 2023/02/14 00:00 [received] 2023/03/16 00:00 [accepted] 2023/03/31 06:41 [medline] 2023/03/29 23:54 [entrez] 2023/03/30 06:00 [pubmed]
 2022/04/30 00:00 [received] 2022/08/14 00:00 [revised] 2022/12/22 00:00 [accepted] 2022/12/27 06:00 [pubmed] 2023/01/18 06:00 [medline] 2022/12/26 19:15 [entrez]
 2023/03/08 20:53 [entrez] 2023/03/09 06:00 [pubmed] 2023/03/11 06:00 [medline]
 2022/12/30 06:00 [pubmed] 2023/01/17 06:00 [medline] 2022/12/29 14:04 [entrez]
 2022/09/16 00:00 [received] 2022/11/07 00:00 [revised] 2022/12/18 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/04/04 06:42 [medline] 2023/01/18 06:00 [pubmed] 2023/01/17 19:21 [entrez]
 2023/02/14 00:00 [received] 2023/03/27 00:00 [revised] 2023/03/28 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/04/03 06:00 [pubmed] 2023/04/02 18:05 [entrez]
 2023/03/03 00:00 [received] 2023/03/20 00:00 [accepted] 2023/05/30 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 20:31 [entrez]
 2023/06/19 13:08 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 00:24 [entrez]
 2022/04/17 00:00 [received] 2022/11/28 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/02/08 06:00 [medline] 2022/12/12 10:11 [entrez]
 2023/05/08 06:41 [medline] 2022/12/17 06:00 [pubmed] 2022/12/16 06:33 [entrez]
 2023/03/28 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/06/04 01:08 [pubmed] 2023/06/03 18:07 [entrez]
 2023/02/15 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/02 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 22:39 [entrez]
 2023/06/30 06:43 [medline] 2023/06/28 19:15 [pubmed] 2023/06/28 14:03 [entrez]
 2022/06/01 00:00 [received] 2022/09/09 00:00 [accepted] 2022/09/08 00:00 [revised] 2022/10/17 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/10/16 23:18 [entrez]
 2022/04/26 00:00 [received] 2022/10/12 00:00 [accepted] 2023/04/13 06:42 [medline] 2022/11/23 06:00 [pubmed] 2022/11/22 23:38 [entrez]
 2022/05/27 00:00 [received] 2022/09/09 00:00 [accepted] 2022/10/29 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/10/28 21:43 [entrez]
 2023/07/17 00:00 [accepted] 2023/08/18 06:42 [medline] 2023/08/08 12:42 [pubmed] 2023/08/08 11:18 [entrez]
 2022/12/29 00:00 [received] 2023/04/14 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 06:42 [pubmed] 2023/05/08 03:45 [entrez]
 2022/01/04 00:00 [received] 2022/06/13 00:00 [revised] 2022/11/09 00:00 [accepted] 2023/01/15 06:00 [pubmed] 2023/02/18 06:00 [medline] 2023/01/14 18:15 [entrez]
 2022/12/15 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/14 07:23 [entrez]
 2022/08/24 00:00 [received] 2022/09/27 00:00 [revised] 2022/10/08 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/03/30 02:03 [entrez] 2023/03/31 06:00 [pubmed]
 2023/06/01 06:42 [medline] 2023/05/29 06:41 [pubmed] 2023/05/29 04:17 [entrez]
 2023/01/30 00:00 [received] 2023/04/18 00:00 [revised] 2023/05/08 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/30 01:06 [pubmed] 2023/05/29 18:02 [entrez]
 2021/08/24 00:00 [received] 2022/12/07 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/15 18:29 [entrez]
 2023/06/19 13:08 [medline] 2023/05/17 06:42 [pubmed] 2023/05/17 03:50 [entrez]
 2023/01/04 00:00 [received] 2023/02/17 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 18:13 [entrez]
 2022/11/28 00:00 [received] 2022/12/28 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/23 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/22 18:14 [entrez]
 2022/09/24 00:00 [received] 2023/03/09 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/31 14:05 [entrez] 2023/04/01 06:00 [pubmed]
 2023/01/18 06:00 [pubmed] 2023/02/07 06:00 [medline] 2023/01/17 16:03 [entrez]
 2022/07/17 00:00 [received] 2023/02/08 00:00 [accepted] 2023/05/15 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 23:22 [entrez]
 2023/05/10 00:00 [received] 2023/05/31 00:00 [revised] 2023/06/06 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/08 01:10 [entrez]
 2023/05/25 06:42 [medline] 2022/12/16 06:00 [pubmed] 2022/12/15 01:43 [entrez]
 2022/06/30 00:00 [received] 2023/02/09 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/21 06:44 [pubmed] 2023/07/21 04:13 [entrez]
 2023/04/17 00:00 [revised] 2023/02/21 00:00 [received] 2023/05/28 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/19 06:41 [pubmed] 2023/06/19 02:06 [entrez]
 2022/12/14 06:00 [pubmed] 2023/03/21 06:00 [medline] 2022/12/13 07:42 [entrez]
 2023/06/01 00:00 [revised] 2023/02/13 00:00 [received] 2023/06/09 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/13 13:12 [pubmed] 2023/06/13 10:52 [entrez]
 2023/01/22 00:00 [received] 2023/05/22 00:00 [accepted] 2023/07/05 06:42 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:49 [entrez]
 2022/11/22 00:00 [revised] 2022/07/23 00:00 [received] 2022/12/20 00:00 [accepted] 2023/01/05 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/04 21:13 [entrez]
 2022/09/28 00:00 [received] 2022/10/26 00:00 [accepted] 2022/12/14 21:52 [entrez] 2022/12/15 06:00 [pubmed] 2022/12/17 06:00 [medline]
 2022/12/23 00:00 [received] 2023/02/24 00:00 [revised] 2023/02/27 00:00 [accepted] 2023/03/11 01:19 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2023/01/09 00:00 [revised] 2022/10/29 00:00 [received] 2023/02/09 00:00 [accepted] 2023/03/15 14:12 [entrez] 2023/03/16 06:00 [pubmed] 2023/03/21 06:00 [medline]
 2023/04/20 00:00 [received] 2023/05/07 00:00 [revised] 2023/05/15 00:00 [accepted] 2023/07/28 06:43 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 19:25 [entrez]
 2022/09/25 00:00 [received] 2022/11/04 00:00 [accepted] 2022/11/03 00:00 [revised] 2022/11/10 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/09 11:15 [entrez]
 2021/10/25 00:00 [received] 2022/01/23 00:00 [accepted] 2022/02/03 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/02/02 12:15 [entrez]
 2024/09/08 00:00 [pmc-release] 2023/09/11 06:43 [medline] 2023/09/08 12:43 [pubmed] 2023/09/08 07:23 [entrez]
 2023/09/14 06:42 [medline] 2023/08/15 12:43 [pubmed] 2023/08/15 11:27 [entrez]
 2023/03/15 00:00 [received] 2023/06/12 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:02 [entrez]
 2023/06/04 00:00 [revised] 2022/12/23 00:00 [received] 2023/06/21 00:00 [accepted] 2023/09/14 06:42 [medline] 2023/07/05 06:42 [pubmed] 2023/07/05 00:43 [entrez]
 2022/12/25 00:00 [received] 2023/01/11 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/02/25 01:23 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/12/05 00:00 [received] 2023/02/16 00:00 [accepted] 2023/02/16 00:00 [revised] 2023/03/02 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/03/01 00:18 [entrez]
 2023/06/28 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/08 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/07/29 11:49 [pubmed] 2023/07/29 01:45 [entrez]
 2023/02/15 00:00 [received] 2023/06/10 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/06/26 13:07 [pubmed] 2023/06/26 11:12 [entrez]
 2023/07/12 06:42 [medline] 2023/05/18 13:09 [pubmed] 2023/05/18 09:23 [entrez]
 2022/08/02 00:00 [received] 2022/12/14 00:00 [accepted] 2023/02/15 21:42 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/18 06:00 [medline]
 2021/08/16 06:00 [pubmed] 2022/12/21 06:00 [medline] 2021/08/15 20:57 [entrez]
 2022/09/26 00:00 [received] 2022/11/22 00:00 [revised] 2022/12/05 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2022/12/28 06:00 [medline] 2022/12/09 19:35 [entrez]
 2022/12/12 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/02/11 01:21 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/03/31 00:00 [received] 2023/04/22 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:29 [entrez]
 2022/11/22 00:00 [received] 2023/04/15 00:00 [revised] 2023/04/22 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/06 19:42 [pubmed] 2023/05/06 18:00 [entrez]
 2022/09/28 00:00 [received] 2023/01/17 00:00 [revised] 2023/02/04 00:00 [accepted] 2023/02/09 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/08 19:23 [entrez]
 2023/01/13 00:00 [received] 2023/07/14 00:00 [revised] 2023/07/15 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/24 00:41 [pubmed] 2023/07/23 18:01 [entrez]
 2021/09/29 00:00 [received] 2022/04/14 00:00 [revised] 2022/04/22 00:00 [accepted] 2022/09/27 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/09/26 15:48 [entrez]
 2022/11/29 00:00 [received] 2023/04/24 00:00 [accepted] 2023/05/24 06:42 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 12:21 [entrez]
 2023/06/30 06:42 [medline] 2023/04/21 00:41 [pubmed] 2023/04/20 18:52 [entrez]
 2022/10/17 00:00 [received] 2023/02/07 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/07/14 13:05 [medline] 2023/05/10 00:41 [pubmed] 2023/05/09 18:42 [entrez]
 2021/09/06 00:00 [received] 2022/06/14 00:00 [accepted] 2022/08/03 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/08/02 11:20 [entrez]
 2023/03/28 00:00 [received] 2023/05/11 00:00 [revised] 2023/05/30 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/01 01:08 [pubmed] 2023/07/31 18:52 [entrez]
 2022/11/19 00:00 [received] 2023/02/09 00:00 [accepted] 2023/04/06 10:16 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 06:03 [entrez]
 2022/07/30 00:00 [received] 2023/06/19 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/07/01 11:41 [pubmed] 2023/06/30 23:32 [entrez]
 2023/06/19 13:08 [medline] 2022/12/02 06:00 [pubmed] 2022/12/01 11:12 [entrez]
 2022/07/20 00:00 [accepted] 2022/08/30 06:00 [pubmed] 2023/02/14 06:00 [medline] 2022/08/29 06:26 [entrez]
 2022/11/22 00:00 [received] 2023/03/20 00:00 [accepted] 2023/04/25 10:20 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:45 [entrez]
 2022/12/20 00:00 [received] 2023/01/30 00:00 [revised] 2023/02/01 00:00 [accepted] 2023/02/08 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/02/07 19:11 [entrez]
 2022/12/28 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/02/11 01:19 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/03/10 00:00 [received] 2023/03/29 00:00 [revised] 2023/04/11 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:54 [entrez]
 2022/12/13 00:00 [revised] 2022/10/17 00:00 [received] 2022/12/23 00:00 [accepted] 2023/06/07 06:42 [medline] 2023/01/05 06:00 [pubmed] 2023/01/04 02:23 [entrez]
 2023/07/06 06:42 [medline] 2022/11/04 06:00 [pubmed] 2022/11/03 08:22 [entrez]
 2022/11/25 00:00 [revised] 2022/08/05 00:00 [received] 2022/12/01 00:00 [accepted] 2022/12/14 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/13 08:03 [entrez]
 2022/11/02 00:00 [received] 2023/05/21 00:00 [revised] 2023/06/02 00:00 [accepted] 2023/06/20 06:42 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 18:11 [entrez]
 2023/08/25 06:42 [medline] 2022/07/09 06:00 [pubmed] 2022/07/08 03:04 [entrez]
 2022/12/15 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/25 00:00 [accepted] 2023/06/02 06:42 [medline] 2023/04/02 06:00 [pubmed] 2023/04/01 19:30 [entrez]
 2023/02/03 06:00 [pubmed] 2023/02/18 06:00 [medline] 2023/02/02 06:13 [entrez]
 2021/08/20 00:00 [received] 2023/01/16 00:00 [accepted] 2023/09/08 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 11:22 [entrez]
 2023/03/06 00:00 [received] 2023/06/21 00:00 [revised] 2023/07/11 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/07/29 06:42 [pubmed] 2023/07/28 18:03 [entrez]
 2022/07/25 00:00 [received] 2023/01/09 00:00 [accepted] 2023/01/25 13:33 [entrez] 2023/01/26 06:00 [pubmed] 2023/01/28 06:00 [medline]
 2023/02/13 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/08 23:41 [entrez] 2023/03/09 06:00 [pubmed] 2023/03/11 06:00 [medline]
 2023/04/03 00:00 [received] 2023/05/24 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/30 01:06 [pubmed] 2023/05/29 18:01 [entrez]
 2022/11/01 00:00 [received] 2022/11/24 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2023/01/10 00:00 [received] 2023/06/13 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 18:05 [entrez]
 2021/11/22 00:00 [received] 2022/03/15 00:00 [revised] 2022/03/17 00:00 [accepted] 2023/06/08 06:42 [medline] 2022/05/28 06:00 [pubmed] 2022/05/27 01:03 [entrez]
 2022/02/07 00:00 [received] 2023/02/01 00:00 [revised] 2023/03/22 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/04/19 06:00 [pubmed] 2023/04/18 06:00 [entrez]
 2022/10/18 00:00 [received] 2023/03/13 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/26 06:00 [pubmed] 2023/03/25 19:01 [entrez]
 2021/09/24 00:00 [received] 2022/09/05 00:00 [revised] 2022/11/19 00:00 [accepted] 2023/02/27 06:00 [pubmed] 2023/03/10 06:00 [medline] 2023/02/26 18:07 [entrez]
 2023/01/26 00:00 [received] 2023/06/05 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 04:21 [entrez]
 2023/02/22 00:00 [received] 2023/02/22 00:00 [accepted] 2023/03/20 11:04 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/23 06:00 [medline]
 2022/04/14 00:00 [received] 2022/08/30 00:00 [accepted] 2023/10/31 00:00 [pmc-release] 2022/10/31 21:41 [entrez] 2022/11/01 06:00 [pubmed] 2022/11/03 06:00 [medline]
 2022/07/26 00:00 [received] 2023/02/13 00:00 [accepted] 2023/02/24 00:51 [entrez] 2023/02/25 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/08/12 00:00 [received] 2023/04/03 00:00 [accepted] 2023/04/13 06:43 [medline] 2023/04/11 23:24 [entrez] 2023/04/12 06:00 [pubmed]
 2022/12/07 00:00 [revised] 2022/08/18 00:00 [received] 2022/12/07 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2022/12/21 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/20 05:43 [entrez]
 2023/03/10 00:00 [received] 2023/05/08 00:00 [revised] 2023/05/26 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:01 [entrez]
 2023/05/24 00:00 [received] 2023/08/07 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:29 [entrez]
 2022/07/19 00:00 [received] 2022/11/22 00:00 [accepted] 2023/01/30 21:44 [entrez] 2023/01/31 06:00 [pubmed] 2023/02/02 06:00 [medline]
 2022/11/21 00:00 [received] 2023/03/31 00:00 [accepted] 2023/02/24 00:00 [revised] 2023/07/21 06:43 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 11:23 [entrez]
 2022/12/18 00:00 [received] 2023/01/09 00:00 [revised] 2023/01/10 00:00 [accepted] 2023/01/21 01:27 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/06/06 00:00 [received] 2022/09/16 00:00 [accepted] 2022/11/21 21:43 [entrez] 2022/11/22 06:00 [pubmed] 2022/11/24 06:00 [medline]
 2022/09/03 00:00 [revised] 2021/11/08 00:00 [received] 2022/09/06 00:00 [accepted] 2022/09/12 06:00 [pubmed] 2023/01/31 06:00 [medline] 2022/09/11 03:42 [entrez]
 2023/03/22 00:00 [received] 2023/07/13 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 23:29 [entrez]
 2023/02/10 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/13 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/04/24 00:41 [pubmed] 2023/04/23 19:30 [entrez]
 2023/01/11 00:00 [received] 2023/02/18 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/04/05 06:42 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 20:28 [entrez]
 2021/08/06 00:00 [revised] 2021/05/07 00:00 [received] 2021/09/02 00:00 [accepted] 2021/09/07 06:00 [pubmed] 2023/02/14 06:00 [medline] 2021/09/06 09:51 [entrez]
 2023/09/21 00:00 [pmc-release] 2023/03/21 13:43 [entrez] 2023/03/22 06:00 [pubmed] 2023/03/24 06:00 [medline]
 2022/07/26 00:00 [received] 2023/01/13 00:00 [accepted] 2023/03/28 19:05 [medline] 2023/01/26 06:00 [pubmed] 2023/01/25 11:21 [entrez]
 2023/08/08 06:42 [medline] 2023/08/07 06:41 [pubmed] 2023/08/07 00:13 [entrez]
 2022/11/06 00:00 [received] 2022/12/19 00:00 [revised] 2022/12/28 00:00 [accepted] 2023/01/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/05 18:06 [entrez]
 2022/06/09 00:00 [received] 2023/03/27 00:00 [accepted] 2023/03/23 00:00 [revised] 2023/04/11 06:42 [medline] 2023/04/08 23:14 [entrez] 2023/04/09 06:00 [pubmed]
 2022/10/11 00:00 [received] 2023/01/04 00:00 [accepted] 2024/03/15 00:00 [pmc-release] 2023/01/26 06:00 [pubmed] 2023/03/10 06:00 [medline] 2023/01/25 10:32 [entrez]
 2023/06/07 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 23:21 [entrez]
 2022/12/02 00:00 [received] 2023/04/19 00:00 [accepted] 2023/04/24 06:41 [medline] 2023/04/21 00:42 [pubmed] 2023/04/20 23:24 [entrez]
 2023/04/06 00:00 [revised] 2022/12/30 00:00 [received] 2023/04/12 00:00 [accepted] 2023/06/23 06:42 [medline] 2023/04/22 19:42 [pubmed] 2023/04/22 12:12 [entrez]
 2022/03/27 00:00 [received] 2022/10/24 00:00 [accepted] 2022/12/17 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/12/16 21:12 [entrez]
 2023/06/09 00:00 [revised] 2023/04/18 00:00 [received] 2023/06/15 00:00 [accepted] 2023/09/08 06:42 [medline] 2023/06/19 13:08 [pubmed] 2023/06/19 11:11 [entrez]
 2023/03/16 00:00 [received] 2023/05/03 00:00 [revised] 2023/05/14 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/05 00:41 [pubmed] 2023/06/04 18:01 [entrez]
 2022/05/04 00:00 [received] 2022/09/06 00:00 [accepted] 2022/11/05 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/04 00:41 [entrez]
 2023/09/01 06:42 [medline] 2023/07/28 13:10 [pubmed] 2023/07/28 09:03 [entrez]
 2023/05/02 00:00 [revised] 2023/02/13 00:00 [received] 2023/05/03 00:00 [accepted] 2023/05/23 06:42 [medline] 2023/05/22 13:04 [pubmed] 2023/05/22 06:03 [entrez]
 2022/02/24 00:00 [received] 2022/05/18 00:00 [revised] 2022/05/18 00:00 [accepted] 2023/06/01 06:42 [medline] 2022/08/19 06:00 [pubmed] 2022/08/18 08:04 [entrez]
 2021/04/24 00:00 [received] 2021/06/29 00:00 [revised] 2021/07/02 00:00 [accepted] 2024/02/01 00:00 [pmc-release] 2021/10/13 06:00 [pubmed] 2023/01/11 06:00 [medline] 2021/10/12 05:49 [entrez]
 2023/02/20 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/26 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 19:28 [entrez]
 2023/02/09 00:00 [received] 2023/03/14 00:00 [revised] 2023/04/18 00:00 [accepted] 2023/06/14 06:42 [medline] 2023/04/24 00:41 [pubmed] 2023/04/23 19:31 [entrez]
 2022/07/11 00:00 [received] 2022/12/13 00:00 [accepted] 2023/03/06 21:43 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/09 06:00 [medline]
 2022/09/07 00:00 [received] 2022/12/29 00:00 [revised] 2023/02/03 00:00 [accepted] 2024/02/06 00:00 [pmc-release] 2023/04/11 06:42 [medline] 2023/02/07 06:00 [pubmed] 2023/02/06 09:53 [entrez]
 2022/09/29 00:00 [received] 2023/07/18 00:00 [accepted] 2023/09/07 06:42 [medline] 2023/08/07 13:10 [pubmed] 2023/08/07 09:13 [entrez]
 2022/10/07 00:00 [received] 2022/11/20 00:00 [revised] 2022/12/07 00:00 [accepted] 2022/12/25 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/24 18:15 [entrez]
 2022/10/07 00:00 [received] 2022/11/07 00:00 [accepted] 2023/01/19 21:42 [entrez] 2023/01/20 06:00 [pubmed] 2023/01/24 06:00 [medline]
 2022/10/17 00:00 [received] 2022/11/17 00:00 [revised] 2022/11/21 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/01/18 06:00 [medline] 2022/12/05 18:23 [entrez]
 2023/01/12 13:54 [entrez] 2023/01/13 06:00 [pubmed] 2023/01/17 06:00 [medline]
 2022/06/30 00:00 [received] 2023/01/13 00:00 [accepted] 2023/02/14 13:33 [entrez] 2023/02/15 06:00 [pubmed] 2023/02/17 06:00 [medline]
 2023/02/01 00:00 [received] 2023/04/20 00:00 [accepted] 2023/05/05 06:42 [medline] 2023/05/04 00:42 [pubmed] 2023/05/03 23:40 [entrez]
 2022/08/29 00:00 [received] 2022/12/17 00:00 [accepted] 2023/01/11 23:37 [entrez] 2023/01/12 06:00 [pubmed] 2023/01/14 06:00 [medline]
 2022/07/21 00:00 [received] 2023/02/11 00:00 [accepted] 2023/04/10 06:42 [medline] 2023/04/06 23:17 [entrez] 2023/04/07 06:00 [pubmed]
 2022/06/14 00:00 [received] 2023/02/01 00:00 [accepted] 2024/05/01 00:00 [pmc-release] 2023/05/12 07:06 [medline] 2023/04/21 00:41 [pubmed] 2023/04/20 21:03 [entrez]
 2022/10/26 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 03:03 [entrez]
 2023/06/26 06:42 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 11:33 [entrez]
 2022/06/17 00:00 [received] 2023/01/10 00:00 [accepted] 2023/04/26 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 21:42 [entrez]
 2023/07/29 00:00 [received] 2023/08/10 00:00 [revised] 2023/08/11 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:47 [pubmed] 2023/08/26 01:17 [entrez]
 2022/03/24 00:00 [received] 2022/08/12 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/08/21 06:00 [pubmed] 2022/12/27 06:00 [medline] 2022/08/20 06:02 [entrez]
 2022/12/12 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/03 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 18:02 [entrez]
 2023/06/30 06:42 [medline] 2023/06/28 19:15 [pubmed] 2023/06/28 17:03 [entrez]
 2023/07/01 00:00 [received] 2023/08/11 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:46 [pubmed] 2023/08/26 01:05 [entrez]
 2022/08/10 00:00 [received] 2022/10/06 06:00 [pubmed] 2023/01/20 06:00 [medline] 2022/10/05 04:32 [entrez]
 2022/07/18 00:00 [received] 2022/12/15 00:00 [accepted] 2022/12/30 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/12/29 18:17 [entrez]
 2023/04/26 00:00 [revised] 2023/02/26 00:00 [received] 2023/06/07 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/06/12 13:06 [pubmed] 2023/06/12 09:44 [entrez]
 2022/12/21 00:00 [received] 2023/03/27 00:00 [accepted] 2023/03/26 00:00 [revised] 2023/05/18 06:42 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 11:13 [entrez]
 2022/11/01 00:00 [received] 2022/12/11 00:00 [revised] 2022/12/15 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2023/01/03 06:00 [pubmed] 2023/02/11 06:00 [medline] 2023/01/02 18:05 [entrez]
 2022/08/17 00:00 [received] 2023/01/04 00:00 [revised] 2023/01/05 00:00 [accepted] 2023/01/15 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/14 18:11 [entrez]
 2022/12/22 00:00 [received] 2023/01/26 00:00 [revised] 2023/01/28 00:00 [accepted] 2023/02/11 01:35 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/06/08 06:42 [medline] 2023/06/06 13:10 [pubmed] 2023/06/06 10:53 [entrez]
 2022/03/10 00:00 [received] 2023/02/22 00:00 [accepted] 2023/04/26 06:42 [medline] 2023/04/25 00:41 [pubmed] 2023/04/24 09:42 [entrez]
 2022/09/21 00:00 [received] 2022/11/24 00:00 [accepted] 2022/12/02 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/01 23:51 [entrez]
 2023/03/07 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/03/06 17:32 [entrez]
 2022/06/17 00:00 [received] 2022/08/28 00:00 [revised] 2023/01/03 00:00 [accepted] 2023/01/13 06:00 [pubmed] 2023/02/03 06:00 [medline] 2023/01/12 22:01 [entrez]
 2022/07/20 00:00 [received] 2023/01/02 00:00 [accepted] 2023/02/24 13:46 [entrez] 2023/02/25 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/05/11 06:42 [medline] 2023/05/10 00:41 [pubmed] 2023/05/09 19:03 [entrez]
 2022/12/30 00:00 [received] 2023/02/28 00:00 [accepted] 2023/01/07 00:00 [revised] 2024/08/01 00:00 [pmc-release] 2023/08/04 06:43 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 08:57 [entrez]
 2022/06/08 00:00 [received] 2022/08/29 00:00 [accepted] 2022/11/17 21:52 [entrez] 2022/11/18 06:00 [pubmed] 2022/11/22 06:00 [medline]
 2022/09/14 00:00 [received] 2022/12/17 00:00 [revised] 2022/12/24 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/12/30 19:13 [entrez]
 2022/10/30 00:00 [received] 2023/01/12 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/02/26 06:00 [pubmed] 2023/02/25 10:53 [entrez]
 2023/01/29 00:00 [received] 2023/02/20 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/27 12:42 [pubmed] 2023/04/27 10:33 [entrez]
 2022/10/19 00:00 [received] 2023/02/07 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 18:07 [entrez]
 2023/02/02 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/28 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:16 [entrez] 2023/04/14 06:00 [pubmed]
 2023/01/23 00:00 [received] 2023/02/24 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 18:02 [entrez]
 2022/12/04 00:00 [revised] 2022/03/04 00:00 [received] 2022/12/06 00:00 [accepted] 2022/12/25 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/24 06:42 [entrez]
 2023/01/07 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 23:16 [entrez]
 2022/10/22 00:00 [received] 2022/11/26 00:00 [revised] 2022/12/05 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/12/12 18:22 [entrez]
 2022/03/14 00:00 [received] 2022/09/06 00:00 [accepted] 2022/11/14 21:47 [entrez] 2022/11/15 06:00 [pubmed] 2022/11/18 06:00 [medline]
 2022/12/27 00:00 [received] 2023/03/24 00:00 [revised] 2023/03/28 00:00 [accepted] 2023/04/25 10:20 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 18:14 [entrez]
 2022/04/11 00:00 [received] 2023/01/04 00:00 [revised] 2023/01/06 00:00 [accepted] 2023/01/13 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/01/12 19:20 [entrez]
 2022/07/22 00:00 [received] 2022/12/13 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/07 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/06 18:16 [entrez]
 2022/11/29 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/06/28 01:06 [pubmed] 2023/06/27 19:11 [entrez]
 2023/09/12 06:42 [medline] 2023/08/07 13:11 [pubmed] 2023/08/07 11:34 [entrez]
 2022/11/14 00:00 [received] 2023/03/12 00:00 [revised] 2023/03/23 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 20:29 [entrez]
 2022/04/07 00:00 [received] 2022/09/07 00:00 [accepted] 2022/11/14 21:47 [entrez] 2022/11/15 06:00 [pubmed] 2022/11/18 06:00 [medline]
 2023/01/02 00:00 [received] 2023/01/31 00:00 [revised] 2023/02/06 00:00 [accepted] 2023/02/25 02:46 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/08/25 00:00 [received] 2022/11/15 00:00 [revised] 2022/11/20 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/05 18:26 [entrez]
 2022/12/20 00:00 [revised] 2022/08/03 00:00 [received] 2023/01/01 00:00 [accepted] 2023/01/27 08:23 [entrez] 2023/01/28 06:00 [pubmed] 2023/01/31 06:00 [medline]
 2022/11/24 00:00 [received] 2023/01/06 00:00 [accepted] 2023/01/13 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/01/12 11:20 [entrez]
 2023/01/30 00:00 [received] 2023/06/13 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/08/11 00:41 [pubmed] 2023/08/10 21:37 [entrez]
 2021/09/14 00:00 [received] 2023/06/08 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/14 13:06 [pubmed] 2023/07/13 23:52 [entrez]
 2022/07/06 00:00 [received] 2023/01/27 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/03/09 06:00 [pubmed] 2023/03/25 06:00 [medline] 2023/03/08 09:13 [entrez]
 2022/08/04 00:00 [received] 2022/10/11 00:00 [revised] 2023/02/27 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 19:03 [entrez]
 2023/06/05 06:42 [medline] 2023/06/02 19:13 [pubmed] 2023/06/02 14:04 [entrez]
 2023/02/03 00:00 [received] 2023/03/15 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/04/17 03:53 [entrez] 2023/04/18 06:00 [pubmed]
 2022/12/09 00:00 [received] 2023/06/15 00:00 [revised] 2023/06/22 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 18:03 [entrez]
 2022/07/11 00:00 [received] 2023/02/10 00:00 [revised] 2023/05/06 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/05/27 09:42 [pubmed] 2023/05/26 18:09 [entrez]
 2023/01/11 00:00 [revised] 2023/01/18 00:00 [revised] 2022/12/01 00:00 [received] 2023/01/19 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/01/23 06:00 [pubmed] 2023/01/22 06:42 [entrez]
 2022/12/09 00:00 [received] 2023/08/17 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/10 00:41 [pubmed] 2023/09/09 23:34 [entrez]
 2022/09/02 00:00 [received] 2022/10/25 00:00 [revised] 2023/01/28 00:00 [accepted] 2023/02/04 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/02/03 19:33 [entrez]
 2023/01/27 00:00 [received] 2023/03/13 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 18:05 [entrez]
 2022/08/03 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/22 06:42 [medline] 2023/05/22 13:03 [pubmed] 2023/05/22 09:13 [entrez]
 2022/09/23 00:00 [received] 2023/01/12 00:00 [accepted] 2023/03/29 06:05 [medline] 2023/03/27 21:43 [entrez] 2023/03/28 06:00 [pubmed]
 2022/11/23 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/02/11 01:37 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/06/19 13:08 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 07:43 [entrez]
 2022/08/10 00:00 [received] 2023/04/06 00:00 [revised] 2023/04/10 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 18:06 [entrez]
 2023/05/01 00:00 [received] 2023/07/17 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/08 00:42 [pubmed] 2023/09/07 21:22 [entrez]
 2023/05/04 12:42 [medline] 2023/01/25 06:00 [pubmed] 2023/01/24 11:33 [entrez]
 2022/05/12 00:00 [received] 2023/01/10 00:00 [revised] 2023/03/29 00:00 [accepted] 2024/05/02 00:00 [pmc-release] 2023/05/05 06:42 [medline] 2023/04/22 10:42 [pubmed] 2023/04/21 18:42 [entrez]
 2022/11/04 00:00 [received] 2022/12/17 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/04/03 01:53 [entrez] 2023/04/04 06:00 [pubmed]
 2023/02/07 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/03/30 01:06 [entrez] 2023/03/31 06:00 [pubmed]
 2024/06/05 00:00 [pmc-release] 2023/07/14 13:07 [medline] 2023/06/05 13:05 [pubmed] 2023/06/05 11:33 [entrez]
 2022/08/01 00:00 [received] 2022/10/31 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/12/01 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/11/30 18:03 [entrez]
 2022/05/12 00:00 [received] 2022/10/29 00:00 [revised] 2022/11/02 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 22:00 [entrez]
 2023/01/04 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/13 00:00 [accepted] 2023/08/15 06:42 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 18:11 [entrez]
 2022/11/23 00:00 [received] 2023/01/11 00:00 [accepted] 2023/02/10 03:12 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2023/02/01 00:00 [received] 2023/04/20 00:00 [accepted] 2023/05/02 06:42 [medline] 2023/05/01 00:42 [pubmed] 2023/04/30 23:14 [entrez]
 2022/06/19 00:00 [received] 2022/12/20 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/01/17 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/16 19:23 [entrez]
 2023/01/05 00:00 [received] 2023/06/05 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 23:24 [entrez]
 2022/11/10 00:00 [received] 2022/12/20 00:00 [accepted] 2023/01/30 03:48 [entrez] 2023/01/31 06:00 [pubmed] 2023/02/01 06:00 [medline]
 2023/04/27 00:00 [revised] 2022/11/23 00:00 [received] 2023/08/17 06:43 [medline] 2023/06/05 06:42 [pubmed] 2023/06/05 00:14 [entrez]
 2023/07/13 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:33 [entrez]
 2022/07/08 00:00 [received] 2022/09/29 00:00 [revised] 2023/01/19 00:00 [accepted] 2023/02/09 02:26 [entrez] 2023/02/10 06:00 [pubmed] 2023/02/10 06:01 [medline]
 2022/12/26 00:00 [received] 2023/02/10 00:00 [accepted] 2023/03/20 04:05 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2022/06/16 00:00 [received] 2023/04/10 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:16 [entrez]
 2022/10/18 00:00 [received] 2023/04/20 00:00 [revised] 2023/07/11 00:00 [accepted] 2023/08/22 06:43 [medline] 2023/08/22 06:42 [pubmed] 2023/08/22 03:42 [entrez]
 2023/04/04 00:00 [received] 2023/06/30 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:31 [entrez]
 2022/11/12 00:00 [received] 2023/06/23 00:00 [accepted] 2023/07/08 19:41 [medline] 2023/07/08 19:41 [pubmed] 2023/07/08 11:09 [entrez]
 2023/05/12 07:06 [medline] 2023/05/12 07:06 [pubmed] 2023/05/12 04:23 [entrez]
 2023/04/15 06:01 [medline] 2023/04/14 01:47 [entrez] 2023/04/15 06:00 [pubmed]
 2022/09/12 00:00 [received] 2023/01/26 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:13 [entrez]
 2022/06/15 00:00 [received] 2022/12/06 00:00 [accepted] 2023/04/24 06:43 [medline] 2023/04/24 06:42 [pubmed] 2023/04/24 03:36 [entrez]
 2023/07/28 13:11 [medline] 2023/07/28 13:11 [pubmed] 2023/07/28 09:13 [entrez]
 2023/07/14 13:09 [medline] 2023/07/14 13:08 [pubmed] 2023/07/14 07:09 [entrez]
 2023/08/05 00:00 [received] 2023/08/24 00:00 [accepted] 2023/08/23 00:00 [revised] 2023/09/07 12:42 [medline] 2023/09/07 12:42 [pubmed] 2023/09/07 11:06 [entrez]
 2022/10/13 00:00 [received] 2022/10/26 00:00 [accepted] 2022/11/28 04:46 [entrez] 2022/11/29 06:00 [pubmed] 2022/11/29 06:01 [medline]
 2023/01/17 00:00 [received] 2023/03/14 00:00 [accepted] 2023/04/18 06:01 [medline] 2023/04/17 03:27 [entrez] 2023/04/18 06:00 [pubmed]
 2022/09/20 00:00 [received] 2023/03/30 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/05 19:11 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 12:08 [entrez]
 2022/07/25 00:00 [received] 2023/01/11 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/04/15 06:01 [medline] 2023/04/14 02:28 [entrez] 2023/04/15 06:00 [pubmed]
 2022/11/22 00:00 [received] 2023/04/07 00:00 [revised] 2023/04/14 00:00 [accepted] 2023/05/16 06:43 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:11 [entrez]
 2022/07/28 00:00 [received] 2022/12/09 00:00 [accepted] 2023/01/26 02:43 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/27 06:01 [medline]
 2023/03/10 02:37 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2023/08/07 13:09 [pubmed] 2023/08/07 13:09 [medline] 2023/08/07 09:13 [entrez]
 2023/09/11 12:41 [medline] 2023/09/11 12:41 [pubmed] 2023/09/11 07:14 [entrez]
 2023/07/25 06:44 [medline] 2023/07/25 06:43 [pubmed] 2023/07/25 01:20 [entrez]
 2022/11/30 00:00 [received] 2023/03/15 00:00 [accepted] 2023/04/27 06:43 [medline] 2023/04/27 06:42 [pubmed] 2023/04/27 02:09 [entrez]
 2022/12/02 02:39 [entrez] 2022/12/03 06:00 [pubmed] 2022/12/03 06:01 [medline]
 2023/07/19 19:07 [medline] 2023/07/19 19:07 [pubmed] 2023/07/19 16:53 [entrez]
 2022/07/28 11:24 [entrez] 2022/07/29 06:00 [pubmed] 2022/07/29 06:01 [medline]
 2023/07/02 00:00 [received] 2023/07/05 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:11 [entrez]
 2023/04/16 00:00 [received] 2023/06/09 00:00 [accepted] 2023/07/14 13:09 [medline] 2023/07/14 13:08 [pubmed] 2023/07/14 03:56 [entrez]
 2023/04/14 00:00 [received] 2023/06/28 00:00 [revised] 2023/08/10 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:00 [entrez]
 2023/04/29 00:00 [received] 2023/06/21 00:00 [accepted] 2023/06/20 00:00 [revised] 2023/07/03 00:41 [medline] 2023/07/03 00:41 [pubmed] 2023/07/02 23:34 [entrez]
 2023/05/16 00:00 [received] 2023/07/11 00:00 [revised] 2023/08/21 00:00 [accepted] 2023/09/04 00:41 [medline] 2023/09/04 00:41 [pubmed] 2023/09/03 18:08 [entrez]
 2022/10/06 00:00 [received] 2022/12/22 00:00 [accepted] 2023/01/30 04:33 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/06/20 00:00 [accepted] 2023/07/08 10:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 21:22 [entrez]
 2023/02/20 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/20 03:47 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2023/01/20 00:00 [received] 2023/01/26 00:00 [accepted] 2023/03/10 02:35 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2023/01/12 00:00 [received] 2023/02/16 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/05 19:11 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 12:08 [entrez]
 2023/04/28 00:00 [received] 2023/04/28 00:00 [accepted] 2023/05/31 13:12 [medline] 2023/05/31 13:11 [pubmed] 2023/05/31 10:28 [entrez]
 2023/01/24 00:00 [received] 2023/02/15 00:00 [revised] 2023/02/25 00:00 [accepted] 2023/03/11 01:21 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/12 06:01 [medline]
 2022/09/14 00:00 [received] 2023/01/16 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/04/24 06:43 [medline] 2023/04/24 06:42 [pubmed] 2023/04/24 03:58 [entrez]
 2023/03/22 00:00 [received] 2023/04/21 00:00 [revised] 2023/04/26 00:00 [accepted] 2023/05/26 13:10 [medline] 2023/05/26 13:09 [pubmed] 2023/05/26 09:23 [entrez]
 2022/11/10 00:00 [received] 2023/04/04 00:00 [revised] 2023/04/20 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:12 [entrez]
 2023/02/16 21:12 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/17 06:01 [medline]
 2022/09/29 00:00 [received] 2022/11/01 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2022/11/29 06:01 [medline] 2022/11/28 23:49 [entrez]
 2023/02/16 00:00 [received] 2023/06/12 00:00 [revised] 2023/07/23 00:00 [accepted] 2023/07/28 01:08 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 18:03 [entrez]
 2022/07/08 00:00 [received] 2023/04/14 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 13:04 [entrez]
 2023/02/16 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 12:02 [entrez]
 2023/03/29 00:00 [received] 2023/06/06 00:00 [accepted] 2023/06/21 19:16 [medline] 2023/06/21 19:15 [pubmed] 2023/06/21 12:02 [entrez]
 2022/12/06 00:00 [received] 2023/04/03 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 02:32 [entrez]
 2021/05/19 00:00 [received] 2022/06/07 00:00 [revised] 2022/11/02 00:00 [accepted] 2023/01/05 02:36 [entrez] 2023/01/06 06:00 [pubmed] 2023/01/06 06:01 [medline]
 2022/08/24 00:00 [received] 2022/12/23 00:00 [accepted] 2023/01/30 04:01 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/01/24 00:00 [received] 2023/01/25 00:00 [accepted] 2023/02/24 02:41 [entrez] 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline]
 2023/06/08 00:00 [received] 2023/08/03 00:00 [accepted] 2023/09/08 12:42 [medline] 2023/09/08 12:42 [pubmed] 2023/09/08 11:16 [entrez]
 2023/07/13 00:00 [received] 2023/08/04 00:00 [accepted] 2023/08/13 00:43 [medline] 2023/08/13 00:43 [pubmed] 2023/08/12 18:07 [entrez]
 2023/08/01 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 05:13 [entrez]
 2023/02/16 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/17 12:42 [medline] 2023/08/17 12:42 [pubmed] 2023/08/17 11:08 [entrez]
 2023/06/23 00:00 [received] 2023/06/27 00:00 [accepted] 2023/08/24 06:44 [medline] 2023/08/24 06:43 [pubmed] 2023/08/24 04:13 [entrez]
 2023/04/29 00:00 [received] 2023/06/30 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 03:51 [entrez]

 2023/08/07 00:00 [received] 2023/08/13 00:00 [accepted] 2023/08/30 12:42 [medline] 2023/08/30 12:42 [pubmed] 2023/08/30 09:53 [entrez]
 2022/11/21 00:00 [received] 2022/12/13 00:00 [accepted] 2023/01/26 02:40 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/27 06:01 [medline]
 2022/09/05 00:00 [received] 2023/02/14 00:00 [revised] 2023/02/15 00:00 [accepted] 2023/04/19 06:00 [pubmed] 2023/04/19 06:00 [medline] 2023/04/18 06:00 [entrez]
 2022/12/03 00:00 [received] 2023/01/09 00:00 [accepted] 2023/02/13 03:56 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2023/09/01 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 04:44 [entrez]
 2022/12/18 00:00 [received] 2023/01/03 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/21 01:31 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2023/01/04 00:00 [received] 2023/01/12 00:00 [accepted] 2023/02/16 02:26 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/17 06:01 [medline]
 2022/11/05 00:00 [received] 2023/03/11 00:00 [accepted] 2023/03/22 12:18 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/23 06:01 [medline]
 2022/08/15 00:00 [received] 2023/03/29 00:00 [accepted] 2023/05/02 06:43 [medline] 2023/05/02 06:42 [pubmed] 2023/05/02 01:56 [entrez]
 2024/07/01 00:00 [pmc-release] 2023/07/13 19:16 [medline] 2023/07/13 19:15 [pubmed] 2023/07/13 15:23 [entrez]
 2023/05/26 00:00 [received] 2023/05/31 00:00 [accepted] 2023/06/30 13:12 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 10:12 [entrez]
 2023/03/10 23:53 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:00 [medline]
 2021/08/28 00:00 [received] 2021/09/18 00:00 [revised] 2022/05/18 00:00 [accepted] 2023/02/06 03:31 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:01 [medline]

 2023/07/05 00:00 [received] 2023/08/15 00:00 [accepted] 2023/09/08 12:42 [medline] 2023/09/08 12:42 [pubmed] 2023/09/08 11:16 [entrez]
 2023/05/14 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/28 06:43 [medline] 2023/07/28 06:42 [pubmed] 2023/07/28 04:31 [entrez]
 2023/03/01 00:00 [received] 2023/05/16 00:00 [revised] 2023/05/21 00:00 [accepted] 2023/06/27 19:13 [medline] 2023/06/27 19:13 [pubmed] 2023/06/27 16:03 [entrez]
 2023/07/01 00:00 [revised] 2022/08/04 00:00 [received] 2023/07/08 00:00 [accepted] 2023/09/08 06:42 [medline] 2023/09/08 06:42 [pubmed] 2023/09/08 02:23 [entrez]
 2022/12/01 00:00 [received] 2023/03/10 00:00 [revised] 2023/03/23 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 03:56 [entrez]
 2023/01/05 00:00 [received] 2023/02/28 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 03:48 [entrez] 2023/04/04 06:00 [pubmed]
 2022/10/21 00:00 [received] 2023/01/09 00:00 [accepted] 2023/02/16 02:23 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/17 06:01 [medline]
 2023/03/19 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:59 [entrez]
 2022/12/29 00:00 [received] 2023/05/04 00:00 [accepted] 2023/07/12 06:43 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 03:49 [entrez]
 2023/02/10 00:00 [received] 2023/04/05 00:00 [accepted] 2023/04/13 23:31 [entrez] 2023/04/14 06:00 [pubmed] 2023/04/14 06:00 [medline]
 2023/08/02 00:00 [received] 2023/08/15 00:00 [accepted] 2023/09/14 12:42 [medline] 2023/09/14 12:42 [pubmed] 2023/09/14 11:12 [entrez]
 2022/12/26 07:35 [entrez] 2022/12/27 06:00 [pubmed] 2022/12/27 06:01 [medline]
 2023/06/12 06:42 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 03:45 [entrez]
 2023/05/24 00:00 [received] 2023/07/22 00:00 [revised] 2023/08/11 00:00 [accepted] 2023/08/31 06:42 [medline] 2023/08/31 06:41 [pubmed] 2023/08/31 04:10 [entrez]
 2023/08/26 05:42 [medline] 2023/08/26 05:42 [pubmed] 2023/08/25 23:35 [entrez]
 2023/03/04 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/18 00:00 [accepted] 2023/06/02 13:17 [medline] 2023/06/02 13:16 [pubmed] 2023/06/02 10:58 [entrez]
 2023/08/15 06:42 [medline] 2023/08/15 06:42 [pubmed] 2023/08/15 04:13 [entrez]
 2022/07/28 11:24 [entrez] 2022/07/29 06:00 [pubmed] 2022/07/29 06:01 [medline]
 2023/07/06 13:14 [medline] 2023/07/06 13:14 [pubmed] 2023/07/06 06:39 [entrez]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2022/07/07 00:00 [received] 2022/11/16 00:00 [accepted] 2023/01/09 04:00 [entrez] 2023/01/10 06:00 [pubmed] 2023/01/10 06:01 [medline]
 2023/04/18 06:00 [pubmed] 2023/04/18 06:00 [medline] 2023/04/17 04:53 [entrez]
 2023/02/02 00:00 [received] 2023/05/10 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:35 [entrez]
 2023/02/02 00:00 [received] 2023/03/01 00:00 [accepted] 2023/06/07 13:11 [medline] 2023/06/07 13:10 [pubmed] 2023/06/07 09:40 [entrez]
 2023/08/24 13:43 [medline] 2023/08/24 13:43 [pubmed] 2023/08/24 09:23 [entrez]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2023/05/04 00:00 [received] 2023/07/11 00:00 [accepted] 2023/08/16 06:44 [medline] 2023/08/16 06:43 [pubmed] 2023/08/16 03:56 [entrez]
 2023/05/03 00:00 [received] 2023/06/05 00:00 [revised] 2023/06/08 00:00 [accepted] 2023/06/16 01:08 [pubmed] 2023/06/16 01:08 [medline] 2023/06/15 18:05 [entrez]
 2023/02/03 19:02 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/04 06:00 [medline]

 2023/06/11 00:00 [received] 2023/08/24 00:00 [accepted] 2023/08/29 12:43 [medline] 2023/08/29 12:43 [pubmed] 2023/08/29 11:12 [entrez]
 2023/07/19 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:09 [entrez]
 2023/02/23 00:00 [received] 2023/05/02 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:50 [entrez]
 2023/06/27 00:00 [received] 2023/07/28 00:00 [accepted] 2023/08/31 06:42 [medline] 2023/08/31 06:41 [pubmed] 2023/08/31 04:11 [entrez]
 2023/01/10 00:00 [received] 2023/05/15 00:00 [revised] 2023/05/25 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 03:45 [entrez]
 2022/10/12 00:00 [received] 2022/12/16 00:00 [accepted] 2023/01/23 05:09 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2023/08/10 18:42 [medline] 2023/08/10 18:42 [pubmed] 2023/08/10 12:03 [entrez]
 2023/06/20 00:00 [received] 2023/08/15 00:00 [accepted] 2023/09/14 12:41 [medline] 2023/09/14 12:41 [pubmed] 2023/09/14 11:12 [entrez]
 2023/01/31 00:00 [received] 2023/08/01 00:00 [accepted] 2023/08/25 06:43 [medline] 2023/08/25 06:42 [pubmed] 2023/08/25 03:49 [entrez]
 2023/05/09 00:00 [received] 2023/05/19 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 05:04 [entrez]
 2023/01/06 00:00 [received] 2023/02/17 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:02 [entrez] 2023/04/04 06:00 [pubmed]
 2023/05/14 00:00 [received] 2023/05/24 00:00 [accepted] 2023/06/22 13:10 [medline] 2023/06/22 13:09 [pubmed] 2023/06/22 09:47 [entrez]
 2023/05/07 00:00 [revised] 2022/11/15 00:00 [received] 2023/05/15 00:00 [accepted] 2023/07/04 06:42 [pubmed] 2023/07/04 06:42 [medline] 2023/07/04 00:03 [entrez]
 2022/03/28 00:00 [received] 2022/08/23 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2022/12/13 06:01 [medline] 2022/12/12 09:02 [entrez]
 2023/03/03 00:00 [received] 2023/06/26 00:00 [revised] 2023/07/14 00:00 [accepted] 2023/09/11 06:44 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 04:36 [entrez]
 2023/04/13 00:00 [received] 2023/05/08 00:00 [revised] 2023/05/19 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:18 [entrez]
 2023/09/07 18:42 [medline] 2023/09/07 18:42 [pubmed] 2023/09/07 12:03 [entrez]
 2020/12/03 00:00 [received] 2021/04/28 00:00 [accepted] 2023/08/23 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 04:18 [entrez]
 2023/07/24 19:10 [medline] 2023/07/24 19:10 [pubmed] 2023/07/24 14:52 [entrez]
 2023/08/02 06:42 [medline] 2023/08/02 06:42 [pubmed] 2023/08/02 01:54 [entrez]
 2023/06/26 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/31 06:42 [pubmed] 2023/07/31 05:16 [entrez]
 2023/03/30 00:00 [received] 2023/06/20 00:00 [accepted] 2023/07/19 06:43 [medline] 2023/07/19 06:42 [pubmed] 2023/07/19 04:01 [entrez]
 2023/02/14 00:00 [received] 2023/07/10 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/09 10:41 [medline] 2023/09/09 10:41 [pubmed] 2023/09/08 18:10 [entrez]
 2023/06/30 00:00 [received] 2023/08/06 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/08/27 05:43 [pubmed] 2023/08/27 05:43 [medline] 2023/08/26 19:28 [entrez]
 2023/04/08 06:01 [medline] 2023/04/07 02:31 [entrez] 2023/04/08 06:00 [pubmed]
 2023/06/26 00:00 [accepted] 2023/07/28 06:43 [medline] 2023/07/28 06:42 [pubmed] 2023/07/28 04:31 [entrez]
 2023/09/11 06:43 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 03:33 [entrez]
 2023/06/20 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:54 [entrez]
 2023/02/09 00:00 [received] 2023/06/15 00:00 [accepted] 2023/07/19 13:08 [medline] 2023/07/19 13:07 [pubmed] 2023/07/19 11:08 [entrez]
 2022/10/12 00:00 [received] 2023/01/27 00:00 [accepted] 2023/02/27 05:38 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2023/06/03 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/11 00:42 [medline] 2023/09/11 00:42 [pubmed] 2023/09/10 18:12 [entrez]
 2023/06/26 00:00 [received] 2023/07/02 00:00 [accepted] 2023/07/09 01:07 [medline] 2023/07/09 01:07 [pubmed] 2023/07/08 23:24 [entrez]
 2023/06/07 00:00 [received] 2023/08/14 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/09/08 06:42 [pubmed] 2023/09/08 04:03 [entrez]
 2022/08/12 00:00 [received] 2022/12/12 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 03:45 [entrez] 2023/04/04 06:00 [pubmed]
 2022/12/20 00:00 [received] 2023/06/23 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 04:45 [entrez]
 2023/01/13 00:00 [received] 2023/06/22 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/08/11 06:44 [medline] 2023/08/11 06:43 [pubmed] 2023/08/11 04:05 [entrez]
 2023/01/16 00:00 [received] 2023/02/20 00:00 [revised] 2023/03/05 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/08/08 06:42 [pubmed] 2023/08/08 01:03 [entrez]
 2023/02/14 00:00 [received] 2023/06/02 00:00 [accepted] 2023/06/11 01:06 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 23:04 [entrez]
 2022/07/25 00:00 [received] 2022/10/12 00:00 [revised] 2023/02/21 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 03:45 [entrez] 2023/04/04 06:00 [pubmed]
 2023/01/31 00:00 [received] 2023/03/27 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 15:44 [entrez]
 2023/03/24 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:34 [entrez]
 2023/02/21 00:00 [received] 2023/05/30 00:00 [accepted] 2023/07/06 06:43 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 04:18 [entrez]
 2023/03/05 00:00 [received] 2023/05/13 00:00 [accepted] 2023/05/25 01:08 [medline] 2023/05/25 01:07 [pubmed] 2023/05/24 23:54 [entrez]
 2023/08/25 00:00 [accepted] 2023/09/14 06:43 [medline] 2023/09/14 06:42 [pubmed] 2023/09/14 04:06 [entrez]
 2022/05/30 00:00 [received] 2022/11/23 00:00 [accepted] 2023/02/13 03:25 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2023/03/06 00:00 [received] 2023/08/02 00:00 [accepted] 2023/08/29 06:44 [medline] 2023/08/29 06:43 [pubmed] 2023/08/29 03:36 [entrez]
 2022/08/16 00:00 [received] 2022/10/21 00:00 [revised] 2022/10/25 00:00 [accepted] 2022/11/25 03:04 [entrez] 2022/11/26 06:00 [pubmed] 2022/11/26 06:01 [medline]
 2023/05/02 00:00 [received] 2023/06/12 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 03:51 [entrez]
 2023/05/02 00:00 [received] 2023/08/20 00:00 [accepted] 2023/09/01 00:42 [medline] 2023/09/01 00:42 [pubmed] 2023/08/31 18:03 [entrez]
 2023/08/21 12:43 [pubmed] 2023/08/21 12:43 [medline] 2023/08/21 07:22 [entrez]
 2023/08/04 06:43 [medline] 2023/08/04 06:43 [pubmed] 2023/08/04 04:33 [entrez]
 2023/02/13 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:42 [entrez] 2023/03/30 06:00 [pubmed]
 2023/04/18 13:02 [entrez] 2023/04/19 06:00 [pubmed] 2023/04/19 06:00 [medline]
 2023/02/13 00:00 [received] 2023/03/18 00:00 [accepted] 2023/05/25 19:13 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 14:18 [entrez]
 2022/02/21 00:00 [received] 2022/08/18 00:00 [accepted] 2023/08/30 06:48 [medline] 2023/08/30 06:47 [pubmed] 2023/08/30 03:47 [entrez]
 2023/04/03 00:00 [received] 2023/08/05 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/08/29 00:41 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 18:01 [entrez]
 2023/07/12 13:07 [pubmed] 2023/07/12 13:07 [medline] 2023/07/12 06:35 [entrez]
 2023/09/04 06:42 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 00:54 [entrez]
 2021/05/20 00:00 [received] 2021/11/23 00:00 [revised] 2022/05/30 00:00 [accepted] 2023/07/12 06:43 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 03:56 [entrez]
 2023/07/29 21:46 [medline] 2023/07/29 21:45 [pubmed] 2023/07/29 08:22 [entrez]
 2023/06/30 13:11 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 06:35 [entrez]
 2023/01/26 00:00 [received] 2023/04/21 00:00 [accepted] 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:27 [entrez]
 2022/10/24 00:00 [received] 2023/01/25 00:00 [accepted] 2023/03/11 06:01 [medline] 2023/03/11 06:00 [pubmed] 2023/03/10 23:28 [entrez]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/03/26 00:00 [received] 2023/06/06 00:00 [accepted] 2023/07/05 13:06 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 10:44 [entrez]
 2022/12/09 00:00 [received] 2023/01/24 00:00 [accepted] 2023/02/27 05:39 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2022/06/29 00:00 [received] 2022/12/07 00:00 [accepted] 2022/12/29 02:38 [entrez] 2022/12/30 06:00 [pubmed] 2022/12/30 06:01 [medline]
 2023/07/11 00:00 [accepted] 2023/08/23 12:42 [medline] 2023/08/23 12:42 [pubmed] 2023/08/23 11:16 [entrez]
 2023/01/31 00:00 [received] 2023/03/06 00:00 [revised] 2023/03/07 00:00 [accepted] 2023/03/24 02:21 [entrez] 2023/03/25 06:00 [pubmed] 2023/03/25 06:01 [medline]
 2023/01/19 00:00 [received] 2023/04/19 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:50 [entrez]
 2022/12/23 00:00 [received] 2023/02/09 00:00 [accepted] 2023/03/13 03:50 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2023/05/17 19:12 [medline] 2023/05/17 19:12 [pubmed] 2023/05/17 12:23 [entrez]

 2023/02/08 00:00 [received] 2023/02/28 00:00 [revised] 2023/03/01 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:21 [entrez] 2023/03/30 06:00 [pubmed]
 2022/10/27 00:00 [received] 2023/01/18 00:00 [accepted] 2023/02/03 01:53 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/04 06:01 [medline]
 2023/05/23 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/04 06:44 [medline] 2023/08/04 06:43 [pubmed] 2023/08/04 03:57 [entrez]
 2023/05/06 00:00 [received] 2023/07/28 00:00 [revised] 2023/07/31 00:00 [accepted] 2023/08/03 01:06 [pubmed] 2023/08/03 01:06 [medline] 2023/08/02 19:13 [entrez]
 2023/06/12 00:00 [received] 2023/06/18 00:00 [accepted] 2023/07/29 11:43 [medline] 2023/07/29 11:42 [pubmed] 2023/07/29 01:19 [entrez]
 2022/10/03 00:00 [received] 2023/01/09 00:00 [accepted] 2023/03/24 02:14 [entrez] 2023/03/25 06:00 [pubmed] 2023/03/25 06:01 [medline]
 2023/05/21 00:00 [received] 2023/07/06 19:12 [medline] 2023/07/06 19:12 [pubmed] 2023/07/06 14:52 [entrez]
 2021/05/30 00:00 [received] 2022/09/05 00:00 [accepted] 2023/06/19 06:42 [medline] 2023/06/19 06:41 [pubmed] 2023/06/19 02:59 [entrez]
 2023/04/19 12:42 [medline] 2023/04/19 12:42 [pubmed] 2023/04/19 09:12 [entrez]
 2023/09/04 18:41 [medline] 2023/09/04 18:41 [pubmed] 2023/09/04 12:42 [entrez]
 2023/06/18 00:00 [received] 2023/07/18 00:00 [revised] 2023/07/19 00:00 [accepted] 2023/08/20 00:41 [medline] 2023/08/20 00:41 [pubmed] 2023/08/19 22:02 [entrez]
 2023/06/14 13:07 [medline] 2023/06/14 13:07 [pubmed] 2023/06/14 11:14 [entrez]
 2022/11/14 00:00 [received] 2023/01/24 00:00 [accepted] 2023/03/06 03:41 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/04/11 00:00 [received] 2023/06/09 00:00 [accepted] 2023/07/26 06:44 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 03:52 [entrez]
 2023/08/07 06:41 [medline] 2023/08/07 06:41 [pubmed] 2023/08/07 03:10 [entrez]
 2023/03/31 00:00 [received] 2023/05/15 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:59 [entrez]
 2022/12/27 00:00 [received] 2023/02/16 00:00 [revised] 2023/03/23 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:27 [entrez]
 2023/01/13 00:00 [received] 2023/02/15 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:20 [entrez]
 2023/02/16 11:16 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/22 06:00 [medline]
 2023/01/05 00:00 [received] 2023/02/27 00:00 [accepted] 2023/04/01 06:01 [medline] 2023/03/31 02:10 [entrez] 2023/04/01 06:00 [pubmed]
 2023/01/10 00:00 [received] 2023/03/02 00:00 [accepted] 2023/04/25 06:43 [medline] 2023/04/25 06:42 [pubmed] 2023/04/25 02:05 [entrez]
 2022/07/20 00:00 [received] 2022/12/04 00:00 [accepted] 2023/01/30 03:45 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/10/19 00:00 [received] 2023/02/22 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/04/30 00:42 [pubmed] 2023/04/30 00:42 [medline] 2023/04/29 19:25 [entrez]
 2023/07/19 06:43 [medline] 2023/07/19 06:43 [pubmed] 2023/07/19 04:42 [entrez]
 2022/11/30 00:00 [received] 2023/05/23 00:00 [accepted] 2023/08/02 06:43 [medline] 2023/08/02 06:42 [pubmed] 2023/08/02 04:01 [entrez]
 2022/05/04 00:00 [received] 2022/10/02 00:00 [revised] 2023/02/06 00:00 [accepted] 2023/03/02 02:16 [entrez] 2023/03/03 06:00 [pubmed] 2023/03/03 06:01 [medline]
 2023/01/28 00:00 [received] 2023/07/03 00:00 [accepted] 2023/07/21 01:11 [medline] 2023/07/21 01:11 [pubmed] 2023/07/20 18:23 [entrez]
 2022/08/28 00:00 [received] 2023/01/25 00:00 [revised] 2023/02/21 00:00 [accepted] 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:30 [entrez]
 2021/08/25 00:00 [received] 2021/10/31 00:00 [revised] 2021/12/06 00:00 [accepted] 2023/02/06 03:31 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:01 [medline]
 2021/09/20 00:00 [received] 2022/03/14 00:00 [revised] 2022/03/27 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/07/31 06:42 [pubmed] 2023/07/31 04:58 [entrez]
 2023/04/19 00:00 [received] 2023/05/19 00:00 [revised] 2023/05/25 00:00 [accepted] 2023/06/10 15:14 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:08 [entrez]
 2022/12/24 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/25 00:00 [accepted] 2023/05/05 00:43 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 22:00 [entrez]
 2021/03/20 00:00 [received] 2022/10/08 00:00 [accepted] 2023/10/01 00:00 [pmc-release] 2023/08/28 06:43 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 04:54 [entrez]
 2022/07/01 00:00 [received] 2022/11/07 00:00 [accepted] 2023/07/03 13:06 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:39 [entrez]
 2023/04/24 06:41 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 05:33 [entrez]
 2023/05/29 00:00 [received] 2023/06/24 00:00 [revised] 2023/07/03 00:00 [accepted] 2023/08/12 10:42 [medline] 2023/08/12 10:42 [pubmed] 2023/08/11 21:57 [entrez]
 2022/12/24 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/25 00:00 [accepted] 2023/07/03 00:41 [pubmed] 2023/07/03 00:41 [medline] 2023/07/02 22:01 [entrez]
 2023/04/20 00:00 [received] 2023/07/12 00:00 [accepted] 2023/07/02 00:00 [revised] 2023/09/04 01:22 [medline] 2023/09/04 01:22 [pubmed] 2023/09/02 11:04 [entrez]
 2023/03/09 00:00 [received] 2023/07/05 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/11 00:42 [medline] 2023/09/11 00:42 [pubmed] 2023/09/10 18:12 [entrez]
 2023/04/19 00:00 [received] 2023/07/19 00:00 [accepted] 2023/08/29 06:44 [medline] 2023/08/29 06:43 [pubmed] 2023/08/29 03:36 [entrez]
 2023/04/19 00:00 [received] 2023/06/21 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/20 00:41 [medline] 2023/08/20 00:41 [pubmed] 2023/08/19 18:04 [entrez]
 2023/01/15 00:00 [received] 2023/02/07 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/02/25 03:04 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/05/24 00:00 [received] 2022/06/06 00:00 [accepted] 2023/02/23 10:00 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/05/23 00:00 [received] 2023/07/02 00:00 [revised] 2023/07/05 00:00 [accepted] 2023/07/29 11:48 [medline] 2023/07/29 11:47 [pubmed] 2023/07/29 01:38 [entrez]
 2023/06/05 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:10 [entrez]
 2023/03/17 00:00 [received] 2023/07/25 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/29 00:42 [medline] 2023/08/29 00:42 [pubmed] 2023/08/28 18:52 [entrez]
 2023/03/28 23:17 [entrez] 2023/03/29 06:00 [pubmed] 2023/03/29 06:00 [medline]
 2022/12/11 00:00 [received] 2023/05/08 00:00 [revised] 2023/06/08 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:56 [entrez]
 2023/06/20 00:00 [received] 2023/07/19 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/07/29 11:54 [medline] 2023/07/29 11:53 [pubmed] 2023/07/29 01:09 [entrez]
 2023/08/29 06:43 [medline] 2023/08/29 06:43 [pubmed] 2023/08/29 00:33 [entrez]
 2023/08/28 06:42 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 00:43 [entrez]
 2023/05/09 00:00 [accepted] 2023/06/06 19:13 [medline] 2023/06/06 19:13 [pubmed] 2023/06/06 15:13 [entrez]
 2022/06/26 00:00 [received] 2022/12/31 00:00 [accepted] 2023/02/17 06:01 [medline] 2023/02/17 06:00 [pubmed] 2023/02/16 23:30 [entrez]
 2023/04/13 00:00 [received] 2023/05/31 00:00 [revised] 2023/06/18 00:00 [accepted] 2023/06/27 01:06 [pubmed] 2023/06/27 01:06 [medline] 2023/06/26 18:09 [entrez]
 2023/06/20 19:14 [medline] 2023/06/20 19:14 [pubmed] 2023/06/20 17:03 [entrez]
 2023/04/03 00:00 [received] 2023/05/15 00:00 [accepted] 2023/06/19 06:43 [medline] 2023/06/19 06:42 [pubmed] 2023/06/19 02:52 [entrez]
 2023/04/22 00:00 [received] 2023/05/18 00:00 [revised] 2023/05/19 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:29 [entrez]
 2023/03/15 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/05/16 06:43 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:15 [entrez]
 2021/02/11 00:00 [received] 2021/04/28 00:00 [revised] 2021/10/04 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:14 [entrez]
 2022/10/24 00:00 [received] 2022/12/30 00:00 [accepted] 2023/02/10 02:57 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/07/13 06:43 [medline] 2023/07/13 06:42 [pubmed] 2023/07/13 02:08 [entrez]
 2022/11/17 00:00 [received] 2023/01/31 00:00 [accepted] 2023/03/06 03:52 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2022/11/04 00:00 [received] 2022/12/23 00:00 [accepted] 2023/02/10 03:15 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2022/12/21 00:00 [received] 2023/01/03 00:00 [accepted] 2023/04/07 06:41 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 04:23 [entrez]
 2023/02/13 00:00 [received] 2023/02/28 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:52 [entrez] 2023/03/30 06:00 [pubmed]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/07/11 00:00 [received] 2023/02/25 04:51 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/08/24 00:00 [accepted] 2023/09/13 00:42 [medline] 2023/09/13 00:42 [pubmed] 2023/09/12 19:13 [entrez]
 2023/09/07 12:42 [pubmed] 2023/09/07 12:42 [medline] 2023/09/07 09:13 [entrez]
 2021/07/17 00:00 [received] 2021/10/20 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:25 [entrez]
 2022/07/05 00:00 [received] 2022/11/23 00:00 [revised] 2023/01/05 00:00 [accepted] 2023/02/23 10:33 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/04/19 00:00 [received] 2023/08/22 00:00 [revised] 2023/08/31 00:00 [accepted] 2023/09/08 18:41 [medline] 2023/09/08 18:41 [pubmed] 2023/09/08 18:05 [entrez]
 2023/09/01 00:41 [medline] 2023/09/01 00:41 [pubmed] 2023/08/31 19:24 [entrez]
 2023/05/30 00:00 [received] 2023/07/04 00:00 [accepted] 2023/07/03 00:00 [revised] 2023/07/12 01:07 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 23:25 [entrez]
 2022/02/13 00:00 [received] 2022/09/22 00:00 [accepted] 2023/05/03 06:43 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 02:02 [entrez]
 2022/12/12 00:00 [received] 2023/06/06 00:00 [accepted] 2023/06/23 01:11 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 23:27 [entrez]
 2023/02/16 19:02 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/17 06:00 [medline]
 2023/01/16 00:00 [received] 2023/03/15 00:00 [accepted] 2023/04/24 06:43 [medline] 2023/04/24 06:42 [pubmed] 2023/04/24 03:28 [entrez]
 2023/02/23 00:00 [received] 2023/03/23 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/10 15:14 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:08 [entrez]
 2022/06/27 00:00 [received] 2023/02/13 00:00 [accepted] 2023/03/20 04:03 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2022/05/05 00:00 [received] 2022/11/16 00:00 [accepted] 2023/01/31 19:12 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/01 06:00 [medline]
 2022/07/17 00:00 [received] 2022/09/29 00:00 [revised] 2022/10/27 00:00 [accepted] 2023/03/22 08:03 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/23 06:00 [medline]
 2023/05/25 00:00 [received] 2023/07/22 00:00 [accepted] 2023/09/04 06:44 [medline] 2023/09/04 06:43 [pubmed] 2023/09/04 05:04 [entrez]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/05/13 00:00 [received] 2023/06/23 00:00 [accepted] 2023/06/22 00:00 [revised] 2023/07/12 13:07 [medline] 2023/07/12 13:07 [pubmed] 2023/07/12 11:09 [entrez]
 2022/12/10 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/21 01:31 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2022/03/29 00:00 [received] 2022/10/09 00:00 [accepted] 2023/02/02 02:07 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/03 06:01 [medline]
 2023/05/13 00:00 [received] 2023/08/14 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/08/25 00:42 [pubmed] 2023/08/25 00:42 [medline] 2023/08/24 19:23 [entrez]
 2022/04/10 00:00 [received] 2022/06/22 00:00 [accepted] 2023/03/08 01:44 [entrez] 2023/03/09 06:00 [pubmed] 2023/03/09 06:01 [medline]
 2023/02/24 00:00 [received] 2023/06/20 00:00 [revised] 2023/06/30 00:00 [accepted] 2023/07/03 00:41 [pubmed] 2023/07/03 00:41 [medline] 2023/07/02 19:26 [entrez]
 2023/05/29 00:42 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 18:53 [entrez]
 2023/04/30 00:00 [received] 2023/06/26 00:00 [revised] 2023/07/31 00:00 [accepted] 2023/08/27 05:43 [medline] 2023/08/27 05:43 [pubmed] 2023/08/26 21:58 [entrez]
 2023/03/27 18:52 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2022/09/12 00:00 [received] 2022/11/20 00:00 [revised] 2022/11/25 00:00 [accepted] 2023/05/28 13:09 [medline] 2023/05/28 13:09 [pubmed] 2023/05/28 10:33 [entrez]
 2022/04/01 00:00 [received] 2022/09/20 00:00 [revised] 2023/02/21 00:00 [accepted] 2023/03/13 04:11 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2023/04/12 00:00 [received] 2023/07/29 00:00 [revised] 2023/08/10 00:00 [accepted] 2023/09/01 00:41 [medline] 2023/09/01 00:41 [pubmed] 2023/08/31 18:05 [entrez]
 2023/02/25 00:00 [received] 2023/05/30 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:09 [entrez]
 2022/09/27 00:00 [received] 2023/01/01 00:00 [accepted] 2023/02/27 05:38 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2023/06/23 06:42 [medline] 2023/06/23 06:42 [pubmed] 2023/06/23 02:11 [entrez]
 2023/02/26 00:00 [received] 2023/03/15 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:15 [entrez]
 2023/07/12 00:00 [received] 2023/08/06 00:00 [revised] 2023/08/09 00:00 [accepted] 2023/08/26 10:42 [medline] 2023/08/26 10:41 [pubmed] 2023/08/26 01:09 [entrez]
 2023/04/21 00:00 [received] 2023/07/11 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:11 [entrez]
 2023/04/13 00:00 [received] 2023/07/04 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/08/07 06:41 [pubmed] 2023/08/07 04:48 [entrez]
 2023/03/02 00:00 [received] 2023/07/07 00:00 [accepted] 2023/07/17 15:09 [medline] 2023/07/17 15:09 [pubmed] 2023/07/17 11:08 [entrez]
 2023/07/10 06:42 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:53 [entrez]
 2022/07/29 00:00 [received] 2022/12/18 00:00 [accepted] 2023/02/06 03:30 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:01 [medline]
 2023/03/14 00:00 [received] 2023/05/15 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/08/21 18:42 [medline] 2023/08/21 18:42 [pubmed] 2023/08/21 18:01 [entrez]
 2023/07/22 21:07 [medline] 2023/07/22 21:07 [pubmed] 2023/07/22 08:03 [entrez]
 2022/12/15 00:00 [received] 2023/01/19 00:00 [revised] 2023/01/20 00:00 [accepted] 2023/02/27 04:44 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2022/12/22 00:00 [received] 2023/02/05 00:00 [revised] 2023/02/06 00:00 [accepted] 2023/02/25 03:07 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/07/26 00:00 [accepted] 2023/08/30 00:41 [medline] 2023/08/30 00:41 [pubmed] 2023/08/29 21:03 [entrez]
 2023/08/21 12:42 [medline] 2023/08/21 12:42 [pubmed] 2023/08/21 10:35 [entrez]
 2023/04/16 00:00 [received] 2023/07/04 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/07/22 10:42 [medline] 2023/07/22 10:42 [pubmed] 2023/07/21 21:00 [entrez]
 2022/05/02 00:00 [received] 2023/06/22 00:00 [revised] 2023/07/03 00:00 [accepted] 2023/07/16 01:06 [pubmed] 2023/07/16 01:06 [medline] 2023/07/15 18:06 [entrez]

 2022/12/15 00:00 [received] 2023/01/21 00:00 [revised] 2023/01/25 00:00 [accepted] 2023/02/25 03:18 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/06/29 01:08 [medline] 2023/06/29 01:08 [pubmed] 2023/06/28 23:28 [entrez]
 2022/09/01 00:00 [received] 2023/07/01 00:00 [accepted] 2023/05/30 00:00 [revised] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 23:24 [entrez]
 2023/04/06 00:00 [received] 2023/06/12 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/07/14 13:07 [pubmed] 2023/07/14 13:07 [medline] 2023/07/13 19:22 [entrez]
 2022/08/06 00:00 [received] 2022/10/17 00:00 [accepted] 2023/06/08 06:43 [medline] 2023/06/08 06:42 [pubmed] 2023/06/08 04:23 [entrez]
 2023/05/18 06:42 [medline] 2023/05/18 06:42 [pubmed] 2023/05/18 00:43 [entrez]
 2022/12/29 00:00 [received] 2023/01/14 00:00 [revised] 2023/01/19 00:00 [accepted] 2023/02/25 01:43 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/01/05 00:00 [received] 2023/01/23 00:00 [revised] 2023/01/24 00:00 [accepted] 2023/02/25 01:26 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/10/15 00:00 [received] 2023/01/18 00:00 [accepted] 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 04:04 [entrez]
 2023/03/04 00:00 [accepted] 2023/05/12 01:08 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 19:30 [entrez]
 2022/05/27 00:00 [received] 2022/11/04 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 03:44 [entrez]
 2021/11/21 00:00 [received] 2022/12/29 00:00 [accepted] 2023/03/27 03:39 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2022/11/30 00:00 [received] 2023/01/08 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/21 01:31 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2022/12/20 00:00 [received] 2023/05/20 00:00 [accepted] 2023/07/19 06:43 [medline] 2023/07/19 06:42 [pubmed] 2023/07/19 03:57 [entrez]
 2023/04/19 00:00 [received] 2023/06/11 00:00 [accepted] 2023/06/08 00:00 [revised] 2023/07/05 13:05 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 11:17 [entrez]
 2022/12/23 00:00 [received] 2023/02/07 00:00 [accepted] 2023/03/13 03:45 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/02/19 00:00 [received] 2023/04/07 00:00 [accepted] 2023/05/16 01:10 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 19:39 [entrez]
 2023/03/27 00:00 [revised] 2023/02/19 00:00 [received] 2023/03/28 00:00 [accepted] 2023/04/12 06:14 [entrez] 2023/04/13 06:00 [pubmed] 2023/04/13 06:00 [medline]
 2023/01/25 00:00 [received] 2023/02/22 00:00 [accepted] 2023/03/27 03:53 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2023/08/08 00:00 [accepted] 2023/04/13 00:00 [received] 2023/07/17 00:00 [revised] 2023/09/13 00:42 [medline] 2023/09/13 00:42 [pubmed] 2023/09/12 21:12 [entrez]
 2022/11/11 00:00 [received] 2023/07/11 00:00 [revised] 2023/07/15 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:58 [entrez]
 2023/03/31 00:00 [received] 2023/05/09 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/06/15 06:43 [medline] 2023/06/15 06:42 [pubmed] 2023/06/15 01:02 [entrez]
 2023/03/06 06:00 [pubmed] 2023/03/06 06:00 [medline] 2023/03/05 14:28 [entrez]
 2023/03/30 00:00 [received] 2023/05/18 00:00 [accepted] 2023/07/24 06:44 [medline] 2023/07/24 06:43 [pubmed] 2023/07/24 04:29 [entrez]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/02/27 00:00 [revised] 2022/08/25 00:00 [received] 2023/03/07 00:00 [accepted] 2023/04/05 08:04 [entrez] 2023/04/06 06:00 [pubmed] 2023/04/06 06:00 [medline]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2023/01/18 00:00 [received] 2023/08/01 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/14 18:10 [entrez]
 2022/11/11 00:00 [received] 2023/05/17 00:00 [accepted] 2023/06/24 11:43 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 23:30 [entrez]
 2022/08/05 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/20 00:00 [accepted] 2023/03/22 00:13 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/23 06:00 [medline]
 2023/04/21 00:00 [received] 2023/06/20 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/08/07 06:41 [pubmed] 2023/08/07 04:28 [entrez]
 2022/11/01 00:00 [received] 2023/01/04 00:00 [accepted] 2023/02/10 03:08 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2023/06/15 00:00 [received] 2023/08/29 00:00 [revised] 2023/08/30 00:00 [accepted] 2023/09/10 00:41 [medline] 2023/09/10 00:41 [pubmed] 2023/09/09 18:07 [entrez]
 2023/07/12 13:07 [pubmed] 2023/07/12 13:07 [medline] 2023/07/12 06:43 [entrez]
 2023/06/19 00:00 [received] 2023/08/08 00:00 [revised] 2023/08/21 00:00 [accepted] 2023/09/09 11:46 [medline] 2023/09/09 11:45 [pubmed] 2023/09/09 01:08 [entrez]
 2023/07/17 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:08 [entrez]
 2023/08/23 18:42 [medline] 2023/08/23 18:42 [pubmed] 2023/08/23 12:33 [entrez]
 2023/08/03 13:09 [medline] 2023/08/03 13:09 [pubmed] 2023/08/03 11:23 [entrez]
 2023/01/18 00:00 [received] 2023/05/16 00:00 [accepted] 2023/04/29 00:00 [revised] 2023/06/06 13:09 [medline] 2023/06/06 13:09 [pubmed] 2023/06/06 11:07 [entrez]
 2022/12/20 00:00 [received] 2023/01/02 00:00 [accepted] 2023/01/12 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/11 11:15 [entrez]
 2023/05/03 00:00 [accepted] 2023/05/20 09:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 21:38 [entrez]
 2023/01/16 00:00 [received] 2023/02/09 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 03:48 [entrez] 2023/04/04 06:00 [pubmed]
 2023/06/07 00:00 [received] 2023/06/19 00:00 [accepted] 2023/07/12 06:43 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 03:52 [entrez]
 2023/06/13 00:00 [revised] 2023/04/17 00:00 [received] 2023/09/04 06:42 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 08:33 [entrez]
 2022/09/08 00:00 [received] 2022/12/06 00:00 [revised] 2022/12/06 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/09 04:38 [entrez]
 2023/06/23 00:00 [received] 2023/08/10 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 18:08 [entrez]
 2023/07/06 00:00 [revised] 2023/05/15 00:00 [received] 2023/07/22 00:00 [accepted] 2023/08/25 06:42 [medline] 2023/08/25 06:42 [pubmed] 2023/08/25 03:09 [entrez]
 2023/03/14 00:00 [received] 2023/06/12 00:00 [revised] 2023/06/27 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/07/27 06:42 [pubmed] 2023/07/27 01:13 [entrez]
 2023/07/19 00:00 [revised] 2023/02/04 00:00 [received] 2023/07/19 00:00 [accepted] 2023/07/20 13:06 [pubmed] 2023/07/20 13:06 [medline] 2023/07/20 08:44 [entrez]
 2021/12/15 00:00 [received] 2022/07/02 00:00 [revised] 2022/08/10 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 03:46 [entrez]
 2022/09/25 00:00 [received] 2023/05/15 00:00 [accepted] 2023/06/30 13:12 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 09:54 [entrez]
 2023/03/02 00:00 [received] 2023/03/28 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/06/23 13:08 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 10:30 [entrez]
 2022/11/26 00:00 [received] 2023/04/17 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/06/22 13:10 [medline] 2023/06/22 13:09 [pubmed] 2023/06/22 09:49 [entrez]
 2023/03/10 00:00 [received] 2023/04/28 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 15:48 [entrez]
 2023/02/13 23:02 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2023/01/02 00:00 [accepted] 2023/02/03 01:59 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/04 06:01 [medline]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/05/23 00:00 [received] 2023/08/10 00:00 [accepted] 2023/09/11 06:44 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 04:49 [entrez]
 2023/05/31 00:00 [received] 2023/06/24 00:00 [revised] 2023/06/26 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:12 [entrez]
 2023/07/28 00:00 [received] 2023/08/21 00:00 [accepted] 2023/09/04 18:41 [medline] 2023/09/04 18:41 [pubmed] 2023/09/04 12:42 [entrez]
 2023/06/15 00:00 [received] 2023/07/03 00:00 [accepted] 2023/08/10 06:43 [medline] 2023/08/10 06:42 [pubmed] 2023/08/10 04:32 [entrez]
 2023/01/15 00:00 [received] 2023/06/23 00:00 [accepted] 2023/08/10 06:43 [medline] 2023/08/10 06:42 [pubmed] 2023/08/10 03:59 [entrez]
 2023/07/28 06:44 [medline] 2023/07/28 06:43 [pubmed] 2023/07/28 04:05 [entrez]
 2023/04/06 00:00 [received] 2023/05/26 00:00 [revised] 2023/07/16 00:00 [accepted] 2023/07/28 01:08 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 18:03 [entrez]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/04/26 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 13:19 [entrez]
 2022/12/19 00:00 [received] 2023/04/14 00:00 [accepted] 2023/06/21 13:05 [medline] 2023/06/21 13:04 [pubmed] 2023/06/21 11:13 [entrez]
 2023/02/16 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:59 [entrez]
 2022/12/10 00:00 [received] 2023/02/02 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 02:02 [entrez] 2023/03/30 06:00 [pubmed]
 2023/02/01 00:00 [received] 2023/02/17 00:00 [revised] 2023/02/21 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:18 [entrez] 2023/03/30 06:00 [pubmed]
 2022/11/02 00:00 [received] 2022/12/13 00:00 [accepted] 2023/01/30 04:01 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/12/01 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/21 01:31 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2023/04/24 00:00 [received] 2023/06/10 00:00 [revised] 2023/06/11 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:31 [entrez]
 2023/07/05 19:13 [medline] 2023/07/05 19:12 [pubmed] 2023/07/05 15:42 [entrez]
 2023/03/28 06:01 [medline] 2023/03/27 21:43 [entrez] 2023/03/28 06:00 [pubmed]
 2023/07/25 06:43 [medline] 2023/07/24 13:06 [pubmed] 2023/07/24 10:03 [entrez]
 2023/01/15 00:00 [received] 2023/03/10 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:49 [entrez]
 2023/08/10 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:41 [entrez]
 2023/03/22 00:00 [received] 2023/07/20 00:00 [accepted] 2023/08/04 01:07 [medline] 2023/08/04 01:07 [pubmed] 2023/08/03 21:03 [entrez]
 2022/12/19 00:00 [received] 2023/02/27 00:00 [accepted] 2023/06/08 06:43 [medline] 2023/06/08 06:42 [pubmed] 2023/06/08 04:23 [entrez]
 2023/02/28 01:02 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:00 [medline]
 2022/12/26 00:00 [received] 2023/05/03 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:15 [entrez]
 2022/08/05 00:00 [received] 2023/02/21 00:00 [accepted] 2023/03/18 12:19 [entrez] 2023/03/19 06:00 [pubmed] 2023/03/19 06:00 [medline]
 2022/10/04 00:00 [received] 2022/12/20 00:00 [accepted] 2023/01/15 14:06 [entrez] 2023/01/16 06:00 [pubmed] 2023/01/16 06:00 [medline]
 2023/07/28 13:11 [pubmed] 2023/07/28 13:11 [medline] 2023/07/28 07:23 [entrez]
 2023/04/11 00:00 [received] 2023/07/24 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 04:35 [entrez]
 2023/03/09 00:00 [received] 2023/08/11 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/08/29 00:41 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 18:01 [entrez]
 2023/04/19 00:00 [received] 2023/07/18 00:00 [revised] 2023/08/04 00:00 [accepted] 2023/08/28 00:41 [medline] 2023/08/28 00:41 [pubmed] 2023/08/27 18:08 [entrez]
 2023/05/04 00:00 [received] 2023/06/06 00:00 [revised] 2023/06/06 00:00 [accepted] 2023/08/03 13:09 [medline] 2023/08/03 13:09 [pubmed] 2023/08/03 08:03 [entrez]
 2023/04/24 00:00 [received] 2023/06/12 00:00 [revised] 2023/07/22 00:00 [accepted] 2023/07/29 06:42 [medline] 2023/07/29 06:42 [pubmed] 2023/07/28 18:09 [entrez]
 2023/07/18 00:00 [revised] 2023/07/11 00:00 [received] 2023/07/19 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 00:04 [entrez]
 2023/04/17 00:00 [received] 2023/06/14 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:47 [entrez]
 2023/04/17 00:00 [received] 2023/06/13 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:26 [entrez]
 2023/04/12 00:00 [received] 2023/05/31 00:00 [accepted] 2023/07/03 13:07 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:23 [entrez]
 2022/11/22 00:00 [received] 2023/05/10 00:00 [accepted] 2023/05/01 00:00 [revised] 2023/06/21 13:04 [pubmed] 2023/06/21 13:04 [medline] 2023/06/21 07:02 [entrez]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2023/01/07 00:00 [received] 2023/03/19 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:47 [entrez]
 2023/02/17 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:21 [entrez] 2023/03/30 06:00 [pubmed]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/12/06 00:00 [received] 2023/01/16 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/25 01:44 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/07/14 00:00 [received] 2023/08/12 00:00 [revised] 2023/08/18 00:00 [accepted] 2023/08/26 10:43 [medline] 2023/08/26 10:42 [pubmed] 2023/08/26 01:07 [entrez]
 2023/04/14 00:00 [received] 2023/07/16 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/15 00:42 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 18:06 [entrez]
 2023/02/25 00:00 [received] 2023/03/14 00:00 [revised] 2023/03/27 00:00 [accepted] 2023/07/08 10:43 [medline] 2023/07/08 10:42 [pubmed] 2023/07/08 01:12 [entrez]
 2023/06/28 13:09 [medline] 2023/06/28 13:09 [pubmed] 2023/06/28 06:34 [entrez]
 2023/06/20 06:42 [medline] 2023/06/20 06:42 [pubmed] 2023/06/20 04:33 [entrez]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2022/11/29 00:00 [received] 2023/03/02 00:00 [accepted] 2023/04/21 06:42 [medline] 2023/04/21 06:41 [pubmed] 2023/04/21 02:29 [entrez]
 2023/03/17 00:00 [accepted] 2023/04/20 06:42 [medline] 2023/04/20 06:41 [pubmed] 2023/04/20 02:23 [entrez]
 2022/11/05 00:00 [received] 2023/02/10 00:00 [accepted] 2023/03/27 03:53 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2022/05/16 00:00 [received] 2022/07/19 00:00 [revised] 2022/08/12 00:00 [accepted] 2023/03/17 02:46 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/18 06:01 [medline]
 2023/01/06 00:00 [received] 2023/02/27 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/03/11 01:22 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/12 06:01 [medline]
 2022/12/14 00:00 [received] 2023/01/28 00:00 [revised] 2023/02/02 00:00 [accepted] 2023/02/24 09:33 [entrez] 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline]
 2022/10/25 06:00 [pubmed] 2022/10/25 06:01 [medline] 2022/10/24 04:53 [entrez]
 2023/09/12 06:42 [medline] 2023/09/12 06:42 [pubmed] 2023/09/12 05:28 [entrez]
 2023/06/02 00:00 [received] 2023/07/26 00:00 [accepted] 2023/09/11 06:44 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 05:03 [entrez]
 2023/07/09 00:00 [accepted] 2023/08/14 06:44 [medline] 2023/08/14 06:43 [pubmed] 2023/08/14 04:34 [entrez]
 2023/06/04 00:00 [received] 2023/07/07 00:00 [accepted] 2023/08/08 06:43 [medline] 2023/08/08 06:42 [pubmed] 2023/08/08 03:33 [entrez]
 2022/04/11 00:00 [received] 2022/06/01 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 04:13 [entrez] 2023/04/11 06:00 [pubmed]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2023/03/06 00:00 [received] 2023/08/06 00:00 [revised] 2023/09/03 00:00 [accepted] 2023/09/14 18:10 [entrez]
 2023/05/03 00:00 [received] 2023/08/04 00:00 [revised] 2023/08/26 00:00 [accepted] 2023/09/09 10:42 [medline] 2023/09/09 10:42 [pubmed] 2023/09/08 18:10 [entrez]
 2023/03/14 00:00 [received] 2023/06/20 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 18:02 [entrez]
 2023/05/16 00:00 [received] 2023/06/03 00:00 [revised] 2023/06/05 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:06 [entrez]
 2023/02/22 00:00 [received] 2023/03/16 00:00 [revised] 2023/03/24 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/13 01:11 [entrez] 2023/04/14 06:00 [pubmed]
 2022/10/29 06:00 [pubmed] 2022/10/29 06:01 [medline] 2022/10/28 21:43 [entrez]
 2023/08/01 00:00 [received] 2023/08/04 00:00 [accepted] 2023/09/07 00:41 [medline] 2023/09/07 00:41 [pubmed] 2023/09/06 21:56 [entrez]
 2023/05/26 06:42 [medline] 2023/05/25 01:07 [pubmed] 2023/05/24 20:59 [entrez]
 2023/02/27 00:00 [revised] 2022/03/30 00:00 [received] 2023/03/06 00:00 [accepted] 2023/03/10 06:00 [pubmed] 2023/03/10 06:00 [medline] 2023/03/09 21:42 [entrez]
 2023/08/09 00:00 [received] 2023/08/11 00:00 [accepted] 2023/09/08 06:44 [medline] 2023/09/08 06:43 [pubmed] 2023/09/08 04:07 [entrez]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/09/07 12:42 [medline] 2023/09/07 12:42 [pubmed] 2023/09/07 07:23 [entrez]
 2023/06/07 00:00 [received] 2023/07/16 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/08/12 10:44 [medline] 2023/08/12 10:44 [pubmed] 2023/08/12 01:01 [entrez]
 2023/05/30 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:10 [entrez]
 2022/08/01 00:00 [received] 2022/12/23 00:00 [accepted] 2023/01/30 04:25 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/06/12 00:00 [received] 2023/08/08 00:00 [revised] 2023/08/26 00:00 [accepted] 2023/09/09 11:43 [medline] 2023/09/09 11:42 [pubmed] 2023/09/09 01:07 [entrez]
 2023/02/10 00:00 [received] 2023/07/20 00:00 [accepted] 2023/09/08 06:44 [medline] 2023/09/08 06:43 [pubmed] 2023/09/08 03:54 [entrez]
 2023/07/25 06:44 [medline] 2023/07/25 06:43 [pubmed] 2023/07/25 01:21 [entrez]
 2022/03/17 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/30 00:42 [medline] 2023/08/30 00:41 [pubmed] 2023/08/29 23:49 [entrez]
 2022/10/10 00:00 [received] 2022/12/30 00:00 [accepted] 2023/01/23 05:02 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2023/07/28 13:11 [pubmed] 2023/07/28 13:11 [medline] 2023/07/28 07:13 [entrez]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/01/16 00:00 [received] 2023/07/24 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/03 00:41 [medline] 2023/09/03 00:41 [pubmed] 2023/09/02 18:15 [entrez]
 2021/06/05 00:00 [received] 2020/11/10 00:00 [revised] 2022/01/02 00:00 [accepted] 2023/06/22 13:10 [medline] 2023/06/22 13:09 [pubmed] 2023/06/22 09:56 [entrez]
 2023/01/23 00:00 [received] 2023/03/06 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/04/27 12:43 [medline] 2023/04/27 12:42 [pubmed] 2023/04/27 10:33 [entrez]
 2023/04/03 00:00 [received] 2023/05/25 00:00 [accepted] 2023/07/03 13:07 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:25 [entrez]
 2023/06/08 00:00 [received] 2023/09/01 00:00 [accepted] 2023/09/08 12:42 [medline] 2023/09/08 12:42 [pubmed] 2023/09/08 11:10 [entrez]
 2021/01/07 06:00 [pubmed] 2021/01/07 06:01 [medline] 2021/01/06 05:28 [entrez]
 2023/07/24 19:09 [pubmed] 2023/07/24 19:09 [medline] 2023/07/24 13:33 [entrez]
 2023/05/24 00:00 [received] 2023/07/01 00:00 [revised] 2023/07/10 00:00 [accepted] 2023/07/17 00:41 [medline] 2023/07/17 00:41 [pubmed] 2023/07/16 18:05 [entrez]
 2023/07/05 13:06 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 09:54 [entrez]
 2023/01/29 00:00 [received] 2023/03/20 00:00 [accepted] 2023/04/28 06:43 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 02:24 [entrez]
 2023/03/06 00:00 [received] 2023/04/07 00:00 [accepted] 2023/05/16 06:42 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:10 [entrez]
 2022/03/06 00:00 [received] 2022/12/12 00:00 [accepted] 2023/01/23 23:40 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2023/03/22 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/13 00:00 [accepted] 2023/06/22 01:07 [pubmed] 2023/06/22 01:07 [medline] 2023/06/21 18:05 [entrez]
 2022/09/16 00:00 [received] 2023/03/08 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/05/16 01:10 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 19:38 [entrez]
 2023/04/17 00:00 [received] 2023/05/15 00:00 [accepted] 2023/06/19 06:43 [medline] 2023/06/19 06:42 [pubmed] 2023/06/19 02:43 [entrez]
 2022/11/17 00:00 [received] 2023/01/27 00:00 [accepted] 2023/02/16 06:01 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 23:28 [entrez]
 2023/01/10 00:00 [received] 2023/04/12 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/07/19 19:07 [pubmed] 2023/07/19 19:07 [medline] 2023/07/19 18:03 [entrez]
 2023/01/18 00:00 [received] 2023/06/03 00:00 [accepted] 2023/07/16 19:17 [medline] 2023/07/16 19:16 [pubmed] 2023/07/16 14:55 [entrez]
 2023/05/19 00:00 [revised] 2023/01/28 00:00 [received] 2023/06/05 00:00 [accepted] 2023/06/30 19:14 [pubmed] 2023/06/30 19:14 [medline] 2023/06/30 13:44 [entrez]
 2023/03/27 00:00 [received] 2023/06/03 00:00 [accepted] 2023/06/01 00:00 [revised] 2023/06/21 13:04 [pubmed] 2023/06/21 13:04 [medline] 2023/06/21 11:08 [entrez]
 2023/06/10 15:14 [medline] 2023/06/10 15:14 [pubmed] 2023/06/09 22:33 [entrez]
 2023/05/06 09:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/06 03:39 [entrez]
 2022/11/19 00:00 [received] 2023/02/22 00:00 [accepted] 2023/04/28 06:43 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 02:38 [entrez]
 2023/03/18 00:00 [received] 2023/05/01 00:00 [revised] 2023/05/03 00:00 [accepted] 2023/05/13 15:14 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:34 [entrez]
 2023/05/19 00:00 [received] 2023/07/07 00:00 [accepted] 2023/08/25 06:43 [medline] 2023/08/25 06:42 [pubmed] 2023/08/25 03:53 [entrez]
 2023/08/24 06:42 [pubmed] 2023/08/24 06:42 [medline] 2023/08/24 02:09 [entrez]
 2022/11/30 00:00 [received] 2023/07/06 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 00:04 [entrez]
 2022/12/30 00:00 [received] 2023/06/14 00:00 [accepted] 2023/07/06 13:14 [medline] 2023/07/06 13:14 [pubmed] 2023/07/06 11:12 [entrez]
 2023/04/28 00:00 [received] 2023/06/12 00:00 [accepted] 2023/06/22 01:07 [pubmed] 2023/06/22 01:07 [medline] 2023/06/21 23:27 [entrez]
 2023/02/22 00:00 [received] 2023/06/07 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/06/19 13:08 [pubmed] 2023/06/19 11:08 [entrez]
 2023/04/14 00:00 [received] 2023/05/23 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/10 15:14 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:08 [entrez]
 2023/05/08 00:00 [received] 2023/05/23 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/10 15:15 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:02 [entrez]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/12/09 00:00 [received] 2023/01/20 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/02/24 11:55 [entrez] 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline]
 2021/03/06 00:00 [received] 2021/10/09 00:00 [revised] 2021/12/31 00:00 [accepted] 2023/02/01 01:51 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/02 06:01 [medline]
 2022/12/12 00:00 [received] 2022/12/29 00:00 [accepted] 2023/01/30 03:50 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/12/15 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/01/26 06:00 [pubmed] 2023/01/26 06:01 [medline] 2023/01/25 18:16 [entrez]
 2022/09/14 00:00 [received] 2022/11/17 00:00 [accepted] 2023/01/13 02:05 [entrez] 2023/01/14 06:00 [pubmed] 2023/01/14 06:01 [medline]
 2022/01/20 00:00 [received] 2022/06/15 00:00 [accepted] 2022/02/16 00:01 [medline] 2022/02/16 00:00 [pubmed] 2023/05/18 16:53 [entrez]
 2023/03/10 00:00 [received] 2023/08/16 00:00 [accepted] 2023/09/12 12:42 [medline] 2023/09/12 12:42 [pubmed] 2023/09/12 11:23 [entrez]
 2023/05/25 00:00 [received] 2023/07/25 00:00 [accepted] 2023/07/25 00:00 [revised] 2023/08/31 12:43 [medline] 2023/08/31 12:43 [pubmed] 2023/08/31 11:07 [entrez]
 2023/04/27 00:00 [received] 2023/07/25 00:00 [accepted] 2023/08/28 06:43 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 05:01 [entrez]
 2022/10/10 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/08/02 01:07 [medline] 2023/08/02 01:07 [pubmed] 2023/08/01 23:14 [entrez]
 2024/02/16 00:00 [pmc-release] 2023/07/03 13:07 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:47 [entrez]
 2023/06/20 19:15 [medline] 2023/06/20 19:15 [pubmed] 2023/06/20 13:52 [entrez]
 2023/02/09 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/05 00:00 [accepted] 2023/06/20 06:43 [medline] 2023/06/20 06:42 [pubmed] 2023/06/20 02:29 [entrez]
 2021/12/09 00:00 [received] 2021/12/23 00:00 [accepted] 2023/06/08 06:43 [medline] 2023/06/08 06:42 [pubmed] 2023/06/08 04:18 [entrez]
 2023/05/24 13:08 [pubmed] 2023/05/24 13:08 [medline] 2023/05/24 10:04 [entrez]
 2022/11/08 00:00 [received] 2023/02/07 00:00 [accepted] 2023/03/13 03:48 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2023/03/07 02:01 [entrez] 2023/03/08 06:00 [pubmed] 2023/03/08 06:01 [medline]
 2022/11/08 00:00 [received] 2022/12/12 00:00 [accepted] 2023/01/23 04:51 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2022/09/29 00:00 [received] 2022/11/02 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2022/11/18 06:01 [medline] 2022/11/17 13:57 [entrez]
 2023/03/31 00:00 [received] 2023/07/20 00:00 [accepted] 2023/09/08 06:44 [medline] 2023/09/08 06:43 [pubmed] 2023/09/08 03:54 [entrez]
 2023/03/03 00:00 [received] 2023/03/13 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 04:02 [entrez] 2023/04/11 06:00 [pubmed]
 2023/06/21 00:00 [received] 2023/08/04 00:00 [revised] 2023/08/11 00:00 [accepted] 2023/08/26 10:47 [medline] 2023/08/26 10:46 [pubmed] 2023/08/26 01:19 [entrez]
 2023/02/21 00:00 [received] 2023/07/07 00:00 [accepted] 2023/08/21 06:44 [medline] 2023/08/21 06:43 [pubmed] 2023/08/21 04:35 [entrez]
 2023/08/13 00:42 [medline] 2023/08/13 00:42 [pubmed] 2023/08/12 08:13 [entrez]
 2023/03/14 00:00 [received] 2023/06/01 00:00 [revised] 2023/07/06 00:00 [accepted] 2023/08/09 06:44 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 03:56 [entrez]
 2023/03/03 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/25 00:00 [accepted] 2023/07/04 01:05 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 18:03 [entrez]
 2023/03/14 00:00 [received] 2023/05/08 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:00 [entrez]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2023/02/08 00:00 [received] 2023/04/07 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:12 [entrez]
 2023/03/01 00:00 [received] 2023/03/23 00:00 [revised] 2023/03/23 00:00 [accepted] 2023/04/24 06:43 [medline] 2023/04/24 06:42 [pubmed] 2023/04/24 03:54 [entrez]
 2023/01/10 00:00 [received] 2023/04/03 00:00 [accepted] 2023/03/28 00:00 [revised] 2023/04/18 11:23 [entrez] 2023/04/19 06:00 [pubmed] 2023/04/19 06:00 [medline]
 2023/02/12 06:00 [pubmed] 2023/02/12 06:00 [medline] 2023/02/11 10:02 [entrez]
 2021/10/08 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/11 00:00 [accepted] 2023/07/17 00:42 [pubmed] 2023/07/17 00:42 [medline] 2023/07/16 18:08 [entrez]
 2023/05/18 00:00 [received] 2023/07/25 00:00 [accepted] 2023/08/24 06:43 [medline] 2023/08/24 06:42 [pubmed] 2023/08/24 04:13 [entrez]
 2023/07/14 13:08 [medline] 2023/07/14 13:08 [pubmed] 2023/07/14 08:32 [entrez]
 2023/06/07 00:00 [received] 2023/06/23 00:00 [revised] 2023/06/24 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:01 [entrez]
 2023/02/13 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 04:28 [entrez]
 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2023/02/06 00:00 [revised] 2022/09/16 00:00 [received] 2023/04/11 00:00 [accepted] 2023/04/19 06:00 [pubmed] 2023/04/19 06:00 [medline] 2023/04/18 05:43 [entrez]
 2023/01/29 00:00 [received] 2023/03/13 00:00 [accepted] 2023/04/14 06:01 [medline] 2023/04/13 01:55 [entrez] 2023/04/14 06:00 [pubmed]
 2023/02/16 00:00 [accepted] 2023/04/12 11:12 [entrez] 2023/04/13 06:00 [pubmed] 2023/04/13 06:00 [medline]
 2022/11/23 00:00 [received] 2023/01/12 00:00 [accepted] 2023/02/07 06:01 [medline] 2023/02/07 06:00 [pubmed] 2023/02/06 23:16 [entrez]
 2022/10/18 00:00 [received] 2022/12/21 00:00 [accepted] 2023/01/30 03:47 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/12/06 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/09 00:00 [accepted] 2023/07/16 01:06 [pubmed] 2023/07/16 01:06 [medline] 2023/07/15 18:06 [entrez]
 2022/12/20 00:00 [received] 2023/03/09 00:00 [accepted] 2023/03/27 06:01 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 14:13 [entrez]
 2023/02/23 00:00 [received] 2023/04/21 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:50 [entrez]
 2023/03/06 03:51 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2022/10/14 00:00 [received] 2022/12/20 00:00 [revised] 2023/01/06 00:00 [accepted] 2023/02/03 06:00 [pubmed] 2023/02/03 06:00 [medline] 2023/02/02 19:21 [entrez]
 2022/08/30 00:00 [received] 2023/01/18 00:00 [accepted] 2023/02/01 01:46 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/02 06:01 [medline]
 2023/05/09 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/03 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:06 [entrez]
 2023/04/12 00:00 [received] 2023/07/06 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/07/31 00:41 [medline] 2023/07/31 00:41 [pubmed] 2023/07/30 18:07 [entrez]
 2022/10/11 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/27 03:45 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2022/11/02 00:00 [received] 2023/01/13 00:00 [accepted] 2023/02/23 09:54 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2022/03/18 00:00 [received] 2023/01/02 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/02/23 09:19 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/07/14 13:09 [medline] 2023/07/14 13:08 [pubmed] 2023/07/14 07:09 [entrez]
 2023/06/09 00:00 [received] 2023/06/19 00:00 [accepted] 2023/06/30 01:06 [pubmed] 2023/06/30 01:06 [medline] 2023/06/29 18:05 [entrez]
 2023/05/10 00:00 [received] 2023/07/18 00:00 [accepted] 2023/06/25 00:00 [revised] 2023/08/01 13:08 [medline] 2023/08/01 13:08 [pubmed] 2023/08/01 06:53 [entrez]
 2023/03/27 00:00 [received] 2023/05/18 00:00 [accepted] 2023/06/19 06:43 [medline] 2023/06/19 06:42 [pubmed] 2023/06/19 02:42 [entrez]
 2023/06/30 13:11 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 06:53 [entrez]
 2022/12/18 00:00 [received] 2023/02/03 00:00 [revised] 2023/02/03 00:00 [accepted] 2023/02/23 09:15 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/03/25 00:00 [received] 2023/06/14 00:00 [accepted] 2023/07/21 06:43 [medline] 2023/07/21 06:43 [pubmed] 2023/07/21 03:57 [entrez]
 2022/07/09 00:00 [received] 2023/05/23 00:00 [revised] 2023/05/30 00:00 [accepted] 2023/06/22 01:08 [medline] 2023/06/22 01:07 [pubmed] 2023/06/21 18:04 [entrez]
 2023/04/10 06:42 [medline] 2021/06/05 06:00 [pubmed] 2021/06/04 05:31 [entrez]
 2022/05/10 00:00 [received] 2022/11/21 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:04 [entrez] 2023/04/04 06:00 [pubmed]
 2023/03/13 01:13 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:00 [medline]
 2023/06/27 00:00 [received] 2023/08/02 00:00 [revised] 2023/08/04 00:00 [accepted] 2023/08/15 00:42 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 18:02 [entrez]
 2023/05/29 00:00 [received] 2023/08/08 00:00 [accepted] 2023/09/07 06:43 [medline] 2023/09/07 06:42 [pubmed] 2023/09/07 04:12 [entrez]
 2022/12/01 00:00 [received] 2023/03/10 00:00 [revised] 2023/03/27 00:00 [accepted] 2023/08/27 05:43 [medline] 2023/08/27 05:43 [pubmed] 2023/08/26 21:58 [entrez]
 2022/09/08 00:00 [received] 2023/05/26 00:00 [revised] 2023/05/30 00:00 [accepted] 2023/07/12 01:07 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 20:22 [entrez]
 2022/11/26 00:00 [received] 2023/01/16 00:00 [accepted] 2023/02/23 09:23 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/08/16 00:00 [revised] 2023/06/21 00:00 [received] 2023/08/21 00:00 [accepted] 2023/08/29 00:41 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 23:52 [entrez]
 2022/05/25 00:00 [received] 2023/04/13 00:00 [revised] 2023/06/05 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:55 [entrez]
 2023/05/13 00:00 [received] 2023/08/09 00:00 [accepted] 2023/09/11 06:44 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 04:27 [entrez]
 2022/08/05 00:00 [received] 2022/12/12 00:00 [accepted] 2023/01/24 01:47 [entrez] 2023/01/25 06:00 [pubmed] 2023/01/25 06:01 [medline]
 2023/08/25 06:42 [pubmed] 2023/08/25 06:42 [medline] 2023/08/25 04:13 [entrez]
 2023/08/11 00:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 23:26 [entrez]
 2023/03/17 03:13 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/18 06:01 [medline]
 2023/06/21 00:00 [accepted] 2023/08/17 12:41 [medline] 2023/08/17 12:41 [pubmed] 2023/08/17 11:06 [entrez]
 2023/05/05 00:00 [received] 2023/07/12 00:00 [accepted] 2023/07/27 01:09 [medline] 2023/07/27 01:09 [pubmed] 2023/07/26 20:52 [entrez]
 2023/03/01 00:00 [received] 2023/03/22 00:00 [revised] 2023/03/24 00:00 [accepted] 2023/05/16 06:43 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:15 [entrez]
 2023/07/11 00:00 [accepted] 2023/07/31 13:09 [medline] 2023/07/31 13:09 [pubmed] 2023/07/31 11:05 [entrez]
 2020/12/31 00:00 [received] 2023/02/13 00:00 [accepted] 2023/03/10 23:38 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2023/03/19 00:00 [received] 2023/07/24 00:00 [accepted] 2023/08/08 12:42 [medline] 2023/08/08 12:42 [pubmed] 2023/08/08 11:13 [entrez]
 2022/11/14 00:00 [received] 2023/03/23 00:00 [accepted] 2023/05/15 19:12 [medline] 2023/05/15 19:12 [pubmed] 2023/05/15 13:26 [entrez]
 2022/11/23 00:00 [received] 2023/03/09 00:00 [revised] 2023/05/12 00:00 [accepted] 2023/06/19 06:42 [medline] 2023/06/19 06:41 [pubmed] 2023/06/19 02:38 [entrez]
 2023/05/04 00:00 [received] 2023/06/05 00:00 [accepted] 2023/08/01 01:08 [medline] 2023/08/01 01:08 [pubmed] 2023/07/31 19:23 [entrez]
 2023/05/01 00:00 [received] 2023/05/28 00:00 [revised] 2023/05/29 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:24 [entrez]
 2022/09/08 00:00 [received] 2023/04/11 00:00 [accepted] 2023/05/26 06:42 [medline] 2023/05/26 06:42 [pubmed] 2023/05/26 03:45 [entrez]
 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 18:42 [entrez]
 2022/12/15 00:00 [received] 2023/03/14 00:00 [accepted] 2023/04/18 06:01 [medline] 2023/04/17 03:27 [entrez] 2023/04/18 06:00 [pubmed]
 2023/01/26 02:37 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/27 06:01 [medline]
 2023/03/31 00:00 [received] 2023/04/19 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/05/13 15:13 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:34 [entrez]
 2023/07/10 19:08 [medline] 2023/07/10 19:08 [pubmed] 2023/07/10 13:35 [entrez]
 2022/07/05 00:00 [received] 2023/02/02 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 03:45 [entrez] 2023/04/11 06:00 [pubmed]
 2023/02/26 00:00 [received] 2023/05/16 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/07/03 13:07 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:16 [entrez]
 2023/06/08 00:00 [received] 2023/06/21 00:00 [accepted] 2023/07/20 01:07 [medline] 2023/07/20 01:07 [pubmed] 2023/07/19 21:37 [entrez]
 2022/10/20 00:00 [received] 2022/10/20 00:00 [accepted] 2022/10/21 06:00 [pubmed] 2022/10/21 06:01 [medline] 2022/10/20 09:43 [entrez]
 2023/06/01 00:00 [received] 2023/06/29 00:00 [accepted] 2023/07/11 01:07 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 23:29 [entrez]
 2023/05/08 06:41 [medline] 2022/05/07 06:00 [pubmed] 2022/05/06 04:03 [entrez]
 2023/04/09 00:00 [received] 2023/05/07 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/06/05 00:41 [pubmed] 2023/06/04 18:03 [entrez]
 2023/07/10 19:08 [medline] 2023/07/10 19:08 [pubmed] 2023/07/10 12:04 [entrez]
 2022/07/08 02:32 [entrez] 2022/07/09 06:00 [pubmed] 2022/07/09 06:01 [medline]
 2022/08/19 00:00 [received] 2023/02/19 00:00 [accepted] 2023/03/31 06:01 [medline] 2023/03/30 02:58 [entrez] 2023/03/31 06:00 [pubmed]
 2023/04/06 00:00 [received] 2023/07/20 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/09/06 06:43 [medline] 2023/09/06 06:42 [pubmed] 2023/09/06 03:46 [entrez]
 2023/07/17 00:00 [revised] 2022/11/21 00:00 [received] 2023/08/10 00:00 [accepted] 2023/08/14 12:43 [pubmed] 2023/08/14 12:43 [medline] 2023/08/14 10:43 [entrez]
 2023/05/23 00:00 [received] 2023/07/22 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/12 10:42 [medline] 2023/08/12 10:42 [pubmed] 2023/08/11 18:02 [entrez]
 2023/02/08 00:00 [received] 2023/07/22 00:00 [accepted] 2023/08/03 13:09 [medline] 2023/08/03 13:09 [pubmed] 2023/08/03 11:05 [entrez]
 2023/03/26 00:00 [received] 2023/05/28 00:00 [accepted] 2023/07/27 06:44 [medline] 2023/07/27 06:43 [pubmed] 2023/07/27 04:25 [entrez]
 2023/04/19 00:00 [received] 2023/07/05 00:00 [accepted] 2023/07/19 01:06 [medline] 2023/07/19 01:06 [pubmed] 2023/07/18 23:33 [entrez]
 2023/05/09 00:00 [received] 2023/06/05 00:00 [revised] 2023/06/08 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:09 [entrez]
 2023/04/22 00:00 [received] 2023/05/14 00:00 [revised] 2023/05/15 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:18 [entrez]
 2022/11/16 00:00 [received] 2022/12/20 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/04/06 03:43 [entrez] 2023/04/07 06:00 [pubmed] 2023/04/07 06:00 [medline]
 2023/09/11 06:43 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 05:27 [entrez]
 2023/08/04 06:43 [pubmed] 2023/08/04 06:43 [medline] 2023/08/04 02:23 [entrez]
 2023/06/05 00:00 [received] 2023/08/17 00:00 [accepted] 2023/08/16 00:00 [revised] 2023/08/28 12:43 [medline] 2023/08/28 12:43 [pubmed] 2023/08/28 11:05 [entrez]
 2023/05/12 00:00 [received] 2023/07/11 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/25 00:42 [medline] 2023/08/25 00:42 [pubmed] 2023/08/24 18:03 [entrez]
 2023/04/26 00:00 [received] 2023/07/08 00:00 [revised] 2023/07/09 00:00 [accepted] 2023/08/09 06:44 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 04:07 [entrez]
 2023/03/19 00:00 [received] 2023/06/07 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/07/29 11:45 [medline] 2023/07/29 11:44 [pubmed] 2023/07/29 01:12 [entrez]
 2023/04/05 00:00 [received] 2023/06/23 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/07/28 01:08 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 18:03 [entrez]
 2022/08/09 00:00 [received] 2023/03/21 00:00 [revised] 2023/05/02 00:00 [accepted] 2024/05/26 00:00 [pmc-release] 2023/07/21 06:44 [medline] 2023/07/21 06:43 [pubmed] 2023/07/21 04:03 [entrez]
 2022/10/29 00:00 [received] 2023/03/23 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:56 [entrez]
 2022/10/03 00:00 [received] 2023/02/28 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 04:26 [entrez] 2023/04/11 06:00 [pubmed]
 2022/09/06 00:00 [received] 2023/03/22 00:00 [accepted] 2023/04/07 06:01 [medline] 2023/04/06 23:50 [entrez] 2023/04/07 06:00 [pubmed]
 2023/01/15 00:00 [received] 2023/02/27 00:00 [accepted] 2023/03/31 06:01 [medline] 2023/03/30 02:46 [entrez] 2023/03/31 06:00 [pubmed]
 2022/11/17 00:00 [received] 2023/02/09 00:00 [accepted] 2023/03/20 04:05 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2022/07/29 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/17 02:50 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/18 06:01 [medline]
 2022/01/27 00:00 [received] 2022/04/11 00:00 [accepted] 2023/02/01 01:51 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/02 06:01 [medline]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/11/09 00:00 [received] 2022/12/27 00:00 [revised] 2023/01/13 00:00 [accepted] 2023/01/21 01:31 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2023/03/01 00:00 [received] 2023/09/02 00:00 [revised] 2023/09/06 00:00 [accepted] 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 18:01 [entrez]
 2019/12/04 00:00 [received] 2020/05/11 00:00 [accepted] 2023/04/18 06:42 [medline] 2022/03/09 06:00 [pubmed] 2022/03/08 05:36 [entrez]
 2023/08/22 06:42 [medline] 2023/08/21 12:42 [pubmed] 2023/08/21 11:09 [entrez]
 2023/07/05 00:00 [received] 2023/08/03 00:00 [revised] 2023/08/09 00:00 [accepted] 2023/08/13 00:43 [pubmed] 2023/08/13 00:43 [medline] 2023/08/12 19:27 [entrez]
 2023/09/01 12:43 [medline] 2023/09/01 12:43 [pubmed] 2023/09/01 06:46 [entrez]
 2023/03/28 00:00 [received] 2023/07/25 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/08/27 05:43 [pubmed] 2023/08/27 05:43 [medline] 2023/08/26 19:25 [entrez]
 2023/07/17 00:00 [revised] 2023/03/14 00:00 [received] 2023/08/08 00:00 [accepted] 2023/08/24 06:42 [medline] 2023/08/24 06:42 [pubmed] 2023/08/24 04:15 [entrez]
 2023/08/04 06:43 [medline] 2023/08/04 06:43 [pubmed] 2023/08/04 02:33 [entrez]
 2023/06/05 19:10 [pubmed] 2023/06/05 19:10 [medline] 2023/06/05 12:27 [entrez]
 2023/03/08 00:00 [revised] 2022/07/11 00:00 [received] 2023/04/30 00:00 [accepted] 2023/05/19 06:42 [medline] 2023/05/19 06:42 [pubmed] 2023/05/19 03:43 [entrez]
 2021/12/21 00:00 [received] 2022/03/04 00:00 [revised] 2022/04/25 00:00 [accepted] 2023/04/24 06:43 [medline] 2023/04/24 06:42 [pubmed] 2023/04/24 04:03 [entrez]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/10/25 00:00 [received] 2022/11/29 00:00 [accepted] 2022/12/24 06:01 [medline] 2022/12/24 06:00 [pubmed] 2022/12/23 23:43 [entrez]
 2023/04/17 00:00 [received] 2023/06/21 00:00 [accepted] 2023/07/26 06:44 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 03:46 [entrez]
 2023/08/02 06:42 [pubmed] 2023/08/02 06:42 [medline] 2023/08/02 01:53 [entrez]
 2023/04/20 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/08/31 06:43 [medline] 2023/08/31 06:42 [pubmed] 2023/08/31 04:06 [entrez]
 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 09:13 [entrez]
 2022/06/27 00:00 [received] 2022/12/30 00:00 [accepted] 2023/02/10 03:15 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2022/07/23 00:00 [received] 2022/09/23 00:00 [revised] 2022/10/03 00:00 [accepted] 2022/10/14 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/10/13 19:37 [entrez]
 2023/08/09 00:00 [revised] 2022/08/16 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/14 12:42 [medline] 2023/08/14 12:42 [pubmed] 2023/08/14 07:23 [entrez]
 2023/05/12 00:00 [received] 2023/07/31 00:00 [accepted] 2023/08/13 00:41 [medline] 2023/08/13 00:41 [pubmed] 2023/08/12 11:09 [entrez]
 2023/05/12 00:00 [revised] 2022/10/10 00:00 [received] 2023/05/28 00:00 [accepted] 2023/06/10 15:13 [pubmed] 2023/06/10 15:13 [medline] 2023/06/10 03:42 [entrez]
 2022/12/28 00:00 [received] 2023/05/08 00:00 [accepted] 2023/06/05 19:11 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 12:13 [entrez]
 2023/03/29 00:00 [received] 2023/04/17 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:19 [entrez]
 2023/03/03 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/05/16 06:43 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:09 [entrez]
 2022/10/23 00:00 [received] 2023/03/20 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 02:41 [entrez]
 2023/03/17 08:44 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/18 06:00 [medline]
 2023/01/06 00:00 [accepted] 2023/03/10 02:30 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2022/11/25 00:00 [received] 2023/01/31 00:00 [accepted] 2023/03/10 02:26 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2023/02/23 02:10 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/03/28 00:00 [revised] 2022/09/19 00:00 [received] 2023/04/26 00:00 [accepted] 2023/05/01 06:42 [pubmed] 2023/05/01 06:42 [medline] 2023/05/01 00:22 [entrez]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2023/07/14 00:00 [received] 2023/08/30 00:00 [revised] 2023/09/11 00:00 [accepted] 2023/09/14 19:18 [entrez]
 2022/10/04 00:00 [received] 2022/11/17 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2022/12/20 06:01 [medline] 2022/12/19 11:19 [entrez]
 2023/01/14 00:00 [received] 2023/04/22 00:00 [accepted] 2023/08/16 06:44 [medline] 2023/08/16 06:43 [pubmed] 2023/08/16 03:49 [entrez]
 2023/06/12 13:07 [medline] 2023/06/12 13:07 [pubmed] 2023/06/12 09:03 [entrez]
 2021/11/03 00:00 [received] 2022/02/25 00:00 [revised] 2022/04/05 00:00 [accepted] 2023/05/24 13:09 [medline] 2023/05/24 13:08 [pubmed] 2023/05/24 11:45 [entrez]
 2023/09/11 06:42 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 03:35 [entrez]
 2022/03/03 06:00 [pubmed] 2022/03/03 06:00 [medline] 2022/03/02 08:41 [entrez]
 2023/06/26 06:41 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 21:38 [entrez]
 2023/05/30 00:00 [received] 2023/08/10 00:00 [accepted] 2023/08/08 00:00 [revised] 2023/08/17 12:43 [medline] 2023/08/17 12:43 [pubmed] 2023/08/17 11:04 [entrez]
 2022/01/07 00:00 [received] 2022/10/12 00:00 [accepted] 2022/12/03 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/02 21:12 [entrez]
 2023/07/02 00:00 [received] 2023/07/24 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:11 [entrez]
 2023/01/28 00:00 [received] 2023/02/10 00:00 [revised] 2023/02/15 00:00 [accepted] 2023/02/25 01:32 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/05/08 00:00 [received] 2023/05/24 00:00 [revised] 2023/05/29 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:12 [entrez]
 2022/08/18 00:00 [received] 2022/12/20 00:00 [accepted] 2023/02/06 03:39 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:01 [medline]
 2023/02/04 00:00 [received] 2023/06/20 00:00 [accepted] 2023/07/22 10:42 [medline] 2023/07/22 10:42 [pubmed] 2023/07/21 21:03 [entrez]
 2022/11/06 00:00 [received] 2023/01/10 00:00 [accepted] 2023/02/13 03:56 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2023/02/15 00:00 [received] 2023/04/16 00:00 [revised] 2023/04/20 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:06 [entrez]
 2023/04/11 00:00 [received] 2023/05/15 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/09 01:09 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 21:56 [entrez]
 2022/11/01 00:00 [received] 2022/11/01 00:00 [accepted] 2023/02/13 03:45 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/05/27 00:00 [revised] 2023/03/30 00:00 [received] 2023/06/01 00:00 [accepted] 2023/06/26 13:07 [medline] 2023/06/26 13:07 [pubmed] 2023/06/26 06:51 [entrez]
 2022/11/20 00:00 [received] 2023/04/18 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/06/03 11:42 [pubmed] 2023/06/03 11:42 [medline] 2023/06/02 18:01 [entrez]
 2023/03/01 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/02/28 02:39 [entrez]
 2022/10/03 00:00 [received] 2023/07/14 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/07/31 19:15 [medline] 2023/07/31 19:15 [pubmed] 2023/07/31 18:01 [entrez]
 2023/07/26 13:07 [medline] 2023/07/26 13:07 [pubmed] 2023/07/26 11:12 [entrez]
 2022/10/12 00:00 [received] 2022/11/15 00:00 [revised] 2022/11/15 00:00 [accepted] 2023/03/06 03:38 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/08/17 12:42 [medline] 2023/08/17 12:42 [pubmed] 2023/08/17 10:55 [entrez]
 2022/11/28 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/22 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:57 [entrez]
 2023/04/24 00:00 [received] 2023/07/12 00:00 [accepted] 2023/07/06 00:00 [revised] 2023/09/04 01:22 [medline] 2023/09/04 01:22 [pubmed] 2023/09/02 11:04 [entrez]
 2022/11/07 00:00 [received] 2023/01/13 00:00 [accepted] 2023/02/24 02:31 [entrez] 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline]
 2023/03/16 00:00 [received] 2023/05/23 00:00 [accepted] 2023/06/23 13:08 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 10:36 [entrez]
 2022/09/26 00:00 [received] 2023/01/26 00:00 [revised] 2023/02/10 00:00 [accepted] 2023/04/04 03:13 [entrez] 2023/04/05 06:00 [pubmed] 2023/04/05 06:00 [medline]
 2023/02/11 00:00 [received] 2023/03/24 00:00 [revised] 2023/04/14 00:00 [accepted] 2023/05/03 06:43 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 02:02 [entrez]
 2020/07/26 00:00 [received] 2020/11/15 00:00 [accepted] 2023/04/07 10:18 [medline] 2023/04/05 13:48 [entrez] 2023/04/06 06:00 [pubmed]
 2023/06/17 00:00 [received] 2023/06/30 00:00 [accepted] 2023/07/28 06:43 [medline] 2023/07/28 06:42 [pubmed] 2023/07/28 04:19 [entrez]
 2023/01/26 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/03 02:32 [entrez] 2023/03/04 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2023/03/22 00:00 [received] 2023/05/08 00:00 [accepted] 2023/05/03 00:00 [revised] 2023/05/16 13:09 [medline] 2023/05/16 13:09 [pubmed] 2023/05/16 11:17 [entrez]
 2023/01/20 00:00 [received] 2023/01/22 00:00 [accepted] 2023/02/01 02:53 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/02 06:00 [medline]
 2023/01/20 00:00 [received] 2023/05/02 00:00 [accepted] 2023/05/30 13:08 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:20 [entrez]
 2023/09/13 06:41 [medline] 2023/09/13 06:41 [pubmed] 2023/09/13 00:52 [entrez]
 2023/01/22 00:00 [received] 2023/01/23 00:00 [accepted] 2023/02/23 09:36 [entrez] 2023/02/24 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2017/02/06 06:00 [pubmed] 2017/02/06 06:01 [medline] 2017/02/03 06:00 [entrez]
 2023/08/25 06:42 [pubmed] 2023/08/25 06:42 [medline] 2023/08/25 04:13 [entrez]
 2023/06/09 00:00 [received] 2023/07/24 00:00 [revised] 2023/08/12 00:00 [accepted] 2023/08/27 05:43 [medline] 2023/08/27 05:43 [pubmed] 2023/08/26 18:03 [entrez]
 2023/07/21 00:00 [revised] 2023/05/08 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/16 06:42 [pubmed] 2023/08/16 06:42 [medline] 2023/08/16 04:43 [entrez]
 2023/08/08 00:00 [received] 2023/08/09 18:42 [medline] 2023/08/09 18:42 [pubmed] 2023/08/09 12:33 [entrez]
 2023/05/09 00:00 [received] 2023/06/29 00:00 [revised] 2023/07/25 00:00 [accepted] 2023/08/04 01:07 [medline] 2023/08/04 01:07 [pubmed] 2023/08/03 18:04 [entrez]
 2023/02/16 00:00 [received] 2023/07/21 00:00 [accepted] 2023/07/27 13:10 [medline] 2023/07/27 13:10 [pubmed] 2023/07/27 11:07 [entrez]
 2023/03/18 00:00 [received] 2023/06/21 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/24 06:41 [pubmed] 2023/07/24 04:31 [entrez]
 2023/02/23 00:00 [received] 2023/05/17 00:00 [accepted] 2023/06/14 01:11 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 23:30 [entrez]
 2023/01/13 00:00 [received] 2023/03/03 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:30 [entrez]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/09/15 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/24 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/02/05 06:00 [pubmed] 2023/02/04 18:16 [entrez]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2021/05/18 00:00 [received] 2021/06/27 00:00 [accepted] 2023/04/29 06:04 [pubmed] 2023/04/29 06:04 [medline] 2023/04/28 19:27 [entrez]
 2023/04/11 00:00 [received] 2023/07/26 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/09/08 00:42 [medline] 2023/09/08 00:42 [pubmed] 2023/09/07 18:11 [entrez]
 2023/03/17 00:00 [received] 2023/07/27 00:00 [accepted] 2023/08/14 12:42 [medline] 2023/08/14 12:42 [pubmed] 2023/08/14 11:23 [entrez]
 2023/01/07 00:00 [received] 2023/05/07 00:00 [accepted] 2023/07/27 13:10 [medline] 2023/07/27 13:10 [pubmed] 2023/07/27 11:09 [entrez]
 2022/09/24 00:00 [received] 2023/05/24 00:00 [accepted] 2023/06/01 13:09 [medline] 2023/06/01 13:09 [pubmed] 2023/06/01 11:15 [entrez]
 2023/02/13 00:00 [received] 2023/04/01 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/05/22 19:12 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 12:16 [entrez]
 2023/02/27 00:00 [received] 2023/04/19 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 15:36 [entrez]
 2022/12/28 00:00 [received] 2023/03/09 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:49 [entrez]
 2023/03/25 08:02 [entrez] 2023/03/26 06:00 [pubmed] 2023/03/26 06:00 [medline]
 2023/05/13 00:00 [received] 2023/08/05 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/04 00:41 [medline] 2023/09/04 00:41 [pubmed] 2023/09/03 18:03 [entrez]
 2023/06/02 00:00 [received] 2023/07/05 00:00 [revised] 2023/07/11 00:00 [accepted] 2023/07/29 11:54 [medline] 2023/07/29 11:53 [pubmed] 2023/07/29 01:20 [entrez]
 2023/03/20 00:00 [received] 2023/06/29 00:00 [accepted] 2023/06/20 00:00 [revised] 2023/07/14 13:06 [medline] 2023/07/14 13:06 [pubmed] 2023/07/13 23:16 [entrez]
 2022/11/30 00:00 [received] 2023/05/13 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 12:00 [entrez]
 2023/02/02 00:00 [received] 2023/05/11 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:08 [entrez]
 2023/05/11 00:00 [accepted] 2023/05/31 01:09 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 22:12 [entrez]
 2022/09/25 00:00 [received] 2022/12/20 00:00 [accepted] 2023/05/24 13:09 [medline] 2023/05/24 13:08 [pubmed] 2023/05/24 11:42 [entrez]
 2023/03/02 13:02 [entrez] 2023/03/03 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/12/08 00:00 [received] 2023/01/06 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/02/11 01:28 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/12 06:01 [medline]
 2023/02/07 06:00 [pubmed] 2023/02/07 06:00 [medline] 2023/02/06 10:44 [entrez]
 2023/09/15 00:41 [medline] 2023/09/15 00:41 [pubmed] 2023/07/30 00:00 [received] 2023/09/10 00:00 [revised] 2023/09/11 00:00 [accepted] 2023/09/14 19:19 [entrez]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2023/04/28 00:00 [received] 2023/06/18 00:00 [revised] 2023/09/02 00:00 [accepted] 2023/09/14 18:10 [entrez]
 2023/08/22 00:00 [revised] 2023/02/12 00:00 [received] 2023/09/10 00:00 [accepted] 2023/09/14 06:42 [medline] 2023/09/14 06:42 [pubmed] 2023/09/14 00:44 [entrez]
 2023/03/15 00:00 [received] 2023/07/10 00:00 [accepted] 2023/07/20 01:07 [medline] 2023/07/20 01:07 [pubmed] 2023/07/19 21:37 [entrez]
 2023/05/29 00:00 [received] 2023/07/07 00:00 [accepted] 2023/07/05 00:00 [revised] 2023/07/19 13:06 [medline] 2023/07/19 13:06 [pubmed] 2023/07/19 11:04 [entrez]
 2023/01/09 00:00 [received] 2023/03/06 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 04:02 [entrez] 2023/04/11 06:00 [pubmed]
 2023/05/25 00:00 [received] 2023/07/12 00:00 [revised] 2023/09/03 00:00 [accepted] 2023/09/09 10:41 [medline] 2023/09/09 10:41 [pubmed] 2023/09/08 18:10 [entrez]
 2023/07/29 00:00 [received] 2023/08/24 00:00 [accepted] 2023/09/03 18:42 [medline] 2023/09/03 18:42 [pubmed] 2023/09/03 14:49 [entrez]
 2021/09/23 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/04 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 18:08 [entrez]
 2023/06/04 00:00 [received] 2023/07/16 00:00 [revised] 2023/08/04 00:00 [accepted] 2023/08/21 18:42 [medline] 2023/08/21 18:42 [pubmed] 2023/08/21 18:01 [entrez]
 2023/02/26 00:00 [received] 2023/08/05 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/17 00:41 [medline] 2023/08/17 00:41 [pubmed] 2023/08/16 18:08 [entrez]
 2023/07/26 13:07 [medline] 2023/07/26 13:07 [pubmed] 2023/07/26 07:32 [entrez]
 2023/01/19 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/10 13:06 [medline] 2023/07/10 13:06 [pubmed] 2023/07/10 11:16 [entrez]
 2023/05/07 00:00 [received] 2023/05/27 00:00 [revised] 2023/06/04 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:07 [entrez]
 2022/11/01 00:00 [received] 2023/06/10 15:14 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 03:39 [entrez]
 2023/03/04 00:00 [received] 2023/03/26 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/05/16 06:43 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:15 [entrez]
 2023/02/11 00:00 [received] 2023/03/17 00:00 [accepted] 2023/05/08 06:43 [medline] 2023/05/08 06:42 [pubmed] 2023/05/08 04:18 [entrez]
 2022/05/30 00:00 [received] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:29 [entrez]
 2022/11/30 00:00 [received] 2023/03/15 00:00 [accepted] 2023/04/28 06:43 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 02:24 [entrez]
 2022/12/23 00:00 [received] 2023/01/19 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/02/25 01:27 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/08/01 00:00 [received] 2023/08/05 00:00 [accepted] 2023/08/10 00:42 [pubmed] 2023/08/10 00:42 [medline] 2023/08/09 19:28 [entrez]
 2023/06/30 13:11 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 06:42 [entrez]
 2022/11/15 00:00 [received] 2023/03/21 00:00 [accepted] 2023/04/24 06:43 [medline] 2023/04/24 06:42 [pubmed] 2023/04/24 03:46 [entrez]
 2023/06/15 00:00 [received] 2023/08/31 00:00 [accepted] 2023/09/06 12:42 [medline] 2023/09/06 12:42 [pubmed] 2023/09/06 11:09 [entrez]
 2022/09/08 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/31 06:01 [medline] 2023/03/30 02:58 [entrez] 2023/03/31 06:00 [pubmed]
 2023/04/30 00:00 [received] 2023/05/18 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 12:04 [entrez]
 2023/01/13 00:00 [received] 2023/02/16 00:00 [revised] 2023/02/21 00:00 [accepted] 2023/03/11 01:20 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/12 06:01 [medline]
 2022/12/09 00:00 [received] 2023/04/18 00:00 [accepted] 2023/05/13 15:13 [pubmed] 2023/05/13 15:13 [medline] 2023/05/12 21:37 [entrez]
 2022/11/30 00:00 [received] 2023/01/30 00:00 [accepted] 2023/04/01 06:01 [medline] 2023/03/31 02:10 [entrez] 2023/04/01 06:00 [pubmed]
 2023/03/06 00:00 [received] 2023/06/04 00:00 [accepted] 2023/07/12 06:43 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 03:48 [entrez]
 2022/09/22 00:00 [received] 2022/12/22 00:00 [accepted] 2023/01/26 02:53 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/27 06:01 [medline]
 2021/07/11 00:00 [received] 2022/03/29 00:00 [revised] 2022/03/31 00:00 [accepted] 2023/03/27 03:30 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2023/04/22 10:43 [medline] 2023/04/22 10:42 [pubmed] 2023/04/21 23:25 [entrez]
 2023/02/03 00:00 [received] 2023/03/24 00:00 [accepted] 2023/05/12 01:08 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 19:25 [entrez]
 2022/06/13 00:00 [received] 2023/01/31 00:00 [revised] 2023/04/10 00:00 [accepted] 2023/05/04 00:42 [pubmed] 2023/05/04 00:42 [medline] 2023/05/03 19:19 [entrez]
 2022/07/30 00:00 [received] 2023/01/19 00:00 [accepted] 2023/02/24 02:31 [entrez] 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline]
 2023/02/27 00:00 [received] 2023/04/11 00:00 [revised] 2023/04/13 00:00 [accepted] 2023/09/10 00:42 [medline] 2023/09/10 00:41 [pubmed] 2023/09/09 21:00 [entrez]
 2023/05/03 00:00 [received] 2023/05/04 00:00 [accepted] 2023/05/30 13:07 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 06:23 [entrez]
 2023/01/10 13:13 [entrez] 2023/01/11 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2022/12/17 00:00 [received] 2023/07/16 00:00 [accepted] 2023/08/10 00:42 [medline] 2023/08/10 00:42 [pubmed] 2023/08/09 18:04 [entrez]
 2022/12/21 00:00 [received] 2023/01/23 00:00 [accepted] 2023/03/06 03:41 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2022/12/10 06:00 [pubmed] 2022/12/10 06:01 [medline] 2022/12/09 00:53 [entrez]
 2022/10/28 00:00 [received] 2023/01/20 00:00 [revised] 2023/02/04 00:00 [accepted] 2023/02/25 01:48 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/03/14 00:00 [received] 2023/05/05 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:11 [entrez]
 2023/09/11 06:43 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 03:35 [entrez]
 2023/03/05 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/19 06:44 [medline] 2023/07/19 06:43 [pubmed] 2023/07/19 03:56 [entrez]
 2023/05/17 00:00 [received] 2023/06/20 00:00 [revised] 2023/06/25 00:00 [accepted] 2023/07/03 00:41 [pubmed] 2023/07/03 00:41 [medline] 2023/07/02 18:09 [entrez]
 2022/12/20 00:00 [received] 2023/04/11 00:00 [accepted] 2023/05/26 06:42 [medline] 2023/05/24 13:08 [pubmed] 2023/05/24 11:41 [entrez]
 2022/04/27 00:00 [received] 2022/10/13 00:00 [revised] 2022/11/05 00:00 [accepted] 2022/11/26 06:00 [pubmed] 2022/12/22 06:00 [medline] 2022/11/25 19:26 [entrez]
 2023/03/13 00:00 [revised] 2022/09/12 00:00 [received] 2023/04/12 00:00 [accepted] 2023/05/03 12:42 [medline] 2023/05/03 12:42 [pubmed] 2023/05/03 06:03 [entrez]
 2023/02/21 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/08 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:23 [entrez] 2023/03/30 06:00 [pubmed]
 2022/09/27 00:00 [received] 2022/12/07 00:00 [accepted] 2023/02/06 03:30 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2023/01/03 00:00 [received] 2023/02/08 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/06/06 01:11 [pubmed] 2023/06/06 01:11 [medline] 2023/06/05 19:22 [entrez]
 2023/07/18 06:43 [medline] 2023/07/18 06:42 [pubmed] 2023/07/18 03:39 [entrez]
 2023/04/04 00:00 [received] 2023/07/02 00:00 [revised] 2023/07/02 00:00 [accepted] 2023/08/19 11:42 [pubmed] 2023/08/19 11:42 [medline] 2023/08/18 19:23 [entrez]
 2022/10/10 00:00 [received] 2022/11/18 00:00 [accepted] 2023/01/23 04:34 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2023/05/25 00:00 [received] 2023/07/18 00:00 [accepted] 2023/08/29 12:42 [medline] 2023/08/28 06:41 [pubmed] 2023/08/28 04:58 [entrez]
 2023/01/04 20:54 [entrez] 2023/01/05 06:00 [pubmed] 2023/01/07 06:00 [medline]
 2022/10/21 00:00 [received] 2023/01/18 00:00 [accepted] 2023/02/23 09:27 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/08/26 10:41 [pubmed] 2023/08/26 10:41 [medline] 2023/08/26 00:53 [entrez]
 2023/01/04 00:00 [received] 2023/02/17 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 03:48 [entrez] 2023/04/04 06:00 [pubmed]
 2023/02/07 00:09 [entrez] 2023/02/08 06:00 [pubmed] 2023/02/08 06:01 [medline]
 2022/07/08 02:32 [entrez] 2022/07/09 06:00 [pubmed] 2022/07/09 06:01 [medline]
 2023/06/11 00:00 [received] 2023/06/27 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 21:38 [entrez]
 2023/08/29 00:00 [accepted] 2023/09/12 12:42 [medline] 2023/09/12 12:42 [pubmed] 2023/09/12 11:13 [entrez]
 2023/08/10 00:42 [medline] 2023/08/10 00:42 [pubmed] 2023/08/09 22:22 [entrez]
 2023/04/27 00:00 [received] 2023/06/12 00:00 [accepted] 2023/07/07 01:05 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 21:13 [entrez]
 2022/09/18 00:00 [received] 2023/06/13 00:00 [accepted] 2023/07/20 01:06 [medline] 2023/07/20 01:06 [pubmed] 2023/07/19 21:37 [entrez]
 2023/07/17 00:00 [revised] 2023/01/13 00:00 [received] 2023/07/27 00:00 [accepted] 2023/08/01 01:08 [pubmed] 2023/08/01 01:08 [medline] 2023/07/31 23:50 [entrez]
 2023/04/28 12:43 [medline] 2023/04/28 12:43 [pubmed] 2023/04/28 07:03 [entrez]
 2022/12/31 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/05 06:01 [medline] 2023/03/05 06:00 [pubmed] 2023/03/04 11:18 [entrez]

 2023/01/05 00:00 [received] 2023/03/30 00:00 [accepted] 2023/07/12 06:42 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 11:18 [entrez]
 2023/03/16 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:35 [entrez]
 2021/12/11 00:00 [received] 2022/04/20 00:00 [accepted] 2023/03/13 04:27 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2022/12/03 00:00 [received] 2023/03/28 00:00 [accepted] 2023/04/18 06:00 [pubmed] 2023/04/18 06:00 [medline] 2023/04/17 21:22 [entrez]
 2023/02/07 00:00 [received] 2023/03/27 00:00 [accepted] 2023/04/16 06:01 [medline] 2023/04/16 06:00 [pubmed] 2023/04/15 23:21 [entrez]
 2023/05/16 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/09 00:00 [accepted] 2023/08/25 00:41 [medline] 2023/08/25 00:41 [pubmed] 2023/08/24 18:04 [entrez]
 2023/05/08 00:00 [received] 2023/07/30 00:00 [accepted] 2023/08/10 00:42 [medline] 2023/08/10 00:42 [pubmed] 2023/08/09 21:12 [entrez]
 2022/10/14 00:00 [received] 2023/04/22 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:41 [entrez]
 2022/09/14 00:00 [received] 2022/11/10 00:00 [revised] 2022/11/10 00:00 [accepted] 2023/03/18 06:01 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 09:45 [entrez]
 2023/07/07 00:00 [received] 2023/08/17 00:00 [accepted] 2023/08/16 00:00 [revised] 2023/08/28 12:43 [medline] 2023/08/28 12:43 [pubmed] 2023/08/28 11:05 [entrez]
 2023/06/22 00:00 [revised] 2022/11/09 00:00 [received] 2023/07/27 00:00 [accepted] 2023/07/31 13:07 [pubmed] 2023/07/31 13:07 [medline] 2023/07/31 07:32 [entrez]
 2023/05/25 00:00 [received] 2023/06/20 00:00 [revised] 2023/06/23 00:00 [accepted] 2023/07/29 11:47 [medline] 2023/07/29 11:46 [pubmed] 2023/07/29 01:26 [entrez]
 2023/05/10 00:00 [received] 2023/06/30 00:00 [revised] 2023/07/10 00:00 [accepted] 2023/07/29 11:53 [medline] 2023/07/29 11:52 [pubmed] 2023/07/29 01:09 [entrez]
 2023/04/11 00:00 [received] 2023/07/11 00:00 [accepted] 2023/07/22 21:06 [medline] 2023/07/22 21:06 [pubmed] 2023/07/22 11:04 [entrez]
 2022/11/27 00:00 [received] 2023/03/27 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:22 [entrez]
 2023/01/27 00:00 [received] 2023/05/02 00:00 [accepted] 2023/05/26 13:10 [medline] 2023/05/26 13:09 [pubmed] 2023/05/26 12:04 [entrez]
 2022/12/10 00:00 [received] 2023/03/28 00:00 [accepted] 2023/05/04 06:43 [medline] 2023/05/04 06:42 [pubmed] 2023/05/04 02:20 [entrez]
 2022/10/04 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/20 03:47 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline] 2023/02/13 11:18 [entrez]
 2022/10/26 00:00 [received] 2022/12/11 00:00 [revised] 2023/01/07 00:00 [accepted] 2023/02/11 01:26 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/12 06:01 [medline]
 2022/10/10 00:00 [received] 2022/11/21 00:00 [revised] 2022/12/12 00:00 [accepted] 2022/12/26 04:32 [entrez] 2022/12/27 06:00 [pubmed] 2022/12/27 06:01 [medline]
 2023/07/24 00:00 [received] 2023/07/31 00:00 [revised] 2023/08/12 00:00 [accepted] 2023/08/21 18:42 [medline] 2023/08/21 18:42 [pubmed] 2023/08/21 18:01 [entrez]
 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 04:42 [entrez]
 2022/08/27 00:00 [received] 2022/11/15 00:00 [revised] 2022/12/17 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/07/31 06:42 [pubmed] 2023/07/31 01:24 [entrez]
 2023/01/10 00:00 [received] 2023/06/10 00:00 [accepted] 2023/07/05 13:06 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 10:35 [entrez]
 2023/02/13 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:43 [entrez] 2023/03/30 06:00 [pubmed]
 2023/01/17 00:00 [received] 2023/03/07 00:00 [revised] 2023/03/16 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:21 [entrez] 2023/03/30 06:00 [pubmed]
 2023/01/10 00:00 [received] 2023/01/31 00:00 [revised] 2023/02/08 00:00 [accepted] 2023/02/28 01:32 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:01 [medline]
 2022/04/13 00:00 [received] 2022/12/28 00:00 [accepted] 2023/02/03 01:57 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/04 06:01 [medline]
 2022/08/18 00:00 [received] 2022/10/14 00:00 [accepted] 2022/11/06 06:00 [pubmed] 2022/11/06 06:01 [medline] 2022/11/05 12:28 [entrez]
 2023/01/13 00:00 [received] 2023/02/14 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:42 [entrez] 2023/03/30 06:00 [pubmed]
 2023/06/09 00:00 [revised] 2023/02/09 00:00 [received] 2023/08/20 00:00 [accepted] 2023/09/06 18:42 [medline] 2023/09/06 18:42 [pubmed] 2023/09/06 14:03 [entrez]
 2023/09/12 06:42 [medline] 2023/09/12 06:42 [pubmed] 2023/09/12 05:28 [entrez]
 2023/07/03 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/01 00:00 [accepted] 2023/08/26 10:43 [medline] 2023/08/26 10:42 [pubmed] 2023/08/26 01:01 [entrez]
 2023/06/22 00:00 [revised] 2022/09/13 00:00 [received] 2023/07/11 00:00 [accepted] 2023/08/09 06:43 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 05:42 [entrez]
 2022/10/03 00:00 [received] 2023/07/24 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/06 05:42 [medline] 2023/08/06 05:42 [pubmed] 2023/08/05 18:07 [entrez]
 2023/05/24 00:00 [received] 2023/06/25 00:00 [revised] 2023/06/27 00:00 [accepted] 2023/07/29 11:52 [medline] 2023/07/29 11:51 [pubmed] 2023/07/29 01:09 [entrez]
 2023/04/19 00:00 [received] 2023/06/29 00:00 [accepted] 2023/07/17 15:10 [medline] 2023/07/17 15:09 [pubmed] 2023/07/17 11:10 [entrez]
 2022/10/20 00:00 [received] 2023/05/11 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 12:04 [entrez]
 2023/02/23 00:00 [received] 2023/06/08 00:00 [accepted] 2023/06/26 13:07 [medline] 2023/06/26 13:07 [pubmed] 2023/06/26 11:09 [entrez]
 2023/06/24 21:05 [medline] 2023/06/24 21:05 [pubmed] 2023/06/24 14:42 [entrez]
 2022/12/06 00:00 [received] 2023/03/10 00:00 [accepted] 2023/04/01 06:01 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 11:22 [entrez]
 2022/10/24 00:00 [received] 2022/11/28 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2022/12/20 06:01 [medline] 2022/12/19 11:19 [entrez]
 2023/06/28 00:00 [received] 2023/07/18 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/28 00:41 [medline] 2023/08/28 00:41 [pubmed] 2023/08/27 18:08 [entrez]
 2023/06/24 00:00 [received] 2023/07/29 00:00 [revised] 2023/08/12 00:00 [accepted] 2023/08/27 05:43 [medline] 2023/08/27 05:43 [pubmed] 2023/08/26 18:03 [entrez]
 2023/02/06 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/02 06:44 [medline] 2023/08/02 06:43 [pubmed] 2023/08/02 03:59 [entrez]
 2022/07/27 00:00 [received] 2023/01/26 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/04/04 03:13 [entrez] 2023/04/05 06:00 [pubmed] 2023/04/05 06:00 [medline]
 2023/05/15 00:00 [received] 2023/06/26 00:00 [revised] 2023/06/26 00:00 [accepted] 2023/07/22 10:42 [medline] 2023/07/22 10:42 [pubmed] 2023/07/21 20:59 [entrez]
 2021/06/30 00:00 [received] 2021/11/08 00:00 [accepted] 2023/07/04 01:05 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 23:25 [entrez]
 2022/11/24 00:00 [received] 2023/01/16 00:00 [accepted] 2023/01/31 01:48 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/01 06:01 [medline]
 2023/09/12 06:41 [medline] 2023/09/12 06:41 [pubmed] 2023/09/12 05:28 [entrez]
 2022/09/24 00:00 [received] 2023/01/25 00:00 [accepted] 2023/03/07 02:02 [entrez] 2023/03/08 06:00 [pubmed] 2023/03/08 06:01 [medline]
 2023/02/01 00:00 [received] 2023/07/20 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/09/04 06:41 [pubmed] 2023/09/04 04:55 [entrez]
 2023/03/29 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/24 11:43 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 23:30 [entrez]
 2023/05/19 00:00 [received] 2023/08/18 00:00 [revised] 2023/08/21 00:00 [accepted] 2023/09/02 05:42 [pubmed] 2023/09/02 05:42 [medline] 2023/09/01 19:23 [entrez]
 2023/05/26 00:00 [received] 2023/07/06 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/07/29 11:52 [medline] 2023/07/29 11:51 [pubmed] 2023/07/29 01:13 [entrez]
 2023/07/24 06:42 [medline] 2023/07/20 19:14 [pubmed] 2023/07/20 12:24 [entrez]
 2023/04/25 00:00 [received] 2023/05/31 00:00 [revised] 2023/06/18 00:00 [accepted] 2023/06/27 01:06 [pubmed] 2023/06/27 01:06 [medline] 2023/06/26 18:09 [entrez]
 2023/02/10 00:00 [received] 2023/05/09 00:00 [revised] 2023/06/02 00:00 [accepted] 2023/06/20 19:14 [medline] 2023/06/20 19:14 [pubmed] 2023/06/20 12:36 [entrez]
 2023/05/02 00:00 [revised] 2023/03/10 00:00 [received] 2023/05/16 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/29 06:42 [pubmed] 2023/05/29 01:02 [entrez]
 2022/12/20 00:00 [received] 2023/02/14 00:00 [accepted] 2023/03/27 03:26 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2022/06/06 00:00 [received] 2022/10/20 00:00 [revised] 2022/11/10 00:00 [accepted] 2023/01/19 04:44 [entrez] 2023/01/20 06:00 [pubmed] 2023/01/20 06:00 [medline]
 2022/10/09 00:00 [received] 2022/11/18 00:00 [revised] 2022/11/22 00:00 [accepted] 2022/11/28 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/11/27 19:26 [entrez]
 2023/03/08 00:00 [received] 2023/08/08 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:36 [entrez]
 2023/04/20 00:00 [received] 2023/08/09 18:42 [medline] 2023/08/09 18:42 [pubmed] 2023/08/09 13:03 [entrez]
 2023/01/16 00:00 [received] 2023/05/08 00:00 [revised] 2023/07/16 00:00 [accepted] 2023/07/31 00:41 [medline] 2023/07/31 00:41 [pubmed] 2023/07/30 18:07 [entrez]
 2022/12/06 00:00 [received] 2023/01/21 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/05/19 01:04 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 22:00 [entrez]
 2022/11/28 00:00 [received] 2023/03/29 00:00 [revised] 2023/04/18 00:00 [accepted] 2023/06/28 06:42 [medline] 2023/04/24 00:41 [pubmed] 2023/04/23 19:25 [entrez]
 2023/01/20 00:00 [received] 2023/02/21 00:00 [revised] 2023/02/27 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/03/30 01:06 [entrez] 2023/03/31 06:00 [pubmed]
 2023/02/09 00:00 [received] 2023/02/22 00:00 [revised] 2023/02/26 00:00 [accepted] 2023/03/09 06:00 [pubmed] 2023/03/09 06:01 [medline] 2023/03/08 18:11 [entrez]
 2023/02/02 03:56 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2022/07/07 00:00 [received] 2022/11/01 00:00 [revised] 2022/12/07 00:00 [accepted] 2023/01/03 01:58 [entrez] 2023/01/04 06:00 [pubmed] 2023/01/04 06:01 [medline]
 2023/09/12 00:00 [accepted] 2023/09/14 06:43 [medline] 2023/09/14 06:42 [pubmed] 2023/09/14 03:59 [entrez]
 2023/05/21 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/06 01:08 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 23:32 [entrez]
 2023/08/01 00:00 [received] 2023/09/07 00:00 [accepted] 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 23:47 [entrez]
 2023/07/09 00:00 [received] 2023/07/30 00:00 [accepted] 2023/07/27 00:00 [revised] 2023/08/06 05:42 [medline] 2023/08/06 05:42 [pubmed] 2023/08/05 11:13 [entrez]
 2023/01/24 00:00 [received] 2023/02/13 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/03/11 01:16 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/11/26 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/14 00:00 [accepted] 2023/02/11 01:09 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2022/10/19 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 19:24 [entrez]
 2022/09/16 00:00 [received] 2022/12/23 00:00 [accepted] 2023/01/07 23:25 [entrez] 2023/01/08 06:00 [pubmed] 2023/01/11 06:00 [medline]
 2023/05/16 00:00 [received] 2023/08/07 00:00 [accepted] 2023/08/15 12:43 [medline] 2023/08/15 12:43 [pubmed] 2023/08/15 11:10 [entrez]
 2022/08/16 00:00 [received] 2023/06/11 00:00 [revised] 2023/07/03 00:00 [accepted] 2023/08/04 01:08 [medline] 2023/08/04 01:08 [pubmed] 2023/08/03 21:56 [entrez]
 2023/03/25 00:00 [received] 2023/06/22 00:00 [accepted] 2023/07/03 13:06 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:10 [entrez]
 2023/02/10 00:00 [received] 2023/04/19 00:00 [accepted] 2023/05/17 13:10 [medline] 2023/05/17 13:09 [pubmed] 2023/05/17 11:09 [entrez]
 2023/01/06 00:00 [received] 2023/02/13 00:00 [accepted] 2023/03/17 02:55 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/18 06:01 [medline]
 2022/09/06 00:00 [revised] 2022/03/27 00:00 [received] 2022/10/12 00:00 [accepted] 2022/10/29 06:00 [pubmed] 2023/02/14 06:00 [medline] 2022/10/28 01:02 [entrez]
 2022/12/06 00:00 [received] 2023/04/17 00:00 [accepted] 2023/05/12 01:07 [pubmed] 2023/05/12 01:07 [medline] 2023/05/11 21:22 [entrez]
 2023/06/05 19:10 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 12:44 [entrez]
 2023/03/23 00:27 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2023/03/17 00:00 [received] 2023/07/05 00:00 [accepted] 2023/07/04 00:00 [revised] 2023/07/18 01:09 [medline] 2023/07/18 01:09 [pubmed] 2023/07/17 23:36 [entrez]
 2022/11/03 00:00 [received] 2023/05/04 00:00 [accepted] 2023/05/25 06:42 [medline] 2023/05/24 01:06 [pubmed] 2023/05/23 23:52 [entrez]
 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 13:09 [entrez]
 2023/01/12 00:00 [received] 2023/03/23 00:00 [accepted] 2023/06/13 01:14 [medline] 2023/06/13 01:14 [pubmed] 2023/06/12 18:43 [entrez]
 2023/04/06 00:00 [received] 2023/04/10 00:00 [accepted] 2023/05/09 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 04:16 [entrez]
 2022/12/21 00:00 [received] 2023/02/04 00:00 [accepted] 2023/02/09 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/02/08 11:21 [entrez]
 2023/02/28 00:00 [received] 2023/03/01 00:00 [accepted] 2023/04/01 06:01 [medline] 2023/03/31 02:10 [entrez] 2023/04/01 06:00 [pubmed]
 2023/01/06 00:00 [received] 2023/06/30 00:00 [revised] 2023/07/12 00:00 [accepted] 2023/07/29 06:42 [medline] 2023/07/29 06:42 [pubmed] 2023/07/28 18:09 [entrez]
 2023/05/02 00:00 [accepted] 2023/06/09 13:42 [medline] 2023/06/09 13:42 [pubmed] 2023/06/09 11:03 [entrez]
 2022/08/31 00:00 [received] 2023/02/10 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/04/04 06:42 [medline] 2023/03/01 06:00 [pubmed] 2023/02/28 23:54 [entrez]
 2023/02/27 00:00 [received] 2023/05/30 00:00 [revised] 2023/07/23 00:00 [accepted] 2023/08/08 18:42 [medline] 2023/08/08 18:42 [pubmed] 2023/08/08 18:00 [entrez]
 2022/04/23 00:00 [received] 2022/09/01 00:00 [accepted] 2022/09/21 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/20 11:16 [entrez]
 2024/04/27 00:00 [pmc-release] 2023/07/12 06:43 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 03:45 [entrez]

 2022/11/18 06:00 [pubmed] 2022/11/18 06:01 [medline] 2022/11/17 13:55 [entrez]
 2023/04/04 00:00 [received] 2023/04/24 00:00 [revised] 2023/04/26 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:28 [entrez]
 2023/02/01 00:00 [received] 2023/05/31 00:00 [accepted] 2023/07/12 01:07 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 21:22 [entrez]
 2023/06/15 00:00 [accepted] 2023/07/18 06:43 [medline] 2023/07/18 06:42 [pubmed] 2023/07/18 03:40 [entrez]
 2022/12/14 00:00 [received] 2023/02/20 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:17 [entrez] 2023/04/04 06:00 [pubmed]
 2023/06/30 19:14 [medline] 2023/06/30 19:14 [pubmed] 2023/06/30 12:03 [entrez]
 2022/09/17 00:00 [received] 2022/12/14 00:00 [revised] 2023/03/11 00:00 [accepted] 2023/07/28 01:08 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 22:01 [entrez]
 2022/10/28 00:00 [received] 2023/07/30 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/09/08 06:42 [pubmed] 2023/09/08 03:59 [entrez]
 2023/05/02 00:00 [received] 2023/07/02 00:00 [revised] 2023/07/15 00:00 [accepted] 2023/08/19 11:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 18:03 [entrez]
 2023/08/16 12:43 [pubmed] 2023/08/16 12:43 [medline] 2023/08/16 08:23 [entrez]
 2023/02/11 00:00 [received] 2023/06/19 00:00 [accepted] 2023/06/14 00:00 [revised] 2023/07/19 13:06 [medline] 2023/07/19 13:06 [pubmed] 2023/07/19 09:03 [entrez]
 2023/06/12 13:07 [medline] 2023/06/12 13:07 [pubmed] 2023/06/12 11:42 [entrez]
 2022/10/28 00:00 [received] 2023/01/09 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/22 14:36 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/23 06:01 [medline]
 2022/08/19 00:00 [received] 2022/10/28 00:00 [accepted] 2022/11/19 06:00 [pubmed] 2022/11/19 06:01 [medline] 2022/11/18 11:15 [entrez]
 2023/03/13 00:00 [received] 2023/05/18 00:00 [revised] 2023/08/06 00:00 [accepted] 2023/08/14 00:42 [medline] 2023/08/14 00:42 [pubmed] 2023/08/13 18:01 [entrez]
 2023/05/15 00:00 [received] 2023/07/04 00:00 [accepted] 2023/08/10 06:44 [medline] 2023/08/10 06:43 [pubmed] 2023/08/10 04:29 [entrez]
 2023/06/09 00:00 [received] 2023/07/14 00:00 [revised] 2023/07/17 00:00 [accepted] 2023/07/29 11:51 [medline] 2023/07/29 11:50 [pubmed] 2023/07/29 01:09 [entrez]
 2023/01/05 00:00 [received] 2023/05/19 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/07/28 01:08 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 18:03 [entrez]
 2023/03/24 00:00 [received] 2023/05/16 00:00 [accepted] 2023/07/03 13:06 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:25 [entrez]
 2023/02/13 00:00 [received] 2023/02/26 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:32 [entrez] 2023/03/30 06:00 [pubmed]
 2022/04/29 00:00 [received] 2023/02/18 00:00 [accepted] 2023/03/16 01:58 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/11/24 00:00 [received] 2023/01/16 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 09:31 [entrez]
 2023/03/29 06:01 [medline] 2023/03/29 06:00 [pubmed] 2023/03/28 23:30 [entrez]
 2023/02/24 06:01 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 11:41 [entrez]
 2023/01/09 03:32 [entrez] 2023/01/10 06:00 [pubmed] 2023/01/10 06:01 [medline]
 2023/09/13 12:43 [medline] 2023/09/13 12:43 [pubmed] 2023/09/13 08:03 [entrez]
 2022/11/09 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 02:34 [entrez]

 2022/11/29 00:00 [received] 2023/08/15 00:00 [revised] 2023/08/15 00:00 [accepted] 2023/09/01 00:41 [medline] 2023/09/01 00:41 [pubmed] 2023/08/31 18:05 [entrez]
 2023/03/31 00:00 [received] 2023/07/18 00:00 [accepted] 2023/08/31 00:42 [medline] 2023/08/31 00:42 [pubmed] 2023/08/30 21:37 [entrez]
 2023/04/15 00:00 [received] 2023/07/01 00:00 [revised] 2023/07/14 00:00 [accepted] 2023/07/30 01:06 [medline] 2023/07/30 01:06 [pubmed] 2023/07/29 18:04 [entrez]
 2023/03/21 00:00 [received] 2023/05/11 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:15 [entrez]
 2023/05/08 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:04 [entrez]
 2023/03/06 00:00 [received] 2023/04/21 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:12 [entrez]
 2023/01/04 00:00 [received] 2023/04/03 00:00 [accepted] 2023/05/14 13:11 [medline] 2023/05/14 13:10 [pubmed] 2023/05/14 11:54 [entrez]
 2022/11/14 00:00 [received] 2022/12/30 00:00 [revised] 2022/12/30 00:00 [accepted] 2023/01/21 01:32 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2023/03/16 00:00 [received] 2023/07/17 00:00 [accepted] 2023/08/23 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 04:24 [entrez]
 2022/12/05 00:00 [received] 2023/06/15 00:00 [accepted] 2023/07/06 13:14 [medline] 2023/07/06 13:14 [pubmed] 2023/07/06 11:12 [entrez]
 2023/08/03 00:00 [received] 2023/08/20 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/09/09 11:43 [medline] 2023/09/09 11:42 [pubmed] 2023/09/09 01:08 [entrez]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2023/03/13 00:00 [received] 2023/07/25 00:00 [revised] 2023/09/01 00:00 [accepted] 2023/09/14 18:10 [entrez]
 2022/12/22 00:00 [received] 2023/02/13 00:00 [accepted] 2023/03/20 04:00 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2023/04/11 00:00 [received] 2023/06/15 00:00 [revised] 2023/07/13 00:00 [accepted] 2023/08/30 06:47 [medline] 2023/08/30 06:47 [pubmed] 2023/08/30 05:42 [entrez]
 2023/05/11 00:00 [accepted] 2023/06/14 06:43 [medline] 2023/06/14 06:42 [pubmed] 2023/06/14 03:51 [entrez]
 2023/04/18 06:01 [medline] 2023/04/17 04:09 [entrez] 2023/04/18 06:00 [pubmed]
 2023/04/03 10:14 [entrez] 2023/04/04 06:00 [pubmed] 2023/04/04 06:00 [medline]
 2023/09/14 12:41 [medline] 2023/09/14 12:41 [pubmed] 2023/09/14 09:23 [entrez]
 2023/01/18 00:00 [received] 2023/05/08 00:00 [accepted] 2023/06/09 06:42 [medline] 2023/06/07 13:10 [pubmed] 2023/06/07 09:37 [entrez]
 2023/06/15 19:14 [medline] 2023/06/15 19:14 [pubmed] 2023/06/15 16:32 [entrez]
 2023/08/17 06:44 [medline] 2023/08/17 06:43 [pubmed] 2023/08/17 04:27 [entrez]
 2023/02/10 00:00 [received] 2023/03/11 00:00 [revised] 2023/03/17 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 15:37 [entrez]
 2023/03/10 00:00 [received] 2023/05/21 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/06/22 01:07 [medline] 2023/06/22 01:07 [pubmed] 2023/06/21 18:02 [entrez]
 2023/07/04 00:00 [received] 2023/07/23 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/08/26 10:45 [medline] 2023/08/26 10:44 [pubmed] 2023/08/26 01:28 [entrez]
 2022/11/09 00:00 [accepted] 2022/12/02 06:01 [medline] 2022/12/02 06:00 [pubmed] 2022/12/01 11:19 [entrez]
 2022/07/27 00:00 [received] 2023/08/02 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/28 00:41 [medline] 2023/08/28 00:41 [pubmed] 2023/08/27 18:08 [entrez]
 2024/02/06 00:00 [pmc-release] 2023/02/06 11:34 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:00 [medline]
 2022/09/09 00:00 [received] 2023/03/27 00:00 [accepted] 2023/05/04 06:43 [medline] 2023/05/04 06:42 [pubmed] 2023/05/04 02:18 [entrez]
 2022/11/22 00:00 [received] 2023/03/23 00:00 [accepted] 2023/05/16 01:10 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 19:32 [entrez]
 2023/05/31 00:00 [received] 2023/06/28 00:00 [revised] 2023/08/03 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 18:42 [entrez]
 2023/04/26 00:00 [received] 2023/06/28 00:00 [revised] 2023/07/26 00:00 [accepted] 2023/08/12 10:41 [medline] 2023/08/12 10:41 [pubmed] 2023/08/11 20:33 [entrez]
 2023/07/09 00:00 [revised] 2023/04/08 00:00 [received] 2023/08/07 00:00 [accepted] 2023/08/11 06:43 [pubmed] 2023/08/11 06:43 [medline] 2023/08/11 05:31 [entrez]
 2023/04/12 00:00 [received] 2023/06/29 00:00 [accepted] 2023/06/28 00:00 [revised] 2023/07/18 13:09 [medline] 2023/07/18 13:09 [pubmed] 2023/07/18 11:07 [entrez]
 2023/08/24 06:42 [medline] 2023/07/11 06:42 [pubmed] 2023/07/11 02:33 [entrez]
 2023/02/10 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/14 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/04/22 10:42 [pubmed] 2023/04/21 18:05 [entrez]
 2022/10/10 00:00 [received] 2022/12/19 00:00 [revised] 2022/12/30 00:00 [accepted] 2023/04/08 06:01 [medline] 2023/04/07 02:30 [entrez] 2023/04/08 06:00 [pubmed]
 2023/01/15 00:00 [received] 2023/02/16 00:00 [revised] 2023/02/25 00:00 [accepted] 2023/03/11 01:17 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/03/28 00:00 [received] 2022/12/06 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/04/03 06:42 [medline] 2023/03/05 06:00 [pubmed] 2023/03/04 12:36 [entrez]
 2022/06/24 00:00 [received] 2022/12/19 00:00 [accepted] 2023/01/13 02:05 [entrez] 2023/01/14 06:00 [pubmed] 2023/01/14 06:01 [medline]
 2023/01/10 00:00 [received] 2023/06/25 00:00 [revised] 2023/06/28 00:00 [accepted] 2023/07/04 01:05 [medline] 2023/07/04 01:05 [pubmed] 2023/07/03 18:04 [entrez]
 2023/09/14 12:42 [medline] 2023/09/14 12:42 [pubmed] 2023/09/14 08:23 [entrez]
 2023/07/11 00:00 [accepted] 2023/08/29 00:41 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 23:28 [entrez]
 2023/01/30 00:00 [received] 2023/07/21 00:00 [accepted] 2023/08/25 00:42 [medline] 2023/08/25 00:42 [pubmed] 2023/08/24 23:40 [entrez]
 2023/07/23 00:00 [revised] 2023/03/05 00:00 [received] 2023/07/24 00:00 [accepted] 2023/08/23 12:44 [pubmed] 2023/08/23 12:44 [medline] 2023/08/23 07:54 [entrez]
 2023/04/18 00:00 [received] 2023/07/06 00:00 [accepted] 2023/08/02 06:44 [medline] 2023/08/02 06:43 [pubmed] 2023/08/02 03:59 [entrez]
 2022/10/17 00:00 [received] 2023/05/05 00:00 [accepted] 2023/05/22 13:04 [medline] 2023/05/22 13:04 [pubmed] 2023/05/22 07:52 [entrez]
 2023/02/20 00:00 [received] 2023/04/03 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:12 [entrez]
 2023/02/27 00:00 [received] 2023/04/05 00:00 [accepted] 2023/05/12 01:08 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 19:17 [entrez]
 2022/08/20 00:00 [received] 2023/01/09 00:00 [accepted] 2022/11/22 00:00 [revised] 2023/04/24 06:41 [medline] 2023/01/26 06:00 [pubmed] 2023/01/25 11:20 [entrez]
 2023/06/08 00:00 [received] 2023/06/29 00:00 [revised] 2023/07/03 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/29 11:47 [pubmed] 2023/07/29 01:45 [entrez]
 2023/02/25 00:00 [received] 2023/05/24 00:00 [accepted] 2023/07/03 13:06 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:38 [entrez]
 2023/02/01 00:00 [received] 2023/04/29 00:00 [revised] 2023/05/18 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:49 [entrez]
 2022/07/01 00:00 [received] 2023/04/14 00:00 [accepted] 2023/05/22 19:12 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 12:15 [entrez]
 2022/02/28 00:00 [received] 2023/03/28 00:00 [accepted] 2023/04/12 06:42 [medline] 2023/04/10 23:43 [entrez] 2023/04/11 06:00 [pubmed]
 2023/01/13 00:00 [received] 2023/02/09 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/02/25 01:32 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/03/13 00:00 [received] 2023/03/14 00:00 [accepted] 2023/07/24 13:06 [medline] 2023/07/24 13:06 [pubmed] 2023/07/24 11:16 [entrez]
 2025/01/10 00:00 [pmc-release] 2023/01/10 20:43 [entrez] 2023/01/11 06:00 [pubmed] 2023/01/13 06:00 [medline]
 2023/04/27 00:00 [received] 2023/07/21 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 18:08 [entrez]
 2023/06/21 00:00 [received] 2024/08/10 00:00 [pmc-release] 2023/08/16 06:44 [medline] 2023/08/16 06:43 [pubmed] 2023/08/16 03:53 [entrez]
 2023/05/17 00:00 [received] 2023/07/11 00:00 [accepted] 2023/07/23 01:11 [medline] 2023/07/23 01:11 [pubmed] 2023/07/22 23:02 [entrez]
 2023/06/27 06:42 [medline] 2023/06/27 06:42 [pubmed] 2023/06/27 02:14 [entrez]
 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline] 2023/02/24 23:24 [entrez]
 2023/08/24 13:43 [medline] 2023/08/24 13:42 [pubmed] 2023/08/24 09:33 [entrez]
 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:46 [entrez]
 2023/03/27 00:00 [received] 2023/05/30 00:00 [accepted] 2023/06/16 01:08 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 21:23 [entrez]
 2024/08/21 00:00 [pmc-release] 2023/08/21 12:42 [medline] 2023/08/21 12:42 [pubmed] 2023/08/21 11:33 [entrez]
 2023/03/08 00:00 [received] 2023/05/01 00:00 [revised] 2023/05/02 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:10 [entrez]
 2022/09/16 00:00 [received] 2023/03/09 00:00 [accepted] 2023/01/23 00:00 [revised] 2023/05/18 13:09 [medline] 2023/05/18 13:09 [pubmed] 2023/05/18 11:06 [entrez]
 2022/08/31 00:00 [received] 2022/12/12 00:00 [accepted] 2023/04/19 06:01 [medline] 2023/04/18 01:44 [entrez] 2023/04/19 06:00 [pubmed]
 2023/03/28 00:00 [received] 2023/08/04 00:00 [accepted] 2023/09/14 06:43 [medline] 2023/09/14 06:42 [pubmed] 2023/09/14 04:12 [entrez]
 2023/04/29 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/08/29 00:41 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 18:01 [entrez]
 2023/05/08 18:42 [medline] 2023/05/08 18:42 [pubmed] 2023/05/08 14:53 [entrez]
 2023/06/04 00:00 [received] 2023/07/09 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/10 00:41 [medline] 2023/09/10 00:41 [pubmed] 2023/09/09 18:04 [entrez]
 2023/06/29 00:00 [revised] 2023/01/25 00:00 [received] 2023/08/01 00:00 [accepted] 2023/08/14 06:42 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 03:09 [entrez]
 2023/07/20 06:43 [medline] 2023/07/20 06:42 [pubmed] 2023/07/20 03:47 [entrez]
 2023/05/10 00:00 [accepted] 2023/06/14 06:43 [medline] 2023/06/14 06:42 [pubmed] 2023/06/14 03:51 [entrez]
 2023/04/23 00:00 [received] 2023/06/01 00:00 [accepted] 2023/06/10 15:14 [pubmed] 2023/06/10 15:14 [medline] 2023/06/09 18:11 [entrez]
 2023/04/05 00:00 [received] 2023/08/08 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/09/03 00:41 [medline] 2023/09/03 00:41 [pubmed] 2023/09/02 18:15 [entrez]
 2023/08/03 00:00 [revised] 2023/03/29 00:00 [received] 2023/08/08 00:00 [accepted] 2023/08/17 00:42 [medline] 2023/08/17 00:42 [pubmed] 2023/08/16 23:45 [entrez]
 2023/05/22 00:00 [revised] 2023/03/09 00:00 [received] 2023/05/23 00:00 [accepted] 2023/06/05 19:10 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 12:27 [entrez]
 2022/12/05 00:00 [received] 2023/03/16 00:00 [revised] 2023/03/17 00:00 [accepted] 2023/04/14 06:01 [medline] 2023/04/13 01:19 [entrez] 2023/04/14 06:00 [pubmed]
 2022/10/13 00:00 [received] 2023/01/24 00:00 [accepted] 2023/02/09 02:21 [entrez] 2023/02/10 06:00 [pubmed] 2023/02/10 06:01 [medline]
 2023/04/13 00:00 [received] 2023/07/28 00:00 [accepted] 2023/08/15 06:43 [medline] 2023/08/15 06:42 [pubmed] 2023/08/15 03:38 [entrez]
 2023/07/29 00:00 [revised] 2023/03/03 00:00 [received] 2023/08/02 00:00 [accepted] 2023/08/11 06:42 [medline] 2023/08/11 06:42 [pubmed] 2023/08/11 02:13 [entrez]
 2023/01/05 00:00 [accepted] 2023/02/06 11:20 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:00 [medline]
 2023/03/09 00:00 [received] 2023/08/14 00:00 [accepted] 2023/07/05 00:00 [revised] 2023/08/27 18:41 [medline] 2023/08/27 18:41 [pubmed] 2023/08/27 14:51 [entrez]
 2022/11/16 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/11/29 11:24 [entrez]
 2022/10/20 00:00 [received] 2023/03/28 00:00 [revised] 2023/04/01 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:17 [entrez]
 2023/03/24 00:00 [received] 2023/07/26 00:00 [accepted] 2023/07/24 00:00 [revised] 2023/08/03 01:06 [medline] 2023/08/03 01:06 [pubmed] 2023/08/02 23:22 [entrez]
 2023/08/07 13:11 [medline] 2023/08/07 13:10 [pubmed] 2023/08/07 11:03 [entrez]
 2022/11/07 00:00 [received] 2023/02/02 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/07/08 10:42 [pubmed] 2023/07/07 20:58 [entrez]
 2023/08/29 12:44 [medline] 2023/08/28 12:43 [pubmed] 2023/08/28 10:53 [entrez]
 2023/07/20 01:06 [medline] 2023/07/20 01:06 [pubmed] 2023/07/19 21:59 [entrez]
 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 05:03 [entrez]
 2022/09/01 00:00 [received] 2023/02/16 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:44 [entrez]
 2023/03/21 12:13 [entrez] 2023/03/22 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2022/10/08 00:00 [received] 2023/02/06 00:00 [revised] 2023/03/14 00:00 [accepted] 2023/04/26 06:42 [medline] 2023/03/26 06:00 [pubmed] 2023/03/25 19:08 [entrez]
 2023/07/22 10:42 [pubmed] 2023/07/22 10:42 [medline] 2023/07/21 19:32 [entrez]
 2023/02/19 00:00 [received] 2023/07/09 00:00 [revised] 2023/07/25 00:00 [accepted] 2023/08/01 01:08 [pubmed] 2023/08/01 01:08 [medline] 2023/07/31 19:12 [entrez]
 2023/05/10 00:00 [revised] 2022/12/16 00:00 [received] 2023/05/12 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/06/07 06:42 [pubmed] 2023/06/07 05:28 [entrez]
 2022/12/30 00:00 [received] 2023/05/11 00:00 [revised] 2023/05/20 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/06/02 01:07 [pubmed] 2023/06/01 18:06 [entrez]
 2023/04/16 00:00 [received] 2023/05/04 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:32 [entrez]
 2021/07/04 00:00 [received] 2022/01/01 00:00 [revised] 2022/08/30 00:00 [accepted] 2023/05/09 18:42 [medline] 2023/05/09 18:41 [pubmed] 2023/05/09 15:16 [entrez]
 2022/08/18 00:00 [received] 2022/11/23 00:00 [revised] 2022/12/29 00:00 [accepted] 2023/02/28 06:55 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:00 [medline]
 2022/12/12 00:00 [received] 2023/01/08 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 02:54 [entrez]
 2022/05/24 00:00 [received] 2022/11/07 00:00 [revised] 2022/11/15 00:00 [accepted] 2022/11/27 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/11/26 19:26 [entrez]
 2023/08/24 00:00 [accepted] 2023/09/08 00:41 [medline] 2023/09/08 00:41 [pubmed] 2023/09/07 23:38 [entrez]
 2023/06/30 00:00 [accepted] 2023/08/16 12:42 [medline] 2023/08/16 12:42 [pubmed] 2023/08/16 11:03 [entrez]
 2023/07/12 06:42 [medline] 2023/07/11 13:11 [pubmed] 2023/07/11 07:42 [entrez]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2023/07/21 19:10 [medline] 2023/07/21 19:10 [pubmed] 2023/07/21 14:04 [entrez]
 2023/05/31 13:12 [medline] 2023/05/31 13:12 [pubmed] 2023/05/31 10:22 [entrez]
 2022/10/30 00:00 [received] 2023/01/30 00:00 [accepted] 2023/03/27 03:53 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2023/09/01 12:43 [medline] 2023/09/01 12:43 [pubmed] 2023/09/01 10:35 [entrez]
 2023/06/01 00:00 [received] 2023/06/10 00:00 [accepted] 2023/07/11 01:08 [medline] 2023/07/11 01:08 [pubmed] 2023/07/10 23:26 [entrez]
 2023/05/23 00:00 [received] 2023/06/29 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/13 01:06 [pubmed] 2023/07/12 23:51 [entrez]
 2023/03/16 00:00 [received] 2023/05/10 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/05/29 00:42 [pubmed] 2023/05/28 18:02 [entrez]
 2023/02/07 00:00 [received] 2023/03/10 00:00 [revised] 2023/03/17 00:00 [accepted] 2023/04/12 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:10 [entrez]
 2021/07/01 00:00 [received] 2022/01/28 00:00 [accepted] 2022/02/12 06:00 [pubmed] 2023/03/21 06:00 [medline] 2022/02/11 08:46 [entrez]
 2023/04/13 00:00 [received] 2023/05/09 00:00 [revised] 2023/05/20 00:00 [accepted] 2023/06/10 15:14 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:09 [entrez]
 2023/03/13 00:00 [received] 2023/07/22 00:00 [accepted] 2023/08/09 06:43 [medline] 2023/08/08 00:42 [pubmed] 2023/08/07 23:39 [entrez]
 2022/08/24 00:00 [received] 2022/11/22 00:00 [revised] 2022/12/26 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/09 04:36 [entrez]
 2023/06/22 00:00 [received] 2023/07/24 00:00 [revised] 2023/07/26 00:00 [accepted] 2023/08/12 10:47 [medline] 2023/08/12 10:46 [pubmed] 2023/08/12 01:01 [entrez]
 2023/04/12 00:00 [received] 2023/05/27 00:00 [revised] 2023/06/20 00:00 [accepted] 2023/07/29 11:43 [medline] 2023/07/29 11:42 [pubmed] 2023/07/29 01:12 [entrez]
 2023/04/30 00:00 [received] 2023/05/29 00:00 [accepted] 2023/07/03 13:06 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:34 [entrez]
 2022/08/22 00:00 [received] 2022/12/22 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:13 [entrez]
 2023/06/11 00:00 [received] 2023/07/03 00:00 [revised] 2023/07/05 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:12 [entrez]
 2023/06/16 00:00 [revised] 2023/04/14 00:00 [received] 2023/06/20 00:00 [accepted] 2023/06/30 06:42 [medline] 2023/06/30 06:42 [pubmed] 2023/06/30 02:15 [entrez]
 2023/05/31 00:00 [revised] 2023/05/08 00:00 [received] 2023/06/05 00:00 [accepted] 2023/06/16 01:08 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 23:44 [entrez]
 2023/02/26 00:00 [received] 2023/07/22 00:00 [revised] 2023/07/31 00:00 [accepted] 2023/08/19 11:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 22:01 [entrez]

 2022/07/18 00:00 [received] 2023/01/10 00:00 [accepted] 2023/02/03 00:05 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/04 06:01 [medline]
 2022/10/13 00:00 [received] 2022/10/17 00:00 [accepted] 2023/06/19 13:08 [medline] 2022/11/11 06:00 [pubmed] 2022/11/10 22:04 [entrez]
 2023/03/02 00:00 [received] 2023/06/08 00:00 [revised] 2023/07/23 00:00 [accepted] 2023/08/20 00:41 [medline] 2023/08/20 00:41 [pubmed] 2023/08/19 18:04 [entrez]
 2022/12/17 00:00 [received] 2023/03/15 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:15 [entrez]
 2023/06/23 00:00 [accepted] 2023/07/25 06:44 [medline] 2023/07/25 06:43 [pubmed] 2023/07/25 03:39 [entrez]
 2023/02/08 02:39 [entrez] 2023/02/09 06:00 [pubmed] 2023/02/09 06:01 [medline]
 2022/05/24 06:01 [medline] 2022/05/24 06:00 [pubmed] 2022/05/23 22:05 [entrez]
 2023/05/09 00:00 [accepted] 2023/06/27 13:11 [medline] 2023/06/27 13:11 [pubmed] 2023/06/27 11:03 [entrez]
 2023/01/11 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/05 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 19:07 [entrez]
 2023/06/28 00:00 [received] 2023/08/13 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/09/07 00:41 [medline] 2023/09/07 00:41 [pubmed] 2023/09/06 18:07 [entrez]

 2022/12/25 00:00 [received] 2023/03/13 00:00 [accepted] 2023/04/05 06:01 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 20:42 [entrez]
 2023/03/29 00:00 [received] 2023/06/16 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:28 [entrez]
 2022/06/27 00:00 [received] 2023/01/12 00:00 [accepted] 2023/02/23 09:27 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/09/07 12:42 [medline] 2023/09/07 12:42 [pubmed] 2023/09/07 10:13 [entrez]
 2023/08/01 00:00 [revised] 2023/05/09 00:00 [received] 2023/08/15 00:00 [accepted] 2023/09/01 06:43 [medline] 2023/09/01 06:43 [pubmed] 2023/09/01 00:43 [entrez]
 2023/01/08 00:00 [received] 2023/08/08 00:00 [accepted] 2023/08/11 00:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 23:33 [entrez]
 2023/01/05 00:00 [received] 2023/07/18 00:00 [revised] 2023/08/05 00:00 [accepted] 2023/08/10 00:42 [pubmed] 2023/08/10 00:42 [medline] 2023/08/09 19:26 [entrez]
 2023/06/29 19:12 [medline] 2023/06/29 19:12 [pubmed] 2023/06/29 12:33 [entrez]
 2023/04/06 12:14 [entrez] 2023/04/07 06:00 [pubmed] 2023/04/07 06:00 [medline]
 2023/03/22 01:56 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/23 06:01 [medline]
 2023/05/09 00:00 [received] 2023/08/17 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/08/30 00:41 [medline] 2023/08/30 00:41 [pubmed] 2023/08/29 19:13 [entrez]
 2023/07/06 06:42 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 00:33 [entrez]
 2023/08/03 19:14 [medline] 2023/08/03 19:14 [pubmed] 2023/08/03 13:33 [entrez]
 2023/05/06 00:00 [received] 2023/06/03 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/06/25 01:08 [pubmed] 2023/06/25 01:08 [medline] 2023/06/24 19:16 [entrez]
 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 13:09 [entrez]
 2023/03/31 06:01 [medline] 2023/03/30 02:52 [entrez] 2023/03/31 06:00 [pubmed]
 2023/07/11 06:42 [pubmed] 2023/07/11 06:42 [medline] 2023/07/11 02:25 [entrez]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/11/30 00:00 [received] 2022/12/28 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/21 01:24 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/11/23 00:00 [received] 2023/05/31 00:00 [revised] 2023/07/10 00:00 [accepted] 2023/08/10 00:42 [medline] 2023/08/10 00:42 [pubmed] 2023/08/09 18:04 [entrez]
 2022/03/28 00:00 [received] 2022/11/17 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/02/27 04:03 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2023/05/07 00:00 [received] 2023/06/16 00:00 [revised] 2023/06/30 00:00 [accepted] 2023/07/29 11:52 [medline] 2023/07/29 11:51 [pubmed] 2023/07/29 01:27 [entrez]
 2023/05/12 00:00 [received] 2023/06/01 00:00 [accepted] 2023/06/22 01:07 [pubmed] 2023/06/22 01:07 [medline] 2023/06/21 18:07 [entrez]
 2023/05/11 00:00 [received] 2023/06/06 00:00 [accepted] 2023/06/05 00:00 [revised] 2023/06/14 13:06 [medline] 2023/06/14 13:06 [pubmed] 2023/06/14 11:06 [entrez]
 2023/02/26 00:00 [received] 2023/05/16 00:00 [revised] 2023/06/10 00:00 [accepted] 2023/07/14 13:07 [medline] 2023/07/14 13:07 [pubmed] 2023/07/13 21:57 [entrez]
 2023/07/19 00:00 [revised] 2023/05/18 00:00 [received] 2023/07/20 00:00 [accepted] 2023/08/02 13:09 [medline] 2023/08/02 13:09 [pubmed] 2023/08/02 10:44 [entrez]
 2023/05/30 00:00 [received] 2023/06/14 00:00 [revised] 2023/06/27 00:00 [accepted] 2023/07/29 11:54 [medline] 2023/07/29 11:53 [pubmed] 2023/07/29 01:06 [entrez]
 2023/02/12 00:00 [received] 2023/04/18 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:11 [entrez]
 2022/06/09 00:00 [received] 2022/12/08 00:00 [accepted] 2023/02/10 03:25 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2022/11/22 00:00 [received] 2022/12/28 00:00 [accepted] 2023/01/30 03:50 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/02/20 00:00 [received] 2023/05/24 00:00 [accepted] 2023/06/14 01:10 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 23:29 [entrez]
 2023/03/16 02:25 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/06/14 00:00 [received] 2022/11/23 00:00 [accepted] 2023/02/22 17:35 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/23 06:01 [medline]
 2023/03/13 00:00 [received] 2023/07/07 00:00 [accepted] 2023/09/07 06:43 [medline] 2023/09/07 06:42 [pubmed] 2023/09/07 04:10 [entrez]
 2023/03/10 00:00 [received] 2023/06/07 00:00 [accepted] 2023/06/24 21:04 [medline] 2023/06/24 21:03 [pubmed] 2023/06/24 11:05 [entrez]
 2023/03/29 00:00 [received] 2023/05/10 00:00 [accepted] 2023/06/08 13:08 [medline] 2023/06/08 13:07 [pubmed] 2023/06/08 11:15 [entrez]
 2022/03/09 00:00 [received] 2022/07/23 00:00 [accepted] 2023/02/13 03:20 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2023/01/11 00:00 [revised] 2022/11/21 00:00 [received] 2023/01/12 00:00 [accepted] 2023/01/20 06:33 [entrez] 2023/01/21 06:00 [pubmed] 2023/01/21 06:00 [medline]
 2023/02/14 00:00 [received] 2023/08/07 00:00 [revised] 2023/08/22 00:00 [accepted] 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 18:02 [entrez]
 2023/03/21 00:00 [received] 2023/05/02 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:50 [entrez]
 2022/10/11 00:00 [received] 2023/01/26 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/03/31 00:02 [entrez] 2023/04/01 06:00 [pubmed] 2023/04/01 06:00 [medline]
 2022/08/28 00:00 [received] 2023/01/25 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/02/23 02:07 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/02/02 13:43 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/07 06:00 [medline]
 2022/10/26 00:00 [received] 2022/12/29 00:00 [revised] 2023/02/09 00:00 [accepted] 2023/02/23 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/22 18:15 [entrez]
 2023/01/30 03:51 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2023/04/10 00:00 [received] 2023/05/19 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/07/27 06:44 [medline] 2023/07/27 06:43 [pubmed] 2023/07/27 04:30 [entrez]
 2022/05/13 00:00 [received] 2023/04/28 00:00 [accepted] 2023/08/18 12:42 [medline] 2023/08/18 12:42 [pubmed] 2023/08/18 11:13 [entrez]
 2023/05/13 00:00 [received] 2023/06/16 00:00 [accepted] 2023/07/08 19:43 [medline] 2023/07/08 19:42 [pubmed] 2023/07/08 11:08 [entrez]
 2023/03/31 00:00 [received] 2023/04/30 00:00 [revised] 2023/05/05 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:09 [entrez]
 2022/10/02 00:00 [received] 2023/02/16 00:00 [accepted] 2023/03/28 19:06 [medline] 2023/03/25 00:26 [entrez] 2023/03/26 06:00 [pubmed]
 2023/05/08 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 14:44 [entrez]
 2022/04/21 00:00 [received] 2022/09/02 00:00 [revised] 2022/09/06 00:00 [accepted] 2023/04/04 06:42 [medline] 2022/09/27 06:00 [pubmed] 2022/09/26 15:02 [entrez]
 2023/06/28 00:00 [revised] 2023/04/30 00:00 [received] 2023/06/30 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 03:09 [entrez]
 2023/06/19 00:00 [received] 2023/08/02 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/09/07 06:42 [pubmed] 2023/09/07 04:15 [entrez]
 2022/12/16 00:00 [received] 2023/01/16 00:00 [revised] 2023/01/16 00:00 [accepted] 2023/02/25 01:25 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/12/01 00:00 [received] 2023/02/13 00:00 [accepted] 2023/03/20 04:05 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2023/02/16 00:00 [received] 2023/06/22 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/23 01:11 [pubmed] 2023/07/22 18:06 [entrez]
 2023/05/02 00:00 [received] 2023/08/25 18:42 [medline] 2023/08/25 18:42 [pubmed] 2023/08/25 15:32 [entrez]
 2023/04/26 00:00 [received] 2023/05/16 00:00 [accepted] 2023/06/09 01:09 [pubmed] 2023/06/09 01:09 [medline] 2023/06/08 21:53 [entrez]


 2022/12/29 00:00 [received] 2023/02/14 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/03/29 06:01 [medline] 2023/03/28 16:12 [entrez] 2023/03/29 06:00 [pubmed]
 2023/01/12 00:00 [received] 2023/04/27 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/06 19:42 [pubmed] 2023/05/06 18:00 [entrez]
 2023/04/17 00:00 [received] 2023/05/25 00:00 [revised] 2023/05/26 00:00 [accepted] 2023/07/01 11:41 [medline] 2023/07/01 11:41 [pubmed] 2023/06/30 21:53 [entrez]
 2022/11/13 00:00 [received] 2023/05/03 00:00 [accepted] 2023/05/23 01:07 [medline] 2023/05/23 01:06 [pubmed] 2023/05/22 23:21 [entrez]
 2022/12/07 00:00 [received] 2023/04/14 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:10 [entrez]
 2022/10/03 00:00 [received] 2023/03/06 00:00 [accepted] 2023/04/15 06:01 [medline] 2023/04/14 02:39 [entrez] 2023/04/15 06:00 [pubmed]
 2022/06/07 00:00 [received] 2022/11/17 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:58 [entrez]
 2022/07/02 00:00 [received] 2023/01/03 00:00 [accepted] 2023/02/10 03:18 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2023/06/08 00:00 [received] 2023/07/01 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 18:07 [entrez]
 2023/02/27 00:00 [received] 2023/03/30 00:00 [revised] 2023/03/31 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:53 [entrez]
 2022/11/07 00:00 [received] 2023/01/11 00:00 [revised] 2023/02/15 00:00 [accepted] 2023/08/17 06:43 [medline] 2023/08/17 06:42 [pubmed] 2023/08/17 04:24 [entrez]
 2022/12/01 00:00 [received] 2022/12/07 00:00 [revised] 2022/12/08 00:00 [accepted] 2024/02/01 00:00 [pmc-release] 2023/01/05 06:00 [pubmed] 2023/02/01 06:00 [medline] 2023/01/04 21:54 [entrez]
 2022/12/28 00:00 [received] 2023/03/20 00:00 [accepted] 2023/03/30 06:00 [pubmed] 2023/03/30 06:00 [medline] 2023/03/29 21:12 [entrez]
 2022/10/07 03:03 [entrez] 2022/10/08 06:00 [pubmed] 2022/10/08 06:01 [medline]

 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:05 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2023/02/23 02:10 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/07/26 00:00 [received] 2023/08/13 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 18:17 [entrez]
 2023/04/18 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/08 00:00 [accepted] 2023/08/01 06:44 [medline] 2023/08/01 06:44 [pubmed] 2023/08/01 03:52 [entrez]
 2023/01/23 11:33 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:00 [medline]
 2023/05/17 00:00 [received] 2023/08/17 00:00 [accepted] 2023/09/13 12:42 [medline] 2023/09/13 12:42 [pubmed] 2023/09/13 07:13 [entrez]
 2023/07/28 06:44 [medline] 2023/07/28 06:43 [pubmed] 2023/07/28 04:27 [entrez]
 2023/03/07 00:00 [received] 2023/04/07 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/05/13 15:13 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:24 [entrez]
 2022/12/01 00:00 [received] 2022/12/31 00:00 [accepted] 2023/02/10 03:06 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2023/01/23 00:00 [received] 2023/07/26 00:00 [revised] 2023/07/29 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 04:46 [entrez]
 2023/03/04 00:00 [received] 2023/06/26 00:00 [revised] 2023/07/16 00:00 [accepted] 2023/08/04 01:07 [medline] 2023/08/04 01:07 [pubmed] 2023/08/03 18:09 [entrez]
 2023/01/25 00:32 [entrez] 2023/01/26 06:00 [pubmed] 2023/01/26 06:00 [medline]
 2023/07/19 13:06 [pubmed] 2023/07/19 13:06 [medline] 2023/07/19 11:14 [entrez]
 2023/08/07 13:09 [pubmed] 2023/08/07 13:09 [medline] 2023/08/07 06:49 [entrez]
 2023/07/21 00:00 [revised] 2023/05/24 00:00 [received] 2023/08/17 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/22 06:42 [pubmed] 2023/08/22 05:32 [entrez]
 2023/06/17 00:00 [received] 2023/07/30 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/15 00:42 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 18:06 [entrez]
 2023/04/03 00:00 [received] 2023/07/05 00:00 [accepted] 2023/07/11 13:10 [medline] 2023/07/11 13:10 [pubmed] 2023/07/11 11:11 [entrez]
 2023/07/19 00:00 [revised] 2023/03/23 00:00 [received] 2023/09/05 00:00 [accepted] 2023/09/07 00:42 [pubmed] 2023/09/07 00:42 [medline] 2023/09/06 19:24 [entrez]

 2023/05/23 00:00 [received] 2023/08/04 00:00 [accepted] 2023/08/25 00:42 [medline] 2023/08/25 00:42 [pubmed] 2023/08/24 23:41 [entrez]
 2023/04/14 00:00 [received] 2023/06/10 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/07/13 19:16 [medline] 2023/07/13 19:15 [pubmed] 2023/07/13 15:22 [entrez]
 2023/04/22 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/15 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 18:04 [entrez]
 2023/05/01 06:42 [medline] 2023/02/26 06:00 [pubmed] 2023/02/25 06:52 [entrez]
 2023/02/06 11:23 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:00 [medline]
 2022/09/06 00:00 [received] 2023/01/02 00:00 [accepted] 2022/12/20 00:00 [revised] 2023/01/26 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/01/25 11:15 [entrez]
 2022/03/14 00:00 [received] 2022/12/06 00:00 [revised] 2022/12/07 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/02/18 06:00 [medline] 2023/01/07 16:01 [entrez]
 2022/10/11 00:00 [revised] 2022/04/15 00:00 [received] 2022/10/13 00:00 [accepted] 2022/11/11 06:00 [pubmed] 2022/12/29 06:00 [medline] 2022/11/10 01:22 [entrez]
 2022/09/20 00:00 [received] 2022/12/28 00:00 [accepted] 2023/01/30 04:25 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/11/10 00:00 [received] 2023/04/23 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/08 19:14 [medline] 2023/06/08 19:14 [pubmed] 2023/06/08 12:36 [entrez]
 2021/12/07 00:00 [received] 2022/02/01 00:00 [revised] 2022/03/02 00:00 [accepted] 2023/07/11 06:42 [medline] 2023/06/06 06:42 [pubmed] 2023/06/06 03:40 [entrez]
 2023/03/23 00:00 [received] 2023/05/17 00:00 [accepted] 2023/03/23 00:00 [revised] 2023/05/26 13:09 [medline] 2023/05/26 13:09 [pubmed] 2023/05/26 11:04 [entrez]
 2023/02/08 00:00 [received] 2023/04/30 00:00 [accepted] 2023/04/21 00:00 [revised] 2023/05/25 13:07 [medline] 2023/05/25 13:07 [pubmed] 2023/05/25 11:27 [entrez]
 2022/11/15 00:00 [received] 2023/02/16 00:00 [revised] 2023/03/26 00:00 [accepted] 2023/04/26 00:42 [pubmed] 2023/04/26 00:42 [medline] 2023/04/25 19:13 [entrez]
 2023/02/01 00:00 [received] 2023/03/06 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/04/10 03:48 [entrez] 2023/04/11 06:00 [pubmed]
 2022/05/10 00:00 [received] 2023/03/17 00:00 [revised] 2023/03/20 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 20:29 [entrez]
 2023/06/26 00:00 [received] 2023/07/19 00:00 [revised] 2023/07/19 00:00 [accepted] 2023/07/31 11:43 [medline] 2023/07/29 11:51 [pubmed] 2023/07/29 01:07 [entrez]
 2022/04/05 00:00 [received] 2022/07/11 00:00 [revised] 2022/08/22 00:00 [accepted] 2022/11/28 06:00 [pubmed] 2023/02/07 06:00 [medline] 2022/11/27 19:28 [entrez]
 2023/06/01 00:00 [received] 2023/06/22 00:00 [accepted] 2023/08/30 06:49 [medline] 2023/08/30 06:48 [pubmed] 2023/08/30 03:47 [entrez]
 2023/03/24 00:00 [received] 2023/07/21 00:00 [revised] 2023/07/30 00:00 [accepted] 2023/08/19 11:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 18:03 [entrez]
 2023/04/24 00:00 [received] 2023/07/05 00:00 [accepted] 2023/08/16 06:44 [medline] 2023/08/16 06:43 [pubmed] 2023/08/16 03:45 [entrez]
 2023/04/13 00:00 [received] 2023/06/27 00:00 [accepted] 2023/08/02 06:43 [medline] 2023/08/02 06:42 [pubmed] 2023/08/02 03:52 [entrez]
 2023/07/19 06:43 [medline] 2023/07/19 06:42 [pubmed] 2023/07/19 03:58 [entrez]
 2023/06/06 00:00 [received] 2023/07/20 00:00 [accepted] 2023/08/31 00:42 [medline] 2023/08/31 00:41 [pubmed] 2023/08/30 23:46 [entrez]




 2022/10/03 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/05/11 06:42 [medline] 2023/05/11 06:42 [pubmed] 2023/05/11 00:13 [entrez]
 2022/11/29 00:00 [received] 2023/01/25 00:00 [accepted] 2023/02/23 09:36 [entrez] 2023/02/24 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/07/22 00:00 [received] 2022/12/08 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/12 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/11 04:35 [entrez]
 2023/05/02 00:00 [received] 2023/07/17 00:00 [revised] 2023/08/02 00:00 [accepted] 2023/08/29 12:42 [medline] 2023/08/29 12:42 [pubmed] 2023/08/29 09:43 [entrez]
 2023/08/09 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/22 06:42 [pubmed] 2023/08/22 05:45 [entrez]
 2022/09/30 00:00 [received] 2022/12/02 00:00 [revised] 2022/12/07 00:00 [accepted] 2023/02/28 19:04 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:01 [medline]
 2023/06/03 00:00 [received] 2023/08/16 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/08/26 05:41 [pubmed] 2023/08/26 05:41 [medline] 2023/08/25 19:28 [entrez]
 2022/12/04 00:00 [received] 2023/01/07 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/01/21 01:34 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2023/01/20 00:00 [received] 2023/05/08 00:00 [accepted] 2023/05/24 01:06 [medline] 2023/05/24 01:06 [pubmed] 2023/05/23 21:23 [entrez]
 2023/06/20 00:00 [received] 2023/07/13 00:00 [revised] 2023/07/20 00:00 [accepted] 2023/08/26 10:45 [medline] 2023/08/26 10:44 [pubmed] 2023/08/26 01:01 [entrez]
 2023/05/13 00:00 [received] 2023/06/12 00:00 [revised] 2023/06/14 00:00 [accepted] 2023/06/29 06:42 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:31 [entrez]
 2023/01/13 00:00 [received] 2023/02/19 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 02:01 [entrez] 2023/03/30 06:00 [pubmed]
 2023/02/07 00:00 [received] 2023/04/19 00:00 [revised] 2023/04/21 00:00 [accepted] 2023/05/13 15:14 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:34 [entrez]
 2023/01/26 00:00 [received] 2023/03/14 00:00 [revised] 2023/03/16 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:23 [entrez] 2023/03/30 06:00 [pubmed]
 2022/12/03 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/02/11 01:20 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/04/04 00:00 [received] 2023/04/26 00:00 [accepted] 2023/07/26 06:42 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 21:23 [entrez]
 2023/01/02 00:00 [received] 2023/06/08 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/14 13:08 [pubmed] 2023/07/14 11:13 [entrez]
 2023/06/03 00:00 [received] 2023/07/18 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/04 01:07 [medline] 2023/08/04 01:07 [pubmed] 2023/08/03 18:09 [entrez]
 2022/12/28 00:00 [received] 2023/03/14 00:00 [revised] 2023/04/10 00:00 [accepted] 2023/04/28 06:43 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:47 [entrez]
 2022/12/08 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/08 00:00 [accepted] 2023/01/20 09:33 [entrez] 2023/01/21 06:00 [pubmed] 2023/01/21 06:01 [medline]
 2023/08/25 18:42 [medline] 2023/08/25 18:42 [pubmed] 2023/08/25 13:23 [entrez]
 2023/02/04 00:00 [revised] 2022/04/26 00:00 [received] 2023/03/06 00:00 [accepted] 2023/03/18 06:00 [pubmed] 2023/03/18 06:00 [medline] 2023/03/17 17:32 [entrez]
 2023/07/25 06:42 [pubmed] 2023/07/25 06:42 [medline] 2023/07/25 05:43 [entrez]
 2023/09/08 00:42 [medline] 2023/09/08 00:42 [pubmed] 2023/09/07 18:12 [entrez]
 2023/07/05 19:12 [medline] 2023/07/05 19:12 [pubmed] 2023/07/05 14:33 [entrez]
 2022/12/06 00:00 [received] 2023/03/10 00:00 [revised] 2023/03/12 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 22:00 [entrez]
 2022/11/09 00:00 [received] 2023/02/07 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 03:46 [entrez] 2023/04/11 06:00 [pubmed]
 2023/02/07 01:56 [entrez] 2023/02/08 06:00 [pubmed] 2023/02/08 06:01 [medline]
 2023/07/09 00:00 [revised] 2023/04/15 00:00 [received] 2023/07/17 00:00 [accepted] 2023/07/27 06:43 [pubmed] 2023/07/27 06:43 [medline] 2023/07/27 02:33 [entrez]
 2023/04/21 00:00 [received] 2023/07/15 00:00 [accepted] 2023/09/13 18:42 [medline] 2023/09/13 18:42 [pubmed] 2023/09/13 12:13 [entrez]
 2022/12/31 00:00 [received] 2023/08/01 00:00 [revised] 2023/08/15 00:00 [accepted] 2023/09/04 00:41 [medline] 2023/09/04 00:41 [pubmed] 2023/09/03 18:09 [entrez]
 2023/03/27 00:00 [received] 2023/07/24 00:00 [accepted] 2023/08/29 06:44 [medline] 2023/08/29 06:43 [pubmed] 2023/08/29 03:36 [entrez]
 2023/08/11 06:43 [medline] 2023/08/11 06:43 [pubmed] 2023/08/11 00:03 [entrez]
 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:03 [entrez]
 2022/12/19 00:00 [received] 2023/02/18 00:00 [accepted] 2023/03/21 02:07 [entrez] 2023/03/22 06:00 [pubmed] 2023/03/22 06:01 [medline]
 2023/08/11 00:42 [pubmed] 2023/08/11 00:42 [medline] 2023/08/10 19:12 [entrez]
 2023/02/24 00:00 [received] 2023/05/14 00:00 [revised] 2023/06/07 00:00 [accepted] 2023/09/04 06:44 [medline] 2023/09/04 06:43 [pubmed] 2023/09/04 05:14 [entrez]
 2022/08/07 00:00 [received] 2022/10/10 00:00 [revised] 2022/11/01 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/03/28 06:00 [medline] 2022/12/08 10:24 [entrez]
 2023/06/13 00:00 [accepted] 2023/07/15 10:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 23:28 [entrez]
 2023/01/29 00:00 [received] 2023/04/29 00:00 [accepted] 2023/05/05 06:42 [medline] 2023/05/04 00:42 [pubmed] 2023/05/03 23:33 [entrez]
 2023/07/04 00:00 [received] 2023/07/18 00:00 [revised] 2023/07/25 00:00 [accepted] 2023/08/26 10:43 [medline] 2023/08/26 10:42 [pubmed] 2023/08/26 01:01 [entrez]
 2023/04/25 00:00 [received] 2023/06/22 00:00 [accepted] 2023/08/01 06:44 [medline] 2023/07/31 06:42 [pubmed] 2023/07/31 04:53 [entrez]
 2023/01/31 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/14 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:41 [entrez] 2023/03/30 06:00 [pubmed]
 2022/11/25 00:00 [received] 2023/02/10 00:00 [accepted] 2023/03/20 04:08 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2023/02/21 18:22 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/07/17 06:42 [medline] 2023/07/16 06:42 [pubmed] 2023/07/16 03:09 [entrez]
 2023/02/07 00:00 [received] 2023/06/07 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/07/27 06:42 [pubmed] 2023/07/27 00:03 [entrez]
 2022/12/13 00:00 [received] 2023/03/12 00:00 [revised] 2023/03/13 00:00 [accepted] 2023/04/03 06:42 [medline] 2023/03/25 06:00 [pubmed] 2023/03/24 19:10 [entrez]
 2022/11/27 00:00 [received] 2022/12/23 00:00 [revised] 2023/01/08 00:00 [accepted] 2023/01/26 02:39 [entrez] 2023/01/27 06:00 [pubmed] 2023/01/27 06:01 [medline]
 2023/09/14 18:43 [medline] 2023/09/14 18:43 [pubmed] 2023/09/14 12:53 [entrez]
 2023/04/04 00:00 [received] 2023/06/14 00:00 [accepted] 2023/07/14 13:09 [medline] 2023/07/14 13:08 [pubmed] 2023/07/14 11:12 [entrez]

 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:38 [entrez]
 2023/02/05 00:00 [received] 2023/05/26 00:00 [accepted] 2023/07/06 06:43 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 04:11 [entrez]
 2022/08/15 00:00 [received] 2023/03/28 00:00 [accepted] 2023/03/27 00:00 [revised] 2023/04/11 06:00 [pubmed] 2023/04/11 06:00 [medline] 2023/04/10 23:17 [entrez]

 2023/07/13 19:15 [medline] 2023/07/13 19:15 [pubmed] 2023/07/13 14:33 [entrez]

 2023/02/14 00:00 [received] 2023/04/30 00:00 [revised] 2023/05/01 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 20:55 [entrez]
 2023/05/18 06:42 [medline] 2023/05/17 06:42 [pubmed] 2023/05/17 04:33 [entrez]

 2023/07/03 13:06 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:43 [entrez]
 2023/06/02 06:42 [medline] 2022/03/25 06:00 [pubmed] 2022/03/24 12:13 [entrez]
 2022/10/13 00:00 [received] 2022/11/29 00:00 [accepted] 2023/01/23 05:12 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2023/03/25 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/28 06:44 [medline] 2023/06/28 06:43 [pubmed] 2023/06/28 01:06 [entrez]

 2023/06/18 00:00 [received] 2023/07/19 00:00 [revised] 2023/07/20 00:00 [accepted] 2023/08/14 00:42 [medline] 2023/08/14 00:42 [pubmed] 2023/08/13 19:27 [entrez]
 2022/12/31 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:14 [pubmed] 2023/06/09 23:32 [entrez]
 2023/05/28 00:00 [received] 2023/06/22 00:00 [revised] 2023/06/25 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:14 [entrez]
 2023/08/02 00:00 [received] 2023/08/04 00:00 [accepted] 2023/09/03 00:41 [medline] 2023/09/03 00:41 [pubmed] 2023/09/02 18:05 [entrez]
 2023/03/10 00:00 [received] 2023/05/02 00:00 [accepted] 2023/05/25 06:42 [medline] 2023/05/24 01:06 [pubmed] 2023/05/23 23:58 [entrez]
 2023/01/30 00:00 [received] 2023/04/13 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 18:07 [entrez]
 2022/09/26 00:00 [received] 2022/12/17 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/01/30 06:00 [pubmed] 2023/03/09 06:00 [medline] 2023/01/29 18:09 [entrez]
 2022/08/23 00:00 [received] 2023/03/06 00:00 [revised] 2023/06/23 00:00 [accepted] 2023/07/19 19:08 [pubmed] 2023/07/19 19:08 [medline] 2023/07/19 18:03 [entrez]
 2023/08/15 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 02:43 [entrez]
 2022/12/30 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/11 01:20 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/02/03 00:00 [received] 2023/07/12 00:00 [accepted] 2023/07/01 00:00 [revised] 2023/08/31 12:44 [medline] 2023/08/31 12:44 [pubmed] 2023/08/31 11:12 [entrez]
 2023/04/09 00:00 [received] 2023/05/21 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:08 [entrez]
 2023/01/05 00:00 [received] 2023/02/06 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/02/25 01:33 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/04/14 00:00 [received] 2023/05/24 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/06/17 05:11 [pubmed] 2023/06/17 05:11 [medline] 2023/06/16 18:05 [entrez]
 2023/05/13 00:00 [received] 2023/05/25 00:00 [revised] 2023/05/30 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 18:08 [entrez]
 2023/08/28 06:42 [medline] 2023/08/25 00:41 [pubmed] 2023/08/24 20:57 [entrez]
 2023/03/03 00:00 [received] 2023/04/13 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 19:30 [entrez]
 2023/06/07 06:42 [medline] 2023/03/29 06:00 [pubmed] 2023/03/28 12:52 [entrez]

 2023/04/22 00:00 [received] 2023/06/07 00:00 [revised] 2023/06/09 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:22 [entrez]
 2022/10/20 00:00 [revised] 2022/08/11 00:00 [received] 2022/10/25 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/04/13 06:42 [medline] 2022/11/27 06:00 [pubmed] 2022/11/26 18:30 [entrez]
 2023/05/23 00:00 [received] 2023/06/16 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/07/29 11:45 [medline] 2023/07/29 11:44 [pubmed] 2023/07/29 01:03 [entrez]
 2023/05/22 00:00 [revised] 2022/12/12 00:00 [received] 2023/06/16 00:00 [accepted] 2023/06/22 06:42 [pubmed] 2023/06/22 06:42 [medline] 2023/06/22 02:43 [entrez]
 2022/11/09 06:00 [pubmed] 2022/11/09 06:01 [medline] 2022/11/08 23:44 [entrez]
 2022/08/11 00:00 [received] 2023/06/28 00:00 [revised] 2023/07/02 00:00 [accepted] 2023/07/15 10:42 [pubmed] 2023/07/15 10:42 [medline] 2023/07/14 18:05 [entrez]
 2023/01/21 00:00 [received] 2023/08/03 00:00 [accepted] 2023/08/19 11:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 20:53 [entrez]
 2023/04/25 00:00 [received] 2023/06/26 00:00 [accepted] 2023/08/05 05:42 [medline] 2023/08/05 05:42 [pubmed] 2023/08/04 21:42 [entrez]
 2023/05/04 00:00 [received] 2023/06/18 00:00 [revised] 2023/07/21 00:00 [accepted] 2023/07/28 01:08 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 18:03 [entrez]
 2023/02/03 00:00 [received] 2023/03/30 00:00 [accepted] 2023/05/04 06:43 [medline] 2023/05/04 06:42 [pubmed] 2023/05/04 02:08 [entrez]
 2023/02/13 03:47 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2022/10/03 00:00 [received] 2022/11/28 00:00 [accepted] 2023/01/23 04:42 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2023/07/30 00:00 [revised] 2023/06/25 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/29 12:43 [medline] 2023/08/29 12:43 [pubmed] 2023/08/29 06:44 [entrez]
 2022/10/06 00:00 [received] 2023/05/22 00:00 [accepted] 2023/06/23 01:11 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 23:20 [entrez]
 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline] 2023/02/13 23:29 [entrez]
 2022/11/19 21:04 [entrez] 2022/11/20 06:00 [pubmed] 2022/11/23 06:00 [medline]
 2023/06/28 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/31 06:43 [pubmed] 2023/07/31 04:38 [entrez]
 2023/01/31 00:00 [received] 2023/02/02 00:00 [accepted] 2023/03/13 06:01 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 23:09 [entrez]
 2023/01/20 03:13 [entrez] 2023/01/21 06:00 [pubmed] 2023/01/24 06:00 [medline]
 2022/10/28 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/06 03:47 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/02/23 00:00 [received] 2023/06/06 00:00 [accepted] 2023/07/28 01:09 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 20:42 [entrez]
 2023/02/28 00:00 [received] 2023/03/30 00:00 [revised] 2023/04/01 00:00 [accepted] 2023/04/14 06:01 [medline] 2023/04/13 01:08 [entrez] 2023/04/14 06:00 [pubmed]
 2023/02/07 01:58 [entrez] 2023/02/08 06:00 [pubmed] 2023/02/08 06:01 [medline]

 2022/11/19 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/11/18 07:52 [entrez]
 2023/03/08 00:00 [received] 2023/03/16 00:00 [accepted] 2023/04/18 06:01 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 21:58 [entrez]
 2022/09/12 00:00 [received] 2022/12/23 00:00 [accepted] 2023/03/10 02:41 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]


 2023/06/18 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/10 00:00 [accepted] 2023/07/31 11:43 [medline] 2023/07/29 11:50 [pubmed] 2023/07/29 01:22 [entrez]
 2023/04/21 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/17 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:25 [entrez]
 2023/03/03 00:00 [received] 2023/03/16 00:00 [revised] 2023/03/17 00:00 [accepted] 2023/03/31 06:41 [medline] 2023/03/30 01:06 [entrez] 2023/03/31 06:00 [pubmed]
 2022/07/24 00:00 [received] 2022/11/07 00:00 [revised] 2022/11/08 00:00 [accepted] 2023/05/22 06:42 [medline] 2022/11/26 06:00 [pubmed] 2022/11/25 01:03 [entrez]
 2023/04/12 00:00 [received] 2023/07/18 00:00 [accepted] 2023/07/29 06:42 [medline] 2023/07/29 06:42 [pubmed] 2023/07/28 23:29 [entrez]
 2023/04/03 00:00 [received] 2023/04/27 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/05/16 01:08 [pubmed] 2023/05/15 19:21 [entrez]
 2023/08/23 00:00 [revised] 2023/02/06 00:00 [received] 2023/08/23 00:00 [accepted] 2023/08/25 18:42 [medline] 2023/08/25 18:42 [pubmed] 2023/08/25 13:53 [entrez]
 2023/02/27 00:00 [received] 2023/05/15 00:00 [revised] 2023/08/17 00:00 [accepted] 2023/09/07 06:42 [medline] 2023/08/25 00:42 [pubmed] 2023/08/24 19:23 [entrez]
 2023/05/30 00:00 [received] 2023/06/29 00:00 [revised] 2023/07/10 00:00 [accepted] 2023/07/29 11:46 [medline] 2023/07/29 11:45 [pubmed] 2023/07/29 01:39 [entrez]
 2023/05/22 00:00 [received] 2023/07/09 00:00 [revised] 2023/07/12 00:00 [accepted] 2023/07/31 11:42 [medline] 2023/07/29 11:45 [pubmed] 2023/07/29 01:07 [entrez]
 2023/06/05 06:42 [pubmed] 2023/06/05 06:42 [medline] 2023/06/05 05:28 [entrez]
 2022/11/17 00:00 [received] 2023/03/24 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/04/23 00:41 [pubmed] 2023/04/22 18:08 [entrez]
 2023/03/22 00:00 [received] 2023/05/16 00:00 [accepted] 2023/06/20 06:41 [medline] 2023/06/19 06:41 [pubmed] 2023/06/19 03:06 [entrez]
 2023/03/04 00:00 [received] 2023/05/25 00:00 [accepted] 2023/06/20 06:43 [medline] 2023/06/20 06:42 [pubmed] 2023/06/20 02:26 [entrez]
 2023/03/09 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/04 00:00 [accepted] 2023/08/15 00:42 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 18:06 [entrez]
 2023/02/12 00:00 [received] 2023/03/07 00:00 [accepted] 2023/05/31 13:12 [medline] 2023/05/31 13:11 [pubmed] 2023/05/31 06:32 [entrez]
 2023/03/21 00:00 [received] 2023/04/27 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/08 00:41 [pubmed] 2023/05/07 19:29 [entrez]
 2022/12/23 00:00 [received] 2023/01/18 00:00 [revised] 2023/01/19 00:00 [accepted] 2023/02/28 01:29 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:01 [medline]
 2023/06/15 00:00 [received] 2023/07/26 00:00 [revised] 2023/08/09 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/09 11:44 [pubmed] 2023/09/09 01:10 [entrez]
 2022/09/09 00:00 [received] 2023/03/23 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/04/12 06:00 [pubmed] 2023/04/11 23:25 [entrez]
 2023/02/18 00:00 [revised] 2022/10/09 00:00 [received] 2023/03/12 00:00 [accepted] 2023/03/26 06:00 [pubmed] 2023/03/26 06:00 [medline] 2023/03/25 16:03 [entrez]
 2023/08/21 00:00 [revised] 2023/06/06 00:00 [received] 2023/09/07 00:00 [accepted] 2023/09/14 06:42 [medline] 2023/09/14 06:42 [pubmed] 2023/09/14 03:56 [entrez]
 2023/06/20 00:00 [received] 2023/08/06 00:00 [revised] 2023/08/10 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 19:21 [entrez]
 2023/01/14 00:00 [received] 2023/05/24 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/06/25 01:08 [pubmed] 2023/06/25 01:08 [medline] 2023/06/24 19:17 [entrez]
 2023/03/04 00:00 [received] 2023/04/20 00:00 [accepted] 2023/08/25 06:42 [medline] 2023/04/28 12:42 [pubmed] 2023/04/28 11:08 [entrez]
 2023/01/16 00:00 [received] 2023/04/20 00:00 [accepted] 2023/05/26 06:42 [medline] 2023/05/26 06:42 [pubmed] 2023/05/26 03:50 [entrez]
 2023/09/08 18:41 [medline] 2023/09/08 18:41 [pubmed] 2023/09/08 12:23 [entrez]
 2023/07/04 00:00 [received] 2023/08/26 00:00 [accepted] 2023/08/25 00:00 [revised] 2023/09/11 12:43 [medline] 2023/09/11 12:43 [pubmed] 2023/09/11 11:15 [entrez]
 2022/09/28 00:00 [received] 2022/12/28 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/03/31 00:02 [entrez] 2023/04/01 06:00 [pubmed] 2023/04/01 06:00 [medline]
 2023/03/10 00:00 [received] 2023/04/28 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:09 [entrez]
 2022/09/19 00:00 [received] 2023/06/26 00:00 [revised] 2023/07/30 00:00 [accepted] 2023/08/06 05:42 [pubmed] 2023/08/06 05:42 [medline] 2023/08/05 19:16 [entrez]
 2023/02/08 00:00 [received] 2023/06/20 00:00 [accepted] 2023/08/02 19:16 [medline] 2023/08/02 19:15 [pubmed] 2023/08/02 13:43 [entrez]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2022/09/28 00:00 [received] 2023/08/14 00:00 [accepted] 2023/09/14 23:31 [entrez]
 2023/07/07 00:00 [revised] 2023/04/06 00:00 [received] 2023/07/18 00:00 [accepted] 2023/08/08 06:42 [pubmed] 2023/08/08 06:42 [medline] 2023/08/08 01:12 [entrez]
 2023/05/12 00:00 [received] 2023/07/06 00:00 [revised] 2023/07/13 00:00 [accepted] 2023/07/29 11:43 [medline] 2023/07/29 11:42 [pubmed] 2023/07/29 01:09 [entrez]
 2023/07/09 00:00 [revised] 2023/05/10 00:00 [received] 2023/07/18 00:00 [accepted] 2023/07/24 06:43 [pubmed] 2023/07/24 06:43 [medline] 2023/07/24 04:13 [entrez]
 2021/11/13 06:00 [pubmed] 2021/11/13 06:00 [medline] 2021/11/12 03:02 [entrez]
 2022/04/27 06:00 [pubmed] 2022/04/27 06:00 [medline] 2022/04/26 17:03 [entrez]
 2023/07/03 00:00 [accepted] 2023/08/18 12:42 [medline] 2023/08/18 12:42 [pubmed] 2023/08/18 11:04 [entrez]
 2023/11/30 00:00 [pmc-release] 2023/07/03 06:41 [medline] 2023/05/31 13:12 [pubmed] 2023/05/31 10:04 [entrez]
 2023/08/04 06:42 [medline] 2023/07/27 19:10 [pubmed] 2023/07/27 15:23 [entrez]
 2023/06/07 00:00 [received] 2023/07/13 00:00 [accepted] 2023/08/15 06:42 [medline] 2023/08/14 06:41 [pubmed] 2023/08/14 04:26 [entrez]
 2023/08/02 13:09 [pubmed] 2023/08/02 13:09 [medline] 2023/08/02 06:33 [entrez]
 2024/01/01 00:00 [pmc-release] 2022/12/19 04:00 [entrez] 2022/12/20 06:00 [pubmed] 2022/12/20 06:01 [medline]
 2023/03/15 00:00 [received] 2023/06/05 00:00 [accepted] 2023/06/21 13:04 [medline] 2023/06/21 13:04 [pubmed] 2023/06/21 11:10 [entrez]
 2022/12/24 00:00 [received] 2023/03/30 00:00 [accepted] 2023/05/08 06:43 [medline] 2023/05/08 06:42 [pubmed] 2023/05/08 04:17 [entrez]
 2022/11/09 00:00 [received] 2023/01/19 00:00 [accepted] 2023/02/11 06:01 [medline] 2023/02/11 06:00 [pubmed] 2023/02/10 11:22 [entrez]
 2022/12/15 00:00 [received] 2023/07/06 00:00 [accepted] 2023/08/23 06:42 [medline] 2023/08/22 13:42 [pubmed] 2023/08/22 07:17 [entrez]
 2023/05/03 00:00 [received] 2023/07/10 00:00 [accepted] 2023/07/22 10:41 [medline] 2023/07/22 10:41 [pubmed] 2023/07/21 21:03 [entrez]
 2022/10/05 00:00 [received] 2022/12/12 00:00 [accepted] 2023/07/30 01:07 [medline] 2023/07/30 01:06 [pubmed] 2023/07/29 20:57 [entrez]
 2022/12/17 00:00 [received] 2023/07/06 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/07/17 00:41 [medline] 2023/07/17 00:41 [pubmed] 2023/07/16 19:29 [entrez]
 2023/07/13 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:34 [entrez]
 2023/07/10 00:00 [accepted] 2023/07/12 06:43 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 03:51 [entrez]
 2023/03/09 00:00 [received] 2023/04/18 00:00 [revised] 2023/04/30 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/07 00:42 [pubmed] 2023/05/06 18:11 [entrez]
 2022/09/09 00:00 [received] 2023/01/28 00:00 [revised] 2023/03/30 00:00 [accepted] 2023/05/04 06:43 [medline] 2023/05/04 06:42 [pubmed] 2023/05/04 02:07 [entrez]

 2022/10/03 00:00 [received] 2023/01/24 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/03/24 00:03 [entrez] 2023/03/25 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2022/09/16 00:00 [received] 2022/09/24 00:00 [accepted] 2023/03/09 02:09 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/10 06:01 [medline]
 2023/02/17 06:00 [pubmed] 2023/02/17 06:01 [medline] 2023/02/16 18:13 [entrez]
 2023/03/25 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/08/28 06:42 [medline] 2023/04/21 18:42 [pubmed] 2023/04/21 15:07 [entrez]
 2023/09/11 06:42 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 02:02 [entrez]

 2022/11/09 00:00 [received] 2022/11/29 00:00 [accepted] 2023/01/14 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/01/13 21:42 [entrez]
 2023/08/23 06:42 [medline] 2023/08/21 18:41 [pubmed] 2023/08/21 15:13 [entrez]

 2022/05/23 00:00 [received] 2022/09/21 00:00 [revised] 2022/10/13 00:00 [accepted] 2022/10/22 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/10/21 19:25 [entrez]
 2023/06/01 06:42 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 20:33 [entrez]
 2023/05/18 19:12 [medline] 2023/05/18 19:12 [pubmed] 2023/05/18 12:03 [entrez]
 2022/12/06 00:00 [received] 2023/02/07 00:00 [accepted] 2023/02/22 14:25 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2023/03/25 00:00 [received] 2023/07/20 00:00 [revised] 2023/08/16 00:00 [accepted] 2023/08/21 18:42 [medline] 2023/08/21 18:42 [pubmed] 2023/08/21 18:01 [entrez]
 2023/05/24 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/25 00:00 [accepted] 2023/07/29 11:45 [medline] 2023/07/29 11:44 [pubmed] 2023/07/29 01:06 [entrez]
 2022/12/06 00:00 [received] 2022/12/29 00:00 [revised] 2023/01/16 00:00 [accepted] 2023/02/11 01:08 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/12 06:01 [medline]
 2022/12/14 00:00 [received] 2023/05/31 00:00 [accepted] 2023/06/28 13:09 [medline] 2023/06/28 13:08 [pubmed] 2023/06/28 09:20 [entrez]
 2023/04/09 00:00 [received] 2023/05/28 00:00 [revised] 2023/05/29 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:01 [entrez]
 2022/06/20 00:00 [received] 2022/10/20 00:00 [revised] 2022/11/01 00:00 [accepted] 2022/12/26 04:00 [entrez] 2022/12/27 06:00 [pubmed] 2022/12/27 06:01 [medline]
 2023/02/04 00:00 [received] 2023/06/07 00:00 [accepted] 2023/06/30 01:06 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 23:33 [entrez]
 2023/07/14 13:06 [medline] 2023/06/19 06:42 [pubmed] 2023/06/19 04:13 [entrez]
 2023/04/12 06:42 [medline] 2023/04/10 20:54 [entrez] 2023/04/11 06:00 [pubmed]
 2022/11/22 00:00 [received] 2023/02/20 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/06/05 06:43 [medline] 2023/04/02 06:00 [pubmed] 2023/04/01 18:01 [entrez]
 2022/11/28 00:00 [revised] 2022/09/14 00:00 [received] 2022/11/28 00:00 [accepted] 2022/12/02 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/12/01 00:33 [entrez]
 2023/05/01 00:00 [received] 2023/06/14 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/06/21 13:04 [pubmed] 2023/06/21 11:09 [entrez]
 2023/01/31 06:00 [pubmed] 2023/01/31 06:00 [medline] 2023/01/30 02:33 [entrez]
 2022/09/10 00:00 [received] 2022/11/18 00:00 [accepted] 2022/11/16 00:00 [revised] 2022/11/28 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/11/27 23:26 [entrez]
 2023/04/10 00:00 [received] 2023/07/31 00:00 [revised] 2023/08/03 00:00 [accepted] 2023/08/19 11:42 [pubmed] 2023/08/19 11:42 [medline] 2023/08/18 19:28 [entrez]
 2023/03/24 00:00 [received] 2023/06/15 00:00 [accepted] 2023/06/14 00:00 [revised] 2023/06/30 01:06 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 23:32 [entrez]
 2022/10/01 00:00 [received] 2023/07/03 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/07/17 19:08 [pubmed] 2023/07/17 19:08 [medline] 2023/07/17 18:05 [entrez]
 2024/01/01 00:00 [pmc-release] 2023/06/28 13:10 [medline] 2023/06/28 13:09 [pubmed] 2023/06/28 09:19 [entrez]
 2023/03/17 00:00 [received] 2023/06/19 00:00 [accepted] 2023/07/07 01:05 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 21:13 [entrez]
 2023/05/24 00:00 [received] 2023/08/28 00:00 [accepted] 2023/08/27 00:00 [revised] 2023/09/09 21:42 [medline] 2023/09/09 21:42 [pubmed] 2023/09/09 11:10 [entrez]
 2023/01/19 00:00 [received] 2023/04/10 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/04/27 12:42 [pubmed] 2023/04/27 11:14 [entrez]
 2023/05/16 00:00 [received] 2023/07/25 00:00 [revised] 2023/07/25 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:45 [pubmed] 2023/08/26 01:05 [entrez]
 2023/04/25 00:00 [received] 2023/07/28 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/01 01:08 [pubmed] 2023/08/01 01:08 [medline] 2023/07/31 19:10 [entrez]
 2023/04/18 06:42 [medline] 2023/04/15 20:57 [entrez] 2023/04/16 06:00 [pubmed]
 2023/03/28 00:00 [received] 2023/07/05 00:00 [accepted] 2023/07/22 21:06 [medline] 2023/07/22 21:06 [pubmed] 2023/07/22 11:14 [entrez]
 2023/09/14 12:42 [medline] 2023/09/14 12:42 [pubmed] 2023/09/14 08:23 [entrez]
 2023/01/11 00:00 [received] 2023/02/27 00:00 [accepted] 2023/05/30 06:42 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 10:07 [entrez]
 2021/12/13 00:00 [received] 2022/06/17 00:00 [accepted] 2022/06/28 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/06/27 18:30 [entrez]
 2022/10/10 00:00 [received] 2023/04/03 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 12:00 [entrez]
 2022/11/02 00:00 [received] 2023/04/24 00:00 [revised] 2023/05/15 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/21 01:05 [pubmed] 2023/05/20 19:27 [entrez]
 2025/01/23 00:00 [pmc-release] 2023/01/23 21:02 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/26 06:00 [medline]
 2023/07/13 00:00 [received] 2023/08/26 00:00 [revised] 2023/08/30 00:00 [accepted] 2023/09/07 00:41 [medline] 2023/09/07 00:41 [pubmed] 2023/09/06 19:24 [entrez]
 2023/08/09 00:00 [accepted] 2023/09/06 00:41 [medline] 2023/09/06 00:41 [pubmed] 2023/09/05 23:37 [entrez]
 2023/05/13 00:00 [received] 2023/07/18 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/08/11 06:42 [pubmed] 2023/08/11 03:59 [entrez]
 2022/11/26 00:00 [received] 2023/03/16 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:16 [entrez]
 2022/07/20 00:00 [received] 2022/12/22 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/03/31 06:01 [medline] 2023/03/30 02:59 [entrez] 2023/03/31 06:00 [pubmed]
 2022/08/27 00:00 [received] 2022/12/26 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/02/04 06:00 [pubmed] 2023/02/03 19:30 [entrez]
 2022/12/28 06:00 [pubmed] 2022/12/28 06:01 [medline] 2022/12/27 11:15 [entrez]
 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:53 [entrez]
 2023/03/07 00:00 [received] 2023/08/14 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/11 00:42 [medline] 2023/09/11 00:42 [pubmed] 2023/09/10 18:04 [entrez]
 2023/03/14 06:01 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 12:20 [entrez]
 2023/01/20 03:13 [entrez] 2023/01/21 06:00 [pubmed] 2023/01/24 06:00 [medline]
 2023/03/07 00:00 [received] 2023/07/25 00:00 [accepted] 2023/08/23 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 03:57 [entrez]
 2022/09/08 00:00 [received] 2022/09/14 00:00 [accepted] 2022/10/04 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/10/03 21:52 [entrez]
 2022/09/24 11:27 [entrez] 2022/09/25 06:00 [pubmed] 2022/09/28 06:00 [medline]
 2022/02/14 00:00 [received] 2022/04/24 00:00 [revised] 2022/04/25 00:00 [accepted] 2022/06/16 06:00 [pubmed] 2023/03/10 06:00 [medline] 2022/06/15 02:32 [entrez]
 2023/03/13 00:00 [received] 2023/07/11 00:00 [accepted] 2023/07/17 15:09 [medline] 2023/07/17 15:09 [pubmed] 2023/07/17 11:15 [entrez]
 2022/02/18 00:00 [received] 2022/03/20 00:00 [revised] 2022/04/01 00:00 [accepted] 2023/05/19 06:42 [medline] 2022/06/17 06:00 [pubmed] 2022/06/16 05:23 [entrez]
 2023/08/07 06:42 [medline] 2023/08/07 06:41 [pubmed] 2023/08/07 04:44 [entrez]
 2023/02/02 09:15 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/03 06:00 [medline]
 2023/05/11 00:00 [received] 2023/07/11 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 18:01 [entrez]
 2023/04/12 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/08/11 00:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 18:06 [entrez]
 2022/08/22 00:00 [received] 2023/03/21 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/12 23:43 [entrez] 2023/04/13 06:00 [pubmed]
 2023/06/14 00:00 [received] 2023/08/27 00:00 [accepted] 2023/09/13 12:43 [medline] 2023/09/13 12:43 [pubmed] 2023/09/13 11:22 [entrez]
 2022/10/18 00:00 [received] 2023/05/18 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 23:18 [entrez]
 2023/05/03 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:25 [entrez]
 2022/12/11 00:00 [received] 2023/04/03 00:00 [revised] 2023/04/14 00:00 [accepted] 2023/05/08 06:41 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 19:25 [entrez]
 2019/11/04 00:00 [received] 2020/03/20 00:00 [accepted] 2022/09/28 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/09/27 19:26 [entrez]
 2022/07/14 00:00 [received] 2023/01/29 00:00 [accepted] 2023/01/09 00:00 [revised] 2023/04/03 06:41 [medline] 2023/03/30 11:53 [entrez] 2023/03/31 06:00 [pubmed]
 2022/04/07 00:00 [received] 2022/11/02 00:00 [revised] 2022/12/17 00:00 [accepted] 2024/02/01 00:00 [pmc-release] 2022/12/22 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/12/21 19:09 [entrez]
 2023/04/23 00:00 [received] 2023/05/24 00:00 [revised] 2023/05/31 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 03:56 [entrez]
 2022/03/19 00:00 [received] 2022/09/16 00:00 [accepted] 2023/05/16 13:11 [medline] 2023/05/16 13:10 [pubmed] 2023/05/16 09:03 [entrez]
 2022/10/03 06:00 [pubmed] 2023/02/11 06:00 [medline] 2022/10/02 20:52 [entrez]
 2023/04/23 00:00 [received] 2023/05/12 00:00 [revised] 2023/05/16 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/05/28 19:10 [pubmed] 2023/05/28 18:00 [entrez]
 2022/07/08 02:32 [entrez] 2022/07/09 06:00 [pubmed] 2022/07/09 06:01 [medline]
 2023/05/05 00:00 [received] 2023/07/11 00:00 [revised] 2023/08/24 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/09/08 06:42 [pubmed] 2023/09/08 03:59 [entrez]
 2022/12/03 00:00 [received] 2023/03/19 00:00 [accepted] 2023/04/05 23:23 [entrez] 2023/04/06 06:00 [pubmed] 2023/04/06 06:00 [medline]
 2023/07/12 00:00 [revised] 2023/04/03 00:00 [received] 2023/09/01 06:43 [medline] 2023/09/01 06:43 [pubmed] 2023/09/01 00:23 [entrez]
 2022/10/29 00:00 [received] 2023/05/22 00:00 [accepted] 2023/06/23 06:42 [medline] 2023/06/22 01:07 [pubmed] 2023/06/21 23:35 [entrez]
 2023/02/02 00:00 [received] 2023/05/09 00:00 [revised] 2023/05/13 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/05/26 01:05 [pubmed] 2023/05/25 18:06 [entrez]
 2022/07/20 00:00 [received] 2023/02/07 00:00 [accepted] 2024/08/08 00:00 [pmc-release] 2023/08/09 06:43 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 21:41 [entrez]
 2022/10/29 00:00 [received] 2023/01/04 00:00 [accepted] 2023/02/17 02:16 [entrez] 2023/02/18 06:00 [pubmed] 2023/02/18 06:01 [medline]
 2022/11/23 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/13 04:16 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2023/02/22 20:57 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/25 06:00 [medline]
 2022/09/27 00:00 [received] 2023/08/17 00:00 [accepted] 2023/09/13 06:43 [medline] 2023/09/13 06:42 [pubmed] 2023/09/13 04:00 [entrez]
 2023/07/27 00:00 [received] 2023/07/28 00:00 [accepted] 2023/08/24 06:43 [medline] 2023/08/24 06:42 [pubmed] 2023/08/24 04:11 [entrez]
 2023/07/03 00:00 [revised] 2023/02/14 00:00 [received] 2023/08/03 00:00 [accepted] 2023/08/10 06:43 [pubmed] 2023/08/10 06:43 [medline] 2023/08/10 02:12 [entrez]
 2022/12/06 00:00 [received] 2023/02/13 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 19:19 [entrez]
 2022/11/25 00:00 [received] 2023/01/05 00:00 [accepted] 2023/02/10 03:09 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2022/07/21 00:00 [received] 2022/12/08 00:00 [accepted] 2022/12/22 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/21 11:17 [entrez]
 2023/12/20 00:00 [pmc-release] 2023/06/22 06:42 [medline] 2023/06/20 19:15 [pubmed] 2023/06/20 14:03 [entrez]
 2023/06/06 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 04:57 [entrez]
 2023/02/28 00:00 [received] 2023/04/05 00:00 [accepted] 2023/05/09 06:42 [medline] 2023/05/08 06:42 [pubmed] 2023/05/08 04:16 [entrez]
 2023/05/01 12:43 [medline] 2023/05/01 12:43 [pubmed] 2023/05/01 10:53 [entrez]
 2023/07/28 06:44 [medline] 2023/07/28 06:43 [pubmed] 2023/07/28 04:27 [entrez]
 2023/04/05 00:00 [received] 2023/05/03 00:00 [revised] 2023/05/05 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:09 [entrez]
 2023/01/31 02:53 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/02 06:00 [medline]
 2023/04/01 00:00 [received] 2023/05/05 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:07 [entrez]
 2023/05/01 12:43 [medline] 2023/05/01 12:43 [pubmed] 2023/05/01 07:12 [entrez]

 2022/09/23 00:00 [received] 2022/11/30 00:00 [revised] 2022/12/30 00:00 [accepted] 2023/01/13 06:00 [pubmed] 2023/02/01 06:00 [medline] 2023/01/12 18:09 [entrez]
 2022/04/12 00:00 [received] 2022/12/07 00:00 [revised] 2022/12/20 00:00 [accepted] 2023/01/10 01:37 [entrez] 2023/01/11 06:00 [pubmed] 2023/01/11 06:01 [medline]
 2022/08/08 00:00 [received] 2022/08/29 00:00 [accepted] 2022/08/08 00:00 [revised] 2022/09/11 06:00 [pubmed] 2023/03/24 06:00 [medline] 2022/09/10 00:02 [entrez]
 2022/03/15 00:00 [received] 2022/10/11 00:00 [accepted] 2022/11/13 06:00 [pubmed] 2023/02/25 06:00 [medline] 2022/11/12 00:16 [entrez]
 2023/04/14 00:00 [received] 2023/07/12 00:00 [revised] 2023/07/17 00:00 [accepted] 2023/08/01 01:08 [medline] 2023/08/01 01:08 [pubmed] 2023/07/31 18:10 [entrez]
 2023/06/21 00:00 [revised] 2023/04/21 00:00 [received] 2023/06/27 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 02:00 [entrez]
 2023/03/31 00:00 [accepted] 2023/05/03 06:43 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 01:57 [entrez]
 2023/03/01 00:00 [revised] 2022/12/23 00:00 [received] 2023/03/20 00:00 [accepted] 2023/06/14 06:42 [medline] 2023/04/14 06:00 [pubmed] 2023/04/13 04:24 [entrez]
 2023/03/13 04:00 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2022/11/18 00:00 [received] 2023/01/30 00:00 [accepted] 2023/03/13 03:48 [entrez] 2023/03/14 06:00 [pubmed] 2023/03/14 06:01 [medline]
 2023/02/14 00:52 [entrez] 2023/02/15 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2022/07/20 00:00 [received] 2023/01/23 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/03/06 03:41 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/04/18 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/11 13:17 [pubmed] 2023/05/11 11:14 [entrez]
 2023/05/09 00:00 [received] 2023/05/21 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/08/23 06:42 [medline] 2023/06/01 01:08 [pubmed] 2023/05/31 22:01 [entrez]
 2023/04/11 00:00 [received] 2023/05/30 00:00 [accepted] 2023/05/29 00:00 [revised] 2023/08/14 06:42 [medline] 2023/06/08 13:08 [pubmed] 2023/06/08 11:09 [entrez]
 2022/08/17 00:00 [revised] 2021/12/09 00:00 [received] 2023/03/29 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 06:03 [entrez]
 2023/03/29 00:00 [received] 2023/04/27 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:12 [pubmed] 2023/05/13 01:28 [entrez]
 2023/03/31 06:01 [medline] 2023/03/30 02:53 [entrez] 2023/03/31 06:00 [pubmed]
 2023/01/25 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/04/10 06:42 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 20:27 [entrez]
 2023/03/07 00:00 [revised] 2022/11/03 00:00 [received] 2023/03/10 00:00 [accepted] 2023/05/10 06:42 [medline] 2023/03/23 06:00 [pubmed] 2023/03/22 01:42 [entrez]
 2022/09/10 00:00 [revised] 2022/10/14 00:00 [revised] 2022/04/15 00:00 [received] 2022/10/18 00:00 [accepted] 2022/10/20 06:00 [pubmed] 2023/01/04 06:00 [medline] 2022/10/19 11:44 [entrez]
 2022/11/02 00:00 [received] 2022/12/05 00:00 [revised] 2023/01/01 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/07 18:22 [entrez]
 2022/11/30 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/29 03:03 [entrez]
 2023/07/26 13:07 [medline] 2023/07/26 13:07 [pubmed] 2023/07/26 08:33 [entrez]
 2023/04/01 00:00 [received] 2023/06/26 00:00 [revised] 2023/06/28 00:00 [accepted] 2023/07/11 19:12 [pubmed] 2023/07/11 19:12 [medline] 2023/07/11 17:59 [entrez]
 2021/05/13 06:00 [pubmed] 2023/03/22 06:00 [medline] 2021/05/12 08:43 [entrez]
 2022/11/30 00:00 [received] 2022/12/23 00:00 [revised] 2023/01/05 00:00 [accepted] 2023/01/21 01:14 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2022/10/12 00:00 [received] 2023/06/29 00:00 [accepted] 2023/09/02 05:42 [medline] 2023/09/02 05:42 [pubmed] 2023/09/01 21:38 [entrez]
 2023/01/30 00:00 [received] 2023/07/18 00:00 [accepted] 2023/08/01 13:10 [medline] 2023/08/01 13:10 [pubmed] 2023/08/01 11:11 [entrez]
 2022/08/15 00:00 [received] 2022/10/10 00:00 [revised] 2022/10/13 00:00 [accepted] 2022/11/22 01:47 [entrez] 2022/11/23 06:00 [pubmed] 2022/11/23 06:01 [medline]
 2023/01/08 06:00 [pubmed] 2023/02/08 06:00 [medline] 2023/01/07 16:16 [entrez]
 2023/08/28 06:41 [medline] 2023/08/25 00:41 [pubmed] 2023/08/24 20:57 [entrez]
 2023/04/11 00:00 [received] 2023/06/22 00:00 [accepted] 2023/07/31 06:44 [medline] 2023/07/31 06:43 [pubmed] 2023/07/31 05:11 [entrez]
 2023/01/26 00:00 [received] 2023/06/19 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/07/26 01:06 [pubmed] 2023/07/26 01:06 [medline] 2023/07/25 19:14 [entrez]
 2023/07/19 06:43 [medline] 2023/06/23 06:42 [pubmed] 2023/06/23 05:53 [entrez]
 2022/08/05 00:00 [received] 2023/01/24 00:00 [accepted] 2023/02/10 23:44 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/11 06:01 [medline]
 2023/01/30 03:57 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]



 2021/01/30 00:00 [received] 2021/04/30 00:00 [revised] 2021/06/27 00:00 [accepted] 2023/06/22 13:09 [medline] 2023/06/22 13:08 [pubmed] 2023/06/22 09:56 [entrez]
 2023/05/17 13:11 [medline] 2023/05/17 13:10 [pubmed] 2023/05/17 11:06 [entrez]
 2023/02/28 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/18 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 05:53 [entrez]

 2023/07/05 00:00 [received] 2023/08/23 00:00 [accepted] 2023/08/30 12:43 [medline] 2023/08/30 12:43 [pubmed] 2023/08/30 11:07 [entrez]
 2023/05/30 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/06 03:39 [entrez]
 2022/12/19 00:00 [received] 2023/02/21 00:00 [accepted] 2023/03/24 02:15 [entrez] 2023/03/25 06:00 [pubmed] 2023/03/25 06:01 [medline]
 2022/04/30 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/16 00:00 [accepted] 2023/02/23 09:21 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2022/04/05 00:00 [received] 2022/08/08 00:00 [accepted] 2023/03/29 06:05 [medline] 2022/11/13 06:00 [pubmed] 2022/11/12 11:20 [entrez]
 2023/08/17 00:00 [received] 2023/08/21 00:00 [accepted] 2023/09/13 00:42 [medline] 2023/09/13 00:42 [pubmed] 2023/09/12 21:23 [entrez]
 2022/10/02 00:00 [received] 2023/04/27 00:00 [accepted] 2024/05/11 00:00 [pmc-release] 2023/09/11 06:42 [medline] 2023/05/11 00:41 [pubmed] 2023/05/10 23:32 [entrez]
 2023/08/15 06:42 [medline] 2023/08/14 12:41 [pubmed] 2023/08/14 11:32 [entrez]
 2023/06/15 00:00 [received] 2023/07/03 00:00 [revised] 2023/07/03 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:58 [entrez]
 2023/03/24 00:00 [received] 2023/04/14 00:00 [accepted] 2023/05/23 13:06 [medline] 2023/05/23 13:05 [pubmed] 2023/05/23 07:22 [entrez]
 2023/01/31 00:00 [received] 2023/03/28 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/05 06:42 [pubmed] 2023/05/05 03:49 [entrez]
 2023/03/22 01:56 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/23 06:01 [medline]
 2023/02/03 00:00 [accepted] 2023/03/09 02:08 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/10 06:01 [medline]
 2022/10/05 00:00 [received] 2023/01/09 00:00 [accepted] 2023/02/13 03:24 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2023/04/12 00:00 [received] 2023/07/06 00:00 [revised] 2023/08/27 00:00 [accepted] 2023/09/05 00:41 [medline] 2023/09/05 00:41 [pubmed] 2023/09/04 18:04 [entrez]
 2023/07/08 00:00 [received] 2023/08/11 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/08/26 10:47 [medline] 2023/08/26 10:46 [pubmed] 2023/08/26 01:34 [entrez]
 2023/05/02 00:00 [received] 2023/06/27 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/07/29 11:48 [medline] 2023/07/29 11:47 [pubmed] 2023/07/29 01:06 [entrez]
 2023/01/19 00:00 [received] 2023/03/05 00:00 [revised] 2023/04/16 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/26 00:42 [pubmed] 2023/04/25 18:02 [entrez]
 2023/07/05 00:00 [accepted] 2023/08/24 06:42 [medline] 2023/08/05 05:42 [pubmed] 2023/08/04 23:23 [entrez]
 2022/11/02 00:00 [received] 2022/12/09 00:00 [accepted] 2023/05/10 18:42 [medline] 2023/05/10 18:41 [pubmed] 2023/05/10 13:03 [entrez]
 2021/02/23 00:00 [received] 2023/01/24 00:00 [revised] 2023/02/11 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:32 [entrez]
 2023/02/22 00:00 [received] 2023/03/28 00:00 [accepted] 2023/04/11 14:32 [entrez] 2023/04/12 06:00 [pubmed] 2023/04/12 06:00 [medline]
 2022/05/26 00:00 [received] 2022/09/30 00:00 [revised] 2022/10/22 00:00 [accepted] 2022/11/21 04:14 [entrez] 2022/11/22 06:00 [pubmed] 2022/11/22 06:01 [medline]
 2022/02/08 00:00 [received] 2023/04/05 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/05/03 00:41 [pubmed] 2023/05/02 23:28 [entrez]
 2022/10/21 06:00 [pubmed] 2022/11/22 06:00 [medline] 2022/10/20 03:12 [entrez]
 2023/02/06 00:00 [received] 2023/07/21 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/11 00:42 [medline] 2023/09/11 00:42 [pubmed] 2023/09/10 18:12 [entrez]
 2023/01/09 00:00 [received] 2023/01/25 00:00 [revised] 2023/02/17 00:00 [accepted] 2023/03/11 01:16 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/11/30 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/19 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/05/12 13:08 [pubmed] 2023/05/12 06:52 [entrez]
 2022/12/09 00:00 [revised] 2022/07/20 00:00 [received] 2022/12/09 00:00 [accepted] 2023/03/29 06:05 [medline] 2022/12/15 06:00 [pubmed] 2022/12/14 06:02 [entrez]
 2023/02/10 00:00 [received] 2023/06/16 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/07/06 19:12 [pubmed] 2023/07/06 13:34 [entrez]
 2023/03/25 00:00 [received] 2023/04/26 00:00 [revised] 2023/05/05 00:00 [accepted] 2023/05/15 11:42 [medline] 2023/05/13 15:13 [pubmed] 2023/05/13 01:31 [entrez]
 2022/11/15 00:00 [received] 2022/12/18 00:00 [accepted] 2022/12/25 06:00 [pubmed] 2023/02/25 06:00 [medline] 2022/12/24 19:13 [entrez]

 2022/03/12 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/03/11 05:31 [entrez]
 2023/01/19 00:00 [received] 2023/05/18 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/15 06:41 [medline] 2023/05/26 01:05 [pubmed] 2023/05/25 19:26 [entrez]
 2023/05/20 00:00 [received] 2023/07/07 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/21 06:41 [pubmed] 2023/08/21 04:39 [entrez]
 2023/02/15 07:43 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/17 06:00 [medline]
 2022/09/20 00:00 [received] 2023/04/03 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/05/24 01:06 [pubmed] 2023/05/23 21:23 [entrez]
 2024/09/05 00:00 [pmc-release] 2023/09/05 12:42 [medline] 2023/09/05 12:42 [pubmed] 2023/09/05 11:34 [entrez]
 2022/10/18 07:14 [entrez] 2022/10/19 06:00 [pubmed] 2022/10/19 06:01 [medline]
 2022/12/31 00:00 [revised] 2022/01/06 00:00 [received] 2023/03/23 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/04/04 06:00 [pubmed] 2023/04/03 01:52 [entrez]
 2023/06/12 00:00 [received] 2023/07/10 00:00 [revised] 2023/07/12 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/31 06:42 [pubmed] 2023/07/31 04:39 [entrez]
 2023/08/03 00:00 [received] 2023/08/20 00:00 [revised] 2023/08/21 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/09 11:42 [pubmed] 2023/09/09 01:16 [entrez]
 2023/06/08 00:00 [revised] 2023/03/31 00:00 [received] 2023/06/16 00:00 [accepted] 2023/07/14 13:06 [medline] 2023/07/12 13:07 [pubmed] 2023/07/12 11:43 [entrez]
 2023/06/14 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 07:32 [entrez]
 2023/07/21 00:00 [received] 2023/08/09 00:00 [accepted] 2023/08/13 00:43 [pubmed] 2023/08/13 00:43 [medline] 2023/08/12 19:25 [entrez]
 2023/07/10 19:09 [medline] 2023/07/10 19:08 [pubmed] 2023/07/10 13:12 [entrez]
 2023/04/19 00:00 [received] 2023/05/21 00:00 [revised] 2023/05/26 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:12 [entrez]
 2022/06/23 00:00 [received] 2022/12/06 00:00 [revised] 2022/12/23 00:00 [accepted] 2023/01/19 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/18 18:04 [entrez]
 2022/08/25 00:00 [accepted] 2022/09/08 06:00 [pubmed] 2022/09/08 06:00 [medline] 2022/09/07 23:32 [entrez]
 2023/01/10 00:00 [received] 2023/07/11 00:00 [accepted] 2023/08/01 13:10 [medline] 2023/08/01 13:10 [pubmed] 2023/08/01 11:13 [entrez]
 2022/09/20 00:00 [received] 2023/05/14 00:00 [accepted] 2023/07/04 06:43 [medline] 2023/07/04 06:42 [pubmed] 2023/07/04 05:26 [entrez]
 2023/03/28 06:00 [pubmed] 2023/03/28 06:00 [medline] 2023/03/27 23:33 [entrez]
 2022/07/03 00:00 [received] 2022/12/19 00:00 [revised] 2022/12/27 00:00 [accepted] 2023/03/09 06:23 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/10 06:00 [medline]
 2023/01/24 00:00 [received] 2023/02/21 00:00 [accepted] 2023/03/09 06:01 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 11:18 [entrez]
 2023/02/08 05:12 [entrez] 2023/02/09 06:00 [pubmed] 2023/02/10 06:00 [medline]
 2022/07/25 00:00 [received] 2022/10/11 00:00 [revised] 2022/11/08 00:00 [accepted] 2022/11/16 06:00 [pubmed] 2023/01/04 06:00 [medline] 2022/11/15 22:04 [entrez]

 2023/05/05 00:00 [received] 2023/06/24 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/07/27 06:42 [medline] 2023/07/27 06:42 [pubmed] 2023/07/27 01:13 [entrez]
 2023/04/23 00:00 [received] 2023/05/16 00:00 [accepted] 2023/07/11 01:07 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 23:22 [entrez]
 2023/06/07 06:42 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 15:52 [entrez]
 2022/12/10 00:00 [received] 2023/03/17 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 02:40 [entrez]
 2023/02/08 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/13 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:42 [entrez] 2023/03/30 06:00 [pubmed]
 2023/02/23 00:00 [revised] 2022/12/23 00:00 [received] 2023/02/24 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 00:25 [entrez]
 2022/09/21 00:00 [received] 2022/12/02 00:00 [accepted] 2023/01/30 04:11 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/11/02 00:00 [received] 2023/01/06 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/01/20 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/19 19:23 [entrez]
 2022/05/17 00:00 [received] 2022/08/06 00:00 [accepted] 2022/09/09 06:00 [pubmed] 2023/01/13 06:00 [medline] 2022/09/08 11:21 [entrez]
 2023/03/10 00:00 [received] 2023/06/01 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 04:55 [entrez]
 2023/06/02 00:00 [accepted] 2023/07/05 13:06 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 10:36 [entrez]
 2023/05/10 00:00 [received] 2023/05/18 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:24 [entrez]
 2022/11/29 00:00 [received] 2023/03/13 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 15:44 [entrez]
 2022/10/21 00:00 [received] 2023/02/11 00:00 [accepted] 2023/03/01 11:21 [entrez] 2023/03/02 06:00 [pubmed] 2023/03/02 06:00 [medline]
 2022/12/15 00:00 [accepted] 2023/01/02 04:00 [entrez] 2023/01/03 06:00 [pubmed] 2023/01/03 06:01 [medline]
 2023/02/02 00:00 [received] 2023/05/19 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:47 [entrez]
 2023/03/01 00:00 [received] 2023/05/05 00:00 [accepted] 2023/06/05 13:05 [medline] 2023/06/05 13:04 [pubmed] 2023/06/05 11:59 [entrez]
 2023/02/09 00:00 [received] 2023/03/10 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:38 [entrez] 2023/03/30 06:00 [pubmed]
 2022/12/15 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/01/26 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/25 18:14 [entrez]
 2023/05/13 00:00 [received] 2023/08/20 00:00 [revised] 2023/08/27 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/09 11:45 [pubmed] 2023/09/09 01:12 [entrez]
 2023/04/29 00:00 [received] 2023/05/25 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/09/07 06:42 [pubmed] 2023/09/07 04:16 [entrez]
 2022/12/01 05:07 [entrez] 2022/12/02 06:00 [pubmed] 2022/12/02 06:01 [medline]
 2023/05/15 00:00 [received] 2023/05/31 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/08 00:41 [medline] 2023/09/08 00:41 [pubmed] 2023/09/07 18:12 [entrez]
 2023/03/08 00:00 [received] 2023/03/26 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/13 01:12 [entrez] 2023/04/14 06:00 [pubmed]
 2022/07/12 00:00 [revised] 2022/04/12 00:00 [received] 2022/08/14 00:00 [accepted] 2022/09/09 06:00 [pubmed] 2023/02/18 06:00 [medline] 2022/09/08 09:04 [entrez]
 2022/09/21 00:00 [received] 2023/01/25 00:00 [revised] 2023/02/06 00:00 [accepted] 2023/02/25 02:49 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/10/26 00:00 [received] 2023/05/01 00:00 [revised] 2023/05/05 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/05/31 01:09 [pubmed] 2023/05/30 18:02 [entrez]
 2022/12/21 00:00 [received] 2023/02/16 00:00 [revised] 2023/02/17 00:00 [accepted] 2023/03/28 17:14 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 19:30 [entrez]
 2023/01/31 00:00 [received] 2023/04/04 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/05/09 06:42 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 19:22 [entrez]
 2023/05/14 00:00 [received] 2023/06/20 00:00 [revised] 2023/06/23 00:00 [accepted] 2023/07/25 06:44 [medline] 2023/07/25 06:43 [pubmed] 2023/07/25 04:44 [entrez]
 2023/03/16 00:00 [received] 2023/03/31 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 10:15 [entrez]
 2023/05/03 06:43 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 01:57 [entrez]
 2023/01/04 00:00 [received] 2023/02/16 00:00 [revised] 2023/07/10 06:42 [medline] 2023/03/28 06:00 [pubmed] 2023/03/27 03:59 [entrez]
 2024/03/01 00:00 [pmc-release] 2023/03/02 06:00 [pubmed] 2023/03/02 06:01 [medline] 2023/03/01 14:52 [entrez]
 2023/05/11 00:00 [received] 2023/08/07 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:35 [entrez]
 2023/05/26 00:00 [received] 2023/05/28 00:00 [accepted] 2023/06/01 01:08 [medline] 2023/06/01 01:08 [pubmed] 2023/05/31 23:46 [entrez]
 2023/03/21 00:00 [received] 2023/07/24 00:00 [accepted] 2023/08/28 06:43 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 05:00 [entrez]
 2023/06/13 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/07/28 13:10 [pubmed] 2023/07/28 11:12 [entrez]
 2023/04/01 00:00 [received] 2023/06/05 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:29 [entrez]

 2023/01/21 00:00 [received] 2023/05/02 00:00 [revised] 2023/05/04 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/26 13:09 [pubmed] 2023/05/26 12:04 [entrez]
 2022/12/30 00:00 [received] 2023/02/09 00:00 [accepted] 2023/03/09 02:13 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/11 06:00 [medline]
 2023/06/08 00:00 [received] 2023/08/06 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/08/12 10:42 [pubmed] 2023/08/11 19:23 [entrez]
 2023/03/16 00:00 [received] 2023/05/30 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:18 [entrez]
 2023/01/30 00:00 [received] 2023/03/17 00:00 [accepted] 2023/04/24 06:41 [medline] 2023/04/21 06:41 [pubmed] 2023/04/21 02:14 [entrez]
 2022/12/06 00:00 [received] 2023/01/31 00:00 [accepted] 2022/12/07 00:00 [revised] 2024/08/01 00:00 [pmc-release] 2023/08/04 06:43 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 16:48 [entrez]
 2022/11/25 00:00 [received] 2023/01/09 00:00 [accepted] 2023/02/13 03:24 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2022/10/29 00:00 [received] 2023/01/07 00:00 [revised] 2023/01/08 00:00 [accepted] 2023/01/17 06:00 [pubmed] 2023/02/01 06:00 [medline] 2023/01/16 18:06 [entrez]
 2022/04/13 00:00 [received] 2022/07/14 00:00 [revised] 2022/07/14 00:00 [accepted] 2022/11/06 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/11/05 20:02 [entrez]
 2023/06/01 06:42 [medline] 2023/04/19 06:00 [pubmed] 2023/04/18 05:43 [entrez]
 2023/06/20 00:00 [received] 2023/07/20 00:00 [revised] 2023/07/26 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/08/12 10:44 [pubmed] 2023/08/12 01:23 [entrez]
 2023/03/17 00:00 [received] 2023/05/22 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 04:50 [entrez]
 2023/06/30 06:42 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 19:13 [entrez]
 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 13:08 [entrez]
 2022/07/22 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/08/29 12:44 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 02:34 [entrez]
 2022/03/25 00:00 [received] 2022/06/22 00:00 [accepted] 2022/06/30 06:00 [pubmed] 2023/01/05 06:00 [medline] 2022/06/29 03:33 [entrez]
 2023/07/08 00:00 [received] 2023/07/21 00:00 [accepted] 2023/08/16 00:42 [medline] 2023/08/16 00:42 [pubmed] 2023/08/15 18:02 [entrez]
 2022/08/01 00:00 [received] 2022/08/27 00:00 [revised] 2022/10/04 00:00 [accepted] 2023/08/09 06:44 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 03:56 [entrez]
 2023/07/10 00:00 [accepted] 2023/08/31 06:42 [medline] 2023/08/04 13:10 [pubmed] 2023/08/04 11:10 [entrez]
 2023/03/14 00:00 [received] 2023/04/19 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/05/26 01:05 [pubmed] 2023/05/25 18:09 [entrez]
 2023/02/27 00:00 [received] 2023/03/24 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:29 [entrez]
 2023/03/10 02:37 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2022/12/31 00:00 [received] 2023/01/24 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/02/25 01:05 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/01/05 00:00 [received] 2023/01/26 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/02/11 06:00 [pubmed] 2023/03/09 06:00 [medline] 2023/02/10 18:22 [entrez]
 2023/05/06 00:00 [received] 2023/08/08 00:00 [accepted] 2023/08/22 00:41 [medline] 2023/08/22 00:41 [pubmed] 2023/08/21 23:51 [entrez]
 2023/07/31 00:00 [revised] 2023/04/06 00:00 [received] 2023/08/17 00:00 [accepted] 2023/08/19 11:42 [pubmed] 2023/08/19 11:42 [medline] 2023/08/18 19:42 [entrez]
 2022/12/11 00:00 [accepted] 2023/01/20 06:00 [pubmed] 2023/02/17 06:00 [medline] 2023/01/19 11:24 [entrez]
 2021/12/15 06:00 [pubmed] 2023/03/03 06:00 [medline] 2021/12/14 05:58 [entrez]
 2019/03/03 00:00 [received] 2019/09/06 00:00 [accepted] 2020/10/13 00:01 [medline] 2020/10/13 00:00 [pubmed] 2023/06/14 03:53 [entrez]
 2023/05/21 00:00 [received] 2023/06/18 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:12 [entrez]
 2022/11/17 00:00 [received] 2023/02/10 00:00 [revised] 2023/02/19 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 19:11 [entrez]
 2023/01/21 06:00 [pubmed] 2023/01/21 06:00 [medline] 2023/01/20 04:12 [entrez]
 2020/01/30 00:00 [received] 2020/05/05 00:00 [accepted] 2023/03/31 06:42 [medline] 2022/03/09 06:00 [pubmed] 2022/03/08 05:36 [entrez]
 2023/06/17 00:00 [received] 2023/07/25 00:00 [revised] 2023/08/02 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/08/17 18:42 [pubmed] 2023/08/17 12:36 [entrez]
 2023/03/23 00:00 [received] 2023/06/29 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/03 00:41 [medline] 2023/09/03 00:41 [pubmed] 2023/09/02 18:16 [entrez]
 2022/06/21 00:00 [received] 2022/11/28 00:00 [revised] 2022/11/29 00:00 [accepted] 2022/12/13 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/12/12 18:22 [entrez]
 2023/06/20 00:00 [revised] 2023/06/15 00:00 [received] 2023/06/23 00:00 [accepted] 2023/07/14 13:06 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 00:05 [entrez]
 2022/07/24 00:00 [received] 2022/11/17 00:00 [revised] 2022/11/18 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2022/11/29 06:01 [medline] 2022/11/28 04:07 [entrez]
 2022/08/31 00:00 [received] 2023/02/28 00:00 [accepted] 2023/01/09 00:00 [revised] 2023/03/18 00:20 [entrez] 2023/03/19 06:00 [pubmed] 2023/03/19 06:00 [medline]
 2023/07/09 00:00 [received] 2023/07/10 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/07/12 13:07 [pubmed] 2023/07/12 07:43 [entrez]
 2023/01/10 00:00 [received] 2023/01/12 00:00 [accepted] 2023/08/08 06:42 [medline] 2023/01/21 06:00 [pubmed] 2023/01/20 06:33 [entrez]
 2023/07/17 06:42 [medline] 2022/12/09 06:00 [pubmed] 2022/12/08 10:14 [entrez]
 2023/04/26 00:00 [received] 2023/05/27 00:00 [revised] 2023/05/31 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:13 [entrez]
 2023/08/17 00:00 [received] 2023/09/03 00:00 [accepted] 2023/09/07 00:42 [pubmed] 2023/09/07 00:42 [medline] 2023/09/06 19:23 [entrez]
 2023/04/14 00:00 [received] 2023/06/04 00:00 [revised] 2023/06/10 00:00 [accepted] 2023/08/29 12:44 [medline] 2023/08/21 00:41 [pubmed] 2023/08/20 18:06 [entrez]
 2023/05/19 00:00 [received] 2023/07/03 00:00 [accepted] 2023/07/07 13:04 [medline] 2023/07/07 13:04 [pubmed] 2023/07/07 11:17 [entrez]
 2022/11/29 00:00 [received] 2022/12/15 00:00 [revised] 2022/12/19 00:00 [accepted] 2023/06/29 13:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:58 [entrez]
 2023/03/03 00:00 [received] 2023/03/28 00:00 [accepted] 2023/05/12 01:08 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 19:26 [entrez]
 2023/01/24 00:00 [received] 2023/03/09 00:00 [accepted] 2023/04/11 06:01 [medline] 2023/04/10 03:53 [entrez] 2023/04/11 06:00 [pubmed]
 2023/04/10 06:42 [medline] 2023/04/07 03:15 [entrez] 2023/04/08 06:00 [pubmed]
 2022/08/29 00:00 [received] 2022/12/29 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:18 [entrez] 2023/04/04 06:00 [pubmed]
 2023/02/12 00:00 [received] 2023/02/24 00:00 [revised] 2023/03/09 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:21 [entrez] 2023/03/30 06:00 [pubmed]
 2022/12/08 00:00 [received] 2023/02/24 00:00 [accepted] 2023/03/28 19:06 [medline] 2023/03/27 03:16 [entrez] 2023/03/28 06:00 [pubmed]
 2022/09/27 00:00 [received] 2022/12/12 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 09:04 [entrez]
 2022/11/15 00:00 [received] 2022/12/24 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/02/05 20:58 [entrez] 2023/02/06 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2023/02/03 07:13 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2022/10/17 00:00 [received] 2022/12/21 00:00 [accepted] 2022/12/20 00:00 [revised] 2022/12/29 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/28 23:29 [entrez]
 2022/07/07 00:00 [accepted] 2022/08/10 06:00 [pubmed] 2022/12/28 06:00 [medline] 2022/08/09 23:31 [entrez]
 2023/07/04 00:00 [revised] 2023/05/24 00:00 [received] 2023/07/09 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 03:29 [entrez]
 2023/07/15 00:00 [received] 2023/08/16 00:00 [accepted] 2023/08/21 00:41 [pubmed] 2023/08/21 00:41 [medline] 2023/08/20 19:27 [entrez]
 2023/05/30 00:00 [received] 2023/08/07 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/18 00:42 [medline] 2023/08/18 00:42 [pubmed] 2023/08/17 18:05 [entrez]
 2023/05/21 00:00 [revised] 2023/02/02 00:00 [received] 2023/07/27 00:00 [accepted] 2023/07/28 13:10 [pubmed] 2023/07/28 13:10 [medline] 2023/07/28 11:15 [entrez]
 2023/04/02 00:00 [received] 2023/04/22 00:00 [revised] 2023/04/27 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/07/11 13:10 [pubmed] 2023/07/11 10:44 [entrez]
 2023/02/28 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/12 00:00 [accepted] 2023/07/24 06:41 [medline] 2023/06/27 01:06 [pubmed] 2023/06/26 19:13 [entrez]
 2023/01/30 00:00 [received] 2023/03/27 00:00 [revised] 2023/05/11 00:00 [accepted] 2023/07/12 06:42 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 18:08 [entrez]
 2023/03/10 00:00 [received] 2023/03/22 00:00 [accepted] 2023/05/19 19:15 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 13:05 [entrez]
 2023/04/28 12:43 [medline] 2023/04/28 12:43 [pubmed] 2023/04/28 09:03 [entrez]
 2023/04/19 06:41 [medline] 2023/04/17 12:23 [entrez] 2023/04/18 06:00 [pubmed]
 2023/04/17 06:41 [medline] 2023/04/08 06:00 [pubmed] 2023/04/07 06:43 [entrez]
 2024/03/01 00:00 [pmc-release] 2023/03/20 04:13 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/21 06:01 [medline]
 2023/01/26 00:00 [received] 2023/02/03 00:00 [accepted] 2023/03/06 04:05 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/08 06:00 [medline]
 2022/12/29 00:00 [received] 2023/01/18 00:00 [revised] 2023/02/02 00:00 [accepted] 2023/02/25 02:37 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/11/19 00:00 [received] 2022/12/14 00:00 [revised] 2022/12/17 00:00 [accepted] 2023/02/25 02:36 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/11/24 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/01/21 01:30 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/11/18 00:00 [revised] 2022/06/10 00:00 [received] 2022/12/05 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/01/21 06:00 [pubmed] 2023/01/20 01:02 [entrez]
 2022/11/27 00:00 [accepted] 2022/12/19 06:00 [pubmed] 2023/02/18 06:00 [medline] 2022/12/18 23:22 [entrez]
 2020/09/28 00:00 [received] 2021/12/29 00:00 [revised] 2022/11/11 00:00 [accepted] 2023/05/01 06:42 [medline] 2022/12/11 06:00 [pubmed] 2022/12/10 22:07 [entrez]
 2023/07/10 06:42 [medline] 2022/09/01 06:00 [pubmed] 2022/08/31 19:02 [entrez]
 2022/07/17 00:00 [received] 2023/06/01 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/09/13 06:42 [medline] 2023/09/13 06:41 [pubmed] 2023/09/13 04:02 [entrez]
 2023/09/04 12:42 [medline] 2023/09/04 12:42 [pubmed] 2023/09/04 07:03 [entrez]
 2023/08/23 12:44 [medline] 2023/08/23 12:44 [pubmed] 2023/08/23 08:25 [entrez]
 2023/06/28 00:00 [accepted] 2023/07/31 06:44 [medline] 2023/07/31 06:43 [pubmed] 2023/07/31 04:38 [entrez]
 2023/03/08 00:00 [received] 2023/06/23 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/28 06:43 [pubmed] 2023/07/28 04:30 [entrez]
 2023/07/27 01:09 [medline] 2023/07/27 01:09 [pubmed] 2023/07/26 22:33 [entrez]
 2023/06/30 06:42 [medline] 2023/06/28 13:09 [pubmed] 2023/06/28 11:07 [entrez]
 2023/06/28 13:08 [medline] 2023/06/28 13:08 [pubmed] 2023/06/28 08:33 [entrez]
 2023/02/13 00:00 [received] 2023/05/29 00:00 [revised] 2023/05/31 00:00 [accepted] 2023/06/28 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:08 [entrez]
 2023/03/01 00:00 [received] 2023/05/19 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/06/22 13:09 [pubmed] 2023/06/22 09:44 [entrez]
 2023/02/21 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/17 00:00 [accepted] 2023/04/14 06:01 [medline] 2023/04/13 01:06 [entrez] 2023/04/14 06:00 [pubmed]
 2023/02/14 00:00 [received] 2023/03/05 00:00 [revised] 2023/03/08 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:23 [entrez] 2023/03/30 06:00 [pubmed]
 2022/03/28 00:00 [received] 2022/10/04 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/03/23 13:42 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/24 06:00 [medline]
 2023/01/01 00:00 [received] 2023/02/18 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/03/11 01:35 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2023/01/03 00:00 [received] 2023/02/22 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/10 06:00 [pubmed] 2023/03/09 18:14 [entrez]
 2023/02/27 00:00 [revised] 2022/11/10 00:00 [received] 2023/03/02 00:00 [accepted] 2023/03/08 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/03/07 08:12 [entrez]
 2023/02/16 11:03 [entrez] 2023/02/17 06:00 [pubmed] 2023/02/17 06:01 [medline]
 2022/12/19 00:00 [received] 2023/01/21 00:00 [accepted] 2023/02/09 10:53 [entrez] 2023/02/10 06:00 [pubmed] 2023/02/10 06:00 [medline]
 2023/01/01 00:00 [received] 2023/01/25 00:00 [accepted] 2023/01/25 00:00 [revised] 2023/02/07 11:23 [entrez] 2023/02/08 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2023/02/07 01:57 [entrez] 2023/02/08 06:00 [pubmed] 2023/02/08 06:01 [medline]
 2023/01/30 04:12 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/09/30 00:00 [received] 2022/12/09 00:00 [revised] 2023/01/15 00:00 [accepted] 2023/01/22 06:00 [pubmed] 2023/03/09 06:00 [medline] 2023/01/21 19:26 [entrez]
 2022/10/11 00:00 [received] 2022/12/30 00:00 [accepted] 2023/01/05 11:16 [entrez] 2023/01/06 06:00 [pubmed] 2023/01/06 06:01 [medline]
 2022/09/27 00:00 [revised] 2022/07/28 00:00 [received] 2022/10/27 00:00 [accepted] 2022/11/01 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/10/31 05:32 [entrez]
 2022/07/06 00:00 [revised] 2021/11/01 00:00 [received] 2022/07/17 00:00 [accepted] 2022/08/09 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/08/08 01:02 [entrez]
 2021/01/18 00:00 [received] 2021/05/27 00:00 [accepted] 2022/02/17 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/02/16 08:43 [entrez]
 2022/01/28 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/01/27 17:14 [entrez]
 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:54 [entrez]
 2023/05/06 00:00 [received] 2023/08/20 00:00 [revised] 2023/08/30 00:00 [accepted] 2023/09/10 00:41 [medline] 2023/09/10 00:41 [pubmed] 2023/09/09 18:07 [entrez]
 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 04:39 [entrez]
 2022/10/25 00:00 [received] 2023/03/07 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 05:10 [entrez]
 2023/02/16 00:00 [received] 2023/07/17 00:00 [accepted] 2023/08/07 06:43 [medline] 2023/08/07 06:42 [pubmed] 2023/08/07 04:35 [entrez]
 2023/05/25 00:00 [revised] 2022/08/18 00:00 [received] 2023/06/29 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 05:43 [entrez]
 2023/05/03 00:00 [received] 2023/06/20 00:00 [revised] 2023/06/26 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:05 [pubmed] 2023/07/14 01:02 [entrez]

 2023/03/01 00:00 [received] 2023/04/05 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/26 12:42 [pubmed] 2023/04/26 11:32 [entrez]
 2024/03/27 00:00 [pmc-release] 2023/05/03 06:42 [medline] 2023/04/04 06:00 [pubmed] 2023/04/03 10:43 [entrez]
 2022/12/29 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/14 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:52 [entrez] 2023/03/30 06:00 [pubmed]
 2023/01/05 00:00 [received] 2023/02/09 00:00 [accepted] 2023/03/17 02:40 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/18 06:01 [medline]
 2023/02/27 12:54 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2022/11/09 00:00 [received] 2023/01/20 00:00 [accepted] 2023/02/27 04:55 [entrez] 2023/02/28 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/12/21 00:00 [received] 2023/01/20 00:00 [revised] 2023/01/23 00:00 [accepted] 2023/02/25 01:26 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/12/02 00:00 [received] 2023/01/10 00:00 [accepted] 2023/02/13 03:55 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2022/10/09 00:00 [received] 2023/01/18 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/02/11 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/10 19:25 [entrez]
 2022/08/12 00:00 [received] 2023/01/09 00:00 [accepted] 2023/02/10 03:12 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2022/07/20 00:00 [revised] 2022/01/18 00:00 [received] 2023/01/14 00:00 [accepted] 2023/04/07 06:42 [medline] 2023/02/06 06:00 [pubmed] 2023/02/05 20:02 [entrez]
 2022/07/30 00:00 [received] 2022/12/22 00:00 [accepted] 2023/01/04 06:00 [pubmed] 2023/02/15 06:00 [medline] 2023/01/03 23:20 [entrez]
 2022/02/23 00:00 [received] 2022/04/14 00:00 [revised] 2022/04/19 00:00 [accepted] 2023/05/19 06:42 [medline] 2022/06/04 06:00 [pubmed] 2022/06/03 07:33 [entrez]
 2022/08/08 00:00 [received] 2023/09/03 00:00 [revised] 2023/09/07 00:00 [accepted] 2023/09/13 00:42 [medline] 2023/09/13 00:42 [pubmed] 2023/09/12 21:51 [entrez]
 2023/07/27 00:00 [received] 2023/08/23 00:00 [revised] 2023/08/25 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/09 11:44 [pubmed] 2023/09/09 01:13 [entrez]
 2023/06/02 00:00 [received] 2023/07/18 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/23 01:11 [pubmed] 2023/07/22 23:25 [entrez]
 2022/10/11 00:00 [received] 2023/01/09 00:00 [accepted] 2023/06/02 06:42 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 18:23 [entrez]
 2022/02/15 00:00 [received] 2022/05/16 00:00 [accepted] 2023/09/04 06:42 [medline] 2022/06/30 06:00 [pubmed] 2022/06/29 15:42 [entrez]
 2023/09/07 06:42 [medline] 2023/08/17 18:42 [pubmed] 2023/08/17 17:32 [entrez]
 2023/04/06 00:00 [received] 2023/05/11 00:00 [accepted] 2023/07/03 13:05 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:10 [entrez]
 2023/04/26 00:00 [received] 2023/05/29 00:00 [revised] 2023/05/30 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:13 [entrez]
 2023/06/06 00:00 [received] 2023/08/30 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/10 00:42 [pubmed] 2023/09/09 23:15 [entrez]
 2022/09/28 00:00 [received] 2022/11/11 00:00 [revised] 2022/11/29 00:00 [accepted] 2023/01/08 06:00 [pubmed] 2023/01/13 06:00 [medline] 2023/01/07 18:05 [entrez]
 2023/01/24 00:00 [received] 2023/03/06 00:00 [accepted] 2023/04/18 06:41 [medline] 2023/04/17 03:35 [entrez] 2023/04/18 06:00 [pubmed]
 2022/11/03 00:00 [revised] 2022/09/19 00:00 [received] 2022/11/08 00:00 [accepted] 2022/11/26 06:00 [pubmed] 2023/01/24 06:00 [medline] 2022/11/25 13:52 [entrez]
 2023/07/19 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/08/29 12:43 [pubmed] 2023/08/29 11:15 [entrez]
 2022/03/10 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/03/09 20:08 [entrez]
 2023/05/03 06:43 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 01:58 [entrez]
 2023/02/13 00:00 [received] 2023/05/23 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/28 01:07 [pubmed] 2023/05/27 23:17 [entrez]
 2022/08/24 00:00 [received] 2022/12/07 00:00 [revised] 2022/12/13 00:00 [accepted] 2022/12/20 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/12/19 19:23 [entrez]
 2023/04/06 00:00 [revised] 2022/10/10 00:00 [received] 2023/04/17 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/05/04 12:42 [pubmed] 2023/05/04 07:03 [entrez]
 2023/03/03 00:00 [received] 2023/06/22 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/10 00:42 [medline] 2023/09/10 00:42 [pubmed] 2023/09/09 18:04 [entrez]
 2022/11/16 00:00 [received] 2023/05/26 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:09 [entrez]
 2022/05/19 00:00 [received] 2022/09/19 00:00 [accepted] 2022/10/06 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/10/05 11:24 [entrez]
 2022/06/12 00:00 [received] 2022/12/25 00:00 [accepted] 2023/04/18 06:41 [medline] 2022/12/29 06:00 [pubmed] 2022/12/28 11:20 [entrez]
 2022/08/21 00:00 [received] 2022/11/06 00:00 [accepted] 2022/12/03 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/02 21:07 [entrez]
 2023/01/22 00:00 [accepted] 2023/02/22 06:01 [medline] 2023/02/22 06:00 [pubmed] 2023/02/21 17:08 [entrez]
 2022/05/29 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/01/07 06:00 [pubmed] 2023/01/06 11:22 [entrez]
 2022/06/13 00:00 [received] 2022/09/21 00:00 [revised] 2022/10/10 00:00 [accepted] 2023/02/23 09:25 [entrez] 2023/02/24 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2021/11/26 00:00 [received] 2022/03/31 00:00 [accepted] 2022/03/10 00:00 [revised] 2022/04/17 06:00 [pubmed] 2023/01/27 06:00 [medline] 2022/04/16 05:24 [entrez]
 2023/03/09 01:53 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/11 06:00 [medline]
 2023/04/28 00:00 [received] 2023/06/22 00:00 [revised] 2023/07/11 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 18:05 [entrez]
 2023/05/12 00:00 [received] 2023/06/29 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:06 [pubmed] 2023/07/14 01:16 [entrez]
 2023/02/26 00:00 [received] 2023/05/23 00:00 [accepted] 2023/07/11 01:07 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 23:27 [entrez]
 2024/01/05 00:00 [pmc-release] 2023/07/06 06:43 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 04:21 [entrez]
 2023/01/08 00:00 [received] 2023/04/06 00:00 [accepted] 2023/06/12 13:07 [medline] 2023/06/12 13:07 [pubmed] 2023/06/12 09:03 [entrez]
 2023/04/21 00:00 [received] 2023/05/08 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:20 [entrez]
 2023/03/05 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:25 [entrez]
 2022/11/12 00:00 [received] 2023/01/05 00:00 [revised] 2023/02/21 00:00 [accepted] 2023/04/05 06:42 [medline] 2023/04/04 01:56 [entrez] 2023/04/05 06:00 [pubmed]
 2023/02/20 00:00 [received] 2023/03/10 00:00 [revised] 2023/03/12 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:59 [entrez] 2023/03/30 06:00 [pubmed]
 2023/03/01 18:03 [entrez] 2023/03/02 06:00 [pubmed] 2023/03/02 06:00 [medline]
 2022/09/02 00:00 [received] 2022/12/20 00:00 [accepted] 2023/01/23 04:54 [entrez] 2023/01/24 06:00 [pubmed] 2023/01/24 06:01 [medline]
 2022/08/01 00:00 [received] 2022/09/17 00:00 [accepted] 2023/01/21 06:00 [pubmed] 2023/03/21 06:00 [medline] 2023/01/20 08:43 [entrez]
 2022/09/14 00:00 [received] 2022/09/29 00:00 [accepted] 2022/10/30 06:00 [pubmed] 2023/03/25 06:00 [medline] 2022/10/29 19:23 [entrez]
 2022/08/03 00:00 [received] 2022/10/12 00:00 [accepted] 2022/09/06 00:00 [revised] 2022/10/18 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/10/17 23:29 [entrez]
 2023/06/02 00:00 [accepted] 2023/06/28 13:08 [medline] 2023/06/28 13:08 [pubmed] 2023/06/28 11:16 [entrez]
 2023/06/15 00:00 [received] 2023/07/29 00:00 [revised] 2023/07/29 00:00 [accepted] 2023/09/07 06:42 [medline] 2023/08/03 01:06 [pubmed] 2023/08/02 19:13 [entrez]
 2023/05/31 00:00 [received] 2023/07/03 00:00 [revised] 2023/07/13 00:00 [accepted] 2023/07/29 11:48 [medline] 2023/07/29 11:47 [pubmed] 2023/07/29 01:27 [entrez]
 2023/07/28 06:43 [medline] 2023/07/28 06:43 [pubmed] 2023/07/28 03:43 [entrez]
 2023/07/25 06:43 [medline] 2023/07/25 06:42 [pubmed] 2023/07/25 01:20 [entrez]
 2023/01/27 00:00 [received] 2023/05/19 00:00 [accepted] 2023/07/25 01:09 [medline] 2023/07/25 01:09 [pubmed] 2023/07/24 21:43 [entrez]
 2023/06/12 00:00 [revised] 2023/02/13 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/11 13:11 [pubmed] 2023/07/11 13:11 [medline] 2023/07/11 08:23 [entrez]
 2023/04/29 00:00 [received] 2023/06/12 00:00 [accepted] 2023/06/09 00:00 [revised] 2023/06/24 11:42 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 23:29 [entrez]
 2023/03/06 00:00 [received] 2023/04/09 00:00 [revised] 2023/04/20 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/04/28 00:42 [pubmed] 2023/04/27 18:09 [entrez]
 2023/02/04 00:00 [received] 2023/03/13 00:00 [accepted] 2023/04/18 06:01 [medline] 2023/04/17 03:24 [entrez] 2023/04/18 06:00 [pubmed]
 2022/04/29 00:00 [received] 2022/06/09 00:00 [revised] 2022/07/05 00:00 [accepted] 2023/04/15 06:01 [medline] 2023/04/14 02:24 [entrez] 2023/04/15 06:00 [pubmed]
 2023/01/05 00:00 [received] 2023/03/21 00:00 [revised] 2023/03/29 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/04/07 06:00 [pubmed] 2023/04/06 18:09 [entrez]
 2023/01/18 00:00 [received] 2023/02/11 00:00 [accepted] 2023/03/01 23:45 [entrez] 2023/03/02 06:00 [pubmed] 2023/03/02 06:00 [medline]
 2023/01/16 00:00 [revised] 2022/07/01 00:00 [received] 2023/01/17 00:00 [accepted] 2023/04/05 06:42 [medline] 2023/02/11 06:00 [pubmed] 2023/02/10 04:22 [entrez]
 2022/12/23 10:33 [entrez] 2022/12/24 06:00 [pubmed] 2022/12/28 06:00 [medline]
 2022/08/01 00:00 [received] 2022/11/22 00:00 [accepted] 2023/03/29 06:05 [medline] 2022/12/05 06:00 [pubmed] 2022/12/04 23:20 [entrez]
 2022/08/11 00:00 [received] 2022/10/06 00:00 [accepted] 2023/06/16 06:42 [medline] 2022/10/23 06:00 [pubmed] 2022/10/22 01:43 [entrez]
 2022/09/26 00:00 [revised] 2022/03/21 00:00 [received] 2022/10/09 00:00 [accepted] 2022/10/20 06:00 [pubmed] 2023/02/07 06:00 [medline] 2022/10/19 09:03 [entrez]
 2022/04/20 00:00 [accepted] 2022/05/10 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/05/09 23:24 [entrez]
 2022/01/01 06:00 [pubmed] 2023/01/18 06:00 [medline] 2021/12/31 12:07 [entrez]
 2021/08/28 06:00 [pubmed] 2023/01/07 06:00 [medline] 2021/08/27 05:34 [entrez]
 2023/08/28 00:00 [revised] 2023/07/18 00:00 [received] 2023/08/30 00:00 [accepted] 2023/09/14 12:41 [medline] 2023/09/14 12:41 [pubmed] 2023/09/14 09:33 [entrez]
 2023/06/04 00:00 [revised] 2023/03/29 00:00 [received] 2023/06/18 00:00 [accepted] 2023/07/10 13:05 [pubmed] 2023/07/10 13:05 [medline] 2023/07/10 06:53 [entrez]
 2023/05/16 00:00 [received] 2023/08/18 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/08/31 00:41 [medline] 2023/08/31 00:41 [pubmed] 2023/08/30 18:00 [entrez]
 2023/05/17 00:00 [received] 2023/06/26 00:00 [accepted] 2023/07/27 06:43 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 03:53 [entrez]
 2023/01/31 00:00 [received] 2023/05/10 00:00 [accepted] 2023/07/11 13:10 [medline] 2023/07/11 13:10 [pubmed] 2023/07/11 09:03 [entrez]
 2024/02/01 00:00 [pmc-release] 2023/07/03 13:07 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:47 [entrez]
 2022/10/08 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/10 00:00 [accepted] 2023/06/24 11:42 [pubmed] 2023/06/24 11:42 [medline] 2023/06/23 19:17 [entrez]
 2023/06/14 13:07 [medline] 2023/06/14 13:07 [pubmed] 2023/06/14 12:03 [entrez]
 2023/04/10 00:00 [received] 2023/05/05 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:21 [entrez]
 2022/11/15 00:00 [received] 2023/02/02 00:00 [revised] 2023/02/06 00:00 [accepted] 2023/04/18 05:03 [entrez] 2023/04/19 06:00 [pubmed] 2023/04/19 06:00 [medline]
 2023/02/14 00:00 [received] 2023/03/06 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:43 [entrez] 2023/03/30 06:00 [pubmed]
 2023/01/06 00:00 [received] 2023/02/17 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:17 [entrez] 2023/03/30 06:00 [pubmed]
 2023/04/14 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 07:55 [entrez]
 2023/02/08 00:00 [revised] 2022/11/04 00:00 [received] 2023/02/24 00:00 [accepted] 2023/07/19 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 00:53 [entrez]
 2022/11/22 00:00 [received] 2023/02/19 00:00 [revised] 2023/03/04 00:00 [accepted] 2023/03/31 06:42 [medline] 2023/03/11 06:00 [pubmed] 2023/03/10 19:26 [entrez]
 2022/12/01 00:00 [received] 2023/01/30 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/02/25 04:18 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/07/15 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/06 00:00 [accepted] 2023/01/16 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/15 19:27 [entrez]
 2022/06/21 00:00 [received] 2022/11/05 00:00 [revised] 2022/12/11 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/12/15 19:24 [entrez]
 2022/04/23 00:00 [received] 2022/07/22 00:00 [accepted] 2022/09/17 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/16 11:20 [entrez]
 2022/05/17 00:00 [received] 2022/08/31 00:00 [accepted] 2022/08/26 00:00 [revised] 2022/09/17 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/09/16 11:19 [entrez]
 2023/07/10 06:42 [medline] 2022/06/18 06:00 [pubmed] 2022/06/17 10:23 [entrez]
 2023/05/22 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/16 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/07/24 00:41 [pubmed] 2023/07/23 18:07 [entrez]
 2023/07/03 00:00 [revised] 2023/02/26 00:00 [received] 2023/08/08 00:00 [accepted] 2023/08/11 12:43 [pubmed] 2023/08/11 12:43 [medline] 2023/08/11 07:53 [entrez]
 2023/05/09 00:00 [received] 2023/07/22 00:00 [accepted] 2023/08/06 05:41 [medline] 2023/08/06 05:41 [pubmed] 2023/08/05 11:13 [entrez]
 2023/07/09 00:00 [revised] 2023/03/17 00:00 [received] 2023/07/24 06:42 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 05:06 [entrez]

 2023/05/04 00:00 [received] 2023/05/24 00:00 [revised] 2023/05/29 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:15 [entrez]
 2023/01/06 00:00 [received] 2023/04/27 00:00 [revised] 2023/05/19 00:00 [accepted] 2023/06/01 13:09 [medline] 2023/06/01 13:09 [pubmed] 2023/06/01 11:42 [entrez]
 2022/12/05 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/04/28 06:41 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 10:30 [entrez]
 2022/09/19 00:00 [received] 2023/02/02 00:00 [accepted] 2023/05/08 10:17 [medline] 2023/02/09 06:00 [pubmed] 2023/02/08 04:03 [entrez]
 2022/12/05 00:00 [revised] 2022/09/06 00:00 [received] 2023/01/25 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/01/27 06:00 [pubmed] 2023/01/26 21:44 [entrez]
 2022/09/06 00:00 [received] 2022/12/19 00:00 [accepted] 2023/04/11 06:41 [medline] 2023/01/11 06:00 [pubmed] 2023/01/10 18:42 [entrez]
 2022/07/09 00:00 [received] 2022/10/19 00:00 [accepted] 2023/01/09 04:18 [entrez] 2023/01/10 06:00 [pubmed] 2023/01/10 06:01 [medline]
 2023/04/19 06:41 [medline] 2023/01/03 06:00 [pubmed] 2023/01/02 06:02 [entrez]
 2022/05/23 00:00 [received] 2022/10/24 00:00 [accepted] 2022/12/29 10:32 [entrez] 2022/12/30 06:00 [pubmed] 2023/01/03 06:00 [medline]
 2022/12/01 06:00 [pubmed] 2023/02/11 06:00 [medline] 2022/11/30 02:53 [entrez]
 2022/08/24 00:00 [received] 2022/10/26 00:00 [revised] 2022/11/10 00:00 [accepted] 2023/05/03 06:42 [medline] 2022/11/22 06:00 [pubmed] 2022/11/21 06:43 [entrez]

 2022/07/07 00:00 [received] 2022/10/26 00:00 [revised] 2022/11/04 00:00 [accepted] 2022/11/12 06:00 [pubmed] 2022/11/30 06:00 [medline] 2022/11/11 19:33 [entrez]
 2022/08/30 00:00 [received] 2022/09/27 00:00 [accepted] 2022/09/26 00:00 [revised] 2022/10/13 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/10/12 11:15 [entrez]
 2023/02/26 00:00 [received] 2023/04/06 00:00 [revised] 2023/04/10 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:14 [entrez]
 2022/11/05 00:00 [received] 2023/02/28 00:00 [accepted] 2023/03/23 14:22 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2023/03/07 00:00 [received] 2023/06/13 00:00 [accepted] 2023/06/10 00:00 [revised] 2023/06/23 13:07 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 11:07 [entrez]
 2023/02/25 00:00 [received] 2023/03/12 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:26 [entrez] 2023/04/14 06:00 [pubmed]
 2022/12/01 00:00 [received] 2023/02/07 00:00 [accepted] 2023/02/27 05:30 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2023/07/13 00:00 [received] 2023/08/16 00:00 [revised] 2023/08/18 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/26 10:42 [pubmed] 2023/08/26 01:17 [entrez]
 2023/05/14 00:00 [received] 2023/06/12 00:00 [revised] 2023/06/19 00:00 [accepted] 2023/06/27 01:06 [pubmed] 2023/06/27 01:06 [medline] 2023/06/26 18:09 [entrez]
 2023/03/27 00:00 [received] 2023/05/12 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/06/09 06:42 [pubmed] 2023/06/09 04:18 [entrez]
 2022/12/31 00:00 [received] 2023/06/21 00:00 [accepted] 2023/07/14 13:08 [medline] 2023/07/13 01:06 [pubmed] 2023/07/12 23:50 [entrez]
 2022/12/06 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/22 00:00 [accepted] 2023/02/25 03:17 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/12/06 00:00 [received] 2023/01/27 00:00 [revised] 2023/02/03 00:00 [accepted] 2023/02/25 03:04 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/08/11 00:00 [revised] 2022/03/17 00:00 [received] 2022/08/17 00:00 [accepted] 2023/04/04 06:42 [medline] 2022/09/13 06:00 [pubmed] 2022/09/12 02:52 [entrez]
 2023/08/23 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 04:06 [entrez]
 2023/04/21 06:41 [medline] 2023/04/20 00:41 [pubmed] 2023/04/19 20:43 [entrez]
 2023/02/17 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/14 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:39 [entrez] 2023/03/30 06:00 [pubmed]
 2023/03/14 00:00 [received] 2023/03/14 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/04/09 06:00 [pubmed] 2023/04/08 18:53 [entrez]
 2022/10/03 00:00 [received] 2023/02/06 00:00 [accepted] 2023/05/14 19:14 [medline] 2023/05/14 19:13 [pubmed] 2023/05/14 12:15 [entrez]
 2023/01/31 00:00 [received] 2023/03/15 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/04/13 01:16 [entrez] 2023/04/14 06:00 [pubmed]
 2023/08/23 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 04:05 [entrez]
 2022/11/30 00:00 [received] 2023/01/01 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/01/21 01:50 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2022/11/01 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/04/10 06:42 [medline] 2023/03/10 06:00 [pubmed] 2023/03/09 19:34 [entrez]
 2023/01/25 00:00 [received] 2023/02/09 00:00 [accepted] 2023/04/25 10:20 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 19:22 [entrez]
 2022/07/13 00:00 [received] 2022/12/13 00:00 [accepted] 2023/01/27 02:15 [entrez] 2023/01/28 06:00 [pubmed] 2023/01/28 06:01 [medline]
 2023/07/12 06:42 [medline] 2023/06/07 06:42 [pubmed] 2023/06/07 03:42 [entrez]
 2023/02/08 00:00 [received] 2023/04/18 00:00 [revised] 2023/04/20 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/04/24 00:41 [pubmed] 2023/04/23 19:29 [entrez]
 2023/02/23 00:00 [received] 2023/05/21 00:00 [revised] 2023/06/05 00:00 [accepted] 2023/08/23 06:42 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 19:15 [entrez]
 2023/02/28 00:00 [received] 2023/06/06 00:00 [accepted] 2023/07/03 13:07 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:25 [entrez]
 2022/05/02 00:00 [received] 2023/04/12 00:00 [accepted] 2023/05/11 13:19 [medline] 2023/05/11 13:18 [pubmed] 2023/05/11 11:13 [entrez]
 2023/06/28 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 20:33 [entrez]
 2023/05/01 00:00 [received] 2023/07/27 00:00 [accepted] 2023/08/31 06:43 [medline] 2023/08/31 06:42 [pubmed] 2023/08/31 04:12 [entrez]
 2023/01/05 00:00 [received] 2023/07/23 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/08/17 00:42 [pubmed] 2023/08/16 18:06 [entrez]
 2022/11/07 00:00 [received] 2022/12/18 00:00 [revised] 2023/01/09 00:00 [accepted] 2023/06/14 06:43 [medline] 2023/06/14 06:42 [pubmed] 2023/06/14 04:00 [entrez]
 2023/01/17 00:00 [received] 2023/04/27 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/11 01:06 [pubmed] 2023/06/10 23:13 [entrez]
 2022/06/19 00:00 [received] 2023/03/06 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 23:48 [entrez]
 2022/11/14 00:00 [received] 2023/03/14 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:46 [entrez]
 2022/12/29 00:00 [received] 2023/03/16 00:00 [accepted] 2023/04/15 06:01 [medline] 2023/04/14 02:35 [entrez] 2023/04/15 06:00 [pubmed]
 2022/11/20 00:00 [received] 2023/01/06 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/04/15 06:01 [medline] 2023/04/14 02:24 [entrez] 2023/04/15 06:00 [pubmed]
 2022/11/26 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/12 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/17 06:00 [pubmed] 2023/03/16 20:33 [entrez]
 2022/12/20 00:00 [received] 2023/01/20 00:00 [accepted] 2023/03/06 03:41 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/01/01 00:00 [received] 2023/02/18 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/03/02 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/03/01 19:27 [entrez]
 2022/08/01 00:00 [received] 2022/10/18 00:00 [revised] 2023/02/03 00:00 [accepted] 2023/02/28 02:29 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:01 [medline]
 2023/01/13 17:43 [entrez] 2023/01/14 06:00 [pubmed] 2023/01/18 06:00 [medline]
 2022/06/22 00:00 [received] 2022/09/20 00:00 [revised] 2022/10/31 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/01/04 06:00 [pubmed] 2023/01/03 00:43 [entrez]
 2022/08/18 00:00 [accepted] 2023/09/08 06:43 [medline] 2022/08/27 06:00 [pubmed] 2022/08/26 11:23 [entrez]
 2022/08/09 06:01 [medline] 2022/08/09 06:00 [pubmed] 2022/08/08 06:53 [entrez]
 2023/07/02 00:00 [received] 2023/08/02 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:29 [entrez]
 2023/02/14 00:00 [received] 2023/04/03 00:00 [accepted] 2023/08/16 06:42 [medline] 2023/08/15 12:43 [pubmed] 2023/08/15 09:13 [entrez]
 2023/06/07 00:00 [received] 2023/07/14 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/08/12 10:46 [medline] 2023/08/12 10:45 [pubmed] 2023/08/12 01:15 [entrez]
 2023/05/02 00:00 [revised] 2022/11/01 00:00 [received] 2023/06/23 00:00 [accepted] 2023/08/07 06:41 [medline] 2023/07/18 06:42 [pubmed] 2023/07/18 02:33 [entrez]
 2023/04/27 00:00 [received] 2023/07/03 00:00 [revised] 2023/07/07 00:00 [accepted] 2023/08/17 06:43 [medline] 2023/07/17 00:42 [pubmed] 2023/07/16 18:08 [entrez]
 2023/01/10 00:00 [received] 2023/05/11 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 21:22 [entrez]
 2023/04/20 00:00 [received] 2023/05/25 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 13:11 [entrez]
 2023/05/24 06:42 [medline] 2023/04/26 12:42 [pubmed] 2023/04/26 10:32 [entrez]
 2023/03/01 00:00 [received] 2023/03/26 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/04/17 06:00 [pubmed] 2023/04/16 21:58 [entrez]
 2022/12/02 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/07 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 19:08 [entrez]
 2023/02/08 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/03/11 01:27 [entrez] 2023/03/12 06:00 [pubmed] 2023/03/15 06:00 [medline]
 2022/12/03 00:00 [received] 2023/01/20 00:00 [accepted] 2023/02/23 09:31 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2022/08/25 00:00 [received] 2022/12/20 00:00 [revised] 2023/01/03 00:00 [accepted] 2023/01/13 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/12 18:10 [entrez]
 2022/11/01 00:00 [received] 2022/11/14 00:00 [accepted] 2023/06/19 13:09 [medline] 2022/12/17 06:00 [pubmed] 2022/12/16 22:05 [entrez]
 2022/12/10 06:00 [pubmed] 2023/03/16 06:00 [medline] 2022/12/09 03:33 [entrez]
 2023/06/22 06:41 [medline] 2022/06/28 06:00 [pubmed] 2022/06/27 22:42 [entrez]
 2022/01/24 00:00 [received] 2023/03/21 00:00 [revised] 2023/08/03 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:49 [entrez]
 2022/07/22 00:00 [received] 2023/08/06 00:00 [accepted] 2023/09/13 06:43 [medline] 2023/09/13 06:42 [pubmed] 2023/09/13 03:57 [entrez]
 2023/06/13 00:00 [received] 2023/07/12 00:00 [revised] 2023/07/13 00:00 [accepted] 2023/09/01 00:43 [medline] 2023/09/01 00:42 [pubmed] 2023/08/31 20:36 [entrez]
 2023/03/17 00:00 [received] 2023/08/17 00:00 [accepted] 2023/08/28 12:43 [medline] 2023/08/28 12:43 [pubmed] 2023/08/28 11:07 [entrez]
 2023/04/03 00:00 [received] 2023/07/17 00:00 [revised] 2023/07/30 00:00 [accepted] 2023/08/03 01:07 [medline] 2023/08/03 01:06 [pubmed] 2023/08/02 19:16 [entrez]
 2023/01/14 00:00 [received] 2023/06/07 00:00 [revised] 2023/07/10 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/07/15 10:42 [pubmed] 2023/07/14 19:22 [entrez]
 2023/05/02 00:00 [received] 2023/06/10 00:00 [revised] 2023/06/16 00:00 [accepted] 2023/08/25 06:42 [medline] 2023/07/13 01:06 [pubmed] 2023/07/12 18:06 [entrez]
 2022/09/28 00:00 [received] 2023/06/16 00:00 [accepted] 2023/07/12 01:08 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 23:42 [entrez]
 2022/08/09 00:00 [received] 2023/06/05 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/07/11 19:12 [pubmed] 2023/07/11 16:43 [entrez]
 2023/04/10 00:00 [received] 2023/05/30 00:00 [accepted] 2023/06/28 06:42 [medline] 2023/06/27 01:06 [pubmed] 2023/06/26 23:34 [entrez]
 2023/04/22 00:00 [received] 2023/05/16 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:18 [entrez]
 2023/04/12 00:00 [received] 2023/04/13 00:00 [accepted] 2023/06/14 06:42 [medline] 2023/04/24 18:42 [pubmed] 2023/04/24 02:22 [entrez]
 2023/03/13 00:00 [revised] 2021/08/16 00:00 [received] 2023/03/20 00:00 [accepted] 2023/06/13 06:42 [medline] 2023/04/09 06:00 [pubmed] 2023/04/08 09:33 [entrez]
 2023/03/18 04:12 [entrez] 2023/03/19 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2022/06/07 00:00 [received] 2022/09/30 00:00 [revised] 2022/10/31 00:00 [accepted] 2022/12/12 11:32 [entrez] 2022/12/13 06:00 [pubmed] 2022/12/13 06:01 [medline]
 2022/05/17 00:00 [received] 2022/09/20 00:00 [revised] 2022/11/21 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/08 23:34 [entrez]
 2022/09/20 00:00 [revised] 2021/07/22 00:00 [received] 2022/11/01 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2022/12/28 06:00 [medline] 2022/11/28 07:33 [entrez]
 2022/04/14 00:00 [received] 2022/10/17 00:00 [revised] 2022/10/31 00:00 [accepted] 2022/11/07 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/11/06 19:33 [entrez]
 2022/10/07 03:03 [entrez] 2022/10/08 06:00 [pubmed] 2022/10/08 06:01 [medline]
 2022/03/10 00:00 [received] 2022/05/10 00:00 [accepted] 2022/07/01 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/06/30 13:44 [entrez]
 2023/08/04 06:43 [medline] 2022/03/31 06:00 [pubmed] 2022/03/30 17:04 [entrez]
 2023/08/23 18:42 [medline] 2023/08/23 18:42 [pubmed] 2023/08/23 12:32 [entrez]
 2023/08/16 06:43 [medline] 2023/08/15 12:42 [pubmed] 2023/08/15 11:09 [entrez]
 2023/06/08 00:00 [received] 2023/07/27 00:00 [accepted] 2023/08/04 13:11 [medline] 2023/08/04 13:11 [pubmed] 2023/08/04 11:12 [entrez]
 2023/07/26 06:42 [medline] 2023/07/26 06:42 [pubmed] 2023/07/26 03:13 [entrez]

 2023/06/12 06:42 [medline] 2023/06/09 13:42 [pubmed] 2023/06/09 08:03 [entrez]
 2023/05/31 06:42 [medline] 2023/05/29 13:04 [pubmed] 2023/05/29 09:03 [entrez]
 2023/03/24 00:00 [received] 2023/04/18 00:00 [accepted] 2023/06/26 06:42 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 23:27 [entrez]
 2023/02/03 00:00 [received] 2023/04/14 00:00 [revised] 2023/04/24 00:00 [accepted] 2023/06/14 06:42 [medline] 2023/04/30 00:42 [pubmed] 2023/04/29 19:29 [entrez]
 2023/05/01 06:42 [medline] 2023/04/28 12:43 [pubmed] 2023/04/28 09:29 [entrez]
 2023/07/28 06:42 [medline] 2023/04/20 18:41 [pubmed] 2023/04/20 15:33 [entrez]
 2023/02/16 00:00 [received] 2023/03/09 00:00 [revised] 2023/03/11 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:18 [entrez] 2023/03/30 06:00 [pubmed]
 2023/01/11 00:00 [received] 2023/02/11 00:00 [revised] 2023/02/17 00:00 [accepted] 2023/02/25 04:21 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/11/09 00:00 [received] 2023/01/28 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/05/09 06:42 [medline] 2023/02/10 06:00 [pubmed] 2023/02/09 18:22 [entrez]
 2023/01/09 00:00 [revised] 2021/11/26 00:00 [received] 2023/01/17 00:00 [accepted] 2023/06/09 06:42 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 02:32 [entrez]
 2022/11/16 00:00 [received] 2022/11/26 00:00 [revised] 2022/11/26 00:00 [accepted] 2022/12/10 06:00 [pubmed] 2023/01/18 06:00 [medline] 2022/12/09 18:14 [entrez]
 2022/08/25 00:00 [revised] 2021/12/03 00:00 [received] 2022/09/07 00:00 [accepted] 2022/10/11 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/10/10 05:53 [entrez]
 2021/11/15 00:00 [received] 2022/08/26 00:00 [accepted] 2023/03/29 06:05 [medline] 2022/09/21 06:00 [pubmed] 2022/09/20 11:17 [entrez]
 2023/03/14 00:00 [received] 2023/07/25 00:00 [revised] 2023/08/10 00:00 [accepted] 2023/09/06 00:41 [medline] 2023/09/06 00:41 [pubmed] 2023/09/05 21:13 [entrez]
 2022/10/19 00:00 [received] 2022/11/21 00:00 [accepted] 2023/04/03 06:41 [medline] 2022/12/23 06:00 [pubmed] 2022/12/22 06:54 [entrez]
 2023/02/25 00:00 [received] 2023/03/30 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:09 [entrez]
 2022/10/18 00:00 [received] 2023/03/14 00:00 [revised] 2023/03/31 00:00 [accepted] 2023/07/31 06:42 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 19:25 [entrez]
 2022/10/10 00:00 [accepted] 2022/10/27 06:00 [pubmed] 2023/01/14 06:00 [medline] 2022/10/26 11:21 [entrez]
 2023/02/08 00:00 [received] 2023/03/01 00:00 [revised] 2023/03/03 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:18 [entrez] 2023/03/30 06:00 [pubmed]
 2024/01/01 00:00 [pmc-release] 2023/01/17 09:32 [entrez] 2023/01/18 06:00 [pubmed] 2023/01/20 06:00 [medline]
 2022/10/14 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/28 00:00 [accepted] 2023/02/23 06:00 [pubmed] 2023/03/10 06:00 [medline] 2023/02/22 09:02 [entrez]
 2023/07/27 00:00 [received] 2023/07/28 00:00 [accepted] 2023/08/24 06:43 [medline] 2023/08/24 06:42 [pubmed] 2023/08/24 04:11 [entrez]
 2023/03/24 00:00 [revised] 2022/10/12 00:00 [received] 2023/03/29 00:00 [accepted] 2023/06/06 06:42 [medline] 2023/04/09 06:00 [pubmed] 2023/04/08 09:52 [entrez]

 2023/07/10 00:00 [received] 2023/07/22 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/08/26 10:48 [medline] 2023/08/26 10:47 [pubmed] 2023/08/26 01:28 [entrez]
 2022/08/08 00:00 [received] 2022/10/24 00:00 [revised] 2022/12/01 00:00 [revised] 2022/12/05 00:00 [accepted] 2023/03/27 03:37 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2023/02/15 00:00 [received] 2023/03/13 00:00 [accepted] 2023/04/18 06:01 [medline] 2023/04/17 03:39 [entrez] 2023/04/18 06:00 [pubmed]
 2023/04/14 06:41 [medline] 2023/04/13 05:23 [entrez] 2023/04/14 06:00 [pubmed]
 2023/03/29 06:05 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 04:12 [entrez]
 2022/09/08 00:00 [received] 2023/03/11 00:00 [revised] 2023/04/18 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/06/06 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 18:04 [entrez]
 2022/06/16 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/10 06:43 [medline] 2023/08/09 01:05 [pubmed] 2023/08/08 23:16 [entrez]
 2022/07/20 00:00 [received] 2022/09/13 00:00 [revised] 2022/10/27 00:00 [accepted] 2022/11/15 06:00 [pubmed] 2022/11/30 06:00 [medline] 2022/11/14 18:20 [entrez]
 2023/06/30 00:00 [revised] 2023/05/16 00:00 [received] 2023/07/06 00:00 [accepted] 2023/09/08 06:43 [medline] 2023/07/12 01:07 [pubmed] 2023/07/11 20:43 [entrez]
 2023/05/05 00:00 [received] 2023/05/18 00:00 [revised] 2023/05/22 00:00 [accepted] 2023/06/10 15:14 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:03 [entrez]
 2024/02/14 00:00 [pmc-release] 2023/08/28 07:16 [medline] 2023/08/14 18:42 [pubmed] 2023/08/14 15:13 [entrez]
 2023/04/19 00:00 [revised] 2022/11/17 00:00 [received] 2023/05/09 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/12 07:06 [pubmed] 2023/05/12 05:29 [entrez]
 2023/07/25 06:43 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 22:43 [entrez]
 2023/02/03 00:00 [received] 2023/05/29 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/06/08 01:08 [pubmed] 2023/06/07 23:30 [entrez]
 2023/03/07 00:00 [revised] 2022/07/26 00:00 [received] 2023/03/20 00:00 [accepted] 2023/05/18 06:42 [medline] 2023/05/15 19:12 [pubmed] 2023/05/15 14:12 [entrez]
 2023/01/13 00:00 [received] 2023/04/25 00:00 [accepted] 2023/04/20 00:00 [revised] 2023/05/08 10:17 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 23:14 [entrez]
 2023/02/27 00:00 [received] 2023/04/05 00:00 [accepted] 2023/04/04 00:00 [revised] 2023/06/16 06:42 [medline] 2023/04/14 06:00 [pubmed] 2023/04/13 11:14 [entrez]
 2022/09/19 00:00 [received] 2023/01/24 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline] 2023/03/16 02:14 [entrez]
 2023/02/10 00:00 [revised] 2022/11/09 00:00 [received] 2023/03/07 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 08:03 [entrez]
 2022/10/14 00:00 [received] 2023/01/14 00:00 [accepted] 2023/02/13 03:15 [entrez] 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline]
 2022/04/08 00:00 [received] 2022/06/27 00:00 [revised] 2023/02/02 11:35 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/07 06:00 [medline]
 2023/02/03 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/02/02 00:13 [entrez]
 2022/12/23 00:00 [received] 2023/01/05 00:00 [revised] 2023/01/07 00:00 [accepted] 2023/01/21 01:50 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2022/08/25 00:00 [received] 2022/10/24 00:00 [revised] 2022/12/18 00:00 [accepted] 2023/01/07 06:00 [pubmed] 2023/03/07 06:00 [medline] 2023/01/06 18:13 [entrez]
 2022/12/27 06:13 [entrez] 2022/12/28 06:00 [pubmed] 2022/12/29 06:00 [medline]
 2021/05/14 06:00 [pubmed] 2023/01/26 06:00 [medline] 2021/05/13 20:08 [entrez]
 2023/03/09 00:00 [received] 2023/06/21 00:00 [revised] 2023/07/24 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/09/06 06:42 [pubmed] 2023/09/06 03:35 [entrez]
 2023/09/15 00:42 [medline] 2023/09/15 00:42 [pubmed] 2023/03/29 00:00 [received] 2023/09/05 00:00 [accepted] 2023/08/21 00:00 [revised] 2023/09/14 23:15 [entrez]
 2022/11/10 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/14 00:42 [pubmed] 2023/08/13 18:40 [entrez]
 2023/06/27 00:00 [revised] 2023/05/26 00:00 [received] 2023/07/03 00:00 [accepted] 2023/08/18 06:42 [medline] 2023/07/26 06:43 [pubmed] 2023/07/26 05:27 [entrez]
 2023/03/12 00:00 [received] 2023/06/12 00:00 [accepted] 2023/07/13 19:16 [medline] 2023/07/13 19:15 [pubmed] 2023/07/13 15:23 [entrez]
 2023/02/19 00:00 [received] 2023/06/27 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/07/09 01:07 [pubmed] 2023/07/08 18:02 [entrez]
 2022/09/16 00:00 [received] 2023/06/12 00:00 [accepted] 2023/06/07 00:00 [revised] 2023/07/03 06:41 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 23:15 [entrez]
 2022/10/19 00:00 [received] 2023/06/02 00:00 [accepted] 2023/06/20 06:42 [medline] 2023/06/20 06:41 [pubmed] 2023/06/20 02:29 [entrez]
 2023/03/15 00:00 [received] 2023/06/13 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/06/18 01:07 [pubmed] 2023/06/17 23:22 [entrez]
 2023/04/09 00:00 [received] 2023/05/25 00:00 [accepted] 2023/06/16 13:11 [medline] 2023/06/16 13:10 [pubmed] 2023/06/16 11:22 [entrez]
 2023/04/14 00:00 [revised] 2022/12/14 00:00 [received] 2023/05/04 00:00 [accepted] 2023/07/19 06:43 [medline] 2023/05/26 13:09 [pubmed] 2023/05/26 08:03 [entrez]
 2020/08/24 00:00 [received] 2021/06/22 00:00 [revised] 2021/06/29 00:00 [accepted] 2023/05/17 01:08 [medline] 2023/05/17 01:07 [pubmed] 2023/05/16 21:18 [entrez]
 2023/03/27 00:00 [revised] 2022/11/21 00:00 [received] 2023/04/12 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 13:42 [pubmed] 2023/05/08 07:04 [entrez]
 2022/10/16 00:00 [received] 2023/04/05 00:00 [accepted] 2023/05/08 06:41 [medline] 2023/05/05 06:42 [pubmed] 2023/05/05 03:49 [entrez]
 2022/09/22 00:00 [received] 2023/04/19 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/30 00:42 [pubmed] 2023/04/29 23:14 [entrez]
 2022/10/19 00:00 [received] 2023/04/04 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/04/14 23:36 [entrez] 2023/04/15 06:00 [pubmed]
 2022/06/16 00:00 [received] 2023/03/15 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:09 [entrez] 2023/04/04 06:00 [pubmed]
 2022/11/06 00:00 [received] 2023/01/03 00:00 [accepted] 2023/03/10 06:00 [pubmed] 2023/03/10 06:01 [medline] 2023/03/09 02:11 [entrez]
 2022/12/30 00:00 [received] 2023/02/01 00:00 [revised] 2023/02/02 00:00 [accepted] 2023/02/25 02:38 [entrez] 2023/02/26 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2023/02/24 02:58 [entrez] 2023/02/25 06:00 [pubmed] 2023/02/25 06:01 [medline]
 2022/02/15 00:00 [received] 2022/05/26 00:00 [accepted] 2022/08/26 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/08/25 11:24 [entrez]
 2023/05/24 00:00 [received] 2023/08/28 00:00 [revised] 2023/09/08 00:00 [accepted] 2023/09/14 18:43 [medline] 2023/09/14 18:43 [pubmed] 2023/09/14 14:53 [entrez]
 2023/08/03 13:09 [medline] 2023/08/03 13:09 [pubmed] 2023/08/03 11:13 [entrez]
 2023/06/24 00:00 [received] 2023/07/19 00:00 [revised] 2023/07/19 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/07/28 01:08 [pubmed] 2023/07/27 18:08 [entrez]
 2023/03/19 00:00 [received] 2023/05/26 00:00 [revised] 2023/06/12 00:00 [accepted] 2023/07/07 01:05 [pubmed] 2023/07/07 01:05 [medline] 2023/07/06 19:29 [entrez]
 2023/07/03 06:41 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 07:22 [entrez]
 2023/04/04 00:00 [accepted] 2023/06/12 06:42 [medline] 2023/05/20 19:13 [pubmed] 2023/05/20 14:59 [entrez]
 2022/04/28 00:00 [received] 2023/03/30 00:00 [accepted] 2023/04/20 06:41 [medline] 2023/04/19 06:41 [pubmed] 2023/04/19 00:01 [entrez]
 2022/10/06 00:00 [received] 2023/03/31 00:00 [accepted] 2023/04/17 06:41 [medline] 2023/04/13 14:04 [entrez] 2023/04/14 06:00 [pubmed]
 2022/09/13 00:00 [received] 2023/02/08 00:00 [accepted] 2023/07/19 06:42 [medline] 2023/04/12 06:00 [pubmed] 2023/04/11 09:33 [entrez]
 2023/01/29 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/05/01 06:41 [medline] 2023/04/11 06:00 [pubmed] 2023/04/10 19:24 [entrez]
 2022/12/24 00:00 [received] 2023/02/27 00:00 [revised] 2023/02/28 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:50 [entrez] 2023/03/30 06:00 [pubmed]
 2022/12/28 00:00 [received] 2023/01/28 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/02/11 01:24 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2022/08/26 00:00 [received] 2022/12/14 00:00 [accepted] 2022/12/26 06:00 [pubmed] 2023/03/08 06:00 [medline] 2022/12/25 23:17 [entrez]
 2023/05/05 06:42 [medline] 2022/12/02 06:00 [pubmed] 2022/12/01 01:23 [entrez]
 2022/07/06 00:00 [received] 2023/07/12 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/04 00:41 [medline] 2023/09/04 00:41 [pubmed] 2023/09/03 18:11 [entrez]
 2023/08/31 06:41 [medline] 2023/08/29 06:43 [pubmed] 2023/08/29 00:43 [entrez]
 2023/04/03 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/13 00:00 [accepted] 2023/08/01 06:45 [medline] 2023/06/23 01:10 [pubmed] 2023/06/22 19:17 [entrez]
 2023/04/14 00:00 [received] 2023/04/28 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/10 15:13 [pubmed] 2023/06/10 01:13 [entrez]
 2023/04/09 00:00 [revised] 2022/12/10 00:00 [received] 2023/04/21 00:00 [accepted] 2023/07/25 06:43 [medline] 2023/05/15 06:42 [pubmed] 2023/05/15 01:02 [entrez]
 2023/04/11 06:01 [medline] 2023/04/10 04:11 [entrez] 2023/04/11 06:00 [pubmed]
 2022/12/01 00:00 [received] 2023/01/25 00:00 [accepted] 2023/03/06 03:41 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/02/08 06:00 [pubmed] 2023/02/10 06:00 [medline] 2023/02/07 10:07 [entrez]
 2023/01/05 06:00 [pubmed] 2023/01/31 06:00 [medline] 2023/01/04 12:02 [entrez]
 2022/06/10 00:00 [received] 2022/09/27 00:00 [revised] 2022/10/17 00:00 [accepted] 2022/10/23 06:00 [pubmed] 2022/12/06 06:00 [medline] 2022/10/22 19:23 [entrez]
 2023/07/25 00:00 [revised] 2023/06/19 00:00 [received] 2023/08/24 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 00:03 [entrez]
 2022/08/17 00:00 [received] 2023/03/27 00:00 [accepted] 2023/06/02 06:42 [medline] 2023/06/01 01:08 [pubmed] 2023/05/31 22:04 [entrez]
 2024/04/01 00:00 [pmc-release] 2023/04/13 06:42 [medline] 2023/04/12 08:43 [entrez] 2023/04/13 06:00 [pubmed]
 2022/05/09 00:00 [received] 2022/10/14 00:00 [accepted] 2022/12/01 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/30 21:41 [entrez]
 2023/07/27 00:00 [revised] 2023/05/25 00:00 [received] 2023/07/31 00:00 [accepted] 2023/08/11 12:42 [medline] 2023/08/11 12:42 [pubmed] 2023/08/11 10:43 [entrez]
 2023/07/31 06:43 [medline] 2023/07/29 11:45 [pubmed] 2023/07/29 02:43 [entrez]
 2022/10/28 00:00 [revised] 2022/03/15 00:00 [received] 2022/12/01 00:00 [accepted] 2023/01/11 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/10 10:08 [entrez]
 2022/10/21 00:00 [revised] 2022/04/14 00:00 [received] 2022/10/26 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/11/17 13:34 [entrez]
 2023/03/02 00:00 [received] 2023/03/27 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/04/21 00:42 [pubmed] 2023/04/20 18:05 [entrez]
 2022/09/01 00:00 [revised] 2022/05/30 00:00 [received] 2022/09/19 00:00 [accepted] 2022/10/20 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/10/19 02:22 [entrez]
 2023/02/23 09:59 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2023/01/31 23:40 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/01 06:01 [medline]
 2023/06/28 06:42 [medline] 2023/06/02 06:42 [pubmed] 2023/06/02 05:28 [entrez]
 2023/04/27 06:42 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 09:03 [entrez]
 2023/05/16 00:00 [received] 2023/08/17 00:00 [revised] 2023/08/19 00:00 [accepted] 2023/09/06 06:42 [medline] 2023/08/25 00:41 [pubmed] 2023/08/24 19:26 [entrez]
 2022/12/02 00:00 [received] 2023/01/26 00:00 [accepted] 2023/03/06 03:41 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/06/24 00:00 [received] 2023/07/28 00:00 [accepted] 2023/07/27 00:00 [revised] 2023/08/13 18:41 [medline] 2023/08/13 18:41 [pubmed] 2023/08/13 14:51 [entrez]
 2023/04/27 00:00 [received] 2023/06/05 00:00 [revised] 2023/06/07 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:34 [entrez]
 2023/04/24 00:00 [received] 2023/05/30 00:00 [accepted] 2023/06/23 13:07 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 11:16 [entrez]
 2023/03/07 00:00 [received] 2023/05/12 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/08/01 06:45 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 19:24 [entrez]
 2022/12/12 00:00 [received] 2023/02/15 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/05/15 19:12 [pubmed] 2023/05/15 13:17 [entrez]
 2023/02/04 00:00 [received] 2023/03/25 00:00 [revised] 2023/03/28 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:35 [entrez]
 2022/08/15 00:00 [received] 2022/12/16 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/03/04 06:00 [medline] 2023/01/26 19:22 [entrez]
 2022/10/17 00:00 [received] 2022/12/01 00:00 [accepted] 2023/01/04 06:00 [pubmed] 2023/02/02 06:00 [medline] 2023/01/03 11:22 [entrez]
 2022/09/16 00:00 [revised] 2022/07/27 00:00 [received] 2022/09/20 00:00 [accepted] 2023/04/04 06:42 [medline] 2022/10/27 06:00 [pubmed] 2022/10/26 06:03 [entrez]
 2022/12/05 00:00 [received] 2023/03/08 00:00 [revised] 2023/03/27 00:00 [accepted] 2023/06/26 06:41 [medline] 2023/06/24 11:42 [pubmed] 2023/06/23 20:57 [entrez]
 2023/07/31 06:42 [medline] 2023/07/27 19:10 [pubmed] 2023/07/27 14:33 [entrez]
 2023/07/01 00:00 [received] 2023/07/06 00:00 [accepted] 2023/07/06 00:00 [revised] 2023/08/11 06:43 [medline] 2023/07/15 21:06 [pubmed] 2023/07/15 11:02 [entrez]
 2023/01/20 00:00 [received] 2023/04/21 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/20 06:42 [medline] 2023/06/19 06:42 [pubmed] 2023/06/19 02:38 [entrez]
 2023/04/20 00:00 [revised] 2022/12/12 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/01 13:10 [medline] 2023/06/01 13:10 [pubmed] 2023/06/01 06:23 [entrez]
 2022/11/16 00:00 [received] 2023/04/26 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/05/15 06:42 [pubmed] 2023/05/15 04:12 [entrez]
 2022/10/16 00:00 [received] 2023/01/15 00:00 [revised] 2023/01/15 00:00 [accepted] 2023/01/21 06:00 [pubmed] 2023/02/09 06:00 [medline] 2023/01/20 19:25 [entrez]
 2022/07/19 00:00 [received] 2022/12/14 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/16 03:04 [entrez] 2023/01/17 06:00 [pubmed] 2023/01/18 06:00 [medline]
 2022/09/21 00:00 [received] 2022/12/09 00:00 [accepted] 2022/12/21 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/12/20 11:04 [entrez]
 2023/07/09 00:00 [received] 2023/07/09 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 04:46 [entrez]
 2023/07/27 00:00 [received] 2023/08/07 00:00 [revised] 2023/08/08 00:00 [accepted] 2023/08/28 07:16 [medline] 2023/08/26 10:44 [pubmed] 2023/08/26 01:14 [entrez]
 2023/08/23 06:42 [medline] 2023/08/22 13:42 [pubmed] 2023/08/22 07:27 [entrez]
 2023/07/07 00:00 [received] 2023/08/05 00:00 [revised] 2023/08/06 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/14 00:42 [pubmed] 2023/08/13 18:40 [entrez]
 2023/06/18 00:00 [received] 2023/06/21 00:00 [revised] 2023/06/25 00:00 [accepted] 2023/08/10 06:44 [medline] 2023/08/10 06:43 [pubmed] 2023/08/10 04:01 [entrez]
 2023/06/30 00:00 [received] 2023/07/18 00:00 [revised] 2023/07/20 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/29 11:49 [pubmed] 2023/07/29 01:24 [entrez]
 2023/01/30 00:00 [received] 2023/07/06 00:00 [accepted] 2023/07/04 00:00 [revised] 2023/07/15 21:06 [medline] 2023/07/15 21:06 [pubmed] 2023/07/15 11:13 [entrez]
 2023/05/10 00:00 [accepted] 2023/06/14 06:43 [medline] 2023/06/14 06:42 [pubmed] 2023/06/14 03:51 [entrez]
 2023/02/07 00:00 [received] 2023/03/12 00:00 [revised] 2023/03/18 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 17:59 [entrez]

 2023/01/28 07:33 [entrez] 2023/01/29 06:00 [pubmed] 2023/02/01 06:00 [medline]
 2023/04/24 06:41 [medline] 2022/12/22 06:00 [pubmed] 2022/12/21 02:23 [entrez]
 2022/10/03 00:00 [received] 2022/11/16 00:00 [accepted] 2022/11/22 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/11/21 19:34 [entrez]
 2022/11/16 06:00 [pubmed] 2022/12/24 06:00 [medline] 2022/11/15 14:04 [entrez]
 2023/03/08 00:00 [received] 2023/07/25 00:00 [accepted] 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:45 [entrez]
 2023/06/08 00:00 [received] 2023/07/24 00:00 [revised] 2023/08/02 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/08/12 10:51 [pubmed] 2023/08/12 01:24 [entrez]
 2023/02/13 00:00 [received] 2023/05/15 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/06/02 01:07 [pubmed] 2023/06/01 23:39 [entrez]
 2023/02/10 00:00 [received] 2023/04/14 00:00 [accepted] 2023/05/18 06:42 [medline] 2023/05/17 01:07 [pubmed] 2023/05/16 21:03 [entrez]
 2023/05/29 06:42 [medline] 2023/05/04 12:41 [pubmed] 2023/05/04 09:05 [entrez]
 2023/03/02 00:00 [received] 2023/04/04 00:00 [revised] 2023/04/11 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:17 [entrez]
 2022/12/14 00:00 [received] 2023/03/26 00:00 [accepted] 2023/04/19 06:41 [medline] 2023/04/04 06:00 [pubmed] 2023/04/03 06:13 [entrez]
 2023/02/09 00:00 [received] 2023/03/17 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/04/10 06:42 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 20:26 [entrez]
 2023/03/31 06:42 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 00:39 [entrez]
 2022/05/06 00:00 [received] 2023/01/24 00:00 [accepted] 2023/01/19 00:00 [revised] 2023/05/11 06:42 [medline] 2023/02/09 06:00 [pubmed] 2023/02/08 23:30 [entrez]
 2022/12/21 00:00 [revised] 2022/08/22 00:00 [received] 2023/01/16 00:00 [accepted] 2023/01/26 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/01/25 10:23 [entrez]
 2022/12/07 00:00 [revised] 2022/09/21 00:00 [received] 2023/01/06 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 23:27 [entrez]
 2022/01/10 00:00 [received] 2022/12/09 00:00 [revised] 2022/12/16 00:00 [accepted] 2023/01/01 06:00 [pubmed] 2023/03/08 06:00 [medline] 2022/12/31 18:03 [entrez]
 2022/11/01 00:00 [received] 2022/12/06 00:00 [revised] 2022/12/12 00:00 [accepted] 2024/01/01 00:00 [pmc-release] 2022/12/18 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/12/17 19:24 [entrez]
 2022/08/08 00:00 [received] 2022/10/26 00:00 [revised] 2022/10/29 00:00 [accepted] 2022/11/12 06:00 [pubmed] 2022/11/30 06:00 [medline] 2022/11/11 18:21 [entrez]
 2023/03/08 00:00 [received] 2023/05/02 00:00 [accepted] 2023/09/14 06:42 [medline] 2023/06/06 13:09 [pubmed] 2023/06/06 10:53 [entrez]
 2023/01/21 00:00 [received] 2023/03/19 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/28 23:40 [entrez] 2023/03/29 06:00 [pubmed]
 2023/06/02 06:42 [medline] 2023/04/25 00:41 [pubmed] 2023/04/24 11:25 [entrez]
 2023/02/13 00:00 [received] 2023/03/31 00:00 [revised] 2023/05/01 00:00 [accepted] 2023/05/26 19:15 [medline] 2023/05/26 19:14 [pubmed] 2023/05/26 12:21 [entrez]
 2022/10/28 00:00 [received] 2023/01/10 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/23 19:22 [entrez]
 2023/02/28 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:26 [entrez] 2023/04/04 06:00 [pubmed]
 2023/08/16 00:42 [medline] 2023/08/16 00:42 [pubmed] 2023/08/15 21:13 [entrez]
 2023/02/18 00:00 [received] 2023/03/26 00:00 [revised] 2023/05/14 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 18:02 [entrez]
 2022/08/25 00:00 [received] 2022/11/02 00:00 [revised] 2022/12/12 00:00 [accepted] 2023/01/12 01:56 [entrez] 2023/01/13 06:00 [pubmed] 2023/01/13 06:01 [medline]
 2022/11/29 00:00 [received] 2023/02/28 00:00 [revised] 2023/03/09 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/05/19 06:42 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 18:00 [entrez]
 2022/06/08 00:00 [received] 2022/10/27 00:00 [accepted] 2022/12/15 06:00 [pubmed] 2023/02/03 06:00 [medline] 2022/12/14 12:12 [entrez]
 2022/08/07 00:00 [received] 2022/10/30 00:00 [revised] 2022/11/01 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/02/04 06:00 [medline] 2022/12/08 23:25 [entrez]
 2023/06/28 13:09 [medline] 2023/06/28 13:09 [pubmed] 2023/06/28 09:32 [entrez]
 2022/09/06 00:00 [received] 2023/06/28 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/09/12 06:42 [medline] 2023/09/11 06:43 [pubmed] 2023/09/11 04:28 [entrez]
 2022/10/25 00:00 [received] 2023/03/11 00:00 [revised] 2023/03/27 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/07/17 00:41 [pubmed] 2023/07/16 18:52 [entrez]
 2022/09/05 00:00 [received] 2022/09/24 00:00 [revised] 2022/09/27 00:00 [accepted] 2022/12/29 20:33 [entrez] 2022/12/30 06:00 [pubmed] 2023/01/03 06:00 [medline]
 2023/05/17 00:00 [received] 2023/07/20 00:00 [revised] 2023/08/28 00:00 [accepted] 2023/09/04 00:41 [medline] 2023/09/04 00:41 [pubmed] 2023/09/03 18:03 [entrez]
 2023/08/14 00:00 [revised] 2023/04/06 00:00 [received] 2023/08/15 00:00 [accepted] 2023/09/01 06:42 [medline] 2023/09/01 06:42 [pubmed] 2023/09/01 04:33 [entrez]
 2022/08/01 00:00 [received] 2023/07/25 00:00 [accepted] 2023/08/29 12:44 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 04:54 [entrez]
 2023/05/30 00:00 [received] 2023/06/26 00:00 [revised] 2023/06/29 00:00 [accepted] 2023/07/29 11:54 [medline] 2023/07/29 11:53 [pubmed] 2023/07/29 01:38 [entrez]
 2023/02/22 00:00 [received] 2023/04/23 00:00 [accepted] 2023/05/25 19:13 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 14:10 [entrez]
 2023/02/27 00:00 [received] 2023/04/14 00:00 [revised] 2023/04/15 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:28 [entrez]
 2022/12/02 00:00 [received] 2023/02/19 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/04/03 06:00 [pubmed] 2023/04/02 18:57 [entrez]
 2022/11/17 00:00 [received] 2023/02/05 00:00 [accepted] 2023/02/17 00:00 [entrez] 2023/02/18 06:00 [pubmed] 2023/02/18 06:01 [medline]
 2022/07/19 00:00 [received] 2023/01/03 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/01/31 06:00 [pubmed] 2023/01/30 11:23 [entrez]
 2022/12/08 00:00 [received] 2023/01/18 00:00 [revised] 2023/01/21 00:00 [accepted] 2023/01/30 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/29 18:06 [entrez]
 2022/09/26 00:00 [revised] 2022/08/09 00:00 [received] 2022/10/10 00:00 [accepted] 2022/10/19 06:00 [pubmed] 2022/12/17 06:00 [medline] 2022/10/18 12:13 [entrez]
 2021/07/18 00:00 [received] 2022/03/04 00:00 [accepted] 2022/06/10 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/06/09 21:41 [entrez]
 2022/02/15 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/02/14 08:53 [entrez]
 2023/02/11 00:00 [received] 2023/06/06 00:00 [accepted] 2023/09/12 00:42 [medline] 2023/09/12 00:42 [pubmed] 2023/09/11 23:41 [entrez]
 2023/02/08 00:00 [received] 2023/07/27 00:00 [revised] 2023/08/03 00:00 [accepted] 2023/09/10 00:42 [medline] 2023/09/10 00:42 [pubmed] 2023/09/09 18:00 [entrez]
 2023/05/07 00:00 [received] 2023/07/25 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/11 00:42 [medline] 2023/08/11 00:42 [pubmed] 2023/08/10 18:06 [entrez]
 2023/07/04 00:00 [received] 2023/07/28 00:00 [accepted] 2023/07/18 00:00 [revised] 2023/08/10 00:43 [medline] 2023/08/10 00:42 [pubmed] 2023/08/09 23:17 [entrez]
 2022/07/16 00:00 [received] 2023/04/27 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 01:06 [pubmed] 2023/06/27 23:34 [entrez]
 2022/11/11 00:00 [received] 2023/03/06 00:00 [accepted] 2023/03/28 19:06 [medline] 2023/03/25 23:26 [entrez] 2023/03/26 06:00 [pubmed]
 2023/02/28 12:33 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/10/10 00:00 [revised] 2022/06/16 00:00 [received] 2022/11/15 00:00 [accepted] 2022/11/25 06:00 [pubmed] 2023/02/14 06:00 [medline] 2022/11/24 00:22 [entrez]
 2023/02/27 00:00 [received] 2023/07/26 00:00 [accepted] 2023/07/23 00:00 [revised] 2023/08/05 05:42 [medline] 2023/08/05 05:42 [pubmed] 2023/08/04 23:26 [entrez]
 2023/02/20 00:00 [received] 2023/06/10 00:00 [accepted] 2023/07/05 06:42 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:38 [entrez]
 2023/03/01 00:00 [received] 2023/05/26 00:00 [accepted] 2023/05/23 00:00 [revised] 2023/06/16 13:10 [medline] 2023/06/16 13:10 [pubmed] 2023/06/16 11:13 [entrez]
 2023/06/08 06:43 [medline] 2023/06/08 06:42 [pubmed] 2023/06/08 04:18 [entrez]
 2023/04/18 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:14 [entrez]
 2023/04/21 00:00 [revised] 2023/01/05 00:00 [received] 2023/05/09 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/12 07:06 [pubmed] 2023/05/12 04:43 [entrez]
 2022/09/12 00:00 [received] 2023/03/11 00:00 [accepted] 2023/03/28 19:05 [medline] 2023/03/25 23:24 [entrez] 2023/03/26 06:00 [pubmed]
 2022/12/29 00:00 [received] 2023/01/22 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/02/28 01:31 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/01 06:01 [medline]
 2022/01/29 00:00 [received] 2023/02/12 00:00 [accepted] 2023/02/14 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/02/13 08:52 [entrez]
 2023/04/28 06:41 [medline] 2023/02/09 06:00 [pubmed] 2023/02/08 11:16 [entrez]
 2022/11/23 00:00 [revised] 2021/10/26 00:00 [received] 2022/12/16 00:00 [accepted] 2024/01/12 00:00 [pmc-release] 2023/01/13 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/12 06:13 [entrez]
 2022/11/14 00:00 [accepted] 2023/01/03 06:00 [pubmed] 2023/01/17 06:00 [medline] 2023/01/02 11:20 [entrez]
 2022/09/15 00:00 [received] 2022/10/20 00:00 [accepted] 2023/04/12 06:42 [medline] 2022/11/03 06:00 [pubmed] 2022/11/02 00:26 [entrez]
 2022/09/28 06:00 [pubmed] 2023/01/05 06:00 [medline] 2022/09/27 07:12 [entrez]
 2023/06/14 00:00 [received] 2023/07/22 00:00 [revised] 2023/08/09 00:00 [accepted] 2023/08/13 00:43 [pubmed] 2023/08/13 00:43 [medline] 2023/08/12 19:25 [entrez]
 2023/06/29 00:00 [revised] 2023/04/21 00:00 [received] 2023/07/03 00:00 [accepted] 2023/07/15 11:42 [medline] 2023/07/15 11:42 [pubmed] 2023/07/15 03:42 [entrez]
 2023/05/10 12:43 [medline] 2023/05/10 12:42 [pubmed] 2023/05/10 11:21 [entrez]
 2023/04/09 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/08/28 06:42 [medline] 2023/05/03 12:42 [pubmed] 2023/05/03 11:09 [entrez]
 2023/02/01 00:00 [received] 2023/03/11 00:00 [revised] 2023/03/23 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 18:00 [entrez]
 2022/11/17 00:00 [received] 2023/01/12 00:00 [revised] 2023/01/12 00:00 [accepted] 2023/02/25 01:07 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2024/01/01 00:00 [pmc-release] 2023/02/23 10:35 [entrez] 2023/02/24 06:00 [pubmed] 2023/02/24 06:01 [medline]
 2022/09/30 00:00 [received] 2023/02/05 00:00 [revised] 2023/02/13 00:00 [accepted] 2023/04/18 10:16 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 10:06 [entrez]
 2022/08/01 00:00 [received] 2023/01/24 00:00 [accepted] 2023/02/04 00:02 [entrez] 2023/02/05 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2022/05/20 00:00 [received] 2022/12/28 00:00 [accepted] 2023/02/02 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/02/01 18:23 [entrez]
 2021/10/20 00:00 [received] 2022/11/27 00:00 [revised] 2023/01/04 00:00 [accepted] 2023/01/23 06:00 [pubmed] 2023/02/22 06:00 [medline] 2023/01/22 18:05 [entrez]
 2022/11/08 00:00 [received] 2022/12/24 00:00 [revised] 2023/01/03 00:00 [accepted] 2023/05/08 10:17 [medline] 2023/01/10 06:00 [pubmed] 2023/01/09 07:43 [entrez]
 2022/06/30 00:00 [received] 2022/09/14 00:00 [accepted] 2023/06/26 06:41 [medline] 2022/10/12 06:00 [pubmed] 2022/10/11 11:24 [entrez]
 2022/07/06 00:00 [revised] 2022/03/09 00:00 [received] 2022/07/08 00:00 [accepted] 2022/08/23 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/08/22 07:33 [entrez]
 2022/07/01 00:00 [received] 2022/10/18 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2023/03/09 06:00 [medline] 2022/11/17 09:54 [entrez]

 2023/03/21 02:05 [entrez] 2023/03/22 06:00 [pubmed] 2023/03/22 06:01 [medline]
 2022/05/17 00:00 [received] 2022/11/28 00:00 [revised] 2022/12/08 00:00 [accepted] 2023/03/23 02:26 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/24 06:01 [medline]
 2023/05/19 00:00 [received] 2023/07/21 06:44 [medline] 2023/07/19 06:42 [pubmed] 2023/07/19 03:44 [entrez]

 2023/07/19 06:43 [medline] 2023/06/20 13:10 [pubmed] 2023/06/20 11:22 [entrez]
 2022/05/31 00:00 [received] 2022/11/08 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/04/18 06:01 [medline] 2023/04/17 03:45 [entrez] 2023/04/18 06:00 [pubmed]
 2022/11/06 00:00 [received] 2023/03/15 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 23:37 [entrez]
 2023/12/27 00:00 [pmc-release] 2022/12/28 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/12/27 11:33 [entrez]
 2023/02/28 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 11:15 [entrez]
 2022/11/17 00:00 [received] 2023/02/06 00:00 [accepted] 2023/03/10 02:32 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]

 2023/01/03 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/02 15:13 [entrez]
 2022/10/13 00:00 [received] 2022/12/22 00:00 [accepted] 2023/02/27 05:22 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2022/11/10 00:00 [received] 2023/02/21 00:00 [revised] 2023/02/24 00:00 [accepted] 2023/04/11 06:42 [medline] 2023/03/16 06:00 [pubmed] 2023/03/15 19:16 [entrez]
 2023/04/18 06:01 [medline] 2023/04/17 04:01 [entrez] 2023/04/18 06:00 [pubmed]
 2023/03/09 00:00 [received] 2023/07/17 00:00 [accepted] 2023/07/20 13:07 [medline] 2023/07/20 13:07 [pubmed] 2023/07/20 11:10 [entrez]
 2022/10/12 00:00 [received] 2022/12/24 00:00 [revised] 2022/12/28 00:00 [accepted] 2023/01/31 07:12 [entrez] 2023/02/01 06:00 [pubmed] 2023/02/02 06:00 [medline]
 2022/10/10 00:00 [received] 2023/01/26 00:00 [accepted] 2024/07/11 00:00 [pmc-release] 2023/07/12 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 21:12 [entrez]
 2022/02/01 00:00 [received] 2022/03/06 00:00 [accepted] 2022/03/21 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/03/20 20:26 [entrez]
 2022/12/08 00:00 [received] 2023/03/13 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/06/02 06:43 [medline] 2023/04/11 06:00 [pubmed] 2023/04/10 18:00 [entrez]
 2022/07/22 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/02/15 02:11 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/16 06:01 [medline]
 2023/06/02 00:00 [received] 2023/07/20 00:00 [revised] 2023/07/25 00:00 [accepted] 2023/08/25 12:43 [medline] 2023/08/25 12:42 [pubmed] 2023/08/25 09:53 [entrez]
 2023/06/05 00:00 [revised] 2023/04/23 00:00 [received] 2023/06/08 00:00 [accepted] 2023/06/14 13:07 [pubmed] 2023/06/14 13:07 [medline] 2023/06/14 11:23 [entrez]
 2022/10/25 00:00 [received] 2023/04/05 00:00 [revised] 2023/05/14 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 18:41 [entrez]
 2023/02/12 00:00 [received] 2023/03/19 00:00 [accepted] 2023/04/25 06:43 [medline] 2023/04/25 06:42 [pubmed] 2023/04/25 02:05 [entrez]
 2022/12/21 00:00 [revised] 2022/04/29 00:00 [received] 2023/01/05 00:00 [accepted] 2023/01/31 06:00 [pubmed] 2023/03/08 06:00 [medline] 2023/01/30 06:22 [entrez]
 2022/07/04 00:00 [received] 2022/10/16 00:00 [revised] 2022/12/01 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/02/02 06:00 [medline] 2022/12/15 18:29 [entrez]
 2022/09/12 00:00 [accepted] 2022/10/22 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/10/21 23:59 [entrez]
 2023/04/18 00:00 [received] 2023/07/03 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 04:54 [entrez]
 2023/06/08 06:42 [medline] 2023/05/24 13:08 [pubmed] 2023/05/24 06:52 [entrez]
 2023/02/16 00:00 [received] 2023/04/18 00:00 [accepted] 2023/05/12 13:08 [medline] 2023/05/12 13:08 [pubmed] 2023/05/12 11:07 [entrez]
 2023/03/22 00:00 [received] 2023/08/16 00:00 [accepted] 2023/09/01 06:43 [medline] 2023/08/31 00:42 [pubmed] 2023/08/30 23:47 [entrez]
 2023/08/31 06:42 [medline] 2023/08/29 00:41 [pubmed] 2023/08/28 20:53 [entrez]
 2022/11/29 00:00 [received] 2023/04/17 00:00 [accepted] 2023/06/20 01:09 [medline] 2023/06/20 01:09 [pubmed] 2023/06/19 22:59 [entrez]
 2023/03/27 10:12 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2023/02/20 00:00 [revised] 2022/03/22 00:00 [received] 2023/02/28 00:00 [accepted] 2023/05/19 06:42 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 22:42 [entrez]
 2023/07/25 00:00 [revised] 2023/02/04 00:00 [received] 2023/07/26 00:00 [accepted] 2024/09/01 00:00 [pmc-release] 2023/09/01 06:43 [medline] 2023/07/29 11:47 [pubmed] 2023/07/29 03:53 [entrez]
 2023/07/20 00:00 [received] 2023/07/25 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/07/29 06:41 [pubmed] 2023/07/28 23:34 [entrez]
 2023/04/26 00:00 [received] 2023/07/01 00:00 [accepted] 2023/06/26 00:00 [revised] 2023/07/28 13:11 [medline] 2023/07/28 13:11 [pubmed] 2023/07/28 11:07 [entrez]
 2022/12/08 00:00 [received] 2023/04/23 00:00 [revised] 2023/05/20 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/05/28 01:07 [pubmed] 2023/05/27 19:26 [entrez]
 2023/02/07 00:00 [received] 2023/03/22 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/04/13 06:00 [pubmed] 2023/04/12 18:22 [entrez]
 2023/07/05 06:42 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 11:13 [entrez]
 2023/02/27 00:00 [received] 2023/05/30 00:00 [accepted] 2023/06/22 01:07 [medline] 2023/06/22 01:07 [pubmed] 2023/06/21 21:03 [entrez]
 2023/03/28 00:00 [received] 2023/05/21 00:00 [revised] 2023/05/23 00:00 [accepted] 2023/06/20 06:42 [medline] 2023/06/05 00:41 [pubmed] 2023/06/04 18:07 [entrez]
 2023/02/25 00:00 [received] 2023/08/03 00:00 [revised] 2023/08/03 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/08/08 00:42 [pubmed] 2023/08/07 19:12 [entrez]
 2022/12/26 00:00 [received] 2023/02/03 00:00 [accepted] 2023/03/10 02:26 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2023/07/03 06:42 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 16:43 [entrez]
 2023/01/10 00:00 [received] 2023/04/12 00:00 [accepted] 2023/12/01 00:00 [pmc-release] 2023/06/05 06:42 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 18:41 [entrez]
 2023/02/09 00:00 [received] 2023/08/08 00:00 [revised] 2023/08/20 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 05:08 [entrez]
 2024/01/01 00:00 [pmc-release] 2021/06/01 06:00 [pubmed] 2022/12/28 06:00 [medline] 2021/05/31 05:25 [entrez]
 2022/10/10 00:00 [received] 2023/02/07 00:00 [revised] 2023/03/22 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/05/16 13:09 [pubmed] 2023/05/16 10:32 [entrez]
 2023/04/22 00:00 [received] 2023/05/16 00:00 [accepted] 2023/06/24 21:04 [medline] 2023/06/24 21:03 [pubmed] 2023/06/24 11:33 [entrez]
 2022/10/24 00:00 [received] 2022/12/15 00:00 [accepted] 2023/01/10 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/09 04:37 [entrez]
 2022/12/16 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/30 13:07 [pubmed] 2023/05/30 11:36 [entrez]
 2023/01/26 00:00 [revised] 2022/10/23 00:00 [received] 2023/03/06 00:00 [accepted] 2023/03/25 06:00 [pubmed] 2023/03/25 06:00 [medline] 2023/03/24 01:32 [entrez]
 2023/01/27 00:00 [received] 2023/02/12 00:00 [accepted] 2023/05/02 00:43 [medline] 2023/05/02 00:42 [pubmed] 2023/05/01 22:12 [entrez]
 2022/10/05 00:00 [received] 2023/03/07 00:00 [accepted] 2023/03/16 00:56 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/21 06:00 [medline]
 2023/01/31 00:00 [accepted] 2023/03/06 03:59 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2022/08/07 00:00 [received] 2023/01/25 00:00 [accepted] 2023/01/19 00:00 [revised] 2023/02/11 06:00 [pubmed] 2023/02/15 06:00 [medline] 2023/02/10 23:24 [entrez]
 2024/02/01 00:00 [pmc-release] 2022/02/17 06:00 [pubmed] 2023/02/14 06:00 [medline] 2022/02/16 05:34 [entrez]
 2023/01/17 00:00 [received] 2023/02/20 00:00 [revised] 2023/02/27 00:00 [accepted] 2023/04/14 06:42 [medline] 2023/03/03 06:00 [pubmed] 2023/03/02 19:24 [entrez]
 2023/01/20 15:43 [entrez] 2023/01/21 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/09/27 00:00 [received] 2022/11/15 00:00 [revised] 2022/12/12 00:00 [accepted] 2022/12/23 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/12/22 18:15 [entrez]
 2023/08/08 00:00 [revised] 2023/07/17 00:00 [received] 2023/08/09 00:00 [accepted] 2023/09/07 12:42 [medline] 2023/09/07 12:42 [pubmed] 2023/09/07 06:44 [entrez]
 2023/02/27 00:00 [received] 2023/05/18 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 23:25 [entrez]
 2023/02/11 00:00 [received] 2023/05/05 00:00 [accepted] 2023/06/09 06:42 [medline] 2023/06/07 13:10 [pubmed] 2023/06/07 09:37 [entrez]
 2022/09/08 00:00 [received] 2023/02/20 00:00 [revised] 2023/03/05 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 20:27 [entrez]
 2023/05/11 00:00 [received] 2023/07/19 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 23:43 [entrez]
 2021/08/11 00:00 [received] 2022/08/22 00:00 [accepted] 2022/08/28 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/08/27 23:28 [entrez]
 2022/11/01 00:00 [received] 2023/04/23 00:00 [revised] 2023/06/02 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:41 [entrez]
 2021/03/12 00:00 [received] 2023/01/17 00:00 [accepted] 2023/02/25 06:00 [pubmed] 2023/03/16 06:00 [medline] 2023/02/24 00:08 [entrez]
 2023/03/01 00:00 [accepted] 2023/04/05 06:01 [medline] 2023/04/04 01:57 [entrez] 2023/04/05 06:00 [pubmed]
 2022/11/29 00:00 [received] 2023/05/05 00:00 [accepted] 2023/07/19 06:43 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 21:43 [entrez]
 2023/02/01 20:53 [entrez] 2023/02/02 06:00 [pubmed] 2023/02/04 06:00 [medline]
 2023/03/28 00:00 [received] 2023/05/13 00:00 [revised] 2023/05/16 00:00 [accepted] 2023/06/03 11:42 [medline] 2023/06/03 11:42 [pubmed] 2023/06/02 22:01 [entrez]
 2022/12/13 00:00 [received] 2023/01/30 00:00 [revised] 2023/02/01 00:00 [accepted] 2023/02/22 14:39 [entrez] 2023/02/23 06:00 [pubmed] 2023/02/23 06:01 [medline]
 2023/06/05 19:11 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 12:22 [entrez]
 2023/04/05 00:00 [received] 2023/08/14 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/08 00:42 [pubmed] 2023/09/07 23:43 [entrez]
 2022/11/11 00:00 [received] 2023/06/30 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/07/06 01:08 [pubmed] 2023/07/05 23:25 [entrez]
 2023/03/20 00:00 [received] 2023/06/26 00:00 [accepted] 2023/08/16 06:43 [medline] 2023/08/14 06:43 [pubmed] 2023/08/14 04:27 [entrez]
 2023/01/25 00:00 [received] 2023/06/03 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:21 [entrez]
 2023/06/19 13:08 [medline] 2023/05/25 13:07 [pubmed] 2023/05/25 08:53 [entrez]
 2022/12/07 00:00 [received] 2023/02/03 00:00 [accepted] 2023/03/10 02:35 [entrez] 2023/03/11 06:00 [pubmed] 2023/03/11 06:01 [medline]
 2023/05/22 00:00 [received] 2023/09/05 00:00 [accepted] 2023/09/04 00:00 [revised] 2023/09/13 12:43 [medline] 2023/09/13 12:43 [pubmed] 2023/09/13 11:17 [entrez]
 2022/12/02 00:00 [received] 2023/03/02 00:00 [accepted] 2023/07/24 06:43 [medline] 2023/07/24 06:42 [pubmed] 2023/07/24 04:55 [entrez]
 2022/10/28 00:00 [received] 2023/07/04 00:00 [revised] 2023/07/27 00:00 [accepted] 2023/08/14 06:44 [medline] 2023/08/14 06:43 [pubmed] 2023/08/14 04:58 [entrez]
 2023/07/20 00:00 [received] 2023/08/11 00:00 [revised] 2023/08/12 00:00 [accepted] 2023/08/21 00:41 [medline] 2023/08/21 00:41 [pubmed] 2023/08/20 18:02 [entrez]
 2022/04/17 00:00 [received] 2022/06/12 00:00 [revised] 2022/06/16 00:00 [accepted] 2023/03/06 03:38 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2022/11/18 00:00 [received] 2023/04/30 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:22 [entrez]
 2023/02/08 20:33 [entrez] 2023/02/09 06:00 [pubmed] 2023/02/09 06:00 [medline]
 2022/04/11 00:00 [received] 2022/08/24 00:00 [revised] 2022/09/01 00:00 [accepted] 2022/11/12 06:00 [pubmed] 2023/03/11 06:00 [medline] 2022/11/11 02:33 [entrez]
 2023/03/25 00:00 [received] 2023/07/07 00:00 [revised] 2023/07/13 00:00 [accepted] 2023/08/28 06:43 [medline] 2023/07/19 01:06 [pubmed] 2023/07/18 19:12 [entrez]
 2022/04/02 00:00 [received] 2022/07/10 00:00 [accepted] 2023/02/06 04:00 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:01 [medline]
 2022/10/31 00:00 [received] 2022/11/28 00:00 [accepted] 2023/01/05 10:22 [entrez] 2023/01/06 06:00 [pubmed] 2023/01/10 06:00 [medline]
 2023/02/08 00:00 [received] 2023/05/11 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/06/26 00:41 [pubmed] 2023/06/25 19:15 [entrez]
 2023/03/20 00:00 [received] 2023/04/12 00:00 [revised] 2023/04/19 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:30 [entrez]
 2023/05/20 00:00 [received] 2023/06/30 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/07/16 01:07 [medline] 2023/07/16 01:07 [pubmed] 2023/07/15 21:59 [entrez]
 2023/06/12 00:00 [revised] 2022/10/24 00:00 [received] 2023/06/16 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/07/03 13:06 [pubmed] 2023/07/03 06:37 [entrez]
 2023/03/24 00:00 [received] 2023/05/08 00:00 [revised] 2023/05/09 00:00 [accepted] 2023/07/10 06:42 [medline] 2023/05/22 00:41 [pubmed] 2023/05/21 19:27 [entrez]
 2023/04/11 06:42 [medline] 2023/04/09 20:52 [entrez] 2023/04/10 06:00 [pubmed]
 2023/04/21 00:00 [received] 2023/05/25 00:00 [revised] 2023/06/06 00:00 [accepted] 2023/08/25 12:41 [medline] 2023/08/25 12:41 [pubmed] 2023/08/25 08:12 [entrez]
 2023/06/08 00:00 [received] 2023/07/19 00:00 [revised] 2023/08/16 00:00 [accepted] 2023/09/01 00:42 [medline] 2023/09/01 00:42 [pubmed] 2023/08/31 18:03 [entrez]
 2022/10/08 00:00 [received] 2023/03/19 00:00 [revised] 2023/04/05 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/05/01 00:41 [pubmed] 2023/04/30 18:08 [entrez]
 2023/04/28 06:43 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 02:40 [entrez]
 2023/03/15 00:00 [received] 2023/04/06 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/05/01 06:41 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:41 [entrez]
 2023/04/18 10:16 [medline] 2023/02/03 06:00 [pubmed] 2023/02/02 12:23 [entrez]
 2023/03/18 00:00 [received] 2023/05/22 00:00 [revised] 2023/06/06 00:00 [accepted] 2023/08/09 06:44 [medline] 2023/08/09 06:43 [pubmed] 2023/08/09 04:02 [entrez]
 2022/11/16 00:00 [received] 2023/03/18 00:00 [revised] 2023/04/28 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/06/12 06:42 [medline] 2023/05/07 00:41 [pubmed] 2023/05/06 19:28 [entrez]
 2022/10/18 00:00 [received] 2023/06/12 00:00 [revised] 2023/07/28 00:00 [accepted] 2023/08/28 00:41 [medline] 2023/08/28 00:41 [pubmed] 2023/08/27 18:04 [entrez]
 2022/08/18 00:00 [received] 2023/01/07 00:00 [revised] 2023/01/07 00:00 [accepted] 2023/01/27 06:00 [pubmed] 2023/01/27 06:01 [medline] 2023/01/26 02:41 [entrez]
 2022/12/23 00:00 [received] 2023/05/18 00:00 [accepted] 2023/07/25 01:09 [medline] 2023/07/25 01:09 [pubmed] 2023/07/24 21:43 [entrez]
 2021/11/04 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/30 06:42 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 23:30 [entrez]
 2023/02/02 00:00 [received] 2023/03/16 00:00 [revised] 2023/04/23 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/08 18:42 [pubmed] 2023/05/08 18:00 [entrez]
 2022/10/21 00:00 [received] 2023/02/10 00:00 [revised] 2023/02/13 00:00 [accepted] 2023/02/17 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/16 19:23 [entrez]
 2022/11/19 00:00 [received] 2023/01/06 00:00 [accepted] 2023/02/10 03:12 [entrez] 2023/02/11 06:00 [pubmed] 2023/02/14 06:00 [medline]
 2022/11/30 00:00 [received] 2022/12/27 00:00 [revised] 2022/12/30 00:00 [accepted] 2023/01/21 01:30 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/22 06:01 [medline]
 2022/07/18 00:00 [received] 2022/12/25 00:00 [revised] 2023/01/02 00:00 [accepted] 2023/01/17 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/01/16 18:07 [entrez]
 2022/08/26 00:00 [revised] 2022/01/29 00:00 [received] 2022/09/05 00:00 [accepted] 2022/09/16 06:00 [pubmed] 2022/12/21 06:00 [medline] 2022/09/15 05:13 [entrez]
 2022/08/23 00:00 [revised] 2022/07/19 00:00 [received] 2022/08/23 00:00 [accepted] 2023/04/07 10:18 [medline] 2022/09/14 06:00 [pubmed] 2022/09/13 07:32 [entrez]
 2023/01/20 00:00 [received] 2023/03/14 00:00 [revised] 2023/03/21 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 18:02 [entrez]
 2022/11/16 00:00 [received] 2023/03/01 00:00 [accepted] 2023/08/07 06:41 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 18:17 [entrez]
 2023/04/17 06:41 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 13:56 [entrez]
 2022/06/21 00:00 [received] 2022/08/11 00:00 [accepted] 2022/10/11 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/10/10 23:31 [entrez]
 2023/08/09 12:56 [medline] 2023/08/09 12:55 [pubmed] 2023/08/09 09:23 [entrez]
 2023/05/09 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 01:23 [entrez]
 2022/12/02 00:00 [received] 2023/03/29 00:00 [revised] 2023/04/07 00:00 [accepted] 2023/04/27 06:43 [medline] 2023/04/27 06:42 [pubmed] 2023/04/27 02:15 [entrez]
 2022/06/07 00:00 [received] 2022/08/05 00:00 [revised] 2022/08/25 00:00 [accepted] 2022/11/29 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/11/28 19:02 [entrez]
 2022/06/01 00:00 [received] 2023/03/31 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/06/19 13:09 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 18:00 [entrez]
 2022/12/25 00:00 [received] 2023/04/15 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 13:19 [entrez]
 2023/03/20 00:00 [received] 2023/04/11 00:00 [revised] 2023/04/18 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:08 [entrez]
 2023/05/10 00:00 [revised] 2022/12/06 00:00 [received] 2023/06/02 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 00:43 [entrez]
 2023/06/20 06:42 [medline] 2023/06/19 00:42 [pubmed] 2023/06/18 20:58 [entrez]

 2023/04/11 06:42 [medline] 2023/04/07 20:57 [entrez] 2023/04/08 06:00 [pubmed]
 2022/08/19 00:00 [revised] 2021/11/13 00:00 [received] 2023/02/02 00:00 [accepted] 2023/06/07 06:42 [medline] 2023/02/15 06:00 [pubmed] 2023/02/14 04:33 [entrez]
 2022/12/01 00:00 [received] 2023/03/22 00:00 [accepted] 2023/04/13 06:01 [medline] 2023/04/12 01:44 [entrez] 2023/04/13 06:00 [pubmed]
 2022/11/29 00:00 [received] 2023/03/23 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/03/30 06:00 [pubmed] 2023/03/29 23:28 [entrez]
 2023/09/07 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 02:07 [entrez]
 2023/03/29 00:00 [received] 2023/06/19 00:00 [accepted] 2023/06/15 00:00 [revised] 2023/07/09 01:07 [medline] 2023/07/09 01:07 [pubmed] 2023/07/08 23:22 [entrez]
 2023/01/02 00:00 [received] 2023/01/12 00:00 [accepted] 2023/01/18 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/01/17 19:20 [entrez]
 2022/01/07 00:00 [received] 2022/03/26 00:00 [revised] 2022/04/04 00:00 [accepted] 2022/05/06 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/05/05 18:05 [entrez]
 2023/03/03 00:00 [received] 2023/04/06 00:00 [revised] 2023/05/18 00:00 [accepted] 2023/06/08 06:43 [medline] 2023/06/08 06:42 [pubmed] 2023/06/08 04:33 [entrez]
 2023/03/04 00:00 [received] 2023/04/01 00:00 [revised] 2023/04/04 00:00 [accepted] 2023/05/15 19:14 [medline] 2023/05/15 19:13 [pubmed] 2023/05/15 13:46 [entrez]
 2023/05/15 06:42 [pubmed] 2023/05/15 06:42 [medline] 2023/05/15 05:29 [entrez]
 2022/12/06 00:00 [received] 2023/01/26 00:00 [revised] 2023/02/10 00:00 [accepted] 2023/02/25 03:20 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/02/21 00:00 [received] 2022/11/14 00:00 [revised] 2022/11/21 00:00 [accepted] 2023/05/22 19:12 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 12:13 [entrez]
 2023/09/01 06:43 [medline] 2023/08/31 00:41 [pubmed] 2023/08/30 20:45 [entrez]
 2023/04/06 00:00 [accepted] 2023/05/12 01:08 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 19:16 [entrez]
 2023/05/09 00:00 [received] 2023/06/09 00:00 [revised] 2023/06/12 00:00 [accepted] 2023/06/28 06:44 [medline] 2023/06/28 06:43 [pubmed] 2023/06/28 01:04 [entrez]
 2023/03/01 02:19 [entrez] 2023/03/02 06:00 [pubmed] 2023/03/02 06:01 [medline]
 2022/08/31 00:00 [received] 2023/03/30 00:00 [accepted] 2023/03/13 00:00 [revised] 2023/07/13 01:06 [medline] 2023/07/13 01:06 [pubmed] 2023/07/12 23:38 [entrez]
 2022/12/01 00:00 [received] 2023/04/16 00:00 [revised] 2023/05/03 00:00 [accepted] 2023/06/14 06:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 19:24 [entrez]
 2023/01/11 14:03 [entrez] 2023/01/12 06:00 [pubmed] 2023/01/14 06:00 [medline]
 2022/07/19 00:00 [received] 2023/06/02 00:00 [accepted] 2023/07/20 01:06 [medline] 2023/07/20 01:06 [pubmed] 2023/07/19 21:37 [entrez]
 2023/07/14 00:00 [received] 2023/07/28 00:00 [revised] 2023/08/04 00:00 [accepted] 2023/08/12 10:45 [medline] 2023/08/12 10:44 [pubmed] 2023/08/12 01:04 [entrez]

 2022/08/29 00:00 [received] 2022/10/18 00:00 [revised] 2022/10/28 00:00 [accepted] 2023/05/03 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 23:22 [entrez]
 2022/08/02 00:00 [received] 2023/01/14 00:00 [revised] 2023/01/18 00:00 [accepted] 2023/02/04 22:01 [entrez] 2023/02/05 06:00 [pubmed] 2023/02/05 06:00 [medline]
 2023/03/03 00:00 [received] 2023/06/27 00:00 [revised] 2023/07/04 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/07/17 19:08 [pubmed] 2023/07/17 18:02 [entrez]
 2022/11/29 00:00 [revised] 2022/08/09 00:00 [received] 2022/12/21 00:00 [accepted] 2023/04/04 06:42 [medline] 2023/02/16 06:00 [pubmed] 2023/02/15 00:42 [entrez]
 2022/03/28 00:00 [received] 2022/06/29 00:00 [accepted] 2022/07/21 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/07/20 11:15 [entrez]
 2022/05/27 06:00 [pubmed] 2023/01/26 06:00 [medline] 2022/05/26 07:32 [entrez]
 2023/01/06 00:00 [received] 2023/04/02 00:00 [accepted] 2023/09/04 06:42 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 05:28 [entrez]
 2023/03/10 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/04 06:44 [medline] 2023/08/04 06:43 [pubmed] 2023/08/04 04:08 [entrez]
 2023/08/31 06:42 [medline] 2022/11/02 06:00 [pubmed] 2022/11/01 03:03 [entrez]
 2023/06/30 00:00 [received] 2023/08/17 00:00 [revised] 2023/08/30 00:00 [accepted] 2023/09/14 00:42 [medline] 2023/09/14 00:42 [pubmed] 2023/09/13 18:05 [entrez]
 2023/04/13 00:00 [received] 2023/07/03 00:00 [accepted] 2023/08/21 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 04:35 [entrez]
 2023/07/09 00:00 [received] 2023/08/11 00:00 [accepted] 2023/09/14 06:43 [medline] 2023/09/13 06:41 [pubmed] 2023/09/13 04:06 [entrez]
 2023/02/20 00:00 [received] 2023/08/13 00:00 [accepted] 2023/08/28 12:42 [medline] 2023/08/28 12:42 [pubmed] 2023/08/28 11:07 [entrez]
 2023/03/03 02:22 [entrez] 2023/03/04 06:00 [pubmed] 2023/03/07 06:00 [medline]
 2022/09/08 00:00 [received] 2023/02/07 00:00 [revised] 2023/02/12 00:00 [accepted] 2023/06/02 06:43 [medline] 2023/03/04 06:00 [pubmed] 2023/03/03 00:52 [entrez]
 2022/12/02 00:00 [received] 2023/01/23 00:00 [accepted] 2023/02/27 05:17 [entrez] 2023/02/28 06:00 [pubmed] 2023/02/28 06:01 [medline]
 2022/12/22 00:00 [received] 2023/02/04 00:00 [revised] 2023/02/07 00:00 [accepted] 2023/02/25 01:04 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/06/26 00:00 [received] 2023/03/15 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:23 [entrez]
 2023/01/29 00:00 [received] 2023/05/03 00:00 [accepted] 2023/06/02 13:17 [medline] 2023/06/02 13:16 [pubmed] 2023/06/02 10:55 [entrez]
 2023/04/13 06:42 [medline] 2023/04/12 01:52 [entrez] 2023/04/13 06:00 [pubmed]
 2021/08/24 00:00 [accepted] 2023/05/10 06:41 [medline] 2022/01/16 06:00 [pubmed] 2022/01/15 05:58 [entrez]
 2023/05/01 06:41 [medline] 2023/03/26 06:00 [pubmed] 2023/03/25 04:03 [entrez]
 2023/05/29 00:00 [received] 2023/08/07 00:00 [accepted] 2023/09/08 06:44 [medline] 2023/09/08 06:43 [pubmed] 2023/09/08 04:00 [entrez]
 2022/07/30 00:00 [received] 2022/08/16 00:00 [accepted] 2022/08/30 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/08/29 23:28 [entrez]
 2023/03/06 04:12 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2022/06/07 00:00 [received] 2022/10/14 00:00 [accepted] 2022/10/28 06:00 [pubmed] 2023/02/16 06:00 [medline] 2022/10/27 07:43 [entrez]
 2022/11/23 00:00 [revised] 2022/08/22 00:00 [received] 2022/11/24 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/02/11 06:00 [medline] 2022/11/29 08:13 [entrez]
 2022/10/26 00:00 [received] 2023/02/09 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 14:34 [entrez]
 2023/06/02 06:43 [medline] 2023/05/31 19:16 [pubmed] 2023/05/31 14:03 [entrez]
 2022/12/21 00:00 [revised] 2022/06/27 00:00 [received] 2023/03/20 00:00 [accepted] 2023/07/21 06:44 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 04:53 [entrez]
 2022/01/20 00:00 [accepted] 2023/04/26 06:42 [medline] 2022/04/14 06:00 [pubmed] 2022/04/13 05:17 [entrez]
 2023/05/31 00:00 [received] 2023/07/13 00:00 [accepted] 2023/07/19 06:42 [medline] 2023/07/18 01:09 [pubmed] 2023/07/17 23:42 [entrez]
 2022/06/29 00:00 [accepted] 2022/11/13 06:00 [pubmed] 2022/12/24 06:00 [medline] 2022/11/12 00:49 [entrez]
 2023/08/07 06:41 [medline] 2023/08/04 19:15 [pubmed] 2023/08/04 14:02 [entrez]
 2023/02/17 00:00 [received] 2023/05/31 00:00 [accepted] 2024/09/01 00:00 [pmc-release] 2023/09/04 06:43 [medline] 2023/07/04 13:08 [pubmed] 2023/07/04 08:03 [entrez]
 2023/02/03 00:00 [received] 2023/05/03 00:00 [revised] 2023/05/12 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/06/05 19:10 [pubmed] 2023/06/05 18:08 [entrez]
 2022/05/12 00:00 [received] 2023/02/27 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 23:15 [entrez]
 2023/01/19 00:00 [received] 2023/04/09 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/06/14 06:42 [medline] 2023/04/21 00:42 [pubmed] 2023/04/20 18:03 [entrez]
 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:56 [entrez]
 2022/05/20 00:00 [received] 2023/05/15 00:00 [accepted] 2023/09/13 06:41 [medline] 2023/07/25 01:09 [pubmed] 2023/07/24 21:43 [entrez]
 2023/06/29 00:00 [received] 2023/08/05 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/08/28 06:43 [medline] 2023/08/26 10:46 [pubmed] 2023/08/26 01:17 [entrez]
 2023/03/27 00:00 [received] 2023/06/05 00:00 [revised] 2023/07/11 00:00 [accepted] 2023/07/12 13:07 [medline] 2023/07/12 13:07 [pubmed] 2023/07/12 07:44 [entrez]
 2023/01/13 00:00 [received] 2023/03/30 00:00 [accepted] 2023/05/22 19:12 [medline] 2023/05/22 19:11 [pubmed] 2023/05/22 12:10 [entrez]
 2023/03/30 00:00 [revised] 2023/02/13 00:00 [received] 2023/04/05 00:00 [accepted] 2023/07/31 06:43 [medline] 2023/05/09 00:42 [pubmed] 2023/05/08 22:43 [entrez]
 2022/09/13 00:00 [received] 2023/02/08 00:00 [accepted] 2023/05/24 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 21:12 [entrez]
 2023/01/19 00:00 [received] 2023/03/24 00:00 [revised] 2023/04/07 00:00 [accepted] 2023/07/15 21:05 [medline] 2023/07/15 21:05 [pubmed] 2023/07/15 10:32 [entrez]
 2023/03/05 00:00 [received] 2023/04/17 00:00 [accepted] 2023/05/25 19:13 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 14:12 [entrez]
 2022/10/23 00:00 [received] 2023/06/29 00:00 [accepted] 2023/09/11 06:42 [medline] 2023/09/08 00:41 [pubmed] 2023/09/07 23:56 [entrez]
 2023/06/01 00:00 [received] 2023/06/27 00:00 [accepted] 2023/08/03 13:08 [medline] 2023/08/03 13:08 [pubmed] 2023/08/03 11:09 [entrez]
 2022/11/07 00:00 [received] 2023/05/10 00:00 [revised] 2023/05/15 00:00 [accepted] 2023/06/13 19:15 [medline] 2023/06/13 19:15 [pubmed] 2023/06/13 13:13 [entrez]
 2022/08/17 00:00 [received] 2022/12/01 00:00 [revised] 2022/12/29 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:47 [entrez]
 2021/09/12 00:00 [received] 2021/10/29 00:00 [accepted] 2023/09/12 06:42 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 03:34 [entrez]
 2023/03/17 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/09 06:43 [medline] 2023/06/09 06:42 [pubmed] 2023/06/09 04:40 [entrez]
 2022/09/22 00:00 [received] 2023/03/18 00:00 [accepted] 2023/05/25 19:13 [medline] 2023/05/25 19:12 [pubmed] 2023/05/25 14:17 [entrez]
 2023/02/24 00:00 [received] 2023/03/24 00:00 [revised] 2023/04/03 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:45 [entrez]
 2023/06/20 00:00 [received] 2023/07/26 00:00 [accepted] 2023/08/24 06:43 [medline] 2023/08/24 06:42 [pubmed] 2023/08/24 04:00 [entrez]
 2022/08/29 00:00 [received] 2022/12/16 00:00 [accepted] 2023/01/13 02:05 [entrez] 2023/01/14 06:00 [pubmed] 2023/01/14 06:01 [medline]
 2023/03/02 00:00 [received] 2023/06/01 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:09 [entrez]
 2023/03/23 00:00 [received] 2023/05/12 00:00 [accepted] 2023/06/16 06:43 [medline] 2023/06/16 06:42 [pubmed] 2023/06/16 04:18 [entrez]
 2022/10/22 00:00 [received] 2023/02/28 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:44 [entrez]
 2023/05/04 12:42 [medline] 2023/05/03 06:42 [pubmed] 2023/05/03 02:03 [entrez]
 2023/06/08 00:00 [received] 2023/06/26 00:00 [revised] 2023/06/30 00:00 [accepted] 2023/07/29 11:49 [medline] 2023/07/29 11:48 [pubmed] 2023/07/29 01:08 [entrez]
 2022/11/12 00:00 [received] 2023/05/23 00:00 [revised] 2023/06/12 00:00 [accepted] 2023/07/11 06:43 [medline] 2023/07/11 06:42 [pubmed] 2023/07/11 03:35 [entrez]
 2023/01/06 00:00 [received] 2023/05/15 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/05/30 01:06 [pubmed] 2023/05/29 23:27 [entrez]
 2023/01/03 00:00 [received] 2023/05/01 00:00 [revised] 2023/05/31 00:00 [accepted] 2023/08/11 06:43 [medline] 2023/06/16 01:08 [pubmed] 2023/06/15 18:03 [entrez]

 2023/09/11 06:43 [medline] 2023/09/08 18:41 [pubmed] 2023/09/08 13:23 [entrez]
 2023/02/19 00:00 [received] 2023/05/16 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/06/17 05:11 [pubmed] 2023/06/16 23:40 [entrez]

 2023/06/19 13:08 [medline] 2022/09/06 06:00 [pubmed] 2022/09/05 05:53 [entrez]
 2022/09/09 00:00 [received] 2023/01/08 00:00 [revised] 2023/01/19 00:00 [accepted] 2023/01/24 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/01/23 19:24 [entrez]
 2022/05/15 00:00 [received] 2022/07/26 00:00 [accepted] 2022/11/29 21:44 [entrez] 2022/11/30 06:00 [pubmed] 2022/12/02 06:00 [medline]
 2023/02/09 00:00 [received] 2023/05/19 00:00 [accepted] 2023/04/17 00:00 [revised] 2023/08/10 06:42 [medline] 2023/06/24 21:03 [pubmed] 2023/06/24 11:04 [entrez]
 2023/03/19 00:00 [received] 2023/04/12 00:00 [accepted] 2023/04/10 00:00 [revised] 2023/07/17 06:42 [medline] 2023/04/27 12:41 [pubmed] 2023/04/27 11:15 [entrez]
 2023/02/09 00:00 [received] 2023/05/03 00:00 [accepted] 2023/04/13 00:00 [revised] 2023/05/25 13:07 [medline] 2023/05/25 13:07 [pubmed] 2023/05/25 11:17 [entrez]
 2021/09/26 00:00 [received] 2022/05/09 00:00 [accepted] 2023/04/24 06:42 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 03:56 [entrez]
 2023/03/29 00:00 [revised] 2022/09/04 00:00 [received] 2023/03/30 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/04/22 19:42 [pubmed] 2023/04/22 09:32 [entrez]
 2023/05/23 00:00 [received] 2023/07/28 00:00 [accepted] 2023/08/25 06:43 [medline] 2023/08/25 06:42 [pubmed] 2023/08/25 03:44 [entrez]
 2023/03/08 00:00 [revised] 2022/10/31 00:00 [received] 2023/03/18 00:00 [accepted] 2023/04/26 06:42 [medline] 2023/03/24 06:00 [pubmed] 2023/03/23 06:32 [entrez]
 2022/05/31 00:00 [accepted] 2023/05/10 06:42 [medline] 2022/06/25 06:00 [pubmed] 2022/06/24 11:19 [entrez]
 2023/08/21 00:00 [revised] 2023/06/12 00:00 [received] 2023/08/21 00:00 [accepted] 2023/08/24 00:42 [medline] 2023/08/24 00:42 [pubmed] 2023/08/23 20:13 [entrez]
 2023/04/21 00:00 [accepted] 2023/05/24 13:08 [pubmed] 2023/05/24 13:08 [medline] 2023/05/24 11:38 [entrez]
 2022/09/24 00:00 [received] 2023/01/20 00:00 [accepted] 2022/12/29 00:00 [revised] 2023/05/01 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 06:42 [entrez]
 2022/05/11 00:00 [accepted] 2023/05/10 06:42 [medline] 2022/06/02 06:00 [pubmed] 2022/06/01 12:24 [entrez]
 2021/08/17 00:00 [received] 2022/09/06 00:00 [revised] 2022/09/09 00:00 [accepted] 2022/10/01 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/30 19:33 [entrez]
 2023/07/06 06:42 [medline] 2022/12/29 06:00 [pubmed] 2022/12/28 07:32 [entrez]
 2022/02/03 00:00 [received] 2022/07/18 00:00 [accepted] 2022/08/06 06:00 [pubmed] 2023/03/15 06:00 [medline] 2022/08/05 23:28 [entrez]
 2023/02/23 00:00 [received] 2023/03/09 00:00 [accepted] 2023/05/30 06:42 [medline] 2023/03/15 06:00 [pubmed] 2023/03/14 20:20 [entrez]
 2023/07/17 00:00 [received] 2023/07/26 00:00 [accepted] 2023/08/24 06:43 [medline] 2023/08/24 06:43 [pubmed] 2023/08/24 02:33 [entrez]
 2023/04/01 00:00 [received] 2023/06/16 00:00 [revised] 2023/06/28 00:00 [accepted] 2023/08/07 06:42 [medline] 2023/07/03 00:41 [pubmed] 2023/07/02 19:25 [entrez]
 2023/08/03 00:00 [revised] 2022/12/04 00:00 [received] 2023/08/08 00:00 [accepted] 2023/08/19 11:43 [medline] 2023/08/19 11:43 [pubmed] 2023/08/19 03:09 [entrez]
 2023/04/21 00:00 [received] 2023/06/12 00:00 [accepted] 2023/06/09 00:00 [revised] 2023/08/11 06:42 [medline] 2023/07/19 13:06 [pubmed] 2023/07/19 11:06 [entrez]
 2023/01/01 00:00 [received] 2023/02/14 00:00 [revised] 2023/02/14 00:00 [accepted] 2024/08/01 00:00 [pmc-release] 2023/07/17 06:42 [medline] 2023/02/24 06:00 [pubmed] 2023/02/23 19:41 [entrez]
 2023/04/19 00:00 [received] 2023/06/10 00:00 [revised] 2023/06/14 00:00 [accepted] 2023/06/29 06:43 [medline] 2023/06/28 06:42 [pubmed] 2023/06/28 01:19 [entrez]
 2022/07/21 00:00 [received] 2023/02/10 00:00 [accepted] 2023/03/09 02:11 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/10 06:01 [medline]
 2023/01/28 00:00 [received] 2023/02/24 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:17 [entrez] 2023/03/30 06:00 [pubmed]
 2023/03/05 00:00 [received] 2023/05/16 00:00 [accepted] 2023/08/22 06:43 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 04:50 [entrez]

 2021/10/13 00:00 [received] 2022/04/03 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/11/17 22:10 [entrez]
 2023/03/01 00:00 [received] 2023/04/13 00:00 [revised] 2023/04/14 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/05/16 06:42 [pubmed] 2023/05/16 01:12 [entrez]
 2022/11/10 00:00 [received] 2023/02/24 00:00 [accepted] 2023/08/04 06:43 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 09:13 [entrez]
 2023/01/05 00:00 [received] 2023/02/19 00:00 [revised] 2023/03/10 00:00 [accepted] 2023/05/08 10:17 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 20:30 [entrez]
 2022/05/11 00:00 [received] 2022/10/23 00:00 [revised] 2022/11/08 00:00 [accepted] 2022/12/16 06:00 [pubmed] 2023/01/17 06:00 [medline] 2022/12/15 18:19 [entrez]
 2022/10/12 00:00 [received] 2023/04/17 00:00 [accepted] 2023/06/08 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:19 [entrez]
 2023/02/10 00:00 [received] 2023/03/17 00:00 [revised] 2023/04/18 00:00 [accepted] 2023/05/09 18:42 [medline] 2023/05/09 18:41 [pubmed] 2023/05/09 15:13 [entrez]
 2022/07/22 00:00 [received] 2022/11/05 00:00 [revised] 2022/11/06 00:00 [accepted] 2022/11/28 06:00 [pubmed] 2023/02/11 06:00 [medline] 2022/11/27 18:13 [entrez]
 2023/08/04 06:43 [medline] 2023/08/03 13:08 [pubmed] 2023/08/03 06:53 [entrez]
 2022/11/30 00:00 [received] 2022/12/28 00:00 [accepted] 2023/02/06 03:25 [entrez] 2023/02/07 06:00 [pubmed] 2023/02/07 06:01 [medline]
 2023/03/28 17:04 [medline] 2022/09/27 06:00 [pubmed] 2022/09/26 15:41 [entrez]
 2023/01/24 00:00 [received] 2023/04/17 00:00 [accepted] 2024/08/08 00:00 [pmc-release] 2023/08/09 06:43 [medline] 2023/06/13 01:13 [pubmed] 2023/06/12 21:38 [entrez]
 2022/11/11 00:00 [accepted] 2022/12/22 06:00 [pubmed] 2023/03/08 06:00 [medline] 2022/12/21 23:29 [entrez]
 2022/12/22 00:00 [received] 2023/05/23 00:00 [accepted] 2023/07/13 19:15 [medline] 2023/07/13 19:14 [pubmed] 2023/07/13 15:20 [entrez]
 2023/02/21 00:00 [received] 2023/05/05 00:00 [revised] 2023/05/05 00:00 [accepted] 2024/05/07 00:00 [pmc-release] 2023/05/19 06:42 [medline] 2023/05/10 00:41 [pubmed] 2023/05/09 19:15 [entrez]
 2022/04/17 00:00 [received] 2023/01/17 00:00 [accepted] 2023/01/15 00:00 [revised] 2023/03/21 11:54 [entrez] 2023/03/22 06:00 [pubmed] 2023/03/22 06:01 [medline]
 2022/12/08 00:00 [received] 2023/02/12 00:00 [accepted] 2023/02/28 20:54 [entrez] 2023/03/01 06:00 [pubmed] 2023/03/03 06:00 [medline]
 2022/11/16 00:00 [received] 2023/01/23 00:00 [accepted] 2023/03/01 00:27 [entrez] 2023/03/02 06:00 [pubmed] 2023/03/02 06:01 [medline]
 2023/03/06 04:22 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/08 06:00 [medline]
 2022/11/25 00:00 [received] 2023/01/19 00:00 [accepted] 2023/03/02 02:19 [entrez] 2023/03/03 06:00 [pubmed] 2023/03/03 06:01 [medline]
 2024/09/06 00:00 [pmc-release] 2023/09/06 12:41 [medline] 2023/09/06 12:41 [pubmed] 2023/09/06 11:33 [entrez]
 2022/05/20 00:00 [received] 2022/12/12 00:00 [accepted] 2023/01/16 23:39 [entrez] 2023/01/17 06:00 [pubmed] 2023/01/19 06:00 [medline]
 2023/04/13 00:00 [received] 2023/07/09 00:00 [revised] 2023/08/11 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/08/15 00:42 [pubmed] 2023/08/14 19:25 [entrez]
 2023/02/06 00:00 [received] 2023/05/23 00:00 [revised] 2023/05/26 00:00 [accepted] 2023/06/10 15:14 [pubmed] 2023/06/10 15:14 [medline] 2023/06/09 18:11 [entrez]
 2023/01/01 14:02 [entrez] 2023/01/02 06:00 [pubmed] 2023/01/04 06:00 [medline]
 2023/09/11 06:43 [medline] 2023/09/11 06:42 [pubmed] 2023/09/11 04:40 [entrez]
 2022/12/22 00:00 [received] 2023/08/15 00:00 [accepted] 2023/09/14 00:00 [revised] 2023/09/01 18:42 [pubmed] 2023/09/01 18:42 [medline] 2023/09/01 13:43 [entrez]
 2022/12/08 00:00 [received] 2023/04/24 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/12 01:07 [pubmed] 2023/05/11 18:04 [entrez]
 2022/12/07 00:00 [received] 2023/01/11 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/02/11 01:25 [entrez] 2023/02/12 06:00 [pubmed] 2023/02/15 06:00 [medline]
 2023/02/03 00:00 [received] 2023/06/12 00:00 [accepted] 2024/10/01 00:00 [pmc-release] 2023/09/04 06:43 [medline] 2023/09/04 06:42 [pubmed] 2023/09/04 05:10 [entrez]
 2023/04/11 00:00 [received] 2023/07/10 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:57 [entrez]
 2022/07/22 00:00 [received] 2023/01/11 00:00 [accepted] 2023/07/03 13:06 [medline] 2023/07/03 13:05 [pubmed] 2023/07/03 11:39 [entrez]
 2021/09/23 00:00 [received] 2022/01/14 00:00 [accepted] 2023/06/23 13:08 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 10:28 [entrez]
 2023/05/02 00:00 [received] 2023/08/01 00:00 [revised] 2023/08/23 00:00 [accepted] 2023/08/26 05:41 [pubmed] 2023/08/26 05:41 [medline] 2023/08/25 19:25 [entrez]
 2022/10/12 00:00 [received] 2023/03/15 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/07/22 10:42 [pubmed] 2023/07/21 18:53 [entrez]
 2023/04/05 00:00 [received] 2023/06/25 00:00 [accepted] 2023/05/17 00:00 [revised] 2023/07/05 13:05 [medline] 2023/07/05 13:05 [pubmed] 2023/07/05 11:04 [entrez]
 2023/02/27 00:00 [received] 2023/04/06 00:00 [revised] 2023/04/07 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 01:25 [entrez]
 2022/09/06 00:00 [received] 2022/10/25 00:00 [revised] 2022/11/21 00:00 [accepted] 2023/11/23 00:00 [pmc-release] 2022/11/24 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/11/23 06:43 [entrez]
 2023/02/24 00:00 [received] 2023/04/10 00:00 [revised] 2023/04/12 00:00 [accepted] 2023/04/28 06:43 [medline] 2023/04/28 06:42 [pubmed] 2023/04/28 01:33 [entrez]
 2021/08/19 00:00 [received] 2021/12/23 00:00 [accepted] 2022/01/18 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/01/17 12:24 [entrez]
 2022/12/05 00:00 [received] 2023/03/29 00:00 [accepted] 2023/05/14 13:11 [medline] 2023/05/14 13:10 [pubmed] 2023/05/14 11:58 [entrez]
 2023/07/03 00:00 [revised] 2023/02/10 00:00 [received] 2023/07/12 00:00 [accepted] 2023/08/02 01:07 [pubmed] 2023/08/02 01:07 [medline] 2023/08/01 23:44 [entrez]
 2023/05/25 00:00 [received] 2023/06/29 00:00 [revised] 2023/07/01 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:17 [entrez]
 2022/12/06 00:00 [received] 2023/02/23 00:00 [accepted] 2023/03/17 06:00 [pubmed] 2023/03/17 06:00 [medline] 2023/03/16 02:31 [entrez]
 2020/03/16 00:00 [received] 2023/06/28 00:00 [accepted] 2023/08/16 06:42 [medline] 2023/06/29 19:11 [pubmed] 2023/06/29 12:08 [entrez]
 2023/03/30 00:00 [received] 2023/05/16 00:00 [revised] 2023/05/30 00:00 [accepted] 2023/06/16 19:16 [medline] 2023/06/16 19:16 [pubmed] 2023/06/16 14:42 [entrez]
 2023/05/01 00:42 [pubmed] 2023/05/01 00:42 [medline] 2023/04/30 23:53 [entrez]
 2022/05/01 00:00 [received] 2022/09/13 00:00 [revised] 2022/10/02 00:00 [accepted] 2022/10/12 06:00 [pubmed] 2022/11/30 06:00 [medline] 2022/10/11 21:45 [entrez]
 2023/05/15 00:00 [revised] 2022/12/07 00:00 [received] 2023/05/18 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/05/31 06:42 [pubmed] 2023/05/31 05:53 [entrez]
 2023/02/13 00:00 [received] 2023/03/02 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 19:34 [entrez]
 2022/09/09 00:00 [received] 2022/10/24 00:00 [accepted] 2023/06/26 06:41 [medline] 2022/11/04 06:00 [pubmed] 2022/11/03 12:18 [entrez]
 2022/12/12 00:00 [received] 2023/05/24 00:00 [accepted] 2023/05/29 06:41 [medline] 2023/05/28 01:07 [pubmed] 2023/05/27 23:19 [entrez]
 2022/06/12 00:00 [received] 2022/12/27 00:00 [revised] 2022/12/30 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/05/18 01:08 [medline] 2023/05/18 01:07 [pubmed] 2023/05/17 20:05 [entrez]
 2023/05/08 00:00 [received] 2023/07/29 00:00 [revised] 2023/08/01 00:00 [accepted] 2023/08/10 00:42 [pubmed] 2023/08/10 00:42 [medline] 2023/08/09 19:25 [entrez]
 2022/06/16 00:00 [received] 2022/09/26 00:00 [revised] 2022/11/23 00:00 [accepted] 2023/01/25 01:44 [entrez] 2023/01/26 06:00 [pubmed] 2023/01/26 06:01 [medline]
 2022/10/18 00:00 [received] 2023/01/18 00:00 [accepted] 2023/08/25 06:42 [medline] 2023/02/12 06:00 [pubmed] 2023/02/11 11:13 [entrez]
 2022/09/09 00:00 [revised] 2022/07/24 00:00 [received] 2022/09/26 00:00 [accepted] 2022/10/14 06:00 [pubmed] 2022/12/15 06:00 [medline] 2022/10/13 08:33 [entrez]
 2022/10/21 00:00 [revised] 2022/08/30 00:00 [received] 2022/10/25 00:00 [accepted] 2024/06/01 00:00 [pmc-release] 2023/06/13 06:42 [medline] 2022/12/15 06:00 [pubmed] 2022/12/14 12:03 [entrez]
 2023/09/01 06:43 [medline] 2023/08/31 00:41 [pubmed] 2023/08/30 18:43 [entrez]
 2023/02/19 00:00 [received] 2023/05/07 00:00 [accepted] 2023/09/12 06:41 [medline] 2023/05/19 13:05 [pubmed] 2023/05/19 11:10 [entrez]
 2021/10/06 00:00 [received] 2022/12/11 00:00 [revised] 2023/01/05 00:00 [accepted] 2024/02/16 00:00 [pmc-release] 2023/02/09 06:00 [pubmed] 2023/02/25 06:00 [medline] 2023/02/08 18:41 [entrez]
 2023/03/03 00:00 [received] 2023/05/13 00:00 [accepted] 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:21 [entrez]
 2022/09/30 00:00 [revised] 2022/05/19 00:00 [received] 2022/10/21 00:00 [accepted] 2023/06/13 06:42 [medline] 2022/12/22 06:00 [pubmed] 2022/12/21 07:03 [entrez]
 2023/02/27 00:00 [revised] 2023/01/17 00:00 [received] 2023/02/27 00:00 [accepted] 2023/05/18 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 15:33 [entrez]
 2023/01/03 00:00 [received] 2023/07/21 00:00 [accepted] 2023/08/28 06:42 [medline] 2023/08/26 05:41 [pubmed] 2023/08/25 23:43 [entrez]
 2022/06/17 00:00 [received] 2023/01/30 00:00 [accepted] 2023/02/15 23:13 [entrez] 2023/02/16 06:00 [pubmed] 2023/02/18 06:00 [medline]
 2023/03/22 00:00 [received] 2023/07/05 00:00 [accepted] 2023/08/22 06:42 [medline] 2023/08/21 06:43 [pubmed] 2023/08/21 04:49 [entrez]
 2023/03/15 00:00 [revised] 2023/01/07 00:00 [received] 2023/03/20 00:00 [accepted] 2023/04/24 06:41 [medline] 2023/04/24 06:41 [pubmed] 2023/04/24 05:03 [entrez]
 2023/06/14 00:00 [received] 2023/07/19 00:00 [accepted] 2023/08/06 05:41 [medline] 2023/08/06 05:41 [pubmed] 2023/08/05 11:06 [entrez]
 2022/06/29 00:00 [received] 2023/02/07 00:00 [accepted] 2023/05/16 01:10 [medline] 2023/05/16 01:09 [pubmed] 2023/05/15 19:32 [entrez]
 2022/11/18 00:00 [received] 2023/03/12 00:00 [revised] 2023/03/13 00:00 [accepted] 2023/06/09 06:42 [medline] 2023/04/24 00:41 [pubmed] 2023/04/23 18:07 [entrez]
 2022/11/22 00:00 [received] 2023/03/23 00:00 [revised] 2023/03/27 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/04/10 06:00 [pubmed] 2023/04/09 18:07 [entrez]
 2023/01/20 00:00 [received] 2023/03/20 00:00 [accepted] 2023/05/01 06:42 [medline] 2023/05/01 06:41 [pubmed] 2023/05/01 03:16 [entrez]
 2022/09/18 00:00 [revised] 2022/06/28 00:00 [received] 2022/11/09 00:00 [accepted] 2022/11/17 06:00 [pubmed] 2023/01/06 06:00 [medline] 2022/11/16 01:42 [entrez]
 2022/10/11 00:00 [received] 2023/01/17 00:00 [revised] 2023/01/30 00:00 [accepted] 2023/02/04 06:00 [pubmed] 2023/02/16 06:00 [medline] 2023/02/03 19:26 [entrez]
 2022/12/20 00:00 [received] 2023/02/10 00:00 [revised] 2023/02/16 00:00 [accepted] 2023/02/23 06:00 [pubmed] 2023/03/23 06:00 [medline] 2023/02/22 14:12 [entrez]
 2023/01/06 00:00 [received] 2023/02/21 00:00 [revised] 2023/02/28 00:00 [accepted] 2023/06/05 06:43 [medline] 2023/05/09 00:42 [pubmed] 2023/05/08 18:53 [entrez]
 2023/07/27 00:00 [accepted] 2023/08/04 13:11 [medline] 2023/08/04 13:11 [pubmed] 2023/08/04 11:07 [entrez]
 2022/04/12 00:00 [received] 2023/07/12 01:07 [pubmed] 2023/07/12 01:07 [medline] 2023/07/11 19:17 [entrez]
 2022/06/03 00:00 [received] 2023/04/01 00:00 [accepted] 2023/04/18 06:42 [medline] 2023/04/14 13:43 [entrez] 2023/04/15 06:00 [pubmed]
 2022/04/01 00:00 [received] 2022/09/07 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/01/15 06:00 [pubmed] 2023/02/07 06:00 [medline] 2023/01/14 12:37 [entrez]
 2023/02/14 06:00 [pubmed] 2023/02/14 06:01 [medline] 2023/02/13 03:47 [entrez]
 2021/09/24 00:00 [received] 2023/04/28 00:00 [revised] 2023/06/21 00:00 [accepted] 2023/08/04 06:42 [medline] 2023/08/03 06:43 [pubmed] 2023/08/03 03:55 [entrez]
 2023/05/15 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 02:22 [entrez]
 2022/01/04 00:00 [received] 2022/05/20 00:00 [accepted] 2023/07/26 06:43 [medline] 2022/06/07 06:00 [pubmed] 2022/06/06 13:16 [entrez]
 2023/01/10 00:00 [received] 2023/02/26 00:00 [accepted] 2023/05/05 06:43 [medline] 2023/05/05 06:42 [pubmed] 2023/05/05 03:56 [entrez]
 2022/06/12 00:00 [received] 2022/09/11 00:00 [revised] 2022/10/17 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/02/14 06:00 [pubmed] 2023/02/13 21:57 [entrez]
 2023/01/07 00:00 [revised] 2022/06/07 00:00 [received] 2023/01/18 00:00 [accepted] 2023/01/21 06:00 [pubmed] 2023/03/04 06:00 [medline] 2023/01/20 22:43 [entrez]
 2023/06/08 06:42 [medline] 2023/05/17 06:42 [pubmed] 2023/05/17 00:52 [entrez]
 2022/11/10 00:00 [received] 2023/05/24 00:00 [accepted] 2023/06/07 13:10 [medline] 2023/06/07 13:10 [pubmed] 2023/06/07 11:12 [entrez]
 2022/06/20 00:00 [received] 2023/03/03 00:00 [accepted] 2023/05/22 06:42 [medline] 2023/05/19 19:14 [pubmed] 2023/05/19 13:34 [entrez]
 2022/10/19 00:00 [received] 2023/01/08 00:00 [accepted] 2023/02/17 02:09 [entrez] 2023/02/18 06:00 [pubmed] 2023/02/18 06:01 [medline]
 2022/12/28 00:00 [revised] 2022/10/21 00:00 [received] 2023/01/19 00:00 [accepted] 2023/04/18 10:16 [medline] 2023/02/01 06:00 [pubmed] 2023/01/31 02:12 [entrez]
 2022/04/26 00:00 [received] 2022/12/02 00:00 [revised] 2022/12/09 00:00 [accepted] 2022/12/17 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/12/16 21:06 [entrez]
 2023/07/03 00:42 [medline] 2023/07/03 00:41 [pubmed] 2023/07/02 20:02 [entrez]
 2023/02/22 06:00 [pubmed] 2023/03/10 06:00 [medline] 2023/02/21 17:36 [entrez]
 2023/05/23 06:42 [medline] 2023/04/18 06:00 [pubmed] 2023/04/17 06:13 [entrez]
 2021/11/15 00:00 [received] 2022/11/16 00:00 [revised] 2023/01/12 00:00 [accepted] 2024/02/02 00:00 [pmc-release] 2023/02/03 18:21 [entrez] 2023/02/04 06:00 [pubmed] 2023/02/08 06:00 [medline]
 2023/08/18 06:43 [medline] 2023/08/17 00:42 [pubmed] 2023/08/16 22:33 [entrez]
 2022/11/01 00:00 [received] 2023/02/24 00:00 [accepted] 2023/02/22 00:00 [revised] 2023/03/17 12:15 [entrez] 2023/03/18 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2023/04/11 00:00 [received] 2023/06/27 00:00 [accepted] 2023/06/23 00:00 [revised] 2023/07/02 19:13 [medline] 2023/07/02 19:13 [pubmed] 2023/07/02 14:54 [entrez]
 2023/04/13 00:00 [received] 2023/06/12 00:00 [accepted] 2023/07/17 06:43 [medline] 2023/07/17 06:42 [pubmed] 2023/07/17 04:45 [entrez]
 2023/03/30 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 04:13 [entrez]
 2023/02/08 00:00 [received] 2023/03/03 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:23 [entrez] 2023/03/30 06:00 [pubmed]
 2023/05/09 06:42 [medline] 2023/03/14 06:00 [pubmed] 2023/03/13 04:34 [entrez]
 2022/12/23 00:00 [received] 2023/02/16 00:00 [accepted] 2023/03/27 03:29 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2022/09/26 00:00 [received] 2023/02/06 00:00 [accepted] 2023/04/01 06:01 [medline] 2023/03/31 02:10 [entrez] 2023/04/01 06:00 [pubmed]
 2022/06/20 00:00 [received] 2023/03/14 00:00 [accepted] 2023/07/03 06:41 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 23:21 [entrez]
 2023/03/20 00:00 [received] 2023/08/25 00:00 [accepted] 2023/09/11 06:41 [medline] 2023/09/08 00:42 [pubmed] 2023/09/07 23:25 [entrez]
 2023/06/27 00:00 [revised] 2023/04/20 00:00 [received] 2023/07/12 00:00 [accepted] 2023/07/25 06:42 [medline] 2023/07/25 06:42 [pubmed] 2023/07/25 03:14 [entrez]
 2023/09/07 06:42 [medline] 2023/09/05 18:42 [pubmed] 2023/09/05 14:03 [entrez]
 2023/04/21 00:00 [received] 2023/07/24 00:00 [revised] 2023/07/26 00:00 [accepted] 2023/08/28 06:43 [medline] 2023/08/28 06:42 [pubmed] 2023/08/28 04:53 [entrez]
 2022/09/21 00:00 [received] 2023/05/26 00:00 [accepted] 2023/06/16 06:42 [medline] 2023/06/15 01:08 [pubmed] 2023/06/14 23:37 [entrez]
 2022/06/03 00:00 [received] 2022/09/26 00:00 [accepted] 2022/11/21 21:43 [entrez] 2022/11/22 06:00 [pubmed] 2022/11/24 06:00 [medline]
 2021/06/09 00:00 [received] 2022/11/05 00:00 [accepted] 2022/12/15 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/12/14 23:28 [entrez]
 2023/03/09 14:05 [entrez] 2023/03/10 06:00 [pubmed] 2023/03/14 06:00 [medline]
 2022/11/25 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/06/23 13:08 [medline] 2023/06/23 13:07 [pubmed] 2023/06/23 10:32 [entrez]
 2023/01/17 00:00 [received] 2023/02/27 00:00 [accepted] 2023/03/27 03:21 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2023/04/02 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/31 00:00 [accepted] 2023/06/11 01:06 [pubmed] 2023/06/11 01:06 [medline] 2023/06/10 18:01 [entrez]
 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:32 [entrez]
 2022/07/03 00:00 [received] 2022/11/09 00:00 [revised] 2022/11/12 00:00 [accepted] 2022/11/20 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/11/19 19:27 [entrez]
 2023/08/14 06:44 [medline] 2023/08/14 06:43 [pubmed] 2023/08/14 05:03 [entrez]
 2022/09/20 00:00 [received] 2023/02/09 00:00 [revised] 2023/03/15 00:00 [accepted] 2023/10/26 00:00 [pmc-release] 2023/05/17 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 21:03 [entrez]
 2022/08/30 00:00 [received] 2022/12/06 00:00 [accepted] 2022/12/19 06:00 [pubmed] 2023/02/25 06:00 [medline] 2022/12/18 14:42 [entrez]
 2023/05/12 00:00 [revised] 2023/02/17 00:00 [received] 2023/05/17 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/05/28 13:10 [pubmed] 2023/05/28 06:12 [entrez]
 2023/01/19 00:00 [received] 2023/05/13 00:00 [revised] 2023/05/13 00:00 [accepted] 2023/05/26 01:05 [medline] 2023/05/26 01:05 [pubmed] 2023/05/25 21:58 [entrez]
 2023/02/08 00:00 [received] 2023/04/21 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/05/05 12:42 [pubmed] 2023/05/05 11:08 [entrez]
 2022/12/09 00:00 [accepted] 2023/05/17 06:42 [medline] 2023/01/09 06:00 [pubmed] 2023/01/08 23:20 [entrez]
 2022/09/16 00:00 [received] 2022/12/03 00:00 [accepted] 2022/12/11 06:00 [pubmed] 2022/12/11 06:00 [medline] 2022/12/10 11:13 [entrez]
 2022/12/30 00:00 [received] 2023/02/02 00:00 [revised] 2023/02/23 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:17 [entrez] 2023/03/30 06:00 [pubmed]
 2022/05/24 00:00 [received] 2022/11/23 00:00 [revised] 2022/12/08 00:00 [accepted] 2023/01/02 04:20 [entrez] 2023/01/03 06:00 [pubmed] 2023/01/03 06:01 [medline]
 2022/11/12 00:00 [revised] 2022/10/06 00:00 [received] 2022/11/28 00:00 [accepted] 2022/12/07 06:00 [pubmed] 2023/03/07 06:00 [medline] 2022/12/06 00:53 [entrez]
 2022/08/19 00:00 [received] 2023/01/30 00:00 [revised] 2023/08/07 00:00 [accepted] 2023/09/01 00:42 [medline] 2023/09/01 00:42 [pubmed] 2023/08/31 18:42 [entrez]
 2022/11/15 00:00 [received] 2023/03/03 00:00 [revised] 2023/03/07 00:00 [accepted] 2023/05/29 06:42 [medline] 2023/03/27 06:00 [pubmed] 2023/03/26 19:08 [entrez]
 2022/06/21 00:00 [received] 2023/02/02 00:00 [accepted] 2023/03/16 02:30 [entrez] 2023/03/17 06:00 [pubmed] 2023/03/17 06:01 [medline]
 2022/06/20 00:00 [received] 2022/09/24 00:00 [accepted] 2022/09/23 00:00 [revised] 2022/11/22 06:00 [pubmed] 2023/03/03 06:00 [medline] 2022/11/21 23:36 [entrez]
 2024/02/28 00:00 [pmc-release] 2023/08/31 06:42 [medline] 2023/08/28 18:41 [pubmed] 2023/08/28 15:23 [entrez]
 2023/02/05 00:00 [revised] 2022/12/08 00:00 [received] 2023/02/07 00:00 [accepted] 2023/04/18 10:16 [medline] 2023/04/11 06:00 [pubmed] 2023/04/10 08:12 [entrez]
 2022/09/30 00:00 [received] 2022/11/18 00:00 [accepted] 2023/08/01 06:45 [medline] 2022/12/03 06:00 [pubmed] 2022/12/02 11:47 [entrez]
 2023/03/02 00:00 [received] 2023/07/31 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/18 00:42 [pubmed] 2023/08/17 23:25 [entrez]
 2022/09/27 00:00 [received] 2022/12/12 00:00 [revised] 2023/01/25 00:00 [accepted] 2023/02/10 06:00 [pubmed] 2023/03/14 06:00 [medline] 2023/02/09 18:13 [entrez]
 2023/05/05 00:00 [received] 2023/05/30 00:00 [revised] 2023/06/01 00:00 [accepted] 2023/06/23 06:42 [medline] 2023/06/05 00:42 [pubmed] 2023/06/04 19:27 [entrez]
 2023/07/10 06:43 [medline] 2023/07/10 06:42 [pubmed] 2023/07/10 05:00 [entrez]
 2022/12/23 00:00 [received] 2023/01/31 00:00 [revised] 2023/01/31 00:00 [accepted] 2023/02/25 01:03 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2022/04/12 00:00 [revised] 2022/01/30 00:00 [received] 2022/04/13 00:00 [accepted] 2023/05/15 06:42 [medline] 2022/04/19 06:00 [pubmed] 2022/04/18 06:45 [entrez]
 2022/11/24 21:04 [entrez] 2022/11/25 06:00 [pubmed] 2022/11/29 06:00 [medline]
 2023/03/14 00:00 [received] 2023/05/16 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 04:27 [entrez]
 2022/12/22 00:00 [received] 2023/02/11 00:00 [revised] 2023/02/22 00:00 [accepted] 2023/04/07 06:41 [medline] 2023/03/09 06:00 [pubmed] 2023/03/08 18:10 [entrez]
 2023/07/31 06:43 [medline] 2023/07/30 06:42 [pubmed] 2023/07/30 01:22 [entrez]
 2022/12/05 00:00 [received] 2023/05/03 00:00 [revised] 2023/05/08 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/06/12 06:42 [pubmed] 2023/06/12 04:03 [entrez]
 2022/12/31 00:00 [received] 2023/03/13 00:00 [revised] 2023/03/19 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/28 15:13 [entrez] 2023/03/29 06:00 [pubmed]
 2022/12/13 00:00 [accepted] 2023/01/12 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/01/11 11:21 [entrez]
 2023/07/25 13:09 [medline] 2023/07/25 13:09 [pubmed] 2023/07/25 09:22 [entrez]
 2023/03/07 00:00 [received] 2023/07/05 00:00 [revised] 2023/07/06 00:00 [accepted] 2023/07/24 06:42 [medline] 2023/07/11 01:07 [pubmed] 2023/07/10 19:22 [entrez]
 2023/05/15 00:00 [received] 2023/05/26 00:00 [accepted] 2023/06/22 06:42 [medline] 2023/06/08 13:07 [pubmed] 2023/06/08 06:53 [entrez]
 2023/03/28 00:00 [received] 2023/05/06 00:00 [revised] 2023/05/06 00:00 [accepted] 2023/05/27 09:43 [medline] 2023/05/27 09:42 [pubmed] 2023/05/27 01:17 [entrez]
 2022/12/26 00:00 [received] 2023/08/16 00:00 [accepted] 2023/09/01 06:43 [medline] 2023/08/31 00:41 [pubmed] 2023/08/30 23:17 [entrez]
 2023/05/19 19:16 [medline] 2023/05/19 19:15 [pubmed] 2023/05/19 13:08 [entrez]
 2023/02/01 00:00 [received] 2023/03/29 00:00 [accepted] 2023/04/20 06:42 [medline] 2023/04/20 06:41 [pubmed] 2023/04/20 02:15 [entrez]
 2022/06/01 00:00 [received] 2022/08/28 00:00 [accepted] 2023/04/04 06:01 [medline] 2023/04/03 04:07 [entrez] 2023/04/04 06:00 [pubmed]
 2023/05/15 19:12 [pubmed] 2023/05/15 19:12 [medline] 2023/05/15 14:39 [entrez]
 2022/05/25 00:00 [received] 2022/10/06 00:00 [accepted] 2022/10/18 06:00 [pubmed] 2023/01/18 06:00 [medline] 2022/10/17 12:04 [entrez]
 2023/09/07 06:43 [medline] 2023/09/07 06:42 [pubmed] 2023/09/07 04:04 [entrez]
 2022/12/30 00:00 [received] 2023/02/03 00:00 [revised] 2023/02/15 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:20 [entrez] 2023/03/30 06:00 [pubmed]
 2023/03/20 05:03 [entrez] 2023/03/21 06:00 [pubmed] 2023/03/22 06:00 [medline]
 2023/01/11 00:00 [received] 2023/04/13 00:00 [revised] 2023/04/26 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 19:24 [entrez]
 2022/05/23 00:00 [received] 2022/09/23 00:00 [accepted] 2023/07/17 06:42 [medline] 2022/10/20 06:00 [pubmed] 2022/10/19 21:43 [entrez]
 2023/04/24 06:41 [medline] 2023/04/20 13:41 [pubmed] 2023/04/20 09:47 [entrez]
 2023/03/24 00:00 [received] 2023/05/22 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:35 [entrez]
 2023/09/08 06:42 [medline] 2023/09/07 12:42 [pubmed] 2023/09/07 11:33 [entrez]
 2023/06/16 06:42 [medline] 2023/05/04 18:41 [pubmed] 2023/05/04 15:03 [entrez]
 2023/03/22 19:43 [entrez] 2023/03/23 06:00 [pubmed] 2023/03/25 06:00 [medline]
 2023/04/04 00:00 [revised] 2023/03/20 00:00 [received] 2023/04/25 00:00 [accepted] 2023/05/02 06:41 [pubmed] 2023/05/02 06:41 [medline] 2023/05/02 04:03 [entrez]
 2022/09/23 00:00 [received] 2022/11/03 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/02/08 06:00 [medline] 2022/12/08 11:57 [entrez]
 2023/02/24 00:00 [received] 2023/04/03 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 03:53 [entrez]
 2022/05/27 00:00 [received] 2022/08/09 00:00 [revised] 2022/08/16 00:00 [accepted] 2022/09/19 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/09/18 19:23 [entrez]
 2022/07/20 00:00 [received] 2022/12/22 00:00 [revised] 2022/12/23 00:00 [accepted] 2023/01/01 06:00 [pubmed] 2023/02/08 06:00 [medline] 2022/12/31 19:12 [entrez]
 2023/02/01 00:00 [revised] 2022/10/20 00:00 [received] 2023/02/07 00:00 [accepted] 2023/05/12 07:06 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 21:02 [entrez]
 2023/01/04 00:00 [received] 2023/02/10 00:00 [accepted] 2023/09/04 06:43 [medline] 2023/02/25 06:00 [pubmed] 2023/02/24 08:23 [entrez]
 2023/07/14 00:00 [revised] 2023/01/23 00:00 [received] 2023/07/23 00:00 [accepted] 2023/08/07 06:41 [medline] 2023/08/07 06:41 [pubmed] 2023/08/07 00:43 [entrez]
 2023/05/31 00:00 [revised] 2022/12/20 00:00 [received] 2023/06/22 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/07/11 13:10 [pubmed] 2023/07/11 11:14 [entrez]
 2023/03/23 00:00 [revised] 2022/12/21 00:00 [received] 2023/03/25 00:00 [accepted] 2023/05/11 06:42 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 10:08 [entrez]
 2023/03/20 00:00 [received] 2023/07/24 00:00 [revised] 2023/08/14 00:00 [accepted] 2023/08/22 00:42 [medline] 2023/08/22 00:42 [pubmed] 2023/08/21 22:03 [entrez]
 2023/03/25 00:00 [received] 2023/05/17 00:00 [revised] 2023/05/24 00:00 [accepted] 2023/06/10 15:15 [medline] 2023/06/10 15:14 [pubmed] 2023/06/10 01:09 [entrez]
 2022/07/06 00:00 [received] 2022/09/05 00:00 [revised] 2022/10/26 00:00 [accepted] 2023/08/31 06:42 [medline] 2022/11/19 06:00 [pubmed] 2022/11/18 11:43 [entrez]
 2024/05/01 00:00 [pmc-release] 2023/05/08 06:41 [medline] 2022/10/28 06:00 [pubmed] 2022/10/27 13:54 [entrez]
 2023/03/24 00:00 [received] 2023/06/12 00:00 [accepted] 2023/08/03 06:43 [medline] 2023/08/02 06:43 [pubmed] 2023/08/02 03:49 [entrez]
 2023/03/07 00:00 [received] 2023/07/19 00:00 [accepted] 2023/07/17 00:00 [revised] 2023/08/01 01:08 [pubmed] 2023/08/01 01:08 [medline] 2023/07/31 23:26 [entrez]
 2022/09/12 00:00 [received] 2023/06/21 00:00 [accepted] 2023/08/14 06:41 [medline] 2023/06/29 13:42 [pubmed] 2023/06/29 11:15 [entrez]
 2023/01/23 00:00 [received] 2023/02/03 00:00 [revised] 2023/02/27 00:00 [accepted] 2023/03/30 06:01 [medline] 2023/03/29 01:46 [entrez] 2023/03/30 06:00 [pubmed]
 2022/11/11 00:00 [received] 2023/01/25 00:00 [accepted] 2023/03/06 03:52 [entrez] 2023/03/07 06:00 [pubmed] 2023/03/07 06:01 [medline]
 2023/05/03 06:42 [medline] 2023/01/31 06:00 [pubmed] 2023/01/30 04:37 [entrez]
 2022/12/09 06:00 [pubmed] 2023/02/17 06:00 [medline] 2022/12/08 09:55 [entrez]
 2023/09/07 06:42 [pubmed] 2023/09/07 06:42 [medline] 2023/09/07 05:31 [entrez]
 2023/04/06 00:00 [revised] 2022/12/01 00:00 [received] 2023/04/16 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 06:41 [pubmed] 2023/05/08 03:46 [entrez]
 2022/11/13 00:00 [received] 2023/08/30 00:00 [accepted] 2023/09/13 06:41 [medline] 2023/09/12 00:42 [pubmed] 2023/09/11 23:22 [entrez]
 2023/01/12 00:00 [revised] 2022/10/28 00:00 [received] 2023/01/19 00:00 [accepted] 2023/04/06 10:16 [medline] 2023/01/25 06:00 [pubmed] 2023/01/24 11:54 [entrez]
 2022/12/21 00:00 [received] 2023/02/20 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 11:16 [entrez]
 2023/01/06 00:00 [received] 2023/02/12 00:00 [revised] 2023/02/14 00:00 [accepted] 2023/02/25 03:07 [entrez] 2023/02/26 06:00 [pubmed] 2023/02/26 06:01 [medline]
 2023/05/12 00:00 [revised] 2023/02/06 00:00 [received] 2023/05/19 00:00 [accepted] 2023/09/07 06:43 [medline] 2023/05/23 19:09 [pubmed] 2023/05/23 13:35 [entrez]
 2022/04/26 00:00 [received] 2022/08/22 00:00 [revised] 2022/09/19 00:00 [accepted] 2023/01/16 06:00 [pubmed] 2023/03/04 06:00 [medline] 2023/01/15 19:12 [entrez]
 2022/11/07 00:00 [revised] 2022/08/15 00:00 [received] 2022/11/10 00:00 [accepted] 2022/11/15 06:00 [pubmed] 2023/01/31 06:00 [medline] 2022/11/14 00:22 [entrez]
 2023/06/11 00:00 [received] 2023/07/18 00:00 [accepted] 2023/07/17 00:00 [revised] 2023/07/26 06:42 [medline] 2023/07/26 06:42 [pubmed] 2023/07/26 00:07 [entrez]
 2022/09/06 00:00 [received] 2022/11/03 00:00 [accepted] 2022/12/09 06:00 [pubmed] 2023/02/07 06:00 [medline] 2022/12/08 11:30 [entrez]
 2022/07/21 00:00 [revised] 2022/03/14 00:00 [received] 2022/10/20 00:00 [accepted] 2024/04/01 00:00 [pmc-release] 2023/04/11 06:42 [medline] 2022/10/26 06:00 [pubmed] 2022/10/25 04:52 [entrez]
 2023/01/04 20:54 [entrez] 2023/01/05 06:00 [pubmed] 2023/01/07 06:00 [medline]
 2022/09/28 00:00 [received] 2023/01/08 00:00 [accepted] 2023/04/17 06:41 [medline] 2023/01/24 06:00 [pubmed] 2023/01/23 21:22 [entrez]
 2023/04/01 00:00 [received] 2023/05/05 00:00 [accepted] 2023/05/04 00:00 [revised] 2023/06/16 06:42 [medline] 2023/05/15 13:06 [pubmed] 2023/05/15 11:13 [entrez]
 2023/06/23 06:42 [medline] 2023/05/25 13:07 [pubmed] 2023/05/25 09:43 [entrez]
 2023/05/19 00:00 [received] 2023/05/19 00:00 [accepted] 2024/05/24 00:00 [pmc-release] 2023/07/05 06:42 [medline] 2023/05/24 19:13 [pubmed] 2023/05/24 17:13 [entrez]
 2023/06/19 00:00 [accepted] 2023/08/02 06:42 [medline] 2023/08/01 01:08 [pubmed] 2023/07/31 20:33 [entrez]
 2022/06/30 00:00 [received] 2022/08/08 00:00 [accepted] 2023/09/04 06:41 [medline] 2023/09/01 06:43 [pubmed] 2023/09/01 04:13 [entrez]
 2023/08/21 06:42 [medline] 2023/08/21 06:42 [pubmed] 2023/08/21 03:33 [entrez]
 2022/10/24 00:00 [received] 2022/12/13 00:00 [accepted] 2023/02/02 02:06 [entrez] 2023/02/03 06:00 [pubmed] 2023/02/03 06:01 [medline]
 2023/01/30 03:56 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/08/25 00:00 [received] 2022/09/27 00:00 [accepted] 2022/08/25 00:00 [revised] 2022/11/03 06:00 [pubmed] 2023/03/24 06:00 [medline] 2022/11/02 12:22 [entrez]
 2023/07/03 13:06 [pubmed] 2023/07/03 13:07 [medline] 2023/07/03 11:46 [entrez]
 2023/04/25 06:43 [medline] 2023/04/25 06:42 [pubmed] 2023/04/25 02:05 [entrez]
 2023/07/28 06:43 [pubmed] 2023/07/28 06:44 [medline] 2023/07/28 04:28 [entrez]
 2023/01/24 00:00 [revised] 2022/12/22 00:00 [received] 2023/02/17 00:00 [accepted] 2023/05/04 12:41 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 02:43 [entrez]
 2023/02/20 00:00 [received] 2023/07/13 00:00 [accepted] 2023/09/01 06:44 [medline] 2023/09/01 06:43 [pubmed] 2023/09/01 04:10 [entrez]
 2023/04/24 06:41 [pubmed] 2023/04/24 06:42 [medline] 2023/04/24 03:44 [entrez]
 2023/01/30 03:55 [entrez] 2023/01/31 06:00 [pubmed] 2023/01/31 06:01 [medline]
 2022/12/15 00:00 [received] 2023/02/04 00:00 [accepted] 2023/02/03 00:00 [revised] 2023/05/18 06:42 [medline] 2023/03/08 06:00 [pubmed] 2023/03/07 23:27 [entrez]
 2021/09/25 00:00 [received] 2021/12/21 00:00 [accepted] 2023/05/26 19:15 [medline] 2023/05/26 19:14 [pubmed] 2023/05/26 12:23 [entrez]
 2022/11/12 00:00 [received] 2023/05/11 00:00 [accepted] 2024/07/01 00:00 [pmc-release] 2023/07/14 13:08 [medline] 2023/06/09 01:09 [pubmed] 2023/06/08 20:52 [entrez]
 2023/07/11 06:42 [medline] 2023/04/21 06:41 [pubmed] 2023/04/21 00:03 [entrez]
 2022/08/09 00:00 [received] 2022/09/24 00:00 [revised] 2022/10/22 00:00 [accepted] 2022/11/03 06:00 [pubmed] 2023/01/25 06:00 [medline] 2022/11/02 20:24 [entrez]
 2022/10/24 00:00 [revised] 2022/08/20 00:00 [received] 2022/10/25 00:00 [accepted] 2022/10/28 06:00 [pubmed] 2023/01/21 06:00 [medline] 2022/10/27 07:23 [entrez]
 2023/04/29 00:00 [revised] 2023/02/20 00:00 [received] 2023/05/02 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/09 18:41 [pubmed] 2023/05/09 13:44 [entrez]
 2023/02/15 00:00 [received] 2023/03/08 00:00 [accepted] 2023/06/12 06:43 [medline] 2023/04/05 06:00 [pubmed] 2023/04/04 11:20 [entrez]
 2023/04/12 06:41 [medline] 2023/02/28 06:00 [pubmed] 2023/02/27 06:31 [entrez]
 2023/01/13 00:00 [revised] 2023/01/04 00:00 [received] 2023/02/02 00:00 [accepted] 2023/04/06 06:41 [medline] 2023/02/12 06:00 [pubmed] 2023/02/11 09:03 [entrez]
 2022/07/29 00:00 [revised] 2022/06/09 00:00 [received] 2022/08/14 00:00 [accepted] 2022/10/15 06:00 [pubmed] 2023/01/27 06:00 [medline] 2022/10/14 10:56 [entrez]
 2023/03/08 00:00 [revised] 2022/12/17 00:00 [received] 2023/04/11 00:00 [accepted] 2023/07/06 06:42 [medline] 2023/05/08 06:42 [pubmed] 2023/05/08 03:45 [entrez]
 2022/11/09 00:00 [received] 2023/01/22 00:00 [revised] 2023/01/23 00:00 [accepted] 2023/02/09 06:00 [pubmed] 2023/03/03 06:00 [medline] 2023/02/08 18:15 [entrez]
 2023/03/18 00:00 [received] 2023/06/06 00:00 [accepted] 2023/07/07 06:42 [medline] 2023/07/06 06:42 [pubmed] 2023/07/06 04:21 [entrez]
 2023/04/03 00:00 [revised] 2022/11/24 00:00 [received] 2023/06/08 00:00 [accepted] 2023/06/19 00:42 [pubmed] 2023/06/19 00:42 [medline] 2023/06/18 23:37 [entrez]
 2023/02/14 00:00 [received] 2023/05/09 00:00 [accepted] 2023/06/26 19:08 [medline] 2023/06/26 19:07 [pubmed] 2023/06/26 12:33 [entrez]
 2023/04/01 00:00 [received] 2023/06/01 00:00 [accepted] 2023/08/15 12:43 [medline] 2023/08/15 12:43 [pubmed] 2023/08/15 09:03 [entrez]
 2022/10/07 00:00 [received] 2023/03/02 00:00 [revised] 2023/03/28 00:00 [accepted] 2023/04/18 13:13 [entrez] 2023/04/19 06:00 [pubmed] 2023/04/19 06:00 [medline]
 2023/03/02 00:00 [received] 2023/04/30 00:00 [accepted] 2023/06/14 01:11 [medline] 2023/06/14 01:10 [pubmed] 2023/06/13 23:44 [entrez]
 2022/03/07 00:00 [received] 2022/09/26 00:00 [accepted] 2022/09/14 00:00 [revised] 2023/03/30 06:11 [medline] 2022/10/13 06:00 [pubmed] 2022/10/12 23:30 [entrez]
 2022/03/09 00:00 [received] 2023/05/19 00:00 [accepted] 2023/07/13 06:42 [medline] 2023/06/30 01:06 [pubmed] 2023/06/29 23:29 [entrez]
 2023/07/03 06:41 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 08:33 [entrez]
 2022/04/25 00:00 [received] 2023/02/07 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/06/09 06:43 [medline] 2023/06/09 06:42 [pubmed] 2023/06/09 04:34 [entrez]
 2023/01/14 00:00 [received] 2023/02/27 00:00 [revised] 2023/03/02 00:00 [accepted] 2023/04/14 06:41 [medline] 2023/04/13 01:24 [entrez] 2023/04/14 06:00 [pubmed]
 2023/01/23 00:00 [revised] 2021/10/27 00:00 [received] 2023/01/30 00:00 [accepted] 2023/04/12 06:42 [medline] 2023/02/02 06:00 [pubmed] 2023/02/01 07:13 [entrez]
 2023/05/23 00:00 [received] 2023/06/28 00:00 [accepted] 2023/07/26 06:43 [medline] 2023/07/25 01:09 [pubmed] 2023/07/24 23:45 [entrez]
 2022/11/23 00:00 [received] 2023/02/13 00:00 [accepted] 2023/05/01 06:43 [medline] 2023/05/01 06:42 [pubmed] 2023/05/01 03:44 [entrez]
 2023/02/28 00:00 [revised] 2022/12/20 00:00 [received] 2023/03/01 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/03/04 06:00 [pubmed] 2023/03/03 07:13 [entrez]
 2023/05/19 00:00 [revised] 2022/10/26 00:00 [received] 2023/07/11 00:00 [accepted] 2023/08/10 06:43 [medline] 2023/08/10 06:43 [pubmed] 2023/08/10 02:13 [entrez]
 2022/11/18 00:00 [received] 2022/12/16 00:00 [accepted] 2023/02/09 02:26 [entrez] 2023/02/10 06:00 [pubmed] 2023/02/10 06:01 [medline]
 2022/10/02 00:00 [received] 2022/12/23 00:00 [accepted] 2022/12/22 00:00 [revised] 2023/01/10 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/01/09 23:20 [entrez]
 2022/10/01 00:00 [received] 2022/10/31 00:00 [accepted] 2023/08/24 06:42 [medline] 2022/11/27 06:00 [pubmed] 2022/11/26 01:46 [entrez]
 2023/06/22 06:42 [medline] 2023/06/20 19:15 [pubmed] 2023/06/20 14:03 [entrez]
 2023/02/23 00:00 [received] 2023/04/28 00:00 [accepted] 2023/05/05 00:43 [medline] 2023/05/05 00:42 [pubmed] 2023/05/04 23:47 [entrez]
 2022/10/29 00:00 [revised] 2022/07/07 00:00 [received] 2022/10/31 00:00 [accepted] 2022/11/02 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/11/01 10:43 [entrez]
 2023/05/17 06:42 [medline] 2023/04/14 06:00 [pubmed] 2023/04/13 12:32 [entrez]
 2022/09/05 00:00 [received] 2022/09/27 00:00 [revised] 2022/09/29 00:00 [accepted] 2022/10/08 06:00 [pubmed] 2022/12/06 06:00 [medline] 2022/10/07 19:12 [entrez]
 2022/09/20 00:00 [revised] 2022/04/04 00:00 [received] 2022/09/22 00:00 [accepted] 2022/09/25 06:00 [pubmed] 2023/01/31 06:00 [medline] 2022/09/24 01:12 [entrez]
 2022/03/08 00:00 [received] 2022/06/20 00:00 [accepted] 2023/08/16 06:43 [medline] 2022/07/26 06:00 [pubmed] 2022/07/25 11:22 [entrez]
 2022/03/31 00:00 [received] 2022/07/03 00:00 [revised] 2022/07/18 00:00 [accepted] 2022/09/27 06:00 [pubmed] 2023/03/04 06:00 [medline] 2022/09/26 14:54 [entrez]
 2023/07/03 06:41 [medline] 2023/03/18 06:00 [pubmed] 2023/03/17 08:16 [entrez]
 2023/08/23 06:43 [medline] 2023/08/23 06:42 [pubmed] 2023/08/23 04:19 [entrez]
 2023/08/10 06:42 [medline] 2023/07/11 06:42 [pubmed] 2023/07/11 02:23 [entrez]
 2023/02/05 00:00 [received] 2023/03/06 00:00 [accepted] 2023/03/05 00:00 [revised] 2023/04/28 06:41 [medline] 2023/03/22 06:00 [pubmed] 2023/03/21 12:16 [entrez]
 2021/09/16 00:00 [received] 2023/02/02 00:00 [accepted] 2023/04/03 06:42 [medline] 2023/03/22 06:00 [pubmed] 2023/03/21 00:22 [entrez]
 2022/10/22 00:00 [received] 2023/01/27 00:00 [accepted] 2023/01/25 00:00 [revised] 2023/04/27 06:42 [medline] 2023/02/23 06:00 [pubmed] 2023/02/22 10:57 [entrez]
 2022/01/18 00:00 [received] 2022/10/26 00:00 [accepted] 2024/02/01 00:00 [pmc-release] 2023/01/05 06:00 [pubmed] 2023/02/02 06:00 [medline] 2023/01/04 23:22 [entrez]
 2022/12/07 00:00 [revised] 2022/08/25 00:00 [received] 2022/12/09 00:00 [accepted] 2023/01/04 06:00 [pubmed] 2023/02/17 06:00 [medline] 2023/01/03 04:42 [entrez]
 2022/09/26 00:00 [accepted] 2022/11/02 06:01 [medline] 2022/11/02 06:00 [pubmed] 2022/11/01 00:38 [entrez]
 2024/01/01 00:00 [pmc-release] 2022/08/26 06:00 [pubmed] 2023/01/04 06:00 [medline] 2022/08/25 06:03 [entrez]
 2022/08/14 00:00 [received] 2022/10/09 00:00 [revised] 2022/10/30 00:00 [accepted] 2022/11/06 06:00 [pubmed] 2022/12/02 06:00 [medline] 2022/11/05 20:34 [entrez]
 2022/09/14 00:00 [received] 2023/03/03 00:00 [revised] 2023/03/24 00:00 [accepted] 2023/06/01 06:42 [medline] 2023/05/01 00:42 [pubmed] 2023/04/30 18:09 [entrez]
 2023/01/10 00:00 [received] 2023/03/30 00:00 [accepted] 2023/08/28 06:43 [medline] 2023/04/21 00:41 [pubmed] 2023/04/20 21:22 [entrez]
 2023/03/27 00:00 [revised] 2023/01/06 00:00 [received] 2023/03/28 00:00 [accepted] 2023/06/05 06:42 [medline] 2023/04/12 06:00 [pubmed] 2023/04/11 05:32 [entrez]
 2022/10/06 00:00 [received] 2023/03/15 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/04/01 06:00 [pubmed] 2023/03/31 21:12 [entrez]
 2024/09/05 00:00 [pmc-release] 2023/09/05 12:42 [medline] 2023/09/05 12:42 [pubmed] 2023/09/05 11:33 [entrez]
 2022/11/15 00:00 [received] 2023/05/11 00:00 [accepted] 2023/08/02 06:43 [medline] 2023/08/02 06:42 [pubmed] 2023/08/02 04:01 [entrez]
 2022/10/13 00:00 [received] 2022/12/23 00:00 [revised] 2023/01/26 00:00 [accepted] 2023/02/10 06:00 [pubmed] 2023/03/22 06:00 [medline] 2023/02/09 18:19 [entrez]
 2023/09/07 06:43 [medline] 2023/08/11 18:42 [pubmed] 2023/08/11 15:13 [entrez]
 2022/07/27 00:00 [received] 2022/10/27 00:00 [revised] 2022/11/08 00:00 [accepted] 2022/11/30 06:00 [pubmed] 2023/01/19 06:00 [medline] 2022/11/29 21:23 [entrez]
 2021/07/19 00:00 [received] 2023/08/07 00:00 [accepted] 2023/08/21 06:42 [medline] 2023/08/19 11:42 [pubmed] 2023/08/18 23:15 [entrez]
 2023/08/07 06:41 [medline] 2023/08/04 01:08 [pubmed] 2023/08/03 21:38 [entrez]
 2023/03/06 00:00 [revised] 2022/11/29 00:00 [received] 2023/03/16 00:00 [accepted] 2023/03/21 06:00 [pubmed] 2023/03/21 06:00 [medline] 2023/03/20 04:53 [entrez]
 2022/03/15 00:00 [received] 2023/02/07 00:00 [accepted] 2023/04/28 06:42 [medline] 2023/04/28 06:41 [pubmed] 2023/04/28 02:39 [entrez]
 2022/12/12 00:00 [received] 2023/02/22 00:00 [revised] 2023/03/06 00:00 [accepted] 2023/04/07 06:41 [medline] 2023/03/13 06:00 [pubmed] 2023/03/12 20:27 [entrez]
 2022/03/06 00:00 [received] 2022/10/12 00:00 [revised] 2022/12/23 00:00 [accepted] 2022/12/31 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/30 18:06 [entrez]
 2022/03/30 00:00 [received] 2022/08/24 00:00 [accepted] 2022/09/08 06:00 [pubmed] 2023/01/10 06:00 [medline] 2022/09/07 23:29 [entrez]
 2023/08/14 06:42 [medline] 2023/08/11 18:42 [pubmed] 2023/08/11 14:03 [entrez]
 2023/03/23 20:53 [entrez] 2023/03/24 06:00 [pubmed] 2023/03/28 06:00 [medline]
 2022/08/29 00:00 [received] 2022/12/22 00:00 [revised] 2023/01/17 00:00 [accepted] 2023/02/07 06:00 [pubmed] 2023/03/15 06:00 [medline] 2023/02/06 18:03 [entrez]
 2023/06/26 06:41 [medline] 2023/06/25 01:08 [pubmed] 2023/06/24 20:43 [entrez]
 2023/02/08 00:00 [received] 2023/03/03 00:00 [revised] 2023/03/07 00:00 [accepted] 2023/03/30 06:11 [medline] 2023/03/29 01:36 [entrez] 2023/03/30 06:00 [pubmed]
 2024/02/01 00:00 [pmc-release] 2023/01/26 06:00 [pubmed] 2023/02/18 06:00 [medline] 2023/01/25 08:33 [entrez]
 2022/05/30 00:00 [received] 2022/09/25 00:00 [revised] 2022/10/27 00:00 [accepted] 2022/12/06 06:00 [pubmed] 2023/01/04 06:00 [medline] 2022/12/05 18:20 [entrez]
 2023/05/28 00:00 [received] 2023/07/27 00:00 [revised] 2023/07/27 00:00 [accepted] 2023/09/13 06:41 [medline] 2023/08/06 05:42 [pubmed] 2023/08/05 19:14 [entrez]
 2022/02/24 00:00 [received] 2022/09/14 00:00 [accepted] 2022/11/18 06:00 [pubmed] 2023/02/09 06:00 [medline] 2022/11/17 09:54 [entrez]
 2022/12/30 00:00 [received] 2023/01/20 00:00 [revised] 2023/01/25 00:00 [accepted] 2023/04/14 06:01 [medline] 2023/04/13 01:19 [entrez] 2023/04/14 06:00 [pubmed]
 2022/08/04 00:00 [received] 2022/12/13 00:00 [accepted] 2022/12/12 00:00 [revised] 2022/12/25 06:00 [pubmed] 2023/03/22 06:00 [medline] 2022/12/24 11:14 [entrez]
 2022/07/15 00:00 [received] 2022/11/16 00:00 [revised] 2023/03/23 00:00 [accepted] 2023/04/12 06:01 [medline] 2023/04/11 01:46 [entrez] 2023/04/12 06:00 [pubmed]
 2022/12/02 06:00 [pubmed] 2023/02/15 06:00 [medline] 2022/12/01 04:22 [entrez]
 2022/11/05 00:00 [received] 2023/07/16 00:00 [accepted] 2023/05/19 00:00 [revised] 2023/08/04 06:43 [medline] 2023/08/03 13:08 [pubmed] 2023/08/03 11:07 [entrez]
 2023/01/27 00:00 [received] 2023/04/06 00:00 [accepted] 2023/05/08 06:42 [medline] 2023/05/06 09:42 [pubmed] 2023/05/05 20:52 [entrez]
 2022/12/21 00:00 [received] 2023/04/21 00:00 [revised] 2023/04/28 00:00 [accepted] 2023/06/19 13:08 [medline] 2023/05/19 01:04 [pubmed] 2023/05/18 18:05 [entrez]
 2022/06/24 00:00 [received] 2022/09/07 00:00 [accepted] 2023/04/05 06:42 [medline] 2022/09/14 06:00 [pubmed] 2022/09/13 12:03 [entrez]
 2023/03/23 00:00 [received] 2023/06/01 00:00 [accepted] 2023/08/09 06:43 [medline] 2023/08/08 00:42 [pubmed] 2023/08/07 21:23 [entrez]
 2023/05/21 00:00 [revised] 2023/02/06 00:00 [received] 2023/05/31 00:00 [accepted] 2023/09/05 06:42 [medline] 2023/07/03 06:42 [pubmed] 2023/07/03 03:29 [entrez]
 2023/04/15 00:00 [revised] 2023/02/14 00:00 [received] 2023/04/28 00:00 [accepted] 2023/08/04 06:43 [medline] 2023/05/22 06:42 [pubmed] 2023/05/22 01:03 [entrez]
 2022/07/27 00:00 [received] 2022/09/17 00:00 [accepted] 2022/09/16 00:00 [revised] 2022/09/28 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/09/27 11:55 [entrez]
 2022/07/09 00:00 [received] 2023/04/14 00:00 [revised] 2023/04/29 00:00 [accepted] 2023/06/09 06:41 [medline] 2023/05/07 00:42 [pubmed] 2023/05/06 19:28 [entrez]
 2022/09/01 00:00 [revised] 2022/04/23 00:00 [received] 2022/09/16 00:00 [accepted] 2022/09/25 06:00 [pubmed] 2023/01/31 06:00 [medline] 2022/09/24 04:33 [entrez]
 2022/08/05 00:00 [received] 2022/12/01 00:00 [revised] 2023/02/28 00:00 [accepted] 2023/03/27 03:46 [entrez] 2023/03/28 06:00 [pubmed] 2023/03/28 06:01 [medline]
 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 05:01 [entrez]
 2022/07/04 00:00 [received] 2023/06/08 00:00 [accepted] 2023/08/02 01:08 [medline] 2023/08/02 01:07 [pubmed] 2023/08/01 23:15 [entrez]
 2023/02/09 00:00 [received] 2023/03/02 00:00 [accepted] 2023/04/25 06:42 [medline] 2023/03/12 06:00 [pubmed] 2023/03/11 19:28 [entrez]
 2023/04/19 00:00 [received] 2023/05/19 00:00 [revised] 2023/05/19 00:00 [accepted] 2023/07/17 06:42 [medline] 2023/07/14 13:07 [pubmed] 2023/07/14 01:17 [entrez]
 2023/04/18 06:01 [medline] 2023/04/17 04:15 [entrez] 2023/04/18 06:00 [pubmed]
 2023/01/23 00:00 [received] 2023/03/21 00:00 [revised] 2023/04/06 00:00 [accepted] 2023/06/30 13:12 [medline] 2023/06/30 13:11 [pubmed] 2023/06/30 10:10 [entrez]
 2022/09/08 00:00 [received] 2022/12/07 00:00 [revised] 2022/12/28 00:00 [accepted] 2023/01/01 06:00 [pubmed] 2023/02/01 06:00 [medline] 2022/12/31 19:13 [entrez]
 2022/11/22 00:00 [received] 2022/12/23 00:00 [revised] 2023/01/05 00:00 [accepted] 2023/01/21 01:26 [entrez] 2023/01/22 06:00 [pubmed] 2023/01/25 06:00 [medline]
 2022/11/23 00:00 [received] 2023/05/30 00:00 [accepted] 2023/08/14 06:43 [medline] 2023/08/14 06:42 [pubmed] 2023/08/14 04:57 [entrez]
 2022/11/06 00:00 [received] 2023/05/04 00:00 [accepted] 2023/08/31 06:42 [medline] 2023/07/07 01:05 [pubmed] 2023/07/06 21:38 [entrez]
 2022/10/03 00:00 [revised] 2022/07/08 00:00 [received] 2022/10/19 00:00 [accepted] 2022/11/01 06:00 [pubmed] 2023/01/07 06:00 [medline] 2022/10/31 06:43 [entrez]
 2023/08/30 06:48 [medline] 2023/08/30 06:47 [pubmed] 2023/08/30 04:04 [entrez]
 2022/12/23 00:00 [received] 2023/06/02 00:00 [accepted] 2024/10/01 00:00 [pmc-release] 2023/08/30 06:49 [medline] 2023/08/30 06:48 [pubmed] 2023/08/30 04:05 [entrez]
 2022/11/29 06:00 [pubmed] 2023/01/12 06:00 [medline] 2022/11/28 11:33 [entrez]
 2022/04/14 00:00 [revised] 2021/07/19 00:00 [received] 2022/09/02 00:00 [accepted] 2023/05/15 06:42 [medline] 2022/10/27 06:00 [pubmed] 2022/10/26 00:34 [entrez]
 2021/12/22 00:00 [received] 2022/08/08 00:00 [revised] 2022/08/22 00:00 [accepted] 2022/11/08 06:00 [pubmed] 2023/01/11 06:00 [medline] 2022/11/07 19:12 [entrez]
 2022/08/30 00:00 [received] 2023/01/31 00:00 [revised] 2023/05/16 00:00 [accepted] 2023/06/23 06:42 [medline] 2023/06/17 05:11 [pubmed] 2023/06/16 18:41 [entrez]
 2023/03/29 00:00 [accepted] 2023/06/07 06:42 [medline] 2023/05/20 09:42 [pubmed] 2023/05/19 23:26 [entrez]
 2022/09/25 00:00 [received] 2023/05/03 00:00 [accepted] 2023/07/12 06:42 [medline] 2023/07/12 06:42 [pubmed] 2023/07/12 01:03 [entrez]
 2022/10/07 00:00 [received] 2022/12/21 00:00 [revised] 2022/12/22 00:00 [accepted] 2023/02/21 18:37 [entrez] 2023/02/22 06:00 [pubmed] 2023/02/25 06:00 [medline]
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 0 (Antibodies, Viral)


 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors)



 0 (DYSF protein, human) EC 2.4.1.198 (PIGC protein, human) 0 (ZNF638 protein, human)





 4F4X42SYQ6 (Rituximab) A10SJL62JY (ocrelizumab)

 BW9B0ZE037 (Sildenafil Citrate)


 0 (Anti-Bacterial Agents) 0 (Penicillins)



 1406-16-2 (Vitamin D) JL5DK93RCL (Melatonin) 0 (Vitamins)
 0 (Crotonates) 0 (Toluidines) 0 (Hydroxybutyrates)
 0 (Immunosuppressive Agents)
 0 (Antidepressive Agents)








 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Immunologic Factors)

 0 (Immunosuppressive Agents) 0 (Natalizumab) 47M74X9YT5 (Cladribine)




 47M74X9YT5 (Cladribine) 0 (Anticonvulsants)
 U59UGK3IPC (ublituximab) 0 (Antibodies, Monoclonal)



 0 (COVID-19 Vaccines)

 0 (Biomarkers)




 0 (Cytokines)




 0 (Immunoglobulin G)











 0 (Biomarkers)





 0 (Immunoglobulin G)
 0 (Immunosuppressive Agents) 0 (Immunologic Factors)
 0 (Biomarkers)




 0 (Autoantibodies) 0 (Receptors, N-Methyl-D-Aspartate)
 BH3B64OKL9 (4-Aminopyridine)
 Illawarra


 0 (Alarmins)

 0 (Vitamins) 1406-16-2 (Vitamin D)















 G926EC510T (Fingolimod Hydrochloride) 0 (Biomarkers)




 Spinocerebellar ataxia 8










 1406-16-2 (Vitamin D)



 35517-12-5 (W 12)







 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)



 63231-63-0 (RNA)

 0 (Immunosuppressive Agents) XRO4566Q4R (Interferon beta-1a) 5M691HL4BO (Glatiramer Acetate) G926EC510T (Fingolimod Hydrochloride)
 1C058IKG3B (teriflunomide) 0 (Crotonates) XRO4566Q4R (Interferon beta-1a)
 77238-31-4 (Interferon-beta)
 0 (COVID-19 Vaccines) SARS-CoV-2 variants


 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents) Melanoma, Cutaneous Malignant



 0 (Oligoclonal Bands)


 0 (Oligoclonal Bands)

 3A189DH42V (Alemtuzumab)




 0 (RNA, Messenger) 63231-63-0 (RNA) EC 2.3.1.- (NAT8L protein, human) EC 2.3.1.- (Acetyltransferases)




 0 (Immunologic Factors) A10SJL62JY (ocrelizumab)


 0 (Contraceptives, Oral)

 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)



 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)
 0 (Cholesterol, HDL)





 0 (Natalizumab) 0 (Antibodies) 0 (Immunologic Factors)
 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors)



 0 (Biomarkers)





 0 (Natalizumab) 0 (Immunologic Factors)






 K4H93P747O (nabiximols) 19GBJ60SN5 (Cannabidiol) 7J8897W37S (Dronabinol) 0 (Cannabinoids) 0 (Drug Combinations)
 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors) 0 (Antibodies, Monoclonal, Humanized) Mediastinal Fibrosis
 5M691HL4BO (Glatiramer Acetate)
 A10SJL62JY (ocrelizumab) 4F4X42SYQ6 (Rituximab)







 0 (Apolipoprotein A-I) 0 (Cholesterol, LDL) 97C5T2UQ7J (Cholesterol) 0 (Cholesterol, HDL) 0 (Apolipoproteins B) 0 (Apolipoproteins E) 0 (Biomarkers) 0 (Apolipoproteins C)


 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)
 VTD58H1Z2X (Dopamine) 333DO1RDJY (Serotonin)




 G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab) 0 (Immunosuppressive Agents)
 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors)
 1C6V77QF41 (Cholecalciferol) 0 (MicroRNAs) 0 (MIRN155 microRNA, human)

 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride)


 H789N3FKE8 (Baclofen)
 0 (Oligoclonal Bands)
 A10SJL62JY (ocrelizumab) 0 (Biomarkers)

 E1UOL152H7 (Iron) 0 (Immunoglobulin G)
 3A189DH42V (Alemtuzumab)





 0 (Forkhead Transcription Factors) 0 (IKZF2 protein, human)
 0 (Brain-Derived Neurotrophic Factor) 130068-27-8 (Interleukin-10) 9061-61-4 (Nerve Growth Factor) 0 (Core Binding Factor Alpha 2 Subunit) 0 (RNA, Long Noncoding) 0 (RNA, Messenger) 0 (RUNX1 protein, human)
 0 (Nerve Tissue Proteins)

 0 (Autoantibodies) 4F4X42SYQ6 (Rituximab)

 0 (Biomarkers)


 0 (Immunosuppressive Agents) 0 (Immunologic Factors)



 47M74X9YT5 (Cladribine) 0 (MicroRNAs) 0 (Biomarkers)



 0 (Nerve Growth Factors) 0 (Biomarkers)
 8021PR16QO (theanine) 0 (Antioxidants) 5N16U7E0AO (Cuprizone) EC 1.11.1.9 (Glutathione Peroxidase) EC 1.15.1.1 (Superoxide Dismutase)

 0 (Antibodies, Monoclonal) 0 (Immunologic Factors) 0 (Natalizumab)

 0 (Antioxidants)
 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride) 5M691HL4BO (Glatiramer Acetate) FO2303MNI2 (Dimethyl Fumarate)





 0 (Antioxidants) 877GWI46C2 (crocin) 5N16U7E0AO (Cuprizone)


 FO2303MNI2 (Dimethyl Fumarate)






 0 (Antihypertensive Agents) 0 (Hypoglycemic Agents) 0 (Lipids)



 77238-31-4 (Interferon-beta)

 3A189DH42V (Alemtuzumab)
 0H73WJJ391 (Topiramate)

 1C058IKG3B (teriflunomide) E1UOL152H7 (Iron) 0 (TSPO protein, human) 0 (Receptors, GABA)

 3A189DH42V (Alemtuzumab)

 5M691HL4BO (Glatiramer Acetate) 0 (Immunosuppressive Agents)
 0 (Antibodies, Monoclonal, Humanized) A10SJL62JY (ocrelizumab)
 EC 3.2.1.14 (Chitinases) 0 (Biomarkers)

 0 (Sulfoglycosphingolipids) 0 (Biomarkers) 0 (Protein Isoforms)
 4F4X42SYQ6 (Rituximab)






 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 RR6P8L282I (siponimod) 0 (Pharmaceutical Preparations) 0 (Sphingosine-1-Phosphate Receptors)
 G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab) 0 (Immunosuppressive Agents)
 0 (MicroRNAs)
 BF4C9Z1J53 (Amantadine)

 5M691HL4BO (Glatiramer Acetate) 0 (Glia Maturation Factor)


 0 (Receptors, Antigen, T-Cell)

 1406-16-2 (Vitamin D)
 0 (Biomarkers)
 0 (Biomarkers)


 0 (Crotonates) 0 (Immunosuppressive Agents) 1C058IKG3B (teriflunomide) 0 (Toluidines)




 0 (Biomarkers)
 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride)





 0 (Immunologic Factors) XRO4566Q4R (Interferon beta-1a)
 0 (Antibodies, Monoclonal, Humanized) 0 (Immunologic Factors) 0 (Natalizumab) A10SJL62JY (ocrelizumab)
 01ZG3TPX31 (Bupropion)


 0 (Natalizumab) 0 (Immunologic Factors)





 EC 2.7.11.1 (EIF2AK4 protein, human) EC 2.7.11.1 (Protein Serine-Threonine Kinases)






 80497-65-0 (Anti-Mullerian Hormone) 8N3DW7272P (Cyclophosphamide)

 Z80293URPV (ozanimod) 5G7AKV2MKP (ponesimod)


 0 (Immune Checkpoint Inhibitors) 0 (Natalizumab)
 0 (Medical Marijuana)
 0 (NK Cell Lectin-Like Receptor Subfamily K)
 EC 3.4.21.- (Granzymes)





 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors)




 0 (Biomarkers) 0 (CXCL13 protein, human) 0 (Chemokine CXCL13)
 XRO4566Q4R (Interferon beta-1a) 0 (Antiviral Agents)
 FO2303MNI2 (Dimethyl Fumarate) 0 (diroximel fumarate) 5G7AKV2MKP (ponesimod) 1C058IKG3B (teriflunomide)

 0 (Natalizumab)
 0 (Oligoclonal Bands) 0 (Immunoglobulin G) 0 (Immunoglobulin kappa-Chains)

 G926EC510T (Fingolimod Hydrochloride) 82115-62-6 (Interferon-gamma)






 EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)

 X72A60C9MT (Lutein) 0 (Zeaxanthins) 0 (Macular Pigment)
 1C058IKG3B (teriflunomide)
 0 (Biomarkers)





 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)

 0 (Biomarkers)



 0 (Natalizumab) 0 (Immunologic Factors)
 A10SJL62JY (ocrelizumab) 1406-16-2 (Vitamin D)

 E1UOL152H7 (Iron)
 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)











 A10SJL62JY (ocrelizumab)



 0 (Immunosuppressive Agents) AU0V1LM3JT (Gadolinium) 5M691HL4BO (Glatiramer Acetate) 77238-31-4 (Interferon-beta)
 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents) 0 (Natalizumab)

 XRO4566Q4R (Interferon beta-1a)
 9001-32-5 (Fibrinogen)




 0 (Carbapenems) 0 (Anti-Bacterial Agents) 0 (beta-Lactams)




 0 (Lysophosphatidylcholines)
 A10SJL62JY (ocrelizumab)
 3A189DH42V (Alemtuzumab)
 M0TTH61XC5 (ibudilast) 0 (Pyridines)


 27YG812J1I (Arachidonic Acid)
 0 (Adrenal Cortex Hormones)


 9NEZ333N27 (Sodium)



 1C058IKG3B (teriflunomide) M95KG522R0 (ofatumumab) 0 (Nitriles)
 W8O17SJF3T (Memantine) K76S41V71X (acetylleucine)


 0 (Antibodies, Monoclonal) 0 (Natalizumab)
 0 (Cytokines)
 0 (Antibodies, Monoclonal) 0 (Antineoplastic Agents)
 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Immunologic Factors)
 0 (Natalizumab) 0 (Immunologic Factors)
 0 (Biomarkers)
 G926EC510T (Fingolimod Hydrochloride)
 0 (Immunologic Factors) 0 (Natalizumab)




 0 (Natalizumab) 0 (Immunologic Factors)

 0 (Anti-Bacterial Agents)




 0 (Androgens)




 0 (Natalizumab) 0 (Immunologic Factors)
 0 (Natalizumab) 0 (Immunologic Factors)



 G926EC510T (Fingolimod Hydrochloride)

 G926EC510T (Fingolimod Hydrochloride) FO2303MNI2 (Dimethyl Fumarate)
 0 (Immunosuppressive Agents)


 0 (Immunosuppressive Agents)
 0 (Biomarkers) 0 (Oligoclonal Bands)
 0 (Immunomodulating Agents)


 0 (Oligoclonal Bands)
 0 (Immunosuppressive Agents)
 0 (Crotonates) 0 (Toluidines)





 3A189DH42V (Alemtuzumab)
 RR6P8L282I (siponimod) 0 (Sphingosine-1-Phosphate Receptors)
 9NEZ333N27 (Sodium)
 G926EC510T (Fingolimod Hydrochloride)




 3A189DH42V (Alemtuzumab) 0 (Antibodies, Monoclonal)



 3A189DH42V (Alemtuzumab) 0 (fibrin fragment D) 0 (Fibrin Fibrinogen Degradation Products) 0 (Immunologic Factors)


 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 0 (COVID-19 Vaccines) 0 (RNA, Viral)
 1C058IKG3B (teriflunomide) 0 (Crotonates) 0 (Toluidines) 0 (Neurofilament Proteins)


 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Tablets)
 0 (Biomarkers) 0 (MicroRNAs) 0 (MIRN485 microRNA, human)


 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 2880D3468G (Levamisole)

 5M691HL4BO (Glatiramer Acetate) 0 (Immunosuppressive Agents)
 Y4S76JWI15 (Methanol)



 0 (Glial Fibrillary Acidic Protein) 0 (Neurofilament Proteins) 0 (Biomarkers)

 0 (Interleukin-8) 0 (Cytokines)


 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents)


 0 (Adjuvants, Immunologic)
 0 (Immunoglobulin G) 0 (Antibodies, Viral) 0 (Antigens, Viral)

 0 (Immunosuppressive Agents) 4F4X42SYQ6 (Rituximab)

 0 (Antibodies, Monoclonal) 0 (Antineoplastic Agents) 0 (Immunoglobulin G)
 G926EC510T (Fingolimod Hydrochloride)
 0 (Biomarkers)
 XRO4566Q4R (Interferon beta-1a) 77238-31-4 (Interferon-beta)


 0 (Immunomodulating Agents)
 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride) 77238-31-4 (Interferon-beta)
 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors)
 0 (Antibodies, Monoclonal) 0 (Antineoplastic Agents) U59UGK3IPC (ublituximab)

 E1UOL152H7 (Iron)

 0 (Interleukin-6) 0 (HLA-DRB1 Chains) 0 (HLA Antigens) 0 (Proto-Oncogene Proteins c-bcl-2)
 K4H93P747O (nabiximols)

 5M691HL4BO (Glatiramer Acetate) 0 (Natalizumab) 47M74X9YT5 (Cladribine)

 H789N3FKE8 (Baclofen)


 BH3B64OKL9 (4-Aminopyridine) 614OI1Z5WI (Valproic Acid) 9NEZ333N27 (Sodium)
 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Tablets)

 FO2303MNI2 (Dimethyl Fumarate) 0 (Antipsychotic Agents) Wells syndrome
 0 (Aquaporin 4)
 0 (Biomarkers)
 FB33469R8E (Estriol)


 0 (Tissue Inhibitor of Metalloproteinase-1) 0 (Aquaporin 4) 0 (Biomarkers)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 5M691HL4BO (Glatiramer Acetate) 0 (Immunosuppressive Agents)

 0 (Amides) 0 (Protons)


 0 (Anticonvulsants) 0 (Antidepressive Agents)

 4F4X42SYQ6 (Rituximab)
 0 (RNA, Long Noncoding) EC 3.4.- (Amyloid Precursor Protein Secretases) EC 3.4.23.- (Aspartic Acid Endopeptidases) EC 3.4.23.46 (BACE1 protein, human)
 0 (Antibodies, Monoclonal) 0 (Antineoplastic Agents) 1C058IKG3B (teriflunomide)
 0 (Biomarkers) 0 (Immunoglobulins)



 690G0D6V8H (Ketamine) R60L0SM5BC (Midazolam)
 0 (Phosphates)
 0 (Myelin Proteins) 0 (Antigens)

 1406-16-2 (Vitamin D)

 AU0V1LM3JT (Gadolinium) 0 (Contrast Media)
 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Tablets)
 47M74X9YT5 (Cladribine) 0 (Tablets)
 3A189DH42V (Alemtuzumab) 0 (Antibodies, Monoclonal, Humanized)
 0 (Steroids)
 0 (Cannabinoids)
 0 (Oligoclonal Bands)

 47M74X9YT5 (Cladribine) 0 (Tablets) 0 (Immunosuppressive Agents)
 K4H93P747O (nabiximols)



 G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab) A10SJL62JY (ocrelizumab) 0 (Immunosuppressive Agents) 0 (Immunologic Factors)
 0 (Glial Fibrillary Acidic Protein) 0 (Biomarkers)



 19GBJ60SN5 (Cannabidiol) 7J8897W37S (Dronabinol) 0 (Drug Combinations) K4H93P747O (nabiximols)




 0 (Biomarkers)

 XRO4566Q4R (Interferon beta-1a) 77238-31-4 (Interferon-beta)
 0 (Immunosuppressive Agents)


 DLG4EML025 (secukinumab) G926EC510T (Fingolimod Hydrochloride) 0 (Antibodies, Monoclonal, Humanized)



 1C058IKG3B (teriflunomide) 0 (Immunosuppressive Agents) 0 (Nitriles)
 0 (Biomarkers) 0 (Glial Fibrillary Acidic Protein) 4QWG6N8QKH (Hydroxychloroquine) 0 (Neurofilament Proteins)
 FO2303MNI2 (Dimethyl Fumarate)
 0 (Oligoclonal Bands) 0 (Biomarkers) EC 3.2.1.14 (Chitinases)
 0 (Neuroprotective Agents) 0 (Toll-Like Receptor 7) O8M467C50G (vesatolimod)





 059QF0KO0R (Water) 0 (Biomarkers)


 0 (Proteome)




 0 (Pharmaceutical Preparations)


 0 (asarone) 3A592W8XKE (astragaloside A) 9012-76-4 (Chitosan)

 5M691HL4BO (Glatiramer Acetate) FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)





 H789N3FKE8 (Baclofen) 0 (Muscle Relaxants, Central)



 0 (Myelin Basic Protein)

 62031-54-3 (Fibroblast Growth Factors)



 0 (Biomarkers) 1406-16-2 (Vitamin D)

 0 (Immunologic Factors)

 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride) FO2303MNI2 (Dimethyl Fumarate)




 0 (TMC8 protein, human) 0 (Membrane Proteins)
 130068-27-8 (Interleukin-10) 0 (Receptors, Interleukin-10)
 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors)

 0 (Immunoglobulin kappa-Chains)
 FO2303MNI2 (Dimethyl Fumarate) 0 (Myelin Basic Protein)


 0 (Interleukin-2)
 H6241UJ22B (Selenium) 0 (Coffee) S7UI8SM58A (Carnitine) 0 (Cytokines)
 0 (Antigens, CD) 147205-72-9 (CD40 Ligand)

 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 XRO4566Q4R (Interferon beta-1a) 0 (Natalizumab) AU0V1LM3JT (Gadolinium) 0 (Immunosuppressive Agents)

 M95KG522R0 (ofatumumab) 0 (Natalizumab)
 K4H93P747O (nabiximols)












 0 (COVID-19 Vaccines)
 0 (Protons) 059QF0KO0R (Water)

 EC 3.4.21.46 (Complement Factor D) 0 (Lipoproteins)



 0 (Tyrosine Protein Kinase Inhibitors)



 M95KG522R0 (ofatumumab) FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)






 0 (Hepatocyte Nuclear Factor 4) 0 (Sp1 protein, human) 0 (HNF4A protein, human)
 0 (Natalizumab) 0 (Immunologic Factors)
 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents)

 0 (RNA, Circular) 63231-63-0 (RNA)

 P6YC3EG204 (Vitamin B 12) 935E97BOY8 (Folic Acid) 0 (Vitamins)
 AU0V1LM3JT (Gadolinium) 9035-58-9 (Thromboplastin) 0 (F3 protein, human)



 0 (Immunosuppressive Agents)

 0 (Autoantibodies) 0 (Biomarkers)
 0 (Cytokines) 0 (Interleukin-27) 0 (MYDGF protein, human)

 EC 3.4.24.35 (Matrix Metalloproteinase 9) 0 (Interleukin-17)

 0 (Antibodies, Monoclonal) 0 (Antineoplastic Agents)
 PQ6CK8PD0R (Ascorbic Acid) 0 (Metals) 0 (Biomarkers)





 G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab) 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors) 0 (Immunosuppressive Agents)

 1C058IKG3B (teriflunomide) 4QWG6N8QKH (Hydroxychloroquine) G162GK9U4W (Leflunomide)

 0 (Tumor Necrosis Factor-alpha)
 FO2303MNI2 (Dimethyl Fumarate)

 1406-16-2 (Vitamin D) 0 (Vitamins)
 5M691HL4BO (Glatiramer Acetate) G926EC510T (Fingolimod Hydrochloride)

 0 (Natalizumab) 0 (Immunologic Factors)
 0 (Autoantibodies) Hashimoto's encephalitis

 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized)
 G926EC510T (Fingolimod Hydrochloride) FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents) 0 (Immunologic Factors)
 0 (Natalizumab)


 0 (Sphingosine-1-Phosphate Receptors) 5G7AKV2MKP (ponesimod) 0 (Immunologic Factors) 0 (Thiazoles) NGZ37HRE42 (Sphingosine)



 0 (COVID-19 Vaccines)


 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride) 5M691HL4BO (Glatiramer Acetate) 0 (Natalizumab) FO2303MNI2 (Dimethyl Fumarate)
 0 (Cytokines) 130068-27-8 (Interleukin-10) 0 (Interleukin-13) 0 (Interleukin-17) 0 (Interleukin-2) 207137-56-2 (Interleukin-4) 0 (Interleukin-5) 0 (Interleukin-9) 0 (Interleukins)



 0 (Contrast Media)


 WI4X0X7BPJ (Hydrocortisone)
 0 (Tea)


 WYQ7N0BPYC (Acetylcysteine) 0 (Biomarkers) GAN16C9B8O (Glutathione)
 9002-68-0 (Follicle Stimulating Hormone)

 1C058IKG3B (teriflunomide) G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents) FO2303MNI2 (Dimethyl Fumarate) 0 (CXCL13 protein, human) 0 (Chemokine CXCL13)


 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors)
 0 (Glial Fibrillary Acidic Protein) 0 (Neurofilament Proteins) 0 (Biomarkers)

 0 (Neurofilament Proteins) 0 (Biomarkers) 0 (Contactins)
 0 (Antigens, CD20) 0 (Antibodies, Monoclonal, Humanized)
 0 (Immunoglobulin kappa-Chains) 0 (Immunoglobulin Light Chains) 0 (Biomarkers) 0 (Oligoclonal Bands)

 8N3DW7272P (Cyclophosphamide)


 0 (Interleukin-17) 0 (Tumor Necrosis Factor-alpha) 0 (Intercellular Signaling Peptides and Proteins)


 0 (Receptors, IgG)

 0 (Biosimilar Pharmaceuticals)






 4F4X42SYQ6 (Rituximab) 0 (Immunoglobulins, Intravenous)
 XRO4566Q4R (Interferon beta-1a)
 0 (Azetidines) 0 (Benzyl Compounds) RR6P8L282I (siponimod)







 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents)
 3A189DH42V (Alemtuzumab) 0 (Antibodies, Monoclonal, Humanized)

 1C058IKG3B (teriflunomide)




 0 (GPC5 protein, human) 0 (Glypicans)







 E1UOL152H7 (Iron)




 E1UOL152H7 (Iron)
 0 (Reactive Oxygen Species) 8L70Q75FXE (Adenosine Triphosphate)


 0 (Immune Checkpoint Inhibitors)
 Inflammatory Bowel Disease 7

 A10SJL62JY (ocrelizumab)


 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Immunologic Factors) SOA12P041N (nitazoxanide) G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab)

 0 (Epitopes, T-Lymphocyte) 0 (Vaccines)
 0 (Natalizumab) 4F4X42SYQ6 (Rituximab) A10SJL62JY (ocrelizumab) 0 (Immunologic Factors)

 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors) 0 (Antibodies, Monoclonal, Humanized)
 0 (Interleukin-17) EC 2.7.10.2 (Janus Kinases) 0 (STAT Transcription Factors)
 G926EC510T (Fingolimod Hydrochloride) 0 (MicroRNAs) 0 (Biomarkers)

 0 (Cannabinoids) 7J8897W37S (Dronabinol) 19GBJ60SN5 (Cannabidiol)
 AU0V1LM3JT (Gadolinium) 0 (Contrast Media)







 1C058IKG3B (teriflunomide) 0 (Crotonates) 0 (Toluidines)
 0 (Biomarkers) 0 (CXCL13 protein, human) 0 (Chemokine CXCL13)
 47M74X9YT5 (Cladribine) 0 (Influenza Vaccines) 0 (Immunosuppressive Agents) 0 (Tablets)
 0 (Glia Maturation Factor) 0 (Cytokines) Y4S76JWI15 (Methanol)
 BH3B64OKL9 (4-Aminopyridine) 0 (Potassium Channel Blockers)
 0 (Natalizumab) FO2303MNI2 (Dimethyl Fumarate)
 0 (Oligoclonal Bands)
 1406-16-2 (Vitamin D) 0 (Antioxidants) 0 (Vitamins)
 97C5T2UQ7J (Cholesterol)

 0 (CXCL13 protein, human) 0 (Chemokine CXCL13)

 M95KG522R0 (ofatumumab) 0 (Antibodies, Monoclonal, Humanized)





 0 (Antibodies, Monoclonal) 4F4X42SYQ6 (Rituximab) 0 (Natalizumab) 3A189DH42V (Alemtuzumab)



 0 (Brain-Derived Neurotrophic Factor) 0 (Neuroprotective Agents)




 0 (HLA-DRB1 Chains)


 0 (Insulins)

 S88TT14065 (Oxygen)

 1C058IKG3B (teriflunomide)
 0 (Glial Fibrillary Acidic Protein) 0 (Biomarkers)
 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) 0 (Antigens)

 0 (Cytokines)



 0 (Immunodominant Epitopes) 0 (Mannans) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Peptide Fragments) 0 (myelin oligodendrocyte glycoprotein (35-55))

 0 (Biomarkers)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 0 (Antioxidants) 0 (Anti-Inflammatory Agents)



 0 (Endocannabinoids) 0 (Biomarkers)
 AU0V1LM3JT (Gadolinium) 0 (Contrast Media) K2I13DR72L (Gadolinium DTPA) 0 (Organometallic Compounds)


 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors)

 3A189DH42V (Alemtuzumab)

 0 (Autoantibodies)
 5G7AKV2MKP (ponesimod) 0 (Receptors, Lysosphingolipid) 0 (Thiazoles)


 G926EC510T (Fingolimod Hydrochloride) 0 (Contrast Media) AU0V1LM3JT (Gadolinium)

 0 (HLA-DR Antigens)


 0 (Autoantibodies)
 0 (Oligoclonal Bands) 0 (Immunoglobulin G) 0 (Albumins)
 XRO4566Q4R (Interferon beta-1a) 0 (sampeginterferon beta-1a)

 0 (Particulate Matter)



 0 (Neurofilament Proteins) 0 (Biomarkers)


 0 (Ion Channels) 0 (Cytokines)

 0 (STAT2 protein, human) 0 (STAT2 Transcription Factor)
 0 (Aquaporin 4) 0 (Oligoclonal Bands) 0 (Immunoglobulin G)
 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)

 ZA45457L1K (evobrutinib) 0 (Pyrimidines)
 9008-11-1 (Interferons) 0 (Immunoglobulin A)

 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents)


 WI4X0X7BPJ (Hydrocortisone)

 FO2303MNI2 (Dimethyl Fumarate) 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents)
 5M691HL4BO (Glatiramer Acetate) 0 (Natalizumab) 9008-11-1 (Interferons) 77238-31-4 (Interferon-beta) 0 (Immunosuppressive Agents)
 0 (Cyclotides) 0 (Plant Proteins)
 EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase) 0 (Protein Kinase Inhibitors)

 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)


 0 (Contrast Media) AU0V1LM3JT (Gadolinium) 0 (Organometallic Compounds) K2I13DR72L (Gadolinium DTPA)
 A10SJL62JY (ocrelizumab) 0 (Antilymphocyte Serum)



 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)
 0 (Biomarkers)

 0 (DNA, Mitochondrial)
 5M691HL4BO (Glatiramer Acetate) 77238-31-4 (Interferon-beta)





 0 (Antibodies, Monoclonal)


 0 (alpha-Synuclein) 0 (beta-Synuclein) 0 (Amyloidogenic Proteins)
 0 (alpha-Synuclein) 0 (Interleukin-6) 0 (Biomarkers)
 0 (Coffee) 0 (Tea)
 G926EC510T (Fingolimod Hydrochloride) 0 (Immunologic Factors) 0 (Immunosuppressive Agents) 0 (Natalizumab)
 0 (Antigens, CD20)
 0 (Acids)
 0 (Immunosuppressive Agents) 5M691HL4BO (Glatiramer Acetate) G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab)





 0 (Glial Fibrillary Acidic Protein) 0 (Biomarkers)

 1C058IKG3B (teriflunomide) 0 (Crotonates) 0 (Toluidines)
 SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one) 0 (Antineoplastic Agents) 9007-49-2 (DNA)
 0 (Brain-Derived Neurotrophic Factor) 0 (Biomarkers)


 0 (ischemia-modified albumin) 0 (Biomarkers) G926EC510T (Fingolimod Hydrochloride) 0 (Disulfides) 0 (Sulfhydryl Compounds) 0 (Serum Albumin)



 73710-32-4 (methyl 4-azidophenylacetimidate) 0 (Receptors, Calcitriol)

 0 (Biomarkers) 0 (RNA, Long Noncoding) 0 (HAR1 noncoding RNA, human)



 0 (Natalizumab) 0 (Immunologic Factors)

 9012-63-9 (Cholera Toxin)

 0 (Antibodies, Viral)




 7J8897W37S (Dronabinol)



 47M74X9YT5 (Cladribine) 0 (Proteome) 0 (Immunoglobulin Heavy Chains)




 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized)
 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)
 0 (Gonadal Steroid Hormones) 0 (Neuroprotective Agents) JL5DK93RCL (Melatonin)



 G926EC510T (Fingolimod Hydrochloride)
 0 (Antibodies, Viral) 0 (Immunoglobulin M)

 0 (COVID-19 Vaccines)




 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Tablets)
 47M74X9YT5 (Cladribine) 3A189DH42V (Alemtuzumab) 0 (RC3H1 protein, human) 0 (RNA-Binding Proteins) EC 2.3.2.27 (Ubiquitin-Protein Ligases)


 A10SJL62JY (ocrelizumab) 0 (Natalizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Immunologic Factors)
 0 (Neurotransmitter Agents) 3KX376GY7L (Glutamic Acid)


 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Biomarkers)



 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Tablets)

 0 (N,N-diethyl-2-(2-(4-(2-fluoroethoxy)phenyl)-5,7-dimethylpyrazolo(1,5-a)pyrimidin-3-yl)acetamide)




 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Autoantibodies)


 0 (Anti-Anxiety Agents) R3UK8X3U3D (Modafinil)
 0 (Biomarkers)
 0 (Natalizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Immunologic Factors)


 EC 3.1.1.7 (Acetylcholinesterase)



 9Y8NXQ24VQ (Propranolol) X4W3ENH1CV (Norepinephrine) 0 (Receptors, Adrenergic)


 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Autoantibodies)
 5M691HL4BO (Glatiramer Acetate) 77238-31-4 (Interferon-beta)
 0 (benzisothiazole) O0P4I5851I (Lurasidone Hydrochloride) 982-24-1 (Clopenthixol)

 A10SJL62JY (ocrelizumab) 0 (COVID-19 Vaccines) 0 (Antibodies, Viral)

 0 (RNF10 protein, human) 0 (Carrier Proteins) 0 (CEP78 protein, human) 0 (Cell Cycle Proteins)



 0 (Interleukin-2) 0 (Antibodies) SARS-CoV-2 variants
 0 (Analgesics, Opioid)



 0 (Anti-Inflammatory Agents) 0 (Cytokines)




 0 (Fibronectins) 0 (Leptin) 0 (UCHL1 protein, human) EC 3.4.19.12 (Ubiquitin Thiolesterase)

 0 (Biomarkers) 0 (Blood Proteins) 0 (TAPBPL protein, human) 0 (Immunoglobulins) 0 (Membrane Proteins)
 G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab) 0 (Immunosuppressive Agents) 0 (Immunologic Factors)

 0 (COVID-19 Vaccines) Italian people
 G926EC510T (Fingolimod Hydrochloride) 65M2UDR9AG (Etretinate)
 EC 2.7.1.105 (PFKFB3 protein, human) EC 2.7.1.105 (Phosphofructokinase-2)
 G926EC510T (Fingolimod Hydrochloride) 0 (Immunologic Factors)





 9007-49-2 (DNA) 0 (BTNL2 protein, human) 0 (Butyrophilins) EC 3.6.1.- (ASAP2 protein, human) 0 (GTPase-Activating Proteins) 0 (ZNF8 protein, human) 0 (Kruppel-Like Transcription Factors)


 0 (Sphingosine-1-Phosphate Receptors) 0 (Receptors, Lysosphingolipid) G926EC510T (Fingolimod Hydrochloride) 0 (Tetrahydroisoquinolines) NGZ37HRE42 (Sphingosine)
 5N16U7E0AO (Cuprizone) 0 (TRPV Cation Channels) 0 (TRPV1 protein, human) 0 (TRPV1 protein, mouse) 0 (TRPV1 receptor) S07O44R1ZM (Capsaicin)

 XRO4566Q4R (Interferon beta-1a) 0 (Epstein-Barr Virus Nuclear Antigens) 0 (Antigens, Viral) 0 (Antibodies, Viral) 0 (Immunoglobulin G) 0 (Antiviral Agents)
 0 (Glucocorticoids) 7S5I7G3JQL (Dexamethasone)
 0 (Blood Proteins) 0 (Biomarkers)

 0 (Brain-Derived Neurotrophic Factor) 7171WSG8A2 (BDNF protein, human)

 AU0V1LM3JT (Gadolinium) 0 (Contrast Media) 0 (Biomarkers) 0 (Glial Fibrillary Acidic Protein) 0 (Neurofilament Proteins)
 0 (Air Pollutants) 0 (HLA-DRB1 Chains) 0 (Particulate Matter)
 0 (Kelch-Like ECH-Associated Protein 1) 0 (NF-E2-Related Factor 2)
 0 (Steroids) 0 (Anticoagulants)
 0 (MicroRNAs) 0 (Biomarkers) 0 (MIRN486 microRNA, human) 0 (MIRN25 microRNA, human)


 0 (Natalizumab)
 0 (Cytokines) 1C058IKG3B (teriflunomide) 130068-27-8 (Interleukin-10) 0 (Interleukin-6) 0 (Anti-Inflammatory Agents)
 0 (Adipokines) 0 (Leptin) 0 (Resistin) 0 (Adiponectin)


 0 (Contrast Media)



 0 (alpha-Crystallins) 0 (Autoantigens)



 5M691HL4BO (Glatiramer Acetate) 77238-31-4 (Interferon-beta)
 N12000U13O (Doxycycline)

 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents)
 0 (Biomarkers)






 0 (Tobacco Smoke Pollution)

 0 (Aquaporin 4)



 U59UGK3IPC (ublituximab) 0 (Antigens, CD20) 0 (Antibodies, Monoclonal) 4F4X42SYQ6 (Rituximab) 0 (Antineoplastic Agents)
 4ZI204Y1MC (acetoacetic acid) 0 (Acetoacetates) 1364PS73AF (Acetone) K3Z4F929H6 (Lysine) 452VLY9402 (Serine)
 0 (Natalizumab) 0 (Peptides)
 EN464416SI (Ethidium) 0 (Cytokines)
 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (Tablets)



 A10SJL62JY (ocrelizumab) 0 (Transmembrane Activator and CAML Interactor Protein) 0 (Cytokines)





 0 (RNA, Viral)

 0 (Biomarkers)

 0 (Immunoglobulin kappa-Chains) 0 (Oligoclonal Bands) 0 (Immunoglobulin G) 0 (Biomarkers)
 0 (Immunosuppressive Agents)
 0 (Interleukin-17) 106441-73-0 (Osteopontin) 0 (Spp1 protein, mouse)
 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized) SML2Y3J35T (Colchicine)
 4F4X42SYQ6 (Rituximab) 0 (Cytokines) 0 (Autoantibodies)

 A10SJL62JY (ocrelizumab) EC 3.6.1.- (Septins) 0 (Antibodies, Viral) 0 (Epstein-Barr Virus Nuclear Antigens)
 0 (Adjuvants, Immunologic) XRO4566Q4R (Interferon beta-1a)



 PKI06M3IW0 (Rivastigmine)
 0 (Biomarkers) 0 (Neurofilament Proteins)
 EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta) 53AXN4NNHX (semaglutide) EC 2.7.1.- (Phosphatidylinositol 3-Kinases) 89750-14-1 (Glucagon-Like Peptide 1) 0 (Neuroprotective Agents)
 0 (beta Catenin) EC 2.7.11.26 (Glycogen Synthase Kinase 3) 9FN79X2M3F (Lithium) G4962QA067 (Lithium Chloride) 15XUH0X66N (Tolonium Chloride) 0 (Enzyme Inhibitors)

 77238-31-4 (Interferon-beta)
 0 (Immunoglobulin kappa-Chains) 0 (Immunoglobulin G) 0 (Biomarkers) 0 (Oligoclonal Bands)
 0 (Contrast Media)

 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors) 0 (Anti-Inflammatory Agents)
 1C6V77QF41 (Cholecalciferol)

 0 (Sphingosine 1 Phosphate Receptor Modulators) 0 (Antibodies, Viral) COVID-19 breakthrough infections
 0 (Neurofilament Proteins) 0 (Biomarkers)






 0 (Cytokines)
 0 (Intrinsically Disordered Proteins) 0 (Myelin Proteins) 0 (Membrane Proteins)
 0 (Immunosuppressive Agents) A10SJL62JY (ocrelizumab) G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab)


 06LU7C9H1V (Triiodothyronine)




 A10SJL62JY (ocrelizumab) 0 (Antithyroid Agents) 0 (Antibodies, Monoclonal, Humanized)






 0 (Aquaporin 4)
 0 (Interleukin-17) 0 (Cytokines) 82115-62-6 (Interferon-gamma) 0 (Transforming Growth Factor beta)
 0 (Aquaporin 4) 0 (Autoantibodies)
 0 (Contrast Media)

 0 (Antibodies, Monoclonal, Humanized) 0 (Nucleosides) A10SJL62JY (ocrelizumab) 0 (Hepatitis B Antibodies)
 1406-16-2 (Vitamin D) 0 (Vitamins) 0 (Nerve Growth Factors)

 K9P6MC7092 (oxybutynin)






 77238-31-4 (Interferon-beta) Complement Factor I Deficiency
 FO2303MNI2 (Dimethyl Fumarate) 0 (Anti-Inflammatory Agents)
 G926EC510T (Fingolimod Hydrochloride)
 0 (Antioxidants) 0 (Cholesterol, LDL) 0 (Lipoproteins) 89750-14-1 (Glucagon-Like Peptide 1) 0 (Lipoproteins, LDL)
 0 (Retinoids)
 0 (Biomarkers) 0 (Brain-Derived Neurotrophic Factor) 0 (Glial Fibrillary Acidic Protein) 0 (Neuroprotective Agents) 7171WSG8A2 (BDNF protein, human) 0 (GFAP protein, human)


 47M74X9YT5 (Cladribine)


 0 (Immune Checkpoint Inhibitors) 0 (Antineoplastic Agents, Immunological)




 47M74X9YT5 (Cladribine) G926EC510T (Fingolimod Hydrochloride) 1C058IKG3B (teriflunomide) 0 (Immunosuppressive Agents) FO2303MNI2 (Dimethyl Fumarate) 0 (Tablets)

 3A189DH42V (Alemtuzumab) XRO4566Q4R (Interferon beta-1a)





 0 (Antibodies) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Oligoclonal Bands) 0 (Myelin-Oligodendrocyte Glycoprotein)
 EH28UP18IF (Isotretinoin) 0 (Anti-Bacterial Agents) 0 (Dermatologic Agents)




 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents) 0 (Drugs, Generic)
 147205-72-9 (CD40 Ligand)
 XRO4566Q4R (Interferon beta-1a) 77238-31-4 (Interferon-beta)
 0 (Natalizumab) A10SJL62JY (ocrelizumab) 4F4X42SYQ6 (Rituximab) SOA12P041N (nitazoxanide)
 0 (Receptors, Antigen, T-Cell)

 0 (Tetanus Toxoid)

 0 (COVID-19 Vaccines) 0 (Antibodies, Viral)
 0 (Sphingosine 1 Phosphate Receptor Modulators) 0 (Sphingosine-1-Phosphate Receptors)

 0 (Amyloid) 0 (Amyloidogenic Proteins) 0 (Autoantigens) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Peptide Fragments)
 BH3B64OKL9 (4-Aminopyridine) 0 (Potassium Channel Blockers) X4W7ZR7023 (Methylprednisolone)



 0 (Receptors, GABA) 0 (Immunoglobulin G) 0 (TSPO protein, human)
 0 (Biomarkers) 0 (Neurofilament Proteins)

 6SO6U10H04 (Biotin) 0 (Hormones)



 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 4F4X42SYQ6 (Rituximab) SARS-CoV-2 variants
 E1UOL152H7 (Iron)
 63231-63-0 (RNA)
 0 (Programmed Cell Death 1 Receptor)
 0 (Interleukin-3)
 RWP5GA015D (Potassium)






 0 (Antibodies, Neutralizing)
 0 (Glucocorticoids) 0 (Immunosuppressive Agents)
 0 (Interleukin-17) 0 (Interleukin-23)
 0 (Natalizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Peptides)

 0 (Neurotransmitter Agents) 0 (Cholinergic Agents)
 25167-62-8 (Docosahexaenoic Acids) 0 (Endocannabinoids) 0 (N-docosahexaenoylethanolamide)

 0 (Cannabinoids) 0 (Endocannabinoids) 0 (Receptors, Cannabinoid)

 0 (Interleukin-17) 01K63SUP8D (Fluoxetine) 0 (Interleukin-6) 0 (Cytokines) 82115-62-6 (Interferon-gamma)

 G926EC510T (Fingolimod Hydrochloride) 0 (Sphingosine 1 Phosphate Receptor Modulators) 0 (Sphingosine-1-Phosphate Receptors) 0 (Antibodies, Monoclonal)
 0 (Receptors, GABA) 0 (TSPO protein, human)

 0 (DNA, Mitochondrial) 0 (Autoantibodies)

 0 (Antibodies, Monoclonal) 0 (Antibodies, Monoclonal, Humanized) 0 (Antineoplastic Agents) A10SJL62JY (ocrelizumab)

 0 (Armadillo Domain Proteins) 0 (Cytoskeletal Proteins) 0 (RNA Splicing Factors) 0 (SARM1 protein, mouse) 0 (SF3B2 protein, human)
 0 (BIBP COVID-19 vaccine) 0 (RNA, Viral) 4F4X42SYQ6 (Rituximab) 0 (Vaccines)
 0 (Cytokines) 0 (Immunosuppressive Agents) 0 (MicroRNAs) 0 (MIRN223 microRNA, human)


 0 (Amyloid beta-Peptides) EC 3.4.- (Amyloid Precursor Protein Secretases) EC 3.4.23.- (Aspartic Acid Endopeptidases) EC 3.4.23.46 (BACE1 protein, human)
 0 (Proteome) 0 (Cerebrospinal Fluid Proteins)
 5M691HL4BO (Glatiramer Acetate) FO2303MNI2 (Dimethyl Fumarate) 77238-31-4 (Interferon-beta) WUB601BHAA (N,N-Dimethyltryptamine) 0 (Immunoglobulin A) 0 (Immunoglobulin G) 0 (Antibodies, Viral)
 0 (C9orf72 Protein) 0 (C9orf72 protein, human)

 BBX060AN9V (Hydrogen Peroxide) 0 (DNA, Mitochondrial)
 0 (DNA, Viral) 0 (Toll-Like Receptor 10) 0 (TLR10 protein, human)
 0 (COVID-19 Vaccines) 0 (Vaccines) COVID-19 breakthrough infections
 0 (Antigens, Viral) 0 (Antibodies, Viral)

 0 (Biomarkers) 0 (Myelin Basic Protein) 0 (Myelin-Oligodendrocyte Glycoprotein)
 0 (Interleukin-17)


 0 (COVID-19 Vaccines) 0 (Antibodies, Viral)
 25167-62-8 (Docosahexaenoic Acids) 0 (Interleukin-2) 207137-56-2 (Interleukin-4) 5688UTC01R (Tretinoin) 0 (Cytokines) 0 (GATA3 protein, human) 0 (GATA3 Transcription Factor)
 0 (Glia Maturation Factor)



 0 (HLA-DRB1 Chains)
 0 (NF-kappa B) 0 (NF-E2-Related Factor 2) 0 (bcl-2-Associated X Protein)
 0 (Micelles) M0TTH61XC5 (ibudilast) 0 (Nasal Sprays)
 059QF0KO0R (Water)
 SOA12P041N (nitazoxanide) 0 (Natalizumab) 3A189DH42V (Alemtuzumab)
 0 (2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole) 0 (Thiazoles) 0 (Aniline Compounds)


 G926EC510T (Fingolimod Hydrochloride) 0 (Antibodies) 0 (Receptors, Lysosphingolipid) 0 (S1PR1 protein, human) 0 (Sphingosine-1-Phosphate Receptors)


 0 (Blood Proteins) AU0V1LM3JT (Gadolinium)
 0 (Galectin 3) 0 (Phosphatidylcholines)


 MLT3645I99 (bisphenol A) 0 (Estrogens) 0 (Benzhydryl Compounds) 80-09-1 (bis(4-hydroxyphenyl)sulfone) 0 (Endocrine Disruptors)
 0 (Antibodies) 0 (Biomarkers)
 0 (Immunosuppressive Agents) G926EC510T (Fingolimod Hydrochloride) FO2303MNI2 (Dimethyl Fumarate) 1C058IKG3B (teriflunomide)

 0 (Immunoglobulin kappa-Chains) 0 (Neurofilament Proteins) 0 (Biomarkers)


 0 (Antibodies, Viral) 0 (Immunoglobulin G) 0 (Epstein-Barr Virus Nuclear Antigens)
 0 (Forkhead Transcription Factors) 0 (CD4 Antigens)

 0 (Gonadal Steroid Hormones) 0 (Estrogens)

 ZA45457L1K (evobrutinib)


 WI4X0X7BPJ (Hydrocortisone) JL5DK93RCL (Melatonin) 0 (Receptors, Melatonin)

 IT942ZTH98 (Curcumin) 0 (Polyphenols) 0 (Antioxidants) 0 (Anti-Inflammatory Agents)





 059QF0KO0R (Water)
 0 (Tumor Necrosis Factor-alpha) 0 (Antirheumatic Agents) 0 (Tumor Necrosis Factor Inhibitors)


 0 (Antigens, CD20) 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors) A10SJL62JY (ocrelizumab) M95KG522R0 (ofatumumab) U59UGK3IPC (ublituximab) 0 (Antibodies, Monoclonal)

 0 (Natalizumab) 0 (Integrin alpha4beta1) SOA12P041N (nitazoxanide)

 0 (HLA-DRB1 Chains)
 1C058IKG3B (teriflunomide) G926EC510T (Fingolimod Hydrochloride) 0 (Crotonates) FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 0 (Antibodies, Monoclonal) 130068-27-8 (Interleukin-10) 0 (elezanumab)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)
 EC 3.5.1.- (Sirtuin 1) EC 3.5.1.- (SIRT1 protein, human)

 1406-16-2 (Vitamin D) 0 (Vitamins)
 1406-16-2 (Vitamin D)


 0 (Peptidomimetics)
 0 (Natalizumab) A10SJL62JY (ocrelizumab) 0 (Immunologic Factors)


 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors) 0 (Antibodies, Monoclonal, Humanized)
 0 (DNA, Viral)
 YY9FVM7NSN (Hydrogen Sulfide) 0 (NF-kappa B) 5N16U7E0AO (Cuprizone) FWU2KQ177W (sodium bisulfide) 0 (MicroRNAs)





 J41CSQ7QDS (Zinc) 0 (Trace Elements)



 0 (Receptors, Progesterone)

 EC 2.7.10.2 (SYK protein, human) EC 2.7.10.2 (Syk Kinase)
 Q369O8926L (Resveratrol)


 0 (Pathogen-Associated Molecular Pattern Molecules)
 0 (remibrutinib) EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase) 0 (Antigen-Antibody Complex) 0 (Anti-Inflammatory Agents)


 0 (Contrast Media) AU0V1LM3JT (Gadolinium) 0 (Organometallic Compounds) K2I13DR72L (Gadolinium DTPA)

 0 (COVID-19 Vaccines) 0 (Antibodies, Viral) 0 (Immunoglobulin G)
 0 (Biomarkers) 0 (Neurofilament Proteins)

 X72A60C9MT (Lutein) 0 (Macular Pigment)

 0 (COVID-19 Vaccines) 0 (RNA, Viral) 0 (Antibodies, Viral)
 0 (Ligands) 0 (Chemokines) 0 (Cytokines) 0 (Chemokines, CXC) 0 (Receptors, Chemokine)


 0 (mRNA Vaccine) SOA12P041N (nitazoxanide) 0 (COVID-19 Vaccines) 0 (Natalizumab) G926EC510T (Fingolimod Hydrochloride) 0 (RNA, Messenger)


 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
 0 (Fatty Acids, Volatile)



 0 (Biomarkers) 0 (Neurofilament Proteins) 0 (Receptors, GABA) 0 (TSPO protein, human) 0 (neurofilament protein L)
 0 (Natalizumab) A10SJL62JY (ocrelizumab) G926EC510T (Fingolimod Hydrochloride)
 0 (Smoke)



 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Peptide Fragments) 0 (Peptides) 0 (Vaccines)




 S88TT14065 (Oxygen)


 0 (Myelin Basic Protein) EC 3.4.25.1 (Proteasome Endopeptidase Complex) 0 (Ligands) 0 (Peptide Fragments) 0 (Peptides) 0 (Immunodominant Epitopes) 0 (HLA-A Antigens)
 0 (Tumor Necrosis Factor-alpha) 0 (Tumor Necrosis Factor Inhibitors) 0 (Cytokines)

 8N3DW7272P (Cyclophosphamide)


 0 (Cytokines)

 0 (Myelin Proteins)
 0 (Contrast Media) AU0V1LM3JT (Gadolinium)
 0 (COVID-19 Vaccines)

 0 (COVID-19 Vaccines)

 0 (Aquaporin 4) 0 (Autoantibodies) 0 (MOG protein, human)
 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 SOA12P041N (nitazoxanide) 0 (Natalizumab) 0 (Biomarkers)


 0 (Cytokines)
 4F4X42SYQ6 (Rituximab)
 0 (Biomarkers)
 9061-61-4 (Nerve Growth Factor)
 0 (Natalizumab)
 77238-31-4 (Interferon-beta) 0 (Biosimilar Pharmaceuticals) XRO4566Q4R (Interferon beta-1a) 0 (Biomarkers)
 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 0 (Cytokines) 0 (RNA, Messenger) 0 (Immunoglobulin G) 0 (Antibodies, Viral) COVID-19 vaccine booster shot

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Aquaporin 4)
 0 (COVID-19 Vaccines)
 3KX376GY7L (Glutamic Acid)


 0 (Liposomes) 0 (Phosphatidylserines)
 0 (Immunoglobulin kappa-Chains) 0 (Immunoglobulin lambda-Chains) 0 (Immunoglobulin Light Chains) 0 (Albumins)

 BG3F62OND5 (Carboplatin)



 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Immunoglobulin G) 0 (Autoantibodies)
 A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized) 0 (Immunoglobulin M)
 0 (Cytokines) 0 (Chemokines) 0 (Pokeweed Mitogens)
 0 (Nanocapsules)
 0 (Biomarkers) 0 (Chemokine CXCL13) 0 (CXCL13 protein, human) 0 (CHI3L1 protein, human) 0 (Chitinase-3-Like Protein 1)
 0 (Biomarkers)
 1406-16-2 (Vitamin D)

 Q369O8926L (Resveratrol) 0 (Neuroprotective Agents)
 EC 3.4.24.69 (Botulinum Toxins, Type A) 0 (Neuromuscular Agents)
 Australians
 0 (Immunoglobulin G) 0 (Allergens)
 G926EC510T (Fingolimod Hydrochloride) DPT0O3T46P (pembrolizumab) 0 (Natalizumab)

 0 (Dihydroorotate Dehydrogenase) 5ML58O200F (ilepcimide)


 0 (Immunoglobulin G)



 0 (TREM2 protein, human) 0 (Membrane Glycoproteins) 0 (Receptors, Immunologic) 0 (Trem2 protein, mouse)
 0 (Biomarkers) 0 (Oligoclonal Bands) 0 (Immunoglobulin Light Chains) 0 (Immunoglobulin kappa-Chains)
 19GBJ60SN5 (Cannabidiol) 7J8897W37S (Dronabinol) 0 (Drug Combinations)
 0 (Dust) 2P299V784P (Lead) 0 (Metals, Heavy) 12597-69-2 (Steel)
 0 (Antibodies, Monoclonal) 0 (Antibodies, Viral)

 0 (Biomarkers) 0 (Neurofilament Proteins) 0 (Glial Fibrillary Acidic Protein)

 0 (Reactive Oxygen Species)
 3F752311CD (beta-hydroxyisovaleric acid) 0 (PPAR-beta) 0 (Valerates)

 0 (GABA Agonists) 56-12-2 (gamma-Aminobutyric Acid)





 0 (Cholinergic Agents) N9YNS0M02X (Acetylcholine)
 0 (Immunoglobulin G) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Myelin-Oligodendrocyte Glycoprotein)

 77238-31-4 (Interferon-beta) XRO4566Q4R (Interferon beta-1a) 3WJQ0SDW1A (Polyethylene Glycols)
 1406-16-2 (Vitamin D)
 0 (BNT162 Vaccine) 4F4X42SYQ6 (Rituximab) 0 (Antibodies) 0 (RNA, Messenger)
 0 (Biomarkers) 0 (Neurofilament Proteins)
 66772-14-3 (1,25-dihydroxyvitamin D) EC 1.14.15.16 (Vitamin D3 24-Hydroxylase) 82115-62-6 (Interferon-gamma) 81627-83-0 (Macrophage Colony-Stimulating Factor) 1406-16-2 (Vitamin D) 0 (Vitamins) EC 1.14.15.16 (CYP24A1 protein, human)
 EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 4)


 0 (Antioxidants) E1UOL152H7 (Iron) 9007-73-2 (Ferritins) GAN16C9B8O (Glutathione)

 Oculocerebral hypopigmentation syndrome type Preus
 EC 3.2.1.14 (Chitinases) 0 (Biomarkers)


 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies)
 0 (syncytin)
 0 (COVID-19 Vaccines)



 0 (Heterogeneous Nuclear Ribonucleoprotein A1) 0 (RNA-Binding Proteins) 0 (RNA, Small Interfering)


 0 (Transcription Factor AP-1)
 77238-31-4 (Interferon-beta) 9008-11-1 (Interferons) 0 (Antiviral Agents)



 0 (CXCL10 protein, human) 0 (Chemokine CXCL10)
 3A189DH42V (Alemtuzumab) 0 (Iodine Radioisotopes)
 G926EC510T (Fingolimod Hydrochloride)
 IY9XDZ35W2 (Glucose)
 0 (Immunoglobulin kappa-Chains)

 63231-63-0 (RNA) 1C058IKG3B (teriflunomide) 3A189DH42V (Alemtuzumab) 0 (COVID-19 Vaccines) 0 (BNT162 Vaccine) 0 (Antibodies, Viral)
 47M74X9YT5 (Cladribine) 0 (Influenza Vaccines)
 5N16U7E0AO (Cuprizone)

 SY7Q814VUP (Calcium) 1406-16-2 (Vitamin D) 0 (Calcium, Dietary) P6YZ13C99Q (Calcifediol)
 0 (Tumor Necrosis Factor-alpha) 0 (Cytokines)

 0 (Antibodies, Monoclonal, Humanized) 0 (Immunologic Factors) XRO4566Q4R (Interferon beta-1a) A10SJL62JY (ocrelizumab)

 CPD4NFA903 (Aluminum)


 E1UOL152H7 (Iron)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Aquaporin 4)


 EC 3.4.24.69 (abobotulinumtoxinA) EC 3.4.24.69 (Botulinum Toxins, Type A) 0 (Neuromuscular Agents)
 789U1901C5 (Copper) 0 (RNA, Small Untranslated) 0 (MicroRNAs) 0 (Biomarkers) J41CSQ7QDS (Zinc) E1UOL152H7 (Iron)
 0 (Nucleocapsid Proteins)

 0 (BIBP COVID-19 vaccine) 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 0 (Antibodies, Viral) 0 (Immunoglobulin G) 0 (Vaccines, Inactivated)
 G926EC510T (Fingolimod Hydrochloride)



 0 (BIBP COVID-19 vaccine) 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 0 (Vaccines) SARS-CoV-2 variants

 0 (Drugs, Chinese Herbal) 0 (Polysaccharides)
 0 (Sphingosine-1-Phosphate Receptors) 26993-30-6 (sphingosine 1-phosphate) Z80293URPV (ozanimod) 0 (Indans) 0 (Oxadiazoles) NGZ37HRE42 (Sphingosine)

 5N16U7E0AO (Cuprizone) 0 (Immunoglobulins)
 0 (HLA-DRB1 Chains) 0 (VDR protein, human) 0 (Receptors, Calcitriol) Slovak people
 G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents) 126880-86-2 (L-Selectin) 0 (Pharmaceutical Preparations) NGZ37HRE42 (Sphingosine) 0 (S1PR1 protein, human)
 0 (Potassium Channels) 5N16U7E0AO (Cuprizone) BH3B64OKL9 (4-Aminopyridine)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)






 47M74X9YT5 (Cladribine) 0 (Immunosuppressive Agents) 0 (RASGRP2 protein, human) 0 (Guanine Nucleotide Exchange Factors)

 U015TT5I8H (Bismuth) 3M4G523W1G (Silver) CPD4NFA903 (Aluminum) 8002-74-2 (Paraffin) FXS1BY2PGL (Mercury) 0 (Hazardous Substances)
 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents)
 S88TT14065 (Oxygen)
 0 (Natalizumab) 0 (COVID-19 Vaccines) 47M74X9YT5 (Cladribine) G926EC510T (Fingolimod Hydrochloride) 0 (Antibodies, Viral)
 VNM47R2QSQ (icariin) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (Inflammasomes)
 0 (CD28 Antigens) G926EC510T (Fingolimod Hydrochloride) 0 (Immunosuppressive Agents)


 0 (PLX5622)


 0 (Natalizumab) A10SJL62JY (ocrelizumab) SOA12P041N (nitazoxanide) 0 (Immunologic Factors)


 0 (Protein Isoforms) 0 (Transforming Growth Factor beta) 0 (Transforming Growth Factor beta1) 0 (Transforming Growth Factor beta3)
 0 (Radiopharmaceuticals) 0 (Fluorine Radioisotopes)


 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 4F4X42SYQ6 (Rituximab) 0 (Antibodies, Viral)
 0 (Fatty Acids) 0 (Fatty Acids, Monounsaturated) 0 (Elovl6 protein, mouse)

 0 (COVID-19 Vaccines) 0 (RNA, Messenger) 0 (mRNA Vaccines) 0 (Immunoglobulin G) 0 (Antibodies, Viral)
 0 (Antiviral Agents)
 0 (Ceramides) 0 (Immunoglobulin G)
 4F4X42SYQ6 (Rituximab) 0 (Immunologic Factors)




 OF5P57N2ZX (Alanine) 0 (Biomarkers) 0 (Galectin 3) EC 2.6.1.- (Transaminases)


 0 (Antibodies, Monoclonal) 4F4X42SYQ6 (Rituximab) 0 (Antineoplastic Agents)
 0 (Proteins) 0 (Autoantibodies) Hashimoto's encephalitis

 0 (Biomarkers)




 EC 1.- (TET1 protein, human) EC 1.- (Mixed Function Oxygenases) 0 (Proto-Oncogene Proteins)
 0 (Natalizumab) 0 (Vaccines, Attenuated) 0 (Chickenpox Vaccine)

 0 (Peptides)
 Q9L0O73W7L (Coconut Oil) BQM438CTEL (epigallocatechin gallate)

 0 (MCAM protein, human) 0 (CD146 Antigen)

 11096-26-7 (Erythropoietin) X4W7ZR7023 (Methylprednisolone)

 3A189DH42V (Alemtuzumab) 0 (Receptors, GABA-A)
 EC 1.14.13.- (Cytochrome P-450 CYP2E1) CYS9AKD70P (Isoflurane) 9035-51-2 (Cytochrome P-450 Enzyme System) BH3B64OKL9 (4-Aminopyridine) 0 (Oxides)
 0 (Xbp1 protein, mouse) 0 (Nucleic Acids) 0 (NR3C2 protein, human) 0 (NCOR2 protein, human) 0 (XBP1 protein, human) 0 (Nr3c2 protein, mouse) 0 (Ncor2 protein, mouse)

 0 (Antigens, CD20) 4F4X42SYQ6 (Rituximab) 0 (Antineoplastic Agents, Immunological)

 0 (Peptides) 0 (Glycoproteins)
 G926EC510T (Fingolimod Hydrochloride) 5M691HL4BO (Glatiramer Acetate) 0 (Immunosuppressive Agents) 77238-31-4 (Interferon-beta)

 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)


 9M998304JB (sephin1)
 47M74X9YT5 (Cladribine) 0 (Tablets) 0 (Antigens, CD20) 0 (Antigens, CD19) 0 (Immunoglobulin G) 0 (Immunoglobulin M)
 1406-16-2 (Vitamin D) 0 (Vitamins) 0 (Cytokines) 0 (Chemokines)



 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 0 (Vaccines)



 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 95QN29S1ID (Clemastine) 0 (NF-E2-Related Factor 2) 0 (NLR Proteins) EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) EC 1.14.14.18 (Heme Oxygenase-1) 0 (Nlrp3 protein, rat)
 0 (Immunoglobulin G) 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Autoantibodies)


 0 (COVID-19 Vaccines)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Anti-Inflammatory Agents) 0 (Peptide Fragments)
 0 (CCR6 protein, mouse) 0 (Chemokines) 0 (Receptors, CCR6) 0 (CCL20 protein, mouse)
 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents) 0 (Biomarkers)

 0 (Natalizumab) 0 (Biomarkers) 0 (Neurofilament Proteins)
 0 (Myelin-Oligodendrocyte Glycoprotein)
 2SCD8Q63PF (NVX-CoV2373 adjuvated lipid nanoparticle) 0 (COVID-19 Vaccines) JT2NS6183B (Ad26COVS1) 0 (BNT162 Vaccine) B5S3K2V0G8 (ChAdOx1 nCoV-19) 0 (Viral Vaccines) 0 (Immunoglobulin G) 0 (Antibodies, Viral)
 0 (COVID-19 Vaccines)
 0 (Lipocalin-2)
 0 (TSPO protein, human) 0 (Receptors, GABA)
 EC 3.4.24.69 (Botulinum Toxins, Type A) 0 (Neuromuscular Agents)
 0 (MicroRNAs) 124671-05-2 (RHOA protein, human) EC 3.6.5.2 (rhoA GTP-Binding Protein) EC 2.7.11.1 (ROCK1 protein, human) EC 2.7.11.1 (rho-Associated Kinases)


 4F4X42SYQ6 (Rituximab) G926EC510T (Fingolimod Hydrochloride) 0 (COVID-19 Vaccines) 0 (Antibodies, Viral) 0 (Immunoglobulin G) 0 (RNA, Messenger)
 0 (Glial Fibrillary Acidic Protein)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantigens)
 O5GA75RST7 (EBV-encoded nuclear antigen 1) 0 (alpha-Crystallins)
 5N16U7E0AO (Cuprizone) 0 (Glucagon-Like Peptide-1 Receptor)
 0 (Lysophosphatidylcholines)
 0 (Bacterial Toxins)
 0 (COVID-19 Vaccines)


 0 (Cannabinoids)


 FO2303MNI2 (Dimethyl Fumarate) 0 (Immunosuppressive Agents) 1C058IKG3B (teriflunomide)
 0 (Receptors, Purinergic P2X7) 0 (Integrin beta3) SY7Q814VUP (Calcium)
 EC 2.3.2.27 (Ubiquitin-Protein Ligases) 0 (Ubiquitins)
 0 (Antibodies) 0 (Aquaporin 4) 0 (Autoantibodies)

 3A189DH42V (Alemtuzumab)
 0 (Natalizumab) 0 (Antibodies, Monoclonal, Humanized)
 X4W3ENH1CV (Norepinephrine)
 47M74X9YT5 (Cladribine) 0 (Neurofilament Proteins) 0 (Biomarkers)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Aquaporin 4) 0 (Immunoglobulin G)

 0 (Beclin-1) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) 0 (Biomarkers)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Immunoglobulin G)
 0 (Tyrosine Protein Kinase Inhibitors)
 EC 3.6.4.13 (DEAD-box RNA Helicases) 0 (Forkhead Transcription Factors) EC 3.6.1.- (DDX39B protein, human) 0 (FOXP3 protein, human)
 0 (Blood Glucose) 0 (Lipids) 0 (Insulin)
 0 (MicroRNAs) 0 (3' Untranslated Regions)
 0 (Biomarkers) 0 (XCL1 protein, human) 0 (Chemokines, C)



 0 (Fatty Acids, Volatile)


 0 (Interleukin-17) 0 (Cytokines)

 0 (STAT5 Transcription Factor) EC 2.7.10.2 (Janus Kinase 2)
 0 (Adrenal Cortex Hormones) 0 (Immunosuppressive Agents)
 0 (Triggering Receptor Expressed on Myeloid Cells-1) 0 (Carrier Proteins) 0 (TREM1 protein, mouse)
 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Immunoglobulin G) 0 (Autoantibodies)
 1C058IKG3B (teriflunomide) 0 (Immunosuppressive Agents) A10SJL62JY (ocrelizumab) 0 (Antibodies, Monoclonal, Humanized)
 0 (Tumor Necrosis Factor Inhibitors)

 0 (Antioxidants) 0 (Cholesterol, LDL) EC 3.1.8.1 (Aryldialkylphosphatase) 0 (Apolipoprotein A-II) 0 (Apolipoproteins C) EC 3.1.8.1 (PON1 protein, human)

 0 (HLA-DRB1 Chains) 0 (HLA Antigens)
 5N16U7E0AO (Cuprizone)
 C5529G5JPQ (ginger extract) 31C4KY9ESH (Nitric Oxide) 0 (Cytokines) 82115-62-6 (Interferon-gamma) 0 (Anti-Inflammatory Agents)
 0 (COVID-19 Vaccines) 47M74X9YT5 (Cladribine) 0 (RNA, Messenger) G926EC510T (Fingolimod Hydrochloride) 0 (Antibodies, Viral)




 0 (Oligoclonal Bands) 0 (Immunoglobulin G)

 0 (COVID-19 Vaccines) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Myelin-Oligodendrocyte Glycoprotein)


 0 (Anti-Bacterial Agents)
 30KYC7MIAI (Aspartic Acid) 4SR0Q8YD1X (D-Aspartic Acid) 0 (Excitatory Amino Acids) 3KX376GY7L (Glutamic Acid) 0 (Cytokines)
 0 (Natalizumab) FO2303MNI2 (Dimethyl Fumarate)
 0 (COVI-VAC) G926EC510T (Fingolimod Hydrochloride) 0 (COVID-19 Vaccines) 0 (BNT162 Vaccine) 0 (Immunosuppressive Agents) 0 (Antibodies, Viral) 0 (RNA, Messenger) 0 (Antibodies, Neutralizing) SARS-CoV-2 variants
 A10SJL62JY (ocrelizumab) 0 (COVID-19 Vaccines) 4F4X42SYQ6 (Rituximab) 0 (Spike Glycoprotein, Coronavirus) 0 (BNT162 Vaccine) 0 (Antibodies, Monoclonal, Humanized) 0 (Antibodies, Viral) 0 (spike protein, SARS-CoV-2)
 AU0V1LM3JT (Gadolinium) 0 (Contrast Media) K2I13DR72L (Gadolinium DTPA)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)
 0 (Iridoids) 0 (oleacein)
 82115-62-6 (Interferon-gamma)


 0 (MicroRNAs) 0 (MIRN155 microRNA, human)


 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Lipids)
 5N16U7E0AO (Cuprizone) 0 (Tumor Necrosis Factor-alpha) 0 (Neuroprotective Agents) 0 (Brain-Derived Neurotrophic Factor) 0 (Chalcones)
 J1K406072N (cannabigerol) 31C4KY9ESH (Nitric Oxide) 0 (Cytokines) 0 (Tumor Necrosis Factor-alpha) 0 (Lipopolysaccharides)
 130068-27-8 (Interleukin-10) 0 (IL10 protein, mouse)
 0 (COVID-19 Vaccines) 0 (Viral Vaccines)
 5N16U7E0AO (Cuprizone) 0 (Receptors, Purinergic P1)
 0 (Fatty Acids, Unsaturated)
 0 (HLA-DRB1 Chains) 0 (Receptors, Antigen, T-Cell) 0 (HLA Antigens)

 5N16U7E0AO (Cuprizone)
 0 (Cytokines) 0 (B-Cell Activating Factor)
 0 (Myelin Basic Protein) 0 (Myelin Proteolipid Protein) 0 (Protein Isoforms)
 4F4X42SYQ6 (Rituximab) 0 (Biosimilar Pharmaceuticals) 0 (Antibodies, Monoclonal) 0 (Antineoplastic Agents)
 0 (Lysophosphatidylcholines) 95QN29S1ID (Clemastine) 5N16U7E0AO (Cuprizone)
 8DUH1N11BX (Tryptophan) 343-65-7 (Kynurenine) H030S2S85J (Kynurenic Acid) F6F0HK1URN (Quinolinic Acid)
 0 (Autoantibodies) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4)
 EC 3.4.21.- (Granzymes) 0 (Programmed Cell Death 1 Receptor) 126465-35-8 (Perforin) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Cytokines)
 0 (Autoantibodies)
 0 (Interleukin-3)
 0 (Sphingosine-1-Phosphate Receptors) 26993-30-6 (sphingosine 1-phosphate) 5N16U7E0AO (Cuprizone) 0 (Receptors, Lysosphingolipid) 0 (beta-Arrestins)
 0 (Biomarkers) 0 (Neurofilament Proteins)

 0 (Interleukin-17) 0 (Cytokines) 0 (Anti-Inflammatory Agents) 0 (Artemisinins) 0 (RNA, Messenger)
 G926EC510T (Fingolimod Hydrochloride) 0 (Sphingosine-1-Phosphate Receptors) RR6P8L282I (siponimod) 0 (Sphingosine 1 Phosphate Receptor Modulators) NGZ37HRE42 (Sphingosine)

 0 (CD28 Antigens)
 EC 3.2.2.5 (CD38 protein, human)
 0 (Anti-Inflammatory Agents)

 0 (Autoantigens) 0 (Adhesins, Bacterial) 0 (Autoantibodies) 0 (Myelin Proteins) 0 (Peptides) 0 (Myelin-Oligodendrocyte Glycoprotein)
 0 (Oligoclonal Bands) 0 (Immunoglobulin G)
 5N16U7E0AO (Cuprizone)
 0 (Interleukin-17) 001E35HGVF (magnolol) 0 (STAT3 Transcription Factor) 0 (Cytokines)

 0 (Receptors, Tumor Necrosis Factor, Type I) 0 (Cytokines) 0 (Tumor Necrosis Factor-alpha)

 0 (Cytokines) 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) 0 (Tumor Necrosis Factor-alpha) 130068-27-8 (Interleukin-10) 0 (Interleukin-17) 82115-62-6 (Interferon-gamma)
 0 (Myelin Basic Protein) 0 (myelin basic protein 85-99) 0 (Tumor Necrosis Factor-alpha) 0 (MBP protein, human)
 0 (Oligoclonal Bands) 0 (Immunoglobulin G)
 67763-96-6 (Insulin-Like Growth Factor I)


 0 (COVID-19 Vaccines) EPK39PL4R4 (2019-nCoV Vaccine mRNA-1273) JT2NS6183B (Ad26COVS1) 0 (BNT162 Vaccine)
 0 (MicroRNAs)


 213431586X (bornyl acetate) 0 (Neuroprotective Agents) 0 (Anti-Inflammatory Agents)
 10216-23-6 (sphingosine phosphorylcholine) 0 (Lipopolysaccharides)

 0 (Glial Fibrillary Acidic Protein) 0 (Biomarkers)


 0 (Homeodomain Proteins)
 0 (TRPA1 Cation Channel) 0 (Transient Receptor Potential Channels)

 A10SJL62JY (ocrelizumab)
 0 (Lipopolysaccharides) EC 3.4.21.- (Kallikreins)
 0 (Antigens, Viral) FO2303MNI2 (Dimethyl Fumarate) 0 (Immunoglobulin G) 0 (Antibodies, Viral) 0 (Capsid Proteins)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Immunoglobulin G)

 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
 0 (MicroRNAs) 0 (Mirn23b microRNA, mouse)
 0 (Immunomodulating Agents)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Receptors, Fc) 9007-36-7 (Complement System Proteins) 0 (Antibodies, Monoclonal)
 0 (ELAV Proteins) 0 (Elavl1 protein, mouse) 0 (Elavl4 protein, mouse)
 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine) 0 (Liposomes) 0 (Angiopoietin-1)
 0 (COVID-19 Vaccines) G926EC510T (Fingolimod Hydrochloride) 0 (Adaptor Proteins, Signal Transducing) 0 (Antibodies, Viral)
 0 (Immunoglobulin G) 9007-36-7 (Complement System Proteins)
 9008-11-1 (Interferons)

 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (AQP4 protein, human) 0 (MOG protein, human)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies)
 0 (Biomarkers) 0 (Glial Fibrillary Acidic Protein) 0 (Neurofilament Proteins) 0 (neurofilament protein L)
 0 (Myelin-Oligodendrocyte Glycoprotein)
 12001-79-5 (Vitamin K)
 9008-11-1 (Interferons) 0 (Proteins) 0 (Ifit2 protein, mouse) 0 (RNA-Binding Proteins) 0 (Apoptosis Regulatory Proteins)
 0 (Antibodies, Viral) 0 (Antiviral Agents)


 29106-49-8 (procyanidin B2) 0 (Proanthocyanidins) 0 (Cytokines)
 0 (Nanocapsules) 5688UTC01R (Tretinoin) 0 (Lipids)

 0 (BCG Vaccine) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Peptides) 0 (Peptide Fragments)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Myelin Proteolipid Protein) 0 (Antibodies)
 47M74X9YT5 (Cladribine) 0 (Tablets) 0 (Immunosuppressive Agents)
 0 (Antibodies, Monoclonal) 0 (Antigens, CD19) 0 (Myelin-Oligodendrocyte Glycoprotein)
 EC 1.15.1.1 (Superoxide Dismutase) EC 1.15.1.1 (Superoxide Dismutase-1)
 0 (Antigens, CD20)
 0 (Receptors, Aryl Hydrocarbon)
 0 (Receptors, Tumor Necrosis Factor, Type I) 0 (Receptors, Tumor Necrosis Factor, Type II) 0 (Tumor Necrosis Factor-alpha)
 0 (Biomarkers) 0 (Neurofilament Proteins) 0 (neurofilament protein L)
 5M691HL4BO (Glatiramer Acetate) 0 (Peptides)

 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Immunoglobulin G) 0 (Myelin-Oligodendrocyte Glycoprotein)
 0 (COVID-19 Vaccines)

 0 (Sulfoglycosphingolipids) 0 (Antibodies) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Glycolipids)
 EC 2.7.1.74 (Deoxycytidine Kinase)
 0 (Cytokines) 0 (MicroRNAs) 0 (MIRN485 microRNA, mouse) 0 (STAT3 Transcription Factor)
 0 (COVID-19 Vaccines) 0 (Antibodies, Neutralizing) 0 (Antibodies, Viral)

 0 (Biomarkers)
 9B1J4V995Q (carvacrol) 0 (Interleukin-17) 0 (Tumor Necrosis Factor-alpha) 0 (NF-kappa B) 0 (Interleukin-1)
 0 (Immunoglobulin G)
 0 (Antibodies, Viral) 26993-30-6 (sphingosine 1-phosphate) 0 (Myelin-Oligodendrocyte Glycoprotein) SARS-CoV-2 variants
 0 (RNA, Untranslated)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Aquaporin 4)
 0 (Antibodies, Catalytic) 0 (Autoantibodies) EC 1.11.1.6 (Catalase) 9007-49-2 (DNA) 0 (Histones) BBX060AN9V (Hydrogen Peroxide) 0 (Myelin-Oligodendrocyte Glycoprotein)
 0 (Cannabinoids) 0 (Cannabinoid Receptor Agonists)
 A10SJL62JY (ocrelizumab) 0 (Immunologic Factors) 0 (Antibodies, Monoclonal, Humanized) 0 (Receptors, Antigen, T-Cell)
 EC 3.2.1.22 (alpha-Galactosidase)
 0 (MicroRNAs) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) 0 (Biomarkers) EC 3.1.3.67 (PTEN protein, human) EC 3.1.3.67 (PTEN Phosphohydrolase) EC 2.7.4.8 (MAGI2 protein, human) 0 (Adaptor Proteins, Signal Transducing) EC 2.7.4.8 (Guanylate Kinases)
 0 (BIBP COVID-19 vaccine) B5S3K2V0G8 (ChAdOx1 nCoV-19) 0 (COVID-19 Vaccines) 0 (Vaccines, Inactivated)

 0 (Epitopes) 0 (Autoantigens)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies)
 0 (Immunoglobulin G) 47M74X9YT5 (Cladribine) 0 (Antigens, CD20) 0 (RNA, Messenger)
 EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 4) 0 (Phosphodiesterase 4 Inhibitors) 0 (Anti-Inflammatory Agents)

 0 (tau Proteins)
 0 (COVID-19 Vaccines) 0 (RNA, Messenger)
 0 (Gonadal Steroid Hormones) 3XMK78S47O (Testosterone) 4TI98Z838E (Estradiol)
 343-65-7 (Kynurenine) 8DUH1N11BX (Tryptophan)
 0 (GPR17 protein, mouse) 0 (Nerve Tissue Proteins) 0 (Receptors, G-Protein-Coupled) 0 (tau Proteins)
 0 (Histocompatibility Antigens Class I)
 49QAH60606 (baicalein) 0 (Chemokines, CXC) 0 (Immunoglobulin G) 0 (Cxcr6 protein, mouse) 0 (Receptors, CXCR6)
 0 (Biomarkers) 0 (Glial Fibrillary Acidic Protein) 0 (neurofilament protein L) 0 (Neurofilament Proteins)
 5N16U7E0AO (Cuprizone) 73Y7P0K73Y (Thioctic Acid) 0K47UL67F2 (Carvedilol)
 9004-61-9 (Hyaluronic Acid) 0 (Glycosaminoglycans) 9007-28-7 (Chondroitin Sulfates)
 0 (Sphingosine 1 Phosphate Receptor Modulators) 0 (COVID-19 Vaccines) 0 (Sphingosine-1-Phosphate Receptors) 0 (Antibodies, Monoclonal) 0 (Immunoglobulin G) 0 (Antibodies, Viral)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Immunoglobulin G) 0 (Immunoglobulin A) 0 (Immunoglobulin M)
 5N16U7E0AO (Cuprizone) 0 (Receptors, Muscarinic)
 0 (Immunoglobulin kappa-Chains) 0 (Oligoclonal Bands) 0 (Biomarkers)
 57WA9QZ5WH (Nimodipine) 0 (Calcium Channel Blockers) 0 (Calcium Channels, L-Type) 0 (MicroRNAs)
 G926EC510T (Fingolimod Hydrochloride) 0 (Sphingosine 1 Phosphate Receptor Modulators) 0 (COVID-19 Vaccines) 0 (Sphingosine-1-Phosphate Receptors) NGZ37HRE42 (Sphingosine)
 0 (Anti-Inflammatory Agents) 0I8Y3P32UF (Berberine) 0 (Cytokines) 0 (Transcription Factors)
 0 (COVID-19 Vaccines) 0 (Natalizumab)
 47M74X9YT5 (Cladribine) 0 (Epstein-Barr Virus Nuclear Antigens)
 0 (Egr2 protein, mouse) 0 (Transcription Factors)
 0 (MicroRNAs) 0 (Mirn155 microRNA, mouse)
 0 (COVID-19 Vaccines) 0 (Antibodies, Viral) WUB601BHAA (N,N-Dimethyltryptamine) 0 (RNA, Messenger)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Histocompatibility Antigens Class II)

 0 (Aquaporin 4) 0 (Autoantibodies)
 0 (Biomarkers)
 0 (Ataxin-1) 0 (Atxn1 protein, mouse)
 0 (Programmed Cell Death 1 Receptor) 0 (B7-H1 Antigen)
 EC 3.6.1.- (Myosin Type I)
 130068-27-8 (Interleukin-10) 0 (Transforming Growth Factor beta1) 0 (NSC 74859) 0 (Interleukin-17) 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (RNA, Messenger) 0 (Forkhead Transcription Factors)
 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) G926EC510T (Fingolimod Hydrochloride) 0 (Galectin 3) 0 (Tumor Necrosis Factor-alpha)
 0 (Anti-Inflammatory Agents) 0 (Cytokines) 0 (Myelin-Oligodendrocyte Glycoprotein)
 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Autoantibodies)
 0 (Oligoclonal Bands) 0 (Immunoglobulin kappa-Chains) 0 (Immunoglobulin Light Chains) 0 (Immunoglobulin lambda-Chains) 0 (Biomarkers)
 0 (COVID-19 Vaccines) 0 (Autoantibodies)

 G926EC510T (Fingolimod Hydrochloride) 26993-30-6 (sphingosine 1-phosphate) 0 (Immunosuppressive Agents) Y9449Q51XH (Bezafibrate) 0 (Propylene Glycols) 0 (Fatty Acids)
 0 (SLC1A3 protein, human) 0 (Amino Acid Transport System X-AG) 48TCX9A1VT (Cystine) 0 (Antioxidants) 3KX376GY7L (Glutamic Acid) 0 (SLC7A11 protein, human) 0 (Amino Acid Transport System y+)
 EC 2.1.1.43 (Histone-Lysine N-Methyltransferase) 0 (RNA, Messenger) EC 2.1.1.43 (SETDB1 protein, human) EC 2.3.2.27 (TRIM28 protein, human) EC 2.3.2.27 (Tripartite Motif-Containing Protein 28)
 G926EC510T (Fingolimod Hydrochloride) 0 (Natalizumab) FO2303MNI2 (Dimethyl Fumarate) A10SJL62JY (ocrelizumab) 0 (Immunosuppressive Agents) 0 (Immunologic Factors)
 0 (Fibronectins) EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta) 0 (Myelin-Oligodendrocyte Glycoprotein)
 0 (SLC20A2 protein, human) 0 (Sodium-Phosphate Cotransporter Proteins, Type III) 0 (GPNMB protein, human) 0 (Membrane Glycoproteins) EC 1.1.- (DHRS11 protein, human) EC 1.1.- (17-Hydroxysteroid Dehydrogenases) 0 (TSFM protein, human)
 EC 3.4.21.- (High-Temperature Requirement A Serine Peptidase 1) Cerebral Autosomal Recessive Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
 0 (BNT162 Vaccine) 0 (COVID-19 Vaccines) 0 (Immunosuppressive Agents) 0 (RNA, Viral) 0 (Steroids)
 0 (Receptors, Tumor Necrosis Factor, Type I) 0 (Receptors, Tumor Necrosis Factor, Type II) 0 (Tumor Necrosis Factor Inhibitors) 0 (Tumor Necrosis Factor-alpha) 0 (Antibodies)
 0 (NF-kappa B) 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) 139874-52-5 (NF-KappaB Inhibitor alpha) SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one) 0 (Tumor Necrosis Factor-alpha) 0 (Interleukin-6) 0 (Protein Kinase Inhibitors) EC 2.7.11.24 (Mitogen-Activated Protein Kinases) 0 (RNA, Messenger)
 0 (MicroRNAs) 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (Vitamins) 11103-57-4 (Vitamin A) 12001-79-5 (Vitamin K)
 0 (RNA, Ribosomal, 16S) 85U4C366QS (oxymatrine) 0N7609K889 (Sulfadiazine)




































































































































































































 0 (Cytokines) 0 (Intercellular Signaling Peptides and Proteins) 0 (Biomarkers)













































































































































 GPL8T5ZO3M (7-deazaguanine) 72496-59-4 (queuine) 9014-25-9 (RNA, Transfer) EC 2.4.2.- (Pentosyltransferases)

















































































 0 (Chromatin)


















































































































































 M95KG522R0 (ofatumumab) 0 (Antibodies, Monoclonal, Humanized)















































 7440-57-5 (Gold) 0 (Peptides)





















 0 (Aquaporin 4) 4F4X42SYQ6 (Rituximab) MRK240IY2L (Azathioprine) 0 (Immunoglobulins, Intravenous) 0 (Immunoglobulin G) 0 (Autoantibodies) 0 (Immunosuppressive Agents) 0 (Enzyme Inhibitors) 0 (Myelin-Oligodendrocyte Glycoprotein)


 0 (Immunoglobulin Light Chains) 0 (Immunoglobulin lambda-Chains) 0 (Biomarkers)



 EC 3.5.1.- (Sirtuin 3) EC 3.5.1.- (SIRT3 protein, human)




 0 (Culture Media, Conditioned)





























 0 (Calreticulin) 139873-08-8 (Calnexin) 0 (Calcium-Binding Proteins) 0 (Ribonucleoproteins)



































































 0 (Cytokines)



 9007-36-7 (Complement System Proteins) 0 (Biomarkers)




 0 (Anti-Bacterial Agents) 0 (Antibodies) 0 (Antioxidants)







































































 0 (NF1 protein, human)





 0 (Autoantibodies)




 0 (plexin) 0 (Receptors, Cell Surface) 0 (Semaphorins) 0 (Single-Domain Antibodies) 0 (Cell Adhesion Molecules)








 0 (Membrane Proteins) 0 (Nerve Tissue Proteins) 0 (Nogo Proteins) 0 (LINGO1 protein, human)


 1C058IKG3B (teriflunomide) 0 (Crotonates) 0 (Hydroxybutyrates)





 0 (Peptides) 0 (Transcription Factors)




 0 (Autoantibodies)







 0 (Dietary Fiber) 0 (Fatty Acids, Volatile)





 0 (Interleukin-17) 0 (Interleukin-6) 0 (Interleukins) 0 (Cytokines) 0 (Interleukin-1)












































 1406-16-2 (Vitamin D)














 0 (Macrophage Migration-Inhibitory Factors) 70ETD81LF0 (5-hydroxymethylfurfural)
 1406-16-2 (Vitamin D) 0 (Vitamins)

 1406-16-2 (Vitamin D) 0 (Vitamins)
 130068-27-8 (Interleukin-10) 0 (Receptors, Aryl Hydrocarbon) 0 (AHR protein, human) 0 (IL10 protein, human)










 0 (Immunoglobulin M) 0 (Sulfoglycosphingolipids) 0 (Lipids)
 0 (Antiviral Agents)



 M95KG522R0 (ofatumumab) 0 (Antibodies, Monoclonal)

































 0 (COVID-19 Vaccines)



 0 (Cell Adhesion Molecules, Neuronal) 0 (IgLON5 protein, human)





 19GBJ60SN5 (Cannabidiol) 0 (PPAR gamma)


 0 (Sulfoglycosphingolipids)
 EC 2.7.1.- (Phosphatidylinositol 3-Kinases) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 2.7.11.1 (TOR Serine-Threonine Kinases) 0 (AXL receptor tyrosine kinase, mouse) 0 (Axl Receptor Tyrosine Kinase)




 0 (Nanocapsules) 0 (Anti-Inflammatory Agents) 0 (Lipopolysaccharides) 0 (Cytokines)


 0 (COVID-19 Vaccines) 0 (mRNA Vaccine)






 EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase) G926EC510T (Fingolimod Hydrochloride)
 0 (Fibrinolytic Agents) FO2303MNI2 (Dimethyl Fumarate) EC 3.4.21.5 (Thrombin)
 0 (Histocompatibility Antigens Class II) 0 (Autoantigens)
 0 (Receptors, Galanin) 88813-36-9 (Galanin) 0 (Receptor, Galanin, Type 2) 0 (RNA, Messenger)

 0 (Nucleic Acids) 0 (MicroRNAs) 0 (Alarmins)
 0 (Hepatitis B Vaccines) 0 (Hepatitis B Antibodies)










 0 (Antigens) 0 (Receptors, Antigen, T-Cell)






 4F4X42SYQ6 (Rituximab) A10SJL62JY (ocrelizumab) 0 (Immunoglobulin G) 0 (Immunoglobulin A)



















































 8N3DW7272P (Cyclophosphamide)
 0 (Keap1 protein, mouse) 0 (Kelch-Like ECH-Associated Protein 1) 0 (NF-E2-Related Factor 2) EC 2.3.2.27 (Ubiquitin-Protein Ligases) 0 (NFE2L2 protein, human)

 5N16U7E0AO (Cuprizone)
 0 (Antibodies) 0 (Biological Products) 0 (Natalizumab)


 0 (Contraceptives, Oral)





 0 (Autoantibodies) 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein)






 0 (Myeloid Differentiation Factor 88)















 E0399OZS9N (Cyclic AMP) 0 (Receptors, G-Protein-Coupled)












 0 (Chemokines, CXC) 0 (Receptors, Scavenger) 0 (Receptors, CXCR6) 0 (Receptors, Virus) 0 (Chemokine CXCL16) 0 (CXCR6 protein, human) 0 (CXCL16 protein, human)
 0 (COVID-19 Vaccines) 0 (Myelin-Oligodendrocyte Glycoprotein)

 0 (Autoantigens)
 0 (Chemokine CX3CL1)



 BH3B64OKL9 (4-Aminopyridine) EC 3.4.- (Amyloid Precursor Protein Secretases) 0 (Peptides)





 0 (Cell-Free Nucleic Acids) 0 (MicroRNAs) 0 (Biomarkers)












 0 (Interferon Type I)
 0 (COVID-19 Vaccines) NGZ37HRE42 (Sphingosine) 0 (Antibodies, Neutralizing) 0 (Antibodies, Viral)







 9DLQ4CIU6V (Proline) 5GZ3E0L9ZU (Azetidinecarboxylic Acid) 0 (Amino Acids)


 6SO6U10H04 (Biotin) 0 (Myelin Basic Protein) 0 (Proteins)

 0 (anti-aquaporin 4 autoantibody) 0 (Autoantibodies) 0 (Aquaporin 4)





















 EC 2.7.11.24 (Mitogen-Activated Protein Kinase 14) 6X80438640 (benzamide) 0 (Benzamides) 0 (Protein Kinase Inhibitors) 0 (Pharmaceutical Preparations)



 0 (Oligoclonal Bands) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Immunoglobulin G)



 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) 0 (RNA, Ribosomal, 16S)

 0 (HMGB1 Protein)




















 AAN7QOV9EA (Eicosapentaenoic Acid) 25167-62-8 (Docosahexaenoic Acids) 0 (Fatty Acids, Omega-3) 0 (Fatty Acids, Unsaturated) 27YG812J1I (Arachidonic Acid) 0 (Linoleic Acids)

 0 (Natalizumab) SOA12P041N (nitazoxanide) 126547-89-5 (Intercellular Adhesion Molecule-1) 143198-26-9 (Integrin alpha4)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Aquaporin 4) 0 (Immunoglobulin G)
 0 (Aquaporin 4) 0 (Biomarkers) 0 (Autoantibodies) 0 (Immunoglobulin G) 0 (Myelin-Oligodendrocyte Glycoprotein)

 0 (Interferon-alpha) 0 (Cytokines)



 5M691HL4BO (Glatiramer Acetate) 0 (Peptides)

 0 (Hepatitis A Virus Cellular Receptor 2) 0 (Ligands) 0 (Mucins) 0 (Membrane Proteins) 0 (Immunoglobulins)
 0 (Antibodies)
 0 (Cytokines)




















 FI96A8X663 (Rilpivirine) 0 (Anti-HIV Agents) 0 (Pyridones) 0 (Vaccines)










 0 (RNA Precursors)

 0 (Autoantigens)


 0 (Photosensitizing Agents)

 VTD58H1Z2X (Dopamine)

 997-55-7 (N-acetylaspartate) 30KYC7MIAI (Aspartic Acid) EC 3.5.1.98 (Histone Deacetylases)

 0 (Immunologic Factors) 0 (Adjuvants, Immunologic)
 82115-62-6 (Interferon-gamma) 0 (B7-H1 Antigen)



 0 (2-methoxyestradiol-3,17-O,O-bis(sulfamate)) 6I2QW73SR5 (2-Methoxyestradiol) 9NFU33906Q (sulfamic acid) 0 (Pharmaceutical Preparations)

 BZ114NVM5P (Mitoxantrone) GAN16C9B8O (Glutathione) 0 (Lipids)
 EC 1.14.19.1 (Stearoyl-CoA Desaturase) 0 (Fatty Acids)




 0 (Amyloid beta-Peptides)














 0 (HHLA2 protein, human) 0 (Immunoglobulins) 0 (RNA, Viral)

 0 (Cytokines)





 0 (BNT162 Vaccine) 0 (Antibodies, Monoclonal) 0 (Antilymphocyte Serum) 0 (RNA, Messenger)





 Q369O8926L (Resveratrol) 0 (Cytokines)





 2679MF687A (Niacin) 0 (Amyloid beta-Peptides)






 0 (COVID-19 Vaccines) 0 (BNT162 Vaccine) 0 (Immunomodulating Agents) 0 (Antibodies, Viral)






 X4W7ZR7023 (Methylprednisolone)


 0 (Antibodies, Monoclonal)


 0 (Epstein-Barr Virus Nuclear Antigens)


 Akkermansia muciniphila






 0 (Alkaloids) 0 (Neuroprotective Agents) 0 (Matrines)
 0 (Toll-Like Receptors) 0 (Cytokines)




 0 (Neurofilament Proteins) 0 (Biomarkers)
 0 (Progestins) 4G7DS2Q64Y (Progesterone)

 4F4X42SYQ6 (Rituximab)
 1406-16-2 (Vitamin D) 0 (Vitamins) SY7Q814VUP (Calcium)





 0 (Interleukin-17) 0 (Cytokines)







 0 (Myelin Proteins) 4QD397987E (Histidine)
 EC 3.5.3.6 (arginine deiminase) EC 3.- (Hydrolases)

 0 (Antioxidants) 0 (Organoselenium Compounds)






 0 (NF-E2-Related Factor 2) 97C5T2UQ7J (Cholesterol)

 EC 1.14.14.25 (Cholesterol 24-Hydroxylase) 97C5T2UQ7J (Cholesterol)





 0 (MicroRNAs) 0 (Biomarkers)





 EC 3.1.6.- (Sulfatases) EC 3.1.6.- (SUMF1 protein, human) EC 1.8.- (Oxidoreductases Acting on Sulfur Group Donors)




 0 (Receptors, AMPA) 3KX376GY7L (Glutamic Acid)



 0 (Basic Helix-Loop-Helix Transcription Factors) 9042-14-2 (Dextran Sulfate)


 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (Interleukin-11)

 0 (Chemokines, CC) 0 (CCL13 protein, human) 0 (Monocyte Chemoattractant Proteins)







 EC 1.11.1.7 (Peroxidase) 0 (Imidazoles) 0 (Benzimidazoles)






 0 (Arrestin) 0 (Receptors, G-Protein-Coupled) 0 (beta-Arrestins) EC 3.6.5.5 (Dynamins) 0 (Clathrin) 0 (Caveolins) 0 (GPR15 protein, human) 0 (Receptors, Peptide)




 0 (Receptors, sigma)
 0 (Aquaporin 4)

 0 (Chitinase-3-Like Protein 1) EC 3.2.1.14 (Chitinases) 0 (Synapsins)
 0 (Cytokines) 0 (Chemokine CX3CL1) 0 (CX3CL1 protein, human)

 26993-30-6 (sphingosine 1-phosphate) G926EC510T (Fingolimod Hydrochloride) NGZ37HRE42 (Sphingosine) 0 (Lysophospholipids) 0 (Sphingolipids) 0 (Receptors, Lysosphingolipid)
 5N16U7E0AO (Cuprizone) 0 (Sulfates) 9050-30-0 (Heparitin Sulfate)
 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) 0 (Interleukin-15) 0 (Interleukin-27) 0 (Tumor Necrosis Factor-alpha)
 0 (Autoantibodies) 0 (Aquaporin 4) 0 (Immunoglobulin G)



 EC 3.4.21.- (Lactoferrin) 0 (Neuroprotective Agents) E1UOL152H7 (Iron)




 0 (Autoantibodies) Hashimoto's encephalitis



 1406-16-2 (Vitamin D) 0 (Vitamins)










 0 (Interferon Lambda) 9008-11-1 (Interferons) 0 (Antiviral Agents)




 8SSC91326P (Donepezil) PKI06M3IW0 (Rivastigmine)
 0 (Inflammasomes) EC 3.4.22.36 (Caspase 1) 0 (Interleukin-1beta) 0 (NLR Family, Pyrin Domain-Containing 3 Protein)


 0 (Immunomodulating Agents) 0 (Receptor, Nerve Growth Factor)






 0 (Glucocorticoids)
 0 (Receptors, Tumor Necrosis Factor, Type II) 0 (Receptors, Tumor Necrosis Factor, Type I) 0 (Tumor Necrosis Factor-alpha) 0 (Cytokines)




 5N16U7E0AO (Cuprizone) Q369O8926L (Resveratrol)


 0 (Histones) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (MicroRNAs) 0 (Antibodies, Catalytic) 9007-49-2 (DNA)


 7G33012534 (Sodium Oxybate) 0 (Natalizumab) GR120KRT6K (Vigabatrin) 0 (Pharmaceutical Preparations)

 0 (Biomarkers)

 Akkermansia muciniphila
 0 (Interleukin-17) 0 (Tumor Necrosis Factor-alpha) 0 (Interleukin-6) 0 (NF-kappa B) 0 (Lipopolysaccharides) 0 (Myeloid Differentiation Factor 88) 0 (Toll-Like Receptor 4) 0 (Cytokines) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Forkhead Transcription Factors) 0 (RNA, Messenger)


 74T7185BMM (inebilizumab) 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Biomarkers) 0 (Autoantibodies)


 5N16U7E0AO (Cuprizone) 0 (Polysaccharides) EC 3.1.3.48 (Protein Tyrosine Phosphatases) EC 3.1.3.48 (Ptprz1 protein, mouse)

 H6241UJ22B (Selenium)
 0 (Cytokines) 0 (Interleukin-17) FO2303MNI2 (Dimethyl Fumarate) EC 3.4.21.- (Granzymes) EC 2.7.7.- (Nucleotidyltransferases) Amyotrophic lateral sclerosis 1
 EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases) 0 (Endocannabinoids)


 0 (Orexins) EC 2.7.10.1 (ErbB Receptors) EC 2.7.10.1 (EGFR protein, human)








 0 (Antibodies, Viral)



 FO2303MNI2 (Dimethyl Fumarate) 817L1N4CKP (malic acid) 0 (Xenobiotics) WYQ7N0BPYC (Acetylcysteine) 0 (Immunosuppressive Agents)


 0 (Potassium Channels) 0 (Cyclic Nucleotide-Gated Cation Channels) 0 (Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels)

 0 (Cytokines) 0 (Interleukin-33) 207137-56-2 (Interleukin-4) 0 (IL4 protein, human)







 0 (Autoantibodies) 0 (Autoantigens) 0 (Immunoglobulin G)

 0 (Receptors, Aryl Hydrocarbon)
 130068-27-8 (Interleukin-10) L497I37F0C (royal jelly) 0 (Interleukin-17) 0 (Transforming Growth Factor beta) 0 (Interleukin-23)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Epitopes)



 0 (Interleukin-6)

 0 (Nerve Growth Factors)

 0 (Myelin Proteins) 0 (Nogo Proteins) 0 (Nerve Growth Factors) 0 (Nogo Receptors)
 0 (Ion Channels)



 9NEZ333N27 (Sodium) 0 (Pharmaceutical Preparations)




 5S6W795CQM (Naltrexone) 0 (Analgesics, Opioid) 0 (Narcotic Antagonists)


 EC 3.1.3.16 (Protein Phosphatase 2)
 0 (MicroRNAs) 0 (MIRN183 microRNA, human)
 0 (Nucleosides) 0 (Antineoplastic Agents) 0 (Membrane Transport Proteins) 0 (Antimetabolites)

 0 (Inflammasomes)


 EC 2.7.10.1 (Receptor, trkB) 0 (Brain-Derived Neurotrophic Factor) 0 (N,N',N'-tris(2-hydroxyethyl)-1,3,5-benzenetricarboxamide) 0 (Benzamides)


 0 (Biomarkers) 0 (Autoantibodies)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 0 (Receptors, Cannabinoid) 0 (Cannabinoids) 0 (Cannabinoid Receptor Antagonists)



 0 (RNA, Viral) 0 (Aquaporin 4)
 9008-11-1 (Interferons)



 0 (Autoantigens)


 2P471X1Z11 (Omalizumab) 5B2546MB5Z (elagolix)


 0 (Cannabinoids) 0 (Endocannabinoids) 0 (Receptors, Cannabinoid)


 0 (ABCB1 protein, human) 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
 H030S2S85J (Kynurenic Acid) 8DUH1N11BX (Tryptophan)

 9001-32-5 (Fibrinogen) 0 (Tlr9 protein, rat) 0 (Toll-Like Receptor 9) 0 (fibrinogen-like protein 2, rat)



 0 (Biomarkers) 0 (Glial Fibrillary Acidic Protein)

 839I73S42A (Liraglutide)
 E1UOL152H7 (Iron)

 0 (Receptor, Anaphylatoxin C5a)







 0 (Pituitary Adenylate Cyclase-Activating Polypeptide) 0 (Biomarkers)

 PLG39H7695 (Paraquat) 0 (Antioxidants) FO2303MNI2 (Dimethyl Fumarate)


 0 (Immunomodulating Agents)




 0 (Vitamins) 11103-57-4 (Vitamin A) 12001-79-5 (Vitamin K)

 0 (HLA-DR Antigens) 0 (Peptides) 0 (Epitopes)


 0 (Aquaporin 4)
 0 (Autoantibodies) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4)

 0 (Carrier Proteins) 0 (Interleukin-18) 0 (Antibodies, Monoclonal)
 19GBJ60SN5 (Cannabidiol)
 0 (Hypoxia-Inducible Factor 1, alpha Subunit) 0 (HIF1A protein, human)

 63231-63-0 (RNA) 0 (RNA-Binding Proteins) 0 (RNA, Messenger)
 0 (Pharmaceutical Preparations)








 L497I37F0C (royal jelly) 0 (Fatty Acids) 0 (Anti-Bacterial Agents) 0 (Biomarkers)


 MRK240IY2L (Azathioprine)

 7864XYD3JJ (Acrolein) 0 (Tobacco Smoke Pollution)


 0 (Receptors, Purinergic P2X7) 0 (Purinergic P2X Receptor Antagonists)






 EC 2.7.- (Protein Kinases) EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta) EC 2.7.1.- (Phosphatidylinositol 3-Kinases)

 0 (Autoantibodies)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Immunoglobulin G)







 0 (Inflammasomes)

 0 (Antioxidants) 0 (Kelch-Like ECH-Associated Protein 1) 0 (Reactive Oxygen Species) 0 (NF-E2-Related Factor 2)
 0 (Anion Transport Proteins) 0 (Lysophospholipids) NGZ37HRE42 (Sphingosine) 26993-30-6 (sphingosine 1-phosphate) 0 (Sphingosine-1-Phosphate Receptors) 0 (Spns2 protein, mouse) 0 (SLF1081851) 0 (2-Aminobenzoxazole)



 0 (Blood Glucose) 0 (Anti-Inflammatory Agents)


 31C4KY9ESH (Nitric Oxide) 0 (Air Pollutants) 0 (Particulate Matter) 1406-16-2 (Vitamin D)
 0 (Helminth Proteins) 0 (Peptides)
 0 (Cytokines)

 3CN01F5ZJ5 (chrysin) 0 (Antioxidants) 0 (Flavonoids)


 0 (RNA, Long Noncoding) 0 (MicroRNAs)

 0 (Air Pollutants) 0 (Environmental Pollutants) 0 (Particulate Matter)
 BQM438CTEL (epigallocatechin gallate) EC 2.7.11.26 (Glycogen Synthase Kinase 3) EC 2.7.1.- (Phosphatidylinositol 3-Kinases)

 0 (Biomarkers) 0 (S100 Calcium Binding Protein beta Subunit) 0 (S100B protein, human)

 0 (NF-E2-Related Factor 2) 0 (Antioxidants)
 S7V92P67HO (Arsenic Trioxide) 789U1901C5 (Copper) 0 (Reactive Oxygen Species) BBX060AN9V (Hydrogen Peroxide)
 0 (Biomarkers)
 EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase) 0 (Protein Kinase Inhibitors)



 0 (Receptor, Bradykinin B2) 0 (Receptor, Bradykinin B1) 0 (Peptides)
 0 (Vascular Endothelial Growth Factor A) EC 1.14.11.29 (Hypoxia-Inducible Factor-Proline Dioxygenases) EC 1.14.11.- (Prolyl Hydroxylases) EC 1.14.11.2 (Procollagen-Proline Dioxygenase) 0 (Hypoxia-Inducible Factor 1, alpha Subunit)


 0 (Radiopharmaceuticals) GZ5I74KB8G (Fluorine-18)
 0 (Neuroprotective Agents) VTD58H1Z2X (Dopamine) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) 8O1CR18L82 (hyperoside) BBX060AN9V (Hydrogen Peroxide) 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Immunoglobulin G)

 0 (Grape Seed Extract) 0 (Interleukin-17) 0 (Interleukin-1beta) 0 (Tumor Necrosis Factor-alpha) 0 (Interleukin-6) 82115-62-6 (Interferon-gamma) 187348-17-0 (Interleukin-12) 0 (Cytokines)

 0 (Biomarkers)


 0 (Neuroprotective Agents) 0 (Anti-Inflammatory Agents, Non-Steroidal)




 0 (Ephrins)
 0 (Cytokines) 0 (Anti-Inflammatory Agents) 0 (Interleukins)
 0 (Vitamins)



 0 (BCG Vaccine)
 FO2303MNI2 (Dimethyl Fumarate) EC 3.4.24.17 (Matrix Metalloproteinase 3) 0 (Interleukin-6)

 0 (Ion Channels)






 0 (Fatty Acids, Volatile) 0 (Butyrates) 0 (Propionates) 0 (Acetates)


 EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinase 2) EC 2.7.11.1 (RIPK2 protein, human)

 0 (Ankyrins) 0 (TRPA1 protein, human) 0 (TRPA1 Cation Channel)
 0 (Analgesics, Opioid) 26993-30-6 (sphingosine 1-phosphate) NGZ37HRE42 (Sphingosine) 0 (Lysophospholipids) 0 (Receptors, Lysosphingolipid)
 0 (Neuroprotective Agents) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 2.7.1.- (Phosphatidylinositol 3-Kinases) 0 (Artemisinins)



 0 (Retinoid X Receptors)




 Akkermansia muciniphila




 0 (Amyloid beta-Peptides)



 0 (Sphingosine-1-Phosphate Receptors) GZ5I74KB8G (Fluorine-18) 0 (Fluorine Radioisotopes) 0 (Radiopharmaceuticals)
 0 (Cytokines) 0 (Stat3 protein, mouse) 0 (STAT3 Transcription Factor)


 619G5K328Y (ceric oxide) K679OBS311 (Carboxymethylcellulose Sodium) 5M691HL4BO (Glatiramer Acetate) 30K4522N6T (Cerium)
 45IUB1PX8R (monomethyl fumarate) 0 (Antioxidants) 0 (Reactive Oxygen Species) 0U46U6E8UK (NAD) 0RQ6CXO9KD (citraconic acid) 0 (Neuroprotective Agents) 0 (NF-E2-Related Factor 2)
 31YO63LBSN (Nivolumab)
 0 (Biological Products)
 0 (NF-E2-Related Factor 2) R4KO0DY52L (Chlorhexidine) 0 (Kelch-Like ECH-Associated Protein 1) 0 (Reactive Oxygen Species)





 0 (Amyloidogenic Proteins) 0 (Amyloid) 0 (Amyloid beta-Peptides)



 0 (Cytokines) 0 (Suppressor of Cytokine Signaling Proteins) 0 (SOCS4 protein, mouse)


 1406-16-2 (Vitamin D) 0 (Vitamins)


 0 (Cell-Free Nucleic Acids) 0 (Biomarkers, Tumor)


 0 (COVID-19 Vaccines) 0 (RNA, Messenger)
 0 (Histones) 0 (Myelin Basic Protein) 9007-49-2 (DNA) 0 (Autoantibodies)


 0 (Histones) 0 (Myelin Basic Protein) 9007-49-2 (DNA) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Antibodies, Catalytic) 0 (Immunoglobulin G)

 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) 54ST71P9EE (4-methylhistamine) 0 (Interleukin-6) 0 (Receptors, Histamine H4) 0 (Tumor Necrosis Factor-alpha) 0 (NF-kappa B) 0 (Adaptor Proteins, Signal Transducing) 0 (Antigens, CD19)

 9006-59-1 (Ovalbumin)
 G926EC510T (Fingolimod Hydrochloride) 5N16U7E0AO (Cuprizone)


 0 (Immunosuppressive Agents) 9PHQ9Y1OLM (Prednisolone) Primary angiitis of the central nervous system


 EC 1.11.1.7 (Peroxidase)


 G926EC510T (Fingolimod Hydrochloride) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) 0 (Receptors, Lysosphingolipid) 0 (Sphingosine-1-Phosphate Receptors) 2ZD004190S (Threonine) 0 (S1PR1 protein, human)


 0 (Reactive Oxygen Species)
 0 (Leukocyte L1 Antigen Complex) 0 (Calgranulin A) 0 (Calgranulin B) 0 (Biomarkers)

 0 (Biomarkers) 0 (Glial Fibrillary Acidic Protein) 74T7185BMM (inebilizumab) 0 (Antibodies, Monoclonal, Humanized)
 0 (wuzi yanzong) 3TGX09BD5B (acteoside) G01BQC0879 (schizandrin) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 2.7.1.- (Phosphatidylinositol 3-Kinases) 19YRN3ZS9P (Ellagic Acid) 5688UTC01R (Tretinoin)
 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (NF-kappa B)


 0 (CTLA-4 Antigen)

 059QF0KO0R (Water)

 H789N3FKE8 (Baclofen) 0 (Muscle Relaxants, Central)




 0 (Interleukin-17) 0 (Interleukin-23)

 0 (Cytokines) 0 (Autoantibodies)


 0 (Insulin)


 9007-49-2 (DNA) 0 (Histocompatibility Antigens Class II) 0 (Mutant Proteins)
 0 (Blood Glucose) AYI8EX34EU (Creatinine) 8N3DW7272P (Cyclophosphamide) 268B43MJ25 (Uric Acid)

 059QF0KO0R (Water)
 3IK6592UBW (shikonin) 0 (Anti-Inflammatory Agents) 0 (Naphthoquinones)
 0 (Autoantibodies)



 0 (Actins) 0 (belumosudil) G926EC510T (Fingolimod Hydrochloride) EC 2.7.11.1 (rho-Associated Kinases) EC 3.6.5.2 (rhoA GTP-Binding Protein) 124671-05-2 (RHOA protein, human) 138381-45-0 (Y 27632)
 EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase) 0 (Tyrosine Protein Kinase Inhibitors)



 FO2303MNI2 (Dimethyl Fumarate) 0 (NF-E2-Related Factor 2)







 0 (Cytokines)

 789U1901C5 (Copper)
 EC 3.4.19.12 (COP9 Signalosome Complex) 0 (Intracellular Signaling Peptides and Proteins) EC 3.4.- (Peptide Hydrolases) EC 3.4.-.- (COPS5 protein, human)

 9008-11-1 (Interferons)
 0 (Transcription Factors)


 0 (Autoantigens) 0 (Liposomes)

 56-12-2 (gamma-Aminobutyric Acid) 0 (Receptors, GABA)

 0 (Dipeptidyl-Peptidase IV Inhibitors) EC 3.4.14.5 (Dipeptidyl Peptidase 4) 9007-92-5 (Glucagon)







 0 (Autoantigens) 0 (Adjuvants, Immunologic) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Peptides)
 0 (Cyclotides) K848JZ4886 (Cysteine)
 EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 7) 0 (Phosphodiesterase Inhibitors) 47341-71-9 (diethylstilbestrol monophosphate) EC 3.1.4.17 (3',5'-Cyclic-AMP Phosphodiesterases) 0 (Nucleotides, Cyclic)
 0 (Antioxidants) 0 (Neuroprotective Agents) 0 (Amyloid beta-Peptides) 0 (Plant Extracts) EC 1.15.1.1 (Superoxide Dismutase)



 V27W9254FZ (Cortisone)

 FO2303MNI2 (Dimethyl Fumarate) 0 (Kelch-Like ECH-Associated Protein 1) 0 (Galectin 1) 0 (NF-E2-Related Factor 2) 45IUB1PX8R (monomethyl fumarate) 0RQ6CXO9KD (citraconic acid)

 0 (MicroRNAs) 0 (Biomarkers) 0 (MIRN15 microRNA, human)






 0 (Amyloid beta-Protein Precursor) 0 (tau Proteins) 0 (APP protein, human) 0 (APP protein, mouse)
 EC 2.7.1.- (Phosphatidylinositol 3-Kinases) EC 2.7.10.2 (Janus Kinases) EC 2.7.1.137 (Phosphatidylinositol 3-Kinase) 0 (Polyphenols) 0 (Alkaloids) 0 (Biological Products)

 0 (Biomarkers) 0 (Neurofilament Proteins)





 0 (Nerve Growth Factors)

 0 (Epitopes, T-Lymphocyte) 0 (Vaccines, Subunit)
 0 (spike protein, SARS-CoV-2) 0 (Spike Glycoprotein, Coronavirus) 0 (CR3022) 0 (Antibodies, Monoclonal) SARS-CoV-2 variants
 0 (Contrast Media) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) AU0V1LM3JT (Gadolinium) 0 (Aquaporin 4) 0 (Immunoglobulin G)

 0 (Capsid Proteins)
 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Autoantibodies)
 0 (Flavonoids)

 0 (NF-kappa B) 0 (Nestin) 0 (Cytokines) 0 (SARM1 protein, mouse) 0 (Cytoskeletal Proteins) 0 (Armadillo Domain Proteins)

 0 (Aquaporin 4) MRK240IY2L (Azathioprine)

 0 (Autoantibodies) 0 (Nerve Tissue Proteins) 0 (Recombinant Proteins) 0 (anti-Yo autoantibodies) 0 (CDR2L antigen, human) 0 (CDR2 protein, human)


 W8O17SJF3T (Memantine) BF4C9Z1J53 (Amantadine)






 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
 9004-61-9 (Hyaluronic Acid) 0 (Extracellular Matrix Proteins) 9007-34-5 (Collagen)

 0 (1,2-indanedione) 0 (Interleukin-6 Inhibitors) YL5FZ2Y5U1 (Methotrexate) 0 (Interleukin-6)


 CPD4NFA903 (Aluminum) 0 (Antioxidants) EC 3.1.1.7 (Acetylcholinesterase) 19GBJ60SN5 (Cannabidiol) 0 (Oils) 7J8897W37S (Dronabinol)




 0 (integrin beta7) 0 (Integrins) 143198-26-9 (Integrin alpha4)

 EC 1.14.99.1 (Cyclooxygenase 2) 3K9958V90M (Ethanol) 0 (SLC39A14 protein, mouse) 0 (Cation Transport Proteins) Prevotella histicola


 0 (Cytokines)

 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (Amyloid beta-Peptides) 0 (Cytokines) EC 3.4.22.- (Caspases)


 0 (MicroRNAs) 0 (Biomarkers) 0 (Mirn128 microRNA, mouse)

 0 (HLA-DRB1 Chains)




 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (Lipids)

 0 (RNA, Ribosomal, 16S) 0 (Adjuvants, Immunologic) 9007-81-2 (Freund's Adjuvant) 0 (Anti-Bacterial Agents) 0 (Immunoglobulin G)
 0 (Antioxidants) 0 (Anti-Inflammatory Agents) 7YNJ3PO35Z (Hydrogen)


 37341-29-0 (Immunoglobulin E)
 0 (Cannabinoids) 7J8897W37S (Dronabinol) 0 (Cannabinoid Receptor Agonists) 0 (Receptors, Cannabinoid) 0 (Receptor, Cannabinoid, CB1)

 FO2303MNI2 (Dimethyl Fumarate) 0 (NF-E2-Related Factor 2)


 268B43MJ25 (Uric Acid) 0 (Antioxidants)
 0 (Cytokines) 0 (Anti-Inflammatory Agents)
 0 (Contrast Media) AU0V1LM3JT (Gadolinium)

 0 (Aquaporin 4) A3ULP0F556 (eculizumab) 0 (Immunoglobulin G) 74T7185BMM (inebilizumab) YB18NF020M (satralizumab)

 0 (Pharmaceutical Preparations) 0 (Central Nervous System Depressants)

 0 (Amyloid beta-Peptides) 0 (Amyloid beta-Protein Precursor) 0 (bcl-2-Associated X Protein) EC 3.4.22.- (Caspase 3) EC 2.7.11.1 (Rock2 protein, mouse)
 0 (Antidepressive Agents)
 5N16U7E0AO (Cuprizone) 67763-96-6 (Insulin-Like Growth Factor I) 0 (Igf1r protein, mouse) EC 2.7.10.1 (Receptor, IGF Type 1)
 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (STA-21) 0 (Cytokines) 0 (Anti-Inflammatory Agents)
 0 (BNT162 Vaccine)



 8L70Q75FXE (Adenosine Triphosphate)
 8DUH1N11BX (Tryptophan) 0 (Indoles)


 0 (Carbohydrates)

 614OI1Z5WI (Valproic Acid) 0 (Interleukin-6) 0 (Tumor Necrosis Factor-alpha) 0 (Phosphodiesterase Inhibitors) M0TTH61XC5 (ibudilast)



 0 (RNA, Viral)


 EC 3.4.24.69 (Botulinum Toxins, Type A) 0 (Cholinergic Antagonists)
 0 (RNA, Viral)


 EC 3.1.4.12 (Sphingomyelin Phosphodiesterase) 0 (Saposins) EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1) Combined Saposin Deficiency

 G926EC510T (Fingolimod Hydrochloride) EC 3.5.1.98 (Histone Deacetylases) 0 (Lipopolysaccharides) 0 (NF-kappa B) 0 (RANK Ligand) 0 (Repressor Proteins)
 0 (Actins) 0 (CLEC16A protein, human) 0 (DNA-Binding Proteins) 0 (Lectins, C-Type) 0 (Membrane Proteins) 0 (Monosaccharide Transport Proteins) 0 (Nuclear Proteins) 0 (Transcription Factors) 0 (TRIM27 protein, human) EC 2.3.2.27 (Ubiquitin-Protein Ligases) 0 (Ubiquitins)

 26993-30-6 (sphingosine 1-phosphate) NGZ37HRE42 (Sphingosine)
 0 (Fatty Acids, Omega-3)
 0 (NF-E2-Related Factor 2) 722KLD7415 (Pyruvaldehyde) 3A3U0GI71G (Magnesium Oxide) 0 (Cytokines)

 0 (Oligonucleotides)


 0 (Autoantibodies) 0 (Aquaporin 4)



 0 (RNA, Circular) 63231-63-0 (RNA)
 0 (Glial Fibrillary Acidic Protein) 0 (Aquaporin 4) 0 (Biomarkers) 0 (Autoantibodies) 0 (Immunoglobulin G)




 0 (Phenanthrenes) NI40JAQ945 (Tetradecanoylphorbol Acetate) 0 (Fluorenes)


 8D239QDW64 (glyceryl 2-arachidonate) 0 (Endocannabinoids) 0 (Neuroprotective Agents)
 0 (COVID-19 Vaccines) 0 (Antibodies) 0 (Antibodies, Viral)
 Australians


 0 (Connexin 43) 0 (Interleukin-6) 0 (Glucosides) 0 (Interleukin-2)
 FO2303MNI2 (Dimethyl Fumarate) 0 (NF-E2-Related Factor 2) 0 (Zebrafish Proteins) 0 (Antioxidants)
 0 (Ligands) 0 (Lipids)
 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
 0 (Reactive Oxygen Species) 144416-78-4 (LMP-2 protein)
 451W47IQ8X (Sodium Chloride)










 0 (Nucleic Acids) 0 (RNA, Double-Stranded)
 0 (Amyloid) 0 (Amyloid beta-Peptides) 0 (APP protein, human)
 EC 3.1.25.1 (Deoxyribonuclease (Pyrimidine Dimer)) EC 3.1.25.1 (NTHL1 protein, human) 0 (RNA, Messenger) 0 (Tuberous Sclerosis Complex 2 Protein) 0 (Tumor Suppressor Proteins) 0 (polycystic kidney disease 1 protein) 0 (TRPP Cation Channels)





 0 (FTY 720P) NGZ37HRE42 (Sphingosine) G926EC510T (Fingolimod Hydrochloride) 0 (Propylene Glycols) 0 (Ligands) 0 (Receptors, Lysosphingolipid) 0 (Sphingosine-1-Phosphate Receptors) 8L70Q75FXE (Adenosine Triphosphate) 0 (Immunosuppressive Agents) 0 (STAT3 protein, human) 0 (STAT3 Transcription Factor)
 45IUB1PX8R (monomethyl fumarate) 0 (Esters) 0 (Interleukin-6) 0 (Tumor Necrosis Factor-alpha) 0RQ6CXO9KD (citraconic acid) FO2303MNI2 (Dimethyl Fumarate) GAN16C9B8O (Glutathione)

 JL5DK93RCL (Melatonin) 0 (Autoantibodies)



 12001-76-2 (Vitamin B Complex) 1406-16-2 (Vitamin D)




 1406-16-2 (Vitamin D) AYI8EX34EU (Creatinine) 0 (Vitamins)
 0 (Membrane Glycoproteins) EC 1.14.13.39 (Nitric Oxide Synthase Type II) 0 (Receptors, Immunologic) 0 (Trem2 protein, mouse) EC 1.14.13.39 (Nos2 protein, mouse)
 A10SJL62JY (ocrelizumab)
 EC 3.1.1.8 (Butyrylcholinesterase) EC 3.1.1.7 (Acetylcholinesterase) 0 (Cholinesterase Inhibitors) 0 (Enzyme Inhibitors) EC 2.5.1.18 (Glutathione Transferase) 0 (Piperazines)

 9100L32L2N (Metformin) 0 (Hypoglycemic Agents) IY9XDZ35W2 (Glucose) EC 2.7.11.31 (AMP-Activated Protein Kinases)



 acute flaccid myelitis
 5N16U7E0AO (Cuprizone) 0 (Receptors, Aryl Hydrocarbon) 0 (Ahr protein, mouse)

 EC 5.3.99.2 (prostaglandin R2 D-isomerase)
 0 (Particulate Matter) 0 (Air Pollutants) 0 (Environmental Pollutants)
 0 (Estrogen Receptor alpha) 0 (Lymphotoxin beta Receptor) 0 (TNF Receptor-Associated Factor 3) 0 (Estrogens)
 UP7QBP99PN (apremilast) 0 (Tumor Necrosis Factor-alpha) 0 (Interleukin-17) 0 (Biological Factors) 0 (Biological Products)
 Diffuse alopecia




 EC 6.2.1.- (Acsl4 protein, mouse) 0 (Lipids) EC 6.2.1.3 (long-chain-fatty-acid-CoA ligase) 0 (Reactive Oxygen Species)
 EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein) 0 (MicroRNAs) 0 (MIRN367 microRNA, mouse) EC 2.1.1.43 (Ezh2 protein, mouse)


 L6UH7ZF8HC (Risperidone) 0 (Antipsychotic Agents) G926EC510T (Fingolimod Hydrochloride)
 0 (Vaccines)
 FO2303MNI2 (Dimethyl Fumarate) 0 (Connexin 43) 45IUB1PX8R (monomethyl fumarate) 0RQ6CXO9KD (citraconic acid)

 0 (Chromatin) 614OI1Z5WI (Valproic Acid) 0 (RNA, Messenger)
 1C058IKG3B (teriflunomide) 0 (Crotonates) 0 (Hydroxybutyrates) 0 (Nitriles)
 0 (Contrast Media)
 0 (Environmental Pollutants)



 0 (Tumor Suppressor Proteins) W36ZG6FT64 (Sirolimus)

 EC 1.15.1.1 (Superoxide Dismutase-1)

 0 (spike protein, SARS-CoV-2) EC 3.4.17.23 (Angiotensin-Converting Enzyme 2) EC 3.4.15.1 (Peptidyl-Dipeptidase A)
 0 (Anticonvulsants)
 0 (Antigens, CD34) 0 (Cell Adhesion Molecules) EC 3.4.21.59 (Tryptases) 0 (Vimentin)


 0 (FUS protein, human) 0 (Heterogeneous-Nuclear Ribonucleoproteins) 0 (PCBP2 protein, human) 0 (RNA-Binding Protein FUS) 0 (RNA-Binding Proteins) Amyotrophic lateral sclerosis 1




 0 (Tuberous Sclerosis Complex 1 Protein) 0 (Tuberous Sclerosis Complex 2 Protein) 0 (Tumor Suppressor Proteins) 0 (TSC1 protein, human) 0 (TSC2 protein, human)
 0 (Tumor Suppressor Proteins) 0 (Tuberous Sclerosis Complex 1 Protein) 0 (Tuberous Sclerosis Complex 2 Protein) 0 (RHEB protein, human) 0 (Ras Homolog Enriched in Brain Protein)

 0 (Autoantibodies) 9014-25-9 (RNA, Transfer) Antisynthetase syndrome



 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein)

 0 (Oxysterols)
 4F4X42SYQ6 (Rituximab) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (Autoantibodies) 0 (Immunoglobulin G)
 0 (Muscarinic Antagonists)

 J1K406072N (cannabigerol) 0 (Cannabinoids)





 0 (Spin Labels) 1406-16-2 (Vitamin D)
 0 (Immunotoxins) 0 (Diphtheria Toxin)


 0 (Myelin Basic Protein) 0 (Unilamellar Liposomes) 0 (Lipids) 97C5T2UQ7J (Cholesterol)

 9HW64Q8G6G (Everolimus)

 0 (Codon, Nonsense) 0 (Tumor Suppressor Proteins) 0 (Tuberous Sclerosis Complex 2 Protein) 0 (Tuberous Sclerosis Complex 1 Protein) Tuberous Sclerosis 2
 9HW64Q8G6G (Everolimus) W36ZG6FT64 (Sirolimus) EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)

 0 (68Ga-FAPI)
 0 (Tumor Suppressor Proteins) 0 (Tuberous Sclerosis Complex 2 Protein) 0 (Tuberous Sclerosis Complex 1 Protein)




 0 (COVID-19 Vaccines) 0 (Immunomodulating Agents) 0 (Immunosuppressive Agents)





 0 (Inflammasomes) EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (Nlrp3 protein, mouse) 0 (Gsdmd protein, mouse) EC 2.7.11.1 (Irak1 protein, mouse)
 0 (Glucocorticoids) VB0R961HZT (Prednisone)
 19GBJ60SN5 (Cannabidiol) 0 (PPAR gamma) 0 (Neuroprotective Agents)
 0 (Propionates) 0 (Histones) 0 (Receptors, G-Protein-Coupled) BBX060AN9V (Hydrogen Peroxide)


 0 (Neuromuscular Agents) EC 3.4.24.69 (Botulinum Toxins, Type A)
 9042-14-2 (Dextran Sulfate) EC 2.7.10.2 (Janus Kinases) 0 (STAT Transcription Factors) 0 (Suppressor of Cytokine Signaling Proteins) 0 (Socs3 protein, mouse) 0 (Suppressor of Cytokine Signaling 3 Protein)
 G926EC510T (Fingolimod Hydrochloride) 9012-76-4 (Chitosan)
 EC 3.4.21.- (PCSK9 protein, human) EC 3.4.21.- (Proprotein Convertase 9) 0 (PCSK9 Inhibitors)
 0 (MTOR Inhibitors)



 0 (Tumor Necrosis Factor-alpha) RR6P8L282I (siponimod)





 FYS6T7F842 (Adalimumab) 0 (Antibodies, Monoclonal) 0 (Biological Products) 2ZM8CX04RZ (Insulin Glargine) P188ANX8CK (Trastuzumab) 9008-11-1 (Interferons)
 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (NLR Proteins)

 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)











 0 (DNA, Mitochondrial)
 0 (Tuberous Sclerosis Complex 2 Protein) 0 (Tuberous Sclerosis Complex 1 Protein)
 EC 3.1.2.- (Protein Deglycase DJ-1)

 EC 1.15.1.1 (Superoxide Dismutase-1) EC 1.15.1.1 (Superoxide Dismutase)

 9HW64Q8G6G (Everolimus)


 0 (HLA Antigens) 0 (Histocompatibility Antigens Class II) 0 (HLA-DRB1 Chains)

 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (Transcription Factors) 0 (Receptors, Retinoic Acid) 5688UTC01R (Tretinoin) 0 (Ligands)


 997-55-7 (N-acetylaspartate)



 9001-32-5 (Fibrinogen)
 0 (Aquaporin 4) 0 (Immunoglobulin G) 0 (Autoantibodies)
 0 (Tumor Necrosis Factor-alpha) EC 2.7.- (Protein Kinases) FO2303MNI2 (Dimethyl Fumarate) EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases) EC 2.7.11.1 (Ripk3 protein, mouse) EC 2.7.11.1 (Ripk1 protein, mouse) EC 2.7.- (MLKL protein, mouse)


 45IUB1PX8R (monomethyl fumarate) 0 (diroximel fumarate) 0 (Fumarates)
 J1DOI7UV76 (Phencyclidine) G926EC510T (Fingolimod Hydrochloride) 0 (Brain-Derived Neurotrophic Factor) 0 (Cytokines)

 0 (Aquaporin 4) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Immunoglobulin G)

 77238-31-4 (Interferon-beta) 0 (Transforming Growth Factor beta)
 BZ114NVM5P (Mitoxantrone) 0 (Antineoplastic Agents) 9035-51-2 (Cytochrome P-450 Enzyme System)




 0 (C9orf72 Protein) 0 (C9orf72 protein, human)


 147604-77-1 (tenascin R) 0 (Autoantibodies)
 Primary angiitis of the central nervous system




 0 (RNA-Binding Proteins) 0 (RNA-Binding Protein FUS) 0 (FXR1 protein, human) 0 (FMR1 protein, human) 139135-51-6 (Fragile X Mental Retardation Protein)
 789U1901C5 (Copper) 42Z2K6ZL8P (Manganese)

 0 (Janus Kinase Inhibitors) EC 2.7.10.2 (Janus Kinases)
 9HW64Q8G6G (Everolimus) HU9DX48N0T (Mycophenolic Acid) WM0HAQ4WNM (Tacrolimus) EC 2.7.11.1 (TOR Serine-Threonine Kinases)





 19GBJ60SN5 (Cannabidiol) 0 (Cannabinoid Receptor Agonists) 0 (Hallucinogens)




 0 (Tuberous Sclerosis Complex 1 Protein) EC 2.7.11.1 (TOR Serine-Threonine Kinases)
 0 (Antibodies, Monoclonal) 0 (Cytokines) 0 (Interleukin Receptor Common gamma Subunit)





 Amyotrophic lateral sclerosis 1


 0 (HLA Antigens)
 19GBJ60SN5 (Cannabidiol) 9HW64Q8G6G (Everolimus) W36ZG6FT64 (Sirolimus)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies) 0 (Immunoglobulin G)


 0 (Autoantibodies)

 0 (Antibodies, Antineutrophil Cytoplasmic)





 0 (MicroRNAs) 0 (Neural Cell Adhesion Molecule L1)

 4F4X42SYQ6 (Rituximab)

 0 (Antineoplastic Agents) 9HW64Q8G6G (Everolimus) 51110-01-1 (Somatostatin)

 W36ZG6FT64 (Sirolimus) 0 (MTOR Inhibitors) 0 (Ointments) 0 (Immunosuppressive Agents) EC 2.7.1.1 (MTOR protein, human) EC 2.7.11.1 (TOR Serine-Threonine Kinases)

 0 (Autoantibodies) 0 (Aquaporins) 0 (Aquaporin 4)
 0 (Interleukin 1 Receptor Antagonist Protein) 0 (Interleukin-1)
 0 (Inflammasomes) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) SX6K58TVWC (Glyburide) FO2303MNI2 (Dimethyl Fumarate) 0 (NF-E2-Related Factor 2) 0 (Antioxidants)

 0 (Glucagon-Like Peptide-1 Receptor) O3FX965V0I (Acetazolamide) 89750-14-1 (Glucagon-Like Peptide 1)
 0 (wuzi yanzong) EC 3.1.- (Endoribonucleases) 0 (Endoplasmic Reticulum Chaperone BiP) EC 3.4.22.- (Caspase 12) EC 2.7.11.1 (Protein Serine-Threonine Kinases) 0 (Neuroprotective Agents)
 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (lysophosphatidylethanolamine) 0 (Lipids)

 4F4X42SYQ6 (Rituximab)

 516-35-8 (Taurochenodeoxycholic Acid) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) 0 (Lipopolysaccharides) EC 1.14.99.1 (Cyclooxygenase 2) 0 (NF-kappa B) 0 (RNA, Messenger) 0 (Gpbar1 protein, mouse) 0 (Receptors, G-Protein-Coupled)


 RR6P8L282I (siponimod)


 0 (Biomarkers)




















 9002-62-4 (Prolactin) 0 (RNA, Viral) 0 (Anti-Inflammatory Agents)




 0 (Intracellular Signaling Peptides and Proteins) GMW67QNF9C (Leucine)

 0 (Immunologic Factors) 0 (Adrenal Cortex Hormones)
 6804DJ8Z9U (Capecitabine) YF1K15M17Y (Temozolomide)





 0 (DNA-Binding Proteins) 0 (Cyclins) 0 (TDP-43 protein, mouse)
 0 (HLA Antigens) 0 (Histocompatibility Antigens Class II) 0 (Irf5 protein, mouse) 0 (Interferon Regulatory Factors)



 0 (Angiotensin-Converting Enzyme Inhibitors)



 0 (Autoantibodies)

 EC 1.15.1.1 (Superoxide Dismutase-1) 0 (Protein Aggregates) 0 (C9orf72 Protein) 0 (DNA-Binding Proteins) Amyotrophic lateral sclerosis 1

 0 (C9orf72 Protein) 0 (DNA-Binding Proteins)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)







 0 (Immunosuppressive Agents) 8N3DW7272P (Cyclophosphamide)
 EC 1.15.1.1 (Superoxide Dismutase-1) S798V6YJRP (Edaravone) EC 1.15.1.1 (Superoxide Dismutase)



 0 (Antigen-Antibody Complex) 0 (Antigens)




 0 (Biomarkers)

 G926EC510T (Fingolimod Hydrochloride) 0 (NF-kappa B) EC 2.7.- (Protein Kinases) KVI301NA53 (Pyridostigmine Bromide)

 0 (Tumor Necrosis Factor Inhibitors) OP401G7OJC (Etanercept) 0 (Antibodies, Monoclonal)











 S79426A41Z (Fluphenazine) 0 (Antipsychotic Agents)







 EC 1.15.1.1 (Superoxide Dismutase-1) EC 1.15.1.1 (Superoxide Dismutase)
 EC 1.15.1.1 (Superoxide Dismutase-1) 11062-77-4 (Superoxides) EC 1.15.1.1 (Superoxide Dismutase)

 0 (RNA, Messenger) Amyotrophic lateral sclerosis 1




 0 (DNA-Binding Proteins) 0 (TDP-43 protein, mouse) EC 2.7.1.- (NLK protein, human) EC 2.7.11.1 (Nlk protein, mouse) Amyotrophic lateral sclerosis 1


 0 (Air Pollutants) 0 (Particulate Matter)



 0 (Immunosuppressive Agents) 0 (Biomarkers)





 0 (Apolipoprotein E4) 0 (Amyloid beta-Peptides) 0 (Apolipoprotein E2) 0 (Apolipoproteins E)


 0 (RNA-Binding Protein FUS) EC 2.7.1.- (Phosphatidylinositol 3-Kinases)

 63231-63-0 (RNA)

 63231-63-0 (RNA)
 A288AR3C9H (25-hydroxyvitamin D) 0 (Vitamin D-Binding Protein) 1406-16-2 (Vitamin D) P6YZ13C99Q (Calcifediol) 0 (Vitamins) 0 (GSDMA protein, human) 0 (Pore Forming Cytotoxic Proteins)
 0 (Interleukin-17) 0 (Interleukin-23) 0 (IL17A protein, human) 0 (IL17F protein, human)




 0 (Autoantibodies)

 EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
 0 (beta Catenin) 0 (MicroRNAs) 0 (RNA, Long Noncoding) 0 (ZEB1 protein, human) 0 (Zinc Finger E-box-Binding Homeobox 1)
 0 (DNA-Binding Proteins) 0 (TDP-43 protein, mouse)








 156621-71-5 (osteoblast cadherin) 0 (Cadherins)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 0 (Mitochondrial Proteins) 0 (CHCHD10 protein, human)



 343-65-7 (Kynurenine) 8DUH1N11BX (Tryptophan) 0 (Autoantibodies) 0 (Aquaporin 4) 0 (Immunoglobulin G) G2X3B3O37U (3-aminobenzoic acid)




 0 (DNA-Binding Proteins)
 0 (beta Catenin) 0 (Ligands) 9007-49-2 (DNA) 0 (RNA, Messenger)
 0 (DNA-Binding Proteins) 0 (TARDBP protein, human)



 0 (Proteins) 63231-63-0 (RNA) 0 (Nucleotides)



 0 (Chloride Channels) 0 (Mitochondrial Proteins) 0 (Clcc1 protein, mouse)
 0 (DNA, Mitochondrial)

 0 (Interleukin-6)


 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Aquaporin 4) 0 (COVID-19 Vaccines) 0 (BNT162 Vaccine)
 0 (Transforming Growth Factor beta1) EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type I)
 0 (Amphiregulin)




 0 (TCIRG1 protein, human) EC 3.6.1.- (Vacuolar Proton-Translocating ATPases) 0 (SLC29A3 protein, human) 0 (Nucleoside Transport Proteins) Dysosteosclerosis

 0 (C9orf72 Protein) 0 (C9orf72 protein, human) 0 (Dipeptides) EC 3.6.4.- (DNA Helicases) EC 3.6.4.12 (G3BP1 protein, human) 0 (Histones) EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases) 0 (Poly-ADP-Ribose Binding Proteins) EC 3.6.4.13 (RNA Helicases) 0 (RNA Recognition Motif Proteins)
 0 (MicroRNAs) 0 (RNA-Binding Proteins)



 62031-54-3 (Fibroblast Growth Factors)



 0 (Prealbumin) 0 (Biomarkers) 0 (Neurofilament Proteins) Amyloidosis, Hereditary, Transthyretin-Related

 0 (Insulins)

 0 (Receptor, Notch3) 0 (Receptors, Notch) 0 (NOTCH3 protein, human)
 N9YNS0M02X (Acetylcholine) 207ZZ9QZ49 (Methylphenidate) 6M3C89ZY6R (Nicotine) X4W3ENH1CV (Norepinephrine) 947S0YZ36I (Reboxetine)
 563KS2PQY5 (Lacosamide)

 0 (Interleukin-18) 0 (Ribosomal Proteins)

 0 (Antioxidants) EC 2.7.1.- (Phosphatidylinositol 3-Kinases) 0 (Phenols) 0 (Polyphenols) 0 (Free Radicals) 0 (Anti-Inflammatory Agents)





 0 (Amyloidogenic Proteins)


 0 (Cyanobacteria Toxins) 0 (Amino Acids, Diamino) 0 (Amino Acids)
 4F4X42SYQ6 (Rituximab) 0 (Biosimilar Pharmaceuticals) 0 (Antibodies, Monoclonal, Murine-Derived) 0 (Immunosuppressive Agents) 0 (Antineoplastic Agents)


 Familial cylindromatosis

 0 (Intrinsically Disordered Proteins) 059QF0KO0R (Water) 0 (FUS protein, human) 0 (RNA-Binding Protein FUS)







 290YE8AR51 (Trichloroethylene) 0 (Solvents)

 0 (Interleukin-8) 0 (Pulmonary Surfactant-Associated Protein D) 0 (Biomarkers)
 0 (NF-kappa B) Q0CH43PGXS (fasudil) 0 (Toll-Like Receptor 4) 0 (Nerve Growth Factors)



 0 (Immunoglobulin G) 0 (Autoantibodies) 0 (Myelin-Oligodendrocyte Glycoprotein)

 0 (hydronidone) 5968Y6H45M (entecavir) 0 (Pyridones)

 9007-34-5 (Collagen) 0 (Microtubule Proteins) 0 (SPAG17 protein, mouse) 0 (SPAG17 protein, human)
 EC 2.7.11.1 (TOR Serine-Threonine Kinases) 0 (TSC2 protein, human) 0 (Tsc2 protein, mouse) EC 2.7.1.1 (MTOR protein, human) EC 2.7.1.1 (mTOR protein, mouse) Tuberous Sclerosis 2

 0 (Immunoglobulins, Intravenous)


 MQE6XG29YI (rosmarinic acid) 0 (Cinnamates) 0 (Neuroprotective Agents)


 11056-06-7 (Bleomycin) 80168379AG (Doxorubicin) 5V9KLZ54CY (Vinblastine)

 0 (Cytokines)

 0 (Biomarkers)



 1MTK0BPN8V (sotrovimab) 0 (Antibodies, Neutralizing) SARS-CoV-2 variants


 0 (C9orf72 Protein) 63231-63-0 (RNA) 0 (Dipeptides) 0 (ZNF598 protein, human) 0 (Carrier Proteins)
 0 (Anti-Bacterial Agents) 0 (Biomarkers)


 EC 3.6.1.- (GTP Phosphohydrolases) 0 (Mitochondrial Proteins)
 0 (spike protein, SARS-CoV-2) 0 (Spike Glycoprotein, Coronavirus)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1) EC 2.7.11.26 (Glycogen Synthase Kinase 3) EC 2.7.11.1 (TOR Serine-Threonine Kinases) EC 3.1.3.16 (Protein Phosphatase 1)
 0 (CD19 molecule, human) 0 (Receptors, Complement 3d)


 0 (Biomarkers) 0 (Neurofilament Proteins)


 UX6OWY2V7J (Codeine) CD35PMG570 (Oxycodone) 0 (Analgesics, Opioid)
 I5Y540LHVR (Cocaine)



 0RH81L854J (Glutamine) 3KX376GY7L (Glutamic Acid) 0 (Neurotransmitter Agents) 56-12-2 (gamma-Aminobutyric Acid)










 0 (Aquaporin 4) 0 (Antibodies, Antinuclear) 0 (Immunoglobulin G) 0 (Autoantibodies)
 0 (Apolipoprotein E4) 0 (Autoantibodies) 0 (Immunoglobulin Isotypes) 0 (Immunoglobulin M) 0 (Membrane Proteins) 0 (Nerve Tissue Proteins) 0 (TENM3 protein, human)

 SARS-CoV-2 variants
 0 (Excipients)

 EC 1.14.14.1 (Cytochrome P-450 CYP3A) 0 (Tryptamines) CJ0O37KU29 (Verapamil) EC 1.14.14.55 (CYP3A4 protein, human)
 0 (Procollagen Type I)
 0 (Immune Checkpoint Inhibitors) 0 (Autoantibodies)
 0 (Interleukin-6) 0 (Cytokines) 0 (Biomarkers) 0 (Receptors, IgG)
 0 (sRAGE protein, human) 0 (Receptor for Advanced Glycation End Products) 0 (HMGB1 protein, human) 0 (HMGB1 Protein)









 0 (RNA, Ribosomal, 16S)
 P1QW714R7M (Imiquimod) 0 (Receptors, Antigen, T-Cell) 0 (CCR4 protein, human) 0 (Receptors, CCR4)


 C3VX249T6L (ravulizumab) 0 (Aquaporin 4) 0 (Complement Inactivating Agents)


 0 (Neurofilament Proteins) 0 (Biomarkers)

 0 (laminin 1) 0 (Extracellular Matrix Proteins) 0 (Receptors, Antigen, T-Cell) 9007-34-5 (Collagen)


 0 (Antibodies, Antineutrophil Cytoplasmic)
 19GBJ60SN5 (Cannabidiol) 0 (Anticonvulsants) 0 (Cannabinoids)
 0 (C9orf72 Protein) EC 2.7.11.1 (TOR Serine-Threonine Kinases) 0 (RNA, Messenger) W36ZG6FT64 (Sirolimus) 0 (STAU1 protein, human) 0 (Cytoskeletal Proteins) 0 (RNA-Binding Proteins)
 EC 2.7.1.- (Phosphatidylinositol 3-Kinases) EC 2.3.1.- (Acetyltransferases) EC 2.3.1.88 (NAT10 protein, human) EC 2.3.1.88 (N-Terminal Acetyltransferases)
 0 (Amyloid beta-Peptides) 0 (Glycation End Products, Advanced) 0 (Receptor for Advanced Glycation End Products) 0 (AGER protein, human)
 0 (Membrane Proteins)

 0 (Immunoglobulins, Intravenous) 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)

 0 (dectin 1) 0 (Lectins, C-Type) 0 (Receptors, Antigen, T-Cell, gamma-delta)

 0 (CXCR5 protein, human) 0 (Programmed Cell Death 1 Receptor) 0 (Receptors, CXCR5)
 0 (Amyloid beta-Peptides) JP2EN8WORU (nitarsone) 0 (Creb1 protein, mouse)


 0 (Glucosides) 0 (Interferon Type I) 0 (Cytokines) 11056-06-7 (Bleomycin)
 0 (Lipopolysaccharides) 0 (NF-kappa B) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (Nlrp3 protein, mouse) O3Y80ZF13F (Thymopentin)

 0 (Biomarkers)




 0 (Receptors, N-Methyl-D-Aspartate) 3KX376GY7L (Glutamic Acid)
 0 (C9orf72 Protein) 0 (DNA Transposable Elements) 0 (C9orf72 protein, human)
 0 (Transcription Factors)
 0 (Biomarkers)


 0 (Biomarkers)

 6867Q6IKOD (florbetapir) 0 (Amyloid beta-Peptides) 0 (Amyloid)


 0 (Biomarkers)

 FYY3R43WGO (Minocycline) 0 (Anti-Inflammatory Agents)
 0 (Brain-Derived Neurotrophic Factor) EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) EC 2.7.1.- (Phosphatidylinositol 3-Kinases) 0 (Lipopolysaccharides) EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases) EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)

 0 (Plasminogen Activator Inhibitor 1) 0 (Thrombomodulin) 9013-56-3 (Factor XIII) 0 (Antithrombins) Thrombophilia, hereditary
 0 (Biomarkers)

 0 (Aquaporin 4) 0 (Autoantibodies)

 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)
 0 (Huntingtin Protein)
 73B0K5S26A (belimumab) 38RL9AE51Q (anifrolumab) 0 (Antibodies, Monoclonal, Humanized)

 0 (Glucocorticoids)
 0 (Antibodies) 0 (Epitopes) 0 (RGS8 protein, human) 0 (RGS Proteins)
 0 (Myelin-Oligodendrocyte Glycoprotein) 0 (Autoantibodies)
 EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) 0 (wuzi yanzong) EC 2.7.1.- (Phosphatidylinositol 3-Kinases) EC 2.7.1.137 (Phosphatidylinositol 3-Kinase) 0 (Antioxidants) 5688UTC01R (Tretinoin)
 0 (Immunosuppressive Agents)

 0 (Immune Checkpoint Inhibitors)



 0 (Autoantibodies) 0 (Receptors, G-Protein-Coupled)
 0 (MicroRNAs) 0 (Biomarkers) 0 (DNA, Viral)


 0 (Amyloid beta-Peptides)
 0 (Endothelin-1) 0 (Biomarkers)

 SARS-CoV-2 variants



 Hashimoto's encephalitis

 0 (DNA, Mitochondrial)



 0 (DMPK protein, human) EC 2.7.11.1 (Myotonin-Protein Kinase) 0 (Oligonucleotides, Antisense) 63231-63-0 (RNA) 0 (RNA, Messenger)
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 ClinicalTrials.gov/NCT01412333 ClinicalTrials.gov/NCT01247324








 ANZCTR/ACTRN12605000455662

































 ClinicalTrials.gov/NCT04413032


































































 ClinicalTrials.gov/NCT03157830







 ClinicalTrials.gov/NCT04377555



 ClinicalTrials.gov/NCT03073603

























 ClinicalTrials.gov/NCT02425644 ClinicalTrials.gov/NCT02634307













 ClinicalTrials.gov/NCT04843813


 ClinicalTrials.gov/NCT03222973





















 ClinicalTrials.gov/NCT05110586







 ClinicalTrials.gov/NCT03490240











 ClinicalTrials.gov/NCT03512886















































 ClinicalTrials.gov/NCT00211887



















 ClinicalTrials.gov/NCT05057676































 ClinicalTrials.gov/NCT01064401














 ClinicalTrials.gov/NCT00355134
 ClinicalTrials.gov/NCT03718247

































 ClinicalTrials.gov/NCT04979546































 ClinicalTrials.gov/NCT05367947









 ClinicalTrials.gov/NCT04655222








 ClinicalTrials.gov/NCT02913157







 ClinicalTrials.gov/NCT02425644

















 ClinicalTrials.gov/NCT01416181 ClinicalTrials.gov/NCT00906399 ClinicalTrials.gov/NCT01064401 ClinicalTrials.gov/NCT01247324 ClinicalTrials.gov/NCT01412333 ClinicalTrials.gov/NCT01194570
















 ClinicalTrials.gov/NCT03826095








 ClinicalTrials.gov/NCT02959658


 ClinicalTrials.gov/NCT02424396



 ClinicalTrials.gov/NCT02739542









































 ClinicalTrials.gov/NCT04380220
















































 ClinicalTrials.gov/NCT03268239

























































 IRCT/IRCT20210808052109N1





























 ANZCTR/ACTRN12605000455662 ClinicalTrials.gov/NCT02889965





 ClinicalTrials.gov/NCT02201108
















































































 ClinicalTrials.gov/NCT03387670



 ClinicalTrials.gov/NCT03233230 ClinicalTrials.gov/NCT02975336












































 ClinicalTrials.gov/NCT03490240






















 ClinicalTrials.gov/NCT03949296
























































 ClinicalTrials.gov/NCT04539002




















 ClinicalTrials.gov/NCT02427997


















































 ClinicalTrials.gov/NCT05403463





























 ClinicalTrials.gov/NCT05229861





































 ClinicalTrials.gov/NCT04929145








 EudraCT/2016-002020-86 ClinicalTrials.gov/NCT03269071
























 ClinicalTrials.gov/NCT04413032











 ClinicalTrials.gov/NCT00050778 ClinicalTrials.gov/NCT00530348 ClinicalTrials.gov/NCT00548405





















































































































 ClinicalTrials.gov/NCT03233230 ClinicalTrials.gov/NCT02975349 ClinicalTrials.gov/NCT02975336




























 ClinicalTrials.gov/NCT04762017



































 GEO/GSE213739 GEO/GSE113973





 ClinicalTrials.gov/NCT03322761


















































































 ClinicalTrials.gov/NCT03039400

















































 ClinicalTrials.gov/NCT05019248





 ClinicalTrials.gov/NCT01247324 ClinicalTrials.gov/NCT01412333 ClinicalTrials.gov/NCT01194570


 IRCT/IRCT20171106037286N2































 ClinicalTrials.gov/NCT04171908































 ClinicalTrials.gov/NCT04633759 ClinicalTrials.gov/NCT04548154
















 ClinicalTrials.gov/NCT01962571














 ClinicalTrials.gov/NCT03364036

























































 GEO/GSE145773
 ClinicalTrials.gov/NCT03919058
























 ClinicalTrials.gov/NCT02544373










 ClinicalTrials.gov/NCT04844489

























































































































 ClinicalTrials.gov/NCT01247324












 ClinicalTrials.gov/NCT04356248













































































































































 ClinicalTrials.gov/NCT00548405 ClinicalTrials.gov/NCT00530348 ClinicalTrials.gov/NCT00930553

















 figshare/10.6084/m9.figshare.c.6781091

























































































 ClinicalTrials.gov/NCT03319732






























































 ClinicalTrials.gov/NCT02386566














 ClinicalTrials.gov/NCT05558683


















































 ClinicalTrials.gov/NCT03961204
































 ClinicalTrials.gov/NCT04389970
















































































 ClinicalTrials.gov/NCT04217564









 ClinicalTrials.gov/NCT04838886























































 ClinicalTrials.gov/NCT01485003
 ClinicalTrials.gov/NCT04988880



































































 ClinicalTrials.gov/NCT01982942










































 ClinicalTrials.gov/NCT04585659




 ClinicalTrials.gov/NCT03560739



 ClinicalTrials.gov/NCT03650114




















 ClinicalTrials.gov/NCT01490502

































 ClinicalTrials.gov/NCT04673240






































































 ClinicalTrials.gov/NCT02975349













 ClinicalTrials.gov/NCT03161028


 ClinicalTrials.gov/NCT00835770 ClinicalTrials.gov/NCT00451451













 ClinicalTrials.gov/NCT01485003









 ClinicalTrials.gov/NCT02664623

















































 ClinicalTrials.gov/NCT02301260





















































 ClinicalTrials.gov/NCT03758820
































































 ClinicalTrials.gov/NCT03122652





























 ClinicalTrials.gov/NCT02623946

































 ClinicalTrials.gov/NCT05474209














































 ClinicalTrials.gov/NCT02047097































 ClinicalTrials.gov/NCT05060354














 ClinicalTrials.gov/NCT04115488





























































































































































































 ClinicalTrials.gov/NCT02576717












 ClinicalTrials.gov/NCT04580381
















































































 DRKS/DRKS00022998



















 ClinicalTrials.gov/NCT01681602
 ClinicalTrials.gov/NCT05462678



















 ClinicalTrials.gov/NCT05605951














 ClinicalTrials.gov/NCT03718247




















 ClinicalTrials.gov/NCT04331899























 ClinicalTrials.gov/NCT03244696











 ClinicalTrials.gov/NCT02200770














































































































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 Multiple sclerosis progression: time for a new mechanism-driven framework.
 Ageing and multiple sclerosis.
 Potential drug targets for multiple sclerosis identified through Mendelian randomization analysis.
 Updates and advances in multiple sclerosis neurotherapeutics.
 Chickenpox and multiple sclerosis: A Mendelian randomization study.
 Pediatric Multiple Sclerosis.
 Epstein-Barr virus as a cause of multiple sclerosis: opportunities for prevention and therapy.
 Family planning considerations in people with multiple sclerosis.
 Diagnosis and treatment of progressive multiple sclerosis: A position paper.
 Immunopathogenesis, Diagnosis, and Treatment of Multiple Sclerosis: A Clinical Update.
 Epstein-Barr virus as a leading cause of multiple sclerosis: mechanisms and implications.
 Present and future of the diagnostic work-up of multiple sclerosis: the imaging perspective.
 Multiple Sclerosis Pathogenesis and Updates in Targeted Therapeutic Approaches.
 Real-world evaluation of ocrelizumab in multiple sclerosis: A systematic review.
 Palliative care in multiple sclerosis.
 Multiple sclerosis and anxiety: Is there an untapped opportunity for exercise?
 Polypharmacy in Multiple Sclerosis: Prevalence, Risks, and Mitigation Strategies.
 Locus for severity implicates CNS resilience in progression of multiple sclerosis.
 [Multiple sclerosis treatments].
 Imaging cortical lesions in multiple sclerosis.
 Multiple sclerosis: role of meningeal lymphoid aggregates in progression independent of relapse activity.
 It's not multiple sclerosis, what is it?!
 Association of obesity with disease outcome in multiple sclerosis.
 Rituximab vs Ocrelizumab in Relapsing-Remitting Multiple Sclerosis.
 Autonomic nervous system disorders in multiple sclerosis.
 Sexual dysfunction therapeutic approaches in patients with multiple sclerosis: a systematic review.
 Migraine and multiple sclerosis: The final answer?
 The State of the Art of Pediatric Multiple Sclerosis.
 Antibiotic use and multiple sclerosis: A systematic review and meta-analysis.
 Measuring Pathology in Patients with Multiple Sclerosis Using Positron Emission Tomography.
 Assessing heterogeneity of treatment effect in multiple sclerosis trials.
 Treatment of autoimmunity: The impact of disease-modifying therapies in multiple sclerosis and comorbid autoimmune disorders.
 Melatonin and vitamin D, two sides of the same coin, better to land on its edge to improve multiple sclerosis.
 Paradigm shifts in multiple sclerosis management: Implications for daily clinical practice.
 Discontinuing disease-modifying multiple sclerosis therapies.
 Neuro-immune crosstalk in depressive symptoms of multiple sclerosis.
 Improving the efficiency of clinical trials in multiple sclerosis.
 Extracellular vesicles as contributors in the pathogenesis of multiple sclerosis.
 Could Mathematics be the Key to Unlocking the Mysteries of Multiple Sclerosis?
 Thalamic asymmetry in Multiple Sclerosis.
 Building a monitoring matrix for the management of multiple sclerosis.
 Pediatric multiple sclerosis: The 2022 ECTRIMS lecture.
 Towards a phenotypic understanding of multiple sclerosis depression.
 The Gut-Brain Axis as a Therapeutic Target in Multiple Sclerosis.
 Ocrelizumab in pediatric multiple sclerosis.
 Towards equitable access to treatment for multiple sclerosis.
 Cost, efficacy, and safety comparison between early intensive and escalating strategies for multiple sclerosis: A systematic review and meta-analysis.
 Boosting multiple sclerosis lesion segmentation through attention mechanism.
 Association between multiple sclerosis and cancer risk: An extensive review/meta and Mendelian randomization analyses.
 [Diagnostic work-up, findings, and documentation of multiple sclerosis].
 Prognostic uncertainty in multiple sclerosis: A concept analysis.
 Seizure risk in multiple sclerosis patients treated with disease-modifying therapy: A systematic review and network meta-analysis.
 Ublituximab (Briumvi) for relapsing multiple sclerosis.
 Management of Possible Multiple Sclerosis.
 Enhancing involvement of people with multiple sclerosis in clinical trial design.
 Concurrent diagnoses of Tuberous sclerosis and multiple sclerosis.
 Navigating the landscape of COVID-19 for Multiple Sclerosis patients and clinicians.
 An Update on the Measurement of Motor Cerebellar Dysfunction in Multiple Sclerosis.
 Radiologically Isolated Syndrome and the Multiple Sclerosis Prodrome in Pediatrics: Early Features of the Spectrum of Demyelination.
 Etiology, effects and management of comorbidities in multiple sclerosis: recent advances.
 It is time to define cognitive phenotypes in multiple sclerosis.
 Real-world operation of multiple sclerosis centres in Central-Eastern European countries covering 107 million inhabitants.
 Does assisted reproductive technology increase risk of multiple sclerosis?
 The role of iron metabolism in the pathogenesis and treatment of multiple sclerosis.
 [Gut microbiota in patients with relapsing-remitting multiple sclerosis].
 Prevalence of dysphagia in patients with multiple sclerosis: A systematic review and meta-analysis.
 The association between the Multiple Sclerosis Screening Questionnaire and objective measures of cognition: a systematic literature review and meta-analysis.
 Hepatotoxicity of Drugs Used in Multiple Sclerosis, Diagnostic Challenge, and the Role of HLA Genotype Susceptibility.
 A distinctive IgG-mediated pathogenesis for primary progressive multiple sclerosis?
 Quantitative Meta-analyses of Cognitive Abilities in Children With Pediatric-onset Multiple Sclerosis.
 Yoga and Multiple Sclerosis: Maintaining engagement in physical activity.
 Opportunities and challenges: mesenchymal stem cells in the treatment of multiple sclerosis.
 Smartphone monitoring of cognition in people with multiple sclerosis: A systematic review.
 Trigeminal neuralgia in multiple sclerosis: Association with demyelination and progression.
 Haematopoietic Stem Cell Transplantation for the Treatment of Multiple Sclerosis: Recent Advances.
 May Mediterranean diet contribute to reduce risk of multiple sclerosis?
 Time to Change the Current Clinical Classification of Multiple Sclerosis?
 Instruments measuring change in cognitive function in multiple sclerosis: A systematic review.
 Real world data on treatment of pediatric onset multiple sclerosis.
 Excess Treatment Costs of Multiple Sclerosis: What Can We Learn From Longitudinal Population-Based Data?
 Emerging role of extracellular vesicles in multiple sclerosis: From cellular surrogates to pathogenic mediators and beyond.
 Current advances in stem cell therapy in the treatment of multiple sclerosis.
 Commercial volumetric MRI reporting tools in multiple sclerosis: a systematic review of the evidence.
 An Updated Review of Epigenetic-Related Mechanisms and their Contribution to Multiple Sclerosis Disease.
 Tumefactive multiple sclerosis presents with painless progressive hemiparesis and aphasia.
 Apraxia of lid opening in multiple sclerosis.
 Cerebrospinal fluid immunoglobulins in primary progressive multiple sclerosis are pathogenic.
 Sleep counts! Role and impact of sleep in the multimodal management of multiple sclerosis.
 Recent Progress in the Identification of Early Transition Biomarkers from Relapsing-Remitting to Progressive Multiple Sclerosis.
 The benefits and risks of escalation versus early highly effective treatment in patients with multiple sclerosis.
 The manifestation of affective symptoms in multiple sclerosis and discussion of the currently available diagnostic assessment tools.
 Making Sure Multiple Sclerosis Counts and Is Counted for All-An Update on Multiple Sclerosis Prevalence by Race and Ethnicity in the United States.
 Advanced brain MRI may help understand the link between migraine and multiple sclerosis.
 Overlapping anti-NMDAR encephalitis and multiple sclerosis: A case report and literature review.
 Current advances in the pharmacological prevention and management of cognitive dysfunction in multiple sclerosis.
 Epidemiological study of multiple sclerosis in the Illawarra region.
 Impact of a specific consultation for patients with progressive forms of multiple sclerosis on the response to their unmet care needs: a cross-sectional study.
 Worldwide Disparity in the Effectiveness of the Diagnostic Process in Multiple Sclerosis.
 Role of DAMPs and cell death in autoimmune diseases: the example of multiple sclerosis.
 How to measure the treatment response in progressive multiple sclerosis: Current perspectives and limitations in clinical settings'.
 Clinical and Imaging Outcomes after Vitamin D Supplementation in Patients with Multiple Sclerosis: A Systematic Review.
 The global prevalence of sexual dysfunction in women with multiple sclerosis: a systematic review and meta-analysis.
 Challenges To Multiple Sclerosis Care In Pakistan.
 Characterization of a late-onset multiple sclerosis Portuguese cohort.
 To predict or not to predict: Multiple sclerosis and B-cell subset-specific genetic risk scores.
 Effect of Metabolic and Bariatric Surgery on the Clinical Course of Multiple Sclerosis in Patients with Severe Obesity: a Systematic Review.
 Potential Protective Role of Pregnancy and Breastfeeding in Delaying Onset Symptoms Related to Multiple Sclerosis.
 A systematic review and meta-analysis exploring the efficacy of mindfulness-based interventions on quality of life in people with multiple sclerosis.
 The economic impact of comorbidity in multiple sclerosis.
 Optical coherence tomography (OCT) measurements and cognitive performance in multiple sclerosis: a systematic review and meta-analysis.
 [Research status and prospect of remyelination in multiple sclerosis based on "inflammation-tissue" homeostatic coupling].
 Contemporary study of multiple sclerosis disability in South East Wales.
 Multiple sclerosis diagnostic delay and its associated factors in Upper Egyptian patients.
 Radiological Disease Activity in Secondary Progressive Multiple Sclerosis.
 Polygenicity of Comorbid Depression in Multiple Sclerosis.
 The challenge of pregnancy in women with multiple sclerosis.
 Prognostic significance of neurofilament light in Fingolimod therapy for Multiple Sclerosis: A systemic review and meta-analysis based on randomized control trials.
 Recurrent disability progression endpoints in multiple sclerosis clinical trials.
 Personality as a Predictor of Disability in Multiple Sclerosis.
 The effect of exercise on cognitive function in people with multiple sclerosis: a systematic review and meta-analysis of randomized controlled trials.
 Case Report: Multiple Sclerosis Presenting as Unilateral Gaze-evoked Nystagmus.
 Coexistence of multiple sclerosis and spinocerebellar ataxia type-8.
 Unmet needs and gaps in the identification of secondary progression in multiple sclerosis: a Southern Italy healthcare professionals' perspective.
 A true isolated cognitive relapse in multiple sclerosis.
 Effects of music therapy intervention on gait disorders in persons with multiple sclerosis: A systematic review of clinical trials.
 The evaluation of small fibers in multiple sclerosis.
 [Cognitive impairment in multiple sclerosis: when to think about it?].
 A neural stem-cell treatment for progressive multiple sclerosis.
 The prevalence of restless legs syndrome (RLS) in patients with multiple sclerosis (MS): a systematic review and meta-analysis-an update.
 Neuron-generating stem cells hold promise for multiple sclerosis.
 A letter to the editor concerning "Geochemistry of multiple sclerosis in Finland".
 Association between multiple sclerosis and epilepsy: A systematic review and meta-analysis.
 Vitamin D genetic risk scores in multiple sclerosis.
 Diagnosis of multiple sclerosis using optical coherence tomography supported by artificial intelligence.
 The Barancik lecture: Comorbidity in multiple sclerosis-Looking backward, looking forward.
 A novel eye-movement impairment in multiple sclerosis indicating widespread cortical damage.
 Rapid, non-contact multifocal visual assessment in multiple sclerosis.
 The importance of assessing sleep disorders in multiple sclerosis.
 A first step towards preventive medicine in multiple sclerosis.
 Use of Telemedicine Among People with Multiple Sclerosis Before and During the COVID-19 Pandemic.
 The relation of sarcopenia and disability in multiple sclerosis.
 Aging with multiple sclerosis: Clinical characterization of an elderly population, a cross-sectional study.
 Associations between multiple sclerosis and in-hospital outcomes of patients with hemorrhagic stroke.
 Late-onset multiple sclerosis in Iran: A report on demographic and disease characteristics.
 Alopecia associated with dimethyl fumarate treatment for multiple sclerosis.
 Predictors of severity and outcome of multiple sclerosis relapses.
 Optical Coherence Tomography, Retinal Atrophy, and Neurodegeneration in Progressive Multiple Sclerosis: Sprinting to the Finish.
 The Mismeasure of Change: Better Cognitive Measurement Instruments Are Urgently Needed for Multiple Sclerosis Research.
 In Silico Drug Repurposing in Multiple Sclerosis Using scRNA-Seq Data.
 Is Autologous Hematopoietic Stem Cell Transplant Better Than High-Efficacy Disease-Modifying Therapies for Relapsing Multiple Sclerosis?
 Current and future trends in multiple sclerosis management: Near East perspective.
 The role of multiple sclerosis therapies on the dynamic of human gut microbiota.
 Early spinal cord pseudoatrophy in interferon-beta-treated multiple sclerosis.
 Characteristics and management of multiple sclerosis patients during the Omicron era: is there a concern about the MS course in the face of the new variant of COVID-19?
 Targeted exercise for African-Americans with multiple sclerosis: Project TEAAMS.
 The interaction between metaplastic neuromodulation and fatigue in multiple sclerosis.
 Soft Palate Malignant Melanoma as an Adverse Effect of Fingolimod in Multiple Sclerosis: A Case Report and Literature Review.
 The National Multiple Sclerosis Registry System of Iran (NMSRI): aspects and methodological dimensions.
 Exploring the relation between reserve and fatigue in multiple sclerosis.
 Is may be Time to Update the Current Definitions of the Types of Multiple Sclerosis.
 Characteristics of the Manifestation of Multiple Sclerosis in Children in Lithuania.
 Episodic Facial Paresis-An Isolated Presenting Symptom of Multiple Sclerosis.
 Predictive models of multiple sclerosis-related cognitive performance using routine clinical practice predictors.
 Predictive factors of multiple sclerosis relapse after the first demyelinating event: A 5-year follow-up.
 Word finding, prosody and social cognition in multiple sclerosis.
 Primary Central Nervous System Vasculitis Following Alemtuzumab Treatment for Multiple Sclerosis: A Case Report and Literature Review.
 Prospective memory in multiple sclerosis: clinical utility of the Miami Prospective Memory Test.
 Letter to editors: - Multiple sclerosis and related disorders - Netravathi et al., 2022.
 New Contrast Enhancement Method for Multiple Sclerosis Lesion Detection.
 Beyond borders: Do geographic correlations suggest shared environmental factors in inflammatory bowel diseases, Hodgkin lymphoma, and multiple sclerosis.
 NAT8L mRNA oxidation is linked to neurodegeneration in multiple sclerosis.
 Multiple sclerosis optic neuritis and trans-synaptic pathology on cortical thinning in people with multiple sclerosis.
 Assessing cognitive changes in multiple sclerosis: criteria for a reliable decision.
 Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression.
 Early onset multiple sclerosis and the effect of disease onset age on neurological disability in multiple sclerosis.
 Relapsing-remitting and primary progressive multiple sclerosis treated with ocrelizumab: A comparative study.
 Time to Rebaseline Cognitive Performance in People with Multiple Sclerosis?
 Genetic Variant Tied to Disability in People With Multiple Sclerosis.
 Misconceptions about multiple sclerosis and pregnancy in the Qassim region in 2021-2022: a cross-sectional study.
 The borderland of multiple sclerosis and functional neurological disorder: A call for clinical research and vigilance.
 Fingolimod significantly reduces MRI activity in paediatric-onset multiple sclerosis (MS).
 BIANCA-MS: An optimized tool for automated multiple sclerosis lesion segmentation.
 Inverse association between Mediterranean diet and risk of multiple sclerosis.
 Cognitive trajectories in relapsing-remitting multiple sclerosis: Evidence of multiple evolutionary trends.
 Comparison of multiple sclerosis patients with or without rebound activity after fingolimod cessation: Five-year clinical outcomes.
 Metabolic syndrome parameters and multiple sclerosis disease outcomes: A Portuguese cross-sectional study.
 Epidemiology of multiple sclerosis in the Campania Region (Italy): Derivation and validation of an algorithm to calculate the 2015-2020 incidence.
 Editorial for "A Multicenter Longitudinal MRI Study Assessing LeMan-PV Software Accuracy in the Detection of White Matter Lesions in Multiple Sclerosis Patients".
 Health-related quality of life in Japanese patients with multiple sclerosis.
 Stroke Outcomes and Hyperacute Treatment Utilization in Multiple Sclerosis.
 Retinal Periphlebitis May Be a Marker for Subphenotype in Multiple Sclerosis.
 Natalizumab treatment of multiple sclerosis - a Danish nationwide study with 13 years of follow-up.
 Rituximab in the treatment of multiple sclerosis. Experience of a tertiary care hospital in Mexico.
 Clinical correlates of state and trait anxiety in multiple sclerosis.
 External validation of a clinical prediction model in multiple sclerosis.
 Altered functional connectivity during performance feedback processing in multiple sclerosis.
 Consensus for the Early Identification of Secondary Progressive Multiple Sclerosis in Portugal: a Delphi Panel.
 A systematic review of Mendelian randomization studies on multiple sclerosis.
 Enlarged choroid plexus related to cortical atrophy in multiple sclerosis.
 Views of Multiple Sclerosis Patients About Key Elements for a Decision Aid: A Qualitative Study.
 Responsiveness of Persian 12-Item multiple sclerosis walking scale: a replication study.
 Trans-Synaptic Degeneration Following Acute Optic Neuritis in Multiple Sclerosis.
 On a 5-year-old girl with multiple sclerosis treated with natalizumab.
 Extracting Phonetic Posterior-Based Features for Detecting Multiple Sclerosis From Speech.
 [Multidisciplinary support is essential for the management of multiple sclerosis].
 The Effect of Acupressure Applied to Patients With Multiple Sclerosis on Fatigue.
 Engagement in volunteering activities by persons with multiple sclerosis in Switzerland.
 Negative and positive personification of multiple sclerosis: Role in psychological adaptation.
 Pediatric onset primary progressive multiple sclerosis with predominant cognitive presentation: a longitudinal MRI and cognitive follow-up.
 Resting-state functional connectivity in multiple sclerosis patients receiving nabiximols for spasticity.
 Viral pericarditis following ocrelizumab in a multiple sclerosis patient.
 [Nicolau syndrome due to self-injectable drugs in multiple sclerosis].
 Non-late-onset neutropaenia following treatment of multiple sclerosis with ocrelizumab.
 Palliative Care for Patients With Multiple Sclerosis: Recommendations Emerging From a Case Study.
 Multiple Sclerosis Heritability Estimation on Sardinian Ascertained Extended Families Using Bayesian Liability Threshold Model.
 Atypical presentation of juvenile multiple sclerosis in a patient with COVID-19.
 Facial emotion impairment in multiple sclerosis is linked to modifying observation strategies of emotional faces.
 Improvement in time to multiple sclerosis diagnosis: 25-year retrospective analysis from New York State MS Consortium (NYSMSC).
 Comparing functional impact of multiple sclerosis on two populations in France, in the Caribbean Sea and in Europe, in regard of care level.
 Longitudinal assessment of cervical spinal cord compartments in multiple sclerosis.
 Cholesterol pathway biomarkers are associated with neuropsychological measures in multiple sclerosis.
 Dilated Virchow Robin spaces in multiple sclerosis - a generalised marker of disease?
 Percentage brain volume change in multiple sclerosis mainly reflects white matter and cortical volume.
 Complicated Monkeypox Infection in a Patient With Multiple Sclerosis and Fingolimod Treatment.
 Monoaminergic network abnormalities: a marker for multiple sclerosis-related fatigue and depression.
 Multimodal diagnostics in multiple sclerosis: predicting disability and conversion from relapsing-remitting to secondary progressive disease course - protocol for systematic review and meta-analysis.
 Prevalence and risk of developing sexual dysfunction in women with multiple sclerosis (MS): a systematic review and meta-analysis.
 Association between early treatment of multiple sclerosis and patient-reported outcomes: a nationwide observational cohort study.
 Discontinuation of first-line disease-modifying therapy in relapse onset multiple sclerosis.
 A decade of fingolimod in multiple sclerosis: Insights from a large real-world cohort study.
 Ocrelizumab-treated patients with relapsing multiple sclerosis show volume loss rates similar to healthy aging.
 Cholecalciferol Supplementation Induced Up-Regulation of SARAF Gene and Down-Regulated miR-155-5p Expression in Slovenian Patients with Multiple Sclerosis.
 Peripheral Vestibular System Involvement in Multiple Sclerosis and Associations with the Disease Severity.
 Trends in the Epidemiology and Treatment of Pediatric-Onset Multiple Sclerosis in Alberta, Canada.
 Brain volume loss in multiple sclerosis is independent of disease activity and might be prevented by early disease-modifying therapy.
 Global Barriers to the Diagnosis of Multiple Sclerosis: Data From the Multiple Sclerosis International Federation Atlas of MS, Third Edition.
 Spasticity treatment patterns among people with multiple sclerosis: a Swedish cohort study.
 Performance of McDonald 2017 multiple sclerosis diagnostic criteria and evaluation of genetic ancestry in patients with a first demyelinating event in Argentina.
 Ocrevus reduces TH40 cells, a biomarker of systemic inflammation, in relapsing multiple sclerosis (RMS) and in progressive multiple sclerosis (PMS).
 Variability of the response to immunotherapy among subgroups of patients with multiple sclerosis.
 Cerebrospinal fluid-related tissue damage in multiple sclerosis patients with iron rim lesions.
 A real-life study of alemtuzumab in persons with multiple sclerosis: Kuwait's experience.
 Reliable change indices for cognitive assessment of patients with multiple sclerosis.
 Incorporating the Central Vein Sign Into the Diagnostic Criteria for Multiple Sclerosis.
 Environmental Influences on Risk and Disease Course in Pediatric Multiple Sclerosis.
 An investigation of the effect of brain atrophy on brain injury in multiple sclerosis.
 ‶You look really good, I don't know why you came here″: persons with multiple sclerosis´ perspectives on social support.
 Decreased frequency of regulatory T cells and level of helios gene expression in secondary progressive multiple sclerosis patients: Evidence about the development of multiple sclerosis.
 Diagnostic and prognostic value of the RUNXOR/RUNX1 axis in multiple sclerosis.
 Quality of care provided by Multiple Sclerosis Centers during Covid-19 pandemic: Results of an Italian multicenter patient-centered survey.
 Supporting brain health in multiple sclerosis: exploring the potential of neuroeducation combined with practical mindfulness exercises in the management of neuropsychological symptoms.
 Neuroimmunological Disorders: The Gender Effect.
 Hyperreflective dots in the avascular outer retina in relapsing-remitting multiple sclerosis.
 The role of systemic ımmune ınflammatory ındex in showing active lesion ın patients with multiple sclerosis : SII and other inflamatuar biomarker in radiological active multiple sclerosis patients.
 The one-and-a-half syndrome: a distinctive clinical finding in a patient with multiple sclerosis.
 Narrative recall in relapsing-remitting multiple sclerosis: A potentially useful speech task for detecting subtle cognitive changes.
 Initial clinical and radiological features of patients with multiple sclerosis in Oman.
 Cognitive function in primary and secondary progressive multiple sclerosis: A multiparametric magnetic resonance imaging study.
 Sensitivity of conventional cognitive tests in multiple sclerosis: Application of item response theory.
 Dilatation of the bridging cerebral veins in multiple sclerosis correlates with fatigue and suggests an increase in pressure.
 Molecular signature associated with cladribine treatment in patients with multiple sclerosis.
 Understanding visual-spatial perceptual deficits in individuals with multiple sclerosis: an analysis of patient performance on the Hooper Visual Organization Test and Visual Form Discrimination.
 Using Redcap to Support the Development of a Learning Healthcare System for Patients with Multiple Sclerosis.
 User Needs of Young Czech Adults with Multiple Sclerosis in a Lifestyle App Design.
 Evaluation of neurotrophic factor secreting mesenchymal stem cells in progressive multiple sclerosis.
 L-Theanine Improves Locomotor Function in a Model of Multiple Sclerosis Mice.
 Assisted reproductive technology treatment and risk of multiple sclerosis - a Danish cohort study.
 Comparative effectiveness of natalizumab on cognition in multiple sclerosis: A cohort study.
 Do cardiovascular disease comorbidities affect the cognitive function of Multiple Sclerosis patients?
 Evaluation of antioxidant parameters of multiple sclerosis patients' serum according to the disease course.
 Effects of disease-modifying therapies on lipid parameters in patients with multiple sclerosis.
 Dilated Virchow-Robin spaces are a marker for arterial disease in multiple sclerosis.
 Prevalence of poor nutrition status in multiple sclerosis patients assessed by different diagnostic tools.
 Assessment of cognitive performance in multiple sclerosis using smartphone-based training games: a feasibility study.
 The influence of the COVID-19 pandemic on the prescription of multiple sclerosis medication in Germany.
 3d Virtual Histology Reveals Pathological Alterations of Cerebellar Granule Cells in Multiple Sclerosis.
 Protective effect of crocin on cuprizone-induced model of multiple sclerosis in mice.
 MRI lesions can often precede trigeminal neuralgia symptoms by years in multiple sclerosis.
 Psychotherapy and professional psychological support in multiple sclerosis: Uncovering patients' patterns of access and preferences.
 Dimethyl fumarate treatment of primary progressive multiple sclerosis: results of an open-label extension study.
 NUTRISEP: Assessment of the nutritional status of patients with multiple sclerosis and link to fatigue.
 Early depressive symptoms and disability accrual in Multiple Sclerosis: a UK MS Register study.
 Pregnancy planning and management for women with multiple sclerosis: what has changed over the last 15 years? An Italian single-center experience.
 Exploring physicians' prescribing behavior in patients with multiple sclerosis in Saudi Arabia: a sequential explanatory mixed-methods.
 T(1) /T(2) ratio from 3T MRI improves multiple sclerosis cortical lesion contrast.
 A new tool to investigate anorectal disorders in patients with multiple sclerosis: STAR-Q.
 Management of vascular risk in people with multiple sclerosis at the time of diagnosis in England: A population-based study.
 The adaptation model of immunity: A new insight into aetiology and treatment of multiple sclerosis.
 Formal help for persons with multiple sclerosis-Background factors associated with usage of personal assistance and home help in Sweden.
 Pontine capillary telangiectasia mimicking active demyelinating plaque in a patient with multiple sclerosis.
 Interferon beta treatment is a potent and targeted epigenetic modifier in multiple sclerosis.
 Synergy between health technology assessments and clinical guidelines for multiple sclerosis.
 Health economic outcomes of switching to alemtuzumab from other disease-modifying therapies in people with multiple sclerosis in the USA.
 Teaching Video NeuroImage: Dramatic Response to Topiramate in Acquired Pendular Nystagmus From Multiple Sclerosis.
 Alexithymia and Coping With Stress in Patients With Multiple Sclerosis: A Comparative Study.
 Longitudinal stability of progression-related microglial activity during teriflunomide treatment in patients with multiple sclerosis.
 Multicenter data harmonization for regional brain atrophy and application in multiple sclerosis.
 Alemtuzumab treatment exemplifies discordant immune effects of blood and cerebrospinal fluid in multiple sclerosis.
 Recommendations for the coordination of Neurology and Neuroradiology Departments in the management of patients with multiple sclerosis.
 Glatiramer acetate or IFN-β bridging therapy in women with relapsing multiple sclerosis planning a pregnancy.
 Safety and patient experience with at-home infusion of ocrelizumab for multiple sclerosis.
 Chitinase-3-like 1-protein in CSF: a novel biomarker for progression in patients with multiple sclerosis.
 Reduced alpha2 power is associated with slowed information processing speed in multiple sclerosis.
 Cerebrospinal fluid sulfatide isoforms lack diagnostic utility in separating progressive from relapsing-remitting multiple sclerosis.
 The Impact of SARS-CoV-2 Infection in Unvaccinated Multiple Sclerosis Patients on Disease-Modifying Therapies.
 Relationship of Motor Impairment with Cognitive and Emotional Alterations in Patients with Multiple Sclerosis.
 Investigating the potential link between lunar cycle and multiple sclerosis relapses: a call for further studies.
 Validation of an iPad version of the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS).
 Mixed B- and T-lymphocyte Vitreous Infiltrate in Multiple Sclerosis Associated Uveitis.
 Regional Analysis of Inner Retinal Layer Changes in Multiple Sclerosis with and without Optic Neuritis.
 Longitudinal associations between quality of diet and disability over 7.5 years in an international sample of people with multiple sclerosis.
 Medication adherence and health outcomes in persons with multiple sclerosis treated with dimethyl fumarate.
 First in vivo fluorine-19 magnetic resonance imaging of the multiple sclerosis drug siponimod.
 Discontinuation of second- versus first-line disease-modifying treatment in middle-aged patients with multiple sclerosis.
 MicroRNAs expression in peripheral blood mononuclear cells of patients with multiple sclerosis propose.
 Effectiveness of acupuncture for fatigue in patients with relapsing-remitting multiple sclerosis: a randomized controlled trial.
 Reliability of the five times sit to stand test performed remotely by multiple sclerosis patients.
 Exploring the effect of glatiramer acetate on cerebral gray matter atrophy in multiple sclerosis.
 Functional Disability and Brain MRI Volumetry Results among Multiple Sclerosis Patients during 5-Year Follow-Up.
 Influence of Cardiovascular Risk Factors in Early Relapsing-Remitting Multiple Sclerosis: A Retrospective Analysis.
 Lesion-Specific Metabolic Alterations in Relapsing-Remitting Multiple Sclerosis Via 7 T Magnetic Resonance Spectroscopic Imaging.
 The importance of the patient's perspective in decision-making in multiple sclerosis: Results of the OwnMS patient perspectives study.
 Modifiable risk factors of COVID-19 in patients with multiple sclerosis: a single-centre case-control study.
 Demographic and disease-related factors impact on cerebrospinal fluid neurofilament light chain levels in multiple sclerosis.
 ATR-FTIR spectroscopy of plasma supported by multivariate analysis discriminates multiple sclerosis disease.
 Real-world annualized relapse rates from contemporary multiple sclerosis clinics in the UK: a retrospective multicentre cohort study.
 Slowing processing speed is associated with cognitive fatigue in newly diagnosed multiple sclerosis patients.
 Teriflunomide Concentrations in Cerebrospinal Fluid and Plasma in Patients with Multiple Sclerosis: A Pharmacokinetic Study.
 Cortical lesions at diagnosis predict long-term cognitive impairment in multiple sclerosis: A 20-year study.
 Characterizing fatigue phenotypes with other symptoms and clinically relevant outcomes among people with multiple sclerosis.
 Assessment of cognitive function and its predictors in patients with multiple sclerosis: a case-control study.
 Assessment of differential item functioning of the PHQ-9, HADS-D and PROMIS-depression scales in persons with and without multiple sclerosis.
 Specific myeloid signatures in peripheral blood differentiate active and rare clinical phenotypes of multiple sclerosis.
 Demographic Features and Clinical Course of Patients With Pediatric-Onset Multiple Sclerosis on Newer Disease-Modifying Treatments.
 Spinal cord and brain corticospinal tract lesions are associated with motor progression in tumefactive multiple sclerosis.
 Considerations regarding noncredible performance in the neuropsychological assessment of patients with multiple sclerosis: A case series.
 "It's on the tip of my tongue!" exploring confrontation naming difficulties in patients with multiple sclerosis.
 Autologous hematopoietic stem cell transplantation of patients with aggressive relapsing-remitting multiple sclerosis: Danish nation-wide experience.
 Impact of depression on the perception of fatigue and information processing speed in a cohort of multiple sclerosis patients.
 Quantitative comparison of the efficacy of clinical drug treatments for primary progressive multiple sclerosis.
 Evaluating the efficacy and safety of transitioning patients with multiple sclerosis from natalizumab to ocrelizumab (OCTAVE).
 The effects of bupropion on sexual dysfunction in female patients with multiple sclerosis: A double-blind randomized clinical trial.
 [Multidisciplinary and multimodal rehabilitation care for patients suffering from multiple sclerosis].
 Psychometrically valid interpretation of cognitive assessments is a prerequisite for classification of cognitive phenotypes in multiple sclerosis.
 Real-world use of natalizumab in Austria: data from the Austrian Multiple Sclerosis Treatment Registry (AMSTR).
 Reliable brain morphometry from contrast-enhanced T1w-MRI in patients with multiple sclerosis.
 The insula modulates the effects of aerobic training on cardiovascular function and ambulation in multiple sclerosis.
 In-person and remote administrations of the symbol digit modalities test are interchangeable among persons with multiple sclerosis.
 Demographics and baseline disease characteristics of Black and Hispanic patients with multiple sclerosis in the open-label, single-arm, multicenter, phase IV CHIMES trial.
 Anterior horn atrophy in the cervical spinal cord: A new biomarker in progressive multiple sclerosis.
 Identification of Key Ferroptosis-Related Genes in the Peripheral Blood of Patients with Relapsing-Remitting Multiple Sclerosis and Its Diagnostic Value.
 Fatigue and its relation to general cognition, social cognition and social activity in multiple sclerosis and stroke.
 Risk of new disease activity in patients with multiple sclerosis who continue or discontinue disease-modifying therapies (DISCOMS): a multicentre, randomised, single-blind, phase 4, non-inferiority trial.
 Towards a more precise rating of neurological disability in multiple sclerosis: A new automatic and linear quantification of limbs function.
 Single-timepoint low-dimensional characterization and classification of acute versus chronic multiple sclerosis lesions using machine learning.
 Usefulness of masseter vestibular evoked myogenic potentials in identifying brainstem dysfunction among individuals with multiple sclerosis.
 Acquired stuttering as the sole manifestation of relapse in multiple sclerosis secondary to involvement of the left frontal aslant tract.
 Anti-Müllerian hormone and pregnancy after autologous hematopoietic stem cell transplantation for multiple sclerosis.
 Abnormal thalamic functional connectivity correlates with cardiorespiratory fitness and physical activity in progressive multiple sclerosis.
 Comparative efficacy and safety of ozanimod and ponesimod for relapsing multiple sclerosis: A matching-adjusted indirect comparison.
 Remote administration of BICAMS measures and the Trail-Making Test to assess cognitive impairment in multiple sclerosis.
 Structural and functional magnetic resonance imaging correlates of fatigue and dual-task performance in progressive multiple sclerosis.
 Immune checkpoint inhibitors: A potential bright spot in the treatment of progressive multifocal leukoencephalopathy in multiple sclerosis.
 Characterizing cannabis use in a sample of adults with multiple sclerosis and chronic pain: An observational study.
 Specific alterations in NKG2D(+) T lymphocytes in relapsing-remitting and progressive multiple sclerosis patients.
 Granzyme B + CD8 + T cells with terminal differentiated effector signature determine multiple sclerosis progression.
 Characteristics and consequences of falls among people with multiple sclerosis who use wheelchairs or scooters: Differences between injurious and non-injurious falls.
 Personalized maps of T1 relaxometry abnormalities provide correlates of disability in multiple sclerosis patients.
 [Knee range of motion as a marker of the effectiveness of medical intervention in multiple sclerosis].
 Physical activity as a correlate of symptoms, quality of life, comorbidity, and disability status in Hispanics with multiple sclerosis.
 Evaluation of the feasibility and acceptability of an integrative group psychological intervention for people with Multiple Sclerosis: A study protocol.
 Clinical and fringe benefits of rituximab in multiple sclerosis treatment in a poor resource setting: Case series and cost analysis.
 Subjective valuation of performance feedback is robust to trait cognitive fatigue in multiple sclerosis.
 The effect of self-acupressure on quality of life, physical and cognitive function in relapsing remitting multiple sclerosis patients: A randomized controlled study.
 Argentinean consensus recommendations for the use of telemedicine in clinical practice in adult people with multiple sclerosis.
 The impact of cognitive impairment on disease burden in Chinese patients with multiple sclerosis: A model simulation study.
 Cerebrospinal fluid neurofilament light chains and CXCL13 as predictive factors for clinical course of multiple sclerosis.
 Prolonged Interferon-Stimulated Gene and Protein Signatures in Multiple Sclerosis Induced by PEGylated IFN-β-1a Compared to Non-PEGylated IFN-β-1a.
 Matching-Adjusted Indirect Comparisons of Diroximel Fumarate, Ponesimod, and Teriflunomide for Relapsing Multiple Sclerosis.
 IFN-β Causing Focal Segmental Glomerulosclerosis in a Multiple Sclerosis Patient-A Case Report.
 Decrease of natalizumab drug levels after switching from intravenous to subcutaneous administration in patients with multiple sclerosis.
 Evaluation of CSF kappa free light chains for the diagnosis of multiple sclerosis (MS): a comparison with oligoclonal bands (OCB) detection via isoelectric focusing (IEF) coupled with immunoblotting.
 Healthcare utilization and satisfaction among enrolees in an online course about multiple sclerosis: A cross-sectional study.
 Assessment of Functional Capacity of Immune System in Patients with Multiple Sclerosis using QuantiFERON Monitor.
 Trail Making Test Could Predict Impairment in Cognitive Domains in Patients with Multiple Sclerosis: A Study of Diagnostic Accuracy.
 ADAMS project: a genetic Association study in individuals from Diverse Ancestral backgrounds with Multiple Sclerosis based in the UK.
 Evaluating the feasibility and preliminary efficacy of a Cognitive Occupation-Based programme for people with Multiple Sclerosis (COB-MS): an update to the protocol for a feasibility cluster-randomised controlled trial.
 Neuropathic pain, cognitive fusion, and alexithymia in patients with multiple sclerosis: Cross-sectional evidence for an explanatory model of anxiety symptoms.
 Medication adherence to disease-modifying therapies among a cohort of Jordanian patients with relapsing-remitting multiple sclerosis: a multicentre cross-sectional study.
 Mesenchymal stem cell-neural progenitors are enriched in cell signaling molecules implicated in their therapeutic effect in multiple sclerosis.
 Pearls & Oy-sters: CSF1R-Related Leukoencephalopathy With Spinal Cord Lesions Mimicking Multiple Sclerosis.
 Incidental demyelination in magnetic resonance imaging and 10-year risk of multiple sclerosis: A data lake cohort study.
 Randomized, Placebo-Controlled, Single-Blind Study of Lutein Supplementation on Carotenoid Status and Cognition in Persons with Multiple Sclerosis.
 Establishing clinically meaningful within-individual improvement thresholds for eight patient-reported outcome measures in people with relapsing-remitting multiple sclerosis.
 Genetically determined serum serine level has a novel causal effect on multiple sclerosis risk and predicts disability progression.
 Lesion-level correspondence and longitudinal properties of paramagnetic rim and slowly expanding lesions in multiple sclerosis.
 Automated Registration and Color Labeling of Serial 3D Double Inversion Recovery MR Imaging for Detection of Lesion Progression in Multiple Sclerosis.
 Commentary: Solomon AJ et al. Differential diagnosis of suspected multiple sclerosis: An updated consensus approach. Lancet Neurol 2023; 22(8): 750-768.
 Influence of physicians' risk perception on switching treatments between high- efficacy and non-high-efficacy disease‑modifying therapies in multiple sclerosis.
 Effect of the COVID-19 pandemic on disease activity in multiple sclerosis patients treated with hematopoietic stem cell transplantation.
 Primary central nervous system lymphoma in a patient with multiple sclerosis using fingolimod.
 Optimal sensor location and direction to accurately classify people with early-stage multiple sclerosis using gait stability.
 Serum neurofilament light chain is more strongly associated with T2 lesion volume than with number of T2 lesions in patients with multiple sclerosis.
 Oral health-related quality of life is more strongly correlated with mental health than with oral health in relapsing-remitting multiple sclerosis.
 Disease activity after discontinuation of disease-modifying therapies in patients with multiple sclerosis in Argentina: data from the nationwide registry RelevarEM.
 Training reactive balance using trips and slips in people with multiple sclerosis: A blinded randomised controlled trial.
 Switching from natalizumab administration at the day hospital to administration at home. A 1 year prospective study of patient experience and quality of life in 30 consecutive patients with multiple sclerosis (TYSAD-35).
 Effectiveness of ocrelizumab on clinical and MRI outcome measures in multiple sclerosis across black and white cohorts: A single-center retrospective study.
 Functional and structural brain MRI changes associated with cognitive worsening in multiple sclerosis: a 3-year longitudinal study.
 Exploring (peri-) lesional and structural connectivity tissue damage through T1/T2-weighted ratio in iron rim multiple sclerosis lesions.
 Use of follow-on fingolimod for multiple sclerosis: Analysis of effectiveness and patient reported outcomes in a real-world clinical setting.
 Rs205764 and rs547311 in linc00513 may influence treatment responses in multiple sclerosis patients: A pharmacogenomics Egyptian study.
 Communicating the relevance of neurodegeneration and brain atrophy to multiple sclerosis patients: patient, provider and researcher perspectives.
 Trajectories of disease-modifying therapies and associated sickness absence and disability pension among 1923 people with multiple sclerosis in Sweden.
 Disruption of specific white matter tracts is associated with neurogenic lower urinary tract dysfunction in women with multiple sclerosis.
 Association between age and inflammatory disease activity on magnetic resonance imaging in relapse onset multiple sclerosis during long-term follow-up.
 Lesion follows function: video-oculography compared with MRI to diagnose internuclear ophthalmoplegia in patients with multiple sclerosis.
 The effect of Transcutaneous Electrical Nerve Stimulation (TENS) and Interferential Currents (IFC) on pain, functional capacity, and quality of life in patients with multiple sclerosis: A randomized controlled, single-blinded study.
 Working memory dysfunction differs between secondary progressive and relapsing multiple sclerosis: Effects of clinical phenotype, age, disease duration, and disability.
 Turning and multitask gait unmask gait disturbance in mild-to-moderate multiple sclerosis: Underlying specific cortical thinning and connecting fibers damage.
 Quantitative susceptibility mapping of the normal-appearing white matter as a potential new marker of disability progression in multiple sclerosis.
 Latin American consensus recommendations on the risk of infections in people with multiple sclerosis treated with disease modifying drugs.
 Case Report: Recurrent Severe Uveitis Secondary to Primary Progressive Multiple Sclerosis Responsive to Ocrelizumab.
 Eight-and-a-half syndrome as the first presentation of multiple sclerosis in an Asian male: a case report.
 [Traumatic brain injury before the multiple sclerosis onset: a relationship with the progression of neurological disorders and pathobiochemical markers of the cerebrospinal fluid].
 Primary results of a phase-III, randomized controlled trial of the Behavioral Intervention for increasing Physical Activity in Multiple Sclerosis project.
 The independent contribution of brain, spinal cord and gadolinium MRI in treatment decision in multiple sclerosis: A population-based retrospective study.
 Assessing the utility of magnetic resonance imaging-based "SuStaIn" disease subtyping for precision medicine in relapsing-remitting and secondary progressive multiple sclerosis.
 Trans-synaptic degeneration in the optic pathway: Exploring the role of lateral geniculate nucleus in early stages of relapsing-remitting multiple sclerosis.
 The spatio-temporal relationship between concurrent lesion and brain atrophy changes in early multiple sclerosis: A post-hoc analysis of the REFLEXION study.
 The rate of force relaxation scaling factor is highly sensitive to detect upper and lower extremity motor deficiencies in mildly affected people with multiple sclerosis.
 Selective vulnerability of brainstem and cervical spinal cord regions in people with non-progressive multiple sclerosis of Black or African American and European ancestry.
 Distinct hemodynamic and functional connectivity features of fatigue in clinically isolated syndrome and multiple sclerosis: accounting for the confounding effect of concurrent depression symptoms.
 Improvements in one severe progressive multiple sclerosis patient quality of life after an intensity fluid dynamic treatment.
 Spinal cord lesions and brain grey matter atrophy independently predict clinical worsening in definite multiple sclerosis: a 5-year, multicentre study.
 Probable Encephalopathy and Spasticity in a Multiple Sclerosis Patient Following Carbapenem Administration: A Case Report and Brief Literature Review.
 ADC restriction is not associated with clinical response to plasma exchange following a cerebral attack of multiple sclerosis.
 Effects of multi-task training on motor and cognitive performances in multiple sclerosis patients without clinical disability: a single-blinded randomized controlled trial.
 Feasibility of remotely delivered and supported aerobic walking exercise training for cognitive processing speed impairment in fully-ambulatory persons with multiple sclerosis.
 Macular ganglion cell-inner plexiform layer defect patterns in multiple sclerosis patients without optic neuritis: A Spectral-Domain-Optical Coherence Tomography Cross-Sectional, Case-Control, Pilot Study.
 Magnetization transfer ratio for assessing remyelination after transcranial ultrasound stimulation in the lysolecithin rat model of multiple sclerosis.
 Blood neurofilament light levels predict non-relapsing progression following anti-CD20 therapy in relapsing and primary progressive multiple sclerosis: findings from the ocrelizumab randomised, double-blind phase 3 clinical trials.
 Longitudinal assessment of neurocognitive function in people with relapsing multiple sclerosis initiating alemtuzumab in routine clinical practice: LEM-COG study results.
 Effects of Ibudilast on Retinal Atrophy in Progressive Multiple Sclerosis Subtypes: Post Hoc Analyses of the SPRINT-MS Trial.
 Multi-arm U-Net with dense input and skip connectivity for T2 lesion segmentation in clinical trials of multiple sclerosis.
 Quantification and Proximal-to-Distal Distribution Pattern of Tibial Nerve Lesions in Relapsing-Remitting Multiple Sclerosis : Assessment by MR Neurography.
 Association of Arachidonic Acid-Derived Lipid Mediators With Disease Severity in Patients With Relapsing and Progressive Multiple Sclerosis.
 A Case of Psychosis in a Patient Concurrently Diagnosed With Multiple Sclerosis Treated Successfully With Corticosteroids.
 Network analysis characterizes key associations between subjective fatigue and specific depressive symptoms in early relapsing-remitting multiple sclerosis.
 Using quantitative magnetic resonance imaging to track cerebral alterations in multiple sclerosis brain: A longitudinal study.
 Influence of Residual Quadrupolar Interaction on Quantitative Sodium Brain Magnetic Resonance Imaging of Patients With Multiple Sclerosis.
 Repetitive transcranial magnetic stimulation for treatment of limb spasticity following multiple sclerosis: a systematic review and meta-analysis.
 Therapy effect on AI-derived thalamic atrophy using clinical routine MRI protocol: A longitudinal, multi-center, propensity-matched multiple sclerosis study.
 Association of Choroid Plexus Inflammation on MRI With Clinical Disability Progression Over 5 Years in Patients With Multiple Sclerosis.
 Evaluating the impact of early vs delayed ofatumumab initiation and estimating the long-term outcomes of ofatumumab vs teriflunomide in relapsing multiple sclerosis patients in Spain.
 Acetyl-DL-leucine in combination with memantine improves acquired pendular nystagmus caused by multiple sclerosis: a case report.
 Patient and nurse preference for Sensoready autoinjector pen versus other autoinjectors in multiple sclerosis: results from a pilot multicenter survey.
 Patient-reported outcome measurements in a selective cohort of relapsing-remitting multiple sclerosis patients: relationships with physical disability, cognitive impairment, and MRI-derived metrics.
 [The use of monoclonal antibodies in the treatment of patients with high-active multiple sclerosis in real clinical practice].
 Changes in serum cytokine profile and deficit severity in patients with relapsing-remitting multiple sclerosis.
 [A case of primary progressive multiple sclerosis with improvement in cognitive impairment by anti-CD20 monoclonal antibody therapy].
 Ocrelizumab in pediatric patients with MS: Efficacy, tolerability, and safety.
 Extended-interval dosing of natalizumab in NOVA.
 Serum NfL as an MS biomarker.
 Obstetric and Gynecologic Disorders and the Nervous System.
 Natalizumab extended-interval dosing in a real-life setting.
 Individual reserve in aging and neurological disease.
 Neuronal activity and NIBS in developmental myelination and remyelination - Current state of knowledge.
 Should trigeminal neuralgia be considered a clinically isolated syndrome?
 [Clinical factors and response to therapy with disease-modifying drugs for multiple sclerosis: the experience of the Tomsk region].
 Recurrent skin infections associated with natalizumab treatment.
 Repair what is lost: Neuroprotection through neural stem cells in progressive MS.
 Interferon-beta exposure in-utero and the risk of infections in early childhood.
 The uncertainty period preceding the clinical defined SPMS diagnosis and the applicability of objective classifiers - A Danish single center study.
 A bibliometric evaluation of the top 100 cited articles on ocrelizumab.
 Fatigability-related oscillatory brain activity changes in people with MS.
 Is breastfeeding in MS harmful or not? An answer from real-world Czech data.
 Androgens show sex-dependent differences in myelination in immune and non-immune murine models of CNS demyelination.
 CSF lymphocytic pleocytosis does not predict a less favourable long-term prognosis in MS.
 Patient reported outcomes in a secondary progressive MS cohort related to cognition, MRI and physical outcomes.
 Silent findings: Examination of asymptomatic demyelination in a pediatric US cohort.
 Analysis of determinants of treatment change in adult paediatric-onset MS patients.
 Natalizumab wearing-off symptoms: effect of extend interval dosing during Sars-CoV-2 pandemic.
 Extended-interval dosing of natalizumab in NOVA - Authors' reply.
 Choroid plexus volume is enlarged in clinically isolated syndrome patients with optic neuritis.
 The impact of relapse definition and measures of durability on MS clinical trial outcomes.
 Fatigue and health-related quality of life depend on the disability status and clinical course in RRMS.
 Leptomeningeal enhancement under different MS immunotherapies: A monocentric retrospective cohort study of 214 patients.
 Brief international cognitive assessment for MS (BICAMS) and global brain volumes in early stages of MS - A longitudinal correlation study.
 Stability of longitudinal DTI metrics in MS with treatment of injectables, fingolimod and dimethyl fumarate.
 Quality of life should be the primary outcome for disease-modifying therapy trials in MS-Yes.
 Relation between retina, cognition and brain volumes in MS: a consequence of asymptomatic optic nerve lesions.
 Presymptomatic MS or radiologically isolated syndrome should be actively monitored and treated: Yes.
 Quality of life should be the primary outcome for disease modifying therapy trials in MS-No.
 Intrathecal versus Peripheral Inflammatory Protein Profile in MS Patients at Diagnosis: A Comprehensive Investigation on Serum and CSF.
 Discontinuation of disease-modifying therapy in MS patients over 60 years old and its impact on relapse rate and disease progression.
 Are we ready to define cognitive worsening in MS? How different cutoffs detect future cognitive worsening after six years of follow-up.
 Death following rapidly progressive demyelinating disorder in a young female-a case report.
 Variation in processes and reporting of cerebrospinal fluid oligoclonal banding and associated tests and calculated indices across Canadian clinical laboratories.
 Quality of life should be the primary outcome for disease-modifying therapy trials in MS: Commentary.
 MS becomes a treatable disease: 30 years later.
 Prevalence and prognostic value of prodromal symptoms in relapsing-remitting multiple sclerosis.
 Threshold definitions for significant change on the timed 25-foot walk and nine-hole peg test in primary progressive multiple sclerosis.
 Identification of Key Genes and Regulatory Pathways in Multiple Sclerosis Brain Samples: A Meta-Analysis of Micro-Array Datasets.
 Automatic segmentation of the choroid plexuses: Method and validation in controls and patients with multiple sclerosis.
 Evaluation of a web-based program for the adoption of wellness behaviors to self-manage fatigue and improve quality of life among people with multiple sclerosis: A randomized waitlist-control trial.
 Alemtuzumab treatment in real clinical practice: Experience in a multicenter cohort.
 Macular edema after siponimod treatment for multiple sclerosis: a case report and literature review.
 Influence of image contrasts and reconstruction methods on the classification of multiple sclerosis-like lesions in simulated sodium magnetic resonance imaging.
 Index of cardiac-electrophysiological balance in relapsing-remitting multiple sclerosis patients treated with fingolimod.
 Does initial high efficacy therapy in multiple sclerosis surpass escalation treatment strategy? A comparison of patients with relapsing-remitting multiple sclerosis in the Czech and Swedish national multiple sclerosis registries.
 Neuromuscular rate of force development discriminates fallers in ambulatory persons with multiple sclerosis - an exploratory study.
 The association between white matter tract structural connectivity and information processing speed in relapsing-remitting multiple sclerosis.
 Differential diagnosis of suspected multiple sclerosis: an updated consensus approach.
 Severe autoimmune intravascular hemolytic anemia in patients receiving alemtuzumab for multiple sclerosis.
 [A clinical case of multiple sclerosis with an episode of schizophrenia-like syndrome].
 Optical coherence tomography as a prognostic tool for disability progression in MS: a systematic review.
 Validation of the Spanish version of DYsphagia in MUltiple Sclerosis questionnaire (DYMUS).
 D-dimer elevation after first alemtuzumab administration in a multiple sclerosis patient: case report.
 Effects of diet on MS onset and course.
 Obesity, gut microbiota, and multiple sclerosis: Unraveling the connection.
 Gut Microbiota Changes during Dimethyl Fumarate Treatment in Patients with Multiple Sclerosis.
 SARS-CoV-2 pandemic as a model to assess the relationship between intercurrent viral infections and disease activity in Multiple Sclerosis: A propensity score matched case-control study.
 The contribution of neurofilament light chain to better characterize pediatric multiple sclerosis (editorial on: Plasma neurofilament light chain in children with relapsing MS receiving teriflunomide or placebo: A post hoc analysis of the randomized TERIKIDS trial).
 Neuraxial Use Among Total Knee and Hip Arthroplasty Patients With Multiple Sclerosis or Myasthenia Gravis.
 Association of volumetric MRI measures and disability in MS patients of the same age: Descriptions from a birth year cohort.
 Safety and effectiveness of cladribine tablets for multiple sclerosis: Results from a single-center real-world cohort.
 miRNA Signature in CSF From Patients With Primary Progressive Multiple Sclerosis.
 Addressing me in the context of my disease: Why it is so complicated.
 Does multiple sclerosis have a zoonotic origin? Correlations with lymphocytic choriomeningitis virus infection.
 Simple parameters from complete blood count predict lymphopenia, adverse effects and efficacy in people with MS treated with dimethyl fumarate.
 Levamisole-associated multifocal inflammatory encephalopathy: clinical and MRI characteristics, and diagnostic algorithm.
 [A therapeutic education program for patients with multiple sclerosis].
 Normocomplementemic urticarial vasculitis in a patient with multiple sclerosis on glatiramer acetate.
 The first MS attack after methanol toxicity in a young man: a case report.
 Deciphering multiple sclerosis disability with deep learning attention maps on clinical MRI.
 Polypharmacy in multiple sclerosis: More is not necessarily better.
 Longitudinal Changes in Cognitive Test Scores in Patients With Relapsing-Remitting Multiple Sclerosis: An Analysis of the DECIDE Dataset.
 A multimodal marker for cognitive functioning in multiple sclerosis: the role of NfL, GFAP and conventional MRI in predicting cognitive functioning in a prospective clinical cohort.
 EDSS and infratentorial white matter lesion volume are considered predictors of fatigue severity in RRMS.
 Genetic regulation of IL-8 influences disease presentation of multiple sclerosis.
 Multi-Disease Validation of the RUDAS for Cognitive Screening in Alzheimer's Disease, Parkinson's Disease, and Multiple Sclerosis.
 Choroid plexus enlargement in paediatric multiple sclerosis: clinical relevance and effect of sex.
 Effectiveness and safety profile of cladribine in an Italian real-life cohort of relapsing-remitting multiple sclerosis patients: a monocentric longitudinal observational study.
 A taxonomic approach to cognitive diagnostics is viable and achievable in MS.
 Relapse-associated worsening in a real-life multiple sclerosis cohort: the role of age and pyramidal phenotype.
 A review on plant-based remedies for the treatment of multiple sclerosis.
 Antibodies to expanded virus antigen panels show elevated diagnostic sensitivities in multiple sclerosis and optic neuritis.
 Sexual problems in MS: Sex differences and their impact on quality of life.
 Cost-Utility Analysis Comparing Ocrelizumab Versus Rituximab in the Treatment of Relapsing-Remitting Multiple Sclerosis: The Colombian Perspective.
 TUFM variants lead to white matter abnormalities mimicking multiple sclerosis.
 Systematic literature review of immunoglobulin trends for anti-CD20 monoclonal antibodies in multiple sclerosis.
 Baseline retinal nerve fiber layer thickness as a predictor of multiple sclerosis progression: New insights from the FREEDOMS II study.
 Serum neurofilament light chain in relapsing multiple sclerosis patients on a ketogenic diet.
 Treatment of Patients with Multiple Sclerosis Transitioning Between Relapsing and Progressive Disease.
 Patients experiences when receiving diagnosis of multiple sclerosis: A qualitative systematic review.
 "Can I exercise? Would it help? Would it not?": exploring the experiences of people with relapsing remitting multiple sclerosis engaging with physical activity during a relapse: a qualitative study.
 First-line disease modifying treatments in pediatric-onset multiple sclerosis in Greece: therapy initiation at more advanced age is the main cause of treatment failure, in a retrospective observational study, with a cohort from a single Multiple Sclerosis Center.
 Initiation Patterns of Disease-Modifying Therapies for Multiple Sclerosis Among US Adults and Children, 2001 Through 2020.
 Ocrelizumab extended-interval dosing in multiple sclerosis during SARS-CoV-2 pandemic: a real-world experience.
 Ublituximab: First Approval.
 Secondary Progressive Multiple Sclerosis: A Review of Clinical Characteristics, Definition, Prognostic Tools, and Disease-Modifying Therapies.
 Enlarged choroid plexus related to iron rim lesions and deep gray matter atrophy in relapsing-remitting multiple sclerosis.
 Digital Phenotypes of Instability and Fatigue Derived From Daily Standing Transitions in Persons With Multiple Sclerosis.
 Gene-environment interactions increase the risk of paediatric-onset multiple sclerosis associated with household chemical exposures.
 Change in upper limb function in people with multiple sclerosis treated with nabiximols: a quantitative kinematic pilot study.
 A journey with no roadmap-The need for validated criteria of the MS prodrome.
 Safety and Monitoring of the Treatment with Disease-Modifying Therapies (DMTs) for Multiple Sclerosis (MS).
 Deep gray matter substructure volumes and depressive symptoms in a large multiple sclerosis cohort.
 Nanosuspension-based microneedle skin patch of baclofen for sustained management of multiple sclerosis-related spasticity.
 Experiences of receiving a diagnosis of multiple sclerosis: a meta-synthesis of qualitative studies.
 Comparing the risk of serious infections in patients with and without MS: A German claims data analysis.
 Refractory Convulsive Status Epilepticus Provoked by Intoxication with Dalfampridine in a Patient with Multiple Sclerosis and Depression Disorder: A Case Report and Literature Review.
 A plain language summary on the effectiveness of cladribine tablets compared with other oral treatments for multiple sclerosis: results from the MSBase registry.
 [Multiple sclerosis and fatigue. It is necessary to improve].
 Dimethyl fumarate induced Wells syndrome. A case report.
 Differentiation between multiple sclerosis and neuromyelitis optica spectrum disorder using a deep learning model.
 Biosensing strategies (approaches) for diagnosis and monitoring of multiple sclerosis.
 Neuroprotection in Cerebral Cortex Induced by the Pregnancy Hormone Estriol.
 [Characteristics and dynamics of pathological changes in visual evoked potentials in multiple sclerosis].
 Associations among stressors across the lifespan, disability, and relapses in adults with multiple sclerosis.
 Granulocyte activation markers in cerebrospinal fluid differentiate acute neuromyelitis spectrum disorder from multiple sclerosis.
 The Treatment of Acute Optic Neuritis.
 Immunosenescence: the role of age in multiple sclerosis.
 Safety evaluations of offspring breastfed by mothers receiving glatiramer acetate for relapsing multiple sclerosis.
 Multiple sclerosis: Exploring the limits and implications of genetic and environmental susceptibility.
 CEST 2022 - Differences in APT-weighted signal in T1 weighted isointense lesions, black holes and normal-appearing white matter in people with relapsing-remitting multiple sclerosis.
 Evaluating the impact of patient-reported outcome measures on depression and anxiety levels in people with multiple sclerosis: a study protocol for a randomized controlled trial.
 Using The Virtual Brain to study the relationship between structural and functional connectivity in patients with multiple sclerosis: a multicenter study.
 Polypharmacy and multiple sclerosis: A population-based study.
 Fully Automatic Method for Reliable Spinal Cord Compartment Segmentation in Multiple Sclerosis.
 PET-measurable innate immune cell activation reduction in chronic active lesions in PPMS brain after rituximab treatment: a case report.
 Long non-coding RNAs BACE1-AS and BC200 in multiple sclerosis and their relation to cognitive function: A gene expression analysis.
 [Efficacy and safety of divozilimab during 24-week treatment of multiple sclerosis patients in randomized double-blind placebo-controlled clinical trial BCD-132-2].
 Peripheral Nerve Involvement at First Diagnosis of Multiple Sclerosis: A Prospective MR Neurography Study.
 [Optic neuropathies as an interdisciplinary subject of research].
 Fast-DIR: A new step for revolutionizing multiple sclerosis detection and patient experience.
 Association between chronic cerebrospinal venous insufficiency and multiple sclerosis: a systematic review and meta-analysis.
 Low-dose ketamine infusion for the treatment of multiple sclerosis fatigue (INKLING-MS): Study protocol for a randomized, double-blind, active placebo-controlled phase II trial.
 Vascular disease risk factors in multiple sclerosis: Effect on metabolism and brain volumes.
 The Fulcrum of Demyelination in Multiple Sclerosis.
 The prevalence and incidence of multiple sclerosis over the past 20 years in northern Japan.
 Effect of Vitamin D Supplementation on Fatigue in Multiple Sclerosis: A Systematic Review and Meta-Analysis.
 Response letter for the comment made on our article entitled "Does the inclusion of societal costs change the economic evaluations recommendations? A systematic review for multiple sclerosis disease", published online last May in the European Journal of Health Economics, doi: 10.1007/s10198-022-01471-9.
 Evolution of acute "black hole" lesions in patients with relapsing-remitting multiple sclerosis.
 Real-world experience of cladribine treatment in relapsing-remitting multiple sclerosis: A Danish nationwide study.
 Reduction in grey matter atrophy in patients with relapsing multiple sclerosis following treatment with cladribine tablets.
 Case Report: Delayed Alemtuzumab-Induced Concurrent Neutropenia and Thrombocytopenia in Relapsing-Remitting Multiple Sclerosis.
 Therapeutic Plasma Exchange (TPE) Complications in Patients With Multiple Sclerosis (MS) and Clinically Isolated Syndrome (CIS): A Report From a Tertiary Center.
 Are Cannabis and Cannabinoids Effective for Symptomatic Treatment in People With Multiple Sclerosis?: A Cochrane Review Summary With Commentary.
 [Performance of the revised 2017 McDonald criteria].
 Cancer risk and mortality in multiple sclerosis: The need for vigilance.
 [New neuroimaging methods in assessing the activity of neuroinflammation in multiple sclerosis].
 Non-interventional, prospective, observational study on spasticity-associated symptom control with nabiximols as add-on therapy in patients with multiple sclerosis spasticity in Austria.
 Association of chronic periodontitis with multiple sclerosis: A systematic review and meta-analysis.
 Cryopreservation of ovarian tissue as fertility preservation in young women with multiple sclerosis before stem cell transplantation.
 Three Dimensional Brain Parameters of Multiple Sclerosis (MS) Patients.
 The comparative effectiveness of fingolimod, natalizumab, and ocrelizumab in relapsing-remitting multiple sclerosis.
 Glial fibrillary acidic protein and multiple sclerosis progression independent of acute inflammation.
 Investigation of in-phase bilateral exercise effects on corticospinal plasticity in relapsing remitting multiple sclerosis: A registered report single-case concurrent multiple baseline design across five subjects.
 The Role of Diet in Multiple Sclerosis: Food for Thought.
 The Heterogeneous Multiple Sclerosis Lesion: How Can We Assess and Modify a Degenerating Lesion?
 Efficacy of nabiximols oromucosal spray on spasticity in people with multiple sclerosis: Treatment effects on Spasticity Numeric Rating Scale, muscle spasm count, and spastic muscle tone in two randomized clinical trials.
 Safety and efficacy of tolebrutinib, an oral brain-penetrant BTK inhibitor, in relapsing multiple sclerosis: A phase 2b, randomized, double-blind, placebo-controlled trial by Daniel S Reich et Al.
 Lessons from immunotherapies in multiple sclerosis.
 Depressive symptoms, anxiety and cognitive impairment: emerging evidence in multiple sclerosis.
 Reliability of brain atrophy measurements in multiple sclerosis using MRI: an assessment of six freely available software packages for cross-sectional analyses.
 "Brain age" predicts disability accumulation in multiple sclerosis.
 Recurrent Optic Neuritis and Perineuritis Followed by an Unexpected Discovery: From the National Multiple Sclerosis Society Case Conference Proceedings.
 Impact of interferon beta exposure on birth outcome and child development - Results from the post-authorisation safety study PRIMA.
 Long-term results of autografting persons with multiple sclerosis are better in those not exposed to prior disease-modifying therapies.
 Decision Making About Disease-Modifying Treatments for Relapsing-Remitting Multiple Sclerosis: Stated Preferences and Real-World Choices.
 The outcomes of total hip arthroplasty in patients with and without multiple sclerosis: a retrospective cohort study.
 A case of psoriasis and multiple sclerosis succesfully treated with concomitant fingolimod and secukinumab.
 COVID-19 and its implications on the clinico-radiological course of multiple sclerosis: A case-control study.
 Psychiatric symptoms in multiple sclerosis: a biological perspective on synaptic and network dysfunction.
 Personalized Longitudinal Assessment of Multiple Sclerosis Using Smartphones.
 Teriflunomide modulates both innate and adaptive immune capacities in multiple sclerosis.
 Serum neurofilament-light and glial fibrillary acidic protein levels in hydroxychloroquine-treated primary progressive multiple sclerosis.
 Impact of Dimethylfumarate on Sleep in Multiple Sclerosis Patients: An Actigraphic Study.
 Oligoclonal band versus chitinase-3-like protein-1 in CSF of newly diagnosed relapsing remitting multiple sclerosis.
 Neuroprotective effect of Vesatolimod in an experimental autoimmune encephalomyelitis mice model.
 Evaluation of the relationship between the morphometric structure of the pituitary gland and fatigue in patients with multiple sclerosis.
 Limited diagnostic utility of serologic testing for neurologic manifestations of systemic disease in the evaluation of suspected multiple sclerosis: A single-center observational study.
 Cognitive skill learning in multiple sclerosis: A meaningful component of the neuropsychological profile.
 Chlamydia pneumonia infection and risk of multiple sclerosis: A meta-analysis.
 The relevance of fatigue to relapse rate in multiple sclerosis: Applying patient preference data to the OPTIMUM trial.
 MWF of the corpus callosum is a robust measure of remyelination: Results from the ReBUILD trial.
 [Changes in venous circulation in patients with multiple sclerosis].
 Is the central vein sign a useful diagnostic marker for paediatric-onset multiple sclerosis?
 Brain proteome-wide association study linking-genes in multiple sclerosis pathogenesis.
 A proposed new taxonomy of cognitive phenotypes in multiple sclerosis: The International Classification of Cognitive Disorders in MS (IC-CoDiMS).
 Cognitive impairment in people with multiple sclerosis: Perception vs. performance - factors that drive perception of impairment differ for patients and clinicians.
 Longitudinal stability of inter-eye differences in optical coherence tomography measures for identifying unilateral optic nerve lesions in multiple sclerosis.
 Functional assessment of the dural lymphatic vessels using dynamic contrast MRI in multiple sclerosis.
 Multiple sclerosis, disease-modifying drugs and risk for adverse perinatal and pregnancy outcomes: Results from a population-based cohort study.
 Employment status, productivity loss, and associated factors among people with multiple sclerosis.
 Multiple sclerosis: Neuroimmune crosstalk and therapeutic targeting.
 Nose to brain delivery of Astragaloside IV by β-Asarone modified chitosan nanoparticles for multiple sclerosis therapy.
 Factors contributing to falls in people with multiple sclerosis: The exploration of the moderation and mediation effects.
 Multiple sclerosis and glatiramer acetate: Risk factors for central retinal vein occlusion?
 Seeking neuroprotection in multiple sclerosis: an ongoing challenge.
 Where's the Vision? The Importance of Visual Outcomes in Neurologic Disorders: The 2021 H. Houston Merritt Lecture.
 Intermediate outcomes for clinical trials of multiple sclerosis rehabilitation interventions: Conceptual and practical considerations.
 Genome-wide study of longitudinal brain imaging measures of multiple sclerosis progression across six clinical trials.
 Effects of Myopia on Rates of Change in Optical Coherence Tomography Measured Retinal Layer Thicknesses in People with Multiple Sclerosis and Healthy Controls.
 Effects of intrathecal Baclofen in reducing tremors in patients with multiple sclerosis.
 Evaluation of transorbital sonography measures of optic nerve diameter in the context of global and regional brain volume in multiple sclerosis.
 NODDI, diffusion tensor microstructural abnormalities and atrophy of brain white matter and gray matter contribute to cognitive impairment in multiple sclerosis.
 Ultrasound measures of muscle morphology in people with multiple sclerosis are associated with muscle performance and functional mobility.
 Location, location, location: myelin repair and proximity to ventricular CSF in multiple sclerosis.
 Patterns of brain atrophy in recently-diagnosed relapsing-remitting multiple sclerosis.
 FGF/FGFR system in the central nervous system demyelinating disease: Recent progress and implications for multiple sclerosis.
 Time restricted eating facilitates weight loss and improves cardiometabolic profile in a female veteran with multiple sclerosis: A case report.
 An evaluation of the role of community care in meeting the needs of people with multiple sclerosis in Ireland.
 Multiple sclerosis and age at primary EBV infection.
 Molecular biomarkers and cognitive impairment in multiple sclerosis: State of the field, limitations, and future direction - A systematic review and meta-analysis.
 Limb apraxia in individuals with multiple sclerosis: Is there a role of semi-immersive virtual reality in treating the Cinderella of neuropsychology?
 Improving the decision to switch from first- to second-line therapy in multiple sclerosis: A dynamic scoring system.
 In vivo characterization of microglia and myelin relation in multiple sclerosis by combined (11)C-PBR28 PET and synthetic MRI.
 Using an animal model to predict the effective human dose for oral multiple sclerosis drugs.
 Is there a relationship between respiratory function and trunk control and functional mobility in patients with relapsing-remitting multiple sclerosis?
 Multicenter Evaluation of AI-generated DIR and PSIR for Cortical and Juxtacortical Multiple Sclerosis Lesion Detection.
 Evaluating the central vein sign in paediatric-onset multiple sclerosis: A case series study.
 Topological reorganization of brain network might contribute to the resilience of cognitive functioning in mildly disabled relapsing remitting multiple sclerosis.
 Parity is associated with long-term differences in DNA methylation at genes related to neural plasticity in multiple sclerosis.
 Under the influence: environmental factors as modulators of neuroinflammation through the IL-10/IL-10R axis.
 Sustained Low Relapse Rate With Highly Variable B-Cell Repopulation Dynamics With Extended Rituximab Dosing Intervals in Multiple Sclerosis.
 Is the Optic Nerve Overdue as a Criterion to Support the Diagnosis of Multiple Sclerosis?
 High levels of kappa free light chain synthesis predict cognitive decline in relapsing-remitting multiple sclerosis.
 Intrathecal CD8(+)CD20(+) T Cells in Primary Progressive Multiple Sclerosis.
 Beyond the simplicity of theory of mind deficit in multiple sclerosis: from kinetic perception to socio-emotional abstraction and mentalizing.
 The role of diet in multiple sclerosis onset and course: results from a nationwide retrospective birth-year cohort.
 A randomized double-blind placebo-controlled trial of low-dose interleukin-2 in relapsing-remitting multiple sclerosis.
 A coffee enriched with guarana, selenium, and l-carnitine (GSC) has nutrigenomic effects on oxi-inflammatory markers of relapsing-remitting multiple sclerosis patients: A pilot study.
 Beyond the B-cell as a treatment target in multiple sclerosis.
 [Microbiota markers level in the blood and cerebrospinal fluid of patients with different types of multiple sclerosis and radiologically isolated syndrome].
 Dimethyl Fumarate Delays Multiple Sclerosis in Radiologically Isolated Syndrome.
 Treatments of paediatric multiple sclerosis: Efficacy and tolerance in a longitudinal follow-up study.
 Changes in physiotherapy services and use of technology for people with multiple sclerosis during the COVID-19 pandemic.
 Cost-consequence analysis of ofatumumab for the treatment of relapsing-remitting multiple sclerosis in Canada.
 Nabiximols oromucosal spray in patients with multiple sclerosis-related bladder dysfunction: A prospective study.
 Automatic detection of active and inactive multiple sclerosis plaques using the Bayesian approach in susceptibility-weighted imaging.
 Evidence of publication bias in multiple sclerosis clinical trials: a comparative analysis of published and unpublished studies registered in ClinicalTrials.gov.
 Quantitation of neurofilament light chain protein in serum and cerebrospinal fluid from patients with multiple sclerosis using the MSD R-PLEX NfL assay.
 How does neurovascular unit dysfunction contribute to multiple sclerosis?
 A self-management intervention for people with multiple sclerosis: The development of a programme theory in the field of rehabilitation nursing.
 Platelets and platelet-derived vesicles as an innovative cellular and subcellular platform for managing multiple sclerosis.
 Physical activity behavior in persons newly diagnosed with multiple sclerosis: Applying the Capability - Opportunity - Motivation - Behavior (COM-B) model.
 Metabolomic profiles in relapsing-remitting and progressive multiple sclerosis compared to healthy controls: a five-year follow-up study.
 Psychophysical Evaluation of Visual vs. Computer-Aided Detection of Brain Lesions on Magnetic Resonance Images.
 Prospective outcome analysis of multiple sclerosis cases reveals candidate prognostic cerebrospinal fluid markers.
 Using the Instrumented Sway System (ISway) to Identify and Compare Balance Domain Deficits in People With Multiple Sclerosis.
 Autologous hematopoietic stem cell transplantation significantly alters circulating ceramides in peripheral blood of relapsing-remitting multiple sclerosis patients.
 Immune response to COVID-19 vaccines in patients with multiple sclerosis treated with disease-modifying therapies.
 Optimized three-dimensional ultrashort echo time: Magnetic resonance fingerprinting for myelin tissue fraction mapping.
 Life Experiences of Patients With Multiple Sclerosis About Their Spasticity: A Phenomenological Study.
 Influence of eight weeks of combined training on adipsin and lipoprotein profile and possible relations with depression, anxiety and stress in women with multiple sclerosis.
 Volumetric changes in hypothalamic subunits in patients with relapsing remitting multiple sclerosis.
 A Comprehensive Exploration of the Transcriptomic Landscape in Multiple Sclerosis: A Systematic Review.
 In vivo quantification of brain soma and neurite density abnormalities in multiple sclerosis.
 Bruton tyrosine kinase inhibitors for multiple sclerosis.
 Pediatric tumefactive multiple sclerosis case (with baló-like lesions), diagnostic and treatment challenges.
 [The need to validate translations into Russian of objective neurological scales, symptoms and syndromes].
 Lived experience of persons with multiple sclerosis: A qualitative interview study.
 To wait, or too late? Modeling the effects of delayed ofatumumab treatment in relapsing-remitting multiple sclerosis.
 Capturing cognitive changes in multiple sclerosis by performance-based functional and virtual reality assessments.
 Overlap autoimmune syndrome: primary progressive multiple sclerosis, primary biliary cirrhosis, Raynaud phenomena with digital necrosis.
 Differential Associations of Mobility With Fronto-Striatal Integrity and Lesion Load in Older Adults With and Without Multiple Sclerosis.
 [Neurology meets Urology : Overview of urologically relevant neurological diseases].
 Effect of support based on family centered empowerment model on care burden in family caregivers of patients with multiple sclerosis.
 An intervention design for promoting quality of life among patients with multiple sclerosis: a protocol with a planning approach for a mixed methods study.
 HNF4α, SP1 and c-myc are master regulators of CNS autoimmunity.
 Fingerprick blood samples to measure serum natalizumab concentrations.
 Cladribine and pregnancy in women with multiple sclerosis: The first cohort study.
 In vivo confocal microscopy of corneal nerve fiber damage in early course of multiple sclerosis.
 The circular RNA landscape in multiple sclerosis: Disease-specific associated variants and exon methylation shape circular RNA expression profile.
 Acute attack in a patient with multiple sclerosis 2 days after COVID vaccination: a case report.
 Association of serum homocysteine, folate, and vitamin B(12) and mood following the Swank and Wahls elimination dietary interventions in relapsing-remitting multiple sclerosis: Secondary analysis of the WAVES trial.
 Tissue factor as a potential coagulative/vascular marker in relapsing-remitting multiple sclerosis.
 Application of diagnostic criteria for optic neuritis - Authors' reply.
 Central vein sign and paramagnetic rim sign: From radiologically isolated syndrome to multiple sclerosis.
 Microstructural alterations in different types of lesions and their perilesional white matter in relapsing-remitting multiple sclerosis based on diffusion kurtosis imaging.
 Moving toward personalized B cell depletion in multiple sclerosis?
 Quantitative MRI identifies lesional and non-lesional abnormalities in MOGAD.
 Dual role of peripheral B cells in multiple sclerosis: emerging remote players in demyelination and novel diagnostic biomarkers.
 Defective Induction of IL-27-Mediated Immunoregulation by Myeloid DCs in Multiple Sclerosis.
 Application of diagnostic criteria for optic neuritis.
 The effect of ginger (Zingiber officinale) supplementation on clinical, biochemical, and anthropometric parameters in patients with multiple sclerosis: a double-blind randomized controlled trial.
 Participant diversity in clinical trials of rehabilitation interventions for people with multiple sclerosis: A scoping review.
 [Efficacy and safety of antiCD20 monoclonal antibody divozilimab during 48-week treatment of multiple sclerosis patients in randomized double-blind placebo-controlled clinical trial BCD-132-4/MIRANTIBUS].
 Multifaceted Analysis of Cerebrospinal Fluid and Serum from Progressive Multiple Sclerosis Patients: Potential Role of Vitamin C and Metal Ion Imbalance in the Divergence of Primary Progressive Multiple Sclerosis and Secondary Progressive Multiple Sclerosis.
 Not all roads lead to the immune system: the genetic basis of multiple sclerosis severity.
 Experiences of health tracking in mobile apps for multiple sclerosis: A qualitative content analysis of user reviews.
 "Oh it's changed, it's changed 10-fold": understanding the experience of self-concept change from the perspectives of people with multiple sclerosis.
 Preliminary validity of the Draw a Shape Test for upper extremity assessment in multiple sclerosis.
 In vivo MRI is sensitive to remyelination in a nonhuman primate model of multiple sclerosis.
 Effectiveness and safety of switching from fingolimod and natalizumab to rituximab in patients with relapsing remitting multiple sclerosis.
 Family planning and multiple sclerosis: A qualitative study of patient experiences to understand information needs and promote informed decision-making.
 Subacute cutaneous lupus erythematosus as a rare complication of disease-modifying therapy administration in multiple sclerosis: case report.
 Disability in multiple sclerosis is associated with vascular factors: An ultrasound study.
 Tumor Necrosis Factor α Blockers and the Risk of Multiple Sclerosis.
 Electronic health record data for assessing risk of hospitalization for COVID-19: Methodological considerations applied to multiple sclerosis.
 Mobile apps used for people living with multiple sclerosis: A scoping review.
 Engagement with three or more healthy lifestyle behaviours is associated with improved quality of life over 7.5 years in people with multiple sclerosis.
 Hematopoietic Stem Cell Transplantation in People With Active Secondary Progressive Multiple Sclerosis.
 A qualitative investigation of reasoning behind decisions to decline participation in a research intervention: A study-within-a-trial.
 Characterizing the 'feel-good experience' in multiple sclerosis patients treated with natalizumab or other therapies.
 Presence of neural surface and onconeural autoantibodies in cerebrospinal fluid and serum in neurological diseases presents a potential risk for misdiagnosis.
 The effectiveness of nontraditional or home-based programing on ADL performance of individuals living with multiple sclerosis: A systematic review.
 Immune Profiling Reveals the T-Cell Effect of Ocrelizumab in Early Relapsing-Remitting Multiple Sclerosis.
 Effect of smoking on disease activity in multiple sclerosis patients treated with dimethyl fumarate or fingolimod.
 Effects of horizontal versus vertical switching of disease-modifying treatment after platform drugs on disease activity in patients with relapsing-remitting multiple sclerosis in Austria.
 Enhanced pathogenicity of Th17 cells due to natalizumab treatment: Implications for MS disease rebound.
 Acquired Demyelinating Syndromes of the Central Nervous System in Children: The Importance of Regular Follow-up in the First Year After Onset.
 Faster progression to multiple sclerosis disability is linked to neuronal pathways associated with neurodegeneration: An ethnicity study.
 Ponesimod: An Oral Second-Generation Selective Sphingosine 1-Phosphate Receptor Modulator for the Treatment of Multiple Sclerosis.
 Methods for comparative effectiveness based on time to confirmed disability progression with irregular observations in multiple sclerosis.
 Experiences of people with multiple sclerosis participating in a social cognitive behavior change physical activity intervention.
 Longitudinal epidemiology of multiple sclerosis in Townsville, Queensland, Australia, 2012-2022.
 Summary of Safety and Efficacy of COVID Vaccination in Patients with Multiple Sclerosis.
 Accurate Diagnosis of Cortical and Infratentorial Lesions in Multiple Sclerosis Using Accelerated Fluid and White Matter Suppression Imaging.
 Retinal ganglion cell loss is associated with future disability worsening in early relapsing-remitting multiple sclerosis.
 Disease-modifying therapy for multiple sclerosis: Implications for gut microbiota.
 The comparative analysis of selected interleukins and proinflammatory factors in CSF among de novo diagnosed patients with RRMS.
 Magnetic resonance imaging approaches for studying mouse models of multiple sclerosis: A mini review.
 Cognitive reserve as a moderating factor between EDSS and cognition in multiple sclerosis.
 A review of current rehabilitation practices and their benefits in patients with multiple sclerosis.
 Contrast-Enhanced 3D Spin Echo T1-Weighted Sequence Outperforms 3D Gradient Echo T1-Weighted Sequence for the Detection of Multiple Sclerosis Lesions on 3.0 T Brain MRI.
 Cerebral organoids in primary progressive multiple sclerosis reveal stem cell and oligodendrocyte differentiation defect.
 Effect of MS14® on physical activity of multiple sclerosis patients: A randomized triple-blind placebo-controlled clinical trial.
 Impact of the covid-19 pandemic on the psychological status and cortisol level of multiple sclerosis patients.
 What's your cup of tea? The role of herbal compounds in the management of multiple sclerosis.
 The psychological impact of the COVID-19 pandemic on people with multiple sclerosis.
 Carotenoids contribution in rapid diagnosis of multiple sclerosis by Raman spectroscopy.
 Effects of N-acetylcysteine on oxidative stress biomarkers, depression, and anxiety symptoms in patients with multiple sclerosis.
 Validation and cross-cultural adaptation of the Multiple Sclerosis Intimacy and Sexuality Questionnaire-15 (MSISQ-15) into Spanish.
 A prospective study of disease modifying therapy and retinal atrophy in relapsing-remitting multiple sclerosis.
 Serum Levels of CXCL13 Are Associated With Teriflunomide Response in Patients With Multiple Sclerosis.
 The importance of gut-brain axis and use of probiotics as a treatment strategy for multiple sclerosis.
 Feeding the gut microbiome: impact on multiple sclerosis.
 Efficacy and safety of repeated low-dose rituximab therapy in relapsing-remitting multiple sclerosis: A retrospective case series study.
 Serum NfL but not GFAP predicts cognitive decline in active progressive multiple sclerosis patients.
 Association between intelligence quotient scores and body mass index in pediatric multiple sclerosis.
 Neuroaxonal and Glial Markers in Patients of the Same Age With Multiple Sclerosis.
 Learning multiple sclerosis immunopathogenesis from anti-CD20 therapy.
 Free light chains as a reliable biomarker of intrathecal synthesis in the diagnosis of CNS inflammatory diseases.
 Diagnostic performance of artificial intelligence in multiple sclerosis: a systematic review and meta-analysis.
 SARS-CoV-2-infection in the setting of autotransplants for multiple sclerosis.
 Multiple sclerosis and the incidence of venous thromboembolism: a systematic review and meta-analysis.
 Locomotor Strategy to Perform 6-Minute Walk Test in People with Multiple Sclerosis: A Prospective Observational Study.
 iPSC-derived reactive astrocytes from patients with multiple sclerosis protect cocultured neurons in inflammatory conditions.
 Pregnancy and neuromyelitis optica spectrum disorders: 2022 recommendations from the French Multiple Sclerosis Society.
 Psychometric properties of the Croatian version of the Multiple Sclerosis Walking Scale (MSWS-12).
 Fc multimers effectively treat murine models of multiple sclerosis.
 Comparing virtual reality exergaming with conventional exercise in rehabilitation of people with multiple sclerosis: A systematic review.
 A place for biosimilars in the changing multiple sclerosis treatment landscape.
 The psychological benefits of neuropsychological assessment feedback as a psycho-educational therapeutic intervention: A randomized-controlled trial with cross-over in multiple sclerosis.
 Task-oriented training for upper limb functions in patients with multiple sclerosis: Systematic review and meta-analysis.
 Assessment of Motor Evoked Potentials in Multiple Sclerosis.
 Clinical utility of the Trendelenburg Test in people with multiple sclerosis.
 Healthcare complexities during community crises: Recommendation for access to healthcare for Australians with multiple sclerosis.
 Association between cognitive impairment and motor dysfunction among patients with multiple sclerosis: a cross-sectional study.
 It's not always an infection: Pyoderma gangrenosum of the urogenital tract in two patients with multiple sclerosis treated with rituximab.
 Assessment of adherence to, and persistence with, an electromechanical autoinjector for subcutaneous interferon beta-1a injections for multiple sclerosis treatment over 3 years.
 Effects of baseline age and disease duration on the efficacy and safety of siponimod in patients with active SPMS: Post hoc analyses from the EXPAND study.
 Conceptualization, use, and outcomes associated with compassion in the care of people with multiple sclerosis: a scoping review.
 In multiple sclerosis, a Functional Independence Measure ≥ 107 is the best predictor of outcome after clean intermittent catheterization training.
 Mapping two decades of multiple sclerosis rehabilitation trials: A systematic scoping review and call to action to advance the study of race and ethnicity in rehabilitation research.
 Factors associated with material deprivation in persons with multiple sclerosis in Switzerland: Cross-sectional data from the Swiss Multiple Sclerosis Registry.
 Chest-Based Wearables and Individualized Distributions for Assessing Postural Sway in Persons With Multiple Sclerosis.
 Results of the MOVE MS Program: A Feasibility Study on Group Exercise for Individuals with Multiple Sclerosis.
 Personalized monitoring of ambulatory function with a smartphone 2-minute walk test in multiple sclerosis.
 Safety and efficacy of cladribine in multiple sclerosis: a systematic review and meta-analysis.
 An unforeseen reality: Hemophagocytic lymphohistiocytosis following alemtuzumab treatment for a multiple sclerosis.
 Cognitive impairment in multiple sclerosis: "classic" knowledge and recent acquisitions.
 Liquid chromatography-tandem mass spectrometry method for determination of total and free teriflunomide concentration in serum of patients with multiple sclerosis.
 A gene regulatory network approach harmonizes genetic and epigenetic signals and reveals repurposable drug candidates for multiple sclerosis.
 Sexuality experiences of women with multiple sclerosis reporting overactive bladder: a qualitative study.
 Effects of repetitive twice-weekly transcranial direct current stimulations on fatigue and fatigability in people with multiple sclerosis.
 Inflammatory Activity After Diverse Fertility Treatments: A Multicenter Analysis in the Modern Multiple Sclerosis Treatment Era.
 [Multiple sclerosis in the Republic of Bashkortostan: population-specific genetic predictors and the results of a 20-year clinical follow-up study].
 Nanoparticulate MgH(2) ameliorates anxiety/depression-like behaviors in a mouse model of multiple sclerosis by regulating microglial polarization and oxidative stress.
 Health related quality of life in the domain of physical activity predicts confirmed disability progression in people with relapsing remitting multiple sclerosis.
 Magnetization transfer saturation reveals subclinical optic nerve injury in pediatric-onset multiple sclerosis.
 Confidence communicating about multiple sclerosis among enrolees in an online course.
 Effect of an educational intervention based on the theory of planned behavior on improving medication adherence in patients with multiple sclerosis treated with injectable disease-modifying drugs: randomized controlled trial.
 Neurodegeneration in multiple sclerosis.
 Subjective Report, Objective Neurocognitive Performance, and "Invisible Symptoms" in Multiple Sclerosis.
 CSF Markers of Oxidative Stress Are Associated with Brain Atrophy and Iron Accumulation in a 2-Year Longitudinal Cohort of Early MS.
 Resting-State Functional Connectivity in Relapsing-Remitting Multiple Sclerosis with Mild Disability: A Data-Driven, Whole-Brain Multivoxel Pattern Analysis Study.
 Brain age gap in neuromyelitis optica spectrum disorders and multiple sclerosis.
 Exploring an 8-Week Online Adaptive Yoga Program for Multiple Sclerosis: A Pilot Study.
 Similar geographic distributions of death rates from inflammatory bowel disease and Hodgkin lymphoma or multiple sclerosis.
 Potential biological contributers to the sex difference in multiple sclerosis progression.
 Mechanisms of metabolic stress induced cell death of human oligodendrocytes: relevance for progressive multiple sclerosis.
 Accelerated Simultaneous T(2) and T(2)* Mapping of Multiple Sclerosis Lesions Using Compressed Sensing Reconstruction of Radial RARE-EPI MRI.
 Risk of fracture in neuromyelitis optica spectrum disorder and multiple sclerosis: a nationwide cohort study in South Korea.
 Neurologic disease activity in people with multiple sclerosis treated with immune checkpoint inhibitors.
 Well-being and flourishing mental health in adults with inflammatory bowel disease, multiple sclerosis and rheumatoid arthritis in Manitoba, Canada: a cross-sectional study.
 Pathology-supported genetic testing presents opportunities for improved disability outcomes in multiple sclerosis.
 Real-world evidence of ocrelizumab-treated relapsing multiple sclerosis cohort shows changes in progression independent of relapse activity mirroring phase 3 trials.
 Functional alteration due to structural damage is network dependent: insight from multiple sclerosis.
 Sexual dysfunction in Brazilian patients with multiple sclerosis.
 Prediction of relapse activity when switching to cladribine for multiple sclerosis.
 A neuropsychologically based employment intervention for women with multiple sclerosis: A quasi-randomized controlled trial.
 Designing and Characterization of Tregitope-Based Multi-Epitope Vaccine Against Multiple Sclerosis: An Immunoinformatic Approach.
 Clinical and economic evaluations of natalizumab, rituximab, and ocrelizumab for the management of relapsing-remitting multiple sclerosis in Saudi Arabia.
 Enhancing diversity of clinical trial populations in multiple sclerosis.
 Ocrelizumab concentration and antidrug antibodies are associated with B-cell count in multiple sclerosis.
 Shared Genetic Risk Factors for Multiple Sclerosis/Psoriasis Suggest Involvement of Interleukin-17 and Janus Kinase-Signal Transducers and Activators of Transcription Signaling.
 miRNA 548a-3p as biomarker of NEDA-3 at 2 years in multiple sclerosis patients treated with fingolimod.
 Association Between Frailty and Free-Living Walking Performance in People With Multiple Sclerosis.
 Effectiveness and Safety of Cannabinoids as an Add-On Therapy in the Treatment of Resistant Spasticity in Multiple Sclerosis: A Systematic Review.
 Lesion location across diagnostic regions in multiple sclerosis.
 [Family Planning in Women Diagnosed with Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder].
 Heterogeneity on long-term disability trajectories in patients with secondary progressive MS: a latent class analysis from Big MS Data network.
 Long-term dietary acid load is associated with depression in multiple sclerosis, but less evidence was found with fatigue and anxiety.
 Immediate effects of wearing textured versus smooth insoles on standing balance and spatiotemporal gait patterns when walking over even and uneven surfaces in people with multiple sclerosis.
 Association between clinic-level quality of care and patient-level outcomes in multiple sclerosis.
 Direct Health Care Costs Associated With Multiple Sclerosis: A Population-Based Cohort Study in British Columbia, Canada, 2001-2020.
 Clinical course of multiple sclerosis and patient experiences during breast cancer treatment.
 Plasma neurofilament light chain in children with relapsing MS receiving teriflunomide or placebo: A post hoc analysis of the randomized TERIKIDS trial.
 The CXCL13 Index as a Predictive Biomarker for Activity in Clinically Isolated Syndrome.
 A plain language summary of the impact of vaccines against flu and chickenpox in people with multiple sclerosis treated with cladribine tablets.
 Translational Significance of GMF-β Inhibition by Indazole-4-yl-methanol in Enteric Glial Cells for Treating Multiple Sclerosis.
 Fampridine for gait imbalance in patients with multiple sclerosis (MS): a systematic review and meta-analysis.
 Pregnancy outcomes after early fetal exposure to injectable first-line treatments, dimethyl fumarate, or natalizumab in Danish women with multiple sclerosis.
 Oligoclonal Band Status and Features of Radiological and Clinical Findings in Patients with Multiple Sclerosis in Lithuania.
 Vitamin D-An Effective Antioxidant in an Animal Model of Progressive Multiple Sclerosis.
 Cholesterol pathway associated with MS disability.
 Understanding humoral immunity and multiple sclerosis severity in Black, and Latinx patients.
 CSF Concentrations of CXCL13 and sCD27 Before and After Autologous Hematopoietic Stem Cell Transplantation for Multiple Sclerosis.
 Adverse events in MS patients fulfilling or not inclusion criteria of the respective clinical trial - The problem of generalizability.
 Usability validation of the Sensoready(®) pen in patients with relapsing multiple sclerosis.
 A new look at cognitive functioning in pediatric MS.
 Leukocyte telomere length in women with multiple sclerosis: Comparison with healthy women during pregnancy and puerperium.
 Multiple sclerosis-related heat sensitivity linked to absence of DMT prescription and subjective hand impairment but not autonomic or corticospinal dysfunction.
 Healthier living with MS: The key role of self-efficacy and emotion regulation.
 A qualitative evaluation of a clinic versus home exercise rehabilitation program for adults with multiple sclerosis: The tele-exercise and multiple sclerosis (TEAMS) study.
 A systematic review of the safety and efficacy of monoclonal antibodies for progressive multiple sclerosis.
 A 28-Year-Old Woman With Left-Sided Weakness and Atypical MRI Lesions: From the National Multiple Sclerosis Society Case Conference Proceedings.
 A Multicenter Longitudinal MRI Study Assessing LeMan-PV Software Accuracy in the Detection of White Matter Lesions in Multiple Sclerosis Patients.
 Comparison of goals set by people with multiple sclerosis during two fatigue management interventions.
 The Role of BDNF in Multiple Sclerosis Neuroinflammation.
 Association of multiple-sclerosis-related mortality with COVID-19 and other common infections: a multiple causes of death analysis.
 The bidirectional effect of stress and functionality in multiple sclerosis and the interaction role of anxiety, coping and social support.
 Time to reconsider the classification of multiple sclerosis.
 Blood pressure and cognition in older adults with multiple sclerosis: preliminary examination.
 Multiple sclerosis risk variants influence the peripheral B-cell compartment early in life in the general population.
 Validity of the 30-Second Sit-to-Stand test as a measure of lower extremity function in persons with multiple sclerosis: Preliminary evidence.
 Central nervous system demyelinating diseases: glial cells at the hub of pathology.
 Insulin resistance is associated with cognitive dysfunction in multiple sclerosis patients: A cross-sectional study.
 Multiple sclerosis in Indigenous Peoples of the Americas: A systematic review of incidence, prevalence, and outcomes.
 Reduced brain oxygen metabolism in patients with multiple sclerosis: Evidence from dual-calibrated functional MRI.
 Effect of immersive virtual reality training on hand-to-mouth task performance in people with Multiple Sclerosis: A quantitative kinematic study.
 Neuropathy in multiple sclerosis patients treated with teriflunomide.
 Early neurofilament light and glial fibrillary acidic protein levels improve predictive models of multiple sclerosis outcomes.
 Design principles of microparticle size and immunomodulatory factor formulation dictate antigen-specific amelioration of multiple sclerosis in a mouse model.
 [Severity of COVID-19 in patients with multiple sclerosis in Argentina].
 The effect of probiotics on immune responses and their therapeutic application: A new treatment option for multiple sclerosis.
 Multimodal-neuroimaging machine-learning analysis of motor disability in multiple sclerosis.
 Significant retinal microvascular impairments in multiple sclerosis assessed through optical coherence tomography angiography.
 Effects of Calorie Restriction on Multiple Sclerosis: A Review of the Preclinical and Clinical Studies.
 Competitive ELISA for the identification of 35-55 myelin oligodendrocyte glycoprotein immunodominant epitope conjugated with mannan.
 Presymptomatic MS or radiologically isolated syndrome (RIS) should be actively monitored and treated - NO.
 [15th Post-ECTRIMS Meeting: a review of the latest developments presented at the 2022 ECTRIMS Congress (Part I)].
 Imaging of Central Nervous System Demyelinating Disorders.
 Paramagnetic rim lesions are associated with greater incidence of relapse and worse cognitive recovery following relapse.
 Efforts Towards Repurposing of Antioxidant Drugs and Active Compounds for Multiple Sclerosis Control.
 Experimental Analysis of Tear Fluid and Its Processing for the Diagnosis of Multiple Sclerosis.
 Using participatory action research to develop a new self-management program: Results from the design stage of Managing My MS My Way.
 Evaluation of multiple sclerosis severity using a new OCT tool.
 The peripheral endocannabinoid system and its association with biomarkers of inflammation in untreated patients with multiple sclerosis.
 MR Imaging Signs of Gadolinium Retention Are Not Associated with Long-Term Motor and Cognitive Outcomes in Multiple Sclerosis.
 Multiple Sclerosis and Depression: Translation and Adaptation of the Spanish Version of the Chicago Multiscale Depression Inventory and the Study of Factors Associated with Depressive Symptoms.
 Successful treatment of a pure red cell aplasia patient following ABO-mismatched hematopoietic stem cell transplantation from a sibling donor with multiple sclerosis.
 2 grams versus 1 gram rituximab as maintenance schedule in multiple sclerosis, neuromyelitis optica spectrum disorders and related diseases: What B-cell repopulation data tell us.
 Quantitative magnetic resonance imaging biomarkers for cortical pathology in multiple sclerosis at 7 T.
 Comparative efficacy of therapies for relapsing multiple sclerosis: a systematic review and network meta-analysis.
 Formative evaluation of an exercise training program for persons with multiple sclerosis who are wheelchair users.
 [Neuromyelitis optica].
 Pharmacokinetic-Pharmacodynamic Modeling of the Ponesimod Effect on Heart Rate in Patients With Multiple Sclerosis.
 Presymptomatic MS or radiologically isolated syndrome should be actively monitored and treated: Commentary.
 Investigating the influence of an effort-reward interaction on cognitive fatigue in individuals with multiple sclerosis.
 [A case of multiple sclerosis with a tumefactive lesion during long-term treatment with fingolimod, leading to decompressive craniotomy].
 Application of diagnostic criteria for optic neuritis.
 People with Primary Progressive Multiple Sclerosis Have a Lower Number of Central Memory T Cells and HLA-DR(+) Tregs.
 Tools for comprehensive evaluation of sexual function in patients with multiple sclerosis.
 Correlation of brain segmental volume changes with clinical parameters: a longitudinal study in multiple sclerosis patients.
 B cell targeted therapies in inflammatory autoimmune disease of the central nervous system.
 Diagnostic significance of IgG and albumin indices versus oligoclonal band types in demyelinating disorders.
 [Long-term Efficacy and Safety of Sampeginterferon-β1a in the Treatment of Relapsing Remitting Multiple Sclerosis: a Randomized, Double-Blind Clinical Trial 104-Week Results].
 Mobility and balance rehabilitation in multiple sclerosis: A systematic review and dose-response meta-analysis.
 Airborne Pollution: A Potential Risk Factor for Multiple Sclerosis in Colder Climates.
 Tissue-resident memory T cells in the multiple sclerosis brain and their relationship to Epstein-Barr virus infected B cells.
 Breastfeeding in Mothers with Multiple Sclerosis: The German Experience.
 Neuroimaging Technology in Exercise Neurorehabilitation Research in Persons with MS: A Scoping Review.
 A Comparison of Two Analytical Approaches for the Quantification of Neurofilament Light Chain, a Biomarker of Axonal Damage in Multiple Sclerosis.
 Chasing shadows: Cytologically detected shadow cells in the cerebrospinal fluid of patients with multiple sclerosis.
 Age-related blood transcriptional regulators affect disease progression in pediatric multiple sclerosis.
 Influence of inflammatory processes on thalamocortical activity.
 Understanding the Role of the Choroid Plexus in Multiple Sclerosis as an MRI Biomarker of Disease Activity.
 Cardiovascular risk factors in secondary progressive multiple sclerosis: A cross-sectional analysis from the MS-STAT2 randomized controlled trial.
 Multiple Sclerosis Followed by Neuromyelitis Optica Spectrum Disorder: From the National Multiple Sclerosis Society Case Conference Proceedings.
 [Actual adherence to dimethyl fumarate in patients with relapsing-remitting multiple sclerosis].
 Longitudinal Effects of Sex, Aging, and Multiple Sclerosis Diagnosis on Function.
 A plain language summary of what clinical studies can tell us about the safety of evobrutinib - a potential treatment for multiple sclerosis.
 Nephrotic-range proteinuria and membranoproliferative glomerulonephritis-like pattern caused by interferon-β1b in a patient with multiple sclerosis.
 A systematic review and meta-analysis of the effects of non-pharmacological interventions on quality of life in adults with multiple sclerosis.
 Eyebrow alopecia associated with cladribine treatment for multiple sclerosis.
 Developing evidence-based guidelines for the safety of symptomatic drugs in multiple sclerosis during pregnancy and breastfeeding: A systematic review and Delphi consensus.
 Discovering functional connectivity features characterizing multiple sclerosis phenotypes using explainable artificial intelligence.
 The role of plasma cortisol in dementia, epilepsy, and multiple sclerosis: A Mendelian randomization study.
 Cognitive impairment in multiple sclerosis: Utility of electroencephalography.
 Cost-effectiveness of cladribine tablets and dimethyl fumarate in the treatment of relapsing remitting multiple sclerosis in Spain.
 Disease-modifying therapies and cost-of-illness progression among people newly diagnosed with multiple sclerosis: a national register-based cohort study covering treatment initiation with interferons, glatiramer acetate or natalizumab.
 Plant-based production of an orally active cyclotide for the treatment of multiple sclerosis.
 Bruton's tyrosine kinase as a promising therapeutic target for multiple sclerosis.
 Spinning Gold out of Straw: Using Modern AI Methods to Create Sequences for Cortical and Juxtacortical Multiple Sclerosis Lesion Detection When Only Conventional Imaging Is Available.
 Differentiating Multiple Sclerosis From AQP4-Neuromyelitis Optica Spectrum Disorder and MOG-Antibody Disease With Imaging.
 Disease severity classification using passively collected smartphone-based keystroke dynamics within multiple sclerosis.
 Dendritic Cells as a Nexus for the Development of Multiple Sclerosis and Models of Disease.
 Skin Thickening of the Scalp and High Signal Intensity of Dentate Nucleus in Multiple Sclerosis: Association With Linear Versus Macrocyclic Gadolinium-Based Contrast Agents Administration.
 Effect of Previous Disease-Modifying Therapy on Treatment Effectiveness for Patients Treated With Ocrelizumab.
 Epstein-Barr Virus and Multiple Sclerosis: A Convoluted Interaction and the Opportunity to Unravel Predictive Biomarkers.
 Neural bases of motor fatigue in multiple sclerosis: A multimodal approach using neuromuscular assessment and TMS-EEG.
 Is Mediterranean diet associated with multiple sclerosis related symptoms and fatigue severity?
 Central Vein Sign in Pediatric Multiple Sclerosis and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.
 The future of diagnosis in clinical neurosciences: Comparing multiple sclerosis and schizophrenia.
 Minimizing the effect of white matter lesions on deep learning based tissue segmentation for brain volumetry.
 Leukocyte Telomere Length Predicts Severe Disability in Relapsing-Remitting Multiple Sclerosis and Correlates with Mitochondrial DNA Copy Number.
 Global DNA Methylation and Hydroxymethylation Levels in PBMCs Are Altered in RRMS Patients Treated with IFN-β and GA-A Preliminary Study.
 The reliability and validity of the Figure of 8 walk test in mildly disabled persons with multiple sclerosis.
 Sleep in multiple sclerosis: a systematic review and meta-analysis of polysomnographic findings.
 Identifying prospective memory deficits in multiple sclerosis: Preliminary evaluation of the criterion and ecological validity of a single item version of the memory for intentions test (MIST).
 A dense residual U-net for multiple sclerosis lesions segmentation from multi-sequence 3D MR images.
 Effect of Acupuncture on Sensorimotor Function and Mobility in Patients with Multiple Sclerosis: A Pilot Study.
 Oral and monoclonal antibody treatments for relapsing forms of multiple sclerosis: Effectiveness and value.
 Incidence and prevalence of multiple sclerosis in China and other Asian countries.
 In Vivo Corneal Confocal Microscopy in Multiple Sclerosis: Can it Differentiate Disease Relapse in Multiple Sclerosis?
 Differential involvement of amyloidogenic evolvability in oligodendropathies; Multiple Sclerosis and Multiple System Atrophy.
 Predictive value of α-synuclein expression in peripheral blood of multiple sclerosis patients: A two-dimensional assessment of a selected biomarker.
 A case-control study of drinking beverages and the risk of multiple sclerosis in Iran.
 Switching to natalizumab or fingolimod in multiple sclerosis: Comparative effectiveness and effect of pre-switch disease activity.
 Anti-CD20 therapies in pregnancy and breast feeding: a review and ABN guidelines.
 Higher Dietary Acid Load Might Be a Potent Derivative Factor for Multiple Sclerosis: The Results from a Case-Control Study.
 [Therapeutic Strategies and Disease-Modifying Therapies for Multiple Sclerosis].
 Pregnancy and multiple sclerosis: 2022 recommendations from the French multiple sclerosis society.
 Patients with multiple sclerosis choose a collaborative role in making treatment decision: results from the Italian multicenter SWITCH study.
 European Committee for Treatment and Research in Multiple Sclerosis and European Academy of Neurology consensus on vaccination in people with multiple sclerosis: Improving immunization strategies in the era of highly active immunotherapeutic drugs.
 The feasibility of a flexible exercise participation programme (FEPP) for individuals with multiple sclerosis.
 Randomized controlled trial of the behavioral intervention for increasing physical activity in multiple sclerosis project: Secondary, patient-reported outcomes.
 NfL and GFAP in serum are associated with microstructural brain damage in progressive multiple sclerosis.
 Multiple sclerosis in 2022: old players, new insights.
 Effectiveness and safety of switching to teriflunomide in older patients with relapsing multiple sclerosis: A real-world retrospective multicenter analysis.
 The small molecule Erk1/2 signaling pathway inhibitor PD98059 improves DNA repair in an experimental autoimmune encephalomyelitis SJL/J mouse model of multiple sclerosis.
 Serum and cerebrospinal fluid BDNF concentrations are associated with neurological and cognitive improvement in multiple sclerosis: A pilot study.
 The Role of Gut Microbiome in the Pathogenesis of Multiple Sclerosis and Related Disorders.
 The moderating roles of self-efficacy and depression in dual-task walking in multiple sclerosis: A test of self-awareness theory.
 Neurocognitive impairment in multiple sclerosis and its association with thiol-disulfide homeostasis and ischemia-modified albumin.
 Sexual dysfunction in female and male people with multiple sclerosis: disability, depression and hormonal status matter.
 Quality of life of MS patients in Trinidad and Tobago: Anomaly or adaptation?
 Myelinodegeneration vs. Neurodegeneration in MS Progressive Forms.
 Vitamin D Receptor Gene Polymorphism Predicts the Outcome of Multidisciplinary Rehabilitation in Multiple Sclerosis Patients.
 Predictors of patient-reported fatigue symptom severity in a nationwide multiple sclerosis cohort.
 The expression profile of HAR1A and HAR1B in the peripheral blood cells of multiple sclerosis patients.
 Multiple sclerosis iron rim lesions are linked to impaired cervical spinal cord integrity using the T1/T2-weighted ratio.
 Pathological ultrastructural alterations of myelinated axons in normal appearing white matter in progressive multiple sclerosis.
 Cell-Specific Aging in Multiple Sclerosis.
 Exploratory clinical efficacy and patient-reported outcomes from NOVA: A randomized controlled study of intravenous natalizumab 6-week dosing versus continued 4-week dosing for relapsing-remitting multiple sclerosis.
 The effect of distance nurse-led fatigue management on fatigue, sleep quality, and self-efficacy in patients with multiple sclerosis: a quasi-experimental study.
 Tr1 cell-mediated protection against autoimmune disease by intranasal administration of a fusion protein targeting cDC1 cells.
 Improved detection of juxtacortical lesions using highly accelerated double inversion-recovery MRI in patients with multiple sclerosis.
 Anti-SARS-CoV-2 humoral and cellular responses in multiple sclerosis patients treated with anti-CD20 monoclonal antibodies.
 A pilot, randomized, placebo-controlled study of mindfulness meditation in treating insomnia in multiple sclerosis.
 Neuropsychiatric Status of Patients With Multiple Sclerosis Across Disease Duration Intervals.
 Is there a relationship between fall status, cognition and cerebellar lobule volume in patients with multiple sclerosis?
 Association between cognition and gait in multiple sclerosis: A smartphone-based longitudinal analysis.
 Cannabis-based products and multiple sclerosis-related pain: The role of routes of administration.
 Ferroptosis drives immune-mediated neurodegeneration in multiple sclerosis.
 Cancer related mortality in multiple sclerosis. A population based cohort study.
 Ongoing increase in incidence and prevalence of multiple sclerosis in south-eastern Iran: A three decade study.
 Cladribine treatment specifically affects peripheral blood memory B cell clones and clonal expansion in multiple sclerosis patients.
 Disability outcomes in early-stage African American and White people with multiple sclerosis.
 Is Clostridium perfringens epsilon toxin associated with multiple sclerosis?
 Healthcare utilisation and perceived healthcare accessibility and quality amongst people living with multiple sclerosis enroled in an online course.
 Laser-activated autologous adipose tissue-derived stromal vascular fraction restores spinal cord architecture and function in multiple sclerosis cat model.
 Hailey-Hailey disease (benign familial pemphigus) responsive to treatment with ocrelizumab for multiple sclerosis.
 A Prospective, Observational Study Assessing Effectiveness, Safety, and QoL of Greek Patients with Multiple Sclerosis Under Treatment with Fingolimod.
 Influence of hormones in multiple sclerosis: focus on the most important hormones.
 Impaired foot vibration sensitivity is related to altered plantar pressures during walking in people with multiple sclerosis.
 Association between human herpesviruses and multiple sclerosis: A systematic review and meta-analysis.
 Reproductive issues and multiple sclerosis: 20 questions.
 Progression of Mycosis Fungoides After Fingolimod Treatment for Multiple Sclerosis and Targeted Next-Generation Sequencing Demonstrating Potential Links Between the Two Diseases.
 Severe Neuroinvasive West Nile Virus in Association With Anti-CD20 Monotherapy for Multiple Sclerosis.
 Discrimination of multiple sclerosis using OCT images from two different centers.
 Risk of COVID-19 in people with multiple sclerosis who are seronegative following vaccination.
 Self-management of falls in people with multiple sclerosis: A scoping review.
 The association between hope and employment among individuals with multiple sclerosis: A hierarchical logistic regression model.
 Stability of sensor-based gait parameters reassessed after a period of one year in people with multiple sclerosis.
 The Mediating Role of Stigma, Internalized Shame, and Autonomous Motivation in the Relationship Between Depression, Anxiety, and Psychological Help-Seeking Attitudes in Multiple Sclerosis.
 Long-term follow-up of patients with relapsing multiple sclerosis from the CLARITY/CLARITY Extension cohort of CLASSIC-MS: An ambispective study.
 Transcriptome alterations in peripheral blood B cells of patients with multiple sclerosis receiving immune reconstitution therapy.
 Relationship between subjective report and objective assessment of neurocognitive functioning in persons with multiple sclerosis.
 A pro-inflammatory diet in people with multiple sclerosis is associated with an increased rate of relapse and increased FLAIR lesion volume on MRI in early multiple sclerosis: A prospective cohort study.
 Progressive multifocal leukoencephalopathy in a patient with relapsing multiple sclerosis treated with ocrelizumab: A case report.
 Exploring the Role of Neurotransmitters in Multiple Sclerosis: An Expanded Review.
 Effects of constraint induced movement therapy in patients with multiple sclerosis: A systematic review.
 Development of an international, multidisciplinary, patient-centered Standard Outcome Set for Multiple Sclerosis: The S.O.S.MS project.
 Immunomodulatory effects of ocrelizumab and candidate biomarkers for monitoring treatment response in multiple sclerosis.
 Cholesterol metabolism: Towards a therapeutic approach for multiple sclerosis.
 Mechanical filtration of the cerebrospinal fluid: procedures, systems, and applications.
 The effects of online exercise training on physical functions and quality of life in patients with pediatric-onset multiple sclerosis.
 Revealing the immune cell subtype reconstitution profile in patients from the CLARITY study using deconvolution algorithms after cladribine tablets treatment.
 DNA Methylation Signatures of Multiple Sclerosis Occur Independently of Known Genetic Risk and Are Primarily Attributed to B Cells and Monocytes.
 Positron Emission Tomography with [(18) F]-DPA-714 Unveils a Smoldering Component in Most Multiple Sclerosis Lesions which Drives Disease Progression.
 Conceiving complexity: Biological mechanisms underpinning the lasting effect of pregnancy on multiple sclerosis outcomes.
 Characterizing microglial gene expression in a model of secondary progressive multiple sclerosis.
 Experiences of individuals with multiple sclerosis and stroke using transcutaneous foot drop electrical stimulators: a systematic review and meta-synthesis of qualitative studies.
 Relationship between paramagnetic rim lesions and slowly expanding lesions in multiple sclerosis.
 Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria.
 The "Managing Fatigue" programme - Experiences shared by MS participants.
 Explainable artificial intelligence toward usable and trustworthy computer-aided diagnosis of multiple sclerosis from Optical Coherence Tomography.
 Fronto-striatal damage may contribute to resistance to fatigue-lowering medications in multiple sclerosis.
 Neutrophil to lymphocyte ratio may be a useful marker in distinguishing MOGAD and MS and platelet to lymphocyte ratio associated with MOGAD activity.
 Concomitant diagnosis of multiple sclerosis and human immunodeficiency virus (HIV) infection: case report and the review of literature.
 Inflammation in multiple sclerosis: consequences for remyelination and disease progression.
 Clostridium epsilon toxin is excessive in multiple sclerosis and provokes multifocal lesions in mouse models.
 Saliva and Serum Acetylcholinesterase Activity in Multiple Sclerosis.
 Coping with multiple sclerosis: reconciling significant aspects of health-related quality of life.
 Validity and reliability of the Tampa Kinesiophobia-Fatigue Scale in patients with multiple sclerosis.
 Protocol for an exploratory, randomised, single-blind clinical trial of aerobic exercise to promote remyelination in multiple sclerosis.
 Adrenoceptors as potential target for add-on immunomodulatory therapy in multiple sclerosis.
 MeTooMS: Sexual, physical, and emotional abuse experience among women with multiple sclerosis.
 Postpartum relapse risk in multiple sclerosis: a systematic review and meta-analysis.
 Update on the diagnosis and treatment of neuromyelits optica spectrum disorders (NMOSD) - revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part I: Diagnosis and differential diagnosis.
 [Esclerosis multiple. Lactancia. Lactante. Planificacion familiar. Posparto. Tratamiento modificador de la enfermedad.].
 In silico repurposing of CNS drugs for multiple sclerosis.
 Respiratory issues in patients with multiple sclerosis as a risk factor during SARS-CoV-2 infection: a potential role for exercise.
 Ocrelizumab Concentration Is a Good Predictor of SARS-CoV-2 Vaccination Response in Patients with Multiple Sclerosis.
 Automatic Intelligent System Using Medical of Things for Multiple Sclerosis Detection.
 A deep transcriptome meta-analysis reveals sex differences in multiple sclerosis.
 A qualitative exploration of the rehabilitation perceptions and experiences of persons with early multiple sclerosis.
 New Approaches to Challenge Old Assumptions-B-Cell Depletion in Multiple Sclerosis.
 Astrocyte-Derived Exosomes Differentially Shape T Cells' Immune Response in MS Patients.
 Humoral and cellular responses to repeated COVID-19 exposure in multiple sclerosis patients receiving B-cell depleting therapies: a single-center, one-year, prospective study.
 Prescription opioid use in multiple sclerosis.
 Gamma Knife Stereotactic Radiosurgery for Trigeminal Neuralgia Secondary to Multiple Sclerosis: A Case-Control Study.
 Similar Time Trends of Hodgkin Lymphoma, Multiple Sclerosis, and Inflammatory Bowel Disease.
 Comments on Letter to the Editor by Ph.D. Jussi Sipilä regarding our paper "Geochemistry of multiple sclerosis in Finland".
 Role of Microglial Cells in the Pathophysiology of MS: Synergistic or Antagonistic?
 Prominent epigenetic and transcriptomic changes in CD4(+) and CD8(+) T cells during and after pregnancy in women with multiple sclerosis and controls.
 Treadmill training with virtual reality to enhance gait and cognitive function among people with multiple sclerosis: a randomized controlled trial.
 Association of adverse childhood experiences with adulthood multiple sclerosis: A systematic review of observational studies.
 Unsupervised anomaly detection in brain MRI: Learning abstract distribution from massive healthy brains.
 UCHL1, besides leptin and fibronectin, also could be a sensitive marker of the relapsing-remitting type of multiple sclerosis.
 Social relations and leisure activities as predictors of wellbeing among older adults with multiple sclerosis: A cross-sectional survey study in Denmark.
 Novel plasma and brain proteins that are implicated in multiple sclerosis.
 Comparative effectiveness in multiple sclerosis: A methodological comparison.
 An investigation of auditory processing in relapsing-remitting multiple sclerosis.
 COVID-19 vaccine hesitancy among Italian people with multiple sclerosis.
 Generalized pustular psoriasis occurring in a patient with multiple sclerosis during treatment with fingolimod.
 Targeting T Cell Metabolism as a Novel Approach for Treatment of MS: With a Focus on PFKFB3 Inhibitors.
 Case Report: Severe rebound after withdrawal of fingolimod in a patient with neuromyelitis optica spectrum disorder.
 Introducing radiomics model to predict active plaque in multiple sclerosis patients using magnetic resonance images.
 Early non-disabling relapses are important predictors of disability accumulation in people with relapsing-remitting multiple sclerosis.
 Conversion Predictors of Clinically Isolated Syndrome to Multiple Sclerosis in Mexican Patients: A Prospective Study.
 How to explore and explain autonomic changes in multiple sclerosis.
 Hypnotherapy as a Nonpharmacological Treatment for the Psychological Symptoms of Multiple Sclerosis.
 [A comparison of DNA methylation profiles of blood mononuclear cells in patients with multiple sclerosis in remission and relapse].
 χ-Separation Imaging for Diagnosis of Multiple Sclerosis versus Neuromyelitis Optica Spectrum Disorder.
 Integration of epigenetic and genetic profiles identifies multiple sclerosis disease-critical cell types and genes.
 Exploration of Tetrahydroisoquinoline- and Benzo[c]azepine-Based Sphingosine 1-Phosphate Receptor 1 Agonists for the Treatment of Multiple Sclerosis.
 Activation of TRPV1 receptor facilitates myelin repair following demyelination via the regulation of microglial function.
 Virus exposure and neurodegenerative disease risk across national biobanks.
 Interferon β1a treatment does not influence serum Epstein-Barr virus antibodies in patients with multiple sclerosis.
 T Cell Energy Metabolism Is a Target of Glucocorticoids in Mice, Healthy Humans, and MS Patients.
 Analytical validation of a multi-protein, serum-based assay for disease activity assessments in multiple sclerosis.
 Effects of aerobic, resistance, and combined exercise training on health-related quality of life in multiple sclerosis: Systematic review and meta-analysis.
 [BDNF gene RS6265 polymorphism in patients with multiple sclerosis of Tomsk region].
 Pain and cognitive performance in adults with multiple sclerosis: A systematic review.
 Relevance of dedicated multiple sclerosis serum biomarkers in predicting contrast enhancement with gadolinium: Results from the REDUCE-GAD trial.
 Association between exposure to combustion-related air pollution and multiple sclerosis risk.
 Shared genetics and causal associations between COVID-19 and multiple sclerosis.
 Cerebral venous thrombosis after high-dose steroid in patient with multiple sclerosis: A case report.
 Early miR-320b and miR-25-3p miRNA levels correlate with multiple sclerosis severity at 10 years: a cohort study.
 Multiple sclerosis: Motor dysfunction.
 Knowledge and worries on motherhood choice in multiple sclerosis - a cross-sectional study on patient-reported outcome measures.
 Long-term effects of natalizumab on MRI activity and clinical outcomes in Japanese patients with relapsing-remitting multiple sclerosis.
 Antigen B modulates anti-inflammatory cytokines in the EAE model of multiple sclerosis.
 Adipokines in multiple sclerosis patients are related to clinical and radiological measures.
 Optical coherence tomography angiography measurements in multiple sclerosis: a systematic review and meta-analysis.
 Lexical Characteristics of the Speech Intelligibility Test: Effects on Transcription Intelligibility for Speakers With Multiple Sclerosis and Parkinson's Disease.
 Longitudinal Assessment of Multiple Sclerosis Lesion Load With Synthetic Magnetic Resonance Imaging-A Multicenter Validation Study.
 Effect of Robot-Assisted Gait Training on Multiple Sclerosis: A Systematic Review and Meta-analysis of Randomized Controlled Trials.
 Inner Retinal Layer Changes Reflect Changes in Ambulation Score in Patients with Primary Progressive Multiple Sclerosis.
 Effect of using of a lower-extremity exoskeleton on disability of people with multiple sclerosis.
 α-Crystallin B autoimmunity and multiple sclerosis.
 Diffusion tensor imaging metrics associated with future disability in multiple sclerosis.
 Investigating the Long-term Effect of Pregnancy on the Course of Multiple Sclerosis Using Causal Inference.
 Car accidents in drivers with Parkinson's disease or multiple sclerosis: A Swedish nationwide study.
 Impact of COVID-19 on prescribing patterns and treatment selection of disease modifying therapies in multiple sclerosis.
 Literature Commentary.
 Occurrence and Severity of Coronavirus Disease 2019 Are Associated With Clinical Disability Worsening in Patients With Multiple Sclerosis.
 Safety and Effectiveness of Cladribine in Multiple Sclerosis: Real-World Clinical Experience From 5 Tertiary Hospitals in Portugal.
 Brain and immune system-derived extracellular vesicles mediate regulation of complement system, extracellular matrix remodeling, brain repair and antigen tolerance in Multiple sclerosis.
 Relationship between medical history and multiple sclerosis: A-case-control study.
 High intensity exercise training on functional outcomes in persons with multiple sclerosis: A systematic review.
 Interoceptive and metacognitive facets of fatigue in multiple sclerosis.
 Deep learning-based PET/MR radiomics for the classification of annualized relapse rate in multiple sclerosis.
 Multiple sclerosis incidence temporal trend in the Northeast of Iran: Using the Empirical Bayesian method.
 Validation of the Czech Version of the Dysphagia in Multiple Sclerosis Questionnaire (DYMUS).
 Influence of oral tobacco versus smoking on multiple sclerosis disease activity and progression.
 The clinical-radiological paradox in multiple sclerosis: myth or truth?
 Frequency of NMOSD misdiagnosis in a cohort from Latin America: Impact and evaluation of different contributors.
 Effect of different types of exercise on fitness in people with multiple sclerosis: A network meta-analysis.
 Cognitive rehabilitation and mindfulness reduce cognitive complaints in multiple sclerosis (REMIND-MS): A randomized controlled trial.
 [Communicating about the flare-up and its treatment].
 Ublituximab: A new FDA-approved anti-CD20 mAb for relapsing forms of multiple sclerosis.
 A metabolome-wide Mendelian randomization study prioritizes potential causal circulating metabolites for multiple sclerosis.
 Peptide Mimotope-Enabled Quantification of Natalizumab Arm Exchange During Multiple Sclerosis Treatment.
 Toxoplasma gondii attenuates the ethidium bromide induced demyelination lesions in multiple sclerosis model rats.
 Cladribine tablets for highly active relapsing-remitting multiple sclerosis in Poland: a real-world, multi-centre, retrospective, cohort study during the COVID-19 pandemic.
 Links between Neuroanatomy and Neurophysiology with Turning Performance in People with Multiple Sclerosis.
 TCA cycle deficiency in multiple sclerosis.
 Work Barriers and Job Adjustments of People with Multiple Sclerosis: A Systematic Review.
 Ocrelizumab Treatment Modulates B-Cell Regulating Factors in Multiple Sclerosis.
 [15th Post-ECTRIMS Meeting: a review of the latest developments presented at the 2022 ECTRIMS Congress (Part II)].
 [Multiple sclerosis, work and job retention].
 Does memory rehabilitation improve health outcomes in people with multiple sclerosis? A Cochrane Review summary with commentary.
 Prevalence, incidence and clinical features of neuromyelitis optica spectrum disorders in northern Japan.
 ["I survive well"].
 Sars-CoV2 infection in pregnant women with multiple sclerosis.
 Cycling in primary progressive multiple sclerosis (CYPRO): study protocol for a randomized controlled superiority trial evaluating the effects of high-intensity interval training in persons with primary progressive multiple sclerosis.
 Somatosensory evoked potentials and magnetic resonance imaging of the central nervous system in early multiple sclerosis.
 ECTRIMS/EAN consensus on vaccination in people with multiple sclerosis: Improving immunization strategies in the era of highly active immunotherapeutic drugs.
 Cerebrospinal fluid kappa free light chains for the diagnosis of multiple sclerosis: A systematic review and meta-analysis.
 Adherence and persistence to self-administered disease-modifying therapies in patients with multiple sclerosis: A multisite analysis.
 Osteopontin expression and the effect of anti-VLA-4 mAb treatment in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis.
 Familial Mediterranean Fever and multiple sclerosis treated with ocrelizumab: Case report.
 B-Cell-Directed Therapies: A New Era in Multiple Sclerosis Treatment.
 Applying multidimensional computerized adaptive testing to the MSQOL-54: a simulation study.
 The concentrations of antibodies to Epstein-Barr virus decrease during ocrelizumab treatment.
 Temporal evolution of new T1-weighted hypo-intense lesions and central brain atrophy in patients with a first clinical demyelinating event treated with subcutaneous interferon β-1a.
 CNS resilience in the progression of MS.
 Disability accrual in primary and secondary progressive multiple sclerosis.
 Role of selective attention in fatigue in neurological disorders.
 Rivastigmine for Cognitive Impairment in Multiple Sclerosis: A Prospective Randomized Open Label study with Blinded End-Point Assessment.
 Neurofilament light chains in serum as biomarkers of axonal damage in early MS lesions: a histological-serological correlative study.
 Semaglutide, a novel glucagon-like peptide-1 agonist, amends experimental autoimmune encephalomyelitis-induced multiple sclerosis in mice: Involvement of the PI3K/Akt/GSK-3β pathway.
 Evaluation of in vivo lithium chloride effects as a GSK3-β inhibitor on human adipose derived stem cells differentiation into oligodendrocytes and re-myelination in an animal model of multiple sclerosis.
 Prediction of the information processing speed performance in multiple sclerosis using a machine learning approach in a large multicenter magnetic resonance imaging data set.
 Pediatric Multiple Sclerosis-Experience of a Tertiary Care Center.
 Cerebrospinal fluid kappa free light chains for the diagnosis of multiple sclerosis: A consensus statement.
 Contrast-enhanced double inversion recovery sequence for patients with multiple sclerosis: feasibility of subtraction images between pre- and post-contrast images.
 A backpack-based myeloid cell therapy for multiple sclerosis.
 The potential therapeutic effect of statins in multiple sclerosis: beneficial or detrimental effects.
 Efficacy of ultraviolet B radiation versus vitamin D(3) on postural control and cognitive functions in relapsing-remitting multiple sclerosis: A randomized controlled study.
 Neural correlates of digital measures shown by structural MRI: a post-hoc analysis of a smartphone-based remote assessment feasibility study in multiple sclerosis.
 SARS-CoV-2 omicron breakthrough infections in patients with multiple sclerosis.
 Association of Serum Neurofilament Light Chain Levels at Disease Onset With Disability Worsening in Patients With a First Demyelinating Multiple Sclerosis Event Not Treated With High-Efficacy Drugs.
 [Not Available].
 The NHANES Biological Age Index demonstrates accelerated aging in MS patients.
 Mobile App Interventions for Parkinson's Disease, Multiple Sclerosis and Stroke: A Systematic Literature Review.
 Neurophysiological MEG markers of cognitive impairment and performance validity in multiple sclerosis.
 The impact of stigma on perceived quality of life and experience of anxiety and depression in individuals diagnosed with MS.
 Multiple sclerosis mortality in New Zealand: a nationwide prospective study.
 Implications of immunometabolism for smouldering MS pathology and therapy.
 Structural dynamics of moonlighting intrinsically disordered proteins - A black box in multiple sclerosis.
 Previous disease-modifying treatments influence T lymphocyte kinetics in people with multiple sclerosis switching to ocrelizumab.
 Observed associations between indicators of socioeconomic status and risk of multiple sclerosis in Sweden are explained by a few lifestyle-related factors.
 Gut microbiome composition is associated with long-term disability worsening in multiple sclerosis.
 A Phase 1b, Open-Label Study to Evaluate the Safety and Tolerability of the Putative Remyelinating Agent, Liothyronine, in Individuals with MS.
 People with multiple sclerosis and unilateral peripheral vestibular loss demonstrate similar alterations in head and trunk turning kinematics compared to healthy controls.
 Self-reported restrictions in different life domains and associated factors among people with multiple sclerosis in Sweden.
 Editorial: Environmental factors influencing the immune functions during multiple sclerosis.
 Toe clearance facilitation to improve walking in multiple sclerosis: The effect of cyclical focal muscle vibration.
 Letter to the Editor: Remission of Graves' Disease After Initiation of Ocrelizumab in Patients with Multiple Sclerosis.
 Choroid plexuses at the interface of peripheral immunity and tissue repair in multiple sclerosis.
 More gain, less pain: How resistance training affects immune system functioning in multiple sclerosis patients: A review.
 Neural stem cell transplantation in patients with progressive multiple sclerosis: an open-label, phase 1 study.
 Sensorimotor network dynamics predict decline in upper and lower limb function in people with multiple sclerosis.
 No seasonality in the risk of multiple sclerosis in an equatorial country: A case-control ecological study.
 Cell-based experimental strategies for myelin repair in multiple sclerosis.
 Utility of the tibial nerve somatosensory evoked potentials in differentiating between neuromyelitis optica spectrum disorders and multiple sclerosis.
 Immunosuppressive Effects of Two Probiotics, Lactobacillus paracasei DSM 13434 and Lactobacillus plantarum DSM 15312, on CD4+ T Cells of Multiple Sclerosis Patients.
 A national case-control study investigating demographic and environmental factors associated with NMOSD.
 Effect of GBCA Use on Detection and Diagnostic Performance of the Central Vein Sign: Evaluation Using a 3-T FLAIR* Sequence in Patients With Suspected Multiple Sclerosis.
 Translingual neurostimulation combined with physical therapy to improve walking and balance in multiple sclerosis (NeuroMSTraLS): Study protocol for a randomized controlled trial.
 OCRELIZUMAB THERAPY IN PATIENTS WITH ANTI-HBC ANTIBODIES - A PRELIMINARY STUDY.
 The Role of Vitamin D in Neuroprotection in Multiple Sclerosis: An Update.
 Contribution of Intravital Neuroimaging to Study Animal Models of Multiple Sclerosis.
 The relationship between severity of overactive bladder symptoms and cognitive dysfunction, anxiety and depression in female patients with multiple sclerosis: Running head: OAB-V8, BICAMS and HAD scale in MS.
 Coping as a Moderator of Associations Between Symptoms and Functional and Affective Outcomes in the Daily Lives of Individuals With Multiple Sclerosis.
 Correlation between patient-reported manual ability and three objective measures of upper limb function in people with multiple sclerosis.
 Discrepancies between self-report and objective sleep outcomes are associated with cognitive impairment and fatigue in people with multiple sclerosis and insomnia.
 Impact of adherence to disease modifying therapies on long-term clinical and economic outcomes in multiple sclerosis: A claims analysis of real-world data.
 Assessment of muscle fatigue in multiple sclerosis patients in electromyographic examinations.
 Study for the validation of the FeetMe® integrated sensor insole system compared to GAITRite® system to assess gait characteristics in patients with multiple sclerosis.
 Thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta treatment for multiple sclerosis.
 Dimethyl Fumarate and Intestine: From Main Suspect to Potential Ally against Gut Disorders.
 The association between fingolimod and mental health outcomes in a cohort of Multiple Sclerosis patients with stress.
 Endothelial Function in Patients with Multiple Sclerosis: The Role of GLP-1 Agonists, Lipoprotein Subfractions, and Redox Balance.
 Profiling cognitive-motor interference in a large sample of persons with progressive multiple sclerosis and impaired processing speed: results from the CogEx study.
 Brain-derived neurotrophic factor, neurofilament light and glial fibrillary acidic protein do not change in response to aerobic training in people with MS-related fatigue - a secondary analysis of a randomized controlled trial.
 Reliability and acceptance of dreaMS, a software application for people with multiple sclerosis: a feasibility study.
 Automatic segmentation of the thalamus using a massively trained 3D convolutional neural network: higher sensitivity for the detection of reduced thalamus volume by improved inter-scanner stability.
 Oral Cladribine Impairs Intermediate, but Not Conventional, Monocyte Transmigration in Multiple Sclerosis Patients across a Model Blood-Brain Barrier.
 The natural history of primary progressive multiple sclerosis: insights from the German NeuroTransData registry.
 Impact of the first Gulf war on multiple sclerosis risk in Kuwait: a quasi-experimental study.
 Tolerability of immune checkpoint inhibitors in patients with cancer and pre-existing multiple sclerosis.
 Pathophysiology of multiple sclerosis damage and repair: Linking cerebral hypoperfusion to the development of irreversible tissue loss in multiple sclerosis using magnetic resonance imaging.
 Explaining the burden of psychosocial factors on the worsening symptoms of MS: a qualitative study of patients' experiences.
 Neuro rehabilitation effectiveness based on virtual reality and tele rehabilitation in people with multiple sclerosis in Argentina: Reavitelem study.
 Effect of deep gray matter atrophy on information processing speed in early relapsing-remitting multiple sclerosis.
 Comparative effectiveness of cladribine tablets versus other oral disease-modifying treatments for multiple sclerosis: Results from MSBase registry.
 Cross-Trait Mendelian Randomization Study to Investigate Whether Migraine Is a Risk Factor for Multiple Sclerosis.
 Alemtuzumab for multiple sclerosis.
 Siblings reduce multiple sclerosis risk by preventing delayed primary Epstein-Barr virus infection.
 Preliminary race-ethnicity-based analyses of fall risk among people with multiple sclerosis.
 Body temperatures, thermal comfort, and neuropsychological responses to air temperatures ranging between 12°C and 39°C in people with Multiple Sclerosis.
 Double inversion recovery to detect cervical spinal cord multiple sclerosis lesions.
 Multisite chronic pain and the risk of autoimmune diseases: A Mendelian randomization study.
 Socioeconomic, Clinical, and Laboratory Parameters Differentiating Pediatric Patients With MOG Antibody-Associated Disease and Multiple Sclerosis.
 Isotretinoin use for acne is not associated with an increased risk of migraine, fibromyalgia, multiple sclerosis, or neuropathy: A matched, retrospective cohort study.
 Pilot Lightweight Denoising Algorithm for Multiple Sclerosis on Spine MRI.
 Diverticulitis, AAA, Multiple Sclerosis, Iron Deficiency Anemia, Testicular Torsion.
 Incidence of Optic Neuritis and the Associated Risk of Multiple Sclerosis for Service Members of U.S. Armed Forces.
 The societal costs of multiple sclerosis in Lebanon: a cross-sectional study.
 The consequences of switching from Gilenya® to generics for fingolimod.
 Anti-CD40L antibody frexalimab slows new brain lesions in multiple sclerosis.
 Patient-reported outcomes are the strongest predictors of disease disability in intramuscular interferon β-1a users.
 Disease Evolution in Women With Highly Active MS Who Suspended Natalizumab During Pregnancy vs Rituximab/Ocrelizumab Before Conception.
 Late Component of the Trigemino-Cervical Reflex: Clinical and Neuroradiological Correlations.
 Cerebellar connectome alterations and associated genetic signatures in multiple sclerosis and neuromyelitis optica spectrum disorder.
 Side effects following vaccination in multiple sclerosis: a prospective, multi-centre cohort study.
 Neuropathologically informed imaging of cortical grey matter lesions in MS - A pilot study.
 A retrospective evaluation of seroconversion after COVID-19 during the early Omicron wave in fully vaccinated multiple sclerosis patients receiving anti-CD20 therapies.
 An update on the use of sphingosine 1-phosphate receptor modulators for the treatment of relapsing multiple sclerosis.
 The increased perceived exertion during the six minute walking test is not accompanied by changes in cost of walking, gait characteristics or muscle fatigue in persons with multiple sclerosis.
 Citrullinated human and murine MOG(35-55) display distinct biophysical and biochemical behavior.
 Fampridine in multiple sclerosis patients with acute phase of cervical transverse myelitis: a double-blind, randomized placebo-controlled trial.
 The Role of MRI in Differentiating Demyelinating and Inflammatory (not Infectious) Myelopathies.
 Diversification and expansion of the EBV-reactive cytotoxic T lymphocyte repertoire following autologous haematopoietic stem cell transplant for multiple sclerosis.
 Characterizing multiple sclerosis disease progression using a combined structural and functional connectivity metric.
 Early prognosticators of later TSPO-PET-measurable microglial activation in multiple sclerosis.
 Challenges and Opportunities for the Promising Biomarker Blood Neurofilament Light Chain.
 Epidemiology of demyelinating diseases in Mexico: A registry-based study.
 Biotin induced biochemical hyperthyroidism: a case report and review of the literature.
 Differential vulnerability of thalamic nuclei in multiple sclerosis.
 A systematic literature review of ankle-foot orthosis and functional electrical stimulation foot-drop treatments for persons with multiple sclerosis.
 Impact of menopause on relapse rate and disability level in patients with multiple sclerosis (MS): a systematic review and meta-analysis.
 T cell responses to SARS-CoV-2 vaccination differ by disease-modifying therapy for multiple sclerosis.
 B cell depletion therapy does not resolve chronic active multiple sclerosis lesions.
 Comparing RNA-sequencing datasets from astrocytes, oligodendrocytes, and microglia in multiple sclerosis identifies novel dysregulated genes relevant to inflammation and myelination.
 The association between PD-1 gene polymorphisms and susceptibility to multiple sclerosis.
 IL-3 worsens MS.
 Neuron-oligodendrocyte potassium shuttling at nodes of Ranvier protects against inflammatory demyelination.
 The radiologically isolated syndrome: revised diagnostic criteria.
 75th Annual Meeting of the American Academy of Neurology (AAN 2023).
 Does the inclusion of societal costs change the economic evaluations recommendations? A systematic review for multiple sclerosis disease.
 Illness intrusiveness: A key part of the cognition-mood link in multiple sclerosis.
 Gender differences in earnings among people with multiple sclerosis and associations with type of occupation and family composition: A population-based study with matched references.
 The roles of fungus in CNS autoimmune and neurodegeneration disorders.
 Long-lasting neutralizing antibodies and T cell response after the third dose of mRNA anti-SARS-CoV-2 vaccine in multiple sclerosis.
 Ratio of lymphocyte to monocyte area under the curve as a novel predictive factor for severe infection in multiple sclerosis.
 Antigen-independent IL-17A production by bystander-activated CD4(+)IL-1R1(+) cells in patients with multiple sclerosis.
 Liquid chromatography - tandem mass spectrometry method for determination of natalizumab in serum and cerebrospinal fluid of patients with multiple sclerosis.
 Drug-induced microglial phagocytosis in multiple sclerosis and experimental autoimmune encephalomyelitis and the underlying mechanisms.
 Correspondence among gray matter atrophy and atlas-based neurotransmitter maps is clinically relevant in multiple sclerosis.
 Role of omega-3 endocannabinoids in the modulation of T-cell activity in a multiple sclerosis experimental autoimmune encephalomyelitis (EAE) model.
 Mechanisms of Demyelination and Remyelination Strategies for Multiple Sclerosis.
 Cannabinoids in neuroinflammatory disorders: Focusing on multiple sclerosis, Parkinsons, and Alzheimers diseases.
 Immune Cell Contributors to the Female Sex Bias in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis.
 [The influence of fluoxetine on neuroimmune interaction in multiple sclerosis].
 Efficacy of surgical treatment in patients with trigeminal neuralgia secondary to multiple sclerosis: A prospective study of 18 cases with evaluation of outcome and complications by independent evaluators.
 Molecular and neuroimmune pharmacology of S1P receptor modulators and other disease-modifying therapies for multiple sclerosis.
 Comparison of Translocator Protein Expression Between Tumefactive Multiple Sclerosis and Glioblastoma.
 The association between cognition and gait disturbance in central nervous system demyelinating disorder with mild disability.
 [Hereditary optic neuropathy associated with demyelinating diseases of the central nervous system].
 An overall view of the most common experimental models for multiple sclerosis.
 Ocrelizumab effect on humoral and cellular immunity in multiple sclerosis and its clinical correlates: a 3-year observational study.
 Synapse Dysfunctions in Multiple Sclerosis.
 Downregulation of SF3B2 protects CNS neurons in models of multiple sclerosis.
 Effectiveness of BBIBP-CorV vaccine in preventing SARS-CoV2 infection and severe outcomes in people living with multiple sclerosis: A population-based study.
 Targeting miR-223 enhances myeloid-derived suppressor cell suppressive activities in multiple sclerosis patients.
 Ultrastructural Axon-Myelin Unit Alterations in Multiple Sclerosis Correlate with Inflammation.
 Factors and strategies affecting motor imagery ability in people with multiple sclerosis: a systematic review.
 BACE1 influences clinical manifestations and central inflammation in relapsing remitting multiple sclerosis.
 Neurodegeneration and humoral response proteins in cerebrospinal fluid associate with pediatric-onset multiple sclerosis and not monophasic demyelinating syndromes in childhood.
 Antibodies against SARS-CoV-2 S and N proteins in relapsing-remitting multiple sclerosis patients treated with disease-modifying therapies.
 No Association of Multiple Sclerosis with C9orf72 Hexanucleotide Repeat Size in an Austrian Cohort.
 [Not Available].
 Early derangement of axonal mitochondria occurs in a mouse model of progressive but not relapsing-remitting multiple sclerosis.
 Toll-like receptor 10 is down-regulated in serum of patients with relapsing-remitting multiple sclerosis but not associated with Epstein-Barr virus.
 Vaccine-breakthrough SARS-CoV-2 infections in people with multiple sclerosis and related conditions: An observational study by the New York COVID-19 Neuro-Immunology Consortium (NYCNIC-2).
 Immunoglobulin γ marker genes as effect modifiers of Epstein-Barr virus-multiple sclerosis association.
 An Exploration of Yoga in Occupational Therapy Practice for Multiple Sclerosis.
 Myelin Basic Protein in Oligodendrocyte-Derived Extracellular Vesicles as a Diagnostic and Prognostic Biomarker in Multiple Sclerosis: A Pilot Study.
 Th17/IL-17 Axis in HTLV-1-Associated Myelopathy Tropical Spastic Paraparesis and Multiple Sclerosis: Novel Insights into the Immunity During HAMTSP.
 Increased Risk for Acute Periapical Abscesses in Multiple Sclerosis Patients and the Possible Association with Epstein-Barr Virus.
 Plasma exchange in inflammatory demyelinating disorders of the central nervous system: reasonable use in the clinical practice.
 T cell responses to COVID-19 infection and vaccination in patients with multiple sclerosis receiving disease-modifying therapy.
 The immunomodulatory effects of all-trans retinoic acid and docosahexaenoic acid combination treatment on the expression of IL-2, IL-4, T-bet, and GATA3 genes in PBMCs of multiple sclerosis patients.
 The impact of cigarette smoking on cognitive processing speed and brain atrophy in multiple sclerosis.
 Establishment of regression-based normative isometric strength values for major lower limb muscle groups in persons with multiple sclerosis.
 Progressive motor impairment from "critical" demyelinating lesions of the cervicomedullary junction.
 DYMUS-Hr self-assessment questionnaire (Croatian version) for dysphagia in multiple sclerosis-validity, reliability, and cross-cultural adaptation.
 Rare and low-frequency coding genetic variants contribute to pediatric-onset multiple sclerosis.
 Suppression of MAPK/NF-kB and activation of Nrf2 signaling by Ajugarin-I in EAE model of multiple sclerosis.
 Nose to brain delivery of ibudilast micelles for treatment of multiple sclerosis in an experimental autoimmune encephalomyelitis animal model.
 Associations between myelin water imaging and measures of fall risk and functional mobility in multiple sclerosis.
 Real-world cost of care and site of care in patients with multiple sclerosis initiating infused disease-modifying therapies.
 Periventricular remyelination failure in multiple sclerosis: a substrate for neurodegeneration.
 Understanding the Health and Well-being of Women With Multiple Sclerosis.
 Letter to the Editor: Lazzaro responds to Rodríguez‑Sánchez et al.
 S1PR1 modulators in multiple sclerosis: Efficacy, safety, comparison, and chemical structure insights.
 The role of specialist nurses in detecting spasticity and related symptoms in multiple sclerosis.
 Escape, expand, embrace: the transformational lived experience of rediscovering the self and the other while dancing with Parkinson's or Multiple Sclerosis.
 Clinical validation of a multi-protein, serum-based assay for disease activity assessments in multiple sclerosis.
 Elevated Galectin-3 Is Associated with Aging, Multiple Sclerosis, and Oxidized Phosphatidylcholine-Induced Neurodegeneration.
 Structured Reporting in Multiple Sclerosis - Consensus-Based Reporting Templates for Magnetic Resonance Imaging of the Brain and Spinal Cord.
 Mediterranean diet is linked to less objective disability in multiple sclerosis.
 Effects of perinatal exposure to bisphenol A or S in EAE model of multiple sclerosis.
 High serum neurofilament levels are observed close to disease activity events in pediatric-onset MS and MOG antibody-associated diseases.
 Real-life outcomes for oral disease-modifying treatments of relapsing-remitting multiple sclerosis patients: Adherence and adverse event profiles from Marmara University.
 New consensus guidelines on vaccination in multiple sclerosis.
 Kappa free light chain and neurofilament light independently predict early multiple sclerosis disease activity-a cohort study.
 Polygenic risk score association with multiple sclerosis susceptibility and phenotype in Europeans.
 Quantitative magnetic resonance mapping of the myelin bilayer reflects pathology in multiple sclerosis brain tissue.
 Increased cytomegalovirus immune responses at disease onset are protective in the long-term prognosis of patients with multiple sclerosis.
 Presentation of Human Neural Stem Cell Antigens Drives Regulatory T Cell Induction.
 Axonal response of mitochondria to demyelination and complex IV activity within demyelinated axons in experimental models of multiple sclerosis.
 The impact of menopause on multiple sclerosis.
 Obesity increases blood-brain barrier permeability and aggravates the mouse model of multiple sclerosis.
 Characterisation of the safety profile of evobrutinib in over 1000 patients from phase II clinical trials in multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus: an integrated safety analysis.
 Validity, reliability and minimal detectable change of Mini-BESTest Turkish version in neurological disorders.
 Optical coherence tomography reflects clinically relevant gray matter damage in patients with multiple sclerosis.
 Inhibiting nighttime melatonin and boosting cortisol increase patrolling monocytes, phagocytosis, and myelination in a murine model of multiple sclerosis.
 Epsilon toxin-producing Clostridium perfringens colonize the multiple sclerosis gut microbiome overcoming CNS immune privilege.
 Dietary Polyphenols, Microbiome, and Multiple Sclerosis: From Molecular Anti-Inflammatory and Neuroprotective Mechanisms to Clinical Evidence.
 T cell-microbiome communication influences disease in MS model.
 Motherhood Experiences of Women With Multiple Sclerosis: A Thematic Meta-Synthesis.
 Emerging Perspectives on MRI Application in Multiple Sclerosis: Moving from Pathophysiology to Clinical Practice.
 Association of paramagnetic rim lesions and retinal layer thickness in patients with multiple sclerosis.
 Myopia in late adolescence and subsequent multiple sclerosis among men.
 Myelin heterogeneity for assessing normal appearing white matter myelin damage in multiple sclerosis.
 Therapeutic consequences in patients with both inflammatory rheumatic diseases and multiple sclerosis.
 Changes in stiffness of the optic nerve and involvement of neurofilament light chains in the course of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis.
 The Preference-Based Multiple Sclerosis Index: an assessment of its psychometric properties and translation into Turkish.
 Anti-CD20 therapies in multiple sclerosis: From pathology to the clinic.
 The association between brain volume loss and disability in multiple sclerosis: A systematic review.
 Natalizumab Promotes Activation of Peripheral Monocytes in Patients With Multiple Sclerosis.
 Population-Based Estimates for the Prevalence of Multiple Sclerosis in the United States by Race, Ethnicity, Age, Sex, and Geographic Region.
 HLA-DRB1*1501 influences long-term disability progression and tissue damage on MRI in relapse-onset multiple sclerosis.
 Comparative adherence trajectories of oral disease-modifying agents in multiple sclerosis.
 Phase 1 Evaluation of Elezanumab (Anti-Repulsive Guidance Molecule A Monoclonal Antibody) in Healthy and Multiple Sclerosis Participants.
 MRI pattern in acute optic neuritis: Comparing multiple sclerosis, NMO and MOGAD.
 The role of SIRT1 level and SIRT1 gene polymorphisms in optic neuritis patients with multiple sclerosis.
 Developing a patient care pathway for emotional support around the point of multiple sclerosis diagnosis: A stakeholder engagement study.
 Radiological Benefits of Vitamin D Status and Supplementation in Patients with MS-A Two-Year Prospective Observational Cohort Study.
 Multiple Sclerosis Pathogenesis: Possible Interplay between Vitamin D Status and Epstein Barr Virus Infection.
 Tissue-resident immune cells in the pathogenesis of multiple sclerosis.
 ALFF response interaction with learning during feedback in individuals with multiple sclerosis.
 A Phase 1 randomized study on the safety and pharmacokinetics of OCS-05, a neuroprotective disease modifying treatment for Acute Optic Neuritis and Multiple Sclerosis.
 Switch to ocrelizumab in MS patients treated with natalizumab in extended interval dosing at high risk of PML: A 96-week follow-up pilot study.
 Multi-omics analysis of magnetically levitated plasma biomolecules.
 Standard versus innovative robotic balance assessment for people with multiple sclerosis: a correlational study.
 Organizing pneumonia following ocrelizumab use in a patient with multiple sclerosis: A case report.
 Is there a role for herpes simplex virus type 1 in multiple sclerosis?
 Modulating miR-146a Expression by Hydrogen Sulfide Ameliorates Motor Dysfunction and Axonal Demyelination in Cuprizone-Induced Multiple Sclerosis.
 Insufficient sleep during adolescence and risk of multiple sclerosis: results from a Swedish case-control study.
 Validation of the French version of the Multiple Sclerosis Intimacy and Sexuality Questionnaire 15 Tools which help nurse for assessing the effect of perceived multiple sclerosis symptoms on sexual activity and satisfaction.
 Discovery of grey matter lesion-related immune genes for diagnostic prediction in multiple sclerosis.
 Chronic pruritus in multiple sclerosis and clinical correlates.
 Ferroptosis and central nervous system demyelinating diseases.
 Zinc and Central Nervous System Disorders.
 The Effect of Distance Empowerment Program on Self-efficacy Among Multiple Sclerosis Patients.
 Study protocol for an online lifestyle modification education course for people living with multiple sclerosis: the multiple sclerosis online course (MSOC).
 Depression, Anxiety, and Physical Activity in Older Adults With Multiple Sclerosis.
 Association of Val660Leu, progesterone receptor polymorphic variant, with susceptibility to RRMS disease.
 Shared decision making in the treatment of multiple sclerosis: A consensus based on Delphi methodology.
 Microglia rely on SYK signalling to mount neuroprotective responses in models of Alzheimer's disease and multiple sclerosis.
 Resveratrol-loaded macrophage exosomes alleviate multiple sclerosis through targeting microglia.
 Glia Connect Inflammation and Neurodegeneration in Multiple Sclerosis.
 The Role of Gut Dysbiosis and Potential Approaches to Target the Gut Microbiota in Multiple Sclerosis.
 Analysis of Differential TLR Activation in a Mouse Model of Multiple Sclerosis.
 Remibrutinib (LOU064) inhibits neuroinflammation driven by B cells and myeloid cells in preclinical models of multiple sclerosis.
 Concurrent multi-session anodal trans-cranial direct current stimulation enhances pelvic floor muscle training effectiveness for female patients with multiple sclerosis suffering from urinary incontinence and pelvic floor dysfunction: a randomized clinical trial study.
 Handling related publications reporting real-world evidence in network meta-analysis: a case study in multiple sclerosis.
 Gadolinium-based contrast agent exposures and physical and cognitive disability in multiple sclerosis.
 Diagnostic Performance of Adding the Optic Nerve Region Assessed by Optical Coherence Tomography to the Diagnostic Criteria for Multiple Sclerosis.
 Humoral immune responses remain quantitatively impaired but improve qualitatively in anti-CD20-treated patients with multiple sclerosis after three or four COVID-19 vaccinations.
 High serum neurofilament light chain levels correlate with brain atrophy and physical disability in multiple sclerosis.
 Speech deficits in multiple sclerosis: a narrative review of the existing literature.
 Neuroprotective influence of macular xanthophylls and retinal integrity on cognitive function among persons with multiple sclerosis.
 Pathways between multiple sclerosis, sleep disorders, and cognitive function: Longitudinal findings from The Nurses' Health Study.
 Predictors for insufficient SARS-CoV-2 vaccination response upon treatment in multiple sclerosis.
 The presence of cerebellar B cell aggregates is associated with a specific chemokine profile in the cerebrospinal fluid in a mouse model of multiple sclerosis.
 Structural covariance in subcortical regions in multiple sclerosis and neuromyelitis optica spectrum disorders: An MRI-based study with automated brain volumetry.
 MHC class I and MHC class II reporter mice enable analysis of immune oligodendroglia in mouse models of multiple sclerosis.
 Symptomatic COVID-19 course and outcomes after three mRNA vaccine doses in multiple sclerosis patients treated with high-efficacy DMTs.
 The correlation between 9-HPT and patient-reported measures of upper limb function in multiple sclerosis: a systematic review and meta-analysis.
 Efficacy of Diet on Fatigue and Quality of Life in Multiple Sclerosis: A Systematic Review and Network Meta-analysis of Randomized Trials.
 Possible role of the NLRP3 inflammasome and the gut-brain axis in multiple sclerosis-related depression.
 Changes in Gut Microbiota and Multiple Sclerosis: A Systematic Review.
 Exercise Therapy in Early Multiple Sclerosis Improves Physical Function But Not Cognition: Secondary Analyses From a Randomized Controlled Trial.
 Spinal cord reserve in multiple sclerosis.
 Effects and optimal dosage of resistance training on strength, functional capacity, balance, general health perception, and fatigue in people with multiple sclerosis: a systematic review and meta-analysis.
 Association of serum neurofilament light with microglial activation in multiple sclerosis.
 Comparative Effectiveness of Autologous Hematopoietic Stem Cell Transplant vs Fingolimod, Natalizumab, and Ocrelizumab in Highly Active Relapsing-Remitting Multiple Sclerosis.
 The impact of the Australian Black Summer Bushfires and the COVID-19 pandemic on wellbeing in persons with multiple sclerosis; preparation for future and ongoing crises.
 The association between disability progression, relapses, and treatment in early relapse onset MS: an observational, multi-centre, longitudinal cohort study.
 Twelve Weeks of Intermittent Caloric Restriction Diet Mitigates Neuroinflammation in Midlife Individuals with Multiple Sclerosis: A Pilot Study with Implications for Prevention of Alzheimer's Disease.
 GPX4 aggravates experimental autoimmune encephalomyelitis by inhibiting the functions of CD4(+) T cells.
 Tolerogenic Nanovaccine for Prevention and Treatment of Autoimmune Encephalomyelitis.
 Eye-tracking control of an adjustable electric bed: construction and validation by immobile patients with multiple sclerosis.
 Validity and reliability of physical activity measures in multiple sclerosis.
 Upper limb contribution during tandem gait in multiple sclerosis: An early marker of balance impairments.
 Rehabilitation treatment of multiple sclerosis.
 Acute intermittent hypoxia alters disease course and promotes CNS repair including resolution of inflammation and remyelination in the experimental autoimmune encephalomyelitis model of MS.
 Signaling mechanisms involved in the regulation of remyelination in multiple sclerosis: a mini review.
 Cell reprogramming for oligodendrocytes: A review of protocols and their applications to disease modeling and cell-based remyelination therapies.
 Myelin Basic Protein Fragmentation by Engineered Human Proteasomes with Different Catalytic Phenotypes Revealed Direct Peptide Ligands of MS-Associated and Protective HLA Class I Molecules.
 Role of tumor necrosis factor-alpha in the central nervous system: a focus on autoimmune disorders.
 Global, regional, and national burden of multiple sclerosis from 1990 to 2019: Findings of global burden of disease study 2019.
 Cyclophosphamide for severe acute forms of central nervous system inflammatory disorders.
 Multiple sclerosis as a model to investigate SARS-CoV-2 effect on brain atrophy.
 Microglia subtypes in acute, subacute, and chronic multiple sclerosis.
 Seasonal Changes in Serum Metabolites in Multiple Sclerosis Relapse.
 Risk factors for multiple sclerosis in the context of Epstein-Barr virus infection.
 Loss of the Novel Myelin Protein CMTM5 in Multiple Sclerosis Lesions and Its Involvement in Oligodendroglial Stress Responses.
 Editorial Comment: Gadolinium-Based Contrast Agent and the Central Vein Sign.
 Safety of COVID-19 vaccines in multiple sclerosis: A systematic review and meta-analysis.
 Multiple sclerosis and circadian rhythms: Can diet act as a treatment?
 Impact of COVID-19 vaccination or infection on disease activity in a radiologically isolated syndrome cohort: The VaxiRIS study.
 [Telephone assistance for neurological diseases: a systematic review].
 Volumetric brain changes in MOGAD: A cross-sectional and longitudinal comparative analysis.
 Marked central canal T2-hyperintensity in MOGAD myelitis and comparison to NMOSD and MS.
 Reinforcer pathology, probabilistic choice, and medication adherence in patients with multiple sclerosis.
 Serum Neurofilaments are a reliable biomarker to early detect PML in Multiple Sclerosis patients.
 Autologous haematopoietic stem cell transplantation for immune-mediated neurological diseases: what, how, who and why?
 Metabolic costs of walking and arm reaching in persons with mild multiple sclerosis.
 The gut microbiota in multiple sclerosis varies with disease activity.
 Efficacy of Rituximab Outlasts B-Cell Repopulation in Multiple Sclerosis: Time to Rethink Dosing?
 Deciphering crucial genes in multiple sclerosis pathogenesis and drug repurposing: A systems biology approach.
 Genetically Engineered Artificial Microvesicles Carrying Nerve Growth Factor Restrains the Progression of Autoimmune Encephalomyelitis in an Experimental Mouse Model.
 Radiological abnormalities in progressive multifocal leukoencephalopathy: Identifying typical and atypical imaging patterns for early diagnosis and differential considerations.
 Evaluating the Utility of Proteomics for the Identification of Circulating Pharmacodynamic Biomarkers of IFNβ-1a Biologics.
 Longitudinal characterisation of B and T-cell immune responses after the booster dose of COVID-19 mRNA-vaccine in people with multiple sclerosis using different disease-modifying therapies.
 Comparison of spouse and patient personality change judgments following MS onset.
 Characteristics of pediatric patients with multiple sclerosis and related disorders infected with SARS-CoV-2.
 The Psychological Impact of COVID-19 Pandemic on Persons with Multiple Sclerosis in Saudi Arabia.
 Smouldering Lesion in MS: Microglia, Lymphocytes and Pathobiochemical Mechanisms.
 Genetic Basis of Inflammatory Demyelinating Diseases of the Central Nervous System: Multiple Sclerosis and Neuromyelitis Optica Spectrum.
 Quality of life and mental health in multiple sclerosis patients during the COVID-19 Pandemic.
 Liposome-based nanoparticles impact on regulatory and effector phenotypes of macrophages and T cells in multiple Sclerosis patients.
 Validation of ELISA assays for the calculation of FLC indices for the diagnosis of intrathecal immunoglobulin synthesis.
 A Thematic Survey on the Reporting Quality of Randomized Controlled Trials in Rehabilitation: The Case of Multiple Sclerosis.
 Carboplatin ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by inducing T cell apoptosis.
 Regional white matter and gray matter damage and cognitive performances in multiple sclerosis according to sex.
 Assessment of intelligence quotient in patients with neuromyelitis optica spectrum disease and multiple sclerosis.
 Association of daily physical activity with brain volumes and cervical spinal cord areas in multiple sclerosis.
 Clinical features of MOGAD with brainstem involvement in the initial attack versus NMOSD and MS.
 Impact of extended interval dosing of ocrelizumab on immunoglobulin levels in multiple sclerosis.
 Immune profiling in multiple sclerosis: a single-center study of 65 cytokines, chemokines, and related molecules in cerebrospinal fluid and serum.
 Trojan Horse Nanocapsule Enabled In Situ Modulation of the Phenotypic Conversion of Th17 Cells to Treg Cells for the Treatment of Multiple Sclerosis in Mice.
 CSF CXCL13 and Chitinase 3-like-1 Levels Predict Disease Course in Relapsing Multiple Sclerosis.
 Annual Plasma Neurofilament Dynamics Is a Sensitive Biomarker of Disease Activity in Patients with Multiple Sclerosis.
 COVID-19 and Multiple Sclerosis: A Complex Relationship Possibly Aggravated by Low Vitamin D Levels.
 The effect of telenursing education of self-care on health-promoting behaviors in patients with multiple sclerosis during the COVID-19 pandemic: A clinical trial study.
 Nanoparticles Enhance Solubility and Neuroprotective Effects of Resveratrol in Demyelinating Disease.
 Intravesical injections of botulinum neurotoxin A to treat overactive bladder and/or detrusor overactivity related to multiple sclerosis: 5-Year continuation rate and specific risk factors for discontinuation-A study from the neuro-urology committee of the French Association of Urology.
 Physical activity participation in Australians with multiple sclerosis: associations with geographical remoteness.
 The prevalence of IgG antibodies against milk and milk antigens in patients with multiple sclerosis.
 Management approach including pembrolizumab for fingolimod-associated progressive multifocal leukoencephalopathy in a patient with relapsing-remitting multiple sclerosis.
 Retinal layer thickness predicts disability accumulation in early relapsing multiple sclerosis.
 Drug repurposing of ilepcimide that ameliorates experimental autoimmune encephalomyelitis via restricting inflammatory response and oxidative stress.
 Unraveling the heterogeneous pathological substrates of relapse-onset multiple sclerosis: a multiparametric voxel-wise 3 T MRI study.
 Appointment attendance behaviors in multiple sclerosis: Understanding the factors that differ between no shows, short notice cancellations, and attended appointments.
 Selective emergence of antibody-secreting cells in the multiple sclerosis brain.
 S1PR-1/5 modulator RP-101074 shows beneficial effects in a model of central nervous system degeneration.
 Identification of protein-protein interaction bridges for multiple sclerosis.
 Wobbly hedgehog syndrome- a progressive neurodegenerative disease.
 TREM2-dependent microglial function is essential for remyelination and subsequent neuroprotection.
 Biochemical biomarkers for multiple sclerosis.
 The effect of tetrahydrocannabinol:cannabidiol oromucosal spray on cognition: a systematic review.
 Human exposure to dust and heavy metals in industrial regions and its relationship with the prevalence of multiple sclerosis disease.
 Anti-SARS-CoV-2 monoclonal antibodies for the treatment of active COVID-19 in multiple sclerosis: An observational study.
 Physiotherapist and participant perspectives from a randomized-controlled trial of physiotherapist-supported online vs. paper-based exercise programs for people with moderate to severe multiple sclerosis.
 Emerging imaging and liquid biomarkers in multiple sclerosis.
 Corpus callosum damage to account for cognitive, affective, and social-cognitive dysfunctions in multiple sclerosis: A model of callosal disconnection syndrome?
 Anti-CD20 treatment and neutrophil function in central nervous system demyelinating diseases.
 Suppression of Experimental Autoimmune Encephalomyelitis in Mice by β-Hydroxy β-Methylbutyrate, a Body-Building Supplement in Humans.
 Comprehensible Machine-Learning-Based Models for the Pre-Emptive Diagnosis of Multiple Sclerosis Using Clinical Data: A Retrospective Study in the Eastern Province of Saudi Arabia.
 Effects of GABAergic Agents on Multiple Sclerosis. A Narrative Review of In-vivo Models.
 Long-term clinical, imaging and cognitive outcomes association with MS immunopathology.
 The nine hole peg test as an outcome measure in progressive MS trials.
 Self-efficacy trajectories of individuals newly diagnosed with multiple sclerosis.
 Automatic Assessment of the 2-Minute Walk Distance for Remote Monitoring of People with Multiple Sclerosis.
 Identifying shared genetic loci and common risk genes of rheumatoid arthritis associated with three autoimmune diseases based on large-scale cross-trait genome-wide association studies.
 Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis.
 Retina thickness in clinically affected and unaffected eyes in patients with aquaporin-4 immunoglobulin G antibody seropositive neuromyelitis optica spectrum disorders: a systematic review and meta-analysis.
 Low socioeconomic status was associated with a higher mortality risk in multiple sclerosis.
 Recurrent encephalopathy associated with pegylated beta-interferon treatment.
 Association of Vitamin D Polygenic Risk Scores and Disease Outcome in People With Multiple Sclerosis.
 Immune response to SARS-CoV-2 mRNA vaccination in multiple sclerosis patients after rituximab treatment interruption.
 Validity of serum neurofilament light chain as a prognostic biomarker of disease activity in multiple sclerosis.
 The CYP24A1 gene variant rs2762943 is associated with low serum 1,25-dihydroxyvitamin D levels in multiple sclerosis patients.
 Identification of the shared gene signatures and molecular mechanisms between multiple sclerosis and non-small cell lung cancer.
 Using the EQ-5D-5L to investigate quality-of-life impacts of disease-modifying therapy policies for people with multiple sclerosis (MS) in New Zealand.
 Dissecting shared genetic architecture between obesity and multiple sclerosis.
 Ferroptosis induces detrimental effects in chronic EAE and its implications for progressive MS.
 Individual Differences in the Patient Experience of Relapsing Multiple Sclerosis (RMS): A Multi-Country Qualitative Exploration of Drivers of Treatment Preferences Among People Living with RMS.
 Cross-syndrome: myasthenia gravis and the demyelinating diseases of the central nervous system combination. Systematic literature review and case reports.
 Chitinase Signature in the Plasticity of Neurodegenerative Diseases.
 Strengthening the link: Diet quality and disability in MS.
 Treatment of relapsing multiple sclerosis in Hungary - consensus recommendation from the Hungarian neuroimmunology society.
 Clinical and MRI measures to identify non-acute MOG-antibody disease in adults.
 Transgenic expression of the HERV-W envelope protein leads to polarized glial cell populations and a neurodegenerative environment.
 Multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) following COVID-19 vaccines: A systematic review.
 Effect of Dynamic Neuromuscular Stabilization on Balance, Trunk Function, Falling, and Spasticity in People With Multiple Sclerosis: A Randomized Controlled Trial.
 Exploring COVID-19 experiences for persons with multiple sclerosis and carers: An Australian qualitative study.
 Energy expenditure and perceived effort during uphill and downhill walking in people with multiple sclerosis.
 hnRNP A1 dysfunction in oligodendrocytes contributes to the pathogenesis of multiple sclerosis.
 Cognitive fatigue-related sensory gating deficits in people with multiple sclerosis.
 Assessing everyday functional activity in cognitively impaired people with multiple sclerosis: The use of Actual Reality(TM).
 Shared Molecular Signatures Across Zika Virus Infection and Multiple Sclerosis Highlight AP-1 Transcription Factor as a Potential Player in Post-ZIKV MS-Like Phenotypes.
 The value of Interferon β in multiple sclerosis and novel opportunities for its anti-viral activity: a narrative literature review.
 Association of Early Progression Independent of Relapse Activity With Long-term Disability After a First Demyelinating Event in Multiple Sclerosis.
 Epstein-Barr virus and multiple sclerosis.
 The biological sample collection of the OFSEP French MS registry: An essential tool dedicated to researchers.
 CXCL10 Is Associated with Increased Cerebrospinal Fluid Immune Cell Infiltration and Disease Duration in Multiple Sclerosis.
 [Alemtuzumab-induced Graves' disease].
 Repurposing drugs against Alzheimer's disease: can the anti-multiple sclerosis drug fingolimod (FTY720) effectively tackle inflammation processes in AD?
 Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis.
 Kappa Free Light Chain Index Predicts Disease Course in Clinically and Radiologically Isolated Syndromes.
 Prevalence of comorbidities in patients with multiple sclerosis using administrative data from 2007 to 2016 in Iran.
 In-depth characterization of long-term humoral and cellular immune responses to COVID-19m-RNA vaccination in multiple sclerosis patients treated with teriflunomide or alemtuzumab.
 Immune Response to Seasonal Influenza Vaccination in Multiple Sclerosis Patients Receiving Cladribine.
 Treadmill aerobic training improve beam-walking test, up-regulate expression of main proteins of myelin and myelination in the hippocampus of cuprizone-fed mice.
 Evaluation of Cell-Specific Epigenetic Age Acceleration in People With Multiple Sclerosis.
 Causal association of genetically determined circulating vitamin D metabolites and calcium with multiple sclerosis in participants of European descent.
 TNF-α/STAT1/CXCL10 mutual inflammatory axis that contributes to the pathogenesis of experimental models of multiple sclerosis: A promising signaling pathway for targeted therapies.
 Systematic overviews of partnership principles and strategies identified from health research about spinal cord injury and related health conditions: A scoping review.
 Association of Higher Ocrelizumab Exposure With Reduced Disability Progression in Multiple Sclerosis.
 Differential activity of transcription factor Sox9 in early and adult oligodendroglial progenitor cells.
 Aluminium in the Human Brain: Routes of Penetration, Toxicity, and Resulting Complications.
 Effects of exergaming on cognition, lower limb functional coordination, and stepping time in people with multiple sclerosis: a randomized controlled trial.
 Development and psychometric properties of a self-assessed knowledge questionnaire for caregivers of people with multiple sclerosis (CareKoMS): a cross-sectional study.
 Clinical correlates of R1 relaxometry and magnetic susceptibility changes in multiple sclerosis: a multi-parameter quantitative MRI study of brain iron and myelin.
 Comparison of MRI T2-lesion evolution in pediatric MOGAD, NMOSD, and MS.
 Single-Cell Transcriptomics Identifies Brain Endothelium Inflammatory Networks in Experimental Autoimmune Encephalomyelitis.
 Systematic review and meta-analysis of reflexology for people with multiple sclerosis: Systematic Review and Meta-Analysis.
 AbobotulinumtoxinA is effective in patients with urinary incontinence due to neurogenic detrusor overactivity regardless of spinal cord injury or multiple sclerosis etiology: Pooled analysis of two phase III randomized studies (CONTENT1 and CONTENT2).
 Investigation of Relationship Between Small Noncoding RNA (sncRNA) Expression Levels and Serum Iron, Copper, and Zinc Levels in Clinical Diagnosed Multiple Sclerosis Patients.
 Sequence similarity between SARS-CoV-2 nucleocapsid and multiple sclerosis-associated proteins provides insight into viral neuropathogenesis following infection.
 Orthotic shorts for improving gait and walking in multiple sclerosis: a feasibility study.
 Third COVID-19 vaccine dose for people with multiple sclerosis who did not seroconvert following two doses of BBIBP-CorV (Sinopharm) inactivated vaccine: A pilot study on safety and immunogenicity.
 Multiple Sclerosis Disease Activity and Disability Following Cessation of Fingolimod for Pregnancy.
 Wearable Sensor Technologies to Assess Motor Functions in People With Multiple Sclerosis: Systematic Scoping Review and Perspective.
 Central and peripheral myeloid-derived suppressor cell-like cells are closely related to the clinical severity of multiple sclerosis.
 COVID-19: The Course, Vaccination and Immune Response in People with Multiple Sclerosis: Systematic Review.
 Effect of multiple sclerosis disease-modifying therapies on the real-world effectiveness of two doses of BBIBP-CorV (Sinopharm) vaccine.
 The immunomodulatory roles of the gut microbiome in autoimmune diseases of the central nervous system: Multiple sclerosis as a model.
 Progress in Mechanism of Astragalus membranaceus and Its Chemical Constituents on Multiple Sclerosis.
 In vitro assessment of the binding and functional responses of ozanimod and its plasma metabolites across human sphingosine 1-phosphate receptors.
 Semi-supervised clustering of quaternion time series: Application to gait analysis in multiple sclerosis using motion sensor data.
 Immunoglobulin directly enhances differentiation of oligodendrocyte-precursor cells and remyelination.
 Analysis of Cdx2 VDR gene polymorphism rs11568820 in association with multiple sclerosis in Slovaks.
 Targeting L-Selectin Lymphocytes to Deliver Immunosuppressive Drug in Lymph Nodes for Durable Multiple Sclerosis Treatment.
 Potassium channels at the crossroads of neuroinflammation and myelination in experimental models of multiple sclerosis.
 COVID-19 and the Pandemic-Related Aspects in Pediatric Demyelinating Disorders.
 Fall risk is related to cognitive functioning in ambulatory multiple sclerosis patients.
 Unwrapping the "black box" of balance training in people with multiple sclerosis - A descriptive systematic review of intervention components, progression, and intensity.
 Effectiveness of a Cognitive-Motor Training Program in Reducing Attentional Cost During Walking in Patients With Multiple Sclerosis.
 Monitoring recovery after CNS demyelination, a novel tool to de-risk pro-remyelinating strategies.
 Struggling to Keep Up and Have a Good Life: A Qualitative Study of Living With Impaired Balance Control Due to Multiple Sclerosis.
 Gut-Microbiota, and Multiple Sclerosis: Background, Evidence, and Perspectives.
 Cladribine Effects on T and B Cells and T Cell Reactivity in Multiple Sclerosis.
 sEMG-controlled forearm bracelet and serious game-based rehabilitation for training manual dexterity in people with multiple sclerosis: a randomised controlled trial.
 Potentially toxic elements in the brains of people with multiple sclerosis.
 Delayed hypersensitivity to dimethyl fumarate: Report of 1 case and literature review.
 Oxygen treatment reduces neurological deficits and demyelination in two animal models of multiple sclerosis.
 A prospective study of cellular immune response to booster COVID-19 vaccination in multiple sclerosis patients treated with a broad spectrum of disease-modifying therapies.
 Icariin ameliorates behavioral deficits and neuropathology in a mouse model of multiple sclerosis.
 Increased Percentage of CD8(+)CD28(-) Regulatory T Cells With Fingolimod Therapy in Multiple Sclerosis.
 Shared genetic loci between Alzheimer's disease and multiple sclerosis: Crossroads between neurodegeneration and immune system.
 The Canadian Multiple Sclerosis Pregnancy Study: First-trimester miscarriages in women with multiple sclerosis.
 Microglia and meningeal macrophages depletion delays the onset of experimental autoimmune encephalomyelitis.
 The effects of cognition, quality of life, and fatigue on olfactory function in patients with multiple sclerosis.
 The association between tobacco smoking and depression and anxiety in people with multiple sclerosis: A systematic review.
 Natalizumab continuation versus switching to ocrelizumab after PML risk stratification in RRMS patients: a natural experiment.
 Physical function across the lifespan in adults with multiple sclerosis: An application of the Short Physical Performance Battery.
 Virtual reality-based therapy improves balance and reduces fear of falling in patients with multiple sclerosis. a systematic review and meta-analysis of randomized controlled trials.
 Transforming growth factor β (TGF-β) pathway in the immunopathogenesis of multiple sclerosis (MS); molecular approaches.
 Design, Radiosynthesis, and Evaluation of New Fluorinated Analogs of MeDAS for Myelin PET Imaging.
 Novel evaluation indicators of MOG(35∼55) induced experimental autoimmune encephalomyelitis in C57BL/6J mice.
 The effect of applying the nursing process based on the Theory of Goal Attainment on activities of daily living and quality of life in persons with multiple sclerosis during COVID-19 pandemic: a clinical trial.
 Antibody response elicited by the SARS-CoV-2 vaccine booster in patients with multiple sclerosis: Who gains from it?
 Fatty acid elongation by ELOVL6 hampers remyelination by promoting inflammatory foam cell formation during demyelination.
 Prefrontal hemodynamics during forward and backward walking, with and without a cognitive task, in people with multiple sclerosis.
 Dynamic Evolution of Humoral and T-Cell Specific Immune Response to COVID-19 mRNA Vaccine in Patients with Multiple Sclerosis Followed until the Booster Dose.
 The repertoire of CSF antiviral antibodies in patients with neuroinflammatory diseases.
 Ceramide is implicated in humoral peripheral and intrathecal autoimmune response in MS patients.
 Predictors of hospitalization due to infection in rituximab-treated MS patients.
 Higher diet quality is associated with short and long-term benefits on SF-6D health state utilities: a 5-year cohort study in an international sample of people with multiple sclerosis.
 [Relationship of patients with multiple sclerosis to vaccination against COVID-19].
 Skeletal Muscle Dysfunction in People With Multiple Sclerosis: A Physiological Target for Improving Physical Function and Mobility.
 Enhancing cognitive rehabilitation in multiple sclerosis with a disease-specific tool.
 Investigation of anti-galectin-8 levels in patients with multiple sclerosis: A consort-clinical study.
 Impact of Multiple Sclerosis on Foot Health and Quality of Life: A Prospective Case-Control Investigation.
 Reliability, Validity, and Responsiveness of the Patient-Specific Functional Scale for Measuring Mobility-Related Goals in People With Multiple Sclerosis.
 Anti-CD20 monoclonal antibody (mAb) therapy and colitis: A case series and review.
 Cerebrospinal fluid proteomics indicates immune dysregulation and neuronal dysfunction in antibody associated autoimmune encephalitis.
 Feasibility and usability of a new home-based immersive virtual reality headset-based dexterity training in multiple sclerosis.
 Cerebrospinal fluid inflammatory biomarkers for disease progression in Alzheimer's disease and multiple sclerosis: a systematic review.
 Myelin insulation as a risk factor for axonal degeneration in autoimmune demyelinating disease.
 Telerehabilitation versus virtual reality supported task-oriented circuit therapy on upper limbs and trunk functions in patients with multiple sclerosis: A randomized controlled study.
 [Psychometric Evaluation of the 'German Neurological Fatigue Index for Multiple Sclerosis (NFI-MS-G)' in a Sample of Rehabilitation Patients with Multiple Sclerosis].
 Predicting sense of coherence among caregiving partners of persons with multiple sclerosis.
 From methylation to myelination: epigenomic and transcriptomic profiling of chronic inactive demyelinated multiple sclerosis lesions.
 Investigation of the safety of live attenuated varicella-zoster virus vaccination in patients with relapse-remitting multiple sclerosis treated with natalizumab: A case series and review of the literature.
 A Vision-Based Framework for Predicting Multiple Sclerosis and Parkinson's Disease Gait Dysfunctions-A Deep Learning Approach.
 Identification of potential functional peptides involved in demyelinating injury in the central nervous system.
 Improvements in gait and balance in patients with multiple sclerosis after treatment with coconut oil and epigallocatechin gallate. A pilot study.
 A registered report of a crossover study on the effects of face masks on walking adaptability in people with Parkinson's disease and multiple sclerosis.
 MCAM+ brain endothelial cells contribute to neuroinflammation by recruiting pathogenic CD4+ T lymphocytes.
 Criterion validity of muscle strain analyses of skeletal muscle function in patients with multiple sclerosis.
 Treatment With Erythropoietin for Patients With Optic Neuritis: Long-term Follow-up.
 Experimental encephalomyelitis at age 90, still relevant and elucidating how viruses trigger disease.
 Anti-GABA-A Receptor Antibody-Mediated Epilepsia Partialis Continua After Treatment With Alemtuzumab: A Case Report.
 Metabolic Stability of the Demyelination Positron Emission Tomography Tracer [(18)F]3-Fluoro-4-Aminopyridine and Identification of Its Metabolites.
 Identification of astrocyte regulators by nucleic acid cytometry.
 Complementary use of statistical parametric mapping and gait profile score to describe walking alterations in multiple sclerosis: a cross-sectional study.
 Targeting CD20 in multiple sclerosis - review of current treatment strategies.
 Oral Pathobionts Promote MS-like Symptoms in Mice.
 Unraveling the Connection of Epstein-Barr Virus and Its Glycoprotein M(146-157) Peptide with Neurological Ailments.
 Retrospective analysis of effectiveness of fingolimod in real life setting in Turkey (REFINE).
 Family health conditions and parental occupational status modify the relationship between pediatric-onset multiple sclerosis and parental health-related quality of life.
 Optic neuritis: current challenges in diagnosis and management.
 Retrospective Cohort Study of Patient-Reported Urinary Tract Infection Signs and Symptoms Among Individuals With Neurogenic Bladder.
 Oxygen cost of walking and its relationship with body composition in multiple sclerosis.
 Insights into the mechanism of oligodendrocyte protection and remyelination enhancement by the integrated stress response.
 Specific Patterns of Immune Cell Dynamics May Explain the Early Onset and Prolonged Efficacy of Cladribine Tablets: A MAGNIFY-MS Substudy.
 1,25(OH)(2)D3 Differently Modulates the Secretory Activity of IFN-DC and IL4-DC: A Study in Cells from Healthy Donors and MS Patients.
 High-Resolution Motion-corrected 7.0-T MRI to Derive Morphologic Measures from the Human Cerebellum in Vivo.
 Decentralised clinical trials in multiple sclerosis research.
 Burden and resources in caregivers of people with multiple sclerosis: A qualitative study.
 Serology results after COVID vaccine in multiple sclerosis patients treated with fingolimod.
 Reliability, validity and clinical usability of a robotic assessment of finger proprioception in persons with multiple sclerosis.
 The potential for treg-enhancing therapies in nervous system pathologies.
 Remote Observational Research for Multiple Sclerosis: A Natural Experiment.
 Modulation of p38 MAPK and Nrf2/HO-1/NLRP3 inflammasome signaling and pyroptosis outline the anti-neuroinflammatory and remyelinating characters of Clemastine in EAE rat model.
 Tumefactive Demyelination in MOG Ab-Associated Disease, Multiple Sclerosis, and AQP-4-IgG-Positive Neuromyelitis Optica Spectrum Disorder.
 Deviation From Normative Whole Brain and Deep Gray Matter Growth in Children With MOGAD, MS, and Monophasic Seronegative Demyelination.
 Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.
 Improving risk prediction for target subpopulations: Predicting suicidal behaviors among multiple sclerosis patients.
 Experiences of persons with multiple sclerosis with the Covid-19 vaccination: A cross-sectional study of the Swiss Multiple Sclerosis Registry.
 The Neutrophil-to-Lymphocyte Ratio and the Monocyte-to-Lymphocyte Ratio Predict Expanded Disability Status Scale Score at One Year in Pediatric Neuromyelitis Optica Spectrum Disorder but not in Multiple Sclerosis.
 Cell therapy procedure using anti-inflammatory macrophage M2 can potentially reduce Clinical Score in animals with Experimental Autoimmune Encephalomyelitis: A preclinical systematic review and meta-analysis study.
 CCL20/CCR6 chemokine signaling is not essential for pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.
 Dimethyl fumarate-related immune and transcriptional signature is associated with clinical response in multiple sclerosis-treated patients.
 Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions.
 Serum neurofilament light levels in natalizumab-treated patients with multiple sclerosis who switch to extended interval dosing from every-4-week dosing in real-world clinical practice.
 Imaging CD19+ B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model using Positron Emission Tomography.
 NVX-CoV2373-induced T- and B-cellular immunity in immunosuppressed people with multiple sclerosis that failed to respond to mRNA and viral vector SARS-CoV-2 vaccines.
 Sudden Death Associated With Possible Flare-Ups of Multiple Sclerosis After COVID-19 Vaccination and Infection: A Case Report and Literature Review.
 Lipocalin-2 promotes adipose-macrophage interactions to shape peripheral and central inflammatory responses in experimental autoimmune encephalomyelitis.
 TSPO-Detectable Chronic Active Lesions Predict Disease Progression in Multiple Sclerosis.
 Trends in Botulinum Toxin Use among Patients with Multiple Sclerosis: A Population-Based Study.
 Dysregulation of miR-193a serves as a potential contributor to MS pathogenesis via affecting RhoA and Rock1.
 Sleep Disorders in Patients with Neurologic Disease.
 Physical Activity in Multiple Sclerosis: Meeting the Guidelines at the Time of the COVID-19 Pandemic.
 Humoral immunity to SARS-CoV-2 mRNA vaccination in multiple sclerosis: the relevance of time since last rituximab infusion and first experience from sporadic revaccinations.
 Schwann Cell Remyelination in the Multiple Sclerosis Central Nervous System.
 Enhancing the functionality of self-assembled immune signals using chemical crosslinks.
 Cross-reactive EBNA1 immunity targets alpha-crystallin B and is associated with multiple sclerosis.
 The Effects of NLY01, a Novel Glucagon-Like Peptide-1 Receptor Agonist, on Cuprizone-Induced Demyelination and Remyelination: Challenges and Future Perspectives.
 Cis-p-tau plays crucial role in lysolecithin-induced demyelination and subsequent axonopathy in mouse optic chiasm.
 Clostridium perfringens Epsilon Toxin Binds to and Kills Primary Human Lymphocytes.
 Multiple sclerosis and COVID-19: A retrospective study in Iran.
 Worldwide prevalence of neuromyelitis optica spectrum disorder (NMOSD) and neuromyelitis optica (NMO): a systematic review and meta-analysis.
 Vascular function and cognition in persons with multiple sclerosis: Preliminary examination.
 Symptom severity is a major determinant of cannabis-based products use among people with multiple sclerosis.
 Hsp65-producing Lactococcus lactis inhibits experimental autoimmune encephalomyelitis by preventing cell migration into spinal cord.
 Higher throughput workflow with sensitive, reliable and automatic quantification of myelination in vitro suitable for drug screening.
 Dimethyl Fumarate or Teriflunomide for Relapsing-Remitting Multiple Sclerosis: A Meta-analysis of Post-marketing Studies.
 Astroglial Cell-to-Cell Interaction with Autoreactive Immune Cells in Experimental Autoimmune Encephalomyelitis Involves P2X7 Receptor, β(3)-Integrin, and Connexin-43.
 RNF157 attenuates CD4(+) T cell-mediated autoimmune response by promoting HDAC1 ubiquitination and degradation.
 Estimated prevalence of AQP4 positive neuromyelitis optica spectrum disorder and MOG antibody associated disease in São Paulo, Brazil.
 [Family planning in men and women with multiple sclerosis. Analysis of the Andalusian Registry (2018-2022)].
 Comparative efficacy and safety of disease-modifying therapies in patients with relapsing multiple sclerosis: A systematic review and network meta-analysis.
 [Differential diagnosis of immune reconstitution inflammatory syndrome and progressive multifocal leukoencephalopathy after natalizumab withdrawal].
 Chemogenetic activation of locus coeruleus neurons ameliorates the severity of multiple sclerosis.
 Serum Neurofilament Light Chain as Biomarker for Cladribine-Treated Multiple Sclerosis Patients in a Real-World Setting.
 Corpus callosum involvement in MOG antibody-associated disease in comparison to AQP4-IgG-seropositive neuromyelitis optica spectrum disorder and multiple sclerosis.
 Complexity and pitfalls in maximal exercise testing for persons with multiple sclerosis.
 Altered Expression of Autophagy Biomarkers in Hippocampal Neurons in a Multiple Sclerosis Animal Model.
 Smartphone accelerometry for quantifying core stability and developing exercise training progressions in people with multiple sclerosis.
 Relevance of kappa free light chains index in patients with aquaporin-4 or myelin-oligodendrocyte-glycoprotein antibodies.
 Targeting B Cells and Microglia in Multiple Sclerosis With Bruton Tyrosine Kinase Inhibitors: A Review.
 The RNA helicase DDX39B activates FOXP3 RNA splicing to control T regulatory cell fate.
 Replacing sitting with light-intensity physical activity throughout the day versus 1 bout of vigorous-intensity exercise: similar cardiometabolic health effects in multiple sclerosis. A randomised cross-over study.
 In silico prioritisation of microRNA-associated common variants in multiple sclerosis.
 XCL1, a serum biomarker in neurological diseases; HTLV-1-associated myelopathy and multiple sclerosis.
 Adherence to physical rehabilitation delivered via tele-rehabilitation for people with multiple sclerosis: a scoping review protocol.
 Social Network Characteristics and Correlations With Cognitive, Psychosocial, and Speech Function and Communication Participation for Adults With Multiple Sclerosis: A Pilot Study.
 Diet, Physical Activity, and Stress Among Wheelchair Users With Multiple Sclerosis: Examining Individual and Co-Occurring Behavioral Risk Factors.
 Role of microbiota short-chain fatty acids in the pathogenesis of autoimmune diseases.
 Global burden and cross-country inequalities in autoimmune diseases from 1990 to 2019.
 Role of Contrast-Enhanced MRI in Differentiating Tumefactive Demyelinating Lesions and Gliomas.
 Proinflammatory IL-17 levels in serum/cerebrospinal fluid of patients with neurodegenerative diseases: a meta-analysis study.
 Determination of five times-sit-to-stand test performance in patients with multiple sclerosis: validity and reliability.
 JAK2/STAT5 inhibition protects mice from experimental autoimmune encephalomyelitis by modulating T cell polarization.
 French recommendations for the management of non-infectious chronic uveitis.
 PET imaging of TREM1 identifies CNS-infiltrating myeloid cells in a mouse model of multiple sclerosis.
 Peripapillary hyper-reflective ovoid mass-like structures (PHOMS) in AQP4-IgG-positive neuromyelitis optica spectrum disease (NMOSD) and MOG-IgG-associated disease (MOGAD).
 Focal segmental glomerulosclerosis in a patient with multiple sclerosis treated with Teriflunomide and Ocrelizumab.
 Risk of Multiple Sclerosis Among Users of Antitumor Necrosis Factor α in 4 Canadian Provinces: A Population-Based Study.
 Single-Cell Sequencing in Neurodegenerative Disorders.
 Antioxidant defense enzymes in multiple sclerosis: A 5-year follow-up study.
 Discriminating spatialised speech in complex environments in multiple sclerosis.
 A role for HLA in mediating long-term multiple sclerosis outcomes?
 Effects of Bone Marrow Mesenchymal Stem Cells on Myelin Repair and Emotional Changes of a Cuprizone-Induced Demyelination Model.
 The Anti-inflammatory Effect of Ginger Extract on the Animal Model of Multiple Sclerosis.
 mRNA versus inactivated virus COVID-19 vaccines in multiple sclerosis: Humoral responses and protectivity-Does it matter?
 Accelerometer measured physical activity and sedentary time in individuals with multiple sclerosis versus age matched controls: A systematic review and meta-analysis.
 Sleep-disordered breathing and neurocognitive function in multiple sclerosis: Differential associations across cognitive domains.
 Frailty and relapse activity in multiple sclerosis: A longitudinal observation.
 Reliability and validity of the incremental shuttle walk test in patients with fully ambulatory multiple sclerosis.
 No evidence of oligoclonal bands, intrathecal immunoglobulin synthesis and B cell recruitment in acute ischemic stroke.
 The role of feedback in the robotic-assisted upper limb rehabilitation in people with multiple sclerosis: a systematic review.
 Evaluation of the safety profile of COVID-19 vaccines in patients with MS, NMOSD, and MOGAD.
 Split-Belt Treadmill Adaptation Improves Spatial and Temporal Gait Symmetry in People with Multiple Sclerosis.
 Development of a Long-Term Cross-Sectoral Case and Care Management Manual for Patients With Severe Multiple Sclerosis and Their Caregivers.
 Multidrug resistance in pathogens of community-acquired urinary tract infections in Turkey: a multicentre prospective observational study.
 Cerebrospinal fluid, brain, and spinal cord levels of L-aspartate signal excitatory neurotransmission abnormalities in multiple sclerosis patients and experimental autoimmune encephalomyelitis mouse model.
 Decision Curve Analysis for Personalized Treatment Choice between Multiple Options.
 Three to four mRNA COVID-19 vaccines in multiple sclerosis patients on immunosuppressive drugs: Seroconversion and variant neutralization.
 Immunity following SARS-CoV-2 vaccination in autoimmune neurological disorders treated with rituximab or ocrelizumab.
 MRI detection of brain gadolinium retention in multiple sclerosis: Magnetization transfer vs. T1-weighted imaging.
 MOG Antibody-Associated Disease and Thymic Hyperplasia: From the National Multiple Sclerosis Society Case Conference Proceedings.
 Treatment with the Olive Secoiridoid Oleacein Protects against the Intestinal Alterations Associated with EAE.
 Blocking the IFN-gamma signal in the choroid plexus confers resistance to experimental autoimmune encephalomyelitis.
 Temporal trends in the prevalence of autoimmune diseases from 1990 to 2019.
 Resting-state functional MRI in multicenter studies on multiple sclerosis: a report on raw data quality and functional connectivity features from the Italian Neuroimaging Network Initiative.
 Roles of the miR-155 in Neuroinflammation and Neurological Disorders: A Potent Biological and Therapeutic Target.
 Prognostic models for predicting clinical disease progression, worsening and activity in people with multiple sclerosis.
 Advanced Structural Magnetic Resonance Imaging of the Spinal Cord: Technical Aspects and Clinical Use.
 TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury.
 The neuroprotective effects of Chalcones from Ashitaba on cuprizone-induced demyelination via modulation of brain-derived neurotrophic factor and tumor necrosis factor α.
 Therapeutic Potential of Phytocannabinoid Cannabigerol for Multiple Sclerosis: Modulation of Microglial Activation In Vitro and In Vivo.
 IL-10-providing B cells govern pro-inflammatory activity of macrophages and microglia in CNS autoimmunity.
 The Potential Role of SARS-CoV-2 Infection and Vaccines in Multiple Sclerosis Onset and Reactivation: A Case Series and Literature Review.
 Roles of Adenosine Receptor (subtypes A(1) and A(2A)) in Cuprizone-Induced Hippocampal Demyelination.
 Several serum lipid metabolites are associated with relapse risk in pediatric-onset multiple sclerosis.
 Risk HLA Variants Affect the T-Cell Repertoire in Multiple Sclerosis.
 Validity of 2 Fall Prevention Strategy Scales for People With Stroke, Parkinson's Disease, and Multiple Sclerosis.
 Key role of the gut-microbiota-brain axis via the subdiaphragmatic vagus nerve in demyelination of the cuprizone-treated mouse brain.
 Dual Role of B Cells in Multiple Sclerosis.
 Involvement of Degenerating 21.5 kDa Isoform of Myelin Basic Protein in the Pathogenesis of the Relapse in Murine Relapsing-Remitting Experimental Autoimmune Encephalomyelitis and MS Autopsied Brain.
 Current evidence of rituximab in the treatment of multiple sclerosis.
 Pharmacological treatment promoting remyelination enhances motor function after internal capsule demyelination in mice.
 Relationship of tryptophan metabolites with the type and severity of multiple sclerosis.
 Optic neuritis and autoimmune optic neuropathies: advances in diagnosis and treatment.
 Characterization of antigen-specific CD8+ memory T cell subsets in peripheral blood of patients with multiple sclerosis.
 Central Nervous System Neuroimmunologic Complications of COVID-19.
 Interleukin-3 coordinates glial-peripheral immune crosstalk to incite multiple sclerosis.
 Visualizing Sphingosine-1-Phosphate Receptor 1(S1P(1)) Signaling During Central Nervous System De- and Remyelination.
 Serum neurofilament light chain reference database for individual application in paediatric care: a retrospective modelling and validation study.
 Immunization status in patients with multiple sclerosis: A cross-sectional, monocenter study in Austria.
 Tehranolid and Artemisinin Effects on Ameliorating Experimental Autoimmune Encephalomyelitis by Modulating Inflammation and Remyelination.
 Rationale for Use of Sphingosine-1-Phosphate Receptor Modulators in COVID-19 Patients: Overview of Scientific Evidence.
 Validation of the EQ-5D-5L and psychosocial bolt-ons in a large cohort of people living with multiple sclerosis in Australia.
 CD28-signaling can be partially compensated in CD28-knockout mice but is essential for virus elimination in a murine model of multiple sclerosis.
 The potential of CD38 protein as a target for autoimmune diseases.
 Alterations in Lymphocytic Metabolism-An Emerging Hallmark of MS Pathophysiology?
 Inflammation and Epstein-Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection.
 Glucopeptides derived from myelin-relevant proteins and hyperglucosylated nontypeable Haemophilus influenzae bacterial adhesin cross-react with multiple sclerosis specific antibodies: A step forward in the identification of native autoantigens in multiple sclerosis.
 The Interpretation of Mirror Pattern Bands During Oligoclonal Immunoglobulin Isoelectric Focusing Electrophoresis: A Retrospective Study.
 Influx of T cells into corpus callosum increases axonal injury, but does not change the course of remyelination in toxic demyelination.
 Magnolol as STAT3 inhibitor for treating multiple sclerosis by restricting Th17 cells.
 Long Latency Reflexes in Clinical Neurology: A Systematic Review.
 Small-molecule modulators of tumor necrosis factor signaling.
 Dynamic balance during walking in people with multiple sclerosis: A cross-sectional study.
 Inflammatory Cytokines Associated with Multiple Sclerosis Directly Induce Alterations of Neuronal Cytoarchitecture in Human Neurons.
 Citrullination of myelin basic protein induces a Th17-cell response in healthy individuals and enhances the presentation of MBP85-99 in patients with multiple sclerosis.
 Assessment of oligoclonal bands in cerebrospinal fluid and serum of dogs with meningoencephalitis of unknown origin.
 Insulin-like growth factor-1 receptor controls the function of CNS-resident macrophages and their contribution to neuroinflammation.
 A smart tablet application to quantitatively assess the dominant hand dexterity.
 Effect of exergaming in people with restless legs syndrome with multiple sclerosis: A single-blind randomized controlled trial.
 Incidence of multiple sclerosis relapses and pseudo-relapses following COVID-19 vaccination.
 MicroRNAs and their Implications in CD4+ T-cells, Oligodendrocytes and Dendritic Cells in Multiple Sclerosis Pathogenesis.
 Remyelination by surviving oligodendrocytes is inefficient in the inflamed mammalian cortex.
 Cognitive impairment, fatigue and depression in multiple sclerosis: Is there a difference between benign and non-benign MS?
 Neuroprotective effects of bornyl acetate on experimental autoimmune encephalomyelitis via anti-inflammatory effects and maintaining blood-brain-barrier integrity.
 Sphingosylphosphorylcholine inhibits plasma cell differentiation and ameliorates experimental autoimmune encephalomyelitis.
 Effect of a Fructose-Rich Diet on Gut Microbiota and Immunomodulation: Potential Factors for Multiple Sclerosis.
 Effect of Estimated Blood Volume and Body Mass Index on GFAP and NfL Levels in the Serum and CSF of Patients With Multiple Sclerosis.
 Supporting the differential diagnosis of connective tissue diseases with neurological involvement by blood and cerebrospinal fluid flow cytometry.
 Genetic susceptibility for autoimmune diseases and white blood cell count.
 Chronic demyelination of rabbit lesions is attributable to failed oligodendrocyte progenitor cell repopulation.
 Neuropathic-like Nociception and Spinal Cord Neuroinflammation Are Dependent on the TRPA1 Channel in Multiple Sclerosis Models in Mice.
 The causal relationship between multiple autoimmune diseases and nasal polyps.
 Ocrelizumab Impairs the Phenotype and Function of Memory CD8(+) T Cells: A 1-Year Longitudinal Study in Patients With Multiple Sclerosis.
 Systemic Inflammation Leads to Changes in the Intracellular Localization of KLK6 in Oligodendrocytes in Spinal Cord White Matter.
 Dimethyl Fumarate Treatment Reduces the Amount but Not the Avidity of the Epstein-Barr Virus Capsid-Antigen-Specific Antibody Response in Multiple Sclerosis: A Pilot Study.
 Serum Neurofilament Identifies Patients With Multiple Sclerosis With Severe Focal Axonal Damage in a 6-Year Longitudinal Cohort.
 MOG and AQP4 Antibodies among Children with Multiple Sclerosis and Controls.
 Genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets.
 Respiratory tract Moraxella catarrhalis and Klebsiella pneumoniae can promote pathogenicity of myelin-reactive Th17 cells.
 Exosomal miR-23b-3p from bone mesenchymal stem cells alleviates experimental autoimmune encephalomyelitis by inhibiting microglial pyroptosis.
 Understanding COVID-19 Risk in Patients With Immune-Mediated Inflammatory Diseases: A Population-Based Analysis of SARS-CoV-2 Testing.
 Dissection of complement and Fc-receptor-mediated pathomechanisms of autoantibodies to myelin oligodendrocyte glycoprotein.
 Posttranscriptional Regulation of Gene Expression Participates in the Myelin Restoration in Mouse Models of Multiple Sclerosis: Antisense Modulation of HuR and HuD ELAV RNA Binding Protein.
 Novel nano-carriers with N-formylmethionyl-leucyl-phenylalanine-modified liposomes improve effects of C16-angiopoietin 1 in acute animal model of multiple sclerosis.
 CD19+ B cell values predict the increase of anti-SARS CoV2 antibodies in fingolimod-treated and COVID-19-vaccinated patients with multiple sclerosis.
 Multiple sclerosis plasma IgG aggregates induce complement-dependent neuronal apoptosis.
 IFN-Induced Protein with Tetratricopeptide Repeats 2 Limits Autoimmune Inflammation by Regulating Myeloid Cell Activation and Metabolic Activity.
 Meningeal inflammation as a driver of cortical grey matter pathology and clinical progression in multiple sclerosis.
 White blood cell count profiles in anti-aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorder and anti-myelin oligodendrocyte glycoprotein antibody-associated disease.
 Cross-cultural adaptation, translation, and validation of the Arabic version of the short form of Neurogenic Bladder Symptoms Score.
 Significance of Myelin Oligodendrocyte Glycoprotein Antibodies in CSF: A Retrospective Multicenter Study.
 Clinically relevant increases in serum neurofilament light chain and glial fibrillary acidic protein in patients with Susac syndrome.
 Acute optic neuritis: What are the clues to the aetiological diagnosis in real life?
 The emerging relationship between vitamin K and neurodegenerative diseases: a review of current evidence.
 Ifit2 restricts murine coronavirus spread to the spinal cord white matter and its associated myelin pathology.
 Anti-EBV antibodies: Roles in diagnosis, pathogenesis, and antiviral therapy.
 Serious Adverse Events Have Not Been Reported with Spinal Intrathecal Injection of Mesenchymal Stem Cells: A Systematic Review.
 Evaluation of the Aggregated Time Savings in Adopting Fast Brain MRI Techniques for Outpatient Brain MRI.
 Oral administration of procyanidin B2 3,3"-di-O-gallate ameliorates experimental autoimmune encephalomyelitis through immunosuppressive effects on CD4(+) T cells by regulating glycolysis.
 Functionalized retinoic acid lipid nanocapsules promotes a two-front attack on inflammation and lack of demyelination on neurodegenerative disorders.
 Visually Evoked Potential as Prognostic Biomarker for Neuroaxonal Damage in Multiple Sclerosis From a Multicenter Longitudinal Cohort.
 Bacillus Calmette-Guérin Tokyo-172 vaccine provides age-related neuroprotection in actively induced and spontaneous experimental autoimmune encephalomyelitis models.
 Proteolipid Protein-Induced Mouse Model of Multiple Sclerosis Requires B Cell-Mediated Antigen Presentation.
 Expert opinion on the long-term use of cladribine tablets for multiple sclerosis: Systematic literature review of real-world evidence.
 CAR-T Cell-Mediated B-Cell Depletion in Central Nervous System Autoimmunity.
 Neuronal deletion of MnSOD in mice leads to demyelination, inflammation and progressive paralysis that mimics phenotypes associated with progressive multiple sclerosis.
 Differential effects of anti-CD20 therapy on CD4 and CD8 T cells and implication of CD20-expressing CD8 T cells in MS disease activity.
 The activity of the aryl hydrocarbon receptor in T cells tunes the gut microenvironment to sustain autoimmunity and neuroinflammation.
 Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS.
 Elevated neurofilament light chain CSF/serum ratio indicates impaired CSF outflow in idiopathic intracranial hypertension.
 Immunomodulatory therapy with glatiramer acetate reduces endoplasmic reticulum stress and mitochondrial dysfunction in experimental autoimmune encephalomyelitis.
 Assessing the Equivalence of Brain-Derived Measures from Two 3D T1-Weighted Acquisitions: One Covering the Brain and One Covering the Brain and Spinal Cord.
 Diagnostic implications of MOG-IgG detection in sera and cerebrospinal fluids.
 Association Between Anti-CD20 Therapies and COVID-19 Severity Among Patients With Relapsing-Remitting and Progressive Multiple Sclerosis.
 Association Between Neighborhood Socioeconomic Status and 30-Day Mortality and Readmission for Patients With Common Neurologic Conditions.
 Anti-Glycolipid Antibody Examination in Five EAE Models and Theiler's Virus Model of Multiple Sclerosis: Detection of Anti-GM1, GM3, GM4, and Sulfatide Antibodies in Relapsing-Remitting EAE.
 Targeting deoxycytidine kinase improves symptoms in mouse models of multiple sclerosis.
 miR-485 regulates Th17 generation and pathogenesis in experimental autoimmune encephalomyelitis through targeting STAT3.
 Serological response to SARS-CoV-2 vaccines in patients with multiple sclerosis in Argentina.
 Mesenchymal Stem Cell-Derived Extracellular Vesicles: An Emerging Diagnostic and Therapeutic Biomolecules for Neurodegenerative Disabilities.
 Diabetes Mellitus is Associated With Higher Serum Neurofilament Light Chain Levels in the General US Population.
 Effect of Carvacrol on histological analysis and expression of genes involved in an animal model of multiple sclerosis.
 Risk of a first clinical diagnosis of central nervous system demyelination in relation to human herpesviruses in the context of Epstein-Barr virus.
 COVID-19 infection after SARS-CoV-2 mRNA vaccination in Multiple Sclerosis, AQP4-antibody NMOSD and MOGAD patients during the Omicron subvariant BA.1/2 wave in Singapore.
 Non-coding RNAs in immunoregulation and autoimmunity: Technological advances and critical limitations.
 The epidemiology and burden of neuromyelitis optica spectrum disorder, multiple sclerosis, and MOG antibody-associated disease in a province in Thailand: A population-based study.
 Autoantibody-Abzymes with Catalase Activity in Experimental Autoimmune Encephalomyelitis Mice.
 Cannabis and Cannabinoids in Multiple Sclerosis: From Experimental Models to Clinical Practice-A Review.
 Effect of Ocrelizumab on B- and T-Cell Receptor Repertoire Diversity in Patients With Relapsing Multiple Sclerosis From the Randomized Phase III OPERA Trial.
 How relevant are cerebral white matter lesions in the D313Y variant of the α-galactosidase A gene? Neurological, cardiological, laboratory, and MRI data of 21 patients within a follow-up of 3 years.
 MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights.
 CNS demyelinating disease following inactivated or viral vector SARS-CoV-2 vaccines: A case series.
 A 3-DoF robotic platform for the rehabilitation and assessment of reaction time and balance skills of MS patients.
 Molecular mimicry between Zika virus and central nervous system inflammatory demyelinating disorders: the role of NS5 Zika virus epitope and PLP autoantigens.
 The neuro-ophthalmological manifestations of NMOSD and MOGAD-a comprehensive review.
 Longitudinal Postvaccine SARS-CoV-2 Immunoglobulin G Titers, Memory B-Cell Responses, and Risk of COVID-19 in Multiple Sclerosis Over 1 Year.
 Selective PDE4 subtype inhibition provides new opportunities to intervene in neuroinflammatory versus myelin damaging hallmarks of multiple sclerosis.
 Effect of lesion temperature on the durability of percutaneous radiofrequency rhizotomies to treat trigeminal neuralgia.
 Abnormal Hyperphosphorylation of Tau in Canine Immune-mediated Meningoencephalitis.
 Safety and effectiveness of the booster dose of mRNA COVID-19 vaccines in people with multiple sclerosis: A monocentric experience.
 Rat Ovarian Function Is Impaired during Experimental Autoimmune Encephalomyelitis.
 The serum kynurenine pathway metabolic profile is associated with overweight and obesity in multiple sclerosis.
 Identification of Tau protein as a novel marker for maturation and pathological changes of oligodendrocytes.
 Antigen recognition detains CD8(+) T cells at the blood-brain barrier and contributes to its breakdown.
 The Small-Molecule compound baicalein alleviates experimental autoimmune encephalomyelitis by suppressing pathogenetic CXCR6(+) CD4 cells.
 Serum GFAP and NfL Levels Differentiate Subsequent Progression and Disease Activity in Patients With Progressive Multiple Sclerosis.
 Remyelinating activities of Carvedilol or alpha lipoic acid in the Cuprizone-Induced rat model of demyelination.
 Brain inflammation induces alterations in glycosaminoglycan metabolism and subsequent changes in CS-4S and hyaluronic acid.
 Longitudinal adaptive immune responses following sequential SARS-CoV-2 vaccinations in MS patients on anti-CD20 therapies and sphingosine-1-phosphate receptor modulators.
 BTN2A2-Ig protein inhibits the differentiation of pathogenic Th17 cells and attenuates EAE in mice.
 Immunoglobulin A Antibodies Against Myelin Oligodendrocyte Glycoprotein in a Subgroup of Patients With Central Nervous System Demyelination.
 Immunoreactivity of Kir3.1, muscarinic receptors 2 and 3 on the brainstem, vagus nerve and heart tissue under experimental demyelination.
 Kappa Free Light Chain Biomarkers Are Efficient for the Diagnosis of Multiple Sclerosis: A Large Multicenter Cohort Study.
 Impact of the Voltage-Gated Calcium Channel Antagonist Nimodipine on the Development of Oligodendrocyte Precursor Cells.
 The impact of sphingosine-1-phosphate receptor modulators on COVID-19 and SARS-CoV-2 vaccination.
 Berberine promotes immunological outcomes and decreases neuroinflammation in the experimental model of multiple sclerosis through the expansion of Treg and Th2 cells.
 Progressive multifocal leukoencephalopathy or severe multiple sclerosis relapse following COVID-19 vaccine: a diagnostic challenge.
 EBNA1 Inhibitors Block Proliferation of Spontaneous Lymphoblastoid Cell Lines From Patients With Multiple Sclerosis and Healthy Controls.
 Transcription factor EGR2 controls homing and pathogenicity of T(H)17 cells in the central nervous system.
 MicroRNA-155 Plays Selective Cell-Intrinsic Roles in Brain-Infiltrating Immune Cell Populations during Neuroinflammation.
 Humoral Immune Response Following SARS-CoV-2 mRNA Vaccination and Infection in Pediatric-Onset Multiple Sclerosis.
 Bioengineered particles expand myelin-specific regulatory T cells and reverse autoreactivity in a mouse model of multiple sclerosis.
 Gut dysbiosis in autoimmune diseases: Association with mortality.
 Epidemiologic and clinical characteristics of neuromyelitis optica spectrum disorder patients, A seven years follow-up study from Iran.
 Serum Neurofilament light chain (NfL) levels in children with and without neurologic diseases.
 Ataxin-1 controls the expression of specific noncoding RNAs in B cells upon autoimmune demyelination.
 PD-L1 positive astrocytes attenuate inflammatory functions of PD-1 positive microglia in models of autoimmune neuroinflammation.
 Elevation of truncated (48 kDa) form of unconventional myosin 1C in blood serum correlates with severe Covid-19.
 S3I-201, a selective stat3 inhibitor, ameliorates clinical symptoms in a mouse model of experimental autoimmune encephalomyelitis through the regulation of multiple intracellular signalling in Th1, Th17, and treg cells.
 GM-CSF Promotes the Survival of Peripheral-Derived Myeloid Cells in the Central Nervous System for Pain-Induced Relapse of Neuroinflammation.
 Increased NLRP3 Inflammasome Activation and Pyroptosis in Patients With Multiple Sclerosis With Fingolimod Treatment Failure.
 Bacillus amyloliquifaciens-Supplemented Camel Milk Suppresses Neuroinflammation of Autoimmune Encephalomyelitis in a Mouse Model by Regulating Inflammatory Markers.
 Cognition in patients with neuromyelitis optica spectrum disorders: A prospective multicentre study of 217 patients (CogniNMO-Study).
 Determination of sensitivities and specificities of cerebrospinal fluid free light chains to diagnose multiple sclerosis- a multicentric case-control study.
 mRNA COVID-19 Vaccination Does Not Exacerbate Symptoms or Trigger Neural Antibody Responses in Multiple Sclerosis.
 Renal function and neurodegenerative diseases : a two-sample Mendelian randomization study.
 Very-long-chain fatty acids induce glial-derived sphingosine-1-phosphate synthesis, secretion, and neuroinflammation.
 Glial Glutamate Transporter-Mediated Plasticity: System x(c)(-)/xCT/SLC7A11 and EAAT1/2 in Brain Diseases.
 Pregnancy Is Associated with Impaired Transcription of Human Endogenous Retroviruses and of TRIM28 and SETDB1, Particularly in Mothers Affected by Multiple Sclerosis.
 Comparison Between Dimethyl Fumarate, Fingolimod, and Ocrelizumab After Natalizumab Cessation.
 Perivascular PDGFRB+ cells accompany lesion formation and clinical evolution differentially in two different EAE models.
 Prioritization of Drug Targets for Neurodegenerative Diseases by Integrating Genetic and Proteomic Data From Brain and Blood.
 Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL): A challenging diagnosis and a rare multiple sclerosis mimic.
 Safety of SARS-CoV2 vaccination and COVID-19 short-term outcome in pediatric acquired demyelinating disorders of central nervous system: A single center experience.
 Co-modulation of TNFR1 and TNFR2 in an animal model of multiple sclerosis.
 Mitogen-activated protein kinase inhibitor PD98059 improves neuroimmune dysfunction in experimental autoimmune encephalomyelitis in SJL/J mice through the inhibition of nuclear factor-kappa B signaling in B cells.
 Vitamins A and D Enhance the Expression of Ror-γ-Targeting miRNAs in a Mouse Model of Multiple Sclerosis.
 Oxymatrine ameliorates experimental autoimmune encephalomyelitis by rebalancing the homeostasis of gut microbiota and reducing blood-brain barrier disruption.
 Developing Hypoimmunogenic Human iPSC-Derived Oligodendrocyte Progenitor Cells as an Off-The-Shelf Cell Therapy for Myelin Disorders.
 Tumefactive Multiple Sclerosis: Challenges With Treatment Modalities.
 Cerebrospinal fluid cytokines after autologous haematopoietic stem cell transplantation and intrathecal rituximab treatment for multiple sclerosis.
 Are highly active and aggressive multiple sclerosis the same entity?
 Narrative review based on fingolimod therapy in pediatric MS.
 Patient-reported outcomes in multiple sclerosis: a prospective registry cohort study.
 Pain and participation in social activities in people with relapsing remitting and progressive multiple sclerosis.
 Autoimmune liver disease and multiple sclerosis: state of the art and future perspectives.
 Fingolimod-related atrioventricular block in paediatric age group with multiple sclerosis: two case reports.
 The role of fibronectin in multiple sclerosis and the effect of drug delivery across the blood-brain barrier.
 Cognitive performance in multiple sclerosis: what is the role of the gamma-aminobutyric acid system?
 Application of oligoclonal bands and other cerebrospinal fluid variables in multiple sclerosis and other neuroimmunological diseases: a narrative review.
 Examining the Sensory Processing Skills and Occupational Performance of People with Multiple Sclerosis.
 CDP-choline to promote remyelination in multiple sclerosis: the need for a clinical trial.
 Modifiable risk factors for multiple sclerosis have consistent directions of effect across diverse ethnic backgrounds: a nested case-control study in an English population-based cohort.
 Multiple sclerosis with megacystic presentation: A case report.
 Gut microbiome-modulated dietary strategies in EAE and multiple sclerosis.
 Antibodies from serum and CSF of multiple sclerosis patients bind to oligodendroglial and neuronal cell-lines.
 A potential protective role of the nuclear receptor-related factor 1 (Nurr1) in multiple sclerosis motor cortex: a neuropathological study.
 Health Disparities in Multiple Sclerosis among Hispanic and Black Populations in the United States.
 Ozanimod Therapy in a Patient With Ulcerative Colitis and Multiple Sclerosis: Hitting 2 Birds With 1 Stone.
 The Impact of Stopping Medications and Introducing a Whole Food Plant-Based Diet on Patients Living with Multiple Sclerosis - A Report of Two Cases.
 Neuro-Behcet's disease misdiagnosed and treated as multiple sclerosis: a deceiving masquerader.
 Factor XI as a therapeutic target in neuroinflammatory disease.
 Understanding the spectrum of non-motor symptoms in multiple sclerosis: insights from animal models.
 Severity and worsening of fatigue among individuals with multiple sclerosis.
 Dupilumab in patients with moderate to severe atopic dermatitis and multiple sclerosis.
 Uveitis in the Setting of Co-Existing Systemic Sarcoidosis and Multiple Sclerosis.
 Safety, immunogenicity, efficacy, and acceptability of COVID-19 vaccination in people with multiple sclerosis: a narrative review.
 Editorial: Insights in multiple sclerosis and neuroimmunology: 2021.
 Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.
 Neuron-binding antibody responses are associated with Black ethnicity in multiple sclerosis during natalizumab treatment.
 Serum levels of neurofilament light chains in pediatric multiple sclerosis: a systematic review and meta-analysis.
 The prevalence of insomnia in multiple sclerosis: A meta-analysis.
 Subtypes of relapsing-remitting multiple sclerosis identified by network analysis.
 Amantadine toxicity causing visual hallucinations.
 Erratum: Omics approaches to understanding the efficacy and safety of disease-modifying treatments in multiple sclerosis.
 Editorial: Women in multiple sclerosis and other demyelinating disorders: A global perspective.
 Detection of grey matter microstructural substrates of neurodegeneration in multiple sclerosis.
 Erratum: Protocol for a cross-sectional study: effects of a multiple sclerosis relapse therapy with methylprednisolone on offspring neurocognitive development and behavior (MS-children).
 The Influence of Conventional and Innovative Rehabilitation Methods on Brain Plasticity Induction in Patients with Multiple Sclerosis.
 Antibodies against the flotillin-1/2 complex in patients with multiple sclerosis.
 Sexual Dysfunction in Multiple Sclerosis: The Role of Executive Function.
 Association between vitamin D deficiency and multiple sclerosis- MRI significance: A scoping review.
 Erratum: Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis.
 Multiple Sclerosis in Pregnancy: A Commentary on Disease Modification and Symptomatic Drug Therapies.
 Stress indicators in minorities with multiple sclerosis.
 Development and usability testing of your MS questionnaire: A patient-based digital tool to monitor symptoms of multiple sclerosis.
 Multiple sclerosis and lower urinary tract symptoms: A survey of prevalence, characteristic and urological evaluations.
 Exercise Self-Efficacy and Fatigue as Predictors of Adherence to Home-Based Exercise Among Patients with Multiple Sclerosis.
 Fingolimod-induced bladder lymphoma in a patient with multiple sclerosis.
 Microstates in multiple sclerosis: an electrophysiological signature of altered large-scale networks functioning?
 Oxidative stress in multiple sclerosis-Emerging imaging techniques.
 Editorial: Fatigue in multiple sclerosis-A current perspective.
 Treatment Patterns and Unmet Need for Patients with Progressive Multiple Sclerosis in the United States: Survey Results from 2016 to 2021.
 Should autologous hematopoietic stem cell transplantation be offered as a first-line disease modifying therapy to patients with multiple sclerosis?
 Teriflunomide-Induced Palmoplantar Pustular Psoriasis: Case Report and Review of the Literature.
 Paroxysmal hemidystonia as the initial presentation of multiple sclerosis: an illustrative video depicting hyperventilation-triggered dystonia.
 Corrigendum: Adaptive and innate immune responses in multiple sclerosis with anti-CD20 therapy: gene expression and protein profiles.
 Comparison of recent updates in genetics, immunology, biomarkers, and neuroimaging of primary-progressive and relapsing-remitting multiple sclerosis and the role of ocrelizumab in the management of their refractory cases.
 Ocrelizumab.
 Honing in on magnetic resonance imaging predictors of multiple sclerosis pathology.
 Sex, aging and immunity in multiple sclerosis and experimental autoimmune encephalomyelitis: An intriguing interaction.
 Mobility and Dual Tasking in the Everyday Lives of Adults with Multiple Sclerosis: A Qualitative Exploration.
 Attitudes of people with multiple sclerosis toward brain donation.
 Comparing Clinical and Radiological Features in Familial and Sporadic Multiple Sclerosis.
 A Systematic Review and Meta-Analysis of the Brief Cognitive Assessment for Multiple Sclerosis (BICAMS) International Validations.
 Corrigendum: Case report: Pragmatic impairment in multiple sclerosis after worsening of clinical symptoms.
 Bilateral exudative retinal detachment, unusual pattern of uveitis with multiple sclerosis.
 Overview of diet and autoimmune demyelinating optic neuritis: a narrative review.
 Cryptococcal Meningoencephalitis Mimicking a Multiple Sclerosis Flare in a Patient Taking Fingolimod.
 Editorial: Animal models of multiple sclerosis: can they advance future therapies?
 Association Between Multiple Sclerosis and the Symptoms of Vertigo and Facial Nerve Palsy.
 Disease-Modifying Therapy in Multiple Sclerosis: Evaluation of Patients Satisfaction in Iranian Multiple Sclerosis Population.
 Natalizumab.
 Neurofilament Light Chain in Adult and Pediatric Multiple Sclerosis: A Promising Biomarker to Better Characterize Disease Activity and Personalize MS Treatment.
 The impact of disease modifying therapies on cognitive functions typically impaired in multiple sclerosis patients: a clinician's review.
 The risk of secondary progressive multiple sclerosis is geographically determined but modifiable.
 Cognitive orientation to daily occupational performance approach in people with multiple sclerosis: A pilot study.
 A case report of carbamazepine-induced oropharyngeal dysphagia in a patient with primary progressive multiple sclerosis.
 Neurophysiological and clinical biomarkers of secondary progressive multiple sclerosis: A cross-sectional study.
 Omics approaches to understanding the efficacy and safety of disease-modifying treatments in multiple sclerosis.
 Single-cell transcriptomics combined with proteomics of intrathecal IgG reveal transcriptional heterogeneity of oligoclonal IgG-secreting cells in multiple sclerosis.
 Case report: Chorea and cognitive decline in a young woman: instrumental and genetic assessment of a case originally diagnosed as multiple sclerosis.
 Kikuchi-Fujimoto disease preceding diagnosis of relapsing-remitting multiple sclerosis.
 Response to Letter to the Editor Regarding "Real-World Analysis Affirms the High Persistence and Adherence Observed with Diroximel Fumarate in Patients with Multiple Sclerosis".
 Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis.
 Standalone Performance Validity Tests May Be Differentially Related to Measures of Working Memory, Processing Speed, and Verbal Memory in Patients With Multiple Sclerosis.
 Anti-NMDA receptor encephalitis in a 73-year-old female with secondary progressive multiple sclerosis: A case report.
 Online occupational therapy in the caregivers of people with Multiple sclerosis: a randomized control trial.
 Moving forward through the in silico modeling of multiple sclerosis: Treatment layer implementation and validation.
 Impaired intestinal permeability in patients with multiple sclerosis.
 Microglia depletion as a therapeutic strategy: friend or foe in multiple sclerosis models?
 The association between weight during early life and multiple sclerosis onset in a nationwide Dutch birth year cohort.
 Effect of Nordic Walking Training on Walking Capacity and Quality of Life for People With Multiple Sclerosis.
 Endocrine and multiple sclerosis outcomes in patients with autoimmune thyroid events in the alemtuzumab CARE-MS studies.
 Virtual Management of Multiple Sclerosis: Providing Access or Just Phoning it in?
 Microglia in the context of multiple sclerosis.
 Multiple sclerosis: 2023 update.
 The role of Fecal Microbiota Transplantation (FMT) in treating patients with multiple sclerosis.
 Reasons for Engaging in Complementary and Alternative Medicine Among Highly Educated Women With Multiple Sclerosis.
 Physical activity is related to disease severity and fatigue, but not to relapse rate in persons with relapsing remitting multiple sclerosis - a self-reported questionnaire based study.
 Cerebrospinal fluid soluble CD27 is associated with CD8(+) T cells, B cells and biomarkers of B cell activity in relapsing-remitting multiple sclerosis.
 Ocrelizumab-induced colitis and cytomegalovirus infection and their disadvantageous interaction with underlying multiple sclerosis.
 Uhthoff Phenomenon.
 The incidence and prevalence of crude and familial multiple sclerosis in Tehran, Iran in 2021.
 Thoughts on Fatigue in Multiple Sclerosis Patients.
 Advanced central nervous system imaging biomarkers in radiologically isolated syndrome: a mini review.
 Decision trees to evaluate the risk of developing multiple sclerosis.
 The peripheral profile of the chitinase 3-like-1 in benign multiple sclerosis - a single centre's experience.
 The quality of life in patients with multiple sclerosis - Association with depressive symptoms and physical disability: A prospective and observational study.
 Pathogenic myelin specific antibodies in multiple sclerosis target conformational proteolipid protein 1 anchored membrane domains.
 Letter to the Editor Regarding: "Real-World Analysis Affirms the High Persistence and Adherence Observed with Diroximel Fumarate in Patients with Multiple Sclerosis".
 Early urinary candidate biomarkers and clinical outcomes of intervention in a rat model of experimental autoimmune encephalomyelitis.
 Juvenile multiple sclerosis: addressing epidemiology, diagnosis, therapeutic, and prognostic updates along with cognitive dysfunction and quality of life.
 A virtual reality program to assess cognitive function in multiple sclerosis: A pilot study.
 Editorial: Shared decision-making in neurology.
 The small molecule fibroblast growth factor receptor inhibitor infigratinib exerts anti-inflammatory effects and remyelination in a model of multiple sclerosis.
 Biomechanical changes of the common carotid artery and internal jugular vein in patients with multiple sclerosis.
 Vaccine response in people with multiple sclerosis treated with fumarates.
 The Relationship between Body Image, Disability and Mental Health in Patients with Multiple Sclerosis.
 CD8+ T cells recognizing a neuron-restricted antigen injure axons in a model of multiple sclerosis.
 Radiotherapy Improves the Disability in Patients with Secondary Progressive Multiple Sclerosis.
 Multiple sclerosis: Implications for the primary care NP.
 Understanding who benefits most from cognitive rehabilitation for multiple sclerosis: A secondary data analysis.
 OCT and OCT-A biomarkers in multiple sclerosis - review.
 A case series in individuals with multiple sclerosis using direct current electrical stimulation to inhibit spasticity and improve functional outcomes.
 Managing cognitive impairment and its impact in multiple sclerosis: An Australian multidisciplinary perspective.
 Protective effect of exogenous peroxiredoxin 6 and thymic peptide thymulin on BBB conditions in an experimental model of multiple sclerosis.
 Examine the Role of Psychological Resilience in Predicting Social and Professional Performance in Patients with Diabetes, Multiple Sclerosis, and Rheumatism.
 A Case Report of Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy Misdiagnosed as Multiple Sclerosis.
 Do the current MS clinical course descriptors need to change and if so how? A survey of the MS community.
 Vaginal Herpes Zoster While Under Treatment for Relapsing-Remitting Multiple Sclerosis With Diroximel Fumarate.
 What Is the True Impact of Cognitive Impairment for People Living with Multiple Sclerosis? A Commentary of Symposium Discussions at the 2020 European Charcot Foundation.
 Opinion: The role of the registered dietitian nutritionist in multiple sclerosis care in the United States.
 Disease modifying treatment for pediatric onset multiple sclerosis: Ethical considerations and strategies to navigate parental refusal.
 Jean-Martin Charcot (1825-1893) and the first classification of multiple sclerosis in the medical literature.
 Unleashing nature's potential and limitations: Exploring molecular targeted pathways and safe alternatives for the treatment of multiple sclerosis (Review).
 Infections among individuals with multiple sclerosis, Alzheimer's disease and Parkinson's disease.
 The psychometric properties of the Persian version of the Multiple Sclerosis Self-Management Scale-Revised: A cross-sectional methodological study.
 Regulation of the programmed cell death protein 1/programmed cell death ligand 1 axis in relapsing-remitting multiple sclerosis.
 Probiotic Influences on Motor Skills: A Review.
 Half-dose ocrelizumab in selected patients with relapsing-remitting multiple sclerosis.
 Polygenic risk score prediction of multiple sclerosis in individuals of South Asian ancestry.
 Multiple sclerosis and breast cancer risk: a meta-analysis of observational and Mendelian randomization studies.
 Wall-Eyed Bilateral Internuclear Ophthalmoplegia as an Early Presentation of Multiple Sclerosis.
 When 'good' is not good enough: a retrospective Rasch analysis study of the Berg Balance Scale for persons with Multiple Sclerosis.
 The relationship between coping strategies with sexual satisfaction and sexual intimacy in women with multiple sclerosis.
 Oral cladribine treatment and idiosyncratic drug-induced liver injury in multiple sclerosis.
 Impact of treatment with dimethyl fumarate on sleep quality in patients with relapsing-remitting multiple sclerosis: A multicentre Italian wearable tracker study.
 Functional connectome fingerprinting and stability in multiple sclerosis.
 Effects of socioeconomic status on excess mortality in patients with multiple sclerosis in France: A retrospective observational cohort study.
 Do magnetic resonance imaging features differ between persons with multiple sclerosis of various races and ethnicities?
 Barriers to accessing multiple sclerosis disease-modifying therapies in the Middle East and North Africa region: A regional survey-based study.
 Comparing face-to-face and videoconference assessment of the Brief Repeatable Battery of Neuropsychological Tests in people with multiple sclerosis.
 Adaptation and validation of the Greek version of the Speech Pathology-Specific Questionnaire for Persons with Multiple Sclerosis (SMS).
 Longitudinal Optical Coherence Tomography Measurement of Retinal Ganglion Cell and Nerve Fiber Layer to Assess Benign Course in Multiple Sclerosis.
 The relationship between dietary profile and adherence to the Mediterranean diet with EDSS and quality of life in multiple sclerosis patients: a retrospective cross-sectional study.
 Navigating the journey of multiple sclerosis management in Africa, overcoming hurdles and harnessing opportunities: a review.
 Newly Diagnosed Tumefactive Demyelinating Lesion and Multiple Sclerosis After COVID-19 Infection.
 Restless Legs Syndrome and fatigue in multiple sclerosis: A cross-sectional clinical study.
 Social determinants of health and disparate disability accumulation in a cohort of Black, Hispanic, and White patients with multiple sclerosis.
 Thrombotic Microangiopathy after a 15-year Treatment with Interferon Beta-1b in a Patient with Multiple Sclerosis: A Case Report and Review of Literature.
 Serum CXCL5 as a biomarker in multiple sclerosis and neuromyelitis optica spectrum disorder.
 Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review.
 Classification and management of sexual dysfunctions in multiple sclerosis patients: A review of current literature.
 A review on multiple sclerosis prognostic findings from imaging, inflammation, and mental health studies.
 Podcast on the Art of the Patient Conversation: Healthcare Provider Perspectives to Improve Outcomes in Multiple Sclerosis.
 Rest-Activity Rhythm, Pain, and Motor Activity in Multiple Sclerosis.
 Restless leg syndrome in multiple sclerosis: a case-control study.
 Risk of cervical pre-cancer and cancer in women with multiple sclerosis exposed to high efficacy disease modifying therapies.
 Changes in diffusion tensor imaging indices in basal ganglia and thalamus of patients with Relapsing-Remitting Multiple Sclerosis and relation with clinical conditions: A case-control study.
 Effectiveness of Ocrelizumab in Primary Progressive Multiple Sclerosis: a Multicenter, Retrospective, Real-world Study (OPPORTUNITY).
 Adoptive T-cell therapy targeting Epstein-Barr virus as a treatment for multiple sclerosis.
 Influence of exercise on quantity and deformability of immune cells in multiple sclerosis.
 Cognitive rehabilitation in multiple sclerosis: Three digital ingredients to address current and future priorities.
 Cognitive impairment in Neuromyelitis Optica Spectrum Disorder: A retrospective study using the Brief International cognitive Assessment for Multiple Sclerosis (BICAMS).
 Glatiramer.
 Countermovement Jumps Detect Subtle Motor Deficits in People with Multiple Sclerosis below the Clinical Threshold.
 Ultrasound-Guided Percutaneous Neuromodulation in Multiple Sclerosis: A Case Report.
 The instrumented single leg stance test detects early balance impairment in people with multiple sclerosis.
 Reactive nitrogen species as therapeutic targets for autophagy/mitophagy modulation to relieve neurodegeneration in multiple sclerosis: Potential application for drug discovery.
 Multiple Sclerosis: Diagnosis, Management, and Future Opportunities.
 Treatment of multiple sclerosis with rituximab: A Spanish multicenter experience.
 The pathogenesis of multiple sclerosis: a series of unfortunate events.
 Graph theoretical approach to brain remodeling in multiple sclerosis.
 Top Ten Tips Palliative Care Clinicians Should Know about Multiple Sclerosis.
 The lived experience of physical exertion for persons with advanced multiple sclerosis: making connections with the world.
 Sleepiness in neurological disorders.
 A safety review of current monoclonal antibodies used to treat multiple sclerosis.
 Case report: First manifestation of multiple sclerosis temporally correlated with COVID-19 vaccination.
 Teriflunomide treatment outcomes in multiple sclerosis: A Portuguese real-life experience.
 Development of a new immersive virtual reality (VR) headset-based dexterity training for patients with multiple sclerosis: Clinical and technical aspects.
 How does Nogo receptor influence demyelination and remyelination in the context of multiple sclerosis?
 Neuroimmune, clinical and treatment challenges in multiple sclerosis-related psychoses.
 The cerebrospinal fluid immune cell landscape in animal models of multiple sclerosis.
 A Unique Multiplex ELISA to Profile Growth Factors and Cytokines in Cerebrospinal Fluid.
 Arginine vasopressin hormone receptor antagonists in experimental autoimmune encephalomyelitis rodent models: A new approach for human multiple sclerosis treatment.
 Cognitive Imapirment in Multiple Sclerosis: Relation to Dysability, Duration and Type of Disease.
 Disease-modifying therapies for relapsing/active secondary progressive multiple sclerosis - a review of population-specific evidence from randomized clinical trials.
 Physical Activity and Quality of Life in Persons Newly Diagnosed With Multiple Sclerosis: A Cross-sectional Study.
 Depression, anxiety, insomnia and dysmenorrhoea in stressed fingolimod-treated women with multiple sclerosis.
 The effectiveness of teriflunomide in patients with multiple sclerosis in China: a real-world comparison to no DMT treatment in the first year after diagnosis.
 Arbaclofen extended-release tablets for spasticity in multiple sclerosis: open-label extension study.
 Interferon beta-1a vs. glatiramer acetate: changes of innate immunity in a group of women with multiple sclerosis.
 Fingolimod induced fulminant liver failure requiring liver transplantation: A case report.
 Effect of vitamin A on recovery from the acute phase of multiple sclerosis-related optic neuritis, double-blind, randomized, placebo-controlled trial.
 Psychometric properties of the Persian version of emotions and attitudes towards MRI" (MRI-EMA).
 The Diversity of Astrocyte Activation during Multiple Sclerosis: Potential Cellular Targets for Novel Disease Modifying Therapeutics.
 Disease-modifying treatments for patients with multiple sclerosis in Spain.
 Clinical and Epidemiological Findings of Pediatric Onset Multiple Sclerosis in East-Azerbaijan, Iran; A Population-based Study.
 Larger lesion volume in people with multiple sclerosis is associated with increased transition energies between brain states and decreased entropy of brain activity.
 Outcomes of importance to people with multiple sclerosis, Parkinson's disease and stroke following a falls prevention intervention: a qualitative study to inform a core outcome set.
 Prodromes in demyelinating disorders, amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer's dementia.
 [Translated Article] Disease-modifying treatments for patients with multiple sclerosis in Spain.
 Longitudinal analysis of new multiple sclerosis lesions with magnetization transfer and diffusion tensor imaging.
 Multiple sclerosis and quality of life: The role of cognitive impairment on quality of life in people with multiple sclerosis.
 Sleep disturbance and fatigue in multiple sclerosis: A systematic review and meta-analysis.
 The prevalence of depression and anxiety among Iranian people with multiple sclerosis: A systematic review and meta-analysis.
 Data Resource Profile: The Multiple Sclerosis Documentation System 3D and AOK PLUS Linked Database (MSDS-AOK PLUS).
 Oxidative stress-related risk of the multiple sclerosis development.
 Neuroprotection in an Experimental Model of Multiple Sclerosis via Opening of Big Conductance, Calcium-Activated Potassium Channels.
 Cellular and Molecular Evidence of Multiple Sclerosis Diagnosis and Treatment Challenges.
 Activated leukocyte cell adhesion molecule on human oligodendrocytes mediates CD4 T cell adhesion.
 Health outcomes of sensory hypersensitivities in myalgic encephalomyelitis/chronic fatigue syndrome and multiple sclerosis.
 Proteomics and relationship with axonal pathology in multiple sclerosis: 5-year diffusion tensor imaging study.
 Cognitive Impairment in Multiple Sclerosis.
 Neuropsychological rehabilitation in patients with relapsing-remitting multiple sclerosis: a systematic review.
 Barriers to and Facilitators of Adjustment Among Iranian Multiple Sclerosis Patients: A Qualitative Study.
 Cognitive Reserve Moderates the Effects of Fatigue and Depressive Symptoms in Multiple Sclerosis.
 Co-occurrence of Multiple Sclerosis and Severe Aplastic Anemia: A Report of Two Cases Successfully Treated with Allogeneic Hematopoietic Stem Cell Transplantation.
 Modulation of cytokine release from peripheral blood mononuclear cells from multiple sclerosis patients by coenzyme A and soraphen A.
 Pausing and fluency in speech of patients with relapsing-remitting multiple sclerosis.
 Remyelination in multiple sclerosis from the miRNA perspective.
 Monoclonal Antibodies in Pregnancy and Breastfeeding in Patients with Multiple Sclerosis: A Review and an Updated Clinical Guide.
 The Value of Various Post-Processing Modalities of Diffusion Weighted Imaging in the Detection of Multiple Sclerosis.
 Time perspective of patients with multiple sclerosis.
 Association between multiple sclerosis and prostate cancer risk: A systematic review and meta‑analysis.
 [A listening and psychological support line for people with MS].
 An appraisal of emerging therapeutic targets for multiple sclerosis derived from current preclinical models.
 The interplay between T helper cells and brain barriers in the pathogenesis of multiple sclerosis.
 The protective role of breastfeeding in multiple sclerosis: Latest evidence and practical considerations.
 Relevance and Impact of Social Support on Quality of Life for Persons With Multiple Sclerosis.
 Understanding others is knowledge, understanding oneself is enlightenment.
 Metabolomic Changes in Patients Affected by Multiple Sclerosis and Treated with Fingolimod.
 The Psychosocial Impact of Parental Multiple Sclerosis on Children and Adolescents: A Systematic Review.
 The Immunomodulatory Aspect of Quercetin Penta Acetate on Th17 Cells Proliferation and Gene Expression in Multiple Sclerosis.
 Associations Between Cognitive Impairment and Neuroimaging in Patients with Multiple Sclerosis.
 Exosomal profiling should be used to monitor disease activity in MS patients: Yes.
 Economic Burden of Multiple Sclerosis Drugs in Iran during 2011-2019.
 Vitamin D and neurodegenerative diseases.
 Balance rehabilitation for patients with Multiple Sclerosis using a Kinect®-based virtual training program.
 Non-pharmacological randomized intervention trial for the management of neuropsychological symptoms in outpatients with progressive multiple sclerosis.
 Cerebral lesions sites in neurosarcoidosis: a lesion mapping study.
 The Relationship Between Social Support and Family Functioning Among Married Multiple Sclerosis Patients in Iran with the Mediating Role of Spiritual Experiences and Moral Foundations.
 Microstructural changes precede depression in patients with relapsing-remitting Multiple Sclerosis.
 [The role of clinical, demographic and psychological characteristics of people with multiple sclerosis in their physical health related quality of life].
 Autonomic response to walk tests is useful for assessing outcome measures in people with multiple sclerosis.
 Measurement Properties' Evaluation of the Arabic Version of the Patient-Specific Functional Scale in Patients with Multiple Sclerosis.
 Self-reported ongoing adherence to diet is associated with lower depression, fatigue, and disability, in people with multiple sclerosis.
 Quantitative magnetic resonance imaging reflects different levels of histologically determined myelin densities in multiple sclerosis, including remyelination in inactive multiple sclerosis lesions.
 REal-World effectIveNess of claDribine for patients with multiple sclerosis: a Sicilian multicentric experience (REWIND study).
 Remyelination in multiple sclerosis, along with its immunology and association with gut dysbiosis, lifestyle, and environmental factors.
 Sacral Neuromodulation Therapy for Urinary and Fecal Incontinence in Patients With Multiple Sclerosis: Report of 6 Cases and Literature Review.
 Practical recommendations on treatment of multiple sclerosis with Cladribine: an Israeli Experts Group‏ Viewpoint.
 Personality Traits Predict 7-Year Risk of Diagnosis of Multiple Sclerosis: A Prospective Study.
 Correlation of disability with quality of life in patients with multiple sclerosis treated with natalizumab: primary results and post hoc analysis of the TYSabri ImPROvement study (PROTYS).
 Research on ferroptosis as a therapeutic target for the treatment of neurodegenerative diseases.
 COVID-19 and its implications on the clinico-radiological course of multiple sclerosis: A case-control study.
 TGN020 application against aquaporin 4 improved multiple sclerosis by inhibiting astrocytes, microglia, and NLRP3 inflammasome in a cuprizone mouse model.
 Kerstin Hellwig: educating on multiple sclerosis and pregnancy.
 Inflammasome assembly in neurodegenerative diseases.
 Cognitive deficits in multiple sclerosis: Auditory and visual attention and inhibitory control.
 Mindfulness and Multiple Sclerosis: A Patient Guide.
 Aglycosylated extracellular loop of inwardly rectifying potassium channel 4.1 (KCNJ10) provides a target for autoimmune neuroinflammation.
 In vivo cortical glutathione response to oral fumarate therapy in relapsing-remitting multiple sclerosis: A single-arm open-label phase IV trial using 7-Tesla (1)H MRS.
 The toxic metal hypothesis for neurological disorders.
 Achieving no evidence of disease activity-3 in highly active multiple sclerosis patients treated with cladribine and monoclonal antibodies.
 Do fatigue and depression have a bivariate association with device-measured physical activity behavior in persons with multiple sclerosis?
 Aneurysmal subarachnoid hemorrhage in a patient with dual autoimmune disorders. Perioperative challenges and management.
 Choroid Plexus Volume Change-A Candidate for a New Radiological Marker of MS Progression.
 Impact of reflex locomotion and the Bobath concept on clinical and biomolecular parameters in people with multiple sclerosis: study protocol for a randomized controlled trial.
 Diagnostic challenge in children with an acquired demyelinating syndrome: an illustrative case report.
 Investigating the effectiveness of cognitive behavioral group therapy on psycho-social and emotional adaptability and cognitive flexibility in people with multiple sclerosis in Hamedan, Iran.
 Anthropometric indices, nutrient intakes and health-related characteristics of patients with multiple sclerosis: a cross-sectional study.
 Natalizumab in cerebrospinal fluid and breastmilk of patients with multiple sclerosis.
 Real-world persistence to first-line DMTs in relapsing-remitting multiple sclerosis.
 Development of an integrated conceptual model of multiple sclerosis spasticity.
 From bedside to bench: how existing therapies inform the relationship between Epstein-Barr virus and multiple sclerosis.
 Effects of Tele-Pilates and Tele-Yoga on Biochemicals, Physical, and Psychological Parameters of Females with Multiple Sclerosis.
 MRI changes in chronic crystal methamphetamine abuse.
 Correction to "Comparative adherence trajectories of oral disease-modifying agents in multiple sclerosis".
 The microglial hypothesis of multiple sclerosis.
 Relationship between miRNA-21, miRNA-155, and miRNA-182 expression and inflammatory factors in cerebrospinal fluid from patients with multiple sclerosis.
 Lhermitte Sign.
 EEG-Neurofeedback as a Potential Therapeutic Approach for Cognitive Deficits in Patients with Dementia, Multiple Sclerosis, Stroke and Traumatic Brain Injury.
 Insights into the genetic architecture of multiple sclerosis severity.
 U-fiber diffusion kurtosis and susceptibility characteristics in relapsing-remitting multiple sclerosis may be related to cognitive deficits and neurodegeneration.
 Comorbid Conditions and Physical Function in Adults With Multiple Sclerosis.
 Effectiveness of various diet patterns among patients with multiple sclerosis.
 Negotiating with digital self-monitoring: A qualitative study on how patients with multiple sclerosis use and experience digital self-monitoring within a scientific study.
 An Interpretable Machine Learning Model to Predict Cortical Atrophy in Multiple Sclerosis.
 Confirmation of CD19+ B-Lymphocyte Depletion Prior to Intake of the Second Dose of Ocrelizumab in Multiple Sclerosis Patients.
 Protein biomarkers in multiple sclerosis.
 Sexual Rehabilitation and Relational Satisfaction in People with Multiple Sclerosis and their Partners.
 Current Updates on the Diagnosis and Management of Multiple Sclerosis for the General Neurologist.
 REMISSION OF HEREDITARY ANGIOEDEMA ATTACKS ASSOCIATED WITH STARTING TERIFLUNOMIDE IN A PATIENT WITH MULTIPLE SCLEROSIS.
 Treatment Courses of Patients Newly Diagnosed with Multiple Sclerosis in 2012-2018.
 Clinical use of dimethyl fumarate in multiple sclerosis treatment: an update to include China, using a modified Delphi method.
 Effectiveness of teriflunomide on No Evidence of Disease Activity and cognition in relapsing remitting multiple sclerosis: results of the NEDA3PLUS study.
 Editorial: Highlights in nano-based drug delivery 2021/22.
 Dance for Multiple Sclerosis: A Systematic Review.
 The therapeutic value of treatment for multiple sclerosis: analysis of health technology assessments of three European countries.
 Neurite Orientation Dispersion and Density Imaging in Multiple Sclerosis: A Systematic Review.
 Natural products targeting cellular processes common in Parkinson's disease and multiple sclerosis.
 Blockade of proteinase-activated receptor 2 (PAR 2) attenuates neuroinflammation in experimental autoimmune encephalomyelitis.
 Age and asymmetry of corticospinal excitability, but not cardiorespiratory fitness, predict cognitive impairments in multiple sclerosis.
 Markers of Epstein-Barr Virus Infection in Patients with Multiple Sclerosis.
 The complex relation between visual complaints and decline in visual, visuoperceptual and cognitive functions in people with multiple sclerosis.
 Impact of aging on treatment considerations for multiple sclerosis patients.
 Epidemiological Insights on Medication Concurrency and Polypharmacy in People With Multiple Sclerosis in Greece.
 Ovarian reserve in patients with multiple sclerosis: A systematic review and meta-analysis.
 Exploring the socio-ecological factors impacting lifestyle management of multiple sclerosis: A scoping review.
 Measuring Fatigue in Multiple Sclerosis: There may be Trouble Ahead.
 Effects of vortioxetine on cognition and fatigue in patients with multiple sclerosis and depression: a case series study.
 Pathology of myelin oligodendrocyte glycoprotein antibody-associated disease: a comparison with multiple sclerosis and aquaporin 4 antibody-positive neuromyelitis optica spectrum disorders.
 Ultra-processed foods consumption is associated with multiple sclerosis severity.
 Laboratory evaluation for the differential diagnosis of possible multiple sclerosis in the United States: A physician survey.
 The familial risk and heritability of multiple sclerosis and its onset phenotypes: A case-control study.
 COVID-19 Vaccination and Disease Course in People with Multiple Sclerosis in Greece.
 The Role of Exercise on Fatigue Among Patients With Multiple Sclerosis in the King Fahad Hospital, Madinah, Saudi Arabia: An Analytical Cross-Sectional Study.
 New opportunities for treatment and prevention of neurodegenerative diseases with PTP1B inhibitors.
 A plain language summary on assessing the long-term effectiveness of cladribine tablets in people living with relapsing multiple sclerosis: The CLASSIC-MS study.
 Deeply 3D-T1-TFE hypointense voxels are characteristic of phase-rim lesions in multiple sclerosis.
 Before attributing subdural empyema to SARS-CoV-2-differential causes must be ruled out.
 Schilder's disease.
 Commentary: Progressive multifocal leukoencephalopathy genetic risk variants for pharmacovigilance of immunosuppressant therapies.
 Editorial: Knocking on neuroimmunology's doors: an entrechat concerning the immune system balance and its cell metabolism orchestration.
 Queuine Analogues Incorporating the 7-Aminomethyl-7-deazaguanine Core: Structure-Activity Relationships in the Treatment of Experimental Autoimmune Encephalomyelitis.
 Hypothesis: Viral infections of pregnant women may be early triggers of childhood type 1 diabetes and other autoimmune disease.
 Expectations about the management of sexual dysfunction in women with multiple sclerosis and association with clinical characteristics.
 Rehabilitation on cerebellar ataxic patients with multiple sclerosis: A systematic review.
 Multiple sclerosis risk among anti-tumor necrosis factor alpha users: A methodological review of observational studies based on real-world data.
 Microbiota, diet, and the gut-brain axis in multiple sclerosis and stroke.
 Assessing Muscle Fatigue in Multiple Sclerosis using the Sample Entropy of Electromyographic Signals: A Proof of Concept.
 A step toward restoring hand functions in patients with multiple sclerosis-a study protocol.
 Evaluation of the prevalence of bovine leukemia virus DNA in peripheral blood mononuclear cells of multiple sclerosis patients.
 Triggering multiple sclerosis at conception and early gestation: The variation in ultraviolet radiation is as important as its intensity.
 Epstein-Barr virus and multiple sclerosis: moving from questions of association to questions of mechanism.
 Prominent role of executive functioning on the Phonemic Fluency Test in people with multiple sclerosis.
 An Overview of the History, Pathophysiology, and Pharmacological Interventions of Multiple Sclerosis.
 Addressing Health-Related Quality of Life Among Children With Multiple Sclerosis.
 Exploring the impact of ketogenic diet on multiple sclerosis: obesity, anxiety, depression, and the glutamate system.
 Personality Traits and Fatigue in Multiple Sclerosis: A Narrative Review.
 The impact of ketogenic diet on the onset and progression of multiple sclerosis.
 Characteristics, comorbidities, and complications in multiple sclerosis (MS) and non-MS patients undergoing lumbar fusion for deformity.
 The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS.
 ADAR Expression and Single Nucleotide Variants in Multiple Sclerosis Patients Affect the Response to Interferon Beta Therapy.
 Defining progression independent of relapse activity (PIRA) in adult patients with relapsing multiple sclerosis: A systematic review(✰).
 Climate Change and the Urgent Need to Prepare Persons With Multiple Sclerosis for Extreme Hurricanes.
 Association of multiple sclerosis with chronic fatigue syndrome, restless legs syndrome, and various sleep disorders, along with the recent updates.
 Summary of Research: Caregiver Involvement in MS: Duty or Disruption?
 Multiple sclerosis lesion segmentation: revisiting weighting mechanisms for federated learning.
 Recent Progress in Multiple Sclerosis Treatment Using Immune Cells as Targets.
 Distinct Neuropsychological Correlates of Apathy Sub-Domains in Multiple Sclerosis.
 Feasibility and acceptability of time-restricted eating in a group of adults with multiple sclerosis.
 Resilience, Stress, Well-Being, and Sleep Quality in Multiple Sclerosis.
 Assessing the impacts of L-carnitine and modafinil on fatigue in Iraqi multiple sclerosis patients.
 Statement of Retraction: Elevated CSF concentration of CCL3 and CCL4 in relapsing remitting multiple sclerosis patients.
 Association of Higher Ocrelizumab Exposure With Reduced Disability Progression in Multiple Sclerosis.
 Mycobacterium abscessus Meningitis Associated with Stem Cell Treatment During Medical Tourism.
 Should we treat pediatric radiologically isolated syndrome? An 18-year follow-up case report.
 A Case of Prolonged Fever in a Patient Infected With COVID-19 on Ofatumumab.
 Early postpartum treatment strategies and early postpartum relapses in women with active multiple sclerosis.
 Bruton's tyrosine kinase inhibitors in the treatment of multiple sclerosis.
 A mixed-methods feasibility case series of a job retention vocational rehabilitation intervention for people with multiple sclerosis.
 Estimation of white matter hyperintensities with synthetic MRI myelin volume fraction in patients with multiple sclerosis and non-multiple-sclerosis white matter hyperintensities: A pilot study among the Indian population.
 Validation of Persian Multiple Sclerosis quality of life-29 (P-MSQOL-29) questionnaire.
 Thyroid autoimmunity following alemtuzumab treatment in multiple sclerosis patients: a prospective study.
 Long-term trajectories of ambulatory impairment in multiple sclerosis.
 Neuroinflammatory disorders of the brain and inner ear: a systematic review of auditory function in patients with migraine, multiple sclerosis, and neurodegeneration to support the idea of an innovative 'window of discovery'.
 The multiple sclerosis self-concept change scale: Development and validation of a new measure.
 Prospective analyses of alertness, sleep, and fitness to drive one year after de novo multiple sclerosis diagnosis.
 Ofatumumab and Early Immunological Cells Subset Characterization in Naïve Relapsing Multiple Sclerosis Patients: A Real-World Study.
 The association between perceived social support and cognition in older adults with and without multiple sclerosis.
 Short-term brain atrophy evolution after initiation of immunotherapy in a real-world multiple sclerosis cohort.
 Examining electroencephalogram signatures of people with multiple sclerosis using a nonlinear dynamics approach: a systematic review and bibliographic analysis.
 How does the brain age in individuals with multiple sclerosis? A systematic review.
 Alzheimer's disease and multiple sclerosis: a possible connection through the viral demyelinating neurodegenerative trigger (vDENT).
 Multiple sclerosis and autoimmune diseases - a case control study.
 Psychometric Properties and Clinical Utility of the Distress Thermometer in Caregivers of Persons With Multiple Sclerosis.
 Cannabinoids and Multiple Sclerosis: A Critical Analysis of Therapeutic Potentials and Safety Concerns.
 A Preclinical Investigation on the Role of IgG Antibodies against Coagulant Components in Multiple Sclerosis.
 Examining the Influence of Cognition on the Relationship Between Backward Walking and Falls in Persons With Multiple Sclerosis.
 Graph-Based Analysis of Brain Connectivity in Multiple Sclerosis Using Functional MRI: A Systematic Review.
 Exploring the Relationship between Antioxidant Enzymes, Oxidative Stress Markers, and Clinical Profile in Relapsing-Remitting Multiple Sclerosis.
 Multiple sclerosis and bowel symptoms: Frequency and barriers to their management.
 A Deep Learning Approach for Predicting Multiple Sclerosis.
 The effect of balance, walking capacity, and fear of falling on the level of community integration in individuals with Multiple Sclerosis: A cross-sectional study.
 Immunoablative therapy followed by autologous hematopoietic stem cell transplantation as the first-line disease-modifying therapy in patients with multiple sclerosis.
 Longitudinal Olfactory Patterns in Multiple Sclerosis: A Scoping Review and Implication for Use in Management of Disease.
 How does multiple sclerosis affect sexual satisfaction in patients' spouses?
 New Onset Multiple Sclerosis Post-COVID-19 Vaccination and Correlation With Possible Predictors in a Case-Control Study.
 Gene network reveals LASP1, TUBA1C, and S100A6 are likely playing regulatory roles in multiple sclerosis.
 A global online study of haematopoietic stem cell transplantation in multiple sclerosis and other neurodegenerative disorders.
 Epidemiological and Immune Profile Analysis of Italian Subjects with Endometriosis and Multiple Sclerosis.
 Multiple Sclerosis: Inflammatory and Neuroglial Aspects.
 Expert opinion on COVID-19 vaccines and cladribine tablets in MS: A plain language summary.
 Clinical and radiologic characteristics associated with multiple sclerosis misdiagnosis at a tertiary referral center in the United States.
 Unraveling the link: exploring the causal relationship between diabetes, multiple sclerosis, migraine, and Alzheimer's disease through Mendelian randomization.
 Diffusion-Weighted Images and Contrast-Enhanced MRI in the Diagnosis of Different Stages of Multiple Sclerosis of the Central Nervous System.
 Fingolimod-Associated Macular Edema in the Treatment of Multiple Sclerosis.
 The effectiveness of group intervention focused on intolerance of uncertainty on psychological distress and quality of life in multiple sclerosis patients.
 "No association between disease modifying treatment and fatigue in multiple sclerosis".
 Effects of backward walking training on balance, gait, and functional mobility in people with multiple sclerosis: A randomized controlled study.
 Reliability and Validity of The Fullerton Advanced Balance Scale in People with Multiple Sclerosis.
 Multiple Sclerosis-Related Dietary and Nutritional Issues: An Updated Scoping Review with a Focus on Pediatrics.
 Sex and Gender Differences in Neurodegenerative Diseases: Challenges for Therapeutic Opportunities.
 Initial High-Efficacy Disease-Modifying Therapy in Multiple Sclerosis: A Nationwide Cohort Study.
 Clinimetrics: Multiple Sclerosis Walking Scale-12 (MSWS-12).
 Epigenetics of neurological diseases.
 Self-reported behaviour change among multiple sclerosis community members and interested laypeople 6 months following participation in a free online course about multiple sclerosis.
 Corrigendum: Polysialic acid promotes remyelination in cerebellar slice cultures by Siglec-E-dependent modulation of microglia polarization.
 Establishing the Test-Retest Reliability and Minimal Detectable Change of the Multiple Sclerosis Resiliency Scale.
 The CLARION study: first report on safety findings in patients newly initiating treatment with cladribine tablets or fingolimod for multiple sclerosis.
 Safety and Discontinuation Rate of Dimethyl Fumarate (Zadiva(®)) in Patients with Multiple Sclerosis: An Observational Retrospective Study.
 Three Doses of COVID-19 Vaccines: A Retrospective Study Evaluating the Safety and the Immune Response in Patients with Multiple Sclerosis.
 Treatment preferences in relation to fatigue of patients with relapsing multiple sclerosis: A discrete choice experiment.
 Multi-Criterial Model for Weighting Biological Risk Factors in Multiple Sclerosis: Clinical and Health Insurance Implications.
 Differences in metacognition between multiple sclerosis phenotypes: cognitive impairment and fatigue are key factors.
 Corrigendum: Brain network correlates of epilepsy occurrence in multiple sclerosis and neuroinflammation.
 Cerebrospinal fluid camk2a levels at baseline predict long-term progression in multiple sclerosis.
 Intravenous immunoglobulin treatment during pregnancy and the post-partum period in women with multiple sclerosis: A prospective analysis.
 Predicting employment deterioration with the Processing Speed Test (PST) and SDMT in multiple sclerosis.
 Orchestrating a New Path for Multiple Sclerosis: Achieving Physical, Cognitive, and Emotional Rehabilitation Goals Through Physical and Music Therapy.
 Characterizing causal relationships of visceral fat and body shape on multiple sclerosis risk.
 The Effect of Aerobic Training With the Consumption of Probiotics on the Myelination of Nerve Fibers in Cuprizone-induced Demyelination Mouse Model of Multiple Sclerosis.
 The Heart-Brain Interplay in Multiple Sclerosis from Pathophysiology to Clinical Practice: A Narrative Review.
 Regional contribution of vascular dysfunction in white matter dementia: clinical and neuropathological insights.
 The prevalence of multiple sclerosis (MS) in Oceania, a systematic review, and meta-analysis.
 Statement of Retraction: The Association of Interleukin-16 Gene Polymorphisms with IL-16 Serum Levels and Risk of Multiple Sclerosis.
 Unilateral Pendular Nystagmus in Multiple Sclerosis: A Case Series.
 Genetic deletion of c-Jun amino-terminal kinase 3 (JNK3) modestly increases disease severity in a mouse model of multiple sclerosis.
 Validity of 2 Fall Prevention Strategy Scales for People With Stroke, Parkinson's Disease, and Multiple Sclerosis: Erratum.
 Comparative in-silico analysis of microbial dysbiosis discern potential metabolic link in neurodegenerative diseases.
 Hippocampal area CA2: interneuron disfunction during pathological states.
 Impact of nutrition counseling on anthropometry and dietary intake of multiple sclerosis patients at Kasr Alainy Multiple Sclerosis Unit, Cairo, Egypt 2019-2020: randomized controlled clinical trial.
 Predicting the final clinical phenotype after the first attack of optic neuritis.
 Increased flexibility of brain dynamics in patients with multiple sclerosis.
 Aging in multiple sclerosis: from childhood to old age, etiopathogenesis, and unmet needs: a narrative review.
 COVID-19 Vaccine Response in People with Multiple Sclerosis Treated with Dimethyl Fumarate, Diroximel Fumarate, Natalizumab, Ocrelizumab, or Interferon Beta Therapy.
 The effects of different types of smoking on recovery from attack in hospitalized multiple sclerosis patients.
 AI-based detection of contrast-enhancing MRI lesions in patients with multiple sclerosis.
 Experiences of persons with multiple sclerosis of a collaborative care programme: A qualitative study.
 Physical fitness moderates the association between brain network impairment and both motor function and cognition in progressive multiple sclerosis.
 Anomia in left hemisphere stroke, multiple sclerosis and Parkinson's disease - a comparative study.
 Effects of Pilates-based telerehabilitation on physical performance and quality of life in patients with multiple sclerosis.
 The impact of disease-modifying therapies on immunoglobulin blood levels in patients with multiple sclerosis: a retrospective cross-sectional study.
 A Case Report of Pediatric Patient with Tuberous Sclerosis and Radiologically Isolated Syndrome.
 Objective assessment of dysarthric disorders in patients with multiple sclerosis depending on sex, age, and type of text read.
 Cost-utility analysis of multiple sclerosis rehabilitation in Iran.
 Transcriptional upregulation of galectin-3 in multiple sclerosis.
 Neuroglial components of brain lesions may provide new therapeutic strategies for multiple sclerosis.
 Cortical morphological changes in multiple sclerosis patients: a study of cortical thickness, sulcal depth, and local gyrification index.
 Effect of resistance exercise training on plasma neurofilaments in multiple sclerosis: a proof of concept for future designs.
 Survival and Its Correlates in Multiple Sclerosis Patients under a Universal Health Insurance Program in Taiwan: An 18-Year Nationwide Cohort Study.
 Iron Rim Lesions as a Specific and Prognostic Biomarker of Multiple Sclerosis: 3T-Based Susceptibility-Weighted Imaging.
 Pneumococcal Vaccination Practices in Patients With Multiple Sclerosis Receiving Anti-CD20 Monoclonal Antibodies After Pharmacy and Nursing Collaboration.
 Brain and Spinal Cord MRI Findings in Thai Multiple Sclerosis Patients.
 Drug Repurposing for Identification of S1P1 Agonists with Potential Application in Multiple Sclerosis Using In Silico Drug Design Approaches.
 Microvascular impairments detected by optical coherence tomography angiography in multiple sclerosis patients: A systematic review and meta-analysis.
 Difficult differential diagnosis of ectopic germinoma from multiple sclerosis: A case report and literature review.
 Lower corticospinal excitability and greater fatigue among people with multiple sclerosis experiencing pain.
 Pain in patients with multiple sclerosis.
 Comparing two relaxation procedures to ease fatigue in multiple sclerosis: a single-blind randomized controlled trial.
 Real-life evaluation of the 2017 McDonald criteria for relapsing-remitting multiple sclerosis after a clinically isolated syndrome confirms a gain in time-to-diagnosis.
 Distinct characteristics and severity of brain magnetic resonance imaging lesions in women and men with multiple sclerosis assessed using verified texture analysis measures.
 Multiple Sclerosis Is Associated With Achalasia and Diffuse Esophageal Spasm.
 Risk Factors for Multiple Sclerosis Development After Optic Neuritis Diagnosis Using a Nationwide Health Records Database.
 MRI Markers of Degenerative Disc Disease in Young Patients With Multiple Sclerosis.
 The interaction between Epstein-Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities.
 Clinical and Demographic Characteristics of Immigrant and Local Multiple Sclerosis Patients in Turkey.
 The diagnostic utility of IgG index and oligoclonal bands for multiple sclerosis in a neurology hospital patient population.
 SARS-CoV-2-specific antibody responses following BNT162b2 vaccination in individuals with multiple sclerosis receiving different disease-modifying treatments.
 Vitamin D Receptor Polymorphisms Among the Turkish Population are Associated with Multiple Sclerosis.
 Large-scale cross-sectional online survey on patient-neurologist communication, burden of disease assessment and disease monitoring in people with multiple sclerosis.
 Treatment with Cladribine Tablets Beyond Year 4: A Position Statement by Southeast European Multiple Sclerosis Centers.
 A cultural training for the improvement of cognitive and affective Theory of Mind in people with Multiple Sclerosis: a pilot randomized controlled study.
 Editorial: Demyelinating neurological syndromes: The role of autoimmunity.
 Depression and Anxiety in Association with Polypharmacy in Patients with Multiple Sclerosis.
 IgM to phosphatidylcholine in multiple sclerosis patients: from the diagnosis to the treatment.
 High CD4+:CD8+ ratios with herpes zoster infections in patients with multiple sclerosis on dimethyl fumarate.
 The Efficacy of Spinal Cord Stimulators in the Reduction of Multiple Sclerosis Spasticity: A Narrative Systematic Review.
 Reduced clinical connectome fingerprinting in multiple sclerosis predicts fatigue severity.
 Visual evoked potentials waveform analysis to measure intracortical damage in a preclinical model of multiple sclerosis.
 Multiple Sclerosis and Use of Medical Cannabis: A Retrospective Review of a Neurology Outpatient Population.
 Influence of Transcranial Direct Current Stimulation and Exercise on Physical Capacity and Gait in Multiple Sclerosis: A Cross-Over Pilot Study.
 Abnormal expression of MAPK14-related lncRNAs in the peripheral blood of patients with multiple sclerosis.
 Sleep in multiple sclerosis and neuromyelitis optica spectrum disorder-the SEMN study.
 Incremental validity of brief and abbreviated neuropsychological tests toward predicting functional outcomes in multiple sclerosis.
 Flu-like syndrome due to interferon-beta injections does not increase anxiety, depression, and lost working days in multiple sclerosis patients during the Sars-CoV-2 pandemic.
 Lacunes are associated with late-stage multiple sclerosis comorbidities.
 Interest in Telerehabilitation Among Patients with Mild to Severe Multiple Sclerosis: Results of the Czech Republic.
 Muscle Coactivation Index during Walking in People with Multiple Sclerosis with Mild Disability, a Cross-Sectional Study.
 Accounting for uncertainty in training data to improve machine learning performance in predicting new disease activity in early multiple sclerosis.
 Standardized Systematic Description of Provision of Care for Multiple Sclerosis at a Local Level: A Demonstration Study.
 High-resolution diffusion tensor imaging and T2 mapping detect regional changes within the hippocampus in multiple sclerosis.
 Relationship between motor performance and cortical activity of older neurological disorder patients with dyskinesia using fNIRS: A systematic review.
 [Over one year of B‑cell targeted therapy with Ofatumumab s.c.: first results of a prospective, patient-centered real-world observational study].
 Assisted Reproductive Techniques in Multiple Sclerosis: Recommendations from an Expert Panel.
 Regionally restricted modulation of Sam68 expression and Arhgef9 alternative splicing in the hippocampus of a murine model of multiple sclerosis.
 The relationship between sleep disorders with patients' demographic-clinical characteristics and quality of life in patients with multiple sclerosis.
 Long-Term Effectiveness and Safety of Natalizumab in African American and Hispanic/Latino Patients with Early Relapsing-Remitting Multiple Sclerosis: STRIVE Data Analysis.
 An expert patient program to improve the empowerment and quality of life of people with multiple sclerosis: protocol for a multicenter pre-post intervention study.
 CORRIGENDUM to Progressive multifocal leukoencephalopathy outcomes in patients with multiple sclerosis treated with dimethyl fumarate.
 Detecting seasonal trends in optic neuritis within the Ottawa region.
 Impact of Menopause in Patients with Multiple Sclerosis: Current Perspectives.
 Distribution of Iron, Copper, Zinc and Cadmium in Glia, Their Influence on Glial Cells and Relationship with Neurodegenerative Diseases.
 Correlation of fatigue with disability and accelerometer-measured daily physical activity in patients with relapsing-remitting MS.
 Maternal Multiple Sclerosis and Health Outcomes Among the Children: A Systematic Review.
 Women in the field of multiple sclerosis: How they contributed to paradigm shifts.
 Expert opinion on the pharmacological management of multiple sclerosis in women of childbearing age in Iraq.
 Trans-synaptic degeneration as a mechanism of neurodegeneration in multiple sclerosis.
 Artificial intelligence and multiple sclerosis: ChatGPT model.
 Serum amino acid profiling in differentiating clinical outcomes of multiple sclerosis.
 Dysfunction of basal ganglia functional connectivity associated with subjective and cognitive fatigue in multiple sclerosis.
 The mediating role of psychological flexibility in the relationship between resilience and distress and quality of life in people with multiple sclerosis.
 Roadmap for understanding mechanisms on how Epstein-Barr virus triggers multiple sclerosis and for translating these discoveries in clinical trials.
 RNA-binding proteins as a common ground for neurodegeneration and inflammation in amyotrophic lateral sclerosis and multiple sclerosis.
 Ayurvedic management of neurological deficits post COVID-19 vaccination - A report of two cases.
 A syndemics approach to exercise is medicine.
 Therapy of women with multiple sclerosis: an analysis of the use of drugs that may have adverse effects on the unborn child in the event of (unplanned) pregnancy.
 A collaborative approach to designing an online nutrition education program for people with multiple sclerosis.
 Clinical relevance of thymic and bone marrow outputs in multiple sclerosis patients treated with alemtuzumab.
 Cutaneous presentation of cryptococcal infection with subclinical central nervous system involvement secondary to fingolimod therapy.
 A short washout period from fingolimod to anti-CD20 therapy is safe and decreases the risk of reactivation.
 A scalable approach for continuous time Markov models with covariates.
 The role of the gut microbiota and fecal microbiota transplantation in neuroimmune diseases.
 Plasma exchange in neurology patients-experience from single center in Montenegro.
 Neurosarcoidosis in an adult man with a family history of MS: A case report.
 Background and roles: myosin in autoimmune diseases.
 Management of Adverse Radiation Effect Associated with Stereotactic Radiosurgery of Brain Metastasis in Multiple Sclerosis.
 Pseudocystic demyelination in multiple sclerosis.
 Inverse association between age and inflammatory disease activity in multiple sclerosis.
 Immunological role of sulfatide in the pathogenesis of multiple sclerosis.
 Measuring disability in multiple sclerosis: the WHODAS 2.0.
 Prognostic value of spinal cord lesion measures in early relapsing-remitting multiple sclerosis.
 Effects on Corticospinal Tract Homology of Faremus Personalized Neuromodulation Relieving Fatigue in Multiple Sclerosis: A Proof-of-Concept Study.
 Estimating the disutility of relapse in relapsing-remitting and secondary progressive multiple sclerosis using the EQ-5D-5L, AQoL-8D, EQ-5D-5L-psychosocial, and SF-6D: implications for health economic evaluation models.
 Comparison of OX40 expression in patients with multiple sclerosis and neuromyelitis optica as an approach to diagnosis.
 Brain MRI disease burden and sex differences in cognitive performance of patients with multiple sclerosis.
 Low protection from breakthrough SARS-CoV-2 infection and mild disease course in ocrelizumab-treated patients with multiple sclerosis after three mRNA vaccine doses.
 Disease phenotype prediction in multiple sclerosis.
 Association between cognitive impairment and the disability in people with multiple sclerosis.
 The Role of Microorganisms in the Etiopathogenesis of Demyelinating Diseases.
 Neuromuscular electrical stimulation in conjunction with conventional swallowing therapy in the treatment of dysphagia caused by Multiple sclerosis: A single case experimental design.
 Gastrointestinal Dysfunction in Multiple Sclerosis and Related Conditions.
 Utility of the visual system to monitor neurodegeneration in multiple sclerosis.
 Unless Something Goes Wrong: Making Art to Understand and Mitigate the Risk of Therapeutic Inertia in the Treatment of Multiple Sclerosis.
 An Immersive Virtual Kitchen Training System for People with Multiple Sclerosis: A Development and Validation Study.
 Subjective well-being of adults with multiple sclerosis during COVID-19: Evaluating stress-appraisal-coping and person-environment factors.
 MicroRNA‑155 modulation of CD8(+) T‑cell activity personalizes response to disease‑modifying therapies of patients with relapsing‑remitting multiple sclerosis.
 Medication self-management toolkits for adults with multiple sclerosis: A scoping review.
 Early Treatment for Multiple Sclerosis: Time Is Brain.
 Corrigendum: Evaluation of cerebrospinal fluid neurofilament light chain levels in multiple sclerosis and non-demyelinating diseases of the central nervous system: clinical and biochemical perspective.
 Correspondence on COVID-19 vaccination uptake in people with multiple sclerosis.
 Third wave cognitive behavioural therapies for people with multiple sclerosis: a scoping review.
 A case of Balò's concentric sclerosis showing the attenuation of the Balò lesion after ofatumumab treatment: A case report.
 Isolated Third Nerve Palsy as Presenting Symptom in Multiple Sclerosis Relapse.
 Emerging role of neuregulin-1beta1 in pathogenesis and progression of multiple sclerosis.
 Retrospective cohort study to devise a treatment decision score predicting adverse 24-month radiological activity in early multiple sclerosis.
 Self-management interventions for people with multiple sclerosis: A systematic review and meta-analysis protocol.
 Comparative analysis of dimethyl fumarate and teriflunomide in relapsing-remitting multiple sclerosis.
 Altered social cognition in early relapsing remitting multiple sclerosis.
 Agreement between video-based clinician-rated tools and patient-reported outcomes on gait assessment in individuals with multiple sclerosis.
 Course of therapy in patients with active relapsing-remitting multiple sclerosis despite first-line treatment.
 Brain and cognitive reserve mitigate balance dysfunction in multiple sclerosis.
 Adiponectin Alleviates Cell Injury due to Cerebrospinal Fluid from Multiple Sclerosis Patients by Inhibiting Oxidative Stress and Proinflammatory Response.
 Clinical Characteristics of Headache in Multiple Sclerosis Patients: A Cross-Sectional Study.
 MiR-142-3p is a Critical Modulator of TNF-mediated Neuronal Toxicity in Multiple Sclerosis.
 Interferon beta-1a sc at 25 years: a mainstay in the treatment of multiple sclerosis over the period of one generation.
 Effect of ibudilast on thalamic magnetization transfer ratio and volume in progressive multiple sclerosis.
 Sex-related differences in upper limb motor function in healthy subjects and multiple sclerosis patients: a multiparametric MRI study.
 Vascular dysfunction in multiple sclerosis: Scoping review of current evidence for informing future research directions.
 Assessing treatment switch among patients with multiple sclerosis: A machine learning approach.
 Association of Blood Levels of Vitamin D and Its Binding Protein with Clinical Phenotypes of Multiple Sclerosis.
 Toxoplasma gondii and multiple sclerosis: a population-based case-control seroprevalence study, Central Anatolia, Turkey.
 Tremor in Patients with Relapsing-Remitting Multiple Sclerosis: Clinical Characteristics and Impact on Quality of Life.
 Mortality of multiple sclerosis in Iceland population-based mortality of MS in incidence and prevalence cohorts.
 Patterns of inflammation, microstructural alterations, and sodium accumulation define multiple sclerosis subtypes after 15 years from onset.
 Assessing the psychometric properties of persian version of Zarit Burden interview among family caregivers of patients with multiple sclerosis.
 The signal intensity variation of multiple sclerosis (MS) lesions on magnetic resonance imaging (MRI) as a potential biomarker for patients' disability: A feasibility study.
 Good multiple sclerosis (MS) care and how to get there in Canada: Perspectives of Canadian healthcare providers working with persons with MS.
 Feasibility and scalability of a fitness tracker study: Results from a longitudinal analysis of persons with multiple sclerosis.
 Clinical and MRI characteristics of multiple sclerosis in Iranian Children and Adolescents.
 Health-Related Quality of Life and Physical Activity in Older Adults With Multiple Sclerosis.
 Early Predictors of Disability and Cognition in Multiple Sclerosis Patients: A Long-Term Retrospective Analysis.
 The role of multiple sclerosis subtype in microvascular decompression outcomes for patients with trigeminal neuralgia.
 Attentional networks in neurodegenerative diseases: anatomical and functional evidence from the Attention Network Test.
 In Vitro and Ex Vivo Methodologies for T-Cell Trafficking Through Blood-Brain Barrier After TLR Activation.
 High Epstein-Barr virus capsid antigen IgG level associates with the carriership of CD8+ T cell somatic mutations in the STAT3 SH2 domain.
 Predictors of performance and perceived fatigability in people with multiple sclerosis.
 Intervention fidelity and adaptation in a multi-site exercise training intervention for adults with multiple sclerosis.
 Lifespan neurodegeneration of the human brain in multiple sclerosis.
 Within-person fluctuations over three years in depression, anxiety, fatigue, and health-related quality of life in multiple sclerosis.
 Effect of Disease-Modifying Therapies on COVID-19 Vaccination Efficacy in Multiple Sclerosis Patients: A Comprehensive Review.
 Reconsidering the route of drug delivery in refractory multiple sclerosis: Toward a more effective drug accumulation in the central nervous system.
 Effect of Remote Ischemic Conditioning on Heart Rate Responses to Walking in People with Multiple Sclerosis.
 Prioritizing Components of a Dyadic Physical Activity Intervention for People With Moderate to Severe Multiple Sclerosis and Their Care Partners: A Modified e-Delphi Study.
 The Place of Immune Reconstitution Therapy in the Management of Relapsing Multiple Sclerosis in France: An Expert Consensus.
 Polysialic acid promotes remyelination in cerebellar slice cultures by Siglec-E-dependent modulation of microglia polarization.
 Caudate volume and symptoms of apathy in older adults with multiple sclerosis.
 Drug-induced liver injury by glatiramer acetate leading to liver transplant: A case report.
 Teriflunomide: an oral therapy for first-line treatment of children and adolescents living with relapsing-remitting multiple sclerosis.
 Therapeutic potential of blocking GAPDH nitrosylation with CGP3466b in experimental autoimmune encephalomyelitis.
 Peptide mediated targeted delivery of gold nanoparticles into the demyelination site ameliorates myelin impairment and gliosis.
 Real-world challenges in the diagnosis of primary progressive multiple sclerosis.
 Association between MEF2 family gene polymorphisms and susceptibility to multiple sclerosis in Chinese population.
 The macular retinal ganglion cell layer as a biomarker for diagnosis and prognosis in multiple sclerosis: A deep learning approach.
 Percutaneous tibial nerve stimulation in the treatment of neurogenic detrusor overactivity in multiple sclerosis patients: a historically controlled study.
 COVID-19 and Health Outcomes in People with Multiple Sclerosis: A Population-Based Study in Italy.
 Altered Lnc-EGFR, SNHG1, and LincRNA-Cox2 Profiles in Patients with Relapsing-Remitting Multiple Sclerosis: Impact on Disease Activity and Progression.
 Functional neurological symptoms are a frequent and relevant comorbidity in patients with multiple sclerosis.
 Thin-slice Two-dimensional T2-weighted Imaging with Deep Learning-based Reconstruction: Improved Lesion Detection in the Brain of Patients with Multiple Sclerosis.
 Participant Perspectives on Community Qigong for People with Multiple Sclerosis.
 Solifenacin versus posterior tibial nerve stimulation for overactive bladder in patients with multiple sclerosis.
 Axonal and myelin changes and their inter-relationship in the optic radiations in people with multiple sclerosis.
 Multiparametric magnetic resonance imaging for detection of pathological changes in the central nervous system of a mouse model of multiple sclerosis in vivo.
 B cell depletion modulates glial responses and enhances blood vessel integrity in a model of multiple sclerosis.
 Serum Neurofilament Light Trajectories and Their Relation to Subclinical Radiological Disease Activity in Relapsing Multiple Sclerosis Patients in the APLIOS Trial.
 Associations between Toxoplasma gondii Infection and Multiple Sclerosis: A Case-Control Seroprevalence Study.
 Feasibility of Telerehabilitation-Based Pelvic Floor Muscle Training for Urinary Incontinence in People With Multiple Sclerosis: A Randomized, Controlled, Assessor-Blinded Study.
 Efficacy and safety of "Jollab Monzej" as a traditional persian compound medicine for the treatment of multiple sclerosis-related fatigue: A randomized placebo-controlled trial.
 Efficacy and safety of four-year ofatumumab treatment in relapsing multiple sclerosis: The ALITHIOS open-label extension.
 Dietary patterns and risk of multiple sclerosis: Results of a double-center case-control study in Iran.
 Uhthoff's phenomenon as the initial symptom in neuromyelitis optica spectrum disorders: a case report.
 Risk of breakthrough COVID-19 after vaccination among people with multiple sclerosis on disease-modifying therapies.
 Therapeutic Response in Pediatric Neuromyelitis Optica Spectrum Disorder.
 Menopausal transition in multiple sclerosis: relationship with disease activity and brain volume measurements.
 High-Dose Intravenous Steroid Treatment Seems to Have No Long-Term Negative Effect on Bone Mineral Density of Young and Newly Diagnosed Multiple Sclerosis Patients: A Pilot Study.
 Free Light Chains κ and λ as New Biomarkers of Selected Diseases.
 Association between improved metabolic risk factors and perceived fatigue during dietary intervention trial in relapsing-remitting multiple sclerosis: A secondary analysis of the WAVES trial.
 Childbirth delivery mode and the risk of multiple sclerosis: a prospective population-based study.
 Efficacy of non-invasive brain stimulation on cognitive and motor functions in multiple sclerosis: A systematic review and meta-analysis.
 Role of Sirtuin 3 in Degenerative Diseases of the Central Nervous System.
 Co-registration with subtraction and color-coding or fusion improves the detection of new and growing lesions on follow-up MRI examination of patients with multiple sclerosis.
 Extracellular vesicles, the emerging mirrors of brain physiopathology.
 Circadian rhythm alterations affecting the pathology of neurodegenerative diseases.
 Higher frequency of Human herpesvirus-6 (HHV-6) viral DNA simultaneously with low frequency of Epstein-Barr virus (EBV) viral DNA in a cohort of multiple sclerosis patients from Rio de Janeiro, Brazil.
 Mesenchymal stem cell-derived neural progenitors attenuate proinflammatory microglial activation via paracrine mechanisms.
 Sexual dysfunction in multiple sclerosis: The impact of different MSISQ-19 cut-offs on prevalence and associated risk factors.
 Correction to: Physical fitness moderates the association between brain network impairment and both motor function and cognition in progressive multiple sclerosis.
 T2-fluid attenuated inversion recovery mismatch in tumefactive multiple sclerosis.
 Abnormal phosphorylation of protein tyrosine in neurodegenerative diseases.
 High-dose vitamin D(3) supplementation in relapsing-remitting multiple sclerosis: a randomised clinical trial.
 Use of gadolinium-based contrast agents in multiple sclerosis: a review by the ESMRMB-GREC and ESNR Multiple Sclerosis Working Group.
 Microchimerism in multiple sclerosis: The association between sex of offspring and MRI features in women with multiple sclerosis.
 Bryostatin-1: a promising compound for neurological disorders.
 Drugs to Treat Neuroinflammation in Neurodegenerative Disorders.
 Utility of optical coherence tomography in patients of central immune mediated demyelinating diseases - A prospective study.
 [Clinical presentation of the first demyelinating event in pediatrics].
 Editorial: Artificial intelligence-based computer-aided diagnosis applications for brain disorders from medical imaging data, volume II.
 Editorial: Dysregulation of Th17 and Treg cells in autoimmune diseases.
 The rising role of magnetic resonance imaging biomarkers in diagnosing multiple sclerosis.
 Editorial for "Methods for Brain Atrophy MR Quantification in Multiple Sclerosis: Application to the Multicenter INNI Dataset".
 FTY720 in immuno-regenerative and wound healing technologies for muscle, epithelial and bone regeneration.
 GM-CSF is a marker of compartmentalised intrathecal inflammation in multiple sclerosis.
 Editorial: Immune Mechanisms in white matter lesions: Clinical and pathophysiological implications.
 RETRACTED ARTICLE: The Association of Interleukin-16 Gene Polymorphisms with IL-16 Serum Levels and Risk of Multiple Sclerosis.
 Pseudocystic inflammatory demyelinating lesions in multiple sclerosis: A clinical, radiological, and pathological description.
 Early use of high efficacy therapies in pediatric forms of relapsing-remitting multiple sclerosis: A real-life observational study.
 The Patient-Determined Disease Steps scale is not interchangeable with the Expanded Disease Status Scale in mild to moderate multiple sclerosis.
 Patient-reported outcomes and pharmacist actions in patients with multiple sclerosis managed by health-system specialty pharmacies.
 Cladribine tablets in people with relapsing multiple sclerosis: A real-world multicentric study from southeast European MS centers.
 Efficacy and safety of tixagevimab-cilgavimab (Evusheld®) in people with Multiple Sclerosis on Ocrelizumab: preliminary evidence.
 Multiple sclerosis and ulcerative colitis: A systematic review and meta-analysis.
 Dietary Patterns and Their Associations with Symptom Levels Among People with Multiple Sclerosis: A Real-World Digital Study.
 Effectiveness of exercise interventions in animal models of multiple sclerosis.
 Online Delivery of the Individualized Reduction of Falls Intervention for Persons With Multiple Sclerosis Who Use a Wheelchair or Scooter Full-time: A Pilot Study.
 Antibodies to calnexin and mutated calreticulin are common in human sera.
 Factors Associated With Treatment-Related Changes in Voice Volume in People With Multiple Sclerosis.
 Early beginning of alemtuzumab: Changing the multiple sclerosis treatment paradigm. Interim analysis of the LEMVIDA study.
 Upper limb dysfunction in people with early-stage Multiple Sclerosis: Perceived performance can be misleading.
 Is the ganglion cell layer thickness to macular thickness ratio a new biomarker for multiple sclerosis?
 TREM-2 Drives Development of Multiple Sclerosis by Promoting Pathogenic Th17 Polarization.
 COVID-19 vaccination uptake in people with multiple sclerosis compared to the general population.
 Reduced Cone Density Is Associated with Multiple Sclerosis.
 Cardiogenic shock due to reverse takotsubo syndrome triggered by multiple sclerosis brainstem lesions: a case report and mini review.
 Clinical efficacy of botulinum toxin type A in patients with traumatic brain injury, spinal cord injury, or multiple sclerosis: An observational longitudinal study.
 The relationship between depression and cognitive performance in multiple sclerosis: a meta-analysis.
 Multiple sclerosis is associated with adverse outcomes following hip and knee arthroplasty: A systematic review and meta-analysis of observational studies.
 Absence of Oligoclonal Bands in Multiple Sclerosis: A Call for Differential Diagnosis.
 Pathogenic Role of Fibrinogen in the Neuropathology of Multiple Sclerosis: A Tale of Sorrows and Fears.
 Lexical and syntactic deficits analyzed via automated natural language processing: the new monitoring tool in multiple sclerosis.
 Multiple sclerosis health-related quality of life utility values from the UK MS register.
 The Relationship between Diurnal Measures of Tonic Alertness and Self-Reported Fatigue in Persons with Multiple Sclerosis-A Retrospective Data Analysis.
 Effects of Dry Needling on Spasticity in Multiple Sclerosis Evaluated Through the Rate-Dependent Depression of the H Reflex: A Case Report.
 Multiple sclerosis versus cerebral small vessel disease in MRI: a practical approach using qualitative and quantitative signal intensity differences in white matter lesions.
 Clinically Manifest Infections Do Not Increase the Relapse Risk in People with Multiple Sclerosis Treated with Disease-Modifying Therapies: A Prospective Study.
 Predictors of long-term disability in multiple sclerosis patients using routine magnetic resonance imaging data: A 15-year retrospective study.
 The Relationship Between Retinal Neurodegenerative Changes and Overactive Bladder Syndrome in Multiple Sclerosis.
 Smoking affects epigenetic ageing of lung bronchoalveolar lavage cells in Multiple Sclerosis.
 Fibroblast growth factor 9 (FGF9) mediated neurodegeneration: implications for progressive multiple sclerosis?
 Influence of cardiorespiratory fitness and MRI measures of neuroinflammation on hippocampal volume in multiple sclerosis.
 Feasibility of detecting atrophy relevant for disability and cognition in multiple sclerosis using 3D-FLAIR.
 Differentiating neurosarcoidosis from multiple sclerosis using combined analysis of basic CSF parameters and MRZ reaction.
 Effect of disease-modifying treatment on spinal cord lesion formation in multiple sclerosis: A retrospective observational study.
 Curcumin's spice-infused therapeutic promise: disease severity alleviation in a mouse model of multiple sclerosis via modulation of immune responses.
 Deep brain stimulation in multiple sclerosis-associated tremor. A large, retrospective, longitudinal open label study, with long-term follow-up.
 Feasibility and efficacy of an at-home, smart-device aided mindfulness program in people with Multiple Sclerosis.
 Randomized controlled trial of the behavioral intervention for physical activity in multiple sclerosis project: Social cognitive theory variables as mediators.
 A Cognitive Occupation-Based programme for people with MS: acceptability, feasibility, and experiences of people with multiple sclerosis.
 Efficacy and safety of rituximab in multiple sclerosis: a systematic review and meta-analysis.
 Cerebrospinal Fluid Chloride Is Associated with Disease Activity of Relapsing-Remitting Multiple Sclerosis: A Retrospective Cohort Study.
 Comparative Analysis of Apigenin-3 Acetate versus Apigenin and Methyl-Prednisolone in Inhibiting Proliferation and Gene Expression of Th1 Cells in Multiple Sclerosis.
 Swept-Source Optical Coherence Tomography Thresholds in Differentiating Clinical Outcomes in a Real-World Cohort of Treatment-Naïve Multiple Sclerosis Patients.
 Validity of an inertial sensor-based system for the assessment of spatio-temporal parameters in people with multiple sclerosis.
 Traumatic Events Exposure and Post Traumatic Stress Disorder in Caregivers of Patients with Bipolar Disorder, Bipolar Disorder and Comorbid Post Traumatic Stress Disorder and Multiple Sclerosis.
 In-vivo characterization of macro- and microstructural injury of the subventricular zone in relapsing-remitting and progressive multiple sclerosis.
 Cerebrospinal Fluid Biomarkers in Differential Diagnosis of Multiple Sclerosis and Systemic Inflammatory Diseases with Central Nervous System Involvement.
 Radiological features of late-onset multiple sclerosis: A systematic review and meta-analysis.
 Smoking, early menopause and multiple sclerosis disease course.
 Diet-related inflammation increases the odds of multiple sclerosis: Results from a large population-based prevalent case-control study in Jordan.
 Impact of COVID-19 and system recovery in delivering healthcare to people with multiple sclerosis: a population-based Study.
 First-in-human clinical trial of the NKT cell-stimulatory glycolipid OCH in multiple sclerosis.
 Socioeconomic status of the elderly MS population compared to the general population: a nationwide Danish matched cross-sectional study.
 Alemtuzumab-Related Lymphocyte Subset Dynamics and Disease Activity or Autoimmune Adverse Events: Real-World Evidence.
 Association of age and inflammatory disease activity in the pivotal natalizumab clinical trials in relapsing-remitting multiple sclerosis.
 Results of treatment with alemtuzumab in a Spanish cohort of patients with multiple sclerosis in the real world: The RealMS study.
 Multiple sclerosis patients treated with cladribine tablets: expert opinion on practical management after year 4.
 Induction of antigen-specific tolerance by hepatic AAV immunotherapy regardless of T cell epitope usage or mouse strain background.
 Clinical spectrum of first episode of optic neuritis in a tertiary care hospital in Southern India - A retrospective analysis.
 Correction to: Fall risk is related to cognitive functioning in ambulatory multiple sclerosis patients.
 Adaptive and innate immune responses in multiple sclerosis with anti-CD20 therapy: Gene expression and protein profiles.
 Risk Factors for Chronic Prescription Opioid Use in Multiple Sclerosis.
 An investigation of the association between focal damage and global network properties in cognitively impaired and cognitively preserved patients with multiple sclerosis.
 Mood Symptoms With Uhthoff Phenomenon as the Initial Presentation in a Man With Multiple Sclerosis.
 Editorial for "Evaluation of the Blood Brain Barrier, Demyelination, and Neurodegeneration of Paramagnetic Rim Lesions in Multiple Sclerosis on 7 Tesla MRI".
 Expression of Concern: Evaluation of the Safety and Efficacy of Sildenafil Citrate for Erectile Dysfunction in Men With Multiple Sclerosis: A Double-Blind, Placebo Controlled, Randomized Study.
 Establishment of comorbidity target pools and prediction of drugs candidate for multiple sclerosis and autoimmune thyroid diseases based on GWAS and transcriptome data.
 Pregnancy-related healthcare utilization among women with multiple sclerosis.
 Correction to: Clinical correlates of R1 relaxometry and magnetic susceptibility changes in multiple sclerosis: a multi-parameter quantitative MRI study of brain iron and myelin.
 Retinal Blood Vessel Analysis Using Optical Coherence Tomography (OCT) in Multiple Sclerosis.
 Impact of Anti-CD20 therapies on the immune homeostasis of gastrointestinal mucosa and their relationship with de novo intestinal bowel disease in multiple sclerosis: a review.
 Arterial stiffness in persons with multiple sclerosis and controls: Does aerobic fitness account for group differences?
 Treatment Options for Epstein-Barr Virus-Related Disorders of the Central Nervous System.
 Whole blood miRNAs in relapsing MS patients treated with dimethyl fumarate in the phase 4 TREMEND trial.
 Cause or consequence? The role of IL-1 family cytokines and receptors in neuroinflammatory and neurodegenerative diseases.
 CRISPR/Cas9 genome editing demonstrates functionality of the autoimmunity-associated SNP rs12946510.
 Antiplatelet drugs: Potential therapeutic options for the management of neurodegenerative diseases.
 Pathogenic Microglia Orchestrate Neurotoxic Properties of Eomes-Expressing Helper T Cells.
 Free complement and complement containing extracellular vesicles as potential biomarkers for neuroinflammatory and neurodegenerative disorders.
 Refractory Eosinophilic Fasciitis: Good Response to Ocrelizumab in a Patient with Multiple Sclerosis Under Treatment with Natalizumab.
 Inflammatory and neurodegenerative serum protein biomarkers increase sensitivity to detect disease activity in multiple sclerosis.
 Preparation, Characterization, in-vitro and in-vivo Pharmacokinetic Evaluation of Thermostable Dimethyl Fumarate Cocrystals.
 Cathepsin-B inhibitor CA-074 attenuates retinopathy and optic neuritis in experimental autoimmune encephalomyelitis induced in SJL/J mice.
 Limosilactobacillus reuteri in immunomodulation: molecular mechanisms and potential applications.
 Community-based neuropalliative care.
 New algorithmic approach for easier and faster extended disability status scale calculation.
 Antibody response to SARS-CoV-2 vaccines in patients with relapsing multiple sclerosis treated with evobrutinib: A Bruton's tyrosine kinase inhibitor.
 The role of autoimmune antibodies to predict secondary autoimmunity in patients with relapsing-remitting multiple sclerosis treated with alemtuzumab: A nationwide prospective survey.
 Correction: An intervention design for promoting quality of life among patients with multiple sclerosis: a protocol with a planning approach for a mixed methods study.
 Synaptic pathology in multiple sclerosis: a role for Nogo-A signaling in astrocytes?
 The Potential to Inform Statin Use in Multiple Sclerosis Through Human Genetics [re: WNL-2023-000524].
 Robust real-world evidence: optimising disease-modifying treatments for multiple sclerosis.
 Quantifying Fatigue Using Electrophysiological Techniques and Non-invasive Brain Stimulation in People With Multiple Sclerosis- A Review and Discussion.
 Risk of secondary progressive multiple sclerosis after early worsening of disability.
 Networks of microstructural damage predict disability in multiple sclerosis.
 Changes in employment status over time in multiple sclerosis following a first episode of central nervous system demyelination, a Markov multistate model study.
 The Czech National MS Registry (ReMuS): Data trends in multiple sclerosis patients whose first disease-modifying therapies were initiated from 2013 to 2021.
 Genetically Determined Levels of mTOR-Dependent Circulating Proteins and Risk of Multiple Sclerosis.
 Cyclophosphamide.
 The Use of Stem Cells as a Potential Treatment Method for Selected Neurodegenerative Diseases: Review.
 Processing speed and memory test performance are associated with different brain region volumes in Veterans and others with progressive multiple sclerosis.
 Clinical and Demographic Characteristics and Two-Year Efficacy and Safety Data of 508 Multiple Sclerosis Patients with Fingolimod Treatment.
 Fertility, pregnancy and childbirth in women with multiple sclerosis: a population-based study from 2018 to 2020.
 Efficacy of Dimethyl Fumarate in Young Adults with Relapsing-Remitting Multiple Sclerosis: Analysis of the DEFINE, CONFIRM, and ENDORSE Studies.
 Hydroxyfasudil regulates immune balance and suppresses inflammatory responses in the treatment of experimental autoimmune encephalomyelitis.
 Trajectories of cognitive processing speed and physical disability over 11 years following initiation of a first multiple sclerosis disease-modulating therapy.
 Interleukins (IL-23 and IL-27) serum levels: Relationships with gene polymorphisms and disease patterns in multiple sclerosis patients under treatment with interferon and glatiramer acetate.
 Outcome of COVID-19 Infection in Patients With Multiple Sclerosis Who Received Disease-Modifying Therapies: A Systematic Review and Meta-Analysis.
 A dynamic interpretation of κFLC index for the diagnosis of multiple sclerosis: a change of perspective.
 The impact of hybrid immunity on immune responses after SARS-CoV-2 vaccination in persons with multiple sclerosis treated with disease-modifying therapies.
 Mycobacterium avium subsp. paratuberculosis Antigens Elicit a Strong IgG4 Response in Patients with Multiple Sclerosis and Exacerbate Experimental Autoimmune Encephalomyelitis.
 Current Status of Oral Disease-Modifying Treatment Effects on Cognitive Outcomes in Multiple Sclerosis: A Scoping Review.
 Missed diagnosis of Fabry disease: should we screen patients with multiple sclerosis?
 Clinical evaluation of white matter lesions on 3D inversion recovery ultrashort echo time MRI in multiple sclerosis.
 Assessing the Health Economic Outcomes from Commercially Insured Relapsing Multiple Sclerosis Patients Who Switched from Other Disease-Modifying Therapies to Teriflunomide, in the United States.
 The prevalence and risk factors of anxiety in multiple sclerosis: A systematic review and meta-analysis.
 Disease associations of excessive daytime sleepiness in multiple sclerosis: A prospective study.
 Correction to: Improvements in Cognitive Processing Speed, Disability, and Patient‑Reported Outcomes in Patients with Early Relapsing‑Remitting Multiple Sclerosis Treated with Natalizumab: Results of a 4‑year, Real‑World, Open‑Label Study.
 Clinical-Radiological Mismatch in Multiple Sclerosis Patients during Acute Relapse: Discrepancy between Clinical Symptoms and Active, Topographically Fitting MRI Lesions.
 The efficacy and safety of ginger supplementation in patients with multiple sclerosis: A rationale and study protocol for a double-blind randomized controlled trial.
 Chloride intracellular channel protein-1 (CLIC1) antibody in multiple sclerosis patients with predominant optic nerve and spinal cord involvement.
 Influence of natalizumab on resting-state connectivity in patients with multiple sclerosis.
 Nabiximols is Efficient as Add-On Treatment for Patients with Multiple Sclerosis Spasticity Refractory to Standard Treatment: A Systematic Review and Meta-Analysis of Randomised Clinical Trials.
 Sexual Motivation in Persons with Multiple Sclerosis: A Controlled Cross-Sectional Study.
 Prognostic Role of Visual Evoked Potentials in Non-Neuritic Eyes at Multiple Sclerosis Diagnosis.
 The Tryptophan-Kynurenine Metabolic System Is Suppressed in Cuprizone-Induced Model of Demyelination Simulating Progressive Multiple Sclerosis.
 COVID-19 Vaccine Status, Intent, Hesitancy, and Disease-Related Beliefs in People with Multiple Sclerosis.
 Personalized dietary advices provided by a dietitian increase calcium intake in outpatients with multiple sclerosis-Results from a randomized, controlled, single-blind trial.
 Real-World Analysis Affirms the High Persistence and Adherence Observed with Diroximel Fumarate in Patients with Multiple Sclerosis.
 Sexual Dysfunction in People with Multiple Sclerosis: The Role of Disease Severity, Illness Perception, and Depression.
 The spectral slope as a marker of excitation/inhibition ratio and cognitive functioning in multiple sclerosis.
 The impact of medical insurance on health care access and quality for people with multiple sclerosis in the United States: A scoping review.
 Neurogenic Lower Urinary Tract Symptoms, Fatigue, and Depression-Are There Correlations in Persons with Multiple Sclerosis?
 Risk of cancer with immunosuppressants compared to immunomodulators in multiple sclerosis: A nested case-control study within the French nationwide claims database.
 Higher dietary quality is prospectively associated with lower MRI FLAIR lesion volume, but not with hazard of relapse, change in disability or black hole volume in people with Multiple Sclerosis.
 Multiple Sclerosis-A Demyelinating Disorder and Its Dental Considerations-A Literature Review with Own Case Report.
 Real-World Clinical and Economic Outcomes Among Persons With Multiple Sclerosis Initiating First- Versus Second- or Later-Line Treatment With Ocrelizumab.
 Articulatory speech measures can be related to the severity of multiple sclerosis.
 Brain MRI activity during the year before pregnancy can predict long-term clinical worsening in patients with Multiple Sclerosis.
 Can a previously co-designed device be used by others? A service evaluation of the use of the Sativex spray holder for individuals with multiple sclerosis.
 Cost Per Relapse Avoided for Ozanimod Versus Other Selected Disease-Modifying Therapies for Relapsing-Remitting Multiple Sclerosis in the United States.
 Sphingosine-1 Phosphate Receptor Modulators Increase In Vitro Melanoma Cell Line Proliferation at Therapeutic Doses Used in Patients with Multiple Sclerosis.
 Higher MRI lesion load in multiple sclerosis is related to the N-glycosylation changes of cerebrospinal fluid immunoglobulin G.
 Real world study of ocrelizumab in multiple sclerosis: Kuwait experience.
 The socioeconomic impact of disability progression in multiple sclerosis: A retrospective cohort study of the German NeuroTransData (NTD) registry.
 Alpha Calcitonin Gene-related Peptide, Neuropeptide Y, and Substance P as Biomarkers for Diagnosis and Disease Activity and Severity in Multiple Sclerosis.
 Navigating the challenges of diagnosing multiple sclerosis.
 Neuro-image: developmental venous anomaly and central vein sign in multiple sclerosis.
 Multiple sclerosis patients' response to COVID-19 pandemic and vaccination: correspondence.
 Distinct intrathecal inflammatory signatures following relapse and anti-COVID-19 mRNA vaccination in multiple sclerosis.
 Pathways to healing: Plants with therapeutic potential for neurodegenerative diseases.
 Stat1 is an inducible transcriptional repressor of neural stem cells self-renewal program during neuroinflammation.
 Podcast on the Challenges and Recommendations to Address Unmet Needs in MS for LGBTQ+ Populations in the United States.
 The X-linked histone demethylases KDM5C and KDM6A as regulators of T cell-driven autoimmunity in the central nervous system.
 A Dual Role of Osteopontin in Modifying B Cell Responses.
 Neurological comorbidities and novel mutations in Turkish cases with neurofibromatosis type 1.
 Nanopore sequencing identifies differentially methylated genes in the central nervous system in experimental autoimmune encephalomyelitis.
 Reelin through the years: From brain development to inflammation.
 Methionine-PET to differentiate between brain lesions appearing similar on conventional CT/MRI scans.
 Adamantanes for the treatment of neurodegenerative diseases in the presence of SARS-CoV-2.
 Mechanistic study on the possible role of embelin in treating neurodegenerative disorders.
 Graves' disease induced by IFN-β1a therapy: A case report, review of literature and new insights into the pathogenesis.
 Pre-training working memory/information processing capabilities and brain atrophy limit the improving effects of cognitive training.
 Targeting T-cell integrins in autoimmune and inflammatory diseases.
 Disease-modifying therapies do not affect sleep quality or daytime sleepiness in a large Australian MS cohort.
 Evaluation of risk management in a natalizumab home infusion procedure.
 Nanobody inhibitors of Plexin-B1 identify allostery in plexin-semaphorin interactions and signaling.
 Virological Markers in Epstein-Barr Virus-Associated Diseases.
 Acute superior mesenteric artery syndrome with complete foregut obstruction following Nissen fundoplication.
 Clinical features and visual outcomes of pediatric optic neuritis in the Indian population: A prospective study.
 Osteopontin associates with brain T(RM)-cell transcriptome and compartmentalization in donors with and without multiple sclerosis.
 Painful Small Fiber Neuropathy Associated With Teriflunomide: A Case Series and Literature Review Related to Teriflunomide and Leflunomide.
 Demyelination induced galactorrhea: an atypical presentation of multiple sclerosis.
 N-acetylglucosamine inhibits inflammation and neurodegeneration markers in multiple sclerosis: a mechanistic trial.
 An update on optic neuritis.
 Nogo-A and LINGO-1: Two Important Targets for Remyelination and Regeneration.
 Pathogenic Role of Adipose Tissue-Derived Mesenchymal Stem Cells in Obesity and Obesity-Related Inflammatory Diseases.
 The Efficacy of the Speed of Processing Training Program in Improving Functional Outcome: From Restoration to Generalization.
 Teriflunomide as a therapeutic means for myelin repair.
 Matrine Mediated Immune Protection in MS by Regulating Gut Microbiota and Production of SCFAs.
 Impact of Pilates suspension with self-awareness on gait and metacognition in multiple sclerosis: Randomized, single-blinded and parallel-group trial.
 Clinical characteristics of intermediate uveitis in adults according to criteria of the SUN working group.
 Central Versus Peripheral Drug Exposure Ratio, a Key Differentiator for Siponimod Over Fingolimod?
 Mesenchymal stem cell therapy for neurological disorders: The light or the dark side of the force?
 Adropin and MOTS-c as new peptides: Do levels change in neurodegenerative diseases and ischemic stroke?
 Multiparametric quantitative MRI reveals progressive cortical damage over time in clinically stable relapsing-remitting MS.
 A Weakly Supervised Gradient Attribution Constraint for Interpretable Classification and Anomaly Detection.
 Inflammation-Mediated Responses in the Development of Neurodegenerative Diseases.
 Fingolimod-associated progressive multifocal leukoencephalopathy in a multiple sclerosis patient with a good response to filgrastim.
 Immunopathogenesis of viral infections in neurological autoimmune disease.
 Toward Precision Medicine Using a "Digital Twin" Approach: Modeling the Onset of Disease-Specific Brain Atrophy in Individuals with Multiple Sclerosis.
 The Role of Myeloid-Derived Suppressor Cells in Multiple Sclerosis and Its Animal Model.
 Editorial: Understanding and targeting neuro-immune interactions within disease and inflammation.
 A woman with progressive motor and cognitive complaints.
 Editorial: Automatic methods for multiple sclerosis new lesions detection and segmentation.
 Associations between Social Support and Cognitive Performance among Persons with MS.
 [Ocrelizumab-associated severe neutropenia: an underestimated complication of treatment of multiple sclerosis with anti-CD20 antibodies?].
 Complex regulatory effects of gut microbial short-chain fatty acids on immune tolerance and autoimmunity.
 Cognitive enrichment and education quality moderate cognitive dysfunction in black and white adults with multiple sclerosis.
 Heart rate variability and fatigue in MS: two parallel pathways representing disseminated inflammatory processes?
 Idiopathic Optic Neuritis Should Neither Be Defined as a Subtype nor an Early Sign of Multiple Sclerosis.
 Baclofen.
 Correction to: Pediatric tumefactive multiple sclerosis case (with baló‑like lesions), diagnostic and treatment challenges.
 Autoimmune Neuroinflammatory Diseases: Role of Interleukins.
 Visual function resists early neurodegeneration in the visual system in primary progressive multiple sclerosis.
 Medication Adherence Status and Its Association With Quality of Life Among Individuals With Neurological Conditions in Saudi Arabia.
 Shared miRNA landscapes of COVID-19 and neurodegeneration confirm neuroinflammation as an important overlapping feature.
 Blepharospasm and Sixth Nerve Palsy as the Presenting Sign of Multiple Sclerosis.
 Atypical multiple sclerosis associated with indolent systemic mastocytosis treated by cladribine.
 Similar neural pathways link psychological stress and brain-age in health and multiple sclerosis.
 Emotional competencies in multiple sclerosis.
 Experiences of integrating and sustaining physical activity in life with multiple sclerosis, Alzheimer's disease, and ischaemic heart disease: a scoping review.
 Clinical significance and prognostic value of serum autoantibody tests in multiple sclerosis.
 Effects of Dietary Modification Based on Complementary and Alternative Iranian Medicine in Patients with Secondary-Progressive Multiple Sclerosis: A Randomized Controlled Clinical Trial.
 Multiple Sclerosis in Mongolia; the First Study Exploring Predictors of Disability and Depression in Mongolian MS Patients.
 Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder: Onset Following Acute COVID-19 Infection, a Case Series.
 Immune cell subpopulations and serum neurofilament light chain are associated with increased risk of disease worsening in multiple sclerosis.
 Predictive value of brain atrophy, serum biomarkers and information processing speed for early disease progression in multiple sclerosis.
 Low Doses of β-Caryophyllene Reduced Clinical and Paraclinical Parameters of an Autoimmune Animal Model of Multiple Sclerosis: Investigating the Role of CB(2) Receptors in Inflammation by Lymphocytes and Microglial.
 Self-reported fatigue impact is associated with frequency of falls and injurious falls in people with multiple sclerosis.
 Clinical associations and characteristics of the polyspecific intrathecal immune response in elderly patients with non-multiple sclerosis chronic autoimmune-inflammatory neurological diseases - a retrospective cross-sectional study.
 Coping of Chronically-Ill Patients during the COVID-19 Pandemic: Comparison between Four Groups.
 A highly challenging balance training intervention for people with multiple sclerosis: a feasibility trial.
 Alternative medicine therapies in neurological disorders: Prevalence, reasons and associated factors. A systematic review.
 Correction to: Concomitant diagnosis of multiple sclerosis and human immunodeficiency virus (HIV) infection: case report and the review of literature.
 Correction to: Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder: Onset Following Acute COVID-19 Infection, a Case Series.
 Correction: Association Between Body Mass Index and Response to Disease-Modifying Therapies in Patients With Relapsing-Remitting Multiple Sclerosis at King Abdulaziz University Hospital: A Retrospective Study.
 Letter to the editor: Classification and management of sexual dysfunctions in multiple sclerosis patients: A review of current literature, Campetella et al.
 The effects of curcumin on astrocytes in common neurodegenerative conditions.
 Methylprednisolone.
 Anti-inflammatory-antioxidant modifications and synbiotics improved health-related conditions in patients with progressive forms of multiple sclerosis: A single-center, randomized clinical trial.
 Long-term effectiveness of a cognitive behavioural therapy (CBT) in the management of fatigue in patients with relapsing remitting multiple sclerosis (RRMS): a multicentre, randomised, open-label, controlled trial versus standard care.
 Intravenous transplantation of bone marrow-derived mesenchymal stromal cells in patients with multiple sclerosis, a phase I/IIa, double blind, randomized controlled study.
 Expert Narrative Review of the Safety of Cladribine Tablets for the Management of Relapsing Multiple Sclerosis.
 Identifying Optical Coherence Tomography Markers for Multiple Sclerosis Diagnosis and Management.
 Significance of Post-Traumatic Growth and Mental Health for Coping in Multiple Sclerosis Caregivers.
 Altered amide proton transfer weighted and diffusion signals in patients with multiple sclerosis: correlation with neurofilament light chain and disease duration.
 Combining Clinical and Genetic Data to Predict Response to Fingolimod Treatment in Relapsing Remitting Multiple Sclerosis Patients: A Precision Medicine Approach.
 Assessing 'no evidence of disease activity' status in patients with relapsing-remitting multiple sclerosis: a long-term follow-up.
 Impaired lung function in multiple sclerosis: a single-center observational study in 371 persons.
 Influence of Disease Modifying Treatment, Severe Acute Respiratory Syndrome Coronavirus 2 Variants and Vaccination on Coronavirus Disease 2019 Risk and Outcome in Multiple Sclerosis and Neuromyelitis Optica.
 Gait initiation in multiple sclerosis patients with and without functional loss.
 Regulation of microglia function by neural stem cells.
 Recombinant Antibody Fragments for Neurological Disorders: An Update.
 Air Pollution and Its Adverse Effects on the Central Nervous System.
 Persistent SARS-CoV-2 Infection in a Multiple Sclerosis Patient on Ocrelizumab: A Case Report.
 Effects of pelvic floor muscle training applied with telerehabilitation in patients with multiple sclerosis having lower urinary track symptoms: A randomized controlled trial.
 Evaluation of Inflammation in the Peripheral Multiple Sclerosis Retina Using Ultra-Widefield Optical Coherence Tomography: A Pilot Study.
 Differential impact of environmental factors on systemic and localized autoimmunity.
 A Comprehensive Evaluation of Multiple Sclerosis-Related Fatigue with a Special Focus on Fatigability.
 Frequency of Registered Cases of Multiple Sclerosis.
 Longitudinal deep network for consistent OCT layer segmentation.
 Personalized estimates of morphometric similarity in multiple sclerosis and neuromyelitis optica spectrum disorders.
 Hepatobiliary Adverse Reactions during Treatment with Cladribine: Analysis of Data from the European Spontaneous Reporting System.
 Cost-effectiveness Analysis of Ocrelizumab for the Treatment of Relapsing and Primary Progressive Multiple Sclerosis in Portugal.
 Evaluation of the use of high-efficacy treatments (HETs) in patients with relapsing-remitting multiple sclerosis in Argentina.
 Serum Glial Fibrillary Acidic Protein Compared With Neurofilament Light Chain as a Biomarker for Disease Progression in Multiple Sclerosis.
 Serum neurofilament light-chain levels and long-term treatment outcomes in relapsing-remitting multiple sclerosis patients: A post hoc analysis of the randomized CombiRx trial.
 Detecting disability using self-reported and clinical assessments in early-stage relapsing-remitting multiple sclerosis: Looking for a complementary approach.
 BMAL1 loss in oligodendroglia contributes to abnormal myelination and sleep.
 Ultra-High Performance Liquid Chromatography Method for Bioanalysis of Fampridine Using Dried Blood Spot (DBS) Methodology: Application to Pharmacokinetic Study in Albino Rats.
 Pregnancy and fetal outcomes following maternal exposure to glatiramer acetate in all three trimesters of pregnancy.
 Functional connectivity modifications in monoaminergic circuits occur in fatigued MS patients treated with fampridine and amantadine.
 5-HMF attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis mice by inhibiting the MIF-CD74 interaction.
 Molecular insights into the pathogenic impact of vitamin D deficiency in neurological disorders.
 Classification of multiple sclerosis women with voiding dysfunction using machine learning: Is functional connectivity or structural connectivity a better predictor?
 How Does Vitamin D Affect Immune Cells Crosstalk in Autoimmune Diseases?
 Aryl hydrocarbon receptor activity downstream of IL-10 signaling is required to promote regulatory functions in human dendritic cells.
 The effect of cladribine on immunoglobulin levels compared to B cell targeting therapies in multiple sclerosis.
 Antibody response to SARS-CoV-2 vaccination or infection in a prospective cohort of children with neuroinflammatory diseases.
 Immune-mediated colitis associated with ocrelizumab: A new safety risk.
 The Benefits and Risks of Switching from Fingolimod to Siponimod for the Treatment of Relapsing-Remitting and Secondary Progressive Multiple Sclerosis.
 Pyruvate Dehydrogenase-Dependent Metabolic Programming Affects the Oligodendrocyte Maturation and Remyelination.
 Oligodendrocyte progenitor cells differentiation induction with MAPK/ERK inhibitor fails to support repair processes in the chronically demyelinated CNS.
 Health-economic benefits of anti-CD20 treatments in relapsing multiple sclerosis estimated using a treatment-sequence model.
 Premorbid cognitive functioning influences differences between self-reported cognitive difficulties and cognitive assessment in multiple sclerosis.
 Brain region dependent molecular signatures and myelin repair following chronic demyelination.
 Development of an ultrasensitive microfluidic assay for the analysis of Glial fibrillary acidic protein (GFAP) in blood.
 Identification of the Lipid Antigens Recognized by rHIgM22, a Remyelination-Promoting Antibody.
 Virus-Specific T-Cell Therapy for Viral Infections of the Central Nervous System: A Review.
 Acthar Gel (RCI): A Narrative Literature Review of Clinical and Economic Evidence.
 Pneumocystis jirovecii pneumonia complicated a case of SARS-CoV-2 infection and multiple sclerosis after treatment with rituximab.
 Correlation and differences of patient-reported outcomes vs. Likert-Rating of MS symptoms in a real-world cohort using a digital patient app.
 Assessment of the treating physicians' first-hand experience with handling and satisfaction of ofatumumab therapy: findings from the PERITIA survey conducted in Europe.
 Serum Neurofilaments and OCT Metrics Predict EDSS-Plus Score Progression in Early Relapse-Remitting Multiple Sclerosis.
 Pinch Strength Measurements in Adolescents With Pediatric Multiple Sclerosis.
 Primary Hyperparathyroidism overlapping with Multiple Sclerosis: a catastrophic marriage.
 Sixteen syndrome: a rare presentation of central demyelination.
 Post-vaccination SARS-Cov-2 T-cell receptor repertoires in patients with multiple sclerosis and related disorders.
 Carboxylic Acid-Containing Indanyl Compounds as S1P5 Modulators for Treating Neurodegenerative Diseases.
 Alemtuzumab induced acquired hemophilia A in multiple sclerosis: a case report.
 The Location of the Abducens Nucleus and Facial Nerve Fascicle: Letter to the Editor Regarding the Article "Association Between Multiple Sclerosis and the Symptoms of Vertigo and Facial Nerve Palsy".
 Author Correction: Inhibiting nighttime melatonin and boosting cortisol increase patrolling monocytes, phagocytosis, and myelination in a murine model of multiple sclerosis.
 A Grave Set of Diagnoses: A Case of Mania with Comorbid Autoimmune Thyroiditis Precipitated by Multiple Sclerosis Treatment.
 Epstein-Barr virus and multiple sclerosis: the dawn of a new age.
 Diffusion-based structural connectivity patterns of multiple sclerosis phenotypes.
 Teriflunomide and Time to Clinical Multiple Sclerosis in Patients With Radiologically Isolated Syndrome: The TERIS Randomized Clinical Trial.
 Investigating the Effect of Cigarette Smoking on Serum Uric Acid Levels in Multiple Sclerosis Patients: A Cross Sectional Study.
 Multiple sclerosis imaging in clinical practice: a European-wide survey of 428 centers and conclusions by the ESNR Working Group.
 The Clinical and Economic Impact of Employees Who Are Care Partners of Patients with Multiple Sclerosis by Disease Severity.
 The prevalence of major depression and generalized anxiety disorder in patients with multiple sclerosis in Saudi Arabia: a cross-sectional multicentered study.
 Real-world use of cladribine tablets (completion rates and treatment persistence) in patients with multiple sclerosis in England: The CLARENCE study.
 Translation, cross-cultural adaptation, and validation of the Persian version of Everyday Memory Questionnaire-Revised (EMQ-R) in patients with multiple sclerosis.
 Impact of the autonomic dysfunction on the quality of life in people with NMOSD and MS: An international cross-sectional study.
 Non-invasive brain stimulation for spasticity rehabilitation in multiple sclerosis: A systematic review of randomized controlled trials.
 An Exploratory Study of Community Mobility in Adults With Multiple Sclerosis Across Different Ambulation Levels.
 Neuromyelitis Optica: A Case Report From a Radiological Perspective.
 Tumefactive demyelinating disorders as stroke mimics: Description of cases and systematic review of the literature.
 Multiple sclerosis is associated with worse COVID-19 outcomes compared to the general population: A population-based study.
 Intersite brain MRI volumetric biases persist even in a harmonized multisubject study of multiple sclerosis.
 Evaluation of the Blood-Brain Barrier, Demyelination, and Neurodegeneration in Paramagnetic Rim Lesions in Multiple Sclerosis on 7 Tesla MRI.
 Effectiveness of Repetitive Transcranial Magnetic Stimulation (rTMS) Add-On Therapy to a Standard Treatment in Individuals with Multiple Sclerosis and Concomitant Symptoms of Depression-Results from a Randomized Clinical Trial and Pilot Study.
 Neuroimaging Correlates of Patient-Reported Outcomes in Multiple Sclerosis.
 Evolution of the RebiSmart(®) Electromechanical Autoinjector to Improve Usability in Support of Adherence to Subcutaneous Interferon Beta-1a Therapy for People Living with Multiple Sclerosis.
 Disease-Modifying Therapies in Multiple Sclerosis: A Focused Review of Rituximab.
 The Association of Health Locus of Control with Clinical and Psychosocial Aspects of Living with Multiple Sclerosis.
 Cortical thickness and cognition in older people with multiple sclerosis.
 Neurological Complications Following COVID-19 Vaccination.
 Successful treatment with subcutaneous ofatumumab in an adolescent patient with refractory myelin oligodendrocyte glycoprotein-immunoglobulin G-associated disease (MOGAD).
 Multiple sclerosis lesions that impair memory map to a connected memory circuit.
 Retraction Note: Protective effects of melatonin against mitochondrial injury in a mouse model of multiple sclerosis.
 Progressive Orthopnea and Bendopnea Due to Diaphragmatic Paralysis Associated With IgLON5 Autoimmunity.
 MS@Work in Flanders: The Development of a MS Toolkit for a Stable Employment.
 Corrigendum to "Longitudinal stability of inter-eye differences in optical coherence tomography measures for identifying unilateral optic nerve lesions in multiple sclerosis" [Journal of the Neurological Sciences 449C (2023) Start page-End page/JOTNS D-23-00048R2].
 Patient iPSC models reveal glia-intrinsic phenotypes in multiple sclerosis.
 Clinical Practice Guidelines for the Detection and Treatment of Depression in Multiple Sclerosis: A Systematic Review.
 Motor Evoked Potential-A Pilot Study Looking at Reliability and Clinical Correlations in Multiple Sclerosis.
 Cannabidiol goes nuclear: The role of PPARγ.
 Cervical myelitis: a practical approach to its differential diagnosis on MR imaging.
 A Novel Sensory Wave (P25) in Myelin Oligodendrocyte Glycoprotein-induced Experimental Autoimmune Encephalomyelitis Murine Model.
 Adult-onset depletion of sulfatide leads to axonal degeneration with relative myelin sparing.
 AXL-Induced Autophagy mitigates experimental autoimmune encephalomyelitis by suppressing microglial inflammation via the PI3K/AKT/mTOR signaling pathway.
 Results on SARS-CoV-2 mRNA Vaccine Booster from an Open-Label Multicenter Study in Ofatumumab-Treated Participants with Relapsing Multiple Sclerosis.
 Intrapsychic and Interpersonal Realms in Patients with Multiple Sclerosis and Their Comparison with Normal Individuals: A Look at Object Relations and Anger Management.
 Anti-inflammatory effects of umbilical cord mesenchymal stem cell and Autologous conditioned serum on oligodendrocyte, astrocyte, and microglial specific gene in cuprizone animal model.
 Inflammatory Bowel Disease and Neurodegenerative Diseases.
 Lipid nanocapsules for the nose-to-brain delivery of the anti-inflammatory bioactive lipid PGD(2)-G.
 Assisted Reproductive Technology and Disease Management in Infertile Women with Multiple Sclerosis.
 Ultrahigh-field MRI: where it really makes a difference.
 Bilateral Optic Neuritis and Hypophysitis With Diabetes Insipidus 1 Month After COVID-19 mRNA Vaccine: Case Report and Literature Review.
 Outcomes and Health Care Service Use in Adults 50 Years or Older With and Without Multiple Sclerosis: A 6-Year Observational Analysis.
 Feasibility of diffusion kurtosis imaging in evaluating cervical spinal cord injury in multiple sclerosis.
 THE EFFECT OF A SIX-WEEK SENSORY-MOTOR EXERCISE PROGRAM ON THE BALANCE AND FATIGUE SEVERITY IN WOMEN WITH MULTIPLE SCLEROSIS.
 Central vein sign and diffusion MRI differentiate microstructural features within white matter lesions of multiple sclerosis patients with comorbidities.
 Combining retinal structural and vascular measurements improves discriminative power for multiple sclerosis patients.
 Clinical efficacy and safety of melatonin supplementation in multiple sclerosis: a systematic review.
 Bruton's tyrosine kinase inhibition reduces disease severity in a model of secondary progressive autoimmune demyelination.
 Dimethyl fumarate possesses antiplatelet and antithrombotic properties.
 Autophagy pathways in autoimmune diseases.
 Detection of galanin receptors in the spinal cord in experimental autoimmune encephalomyelitis.
 Frequency and Predictors of Relapses following SARS-CoV-2 Vaccination in Patients with Multiple Sclerosis: Interim Results from a Longitudinal Observational Study.
 Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.
 HBV and VZV seroprotection loss in MS patients under DMT.
 The Prevalence of Diabetes Mellitus Type II (DMII) in the Multiple Sclerosis Population: A Systematic Review and Meta-Analysis.
 The Blood Concentration of Metallic Nanoparticles Is Related to Cognitive Performance in People with Multiple Sclerosis: An Exploratory Analysis.
 The risk of dementia in multiple sclerosis and neuromyelitis optica spectrum disorder.
 Shared imaging markers of fatigue across multiple sclerosis, aquaporin-4 antibody neuromyelitis optica spectrum disorder and MOG antibody disease.
 Effects of Peripheral Cooling on Upper Limb Tremor Severity and Functional Capacity in Persons with MS.
 Assessment of relationships between bullous pemphigoid and neurological diseases: A bidirectional two-sample Mendelian randomization study.
 MRI to differentiate multiple sclerosis, neuromyelitis optica, and myelin oligodendrocyte glycoprotein antibody disease.
 Effect of Tai-chi on balance, mood, cognition, and quality of life in women with multiple sclerosis: A one-year prospective study.
 Electrodiagnostic Evaluation of Motor Neuron Disease.
 Quantitative cone contrast threshold testing in patients with differing pathophysiological mechanisms causing retinal diseases.
 Antigenic mimicry - The key to autoimmunity in immune privileged organs.
 A retrospective claims analysis of fatigue in patients with multiple sclerosis on disease-modifying therapy.
 Association of body mass index and physical activity with fatigue, depression, and anxiety among Iranian patients with multiple sclerosis.
 A Perplexing Case of Bladder Mass Biopsy-Proven Neurosarcoidosis.
 Brain network correlates of epilepsy occurrence in multiple sclerosis and neuroinflammation.
 Erratum to "Multiple Sclerosis-associated Bacterial Ligand 654" [Archives of Medical Research 53/2(February 2022) 157-162/ARCMED_2021_2713].
 [Melanosis of the bladder-a rare diagnosis].
 Predictors of hypogammaglobulinemia and serious infections among patients receiving ocrelizumab or rituximab for treatment of MS and NMOSD.
 Disease modifying therapy and pregnancy outcomes in multiple sclerosis: A systematic review and meta-analysis.
 Interferon.
 Tourette syndrome and multiple sclerosis: a case report.
 Learning from pseudo-labels: deep networks improve consistency in longitudinal brain volume estimation.
 Proportion and characteristics of secondary progressive multiple sclerosis in five European registries using objective classifiers.
 Predicting physical activity for people with multiple sclerosis: The role of exercise-related cognitive errors.
 Curcumin and targeting of molecular and metabolic pathways in multiple sclerosis.
 Patterns of attention deficit in relapsing and progressive phenotypes of multiple sclerosis.
 Neuronal binding by antibodies can be influenced by low pH stress during the isolation procedure.
 Social cognitive disruptions in multiple sclerosis: The role of executive (dys)function.
 Novel Moving Steady-State Visual Evoked Potential Stimulus to Assess Afferent and Efferent Dysfunction in Multiple Sclerosis.
 Dilated Virchow-Robin Spaces are a Marker for Arterial Disease in Multiple Sclerosis.
 Trigeminal Neuralgia as A Primary Demyelinating Disease: Potential Multimodal Evidence and Remaining Controversies.
 An updated systematic review and quantitative synthesis of physical activity levels in multiple sclerosis.
 Multiple sclerosis is associated with differences in semantic memory structure.
 Analysis of metabolic syndrome and cognitive functional analysis in schizophrenic patients based on psychological intervention.
 A Predictive Autoantibody Signature in Multiple Sclerosis.
 Lifespan Neurodegeneration Of The Human Brain In Multiple Sclerosis.
 Exposure to systemic antibiotics in outpatient care and the risk of multiple sclerosis.
 Effect of Backward and Forward Walking on Lower Limb Strength, Balance, and Gait in Multiple Sclerosis: A Randomized Feasibility Trial.
 The Role of Fecal Microbiota Transplantation in the Treatment of Neurodegenerative Diseases: A Review.
 Real-world use of ofatumumab to treat multiple sclerosis 9 months post-FDA approval during COVID-19 pandemic.
 Patient and Clinician Perspectives of Physical Therapy for Walking Difficulties in Multiple Sclerosis.
 The Early Initiation Advantages of Physical Therapy in Multiple Sclerosis-A Pilot Study.
 Comparative effectiveness of cladribine tablets versus fingolimod in the treatment of highly active multiple sclerosis: A real-world study.
 Intrathecal kappa free light chain synthesis is associated with worse prognosis in relapsing-remitting multiple sclerosis.
 The Impact of Neuroimmunologic Disease and Developing Nervous System.
 A Fully Automatic Method to Segment Choroid Plexuses in Multiple Sclerosis Using Conventional MRI Sequences.
 ABC Transporter C1 Prevents Dimethyl Fumarate from Targeting Alzheimer's Disease.
 Early metabolic alterations in the normal‑appearing grey and white matter of patients with clinically isolated syndrome suggestive of multiple sclerosis: A proton MR spectroscopic study.
 Evaluation of frequency, severity, and independent risk factors for recurrence of disease activity after fingolimod discontinuation in a large real-world cohort of patients with multiple sclerosis.
 Combining in vivo proton exchange rate (k (ex)) MRI with quantitative susceptibility mapping to further stratify the gadolinium-negative multiple sclerosis lesions.
 Data monitoring roadmap. The experience of the Italian Multiple Sclerosis and Related Disorders Register.
 Investigating Relationships Among Interoceptive Awareness, Emotional Susceptibility, and Fatigue in Persons With Multiple Sclerosis.
 Non-equivalent, but still valid: Establishing the construct validity of a consumer fitness tracker in persons with multiple sclerosis.
 No Increase in Symptoms Toward the End of the Ocrelizumab Infusion Cycle in Patients With Multiple Sclerosis: Symptom Burden on Ocrelizumab: A Longitudinal Study (SymBOLS).
 Real-World Safety and Effectiveness After 5 Years of Dimethyl Fumarate Treatment in Black and Hispanic Patients with Multiple Sclerosis in ESTEEM.
 Multicentre Observational Study of Treatment Satisfaction with Cladribine Tablets in the Management of Relapsing Multiple Sclerosis in the Arabian Gulf: The CLUE Study.
 Corneal axonal loss as an imaging biomarker of neurodegeneration in multiple sclerosis: a longitudinal study.
 Methods for Brain Atrophy MR Quantification in Multiple Sclerosis: Application to the Multicenter INNI Dataset.
 Cross-talk between B cells, microglia and macrophages, and implications to central nervous system compartmentalized inflammation and progressive multiple sclerosis.
 Peripapillary hyper-reflective ovoid mass-like structures (PHOMS): clinical significance, associations, and prognostic implications in ophthalmic conditions.
 Acetyl-L-carnitine and Amyotrophic Lateral Sclerosis: current evidence and potential use.
 A case of anti-myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG) associated disorder (MOGAD) with clinical manifestations of acute disseminated encephalomyelitis: Secondary to mycoplasma pneumoniae infection.
 Distinctive transcriptomic and epigenomic signatures of bone marrow-derived myeloid cells and microglia in CNS autoimmunity.
 Moving intra-individual variability (IIV) towards clinical utility: IIV measured using a commercial testing platform.
 A Systematic Review of the Validity and Reliability of the Patient-Determined Disease Steps Scale.
 Deep learning network with differentiable dynamic programming for retina OCT surface segmentation.
 Let Us Talk Money: Subjectively Reported Financial Performance of People Living with Neurodegenerative Diseases-A Systematic Review.
 Cladribine Tablets Mode of Action, Learning from the Pandemic: A Narrative Review.
 Compromised Myelin and Axonal Molecular Organization Following Adult-Onset Sulfatide Depletion.
 Effect of Hematopoietic Stem Cell Transplantation and Post-Transplantation Cyclophosphamide on the Microglia Phenotype in Rats with Experimental Allergic Encephalomyelitis.
 The KEAP1-NRF2 System and Neurodegenerative Diseases.
 Influence of Transfer Quality and Wheelchair Type on Fear of Falling Among Full-Time Wheelchair Users.
 Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination.
 Natalizumab-immunogenicity evaluation in patients with infusion related events or disease exacerbations.
 The GABA and GABA-Receptor System in Inflammation, Anti-Tumor Immune Responses, and COVID-19.
 Dietary protection against the visual and motor deficits induced by experimental autoimmune encephalomyelitis.
 Influence of menstrual cycle and hormonal contraceptive use on MS symptom fluctuations: A pilot study.
 Addressing smoking in persons with Multiple Sclerosis: State of the science and need for a targeted intervention.
 A Birth Year Cohort and What It Can Reveal About Lipid Mediators as Putative Biomarkers of Progression in Multiple Sclerosis.
 Baclofen Toxicity.
 Cladribine.
 A 10-Year Single-Center Study of the Clinical Characteristics of Optic Neuritis-Related NMOSD, MS, and Double Seronegative Optic Neuritis, Together with Factors Predicting Visual Outcomes.
 Clinical characteristics and prognosis of optic neuritis in Taiwan - a hospital-based cohort study.
 Dyspnea and Bronchoconstriction in a Young Patient With Multiple Sclerosis Treated With Ponesimod.
 Imaging immunomodulatory treatment responses in a multiple sclerosis mouse model using hyperpolarized (13)C metabolic MRI.
 Shared decision-making in multiple sclerosis physical symptomatic care: a systematic review.
 Preserved T cell but attenuated antibody response in MS patients on fingolimod and ocrelizumab following 2nd and 3rd SARS-CoV-2 mRNA vaccine.
 Nogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model.
 Driving time-based identification of gaps in specialised care coverage: An example of neuroinflammatory diseases in Germany.
 MYD88 L265P mutation in neurologic autoimmunity without evidence of malignancy.
 Short- and Long-Term Humoral and Cellular Immune Responses to SARS-CoV-2 Vaccination in Patients with Multiple Sclerosis Treated with Disease-Modifying Therapies.
 Remyelination and Ageing: Ethical Considerations of Using Surgically Joined Animals in Research.
 Life and death of tolerogenic dendritic cells.
 Paramagnetic rim and core sign lesions in paediatric multiple sclerosis patients.
 Emerging roles of GPR109A in regulation of neuroinflammation in neurological diseases and pain.
 Dexamethasone.
 Correction: Real-world use of natalizumab in Austria: data from the Austrian Multiple Sclerosis Treatment Registry (AMSTR).
 [Social support and accompaniment for patients with disabilities].
 Using modified Ashworth scale for assessing multiple sclerosis-associated spasticity: a high time for a paradigm shift.
 IL-17 receptor goes solo in autoimmune inflammation.
 Short PDE4 Isoforms as Drug Targets in Disease.
 Efficacy and Safety of Proposed Biosimilar Natalizumab (PB006) in Patients With Relapsing-Remitting Multiple Sclerosis: The Antelope Phase 3 Randomized Clinical Trial.
 Development and multi-center validation of a fully automated digital immunoassay for neurofilament light chain: toward a clinical blood test for neuronal injury.
 Genome-wide analyses reveal widespread genetic overlap between neurological and psychiatric disorders and a convergence of biological associations related to the brain.
 Diagnostic Potential of Two Novel Biomarkers for Neuromyelitis Optica Spectrum Disorder and Multiple Sclerosis.
 GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses.
 Cognitive Contributors of Backward Walking in Persons with Multiple Sclerosis.
 The effect of COVID-19 lockdowns on exercise and the role of online exercise in Australians with multiple sclerosis.
 Change in Insomnia and Depressive Symptoms During COVID-19: A Prospective Longitudinal Study of Iranian Women with Multiple Sclerosis.
 Ketogenic diet attenuates neuroinflammation and induces conversion of M1 microglia to M2 in an EAE model of multiple sclerosis by regulating the NF-κB/NLRP3 pathway and inhibiting HDAC3 and P2X7R activation.
 Characteristics of multiple sclerosis and demyelinating disease in an Asian American population.
 Temporal pattern of cortical hypoxia in Multiple Sclerosis and its significance on neuropsychological and clinical measures of disability.
 Iron in multiple sclerosis - Neuropathology, immunology, and real-world considerations.
 The validation of the Italian version of multiple sclerosis neuropsychological screening questionnaire in Huntington's disease.
 Diet-microbiome-immune interplay in multiple sclerosis: Understanding the impact of phytoestrogen metabolizing gut bacteria.
 Multiple Sclerosis.
 The relationship between plasma prolactin levels and clinical manifestations with neuromyelitis optica spectrum disorders.
 Green tea EGCG inhibits naïve CD4(+) T cell division and progression in mice: An integration of network pharmacology, molecular docking and experimental validation.
 Role of the CXCR6/CXCL16 axis in autoimmune diseases.
 Acute central nervous system inflammation following COVID-19 vaccination: An observational cohort study.
 Cannabidiol Attenuates In Vivo Leukocyte Recruitment to the Spinal Cord Microvasculature at Peak Disease of Experimental Autoimmune Encephalomyelitis.
 Persistent virus-specific and clonally expanded antibody-secreting cells respond to induced self-antigen in the CNS.
 Fractalkine enhances oligodendrocyte regeneration and remyelination in a demyelination mouse model.
 Rapid whole-brain myelin imaging with selective inversion recovery and compressed SENSE.
 Real-time associations among MS symptoms and cognitive dysfunction using ecological momentary assessment.
 Distinct myeloid population phenotypes dependent on TREM2 expression levels shape the pathology of traumatic versus demyelinating CNS disorders.
 Synthesis and Biological Study of 4-Aminopyridine-Peptide Derivatives Designed for the Treatment of Neurodegenerative Disorders.
 Association between atopic dermatitis, autoimmune illnesses, Epstein-Barr virus, and cytomegalovirus.
 Ivermectin Protects Against Experimental Autoimmune Encephalomyelitis in Mice by Modulating the Th17/Treg Balance Involved in the IL-2/STAT5 Pathway.
 Effects of Functional Electrical Stimulation Cycling Combined With Arm Cranking Exercise on Cardiorespiratory Fitness in People With Central Nervous System Disorders: A Systematic Review and Meta-analysis.
 A systematic review: Virtual-reality-based techniques for human exercises and health improvement.
 rTMS ameliorates depression/anxiety-like behaviors in experimental autoimmune encephalitis by inhibiting neurotoxic reactive astrocytes.
 Liquid Biopsy in Neurological Diseases.
 Eight-and-a-half syndrome as manifestation of acute disseminated adenovirus encephalomyelitis.
 The Effect of Smoking on Inactivated and mRNA Vaccine Responses Applied to Prevent COVİD-19 in Multiple Sclerosis.
 Non-invasive brain stimulation on clinical symptoms in multiple sclerosis patients: A systematic review and meta-analysis.
 The effect of exercise and physical activity-interventions on step count and intensity level in individuals with multiple sclerosis: a systematic review and meta-analysis of randomized controlled trials.
 Cellular mechanisms of fibrin (ogen): insight from neurodegenerative diseases.
 Glucose metabolic reprogramming in autoimmune diseases.
 Can ChatGPT explain it? Use of artificial intelligence in multiple sclerosis communication.
 Progressive Multifocal Leukoencephalopathy.
 Tizanidine.
 Myoclonus.
 Berg Balance Testing.
 Erucic Acid: A Possible Therapeutic Agent for Neurodegenerative Diseases.
 Breaking down the cellular responses to type I interferon neurotoxicity in the brain.
 Evaluation of immunological responses to third COVID-19 vaccine among people treated with sphingosine receptor-1 modulators and anti-CD20 therapy.
 Prognostic value of single-subject grey matter networks in early multiple sclerosis.
 Editorial for "A Fully-Automatic Method to Segment Choroid Plexuses in Multiple Sclerosis Using Conventional MRI Sequences".
 Multiple Sclerosis in a Patient With Neurogenic Locus Notch Homolog Protein 3 Mutation.
 Atrophy and Severe Kinking of Trigeminal Nerve Root by Duplicate Trunks of Superior Cerebellar Artery in an Elderly Patient with Trigeminal Neuralgia.
 Targeting Neuroinflammation to Alleviate Chronic Olfactory Dysfunction in Long COVID: A Role for Investigating Disease-Modifying Therapy (DMT)?
 Cerebral enhancement in MOG antibody-associated disease.
 Genome-Wide Expression Profile in People with Optic Neuritis Associated with Multiple Sclerosis.
 L-Proline Prevents Endoplasmic Reticulum Stress in Microglial Cells Exposed to L-azetidine-2-carboxylic Acid.
 Probiotic-Fermented Camel Milk Attenuates Neurodegenerative Symptoms via SOX5/miR-218 Axis Orchestration in Mouse Models.
 Non-Immersive Virtual Reality Telerehabilitation System Improves Postural Balance in People with Chronic Neurological Diseases.
 Identification of Myelin Basic Protein Proximity Interactome Using TurboID Labeling Proteomics.
 The Lung Microbiome: A New Frontier for Lung and Brain Disease.
 Treatment De-escalation in AQP4-Ab Neuromyelitis Optica Spectrum Disorder.
 Application of Statistical Methods for Central Statistical Monitoring and Implementations on the German Multiple Sclerosis Registry.
 The role of biogenic amines in the modulation of monocytes in autoimmune neuroinflammation.
 A Dual Therapy of Nanostructured Lipid Carrier Loaded with Teriflunomide-A Dihydro-Orotate Dehydrogenase Inhibitor and an miR-155-Antagomir in Cuprizone-Induced C57BL/6J Mouse.
 1,2-(13)C(2)-Glucose Tracing Approach to Assess Metabolic Alterations of Human Monocytes under Neuroinflammatory Conditions.
 Assessment of Outer Retina and Choroid Using Swept Source Optical Coherence Tomography and Angiography in Patients With Multiple Sclerosis.
 Implementing physical activity vital sign as a self-reported measure of physical activity in patients with multiple sclerosis in a clinical setting.
 Blended versus face-to-face cognitive behavioural therapy for severe fatigue in patients with multiple sclerosis: A non-inferiority RCT.
 The Interaural Time Difference for High-Pass Filtered Noise and Its Relationship With Brainstem Dysfunction and Disability in Multiple Sclerosis.
 Self-Report Measures of Fatigue for People With Multiple Sclerosis: A Systematic Review.
 The ethical matrix as a method for involving people living with disease and the wider public (PPI) in near-term artificial intelligence research.
 Complement activation and increased anaphylatoxin receptor expression are associated with cortical grey matter lesions and the compartmentalised inflammatory response of multiple sclerosis.
 The sequence of regional structural disconnectivity due to multiple sclerosis lesions.
 Treatment Effect on Brain Atrophy Correlates with Treatment Effect on Cognition in Multiple Sclerosis.
 Association between Expanded Disability Status Scale score and dietary antioxidant capacity in patients with multiple sclerosis.
 A DFT study on the probability of using the heteroatom decorated graphitic carbonitride (g-C(3)N(4)) species for delivering of three novel Multiple sclerosis drugs.
 Overall and patient-specific comparative effectiveness of dimethyl fumarate versus teriflunomide: A novel approach to precision medicine applied to the German NeuroTrans Data Multiple Sclerosis Registry.
 Feasibility, Outcomes, and Perceptions of a Virtual Group Exercise Program in Multiple Sclerosis.
 Identification of commensal gut microbiota signatures as predictors of clinical severity and disease progression in multiple sclerosis.
 Factors Associated with Therapeutic Adherence in Multiple Sclerosis in Spain.
 Overview of the Gut Microbiome.
 Curcumin, inflammation, and neurological disorders: How are they linked?
 Novel 4-chloro-N-phenyl Benzamide Derivatives as p38α Mitogenactivated Protein Kinase Inhibitors for Treating Cancer, COVID-19, and Other Diseases.
 Microglia regulation of central nervous system myelin health and regeneration.
 Neurologists' lived experiences of communicating the diagnosis of a motor neurodegenerative condition: an interpretative phenomenological analysis.
 L-serine: Neurological Implications and Therapeutic Potential.
 Comparing clinical and imaging features of patients with MOG antibody-positivity and with and without oligoclonal bands.
 Immune Regulatory Functions of Macrophages and Microglia in Central Nervous System Diseases.
 Viral-induced neuroinflammation: Different mechanisms converging to similar exacerbated glial responses.
 Therapeutic potential of extracellular vesicles in neurodegenerative disorders.
 Efficacy of Heshouwu () on gut mircobiota in mice with autoimmune encephalomyelitis.
 Dual role of Exosome in neurodegenerative diseases: a review study.
 The role of high mobility group box 1 in neuroinflammatory related diseases.
 Paroxysmal painful tonic spasms in neuromyelitis optica spectrum disorder.
 Relieving Administrative Burden on Clinical Staff with Streamlined Workflows And Speech-Recognition Software.
 The Development of Ofatumumab, a Fully Human Anti-CD20 Monoclonal Antibody for Practical Use in Relapsing Multiple Sclerosis Treatment.
 Cannabinoid Hyperemesis Syndrome.
 Mapping brain microstructure in vivo in health and disease using diffusion MRI.
 Ferroptosis: A potential therapeutic target in autoimmune disease (Review).
 Revisiting the critical roles of reactive astrocytes in neurodegeneration.
 Prednisone.
 Bilateral Internuclear Ophthalmoplegia Caused by Dengue Fever.
 Intention Tremor.
 Transition of Care to Adult Neuroimmunology.
 [Recent Advances in Novel Therapies for Neurological Diseases: An Overview and Future Scope].
 Interferon-Induced Retinopathy.
 Mapping the relationship of white matter lesions to depression in multiple sclerosis.
 Predictors and correlates of emotionalism across acquired and progressive neurological conditions: A systematic review.
 Therapeutic effect of combination vitamin D3 and siponimod on remyelination and modulate microglia activation in cuprizone mouse model of multiple sclerosis.
 Indoleamine 2,3-Dioxygenase as a Therapeutic Target for Alzheimer's Disease and Geriatric Depression.
 Chlamydia Pneumonia.
 NLRX1: versatile functions of a mitochondrial NLR protein that controls mitophagy.
 Role of the immune system in amyotrophic lateral sclerosis. Analysis of the natural killer cells and other circulating lymphocytes in a cohort of ALS patients.
 DHA/EPA (Omega-3) and LA/GLA (Omega-6) as Bioactive Molecules in Neurodegenerative Diseases.
 How far MS lesion detection and segmentation are integrated into the clinical workflow? A systematic review.
 High levels of endothelial ICAM-1 prohibit natalizumab mediated abrogation of CD4(+) T cell arrest on the inflamed BBB under flow in vitro.
 Identifying specific myelopathy etiologies in the evaluation of suspected myelitis: A retrospective analysis.
 Decipher potential biomarkers of diagnosis and disease activity for NMOSD with AQP4 using LC-MS/MS and Simoa.
 Common comorbid and secondary conditions leading to hospitalization in multiple sclerosis patients in the United States.
 The Role of Interferon-α in Neurodegenerative Diseases: A Systematic Review.
 Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants.
 Assessing robustness and generalization of a deep neural network for brain MS lesion segmentation on real-world data.
 DAPTA, a C-C Chemokine Receptor 5 (CCR5), Leads to the Downregulation of Notch/NF-κB Signaling and Proinflammatory Mediators in CD40(+) Cells in Experimental Autoimmune Encephalomyelitis Model in SJL/J Mice.
 Prophylactic Glatiramer Acetate Treatment Positively Attenuates Spontaneous Opticospinal Encephalomyelitis.
 Do clinical trials prepare to fail by failing to prepare? An examination of MS trials and recommendations for patient-reported outcome measure selection.
 T-cell immunoglobulin and mucin-domain containing-3 (TIM-3): Solving a key puzzle in autoimmune diseases.
 Transverse myelitis in children and adults.
 T follicular helper cells and T follicular regulatory cells in autoimmune diseases.
 Assessment of Microglial Activation in Alzheimer Disease Using 18 F-PBR06 PET.
 Bilateral Vocal Cord Paralysis.
 Adult-Onset Neuroepidemiology in Finland: Lessons to Learn and Work to Do.
 Specialty care after transition to long-term care in nursing home.
 Chelation Therapy Associated with Antioxidant Supplementation Can Decrease Oxidative Stress and Inflammation in Multiple Sclerosis: Preliminary Results.
 Early Magnetic Resonance Imaging Features of New Paramagnetic Rim Lesions in Multiple Sclerosis.
 Correction to: Argentinean consensus recommendations for the use of telemedicine in clinical practice in adult people with multiple sclerosis.
 Comparison of physical performance, gait, balance, falls efficacy, and step reaction time in individuals with multiple sclerosis.
 Dietary wheat amylase trypsin inhibitors exacerbate CNS inflammation in experimental multiple sclerosis.
 Best practices in phase III clinical trials on DMTs for multiple sclerosis: a systematic analysis and appraisal of published trials.
 The effect of cooling garments to improve physical function in people with multiple sclerosis: A systematic review and meta-analysis.
 Functional and structural readouts for early detection of retinal involvement in multiple sclerosis.
 Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells.
 Differential DNA methylation associated with multiple sclerosis and disease modifying treatments in an underrepresented minority population.
 The microRNAs (miRs) overexpressing mesenchymal stem cells (MSCs) therapy in neurological disorders; hope or hype.
 Capturing primary ozonides for a syn-dihydroxylation of olefins.
 Correction: Uveitis and Multiple Sclerosis: Potential Common Causal Mutations.
 Microbiome in Anxiety and Other Psychiatric Disorders.
 Postural Orthostatic Tachycardia Syndrome in Spinal Cord Injury.
 Cerebellar Contributions to Motor and Cognitive Control in Multiple Sclerosis.
 [Pharmacotherapy: New drugs and vaccines in 2022].
 Neutrophil extracellular traps in central nervous system pathologies: A mini review.
 Optic neuritis associated with seronegative autoimmune encephalitis: a case report.
 EBV and Lymphomagenesis.
 Vacuole Membrane Protein 1 (VMP1) Restricts NLRP3 Inflammasome Activation by Modulating SERCA Activity and Autophagy.
 Immune Globulin.
 Glial aging and its impact on central nervous system myelin regeneration.
 Get With the Guidelines on MS Imaging by Leveraging Peer Learning.
 Overview of myelin, major myelin lipids, and myelin-associated proteins.
 Transverse Myelitis.
 Set Up and Execution of an Effective Standardized Patient Program in Medical Simulation.
 Early Splicing Complexes and Human Disease.
 Effect of Music Based Therapy Rhythmic Auditory Stimulation (RAS) Using Wearable Device in Rehabilitation of Neurological Patients: A Systematic Review.
 The Role of Viral Infections in the Onset of Autoimmune Diseases.
 Can the Therapeutic Spectrum of Probiotics be Extended: Exploring Potential of Gut Microbiome.
 Sphingosine 1-Phosphate Lyase in the Developing and Injured Nervous System: a Dichotomy?
 Fourier-transform infrared spectroscopy: A universal optical sensing technique with auspicious application prospects in the diagnosis and management of autoimmune diseases.
 Therapeutic targeting of gut-originating regulatory B cells in neuroinflammatory diseases.
 Neurofilaments - Small proteins of physiological significance and predictive power for future neurodegeneration and cognitive decline across the life span.
 Virus-Based Biological Systems as Next-Generation Carriers for the Therapy of Central Nervous System Diseases.
 N-Acetylaspartate Drives Oligodendroglial Differentiation via Histone Deacetylase Activation.
 Progressive multifocal leukoencephalopathy with natalizumab extended or standard interval dosing in the United States and the rest of the world.
 History of the discovery and development of Biomodulina T (InmunyVital®), a useful immunomodulator with a broad range of clinical applications.
 Interferon-gamma ameliorates experimental autoimmune encephalomyelitis by inducing homeostatic adaptation of microglia.
 Hopelessness in Patients with Early-Stage Relapsing-Remitting Multiple Sclerosis.
 Effects of inpatient energy management education and high-intensity interval training on health-related quality of life in persons with multiple sclerosis: A randomized controlled superiority trial with six-month follow-up.
 Effects of concurrent training and CoQ10 on neurotrophic factors and physical function in people with Multiple Sclerosis: a pilot study.
 2-Methoxyestradiol-3,17-O,O-bis-sulfamate inhibits store-operated Ca(2+) entry in T lymphocytes and prevents experimental autoimmune encephalomyelitis.
 Factors Influencing COVID-19 Vaccine Hesitancy among Patients with Serious Chronic Illnesses during the Initial Australian Vaccine Rollout: A Multi-Centre Qualitative Analysis Using the Health Belief Model.
 A Clinically Relevant Dosage of Mitoxantrone Disrupts the Glutathione and Lipid Metabolic Pathways of the CD-1 Mice Brain: A Metabolomics Study.
 Fatty acid desaturation by stearoyl-CoA desaturase-1 controls regulatory T cell differentiation and autoimmunity.
 Chemical exchange saturation transfer MRI detects myelin changes in cuprizone mouse model at 3T.
 MOG antibodies in adults with a first demyelinating event suggestive of multiple sclerosis.
 Unveiling the role of gut-brain axis in regulating neurodegenerative diseases: A comprehensive review.
 Neutrophil biology in injuries and diseases of the central and peripheral nervous systems.
 Cellular senescence and neurodegeneration.
 Chronic effects of the sympathetic nervous system in inflammatory models.
 Automatic Segmentation of Retinal Layers in Multiple Neurodegenerative Disorder Scenarios.
 Hepatitis B reactivation is a rare event among patients with resolved infection undergoing anti-CD20 antibodies in monotherapy without antiviral prophylaxis: results from the HEBEM study.
 Molecular Targets Underlying the Neuroprotective Effects of Boswellic acid: A Systematic Review.
 STING-Triggered CNS Inflammation in Human Neurodegenerative Diseases.
 TSPO PET brain inflammation imaging: A transdiagnostic systematic review and meta-analysis of 156 case-control studies.
 Blending citizen science with natural language processing and machine learning: Understanding the experience of living with multiple sclerosis.
 A genome-wide in vivo CRISPR screen identifies essential regulators of T cell migration to the CNS in a multiple sclerosis model.
 SARS-CoV-2 vaccination and infection in ozanimod-treated participants with relapsing multiple sclerosis.
 Mood Symptoms and Chronic Fatigue Syndrome Due to Relapsing-Remitting Multiple Sclerosis Are Associated with Immune Activation and Aberrations in the Erythron.
 Health Effects of Vitamin D Supplementation: Lessons Learned From Randomized Controlled Trials and Mendelian Randomization Studies.
 Characterizing internet search patterns for neurologic and neurosurgical conditions following celebrity diagnosis.
 The reliability and validity of the 30-second chair stand test and modified four square step test in persons with multiple sclerosis.
 [Consensus recommendations on regional interdisciplinary standardization of MRI diagnostics for multiple sclerosis in the metropolitan area of Essen].
 CancerHERVdb: Human Endogenous Retrovirus (HERV) Expression Database for Human Cancer Accelerates Studies of the Retrovirome and Predictions for HERV-Based Therapies.
 Automated Vowel Articulation Analysis in Connected Speech Among Progressive Neurological Diseases, Dysarthria Types, and Dysarthria Severities.
 The role of the CD8+ T cell compartment in ageing and neurodegenerative disorders.
 Serum glial fibrillary acidic protein in natalizumab-treated relapsing-remitting multiple sclerosis: An alternative to neurofilament light.
 Case Report and Clinical Reasoning: Fulminant Liver Failure and Invasive Aspergillosis Following Ocrelizumab Treatment in a 21 Year-Old Woman.
 Pharmacological targeting of coagulation factor XI attenuates experimental autoimmune encephalomyelitis in mice.
 Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice.
 Real-World Effectiveness of Natalizumab Extended Interval Dosing in a French Cohort.
 Prior cycles of anti-CD20 antibodies affect antibody responses after repeated SARS-CoV-2 mRNA vaccination.
 Is vaccine response to SARS-CoV-2 preserved after switching to anti-CD20 therapies in patients with multiple sclerosis or related disorders?
 Cerebral microbleeds. Utility of SWI sequences.
 Assay of Sphingosine 1-phosphate Transporter Spinster Homolog 2 (Spns2) Inhibitors.
 Cannabis Use and Associated Gastrointestinal Disorders: A Literature Review.
 Recurrent Catatonia and Demyelinating Disorders.
 Breaking the circulus vitiosus of neuroinflammation: Resveratrol attenuates the human glial cell response to cytokines.
 Modulation of microglial metabolism facilitates regeneration in demyelination.
 Modified Ashworth Scale.
 Neuroprotective Potential of Hesperidin as Therapeutic Agent in the Treatment of Brain Disorders: Preclinical Evidence-based Review.
 Aseptic pleocytosis eight days after the first dose of a vector-based SARS-CoV-2 vaccine.
 Corrigendum to 'To be or not to be vaccinated: The risk of MS or NMOSD relapse after COVID-19 vaccination and infection'[Multiple sclerosis and related disorders vol. 65 (2022) 104014].
 The Promise of Niacin in Neurology.
 Prognosis in chronic progressive neurologic disease: a narrative review.
 Cladribine.
 Deep Learning Algorithms for Brain Imaging: From Black Box to Clinical Toolbox?
 Targeted evolution of adeno-associated virus capsids for systemic transgene delivery to microglia and tissue-resident macrophages.
 Neuromyelitis Optica (NMO, Devics Disease).
 Interplay between activation of endogenous retroviruses and inflammation as common pathogenic mechanism in neurological and psychiatric disorders.
 Immunogenicity and safety of mixed COVID-19 vaccine regimens in patients with immune-mediated inflammatory diseases: a single-centre prospective cohort study.
 Predictors of Long-Term Visual Acuity in a Modern Cohort of Patients With Acute Idiopathic and Multiple Sclerosis-Associated Optic Neuritis.
 Combining robot-assisted therapy with virtual reality or using it alone? A systematic review on health-related quality of life in neurological patients.
 A systematic review of the symptomatic management of Lhermitte's phenomenon.
 VDR Gene Single Nucleotide Polymorphisms and Autoimmunity: A Narrative Review.
 An Updated Evaluation of Intrathecal IgG Synthesis Markers in Relation to Oligoclonal Bands.
 Hypogammaglobulinemia secondary to B-cell depleting therapies in neuroimmunology: Comparing management strategies.
 In Vitro Effects of Methylprednisolone over Oligodendroglial Cells: Foresight to Future Cell Therapies.
 Total Hip Arthroplasty in Patients With Neurological Conditions: A Systematic Review.
 Investigation of sexual dysfunction and depression prevalence in neuromyelitis optica spectrum disorder.
 Monoclonal antibodies for the management of central nervous system diseases: clinical success and future strategies.
 [Role of the MS nurse specialist in the patient's care pathway].
 Psychosocial difficulties experienced by MS patients in their quality of life: A comparative study of two countries.
 A common mechanism links Epstein-Barr virus infections and autoimmune diseases.
 Microglial Metabolic Reprogramming: Emerging Insights and Therapeutic Strategies in Neurodegenerative Diseases.
 Rituximab for Pediatric Central Nervous System Inflammatory Disorders in Alberta, Canada.
 Physiological benefits of Akkermansia muciniphila under high-altitude hypoxia.
 Effect of the Combination of Different Therapies on Oxidative Stress in the Experimental Model of Multiple Sclerosis.
 The added value of spinal cord lesions to disability accrual in multiple sclerosis.
 A prospective observational longitudinal study with a two-year follow-up of multiple sclerosis patients on Cladribine.
 Multiway sparse distance weighted discrimination.
 Effectiveness of multiple disease-modifying therapies in relapsing-remitting multiple sclerosis: causal inference to emulate a multiarm randomised trial.
 Therapeutic implications of phosphorylation- and dephosphorylation-dependent factors of cAMP-response element-binding protein (CREB) in neurodegeneration.
 Matrine exerts its neuroprotective effects by modulating multiple neuronal pathways.
 Counting the Toll of Inflammation on Schizophrenia-A Potential Role for Toll-like Receptors.
 The many "Neurofaces" of Prohibitins 1 and 2: Crucial for the healthy brain, dysregulated in numerous brain disorders.
 T cells in the brain inflammation.
 Role of Peptidylarginine Deiminase 4 in Central Nervous System Diseases.
 Colitis in ocrelizumab-treated patients: The dilemma of causation versus association in immune-mediated iatrogenicity.
 Neurofilament light chain as neuronal injury marker - what is needed to facilitate implementation in clinical laboratory practice?
 Progestogen-Mediated Neuroprotection in Central Nervous System Disorders.
 Attenuation of immune activation in patients with multiple sclerosis on a wheat-reduced diet: a pilot crossover trial.
 Addressing the key issue: Antigen-specific targeting of B cells in autoimmune diseases.
 Vitamin D-induced hypercalcaemia and acute kidney injury in sarcoidosis.
 Farnesol brain transcriptomics in CNS inflammatory demyelination.
 Sleep Disturbances in Autoimmune Neurological Diseases.
 Neuronal activity and remyelination: new insights into the molecular mechanisms and therapeutic advancements.
 Painful tonic spasms in a patient with neuromyelitis optica spectrum disorder: A case report.
 Alterations in oligodendrocyte transcriptional networks reveal region-specific vulnerabilities to neurological disease.
 Therapeutic potential of targeting IL-17 and its receptor signaling in neuroinflammation.
 Correction to: Communicating the relevance of neurodegeneration and brain atrophy to multiple sclerosis patients: patient, provider and researcher perspectives.
 Myelin dystrophy in the aging prefrontal cortex leads to impaired signal transmission and working memory decline: a multiscale computational study.
 Nuclear orphan receptors: A novel therapeutic agent in neuroinflammation.
 Correction to: Resting-state functional MRI in multicenter studies on multiple sclerosis: a report on raw data quality and functional connectivity features from the Italian Neuroimaging Network Initiative.
 [Neurology: what's new in 2022].
 Meningeal T cells function in the central nervous system homeostasis and neurodegenerative diseases.
 Predicting Cognitive Decline in Primary Progressive Aphasia: Can Brain Networks Be Crystal Balls?
 Isobaric Incorporation of C13-Histidine for the Assessment of Remyelination.
 The Role of Peptidyl Arginine Deiminase IV(PADI4) in Cancers.
 Dissecting the Relationship Between Neuropsychiatric and Neurodegenerative Disorders.
 Neuropharmacology of Organoselenium Compounds in Mental Disorders and Degenerative Diseases.
 Looking at the Full Picture: Utilizing Topic Modeling to Determine Disease-Associated Microbiome Communities.
 Siponimod-Related Bilateral Macular Edema: A Transient and Completely Reversible Disorder.
 HACA3: A unified approach for multi-site MR image harmonization.
 Socioeconomic, health-care access and clinical determinants of disease severity in Multiple Sclerosis in Chile.
 The impact of the COVID-19 pandemic on neuropsychiatric and sleep disorders, and quality of life in individuals with neurodegenerative and demyelinating diseases: a systematic review and meta-analysis of observational studies.
 Inhibiting the NLRP3 Inflammasome with MCC950 Alleviates Neurological Impairment in the Brain of EAE Mice.
 Astrocyte-oligodendrocyte interaction regulates central nervous system regeneration.
 Mesenchymal stem cell secretome and extracellular vesicles for neurodegenerative diseases: Risk-benefit profile and next steps for the market access.
 The potential of CYP46A1 as a novel therapeutic target for neurological disorders: An updated review of mechanisms.
 Do patients diagnosed with a neurological disease present increased risk of suicide?
 Turning When Using Smartphone in Persons With and Those Without Neurologic Conditions: Observational Study.
 Denoising of diffusion MRI in the cervical spinal cord - effects of denoising strategy and acquisition on intra-cord contrast, signal modeling, and feature conspicuity.
 Exploring the impact of exercise and essential amino acid plus cholecalciferol supplementation on physical fitness and body composition in multiple sclerosis: A case study.
 Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies.
 Exosomal microRNAs as diagnostic biomarkers and therapeutic applications in neurodegenerative diseases.
 Application of mesenchymal stem cells (MSCs) in neurodegenerative disorders: History, findings, and prospective challenges.
 Neuroaxonal and cellular damage/protection by prostanoid receptor ligands, fatty acid derivatives and associated enzyme inhibitors.
 Fecal Microbiota Underlying the Coexistence of Schizophrenia and Multiple Sclerosis in Chinese Patients.
 Multiplex Analysis of Cerebrospinal Fluid and Serum Exosomes MicroRNAs of Untreated Relapsing Remitting Multiple Sclerosis (RRMS) and Proposing Noninvasive Diagnostic Biomarkers.
 Developing a Blood Cell-Based Diagnostic Test for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Using Peripheral Blood Mononuclear Cells.
 Association between SUMF1 polymorphisms and COVID-19 severity.
 Processing speed test: Results from a Japanese normative sample of healthy participants compared with a US normative sample.
 Pearls & Oy-sters: Hemorrhagic Myelitis Following SARS-CoV-2 Infection.
 Discussing sexuality with patients with neurological diseases: A survey among neurologists working in Saudi Arabia.
 Increased physical activity, higher educational attainment, and the use of mobility aid are associated with self-esteem in people with physical disabilities.
 Endocytosis of AMPA receptors: Role in neurological conditions.
 Inhibition of pro-inflammatory signaling in human primary macrophages by enhancing arginase-2 via target site blockers.
 Editorial: Complement in nervous system disease.
 Update on the role of T cells in cognitive impairment.
 Musculin does not modulate the disease course of Experimental Autoimmune Encephalomyelitis and DSS colitis.
 Aerobic exercise does not affect serum neurofilament light in patients with mild Alzheimer's disease.
 Motor, cognitive, and combined rehabilitation approaches on MS patients' cognitive impairment.
 IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system.
 Neuroprotective Role of Klotho on Dementia.
 CCL13 and human diseases.
 Use of cannabidiol (CBD) for the treatment of cognitive impairment in psychiatric and neurological illness: A narrative review.
 Wobbly hedgehog syndrome- a progressive neurodegenerative disease.
 Dimethyl Fumarate as Potential Treatment for Alzheimer's Disease: Rationale and Clinical Trial Design.
 Susac syndrome - the current review of knowledge and own experience presentation.
 Interferons in COVID-19: missed opportunities to prove efficacy in clinical phase III trials?
 Adalimumab-induced central nervous system demyelination in a patient with rheumatoid arthritis.
 Biotin Deficiency.
 Design, synthesis, and biological activity studies on benzimidazole derivatives targeting myeloperoxidase.
 Quantitative analysis of disease-related metabolic dysregulation of human microbiota.
 Strategies for Manipulating Microglia to Determine Their Role in the Healthy and Diseased Brain.
 Dietary energy restriction in neurological diseases: what's new?
 Olfactory function in Susac syndrome.
 Calreticulin: Endoplasmic reticulum Ca(2+) gatekeeper.
 Cerebral Vasculitis Revealing Systemic Sarcoidosis: A Case Report and Review of the Literature.
 Endocytic proteins mediating GPR15 receptor internalization provide insight into the underlying mechanisms.
 FOXP3 (+) regulatory T cells use heparanase to access IL-2 bound to ECM in inflamed tissues.
 The Acute Optic Neuritis Network (ACON): Study protocol of a non-interventional prospective multicenter study on diagnosis and treatment of acute optic neuritis.
 The economic burden of diseases in the Nordic countries: A systematic review.
 Structural brain changes in patients with post-COVID fatigue: a prospective observational study.
 Targeting Sigma Receptors for the Treatment of Neurodegenerative and Neurodevelopmental Disorders.
 The importance of autologous hematopoietic stem cell transplantation in severe cases of neuromyelitis optica spectrum disorder.
 Neurodegeneration in the retina of motoneuron diseases: a longitudinal study in amyotrophic lateral sclerosis and Kennedy's disease.
 Astrocytic Chitinase-3-like protein 1 in neurological diseases: Potential roles and future perspectives.
 The Cytokine CX3CL1 and ADAMs/MMPs in Concerted Cross-Talk Influencing Neurodegenerative Diseases.
 Three-dimensional multi-parameter brain mapping using MR fingerprinting.
 The role of sphingosine 1-phosphate metabolism in brain health and disease.
 Low sulfated heparan sulfate mimetic differentially affects repair in immune-mediated and toxin-induced experimental models of demyelination.
 Granulocyte-macrophage colony-stimulating factor-stimulated human macrophages demonstrate enhanced functions contributing to T-cell activation.
 Factors associated with the misdiagnosis of neuromyelitis optica spectrum disorder.
 Cost-effectiveness analysis of hydrophilic-coated catheters in long-term intermittent catheter users in the UK.
 Highly Sensitive 3-Tesla Real Inversion Recovery MRI Detects Leptomeningeal Contrast Enhancement in Chronic Active Multiple Sclerosis.
 Ketogenic diet in relapsing multiple sclerosis: Patient perceptions, post-trial diet adherence & outcomes.
 Lactoferrin for Mental Health: Neuro-Redox Regulation and Neuroprotective Effects across the Blood-Brain Barrier with Special Reference to Neuro-COVID-19.
 Osteopontin Is Associated with Multiple Sclerosis Relapses.
 Exploring the Role of Plasma Lipids and Statins Interventions on Multiple Sclerosis Risk and Severity: A Mendelian Randomization Study.
 Characterization of Depression- and Anxiety-Like Behaviours in a Mouse Model of Relapsing-Remitting Multiple Sclerosis.
 CLIPPERS: Multiparametric and quantitative MRI features.
 Challenging diagnosis and treatment decision of a long-history autoantibody-negative autoimmune encephalitis: Expert commentary.
 Tropical spastic paraparesis.
 Novel Gastroprotective and Thermostable Cocrystal of Dimethyl Fumarate: Its Preparation, Characterization, and In Vitro and In Vivo Evaluation.
 The Role of Gut Microbiota in Glaucoma Progression and Other Retinal Diseases.
 Maternal vitamin D deficiency and brain functions: a never-ending story.
 Evidence from ClinicalTrials.gov on the growth of Digital Health Technologies in neurology trials.
 Deconfounded Dimension Reduction via Partial Embeddings.
 Tinetti Gait and Balance Test.
 Peginterferon Beta.
 Neuroanatomy, Optic Tract.
 Gut Microbiota and Neuropsychiatric Disorders.
 Correction to: Effectiveness and safety profile of cladribine in an Italian real-life cohort of relapsing-remitting multiple sclerosis patients: a monocentric longitudinal observational study.
 CCR6 as a Potential Target for Therapeutic Antibodies for the Treatment of Inflammatory Diseases.
 Alemtuzumab.
 Effect of Substituents on Solubility, Medicinal, Absorption, Emission and Cationic/Anionic Detection Properties of Anthraquinone Derivatives.
 Interferon lambda as a potential treatment for COVID-19.
 Recent advances in the development of RIPK2 modulators for the treatment of inflammatory diseases.
 SAPHO Syndrome Complicated by Lesions of the Central Nervous System Successfully Treated with Brodalumab.
 Interactions Between Astrocytes and Oligodendroglia in Myelin Development and Related Brain Diseases.
 White matter disease derived from vascular and demyelinating origins.
 Endophytic fungi: a potential source for drugs against central nervous system disorders.
 Methods to Study Inflammasome Activation in the Central Nervous System: Immunoblotting and Immunohistochemistry.
 A Perplexing case of isolated abducens nerve palsy in a primigravida woman: A case report.
 Etiology of spastic foot drop among 16 patients undergoing electrodiagnostic studies: patient series.
 ProBDNF and its receptors in immune-mediated inflammatory diseases: novel insights into the regulation of metabolism and mitochondria.
 Augmentation of a neuroprotective myeloid state by hematopoietic cell transplantation.
 Acute Disseminated Encephalomyelitis Post COVID-19 Pneumonia.
 Implementing functional electrical stimulation clinical practice guidelines to support mobility: A stakeholder consultation.
 SARS-CoV-2 mRNA vaccination induces an antigen-specific T cell response correlating with plasma interferon-gamma in B cell depleted patients.
 Immune Response to Initial and Booster SARS-CoV-2 mRNA Vaccination in Patients Treated with Siponimod-Final Analysis of a Nonrandomized Controlled Clinical Trial (AMA-VACC).
 Proline Isomerization: From the Chemistry and Biology to Therapeutic Opportunities.
 Screening for osteoporosis in people with MS: A new risk score.
 TNF and TNF receptors as therapeutic targets for rheumatic diseases and beyond.
 Investigating Causality and Shared Genetic Architecture between Neurodegenerative Disorders and Inflammatory Bowel Disease.
 Therapeutic Implications of Some Natural Products for Neuroimmune Diseases: A Narrative of Clinical Studies Review.
 Differentiating Neurodegenerative Disease from Compressive Cervical Myelopathy Using Motor Evoked Potentials.
 Masitinib analogues with the N-methylpiperazine group replaced - A new hope for the development of anti-COVID-19 drugs.
 Neurobehavioral, biochemical and histological assessment of the effects of resveratrol on cuprizone-induced demyelination in mice: role of autophagy modulation.
 Is telehealth an effective and feasible option for improving falls-related outcomes in community-dwelling adults with neurological conditions? A systematic review and meta-analysis.
 Accelerometry measures of physical activity and sedentary behavior: Associations with cognitive functioning in MS.
 Experimental Autoimmune Encephalomyelitis of Mice: IgGs from the Sera of Mice Hydrolyze miRNAs.
 Whole-body cryotherapy as a treatment for chronic medical conditions?
 Seasonal Variation in Neurologic Hospitalizations in the United States.
 Physician experiences with and perceptions of risk evaluation and mitigation strategy programs with elements to assure safe use.
 Functions of Astrocytes under Normal Conditions and after a Brain Disease.
 Exosomes as biomarkers and therapeutic delivery for autoimmune diseases: Opportunities and challenges.
 Physiology, Deep Tendon Reflexes.
 The role of the probiotic Akkermansia muciniphila in brain functions: insights underpinning therapeutic potential.
 Therapeutic effect of the total saponin from Panax Japonicus on experimental autoimmune encephalomyelitis by attenuating inflammation and regulating gut microbiota in mice.
 The gut microbiota-brain axis in neurological disorder.
 Isolated Sixth Nerve Palsies in a Child With Familial Hemophagocytic Lymphohistiocytosis Type 2.
 Serum neurofilament light chain levels at attack predict post-attack disability worsening and are mitigated by inebilizumab: analysis of four potential biomarkers in neuromyelitis optica spectrum disorder.
 Vaccines and the Risk of Hospitalization for Multiple Sclerosis Flare-Ups.
 The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer's disease.
 Brain-specific glycosylation of protein tyrosine phosphatase receptor type Z (PTPRZ) marks a demyelination-associated astrocyte subtype.
 Association analysis between symptomology and herpesvirus IgG antibody concentrations in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and multiple sclerosis.
 Association of Selenium Levels with Neurodegenerative Disease: A Systemic Review and Meta-Analysis.
 Therapy of autoimmune inflammation in sporadic amyotrophic lateral sclerosis: Dimethyl fumarate and H-151 downregulate inflammatory cytokines in the cGAS-STING pathway.
 The pursuit of mechanistic links between sleep disturbances and pain: are we getting warmer?
 Intermittent fasting: A promising dietary intervention for autoimmune diseases.
 The role of the ATP-Binding Cassette A1 (ABCA1) in neurological disorders: a mechanistic review.
 Does EGFR Signaling Mediate Orexin System Activity in Sleep Initiation?
 Paroxysmal Neuropathic Pruritus in Patients With Chiari Malformation Type I: A Rare Phenotype.
 Regaining Autonomy in a Holding Environment: Patients' Perspectives on the Existential Communication with Physicians When Suffering from a Severe, Chronic Illness: A Qualitative Nordic Study.
 Accelerometry applications and methods to assess standing balance in older adults and mobility-limited patient populations: a narrative review.
 Effectiveness of dialectical behavior therapy as a transdiagnostic treatment for improving cognitive functions: a systematic review.
 7T MRI in transient ischemic attacks: Have we only seen the tip of the iceberg?
 The effect of statins on the differentiation and function of central nervous system cells.
 Familial Mediterranean Fever and Transverse Myelitis: A Causal Relation?
 The Role of Ketogenic Diet in the Treatment of Neuroblastoma.
 Clinical usefulness of testing for severe acute respiratory syndrome coronavirus 2 antibodies.
 Volvulus.
 The Role of monosodium glutamate (MSG) in Epilepsy and other Neurodegenerative Diseases: Phytochemical-based Therapeutic Approaches and Mechanisms.
 Type 2 immunity in the brain and brain borders.
 Metabolism, pharmacokinetics and excretion of [(14)C]dimethyl fumarate in healthy volunteers: an example of xenobiotic biotransformation following endogenous metabolic pathways.
 Active constituents of saffron (Crocus sativus L.) and their prospects in treating neurodegenerative diseases (Review).
 CNS Ageing in Health and Neurodegenerative Disorders.
 Optimized synthesis and pharmacological evaluation of HCN channel inhibitor EC18.
 Customer-centric product presentations for monoclonal antibodies.
 Interleukin-4 as a therapeutic target.
 Accelerating Digitalization in Healthcare with the InSilicoTrials Cloud-Based Platform: Four Use Cases.
 Advanced methods and novel biomarkers in autoimmune diseases ‑ a review of the recent years progress in systemic lupus erythematosus.
 Hepatitis C: A Rare Cause of Subacute Paralysis.
 A Critical Perspective on the Supplementation of Akkermansia muciniphila: Benefits and Harms.
 Does the functional polymorphism-1562C/T of MMP-9 gene influence brain disorders?
 IL-17A Facilitates Entry of Autoreactive T-Cells and Granulocytes into the CNS During EAE.
 Hemiplegic Migraine with Concurrent SARS-CoV-2 Infection Leads to Motor Vehicle Collision: a Case Report.
 Brain-reactive autoantibodies in neuropsychiatric systemic lupus erythematosus.
 Scanner agnostic large-scale evaluation of MS lesion delineation tool for clinical MRI.
 The Ah Receptor from Toxicity to Therapeutics: Report from the 5th AHR Meeting at Penn State University, USA, June 2022.
 Additive beneficial effects of aerobic training and royal jelly on hippocampal inflammation and function in experimental autoimmune encephalomyelitis rats.
 Pathogenesis, Clinical Features, and Treatment of Patients with Myelin Oligodendrocyte Glycoprotein (MOG) Autoantibody-Associated Disorders Focusing on Optic Neuritis with Consideration of Autoantibody-Binding Sites: A Review.
 Diagnosis and treatment of Watershed strokes: a narrative review.
 Neuro faces of beneficial T cells: essential in brain, impaired in aging and neurological diseases, and activated functionally by neurotransmitters and neuropeptides.
 Severe disease reactivation in seropositive neuromyelitis optica spectrum disorders patients after stopping eculizumab treatment.
 Immunomodulatory Aspects of Therapeutic Plasma Exchange in Neurological Disorders-A Pilot Study.
 Automated detection of hyperreflective foci in the outer nuclear layer of the retina.
 Neurotrophic Factors as Regenerative Therapy for Neurodegenerative Diseases: Current Status, Challenges and Future Perspectives.
 Implications from proteomic studies investigating circadian rhythm disorder-regulated neurodegenerative disease pathology.
 Unveiling the modulation of Nogo receptor in neuroregeneration and plasticity: Novel aspects and future horizon in a new frontier.
 Restoration of metal homeostasis: a potential strategy against neurodegenerative diseases.
 WNT-β Catenin Signaling as a Potential Therapeutic Target for Neurodegenerative Diseases: Current Status and Future Perspective.
 Epidemiology of small intestinal bacterial overgrowth.
 Genetic insights into the association between inflammatory bowel disease and Alzheimer's disease.
 Sodium in the skin: a summary of the physiology and a scoping review of disease associations.
 When You SPRINT, It's Good to Know the Goal as Well as the Goal Line.
 Factors associated with depressive mood at the onset of multiple sclerosis - an analysis of 781 patients of the German NationMS cohort.
 Reply: Do we need new MRI criteria for diagnosing radiologically isolated syndrome?
 Machine learning assisted-nanomedicine using magnetic nanoparticles for central nervous system diseases.
 The Utilization of Low Dose Naltrexone for Chronic Pain.
 Enhancing neurorehabilitation by targeting beneficial plasticity.
 Interferon Beta.
 Protein Phosphatase 2A: Role in T Cells and Diseases.
 MicroRNA-183/96/182 cluster in immunity and autoimmunity.
 Nucleoside-based anticancer drugs: Mechanism of action and drug resistance.
 Cannabis Unveiled: An Exploration of Marijuana's History, Active Compounds, Effects, Benefits, and Risks on Human Health.
 The regulation of self-tolerance and the role of inflammasome molecules.
 Vision as a piece of the head trauma puzzle.
 Telerehabilitation during the COVID-19 pandemic, what are the determinants of satisfaction for chronic diseases? a retrospective study.
 Design, synthesis and biological characterization of novel activators of the TrkB neurotrophin receptor.
 The intestinal barrier in disorders of the central nervous system.
 Optical coherence tomography angiography in neuro-ophthalmology.
 Immunosensors for Autoimmune-Disease-Related Biomarkers: A Literature Review.
 Neuroprotective effects of coenzyme Q10 on neurological diseases: a review article.
 Neuro-Ophthalmic Visual Impairment in the Setting of COVID-19.
 Auto-STEED: A data mining tool for automated extraction of experimental parameters and risk of bias items from in vivo publications.
 Impact of Cannabinoid Receptors in the Design of Therapeutic Agents against Human Ailments.
 Real-world application of plasmapheresis for neurological disease: Results from the Japan-Plasmapheresis Outcome and Practice Patterns Study.
 Is it ethical to use teriflunomide as an active comparator in phase 3 trials?
 Clinical studies with Cannabis in India - A need for guidelines for the investigators and ethics committees.
 A Clinical Approach to Existing and Emerging Therapeutics in Neuromyelitis Optica Spectrum Disorder.
 Interferon production by Viral, Bacterial & Yeast system: A comparative overview in 2023.
 Energy minimization segmentation model based on MRI images.
 Neurological Health: Not Merely the Absence of Disease: Current Wellbeing Instruments Across the Spectrum of Neurology.
 Hematopoietic Stem Cell Transplantation for the Treatment of Autoimmune Neurological Diseases: An Update.
 Neutrophil extracellular trap: A key player in the pathogenesis of autoimmune diseases.
 Biosensors, Recent Advances in Determination of BDNF and NfL.
 GPR109A expressed on medullary thymic epithelial cells affects thymic Treg development.
 Incorporating Dynamic Pricing in Cost-Effectiveness Analysis: Are Known Unknowns Valuable?
 Validity of chronic disease diagnoses in Icelandic healthcare registries.
 Clinical comparative analysis of monophasic and multiphasic acute disseminated encephalomyelitis in adults.
 Zebrafish as an Animal Model in Cannabinoid Research.
 An open-source tool for longitudinal whole-brain and white matter lesion segmentation.
 Additional advances related to the health benefits associated with kombucha consumption.
 ABCB1 gene variants as risk factors and modulators of age of onset of demyelinating disease in Mexican patients.
 The gut microbiota-induced kynurenic acid recruits GPR35-positive macrophages to promote experimental encephalitis.
 A multicenter study of radiologically isolated syndrome in children and adolescents: Can we predict the course?
 Expression of fibrinogen-like protein 2 (Fgl2) on Toll-like receptor 9 (TLR9) expression in autoimmune myelitis.
 Defining the natural history of tumefactive demyelination: A retrospective cohort of 257 patients.
 In vitro evaluation of the activity of teriflunomide against SARS-CoV-2 and the human coronaviruses 229E and OC43.
 Evaluating patient-reported outcome measures (PROMs) for future clinical trials in adult patients with optic neuritis.
 Toward a serum biomarker of disease activity in Susac syndrome.
 Editorial for "Deep Learning for Noninvasive Assessment of H3 K27M Mutation Status in Diffuse Midline Gliomas Using MR Imaging".
 A second case of liraglutide-type localised amyloidosis.
 Iron and Ferroptosis More than a Suspect: Beyond the Most Common Mechanisms of Neurodegeneration for New Therapeutic Approaches to Cognitive Decline and Dementia.
 Paraneoplastic autoimmune Laminin-332 syndrome (PALS): Anti-Laminin-332 mucous membrane pemphigoid as a prototype.
 The role of C5a receptors in autoimmunity.
 Multinomial classification of NLRP3 inhibitory compounds based on large scale machine learning approaches.
 An Overview of Reviews on the Effects of Acceptance and Commitment Therapy (ACT) on Depression and Anxiety.
 Age-related changes in mice behavior and the contribution of lipocalin-2.
 Microglial activating transcription factor 3 upregulation: An indirect target to attenuate inflammation in the nervous system.
 Role of Gamma Knife Radiosurgery in the Management of Functional Disorders - A Literature Review.
 Interactive statistical monitoring to optimize review of potential clinical trial issues during study conduct.
 Optimal Selection of IFN-α-Inducible Genes to Determine Type I Interferon Signature Improves the Diagnosis of Systemic Lupus Erythematosus.
 Role of endocrine PACAP in age-related diseases.
 Augmented Reality-Assisted Percutaneous Rhizotomy for Trigeminal Neuralgia.
 Dimethyl fumarate attenuates paraquat-induced pulmonary oxidative stress, inflammation and fibrosis in mice.
 The KEAP1-NRF2 system and neurodegenerative diseases.
 Clinical and MRI features of gait and balance disorders in neurodegenerative diseases.
 Gut immune cell trafficking: inter-organ communication and immune-mediated inflammation.
 Acute coronary syndrome in an anomalous mid-LAD right coronary artery: Don't forget to look twice before turning left.
 Navigating the landscape of Rho GTPase signalling system in autoimmunity: A bibliometric analysis spanning over three decades (1990 to 2023).
 The novel small molecule TPN10518 alleviates EAE pathogenesis by inhibiting AP1 to depress Th1/Th17 cell differentiation.
 How myeloid cells shape experimental autoimmune encephalomyelitis: At the crossroads of outside-in immunity.
 Nutrient Therapy for the Improvement of Fatigue Symptoms.
 Loss of optic nerve oligodendrocytes during maturation alters retinal organization.
 Autoimmune susceptible HLA class II motifs facilitate the presentation of modified neoepitopes to potentially autoreactive T cells.
 Spinal Dural Arterio-Venous Fistula: A Vital Differential Diagnosis to Consider for Myelopathy.
 Nervonic acid and its sphingolipids: Biological functions and potential food applications.
 [Clinical phenotypes of optic nerve damage in patients with neuromyelitis optica spectrum disorder].
 Current perspectives on the diagnosis and management of acute transverse myelitis.
 Delivery route considerations for designing antigen-specific biomaterial strategies to combat autoimmunity.
 A natural goldmine of binding proteins and soluble receptors simplified their translation to blockbuster drugs, all in one decade.
 Effects of Cannabidiol on Innate Immunity: Experimental Evidence and Clinical Relevance.
 Relationship between Hypoxic and Immune Pathways Activation in the Progression of Neuroinflammation: Role of HIF-1α and Th17 Cells.
 Gut Microbial-Derived Metabolites as Immune Modulators of T Helper 17 and Regulatory T Cells.
 RNA-binding proteins in autoimmunity: From genetics to molecular biology.
 The Value of New: Consideration of Product Novelty in Health Technology Assessments of Pharmaceuticals.
 Intravascular Endothelial Hyperplasia of the Foot.
 Splenium of the Corpus Callosum Infarct Associated With COVID-19: Case Report.
 A comprehensive review on the impact of calcium and vitamin D insufficiency and allied metabolic disorders in females.
 Simultaneous intervention against oxidative stress and inflammation by targeting Nrf2/ARE and NLRP3 inflammasome pathway mitigates thioacetamide-induced liver fibrosis in rat.
 Involvement of NRON and TUG1 long noncoding RNAs in inflammation and the pathogenesis of EAE.
 Neuromyelitis Optica Spectrum Disorder Mimicking Pontine Stroke: A Case Report and Systematic Literature Review.
 Research trends and hotspots of neuropathic pain in neurodegenerative diseases: a bibliometric analysis.
 Objectively-captured Changes in Trigeminal Fibers before and after Microvascular Decompression Using 3D T2-SPACE MRI Might Relate to Eventual Residual Symptoms.
 The Potential Effect of Royal Jelly on Biomarkers Related to COVID-19 Infection and Severe Progression.
 Use of a Commercial 7-T MRI Scanner for Clinical Brain Imaging: Indications, Protocols, Challenges, and Solutions-A Single-Center Experience.
 Opiate Antagonists for Chronic Pain: A Review on the Benefits of Low-Dose Naltrexone in Arthritis versus Non-Arthritic Diseases.
 Emerging trends and research foci of neuromyelitis optica spectrum disorder: a 20-year bibliometric analysis.
 Accurate and Reliable Classification of Unstructured Reports on Their Diagnostic Goal Using BERT Models.
 The Tobacco Smoke Component, Acrolein, as a Major Culprit in Lung Diseases and Respiratory Cancers: Molecular Mechanisms of Acrolein Cytotoxic Activity.
 Transcriptomic atlas and interaction networks of brain cells in mouse CNS demyelination and remyelination.
 An Adaptive Pedaling Assistive Device for Asymmetric Torque Assistant in Cycling.
 From lead to clinic: A review of the structural design of P2X7R antagonists.
 The microbiome-gut-brain axis in epilepsy: pharmacotherapeutic target from bench evidence for potential bedside applications.
 Corrigendum to: Use of electronic medical records to monitor the safe and effective prescribing of medicinal cannabis: is it feasible?
 Targeting the gut-microbiota-brain axis in irritable bowel disease to improve cognitive function - recent knowledge and emerging therapeutic opportunities.
 Sphingosine-1-phosphate Signalling in Aneurysmal Subarachnoid Haemorrhage: Basic Science to Clinical Translation.
 Insights into the mechanism of oligodendrocyte protection and remyelination enhancement by the integrated stress response.
 On multi-path longitudinal spin relaxation in brain tissue.
 Unwinding the modalities of necrosome activation and necroptosis machinery in neurological diseases.
 Pleotropic effects of statins: the dilemma of wider utilization of statin.
 Targeting B cells and plasma cells in autoimmune diseases: From established treatments to novel therapeutic approaches.
 Inline dual-echo T2 quantification in brain using a fast mapping reconstruction technique.
 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis: an update.
 Characteristics of peer-based interventions for individuals with neurological conditions: a scoping review.
 PKC modulator bryostatin-1 therapeutically targets CNS innate immunity to attenuate neuroinflammation and promote remyelination.
 Quantitative evaluation of the thickened dura mater impacting clinical signs in immune-mediated hypertrophic pachymeningitis.
 Novel TRPM7 inhibitors with potent anti-inflammatory effects in vivo.
 Bibliometric analyses of global output on neuromyelitis optica spectrum disorder.
 Challenges in tolerogenic dendritic cell therapy for autoimmune diseases: the route of administration.
 Stellate ganglion block to mitigate thalamic pain syndrome of an oncological origin.
 Inflammasomes: Mechanisms of Action and Involvement in Human Diseases.
 Intrathecal Catheter.
 Beyond Antioxidation: Keap1-Nrf2 in the Development and Effector Functions of Adaptive Immune Cells.
 2-Aminobenzoxazole Derivatives as Potent Inhibitors of the Sphingosine-1-Phosphate Transporter Spinster Homolog 2 (Spns2).
 Biosynthesis of Phytocannabinoids and Structural Insights: A Review.
 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease.
 Cinnamein Inhibits the Induction of Nitric Oxide and Proinflammatory Cytokines in Macrophages, Microglia and Astrocytes.
 Anti-inflammatory effects of vagus nerve stimulation in pediatric patients with epilepsy.
 Therapeutic Plasma Exchange in Certain Immune-Mediated Neurological Disorders: Focus on a Novel Nanomembrane-Based Technology.
 Neural stem cells and oligodendrocyte progenitor cells compete for remyelination in the corpus callosum.
 UV radiation and air pollution as drivers of major autoimmune conditions.
 The helminth derived peptide FhHDM-1 redirects macrophage metabolism towards glutaminolysis to regulate the pro-inflammatory response.
 COVID-19: A trigger of autoimmune diseases.
 Analyzing global features of magnetic resonance images in widespread neurodegenerative diseases: new hope to understand brain mechanism and robust neurodegenerative disease diagnosis.
 A Comprehensive Review on Therapeutic Potential of Chrysin in Brain Related Disorders.
 Genomic associations with antibody response to an oral cholera vaccine.
 Influence of Pre-Analytic Conditions on Quantity of Lymphocytes.
 Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes.
 Home Use of Mechanical Insufflation/Exsufflation in Adult Patients in Western Switzerland.
 The effect of long-term exposure to toxic air pollutants on the increased risk of malignant brain tumors.
 Epigallocatechin Gallate: A Multifaceted Molecule for Neurological Disorders and Neurotropic Viral Infections.
 Knowledge mapping of COVID-19 and autoimmune diseases: a visual and bibliometric analysis.
 The S100B Protein: A Multifaceted Pathogenic Factor More Than a Biomarker.
 Mitochondrial dysfunction in neurodegenerative disorders: Potential therapeutic application of mitochondrial transfer to central nervous system-residing cells.
 Targeting the Nrf2 signaling pathway using phytochemical ingredients: A novel therapeutic road map to combat neurodegenerative diseases.
 Optimal combination of arsenic trioxide and copper ions to prevent autoimmunity in a murine HOCl-induced model of systemic sclerosis.
 Associations of sNfL with clinico-radiological measures in a large MS population.
 Absorption, Metabolism, and Excretion of [(14)C]-Tolebrutinib After Oral Administration in Humans, Contribution of the Metabolites to Pharmacological Activity.
 [Work Participation after Multimodal Rehabilitation due to Neurological Diseases - Representative Analyses Using Routine Data of the German Pension Insurance].
 E-WE thrombin, a protein C activator, reduces disease severity and spinal cord inflammation in relapsing-remitting murine experimental autoimmune encephalomyelitis.
 Machine learning based estimation of dynamic balance and gait adaptability in persons with neurological diseases using inertial sensors.
 Kinins and their B(1) and B(2) receptors as potential therapeutic targets for pain relief.
 HIF prolyl hydroxylase 2/3 deletion disrupts astrocytic integrity and exacerbates neuroinflammation.
 Serum neurofilament and glial fibrillary acidic protein in idiopathic and seropositive transverse myelitis.
 New onset or relapsing neuromyelitis optica temporally associated with SARS-CoV-2 infection and COVID-19 vaccination: a systematic review.
 Human biodistribution and radiation dosimetry of the demyelination tracer [(18)F]3F4AP.
 Neuroprotective effect of hyperoside in MPP(+)/MPTP -induced dopaminergic neurodegeneration.
 Prognostic relevance of quantitative and longitudinal MOG antibody testing in patients with MOGAD: a multicentre retrospective study.
 Cost-Analysis of Subcutaneous vs Intravenous Administration of Natalizumab Based on Patient Care Pathway in Multiple Sclerosis in Spain.
 Grape Seed Extract Attenuates Demyelination in Experimental Autoimmune Encephalomyelitis Mice by Inhibiting Inflammatory Response of Immune Cells.
 The Role of Gut Microbiota in Various Neurological and Psychiatric Disorders-An Evidence Mapping Based on Quantified Evidence.
 Optical coherence tomography as retinal imaging biomarker of neuroinflammation/neurodegeneration in systemic disorders in adults and children.
 [Myalgic Encephalitis/Chronic Fatigue Syndrome: Diagnostic and Therapeutic Approach and Biological Research].
 Chronic inflammation in high-fat diet-fed mice: Unveiling the early pathogenic connection between liver and adipose tissue.
 From the Bush to the Brain: Preclinical Stages of Ethnobotanical Anti-Inflammatory and Neuroprotective Drug Discovery-An Australian Example.
 Factors regulating the differences in frequency of infiltration of Th17 and Treg of the blood-brain barrier.
 Characterizing the Use of Nabiximols (Δ9-Tetrahydrocannabinol-Cannabidiol) Buccal Spray in Pediatric Patients.
 Preoperative Characteristics and Postoperative Pain Outcomes in Trigeminal Neuralgia With Concomitant Autoimmune Disease.
 Association between Periodontitis Extent, Severity, and Progression Rate with Systemic Diseases and Smoking: A Retrospective Study.
 Interactions between Guidance Cues and Neuronal Activity: Therapeutic Insights from Mouse Models.
 Interleukin-35 and Interleukin-37 anti-inflammatory effect on inflammatory bowel disease: Application of non-coding RNAs in IBD therapy.
 The Role of Diet as a Modulator of the Inflammatory Process in the Neurological Diseases.
 Vitamin D: immune function, inflammation, infections and auto-immunity.
 An insight into the neuroprotective and anti-neuroinflammatory effects and mechanisms of Moringa oleifera.
 A Case Series of Trigeminal Neuralgia With Pure Venous Compression: Postoperative Outcomes Associated With Intraoperative Venous Transposition Versus Coagulation.
 Implications of the non-specific effect induced by Bacillus Calmette-Guerin (BCG) vaccine on vaccine recommendations.
 Dimethyl Fumarate Inhibits Fibroblast Like Synoviocytes-mediated Inflammation and Joint Destruction in Rheumatoid Arthritis.
 Naringenin stimulates aromatase expression and alleviates the clinical and histopathological findings of experimental autoimmune encephalomyelitis in C57bl6 mice.
 Mechanosensitive Piezo1 channel in physiology and pathophysiology of the central nervous system.
 Molecular Insights into Royal Jelly Anti-Inflammatory Properties and Related Diseases.
 Efficacy of rehabilitation interventions evaluated in common neurological conditions in improving participation outcomes: A systematic review.
 Type-B monoamine oxidase inhibitors in neurological diseases: clinical applications based on preclinical findings.
 Progressive Multifocal Leukoencephalopathy: Pathogenesis, Diagnostic Tools, and Potential Biomarkers of Response to Therapy.
 Delphi consensus study and clinical practice guideline development for functional electrical stimulation to support upright mobility in people with an upper motor neuron lesion.
 Role of Serum/Glucocorticoid-Regulated Kinase 1 (SGK1) in Immune and Inflammatory Diseases.
 Short chain fatty acids, a possible treatment option for autoimmune diseases.
 A dual-task-embedded virtual reality system for intelligent quantitative assessment of cognitive processing speed.
 Upscaling human mesenchymal stromal cell production in a novel vertical-wheel bioreactor enhances extracellular vesicle secretion and cargo profile.
 RIPK2 as a promising druggable target for autoimmune diseases.
 Autoimmune diseases and gut microbiota: a bibliometric and visual analysis from 2004 to 2022.
 Transient receptor potential Ankyrin-1 (TRPA1) agonists suppress myelination and induce demyelination in organotypic cortical slices.
 Targeting neuroinflammation in neuropathic pain and opioid use.
 Repurposing artemisinins as neuroprotective agents: a focus on the PI3k/Akt signalling pathway.
 Use of a physiological profile to document upper limb motor impairment in ageing and in neurological conditions.
 Deep learning-regularized, single-step quantitative susceptibility mapping quantification.
 The impact of the gut microbiome on extra-intestinal autoimmune diseases.
 Computational refinement identifies functional destructive single nucleotide polymorphisms associated with human retinoid X receptor gene.
 Dysregulated translational factors and epigenetic regulations orchestrate in B cells contributing to autoimmune diseases.
 Rates of John Cunningham virus seroconversion greatly reduced in natalizumab-treated patients during COVID-19-related lockdowns.
 mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model.
 Electroacupuncture at ST36 acupoint regulates stem cells during experimental autoimmune encephalomyelitis.
 Akkermansia muciniphila in neuropsychiatric disorders: friend or foe?
 A Case Series of Stereotactic Radiosurgery First for Trigeminal Neuralgia: A History of Stereotactic Radiosurgery Does Not Complicate Microvascular Decompression.
 Paracentral Acute Middle Maculopathy Associated with Severe Anti-Mog (Myelin Oligodendrocyte Glycoprotein)-Positive Optic Neuritis.
 Who Benefits the Most From Different Psychological Chronic Pain Treatments? An Exploratory Analysis of Treatment Moderators.
 Optic Neuritis After COVID-19 Vaccination: An Analysis of the Vaccine Adverse Event Reporting System.
 Why Are Perivascular Spaces Important?
 A patent review of human dihydroorotate dehydrogenase (hDHODH) inhibitors as anticancer agents and their other therapeutic applications (1999-2022).
 The Role and Clinical Relevance of Osteopontin in Allergic Airway Diseases.
 Validation of Recombinant Heparan Sulphate Reagents for CNS Repair.
 Discovery of a Promising Fluorine-18 Positron Emission Tomography Radiotracer for Imaging Sphingosine-1-Phosphate Receptor 1 in the Brain.
 Regulatory T cells promote functional recovery after spinal cord injury by alleviating microglia inflammation via STAT3 inhibition.
 Loss of Tyro3 causes anxiety-relevant behavioural changes in female mice.
 Chemokine Receptors-Structure-Based Virtual Screening Assisted by Machine Learning.
 Synthesis of cubosomes containing cerium oxide nanoparticles from Lactobacillus acidophilus loaded with glatiramer acetate and carboxymethylcellulose coating.
 MMF induces antioxidative and anaplerotic pathways and is neuroprotective in hyperexcitability in vitro.
 Neurology of cancer immunotherapy.
 Stem Cells and Natural Agents in the Management of Neurodegenerative Diseases: A New Approach.
 Chlorhexidine as a Keap1-Nrf2 inhibitor: a new target for an old drug for Parkinson's disease therapy.
 RDKG-115: Assisting drug repurposing and discovery for rare diseases by trimodal knowledge graph embedding.
 Chronic encephalomyelitis virus exhibits cellular tropism and evades pDCs by binding to sialylated integrins as the cell surface receptors.
 Anti-inflammatory Effects of Siponimod in a Mouse Model of Excitotoxicity-Induced Retinal Injury.
 Electrophysiological In Vitro Study of Long-Range Signal Transmission by Astrocytic Networks.
 Glatiramer.
 Quantitation of Tissue Amyloid via Fluorescence Spectroscopy Using Controlled Concentrations of Thioflavin-S.
 A prospective survey on therapeutic inertia in psoriatic arthritis (OPTI'PsA).
 The role of the blood-brain barrier during neurological disease and infection.
 Acute truncal ataxia without nystagmus in patients with acute vertigo.
 In Semliki Forest virus encephalitis, suppressor of cytokine signaling 4 (SOCS4) is an essential modulator of immune responses that mediates the balance between immunopathology and virus clearance.
 Clinicians' implicit and explicit attitudes about the legitimacy of functional neurological disorders correlate with referral decisions.
 Repurposing MS immunotherapies for CIDP and other autoimmune neuropathies: unfulfilled promise or efficient strategy?
 The preventive role of vitamin D in the prevention and management of Fibromyalgia syndrome.
 Comparison of Clinical Guidelines for Authorization of MRI in the Evaluation of Neck Pain and Cervical Radiculopathy in the United States.
 Measurement properties of outcome measures used in neurological telerehabilitation: A systematic review using COSMIN checklist.
 Cell-free DNA-based liquid biopsies in neurology.
 Appropriate Magnetic Resonance Imaging Ordering.
 Overlapping genetic susceptibility of seven autoimmune diseases:SPU tests based on genome-wide association summary statistics.
 New onset of Susac syndrome after mRNA COVID-19 vaccine: a case report.
 EAE of Mice: Enzymatic Cross Site-Specific Hydrolysis of H2A Histone by IgGs against H2A, H1, H2B, H3, and H4 Histones and Myelin Basic Protein.
 Italian cross-cultural adaptation of the Quality of Communication questionnaire and the 4-item advance care planning engagement questionnaire.
 Association between vaccination and the risk of central demyelination: results from a case-referent study.
 EAE of Mice: Enzymatic Cross Site-Specific Hydrolysis of H2B Histone by IgGs against H1, H2A, H2B, H3, and H4 Histones and Myelin Basic Protein.
 Fish consumption in multiple health outcomes: an umbrella review of meta-analyses of observational and clinical studies.
 Histamine H4 Receptor Agonist, 4-Methylhistamine, Aggravates Disease Progression and Promotes Pro-Inflammatory Signaling in B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model.
 Real-world application of the 2022 diagnostic criteria for first-ever episode of optic neuritis.
 Ovalbumin-specific CD4(+) and CD8(+) T cells contribute to different susceptibility for Theiler's murine encephalomyelitis virus persistence.
 Ameliorative effects of Fingolimod (FTY720) on microglial activation and psychosis-related behavior in short term cuprizone exposed mice.
 Multiple Brain Tumor Classification with Dense CNN Architecture Using Brain MRI Images.
 A Retrospective Medical Record Review of Adults with Non-Cancer Diagnoses Prescribed Medicinal Cannabis.
 A case of childhood unilateral relapsing primary angiitis of the central nervous system.
 Chemical and biophysical characterization of novel potassium channel blocker 3-fluoro-5-methylpyridin-4-amine.
 Primary healthcare needs and service utilisation of people with disability: a data linkage protocol.
 Myeloperoxidase PET Imaging Tracks Intracellular and Extracellular Treatment Changes in Experimental Myocardial Infarction.
 Fast tracking informative clinical trials: lessons for mental health.
 A comparative analysis of demographic, clinical and imaging features of myelin oligodendrocyte glycoprotein antibody positive, aquaporin 4 antibody positive, and double seronegative demyelinating disorders - An Indian tertiary care center prospective study.
 S1P1 Threonine 236 Phosphorylation Mediates the Invasiveness of Triple-Negative Breast Cancer and Sensitivity to FTY720.
 Maternal-fetal outcomes in patients with immune mediated inflammatory diseases, with consideration of comorbidities: a retrospective cohort study in a large U.S. healthcare system.
 Therapeutic Potential of Natural Compounds in Neurodegenerative Diseases: Insights from Clinical Trials.
 Molecular mechanisms of ferroptosis and their involvement in brain diseases.
 Circulating Calprotectin (cCLP) in autoimmune diseases.
 Cognition and Quality of Life of People with Spinal Cord Injury.
 Attack adjudication in neuromyelitis optica spectrum disorder: Substantiation of criteria by magnetic resonance imaging and biomarkers in N-MOmentum.
 An optimal combination of five main monomer components in Wuzi Yanzong Pill that prevents neural tube defects and reduces apoptosis and oxidative stress.
 Identification of D359-0396 as a novel inhibitor of the activation of NLRP3 inflammasome.
 Characteristics of hypersomnia due to inflammatory demyelinating diseases of the central nervous system.
 Tailoring Rituximab According to CD27-Positive B-Cell versus CD19-Positive B-Cell Monitoring in Neuromyelitis Optica Spectrum Disorder and MOG-Associated Disease: Results from a Single-Center Study.
 T-cell tolerant fraction as a predictor of immune-related adverse events.
 Association Between Autoimmune Diseases and Sarcopenia: A Two-Sample Mendelian Randomization Study.
 REUSED: A deep neural network method for rapid whole-brain high-resolution myelin water fraction mapping from extremely under-sampled MRI.
 Oral Antispasticity Drugs and Non-Progressive Neurological Diseases: A Meta-Analysis on Safety and Efficacy.
 Decompression for lumbar spinal stenosis at the intrathecal catheter insertion site during intrathecal baclofen therapy: a case report.
 Mesenchymal stromal cell-derived secretome-based therapy for neurodegenerative diseases: overview of clinical trials.
 Predictive role of blood-based indicators in neuromyelitis optica spectrum disorders.
 Dimethyl fumarate abrogates striatal endoplasmic reticulum stress in experimentally induced late-stage Huntington's disease: Focus on the IRE1α/JNK and PERK/CHOP trajectories.
 In situ Microinflammation Detection Using Gold Nanoclusters and a Tissue-clearing Method.
 The role of IL-23/IL-17 axis in ischemic stroke from the perspective of gut-brain axis.
 CNS demyelinating events in primary Sjögren's syndrome: A single-center case series on the clinical phenotype.
 Covid-19 a triggering factor of autoimmune and multi-inflammatory diseases.
 High-throughput screening for myelination promoting compounds using human stem cell-derived oligodendrocyte progenitor cells.
 Impact of Treating Depression on Associated Comorbidities: A Systematic Literature Review.
 Diabetes Mellitus and Energy Dysmetabolism in Alzheimer's Disease: Understanding the Relationships and Potential Therapeutic Targets.
 The Effect of Cerebellar rTMS on Modulating Motor Dysfunction in Neurological Disorders: a Systematic Review.
 A computational study to target necroptosis via RIPK1 inhibition.
 Simultaneous detection of DNA variation and methylation at HLA class II locus and immune gene promoters using targeted SureSelect Methyl-Sequencing.
 Serum Electrolyte and Metabolic Changes During Conditioning of Autologous Hematopoietic Stem Cell Transplantation in Patients with Autoimmune Diseases: A Prospective Study in a Single Institution.
 Secondary Central Nervous System Demyelinating Disorders in the Elderly: A Narrative Review.
 Mapping tissue microstructure across the human brain on a clinical scanner with soma and neurite density image metrics.
 Recent advances in shikonin for the treatment of immune-related diseases: Anti-inflammatory and immunomodulatory mechanisms.
 Synthetic Cell-Based Immunotherapies for Neurologic Diseases.
 Real world evidence of improved attention and cognition during physical therapy paired with neuromodulation: a brain vital signs study.
 Smooth pursuit eye movements contribute to anticipatory force control during mechanical stopping of moving objects.
 Functional MRI in neuro-urology: A narrative review.
 Comparative transcriptome profile of mouse macrophages treated with the RhoA/Rock pathway inhibitors Y27632, Fingolimod (Gilenya), and Rezurock (Belumosudil, SLx-2119).
 Bruton's Tyrosine Kinase Inhibitors (BTKIs): Review of Preclinical Studies and Evaluation of Clinical Trials.
 Short-term exposure to dimethyl fumarate (DMF) inhibits LPS-induced IκBζ expression in macrophages.
 Is percutaneous balloon compression better than microvascular decompression to treat trigeminal neuralgia? A systematic review and meta-analysis.
 Involvement of trained immunity during autoimmune responses.
 Dimethyl fumarate protects against hepatic ischemia-reperfusion injury by alleviating ferroptosis via the NRF2/SLC7A11/HO-1 axis.
 Oral health in patients with neurodegenerative and cerebrovascular disease: a retrospective study.
 Brain Atrophy as an Outcome of Disease-Modifying Therapy for Remitting-Relapsing Multiple Sclerosis.
 Investigating the Needs of Caregivers of Patients Suffering from Chronic Diseases: A Mixed-Method Study.
 A Preliminary Study of Pharmacokinetics and Pharmacodynamics of Oral Fingolimod in Dogs.
 Bifidobacterium breve Probiotic Compared to Lactobacillus casei Causes a Better Reduction in Demyelination and Oxidative Stress in Cuprizone-Induced Demyelination Model of Rat.
 Immunohistochemical evaluation of fibrin/fibrinogen, d-dimers, and intravascular thrombosis in brains of dogs with meningoencephalitis of unknown origin.
 Epstein-Barr virus and genetic risk variants as determinants of T-bet(+) B cell-driven autoimmune diseases.
 The developing role of extracellular vesicles in autoimmune diseases: special attention to mesenchymal stem cell-derived extracellular vesicles.
 Blood RNA-Seq profiling reveals a set of circular RNAs differentially expressed in frail individuals.
 Myelopathy due to copper deficiency: A case series and review of the literature.
 Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.
 Perspectives on Neuronutrition in Prevention and Treatment of Neurological Disorders.
 Role of stimulator of interferon genes (STING) in the enteric nervous system in health and disease.
 Transcription factor combinations that define human astrocyte identity encode significant variation of maturity and function.
 Prevalence and severity of restless leg syndrome in patients with spinal cord injuries.
 Pharmacotherapeutic potential of walnut (Juglans spp.) in age-related neurological disorders.
 A new platform for autoimmune diseases. Inducing tolerance with liposomes encapsulating autoantigens.
 Spatially informed Bayesian neural network for neurodegenerative diseases classification.
 GABAergic regulation of cell proliferation within the adult mouse spinal cord.
 Siponimod exerts neuroprotective effects on the retina and higher visual pathway through neuronal S1PR1 in experimental glaucoma.
 The many facets of CD26/dipeptidyl peptidase 4 and its inhibitors in disorders of the CNS - a critical overview.
 The safety and accuracy of home-based ballistic resistance training for people with neurological conditions.
 Palliative Care Knowledge and Attitudes Among Patients With Neuroinflammatory Diseases.
 Investigating the Needs of Patients Suffering from Chronic Diseases: A Cross-Sectional Study.
 Two-carba cyclic phosphatidic acid treatment promotes phenotypic switch from M1 to M2 microglia and prevents behavioral abnormalities in a mouse model of neuropsychiatric systemic lupus erythematosus.
 The effect of acute urinary retention on the results of transurethral resection of the prostate.
 Vestibular Dysfunction.
 [Headache registry in Szeged: Experiences regarding to migraine patients].
 Adjuvant Activity of Mycobacterium paratuberculosis in Enhancing the Immunogenicity of Autoantigens During Experimental Autoimmune Encephalomyelitis.
 Insights into the synthesis strategies of plant-derived cyclotides.
 Phosphodiesterase 7 as a therapeutic target - Where are we now?
 Antioxidant properties of Trifolium resupinatum and its therapeutic potential for Alzheimer's disease.
 Psychosocial group therapy interventions for patients with physical disabilities: A scoping review of implementation considerations.
 Inhibition of Microglial Activation by Amitriptyline and Doxepin in Interferon-β Pre-Treated Astrocyte-Microglia Co-Culture Model of Inflammation.
 Current Advances of Plant-Based Vaccines for Neurodegenerative Diseases.
 Analysis of the effect of cortisone on the QT interval.
 One-year prediction of cognitive decline following cognitive-stimulation from real-world data.
 Identification of galectin-1 and other cellular targets of alpha,beta-unsaturated carbonyl compounds, including dimethylfumarate, by use of click-chemistry probes.
 Semisupervised white matter hyperintensities segmentation on MRI.
 The role of microRNAs in neurodegenerative diseases: a review.
 Glial Sphingosine-mediated Epigenetic Regulation Stabilizes Synaptic Function in Drosophila Models of Alzheimer's Disease.
 Autoimmune diseases and new-onset atrial fibrillation: a UK Biobank study.
 Large-Scale Integration of Single-Cell RNA-Seq Data Reveals Astrocyte Diversity and Transcriptomic Modules across Six Central Nervous System Disorders.
 Neural network algorithms predict new diffusion MRI data for multi-compartmental analysis of brain microstructure in a clinical setting.
 Valuation of Costs in Health Economics During Financial and Economic Crises: A Case Study from Lebanon.
 Carotenoids: Role in Neurodegenerative Diseases Remediation.
 Methods to Study Mitochondria: Techniques Used to Study the Effects of Age-Related Diseases Including Alzheimer's.
 The pivotal role of JAK/STAT and IRS/PI3K signaling pathways in neurodegenerative diseases: Mechanistic approaches to polyphenols and alkaloids.
 Corrigendum: Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody.
 Serum neurofilament light chain cut-off definition for clinical diagnosis and prognosis of amyotrophic lateral sclerosis.
 Siponimod Therapy and CYP2C9 Genotype.
 Cannabis-Based Medicine for Neuropathic Pain and Spasticity-A Multicenter, Randomized, Double-Blinded, Placebo-Controlled Trial.
 A specific anti-COVID-19 BNT162b2 vaccine-induced early innate immune signature positively correlates with the humoral protective response in healthy and multiple sclerosis vaccine recipients.
 Multiple Micronodular Pneumocyte Hyperplasia (MMPH): A Less-Known Presentation of Tuberous Sclerosis Complex Related Lung Disease.
 Tuberous sclerosis associated lymphangioleiomyomatosis: A case report.
 Priming mesenchymal stromal cells with neurotrophic factors boosts the neuro-regenerative potential of their secretome.
 DeepSTI: Towards tensor reconstruction using fewer orientations in susceptibility tensor imaging.
 Lymph node targeted multi-epitope subunit vaccine promotes effective immunity to EBV in HLA-expressing mice.
 Towards an optimal monoclonal antibody with higher binding affinity to the receptor-binding domain of SARS-CoV-2 spike proteins from different variants.
 Non-demyelinating disorders mimicking and misdiagnosed as NMOSD: a literature review.
 Mendelian Randomization Analyses of Chronic Immune-Mediated Diseases, Circulating Inflammatory Biomarkers, and Cytokines in Relation to Liver Cancer.
 The autophagy machinery interacts with EBV capsids during viral envelope release.
 A score that predicts aquaporin-4 IgG positivity in patients with longitudinally extensive transverse myelitis.
 Total Flavonoids of Astragalus Inhibit Activated CD4[Formula: see text] T Cells and Regulate Differentiation of Th17/Th1/Treg Cells in Experimental Autoimmune Encephalomyelitis Mice by JAK/STAT and NF[Formula: see text]B Signaling Pathways.
 Retrospective comparison of percutaneous balloon compression and radiofrequency-thermocoagulation in the management of trigeminal neuralgia.
 SARM1 promotes the neuroinflammation and demyelination through IGFBP2/NF-κB pathway in experimental autoimmune encephalomyelitis mice.
 Identification of schizophrenia symptom-related gene modules by postmortem brain transcriptome analysis.
 High-efficacy therapies reduce clinical and radiological events more effectively than traditional treatments in neuromyelitis optica spectrum disorder.
 Physical health of Post-9/11 U.S. Military veterans in the context of Healthy People 2020 targeted topic areas: Results from the Comparative Health Assessment Interview Research Study.
 A cerebellar degeneration-related protein 2-like cell-based assay for anti-Yo detection in patients with paraneoplastic cerebellar degeneration.
 A review article on neuroprotective, immunomodulatory, and anti-inflammatory role of vitamin-D3 in elderly COVID-19 patients.
 Listening to the patients' voice: a conceptual framework of the walking experience.
 Aminoadamantanes: from treatment of Parkinson's and Alzheimer's disease to symptom amelioration of long COVID-19 syndrome?
 Curcumin-Based Nanomedicines in the Treatment of Inflammatory and Immunomodulated Diseases: An Evidence-Based Comprehensive Review.
 Skin-related complications following deep brain stimulation surgery: A single-center retrospective analysis of 525 patients who underwent DBS surgery.
 [A view of care pathways approved by Italian Regions, to face the challenge of the community-based healthcare: a quali-quantitative analysis of the Pdta Net database.].
 Toulouse-Piéron Cancellation Test: Normative scores for the portuguese population.
 Role of Th17 and IL-17 Cytokines on Inflammatory and Auto-immune Diseases.
 CXCR1 drives the pathogenesis of EAE and ARDS via boosting dendritic cells-dependent inflammation.
 Small molecule inhibitors of NLRP3 inflammasome and GSK-3β in the management of traumatic brain injury: A review.
 Hyaluronan hydrates and compartmentalises the CNS/PNS extracellular matrix and provides niche environments conducive to the optimisation of neuronal activity.
 Dissecting regulatory T cell expansion using polymer microparticles presenting defined ratios of self-antigen and regulatory cues.
 Leveraging decagonal in-silico strategies for uncovering IL-6 inhibitors with precision.
 Metabolism-related brain morphology accelerates aging and predicts neurodegenerative diseases and stroke: a UK Biobank study.
 Low-Dose Naltrexone (LDN) for Chronic Pain at a Single Institution: A Case Series.
 Cannabis sativa-based oils against aluminum-induced neurotoxicity.
 Molecular mechanisms of syncytin-1 in tumors and placental development related diseases.
 Association between genetically determined telomere length and health-related outcomes: A systematic review and meta-analysis of Mendelian randomization studies.
 Mode of binding, kinetic and thermodynamic properties of a lipid-like drug (Fingolimod) interacting with Human Serum Albumin.
 Respiratory symptoms are common in stiff person syndrome spectrum disorders and are associated with number of body regions involved.
 Alpha4 beta7 integrin controls Th17 cell trafficking in the spinal cord leptomeninges during experimental autoimmune encephalomyelitis.
 Data-driven characterization of walking after a spinal cord injury using inertial sensors.
 Prevotella histicola suppresses ferroptosis to mitigate ethanol-induced gastric mucosal lesions in mice.
 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease and COVID-19: A Systematic Review.
 The Effects of SARS-CoV-2 Infection on the Cognitive Functioning of Patients with Pre-Existing Dementia.
 Study of Effector CD8+ T Cell Interactions with Cortical Neurons in Response to Inflammation in Mouse Brain Slices and Neuronal Cultures.
 Astrocytic TIMP-1 regulates production of Anastellin, a novel inhibitor of oligodendrocyte differentiation and FTY720 responses.
 Role of NLRP3 Inflammasome and Its Inhibitors as Emerging Therapeutic Drug Candidate for Alzheimer's Disease: a Review of Mechanism of Activation, Regulation, and Inhibition.
 Prevalence, risk factors, clinical and biochemical characteristics of Alemtuzumab-induced Graves' disease.
 Quantifying the Association between Objectively Measured Physical Activity and Multiple Sclerosis in the UK Biobank.
 Exploring the impact of miR-128 in inflammatory diseases: A comprehensive study on autoimmune diseases.
 AXL(+)SIGLEC6(+) dendritic cells in cerebrospinal fluid and brain tissues of patients with autoimmune inflammatory demyelinating disease of CNS.
 In Silico Analysis: HLA-DRB1 Gene's Variants and Their Clinical Impact.
 Neurological Manifestations of Histiocytic Disorders.
 Satisfaction analysis of overground gait exoskeletons in people with neurological pathology. a systematic review.
 Digital health for chronic disease management: An exploratory method to investigating technology adoption potential.
 Percutaneous Rhizotomy of the Gasserian Ganglion in Patients With Mass Lesion-Associated Trigeminal Neuralgia: A Case Series.
 Lipid metabolism in Th17 cell function.
 Controlling the Impact of Helicobacter pylori-Related Hyperhomocysteinemia on Neurodegeneration.
 Adjuvant Injections Altered the Ileal and Fecal Microbiota Differently with Changes in Immunoglobulin Isotypes and Antimycobacterial Antibody Responses.
 Molecular Hydrogen: an Emerging Therapeutic Medical Gas for Brain Disorders.
 Neurological manifestations of COVID-19: a retrospective observational study based on 1060 patients with a narrative review.
 A longitudinal study of distress symptoms and work impairment in immune-mediated inflammatory diseases.
 Relationship between autoimmune diseases and serum basal immunoglobulin E levels in patients with common variable immunodeficiency.
 Mechanisms of cannabinoid tolerance.
 Neurodegenerative and Neurodevelopmental Diseases and the Gut-Brain Axis: The Potential of Therapeutic Targeting of the Microbiome.
 Mechanism of action and therapeutic potential of dimethyl fumarate in ischemic stroke.
 Radiosynthesis automation, non-human primate biodistribution and dosimetry of K (+) channel tracer [ (11) C]3MeO4AP.
 Experience and perception of utilizing virtual clinic in neurological assessment in Saudi Arabia.
 A study of the relationship between serum uric acid levels and pain in patients with migraine.
 Synthesis and Comprehensive in Vivo Activity Profiling of Olean-12-en-28-ol, 3β-Pentacosanoate in Experimental Autoimmune Encephalomyelitis: A Natural Remyelinating and Anti-Inflammatory Agent.
 Use of metal-based contrast agents for in vivo MR and CT imaging of phagocytic cells in neurological pathologies.
 Preliminary PET imaging of [(11) C]evobrutinib in mouse models of colorectal cancer, SARS-CoV-2, and lung damage: Radiosynthesis via base-aided palladium-NiXantphos-mediated (11) C-carbonylation.
 International Delphi Consensus on the Management of AQP4-IgG+ NMOSD: Recommendations for Eculizumab, Inebilizumab, and Satralizumab.
 Preparation of Primary Mixed Glial Cell Cultures from Adult Mouse Spinal Cord Tissue.
 Costs and Utilization of New-to-Market Neurologic Medications.
 The causal role of circulating amino acids on neurodegenerative disorders: A two-sample Mendelian randomization study.
 [Knock-down of ROCK2 gene improves cognitive function and reduces neuronal apoptosis in AD mice by promoting mitochondrial fusion and inhibiting its division].
 Synthesizing cross-design evidence and cross-format data using network meta-regression.
 IGF1R expression by adult oligodendrocytes is not required in the steady-state but supports neuroinflammation.
 STA-21, a small molecule STAT3 inhibitor, ameliorates experimental autoimmune encephalomyelitis by altering Th-17/Treg balance.
 Neurological autoimmune diseases following vaccinations against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2): A follow-up study.
 Corrigendum to "CLIPPERS: Multiparametric and quantitative MRI features" [Radiology Case Reports 18 (2023) 368-376].
 Author Correction: Vitamin D status and severity of COVID-19.
 Overcoming Early Career Setbacks.
 Epstein-Barr Virus-Positive Lymphomas Exploit Ectonucleotidase Activity To Limit Immune Responses and Prevent Cell Death.
 The role of the indoles in microbiota-gut-brain axis and potential therapeutic targets: A focus on human neurological and neuropsychiatric diseases.
 SAkuraBONSAI: Protocol design of a novel, prospective study to explore clinical, imaging, and biomarker outcomes in patients with AQP4-IgG-seropositive neuromyelitis optica spectrum disorder receiving open-label satralizumab.
 Central nervous system complications in SARS-CoV-2-infected patients.
 The Impact of a Very-Low-Calorie Ketogenic Diet in the Gut Microbiota Composition in Obesity.
 Implication of cognitive-behavioral stress management on anxiety, depression, and quality of life in acute myocardial infarction patients after percutaneous coronary intervention: a multicenter, randomized, controlled study.
 Phosphodiesterase inhibitor, ibudilast alleviates core behavioral and biochemical deficits in the prenatal valproic acid exposure model of autism spectrum disorder.
 Isolated Area Postrema Syndrome Preceding the Diagnosis of Giant Cell Arteritis: A Case Report.
 Mental Illnesses in Inflammatory Bowel Diseases: mens sana in corpore sano.
 Applications of generative adversarial networks in neuroimaging and clinical neuroscience.
 SARS-CoV2 entry factors are expressed in primary human glioblastoma and recapitulated in cerebral organoid models.
 Parenting with a physical disability: A scoping review of assessment methods.
 Palliative care to support the needs of adults with neurological disease.
 Treatment of neurogenic detrusor overactivity and overactive bladder with Botox (onabotulinumtoxinA): Development, insights, and impact.
 Vagus nerve inflammation contributes to dysautonomia in COVID-19.
 Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases.
 Is functional electrical stimulation effective in improving walking in adults with lower limb impairment due to an upper motor neuron lesion? An umbrella review.
 A zebrafish model of combined saposin deficiency identifies acid sphingomyelinase as a potential therapeutic target.
 Immunity orchestrates a bridge in gut-brain axis of neurodegenerative diseases.
 FTY720 Attenuates LPS-Induced Inflammatory Bone Loss by Inhibiting Osteoclastogenesis via the NF-κB and HDAC4/ATF Pathways.
 CLEC16A interacts with retromer and TRIM27, and its loss impairs endosomal trafficking and neurodevelopment.
 Identifying Suitable Targets for Alzheimer's Disease and Other Eight Common Neurological Disorders Using the Human Plasma Proteome: A Mendelian Randomization Study.
 Immune System and Brain/Intestinal Barrier Functions in Psychiatric Diseases: Is Sphingosine-1-Phosphate at the Helm?
 Modulation of inflammation and immunity by omega-3 fatty acids: a possible role for prevention and to halt disease progression in autoimmune, viral, and age-related disorders.
 Methylglyoxal suppresses microglia inflammatory response through NRF2-IκBζ pathway.
 Diagnosis and Management of Marchiafava-Bignami Disease, a Rare Neurological Complication of Long-term Alcohol Abuse.
 Exploring the Potential of Aptamers in Targeting Neuroinflammation and Neurodegenerative Disorders: Opportunities and Challenges.
 Prevalence and adverse consequences of delayed diagnosis and misdiagnosis in thrombotic antiphospholipid syndrome. An observational cohort study and a review of the literature.
 Factors Associated With No-Show to Ambulatory Tele-Video Neurology Visits.
 Familial neuromyelitis optica spectrum disorders: Case series and systematic review.
 Monoclonal Antibodies.
 Infectious mononucleosis is associated with an increased incidence of Crohn's disease: results from a cohort study of 31 862 outpatients in Germany.
 A scoping review to identify process and outcome measures used in acceptance and commitment therapy research, with adults with acquired neurological conditions.
 Recent insights into the roles of circular RNAs in human brain development and neurologic diseases.
 Glial fibrillary acidic protein as a biomarker in neuromyelitis optica spectrum disorder: a current review.
 Effects of sub-chronic nabiximols on biological markers of individuals undergoing a clinical trial for the treatment of cannabis use disorder.
 Performance of a Mobile 3D Camera to Evaluate Simulated Pathological Gait in Practical Scenarios.
 The choroid plexus acts as an immune cell reservoir and brain entry site in experimental autoimmune encephalomyelitis.
 Self-evidence-based digital care programme improves health-related quality of life in adults with a variety of autoimmune diseases and long COVID: a retrospective study.
 Immunomodulatory Effects of New Phenanthrene Derivatives from Dendrobium crumenatum.
 Evaluation of BAFF, APRIL and CD40L in Ocrelizumab-Treated pwMS and Infectious Risk.
 Analysis of heat stroke and heat exhaustion cases in EudraVigilance pharmacovigilance database.
 Inhibiting degradation of 2-arachidonoylglycerol as a therapeutic strategy for neurodegenerative diseases.
 [Antibody production capacity after COVID-19 vaccination in immune-mediated neuromuscular diseases under immunotherapy].
 Higher consumption of ultra-processed foods and increased likelihood of central nervous system demyelination in a case-control study of Australian adults.
 Robot-assisted laparoscopic cystectomy with non-continent urinary diversion for neurogenic lower urinary tract dysfunction: Midterm outcomes.
 The Cognitive and Behavioural Responses to Symptoms Questionnaire (CBRQ): Development, reliability and validity across several long-term conditions.
 The protective effect of total glucosides of white paeony capsules on experimental autoimmune encephalomyelitis.
 Developmental impacts of Nrf2 activation by dimethyl fumarate (DMF) in the developing zebrafish (Danio rerio) embryo.
 Surface-modified lipid nanocarriers for crossing the blood-brain barrier (BBB): A current overview of active targeting in brain diseases.
 Mesenchymal stem cells (MSCs) and MSC-derived exosomes in animal models of central nervous system diseases: Targeting the NLRP3 inflammasome.
 LMP2 deficiency causes abnormal metabolism, oxidative stress, neuroinflammation, myelin loss and neurobehavioral dysfunctions.
 Salt sensitivity includes effects on immune cell signalling and metabolism.
 Injury-induced activation of the endocannabinoid system promotes axon regeneration.
 Letter to the editor regarding "Stabilization of leukocytes from cerebrospinal fluid for central immunophenotypic evaluation in multicenter clinical trials".
 Difficulties in Differentiating Osteosclerosis in Patients With Multifocal Micronodular Pneumocyte Hyperplasia and Cancer.
 Recurrent Tumefactive Central Nervous System Lesions Due to BRIP1-Related Fanconi Anemia.
 Pediatric anti-NMDA-receptor autoimmune encephalitis in siblings: Developmental, Electrophysiologic, and Genetic Implications.
 Multiple pathways of lipid dysregulation in amyotrophic lateral sclerosis.
 Clinical diagnostic utility of transcranial magnetic stimulation in neurological disorders. Updated report of an IFCN committee.
 First-in-Human Studies of Pharmacokinetics and Safety of Utreloxastat (PTC857), a Novel 15-Lipooxygenase Inhibitor for the Treatment of Amyotrophic Lateral Sclerosis.
 Effects of Palliative Care for Progressive Neurologic Diseases: A Systematic Review and Meta-Analysis.
 Amplifying the Effects of Contrast Agents on Magnetic Resonance Images Using a Deep Learning Method Trained on Synthetic Data.
 Nanoparticle Delivery of Immunostimulatory Alu RNA for Cancer Immunotherapy.
 The complex pathway between amyloid β and cognition: implications for therapy.
 Concurrent Reduced Expression of Contiguous PKD1, TSC2 and NTHL1 Leading to Kidney Diseases and Multiple Diverse Renal Cancers.
 Delayed oculomotor response associates with optic neuritis in youth with demyelinating disorders.
 mcLARO: Multi-contrast learned acquisition and reconstruction optimization for simultaneous quantitative multi-parametric mapping.
 Factors correlated with neuropathic pain among industrial workers in Vietnam: a multi-site cross-sectional study.
 Drug-Repurposing Strategy for Dimethyl Fumarate.
 A Comparison Between Somatosensory Evoked Potentials and Spine MRI in the Diagnosis of Non-compressive Myelopathy: Which Is More Accurate?
 FTY720-P, a Biased S1PR Ligand, Increases Mitochondrial Function through STAT3 Activation in Cardiac Cells.
 Immune cell targeted fumaric esters support a role of GPR109A as a primary target of monomethyl fumarate in vivo.
 Magnetic transferrin nanoparticles (MTNs) assay as a novel isolation approach for exosomal biomarkers in neurological diseases.
 Melatonin: a potential therapeutic approach for the management of primary Sjögren's syndrome.
 Association between autoimmune diseases of the nervous system and schizophrenia: A systematic review and meta-analysis of cohort studies.
 Telemedicine for neurological diseases: A systematic review and meta-analysis.
 Gender Representation Among Physician Authors of Practice Guidelines Developed, Endorsed, or Affirmed by the American Academy of Neurology.
 Efficacy of B-vitamins and vitamin D therapy in improving depressive and anxiety disorders: a systematic review of randomized controlled trials.
 A workflow for the development of template-assisted membrane crystallization downstream processing for monoclonal antibody purification.
 COVID-19 vaccine safety in Scotland - background rates of adverse events of special interest.
 Subclinical damage to the contralateral eye in unilateral optic neuritis: A longitudinal study.
 Nogo-A antibody delivery through the olfactory mucosa mitigates experimental autoimmune encephalomyelitis in the mouse CNS.
 A Mendelian randomization study on causal effects of 25(OH) vitamin D levels on diabetic nephropathy.
 Inducible nitric oxide synthase deficiency promotes murine-β-coronavirus induced demyelination.
 Effects of an Ocrevus Rapid Infusion Protocol: A Literature Review and Quality Improvement Project.
 Piperazine derivatives with potent drug moiety as efficient acetylcholinesterase, butyrylcholinesterase, and glutathione S-transferase inhibitors.
 Prenatal exposure to environmental air pollution and psychosocial stress jointly contribute to the epigenetic regulation of the serotonin transporter gene in newborns.
 Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes.
 Neutralizing RGMa with Elezanumab Promotes Cerebroprotection and Recovery in Rabbit Middle Cerebral Artery Occlusion.
 Erratum: Clinical and Demographic Characteristics and Two-Year Efficacy and Safety Data of 508 Multiple Sclerosis Patients with Fingolimod Treatment.
 Interpersonal Values of Patients Participating in Phase II-III Clinical Trials: Implications for Clinical Trial Representativeness.
 Comparison of acute flaccid myelitis and transverse myelitis in children and evaluation of diagnostic criteria.
 Microglial aryl hydrocarbon receptor enhances phagocytic function via SYK and promotes remyelination in the cuprizone mouse model of demyelination.
 Tixagevimab and Cilgavimab (Evusheld™) Prophylaxis Prevents Breakthrough COVID-19 Infections in Immunosuppressed Population: 6-Month Prospective Study.
 Oligodendrocyte-lineage cell exocytosis and L-type prostaglandin D synthase promote oligodendrocyte development and myelination.
 Particulate matter and ultrafine particles in urban air pollution and their effect on the nervous system.
 Estrogen receptor alpha signaling in dendritic cells modulates autoimmune disease phenotype in mice.
 Biologic and Small-Molecule Therapies for Moderate-to-Severe Psoriasis: Focus on Psoriasis Comorbidities.
 Immune-mediated diseases and subsequent risk of alopecia areata in a prospective study of US women.
 Familial autoimmunity in patients with idiopathic inflammatory myopathies.
 A global assessment of incidence trends of autoimmune diseases from 1990 to 2019 and predicted changes to 2040.
 Dual combined antiviral treatment with remdesivir and nirmatrelvir/ritonavir in patients with impaired humoral immunity and persistent SARS-CoV-2 infection.
 Suboptimal Sleep Duration is Associated with Poorer Neuroimaging Brain Health Profiles.
 Inhibition of ACSL4 Alleviates Parkinsonism Phenotypes by Reduction of Lipid Reactive Oxygen Species.
 Mesenchymal stem cell-derived exosomal microRNA-367-3p alleviates experimental autoimmune encephalomyelitis via inhibition of microglial ferroptosis by targeting EZH2.
 On the Chemical and Biological Characteristics of Multifunctional Compounds for the Treatment of Parkinson's Disease.
 The Effects of HSOP on Cognition, Depression, and Activities of Daily Living in Older Adults with Cognitive Issues.
 Efficacy and safety of adjunctive therapy with fingolimod in patients with schizophrenia: A randomized, double-blind, placebo-controlled clinical trial.
 Mendelian randomisation identifies priority groups for prophylactic EBV vaccination.
 Experimental Investigations of Monomethyl and Dimethyl Fumarate in an Astrocyte-Microglia Co-Culture Model of Inflammation.
 Undersampled single-shell to MSMT fODF reconstruction using CNN-based ODE solver.
 Dysregulation of the chromatin environment leads to differential alternative splicing as a mechanism of disease in a human model of autism spectrum disorder.
 The Beneficial Clinical Effects of Teriflunomide in Experimental Autoimmune Myasthenia Gravis and the Investigation of the Possible Immunological Mechanisms.
 Reproducibility and Optimal Arterial Input Function Selection in Dynamic Contrast-Enhanced Perfusion MRI in the Healthy Brain.
 Impacts of Climate Change and Air Pollution on Neurologic Health, Disease, and Practice: A Scoping Review.
 Amyotrophic Lateral Sclerosis.
 Multiple fibrofolliculomas within a fibrous cephalic plaque in a patient with tuberous sclerosis.
 Pachydermodactyly, mimicker of rheumatoid hands, presents in a patient with Tuberous Sclerosis.
 Tuberous Sclerosis Complex in a 17-month-old: A Case Report.
 Biotinidase Deficiency.
 Susceptibility and disease modifier genes in amyotrophic lateral sclerosis: from genetic associations to therapeutic implications.
 Measuring Ambulatory Racial and Ethnic Neurologic Disparities With the Axon Registry.
 Structural and non-structural proteins in SARS-CoV-2: potential aspects to COVID-19 treatment or prevention of progression of related diseases.
 Association Between Antiepileptic Drugs and Incident Parkinson Disease.
 Identification and protective role of CD34(+) stromal cells/telocytes in experimental autoimmune encephalomyelitis (EAE) mouse spleen.
 TSC2/PKD1 contiguous deletion syndrome in a pregnant woman: A case report.
 Encapsulating Peritoneal Sclerosis.
 Mutated FUS in familial amyotrophic lateral sclerosis involves multiple hnRNPs in the formation of neuronal cytoplasmic inclusions.
 Late diagnosis of tuberous sclerosis complex in a 40-year-old female presenting with abdominal pain: a case report.
 Epilepsy surgery for dominant-side mesial temporal lobe epilepsy without hippocampal sclerosis.
 Multiple Cardiac Rhabdomyomas in Dizygotic Twins.
 Wuzi Yanzong Pill relieves MPTP-induced motor dysfunction and neuron loss by inhibiting NLRP3 inflammasome-mediated neuroinflammation.
 Refractive Errors, Retinal Findings, and Genotype of Tuberous Sclerosis Complex: A Retrospective Cohort Study.
 Pathogenic RHEB Somatic Variant in a Child With Tuberous Sclerosis Complex Without Pathogenic Variants in TSC1 or TSC2.
 Multiple Interventions to Thoracoabdominal Aortic Aneurysm in a Child With Tuberous Sclerosis.
 Overlap syndrome with antibodies against multiple transfer-RNA components presenting antisynthetase syndrome.
 Incidental finding of tuberous sclerosis complex in a woman with hematuria: A case report of renal angiomyolipoma and review of the literature.
 Usefulness of Next-Generation Sequencing in Excluding Bovine Leukemia Virus as a Cause of Adult Camel Leukosis in Dromedaries.
 Alterations in Aquaporin-4-IgG Serostatus in 986 Patients: A Laboratory-Based Longitudinal Analysis.
 An Epstein-Barr virus protein interaction map reveals NLRP3 inflammasome evasion via MAVS UFMylation.
 Pregabalin in the Treatment of Peripheral and Central Chronic Neuropathic Pain.
 Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis.
 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) in Chile: lessons learned from challenging cases.
 [Short version of the S2k guideline on drug therapy of neurogenic lower urinary tract dysfunction (NLUTD)].
 The protective effects of sesamol and/or the probiotic, Lactobacillus rhamnosus, against aluminum chloride-induced neurotoxicity and hepatotoxicity in rats: Modulation of Wnt/β-catenin/GSK-3β, JAK-2/STAT-3, PPAR-γ, inflammatory, and apoptotic pathways.
 Bioactivity of the cannabigerol cannabinoid and its analogues - the role of 3-dimensional conformation.
 SARS-CoV-2 antibodies in inflammatory neurological conditions: a multicentre retrospective comparative study.
 Neurological manifestations of SARS-CoV-2: complexity, mechanism and associated disorders.
 Perspectives on how to build bridges between regulation, health technology assessment and clinical guideline development: a qualitative focus group study with European experts.
 Timing and Predictors of T2-Lesion Resolution in Patients With Myelin-Oligodendrocyte-Glycoprotein-Antibody-Associated Disease.
 Clinical Practice Guidelines for Cannabis and Cannabinoid-Based Medicines in the Management of Chronic Pain and Co-Occurring Conditions.
 Effect of vitamin D supplementation on cerebral blood flow in male patients with adrenoleukodystrophy.
 Diphtheria toxin-derived, anti-PD-1 immunotoxin, a potent and practical tool to selectively deplete PD-1(+) cells.
 MRI features of idiopathic intracranial hypertension are not prognostic of visual and headache outcome.
 Immune-mediated inflammatory diseases and the risk of valvular heart disease: a Mendelian randomization study.
 Shaping membrane interfaces in lipid vesicles mimicking the cytoplasmic leaflet of myelin through variation of cholesterol and myelin basic protein contents.
 Prevalence and Mortality Risk of Neurological Disorders during the COVID-19 Pandemic: An Umbrella Review of the Current Evidence.
 Cardiac rhabdomyomas: clinical progression, efficacy and safety of everolimus treatment.
 A rare case of signet ring cell carcinoma with diffuse cutaneous systemic sclerosis: A case report.
 Establishment of human induced pluripotent stem cell lines, KMUGMCi006, from a patient with Tuberous sclerosis complex (TSC) bearing mosaic nonsense mutations in the Tuberous sclerosis complex 2 (TSC2) gene.
 Paradigm shift in the treatment of tuberous sclerosis: Effectiveness of everolimus.
 Implications of miRNAs dysregulation in amyotrophic lateral sclerosis: Challenging for clinical applications.
 68 Ga-FAPI-04 PET/MRI in a Case of Tuberous Sclerosis Complex With Extrarenal Retroperitoneal Angiomyolipoma.
 Comprehensive genetic and phenotype analysis of 95 individuals with mosaic tuberous sclerosis complex.
 Retinal astrocytic hamartoma complicated by branch retinal vein occlusion in a patient with tuberous sclerosis complex.
 Considerations for Hand Surgery in Patients With Scleroderma.
 Misdiagnosis in Amyotrophic Lateral Sclerosis.
 Subependymal giant cell astrocytoma in the absence of tuberous sclerosis: illustrative case.
 Disease activity in patients with immune-mediated inflammatory diseases after SARS-CoV-2 vaccinations.
 Potential angiogenic, immunomodulatory, and antifibrotic effects of mesenchymal stem cell-derived extracellular vesicles in systemic sclerosis.
 Lack of Causal Associations of Inflammatory Bowel Disease with Parkinson's Disease and Other Neurodegenerative Disorders.
 Engaging Multistakeholder Perspectives to Identify Patient-Centered Research Priorities Regarding Vaccine Uptake Among Adults With Autoimmune Conditions.
 Vascular comorbidity is associated with decreased cognitive functioning in inflammatory bowel disease.
 Online Health Information Seeking by Individuals With Physical Disabilities Caused by Neurological Conditions in Saudi Arabia.
 IRAK-M suppresses the activation of microglial NLRP3 inflammasome and GSDMD-mediated pyroptosis through inhibiting IRAK1 phosphorylation during experimental autoimmune encephalomyelitis.
 Predictors of Glucocorticoid Use for Acute Optic Neuritis in the United States, 2005-2019.
 Neuroprotection by the cannabidiol aminoquinone VCE-004.8 in experimental ischemic stroke in mice.
 Propionate exerts neuroprotective and neuroregenerative effects in the peripheral nervous system.
 The relation between cognitive-behavioural responses to symptoms in patients with long term medical conditions and the outcome of cognitive behavioural therapy for fatigue - A secondary analysis of four RCTs.
 Anti-CD20 monoclonal antibody therapy in postpartum women with neurological conditions.
 Botulinum Toxin Utilization, Treatment Patterns, and Healthcare Costs Among Patients with Spasticity or Cervical Dystonia in the US.
 Socs3 expression in myeloid cells modulates the pathogenesis of dextran sulfate sodium (DSS)-induced colitis.
 CDX-modified chitosan nanoparticles remarkably reduce therapeutic dose of fingolimod in the EAE model of mice.
 Causal relationship between PCSK9 inhibitor and autoimmune diseases: a drug target Mendelian randomization study.
 Association of multiple retinal nodular hamartomas and "confetti" skin lesions with end-stage renal disease in patients with tuberous sclerosis.
 Prenatal diagnosis of tuberous sclerosis complex: Echocardiography, cranial magnetic resonance, and genetic testing of 40 cases with fetal cardiac tumors.
 Brain expression quantitative trait locus and network analyses reveal downstream effects and putative drivers for brain-related diseases.
 Progressive Systemic Sclerosis With Negative Antinuclear Antibodies and Absence of Raynaud's Phenomenon: A Case Report and Literature Review.
 Siponimod As a Novel Inhibitor of Retinal Angiogenesis: In Vitro and In Vivo Evidence of Therapeutic Efficacy.
 Systematic, comprehensive, evidence-based approach to identify neuroprotective interventions for motor neuron disease: using systematic reviews to inform expert consensus.
 The implications of physiological biomolecular condensates in amyotrophic lateral sclerosis.
 Anti-RuvBL1/2 Autoantibodies Detection in a Patient with Overlap Systemic Sclerosis and Polymyositis.
 Tuberous Sclerosis Complex-Varied Presentations in Family Clusters.
 Association of caesarean delivery with offspring health outcomes in full-cohort versus sibling-comparison studies: a comparative meta-analysis and simulation study.
 Using real-world evidence data and digital monitoring to analyze the hepatotoxic profiles of biologics across more than two million patients.
 Divergent functional outcomes of NLRP3 blockade downstream of multi-inflammasome activation: therapeutic implications for ALS.
 Cerebrovascular disease in patients with COVID-19 infection: a case series from Lebanon.
 Leigh syndrome mimicking neuromyelitis optica spectrum disorder (NMOSD).
 Case report: JAK inhibition as promising treatment option of fatal RVCLS due to TREX1 mutation (pVAL235Glyfs(*)6).
 Esophageal motility in systemic sclerosis before and after autologous hematopoietic cell transplantation.
 Orbital Perivascular Epithelioid Cell Tumor in a Case of Tuberous Sclerosis.
 Primary care blood tests show lipid profile changes in pre-symptomatic amyotrophic lateral sclerosis.
 Candlenut oil-induced sclerosing lipogranuloma of the penis: A case report.
 Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis.
 Shear wave elastography-based skin assessment system for systemic sclerosis: a supplement or alternative to conventional ultrasound?
 Pathological Factors Affecting the R2* Values of the Kidney in Blood Oxygenation Level-dependent MR Imaging: A Retrospective Study.
 Amyotrophic Lateral Sclerosis Risk Genes and Suppressor.
 Unwinding the role of Wnt signaling cascade and molecular triggers of motor neuron degeneration in amyotrophic lateral sclerosis (ALS).
 Percutaneous revascularization for the treatment of refractory digital ischemia in systemic sclerosis.
 The effects of nuclear DNA mutations on mitochondrial function.
 An Integral Approach to the Molecular Diagnosis of Tuberous Sclerosis Complex: The Role of Mosaicism and Splicing Variants.
 Molecular and Physiological Determinants of Amyotrophic Lateral Sclerosis: What the DJ-1 Protein Teaches Us.
 Prevalence of anti-synthetase antibodies among systemic sclerosis patients.
 Astrocytic K(+) clearance during disease progression in amyotrophic lateral sclerosis.
 Is External Cervical Resorption an Established Manifestation of Systemic Sclerosis? A Case Report.
 A case of massive fetal cardiac rhabdomyoma: ultrasound features and management.
 Pathomechanistic Networks of Motor System Injury in Amyotrophic Lateral Sclerosis.
 Assessing the duration of EDSS improvement after a therapy start: A novel approach applied to the long-term extension of the PRISMS study.
 Identifying shared genetic architecture between rheumatoid arthritis and other conditions: a phenome-wide association study with genetic risk scores.
 A Pilot Study on Cannabidiol (CBD) and Eccentric Exercise: Impact on Inflammation, Performance, and Pain.
 Virtual Screening Strategy to Identify Retinoic Acid-Related Orphan Receptor γt Modulators.
 Simultaneous Multislice Accelerated TSE for Improved Spatiotemporal Resolution and Diagnostic Accuracy in Magnetic Resonance Neurography: A Feasibility Study.
 Two different isoforms of osteopontin modulate myelination and axonal integrity.
 Renewal of oligodendrocyte lineage reverses dysmyelination and CNS neurodegeneration through corrected N-acetylaspartate metabolism.
 Sclerotic Bone Lesions as a Clue in the Diagnosis of Three Generations of Tuberous Sclerosis Complex: Case Report and Review of Literature.
 The paradigm of amyloid precursor protein in amyotrophic lateral sclerosis: The potential role of the (682)YENPTY(687) motif.
 Clinical, Radiologic, and Immunologic Features of Patients With CTLA4 Deficiency With Neurologic Involvement.
 Defining blood-induced microglia functions in neurodegeneration through multiomic profiling.
 Neuromyelitis optica spectrum disorders with a benign course. Analysis of 544 patients.
 Dimethyl fumarate inhibits necroptosis and alleviates systemic inflammatory response syndrome by blocking the RIPK1-RIPK3-MLKL axis.
 The association between Parkinson's disease and autoimmune diseases: A systematic review and meta-analysis.
 The Efficacity of the NeuroAssist Robotic System for Motor Rehabilitation of the Upper Limb-Promising Results from a Pilot Study.
 Comparative pharmacokinetics and bioavailability of monomethyl fumarate following a single oral dose of Bafiertam® (monomethyl fumarate) versus Vumerity® (diroximel fumarate).
 Fingolimod ameliorates schizophrenia-like cognitive impairments induced by phencyclidine in male rats.
 Synthetic MRI with Magnetic Resonance Spin TomogrAphy in Time-Domain (MR-STAT): Results from a Prospective Cross-Sectional Clinical Trial.
 Clinical and radiological profile of neuromyelitis optica spectrum disorders in a Pakistani cohort.
 Suitability of Goal Attainment Scaling in Older Adult Populations with Neurodegenerative Disease Experiencing Cognitive Impairment: A Systematic Review and Meta-Analysis.
 Stability and Activity of Interferon Beta to Treat Idiopathic Pulmonary Fibrosis with Different Nebulizer Technologies.
 Autophagy (but not metabolism) is a key event in mitoxantrone-induced cytotoxicity in differentiated AC16 cardiac cells.
 The Role of CCL24 in Systemic Sclerosis.
 Anti-PL12 Anti-Synthetase Syndrome and Amyotrophic Lateral Sclerosis: A Case Report of a Rare Comorbidity.
 Inclusion body myositis in an older patient following a fall.
 Systemic sclerosis.
 C9orf72 ALS mutation carriers show extensive cortical and subcortical damage compared to matched wild-type ALS patients.
 Systemic sclerosis with interstitial lung disease and myocardial infarction: a case report.
 Discovery of Biomarkers for Amyotrophic Lateral Sclerosis from Human Cerebrospinal Fluid Using Mass-Spectrometry-Based Proteomics.
 Tenascin-R Autoimmunity: Isolated Tremor Reversed with Immunotherapy.
 Central Nervous System Vasculitis: Primary Angiitis of the Central Nervous System and Central Nervous System Manifestations of Systemic Vasculitis.
 Tuberous Sclerosis.
 Preventative Care in Scleroderma: What Is the Best Approach to Vaccination?
 Molecular mechanisms of amyotrophic lateral sclerosis as broad therapeutic targets for gene therapy applications utilizing adeno-associated viral vectors.
 Treatment-Resistant Epilepsy and Tuberous Sclerosis Complex: Treatment, Maintenance, and Future Directions.
 The Fragile X Protein Family in Amyotrophic Lateral Sclerosis.
 Interplay of Metallome and Metabolome in Amyotrophic Lateral Sclerosis: A Study on Cerebrospinal Fluid of Patients Carrying Disease-Related Gene Mutations.
 Detection of episodic nocturnal hypercapnia in patients with neurodegenerative disorders.
 JAK inhibitors and autoimmune rheumatic diseases.
 A mechanistic target of rapamycin inhibitor, everolimus safely ameliorated lupus nephritis in a patient complicated with tuberous sclerosis.
 Cognitive and neuropsychiatric endophenotypes in amyotrophic lateral sclerosis.
 Role of Oxidative Stress on the Etiology and Pathophysiology of Amyotrophic Lateral Sclerosis (ALS) and Its Relation with the Enteric Nervous System.
 Split Phenomenon of Fasciculation between Antagonistic Muscles in Amyotrophic Lateral Sclerosis: An Ultrasound Study.
 Involvement of Lipids in the Pathogenesis of Amyotrophic Lateral Sclerosis.
 Evaluation of an educational conference for persons affected by hereditary frontotemporal degeneration and amyotrophic lateral sclerosis.
 Balancing risks and benefits of cannabis use: umbrella review of meta-analyses of randomised controlled trials and observational studies.
 Skeletal Fluorosis in a Patient With Computer Cleaner Inhalant Abuse.
 Pulmonary Nodules in Juvenile Systemic Sclerosis: A Case-Series from the National Registry for Childhood Onset Scleroderma (NRCOS).
 Tuberous Sclerosis Complex: Prenatal Diagnosis Using Ultrasound and Magnetic Resonance Imaging-A Report of Two Cases.
 Diffusion basis spectrum imaging detects pathological alterations in substantia nigra and white matter tracts with early-stage Parkinson's disease.
 Proteomic analysis of murine Tsc1-deficient neural stem progenitor cells.
 Blocking common γ chain cytokine signaling ameliorates T cell-mediated pathogenesis in disease models.
 Association of Very Early Treatment Initiation With the Risk of Long-Term Disability in Patients With a First Demyelinating Event.
 Assessing Osteolytic Lesion Size on Sequential CT Scans Is a Reliable Study Endpoint for Bone Remineralization in Newly Diagnosed Multiple Myeloma.
 Osteopathia Striata with Cranial Sclerosis.
 Physical activity as an exogenous risk factor for amyotrophic lateral sclerosis: a review of the evidence.
 Differences in morphology of temporomandibular joint ankylosis of traumatic and infective origin.
 Sleep disorders and white matter integrity in patients with sporadic amyotrophic lateral sclerosis.
 Determining the neurocognitive profile of children with tuberous sclerosis complex within the Western Cape region of South Africa.
 The linkage of depressive and anxiety disorders with the expected labor market affiliation (ELMA): a longitudinal multi-state study of Danish employees.
 HLA and amyotrophic lateral sclerosis: a systematic review and meta-analysis.
 Pharmacokinetic Drug-Drug Interaction With Coadministration of Cannabidiol and Everolimus in a Phase 1 Healthy Volunteer Trial.
 Mapping the sociodemographic distribution and self-reported justifications for non-compliance with COVID-19 guidelines in the United Kingdom.
 MOG-IgG positive optic neuritis after SARS-CoV-2 infection.
 Myasthenia gravis patients exhibiting an eyelid myotonia-like phenomenon.
 Contactin-associated protein 2 autoantibodies can be associated with multifocal motor-like neuropathy: a case report.
 Comprehensive autoantibody profiling in systemic autoimmunity by a highly-sensitive multiplex protein array.
 Abnormal Brain Protein Abundance and Cross-tissue mRNA Expression in Amyotrophic Lateral Sclerosis.
 Importance of numerical density of tubulointerstitium infiltrates in the prognosis of antineutrophil cytoplasmic antibodies-associated glomerulonephritis.
 Pathological combinations in neurodegenerative disease are heterogeneous and disease-associated.
 Genetic and clinical analysis of TP73 gene in amyotrophic lateral sclerosis patients from Chinese mainland.
 Molecular Mechanisms Behind the Role of Plasmacytoid Dendritic Cells in Systemic Sclerosis.
 Mesenchymal stem cell therapy in amyotrophic lateral sclerosis (ALS) patients: A comprehensive review of disease information and future perspectives.
 Therapeutic mechanism of baicalein in peritoneal dialysis-associated peritoneal fibrosis based on network pharmacology and experimental validation.
 L1CAM immunocapture generates a unique extracellular vesicle population with a reproducible miRNA fingerprint.
 Mesenchymal Stem Cell-Based Therapy as a New Approach for the Treatment of Systemic Sclerosis.
 Advances in biological and targeted therapies for systemic sclerosis.
 Potential benefits of medium chain fatty acids in aging and neurodegenerative disease.
 Neuroendocrine neoplasms in the context of inherited tumor syndromes: a reappraisal focused on targeted therapies.
 Multimodal imaging in a case of bilateral astrocytic hamartoma with retinitis pigmentosa.
 Analysis of current data on the use of topical mTOR inhibitors in the treatment of facial angiofibromas in tuberous sclerosis complex-An update.
 Prevalence and determinants of language impairment in non-demented amyotrophic lateral sclerosis patients.
 Diagnostic value of intereye difference metrics for optic neuritis in aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders.
 Constitutive IL-1RA production by modified immune cells protects against IL-1-mediated inflammatory disorders.
 Dimethyl fumarate-mediated Nrf2/ARE pathway activation and glibenclamide-mediated NLRP3 inflammasome cascade inhibition alleviate type II diabetes-associated fatty liver in rats by mitigating oxidative stress and inflammation.
 Consensus Paper: Ataxic Gait.
 Treatment with GLP-1 receptor agonists is associated with significant weight loss and favorable headache outcomes in idiopathic intracranial hypertension.
 Wuzi Yanzong Pill Plays A Neuroprotective Role in Parkinson's Disease Mice via Regulating Unfolded Protein Response Mediated by Endoplasmic Reticulum Stress.
 1-Oleoyl-lysophosphatidylethanolamine stimulates RORγt activity in T(H)17 cells.
 Effects of a More Selective Arteriovenous Fistula Strategy on Vascular Access Outcomes.
 Infectious risk when prescribing rituximab in patients with hypogammaglobulinemia acquired in the setting of autoimmune diseases.
 Single-cell analysis reveals inflammatory interactions driving macular degeneration.
 Taurochenodeoxycholic acid reduces astrocytic neuroinflammation and alleviates experimental autoimmune encephalomyelitis in mice.
 Internal tremors and vibrations in long COVID: a cross-sectional study.
 Examining the National Representativeness of the Axon Registry: A Neurology-Specific Patient Registry.
 Effect of Siponimod on Brain and Spinal Cord Imaging Markers of Neurodegeneration in the Theiler's Murine Encephalomyelitis Virus Model of Demyelination.
 Peripherin is a biomarker of axonal damage in peripheral nervous system disease.
 A multi-sensor wearable system for the assessment of diseased gait in real-world conditions.
 Defining the Riddle in Order to Solve It: There Is More Than One "Parkinson's Disease".
 Burden of Common Neurologic Diseases in Asian Countries, 1990-2019: An Analysis for the Global Burden of Disease Study 2019.
 Extracellular Matrix-Derived Damage-Associated Molecular Patterns: Implications in Systemic Sclerosis and Fibrosis.
 Traditional Chinese Medicine Integrated Responsive Microneedles for Systemic Sclerosis Treatment.
 Tuberous sclerosis complex: a case report and literature review.
 Real life data on nintedanib safety: idiopathic pulmonary fibrosis versus systemic sclerosis-interstitial lung disease and strategies adopted to manage adverse effects.
 Increased CD8+ tissue resident memory T cells, regulatory T cells, and activated natural killer cells in systemic sclerosis lungs.
 Differences in pharyngeal swallow event timing: Healthy aging, Parkinson disease, and amyotrophic lateral sclerosis.
 [Asymptomatic course of rhabdomyoma of the heart].
 Serum chloride as a respiratory failure marker in amyotrophic lateral sclerosis.
 De novo mutation of the TSC2 gene in patient with Tuberous Sclerosis Complex-Associated Neuropsychiatric Disorders (TAND) Phenotype: a case report.
 A Systematic Review of Aminaphtone from Pathophysiology to Clinical Applications: Focus on New Rheumatological Acquisitions.
 Pilot study on the influence of acute alcohol exposure on biophysical parameters of leukocytes.
 High fever in myelin oligodendrocyte glycoprotein-associated disorder (MOGAD): A diagnostic challenge.
 Sequence- and structure-specific RNA oligonucleotide binding attenuates heterogeneous nuclear ribonucleoprotein A1 dysfunction.
 Time-of-day influences resting-state functional cortical connectivity.
 Total Tau Level in Cerebrospinal Fluid as a Predictor of Survival in Creutzfeldt-Jakob Disease: A Retrospective Analysis.
 Non-cirrhotic Portal Hypertension as the Initial Presentation of Limited Cutaneous Scleroderma: A Case Report.
 Quantitative Characterization of Gait Patterns in Individuals with Spinocerebellar Ataxia 38.
 Mini-Review: Role of Drugs Affecting Renin-Angiotensin System (RAS) in Traumatic Brain Injury (TBI): What We Know and What We Should Know.
 Tele-Global Examination of Mental State (Tele-GEMS): an open tool for the remote neuropsychological screening.
 The effects of prolactin on the immune system, its relationship with the severity of COVID-19, and its potential immunomodulatory therapeutic effect.
 Lichen Sclerosus.
 Sclerotherapy and its complications: a literature review and a case report.
 Shared genetic risk loci between Alzheimer's disease and related dementias, Parkinson's disease, and amyotrophic lateral sclerosis.
 Cardiac Rhabdomyoma.
 Cognitive outcomes in anti-LGI-1 encephalitis.
 Cell therapy in ALS: An update on preclinical and clinical studies.
 Early Immunotherapy and Longer Corticosteroid Treatment Are Associated With Lower Risk of Relapsing Disease Course in Pediatric MOGAD.
 Tuberous sclerosis complex mutations in patients with pancreatic neuroendocrine tumors. Observations on phenotypic and treatment-related associations.
 Comparison of spinal magnetic resonance imaging and classical clinical factors in predicting motor capacity in amyotrophic lateral sclerosis.
 The value of integration of bone scan and targeted SPECT/CT in diagnosis of primary hyperparathyroidism with multiple bone brown tumor.
 The Efficacy and Safety of Rapamycin in Children with Tuberous Sclerosis: A Cross-sectional Study.
 Far-field potential of the compound muscle action potential as a reliable marker in amyotrophic lateral sclerosis.
 Development of a robust UPLC-MS/MS method for the quantification of riluzole in human plasma and its application in pharmacokinetics.
 TDP-43 pathology and functional deficits in wild-type and ALS/FTD mutant cyclin F mouse models.
 A Summary on the Genetics of Systemic Lupus Erythematosus, Rheumatoid Arthritis, Systemic Sclerosis, and Sjögren's Syndrome.
 Postoperative seizure and memory outcome of temporal lobe epilepsy with hippocampal sclerosis: A systematic review.
 Morphological Features of Language Regions in Individuals with Tuberous Sclerosis Complex.
 Prevalence of polyneuropathies among systemic sclerosis patients and impact on health-related quality of life.
 Renal Disease and Systemic Sclerosis: an Update on Scleroderma Renal Crisis.
 Physical Activity in People With Motor Neuron Disease: Validity of the Physical Activity Scale for the Elderly as a Measuring Tool.
 Primary lateral sclerosis natural history study - planning, designing, and early enrollment.
 Predictors of Peak Expiratory Cough Flow in Individuals with Amyotrophic Lateral Sclerosis.
 Differentially expressed genes in systemic sclerosis: Towards predictive medicine with new molecular tools for clinicians.
 Wheel Running Adversely Affects Disease Onset and Neuromuscular Interplay in Amyotrophic Lateral Sclerosis Slow Progression Mouse Model.
 Intercellular transmission of pathogenic proteins in ALS: Exploring the pathogenic wave.
 Generalized early inflammatory morphea mimicking interstitial T-cell lymphoma: A diagnostic pitfall.
 Cryptic exon detection and transcriptomic changes revealed in single-nuclei RNA sequencing of C9ORF72 patients spanning the ALS-FTD spectrum.
 Visual Outcomes Following Plasma Exchange for Optic Neuritis: An International Multicenter Retrospective Analysis of 395 Optic Neuritis Attacks.
 Mesenchymal Stem/Stromal Cell-Based Therapies in Systemic Rheumatic Disease: From Challenges to New Approaches for Overcoming Restrictions.
 UPLC-MS based integrated plasma proteomic and metabolomic profiling of TSC-RAML and its relationship with everolimus treatment.
 Nitric Oxide/Nitric Oxide Synthase System in the Pathogenesis of Neurodegenerative Disorders-An Overview.
 Immunologic and nonimmunologic sclerodermal skin conditions - review.
 Cutaneous Angiofibroma.
 Indications for genetic study in gastro-entero-pancreatic and thoracic neuroendocrine tumors.
 Reversing Dysdynamism to Interrupt Mitochondrial Degeneration in Amyotrophic Lateral Sclerosis.
 Pharmacological treatment of systemic sclerosis-associated interstitial lung disease: an updated review and current approach to patient care.
 Ultrasound-enhanced brain delivery of edaravone provides additive amelioration on disease progression in an ALS mouse model.
 Whole genome sequencing analysis reveals post-zygotic mutation variability in monozygotic twins discordant for amyotrophic lateral sclerosis.
 Astrocyte-derived complement C3 is activated in patients with tuberous sclerosis complex and mediates immune injury: an integrated bioinformatics analysis.
 Neuronal overexpression of hTDP-43 in Caenorhabditis elegans impairs motor function.
 Immune complexome analysis of a rich variety of serum immune complexes identifies disease-characteristic immune complex antigens in systemic sclerosis.
 [Methodology and clinical use of superb microvascular imaging in assessing micro-circulation changes of fingertips in systemic sclerosis].
 Comparing therapeutic modulators of the SOD1 G93A Amyotrophic Lateral Sclerosis mouse pathophysiology.
 Home-based rehabilitation improves functional capacity and quality of life in women with systemic sclerosis: A preliminary study.
 Global Prevalence and Incidence of Amyotrophic Lateral Sclerosis: A Systematic Review.
 Amyotrophic lateral sclerosis: a neurodegenerative disorder poised for successful therapeutic translation.
 Long-term safety and effectiveness of eculizumab in patients with aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder: a 2-year interim analysis of post-marketing surveillance in Japan.
 Fingolimod mitigates memory loss in a mouse model of Gulf War Illness amid decreasing the activation of microglia, protein kinase R, and NFκB.
 Patient Experiences With Prescription Cannabinoids in Germany: Protocol for a Mixed Methods, Exploratory, and Anonymous Web-Based Survey.
 Exposure to specific tumour necrosis factor inhibitors and risk of demyelinating and inflammatory neuropathy in cohorts of patients with inflammatory arthritis: a collaborative observational study across five Nordic rheumatology registers.
 ANGPTL2 binds MAG to efficiently enhance oligodendrocyte differentiation.
 Male Breast Imaging Uncovers Lymphoma.
 Immune cell population and cytokine profiling suggest age dependent differences in the response to SARS-CoV-2 infection.
 Efficacy and Safety of Antidepressants in Patients With Comorbid Depression and Medical Diseases: An Umbrella Systematic Review and Meta-Analysis.
 Statistical analysis plan for the motor neuron disease systematic multi-arm adaptive randomised trial (MND-SMART).
 Inferring the genetic relationship between brain imaging-derived phenotypes and risk of complex diseases by Mendelian randomization and genome-wide colocalization.
 Progressive post infectious neurological syndromes with a poor outcome: Long term follow-up and neurofilament light chain quantification.
 Transition of cluster headache phenotype: An interview-based study.
 Patient perceptions of copay card utilization and policies.
 A multi-layer mean-field model of the cerebellum embedding microstructure and population-specific dynamics.
 Periventricular gradients in NAWM abnormalities differ in MS, NMOSD and MOGAD.
 Fluphenazine-Induced Neurotoxicity with Acute Almost Transient Parkinsonism and Permanent Memory Loss: Lessons from a Case Report.
 Differential Diagnosis of Tumor-like Brain Lesions.
 Virtual brain simulations reveal network-specific parameters in neurodegenerative dementias.
 Parallel processing relies on a distributed, low-dimensional cortico-cerebellar architecture.
 The Prevalence of Migraine in Inflammatory Bowel Disease, a Systematic Review and Meta-Analysis.
 Don't plan, just do it: Cognitive and sensorimotor contributions to manual dexterity.
 Insights into migraine attacks from neuroimaging.
 Association of vitiligo with multiple cutaneous and extra-cutaneous autoimmune diseases: a nationwide cross-sectional study.
 Rapid and Robust Multi-Phenotypic Assay System for ALS Using Human iPS Cells with Mutations in Causative Genes.
 Activating mitofusins interrupts mitochondrial degeneration and delays disease progression in SOD1 mutant amyotrophic lateral sclerosis.
 Amyotrophic Lateral Sclerosis Mimic Syndrome in a 24-Year-Old Man with Chiari 1 Malformation and Syringomyelia: A Clinical Case.
 Identifying Candidate Genes Associated with Sporadic Amyotrophic Lateral Sclerosis via Integrative Analysis of Transcriptome-Wide Association Study and Messenger RNA Expression Profile.
 Mitochondria: It is all about energy.
 Genetic Modifiers of Age at Onset for Amyotrophic Lateral Sclerosis: A Genome-Wide Association Study.
 The Role of Autophagy and Apoptosis in Affected Skin and Lungs in Patients with Systemic Sclerosis.
 The role of trichoscopy beyond hair and scalp diseases. A review.
 Reduction of nemo-like kinase increases lysosome biogenesis and ameliorates TDP-43-related neurodegeneration.
 Skeletal muscle in amyotrophic lateral sclerosis.
 The association between longitudinal declines in speech sound accuracy and speech intelligibility in speakers with amyotrophic lateral sclerosis.
 Long-term air pollution and risk of amyotrophic lateral sclerosis mortality in the Women's Health Initiative cohort.
 Factors influencing decisions people with motor neuron disease make about gastrostomy placement and ventilation: A qualitative evidence synthesis.
 Novel aspects of muscle involvement in immune-mediated inflammatory arthropathies and connective tissue diseases.
 The Role of Mitophagy in Various Neurological Diseases as a Therapeutic Approach.
 Protein biomarkers of disease progression in patients with systemic sclerosis associated interstitial lung disease.
 Presence of Rare Variants is Associated with Poorer Survival in Chinese Patients with Amyotrophic Lateral Sclerosis.
 Senataxin: A key actor in RNA metabolism, genome integrity and neurodegeneration.
 The role of neurofilament light in genetic frontotemporal lobar degeneration.
 Phenome-wide genetic-correlation analysis and genetically informed causal inference of amyotrophic lateral sclerosis.
 pTDP-43 aggregates accumulate in non-central nervous system tissues prior to symptom onset in amyotrophic lateral sclerosis: a case series linking archival surgical biopsies with clinical phenotypic data.
 AD and non-AD mediators of the pathway between the APOE genotype and cognition.
 Definitions, phenomenology, diagnosis, and management of the disorders of laughter and crying in amyotrophic lateral sclerosis (ALS): Consensus from ALS and Motor Neuron Disease Scientific Department of the Brazilian Academy of Neurology.
 ALS-plus related clinical and genetic study from China.
 PIKFYVE inhibition mitigates disease in models of diverse forms of ALS.
 Chimeric antigen receptor T cell therapy for the treatment of systemic rheumatic diseases: a comprehensive review of recent literature.
 Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases.
 Causes of death among United States decedents with ALS: An eye toward delaying mortality.
 Translation dysregulation in neurodegenerative diseases: a focus on ALS.
 Genetic correlates of vitamin D-binding protein and 25-hydroxyvitamin D in neonatal dried blood spots.
 The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases.
 The correlation between neuropathology levels and cognitive performance in centenarians.
 Association between esophageal motor disorders and pulmonary involvement in patients affected by systemic sclerosis: a retrospective study.
 Systemic sclerosis associated interstitial lung disease: a survey of current practices in France.
 French recommendations for the diagnosis and management of lymphangioleiomyomatosis.
 Juvenile and adult-onset scleroderma: Different clinical phenotypes.
 Long-term survival benefits of intrathecal autologous bone marrow-derived mesenchymal stem cells (Neuronata-R®: lenzumestrocel) treatment in ALS: Propensity-score-matched control, surveillance study.
 Developmental effects of constitutive mTORC1 hyperactivity and environmental enrichment on structural synaptic plasticity and behaviour in a rat model of autism spectrum disorder.
 Identification of a novel pathway in sporadic Amyotrophic Lateral Sclerosis mediated by the long non-coding RNA ZEB1-AS1.
 Immunotherapy targeting the C-terminal domain of TDP-43 decreases neuropathology and confers neuroprotection in mouse models of ALS/FTD.
 Incidence, prevalence, and co-occurrence of autoimmune disorders over time and by age, sex, and socioeconomic status: a population-based cohort study of 22 million individuals in the UK.
 Comparison of Two Therapeutic Approaches of Cerebellar Transcranial Direct Current Stimulation in a Sardinian Family Affected by Spinocerebellar Ataxia 38: a Clinical and Computerized 3D Gait Analysis Study.
 Incidence of Bell's palsy after coronavirus disease (COVID-19) vaccination: a systematic review and meta-analysis.
 Effect of geometric distortion correction on thickness and volume measurements of cortical parcellations in 3D T1w gradient echo sequences.
 The human placenta shapes the phenotype of decidual macrophages.
 Ataxin-2 polyglutamine expansions aberrantly sequester TDP-43, drive ribonucleoprotein condensate transport dysfunction and suppress local translation.
 A structured evaluation of cryopreservation in generating single-cell transcriptomes from cerebrospinal fluid.
 Neoehrlichia mikurensis-An emerging opportunistic tick-borne infection in immunosuppressed patients.
 Cadherin-11 and Its Role in Tissue Fibrosis.
 Modelling accessibility of adult neurology care in Australia, 2020-2034.
 Non-infectious meningitis and CNS demyelinating diseases: A conceptual review.
 Impact of percutaneous endoscopic gastrostomy on pediatric bone marrow transplantation outcomes: Retrospectice single-center cohort study.
 Frontotemporal Dementia-Related V57E Mutation Impairs Mitochondrial Function and Alters the Structural Properties of CHCHD10.
 Serum neurofilament light and white matter characteristics in the general population: a longitudinal analysis.
 Early biochemical analysis of COVID-19 patients helps severity prediction.
 Endothelial Indoleamine-2,3-Dioxygenase-1 is not Critically Involved in Regulating Antitumor Immunity in the Central Nervous System.
 Decreased kynurenine in cerebrospinal fluid and potential role in neuromyelitis optica spectrum disorder.
 Comparative Proteomics Analysis of Growth-Primed Adult Dorsal Root Ganglia Reveals Key Molecular Mediators for Peripheral Nerve Regeneration.
 Multiple roles of ALK3 in osteoarthritis.
 Acoustic Measures of Dysphonia in Amyotrophic Lateral Sclerosis.
 Superior Global Cognition in Oldest-Old Is Associated with Resistance to Neurodegenerative Pathologies: Results from The 90+ Study.
 SYF2 suppression mitigates neurodegeneration in models of diverse forms of ALS.
 Genome-wide DNA methylation and transcriptome expression profiles of peripheral blood mononuclear cells in patients with systemic sclerosis with interstitial lung disease.
 Aggregation-prone TDP-43 sequesters and drives pathological transitions of free nuclear TDP-43.
 Anti-Ku antibody-positive systemic sclerosis and idiopathic inflammatory myopathies overlap syndrome in children: a report of two cases and a review of the literature.
 Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody.
 Cat Eye Syndrome with a Unique Liver and Dermatological Presentation.
 Advances in Nucleotide Repeat Expansion Diseases: Transcription Gets in Phase.
 The Muscular Dystrophy Association's neuroMuscular ObserVational Research Data Hub (MOVR): Design, Methods, and Initial Observations.
 How to mitigate the inhibitory effect of organizational inertia on corporate digital entrepreneurship?
 Frameshift mutation in SQSTM1 causes proximal myopathy with rimmed vacuoles: A case report.
 Disruption of ER ion homeostasis maintained by an ER anion channel CLCC1 contributes to ALS-like pathologies.
 Evaluating genomic signatures of aging in brain tissue as it relates to Alzheimer's disease.
 Differential Item Functioning on the Cochin Hand Function Scale among People with Systemic Sclerosis by Language, Sex, and Disease Subtype: a Scleroderma Patient-centered Intervention Network (SPIN) Cohort Study.
 IL-6 trans-signaling in a humanized mouse model of scleroderma.
 Risk of autoimmune diseases following COVID-19 and the potential protective effect from vaccination: a population-based cohort study.
 Assessing real-world gait with digital technology? Validation, insights and recommendations from the Mobilise-D consortium.
 Acute Inflammatory Diseases of the Central Nervous System After SARS-CoV-2 Vaccination.
 Microglia regulate central nervous system myelin growth and integrity.
 Droplet-based forward genetic screening of astrocyte-microglia cross-talk.
 Generation of a C. elegans tdp-1 null allele and humanized TARDBP containing human disease-variants.
 Disturb mitochondrial associated proteostasis: Neurodegeneration and imperfect ageing.
 Radiologic findings of osteonecrosis, osteoradionecrosis, osteomyelitis and jaw metastatic disease with cone beam CT.
 Qualitative and Quantitative Evaluation of Morpho-Metabolic Changes in Bone Cartilage Complex of Knee Joint in Osteoarthritis Using Simultaneous 18F-NaF PET/MRI-A Pilot Study.
 Osteopetrosis: Gene-based nosology and significance Dysosteosclerosis.
 Human brain single nucleus cell type enrichments in neurodegenerative diseases.
 c-Jun N-Terminal Kinase Promotes Stress Granule Assembly and Neurodegeneration in C9orf72-Mediated ALS and FTD.
 Roles of RNA-binding proteins in neurological disorders, COVID-19, and cancer.
 Design and Statistical Innovations in a Platform Trial for Amyotrophic Lateral Sclerosis.
 Nutritional considerations for a new era: A CF foundation position paper.
 Patient-reported outcome measures in drugs for neurological conditions approved by European Medicines Agency 2017-2022.
 Culture Protocol and Transcriptomic Analysis of Murine SVZ NPCs and OPCs.
 Severe neuromuscular immune-related adverse events of immune checkpoint inhibitors at national cancer center in Korea.
 Characterization by Gene Expression Analysis of Two Groups of Dopaminergic Cells Isolated from the Mouse Olfactory Bulb.
 The role of DNA methylation in progression of neurological disorders and neurodegenerative diseases as well as the prospect of using DNA methylation inhibitors as therapeutic agents for such disorders.
 Serum neurofilament light chain as a reliable biomarker of hereditary transthyretin-related amyloidosis-A Swiss reference center experience.
 Human astrocytes and microglia show augmented ingestion of synapses in Alzheimer's disease via MFG-E8.
 Associations between individual depressive symptoms and immunometabolic characteristics in major depression.
 Lack of STAT1 co-operative DNA binding protects against adverse cardiac remodelling in acute myocardial infarction.
 Exome-based gene panel analysis in a cohort of acute juvenile ischemic stroke patients:relevance of NOTCH3 and GLA variants.
 Acetylcholine and noradrenaline enhance foraging optimality in humans.
 Oral lacosamide for the treatment of refractory trigeminal neuralgia: A retrospective analysis of 86 cases.
 The impact of the secondary infections in ICU patients affected by COVID-19 during three different phases of the SARS-CoV-2 pandemic.
 Randomized, double-blind, placebo-controlled trial of rapamycin in amyotrophic lateral sclerosis.
 Associations between sleep-related symptoms, obesity, cardiometabolic conditions, brain structural alterations and cognition in the UK biobank.
 Phenolic metabolites as therapeutic in inflammation and neoplasms: Molecular pathways explaining their efficacy.
 Cognitive reserve in ALS: The role of occupational skills and requirements.
 Ageing-Induced Decline in Primary Myeloid Cell Phagocytosis Is Unaffected by Optineurin Insufficiency.
 Status epilepticus and early development: Neuronal injury, neurodegeneration, and their consequences.
 Myocardial Involvement in Systemic Autoimmune Rheumatic Diseases.
 The long-term neurodevelopmental outcomes of febrile seizures and underlying mechanisms.
 Probing the interactions between amyloidogenic proteins and bio-membranes.
 A Hidden Condition: Multiple Tarlov Cysts Unveiled in a Young Woman Seeking Primary Care for Debilitating Low Back Pain.
 Automated subfield volumetric analysis of amygdala, hippocampus, and thalamic nuclei in mesial temporal lobe epilepsy.
 Freshwater Cyanobacterial Toxins, Cyanopeptides and Neurodegenerative Diseases.
 Review of an Anti-CD20 Monoclonal Antibody for the Treatment of Autoimmune Diseases of the Skin.
 The cholesterol depleting agent, (2-Hydroxypropyl)-ß-cyclodextrin, does not affect disease progression in SOD1(G93A) mice.
 Exploring microglia and their phenomenal concatenation of stress responses in neurodegenerative disorders.
 Autosomal dominant genodermatoses in adults being heralded by superimposed skin lesions in children.
 Safety, Efficacy and Mid-Term Outcome for Transarterial Embolization (TAE) of Renal Angiomyolipoma (AML) Using Ethylene Vinyl Alcohol Copolymer Liquid Embolic Agent (EVOH).
 Benchmarking of force fields to characterize the intrinsically disordered R2-FUS-LC region.
 TDP-43 pathology in Drosophila induces glial-cell type specific toxicity that can be ameliorated by knock-down of SF2/SRSF1.
 Chlamydia psittaci Pneumonia Complicated with Lower Extremity Atherosclerotic Occlusive Disease.
 Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice.
 Pathogenesis of Neurodegenerative Diseases and the Protective Role of Natural Bioactive Components.
 Evaluation of risk in chronic cutaneous inflammatory conditions for malignant transformation.
 HtrA1 prevents and reverses α-synuclein aggregation, rendering it non-toxic and seeding incompetent.
 The HFE p.H63D (p.His63Asp) Polymorphism Is a Modifier of ALS Outcome in Italian and French Patients with SOD1 Mutations.
 Trichloroethylene: An Invisible Cause of Parkinson's Disease?
 GRADE concept 4: rating the certainty of evidence when study interventions or comparators differ from PICO targets.
 Mediators of systemic sclerosis-associated interstitial lung disease (SSc-ILD): systematic review and meta-analyses.
 Fasudil alleviates cerebral ischemia‑reperfusion injury by inhibiting inflammation and improving neurotrophic factor expression in rats.
 Investigating the association between neoplasms and MOG antibody-associated disease.
 Hospital-Diagnosed Infections, Autoimmune Diseases, and Subsequent Dementia Incidence.
 Emotional demands and all-cause and diagnosis-specific long-term sickness absence: a prospective cohort study in Sweden.
 Neuromyelitis optica spectrum disorders: a review with a focus on children and adolescents.
 Validity, Reliability, and Differential Item Functioning of English and French Versions of the 10-Item Connor-Davidson Resilience Scale in Systemic Sclerosis: A Scleroderma Patient-Centered Intervention Network Cohort Study.
 A Pharmacokinetic Drug-Drug Interactions Study between Entecavir and Hydronidone, a Potential Novel Antifibrotic Small Molecule, in Healthy Male Volunteers.
 'Intensive palliative care': a qualitative study of issues related to nurses' care of people with amyotrophic lateral sclerosis at end-of-life.
 Reduced SPAG17 Expression in Systemic Sclerosis Triggers Myofibroblast Transition and Drives Fibrosis.
 Knockout of TSC2 in Nav1.8+ neurons predisposes to the onset of normal weight obesity.
 Evaluation of eight registration algorithms applied to the insula and insular gyri.
 Rapid improvement of systemic sclerosis-associated intestinal pseudo-obstruction with intravenous immunoglobulin administration.
 Seizure reduction in TSC2-mutant mouse model by an mTOR catalytic inhibitor.
 Transplantation of in vitro prefabricated adipose organoids attenuates skin fibrosis by restoring subcutaneous fat and inducing dermal adipogenesis.
 Molecular mechanisms of neuroprotective offerings by rosmarinic acid against neurodegenerative and other CNS pathologies.
 Evaluation of clinical signs and magnetic resonance imaging findings in patients with temporomandibular disorders.
 Inflammatory Process on Knee Osteoarthritis in Cyclists.
 Mediastinal Mass Discovered in the Second Trimester, a Rare Presentation of Hodgkin's Lymphoma in Pregnancy.
 Molecular Determinants of Mitochondrial Shape and Function and Their Role in Glaucoma.
 The role of mononuclear phagocyte system in IgA nephropathy: pathogenesis and prognosis.
 An impaired splicing program underlies differentiation defects in hSOD1(G93A) neural progenitor cells.
 NORHA: A NORmal Hippocampal Asymmetry Deviation Index Based on One-Class Novelty Detection and 3D Shape Features.
 Efficacy and Satisfaction of Low Doses UVA1 Phototherapy: A Spanish Experience from a Single Centre.
 Bifurcation analysis of motoneuronal excitability mechanisms under normal and ALS conditions.
 Serum neurofilament light chain in functionally relevant coronary artery disease and adverse cardiovascular outcomes.
 Sotrovimab in Hospitalized Patients with SARS-CoV-2 Omicron Variant Infection: a Propensity Score-Matched Retrospective Cohort Study.
 Sodium as an Important Regulator of Immunometabolism.
 Risk of myocardial infarction in Parkinson's disease: A systematic review and meta-analysis.
 Single-molecule imaging reveals distinct elongation and frameshifting dynamics between frames of expanded RNA repeats in C9ORF72-ALS/FTD.
 Plasma neurofilament light significantly decreases following treatment in Lyme neuroborreliosis and is not associated with persistent symptoms.
 Comparative analysis of freezing of gait in distinct Parkinsonism types by diffusion tensor imaging method and cognitive profiles.
 Peri-Operative Risk Factors Associated with Post-Operative Cognitive Dysfunction (POCD): An Umbrella Review of Meta-Analyses of Observational Studies.
 Mitofusin 1 overexpression rescues the abnormal mitochondrial dynamics caused by the Mitofusin 2 K357T mutation in vitro.
 Haemorrhage of human foetal cortex associated with SARS-CoV-2 infection.
 Cerebral Cortical Encephalitis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.
 Presymptomatic geographical distribution of ALS patients suggests the involvement of environmental factors in the disease pathogenesis.
 Phosphorylation of PBX2, a novel downstream target of mTORC1, is determined by GSK3 and PP1.
 Multiparameter analysis of human B lymphocytes identifies heterogeneous CD19(+) CD21(lo) subsets.
 Neurology ethics at the end of life.
 A roadmap to ALS prevention: strategies and priorities.
 Prognostic performance of blood neurofilament light chain protein in hospitalized COVID-19 patients without major central nervous system manifestations: an individual participant data meta-analysis.
 Renal injury in relation to obesity and the additive effect of hypertension in female and male obese and lean ZSF1 rats.
 Precision diagnosis and staging of TDP-43 proteinopathies: harnessing the power of artificial intelligence.
 Prescription of oxycodone versus codeine after childbirth and risk of persistent opioid use: a population-based cohort study.
 Upper gastrointestinal bleeding from gastric antral vascular ectasia following cocaine use: case presentation and review of literature.
 Clinicopathological Impacts of Expression of Neuronal Markers in Lymphangioleiomyomatosis.
 Brain-protective mechanisms of autophagy associated circRNAs: Kick starting self-cleaning mode in brain cells via circRNAs as a potential therapeutic approach for neurodegenerative diseases.
 The major TMEM106B dementia risk allele affects TMEM106B protein levels and myelin lipid homeostasis in the ageing human hippocampus.
 Glial Glutamine Homeostasis in Health and Disease.
 Defining the molecular correlate of arteriolar hyalinosis in kidney disease progression by integration of single cell transcriptomic analysis and pathology scoring.
 Traumatic Brain Injury in a Well: A Modular Three-Dimensional Printed Tool for Inducing Traumatic Brain Injury In vitro.
 C9orf72 gene networks in the human brain correlate with cortical thickness in C9-FTD and implicate vulnerable cell types.
 Automation and deep (machine) learning in temporomandibular joint disorder radiomics: A systematic review.
 Pharmacological diversity amongst approved and emerging antiseizure medications for the treatment of developmental and epileptic encephalopathies.
 omicSynth: an Open Multi-omic Community Resource for Identifying Druggable Targets across Neurodegenerative Diseases.
 A dual MTOR/NAD+ acting gerotherapy.
 Left- vs right-sided migraine: a scoping review.
 Association of pain and clinical factors on disability and quality of life in systemic sclerosis: A cross-sectional study from Turkish League Against Rheumatism Network.
 Validation of a New Semiautomated Segmentation Pipeline Based on the Spinal Cord Toolbox DeepSeg Algorithm to Estimate the Cervical Canal Area.
 Time-Dependent Analysis of Sicca Symptoms and Anti-Ro/SSA and Anti-La/SSB Antibodies in Patients with AQP4-IgG-Positive Neuromyelitis Optica Spectrum Disorder.
 Factors predisposing to humoral autoimmunity against brain-antigens in health and disease: Analysis of 49 autoantibodies in over 7000 subjects.
 Childhood trauma in patients with epileptic vs nonepileptic seizures.
 History of cerebrovascular disease but not dementia increases the risk for secondary vascular events during SARS-CoV-2 infection with presumed Omicron variant: a retrospective observational study.
 Reversible cerebral vasoconstriction syndrome: strategies to early diagnosis and the role of transcranial color-coded doppler ultrasonography (TCCD).
 Cleveland Clinic Cognitive Battery (C3B): Normative, Reliability, and Validation Studies of a Self-Administered Computerized Tool for Screening Cognitive Dysfunction in Primary Care.
 Cluster headache polygenetic risk and known functional variants of CYP3A4 are not associated with treatment response.
 The effects of time-restricted eating and weight loss on bone metabolism and health: a 6-month randomized controlled trial.
 Immune checkpoint inhibitor-associated central nervous system autoimmunity.
 Peripheral monocytes and soluble biomarkers in autoimmune encephalitis.
 The soluble receptor for advanced glycation end products is potentially predictive of pulmonary arterial hypertension in systemic sclerosis.
 Proposed Response Parameters for Twelve-Month Drug Trial in Juvenile Systemic Sclerosis: Results of the Hamburg International Consensus Meetings.
 Altered metabolic-functional coupling in the epileptogenic network could predict surgical outcomes of mesial temporal lobe epilepsy.
 Intratumoral Hemorrhage in Vestibular Schwannomas After Stereotactic Radiosurgery: Multi-Institutional Study.
 Abl kinase-mediated FUS Tyr526 phosphorylation alters nucleocytoplasmic FUS localization in FTLD-FUS.
 The therapeutic potential of purified cannabidiol.
 Diagnostic imaging of retinal astrocytomas: A case-series.
 Large-scale multitrait genome-wide association analyses identify hundreds of glaucoma risk loci.
 Exploring research team members' and trial participants' perceptions of acceptability and implementation within one videoconference-based supportive care program for individuals affected by systemic sclerosis during COVID-19: a qualitative interview study.
 Impact of Different Artificial Intelligence User Interfaces on Lung Nodule and Mass Detection on Chest Radiographs.
 Impact of High Salt-Intake on a Natural Gut Ecosystem in Wildling Mice.
 CCR4(+) CD8(+) T cells clonally expand to differentiated effectors in murine psoriasis and in human psoriatic arthritis.
 Assisted ambulation to improve health outcomes for older medical inpatients (AMBULATE): study protocol for a randomized controlled trial.
 Autoimmune Encephalitis Criteria in Clinical Practice.
 Ravulizumab in Aquaporin-4-Positive Neuromyelitis Optica Spectrum Disorder.
 Cdon ablation in motor neurons causes age-related motor neuron degeneration and impaired sciatic nerve repair.
 Dual ankyrinG and subpial autoantibodies in a man with well-controlled HIV infection with steroid-responsive meningoencephalitis: A case report.
 Neurofilament light (NfL) as biomarker in serum and CSF in status epilepticus.
 Multimodal Analysis of the Visual Pathways in Friedreich's Ataxia Reveals Novel Biomarkers.
 Adhesion to laminin-1 and collagen IV induces the formation of Ca(2+) microdomains that sensitize mouse T cells for activation.
 Clinical surrogates of dysautonomia predict lethal outcome in COVID-19 on intensive care unit.
 Somatic symptoms and related disorders in a large cohort of people with epilepsy: A cohort study.
 Clinicopathologic features in childhood-onset lupus nephritis with antineutrophil cytoplasmic antibody positivity--a multi-center retrospective study.
 Therapeutic and clinical foundations of cannabidiol therapy for difficult-to-treat seizures in children and adults with refractory epilepsies.
 Staufen Impairs Autophagy in Neurodegeneration.
 Regulatory roles of NAT10 in airway epithelial cell function and metabolism in pathological conditions.
 Receptors for Advanced Glycation End Products (RAGE): Promising Targets Aiming at the Treatment of Neurodegenerative Conditions.
 Multiple Fibroblast Subtypes Contribute to Matrix Deposition in Pulmonary Fibrosis.
 Point-Of-Care Ultrasonography for Identification of Skin and Soft Tissue Abscess in Adult and Pediatric Patients; a Systematic Review and Meta-Analysis.
 Intravenous immunoglobulin treatment for acute attacks in myelin oligodendrocyte glycoprotein antibody disease.
 COVID19-associated new-onset movement disorders: a follow-up study.
 Dectin-1 signaling on colonic γδ T cells promotes psychosocial stress responses.
 Whole-brain diffusion tensor imaging predicts 6-month functional outcome in acute intracerebral haemorrhage.
 CXCR5(+)PD-1(++) CD4(+) T cells colonize infant intestines early in life and promote B cell maturation.
 Jacob-induced transcriptional inactivation of CREB promotes Aβ-induced synapse loss in Alzheimer's disease.
 Framework for Patient Experience Value Elements in Rare Disease: A Case Study Demonstrating the Applicability of Combined Qualitative and Quantitative Methods.
 Validation of STOP, STOP-BANG, STOP-BAG, STOP-B28, and GOAL screening tools for identification of obstructive sleep apnea in patients with Parkinson disease.
 Total glucosides of paeony alleviates scleroderma by inhibiting type I interferon responses.
 Thymopentin (TP-5) prevents lipopolysaccharide-induced neuroinflammation and dopaminergic neuron injury by inhibiting the NF-κB/NLRP3 signaling pathway.
 Visual dysfunction is a better predictor than retinal thickness for dementia in Parkinson's disease.
 Review and standard operating procedures for collection of biospecimens and analysis of biomarkers in new onset refractory status epilepticus.
 Association of age with 1-year outcome in patients with acute ischaemic stroke treated with thrombectomy: real-world analysis in 18 506 patients.
 Rapid Immunodot AQP4 Assay for Neuromyelitis Optica Spectrum Disorder.
 Therapeutic plasma exchange in the management of stiff person syndrome spectrum disorders: a case series and review of the literature.
 Dynamics of progressive degeneration of major spinal pathways following spinal cord injury: A longitudinal study.
 Development of a Dihydroquinoline-Pyrazoline GluN2C/2D-Selective Negative Allosteric Modulator of the N-Methyl-d-aspartate Receptor.
 Radiogenomics of C9orf72 Expansion Carriers Reveals Global Transposable Element Derepression and Enables Prediction of Thalamic Atrophy and Clinical Impairment.
 A genome-wide association study of blood cell morphology identifies cellular proteins implicated in disease aetiology.
 Multicohort cross-sectional study of cognitive and behavioural digital biomarkers in neurodegeneration: the Living Lab Study protocol.
 Evaluation of Measurement Properties and Differential Item Functioning in the English and French Versions of the University of California, Los Angeles, Loneliness Scale-6: A Scleroderma Patient-Centered Intervention Network (SPIN) Study.
 De novo collapsing glomerulopathy after kidney transplantation: Description of two cases.
 Transferability of Alzheimer's disease progression subtypes to an independent population cohort.
 School performance and psychiatric comorbidity in childhood absence epilepsy: A Danish cohort study.
 Cerebral blood flow, amyloid burden, and cognition in cognitively normal individuals.
 Adipose tissue coregulates cognitive function.
 Meaning of Family Reported Outcome Measure (FROM-16) severity score bands: a cross-sectional online study in the UK.
 A unified classification approach rating clinical utility of protein biomarkers across neurologic diseases.
 Cohort profile: rationale and methods of UK Biobank repeat imaging study eye measures to study dementia.
 Minocycline as Treatment for Psychiatric and Neurological Conditions: A Systematic Review and Meta-Analysis.
 BDNF-induced phrenic motor facilitation shifts from PKCθ to ERK dependence with mild systemic inflammation.
 Stereoelectroencephalography-based research on the value of drug-resistant temporal lobe epilepsy auras: A retrospective single-center study.
 Endothelial dysfunction, thrombophilia, and nailfold capillaroscopic features in livedoid vasculopathy.
 Inflammatory Diseases, Inflammatory Biomarkers, and Alzheimer Disease: An Observational Analysis and Mendelian Randomization.
 Clinical Profile and Risk Factors for Severe COVID-19 in Hospitalized Patients from Rio de Janeiro, Brazil: Comparison between the First and Second Pandemic Waves.
 Clinical and epidemiological correlates of treatment change in patients with NMOSD: insights from the CIRCLES cohort.
 Absence of self-reported neuropsychiatric and somatic symptoms after Omicron variant SARS-CoV-2 breakthrough infections.
 Pregnancy and post-partum in patients with myelin-oligodendrocyte glycoprotein antibody-associated disease.
 Soluble mutant huntingtin drives early human pathogenesis in Huntington's disease.
 Belimumab versus anifrolumab in adults with systemic lupus erythematosus: an indirect comparison of clinical response at 52 weeks.
 Disentangling the genetic overlap and causal relationships between primary open-angle glaucoma, brain morphology and four major neurodegenerative disorders.
 Glucocorticoids prescribing practices in systemic sclerosis: an analysis of the EUSTAR database.
 Utility of Protein Microarrays for Detection of Classified and Novel Antibodies in Autoimmune Neurologic Disease.
 Do Early Relapses Predict the Risk of Long-Term Relapsing Disease in an Adult and Paediatric Cohort with MOGAD?
 Wuzi Yanzong Pill protects neural tube defects by activating PI3K/Akt signaling pathway.
 Risk and course of COVID-19 in immunosuppressed patients with myasthenia gravis.
 High ultra-processed food consumption is associated with elevated psychological distress as an indicator of depression in adults from the Melbourne Collaborative Cohort Study.
 Progressive Multifocal Leukoencephalopathy Treated by Immune Checkpoint Inhibitors.
 Cognitive correlates of antisaccade behaviour across multiple neurodegenerative diseases.
 Divergent patterns of healthy aging across human brain regions at single-cell resolution reveal links to neurodegenerative disease.
 VAPB-mediated ER-targeting stabilizes IRS-1 signalosomes to regulate insulin/IGF signaling.
 Autoantibodies targeting G protein-coupled receptors: An evolving history in autoimmunity. Report of the 4th international symposium.
 miRNAs in Neurological Manifestation in Patients Co-Infected with SARS-CoV-2 and Herpesvírus 6 (HHV-6).
 Efficacy of low carbohydrate and ketogenic diets in treating mood and anxiety disorders: systematic review and implications for clinical practice.
 Genome-wide structural variant analysis identifies risk loci for non-Alzheimer's dementias.
 Regional transcriptional vulnerability to basal forebrain functional dysconnectivity in mild cognitive impairment patients.
 Endothelin-1 as a Biomarker of Idiopathic Pulmonary Fibrosis and Interstitial Lung Disease Associated with Autoimmune Diseases.
 Patient-reported impact of symptoms in lung cancer (PRISM-LC).
 Incidence and Long-term Functional Outcome of Neurologic Disorders in Hospitalized Patients With COVID-19 Infected With Pre-Omicron Variants.
 Comparative features and outcomes of major neurological complications of COVID-19.
 Comorbidities in Early-Onset Sporadic versus Presenilin-1 Mutation-Associated Alzheimer's Disease Dementia: Evidence for Dependency on Alzheimer's Disease Neuropathological Changes.
 Friedreich's Ataxia-Health Index: Development and Validation of a Novel Disease-Specific Patient-Reported Outcome Measure.
 Autoimmune Encephalitis Misdiagnosis in Adults.
 Cost-effectiveness models for Alzheimer's disease and related dementias: IPECAD modeling workshop cross-comparison challenge.
 Mitochondrial haplogroups and cognitive progression in Parkinson's disease.
 Multi-omic longitudinal study reveals immune correlates of clinical course among hospitalized COVID-19 patients.
 Global synergistic actions to improve brain health for human development.
 Anomalies in the review process and interpretation of the evidence in the NICE guideline for chronic fatigue syndrome and myalgic encephalomyelitis.
 Antisense oligonucleotide targeting DMPK in patients with myotonic dystrophy type 1: a multicentre, randomised, dose-escalation, placebo-controlled, phase 1/2a trial.


















 Les traitements de la sclérose en plaques.






























 Diagnostik, Befunde und Dokumentation bei multipler Sklerose.














 Mikrobiota kishechnika u patsientov s remittiruyushchim rasseyannym sklerozom.





























































 Troubles cognitifs dans la sclérose en plaques : quand y penser ?































































 Retinale Periphlebitis – Marker eines Subphänotyps der Multiplen Sklerose.

 Rituximab en el tratamiento de esclerosis múltiple. Experiencia de un hospital de tercer nivel en México.











 Un accompagnement multidisciplinaire indispensable pour la prise en charge de la sclérose en plaques.






 Síndrome de Nicolau por fármacos autoinyectables en la esclerosis múltiple.


































































































































 Une prise en charge rééducative pluridisciplinaire et multimodale des patients souffrant de sclérose en plaques.

























 Diapazon dvizheniya v kolennom sustave kak marker effektivnosti meditsinskogo vmeshatel'stva pri rasseyannom skleroze.























































 Cherepno-mozgovaya travma do debyuta rasseyannogo skleroza: svyaz' s progressirovaniem nevrologicheskikh rasstroistv i patobiokhimicheskimi pokazatelyami tserebrospinal'noi zhidkosti.

































 Primenenie monoklonal'nykh antitel v lechenii bol'nykh vysokoaktivnym rasseyannym sklerozom v real'noi klinicheskoi praktike.










 Klinicheskie faktory i otvet na terapiyu preparatami, izmenyayushchimi techenie rasseyannogo skleroza: opyt Tomskoi oblasti.













































 Rasseyannyi skleroz s epizodom shizofrenopodobnogo sindroma.
















 Un programme d’éducation thérapeutique pour les patients atteints de sclérose en plaques.









































 Esclerosis múltiple y fatiga. Es necesario mejorar.
 Síndrome de Wells secundario a dimetilfumarato. A propósito de un caso clínico.



 Kharakteristika i dinamika patologicheskikh izmenenii zritel'nykh vyzvannykh potentsialov pri rasseyannom skleroze.













 Effektivnost' i bezopasnost' 24 nedel' primeneniya divozilimaba sredi patsientov s rasseyannym sklerozom v ramkakh randomizirovannogo dvoinogo slepogo platsebo-kontroliruemogo klinicheskogo issledovaniya BCD-132-2.

 Opticheskie neiropatii kak predmet mezhdistsiplinarnogo izucheniya.














 Leistungsfähigkeit der McDonald-Kriterien von 2017.

 Novye metody neirovizualizatsii otsenki aktivnosti neirovospaleniya pri rasseyannom skleroze.



































 Izmeneniya venoznogo krovoobrashcheniya u patsientov s rasseyannym sklerozom.















































 Issledovanie soderzhaniya markerov mikrobioty v tsel'noi krovi i tserebrospinal'noi zhidkosti patsientov s razlichnymi tipami techeniya rasseyannogo skleroza i lits s radiologicheski izolirovannym sindromom.


























 K voprosu o neobkhodimosti validizatsii perevodov na russkii yazyk ob"ektivnykh nevrologicheskikh shkal, simptomov i sindromov.





 „Neurology meets Urology“ : Übersicht urologisch relevanter neurologischer Erkrankungen.




















 Effektivnost' i bezopasnost' 48 nedel'nogo primeneniya monoklonal'nogo antitela protiv CD20 divozilimaba u patsientov s rasseyannym sklerozom: rezul'taty randomizirovannogo dvoinogo slepogo platsebo-kontroliruemogo klinicheskogo issledovaniya BCD-132-4/MIRANTIBUS.




















































































 Deficiência cognitiva na esclerose múltipla: conhecimentos “clássicos” e aquisições recentes.





 Rasseyannyi skleroz v Respublike Bashkortostan: populyatsionno-spetsificheskie geneticheskie prediktory i rezul'taty 20-letnego klinicheskogo nablyudeniya.





















 Disfunção sexual em pacientes brasileiros com esclerose múltipla.























































 Infección grave por COVID-19 en pacientes con esclerosis múltiple en la Argentina.






 XV Reunión Post-ECTRIMS: revisión de las novedades presentadas en el Congreso ECTRIMS 2022 (I).














 Neuromyélite optique.







 Correlação das alterações do volume segmentar cerebral com parâmetros clínicos: um estudo longitudinal em pacientes com esclerose múltipla.


 Dolgosrochnye dannye po effektivnosti i bezopasnosti preparata sampeginterferon-β1a u patsientov s remittiruyushchim rasseyannym sklerozom: rezul'taty 104-nedel'nogo randomizirovannogo dvoinogo slepogo klinicheskogo issledovaniya.












 Adhesión real al dimetilfumarato en pacientes con esclerosis múltiple remitente-recurrente.



































































































































 Fármacos modificadores de la enfermedad en la esclerosis múltiple durante la lactancia: revisión de la evidencia actual.
































 Sravnenie profilei metilirovaniya DNK mononuklearnykh kletok krovi bol'nykh rasseyannym sklerozom v stadiyakh remissii i obostreniya.









 Polimorfizm RS6265 gena BDNF v populyatsii bol'nykh rasseyannym sklerozom Tomskoi oblasti.

































 O paradoxo clínico radiológico na esclerose múltipla: mito ou verdade?



 Bien communiquer sur la poussée et ses traitements.









 XV Reunión Post-ECTRIMS: revisión de las novedades presentadas en el Congreso ECTRIMS 2022 (II).
 Sclérose en plaques, travail et maintien en emploi.


 « Je survis bien ».





























 Pour un meilleur accompagnement des patients atteints de sclérose en plaques.
















































































































 Vliyanie fluoksetina na neiroimmunnoe vzaimodeistvie pri rasseyannom skleroze.




 Nasledstvennaya opticheskaya neiropatiya v sochetanii s demieliniziruyushchimi zabolevaniyami tsentral'noi nervnoi sistemy.












 Multiple Sklerose: Neue Impfempfehlungen.








 Plasmaférese em doenças inflamatórias desmielinizantes do sistema nervoso central: uso coerente na prática clínica.



















 Strukturierte Befundung bei Multipler Sklerose – Konsensbasierte Befundvorlagen für die magnetresonanztomografische Untersuchung des Gehirns und des Rückenmarks.














































 Multipl Skleroz tanılı bir hastada ocrelizumab kullanımını takip eden organize pnömoni : Vaka sunumu.



































































 La asistencia telefónica de las enfermedades neurológicas: una revisión sistemática.










































































































































































 Otnoshenie patsientov s rasseyannym sklerozom k vaktsinatsii protiv COVID-19.











 Psychometrische Prüfung des deutschsprachigen „Neurologischen Fragebogens zur Müdigkeit bei Multipler Sklerose (NFI-MS-G)“ bei Rehabilitanden mit Multipler Sklerose.







































































 Planificación familiar en hombres y mujeres con esclerosis múltiple. Análisis del Registro Andaluz (2018-2022).

 Differentsial'naya diagnostika vospalitel'nogo sindroma vosstanovleniya immuniteta i progressiruyushchei mul'tifokal'noi entsefalopatii pri otmene natalizumaba.





























































































































































 Respuesta serológica a vacunas contra SARS-CoV-2 en pacientes con esclerosis múltiple en Argentina.














 Mimetismo molecular entre o vírus Zika e os distúrbios inflamatórios desmielinizantes do sistema nervoso central: o papel do epítopo NS5 do vírus Zika e dos autoantígenos PLP.





























































































































































 Ocrelizumab induzierte Kolitis und Cytomegalie-Virusinfektion und ihre nachteilige Wechselwirkung mit der zugrunde liegenden Multiplen Sklerose.









































































































 Tratamientos modificadores de la enfermedad en pacientes con esclerosis múltiple en España.




























 Une ligne d’écoute et de soutien psychologique pour les personnes atteintes de SEP.













































































































































































































































































 Über ein Jahr B-Zell-gerichtete Therapie mit Ofatumumab s.c.: erste Ergebnisse einer prospektiven, patientenzentrierten Real-world-Beobachtungsstudie.























































































































































 Presentación clínica de primer evento desmielinizante en pediatría.



























































































 Fascitis eosinofílica refractaria en un paciente con esclerosis múltiple en tratamiento con natalizumab: respuesta al ocrelizumab.











































































 Neurológiai komorbiditások és új mutációk törökországi 1-es típusú neurofibromatosisos esetekben.








































 Ocrelizumab-assoziierte schwere Neutropenie: eine unterschätzte Komplikation der Therapie mit CD20-Antikörpern bei Multipler Sklerose?



































































































































 Zervikale Myelitis: praktische differentialdiagnostische Aspekte im MRT.









 Ultrahochfeld-MRT: wo es wirklich einen Unterschied macht.






























 Melanose der Harnblase – eine Rarität.
















































































 Soutien et accompagnement social des patients en situation de handicap.





















































































































































 Pharmacothérapie - Nouveaux médicaments et vaccins disponibles en 2022.
















































 Konsensusempfehlungen zur regionalen fächerübergreifenden Standardisierung der MRT-Diagnostik bei Multipler Sklerose im Großraum Essen.






































 Rôle de l’infirmière spécialisée SEP dans le parcours de soins du patient.
































 Neurologie : ce qui a changé en 2022.

































































































































































































































































 Klinicheskie fenotipy porazheniya zritel'nogo nerva u patsientov s zabolevaniyami spektra opticheskogo neiromielita.







































































 Berufliche Teilhabe nach einer medizinischen Rehabilitation aufgrund neurologischer Erkrankungen.






























































































































































 Mielopatía por déficit de cobre: serie de casos y revisión de la literatura.

















 Fejfájásregiszter kialakításával szerzett szegedi tapasztalataink migrénes betegek vonatkozásában.















































 Conoscere i percorsi diagnostico-terapeutici assistenziali (Pdta) regionali approvati in Italia per affrontare il cambiamento della assistenza di prossimità: analisi quali-quantitativa del database Pdta Net.











































































































































































































 Kurzfassung der S2k-Leitlinie medikamentöse Therapie der neurogenen Dysfunktion des unteren Harntraktes (NLUTD).




























































































































































































































































































 Definições, fenomenologia, diagnóstico e manejo das desordens do riso e do choro em esclerose lateral amiotrófica (ELA): Consenso do Departamento Científico de ELA e Doença do Neurônio Motor da Academia Brasileira de Neurologia.







































 系统性硬化症合并肺间质病变患者外周血单个核细胞全基因组DNA甲基化和转录组表达谱.








































































 Espectro da neuromielite óptica: uma revisão com ênfase em crianças e adolescentes.


































































































































































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 220
 127
 51
 15
 20
 70
 57
 30
 71
 77
 59
 18
 89
 24
 27
 24
 270
 70
 270
 33
 24
 23
 23
 189
 30
 23
 70
 71
 29
 100
 6
 146
 77
 266
 33
 14
 38
 88
 36
 107
 188
 23
 74
 29
 13
 10
 40
 21
 13
 71
 71
 24
 70
 299
 44
 44
 254
 103
 75
 80
 75
 17
 29
 47
 23
 8
 94
 15
 46
 24
 133
 146
 37
 24
 68
 18
 13
 14
 14
 84
 234
 50
 28
 299
 24
 49
 62
 123
 43
 246
 48
 23
 123
 184
 270
 24
 10
 71
 76
 93
 118
 71
 29
 57
 24
 165
 178
 29
 29
 169
 43
 24
 60
 49
 81
 29
 45
 29
 75
 29
 44
 29
 37
 638
 33
 26
 146
 55
 24
 250
 32
 18
 253
 43
 195
 29
 392
 74
 53
 19
 91
 146
 9
 94
 210
 49
 22
 72
 94
 123
 270
 55
 133
 24
 19
 32
 307
 29
 71
 33
 62
 1869
 45
 14
 74
 10
 80
 29
 43
 93
 36
 18
 26
 15
 22
 72
 70
 13
 14
 220
 28
 71
 25
 14
 94
 10
 11
 37
 165
 15
 55
 23
 31
 45
 70
 13
 353
 39
 37
 2700
 20
 34
 12
 33
 101
 29
 30
 28
 188
 29
 87
 20
 70
 12
 29
 270
 100
 37
 20
 37
 94
 45
 94
 80
 45
 13
 93
 642
 35
 20
 39
 149
 14
 71
 101
 101
 24
 14
 11
 451
 29
 82
 24
 14
 12
 220
 29
 237
 29
 77
 69
 450
 119
 77
 23
 129
 15
 10
 280
 24
 77
 113
 94
 33
 29
 28
 24
 14
 70
 292
 61
 47
 121
 28
 70
 29
 77
 4
 14
 35
 60
 59
 12
 70
 20
 29
 45
 14
 29
 30
 458
 270
 70
 89
 14
 39
 368
 71
 548
 79
 195
 29
 45
 53
 29
 381
 211
 20
 22
 10
 69
 68
 23
 14
 30
 270
 29
 376
 10
 14
 270
 30
 14
 24
 93
 11
 16
 123
 24
 29
 18
 146
 120
 179
 104
 26
 59
 71
 176
 29
 60
 14
 80
 21
 77
 13
 69
 130
 24
 10
 74
 72
 12
 792
 101
 77
 168
 46
 10
 71
 24
 45
 13
 33
 29
 10
 102
 42
 60
 13
 45
 14
 10
 25
 146
 24
 444
 137
 29
 941
 42
 13
 45
 10
 653
 46
 44
 69
 27
 146
 103
 15
 94
 20
 13
 11
 49
 270
 1804
 10
 183
 29
 14
 229
 70
 270
 73
 20
 50
 66
 228
 192
 30
 120
 59
 24
 9
 71
 71
 32
 123
 104
 18
 102
 68
 47
 75
 135
 71
 14
 26
 71
 62
 68
 146
 77
 27
 11
 14
 18
 146
 70
 10
 220
 10
 386
 614
 13
 57
 102
 14
 53
 29
 36
 102
 47
 71
 10
 24
 307
 29
 18
 179
 70
 211
 10
 209
 100
 101
 24
 18
 74
 143
 37
 641
 14
 5
 29

 14
 38
 76
 10
 15
 69
 29
 47
 94
 103
 14
 9
 20
 359
 15
 18
 44
 71
 32
 384
 13
 20
 12
 13
 70
 76
 63
 123
 20
 24
 29
 30
 24
 72
 30
 80
 12
 45
 17
 174
 13
 66
 104
 162
 22
 71
 396
 40
 120
 44
 15
 270
 36
 100
 27
 30
 159
 29
 22
 20
 75
 69
 29
 72
 70
 18
 20
 44
 23
 28
 53
 166
 43
 30
 14
 33
 10
 24
 37
 22
 270
 43
 9
 44
 12
 13
 13
 145
 15
 60
 29
 10
 46
 176
 24
 24
 75
 164
 77
 22
 14
 43
 56
 43
 22
 30
 60
 43
 32
 14
 22
 24
 15
 29
 54
 71
 117
 50
 28
 237
 18
 139
 18
 11
 238
 70
 77
 23
 111
 73
 112
 14
 7
 10
 20
 13
 71
 12
 14
 10
 48
 24
 10
 93
 24
 16
 363
 75
 120
 60
 30
 70
 14
 210
 19
 13
 42
 100
 30
 76
 50
 97
 95
 18
 30
 954
 358
 10
 212
 211
 69
 10
 59
 120
 21
 20
 20
 13
 44
 146
 6
 100
 24
 168
 379
 83
 13
 108
 70
 30
 270
 134
 70
 28
 30
 10
 44
 14
 41
 18
 81
 37
 10
 109
 139
 37
 72
 12
 72
 71
 14
 114
 10
 118
 230
 70
 260
 80
 197
 10
 24
 69
 11
 44
 10
 24
 210
 143
 9
 13
 77
 45
 101
 14
 514
 73
 211
 10
 15
 29
 74
 10
 45
 35
 28
 15
 80
 69
 93
 32
 14
 20
 194
 60
 12
 10
 15
 5
 14
 11
 5
 9


 18
 5
 11

 18

 18
 10
 5
 5
 11
 10
 17


 19
 9
 31

 18
 14
 16
 5

 72
 4

 14
 14
 5
 14
 12
 5
 13
 9

 12
 78
 9
 11
 17
 11
 5
 13
 14

 78
 15

 14
 6


 13

 14
 15
 12
 14
 13
 5
 13
 16

 14


 14


 11
 14
 14
 17
 14


 18

 24

 21

 18

 25
 9

 14
 4

 25
 14
 381



 15
 14
 17

 13


 10
 85
 17
 14

 42
 9
 12

 13
 48

 67
 9
 79
 746
 11
 15

 15
 12
 14
 79

 3
 5
 6
 5


 5
 17
 15
 14
 22
 5
 9
 9
 24
 14
 79
 29

 12

 85
 60
 79
 29

 10
 32

 17
 12
 25
 14
 14
 10

 12
 14
 17


 11
 13
 14
 208
 12
 14

 7




 14
 7

 17
 13
 16
 2612
 17
 35
 16


 16
 5

 4
 14
 14
 11
 47
 17
 7


 47

 79
 9
 78
 12
 42
 16
 12


 5
 10



 5
 381

 16
 16
 13
 10
 25
 68
 27
 17
 13
 25
 12
 13
 25
 25

 29
 52
 9
 116


 38
 3

 14
 11
 10


 85
 25

 12
 5
 91
 160
 132




 5
 39
 14
 9

 14
 13
 14
 17


 16
 78

 12
 12


 22
 232

 13



 32

 13
 11
 3
 41
 19
 10
 12
 16

 5
 25
 14

 14

 15
 11

 14
 25

 79
 12

 14
 14
 453
 29
 12
 15



 39

 14
 14
 18
 135
 79



 13
 4
 7
 9
 12

 15
 25
 10
 12

 14
 17
 10
 78
 25
 85
 12
 17
 15
 13
 13
 12
 14
 44
 10
 29
 14
 15

 32

 10


 29
 14
 79
 79

 78

 17
 14
 15
 57
 25
 15
 11
 25
 13
 12
 78
 14


 25
 14
 15
 14
 9
 12
 45
 13

 17
 15
 15
 12
 79
 79
 79
 10
 24
 100

 198

 17
 25

 12
 12
 9
 11
 14
 19
 20
 9
 29
 25
 79
 14
 10
 14

 52

 382
 46
 17
 17
 81
 381
 5
 14
 12
 232
 14
 10



 16
 12
 14



 65

 11
 13
 25
 9
 13
 16
 103
 9
 69


 14

 47

 12
 60

 14
 25
 13
 12
 14
 14
 12
 16

 16
 39
 17
 25
 11
 8


 232
 14

 13
 14
 25

 14

 12
 15
 232
 12
 14
 9

 15
 13
 78
 15
 16
 9
 18
 76

 17

 12
 16
 14
 27
 14

 382
 9


 14

 11
 11
 8
 29

 18


 13

 19


 26
 44
 13

 43
 16
 10
 12

 3
 10

 23

 45
 450

 18
 16
 6

 78

 32

 11
 12


 29

 78
 11
 11
 78
 10
 9
 17
 22
 17
 14
 5
 17
 25
 12
 233
 38
 2700
 255

 133


 36

 26
 25
 12
 17
 29
 7
 23
 13
 47



 15
 13
 13
 14

 2
 17
 9
 36

 12
 18

 14

 29
 29

 100
 14
 11
 24
 13

 14
 13

 19

 76
 18
 78

 9

 59

 17
 14

 31
 80
 17
 14


 14

 14
 52
 29
 79


 382

 9
 12
 10
 25
 71
 25

 79



 3
 10
 14

 79
 12

 16
 9

 16

 12


 79



 14
 79

 79
 78
 78


 13
 25
 13
 14
 37
 17
 11


 10

 16
 14
 12
 94
 14
 16
 28
 37
 44
 14

 17
 64


 78
 14
 33
 13
 14

 16
 381
 14
 1869

 12
 13



 31
 14
 191
 9

 14
 23
 18







 12

 43
 14
 60
 94
 12
 124

 9
 19


 13
 10

 13
 15
 17
 9
 37
 12
 6
 78
 15

 13
 12
 11
 11
 9
 12
 12


 11

 78
 13
 12
 14


 12
 12
 79
 79
 9

 22

 59

 14
 17
 12
 202
 11
 76
 381
 42

 17

 22
 9

 78

 299
 15
 104
 71
 26
 15

 20

 24
 12
 104
 20



 12
 11
 37
 94
 PP
 1411

 23


 14
 44
 17
 78

 20
 78
 44
 47

 44
 24

 15
 16


 26
 78



 30
 12
 382
 14
 13
 78
 14
 20
 9
 73
 44
 12
 15



 53

 78
 12
 13
 11
 17
 13
 14

 12
 79
 17

 15



 14

 18
 14
 39
 16
 7
 79
 80
 9
 9




 55
 162
 4
 24
 42
 9
 46
 29



 9

 17
 10
 48
 15
 15
 11
 9
 23
 11
 25
 94
 16
 79
 14


 55
 31
 12


 13

 10
 14
 79

 79

 25
 15
 76
 79


 12
 13
 17



 23
 31

 241
 98
 306


 13

 114


 71
 159
 11
 18

 17
 48


 11
 25
 102

 14


 11
 120
 136
 167
 12
 30
 70
 12
 11
 17
 5
 12




 9
 137
 78
 14
 15
 18
 54

 377
 383

 45
 17
 9


 13
 521

 PP




 173


 29
 25
 24
 78
 2023
 13
 76



 12
 26
 16
 16

 25
 2
 13
 12
 12
 16

 96
 14

 9
 120
 446
 25
 14

 12
 11
 71
 38
 104
 71
 14
 11
 14
 77

 101


 7
 75

 3
 14
 9
 5
 9
 77
 11
 21
 44
 94
 18

 270
 68
 16
 56
 28
 80


 13
 13
 2023
 78

 14
 29

 78




 7
 121
 29

 145
 18
 89
 9
 42
 20



 11
 331
 12
 98
 60
 78
 5
 17
 27
 5





 14
 70


 19
 179
 13

 11
 28
 16
 12
 12
 24
 101

 78
 15
 45


 29


 29 Suppl 1
 17


 56
 125
 9


 17
 43
 12
 18

 23
 11
 14
 24
 17
 193
 43

 161
 30
 32
 12


 26




 46
 75


 33
 16
 13


 23
 24
 39
 20
 450
 116
 232
 94
 24

 11
 12
 76
 121
 196
 14
 48

 12
 71
 12

 44
 232


 78
 17

 13

 15
 60
 107
 15
 104
 19
 10
 3
 15


 1519
 52
 10


 24
 23
 15
 18

 42

 90
 15
 12

 119
 14
 17
 78
 33
 1870
 11
 24
 20


 330
 228
 142

 PP


 11
 113
 2


 13

 67
 39

 97
 66
 14
 29
 13

 17
 12
 8

 65

 15
 15
 163
 26


 14
 70
 20


 100
 120

 107
 13

 21
 116
 12
 13
 9
 12
 19

 23
 68
 73
 95
 43

 107
 529

 232
 32


 38
 13
 132
 157

 29
 61
 113
 16
 259
 16


 11
 11
 26
 28
 270

 124
 270
 19
 17
 100
 2571
 23

 30


 109
 78
 23

 14
 29
 949
 38
 25
 266
 11
 14
 45
 247
 18
 2023


 24
 230
 101
 14
 14
 196
 33
 17

 255
 17
 44
 120
 15
 14


 11
 77
 10


 248
 26
 48
 62
 233

 15
 597

 14

 58
 37
 115
 270
 165
 24

 244
 71
 101
 70
 39

 42
 20
 11


 18
 107
 196
 8

 14
 6




 14
 270
 12


 23
 14
 2023
 39

 54
 2696
 39
 5
 14

 15
 4
 383
 11
 12
 74
 19
 14
 2023

 35
 79
 37
 79
 24
 146
 93
 18
 24
 22

 49
 315
 17
 43
 94

 18
 166
 9
 15
 37
 46
 22
 27
 24
 140
 62

 26


 12
 22
 107



 53
 25
 12
 356
 9
 242
 51
 10
 15
 13
 17

 5
 14
 17
 24
 70
 24
 16
 18
 79
 24
 101
 24
 70
 210
 87
 11
 29

 48
 34
 16

 5
 37
 4

 2023
 14
 215
 17
 14
 37
 4
 248
 8
 34
 23
 17
 43

 23
 27
 78
 14
 23
 120
 17
 17
 10
 116


 41
 51
 19
 24
 38

 38
 42
 79
 114

 33

 30
 58
 30
 24
 22
 228

 18
 15
 16
 71
 33
 11
 14
 24
 190

 270
 20
 102
 111
 123

 15
 233
 390
 10

 139
 23
 3
 14
 24
 24
 24
 14
 21
 62
 28
 11


 15
 14

 1412

 11
 14
 13
 12
 42
 23
 251

 29




 86
 75
 53
 36
 86
 45

 453

 16
 3

 12

 7
 66
 13
 14
 8
 14
 11
 17
 224
 14
 47
 61
 22

 24
 20
 102
 38
 14

 24
 21
 109
 14
 10
 43
 62

 13
 314
 71
 79
 14
 50
 38
 94
 7
 29
 2023
 37
 75
 139
 24

 76

 13
 24
 117
 15

 13
 24
 99 Suppl 1
 46

 90
 13

 19



 163
 17
 25
 118

 71
 220
 396
 601
 36
 23
 41
 42

 104
 124
 13

 47


 59

 12
 12
 66
 29
 1807
 15
 231
 194
 44
 48
 41
 164




 28

 51
 30
 101
 28
 16
 29
 31
 37
 146

 851
 270
 24
 18

 28
 11
 24
 381
 14
 16
 13
 12
 43

 13
 24
 10
 14
 12

 15
 244
 22
 8
 29
 313
 169
 5
 12
 11
 15
 108
 15
 17
 14
 17
 14
 13
 231
 14
 319
 26
 25
 19
 22
 41
 14
 17
 11
 44
 165
 10
 17
 129
 33
 118
 28
 14
 109
 137
 22
 45
 2023
 29
 37

 298-299
 261
 122
 20
 43
 29
 15
 35
 71
 73
 14
 48
 42
 223
 18
 34
 39

 1425



 76

 55
 108
 61
 68
 13
 15
 78
 17
 59
 44
 39

 25
 13
 102
 21
 13
 3
 112
 17
 30

 16
 12
 107
 73
 18
 87
 14
 221
 30
 15
 120
 30
 51
 165
 238
 13
 270
 32
 30
 59
 52
 16
 15
 225
 114
 30

 14
 259
 166
 11
 163
 13
 16
 13
 14
 22
 13
 30
 14
 20
 23
 15
 7
 24

 46


 248
 253
 32
 23
 20
 18
 25
 245
 59
 24
 60
 64
 174
 44
 214
 24
 101

 14
 102
 86
 383

 10
 3
 100

 39
 14
 71
 119
 30
 18
 13
 54
 14
 239
 14

 15

 1815
 10
 59
 269
 161
 70
 22
 102
 146
 2023

 16
 85
 2023
 142
 7
 24
 27
 65
 11
 24

 15
 73

 35
 37
 225
 19
 15
 23
 20
 9
 86
 12
 79
 244
 63
 77
 42
 28
 228
 194
 221
 75
 21
 23
 26
 514
 15

 379
 5
 150
 12
 24

 3
 22
 20
 79

 11
 16
 15
 24
 31
 27
 71
 122
 30
 100
 26

 224
 78
 9
 24
 20
 46
 37

 17

 60
 37
 30
 20
 11
 12
 25
 24
 37
 315
 293
 22


 20
 162
 12
 21
 254
 23
 108
 230
 32
 43
 57
 100

 34
 39
 61

 36
 13
 21
 80
 160
 10

 82
 85
 111
 7

 64
 101
 115
 33
 11
 12

 83
 35
 24
 69
 62
 14
 21

 28
 13


 101
 32
 24

 1865
 57
 65

 70
 195
 17
 48
 110
 32
 18
 48
 5
 135
 14
 38
 5
 13
 15
 14
 30
 165
 120
 161

 40
 14
 636
 25
 55
 9
 55
 15
 386
 13

 12
 68
 21
 13
 14
 85
 29
 14

 14
 5
 110
 13
 13

 23
 110
 8
 35
 25
 24

 71
 49
 36

 79
 92
 16
 28
 58
 5
 226
 148
 21

 24
 75
 189
 14
 12
 70
 180
 57
 74
 69
 36
 97
 14
 24
 11
 401
 38
 85
 11
 94
 49

 49
 43
 19
 60
 14

 22
 7
 5
 45

 13
 2
 382
 15
 13
 33

 283-284
 15

 15

 146

 109
 67
 96
 24
 12
 14
 33
 453
 16
 14

 64
 146
 15
 12
 26
 14
 20
 64
 23
 15
 46
 13
 37
 30
 94
 15
 37
 22
 24
 29
 8
 34
 120
 14
 228

 101
 24

 11
 38
 100

 6
 49


 8
 63
 15
 85
 16
 10
 9
 10
 17
 13
 11
 10
 19
 44
 169

 32
 15

 29
 194
 10
 483
 270

 17
 68
 14
 49
 64


 57
 64
 104
 24
 38
 22

 184

 146
 252
 24
 10
 12
 14

 70 Suppl 1
 12
 41
 16
 122
 12
 2023
 134
 55
 16
 36
 101
 22
 16
 96
 12
 9
 13
 17
 4

 24
 279
 76
 43
 11
 19
 75
 24
 13
 15
 7
 14
 280
 22

 24
 32
 12
 43
 14

 24

 133


 216
 26
 22
 43
 13
 3

 5
 142
 9
 19
 81
 44
 186
 85
 19
 10
 18
 14
 14


 15
 83
 60
 15
 57
 178
 179
 401


 18
 42

 3
 293
 212
 5
 179
 47
 14

 18
 16
 165
 10
 12
 66
 93
 30
 48
 80

 17
 15
 12
 10
 14
 14
 33
 13

 120
 63
 20
 10
 613
 379
 2023
 11
 165
 33
 167

 43
 36
 94

 44
 19
 149
 12
 14
 28

 71
 10
 270
 120
 63
 23
 14
 103
 193

 12
 8 Suppl 1
 49
 11
 296
 24
 19
 15
 24

 328
 193
 12
 13

 16
 14

 37

 11
 13
 159
 78
 83
 14
 6
 33
 81

 40
 17
 143
 68
 33
 62

 37
 37

 12
 188
 38
 14
 80
 36
 13
 17
 28
 11

 30
 14
 30
 130
 12
 28
 146
 93

 173
 103
 191
 94
 270
 325
 146
 195
 65

 15

 48

 4

 50
 16


 270
 38
 44
 260
 108
 64
 30
 44
 92
 30
 31 Suppl 1
 30
 135
 14

 17


 5
 37
 55
 13
 5
 15
 53
 24
 13
 93

 13
 270
 38
 16
 5
 64
 32
 359
 93
 39
 21
 69
 11
 29
 270
 24
 270
 20
 42
 7
 19
 302
 119
 94
 64
 94

 16
 37
 14
 43
 14
 13

 11
 271
 42
 50
 9
 13
 89
 13
 24
 129
 138
 150
 100
 12
 270
 5
 29
 80
 10
 92
 62
 10
 94
 83
 270
 335
 93
 5

 9
 22
 24
 9
 3
 177
 24
 12
 101
 30

 13
 80
 19
 146
 4
 19

 22